CORRESPONDENCE

1119

the portal vein and also the infra hepatic portion of the inferior vena cava against the vertebral column. P. CHARI

Chandigarh, India REFERENCE

Malatinsky, J., and Kadlic, T. (1974). Inferior vena caval occlusion in the left lateral position. Br. J. Anaesth., 46, 165. NITROUS OXIDE AND INTRACRANIAL PRESSURE

G. E. COLD

Aarhus, Denmark

TABLE I. A summary of the features of reported cases of possible allergic reactions to methohexitone. No

REFERENCES

Henriksen, H. T., and Balslev-Jorgensen, P. (1973). The effect of nitrous oxide on intracranial pressure in patients with intracranial disorders. Br. J. Anaesth., 45, 486. Scrimshire, D. A., and Tomlin, P. J. (1973). Gas exchange during initial stages of N,O uptake and elimination in a lung model. J. Appl. Physiol., 34, 775. REACTION TO METHOHEXTTONE

Sir,—We wish to report an immediate reaction to methohexitone in a healthy 25-year-old woman who presented for outpatient general anaesthesia for Zadek's operation. She was not taking any drugs, had no complaints or history of disease and gave no personal or family history of allergy. General anaesthesia had been administered on three occasions in the past year for surgery to the great toes. Propanidid had been used as the induction agent on the first two occasions, without untoward effects. Thiopentone was used on the third occasion and the patient experienced nausea and vomiting for 3 days subsequently, although she did not consult her doctor.

No

Source Hainsworth and Bingham (1970) Reichert and Bassett (1972) Driggs and O'Day 1972) (1) (2) (3) (4) (5) (6) Wicks (personal communication) (1) (2) Shafto (1969) Present case

history

Speed of

of other onset Facial drugs allergy < 1 min flush

Oedema of

face

+

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Sir,—The effect of induction of anaesthesia with nitrous oxide in oxygen on cerebral haemodynamics in patients with intracranial lesions has been discussed by Henriksen and Balslev-Jorgensen (1973). In their study a simple semiclosed mask and bag system without carbon dioxide absorption, was used with a fresh gas flow of 9-12 litre/min. As a result of the high nitrous oxide uptake during induction of anaesthesia, an increase in PA,-,, and P A ^ , occur (Scrimshire and Tomlin, 1973). When used in connection with a semiclosed system without carbon dioxide absorption, an increase in Papo, may occur and lead to a dangerous increase in intraventricular pressure (IVP) in patients with intracranial hypertension. In five patients we have measured IVP, systemic arterial pressure, Paco,, Pa 0 ,, end-tidal carbon dioxide % and expiratory minute volume during induction of anaesthesia with nitrous oxide 67% in oxygen. All patients were ventilated with a Servo 900 ventilator, with a constant FIQ, and inspiratory minute volume. The patients were unconscious following brain injury and they were studied 1-12 days after the acute trauma. In all cases we noted an increase in Paco, ranging from 2 to 4 mm Hg, an increase in IVP ranging from 5 to 24 mm Hg, and a decrease in expiratory minute volume ranging from 1.5 to 2 litre/min (15-20% decrease). The largest increase in IVP was recorded in a severely injured patient in whom the IVP before induction was about 20 mm Hg. We believe that an increase in IVP in unconscious braininjured patients, results not only from a direct effect of nitrous oxide, but also from the small increase in Paco, which occurs during nitrous oxide induction. In these deeply unconscious patients, the increase in IVP cannot be associated with excitation, which may occur in conscious subjects during induction of anaesthesia.

Six weeks later, anaesthesia was induced with methohexitone 65 mg. The drug was prepared freshly in a singledose vial and administered via an indwelling needle in the dorsum of the left hand. Within a few seconds a bright red facial flush developed and the peripheral pulses became impalpable. On applying a face mask to deliver oxygen, facial oedema was apparent. An infusion of Hartmann's solution was begun and hydrocortisone succinate 200 mg and mepyramine maleate 5 mg were given i.v. Five min later the facial flush had faded to a dusky blue colour with signs of slow capillary filling, periorbital oedema was more pronounced and the arterial pressure remained unrecordable, although the carotid pulse was palpable throughout and the pupils remained constricted. Twenty min after the injection the arterial systolic pressure was 60 mm Hg, consciousness had returned and the facial colour was normal. At no time was bronchospasm detectable. Thereafter the patient made a slow but uninterrupted recovery. Hypotension persisted for 8 hr and the facial oedema for 2 day. The patient was discharged on the 3rd day. When seen 1 week later the history and the impression of a pleasant induction of anaesthesia were confirmed. The clinical features in this patient resemble the reactions described following the use of Althesin and propanidid. However, the serum chemistry in this patient showed marked differences from those we have seen following apparent anaphylactic reactions to Althesin. Samples of serum obtained from the present patient at 3, 6 and 24 hr after the incident showed a progressive and large decrease in C3 complement component from a normal value of 1415 mg/ litre at 3 hr after the reaction to 550 mg/litre at 24 hr; this decrease was accompanied by a reduction in the C4 complement component (552 mg/litre to 220 mg/litre). In our experience this response differs from the pattern following a reaction to Althesin where there is an initial and rapid decrease in C3 complement component in the first few minutes after induction and a complete restoration to normal values over the next 12-24 hr. The prolonged complement conversion pattern in the present patient is in keeping with the pharmacokinetics of methohexitone, as is the persistence of facial oedema. It seems probable that this patient was exhibiting a true type 1 hypersensitivity (anaphylactic) reaction, following passive sensitization to barbiturates at the previous induc-

