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

We encountered a case of malignant hyperthermia caused by intravenous lidocaine which had been administered as treatment for a ventricular arrhythmia. The patient, a 72-year-old male, was admitted with chronic renal failure and aortic valvular stenosis. His chronic renal failure progressed, and congestive heart failure developed, and ventricular arrhythmias occurred frequently. For the treatment of these arrhythmias, lidocaine was injected and continuous infusion was started. Despite initial improvement in symptoms and laboratory data following hemofiltration, refractory ventricular tachycardia occurred. The patient was treated with large doses of lidocaine. His body temperature rose to a maximum of 41.7 degrees C, and generalized muscular twitching was observed before he lost consciousness. Serum and urinary myoglobin levels became elevated. This abnormally high fever was relieved only by dantrolene sodium. After we made a diagnosis of malignant hyperthermia and stopped the lidocaine infusion, the high fever resolved quickly. It is important to note that malignant hyperthermia can be caused by lidocaine and amide-linked local anesthetics.
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PMID:Malignant hyperthermia caused by intravenous lidocaine for ventricular arrhythmia. 147 68

We studied the effects of succinylcholine (SCC) on serum levels of myoglobin (Mb) and CK in children under halothane or enflurane anesthesia. Forty-five children, aged 2 years 11 months to 12 years 6 months were subjected to this study. They were divided into four groups; the two groups were injected with SCC 1 mg.kg-1 intravenously to facilitate tracheal intubation and maintained with halothane (Group SH) or with enflurane (Group SE). The other two groups were intubated without the aid of SCC and maintained with halothane (Group H), or with enflurane (Group E). Mb was analyzed by an antibody radioimmunoassay technique and CK was analyzed by a modified Rosalki's method. While Mb increased in all four groups, the increase was pronounced in the SCC groups (60 min value of Group SH 2192 +/- 639 ng.ml-1, Group SE 1722 +/- 436 ng.ml-1, mean +/- SE), and the increase was significantly smaller in SCC free groups (Group H 40 +/- 12 ng.ml-1, Group E 43 +/- 9 ng.ml-1). The CK value increased only in the SCC groups to 174.1 +/- 32.8 IU.l-1 in Group SH, and to 193.6 +/- 35.7 IU.l-1 in Group SE at 60 min, respectively. These results indicate that increases in Mb and CK values were mainly induced by SCC injection and that SCC might play some roles in development of malignant hyperthermia.
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PMID:[Effects of succinylcholine on serum levels of myoglobin and CK in children under halothane or enflurane anesthesia]. 224 8

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

Malignant hyperthermia (MH) is a pharmacogenetic disease in man and animals. It primarily involves skeletal muscle tissue, but other tissues might be affected to a lesser degree. Calcium homeostasis in muscle cells is upset in susceptible individuals, so that various agents and circumstances can increase the free, ionised intracellular calcium concentration to damaging levels. The primary defect is not known at present, but is believed to involve an abnormally sensitive calcium-induced calcium release mechanism. Thus small, localised increases in calcium concentration releases more calcium so that a vicious cycle is triggered. The increased calcium concentration causes multiple effects in the muscles by stimulating contraction and a hypermetabolic state, clinically observed as rigidity and fever. If demands on the homeostatic mechanisms to lower the calcium concentration become exhausted, and metabolism is insufficient to supply enough phosphocreatine and ATP, membrane potentials cannot be maintained, and permeability of the cell membranes increase. This causes loss of phosphate and H+ as well as K+ and Mg++, and later myoglobin and creatine kinase. Thereby oxidative metabolism is further impeded with formation of lactate as a result. The ensuing acidosis stimulates sympathetic innervation, resulting in tachycardia, high blood pressure, and vasoconstriction. Hyperkalemia causes arrhythmia. Dantrolene inhibits the release of calcium and can halt the process if given before depletion of the energy rich phosphates is too advanced.
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PMID:Pathophysiology of malignant hyperthermia. 269 55

A 33 year old woman, with myotonia atrophica and a known susceptibility to malignant hyperthermia, presented during her second pregnancy with multiple episodes of hyperthermia. They were associated with a rapid rise in the serum creatine phosphokinase (CPK) level, and not with infection or a myotonic crisis. Because of the obstetric conditions, caesarean section was planned. Preoperative oral dantrolene was used as prophylaxis. Six days after the start of this treatment, CPK and serum myoglobin levels were back within the normal range. There were no side-effects for the mother nor for the foetus. There were no further increases in either CPK or serum myoglobin levels during surgery or afterwards, but the rectal temperature remained markedly raised for 48 h after the delivery. Oral dantrolene was given during the first nine postoperative days. The occurrence of episodes of high fever during pregnancy linked to MHS and myotonia atrophica is discussed, as well as the anaesthetic management of such a patient. Side-effects of dantrolene for the mother or the foetus are also considered, especially as foetal levels of this drug would seem not to reach therapeutic levels. It would appear interesting to measure maternal dantrolene blood levels, especially if high doses are administered, to avoid reaching therapeutic levels in the foetus.
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PMID:[Oral dantrolene in a parturient with myotonic dystrophy and susceptibility to malignant hyperthermia]. 320 29

