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Query: UMLS:C0035400 (Reye's syndrome)
 879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The encephalopathy of Reye's syndrome is frequently complicated by increased intracranial pressure (ICP) which may lead to death or severe neurologic sequelae. An understanding of the pathophysiology of increased ICP is necessary to prevent further increases in pressure and to reduce pressure while maintaining adequate cerebral perfusion. Four of seven children with Reye's syndrome and increased ICP survived after reduction of increased ICP by controlled hyperventilation and osmotherapy while being monitored with the Richmond intracranial bolt. Careful anesthetic and critical-care management, appropriate, reliable monitoring, and pentobarbital therapy may constitute the most successful therapy to date for patients with Reye's syndrome and increased ICP.
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PMID:Critical care and anesthetic management of Reye's syndrome. 45 52

Reye's syndrome (encephalopathy and fatty liver) is generally considered a disease of children. Four patients, aged 16, 18, 19, and 23 years, with Reye's syndrome were initially seen by internists. A viral prodrome followed by vomiting and encephalopathy without focal neurological signs or jaundice clinically suggested Reye's syndrome. Normal findings of CSF examination (except for increased opening pressure), abnormal findings of liver function tests, and increased blood ammonia further supported the diagnosis. None was hypoglycemic. Reye's syndrome was related to influenza B virus in three patients and to Varicella in another. Three patients survived. Reye's syndrome may be seen intially by general practitioners, emergency room physicians, internists, or psychiatrists. The importance of considering this syndrome in the differential diagnosis of unexplained encephalopathy in adults is stressed.
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PMID:Reye's syndrome in nonpediatric age groups. 48 May 58

A new concept of neurointensive care is presented which is based on earily measured parameters such as intracranial pressure (ICP), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) (CPP = MAP - ICP). ICP should preferably be measured by a subarachnoid hollow screw (Richmond screw). Of chief importance in neurointensive care (after adequate neurodiagnosis) is the avoidance or treatment of cerebral edema and maintenance of sufficient CPP, which should be above 50 mm Hg in older children. This is achieved by controlled hyperventilation under curare, generous oxygenation, control of body temperature, dexamethasone and possibly barbiturates in very high doses (phenobarbital and thiopentone). This kind of neurointensive care should be administered in all types of severe CNS accidents which are followed by substantial cerebral edema (head injuries, near drowning, Reye's syndrome, hypoxic encephalopathy, encephalitis, meningitis and intracranial bleeding). To obtain the indication for ICP monitoring, the depth of the disturbance of consciousness is measured by the Glasgow Coma Scale. Children with the aforementioned affections and a Glasgow Coma Scale below 6 to 8 should be treated as outlined above. The data published in the literature and our own experience point very much in this direction, especially for severe head injury, Reye's syndrome and near drowning.
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PMID:[Continuous monitoring of intracranial pressure and new aspects of neurologic intensive care for children]. 52

Reye's syndrome or encephalopathy with fatty infiltration of the liver occurs mainly in childhood and to a lesser degree in adult age. This report concerns a rare adult case of this syndrome in Europe. The different diagnostic steps are described, with special emphasis on the enzymatic disturbances of the Krebs-Henseleit cycle and on the morphological criteria needed to confirm the diagnosis.
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PMID:Reye's syndrome in an adult. 54 59

The authors studied four children with Reye's syndrome aged 16 months, 6 years, 8 years and 11 years respectively with severe liver failure and progressive coma. The laboratory investigations in all of them showed a marked elevation of serum transaminases, hyperammoniaemia and a prolongation of the prothrombin time. The electroencephalograms showed a grossly abnormal picture with generalised continuous delta activity. Three children survived with return to normal of the liver function tests whilst the fourth child died. In the last two patients an electroencephalogram carried out every six hours has enabled certain prognostic features to be determined. Improvement in the E.E.G. correlates closely with clinical improvement and vice versa. The authors also advocate serial E.E.G. recordings in Reye's syndrome. The role of hyperammonaemia in the genesis of encephalopathy and the electroencephalographic changed is discussed. The role played by raised intracranial pressure is stressed and the importance of controlling it in order to prevent further damage and improve the prognosis of this serious illness.
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PMID:[Reye's syndrome a clinical and electrophysiological study of four patients (author's transl)]. 61 96

