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)

Two patients in a family of exertion-induced heat stroke were reported. Case 1: A 23-year-old male, paternal cousin of case 2, was admitted to our hospital because of loss of consciousness during running under a burning sun. On physical and neurological examinations, he was deeply comatose with high fever, tachycardia, and increased deep tendon reflexes. Laboratory findings disclosed rhabdomyolysis, acute renal failure, disseminated intravascular coagulation, liver injury, and brain edema. He recovered after intensive cooling, some antibiotics, glycerol and sodium dantrolene administration. Case 2: A 19-year-old male experienced loss of consciousness and high fever during playing soccer at 15 years of age, and was admitted to a hospital. On admission, he had high fever of 38.7 degrees C, and increased serum CK level. He recovered two weeks after admission. He was readmitted to our hospital to evaluate the predisposition for malignant hyperthermia. His physical and neurological examinations showed no abnormalities. Routine laboratory findings were within normal limits. Muscle biopsy findings of cases 1 and 2 were mildly increased number of fibers with centrally placed nuclei. Caffeine test on skinned muscle fibers from the biopsies showed normal response in both type 1 and 2 fibers. The present patients were diagnosed as having exertion-induced heat stroke, but with no increased muscle fiber sensitivity to caffeine, suggesting that the pathomechanism differs from that of malignant hyperthermia induced by malfunction of sarcoplasmic reticulum.
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PMID:[Two familial cases with exertion-induced heat stroke--relationship to malignant hyperthermia]. 139 27

A middle aged man developed very high fever, status epilepticus, and terminal acute renal failure with myoglobinuria after surgery. A post mortem examination showed widespread muscle necrosis with hypercontraction bands. Muscle enzyme studies and electron microscopic examination disclosed central core disease, a condition closely related to malignant hyperpyrexia. This condition is a genetically inherited disorder which can be triggered by certain volatile anaesthetic agents or Suxamethonium. In this patient the condition may have been triggered by either the Isoflurane or the postoperative status epilepticus.
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PMID:Malignant hyperpyrexia: a rare cause of postoperative death. 157 80

A patient for fixation of ankle arthrodesis diagnosed as having malignant hyperthermia trait preoperatively is reported. A 17 year old man was anesthetized with enflurane for orthopedic surgery of the knee joint. At that time malignant hyperthermia developed. He was critically ill, but resuscitated and recovered from acute renal failure on 7th day after operation. Ca2+ release test was performed. Ca2+ releasing speed was prominently accelerated in this patient. We could identify him as having malignant hyperthermia trait. Epidural anesthesia with procaine chloride was given cautiously. No drug which may induce malignant hyperthermia was used. Nevertheless, malignant hyperthermia occurred. This disease has various forms of presentation. The mechanism is equivocal, and in some cases, it is difficult to judge it immediately. This patient was managed without complication. We consider that tourniquet and stress provoked signs of malignant hyperthermia in this patient.
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PMID:[The anesthetic management of a patient with the malignant hyperthermia trait diagnosed preoperatively]. 187 46

Striated musculature is considered unusually tolerant to all kinds of injuries, and rhabdomyolysis associated with drug overdose or chronic drug intake is a rare event. This may be because striated musculature, in contrast to other tissues such as liver and kidney, shows little affinity for most drugs. Several different types of drug-induced rhabdomyolysis may be distinguished, and the clinical features of the condition may vary widely, from moderate myalgia to involvement of groups of muscles to involvement of the total skeletal musculature. In clinically asymptomatic rhabdomyolysis, early diagnosis is only made if routine laboratory tests include determination of serum creatine kinase. Determination of myoglobin in serum and urine is more sensitive and allows earlier diagnosis of muscle necrosis. Myoglobinaemia may lead to toxin-induced tubular necrosis, and impairment of renal function or even acute renal failure. About 10% of all cases of acute renal failure are due to rhabdomyolysis. Fulminant rhabdomyolysis may be associated with excessive hyperkalaemia and hypocalcaemia which may induce further life-threatening complications. Therefore, early diagnosis of rhabdomyolysis is most important for prevention of its potentially life-threatening sequelae. Therapy of rhabdomyolysis consists of supportive and specific measures. Early diagnosis may help to prevent life-threatening sequelae like acute renal failure, electrolyte imbalance and shock. Withdrawal of the incriminated drug or detoxification in drug overdose should be followed by supportive measures including infusion therapy and correction of dehydration and electrolyte imbalances. Forced diuresis with sodium bicarbonate may protect the kidney function from acidosis and precipitation of myoglobin in tubules. Elimination of myoglobin from plasma may be enhanced by plasmapheresis. In patients with acute renal failure, haemodialysis is necessary. In malignant hyperthermia, immediate infusion of dantrolene sodium is required. This drug also seems to have a beneficial effect in neuroleptic malignant syndrome. The repair mechanisms of striated musculature function extremely well. The prognosis of muscular atrophy after the acute stage of rhabdomyolysis is excellent. The same is true for the prognosis of acute renal failure. However, the extent of complications or survival of the acute stage of rhabdomyolysis strongly depend on early diagnosis and start of adequate therapy.
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PMID:Clinical features, pathogenesis and management of drug-induced rhabdomyolysis. 265 42

