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

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

Masseter muscle rigidity after suxamethonium, usually occurring in children induced with halothane, is associated with malignant hyperthermia. A case is reported in which masseter muscle rigidity occurred in an adult following vecuronium. From the limited data available, this and two similar reported cases, it appears that non-depolarizing muscle relaxants can, very rarely, cause masseter muscle rigidity in adults. This masseter muscle rigidity may complicate airway management, but is unlikely to progress to generalized rigidity and malignant hyperthermia.
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PMID:Masseter muscle rigidity after vecuronium. 1010 32

The clinical pharmacology of neuromuscular blocking agents is described. During neuromuscular blockade, succinylcholine attaches to receptors in the motor end plate and depolarizes the neuromuscular junction, making the end plate refractory to acetylcholine. The nondepolarizing relaxants have a structure similar to that of succinylcholine and bind to the same receptors. Instead of depolarizing the junction, they block acetylcholine from binding to the receptor and cause channel blockade. As the concentration of nondepolarizing relaxant increases relative to acetylcholine, neuromuscular transmission is compromised. This relationship is used clinically to facilitate recovery from nondepolarizing agents. Succinylcholine is popular because its onset is faster than that of the nondepolarizing relaxants and metabolism by pseudocholinesterase clears it quickly. It is commonly given as an i.v. bolus to facilitate tracheal intubation. The onset of these agents varies widely and is dose dependent. Large doses are usually given to hasten the onset of paralysis; subsequent doses are adjusted according to response. The nondepolarizing agents interact with inhaled anesthetics, magnesium, and many antimicrobials. Drugs like neostigmine, edrophonium, and pyridostigmine antagonize neuromuscular blockade; an anticholinergic drug is typically administered to counteract the cardiovascular effects. The most serious adverse effects of succinylcholine are malignant hyperthermia syndrome, masseter muscle rigidity, and bradycardia. Some nondepolarizing relaxants (atracurium, mivacurium, and pancuronium) are associated with histamine release, occasionally causing serious hypotension and tachycardia. Neuromuscular blocking agents are essential to anesthesia. Older compounds produce greater toxicity than newer compounds, and several of these older compounds therefore are no longer in clinical use.
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PMID:Clinical pharmacology of neuromuscular blocking agents. 1043 10

Malignant hyperthermia susceptibility (MHS), a skeletal muscle disorder, is mostly inherited as an autosomal dominant trait. Exposure of susceptible individuals to volatile halogenated anaesthetics can lead to a MH episode resulting in irreversible tissue damages or to the patient's death if not immediately reversed by dantrolene treatment. A MH episode is characterised by a combination of hyperthermia, skeletal muscle rigidity and hypermetabolism. Porcine stress syndrome has proved to be a valuable model for physiopathological studies of MHS. Malignant hyperthermia syndrome is associated with a failure of the calcium homeostasis in muscular fibres. Dysfunction of the calcium channels: the ryanodine receptor (RyR) and the dihydropyridine receptor (DHPR), which are involved in the release of the Ca2+ stored in sarcoplasmic reticulum has been clearly demonstrated. A biochemical test based on the analysis of the in vitro contracture response of muscular fibres to caffeine and halothane was developed to define the MHS status of patients. Although the genetic analysis of MHS has beneficiated from recent progresses, genetic testing is still far to answer to all testing situations. If in swine, hyperthermia syndrome was always associated with a unique mutation of the RyR1 gene, genetic analysis is far more complicated in human: i) more than 20 different MHS mutations in the RyR1 gene have been described; ii) a mutation of the gene encoding the dihydropyridine receptor has been identified; iii) 4 other potential MHS loci have been reported.
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PMID:[Biology of malignant hyperthermia: a disease of the calcium channels of the skeletal muscle]. 1076 Jul 1

Hyperthermia, skeletal muscle rigidity, rhabdomyolysis, acidosis and multiple system insufficiency characterize malignant hyperthermia. Anaesthetic malignant hyperthermia follows halogenated volatile agents and/or depolarizing muscle relaxants utilization. Diagnosis is based on in vitro muscle contracture in response to halothane and/or caffeine exposure. Neuroleptic malignant syndrome affects patients taking neuroleptic drugs; clinical findings include hyperthermia, extrapyramidal rigidity, acidosis, neurovegetative instability and neurological signs. We report three neuroleptic malignant syndrome patients with positive muscle contracture tests which shows that muscle from neuroleptic malignant syndrome patients may in some instances show alterations similar to those of anaesthetic malignant hyperthermia.
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PMID:[Malignant hyperthermia susceptibility in 3 patients with malignant neuroleptic syndrome]. 1097 14

Malignant hyperthermia is an autosomal-dominant inherited disorder of the skeletal muscle cell characterized by a hypermetabolic response to all commonly used inhalational anaesthetics and depolarizing muscle relaxants. The clinical syndrome includes muscle rigidity, hypercapnia, tachycardia and myoglobinuria as result of increased carbon dioxide production, oxygen consumption and muscle membrane breakdown. In human beings and animals susceptible to malignant hyperthermia, it is generally accepted that an increase in the level of myoplasmic free calcium is the cause of the syndrome. Various hypotheses have been proposed to account for the increase of intracellular calcium levels, e.g. a defect in the calcium release channel of the sarcoplasmic reticulum (ryanodine receptor), an abnormality of the excitation-contraction coupling mechanisms, or alterations in second messenger systems of skeletal muscles. This review gives an overview of the main features of this disease and recent advances in research including pathophysiology, treatment, diagnosis and genetics as well as association with other disorders.
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PMID:Malignant hyperthermia. 1155 40

