Testimonial

True and honest statement of strange and interesting recovery experienced by some of our patients who were suffering from chronic and difficult diseases that did not respond to treatment given earlier by different medical experts.

We accept and treat such patients with chronic and difficult diseases who are hopeless and helpless even after trying many other different medical experts. Speciality homeopathic care integrated, sometimes, with other accepted medical therapies remains the mainstay of our treatment.

The therapeutic results at our centre are peculiar in that they are safe and fast with high success rate. The following statements given by the patients stand the testimony. Only a few important cases have been displayed here to save the precious time of viewers.


  DISEASES OF NERVOUS SYSTEM (BRAIN, SPINAL CORD AND NERVES)

PARALYSIS (Stroke, Hemiplegia) - susheela, Mehdipatnam, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Diabetes, High BP,Left sided Paralysis. Was treated by Neurophysicians of a Corporate Hospital, Mehdipatnam. She had difficult speech ,and could walk only a few steps with much difficulty with walker even after 5 days of their treatment in Acute medical care

MODE OF RECOVERY AT NEW LIFE CENTRE

Maximum recovery of power in left sided limbs in the first week only. Speech regained .She was able to carry on all her activities in the first month only. Fully cured in just 45 days.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Hemiplegia is paralysis of the arm, leg, and trunk on the same side of the body. Hemiplegia is more severe than hemiparesis, where in one half of the body has less marked weakness. Hemiplegia and hemiparesis may be congenital, or they might be acquired conditions resulting from an illness, an injury, or a stroke.

SIGNS AND SYMPTOMS

Hemiplegia means severe weakness of the limbs on one side of the body but the specific features can vary tremendously from person to person. Problems may include :

  • Difficulty with gait.
  • Difficulty with balance while standing or walking.
  • Increasing stiffness of muscles.
  • Muscle spasms.
  • The majority of children who develop hemiplegia also have abnormal mental development.
  • Behavior problems like anxiety, anger, irritability, lack of concentration or comprehension.
  • Emotions — depression.
  • Shoulder pain — Often associated with a loss of external rotation of the glenohumeral joint, commonly due to the increased tone of the Subscapularis muscle and Pectoralis major muscle.
  • Shoulder Subluxation.

CAUSES

The most common cause of hemiplegia is stroke. Strokes can cause a variety of movement disorders, depending on the location and severity of the lesion. Hemiplegia is common when the stroke affects the corticospinal tract. Other causes of hemiplegia include spinal cord injury, specifically Brown-Séquard syndrome, traumatic brain injury, or disease affecting the brain. As a lesion that results in hemiplegia occurs in the brain or spinal cord, hemiplegic muscles display features of the Upper Motor Neuron Syndrome. Features other than weakness include decreased movement control, clonus (a series of involuntary rapid muscle contractions), spasticity, exaggerated deep tendon reflexes and decreased endurance.

The incidence of hemiplegia is much higher in premature babies than term babies. There is also a high incidence of hemiplegia during pregnancy and experts believe that this may be related to either a traumatic delivery, use of forceps or some event which causes brain injury.

Other causes of hemiplegia in adults include trauma, bleeding, brain infections and cancers. Individuals who have uncontrolled diabetes, hypertension or those who smoke have a higher chance of developing a stroke. Weakness on one side of the face may occur and may be due to a viral infection, stroke or a cancer.

COMMON CAUSES BY ETIOLOGY

  • VASCULAR: cerebral hemorrhage, stroke, diabetic neuropathy
  • INFECTIVE: encephalitis, meningitis, brain abscess
  • NEOPLASTIC: glioma-meningioma
  • DEMYELINATION: disseminated sclerosis, lesions to the internal capsule
  • TRAUMATIC: cerebral lacerations, subdural hematoma rare cause of hemiplegia is due to local anaesthetic injections given intra-arterially rapidly, instead of given in a nerve branch.
  • CONGENITAL: cerebral palsy
  • DISSEMINATED: multiple sclerosis
  • PSYCHOLOGICAL: parasomnia (nocturnal hemiplegia)

PATHOGENESIS

The exact cause of hemiplegia is not known in all cases, but it appears that the brain is deprived of oxygen and this results in the death of neurons. When the corticospinal tract is damaged, the injury is usually manifested on the opposite side of the body. For example if one has an injury to the right side of the brain, the hemiplegia will be on the left side of the body. This happens because the motor fibres of corticospinal tract ( also called pyramidal fibres), which take origin from the motor cortex in brain, cross to the opposite side in the lower part of medulla oblangata and then descend down in spinal cord to supply their respective muscles. Depending on the site of lesion in brain, the severity of hemiplegia varies. A lesion in internal capsule where all the motor fibres are condensed in a small area, will cause dense hemiplegia i.e. complete loss of power of all muscles of one half of body while a lesion at cortical or subcortical level will cause varied amount of weakness of one half of the body.

DIAGNOSIS

Hemiplegia is identified by clinical examination by a health professional, such as a physiotherapist or doctor. Radiological studies like a CT scan or magnetic resonance imaging of the brain should be used to confirm injury in the brain and spinal cord, but alone cannot be used to identify movement disorders. Individuals who develop seizures may undergo tests to determine where the focus of excess electrical activity is.

Hemiplegia patients usually show a characteristic gait. The leg on the affected side is extended and internally rotated and is swung in a wide, lateral arc rather than lifted in order to move it forward. The upper limb on the same side is also adducted at the shoulder, flexed at the elbow, and pronated at the wrist with the thumb tucked into the palm and the fingers curled around it.

TREATMENT

Treatment should be based on assessment by the relevant health professionals, including physiotherapists, doctors and occupational therapists. Muscles with severe motor impairment including weakness need these therapists to assist them with specific exercise, and are likely to require help to do this.

Pharmacological

Drugs can be used to treat issues related to the Upper Motor Neuron Syndrome. Drugs like Librium or Valium could be used as a relaxant. Drugs are also given to individuals who have recurrent seizures, which may be a separate but related problem after brain injury.

Surgery

Surgery may be used if the individual develops a secondary issue of contracture, from a severe imbalance of muscle activity. In such cases the surgeon may cut the ligaments and relieve joint contractures. Individuals who are unable to swallow may have a tube inserted into the stomach. This allows food to be given directly into the stomach. The food is in liquid form and instilled at low rates. Some individuals with hemiplegia will benefit from some type of prosthetic device. There are many types of braces and splints available to stabilize a joint, assist with walking and keep the upper body erect.

Rehabilitation

Rehabilitation is the main treatment of individuals with hemiplegia. In all cases, the major aim of rehabilitation is to regain maximum function and quality of life. Both physical and occupational therapy can significantly improve the quality of life.

Physical Therapy

Physical therapy (PT) can help improve muscle strength & coordination, mobility (such as standing and walking), and other physical function using different sensorimotor techniques. Physiotherapists can also help reduce shoulder pain by maintaining shoulder range of motion, as well as using Functional electrical stimulation.[11] Supportive devices, such as braces or slings, can be used to help prevent or treat shoulder subluxation in the hopes to minimize disability and pain. It should be noted that although many individuals suffering from stroke experience both shoulder pain and shoulder subluxation, the two are mutually exclusive. A treatment method that can be implemented with the goal of helping to regain motor function in the affected limb is constraint-induced movement therapy. This consists of constraining the unaffected limb, forcing the affected limb to accomplish tasks of daily living.

Occupational Therapy

Occupational therapy Occupational Therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening hand, shoulder and torso, and participating in activities of daily living (ADLs), such as eating and dressing. Therapists may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your child’s hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual - which may include, environmental modification, use of adaptive equipment, sensory integration, etc.

Constraint-Induced Movement Therapy

Constraint-induced movement therapy (CI or CIMT) is a form of rehabilitation therapy that improves upper extremity function, especially in cases of hemiplegia.

ASSESSMENT TOOLS

There are a variety of standardized assessment scales available to physiotherapists and other health care professionals for use in the ongoing evaluation of the status of a patient’s hemiplegia. The use of standardized assessment scales may help physiotherapists and other health care professionals during the course of their treatment plant to:

  • Prioritize treatment interventions based on specific identifiable motor and sensory deficits.
  • Create appropriate short and long term goals for treatment based on the outcome of the scales, their professional expertise and the desires of the patient.
  • Evaluate the potential burden of care and monitor any changes based on either improving or declining scores.

Some of the most commonly used scales in the assessment of hemiplegia are:

The Fugl-Meyer Assessment of Physical Performance (FMA)

The FMA is often used as a measure of functional or physical impairment following a cerebrovascular accident(CVA). It measures sensory and motor impairment of the upper and lower extremities, balance in several positions, range of motion, and pain. This test is a reliable and valid measure in measuring post-stroke impairments related to stroke recovery. A lower score in each component of the test indicates higher impairment and a lower functional level for that area. The maximum score for each component is 66 for the upper extremities, 34 for the lower extremities, and 14 for balance. Administration of the FMA should be done after reviewing a training manual.

The Chedoke-McMaster Stroke Assessment (CMSA)

This test is a reliable measure of two separate components evaluating both motor impairment and disability. The disability component assesses any changes in physical function including gross motor function and walking ability. The disability inventory can have a maximum score of 100 with 70 from the gross motor index and 30 from the walking index. Each task in this inventory has a maximum score of seven except for the 2 minute walk test which is out of two. The impairment component of the test evaluates the upper and lower extremities, postural control and pain. The impairment inventory focuses on the seven stages of recovery from stroke from flaccid paralysis to normal motor functioning. A training workshop is recommended if the measure is being utilized for the purpose of data collection.

The Stroke Rehabilitation Assessment of Movement (STREAM)

The STREAM consists of 30 test items involving upper-limb movements, lower-limb movements, and basic mobility items. It is a clinical measure of voluntary movements and general mobility (rolling, bridging, sit-to-stand, standing, stepping, walking and stairs) following a stroke. The voluntary movement part of the assessment is measured using a 3-point ordinal scale (unable to perform, partial performance, and complete performance) and the mobility part of the assessment uses a 4-point ordinal scale (unable, partial, complete with aid, complete no aid). The maximum score one can receive on the STREAM is a 70 (20 for each limb score and 30 for mobility score). The higher the score, the better movement and mobility is available for the individual being scored.

PROGNOSIS

Hemiplegia is not a progressive disorder, except in progressive conditions like a growing brain tumour. Once the injury has occurred, the symptoms should not worsen. However, because of lack of mobility, other complications can occur. Complications may include muscle and joint stiffness, loss of aerobic fitness, muscle spasms, bed sores, pressure ulcers and blood clots.

Sudden recovery from hemiplegia is very rare. Many of the individuals will have limited recovery, but the majority will improve from intensive, specialised rehabilitation. Potential to progress may differ in cerebral palsy, compared to adult acquired brain injury. It is vital to integrate the hemiplegic child into society and encourage them in their daily living activities. With time, some individuals may make remarkable progress.

IMAGES

CASE RECORD

PARALYSIS (Stroke, Hemiplegia) - Anjamma, Bhavanipeta, Kamareddy

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Diabetes, High BP, Left sided Paralysis. Was treated by specialists of Kamareddy but without any improvement even after 25 days.

MODE OF RECOVERY AT NEW LIFE CENTRE

Started improving in just three days and the cure was complete in first month

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Hemiplegia is paralysis of the arm, leg, and trunk on the same side of the body. Hemiplegia is more severe than hemiparesis, where in one half of the body has less marked weakness. Hemiplegia and hemiparesis may be congenital, or they might be acquired conditions resulting from an illness, an injury, or a stroke.

SIGNS AND SYMPTOMS

Hemiplegia means severe weakness of the limbs on one side of the body but the specific features can vary tremendously from person to person. Problems may include :

  • Difficulty with gait.
  • Difficulty with balance while standing or walking.
  • Increasing stiffness of muscles.
  • Muscle spasms.
  • The majority of children who develop hemiplegia also have abnormal mental development.
  • Behavior problems like anxiety, anger, irritability, lack of concentration or comprehension.
  • Emotions — depression.
  • Shoulder pain — Often associated with a loss of external rotation of the glenohumeral joint, commonly due to the increased tone of the Subscapularis muscle and Pectoralis major muscle.
  • Shoulder Subluxation.

CAUSES

The most common cause of hemiplegia is stroke. Strokes can cause a variety of movement disorders, depending on the location and severity of the lesion. Hemiplegia is common when the stroke affects the corticospinal tract. Other causes of hemiplegia include spinal cord injury, specifically Brown-Séquard syndrome, traumatic brain injury, or disease affecting the brain. As a lesion that results in hemiplegia occurs in the brain or spinal cord, hemiplegic muscles display features of the Upper Motor Neuron Syndrome. Features other than weakness include decreased movement control, clonus (a series of involuntary rapid muscle contractions), spasticity, exaggerated deep tendon reflexes and decreased endurance.

The incidence of hemiplegia is much higher in premature babies than term babies. There is also a high incidence of hemiplegia during pregnancy and experts believe that this may be related to either a traumatic delivery, use of forceps or some event which causes brain injury.

Other causes of hemiplegia in adults include trauma, bleeding, brain infections and cancers. Individuals who have uncontrolled diabetes, hypertension or those who smoke have a higher chance of developing a stroke. Weakness on one side of the face may occur and may be due to a viral infection, stroke or a cancer.

COMMON CAUSES BY ETIOLOGY

  • VASCULAR: cerebral hemorrhage, stroke, diabetic neuropathy
  • INFECTIVE: encephalitis, meningitis, brain abscess
  • NEOPLASTIC: glioma-meningioma
  • DEMYELINATION: disseminated sclerosis, lesions to the internal capsule
  • TRAUMATIC: cerebral lacerations, subdural hematoma rare cause of hemiplegia is due to local anaesthetic injections given intra-arterially rapidly, instead of given in a nerve branch.
  • CONGENITAL: cerebral palsy
  • DISSEMINATED: multiple sclerosis
  • PSYCHOLOGICAL: parasomnia (nocturnal hemiplegia)

PATHOGENESIS

The exact cause of hemiplegia is not known in all cases, but it appears that the brain is deprived of oxygen and this results in the death of neurons. When the corticospinal tract is damaged, the injury is usually manifested on the opposite side of the body. For example if one has an injury to the right side of the brain, the hemiplegia will be on the left side of the body. This happens because the motor fibres of corticospinal tract ( also called pyramidal fibres), which take origin from the motor cortex in brain, cross to the opposite side in the lower part of medulla oblangata and then descend down in spinal cord to supply their respective muscles. Depending on the site of lesion in brain, the severity of hemiplegia varies. A lesion in internal capsule where all the motor fibres are condensed in a small area, will cause dense hemiplegia i.e. complete loss of power of all muscles of one half of body while a lesion at cortical or subcortical level will cause varied amount of weakness of one half of the body.

DIAGNOSIS

Hemiplegia is identified by clinical examination by a health professional, such as a physiotherapist or doctor. Radiological studies like a CT scan or magnetic resonance imaging of the brain should be used to confirm injury in the brain and spinal cord, but alone cannot be used to identify movement disorders. Individuals who develop seizures may undergo tests to determine where the focus of excess electrical activity is.

Hemiplegia patients usually show a characteristic gait. The leg on the affected side is extended and internally rotated and is swung in a wide, lateral arc rather than lifted in order to move it forward. The upper limb on the same side is also adducted at the shoulder, flexed at the elbow, and pronated at the wrist with the thumb tucked into the palm and the fingers curled around it.

TREATMENT

Treatment should be based on assessment by the relevant health professionals, including physiotherapists, doctors and occupational therapists. Muscles with severe motor impairment including weakness need these therapists to assist them with specific exercise, and are likely to require help to do this.

Pharmacological

Drugs can be used to treat issues related to the Upper Motor Neuron Syndrome. Drugs like Librium or Valium could be used as a relaxant. Drugs are also given to individuals who have recurrent seizures, which may be a separate but related problem after brain injury.

Surgery

Surgery may be used if the individual develops a secondary issue of contracture, from a severe imbalance of muscle activity. In such cases the surgeon may cut the ligaments and relieve joint contractures. Individuals who are unable to swallow may have a tube inserted into the stomach. This allows food to be given directly into the stomach. The food is in liquid form and instilled at low rates. Some individuals with hemiplegia will benefit from some type of prosthetic device. There are many types of braces and splints available to stabilize a joint, assist with walking and keep the upper body erect.

Rehabilitation

Rehabilitation is the main treatment of individuals with hemiplegia. In all cases, the major aim of rehabilitation is to regain maximum function and quality of life. Both physical and occupational therapy can significantly improve the quality of life.

Physical Therapy

Physical therapy (PT) can help improve muscle strength & coordination, mobility (such as standing and walking), and other physical function using different sensorimotor techniques. Physiotherapists can also help reduce shoulder pain by maintaining shoulder range of motion, as well as using Functional electrical stimulation.[11] Supportive devices, such as braces or slings, can be used to help prevent or treat shoulder subluxation in the hopes to minimize disability and pain. It should be noted that although many individuals suffering from stroke experience both shoulder pain and shoulder subluxation, the two are mutually exclusive. A treatment method that can be implemented with the goal of helping to regain motor function in the affected limb is constraint-induced movement therapy. This consists of constraining the unaffected limb, forcing the affected limb to accomplish tasks of daily living.

Occupational Therapy

Occupational therapy Occupational Therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening hand, shoulder and torso, and participating in activities of daily living (ADLs), such as eating and dressing. Therapists may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your child’s hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual - which may include, environmental modification, use of adaptive equipment, sensory integration, etc.

Constraint-Induced Movement Therapy

Constraint-induced movement therapy (CI or CIMT) is a form of rehabilitation therapy that improves upper extremity function, especially in cases of hemiplegia.

ASSESSMENT TOOLS

There are a variety of standardized assessment scales available to physiotherapists and other health care professionals for use in the ongoing evaluation of the status of a patient’s hemiplegia. The use of standardized assessment scales may help physiotherapists and other health care professionals during the course of their treatment plant to:

  • Prioritize treatment interventions based on specific identifiable motor and sensory deficits.
  • Create appropriate short and long term goals for treatment based on the outcome of the scales, their professional expertise and the desires of the patient.
  • Evaluate the potential burden of care and monitor any changes based on either improving or declining scores.

Some of the most commonly used scales in the assessment of hemiplegia are:

The Fugl-Meyer Assessment of Physical Performance (FMA)

The FMA is often used as a measure of functional or physical impairment following a cerebrovascular accident(CVA). It measures sensory and motor impairment of the upper and lower extremities, balance in several positions, range of motion, and pain. This test is a reliable and valid measure in measuring post-stroke impairments related to stroke recovery. A lower score in each component of the test indicates higher impairment and a lower functional level for that area. The maximum score for each component is 66 for the upper extremities, 34 for the lower extremities, and 14 for balance. Administration of the FMA should be done after reviewing a training manual.

The Chedoke-McMaster Stroke Assessment (CMSA)

This test is a reliable measure of two separate components evaluating both motor impairment and disability. The disability component assesses any changes in physical function including gross motor function and walking ability. The disability inventory can have a maximum score of 100 with 70 from the gross motor index and 30 from the walking index. Each task in this inventory has a maximum score of seven except for the 2 minute walk test which is out of two. The impairment component of the test evaluates the upper and lower extremities, postural control and pain. The impairment inventory focuses on the seven stages of recovery from stroke from flaccid paralysis to normal motor functioning. A training workshop is recommended if the measure is being utilized for the purpose of data collection.

The Stroke Rehabilitation Assessment of Movement (STREAM)

The STREAM consists of 30 test items involving upper-limb movements, lower-limb movements, and basic mobility items. It is a clinical measure of voluntary movements and general mobility (rolling, bridging, sit-to-stand, standing, stepping, walking and stairs) following a stroke. The voluntary movement part of the assessment is measured using a 3-point ordinal scale (unable to perform, partial performance, and complete performance) and the mobility part of the assessment uses a 4-point ordinal scale (unable, partial, complete with aid, complete no aid). The maximum score one can receive on the STREAM is a 70 (20 for each limb score and 30 for mobility score). The higher the score, the better movement and mobility is available for the individual being scored.

PROGNOSIS

Hemiplegia is not a progressive disorder, except in progressive conditions like a growing brain tumour. Once the injury has occurred, the symptoms should not worsen. However, because of lack of mobility, other complications can occur. Complications may include muscle and joint stiffness, loss of aerobic fitness, muscle spasms, bed sores, pressure ulcers and blood clots.

Sudden recovery from hemiplegia is very rare. Many of the individuals will have limited recovery, but the majority will improve from intensive, specialised rehabilitation. Potential to progress may differ in cerebral palsy, compared to adult acquired brain injury. It is vital to integrate the hemiplegic child into society and encourage them in their daily living activities. With time, some individuals may make remarkable progress.

IMAGES

MENTAL RETARDATION - Behavioural Disorder - Narsiah, Godavari khani, Karimnagar

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I am Narsiah. This is my son. He does not indicate about his natural calls. His mother has to take care including feeding. He does not go to school, fights with classmates and spits on others. We consulted many doctors including neurophysician and Psychiatrist. CT Scan was done .He was advised to be admitted in the school for the mentally handicapped.

MODE OF RECOVERY AT NEW LIFE CENTRE

Our neighbour’s son was cured of his longstanding joint pains by Dr.Subhash. We also started taking his treatment. My child is now totally cured in all aspects. His behaviour is quite normal. He is attending his school and not spitting on others. He tells us about his needs and natural calls. We are too happy. We did not imagine this miracle. It is a new life to my son. We are at peace.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Intellectual disability (ID) or general learning disability is a generalized disorder appearing before adulthood, characterized by significantly impaired cognitive functioning and deficits in two or more adaptive behaviors. Intellectual disability is also known as mental retardation (MR), although this older term is being used less frequently. It was historically defined as an intelligence quotient score under 70. Once focused almost entirely on cognition, the definition now includes both a component relating to mental functioning and one relating to individuals' functional skills in their environments. As a result, a person with an unusually low IQ may not be considered intellectually disabled. Intellectual disability is subdivided into syndromic intellectual disability, in which intellectual deficits associated with other medical and behavioral signs and symptoms are present, and non-syndromic intellectual disability, in which intellectual deficits appear without other abnormalities.

The terms used for this condition are subject to a process called the euphemism treadmill. This means that whatever term is chosen for this condition, it eventually becomes perceived as an insult. The terms mental retardation and mentally retarded were invented in the middle of the 20th century to replace the previous set of terms, which were deemed to have become offensive. By the end of the 20th century, these terms themselves have come to be widely seen as disparaging, politically incorrect, and in need of replacement.[3] The term intellectual disability is now preferred by most advocates and researchers in most English-speaking countries. As of 2013, the term "mental retardation" is still used by the World Health Organization in the ICD-10 codes, which have a section titled "Mental Retardation" (codes F70–F79). In the next revision, the ICD-11 is expected to replace the term "mental retardation" with "intellectual disability," and the DSM-5 has replaced it with "intellectual disability (intellectual developmental disorder)." Because of its specificity and lack of confusion with other conditions, the term "mental retardation" is still sometimes used in professional medical settings around the world, such as formal scientific research and health insurance paperwork.

SIGNS AND SYMPTONS

The signs and symptoms of intellectual disability are all behavioral. Most people with intellectual disability do not look like they are afflicted with such, especially if the disability is caused by environmental factors such as malnutrition or lead poisoning. The so-called typical appearance ascribed to people with intellectual disability is only present in a minority of cases, all of which are syndromic.

Children with intellectual disability may learn to sit up, to crawl, or to walk later than other children, or they may learn to talk later. Both adults and children with intellectual disability may also exhibit some or all of the following characteristics:

  • Delays in oral language development
  • Deficits in memory skills
  • Difficulty learning social rules
  • Difficulty with problem solving skills
  • Delays in the development of adaptive behaviors such as self-help or self-care skills
  • Lack of social inhibitors

Children with intellectual disability learn more slowly than a typical child. Children may take longer to learn language, develop social skills, and take care of their personal needs, such as dressing or eating. Learning will take them longer, require more repetition, and skills may need to be adapted to their learning levels. Nevertheless, virtually every child is able to learn, develop and become a participating member of the community.

In early childhood, mild intellectual disability (IQ 50–69) may not be obvious, and may not be identified until children begin school. Even when poor academic performance is recognized, it may take expert assessment to distinguish mild intellectual disability from learning disability or emotional/behavioral disorders. People with mild intellectual disability are capable of learning reading and mathematics skills to approximately the level of a typical child aged nine to twelve. They can learn self-care and practical skills, such as cooking or using the local mass transit system. As individuals with intellectual disability reach adulthood, many learn to live independently and maintain gainful employment.

Moderate intellectual disability (IQ 35–49) is nearly always apparent within the first years of life. Speech delays are particularly common signs of moderate MR. People with moderate intellectual disability need considerable supports in school, at home, and in the community in order to participate fully. While their academic potential is limited, they can learn simple health and safety skills and to participate in simple activities. As adults they may live with their parents, in a supportive group home, or even semi-independently with significant supportive services to help them, for example, manage their finances. As adults, they may work in a sheltered workshop.

People with severe or profound intellectual disability need more intensive support and supervision their entire lives. They may learn some activities of daily living. Some require full-time care by an attendant.

CAUSES

Among children, the cause is unknown for one-third to one-half of cases. Down syndrome, velocariofacial syndrome, and fetal alcohol syndrome are the three most common inborn causes. However, doctors have found many other causes. The most common are:

  • Genetic conditions. Sometimes disability is caused by abnormal genes inherited from parents, errors when genes combine, or other reasons. The most prevalent genetic conditions include Down syndrome, Klinefelter's syndrome, Fragile X syndrome (common among boys), Neurofibromatosis, congenital hypothyroidism, Williams syndrome, Phenylketonuria (PKU), and Prader-Willi syndrome. Other genetic conditions include Phelan-McDermid syndrome (22q13del), Mowat-Wilson syndrome, genetic ciliopathy, and Siderius type X-linked intellectual disability (OMIM 300263) as caused by mutations in the PHF8 gene (OMIM 300560). In the rarest of cases, abnormalities with the X or Y chromosome may also cause disability. 48, XXXX and 49, XXXXX syndrome affect a small number of girls worldwide, while boys may be affected by 47, XYY, 49, XXXXY, or 49, XYYYY.
  • Problems during pregnancy. Intellectual disability can result when the fetus does not develop properly. For example, there may be a problem with the way the fetus' cells divide as it grows. A woman who drinks alcohol (see fetal alcohol syndrome) or gets an infection like rubella during pregnancy may also have a baby with intellectual disability.
  • Problems at birth. If a baby has problems during labor and birth, such as not getting enough oxygen, he or she may have developmental disability due to brain damage.
  • Exposure to certain types of disease or toxins. Diseases like whooping cough, measles, or meningitis can cause intellectual disability if medical care is delayed or inadequate. Exposure to poisons like lead or mercury may also affect mental ability.
  • Iodine deficiency, affecting approximately 2 billion people worldwide, is the leading preventable cause of intellectual disability in areas of the developing world where iodine deficiency is endemic. Iodine deficiency also causes goiter, an enlargement of the thyroid gland. More common than full-fledged cretinism, as intellectual disability caused by severe iodine deficiency is called, is mild impairment of intelligence. Certain areas of the world due to natural deficiency and governmental inaction are severely affected. India is the most outstanding, with 500 million suffering from deficiency, 54 million from goiter, and 2 million from cretinism. Among other nations affected by iodine deficiency, China and Kazakhstan have instituted widespread iodization programs, whereas, as of 2006, Russia had not.
  • Malnutrition is a common cause of reduced intelligence in parts of the world affected by famine, such as Ethiopia.
  • Absence of the arcuate fasciculus.

DIAGNOSIS

According to the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), three criteria must be met for a diagnosis of intellectual disability: an IQ below 70, significant limitations in two or more areas of adaptive behavior (as measured by an adaptive behavior rating scale, i.e. communication, self-help skills, interpersonal skills, and more), and evidence that the limitations became apparent before the age of 18.

It is formally diagnosed by an assessment of IQ and adaptive behavior. A third condition requiring onset in childhood is used to distinguish intellectual disability from dementia such as Alzheimer's disease or due to traumatic brain injuries.

Intelligence quotient

The first English-language IQ test, the Stanford-Binet Intelligence Scales, was adapted from a test battery designed for school placement by Alfred Binet in France. Lewis Terman adapted Binet's test and promoted it as a test measuring "general intelligence." Terman's test was the first widely used mental test to report scores in "intelligence quotient" form ("mental age" divided by chronological age, multiplied by 100). Current tests are scored in "deviation IQ" form, with a performance level by a test-taker two standard deviations below the median score for the test-taker's age group defined as IQ 70. Until the most recent revision of diagnostic standards, an IQ of 70 or below was a primary factor for intellectual disability diagnosis, and IQ scores were used to categorize degrees of intellectual disability.

Since current diagnosis of intellectual disability is not based on IQ scores alone, but must also take into consideration a person's adaptive functioning, the diagnosis is not made rigidly. It encompasses intellectual scores, adaptive functioning scores from an adaptive behavior rating scale based on descriptions of known abilities provided by someone familiar with the person, and also the observations of the assessment examiner who is able to find out directly from the person what he or she can understand, communicate, and such like. IQ assessment must be based on a current test. This enables diagnosis to avoid the pitfall of the Flynn Effect, which is a consequence of changes in population IQ test performance changing IQ test norms over time.

Distinction from other disabilities

Clinically, intellectual disability is a subtype of cognitive deficit or disabilities affecting intellectual abilities, which is a broader concept and includes intellectual deficits that are too mild to properly qualify as intellectual disability, or too specific (as in specific learning disability), or acquired later in life through acquired brain injuries or neurodegenerative diseases like dementia. Cognitive deficits may appear at any age. Developmental disability is any disability that is due to problems with growth and development. This term encompasses many congenital medical conditions that have no mental or intellectual components, although it, too, is sometimes used as a euphemism for intellectual disability.

Limitations in more than one areas

Clinically, intellectual disability is a subtype of cognitive deficit or disabilities affecting intellectual abilities, which is a broader concept and includes intellectual deficits that are too mild to properly qualify as intellectual disability, or too specific (as in specific learning disability), or acquired later in life through acquired brain injuries or neurodegenerative diseases like dementia. Cognitive deficits may appear at any age. Developmental disability is any disability that is due to problems with growth and development. This term encompasses many congenital medical conditions that have no mental or intellectual components, although it, too, is sometimes used as a euphemism for intellectual disability.

Limitations in more than one areas

Adaptive behavior, or adaptive functioning, refers to the skills needed to live independently (or at the minimally acceptable level for age). To assess adaptive behavior, professionals compare the functional abilities of a child to those of other children of similar age. To measure adaptive behavior, professionals use structured interviews, with which they systematically elicit information about persons' functioning in the community from people who know them well. There are many adaptive behavior scales, and accurate assessment of the quality of someone's adaptive behavior requires clinical judgment as well. Certain skills are important to adaptive behavior, such as:

  • Daily living skills, such as getting dressed, using the bathroom, and feeding oneself
  • Communication skills, such as understanding what is said and being able to answer
  • Social skills with peers, family members, spouses, adults, and others

MANAGEMENT

By most definitions intellectual disability is more accurately considered a disability rather than a disease. Intellectual disability can be distinguished in many ways from mental illness, such as schizophrenia or depression. Currently, there is no "cure" for an established disability, though with appropriate support and teaching, most individuals can learn to do many things.

There are thousands of agencies around the world that provide assistance for people with developmental disabilities. They include state-run, for-profit, and non-profit, privately run agencies. Within one agency there could be departments that include fully staffed residential homes, day rehabilitation programs that approximate schools, workshops wherein people with disabilities can obtain jobs, programs that assist people with developmental disabilities in obtaining jobs in the community, programs that provide support for people with developmental disabilities who have their own apartments, programs that assist them with raising their children, and many more. There are also many agencies and programs for parents of children with developmental disabilities.

Beyond that there are specific programs that people with developmental disabilities can take part in wherein they learn basic life skills. These "goals" may take a much longer amount of time for them to accomplish, but the ultimate goal is independence. This may be anything from independence in tooth brushing to an independent residence. People with developmental disabilities learn throughout their lives and can obtain many new skills even late in life with the help of their families, caregivers, clinicians and the people who coordinate the efforts of all of these people.

There are four broad areas of intervention that allow for active participation from caregivers, community members, clinicians, and of course, the individual(s) with an intellectual disability. These include psychosocial treatments, behavioral treatments, cognitive-behavioral treatments, and family-oriented strategies Psychosocial treatments are intended primarily for children before and during the preschool years as this is the optimum time for intervention. This early intervention should include encouragement of exploration, mentoring in basic skills, celebration of developmental advances, guided rehearsal and extension of newly acquired skills, protection from harmful displays of disapproval, teasing, or punishment, and exposure to a rich and responsive language environment. A great example of a successful intervention is the Carolina Abecedarian Project that was conducted with over 100 children from low SES families beginning in infancy through pre-school years. Results indicated that by age 2, the children provided the intervention had higher test scores than control group children, and they remained approximately 5 points higher 10 years after the end of the program. By young adulthood, children from the intervention group had better educational attainment, employment opportunities, and fewer behavioral problems than their control-group counterparts.

Core components of behavioral treatments include language and social skills acquisition. Typically, one-to-one training is offered in which a therapist uses a shaping procedure in combination with positive reinforcements to help the child pronounce syllables until words are completed. Sometimes involving pictures and visual aids, therapists aim at improving speech capacity so that short sentences about important daily tasks (e.g. bathroom use, eating, etc.) can be effectively communicated by the child. In a similar fashion, older children benefit from this type of training as they learn to sharpen their social skills such as sharing, taking turns, following instruction, and smiling. At the same time, a movement known as social inclusion attempts to increase valuable interactions between children with an intellectual disability and their non-disabled peers. Cognitive-behavioral treatments, a combination of the previous two treatment types, involves a strategical-metastrategical learning technique[clarification needed] that teaches children math, language, and other basic skills pertaining to memory and learning. The first goal of the training is to teach the child to be a strategical thinker through making cognitive connections and plans. Then, the therapist teaches the child to be metastrategical by teaching them to discriminate among different tasks and determine which plan or strategy suits each task. Finally, family-oriented strategies delve into empowering the family with the skill set they need to support and encourage their child or children with an intellectual disability. In general, this includes teaching assertiveness skills or behavior management techniques as well as how to ask for help from neighbors, extended family, or day-care staff. As the child ages, parents are then taught how to approach topics such as housing/residential care, employment, and relationships. The ultimate goal for every intervention or technique is to give the child autonomy and a sense of independence using the acquired skills he/she has.

Although there is no specific medication for intellectual disability, many people with developmental disabilities have further medical complications and may be prescribed several medications. For example autistic children with developmental delay may be prescribed antipsychotics or mood stabilizers to help with their behavior. Use of psychotropic medications such as benzodiazepines in people with intellectual disability requires monitoring and vigilance as side effects occur commonly and are often misdiagnosed as behavioural and psychiatric problems.

IMAGES

MENTAL RETARDATION - Karthikeya, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

He was hyperactive, dull, cranky and crying. Doctors advised us to take occupational and speech therapy. We spent Rs.4000/- week but in vain We tried Homeopathy also at a corporate centre of Chennai. There was some initial calmness but later the boy became more hyperactive and started crying.

MODE OF RECOVERY AT NEW LIFE CENTRE

The treatment given by NEW LIFE centre at Hyderabad could make him calm, his concentration has increased and he started playing with fellow students and attending his classes. There is no restlessness. Nowadays not getting any complaints about him from the school management.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Intellectual disability (ID) or general learning disability is a generalized disorder appearing before adulthood, characterized by significantly impaired cognitive functioning and deficits in two or more adaptive behaviors. Intellectual disability is also known as mental retardation (MR), although this older term is being used less frequently. It was historically defined as an intelligence quotient score under 70. Once focused almost entirely on cognition, the definition now includes both a component relating to mental functioning and one relating to individuals' functional skills in their environments. As a result, a person with an unusually low IQ may not be considered intellectually disabled. Intellectual disability is subdivided into syndromic intellectual disability, in which intellectual deficits associated with other medical and behavioral signs and symptoms are present, and non-syndromic intellectual disability, in which intellectual deficits appear without other abnormalities.

The terms used for this condition are subject to a process called the euphemism treadmill. This means that whatever term is chosen for this condition, it eventually becomes perceived as an insult. The terms mental retardation and mentally retarded were invented in the middle of the 20th century to replace the previous set of terms, which were deemed to have become offensive. By the end of the 20th century, these terms themselves have come to be widely seen as disparaging, politically incorrect, and in need of replacement.[3] The term intellectual disability is now preferred by most advocates and researchers in most English-speaking countries. As of 2013, the term "mental retardation" is still used by the World Health Organization in the ICD-10 codes, which have a section titled "Mental Retardation" (codes F70–F79). In the next revision, the ICD-11 is expected to replace the term "mental retardation" with "intellectual disability," and the DSM-5 has replaced it with "intellectual disability (intellectual developmental disorder)." Because of its specificity and lack of confusion with other conditions, the term "mental retardation" is still sometimes used in professional medical settings around the world, such as formal scientific research and health insurance paperwork.

SIGNS AND SYMPTONS

The signs and symptoms of intellectual disability are all behavioral. Most people with intellectual disability do not look like they are afflicted with such, especially if the disability is caused by environmental factors such as malnutrition or lead poisoning. The so-called typical appearance ascribed to people with intellectual disability is only present in a minority of cases, all of which are syndromic.

Children with intellectual disability may learn to sit up, to crawl, or to walk later than other children, or they may learn to talk later. Both adults and children with intellectual disability may also exhibit some or all of the following characteristics:

  • Delays in oral language development
  • Deficits in memory skills
  • Difficulty learning social rules
  • Difficulty with problem solving skills
  • Delays in the development of adaptive behaviors such as self-help or self-care skills
  • Lack of social inhibitors

Children with intellectual disability learn more slowly than a typical child. Children may take longer to learn language, develop social skills, and take care of their personal needs, such as dressing or eating. Learning will take them longer, require more repetition, and skills may need to be adapted to their learning levels. Nevertheless, virtually every child is able to learn, develop and become a participating member of the community.

In early childhood, mild intellectual disability (IQ 50–69) may not be obvious, and may not be identified until children begin school. Even when poor academic performance is recognized, it may take expert assessment to distinguish mild intellectual disability from learning disability or emotional/behavioral disorders. People with mild intellectual disability are capable of learning reading and mathematics skills to approximately the level of a typical child aged nine to twelve. They can learn self-care and practical skills, such as cooking or using the local mass transit system. As individuals with intellectual disability reach adulthood, many learn to live independently and maintain gainful employment.

Moderate intellectual disability (IQ 35–49) is nearly always apparent within the first years of life. Speech delays are particularly common signs of moderate MR. People with moderate intellectual disability need considerable supports in school, at home, and in the community in order to participate fully. While their academic potential is limited, they can learn simple health and safety skills and to participate in simple activities. As adults they may live with their parents, in a supportive group home, or even semi-independently with significant supportive services to help them, for example, manage their finances. As adults, they may work in a sheltered workshop.

People with severe or profound intellectual disability need more intensive support and supervision their entire lives. They may learn some activities of daily living. Some require full-time care by an attendant.

CAUSES

Among children, the cause is unknown for one-third to one-half of cases. Down syndrome, velocariofacial syndrome, and fetal alcohol syndrome are the three most common inborn causes. However, doctors have found many other causes. The most common are:

  • Genetic conditions. Sometimes disability is caused by abnormal genes inherited from parents, errors when genes combine, or other reasons. The most prevalent genetic conditions include Down syndrome, Klinefelter's syndrome, Fragile X syndrome (common among boys), Neurofibromatosis, congenital hypothyroidism, Williams syndrome, Phenylketonuria (PKU), and Prader-Willi syndrome. Other genetic conditions include Phelan-McDermid syndrome (22q13del), Mowat-Wilson syndrome, genetic ciliopathy, and Siderius type X-linked intellectual disability (OMIM 300263) as caused by mutations in the PHF8 gene (OMIM 300560). In the rarest of cases, abnormalities with the X or Y chromosome may also cause disability. 48, XXXX and 49, XXXXX syndrome affect a small number of girls worldwide, while boys may be affected by 47, XYY, 49, XXXXY, or 49, XYYYY.
  • Problems during pregnancy. Intellectual disability can result when the fetus does not develop properly. For example, there may be a problem with the way the fetus' cells divide as it grows. A woman who drinks alcohol (see fetal alcohol syndrome) or gets an infection like rubella during pregnancy may also have a baby with intellectual disability.
  • Problems at birth. If a baby has problems during labor and birth, such as not getting enough oxygen, he or she may have developmental disability due to brain damage.
  • Exposure to certain types of disease or toxins. Diseases like whooping cough, measles, or meningitis can cause intellectual disability if medical care is delayed or inadequate. Exposure to poisons like lead or mercury may also affect mental ability.
  • Iodine deficiency, affecting approximately 2 billion people worldwide, is the leading preventable cause of intellectual disability in areas of the developing world where iodine deficiency is endemic. Iodine deficiency also causes goiter, an enlargement of the thyroid gland. More common than full-fledged cretinism, as intellectual disability caused by severe iodine deficiency is called, is mild impairment of intelligence. Certain areas of the world due to natural deficiency and governmental inaction are severely affected. India is the most outstanding, with 500 million suffering from deficiency, 54 million from goiter, and 2 million from cretinism. Among other nations affected by iodine deficiency, China and Kazakhstan have instituted widespread iodization programs, whereas, as of 2006, Russia had not.
  • Malnutrition is a common cause of reduced intelligence in parts of the world affected by famine, such as Ethiopia.
  • Absence of the arcuate fasciculus.

DIAGNOSIS

According to the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), three criteria must be met for a diagnosis of intellectual disability: an IQ below 70, significant limitations in two or more areas of adaptive behavior (as measured by an adaptive behavior rating scale, i.e. communication, self-help skills, interpersonal skills, and more), and evidence that the limitations became apparent before the age of 18.

It is formally diagnosed by an assessment of IQ and adaptive behavior. A third condition requiring onset in childhood is used to distinguish intellectual disability from dementia such as Alzheimer's disease or due to traumatic brain injuries.

Intelligence quotient

The first English-language IQ test, the Stanford-Binet Intelligence Scales, was adapted from a test battery designed for school placement by Alfred Binet in France. Lewis Terman adapted Binet's test and promoted it as a test measuring "general intelligence." Terman's test was the first widely used mental test to report scores in "intelligence quotient" form ("mental age" divided by chronological age, multiplied by 100). Current tests are scored in "deviation IQ" form, with a performance level by a test-taker two standard deviations below the median score for the test-taker's age group defined as IQ 70. Until the most recent revision of diagnostic standards, an IQ of 70 or below was a primary factor for intellectual disability diagnosis, and IQ scores were used to categorize degrees of intellectual disability.

Since current diagnosis of intellectual disability is not based on IQ scores alone, but must also take into consideration a person's adaptive functioning, the diagnosis is not made rigidly. It encompasses intellectual scores, adaptive functioning scores from an adaptive behavior rating scale based on descriptions of known abilities provided by someone familiar with the person, and also the observations of the assessment examiner who is able to find out directly from the person what he or she can understand, communicate, and such like. IQ assessment must be based on a current test. This enables diagnosis to avoid the pitfall of the Flynn Effect, which is a consequence of changes in population IQ test performance changing IQ test norms over time.

Distinction from other disabilities

Clinically, intellectual disability is a subtype of cognitive deficit or disabilities affecting intellectual abilities, which is a broader concept and includes intellectual deficits that are too mild to properly qualify as intellectual disability, or too specific (as in specific learning disability), or acquired later in life through acquired brain injuries or neurodegenerative diseases like dementia. Cognitive deficits may appear at any age. Developmental disability is any disability that is due to problems with growth and development. This term encompasses many congenital medical conditions that have no mental or intellectual components, although it, too, is sometimes used as a euphemism for intellectual disability.

Limitations in more than one areas

Clinically, intellectual disability is a subtype of cognitive deficit or disabilities affecting intellectual abilities, which is a broader concept and includes intellectual deficits that are too mild to properly qualify as intellectual disability, or too specific (as in specific learning disability), or acquired later in life through acquired brain injuries or neurodegenerative diseases like dementia. Cognitive deficits may appear at any age. Developmental disability is any disability that is due to problems with growth and development. This term encompasses many congenital medical conditions that have no mental or intellectual components, although it, too, is sometimes used as a euphemism for intellectual disability.

Limitations in more than one areas

Adaptive behavior, or adaptive functioning, refers to the skills needed to live independently (or at the minimally acceptable level for age). To assess adaptive behavior, professionals compare the functional abilities of a child to those of other children of similar age. To measure adaptive behavior, professionals use structured interviews, with which they systematically elicit information about persons' functioning in the community from people who know them well. There are many adaptive behavior scales, and accurate assessment of the quality of someone's adaptive behavior requires clinical judgment as well. Certain skills are important to adaptive behavior, such as:

  • Daily living skills, such as getting dressed, using the bathroom, and feeding oneself
  • Communication skills, such as understanding what is said and being able to answer
  • Social skills with peers, family members, spouses, adults, and others

MANAGEMENT

By most definitions intellectual disability is more accurately considered a disability rather than a disease. Intellectual disability can be distinguished in many ways from mental illness, such as schizophrenia or depression. Currently, there is no "cure" for an established disability, though with appropriate support and teaching, most individuals can learn to do many things.

There are thousands of agencies around the world that provide assistance for people with developmental disabilities. They include state-run, for-profit, and non-profit, privately run agencies. Within one agency there could be departments that include fully staffed residential homes, day rehabilitation programs that approximate schools, workshops wherein people with disabilities can obtain jobs, programs that assist people with developmental disabilities in obtaining jobs in the community, programs that provide support for people with developmental disabilities who have their own apartments, programs that assist them with raising their children, and many more. There are also many agencies and programs for parents of children with developmental disabilities.

Beyond that there are specific programs that people with developmental disabilities can take part in wherein they learn basic life skills. These "goals" may take a much longer amount of time for them to accomplish, but the ultimate goal is independence. This may be anything from independence in tooth brushing to an independent residence. People with developmental disabilities learn throughout their lives and can obtain many new skills even late in life with the help of their families, caregivers, clinicians and the people who coordinate the efforts of all of these people.

There are four broad areas of intervention that allow for active participation from caregivers, community members, clinicians, and of course, the individual(s) with an intellectual disability. These include psychosocial treatments, behavioral treatments, cognitive-behavioral treatments, and family-oriented strategies Psychosocial treatments are intended primarily for children before and during the preschool years as this is the optimum time for intervention. This early intervention should include encouragement of exploration, mentoring in basic skills, celebration of developmental advances, guided rehearsal and extension of newly acquired skills, protection from harmful displays of disapproval, teasing, or punishment, and exposure to a rich and responsive language environment. A great example of a successful intervention is the Carolina Abecedarian Project that was conducted with over 100 children from low SES families beginning in infancy through pre-school years. Results indicated that by age 2, the children provided the intervention had higher test scores than control group children, and they remained approximately 5 points higher 10 years after the end of the program. By young adulthood, children from the intervention group had better educational attainment, employment opportunities, and fewer behavioral problems than their control-group counterparts.

Core components of behavioral treatments include language and social skills acquisition. Typically, one-to-one training is offered in which a therapist uses a shaping procedure in combination with positive reinforcements to help the child pronounce syllables until words are completed. Sometimes involving pictures and visual aids, therapists aim at improving speech capacity so that short sentences about important daily tasks (e.g. bathroom use, eating, etc.) can be effectively communicated by the child. In a similar fashion, older children benefit from this type of training as they learn to sharpen their social skills such as sharing, taking turns, following instruction, and smiling. At the same time, a movement known as social inclusion attempts to increase valuable interactions between children with an intellectual disability and their non-disabled peers. Cognitive-behavioral treatments, a combination of the previous two treatment types, involves a strategical-metastrategical learning technique[clarification needed] that teaches children math, language, and other basic skills pertaining to memory and learning. The first goal of the training is to teach the child to be a strategical thinker through making cognitive connections and plans. Then, the therapist teaches the child to be metastrategical by teaching them to discriminate among different tasks and determine which plan or strategy suits each task. Finally, family-oriented strategies delve into empowering the family with the skill set they need to support and encourage their child or children with an intellectual disability. In general, this includes teaching assertiveness skills or behavior management techniques as well as how to ask for help from neighbors, extended family, or day-care staff. As the child ages, parents are then taught how to approach topics such as housing/residential care, employment, and relationships. The ultimate goal for every intervention or technique is to give the child autonomy and a sense of independence using the acquired skills he/she has.

Although there is no specific medication for intellectual disability, many people with developmental disabilities have further medical complications and may be prescribed several medications. For example autistic children with developmental delay may be prescribed antipsychotics or mood stabilizers to help with their behavior. Use of psychotropic medications such as benzodiazepines in people with intellectual disability requires monitoring and vigilance as side effects occur commonly and are often misdiagnosed as behavioural and psychiatric problems.

IMAGES

MENTAL RETARDATION FITS(Post encephalitic Sequelae) - D/O Rupender, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

My daughter suffered from Pneumonia during her 2nd year leading to mental retardation. She was getting fits ,4-5 times a day, which are periodically severe with the girl turning blue in her face and hands despite consulting experts. She is retarded both in her physical and mental development.

MODE OF RECOVERY AT NEW LIFE CENTRE

We started getting homeopathyfrom New Life centre about 16 days ago. Now the severity and frequency of fits is very much less. She gets only 1-2 mild fits per day. Blue coloration is not there.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Intellectual disability (ID) or general learning disability is a generalized disorder appearing before adulthood, characterized by significantly impaired cognitive functioning and deficits in two or more adaptive behaviors. Intellectual disability is also known as mental retardation (MR), although this older term is being used less frequently. It was historically defined as an intelligence quotient score under 70. Once focused almost entirely on cognition, the definition now includes both a component relating to mental functioning and one relating to individuals' functional skills in their environments. As a result, a person with an unusually low IQ may not be considered intellectually disabled. Intellectual disability is subdivided into syndromic intellectual disability, in which intellectual deficits associated with other medical and behavioral signs and symptoms are present, and non-syndromic intellectual disability, in which intellectual deficits appear without other abnormalities.

The terms used for this condition are subject to a process called the euphemism treadmill. This means that whatever term is chosen for this condition, it eventually becomes perceived as an insult. The terms mental retardation and mentally retarded were invented in the middle of the 20th century to replace the previous set of terms, which were deemed to have become offensive. By the end of the 20th century, these terms themselves have come to be widely seen as disparaging, politically incorrect, and in need of replacement.[3] The term intellectual disability is now preferred by most advocates and researchers in most English-speaking countries. As of 2013, the term "mental retardation" is still used by the World Health Organization in the ICD-10 codes, which have a section titled "Mental Retardation" (codes F70–F79). In the next revision, the ICD-11 is expected to replace the term "mental retardation" with "intellectual disability," and the DSM-5 has replaced it with "intellectual disability (intellectual developmental disorder)." Because of its specificity and lack of confusion with other conditions, the term "mental retardation" is still sometimes used in professional medical settings around the world, such as formal scientific research and health insurance paperwork.

SIGNS AND SYMPTONS

The signs and symptoms of intellectual disability are all behavioral. Most people with intellectual disability do not look like they are afflicted with such, especially if the disability is caused by environmental factors such as malnutrition or lead poisoning. The so-called typical appearance ascribed to people with intellectual disability is only present in a minority of cases, all of which are syndromic.

Children with intellectual disability may learn to sit up, to crawl, or to walk later than other children, or they may learn to talk later. Both adults and children with intellectual disability may also exhibit some or all of the following characteristics:

  • Delays in oral language development
  • Deficits in memory skills
  • Difficulty learning social rules
  • Difficulty with problem solving skills
  • Delays in the development of adaptive behaviors such as self-help or self-care skills
  • Lack of social inhibitors

Children with intellectual disability learn more slowly than a typical child. Children may take longer to learn language, develop social skills, and take care of their personal needs, such as dressing or eating. Learning will take them longer, require more repetition, and skills may need to be adapted to their learning levels. Nevertheless, virtually every child is able to learn, develop and become a participating member of the community.

In early childhood, mild intellectual disability (IQ 50–69) may not be obvious, and may not be identified until children begin school. Even when poor academic performance is recognized, it may take expert assessment to distinguish mild intellectual disability from learning disability or emotional/behavioral disorders. People with mild intellectual disability are capable of learning reading and mathematics skills to approximately the level of a typical child aged nine to twelve. They can learn self-care and practical skills, such as cooking or using the local mass transit system. As individuals with intellectual disability reach adulthood, many learn to live independently and maintain gainful employment.

Moderate intellectual disability (IQ 35–49) is nearly always apparent within the first years of life. Speech delays are particularly common signs of moderate MR. People with moderate intellectual disability need considerable supports in school, at home, and in the community in order to participate fully. While their academic potential is limited, they can learn simple health and safety skills and to participate in simple activities. As adults they may live with their parents, in a supportive group home, or even semi-independently with significant supportive services to help them, for example, manage their finances. As adults, they may work in a sheltered workshop.

People with severe or profound intellectual disability need more intensive support and supervision their entire lives. They may learn some activities of daily living. Some require full-time care by an attendant.

CAUSES

Among children, the cause is unknown for one-third to one-half of cases. Down syndrome, velocariofacial syndrome, and fetal alcohol syndrome are the three most common inborn causes. However, doctors have found many other causes. The most common are:

  • Genetic conditions. Sometimes disability is caused by abnormal genes inherited from parents, errors when genes combine, or other reasons. The most prevalent genetic conditions include Down syndrome, Klinefelter's syndrome, Fragile X syndrome (common among boys), Neurofibromatosis, congenital hypothyroidism, Williams syndrome, Phenylketonuria (PKU), and Prader-Willi syndrome. Other genetic conditions include Phelan-McDermid syndrome (22q13del), Mowat-Wilson syndrome, genetic ciliopathy, and Siderius type X-linked intellectual disability (OMIM 300263) as caused by mutations in the PHF8 gene (OMIM 300560). In the rarest of cases, abnormalities with the X or Y chromosome may also cause disability. 48, XXXX and 49, XXXXX syndrome affect a small number of girls worldwide, while boys may be affected by 47, XYY, 49, XXXXY, or 49, XYYYY.
  • Problems during pregnancy. Intellectual disability can result when the fetus does not develop properly. For example, there may be a problem with the way the fetus' cells divide as it grows. A woman who drinks alcohol (see fetal alcohol syndrome) or gets an infection like rubella during pregnancy may also have a baby with intellectual disability.
  • Problems at birth. If a baby has problems during labor and birth, such as not getting enough oxygen, he or she may have developmental disability due to brain damage.
  • Exposure to certain types of disease or toxins. Diseases like whooping cough, measles, or meningitis can cause intellectual disability if medical care is delayed or inadequate. Exposure to poisons like lead or mercury may also affect mental ability.
  • Iodine deficiency, affecting approximately 2 billion people worldwide, is the leading preventable cause of intellectual disability in areas of the developing world where iodine deficiency is endemic. Iodine deficiency also causes goiter, an enlargement of the thyroid gland. More common than full-fledged cretinism, as intellectual disability caused by severe iodine deficiency is called, is mild impairment of intelligence. Certain areas of the world due to natural deficiency and governmental inaction are severely affected. India is the most outstanding, with 500 million suffering from deficiency, 54 million from goiter, and 2 million from cretinism. Among other nations affected by iodine deficiency, China and Kazakhstan have instituted widespread iodization programs, whereas, as of 2006, Russia had not.
  • Malnutrition is a common cause of reduced intelligence in parts of the world affected by famine, such as Ethiopia.
  • Absence of the arcuate fasciculus.

DIAGNOSIS

According to the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), three criteria must be met for a diagnosis of intellectual disability: an IQ below 70, significant limitations in two or more areas of adaptive behavior (as measured by an adaptive behavior rating scale, i.e. communication, self-help skills, interpersonal skills, and more), and evidence that the limitations became apparent before the age of 18.

It is formally diagnosed by an assessment of IQ and adaptive behavior. A third condition requiring onset in childhood is used to distinguish intellectual disability from dementia such as Alzheimer's disease or due to traumatic brain injuries.

Intelligence quotient

The first English-language IQ test, the Stanford-Binet Intelligence Scales, was adapted from a test battery designed for school placement by Alfred Binet in France. Lewis Terman adapted Binet's test and promoted it as a test measuring "general intelligence." Terman's test was the first widely used mental test to report scores in "intelligence quotient" form ("mental age" divided by chronological age, multiplied by 100). Current tests are scored in "deviation IQ" form, with a performance level by a test-taker two standard deviations below the median score for the test-taker's age group defined as IQ 70. Until the most recent revision of diagnostic standards, an IQ of 70 or below was a primary factor for intellectual disability diagnosis, and IQ scores were used to categorize degrees of intellectual disability.

Since current diagnosis of intellectual disability is not based on IQ scores alone, but must also take into consideration a person's adaptive functioning, the diagnosis is not made rigidly. It encompasses intellectual scores, adaptive functioning scores from an adaptive behavior rating scale based on descriptions of known abilities provided by someone familiar with the person, and also the observations of the assessment examiner who is able to find out directly from the person what he or she can understand, communicate, and such like. IQ assessment must be based on a current test. This enables diagnosis to avoid the pitfall of the Flynn Effect, which is a consequence of changes in population IQ test performance changing IQ test norms over time.

Distinction from other disabilities

Clinically, intellectual disability is a subtype of cognitive deficit or disabilities affecting intellectual abilities, which is a broader concept and includes intellectual deficits that are too mild to properly qualify as intellectual disability, or too specific (as in specific learning disability), or acquired later in life through acquired brain injuries or neurodegenerative diseases like dementia. Cognitive deficits may appear at any age. Developmental disability is any disability that is due to problems with growth and development. This term encompasses many congenital medical conditions that have no mental or intellectual components, although it, too, is sometimes used as a euphemism for intellectual disability.

Limitations in more than one areas

Clinically, intellectual disability is a subtype of cognitive deficit or disabilities affecting intellectual abilities, which is a broader concept and includes intellectual deficits that are too mild to properly qualify as intellectual disability, or too specific (as in specific learning disability), or acquired later in life through acquired brain injuries or neurodegenerative diseases like dementia. Cognitive deficits may appear at any age. Developmental disability is any disability that is due to problems with growth and development. This term encompasses many congenital medical conditions that have no mental or intellectual components, although it, too, is sometimes used as a euphemism for intellectual disability.

Limitations in more than one areas

Adaptive behavior, or adaptive functioning, refers to the skills needed to live independently (or at the minimally acceptable level for age). To assess adaptive behavior, professionals compare the functional abilities of a child to those of other children of similar age. To measure adaptive behavior, professionals use structured interviews, with which they systematically elicit information about persons' functioning in the community from people who know them well. There are many adaptive behavior scales, and accurate assessment of the quality of someone's adaptive behavior requires clinical judgment as well. Certain skills are important to adaptive behavior, such as:

  • Daily living skills, such as getting dressed, using the bathroom, and feeding oneself
  • Communication skills, such as understanding what is said and being able to answer
  • Social skills with peers, family members, spouses, adults, and others

MANAGEMENT

By most definitions intellectual disability is more accurately considered a disability rather than a disease. Intellectual disability can be distinguished in many ways from mental illness, such as schizophrenia or depression. Currently, there is no "cure" for an established disability, though with appropriate support and teaching, most individuals can learn to do many things.

There are thousands of agencies around the world that provide assistance for people with developmental disabilities. They include state-run, for-profit, and non-profit, privately run agencies. Within one agency there could be departments that include fully staffed residential homes, day rehabilitation programs that approximate schools, workshops wherein people with disabilities can obtain jobs, programs that assist people with developmental disabilities in obtaining jobs in the community, programs that provide support for people with developmental disabilities who have their own apartments, programs that assist them with raising their children, and many more. There are also many agencies and programs for parents of children with developmental disabilities.

Beyond that there are specific programs that people with developmental disabilities can take part in wherein they learn basic life skills. These "goals" may take a much longer amount of time for them to accomplish, but the ultimate goal is independence. This may be anything from independence in tooth brushing to an independent residence. People with developmental disabilities learn throughout their lives and can obtain many new skills even late in life with the help of their families, caregivers, clinicians and the people who coordinate the efforts of all of these people.

There are four broad areas of intervention that allow for active participation from caregivers, community members, clinicians, and of course, the individual(s) with an intellectual disability. These include psychosocial treatments, behavioral treatments, cognitive-behavioral treatments, and family-oriented strategies Psychosocial treatments are intended primarily for children before and during the preschool years as this is the optimum time for intervention. This early intervention should include encouragement of exploration, mentoring in basic skills, celebration of developmental advances, guided rehearsal and extension of newly acquired skills, protection from harmful displays of disapproval, teasing, or punishment, and exposure to a rich and responsive language environment. A great example of a successful intervention is the Carolina Abecedarian Project that was conducted with over 100 children from low SES families beginning in infancy through pre-school years. Results indicated that by age 2, the children provided the intervention had higher test scores than control group children, and they remained approximately 5 points higher 10 years after the end of the program. By young adulthood, children from the intervention group had better educational attainment, employment opportunities, and fewer behavioral problems than their control-group counterparts.

Core components of behavioral treatments include language and social skills acquisition. Typically, one-to-one training is offered in which a therapist uses a shaping procedure in combination with positive reinforcements to help the child pronounce syllables until words are completed. Sometimes involving pictures and visual aids, therapists aim at improving speech capacity so that short sentences about important daily tasks (e.g. bathroom use, eating, etc.) can be effectively communicated by the child. In a similar fashion, older children benefit from this type of training as they learn to sharpen their social skills such as sharing, taking turns, following instruction, and smiling. At the same time, a movement known as social inclusion attempts to increase valuable interactions between children with an intellectual disability and their non-disabled peers. Cognitive-behavioral treatments, a combination of the previous two treatment types, involves a strategical-metastrategical learning technique[clarification needed] that teaches children math, language, and other basic skills pertaining to memory and learning. The first goal of the training is to teach the child to be a strategical thinker through making cognitive connections and plans. Then, the therapist teaches the child to be metastrategical by teaching them to discriminate among different tasks and determine which plan or strategy suits each task. Finally, family-oriented strategies delve into empowering the family with the skill set they need to support and encourage their child or children with an intellectual disability. In general, this includes teaching assertiveness skills or behavior management techniques as well as how to ask for help from neighbors, extended family, or day-care staff. As the child ages, parents are then taught how to approach topics such as housing/residential care, employment, and relationships. The ultimate goal for every intervention or technique is to give the child autonomy and a sense of independence using the acquired skills he/she has.

Although there is no specific medication for intellectual disability, many people with developmental disabilities have further medical complications and may be prescribed several medications. For example autistic children with developmental delay may be prescribed antipsychotics or mood stabilizers to help with their behavior. Use of psychotropic medications such as benzodiazepines in people with intellectual disability requires monitoring and vigilance as side effects occur commonly and are often misdiagnosed as behavioural and psychiatric problems.

IMAGES

LEAK OF BRAIN FLUID - Madhavi, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Four months ago watery fluid started flowing continuously from my right nostril. ENT doctors said it was brain fluid. There was no medicine or any cure for it. I was much scared. The only way out was a complicated surgery that did not guarantee any lasting effect. There was a fear of developing complications too like Meningitis. I was forced to sleep with my head straight. Any little turning of my head would increase the flow soaking the whole pillow wet. It was a hopeless state.

MODE OF RECOVERY AT NEW LIFE CENTRE

Under such conditions I consulted Dr.Subhash and started taking his medicines. The fluid leak has totally stopped in just four months of his treatment. It has been a miraculous cure. There has been no recurrence or any side effects. Now that I am totally cured; I feel one should have faith in homeopathy. Patients suffering from difficult diseases, needing expensive treatment, could also benefit. Experienced homeopaths can only perform. I thank Dr.Subhash Chandar again.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Spontaneous cerebrospinal fluid leak syndrome (SCSFLS) is a medical condition in which the cerebrospinal fluid (CSF) held in and around a human brain and spinal cord leaks out of the surrounding protective sac, the dura, for no apparent reason. The dura, a tough, inflexible tissue, is the outermost of the three layers of the meninges, the system of meninges surrounding the brain and spinal cord. (The other two meningeal layers are the pia mater and the arachnoid mater).

A spontaneous cerebrospinal fluid leak is one of several types of cerebrospinal fluid leaks and occurs due to the presence of one or more holes in the dura. A spontaneous CSF leak, as opposed to traumatically caused CSF leaks, arises idiopathically. A loss of CSF greater than its rate of production leads to a decreased volume inside the skull known as intracranial hypotension. A CSF leak is most often characterized by a severe and disabling headache and a spectrum of various symptoms that occur as a result of intracerebral hemorrhage (ICH). These symptoms can include: dizziness, nausea, fatigue, a metallic taste in the mouth (indicative of a cranial leak), myoclonus, tinnitus, tingling in the limbs, and facial weakness among others. A CT scan can identify the site of a cerebrospinal fluid leakage. Once identified, the leak can often be repaired by an epidural blood patch, an injection of the patient's own blood at the site of the leak, fibrin glue injection or surgery.

SCSFLS afflicts 5 out of every 100,000 people. On average, the condition is developed at the age of 42, and women are twice as likely as men to develop the condition. Some people with SCSFLS chronically leak cerebrospinal fluid despite repeated attempts at patching, leading to long-term disability due to pain and nerve damage. SCSFLS was first described by German neurologist Georg Schaltenbrand in 1938 and by American physician Henry Woltman of the Mayo Clinic in the 1950s.

CLASSIFICATION

SCSFLS is classified into two main types, cranial leaks and spinal leaks. Cranial leaks occur in the head. In some cases, CSF can be seen dripping out of the nose, or ear. Spinal leaks occur when one or more holes form in the dura along the spinal cord. Both cranial and spinal spontaneous CSF leaks cause neurological symptoms as well as spontaneous intracranial hypotension, diminished volume and pressure of the cranium. While referred to as intracranial hypotension the intracranial pressure may be normal, but low-volume CSF is instead the underlying issue. For this reason SCSFLS is referred to as CSF hypovolemia as opposed to CSF hypotension.

SIGNS AND SYMPTOMS

Most people who develop SCSFLS feel a sudden onset of a severe and acute headache. It is a headache usually but not necessarily orthostatic in nature, typically becoming prominent throughout the day, in which usually the pain is worse when the person is vertical and less severe when horizontal. Other symptoms include dizziness and vertigo, facial numbness or weakness, unusually blurry or double vision, neuralgia, fatigue, a metallic taste in the mouth, nausea, or vomiting. Leaking CSF can sometimes be felt or observed as discharge through the nose or ear.[16] Orthostatic headaches can be incapacitating; these ailments often become chronic and can be sufficiently disabling to make those afflicted unable to work. Some patients with CSF leak will develop headaches that begin in the afternoon. This is known as second-half-of-the-day headache. This may be an initial presentation of CSF leak or appear after treatment and likely indicates a slow CSF leak.

Lack of CSF pressure and volume allows the brain to descend through the foramen magnum, or occipital bone, the large opening at the base of the skull. The lower portion of the brain is believed to stretch or impact one or more cranial nerve complexes, thereby causing a variety of sensory symptoms. Nerves that can be affected and their related symptoms are detailed in the table at right.

CAUSES

The two main theories as to the underlying cause of SCSFLS are as a result of a connective tissue disorder or spinal drainage problems.

Connective Tissue Theory

A spontaneous CSF leak is idiopathic; it can arise spontaneously or from an unknown cause. Various scientists and physicians have suggested that this condition may be the result of an underlying connective tissue disorder affecting the spinal dura. It may also run in families and be associated with aortic aneurysms and joint hypermobility. Up to two thirds of those afflicted demonstrate some type of generalized connective tissue disorder. Marfan syndrome, Ehlers-Danlos syndrome and autosomal dominant polycystic kidney disease are the three most common connective tissue disorders associated with SCSFLS.

Roughly 20% of patients with SCSFLS exhibit features of Marfan syndrome, including tall stature, chest divot (pectus excavatum), joint hypermobility and arched palate. However these patients do not exhibit any other Marfan syndrome presentations.

Spinal Drainage Theory

Some other studies have proposed that issues with the spinal venous drainage system may cause a CSF leak. According to this theory, dural holes and intracranial hypotension are symptoms caused by low pressure in the epidural space due to outflow to the heart through the inferior vena cava vein.

Other causes

Patients with a nude (absent) nerve root are at increased risk for developing recurrent CSF leaks. Cranial CSF leaks are as a result of intracranial hypertension in a vast majority of cases. The increased pressure causes a rupture of the cranial dura mater, leading to CSF leak and intracranial hypotension. Lumbar disc herniation has been reported to cause CSF leak in at least one case. Degenerative spinal disc diseases cause a disc to pierce the dura mater, leading to a CSF leak.

Another view of the cause of orthostatic headaches proposes a malformed distribution of craniospinal elasticity as a result of the collapse of the lower spine's CSF space resulting in the collapse of the dura sac.

PATHOPHYSIOLOGY

Cerebrospinal fluid is produced by the choroid plexus in the brain and contained by the dura and arachnoid layers of the meninges. The brain floats in CSF, which also transports nutrients to the brain and spinal cord. As holes form in the spinal dura mater, CSF leaks out into the surrounding space. The CSF is then absorbed into the spinal epidural venous plexus or soft tissues around the spine. Due to the sterile conditions of the soft tissues around the spine there is no risk of meningitis.

DIAGNOSIS

The primary place of first complaint to a physician is a hospital emergency room. Up to 94% of those suffering from SCSFLS are initially misdiagnosed. Incorrect diagnoses include migraines, meningitis, and psychiatric disorders. The average time from onset of symptoms until definitive diagnosis is 13 months. A study found a 0% success rate for proper diagnosis in the emergency department.

Diagnosis of CSF leak can be done through various imaging techniques, chemical tests of bodily fluid discharged from a head orifice, or clinical exam. The use of CT, MRI, and assays are the most common types of CSF leak instrumental tests. Many CSF leaks are occult and do not show up on imaging and chemical assays, thus such diagnostic tools are not definitive to rule out CSF leaks. A clinician may often depend upon patient history and exam to diagnose, for example: discharge of excessive amount of clear fluid from the nose upon bending over, the increase in headache following a Valsalva maneuver or the reduction of headache when the patient takes a prone position are positive indicators.

As most candidates for CSF leak do not have access to imaging and laboratory tools (modern medicine), clinical exam is the most often used means to diagnose CSF leaks. Improved patient response to conservative treatment may further define a positive diagnosis. The lack of clinician awareness of the signs -symptoms and ailments- of a CSF leak is the greatest challenge to proper diagnosis and treatment, in particular: the loss of the orthostatic characteristic of headache and that every chronic CSF leaker will have a unique symptom set that as a whole contributes to the underlying condition, and diagnosis of, a CSF leak.

CT SCAN

Diagnosis of a cerebrospinal fluid leak is performed through a combination of measurement of the CSF pressure and a computed tomography myelogram (CTM) scan of the spinal column for fluid leaks. The opening fluid pressure in the spinal canal is obtained by performing a lumbar puncture, also known as a spinal tap. Once the pressure is measured, radiopaque contrast material is injected into the spinal fluid. The contrast then diffuses out through the dura sac before leaking through dural holes. This allows for a CTM with fluoroscopy to locate and image any sites of dura rupture via contrast seen outside the dura sac in the imagery.

MRI SCAN

Magnetic resonance imaging is historically less effective at directly imaging sites of CSF leak. MRI studies may show pachymeningeal enhancement (when the dura mater looks thick and inflamed) and an Arnold-Chiari malformation in many, but not all, cases. An Arnold-Chiari malformation occurs when the brain sags and has a downward displacement due to the decreased volume and buoyancy of cerebrospinal fluid in which the brain floats. MRIs can present as completely normal, however, and are not the study of choice. An alternate method of locating the site of a CSF leak is to use heavily T2-weighted MR myelography. This has been effective in identifying the sites of a CSF leak without the need for a CT scan, lumbar puncture, and contrast and at locating fluid collections such as CSF pooling. MRIs done on patients sitting upright demonstrated no difference in MRI results compared to those lying down. The use of intrathecal contrast and MR Myelography is also an alternative method of locating CSF leaks with a very high degree of success.

ASSAY

When cranial CSF leak is suspected because of discharge from the nose or ear that is potentially CSF, the fluid can be collected and tested with a beta-2 transferrin assay. This test can positively identify if the fluid is cerebrospinal fluid.

CSF analysis

Patients with CSF leak have been noted to have very low or even negative opening pressures. However, patients with confirmed CSF leaks may also demonstrate completely normal opening pressures. In 18–46% of cases, the CSF pressure is measured within the normal range. Analysis of spinal fluid may demonstrate lymphocytic pleocytosis and elevated protein content or xanthochromia. This is hypothesized to be due to increased permeability of dilated meningeal blood vessels and a decrease of CSF flow in the lumbar subarachnoid space.

Clinical presentation

The diagnostic criteria for SCSFLS is based on the 2004 International Classification of Headache Disorders, 2nd edn (ICHD-II) criteria. However, the presentation of patients with confirmed diagnosis may be very different from that of the clinical diagnostic criteria and cannot be considered authoritative.

TREATMENT

The treatment of choice for this condition is the surgical application of epidural blood patches, which has a 90% success rate in treating dural holes; a rate higher than that of a conservative treatment of bed rest and hydration. Through the injection of a person's own blood into the area of the hole in the dura, an epidural blood patch uses blood's clotting factors to clot the sites of holes. The volume of autologous blood and number of patch attempts for patients is highly variable. One-quarter to one-third of SCSFLS patients do not have relief of symptoms from epidural blood patching.

Fibrin glue sealant

If blood patches alone do not succeed in closing the dural tears, placement of percutaneous fibrin glue can be used in place of blood patching, raising the effectiveness of forming a clot and arresting CSF leakage.

Surgical drain technique

In extreme cases of intractable CSF leak, a surgical lumbar drain has been used. This procedure is believed to decrease spinal CSF volume while increasing intracranial CSF pressure and volume. This procedure restores normal intracranial CSF volume and pressure while promoting the healing of dural tears by lowering the pressure and volume in the dura. This procedure has led to positive results leading to relief of symptoms for up to one year.

Neurosurgical repair

For patients that do not respond to either epidural blood patching or fibrin glue, neurosurgery is available to directly repair leaking meningeal diverticula. The areas of dura leak can be tied together in a process called ligation[disambiguation needed] and then a metal clip can be placed in order to hold the ligation closed. Alternatively, a small compress called a muscle pledget can be placed over the dura leak and then sealed with gel foam and fibrin glue. Primary suturing is rarely able to repair a CSF leak, and in some patients exploration of the dura may be required to properly locate all sites of CSF leak.

Other treatments

The use of an abdominal binder has also been employed as a treatment.

PROGNOSIS

Final outcomes for people with SCSFLS remain poorly studied. Some of those afflicted continue to leak CSF from one or more sites and may suffer from unremitting symptoms for many years. People with chronic SCSFLS may be disabled and unable to work. Recurrent CSF leak at an alternate site after recent repair is common.

COMPLICATIONS

Several complications can occur as a result of SCSFLS including decreased cranial pressure, brain herniation, infection, blood pressure problems, transient paralysis, and coma. The primary and most serious complication of SCSFLS is spontaneous intracranial hypotension, where pressure in the brain is severely decreased. This complication leads to the hallmark symptom of severe orthostatic headaches.

People with cranial CSF leaks have a higher chance of developing meningitis than those with spinal CSF leaks. In addition, if cranial leaks last more than seven days, the chances of developing meningitis are significantly higher. Spinal CSF leaks do not usually result in meningitis due to the mostly aseptic conditions of the spinal dura. When a CSF leak occurs at the temporal bone surgery becomes necessary in order to prevent infection and repair the leak. Orthostatic hypotension is another complication that occurs due to autonomic dysfunction when blood pressure drops significantly. The autonomic dysfunction is caused by compression of the brainstem, which controls breathing and circulation.

An Arnold-Chiari malformation is a downward displacement of lower parts of the brain through the skull opening that occurs due to a lack of CSF volume and pressure. A further, albeit rare, complication of CSF leak is transient quadriplegia due to a sudden and significant loss of CSF. This loss results in hindbrain herniation and causes major compression of the upper cervical spinal cord. The quadriplegia dissipates once the patient lies supine. An extremely rare complication of SCSFLS is third nerve palsy, where the ability to move one's eyes becomes difficult and interrupted due to compression of the third cranial nerve. Although other sources consider 3rd nerve palsy a common manifestation of CSF leaks.

There are documented cases of reversible frontotemporal dementia and coma. Coma due to a CSF leak has been successfully treated by using blood patches and/or fibrin glue and placing the patient in the Trendelenburg position. Empty sella syndrome, a boney structure that surround the pituitary gland, occurs in CSF leak patients.

EPIDEMIOLOGY

A 1994 community-based study indicated that two out of every 100,000 people suffered from SCSFLS, while a 2004 emergency room-based study indicated five per 100,000. SCSFLS generally affects the young and middle aged; the average age for onset is 42.3 years, but onset can range from ages 22 to 61. In an 11-year study women were found to be twice as likely to be affected as men.

Studies have shown that SCSFLS runs in families and it is suspected that genetic similarity in families includes weakness in the dura mater, which leads to SCSFLS. Large scale population-based studies have not yet been conducted. While a majority of SCSFLS cases continue to be undiagnosed or misdiagnosed, an actual increase in occurrence is unlikely.

IMAGES

CASE RECORD

PARALYSIS, DIABETES, High BP.(old case) - Gangaram Koratla, Karimnagar

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

About 9 years ago I developed paralysis of my left sided limbs. In NIMS hospital I could come out of coma. Later I got admitted in a Nature cure hospital. There I could start walking with support.

MODE OF RECOVERY AT NEW LIFE CENTRE

I started taking treatment at New Life Centre about one year ago. I am now able to walk, without anybody’s support, My other problems like Diabetes and Blood pressure are also under control. I have not developed any side effects.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Hemiplegia is paralysis of the arm, leg, and trunk on the same side of the body. Hemiplegia is more severe than hemiparesis, where in one half of the body has less marked weakness. Hemiplegia and hemiparesis may be congenital, or they might be acquired conditions resulting from an illness, an injury, or a stroke.

SIGNS AND SYMPTOMS

Hemiplegia means severe weakness of the limbs on one side of the body but the specific features can vary tremendously from person to person. Problems may include :

  • Difficulty with gait.
  • Difficulty with balance while standing or walking.
  • Increasing stiffness of muscles.
  • Muscle spasms.
  • The majority of children who develop hemiplegia also have abnormal mental development.
  • Behavior problems like anxiety, anger, irritability, lack of concentration or comprehension.
  • Emotions — depression.
  • Shoulder pain — Often associated with a loss of external rotation of the glenohumeral joint, commonly due to the increased tone of the Subscapularis muscle and Pectoralis major muscle.
  • Shoulder Subluxation.

CAUSES

The most common cause of hemiplegia is stroke. Strokes can cause a variety of movement disorders, depending on the location and severity of the lesion. Hemiplegia is common when the stroke affects the corticospinal tract. Other causes of hemiplegia include spinal cord injury, specifically Brown-Séquard syndrome, traumatic brain injury, or disease affecting the brain. As a lesion that results in hemiplegia occurs in the brain or spinal cord, hemiplegic muscles display features of the Upper Motor Neuron Syndrome. Features other than weakness include decreased movement control, clonus (a series of involuntary rapid muscle contractions), spasticity, exaggerated deep tendon reflexes and decreased endurance.

