sufentanil and intracranial pressure

Correspondence 543

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Vco2 following tourniquet deflation

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Hoka and colleagues (Anaesthesia 1992; 47: 65-8) described the changes in oxygen uptake and carbon dioxide output on releasing leg tourniquets during orthopaedic surgery. Their study involved 23 awake patients undergoing lower limb surgery under spinal anaesthesia, and the results demonstrated increases in both parameters that were proportional to tourniquet time. We performed a similar study, measuring the increase in CO, output after tourniquet release in patients under general anaesthesia with controlled ventilation.

Twenty-five fit patients undergoing orthopaedic surgery to the lower limb were studied. Each patient was fasted, premedicated, and anaesthetised with a standardised technique involving thiopentone, vecuronium, fentanyl, o,, and N,O. Ventilation was adjusted to maintain arterial oxygen saturation and end-tidal carbon dioxide values within the normal range. Anaesthetic depth and infusion rates were adjusted to maintain cardiovascular measurements close to the patients’ norm.

Carbon dioxide output was measured over 5 min periods by collecting expired gases from the Manley Pulmovent ventilator in a Douglas bag and then measuring its co, concentration by passing a sample through a Datex Cardiocap monitor. The volume of the 5 min specimen of expired gas was measured with a Wright’s respirometer, allowing the co, output per 5 rnin to be calculated by the following formula:

(volume of sample) x (mixed CO, concentration)

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A control reading was made during tourniquet inflation, and four consecutive 5 min samples were taken after deflation.

The mean tourniquet time was 72 min, with a range of 20-1 16 min. The mean pre-release co2 was somewhat lower than Hoka er al. found, reflecting the lower basal metabolic rate of the anaesthetised subject. In addition, this basal CO, output was found to correlate with age in an inverse linear fashion, with an r value of 0.7. Where our results differ is in

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Tourniquet time (rnin)

Fig. 1. Increase in CO, excretion per kg vs tourniquet time.

the relationship between tourniquet time and the ‘excess co,’ output on tourniquet release. Our results showed minimal extra co, output with tourniquet times below 80 min. However, with longer tourniquet times, extra co, output increased markedly (Fig. I ) .

These results suggest that the metabolic impact of releasing a leg tourniquet after 80 min or less is unlikely to be of importance. However, with longer ischaemic times, the sudden entry of CO, and lactic acid into the circulation may affect the vulnerable patient, particularly if general anaesthesia prevents a compensatory increase in minute volume. Increasing the minute ventilation of paralysed patients for approximately 15 min after prolonged tourniquet times would, therefore, seem a sensible approach.

Killingbeck Hospital, Leeds

M. DRESNER

I would like to thank Professor S. Feldman of the Magill Department of Anaesthetics, Westminster Hospital, for his help in performing this study.

Sufentanil and intracranial pressure

We would like to comment on the article by Weinstabl etal . (Anaesthesia 1991; 46: 837-40) on the effect of sufentanil on intracranial pressure (ICP) in neurosurgical patients.

The mild hyperventilation of all the patients in this study is not quantified in the article, so it is uncertain whether any cerebral vasoconstriction may have masked the effects of sufentanil on the cerebral vasculature. We believe that the title of this article may, strictly speaking, be incomplete. The authors appear to have omitted to consider any effect of residual midazolam. The elimination half-life of this benzodiazepine is 1-4 h and therefore stopping the midazolam infusion 1 h prior to the sufentanil boluses is an inadequate interval. Furthermore since midazolam is known to reduce cerebral blood flow, any residuum may have counteracted any contrary effects of sufentanil [l]. Therefore this study is actually examining the effect of sufentanil plus midazolam on intracranial pressure. We would also be interested to learn how the authors obtained informed consent from patients in a neurosurgical intensive care unit, some of whom had sustained head injury or intracerebral haemorrhage.

A recent abstract presented data suggesting that both sufentanil and fentanyl increase intracranial pressure in resuscitated head trauma patients [2]. Therefore the

controversy as to the effects of sufentanil on intrcranial pressure remains and the article by Weinstabl e ta l . does not appear to resolve it.

Division of Neuroanesthesia, N.A. PACE Parkland Memorial Hospital. M.B. WALKER Dallas, Texas, USA

References [ I ] FORSTER A, JUGE 0, MOREL D. Effects of midazolam on

cerebral blood flow in human volunteers. Anesthesiology 1982; 56: 453-5.

[2] BAILEY PL, SPERRY RJ, REICHMANN MV, PETERSON JC, PETERSON PB, PACE NL, STANLEY TH. Both sufentanil and fentanyl increase intracranial pressure significantly in resuscitated head trauma patients. Anesthesiology 1991; 7 5 A198.

A reply

We welcome the opportunity to reply to the comments of our article on the effect of sufentanil on intracranial pressure in neurosurgical patients.