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OBJECTIVES: To describe varicella complications in healthy and previously ill children hospitalized for varicella and to explore trends in group A beta-hemolytic streptococcus complications of varicella. METHODS: A retrospective record review of children hospitalized for varicella between January 1, 1990, and March 31, 1994, was conducted in nine large acute care hospitals in Los Angeles County, California. RESULTS: We identified 574 children hospitalized for varicella in study hospitals during the 4.25-year study period (estimated risk of hospitalization, approximately 1 in 550 cases of varicella); 53% of the children were healthy before the onset of varicella and 47% were previously ill with underlying cancers or other chronic illnesses. Children were hospitalized for treatment of complications (n = 427, 74%) or for prophylactic antiviral therapy or observation (n = 147, 26%). Systems involved in complications included skin/soft tissue (45%), neurologic (18%), respiratory (14%), gastrointestinal (10%), and hematologic, renal, or hepatic (8% or less). The mean age of children with skin/soft tissue infections was 2.7 years (range < 1 to 16 years) compared with 4.7 years (< 1 to 18 years) for other complications. Children with skin/soft tissue and neurologic complications were more often previously healthy (p < 0.05), whereas those with respiratory complications were more often previously ill (p < 0.001). Hospitalizations for skin/soft tissue infections increased during the study period. The proportion of complications as a result of group A beta-hemolytic streptococcus infection increased from 4.7% before 1993 to 12.2% for the remainder of the study period (p = 0.02). CONCLUSIONS: Prior health status was predictive of the type of complications experienced by children with varicella requiring hospitalization. Our data suggest a recent increase in skin/soft tissue complications of varicella requiring hospitalization and an increase in the proportion of complications related to group A beta-hemolytic streptococcus. Wide-scale vaccine use should reverse this trend and reduce the overall impact of varicella on both healthy and previously ill children.

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STUDY OBJECTIVE: To determine the effect of immediate resuscitative efforts on the neurological outcome of children with submersion injury. DESIGN: A case-control study was designed to determine if immediate resuscitation by rescuers or bystanders reduces the frequency of severe neurological damage or death in children with a documented submersion event. Logistic regression was used calculate an adjusted odds ratio. PARTICIPANTS: The study group consisted of 166 children, aged zero to 14 years, having a submersion event during May 1984 through August 1992, and admitted through various emergency departments to Huntington Memorial Hospital in Pasadena, California. MEASUREMENTS AND MAIN RESULTS: All study subjects had an observed and documented episode of apnea at the time of submersion. Outcomes were evaluated on the basis of neurological impairment or death. Exposure was verified from historical accounts of postsubmersion events provided by family, friends, and/or paramedical personnel. The study factors included age and gender, duration of submersion, hypothermia, presence of apnea, resuscitative efforts, and clinical outcome. Children with a good outcome were 4.75 (adjusted odds ratio (OR)) times more likely to have a history of immediate resuscitation than children with poor outcome (95% confidence interval: 3.44 < OR < 6.06, P = .0001). Various types of resuscitative efforts and potential confounding factors were also evaluated. CPR and mouth-to-mouth resuscitation were the most effective types for the prevention of death or severe anoxic encephalopathy. CONCLUSION: Immediate resuscitation before the arrival of paramedical personnel is associated with a significantly better neurological outcome in children with submersion injury.

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A case of an infant with diarrhea and acidosis associated with methemoglobinemia is presented. Of interest is that the association of diarrhea and acidosis with methemoglobinemia is more common than previously thought and can produce dangerously high methemoglobin levels. A review of the literature of this unusual occurrence along with clues to making the diagnosis are discussed.

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Between July 1985 and December 1986, 29 near-drowned children ranging in age between 6 months and 13 yr were admitted to the Pediatric ICU of Huntington Memorial Hospital. Eight patients suffered cardiopulmonary arrest and had an admission Glasgow Coma Score of 3 or 4. Hemodynamic monitoring was performed on five of these patients. Three received cerebral resuscitation with controlled hyperventilation, hypothermia, pentobarbital, and mannitol because of intracranial hypertension. After CPR, a low cardiac index (CI) and high systemic vascular resistance index (SVRI) were found. When cerebral resuscitative therapy was initiated later, it caused a reduction of SVRI, CI, mean arterial pressure, and cerebral perfusion pressure. Fluid volume therapy and inotropic cardiac support was necessary to maintain adequate cerebral perfusion pressure. These observations indicate that cerebral resuscitative therapy can affect cardiovascular function. The hemodynamic depressive effects might even worsen the outcome. For this reason, it is advisable to obtain CI and pulmonary capillary wedge pressure to optimize cerebral perfusion and potentially neurologic outcome.

