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Query: UMLS:C0024591 (malignant hyperthermia)
 2,353 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report a retrospective study of 11 cases of malignant hyperthermia. The mean age of the patients was 5 months and 3 weeks. Clinical features included severe hyperthermia (greater than 41 degrees C), seizures, coma, collapse, rhabdomyolysis, acute renal failure and functional renal failure. Three infants died. Four patients presented neurological damages. Four recovered fully. The authors discuss the difficulties of diagnosis, the nosological position and the pathophysiology of this syndrome.
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PMID:[Severe hyperthermia syndrome in the infant. Apropos of 11 cases]. 367 Oct 30

This report describes three male patients arrested for aggressive and combative behavior, characteristic of phencyclidine intoxication, in whom severe hyperthermia, respiratory failure, and coma developed. Two days after the malignant hyperthermic event, serum transaminase levels rose acutely to extremely high levels with concomitant elevations in bilirubin levels and a fall in prothrombin activity. Liver biopsy specimens in two patients showed marked perivenular necrosis and collapse. No specific treatment was directed at the phencyclidine intoxication. Two of the three patients survived. Submassive liver necrosis caused by malignant hyperthermia is an unusual complication of phencyclidine abuse.
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PMID:Phencyclidine-induced malignant hyperthermia causing submassive liver necrosis. 674 77

Succinylcholine, a depolarizing muscle relaxant with both activating and desensitizing effects, is used to facilitate endotracheal intubation. The activating effects were found to be above-normal on induction of anesthesia in 7 neurological patients: generalized muscle spasm in 1 myotonic patient, contractures or prolonged contractions in "anatomically" denervated muscles (1 patient), in "functionally" denervated muscles (1 patient) and in "centrally" denervated muscles (4 patients). One of these four presented hyperkalemia and cardiocirculatory collapse. It is important to differentiate these anomalous responses to succinylcholine from those occurring as early signs of rhabdomyolysis or malignant hyperthermia.
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PMID:Increased activation effects of succinylcholine in neurological patients. 686 44

The first 2000 incidents reported to the Australian Incident Monitoring Study were analysed with respect to the role of the capnograph. One hundred and fifty-seven (8%) were first detected by a capnograph and there were a further 18 (1%) in which capnography was contributory. Of the 1256 incidents which occurred in association with general anaesthesia 48% were "human detected" and 52% "monitor detected". The capnograph was ranked second and detected 24% of these monitor detected incidents; this figure would have been nearly 30% if a correctly checked, calibrated capnograph had always been used. The capnograph is a "front-line" monitor for oesophageal intubation, failure of ventilation, anaesthetic circuit faults, gas embolism, sudden circulatory collapse and malignant hyperthermia. It is a valuable "back-up" monitor when other monitors (e.g. low pressure alarm, pulse oximeter) are not in use, are being used incorrectly or fail. Such situations, in order of frequency of detection were: circuit-leak, overpressure of the breathing circuit, bronchospasm, leak of ventilator-driving-gas into the patient circuit, aspiration and/or regurgitation and hypoventilation. There were 20 reports of "failure", over two-thirds of which would not have occurred with appropriate checking and calibration. Seven were due to gas sampling problems and 6 to apnoea alarm failure. Two circuit leaks and 2 faulty unidirectional valves were not detected; on 3 occasions problems occurred due to power failure, calibration problems, or misinterpretation of an alarm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The Australian Incident Monitoring Study. The capnograph: applications and limitations--an analysis of 2000 incident reports. 827 74

The serotonin syndrome is frequently characterized by minor neurologic manifestations that regress rapidly (such as confusion, tremor, ...). Many medications including tricyclic antidepressants, serotonin reuptake inhibitors, tryptophan and the association of monoamine oxidase inhibitors together with a serotoninergic agent have been implicated in this syndrome. In certain cases, and for poorly understood reasons, clinical manifestations can include circulatory collapse, malignant hyperthermia, convulsions and rhabdomyolysis. These forms are often fatal. Treatment, other than the withdrawal of the offending drug, is symptomatic. Dialysis may be of value in withdrawing the drug from the circulatory system. We report a patient with the serotonin syndrome of favorable outcome due to an overdose of moclobemide and clomipramine.
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PMID:Serotonin syndrome due to an overdose of moclobemide and clomipramine. A potentially life-threatening association. 903 53

