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)

In a case-control study of factors contributing to hypothermia all fourteen patients (mean age 80 years) admitted to hospital with hypothermia after being found ill indoors also had some other serious illness. They were more likely than control patients to have been alone when taken ill (93 vs 39% of controls), to live alone (86 vs 43%), and to have been found on the floor (79 vs 14%). They were less likely to have been wearing more than indoor clothing (0 vs 50%), or to have had heating on when found (50 vs 89%), but 93% of patients in both groups had heating available. Healthy young adult volunteers who lay immobile on the ground in air at 5 degrees C lightly clothed cooled progressively by 0.57 degrees C (SD 0.32) (rectal T degrees) in 90 min despite doubling of metabolic rate. With better insulation in bed, core temperature stabilised within 90 min, and when they were in an armchair it fell slowly, with no increase in metabolic rate in either case. The findings suggest that hypothermia indoors resulted largely from collapse due to illness when the patient was alone lightly clothed and not in bed. Eight hypothermic patients found outside (in December and January) were younger (mean age 60 years) than the fourteen found indoors; six of these were chronic alcoholics or acutely intoxicated, and six lacked, or had wandered from, a fixed home.
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PMID:Factors associated with hypothermia in patients admitted to a group of inner city hospitals. 196 5

Environmentally induced hypothermia has a very high mortality. Cardiopulmonary bypass affords the best chance of survival from hypothermia but can be time-consuming to institute. We have utilized percutaneous cardiopulmonary bypass with recently developed bypass catheters to resuscitate a patient with profound hypothermia complicated by circulatory collapse. Percutaneous cardiopulmonary bypass appears to be the treatment of choice for profound hypothermia.
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PMID:Percutaneous cardiopulmonary bypass for the treatment of hypothermic circulatory collapse. 271 35

We identified two siblings with exercise-induced anaphylaxis who share the HLA haplotype A3-B8-DR3 with their atopic father. The index case, a 16-year-old female, noted initial episodes at age 13. Intense pruritus, urticaria, facial edema, choking sensation, nausea, hypothermia, and collapse followed vigorous running but not swimming, cycling, racquetball, solar exposure, or cold exposure. Neither antihistamine, antiserotonin, anticholinergic nor epinephrine therapy was entirely effective or protective; only modification of running prevented episodes. Three similar episodes were noted at age 15 years by a brother who, now age 25, relates a 4-year history of seasonal rhinitis and exercise-related urticaria without anaphylactoid reaction. The remainder of the family (father, 47; mother, 46; brother, 22 years) does not have exercise intolerance. The father has allergic rhinitis; his nephew suffers exercise-induced urticaria without collapse. HLA typing revealed the father to be A1-B8-DR3, A3-B8-DR3; the symptomatic daughter to be A3-B8-DR3, A30-B5-DR8; and the symptomatic son to be A3-B8-DR3, A30-B5-DR8. The asymptomatic mother was A30-B5-DR8, A2-B7-DR5 and the asymptomatic son A1-B8-DR3, A30-B5-DR8. We describe exercise-induced anaphylaxis in a unique familial setting, perhaps linked to the HLA haplotype A3-B8-DR3.
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PMID:Familial exercise-induced anaphylaxis. 347 Oct 98

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

To obtain more detailed information relative to the potential usefulness of using radio frequency (RF) energy in treating hypothermia, anesthetized rhesus monkeys were used in a rewarming study that compared a conventional method (heating pad) with an RF induction coil system. Rectal temperature (Tre) of each subject was monitored, and enzyme and isoenzyme levels were determined from blood samples collected before, during, and up to 48 h after hypothermia in order to assess the effects of each rewarming method. The previously observed postprocedure rise in serum enzymes (most visible at 24 h) was again seen, with no statistically significant difference in the time course of serum enzyme levels between the two treatments for comparable durations of hypothermia. To test the limits of the ability of the RF induction coil system, successively more severe hypothermia was induced in the subjects to the point of cardiovascular collapse (Tre less than 20 degrees C); RF energy was successful in resuscitating the profoundly hypothermic subjects without discernible harmful effects.
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PMID:Rewarming of the hypothermic rhesus monkey with electromagnetic radiation. 361 52

The treatment of accidental hypothermia by extracorporeal circulation and internal rewarming can be life saving in patients unconscious from drug overdose or victims of accidental exposure to severe cold. Advantages are the rapidity of treatment, the provision of circulatory support, and a lessened chance of rewarming collapse, since peripheral vasodilation is paralleled by an increase in cardiac output. A premature diagnosis of clinical death was averted in two patients with rectal temperatures of 25 degrees C or below, and their lives were saved by the use of this technique.
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PMID:Treatment of hypothermia by extracorporeal circulation and internal rewarming. 380 23

