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Clubfoot deformity in Children

 Musculoskeletal System, Neonatology  No Responses »
Aug 102011
 
The most common congenital disorder of the lower extremities, clubfoot, or talipes, is marked primarily by a deformed talus and shortened Achilles tendon, which give the foot a characteristic clublike appearance. In talipes equinovarus, the foot points downward (equinus) and turns inward (varus), and the front of the foot curls toward the heel (forefoot adduction).
Clubfoot, which has an incidence of about 1 per 1,000 live births, usually occurs bilaterally and is twice as common in boys as it is in girls. It may be associated with other birth defects, such as myelomeningocele, spina bifida, and arthrogryposis. Clubfoot is correctable with prompt treatment.
Causes
A combination of genetic and environmental factors in utero appears to cause clubfoot. Heredity is a definite factor in some cases, although the mechanism of transmission is undetermined. If a child is born with clubfoot, his sibling has a 1 in 35 chance of being born with the same anomaly. Children of a parent with clubfoot have 1 chance in 10.
In children without a family history of clubfoot, this anomaly seems linked to arrested development during the 9th and 10th weeks of embryonic life, when the feet are formed. Researchers also suspect muscle abnormalities, leading to variations in length and tendon insertions, as possible causes of clubfoot.
Signs and symptoms
Talipes equinovarus varies in severity. Deformity may be so extreme that the toes touch the inside of the ankle, or it may be only vaguely apparent.
In every case, the talus is deformed, the Achilles tendon shortened, and the calcaneus somewhat shortened and flattened. Depending on the degree of the varus deformity, the calf muscles are shortened and underdeveloped, with soft-tissue contractures at the site of the deformity. The foot is tight in its deformed position and resists manual efforts to push it back into normal position.
Clubfoot is painless, except in older, arthritic patients. In older children, clubfoot may be secondary to paralysis, poliomyelitis, or cerebral palsy, in which case treatment must include Continue reading »
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Reye’s syndrome

 Liver Diseases, Metabolic Disorders  No Responses »
Aug 092011
 
An acute childhood illness, Reye’s syndrome causes fatty infiltration of the liver with concurrent hyperammonemia, encephalopathy, and increased intracranial pressure (ICP). In addition, fatty infiltration of the kidneys, brain, and myocardium may occur.
Reye’s syndrome affects children. It’s most common in patients ages 4 to 12, with a peak incidence at age 6.
The prognosis depends on the severity of central nervous system depression. Previously, mortality was as high as 90%. Today, ICP monitoring and, consequently, early treatment of increased ICP, along with other treatment measures, have cut mortality to about 20%. Death is usually a result of cerebral edema or respiratory arrest. Comatose patients who survive may have residual brain damage.
Causes
Incidence of Reye’s syndrome usually rises during influenza outbreaks and is linked to aspirin use. It almost always follows within 1 to 3 days of an acute viral infection, such as an upper respiratory tract infection, type B influenza, or varicella (chickenpox).
With Reye’s syndrome, damaged hepatic mitochondria disrupt the urea cycle, which normally changes ammonia to urea for its excretion from the body. This results in hyperammonemia, hypoglycemia, and an increase in serum short-chain fatty acids, leading to encephalopathy. Simultaneously, fatty infiltration is found in renal tubular cells, neuronal tissue, and muscle tissue, including the heart.
Signs and symptoms
Reye’s syndrome develops in five stages, but the severity of the child’s signs and symptoms varies with the degree of encephalopathy and cerebral edema. Infants may have atypical presentation.
After the initial viral infection, a brief recovery period follows when the child doesn’t seem seriously ill. A few days later, he develops intractable vomiting, lethargy, rapidly changing mental status (mild to severe agitation, confusion, irritability, delirium), hyperactive reflexes, and rising blood pressure, respiratory rate, and pulse rate.
Reye’s syndrome may progress to coma. As the coma deepens, seizures develop, followed by decreased tendon reflexes and, commonly, respiratory failure. Continue reading »
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Diagnosing autistic disorder

 Genetics, Neurology  No Responses »
Jul 212011
 
Autism is diagnosed when the patient meets the criteria in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition – Text Revision. At least six characteristics from the following three categories must be present, including at least two from the social interaction category and one each from the communication and patterns categories.
Social interaction
Patient displays impairment in social interaction, as shown by at least two of the following:
  • marked impairment in the use of multiple nonverbal behaviors, such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction
  • failure to develop peer relationships appropriate to developmental level
  • no spontaneous sharing of enjoyment, interests, or achievements with others
  • lack of social or emotional reciprocity
  • gross impairment in ability to make peer friendships.
Communication
Patient displays impairment in communication, as shown by at least one of the following:
  • delay in or total lack of development of spoken language
  • in individuals with adequate speech, marked impairment in initiating or sustaining a conversation with others
  • stereotyped and repetitive use of language or idiosyncratic language
  • lack of varied, spontaneous make-believe play or social imitative play appropriate to developmental level.
Patterns
Patient displays restricted, repetitive, and stereotyped patterns of behavior, interests, and Continue reading »
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