Among all the drugs used for general anaesthesia, neuromuscular blockers appear to play a prominent role in the incidence of severe adverse reactions. It now seems likely that most serious adverse drug reactions occurring during anaesthesia are immunological in type. The frequency of life-threatening anaphylactic or anaphylactoid reactions occurring during anaesthesia has been estimated to be between 1 in 1000 and 1 in 25,000 anaesthetic procedures, with the neuromuscular blockers being involved in 80% of cases. The mortality from such serious reactions is reported to be in the range of 3.4 to 6%. The highly immunogenic drug, suxamethonium chloride (succinylcholine), was found to be the most hazardous agent. Drug-specific immunoglobulin E antibodies to suxamethonium chloride and other neuromuscular blockers have been demonstrated. This sensitivity to neuromuscular blockers seems to be a long-lasting phenomenon. During anaesthesia, the clinical features of an allergic reaction are often masked. Tachycardia and circulatory collapse may be the only signs of an allergic reaction, and they are easily misdiagnosed. Bronchospasm is reported to be present in about 40% of cases. Successful management of these patients includes stabilisation during the acute reaction and avoidance of future reactions. The latter is based on the identification of the causative drug and potentially cross-reacting compounds. The use of suxamethonium chloride is associated with many other adverse effects, such as fasciculations, myalgia, potassium release, changes in the heart rate, increases in intragastric and intraocular pressures, and malignant hyperthermia. Because of the dangers of hyperkalaemic cardiac arrest after suxamethonium chloride administration in children with unrecognised muscular dystrophy, there have now been moves to limit the use of this drug in children. Although neuromuscular blockers are designed to specifically block nicotinic cholinergic receptors at the neuromuscular junction, many bind to muscarinic cholinergic receptors on ganglia and smooth muscle, and alter parasympathetically mediated heart rate and airway calibre. Most benzylisoquinolinium muscle relaxants can induce histamine release, especially when they are administered rapidly, which can lead to disturbances of cardiovascular function. In addition, nondepolarising neuromuscular blockers have been implicated in causing generalised weakness following their long term administration to patients on an intensive care unit. The problem with these adverse drug reactions is their unpredictable nature. Therefore, prompt recognition with appropriate therapy can help to improve the outcome.
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PMID:Adverse effects of neuromuscular blockers and their antagonists. 951 17

Among all the drugs used for general anesthesia, neuromuscular blockers appear to play a prominent role in the incidence of severe adverse reactions. It now seems likely that most serious adverse drug reactions occurring during anesthesia are immunological in type. The frequency of life-threatening anaphylactic or anaphylactoid reactions occurring during anesthesia has been estimated to be between 1 in 1000 and 1 in 25,000 anesthetic procedures, with the neuromuscular blockers being involved in 80% of cases. The mortality from such serious reactions is reported to be in the range of 3.4 to 6%. The highly immunogenic drug, suxamethonium chloride (succinylcholine), was found to be the most hazardous agent. Drug-specific immunoglobulin E antibodies to suxamethonium chloride and other neuromuscular blockers have been demonstrated. This sensitivity to neuromuscular blockers seems to be a long-lasting phenomenon. During anesthesia, the clinical features of an allergic reaction are often masked. Tachycardia and circulatory collapse may be the only signs of an allergic reaction, and they are easily misdiagnosed. Bronchospasm is reported to be present in about 40% of cases. Successful management of these patients includes stabilisation during the acute reaction and avoidance of future reactions. The latter is based on the identification of the causative drug and potentially cross-reacting compounds. The use of suxamethonium chloride is associated with many other adverse effects, such as fasciculations, myalgia, potassium release, changes in the heart rate, increases in intragastric and intraocular pressures, and malignant hyperthermia. Because of the dangers of hyperkalemic cardiac arrest suxamethonium chloride administration in children with unrecognised muscular dystrophy, there have now been moves to limit the use of this drug in children. Although neuromuscular blockers are designed to specifically block nicotinic cholinergic receptors at the neuromuscular junction, many bind to muscarinic cholinergic receptors on ganglia and smooth muscle, and alter parasympathetically mediated heart rate and airway calibre. Most benzylisoquinolinium muscle relaxants can induce histamine release, especially when they are administered rapidly, which can lead to disturbances of cardiovascular function. In addition, nondepolarising neuromuscular blockers have been implicated in causing generalised weakness following their long term administration to patients on an intensive care unit. The problem with these adverse drug reactions is their upredictable nature. Therefore, prompt recognition with appropriate therapy can help to improve the outcome.
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PMID:Adverse effects of neuromuscular blockers and their antagonists. 978 39