The incidence of hemiplegia is much higher in premature babies than term babies. There is also a high incidence of hemiplegia during pregnancy and experts believe that this may be related to either a traumatic delivery, use of forceps or some event which causes brain injury.

Other causes of hemiplegia in adults include trauma, bleeding, brain infections and cancers. Individuals who have uncontrolled diabetes, hypertension or those who smoke have a higher chance of developing a stroke. Weakness on one side of the face may occur and may be due to a viral infection, stroke or a cancer.

COMMON CAUSES BY ETIOLOGY

  • VASCULAR: cerebral hemorrhage, stroke, diabetic neuropathy
  • INFECTIVE: encephalitis, meningitis, brain abscess
  • NEOPLASTIC: glioma-meningioma
  • DEMYELINATION: disseminated sclerosis, lesions to the internal capsule
  • TRAUMATIC: cerebral lacerations, subdural hematoma rare cause of hemiplegia is due to local anaesthetic injections given intra-arterially rapidly, instead of given in a nerve branch.
  • CONGENITAL: cerebral palsy
  • DISSEMINATED: multiple sclerosis
  • PSYCHOLOGICAL: parasomnia (nocturnal hemiplegia)

PATHOGENESIS

The exact cause of hemiplegia is not known in all cases, but it appears that the brain is deprived of oxygen and this results in the death of neurons. When the corticospinal tract is damaged, the injury is usually manifested on the opposite side of the body. For example if one has an injury to the right side of the brain, the hemiplegia will be on the left side of the body. This happens because the motor fibres of corticospinal tract ( also called pyramidal fibres), which take origin from the motor cortex in brain, cross to the opposite side in the lower part of medulla oblangata and then descend down in spinal cord to supply their respective muscles. Depending on the site of lesion in brain, the severity of hemiplegia varies. A lesion in internal capsule where all the motor fibres are condensed in a small area, will cause dense hemiplegia i.e. complete loss of power of all muscles of one half of body while a lesion at cortical or subcortical level will cause varied amount of weakness of one half of the body.

DIAGNOSIS

Hemiplegia is identified by clinical examination by a health professional, such as a physiotherapist or doctor. Radiological studies like a CT scan or magnetic resonance imaging of the brain should be used to confirm injury in the brain and spinal cord, but alone cannot be used to identify movement disorders. Individuals who develop seizures may undergo tests to determine where the focus of excess electrical activity is.

Hemiplegia patients usually show a characteristic gait. The leg on the affected side is extended and internally rotated and is swung in a wide, lateral arc rather than lifted in order to move it forward. The upper limb on the same side is also adducted at the shoulder, flexed at the elbow, and pronated at the wrist with the thumb tucked into the palm and the fingers curled around it.

TREATMENT

Treatment should be based on assessment by the relevant health professionals, including physiotherapists, doctors and occupational therapists. Muscles with severe motor impairment including weakness need these therapists to assist them with specific exercise, and are likely to require help to do this.

Pharmacological

Drugs can be used to treat issues related to the Upper Motor Neuron Syndrome. Drugs like Librium or Valium could be used as a relaxant. Drugs are also given to individuals who have recurrent seizures, which may be a separate but related problem after brain injury.

Surgery

Surgery may be used if the individual develops a secondary issue of contracture, from a severe imbalance of muscle activity. In such cases the surgeon may cut the ligaments and relieve joint contractures. Individuals who are unable to swallow may have a tube inserted into the stomach. This allows food to be given directly into the stomach. The food is in liquid form and instilled at low rates. Some individuals with hemiplegia will benefit from some type of prosthetic device. There are many types of braces and splints available to stabilize a joint, assist with walking and keep the upper body erect.

Rehabilitation

Rehabilitation is the main treatment of individuals with hemiplegia. In all cases, the major aim of rehabilitation is to regain maximum function and quality of life. Both physical and occupational therapy can significantly improve the quality of life.

Physical Therapy

Physical therapy (PT) can help improve muscle strength & coordination, mobility (such as standing and walking), and other physical function using different sensorimotor techniques. Physiotherapists can also help reduce shoulder pain by maintaining shoulder range of motion, as well as using Functional electrical stimulation.[11] Supportive devices, such as braces or slings, can be used to help prevent or treat shoulder subluxation in the hopes to minimize disability and pain. It should be noted that although many individuals suffering from stroke experience both shoulder pain and shoulder subluxation, the two are mutually exclusive. A treatment method that can be implemented with the goal of helping to regain motor function in the affected limb is constraint-induced movement therapy. This consists of constraining the unaffected limb, forcing the affected limb to accomplish tasks of daily living.

Occupational Therapy

Occupational therapy Occupational Therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening hand, shoulder and torso, and participating in activities of daily living (ADLs), such as eating and dressing. Therapists may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your child’s hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual - which may include, environmental modification, use of adaptive equipment, sensory integration, etc.

Constraint-Induced Movement Therapy

Constraint-induced movement therapy (CI or CIMT) is a form of rehabilitation therapy that improves upper extremity function, especially in cases of hemiplegia.

ASSESSMENT TOOLS

There are a variety of standardized assessment scales available to physiotherapists and other health care professionals for use in the ongoing evaluation of the status of a patient’s hemiplegia. The use of standardized assessment scales may help physiotherapists and other health care professionals during the course of their treatment plant to:

  • Prioritize treatment interventions based on specific identifiable motor and sensory deficits.
  • Create appropriate short and long term goals for treatment based on the outcome of the scales, their professional expertise and the desires of the patient.
  • Evaluate the potential burden of care and monitor any changes based on either improving or declining scores.

Some of the most commonly used scales in the assessment of hemiplegia are:

The Fugl-Meyer Assessment of Physical Performance (FMA)

The FMA is often used as a measure of functional or physical impairment following a cerebrovascular accident(CVA). It measures sensory and motor impairment of the upper and lower extremities, balance in several positions, range of motion, and pain. This test is a reliable and valid measure in measuring post-stroke impairments related to stroke recovery. A lower score in each component of the test indicates higher impairment and a lower functional level for that area. The maximum score for each component is 66 for the upper extremities, 34 for the lower extremities, and 14 for balance. Administration of the FMA should be done after reviewing a training manual.

The Chedoke-McMaster Stroke Assessment (CMSA)

This test is a reliable measure of two separate components evaluating both motor impairment and disability. The disability component assesses any changes in physical function including gross motor function and walking ability. The disability inventory can have a maximum score of 100 with 70 from the gross motor index and 30 from the walking index. Each task in this inventory has a maximum score of seven except for the 2 minute walk test which is out of two. The impairment component of the test evaluates the upper and lower extremities, postural control and pain. The impairment inventory focuses on the seven stages of recovery from stroke from flaccid paralysis to normal motor functioning. A training workshop is recommended if the measure is being utilized for the purpose of data collection.

The Stroke Rehabilitation Assessment of Movement (STREAM)

The STREAM consists of 30 test items involving upper-limb movements, lower-limb movements, and basic mobility items. It is a clinical measure of voluntary movements and general mobility (rolling, bridging, sit-to-stand, standing, stepping, walking and stairs) following a stroke. The voluntary movement part of the assessment is measured using a 3-point ordinal scale (unable to perform, partial performance, and complete performance) and the mobility part of the assessment uses a 4-point ordinal scale (unable, partial, complete with aid, complete no aid). The maximum score one can receive on the STREAM is a 70 (20 for each limb score and 30 for mobility score). The higher the score, the better movement and mobility is available for the individual being scored.

PROGNOSIS

Hemiplegia is not a progressive disorder, except in progressive conditions like a growing brain tumour. Once the injury has occurred, the symptoms should not worsen. However, because of lack of mobility, other complications can occur. Complications may include muscle and joint stiffness, loss of aerobic fitness, muscle spasms, bed sores, pressure ulcers and blood clots.

Sudden recovery from hemiplegia is very rare. Many of the individuals will have limited recovery, but the majority will improve from intensive, specialised rehabilitation. Potential to progress may differ in cerebral palsy, compared to adult acquired brain injury. It is vital to integrate the hemiplegic child into society and encourage them in their daily living activities. With time, some individuals may make remarkable progress.

IMAGES

PARALYSIS (Stroke, Hemiplegia) - Pandari, Nizamabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

High BP, Left sided Paralysis. Speech not clear. Was treated by specialists of Nizamabad but without any improvement even after 10 days

MODE OF RECOVERY AT NEW LIFE CENTRE

Speech recovered fully and the power in his left limbs was fully recovered in just 15 days only.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Hemiplegia is paralysis of the arm, leg, and trunk on the same side of the body. Hemiplegia is more severe than hemiparesis, where in one half of the body has less marked weakness. Hemiplegia and hemiparesis may be congenital, or they might be acquired conditions resulting from an illness, an injury, or a stroke.

SIGNS AND SYMPTOMS

Hemiplegia means severe weakness of the limbs on one side of the body but the specific features can vary tremendously from person to person. Problems may include :

  • Difficulty with gait.
  • Difficulty with balance while standing or walking.
  • Increasing stiffness of muscles.
  • Muscle spasms.
  • The majority of children who develop hemiplegia also have abnormal mental development.
  • Behavior problems like anxiety, anger, irritability, lack of concentration or comprehension.
  • Emotions — depression.
  • Shoulder pain — Often associated with a loss of external rotation of the glenohumeral joint, commonly due to the increased tone of the Subscapularis muscle and Pectoralis major muscle.
  • Shoulder Subluxation.

CAUSES

The most common cause of hemiplegia is stroke. Strokes can cause a variety of movement disorders, depending on the location and severity of the lesion. Hemiplegia is common when the stroke affects the corticospinal tract. Other causes of hemiplegia include spinal cord injury, specifically Brown-Séquard syndrome, traumatic brain injury, or disease affecting the brain. As a lesion that results in hemiplegia occurs in the brain or spinal cord, hemiplegic muscles display features of the Upper Motor Neuron Syndrome. Features other than weakness include decreased movement control, clonus (a series of involuntary rapid muscle contractions), spasticity, exaggerated deep tendon reflexes and decreased endurance.

The incidence of hemiplegia is much higher in premature babies than term babies. There is also a high incidence of hemiplegia during pregnancy and experts believe that this may be related to either a traumatic delivery, use of forceps or some event which causes brain injury.

Other causes of hemiplegia in adults include trauma, bleeding, brain infections and cancers. Individuals who have uncontrolled diabetes, hypertension or those who smoke have a higher chance of developing a stroke. Weakness on one side of the face may occur and may be due to a viral infection, stroke or a cancer.

COMMON CAUSES BY ETIOLOGY

  • VASCULAR: cerebral hemorrhage, stroke, diabetic neuropathy
  • INFECTIVE: encephalitis, meningitis, brain abscess
  • NEOPLASTIC: glioma-meningioma
  • DEMYELINATION: disseminated sclerosis, lesions to the internal capsule
  • TRAUMATIC: cerebral lacerations, subdural hematoma rare cause of hemiplegia is due to local anaesthetic injections given intra-arterially rapidly, instead of given in a nerve branch.
  • CONGENITAL: cerebral palsy
  • DISSEMINATED: multiple sclerosis
  • PSYCHOLOGICAL: parasomnia (nocturnal hemiplegia)

PATHOGENESIS

The exact cause of hemiplegia is not known in all cases, but it appears that the brain is deprived of oxygen and this results in the death of neurons. When the corticospinal tract is damaged, the injury is usually manifested on the opposite side of the body. For example if one has an injury to the right side of the brain, the hemiplegia will be on the left side of the body. This happens because the motor fibres of corticospinal tract ( also called pyramidal fibres), which take origin from the motor cortex in brain, cross to the opposite side in the lower part of medulla oblangata and then descend down in spinal cord to supply their respective muscles. Depending on the site of lesion in brain, the severity of hemiplegia varies. A lesion in internal capsule where all the motor fibres are condensed in a small area, will cause dense hemiplegia i.e. complete loss of power of all muscles of one half of body while a lesion at cortical or subcortical level will cause varied amount of weakness of one half of the body.

DIAGNOSIS

Hemiplegia is identified by clinical examination by a health professional, such as a physiotherapist or doctor. Radiological studies like a CT scan or magnetic resonance imaging of the brain should be used to confirm injury in the brain and spinal cord, but alone cannot be used to identify movement disorders. Individuals who develop seizures may undergo tests to determine where the focus of excess electrical activity is.

Hemiplegia patients usually show a characteristic gait. The leg on the affected side is extended and internally rotated and is swung in a wide, lateral arc rather than lifted in order to move it forward. The upper limb on the same side is also adducted at the shoulder, flexed at the elbow, and pronated at the wrist with the thumb tucked into the palm and the fingers curled around it.

TREATMENT

Treatment should be based on assessment by the relevant health professionals, including physiotherapists, doctors and occupational therapists. Muscles with severe motor impairment including weakness need these therapists to assist them with specific exercise, and are likely to require help to do this.

Pharmacological

Drugs can be used to treat issues related to the Upper Motor Neuron Syndrome. Drugs like Librium or Valium could be used as a relaxant. Drugs are also given to individuals who have recurrent seizures, which may be a separate but related problem after brain injury.

Surgery

Surgery may be used if the individual develops a secondary issue of contracture, from a severe imbalance of muscle activity. In such cases the surgeon may cut the ligaments and relieve joint contractures. Individuals who are unable to swallow may have a tube inserted into the stomach. This allows food to be given directly into the stomach. The food is in liquid form and instilled at low rates. Some individuals with hemiplegia will benefit from some type of prosthetic device. There are many types of braces and splints available to stabilize a joint, assist with walking and keep the upper body erect.

Rehabilitation

Rehabilitation is the main treatment of individuals with hemiplegia. In all cases, the major aim of rehabilitation is to regain maximum function and quality of life. Both physical and occupational therapy can significantly improve the quality of life.

Physical Therapy

Physical therapy (PT) can help improve muscle strength & coordination, mobility (such as standing and walking), and other physical function using different sensorimotor techniques. Physiotherapists can also help reduce shoulder pain by maintaining shoulder range of motion, as well as using Functional electrical stimulation.[11] Supportive devices, such as braces or slings, can be used to help prevent or treat shoulder subluxation in the hopes to minimize disability and pain. It should be noted that although many individuals suffering from stroke experience both shoulder pain and shoulder subluxation, the two are mutually exclusive. A treatment method that can be implemented with the goal of helping to regain motor function in the affected limb is constraint-induced movement therapy. This consists of constraining the unaffected limb, forcing the affected limb to accomplish tasks of daily living.

Occupational Therapy

Occupational therapy Occupational Therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening hand, shoulder and torso, and participating in activities of daily living (ADLs), such as eating and dressing. Therapists may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your child’s hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual - which may include, environmental modification, use of adaptive equipment, sensory integration, etc.

Constraint-Induced Movement Therapy

Constraint-induced movement therapy (CI or CIMT) is a form of rehabilitation therapy that improves upper extremity function, especially in cases of hemiplegia.

ASSESSMENT TOOLS

There are a variety of standardized assessment scales available to physiotherapists and other health care professionals for use in the ongoing evaluation of the status of a patient’s hemiplegia. The use of standardized assessment scales may help physiotherapists and other health care professionals during the course of their treatment plant to:

  • Prioritize treatment interventions based on specific identifiable motor and sensory deficits.
  • Create appropriate short and long term goals for treatment based on the outcome of the scales, their professional expertise and the desires of the patient.
  • Evaluate the potential burden of care and monitor any changes based on either improving or declining scores.

Some of the most commonly used scales in the assessment of hemiplegia are:

The Fugl-Meyer Assessment of Physical Performance (FMA)

The FMA is often used as a measure of functional or physical impairment following a cerebrovascular accident(CVA). It measures sensory and motor impairment of the upper and lower extremities, balance in several positions, range of motion, and pain. This test is a reliable and valid measure in measuring post-stroke impairments related to stroke recovery. A lower score in each component of the test indicates higher impairment and a lower functional level for that area. The maximum score for each component is 66 for the upper extremities, 34 for the lower extremities, and 14 for balance. Administration of the FMA should be done after reviewing a training manual.

The Chedoke-McMaster Stroke Assessment (CMSA)

This test is a reliable measure of two separate components evaluating both motor impairment and disability. The disability component assesses any changes in physical function including gross motor function and walking ability. The disability inventory can have a maximum score of 100 with 70 from the gross motor index and 30 from the walking index. Each task in this inventory has a maximum score of seven except for the 2 minute walk test which is out of two. The impairment component of the test evaluates the upper and lower extremities, postural control and pain. The impairment inventory focuses on the seven stages of recovery from stroke from flaccid paralysis to normal motor functioning. A training workshop is recommended if the measure is being utilized for the purpose of data collection.

The Stroke Rehabilitation Assessment of Movement (STREAM)

The STREAM consists of 30 test items involving upper-limb movements, lower-limb movements, and basic mobility items. It is a clinical measure of voluntary movements and general mobility (rolling, bridging, sit-to-stand, standing, stepping, walking and stairs) following a stroke. The voluntary movement part of the assessment is measured using a 3-point ordinal scale (unable to perform, partial performance, and complete performance) and the mobility part of the assessment uses a 4-point ordinal scale (unable, partial, complete with aid, complete no aid). The maximum score one can receive on the STREAM is a 70 (20 for each limb score and 30 for mobility score). The higher the score, the better movement and mobility is available for the individual being scored.

PROGNOSIS

Hemiplegia is not a progressive disorder, except in progressive conditions like a growing brain tumour. Once the injury has occurred, the symptoms should not worsen. However, because of lack of mobility, other complications can occur. Complications may include muscle and joint stiffness, loss of aerobic fitness, muscle spasms, bed sores, pressure ulcers and blood clots.

Sudden recovery from hemiplegia is very rare. Many of the individuals will have limited recovery, but the majority will improve from intensive, specialised rehabilitation. Potential to progress may differ in cerebral palsy, compared to adult acquired brain injury. It is vital to integrate the hemiplegic child into society and encourage them in their daily living activities. With time, some individuals may make remarkable progress.

IMAGES

MULTIPLE SCLEROSIS - Saritha

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Numbness, weakness in left arm with stiffness and deformity of two fingers and numbness of trunk from neck to the level of navel.also diabetic. Neurophycisians were not able help and advised me to proceed to CMC Vellore for expert care

MODE OF RECOVERY AT NEW LIFE CENTRE

Started treatment on 31-10-2010 at NEW LIFE. I have recovered to a large extent except for mild degree of diabetes and little numbness. I am now able to continue my studies and work as usual.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Multiple sclerosis (MS), also known as disseminated sclerosis or encephalomyelitis disseminata, is an inflammatory disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged. This damage disrupts the ability of parts of the nervous system to communicate, resulting in a wide range of signs and symptoms, including physical, mental, and sometimes psychiatric problems. MS takes several forms, with new symptoms either occurring in isolated attacks (relapsing forms) or building up over time (progressive forms). Between attacks, symptoms may disappear completely; however, permanent neurological problems often occur, especially as the disease advances.

While the cause is not clear, the underlying mechanism is thought to be either destruction by the immune system or failure of the myelin-producing cells. Proposed causes for this include genetics and environmental factors such as infections. MS is usually diagnosed based on the presenting signs and symptoms and the results of supporting medical tests.

There is no known cure for multiple sclerosis. Treatments attempt to improve function after an attack and prevent new attacks. Medications used to treat MS while modestly effective can have adverse effects and be poorly tolerated. Many people pursue alternative treatments, despite a lack of evidence. The long-term outcome is difficult to predict, with good outcomes more often seen in women, those who develop the disease early in life, those with a relapsing course, and those who initially experienced few attacks. Life expectancy is 5 to 10 years lower than that of an unaffected population.

SIGNS AND SYMPTONS

A person with MS can have almost any neurological symptom or sign; with autonomic, visual, motor, and sensory problems being the most common. The specific symptoms are determined by the locations of the lesions within the nervous system, and may include loss of sensitivity or changes in sensation such as tingling, pins and needles or numbness, muscle weakness, very pronounced reflexes, muscle spasms, or difficulty in moving; difficulties with coordination and balance (ataxia); problems with speech or swallowing, visual problems (nystagmus, optic neuritis or double vision), feeling tired, acute or chronic pain, and bladder and bowel difficulties, among others. Difficulties thinking and emotional problems such as depression or unstable mood are also common. Uhthoff's phenomenon, a worsening of symptoms due to exposure to higher than usual temperatures, and Lhermitte's sign, an electrical sensation that runs down the back when bending the neck, are particularly characteristic of MS. The main measure of disability and severity is the expanded disability status scale (EDSS), with other measures such as the multiple sclerosis functional composite being increasingly used in research.

The condition begins in 85% of cases as a clinically isolated syndrome over a number of days with 45% having motor or sensory problems, 20% having optic neuritis, and 10% having symptoms related to brainstem dysfunction, while the remaining 25% have more than one of the previous difficulties. The course of symptoms occurs in two main patterns initially: either as episodes of sudden worsening that last a few days to months (called relapses, exacerbations, bouts, attacks, or flare-ups) followed by improvement (85% of cases) or as a gradual worsening over time without periods of recovery (10-15% of cases). A combination of these two patterns may also occur or people may start in a relapsing and remitting course that then becomes progressive later on. Relapses are usually not predictable, occurring without warning. Exacerbations rarely occur more frequently than twice per year. Some relapses, however, are preceded by common triggers and they occur more frequently during spring and summer. Similarly, viral infections such as the common cold, influenza, or gastroenteritis increase their risk. Stress may also trigger an attack. Women with MS who become pregnant experience fewer relapses; however, during the first months after delivery the risk increases. Overall, pregnancy does not seem to influence long-term disability. Many events have not been found to affect relapse rates including vaccination, breast feeding, physical trauma, and Uhthoff's phenomenon.

CAUSES

The cause of MS is unknown; however, it is believed to occur as a result of some combination of environmental factors such as infectious agents and genetics. Theories try to combine the data into likely explanations, but none has proved definitive. While there are a number of environmental risk factors and although some are partly modifiable, further research is needed to determine whether their elimination can prevent MS.

Geography

MS is more common in people who live farther from the equator, although exceptions exist. These exceptions include ethnic groups that are at low risk far from the equator such as the Samis, Amerindians, Canadian Hutterites, New Zealand Māori, and Canada's Inuit, as well as groups that have a relatively high risk close to the equator such as Sardinians, Palestinians and Parsis. The cause of this geographical pattern is not clear. While the north-south gradient of incidence is decreasing, as of 2010 it is still present.

MS is more common in regions with northern European populations and the geographic variation may simply reflect the global distribution of these high-risk populations. Decreased sunlight exposure resulting in decreased vitamin D production has also been put forward as an explanation. A relationship between season of birth and MS lends support to this idea, with fewer people born in the northern hemisphere in November as compared to May being affected later in life. Environmental factors may play a role during childhood, with several studies finding that people who move to a different region of the world before the age of 15 acquire the new region's risk to MS. If migration takes place after age 15, however, the person retains the risk of his home country. There is some evidence that the effect of moving may still apply to people older than 15.

Genetics

MS is not considered a hereditary disease; however, a number of genetic variations have been shown to increase the risk. The probability is higher in relatives of an affected person, with a greater risk among those more closely related. In identical twins both are affected about 30% of the time, while around 5% for non-identical twins and 2.5% of siblings are affected with a lower percentage of half-siblings. If both parents are affected the risk in their children is 10 times that of the general population. MS is also more common in some ethnic groups than others.

Specific genes that have been linked with MS include differences in the human leukocyte antigen (HLA) system—a group of genes on chromosome 6 that serves as the major histocompatibility complex (MHC). That changes in the HLA region are related to susceptibility has been known for over thirty years, and additionally this same region has been implicated in the development of other autoimmune diseases such as diabetes type I and systemic lupus erythematosus. The most consistent finding is the association between multiple sclerosis and alleles of the MHC defined as DR15 and DQ6. Other loci have shown a protective effect, such as HLA-C554 and HLA-DRB1*11. Overall, it has been estimated that HLA changes account for between 20 and 60% of the genetic predisposition. Modern genetic methods (genome-wide association studies) have discovered at least twelve other genes outside the HLA locus that modestly increase the probability of MS.

Infectious agents

Many microbes have been proposed as triggers of MS, but none have been confirmed. Moving at an early age from one location in the world to another alters a person's subsequent risk of MS. An explanation for this could be that some kind of infection, produced by a widespread microbe rather than a rare one, is related to the disease. Proposed mechanisms include the hygiene hypothesis and the prevalence hypothesis. The hygiene hypothesis proposes that exposure to certain infectious agents early in life is protective, the disease being a response to a late encounter with such agents. The prevalence hypothesis proposes that the disease is due to an infectious agent more common in regions where MS is common and where in most individuals it causes an ongoing infection without symptoms. Only in a few cases and after many years does it cause demyelination. The hygiene hypothesis has received more support than the prevalence hypothesis.

Evidence for a virus as a cause include: the presence of oligoclonal bands in the brain and cerebrospinal fluid of most people with MS, the association of several viruses with human demyelination encephalomyelitis, and the occurrence of demyelination in animals caused by some viral infection. Human herpes viruses are a candidate group of viruses. Individuals having never been infected by the Epstein-Barr virus are at a reduced risk of getting MS, whereas those infected as young adults are at a greater risk than those having had it at a younger age. Although some consider that this goes against the hygiene hypothesis, since the non-infected have probably experienced a more hygienic upbringing, others believe that there is no contradiction, since it is a first encounter with the causative virus relatively late in life that is the trigger for the disease. Other diseases that may be related include measles, mumps and rubella.

Other

Smoking has been shown to be an independent risk factor for MS. Stress may be a risk factor although the evidence to support this is weak. Association with occupational exposures and toxins—mainly solvents—has been evaluated, but no clear conclusions have been reached. Vaccinations were studied as causal factors; however, most studies show no association. Several other possible risk factors, such as diet and hormone intake, have been looked at; however, evidence on their relation with the disease is "sparse and unpersuasive". Gout occurs less than would be expected and lower levels of uric acid have been found in people with MS. This has led to the theory that uric acid is protective, although its exact importance remains unknown.

PATHOPHYSIOLOGY

The three main characteristics of MS are the formation of lesions in the central nervous system (also called plaques), inflammation, and the destruction of myelin sheaths of neurons. These features interact in a complex and not yet fully understood manner to produce the breakdown of nerve tissue and in turn the signs and symptoms of the disease. Additionally MS is believed to be an immune-mediated disorder that develops from an interaction of the individual's genetics and as yet unidentified environmental causes. Damage is believed to be caused, at least in part, by attack on the nervous system by a person's own immune system.

Lesions

The name multiple sclerosis refers to the scars (sclerae – better known as plaques or lesions) that form in the nervous system. These lesions most commonly affect the white matter in the optic nerve, brain stem, basal ganglia, and spinal cord, or white matter tracts close to the lateral ventricles. The function of white matter cells is to carry signals between grey matter areas, where the processing is done, and the rest of the body. The peripheral nervous system is rarely involved.

To be specific, MS involves the loss of oligodendrocytes, the cells responsible for creating and maintaining a fatty layer—known as the myelin sheath—which helps the neurons carry electrical signals (action potentials). This results in a thinning or complete loss of myelin and, as the disease advances, the breakdown of the axons of neurons. When the myelin is lost, a neuron can no longer effectively conduct electrical signals. A repair process, called remyelination, takes place in early phases of the disease, but the oligodendrocytes are unable to completely rebuild the cell's myelin sheath. Repeated attacks lead to successively less effective remyelinations, until a scar-like plaque is built up around the damaged axons. These scars are the origin of the symptoms and during an attack magnetic resonance imaging (MRI) often shows more than ten new plaques. This could indicate that there are a number of lesions below which the brain is capable of repairing itself without producing noticeable consequences. Another process involved in the creation of lesions is an abnormal increase in the number of astrocytes due to the destruction of nearby neurons. A number of lesion patterns have been described.

Inflamation

Apart from demyelination, the other sign of the disease is inflammation. Fitting with an immunological explanation, the inflammatory process is caused by T cells, a kind of lymphocyte that plays an important role in the body's defenses. T cells gain entry into the brain via disruptions in the blood–brain barrier. The T cells recognize myelin as foreign and attack it, explaining why these cells are also called "autoreactive lymphocytes".

The attack of myelin starts inflammatory processes, which triggers other immune cells and the release of soluble factors like cytokines and antibodies. Further breakdown of the blood–brain barrier, in turn cause a number of other damaging effects such as swelling, activation of macrophages, and more activation of cytokines and other destructive proteins. Inflammation can potentially reduce transmission of information between neurons in at least three ways. The soluble factors released might stop neurotransmission by intact neurons. These factors could lead to or enhance the loss of myelin, or they may cause the axon to break down completely.

Blood brain barrier

The blood–brain barrier is a part of the capillary system that prevents the entry of T cells into the central nervous system. It may become permeable to these types of cells secondary to an infection by a virus or bacteria. After it repairs itself, typically once the infection has cleared, T cells may remain trapped inside the brain. Gadolinium cannot cross a normal BBB and, therefore, Gadolinium-enhanced MRI is used to show BBB breakdowns.

DIAGNOSIS

Multiple sclerosis is typically diagnosed based on the presenting signs and symptoms, in combination with supporting medical imaging and laboratory testing. It can be difficult to confirm, especially early on, since the signs and symptoms may be similar to those of other medical problems. The McDonald criteria, which focus on clinical, laboratory, and radiologic evidence of lesions at different times and in different areas, is the most commonly used method of diagnosis with the Schumacher and Poser criteria being of mostly historical significance. While the above criteria allow for a non-invasive diagnosis, some state that the only definitive proof is an autopsy or biopsy where lesions typical of MS are detected.

Clinical data alone may be sufficient for a diagnosis of MS if an individual has had separate episodes of neurologic symptoms characteristic of the disease. In those who seek medical attention after only one attack, other testing is needed for the diagnosis. The most commonly used diagnostic tools are neuroimaging, analysis of cerebrospinal fluid and evoked potentials. Magnetic resonance imaging of the brain and spine may show areas of demyelination (lesions or plaques). Gadolinium can be administered intravenously as a contrast agent to highlight active plaques and, by elimination, demonstrate the existence of historical lesions not associated with symptoms at the moment of the evaluation. Testing of cerebrospinal fluid obtained from a lumbar puncture can provide evidence of chronic inflammation in the central nervous system. The cerebrospinal fluid is tested for oligoclonal bands of IgG on electrophoresis, which are inflammation markers found in 75–85% of people with MS. The nervous system in MS may respond less actively to stimulation of the optic nerve and sensory nerves due to demyelination of such pathways. These brain responses can be examined using visual- and sensory-evoked potentials.

Clinical Courses

Several subtypes, or patterns of progression, have been described. Subtypes use the past course of the disease in an attempt to predict the future course. They are important not only for prognosis but also for treatment decisions. In 1996, the United States National Multiple Sclerosis Society described four clinical courses:

  • relapsing remitting
  • secondary progressive
  • primary progressive
  • progressive relapsing

The relapsing-remitting subtype is characterized by unpredictable relapses followed by periods of months to years of relative quiet (remission) with no new signs of disease activity. Deficits that occur during attacks may either resolve or leave problems, the latter in about 40% of attacks and being more common the longer a person has had the disease. This describes the initial course of 80% of individuals with MS. When deficits always resolve between attacks, this is sometimes referred to as benign MS, although people will still build up some degree of disability in the long term. On the other hand, the term malignant multiple sclerosis is used to describe people with MS having reached significant level of disability in a short period of time. The relapsing-remitting subtype usually begins with a clinically isolated syndrome (CIS). In CIS, a person has an attack suggestive of demyelination, but does not fulfill the criteria for multiple sclerosis. 30 to 70% of persons experiencing CIS later develop MS.

Secondary progressive MS occurs in around 65% of those with initial relapsing-remitting MS, who eventually have progressive neurologic decline between acute attacks without any definite periods of remission. Occasional relapses and minor remissions may appear. The most common length of time between disease onset and conversion from relapsing-remitting to secondary progressive MS is 19 years. The primary progressive subtype occurs in approximately 10–20% of individuals, with no remission after the initial symptoms. It is characterized by progression of disability from onset, with no, or only occasional and minor, remissions and improvements. The usual age of onset for the primary progressive subtype is later than of the relapsing-remitting subtype. It is similar to the age that secondary progressive usually begins in relapsing-remitting MS, around 40 years of age.

Progressive relapsing MS describes those individuals who, from onset, have a steady neurologic decline but also have clear superimposed attacks. This is the least common of all subtypes.

Unusual types of MS have been described; these include Devic's disease, Balo concentric sclerosis, Schilder's diffuse sclerosis, and Marburg multiple sclerosis. There is debate on whether they are MS variants or different diseases. Multiple sclerosis behaves differently in children, taking more time to reach the progressive stage. Nevertheless, they still reach it at a lower average age than adults usually do.

MANAGEMENT

Although there is no known cure for multiple sclerosis, several therapies have proven helpful. The primary aims of therapy are returning function after an attack, preventing new attacks, and preventing disability. As with any medical treatment, medications used in the management of MS have several adverse effects. Alternative treatments are pursued by some people, despite the shortage of supporting evidence.

Acute Attacks

During symptomatic attacks, administration of high doses of intravenous corticosteroids, such as methylprednisolone, is the usual therapy, with oral corticosteroids seeming to have a similar efficacy and safety profile. Although, in general, effective in the short term for relieving symptoms, corticosteroid treatments do not appear to have a significant impact on long-term recovery. The consequences of severe attacks that do not respond to corticosteroids might be treatable by plasmapheresis.

DISEASE MODIFYING TREATMENTS

Relapsing remitting multiple sclerosis

Eight disease-modifying treatments have been approved by regulatory agencies for relapsing-remitting multiple sclerosis (RRMS) including: interferon beta-1a, interferon beta-1b, glatiramer acetate, mitoxantrone, natalizumab, fingolimod, teriflunomide and dimethyl fumarate. Their cost effectiveness as of 2012 is unclear.

In RRMS they are modestly effective at decreasing the number of attacks. The interferons and glatiramer acetate are first-line treatments and are roughly equivalent, reducing relapses by approximately 30%. Early-initiated long-term therapy is safe and improves outcomes. Natalizumab reduces the relapse rate more than first-line agents; however, due to issues of adverse effects is a second-line agent reserved for those who do not respond to other treatments or with severe disease. Mitoxantrone, whose use is limited by severe adverse effects, is a third-line option for those who do not respond to other medications. Treatment of clinically isolated syndrome (CIS) with interferons decreases the chance of progressing to clinical MS. Efficacy of interferons and glatiramer acetate in children has been estimated to be roughly equivalent to that of adults. The role of some of the newer agents such as fingolimod, teriflunomide, and dimethyl fumarate, as of 2011, is not yet entirely clear.

Progressive multiple sclerosis

No treatment has been shown to change the course of primary progressive MS and as of 2011 only one medication, mitoxantrone, has been approved for secondary progressive MS. In this population tentative evidence supports mitoxantrone moderately slowing the progression of the disease and decreasing rates of relapses over two years.

Adverse effects

The disease-modifying treatments have several adverse effects. One of the most common is irritation at the injection site for glatiramer acetate and the interferons (up to 90% with subcutaneous injections and 33% with intramuscular injections). Over time, a visible dent at the injection site, due to the local destruction of fat tissue, known as lipoatrophy, may develop. Interferons may produce flu-like symptoms; some people taking glatiramer experience a post-injection reaction with flushing, chest tightness, heart palpitations, breathlessness, and anxiety, which usually lasts less than thirty minutes.[64] More dangerous but much less common are liver damage from interferons,systolic dysfunction (12%), infertility, and acute myeloid leukemia (0.8%) from mitoxantrone, and progressive multifocal leukoencephalopathy occurring with natalizumab (occurring in 1 in 600 people treated).

Fingolimod may give rise to hypertension and bradycardia, macular edema, elevated liver enzymes or a reduction in lymphocyte levels. Tentative evidence supports the short term safety of teriflunomide, with common side effects including: headaches, fatigue, nausea, hair loss, and limb pain. There have also been reports of liver failure and PML with its use and it is dangerous for fetal development. Most common side effects of dimethyl fumarate are flushing and gastrointestinal problems. While dimethyl fumarate may lead to a reduction in the white blood cell count there were no reported cases of opportunistic infections during trials.

Associated symptoms

Both medications and neurorehabilitation have been shown to improve some symptoms, though neither changes the course of the disease. Some symptoms have a good response to medication, such as an unstable bladder and spasticity, while others are little changed. For neurologic problems, a multidisciplinary approach is important for improving quality of life; however, it is difficult to specify a 'core team' as many different health services may be needed at different points in time. Multidisciplinary rehabilitation programs increase activity and participation of people with MS but do not influence impairment level. There is limited evidence for the overall efficacy of individual therapeutic disciplines, though there is good evidence that specific approaches, such as exercise, and psychology therapies, in particular cognitive behavioral approaches are effective.

ALTERNATIVE TREATMENTS

Over 50% of people with MS may use complementary and alternative medicine, although percentages vary depending on how alternative medicine is defined. The evidence for the effectiveness for such treatments in most cases is weak or absent. Treatments of unproven benefit used by people with MS include: dietary supplementation and regimens, vitamin D,[81] relaxation techniques such as yoga, herbal medicine (including medical cannabis), hyperbaric oxygen therapy, self-infection with hookworms, reflexology and acupuncture. Regarding the characteristics of users, they are more frequently women, have had MS for a longer time, tend to be more disabled and have lower levels of satisfaction with conventional healthcare.

PROGNOSIS

The expected future course of the disease depends on the subtype of the disease; the individual's sex, age, and initial symptoms; and the degree of disability the person has. Female sex, relapsing-remitting subtype, optic neuritis or sensory symptoms at onset, few attacks in the initial years and especially early age at onset, are associated with a better course.

The average life expectancy is 30 years from onset, which is 5 to 10 years lower than that of unaffected people. Almost 40% of people with MS reach the seventh decade of life. Nevertheless, two-thirds of the deaths are directly related to the consequences of the disease. Suicide is more common, while infections and other complications are especially dangerous for the more disabled. Although most people lose the ability to walk before death, 90% are capable of independent walking at 10 years from onset, and 75% at 15 years.

IMAGES

PARALYSIS (Stroke, Hemiplegia) - Saraswathi, Siddipet, Medak

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Diabetes, Left sided Paralysis. Was treated by specialists of Siddipet and Neurophysicians of a Corporate Hospital, Kachiguda. She was semiconscious,speech difficult. Not swallowing and no power in left limbs even after 23 days of their intensive care.

MODE OF RECOVERY AT NEW LIFE CENTRE

Recovered consciousness, speech and 80% power in left upper limb in just one day. Left leg gained 70% power in 15 days only. Sugar level came down a lot.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Hemiplegia is paralysis of the arm, leg, and trunk on the same side of the body. Hemiplegia is more severe than hemiparesis, where in one half of the body has less marked weakness. Hemiplegia and hemiparesis may be congenital, or they might be acquired conditions resulting from an illness, an injury, or a stroke.

SIGNS AND SYMPTOMS

Hemiplegia means severe weakness of the limbs on one side of the body but the specific features can vary tremendously from person to person. Problems may include :

  • Difficulty with gait.
  • Difficulty with balance while standing or walking.
  • Increasing stiffness of muscles.
  • Muscle spasms.
  • The majority of children who develop hemiplegia also have abnormal mental development.
  • Behavior problems like anxiety, anger, irritability, lack of concentration or comprehension.
  • Emotions — depression.
  • Shoulder pain — Often associated with a loss of external rotation of the glenohumeral joint, commonly due to the increased tone of the Subscapularis muscle and Pectoralis major muscle.
  • Shoulder Subluxation.

CAUSES

The most common cause of hemiplegia is stroke. Strokes can cause a variety of movement disorders, depending on the location and severity of the lesion. Hemiplegia is common when the stroke affects the corticospinal tract. Other causes of hemiplegia include spinal cord injury, specifically Brown-Séquard syndrome, traumatic brain injury, or disease affecting the brain. As a lesion that results in hemiplegia occurs in the brain or spinal cord, hemiplegic muscles display features of the Upper Motor Neuron Syndrome. Features other than weakness include decreased movement control, clonus (a series of involuntary rapid muscle contractions), spasticity, exaggerated deep tendon reflexes and decreased endurance.

The incidence of hemiplegia is much higher in premature babies than term babies. There is also a high incidence of hemiplegia during pregnancy and experts believe that this may be related to either a traumatic delivery, use of forceps or some event which causes brain injury.

Other causes of hemiplegia in adults include trauma, bleeding, brain infections and cancers. Individuals who have uncontrolled diabetes, hypertension or those who smoke have a higher chance of developing a stroke. Weakness on one side of the face may occur and may be due to a viral infection, stroke or a cancer.

COMMON CAUSES BY ETIOLOGY

  • VASCULAR: cerebral hemorrhage, stroke, diabetic neuropathy
  • INFECTIVE: encephalitis, meningitis, brain abscess
  • NEOPLASTIC: glioma-meningioma
  • DEMYELINATION: disseminated sclerosis, lesions to the internal capsule
  • TRAUMATIC: cerebral lacerations, subdural hematoma rare cause of hemiplegia is due to local anaesthetic injections given intra-arterially rapidly, instead of given in a nerve branch.
  • CONGENITAL: cerebral palsy
  • DISSEMINATED: multiple sclerosis
  • PSYCHOLOGICAL: parasomnia (nocturnal hemiplegia)

PATHOGENESIS

The exact cause of hemiplegia is not known in all cases, but it appears that the brain is deprived of oxygen and this results in the death of neurons. When the corticospinal tract is damaged, the injury is usually manifested on the opposite side of the body. For example if one has an injury to the right side of the brain, the hemiplegia will be on the left side of the body. This happens because the motor fibres of corticospinal tract ( also called pyramidal fibres), which take origin from the motor cortex in brain, cross to the opposite side in the lower part of medulla oblangata and then descend down in spinal cord to supply their respective muscles. Depending on the site of lesion in brain, the severity of hemiplegia varies. A lesion in internal capsule where all the motor fibres are condensed in a small area, will cause dense hemiplegia i.e. complete loss of power of all muscles of one half of body while a lesion at cortical or subcortical level will cause varied amount of weakness of one half of the body.

DIAGNOSIS

Hemiplegia is identified by clinical examination by a health professional, such as a physiotherapist or doctor. Radiological studies like a CT scan or magnetic resonance imaging of the brain should be used to confirm injury in the brain and spinal cord, but alone cannot be used to identify movement disorders. Individuals who develop seizures may undergo tests to determine where the focus of excess electrical activity is.

Hemiplegia patients usually show a characteristic gait. The leg on the affected side is extended and internally rotated and is swung in a wide, lateral arc rather than lifted in order to move it forward. The upper limb on the same side is also adducted at the shoulder, flexed at the elbow, and pronated at the wrist with the thumb tucked into the palm and the fingers curled around it.

TREATMENT

Treatment should be based on assessment by the relevant health professionals, including physiotherapists, doctors and occupational therapists. Muscles with severe motor impairment including weakness need these therapists to assist them with specific exercise, and are likely to require help to do this.

Pharmacological

Drugs can be used to treat issues related to the Upper Motor Neuron Syndrome. Drugs like Librium or Valium could be used as a relaxant. Drugs are also given to individuals who have recurrent seizures, which may be a separate but related problem after brain injury.

Surgery

Surgery may be used if the individual develops a secondary issue of contracture, from a severe imbalance of muscle activity. In such cases the surgeon may cut the ligaments and relieve joint contractures. Individuals who are unable to swallow may have a tube inserted into the stomach. This allows food to be given directly into the stomach. The food is in liquid form and instilled at low rates. Some individuals with hemiplegia will benefit from some type of prosthetic device. There are many types of braces and splints available to stabilize a joint, assist with walking and keep the upper body erect.

Rehabilitation

Rehabilitation is the main treatment of individuals with hemiplegia. In all cases, the major aim of rehabilitation is to regain maximum function and quality of life. Both physical and occupational therapy can significantly improve the quality of life.

Physical Therapy

Physical therapy (PT) can help improve muscle strength & coordination, mobility (such as standing and walking), and other physical function using different sensorimotor techniques. Physiotherapists can also help reduce shoulder pain by maintaining shoulder range of motion, as well as using Functional electrical stimulation.[11] Supportive devices, such as braces or slings, can be used to help prevent or treat shoulder subluxation in the hopes to minimize disability and pain. It should be noted that although many individuals suffering from stroke experience both shoulder pain and shoulder subluxation, the two are mutually exclusive. A treatment method that can be implemented with the goal of helping to regain motor function in the affected limb is constraint-induced movement therapy. This consists of constraining the unaffected limb, forcing the affected limb to accomplish tasks of daily living.

Occupational Therapy

Occupational therapy Occupational Therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening hand, shoulder and torso, and participating in activities of daily living (ADLs), such as eating and dressing. Therapists may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your child’s hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual - which may include, environmental modification, use of adaptive equipment, sensory integration, etc.

Constraint-Induced Movement Therapy

Constraint-induced movement therapy (CI or CIMT) is a form of rehabilitation therapy that improves upper extremity function, especially in cases of hemiplegia.

ASSESSMENT TOOLS

There are a variety of standardized assessment scales available to physiotherapists and other health care professionals for use in the ongoing evaluation of the status of a patient’s hemiplegia. The use of standardized assessment scales may help physiotherapists and other health care professionals during the course of their treatment plant to:

  • Prioritize treatment interventions based on specific identifiable motor and sensory deficits.
  • Create appropriate short and long term goals for treatment based on the outcome of the scales, their professional expertise and the desires of the patient.
  • Evaluate the potential burden of care and monitor any changes based on either improving or declining scores.

Some of the most commonly used scales in the assessment of hemiplegia are:

The Fugl-Meyer Assessment of Physical Performance (FMA)

The FMA is often used as a measure of functional or physical impairment following a cerebrovascular accident(CVA). It measures sensory and motor impairment of the upper and lower extremities, balance in several positions, range of motion, and pain. This test is a reliable and valid measure in measuring post-stroke impairments related to stroke recovery. A lower score in each component of the test indicates higher impairment and a lower functional level for that area. The maximum score for each component is 66 for the upper extremities, 34 for the lower extremities, and 14 for balance. Administration of the FMA should be done after reviewing a training manual.

The Chedoke-McMaster Stroke Assessment (CMSA)

This test is a reliable measure of two separate components evaluating both motor impairment and disability. The disability component assesses any changes in physical function including gross motor function and walking ability. The disability inventory can have a maximum score of 100 with 70 from the gross motor index and 30 from the walking index. Each task in this inventory has a maximum score of seven except for the 2 minute walk test which is out of two. The impairment component of the test evaluates the upper and lower extremities, postural control and pain. The impairment inventory focuses on the seven stages of recovery from stroke from flaccid paralysis to normal motor functioning. A training workshop is recommended if the measure is being utilized for the purpose of data collection.

The Stroke Rehabilitation Assessment of Movement (STREAM)

The STREAM consists of 30 test items involving upper-limb movements, lower-limb movements, and basic mobility items. It is a clinical measure of voluntary movements and general mobility (rolling, bridging, sit-to-stand, standing, stepping, walking and stairs) following a stroke. The voluntary movement part of the assessment is measured using a 3-point ordinal scale (unable to perform, partial performance, and complete performance) and the mobility part of the assessment uses a 4-point ordinal scale (unable, partial, complete with aid, complete no aid). The maximum score one can receive on the STREAM is a 70 (20 for each limb score and 30 for mobility score). The higher the score, the better movement and mobility is available for the individual being scored.

PROGNOSIS

Hemiplegia is not a progressive disorder, except in progressive conditions like a growing brain tumour. Once the injury has occurred, the symptoms should not worsen. However, because of lack of mobility, other complications can occur. Complications may include muscle and joint stiffness, loss of aerobic fitness, muscle spasms, bed sores, pressure ulcers and blood clots.

Sudden recovery from hemiplegia is very rare. Many of the individuals will have limited recovery, but the majority will improve from intensive, specialised rehabilitation. Potential to progress may differ in cerebral palsy, compared to adult acquired brain injury. It is vital to integrate the hemiplegic child into society and encourage them in their daily living activities. With time, some individuals may make remarkable progress.

IMAGES

PARALYSIS (Stroke, Hemiplegia) - Krishna Kumari, L.S.Hatcheries, Tarnaka, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I was admitted in a corporate hospital in 2008 near LB Nagar. After 3 weeks of acute medical care I could stand and walk only a few steps with difficulty.

MODE OF RECOVERY AT NEW LIFE CENTRE

Maximum recovery in just 10 days and complete cure in two months

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Hemiplegia is paralysis of the arm, leg, and trunk on the same side of the body. Hemiplegia is more severe than hemiparesis, where in one half of the body has less marked weakness. Hemiplegia and hemiparesis may be congenital, or they might be acquired conditions resulting from an illness, an injury, or a stroke.

SIGNS AND SYMPTOMS

Hemiplegia means severe weakness of the limbs on one side of the body but the specific features can vary tremendously from person to person. Problems may include :

  • Difficulty with gait.
  • Difficulty with balance while standing or walking.
  • Increasing stiffness of muscles.
  • Muscle spasms.
  • The majority of children who develop hemiplegia also have abnormal mental development.
  • Behavior problems like anxiety, anger, irritability, lack of concentration or comprehension.
  • Emotions — depression.
  • Shoulder pain — Often associated with a loss of external rotation of the glenohumeral joint, commonly due to the increased tone of the Subscapularis muscle and Pectoralis major muscle.
  • Shoulder Subluxation.

CAUSES

The most common cause of hemiplegia is stroke. Strokes can cause a variety of movement disorders, depending on the location and severity of the lesion. Hemiplegia is common when the stroke affects the corticospinal tract. Other causes of hemiplegia include spinal cord injury, specifically Brown-Séquard syndrome, traumatic brain injury, or disease affecting the brain. As a lesion that results in hemiplegia occurs in the brain or spinal cord, hemiplegic muscles display features of the Upper Motor Neuron Syndrome. Features other than weakness include decreased movement control, clonus (a series of involuntary rapid muscle contractions), spasticity, exaggerated deep tendon reflexes and decreased endurance.

The incidence of hemiplegia is much higher in premature babies than term babies. There is also a high incidence of hemiplegia during pregnancy and experts believe that this may be related to either a traumatic delivery, use of forceps or some event which causes brain injury.

Other causes of hemiplegia in adults include trauma, bleeding, brain infections and cancers. Individuals who have uncontrolled diabetes, hypertension or those who smoke have a higher chance of developing a stroke. Weakness on one side of the face may occur and may be due to a viral infection, stroke or a cancer.

COMMON CAUSES BY ETIOLOGY

  • VASCULAR: cerebral hemorrhage, stroke, diabetic neuropathy
  • INFECTIVE: encephalitis, meningitis, brain abscess
  • NEOPLASTIC: glioma-meningioma
  • DEMYELINATION: disseminated sclerosis, lesions to the internal capsule
  • TRAUMATIC: cerebral lacerations, subdural hematoma rare cause of hemiplegia is due to local anaesthetic injections given intra-arterially rapidly, instead of given in a nerve branch.
  • CONGENITAL: cerebral palsy
  • DISSEMINATED: multiple sclerosis
  • PSYCHOLOGICAL: parasomnia (nocturnal hemiplegia)

PATHOGENESIS

The exact cause of hemiplegia is not known in all cases, but it appears that the brain is deprived of oxygen and this results in the death of neurons. When the corticospinal tract is damaged, the injury is usually manifested on the opposite side of the body. For example if one has an injury to the right side of the brain, the hemiplegia will be on the left side of the body. This happens because the motor fibres of corticospinal tract ( also called pyramidal fibres), which take origin from the motor cortex in brain, cross to the opposite side in the lower part of medulla oblangata and then descend down in spinal cord to supply their respective muscles. Depending on the site of lesion in brain, the severity of hemiplegia varies. A lesion in internal capsule where all the motor fibres are condensed in a small area, will cause dense hemiplegia i.e. complete loss of power of all muscles of one half of body while a lesion at cortical or subcortical level will cause varied amount of weakness of one half of the body.

DIAGNOSIS

Hemiplegia is identified by clinical examination by a health professional, such as a physiotherapist or doctor. Radiological studies like a CT scan or magnetic resonance imaging of the brain should be used to confirm injury in the brain and spinal cord, but alone cannot be used to identify movement disorders. Individuals who develop seizures may undergo tests to determine where the focus of excess electrical activity is.

Hemiplegia patients usually show a characteristic gait. The leg on the affected side is extended and internally rotated and is swung in a wide, lateral arc rather than lifted in order to move it forward. The upper limb on the same side is also adducted at the shoulder, flexed at the elbow, and pronated at the wrist with the thumb tucked into the palm and the fingers curled around it.

TREATMENT

Treatment should be based on assessment by the relevant health professionals, including physiotherapists, doctors and occupational therapists. Muscles with severe motor impairment including weakness need these therapists to assist them with specific exercise, and are likely to require help to do this.

Pharmacological

Drugs can be used to treat issues related to the Upper Motor Neuron Syndrome. Drugs like Librium or Valium could be used as a relaxant. Drugs are also given to individuals who have recurrent seizures, which may be a separate but related problem after brain injury.

Surgery

Surgery may be used if the individual develops a secondary issue of contracture, from a severe imbalance of muscle activity. In such cases the surgeon may cut the ligaments and relieve joint contractures. Individuals who are unable to swallow may have a tube inserted into the stomach. This allows food to be given directly into the stomach. The food is in liquid form and instilled at low rates. Some individuals with hemiplegia will benefit from some type of prosthetic device. There are many types of braces and splints available to stabilize a joint, assist with walking and keep the upper body erect.

Rehabilitation

Rehabilitation is the main treatment of individuals with hemiplegia. In all cases, the major aim of rehabilitation is to regain maximum function and quality of life. Both physical and occupational therapy can significantly improve the quality of life.

Physical Therapy

Physical therapy (PT) can help improve muscle strength & coordination, mobility (such as standing and walking), and other physical function using different sensorimotor techniques. Physiotherapists can also help reduce shoulder pain by maintaining shoulder range of motion, as well as using Functional electrical stimulation.[11] Supportive devices, such as braces or slings, can be used to help prevent or treat shoulder subluxation in the hopes to minimize disability and pain. It should be noted that although many individuals suffering from stroke experience both shoulder pain and shoulder subluxation, the two are mutually exclusive. A treatment method that can be implemented with the goal of helping to regain motor function in the affected limb is constraint-induced movement therapy. This consists of constraining the unaffected limb, forcing the affected limb to accomplish tasks of daily living.

Occupational Therapy

Occupational therapy Occupational Therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening hand, shoulder and torso, and participating in activities of daily living (ADLs), such as eating and dressing. Therapists may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your child’s hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual - which may include, environmental modification, use of adaptive equipment, sensory integration, etc.

Constraint-Induced Movement Therapy

Constraint-induced movement therapy (CI or CIMT) is a form of rehabilitation therapy that improves upper extremity function, especially in cases of hemiplegia.

ASSESSMENT TOOLS

There are a variety of standardized assessment scales available to physiotherapists and other health care professionals for use in the ongoing evaluation of the status of a patient’s hemiplegia. The use of standardized assessment scales may help physiotherapists and other health care professionals during the course of their treatment plant to:

  • Prioritize treatment interventions based on specific identifiable motor and sensory deficits.
  • Create appropriate short and long term goals for treatment based on the outcome of the scales, their professional expertise and the desires of the patient.
  • Evaluate the potential burden of care and monitor any changes based on either improving or declining scores.

Some of the most commonly used scales in the assessment of hemiplegia are:

The Fugl-Meyer Assessment of Physical Performance (FMA)

The FMA is often used as a measure of functional or physical impairment following a cerebrovascular accident(CVA). It measures sensory and motor impairment of the upper and lower extremities, balance in several positions, range of motion, and pain. This test is a reliable and valid measure in measuring post-stroke impairments related to stroke recovery. A lower score in each component of the test indicates higher impairment and a lower functional level for that area. The maximum score for each component is 66 for the upper extremities, 34 for the lower extremities, and 14 for balance. Administration of the FMA should be done after reviewing a training manual.

The Chedoke-McMaster Stroke Assessment (CMSA)

This test is a reliable measure of two separate components evaluating both motor impairment and disability. The disability component assesses any changes in physical function including gross motor function and walking ability. The disability inventory can have a maximum score of 100 with 70 from the gross motor index and 30 from the walking index. Each task in this inventory has a maximum score of seven except for the 2 minute walk test which is out of two. The impairment component of the test evaluates the upper and lower extremities, postural control and pain. The impairment inventory focuses on the seven stages of recovery from stroke from flaccid paralysis to normal motor functioning. A training workshop is recommended if the measure is being utilized for the purpose of data collection.

The Stroke Rehabilitation Assessment of Movement (STREAM)

The STREAM consists of 30 test items involving upper-limb movements, lower-limb movements, and basic mobility items. It is a clinical measure of voluntary movements and general mobility (rolling, bridging, sit-to-stand, standing, stepping, walking and stairs) following a stroke. The voluntary movement part of the assessment is measured using a 3-point ordinal scale (unable to perform, partial performance, and complete performance) and the mobility part of the assessment uses a 4-point ordinal scale (unable, partial, complete with aid, complete no aid). The maximum score one can receive on the STREAM is a 70 (20 for each limb score and 30 for mobility score). The higher the score, the better movement and mobility is available for the individual being scored.

PROGNOSIS

Hemiplegia is not a progressive disorder, except in progressive conditions like a growing brain tumour. Once the injury has occurred, the symptoms should not worsen. However, because of lack of mobility, other complications can occur. Complications may include muscle and joint stiffness, loss of aerobic fitness, muscle spasms, bed sores, pressure ulcers and blood clots.

Sudden recovery from hemiplegia is very rare. Many of the individuals will have limited recovery, but the majority will improve from intensive, specialised rehabilitation. Potential to progress may differ in cerebral palsy, compared to adult acquired brain injury. It is vital to integrate the hemiplegic child into society and encourage them in their daily living activities. With time, some individuals may make remarkable progress.

IMAGES

CASE RECORD

  DISEASES OF MUSCULOSKELETAL SYSTEM (BONES, JOINTS, MUSCLES)

RHEUMATOID ARTHRITIS - Shashikala, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I was suffering from severe pains in multiple joints, Nasal allergy and Headache for the past five years. Visited many orthopaedic surgeons in corporate hospitals, underwent operation for my sinus problem. But there was no lasting relief.I was not able to carry on my daily activities both in my house and at school

MODE OF RECOVERY AT NEW LIFE CENTRE

My nasal problem and the headache have disappeared with the treatment given by New life centre and my joint pains have decreased by 70 % in just three months. I am now able to attend my duty regularly.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Rheumatoid arthritis (RA) is an autoimmune disease that results in a chronic, systemic inflammatory disorder that may affect many tissues and organs, but principally attacks flexible (synovial) joints. It can be a disabling and painful condition, which can lead to substantial loss of functioning and mobility if not adequately treated.

The process involves an inflammatory response of the capsule around the joints (synovium) secondary to swelling (turgescence) of synovial cells, excess synovial fluid, and the development of fibrous tissue (pannus) in the synovium. The pathology of the disease process often leads to the destruction of articular cartilage and ankylosis (fusion) of the joints. RA can also produce diffuse inflammation in the lungs, the membrane around the heart (pericardium), the membranes of the lung (pleura), and white of the eye (sclera), and also nodular lesions, most common in subcutaneous tissue. Although the cause of RA is unknown, autoimmunity plays a big part, and RA is a systemic autoimmune disease. It is a clinical diagnosis made on the basis of symptoms, physical exam, radiographs (X-rays) and labs.

Treatments are pharmacological and non-pharmacological. Non-pharmacological treatment includes physical therapy, orthoses, occupational therapy and nutritional therapy but these don't stop the progression of joint destruction. Analgesics (painkillers) and anti-inflammatory drugs, including steroids, suppress symptoms, but don't stop the progression of joint destruction either. Disease-modifying antirheumatic drugs (DMARDs) slow or halt the progress of the disease. The newer biologics are DMARDs. The evidence for complementary and alternative medicine (CAM) treatments for RA related pain is weak, with the lack of high quality evidence leading to the conclusions that their use is currently not supported by the evidence. Patients should inform their health care provider of any CAM treatments and continue taking traditional treatments.

About 0.6% of the United States adult population has RA, women two to three times as often as men. Onset is most frequent during middle age, but people of any age can be affected.

SIGNS AND SYMPTOMS

RA primarily affects joints, however it also affects other organs in 15–25% of individuals. It can be difficult to determine whether disease manifestations are directly caused by the rheumatoid process itself, or from side effects of the medications used to treat it – for example, lung fibrosis from methotrexate or osteoporosis from corticosteroids.

JOINTS

Arthritis of joints involves inflammation of the synovial membrane. Joints become swollen, tender and warm, and stiffness limits their movement. With time, multiple joints are affected (it is a polyarthritis). Most commonly involved are the small joints of the hands, feet and cervical spine, but larger joints like the shoulder and knee can also be involved. 1089 Synovitis can lead to tethering of tissue with loss of movement and erosion of the joint surface causing deformity and loss of function.

RA typically manifests with signs of inflammation, with the affected joints being swollen, warm, painful and stiff, particularly early in the morning on waking or following prolonged inactivity. Increased stiffness early in the morning is often a prominent feature of the disease and typically lasts for more than an hour. Gentle movements may relieve symptoms in early stages of the disease. These signs help distinguish rheumatoid from non-inflammatory problems of the joints, often referred to as osteoarthritis or "wear-and-tear" arthritis. In arthritis of non-inflammatory causes, signs of inflammation and early morning stiffness are less prominent with stiffness typically less than 1 hour, and movements induce pain caused by mechanical arthritis. The pain associated with RA is induced at the site of inflammation and classified as nociceptive as opposed to neuropathic. The joints are often affected in a fairly symmetrical fashion, although this is not specific, and the initial presentation may be asymmetrical.

As the pathology progresses the inflammatory activity leads to tendon tethering and erosion and destruction of the joint surface, which impairs range of movement and leads to deformity. The fingers may suffer from almost any deformity depending on which joints are most involved. Specific deformities, which also occur in osteoarthritis, include ulnar deviation, boutonniere deformity, swan neck deformity and "Z-thumb." "Z-thumb" or "Z-deformity" consists of hyperextension of the interphalangeal joint, fixed flexion and subluxation of the metacarpophalangeal joint and gives a "Z" appearance to the thumb. 1089 The hammer toe deformity may be seen. In the worst case, joints are known as arthritis mutilans due to the mutilating nature of the deformities.

SKIN

The rheumatoid nodule, which is sometimes cutaneous, is the feature most characteristic of RA. It is a type of inflammatory reaction known to pathologists as a "necrotizing granuloma". The initial pathologic process in nodule formation is unknown but may be essentially the same as the synovitis, since similar structural features occur in both. The nodule has a central area of fibrinoid necrosis that may be fissured and which corresponds to the fibrin-rich necrotic material found in and around an affected synovial space. Surrounding the necrosis is a layer of palisading macrophages and fibroblasts, corresponding to the intimal layer in synovium and a cuff of connective tissue containing clusters of lymphocytes and plasma cells, corresponding to the subintimal zone in synovitis. The typical rheumatoid nodule may be a few millimetres to a few centimetres in diameter and is usually found over bony prominences, such as the olecranon, the calcaneal tuberosity, the metacarpophalangeal joint, or other areas that sustain repeated mechanical stress. Nodules are associated with a positive RF (rheumatoid factor) titer and severe erosive arthritis. Rarely, these can occur in internal organs or at diverse sites on the body.

Several forms of vasculitis occur in RA. A benign form occurs as microinfarcts around the nailfolds. More severe forms include livedo reticularis, which is a network (reticulum) of erythematous to purplish discoloration of the skin caused by the presence of an obliterative cutaneous capillaropathy

Other, rather rare, skin associated symptoms include pyoderma gangrenosum, Sweet's syndrome, drug reactions, erythema nodosum, lobe panniculitis, atrophy of finger skin, palmar erythema, diffuse thinning (rice paper skin), and skin fragility (often worsened by corticosteroid use).

LUNGS

Fibrosis of the lungs is a recognized response to rheumatoid disease. It is also a rare but well recognized consequence of therapy (for example with methotrexate and leflunomide). Caplan's syndrome describes lung nodules in individuals with RA and additional exposure to coal dust. Pleural effusions are also associated with RA. Another complication of RA is Rheumatoid Lung Disease. It is estimated that about one quarter of Americans with RA develop Rheumatoid Lung Disease.

KIDNEYS

Renal amyloidosis can occur as a consequence of chronic inflammation. RA may affect the kidney glomerulus directly through a vasculopathy or a mesangial infiltrate but this is less well documented (though this is not surprising, considering immune complex-mediated hypersensitivities are known for pathogenic deposition of immune complexes in organs where blood is filtered at high pressure to form other fluids, such as urine and synovial fluid). Treatment with Penicillamine and gold salts are recognized causes of membranous nephropathy.

Heart and blood vessels

People with RA are more prone to atherosclerosis, and risk of myocardial infarction (heart attack) and stroke is markedly increased. Other possible complications that may arise include: pericarditis, endocarditis, left ventricular failure, valvulitis and fibrosis. Many people with RA do not experience the same chest pain that others feel when they have angina or myocardial infarction. To reduce cardiovascular risk, it is crucial to maintain optimal control of the inflammation caused by RA (which may be involved in causing the cardiovascular risk), and to use exercise and medications appropriately to reduce other cardiovascular risk factors such as blood lipids and blood pressure. Doctors who treat RA patients should be sensitive to cardiovascular risk when prescribing anti-inflammatory medications, and may want to consider prescribing routine use of low doses of aspirin if the gastrointestinal effects are tolerable.

OTHER

Ocular

The eye is directly affected in the form of episcleritis which when severe can very rarely progress to perforating scleromalacia. Rather more common is the indirect effect of keratoconjunctivitis sicca, which is a dryness of eyes and mouth caused by lymphocyte infiltration of lacrimal and salivary glands. When severe, dryness of the cornea can lead to keratitis and loss of vision. Preventive treatment of severe dryness with measures such as nasolacrimal duct blockage is important.

Hepatic

Cytokine production in joints and/or hepatic (liver) Kupffer cells leads to increased activity of hepatocytes with increased production of acute-phase proteins, such as C-reactive protein, and increased release of enzymes such as alkaline phosphatase into the blood. In Felty's syndrome, Kupffer cell activation is so marked that the resulting increase in hepatocyte activity is associated with nodular hyperplasia of the liver, which may be palpably enlarged. Although Kupffer cells are within the hepatic parenchyma, they are separate from hepatocytes. As a result there is little or no microscopic evidence of hepatitis (immune-mediated destruction of hepatocytes). Hepatic involvement in RA is essentially asymptomatic.

Hematological

Anemia is by far the most common abnormality of the blood cells which can be caused by a variety of mechanisms. The chronic inflammation caused by RA leads to raised hepcidin levels, leading to anemia of chronic disease where iron is poorly absorbed and also sequestered into macrophages. RA may also cause a warm autoimmune hemolytic anemia. The red cells are of normal size and colour (normocytic and normochromic). A low white blood cell count (neutropenia) usually only occurs in patients with Felty's syndrome with an enlarged liver and spleen. The mechanism of neutropenia is complex. An increased platelet count (thrombocytosis) occurs when inflammation is uncontrolled.

Neurological

Peripheral neuropathy and mononeuritis multiplex may occur. The most common problem is carpal tunnel syndrome caused by compression of the median nerve by swelling around the wrist. Atlanto-axial subluxation can occur, owing to erosion of the odontoid process and/or transverse ligaments in the cervical spine's connection to the skull. Such an erosion (>3mm) can give rise to vertebrae slipping over one another and compressing the spinal cord. Clumsiness is initially experienced, but without due care this can progress to quadriplegia.

Constitutional symptoms

Constitutional symptoms including fatigue, low grade fever, malaise, morning stiffness, loss of appetite and loss of weight are common systemic manifestations seen in patients with active RA.

Osteoporosis

Local osteoporosis occurs in RA around inflamed joints. It is postulated to be partially caused by inflammatory cytokines. More general osteoporosis is probably contributed to by immobility, systemic cytokine effects, local cytokine release in bone marrow and corticosteroid therapy.

Lymphoma

The incidence of lymphoma is increased in RA, although it is still uncommon.

CAUSES

RA is a form of autoimmunity, the causes of which are still not completely known. It is a systemic (whole body) disorder principally affecting synovial tissues. There is no evidence that physical and emotional effects or stress could be a trigger for the disease. The many negative findings suggest that either the trigger varies, or that it might in fact be a chance event inherent with the immune response.

Half of the risk for RA is believed to be genetic. It is strongly associated with the inherited tissue type major histocompatibility complex (MHC) antigen HLA-DR4 (most specifically DR0401 and 0404), and the genes PTPN22 and PADI4—hence family history is an important risk factor. Inheriting the PTPN22 gene has been shown to double a person's susceptibility to RA. PADI4 has been identified as a major risk factor in people of Asian descent, but not in those of European descent.[25] First-degree relatives prevalence rate is 2–3% and disease genetic concordance in monozygotic twins is approximately 15–20%.

Smoking is the most significant non-genetic risk with RA being up to three times more common in smokers than non-smokers, particularly in men, heavy smokers, and those who are rheumatoid factor positive. Modest alcohol consumption may be protective.

Epidemiological studies have confirmed a potential association between RA and two herpesvirus infections:Epstein-Barr virus (EBV) and Human Herpes Virus 6 (HHV-6). Individuals with RA are more likely to exhibit an abnormal immune response to EBV and have high levels of anti-EBV antibodies.

Vitamin D deficiency is common in those with RA and may be causally associated. Some trials have found a decreased risk for RA with vitamin D supplementation while others have not.

Vitamin D deficiency is more common in patients with rheumatoid arthritis than in the general population. However, whether vitamin D deficiency is a cause or a consequence of the disease remains unclear. 1α,25-dihydroxyvitamin D3 (1,25D), an active metabolite of vitamin D, effects bone metabolism indirectly through control of calcium and phosphate homeostasis. Interaction between 1,25D and the vitamin D receptor (VDR) effects the production of RANKL and delays osteoclastogenesis.

PATHOPHYSIOLOGY

The key pieces of evidence relating to pathogenesis are:

  • A genetic link with HLA-DR4 and related allotypes of MHC Class II and the T cell-associated protein PTPN22.
  • An undeniable link to the pathogenesis of vascular disease of many types, including the possibility of a strong causal connection to rheumatoid vasculitis, a typical feature of this condition.
  • A remarkable deceleration of disease progression in many cases by blockade of the cytokine TNF (alpha).
  • A similar dramatic response in many cases to depletion of B lymphocytes, but no comparable response to depletion of T lymphocytes.
  • A more or less random pattern of whether and when predisposed individuals are affected.
  • The presence of autoantibodies to IgGFc, known as rheumatoid factors (RF), and antibodies to citrullinated peptides (ACPA).

These data suggest that the disease involves abnormal B cell–T cell interaction, with presentation of antigens by B cells to T cells via HLA-DR eliciting T cell help and consequent production of RF and ACPA. Inflammation is then driven either by B cell or T cell products stimulating release of TNF and other cytokines. The process may be facilitated by an effect of smoking on citrullination but the stochastic (random) epidemiology suggests that the rate limiting step in genesis of disease in predisposed individuals may be an inherent stochastic process within the immune response such as immunoglobulin or T cell receptor gene recombination and mutation. (See entry under autoimmunity for general mechanisms.)

If TNF release is stimulated by B cell products in the form of RF or ACPA -containing immune complexes, through activation of immunoglobulin Fc receptors, then RA can be seen as a form of Type III hypersensitivity. If TNF release is stimulated by T cell products such as interleukin-17 it might be considered closer to type IV hypersensitivity although this terminology may be getting somewhat dated and unhelpful.[39] The debate on the relative roles of immune complexes and T cell products in inflammation in RA has continued for 30 years. There is little doubt that both B and T cells are essential to the disease. However, there is good evidence for neither cell being necessary at the site of inflammation. This tends to favour immune complexes (based on antibody synthesised elsewhere) as the initiators, even if not the sole perpetuators of inflammation. Moreover, work by Thurlings and others in Paul-Peter Tak's group and also by Arthur Kavanagh's group suggest that if any immune cells are relevant locally they are the plasma cells, which derive from B cells and produce in bulk the antibodies selected at the B cell stage.

Although TNF appears to be the dominant, other cytokines (chemical mediators) are likely to be involved in inflammation in RA. Blockade of TNF does not benefit all patients or all tissues (lung disease and nodules may get worse). Blockade of IL-1, IL-15 and IL-6 also have beneficial effects and IL-17 may be important. Constitutional symptoms such as fever, malaise, loss of appetite and weight loss are also caused by cytokines released into the blood stream.

As with most autoimmune diseases, it is important to distinguish between the cause(s) that trigger the process, and those that may permit it to persist and progress.

ABNORMAL IMMUNE RESPONSE

The factors that allow an abnormal immune response, once initiated, to become permanent and chronic, are becoming more clearly understood. The genetic association with HLA-DR4, as well as the newly discovered associations with the gene PTPN22 and with two additional genes, all implicate altered thresholds in regulation of the adaptive immune response. It has also become clear from recent studies that these genetic factors may interact with the most clearly defined environmental risk factor for RA, namely cigarette smoking Other environmental factors also appear to modulate the risk of acquiring RA, and hormonal factors in the individual may explain some features of the disease, such as the higher occurrence in women, the not-infrequent onset after child-birth, and the (slight) modulation of disease risk by hormonal medications. Exactly how altered regulatory thresholds allow the triggering of a specific autoimmune response remains uncertain. However, one possibility is that negative feedback mechanisms that normally maintain tolerance of self are overtaken by aberrant positive feedback mechanisms for certain antigens such as IgG Fc (bound by RF) and citrullinated fibrinogen (bound by ACPA) (see entry on autoimmunity).

Once the abnormal immune response has become established (which may take several years before any symptoms occur), plasma cells derived from B lymphocytes produce rheumatoid factors and ACPA of the IgG and IgM classes in large quantities. These are not deposited in the way that they are in systemic lupus. Rather, they activate macrophages through Fc receptor and complement binding, which seems to play an important role in the intense inflammatory response present in RA. This contributes to inflammation of the synovium, in terms of edema, vasodilation and infiltration by activated T-cells (mainly CD4 in nodular aggregates and CD8 in diffuse infiltrates). Synovial macrophages and dendritic cells further function as antigen presenting cells by expressing MHC class II molecules, leading to an established local immune reaction in the tissue. The disease progresses in concert with formation of granulation tissue at the edges of the synovial lining (pannus) with extensive angiogenesis and production of enzymes that cause tissue damage. Modern pharmacological treatments of RA target these mediators. Once the inflammatory reaction is established, the synovium thickens, the cartilage and the underlying bone begins to disintegrate and evidence of joint destruction accrues.

DIAGNOSIS

Imaging

X-rays of the hands and feet are generally performed in people with a polyarthritis. In RA, there may be no changes in the early stages of the disease, or the x-ray may demonstrate juxta-articular osteopenia, soft tissue swelling and loss of joint space. As the disease advances, there may be bony erosions and subluxation. X-rays of other joints may be taken if symptoms of pain or swelling occur in those joints.

Other medical imaging techniques such as magnetic resonance imaging (MRI) and ultrasound are also used in RA

There have been technical advances in ultrasonography. High-frequency transducers (10 MHz or higher) have improved the spatial resolution of ultrasound images; these images can depict 20% more erosions than conventional radiography. Also, color Doppler and power Doppler ultrasound, which show vascular signals of active synovitis depending on the degree of inflammation, are useful in assessing synovial inflammation. This is important, since in the early stages of RA, the synovium is primarily affected, and synovitis seems to be the best predictive marker of future joint damage.

Blood tests

When RA is clinically suspected, immunological studies are required, such as testing for the presence of rheumatoid factor (RF, a non-specific antibody). A negative RF does not rule out RA; rather, the arthritis is called seronegative. This is the case in about 15% of patients. During the first year of illness, rheumatoid factor is more likely to be negative with some individuals converting to seropositive status over time. RF is also seen in other illnesses, for example Sjögren's syndrome, hepatitis C, systemic lupus erythematosus, chronic infections and in approximately 10% of the healthy population, therefore the test is not very specific.

Because of this low specificity, new serological tests have been developed, which test for the presence of the anti-citrullinated protein antibodies (ACPAs) or anti-CCP. Like RF, these tests are positive in only a proportion (67%) of all RA cases, but are rarely positive if RA is not present, giving it a specificity of around 95%. As with RF, there is evidence for ACPAs being present in many cases even before onset of clinical disease.

The most common tests for ACPAs are the anti-CCP (cyclic citrullinated peptide) test and the Anti-MCV assay (antibodies against mutated citrullinated Vimentin). Recently a serological point-of-care test (POCT) for the early detection of RA has been developed. This assay combines the detection of rheumatoid factor and anti-MCV for diagnosis of RA and shows a sensitivity of 72% and specificity of 99.7%.

Also, several other blood tests are usually done to allow for other causes of arthritis, such as lupus erythematosus. The erythrocyte sedimentation rate (ESR), C-reactive protein, full blood count, renal function, liver enzymes and other immunological tests (e.g., antinuclear antibody/ANA) are all performed at this stage. Elevated ferritin levels can reveal hemochromatosis, a mimic of RA, or be a sign of Still's disease, a seronegative, usually juvenile, variant of rheumatoid arthritis.

CRITERIA

In 2010 the 2010 ACR / EULAR Rheumatoid Arthritis Classification Criteria were introduced.

These new classification criteria overruled the "old" ACR criteria of 1987 and are adapted for early RA diagnosis. The "new" classification criteria, jointly published by the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR) establish a point value between 0 and 10. Every patient with a point total of 6 or higher is unequivocally classified as an RA patient, provided he has synovitis in at least one joint and given that there is no other diagnosis better explaining the synovitis. Four areas are covered in the diagnosis:

  • joint involvement, designating the metacarpophalangeal joints, proximal interphalangeal joints, the interphalangeal joint of the thumb, second through fifth metatarsophalangeal joint and wrist as small joints, and shoulders, elbows, hip joints, knees, and ankles as large joints:
  • Involvement of 1 large joint gives 0 points
  • Involvement of 2–10 large joints gives 1 point
  • Involvement of 1–3 small joints (with or without involvement of large joints) gives 2 points
  • Involvement of 4–10 small joints (with or without involvement of large joints) gives 3 points
  • Involvement of more than 10 joints (with involvement of at least 1 small joint) gives 5 points
  • serological parameters – including the rheumatoid factor as well as ACPA – "ACPA" stands for "anti-citrullinated protein antibody":
  • Negative RF and negative ACPA gives 0 points
  • Low-positive RF or low-positive ACPA gives 2 points
  • High-positive RF or high-positive ACPA gives 3 points
  • acute phase reactants: 1 point for elevated erythrocyte sedimentation rate, ESR, or elevated CRP value (c-reactive protein)
  • duration of arthritis: 1 point for symptoms lasting six weeks or longer

The new criteria accommodate to the growing understanding of RA and the improvements in diagnosing RA and disease treatment. In the "new" criteria serology and autoimmune diagnostics carries major weight, as ACPA detection is appropriate to diagnose the disease in an early state, before joints destructions occur. Destruction of the joints viewed in radiological images was a significant point of the ACR criteria from 1987. This criterion no longer is regarded to be relevant, as this is just the type of damage that treatment is meant to avoid.

