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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypothermia may occur in association with hypoglycemia, and indeed may be the only sign. Two cases are presented. In one, the patient presented with hypoglycemic encephalopathy. In the insulin dependent diabetic, the condition is life-threatening. Subnormal temperature is a clue to hypoglycemia in the alcoholic. The mechanism of hypothermia has been extensively studied, but remains unclear.
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PMID:Hypothermia--a sign of hypoglycemia. 101 86

The retrospective electroclinical evaluation of anoxia by near-drowning in 23 children observed between 1985 and 1989 revealed 2 groups, each with a distinct evolution: the first group, with good prognosis of 17 children, which recovered consciousness without neurological complications between 2 d and 1 wk after the accident. The second group of 6 children with a poor outcome--either i), death; or ii), state of permanent injury; or iii), a high level of clinical deficits. The gravity of the early clinical state, the estimated duration of cardiorespiratory arrest, the severity of the hypothermia, the seizures and the paroxysmic activity, do not determine the severity of near-drowning encephalopathy. The EEG patterns described in correlation with the group and the clinical outcome permitted determination of prognostic criteria. A good prognostic consisted of the following: moderate background activity, sleep patterns, response to auditory and painful stimulations, and numerous beta rhythms. A bad outcome was defined by: high voltage, rhythmic delta waves; biphasic sharp waves; monotonous EEG, "burst-suppression" pattern, absence of beta rhythms. The importance of EEG recordings is emphasized performed as early as possible and until 3 or 7 d after the near-drowning. Any modification in the EEG, with attenuation or disappearance of fast frequencies and painful reactivity, appearance or enhancement of slow and biphasic sharp waves, are ominous signs and may be accompanied by the appearance of cerebral oedema and decerebration.
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PMID:[Cerebral anoxia in near-drowning of children. The prognostic value of EEG]. 192 39

Protein energy malnutrition and infection are largely responsible for the very high postneonatal and toddler mortality ratios of developing countries. Availability of food is just one environmental factor in the aetiology of protein energy malnutrition--many others such as size at birth, infection and culture play a role. Diet needs as careful prescription as any other form of therapy, but in the severely malnourished child it is only one aspect of management; care is necessary to avoid or detect 6 complications: hypothermia, hypoglycaemia, encephalopathy, intractable diarrhoea, cardiac failure, and infection. Prevention should be incorporated within the child health services as a whole and delivered with them; however central government, and the food industry from farming to retailing, play an at least as important role as health care professionals.
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PMID:Protein energy malnutrition: problems and priorities. 195 28

Sepsis, an important cause of hospital mortality, continues to be a diagnostic and therapeutic challenge. To define more clearly the impact of encephalopathy on the course of sepsis, the various clinical signs of sepsis, blood culture results, and mortality rates were examined in relation to mental status in septic patients. Patients were classified as having an acutely altered mental status due to sepsis (AAMS), preexisting altered mental status (PAMS), or normal mental status (NMS). Twenty-three (307/1333) percent of the study patients had an acutely altered sensorium secondary to sepsis. Patients with AAMS had a higher mortality (49%) than patients with PAMS (41%) or patients with NMS (26%) (p less than .000001). Multivariate analysis disclosed that altered mental status, hypothermia, hypotension, thrombocytopenia, and the absence of shaking chills were independent predictors of increased mortality in the sepsis syndrome. Patients with Gram-negative bacteremia (28%) were as likely to have AAMS as patients with Gram-positive bacteremia (25%) or patients with negative blood cultures (23%). In summary, alterations in mental status are common in septic patients, and are associated with significantly higher mortality.
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PMID:Impact of encephalopathy on mortality in the sepsis syndrome. The Veterans Administration Systemic Sepsis Cooperative Study Group. 237 91

