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

The respiratory pathophysiology of A2 influenza infection was studied in mice treated with small-particle aerosols (SPA) of rimantadine or ribavirin. Untreated infections in mice resulted in survival rates of 15% or less and were characterized by (i) severe hypoventilation (decreased P(O2) and increased P(CO2)), (ii) compensated respiratory acidosis (increased P(CO2) and HCO(3) (-), with normal pH), (iii) pneumonia with increased ratio of wet/dry lung weight, and (iv) hypothermia. Treatment with SPA of rimantadine (21 mg/kg per day for 4 days) beginning 72 h after virus challenge significantly improved survival rate (80%) but failed to alter lung pathology from that found in infected, untreated mice. Rimantadine treatment decreased somewhat the severity of hypoventilation, respiratory acidosis, lung wet weight, hypothermia, and lung virus titers from that observed in infected, untreated mice. SPA of ribavirin (26 mg/kg per day for 4 days) initiated 6 h after SPA exposure of mice to virus significantly improved survival rate (95%) and reduced lung virus titers and lung pathology. Gas exchange and pulmonary edema in ribavirin-treated, infected mice were significantly improved over those of infected, untreated controls. The mechanisms for increased survival rates induced by SPA of rimantadine remain uncertain, since increased survival rates could not be ascribed entirely to improvements in lung functions. In contrast, however, ribavirin treatment appeared to improve survival rates by reducing major lung pathology and pulmonary dysfunction. This was probably mediated through the antiviral effects of ribavirin.
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PMID:Effects of small-particle aerosols of rimantadine and ribavirin on arterial blood pH and gas tensions and lung water content of A2 influenza-infected mice. 1 87

Circulation was maintained in profoundly hypothermic dogs for 8 h at temperatures below 10 degrees C. During cooling to 5 degrees C cardiac output and blood pressure decreased and peripheral resistance rose. Thereafter, circulatory dynamics remained relatively stable over the next 6 h with a gradual decline in blood pressure. The proportion of blood flow to the heart and brain increased with cooling and remained elevated throughout the hypothermia period. Despite continued circulation, pulmonary edema developed after 5-7 h and the dogs were nonviable when rewarmed.
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PMID:Hemodynamics and blood flow distribution following prolonged circulation at 5 degrees C. 24 Feb 78

The effects of induced hypocapnia, hypothermia, and hypertension were surveyed in a primate model of acute stroke during and following a 48-hour period of intensive care. The results were compared to a group of nine control animals previously studied. Hypocapnia (PaCO2=25 torr) was examined in five animals and did not appear to alter the expected mortality, degree of neurological deficit, or frequency of infarction. There was, however, a suggestion that the size of infarction may be reduced. Hypothermia (29 degrees C) in five animals had a detrimental effect in that no animals survived following the intensive care period and all had infarction with massive edema. We speculate that hypothermia caused a sufficient increase in blood viscosity as to compromise collateral flow, thereby accounting for this detrimental effect. Induced hypertension (to 20% above control levels) was abandoned after three animals because of severe systemic effects (cardiac failure and pulmonary edema) resulting in death during the period of intensive care.
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PMID:Failure of prolonged hypocapnia, hypothermia, or hypertension to favorably alter acute stroke in primates. 40 43

The phenomenon called paradoxical undressing has been described from 33 cases of hypothermia collected from Swedish police reports. The cases were almost evenly distributed with regard to sex, age, and geographical distribution. The cases occurred more frequently in open land although cases from town areas were also found. Most incidents were recorded from November to February at low ambient temperatures, although cases were also reported at temperatures above 0 degree C. Arteriosclerosis and chronic alcoholism were important concomitant illnesses, the latter being frequent in middle-aged men. Epilepsy, diabetes, and pregnancy were present in single cases. Ethanol and other drugs were present in 67% of the males and in 78% of the females, ethanol predominating in men and various psychotropic agents in women. The mean blood ethanol concentration in males was 0.16% and in females, 0.18%. Most frequent findings at necropsy were purple spots or discoloration on the extremities, pulmonary edema, and gastric hemorrhages. It is concluded that paradoxical undressing might be explained by changes in peripheral vasoconstriction in the deeply hypothermic person. It represents the last effort of the victim and is followed almost immediately by unconsciousness and death.
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PMID:"Paradoxical undressing" in fatal hypothermia. 54 27

A series of 22 cases of fatal accidental or suicidal hypothermia is presented. Necropsy findings on which the diagnosis can be based were analysed. Purple skin and swelling of face, hands and feet, as well as violet patches on elbows or knees were the most frequent external signs (Frequency 54--59%). The most conspicuous internal macroscopic signs were gastric erosions or haemorrhages, which were seen in half of the cases. Other less frequent signs were pulmonary oedema and acute renal and hepatic degeneration. Microscopically the myocardium showed small degenerative foci and/or fuchsinophilic fibres in two thirds of the cases. The myocardium was macroscopically normal. Histamine and serotonin assays from urine did not indicate increased excretion during exposure. Catecholamine concentrations in urine were high (greater than 0.1 mug/ml) in most hypothermia deaths indicating increased excretion due to cold. The best diagnostic signs seem to be purple skin and oedema in face and ears, stomach erosions, degenerative foci in myocardium and high concentration of catecholamines in the urine.
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PMID:Necropsy findings in fatal hypothermia cases. 97 1

