Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024591 (malignant hyperthermia)
 2,353 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 25-year-old man admitted with severe upper torso trauma displayed masseter muscle spasm after suxamethonium given during resuscitation. Anaesthesia was initially maintained with intravenous agents during transfer and X-ray angiography. However, during surgery to correct a brachial artery injury, malignant hyperthermia was triggered when isoflurane was given, 2.5 h after the suxamethonium. He responded to treatment, including dantrolene administration. Peak serum and urine myoglobin were 12,947 micrograms.l-1 and 54,571 micrograms.l-1, respectively, while maximum serum creatinine kinase was 17,300 IU. The patient made an uneventful recovery and later proved positive for malignant hyperthermia susceptibility on muscle contracture tests.
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PMID:Suxamethonium, masseter spasm and later malignant hyperthermia. 1002 82

Early clinical signs, triggering agents, time to onset of reaction, mortality and methods of treatment were identified in 123 suspected malignant hyperthermia reactions. In vitro contracture test results were compared with clinical signs and the Malignant Hyperthermia Clinical Grading Scale. Increased end-tidal carbon dioxide is the earliest sign when not preceded by masseter spasm. Earlier diagnosis reduces the incidence of rigidity and severe metabolic acidosis. The combination of suxamethonium and a potent volatile anaesthetic agent triggers an earlier reaction compared with a volatile agent alone. There has been zero mortality since 1981, essentially due to a combination of advanced monitoring capability, increased anaesthetist awareness of malignant hyperthermia, and dantrolene availability. DNA analysis has identified nine New Zealand families with ryanodine receptor gene mutations. A positive DNA test indicates malignant hyperthermia susceptibility with "causative" mutations but discordance requires that negative DNA tests are confirmed with in vitro contracture test. This test also demonstrated the shortcomings of the Malignant Hyperthermia Clinical Grading Scale.
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PMID:Suspected malignant hyperthermia reactions in New Zealand. 1263 9

Malignant hyperthermia is a potentially fatal pharmacogenetic disease triggered by volatile anesthetics and/or succinylcholine. Dysregulation of intracellular calcium homeostasis is the trigger of the acute crisis. Malignant hyperthermia crisis correspond to an hypermetabolic state, which occurred acutely and interesting skeletal muscular cell. Early manifestations grouped tachycardia, tachypnea, masseter spasm, mixed acidosis and raise of the end expiratory CO2 pressure. Hyperthermia is a late sign, rhabdomyolysis is a sign of the severity of the malignant hyperthermia. The successful treatment is based on an early diagnosis, immediately interruption of triggering agents, intravenous administration of Dantrolene in sufficient dosage and starting of adequate symptomatic treatment. Prevention of this complication is based on asking the patient about genetic predisposition to malignant hyperthermia. Confirmation of the susceptibility to malignant hyperthermia can be provided by in vitro contracture test with halothane or caffeine after muscle biopsy.
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PMID:[Malignant hyperthermia]. 1261 49

We report anesthetic management of a patient suspected of malignant hyperthermia with difficult tracheal intubation. A 64-year-old man was scheduled for a fixation of humerus bone fractures in prone position. He had a history of difficult tracheal intubation due to masseter spasm, and his niece was suspected to be malignant hyperthermia. Anesthesia was induced with propofol using a target controlled infusion. No muscle relaxant was given and spontaneous breathing was maintained. Trials for tracheal intubation failed whenever using a standard laryngoscope, a bronchofiberscope, a laryngeal mask airway or an intubating laryngeal mask airway. Resecting the epiglottic elevating bar of an intubating laryngeal mask airway enabled fiberoptic tracheal intubation. No symptom suggesting malignant hyperthermia developed.
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PMID:[Difficult tracheal intubation in a patient suspected of malignant hyperthermia]. 1264 73

Myotonia congenita (MC) is caused by a defect in the skeletal muscle chloride channel function, which may cause sustained membrane depolarisation. We describe a previously healthy 32-year-old woman who developed a life-threatening muscle spasm and secondary ventilation difficulties following a preoperative injection of suxamethonium. The muscle spasms disappeared spontaneously and the surgery proceeded without further problems. When subsequently questioned, she reported minor symptoms suggesting a myotonic condition. Myotonia was found on clinical examination and EMG. The diagnosis MC was confirmed genetically. Neither the patient nor the anaesthetist were aware of the diagnosis before this potentially lethal complication occurred. We give a brief overview of ion channel disorders including malignant hyperthermia and their anaesthetic considerations.
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PMID:Anaesthetic complications associated with myotonia congenita: case study and comparison with other myotonic disorders. 1567 99

