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)

Violent shaking causes severe injury in infants, but the diagnosis of shaken baby syndrome is often difficult to make because of the lack of obvious external signs. Consultations by other specialists may not be helpful, since the findings of most organ systems, taken in isolation, are usually nonspecific. Shaken baby syndrome should be considered in infants presenting with seizures, failure to thrive, vomiting associated with lethargy or drowsiness, hypothermia, bradycardia, hypertension or hypotension, respiratory irregularities, coma or death. Shaken babies are usually less than one year old, and most are under six months of age. Head injury (notably subdural hemorrhage) and retinal hemorrhages are the hallmarks of the syndrome.
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PMID:Shaken baby syndrome. 218 31

The central anticholinergic syndrome (CAS) includes central signs (somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium, stupor, coma) and peripheral signs (dry mouth, dry skin, tachycardia, visual disturbances and difficulty in micturition). It occurs when central cholinergic sites are occupied by specific drugs and also as a result of an insufficient release of acetylcholine. The CAS can be caused by atropine sulphate, hyoscine (scopolamine), promethazine, benzodiazepines, opioids, halothane, influrane, ketamine. The incidence of CAS during the postoperative period depends on choice and dose of anaesthetic agents, type of surgery, patient's condition and diagnostic criteria. It is close to 10% following general anaesthesia and 4% following regional anaesthesia with sedation. The differential diagnosis of CAS includes an overdose of anaesthetic drugs or an alteration in pharmacokinetics, altered hydratation, electrolyte or acid-base state, hypoglycaemia, hypoxia, hypercapnia, hypocapnia, hyperthermia, hypothermia, hormonal disorders, neurological damage resulting from surgery, embolism, haemorrhage or trauma. The diagnosis of CAS is often determined by a process of exclusion and not actually made until a positive therapeutic response to physostigmine, a centrally active anticholinesterase agent has taken place.
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PMID:[Central anticholinergic syndrome during postoperative period]. 219 41

Myxedema coma, an extreme expression of hypothyroidism, represents a medical emergency with high mortality. Hypothermia and cerebro-vascular accidents should be taken into account for correct differential diagnosis. The treatment of myxedema coma is based on prevention of the precipitating factors and on the administration of generous doses of L-thyroxine and/or triiodothyronine, associated with steroids and drugs for respiratory and cardio-vascular complications.
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PMID:[Myxedema coma]. 220 66

In the attempt to correlate clinical findings with serum levels of aldrin, sixteen patients were followed-up after acute intoxication by this agent. Eight of them, males and females, aged from 1 to 37 years, presented no or light symptoms (some discomfort and nausea). The serum of one of these patients was found to contain 16.6 ppb of aldrin and that of another, 1.41 ppb of dieldrin. A group of five patients, aged from two to 30 years, showed symptoms of moderate severity, reporting nausea, vomiting, drowsiness, dyspnea, sweating, mild jerking, rise in blood pressure and convulsions. Of these cases, two were accidental and three were attempted suicides, the majority achieving complete recovery within 24 hours. Serum levels of aldrin were between 6.98 ppb and 26.3 ppb and of dieldrin between 82.00 and 314.18 ppb. We found three severe cases, aged from 21 to 35 years, two attempted suicides and one occupational case. Two of these patients died and one of them presented hypothermia, coma, absence of reflexes and generalized convulsions, and another presented abdominal pain, paleness, sweating, cold extremities, dyspnea, hyperthermia and generalized convulsions. In the first one that died the serum levels were: of aldrin 30.00 ppb and of dieldrin 720 ppb. In the other levels of 747.3 ppb of aldrin and 1,314.00 ppb of dieldrin were found. The third had less serious symptoms and presented serum levels of aldrin of 31.05 ppb and of dieldrin 147.11 ppb.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute poisoning by aldrin: relationship between serum levels and toxic effects in humans]. 221 74