The criteria are not intended for the diagnosis for routine clinical care; they were primarily intended to categorize research (classification criteria). In clinical practice, the following criteria apply:

  • two or more swollen joints
  • morning stiffness lasting more than one hour for at least six weeks
  • the detection of rheumatoid factors or autoantibodies against ACPA such as autoantibodies to mutated citrullinated vimentin can confirm the suspicion of RA. A negative autoantibody result does not exclude a diagnosis of RA.

DIFFERENTIAL DIAGNOSIS

Several other medical conditions can resemble RA, and usually need to be distinguished from it at the time of diagnosis:

  • Crystal induced arthritis (gout, and pseudogout) – usually involves particular joints (knee, MTP1, heels) and can be distinguished with aspiration of joint fluid if in doubt. Redness, asymmetric distribution of affected joints, pain occurs at night and the starting pain is less than an hour with gout.
  • Osteoarthritis – distinguished with X-rays of the affected joints and blood tests, age (mostly older patients), starting pain less than an hour, a-symmetric distribution of affected joints and pain worsens when using joint for longer periods.
  • Systemic lupus erythematosus (SLE) – distinguished by specific clinical symptoms and blood tests (antibodies against double-stranded DNA)
  • One of the several types of psoriatic arthritis resembles RA – nail changes and skin symptoms distinguish between them
  • Lyme disease causes erosive arthritis and may closely resemble RA – it may be distinguished by blood test in endemic areas
  • Reactive arthritis (previously Reiter's disease) – asymmetrically involves heel, sacroiliac joints, and large joints of the leg. It is usually associated with urethritis, conjunctivitis, iritis, painless buccal ulcers, and keratoderma blennorrhagica.
  • Ankylosing spondylitis – this involves the spine, although a RA-like symmetrical small-joint polyarthritis may occur in the context of this condition.
  • Hepatitis C – RA-like symmetrical small-joint polyarthritis may occur in the context of this condition. Hepatitis C may also induce Rheumatoid Factor auto-antibodies

Rarer causes that usually behave differently but may cause joint pains:

  • Sarcoidosis, amyloidosis, and Whipple's disease can also resemble RA.
  • Hemochromatosis may cause hand joint arthritis.
  • Acute rheumatic fever can be differentiated from RA by a migratory pattern of joint involvement and evidence of antecedent streptococcal infection. Bacterial arthritis (such as streptococcus) is usually asymmetric, while RA usually involves both sides of the body symmetrically.
  • Gonococcal arthritis (another bacterial arthritis) is also initially migratory and can involve tendons around the wrists and ankles.

MANAGEMENT

There is no cure for RA, but treatments can improve symptoms and slow the progress of the disease. Disease-modifying treatment has the best results when it is started early and aggressively.

The goals of treatment are to minimize symptoms such as pain and swelling, to prevent bone deformity (for example, bone erosions visible in X-rays), and to maintain day-to-day functioning. This can often be achieved using two main classes of medications: analgesics such as NSAIDs, and disease-modifying antirheumatic drugs (DMARDs). RA should generally be treated with at least one specific anti-rheumatic medication. The use of benzodiazepines (such as diazepam) to treat the pain is not recommended as it does not appear to help and is associated with risks. Analgesics, other than NSAIDs, offer lesser, but some benefit with respect to pain. whilst not causing the same level of gastrointestinal irritation.

Lifestyle

Regular exercise is recommended as both safe and useful to maintain muscles strength and overall physical function. It is uncertain if specific dietary measures have an effect

Disease modifying agents

Disease-modifying antirheumatic drugs (DMARD) are the primary treatment for RA. They are a diverse collection of drugs, grouped by use and convention. They have been found to improve symptoms, decrease joint damage, and improve overall functional abilities. They should be started very early in the disease as when they result in disease remission in approximately half of people and improved outcomes overall.

The most commonly used agent is methotrexate with other frequently used agents including sulfasalazine and leflunomide. Sodium aurothiomalate (Gold) and cyclosporin are less commonly used due to more common adverse effects. Agents may be used in combinations.

Methotrexate is the most important and useful DMARD and is usually the first treatment. Adverse effects should be monitored regularly with toxicity including gastrointestinal, hematologic, pulmonary, and hepatic. Side effects such as nausea, vomiting or abdominal pain can be reduced by taking folic acid. The most common undesirable affect is that it increases liver enzymes in almost 15% of people. It is thus recommended that those who consistently demonstrate abnormal levels of liver enzymes or have a history of liver disease or alcohol use undergo liver biopsies. Methotrexate is also considered a teratogenic and as such, it is recommended women of childbearing age should use contraceptives to avoid pregnancy and to discontinue its use if pregnancy is planned.

Biological agents should generally only be used if methotrexate and other conventional agents are not effective after a trial of three months. These agents include: tumor necrosis factor alpha (TNFα) blockers such as infliximab; interleukin 1 blockers such as anakinra, monoclonal antibodies against B cells such as rituximab, T cell costimulation blocker such as abatacept among others. They are often used in combination with either methotrexate or leflunomide.

TNF blockers and methotrexate appear to have similar effectiveness when used alone and better results are obtained when used together. TNF blockers appear to have equivalent effectiveness with etanercept appearing to be the safest. Abatacept appears effective for RA with 20% more people improving with treatment than without. There however is a lack of evidence to distinguish between the biologics available for RA. Issues with the biologics include their high cost and association with infections including tuberculosis.

Anti-inflammatory agents

NSAIDs reduce both pain and stiffness in those with RA. Generally they appear to have no effect on people's long term disease course and thus are no longer first line agents. NSAIDs should be used with caution in those with gastrointestinal, cardiovascular, or kidney problems.

COX-2 inhibitors, such as celecoxib, and NSAIDs are equally effective.[74] They have a similar gastrointestinal risk as an NSAIDs plus a proton pump inhibitor. In the elderly there is less gastrointestinal intolerance to celecoxib than to NSAIDs alone. There however is an increased risk of myocardial infarction with COX-2 inhibitors. Anti-ulcer medications are not recommended routinely but only in those high risk of gastrointestinal problems.

Glucocorticoids can be used in the short term for flare-ups, while waiting for slow-onset drugs to take effect. Injection of glucocorticoids into individual joints is also effective. While long-term use reduces joint damage it also results in osteoporosis and susceptibility to infections, and thus is not recommended.

Surgery

In early phases of the disease, an arthroscopic or open synovectomy may be performed. It consists of the removal of the inflamed synovia and prevents a quick destruction of the affected joints. Severely affected joints may require joint replacement surgery, such as knee replacement. Postoperatively, physiotherapy is always necessary.

Alternative medicine

There has been an increasing interest in the use of complementary and alternative medicine interventions for the treatment of pain in rheumatoid arthritis. While there have been multiple studies showing beneficial effects in RA on a wide variety of CAM modalities, these studies are often affected by publication bias and are generally not high quality evidence such as randomized controlled trials (RCTs), making definitive conclusions difficult to reach.

The National Center for Complementary and Alternative Medicine has concluded, "In general, there is not enough scientific evidence to prove that any complementary health approaches are beneficial for RA, and there are safety concerns about some of them. Some mind and body practices and dietary supplements may help people with RA manage their symptoms and therefore may be beneficial additions to conventional RA treatments, but there is not enough evidence to draw conclusions." A systematic review of CAM modalities (excluding fish oil) found "The major limitation in reviewing the evidence for CAMs is the paucity of RCTs in the area. The available evidence does not support their current use in the management of RA." One review suggests that of the various alternative medicine treatments evaluated, only acupuncture, bee venom acupuncture, herbal remedies, dietary omega-3 fatty acids, and pulsed electromagnetic field therapy have been studied with RCTs and show promise in treating the pain of RA, though no definitive conclusions could be reached.

Dietary supplements

The American College of Rheumatology states that no herbal medicines have health claims supported by high quality evidence and thus they do not recommend their use. There is no scientific basis to suggest that herbal supplements advertised as "natural" are safer for use than conventional medications as both are chemicals. Herbal medications, although labelled "natural", may be toxic or fatal if consumed. Some evidence supports omega-3 fatty acids and gamma-linolenic acid in RA. The benefit from omega-3 appears modest but consistent, though the current evidence is not strong enough to determine that supplementation with omega-3 polyunsaturated fatty acids (found in fish oil) is an effective treatment for RA. Gamma-linolenic acid, which may reduce pain, tender joint count and stiffness, is generally safe.

Dietary supplements

The American College of Rheumatology states that no herbal medicines have health claims supported by high quality evidence and thus they do not recommend their use. There is no scientific basis to suggest that herbal supplements advertised as "natural" are safer for use than conventional medications as both are chemicals. Herbal medications, although labelled "natural", may be toxic or fatal if consumed. Some evidence supports omega-3 fatty acids and gamma-linolenic acid in RA. The benefit from omega-3 appears modest but consistent, though the current evidence is not strong enough to determine that supplementation with omega-3 polyunsaturated fatty acids (found in fish oil) is an effective treatment for RA. Gamma-linolenic acid, which may reduce pain, tender joint count and stiffness, is generally safe.

The following show promise as treatments for RA, based on preliminary studies: boswellic acid, curcumin, Devil's claw, Euonymus alatus, and Thunder god vine (Tripterygium wilfordii).

Herbal supplements can often have significant side effects, and can interact with prescription medications being taken at the same time. These risks are often exacerbated by the false general belief by patients that herbal supplements are always safe and the hesitancy by patients in reporting the use of herbal supplements to physicians. NCCAM has noted that, "In particular, the herb thunder god vine (Tripterygium wilfordii) can have serious side effects."

Manual therapies

The evidence for acupuncture is inconclusive with it appearing to be equivalent to sham acupuncture.

Prevention

There is no known prevention for the contraction. Reduction of risk factors and aggressive treatment after diagnosis are recommended actions.

PROGNOSIS

The course of the disease varies greatly. Some people have mild short-term symptoms, but in most the disease is progressive for life. Around 20%–30% will have subcutaneous nodules (known as rheumatoid nodules); this is associated with a poor prognosis.

Prognostic factors

Poor prognostic factors include persistent synovitis, early erosive disease, extra-articular findings (including subcutaneous rheumatoid nodules), positive serum RF findings, positive serum anti-CCP autoantibodies, carriership of HLA-DR4 "Shared Epitope" alleles, family history of RA, poor functional status, socioeconomic factors, elevated acute phase response (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]), and increased clinical severity.

Mortality

RA is known to reduce the lifespan of patients by anywhere from three to 12 years. A new line of research does, however, show that the use of new biologic drug therapies extend the lifespan of patients with RA and reduce the risk and progression of atherosclerosis. According to the UK's National Rheumatoid Arthritis Society, "Young age at onset, long disease duration, the concurrent presence of other health problems (called co-morbidity), and characteristics of severe RA—such as poor functional ability or overall health status, a lot of joint damage on x-rays, the need for hospitalisation or involvement of organs other than the joints—have been shown to associate with higher mortality". Positive responses to treatment may indicate a better prognosis. A 2005 study by the Mayo Clinic noted that RA sufferers suffer a doubled risk of heart disease, independent of other risk factors such as diabetes, alcohol abuse, and elevated cholesterol, blood pressure and body mass index. The mechanism by which RA causes this increased risk remains unknown; the presence of chronic inflammation has been proposed as a contributing factor.

EPIDEMIOLOGY

RA affects between 0.5 and 1% of adults in the developed world with between 5 and 50 per 100,000 people newly developing the condition each year. In 2010 it resulted in about 49,000 deaths globally.

Onset is uncommon under the age of 15 and from then on the incidence rises with age until the age of 80. Women are affected three to five times as often as men.

Some Native American groups have higher prevalence rates (5–6%) and people from the Caribbean region have lower prevalence rates.

The age at which the disease most commonly starts is in women between 40 and 50 years of age, and for men somewhat later. RA is a chronic disease, and although rarely, a spontaneous remission may occur, the natural course is almost invariably one of persistent symptoms, waxing and waning in intensity, and a progressive deterioration of joint structures leading to deformations and disability.

IMAGES

CERVICAL AND LUMBAR SPONDYLOSYS - severe degree - G.Srihari, Head Master, Secunderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Pain, numbness and weakness in my limbs, neck and back gradually increased over a period of seven years. Moving in the house without other’s support was difficult,I could not take care of my own needs. Neurosurgeons advised me immediate operation. I was also diabetic.

MODE OF RECOVERY AT NEW LIFE CENTRE

The pain, numbness and weakness in my limbs, neck and back gradually decreased over a period of few weeks and I am now free from all the complaints and am quite healthy and active. Diabetes is also under control.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Spondylosis is a term referring to degenerative osteoarthritis of the joints between the center of the spinal vertebrae and/or neural foramina. If this condition occurs in the zygapophysial joints, it can be considered facet syndrome. If severe, it may cause pressure on nerve roots with subsequent sensory and/or motor disturbances, such as pain, paresthesia, or muscle weakness in the limbs.

When the space between two adjacent vertebrae narrows, compression of a nerve root emerging from the spinal cord may result in radiculopathy (sensory and motor disturbances, such as severe pain in the neck, shoulder, arm, back, and/or leg, accompanied by muscle weakness). Less commonly, direct pressure on the spinal cord (typically in the cervical spine) may result in myelopathy, characterized by global weakness, gait dysfunction, loss of balance, and loss of bowel and/or bladder control. The patient may experience a phenomenon of shocks (paresthesia) in hands and legs because of nerve compression and lack of blood flow. If vertebrae of the neck are involved it is labelled cervical spondylosis. Lower back spondylosis is labeled lumbar spondylosis.

CAUSES

Spondylosis can affect a person at any age; however, older people are more susceptible.

DIAGNOSIS

  • Spurling's test is performed by laterally flexing the patient's head and placing downward pressure on it. A positive sign is neck or shoulder pain on the ipsilateral side, that is, the side to which the head is laterally flexed. This is somewhat predictive of cervical spondylosis.
  • Lhermitte sign, feeling of electrical shock with neck flexion;
  • reduced range of motion of the neck, the most frequent objective finding on physical examination
  • MRI testing. This test is non-invasive and provides the only definitive positive diagnosis.

TREATMENT

Treatment is usually conservative in nature. Patient education on lifestyle modifications and nonsteroidal anti-inflammatory drugs (NSAIDs) and physical therapy have been shown to manage such conditions. Other alternative therapies such as massage, trigger-point therapy, yoga and acupuncture may be of limited benefit. Surgery is occasionally performed.

Many of the treatments for cervical spondylosis have not been subjected to rigorous, controlled trials. Surgery is advocated for cervical radiculopathy in patients who have intractable pain, progressive symptoms, or weakness that fails to improve with conservative therapy. Surgical indications for cervical spondylosis with myelopathy (CSM) remain somewhat controversial, but "most clinicians recommend operative therapy over conservative therapy for moderate-to-severe myelopathy." (Baron, M.E.)

Physical therapy may be effective for restoring range of motion, flexibility, and core strengthening. Decompressive therapies (i.e. manual mobilization, mechanical traction) may also help alleviate pain. However, physical therapy and chiropractic cannot "cure" the degeneration, and some people view that strong compliance with postural modification is necessary to realize maximum benefit from decompression, adjustments, and flexibility rehabilitation.

It is often argued, however, that the cause of spondylosis is simply old age, and that posture modification treatment is often practiced by those who have a financial interest (such as Worker's Compensation) in proving that it is caused by work conditions and poor physical habits. Understanding anatomy is the key to conservative management of spondylosis.

SURGERY

A major problem related to this disease is vertebrobasilar insufficiency. This is a result of the vertebral artery becoming occluded as it passes up in the transverse foramen. The spinal joints become stiff in cervical spondylosis. Thus the chondrocytes which maintain the disc become deprived of nutrition and die. The weakened disc bulges and grows out as a result of incoming osteophytes.

  • Laminectomy

IMAGES

CASE RECORD

DISC PROLAPSE - Sciatica - Ramesh, Area Manager, Escorts, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

There was severe backache with radiation of pain to leg. No relief even after three weeks of rest as advised by orthopaedic surgeon Neurosurgeon advised me a costly and risky operation.

MODE OF RECOVERY AT NEW LIFE CENTRE

Homeopathic treatment given by New Life health care could provide me rapid and safe relief and I was able to attend my job in just two weeks.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Sciatica (sciatic neuritis, sciatic neuralgia, or lumbar radiculopathy) is a set of symptoms including pain caused by general compression or irritation of one of five spinal nerve roots of each sciatic nerve—or by compression or irritation of the left or right or both sciatic nerves. Symptoms include lower back pain, buttock pain, and numbness, pain or weakness in various parts of the leg and foot. Other symptoms include a "pins and needles" sensation, or tingling and difficulty moving or controlling the leg. Typically, symptoms only manifest on one side of the body. The pain may radiate above the knee, but does not always.

Sciatica is a relatively common form of low back and leg pain, but the true meaning of the term is often misunderstood. Sciatica is a set of symptoms rather than a diagnosis for what is irritating the root of the nerve to cause the pain. Treatment for sciatica or sciatic symptoms often differs, depending on underlying causes and pain levels. Causes include compression of the sciatic nerve roots by a herniated (torn) or protruding disc in the lower back.

DEFINITION

The term sciatica describes a symptom rather than a specific disease. Some use it to mean any pain starting in the lower back and going down the leg. Others use the term more specifically to mean a nerve dysfunction caused by compression of one or more lumbar or sacral nerve roots from a spinal disc herniation. Pain typically occurs in the distribution of a dermatome and goes below the knee to the foot. It may be associated with neurological dysfunction, such as weakness. The pain is characteristically of shooting type, quickly traveling along the course of the nerve.

CAUSES

Spinal disc herniation

Spinal disc herniation pressing on one of the lumbar or sacral nerve roots is the primary cause of sciatica, being present in about 90% of cases. Sciatica caused by pressure from a disc herniation and swelling of surrounding tissue can spontaneously subside if the tear in the disc heals and the pulposus extrusion and inflammation cease.

Spinal stenosis

Other compressive spinal causes include lumbar spinal stenosis, a condition in which the spinal canal (the spaces the spinal cord runs through) narrows and compresses the spinal cord, cauda equina, or sciatic nerve roots. This narrowing can be caused by bone spurs, spondylolisthesis, inflammation, or herniated disc, which decreases available space for the spinal cord, thus pinching and irritating nerves from the spinal cord that travel to the sciatic nerves.

Piriformis syndrome

Piriformis syndrome is a controversial condition that, depending on the analysis, varies from a "very rare" cause to contributing to up to 8% of low back or buttock pain.[7] In 15% of the population, the sciatic nerve runs through, or under the piriformis muscle rather than beneath it. When the muscle shortens or spasms due to trauma or overuse, it's posited that this causes compression of the sciatic nerve. It has colloquially been referred to as "wallet sciatica" since a wallet carried in a rear hip pocket compresses the buttock muscles and sciatic nerve when the bearer sits down. Piriformis syndrome cause sciatica when the nerve root is normal.

Pregnancy

Sciatica may also occur during pregnancy as a result of the weight of the fetus pressing on the sciatic nerve during sitting or during leg spasms. While most cases do not directly harm the fetus or the mother, indirect harm may come from the numbing effect on the legs, which can cause loss of balance and falling. There is no standard treatment for pregnancy induced sciatica.

Other

Sciatica can also be caused by tumours impinging on the spinal cord or the nerve roots. Severe back pain extending to the hips and feet, loss of bladder or bowel control, or muscle weakness may result from spinal tumours or cauda equina syndrome. Trauma to the spine, such as from a car accident, may also lead to sciatica.

PATHOPHYSIOLOGY

Sciatica is generally caused by the compression of lumbar nerves L3, L4, or L5 or sacral nerves S1, S2, or S3, or by compression of the sciatic nerve itself. When sciatica is caused by compression of a dorsal nerve root (radix), it is considered a lumbar radiculopathy (or radiculitis when accompanied with an inflammatory response). This can occur as a result of a spinal disk bulge or spinal disc herniation (a herniated intervertebral disc), or from roughening, enlarging, or misalignment (spondylolisthesis) of the vertebrae, or as a result of degenerated discs that can reduce the diameter of the lateral foramen (natural hole) through which nerve roots exit the spine. The intervertebral discs consist of an anulus fibrosus, which forms a ring surrounding the inner nucleus pulposus. When there is a tear in the anulus fibrosus, the nucleus pulposus (pulp) may extrude through the tear and press against spinal nerves within the spinal cord, cauda equina, or exiting nerve roots, causing inflammation, numbness, or excruciating pain. Inflammation in the spinal canal can also spread to adjacent facet joints and cause lower back pain and/or referred pain in the posterior thigh(s). Pseudosciatic pain can also be caused by compression of peripheral sections of the nerve, usually from soft tissue tension in the piriformis or related muscles.

The spinal discs are composed of a tough spongiform ring of cartilage ("anulus fibrosus") with a more malleable center ("nucleus pulposus"). The discs separate the vertebrae, thereby allowing room for the nerve roots to properly exit through the spaces between the vertebrae. The discs cushion the spine from compressive forces, but are weak to pressure applied during rotational movements. That is why a person who bends to one side, at a bad angle to pick something up, may more likely herniate a spinal disc than a person jumping from a ladder and landing on their feet.

Herniation of a disc occurs when the liquid center of the disc bulges outwards, tearing the external ring of fibers, extrudes into the spinal canal, and compresses a nerve root against the lamina or pedicle of a vertebra, thus causing sciatica. This extruded liquid from the "nucleus pulposus" may cause inflammation and swelling of surrounding tissue, which may cause further compression of the nerve root in the confined space in the spinal canal.

DIAGNOSIS

Sciatica is typically diagnosed by physical examination, and the history of the symptoms. Generally if a person reports the typical radiating pain in one leg as well as one or more neurological indications of nerve root tension or neurological deficit, sciatica can be diagnosed.

The most applied diagnostic test is the straight leg raise to produce Lasègue's sign, which is considered positive if pain in the distribution of the sciatic nerve is reproduced with between 30 and 70 degrees passive flexion of the straight leg. While this test is positive in about 90% of people with sciatica, approximately 75% of people with a positive test do not have sciatica.

Imaging tests such as computerised tomography or magnetic resonance imaging can help with the diagnosis of lumbar disc herniation. The utility of MR neurography in the diagnoses of piriformis syndrome is controversial.

MANAGEMENT

When the cause of sciatica is lumbar disc herniation, most cases resolve spontaneously over weeks to months. Initially treatment in the first 6–8 weeks should be conservative. There does not appear to be a significant difference in outcomes between advice to stay active and recommendations of bed rest. Similarly, physical therapy (exercises) has not been found better than bed rest.

Medication

Although medicines are commonly prescribed for the treatment of sciatica, evidence for analgesics is poor. Specifically, NSAIDs do not appear to improve immediate pain and all NSAIDs appear about equivalent. Evidence is also lacking in use of opioids and muscle relaxants. In those with sciatica due to piriformis syndrome, botulism toxin injections may improve pain and or function. There is little evidence for steroids, either epidural or by pill.

Surgery

Surgery for unilateral sciatica involves the removal of part of the disc, known as a discectomy. While it results in short term benefits, long term benefits appear equivalent to conservative care. Treatment of the underlying cause of the compression is needed in cases of epidural abscess, epidural tumors, and cauda equina syndrome.

Alternative medicine

Moderate quality evidence suggests that spinal manipulation is an effective treatment for acute sciatica. For chronic sciatica the evidence is poor. Spinal manipulation has been found generally safe for the treatment of disc-related pain; however, case reports have found an association with cauda equina syndrome and it is contraindicated when there are progressive neurological deficits.

EPIDEMIOLOGY

Depending on how it is defined, 1.6% to 43% of people have sciatica.

IMAGES

INJURY TO SPINE-Severe backache - Chinapu Reddy, Tarnaka, Secunderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

In 2006 I fell down vertically from a water tanker onto a metal pipe of tractor trolly. The pain gradually increased to cripple me in all my activities Any movement in any position was highly painful and there was no relief even after four years of treatment by experts. MRI of Spine revealed severe damage to my vertebrae and I was advised operation followed by rest for 18 months by three surgeons. The proposed operation was learnt to be not safe.

MODE OF RECOVERY AT NEW LIFE CENTRE

In 2010 I started taking homeopathy from NEW LIFE centre. The relief started in the very first week and the recovery was maximum in fourth month. The severity of pain in my back and legs disappeared to a large extent and I could carry on my daily activities as usual.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Spondylosis is a term referring to degenerative osteoarthritis of the joints between the center of the spinal vertebrae and/or neural foramina. If this condition occurs in the zygapophysial joints, it can be considered facet syndrome. If severe, it may cause pressure on nerve roots with subsequent sensory and/or motor disturbances, such as pain, paresthesia, or muscle weakness in the limbs.

When the space between two adjacent vertebrae narrows, compression of a nerve root emerging from the spinal cord may result in radiculopathy (sensory and motor disturbances, such as severe pain in the neck, shoulder, arm, back, and/or leg, accompanied by muscle weakness). Less commonly, direct pressure on the spinal cord (typically in the cervical spine) may result in myelopathy, characterized by global weakness, gait dysfunction, loss of balance, and loss of bowel and/or bladder control. The patient may experience a phenomenon of shocks (paresthesia) in hands and legs because of nerve compression and lack of blood flow. If vertebrae of the neck are involved it is labelled cervical spondylosis. Lower back spondylosis is labeled lumbar spondylosis.

CAUSES

Spondylosis can affect a person at any age; however, older people are more susceptible.

DIAGNOSIS

  • Spurling's test is performed by laterally flexing the patient's head and placing downward pressure on it. A positive sign is neck or shoulder pain on the ipsilateral side, that is, the side to which the head is laterally flexed. This is somewhat predictive of cervical spondylosis.
  • Lhermitte sign, feeling of electrical shock with neck flexion;
  • reduced range of motion of the neck, the most frequent objective finding on physical examination
  • MRI testing. This test is non-invasive and provides the only definitive positive diagnosis.

TREATMENT

Treatment is usually conservative in nature. Patient education on lifestyle modifications and nonsteroidal anti-inflammatory drugs (NSAIDs) and physical therapy have been shown to manage such conditions. Other alternative therapies such as massage, trigger-point therapy, yoga and acupuncture may be of limited benefit. Surgery is occasionally performed.

Many of the treatments for cervical spondylosis have not been subjected to rigorous, controlled trials. Surgery is advocated for cervical radiculopathy in patients who have intractable pain, progressive symptoms, or weakness that fails to improve with conservative therapy. Surgical indications for cervical spondylosis with myelopathy (CSM) remain somewhat controversial, but "most clinicians recommend operative therapy over conservative therapy for moderate-to-severe myelopathy." (Baron, M.E.)

Physical therapy may be effective for restoring range of motion, flexibility, and core strengthening. Decompressive therapies (i.e. manual mobilization, mechanical traction) may also help alleviate pain. However, physical therapy and chiropractic cannot "cure" the degeneration, and some people view that strong compliance with postural modification is necessary to realize maximum benefit from decompression, adjustments, and flexibility rehabilitation.

It is often argued, however, that the cause of spondylosis is simply old age, and that posture modification treatment is often practiced by those who have a financial interest (such as Worker's Compensation) in proving that it is caused by work conditions and poor physical habits. Understanding anatomy is the key to conservative management of spondylosis.

SURGERY

A major problem related to this disease is vertebrobasilar insufficiency. This is a result of the vertebral artery becoming occluded as it passes up in the transverse foramen. The spinal joints become stiff in cervical spondylosis. Thus the chondrocytes which maintain the disc become deprived of nutrition and die. The weakened disc bulges and grows out as a result of incoming osteophytes.

  • Laminectomy

IMAGES

CASE RECORD

SEVERE PAIN IN BACK AND LEGS - Saritha, Principal, G. Model School, Hyderabad.

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I had severe crushing pain in my legs along with backache. No beneficial effect with the medicines given by Orthopaedic surgeons. Any short walk was a hell and demanded the support of two people on either side. Every step was highly painful.The gravity of my pain limited my activity to the bed and bathroom only and I could not do any other work for the past one year. I never thought I could walk in my life again.

MODE OF RECOVERY AT NEW LIFE CENTRE

Mr Suresh,a parent of one student who observed my condition brought me to Dr Subhash Chandar.I can now walk freely without any pain after taking homeopathy. I can attend all my domestic and official work easily. It is a fact that something impossible has been made possible in my case.I have experienced it and realised it. I am very much indebted to the doctor for his unique treatment.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Lumbosacral spondylosis is a basic term used by medical professionals to describe common, age-related degeneration in the lower back at the site where the last vertebra of the lumbar spine (L5) and the first vertebra of the sacral spine (S1) connect. This area is especially prone to deterioration because the lower back supports upright posture and many different bending and twisting movements, and also because it supports such a large amount of weight.

SIGNS AND SYMPTOMS

Specific conditions that fall under the umbrella term of lumbosacral spondylosis can include herniated discs, bulging discs, bone spurs and osteoarthritis, all of which are spinal abnormalities that run the risk of protruding into the spinal canal and exerting pressure on spinal nerves. The sciatic nerve is often compressed at the meeting of the L5 and S1 vertebrae. Common symptoms of sciatic nerve compression include tingling, numbness, weakness and pain that can spread through the following areas:

  • Lower back
  • Tailbone
  • Buttocks
  • Hip joints
  • Toes
  • Back of thighs (hamstrings)
  • Calves
  • Feet

TREATMENT

While you would not directly treat spondylosis itself since the term does not specifically pinpoint a condition that’s treatable, you can certainly treat the herniated disc, joint or vertebra that is part of overall spine degeneration. The majority of patients will find that weeks or months of stretching, low-impact exercise, pain medication, hot-cold therapy and behavior modification can sufficiently manage their symptoms. For the small percentage of patients whose degenerative spine condition worsens over time, there is Laser Spine Institute, the leader in minimally invasive spine surgery. Contact us today to find out more about our outpatient procedures that offer fewer risks and faster recuperation times compared to traditional open spine surgeries.

IMAGES

INJURY TO KNEE- chronic pain - A.Kumar, Bihar

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I met with an accident in 2008.My knee was severely injured Took treatment from orthopaedic experts. But the pain did not disappear totally; I had to take help of walking stick for nearly one year despite taking pain killer tablets and injections.

MODE OF RECOVERY AT NEW LIFE CENTRE

Two doses of homeopathic doses from Dr Subhash worked wonders. My pain has gone completely and there is no recurrence till date even after 5 years.
Similarly my mother, who is in Bihar, used to suffer from pain in the knees. She consulted many doctors who advised her pain killers etc. She was forced to limp with pain despite being on medicines She was shown to Dr Subhash Chandar. She is now perfectly alright after taking his medicine. There is no more of the pain and limping.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Osteoarthritis (OA) also known as degenerative arthritis or degenerative joint disease or osteoarthrosis, is a group of mechanical abnormalities involving degradation of joints, including articular cartilage and subchondral bone. Symptoms may include joint pain, tenderness, stiffness, locking, and sometimes an effusion. A variety of causes—hereditary, developmental, metabolic, and mechanical deficits—may initiate processes leading to loss of cartilage. When bone surfaces become less well protected by cartilage, bone may be exposed and damaged. As a result of decreased movement secondary to pain, regional muscles may atrophy, and ligaments may become more lax.

Treatment generally involves a combination of exercise, lifestyle modification, and analgesics. If pain becomes debilitating, joint replacement surgery may be used to improve the quality of life. OA is the most common form of arthritis, and the leading cause of chronic disability in the United States. It affects about 1.9 million people in Australia, 8 million people in the United Kingdom and nearly 27 million people in the United States.

SIGNS AND SYMPTOMS

The main symptom is pain, causing loss of ability and often stiffness. "Pain" is generally described as a sharp ache or a burning sensation in the associated muscles and tendons. OA can cause a crackling noise (called "crepitus") when the affected joint is moved or touched and people may experience muscle spasms and contractions in the tendons. Occasionally, the joints may also be filled with fluid. Some people report increased pain associated with cold temperature, high humidity, and/or a drop in barometric pressure, but studies have had mixed results.

OA commonly affects the hands, feet, spine, and the large weight bearing joints, such as the hips and knees, although in theory, any joint in the body can be affected. As OA progresses, the affected joints appear larger, are stiff and painful, and usually feel better with gentle use but worse with excessive or prolonged use, thus distinguishing it from rheumatoid arthritis.

In smaller joints, such as at the fingers, hard bony enlargements, called Heberden's nodes (on the distal interphalangeal joints) and/or Bouchard's nodes (on the proximal interphalangeal joints), may form, and though they are not necessarily painful, they do limit the movement of the fingers significantly. OA at the toes leads to the formation of bunions, rendering them red or swollen. Some people notice these physical changes before they experience any pain.OA is the most common cause of a joint effusion of the knee.

CAUSES

Damage from mechanical stress with insufficient self repair by joints is believed to be the primary cause of osteoarthritis. Sources of this stress may include: misalignments of bones caused by congenital or pathogenic causes; mechanical injury; excess body weight; loss of strength in the muscles supporting a joint; and impairment of peripheral nerves, leading to sudden or uncoordinated movements. However exercise, including running in the absence of injury, has not been found to increase the risk. Nor has cracking one's knuckles been found to play a role.

Primary

A number of studies have shown that there is a greater prevalence of the disease among siblings and especially identical twins, indicating a hereditary basis. Although a single factor is not generally sufficient to cause the disease, about half of the variation in susceptibility has been assigned to genetic factors.

As early human ancestors evolved into bipeds, changes occurred in the pelvis, hip joint and spine which increased the risk of osteoarthritis. Additionally genetic variations that increase the risk were likely not selected against because usually problems only occur after reproductive success.

The development of OA is correlated with a history of previous joint injury and with obesity, especially with respect to knees.[16] Since the correlation with obesity has been observed not only for knees but also for non-weight bearing joints and the loss of body fat is more closely related to symptom relief than the loss of body weight, it has been suggested that there may be a metabolic link to body fat as opposed to just mechanical loading.

Changes in sex hormone levels may play a role in the development of OA as it is more prevalent among post-menopausal women than among men of the same age. A study of mice found natural female hormones to be protective while injections of the male hormone dihydrotestosterone reduced protection.

Secondary

This type of OA is caused by other factors but the resulting pathology is the same as for primary OA:

  • Alkaptonuria
  • Congenital disorders of joints
  • Diabetes
  • Ehlers-Danlos Syndrome
  • Hemochromatosis and Wilson's disease
  • Inflammatory diseases (such as Perthes' disease), (Lyme disease), and all chronic forms of arthritis (e.g. costochondritis, gout, and rheumatoid arthritis). In gout, uric acid crystals cause the cartilage to degenerate at a faster pace.
  • Injury to joints or ligaments (such as the ACL), as a result of an accident or orthopedic operations.
  • Ligamentous deterioration or instability may be a factor.
  • Marfan syndrome
  • Obesity
  • Septic arthritis (infection of a joint)

PATHOPHYSIOLOGY

Primary OA is a chronic degenerative disorder related to but not caused by aging, as there are people well into their nineties who have no clinical or functional signs of the disease. As a person ages, the water content of the cartilage decreases as a result of a reduced proteoglycan content, thus causing the cartilage to be less resilient. The water content of healthy cartilage is finely balanced by compressive force driving water out & swelling pressure drawing water in. Collagen fibres exert the compressive force, whereas the Gibbs–Donnan effect & cartilage proteoglycans create osmotic pressure which tends to draw water in.[22] However during onset of OA there is an increase in cartilage water content. This increase occurs because whilst there is an overall loss of proteoglycans,[24][28] it is outweighed by a loss of collagen. Without the protective effects of the proteoglycans, the collagen fibers of the cartilage can become susceptible to degradation and thus exacerbate the degeneration. Inflammation of the surrounding joint capsule can also occur, though often mild (compared to what occurs in rheumatoid arthritis). This can happen as breakdown products from the cartilage are released into the synovial space, and the cells lining the joint attempt to remove them. New bone outgrowths, called "spurs" or osteophytes, can form on the margins of the joints, possibly in an attempt to improve the congruence of the articular cartilage surfaces. These bone changes, together with the inflammation, can be both painful and debilitating.

DIAGNOSIS

Diagnosis is made with reasonable certainty based on history and clinical examination. X-rays may confirm the diagnosis. The typical changes seen on X-ray include: joint space narrowing, subchondral sclerosis (increased bone formation around the joint), subchondral cyst formation, and osteophytes. Plain films may not correlate with the findings on physical examination or with the degree of pain. Usually other imaging techniques are not necessary to clinically diagnose OA.

In 1990, the American College of Rheumatology, using data from a multi-center study, developed a set of criteria for the diagnosis of hand OA based on hard tissue enlargement and swelling of certain joints. These criteria were found to be 92% sensitive and 98% specific for hand OA versus other entities such as rheumatoid arthritis and spondyloarthropathies.

Related pathologies whose names may be confused with OA include pseudo-arthrosis. This is derived from the Greek words pseudo, meaning "false", and arthrosis, meaning "joint." Radiographic diagnosis results in diagnosis of a fracture within a joint, which is not to be confused with OA which is a degenerative pathology affecting a high incidence of distal phalangeal joints of female patients. A polished ivory-like appearance may also develop on the bones of the affected joints, reflecting a change called eburnation.

CLASSIFICATION

OA can be classified into either primary or secondary depending on whether or not there is an identifiable underlying cause.

Both primary generalized nodal OA and erosive OA (EOA, also called inflammatory OA) are sub-sets of primary OA. EOA is a much less common, and more aggressive inflammatory form of OA which often affects the distal interphalangeal joints of the hand and has characteristic articular erosive changes on x-ray.

MANAGEMENT

Lifestyle modification (such as weight loss and exercise) and analgesics are the mainstay of treatment. Acetaminophen (also known as paracetamol) is recommended first line with NSAIDs being used as add on therapy only if pain relief is not sufficient. This is due to the relative greater safety of acetaminophen.

Lifestyle modification

For overweight people, weight loss may be an important factor. Patient education has been shown to be helpful in the self-management of arthritis. It decreases pain, improves function, reduces stiffness and fatigue, and reduces medical usage. Patient education can provide on average 20% more pain relief when compared to NSAIDs alone in patients with hip OA.[

Physical measures

Moderate exercise is beneficial with respect to pain and function in those with osteoathritis of the knee and hip. These exercises should occur at least three times per week. While some evidence supports certain physical therapies evidence for a combined program is limited. There is not enough evidence to determine the effectiveness of massage therapy.

The use of orthoses (which include splints, braces or insoles) have been studied. Lateral wedge insoles do not appear to be useful in osteoarthritis of the knee. Knee braces may be useful.

The evidence for manual therapy is inconclusive. Functional, gait, and balance training has been recommended to address impairments of position sense, balance, and strength in individuals with lower extremity arthritis as these can contribute to higher falls in older individuals.

Medication

The analgesic acetaminophen is the first line treatment for OA. For mild to moderate symptoms effectiveness is similar to non-steroidal anti-inflammatory drugs (NSAIDs), though for more severe symptoms NSAIDs may be more effective. NSAIDs such as naproxen while more effective in severe cases are associated with greater side effects such as gastrointestinal bleeding. Another class of NSAIDs, COX-2 selective inhibitors (such as celecoxib) are equally effective to NSAIDs with lower rates of adverse gastrointestinal effects but higher rates of cardiovascular disease such as myocardial infarction. They are also much more expensive. Oral steroids are not recommended in the treatment of OA because of their modest benefit and high rate of adverse effects.

There are several NSAIDs available for topical use including diclofenac. Topical and oral diclofenac work equally well with topical having a greater risk of mild skin reactions but no greater risk of gastrointestinal adverse effects. Opioid analgesics such as morphine and fentanyl reduce pain, but this benefit is outweighed by frequent adverse events and thus they should not routinely be used. Topical capsaicin is controversial with some reviews finding benefit and others not.

Injection of glucocorticoids (such as hydrocortisone) leads to short term pain relief that may last between a few weeks and a few months. Joint injections of hyaluronic acid have not been found to lead to significant improvement. Hyaluronic acid injects have been associated with significant harm. Nevertheless another study about hyaluronic acid injections says efficacy on pain and function, and no adverse effect when compared to saline injections. Injections of platelet rich plasma improves function but not pain and is associated with increased risk.

Surgery

If disability is significant and more conservative management is ineffective, joint replacement surgery or resurfacing may be recommended. Evidence supports joint replacement for both knees and hips. For the knee it improves both pain and functioning. Arthroscopic surgical intervention for OA of the knee however has been found to be no better than placebo at relieving symptoms.

Alternative Medicine

Dietary supplements

Many dietary supplements are sold as treatments for OA and some of them have been found to be effective.

Since glucosamine is a precursor for glycosaminoglycans, and glycosaminoglycans are a major component of cartilage, some have hoped that supplemental glucosamine could beneficially influence cartilage structure, and alleviate arthritis. Its use as a therapy for osteoarthritis appears safe, but there is no good evidence for its effectiveness. There have been multiple clinical trials testing glucosamine as a potential medical therapy for osteoarthritis, but the results have not supported its use.

Phytodolor, SAMe, and SKI 306X (a Chinese herbal mixture) may be effective in improving pain, and there is some evidence to support the use of cat's claw as an anti-inflammatory. There is tentative evidence to support avocado/soybean unsaponifiables (ASU), Boswellia serrata extracts (frankincense), MSM and rose hip.

There is little evidence supporting benefits for some supplements, including: the Ayurvedic herbal preparations with brand names Articulin F and Eazmov, collagen, devil's claw, Duhuo Jisheng Wan (a Chinese herbal preparation), fish liver oil, ginger, the herbal preparation Gitadyl, glucosamine, hyaluronic acid, omega-3 fatty acids, the brand-name product Reumalax, stinging nettle, turmeric, vitamins A, C, and E in combination, vitamin E alone, vitamin K and willow bark. There is insufficient evidence to make a recommendation about the safety and efficacy of these treatments.

Manual therapies

While acupuncture leads to a statistically significant improvement in pain relief, this improvement is small and may be of questionable clinical significance. Waiting list-controlled trials for peripheral joint osteoarthritis do show clinically relevant benefits, but these may be due to placebo effects. Acupuncture does not seem to produce long-term benefits. While electrostimulation techniques such as TENS have been used for twenty years to treat osteoarthritis in the knee, there is no conclusive evidence to show that it reduces pain or disability.

EPIDEMIOLOGY

OA is derived from the Greek word part osteo-, meaning "of the bone", combined with arthritis: arthr-, meaning "joint", and -itis, the meaning of which has come to be associated with inflammation. The -itis of OA could be considered misleading as inflammation is not a conspicuous feature. Some clinicians refer to this condition as osteoarthosis to signify the lack of inflammatory response.

IMAGES

LUMBAR SPONDYLOSYS - backache and sciatica - M.Devi, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I am a teacher. I was having severe pain in my back since last 7 months. I could not sit, stand or walk for long periods. I could not even sleep peacefully. Orthopaedic surgeons took an X- Ray and MRI and advised me rest and pain killers. I was sleepy with their tablets but my pain did not subside and consequently could not attend my duty.

MODE OF RECOVERY AT NEW LIFE CENTRE

My neighbour who got cured with homeopathy insisted on us to visit Dr.Subhash Chandar for a safe, real and fast cure. When I visited the doctor my condition did not allow me to sit .I lied down on a bed. I was doubting a cure of my serious and painful condition by homeopathy.But miraculously,my pain has disappeared completely after taking his treatment. There is no recurrence even after 18 months of time. He is a God.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Lumbosacral spondylosis is a basic term used by medical professionals to describe common, age-related degeneration in the lower back at the site where the last vertebra of the lumbar spine (L5) and the first vertebra of the sacral spine (S1) connect. This area is especially prone to deterioration because the lower back supports upright posture and many different bending and twisting movements, and also because it supports such a large amount of weight.

SIGNS AND SYMPTOMS

Specific conditions that fall under the umbrella term of lumbosacral spondylosis can include herniated discs, bulging discs, bone spurs and osteoarthritis, all of which are spinal abnormalities that run the risk of protruding into the spinal canal and exerting pressure on spinal nerves. The sciatic nerve is often compressed at the meeting of the L5 and S1 vertebrae. Common symptoms of sciatic nerve compression include tingling, numbness, weakness and pain that can spread through the following areas:

  • Lower back
  • Tailbone
  • Buttocks
  • Hip joints
  • Toes
  • Back of thighs (hamstrings)
  • Calves
  • Feet

TREATMENT

While you would not directly treat spondylosis itself since the term does not specifically pinpoint a condition that’s treatable, you can certainly treat the herniated disc, joint or vertebra that is part of overall spine degeneration. The majority of patients will find that weeks or months of stretching, low-impact exercise, pain medication, hot-cold therapy and behavior modification can sufficiently manage their symptoms. For the small percentage of patients whose degenerative spine condition worsens over time, there is Laser Spine Institute, the leader in minimally invasive spine surgery. Contact us today to find out more about our outpatient procedures that offer fewer risks and faster recuperation times compared to traditional open spine surgeries.

IMAGES

OSTEOARTHRITIS - Knee Joint Pain - Rajaiah, Godavari Khani

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Pain in both knees for 5 years. Consulted experts of Karimnagar, Godavarikhani and Huzurabad but in vain. I could not attend my duty in Singareni collieries for some months.

MODE OF RECOVERY AT NEW LIFE CENTRE

Treatment by Dr.Subhash Chandar relieved my pains by about 75% in just 2 months only. The pains have not recurred even after 3 years of his treatment. I am happy and performing my duty in coal mines regularly.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Osteoarthritis (OA) also known as degenerative arthritis or degenerative joint disease or osteoarthrosis, is a group of mechanical abnormalities involving degradation of joints, including articular cartilage and subchondral bone. Symptoms may include joint pain, tenderness, stiffness, locking, and sometimes an effusion. A variety of causes—hereditary, developmental, metabolic, and mechanical deficits—may initiate processes leading to loss of cartilage. When bone surfaces become less well protected by cartilage, bone may be exposed and damaged. As a result of decreased movement secondary to pain, regional muscles may atrophy, and ligaments may become more lax.

Treatment generally involves a combination of exercise, lifestyle modification, and analgesics. If pain becomes debilitating, joint replacement surgery may be used to improve the quality of life. OA is the most common form of arthritis, and the leading cause of chronic disability in the United States. It affects about 1.9 million people in Australia, 8 million people in the United Kingdom and nearly 27 million people in the United States.

SIGNS AND SYMPTOMS

The main symptom is pain, causing loss of ability and often stiffness. "Pain" is generally described as a sharp ache or a burning sensation in the associated muscles and tendons. OA can cause a crackling noise (called "crepitus") when the affected joint is moved or touched and people may experience muscle spasms and contractions in the tendons. Occasionally, the joints may also be filled with fluid. Some people report increased pain associated with cold temperature, high humidity, and/or a drop in barometric pressure, but studies have had mixed results.

OA commonly affects the hands, feet, spine, and the large weight bearing joints, such as the hips and knees, although in theory, any joint in the body can be affected. As OA progresses, the affected joints appear larger, are stiff and painful, and usually feel better with gentle use but worse with excessive or prolonged use, thus distinguishing it from rheumatoid arthritis.

In smaller joints, such as at the fingers, hard bony enlargements, called Heberden's nodes (on the distal interphalangeal joints) and/or Bouchard's nodes (on the proximal interphalangeal joints), may form, and though they are not necessarily painful, they do limit the movement of the fingers significantly. OA at the toes leads to the formation of bunions, rendering them red or swollen. Some people notice these physical changes before they experience any pain.OA is the most common cause of a joint effusion of the knee.

CAUSES

Damage from mechanical stress with insufficient self repair by joints is believed to be the primary cause of osteoarthritis. Sources of this stress may include: misalignments of bones caused by congenital or pathogenic causes; mechanical injury; excess body weight; loss of strength in the muscles supporting a joint; and impairment of peripheral nerves, leading to sudden or uncoordinated movements. However exercise, including running in the absence of injury, has not been found to increase the risk. Nor has cracking one's knuckles been found to play a role.

Primary

A number of studies have shown that there is a greater prevalence of the disease among siblings and especially identical twins, indicating a hereditary basis. Although a single factor is not generally sufficient to cause the disease, about half of the variation in susceptibility has been assigned to genetic factors.

As early human ancestors evolved into bipeds, changes occurred in the pelvis, hip joint and spine which increased the risk of osteoarthritis. Additionally genetic variations that increase the risk were likely not selected against because usually problems only occur after reproductive success.

The development of OA is correlated with a history of previous joint injury and with obesity, especially with respect to knees.[16] Since the correlation with obesity has been observed not only for knees but also for non-weight bearing joints and the loss of body fat is more closely related to symptom relief than the loss of body weight, it has been suggested that there may be a metabolic link to body fat as opposed to just mechanical loading.

Changes in sex hormone levels may play a role in the development of OA as it is more prevalent among post-menopausal women than among men of the same age. A study of mice found natural female hormones to be protective while injections of the male hormone dihydrotestosterone reduced protection.

Secondary

This type of OA is caused by other factors but the resulting pathology is the same as for primary OA:

  • Alkaptonuria
  • Congenital disorders of joints
  • Diabetes
  • Ehlers-Danlos Syndrome
  • Hemochromatosis and Wilson's disease
  • Inflammatory diseases (such as Perthes' disease), (Lyme disease), and all chronic forms of arthritis (e.g. costochondritis, gout, and rheumatoid arthritis). In gout, uric acid crystals cause the cartilage to degenerate at a faster pace.
  • Injury to joints or ligaments (such as the ACL), as a result of an accident or orthopedic operations.
  • Ligamentous deterioration or instability may be a factor.
  • Marfan syndrome
  • Obesity
  • Septic arthritis (infection of a joint)

PATHOPHYSIOLOGY

Primary OA is a chronic degenerative disorder related to but not caused by aging, as there are people well into their nineties who have no clinical or functional signs of the disease. As a person ages, the water content of the cartilage decreases as a result of a reduced proteoglycan content, thus causing the cartilage to be less resilient. The water content of healthy cartilage is finely balanced by compressive force driving water out & swelling pressure drawing water in. Collagen fibres exert the compressive force, whereas the Gibbs–Donnan effect & cartilage proteoglycans create osmotic pressure which tends to draw water in.[22] However during onset of OA there is an increase in cartilage water content. This increase occurs because whilst there is an overall loss of proteoglycans,[24][28] it is outweighed by a loss of collagen. Without the protective effects of the proteoglycans, the collagen fibers of the cartilage can become susceptible to degradation and thus exacerbate the degeneration. Inflammation of the surrounding joint capsule can also occur, though often mild (compared to what occurs in rheumatoid arthritis). This can happen as breakdown products from the cartilage are released into the synovial space, and the cells lining the joint attempt to remove them. New bone outgrowths, called "spurs" or osteophytes, can form on the margins of the joints, possibly in an attempt to improve the congruence of the articular cartilage surfaces. These bone changes, together with the inflammation, can be both painful and debilitating.

DIAGNOSIS

Diagnosis is made with reasonable certainty based on history and clinical examination. X-rays may confirm the diagnosis. The typical changes seen on X-ray include: joint space narrowing, subchondral sclerosis (increased bone formation around the joint), subchondral cyst formation, and osteophytes. Plain films may not correlate with the findings on physical examination or with the degree of pain. Usually other imaging techniques are not necessary to clinically diagnose OA.

In 1990, the American College of Rheumatology, using data from a multi-center study, developed a set of criteria for the diagnosis of hand OA based on hard tissue enlargement and swelling of certain joints. These criteria were found to be 92% sensitive and 98% specific for hand OA versus other entities such as rheumatoid arthritis and spondyloarthropathies.

Related pathologies whose names may be confused with OA include pseudo-arthrosis. This is derived from the Greek words pseudo, meaning "false", and arthrosis, meaning "joint." Radiographic diagnosis results in diagnosis of a fracture within a joint, which is not to be confused with OA which is a degenerative pathology affecting a high incidence of distal phalangeal joints of female patients. A polished ivory-like appearance may also develop on the bones of the affected joints, reflecting a change called eburnation.

CLASSIFICATION

OA can be classified into either primary or secondary depending on whether or not there is an identifiable underlying cause.

Both primary generalized nodal OA and erosive OA (EOA, also called inflammatory OA) are sub-sets of primary OA. EOA is a much less common, and more aggressive inflammatory form of OA which often affects the distal interphalangeal joints of the hand and has characteristic articular erosive changes on x-ray.

MANAGEMENT

Lifestyle modification (such as weight loss and exercise) and analgesics are the mainstay of treatment. Acetaminophen (also known as paracetamol) is recommended first line with NSAIDs being used as add on therapy only if pain relief is not sufficient. This is due to the relative greater safety of acetaminophen.

Lifestyle modification

For overweight people, weight loss may be an important factor. Patient education has been shown to be helpful in the self-management of arthritis. It decreases pain, improves function, reduces stiffness and fatigue, and reduces medical usage. Patient education can provide on average 20% more pain relief when compared to NSAIDs alone in patients with hip OA.[

Physical measures

Moderate exercise is beneficial with respect to pain and function in those with osteoathritis of the knee and hip. These exercises should occur at least three times per week. While some evidence supports certain physical therapies evidence for a combined program is limited. There is not enough evidence to determine the effectiveness of massage therapy.

The use of orthoses (which include splints, braces or insoles) have been studied. Lateral wedge insoles do not appear to be useful in osteoarthritis of the knee. Knee braces may be useful.

The evidence for manual therapy is inconclusive. Functional, gait, and balance training has been recommended to address impairments of position sense, balance, and strength in individuals with lower extremity arthritis as these can contribute to higher falls in older individuals.

Medication

The analgesic acetaminophen is the first line treatment for OA. For mild to moderate symptoms effectiveness is similar to non-steroidal anti-inflammatory drugs (NSAIDs), though for more severe symptoms NSAIDs may be more effective. NSAIDs such as naproxen while more effective in severe cases are associated with greater side effects such as gastrointestinal bleeding. Another class of NSAIDs, COX-2 selective inhibitors (such as celecoxib) are equally effective to NSAIDs with lower rates of adverse gastrointestinal effects but higher rates of cardiovascular disease such as myocardial infarction. They are also much more expensive. Oral steroids are not recommended in the treatment of OA because of their modest benefit and high rate of adverse effects.

There are several NSAIDs available for topical use including diclofenac. Topical and oral diclofenac work equally well with topical having a greater risk of mild skin reactions but no greater risk of gastrointestinal adverse effects. Opioid analgesics such as morphine and fentanyl reduce pain, but this benefit is outweighed by frequent adverse events and thus they should not routinely be used. Topical capsaicin is controversial with some reviews finding benefit and others not.

Injection of glucocorticoids (such as hydrocortisone) leads to short term pain relief that may last between a few weeks and a few months. Joint injections of hyaluronic acid have not been found to lead to significant improvement. Hyaluronic acid injects have been associated with significant harm. Nevertheless another study about hyaluronic acid injections says efficacy on pain and function, and no adverse effect when compared to saline injections. Injections of platelet rich plasma improves function but not pain and is associated with increased risk.

Surgery

If disability is significant and more conservative management is ineffective, joint replacement surgery or resurfacing may be recommended. Evidence supports joint replacement for both knees and hips. For the knee it improves both pain and functioning. Arthroscopic surgical intervention for OA of the knee however has been found to be no better than placebo at relieving symptoms.

Alternative Medicine

Dietary supplements

Many dietary supplements are sold as treatments for OA and some of them have been found to be effective.

Since glucosamine is a precursor for glycosaminoglycans, and glycosaminoglycans are a major component of cartilage, some have hoped that supplemental glucosamine could beneficially influence cartilage structure, and alleviate arthritis. Its use as a therapy for osteoarthritis appears safe, but there is no good evidence for its effectiveness. There have been multiple clinical trials testing glucosamine as a potential medical therapy for osteoarthritis, but the results have not supported its use.

Phytodolor, SAMe, and SKI 306X (a Chinese herbal mixture) may be effective in improving pain, and there is some evidence to support the use of cat's claw as an anti-inflammatory. There is tentative evidence to support avocado/soybean unsaponifiables (ASU), Boswellia serrata extracts (frankincense), MSM and rose hip.

There is little evidence supporting benefits for some supplements, including: the Ayurvedic herbal preparations with brand names Articulin F and Eazmov, collagen, devil's claw, Duhuo Jisheng Wan (a Chinese herbal preparation), fish liver oil, ginger, the herbal preparation Gitadyl, glucosamine, hyaluronic acid, omega-3 fatty acids, the brand-name product Reumalax, stinging nettle, turmeric, vitamins A, C, and E in combination, vitamin E alone, vitamin K and willow bark. There is insufficient evidence to make a recommendation about the safety and efficacy of these treatments.

Manual therapies

While acupuncture leads to a statistically significant improvement in pain relief, this improvement is small and may be of questionable clinical significance. Waiting list-controlled trials for peripheral joint osteoarthritis do show clinically relevant benefits, but these may be due to placebo effects. Acupuncture does not seem to produce long-term benefits. While electrostimulation techniques such as TENS have been used for twenty years to treat osteoarthritis in the knee, there is no conclusive evidence to show that it reduces pain or disability.

EPIDEMIOLOGY

OA is derived from the Greek word part osteo-, meaning "of the bone", combined with arthritis: arthr-, meaning "joint", and -itis, the meaning of which has come to be associated with inflammation. The -itis of OA could be considered misleading as inflammation is not a conspicuous feature. Some clinicians refer to this condition as osteoarthosis to signify the lack of inflammatory response.

IMAGES

OSTEOPOROSIS - Fracture of L4 vertebra - K.V.Satyanarayana, subash nagar, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

My father was suffering from severe pain in back and legs. Visited a corporate hospital. MRI of his spine revealed severe degeneration of L4 vertebra. Doctors declined to operate upon him, there was no dependable medicine even. Then he was ailing from severe degree of pain in his back and legs. He was not able to sit, stand or walk without any support. He tended to fall sideways.

MODE OF RECOVERY AT NEW LIFE CENTRE

We approached Dr Subhash of Bowenpally. My father is now relieved of all the pain and he is able to sit, stand or walk without any support. He is attending his work freely on his own .We are all happy.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Osteoporosis is a progressive bone disease that is characterized by a decrease in bone mass and density which can lead to an increased risk of fracture. In osteoporosis, the bone mineral density (BMD) is reduced, bone micro architecture deteriorates, and the amount and variety of proteins in bone are altered. Osteoporosis is defined by the World Health Organization (WHO) as a bone mineral density of 2.5 standard deviations or more below the mean peak bone mass (average of young, healthy adults) as measured by dual-energy X-ray absorptiometry; the term "established osteoporosis" includes the presence of a fragility fracture. The disease may be classified as primary type 1, primary type 2, or secondary. The form of osteoporosis most common in women after menopause is referred to as primary type 1 or postmenopausal osteoporosis. Primary type 2 osteoporosis or senile osteoporosis occurs after age 75 and is seen in both females and males at a ratio of 2:1. Secondary osteoporosis may arise at any age and affect men and women equally. This form results from chronic predisposing medical problems or disease, or prolonged use of medications such as glucocorticoids, when the disease is called steroid- or glucocorticoid-induced osteoporosis.

The risk of osteoporosis fractures can be reduced with lifestyle changes and in those with previous osteoporosis related fractures, medications. Lifestyle change includes diet, exercise, and preventing falls. The utility of calcium and vitamin D is questionable in most. Bisphosphonates are useful in those with previous fractures from osteoporosis but are of minimal benefit in those who have osteoporosis but no previous fractures. Osteoporosis is a component of the frailty syndrome.

SIGNS AND SYMPTOMS

Osteoporosis itself has no symptoms; its main consequence is the increased risk of bone fractures. Osteoporotic fractures occur in situations where healthy people would not normally break a bone; they are therefore regarded as fragility fractures. Typical fragility fractures occur in the vertebral column, rib, hip and wrist.

Fractures

Fractures are the most dangerous aspect of osteoporosis. Debilitating acute and chronic pain in the elderly is often attributed to fractures from osteoporosis and can lead to further disability and early mortality. These fractures may also be asymptomatic. The most common osteoporotic fractures are of the wrist, spine, shoulder and hip. The symptoms of a vertebral collapse ("compression fracture") are sudden back pain, often with radicular pain (shooting pain due to nerve root compression) and rarely with spinal cord compression or cauda equina syndrome. Multiple vertebral fractures lead to a stooped posture, loss of height, and chronic pain with resultant reduction in mobility.

Fractures of the long bones acutely impair mobility and may require surgery. Hip fracture, in particular, usually requires prompt surgery, as serious risks are associated with it, such as deep vein thrombosis and pulmonary embolism, and increased mortality.

Fracture risk calculators assess the risk of fracture based upon several criteria, including BMD, age, smoking, alcohol usage, weight, and gender. Recognized calculators include FRAX and Dubbo.

Falls risk

The increased risk of falling associated with aging leads to fractures of the wrist, spine, and hip. The risk of falling, in turn, is increased by impaired eyesight due to any cause (e.g. glaucoma, macular degeneration), balance disorder, movement disorders (e.g. Parkinson's disease), dementia, and sarcopenia (age-related loss of skeletal muscle). Collapse (transient loss of postural tone with or without loss of consciousness) leads to a significant risk of falls; causes of syncope are manifold, but may include cardiac arrhythmias (irregular heart beat), vasovagal syncope, orthostatic hypotension (abnormal drop in blood pressure on standing up), and seizures. Removal of obstacles and loose carpets in the living environment may substantially reduce falls. Those with previous falls, as well as those with gait or balance disorders, are most at risk.

Risk Factors

Risk factors for osteoporotic fracture can be split between nonmodifiable and (potentially) modifiable. In addition, osteoporosis is a recognized complication in specific diseases and disorders. Medication use is theoretically modifiable, although in many cases, the use of medication that increases osteoporosis risk may be unavoidable. Caffeine is not a risk factor for osteoporosis.

It is more likely for a female to get osteoporosis than a male.

Nonmodifiable

  • The most important risk factors for osteoporosis are advanced age (in both men and women) and female sex; estrogen deficiency following menopause or oophorectomy is correlated with a rapid reduction in bone mineral density, while in men, a decrease in testosterone levels has a comparable (but less pronounced) effect.
  • Race: While osteoporosis occurs in people from all ethnic groups, European or Asian ancestry predisposes for osteoporosis.
  • Heredity: Those with a family history of fracture or osteoporosis are at an increased risk; the heritability of the fracture, as well as low bone mineral density, are relatively high, ranging from 25 to 80%. At least 30 genes are associated with the development of osteoporosis. Early menopause/hysterectomy is another predisposing factor.
  • Those who have already had a fracture are at least twice as likely to have another fracture compared to someone of the same age and sex.
  • Build: A small stature is also a nonmodifiable risk factor associated with the development of osteoporosis.

Potentially modifiable

  • Excess consumption of alcohol: Although small amounts of alcohol are probably beneficial (bone density increases with increasing alcohol intake), chronic heavy drinking (alcohol intake greater than three units/day) probably increases fracture risk despite any beneficial effects on bone density
  • Vitamin D deficiency Low circulating Vitamin D is common among the elderly worldwide. Mild vitamin D insufficiency is associated with increased parathyroid hormone (PTH) production. PTH increases bone resorption, leading to bone loss. A positive association exists between serum 1,25-dihydroxycholecalciferol levels and bone mineral density, while PTH is negatively associated with bone mineral density.
  • Tobacco smoking: Many studies have associated smoking with decreased bone health, but the mechanisms are unclear. Tobacco smoking has been proposed to inhibit the activity of osteoblasts, and is an independent risk factor for osteoporosis. Smoking also results in increased breakdown of exogenous estrogen, lower body weight and earlier menopause, all of which contribute to lower bone mineral density
  • Malnutrition: Nutrition has an important and complex role in maintenance of good bone. Identified risk factors include low dietary calcium and/or phosphorus, magnesium, zinc, boron, iron, fluoride, copper, vitamins A, K, E and C (and D where skin exposure to sunlight provides an inadequate supply). Excess sodium is a risk factor. High blood acidity may be diet-related, and is a known antagonist of bone. Some have identified low protein intake as associated with lower peak bone mass during adolescence and lower bone mineral density in elderly populations. Conversely, some have identified low protein intake as a positive factor, protein is among the causes of dietary acidity. Imbalance of omega-6 to omega-3 polyunsaturated fats is yet another identified risk factor.
  • High dietary protein Research has found an association between diets high in animal protein and increased urinary calcium, and have been linked to an increase in fractures.[26] However, the relevance of this observation to bone density is unclear, since higher protein diets tend to increase absorption of calcium from the diet and are associated with higher bone density. Indeed, it has recently been argued that low protein diets cause poor bone health. No interventional trials have been performed on dietary protein in the prevention and treatment of osteoporosis.
  • Underweight/inactive: Bone remodeling occurs in response to physical stress, so physical inactivity can lead to significant bone loss. Weight bearing exercise can increase peak bone mass achieved in adolescence, and a highly significant correlation between bone strength and muscle strength has been determined. The incidence of osteoporosis is lower in overweight people.
  • Endurance training: In female endurance athletes, large volumes of training can lead to decreased bone density and an increased risk of osteoporosis. This effect might be caused by intense training suppressing menstruation, producing amenorrhea, and it is part of the female athlete triad. However, for male athletes, the situation is less clear, and although some studies have reported low bone density in elite male endurance athletes, others have instead seen increased leg bone density.
  • Heavy metals: A strong association between cadmium and lead with bone disease has been established. Low-level exposure to cadmium is associated with an increased loss of bone mineral density readily in both genders, leading to pain and increased risk of fractures, especially in the elderly and in females. Higher cadmium exposure results in osteomalacia (softening of the bone).
  • Soft drinks: Some studies indicate soft drinks (many of which contain phosphoric acid) may increase risk of osteoporosis, at least in women. Others suggest soft drinks may displace calcium-containing drinks from the diet rather than directly causing osteoporosis.

Evolutionary

Age related bone loss is common among humans due to exhibiting less dense bones than other primate species. Because of the more porous bones of humans, frequency of severe osteoporosis and osteoporosis related fractures is higher. The human vulnerability to osteoporosis is an obvious cost but it can be justified by the advantage of bipedalism inferring that this vulnerability is the byproduct of such. It has been suggested that porous bones help to absorb the increased stress that we have on two surfaces compared to our primate counterparts who have four surfaces to disperse the force. In addition, the porosity allows for more flexibility and a lighter skeleton that is easier to support. One other consideration may be that diets today have much lower amounts of calcium than the diets of other primates or the tetrapedal ancestors to humans which may lead to higher likelihood to show signs of osteoporosis.

Diagnosis

The diagnosis of osteoporosis can be made using conventional radiography and by measuring the bone mineral density (BMD). The most popular method of measuring BMD is dual-energy x-ray absorptiometry. In addition to the detection of abnormal BMD, the diagnosis of osteoporosis requires investigations into potentially modifiable underlying causes; this may be done with blood tests. Depending on the likelihood of an underlying problem, investigations for cancer with metastasis to the bone, multiple myeloma, Cushing's disease and other above-mentioned causes may be performed.

Conventional radiography

Conventional radiography is useful, both by itself and in conjunction with CT or MRI, for detecting complications of osteopenia (reduced bone mass; preosteoporosis), such as fractures; for differential diagnosis of osteopenia; or for follow-up examinations in specific clinical settings, such as soft tissue calcifications, secondary hyperparathyroidism, or osteomalacia in renal osteodystrophy. However, radiography is relatively insensitive to detection of early disease and requires a substantial amount of bone loss (about 30%) to be apparent on X-ray images.

The main radiographic features of generalized osteoporosis are cortical thinning and increased radiolucency. Frequent complications of osteoporosis are vertebral fractures for which spinal radiography can help considerably in diagnosis and follow-up. Vertebral height measurements can objectively be made using plain-film X-rays by using several methods such as height loss together with area reduction, particularly when looking at vertical deformity in T4-L4, or by determining a spinal fracture index that takes into account the number of vertebrae involved. Involvement of multiple vertebral bodies leads to kyphosis of the thoracic spine, leading to what is known as dowager's hump.

IMAGES

RHEUMATIC FEVER - 1 - Boy, GodavariKhani

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

My son had shifting joint pains with fever and cough. Walking was difficult. Hence we were forced to carry that big boy while moving out. Treatment given by specialists of Karimnagar could not help. Suffered many years.

MODE OF RECOVERY AT NEW LIFE CENTRE

Homeopathy given by Dr Subhash relieved his fever and joint pains completely.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Rheumatic fever is an inflammatory disease that occurs following a Streptococcus pyogenes infection, such as streptococcal pharyngitis. Believed to be caused by antibody cross-reactivity that can involve the heart, joints, skin, and brain, the illness typically develops two to three weeks after a streptococcal infection. Acute rheumatic fever commonly appears in children between the ages of 6 and 15, with only 20% of first-time attacks occurring in adults. The illness is so named because of its similarity in presentation to rheumatism.

DIAGNOSIS

Modified Jones criteria were first published in 1944 by T. Duckett Jones, MD. They have been periodically revised by the American Heart Association in collaboration with other groups. According to revised Jones criteria, the diagnosis of rheumatic fever can be made when two of the major criteria, or one major criterion plus two minor criteria, are present along with evidence of streptococcal infection: elevated or rising antistreptolysin O titre or DNAase. Exceptions are chorea and indolent carditis, each of which by itself can indicate rheumatic fever. An April 2013 review article in the Indian Journal of Medical Research stated that echocardiographic and Doppler (E & D) studies, despite some reservations about their utility, have identified a massive burden of rheumatic heart disease, which suggests the inadequacy of the 1992 Jones' criteria. E & D studies have identified subclinical carditis in patients with acute rheumatic fever, as well as in follow-ups of rheumatic heart disease patients who initially presented as having isolated cases of Sydenham's chorea.

Major criteria
  • Polyarthritis: A temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards.
  • Carditis: Inflammation of the heart muscle (myocarditis) which can manifest as congestive heart failure with shortness of breath, pericarditis with a rub, or a new heart murmur.
  • Subcutaneous nodules: Painless, firm collections of collagen fibers over bones or tendons. They commonly appear on the back of the wrist, the outside elbow, and the front of the knees.
  • Erythema marginatum: A long-lasting reddish rash that begins on the trunk or arms as macules, which spread outward and clear in the middle to form rings, which continue to spread and coalesce with other rings, ultimately taking on a snake-like appearance. This rash typically spares the face and is made worse with heat.
  • Sydenham's chorea (St. Vitus' dance): A characteristic series of rapid movements without purpose of the face and arms. This can occur very late in the disease for at least three months from onset of infection.
Minor criteria
  • Fever of 38.2–38.9 °C (100.8–102.0 °F)
  • Arthralgia: Joint pain without swelling (Cannot be included if polyarthritis is present as a major symptom)
  • Raised erythrocyte sedimentation rate or C reactive protein
  • Leukocytosis
  • ECG showing features of heart block, such as a prolonged PR interval (Cannot be included if carditis is present as a major symptom)
  • Previous episode of rheumatic fever or inactive heart disease
Other signs and symptoms
  • Abdominal pain
  • Nose bleeds
  • Preceding streptococcal infection: recent scarlet fever, raised antistreptolysin O or other streptococcal antibody titre, or positive throat culture.

PATHOPHYSIOLOGY

Chronic rheumatic heart disease (RHD) is characterized by repeated inflammation with fibrinous repair. The cardinal anatomic changes of the valve include leaflet thickening, commissural fusion, and shortening and thickening of the tendinous cords. It is caused by an autoimmune reaction to Group A β-hemolytic streptococci (GAS) that results in valvular damage. Fibrosis and scarring of valve leaflets, commissures and cusps leads to abnormalities that can result in valve stenosis or regurgitation. The inflammation caused by rheumatic fever, usually during childhood, is referred to as rheumatic valvulitis. About half of patients with acute rheumatic fever develop inflammation involving valvular endothelium. The majority of morbidity and mortality associated with rheumatic fever is caused by its destructive effects on cardiac valve tissue. The pathogenesis of RHD is complex and not fully understood, but it is known to involve molecular mimicry and genetic predisposition that lead to autoimmune reactions.

Molecular mimicry occurs when epitopes are shared between host antigens and GAS antigens. This causes an autoimmune reaction against native tissues in the heart that are incorrectly recognized as "foreign" due to the cross-reactivity of antibodies generated as a result of epitope sharing. The valvular endothelium is a prominent site of lymphocyte-induced damage. CD4+ T cells are the major effectors of heart tissue autoimmune reactions in RHD. Normally, T cell activation is triggered by the presentation of GAS antigens. In RHD, molecular mimicry results in incorrect T cell activation, and these T lymphocytes can go on to activate B cells, which will begin to produce self-antigen-specific antibodies. This leads to an immune response attack mounted against tissues in the heart that have been misidentified as pathogens. Rheumatic valves display increased expression of VCAM-1, a protein that mediates the adhesion of lymphocytes. Self-antigen-specific antibodies generated via molecular mimicry between human proteins and GAS antigens up-regulate VCAM-1 after binding to the valvular endothelium. This leads to the inflammation and valve scarring observed in rheumatic valvulitis, mainly due to CD4+ T cell infiltration.

While the mechanisms of genetic predisposition remain unclear, a few genetic factors have been found to increase susceptibility to autoimmune reactions in RHD. The dominant contributors are a component of MHC class II molecules, found on lymphocytes and antigen-presenting cells, specifically the DR and DQ alleles on human chromosome 6. Certain allele combinations appear to increase RHD autoimmune susceptibility. Human leukocyte antigen (HLA) class II allele DR7 (HLA-DR7) is most often associated with RHD, and its combination with certain DQ alleles is seemingly associated with the development of valvular lesions. The mechanism by which MHC class II molecules increase a host's susceptibility to autoimmune reactions in RHD is unknown, but it is likely related to the role HLA molecules play in presenting antigens to T cell receptors, thus triggering an immune response. Also found on human chromosome 6 is the cytokine TNF-α which is also associated with RHD. High expression levels of TNF-α may exacerbate valvular tissue inflammation, contributing to RHD pathogenesis. Mannose-binding lectin (MBL) is an inflammatory protein involved in pathogen recognition. Different variants of MBL2 gene regions are associated in RHD. RHD-induced mitral valve stenosis has been associated with MBL2 alleles encoding for high production of MBL. Aortic valve regurgitation in RHD patients has been associated with different MBL2 alleles that encode for low production of MBL. Other genes are also being investigated to better understand the complexity of autoimmune reactions that occur in RHD.

PREVENTION

Prevention of recurrence is achieved by eradicating the acute infection and prophylaxis with antibiotics. The American Heart Association suggests that people with a history of bacterial endocarditis may wish to consider long-term antibiotic prophylaxis.

TREATMENT

The management of acute rheumatic fever is geared toward the reduction of inflammation with anti-inflammatory medications such as aspirin or corticosteroids. Individuals with positive cultures for strep throat should also be treated with antibiotics. Aspirin is the drug of choice and should be given at high doses of 100 mg/kg/day. One should watch for side effects like gastritis and salicylate poisoning. In children and teenagers, the use of aspirin and aspirin-containing products can be associated with Reye's syndrome, a serious and potentially deadly condition. The risks, benefits and alternative treatments must always be considered when administering aspirin and aspirin-containing products in children and teenagers. Ibuprofen for pain and discomfort and corticosteroids for moderate to severe inflammatory reactions manifested by rheumatic fever should be considered in children and teenagers. Steroids are reserved for cases where there is evidence of involvement of heart. The use of steroids may prevent further scarring of tissue and may prevent development of sequelae such as mitral stenosis. Monthly injections of longacting penicillin must be given for a period of five years in patients having one attack of rheumatic fever. If there is evidence of carditis, the length of therapy may be up to 40 years. Another important cornerstone in treating rheumatic fever includes the continual use of low-dose antibiotics (such as penicillin, sulfadiazine, or erythromycin) to prevent recurrence.

Vaccine

No vaccines are currently available to protect against S. pyogenes infection, although there has been research into the development of one. Difficulties in developing a vaccine include the wide variety of strains of S. pyogenes present in the environment and the large amount of time and people that will be needed for appropriate trials for safety and efficacy of the vaccine.

Infection

Patients with positive cultures for Streptococcus pyogenes should be treated with penicillin as long as allergy is not present. This treatment will not alter the course of the acute disease.

The most appropriate treatment stated in the Oxford Handbook of Clinical Medicine for rheumatic fever is benzathine benzylpenicillin.

Inflammation

Patients with significant symptoms may require corticosteroids. Salicylates are useful for pain.

Heart failure

Some patients develop significant carditis which manifests as congestive heart failure. This requires the usual treatment for heart failure: ACE inhibitors, diuretics, beta blockers, and digoxin. Unlike normal heart failure, rheumatic heart failure responds well to corticosteroids.

EPIDEMIOLOGY

Rheumatic fever is common worldwide and responsible for many cases of damaged heart valves. As of 2010 globally it resulted in 345,000 deaths, down from 463,000 in 1990.

In Western countries, it became fairly rare since the 1960s, probably due to widespread use of antibiotics to treat streptococcus infections. While it has been far less common in the United States since the beginning of the 20th century, there have been a few outbreaks since the 1980s. Although the disease seldom occurs, it is serious and has a case-fatality rate of 2–5%.

Rheumatic fever primarily affects children between ages 5 and 17 years and occurs approximately 20 days after strep throat. In up to a third of cases, the underlying strep infection may not have caused any symptoms.

The rate of development of rheumatic fever in individuals with untreated strep infection is estimated to be 3%. The incidence of recurrence with a subsequent untreated infection is substantially greater (about 50%). The rate of development is far lower in individuals who have received antibiotic treatment. Persons who have suffered a case of rheumatic fever have a tendency to develop flare-ups with repeated strep infections.

The recurrence of rheumatic fever is relatively common in the absence of maintenance of low dose antibiotics, especially during the first three to five years after the first episode. Heart complications may be long-term and severe, particularly if valves are involved.

Survivors of rheumatic fever often have to take penicillin to prevent streptococcal infection which could possibly lead to another case of rheumatic fever that could prove fatal.

IMAGES

RHEUMATIC FEVER-2 - Madhusudhan, Ramakrishnapur

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Shifting joint pains with fever since 2 months. I was admitted and treated in Singareni area Hospital but in vain. Any little movement was highly painful and difficult.I was bedridden.

MODE OF RECOVERY AT NEW LIFE CENTRE

My uncle whose backache was cured by Dr subhash took me to hm. My disease disappeared completely with his treatment in one month. Now,I am healthy and active.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Rheumatic fever is an inflammatory disease that occurs following a Streptococcus pyogenes infection, such as streptococcal pharyngitis. Believed to be caused by antibody cross-reactivity that can involve the heart, joints, skin, and brain, the illness typically develops two to three weeks after a streptococcal infection. Acute rheumatic fever commonly appears in children between the ages of 6 and 15, with only 20% of first-time attacks occurring in adults. The illness is so named because of its similarity in presentation to rheumatism.