Alterations in the calcium metabolism are a characteristic paraclinical finding in patients with oliguric acute renal failure associated with rhabdomyolysis. A 20-year-old male operated on under general anesthesia developed non-oliguric acute renal failure due to malignant hyperthermia with rhabdomyolysis (urine myoglobin greater than 20,000 nmol/l; reference range less than 0.85 nmol/l). On the 20th postoperative day hypercalcemia was found, reaching a maximum serum level of 3.74 mmol/l (reference range 2.18-2.65 mmol/l) on the 27th postoperative day. Delayed hypercalcemia in non-oliguric acute renal failure associated with rhabdomyolysis has not been reported previously. This case suggests that prolonged control of the serum calcium level should be performed in patients with rhabdomyolysis, even in the absence of oliguria.
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PMID:Delayed hypercalcemia after non-oliguric acute renal failure associated with rhabdomyolysis. 341 9

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

A case of a severe heat stroke is reported in a 30 yr old white man while running a long-distance race. At the time of admission, moderate hyperthermia (40 degrees C) and coma were two major symptoms found at physical examination. Within 24 h, the clinical picture evolved to multiple organ failure with marked rhabdomyolysis, acute renal failure with hyperkalaemia and lactic acidosis. At this time, were also found a consumptive coagulopathy and acute hepatic failure. After numerous complications, most of them infectious, the patient was discharged after four months in ICU and admitted in a physical rehabilitation department. Muscle biopsy performed three years after the heat stroke showed an abnormal reactivity to caffeine, but a normal reaction to halothane. The relationship between malignant hyperthermia and heat stroke remains uncertain.
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PMID:[A severe form of heat stroke in a long-distance runner]. 377 73

A variety of drugs used in clinical practice may cause myopathy or interfere with neuromuscular transmission. The precise incidence of such disorders is not known, but it is almost certainly higher than is generally suspected. An important aspect of drug-induced muscular disorders is their reversibility if the offending agent is withdrawn, whereas failure to do so may lead to unnecessary morbidity. The study of drug effects on muscle provides a means of investigating the pathological reactions of muscle, and of producing experimental models of naturally occurring myopathies. Drug-induced myopathies may result from a direct toxic effect, which may be local when the drug is injected into a muscle or more diffuse when the drug is taken systemically, or may be secondary to electrolyte disturbances, muscle compression, ischaemia, neural activation or to the development of an immunological reaction directed against muscle. Repeated injections of antibiotics or drugs of addiction may lead to severe muscle fibrosis and contractures. A variety of drugs may cause an acute or subacute painful necrotising myopathy which may be associated with myoglobinuria, at times leading to acute renal failure. Clofibrate and epsilon aminocaproic acid are the drugs most frequently implicated, but a similar syndrome may occur in alcoholics and heroin addicts. Certain hypocholesterolaemic agents may induce myotonia by altering the sterol composition of the muscle cell membrane, while certain drugs including beta-adrenergic blockers and agonists, succinylcholine and diuretics may exacerbate or unmask pre-existing myotonia. In the syndrome of malignant hyperpyrexia, halothane, succinylcholine and various other agents may induce a potentially fatal state of muscular rigidity and hypermetabolism in susceptible individuals as a result of a defect in the calcium transport function of the sarcoplasmic reticulum and possibly of other cellular membranes. In corticosteroid myopathy, which is the most common form of drug-induced myopathy, there is selective atrophy of type 2 muscle fibres and the primary metabolic effect is an inhibition of RNA and protein synthesis, although protein degradation is also increased. Chloroquine and a number of related drugs with amphiphilic cationic properties may induce lysosomal storage myopathy, which may be associated with cardiomyopathy and with a more widespread form of lipidosis.
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PMID:Adverse effects of drugs on muscle. 612 17

Seven episodes of rhabdomyolysis with acute renal failure (ARF) have been observed in 6 patients treated with various short-acting tranquilizers and antidepressants. Clinical features usually included severe hyperthermia, diffuse hypertonicity with or without coma, circulatory failure or unstable blood pressure, and often acute respiratory failure. Serum CPK were always elevated. The type of ARF was prerenal failure without oliguria in 5/7 episodes, and acute tubular necrosis in 2/7 episodes, requiring hemodialyses in one patient. Three patients died. In any case, the tranquilizers and antidepressants responsible for this syndrome were stopped, and electrolyte disorders and acidosis were corrected. Associated acute circulatory failure, septicemia and/or acute hepatic failure required prompt therapy, and artificial ventilation was required in 4 instances. The further use of phenothiazines, butyrophenones, sulpiride and their derivatives should be avoided in any patient having developed such an accident, whose pathophysiology is similar to that described in malignant hyperthermia of various origin.
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PMID:[Rhabdomyolysis with acute renal failure and malignant neuroleptic syndrome]. 613 93

We report three cases of fatal hyperthermia in the course of neuroleptic drug treatment. One patient developed his symptoms within hours after a single drug dose whereas the two others had a prolonged symptomatology which lasted for several days after the administration of different neuroleptic drugs. Biochemical events included diffuse intravascular coagulation, muscle cell necrosis and acute renal failure. Rhabdomyolysis was proved pathologically in two patients but brain lesions were atypical in all three cases. We conclude that the biochemical and pathological abnormalities seen in these patients are those which have been described by some authors in the malignant hyperthermia syndrome after anaesthesia. The symptomatology however can be insidious and the syndrome can develop after withdrawal of the drugs.
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PMID:Fatal complications of neuroleptic drugs. A clinico-pathological study of three cases. 614 81


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