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

Knowledge of the effects of hypothermia has increased greatly over the past 25 yr. Thousands of patients have been cooled intentionally in the operating room, and hundreds of thousands of living hearts have been temporarily stopped by cold cardioplegia and restarted without difficulty or apparent ill-effect. Yet in spite of the acquisition of this vast body of clinical experience an aura of mystery stills surrounds the patient who becomes hypothermic accidentally. The best treatment in any particular case is not always clear, and published accounts do not always give the impression that the hypothermic patient is treated with the same rational approach with which other sick and comatose patients are treated. In summarizing, therefore, conclusions that might be reached from reviewing past experience several important points emerge. The severely hypothermic patient should be treated in an intensive care unit where appropriate monitoring of temperature, cardiovascular function and respiratory function are available, and where full respiratory support including assisted ventilation can be given. The final outcome depends upon the etiology. The young healthy victim of exposure has a good chance of surviving. The patient poisoned by alcohol or barbiturates has a good chance of surviving provided the level of intoxication is not itself lethal. The elderly without severe underlying disease have a good chance of surviving. The patient with severe underlying disease of the endocrine, cardiovascular or neurologic system probably has, at best, a 50% chance of surviving and, at worst, a chance of only 10-20%, depending upon the associated disease. There is no statistical evidence that any one method of rewarming is significantly better than any other. But there is anecdotal evidence that in the absence of full monitoring and support systems slow rewarming is safer than over-energetic external rewarming. Internal rewarming, peritoneal dialysis, hemodialysis, inhalation of warmed oxygen and extracorporeal circulation are effective in severe cases and can be used with safety. The causes of, and triggering mechanism for, ventricular fibrillation are still largely unknown but the onset of ventricular fibrillation in a very cold patient may often be an irreversible complication. The place of modern anti-arrhythmic drugs in the prevention and management of this complication has yet to be elucidated. Cardiopulmonary resuscitation is difficult in profoundly hypothermic patients but should be maintained until a body temperature of 30 degrees C has been achieved.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Accidental hypothermia. 636 3

Treatment resistant intracranial hypertension after severe head injury has a very high mortality with conventional therapy such as hyperventilation and mannitol infusions. In this report, we describe the use of large doses of thiopental as a means of treating such swelling. From a consecutive series of 107 severe head injuries with a Glasgow Coma Score (GCS) of 6 or below, we selected all patients below 40 years age with a progressive increase in intracranial pressure (ICP) to 40 mm Hg. The first 16 patients (mean age 20 years, mean GCS 4.3) were treated with deep barbiturate coma and hypothermia (32-35 degrees Celsius) until stable lowering of ICP was achieved. The next 15 patients received conventional intensive care and were in other respects very similar to the barbiturate group (mean age 26, mean GCS 5.2). After 9-12 months the outcome was classified according to the Glasgow Outcome Scale (GOS). Therapy with barbiturate coma resulted in 6 good/moderate outcomes, 3 severe and 7 dead/vegetative. Conventional treatment resulted in 2 good/moderate outcomes and 13 dead/vegetative. This is a highly significant difference and cannot easily be explained by more severe injuries or complications in the conventional group. Superior control of ICP was achieved by large doses of thiopental and the final outcome was better.
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PMID:The effect of high dose barbiturate decompression after severe head injury. A controlled clinical trial. 638 45

This paper reviews the pathophysiology and therapy of the multiorgan failure which occurs with submersion injury of children. First, the influence of hypothermia, the pulmonary, cardiovascular, neurologic and renal changes and the blood gas, acid-base and bloodvolume and serum electrolyte disturbances are discussed in detail. The therapeutic procedures are separated in the cardiopulmonary resuscitation at the scene of the accident and in the management of the children within the hospital where all near-drowned children should be taken. The intensity of the treatment at the hospital depends on the level of consciousness and on the respiratory and cardiovascular problems of the near-drowned child. For the treatment of comatose children with abnormal patterns of respiration and cardiovascular derangements the routine management and a more aggressive approach to therapy are presented. The rational for the aggressive therapy is to improve cerebral salvage. The urgency for an extensive monitoring system is underlined.
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PMID:[Drowning accidents in childhood]. 642 14

