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)

There is evidence for the occurrence of psychopathological symptoms in the adult form of myotonic dystrophy such as disturbance of concentration and memory, chronic depression, disturbed social behaviour, mental retardation, and hypersomnia. In this report we present a patient suffering from multisystemic myotonic myopathy without a cytosine-thymine-guanine [corrected] repeat expansion on chromosome 19q13.3 and schizophrenia. In this patient, a severe increase of creatine kinase (CK) occurred during treatment with olanzapine and amisulpride. The following risperidone medication was well tolerated without side effects. Susceptibility for malignant hyperthermia was detected by a positive in vitro contracture test. The occurrence of elevated muscle enzymes during treatment with atypical neuroleptics is suspicious as a possible side effect of neuroleptic medication and muscle disease.
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PMID:[Incompatibility of olanzapine and amisulpride in multisystemic myotonic myopathy]. 1157 7

We report a patient with proximal myotonic myopathy who was treated with neuroleptics because of exacerbating schizophrenia. Under therapy with fluanxol, the patient developed muscle stiffness and oculogyric cramps. Treatment with both amisulpride and olanzapine lead to markedly elevated serum creatine kinase levels. An in-vitro contracture test was positive for halothane. Thus, in patients with all kinds of multisystemic myotonic myopathies, a susceptibility for malignant hyperthermia and intolerance towards neuroleptics should be taken into account.
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PMID:Intolerance to neuroleptics and susceptibility for malignant hyperthermia in a patient with proximal myotonic myopathy (PROMM) and schizophrenia. 1173 Dec 82

A case of rhabdomyolysis from malignant hyperthermia occurred during renal transplantation surgery is presented. After the completion of vascular and uretherovesical anostomosis, the patient's heart rate began to rise, sweatiness was observed and body temperature increased to 41 degrees C. Additionally, metabolic and respiratory acidosis and hyperkalemia were detected. Serum creatine kinase and lactic dehydrogenase levels were increased significantly. After external cooling and the administration of dantrolene sodium, body temperature and heart rate were decreased. During this period; furosemide, mannitol and sodium bicarbonate were given. Three hours after the completion of surgery, urine output was begun and urine myoglobin was found to be positive. Renal function improved gradually and serum creatinine level decreased to 1.6 mg/dl on the 14th postoperative day. Malignant hyperthermia can lead to severe rhabdomyolysis and delayed graft function in renal transplant recipients. Early diagnosis and intervention is crucial for protecting renal function.
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PMID:Severe rhabdomyolysis due to malignant hyperthermia during renal transplantation procedure can cause delayed graft function. 1191 7

Rhabdomyolysis is a disorder characterized by acute damage of the sarcolemma of the skeletal muscle leading to release of potentially toxic muscle cell components into the circulation, most notably creatine phosphokinase (CK) and myoglobin, and is frequently accompanied by myoglobinuria. Therefore, the term myoglobinuria is often used interchangeably with the term rhabdomyolysis. This disorder may result in potential life-threatening complications such as acute myoglobinuric renal failure, hyperkalemia and cardiac arrest, disseminated intravascular coagulation, and compartment syndrome. The condition is etiologically heterogeneous and may result from a large variety of diseases affecting muscle membranes, membrane ion channels, and muscle energy supply including acquired causes (e.g., exertion, crush injury and trauma, alcoholism, drugs, and toxins) and hereditary causes (e.g., disorders of carbohydrate metabolism, disorders of lipid metabolism, or diseases of the muscle associated with malignant hyperthermia). In many patients with idiopathic recurrent rhabdomyolysis, specific inherited metabolic defects have not been recognized up to now.
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PMID:[Rhabdomyolysis and myoglobinuria]. 1279 89