With proper nursing care and procedures, small hospitals in rural areas of developing countries can provide good neonatal care and achieve perinatal mortality rates comparable to those found at teaching hospitals. The 1st ingredient of adequate neonatology is the establishment of proper regimens for feeding, observation, and resuscitation of newborns. Even in areas where the majority of births take place at home, good neonatal care is possible as long as local risk factors are identified, all newborns are screened for these factors, and at-risk infants are referred for treatment. Factors that place infants at risk include birthweight under 2 kg or above 4 kg, delivery before 34 weeks' gestation, respiratory distress, severe birth asphyxia or trauma, jaundice, prolonged rupture of the membranes, infant not sucking or febrile, convulsions, congenital malformations, and maternal disease. 4 areas require special knowledge on the part of health personnel: the asphyxiated infant, hypothermia, hypoglycemia, and neonatal sepsis. Health workers must be familiar with proper resuscitation techniques, especially avoidance of excessive suctioning of the pharynx, and be alert to signs of hypoxic ischemic encephalopathy. Premature, small, asphyxiated, and sick infants are at greatest risk of hypothermia, a condition that can be prevented by drying and wrapping newborns immediately. Providers should be alert to signs of hypoglycemia in infants of diabetic mothers, large-for-gestational-age babies, the low- birthweight infant, and sick babies. To prevent sudden infant deaths, all sick newborns should be treated for neonatal sepsis.
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PMID:Neonatology in the developing world. Part 1. 277 46

Brain edema is a fatal complication of fulminant hepatic failure and its pathogenesis remains unclear. To determine its presence in a model of ischemic hepatic failure, rats were subjected to a portacaval anastomosis followed by hepatic artery ligation. Brain water was measured using the sensitive gravimetric method. Preliminary studies revealed marked hypothermia in devascularized animals kept at room temperature (26.9 degrees +/- 2.8 degrees C). An additional group of devascularized rats was kept in an incubator. As expected for hypothermia, such animals had a lower arterial pressure and heart rate; the duration of encephalopathy was markedly prolonged. Water content of the cortical gray matter was only increased in normothermic devascularized rats: 80.14% +/- 0.31%, normal; 80.06% +/- 0.22%, portacaval shunt only; 80.42% +/- 0.26%, devascularized at room temperature; 81.29% +/- 0.38%, devascularized at controlled temperature (p less than 0.001). Such differences could not be detected using the dry-weight technique in whole cerebral hemispheres. Astrocyte changes in the cortical gray matter were noted in both edematous and nonedematous devascularized groups, coupled with the presence of vesicles containing horseradish peroxidase in the endothelial capillary cell. This suggests that in this model, brain edema may be due to both a cytotoxic mechanism and changes in the permeability of the blood-brain barrier. Future studies with this widely used model will require strict control of temperature to allow interpretation of experimental results. A therapeutic role for hypothermia in the management of brain edema deserves further attention.
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PMID:Effect of body temperature on brain edema and encephalopathy in the rat after hepatic devascularization. 291 49

We investigated whether thiamine deficiency (TD), a frequent concomitant of chronic alcoholism, differentially modifies the response to ethanol in two inbred rat strains with highly different genetic susceptibilities to development of TD encephalopathy. Ethanol-induced (3 g/kg i.p.) behavioral impairment and hypothermia were studied after 2, 5 and 7 weeks of TD and after 6 weeks of repletion on normal diet. Controls of the M520/N (TD-sensitive) strain metabolized ethanol more rapidly, had a greater liver to body weight ratio, greater total body water, earlier and lower peak blood ethanol concentrations (BEC), diminished area under the BEC curve and lesser behavioral impairment and hypothermia (even at equivalent BEC values) than those of the F344/N (TD-resistant) strain. In both strains, TD resulted in reduced ethanol metabolic rate and liver to body weight ratio and equivalent ethanol-induced hypothermia and behavioral impairment at lower BEC. Lower and delayed peak BEC and unchanged area under the BEC curve suggest an increased volume of ethanol distribution during TD. Recovery appeared complete after 6 weeks of normal diet. Both strains lost an equivalent proportion of body weight during TD but M520/N rats had lesser decrements in ethanol metabolic rate, had greater reductions in liver weight, peak BEC and baseline body temperature and developed overt encephalopathy whereas F344/N rats did not. Therefore, in the chronic alcoholic, TD may modify ethanol's effects via pharmacokinetic and pharmacodynamic mechanisms. Relatively high ethanol tolerance of the strain with a genetic predisposition to TD encephalopathy is consistent with the hypothesized role of this avitaminosis in the pharmacogenetics of alcoholism.
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PMID:Influence of thiamine deficiency on the response to ethanol in two inbred rat strains. 355 71