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

A report is made of a 44-year-old female who died of malignant hyperthermia during general anesthesia for an operation of left subtrochanteric femoral fracture. Symptoms began with increases in heart rate and blood pressure after the introduction of anesthesia with halothane and were accelerated by the administration of succinylcholine, followed by muscle rigidity and high temperature. The typical wine red urine was observed. The oral temperature of 42 degrees C was recorded within 1 h after succinylcholine. The rectal temperature was 30 degrees C 22 h after death. Severe pulmonary edema and tubular necrosis of the kidney were found by postmortem examination. No latent myopathy was observed. The creatine phosphokinase levels in plasma obtained after the onset of malignant hyperthermia and at the time of autopsy were abnormally high and were 5632 and 34,854 mU/ml, respectively. Plasma myoglobin levels were 130,000 and 2.8 X 10(6) ng/ml, respectively.
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PMID:An autopsy case of malignant hyperthermia. 398 93

A 51-year-old male patient with no history of musculo-skeletal or myopathic abnormalities, but suffering from manic-depressive psychosis, attempted suicide with an overdose of dolpersin hydrochloride (Mydocalm), dipenzepine hydrochloride (Noveril), meprobamate (Mepronox) and nitrazepam (Mogadon). He developed high fever, muscle rigidity, tachycardia, arrhythmias, hypotension and mottled cyanosis, symptoms well-known in persons with malignant hyperthermia, an autosomally inherited disease of skeletal muscle. There is also discussed the manifestation and the symptoms of an acute rhabdomyolysis. The diagnosis was confirmed by chemical pathological laboratory findings, including respiratory and metabolic acidosis, myoglobinaemia accompanied by myoglobin diuresis, and elevated creatine phosphokinase (CPK values up to 2790 U/l). Electron microscopic examination of muscle tissue revealed signs of myolysis and mitochondrial reactions with pleoconic hyperplasia. No inhalation anaesthetics or skeletal muscle relaxants, such as succinyl choline, were used in this case. Therefore, malignant hyperthermia might have been induced by a combination of drugs which were not known to induce this abnormal muscular reaction. However, the muscle relaxant effect of dolpersin hydrochloride may have acted as a possible inducer of the attack.
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PMID:[Possible malignant hyperthermia as reaction to an overdose of myotonolytic, antidepressive and sedative drugs (author's transl)]. 611 87

Administration of succinylcholine to normal individuals results in alterations in muscle membrane integrity expressed as a slight increase in the concentrations of creatine phosphokinase (CK) in serum and appearance of small amounts of myoglobin in the urine, but without clinical symptoms. Subjects with strabismus due to congenital muscular dystrophy may develop more significant rhabdomyolysis expressed as muscle stiffness and weakness, massive myoglobinuria, marked elevation of serum CK and other enzymes, metabolic acidosis, tachycardia and moderate elevation of body temperature. In some cases grave malignant hyperthermia with significant hypoxia, metabolic acidosis, tachycardia and marked abnormalities in serum electrolyte concentrations may cause irreversible damage to the central nervous system and other vital organs and death. A case of difficult anaesthesia for a six year old boy belonging to family affected with muscular dystrophy is presented. More attention must be given to preoperative examination (anamnesis, serum enzymes) or ophthalmological patients and more careful monitoring during anaesthesia and in the early postoperative period must be instituted to prevent and treat complications induced by succinylcholine and volatile anaesthetic agents.
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PMID:Strabismus as a possible sign of subclinical muscular dystrophy predisposing to rhabdomyolysis and myoglobinuria: a study of an affected family. 710 7

A report is made of a 65-year-old male who died of a malignant hyperthermia of 42 degrees C. Symptoms included muscle rigidity at the termination of operation for neck-clipping of an aneurysm of the anterior communicating artery. Latent myopathy was observed in skeletal muscle, and a bleeding focus was present in the left anterior region of the hypothalamus, coinciding with the temperature regulation center. The mechanism of onset of this disease is still poorly understood, but it seems that this disease occurred due to synergic effects of the hypothalamic hemorrhage and the pre-existing myopathy. The serum CPK level at the time of death was abnormally high (250 U), and 3.4% of isozyme CPK1 was detected. The serum myoglobin was 204, 850 ng/ml, a markedly high level, and myoglobinuric nephrosis was present as a result.
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PMID:Malignant hyperthermia. 711 2


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