Suxamethonium-induced jaw stiffness and myalgia associated with atypical cholinesterase: case report.

An 11-year-old boy was given halothane, nitrous oxide and oxygen, pancuronium 0.4 mg and suxamethonium 100 mg for induction of anaesthesia. In response to this a marked jaw stiffness occurred which lasted for two minutes and the anaesthesia were terminated. Four hours of apnoea ensued and he suffered generalized severe myalgia lasting for one week. He was found to have atypical plasma cholinesterase with a dibucaine number of 12, indicating homozygocity. This was verified by study of the family. The case shows that prolonged jaw rigidity and myalgia may occur after suxamethonium in patients with atypical cholinesterase despite pretreatment with pancuronium.

Artery-to-muscle onset time for neuromuscular blocking drugs.

Artery-to-muscle (A-M) onset time for five neuromuscular blocking agents was studied in 50 female patients under light endotracheal anaesthesia. Circulation to the right arm was occluded by a tourniquet and released 1 min after the injection i.v. into the left arm of a myoneural blocking drug. Muscle twitches were recorded in the right hand after stimulation of the ulnar nerve (1 Hz). After releasing the tourniquet the response to single twitches continued without decrease in height (latent onset time). The onset of gradual decreases in twitch height was noted, and the time until 90% depression of twitch height was measured (manifest onset time). The mean latent onset times were: pancuronium 31.9 s, tubocuraine 21 s, alcuronium 17.2 s, fazadinium 8.6 s and suxamethonium 4.8 s. Mean A-M latent onset time was significantly different for each drug (P less than 0.005). Manifest A-M onset times were related to A-M latent onset time except for tubocurarine which exhibited a slower decline in twitch height. A-M latent onset time correlated well with the values for intravenous onset times reported in the literature.

Plasma viscosity and cremophor-containing anaesthetics.

The cremophor-containing anaesthetic agents, Althesin, propanidid and diazepam, were added to plasma in vitro and administered to patients. In vitro these anaesthetics, and cremophor alone in concentrations equal to those obtained in vivo, decreased the viscosity of plasma 45% at shear rate 11.5 s-1. In 11 patients given cremophor-containing anaesthetics to induce anaesthesia, plasma samples obtained 5 min after injection showed a mean decrease in viscosity of 42% compared with the pre-induction values. The effect on viscosity after a single dose disappeared in 50 min. Triton x-100 added to plasma caused a decrease in viscosity similar to that of cremophor. The interaction in vitro of cremophor and Triton x-100 with concentrated urea was found to be identical both in plasma and dextran. This suggests that cremophor acts by increasing the sheet of structured water around the protein molecules, thereby preventing the aggregation of proteins.

Dermatomyositis, suxamethonium action and atypical plasmacholinesterase.

A 19-year-old girl suffering from active dermatomyositis was given suxamethonium 60 mg during anaesthesia for termination of pregnancy. A prolonged suxamethonium action occurred which was explained by the finding of homozygous atypical plasmacholinesterase in her blood. Although no fasciculations were seen immediately after injection of the drug, a period of fasciculations progressing from the extremities to the head and trunk occurred during recovery of muscle tone. No hyperpyrexia or elevation of serum creatine phosphokinase occurred. This was ascribed to the steroid therapy she received. Plasma from four other patients suffering from dermatomyositis was also investigated and one young woman, also pregnant, was found to be heterozygous for the atypical enzyme.

Ten cases of malignant hyperthermia in Norway.

Data are presented on ten cases of anaesthesia-induced malignant hyperthermia in Norway. Seven of the patients died, three recovered. The fatal cases were all boys in the age group 11-20 years. This age and sex distribution suggests that puberty with the increase in androgens is a precipitating factor in malignant hyperthermia. One of the victims who survived was a 4 1/2-year-old pseudohermaphrodite girl with the adrenogenital syndrome. The coincidence of malignant hyperthermia in a patient with such a rare syndrome points to the excessive formation of androgens in patients with this syndrome as a predisposing factor. The indications for surgery were traumatic injuries in five cases, congenital abnormalities in three and appendicitis in two cases. These conditions in themselves may cause an increased sensitivity to suxamethonium. One patient received only hexobarbitone, halothane and suxamethonium. After the last drug jaw rigidity and temperature rise to 41.3 degrees C prompted the anaesthetist to end the anaesthetic. The fact that the patient survived proves that suxamethonium induced jaw rigidity is valuable as a warning. The absence of cardiovascular depression after procaine 3.5 g in one patient is ascribed to the correction of acidosis at the time of infusion of this drug. It is suggested that procaine should be withheld until other measures such as cooling, correction of acidosis and steroid therapy have been tried.

