Reye Syndrome -- United States, 1985

For the 1985 surveillance year,* 91 cases of Reye syndrome (RS) meeting CDC's case definition** were reported. Although delayed reports through June 1986 may increase the number of cases for 1985, the provisional 1985 total is less than half the lowest annual total reported through the National Reye Syndrome Surveillance System (NRSSS) since its initiation in December 1973 (Table 1).

Cases were reported from 31 states. The sex and race distributions were similar to previous years. Of patients for whom this information was reported, 52% were female; 89%, white; 7%, black; and 4%, of Asian or American Indian extraction. Fifty-three percent of RS patients were 0-4 years of age; 20%, 5-9 years of age; 19%, 10-14 years of age; 5%, 15-19 years of age; and 3%, 20 years of age or older. The reported incidence of RS among children in all age groups has decreased in recent years (Figure 4).

Most patients (57%) reported thus far for 1985 were hospitalized in January and February. This primarily reflected the increased incidence of viral respiratory infections among children during those months. The predominant influenza isolate during this period was influenza A(H3N2) (1).

For 84 (92%) of the patients, a prodromal illness occurring within 2 weeks before the onset of vomiting or neurologic symptoms of RS was reported. Fourteen (17%) of these had varicella reported as their prodromal illness, compared with 26 (13%) patients in 1984. For the remainder of patients in 1985, the prodromal illness was characterized by respiratory symptoms (67%), diarrhea without respiratory symptoms (8%), or other signs and symptoms, including fever alone (7%).

The largest percentages of patients were admitted to hospitals in the three precomatose stages of RS: stage I--39%; stage II--28%; or stage 0--9%. The deepest stages of RS attained by the hospitalized patients were: stage I--36% of patients; stage II--23%; stage III--5%; stage IV--4%; and stage V--32%. The short-term outcomes were reported for 87 (96%) of the RS patients; 28 died, for a case-fatality rate of 32%. Reported by Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: The NRSSS provides crude annual comparisons of RS activity, although the number of cases reported underestimates true RS incidence and mortality. Because state health departments and CDC are more likely to become aware of fatal cases, the reported case-fatality ratios are probably overestimated.

During the 1985 surveillance year, the annual RS incidence was the lowest reported since the NRSSS was initiated. In previous years, the RS incidence, at least in part, has reflected the intensity and type of influenza activity. By all surveillance parameters, 1985 influenza activity was comparable in intensity to 1984, and the activity was greater than in 1982 or 1983. However, the predominant isolate was influenza A(H3N2), which has been generally associated with fewer cases of RS than influenza types B or A(H1N1). Nonetheless, the number of RS cases reported in 1985 was markedly lower than in the 3 previous years (1978, 1981, and 1983) that influenza A(H3N2) predominated (Table 1). In addition, varicella-associated RS cases reported annually declined by over 60% during 1981-1984, and the decline appears to be continuing during 1985, despite relatively stable annual varicella activity.

During 1981-1984, the number of reported RS cases consistently declined among children under 10 years of age; no such decrease occurred in the number of patients 10-19 years of age (2). During 1985, the continued decrease in RS incidence among patients 0-9 years of age was accompanied by an even larger decrease in incidence among patients 10-19 years of age (Figure 1).

Between 1981 and 1985, a less rapid decrease in RS incidence among children under 2 years of age has led to an increasing proportion of RS cases in this age group. This may be related, in part, to a long-standing difficulty in the diagnosis of RS in young children. It may be particularly difficult to distinguish RS from anoxic encephalopathy and inborn errors of metabolism in these children (3,4). At a National Institutes of Health Consensus Development Conference on the Diagnosis and Treatment of Reye Syndrome, it was recommended that, although RS diagnosis can be made in most patients without a liver biopsy, biopsy should be considered in very young children (5). It has been suggested, however, that the pathologic changes seen may not always reliably differentiate RS from inborn errors of metabolism (6). Recently, the specificity of light microscopy changes on postmortem examination considered to be characteristic of RS has been challenged (7). Thus, before the diagnosis is established, the possibility of other more reasonable explanations for the cerebral and hepatic abnormalities should be explored, particularly in infants and young children. Histochemical staining and electron-microscopic examination of the liver, as well as a serum amino-acid profile, may help increase the specificity of diagnosis (8,9).

The intensity of RS surveillance usually depends partially on the awareness of the illness among the public and medical personnel and the ease and perceived importance of reporting cases. The low reported RS incidence in 1985 occurred during widespread publicity about the probable increased risk of RS associated with the use of aspirin for teenagers, as well as for younger children, with influenza-like illnesses or chickenpox.

Following the results of the pilot phase of the U.S. Public Health Service study on RS and medications (10), the U.S. Food and Drug Administration has proposed that oral over-the-counter medicine containing aspirin add a label reading: WARNING: Children and teenagers should not use this medicine for chickenpox or flu symptoms before a doctor is consulted about Reye syndrome, a rare but serious disease.

For the 1985-1986 influenza season, increasing numbers of states are reporting influenza virus isolates, predominantly types B and A(H3N2). Physicians and other appropriate personnel in the medical community are encouraged to continue reporting RS cases to CDC through their local and state health departments. RS case-report forms can be obtained from state health departments or the Epidemiology Office, Division of Viral Diseases, Center for Infectious Diseases, CDC, Atlanta, Georgia 30333.

References

1. CDC. Influenza--United States, 1984-1985 season. MMWR 1985;34:440-3.

2. CDC. Reye syndrome--United States, 1984. MMWR 1985;34:13-6.

3. Trauner DA. Reye's syndrome. In: Gluck L, ed. Current problems in pediatrics. Chicago: Year Book Medical Publishers, Inc. 1982;1-31.

4. Crocker JF, Bagnell PC. Reye's syndrome: a clinical review. Can Med Assoc J 1981;124:375-82.

5. National Institutes of Health. Diagnosis and treatment of Reye's syndrome. JAMA 1981;246:2441-4.

6. Huttenlocher PR, Trauner DA. Reye's syndrome in infancy. Pediatrics 1978;62:84-90.

7. Bonnell HJ, Beckwith JB. Fatty liver in sudden childhood death. Implications for Reye's syndrome? Am J Dis Child 1986;140:30-3.

8. Bove, KE, McAdams AJ, Partin JC, Partin JS, Hug G, Schubert WK. The hepatic lesion in Reye's syndrome. Gastroenterology 1975;69:685-97.

9. Romshe CA, Hilty MD, McClung HJ, Kerzner B, Reiner CB. Amino acid pattern in Reye syndrome: comparison with clinically similar entities. J Pediatrics 1981;98:788-90.

10. Hurwitz ES, Barrett MJ, Bregman D, et al. Public Health Service study on Reye's syndrome and medications. Report of the pilot phase. N Engl J Med 1985;313:849-57. *For surveillance purposes, the Reye syndrome year extends from December 1 through November 30 (i.e., the 1985 year runs from December 1, 1984, through November 30, 1985). The data for 1985 are preliminary and include cases reported as of January 15, 1986. **The CDC case definition is (1) acute noninflammatory encephalopathy documented clinically by an alteration in consciousness and, if available, a record of cerebrospinal fluid containing eight leukocytes or fewer per mm((3)), or by histologic specimen demonstrating cerebral edema without perivascular or meningeal inflammation; (2) hepatopathy documented by either a liver biopsy or autopsy considered to be diagnostic of Reye syndrome, or a threefold or greater rise in the levels of either the SGOT, SGPT, or serum ammonia; and (3) no more reasonable explanation for the cerebral or hepatic abnormalities.

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