DIAGNOSIS

Modified Jones criteria were first published in 1944 by T. Duckett Jones, MD. They have been periodically revised by the American Heart Association in collaboration with other groups. According to revised Jones criteria, the diagnosis of rheumatic fever can be made when two of the major criteria, or one major criterion plus two minor criteria, are present along with evidence of streptococcal infection: elevated or rising antistreptolysin O titre or DNAase. Exceptions are chorea and indolent carditis, each of which by itself can indicate rheumatic fever. An April 2013 review article in the Indian Journal of Medical Research stated that echocardiographic and Doppler (E & D) studies, despite some reservations about their utility, have identified a massive burden of rheumatic heart disease, which suggests the inadequacy of the 1992 Jones' criteria. E & D studies have identified subclinical carditis in patients with acute rheumatic fever, as well as in follow-ups of rheumatic heart disease patients who initially presented as having isolated cases of Sydenham's chorea.

Major criteria
  • Polyarthritis: A temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards.
  • Carditis: Inflammation of the heart muscle (myocarditis) which can manifest as congestive heart failure with shortness of breath, pericarditis with a rub, or a new heart murmur.
  • Subcutaneous nodules: Painless, firm collections of collagen fibers over bones or tendons. They commonly appear on the back of the wrist, the outside elbow, and the front of the knees.
  • Erythema marginatum: A long-lasting reddish rash that begins on the trunk or arms as macules, which spread outward and clear in the middle to form rings, which continue to spread and coalesce with other rings, ultimately taking on a snake-like appearance. This rash typically spares the face and is made worse with heat.
  • Sydenham's chorea (St. Vitus' dance): A characteristic series of rapid movements without purpose of the face and arms. This can occur very late in the disease for at least three months from onset of infection.
Minor criteria
  • Fever of 38.2–38.9 °C (100.8–102.0 °F)
  • Arthralgia: Joint pain without swelling (Cannot be included if polyarthritis is present as a major symptom)
  • Raised erythrocyte sedimentation rate or C reactive protein
  • Leukocytosis
  • ECG showing features of heart block, such as a prolonged PR interval (Cannot be included if carditis is present as a major symptom)
  • Previous episode of rheumatic fever or inactive heart disease
Other signs and symptoms
  • Abdominal pain
  • Nose bleeds
  • Preceding streptococcal infection: recent scarlet fever, raised antistreptolysin O or other streptococcal antibody titre, or positive throat culture.

PATHOPHYSIOLOGY

Chronic rheumatic heart disease (RHD) is characterized by repeated inflammation with fibrinous repair. The cardinal anatomic changes of the valve include leaflet thickening, commissural fusion, and shortening and thickening of the tendinous cords. It is caused by an autoimmune reaction to Group A β-hemolytic streptococci (GAS) that results in valvular damage. Fibrosis and scarring of valve leaflets, commissures and cusps leads to abnormalities that can result in valve stenosis or regurgitation. The inflammation caused by rheumatic fever, usually during childhood, is referred to as rheumatic valvulitis. About half of patients with acute rheumatic fever develop inflammation involving valvular endothelium. The majority of morbidity and mortality associated with rheumatic fever is caused by its destructive effects on cardiac valve tissue. The pathogenesis of RHD is complex and not fully understood, but it is known to involve molecular mimicry and genetic predisposition that lead to autoimmune reactions.

Molecular mimicry occurs when epitopes are shared between host antigens and GAS antigens. This causes an autoimmune reaction against native tissues in the heart that are incorrectly recognized as "foreign" due to the cross-reactivity of antibodies generated as a result of epitope sharing. The valvular endothelium is a prominent site of lymphocyte-induced damage. CD4+ T cells are the major effectors of heart tissue autoimmune reactions in RHD. Normally, T cell activation is triggered by the presentation of GAS antigens. In RHD, molecular mimicry results in incorrect T cell activation, and these T lymphocytes can go on to activate B cells, which will begin to produce self-antigen-specific antibodies. This leads to an immune response attack mounted against tissues in the heart that have been misidentified as pathogens. Rheumatic valves display increased expression of VCAM-1, a protein that mediates the adhesion of lymphocytes. Self-antigen-specific antibodies generated via molecular mimicry between human proteins and GAS antigens up-regulate VCAM-1 after binding to the valvular endothelium. This leads to the inflammation and valve scarring observed in rheumatic valvulitis, mainly due to CD4+ T cell infiltration.

While the mechanisms of genetic predisposition remain unclear, a few genetic factors have been found to increase susceptibility to autoimmune reactions in RHD. The dominant contributors are a component of MHC class II molecules, found on lymphocytes and antigen-presenting cells, specifically the DR and DQ alleles on human chromosome 6. Certain allele combinations appear to increase RHD autoimmune susceptibility. Human leukocyte antigen (HLA) class II allele DR7 (HLA-DR7) is most often associated with RHD, and its combination with certain DQ alleles is seemingly associated with the development of valvular lesions. The mechanism by which MHC class II molecules increase a host's susceptibility to autoimmune reactions in RHD is unknown, but it is likely related to the role HLA molecules play in presenting antigens to T cell receptors, thus triggering an immune response. Also found on human chromosome 6 is the cytokine TNF-α which is also associated with RHD. High expression levels of TNF-α may exacerbate valvular tissue inflammation, contributing to RHD pathogenesis. Mannose-binding lectin (MBL) is an inflammatory protein involved in pathogen recognition. Different variants of MBL2 gene regions are associated in RHD. RHD-induced mitral valve stenosis has been associated with MBL2 alleles encoding for high production of MBL. Aortic valve regurgitation in RHD patients has been associated with different MBL2 alleles that encode for low production of MBL. Other genes are also being investigated to better understand the complexity of autoimmune reactions that occur in RHD.

PREVENTION

Prevention of recurrence is achieved by eradicating the acute infection and prophylaxis with antibiotics. The American Heart Association suggests that people with a history of bacterial endocarditis may wish to consider long-term antibiotic prophylaxis.

TREATMENT

The management of acute rheumatic fever is geared toward the reduction of inflammation with anti-inflammatory medications such as aspirin or corticosteroids. Individuals with positive cultures for strep throat should also be treated with antibiotics. Aspirin is the drug of choice and should be given at high doses of 100 mg/kg/day. One should watch for side effects like gastritis and salicylate poisoning. In children and teenagers, the use of aspirin and aspirin-containing products can be associated with Reye's syndrome, a serious and potentially deadly condition. The risks, benefits and alternative treatments must always be considered when administering aspirin and aspirin-containing products in children and teenagers. Ibuprofen for pain and discomfort and corticosteroids for moderate to severe inflammatory reactions manifested by rheumatic fever should be considered in children and teenagers. Steroids are reserved for cases where there is evidence of involvement of heart. The use of steroids may prevent further scarring of tissue and may prevent development of sequelae such as mitral stenosis. Monthly injections of longacting penicillin must be given for a period of five years in patients having one attack of rheumatic fever. If there is evidence of carditis, the length of therapy may be up to 40 years. Another important cornerstone in treating rheumatic fever includes the continual use of low-dose antibiotics (such as penicillin, sulfadiazine, or erythromycin) to prevent recurrence.

Vaccine

No vaccines are currently available to protect against S. pyogenes infection, although there has been research into the development of one. Difficulties in developing a vaccine include the wide variety of strains of S. pyogenes present in the environment and the large amount of time and people that will be needed for appropriate trials for safety and efficacy of the vaccine.

Infection

Patients with positive cultures for Streptococcus pyogenes should be treated with penicillin as long as allergy is not present. This treatment will not alter the course of the acute disease.

The most appropriate treatment stated in the Oxford Handbook of Clinical Medicine for rheumatic fever is benzathine benzylpenicillin.

Inflammation

Patients with significant symptoms may require corticosteroids. Salicylates are useful for pain.

Heart failure

Some patients develop significant carditis which manifests as congestive heart failure. This requires the usual treatment for heart failure: ACE inhibitors, diuretics, beta blockers, and digoxin. Unlike normal heart failure, rheumatic heart failure responds well to corticosteroids.

EPIDEMIOLOGY

Rheumatic fever is common worldwide and responsible for many cases of damaged heart valves. As of 2010 globally it resulted in 345,000 deaths, down from 463,000 in 1990.

In Western countries, it became fairly rare since the 1960s, probably due to widespread use of antibiotics to treat streptococcus infections. While it has been far less common in the United States since the beginning of the 20th century, there have been a few outbreaks since the 1980s. Although the disease seldom occurs, it is serious and has a case-fatality rate of 2–5%.

Rheumatic fever primarily affects children between ages 5 and 17 years and occurs approximately 20 days after strep throat. In up to a third of cases, the underlying strep infection may not have caused any symptoms.

The rate of development of rheumatic fever in individuals with untreated strep infection is estimated to be 3%. The incidence of recurrence with a subsequent untreated infection is substantially greater (about 50%). The rate of development is far lower in individuals who have received antibiotic treatment. Persons who have suffered a case of rheumatic fever have a tendency to develop flare-ups with repeated strep infections.

The recurrence of rheumatic fever is relatively common in the absence of maintenance of low dose antibiotics, especially during the first three to five years after the first episode. Heart complications may be long-term and severe, particularly if valves are involved.

Survivors of rheumatic fever often have to take penicillin to prevent streptococcal infection which could possibly lead to another case of rheumatic fever that could prove fatal.

IMAGES

SPINAL INJURY - Urinary Retention - Savithri, Pirket, Secunderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I met with an accident leading to fracture of my backbone. This resulted in retention of urine and stools.Experts of a corporate hospital operated upon me and put one indwelling pipe and urinary bag.It has been 4 months now.They said it is a hopeless case and takes time.The pipe and urinary bag are still there.Earlier the urinary flow was completely blocked.We changed the pipe periodically. The urine never came out naturally without pipe.

MODE OF RECOVERY AT NEW LIFE CENTRE

I have been coming to NLHC since 3 months. The pipe and urinary bag have been removed one month ago.Urine is now flowing freely after taking your treatment. I am healthy. There is no fever or backache. Earlier the surgeons were not hopeful of any recovery even after one year of time.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Neurogenic bladder dysfunction, sometimes simply referred to as neurogenic bladder, is a dysfunction of the urinary bladder due to disease of the central nervous system or peripheral nerves involved in the control of micturition (urination). Neurogenic bladder usually causes difficulty or full inability to pass urine without use of a catheter or other method.

CAUSES

Any condition that impairs bladder and bladder outlet afferent and efferent signaling can cause neurogenic bladder. It is often associated with spinal cord diseases (such as syringomyelia/hydromyelia), injuries like herniated disks, and neural tube defects including spina bifida. It may also be caused by brain tumors and other diseases of the brain, and by peripheral nerve diseases such as: Diabetes, Alcoholism and Vitamin B12 deficiency. It is a common complication of major surgery in the pelvis, such as for removal of sacrococcygeal teratoma and other tumors.

TREATMENTS

Catheterization methods range from intermittent catheterization, which involves no surgery or permanently attached appliances, to the creation of a stoma, which bypasses the urethra to empty the bladder directly.

Intermittent catheterization is the use, several times a day, of straight catheters (which are usually disposable or single-use products) to empty the bladder. This can be done independently by the patient, or with help, in the case that the patient lacks the dexterity to manage the catheter. For patients that are unable to tolerate disposable straight catheters, a Foley catheter allows continuous drainage of urine into a sterile drainage bag that is worn by the patient.

Other treatments involve creation of a stoma that is continent and readily accepts a catheter. These are known as Mitrofanoff mechanisms. An example of this treatment is the creation of an Indiana pouch. Additionally, a muscarinic agonist like Bethanechol may also be used, particularly in the postpartum or postoperative period. Function of the stoma may be augmented by periodic injections of botulinum toxin to relax one of the two sphincters involved in normal urination. The effect is longer lasting with botulinum toxin type A than with type B. This use of botulinum toxin is discussed at length in the French medical literature.

IMAGES

CASE RECORD

CHIKUNGUNYA - Raghupati, Structural Engineer, Lalapet, Secunderabad.

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I am an engineer. Our family was on a trip to Visakhapatnam. One day, I developed a sudden fever with severe joint pains Local doctors diagnosed it as Chikungunya and prescribed some medicines but there was no relief
My relatives in Vizag who were also affected with the similar disease were still suffering from pains for the last one month despite taking drugs.

MODE OF RECOVERY AT NEW LIFE CENTRE

I came back to Hyderabad and consulted Dr Subhash who lives in neighbouring building only. Surprisingly my fever and joint pains disappeared to a large extent in just two hours of taking his medicine.
My son who was also a patient of Chikungunya fever recovered fully in just one day only. He started playing few hours after taking his dose.
Our recovery is really very fast and safe in contrast to the other similar patients who could not recover even after one month despite visiting expert doctors. The cure is unexpected and truly wonderful. I thank the doctor immensely. I wish that his specialised treatment reaches every corner of the country.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Chikungunya ("Makonde for "that which bends up") virus (CHIKV) is an arthropod-borne virus, of the genus Alphavirus, that is transmitted to humans by virus-carrying Aedes mosquitoes. CHIKV is transmitted similarly to dengue fever and causes an illness with an acute febrile phase lasting two to five days, followed by a longer period of joint pains in the extremities; this pain may persist for years in some cases.

The best means of prevention is overall mosquito control and in addition, the avoidance of bites by any infected mosquitoes. There is no specific treatment but medications can be used to reduce symptoms. Rest and fluids may also be useful.

SIGNS AND SYMPTOMS

The incubation period of chikungunya disease ranges from one to twelve days, typically two to three. The majority of those infected will develop symptoms. Symptoms include a fever up to 40 °C (104 °F), a petechial or maculopapular rash of the trunk and occasionally the limbs, and arthralgia or arthritis affecting multiple joints. Other nonspecific symptoms can include headache, nausea, vomiting, conjunctivitis, slight photophobia and partial loss of taste. Ocular inflammation from chikungunya may present as iridocyclitis. Retinal lesions may also occur. Pedal oedema (swelling of legs) is observed in many patients, the cause of which remains obscure as it is not related to any cardiovascular, renal or hepatic abnormalities.

Typically, the fever lasts for two days and then ends abruptly. However, other symptoms—namely joint pain, intense headache, insomnia and an extreme degree of prostration—last for a variable period; usually for about five to seven days. Patients have complained of joint pains for much longer time periods; some as long as two years, depending on their age. Recovery from the disease varies by age. Younger patients recover within 5 to 15 days; middle-aged patients recover in 1 to 2.5 months. Recovery is longer for the elderly. The severity of the disease as well as its duration is less in younger patients and pregnant women. In pregnant women, no untoward effects are noticed after the infection.

Chronic Disease

Observations during recent epidemics have suggested chikungunya may cause long-term symptoms following acute infection. During the La Reunion outbreak in 2006, greater than 50% of subjects over the age of 45 reported long term musculoskeletal pain with up to 60% of patients reporting prolonged arthralgia 3 years following initial infection. A study of imported cases in France reported that 59% of patients still suffered from arthralgia two years after acute infection. Following a local epidemic of chikungunya in Italy, 66% of patients reported myalgia, arthralgia, or asthenia at one year postacute infection. Long-term symptoms are not an entirely new observation; long-term arthritis was observed following an outbreak in 1979. Common predictors of prolonged symptoms are increased age and prior rheumatological disease. The cause of these chronic symptoms is currently not fully known. Markers of autoimmune or rheumatoid disease have not been found in patients reporting chronic symptoms. However, some evidence from human patients and animal models suggest that chikungunya may be able to establish chronic infections within the host. Viral antigen was detected in a muscle biopsy of a patient suffering a recurrent episode of disease three months after initial onset. Additionally, viral antigen and RNA were found in synovial macrophages of a patient during a relapse of musculoskeletal disease 18 months post initial infection. Several animal models have also suggested that chikungunya virus may establish persistent infections. In a mouse model, viral RNA was detected specifically in joint-associated tissue for at least 16 weeks post-inoculation, and was associated with chronic synovitis. Similarly, another study reported detection of a viral reporter gene in joint tissue of mice for weeks post-inoculation. In a non-human primate model, chikungunya virus was found to persist in the spleen for at least 6 weeks.

VIROLOGY

Chikungunya virus is an alphavirus with a positive sense single-stranded RNA genome of approximately 11.6kb. It is a member of the Semliki Forest Virus complex and is closely related to Ross River Virus, O’Nyong Nyong virus and Semliki Forest Virus. In the United States it is classified as a Category C priority pathogen and work requires Biosafety Level III precautions.

Human epithelial, endothelial, primary fibroblasts and monocyte-derived macrophages are permissive for chikungunya virus in vitro and viral replication is highly cytopathic but susceptible to type I and II interferon. In vivo, chikungunya virus appears to replicate in fibroblasts, skeletal muscle progenitor cells and myofibers.

Type 1 interferon

Upon infection with chikungunya, the host's fibroblasts will produce type 1 (alpha and beta) interferon. Mice that lack the interferon alpha receptor die in 2–3 days upon being exposed to 102 chikungunya PFU, while wild type mice survive even when exposed to as much as 106 PFU of the virus. At the same time, mice that are partially type 1 deficient are mildly affected and experience symptoms such as muscle weakness and lethargy. Partidos et al. 2011 saw similar results with the live attenuated strain CHIKV181/25. However, rather than dying, the type 1 interferon deficient mice were temporarily disabled and the partially type 1 interferon deficient mice did not have any problems.

Several studies have attempted to find the upstream components of the type 1 interferon pathway involved in the host's response to chikungunya infection. So far, no one knows the chikungunya specific pathogen associated molecular pattern. Nonetheless, IPS-1—also known as Cardif, MAVS, and VISA—has been found to be an important factor. In 2011, White et al. found that interfering with IPS-1 decreased the phosphorylation of interferon regulatory factor 3 (IRF3) and the production of IFN-β. Other studies have found that IRF3 and IRF7 are important in an age-dependent manner. Adult mice that lack both of these regulatory factors die upon infection with chikungunya. Neonates, on the other hand, succumb to the virus if they are deficient in one of these factors.

Chikungunya counters the Type I interferon response by producing NS2, a non-structural protein that degrades Rpb and turns off the host cell's ability to transcribe DNA. NS2 interferes with the JAK-STAT signaling pathway and prevents STAT from becoming phosphorylated.

DIAGNOSIS

Common laboratory tests for chikungunya include RT-PCR, virus isolation, and serological tests.

  • Virus isolation provides the most definitive diagnosis, but takes one to two weeks for completion and must be carried out in biosafety level 3 laboratories. The technique involves exposing specific cell lines to samples from whole blood and identifying chikungunya virus-specific responses.
  • RT-PCR using nested primer pairs is used to amplify several chikungunya-specific genes from whole blood. Results can be determined in one to two days.
  • Serological diagnosis requires a larger amount of blood than the other methods, and uses an ELISA assay to measure chikungunya-specific IgM levels. Results require two to three days, and false positives can occur with infection via other related viruses, such as o'nyong'nyong virus and Semliki Forest virus.

PREVENTION

The most effective means of prevention are protection against contact with the disease-carrying mosquitoes and mosquito control. These include using insect repellents with substances such as DEET (N,N-diethyl-meta-toluamide; also known as N,N'-diethyl-3-methylbenzamide or NNDB), icaridin (also known as picaridin and KBR3023), PMD (p-menthane-3,8-diol, a substance derived from the lemon eucalyptus tree), or IR3535. Wearing bite-proof long sleeves and trousers also offers protection.

In addition, garments can be treated with pyrethroids, a class of insecticides that often has repellent properties. Vaporized pyrethroids (for example in mosquito coils) are also insect repellents. Securing screens on windows and doors will help to keep mosquitoes out of the house. In the case of the day-active Aedes aegypti and Aedes albopictus, however, this will have only a limited effect, since many contacts between the mosquitoes and humans occur outside.

Vaccine

There are currently no approved vaccines available. A phase II vaccine trial, used a live, attenuated virus, developing viral resistance in 98% of those tested after 28 days and 85% still showed resistance after one year. However, 8% of people reported transient joint pain and attenuation was found to be due to only two mutations in the E2 glycoprotein. Alternative vaccine strategies have been developed and shown efficacy in mouse models but have so far not reached clinical trials.

TREATMENT

Currently there is no specific treatment. Efforts to improve the symptoms include the use of NSAIDs such as naproxen, paracetamol (acetaminophen) and fluids. Aspirin is not recommended.

Chronic arthritis

In those who have more than two weeks of arthritis, ribavirin may be useful. The effect of chloroquine is not clear. It does not appear to help acute disease but there is tentative evidence that it might help the chronic arthritis. Steroids do not appear useful either.

EPIDEMIOLOGY

Chikungunya virus is an alphavirus closely related to the o'nyong'nyong virus, the Ross River virus in Australia, and the viruses that cause eastern equine encephalitis and western equine encephalitis.

Three genotypes of this virus have been described: West African, East/Central/South African and Asian genotypes.

Chikungunya is generally spread through bites from Aedes aegypti mosquitoes, but recent research by the Pasteur Institute in Paris has suggested chikungunya virus strains in the 2005-2006 Reunion Island outbreak incurred a mutation that facilitated transmission by Asian tiger mosquito (Aedes albopictus).

Concurrent studies by arbovirologists at the University of Texas Medical Branch in Galveston, Texas, confirmed definitively that enhanced chikungunya virus infection of A. albopictus was caused by a point mutation in one of the viral envelope genes (E1). Enhanced transmission of chikungunya virus by A. albopictus could mean an increased risk for chikungunya outbreaks in other areas where the Asian tiger mosquito is present. A recent epidemic in Italy was likely perpetuated by A. albopictus.

In Africa, chikungunya is spread via a sylvatic cycle in which the virus largely resides in other primates in between human outbreaks.

On 28 May 2009 in Changwat Trang of Thailand where the virus is endemic, the provincial hospital decided to deliver by Caesarean section a male baby from his chikungunya-infected mother, Khwanruethai Sutmueang, 28, a Trang native, to prevent mother-fetus virus transmission. However, after delivering the baby, the physicians discovered the baby was already infected with the virus, and put him into intensive care because the infection had left the baby unable to breathe by himself or to drink milk. The physicians presumed the virus might be able to be transmitted from a mother to her fetus, but without laboratory confirmation.

IMAGES

TUBERCULOSIS OF SPINE - C.S.Chary, Mancherial

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I am a driver. I had TB of my spine causing severe backache and fever. T.B. medicines given by specialists and the government did not help. Fever and pain did not subside; I lost my appetite and weight. Orthopaedic surgeons suggested a critical operation. I could not afford it. Suffered two years and lost my job. Any little movement in bed was highly painful. I was confined to bed only.

MODE OF RECOVERY AT NEW LIFE CENTRE

Homeopathy given by Dr.Subhash cured 80% of my pain in just five months. Fever dropped and appetite improved. I am attending my job. I am now healthy and active.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Pott's disease or Pott disease is a presentation of extrapulmonary tuberculosis whereby disease is seen in the spinal vertebrae. Extrapulmonary tuberculosis can affect the spine, a kind of tuberculous arthritis of the intervertebral joints. It is named after Percivall Pott (1714–1788), a British surgeon. The lower thoracic and upper lumbar vertebrae are the areas of the spine most often affected. Scientifically, it is called tuberculous spondylitis and it is most commonly localized in the thoracic portion of the spine. Pott’s disease results from haematogenous spread of tuberculosis from other sites, often pulmonary. The infection then spreads from two adjacent vertebrae into the adjoining intervertebral disc space. If only one vertebra is affected, the disc is normal, but if two are involved, the disc, which is avascular, cannot receive nutrients and collapses. The disc tissue dies and is broken down by caseation, leading to vertebral narrowing and eventually to vertebral collapse and spinal damage. A dry soft tissue mass often forms and superinfection is rare.

SIGNS AND SYMPTOMS

  • Back pains
  • Fever
  • Night sweating
  • Anorexia
  • Spinal mass, sometimes associated with numbness, paraesthesia, or muscle weakness of the legs
  • Difficulty standing

DIAGNOSIS

  • Blood tests
  • Tuberculin skin test
  • Radiographs of the spine
  • Bone scan
  • CT of the spine
  • Bone biopsy
  • MRI

Late Complications

Controlling the spread of tuberculosis infection can prevent tuberculous spondylitis and arthritis. Patients who have a positive PPD test (but not active tuberculosis) may decrease their risk by properly taking medicines to prevent tuberculosis. To effectively treat tuberculosis, it is crucial that patients take their medications exactly as prescribed.

THERAPY

  • Non-operative – antituberculous drugs
  • Analgesics
  • Immobilization of the spine region different types of braces and collars
  • Surgery may be necessary, especially to drain spinal abscesses or debride bony lesions fully or to stabilize the spine. A 2007 review found only just two randomized clinical trial with at least one year-follow up found which compared chemotherapy plus surgery with chemotherapy alone for treating people diagnosed with active tuberculosis of the spine. As such there is no high grade evidence but the results of this study indicates that surgery should not be recommended routinely and clinicians have to selectively judge and decide on which patients to operate.
  • Thoracic spinal fusion with or without instrumentation as a last resort
  • Physical therapy for pain-relieving modalties, postural education and teaching a home exercise program for strength and flexibility

IMAGES

RHEUMATOID ARTHRITICS WITH ASTHMATIC BRONCHITIS - Kavitha Jain, Secunderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I am a driver. I had TB of my spine causing severe backache and fever. T.B. medicines given by specialists and the government did not help. Fever and pain did not subside; I lost my appetite and weight. Orthopaedic surgeons suggested a critical operation. I could not afford it. Suffered two years and lost my job. Any little movement in bed was highly painful. I was confined to bed only.

MODE OF RECOVERY AT NEW LIFE CENTRE

Homeopathy given by Dr.Subhash cured 80% of my pain in just five months. Fever dropped and appetite improved. I am attending my job. I am now healthy and active.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Pott's disease or Pott disease is a presentation of extrapulmonary tuberculosis whereby disease is seen in the spinal vertebrae. Extrapulmonary tuberculosis can affect the spine, a kind of tuberculous arthritis of the intervertebral joints. It is named after Percivall Pott (1714–1788), a British surgeon. The lower thoracic and upper lumbar vertebrae are the areas of the spine most often affected. Scientifically, it is called tuberculous spondylitis and it is most commonly localized in the thoracic portion of the spine. Pott’s disease results from haematogenous spread of tuberculosis from other sites, often pulmonary. The infection then spreads from two adjacent vertebrae into the adjoining intervertebral disc space. If only one vertebra is affected, the disc is normal, but if two are involved, the disc, which is avascular, cannot receive nutrients and collapses. The disc tissue dies and is broken down by caseation, leading to vertebral narrowing and eventually to vertebral collapse and spinal damage. A dry soft tissue mass often forms and superinfection is rare.

SIGNS AND SYMPTOMS

  • Back pains
  • Fever
  • Night sweating
  • Anorexia
  • Spinal mass, sometimes associated with numbness, paraesthesia, or muscle weakness of the legs
  • Difficulty standing

DIAGNOSIS

  • Blood tests
  • Tuberculin skin test
  • Radiographs of the spine
  • Bone scan
  • CT of the spine
  • Bone biopsy
  • MRI

Late Complications

Controlling the spread of tuberculosis infection can prevent tuberculous spondylitis and arthritis. Patients who have a positive PPD test (but not active tuberculosis) may decrease their risk by properly taking medicines to prevent tuberculosis. To effectively treat tuberculosis, it is crucial that patients take their medications exactly as prescribed.

THERAPY

  • Non-operative – antituberculous drugs
  • Analgesics
  • Immobilization of the spine region different types of braces and collars
  • Surgery may be necessary, especially to drain spinal abscesses or debride bony lesions fully or to stabilize the spine. A 2007 review found only just two randomized clinical trial with at least one year-follow up found which compared chemotherapy plus surgery with chemotherapy alone for treating people diagnosed with active tuberculosis of the spine. As such there is no high grade evidence but the results of this study indicates that surgery should not be recommended routinely and clinicians have to selectively judge and decide on which patients to operate.
  • Thoracic spinal fusion with or without instrumentation as a last resort
  • Physical therapy for pain-relieving modalties, postural education and teaching a home exercise program for strength and flexibility

IMAGES

SPONDYLOSIS (HELPLESS EVEN AFTER OPERATION) - Madhusudan, Secunderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I am a driver. I had TB of my spine causing severe backache and fever. T.B. medicines given by specialists and the government did not help. Fever and pain did not subside; I lost my appetite and weight. Orthopaedic surgeons suggested a critical operation. I could not afford it. Suffered two years and lost my job. Any little movement in bed was highly painful. I was confined to bed only.

MODE OF RECOVERY AT NEW LIFE CENTRE

Homeopathy given by Dr.Subhash cured 80% of my pain in just five months. Fever dropped and appetite improved. I am attending my job. I am now healthy and active.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Pott's disease or Pott disease is a presentation of extrapulmonary tuberculosis whereby disease is seen in the spinal vertebrae. Extrapulmonary tuberculosis can affect the spine, a kind of tuberculous arthritis of the intervertebral joints. It is named after Percivall Pott (1714–1788), a British surgeon. The lower thoracic and upper lumbar vertebrae are the areas of the spine most often affected. Scientifically, it is called tuberculous spondylitis and it is most commonly localized in the thoracic portion of the spine. Pott’s disease results from haematogenous spread of tuberculosis from other sites, often pulmonary. The infection then spreads from two adjacent vertebrae into the adjoining intervertebral disc space. If only one vertebra is affected, the disc is normal, but if two are involved, the disc, which is avascular, cannot receive nutrients and collapses. The disc tissue dies and is broken down by caseation, leading to vertebral narrowing and eventually to vertebral collapse and spinal damage. A dry soft tissue mass often forms and superinfection is rare.

SIGNS AND SYMPTOMS

  • Back pains
  • Fever
  • Night sweating
  • Anorexia
  • Spinal mass, sometimes associated with numbness, paraesthesia, or muscle weakness of the legs
  • Difficulty standing

DIAGNOSIS

  • Blood tests
  • Tuberculin skin test
  • Radiographs of the spine
  • Bone scan
  • CT of the spine
  • Bone biopsy
  • MRI

Late Complications

Controlling the spread of tuberculosis infection can prevent tuberculous spondylitis and arthritis. Patients who have a positive PPD test (but not active tuberculosis) may decrease their risk by properly taking medicines to prevent tuberculosis. To effectively treat tuberculosis, it is crucial that patients take their medications exactly as prescribed.

THERAPY

  • Non-operative – antituberculous drugs
  • Analgesics
  • Immobilization of the spine region different types of braces and collars
  • Surgery may be necessary, especially to drain spinal abscesses or debride bony lesions fully or to stabilize the spine. A 2007 review found only just two randomized clinical trial with at least one year-follow up found which compared chemotherapy plus surgery with chemotherapy alone for treating people diagnosed with active tuberculosis of the spine. As such there is no high grade evidence but the results of this study indicates that surgery should not be recommended routinely and clinicians have to selectively judge and decide on which patients to operate.
  • Thoracic spinal fusion with or without instrumentation as a last resort
  • Physical therapy for pain-relieving modalties, postural education and teaching a home exercise program for strength and flexibility

IMAGES

RHEUMATOID ARTHRITICS - Subramanyam, Secunderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I am a driver. I had TB of my spine causing severe backache and fever. T.B. medicines given by specialists and the government did not help. Fever and pain did not subside; I lost my appetite and weight. Orthopaedic surgeons suggested a critical operation. I could not afford it. Suffered two years and lost my job. Any little movement in bed was highly painful. I was confined to bed only.

MODE OF RECOVERY AT NEW LIFE CENTRE

Homeopathy given by Dr.Subhash cured 80% of my pain in just five months. Fever dropped and appetite improved. I am attending my job. I am now healthy and active.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Pott's disease or Pott disease is a presentation of extrapulmonary tuberculosis whereby disease is seen in the spinal vertebrae. Extrapulmonary tuberculosis can affect the spine, a kind of tuberculous arthritis of the intervertebral joints. It is named after Percivall Pott (1714–1788), a British surgeon. The lower thoracic and upper lumbar vertebrae are the areas of the spine most often affected. Scientifically, it is called tuberculous spondylitis and it is most commonly localized in the thoracic portion of the spine. Pott’s disease results from haematogenous spread of tuberculosis from other sites, often pulmonary. The infection then spreads from two adjacent vertebrae into the adjoining intervertebral disc space. If only one vertebra is affected, the disc is normal, but if two are involved, the disc, which is avascular, cannot receive nutrients and collapses. The disc tissue dies and is broken down by caseation, leading to vertebral narrowing and eventually to vertebral collapse and spinal damage. A dry soft tissue mass often forms and superinfection is rare.

SIGNS AND SYMPTOMS

  • Back pains
  • Fever
  • Night sweating
  • Anorexia
  • Spinal mass, sometimes associated with numbness, paraesthesia, or muscle weakness of the legs
  • Difficulty standing

DIAGNOSIS

  • Blood tests
  • Tuberculin skin test
  • Radiographs of the spine
  • Bone scan
  • CT of the spine
  • Bone biopsy
  • MRI

Late Complications

Controlling the spread of tuberculosis infection can prevent tuberculous spondylitis and arthritis. Patients who have a positive PPD test (but not active tuberculosis) may decrease their risk by properly taking medicines to prevent tuberculosis. To effectively treat tuberculosis, it is crucial that patients take their medications exactly as prescribed.

THERAPY

  • Non-operative – antituberculous drugs
  • Analgesics
  • Immobilization of the spine region different types of braces and collars
  • Surgery may be necessary, especially to drain spinal abscesses or debride bony lesions fully or to stabilize the spine. A 2007 review found only just two randomized clinical trial with at least one year-follow up found which compared chemotherapy plus surgery with chemotherapy alone for treating people diagnosed with active tuberculosis of the spine. As such there is no high grade evidence but the results of this study indicates that surgery should not be recommended routinely and clinicians have to selectively judge and decide on which patients to operate.
  • Thoracic spinal fusion with or without instrumentation as a last resort
  • Physical therapy for pain-relieving modalties, postural education and teaching a home exercise program for strength and flexibility

IMAGES

SEVERE SPONDYLOSIS - SRUJIT SING BHALLA, Secunderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I am a driver. I had TB of my spine causing severe backache and fever. T.B. medicines given by specialists and the government did not help. Fever and pain did not subside; I lost my appetite and weight. Orthopaedic surgeons suggested a critical operation. I could not afford it. Suffered two years and lost my job. Any little movement in bed was highly painful. I was confined to bed only.

MODE OF RECOVERY AT NEW LIFE CENTRE

Homeopathy given by Dr.Subhash cured 80% of my pain in just five months. Fever dropped and appetite improved. I am attending my job. I am now healthy and active.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Pott's disease or Pott disease is a presentation of extrapulmonary tuberculosis whereby disease is seen in the spinal vertebrae. Extrapulmonary tuberculosis can affect the spine, a kind of tuberculous arthritis of the intervertebral joints. It is named after Percivall Pott (1714–1788), a British surgeon. The lower thoracic and upper lumbar vertebrae are the areas of the spine most often affected. Scientifically, it is called tuberculous spondylitis and it is most commonly localized in the thoracic portion of the spine. Pott’s disease results from haematogenous spread of tuberculosis from other sites, often pulmonary. The infection then spreads from two adjacent vertebrae into the adjoining intervertebral disc space. If only one vertebra is affected, the disc is normal, but if two are involved, the disc, which is avascular, cannot receive nutrients and collapses. The disc tissue dies and is broken down by caseation, leading to vertebral narrowing and eventually to vertebral collapse and spinal damage. A dry soft tissue mass often forms and superinfection is rare.

SIGNS AND SYMPTOMS

  • Back pains
  • Fever
  • Night sweating
  • Anorexia
  • Spinal mass, sometimes associated with numbness, paraesthesia, or muscle weakness of the legs
  • Difficulty standing

DIAGNOSIS

  • Blood tests
  • Tuberculin skin test
  • Radiographs of the spine
  • Bone scan
  • CT of the spine
  • Bone biopsy
  • MRI

Late Complications

Controlling the spread of tuberculosis infection can prevent tuberculous spondylitis and arthritis. Patients who have a positive PPD test (but not active tuberculosis) may decrease their risk by properly taking medicines to prevent tuberculosis. To effectively treat tuberculosis, it is crucial that patients take their medications exactly as prescribed.

THERAPY

  • Non-operative – antituberculous drugs
  • Analgesics
  • Immobilization of the spine region different types of braces and collars
  • Surgery may be necessary, especially to drain spinal abscesses or debride bony lesions fully or to stabilize the spine. A 2007 review found only just two randomized clinical trial with at least one year-follow up found which compared chemotherapy plus surgery with chemotherapy alone for treating people diagnosed with active tuberculosis of the spine. As such there is no high grade evidence but the results of this study indicates that surgery should not be recommended routinely and clinicians have to selectively judge and decide on which patients to operate.
  • Thoracic spinal fusion with or without instrumentation as a last resort
  • Physical therapy for pain-relieving modalties, postural education and teaching a home exercise program for strength and flexibility

IMAGES

INJURY TO KNEE(OPARATED IN USA BUT PAIN NOT RELIEVED) - NAVIN, USA

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I am a driver. I had TB of my spine causing severe backache and fever. T.B. medicines given by specialists and the government did not help. Fever and pain did not subside; I lost my appetite and weight. Orthopaedic surgeons suggested a critical operation. I could not afford it. Suffered two years and lost my job. Any little movement in bed was highly painful. I was confined to bed only.

MODE OF RECOVERY AT NEW LIFE CENTRE

Homeopathy given by Dr.Subhash cured 80% of my pain in just five months. Fever dropped and appetite improved. I am attending my job. I am now healthy and active.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Pott's disease or Pott disease is a presentation of extrapulmonary tuberculosis whereby disease is seen in the spinal vertebrae. Extrapulmonary tuberculosis can affect the spine, a kind of tuberculous arthritis of the intervertebral joints. It is named after Percivall Pott (1714–1788), a British surgeon. The lower thoracic and upper lumbar vertebrae are the areas of the spine most often affected. Scientifically, it is called tuberculous spondylitis and it is most commonly localized in the thoracic portion of the spine. Pott’s disease results from haematogenous spread of tuberculosis from other sites, often pulmonary. The infection then spreads from two adjacent vertebrae into the adjoining intervertebral disc space. If only one vertebra is affected, the disc is normal, but if two are involved, the disc, which is avascular, cannot receive nutrients and collapses. The disc tissue dies and is broken down by caseation, leading to vertebral narrowing and eventually to vertebral collapse and spinal damage. A dry soft tissue mass often forms and superinfection is rare.

SIGNS AND SYMPTOMS

  • Back pains
  • Fever
  • Night sweating
  • Anorexia
  • Spinal mass, sometimes associated with numbness, paraesthesia, or muscle weakness of the legs
  • Difficulty standing

DIAGNOSIS

  • Blood tests
  • Tuberculin skin test
  • Radiographs of the spine
  • Bone scan
  • CT of the spine
  • Bone biopsy
  • MRI

Late Complications

Controlling the spread of tuberculosis infection can prevent tuberculous spondylitis and arthritis. Patients who have a positive PPD test (but not active tuberculosis) may decrease their risk by properly taking medicines to prevent tuberculosis. To effectively treat tuberculosis, it is crucial that patients take their medications exactly as prescribed.

THERAPY

  • Non-operative – antituberculous drugs
  • Analgesics
  • Immobilization of the spine region different types of braces and collars
  • Surgery may be necessary, especially to drain spinal abscesses or debride bony lesions fully or to stabilize the spine. A 2007 review found only just two randomized clinical trial with at least one year-follow up found which compared chemotherapy plus surgery with chemotherapy alone for treating people diagnosed with active tuberculosis of the spine. As such there is no high grade evidence but the results of this study indicates that surgery should not be recommended routinely and clinicians have to selectively judge and decide on which patients to operate.
  • Thoracic spinal fusion with or without instrumentation as a last resort
  • Physical therapy for pain-relieving modalties, postural education and teaching a home exercise program for strength and flexibility

IMAGES

LUMBAGO (BACKACHE) - MAMATHA BHANSAL, HYDERABAD

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I am a driver. I had TB of my spine causing severe backache and fever. T.B. medicines given by specialists and the government did not help. Fever and pain did not subside; I lost my appetite and weight. Orthopaedic surgeons suggested a critical operation. I could not afford it. Suffered two years and lost my job. Any little movement in bed was highly painful. I was confined to bed only.

MODE OF RECOVERY AT NEW LIFE CENTRE

Homeopathy given by Dr.Subhash cured 80% of my pain in just five months. Fever dropped and appetite improved. I am attending my job. I am now healthy and active.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Pott's disease or Pott disease is a presentation of extrapulmonary tuberculosis whereby disease is seen in the spinal vertebrae. Extrapulmonary tuberculosis can affect the spine, a kind of tuberculous arthritis of the intervertebral joints. It is named after Percivall Pott (1714–1788), a British surgeon. The lower thoracic and upper lumbar vertebrae are the areas of the spine most often affected. Scientifically, it is called tuberculous spondylitis and it is most commonly localized in the thoracic portion of the spine. Pott’s disease results from haematogenous spread of tuberculosis from other sites, often pulmonary. The infection then spreads from two adjacent vertebrae into the adjoining intervertebral disc space. If only one vertebra is affected, the disc is normal, but if two are involved, the disc, which is avascular, cannot receive nutrients and collapses. The disc tissue dies and is broken down by caseation, leading to vertebral narrowing and eventually to vertebral collapse and spinal damage. A dry soft tissue mass often forms and superinfection is rare.

SIGNS AND SYMPTOMS

  • Back pains
  • Fever
  • Night sweating
  • Anorexia
  • Spinal mass, sometimes associated with numbness, paraesthesia, or muscle weakness of the legs
  • Difficulty standing

DIAGNOSIS

  • Blood tests
  • Tuberculin skin test
  • Radiographs of the spine
  • Bone scan
  • CT of the spine
  • Bone biopsy
  • MRI

Late Complications

Controlling the spread of tuberculosis infection can prevent tuberculous spondylitis and arthritis. Patients who have a positive PPD test (but not active tuberculosis) may decrease their risk by properly taking medicines to prevent tuberculosis. To effectively treat tuberculosis, it is crucial that patients take their medications exactly as prescribed.

THERAPY

  • Non-operative – antituberculous drugs
  • Analgesics
  • Immobilization of the spine region different types of braces and collars
  • Surgery may be necessary, especially to drain spinal abscesses or debride bony lesions fully or to stabilize the spine. A 2007 review found only just two randomized clinical trial with at least one year-follow up found which compared chemotherapy plus surgery with chemotherapy alone for treating people diagnosed with active tuberculosis of the spine. As such there is no high grade evidence but the results of this study indicates that surgery should not be recommended routinely and clinicians have to selectively judge and decide on which patients to operate.
  • Thoracic spinal fusion with or without instrumentation as a last resort
  • Physical therapy for pain-relieving modalties, postural education and teaching a home exercise program for strength and flexibility

IMAGES

  DISEASES OF GASTRO INTESTINAL SYSTEM

CHRONIC, SEVERE and UNYIELDING PAIN IN ABDOMEN - C.H.Balakrishna, Nizamabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I used to get severe attacks of colicky pain in my abdomen followed by vomiting. Consulted many experts in Nizamabad but in vain. I was not able to attend my business. Later I visited the leading gastroenterologists. They investigated me and found nothing They also could not help me. Thus I suffered 12 long years.

MODE OF RECOVERY AT NEW LIFE CENTRE

I am now relieved of pain and vomiting in one month after taking treatment from NEW LIFE centre. I am now married and am leading a peaceful life.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Intestinal colic is severe abdominal pain associated with malfunction in the intestines, such as a blockage or air bubble the patient cannot pass. It should not be confused with colic in babies, where the term “colic” is used generally to refer to a baby who is fussing more than usual, possibly because of intestinal colic but also because of other reasons. In addition, humans are not the only creatures affected by colic. The condition is common in horses, where it can be fatal if not treated promptly and aggressively.

An episode of intestinal colic can start with a sharp twinging sensation in the abdomen. Depending on the cause, there may be an urge to defecate and constipation can occur. Patients may be inclined to lie down or squat to relieve the pain, and it will become increasingly painful over time as the abdomen becomes rigid, hot, and swollen. Causes of this condition can include blockages caused by foreign objects or torsion, where intestines loop around each other.

A medical imaging study of the abdomen will show a blockage in the intestines and can also reveal the presence of trapped gas or stool. Palpation of the abdomen may be used to determine the source of the pain and check for tell-tale signs of conditions like appendicitis, which a patient may confuse with colic initially. With more information about the intestinal colic in hand, a doctor can develop a treatment recommendation for the patient, with the goal of addressing the pain while also treating the underlying cause. This may include surgery, the use of careful stretches and poses to address displaced intestines, or medications.

Causes of intestinal colic can vary. Sometimes people develop this condition as a result of swallowing air while eating or consuming high volumes of fermented food. Issues like torsion and displacement can happen spontaneously. Once someone has recovered from this type of colic, a mild diet is usually recommended to rest the intestines. Patients who experience repeat episodes may be advised to make permanent lifestyle and diet changes to prevent recurrence of colic.

In horses, intestinal colic is recognizable in the form of acute and obvious discomfort. The horse may try to lie down or lean, and can nip at the abdomen. Behavioral changes including lethargy or aggression sometimes occur. It is important to get colic treatment promptly for horses, as this condition can become very dangerous in a short period of time. The intestines may rupture, leading to peritonitis and death for the animal.

IMAGES

CHRONIC LIVER DISEASE, HEPATITIS C, CIRRHOSIS OF LIVER - Saroj Sharma, Delhi

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

She was under treatment at various liver speciality hospitals of Delhi for the past ten years for complications like recurrent fever, vomiting of blood, jaundice, swollen body, tapping of fluid from abdomen, anaemia, extreme weakness etc. ultimately they advised an operation called liver transplantation for her survival that could cost about Rs.60,00,000/-

MODE OF RECOVERY AT NEW LIFE CENTRE

We started taking homeopathy from Hyderabad. Luckily she has recovered from all these complications gradually; there is no need for frequent hospital admissions like before and many surgical procedures which were imminent have also been averted just with homeopathy. She is now active and moving freely like a normal person.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Hepatitis C is an infectious disease affecting primarily the liver, caused by the hepatitis C virus (HCV).[1] The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure, liver cancer, or life-threatening esophageal and gastric varices.

HCV is spread primarily by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment, and transfusions. An estimated 150–200 million people worldwide are infected with hepatitis C. The existence of hepatitis C (originally identifiable only as a type of non-A non-B hepatitis) was suggested in the 1970s and proven in 1989. Hepatitis C infects only humans and chimpanzees.

The virus persists in the liver in about 85% of those infected. This chronic infection can be treated with medication: the standard therapy is a combination of peginterferon and ribavirin, with either boceprevir or telaprevir added in some cases. Overall, 50–80% of people treated are cured. Those who develop cirrhosis or liver cancer may require a liver transplant. Hepatitis C is the leading reason for liver transplantation, though the virus usually recurs after transplantation. No vaccine against hepatitis C is available.

SIGNS AND SYMPTOMS

Acute infection

Hepatitis C infection causes acute symptoms in 15% of cases. Symptoms are generally mild and vague, including a decreased appetite, fatigue, nausea, muscle or joint pains, and weight loss[9] and rarely does acute liver failure result. Most cases of acute infection are not associated with jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in individuals who are young and female.

Chronic infection

About 80% of those exposed to the virus develop a chronic infection. This is defined as the presence of detectable viral replication for at least six months. Most experience minimal or no symptoms during the initial few decades of the infection. Chronic hepatitis C can be associated with fatigue[14] and mild cognitive problems. Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.

Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops.[17][18] Usually (80% of the time) this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year. Being infected with hepatits B in additional to hepatitis C increases this risk further.

Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the stomach and esophagus), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy. Ascites occurs at some stage in more than half of those who have a chronic infection.

Extrahepatic complications

The most common problem due to hepatitis C but not involving the liver is mixed cryoglobulinemia (usually the type II form) — an inflammation of small and medium-sized blood vessels. Hepatitis C is also associated with Sjögren's syndrome (an autoimmune disorder); thrombocytopenia; lichen planus; porphyria cutanea tarda; necrolytic acral erythema; insulin resistance; diabetes mellitus; diabetic nephropathy; autoimmune thyroiditis and B-cell lymphoproliferative disorders. Thrombocytopenia is estimated to occur in 0.16% to 45.4% of people with chronic hepatitis C. 20–30% of people infected have rheumatoid factor — a type of antibody. Possible associations include Hyde's prurigo nodularis and membranoproliferative glomerulonephritis. Cardiomyopathy with associated arrhythmias has also been reported. A variety of central nervous system disorders have been reported. Chronic infection seems to be associated with an increased risk of pancreatic cancer.

Occult infection

Persons who have been infected with hepatitis C may appear to clear the virus but remain infected.[34] The virus is not detectable with conventional testing but can be found with ultra-sensitive tests. The original method of detection was by demonstrating the viral genome within liver biopsies, but newer methods include an antibody test for the virus' core protein and the detection of the viral genome after first concentrating the viral particles by ultracentrifugation. A form of infection with persistently moderately elevated serum liver enzymes but without antibodies to hepatitis C has also been reported. This form is known as cryptogenic occult infection.

Several clinical pictures have been associated with this type of infection. It may be found in people with anti-hepatitis-C antibodies but with normal serum levels of liver enzymes; in antibody-negative people with ongoing elevated liver enzymes of unknown cause; in healthy populations without evidence of liver disease; and in groups at risk for HCV infection including those on haemodialysis or family members of people with occult HCV. The clinical relevance of this form of infection is under investigation. The consequences of occult infection appear to be less severe than with chronic infection but can vary from minimal to hepatocellular carcinoma.

The rate of occult infection in those apparently cured is controversial but appears to be low. 40% of those with hepatitis but with both negative hepatitis C serology and the absence of detectable viral genome in the serum have hepatitis C virus in the liver on biopsy. How commonly this occurs in children is unknown.

VIROLOGY

The hepatitis C virus (HCV) is a small, enveloped, single-stranded, positive-sense RNA virus. It is a member of the Hepacivirus genus in the family Flaviviridae. There are seven major genotypes of HCV, which are known as genotypes one to seven. The genotypes are divided into several subtypes with the number of subtypes depending on the genotype. In the United States, about 70% of cases are caused by genotype 1, 20% by genotype 2 and about 1% by each of the other genotypes. Genotype 1 is also the most common in South America and Europe.

The half life of the virus particles in the serum is around 3 hours and may be as short as 45 minutes. In an infected person, about 1012 virus particles are produced each day. In addition to replicating in the liver the virus can multiply in lymphocytes.

TRANSMISSION

The primary route of transmission in the developed world is intravenous drug use (IDU), while in the developing world the main methods are blood transfusions and unsafe medical procedures. The cause of transmission remains unknown in 20% of cases; however, many of these are believed to be accounted for by IDU.

Intravenous drug use

IDU is a major risk factor for hepatitis C in many parts of the world. Of 77 countries reviewed, 25 (including the United States) were found to have prevalences of hepatitis C in the intravenous drug user population of between 60% and 80%. Twelve countries had rates greater than 80%. It is believed that ten million intravenous drug users are infected with hepatitis C; China (1.6 million), the United States (1.5 million), and Russia (1.3 million) have the highest absolute totals. Occurrence of hepatitis C among prison inmates in the United States is 10 to 20 times that of the occurrence observed in the general population; this has been attributed to high-risk behavior in prisons such as IDU and tattooing with nonsterile equipment.

Healthcare exposure

Blood transfusion, transfusion of blood products, or organ transplants without HCV screening carry significant risks of infection. The United States instituted universal screening in 1992 to between one in 10,000 to one in 10,000,000 per unit of blood. This low risk remains as there is a period of about 11–70 days between the potential blood donor's acquiring hepatitis C and the blood's testing positive depending on the method. Some countries do not screen for hepatitis C due to the cost.

Those who have experienced a needle stick injury from someone who was HCV positive have about a 1.8% chance of subsequently contracting the disease themselves. The risk is greater if the needle in question is hollow and the puncture wound is deep. There is a risk from mucosal exposures to blood; but this risk is low, and there is no risk if blood exposure occurs on intact skin.

Hospital equipment has also been documented as a method of transmission of hepatitis C, including reuse of needles and syringes; multiple-use medication vials; infusion bags; and improperly sterilized surgical equipment, among others. Limitations in the implementation and enforcement of stringent standard precautions in public and private medical and dental facilities are known to be the primary cause of the spread of HCV in Egypt, the country with highest rate of infection in the world.

Sexual intercourse

Whether hepatitis C can be transmitted through sexual activity is controversial. While there is an association between high-risk sexual activity and hepatitis C, and multiple sexual partners are a risk factor for hepatitis C, there is no conclusive evidence that hepatitis C can be transmitted by sexual activity, since people who report transmission with sex as their only risk factor may actually have used drugs but denied it. The majority of evidence supports there being no risk for monogamous heterosexual couples. Sexual practices that involve higher levels of trauma to the anogenital mucosa, such as anal penetrative sex, or that occur when there is a concurrent sexually transmitted infection, including HIV or genital ulceration, do present a risk. The United States Department of Veterans Affairs recommends condom use to prevent hepatitis C transmission in those with multiple partners, but not those in monogamous relationships.

Body modification

Tattooing is associated with two to threefold increased risk of hepatitis C. This can be due to either improperly sterilized equipment or contamination of the dyes being used. Tattoos or piercings performed either before the mid-1980s, "underground," or nonprofessionally are of particular concern, since sterile techniques in such settings may be lacking. The risk also appears to be greater for larger tattoos. It is estimated that nearly half of prison inmates share unsterilized tattooing equipment. It is rare for tattoos in a licensed facility to be directly associated with HCV infection.

Shared personal items

Personal-care items such as razors, toothbrushes, and manicuring or pedicuring equipment can be contaminated with blood. Sharing such items can potentially lead to exposure to HCV. Appropriate caution should be taken regarding any medical condition that results in bleeding, such as cuts and sores. HCV is not spread through casual contact, such as hugging, kissing, or sharing eating or cooking utensils. Neither is it transmitted through food or water.

Vertical transmission

Vertical transmission of hepatitis C from an infected mother to her child occurs in less than 10% of pregnancies. There are no measures that alter this risk. It is not clear when during pregnancy transmission occurs, but it may occur both during gestation and at delivery. A long labor is associated with a greater risk of transmission. There is no evidence that breast-feeding spreads HCV; however, to be cautious, an infected mother is advised to avoid breastfeeding if her nipples are cracked and bleeding, or her viral loads are high.

DIAGNOSIS

There are a number of diagnostic tests for hepatitis C, including HCV antibody enzyme immunoassay or ELISA, recombinant immunoblot assay, and quantitative HCV RNA polymerase chain reaction (PCR). HCV RNA can be detected by PCR typically one to two weeks after infection, while antibodies can take substantially longer to form and thus be detected. Chronic hepatitis C is defined as infection with the hepatitis C virus persisting for more than six months based on the presence of its RNA. Chronic infections are typically asymptomatic during the first few decades, and thus are most commonly discovered following the investigation of elevated liver enzyme levels or during a routine screening of high-risk individuals. Testing is not able to distinguish between acute and chronic infections. Diagnosis in the infant is difficult as maternal antibodies may persist for up to 18 months.

Serology

Hepatitis C testing typically begins with blood testing to detect the presence of antibodies to the HCV, using an enzyme immunoassay. If this test is positive, a confirmatory test is then performed to verify the immunoassay and to determine the viral load. A recombinant immunoblot assay is used to verify the immunoassay and the viral load is determined by a HCV RNA polymerase chain reaction. If there are no RNA and the immunoblot is positive, it means that the person tested had a previous infection but cleared it either with treatment or spontaneously; if the immunoblot is negative, it means that the immunoassay was wrong. It takes about 6–8 weeks following infection before the immunoassay will test positive. A number of tests are available as point of care testing which means that results are available within 30 minutes.

Liver enzymes are variable during the initial part of the infection and on average begin to rise at seven weeks after infection. The elevation of liver enzymes does not closely follow disease severity.

Biopsy

Liver biopsies are used to determine the degree of liver damage present; however, there are risks from the procedure. The typical changes seen are lymphocytes within the parenchyma, lymphoid follicles in portal triad, and changes to the bile ducts. There are a number of blood tests available that try to determine the degree of hepatic fibrosis and alleviate the need for biopsy.

Screening

It is believed that only 5–50% of those infected in the United States and Canada are aware of their status. Testing is recommended in those at high risk, which includes injection drug users, those who have received blood transfusions before 1992, those who have been in jail, those on long term hemodialysis, and those with tattoos. Screening is also recommended in those with elevated liver enzymes, as this is frequently the only sign of chronic hepatitis. Routine screening is not currently recommended in the United States. In 2012, the U.S. Centers for Disease Control and Prevention (CDC) added a recommendation for a single screening test for those born between 1945 and 1965.

PREVENTION

As of 2011, no vaccine protects against contracting hepatitis C. However, there are a number under development and some have shown encouraging results. A combination of harm reduction strategies, such as the provision of new needles and syringes and treatment of substance use, decrease the risk of hepatitis C in intravenous drug users by about 75%. The screening of blood donors is important at a national level, as is adhering to universal precautions within healthcare facilities. In countries where there is an insufficient supply of sterile syringes, medications should be given orally rather than via injection (when possible).

TREATMENT

HCV induces chronic infection in 50–80% of infected persons. Approximately 40–80% of these clear with treatment. In rare cases, infection can clear without treatment. Those with chronic hepatitis C are advised to avoid alcohol and medications toxic to the liver, and to be vaccinated for hepatitis A and hepatitis B. Ultrasound surveillance for hepatocellular carcinoma is recommended in those with accompanying cirrhosis.

Medications

In general, treatment is recommended for those with proven HCV infection and signs of liver inflammation. As of 2010, treatments consist of a combination of pegylated interferon alpha and the antiviral drug ribavirin for a period of 24 or 48 weeks, depending on HCV genotype. This produces cure rates of between 70 and 80% for genotype 2 and 3, respectively, and 45 to 70% for other genotypes. When combined with ribavirin, pegylated interferon-alpha-2a may be superior to pegylated interferon-alpha-2b, though the evidence is not strong.

Combining either boceprevir or telaprevir with ribavirin and peginterferon alfa improves antiviral response for hepatitis C genotype 1. Adverse effects with treatment are common, with half of people getting flu like symptoms and a third experiencing emotional problems. Treatment during the first six months is more effective than once hepatitis C has become chronic. If someone develops a new infection and it has not cleared after eight to twelve weeks, 24 weeks of pegylated interferon is recommended. In people with thalassemia, ribavirin appears to be useful but increases the need for transfusions.

Sofosbuvir with ribavirin and interferon appears to be around 90% effective in those with genotype 1, 4, 5, or 6 disease. Sofosbuvir with just ribavirin appears to be 70 to 95% effective in type 2 and 3 disease. This benefit is somewhat offset by a greater rate of adverse effects. Treatments that contain ledipasvir and sofosbuvir for genotype 1 has success rates of around 93 to 99% but is very expensive. In genotype 6 infection, pegylated interferon and ribavirin is effective in 60 to 90% of cases. There is some tentative data for simeprevir use in type 6 disease as well.

Surgery

Cirrhosis due to hepatitis C is a common reason for liver transplantion though the virus usually (80–90% of cases) recurs afterwards. Infection of the graft leads to 10–30% of people developing cirrhosis within five years. Treatment with pegylated interferon and ribavirin post transplant decreases the risk of recurrence to 70%.

Alternative medicine

Alternative medicine Several alternative therapies are claimed by their proponents to be helpful for hepatitis C including milk thistle, ginseng, and colloidal silver. However, no alternative therapy has been shown to improve outcomes in hepatitis C, and no evidence exists that alternative therapies have any effect on the virus at all.

PROGNOSIS

The responses to treatment is measured by sustained viral response and vary by HCV C genotype. A sustained response occurs in about 40–50% in people with HCV genotype 1 given 48 weeks of treatment. A sustained response is seen in 70–80% of people with HCV genotypes 2 and 3 with 24 weeks of treatment. A sustained response occurs about 65% in those with genotype 4 after 48 weeks of treatment. The evidence for treatment in genotype 6 disease is sparse and what evidence there is supports 48 weeks of treatment at the same doses used for genotype 1 disease. Successful treatment decreases the future risk of hepatocellular carcinoma by 75%.

EPIDEMIOLOGY

It is estimated that 150–200 million people, or ~3% of the world's population, are living with chronic hepatitis C. About 3–4 million people are infected per year, and more than 350,000 people die yearly from hepatitis C-related diseases. During 2010 it is estimated that 16,000 people died from acute infections while 196,000 deaths occurred from liver cancer secondary to the infection. Rates have increased substantially in the 20th century due to a combination of intravenous drug abuse and reused but poorly sterilized medical equipment.

Rates are high (>3.5% population infected) in Central and East Asia, North Africa and the Middle East, they are intermediate (1.5%-3.5%) in South and Southeast Asia, sub-Saharan Africa, Andean, Central and Southern Latin America, Caribbean, Oceania, Australasia and Central, Eastern and Western Europe; and they are low (<1.5%) in Asia Pacific, Tropical Latin America and North America.

Among those chronically infected, the risk of cirrhosis after 20 years varies between studies but has been estimated at ~10–15% for men and ~1–5% for women. The reason for this difference is not known. Once cirrhosis is established, the rate of developing hepatocellular carcinoma is ~1–4% per year. Rates of new infections have decreased in the Western world since the 1990s due to improved screening of blood before transfusion.

In the United States, about 2% of people have hepatitis C, with the number of new cases per year stabilized at 17,000 since 2007. The number of deaths from hepatitis C has increased to 15,800 in 2008 and by 2007 had overtaken HIV/AIDS as a cause of death in the USA. This mortality rate is expected to increase, as those infected by transfusion before HCV testing become apparent. In Europe the percentage of people with chronic infections has been estimated to be between 0.13 and 3.26%.

The total number of people with this infection is higher in some countries in Africa and Asia. Countries with particularly high rates of infection include Egypt (22%), Pakistan (4.8%) and China (3.2%). It is believed that the high prevalence in Egypt is linked to a now-discontinued mass-treatment campaign for schistosomiasis, using improperly sterilized glass syringes.

IMAGES

CASE RECORD

SORE MOUTH(Ulcers) - Bheemiah, Karimnagar

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Ulcers in mouth with severe burning pain, also burning while passing urine. Eating and drinking was highly painful and difficult. Treatment by ENT specialists and dental surgeons failed to help me. I suffered four years.

MODE OF RECOVERY AT NEW LIFE CENTRE

Homeopathy cured me in just one month only. I am now able to eat and drink easily without any pain.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

A mouth ulcer (also termed an oral ulcer, or a mucosal ulcer) is an ulcer that occurs on the mucous membrane of the oral cavity. More plainly, a mouth ulcer is a sore or open lesion in the mouth. Mouth ulcers are very common, occurring in association with many diseases and by many different mechanisms, but usually there is no serious underlying cause. The two most common causes of oral ulceration are local trauma (e.g. rubbing from a sharp edge on a filling) and aphthous stomatitis ("canker sores"), a condition characterized by recurrent formation of oral ulcers for largely unknown reasons. Mouth ulcers often cause pain and discomfort, and may alter the person's choice of food while healing occurs (e.g. avoiding acidic or spicy foods and beverages). They may occur singly or multiple ulcers may occur at the same time (a "crop" of ulcers). Once formed, the ulcer may be maintained by inflammation and/or secondary infection. Rarely, a mouth ulcer that does not heal for many weeks may be a sign of oral cancer.

DEFINITION

An ulcer (/ˈʌlsər/; from Latin ulcus, from Greek "ἕλκος" – elkos, "wound") is a break in the skin or mucous membrane with loss of surface tissue, disintegration and necrosis of epithelial tissue. A mucosal ulcer is an ulcer which specifically occurs on a mucous membrane. An ulcer is a tissue defect which has penetrated the epithelial-connective tissue border, with its base at a deep level in the submucosa, or even within muscle or periosteum. An ulcer is a deeper breach of the epithelium than an erosion or an excoriation, and involves damage to both epithelium and lamina propria.

An erosion is a superficial breach of the epithelium, with little damage to the underlying lamina propria. A mucosal erosion is an erosion which specifically occurs on a mucous membrane. Only the superficial epithelial cells of the epidermis or of the mucosa are lost, and the lesion can reach the depth of the basement membrane. Erosions heal without scar formation.

Excoriation is a term sometimes used to describe a breach of the epithelium which is deeper than an erosion but shallower than an ulcer. This type of lesion is tangential to the rete pegs and shows punctiform (small pinhead spots) bleeding, caused by exposed capillary loops.

DIFFERENTIAL DIAGNOSIS

Aphthous stomatitis and local trauma are very common causes of oral ulceration, the many other possible causes are all rare in comparison.

Traumatic ulceration

Traumatic ulceration Most mouth ulcers that are not associated with recurrent aphthous stomatitis are caused by local trauma. The mucous membrane lining of the mouth is thinner than the skin, and easily damaged by mechanical, thermal (heat/cold), chemical or electrical means, or by irradiation.

A small ulcer on the lower labial frenum. Common causes of oral ulceration include rubbing on sharp edges of teeth, fillings, crowns, false teeth (dentures), braces (orthodontic appliances). Accidental biting caused by a lack of awareness of painful stimuli in the mouth (following a local anesthetic e.g. during dental treatment) may cause ulceration which the person becomes aware of as the anesthetic wears off and the full sensation returns. Eating rough foods (e.g. potato chips) can damage the lining of the mouth. Some people cause damage inside their mouths themselves, either through an absent minded habit or as a type of deliberate self harm (factitious ulceration). Examples include biting the cheek, tongue or lips, rubbing a finger nail, pen or tooth pick inside the mouth. Tearing (and subsequent ulceration) of the upper labial frenum may be a sign of child abuse (non-accidental injury). Iatrogenic ulceration can also occur during dental treatment, when incidental abrasions to the soft tissues of the mouth are common. Some dentists apply a protective layer of petroleum jelly to the lips before carrying out dental work to minimize the number of incidental injuries. The lingual frenum is also vulnerable to ulceration by repeated friction during oral sexual activity, in which case the incisal edges of the mandibular teeth can be smoothed to minimize the chance of trauma.

Thermal and electrical burn

Thermal burns usually result from placing hot food or beverages in the mouth. This may occur in those who eat or drink before a local anesthetic has worn off. The normal painful sensation is absent and a burn may occur. Microwave ovens sometimes produce food which is cold externally and very hot internally, and this has led to a rise in the frequency of intra-oral thermal burns. Thermal food burns are usually on the palate or posterior buccal mucosa, and appear as zones of erythema and ulceration with necrotic epithelium peripherally. Electrical burns more commonly affect the oral commissure (corner of the mouth). The lesions are usually initially painless, charred and yellow with little bleeding. Swelling then develops and by the fourth day following the burn the area becomes necrotic and the epithelium sloughs off.

Electrical burns in the mouth are usually caused by chewing on live electrical wiring (an act that is relatively common among young children). Saliva acts as a conducting medium and an electrical arc flows between the electrical source and the tissues, causing extreme heat and possible tissue destruction.

Chemical injury

Caustic chemicals may cause ulceration of the oral mucosa if they are of strong enough concentration and in contact for a sufficient length of time. The holding of medication in the mouth instead of swallowing it occurs mostly in children, those under psychiatric care, or simply because of a lack of understanding. Holding an aspirin tablet next to a painful tooth in an attempt to relieve pulpitis (toothache) is common, and leads to epithelial necrosis. Chewable aspirin tablets also need to be swallowed, and the residue quickly cleared from the mouth. Other caustic medications include eugenol and chlorpromazine. Hydrogen peroxide, used to treat gum disease, is also capable of causing epithelial necrosis at concentrations of 1–3%. Silver nitrate, sometimes used for pain relief from aphthous ulceration, acts as a chemical cauterant and destroys nerve endings, but the mucosal damage is increased. Phenol is used during dental treatment as a cavity sterilizing agent and cauterizing material, and it is also present in some over the counter agents again intended to treat aphthous ulcerations. Mucosal necrosis has been reported to occur with concentrations of 0.5%. Other materials used in endodontics are also caustic, which is part of the reason why use of a rubber dam is now recommended.

Irradiation

As a result of radiotherapy to the mouth, radiation induced stomatitis may develop, which can be associated with mucosal erosions and ulceration. If the salivary glands are irradiated, there may also be xerostomia (dry mouth), making the oral mucosa more vulnerable to frictional damage as the lubricating function of saliva is lost, and mucosal atrophy (thinning) which makes a breach of the epithelium more likely. Radiation to the bones of the jaws causes damage to osteocytes and impairs the blood supply. The affected hard tissues become hypovascular (reduced number of blood vessels), hypocellular (reduced number of cells) and hypoxic (low levels of oxygen). Osteoradionecrosis is the term for when such an area of irradiated bone does not heal from this damage. This usually occurs in the mandible, and causes chronic pain and surface ulceration, sometimes resulting in non healing bone being exposed through a soft tissue defect. Prevention of osteradionecrosis is part of the reason why all teeth of questionable prognosis are removed before the start of a course of radiotherapy.

Aphthous stomatitis

Aphthous stomatitis (also termed recurrent aphthous stomatits, RAS, and commonly called "canker sores") is a very common cause of oral ulceration. 10–25% of the general population suffer from this non-contagious condition. The appearance of aphthous stomatitis varies as there are 3 types, namely minor aphthous ulceration, major aphthous ulceration and herpetiform ulceration. Minor aphthous ulceration is the most common type, presenting with 1–6 small (2-4mm diameter), round/oval ulcers with a yellow-grey color and an erythematous (red) "halo". These ulcers heal with no permanent scarring in about 7–10 days. Ulcers recur at intervals of about 1–4 months. Major aphthous ulceration is less common than the minor type, but produces more severe lesions and symptoms. Major aphthous ulceration presents with larger (>1 cm diameter) ulcers that take much longer to heal (10–40 days) and may leave scarring. The minor and major subtypes of aphthous stomatitis usually produce lesions on the non-keratinized oral mucosa (i.e. the inside of the cheeks, lips, underneath the tongue and the floor of mouth), but less commonly major aphthous ulcers may occur in other parts of the mouth on keratinized mucosal surfaces. The least common type is herpetiform ulceration, so named because the condition resembles primary herpetic gingivostomatitis.

Herpetiform ulcers begin as small blisters (vesicles) which break down into 2-3mm sized ulcers. Herpetiform ulcers appear in "crops" sometimes hundreds in number, which can coalesce to form larger areas of ulceration. This subtype may cause extreme pain, heals with scarring and may recur frequently. The exact cause of aphthous stomatitis is unknown, but there may be a genetic predisposition in some people. Other possible causes include hematinic deficiency (folate, vitamin B, iron), stopping smoking, stress, menstruation, trauma, food allergies or hypersensitivity to sodium lauryl sulphate (found in many brands of toothpaste). Aphthous stomatitis has no clinically detectable signs or symptoms outside the mouth, but the recurrent ulceration can cause much discomfort to sufferers. Treatment is aimed at reducing the pain and swelling and speeding healing, and may involve systemic or topical steroids, analgesics (pain killers), antiseptics, anti-inflammatories or barrier pastes to protect the raw area(s).

Infection

Many infections can cause oral ulceration (see table). The most common are Herpes simplex virus (herpes labialis, primary herpetic gingivostomatitis), Varicella Zoster (chicken pox, shingles), and coxsackie A virus (hand, foot and mouth disease). Human immunodeficiency virus (HIV) creates immunodeficiencies which allow opportunistic infections or neoplasms to proliferate. Bacterial processes leading to ulceration can be caused by Mycobacterium tuberculosis (tuberculosis) and Treponema pallidum (syphilis). Opportunistic activity by combinations of otherwise normal bacterial flora, such as aerobic streptococi, Neisseria, Actinomyces, spirochetes, and Bacteroides species can prolong the ulcerative process. Fungal causes include Coccidioides immitis (valley fever), Cryptococcus neoformans (cryptococcosis), and Blastomyces dermatitidis ("North American Blastomycosis"). Entamoeba histolytica, a parasitic protozoan, is sometimes known to cause mouth ulcers through formation of cysts.

Drug-induced

Many drugs can cause mouth ulcers as a side effect. Common examples are alendronate (a bisphosphonate, commonly prescribed for osteoporosis), cytotoxic drugs (e.g. methotrexate, i.e. chemotherapy), non steroidal anti-inflammatory drugs, nicorandil (may be prescribed for angina) and propylthiouracil (e.g. used for hyperthyroidism). Some recreational drugs can cause ulceration, e.g. cocaine.

Malignancy

Rarely, a persistent, non healing mouth ulcer may be a cancerous lesion. Malignancies in the mouth are usually carcinomas, but lymphomas, sarcomas and others may also be possible. Either the tumor arises in the mouth, or it may grow to involve the mouth, e.g. from the maxillary sinus, salivary glands, nasal cavity or peri-oral skin. The most common type of oral cancer is squamous cell carcinoma. The main causes are long term smoking and alcohol consumption (particularly together) and betel use. Common sites of oral cancer are the lower lip, the floor of the mouth, and the sides and underside of the tongue, but it is possible to have a tumor anywhere in the mouth. Appearances vary greatly, but a typical malignant ulcer would be a persistent, expanding lesion which is totally red (erythroplasia) or speckled red and white (erythroleukoplakia). Malignant lesions also typically feel indurated (hardened) and attached to adjacent structures, with "rolled" margins or a punched out appearance and bleeds easily on gentle manipulation.

Vesiculobullous diseases

Due to various factors (saliva, relative thinness of oromucosa, trauma from teeth, chewing, etc.), vesicles and bullae which form on the mucous membranes of the oral cavity tend to be fragile and quickly break down to leave ulcers.

Some of the viral infections mentioned above are also classified as vesiculobullous diseases. Other example vesiculobullous diseases include pemphigus vulgaris, mucous membrane pemphigoid, bullous pemphigoid, dermatitis herpetiformis, linear IgA disease, and epidermolysis bullosa.

Allergy

Rarely, allergic reactions of the mouth and lips may manifest as erosions, however such reactions usually do not produce frank ulceration. An example of one common allergen is Balsam of Peru, if they have oral exposure to the substance, may experience stomatitis and cheilitis (inflammation, rash, or painful erosion of the lips, oropharyngeal mucosa, or angles of their mouth). Balsam of Peru is used in food and drink for flavoring, in perfumes and toiletries for fragrance, and in medicine and pharmaceutical items for healing properties.

Other causes

A wide range of other diseases may cause mouth ulcers. Hematological causes include anemia, hematinic deficiencies, neutropenia, hypereosinophilic syndrome, leukemia, myelodysplastic syndromes, other white cells dyscrasias and gammopathies. Gastrointestinal causes include celiac disease, Crohn's disease (orofacial granulomatosis), and ulcerative colitis. Dermatological causes include chronic ulcerative stomatitis, erythema multiforme (Stevens-Johnson syndrome), angina bullosa haemorrhagica and lichen planus. Other examples of systemic disease capable of causing mouth ulcers include lupus erythematosus, Sweet syndrome, Reiter syndrome, Behçet syndrome, Wegener's granulomatosis, periarteritis nodosa, giant cell arteritis, diabetes, glucagonoma, sarcoidosis and periodic fever, aphthous stomatitis, pharyngitis and adenitis.

The conditions eosinophilic ulcer and necrotizing sialometaplasia may present as oral ulceration.

Macroglossia, an abnormally large tongue, can be associated with ulceration if the tongue protrudes constantly from the mouth. Caliber persistent artery describes a common vascular anomaly where a main arterial branch extends into superficial submucosal tissues without a reduction of diameter. This commonly occurs in elderly people on the lip and may be associated with ulceration.

PATHOPHYSIOLOGY

The exact pathogenesis is dependent upon the cause. Ulcers and erosions can be the result of a spectrum of conditions including those causing auto-immune epithelial damage, damage because of an immune defect (e.g. HIV, leukemia, infections e.g. herpes viruses) or nutritional disorders (e.g. vitamin deficiencies). Simple mechanisms which predispose the mouth to trauma and ulceration are xerostomia (dry mouth – as saliva usually lubricates the mucous membrane and controls bacterial levels) and epithelial atrophy (thinning, e.g. after radiotherapy), making the lining more fragile and easily breached. Stomatitis is a general term meaning inflammation within the mouth, and often may be associated with ulceration. Pathologically, the mouth represents a transition between the gastrointestinal tract and the skin, meaning that many gastrointestinal and cutaneous conditions can involve the mouth. Some conditions usually associated with the whole gastrointestinal tract may present only in the mouth, e.g. orofacial granulomatosis/oral Crohn's disease. Similarly, cutaneous conditions can also involve the mouth and sometimes only the mouth, sparing the skin. The different conditions mean that many conditions which produce characteristic lesions on the skin produce only non specific lesions in the mouth. The vesicles and bullae of blistering mucocutaneous disorders progress quickly to ulceration in the mouth, because of moisture and trauma from food and teeth. The high bacterial load in the mouth means that ulcers may become secondarily infected. Cytotoxic drugs administered during chemotherapy target cells with fast turnovers such as malignant cells. However, the epithelia of the mouth also has a high turnover rate and makes oral ulceration a common side effect of chemotherapy.

Erosions, which involve the epithelial layer, are red in appearance since the underlying lamina propria shows through. When the full thickness of the epithelium is penetrated (ulceration), the lesion becomes covered with a fibrinous exudate and takes on a yellow-grey color. Because an ulcer is a breach of the normal lining, when seen in cross section, the lesion is a crater. A "halo" may be present, which is a reddening of the surrounding mucosa and is caused by inflammation. There may also be edema (swelling) around the ulcer. Chronic trauma may produce an ulcer with a keratotic (white, thickened mucosa) margin. Malignant lesions may ulcerate either because the tumor infiltrates the mucosa from adjacent tissues, or because the lesion originates within the mucosa itself, and the disorganized growth leads to a break in the normal architecture of the lining tissues. Repeat episodes of mouth ulcers can be indicative of an immunodeficiency, signaling low levels of immunoglobulin in the oral mucous membranes. Chemotherapy, HIV, and mononucleosis are all causes of immunodeficiency/immunosuppression with which oral ulcers may become a common manifestation. Autoimmunity is also a cause of oral ulceration. Mucous membrane pemphigoid, an autoimmune reaction to the epithelial basement membrane, causes desquamation/ulceration of the oral mucosa. Numerous aphthous ulcers could be indicative of an inflammatory autoimmune disease called Behçet's disease. This can later involve skin lesions and uveitis in the eyes. Vitamin C deficiency may lead to scurvy which impairs wound healing, which can contribute to ulcer formation. For a detailed discussion of the pathophysiology of aphthous stomatitis, see Aphthous stomatitis#Causes.

