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)

Patients who suffer severe brain damage may be brain dead, even though their cardiorespiratory function is supported by mechanical ventilation. According to criteria established in the United Kingdom and the United States, if these patients meet the preconditions of apneic coma that is attributable to diagnosed irreversible cause, and the presence of drug intoxication, hypothermia, or metabolic coma is excluded, then documentation of absent brainstem reflexes and apnea despite a PaCO2 of 50 mm Hg or greater will confirm the presence of brain death. If the brain is dead, the patient is dead, regardless of the state of his circulation, and he should be declared dead and removed from the ventilator. If the patient has lost higher cortical function but brainstem function is preserved, he may be in the persistent vegetative state and live for years with apparent sleep-wake cycles but no awareness of any external or internal stimuli. As the prognosis for recovery from the persistent vegetative state is absent, there is no ethical responsibility to continue treatment other than to provide basic nursing care to maintain the dignity of the patient.
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PMID:Brain death and persistent vegetative states. 352 1

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

We report four cases of severe meprobamate intoxication. Maximal plasma levels reached 800 (176), 816 (180), 863 (190) and 923 mumol/l (203 mg/l). All patients survived without sequelae including one patient resuscitated from cardiac arrest. The clinical course was complicated by coma, hypotension, and hypothermia in all patients. Three cases were treated with charcoal hemoperfusion with mean hemoperfusion clearance ranging from 134-164 ml/min compared to 174 ml/min in one case treated with resin filter and the same blood flow of 200 ml/min. In two cases, a mean renal meprobamate clearance of 15 and 23 ml/min was calculated comprising only 9-15% of the hemoperfusion clearance. The amount of meprobamate removed by hemoperfusion ranged from 1.6-6.2 g. In one case, the half-life of plasma meprobamate during hemoperfusion was 2.6 hours compared to 8.3 hours after hemoperfusion. Thus the half-life was reduced more than 3-fold. These data show that hemoperfusion may be indicated in severe meprobamate intoxication.
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PMID:Meprobamate kinetics during and after terminated hemoperfusion in acute intoxications. 366 17

A 74-year-old man with myxedema and hypothermia had increased activities in plasma of creatine kinase (CK; EC 2.7.3.2), aspartate aminotransferase (AST; EC 2.6.1.1), and lactate dehydrogenase (LD; EC 1.1.1.27) and increased proportions of CK-MB (up to 20% of total CK) and LD1 isoenzymes, but no clinical or investigational evidence of associated myocardial infarction. This case illustrates that plasma enzyme activity and isoenzyme profiles in such clinical settings should be interpreted with caution, because increases in CK-MB and LD1 may relate to myxedema coma or hypothermia (or both) rather than to myocardial infarction.
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PMID:Cardiac enzyme changes in myxedema coma. 382 11

Auditory brainstem responses (ABRs) provide a way to evaluate central nervous system function in young, confused, uncooperative or comatose patients. Auditory brainstem responses represent activity in or around the vestibulocochlear (VIII) cranial nerve, cochlear nucleus, superior olivary complex, lateral lemniscus, and inferior colliculus. Many factors affect recording of the auditory brainstem response. These factors include technical factors, chronic alcoholism, demyelinating diseases, ototoxic drugs, barbiturates, hearing loss, otitis media, and hypothermia.
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PMID:Problems in interpreting abnormal auditory brainstem responses in comatose patients. 384 67

Cardiopulmonary arrest is a test of the brain's tolerance to global ischemia. New insights into the pathophysiology of global ischemia have led to the potential use of early prophylactic anticonvulsants, hypothermia, barbiturate coma, glucose manipulations, calcium-blocking agents, and hemodilution. A wide spectrum of neurologic sequelae may follow global ischemia, ranging from brain death, vegetative states, and impairment of higher intellectual function to syndromes of amnesia and cortical blindness, post-anoxic myoclonus, delayed leukoencephalopathy, and spinal stroke. The distinctive features of these sequelae and their pathophysiologic aspects are discussed. Special attention is given to brain death and prognostication.
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PMID:Cardiopulmonary arrest. Pathophysiology and neurologic complications. 390 62