Two patients were rewarmed from hypothermia (esophageal temperature 27.2 degrees C, 27.5 degrees C respectively). The first case suffered from head-injury after alcohol ingestion and was deeply comatose. A metabolic or cardiovascular regulatory response to cold was not observed in this patient. The relationship between esophageal temperature and whole-body-oxygen consumption was quantified with a Q10 of 2.75 during rewarming (27.2-37.2 degrees C). His epinephrine levels were greatly elevated to 1,000 pg/ml whereas norepinephrine levels were only moderately increased to 250 pg/ml. Premature ventricular contractions (PVCs) during intubation or from the pulmonary artery catheter were not observed. The second patient was a 87 year old man with accidental hypothermia. He exhibited shivering at an esophageal temperature of 27.5 degrees C which indicated persistent thermoregulation. In contrast to the first case his norepinephrine levels were elevated to 1,500 pg/ml and his epinephrine levels only to 450 pg/ml. After onset of surface rewarming an additional increase in norepinephrine levels was observed and an increasing rate of PVC's (15/min) recorded, which ceased when temperature returned to normal. Our observations indicate that part of the cardiac complications during rewarming from deep hypothermia may result from thermoregulation and additional catecholamine liberation.
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PMID:[Rewarming from moderate to deep hypothermia: plasma catecholamine content, metabolism and circulatory function. 2 case reports]. 648 85

24 deep toxic comas with respiratory assistance were studied by brain-stem reflex and BAEP. Laboratory analysis showed several simultaneous toxics (phenobarbital, benzodiazepines, tricyclic antidepressants...). Three groups of patients were defined: Twelve patients with normal BAEP and with relatively preserved brain-stem reflex (oculocephalic and oculovestibular are often disturbed but photomotor is present). Eleven patients with delayed BAEP and with more disturbed brain-stem reflex (photomotor is missing 3 times). In 2 cases (one of which is mentioned above in group B) brain-stem reflex and BAEP disappear and these patients die. Cerebral anoxia is associated here with toxics. Causes of delayed latencies (group B) are discussed (hypothermia, toxics). BAEP seems important in diagnosis and prognosis of toxic coma.
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PMID:[Brain stem AEP in toxic comas. Correlation with brain stem reflexes]. 652 61

A 64-year-old woman developed impaired consciousness and vision, sensorimotor paresis, hypothermia, bradycardia, and edema. Symptoms fluctuated with seasonal exacerbations in winter and terminated in coma with respiratory insufficiency at age 69. High CSF protein content and low serum T4 and TSH levels were noted. Treatment with prednisolone and thyroxin considerably improved her consciousness and edema. The patient suddenly expired of pulmonary embolism. Postmortem examination revealed a marked atrophy of pituitary and thyroid glands, while multiple demyelinating plaques were disclosed in the optic tract and cervical cord. A review of the literature indicates that this is the first report of the co-existence of two such disorders.
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PMID:Multiple sclerosis co-existent with myxedema. An autopsy case report. 653 Jun 12

The toxicity of the weed-killer paraquat is related to the formation of superoxyde radicals responsible of a progressive and usually lethal pulmonary fibrosis. Recognition of lipid peroxidation of membrane bilayers by free radicals as the causative factor pointed to oxygen as an important cofactor in the severity of paraquat poisoning. It has been shown that any FiO2 over 21% accelerates this process and increases the the mortality of rats and humans. FiO2 21% gave a significant reduction of mortality in rats (DOUZE 1976). We proposed this therapy (1978-1879) in 6 cases of paraquat poisoning. It was conducted with induction of a barbiturate coma, hypothermia, curarisation and hypo-oxygenation (FiO2 around 14% thanks to the adjunction of nitrogen to assisted ventilation). In 5/6 patients, these technics did not prevent the evolution towards death. This evolution was in fact predicted, according the following prognostic factors: suicide, more than a mouthful ingestion, oesophago-gastric burns detected by endoscopy, organic renal failure, high plasma paraquat level. Associated methods of elimination (Fuller's earth, provoked diarrhea, furosemide, hemoperfusion and hemodialysis) did not change the early established prognosis. The only survival was observed in an accidental poisoning with undetectable plasma paraquat and isolated oral burns: the herbicide had been probably spit out. This survival cannot be related to hypo-oxygenation. This failure is not definitive, according to us: this therapy should be undertaken only after minimal, accidental poisoning possibly evolving to pulmonary fibrosis. It appears unuseful in massive, suicidal poisonings, leading readily to a lethal circulatory failure.
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PMID:[Hypo-oxygenation in paraquat poisoning. Apropos of 6 cases]. 661 25