Blood substrate and hormone concentration were determined in 16 children with Reye syndrome prior to and following administration of hypertonic glucose. Baseline concentrations of lactate, pyruvate, alanine, glutamine, glutamate, proline, hydroxyproline, lysine, and aspartate were elevated (p less than 0.01), whereas citrulline and arginine were low. All substrate concentrations were below or within the normal range following 36 hours of therapy except those of lactate, pyruvate, and aspartate. Urea nitrogen excretion was reduced (p less than 0.05) on the second day of therapy. Plasma concentrations of insulin and growth hormone increased and glucagon decreased during the first day. Cortisol remained elevated throughout the study period. We conclude that the high circulating concentrations of substrates are the result of both increased mobilization and decreased clearance and that hypertonic glucose infusion suppresses substrate mobilization. A primary abnormality of the mitochondria could explain the metabolic perturbations that occurred. A possible relationship between the encephalopathy in this disorder and an insult to both brain and brain capillary mitochondria is discussed.
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PMID:Metabolic response to hypertonic glucose administration in Reye syndrome. 66 61

We report Reye syndrome in an 11-year-old boy whose first symptoms were generalized convulsions and coma without clinical or laboratory evidence of liver disease. Serum glutamic oxaloacetic transaminase and lactate dehydrogenase (LDH) values increased strikingly on the third day after the onset of coma. These enzymatic changes were associated with prolongation of prothrombin time. A rise in blood ammonia concentrations began on the fourth day of coma. The diagnosis of Reye syndrome was confirmed by a liver biopsy and at autopsy. This case demonstrates that encephalopathy in Reye syndrome can develop prior to detectable hepatic involvement, and suggests that factors unrelated to generalized liver damage may occasionally play a role in the pathogenesis of this obscure disorder.
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PMID:Reye syndrome without initial hepatic involvement. 84 16

The encephalopathy of Reye's syndrome is a potentially reversible, treatable problem in many cases. Treatment requires (1) accurate, early diagnosis; (2) the prevention of anoxia; (3) the restitution of body glycogen stores through the administration of glucose; (4) the control of the complicating cerebral edema; (5) the avoidance of counterproductive treatment measures, such as the unwarranted infusion of sodium bicarbonate and the inappropriate use of respiratory depressing anticonvulsants; and (6) the early and aggressive use of exchange transfusion.
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PMID:Hepatic encephalopathy and Reye's syndrome. 85 74

Between December 15, 1973, and Jun 30, 1974, a total of 379 cases of Reye's syndrome was reported to the Center for Disease Control. One hundred forty-seven (40%) were confirmed by either autopsy or biopsy, while 232 were diagnosed by clinical and laboratory parameters. Comparisons of the epidemiologic and demographic characteristics, the hospital course, the outcome, and the laboratory abnormalities of the clinically diagnosed and the pathologically confirmed cases revealed no significant differences. In the epidemiologic setting of influenza B outbreaks, children who have the acute onset of noninflammatory encephalopathy associated with elevated serum transaminase levels, hypoprothrombinemia, and elevated blood ammonia levels should be considered to have Reye's syndrome. Further evaluation of diagnostic criteria is needed, however, for sporadically occurring, nonepidemic cases of noninflammatory encephalopathy associated with hepatic dysfunction.
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PMID:Diagnostic criteria for influenza B-associated Reye's syndrome: clinical vs. pathologic criteria. 91 32

Report of the successful use of a decompressive craniectomy for the encephalopathy of Reye's syndrome with increased intracranial pressure. The patient had failed to respond to all medical management.
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PMID:Decompressive craniectomy for the encephalopathy of Reye's syndrome. 95 59


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