DIAGNOSTIC APPROACH

Diagnosis of mouth ulcers usually consists of a medical history followed by an oral examination as well as examination of any other involved area. The following details may be pertinent: The duration that the lesion has been present, the location, the number of ulcers, the size, the color and whether it is hard to touch, bleeds or has a rolled edge. As a general rule, a mouth ulcer that does not heal within 2 or 3 weeks should be examined by a health care professional who is able to rule out oral cancer (e.g. a dentist, oral physician, oral surgeon/ maxillofacial surgeon). If there have been previous ulcers which have healed, then this again makes cancer unlikely. An ulcer that keeps forming on the same site and then healing may be caused by a nearby sharp surface, and ulcers that heal and then recur at different sites are likely to be RAS. Malignant ulcers are likely to be single in number, and conversely, multiple ulcers are very unlikely to be oral cancer. The size of the ulcers may be helpful in distinguishing the types of RAS, as can the location (minor RAS mainly occurs on non-keratonizing mucosa, major RAS occurs anywhere in the mouth or oropharynx). Induration, contact bleeding and rolled margins are features of a malignant ulcer. There may be nearby causative factor, e.g. a broken tooth with a sharp edge that is traumatizing the tissues. Otherwise, the person may be asked about problems elsewhere, e.g. ulceration of the genital mucous membranes, eye lesions or digestive problems, swollen glands in neck (lymphadenopathy) or a general unwell feeling. The diagnosis comes mostly from the history and examination, but the following special investigations may be involved: blood tests (vitamin deficiency, anemia, leukemia, Epstein-Barr virus, HIV infection, diabetes) microbiological swabs (infection), or urinalysis (diabetes). A biopsy (minor procedure to cut out a small sample of the ulcer to look at under a microscope) with or without immunofluorescence may be required, to rule out cancer, but also if a systemic disease is suspected. Ulcers caused by local trauma are painful to touch and sore. They usually have an irregular border with erythematous margins and the base is yellow. As healing progresses, a keratotic (thickened, white mucosa) halo may occur.

TREATMENT

Treatment is cause related, but also symptomatic if the underlying cause is unknown or not correctable. It is also important to note that most ulcers will heal completely without any intervention. Treatment can range from simply smoothing or removing a local cause of trauma, to addressing underlying factors such as dry mouth or substituting a problem medication. Maintaining good oral hygiene and use of an antiseptic mouthwashes/sprays (e.g. chlorhexidine) can prevent secondary infection and therefore hasten healing. A topical analgesic (e.g. benzydamine mouthwash) may reduce pain. Topical (gels, creams or inhalers) or systemic steroids may be used to reduce inflammation. An antifungal drug may be used to prevent oral candidiasis developing in those who use prolonged steroids. People with mouth ulcers may prefer to avoid hot or spicy foods, which can increase the pain. Self-inflicted ulceration can be difficult to manage, and psychiatric input may be required in some people.

EPIDEMIOLOGY

Oral ulceration is a common cause for people to seek medical or dental advice. A breach of the oral mucosa probably affects most people at various times during life. For a discussion of the epidemiology of aphthous stomatitis, see Aphthous stomatitis#Epidemiology.

IMAGES

CIRRHOSIS OF LIVER - HEPATITIS C - G.S.Agarwal, Nagpur

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I was suffering from hepatitis C, a severe liver disease with all complications like Cirrhosis of liver, Portal hypertension, Ascites, Swelling of abdomen and legs, fever, vomiting of blood,diarrhoea etc. Gastroenterologists advised me two courses of costly antiviral drugs for six months each, but there was no relief. Liver transplant operation was suggested.

MODE OF RECOVERY AT NEW LIFE CENTRE

Later my daughter Dr GeetaAgarwal who learnt about the successful novel treatment of Dr.Subhash Chandar for such diseases through homeopathic journal, directed me to take his treatment. I recovered fully with his treatment in all aspects in a short period and my blood tested negative for the Hepatitis C virus.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Hepatitis C is an infectious disease affecting primarily the liver, caused by the hepatitis C virus (HCV).[1] The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure, liver cancer, or life-threatening esophageal and gastric varices.

HCV is spread primarily by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment, and transfusions. An estimated 150–200 million people worldwide are infected with hepatitis C. The existence of hepatitis C (originally identifiable only as a type of non-A non-B hepatitis) was suggested in the 1970s and proven in 1989. Hepatitis C infects only humans and chimpanzees.

The virus persists in the liver in about 85% of those infected. This chronic infection can be treated with medication: the standard therapy is a combination of peginterferon and ribavirin, with either boceprevir or telaprevir added in some cases. Overall, 50–80% of people treated are cured. Those who develop cirrhosis or liver cancer may require a liver transplant. Hepatitis C is the leading reason for liver transplantation, though the virus usually recurs after transplantation. No vaccine against hepatitis C is available.

SIGNS AND SYMPTOMS

Acute infection

Hepatitis C infection causes acute symptoms in 15% of cases. Symptoms are generally mild and vague, including a decreased appetite, fatigue, nausea, muscle or joint pains, and weight loss[9] and rarely does acute liver failure result. Most cases of acute infection are not associated with jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in individuals who are young and female.

Chronic infection

About 80% of those exposed to the virus develop a chronic infection. This is defined as the presence of detectable viral replication for at least six months. Most experience minimal or no symptoms during the initial few decades of the infection. Chronic hepatitis C can be associated with fatigue[14] and mild cognitive problems. Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.

Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops.[17][18] Usually (80% of the time) this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year. Being infected with hepatits B in additional to hepatitis C increases this risk further.

Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the stomach and esophagus), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy. Ascites occurs at some stage in more than half of those who have a chronic infection.

Extrahepatic complications

The most common problem due to hepatitis C but not involving the liver is mixed cryoglobulinemia (usually the type II form) — an inflammation of small and medium-sized blood vessels. Hepatitis C is also associated with Sjögren's syndrome (an autoimmune disorder); thrombocytopenia; lichen planus; porphyria cutanea tarda; necrolytic acral erythema; insulin resistance; diabetes mellitus; diabetic nephropathy; autoimmune thyroiditis and B-cell lymphoproliferative disorders. Thrombocytopenia is estimated to occur in 0.16% to 45.4% of people with chronic hepatitis C. 20–30% of people infected have rheumatoid factor — a type of antibody. Possible associations include Hyde's prurigo nodularis and membranoproliferative glomerulonephritis. Cardiomyopathy with associated arrhythmias has also been reported. A variety of central nervous system disorders have been reported. Chronic infection seems to be associated with an increased risk of pancreatic cancer.

Occult infection

Persons who have been infected with hepatitis C may appear to clear the virus but remain infected.[34] The virus is not detectable with conventional testing but can be found with ultra-sensitive tests. The original method of detection was by demonstrating the viral genome within liver biopsies, but newer methods include an antibody test for the virus' core protein and the detection of the viral genome after first concentrating the viral particles by ultracentrifugation. A form of infection with persistently moderately elevated serum liver enzymes but without antibodies to hepatitis C has also been reported. This form is known as cryptogenic occult infection.

Several clinical pictures have been associated with this type of infection. It may be found in people with anti-hepatitis-C antibodies but with normal serum levels of liver enzymes; in antibody-negative people with ongoing elevated liver enzymes of unknown cause; in healthy populations without evidence of liver disease; and in groups at risk for HCV infection including those on haemodialysis or family members of people with occult HCV. The clinical relevance of this form of infection is under investigation. The consequences of occult infection appear to be less severe than with chronic infection but can vary from minimal to hepatocellular carcinoma.

The rate of occult infection in those apparently cured is controversial but appears to be low. 40% of those with hepatitis but with both negative hepatitis C serology and the absence of detectable viral genome in the serum have hepatitis C virus in the liver on biopsy. How commonly this occurs in children is unknown.

VIROLOGY

The hepatitis C virus (HCV) is a small, enveloped, single-stranded, positive-sense RNA virus. It is a member of the Hepacivirus genus in the family Flaviviridae. There are seven major genotypes of HCV, which are known as genotypes one to seven. The genotypes are divided into several subtypes with the number of subtypes depending on the genotype. In the United States, about 70% of cases are caused by genotype 1, 20% by genotype 2 and about 1% by each of the other genotypes. Genotype 1 is also the most common in South America and Europe.

The half life of the virus particles in the serum is around 3 hours and may be as short as 45 minutes. In an infected person, about 1012 virus particles are produced each day. In addition to replicating in the liver the virus can multiply in lymphocytes.

TRANSMISSION

The primary route of transmission in the developed world is intravenous drug use (IDU), while in the developing world the main methods are blood transfusions and unsafe medical procedures. The cause of transmission remains unknown in 20% of cases; however, many of these are believed to be accounted for by IDU.

Intravenous drug use

IDU is a major risk factor for hepatitis C in many parts of the world. Of 77 countries reviewed, 25 (including the United States) were found to have prevalences of hepatitis C in the intravenous drug user population of between 60% and 80%. Twelve countries had rates greater than 80%. It is believed that ten million intravenous drug users are infected with hepatitis C; China (1.6 million), the United States (1.5 million), and Russia (1.3 million) have the highest absolute totals. Occurrence of hepatitis C among prison inmates in the United States is 10 to 20 times that of the occurrence observed in the general population; this has been attributed to high-risk behavior in prisons such as IDU and tattooing with nonsterile equipment.

Healthcare exposure

Blood transfusion, transfusion of blood products, or organ transplants without HCV screening carry significant risks of infection. The United States instituted universal screening in 1992 to between one in 10,000 to one in 10,000,000 per unit of blood. This low risk remains as there is a period of about 11–70 days between the potential blood donor's acquiring hepatitis C and the blood's testing positive depending on the method. Some countries do not screen for hepatitis C due to the cost.

Those who have experienced a needle stick injury from someone who was HCV positive have about a 1.8% chance of subsequently contracting the disease themselves. The risk is greater if the needle in question is hollow and the puncture wound is deep. There is a risk from mucosal exposures to blood; but this risk is low, and there is no risk if blood exposure occurs on intact skin.

Hospital equipment has also been documented as a method of transmission of hepatitis C, including reuse of needles and syringes; multiple-use medication vials; infusion bags; and improperly sterilized surgical equipment, among others. Limitations in the implementation and enforcement of stringent standard precautions in public and private medical and dental facilities are known to be the primary cause of the spread of HCV in Egypt, the country with highest rate of infection in the world.

Sexual intercourse

Whether hepatitis C can be transmitted through sexual activity is controversial. While there is an association between high-risk sexual activity and hepatitis C, and multiple sexual partners are a risk factor for hepatitis C, there is no conclusive evidence that hepatitis C can be transmitted by sexual activity, since people who report transmission with sex as their only risk factor may actually have used drugs but denied it. The majority of evidence supports there being no risk for monogamous heterosexual couples. Sexual practices that involve higher levels of trauma to the anogenital mucosa, such as anal penetrative sex, or that occur when there is a concurrent sexually transmitted infection, including HIV or genital ulceration, do present a risk. The United States Department of Veterans Affairs recommends condom use to prevent hepatitis C transmission in those with multiple partners, but not those in monogamous relationships.

Body modification

Tattooing is associated with two to threefold increased risk of hepatitis C. This can be due to either improperly sterilized equipment or contamination of the dyes being used. Tattoos or piercings performed either before the mid-1980s, "underground," or nonprofessionally are of particular concern, since sterile techniques in such settings may be lacking. The risk also appears to be greater for larger tattoos. It is estimated that nearly half of prison inmates share unsterilized tattooing equipment. It is rare for tattoos in a licensed facility to be directly associated with HCV infection.

Shared personal items

Personal-care items such as razors, toothbrushes, and manicuring or pedicuring equipment can be contaminated with blood. Sharing such items can potentially lead to exposure to HCV. Appropriate caution should be taken regarding any medical condition that results in bleeding, such as cuts and sores. HCV is not spread through casual contact, such as hugging, kissing, or sharing eating or cooking utensils. Neither is it transmitted through food or water.

Vertical transmission

Vertical transmission of hepatitis C from an infected mother to her child occurs in less than 10% of pregnancies. There are no measures that alter this risk. It is not clear when during pregnancy transmission occurs, but it may occur both during gestation and at delivery. A long labor is associated with a greater risk of transmission. There is no evidence that breast-feeding spreads HCV; however, to be cautious, an infected mother is advised to avoid breastfeeding if her nipples are cracked and bleeding, or her viral loads are high.

DIAGNOSIS

There are a number of diagnostic tests for hepatitis C, including HCV antibody enzyme immunoassay or ELISA, recombinant immunoblot assay, and quantitative HCV RNA polymerase chain reaction (PCR). HCV RNA can be detected by PCR typically one to two weeks after infection, while antibodies can take substantially longer to form and thus be detected. Chronic hepatitis C is defined as infection with the hepatitis C virus persisting for more than six months based on the presence of its RNA. Chronic infections are typically asymptomatic during the first few decades, and thus are most commonly discovered following the investigation of elevated liver enzyme levels or during a routine screening of high-risk individuals. Testing is not able to distinguish between acute and chronic infections. Diagnosis in the infant is difficult as maternal antibodies may persist for up to 18 months.

Serology

Hepatitis C testing typically begins with blood testing to detect the presence of antibodies to the HCV, using an enzyme immunoassay. If this test is positive, a confirmatory test is then performed to verify the immunoassay and to determine the viral load. A recombinant immunoblot assay is used to verify the immunoassay and the viral load is determined by a HCV RNA polymerase chain reaction. If there are no RNA and the immunoblot is positive, it means that the person tested had a previous infection but cleared it either with treatment or spontaneously; if the immunoblot is negative, it means that the immunoassay was wrong. It takes about 6–8 weeks following infection before the immunoassay will test positive. A number of tests are available as point of care testing which means that results are available within 30 minutes.

Liver enzymes are variable during the initial part of the infection and on average begin to rise at seven weeks after infection. The elevation of liver enzymes does not closely follow disease severity.

Biopsy

Liver biopsies are used to determine the degree of liver damage present; however, there are risks from the procedure. The typical changes seen are lymphocytes within the parenchyma, lymphoid follicles in portal triad, and changes to the bile ducts. There are a number of blood tests available that try to determine the degree of hepatic fibrosis and alleviate the need for biopsy.

Screening

It is believed that only 5–50% of those infected in the United States and Canada are aware of their status. Testing is recommended in those at high risk, which includes injection drug users, those who have received blood transfusions before 1992, those who have been in jail, those on long term hemodialysis, and those with tattoos. Screening is also recommended in those with elevated liver enzymes, as this is frequently the only sign of chronic hepatitis. Routine screening is not currently recommended in the United States. In 2012, the U.S. Centers for Disease Control and Prevention (CDC) added a recommendation for a single screening test for those born between 1945 and 1965.

PREVENTION

As of 2011, no vaccine protects against contracting hepatitis C. However, there are a number under development and some have shown encouraging results. A combination of harm reduction strategies, such as the provision of new needles and syringes and treatment of substance use, decrease the risk of hepatitis C in intravenous drug users by about 75%. The screening of blood donors is important at a national level, as is adhering to universal precautions within healthcare facilities. In countries where there is an insufficient supply of sterile syringes, medications should be given orally rather than via injection (when possible).

TREATMENT

HCV induces chronic infection in 50–80% of infected persons. Approximately 40–80% of these clear with treatment. In rare cases, infection can clear without treatment. Those with chronic hepatitis C are advised to avoid alcohol and medications toxic to the liver, and to be vaccinated for hepatitis A and hepatitis B. Ultrasound surveillance for hepatocellular carcinoma is recommended in those with accompanying cirrhosis.

Medications

In general, treatment is recommended for those with proven HCV infection and signs of liver inflammation. As of 2010, treatments consist of a combination of pegylated interferon alpha and the antiviral drug ribavirin for a period of 24 or 48 weeks, depending on HCV genotype. This produces cure rates of between 70 and 80% for genotype 2 and 3, respectively, and 45 to 70% for other genotypes. When combined with ribavirin, pegylated interferon-alpha-2a may be superior to pegylated interferon-alpha-2b, though the evidence is not strong.

Combining either boceprevir or telaprevir with ribavirin and peginterferon alfa improves antiviral response for hepatitis C genotype 1. Adverse effects with treatment are common, with half of people getting flu like symptoms and a third experiencing emotional problems. Treatment during the first six months is more effective than once hepatitis C has become chronic. If someone develops a new infection and it has not cleared after eight to twelve weeks, 24 weeks of pegylated interferon is recommended. In people with thalassemia, ribavirin appears to be useful but increases the need for transfusions.

Sofosbuvir with ribavirin and interferon appears to be around 90% effective in those with genotype 1, 4, 5, or 6 disease. Sofosbuvir with just ribavirin appears to be 70 to 95% effective in type 2 and 3 disease. This benefit is somewhat offset by a greater rate of adverse effects. Treatments that contain ledipasvir and sofosbuvir for genotype 1 has success rates of around 93 to 99% but is very expensive. In genotype 6 infection, pegylated interferon and ribavirin is effective in 60 to 90% of cases. There is some tentative data for simeprevir use in type 6 disease as well.

Surgery

Cirrhosis due to hepatitis C is a common reason for liver transplantion though the virus usually (80–90% of cases) recurs afterwards. Infection of the graft leads to 10–30% of people developing cirrhosis within five years. Treatment with pegylated interferon and ribavirin post transplant decreases the risk of recurrence to 70%.

Alternative medicine

Alternative medicine Several alternative therapies are claimed by their proponents to be helpful for hepatitis C including milk thistle, ginseng, and colloidal silver. However, no alternative therapy has been shown to improve outcomes in hepatitis C, and no evidence exists that alternative therapies have any effect on the virus at all.

PROGNOSIS

The responses to treatment is measured by sustained viral response and vary by HCV C genotype. A sustained response occurs in about 40–50% in people with HCV genotype 1 given 48 weeks of treatment. A sustained response is seen in 70–80% of people with HCV genotypes 2 and 3 with 24 weeks of treatment. A sustained response occurs about 65% in those with genotype 4 after 48 weeks of treatment. The evidence for treatment in genotype 6 disease is sparse and what evidence there is supports 48 weeks of treatment at the same doses used for genotype 1 disease. Successful treatment decreases the future risk of hepatocellular carcinoma by 75%.

EPIDEMIOLOGY

It is estimated that 150–200 million people, or ~3% of the world's population, are living with chronic hepatitis C. About 3–4 million people are infected per year, and more than 350,000 people die yearly from hepatitis C-related diseases. During 2010 it is estimated that 16,000 people died from acute infections while 196,000 deaths occurred from liver cancer secondary to the infection. Rates have increased substantially in the 20th century due to a combination of intravenous drug abuse and reused but poorly sterilized medical equipment.

Rates are high (>3.5% population infected) in Central and East Asia, North Africa and the Middle East, they are intermediate (1.5%-3.5%) in South and Southeast Asia, sub-Saharan Africa, Andean, Central and Southern Latin America, Caribbean, Oceania, Australasia and Central, Eastern and Western Europe; and they are low (<1.5%) in Asia Pacific, Tropical Latin America and North America.

Among those chronically infected, the risk of cirrhosis after 20 years varies between studies but has been estimated at ~10–15% for men and ~1–5% for women. The reason for this difference is not known. Once cirrhosis is established, the rate of developing hepatocellular carcinoma is ~1–4% per year. Rates of new infections have decreased in the Western world since the 1990s due to improved screening of blood before transfusion.

In the United States, about 2% of people have hepatitis C, with the number of new cases per year stabilized at 17,000 since 2007. The number of deaths from hepatitis C has increased to 15,800 in 2008 and by 2007 had overtaken HIV/AIDS as a cause of death in the USA. This mortality rate is expected to increase, as those infected by transfusion before HCV testing become apparent. In Europe the percentage of people with chronic infections has been estimated to be between 0.13 and 3.26%.

The total number of people with this infection is higher in some countries in Africa and Asia. Countries with particularly high rates of infection include Egypt (22%), Pakistan (4.8%) and China (3.2%). It is believed that the high prevalence in Egypt is linked to a now-discontinued mass-treatment campaign for schistosomiasis, using improperly sterilized glass syringes.

IMAGES

CASE RECORD

LIVER DISEASE - HEPATITIS C - Srikanth, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

In the year 1999, my condition was diagnosed as a liver disease called Hepatitis C.I took a course of costly antiviral drugs procured from USA as prescribed by a leading Gastroenterologist of Hyderabad. There was no relief.

MODE OF RECOVERY AT NEW LIFE CENTRE

I happened to read the news in Deccan Chronical that Dr Subhash Chandar of Mancherial has a new cure for it and started taking his treatment. After about six months of his treatment my blood tested negative for Hepatitis C. which is impossible with any other treatment. I am now healthy in all aspects. My consultant was surprised to see the great change.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Hepatitis C is an infectious disease affecting primarily the liver, caused by the hepatitis C virus (HCV).[1] The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure, liver cancer, or life-threatening esophageal and gastric varices.

HCV is spread primarily by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment, and transfusions. An estimated 150–200 million people worldwide are infected with hepatitis C. The existence of hepatitis C (originally identifiable only as a type of non-A non-B hepatitis) was suggested in the 1970s and proven in 1989. Hepatitis C infects only humans and chimpanzees.

The virus persists in the liver in about 85% of those infected. This chronic infection can be treated with medication: the standard therapy is a combination of peginterferon and ribavirin, with either boceprevir or telaprevir added in some cases. Overall, 50–80% of people treated are cured. Those who develop cirrhosis or liver cancer may require a liver transplant. Hepatitis C is the leading reason for liver transplantation, though the virus usually recurs after transplantation. No vaccine against hepatitis C is available.

SIGNS AND SYMPTOMS

Acute infection

Hepatitis C infection causes acute symptoms in 15% of cases. Symptoms are generally mild and vague, including a decreased appetite, fatigue, nausea, muscle or joint pains, and weight loss[9] and rarely does acute liver failure result. Most cases of acute infection are not associated with jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in individuals who are young and female.

Chronic infection

About 80% of those exposed to the virus develop a chronic infection. This is defined as the presence of detectable viral replication for at least six months. Most experience minimal or no symptoms during the initial few decades of the infection. Chronic hepatitis C can be associated with fatigue[14] and mild cognitive problems. Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.

Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops.[17][18] Usually (80% of the time) this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year. Being infected with hepatits B in additional to hepatitis C increases this risk further.

Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the stomach and esophagus), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy. Ascites occurs at some stage in more than half of those who have a chronic infection.

Extrahepatic complications

The most common problem due to hepatitis C but not involving the liver is mixed cryoglobulinemia (usually the type II form) — an inflammation of small and medium-sized blood vessels. Hepatitis C is also associated with Sjögren's syndrome (an autoimmune disorder); thrombocytopenia; lichen planus; porphyria cutanea tarda; necrolytic acral erythema; insulin resistance; diabetes mellitus; diabetic nephropathy; autoimmune thyroiditis and B-cell lymphoproliferative disorders. Thrombocytopenia is estimated to occur in 0.16% to 45.4% of people with chronic hepatitis C. 20–30% of people infected have rheumatoid factor — a type of antibody. Possible associations include Hyde's prurigo nodularis and membranoproliferative glomerulonephritis. Cardiomyopathy with associated arrhythmias has also been reported. A variety of central nervous system disorders have been reported. Chronic infection seems to be associated with an increased risk of pancreatic cancer.

Occult infection

Persons who have been infected with hepatitis C may appear to clear the virus but remain infected.[34] The virus is not detectable with conventional testing but can be found with ultra-sensitive tests. The original method of detection was by demonstrating the viral genome within liver biopsies, but newer methods include an antibody test for the virus' core protein and the detection of the viral genome after first concentrating the viral particles by ultracentrifugation. A form of infection with persistently moderately elevated serum liver enzymes but without antibodies to hepatitis C has also been reported. This form is known as cryptogenic occult infection.

Several clinical pictures have been associated with this type of infection. It may be found in people with anti-hepatitis-C antibodies but with normal serum levels of liver enzymes; in antibody-negative people with ongoing elevated liver enzymes of unknown cause; in healthy populations without evidence of liver disease; and in groups at risk for HCV infection including those on haemodialysis or family members of people with occult HCV. The clinical relevance of this form of infection is under investigation. The consequences of occult infection appear to be less severe than with chronic infection but can vary from minimal to hepatocellular carcinoma.

The rate of occult infection in those apparently cured is controversial but appears to be low. 40% of those with hepatitis but with both negative hepatitis C serology and the absence of detectable viral genome in the serum have hepatitis C virus in the liver on biopsy. How commonly this occurs in children is unknown.

VIROLOGY

The hepatitis C virus (HCV) is a small, enveloped, single-stranded, positive-sense RNA virus. It is a member of the Hepacivirus genus in the family Flaviviridae. There are seven major genotypes of HCV, which are known as genotypes one to seven. The genotypes are divided into several subtypes with the number of subtypes depending on the genotype. In the United States, about 70% of cases are caused by genotype 1, 20% by genotype 2 and about 1% by each of the other genotypes. Genotype 1 is also the most common in South America and Europe.

The half life of the virus particles in the serum is around 3 hours and may be as short as 45 minutes. In an infected person, about 1012 virus particles are produced each day. In addition to replicating in the liver the virus can multiply in lymphocytes.

TRANSMISSION

The primary route of transmission in the developed world is intravenous drug use (IDU), while in the developing world the main methods are blood transfusions and unsafe medical procedures. The cause of transmission remains unknown in 20% of cases; however, many of these are believed to be accounted for by IDU.

Intravenous drug use

IDU is a major risk factor for hepatitis C in many parts of the world. Of 77 countries reviewed, 25 (including the United States) were found to have prevalences of hepatitis C in the intravenous drug user population of between 60% and 80%. Twelve countries had rates greater than 80%. It is believed that ten million intravenous drug users are infected with hepatitis C; China (1.6 million), the United States (1.5 million), and Russia (1.3 million) have the highest absolute totals. Occurrence of hepatitis C among prison inmates in the United States is 10 to 20 times that of the occurrence observed in the general population; this has been attributed to high-risk behavior in prisons such as IDU and tattooing with nonsterile equipment.

Healthcare exposure

Blood transfusion, transfusion of blood products, or organ transplants without HCV screening carry significant risks of infection. The United States instituted universal screening in 1992 to between one in 10,000 to one in 10,000,000 per unit of blood. This low risk remains as there is a period of about 11–70 days between the potential blood donor's acquiring hepatitis C and the blood's testing positive depending on the method. Some countries do not screen for hepatitis C due to the cost.

Those who have experienced a needle stick injury from someone who was HCV positive have about a 1.8% chance of subsequently contracting the disease themselves. The risk is greater if the needle in question is hollow and the puncture wound is deep. There is a risk from mucosal exposures to blood; but this risk is low, and there is no risk if blood exposure occurs on intact skin.

Hospital equipment has also been documented as a method of transmission of hepatitis C, including reuse of needles and syringes; multiple-use medication vials; infusion bags; and improperly sterilized surgical equipment, among others. Limitations in the implementation and enforcement of stringent standard precautions in public and private medical and dental facilities are known to be the primary cause of the spread of HCV in Egypt, the country with highest rate of infection in the world.

Sexual intercourse

Whether hepatitis C can be transmitted through sexual activity is controversial. While there is an association between high-risk sexual activity and hepatitis C, and multiple sexual partners are a risk factor for hepatitis C, there is no conclusive evidence that hepatitis C can be transmitted by sexual activity, since people who report transmission with sex as their only risk factor may actually have used drugs but denied it. The majority of evidence supports there being no risk for monogamous heterosexual couples. Sexual practices that involve higher levels of trauma to the anogenital mucosa, such as anal penetrative sex, or that occur when there is a concurrent sexually transmitted infection, including HIV or genital ulceration, do present a risk. The United States Department of Veterans Affairs recommends condom use to prevent hepatitis C transmission in those with multiple partners, but not those in monogamous relationships.

Body modification

Tattooing is associated with two to threefold increased risk of hepatitis C. This can be due to either improperly sterilized equipment or contamination of the dyes being used. Tattoos or piercings performed either before the mid-1980s, "underground," or nonprofessionally are of particular concern, since sterile techniques in such settings may be lacking. The risk also appears to be greater for larger tattoos. It is estimated that nearly half of prison inmates share unsterilized tattooing equipment. It is rare for tattoos in a licensed facility to be directly associated with HCV infection.

Shared personal items

Personal-care items such as razors, toothbrushes, and manicuring or pedicuring equipment can be contaminated with blood. Sharing such items can potentially lead to exposure to HCV. Appropriate caution should be taken regarding any medical condition that results in bleeding, such as cuts and sores. HCV is not spread through casual contact, such as hugging, kissing, or sharing eating or cooking utensils. Neither is it transmitted through food or water.

Vertical transmission

Vertical transmission of hepatitis C from an infected mother to her child occurs in less than 10% of pregnancies. There are no measures that alter this risk. It is not clear when during pregnancy transmission occurs, but it may occur both during gestation and at delivery. A long labor is associated with a greater risk of transmission. There is no evidence that breast-feeding spreads HCV; however, to be cautious, an infected mother is advised to avoid breastfeeding if her nipples are cracked and bleeding, or her viral loads are high.

DIAGNOSIS

There are a number of diagnostic tests for hepatitis C, including HCV antibody enzyme immunoassay or ELISA, recombinant immunoblot assay, and quantitative HCV RNA polymerase chain reaction (PCR). HCV RNA can be detected by PCR typically one to two weeks after infection, while antibodies can take substantially longer to form and thus be detected. Chronic hepatitis C is defined as infection with the hepatitis C virus persisting for more than six months based on the presence of its RNA. Chronic infections are typically asymptomatic during the first few decades, and thus are most commonly discovered following the investigation of elevated liver enzyme levels or during a routine screening of high-risk individuals. Testing is not able to distinguish between acute and chronic infections. Diagnosis in the infant is difficult as maternal antibodies may persist for up to 18 months.

Serology

Hepatitis C testing typically begins with blood testing to detect the presence of antibodies to the HCV, using an enzyme immunoassay. If this test is positive, a confirmatory test is then performed to verify the immunoassay and to determine the viral load. A recombinant immunoblot assay is used to verify the immunoassay and the viral load is determined by a HCV RNA polymerase chain reaction. If there are no RNA and the immunoblot is positive, it means that the person tested had a previous infection but cleared it either with treatment or spontaneously; if the immunoblot is negative, it means that the immunoassay was wrong. It takes about 6–8 weeks following infection before the immunoassay will test positive. A number of tests are available as point of care testing which means that results are available within 30 minutes.

Liver enzymes are variable during the initial part of the infection and on average begin to rise at seven weeks after infection. The elevation of liver enzymes does not closely follow disease severity.

Biopsy

Liver biopsies are used to determine the degree of liver damage present; however, there are risks from the procedure. The typical changes seen are lymphocytes within the parenchyma, lymphoid follicles in portal triad, and changes to the bile ducts. There are a number of blood tests available that try to determine the degree of hepatic fibrosis and alleviate the need for biopsy.

Screening

It is believed that only 5–50% of those infected in the United States and Canada are aware of their status. Testing is recommended in those at high risk, which includes injection drug users, those who have received blood transfusions before 1992, those who have been in jail, those on long term hemodialysis, and those with tattoos. Screening is also recommended in those with elevated liver enzymes, as this is frequently the only sign of chronic hepatitis. Routine screening is not currently recommended in the United States. In 2012, the U.S. Centers for Disease Control and Prevention (CDC) added a recommendation for a single screening test for those born between 1945 and 1965.

PREVENTION

As of 2011, no vaccine protects against contracting hepatitis C. However, there are a number under development and some have shown encouraging results. A combination of harm reduction strategies, such as the provision of new needles and syringes and treatment of substance use, decrease the risk of hepatitis C in intravenous drug users by about 75%. The screening of blood donors is important at a national level, as is adhering to universal precautions within healthcare facilities. In countries where there is an insufficient supply of sterile syringes, medications should be given orally rather than via injection (when possible).

TREATMENT

HCV induces chronic infection in 50–80% of infected persons. Approximately 40–80% of these clear with treatment. In rare cases, infection can clear without treatment. Those with chronic hepatitis C are advised to avoid alcohol and medications toxic to the liver, and to be vaccinated for hepatitis A and hepatitis B. Ultrasound surveillance for hepatocellular carcinoma is recommended in those with accompanying cirrhosis.

Medications

In general, treatment is recommended for those with proven HCV infection and signs of liver inflammation. As of 2010, treatments consist of a combination of pegylated interferon alpha and the antiviral drug ribavirin for a period of 24 or 48 weeks, depending on HCV genotype. This produces cure rates of between 70 and 80% for genotype 2 and 3, respectively, and 45 to 70% for other genotypes. When combined with ribavirin, pegylated interferon-alpha-2a may be superior to pegylated interferon-alpha-2b, though the evidence is not strong.

Combining either boceprevir or telaprevir with ribavirin and peginterferon alfa improves antiviral response for hepatitis C genotype 1. Adverse effects with treatment are common, with half of people getting flu like symptoms and a third experiencing emotional problems. Treatment during the first six months is more effective than once hepatitis C has become chronic. If someone develops a new infection and it has not cleared after eight to twelve weeks, 24 weeks of pegylated interferon is recommended. In people with thalassemia, ribavirin appears to be useful but increases the need for transfusions.

Sofosbuvir with ribavirin and interferon appears to be around 90% effective in those with genotype 1, 4, 5, or 6 disease. Sofosbuvir with just ribavirin appears to be 70 to 95% effective in type 2 and 3 disease. This benefit is somewhat offset by a greater rate of adverse effects. Treatments that contain ledipasvir and sofosbuvir for genotype 1 has success rates of around 93 to 99% but is very expensive. In genotype 6 infection, pegylated interferon and ribavirin is effective in 60 to 90% of cases. There is some tentative data for simeprevir use in type 6 disease as well.

Surgery

Cirrhosis due to hepatitis C is a common reason for liver transplantion though the virus usually (80–90% of cases) recurs afterwards. Infection of the graft leads to 10–30% of people developing cirrhosis within five years. Treatment with pegylated interferon and ribavirin post transplant decreases the risk of recurrence to 70%.

Alternative medicine

Alternative medicine Several alternative therapies are claimed by their proponents to be helpful for hepatitis C including milk thistle, ginseng, and colloidal silver. However, no alternative therapy has been shown to improve outcomes in hepatitis C, and no evidence exists that alternative therapies have any effect on the virus at all.

PROGNOSIS

The responses to treatment is measured by sustained viral response and vary by HCV C genotype. A sustained response occurs in about 40–50% in people with HCV genotype 1 given 48 weeks of treatment. A sustained response is seen in 70–80% of people with HCV genotypes 2 and 3 with 24 weeks of treatment. A sustained response occurs about 65% in those with genotype 4 after 48 weeks of treatment. The evidence for treatment in genotype 6 disease is sparse and what evidence there is supports 48 weeks of treatment at the same doses used for genotype 1 disease. Successful treatment decreases the future risk of hepatocellular carcinoma by 75%.

EPIDEMIOLOGY

It is estimated that 150–200 million people, or ~3% of the world's population, are living with chronic hepatitis C. About 3–4 million people are infected per year, and more than 350,000 people die yearly from hepatitis C-related diseases. During 2010 it is estimated that 16,000 people died from acute infections while 196,000 deaths occurred from liver cancer secondary to the infection. Rates have increased substantially in the 20th century due to a combination of intravenous drug abuse and reused but poorly sterilized medical equipment.

Rates are high (>3.5% population infected) in Central and East Asia, North Africa and the Middle East, they are intermediate (1.5%-3.5%) in South and Southeast Asia, sub-Saharan Africa, Andean, Central and Southern Latin America, Caribbean, Oceania, Australasia and Central, Eastern and Western Europe; and they are low (<1.5%) in Asia Pacific, Tropical Latin America and North America.

Among those chronically infected, the risk of cirrhosis after 20 years varies between studies but has been estimated at ~10–15% for men and ~1–5% for women. The reason for this difference is not known. Once cirrhosis is established, the rate of developing hepatocellular carcinoma is ~1–4% per year. Rates of new infections have decreased in the Western world since the 1990s due to improved screening of blood before transfusion.

In the United States, about 2% of people have hepatitis C, with the number of new cases per year stabilized at 17,000 since 2007. The number of deaths from hepatitis C has increased to 15,800 in 2008 and by 2007 had overtaken HIV/AIDS as a cause of death in the USA. This mortality rate is expected to increase, as those infected by transfusion before HCV testing become apparent. In Europe the percentage of people with chronic infections has been estimated to be between 0.13 and 3.26%.

The total number of people with this infection is higher in some countries in Africa and Asia. Countries with particularly high rates of infection include Egypt (22%), Pakistan (4.8%) and China (3.2%). It is believed that the high prevalence in Egypt is linked to a now-discontinued mass-treatment campaign for schistosomiasis, using improperly sterilized glass syringes.

IMAGES

CASE RECORD

  DISEASES OF CARDIOVASCULAR SYSTEM (HEART, ARTERIES, VEINS,)

VARICOSE VEINS and NONHEALING ULCER on leg - 8 years - Satyanarayana, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I was suffering for the past 8 years from painful and enlarged veins in my legs with complications like non- healing varicose ulcers on my legs. The ulcers were painful and discharging fluid, consequently, I suffered many sleepless nights despite visiting many experts including those of NIMS and CARE hospitals. Ultimately an operation costing about Rs.80,000/-was suggested with unpredictable results.

MODE OF RECOVERY AT NEW LIFE CENTRE

The claim of operation was not convincing, hence I started taking homeopathy. The pain, fever, swelling and discharge came down very much in the very first week of taking homeopathy and the ulcer also started healing. My sleep was satisfactory. The ulcer on right foot healed up almost fully in just three months only. Ulcer on the left foot healed in 6 months.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Varicose veins are veins that have become enlarged and tortuous (twisted). The term commonly refers to the veins on the leg, although varicose veins can occur elsewhere. Veins have leaflet valves to prevent blood from flowing backwards (retrograde flow or reflux). Leg muscles pump the veins to return blood to the heart (the skeletal-muscle pump), against the effects of gravity. When veins become varicose, the leaflets of the valves no longer meet properly, and the valves do not work (valvular incompetence). This allows blood to flow backwards and they enlarge even more. Varicose veins are most common in the superficial veins of the legs, which are subject to high pressure when standing. Besides being a cosmetic problem, varicose veins can be painful, especially when standing. Severe long-standing varicose veins can lead to leg swelling, venous eczema, skin thickening (lipodermatosclerosis) and ulceration. Life-threatening complications are uncommon, but varicose veins may be confused with deep vein thrombosis, which may be life-threatening.

Non-surgical treatments include sclerotherapy, elastic stockings, elevating the legs, and exercise. The traditional surgical treatment has been vein stripping to remove the affected veins. Newer, less invasive treatments which seal the main leaking vein are available. Alternative techniques, such as ultrasound-guided foam sclerotherapy, radiofrequency ablation and endovenous laser treatment, are available as well. Because most of the blood in the legs is returned by the deep veins, the superficial veins, which return only about 10% of the total blood of the legs, can usually be removed or ablated without serious harm.

Secondary varicose veins are those developing as collateral pathways, typically after stenosis or occlusion of the deep veins, a common sequel of extensive deep venous thrombosis (DVT). Treatment options are usually support stockings, occasionally sclerotherapy, and rarely limited surgery.

Varicose veins are distinguished from reticular veins (blue veins) and telangiectasias (spider veins), which also involve valvular insufficiency, by the size and location of the veins. Many patients who suffer with varicose veins seek out the assistance of physicians who specialize in vein care or peripheral vascular disease. These physicians include vascular surgeons, phlebologists or interventional radiologists.

SIGNS AND SYMPTOMS

  • Aching, heavy legs (often worse at night and after exercise).
  • Appearance of spider veins (telangiectasia) in the affected leg.
  • Ankle swelling, especially in evening.
  • A brownish-yellow shiny skin discoloration near the affected veins.
  • Redness, dryness, and itchiness of areas of skin, termed stasis dermatitis or venous eczema, because of waste products building up in the leg.
  • Cramps may develop especially when making a sudden move as standing up.
  • Minor injuries to the area may bleed more than normal or take a long time to heal.
  • In some people the skin above the ankle may shrink (lipodermatosclerosis) because the fat underneath the skin becomes hard.
  • Restless legs syndrome appears to be a common overlapping clinical syndrome in patients with varicose veins and other chronic venous insufficiency.
  • Whitened, irregular scar-like patches can appear at the ankles. This is known as atrophie blanche.
Clinical Tests

Clinical tests that may be used include:

  • Trendelenburg test
  • Fegan's test
  • Perthe's test
  • Multiple tornique test
Investigations

Traditionally, varicose veins were only investigated using imaging techniques if there was a clinical suspicion of deep venous insufficiency, if they were recurrent, or if they involved the sapheno-popliteal junction. This practice is not now widely accepted. All patients with varicose veins should now be investigated using Duplex doppler ultrasound scanning. The results from a randomised controlled trial (RCT) on the follow up of patients with and without routine Duplex scan has shown a significant difference in recurrence rate and reoperation rate at 2 and 7 years of follow up.

Complications

Most varicose veins are reasonably benign, but severe varicosities can lead to major complications, due to the poor circulation through the affected limb.

  • Pain, tenderness, heaviness, inability to walk or stand for long hours, thus hindering work
  • Skin conditions / Dermatitis which could predispose skin loss
  • Skin ulcers especially near the ankle, usually referred to as venous ulcers.
  • Development of carcinoma or sarcoma in longstanding venous ulcers. There have been over 100 reported cases of malignant transformation and the rate is reported as 0.4% to 1%.
  • Severe bleeding from minor trauma, of particular concern in the elderly.
  • Blood clotting within affected veins. Termed superficial thrombophlebitis. These are frequently isolated to the superficial veins, but can extend into deep veins becoming a more serious problem.
  • Acute fat necrosis can occur, especially at the ankle of overweight patients with varicose veins. Females are more frequently affected than males.

STAGES

  • C0 no visible or palpable signs of venous disease
  • C1 telangectasia or reticular veins
  • C2 varicose veins
  • C3 edema
  • C4a skin changes due to venous disorders: pigmentation, eczema
  • C4b skin changes due to venous disorders: lipodermatosclerosis, atrophie blanche
  • C5 as C4 but with healed ulcers
  • C6 skin changes with active ulcers (venous insufficiency ulceration)

CAUSES

Varicose veins are more common in women than in men, and are linked with heredity. Other related factors are pregnancy, obesity, menopause, aging, prolonged standing, leg injury, and abdominal straining. Varicose veins are unlikely to be caused by crossing the legs or ankles. Less commonly, but not exceptionally, varicose veins can be due to other causes, as post phlebitic obstruction or incontinence, venous and arteriovenous malformations

Varicose veins could also be caused by elevated levels of homocysteine in the body, which can degrade and inhibit the formation of the three main structural components of the artery: collagen, elastin and the proteoglycans. Homocysteine permanently degrades cysteine disulfide bridges and lysine amino acid residues in proteins, gradually affecting function and structure. Simply put, homocysteine is a 'corrosive' of long-living proteins, i.e. collagen or elastin, or lifelong proteins, i.e. fibrillin. These long-term effects are difficult to establish in clinical trials focusing on groups with existing artery decline. See also for differential diagnosis- 1. Klippel-Trenaunay syndrome, 2. Parkes-Weber syndrome

TREATMENT

Conservative

The symptoms of varicose veins can be controlled to an extent with the following:

  • Elevating the legs often provides temporary symptomatic relief.
  • Advice about regular exercise sounds sensible but is not supported by any evidence.
  • The wearing of graduated compression stockings with variable pressure gradients (Class II or III) has been shown to correct the swelling, nutritional exchange, and improve the microcirculation in legs affected by varicose veins. They also often provide relief from the discomfort associated with this disease. Caution should be exercised in their use in patients with concurrent arterial disease.
  • The wearing of intermittent pneumatic compression devices have been shown to reduce swelling and increase circulation.
  • Diosmin/Hesperidine and other flavonoids.
  • Anti-inflammatory medication such as ibuprofen or aspirin can be used as part of treatment for superficial thrombophlebitis along with graduated compression hosiery – but there is a risk of intestinal bleeding. In extensive superficial thrombophlebitis, consideration should be given to anti-coagulation, thrombectomy or sclerotherapy of the involved vein.
  • Topical gel application, helps in managing symptoms related to varicose veins such as inflammation, pain, swelling, itching and dryness. Topical application-Non invasive and has patient compliance.
Active

Active medical intervention in varicose veins can be divided into surgical and non-surgical treatments. Some doctors favor traditional open surgery, while others prefer the newer methods. Newer methods for treating varicose veins such as Endovenous Thermal Ablation (endovenous laser treatment or radiofrequency ablation), and foam sclerotherapy are not as well studied, especially in the longer term.

Surgical

Several techniques have been performed for over a century, from the more invasive saphenous stripping, to less invasive procedures like ambulatory phlebectomy and CHIVA.

Stripping

Stripping consists of removal of all or part the saphenous vein (great/long or lesser/short) main trunk. The complications include deep vein thrombosis (5.3%), pulmonary embolism (0.06%), and wound complications including infection (2.2%). There is evidence for the Great Saphenous Vein growing back again after stripping. For traditional surgery, reported recurrence rates, which have been tracked for 10 years, range from 5–60%. In addition, since stripping removes the saphenous main trunks, they are no longer available for use as venous bypass grafts in the future (coronary or leg artery vital disease)

Other

Other surgical treatments are:

  • Ambulatory phlebectomy
  • Vein ligation
  • Cryosurgery- A cryoprobe is passed down the long saphenous vein following saphenofemoral ligation. Then the probe is cooled with NO2 or CO2 to a temperature of −85o. The vein freezes to the probe and can be retrogradely stripped after 5 second of freezing. It is a variant of Stripping. The only point of this technique is to avoid a distal incision to remove the stripper.

Non-surgical treatment

Sclerotherapy management

A commonly performed non-surgical treatment for varicose and "spider" leg veins is sclerotherapy in which medicine (sclerosant) is injected into the veins to make them shrink. The medicines that are commonly used as sclerosants are polidocanol (POL), sodium tetradecyl sulphate (STS), Sclerodex (Canada), Hypertonic Saline, Glycerin and Chromated Glycerin. STS (branded Fibrovein in Australia) and Polidocanol (branded Asclera in the United States, Aethoxysklerol in Australia) liquids can be mixed at varying concentrations of sclerosant and varying sclerosant/gas proportions, with air or CO2 or O2 to create foams. Foams may allow more veins to be treated per session with comparable efficacy. Their use in contrast to liquid sclerosant is still somewhat controversial. Sclerotherapy has been used in the treatment of varicose veins for over 150 years. Sclerotherapy is often used for telangiectasias (spider veins) and varicose veins that persist or recur after vein stripping. Sclerotherapy can also be performed using foamed sclerosants under ultrasound guidance to treat larger varicose veins, including the great saphenous and small saphenous veins. A study by Kanter and Thibault in 1996 reported a 76% success rate at 24 months in treating saphenofemoral junction and great saphenous vein incompetence with STS 3% solution. A Cochrane Collaboration review concluded sclerotherapy was better than surgery in the short term (1 year) for its treatment success, complication rate and cost, but surgery was better after 5 years, although the research is weak. A Health Technology Assessment found that sclerotherapy provided less benefit than surgery, but is likely to provide a small benefit in varicose veins without reflux.[25] This Health Technology Assessment monograph includes reviews of the epidemiology, assessment, and treatment of varicose veins, as well as a study on clinical and cost effectiveness of surgery and sclerotherapy. Complications of sclerotherapy are rare but can include blood clots and ulceration. Anaphylactic reactions are "extraordinarily rare but can be life-threatening," and doctors should have resuscitation equipment ready. There has been one reported case of stroke after ultrasound guided sclerotherapy when an unusually large dose of sclerosant foam was injected.

Endovenous thermal ablation

The Australian Medical Services Advisory Committee (MSAC) in 2008 has determined that endovenous laser treatment/ablation (ELA) for varicose veins "appears to be more effective in the short term, and at least as effective overall, as the comparative procedure of junction ligation and vein stripping for the treatment of varicose veins." It also found in its assessment of available literature, that "occurrence rates of more severe complications such as DVT, nerve injury and paraesthesia, post-operative infections and haematomas, appears to be greater after ligation and stripping than after EVLT". Complications for ELA include minor skin burns (0.4%) and temporary paraesthesia (2.1%). The longest study of endovenous laser ablation is 39 months.

Two prospective randomized trials found speedier recovery and fewer complications after radiofrequency ablation (ERA) compared to open surgery. Myers wrote that open surgery for small saphenous vein reflux is obsolete. Myers said these veins should be treated with endovenous techniques, citing high recurrence rates after surgical management, and risk of nerve damage up to 15%. In comparison, ERA has been shown to control 80% of cases of small saphenous vein reflux at 4 years, said Myers. Complications for ERA include burns, paraesthesia, clinical phlebitis, and slightly higher rates of deep vein thrombosis (0.57%) and pulmonary embolism (0.17%). One 3-year study compared ERA, with a recurrence rate of 33%, to open surgery, which had a recurrence rate of 23%.

ELA and ERA require specialized training for doctors and expensive equipment. ELA is performed as an outpatient procedure and does not require the use of an operating theatre, nor does the patient need a general anaesthetic. Doctors must use high frequency ultrasound during the procedure to visualize the anatomical relationships between the saphenous structures. Some practitioners also perform phlebectomy or ultrasound guided sclerotherapy at the time of endovenous treatment. Follow-up treatment to smaller branch varicose veins is often needed in the weeks or months after the initial procedure.

IMAGES

CASE RECORD

HEART DISEASE with SEVERE BREATHLESSNESS and CYANOSIS - Sarojini, Bowenpally, Secunderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Block in blood supply to my heart leading to pain chest and severe breathlessness on exertion. Tried treatment from reputed doctors of Chennai for six years.Recently my fingers and toes started turning blue along with severe shortness of breath even on walking a few steps.

MODE OF RECOVERY AT NEW LIFE CENTRE

I do not have the previous troubles now. I am able to walk freely in the town, can get up and down the stairs without any strain.Many thanks to NLHC. Centre.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Myocardial infarction (from Latin: Infarctus myocardii, MI) or acute myocardial infarction (AMI) is the medical term for an event commonly known as a heart attack. It happens when blood stops flowing properly to part of the heart and the heart muscle is injured due to not receiving enough oxygen. Usually this is because one of the coronary arteries that supplies blood to the heart develops a blockage due to an unstable buildup of white blood cells, cholesterol and fat. The event is called "acute" if it is sudden and serious.

A person having an acute MI usually has sudden chest pain that is felt behind the breast bone and sometimes travels to the left arm or the left side of the neck. Additionally, the person may have shortness of breath, sweating, nausea, vomiting, abnormal heartbeats, and anxiety. Women experience fewer of these symptoms than men, but usually have shortness of breath, weakness, a feeling of indigestion, and fatigue. In many cases, in some estimates as high as 64%, the person does not have chest pain or other symptoms. These are called "silent" myocardial infarctions.

Important risk factors are previous cardiovascular disease, old age, tobacco smoking, high blood levels of certain lipids (low-density lipoprotein cholesterol, triglycerides) and low levels of high density lipoprotein (HDL) cholesterol, diabetes, high blood pressure, lack of physical activity, obesity, chronic kidney disease, excessive alcohol consumption, and the use of cocaine and amphetamines. The main way to determine if a person has had a myocardial infarction are electrocardiograms (ECGs) that trace the electrical signals in the heart and testing the blood for substances associated with damage to the heart muscle. Common blood tests are troponin and creatine kinase (CK-MB). ECG testing is used to differentiate between two types of myocardial infarctions based on the shape of the tracing. An ST section of the tracing higher than the baseline is called an ST elevation MI (STEMI) which usually requires more aggressive treatment.

Immediate treatments for a suspected MI include aspirin, which prevents further blood from clotting, and sometimes nitroglycerin to treat chest pain and oxygen. STEMI is treated by restoring circulation to the heart, called reperfusion therapy, and typical methods are angioplasty, where the arteries are pushed open, and thrombolysis, where the blockage is removed using medications. Non-ST elevation myocardial infarction (NSTEMI) may be managed with medication, although angioplasty may be required if the person is considered to be at high risk. People who have multiple blockages of their coronary arteries, particularly if they also have diabetes, may also be treated with bypass surgery (CABG). Ischemic heart disease, which includes MI, angina, and heart failure when it happens after MI, was the leading cause of death for both men and women worldwide in 2011.

SIGNS AND SYMPTOMS

The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous. Chest pain is the most common symptom of acute MI and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and upper abdomen, where it may mimic heartburn. Levine's sign, in which patients localize the chest pain by clenching their fists over their sternums, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed it had a poor positive predictive value.

Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate blood flow to the brain and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in MIs.

Female, elderly, and diabetic patients report atypical symptoms more frequently than their male and younger counterparts. Women also report more numerous symptoms compared with men (2.6 on average vs. 1.8 symptoms in men). The most common symptoms of MI in women include dyspnea, weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms that may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men. Women may also experience back or jaw pain during an episode.

At least one-fourth of all MIs are silent, without chest pain or other symptoms. These cases can be discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of related complaints. Estimates of the prevalence of silent MIs vary between 22 and 64%. A silent course is more common in the elderly, in patients with diabetes mellitus and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient. In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.

Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.

The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary embolism, aortic dissection, pericardial effusion causing cardiac tamponade, tension pneumothorax, and esophageal rupture. Other noncatastrophic differentials include gastroesophageal reflux and Tietze's syndrome.

CAUSES

Many of the risk factors for myocardial infarction are modifiable and thus many cases may be preventable.

Lifestyle

Smoking appears to be the cause of about 36% and obesity the cause of 20% of coronary artery disease.[26] Lack of exercise has been linked to 7-12% of cases. Job stress appears to play a minor role, accounting for about 3% of cases. Chronic high stress levels may cause some cases.

Tobacco smoking, including secondhand smoke Short-term exposure to air pollution, including carbon monoxide, nitrogen dioxide, and sulfur dioxide, but not ozone. Lack of physical activity, psychosocial factors including, low socioeconomic status, social isolation and negative emotions increase the risk of and are associated with worse outcomes after MI. Socioeconomic factors such as a shorter education and lower income (particularly in women), and unmarried cohabitation are also correlated with a higher risk of MI. Alcohol — prolonged exposure to high quantities of alcohol can increase the risk of heart attack. There is little evidence that dietary saturated fat or polyunsaturated fat intake affects risk. Trans fats do appear to increase risk.

Disease

Diabetes mellitus (type 1 or 2), high blood pressure, dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides Obesity (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).

A number of acute and chronic infections including: Chlamydophila pneumoniae, influenza, Helicobacter pylori, and Porphyromonas gingivalis among others have been linked to atherosclerosis and myocardial infarction. As of 2013, there is no evidence of benefit from antibiotics or vaccination, however, calling the association into question.

Other

At any given age, men are more at risk than women, particularly before menopause, but because in general women live longer than men, ischemic heart disease causes slightly more total deaths in women. Family history of ischaemic heart disease or MI, particularly if one has a first-degree relative (father, brother, mother, sister) who suffered a 'premature' myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65 (women).

Oral contraceptive pill–women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.

An increased incidence of a heart attack is associated with time of day especially in the morning hours, more specifically around 9 am. Old age increases risk of a heart attack.

PATHOPHYSIOLOGY

Acute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-ST-elevated and ST-elevated MIs, which are most frequently (but not always) a manifestation of coronary artery disease. The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery. Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries), typically over decades. Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis. Plaques can become unstable, rupture, and additionally promote the formation of a blood clot that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to MI (necrosis of downstream myocardium).

If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the occluded coronary artery die (chiefly through necrosis) and do not grow back. A collagen scar forms in their place. Recent studies indicate that another form of cell death, apoptosis, also plays a role in the process of tissue damage subsequent to MI. As a result, the patient's heart will be permanently damaged. This myocardial scarring also puts the patient at risk for potentially life-threatening arrhythmias, and may result in the formation of a ventricular aneurysm that can rupture with catastrophic consequences.

Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life-threatening arrhythmia is ventricular tachycardia (V-tach/VT), which can cause sudden cardiac death. However, VT usually results in rapid heart rates that prevent the heart from pumping blood effectively. Cardiac output and blood pressure may fall to dangerous levels, which can lead to further coronary ischemia and extension of the infarct.

The cardiac defibrillator device was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient to depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. This therapy is time-dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest.

Myocardial infarction results from atherosclerosis. Inflammation is known to be an important step in the process of atherosclerotic plaque formation. C-reactive protein (CRP) is a sensitive but nonspecific marker for inflammation. Elevated CRP blood levels, especially measured with high-sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes. Moreover, some drugs for MI might also reduce CRP levels. The use of high-sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician's discretion in patients who already present with other risk factors or known coronary artery disease. Whether CRP plays a direct role in atherosclerosis remains uncertain.

Calcium deposition is another part of atherosclerotic plaque formation. Calcium deposits in the coronary arteries can be detected with CT scans. Several studies have shown that coronary calcium can provide predictive information beyond that of classical risk factors.

Hyperhomocysteinemia (high blood levels of the amino acid homocysteine) in homocysteinuria is associated with premature atherosclerosis; whether elevated homocysteine in the normal range is causal is controversial.

Pathological types

The two main types of acute myocardial infarction, based on pathology, are:

  • Transmural AMI is associated with atherosclerosis involving a major coronary artery. It can be subclassified into anterior, posterior, inferior, lateral, or septal. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply. In addition, on ECG, ST elevation and Q waves are seen.
  • Subendocardial AMI involves a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. The subendocardial area is particularly susceptible to ischemia. In addition, ST depression is seen on ECG.

DIAGNOSIS

A cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is diagnostic of MI. WHO criteria formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with MI if two (probable) or three (definite) of the following criteria are satisfied:

  1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes
  2. Changes in serial ECG tracings
  3. Rise and fall of serum cardiac biomarkers

At autopsy, a pathologist can diagnose an MI based on anatomopathological findings.

Classification

Myocardial infarctions are generally classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI). A STEMI is the combination of symptoms related to poor oxygenation of the heart with elevation of the ST segments on the electrocardiogram followed by an increase in proteins in the blood related to heart muscles death. They make up abut 25 to 40 percent of cases.

The phrase "heart attack" is often used non-specifically to refer to a myocardial infarction and to sudden cardiac death. An MI is different from, but can cause cardiac arrest, which is the stopping of the heartbeat. It is also distinct from heart failure, in which the pumping action of the heart is impaired. However, an MI may lead to heart failure.

A 2007 consensus document classifies MI into five main types:

  • Type 1 – spontaneous MI related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection
  • Type 2 – MI secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension
  • Type 3 – sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by new ST elevation, or new left bundle branch block (LBBB), or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
  • Type 4 – associated with coronary angioplasty or stents:
    • Type 4a – MI associated with Percutaneous coronary intervention (PCI)
    • Type 4b – MI associated with stent thrombosis as documented by angiography or at autopsy
  • Type 5 – MI associated with CABG
Electrocardiogram

For a person to qualify as having an STEMI, the ECG must show new ST elevation in two or more adjacent ECG leads. This must be greater than 2 mm (0.2 mV) for males and greater than 1.5 mm (0.15mV) in females if in leads V2 and V3 or greater than 1 mm (0.1 mV) if it is in other ECG leads. A left bundle branch block that is believed to be new used to be considered the same as ST elevation; however, this is no longer the case. In early STEMIs there may just be peaked T wave with ST elevation developing later.

Cardiac biomarkers

While there are a number of different biomarkers, troponins are considered to be the best.

Imaging

A chest radiograph and routine blood tests may indicate complications or precipitating causes, and are often performed upon arrival to an emergency department. New regional wall motion abnormalities on an echocardiogram are also suggestive of an MI. Echo may be performed in equivocal cases by the on-call cardiologist. In stable patients whose symptoms have resolved by the time of evaluation, technetium (99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiological or pharmacological stress. Thallium may also be used to determine viability of tissue, distinguishing whether nonfunctional myocardium is actually dead or merely in a state of hibernation or of being stunned.

Medical societies recommend that the physician confirm a person is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis. Patients who have a normal ECG and who are able to exercise, for example, do not merit routine imaging. Imaging tests such as stress radionuclide myocardial perfusion imaging or stress echocardiography can confirm a diagnosis when a patient's history, physical exam, ECG, and cardiac biomarkers suggest the likelihood of a problem.

PREVENTION

The risk of a recurrent MI decreases with strict blood pressure management and lifestyle changes, chiefly smoking cessation, regular exercise, a sensible diet for those with heart disease, and limitation of alcohol intake. People are usually started on several long-term medications after an MI, with the aim of preventing further cardiovascular events such MIs, congestive heart failure, or strokes. Unless contraindicated, such medications often include the following:

  • Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent MI. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, but the risk of hemorrhage is increased.
  • Beta blocker therapy such as metoprolol or carvedilol should be started. These have been particularly beneficial in those who are high-risk such as those with left ventricular dysfunction and/or continuing cardiac ischaemia. β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI.
  • ACE inhibitor therapy should be commenced 24–48 hours after MI in those who are hemodynamically stable, particularly with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling.
  • Statin therapy has been shown to reduce mortality and morbidity. The protective effects of statins may be due to more than their LDL lowering effects. The general consensus is that statins have the ability to stabilize plaques and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids.
  • The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death after MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above. Spironolactone, another option, is sometimes preferable to eplerenone due to cost.
  • Evidence supports the consumption of polyunsaturated fats instead of saturated fats as a measure of decreasing coronary heart disease. In high-risk people, no clear-cut decrease in potentially fatal arrhythmias occurs due to omega-3 fatty acids and may actually increase risk in some groups.
  • Giving heparin to people with heart conditions like unstable angina and some forms of heart attacks reduces the risk of having another heart attack. However, heparin also increases the chance of minor bleeding.

MANAGEMENT

An MI requires immediate medical attention. Treatment attempts to save as much viable heart muscle as possible and to prevent further complications, hence the phrase "time is muscle". Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI. Reviews of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use. Other analgesics such as nitrous oxide are of unknown benefit.

STEMI

Immediate

Percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a timely manner. If PCI cannot be performed within 90 to 120 minutes then fibrinolysis, preferably within 30 minutes, is recommended. If after fibrinolysis, significant cardiogenic shock, continued severe chest pain, or less than a 50% improvement in ST elevation after 90 minutes occurs, then rescue PCI is indicated emergently. After PCI, people are generally placed on dual antiplatelet therapy for at least a year (which is generally aspirin and clopidogrel).

Long term

Beta blockers are recommended in those without signs of heart failure or a heart block. If used, they should be started in the first 24 hours.

PROGNOSIS

The prognosis after MI varies greatly depending on a person's health, the extent of the heart damage, and the treatment given.

In those who have an STEMI in the United States, between 5 to 6 percent die before leaving hospital and 7 to 18 percent die within a year.[

Using variables available in the emergency room, people with a higher risk of adverse outcome can be identified. One study found 0.4% of patients with a low-risk profile died after 90 days, whereas in high-risk people it was 21.1%.

Some risk factors for death include: age, hemodynamic parameters (such as heart failure, cardiac arrest on admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation, diabetes, serum creatinine, peripheral vascular disease, and elevation of cardiac markers. Assessment of left ventricular ejection fraction may increase the predictive power. Prognosis is worse if a mechanical complication such as papillary muscle or myocardial free wall rupture occurs. Morbidity and mortality from myocardial infarction has improved over the years due to better treatment.

Complications

Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). Acute complications may include heart failure if the damaged heart is no longer able to pump blood adequately around the body; aneurysm or rupture of the myocardium; mitral regurgitation, in particular if the infarction causes dysfunction of the papillary muscle; Dressler's syndrome; and arrhythmias, such as ventricular fibrillation, ventricular tachycardia, atrial fibrillation, and heart block. Longer-term complications include heart failure, atrial fibrillation, and the increased risk of a second MI.

EPIDEMIOLOGY

Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease; with it being the leading cause of death in high- or middle-income countries and second only to lower respiratory infections in lower-income countries. Worldwide, more than 3 million people have STEMIs and 4 million have NSTEMIs a year. STEMIs occur about twice as often in men as women.

Rates of death from ischemic heart disease (IHD) have slowed or declined in most high-income countries, although cardiovascular disease still accounted for one in three of all deaths in the USA in 2008. In contrast, IHD is becoming a more common cause of death in the developing world. For example in India, IHD had become the leading cause of death by 2004, accounting for 1.46 million deaths (14% of total deaths) and deaths due to IHD were expected to double during 1985–2015. Globally, disability adjusted life years (DALYs) lost to ischemic heart disease are predicted to account for 5.5% of total DALYs in 2030, making it the second-most-important cause of disability (after unipolar depressive disorder), as well as the leading cause of death by this date.

SOCIETY AND CULTURE

In the United States, women who have had an MI are often treated with fewer medical interventions than men.

Economics

In 2011, AMI was one of the top five most expensive conditions seen during inpatient hospitalizations in the U.S., with an aggregate cost of about $11.5 billion for 612,000 hospital stays.

Legal implications

At common law, in general, a myocardial infarction is a disease, but may sometimes be an injury. This can create coverage issues in administration of no-fault insurance schemes such as workers' compensation. In general, a heart attack is not covered; however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion. In addition, in some jurisdictions, heart attacks suffered by persons in particular occupations such as police officers may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person having suffered from an MI may be prevented from participating in activity that puts other people's lives at risk, for example driving a car or flying an airplane.

IMAGES

HEART ATTACK - Shankar Rao, Forest Dept, Mancherial

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Diabetes, High BP, Bypass done for Heart attack about 20 years ago, Second attack in 2012,Three vessels blocked ,Stent advised by cardiologists Pain chest and breathlessness on least exertion / walking a few steps

MODE OF RECOVERY AT NEW LIFE CENTRE

Made smooth,rapid and safe recovery with our treatment in just 1-2 months.
Now, he can walk long distances and get up and down stairs like any ordinary person.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Myocardial infarction (from Latin: Infarctus myocardii, MI) or acute myocardial infarction (AMI) is the medical term for an event commonly known as a heart attack. It happens when blood stops flowing properly to part of the heart and the heart muscle is injured due to not receiving enough oxygen. Usually this is because one of the coronary arteries that supplies blood to the heart develops a blockage due to an unstable buildup of white blood cells, cholesterol and fat. The event is called "acute" if it is sudden and serious.

A person having an acute MI usually has sudden chest pain that is felt behind the breast bone and sometimes travels to the left arm or the left side of the neck. Additionally, the person may have shortness of breath, sweating, nausea, vomiting, abnormal heartbeats, and anxiety. Women experience fewer of these symptoms than men, but usually have shortness of breath, weakness, a feeling of indigestion, and fatigue. In many cases, in some estimates as high as 64%, the person does not have chest pain or other symptoms. These are called "silent" myocardial infarctions.

Important risk factors are previous cardiovascular disease, old age, tobacco smoking, high blood levels of certain lipids (low-density lipoprotein cholesterol, triglycerides) and low levels of high density lipoprotein (HDL) cholesterol, diabetes, high blood pressure, lack of physical activity, obesity, chronic kidney disease, excessive alcohol consumption, and the use of cocaine and amphetamines. The main way to determine if a person has had a myocardial infarction are electrocardiograms (ECGs) that trace the electrical signals in the heart and testing the blood for substances associated with damage to the heart muscle. Common blood tests are troponin and creatine kinase (CK-MB). ECG testing is used to differentiate between two types of myocardial infarctions based on the shape of the tracing. An ST section of the tracing higher than the baseline is called an ST elevation MI (STEMI) which usually requires more aggressive treatment.

Immediate treatments for a suspected MI include aspirin, which prevents further blood from clotting, and sometimes nitroglycerin to treat chest pain and oxygen. STEMI is treated by restoring circulation to the heart, called reperfusion therapy, and typical methods are angioplasty, where the arteries are pushed open, and thrombolysis, where the blockage is removed using medications. Non-ST elevation myocardial infarction (NSTEMI) may be managed with medication, although angioplasty may be required if the person is considered to be at high risk. People who have multiple blockages of their coronary arteries, particularly if they also have diabetes, may also be treated with bypass surgery (CABG). Ischemic heart disease, which includes MI, angina, and heart failure when it happens after MI, was the leading cause of death for both men and women worldwide in 2011.

SIGNS AND SYMPTOMS

The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous. Chest pain is the most common symptom of acute MI and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and upper abdomen, where it may mimic heartburn. Levine's sign, in which patients localize the chest pain by clenching their fists over their sternums, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed it had a poor positive predictive value.

Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate blood flow to the brain and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in MIs.

Female, elderly, and diabetic patients report atypical symptoms more frequently than their male and younger counterparts. Women also report more numerous symptoms compared with men (2.6 on average vs. 1.8 symptoms in men). The most common symptoms of MI in women include dyspnea, weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms that may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men. Women may also experience back or jaw pain during an episode.

At least one-fourth of all MIs are silent, without chest pain or other symptoms. These cases can be discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of related complaints. Estimates of the prevalence of silent MIs vary between 22 and 64%. A silent course is more common in the elderly, in patients with diabetes mellitus and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient. In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.

Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.

The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary embolism, aortic dissection, pericardial effusion causing cardiac tamponade, tension pneumothorax, and esophageal rupture. Other noncatastrophic differentials include gastroesophageal reflux and Tietze's syndrome.

CAUSES

Many of the risk factors for myocardial infarction are modifiable and thus many cases may be preventable.

Lifestyle

Smoking appears to be the cause of about 36% and obesity the cause of 20% of coronary artery disease.[26] Lack of exercise has been linked to 7-12% of cases. Job stress appears to play a minor role, accounting for about 3% of cases. Chronic high stress levels may cause some cases.

Tobacco smoking, including secondhand smoke Short-term exposure to air pollution, including carbon monoxide, nitrogen dioxide, and sulfur dioxide, but not ozone. Lack of physical activity, psychosocial factors including, low socioeconomic status, social isolation and negative emotions increase the risk of and are associated with worse outcomes after MI. Socioeconomic factors such as a shorter education and lower income (particularly in women), and unmarried cohabitation are also correlated with a higher risk of MI. Alcohol — prolonged exposure to high quantities of alcohol can increase the risk of heart attack. There is little evidence that dietary saturated fat or polyunsaturated fat intake affects risk. Trans fats do appear to increase risk.

Disease

Diabetes mellitus (type 1 or 2), high blood pressure, dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides Obesity (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).

A number of acute and chronic infections including: Chlamydophila pneumoniae, influenza, Helicobacter pylori, and Porphyromonas gingivalis among others have been linked to atherosclerosis and myocardial infarction. As of 2013, there is no evidence of benefit from antibiotics or vaccination, however, calling the association into question.

Other

At any given age, men are more at risk than women, particularly before menopause, but because in general women live longer than men, ischemic heart disease causes slightly more total deaths in women. Family history of ischaemic heart disease or MI, particularly if one has a first-degree relative (father, brother, mother, sister) who suffered a 'premature' myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65 (women).

Oral contraceptive pill–women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.

An increased incidence of a heart attack is associated with time of day especially in the morning hours, more specifically around 9 am. Old age increases risk of a heart attack.

PATHOPHYSIOLOGY

Acute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-ST-elevated and ST-elevated MIs, which are most frequently (but not always) a manifestation of coronary artery disease. The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery. Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries), typically over decades. Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis. Plaques can become unstable, rupture, and additionally promote the formation of a blood clot that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to MI (necrosis of downstream myocardium).

If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the occluded coronary artery die (chiefly through necrosis) and do not grow back. A collagen scar forms in their place. Recent studies indicate that another form of cell death, apoptosis, also plays a role in the process of tissue damage subsequent to MI. As a result, the patient's heart will be permanently damaged. This myocardial scarring also puts the patient at risk for potentially life-threatening arrhythmias, and may result in the formation of a ventricular aneurysm that can rupture with catastrophic consequences.

Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life-threatening arrhythmia is ventricular tachycardia (V-tach/VT), which can cause sudden cardiac death. However, VT usually results in rapid heart rates that prevent the heart from pumping blood effectively. Cardiac output and blood pressure may fall to dangerous levels, which can lead to further coronary ischemia and extension of the infarct.

The cardiac defibrillator device was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient to depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. This therapy is time-dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest.

Myocardial infarction results from atherosclerosis. Inflammation is known to be an important step in the process of atherosclerotic plaque formation. C-reactive protein (CRP) is a sensitive but nonspecific marker for inflammation. Elevated CRP blood levels, especially measured with high-sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes. Moreover, some drugs for MI might also reduce CRP levels. The use of high-sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician's discretion in patients who already present with other risk factors or known coronary artery disease. Whether CRP plays a direct role in atherosclerosis remains uncertain.

Calcium deposition is another part of atherosclerotic plaque formation. Calcium deposits in the coronary arteries can be detected with CT scans. Several studies have shown that coronary calcium can provide predictive information beyond that of classical risk factors.

Hyperhomocysteinemia (high blood levels of the amino acid homocysteine) in homocysteinuria is associated with premature atherosclerosis; whether elevated homocysteine in the normal range is causal is controversial.

Pathological types

The two main types of acute myocardial infarction, based on pathology, are:

  • Transmural AMI is associated with atherosclerosis involving a major coronary artery. It can be subclassified into anterior, posterior, inferior, lateral, or septal. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply. In addition, on ECG, ST elevation and Q waves are seen.
  • Subendocardial AMI involves a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. The subendocardial area is particularly susceptible to ischemia. In addition, ST depression is seen on ECG.

DIAGNOSIS

A cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is diagnostic of MI. WHO criteria formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with MI if two (probable) or three (definite) of the following criteria are satisfied:

  1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes
  2. Changes in serial ECG tracings
  3. Rise and fall of serum cardiac biomarkers

At autopsy, a pathologist can diagnose an MI based on anatomopathological findings.

Classification

Myocardial infarctions are generally classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI). A STEMI is the combination of symptoms related to poor oxygenation of the heart with elevation of the ST segments on the electrocardiogram followed by an increase in proteins in the blood related to heart muscles death. They make up abut 25 to 40 percent of cases.

The phrase "heart attack" is often used non-specifically to refer to a myocardial infarction and to sudden cardiac death. An MI is different from, but can cause cardiac arrest, which is the stopping of the heartbeat. It is also distinct from heart failure, in which the pumping action of the heart is impaired. However, an MI may lead to heart failure.

A 2007 consensus document classifies MI into five main types:

  • Type 1 – spontaneous MI related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection
  • Type 2 – MI secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension
  • Type 3 – sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by new ST elevation, or new left bundle branch block (LBBB), or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
  • Type 4 – associated with coronary angioplasty or stents:
    • Type 4a – MI associated with Percutaneous coronary intervention (PCI)
    • Type 4b – MI associated with stent thrombosis as documented by angiography or at autopsy
  • Type 5 – MI associated with CABG
Electrocardiogram

For a person to qualify as having an STEMI, the ECG must show new ST elevation in two or more adjacent ECG leads. This must be greater than 2 mm (0.2 mV) for males and greater than 1.5 mm (0.15mV) in females if in leads V2 and V3 or greater than 1 mm (0.1 mV) if it is in other ECG leads. A left bundle branch block that is believed to be new used to be considered the same as ST elevation; however, this is no longer the case. In early STEMIs there may just be peaked T wave with ST elevation developing later.

Cardiac biomarkers

While there are a number of different biomarkers, troponins are considered to be the best.

Imaging

A chest radiograph and routine blood tests may indicate complications or precipitating causes, and are often performed upon arrival to an emergency department. New regional wall motion abnormalities on an echocardiogram are also suggestive of an MI. Echo may be performed in equivocal cases by the on-call cardiologist. In stable patients whose symptoms have resolved by the time of evaluation, technetium (99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiological or pharmacological stress. Thallium may also be used to determine viability of tissue, distinguishing whether nonfunctional myocardium is actually dead or merely in a state of hibernation or of being stunned.

Medical societies recommend that the physician confirm a person is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis. Patients who have a normal ECG and who are able to exercise, for example, do not merit routine imaging. Imaging tests such as stress radionuclide myocardial perfusion imaging or stress echocardiography can confirm a diagnosis when a patient's history, physical exam, ECG, and cardiac biomarkers suggest the likelihood of a problem.

PREVENTION

The risk of a recurrent MI decreases with strict blood pressure management and lifestyle changes, chiefly smoking cessation, regular exercise, a sensible diet for those with heart disease, and limitation of alcohol intake. People are usually started on several long-term medications after an MI, with the aim of preventing further cardiovascular events such MIs, congestive heart failure, or strokes. Unless contraindicated, such medications often include the following:

  • Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent MI. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, but the risk of hemorrhage is increased.
  • Beta blocker therapy such as metoprolol or carvedilol should be started. These have been particularly beneficial in those who are high-risk such as those with left ventricular dysfunction and/or continuing cardiac ischaemia. β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI.
  • ACE inhibitor therapy should be commenced 24–48 hours after MI in those who are hemodynamically stable, particularly with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling.
  • Statin therapy has been shown to reduce mortality and morbidity. The protective effects of statins may be due to more than their LDL lowering effects. The general consensus is that statins have the ability to stabilize plaques and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids.
  • The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death after MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above. Spironolactone, another option, is sometimes preferable to eplerenone due to cost.
  • Evidence supports the consumption of polyunsaturated fats instead of saturated fats as a measure of decreasing coronary heart disease. In high-risk people, no clear-cut decrease in potentially fatal arrhythmias occurs due to omega-3 fatty acids and may actually increase risk in some groups.
  • Giving heparin to people with heart conditions like unstable angina and some forms of heart attacks reduces the risk of having another heart attack. However, heparin also increases the chance of minor bleeding.

MANAGEMENT

An MI requires immediate medical attention. Treatment attempts to save as much viable heart muscle as possible and to prevent further complications, hence the phrase "time is muscle". Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI. Reviews of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use. Other analgesics such as nitrous oxide are of unknown benefit.

STEMI

Immediate

Percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a timely manner. If PCI cannot be performed within 90 to 120 minutes then fibrinolysis, preferably within 30 minutes, is recommended. If after fibrinolysis, significant cardiogenic shock, continued severe chest pain, or less than a 50% improvement in ST elevation after 90 minutes occurs, then rescue PCI is indicated emergently. After PCI, people are generally placed on dual antiplatelet therapy for at least a year (which is generally aspirin and clopidogrel).

Long term

Beta blockers are recommended in those without signs of heart failure or a heart block. If used, they should be started in the first 24 hours.

PROGNOSIS

The prognosis after MI varies greatly depending on a person's health, the extent of the heart damage, and the treatment given.

In those who have an STEMI in the United States, between 5 to 6 percent die before leaving hospital and 7 to 18 percent die within a year.[

Using variables available in the emergency room, people with a higher risk of adverse outcome can be identified. One study found 0.4% of patients with a low-risk profile died after 90 days, whereas in high-risk people it was 21.1%.

Some risk factors for death include: age, hemodynamic parameters (such as heart failure, cardiac arrest on admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation, diabetes, serum creatinine, peripheral vascular disease, and elevation of cardiac markers. Assessment of left ventricular ejection fraction may increase the predictive power. Prognosis is worse if a mechanical complication such as papillary muscle or myocardial free wall rupture occurs. Morbidity and mortality from myocardial infarction has improved over the years due to better treatment.

Complications

Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). Acute complications may include heart failure if the damaged heart is no longer able to pump blood adequately around the body; aneurysm or rupture of the myocardium; mitral regurgitation, in particular if the infarction causes dysfunction of the papillary muscle; Dressler's syndrome; and arrhythmias, such as ventricular fibrillation, ventricular tachycardia, atrial fibrillation, and heart block. Longer-term complications include heart failure, atrial fibrillation, and the increased risk of a second MI.

EPIDEMIOLOGY

Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease; with it being the leading cause of death in high- or middle-income countries and second only to lower respiratory infections in lower-income countries. Worldwide, more than 3 million people have STEMIs and 4 million have NSTEMIs a year. STEMIs occur about twice as often in men as women.