A patient is reported who developed adult respiratory distress syndrome (ARDS) and severe hypothermia during the decompensated phase of Wernicke encephalopathy. The absence of other causes suggests a neurogenic origin for the hypothermia, possibly as a result of lesions localized in the posterior hypothalamus. A hemodynamic study during normothermia, hypothermia and rewarming showed that at body temperatures inferior to 32 degrees C the increase in pulmonary vascular resistances seems not to be the result of a real vasoconstrictor effect in the pulmonary circulation. The Wernicke-Korsakoff syndrome may have a clinical picture similar to delirium tremens, evolving into coma with complications such as hypothermia and, possibly, ARDS.
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PMID:[Respiratory distress syndrome and hypothermia in Wernicke's encephalopathy]. 408 74

Thirty-eight patients in coma due to head trauma, cerebrovascular accidents, hypoxia, hypoglycaemia, or barbiturate intoxication, and 15 cases of brain death were studied. Cerebral metabolic rate of oxygen (CMRO(2)) was obtained from the arteriovenous oxygen difference and cerebral blood flow (CBF) measured by intra-arterial (133)Xenon method. If hypothermia and CNS depressants were excluded, CMRO(2) below one-third of normal was incompatible with regaining of consciousness, but this was seen in only three comatose patients. Irrespective of the clinical outcome (death, vegetative survival, or recovery), CMRO(2) values of one-third to two-thirds of normal were seen in the majority of coma patients. CMRO(2) measurements were of no practical value to predict the prognosis in coma, even when the effect of temperature and sedatives were considered. In brain death the CBF studies gave indirect evidence of cerebral circulatory arrest. The cerebrospinal fluid (CSF) was obtained for analysis of lactate, pyruvate, and bicarbonate in 29 cases. Increased CSF lactate levels were found in all groups except barbiturate intoxication. The finding of a negative correlation between CSF bicarbonate and log CBF suggests that the CSFpH determines the wide range of CBF in coma.
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PMID:Cerebral blood flow and oxygen uptake, and cerebrospinal fluid biochemistry in severe coma. 483 10

Accidental hypothermia was studied in 11 patients, five of whom died. This condition occurs spontaneously, usually in a cold environment, and should be suspected in the comatose hypotensive patient. It is easily missed because regular clinical thermometers do not record extremely low body temperatures. It is distinguished from other forms of hypothermia by the very low body temperature and by the absence of recognized causes of hypothermia. Ten of the 11 patients were either alcoholic or diabetic. Intravascular thrombosis was the most common complication leading to death.
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PMID:Accidental hypothermia. 549

During acute intoxications, the first EEG may show persistence or abolition of cerebral activity, but the possibility of recovery after isoelectric tracing in toxic comas must be emphasized. EEG patterns frequently suggest the probability of hypnotic tranquilizer poisoning; 4 types of EEG are encountered corresponding to different grades of toxic coma. Recurrent periods of electrical silence alternating with bursts of activity are habitually recorded in carus comas with hypothermia due to acute barbiturate intoxication, with good prognosis. The possibility of a neurological disturbance associated with drug overdose must be raised whenever an asymmetric tracing is encountered. Serial recordings may detect complications such as: a localized lesion, anoxia or, very rarely, typical paroxysmal abnormalities reappearing in comitial patients before emergence from a toxic coma. Paradoxical monomorphic delta activity corresponding to improvement must not be considered as an aggravation. Peculiar EEG findings occur after oral trichlorethylene poisoning, with temporary clinical deterioration and intermittent periods of electrical silence; recovery is possible. An alpha-like pattern after cardiac arrest of toxic origin has a poor prognosis. The appearance of alternating patterns suggests the development of irreversible brain damage.
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PMID:[EEG in the prognosis of toxic coma: reflections apropos of unusual data]. 613 24


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