THE CBAVITY OF AN ATTACK of bronchial spasm in an unconscious patient depends on its intensity. If severe, it is a life-threatening condition and the time available for treatment is limited to only a few minutes. In our combined professional experience we have lost two such patients: the first, while passing a nasogastric tube in a young man who had taken an overdose of barbiturate; the second was a middle-aged female having a cholecystectomy under cyclopropane anaesthesia. Two recent cases of severe bronchial spasm, developed during induction of anaesthesia, were successfully treated with local anaesthetic drugs administered intravenously. The pertinent data from their case histories form the basis of this report. CAS~-BEvom's Case 1A.N., a 64-year-old white housewife, weight 57 kg, was admitted to the hospital on July 24, 1967, for surgical removal of a tumour of the right breast. The patient had a history of borderline glaucoma (not on medication), of chronic dry cough (not productive), and of heavy smoking which had been given up, in the past, at an unspecified date. There was no history of allergies. Physical examination was not remarkable except for signs consistent with the diagnosis of carcinoma of the breast, with involvement of the axillary lymph nodes. On chest roentgenograms, irregular infiltrative densities were seen in the region of the right mid-lung field, the nature of which it was not possible to diagnose at that time. Laboratory studies and electrocardiogram were within normal limits, and the haemoglobin concentration was 13.8 gm per cent.On the morning of surgery the patient was calm, her arterial blood pressure was 100/70 mm Hg, the pulse rate was 80 and the respiratory rate 15 per minute, and the lungs were clear on auscultation.Pre-anaesthetic medication consisted of secobarbital ( Seconal sodium| 100 mg given intramuscularly 1~ hours prior to surgery. Atropine was omitted.Anaesthesia was induced intravenously with approximately 100 mg of thiopenthal sodium in 0.5 per cent solution. The patient was breathing spontaneously, oxygen was administered by mask, and the ventilation was augmented with intermittent positive pressure.To facilitate tracheal intubation, d-tubocurarine chloride 15 mg was injected

In preparation for an appendicectomy the anaesthesia was started with thiopentone 350 mg followed by a dose of 24 mg of tubocurarine, intravenously, in a patient with 39° C (102°F) temperature and a history of sensitivity to detergents; an anaphylactoid reaction resulted. The intradermal sensitivity tests to tubocurarine, performed with the skin at room temperature 30°C (85°F) and at 39°C (102°F), were positive and at higher skin temperature the responses were stronger. It was concluded that tubocurarine may induce anaphylactoid reactions in susceptible individuals and that an increase in body temperature acts as a contributory factor.