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Concept
Reye syndrome
Summary
Reye syndrome is a rapidly worsening brain disease. Symptoms of Reye syndrome may include vomiting, personality changes, confusion, seizures, and loss of consciousness. While liver toxicity typically occurs in the syndrome, jaundice usually does not. Death occurs in 20–40% of those affected with Reye syndrome, and about a third of those who survive are left with a significant degree of brain damage.
The cause of Reye syndrome is unknown. It usually begins shortly after recovery from a viral infection, such as influenza or chickenpox. About 90% of cases in children are associated with aspirin (salicylate) use. Inborn errors of metabolism are also a risk factor. The syndrome is associated with changes on blood tests such as a high blood ammonia level, low blood sugar level, and prolonged prothrombin time. Often, the liver is enlarged in the syndrome.
Prevention is typically by avoiding the use of aspirin in children. When aspirin was withdrawn for use in children in the US and UK in the 1980s, a decrease of more than 90% in rates of Reye syndrome was seen. Early diagnosis of the syndrome improves outcomes. Treatment is supportive; mannitol may be used to help with the brain swelling.
The first detailed description of Reye syndrome was in 1963 by Australian pathologist Douglas Reye. The syndrome most commonly affects children. It affects fewer than one in a million children a year. The general recommendation to use aspirin in children was withdrawn because of Reye syndrome, with use only recommended in Kawasaki disease.
Reye syndrome progresses through five stages:
Stage I
Vasoconstrictive rash on palms of hands and feet
Persistent, heavy vomiting that is not relieved by not eating
Generalized lethargy
Confusion
Nightmares (possible symptom)
No fever usually present
Headaches
Stage II
Deep lethargy
Delirium
Confusion
Combative behavior
Stupor
Hyperventilation
Fatty liver (found on biopsy)
Hyperactive reflexes
Stage III
Continuation of Stage I and II symptoms
Possible coma
Possible cerebral edema
Possible seizures
Rarely, respiratory arrest
Decorticate posturing
Stage IV
Seizures
Decerebrate posturing
Deepening coma
Dilated pupils with minimal response to light
Loss of oculocephalic reflexes
Minimal but still present liver dysfunction
Stage V
Very rapid onset following stage IV
Areflexia
Deep coma
Dilated, nonreactive pupils
Isoelectric EEG
Respiratory arrest
Seizures
Multiple organ failure
Flaccidity
Hyperammonemia (above 300 mg/dL of blood)
Death
The cause of Reye syndrome is unknown.
Official source
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