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

Rat exposure to pure normobaric oxygen induces a specific non alveolar pulmonary edema which leads to massive pleural exudate. This does not induce hypoxemia, and is characterized by both hypovolemia and arterial hypotension with hypothermia. Histological findings shed some light on these special aspects of oxygen toxicity. In the Rat, this toxicity results from hemodynamic changes rather than from pulmonary lesions.
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PMID:[Hypovolemia in the course of pulmonary edema in rats exposed to normobaric oxygen]. 680 15

A sixteen month old girl developed acute respiratory failure from pulmonary oedema, and acute circulatory failure, following postoperative laryngeal obstruction. Her condition deteriorated despite mechanical ventilation with PEEP. She was finally treated with a combination of mild hypothermia, profound muscle paralysis and deep sedation for five days, after which she made a full recovery. This case confirms the previously reported value of such therapy when standard measures fail.
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PMID:A hypothermic regime for acute respiratory failure. 683 27

Cardiovascular failure (shock) associated with acute alcohol ingestion and severe hypothermia (core temperature 23 and 21 degrees C) was studied in 2 patients. In each case, perfusion failure was associated with lactacidemia, severe bradycardia, and agonal respirations. Infusion of fluids and mechanical ventilation reversed shock and prevented a fatal outcome. One case, complicated by renal failure and volume overload with pulmonary edema, was managed with peritoneal dialysis. These findings suggest that perfusion failure associated with severe accidental hypothermia after acute alcohol ingestion is due to a combination of hypovolemia, bradycardia, and respiratory depression.
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PMID:Shock due to profound hypothermia and alcohol ingestion: report of two cases. 727 11

In Norway the number of deaths per year from drowning is approximately nine persons per 100,000, most of them men between 25 and 40 years of age. About 60% of these persons can swim, and 50% of the deaths are related to intake of alcohol. About 6% of the drowned are children, most of them boys. In disaster medicine, drowning is associated with accidents at sea, involving large vessels or small boats, or connected to offshore activities. The important pathological events are directly related to asphyxia, hypoxemia, hypercarbia, pulmonary oedema, and circulatory arrest. This paper describes various aspects of drowning and the pathophysiological processes involved, and discusses differences between drowning and near drowning in fresh water and salt water. Although treatment is basically centred on effective cardiopulmonary resuscitation, there are certain differences with regard to further treatment and fluid/electrolyte management. Hypothermia is often a prominent feature, and if cardiopulmonary resuscitation is successful, hypoxic brain damage may be ameliorated by the fall in body temperature.
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PMID:[Drowning--near drowning]. 826 93

The central autonomic network (CAN) is an integral component of an internal regulation system through which the brain controls visceromotor, neuroendocrine, pain, and behavioral responses essential for survival. It includes the insular cortex, amygdala, hypothalamus, periaqueductal gray matter, parabrachial complex, nucleus of the tractus solitarius, and ventrolateral medulla. Inputs to the CAN are multiple, including viscerosensory inputs relayed on the nucleus of the tractus solitarius and humoral inputs relayed through the circumventricular organs. The CAN controls preganglionic sympathetic and parasympathetic, neuroendocrine, respiratory, and sphincter motoneurons. The CAN is characterized by reciprocal interconnections, parallel organization, state-dependent activity, and neurochemical complexity. The insular cortex and amygdala mediate high-order autonomic control, and their involvement in seizures or stroke may produce severe cardiac arrhythmias and other autonomic manifestations. The paraventricular and other hypothalamic nuclei contain mixed neuronal populations that control specific subsets of preganglionic sympathetic and parasympathetic neurons. Hypothalamic autonomic disorders commonly produce hypothermia or hyperthermia. Hyperthermia and autonomic hyperactivity occur in patients with head trauma, hydrocephalus, neuroleptic malignant syndrome, and fatal familial insomnia. In the medulla, the nucleus of the tractus solitarius and ventrolateral medulla contain a network of respiratory, cardiovagal, and vasomotor neurons. Medullary autonomic disorders may cause orthostatic hypotension, paroxysmal hypertension, and sleep apnea. Neurologic catastrophes, such as subarachnoid hemorrhage, may produce cardiac arrhythmias, myocardial injury, hypertension, and pulmonary edema. Multiple system atrophy affects preganglionic autonomic, respiratory, and neuroendocrine outputs. The CAN may be critically involved in panic disorders, essential hypertension, obesity, and other medical conditions.
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PMID:The central autonomic network: functional organization, dysfunction, and perspective. 841 66