A 45-year-old woman underwent radical neck clipping for cerebral aneurysm under isoflurane anesthesia. Her preoperative examination revealed elevated body temperature which had been normal on admission. Her body temperature increased up to 40.3 degrees C during anesthesia and surgery, and it showed a downward trend at the end of surgery. Malignant hyperthermia was excluded because the patient did not have metabolic acidosis, hypercarbia, hyperpotassemia or abnormal sweating anesthesia. The patient received intravenous dantrolene postoperatively since there was a suspicion of malignant hyperthermia on the basis of hyperthermia and increases in serum creatine kinase (CK) and myoglobin (Mb) levels. Her body temperature and serum CK and Mb levels decreased for a while after administration of dantrolene, but they increased again thereafter. The patient was aggressively cooled with a cooling blanket and hyperthermia and increases in serum CK and Mb levels disappeared in postoperative two weeks. She was discharged on foot without any neurological deficit on the forty-third hospital day. According to the diagnostic criteria for malignant hyperthermia by Larach and his colleague, malignant hyperthermia was somewhat less than likely in our case. The clinical course of the patient also suggested that a possibility of malignant hyperthermia was considerably low. The authors conclude that perioperative hyperthermia in our case must have derived from central hyperthermia following subarachnoid hemorrhage, and that postoperative increases in serum CK and Mb levels might have resulted from acceleration of sympathetic nervous system by subarachnoid hemorrhage.
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PMID:[Central hyperthermia suspected of malignant hyperthermia in a patient undergoing radical neck clipping for cerebral aneurysm]. 1571 69

The perioperative changes in the serum concentration of creatine phosphokinase (CPK) and its isoenzymes MM, MB, and BB and of lactic dehydrogenase (LDH) and its isoenzymes LDH1 to LDH5 were determined during craniotomy in order to distinguish operation-induced changes in these enzymes from those due to acute myocardial infarction and malignant hyperthermia. Twenty-eight male patients, 29 to 76 years of age (mean +/- SD = 58 +/- 13.2 years), undergoing craniotomy for tumor reseaction (n = 26) or cerebral artery aneurysm clipping (n = 2) were included in this study. Ten serial blood samples were obtained from each patient: one sample before and another after induction of anesthesia, and eight samples after the incision, over a period of 70 h. The preinduction serum CPK level of 97 +/- 32 U/L (mean +/- SD) increased gradually and significantly and reached the peak level of 542 +/- 116 U/L 34 h after incision (p <0.05). Whereas all of the CPK isoenzymes increased in terms of U/L after incision, only the MM fraction (expressed as percent of total CPK) increased, and the MB and BB fractions (expressed as percent of total CPK) decreased. The preinduction serum LDH level of 150 +/- 42 U/L (mean +/- SD) increased gradually after incision and reached the peak level of 210 +/- 32 U/L 58 h after incision (p <0.05). LDH2 as a percent of total LDH decreased significantly, but the LDH1/LDH2 ratio did not change. LDH4 and LDH5, as percents of total LDH, increased significantly. The large increases in total serum CPK and the concomitant decrease in MB percent after craniotomy may minimize and/or mask the percentage increase in the MB level following acute myocardial infarction. The perioperative serum CPK level as a marker in the diagnosis of malignant hyperthermia should be interpreted in light of the present results and in conjunction with clinical symptomatology.
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PMID:Changes in serum CPK, LDH, and their isoenzymes in the perioperative period in patients undergoing craniotomy. 1581 62

Progressive muscular dystrophy may produce abnormal reactions to several drugs. There is no consensus of opinion regarding the continuous infusion of propofol in patients with progressive muscular dystrophy. We successfully treated 2 patients with progressive muscular dystrophy who were anesthetized with a continuous infusion of propofol. In case 1, a 19-year-old, 59-kg man with Becker muscular dystrophy and mental retardation was scheduled for dental treatment under general anesthesia. General anesthesia was maintained by a continuous infusion of 6-10 mg/kg propofol per hour and an inhalational mixture of 67% nitrous oxide and 33% oxygen. No complications were observed during or after the operation. In case 2, a 5-year-old, 11-kg boy with Fukuyama type congenital muscular dystrophy and slight mental retardation was scheduled for dental treatment under general anesthesia. General anesthesia was maintained with a continuous infusion of 6-12 mg/kg propofol per hour and an inhalational mixture of 0.5-1.5% sevoflurane in 67% nitrous oxide and 33% oxygen. No complications were observed during or after the operation. It is speculated that a continuous infusion of propofol in progressive muscular dystrophy does not cause malignant hyperthermia because serum levels of creatine phosphokinase and myoglobin decreased after our anesthetic management. Furthermore, our observations suggest that sevoflurane may have some advantages in patients with progressive type muscular dystrophies other than Duchenne muscular dystrophy and Becker muscular dystrophy. In conclusion, our cases suggest that a continuous infusion of propofol for the patients with progressive muscular dystrophy is a safe component of our anesthetic strategy.
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PMID:Continuous infusion propofol general anesthesia for dental treatment in patients with progressive muscular dystrophy. 1585 43