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We compared the levels of hormones and metabolites in the plasma of 37 survivors of Reye's syndrome with the levels in 8 fatal cases, at four time periods within 72 hours of admission. The most prominent differences were found for norepinephrine (NE), which was significantly elevated in fatal cases compared with survivors at all periods. Lactate and dopamine were elevated in the earlier periods. Epinephrine and alpha-amino acid nitrogen were also elevated in fatal cases, but the differences usually were not significant. NE elevation may reflect an increased sympathoadrenal medullary output associated with brain edema, compounded by impaired hepatic clearance of monoamines. Skeletal muscle ischemia from NE-induced vasoconstriction may explain the association between lactic acidemia and the severity of encephalopathy.

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Following reports of a Reye-like syndrome in children resulting from Margosa oil (MO) ingestion, we administered MO to laboratory rats in an attempt to produce an animal model of Reye's syndrome. Male rats were injected intraperitoneally with either MO or corn oil and observed for clinical signs of a toxic response. After 15 h the animals were administered a second dose and the MO-treated animals developed florid neurological symptoms. The animals were then sacrificed and blood samples were analyzed for glucose, ammonia, aspartate aminotransferase, and alanine aminotransferase. Sections of liver, kidney, and brain were examined by light microscopy after Sudan black B, hematoxylin and eosin, and periodic acid-Schiff staining. Liver was additionally examined by electron microscopy. Liver samples were analyzed for hepatic enzyme levels and brain samples were analyzed for water content. There were greatly increased levels of ammonia, aspartate aminotransferase, and alanine aminotransferase and decreased glucose levels in the blood of MO-treated animals. Light microscopy of MO-treated livers revealed fatty infiltration, granularity of the cytoplasm with normal nuclei, and glycogen depletion; electron microscopy revealed mitochondrial pathology in the livers of MO-treated animals. There were no significant morphological changes in brain or kidney specimens although the kidneys did show some fatty infiltration. Hepatic mitochondrial enzyme levels were unchanged and there was no increase in brain water content in the MO-treated animals. Thus, many of the abnormalities seen in Reye's syndrome were seen in this model; however, there were no hepatic enzyme changes despite altered mitochondrial morphology and no evidence of cerebral edema despite a florid encephalopathy. Nonetheless, this model may have important implications for the understanding of the pathogenetic mechanisms of this Reye-like syndrome and, perhaps, Reye's syndrome.

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Discriminant analysis was used to discriminate between Reye syndrome (RS) patients and non-RS cases based either on conventional blood chemistry data obtained upon admission, or on the activities of hepatic mitochondrial enzymes in biopsy or necropsy tissue. The control group for blood chemistry measurements contained children with upper respiratory tract infections, varicella, etc. who did not develop RS, as well as healthy children. Subjects with no liver disorder (e.g., accidental death, sudden infant death, etc.) or with non-RS liver disorders were used as controls for hepatic enzyme studies. Hepatic damage indicators (aspartate aminotransferase, AST; alanine aminotransferase, ALT; and bilirubin) correctly classified 86-96% of non-RS cases and 61-71% of RS. By contrast, AST and ALT had little prognostic value (63% overall correct). Ammonia effectively classified favorable outcome cases (95% correct) but not unfavorable (14% correct). However, when ammonia was included with stage of coma information 88% of the favorable and 85% of the unfavorable outcome cases were correctly classified. Discriminant analysis of hepatic enzymes (glutamate dehydrogenase and monoamine oxidase activity) for a RS and a non-RS group correctly classified 80% of non-RS and 95% of RS specimens. The function was suitable for the direct evaluation of RS-like mitochondrial enzyme changes in rat liver.

