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 10,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The number of children in this report treated with either TBW or exchange transfusions is small. Case mortality rates among children with Reye syndrome in Stage IV coma tends to be exceedingly high, varying from 50 to 100%. Intracranial pressure monitoring with the subarachnoid screw may have been an additional factor in increasing our survival data in three patients in the TBW group, since it provided continuous monitoring of ICP and allowed judicious administration of mannitol intravenously. Survival of five of six patients without neurologic sequelae in the present series has encouraged us to coninue utilization of TBW in children with Stage IV Reye syndrome.
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PMID:Hypothermic total body washout and intracranial pressure monitoring in Stage IV Reye syndrome. 83 85

Intracranial pressure has been monitored in ten patients with Reye syndrome. All of the patients were comatose and all were treated with dexamethasone, mannitol, hyperventilation, and multiple exchange transfusions. Five of these children are alive and well; five died. In each case ICP monitoring allowed for immediate treatment and evaluation of the mode of therapy used to reduce elevated ICP. Exchange transfusions in all patients either reduced the increased ICP or made the pressure rises easier to manage. ICP is not always reflected by lumbar spinal fluid pressure or clinical state. In our hands, ICP monitoring has proved to be a safe technique for the investigation of the significance of raised ICP in the outcome of patients with Reye syndrome and of the effectiveness of a chosen therapy in reducing this pressure.
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PMID:The effects of exchange transfusion on intracranial pressure in patients with Reye syndrome. 105 37

Reye syndrome, a reversible metabolic encephalopathy and hepatopathy, offers a unique opportunity to investigate the pharmacologic mechanisms by which a toxic-metabolic insult to mitochondria is translated into neurochemical and neurologic dysfunction. Similarity of some clinical and metabolic abnormalities between certain inborn errors of organic acid, ammonia, and carbohydrate metabolism and Reye syndrome suggests a common pathophysiologic mechanism at some level. The primary metabolic aberration in Reye syndrome is unknown. Viral, drug, and toxic precipitants in a conductive host alter glial and neuronal function, possibly by direct toxic effects or by altered transmitter metabolism and signal transduction. These events translate into a rather stereotyped progression of the clinical syndrome. Increased ICP, which is a life-threatening epiphenomenon, is the focus of conventional therapy. Investigational treatments, still in preliminary stages, are aimed at early correction of instigating metabolic abnormalities or correction of their consequences on central neurotransmission. Our fragmentary knowledge of neurotransmitter abnormalities in this disorder, which have suggested disparate interpretations, does not allow a cohesive pharmacologic theory of Reye syndrome. The greatest difficulties in interpretation of possible central mechanisms from existing data, which derive largely from peripheral tissues, is in the differentiation of primary from compensatory changes. The unitarian notion that a single pharmacologic disturbance is the source of the encephalopathy is perhaps too simplistic. It is hoped that future studies of disorders such as Reye syndrome will elucidate the intricate relationships between biochemical pathways and neurotransmitter metabolism.
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PMID:Pharmacology of Reye syndrome. 284 66

Monitoring modalities unique to the neurologic intensive care unit include intracranial pressure monitors and neuroelectrophysiologic monitors. Each modality fullfills criteria for accuracy, responsivity during clinical change, and stability over time for trend analysis. Intracranial pressure monitoring may be accomplished by any of three approaches--ventricular catheter, subarachnoid bolt, or epidural pressure transducer. Intracranial pressure control has proved beneficial in at least three different illnesses--acute closed head injury, acute noncommunicating hydrocephalus, and Reye's syndrome. Other illnesses, such as cerebral hemorrhage, near drowning, meningitis, encephalitis, and cerebral mass lesions, are often associated with ICP elevations. Neuroelectrophysiologic monitoring encompassing electroencephalography (EEG), signal-processed EEG, and evoked potentials has proved to be most beneficial to the intensive care setting. Evoked potentials are most useful for monitoring patients in drug-induced coma or muscle paralysis in whom a clinical neurologic examination is unreliable. Focal neurologic deficits, incipient brainstem ischemia, and possibly brain death can be deduced from multimodality-evoked potentials (brainstem auditory and somatosensory). Evoked potential apparatus can be used to record sequential stimuli and trend changes. Signal-processed EEG apparatus (compressed spectral array and cerebral function monitor) are used to assess global or regional EEG activity for longer periods of time. Interpretation of signal-processed EEG recording requires some experience with this technique, but it is much easier to interpret than a standard 16-lead EEG. These monitors are useful in evaluating some forms of abnormal EEG activity and in monitoring gross changes in global or regional electrical activity. Currently available technology offers dynamic insight into the management of acute neurologic illnesses. The technology in evoked potential and signal processed EEG monitoring will eventually reduce the size and complexity of the instrumentation, making its application routine. Intracranial pressure monitoring is already routine in many intensive care units, although its use is occasionally sporadic. We believe that application of appropriate neurologic monitors improves therapy and outcome in neurologically injured and ill patients.
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PMID:Neurologic intensive care unit monitoring. 391 79

