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Discontinuation of ventilation after brain stem death {#article-title-2} Confusion among the public over the difference between brain stem death and a persistent vegetative state can make it difficult to obtain consent to withdraw ventilation. Clinicians who have been faced with this dilemma outline their strategies for coping with such a situation, and a neurologist and a neurosurgeon offer their opinions. # To whom is our duty of care? {#article-title-3} The concept of brain death is not often discussed in the public arena. According to the royal medical colleges in the United Kingdom and their faculties death of the brain stem is a component of brain death, and brain death is death.1 The criteria for brain stem death are well established,2 and their use in intensive care units enables treatment to be withdrawn from patients with brain stem death without recourse to the courts. Conversely, as a result of several high profile cases, persistent vegetative state has been reported on frequently in recent years. The application to the High Court in 1992 to discontinue life sustaining treatment for Tony Bland, who had been injured in the tragedy at Hillsborough football ground, brought the ethical debate to the front pages of the national press. Occasional stories of “miraculous recoveries” from comas are widely reported and may have led to an exaggeration of the small chances that patients have of recovering from a persistent vegetative state among a public that is increasingly well versed in this condition. This contrasts with the inevitable death from asystole which occurs within a few days for patients who are brain dead.3 We have experienced a case in which, although the patient had been declared brain stem dead, the patient's family prevented us from switching off the ventilator. On this occasion our intensive care unit was full, and maintaining this patient on a ventilator might have forced us to transfer any new …

In most surgical specialties there are wide variations in what surgeons do for the same kinds of patient. Reporting studies of surgical variations between adjacent counties of New England, and between New England and old England and other European countries, Wennberg concluded that these differences reflected the practice styles or surgical signatures of different surgeons [6]. In his view wide variations in practice indicate professional uncertainty about the effectiveness of, or necessity for, those interventions that are used at very different rates.

In most Westernised countries injury is the leasing cause not only of death under the age of 45, but also of years of life lost between the ages 1 and 65 years. By these measures injury is ahead of heart disease, stroke and cancer in the UK, West Germany, France, the US and Japan. The proportion of all deaths that are due to accidents varies considerably between countries, higher in Australia and Canada than in the USA and West Germany, and less common in the UK. Road accidents account for about a half of accidental deaths in North America, Australia and West Germany but for only a third in England and Scotland. Road accident deaths per 100000 population vary from 30 in West Germany, Australia, and Canada, through 22 for the USA, to only about 15 in the UK (WHO 1987).

Features of patients transferred to a regional neurosurgical unit in coma after recent head injury were compared with a similar audit seven years previously. There were fewer avoidable adverse factors in the recent series, but some patients received inadequate care of the airway, while in some others major extracranial injuries were overlooked or poorly managed. Only 42% of the comatose patients had had an endotracheal tube inserted; half those in whom neither a tube nor an oral airway had been inserted were transported supine. Systemic hypoxia or hypotension [corrected] were associated with a poor outcome. Even when computed tomography scanners become available in more hospitals, many patients who are unconscious after head injury will still need to be transferred to a neurosurgical unit. Detailed guidelines should be agreed locally to minimise the hazards of transfer of unconscious patients between hospitals. A rota of experienced doctors and nurses at the sending hospital should be responsible for deciding how each individual patient should be managed during transfer, according to the guidelines. Continuing audit of such cases is needed to indicate whether revision of local practice is needed.

The ability to predict outcome in the early stages of severe head injury would have several uses. A computerized system which has been developed in Glasgow to assist clinicians in this task, based on information from over 2500 severely head-injured patients, is described, with particular attention to the testing of the statistical properties of the system, and, more importantly, the assessment of its clinical impact.

Accident is now the commonest cause of death under the age of 45 years in developed countries. Head injuries contribute to many fatal accidents, and are the only common cause of persisting disability in survivors. In Britain, which has less than half the head injury death rate (per unit of population) that prevails in North America, Australia, West Germany or France, there are a million patients attending British hospitals each year with head injury. Many of these are mildly injured, but even so there may be minor sequelae for weeks or months. There are about 7000 deaths each year, and at least 1500 patients leave hospital with permanent brain damage, half of them never to work again; as the average age of these severely injured survivors is under 30 years, they face many years of disability.