Malignant Hyperthermia (MH) has been a recognized complication of general anesthesia after the first case reports in the 1940's. Since then a great deal has been discovered about the genetics, pathophysiology and treatment of this once fatal syndrome. MH is the only clinical entity specifically related to and caused by anesthetic agents. MH once triggered during anesthesia results in a profound hyper metabolic state with rise in the core temperature, increased carbon dioxide production and oxygen consumption. Death will ensue if specific treatment is not started. The incidence of fulminant MH ranges from 1:62,000 to 1: 84,000 of general anesthesia cases if succinylcholine and inhalation agents are used. Massseter muscle spasm on induction of anesthesia, with an incidence of between 1:16,000 and 1:4,000, may be a predromal indication of the development of MH. Anesthetic agents, which may trigger MH in susceptible individuals, are the depolarizing muscle relaxant, succinyl choline and all the volatile anesthetic gasses. Nitrous oxide, intravenous induction agents, benzodiazepines, opioids, and the non-depolarizing relaxants do not trigger MH. MH susceptibility is associated with certain disorders, such as Duchene muscular dystrophy, and triggering agent should not be used in these patients. Inheritance is an autosomal dominant trait with variable penetrance. The pathogenesis of MH involves the loss of control of intracellular calcium ions in skeletal muscle with resultant protracted spasm and hyper metabolism. Clinically this will progress to hypercarbia, hypoxia, hyperthermia, hyperkalemia and death will result if specific treatment is not started. Management involves immediate discontinuation of the triggering anesthetics, hyperventilation with 100% oxygen and most importantly the definitive treatment with intravenous dantrolene.The importance of instigating the use of dantrolene in cases of MH cannot be overemphasized. MH is now treatable when once it would be fatal before the availability of dantrolene. Unless of an emergent nature, surgery should be canceled following the acute phase of MH. The patient should be admitted to intensive care for at least 24 hours and dantrolene continued as recurrence has been described. It is imperative that the patient and their family are counseled, Medalert bracelets provided and registration with the Malignant Hyperthermia Association of the United States (MHAUS), encouraged. The caffeine/halothane testing of muscle biopsies is currently the most definitive test for malignant hyperthermia susceptibility. The routine use in suspected cases or the immediate family of known cases remains a matter of contention.
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PMID:Malignant hyperthermia. 1450 52

We report the case of a 20-year-old woman who developed masseter spasm after receiving succinylcholine for rapid sequence intubation. Sometimes referred to as "jaws of steel," masseter spasm secondary to anesthetic administration may progress to malignant hyperthermia. Although succinylcholine-induced masseter spasm is uncommon, it is important to be prepared to deal with this entity when administering succinylcholine.
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PMID:Masseter spasm after succinylcholine administration. 1763 81

A 3-year-old Thai boy underwent open reduction and internal fixation with K-wire of condylar fracture of humerus under general anesthesia. The patients developed generalized muscle regidity, masseter muscle spasm, elevated creatinine kinase, high temperature (39.3 C), inappropriate tachycardia, and arterial base excess was more than-8 mEq/L. The clinical grading scale of diagnosis of malignant hyperthermia was 58 (grade D6; almost certain malignant hyperthermia). Succinylcholine has been identified as the trigger agent, as other possible trigger agents were not involved. The treatment included hyperventilation, external cooling and cold IV fluids without administration of dantrolene. The patient fully recovered and discharged on day 12. This case report showed an incidence of malignant hyperthermia of approximated 1:150,000 in Thai Anesthesia Incidents Study (THAI Study).
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PMID:Malignant hyperthermia: a case report in Thai Anesthesia Incidents Study (THAI Study). 1686 89

Malignant hyperthermia (MH) is a rare but fatal complication that develops under general anesthesia. Reports on MH in patients over the age of 80 years are unusual. We experienced a case of MH in an 82-year-old patient during esophageal resection. Anesthesia was induced with propofol and succinylcholine, and maintained with sevoflurane. Neither masseter spasm nor rigidity of the limbs was seen during induction. Body temperature (BT) at induction was 36.0 degrees C. Three hours after incision, the level of end-tidal CO2 was elevated to 55 mmHg. We assumed that the rise in end-tidal CO2 had occurred due to secretions in the airway. However, the BT, which had risen at 3 h after incision, continued to rise, and about 60 min later, the BT exceeded 39.0 degrees C. A rise of more than 0.5 degrees C in less than 15 min was seen, and MH was suspected. With dantrolene administration, the BT decreased from 40.9 degrees C at maximum to 37.7 degrees C. With continuous infusion of dantrolene when the patient was transferred to the intensive care unit (ICU), BT remained within the normal range. The next day re-operation was performed, without further complications or recurrence of MH during the postoperative period. Because it is necessary to initiate treatment in the early stage of MH, as soon as possible, although MH prevalence is low in the elderly, it is important to suspect MH when hypercapnia and/or hyperthermia are seen.
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PMID:Malignant hyperthermia developing during esophageal resection in an 82-year-old man. 1901 91

We are reporting a case of endosulfan poisoning, admitted in a state of altered consciousness, vomiting, and seizure. The diagnosis was based on history, physical examination and positive reports from toxicological screening. After 8 hrs of admission, a sudden rise in EtCO(2), respiratory rate, heart rate, blood pressure, and body temperature was noted. Masseter spasm was there and patient's elbow/knees could not be bent upon manipulation. Caffeine halothane contraction test later confirmed it to be malignant hyperthermia (MH). We suggest that if there is a sudden rise in body temperature, stiffness in limbs or massater spasm in a case of endosulfan poisoning, the diagnosis of MH should be considered as one possibility when etiology is not certain.
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PMID:Malignant hyperthermia in endosulfan poisoning. 2273 8


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