THE JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA

Rates of Ca²⁺-induced Ca²⁺ release (CICR) using the skinned fiber method were measured in the muscle fibers biopsied from 75 clinically suspected malignant hyperthermia (MH) patients. Their results were highly correlated to clinical classification (fulminant or abortive). Only 40% of clinically suspected MH (87% of fulminant and 18% of abortive MH) showed accelerated CICR, while others were normal in Ca²⁺ release rates. This suggests that some of the MH cases might be caused by a different mechanism other than the mechanism responded to the accelerated rate of CICR. This gives rise to the further discussion related to the dantrolene efficacy on the MH treatment since dantrolene works specifically on the CICR channel.

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Myocardial ischemia is known as one of the major causes of the serious complication of low-output syndrome during open heart surgery.
Injury associated with ischemia and reperfusion has been attributed in part to the action of neutrophils, interaction of neutrophils with vascular endothelial cells, and cytokines which are mediators to induce and modify reactions between these substances. We investigated cell injury in relation to interleukins 6 and 8 (IL-6 and IL-8), which have recently received much attention as neutrophil activators, by following changes in these factors in patients during open-heart surgery with cardiopulmonary bypass (CPB). Eleven adult patients who underwent open-heart surgery with cardiopulmonary bypass were studied. They were anesthetized with fentanyl at a high dose (100μg/kg-1) plus oxygen inhalation.
The results showed 1) increased CK, CK-MB, neutrophils and granulocyte elastase (GEL) from one hour after reperfusion; 2) increased production of IL-6 and IL-8 one hour after reperfusion; and 3) positive correlation between GEL and the production of IL-8. These results suggest that neutrophils are activated by the production of IL-8, and then cells are injured.

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A healthy 12 year-old male underwent excision of an extensive facial hemangioma under enflurane anesthesia.
Pulmonary edema developed 20 to 30 minutes after the operative field had been inofiltrated with 30ml of adrenaline in saline (1:100, 000). Treatment with PEEP, inotropics and vasodilators quickly resolved the pulmonary symptoms. The trachea was extubated the next day. A combination of epinephrine infiltration and inadequate management of respiratory and metabolic acidosis was thought to have caused the pulmonary edema.

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We administered total intravenous anesthesia with droperidol, fentanyl and ketamine uneventfully for a patient with Becker's muscular dystrophy who had developed rhabdomyolysis after previous enflurane anesthesia.
This patient was a 12-year-old male weighing 44.6kg. A diagnosis of Becker's muscular dystrophy was made when he was 6 years old. At the age of 11, he experienced his first operation for a repair of hypospedias under enflurane-nitrous oxide anesthesia. He developed rhabdomyolysis postoperatively, as substantiated by a marked increase of CPK to 137, 000 unit/e 1, and received diuretic therapy in ICU for 3 days. The second operation was performed when he was 12 under total intravenous anesthesia with droperidol, fentanyl and ketamine without any complication. Neither CPK increase nor myoglobinuria was observed at any time after this anesthesia.
Many reports in the literature suggest that some patients with progressive muscular dystrophy may develop malignant hyperpyrexia and malignant hyperpyrexia-like reactions in response to inhaled anesthetics or suxamethonium, but there has been no previous report about such an adverse reaction to intravenous anesthetics. Because we experienced only one patient with progressive muscular dystrophy, we consider this anesthetic method with intravenous agents to be a good choice for patients with neuromuscular disease.

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