When the brain is examined within a few days of injury it can be surprisingly difficult to establish what has been the cause of death, or to determine with certainty which lesions are primary and which are secondary, apart from clear-cut complications such as intracranial haematoma or infection. Recent reports of continuous measurements of intracranial pressure after head injury (Lundberg, Troupp, and Lorin, 1965; Troupp, 1965 and 1967) suggest that many patients who die after head injury develop very high intracranial pressure before death without necessarily having a focal expanding lesion. The effect of a generalized increase in intracranial pressure on the brain is ultimately to produce a reduced perfusion of blood and the brain will then suffer hypoxic damage. In the belief that this may be one of the mechanisms contributing to brain damage after head injuries (and other lesions causing raised pressure) we have explored various aspects of the relationships between intracranial pressure and cerebral blood flow. The oxygen supply to the brain depends, as in any other tissue, on the equation: available oxygen = haemoglobin x oxygen saturation x blood flow. A reduced oxygen content of the blood is not uncommon after head injury, which makes the brain much more critically dependent on blood flow. Blood loss from associated injuries, which occurs in a third of all cases of head injury admitted to hospital, commonly gives a low haemoglobin. Respiratory difficulties are also frequent after head injury, either due to the unconscious state or to associated chest injuries, and as a result of ventilatory insufficiency the oxygen saturation is then reduced. Blood flow in the brain has a characteristic peculiar to its situation within a rigid closed cavity, namely, its susceptibility to surrounding tissue pressure. Indeed the supply of blood to the brain depends on cerebral perfusion pressure, which is the difference between systemic arterial pressure and intracranial pressure. Cerebral perfusion may be altered not only by systemic hypotension but also by raised intracranial pressure. Whilst hypotension is uncommon in patients suffering from head injury alone, the

SUMMARY The effects of the neuroleptanalgesic drug combinations, droperidol 5 mg+phnoperidine 1.5 mg, and droperidol 5 mg+fentanyl 0.1 mg, on the cerebrospinal fluid (c.s.f.) pressure, have been studied in patients with normal c.s.f. pathways during controlled ventilation. The influence of droperidol 5 mg+fentanyl 0.1 mg on intracranial pressure has also been investigated in patients with intracranial space-occupying lesions. In patients with normal c.s.f. pathways, droperidol and phenoperidine produced only small alterations in c.s.f. pressure in either direction, while a significant decrease in overall mean c.s.f. pressure. Similarly, in patients with intracranial space-occupying lesions, droperidol plus fentanyl produced decreases in c.s.f. pressure in all but one of the cases studied. The striking difference between the effect on c.s.f. pressure of these drugs and of the volatile anaesthetic agents could be of importance to the clinical anaesthetist dealing with head injuries or working in a neurosurgical unit, when under conditions of controlled ventilation these drugs could be used as adjuvants to nitrous oxide-oxygen anaesthesia.

Three weeks after admission to a maternity hospital for observation following minor antepartum haemorrhage, a primiparous patient aged 22 suffered a sudden left hemiplegia and became comatose. Congestive cardiac failure ensued and because of the subsequent severe hypoxaemia she was transferred to the hyperbaric oxygen unit at the Western Infirmary, Glasgow, where it was found possible to improve her condition by means of oxygen at increased pressure. A caesarean section was w successfully performed in the hyperbaric chamber, and a normal live female infant was delivered. Though the patient's general condition improved she never regained consciousness and died almost three months later. Necropsy confirmed the clinical diagnosis of cardiomyopathy of pregnancy with severe ischaemic changes in the brain.

In 1966 we published a preliminary communication indicating that measurements of rCBF in the operating room before and after trial occlusion of the carotid arteries in the neck might provide a better estimate of the risk of permanent ischemia of the cerebral hemisphere than methods already available. On the basis of our experience with those 10 cases it seemed that 25% reduction during trial clamping was a critical level; with a greater reduction of flow than this hemiparesis often occurred. This communication reports our experience with a further 58 patients.

Opinions about the importance of age as a prognostic factor after head injury have varied. For instance, Carlsson et al.1 emphasized a close correlation between increasing age and a decreasing change of mental recovery; but others2 report that age has little influence on the prospects for recovery.

In 1975 Jennett and Bond published an account of a Global Outcome Scale which they developed for use in the assessment of individuals who have had head injuries. The Scale has been used widely in several contries including Britain, Holland, and the United States, and familiarity with it has brought several criticisms. The main ones are, first, that it is a crude measure and not sensitive to subtle changes in patients’ status and, second, that there is little background information about the nature and extent of physical and mental handicaps which make up the first three elements of the Scale. In other words, we wish to know what constitutes good recovery, moderate disability and severe disability. Jennett and others (1978) accept the first of these criticisms, and in a response to it have expanded the categories mentioned above from three to six thereby giving increased sensitivity. In order to deal with the second criticism a careful study of the mental and physical deficits of two groups of brain injured individuals has been carried out. Four kinds of disability have been examined. In a first sample of 150 patients physical, cognitive, and personality deficits have been graded as nil, mild, moderate, or severe, and related to outcome at six months after injury by which time most of these deficits are established. In a second sample, which is still under study, in addition to the deficits examined in the first group, the social consequences of disability are being examined in detail. Results from the first study show that some deficits, albeit mild, were detectable in 97% of the patients examined. Two-thirds had personality change, two-thirds had cognitive change, and 93% had one or other of both of these mental deficits. Physical handicaps were present in 75% of patients, but were less significant than mental handicaps which dominated recovery in just over half the patients in the survey. This pattern was repeated in each of the three outcome categories examined. In more detail, in 30% of patients the only detectable deficit was a change in personality, a figure which increased to 60% in patients without physical deficits or one of only a mild degree, and to a similar extent in those with nil or mild cognitive deficits.