Rates of death from ischemic heart disease (IHD) have slowed or declined in most high-income countries, although cardiovascular disease still accounted for one in three of all deaths in the USA in 2008. In contrast, IHD is becoming a more common cause of death in the developing world. For example in India, IHD had become the leading cause of death by 2004, accounting for 1.46 million deaths (14% of total deaths) and deaths due to IHD were expected to double during 1985–2015. Globally, disability adjusted life years (DALYs) lost to ischemic heart disease are predicted to account for 5.5% of total DALYs in 2030, making it the second-most-important cause of disability (after unipolar depressive disorder), as well as the leading cause of death by this date.

SOCIETY AND CULTURE

In the United States, women who have had an MI are often treated with fewer medical interventions than men.

Economics

In 2011, AMI was one of the top five most expensive conditions seen during inpatient hospitalizations in the U.S., with an aggregate cost of about $11.5 billion for 612,000 hospital stays.

Legal implications

At common law, in general, a myocardial infarction is a disease, but may sometimes be an injury. This can create coverage issues in administration of no-fault insurance schemes such as workers' compensation. In general, a heart attack is not covered; however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion. In addition, in some jurisdictions, heart attacks suffered by persons in particular occupations such as police officers may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person having suffered from an MI may be prevented from participating in activity that puts other people's lives at risk, for example driving a car or flying an airplane.

IMAGES

CASE RECORD

  DISEASES - GENERAL & FEW CANCERS

BLOOD CANCER - (Juvenie Chronic Myeloid Leukemia) - Mahitha, Ramakrishnapur, Adilabad, Now at Salem, Tamilnadu

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Detected at the age of second month of her life. Cancer medicines were given for about two years after which the experts expressed their helplessness for want of any further curative or dependable drug.

MODE OF RECOVERY AT NEW LIFE CENTRE

She started taking our treatment during third year in Aug 2006.There was no evidence of any cancer cells in her blood in Nov.2008, after our treatment. Her cancer is cured and she is totally healthy now.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Leukemia(American English) or leukaemia (British English) is a type of cancer of the blood or bone marrow characterized by an abnormal increase of immature white blood cells called "blasts". Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader group of diseases affecting the blood, bone marrow, and lymphoid system, which are all known as hematological neoplasms.

Leukemia is a treatable disease. Most treatments involve chemotherapy, medical radiation therapy, hormone treatments, or bone marrow transplant. The rate of cure depends on the type of leukemia as well as the age of the patient. Children are more likely to be permanently cured than adults. Even when a complete cure is unlikely, most people with a chronic leukemia and many people with an acute leukemia can be successfully treated for years. Sometimes, leukemia is the effect of another cancer, known as blastic leukemia, which usually involves the same treatment, although it is usually unsuccessful.

Leukemia can affect people at any age. In 2000 approximately 256,000 children and adults around the world had developed some form of leukemia, and 209,000 have died from it. About 90% of all leukemias are diagnosed in adults.

CLASSIFICATION

Clinically and pathologically, leukemia is subdivided into a variety of large groups. The first division is between its acute and chronic forms:

  • Acute leukemia is characterized by a rapid increase in the number of immature blood cells. Crowding due to such cells makes the bone marrow unable to produce healthy blood cells. Immediate treatment is required in acute leukemia due to the rapid progression and accumulation of the malignant cells, which then spill over into the bloodstream and spread to other organs of the body. Acute forms of leukemia are the most common forms of leukemia in children.
  • Chronic leukemia is characterized by the excessive buildup of relatively mature, but still abnormal, white blood cells. Typically taking months or years to progress, the cells are produced at a much higher rate than normal, resulting in many abnormal white blood cells. Whereas acute leukemia must be treated immediately, chronic forms are sometimes monitored for some time before treatment to ensure maximum effectiveness of therapy. Chronic leukemia mostly occurs in older people, but can theoretically occur in any age group.

Additionally, the diseases are subdivided according to which kind of blood cell is affected. This split divides leukemias into lymphoblastic or lymphocytic leukemias and myeloid or myelogenous leukemias:

  • In lymphoblastic or lymphocytic leukemias, the cancerous change takes place in a type of marrow cell that normally goes on to form lymphocytes, which are infection-fighting immune system cells. Most lymphocytic leukemias involve a specific subtype of lymphocyte, the B cell.
  • In myeloid or myelogenous leukemias, the cancerous change takes place in a type of marrow cell that normally goes on to form red blood cells, some other types of white cells, and platelets.

Combining these two classifications provides a total of four main categories. Within each of these four main categories, there are typically several subcategories. Finally, some rarer types are usually considered to be outside of this classification scheme.

  • Acute lymphoblastic leukemia (ALL) is the most common type of leukemia in young children. This disease also affects adults, especially those age 65 and older. Standard treatments involve chemotherapy and radiotherapy. The survival rates vary by age: 85% in children and 50% in adults. Subtypes include precursor B acute lymphoblastic leukemia, precursor T acute lymphoblastic leukemia, Burkitt's leukemia, and acute biphenotypic leukemia.
  • Chronic lymphocytic leukemia (CLL) most often affects adults over the age of 55. It sometimes occurs in younger adults, but it almost never affects children. Two-thirds of affected people are men. The five-year survival rate is 75%. It is incurable, but there are many effective treatments. One subtype is B-cell prolymphocytic leukemia, a more aggressive disease.
  • Acute myelogenous leukemia (AML) occurs more commonly in adults than in children, and more commonly in men than women. AML is treated with chemotherapy. The five-year survival rate is 40%, except for APL (Acute Promyelocytic Leukemia), which is over 90%.[6] Subtypes of AML include acute promyelocytic leukemia, acute myeloblastic leukemia, and acute megakaryoblastic leukemia.
  • Chronic myelogenous leukemia (CML) occurs mainly in adults; a very small number of children also develop this disease. Treatment is with imatinib (Gleevec in United States, Glivec in Europe) or other drugs. The five-year survival rate is 90%. One subtype is chronic myelomonocytic leukemia.
  • Hairy cell leukemia (HCL) is sometimes considered a subset of chronic lymphocytic leukemia, but does not fit neatly into this pattern. About 80% of affected people are adult men. No cases in children have been reported. HCL is incurable, but easily treatable. Survival is 96% to 100% at ten years.
  • T-cell prolymphocytic leukemia (T-PLL) is a very rare and aggressive leukemia affecting adults; somewhat more men than women are diagnosed with this disease. Despite its overall rarity, it is also the most common type of mature T cell leukemia; nearly all other leukemias involve B cells. It is difficult to treat, and the median survival is measured in months.
  • Large granular lymphocytic leukemia may involve either T-cells or NK cells; like hairy cell leukemia, which involves solely B cells, it is a rare and indolent (not aggressive) leukemia.
  • Adult T-cell leukemia is caused by human T-lymphotropic virus (HTLV), a virus similar to HIV. Like HIV, HTLV infects CD4+ T-cells and replicates within them; however, unlike HIV, it does not destroy them. Instead, HTLV "immortalizes" the infected T-cells, giving them the ability to proliferate abnormally. Human T cell lymphotropic virus types I and II (HTLV-I/II) are endemic in certain areas of the world.

SIGNS AND SYMPTOMS

Damage to the bone marrow, by way of displacing the normal bone marrow cells with higher numbers of immature white blood cells, results in a lack of blood platelets, which are important in the blood clotting process. This means people with leukemia may easily become bruised, bleed excessively, or develop pinprick bleeds (petechiae).

White blood cells, which are involved in fighting pathogens, may be suppressed or dysfunctional. This could cause the patient's immune system to be unable to fight off a simple infection or to start attacking other body cells. Because leukemia prevents the immune system from working normally, some patients experience frequent infection, ranging from infected tonsils, sores in the mouth, or diarrhea to life-threatening pneumonia or opportunistic infections.

Finally, the red blood cell deficiency leads to anemia, which may cause dyspnea and pallor.

Some patients experience other symptoms, such as feeling sick, having fevers, chills, night sweats, feeling fatigued and other flu-like symptoms. Some patients experience nausea or a feeling of fullness due to an enlarged liver and spleen; this can result in unintentional weight loss. Blasts affected by the disease may come together and become swollen in the liver or in the lymph nodes causing pain and leading to nausea.

If the leukemic cells invade the central nervous system, then neurological symptoms (notably headaches) can occur. Uncommon neurological symptoms like migraines, seizures, or coma can occur as a result of brain stem pressure. All symptoms associated with leukemia can be attributed to other diseases. Consequently, leukemia is always diagnosed through medical tests.

The word leukemia, which means 'white blood', is derived from the disease's namesake high white blood cell counts that most leukemia patients have before treatment. The high number of white blood cells are apparent when a blood sample is viewed under a microscope. Frequently, these extra white blood cells are immature or dysfunctional. The excessive number of cells can also interfere with the level of other cells, causing a harmful imbalance in the blood count.

Some leukemia patients do not have high white blood cell counts visible during a regular blood count. This less-common condition is called aleukemia. The bone marrow still contains cancerous white blood cells which disrupt the normal production of blood cells, but they remain in the marrow instead of entering the bloodstream, where they would be visible in a blood test. For an aleukemic patient, the white blood cell counts in the bloodstream can be normal or low. Aleukemia can occur in any of the four major types of leukemia, and is particularly common in hairy cell leukemia.

CAUSES

There is no single known cause for any of the different types of leukemia. The few known causes, which are not generally factors within the control of the average person, account for relatively few cases. The cause for most cases of leukemia is unknown. The different leukemias likely have different causes.

Leukemia, like other cancers, results from mutations in the DNA. Certain mutations can trigger leukemia by activating oncogenes or deactivating tumor suppressor genes, and thereby disrupting the regulation of cell death, differentiation or division. These mutations may occur spontaneously or as a result of exposure to radiation or carcinogenic substances.

Among adults, the known causes are natural and artificial ionizing radiation, a few viruses such as human T-lymphotropic virus, and some chemicals, notably benzene and alkylating chemotherapy agents for previous malignancies. Use of tobacco is associated with a small increase in the risk of developing acute myeloid leukemia in adults. Cohort and case-control studies have linked exposure to some petrochemicals and hair dyes to the development of some forms of leukemia. Diet has very limited or no effect, although eating more vegetables may confer a small protective benefit.

Viruses have also been linked to some forms of leukemia. Experiments on mice and other mammals have demonstrated the relevance of retroviruses in leukemia, and human retroviruses have also been identified. The first human retrovirus identified was human T-lymphotropic virus, or HTLV-1, which is known to cause adult T-cell leukemia.

Some people have a genetic predisposition towards developing leukemia. This predisposition is demonstrated by family histories and twin studies. The affected people may have a single gene or multiple genes in common. In some cases, families tend to develop the same kinds of leukemia as other members; in other families, affected people may develop different forms of leukemia or related blood cancers.

In addition to these genetic issues, people with chromosomal abnormalities or certain other genetic conditions have a greater risk of leukemia. For example, people with Down syndrome have a significantly increased risk of developing forms of acute leukemia (especially acute myeloid leukemia), and Fanconi anemia is a risk factor for developing acute myeloid leukemia.

Whether non-ionizing radiation causes leukemia has been studied for several decades. The International Agency for Research on Cancer expert working group undertook a detailed review of all data on static and extremely low frequency electromagnetic energy, which occurs naturally and in association with the generation, transmission, and use of electrical power. They concluded that there is limited evidence that high levels of ELF magnetic (but not electric) fields might cause childhood leukemia. Exposure to significant ELF magnetic fields might result in twofold excess risk for leukemia for children exposed to these high levels of magnetic fields. However, the report also says that methodological weaknesses and biases in these studies have likely caused the risk to be overstated. No evidence for a relationship to leukemia or another form of malignancy in adults has been demonstrated. Since exposure to such levels of ELFs is relatively uncommon, the World Health Organization concludes that ELF exposure, if later proven to be causative, would account for just 100 to 2400 cases worldwide each year, representing 0.2 to 4.9% of the total incidence of childhood leukemia for that year (about 0.03 to 0.9% of all leukemias).

A few cases of maternal-fetal transmission (a baby acquires leukemia because its mother had leukemia during the pregnancy) have been reported.

According to a study conducted at the Center for Research in Epidemiology and Population Health in France, children born to mothers who use fertility drugs to induce ovulation are more than twice as likely to develop leukemia during their childhoods than other children.

DIAGNOSIS

Most forms of leukemia are treated with pharmaceutical medication, typically combined into a multi-drug chemotherapy regimen. Some are also treated with radiation therapy. In some cases, a bone marrow transplant is effective.

Acute lymphoblastic

Management of ALL focuses on control of bone marrow and systemic (whole-body) disease. Additionally, treatment must prevent leukemic cells from spreading to other sites, particularly the central nervous system (CNS) e.g. monthly lumbar punctures. In general, ALL treatment is divided into several phases:

  • Induction chemotherapy to bring about bone marrow remission. For adults, standard induction plans include prednisone, vincristine, and an anthracycline drug; other drug plans may include L-asparaginase or cyclophosphamide. For children with low-risk ALL, standard therapy usually consists of three drugs (prednisone, L-asparaginase, and vincristine) for the first month of treatment.
  • Consolidation therapy or intensification therapy to eliminate any remaining leukemia cells. There are many different approaches to consolidation, but it is typically a high-dose, multi-drug treatment that is undertaken for a few months. Patients with low- to average-risk ALL receive therapy with antimetabolite drugs such as methotrexate and 6-mercaptopurine (6-MP). High-risk patients receive higher drug doses of these drugs, plus additional drugs.
  • CNS prophylaxis (preventive therapy) to stop the cancer from spreading to the brain and nervous system in high-risk patients. Standard prophylaxis may include radiation of the head and/or drugs delivered directly into the spine.
  • Maintenance treatments with chemotherapeutic drugs to prevent disease recurrence once remission has been achieved. Maintenance therapy usually involves lower drug doses, and may continue for up to three years.
  • Alternatively, allogeneic bone marrow transplantation may be appropriate for high-risk or relapsed patients.
Treatment approach

CLL is probably incurable by present treatments. The primary chemotherapeutic plan is combination chemotherapy with chlorambucil or cyclophosphamide, plus a corticosteroid such as prednisone or prednisolone. The use of a corticosteroid has the additional benefit of suppressing some related autoimmune diseases, such as immunohemolytic anemia or immune-mediated thrombocytopenia. In resistant cases, single-agent treatments with nucleoside drugs such as fludarabine, pentostatin, or cladribine may be successful. Younger patients may consider allogeneic or autologous bone marrow transplantation.

Acute myelogenous

Many different anti-cancer drugs are effective for the treatment of AML. Treatments vary somewhat according to the age of the patient and according to the specific subtype of AML. Overall, the strategy is to control bone marrow and systemic (whole-body) disease, while offering specific treatment for the central nervous system (CNS), if involved.

In general, most oncologists rely on combinations of drugs for the initial, induction phase of chemotherapy. Such combination chemotherapy usually offers the benefits of early remission and a lower risk of disease resistance. Consolidation and maintenance treatments are intended to prevent disease recurrence. Consolidation treatment often entails a repetition of induction chemotherapy or the intensification chemotherapy with additional drugs. By contrast, maintenance treatment involves drug doses that are lower than those administered during the induction phase.

Chronic myelogenous

There are many possible treatments for CML, but the standard of care for newly diagnosed patients is imatinib (Gleevec) therapy. Compared to most anti-cancer drugs, it has relatively few side effects and can be taken orally at home. With this drug, more than 90% of patients will be able to keep the disease in check for at least five years, so that CML becomes a chronic, manageable condition.

In a more advanced, uncontrolled state, when the patient cannot tolerate imatinib, or if the patient wishes to attempt a permanent cure, then an allogeneic bone marrow transplantation may be performed. This procedure involves high-dose chemotherapy and radiation followed by infusion of bone marrow from a compatible donor. Approximately 30% of patients die from this procedure.

Hairy Cell

Decision to treat

Patients with hairy cell leukemia who are symptom-free typically do not receive immediate treatment. Treatment is generally considered necessary when the patient shows signs and symptoms such as low blood cell counts (e.g., infection-fighting neutrophil count below 1.0 K/µL), frequent infections, unexplained bruises, anemia, or fatigue that is significant enough to disrupt the patient's everyday life.

Typical treatment approach

Patients who need treatment usually receive either one week of cladribine, given daily by intravenous infusion or a simple injection under the skin, or six months of pentostatin, given every four weeks by intravenous infusion. In most cases, one round of treatment will produce a prolonged remission.

Other treatments include rituximab infusion or self-injection with Interferon-alpha. In limited cases, the patient may benefit from splenectomy (removal of the spleen). These treatments are not typically given as the first treatment because their success rates are lower than cladribine or pentostatin.

T-cell prolymphocytic

Most patients with T-cell prolymphocytic leukemia, a rare and aggressive leukemia with a median survival of less than one year, require immediate treatment.

T-cell prolymphocytic leukemia is difficult to treat, and it does not respond to most available chemotherapeutic drugs. Many different treatments have been attempted, with limited success in certain patients: purine analogues (pentostatin, fludarabine, cladribine), chlorambucil, and various forms of combination chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone CHOP, cyclophosphamide, vincristine, prednisone [COP], vincristine, doxorubicin, prednisone, etoposide, cyclophosphamide, bleomycin VAPEC-B). Alemtuzumab (Campath), a monoclonal antibody that attacks white blood cells, has been used in treatment with greater success than previous options.

Some patients who successfully respond to treatment also undergo stem cell transplantation to consolidate the response.

Juvenile myelomonocytic

Treatment for juvenile myelomonocytic leukemia can include splenectomy, chemotherapy, and bone marrow transplantation.

EPIDEMIOLOGY

In 2010, globally, approximately 281,500 people died of leukemia. In 2000, approximately 256,000 children and adults around the world developed a form of leukemia, and 209,000 died from it. This represents about 3% of the almost seven million deaths due to cancer that year, and about 0.35% of all deaths from any cause. Of the sixteen separate sites the body compared, leukemia was the 12th most common class of neoplastic disease, and the 11th most common cause of cancer-related death.

About 245,000 people in the United States are affected with some form of leukemia, including those that have achieved remission or cure. Approximately 44,270 new cases of leukemia were diagnosed in the year of 2008 in the US. This represents 2.9% of all cancers (excluding simple basal cell and squamous cell skin cancers) in the United States, and 30.4% of all blood cancers.

Among children with some form of cancer, about a third have a type of leukemia, most commonly acute lymphoblastic leukemia. A type of leukemia is the second most common form of cancer in infants (under the age of 12 months) and the most common form of cancer in older children. Boys are somewhat more likely to develop leukemia than girls, and white American children are almost twice as likely to develop leukemia than black American children. Only about 3% cancer diagnoses among adults are for leukemias, but because cancer is much more common among adults, more than 90% of all leukemias are diagnosed in adults.

Race is a risk factor. Hispanics, especially those under the age of 20, are at the highest risk for leukemia, while whites, Native Americans, Asians, and Alaska Natives are at higher risk than blacks.

Sex is also a risk factor. More men than women are diagnosed with leukemia and die from the disease. Around 30 percent more men than women have leukemia.

IMAGES

CASE RECORD

CHRONIC FEVER - Tubercular Meningitis (Six Months) - Lavanya, Metpalli, Karimnagar

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

The fever did not respond despite visiting many experts for 6 months.. Ultimately it was diagnosed as TB Meningitis by Apollo hospital of Karimnagar but it did not subside with their treatment. There was severe headache, lack of appetite and also sleeplessness .

MODE OF RECOVERY AT NEW LIFE CENTRE

I have recovered fully from all the suffering in just one day only with the homeopathic medicines given at New Life centre. I am now active and healthy. It was a miracle.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Tuberculous meningitis is also known as TB meningitis or tubercular meningitis.

Tuberculous meningitis is Mycobacterium tuberculosis infection of the meninges—the system of membranes which envelop's the central nervous system. It is the most common form of CNS tuberculosis.

CLINICAL FEATURES

Fever and headache are the cardinal features. Confusion is a late feature and coma bears a poor prognosis. Meningism is absent in a fifth of patients with TB meningitis. Patients may also have focal neurological deficits.

PATHOLOGY

Mycobacterium tuberculosis of the meninges is the cardinal feature and the inflammation is concentrated towards the base of the brain. When the inflammation is in the brain stem subarachnoid area, cranial nerve roots may be affected. The symptoms will mimic those of space-occupying lesions. Infection begins in the lungs and may spread to the meninges by a variety of routes.

Blood-borne spread certainly occurs and 25% of patients with miliary TB have TB meningitis, presumably by crossing the blood–brain barrier; but a proportion of patients may get TB meningitis from rupture of a cortical focus in the brain (a so-called Rich focus); an even smaller proportion get it from rupture of a bony focus in the spine. It is rare and unusual for TB of the spine to cause TB of the central nervous system, but isolated cases have been described.

DIAGNOSIS

Diagnosis of TB meningitis is made by analysing cerebrospinal fluid collected by lumbar puncture. When collecting CSF for suspected TB meningitis, a minimum of 1ml of fluid should be taken (preferably 5 to 10ml).

The CSF usually has a high protein, low glucose and a raised number of lymphocytes. Acid-fast bacilli are sometimes seen on a CSF smear, but more commonly, M. tuberculosis is grown in culture. A spiderweb clot in the collected CSF is characteristic of TB meningitis, but is a rare finding.

ELISPOT testing is not useful for the diagnosis of acute TB meningitis and is often false negative, but may paradoxically become positive after treatment has started, which helps to confirm the diagnosis.

More than half of cases of TB meningitis cannot be confirmed microbiologically, and these patients are treated on the basis of clinical suspicion only. The culture of TB from CSF takes a minimum of two weeks, and therefore the majority of patients with TB meningitis are started on treatment before the diagnosis is confirmed.

Nucleic acid amplification tests (NAAT)

This is a heterogeneous group of tests that use polymerase chain reaction (PCR) to detect mycobacterial nucleic acid. These test vary in which nucleic acid sequence they detect and vary in their accuracy. The two most common commercially available tests are the amplified mycobacterium tuberculosis direct test (MTD, Gen-Probe) and Amplicor. In 2007, a systematic review of NAAT by the NHS Health Technology Assessment Programme concluded that for diagnosing tuberculous meningitis "Individually, the AMTD test appears to perform the best (sensitivity 74% and specificity 98%) [page 87]". In the NHS meta-analysis, they found the pooled prevalence of TB meningitis to be 29%; however there was much heterogeneity in the reported sensitivities. Using a clinical calculator, these numbers yield a positive predictive value of 94% and a negative predictive value of 90%; however the 30% prevalence may be high due to referral bias. Alternate estimates of disease prevalence can be entered into the clinical calculator to refine the predictive values.These instances vary from patient to patient according to their pathology.

Imaging

Imaging studies such as CT or MRI may show features strongly suggestive of TB meningitis, but cannot diagnose it.

TREATMENT

The treatment of TB meningitis is isoniazid, rifampicin, pyrazinamide and ethambutol for two months, followed by isoniazid and rifampicin alone for a further ten months. Steroids help reduce the risk of death or disabling neurological deficit. Steroids can be used in the first six weeks of treatment, but must be used with caution in individuals who also have HIV. A few patients may require immunomodulatory agents such as thalidomide.

Treatment must be started as soon as there is a reasonable suspicion of the diagnosis. Treatment must not be delayed while waiting for confirmation of the diagnosis.

Hydrocephalus occurs as a complication in about a third of patients with TB meningitis and will require a ventricular shunt. The addition of aspirin may improve mortality, possibly by reducing complications such as infarcts.

IMAGES

DIABETIC GANGRENE - Mrs.Sharma, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

My wife, who is a diabetic patient developed pain in her foot and toes. It did not respond to treatment given by experts in a corporate hospital. So they operated and removed the two toes. But the foot remained painful, swollen and reddish even after six months despite trying all available antibiotics in a corporate hospital .Even homeopathy did not help. They were planning another surgical amputation and remove the foot up to ankle.

MODE OF RECOVERY AT NEW LIFE CENTRE

Then we happened to start the homeopathic treatment given by the doctor of NEW LIFE centre. In just 15 days the pain and swelling had decreased. She is totally healthy now and we have stopped all the antibiotics.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Gangrene is a potentially life-threatening condition that arises when a considerable mass of body tissue dies (necrosis). This may occur after an injury or infection, or in people suffering from any chronic health problem affecting blood circulation. The primary cause of gangrene is reduced blood supply to the affected tissues, which results in cell death. Diabetes and long-term smoking increase the risk of suffering from gangrene.

There are different types of gangrene with different symptoms, such as dry gangrene, wet gangrene, gas gangrene, internal gangrene and necrotizing fasciitis. Treatment options include debridement (or, in severe cases, amputation) of the affected body parts, antibiotics, vascular surgery, maggot therapy or hyperbaric oxygen therapy.

CAUSES

Gangrene is caused by ischemia or infection, such as by the bacteria Clostridium perfringens or by thrombosis (a blood vessel blocked by a blood clot). It is usually the result of critically insufficient blood supply (e.g., peripheral vascular disease) and is often associated with diabetes and long-term tobacco smoking. This condition is most common in the lower extremities. The best treatment for gangrene is revascularization (i.e., restoration of blood flow) of the afflicted organ, which can reverse some of the effects of necrosis and allow healing. Other treatments include debridement and surgical amputation. The method of treatment is generally determined by the location of affected tissue and extent of tissue loss. Gangrene may appear as one effect of foot binding.

TYPES

Dry

Dry gangrene begins at the distal part of the limb due to ischemia, and often occurs in the toes and feet of elderly patients due to arteriosclerosis and thus, is also known as senile gangrene. Dry gangrene is mainly due to arterial occlusion. There is limited putrefaction and bacteria fail to survive. Dry gangrene spreads slowly through portions of tissue where the blood supply is inadequate to keep tissue viable. The affected part is dry, shrunken and dark reddish-black, resembling mummified flesh. The dark coloration is due to liberation of hemoglobin from hemolyzed red blood cells, which is acted upon by hydrogen sulfide (H2S) produced by the bacteria, resulting in formation of black iron sulfide that remains in the tissues. The line of separation usually brings about complete separation, with eventual falling off of the gangrenous tissue if it is not removed surgically, also called autoamputation.

Dry gangrene is actually a form of coagulative necrosis. If blood flow is interrupted for a reason other than severe bacterial infection, the result is a case of dry gangrene. Individuals with impaired peripheral blood flow, such as diabetics, are at greater risk of developing dry gangrene.

The early signs and symptoms of dry gangrene are a dull ache and sensation of coldness in the affected area along with pallor of the flesh. If detected early, the process can sometimes be reversed by vascular surgery. However, if necrosis sets in, the affected tissue must be removed just as with wet gangrene.

Wet

Wet gangrene occurs in naturally moist tissue and organs such as the mouth, bowel, lungs, cervix, and vulva.[citation needed] Bedsores occurring on body parts such as the sacrum, buttocks, and heels — although not necessarily moist areas — are also wet gangrene infections. This condition is characterized by thriving bacteria and has a poor prognosis (compared to dry gangrene) due to septicemia resulting from the free communication between infected fluid and circulatory fluid. In wet gangrene, the tissue is infected by saprogenic microorganisms (Clostridium perfringens or Bacillus fusiformis, for example), which cause tissue to swell and emit a fetid smell. Wet gangrene usually develops rapidly due to blockage of venous (mainly) and/or arterial blood flow. The affected part is saturated with stagnant blood, which promotes the rapid growth of bacteria. The toxic products formed by bacteria are absorbed, causing systemic manifestation of septicemia and finally death. The affected part is edematous, soft, putrid, rotten and dark. The darkness in wet gangrene occurs due to the same mechanism as in dry gangrene. Wet gangrene is coagulative necrosis progressing to liquefactive necrosis.

Gas

Gas gangrene is a bacterial infection that produces gas within tissues. It is a deadly form of gangrene usually caused by Clostridium perfringens bacteria. Infection spreads rapidly as the gases produced by bacteria expand and infiltrate healthy tissue in the vicinity. Because of its ability to quickly spread to surrounding tissues, gas gangrene should be treated as a medical emergency.

Gas gangrene is caused by a bacterial exotoxin-producing clostridial species, which are mostly found in soil and other anaerobes (e.g., Bacteroides and anaerobic streptococci). These environmental bacteria may enter the muscle through a wound and subsequently proliferate in necrotic tissue and secrete powerful toxins. These toxins destroy nearby tissue, generating gas at the same time. A gas composition of 5.9% hydrogen, 3.4% carbon dioxide, 74.5% nitrogen, and 16.1% oxygen was reported in one clinical case.

Gas gangrene can cause necrosis, gas production, and sepsis. Progression to toxemia and shock is often very rapid.

Other
  • Necrotizing fasciitis affects the deeper layers of the skin.
  • Noma is a gangrene of the face.
  • Fournier gangrene usually affects the male genitals and groin.
  • Venous limb gangrene may be caused by heparin-induced thrombocytopenia and thrombosis (HITT).

TREATMENT

Treatment is usually surgical debridement, wound care, and antibiotic therapy, although amputation is necessary in many cases.

"Most amputations are performed for ischemic disease of the lower extremity. Of dysvascular amputations, 15-28% of patients undergo contralateral limb amputations within 3 years. Of elderly persons who undergo amputations, 50% survive the first 3 years."

In the United States, 30,000–40,000 amputations are performed annually. There were an estimated 1.6 million individuals living with the loss of a limb in 2005; these estimates are expected to more than double to 3.6 million such individuals by the year 2050. Antibiotics alone are not effective because they may not penetrate infected tissues sufficiently. Hyperbaric oxygen therapy (HBOT) treatment is used to treat gas gangrene. HBOT increases pressure and oxygen content to allow blood to carry more oxygen to inhibit anaerobic organism growth and reproduction. A regenerative medicine therapy was developed by Dr. Peter DeMarco to treat gangrene using procaine and PVP. He applied his therapy to diabetic patients to avoid amputations. Growth factors, hormones and skin grafts have also been used to accelerate healing for gangrene and other chronic wounds.

Angioplasty should be considered if severe blockage in lower leg vessels (tibial and peroneal artery) leads to gangrene.

IMAGES

  DISEASES OF URINARY SYSTEM (KIDNEY, BLADDER, URETER,PROSTATE &URETHRA)

KIDNEY STONE with SEVERE PAIN - Venkateswar Rao, Santhinagar, Lalaguda, Secunderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I was getting recurrent attacks of severe intolerable pain in my abdomen due to kidney stones. I was forced to undergo blasting twice and operation once costing a total amount of Rs.2.5 lakhs in a span of just three years.

MODE OF RECOVERY AT NEW LIFE CENTRE

I happened to take homeopathy from NEW LIFE HOMEO CARE in the year 2010.I am now relieved of all trouble and there is no recurrence of pain during the following three years. The stones are not forming now.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Chronic kidney disease (CKD), also known as chronic renal disease (CRD), is a progressive loss in renal function over a period of months or years. The symptoms of worsening kidney function are non-specific, and might include feeling generally unwell and experiencing a reduced appetite. Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes and those with a blood relative with chronic kidney disease. Chronic kidney disease may also be identified when it leads to one of its recognized complications, such as cardiovascular disease, anemia or pericarditis. It is differentiated from acute kidney disease in that the reduction in kidney function must be present for over 3 months.

Chronic kidney disease is identified by a blood test for creatinine. Higher levels of creatinine indicate a lower glomerular filtration rate and as a result a decreased capability of the kidneys to excrete waste products. Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis (testing of a urine sample) shows that the kidney is allowing the loss of protein or red blood cells into the urine. To fully investigate the underlying cause of kidney damage, various forms of medical imaging, blood tests and often renal biopsy (removing a small sample of kidney tissue) are employed to find out if there is a reversible cause for the kidney malfunction. Recent professional guidelines classify the severity of chronic kidney disease in five stages, with stage 1 being the mildest and usually causing few symptoms and stage 5 being a severe illness with poor life expectancy if untreated. Stage 5 CKD is often called end stage renal disease (ESRD), end stage renal failure (ESRF), or end-stage kidney disease (ESKD) and is synonymous with the now outdated terms chronic kidney failure (CKF) or chronic renal failure (CRF).

There is no specific treatment unequivocally shown to slow the worsening of chronic kidney disease. If there is an underlying cause to CKD, such as vasculitis, this may be treated directly to slow the damage. In more advanced stages, treatments may be required for anemia and bone disease. Severe CKD requires renal replacement therapy, which may involve a form of dialysis, but ideally constitutes a kidney transplant.

SIGNS AND SYMPTOMS

CKD is initially without specific symptoms and is generally only detected as an increase in serum creatinine or protein in the urine. As the kidney function decreases:

  • Blood pressure is increased due to fluid overload and production of vasoactive hormones created by the kidney via the RAS (renin-angiotensin system), increasing one's risk of developing hypertension and/or suffering from congestive heart failure
  • Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Urea is excreted by sweating and crystallizes on skin ("uremic frost").
  • Potassium accumulates in the blood (known as hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias). Hyperkalemia usually does not develop until the GFR falls to less than 20-25 mL/min/1.73 m2, at which point the kidneys have decreased ability to excrete potassium. Hyperkalemia in CKD can be exacerbated by acidemia (which leads to extracellular shift of potassium) and from lack of insulin.[2]
  • Erythropoietin synthesis is decreased
  • Fluid volume overload — symptoms may range from mild edema to life-threatening pulmonary edema
  • Hyperphosphatemia — due to reduced phosphate excretion, which follows the decrease in glomerular filtration. Hyperphosphatemia is associated to increased cardiovascular risk, being a direct stimulus to vascular calcification.
  • Hypocalcemia — due to 1,25 dihydroxyvitamin D3 deficiency. The 1,25 dihydroxyvitamin D3 deficiency is due to stimulation of fibroblast growth factor-23. Osteocytes are responsible for the increased production of FGF23, which is a potent inhibitor of the enzyme 1-alpha-hydroxylase (responsible for the conversion of 25-hydroxycholecalciferol into 1,25 dihydroxyvitamin D3)
    • Later this progresses to secondary hyperparathyroidism, renal osteodystrophy and vascular calcification that further impairs cardiac function.
  • Metabolic acidosis, due to accumulation of sulfates, phosphates, uric acid etc. This may cause altered enzyme activity by excess acid acting on enzymes and also increased excitability of cardiac and neuronal membranes by the promotion of hyperkalemia due to excess acid (acidemia). Acidosis is also due to decreased capacity of generating enough ammonia from the cells of the proximal tubule.
  • Iron deficiency anemia, which increases in prevalence as kidney function decreases, and is especially prevalent in those requiring haemodialysis. It is multifactoral in cause but includes increased inflammation, reduction in Erythropoietin, hyperuricemia leading to bone marrow suppression.

People with chronic kidney disease suffer from accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients afflicted with chronic kidney disease and cardiovascular disease tend to have significantly worse prognoses than those suffering only from the latter.

Sexual dysfunction is very common in both men and women with chronic kidney disease. A majority of men have a reduced sex drive, difficulty obtaining an erection and reaching orgasm, and the problems get worse with age. A majority of women have trouble with sexual arousal, and painful periods and problems with performing and enjoying sex are common.

CAUSES

The three most common causes of CKD are diabetes mellitus, hypertension, and glomerulonephritis. Together, these cause approximately 75% of all adult cases.

Historically, kidney disease has been classified according to the part of the renal anatomy that is involved.

  • Vascular, includes large vessel disease such as bilateral renal artery stenosis and small vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome and vasculitis
  • Glomerular, comprising a diverse group and subclassified into
    • Primary Glomerular disease such as focal segmental glomerulosclerosis and IgA nephropathy (or nephritis)
    • Secondary Glomerular disease such as diabetic nephropathy and lupus nephritis
  • Tubulointerstitial including polycystic kidney disease, drug and toxin-induced chronic tubulointerstitial nephritis and reflux nephropathy
  • Obstructive such as with bilateral kidney stones and diseases of the prostate
  • On rare cases, pinworms infecting the kidney can also cause nephropathy.
  • non traditional causes of CKD are denoted if the common causes of CKD are not present, e.g. in El Salvador, Nicaragua, ... in rural communities with agriculture.
  • non traditional causes of CKD are denoted if the common causes of CKD are not present, e.g. in El Salvador, Nicaragua, ... in rural communities with agriculture.

DIAGNOSIS

In many CKD patients, previous renal disease or other underlying diseases are already known. A small number present with CKD of unknown cause. In these patients, a cause is occasionally identified retrospectively.

It is important to differentiate CKD from acute renal failure (ARF) because ARF can be reversible. Abdominal ultrasound, in which the size of the kidneys is measured, is commonly performed. Kidneys with CKD are usually smaller (< 9 cm) than normal kidneys, with notable exceptions such as in diabetic nephropathy and polycystic kidney disease. Another diagnostic clue that helps differentiate CKD from ARF is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). If these levels are unavailable (because the patient has been well and has had no blood tests), it is occasionally necessary to treat a patient briefly as having ARF until it has been established that the renal impairment is irreversible.

Additional tests may include nuclear medicine MAG3 scan to confirm blood flows and establish the differential function between the two kidneys. DMSA scans are also used in renal imaging; with both MAG3 and DMSA being used chelated with the radioactive element Technetium-99.

In chronic renal failure treated with standard dialysis, numerous uremic toxins accumulate. These toxins show various cytotoxic activities in the serum, have different molecular weights and some of them are bound to other proteins, primarily to albumin. Such toxic protein bound substances are receiving the attention of scientists who are interested in improving the standard chronic dialysis procedures used today.

Stages

All individuals with a glomerular filtration rate (GFR) <60 mL/min/1.73 m2 for 3 months are classified as having chronic kidney disease, irrespective of the presence or absence of kidney damage. The rationale for including these individuals is that reduction in kidney function to this level or lower represents loss of half or more of the adult level of normal kidney function, which may be associated with a number of complications.

All individuals with kidney damage are classified as having chronic kidney disease, irrespective of the level of GFR. The rationale for including individuals with GFR > 60 mL/min/1.73 m2 is that GFR may be sustained at normal or increased levels despite substantial kidney damage and that patients with kidney damage are at increased risk of the two major outcomes of chronic kidney disease: loss of kidney function and development of cardiovascular disease.

The loss of protein in the urine is regarded as an independent marker for worsening of renal function and cardiovascular disease. Hence, British guidelines append the letter "P" to the stage of chronic kidney disease if there is significant protein loss.

Stage 1

Slightly diminished function; kidney damage with normal or relatively high GFR (≥90 mL/min/1.73 m2). Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies.

Stage 2

Mild reduction in GFR (60–89 mL/min/1.73 m2) with kidney damage. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies.

Stage 3

Moderate reduction in GFR (30–59 mL/min/1.73 m2). British guidelines distinguish between stage 3A (GFR 45–59) and stage 3B (GFR 30–44) for purposes of screening and referral.

Stage 4

Severe reduction in GFR (15–29 mL/min/1.73 m2) Preparation for renal replacement therapy

Stage 5

Established kidney failure (GFR <15 mL/min/1.73 m2, permanent renal replacement therapy (RRT), or end stage renal disease (ESRD)

NDD-CKD vs. ESRD

The term non-dialysis dependent CKD, also abbreviated as NDD-CKD, is a designation used to encompass the status of those persons with an established CKD who do not yet require the life-supporting treatments for renal failure known as renal replacement therapy (including maintenance dialysis or renal transplantation). The condition of individuals with CKD, who require either of the 2 types of renal replacement therapy (dialysis or transplantation), is referred to as the end-stage renal disease (ESRD). Hence, the start of the ESRD is practically the irreversible conclusion of the NDD-CKD. Even though the non-dialysis dependent status refers to the status of persons with earlier stages of CKD (stages 1 to 4), patients with advanced stage of CKD (Stage 5), who have not yet started renal replacement therapy are also referred to as NDD-CKD.

SCREENING

Screening those who neither have symptoms nor risk factors for chronic kidney disease is not recommended. Those who should be screened include: those with hypertension or history of cardiovascular disease, those with diabetes or marked obesity, those aged > 60 years, subjects with indigenous racial origin, those with a history of renal disease in the past, as well as subjects who have relatives who had kidney disease requiring dialysis. Screening should include calculation of estimated GFR/1.73 m2 from the serum creatinine level, and measurement of urine-to-albumin creatinine ratio in a first-morning urine specimen as well as dipstick screen for hematuria. Guidelines for nephrologist referral vary among different countries. Nephrology referral is useful when eGFR/1.73m2 is less than 30 or decreasing by more than 3 mL/min/year, when urine albumin-to-creatinine ratio is more than 30 mg/g, when blood pressure is difficult to control, or when hematuria or other findings suggest either a primarily glomerular disorder or secondary disease amenable to specific treatment. Other benefits of early nephrology referral include proper patient education regarding options for renal replacement therapy as well as pre-emptive transplantation, and timely workup and placement of an arteriovenous fistula in those patients opting for future hemodialysis.

TREATMENT

The presence of chronic kidney disease confers a markedly increased risk of cardiovascular disease, and people with CKD often have other risk factors for heart disease, such as hyperlipidemia. The most common cause of death in people with CKD is therefore cardiovascular disease rather than renal failure. Aggressive treatment of hyperlipidemia is warranted.

Apart from controlling other risk factors, the goal of therapy is to slow down or halt the progression of CKD to stage 5. Control of blood pressure and treatment of the original disease, whenever feasible, are the broad principles of management. Generally, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are used, as they have been found to slow the progression of CKD to stage 5. Although the use of ACE inhibitors and ARBs represents the current standard of care for patients with CKD, patients progressively lose kidney function while on these medications, as seen in the IDNT and RENAL studies, which reported a decrease over time in estimated glomerular filtration rate (an accurate measure of CKD progression, as detailed in the K/DOQI guidelines) in patients treated by these conventional methods.

Currently, several compounds are in development for CKD. These include, but are not limited to, bardoxolone methyl, olmesartan medoxomil, sulodexide, and avosentan.

Replacement of erythropoietin and calcitriol, two hormones processed by the kidney, is often necessary in people with advanced disease. Guidelines recommend treatment with parenteral iron prior to treatment with erythropoietin. A target hemoglobin level of 9–12 g/dL is recommended. Phosphate binders are also used to control the serum phosphate levels, which are usually elevated in advanced chronic kidney disease. Zerenex(TM), a very promising new drug developed by Keryx Biopharma will have the ability to treat both elevated serum phosphate levels and anemia in CKD patients likely reducing or eliminating the need for other drugs i.e. IV iron and ESA's.

When one reaches stage 5 CKD, renal replacement therapy is usually required, in the form of either dialysis or a transplant.

The normalization of hemoglobin has not been found to be of any benefit to the CKD but does significantly improve the patient's quality of life in reducing symptoms such as fatigue and can improve other co-morbidities that might be present, such as chronic heart failure (CHF).[citation needed] Although the evidence for them is limited, phosphodiesterase-5 inhibitors and zinc show potential for helping men with sexual dysfunction.

PROGNOSIS

The prognosis of patients with chronic kidney disease is guarded as epidemiological data has shown that all cause mortality (the overall death rate) increases as kidney function decreases. The leading cause of death in patients with chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5.

While renal replacement therapies can maintain patients indefinitely and prolong life, the quality of life is severely affected. Renal transplantation increases the survival of patients with stage 5 CKD significantly when compared to other therapeutic options; however, it is associated with an increased short-term mortality due to complications of the surgery. Transplantation aside, high intensity home hemodialysis appears to be associated with improved survival and a greater quality of life, when compared to the conventional three times a week hemodialysis and peritoneal dialysis.

Cancer risk

Patients with end-stage renal disease are at increased overall risk for cancer. This risk is particularly high in younger patients and gradually diminishes with age. Medical specialty professional organizations recommend that physicians not perform routine cancer screening in patients with limited life expectancies due to ESRD because evidence does not show that such tests lead to improved patient outcomes.

EPIDEMIOLOGY

Chronic kidney disease globally resulted in 735,000 deaths in 2010 up from 400,000 deaths in 1990.

In Canada 1.9 to 2.3 million people have chronic kidney disease. In the US, the Centers for Disease Control and Prevention found that CKD affected an estimated 16.8% of adults aged 20 years and older, during 1999 to 2004. UK estimates suggest that 8.8% of the population of Great Britain and Northern Ireland have symptomatic CKD.

Chronic kidney disease (CKD) is a major concern in African Americans, mostly due to increased prevalence of hypertension. As an example, 37% of end-stage renal disease cases in African Americans can be attributed to high blood pressure, compared with 19% among caucasians. Treatment efficacy also differs between racial groups. Administration of anti-hypertensive drugs generally halts disease progression in white populations, but has little effect in slowing renal disease among blacks, and additional treatment such as bicarbonate therapy is often required. While lower socioeconomic status contributes to prevalence of CKD, there are still significant differences in CKD prevalence between African Americans and whites when controlling for environmental factors. Studies have shown that there is a true association between history of chronic renal failure in first or second-degree relatives, and risk of disease.[38] In addition, African Americans may have higher serum levels of human leukocyte antigens (HLA). High HLA concentrations can contribute to increased systemic inflammation, which indirectly may lead to heightened susceptibility for developing kidney disease. Lack of nocturnal reduction in blood pressure among groups of African Americans is also offered as an explanation, which lends further credence to a genetic etiology of CKD racial disparities.

A high and so-far unexplained incidence of chronic kidney disease, referred to as the Mesoamerican nephropathy, has been noted among male workers in Central America, mainly in sugar cane fields in the low-lands of El Salvador and Nicaragua. Heat stress from long hours of piece-rate work at high average temperatures (in the range of 96°F) is suspected, as are agricultural chemicals and other factors.

IMAGES

CASE RECORD

KIDNEY FAILURE - MR.Boomiah, Teacher, Mancherial

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

My mother Mrs Rambai developed fever, vomiting swelling of body which was diagnosed as kidney failure by specialists She was also suffering from cough and breathlessness which was ascribed by heart specialists to high BP and accumulation of water in lungs. After discharge the problems repeated and we visited the kidney hospital again. After 20 days of stay we went home and again the same problem repeated.

MODE OF RECOVERY AT NEW LIFE CENTRE

Then we approached Dr Subhash Chandar of Mancherial. My mother recovered from all her sufferings in the very first ten days of his treatment. Her BP also became normal, She is now healthy even after ten years have passed. We thank the doctor immensely for his surprising treatment.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

In medicine, dialysis (from Greek dialusis,"διάλυσις", meaning dissolution, dia, meaning through, and lysis, meaning loosening or splitting) is a process for removing waste and excess water from the blood, and is used primarily as an artificial replacement for lost kidney function in people with renal failure. Dialysis may be used for those with an acute disturbance in kidney function (acute kidney injury, previously acute renal failure), or progressive but chronically worsening kidney function–a state known as chronic kidney disease stage 5 (previously chronic renal failure or end-stage renal disease). The latter form may develop over months or years, but in contrast to acute kidney injury is not usually reversible, and dialysis is regarded as a "holding measure" until a renal transplant can be performed, or sometimes as the only supportive measure in those for whom a transplant would be inappropriate.

The kidneys have important roles in maintaining health. When healthy, the kidneys maintain the body's internal equilibrium of water and minerals (sodium, potassium, chloride, calcium, phosphorus, magnesium, sulfate). The acidic metabolism end-products that the body cannot get rid of via respiration are also excreted through the kidneys. The kidneys also function as a part of the endocrine system, producing erythropoietin and calcitriol. Erythropoietin is involved in the production of red blood cells and calcitriol plays a role in bone formation. Dialysis is an imperfect treatment to replace kidney function because it does not correct the compromised endocrine functions of the kidney. Dialysis treatments replace some of these functions through diffusion (waste removal) and ultrafiltration (fluid removal).

HISTORY

Dr. Willem Kolff, a Dutch physician, constructed the first working dialyzer in 1943 during the Nazi occupation of the Netherlands. Due to the scarcity of available resources, Kolff had to improvise and build the initial machine using sausage casings, beverage cans, a washing machine, and various other items that were available at the time. Over the following two years,[1943-1945] Kolff used his machine to treat 16 patients suffering from acute kidney failure, but the results were unsuccessful. Then, in 1945, a 67-year-old comatose woman regained consciousness following 11 hours of hemodialysis with the dialyzer, and lived for another seven years before dying from an unrelated condition. She was the first-ever patient successfully treated with dialysis.

PRINCIPLE

Dialysis works on the principles of the diffusion of solutes and ultrafiltration of fluid across a semi-permeable membrane. Diffusion is a property of substances in water; substances in water tend to move from an area of high concentration to an area of low concentration. Blood flows by one side of a semi-permeable membrane, and a dialysate, or special dialysis fluid, flows by the opposite side. A semipermeable membrane is a thin layer of material that contains holes of various sizes, or pores. Smaller solutes and fluid pass through the membrane, but the membrane blocks the passage of larger substances (for example, red blood cells, large proteins). This replicates the filtering process that takes place in the kidneys, when the blood enters the kidneys and the larger substances are separated from the smaller ones in the glomerulus.

The two main types of dialysis, hemodialysis and peritoneal dialysis, remove wastes and excess water from the blood in different ways. Hemodialysis removes wastes and water by circulating blood outside the body through an external filter, called a dialyzer, that contains a semipermeable membrane. The blood flows in one direction and the dialysate flows in the opposite. The counter-current flow of the blood and dialysate maximizes the concentration gradient of solutes between the blood and dialysate, which helps to remove more urea and creatinine from the blood. The concentrations of solutes (for example potassium, phosphorus, and urea) are undesirably high in the blood, but low or absent in the dialysis solution, and constant replacement of the dialysate ensures that the concentration of undesired solutes is kept low on this side of the membrane. The dialysis solution has levels of minerals like potassium and calcium that are similar to their natural concentration in healthy blood. For another solute, bicarbonate, dialysis solution level is set at a slightly higher level than in normal blood, to encourage diffusion of bicarbonate into the blood, to act as a pH buffer to neutralize the metabolic acidosis that is often present in these patients. The levels of the components of dialysate are typically prescribed by a nephrologist according to the needs of the individual patient.

In peritoneal dialysis, wastes and water are removed from the blood inside the body using the peritoneal membrane of the peritoneum as a natural semipermeable membrane. Wastes and excess water move from the blood, across the peritoneal membrane, and into a special dialysis solution, called dialysate, in the abdominal cavity which has a composition similar to the fluid portion of blood.

TYPES

There are three primary and two secondary types of dialysis: hemodialysis (primary), peritoneal dialysis (primary), hemofiltration (primary), hemodiafiltration (secondary), and intestinal dialysis (secondary).

Hemodialysis

In hemodialysis, the patient's blood is pumped through the blood compartment of a dialyzer, exposing it to a partially permeable membrane. The dialyzer is composed of thousands of tiny hollow synthetic fibers. The fiber wall acts as the semipermeable membrane. Blood flows through the fibers, dialysis solution flows around the outside of the fibers, and water and wastes move between these two solutions. The cleansed blood is then returned via the circuit back to the body. Ultrafiltration occurs by increasing the hydrostatic pressure across the dialyzer membrane. This usually is done by applying a negative pressure to the dialysate compartment of the dialyzer. This pressure gradient causes water and dissolved solutes to move from blood to dialysate, and allows the removal of several litres of excess fluid during a typical 4-hour treatment. In the United States, hemodialysis treatments are typically given in a dialysis center three times per week (due in the United States to Medicare reimbursement rules); however, as of 2007 over 2,500 people in the United States are dialyzing at home more frequently for various treatment lengths. Studies have demonstrated the clinical benefits of dialyzing 5 to 7 times a week, for 6 to 8 hours. This type of hemodialysis is usually called "nocturnal daily hemodialysis", which a study has shown a significant improvement in both small and large molecular weight clearance and decrease the requirement of taking phosphate binders. These frequent long treatments are often done at home while sleeping, but home dialysis is a flexible modality and schedules can be changed day to day, week to week. In general, studies have shown that both increased treatment length and frequency are clinically beneficial.

Hemo-dialysis was one of the most common procedures performed in U.S. hospitals in 2011, occurring in 909,000 stays (a rate of 29 stays per 10,000 population).

Peritoneal dialysis

In peritoneal dialysis, a sterile solution containing glucose (called dialysate) is run through a tube into the peritoneal cavity, the abdominal body cavity around the intestine, where the peritoneal membrane acts as a partially permeable membrane. The peritoneal membrane or peritoneum is a layer of tissue containing blood vessels that lines and surrounds the peritoneal, or abdominal, cavity and the internal abdominal organs (stomach, spleen, liver, and intestines). Diffusion and osmosis drive waste products and excess fluid through the peritoneum into the dialysate until the dialysate approaches equilibrium with the body's fluids. Then the dialysate is drained, discarded, and replaced with fresh dialysate.

This exchange is repeated 4-5 times per day; automatic systems can run more frequent exchange cycles overnight. Peritoneal dialysis is less efficient than hemodialysis, but because it is carried out for a longer period of time the net effect in terms of removal of waste products and of salt and water are similar to hemodialysis. Peritoneal dialysis is carried out at home by the patient, often without help. This frees patients from the routine of having to go to a dialysis clinic on a fixed schedule multiple times per week. Peritoneal dialysis can be performed with little to no specialized equipment (other than bags of fresh dialysate).

Hemofiltration

Hemofiltration is a similar treatment to hemodialysis, but it makes use of a different principle. The blood is pumped through a dialyzer or "hemofilter" as in dialysis, but no dialysate is used. A pressure gradient is applied; as a result, water moves across the very permeable membrane rapidly, "dragging" along with it many dissolved substances, including ones with large molecular weights, which are not cleared as well by hemodialysis. Salts and water lost from the blood during this process are replaced with a "substitution fluid" that is infused into the extracorporeal circuit during the treatment. Hemodiafiltration is the combining of hemodialysis and hemofiltration in one process.

Hemodiafiltration

Hemodiafiltration is a combination of hemodialysis and hemofiltration.

Intestinal dialysis

In intestinal dialysis, the diet is supplemented with soluble fibres such as acacia fibre, which is digested by bacteria in the colon. This bacterial growth increases the amount of nitrogen that is eliminated in fecal waste. An alternative approach utilizes the ingestion of 1 to 1.5 liters of non-absorbable solutions of polyethylene glycol or mannitol every fourth hour.

STARTING INDICATIONS

The decision to initiate dialysis or hemofiltration in patients with renal failure depends on several factors. These can be divided into acute or chronic indications.

  • Indications for dialysis in the patient with acute kidney injury are summarized with the vowel acronym of "AEIOU":
    • Acidemia from metabolic acidosis in situations in which correction with sodium bicarbonate is impractical or may result in fluid overload.
    • Electrolyte abnormality, such as severe hyperkalemia, especially when combined with AKI.
    • Intoxication, that is, acute poisoning with a dialyzable substance. These substances can be represented by the mnemonic SLIME: salicylic acid, lithium, isopropanol, magnesium-containing laxatives, and ethylene glycol.
    • Overload of fluid not expected to respond to treatment with diuretics
    • Uremia complications, such as pericarditis, encephalopathy, or gastrointestinal bleeding.
  • Chronic indications for dialysis:
    • Symptomatic renal failure.
    • Low glomerular filtration rate (GFR) (renal replacement therapy (RRT) often recommended to commence at a GFR of less than 10-15 mls/min/1.73m2). In diabetics, dialysis is started earlier.
    • Difficulty in medically controlling fluid overload, serum potassium, and/or serum phosphorus when the GFR is very low.

IMAGES

KIDNEY FAILURE & HEART FAILURE - Narsiah, Coal filler,SRP-1 Srirampur, Dist.Adilabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

The quantity of my urine decreased and my whole body started swelling for which I tried treatment at many specialists for about three months but in vain. Doctors said my heart and kidney were not functioning properly and in the X Ray my heart increased three times in size. I was so breathless that I was not able to sleep in lying posture and it was very difficult to walk for more than a few yards .I was forced to sleep in sitting posture for many weeks.

MODE OF RECOVERY AT NEW LIFE CENTRE

My urine output increased on the very next day of starting the treatment of Dr.Subhash Chandar and after four days I was able to lie down peacefully and in about 20 days the swelling of body disappeared. I have now resumed my work as a worker in SingareniColleries

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

In medicine, dialysis (from Greek dialusis,"διάλυσις", meaning dissolution, dia, meaning through, and lysis, meaning loosening or splitting) is a process for removing waste and excess water from the blood, and is used primarily as an artificial replacement for lost kidney function in people with renal failure. Dialysis may be used for those with an acute disturbance in kidney function (acute kidney injury, previously acute renal failure), or progressive but chronically worsening kidney function–a state known as chronic kidney disease stage 5 (previously chronic renal failure or end-stage renal disease). The latter form may develop over months or years, but in contrast to acute kidney injury is not usually reversible, and dialysis is regarded as a "holding measure" until a renal transplant can be performed, or sometimes as the only supportive measure in those for whom a transplant would be inappropriate.

The kidneys have important roles in maintaining health. When healthy, the kidneys maintain the body's internal equilibrium of water and minerals (sodium, potassium, chloride, calcium, phosphorus, magnesium, sulfate). The acidic metabolism end-products that the body cannot get rid of via respiration are also excreted through the kidneys. The kidneys also function as a part of the endocrine system, producing erythropoietin and calcitriol. Erythropoietin is involved in the production of red blood cells and calcitriol plays a role in bone formation. Dialysis is an imperfect treatment to replace kidney function because it does not correct the compromised endocrine functions of the kidney. Dialysis treatments replace some of these functions through diffusion (waste removal) and ultrafiltration (fluid removal).

HISTORY

Dr. Willem Kolff, a Dutch physician, constructed the first working dialyzer in 1943 during the Nazi occupation of the Netherlands. Due to the scarcity of available resources, Kolff had to improvise and build the initial machine using sausage casings, beverage cans, a washing machine, and various other items that were available at the time. Over the following two years,[1943-1945] Kolff used his machine to treat 16 patients suffering from acute kidney failure, but the results were unsuccessful. Then, in 1945, a 67-year-old comatose woman regained consciousness following 11 hours of hemodialysis with the dialyzer, and lived for another seven years before dying from an unrelated condition. She was the first-ever patient successfully treated with dialysis.

PRINCIPLE

Dialysis works on the principles of the diffusion of solutes and ultrafiltration of fluid across a semi-permeable membrane. Diffusion is a property of substances in water; substances in water tend to move from an area of high concentration to an area of low concentration. Blood flows by one side of a semi-permeable membrane, and a dialysate, or special dialysis fluid, flows by the opposite side. A semipermeable membrane is a thin layer of material that contains holes of various sizes, or pores. Smaller solutes and fluid pass through the membrane, but the membrane blocks the passage of larger substances (for example, red blood cells, large proteins). This replicates the filtering process that takes place in the kidneys, when the blood enters the kidneys and the larger substances are separated from the smaller ones in the glomerulus.

The two main types of dialysis, hemodialysis and peritoneal dialysis, remove wastes and excess water from the blood in different ways. Hemodialysis removes wastes and water by circulating blood outside the body through an external filter, called a dialyzer, that contains a semipermeable membrane. The blood flows in one direction and the dialysate flows in the opposite. The counter-current flow of the blood and dialysate maximizes the concentration gradient of solutes between the blood and dialysate, which helps to remove more urea and creatinine from the blood. The concentrations of solutes (for example potassium, phosphorus, and urea) are undesirably high in the blood, but low or absent in the dialysis solution, and constant replacement of the dialysate ensures that the concentration of undesired solutes is kept low on this side of the membrane. The dialysis solution has levels of minerals like potassium and calcium that are similar to their natural concentration in healthy blood. For another solute, bicarbonate, dialysis solution level is set at a slightly higher level than in normal blood, to encourage diffusion of bicarbonate into the blood, to act as a pH buffer to neutralize the metabolic acidosis that is often present in these patients. The levels of the components of dialysate are typically prescribed by a nephrologist according to the needs of the individual patient.

In peritoneal dialysis, wastes and water are removed from the blood inside the body using the peritoneal membrane of the peritoneum as a natural semipermeable membrane. Wastes and excess water move from the blood, across the peritoneal membrane, and into a special dialysis solution, called dialysate, in the abdominal cavity which has a composition similar to the fluid portion of blood.

TYPES

There are three primary and two secondary types of dialysis: hemodialysis (primary), peritoneal dialysis (primary), hemofiltration (primary), hemodiafiltration (secondary), and intestinal dialysis (secondary).

Hemodialysis

In hemodialysis, the patient's blood is pumped through the blood compartment of a dialyzer, exposing it to a partially permeable membrane. The dialyzer is composed of thousands of tiny hollow synthetic fibers. The fiber wall acts as the semipermeable membrane. Blood flows through the fibers, dialysis solution flows around the outside of the fibers, and water and wastes move between these two solutions. The cleansed blood is then returned via the circuit back to the body. Ultrafiltration occurs by increasing the hydrostatic pressure across the dialyzer membrane. This usually is done by applying a negative pressure to the dialysate compartment of the dialyzer. This pressure gradient causes water and dissolved solutes to move from blood to dialysate, and allows the removal of several litres of excess fluid during a typical 4-hour treatment. In the United States, hemodialysis treatments are typically given in a dialysis center three times per week (due in the United States to Medicare reimbursement rules); however, as of 2007 over 2,500 people in the United States are dialyzing at home more frequently for various treatment lengths. Studies have demonstrated the clinical benefits of dialyzing 5 to 7 times a week, for 6 to 8 hours. This type of hemodialysis is usually called "nocturnal daily hemodialysis", which a study has shown a significant improvement in both small and large molecular weight clearance and decrease the requirement of taking phosphate binders. These frequent long treatments are often done at home while sleeping, but home dialysis is a flexible modality and schedules can be changed day to day, week to week. In general, studies have shown that both increased treatment length and frequency are clinically beneficial.

Hemo-dialysis was one of the most common procedures performed in U.S. hospitals in 2011, occurring in 909,000 stays (a rate of 29 stays per 10,000 population).

Peritoneal dialysis

In peritoneal dialysis, a sterile solution containing glucose (called dialysate) is run through a tube into the peritoneal cavity, the abdominal body cavity around the intestine, where the peritoneal membrane acts as a partially permeable membrane. The peritoneal membrane or peritoneum is a layer of tissue containing blood vessels that lines and surrounds the peritoneal, or abdominal, cavity and the internal abdominal organs (stomach, spleen, liver, and intestines). Diffusion and osmosis drive waste products and excess fluid through the peritoneum into the dialysate until the dialysate approaches equilibrium with the body's fluids. Then the dialysate is drained, discarded, and replaced with fresh dialysate.

This exchange is repeated 4-5 times per day; automatic systems can run more frequent exchange cycles overnight. Peritoneal dialysis is less efficient than hemodialysis, but because it is carried out for a longer period of time the net effect in terms of removal of waste products and of salt and water are similar to hemodialysis. Peritoneal dialysis is carried out at home by the patient, often without help. This frees patients from the routine of having to go to a dialysis clinic on a fixed schedule multiple times per week. Peritoneal dialysis can be performed with little to no specialized equipment (other than bags of fresh dialysate).

Hemofiltration

Hemofiltration is a similar treatment to hemodialysis, but it makes use of a different principle. The blood is pumped through a dialyzer or "hemofilter" as in dialysis, but no dialysate is used. A pressure gradient is applied; as a result, water moves across the very permeable membrane rapidly, "dragging" along with it many dissolved substances, including ones with large molecular weights, which are not cleared as well by hemodialysis. Salts and water lost from the blood during this process are replaced with a "substitution fluid" that is infused into the extracorporeal circuit during the treatment. Hemodiafiltration is the combining of hemodialysis and hemofiltration in one process.

Hemodiafiltration

Hemodiafiltration is a combination of hemodialysis and hemofiltration.

Intestinal dialysis

In intestinal dialysis, the diet is supplemented with soluble fibres such as acacia fibre, which is digested by bacteria in the colon. This bacterial growth increases the amount of nitrogen that is eliminated in fecal waste. An alternative approach utilizes the ingestion of 1 to 1.5 liters of non-absorbable solutions of polyethylene glycol or mannitol every fourth hour.

STARTING INDICATIONS

The decision to initiate dialysis or hemofiltration in patients with renal failure depends on several factors. These can be divided into acute or chronic indications.

  • Indications for dialysis in the patient with acute kidney injury are summarized with the vowel acronym of "AEIOU":
    • Acidemia from metabolic acidosis in situations in which correction with sodium bicarbonate is impractical or may result in fluid overload.
    • Electrolyte abnormality, such as severe hyperkalemia, especially when combined with AKI.
    • Intoxication, that is, acute poisoning with a dialyzable substance. These substances can be represented by the mnemonic SLIME: salicylic acid, lithium, isopropanol, magnesium-containing laxatives, and ethylene glycol.
    • Overload of fluid not expected to respond to treatment with diuretics
    • Uremia complications, such as pericarditis, encephalopathy, or gastrointestinal bleeding.
  • Chronic indications for dialysis:
    • Symptomatic renal failure.
    • Low glomerular filtration rate (GFR) (renal replacement therapy (RRT) often recommended to commence at a GFR of less than 10-15 mls/min/1.73m2). In diabetics, dialysis is started earlier.
    • Difficulty in medically controlling fluid overload, serum potassium, and/or serum phosphorus when the GFR is very low.

IMAGES

RECURRENT KIDNEY STONES (EVEN AFTER 3 OPERATIONS) - Venkateshwar Rao, From Lalguda

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

Detected at the age of second month of her life. Cancer medicines were given for about two years after which the experts expressed their helplessness for want of any further curative or dependable drug.

MODE OF RECOVERY AT NEW LIFE CENTRE

She started taking our treatment during third year in Aug 2006.There was no evidence of any cancer cells in her blood in Nov.2008, after our treatment. Her cancer is cured and she is totally healthy now.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

In medicine, dialysis (from Greek dialusis,"διάλυσις", meaning dissolution, dia, meaning through, and lysis, meaning loosening or splitting) is a process for removing waste and excess water from the blood, and is used primarily as an artificial replacement for lost kidney function in people with renal failure. Dialysis may be used for those with an acute disturbance in kidney function (acute kidney injury, previously acute renal failure), or progressive but chronically worsening kidney function–a state known as chronic kidney disease stage 5 (previously chronic renal failure or end-stage renal disease). The latter form may develop over months or years, but in contrast to acute kidney injury is not usually reversible, and dialysis is regarded as a "holding measure" until a renal transplant can be performed, or sometimes as the only supportive measure in those for whom a transplant would be inappropriate.

The kidneys have important roles in maintaining health. When healthy, the kidneys maintain the body's internal equilibrium of water and minerals (sodium, potassium, chloride, calcium, phosphorus, magnesium, sulfate). The acidic metabolism end-products that the body cannot get rid of via respiration are also excreted through the kidneys. The kidneys also function as a part of the endocrine system, producing erythropoietin and calcitriol. Erythropoietin is involved in the production of red blood cells and calcitriol plays a role in bone formation. Dialysis is an imperfect treatment to replace kidney function because it does not correct the compromised endocrine functions of the kidney. Dialysis treatments replace some of these functions through diffusion (waste removal) and ultrafiltration (fluid removal).

HISTORY

Dr. Willem Kolff, a Dutch physician, constructed the first working dialyzer in 1943 during the Nazi occupation of the Netherlands. Due to the scarcity of available resources, Kolff had to improvise and build the initial machine using sausage casings, beverage cans, a washing machine, and various other items that were available at the time. Over the following two years,[1943-1945] Kolff used his machine to treat 16 patients suffering from acute kidney failure, but the results were unsuccessful. Then, in 1945, a 67-year-old comatose woman regained consciousness following 11 hours of hemodialysis with the dialyzer, and lived for another seven years before dying from an unrelated condition. She was the first-ever patient successfully treated with dialysis.

PRINCIPLE

Dialysis works on the principles of the diffusion of solutes and ultrafiltration of fluid across a semi-permeable membrane. Diffusion is a property of substances in water; substances in water tend to move from an area of high concentration to an area of low concentration. Blood flows by one side of a semi-permeable membrane, and a dialysate, or special dialysis fluid, flows by the opposite side. A semipermeable membrane is a thin layer of material that contains holes of various sizes, or pores. Smaller solutes and fluid pass through the membrane, but the membrane blocks the passage of larger substances (for example, red blood cells, large proteins). This replicates the filtering process that takes place in the kidneys, when the blood enters the kidneys and the larger substances are separated from the smaller ones in the glomerulus.

The two main types of dialysis, hemodialysis and peritoneal dialysis, remove wastes and excess water from the blood in different ways. Hemodialysis removes wastes and water by circulating blood outside the body through an external filter, called a dialyzer, that contains a semipermeable membrane. The blood flows in one direction and the dialysate flows in the opposite. The counter-current flow of the blood and dialysate maximizes the concentration gradient of solutes between the blood and dialysate, which helps to remove more urea and creatinine from the blood. The concentrations of solutes (for example potassium, phosphorus, and urea) are undesirably high in the blood, but low or absent in the dialysis solution, and constant replacement of the dialysate ensures that the concentration of undesired solutes is kept low on this side of the membrane. The dialysis solution has levels of minerals like potassium and calcium that are similar to their natural concentration in healthy blood. For another solute, bicarbonate, dialysis solution level is set at a slightly higher level than in normal blood, to encourage diffusion of bicarbonate into the blood, to act as a pH buffer to neutralize the metabolic acidosis that is often present in these patients. The levels of the components of dialysate are typically prescribed by a nephrologist according to the needs of the individual patient.

In peritoneal dialysis, wastes and water are removed from the blood inside the body using the peritoneal membrane of the peritoneum as a natural semipermeable membrane. Wastes and excess water move from the blood, across the peritoneal membrane, and into a special dialysis solution, called dialysate, in the abdominal cavity which has a composition similar to the fluid portion of blood.

TYPES

There are three primary and two secondary types of dialysis: hemodialysis (primary), peritoneal dialysis (primary), hemofiltration (primary), hemodiafiltration (secondary), and intestinal dialysis (secondary).

Hemodialysis

In hemodialysis, the patient's blood is pumped through the blood compartment of a dialyzer, exposing it to a partially permeable membrane. The dialyzer is composed of thousands of tiny hollow synthetic fibers. The fiber wall acts as the semipermeable membrane. Blood flows through the fibers, dialysis solution flows around the outside of the fibers, and water and wastes move between these two solutions. The cleansed blood is then returned via the circuit back to the body. Ultrafiltration occurs by increasing the hydrostatic pressure across the dialyzer membrane. This usually is done by applying a negative pressure to the dialysate compartment of the dialyzer. This pressure gradient causes water and dissolved solutes to move from blood to dialysate, and allows the removal of several litres of excess fluid during a typical 4-hour treatment. In the United States, hemodialysis treatments are typically given in a dialysis center three times per week (due in the United States to Medicare reimbursement rules); however, as of 2007 over 2,500 people in the United States are dialyzing at home more frequently for various treatment lengths. Studies have demonstrated the clinical benefits of dialyzing 5 to 7 times a week, for 6 to 8 hours. This type of hemodialysis is usually called "nocturnal daily hemodialysis", which a study has shown a significant improvement in both small and large molecular weight clearance and decrease the requirement of taking phosphate binders. These frequent long treatments are often done at home while sleeping, but home dialysis is a flexible modality and schedules can be changed day to day, week to week. In general, studies have shown that both increased treatment length and frequency are clinically beneficial.

Hemo-dialysis was one of the most common procedures performed in U.S. hospitals in 2011, occurring in 909,000 stays (a rate of 29 stays per 10,000 population).

Peritoneal dialysis

In peritoneal dialysis, a sterile solution containing glucose (called dialysate) is run through a tube into the peritoneal cavity, the abdominal body cavity around the intestine, where the peritoneal membrane acts as a partially permeable membrane. The peritoneal membrane or peritoneum is a layer of tissue containing blood vessels that lines and surrounds the peritoneal, or abdominal, cavity and the internal abdominal organs (stomach, spleen, liver, and intestines). Diffusion and osmosis drive waste products and excess fluid through the peritoneum into the dialysate until the dialysate approaches equilibrium with the body's fluids. Then the dialysate is drained, discarded, and replaced with fresh dialysate.

This exchange is repeated 4-5 times per day; automatic systems can run more frequent exchange cycles overnight. Peritoneal dialysis is less efficient than hemodialysis, but because it is carried out for a longer period of time the net effect in terms of removal of waste products and of salt and water are similar to hemodialysis. Peritoneal dialysis is carried out at home by the patient, often without help. This frees patients from the routine of having to go to a dialysis clinic on a fixed schedule multiple times per week. Peritoneal dialysis can be performed with little to no specialized equipment (other than bags of fresh dialysate).

Hemofiltration

Hemofiltration is a similar treatment to hemodialysis, but it makes use of a different principle. The blood is pumped through a dialyzer or "hemofilter" as in dialysis, but no dialysate is used. A pressure gradient is applied; as a result, water moves across the very permeable membrane rapidly, "dragging" along with it many dissolved substances, including ones with large molecular weights, which are not cleared as well by hemodialysis. Salts and water lost from the blood during this process are replaced with a "substitution fluid" that is infused into the extracorporeal circuit during the treatment. Hemodiafiltration is the combining of hemodialysis and hemofiltration in one process.

Hemodiafiltration

Hemodiafiltration is a combination of hemodialysis and hemofiltration.

Intestinal dialysis

In intestinal dialysis, the diet is supplemented with soluble fibres such as acacia fibre, which is digested by bacteria in the colon. This bacterial growth increases the amount of nitrogen that is eliminated in fecal waste. An alternative approach utilizes the ingestion of 1 to 1.5 liters of non-absorbable solutions of polyethylene glycol or mannitol every fourth hour.

STARTING INDICATIONS

The decision to initiate dialysis or hemofiltration in patients with renal failure depends on several factors. These can be divided into acute or chronic indications.

  • Indications for dialysis in the patient with acute kidney injury are summarized with the vowel acronym of "AEIOU":
    • Acidemia from metabolic acidosis in situations in which correction with sodium bicarbonate is impractical or may result in fluid overload.
    • Electrolyte abnormality, such as severe hyperkalemia, especially when combined with AKI.
    • Intoxication, that is, acute poisoning with a dialyzable substance. These substances can be represented by the mnemonic SLIME: salicylic acid, lithium, isopropanol, magnesium-containing laxatives, and ethylene glycol.
    • Overload of fluid not expected to respond to treatment with diuretics
    • Uremia complications, such as pericarditis, encephalopathy, or gastrointestinal bleeding.
  • Chronic indications for dialysis:
    • Symptomatic renal failure.
    • Low glomerular filtration rate (GFR) (renal replacement therapy (RRT) often recommended to commence at a GFR of less than 10-15 mls/min/1.73m2). In diabetics, dialysis is started earlier.
    • Difficulty in medically controlling fluid overload, serum potassium, and/or serum phosphorus when the GFR is very low.

IMAGES

  DISEASES OF RESPIRATORY SYSTEM (LUNGS, BRONCHUS, PLEURA)

RECURRENT COLD , COUGH, FEVER & ASTHAMA - Dhruv, Ramanthapur, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

My son used to suffer from recurrent attacks ofcold , cough, fever and asthmasince childhood.Consulted many doctors. Inhalers and antibiotics advised by them did not give any lasting relief-Rajesh

MODE OF RECOVERY AT NEW LIFE CENTRE

The cough and asthma subsided In just 10 days of starting treatment given by New Life. There is no recurrence of the trouble even in cold weather He has become more active and his concentration in studies has improved

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Asthma (from the Greek ἅσθμα, ásthma, "panting") is a common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction and bronchospasm. Common symptoms include wheezing, coughing, chest tightness, and shortness of breath.

Asthma is thought to be caused by a combination of genetic and environmental factors. Its diagnosis is usually based on the pattern of symptoms, response to therapy over time and spirometry. It is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate. Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic) where atopy refers to a predisposition toward developing type 1 hypersensitivity reactions.

Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist (such as salbutamol) and oral corticosteroids. In very severe cases, intravenous corticosteroids, magnesium sulfate, and hospitalization may be required. Symptoms can be prevented by avoiding triggers, such as allergens and irritants, and by the use of inhaled corticosteroids. Long-acting beta agonists (LABA) or leukotriene antagonists may be used in addition to inhaled corticosteroids if asthma symptoms remain uncontrolled. The occurrence of asthma has increased significantly since the 1970s. In 2011, 235–300 million people globally have been diagnosed with asthma, and it caused 250,000 deaths.

SIGNS AND SYMPTOMS

Asthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing. Sputum may be produced from the lung by coughing but is often hard to bring up. During recovery from an attack it may appear pus like due to high levels of white blood cells called eosinophils. Symptoms are usually worse at night and in the early morning or in response to exercise or cold air. Some people with asthma rarely experience symptoms, usually in response to triggers, whereas others may have marked and persistent symptoms.

Associated conditions

A number of other health conditions occur more frequently in those with asthma, including gastro-esophageal reflux disease (GERD), rhinosinusitis, and obstructive sleep apnea. Psychological disorders are also more common, with anxiety disorders occurring in between 16–52% and mood disorders in 14–41%. However, it is not known if asthma causes psychological problems or if psychological problems lead to asthma.

CAUSES

Asthma is caused by a combination of complex and incompletely understood environmental and genetic interactions. These factors influence both its severity and its responsiveness to treatment. It is believed that the recent increased rates of asthma are due to changing epigenetics (heritable factors other than those related to the DNA sequence) and a changing living environment.

Environmental

Many environmental factors have been associated with asthma's development and exacerbation including allergens, air pollution, and other environmental chemicals. Smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms. Low air quality from factors such as traffic pollution or high ozone levels, has been associated with both asthma development and increased asthma severity. Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association. Also, phthalates in PVC are associated with asthma in children and adults. There is an association between acetaminophen (paracetamol) use and asthma.[35] The majority of the evidence does not; however, support a causal role. Use by a mother during pregnancy is also associated with an increased risk.

Asthma is associated with exposure to indoor allergens. Common indoor allergens include: dust mites, cockroaches, animal dander, and mold. Efforts to decrease dust mites have been found to be ineffective. Certain viral respiratory infections, such as respiratory syncytial virus and rhinovirus, may increase the risk of developing asthma when acquired as young children. Certain other infections, however, may decrease the risk.

Hygiene hypothesis

The hygiene hypothesis attempts to explain the increased rates of asthma worldwide as a direct and unintended result of reduced exposure, during childhood, to non-pathogenic bacteria and viruses. It has been proposed that the reduced exposure to bacteria and viruses is due, in part, to increased cleanliness and decreased family size in modern societies. Exposure to bacterial endotoxin in early childhood may prevent the development of asthma, but exposure at an older age may provoke bronchoconstriction. Evidence supporting the hygiene hypothesis includes lower rates of asthma on farms and in households with pets.

Use of antibiotics in early life has been linked to the development of asthma. Also, delivery via caesarean section is associated with an increased risk (estimated at 20–80%) of asthma—this increased risk is attributed to the lack of healthy bacterial colonization that the newborn would have acquired from passage through the birth canal. There is a link between asthma and the degree of affluence.

Genetic

Family history is a risk factor for asthma, with many different genes being implicated. If one identical twin is affected, the probability of the other having the disease is approximately 25%. By the end of 2005, 25 genes had been associated with asthma in six or more separate populations, including GSTM1, IL10, CTLA-4, SPINK5, LTC4S, IL4R and ADAM33, among others. Many of these genes are related to the immune system or modulating inflammation. Even among this list of genes supported by highly replicated studies, results have not been consistent among all populations tested. In 2006 over 100 genes were associated with asthma in one genetic association study alone; more continue to be found.