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 review of 398 neonatal autopsies at Downstate Medical Center revealed 27 cases of kernicterus during the seven-year period from 1971 through 1977. With the current intensive care of the sick newborn, kernicterus continues to occur, mainly in premature infants with relatively low levels of serum bilirubin (mean of 11.5 mg/100 ml). To understand the factors contributing to the development of kernicterus, clinical and pathologic findings in 27 infants with kernicterus were compared to 103 "control" infants with retrospectively. Birth weight, gestational age, sex, and Apgar scores were comparable in both groups. The duration of survival was significantly shorter in infants with kernicterus than in the control infants. The clinical signs and symptoms of kernicterus were nonspecific and the premortem diagnosis of kernicterus was not suspected in most of the cases. There were no significant differences in the peak serum bilirubin values, incidence of hypothermia, hypoglycemia, convulsions, anemia, infection, use of phototherapy, transfusion and exchange transfusion in the two groups. Serum albumin values and bilirubin binding capacity measured by 2-(4-hydroxybenzeneazo)benzoic acid were significantly lower in the kernicteric group although the bilirubin-albumin molar ratio was equal in both groups. The incidences of severe acidosis and hypoxic encephalopathy were significantly higher in the kernicteric infants. In this study, acidosis, hypoxia, hypoalbuminemia, and low bilirubin binding capacity were seen more often in kernicteric infants than in control infants. However, analysis of previously suggested risk factors failed to identify any single factor or combination of factors which could be predictive to the development of kernicterus.
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PMID:Lack of predictive indices in kernicterus: a comparison of clinical and pathologic factors in infants with or without kernicterus. 719 47

To study the molecular basis of ammonia toxicity, highly reproducible models of acute liver failure and acute hyperammonemia in the rabbit were developed. Acute liver failure was induced by two-stage liver devascularization, and acute hyperammonemia by prolonged ammonia infusion such that the plasma ammonia pattern found in acute liver failure was simulated. Clinical symptoms, spectral analysis of the EEG, biochemistry (blood gases, renal function, electrolytes and markers of hepatic injury) and the presence of cerebral edema were studied. During acute liver failure severe encephalopathy developed after 10.2 +/- 1.9 h (n = 6, mean +/- SEM). Other liver-failure-associated abnormalities were cerebral edema, lactic acidosis, renal dysfunction, hypothermia and septicemia. During acute hyperammonemia, severe encephalopathy developed after 18.2 +/- 0.4 h (n = 6, mean +/- SEM). Other abnormalities found were cerebral edema and lactic acidosis. In both animal models comparable EEG changes were observed (a decrease in mean dominant frequency and theta-activity, and an increase in delta activity). However, these changes were not statistically significant, and non-specific as they also occurred in control rabbits despite their clinical wellbeing. This study demonstrates in the rabbit the similarity between encephalopathy due to acute ischemic liver failure and that due to hyperammonemia. An observed difference in hyperammonemia-induced encephalopathy was pronounced ataxia, which did not occur during acute liver failure, whereas hypothermia, sepsis and renal failure occurred exclusively in acute liver failure. Our models appear satisfactory for the study of hepatic encephalopathy and ammonia toxicity.
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PMID:Encephalopathy from acute liver failure and from acute hyperammonemia in the rabbit. A clinical and biochemical study. 817 26


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