BRITISH JOURNAL OF ANAESTHESIA

1120 tion. This view is supported by our serum measurements which showed an apparent consumption of reagin antibody (IgE). Relatively few acute reactions associated with the use of methohexitone have been reported (table I). None have all the features described here, namely: (1) The patient had no history of allergy. (2) No other drug was involved. (3) The reaction was almost instantaneous. (4) A brilliant facial flush was observed. In addition, an immunological process has been demonstrated for the first time. There is an increasing incidence of reports of anaphylactic or histaminoid responses following the use of Althesin and propanidid, but clearly all such incidents should be reported, not just those involving newly introduced agents (Dundee and Clarke, 1973). Sheffield

M. HEIFETZ

H. J. BnucHAHN REFERENCES

Heifetz, M. (1974). Anaesthesic management of reconstruction of the lower portion of the trachea. Anaesthesia, 29, 760. Kamvyssi-Dea, S., Kritikou, P., Exarhos, N., and Skalkeas, G. (1975). Anaesthetic management of reconstruction of the lower portion of the trachea. Br. J. Anaesth., 47, 82.

REFERENCES

Driggs, R. L., and O'Day, R. A. (1972). Acute allergic reaction associated with methohexital anaesthesia. J. Oral. Surg., 30, 906. Dundee, J. W., and Clarke, R. S. J. (1973). Adverse reactions to intravenous anaesthetics. Br. J. Anaesth., 45, 304. Hainsworth, A. M., and Bingham, W. (1970). An allergic circulatory collapse following the administration of muscle relaxants. Anaesthesia, 25, 105. Reichert, E. F., and Basset, P. A. (1972). A rare allergic reaction to sodium methohexital. J. Oral. Surg., 30, 910. Shafto, C. E. (1969). Continuous intravenous anaesthesia for paediatric dentistry. Br. J. Anaesth., 41, 407.

ANAESTHETIC

MANAGEMENT FOR RECONSTRUCTION LOWER TRACHEA

OF

THE

Sir,—We should like to comment on the case report by Kamvyssi-Dea and colleagues (1975) of the anaesthetic management for reconstruction of the lower portion of the trachea. It is the opinion of ourselves and of our surgical colleagues that a combined cervical and right thoracic approach for surgical resection of tracheal stenosis is necessary only when the site of the lesion has not been adequately localized before operation. In our own experience with five patients, a cervical approach was used where the lesion was high whilst a right thoracic approach was used only for lesions which were situated low in the trachea. The need for intubation of the left bronchus was dependent upon the length of the stump above the carina. Kamvyssi-Dea stated that 100% oxygen was used throughout the period of excision, dissection and anastomosis without specifying how anaesthesia was maintained. We assume that intravenous anaesthesia was used, but we regard this as being unsatisfactory for the anaesthetic management of these patients. We have used 1 % halothane in 99 % oxygen and have found that this provides an adequate level of anaesthesia (Heifetz, 1974) and obviates the use of muscle relaxants. One hundred per cent oxygen is unnecessary if the endotracheal tube is left in position and both lungs have been ventilated during surgery. Although Kamvyssi-Dea stated that arterial blood-gases were satisfactory, we would feel that the values should have been reported in the paper. In addition we should like to draw

I

Sir,—We agree absolutely with Dr Heifetz's comments on the techniques used for high and low strictures of the trachea. The transverse cervical incision at the level of the tracheostomy that was mentioned in our case report was approximately 1 cm on each side of the stoma and was performed in order to free and mobilize the cervical trachea. We do not make any cervical incision in the absence of a tracheostomy. At the beginning of the operation, anaesthesia was maintained with nitrous oxide 3 litre/min, oxygen 3 litre/min and halothane 1-2%. Towards the end of the dissection and during the anastomosis of the trachea, oxygen 6 litre/min with halothane 0.5% were administered. As soon as the anastomosis was completed, the halothane was discontinued and anaesthesia was maintained with nitrous oxide and oxygen, and pancuronium was used to provide muscle relaxation. Until this moment, the patient was breathing spontaneously with manual assistance of ventilation. However, in a second case of low tracheal stenosis which we have encountered recently, pancuronium was administered initially and the patient was ventilated through an endobronchial tube. There were no difficulties and the patient was betteT controlled and well oxygenated before the excision and during one-lung anaesthesia. During the period of excision of the trachea in the reported case, which lasted approximately 2 min, the patient was breathing air. The reduction in POQX was transient, from 442 mm Hg to 336 mm Hg. Arterial Pco, increased from 36 mm Hg to 41 mm Hg. (We appreciate that the process of apnoeic oxygenation is different from apnoea persisting for 5 min after ventilation with 100% oxygen.) We are also of the opinion that tracheostomy following reconstruction of the trachea is not desirable for fear of infection or recurrence of stenosis. However, in our patients, a tracheostomy had already been performed and we took advantage of it for aspiration of secretions after operation.

Printtd in Gnat Britain by John Wrixht and Sons Ltd. ax Tht Stontbridf Pros, Briaol BS4 5SU

SONIA KAMVYSSI-DEA

Athens, Greece

Ig) Macmillsn Journals Ltd. 1975

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R. WYATT J. WATKINS

attention to the fact that the process of apnoeic oxygenation is totally different from apnoea persisting for 5 min after ventilation with 100% oxygen. It is our opinion that tracheostomy following resection of a tracheal stenosis is contraindicated for the postoperative management of these patients. Tracheostomy itself has induced the stenosis in some of the cases operated upon in our series and consequently we would take issue with the statement that a tracheostomy should remain for a period of 1 month following tracheal resection.

I

Letter: Nitrous oxide and intracranial pressure.

CORRESPONDENCE 1119 the portal vein and also the infra hepatic portion of the inferior vena cava against the vertebral column. P. CHARI Chandigarh,...
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