Following carotid ligation in the neck, there is a considerable risk of ischemia of the ipsilateral hemisphere. Neurological complications may develop immediately because of poor collateral circulation. More often, this complication develops later, in a period ranging from a few hours to a few days. The reason for the development of delayed complications is not known.

Head injuries are an important aspect of health care which impose considerable burdens on the hospital service; in the UK they comprise 1 in every 10 new patients in accident and emergency departments, and account for 150,000 hospital admissions every year. In Europe most admissions are to accident or general surgery wards, only the minority of obviously serious injuries coming to neurosurgeons. Even after mild injury there is the threat of serious complications which can develop rapidly, and are associated with considerable mortality and morbidity rates. The reason why so many mildly injured patients are admitted to hospital is in the hope that clinical observation will result in early detection of complications.

Hyperbaric oxygen, by increasing the dissolved oxygen content of the blood, might be expected to improve oxygenation in areas of the brain suffering threatened or incomplete ischaemia but which are still being perfused sufficiently for blood to reach them, although in inadequate amounts. It might also increase the period of occlusion of major neck vessels which the brain will tolerate, such as clamping of the carotid artery during surgical procedures. However, previous studies in man [3] and in dogs [1] showed a reduction of 24% and 21% in CBF at 2 ATA; it seemed possible that this vasoconstriction might largely cancel out any beneficial effect if it were also to operate in pathological situations.

Thirty-one cases of ischaemic cerebral stroke occurring in association with childbirth were fully investigated. The pathological basis of non-haemorrhagic carotid territory strokes in pregnant or puerperal women proved to be similar to that in non-pregnant women of the same age group. Over 70% were due to occlusive cerebral arterial disease or ischaemic lesions unrelated to thrombosis of the intracranial venous system. Comparisons are made with some other reported series in which only a minority of the patients were investigated by angiography, but in which intracranial venous occlusion was assumed to be the primary lesion. It seems likely that many of these patients may also have suffered arterial rather than venous lesions.

Mannitol has been shown to be effective in reducing raised intracranial pressure when used in a single large dose [1]. Its use in the control of raised intracranial pressure over longer periods of time, particularly in patients with diffuse brain damage is, however, less well founded and here other effects, for example on cerebral blood flow, may be of importance. This paper briefly reports the results of a clinical study of the effect of small serial doses of Mannitol on intracranial pressure and of an experimental study of the effect of Mannitol on cerebral blood flow.

Changes in cerebral blood flow during incremental increases of intracranial pressure produced by infusion of fluid into the cisterna magna were studied in anaesthetized baboons. Cerebral blood flow remained constant at intracranial pressure levels up to approximately 50 mm Hg. At intracranial pressure levels between 50-96 mm Hg a marked increase in cerebral blood flow occurred, associated with the development of systemic hypertension and changes in cerebrovascular resistance. Further increases of intracranial pressure led to a progressive fall in cerebral blood flow. Prior section of the cervical cord prevented both the increase in cerebral blood flow and the systemic hypertension. Alteration of cerebral perfusion pressure by bleeding during the hyperaemia in a further group of animals suggested that autoregulation was at least partially preserved during this phase. After maximum hyperaemia had occurred, however, autoregulation appeared to be lost. The clinical implications of these findings are discussed.

The mode circulation time was measured using intravenously injected technetium 99(m) and a collimation system devised to discriminate between the right and left sides of the head. The results in 21 normal men were used as a basis of assessing the findings in 205 patients, made up of five diagnostic groups (ischaemia, haematoma, subarachnoid haemorrhage, intracranial tumour, and head injury). The average mode circulation time in the affected hemisphere for the three groups with vascular disease was increased, but even in these groups half the patients had a mode circulation time within 1 SD of normal mean; similar results were found for asymmetry between the hemispheres. In serial measurements in 45 patients no correlation was found between change in mode circulation time and the clinical state. That so many results are within the normal range limits the value of this method.