We previously found mild hypothermia (34-36 degrees C), induced before cardiac arrest, to improve neurologic outcome. In this study we used a reproducible dog model to evaluate mild hypothermia by head cooling during arrest, continued with systemic cooling (34 degrees C) during recirculation and for 1 h after arrest. In four groups of dogs, ventricular fibrillation (no flow) of 12.5 min at 37.5 degrees C was reversed with cardiopulmonary bypass and defibrillation in less than or equal to 5 min, and followed by controlled ventilation to 20 h and intensive care to 96 h. In Study A we resuscitated with normotension and normal hematocrit; Control Group A-I (n = 12) was maintained normothermic, while Treatment Group A-II (n = 10) was treated with hypothermia. In Study B we resuscitated with hypertension and hemodilution. Control Group B-I (n = 12) was maintained normothermic (6 of 12 were not hemodiluted), while Treatment Group B-II (n = 10) was treated with hypothermia. Best overall performance categories (OPCs) achieved between 24 and 96 h postarrest were in Group A-I: OPC 1 (normal) in 0 of 12 dogs, OPC 2 (moderate disability) in 2, OPC 3 (severe disability) in 7, and OPC 4 (coma) in 3 dogs. In Group A-II, OPC 1 was achieved in 5 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.001), OPC 3 in 1, and OPC 4 in 0 dogs. In Group B-I, OPC 1 was achieved in 0 of 12 dogs, OPC 2 in 6, OPC 3 in 5, and OPC 4 in 1 dog. In Group B-II, OPC 1 was achieved in 6 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.05), and OPC 3 or 4 in 0 dogs. Mean neurologic deficit and brain histopathologic damage scores showed similar significant group differences. Morphologic myocardial damage scores were the same in all four groups. We conclude that mild brain cooling during and after insult improves neurologic outcome after cardiac arrest.
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PMID:Mild cerebral hypothermia during and after cardiac arrest improves neurologic outcome in dogs. 229 37

A study on septicemia in the elderly (mean age 80.3 +/- 9.1 years) was carried out during 1982-85. A total of 184 episodes of bacteremia occurred in 175 patients (incidence rate 7.2%); 61% were attributed to community-acquired sepsis. Gram-negative microorganisms accounted for 64% of all episodes and gram-positive for 30%. The overall mortality was 18.3%. Using univariate analysis, significant factors associated with a high mortality were: hospital-acquired sepsis, respiratory infections as source of the sepsis, severe underlying disease, Klebsiella and Proteus as pathogens, comatose state, hypothermia, thrombocytopenia, and serum sodium abnormalities. Using logistic regression analysis the odds ratio for hospital-acquired septicemia and hypothermia were positive and statistically significant, whereas soft tissue and urinary tract infections as sources were negative and significant. The relative low mortality in our study confirms that age alone is not necessarily a poor prognostic indicator of septicemia in the elderly.
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PMID:Septicemia in the elderly: incidence, etiology and prognostic factors. 234 81

We conducted a retrospective review of 55 near-drowning victims (mean age 4.75 years) admitted to the intensive care unit during a 5-year period, to determine the factors that may influence survival both before and after hospital admission. All patients who remained comatose after resuscitation received ventilation for an initial 24 hour period, after which an assessment of central nervous system injury was made. Intracranial pressure was not monitored, and barbiturate therapy was used only for seizure control. Thirty-seven children survived and 18 died; five survivors had profound neurologic damage resulting in a persistent vegetative state: the remaining 32 (58%) survived intact. The major factors that separated intact survivors from those who died and from survivors in a persistent vegetative state were the presence of a detectable heartbeat and hypothermia (less than 33 degrees C) on examination in the emergency department. Thirteen patients with absent vital signs and a temperature of greater than 33 degrees C either died or survived in a persistent vegetative state. Fourteen patients had a combination of absent vital signs and hypothermia and were resuscitated; eight died, two survived in a persistent vegetative state, and four survived intact. All intact survivors had been submerged in cold water for prolonged periods, and all underwent prolonged cardiopulmonary resuscitation. All patients with a detectable pulse, regardless of temperature, survived without neurologic sequelae. The 58% intact survival rate in this series compares favorably with the 50% we reported previously when high-dose barbiturate therapy and hypothermia were used to control intracranial pressure; at the same time, the number of survivors with a persistent vegetative state has been reduced by 50%. We conclude that prolonged in-hospital resuscitation and aggressive treatment of near-drowning victims who initially have absence of vital signs and are not hypothermic either results in eventual death or increases the number of survivors with a persistent vegetative state.
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PMID:Effect of hypothermia and cardiac arrest on outcome of near-drowning accidents in children. 238 Aug 13

