Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five patients suffering from progressive Reye's syndrome were aggressively treated in our ICU. Our protocol consisted of endotracheal intubation, curarization, mechanical ventilation, hypothermia to 31 degrees C, and fluid restriction. Intracranial pressure (ICP) was monitored and remained below 10-20 torr in all patients except one in whom ICP rose only once (for a few minutes) to 27 torr. Pulmonary artery wedge pressure was monitored in 4 patients and was maintained at 4-5 torr. Duration of active intervention as outlined above was 3-4 days. All 5 patients started with clinical stage IV and EEG grade IV or worse. Four patients had complete recovery and one died. In this group of patients, high ICP was not a feature of the disease. We recommend that use of mannitol for active dehydration be reserved for cases with proven rise in ICP, in which case hemodynamics should be carefully monitored.
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PMID:Management of Reye's syndrome. A rational approach to a complex problem. 90 93

Fifteen patients with non-traumatic encephalopathies underwent continuous monitoring of intracranial pressure. These included 11 children with Reye's syndrome, two with viral encephalitis, one with mushroom poisoning, and one with hypoxia from drowning. Elevated intracranial pressure was treated with decadron, hyperventilation, hyperosmolar agents and in some cases hypothermia and barbiturates. The results are discussed.
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PMID:Monitoring and control of intracranial pressure in non-traumatic encephalopathies. 126 50

A four year old girl manifested with seizures, raised intracranial tension and altered consciousness. Laboratory investigations suggested Reye's syndrome. Later she developed fatal hypothermia. Rarity of such a case is highlighted. Probable pathogenesis of hypothermia in Reye's syndrome is discussed.
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PMID:Hypothermia: an unusual manifestation of Reye's syndrome. 226 14

To focus attention on the problem of infant mortality in Lebanon, data were compiled on infant mortality from 1978 to 1986 at the American University of Beirut Medical Center. Causes of death are analyzed for 602 males and 398 females. 54.9% deaths occurred at 1 month of age and 77.4% died within the 1st year. Autopsies were performed on .7%. 37.7% of all neonatal deaths were due to neonatal diseases such as hyaline membrane disease, asphyxia neonatorum, immaturity, necrotizing enterocolitis, hemorrhage, hemolysis, meconium aspiration, and kernicterus. Better prenatal care would reduce this group, or the administration of corticosteroids to the mother 24-48 hours prior to delivery, as well as rapid resuscitation at birth and prevention of the 5 curses: hypoxemia, hypoglycemia, hypothermia, hypotension, and acidosis. Although unavailable in Lebanon, administration of surfactants through an endotracheal tube would also help. Infections constitute 25.1% of deaths; many are preventable through adequate public health measures and strict personal hygiene, i.e., diseases such as sepsis, pneumonia, meningitis, gastroenteritis, hepatitis, encephalitis, and 1-2 cases of the following: diphtheria, measles, peritonitis, tetanus, tuberculosis, cytomegalis inclusion, herpes, parathyphoid, pertussis, poliomyelitis, and shigellosis. Congenital diseases were 21.6%. In utero diagnosis could prevent some diseases and in utero treatment is possible for hydrocephalus and hydronephrosis. Screening programs postnatally could lead to treatment. 5.9% were malignancies such as leukemia, lymphoma, brain tumors, histocytosis, Wilm's tumor, Ewing sarcoma, and Hodgkin's disease. Early diagnosis is critical if mortality is to be reduced in this group, but medical advances are still needed. 2.9% are miscellaneous diseases such as poisoning, rheumatic diseases, marasmus, Reye's syndrome, nephrosis, rickets, and epilepsy. Most of these diseases are preventable, except for rheumatic inflammation of the heart. Recommended necessary steps to reduce infant mortality are: prenatal care, diagnosis and screening, intrauterine surgery; resuscitation and intensive care centers with modern equipment and trained personnel; national vaccination and screening programs; adequate public health measures and hygiene; parental education; and well-equipped hospitals to serve all regardless of income level.
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PMID:Pediatric mortality: an avoidable tragedy. 251 28

Metabolic acidosis has previously been described in the gray baby syndrome, but has not been documented as a presenting feature. Four seriously ill children (bronchiolitis, hypoaldosteronism, dysautonomia, Reye syndrome), ages 4 months to 11 years, received chloramphenicol (CAP) intravenously. After initial stabilization, unexplained metabolic acidosis occurred 40 to 81 hours after beginning CAP. Serum CAP concentrations were 84, 62, 80, and 30 micrograms/ml, respectively, when acidosis was recognized. Hypotension, hypothermia, and abdominal distension occurred a mean of 23 hours after the onset of acidosis. Acidosis resolved and signs of the gray baby syndrome cleared with the decrease in serum CAP concentrations. Metabolic acidosis should be considered an early sign of CAP toxicity, and CAP should be used in reduced doses in severely ill patients, especially those with liver dysfunction.
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PMID:Acidosis as a presenting feature of chloramphenicol toxicity. 395 Aug 30

