History and exam
Key diagnostic factors
common
vomiting
Patients present with persistent and profuse vomiting. May or may not have volume depletion.
altered mental status
May initially start as lethargy and proceed to irritability, delirium, combativeness, disorientation, and coma.
Other diagnostic factors
common
hyperventilation
More commonly present in younger patients.
hepatomegaly
Present in 50% of patients at the time of diagnosis.
abnormal pupillary response
May be helpful in assessing disease severity (stage): dilated/sluggish in stage 2, fixed/dilated in stage 4, unresponsive in stage 5.[2]
hyperreflexia/areflexia
Helpful in assessing disease stage. In stage 2, patients may show hyperreflexive response. Areflexia is seen in stage 5.[2]
diminished pain response
In early stages (1-2), patients are responsive to pain.[2] If unresponsive, patients are considered to be at stage 3 or higher.
seizures
May occur in late stages of disease.
uncommon
absence of, or minimal, jaundice and scleral icterus
Jaundice is typically not a feature of Reye syndrome.
Risk factors
strong
age 5-14 years
white ethnicity
CDC surveillance data for 1980 to 1997 showed that 93% of patients were white, 5% were black, 2% were Asian, and 0.3% were Native American or Native Alaskan.[5]
recent viral infection
Antecedent viral illness during the three week period prior to onset of Reye syndrome was reported in 93% of patients (n=1080) for whom data was available (n=1160).[5]
Of these, 73% had influenza-like illness, 21% had varicella-zoster infection, 14% had viral gastroenteritis, and 5% had viral exanthema.[5]
weak
aspirin (acetylsalicylic acid) and other drug exposure
Aspirin is the drug classically associated with Reye syndrome and has been studied the most.[5] However, studies have not clearly supported or refuted a cause-effect relationship between aspirin intake and Reye syndrome in children.[8]
Other drugs include antiemetics, valproic acid, outdated tetracyclines, zidovudine, didanosine, and acetaminophen.
genetically predisposed individual
Data suggest that an exogenous factor contributes to the mitochondrial dysfunction in certain genetically predisposed individuals with Reye syndrome.[7]
toxin exposure
Aflatoxin, margosa oil, hypoglycin (found in unripe ackee fruit), various pesticides, polyethylene, and various insecticides have been implicated.
winter/spring presentation
In the US, an increase in the number of cases of Reye syndrome was found during the months of December through April, which correlated with the peak occurrences of most viral respiratory infections.[5] Since the 1990s, this seasonal association has diminished. Globally, a seasonal predominance has not been found.[5]
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