Some genetic variants may only cause asthma when they are combined with specific environmental exposures. An example is a specific single nucleotide polymorphism in the CD14 region and exposure to endotoxin (a bacterial product). Endotoxin exposure can come from several environmental sources including tobacco smoke, dogs, and farms. Risk for asthma, then, is determined by both a person's genetics and the level of endotoxin exposure.

Medical conditions

A triad of atopic eczema, allergic rhinitis and asthma is called atopy. The strongest risk factor for developing asthma is a history of atopic disease; with asthma occurring at a much greater rate in those who have either eczema or hay fever. Asthma has been associated with Churg–Strauss syndrome, an autoimmune disease and vasculitis. Individuals with certain types of urticaria may also experience symptoms of asthma.

There is a correlation between obesity and the risk of asthma with both having increased in recent years. Several factors may be at play including decreased respiratory function due to a buildup of fat and the fact that adipose tissue leads to a pro-inflammatory state.

Beta blocker medications such as propranolol can trigger asthma in those who are susceptible. Cardioselective beta-blockers, however, appear safe in those with mild or moderate disease. Other medications that can cause problems are ASA, NSAIDs, and angiotensin-converting enzyme inhibitors.

Exacerbation

Some individuals will have stable asthma for weeks or months and then suddenly develop an episode of acute asthma. Different individuals react to various factors in different ways. Most individuals can develop severe exacerbation from a number of triggering agents.

Home factors that can lead to exacerbation of asthma include dust, animal dander (especially cat and dog hair), cockroach allergens and mold. Perfumes are a common cause of acute attacks in women and children. Both viral and bacterial infections of the upper respiratory tract can worsen the disease. Psychological stress may worsen symptoms—it is thought that stress alters the immune system and thus increases the airway inflammatory response to allergens and irritants.

PATHOPHYSIOLOGY

Asthma is the result of chronic inflammation of the airways which subsequently results in increased contractability of the surrounding smooth muscles. This among other factors leads to bouts of narrowing of the airway and the classic symptoms of wheezing. The narrowing is typically reversible with or without treatment. Occasionally the airways themselves change. Typical changes in the airways include an increase in eosinophils and thickening of the lamina reticularis. Chronically the airways' smooth muscle may increase in size along with an increase in the numbers of mucous glands. Other cell types involved include: T lymphocytes, macrophages, and neutrophils. There may also be involvement of other components of the immune system including: cytokines, chemokines, histamine, and leukotrienes among others.

DIAGNOSIS

While asthma is a well recognized condition, there is not one universal agreed upon definition. It is defined by the Global Initiative for Asthma as "a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation is associated with airway hyper-responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction within the lung that is often reversible either spontaneously or with treatment".

There is currently no precise test with the diagnosis typically based on the pattern of symptoms and response to therapy over time. A diagnosis of asthma should be suspected if there is a history of: recurrent wheezing, coughing or difficulty breathing and these symptoms occur or worsen due to exercise, viral infections, allergens or air pollution. Spirometry is then used to confirm the diagnosis. In children under the age of six the diagnosis is more difficult as they are too young for spirometry.

Spirometry

Spirometry is recommended to aid in diagnosis and management. It is the single best test for asthma. If the FEV1 measured by this technique improves more than 12% following administration of a bronchodilator such as salbutamol, this is supportive of the diagnosis. It however may be normal in those with a history of mild asthma, not currently acting up. As caffeine is a bronchodilator in people with asthma, the use of caffeine before a lung function test may interfere with the results. Single-breath diffusing capacity can help differentiate asthma from COPD. It is reasonable to perform spirometry every one or two years to follow how well a person's asthma is controlled.

Others

The methacholine challenge involves the inhalation of increasing concentrations of a substance that causes airway narrowing in those predisposed. If negative it means that a person does not have asthma; if positive, however, it is not specific for the disease.

Other supportive evidence includes: a ≥20% difference in peak expiratory flow rate on at least three days in a week for at least two weeks, a ≥20% improvement of peak flow following treatment with either salbutamol, inhaled corticosteroids or prednisone, or a ≥20% decrease in peak flow following exposure to a trigger. Testing peak expiratory flow is more variable than spirometry, however, and thus not recommended for routine diagnosis. It may be useful for daily self-monitoring in those with moderate to severe disease and for checking the effectiveness of new medications. It may also be helpful in guiding treatment in those with acute exacerbations.

CLASSIFICATION

Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate. Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic), based on whether symptoms are precipitated by allergens (atopic) or not (non-atopic). While asthma is classified based on severity, at the moment there is no clear method for classifying different subgroups of asthma beyond this system. Finding ways to identify subgroups that respond well to different types of treatments is a current critical goal of asthma research.

Although asthma is a chronic obstructive condition, it is not considered as a part of chronic obstructive pulmonary disease as this term refers specifically to combinations of disease that are irreversible such as bronchiectasis, chronic bronchitis, and emphysema. Unlike these diseases, the airway obstruction in asthma is usually reversible; however, if left untreated, the chronic inflammation from asthma can lead the lungs to become irreversibly obstructed due to airway remodeling. In contrast to emphysema, asthma affects the bronchi, not the alveoli.

Asthma exacerbation

An acute asthma exacerbation is commonly referred to as an asthma attack. The classic symptoms are shortness of breath, wheezing, and chest tightness. While these are the primary symptoms of asthma, some people present primarily with coughing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.

Signs which occur during an asthma attack include the use of accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest. A blue color of the skin and nails may occur from lack of oxygen.

In a mild exacerbation the peak expiratory flow rate (PEFR) is ≥200 L/min or ≥50% of the predicted best. Moderate is defined as between 80 and 200 L/min or 25% and 50% of the predicted best while severe is defined as ≤ 80 L/min or ≤25% of the predicted best.

Acute severe asthma, previously known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and corticosteroids. Half of cases are due to infections with others caused by allergen, air pollution, or insufficient or inappropriate medication use.

Brittle asthma is a kind of asthma distinguishable by recurrent, severe attacks. Type 1 brittle asthma is a disease with wide peak flow variability, despite intense medication. Type 2 brittle asthma is background well-controlled asthma with sudden severe exacerbations.

Exercise-induced

Exercise can trigger bronchoconstriction in both people with and without asthma. It occurs in most people with asthma and up to 20% of people without asthma. In athletes is diagnosed more commonly in elite athletes, with rates varying from 3% for bobsled racers to 50% for cycling and 60% for cross-country skiing. While it may occur with any weather conditions it is more common when it is dry and cold. Inhaled beta2-agonists do not appear to improve athletic performance among those without asthma however oral doses may improve endurance and strength.

Occupational

Asthma as a result of (or worsened by) workplace exposures, is a commonly reported occupational disease. Many cases however are not reported or recognized as such. It is estimated that 5–25% of asthma cases in adults are work–related. A few hundred different agents have been implicated with the most common being: isocyanates, grain and wood dust, colophony, soldering flux, latex, animals, and aldehydes. The employment associated with the highest risk of problems include: those who spray paint, bakers and those who process food, nurses, chemical workers, those who work with animals, welders, hairdressers and timber workers.

Differential diagnosis

Many other conditions can cause symptoms similar to those of asthma. In children, other upper airway diseases such as allergic rhinitis and sinusitis should be considered as well as other causes of airway obstruction including: foreign body aspiration, tracheal stenosis or laryngotracheomalacia, vascular rings, enlarged lymph nodes or neck masses. In adults, COPD, congestive heart failure, airway masses, as well as drug-induced coughing due to ACE inhibitors should be considered. In both populations vocal cord dysfunction may present similarly.

Chronic obstructive pulmonary disease can coexist with asthma and can occur as a complication of chronic asthma. After the age of 65 most people with obstructive airway disease will have asthma and COPD. In this setting, COPD can be differentiated by increased airway neutrophils, abnormally increased wall thickness, and increased smooth muscle in the bronchi. However, this level of investigation is not performed due to COPD and asthma sharing similar principles of management: corticosteroids, long acting beta agonists, and smoking cessation. It closely resembles asthma in symptoms, is correlated with more exposure to cigarette smoke, an older age, less symptom reversibility after bronchodilator administration, and decreased likelihood of family history of atopy.

PREVENTION

The evidence for the effectiveness of measures to prevent the development of asthma is weak. Some show promise including: limiting smoke exposure both in utero and after delivery, breastfeeding, and increased exposure to daycare or large families but none are well supported enough to be recommended for this indication. Early pet exposure may be useful. Results from exposure to pets at other times are inconclusive and it is only recommended that pets be removed from the home if a person has allergic symptoms to said pet. Dietary restrictions during pregnancy or when breast feeding have not been found to be effective and thus are not recommended. Reducing or eliminating compounds known to sensitive people from the work place may be effective. It is not clear if annual influenza vaccinations effects the risk of exacerbations. Immunization; however, is recommended by the World Health Organization.

MANAGEMENT

While there is no cure for asthma, symptoms can typically be improved. A specific, customized plan for proactively monitoring and managing symptoms should be created. This plan should include the reduction of exposure to allergens, testing to assess the severity of symptoms, and the usage of medications. The treatment plan should be written down and advise adjustments to treatment according to changes in symptoms.

The most effective treatment for asthma is identifying triggers, such as cigarette smoke, pets, or aspirin, and eliminating exposure to them. If trigger avoidance is insufficient, the use of medication is recommended. Pharmaceutical drugs are selected based on, among other things, the severity of illness and the frequency of symptoms. Specific medications for asthma are broadly classified into fast-acting and long-acting categories.

Bronchodilators are recommended for short-term relief of symptoms. In those with occasional attacks, no other medication is needed. If mild persistent disease is present (more than two attacks a week), low-dose inhaled corticosteroids or alternatively, an oral leukotriene antagonist or a mast cell stabilizer is recommended. For those who have daily attacks, a higher dose of inhaled corticosteroids is used. In a moderate or severe exacerbation, oral corticosteroids are added to these treatments.

Lifestyle modification

Avoidance of triggers is a key component of improving control and preventing attacks. The most common triggers include allergens, smoke (tobacco and other), air pollution, non selective beta-blockers, and sulfite-containing foods. Cigarette smoking and second-hand smoke (passive smoke) may reduce the effectiveness of medications such as corticosteroids. Laws that limit smoking decrease the number of people hospitalized for asthma. Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms. Overall exercise, however is beneficial in people with stable asthma.

Medications

Medications used to treat asthma are divided into two general classes: quick-relief medications used to treat acute symptoms; and long-term control medications used to prevent further exacerbation.[

Fast–acting
  • Short-acting beta2-adrenoceptor agonists (SABA), such as salbutamol (albuterol USAN) are the first line treatment for asthma symptoms. They are recommended before exercise in those with exercise induced symptoms.
  • Anticholinergic medications, such as ipratropium bromide, provide additional benefit when used in combination with SABA in those with moderate or severe symptoms. Anticholinergic bronchodilators can also be used if a person cannot tolerate a SABA.
  • Older, less selective adrenergic agonists, such as inhaled epinephrine, have similar efficacy to SABAs. They are however not recommended due to concerns regarding excessive cardiac stimulation.
Long–term control
  • Corticosteroids are generally considered the most effective treatment available for long-term control. Inhaled forms such as beclomethasone are usually used except in the case of severe persistent disease, in which oral corticosteroids may be needed. It is usually recommended that inhaled formulations be used once or twice daily, depending on the severity of symptoms.
  • Long-acting beta-adrenoceptor agonists (LABA) such as salmeterol and formoterol can improve asthma control, at least in adults, when given in combination with inhaled corticosteroids. In children this benefit is uncertain. When used without steroids they increase the risk of severe side-effects and even with corticosteroids they may slightly increase the risk.
  • Leukotriene antagonists (such as montelukast and zafirlukast) may be used in addition to inhaled corticosteroids, typically also in conjunction with LABA. Evidence is insufficient to support use in acute exacerbations. In children they appear to be of little benefit when added to inhaled steroids. In those under five years of age, they were the preferred add-on therapy after inhaled corticosteroids by the British Thoracic Society in 2009.
  • Mast cell stabilizers (such as cromolyn sodium) are another non-preferred alternative to corticosteroids.
Delivery methods

Medications are typically provided as metered-dose inhalers (MDIs) in combination with an asthma spacer or as a dry powder inhaler. The spacer is a plastic cylinder that mixes the medication with air, making it easier to receive a full dose of the drug. A nebulizer may also be used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms. However insufficient evidence is available to determine whether a difference exists in those with severe disease.

Adverse effects

Long-term use of inhaled corticosteroids at conventional doses carries a minor risk of adverse effects. Risks include the development of cataracts and a mild regression in stature.

Others
  • Oxygen to alleviate hypoxia if saturations fall below 92%.
  • Oral corticosteroid are recommended with five days of prednisone being the same 2 days of dexamethasone.
  • Magnesium sulfate intravenous treatment has been shown to provide a bronchodilating effect when used in addition to other treatment in severe acute asthma attacks.
  • Heliox, a mixture of helium and oxygen, may also be considered in severe unresponsive cases.
  • Intravenous salbutamol is not supported by available evidence and is thus used only in extreme cases.
  • Methylxanthines (such as theophylline) were once widely used, but do not add significantly to the effects of inhaled beta-agonists. Their use in acute exacerbations is controversial.
  • The dissociative anesthetic ketamine is theoretically useful if intubation and mechanical ventilation is needed in people who are approaching respiratory arrest; however, there is no evidence from clinical trials to support this.

For those with severe persistent asthma not controlled by inhaled corticosteroids and LABAs, bronchial thermoplasty may be an option. It involves the delivery of controlled thermal energy to the airway wall during a series of bronchoscopies. While it may increase exacerbation frequency in the first few months it appears to decrease the subsequent rate. Effects beyond one year are unknown. Evidence suggests that sublingual immunotherapy in those with both allergic rhinitis and asthma improve outcomes.

Alternative medicine

Many people with asthma, like those with other chronic disorders, use alternative treatments; surveys show that roughly 50% use some form of unconventional therapy. There is little data to support the effectiveness of most of these therapies. Evidence is insufficient to support the usage of Vitamin C. There is tentative support for its use in exercise induced brochospasm. Acupuncture is not recommended for the treatment as there is insufficient evidence to support its use. Air ionisers show no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.

"Manual therapies", including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic maneuvers, have insufficient evidence to support their use in treating asthma. The Buteyko breathing technique for controlling hyperventilation may result in a reduction in medications use however does not have any effect on lung function. Thus an expert panel felt that evidence was insufficient to support its use.

PROGNOSIS

The prognosis for asthma is generally good, especially for children with mild disease. Mortality has decreased over the last few decades due to better recognition and improvement in care. Globally it causes moderate or severe disability in 19.4 million people as of 2004 (16 million of which are in low and middle income countries). Of asthma diagnosed during childhood, half of cases will no longer carry the diagnosis after a decade. Airway remodeling is observed, but it is unknown whether these represent harmful or beneficial changes. Early treatment with corticosteroids seems to prevent or ameliorates a decline in lung function.

EPIDEMIOLOGY

As of 2011, 235–330 million people worldwide are affected by asthma, and approximately 250,000-345,000 people die per year from the disease. Rates vary between countries with prevalences between 1 and 18%. It is more common in developed than developing countries. One thus sees lower rates in Asia, Eastern Europe and Africa. Within developed countries it is more common in those who are economically disadvantaged while in contrast in developing countries it is more common in the affluent. The reason for these differences is not well known. Low and middle income countries make up more than 80% of the mortality.

While asthma is twice as common in boys as girls, severe asthma occurs at equal rates. In contrast adult women have a higher rate of asthma than men and it is more common in the young than the old.

Global rates of asthma have increased significantly between the 1960s and 2008 with it being recognized as a major public health problem since the 1970s. Rates of asthma have plateaued in the developed world since the mid-1990s with recent increases primarily in the developing world. Asthma affects approximately 7% of the population of the United States and 5% of people in the United Kingdom. Canada, Australia and New Zealand have rates of about 14–15%.

IMAGES

SEVERE COUGH WITH ASTHAMA IN MENTALLY RETARDED- Yadhagiri, Sanga Reddy

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

My son used to suffer from recurrent attacks ofcold , cough, fever and asthmasince childhood.Consulted many doctors. Inhalers and antibiotics advised by them did not give any lasting relief-Rajesh

MODE OF RECOVERY AT NEW LIFE CENTRE

The cough and asthma subsided In just 10 days of starting treatment given by New Life. There is no recurrence of the trouble even in cold weather He has become more active and his concentration in studies has improved

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Asthma (from the Greek ἅσθμα, ásthma, "panting") is a common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction and bronchospasm. Common symptoms include wheezing, coughing, chest tightness, and shortness of breath.

Asthma is thought to be caused by a combination of genetic and environmental factors. Its diagnosis is usually based on the pattern of symptoms, response to therapy over time and spirometry. It is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate. Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic) where atopy refers to a predisposition toward developing type 1 hypersensitivity reactions.

Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist (such as salbutamol) and oral corticosteroids. In very severe cases, intravenous corticosteroids, magnesium sulfate, and hospitalization may be required. Symptoms can be prevented by avoiding triggers, such as allergens and irritants, and by the use of inhaled corticosteroids. Long-acting beta agonists (LABA) or leukotriene antagonists may be used in addition to inhaled corticosteroids if asthma symptoms remain uncontrolled. The occurrence of asthma has increased significantly since the 1970s. In 2011, 235–300 million people globally have been diagnosed with asthma, and it caused 250,000 deaths.

SIGNS AND SYMPTOMS

Asthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing. Sputum may be produced from the lung by coughing but is often hard to bring up. During recovery from an attack it may appear pus like due to high levels of white blood cells called eosinophils. Symptoms are usually worse at night and in the early morning or in response to exercise or cold air. Some people with asthma rarely experience symptoms, usually in response to triggers, whereas others may have marked and persistent symptoms.

Associated conditions

A number of other health conditions occur more frequently in those with asthma, including gastro-esophageal reflux disease (GERD), rhinosinusitis, and obstructive sleep apnea. Psychological disorders are also more common, with anxiety disorders occurring in between 16–52% and mood disorders in 14–41%. However, it is not known if asthma causes psychological problems or if psychological problems lead to asthma.

CAUSES

Asthma is caused by a combination of complex and incompletely understood environmental and genetic interactions. These factors influence both its severity and its responsiveness to treatment. It is believed that the recent increased rates of asthma are due to changing epigenetics (heritable factors other than those related to the DNA sequence) and a changing living environment.

Environmental

Many environmental factors have been associated with asthma's development and exacerbation including allergens, air pollution, and other environmental chemicals. Smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms. Low air quality from factors such as traffic pollution or high ozone levels, has been associated with both asthma development and increased asthma severity. Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association. Also, phthalates in PVC are associated with asthma in children and adults. There is an association between acetaminophen (paracetamol) use and asthma.[35] The majority of the evidence does not; however, support a causal role. Use by a mother during pregnancy is also associated with an increased risk.

Asthma is associated with exposure to indoor allergens. Common indoor allergens include: dust mites, cockroaches, animal dander, and mold. Efforts to decrease dust mites have been found to be ineffective. Certain viral respiratory infections, such as respiratory syncytial virus and rhinovirus, may increase the risk of developing asthma when acquired as young children. Certain other infections, however, may decrease the risk.

Hygiene hypothesis

The hygiene hypothesis attempts to explain the increased rates of asthma worldwide as a direct and unintended result of reduced exposure, during childhood, to non-pathogenic bacteria and viruses. It has been proposed that the reduced exposure to bacteria and viruses is due, in part, to increased cleanliness and decreased family size in modern societies. Exposure to bacterial endotoxin in early childhood may prevent the development of asthma, but exposure at an older age may provoke bronchoconstriction. Evidence supporting the hygiene hypothesis includes lower rates of asthma on farms and in households with pets.

Use of antibiotics in early life has been linked to the development of asthma. Also, delivery via caesarean section is associated with an increased risk (estimated at 20–80%) of asthma—this increased risk is attributed to the lack of healthy bacterial colonization that the newborn would have acquired from passage through the birth canal. There is a link between asthma and the degree of affluence.

Genetic

Family history is a risk factor for asthma, with many different genes being implicated. If one identical twin is affected, the probability of the other having the disease is approximately 25%. By the end of 2005, 25 genes had been associated with asthma in six or more separate populations, including GSTM1, IL10, CTLA-4, SPINK5, LTC4S, IL4R and ADAM33, among others. Many of these genes are related to the immune system or modulating inflammation. Even among this list of genes supported by highly replicated studies, results have not been consistent among all populations tested. In 2006 over 100 genes were associated with asthma in one genetic association study alone; more continue to be found.

Some genetic variants may only cause asthma when they are combined with specific environmental exposures. An example is a specific single nucleotide polymorphism in the CD14 region and exposure to endotoxin (a bacterial product). Endotoxin exposure can come from several environmental sources including tobacco smoke, dogs, and farms. Risk for asthma, then, is determined by both a person's genetics and the level of endotoxin exposure.

Medical conditions

A triad of atopic eczema, allergic rhinitis and asthma is called atopy. The strongest risk factor for developing asthma is a history of atopic disease; with asthma occurring at a much greater rate in those who have either eczema or hay fever. Asthma has been associated with Churg–Strauss syndrome, an autoimmune disease and vasculitis. Individuals with certain types of urticaria may also experience symptoms of asthma.

There is a correlation between obesity and the risk of asthma with both having increased in recent years. Several factors may be at play including decreased respiratory function due to a buildup of fat and the fact that adipose tissue leads to a pro-inflammatory state.

Beta blocker medications such as propranolol can trigger asthma in those who are susceptible. Cardioselective beta-blockers, however, appear safe in those with mild or moderate disease. Other medications that can cause problems are ASA, NSAIDs, and angiotensin-converting enzyme inhibitors.

Exacerbation

Some individuals will have stable asthma for weeks or months and then suddenly develop an episode of acute asthma. Different individuals react to various factors in different ways. Most individuals can develop severe exacerbation from a number of triggering agents.

Home factors that can lead to exacerbation of asthma include dust, animal dander (especially cat and dog hair), cockroach allergens and mold. Perfumes are a common cause of acute attacks in women and children. Both viral and bacterial infections of the upper respiratory tract can worsen the disease. Psychological stress may worsen symptoms—it is thought that stress alters the immune system and thus increases the airway inflammatory response to allergens and irritants.

PATHOPHYSIOLOGY

Asthma is the result of chronic inflammation of the airways which subsequently results in increased contractability of the surrounding smooth muscles. This among other factors leads to bouts of narrowing of the airway and the classic symptoms of wheezing. The narrowing is typically reversible with or without treatment. Occasionally the airways themselves change. Typical changes in the airways include an increase in eosinophils and thickening of the lamina reticularis. Chronically the airways' smooth muscle may increase in size along with an increase in the numbers of mucous glands. Other cell types involved include: T lymphocytes, macrophages, and neutrophils. There may also be involvement of other components of the immune system including: cytokines, chemokines, histamine, and leukotrienes among others.

DIAGNOSIS

While asthma is a well recognized condition, there is not one universal agreed upon definition. It is defined by the Global Initiative for Asthma as "a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation is associated with airway hyper-responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction within the lung that is often reversible either spontaneously or with treatment".

There is currently no precise test with the diagnosis typically based on the pattern of symptoms and response to therapy over time. A diagnosis of asthma should be suspected if there is a history of: recurrent wheezing, coughing or difficulty breathing and these symptoms occur or worsen due to exercise, viral infections, allergens or air pollution. Spirometry is then used to confirm the diagnosis. In children under the age of six the diagnosis is more difficult as they are too young for spirometry.

Spirometry

Spirometry is recommended to aid in diagnosis and management. It is the single best test for asthma. If the FEV1 measured by this technique improves more than 12% following administration of a bronchodilator such as salbutamol, this is supportive of the diagnosis. It however may be normal in those with a history of mild asthma, not currently acting up. As caffeine is a bronchodilator in people with asthma, the use of caffeine before a lung function test may interfere with the results. Single-breath diffusing capacity can help differentiate asthma from COPD. It is reasonable to perform spirometry every one or two years to follow how well a person's asthma is controlled.

Others

The methacholine challenge involves the inhalation of increasing concentrations of a substance that causes airway narrowing in those predisposed. If negative it means that a person does not have asthma; if positive, however, it is not specific for the disease.

Other supportive evidence includes: a ≥20% difference in peak expiratory flow rate on at least three days in a week for at least two weeks, a ≥20% improvement of peak flow following treatment with either salbutamol, inhaled corticosteroids or prednisone, or a ≥20% decrease in peak flow following exposure to a trigger. Testing peak expiratory flow is more variable than spirometry, however, and thus not recommended for routine diagnosis. It may be useful for daily self-monitoring in those with moderate to severe disease and for checking the effectiveness of new medications. It may also be helpful in guiding treatment in those with acute exacerbations.

CLASSIFICATION

Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate. Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic), based on whether symptoms are precipitated by allergens (atopic) or not (non-atopic). While asthma is classified based on severity, at the moment there is no clear method for classifying different subgroups of asthma beyond this system. Finding ways to identify subgroups that respond well to different types of treatments is a current critical goal of asthma research.

Although asthma is a chronic obstructive condition, it is not considered as a part of chronic obstructive pulmonary disease as this term refers specifically to combinations of disease that are irreversible such as bronchiectasis, chronic bronchitis, and emphysema. Unlike these diseases, the airway obstruction in asthma is usually reversible; however, if left untreated, the chronic inflammation from asthma can lead the lungs to become irreversibly obstructed due to airway remodeling. In contrast to emphysema, asthma affects the bronchi, not the alveoli.

Asthma exacerbation

An acute asthma exacerbation is commonly referred to as an asthma attack. The classic symptoms are shortness of breath, wheezing, and chest tightness. While these are the primary symptoms of asthma, some people present primarily with coughing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.

Signs which occur during an asthma attack include the use of accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest. A blue color of the skin and nails may occur from lack of oxygen.

In a mild exacerbation the peak expiratory flow rate (PEFR) is ≥200 L/min or ≥50% of the predicted best. Moderate is defined as between 80 and 200 L/min or 25% and 50% of the predicted best while severe is defined as ≤ 80 L/min or ≤25% of the predicted best.

Acute severe asthma, previously known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and corticosteroids. Half of cases are due to infections with others caused by allergen, air pollution, or insufficient or inappropriate medication use.

Brittle asthma is a kind of asthma distinguishable by recurrent, severe attacks. Type 1 brittle asthma is a disease with wide peak flow variability, despite intense medication. Type 2 brittle asthma is background well-controlled asthma with sudden severe exacerbations.

Exercise-induced

Exercise can trigger bronchoconstriction in both people with and without asthma. It occurs in most people with asthma and up to 20% of people without asthma. In athletes is diagnosed more commonly in elite athletes, with rates varying from 3% for bobsled racers to 50% for cycling and 60% for cross-country skiing. While it may occur with any weather conditions it is more common when it is dry and cold. Inhaled beta2-agonists do not appear to improve athletic performance among those without asthma however oral doses may improve endurance and strength.

Occupational

Asthma as a result of (or worsened by) workplace exposures, is a commonly reported occupational disease. Many cases however are not reported or recognized as such. It is estimated that 5–25% of asthma cases in adults are work–related. A few hundred different agents have been implicated with the most common being: isocyanates, grain and wood dust, colophony, soldering flux, latex, animals, and aldehydes. The employment associated with the highest risk of problems include: those who spray paint, bakers and those who process food, nurses, chemical workers, those who work with animals, welders, hairdressers and timber workers.

Differential diagnosis

Many other conditions can cause symptoms similar to those of asthma. In children, other upper airway diseases such as allergic rhinitis and sinusitis should be considered as well as other causes of airway obstruction including: foreign body aspiration, tracheal stenosis or laryngotracheomalacia, vascular rings, enlarged lymph nodes or neck masses. In adults, COPD, congestive heart failure, airway masses, as well as drug-induced coughing due to ACE inhibitors should be considered. In both populations vocal cord dysfunction may present similarly.

Chronic obstructive pulmonary disease can coexist with asthma and can occur as a complication of chronic asthma. After the age of 65 most people with obstructive airway disease will have asthma and COPD. In this setting, COPD can be differentiated by increased airway neutrophils, abnormally increased wall thickness, and increased smooth muscle in the bronchi. However, this level of investigation is not performed due to COPD and asthma sharing similar principles of management: corticosteroids, long acting beta agonists, and smoking cessation. It closely resembles asthma in symptoms, is correlated with more exposure to cigarette smoke, an older age, less symptom reversibility after bronchodilator administration, and decreased likelihood of family history of atopy.

PREVENTION

The evidence for the effectiveness of measures to prevent the development of asthma is weak. Some show promise including: limiting smoke exposure both in utero and after delivery, breastfeeding, and increased exposure to daycare or large families but none are well supported enough to be recommended for this indication. Early pet exposure may be useful. Results from exposure to pets at other times are inconclusive and it is only recommended that pets be removed from the home if a person has allergic symptoms to said pet. Dietary restrictions during pregnancy or when breast feeding have not been found to be effective and thus are not recommended. Reducing or eliminating compounds known to sensitive people from the work place may be effective. It is not clear if annual influenza vaccinations effects the risk of exacerbations. Immunization; however, is recommended by the World Health Organization.

MANAGEMENT

While there is no cure for asthma, symptoms can typically be improved. A specific, customized plan for proactively monitoring and managing symptoms should be created. This plan should include the reduction of exposure to allergens, testing to assess the severity of symptoms, and the usage of medications. The treatment plan should be written down and advise adjustments to treatment according to changes in symptoms.

The most effective treatment for asthma is identifying triggers, such as cigarette smoke, pets, or aspirin, and eliminating exposure to them. If trigger avoidance is insufficient, the use of medication is recommended. Pharmaceutical drugs are selected based on, among other things, the severity of illness and the frequency of symptoms. Specific medications for asthma are broadly classified into fast-acting and long-acting categories.

Bronchodilators are recommended for short-term relief of symptoms. In those with occasional attacks, no other medication is needed. If mild persistent disease is present (more than two attacks a week), low-dose inhaled corticosteroids or alternatively, an oral leukotriene antagonist or a mast cell stabilizer is recommended. For those who have daily attacks, a higher dose of inhaled corticosteroids is used. In a moderate or severe exacerbation, oral corticosteroids are added to these treatments.

Lifestyle modification

Avoidance of triggers is a key component of improving control and preventing attacks. The most common triggers include allergens, smoke (tobacco and other), air pollution, non selective beta-blockers, and sulfite-containing foods. Cigarette smoking and second-hand smoke (passive smoke) may reduce the effectiveness of medications such as corticosteroids. Laws that limit smoking decrease the number of people hospitalized for asthma. Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms. Overall exercise, however is beneficial in people with stable asthma.

Medications

Medications used to treat asthma are divided into two general classes: quick-relief medications used to treat acute symptoms; and long-term control medications used to prevent further exacerbation.[

Fast–acting
  • Short-acting beta2-adrenoceptor agonists (SABA), such as salbutamol (albuterol USAN) are the first line treatment for asthma symptoms. They are recommended before exercise in those with exercise induced symptoms.
  • Anticholinergic medications, such as ipratropium bromide, provide additional benefit when used in combination with SABA in those with moderate or severe symptoms. Anticholinergic bronchodilators can also be used if a person cannot tolerate a SABA.
  • Older, less selective adrenergic agonists, such as inhaled epinephrine, have similar efficacy to SABAs. They are however not recommended due to concerns regarding excessive cardiac stimulation.
Long–term control
  • Corticosteroids are generally considered the most effective treatment available for long-term control. Inhaled forms such as beclomethasone are usually used except in the case of severe persistent disease, in which oral corticosteroids may be needed. It is usually recommended that inhaled formulations be used once or twice daily, depending on the severity of symptoms.
  • Long-acting beta-adrenoceptor agonists (LABA) such as salmeterol and formoterol can improve asthma control, at least in adults, when given in combination with inhaled corticosteroids. In children this benefit is uncertain. When used without steroids they increase the risk of severe side-effects and even with corticosteroids they may slightly increase the risk.
  • Leukotriene antagonists (such as montelukast and zafirlukast) may be used in addition to inhaled corticosteroids, typically also in conjunction with LABA. Evidence is insufficient to support use in acute exacerbations. In children they appear to be of little benefit when added to inhaled steroids. In those under five years of age, they were the preferred add-on therapy after inhaled corticosteroids by the British Thoracic Society in 2009.
  • Mast cell stabilizers (such as cromolyn sodium) are another non-preferred alternative to corticosteroids.
Delivery methods

Medications are typically provided as metered-dose inhalers (MDIs) in combination with an asthma spacer or as a dry powder inhaler. The spacer is a plastic cylinder that mixes the medication with air, making it easier to receive a full dose of the drug. A nebulizer may also be used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms. However insufficient evidence is available to determine whether a difference exists in those with severe disease.

Adverse effects

Long-term use of inhaled corticosteroids at conventional doses carries a minor risk of adverse effects. Risks include the development of cataracts and a mild regression in stature.

Others
  • Oxygen to alleviate hypoxia if saturations fall below 92%.
  • Oral corticosteroid are recommended with five days of prednisone being the same 2 days of dexamethasone.
  • Magnesium sulfate intravenous treatment has been shown to provide a bronchodilating effect when used in addition to other treatment in severe acute asthma attacks.
  • Heliox, a mixture of helium and oxygen, may also be considered in severe unresponsive cases.
  • Intravenous salbutamol is not supported by available evidence and is thus used only in extreme cases.
  • Methylxanthines (such as theophylline) were once widely used, but do not add significantly to the effects of inhaled beta-agonists. Their use in acute exacerbations is controversial.
  • The dissociative anesthetic ketamine is theoretically useful if intubation and mechanical ventilation is needed in people who are approaching respiratory arrest; however, there is no evidence from clinical trials to support this.

For those with severe persistent asthma not controlled by inhaled corticosteroids and LABAs, bronchial thermoplasty may be an option. It involves the delivery of controlled thermal energy to the airway wall during a series of bronchoscopies. While it may increase exacerbation frequency in the first few months it appears to decrease the subsequent rate. Effects beyond one year are unknown. Evidence suggests that sublingual immunotherapy in those with both allergic rhinitis and asthma improve outcomes.

Alternative medicine

Many people with asthma, like those with other chronic disorders, use alternative treatments; surveys show that roughly 50% use some form of unconventional therapy. There is little data to support the effectiveness of most of these therapies. Evidence is insufficient to support the usage of Vitamin C. There is tentative support for its use in exercise induced brochospasm. Acupuncture is not recommended for the treatment as there is insufficient evidence to support its use. Air ionisers show no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.

"Manual therapies", including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic maneuvers, have insufficient evidence to support their use in treating asthma. The Buteyko breathing technique for controlling hyperventilation may result in a reduction in medications use however does not have any effect on lung function. Thus an expert panel felt that evidence was insufficient to support its use.

PROGNOSIS

The prognosis for asthma is generally good, especially for children with mild disease. Mortality has decreased over the last few decades due to better recognition and improvement in care. Globally it causes moderate or severe disability in 19.4 million people as of 2004 (16 million of which are in low and middle income countries). Of asthma diagnosed during childhood, half of cases will no longer carry the diagnosis after a decade. Airway remodeling is observed, but it is unknown whether these represent harmful or beneficial changes. Early treatment with corticosteroids seems to prevent or ameliorates a decline in lung function.

EPIDEMIOLOGY

As of 2011, 235–330 million people worldwide are affected by asthma, and approximately 250,000-345,000 people die per year from the disease. Rates vary between countries with prevalences between 1 and 18%. It is more common in developed than developing countries. One thus sees lower rates in Asia, Eastern Europe and Africa. Within developed countries it is more common in those who are economically disadvantaged while in contrast in developing countries it is more common in the affluent. The reason for these differences is not well known. Low and middle income countries make up more than 80% of the mortality.

While asthma is twice as common in boys as girls, severe asthma occurs at equal rates. In contrast adult women have a higher rate of asthma than men and it is more common in the young than the old.

Global rates of asthma have increased significantly between the 1960s and 2008 with it being recognized as a major public health problem since the 1970s. Rates of asthma have plateaued in the developed world since the mid-1990s with recent increases primarily in the developing world. Asthma affects approximately 7% of the population of the United States and 5% of people in the United Kingdom. Canada, Australia and New Zealand have rates of about 14–15%.

IMAGES

  DISEASES OF EAR, NOSE AND THROAT

MENIERES SYNDROME - Anitha, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I developed abnormal sounds in my ears about five years ago. My hearing capacity also came down gradually. In addition, I Suffered periodically from distressing episodes of vomiting leading to giddiness and extreme weakness that necessitated frequent hospitalisation for administration of IV fluids. Consulted leading ENT surgeons and Neurophysicians. They investigated me fully and concluded that my condition was irreparable as the important structures in my ears got hardened. Their medicines could give me little or no relief for short periods only, leading to recurrence of the problem. My condition became miserable The episodes of vomiting and giddiness were more frequent , the abnormal sounds in my ears were distressing and unbearable and my capability to hear normal sounds was very poor.

MODE OF RECOVERY AT NEW LIFE CENTRE

It was a hopeless condition when I consulted New Life Homeo Care.
It has been two months now, since I started taking homeopathic treatment. The episodes of vomiting and giddiness have stopped fully. There was no need to take IV fluids any more. My hearing capability has improved by 50% and the abnormal sounds have also decreased by more than 50%. I am very happy. Thanks

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Ménière's disease also called endolymphatic hydrops, is a disorder of the inner ear that can affect hearing and balance to a varying degree. It is characterized by episodes of vertigo, low-pitched tinnitus, and hearing loss. The hearing loss is fluctuating rather than permanent, meaning that it comes and goes, alternating between ears for some time, then becomes permanent with no return to normal function. It is named after the French physician Prosper Ménière, who, in an article published in 1861, first reported that vertigo was caused by inner ear disorders. The condition affects people differently; it can range in intensity from being a mild annoyance to a lifelong condition.

SIGNS AND SYMPTOMS

Ménière's often begins with one symptom, and gradually progresses. However, not all symptoms must be present to confirm the diagnosis although several symptoms at once is more conclusive than different symptoms at separate times. Other conditions can present themselves with Ménière's-like symptoms, such as syphilis, Cogan's syndrome, autoimmune inner ear disease, dysautonomia, perilymph fistula, multiple sclerosis, acoustic neuroma, and both hypo- and hyperthyroidism.

The symptoms of Ménière's are variable; not all sufferers experience the same symptoms. However, so-called "classic Ménière's" is considered to have the following four symptoms:

  • Attacks of rotational vertigo that can be severe, incapacitating, unpredictable, and last anywhere from minutes to hours, but generally no longer than 24 hours. For some, prolonged attacks can occur, lasting from several days to several weeks, often causing the sufferer to be severely incapacitated. This combines with an increase in volume of tinnitus and temporary, albeit significant, hearing loss. Hearing may improve after an attack, but often becomes progressively worse. Nausea, vomiting, and sweating sometimes accompany vertigo, but are symptoms of vertigo, and not of Ménière's.
  • Fluctuating, progressive, unilateral (in one ear) or bilateral (in both ears) hearing loss, usually in lower frequencies. For some, sounds can appear tinny or distorted, and patients can experience unusual sensitivity to noises.
  • Unilateral or bilateral tinnitus.
  • A sensation of fullness or pressure in one or both ears.

Some may have parasympathetic symptoms, which aren't necessarily symptoms of Ménière's, but rather side effects from other symptoms. These are typically nausea, vomiting, and sweating which are typically symptoms of vertigo, and not of Ménière's. Vertigo may induce nystagmus, or uncontrollable rhythmical and jerky eye movements, usually in the horizontal plane, reflecting the essential role of non-visual balance in coordinating eye movements. Sudden, severe attacks of dizziness or vertigo, known informally as "drop attacks," can cause someone who is standing to suddenly fall. Drop attacks are likely to occur later in the disease, but can occur at any time.

Migraine

There is an increased prevalence of migraine in patients with Ménière’s disease, with some clinical samples showing about one third of patients experiencing migraines. An association with familial history of vestibular migraine has also been demonstrated.

CAUSES

Ménière's disease once was considered idiopathic, but it is now believed to be linked to endolymphatic hydrops, an excess of fluid in the inner ear. It is thought that endolymphatic fluid bursts from its normal channels in the ear and flows into other areas, causing damage. This is called "hydrops." The membranous labyrinth, a system of membranes in the ear, contains a fluid called endolymph. The membranes can become dilated like a balloon when pressure increases and drainage is blocked. This may be related to swelling of the endolymphatic sac or other tissues in the vestibular system of the inner ear, which is responsible for the body's sense of balance. In some cases, the endolymphatic duct may be obstructed by scar tissue, or may be narrow from birth. In some cases there may be too much fluid secreted by the stria vascularis. The symptoms may occur in the presence of a middle ear infection, head trauma, or an upper respiratory tract infection, or by using aspirin, smoking cigarettes, or drinking alcohol. They may be further exacerbated by excessive consumption of salt in some patients. It has also been proposed that Ménière's symptoms in many patients are caused by the deleterious effects of a herpes virus.

Ménière's disease affects about 190 people per 100,000. Recent gender predominance studies show that Ménière's tends to affect women more often than men. Age of onset typically occurs in adult years, with prevalence increasing with age.

Recent research has found that Ménière's disease may potentially be influenced and worsened by obstructive sleep apnea, and that risk factors for reduced vascular function in the brain such as smoking, migraines, and atherosclerosis may play an important role in triggering attacks.

DIAGNOSIS

Doctors establish a diagnosis with complaints and medical history. However, a detailed otolaryngological examination, audiometry, and head MRI scan should be performed to exclude a vestibular schwannoma or superior canal dehiscence which would cause similar symptoms. Some of the same symptoms also occur with benign paroxysmal positional vertigo (BPPV), and with cervical spondylosis (which can affect blood supply to the brain and cause vertigo). There is no definitive test for Ménière's; it is only diagnosed when all other causes have been ruled out. If any cause had been discovered, this would eliminate Ménière's disease, as by its very definition, as an exclusively idiopathic disease—it has no known cause.

MANAGEMENT

Several environmental and dietary changes are thought to reduce the frequency or severity of symptom outbreaks. It is believed that since high salt diets cause water retention, it can lead to an increase (or at least preventing the decrease) of fluid within the inner ear, although the relationship between salt and the inner ear is not fully understood. High-salt intake is thought to alter the concentrations of fluid in the inner ear and Ménière's episodes could be accelerated by high-salt binges. Recommended salt intake is often around one to two grams per day. One source recommends taking two grams of potassium or more daily. Diuretics have traditionally been prescribed to facilitate a low sodium diet although there is no definite supportive evidence.

Additionally, patients may be advised to avoid alcohol, caffeine, and tobacco, all of which can aggravate symptoms of Ménière's. Many patients will have allergy testing done to see if they are candidates for allergy desensitization, as allergies have been shown to aggravate Ménière's symptoms.

Both prescription and over-the-counter medicine can be used to reduce nausea and vomiting during an episode. Included are antihistamines such as meclozine or dimenhydrinate, trimethobenzamide and other antiemetics, betahistine, diazepam, or ginger root. Betahistine, specifically, is of note because it is the only drug listed that has been proposed to prevent symptoms due to its vasodilation effect on the inner ear.

The antiherpes virus drug acyclovir has been used with some success to treat Ménière's disease. The likelihood of the effectiveness of the treatment was found to decrease with increasing duration of the disease, probably because viral suppression does not reverse damage. Morphological changes to the inner ear of Ménière's sufferers have also been found in which it was considered likely to have resulted from attack by a herpes simplex virus. It was considered possible that long term treatment with acyclovir (greater than six months) would be required to produce an appreciable effect on symptoms. Herpes viruses have the ability to remain dormant in nerve cells by a process known as HHV Latency Associated Transcript. Continued administration of the drug should prevent reactivation of the virus and allow for the possibility of an improvement of symptoms. Another consideration is that different strains of a herpes virus can have different characteristics which may result in differences in the precise effects of the virus. Further confirmation that acyclovir can have a positive effect on Ménière's symptoms has been reported.

Studies done over the use of transtympanic micropressure pulses have indicated promise with patients who had not been previously treated by gentamicin or surgery. Other studies suggest less clear results and propose that micropressure devices are simply placebos.

Coping

Sufferers tend to have high stress and anxiety due to the unpredictable nature of the disease. Some patients benefit from non-specific yoga, t'ai chi, and meditation. Greenberg and Nedzelski recommend education to alleviate feelings of depression or helplessness.

Surgery

If symptoms do not improve with typical treatment, more permanent surgery is considered. Unfortunately, because the inner ear deals with both balance and hearing, few surgeries guarantee no hearing loss.

Nondestructive surgeries include those which do not actively remove any functionality, but rather aim to improve the way the ear works. Intratympanic steroid treatments involve injecting steroids (commonly dexamethasone) into the middle ear in order to reduce inflammation and alter inner ear circulation. Surgery to decompress the endolymphatic sac has shown to be effective for temporary relief from symptoms. Most patients see a decrease in vertigo occurrence, while their hearing may be unaffected. This treatment, however, does not address the long-term course of vertigo in Ménière's disease and may require repeated surgery. Danish studies even link this surgery to a very strong placebo effect, and that very little difference occurred in a 9-year followup, but could not deny the efficacy of the treatment.

Conversely, destructive surgeries are irreversible and involve removing entire functionality of most, if not all, of the affected ear. The inner ear itself can be surgically removed via labyrinthectomy although hearing is always completely lost in the affected ear with this operation. Alternatively, a chemical labyrinthectomy, in which a drug (such as gentamicin) that "kills" the vestibular apparatus is injected into the middle ear can accomplish the same results while retaining hearing. In more serious cases surgeons can cut the nerve to the balance portion of the inner ear in a vestibular neurectomy. Hearing is often mostly preserved, however the surgery involves cutting open into the lining of the brain, and a hospital stay of a few days for monitoring would be required. Vertigo (and the associated nausea and vomiting) typically accompany the recovery from destructive surgeries as the brain learns to compensate.

Physiotherapy

Physiotherapists also have a role in the management of Ménière's disease. In vestibular rehabilitation, physiotherapists use interventions aimed at stabilizing gaze, reducing dizziness and increasing postural balance within the context of activities of daily living. After a vestibular assessment is conducted, the physiotherapist tailors the treatment plan to the needs of that specific patient.

The central nervous system (CNS) can be re-trained because of its plasticity, or alterability, as well as its repetitious pathways. During vestibular rehabilitation, physiotherapists take advantage of this characteristic of the CNS by provoking symptoms of dizziness or unsteadiness with head movements while allowing the visual, somatosensory and vestibular systems to interpret the information. This leads to a continuous decrease in symptoms.

Although a significant amount of research has been done regarding vestibular rehabilitation in other disorders, substantially less has been done specifically on Ménière's disease. However, vestibular physiotherapy is currently accepted as part of best practices in the management of this condition.

The Merck Manual has added head trauma as a risk factor due to the research on 300 Ménière's patients over the past fourteen years. Michael Burcon, BPh, DC has established a link between whiplash as a result of vehicular accidents or falling on one's head and Ménière's disease. It takes an average of fifteen years after the trauma before the onset of symptoms. Case history, thermography, MRI, CScan, and/or cervical x-ray and modified Prill relative leg length tests are used for diagnosis and upper cervical specific adjustments are performed for treatment to reduce or eliminate vertigo.

PROGNOSIS

Ménière's disease usually starts confined to one ear, but it often extends to involve both ears over time. The number of patients who end up with bilaterial Ménière's is debated, with ranges spanning from 17% to 75%.

Some Ménière's disease sufferers, in severe cases, may end up losing their jobs, and will be on disability until the disease burns out. However, a majority (60-80%) of sufferers will not need permanent disability and will recover with or without medical help.

Hearing loss usually fluctuates in the beginning stages and becomes more permanent in later stages, although hearing aids and cochlear implants can help remedy damage. Tinnitus can be unpredictable, but patients usually get used to it over time.

Ménière's disease, being unpredictable, has a variable prognosis. Attacks could come more frequently and more severely, less frequently and less severely, and anywhere in between. However, Ménière's is known to "burn out" when vestibular function has been destroyed to a stage where vertigo attacks cease.

Studies done on both right and left ear sufferers show that patients with their right ear affected tend to do significantly worse in cognitive performance. General intelligence was not hindered, and it was concluded that declining performance was related to how long the patient had been suffering from the disease.

IMAGES

CASE RECORD

  DISEASES OF SKIN, HAIR AND NAILS

VITILIGO - LUEKODERMA - Saraswathi, Karimnagar

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I had longstanding white patches over my neck, chest and upper eyelids. The patches were also there over the front aspect of my elbows and knees. I consulted some skin specialists of Karimnagar. There was no change. The doctors expressed their helplessness. Many said that the disease has no cure.

MODE OF RECOVERY AT NEW LIFE CENTRE

Later I took homeopathic treatment from Dr.Subhash Chandar of Mancherial. Many of my patches have disappeared with his medicines. Only 2% of the disease is left and that is here over my neck.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Leukoderma is a cutaneous condition, an acquired condition with localized loss of pigmentation of the skin that may occur after any number of inflammatory skin conditions, burns, intralesional steroid injections, postdermabrasion, etc.

TRADITIONAL THERAPY

Leukoderma is a cutaneous condition, an acquired condition with localized loss of pigmentation of the skin that may occur after any number of inflammatory skin conditions, burns, intralesional steroid injections, postdermabrasion, etc. The change in appearance caused by Vitiligo can affect a person's emotional and psychological well-being and may create difficulty in getting or keeping a job. People with this disorder can experience emotional stress, particularly if Vitiligo develops on visible areas of the body, such as the face, hands, arms, feet, or on the genitals. Talking & chatting with other people who have Vitiligo may also help a person cope.

CAUSES

The cause of vitiligo is unknown, but research suggests that it may arise from autoimmunea condition in which immune system of body destroys its own cells & tissues, genetic, stress. The incidence worldwide is less than 1%. The most common form is non-segmental vitiligo, which tends to appear in symmetric patches, sometimes over large areas of the body. Excessive mental worry, presence of parasites in alimentary canal and mostly improper hygiene too may also be considered to be one of the causes according to Ayurveda. An example of this is ‘virudh ahar sevan’ (as fish & milk together) forms toxic substances which gradually destroys body’s own immunity system. While referring about Leucoderma, it generally appears due to some external accidental causes, which may be a burn, a cut or an ulcer. These external factors basically damage the cells beneath skin, which produce ‘melanin’ pigment. It results to diminished skin colour patches, which later converts white and prominent, forming white patches. Exact cause of Vitiligo remains unknown. However, there are different theories suggesting autoimmune syndrome (a condition whereby the immune system of body destroys body’s own tissues & cells), impaired hepatic function as jaundice, gastric disorder, typhoid fever etc. It is neither infectious nor contagious, it is only a cosmetic problem & it tarnishes the beauty of the human body.

Treatment

The bael fruit is traditionally used to treat this condition. Milk intake to be lowered also. Studies have shown that immunomodulator creams such as Protopic and Elidel also cause repigmentation in some cases, when used with UVB narrowband treatments. A 1997 report suggests that combining vitamin B12 and folic acid supplements with sun exposure caused repigmentation in 52% of cases.

IMAGES

  VIRAL DISEASES

DENGUE FEVER - V.Vignesh s/o - RAJU, Engineer, BSNL, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

My son aged about 8 months suddenly developed fever with vomiting, after admission in a speciality hospital, he was diagnosed as a case of Dengue fever and developed complications like water in lungs and abdomen and unconsciousness. Platelets were transfused. His condition was declared critical.

MODE OF RECOVERY AT NEW LIFE CENTRE

Then we approached Dr.Subhash Chandar. He started his treatment with the consent of the attending consultant. The fever subsided in just one day of starting his treatment and the boy became conscious and active and all the rubber connections like oxygen, IV feeding were removed .There was no need to give platelets again. Dr Subhash Chandar’s treatment has given a new life to my son-.Mr.Raju, AE,BSNL

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Dengue fever , also known as breakbone fever, is a mosquito-borne tropical disease caused by the dengue virus. Symptoms include fever, headache, muscle and joint pains, and a characteristic skin rash that is similar to measles. In a small proportion of cases the disease develops into the life-threatening dengue hemorrhagic fever, resulting in bleeding, low levels of blood platelets and blood plasma leakage, or into dengue shock syndrome, where dangerously low blood pressure occurs.

Dengue is transmitted by several species of mosquito within the genus Aedes, principally A. aegypti. The virus has five different types; infection with one type usually gives lifelong immunity to that type, but only short-term immunity to the others. Subsequent infection with a different type increases the risk of severe complications. As there is no commercially available vaccine, prevention is sought by reducing the habitat and the number of mosquitoes and limiting exposure to bites.

Treatment of acute dengue is supportive, using either oral or intravenous rehydration for mild or moderate disease, and intravenous fluids and blood transfusion for more severe cases. The number of cases of dengue fever has increased dramatically since the 1960s, with between 50 and 528 million people infected yearly. Early descriptions of the condition date from 1779, and its viral cause and the transmission were figured out in the early 20th century. Dengue has become a global problem since the Second World War and is endemic in more than 110 countries. Apart from eliminating the mosquitoes, work is ongoing on a vaccine, as well as medication targeted directly at the virus.

SIGNS AND SYMPTOMS

Typically, people infected with dengue virus are asymptomatic (80%) or only have mild symptoms such as an uncomplicated fever. Others have more severe illness (5%), and in a small proportion it is life-threatening. The incubation period (time between exposure and onset of symptoms) ranges from 3–14 days, but most often it is 4–7 days. Therefore, travelers returning from endemic areas are unlikely to have dengue if fever or other symptoms start more than 14 days after arriving home. Children often experience symptoms similar to those of the common cold and gastroenteritis (vomiting and diarrhea) and have a greater risk of severe complications, though initial symptoms are generally mild but include high fever.

CLINICAL COURSE

The characteristic symptoms of dengue are sudden-onset fever, headache (typically located behind the eyes), muscle and joint pains, and a rash. The alternative name for dengue, "breakbone fever", comes from the associated muscle and joint pains. The course of infection is divided into three phases: febrile, critical, and recovery.

The febrile phase involves high fever, potentially over 40 °C (104 °F), and is associated with generalized pain and a headache; this usually lasts two to seven days. Nausea and vomiting may also occur. A rash occurs in 50–80% of those with symptoms in the first or second day of symptoms as flushed skin, or later in the course of illness (days 4–7), as a measles-like rash. A rash described as "islands of white in a sea of red" has also been described. Some petechiae (small red spots that do not disappear when the skin is pressed, which are caused by broken capillaries) can appear at this point, as may some mild bleeding from the mucous membranes of the mouth and nose. The fever itself is classically biphasic or saddleback in nature, breaking and then returning for one or two days.

In some people, the disease proceeds to a critical phase as fever resolves. During this period there is leakage of plasma from the blood vessels which typically lasts one to two days. This may result in fluid accumulation in the chest and abdominal cavity as well as depletion of fluid from the circulation and decreased blood supply to vital organs. There may also be organ dysfunction and severe bleeding, typically from the gastrointestinal tract. Shock (dengue shock syndrome) and hemorrhage (dengue hemorrhagic fever) occur in less than 5% of all cases of dengue, however those who have previously been infected with other serotypes of dengue virus ("secondary infection") are at an increased risk. This critical phase, while rare, occurs relatively more commonly in children and young adults.

The recovery phase occurs next, with resorption of the leaked fluid into the bloodstream. This usually lasts two to three days. The improvement is often striking, and can be accompanied with severe itching and a slow heart rate. Another rash may occur with either a maculopapular or a vasculitic appearance, which is followed by peeling of the skin. During this stage, a fluid overload state may occur; if it affects the brain, it may cause a reduced level of consciousness or seizures. A feeling of fatigue may last for weeks in adults.

Associated problems

Dengue can occasionally affect several other body systems, either in isolation or along with the classic dengue symptoms. A decreased level of consciousness occurs in 0.5–6% of severe cases, which is attributable either to inflammation of the brain by the virus or indirectly as a result of impairment of vital organs, for example, the liver.

Other neurological disorders have been reported in the context of dengue, such as transverse myelitis and Guillain-Barré syndrome. Infection of the heart and acute liver failure are among the rarer complications.

CAUSES

Dengue fever virus (DENV) is an RNA virus of the family Flaviviridae; genus Flavivirus. Other members of the same genus include yellow fever virus, West Nile virus, St. Louis encephalitis virus, Japanese encephalitis virus, tick-borne encephalitis virus, Kyasanur forest disease virus, and Omsk hemorrhagic fever virus. Most are transmitted by arthropods (mosquitoes or ticks), and are therefore also referred to as arboviruses (arthropod-borne viruses).

The dengue virus genome (genetic material) contains about 11,000 nucleotide bases, which code for the three different types of protein molecules (C, prM and E) that form the virus particle and seven other types of protein molecules (NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5) that are only found in infected host cells and are required for replication of the virus. There are five strains of the virus, called serotypes, of which the first four are referred to as DENV-1, DENV-2, DENV-3 and DENV-4. The distinctions between the serotypes is based on the their antigenicity.

Transmission

Dengue virus is primarily transmitted by Aedes mosquitoes, particularly A. aegypti. These mosquitoes usually live between the latitudes of 35° North and 35° South below an elevation of 1,000 metres (3,300 ft). They typically bite during the day, particularly in the early morning and in the evening, but they are able to bite and thus spread infection at any time of day all during the year. Other Aedes species that transmit the disease include A. albopictus, A. polynesiensis and A. scutellaris. Humans are the primary host of the virus, but it also circulates in nonhuman primates. An infection can be acquired via a single bite. A female mosquito that takes a blood meal from a person infected with dengue fever, during the initial 2–10 day febrile period, becomes itself infected with the virus in the cells lining its gut. About 8–10 days later, the virus spreads to other tissues including the mosquito's salivary glands and is subsequently released into its saliva. The virus seems to have no detrimental effect on the mosquito, which remains infected for life. Aedes aegypti prefers to lay its eggs in artificial water containers, to live in close proximity to humans, and to feed on people rather than other vertebrates.

Dengue can also be transmitted via infected blood products and through organ donation. In countries such as Singapore, where dengue is endemic, the risk is estimated to be between 1.6 and 6 per 10,000 transfusions. Vertical transmission (from mother to child) during pregnancy or at birth has been reported. Other person-to-person modes of transmission have also been reported, but are very unusual. The genetic variation in dengue viruses is region specific, suggestive that establishment into new territories is relatively infrequent, despite dengue emerging in new regions in recent decades.

Predisposition

Severe disease is more common in babies and young children, and in contrast to many other infections it is more common in children that are relatively well nourished. Other risk factors for severe disease include female sex, high body mass index, and viral load. While each serotype can cause the full spectrum of disease, virus strain is a risk factor. Infection with one serotype is thought to produce lifelong immunity to that type, but only short term protection against the other three. The risk of severe disease from secondary infection increases if someone previously exposed to serotype DENV-1 contracts serotype DENV-2 or DENV-3, or if someone previously exposed to DENV-3 acquires DENV-2. Dengue can be life-threatening in people with chronic diseases such as diabetes and asthma.

Polymorphisms (normal variations) in particular genes have been linked with an increased risk of severe dengue complications. Examples include the genes coding for the proteins known as TNFα, mannan-binding lectin, CTLA4, TGFβ, DC-SIGN, PLCE1, and particular forms of human leukocyte antigen from gene variations of HLA-B. A common genetic abnormality in Africans, known as glucose-6-phosphate dehydrogenase deficiency, appears to increase the risk. Polymorphisms in the genes for the vitamin D receptor and FcγR seem to offer protection against severe disease in secondary dengue infection.

MECHANISM

When a mosquito carrying dengue virus bites a person, the virus enters the skin together with the mosquito's saliva. It binds to and enters white blood cells, and reproduces inside the cells while they move throughout the body. The white blood cells respond by producing a number of signaling proteins, such as cytokines and interferons, which are responsible for many of the symptoms, such as the fever, the flu-like symptoms and the severe pains. In severe infection, the virus production inside the body is greatly increased, and many more organs (such as the liver and the bone marrow) can be affected. Fluid from the bloodstream leaks through the wall of small blood vessels into body cavities due to capillary permeability. As a result, less blood circulates in the blood vessels, and the blood pressure becomes so low that it cannot supply sufficient blood to vital organs. Furthermore, dysfunction of the bone marrow due to infection of the stromal cells leads to reduced numbers of platelets, which are necessary for effective blood clotting; this increases the risk of bleeding, the other major complication of dengue fever.

Viral replication

Once inside the skin, dengue virus binds to Langerhans cells (a population of dendritic cells in the skin that identifies pathogens). The virus enters the cells through binding between viral proteins and membrane proteins on the Langerhans cell, specifically the C-type lectins called DC-SIGN, mannose receptor and CLEC5A. DC-SIGN, a non-specific receptor for foreign material on dendritic cells, seems to be the main point of entry. The dendritic cell moves to the nearest lymph node. Meanwhile, the virus genome is translated in membrane-bound vesicles on the cell's endoplasmic reticulum, where the cell's protein synthesis apparatus produces new viral proteins that replicate the viral RNA and begin to form viral particles. Immature virus particles are transported to the Golgi apparatus, the part of the cell where some of the proteins receive necessary sugar chains (glycoproteins). The now mature new viruses bud on the surface of the infected cell and are released by exocytosis. They are then able to enter other white blood cells, such as monocytes and macrophages.

The initial reaction of infected cells is to produce interferon, a cytokine that raises a number of defenses against viral infection through the innate immune system by augmenting the production of a large group of proteins mediated by the JAK-STAT pathway. Some serotypes of dengue virus appear to have mechanisms to slow down this process. Interferon also activates the adaptive immune system, which leads to the generation of antibodies against the virus as well as T cells that directly attack any cell infected with the virus. Various antibodies are generated; some bind closely to the viral proteins and target them for phagocytosis (ingestion by specialized cells and destruction), but some bind the virus less well and appear instead to deliver the virus into a part of the phagocytes where it is not destroyed but is able to replicate further.

Severe disease

It is not entirely clear why secondary infection with a different strain of dengue virus places people at risk of dengue hemorrhagic fever and dengue shock syndrome. The most widely accepted hypothesis is that of antibody-dependent enhancement (ADE). The exact mechanism behind ADE is unclear. It may be caused by poor binding of non-neutralizing antibodies and delivery into the wrong compartment of white blood cells that have ingested the virus for destruction. There is a suspicion that ADE is not the only mechanism underlying severe dengue-related complications, and various lines of research have implied a role for T cells and soluble factors such as cytokines and the complement system.

Severe disease is marked by the problems of capillary permeability (an allowance of fluid and protein normally contained within blood to pass) and disordered blood clotting. These changes appear associated with a disordered state of the endothelial glycocalyx, which acts as a molecular filter of blood components. Leaky capillaries (and the critical phase) are thought to be caused by an immune system response. Other processes of interest include infected cells that become necrotic—which affect both coagulation and fibrinolysis (the opposing systems of blood clotting and clot degradation)—and low platelets in the blood, also a factor in normal clotting.

DIAGNOSIS

The diagnosis of dengue is typically made clinically, on the basis of reported symptoms and physical examination; this applies especially in endemic areas. However, early disease can be difficult to differentiate from other viral infections. A probable diagnosis is based on the findings of fever plus two of the following: nausea and vomiting, rash, generalized pains, low white blood cell count, positive tourniquet test, or any warning sign (see table) in someone who lives in an endemic area. Warning signs typically occur before the onset of severe dengue. The tourniquet test, which is particularly useful in settings where no laboratory investigations are readily available, involves the application of a blood pressure cuff at between the diastolic and systolic pressure for five minutes, followed by the counting of any petechial hemorrhages; a higher number makes a diagnosis of dengue more likely with the cut off being more than 10 to 20 per 1 inch2 (6.25 cm2).

The diagnosis should be considered in anyone who develops a fever within two weeks of being in the tropics or subtropics. It can be difficult to distinguish dengue fever and chikungunya, a similar viral infection that shares many symptoms and occurs in similar parts of the world to dengue. Often, investigations are performed to exclude other conditions that cause similar symptoms, such as malaria, leptospirosis, viral hemorrhagic fever, typhoid fever, meningococcal disease, measles, and influenza.

The earliest change detectable on laboratory investigations is a low white blood cell count, which may then be followed by low platelets and metabolic acidosis. A moderately elevated level of aminotransferase (AST and ALT) from the liver is commonly associated with low platelets and white blood cells. In severe disease, plasma leakage results in hemoconcentration (as indicated by a rising hematocrit) and hypoalbuminemia. Pleural effusions or ascites can be detected by physical examination when large, but the demonstration of fluid on ultrasound may assist in the early identification of dengue shock syndrome. The use of ultrasound is limited by lack of availability in many settings. Dengue shock syndrome is present if pulse pressure drops to ≤ 20 mm Hg along with peripheral vascular collapse. Peripheral vascular collapse is determined in children via delayed capillary refill, rapid heart rate, or cold extremities.

CLASSIFICATION

The World Health Organization's 2009 classification divides dengue fever into two groups: uncomplicated and severe. This replaces the 1997 WHO classification, which needed to be simplified as it had been found to be too restrictive, though the older classification is still widely used including by the World Health Organization's Regional Office for South-East Asia as of 2011. Severe dengue is defined as that associated with severe bleeding, severe organ dysfunction, or severe plasma leakage while all other cases are uncomplicated. The 1997 classification divided dengue into undifferentiated fever, dengue fever, and dengue hemorrhagic fever. Dengue hemorrhagic fever was subdivided further into grades I–IV. Grade I is the presence only of easy bruising or a positive tourniquet test in someone with fever, grade II is the presence of spontaneous bleeding into the skin and elsewhere, grade III is the clinical evidence of shock, and grade IV is shock so severe that blood pressure and pulse cannot be detected. Grades III and IV are referred to as "dengue shock syndrome".

Laboratory tests

The diagnosis of dengue fever may be confirmed by microbiological laboratory testing. This can be done by virus isolation in cell cultures, nucleic acid detection by PCR, viral antigen detection (such as for NS1) or specific antibodies (serology). Virus isolation and nucleic acid detection are more accurate than antigen detection, but these tests are not widely available due to their greater cost. Detection of NS1 during the febrile phase of a primary infection may be greater than 90% however is only 60–80% in subsequent infections. All tests may be negative in the early stages of the disease. PCR and viral antigen detection are more accurate in the first seven days. In 2012 a PCR test was introduced that can run on equipment used to diagnose influenza; this is likely to improve access to PCR-based diagnosis.

These laboratory tests are only of diagnostic value during the acute phase of the illness with the exception of serology. Tests for dengue virus-specific antibodies, types IgG and IgM, can be useful in confirming a diagnosis in the later stages of the infection. Both IgG and IgM are produced after 5–7 days. The highest levels (titres) of IgM are detected following a primary infection, but IgM is also produced in reinfection. IgM becomes undetectable 30–90 days after a primary infection, but earlier following re-infections. IgG, by contrast, remains detectable for over 60 years and, in the absence of symptoms, is a useful indicator of past infection. After a primary infection IgG reaches peak levels in the blood after 14–21 days. In subsequent re-infections, levels peak earlier and the titres are usually higher. Both IgG and IgM provide protective immunity to the infecting serotype of the virus. The laboratory test for IgG and IgM antibodies can cross-react with other flaviviruses and may result in a false positive after recent infections or vaccinations with yellow fever virus or Japanese encephalitis. The detection of IgG alone is not considered diagnostic unless blood samples are collected 14 days apart and a greater than fourfold increase in levels of specific IgG is detected. In a person with symptoms, the detection of IgM is considered diagnostic.

PREVENTION

There are no approved vaccines for the dengue virus. Prevention thus depends on control of and protection from the bites of the mosquito that transmits it. The World Health Organization recommends an Integrated Vector Control program consisting of five elements:

  • Advocacy, social mobilization and legislation to ensure that public health bodies and communities are strengthened;
  • Collaboration between the health and other sectors (public and private);
  • An integrated approach to disease control to maximize use of resources;
  • Evidence-based decision making to ensure any interventions are targeted appropriately; and
  • Capacity-building to ensure an adequate response to the local situation.

The primary method of controlling A. aegypti is by eliminating its habitats. This is done by getting rid of open sources of water, or if this is not possible, by adding insecticides or biological control agents to these areas. Generalized spraying with organophosphate or pyrethroid insecticides, while sometimes done, is not thought to be effective. Reducing open collections of water through environmental modification is the preferred method of control, given the concerns of negative health effects from insecticides and greater logistical difficulties with control agents. People can prevent mosquito bites by wearing clothing that fully covers the skin, using mosquito netting while resting, and/or the application of insect repellent (DEET being the most effective). However, these methods appear not to be sufficiently effective, as the frequency of outbreaks appears to be increasing in some areas, probably due to urbanization increasing the habitat of A. aegypti. The range of the disease appears to be expanding possibly due to climate change.

MANAGEMENT

There are no specific antiviral drugs for dengue, however maintaining proper fluid balance is important. Treatment depends on the symptoms. Those who are able to drink, are passing urine, have no "warning signs" and are otherwise healthy can be managed at home with daily follow up and oral rehydration therapy. Those who have other health problems, have "warning signs" or who cannot manage regular follow up should be cared for in hospital. In those with severe dengue care should be provided in an area where there is access to an intensive care unit.

Intravenous hydration, if required, is typically only needed for one or two days. The rate of fluid administration is titrated to a urinary output of 0.5–1 mL/kg/h, stable vital signs and normalization of hematocrit. The smallest amount of fluid required to achieve this is recommended. Invasive medical procedures such as nasogastric intubation, intramuscular injections and arterial punctures are avoided, in view of the bleeding risk. Paracetamol (acetaminophen) is used for fever and discomfort while NSAIDs such as ibuprofen and aspirin are avoided as they might aggravate the risk of bleeding. Blood transfusion is initiated early in people presenting with unstable vital signs in the face of a decreasing hematocrit, rather than waiting for the hemoglobin concentration to decrease to some predetermined "transfusion trigger" level. Packed red blood cells or whole blood are recommended, while platelets and fresh frozen plasma are usually not. Corticosteroids do not appear to affect outcomes and may cause harm, thus are not recommended.

During the recovery phase intravenous fluids are discontinued to prevent a state of fluid overload. If fluid overload occurs and vital signs are stable, stopping further fluid may be all that is needed. If a person is outside of the critical phase, a loop diuretic such as furosemide may be used to eliminate excess fluid from the circulation.

EPIDEMIOLOGY

Most people with dengue recover without any ongoing problems. The mortality is 1–5% without treatment, and less than 1% with adequate treatment; however severe disease carries a mortality of 26%. Dengue is endemic in more than 110 countries. It infects 50 to 528 million people worldwide a year, leading to half a million hospitalizations, and approximately 25,000 deaths. For the decade of the 2000s, 12 countries in Southeast Asia were estimated to have about 3 million infections and 6,000 deaths annually. It is reported in at least 22 countries in Africa; but is likely present in all of them with 20% of the population at risk.

Infections are most commonly acquired in the urban environment. In recent decades, the expansion of villages, towns and cities in endemic areas, and the increased mobility of people has increased the number of epidemics and circulating viruses. Dengue fever, which was once confined to Southeast Asia, has now spread to Southern China, countries in the Pacific Ocean and America, and might pose a threat to Europe.

Rates of dengue increased 30 fold between 1960 and 2010. This increase is believed to be due to a combination of urbanization, population growth, increased international travel, and global warming. The geographical distribution is around the equator with 70% of the total 2.5 billion people living in endemic areas from Asia and the Pacific. An infection with dengue is second only to malaria as a diagnosed cause of fever among returning travelers. It is the most common viral disease transmitted by arthropods, and has a disease burden estimated at 1,600 disability-adjusted life years per million population. The World Health Organization counts dengue as one of seventeen neglected tropical diseases.

Like most arboviruses, dengue virus is maintained in nature in cycles that involve preferred blood-sucking vectors and vertebrate hosts. The viruses are maintained in the forests of Southeast Asia and Africa by transmission from female Aedes mosquitoes—of species other than A. aegypti—to her offspring and to lower primates. In towns and cities, the virus is primarily transmitted by the highly domesticated A. aegypti. In rural settings the virus is transmitted to humans by A. aegypti and other species of Aedes such as A. albopictus. Both these species have had expanding ranges in the second half of the 20th century. In all settings the infected lower primates or humans greatly increase the number of circulating dengue viruses, in a process called amplification.

IMAGES

CASE RECORD

DENGUE FEVER - Manish s/o - KISHORE, DCTO, Hyderabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

This is my son. One day he developed fever with rash, cold and cough, gradually he became weak and semiconscious. The Child specialist confirmed it as Dengue and declared his condition as critical and Started administering platelets.

MODE OF RECOVERY AT NEW LIFE CENTRE

My relatives who recently recovered with homeopathy from a similar attack advised us to approach Dr.Subhash. Dr.Subhash visited the patient and gave a single dose of homeopathy in the night.
Next morning the fever disappeared and my son was found healthy and active. His platelet count has also risen to 2,36,000. It was a fast and safe recovery.
My relatives and the attending doctor were astonished to observe this fast and wonderful recovery.
Other children suffering from Dengue were still in the same hospital for weeks together spending huge sums of money towards platelet administration etc. We were discharged on fourth day only I thank Dr Subhash very much for his excellent and free treatment. I sincerely wish that his treatment reaches all sections of people.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Dengue fever , also known as breakbone fever, is a mosquito-borne tropical disease caused by the dengue virus. Symptoms include fever, headache, muscle and joint pains, and a characteristic skin rash that is similar to measles. In a small proportion of cases the disease develops into the life-threatening dengue hemorrhagic fever, resulting in bleeding, low levels of blood platelets and blood plasma leakage, or into dengue shock syndrome, where dangerously low blood pressure occurs.

Dengue is transmitted by several species of mosquito within the genus Aedes, principally A. aegypti. The virus has five different types; infection with one type usually gives lifelong immunity to that type, but only short-term immunity to the others. Subsequent infection with a different type increases the risk of severe complications. As there is no commercially available vaccine, prevention is sought by reducing the habitat and the number of mosquitoes and limiting exposure to bites.

Treatment of acute dengue is supportive, using either oral or intravenous rehydration for mild or moderate disease, and intravenous fluids and blood transfusion for more severe cases. The number of cases of dengue fever has increased dramatically since the 1960s, with between 50 and 528 million people infected yearly. Early descriptions of the condition date from 1779, and its viral cause and the transmission were figured out in the early 20th century. Dengue has become a global problem since the Second World War and is endemic in more than 110 countries. Apart from eliminating the mosquitoes, work is ongoing on a vaccine, as well as medication targeted directly at the virus.

SIGNS AND SYMPTOMS

Typically, people infected with dengue virus are asymptomatic (80%) or only have mild symptoms such as an uncomplicated fever. Others have more severe illness (5%), and in a small proportion it is life-threatening. The incubation period (time between exposure and onset of symptoms) ranges from 3–14 days, but most often it is 4–7 days. Therefore, travelers returning from endemic areas are unlikely to have dengue if fever or other symptoms start more than 14 days after arriving home. Children often experience symptoms similar to those of the common cold and gastroenteritis (vomiting and diarrhea) and have a greater risk of severe complications, though initial symptoms are generally mild but include high fever.

CLINICAL COURSE

The characteristic symptoms of dengue are sudden-onset fever, headache (typically located behind the eyes), muscle and joint pains, and a rash. The alternative name for dengue, "breakbone fever", comes from the associated muscle and joint pains. The course of infection is divided into three phases: febrile, critical, and recovery.

The febrile phase involves high fever, potentially over 40 °C (104 °F), and is associated with generalized pain and a headache; this usually lasts two to seven days. Nausea and vomiting may also occur. A rash occurs in 50–80% of those with symptoms in the first or second day of symptoms as flushed skin, or later in the course of illness (days 4–7), as a measles-like rash. A rash described as "islands of white in a sea of red" has also been described. Some petechiae (small red spots that do not disappear when the skin is pressed, which are caused by broken capillaries) can appear at this point, as may some mild bleeding from the mucous membranes of the mouth and nose. The fever itself is classically biphasic or saddleback in nature, breaking and then returning for one or two days.

In some people, the disease proceeds to a critical phase as fever resolves. During this period there is leakage of plasma from the blood vessels which typically lasts one to two days. This may result in fluid accumulation in the chest and abdominal cavity as well as depletion of fluid from the circulation and decreased blood supply to vital organs. There may also be organ dysfunction and severe bleeding, typically from the gastrointestinal tract. Shock (dengue shock syndrome) and hemorrhage (dengue hemorrhagic fever) occur in less than 5% of all cases of dengue, however those who have previously been infected with other serotypes of dengue virus ("secondary infection") are at an increased risk. This critical phase, while rare, occurs relatively more commonly in children and young adults.

The recovery phase occurs next, with resorption of the leaked fluid into the bloodstream. This usually lasts two to three days. The improvement is often striking, and can be accompanied with severe itching and a slow heart rate. Another rash may occur with either a maculopapular or a vasculitic appearance, which is followed by peeling of the skin. During this stage, a fluid overload state may occur; if it affects the brain, it may cause a reduced level of consciousness or seizures. A feeling of fatigue may last for weeks in adults.

Associated problems

Dengue can occasionally affect several other body systems, either in isolation or along with the classic dengue symptoms. A decreased level of consciousness occurs in 0.5–6% of severe cases, which is attributable either to inflammation of the brain by the virus or indirectly as a result of impairment of vital organs, for example, the liver.

Other neurological disorders have been reported in the context of dengue, such as transverse myelitis and Guillain-Barré syndrome. Infection of the heart and acute liver failure are among the rarer complications.

CAUSES

Dengue fever virus (DENV) is an RNA virus of the family Flaviviridae; genus Flavivirus. Other members of the same genus include yellow fever virus, West Nile virus, St. Louis encephalitis virus, Japanese encephalitis virus, tick-borne encephalitis virus, Kyasanur forest disease virus, and Omsk hemorrhagic fever virus. Most are transmitted by arthropods (mosquitoes or ticks), and are therefore also referred to as arboviruses (arthropod-borne viruses).

The dengue virus genome (genetic material) contains about 11,000 nucleotide bases, which code for the three different types of protein molecules (C, prM and E) that form the virus particle and seven other types of protein molecules (NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5) that are only found in infected host cells and are required for replication of the virus. There are five strains of the virus, called serotypes, of which the first four are referred to as DENV-1, DENV-2, DENV-3 and DENV-4. The distinctions between the serotypes is based on the their antigenicity.

Transmission

Dengue virus is primarily transmitted by Aedes mosquitoes, particularly A. aegypti. These mosquitoes usually live between the latitudes of 35° North and 35° South below an elevation of 1,000 metres (3,300 ft). They typically bite during the day, particularly in the early morning and in the evening, but they are able to bite and thus spread infection at any time of day all during the year. Other Aedes species that transmit the disease include A. albopictus, A. polynesiensis and A. scutellaris. Humans are the primary host of the virus, but it also circulates in nonhuman primates. An infection can be acquired via a single bite. A female mosquito that takes a blood meal from a person infected with dengue fever, during the initial 2–10 day febrile period, becomes itself infected with the virus in the cells lining its gut. About 8–10 days later, the virus spreads to other tissues including the mosquito's salivary glands and is subsequently released into its saliva. The virus seems to have no detrimental effect on the mosquito, which remains infected for life. Aedes aegypti prefers to lay its eggs in artificial water containers, to live in close proximity to humans, and to feed on people rather than other vertebrates.

