Correspondence
113
In two previously reported cases’**in which the convulsions immediately followed the administration of Althesin the total dose was injected over 10 and 15 seconds respectively. The later onset of convulsions in the present case may have been due to the slower rate of injection which would give a lower peak blood level of Althesin. Induction with this drug is, in the author’s experience, quite commonly associated with twitching of the legs or arms and, less commonly, with hiccoughs. Usually the twitching is of only a few seconds’ duration and subsides as the depth of anaesthesia is increased. In the case reported here it may well be that the cerebral stimulant effect of Althesin together with that of light halothane anaesthesia3 and that of the mild stimulation summated to produce a generalised seizure. It is of interest that, like the cases reported by Rees and Uppington, the patient did not become cyanosed during the convulsion, nor was there any clinically apparent depression of respiration afterwards. Unfortunately it has not been feasible to recall the patient from his outlying farm to have electroencephalographic studies performed but he gave no medical or family history to suggest a liability toepileptiform seizures. It must beconcluded that it would be wiser to avoid Althesin in known epileptics. Harari Hospital, P.O. Box ST 14, Southerton, Salisbury, Rhodesia
RICHARD G. MCGOWN
References 1. UPPINGTON, J. (1973) Epileptiform convulsion with Althesin. Anaesthesiu, 28, 546. 2. REES, L.J. (1975) Convulsions immediately following Althesin. Anaesthesia, 30,54. 3. EVANS, D.E.N. (1975) Anaesthesia and the epilepticpatient. Anaesthesia,30,34.
Anaesthesia and hypothermia in sickle cell disease Anaesthesia for patients with sickle cell trait (HbAS) is not unduly hazardous although the dangers of sickling cannot be ruled out. Unusual techniques such as hypothermia or extracorporeal circulation in association with anaesthesia could be dangerous in persons with sickle cell trait. A Nigerian patient with an atrio-septa1 defect and who was sickle cell test positive for sickle cell trait was managed under profound hypothermia using an extracorporeal circulation incorporating a heat exchanger without any complications. The patient was cooled by Drew’s technique to a nasopharyngeal temperature of 20°C. Cardiac arrest time was 21 minutes during which the septa1 defect was repaired ; as rewarming started ventricular fibrillation returned and, on defibrillation, the heart went into sinus rhythm. Blood samples taken during cooling and warming showed no sign of sickling. The patient was artificially ventilated overnight and was extubated the following morning. The post-operative course was uneventful and she was discharged 2 weeks later. Hypoxia, circulatory stasis and cooling are factors which in this technique might be expected to contribute to sickling but at no stage was there any evidence of haemolysis, significant biochemical upset, neurological disturbance or any other changes. Department of Anaesthesia, St George’s Hospital,
Hyde Park Corner, London, S W1
S. SOMANATHAN
113
In two previously reported cases’**in which the convulsions immediately followed the administration of Althesin the total dose was injected over 10 and 15 seconds respectively. The later onset of convulsions in the present case may have been due to the slower rate of injection which would give a lower peak blood level of Althesin. Induction with this drug is, in the author’s experience, quite commonly associated with twitching of the legs or arms and, less commonly, with hiccoughs. Usually the twitching is of only a few seconds’ duration and subsides as the depth of anaesthesia is increased. In the case reported here it may well be that the cerebral stimulant effect of Althesin together with that of light halothane anaesthesia3 and that of the mild stimulation summated to produce a generalised seizure. It is of interest that, like the cases reported by Rees and Uppington, the patient did not become cyanosed during the convulsion, nor was there any clinically apparent depression of respiration afterwards. Unfortunately it has not been feasible to recall the patient from his outlying farm to have electroencephalographic studies performed but he gave no medical or family history to suggest a liability toepileptiform seizures. It must beconcluded that it would be wiser to avoid Althesin in known epileptics. Harari Hospital, P.O. Box ST 14, Southerton, Salisbury, Rhodesia
RICHARD G. MCGOWN
References 1. UPPINGTON, J. (1973) Epileptiform convulsion with Althesin. Anaesthesiu, 28, 546. 2. REES, L.J. (1975) Convulsions immediately following Althesin. Anaesthesia, 30,54. 3. EVANS, D.E.N. (1975) Anaesthesia and the epilepticpatient. Anaesthesia,30,34.
Anaesthesia and hypothermia in sickle cell disease Anaesthesia for patients with sickle cell trait (HbAS) is not unduly hazardous although the dangers of sickling cannot be ruled out. Unusual techniques such as hypothermia or extracorporeal circulation in association with anaesthesia could be dangerous in persons with sickle cell trait. A Nigerian patient with an atrio-septa1 defect and who was sickle cell test positive for sickle cell trait was managed under profound hypothermia using an extracorporeal circulation incorporating a heat exchanger without any complications. The patient was cooled by Drew’s technique to a nasopharyngeal temperature of 20°C. Cardiac arrest time was 21 minutes during which the septa1 defect was repaired ; as rewarming started ventricular fibrillation returned and, on defibrillation, the heart went into sinus rhythm. Blood samples taken during cooling and warming showed no sign of sickling. The patient was artificially ventilated overnight and was extubated the following morning. The post-operative course was uneventful and she was discharged 2 weeks later. Hypoxia, circulatory stasis and cooling are factors which in this technique might be expected to contribute to sickling but at no stage was there any evidence of haemolysis, significant biochemical upset, neurological disturbance or any other changes. Department of Anaesthesia, St George’s Hospital,
Hyde Park Corner, London, S W1
S. SOMANATHAN