We experienced two cases of malignant hyperthermia (MH) triggered by sevoflurane. Case 1 was a six-year-old girl, 15.8 kg, undergoing strabismus repair. She had flat back, elevated diaphragm and high arched palate. Anesthesia was induced and maintained with sevoflurane and nitrous oxide in oxygen. Her trachea was intubated without the use of muscle relaxant. Thirty minutes after the induction of anesthesia, ETco2 was over 60 mmHg despite hyperventilation. Muscle rigidity of legs and the rise in temperature were noted. MH was diagnosed and dantrolene i.v. was administered. Her maximum esophageal temperature was 40.2 degrees C. ETco2 and temperature returned to baseline values after dantrolene administration. Creatine phosphokinase (CK) level was 252 U.l-1 preoperatively, and 1690 U.l-1 next day. Case 2 was a year-and-9-month-old boy undergoing accessory ear resection. Anesthesia was induced with sevoflurane and nitrous oxide in oxygen. His trachea was intubated with an aid of vecuronium. Forty minutes after administration of sevoflurane his temperature rose to 38.6 degrees C with heart rate 191 bpm and Spo2 93%, and muscle rigidity of legs. MH was diagnosed and dantrolene was administered. His highest temperature was 39.3 degrees C and was reduced promptly after dantrolene. Postoperatively he was noted to have downslanting palpebral fissures, micrognathia, low set ears, and a single crease of the fifth finger and diagnosed as King syndrome which is reported to have association with MH. Both patients had no history of anesthesia nor abnormal family history. Both of them were rescued with dantrolene and recovered without sequelae.
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PMID:[Two pediatric cases of malignant hyperthermia caused by sevoflurane]. 1175 32

Malignant hyperthermia (MH) is a hypermetabolic syndrome triggered in genetically susceptible individuals when certain potent inhalation anesthetics or succinylcholine are administered. The signs of MH include a greatly increased body metabolism, muscle rigidity and eventual hyperthermia that may exceed 110 degrees F. Death can result from cardiac arrest, brain damage, internal hemorrhaging or failure of other body systems. Dantrolene is given until the manifestations of MH abate. The initial dose is 2.5 mg/kg body weight; and repeated as needed. High-risk patients cannot always be identified by history, and preparation of every OR is essential. Supplies of dantrolene and other medications must be kept in the OR area. If MH develops, acting within minutes may save a life.
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PMID:Malignant hyperthermia: an OR emergency! 1202 57

A case of malignant hyperthermia (mh) in a 27-year-old man is described. In a first anaesthesia using isoflurane and succinylcholine, the end-tidal CO(2) rose from 39 to 49 mmHg 2.75 h post-intubation and the body temperature rose to 39.8 degrees C 14 h post-intubation but was normal again the next day. In a second anaesthesia using the same medication, the maximal end-tidal CO(2) was 44 mmHg and the body temperature rose to 39 degrees C after 9 h. After 4 days, the fever rose to 40 degrees C, and to 42 degrees C when death occurred 10 days after the second anaesthesia. Masseter spasms or muscle rigidity were never present. According to the death certificate, death was due to multi-organ failure from sepsis. At autopsy, the skeletal muscles were pale and oedematous. Histology demonstrated focal necroses in the skeletal muscles, shock kidneys with myoglobin excretion and myoglobin clots in small blood vessels of the lungs. Hence, the postmortem diagnosis "malignant hyperthermia" was established but accusations of medical maltreatment were rejected because of the atypical and protracted clinical course and because uncharacteristic signs of malignant hyperthermia were attributable to the clinically suspected sepsis.
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PMID:Fatal malignant hyperthermia--delayed onset and atypical course. 1237 88

Drug-induced hyperthermia is one condition that anesthesiologists may meet even though it is uncommon, it is life threatening. We report 3 cases of patients at Siriraj Hospital, Mahidol University who developed drug-induced hyperthermia and rhabdomyolysis from different mechanisms. In two of them, the diagnosis was suspected malignant hyperthermia. Rigidity, hyperthermia and tachyarrhythmia developed just after inhalation induction (halothane and sevoflurane) and intubation with succinylcholine. The other case was the result of amphetamine abuse. He also had received both succinylcholine and inhalation agent (isoflurane) but no obvious signs or symptoms were detected during anesthesia. He developed a gradual increase in fever over 13 hours post operation and complained of muscle pain (with leg muscle cramps). All of them showed a marked increase in muscle enzymes and had rhabdomyolysis. As a result of early detection and early manangement, these three patients survived without any permanent damage to vital organs. We conclude that Thai anesthesiologists should be more aware and alert to drug-induced hyperthermia especially as nowadays many teenagers abuse stimulant drugs and "triggering" drugs as antidepressant or serotonin reuptake inhibitors are prescribed more frequently. Early detection and management will decrease morbidity and mortality.
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PMID:Drug-induced hyperthermia and rhabdomyolysis during the perioperative period: report of three patients. 1245 25


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