Rhabdomyolysis is a common and potentially lethal clinical syndrome that results from acute muscle fiber necrosis with leakage of muscle constituents into blood. Myoglobinuria is the most significant consequence, leading to acute renal failure (ARF) in 15%-33% of patients with rhabdomyolysis. Rhabdomyolysis occurs from inherited diseases, toxins, muscle compression or overexertion, or inflammatory processes, among other disorders. In some cases, no cause is found. We describe 475 patients from the Johns Hopkins Hospital inpatient records between January 1993 and December 2001 for the following discharge diagnosis codes: myoglobinuria, rhabdomyolysis, myopathy, toxic myopathy, malignant hyperthermia, neuroleptic malignant syndrome, and polymyositis. Of 1362 patients, 475 patients with an acute neuromuscular illness with serum creatine kinase (CK) more than 5 times the upper limit of normal (>975 IU/L) were included. Patients with recent myocardial infarction or stroke were excluded. The etiology was assigned by chart review. For all, the highest values of serum CK, serum creatinine and urine myoglobin, hemoglobin, and red blood cells were recorded. Forty-one patients had muscle biopsy within at least 2 months from the onset of rhabdomyolysis.Of the 475 patients, 151 were female and 324 were male (median age, 47 yr; range, 4-95 yr). Exogenous toxins were the most common cause of rhabdomyolysis, with illicit drugs, alcohol, and prescribed drugs responsible for 46%. Among the medical drugs, antipsychotics, statins, zidovudine, colchicine, selective serotonin reuptake inhibitors, and lithium were the most frequently involved. In 60% of all cases, multiple factors were present. In 11% of all cases, rhabdomyolysis was recurrent. Underlying myopathy or muscle metabolic defects were responsible for 10% of cases, in which there was a high percentage of recurrence, only 1 etiologic factor, and a low incidence of ARF. In 7%, no cause was found. ARF was present in 218 (46%) patients, and 16 died (3.4%). A linear correlation was found between CK and creatinine and between multiple factors and ARF, but there was no correlation between ARF and death or between multiple factors and death. Urine myoglobin detected by dipstick/ultrafiltration was positive in only 19%. Toxins are the most frequent cause of rhabdomyolysis, but in most cases more than 1 etiologic factor was present. Patients using illicit drugs or on prescribed polytherapy are at risk for rhabdomyolysis. The absence of urine myoglobin, by qualitative assay, does not exclude rhabdomyolysis. With appropriate care, death is rare.
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PMID:Rhabdomyolysis: an evaluation of 475 hospitalized patients. 1626 12

A 61-year-old man showed clinical findings which suggest atypical malignant hyperthermia after pancreatoduodenectomy. He showed no abnormal findings in preoperative examinations. General anesthesia was induced with thiopental, fentanyl, and vecuronium, and epidural anesthesia was also used for the perioperative management. The surgery went on uneventfully and the patient returned to the ward. The laboratory data after the surgery showed extremely high creatine kinase and myoglobin. The patient's body temperature rose up and showed rigidity. We suspected atypical malignant hyperthermia and began its treatment. Four months later, we performed muscle biopsy and Ca-induced Ca release (CICR) test, which presented a typical rising pattern. This is the first case of malignant hyperthermia which occurred after the surgery and accompanied by a typical rise in CICR.
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PMID:[A case of atypical malignant hyperthermia which presented a typical rise in Ca-induced Ca release after the operation]. 1719 Mar 24

A 70-year-old man with lung cancer was scheduled for partial resection of the right lung. Preoperative serum creatine kinase was elevated (1808 IU x l(-1), CK-MM 97%). Acute coronary syndrome was denied by the absence of significant stenosis of coronary artery and the normal segmental wall motion in echocardiography. The other examinations did not reveal the cause of CK elevation. He did not receive dantlorene preoperatively, but the surgical procedure was performed uneventfully without the use of the triggering agents, such as volatile inhalational anesthetic gases and suxamethonium. Thoracic wall was not invaded by the tumor. After the operation, CK went down quickly. It decreased further after the postoperative chemotherapy. We concluded that CK elevation might have been produced by adenocarcinoma itself, judging from the rapid decrease after surgery and the absence of thoracic wall invasion. Though CK elevation may indicate the malignant hyperthermia, we should not delay the surgery too long when there is possibility of CK elevation derived from cancer itself.
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PMID:[How should we manage patients with elevated preoperative creatine kinase? --A case of CK productive lung cancer]. 1757 18


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