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Mitochondrial alterations are known to be constantly associated with Reye's syndrome. Fifty-eight liver specimens from 50 patients who fulfilled the clinical and pathologic criteria were examined by electron microscopy. The degree of mitochondrial injury was graded I, II, and III according to the severity of the alteration of mitochondrial matrix. The results correlated well with clinical parameters--specifically initial clinical stage, peak clinical stage, and clinical outcome. Electron microscopic examination of hepatic mitochondria is therefore potentially useful in evaluating Reye's syndrome patients.

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Five enzymes were measured in 50 liver specimens (18 normal liver, 20 Reye liver, 12 diverse liver disorders other than Reye syndrome). The enzymes were: glutamic dehydrogenase (E.C. 1.4.1.3), monoamine oxidase (E.C. 1.4.3.4), lactate dehydrogenase (E.C. 1.1.1.27), D-glucose-6-phosphate dehydrogenase (E.C. 1.1.1.49), catalase (E.C. 1.11.1.6). The Reye syndrome group showed significant decreases in glutamic dehydrogenase (56%) and monoamine oxidase (70%) compared to normal control tissue and these changes were not characteristic of the non-Reye liver disorder group as a whole. Neither catalase nor lactate dehydrogenase appeared to be altered significantly in the Reye or in the abnormal control group compared with normal controls. Thus, only the prominent decreases in the mitochondrial enzyme activities appeared to be highly characteristic of Reye syndrome. Paradoxically, the means of the five hepatic enzymes and the admission levels of two serum enzymes indicative of liver damage (alanine and aspartate aminotransferase) were remarkably similar for both survivors and nonsurvivors of Reye syndrome.

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The activities of nine enzymes in liver specimens obtained from four children who had died from Reye's syndrome were compared to the corresponding activities of a control group of four children who had died from unrelated causes. At the 95% significance level, the alterations could be classified into three groups. Five activities [lactate dehydrogenase, alanine aminotransferase, glucose 6-phosphatase, cytochrome oxidase, and malate dehydrogenase (mitochondrial plus cytosolic)] showed no change. Three enzymes [glutamate dehydrogenase, isocitrate dehydrogenase (NADP), and monoamine oxidase] were decreased. One activity (glucose 6-phosphate dehydrogenase) was increased. The malate dehydrogenase isozymes were resolved by electrophoresis, and the two bands were stained and measured. The ratio of cytosolic:mitochondrial enzyme was significantly greater in Reye's syndrome than in the control group. These results lend further support to the view that in Reye's syndrome the impairment of hepatic function is largely confined to the mitochondria. The lowered activity of monoamine oxidase means that the abnormalities extend to the outer mitochondrial membrane. Imbalances of the cytosolic:mitochondrial enzyme activities were evaluated in needle biopsy specimens from four other children under conditions where neurologic abnormalities were less severe. Two patients had elevated ratios of both glutamate:lactate dehydrogenase and cytosolic:mitochondrial malate dehydrogenase activities, and a third had only an abnormal malate dehydrogenase ratio. In contrast to these Reye's syndrome patients, a fourth case admitted with a provisional diagnosis of Reye's syndrome showed no abnormality in either ratio in stage IV coma.

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Ninety children with acute epiglottitis were admitted from 1971 - 1977. Lateral extended neck radiograph was found to be a quick, safe and reliable way to establish the diagnosis. Out of 79, 77 (97%) had blood cultures yielding Hemophilus influenzae type b. Immediate institution of airway and antibiotics were the mainstay of treatment. All patients in the series survived. For short-term airway management, as in acute epiglottitis, nasotracheal intubation under general anesthesia was found to be the airway of choice.

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Three patients with initial clinical manifestations and biochemical findings suggestive of a diagnosis of Reye's syndrome had acute renal insufficiency develop and had evidence of consumptive coagulopathy, not generally considered features of the syndrome. As a group, they could not be distinguished, either on the basis of their clinical manifestations or liver pathologic findings, from the 17 patients with Reye's syndrome without renal failure seen in our institution during the same period of time. The use of osmotic diuretics in an effort to decrease cerebral edema may be life threatening in these patients with compromised renal function since hypervolemia, cardiac failure, and worsening of cerebral edema may occur.

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