Groups of 10 male and 10 female rats were dosed orally with 1,2,3,4-, 1,2,4,5-, or 1,2,3,5-tetrachlorobenzene (TCB) at levels that ranged from 200 to 4000 mg/kg, and were observed clinically for 14 d. LD50 values for 1,2,3,4-, 1,2,4,5-, and 1,2,3,5-TCB were found to be 1470, 3105, and 2297 mg/kg, respectively, in male rats. In females, the LD50 values were found to be 1167 and 1727 mg/kg for 1,2,3,4- and 1,2,3,5-TCB, respectively. Clinical signs of toxicity included depression, flaccid muscle tone, prostration, piloerection, loose stool, hypothermia, dacryorrhea, coma, and death. In a subacute study, groups of 10 males and 10 females were fed diets containing 0, 0.5, 5.0, 50, or 500 ppm 1,2,3,4-, 1,2,4,5-, or 1,2,3,5-TCB for 28 d. No deaths or clinical signs of toxicity were observed, and neither growth rate nor food consumption was affected. At 500 ppm, 1,2,4,5- but not 1,2,3,4- or 1,2,3,5-TCB caused a significant increase in the liver weight and serum cholesterol of male and female rats. Hepatic microsomal aniline hydroxylase and ethoxyresorufin deethylase were induced by 500 ppm 1,2,4,5-TCB. Hepatic microsomal aminopyrine demethylase activity was increased by the administration of this compound at 50 ppm and higher in males and at 500 ppm in the females. Rats fed 1,2,3,4- and 1,2,3,5-TCB at 500 ppm also showed a significant increase in aminopyrine demethylase activity. Moderate to severe histological changes were found in the liver, thyroid, kidney, and lungs of rats fed 500 ppm 1,2,4,5-TCB. Histological changes in the tissues produced by the administration of the 1,2,3,4- and 1,2,3,5-isomer were mild even at the highest dose levels. Tissue residue data showed that 1,2,4,5-TCB accumulated at much higher levels than the other two isomers. The results suggest that the position of chlorine substitution can affect the tissue accumulation and toxicity of chlorinated benzenes in rats.
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PMID:Comparative toxicity of 1,2,3,4-, 1,2,4,5-, and 1,2,3,5-tetrachlorobenzene in the rat: results of acute and subacute studies. 662 Apr 5

The criteria of brain death established by Japanese Society of EEG in 1974, necessitates a prerequisite; be applicable only to "acute destructive, primary gross lesion of brain". Namely, because of insufficient clinical data, secondary brain lesion such as post-anoxia, intoxication, metabolic coma and some kinds of CNS infection were excluded for the object to determine brain death. The criteria published by others also describe that etiology of coma should be clarified, and that careful measures are necessary to diagnose brain death if the cause of coma is unknown. In the present study, it was investigated that whether a clinico-pathological entity of brain death could exist universally regardless of the etiology, and by what means it could be defined clinically. The patients suffering from nondestructive, secondary brain lesions and who showed "brain death-like state" were selected for the study. ("Brain death-like state" requires coma, dilated nonreactive pupis and arrest of respiration concomitantly for more than 6 hours.) And 25 patients were collected, whose underlying diseases were post-anoxia or shock, CO intoxication, Paraquat poisoning, near-drowning or suffocation, hepatic coma, accidental hypothermia and sepsis, with or without the episode of cardiac arrest. Though all the patients died from 1 to 13 days after the insult, clinical signs of brain death-like state were not always irreversible. Isoelectric EEG was obtained on that state in 11 patients and repeated EEG revealed no return on those patients. But another 5 patients showed EEG activity when brain death was strongly suspected clinically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain death in secondary brain lesion]. 665 91

Eight cases of hypothyroid coma observed between 1971 and 1981 are reported, and their main clinical, biological and therapeutic features described. Three out of the 8 patients died. Physiopathological and therapeutic comments are made with reference to these cases and previous reports, concerning the hypothermia, cardiac and respiratory function, hyponatraemia and the endocrine disturbances observed in hypothyroid coma.
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PMID:[Myxedema coma. Apropos of 8 cases]. 666 45


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