Early deaths from trauma are often caused by exsanguinating hemorrhage from injuries that appear "irreparable." We explored the limits of deep hypothermic circulatory arrest induced during hemorrhagic shock to enable repair of these injuries in a bloodless field. In 15 dogs, after 30 minutes of hemorrhagic shock (mean arterial pressure, 40 mm Hg), cardiopulmonary bypass (CPB) was used to cool to 15 degrees C in 13-37 minutes. After circulatory arrest of 60 (Group 1), 90 (Group 2), or 120 (Group 3) minutes, reperfusion and rewarming were accomplished by CPB. All dogs survived greater than 72 hours. Best neurologic deficit scores (ND) (0% = normal, 100% = brain death) were 0 +/- 0% (normal) in Group 1, 10 +/- 8% (mild disability) in Group 2, and 27 +/- 24% in Group 3. Outcome in Group 3 dogs ranged from near-normal to comatose. After perfusion-fixation sacrifice, brain histopathologic damage scores correlated with insult time, as did ND scores. Deep hypothermia can allow 60-90 min of circulatory arrest with good neurologic recovery, even after a period of severe hemorrhagic shock. This technique may allow repair of otherwise lethal injuries and survival without brain damage.
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PMID:Therapeutic deep hypothermic circulatory arrest in dogs: a resuscitation modality for hemorrhagic shock with 'irreparable' injury. 238 Oct 1

Several laboratories have reported a significant reduction of ischemia-induced injury to hippocampal neurons in rodents treated with competitive and noncompetitive N-methyl-D-aspartate (NMDA) receptor-channel antagonists. This study examined the effects of the noncompetitive antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) in Mongolian gerbils subjected to 5 min of bilateral carotid artery occlusion. In adult female gerbils, single doses of MK-801 injected 1 hr prior to ischemia significantly (p less than 0.01) reduced damage to CA1 hippocampal neurons. However, the drug rendered the postischemic animals comatose and hypothermic for several hours compared with the saline-treated animals. In subsequent experiments, animals pretreated with MK-801 and maintained normothermic during and after forebrain ischemia demonstrated no amelioration of hippocampal damage. Gerbils not treated with MK-801, but kept hypothermic in the postischemic period to approximately the same degree (34.5 degrees C) and duration (8 hr) as was induced by MK-801 therapy showed significant (p less than 0.01) protection of CA1 neurons against ischemia. The neuroprotective activity of MK-801 against transient global ischemia appears to be largely a consequence of postischemic hypothermia rather than a direct action on NMDA receptor-channels.
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PMID:Hypothermia but not the N-methyl-D-aspartate antagonist, MK-801, attenuates neuronal damage in gerbils subjected to transient global ischemia. 1581 67

Auditory brain-stem responses (ABRs) were studied in 66 subjects with severe head trauma. Middle latency responses (MLRs) were also recorded in 22 of them. Patients were carefully selected to avoid conditions such as pre-existing or acute deafness, hypothermia or ethanol intoxication. In order to evaluate the usefulness of potentials in predicting recovery, patients were classified according to the Glasgow Coma Scale (GCS). ABR tracings were classified into 5 groups and MLR into 2 groups. The recovery was good in the presence of a type 1 ABR, poor in the presence of types 3, 4 and 5. Concerning type 2 ABR, the outcome is related to the MLR type, and to the presence of an electrophysiological improvement within the first 3 months following trauma. The reliability of ABR and MLR in predicting the outcome of severe head injury appears to be greater than other usually considered clinical and instrumental data (age, GCS, CT scan, EEG).
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PMID:Auditory brain-stem (ABRs) and middle latency auditory responses (MLRs) in the prognosis of severely head-injured patients. 242 May 72


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