Acute asthma is well known to provoke complications. We report the case of a patient who needed intubation and mechanical ventilation for acute asthma. Despite a treatment with corticosteroids, bronchodilators, neuromuscular blocking drugs and magnesium sulfate, the situation remained uncontrolled and as a last resort, halothane became necessary. The patient then developed an episode of malignant hyperthermia with fever at 40 degrees C and rhabdomyolysis. At this time, halothane could be stopped and all the symptoms disappeared without modifying the rest of the treatment. Eight days later, he presented with a neuroleptic malignant syndrome following an injection of droperidol. Temperature rose to 42 degrees C, associated with muscle rigidity, sweating, tachycardia and severe circulatory collapse. The use of dantrolene in association with a symptomatic treatment of the collapse led to a favourable outcome in. Unfortunately, in vitro contracture test could not be performed in this case. The links between malignant hyperthermia and neuroleptic malignant syndrome remain unclear. Although these two pathologies share the same physiopathology, symptomatology and treatment, they are clearly individualized. This case seems to be the first description of their occurrence in the same patient.
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PMID:Malignant hyperthermia and neuroleptic malignant syndrome in a patient during treatment for acute asthma. 992

The implications of the collapse of a soldier early in an exercise from exertional heat illness (EHI) are considered. Such soldiers may be at risk from a genetic predisposition. Malignant hyperthermia (MH) and isolated and improbable cases of EHI may be just two different expressions of the same mutated gene sequence. The genetics of MH are complex and present knowledge is incomplete. The use of the in vitro contraction test (IVCT) on cases of EHI, in addition to its proven role in MH, would be helpful in examining the relationship between MH and EHI. It has been shown that some soldiers collapsing with EHI may have subsequent positive IVCTs. The test, however, sometimes produces false positives and, in addition, a positive result could be a consequence of a heat insult rather than an antecedent. Further studies to establish the incidence of positive IVCTs in relatives of EHI probands, and thus test for heritability, are required. There is, at the moment, only one example of proven MH and proven EHI occurring in the same individual. DNA from a 12-year-old boy who suffered MH and later died from the EHI and from his relatives showed relevant mutations as did the DNA of two of three soldiers who survived EHI. Hajj pilgrims, who collapse with heat illness, do not show such mutations, but the etiology is different. The sedentary pilgrims succumbed to a very high external ambient temperature, the active soldiers to a huge output of internal metabolic heat. Only eventual advances in defining the genetics of MH and EHI will resolve the present confusion of the relationship between the two conditions. Meanwhile, there is a need to bypass considerations of the etiology of EHI and to identify the vulnerable and handicapped soldier by exposure after an interval of time to one or more exercise tolerance tests.
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PMID:Collapse from exertional heat illness: implications and subsequent decisions. 1254 51

A young, overweight dog presented with sudden onset lethargy and collapse following exercise in warm environmental conditions. Investigations revealed systolic hypotension, multiform ventricular premature complexes, irregular myocardial echogenicity with poor left ventricular systolic function and a markedly elevated troponin cTnI (180ng/mL, reference range <0.3ng/mL) consistent with severe myocyte damage. Infectious causes of myocarditis were ruled out on the basis of serological and polymerase chain reaction blood tests. Exercise-induced malignant hyperthermia was excluded from the history, an exercise tolerance test and genetic testing for the RYR1 V547A mutation. The diagnosis was myocardial damage secondary to suspected exertional heatstroke, from which the dog recovered uneventfully over a number of weeks and serum troponin normalised. This is the first case report in any species including man, documenting high troponin as a marker of severe myocardial damage following suspected heatstroke.
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PMID:High serum troponin I concentration as a marker of severe myocardial damage in a case of suspected exertional heatstroke in a dog. 1908 37


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