Fulminating hyperthermia and general anaesthesia.

Hawthorne, A. T.; Richardson, Margaret E.; Whitfield, G. T.

doi:10.1136/bmj.4.5633.750

Cited by 10 publications

(4 citation statements)

References 8 publications

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“…This case is not typical, however, as the serum potassium was only marginally raised, there was no overt myopathy or family history, no myoglobinaemia (tests for myoglobinuria were not performed) and the hyperpyrexia was moderate and responded to cooling. There was an unusual difficulty in rewarming, but Hawthorne, Richardson and Whitfield (1968) and Britt and Gordon (1969) reported cases in which hypothermia was noted before death. It would have been interesting to know the blood sugar level in this patient because presumably if the brain is deprived of substrate, glucose metabolism must stop and the temperature fall.…”

Section: Discussionmentioning

confidence: 99%

A Puzzling Case of Cardiac Arrest

Hannah¹

1971

British Journal of Anaesthesia

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A case of cardiac arrest during anaesthesia for appendicectomy is presented. The diagnosis was uncertain and seemed to lie between malignant, hypertonic hyperpyrexia and endotoxic shock, but the features were not typical of either syndrome. This case presented a problem in diagnosis, which was not resolved by postmortem examination. CASE REPORT A 33-year-old Malay soldier was admitted complaining of vague abdominal pain of 2-3 days' duration. He had had one previous admission 8 months previously for a similar pain, which resolved rapidly. Otherwise he had had no serious illnesses or operations and his family history was unremarkable. On examination he was a fit-looking man of normal physique, weighing 120 lb. His temperature was 37.2 °C and diffuse abdominal tenderness was noted. Chest Xray was normal. After observation for 2 days, appendicectomy was proposed. He was premedicated with papaveretum 20 mg and hyoscine 0.4 mg, li hours before induction. Anaesthesia was induced at 14.00 hours with thiopentone 400 mg and suxamethonium bromide (Brevidil) 20 mg. A cuffed, oral, endotracheal tube was passed. Anaesthesia was maintained with nitrous oxide, 33 per cent oxygen and 0.5 per cent halothane, ventilation being controlled using a Manley ventilator, at a tidal volume of 500 ml, and a minute volume of 10 L/min. Relaxation was provided by repeated doses of suxamethonium bromide to a total of 160 mg. As soon as anaesthesia was established, a mass was palpable in the right iliac fossa and the operation proved rather more difficult than had been anticipated, the appendix being inflamed, friable and adherent, and required considerable dissection. Accordingly an intravenous infusion of dextrose-saline was set up and a Ryle's tube passed. At no time was there any abnormal reaction to suxamethonium and the patients jaw and limbs remained relaxed during these manoeuvres. The patient was noted to be hot and the question of postoperative antibiotics was discussed. His pre-operative temperature had been 37.1 *C and he had not previously received any antibiotics. The theatre was airconditioned. Pulse and blood pressure remained satisfactory. At 15.45 the last dose of suxamethonium bromide was given and anaesthesia was thereafter maintained with nitrous oxide, oxygen and 0.5 per cent halothane while the abdomen was closed. At 16.00 hours, after suture of the peritoneum, the pulse suddenly became irregular and rigidity of the limbs was noticed. At 16.05, in spite of pulmonary ventilation with 100 per cent oxygen, the pulse ceased and external cardiac massage

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Section: Discussionmentioning

confidence: 99%

A Puzzling Case of Cardiac Arrest

Hannah¹

1971

British Journal of Anaesthesia

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“…They occur particularly in children and young persons and are often fatal. In most of these unfortunate incidents the anaesthetics used were volatile fluorinated hydrocarbon agents, halothane or methoxyfluorane, but they have also occurred with other anaesthetics (Brown, 1954;Saidman, Havard & Eger, 1964;Cullen, 1966;Davies & Graves, 1966;Hogg & Renwick, 1966;Lavoie, 1966;Relton, Creighton, Johnston, Pelton & Conn, 1966;Thut & Davenport, 1966;Purkis, Horrelt, de Young, Fleming & Langley, 1967;Stephen, 1967;Wilson, Dent, Tralber, McCoy & Allen, 1967;Hawthorne, Richardson & Whitfield, 1968). Recently, lethal pyrexias have also been described in about 17% of pigs anaesthetized with halothane (Harrison, Biebuyck, Terblanche, Dent, Hickman & Saunders, 1968).…”

Section: Discussionmentioning

confidence: 99%

Effects of monoamine oxidase inhibitors on the hypothermia produced in cats by halothane

Summers

1969

British J Pharmacology

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1. In cats, the effects of intraperitoneal injections of four monoamine oxidase (MAO) inhibitors, tranylcypromine, pheniprazine, pargyline, and nialamide, were examined on rectal temiperature and on the hypothermia during anaesthesia produced by a 2 hr period of halothane inhalation. 2. A 2 hr period of halothane inhalation produced a steady fall in temperature amounting to between 20 and 3.50 C. After discontinuation of halothane inhalation, temperature quickly returned to the pre-anaesthetic level but no pyrexia developed. A peculiar stiffness of the leg muscles occurred in several experiments either at the beginning of the inhalation or after its discontinuation.3. An injection of tranylcypromine (5 mg/kg) caused a rise in rectal temperature and prevented the hypothermia of halothane anaesthesia. This effect lasted for at least 4 hr; 20 hr after the injection, halothane again caused hypothermia.4. An injection of pheniprazine (10 mg/kg) usually caused a small rise in temperature which was not sustained. Pheniprazine not only prevented the hypothermia of halothane anaesthesia during the sulbsequent 20 hr, but during the first few hours after the injection halothane inhalation actually produced a steep rise in temperature.5. An injection of pargyline (50 mg/kg) had no effect on temperature but the hypothermia due to halothane inhalation was prevented 1 hr after the injection and attenuated after 20 hr. Injection of 200 mg/kg caused a steady rise in temperature which was accelerated when halothane was administered 1 hr later.6. An injection of nialamide (10, 25 or 50 mg/kg) had no immediate effect on temperature, but pyrexia developed overnight after the two larger doses. The effect on the hypothermia due to halothane inhalation was greater 20 hr after the injection than it was after 1 to 2 hr. Twenty hours after injection of the two larger doses, halothane no longer produced hypothermia but caused a lethal rise in temperature either during or after its inhalation. 7. In rabbits, the effect on temperature of halothane inhalation varied. Either temperature rose slightly or it fell, but not as much as in cats. In one rabbit in which the inhalation had produced a transient rise, pyrexia developed 40 min after discontinuation of halothane.

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“…British Medical3Journal, 1970, 2, 341-343 Rapidly rising body temperature resistant to treatment and usually ending fatally has been described on several occasions during the course of surgical anaesthesia (Saidman et al, 1964;Thut and Davenport, 1966;Stephen, 1967;Wilson et al, 1967;British Medical 7ournal, 1968;Hawthorne et al, 1968). It has been called fulminating hyperpyrexia.…”

Section: Fulminating Hyperpyrexia During Anaesthesia In a Member Of Amentioning

confidence: 99%