The pharmacokinetics of pentobarbital were examined in 11 children with Reye syndrome, hypoxic encephalopathy, or acute head injury. Nine of these patients were hypothermic (less than 32 degrees C). The total systemic clearance and volume of distribution at steady state of pentobarbital were significantly reduced in these patients when compared to previous data in normothermic adult volunteers following intravenous doses of pentobarbital. Pentobarbital elimination half-life was not significantly different from control values. The diminished systemic clearance of pentobarbital may result from decreases in intrinsic enzyme activity that accompany hypothermia, as well as hepatic dysfunction in patients with Reye syndrome. Less extensive distribution of pentobarbital is likely the result of either differences in body fat composition or hypothermia-induced decreases in regional blood flow. The reduced clearance and distribution of pentobarbital may partially explain the enhanced reduction in cerebral metabolism that occurs on addition of hypothermia to barbiturate therapy in patients with elevated intracranial pressure.
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PMID:High-dose pentobarbital pharmacokinetics in hypothermic brain-injured children. 706 21

A retrospective review of 41 patients with post-mortem evidence of acute pancreatitis revealed that 19 patients (46%) showed concomitant evidence of increased intracranial pressure (ICP). A prospective analysis of five patients with increased ICP demonstrated two patients with evidence of acute pancreatitis. The pathogenesis of acute pancreatitis in these patients appears to be dependent on the following risk factors: increased intracranial pressure, steroids, hypovolemia, morphine infusion and hypothermia. These factors increase vagal stimulation, predispose to pancreatic duct obstruction and enhance cellular hypoperfusion. Acute pancreatitis occurring in Reye's Syndrome is probably a consequence of increased ICP and the therapy instituted.
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PMID:Acute pancreatitis and increased intracranial pressure. 727 56

Acute pancreatitis was an unexpected complication during the course of intensive supportive management in five patients with Reye's syndrome. Four of the five patients died and one survived with transient neurologic deficits. Although corticosteroid therapy, fluid restriction, and hypothermia may have contributed to the development of this complication, acute pancreatitis may represent a severe manifestation of visceral metabolic dysfunction in Reye's syndrome.
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PMID:Acute pancreatitis in Reye's syndrome: a fatal complication during intensive supportive care. 735 11

CT/MRI findings, laboratory examinations and prognoses of 42 patients with acute encephalopathy (AE) (Japan Coma Scale > or = 200) were reported. 1. Findings on CT/MRI were divided into the following 7 categories: Group 1 (normal), Group 2 (CT/MRI looked normal in acute phase, but brain atrophy developed and progressed slowly by weeks or months), Group 3 (CT/MRI looked normal within a few days after the onset of AE, but cortical laminar necrosis developed at 4-5 days after the onset), Group 4 (marked brain edema developed within 2 days after the onset of AE), Group 5 (AE with symmetric thalamic lesions), Group 6 (symmetric pallidum, lesions on MRI which appeared after brain edema disappeared), and Group 7 (the brain shrinked during acute phase, which normalized on the follow up CT/MRI). 2. Serum AST elevated in approximately 50% of the patients with AE. Sixty percent of them exhibited DIC, whose prognoses were poor. Cerebrospinal fluids (CSF) neopterin (NP) and/or interleukin (IL)-6 were elevated in all the 8 patients examined. In the two cases whose serum NP and IL-6 were measured at the same time, their values in the CSF were higher than those in the serum in one case, and almost the same in the other. In a patient with a condition mimicking hemorrhagic shock and encephalopathy, serum IL-6 concentration was very high (94,000 pg/ml). 3. Mild hypothermia (around 34 degrees C) combined with methylprednisolone pulse therapy was excellently effective on AE. A 6-year-old boy exhibited tonsillar herniation at admission recovered well to be able to run. 4. Differentiation between Reye syndrome and HSE, and the pathogenesis of AE were also discussed.
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PMID:[Infection-related acute encephalopathy: CT scan/MRI finding, laboratory examination and prognosis]. 1072 91

During the Winter or Influenza season in Japan, there has been an increase in the number of patients presenting with Central Nervous System complaints or symptoms. One of the causes is reported be Influenza encephalitis/encephalopathy. Some of these patients undergo a course of Reye's Syndrome, Acute Necrotizing Encephalopathy (ANE), or Hemorrhagic Shock and Encephalopathy(HSE), of which the pathologic features are still unknown. It is likely that the major underlying feature is cerebral edema, caused by impairments in the blood-brain barrier, which is mediated by inflammatory cytokines. Mild brain hypothermia may be an effective treatment in preventing cerebral edema by preventing the cytokine activation and elevations in brain temperature. A combination of mild brain hypothermia and high-dose corticosteroid therapy is thought to be effective in the treatment of influenza encephalitis/encephalopathy.
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PMID:[Mild brain hypothermia for influenza encephalitis/encephalopathy and its significance]. 1122 26


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