Reye's syndrome is a potentially devastating neurologic illness seen predominantly in children following a viral prodrome. The cause is unknown. The clinical history and laboratory presentation are stereotypical and easy to recognize if the clinician considers the diagnosis. Neurologic dysfunction is characterized by lethargy, obtundation, persistent vomiting, agitated delirium, and coma. Death is secondary to severe cerebral swelling with elevation of intracranial pressure. Although no specific therapy has been clearly demonstrated to be superior in terms of outcome, most clinicians have adopted a management scheme aimed at lowering and controlling the elevated ICP. We have described the management protocol in use at the Children's Hospital of Philadelphia. The protocol is summarized in the Appendix for the convenience of the reader.
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PMID:Management of Reye's syndrome. 391 81

Glycerol is a potent osmotic dehydrating agent with additional effects on brain metabolism. In doses of 0.25-2.0 g/kg glycerol decreases intracranial pressure in numerous disease states, including Reye's syndrome, stroke, encephalitis, meningitis, pseudotumor cerebri, central nervous system tumor, and space occupying lesions. It is also effective in lowering intraocular pressure in glaucoma and shrinking the brain during neurosurgical procedures. Hyperosmolality with rebound cerebral overhydration is of concern, especially in patients with altered blood brain barriers. They may be avoided if glycerol is administered on an intermittent rather than a continuous basis. Intravascular hemolysis does not occur with oral use. When administered intravenously, hemolysis can be minimized by using glycerol 10% in dextrose 5% with normal saline at rates of 6 mg/kg/min or less. However, intravenous doses of 1-2 g/kg every 2 hr can be administered safely in severe cases of elevated ICP. In such patients, glycerol serum concentration, serum osmolality and ICP monitoring are required to optimize glycerol therapy.
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PMID:Glycerol: a review of its pharmacology, pharmacokinetics, adverse reactions, and clinical use. 692 4

This report describes a case of two-yr-old female with severe clinical Reye syndrome (Stage III and over), who was treated with not only conventional therapies but also mild hypothermia therapy. She presented acute episodes of tonic convulsion, hepatic dysfunction and intracranial hypertension. The first treatment consisted of the administration of anticonvulsant and mannitol, which were not effective to control intracranial pressure. Therefore, we induced mild hypothermia to rectal temperature of 33-34 degrees C for ten days to control intracranial hypertension as well as barbiturate therapy and hyperventilation under mechanical ventilation. Although she had hypokalemia, atelectasis of the right upper lung lobe and thrombocytopenia as the side effects during this therapy, we effectively controlled ICP. Glucose fluid therapy is recommended for Reye syndrome. We especially should pay attention to hypokalemia because of hyperventilation, absorption of potassium with insulin and transudation of potassium from the intestine. We determined the initiation and weaning of mild hypothermia therapy by findings of MRI as well as intracranial pressure. MRI findings will contribute to the determination of initiation and weaning of mild hypothermia therapy. Mild hypothermia therapy should be considered in patients with severe clinical Reye syndrome if conventional supportive therapies are not effective.
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PMID:[Successful use of mild hypothermia therapy in a patient with severe clinical Reye syndrome]. 1205 35