Publisher Summary Halothane and trichloroethylene dilate the cerebral blood vessels and the degree of vascular dilatation is proportional to the concentration of the drug administered. These anaesthetic drugs also depress the aerobic metabolism of the brain and lead to a fall in cerebral oxygen consumption. This effect, at least in the case of halothane, is also proportional to the concentration of the drug administered; 0.5 % halothane lowers the oxygen uptake of the cerebral cortex of the dog by 14 % while 2 % halothane causes a fall of 33 %. These appreciable reductions in cerebral oxygen requirements may render partial protection. In summary, halothane and trichloroethylene dilate the cerebral blood vessels and increase cerebral blood flow, provided that systemic blood pressure is not too greatly depressed. These drugs also cause considerable depression of cerebral oxygen uptake. As a result of this combination of flow increase and metabolic depression, cerebral venous oxygenation increases. As a result of the flow increase, cerebrospinal fluid pressure rises. This increase in pCSF may be so great in patients with intracranial tumours as to reduce cerebral perfusion. The value of hyperventilating patients with intracranial space occupying lesions prior to halothane or trichloroethylene administration is stressed.

SUMMARY The effect of methoxyflurane 0.5 per cent and 1.5 per cent on cerebrospinal fluid (c.s.f.) pressure has been studied in patients with normal c.s.f. pathways and in patients with in intracranial space-occupying lesions. In patients with normal c.s.f. pathways, methoxyflurane 0.5 per cent produced variable responses, causing small increases in c.s.f. pressure in some and small decreases in others. On the other hand, methoxyflurane 1.5 per cent caused significant increases in c.s.f. pressure in all patients, increases that were not associated with any alteration in either carbon dioxide tension or central venous pressure. In those patients studied with intracranial space-occupying lesions, both 0.5 per cent and 1.5 per cent methoxyflurane produced increases in c.s.f. pressure which were markedly greater than those found in the patients without space-occupying lesions. The mean rise in c.s.f. pressure was dependent on the concentration of the drug administered, being small with 0.5 per cent methoxyflurane, but much greater with the higher concentration. A possible hazard in such patients is that the administration of methoxyflurane may lead to gradients of intracranial pressure, thus aggravating brain shifts and mid-brain distortion, and if the skull is opened lead to external brain herniation.

Changes in cerebral blood flow with increasing intracranial pressure were studied in anaesthetized baboons during expansion of a subdural balloon in one of two different sites. With an infratentorial balloon, cerebral blood flow bore no clear relation to intracranial pressure, but was linearly related to cerebral perfusion pressure. Apart from an initial change in some animals, cerebrovascular resistance remained constant with increasing intracranial pressure, and autoregulation appeared to be lost from the outset. With a supratentorial balloon, cerebral blood flow remained constant as intracranial pressure was increased to levels around 60 mm Hg, corresponding to a cerebral perfusion pressure range of approximately 100 to 40 mmHg. Cerebrovascular resistance fell progressively, and autoregulation appeared to be effective during this phase. At higher intracranial pressure levels (lower cerebral perfusion pressure levels), autoregulation was lost and cerebral blood flow became directly dependent on cerebral perfusion pressure. The importance of the cause of the increase in intracranial pressure on the response of the cerebral circulation and the relevance of these findings to the clinical situation are discussed.

Raised intracranial pressure (ICP) is the mechanism whereby many clinical conditions eventually threaten brain function and life itself. Neurosurgeons are therefore frequently concerned to recognise whether ICP is raised, and if so to try to reduce the level of pressure. Continuous clinical monitoring of pressure was shown to be feasible by GUILLAUME and JANNY in France in 1951, and a large series of neurosurgical cases was reported from Sweden in 1960 by LUNDBERG. Their observations showed that the level of pressure is often variable so that single estimations of pressure may be misleading; the clinical state of the patient has likewise been shown to be an unreliable guide to ICP. In these circumstances widespread adoption of continuous monitoring of ICP might have been expected, but last year’s conference in Hannover revealed that it has become routine in comparatively few centres. In the Glasgow Institute some 300 patients have now been monitored by the LUNDBERG method, a plastic catheter being introduced into the ventricle via a frontal burr hole and linked through a fluid-filled system to a bedside transducer and chart recorder. Monitoring is continued for 2–5 days as a rule but only one patient has developed intracranial infection and he recovered, which confirms a recent report of an extremely low incidence of infection (0. 5%) with LUNDBERG’s method in almost 1,000 cases (SUNDBARG et al, 1972).

Increased intracranial pressure was induced in anaesthetized dogs by application of liquid nitrogen to the dura mater. Intracranial pressure and cerebral blood flow were measured, together with arterial blood pressure and arterial and cerebral venous blood gases.Carbon dioxide was administered intermittently to test the responsiveness of the cerebral circulation, and hyperbaric oxygen was delivered at intervals in a walk-in hyperbaric chamber, pressurized to two atmospheres absolute.Hyperbaric oxygen caused a 30% reduction of intracranial pressure and a 19% reduction of cerebral blood flow in the absence of changes in arterial PCO(2) or blood pressure, but only as long as administration of carbon dioxide caused an increase in both intracranial pressure and cerebral blood flow. When carbon dioxide failed to influence intracranial pressure or cerebral blood flow then hyperbaric oxygen had no effect. This unresponsive state was reached at high levels of intracranial pressure.