2.2 Brainstem Testing

Brain death describes the situation in which a patient has undergone the irreversible loss of any capacity for consciousness, together with the irreversible loss of the ability to breathe.

Before testing can be considered, there are preconditions that must be satisfied, the most important of which is that there must be a definitive diagnosis of the cause of the brain damage. The patient should also be in an apnoeic coma, with a Glasgow Coma Score of 3 (no eye opening, no verbal response and no localization of pain).

Children: theoretically, the clinical criteria are the same in children, although there are enough concerns about their applicability to make this a very difficult area. In neonates, for example, CNS immaturity raises doubts about the validity of brain stem death tests, and there is much anecdotal evidence of children who have recovered substantial neurological function despite severe insult and prolonged coma.

• Temperature: this must be at least 35 C. • Sedatives: • Neuromuscular blockade • Metabolic Derangement • Normocapnia

There should be no residual depressant drugs in the system, which in practice may mean substantial delay until clearance can be assured. Such patients are usually sedated with short-acting agents whose elimination can be predicted with some confidence. (Observation over four elimination half-lives is commonly recommended). If, however, they have received longer-acting drugs, such as barbiturates (e.g. thiopental) to control convulsive activity, or if there is a suspicion of illicit drug use then the situation can be more difficult. Plasma determinations may be indicated, but if the intracranial catastrophe is obvious and extreme, some clinicians do not believe them to be necessary.

Neuromuscular blockade: This should be excluded (where appropriate) by using a peripheral nerve stimulator.

There must be no endocrine or metabolic disturbance that may contribute to continued coma, and there should be no possibility that impaired circulatory function is compromising cerebral perfusion.

Normocapnia: A high PaCO2 can obtund cerebral function and so must be kept normal (for that patient).

these are carried out by two doctors, both of whom have been registered for more than 5 years, and one of whom must be a consultant. Two sets of tests are performed, although there is no set interval between them. In practice, they are usually done a few hours apart. There has never been a reported case of a patient who initially satisfied the criteria for brain stem death and who subsequently failed to do so. The tests aim to confirm the absence of brain stem reflexes and examine those cranial nerves which are amenable to testing.

II V VII VIII IX X

I: the first nerve (olfactory) cannot be tested. — II: the second nerve (optic), together with the parasympathetic constrictor outflow, is tested by pupillary responses to light (direct and consensual). Pupillary size is not important. — III, IV, VI: the third, fourth and sixth nerves (oculomotor, trochlear and abducens) are not tested.

V, VII: the fifth (trigeminal) and seventh (facial) nerves are tested first by the corneal reflex, and then by the response to painful stimuli applied to the face (supraorbital or infraorbital pressure), to the limbs (nail bed pressure) and to the trunk (sternal stimulation). It is because of the possibility of tetraplegia that a stimulus should be applied above the neck.

VIII: the eighth nerve (auditory/vestibular) is examined by caloric testing. It is important to establish that both drums are visible and intact, after which 30 ml of ice-cold water is instilled via a syringe. Nystagmus is absent if the patient is brain-dead. The assessment of doll’s eye movements, to test whether the eyes move with the head (which is abnormal) instead of maintaining central gaze, is not part of the brain stem death tests as performed in the UK.

IX, X: the ninth (glossopharyngeal) and tenth (vagus) nerves are tested by stimulating the pharynx, larynx and trachea. The patient should neither gag nor cough

the eleventh (accessory) and twelfth (hypoglossal) nerves are not tested.

after ventilation with 100% oxygen for 10 minutes, the patient is disconnected from the ventilator. Oxygen saturation is maintained thereafter by apnoeic oxygenation via a tracheal catheter. In the apnoeic patient, arterial CO2 rises at a rate of about 0.40–0.80 kPa per minute, depending on the metabolic rate, and so it may take some time to reach the arterial blood gas level of 6.65 kPa required by the testing criteria.

There are a number of lesions of the brain stem which may closely mimic irreversible brain death. These include severe Guillain–Barré + Miller–Fisher syndromes, Bickerstaff’s brain stem encephalitis ventral pontine infarction associated with the ‘locked-in syndrome’.

Brain stem encephalitis is characterized by acute progressive cranial nerve dysfunction associated with ataxia, coma and apnoea. There is no structural abnormality of the brain, but the picture is one of brain stem death. It is reversible.

Bilateral ventral pontine lesions may involve both corticospinal and corticobulbar tracts, leading to tetraplegia and the locked-in syndrome Patients are unable to speak or produce facial movements. They can usually blink and move their eyes vertically, and because the tegmentum of the pons is spared, they remain sensate, fully conscious and aware. It is the stuff of nightmares, and meaningful recovery from the locked-in syndrome is extremely rare.

Auditory, visual and somatosensory evoked potentials can be used, as can the EEG and cerebral angiography. None of these is required in the UK.

Clearly the potential donor organs must be oxygenated and well perfused, and this may require some haemodynamic manipulation. The problem arises with the question of ‘anaesthesia’. The legal time of death occurs when brain stem death is confirmed, and so logically a dead patient cannot require anaesthesia except perhaps for muscle relaxants to prevent spinal reflexes). There are, however, those who believe brain stem death testing to be little more than a pragmatic way of providing donor organs for transplant, and some anaesthetists appear to share enough residual unease about the process to make them give a general anaesthetic. The philosophical questions that this raises are interesting and important, but the clinical science oral is probably not the best place to explore them.

Pupillary signs: lateral herniation of the tentorium as a result of increased intracranial pressure (ICP) can compress the oculomotor (III) nerve with ipsilateral pupillary dilatation. This may also be accompanied by ptosis and motor paralysis of the extraocular muscles (apart from the superior oblique and lateral rectus muscles which are supplied by cranial IV + VI) Central tentorial herniation can cause miosis (due to diencephalic damage). If there is midbrain compression, the size of the pupils may remain in the mid-range, but they are unresponsive. Pinpoint and unreactive pupils may signify pontine haemorrhage.

Eye signs: raised ICP obstructs cerebrospinal fluid (CSF) flow in the optic nerve sheath with the development of papilloedema. The lateral rectus is also affected because of the displacement of the sixth cranial nerve (abducens) during its long intracranial course. (As it leaves the posterior margin of the pons, it is crossed by the anterior inferior cerebellar artery. Cerebellar displacement may cause compression of the nerve, paresis and failure of lateral gaze.)

Cranial nerves XIII and XIV: it is unlikely to come from the examiners, but they may well be impressed if you impart information about these two extra cranial nerves which have long been identified but which have not routinely been described in medical texts. (You could mention, e.g., that ‘cranial nerves XIII and XIV are of course not tested as part of brain stem function’.) The thirteenth cranial nerve, also known as Nerve Zero (because it lies more rostrally than the other cranial nerves) or the Nervus Terminalis, has its origins close to the olfactory bulb but is not part of it. It appears to mediate the release of luteinizing hormone and is thought therefore to have some role in the regulation of reproductive behaviour. This hypothesis is reinforced by its projections to septal nuclei and the preoptic areas of the brain, which in mammals are associated with sexual behaviour, including the response to pheromones.