Significant hypothermia is an increasing clinical problem that requires a rapid response with properly trained personnel and techniques. Although the clinical presentation may be such that the victim appears dead, aggressive management may allow successful resuscitation in many instances. Initial management should include CPR if the victim is not breathing or is pulseless. Further core heat loss should be prevented by removing wet garments, insulating the victim, and ventilating with warm humidified air/oxygen to help stabilize core temperature. Core temperature and cardiac rhythm should be monitored in the prehospital setting, if possible, and CPR should be continued during transport. In-hospital management should consist of rapid core rewarming in the severely hypothermic victim with heated humidified oxygen, centrally administered warm IV fluids (43 C), and peritoneal dialysis until extracorporeal rewarming can be accomplished. Postresuscitation complications should be monitored; they include pneumonia, pulmonary edema, cardiac arrhythmias, myoglobinuria, disseminated intravascular thrombosis, and seizures. The decision to terminate resuscitative efforts must be individualized by the physician in charge.
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PMID:Hypothermia. 843 36

From January 1984 to May 1994, 17 of 239 children under 15 years old stung by Tityus serrulatus (15.1%) or Tityus bahiensis (84.9%) presented severe envenoming. Of these 17 patients (1-11 years old; median = 2 yr) 14 were stung by T. serrulatus and three by T. bahiensis. All of them received scorpion antivenom i.v. at times ranging from 45 min. to 5 h after the accident (median = 2 h). On admission, the main clinical manifestations and laboratory and electrocardiographic changes were: vomiting (17), diaphoresis (15), tachycardia (14), prostration (10), tachypnea (8), arterial hypertension (7), arterial hypotension (5), tremors (5), hypothermia (4), hyperglycemia (17), leukocytosis (16/16), hypokalemia (13/17), increased CK-MB enzyme activity (> 6% of the total CK, 11/12), hyperamylasemia (11/14), sinusal tachycardia (16/17) and a myocardial infarction-like pattern (11/17). Six patients stung by T. serrulatus had depressed left ventricular systolic function assessed by means of echocardiography. Of these, five presented pulmonary edema and four had shock. A child aged two-years old presented severe respiratory failure and died 65 h after being stung by T. serrulatus. Severe envenomations caused by T. serrulatus were 26.2 times more frequent than those caused by T. bahiensis (p < 0.001).
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PMID:A comparative study of severe scorpion envenomation in children caused by Tityus bahiensis and Tityus serrulatus. 859 62

The combination of severe hypothermia and noncardiogenic pulmonary edema secondary to an opiate overdose is presented. This case emphasizes the importance of ventilatory support and rewarming techniques available in the emergency department setting.
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PMID:Hypothermia accompanied by noncardiogenic pulmonary edema: a case report. 891 96

The pathophysiology of elevated intracranial pressure (ICP) is assessed from a three cerebral compartment model and from brain compliance. The mechanisms leading to elevated ICP (expanding process, cerebral edema, brain swelling, hydrocephalus) and their consequences (brain herniation, ischemia-anoxia phenomenon, Cushing reaction and neurogenic pulmonary edema) are overviewed. The causes of elevated ICP in children are reported with emphasis on traumatology. Diagnostic procedures include clinical assessment, fundoscopy, cerebral computerized tomography scan and specific problems of cerebrospinal fluid investigation. Methods and results of intracranial pressure monitoring are reported. The treatment of elevated ICP is based upon clinical follow-up and monitoring of ICP. General therapeutic rules consist of adequate position, suppression of any neck, skull and abdominal compression, stimuli limitation and fluid restriction. Specific treatments include mechanical ventilation, sedation and analgesia, barbiturates, anticonvulsant drugs, mannitol, corticosteroids, hypothermia, enteral nutrition, and antibiotics.
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PMID:[Intracranial hypertension in the infant: from its physiopathology to its therapeutic management]. 975 78

To study the mechanisms responsible for ischemia-reperfusion lung injury, we developed an anesthetized rabbit model in which the effects of lung deflation, lung inflation, alveolar gas composition, hypothermia, and neutrophils on reperfusion pulmonary edema could be studied. Rabbits were anesthetized and ventilated, and the left pulmonary hilum was clamped for either 2 or 4 h. Next, the left lung was reperfused and ventilated with 100% oxygen. As indexes of lung injury, we measured arterial oxygenation, extravascular lung water, and the influx of a vascular protein (131I-labeled albumin) into the extravascular space of the lungs. The principal results were that 1) all rabbits with the deflation of the lung during ischemia for 4 h died of fulminant pulmonary edema within 1 h of reperfusion; 2) inflation of the ischemic lung with either 100% oxygen, air, or 100% nitrogen prevented the reperfusion lung injury; 3) hypothermia at 6-8 degreesC also prevented the reperfusion lung injury; 4) although circulating neutrophils declined during reperfusion lung injury, there was no increase in interleukin-8 levels in the plasma or the pulmonary edema fluid, and, furthermore, neutrophil depletion did not prevent the reperfusion injury; and 5) ultrastructural studies demonstrated injury to both the lung endothelium and the alveolar epithelium after reperfusion in deflated lungs, whereas the inflated lungs had no detectable injury. In summary, ischemia-reperfusion injury to the rabbit lung can be prevented by either hypothermia or lung inflation with either air, oxygen, or nitrogen.
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PMID:Ischemia-reperfusion lung injury in rabbits: mechanisms of injury and protection. 988 66


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