Dengue can also be transmitted via infected blood products and through organ donation. In countries such as Singapore, where dengue is endemic, the risk is estimated to be between 1.6 and 6 per 10,000 transfusions. Vertical transmission (from mother to child) during pregnancy or at birth has been reported. Other person-to-person modes of transmission have also been reported, but are very unusual. The genetic variation in dengue viruses is region specific, suggestive that establishment into new territories is relatively infrequent, despite dengue emerging in new regions in recent decades.

Predisposition

Severe disease is more common in babies and young children, and in contrast to many other infections it is more common in children that are relatively well nourished. Other risk factors for severe disease include female sex, high body mass index, and viral load. While each serotype can cause the full spectrum of disease, virus strain is a risk factor. Infection with one serotype is thought to produce lifelong immunity to that type, but only short term protection against the other three. The risk of severe disease from secondary infection increases if someone previously exposed to serotype DENV-1 contracts serotype DENV-2 or DENV-3, or if someone previously exposed to DENV-3 acquires DENV-2. Dengue can be life-threatening in people with chronic diseases such as diabetes and asthma.

Polymorphisms (normal variations) in particular genes have been linked with an increased risk of severe dengue complications. Examples include the genes coding for the proteins known as TNFα, mannan-binding lectin, CTLA4, TGFβ, DC-SIGN, PLCE1, and particular forms of human leukocyte antigen from gene variations of HLA-B. A common genetic abnormality in Africans, known as glucose-6-phosphate dehydrogenase deficiency, appears to increase the risk. Polymorphisms in the genes for the vitamin D receptor and FcγR seem to offer protection against severe disease in secondary dengue infection.

MECHANISM

When a mosquito carrying dengue virus bites a person, the virus enters the skin together with the mosquito's saliva. It binds to and enters white blood cells, and reproduces inside the cells while they move throughout the body. The white blood cells respond by producing a number of signaling proteins, such as cytokines and interferons, which are responsible for many of the symptoms, such as the fever, the flu-like symptoms and the severe pains. In severe infection, the virus production inside the body is greatly increased, and many more organs (such as the liver and the bone marrow) can be affected. Fluid from the bloodstream leaks through the wall of small blood vessels into body cavities due to capillary permeability. As a result, less blood circulates in the blood vessels, and the blood pressure becomes so low that it cannot supply sufficient blood to vital organs. Furthermore, dysfunction of the bone marrow due to infection of the stromal cells leads to reduced numbers of platelets, which are necessary for effective blood clotting; this increases the risk of bleeding, the other major complication of dengue fever.

Viral replication

Once inside the skin, dengue virus binds to Langerhans cells (a population of dendritic cells in the skin that identifies pathogens). The virus enters the cells through binding between viral proteins and membrane proteins on the Langerhans cell, specifically the C-type lectins called DC-SIGN, mannose receptor and CLEC5A. DC-SIGN, a non-specific receptor for foreign material on dendritic cells, seems to be the main point of entry. The dendritic cell moves to the nearest lymph node. Meanwhile, the virus genome is translated in membrane-bound vesicles on the cell's endoplasmic reticulum, where the cell's protein synthesis apparatus produces new viral proteins that replicate the viral RNA and begin to form viral particles. Immature virus particles are transported to the Golgi apparatus, the part of the cell where some of the proteins receive necessary sugar chains (glycoproteins). The now mature new viruses bud on the surface of the infected cell and are released by exocytosis. They are then able to enter other white blood cells, such as monocytes and macrophages.

The initial reaction of infected cells is to produce interferon, a cytokine that raises a number of defenses against viral infection through the innate immune system by augmenting the production of a large group of proteins mediated by the JAK-STAT pathway. Some serotypes of dengue virus appear to have mechanisms to slow down this process. Interferon also activates the adaptive immune system, which leads to the generation of antibodies against the virus as well as T cells that directly attack any cell infected with the virus. Various antibodies are generated; some bind closely to the viral proteins and target them for phagocytosis (ingestion by specialized cells and destruction), but some bind the virus less well and appear instead to deliver the virus into a part of the phagocytes where it is not destroyed but is able to replicate further.

Severe disease

It is not entirely clear why secondary infection with a different strain of dengue virus places people at risk of dengue hemorrhagic fever and dengue shock syndrome. The most widely accepted hypothesis is that of antibody-dependent enhancement (ADE). The exact mechanism behind ADE is unclear. It may be caused by poor binding of non-neutralizing antibodies and delivery into the wrong compartment of white blood cells that have ingested the virus for destruction. There is a suspicion that ADE is not the only mechanism underlying severe dengue-related complications, and various lines of research have implied a role for T cells and soluble factors such as cytokines and the complement system.

Severe disease is marked by the problems of capillary permeability (an allowance of fluid and protein normally contained within blood to pass) and disordered blood clotting. These changes appear associated with a disordered state of the endothelial glycocalyx, which acts as a molecular filter of blood components. Leaky capillaries (and the critical phase) are thought to be caused by an immune system response. Other processes of interest include infected cells that become necrotic—which affect both coagulation and fibrinolysis (the opposing systems of blood clotting and clot degradation)—and low platelets in the blood, also a factor in normal clotting.

DIAGNOSIS

The diagnosis of dengue is typically made clinically, on the basis of reported symptoms and physical examination; this applies especially in endemic areas. However, early disease can be difficult to differentiate from other viral infections. A probable diagnosis is based on the findings of fever plus two of the following: nausea and vomiting, rash, generalized pains, low white blood cell count, positive tourniquet test, or any warning sign (see table) in someone who lives in an endemic area. Warning signs typically occur before the onset of severe dengue. The tourniquet test, which is particularly useful in settings where no laboratory investigations are readily available, involves the application of a blood pressure cuff at between the diastolic and systolic pressure for five minutes, followed by the counting of any petechial hemorrhages; a higher number makes a diagnosis of dengue more likely with the cut off being more than 10 to 20 per 1 inch2 (6.25 cm2).

The diagnosis should be considered in anyone who develops a fever within two weeks of being in the tropics or subtropics. It can be difficult to distinguish dengue fever and chikungunya, a similar viral infection that shares many symptoms and occurs in similar parts of the world to dengue. Often, investigations are performed to exclude other conditions that cause similar symptoms, such as malaria, leptospirosis, viral hemorrhagic fever, typhoid fever, meningococcal disease, measles, and influenza.

The earliest change detectable on laboratory investigations is a low white blood cell count, which may then be followed by low platelets and metabolic acidosis. A moderately elevated level of aminotransferase (AST and ALT) from the liver is commonly associated with low platelets and white blood cells. In severe disease, plasma leakage results in hemoconcentration (as indicated by a rising hematocrit) and hypoalbuminemia. Pleural effusions or ascites can be detected by physical examination when large, but the demonstration of fluid on ultrasound may assist in the early identification of dengue shock syndrome. The use of ultrasound is limited by lack of availability in many settings. Dengue shock syndrome is present if pulse pressure drops to ≤ 20 mm Hg along with peripheral vascular collapse. Peripheral vascular collapse is determined in children via delayed capillary refill, rapid heart rate, or cold extremities.

CLASSIFICATION

The World Health Organization's 2009 classification divides dengue fever into two groups: uncomplicated and severe. This replaces the 1997 WHO classification, which needed to be simplified as it had been found to be too restrictive, though the older classification is still widely used including by the World Health Organization's Regional Office for South-East Asia as of 2011. Severe dengue is defined as that associated with severe bleeding, severe organ dysfunction, or severe plasma leakage while all other cases are uncomplicated. The 1997 classification divided dengue into undifferentiated fever, dengue fever, and dengue hemorrhagic fever. Dengue hemorrhagic fever was subdivided further into grades I–IV. Grade I is the presence only of easy bruising or a positive tourniquet test in someone with fever, grade II is the presence of spontaneous bleeding into the skin and elsewhere, grade III is the clinical evidence of shock, and grade IV is shock so severe that blood pressure and pulse cannot be detected. Grades III and IV are referred to as "dengue shock syndrome".

Laboratory tests

The diagnosis of dengue fever may be confirmed by microbiological laboratory testing. This can be done by virus isolation in cell cultures, nucleic acid detection by PCR, viral antigen detection (such as for NS1) or specific antibodies (serology). Virus isolation and nucleic acid detection are more accurate than antigen detection, but these tests are not widely available due to their greater cost. Detection of NS1 during the febrile phase of a primary infection may be greater than 90% however is only 60–80% in subsequent infections. All tests may be negative in the early stages of the disease. PCR and viral antigen detection are more accurate in the first seven days. In 2012 a PCR test was introduced that can run on equipment used to diagnose influenza; this is likely to improve access to PCR-based diagnosis.

These laboratory tests are only of diagnostic value during the acute phase of the illness with the exception of serology. Tests for dengue virus-specific antibodies, types IgG and IgM, can be useful in confirming a diagnosis in the later stages of the infection. Both IgG and IgM are produced after 5–7 days. The highest levels (titres) of IgM are detected following a primary infection, but IgM is also produced in reinfection. IgM becomes undetectable 30–90 days after a primary infection, but earlier following re-infections. IgG, by contrast, remains detectable for over 60 years and, in the absence of symptoms, is a useful indicator of past infection. After a primary infection IgG reaches peak levels in the blood after 14–21 days. In subsequent re-infections, levels peak earlier and the titres are usually higher. Both IgG and IgM provide protective immunity to the infecting serotype of the virus. The laboratory test for IgG and IgM antibodies can cross-react with other flaviviruses and may result in a false positive after recent infections or vaccinations with yellow fever virus or Japanese encephalitis. The detection of IgG alone is not considered diagnostic unless blood samples are collected 14 days apart and a greater than fourfold increase in levels of specific IgG is detected. In a person with symptoms, the detection of IgM is considered diagnostic.

PREVENTION

There are no approved vaccines for the dengue virus. Prevention thus depends on control of and protection from the bites of the mosquito that transmits it. The World Health Organization recommends an Integrated Vector Control program consisting of five elements:

  • Advocacy, social mobilization and legislation to ensure that public health bodies and communities are strengthened;
  • Collaboration between the health and other sectors (public and private);
  • An integrated approach to disease control to maximize use of resources;
  • Evidence-based decision making to ensure any interventions are targeted appropriately; and
  • Capacity-building to ensure an adequate response to the local situation.

The primary method of controlling A. aegypti is by eliminating its habitats. This is done by getting rid of open sources of water, or if this is not possible, by adding insecticides or biological control agents to these areas. Generalized spraying with organophosphate or pyrethroid insecticides, while sometimes done, is not thought to be effective. Reducing open collections of water through environmental modification is the preferred method of control, given the concerns of negative health effects from insecticides and greater logistical difficulties with control agents. People can prevent mosquito bites by wearing clothing that fully covers the skin, using mosquito netting while resting, and/or the application of insect repellent (DEET being the most effective). However, these methods appear not to be sufficiently effective, as the frequency of outbreaks appears to be increasing in some areas, probably due to urbanization increasing the habitat of A. aegypti. The range of the disease appears to be expanding possibly due to climate change.

MANAGEMENT

There are no specific antiviral drugs for dengue, however maintaining proper fluid balance is important. Treatment depends on the symptoms. Those who are able to drink, are passing urine, have no "warning signs" and are otherwise healthy can be managed at home with daily follow up and oral rehydration therapy. Those who have other health problems, have "warning signs" or who cannot manage regular follow up should be cared for in hospital. In those with severe dengue care should be provided in an area where there is access to an intensive care unit.

Intravenous hydration, if required, is typically only needed for one or two days. The rate of fluid administration is titrated to a urinary output of 0.5–1 mL/kg/h, stable vital signs and normalization of hematocrit. The smallest amount of fluid required to achieve this is recommended. Invasive medical procedures such as nasogastric intubation, intramuscular injections and arterial punctures are avoided, in view of the bleeding risk. Paracetamol (acetaminophen) is used for fever and discomfort while NSAIDs such as ibuprofen and aspirin are avoided as they might aggravate the risk of bleeding. Blood transfusion is initiated early in people presenting with unstable vital signs in the face of a decreasing hematocrit, rather than waiting for the hemoglobin concentration to decrease to some predetermined "transfusion trigger" level. Packed red blood cells or whole blood are recommended, while platelets and fresh frozen plasma are usually not. Corticosteroids do not appear to affect outcomes and may cause harm, thus are not recommended.

During the recovery phase intravenous fluids are discontinued to prevent a state of fluid overload. If fluid overload occurs and vital signs are stable, stopping further fluid may be all that is needed. If a person is outside of the critical phase, a loop diuretic such as furosemide may be used to eliminate excess fluid from the circulation.

EPIDEMIOLOGY

Most people with dengue recover without any ongoing problems. The mortality is 1–5% without treatment, and less than 1% with adequate treatment; however severe disease carries a mortality of 26%. Dengue is endemic in more than 110 countries. It infects 50 to 528 million people worldwide a year, leading to half a million hospitalizations, and approximately 25,000 deaths. For the decade of the 2000s, 12 countries in Southeast Asia were estimated to have about 3 million infections and 6,000 deaths annually. It is reported in at least 22 countries in Africa; but is likely present in all of them with 20% of the population at risk.

Infections are most commonly acquired in the urban environment. In recent decades, the expansion of villages, towns and cities in endemic areas, and the increased mobility of people has increased the number of epidemics and circulating viruses. Dengue fever, which was once confined to Southeast Asia, has now spread to Southern China, countries in the Pacific Ocean and America, and might pose a threat to Europe.

Rates of dengue increased 30 fold between 1960 and 2010. This increase is believed to be due to a combination of urbanization, population growth, increased international travel, and global warming. The geographical distribution is around the equator with 70% of the total 2.5 billion people living in endemic areas from Asia and the Pacific. An infection with dengue is second only to malaria as a diagnosed cause of fever among returning travelers. It is the most common viral disease transmitted by arthropods, and has a disease burden estimated at 1,600 disability-adjusted life years per million population. The World Health Organization counts dengue as one of seventeen neglected tropical diseases.

Like most arboviruses, dengue virus is maintained in nature in cycles that involve preferred blood-sucking vectors and vertebrate hosts. The viruses are maintained in the forests of Southeast Asia and Africa by transmission from female Aedes mosquitoes—of species other than A. aegypti—to her offspring and to lower primates. In towns and cities, the virus is primarily transmitted by the highly domesticated A. aegypti. In rural settings the virus is transmitted to humans by A. aegypti and other species of Aedes such as A. albopictus. Both these species have had expanding ranges in the second half of the 20th century. In all settings the infected lower primates or humans greatly increase the number of circulating dengue viruses, in a process called amplification.

IMAGES

CASE RECORD

CHIKUNGUNYA EPIDEMIC - Madaram Town, Dist.Adilabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

About 86 patients suffering from Chikungunya fever were treated,making use of our novel concept DAHT,in Madaram village of Adilabad district in the year 2006.
In the majority of them the fever disappeared in one day and the joint pains in about four days only.
This is in sharp contrast to the prolonged suffering experienced by many patients who missed our DAHT therapy. Their pains extended over some weeks and months despite all available therapies they could try.
An audiovisual evidence of it has been recorded.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Chikungunya ("Makonde for "that which bends up") virus (CHIKV) is an arthropod-borne virus, of the genus Alphavirus, that is transmitted to humans by virus-carrying Aedes mosquitoes. CHIKV is transmitted similarly to dengue fever and causes an illness with an acute febrile phase lasting two to five days, followed by a longer period of joint pains in the extremities; this pain may persist for years in some cases.

The best means of prevention is overall mosquito control and in addition, the avoidance of bites by any infected mosquitoes. There is no specific treatment but medications can be used to reduce symptoms. Rest and fluids may also be useful.

SIGNS AND SYMPTOMS

The incubation period of chikungunya disease ranges from one to twelve days, typically two to three. The majority of those infected will develop symptoms. Symptoms include a fever up to 40 °C (104 °F), a petechial or maculopapular rash of the trunk and occasionally the limbs, and arthralgia or arthritis affecting multiple joints. Other nonspecific symptoms can include headache, nausea, vomiting, conjunctivitis, slight photophobia and partial loss of taste. Ocular inflammation from chikungunya may present as iridocyclitis. Retinal lesions may also occur. Pedal oedema (swelling of legs) is observed in many patients, the cause of which remains obscure as it is not related to any cardiovascular, renal or hepatic abnormalities.

Typically, the fever lasts for two days and then ends abruptly. However, other symptoms—namely joint pain, intense headache, insomnia and an extreme degree of prostration—last for a variable period; usually for about five to seven days. Patients have complained of joint pains for much longer time periods; some as long as two years, depending on their age. Recovery from the disease varies by age. Younger patients recover within 5 to 15 days; middle-aged patients recover in 1 to 2.5 months. Recovery is longer for the elderly. The severity of the disease as well as its duration is less in younger patients and pregnant women. In pregnant women, no untoward effects are noticed after the infection.

Chronic Disease

Observations during recent epidemics have suggested chikungunya may cause long-term symptoms following acute infection. During the La Reunion outbreak in 2006, greater than 50% of subjects over the age of 45 reported long term musculoskeletal pain with up to 60% of patients reporting prolonged arthralgia 3 years following initial infection. A study of imported cases in France reported that 59% of patients still suffered from arthralgia two years after acute infection. Following a local epidemic of chikungunya in Italy, 66% of patients reported myalgia, arthralgia, or asthenia at one year postacute infection. Long-term symptoms are not an entirely new observation; long-term arthritis was observed following an outbreak in 1979. Common predictors of prolonged symptoms are increased age and prior rheumatological disease. The cause of these chronic symptoms is currently not fully known. Markers of autoimmune or rheumatoid disease have not been found in patients reporting chronic symptoms. However, some evidence from human patients and animal models suggest that chikungunya may be able to establish chronic infections within the host. Viral antigen was detected in a muscle biopsy of a patient suffering a recurrent episode of disease three months after initial onset. Additionally, viral antigen and RNA were found in synovial macrophages of a patient during a relapse of musculoskeletal disease 18 months post initial infection. Several animal models have also suggested that chikungunya virus may establish persistent infections. In a mouse model, viral RNA was detected specifically in joint-associated tissue for at least 16 weeks post-inoculation, and was associated with chronic synovitis. Similarly, another study reported detection of a viral reporter gene in joint tissue of mice for weeks post-inoculation. In a non-human primate model, chikungunya virus was found to persist in the spleen for at least 6 weeks.

VIROLOGY

Chikungunya virus is an alphavirus with a positive sense single-stranded RNA genome of approximately 11.6kb. It is a member of the Semliki Forest Virus complex and is closely related to Ross River Virus, O’Nyong Nyong virus and Semliki Forest Virus. In the United States it is classified as a Category C priority pathogen and work requires Biosafety Level III precautions.

Human epithelial, endothelial, primary fibroblasts and monocyte-derived macrophages are permissive for chikungunya virus in vitro and viral replication is highly cytopathic but susceptible to type I and II interferon. In vivo, chikungunya virus appears to replicate in fibroblasts, skeletal muscle progenitor cells and myofibers.

Type 1 interferon

Upon infection with chikungunya, the host's fibroblasts will produce type 1 (alpha and beta) interferon. Mice that lack the interferon alpha receptor die in 2–3 days upon being exposed to 102 chikungunya PFU, while wild type mice survive even when exposed to as much as 106 PFU of the virus. At the same time, mice that are partially type 1 deficient are mildly affected and experience symptoms such as muscle weakness and lethargy. Partidos et al. 2011 saw similar results with the live attenuated strain CHIKV181/25. However, rather than dying, the type 1 interferon deficient mice were temporarily disabled and the partially type 1 interferon deficient mice did not have any problems.

Several studies have attempted to find the upstream components of the type 1 interferon pathway involved in the host's response to chikungunya infection. So far, no one knows the chikungunya specific pathogen associated molecular pattern. Nonetheless, IPS-1—also known as Cardif, MAVS, and VISA—has been found to be an important factor. In 2011, White et al. found that interfering with IPS-1 decreased the phosphorylation of interferon regulatory factor 3 (IRF3) and the production of IFN-β. Other studies have found that IRF3 and IRF7 are important in an age-dependent manner. Adult mice that lack both of these regulatory factors die upon infection with chikungunya. Neonates, on the other hand, succumb to the virus if they are deficient in one of these factors.

Chikungunya counters the Type I interferon response by producing NS2, a non-structural protein that degrades Rpb and turns off the host cell's ability to transcribe DNA. NS2 interferes with the JAK-STAT signaling pathway and prevents STAT from becoming phosphorylated.

DIAGNOSIS

Common laboratory tests for chikungunya include RT-PCR, virus isolation, and serological tests.

  • Virus isolation provides the most definitive diagnosis, but takes one to two weeks for completion and must be carried out in biosafety level 3 laboratories. The technique involves exposing specific cell lines to samples from whole blood and identifying chikungunya virus-specific responses.
  • RT-PCR using nested primer pairs is used to amplify several chikungunya-specific genes from whole blood. Results can be determined in one to two days.
  • Serological diagnosis requires a larger amount of blood than the other methods, and uses an ELISA assay to measure chikungunya-specific IgM levels. Results require two to three days, and false positives can occur with infection via other related viruses, such as o'nyong'nyong virus and Semliki Forest virus.

PREVENTION

The most effective means of prevention are protection against contact with the disease-carrying mosquitoes and mosquito control. These include using insect repellents with substances such as DEET (N,N-diethyl-meta-toluamide; also known as N,N'-diethyl-3-methylbenzamide or NNDB), icaridin (also known as picaridin and KBR3023), PMD (p-menthane-3,8-diol, a substance derived from the lemon eucalyptus tree), or IR3535. Wearing bite-proof long sleeves and trousers also offers protection.

In addition, garments can be treated with pyrethroids, a class of insecticides that often has repellent properties. Vaporized pyrethroids (for example in mosquito coils) are also insect repellents. Securing screens on windows and doors will help to keep mosquitoes out of the house. In the case of the day-active Aedes aegypti and Aedes albopictus, however, this will have only a limited effect, since many contacts between the mosquitoes and humans occur outside.

Vaccine

There are currently no approved vaccines available. A phase II vaccine trial, used a live, attenuated virus, developing viral resistance in 98% of those tested after 28 days and 85% still showed resistance after one year. However, 8% of people reported transient joint pain and attenuation was found to be due to only two mutations in the E2 glycoprotein. Alternative vaccine strategies have been developed and shown efficacy in mouse models but have so far not reached clinical trials.

TREATMENT

Currently there is no specific treatment. Efforts to improve the symptoms include the use of NSAIDs such as naproxen, paracetamol (acetaminophen) and fluids. Aspirin is not recommended.

Chronic arthritis

In those who have more than two weeks of arthritis, ribavirin may be useful. The effect of chloroquine is not clear. It does not appear to help acute disease but there is tentative evidence that it might help the chronic arthritis. Steroids do not appear useful either.

EPIDEMIOLOGY

Chikungunya virus is an alphavirus closely related to the o'nyong'nyong virus, the Ross River virus in Australia, and the viruses that cause eastern equine encephalitis and western equine encephalitis.

Three genotypes of this virus have been described: West African, East/Central/South African and Asian genotypes.

Chikungunya is generally spread through bites from Aedes aegypti mosquitoes, but recent research by the Pasteur Institute in Paris has suggested chikungunya virus strains in the 2005-2006 Reunion Island outbreak incurred a mutation that facilitated transmission by Asian tiger mosquito (Aedes albopictus).

Concurrent studies by arbovirologists at the University of Texas Medical Branch in Galveston, Texas, confirmed definitively that enhanced chikungunya virus infection of A. albopictus was caused by a point mutation in one of the viral envelope genes (E1). Enhanced transmission of chikungunya virus by A. albopictus could mean an increased risk for chikungunya outbreaks in other areas where the Asian tiger mosquito is present. A recent epidemic in Italy was likely perpetuated by A. albopictus.

In Africa, chikungunya is spread via a sylvatic cycle in which the virus largely resides in other primates in between human outbreaks.

On 28 May 2009 in Changwat Trang of Thailand where the virus is endemic, the provincial hospital decided to deliver by Caesarean section a male baby from his chikungunya-infected mother, Khwanruethai Sutmueang, 28, a Trang native, to prevent mother-fetus virus transmission. However, after delivering the baby, the physicians discovered the baby was already infected with the virus, and put him into intensive care because the infection had left the baby unable to breathe by himself or to drink milk. The physicians presumed the virus might be able to be transmitted from a mother to her fetus, but without laboratory confirmation.

IMAGES

CHIKUNGUNYA FEVER - Raghupati, Structural Engineer, Lalapet, Secunderabad.

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I am an engineer. Our family was on a trip to Visakhapatnam. One day, I developed sudden fever with severe joint pains. Local doctors diagnosed it as Chikungunya and prescribed some medicines but there was no relief.
My relatives in Vizag who were also affected with the similar disease were still suffering from pains for the last one month despite taking drugs.

MODE OF RECOVERY AT NEW LIFE CENTRE

I came back to Hyderabad and consulted Dr Subhash who lives in a neighbouring building. Surprisingly my fever and joint pains disappeared to a large extent in just two hours of taking his medicine.
My son who was also a patient of Chikungunya fever recovered fully in just one day only. He started playing few hours after taking his dose.
Our recovery is really very fast and safe in contrast to the other similar patients who could not recover even after one month despite visiting expert doctors.
The cure is unexpected and truly wonderful. I thank the doctor immensely. I wish that his specialised treatment reaches every corner of the country.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Chikungunya ("Makonde for "that which bends up") virus (CHIKV) is an arthropod-borne virus, of the genus Alphavirus, that is transmitted to humans by virus-carrying Aedes mosquitoes. CHIKV is transmitted similarly to dengue fever and causes an illness with an acute febrile phase lasting two to five days, followed by a longer period of joint pains in the extremities; this pain may persist for years in some cases.

The best means of prevention is overall mosquito control and in addition, the avoidance of bites by any infected mosquitoes. There is no specific treatment but medications can be used to reduce symptoms. Rest and fluids may also be useful.

SIGNS AND SYMPTOMS

The incubation period of chikungunya disease ranges from one to twelve days, typically two to three. The majority of those infected will develop symptoms. Symptoms include a fever up to 40 °C (104 °F), a petechial or maculopapular rash of the trunk and occasionally the limbs, and arthralgia or arthritis affecting multiple joints. Other nonspecific symptoms can include headache, nausea, vomiting, conjunctivitis, slight photophobia and partial loss of taste. Ocular inflammation from chikungunya may present as iridocyclitis. Retinal lesions may also occur. Pedal oedema (swelling of legs) is observed in many patients, the cause of which remains obscure as it is not related to any cardiovascular, renal or hepatic abnormalities.

Typically, the fever lasts for two days and then ends abruptly. However, other symptoms—namely joint pain, intense headache, insomnia and an extreme degree of prostration—last for a variable period; usually for about five to seven days. Patients have complained of joint pains for much longer time periods; some as long as two years, depending on their age. Recovery from the disease varies by age. Younger patients recover within 5 to 15 days; middle-aged patients recover in 1 to 2.5 months. Recovery is longer for the elderly. The severity of the disease as well as its duration is less in younger patients and pregnant women. In pregnant women, no untoward effects are noticed after the infection.

Chronic Disease

Observations during recent epidemics have suggested chikungunya may cause long-term symptoms following acute infection. During the La Reunion outbreak in 2006, greater than 50% of subjects over the age of 45 reported long term musculoskeletal pain with up to 60% of patients reporting prolonged arthralgia 3 years following initial infection. A study of imported cases in France reported that 59% of patients still suffered from arthralgia two years after acute infection. Following a local epidemic of chikungunya in Italy, 66% of patients reported myalgia, arthralgia, or asthenia at one year postacute infection. Long-term symptoms are not an entirely new observation; long-term arthritis was observed following an outbreak in 1979. Common predictors of prolonged symptoms are increased age and prior rheumatological disease. The cause of these chronic symptoms is currently not fully known. Markers of autoimmune or rheumatoid disease have not been found in patients reporting chronic symptoms. However, some evidence from human patients and animal models suggest that chikungunya may be able to establish chronic infections within the host. Viral antigen was detected in a muscle biopsy of a patient suffering a recurrent episode of disease three months after initial onset. Additionally, viral antigen and RNA were found in synovial macrophages of a patient during a relapse of musculoskeletal disease 18 months post initial infection. Several animal models have also suggested that chikungunya virus may establish persistent infections. In a mouse model, viral RNA was detected specifically in joint-associated tissue for at least 16 weeks post-inoculation, and was associated with chronic synovitis. Similarly, another study reported detection of a viral reporter gene in joint tissue of mice for weeks post-inoculation. In a non-human primate model, chikungunya virus was found to persist in the spleen for at least 6 weeks.

VIROLOGY

Chikungunya virus is an alphavirus with a positive sense single-stranded RNA genome of approximately 11.6kb. It is a member of the Semliki Forest Virus complex and is closely related to Ross River Virus, O’Nyong Nyong virus and Semliki Forest Virus. In the United States it is classified as a Category C priority pathogen and work requires Biosafety Level III precautions.

Human epithelial, endothelial, primary fibroblasts and monocyte-derived macrophages are permissive for chikungunya virus in vitro and viral replication is highly cytopathic but susceptible to type I and II interferon. In vivo, chikungunya virus appears to replicate in fibroblasts, skeletal muscle progenitor cells and myofibers.

Type 1 interferon

Upon infection with chikungunya, the host's fibroblasts will produce type 1 (alpha and beta) interferon. Mice that lack the interferon alpha receptor die in 2–3 days upon being exposed to 102 chikungunya PFU, while wild type mice survive even when exposed to as much as 106 PFU of the virus. At the same time, mice that are partially type 1 deficient are mildly affected and experience symptoms such as muscle weakness and lethargy. Partidos et al. 2011 saw similar results with the live attenuated strain CHIKV181/25. However, rather than dying, the type 1 interferon deficient mice were temporarily disabled and the partially type 1 interferon deficient mice did not have any problems.

Several studies have attempted to find the upstream components of the type 1 interferon pathway involved in the host's response to chikungunya infection. So far, no one knows the chikungunya specific pathogen associated molecular pattern. Nonetheless, IPS-1—also known as Cardif, MAVS, and VISA—has been found to be an important factor. In 2011, White et al. found that interfering with IPS-1 decreased the phosphorylation of interferon regulatory factor 3 (IRF3) and the production of IFN-β. Other studies have found that IRF3 and IRF7 are important in an age-dependent manner. Adult mice that lack both of these regulatory factors die upon infection with chikungunya. Neonates, on the other hand, succumb to the virus if they are deficient in one of these factors.

Chikungunya counters the Type I interferon response by producing NS2, a non-structural protein that degrades Rpb and turns off the host cell's ability to transcribe DNA. NS2 interferes with the JAK-STAT signaling pathway and prevents STAT from becoming phosphorylated.

DIAGNOSIS

Common laboratory tests for chikungunya include RT-PCR, virus isolation, and serological tests.

  • Virus isolation provides the most definitive diagnosis, but takes one to two weeks for completion and must be carried out in biosafety level 3 laboratories. The technique involves exposing specific cell lines to samples from whole blood and identifying chikungunya virus-specific responses.
  • RT-PCR using nested primer pairs is used to amplify several chikungunya-specific genes from whole blood. Results can be determined in one to two days.
  • Serological diagnosis requires a larger amount of blood than the other methods, and uses an ELISA assay to measure chikungunya-specific IgM levels. Results require two to three days, and false positives can occur with infection via other related viruses, such as o'nyong'nyong virus and Semliki Forest virus.

PREVENTION

The most effective means of prevention are protection against contact with the disease-carrying mosquitoes and mosquito control. These include using insect repellents with substances such as DEET (N,N-diethyl-meta-toluamide; also known as N,N'-diethyl-3-methylbenzamide or NNDB), icaridin (also known as picaridin and KBR3023), PMD (p-menthane-3,8-diol, a substance derived from the lemon eucalyptus tree), or IR3535. Wearing bite-proof long sleeves and trousers also offers protection.

In addition, garments can be treated with pyrethroids, a class of insecticides that often has repellent properties. Vaporized pyrethroids (for example in mosquito coils) are also insect repellents. Securing screens on windows and doors will help to keep mosquitoes out of the house. In the case of the day-active Aedes aegypti and Aedes albopictus, however, this will have only a limited effect, since many contacts between the mosquitoes and humans occur outside.

Vaccine

There are currently no approved vaccines available. A phase II vaccine trial, used a live, attenuated virus, developing viral resistance in 98% of those tested after 28 days and 85% still showed resistance after one year. However, 8% of people reported transient joint pain and attenuation was found to be due to only two mutations in the E2 glycoprotein. Alternative vaccine strategies have been developed and shown efficacy in mouse models but have so far not reached clinical trials.

TREATMENT

Currently there is no specific treatment. Efforts to improve the symptoms include the use of NSAIDs such as naproxen, paracetamol (acetaminophen) and fluids. Aspirin is not recommended.

Chronic arthritis

In those who have more than two weeks of arthritis, ribavirin may be useful. The effect of chloroquine is not clear. It does not appear to help acute disease but there is tentative evidence that it might help the chronic arthritis. Steroids do not appear useful either.

EPIDEMIOLOGY

Chikungunya virus is an alphavirus closely related to the o'nyong'nyong virus, the Ross River virus in Australia, and the viruses that cause eastern equine encephalitis and western equine encephalitis.

Three genotypes of this virus have been described: West African, East/Central/South African and Asian genotypes.

Chikungunya is generally spread through bites from Aedes aegypti mosquitoes, but recent research by the Pasteur Institute in Paris has suggested chikungunya virus strains in the 2005-2006 Reunion Island outbreak incurred a mutation that facilitated transmission by Asian tiger mosquito (Aedes albopictus).

Concurrent studies by arbovirologists at the University of Texas Medical Branch in Galveston, Texas, confirmed definitively that enhanced chikungunya virus infection of A. albopictus was caused by a point mutation in one of the viral envelope genes (E1). Enhanced transmission of chikungunya virus by A. albopictus could mean an increased risk for chikungunya outbreaks in other areas where the Asian tiger mosquito is present. A recent epidemic in Italy was likely perpetuated by A. albopictus.

In Africa, chikungunya is spread via a sylvatic cycle in which the virus largely resides in other primates in between human outbreaks.

On 28 May 2009 in Changwat Trang of Thailand where the virus is endemic, the provincial hospital decided to deliver by Caesarean section a male baby from his chikungunya-infected mother, Khwanruethai Sutmueang, 28, a Trang native, to prevent mother-fetus virus transmission. However, after delivering the baby, the physicians discovered the baby was already infected with the virus, and put him into intensive care because the infection had left the baby unable to breathe by himself or to drink milk. The physicians presumed the virus might be able to be transmitted from a mother to her fetus, but without laboratory confirmation.

IMAGES

CHIKUNGUNYA - ACUTE ATTACK - Rama, Kamareddy town, Dist.Nizamabad

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I contacted Chikungunya fever. All the joints were highly painful. I could not walk freely even if two people supported me. I could not drink milk or hold anything. Five days of intensive treatment by local doctors of Kamareddy town could not help me.

MODE OF RECOVERY AT NEW LIFE CENTRE

Later I was brought to NLHC of Secunderabad. The doctor gave me one dose of homeopathic medicine. I got great relief in just two hours only. My fever and joint pains subsided by 50%. My nausea disappeared and my appetite improved. I became more active and I could walk better without anybody’s support. Movement of my limbs is not much painful now. The recovery is fast and really miraculous. It is unbelievable that I could find such a great relief in just two hours only. I thank the doctor wholeheartedly and wish him all the success.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Chikungunya ("Makonde for "that which bends up") virus (CHIKV) is an arthropod-borne virus, of the genus Alphavirus, that is transmitted to humans by virus-carrying Aedes mosquitoes. CHIKV is transmitted similarly to dengue fever and causes an illness with an acute febrile phase lasting two to five days, followed by a longer period of joint pains in the extremities; this pain may persist for years in some cases.

The best means of prevention is overall mosquito control and in addition, the avoidance of bites by any infected mosquitoes. There is no specific treatment but medications can be used to reduce symptoms. Rest and fluids may also be useful.

SIGNS AND SYMPTOMS

The incubation period of chikungunya disease ranges from one to twelve days, typically two to three. The majority of those infected will develop symptoms. Symptoms include a fever up to 40 °C (104 °F), a petechial or maculopapular rash of the trunk and occasionally the limbs, and arthralgia or arthritis affecting multiple joints. Other nonspecific symptoms can include headache, nausea, vomiting, conjunctivitis, slight photophobia and partial loss of taste. Ocular inflammation from chikungunya may present as iridocyclitis. Retinal lesions may also occur. Pedal oedema (swelling of legs) is observed in many patients, the cause of which remains obscure as it is not related to any cardiovascular, renal or hepatic abnormalities.

Typically, the fever lasts for two days and then ends abruptly. However, other symptoms—namely joint pain, intense headache, insomnia and an extreme degree of prostration—last for a variable period; usually for about five to seven days. Patients have complained of joint pains for much longer time periods; some as long as two years, depending on their age. Recovery from the disease varies by age. Younger patients recover within 5 to 15 days; middle-aged patients recover in 1 to 2.5 months. Recovery is longer for the elderly. The severity of the disease as well as its duration is less in younger patients and pregnant women. In pregnant women, no untoward effects are noticed after the infection.

Chronic Disease

Observations during recent epidemics have suggested chikungunya may cause long-term symptoms following acute infection. During the La Reunion outbreak in 2006, greater than 50% of subjects over the age of 45 reported long term musculoskeletal pain with up to 60% of patients reporting prolonged arthralgia 3 years following initial infection. A study of imported cases in France reported that 59% of patients still suffered from arthralgia two years after acute infection. Following a local epidemic of chikungunya in Italy, 66% of patients reported myalgia, arthralgia, or asthenia at one year postacute infection. Long-term symptoms are not an entirely new observation; long-term arthritis was observed following an outbreak in 1979. Common predictors of prolonged symptoms are increased age and prior rheumatological disease. The cause of these chronic symptoms is currently not fully known. Markers of autoimmune or rheumatoid disease have not been found in patients reporting chronic symptoms. However, some evidence from human patients and animal models suggest that chikungunya may be able to establish chronic infections within the host. Viral antigen was detected in a muscle biopsy of a patient suffering a recurrent episode of disease three months after initial onset. Additionally, viral antigen and RNA were found in synovial macrophages of a patient during a relapse of musculoskeletal disease 18 months post initial infection. Several animal models have also suggested that chikungunya virus may establish persistent infections. In a mouse model, viral RNA was detected specifically in joint-associated tissue for at least 16 weeks post-inoculation, and was associated with chronic synovitis. Similarly, another study reported detection of a viral reporter gene in joint tissue of mice for weeks post-inoculation. In a non-human primate model, chikungunya virus was found to persist in the spleen for at least 6 weeks.

VIROLOGY

Chikungunya virus is an alphavirus with a positive sense single-stranded RNA genome of approximately 11.6kb. It is a member of the Semliki Forest Virus complex and is closely related to Ross River Virus, O’Nyong Nyong virus and Semliki Forest Virus. In the United States it is classified as a Category C priority pathogen and work requires Biosafety Level III precautions.

Human epithelial, endothelial, primary fibroblasts and monocyte-derived macrophages are permissive for chikungunya virus in vitro and viral replication is highly cytopathic but susceptible to type I and II interferon. In vivo, chikungunya virus appears to replicate in fibroblasts, skeletal muscle progenitor cells and myofibers.

Type 1 interferon

Upon infection with chikungunya, the host's fibroblasts will produce type 1 (alpha and beta) interferon. Mice that lack the interferon alpha receptor die in 2–3 days upon being exposed to 102 chikungunya PFU, while wild type mice survive even when exposed to as much as 106 PFU of the virus. At the same time, mice that are partially type 1 deficient are mildly affected and experience symptoms such as muscle weakness and lethargy. Partidos et al. 2011 saw similar results with the live attenuated strain CHIKV181/25. However, rather than dying, the type 1 interferon deficient mice were temporarily disabled and the partially type 1 interferon deficient mice did not have any problems.

Several studies have attempted to find the upstream components of the type 1 interferon pathway involved in the host's response to chikungunya infection. So far, no one knows the chikungunya specific pathogen associated molecular pattern. Nonetheless, IPS-1—also known as Cardif, MAVS, and VISA—has been found to be an important factor. In 2011, White et al. found that interfering with IPS-1 decreased the phosphorylation of interferon regulatory factor 3 (IRF3) and the production of IFN-β. Other studies have found that IRF3 and IRF7 are important in an age-dependent manner. Adult mice that lack both of these regulatory factors die upon infection with chikungunya. Neonates, on the other hand, succumb to the virus if they are deficient in one of these factors.

Chikungunya counters the Type I interferon response by producing NS2, a non-structural protein that degrades Rpb and turns off the host cell's ability to transcribe DNA. NS2 interferes with the JAK-STAT signaling pathway and prevents STAT from becoming phosphorylated.

DIAGNOSIS

Common laboratory tests for chikungunya include RT-PCR, virus isolation, and serological tests.

  • Virus isolation provides the most definitive diagnosis, but takes one to two weeks for completion and must be carried out in biosafety level 3 laboratories. The technique involves exposing specific cell lines to samples from whole blood and identifying chikungunya virus-specific responses.
  • RT-PCR using nested primer pairs is used to amplify several chikungunya-specific genes from whole blood. Results can be determined in one to two days.
  • Serological diagnosis requires a larger amount of blood than the other methods, and uses an ELISA assay to measure chikungunya-specific IgM levels. Results require two to three days, and false positives can occur with infection via other related viruses, such as o'nyong'nyong virus and Semliki Forest virus.

PREVENTION

The most effective means of prevention are protection against contact with the disease-carrying mosquitoes and mosquito control. These include using insect repellents with substances such as DEET (N,N-diethyl-meta-toluamide; also known as N,N'-diethyl-3-methylbenzamide or NNDB), icaridin (also known as picaridin and KBR3023), PMD (p-menthane-3,8-diol, a substance derived from the lemon eucalyptus tree), or IR3535. Wearing bite-proof long sleeves and trousers also offers protection.

In addition, garments can be treated with pyrethroids, a class of insecticides that often has repellent properties. Vaporized pyrethroids (for example in mosquito coils) are also insect repellents. Securing screens on windows and doors will help to keep mosquitoes out of the house. In the case of the day-active Aedes aegypti and Aedes albopictus, however, this will have only a limited effect, since many contacts between the mosquitoes and humans occur outside.

Vaccine

There are currently no approved vaccines available. A phase II vaccine trial, used a live, attenuated virus, developing viral resistance in 98% of those tested after 28 days and 85% still showed resistance after one year. However, 8% of people reported transient joint pain and attenuation was found to be due to only two mutations in the E2 glycoprotein. Alternative vaccine strategies have been developed and shown efficacy in mouse models but have so far not reached clinical trials.

TREATMENT

Currently there is no specific treatment. Efforts to improve the symptoms include the use of NSAIDs such as naproxen, paracetamol (acetaminophen) and fluids. Aspirin is not recommended.

Chronic arthritis

In those who have more than two weeks of arthritis, ribavirin may be useful. The effect of chloroquine is not clear. It does not appear to help acute disease but there is tentative evidence that it might help the chronic arthritis. Steroids do not appear useful either.

EPIDEMIOLOGY

Chikungunya virus is an alphavirus closely related to the o'nyong'nyong virus, the Ross River virus in Australia, and the viruses that cause eastern equine encephalitis and western equine encephalitis.

Three genotypes of this virus have been described: West African, East/Central/South African and Asian genotypes.

Chikungunya is generally spread through bites from Aedes aegypti mosquitoes, but recent research by the Pasteur Institute in Paris has suggested chikungunya virus strains in the 2005-2006 Reunion Island outbreak incurred a mutation that facilitated transmission by Asian tiger mosquito (Aedes albopictus).

Concurrent studies by arbovirologists at the University of Texas Medical Branch in Galveston, Texas, confirmed definitively that enhanced chikungunya virus infection of A. albopictus was caused by a point mutation in one of the viral envelope genes (E1). Enhanced transmission of chikungunya virus by A. albopictus could mean an increased risk for chikungunya outbreaks in other areas where the Asian tiger mosquito is present. A recent epidemic in Italy was likely perpetuated by A. albopictus.

In Africa, chikungunya is spread via a sylvatic cycle in which the virus largely resides in other primates in between human outbreaks.

On 28 May 2009 in Changwat Trang of Thailand where the virus is endemic, the provincial hospital decided to deliver by Caesarean section a male baby from his chikungunya-infected mother, Khwanruethai Sutmueang, 28, a Trang native, to prevent mother-fetus virus transmission. However, after delivering the baby, the physicians discovered the baby was already infected with the virus, and put him into intensive care because the infection had left the baby unable to breathe by himself or to drink milk. The physicians presumed the virus might be able to be transmitted from a mother to her fetus, but without laboratory confirmation.

IMAGES

LIVER FAILURE - HEPATITIS C - Deepak, Delhi

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

My motherwho was suffering from Hepatitis C, developed Cirrhosis of liver and all its related complications like recurrent fever, swollen abdomen, swollen limbs, vomiting of blood, pain in the abdomen, lack of blood etc.
She was treated by reputed gastroenterologists of Delhi in a liver speciality hospital. She needed frequent hospital admissions, spreading over many years, for many complaints and we spent huge amounts with only temporary palliation of the complaints.
The specialists ultimately advised Liver Transplantation that costs about 50 lakh rupees.

MODE OF RECOVERY AT NEW LIFE CENTRE

In July 2010 we came to know about the novel antiviral treatment of Dr.Subhash Chandar and started taking his treatment.
My mother has recovered from the old complications; a hitherto sick and bedridden patient is now able to move out freely like a normal healthy individual. There are no frequent costly hospital admissions like before.
We are saved from the burden of huge expenditure, worry and tension--.Mr.DS, Delhi.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Hepatitis C is an infectious disease affecting primarily the liver, caused by the hepatitis C virus (HCV).[1] The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure, liver cancer, or life-threatening esophageal and gastric varices.

HCV is spread primarily by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment, and transfusions. An estimated 150–200 million people worldwide are infected with hepatitis C. The existence of hepatitis C (originally identifiable only as a type of non-A non-B hepatitis) was suggested in the 1970s and proven in 1989. Hepatitis C infects only humans and chimpanzees.

The virus persists in the liver in about 85% of those infected. This chronic infection can be treated with medication: the standard therapy is a combination of peginterferon and ribavirin, with either boceprevir or telaprevir added in some cases. Overall, 50–80% of people treated are cured. Those who develop cirrhosis or liver cancer may require a liver transplant. Hepatitis C is the leading reason for liver transplantation, though the virus usually recurs after transplantation. No vaccine against hepatitis C is available.

SIGNS AND SYMPTOMS

Acute infection

Hepatitis C infection causes acute symptoms in 15% of cases. Symptoms are generally mild and vague, including a decreased appetite, fatigue, nausea, muscle or joint pains, and weight loss[9] and rarely does acute liver failure result. Most cases of acute infection are not associated with jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in individuals who are young and female.

Chronic infection

About 80% of those exposed to the virus develop a chronic infection. This is defined as the presence of detectable viral replication for at least six months. Most experience minimal or no symptoms during the initial few decades of the infection. Chronic hepatitis C can be associated with fatigue[14] and mild cognitive problems. Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.

Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops.[17][18] Usually (80% of the time) this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year. Being infected with hepatits B in additional to hepatitis C increases this risk further.

Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the stomach and esophagus), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy. Ascites occurs at some stage in more than half of those who have a chronic infection.

Extrahepatic complications

The most common problem due to hepatitis C but not involving the liver is mixed cryoglobulinemia (usually the type II form) — an inflammation of small and medium-sized blood vessels. Hepatitis C is also associated with Sjögren's syndrome (an autoimmune disorder); thrombocytopenia; lichen planus; porphyria cutanea tarda; necrolytic acral erythema; insulin resistance; diabetes mellitus; diabetic nephropathy; autoimmune thyroiditis and B-cell lymphoproliferative disorders. Thrombocytopenia is estimated to occur in 0.16% to 45.4% of people with chronic hepatitis C. 20–30% of people infected have rheumatoid factor — a type of antibody. Possible associations include Hyde's prurigo nodularis and membranoproliferative glomerulonephritis. Cardiomyopathy with associated arrhythmias has also been reported. A variety of central nervous system disorders have been reported. Chronic infection seems to be associated with an increased risk of pancreatic cancer.

Occult infection

Persons who have been infected with hepatitis C may appear to clear the virus but remain infected.[34] The virus is not detectable with conventional testing but can be found with ultra-sensitive tests. The original method of detection was by demonstrating the viral genome within liver biopsies, but newer methods include an antibody test for the virus' core protein and the detection of the viral genome after first concentrating the viral particles by ultracentrifugation. A form of infection with persistently moderately elevated serum liver enzymes but without antibodies to hepatitis C has also been reported. This form is known as cryptogenic occult infection.

Several clinical pictures have been associated with this type of infection. It may be found in people with anti-hepatitis-C antibodies but with normal serum levels of liver enzymes; in antibody-negative people with ongoing elevated liver enzymes of unknown cause; in healthy populations without evidence of liver disease; and in groups at risk for HCV infection including those on haemodialysis or family members of people with occult HCV. The clinical relevance of this form of infection is under investigation. The consequences of occult infection appear to be less severe than with chronic infection but can vary from minimal to hepatocellular carcinoma.

The rate of occult infection in those apparently cured is controversial but appears to be low. 40% of those with hepatitis but with both negative hepatitis C serology and the absence of detectable viral genome in the serum have hepatitis C virus in the liver on biopsy. How commonly this occurs in children is unknown.

VIROLOGY

The hepatitis C virus (HCV) is a small, enveloped, single-stranded, positive-sense RNA virus. It is a member of the Hepacivirus genus in the family Flaviviridae. There are seven major genotypes of HCV, which are known as genotypes one to seven. The genotypes are divided into several subtypes with the number of subtypes depending on the genotype. In the United States, about 70% of cases are caused by genotype 1, 20% by genotype 2 and about 1% by each of the other genotypes. Genotype 1 is also the most common in South America and Europe.

The half life of the virus particles in the serum is around 3 hours and may be as short as 45 minutes. In an infected person, about 1012 virus particles are produced each day. In addition to replicating in the liver the virus can multiply in lymphocytes.

TRANSMISSION

The primary route of transmission in the developed world is intravenous drug use (IDU), while in the developing world the main methods are blood transfusions and unsafe medical procedures. The cause of transmission remains unknown in 20% of cases; however, many of these are believed to be accounted for by IDU.

Intravenous drug use

IDU is a major risk factor for hepatitis C in many parts of the world. Of 77 countries reviewed, 25 (including the United States) were found to have prevalences of hepatitis C in the intravenous drug user population of between 60% and 80%. Twelve countries had rates greater than 80%. It is believed that ten million intravenous drug users are infected with hepatitis C; China (1.6 million), the United States (1.5 million), and Russia (1.3 million) have the highest absolute totals. Occurrence of hepatitis C among prison inmates in the United States is 10 to 20 times that of the occurrence observed in the general population; this has been attributed to high-risk behavior in prisons such as IDU and tattooing with nonsterile equipment.

Healthcare exposure

Blood transfusion, transfusion of blood products, or organ transplants without HCV screening carry significant risks of infection. The United States instituted universal screening in 1992 to between one in 10,000 to one in 10,000,000 per unit of blood. This low risk remains as there is a period of about 11–70 days between the potential blood donor's acquiring hepatitis C and the blood's testing positive depending on the method. Some countries do not screen for hepatitis C due to the cost.

Those who have experienced a needle stick injury from someone who was HCV positive have about a 1.8% chance of subsequently contracting the disease themselves. The risk is greater if the needle in question is hollow and the puncture wound is deep. There is a risk from mucosal exposures to blood; but this risk is low, and there is no risk if blood exposure occurs on intact skin.

Hospital equipment has also been documented as a method of transmission of hepatitis C, including reuse of needles and syringes; multiple-use medication vials; infusion bags; and improperly sterilized surgical equipment, among others. Limitations in the implementation and enforcement of stringent standard precautions in public and private medical and dental facilities are known to be the primary cause of the spread of HCV in Egypt, the country with highest rate of infection in the world.

Sexual intercourse

Whether hepatitis C can be transmitted through sexual activity is controversial. While there is an association between high-risk sexual activity and hepatitis C, and multiple sexual partners are a risk factor for hepatitis C, there is no conclusive evidence that hepatitis C can be transmitted by sexual activity, since people who report transmission with sex as their only risk factor may actually have used drugs but denied it. The majority of evidence supports there being no risk for monogamous heterosexual couples. Sexual practices that involve higher levels of trauma to the anogenital mucosa, such as anal penetrative sex, or that occur when there is a concurrent sexually transmitted infection, including HIV or genital ulceration, do present a risk. The United States Department of Veterans Affairs recommends condom use to prevent hepatitis C transmission in those with multiple partners, but not those in monogamous relationships.

Body modification

Tattooing is associated with two to threefold increased risk of hepatitis C. This can be due to either improperly sterilized equipment or contamination of the dyes being used. Tattoos or piercings performed either before the mid-1980s, "underground," or nonprofessionally are of particular concern, since sterile techniques in such settings may be lacking. The risk also appears to be greater for larger tattoos. It is estimated that nearly half of prison inmates share unsterilized tattooing equipment. It is rare for tattoos in a licensed facility to be directly associated with HCV infection.

Shared personal items

Personal-care items such as razors, toothbrushes, and manicuring or pedicuring equipment can be contaminated with blood. Sharing such items can potentially lead to exposure to HCV. Appropriate caution should be taken regarding any medical condition that results in bleeding, such as cuts and sores. HCV is not spread through casual contact, such as hugging, kissing, or sharing eating or cooking utensils. Neither is it transmitted through food or water.

Vertical transmission

Vertical transmission of hepatitis C from an infected mother to her child occurs in less than 10% of pregnancies. There are no measures that alter this risk. It is not clear when during pregnancy transmission occurs, but it may occur both during gestation and at delivery. A long labor is associated with a greater risk of transmission. There is no evidence that breast-feeding spreads HCV; however, to be cautious, an infected mother is advised to avoid breastfeeding if her nipples are cracked and bleeding, or her viral loads are high.

DIAGNOSIS

There are a number of diagnostic tests for hepatitis C, including HCV antibody enzyme immunoassay or ELISA, recombinant immunoblot assay, and quantitative HCV RNA polymerase chain reaction (PCR). HCV RNA can be detected by PCR typically one to two weeks after infection, while antibodies can take substantially longer to form and thus be detected. Chronic hepatitis C is defined as infection with the hepatitis C virus persisting for more than six months based on the presence of its RNA. Chronic infections are typically asymptomatic during the first few decades, and thus are most commonly discovered following the investigation of elevated liver enzyme levels or during a routine screening of high-risk individuals. Testing is not able to distinguish between acute and chronic infections. Diagnosis in the infant is difficult as maternal antibodies may persist for up to 18 months.

Serology

Hepatitis C testing typically begins with blood testing to detect the presence of antibodies to the HCV, using an enzyme immunoassay. If this test is positive, a confirmatory test is then performed to verify the immunoassay and to determine the viral load. A recombinant immunoblot assay is used to verify the immunoassay and the viral load is determined by a HCV RNA polymerase chain reaction. If there are no RNA and the immunoblot is positive, it means that the person tested had a previous infection but cleared it either with treatment or spontaneously; if the immunoblot is negative, it means that the immunoassay was wrong. It takes about 6–8 weeks following infection before the immunoassay will test positive. A number of tests are available as point of care testing which means that results are available within 30 minutes.

Liver enzymes are variable during the initial part of the infection and on average begin to rise at seven weeks after infection. The elevation of liver enzymes does not closely follow disease severity.

Biopsy

Liver biopsies are used to determine the degree of liver damage present; however, there are risks from the procedure. The typical changes seen are lymphocytes within the parenchyma, lymphoid follicles in portal triad, and changes to the bile ducts. There are a number of blood tests available that try to determine the degree of hepatic fibrosis and alleviate the need for biopsy.

Screening

It is believed that only 5–50% of those infected in the United States and Canada are aware of their status. Testing is recommended in those at high risk, which includes injection drug users, those who have received blood transfusions before 1992, those who have been in jail, those on long term hemodialysis, and those with tattoos. Screening is also recommended in those with elevated liver enzymes, as this is frequently the only sign of chronic hepatitis. Routine screening is not currently recommended in the United States. In 2012, the U.S. Centers for Disease Control and Prevention (CDC) added a recommendation for a single screening test for those born between 1945 and 1965.

PREVENTION

As of 2011, no vaccine protects against contracting hepatitis C. However, there are a number under development and some have shown encouraging results. A combination of harm reduction strategies, such as the provision of new needles and syringes and treatment of substance use, decrease the risk of hepatitis C in intravenous drug users by about 75%. The screening of blood donors is important at a national level, as is adhering to universal precautions within healthcare facilities. In countries where there is an insufficient supply of sterile syringes, medications should be given orally rather than via injection (when possible).

TREATMENT

HCV induces chronic infection in 50–80% of infected persons. Approximately 40–80% of these clear with treatment. In rare cases, infection can clear without treatment. Those with chronic hepatitis C are advised to avoid alcohol and medications toxic to the liver, and to be vaccinated for hepatitis A and hepatitis B. Ultrasound surveillance for hepatocellular carcinoma is recommended in those with accompanying cirrhosis.

Medications

In general, treatment is recommended for those with proven HCV infection and signs of liver inflammation. As of 2010, treatments consist of a combination of pegylated interferon alpha and the antiviral drug ribavirin for a period of 24 or 48 weeks, depending on HCV genotype. This produces cure rates of between 70 and 80% for genotype 2 and 3, respectively, and 45 to 70% for other genotypes. When combined with ribavirin, pegylated interferon-alpha-2a may be superior to pegylated interferon-alpha-2b, though the evidence is not strong.

Combining either boceprevir or telaprevir with ribavirin and peginterferon alfa improves antiviral response for hepatitis C genotype 1. Adverse effects with treatment are common, with half of people getting flu like symptoms and a third experiencing emotional problems. Treatment during the first six months is more effective than once hepatitis C has become chronic. If someone develops a new infection and it has not cleared after eight to twelve weeks, 24 weeks of pegylated interferon is recommended. In people with thalassemia, ribavirin appears to be useful but increases the need for transfusions.

Sofosbuvir with ribavirin and interferon appears to be around 90% effective in those with genotype 1, 4, 5, or 6 disease. Sofosbuvir with just ribavirin appears to be 70 to 95% effective in type 2 and 3 disease. This benefit is somewhat offset by a greater rate of adverse effects. Treatments that contain ledipasvir and sofosbuvir for genotype 1 has success rates of around 93 to 99% but is very expensive. In genotype 6 infection, pegylated interferon and ribavirin is effective in 60 to 90% of cases. There is some tentative data for simeprevir use in type 6 disease as well.

Surgery

Cirrhosis due to hepatitis C is a common reason for liver transplantion though the virus usually (80–90% of cases) recurs afterwards. Infection of the graft leads to 10–30% of people developing cirrhosis within five years. Treatment with pegylated interferon and ribavirin post transplant decreases the risk of recurrence to 70%.

Alternative medicine

Alternative medicine Several alternative therapies are claimed by their proponents to be helpful for hepatitis C including milk thistle, ginseng, and colloidal silver. However, no alternative therapy has been shown to improve outcomes in hepatitis C, and no evidence exists that alternative therapies have any effect on the virus at all.

PROGNOSIS

The responses to treatment is measured by sustained viral response and vary by HCV C genotype. A sustained response occurs in about 40–50% in people with HCV genotype 1 given 48 weeks of treatment. A sustained response is seen in 70–80% of people with HCV genotypes 2 and 3 with 24 weeks of treatment. A sustained response occurs about 65% in those with genotype 4 after 48 weeks of treatment. The evidence for treatment in genotype 6 disease is sparse and what evidence there is supports 48 weeks of treatment at the same doses used for genotype 1 disease. Successful treatment decreases the future risk of hepatocellular carcinoma by 75%.

EPIDEMIOLOGY

It is estimated that 150–200 million people, or ~3% of the world's population, are living with chronic hepatitis C. About 3–4 million people are infected per year, and more than 350,000 people die yearly from hepatitis C-related diseases. During 2010 it is estimated that 16,000 people died from acute infections while 196,000 deaths occurred from liver cancer secondary to the infection. Rates have increased substantially in the 20th century due to a combination of intravenous drug abuse and reused but poorly sterilized medical equipment.

Rates are high (>3.5% population infected) in Central and East Asia, North Africa and the Middle East, they are intermediate (1.5%-3.5%) in South and Southeast Asia, sub-Saharan Africa, Andean, Central and Southern Latin America, Caribbean, Oceania, Australasia and Central, Eastern and Western Europe; and they are low (<1.5%) in Asia Pacific, Tropical Latin America and North America.

Among those chronically infected, the risk of cirrhosis after 20 years varies between studies but has been estimated at ~10–15% for men and ~1–5% for women. The reason for this difference is not known. Once cirrhosis is established, the rate of developing hepatocellular carcinoma is ~1–4% per year. Rates of new infections have decreased in the Western world since the 1990s due to improved screening of blood before transfusion.

In the United States, about 2% of people have hepatitis C, with the number of new cases per year stabilized at 17,000 since 2007. The number of deaths from hepatitis C has increased to 15,800 in 2008 and by 2007 had overtaken HIV/AIDS as a cause of death in the USA. This mortality rate is expected to increase, as those infected by transfusion before HCV testing become apparent. In Europe the percentage of people with chronic infections has been estimated to be between 0.13 and 3.26%.

The total number of people with this infection is higher in some countries in Africa and Asia. Countries with particularly high rates of infection include Egypt (22%), Pakistan (4.8%) and China (3.2%). It is believed that the high prevalence in Egypt is linked to a now-discontinued mass-treatment campaign for schistosomiasis, using improperly sterilized glass syringes.

IMAGES

CIRRHOSIS OF LIVER - HEPATITIS C - G.S Agarwal, Nagpur

UNBELIEVABLE SUCCESS AT NEW LIFE HOMEO CARE

PAST HISTORY BEFORE COMING TO US

I was suffering from a severe liver disease with all complications like hepatitis C, Cirrhosis of liver, Portal hypertension, Ascites, Fluid in abdomen with Swelling of abdomenand legs, fever, vomiting of blood,diarrhoea etc. Gastroenterologists advised me two courses of costly antiviral drugs for six months each, but there was no relief.

MODE OF RECOVERY AT NEW LIFE CENTRE

Later my daughter Dr GeetaAgarwal who learnt about the successful novel treatment of Dr.Subhash Chandar for such diseases through homeopathic journal, directed me to take his treatment. I recovered fully with his treatment in all aspects in a short period and my blood tested negative for the Hepatitis C virus.

INDEED, ITS A NEW LIFE FOR THE PATIENT

WHAT SCIENCE SAYS

Hepatitis C is an infectious disease affecting primarily the liver, caused by the hepatitis C virus (HCV).[1] The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure, liver cancer, or life-threatening esophageal and gastric varices.

HCV is spread primarily by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment, and transfusions. An estimated 150–200 million people worldwide are infected with hepatitis C. The existence of hepatitis C (originally identifiable only as a type of non-A non-B hepatitis) was suggested in the 1970s and proven in 1989. Hepatitis C infects only humans and chimpanzees.

The virus persists in the liver in about 85% of those infected. This chronic infection can be treated with medication: the standard therapy is a combination of peginterferon and ribavirin, with either boceprevir or telaprevir added in some cases. Overall, 50–80% of people treated are cured. Those who develop cirrhosis or liver cancer may require a liver transplant. Hepatitis C is the leading reason for liver transplantation, though the virus usually recurs after transplantation. No vaccine against hepatitis C is available.

SIGNS AND SYMPTOMS

Acute infection

Hepatitis C infection causes acute symptoms in 15% of cases. Symptoms are generally mild and vague, including a decreased appetite, fatigue, nausea, muscle or joint pains, and weight loss[9] and rarely does acute liver failure result. Most cases of acute infection are not associated with jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in individuals who are young and female.

Chronic infection

About 80% of those exposed to the virus develop a chronic infection. This is defined as the presence of detectable viral replication for at least six months. Most experience minimal or no symptoms during the initial few decades of the infection. Chronic hepatitis C can be associated with fatigue[14] and mild cognitive problems. Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.

Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops.[17][18] Usually (80% of the time) this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year. Being infected with hepatits B in additional to hepatitis C increases this risk further.

Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the stomach and esophagus), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy. Ascites occurs at some stage in more than half of those who have a chronic infection.

Extrahepatic complications

The most common problem due to hepatitis C but not involving the liver is mixed cryoglobulinemia (usually the type II form) — an inflammation of small and medium-sized blood vessels. Hepatitis C is also associated with Sjögren's syndrome (an autoimmune disorder); thrombocytopenia; lichen planus; porphyria cutanea tarda; necrolytic acral erythema; insulin resistance; diabetes mellitus; diabetic nephropathy; autoimmune thyroiditis and B-cell lymphoproliferative disorders. Thrombocytopenia is estimated to occur in 0.16% to 45.4% of people with chronic hepatitis C. 20–30% of people infected have rheumatoid factor — a type of antibody. Possible associations include Hyde's prurigo nodularis and membranoproliferative glomerulonephritis. Cardiomyopathy with associated arrhythmias has also been reported. A variety of central nervous system disorders have been reported. Chronic infection seems to be associated with an increased risk of pancreatic cancer.

Occult infection

Persons who have been infected with hepatitis C may appear to clear the virus but remain infected.[34] The virus is not detectable with conventional testing but can be found with ultra-sensitive tests. The original method of detection was by demonstrating the viral genome within liver biopsies, but newer methods include an antibody test for the virus' core protein and the detection of the viral genome after first concentrating the viral particles by ultracentrifugation. A form of infection with persistently moderately elevated serum liver enzymes but without antibodies to hepatitis C has also been reported. This form is known as cryptogenic occult infection.

Several clinical pictures have been associated with this type of infection. It may be found in people with anti-hepatitis-C antibodies but with normal serum levels of liver enzymes; in antibody-negative people with ongoing elevated liver enzymes of unknown cause; in healthy populations without evidence of liver disease; and in groups at risk for HCV infection including those on haemodialysis or family members of people with occult HCV. The clinical relevance of this form of infection is under investigation. The consequences of occult infection appear to be less severe than with chronic infection but can vary from minimal to hepatocellular carcinoma.

The rate of occult infection in those apparently cured is controversial but appears to be low. 40% of those with hepatitis but with both negative hepatitis C serology and the absence of detectable viral genome in the serum have hepatitis C virus in the liver on biopsy. How commonly this occurs in children is unknown.

VIROLOGY

The hepatitis C virus (HCV) is a small, enveloped, single-stranded, positive-sense RNA virus. It is a member of the Hepacivirus genus in the family Flaviviridae. There are seven major genotypes of HCV, which are known as genotypes one to seven. The genotypes are divided into several subtypes with the number of subtypes depending on the genotype. In the United States, about 70% of cases are caused by genotype 1, 20% by genotype 2 and about 1% by each of the other genotypes. Genotype 1 is also the most common in South America and Europe.

The half life of the virus particles in the serum is around 3 hours and may be as short as 45 minutes. In an infected person, about 1012 virus particles are produced each day. In addition to replicating in the liver the virus can multiply in lymphocytes.

TRANSMISSION

The primary route of transmission in the developed world is intravenous drug use (IDU), while in the developing world the main methods are blood transfusions and unsafe medical procedures. The cause of transmission remains unknown in 20% of cases; however, many of these are believed to be accounted for by IDU.

Intravenous drug use

IDU is a major risk factor for hepatitis C in many parts of the world. Of 77 countries reviewed, 25 (including the United States) were found to have prevalences of hepatitis C in the intravenous drug user population of between 60% and 80%. Twelve countries had rates greater than 80%. It is believed that ten million intravenous drug users are infected with hepatitis C; China (1.6 million), the United States (1.5 million), and Russia (1.3 million) have the highest absolute totals. Occurrence of hepatitis C among prison inmates in the United States is 10 to 20 times that of the occurrence observed in the general population; this has been attributed to high-risk behavior in prisons such as IDU and tattooing with nonsterile equipment.

Healthcare exposure

Blood transfusion, transfusion of blood products, or organ transplants without HCV screening carry significant risks of infection. The United States instituted universal screening in 1992 to between one in 10,000 to one in 10,000,000 per unit of blood. This low risk remains as there is a period of about 11–70 days between the potential blood donor's acquiring hepatitis C and the blood's testing positive depending on the method. Some countries do not screen for hepatitis C due to the cost.

Those who have experienced a needle stick injury from someone who was HCV positive have about a 1.8% chance of subsequently contracting the disease themselves. The risk is greater if the needle in question is hollow and the puncture wound is deep. There is a risk from mucosal exposures to blood; but this risk is low, and there is no risk if blood exposure occurs on intact skin.

Hospital equipment has also been documented as a method of transmission of hepatitis C, including reuse of needles and syringes; multiple-use medication vials; infusion bags; and improperly sterilized surgical equipment, among others. Limitations in the implementation and enforcement of stringent standard precautions in public and private medical and dental facilities are known to be the primary cause of the spread of HCV in Egypt, the country with highest rate of infection in the world.

Sexual intercourse

Whether hepatitis C can be transmitted through sexual activity is controversial. While there is an association between high-risk sexual activity and hepatitis C, and multiple sexual partners are a risk factor for hepatitis C, there is no conclusive evidence that hepatitis C can be transmitted by sexual activity, since people who report transmission with sex as their only risk factor may actually have used drugs but denied it. The majority of evidence supports there being no risk for monogamous heterosexual couples. Sexual practices that involve higher levels of trauma to the anogenital mucosa, such as anal penetrative sex, or that occur when there is a concurrent sexually transmitted infection, including HIV or genital ulceration, do present a risk. The United States Department of Veterans Affairs recommends condom use to prevent hepatitis C transmission in those with multiple partners, but not those in monogamous relationships.

Body modification

Tattooing is associated with two to threefold increased risk of hepatitis C. This can be due to either improperly sterilized equipment or contamination of the dyes being used. Tattoos or piercings performed either before the mid-1980s, "underground," or nonprofessionally are of particular concern, since sterile techniques in such settings may be lacking. The risk also appears to be greater for larger tattoos. It is estimated that nearly half of prison inmates share unsterilized tattooing equipment. It is rare for tattoos in a licensed facility to be directly associated with HCV infection.

Shared personal items

Personal-care items such as razors, toothbrushes, and manicuring or pedicuring equipment can be contaminated with blood. Sharing such items can potentially lead to exposure to HCV. Appropriate caution should be taken regarding any medical condition that results in bleeding, such as cuts and sores. HCV is not spread through casual contact, such as hugging, kissing, or sharing eating or cooking utensils. Neither is it transmitted through food or water.

Vertical transmission

Vertical transmission of hepatitis C from an infected mother to her child occurs in less than 10% of pregnancies. There are no measures that alter this risk. It is not clear when during pregnancy transmission occurs, but it may occur both during gestation and at delivery. A long labor is associated with a greater risk of transmission. There is no evidence that breast-feeding spreads HCV; however, to be cautious, an infected mother is advised to avoid breastfeeding if her nipples are cracked and bleeding, or her viral loads are high.

DIAGNOSIS

There are a number of diagnostic tests for hepatitis C, including HCV antibody enzyme immunoassay or ELISA, recombinant immunoblot assay, and quantitative HCV RNA polymerase chain reaction (PCR). HCV RNA can be detected by PCR typically one to two weeks after infection, while antibodies can take substantially longer to form and thus be detected. Chronic hepatitis C is defined as infection with the hepatitis C virus persisting for more than six months based on the presence of its RNA. Chronic infections are typically asymptomatic during the first few decades, and thus are most commonly discovered following the investigation of elevated liver enzyme levels or during a routine screening of high-risk individuals. Testing is not able to distinguish between acute and chronic infections. Diagnosis in the infant is difficult as maternal antibodies may persist for up to 18 months.

Serology

Hepatitis C testing typically begins with blood testing to detect the presence of antibodies to the HCV, using an enzyme immunoassay. If this test is positive, a confirmatory test is then performed to verify the immunoassay and to determine the viral load. A recombinant immunoblot assay is used to verify the immunoassay and the viral load is determined by a HCV RNA polymerase chain reaction. If there are no RNA and the immunoblot is positive, it means that the person tested had a previous infection but cleared it either with treatment or spontaneously; if the immunoblot is negative, it means that the immunoassay was wrong. It takes about 6–8 weeks following infection before the immunoassay will test positive. A number of tests are available as point of care testing which means that results are available within 30 minutes.

Liver enzymes are variable during the initial part of the infection and on average begin to rise at seven weeks after infection. The elevation of liver enzymes does not closely follow disease severity.

Biopsy

Liver biopsies are used to determine the degree of liver damage present; however, there are risks from the procedure. The typical changes seen are lymphocytes within the parenchyma, lymphoid follicles in portal triad, and changes to the bile ducts. There are a number of blood tests available that try to determine the degree of hepatic fibrosis and alleviate the need for biopsy.

Screening

It is believed that only 5–50% of those infected in the United States and Canada are aware of their status. Testing is recommended in those at high risk, which includes injection drug users, those who have received blood transfusions before 1992, those who have been in jail, those on long term hemodialysis, and those with tattoos. Screening is also recommended in those with elevated liver enzymes, as this is frequently the only sign of chronic hepatitis. Routine screening is not currently recommended in the United States. In 2012, the U.S. Centers for Disease Control and Prevention (CDC) added a recommendation for a single screening test for those born between 1945 and 1965.

PREVENTION

As of 2011, no vaccine protects against contracting hepatitis C. However, there are a number under development and some have shown encouraging results. A combination of harm reduction strategies, such as the provision of new needles and syringes and treatment of substance use, decrease the risk of hepatitis C in intravenous drug users by about 75%. The screening of blood donors is important at a national level, as is adhering to universal precautions within healthcare facilities. In countries where there is an insufficient supply of sterile syringes, medications should be given orally rather than via injection (when possible).

TREATMENT

HCV induces chronic infection in 50–80% of infected persons. Approximately 40–80% of these clear with treatment. In rare cases, infection can clear without treatment. Those with chronic hepatitis C are advised to avoid alcohol and medications toxic to the liver, and to be vaccinated for hepatitis A and hepatitis B. Ultrasound surveillance for hepatocellular carcinoma is recommended in those with accompanying cirrhosis.

Medications

In general, treatment is recommended for those with proven HCV infection and signs of liver inflammation. As of 2010, treatments consist of a combination of pegylated interferon alpha and the antiviral drug ribavirin for a period of 24 or 48 weeks, depending on HCV genotype. This produces cure rates of between 70 and 80% for genotype 2 and 3, respectively, and 45 to 70% for other genotypes. When combined with ribavirin, pegylated interferon-alpha-2a may be superior to pegylated interferon-alpha-2b, though the evidence is not strong.

Combining either boceprevir or telaprevir with ribavirin and peginterferon alfa improves antiviral response for hepatitis C genotype 1. Adverse effects with treatment are common, with half of people getting flu like symptoms and a third experiencing emotional problems. Treatment during the first six months is more effective than once hepatitis C has become chronic. If someone develops a new infection and it has not cleared after eight to twelve weeks, 24 weeks of pegylated interferon is recommended. In people with thalassemia, ribavirin appears to be useful but increases the need for transfusions.

Sofosbuvir with ribavirin and interferon appears to be around 90% effective in those with genotype 1, 4, 5, or 6 disease. Sofosbuvir with just ribavirin appears to be 70 to 95% effective in type 2 and 3 disease. This benefit is somewhat offset by a greater rate of adverse effects. Treatments that contain ledipasvir and sofosbuvir for genotype 1 has success rates of around 93 to 99% but is very expensive. In genotype 6 infection, pegylated interferon and ribavirin is effective in 60 to 90% of cases. There is some tentative data for simeprevir use in type 6 disease as well.

Surgery

Cirrhosis due to hepatitis C is a common reason for liver transplantion though the virus usually (80–90% of cases) recurs afterwards. Infection of the graft leads to 10–30% of people developing cirrhosis within five years. Treatment with pegylated interferon and ribavirin post transplant decreases the risk of recurrence to 70%.

Alternative medicine

Alternative medicine Several alternative therapies are claimed by their proponents to be helpful for hepatitis C including milk thistle, ginseng, and colloidal silver. However, no alternative therapy has been shown to improve outcomes in hepatitis C, and no evidence exists that alternative therapies have any effect on the virus at all.

PROGNOSIS

The responses to treatment is measured by sustained viral response and vary by HCV C genotype. A sustained response occurs in about 40–50% in people with HCV genotype 1 given 48 weeks of treatment. A sustained response is seen in 70–80% of people with HCV genotypes 2 and 3 with 24 weeks of treatment. A sustained response occurs about 65% in those with genotype 4 after 48 weeks of treatment. The evidence for treatment in genotype 6 disease is sparse and what evidence there is supports 48 weeks of treatment at the same doses used for genotype 1 disease. Successful treatment decreases the future risk of hepatocellular carcinoma by 75%.

EPIDEMIOLOGY

It is estimated that 150–200 million people, or ~3% of the world's population, are living with chronic hepatitis C. About 3–4 million people are infected per year, and more than 350,000 people die yearly from hepatitis C-related diseases. During 2010 it is estimated that 16,000 people died from acute infections while 196,000 deaths occurred from liver cancer secondary to the infection. Rates have increased substantially in the 20th century due to a combination of intravenous drug abuse and reused but poorly sterilized medical equipment.

Rates are high (>3.5% population infected) in Central and East Asia, North Africa and the Middle East, they are intermediate (1.5%-3.5%) in South and Southeast Asia, sub-Saharan Africa, Andean, Central and Southern Latin America, Caribbean, Oceania, Australasia and Central, Eastern and Western Europe; and they are low (<1.5%) in Asia Pacific, Tropical Latin America and North America.

Among those chronically infected, the risk of cirrhosis after 20 years varies between studies but has been estimated at ~10–15% for men and ~1–5% for women. The reason for this difference is not known. Once cirrhosis is established, the rate of developing hepatocellular carcinoma is ~1–4% per year. Rates of new infections have decreased in the Western world since the 1990s due to improved screening of blood before transfusion.

In the United States, about 2% of people have hepatitis C, with the number of new cases per year stabilized at 17,000 since 2007. The number of deaths from hepatitis C has increased to 15,800 in 2008 and by 2007 had overtaken HIV/AIDS as a cause of death in the USA. This mortality rate is expected to increase, as those infected by transfusion before HCV testing become apparent. In Europe the percentage of people with chronic infections has been estimated to be between 0.13 and 3.26%.

The total number of people with this infection is higher in some countries in Africa and Asia. Countries with particularly high rates of infection include Egypt (22%), Pakistan (4.8%) and China (3.2%). It is believed that the high prevalence in Egypt is linked to a now-discontinued mass-treatment campaign for schistosomiasis, using improperly sterilized glass syringes.

INDEED, ITS A NEW LIFE FOR THE PATIENT

IMAGES

CASE RECORD