A 19-year old woman ingested an unknown amount of sodium azide (NaN3). The earliest symptoms were nausea and loss of vision. Within a few hours her clinical features were dominated by central nervous system signs, acute pulmonary edema, lactic acidosis, and hypothermia. The patient died within 12 hours, hypotension and shock occurring as preterminal events. This was the first recorded case in which antidotal methemoglobin production was attempted. Sodium nitrite administration resulted in methemoglobinemia but did not appreciably alter the clinical course and may not be of major benefit. Gross examination post-mortem showed marked pulmonary edema, visceral hemorrhage and congestion, and slight cerebral edema. Microscopically, the lungs showed alveolar and interstitial edema and a polymorphonuclear infiltrate. There were petechial hemorrhages and severe nonspecific changes in the brain.
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PMID:Fatal self-administration of sodium azide. 114 58

The advantages of a bloodless field and total cardiac relaxation have popularized the technique of deep hypothermia and total circulatory arrest for the correction of complex congenital cardiac defects in infancy. There is, however, a significant potential for cerebral and pulmonary complications. Presently, the most common technique is that of using a combination of surface cooling and cardiopulmonary bypass cooling and rewarming. Normal neurological development has been claimed with the present technique of hypothermia at 20 degrees C and total circulatory arrest for periods up to an hour; however, there are reports of seizure activity in the early postoperative period. There is also a disturbing incidence of respiratory insufficiency and, occasionally, hemorrhagic pulmonary edema. This study, using growing puppies and subjecting them to deep hypothermia and total circulatory arrest for varying periods of time, disclosed that animals subjected to 60 min of circulatory arrest recovered neurologically; however, there were histological changes of anoxia in the brain. Animals subjected to 30 min of total circulatory arrest were normal neurologically and there was no histological evidence of anoxic damage to brain tissue. Puppies that were continuously on cardiopulmonary bypass had no significant pulmonary changes caused by increasing the inspired oxygen tension in the ventilator; however, striking changes were noted when limited cardiopulmonary bypass was employed for core cooling and total circulatory arrest combined with pulmonary ventilation with 100% oxygen. We conclude from this experimental study that the use of surface cooling and core cooling with subsequent total circulatory arrest at 20 degrees C is a safe procedure, providing the period of time of cardiac arrest is kept around 30 min. We also conclude that the alveolar oxygen tension should be maintained at the lowest level possible during the interval of circulatory arrest to avoid the apparent rapid onset of post-traumatic pulmonary insufficiency.
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PMID:Effect of deep hypothermia, limited cardiopulmonary bypass, and total arrest on growing puppies. 120 92

Injection of ibotenic acid (IA), a glutamate agonist, into the ventral medullary raphe (VMR; especially the nucleus raphe magnus) of the rat produced respiratory failure and death following a predictable course of events. The response to the IA injection was characterized initially by increased respiratory frequency and was followed by pulmonary arterial hypertension, systemic arterial hypoxemia, acidosis, and hypothermia. Within 90 min apnea occurred as a terminal event in all animals. Gravimetric, bronchoalveolar lavage protein, and histological analyses revealed no evidence of pulmonary edema. Intracerebral (VMR) pretreatment with PPP, a sigma receptor agonist, or scopolamine, a muscarinic cholinergic antagonist, prevented pulmonary failure and death even though postmortem histological analysis showed VMR cell loss and gliosis consequent to the cytotoxic IA injection. Based on the results of the study, it is suggested that the VMR has a role in regulation of pulmonary blood flow. Preliminary pharmacological studies suggested that a disruption of glutamatergic and cholinergic mechanisms mediates the lethal pulmonary phenomenon.
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PMID:Respiratory failure without pulmonary edema following injection of a glutamate agonist into the ventral medullary raphe of the rat. 137 23

We report the case of a 59-year-old woman suffering from profound accidental hypothermia promoted by intoxication with codeine, sedatives, and a beta-blocking agent ingested in a suicidal attempt. Treatment was further complicated by ventricular fibrillation and asystole that was refractory to therapeutic interventions. The comatose patient (Glasgow score 3) was found outdoors in rainy weather--environmental temperature approximately 10 degrees C (50 degrees F)--by children. The skin was rosy when the emergency team arrived. The respiratory rate was low and the ECG showed sinus rhythm with a heart rate of 28/min. No arterial pulsations were detectable, even at the carotid and femoral sites. Because catecholamine therapy failed to increase the heart rate, the patient was suspected to be profoundly hypothermic. After confirming core hypothermia with a rectal temperature of 25 degrees C (77 degrees F) at the initial receiving hospital, transfer to an institution with cardiac surgery facilities was initiated. During this transport and after arrival, ventricular fibrillation occurred at decreasing intervals followed by asystole, which was refractory to large doses of epinephrine. The patient was transferred to the operating room under continuous resuscitation maneuvers and cardiopulmonary bypass was instituted via the femoral vessels. After 110 min of extracorporeal circulation (ECC, flow 4.5 l/min) normothermia was achieved and the asystole reverted spontaneously to sinus rhythm. The patient's course was subsequently complicated by worsening pulmonary gas exchange with signs of pulmonary edema on X-ray films and cardiac failure, which was treated successfully with epinephrine and dopamine. No neurological deficits were detectable after consciousness had returned.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Successful therapy of a cardiac arrest during accidental hypothermia using extracorporeal circulation]. 156 99

Three schizophrenic adults with previous histories of using phenothiazine derivatives developed acute pulmonary edema after taking large amounts of these drugs. The clinical manifestations included coma (three), hypothermia (two), tachycardia (two), miosis (two) and hypotension (one). All three patients underwent gastric lavage and were treated supportively. The fulminant pulmonary edema in the three cases resolved within 18 to 40 h. The etiology of pulmonary edema following overdosage of phenothiazines remains unknown. The authors hypothesize that the most likely pathogenesis is a drug-induced neurogenic pulmonary edema resulting from a disturbance of hypothalamic function.
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PMID:Acute pulmonary edema induced by overdosage of phenothiazines. 172 53


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