Suxamethonium apnoea terminated with commercial serumcholinesterase.

A case of prolonged suxamethonium apnoea successfully terminated by the infusion of a commercial preparation of serumcholinesterase is reported. The patient appeared to be homozygous for the dibucaine resistant gene, having only 15% of normal activity in his serum. His dibucaine number was 21, and the Michaelis constant was 5.5 times that of normal sera. One and a half hours after receiving 110 mg suxamethonium for oesophagoscopy, the patient was still apnoeic with no response to ulnar nerve stimulation. Intravenous administration of 90 mg commercial serumcholinesterase, the equivalent to 1000 ml fresh human plasma, restored twitch and tetanic responses and the patient could lift his head 15 min after the beginning of the enzyme injection. The serumcholinesterase activity of the patient's serum increased by 55% (from 15% to 70%) following the injection. This rise was halved over the next 8 days.

The inhibition of cholinesterases by pancuronium.

Pancuronium causes a powerful and highly selective inhibition of human serum cholinesterase in vitro. The inhibition was studied in serum from 14 individuals of both sexes (5-60 years of age) with normal reactions to suxamethonium. Pancuronium, in a concentration of 2.3 x 10(-7) M, caused a 50% inhibition of the enzymatic hydrolysis of acetylcholine, when this substrate was present in a concentration of 10 x 10(-3) M. The same I50 value was also found for a commercial preparation of human serum cholinesterase. The inhibition was reversible and competitive in type. Pancuronium inhibition of the acetylcholinesterase in human red blood cells and from the electric eel was more than one thousand times weaker. Thus pancuronium is one of the most selective inhibitors of serum cholinesterase described so far. The in vivo activity of the serum cholinesterase in four patients receiving pancuronium 0.1 mg/kg decreased, during the first 3 min, by 60-80%, from the pre-induction value. After this a slow recovery occurred with 40% depression remaining at 45 min after the injection. The tachycardia produced by pancuronium may be related to this selective inhibition of serum cholinesterase. It is suggested that relaxants which selectively inhibit serum cholinesterase also selectively block the cardiac muscarinic receptors.

Ketamine-pancuronium induction in patients with aortic stenosis.

In 15 patients with severe aortic stenosis who were to undergo aortic valve replacement, the induction sequence ketamine followed by pancuronium caused a 25% rise in systolic blood pressure. In a similar series, the induction sequence diazepam + morphine followed by pancuronium caused a 22% fall in systolic blood pressure. This shows that the blood pressure rise caused by ketamine is not blocked by pancuronium, although pancuronium may possibly modify the cardiovascular responses to this drug.

Brain damage following collapse of a polyvinyl tube: elasticity and permeability of the cuff.

A 13-year-old boy undergoing tympanoplasty lasting 3 1/2 hours developed serious airway obstruction at the end of surgery leading to permanent brain damage. It appeared that the no. 7 Portex "blue line" endotracheal tube had collapsed under the cuff. This was concluded because deflation of the cuff had promptly relieved the obstruction of the airway. Further support for this conclusion was the finding that shortly after extubation the inflation of 8 ml air caused the tube to collapse. Collapse of these tubes cannot normally be produced unless they have been made to collapse shortly before. Investigation of such tubes in vitro at 37 degrees C showed that overinflation of the cuff caused a symmetrical collapse of the tube wall along the x-ray opaque blue line. The collapse occurred with cuff pressures varying from 310 mmHg up to 460 mmHg for tubes from different batches. During anaesthesia with 66% nitrous oxide, this gas together with carbon dioxide were found to diffuse into the cuff at steady rates of 3.69 vol % and 0.36 vol % per hour, respectively. Corresponding increases in intracuff volumes were found. It is advised that disposable tubes should be carefully inspected before use and that endotracheal cuffs should be deflated periodically during anaesthesia to avoid excessive rise in cuff pressure.