{"id":7547,"date":"2017-07-31T00:27:27","date_gmt":"2017-07-30T20:27:27","guid":{"rendered":"http:\/\/aroxjblog.am\/?p=7547"},"modified":"2017-07-31T00:32:02","modified_gmt":"2017-07-30T20:32:02","slug":"reyes-syndrome","status":"publish","type":"post","link":"https:\/\/aroxjblog.am\/en\/reyes-syndrome\/","title":{"rendered":"Reye\u2019s Syndrome"},"content":{"rendered":"

General Surgery \u2013 DOCTOR EB<\/p>\n

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DEFINITION<\/strong>
\nReye\u2019s syndrome is a postinfectious triad consisting of encephalopathy, fatty liver degeneration, and transaminase elevation.<\/p>\n

EPIDEMIOLOGY & DEMOGRAPHICS<\/strong>
\n\u2022 During the 1970s, 300 to 600 cases were being reported yearly in the U.S.
\n\u2022 Since the mid-1980s, after the understanding that aspirin is associated with Reye\u2019s syndrome, the yearly count has fallen to <20 cases
\n\u2022 Seasonal relation with influenza and varicella outbreaks
\n\u2022 Age: rare in persons aged >18 yr; peak age (in the U.S.) is 6 to 8 yr
\n\u2022 Case-fatality rate: 25% to 50%
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\nETIOLOGY<\/strong>
\n\u2022 Temporal association with influenza and varicella infection
\n\u2022 Epidemiologic association with aspirin or other salicylate use to treat the viral infection
\n\u2022 Possible association with aflatoxin and pesticides
\n\u2022 Pathology<\/p>\n

\u2022 Liver: no inflammation; the striking finding is panlobular microvesicular hepatocyte infiltration on light microscopy and mitochondrial injury on electron microscopy
\n\u2022 Brain: no inflammation but cerebral edema and anoxic degeneration
\n\u2022 Pathogenesis: not fully understood but mitochondrial dysfunction is clearly center stage<\/p>\n

DIFFERENTIAL DIAGNOSIS<\/strong>
\n\u2022 Inborn errors of metabolism (e.g., carnitine deficiency, ornithine transcarbamylase deficiency)
\n\u2022 Salicylate or amiodarone intoxication
\n\u2022 Jamaican vomiting sickness
\n\u2022 Hepatic encephalopathy of any cause
\n\u2022 Table E1-433 describes diseases that present a clinical or pathologic picture resembling
\nReye\u2019s syndrome.<\/p>\n

LABORATORY TESTS<\/strong>
\n\u2022 Elevated transaminase (alanine aminotransferase and aspartate aminotransferase)
\n\u2022 Elevated ammonia level
\n\u2022 Occasional elevation of creatine phosphokinase, lactate dehydrogenase, and bilirubin and prolongation of prothrombin time
\n\u2022 Occasional hypoglycemia (in patients <4 yr)
\n\u2022 Cerebrospinal fluid is normal or contains <8 white blood cells per milliliter
\n\u2022 Rarely a liver biopsy is indicated (in infants or in recurrent cases)
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\nTREATMENT<\/strong>
\n\u2022 Supportive
\n\u2022 Mannitol, glycerol, or hyperventilation for cerebral edema if present
\n\u2022 Interferon-alfa (experimental)
\n\u2022 Prevention
\nInfluenza vaccine
\nVaricella vaccine
\nAvoidance of aspirin in children, especially during influenza and varicella outbreaks<\/p>\n<\/div>\n

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