Group B streptococcal cells, either viable or heat-killed, contain a substance that induced fever in rabbits with maximal responses occurring four hours after intravenous injection. In contrast, supernatant fluids failed to induce significant fever. Group B streptococcal cells also enhanced host susceptibility to lethal shock by endotoxin as much as 40,000-fold. A graph of log streptococcal cell dose used for pretreatment versus log LD50 endotoxin gave a straight line with a slope of approximately -1. Rabbits that received both streptococcal cells and endotoxin showed initial fever followed by hypothermia, labored breathing, watery diarrhea, evidence of vascular collapse, and finally death. Animals that received streptococcal cells or endotoxin alone showed only fevers and mild diarrhea. A possible theory for the cause of death in the neonate infected with group B streptococci is presented.
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PMID:Endotoxin enhancement as a possible etiology of early-onset group B beta-hemolytic streptococcal sepsis in the newborn. 634 11

The light and electron microscopic morphology of 57 cadaver renal allografts was assessed at the time of procurement and again after revascularization. Twenty-two kidneys (39%) did not function immediately after transplantation and 19 of these (86%) contained morphologic evidence of acute tubular necrosis (ATN) in the procurement biopsy. The morphology of the post-transplant biopsy was abnormal in all 22 kidneys with delayed function. There was a wide spectrum of morphologic change between the time of procurement and revascularization in all kidneys with normal function. These changes were mild in nature, were usually confined to proximal tubules, and were of unknown clinical significance. The morphology of kidneys that were damaged by the time of procurement was surprisingly different after storage with simple hypothermia (ice) than after storage with hypothermic pulsatile perfusion. The changes attributed to ice storage included endothelial swelling and vacuolation with obliteration and collapse of capillary lumens, fracture and splitting of peritubular basement membrane, and hyalinization of the renal interstitium. It was unknown whether these morphologic abnormalities were associated with delayed recovery of function of the injured kidneys.
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PMID:Renal allograft acute tubular necrosis. II. A light and electron microscopic study of biopsies taken at procurement and after revascularization. 634 15

Staphylococcal pyrogenic exotoxin (PE) ty pe C enhanced the susceptibility of rabbits to lethal shock by endotoxin by as much as 50,000-fold. A graph of log PE type C dose used for pretreatment versus log 50% lethal dose of endotoxin gave a straight line with a slope of approximately -1. Rabbits that received PE type C alone showed fevers only, but those given both PE ty pe C and endotoxin showed initial fever followed by hypothermia, labored breathing, diarrhea, evidence of vascular collapse, and finally death. When a PE type C dose of 3 micrograms/kg was used, pretreatment of the animals with PE for 2 h before giving the endotoxin was required to obtain maximal susceptibility. However, when 15 micrograms of PE type C per kg was utilized, the endotoxin could be given before, concurrently, or after PE type C. The capacity of PE type C to prepare rabbits for enhanced susceptibility to endotoxin was lost after 24 to 48 h. Animals could be protected from enhanced susceptibility to endotoxin by prior immunization with either PE type C or endotoxin. However, 30% of the rabbits which were immunized with PE type C failed to develop immunity, and after three injections of PE type C, these animals developed gram-negative bacteremia and succumbed. In addition, rabbits with diarrhea initially, possibly caused by Pasteurella infection, died less than 24 h after a single injection of PE type C.
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PMID:Enhancement of host susceptibility to lethal endotoxin shock by staphylococcal pyrogenic exotoxin type C. 704 68

The authors had previously observed a deleterious cerebrovascular effect of prolonged hypothermia in primates and cats. In this study they examined the systemic as well as cerebral hemodynamic and metabolic effects of 24 hours of hypothermia in the dog. With decreases in temperature to 29 C, cardiac output (Q) and whole-body oxygen consumption (VO2) initially decreased 52 and 42 per cent, respectively. Thereafter, despite a stable temperature, both Q and VO2 continued to decrease, and at 24 hours values were 7 and 28 per cent of control, respectively, Cerebral blood flow (CBF) and cerebral oxygen consumption responded similarly. At 24 hours inhomogeneous perfusion of both brain and skeletal muscle was observed. With rewarming, cardiovascular collapse with severe tissue hypoxia and acidosis developed; CBF became grossly inadequate, resulting in depletion of brain energy stores.
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PMID:The detrimental effects of prolonged hypothermia and rewarming in the dog. 736 10


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