Brain death

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Chapter 46 Brain death

Marcus Peck, Martin Smith

Most people die a ‘conventional’ death when their heart stops beating. In others the advent of intensive organ support has complicated the diagnosis of death. Patients who have sustained irreversible structural brain damage as a result of head injury, subarachnoid haemorrhage, stroke or cerebral anoxia lie in a deep coma without the capacity to breathe. Prompt medical attention may have taken over ventilation, but recovery is impossible. It therefore became necessary to reappraise death based on the integrity of the central nervous system.1–3 Brain death describes a state of irreversible loss of brain function, including loss of brainstem function. The ability to certify death under such circumstances allows intensivists to withdraw treatment on ethical, humanitarian and utilitarian grounds. Relatives are relieved of unnecessary prolonged anxiety and false hopes, and the burden on expensive medical resources is reduced. A further benefit for society is the availability of organs for transplantation from heart-beating donors.

DEFINITION OF DEATH

Three distinct mechanisms of death are recognised – cardiac arrest, respiratory arrest and brain death. This distinction is artificial. Cardiorespiratory arrest only results in inevitable death if the period of arrest has been long enough to result in irreversible damage to the brainstem due to lack of perfusion with oxygenated blood. Shorter periods of cardiac or respiratory arrest may result in survival with differing degrees of brain damage. As the neurones of the brainstem are the most resistant to anoxia, patients may retain the ability to breathe but survive with severe, irreversible cortical damage (the persistent vegetative state: PVS). The key feature of both cardiorespiratory death and brainstem death is irreparable brain damage. Death of the brainstem, whether caused by intracranial events or extracranial phenomena such as hypoxia, represents death of a person as a whole.

Dying is a process but death is an event that can be defined in a number of ways. In the UK there is no statutory definition of death, but English law has adopted widely accepted criteria and considers death to be the ‘the irreversible loss of the capacity for consciousness, combined with the irreversible loss of the capacity to breathe’. In Australia, for the purpose of organ harvest, the statutory definition is ‘irreversible cessation of all brain function’.

Brain death results from massive swelling of the traumatised brain, a sustained rise in intracranial pressure equal to or above systemic arterial pressure causing cessation of cerebral circulation, and brainstem herniation. The principal causes in adults are traumatic brain injury (50%), subarachnoid haemorrhage (30%) and severe hypoxic–ischaemic injury (20%). Complete and irreversible loss of brainstem function may also be seen in isolated brainstem injury without the typical features of herniation (e.g. brainstem infarction), which may or may not be accompanied by complete loss of hemispheric function.

PERSISTENT VEGETATIVE STATE

Severe brain damage is distinct from brain death. Comatose patients with severe brain damage may recover, albeit with varying degrees of disability, or remain in persistent coma. PVS is an irreversible condition in patients who have lost cortical activity. Coma has progressed to a state of wakefulness without detectable awareness and the patient is able to breathe spontaneously. PVS is therefore compatible with life if supportive care is provided. This is in contrast to brain death, where there is irreversible loss of the capacity to breathe and independent survival is impossible. PVS is not recognised as death in any jurisdiction and, in most, withdrawal of support to patients with PVS requires legal authority.

ROLE OF THE BRAINSTEM

There is sometimes a lack of clarity between brain death and brainstem death and this reflects differing diagnostic practices.4 In the USA the Uniform Determination of Death Act describes brain death as death of the whole brain and states: ‘an individual who has sustained irreversible cessation of all functions of the entire brain, including the brainstem, is dead’.5 This formulation is one of the most commonly applied worldwide and forms the basis of the legal status in many countries. A notable exception exists in the UK, where a brainstem-based definition of death is in place.2

The brainstem contains the cranial nerve nuclei and respiratory and cardiovascular control centres. It is also the conduit for all ascending and descending pathways that connect the cortex with the rest of the body and is an essential part of the reticulo-activating system (RAS). Awareness depends on the integrity of the RAS. The mechanism of loss of consciousness in brainstem death is related to disruption of the RAS. After onset of brainstem death, brainstem reflexes are lost sequentially in a craniocaudal direction. This process may take several hours to become complete but finally results in apnoea due to failure of the medulla oblongata. Because of the fundamental controlling role of the brainstem, myocardial and other systemic physiological functions deteriorate after the onset of brainstem death.6 Without cardiovascular support most patients confirmed as brain-dead progress to asystolic cardiac arrest within 24–48 hours.

Establishment of brain death criteria

Brain death was first described in 1959 by Mollaret and Goulon,7 two French physicians, who coined the phrase ‘coma dépassé’ (meaning literally a state beyond coma) to describe 23 unconscious apnoeic patients who had lost brainstem reflexes.

In 1968 an ad hoc committee of the Harvard Medical School defined irreversible coma, or brain death, as unresponsiveness and lack of receptivity, the absence of movement and breathing, the absence of brainstem reflexes and coma whose cause has been identified (the Harvard criteria).1 In the following year the committee indicated that brain death could be diagnosed on clinical grounds alone. This was affirmed in 1971 by two neurosurgeons (Mohandas and Chou) who described irreversible loss of brainstem function as the ‘point of no return’ (the Minnesota criteria).8 At this time it was reiterated that brain death could be diagnosed on clinical judgement alone, without the need for a confirmatory electroencephalogram (EEG), so long as certain aetiological preconditions were present.

In 1976 a memorandum from the Conference of Medical Colleges and their Faculties in the UK stated that ‘permanent functional death of the brainstem constitutes brain death’ and that this could be diagnosed clinically in the context of irremediable structural brain damage after certain specified conditions had been excluded.2 The memorandum established a set of guidelines and clinical tests for the diagnosis of brainstem death that became the foundation of practice worldwide. A subsequent memorandum in 1979 concluded that the identification of brain death means that the patient is dead, whether or not the function of some organs, such as the heart beat, is still maintained by artificial means. A further memorandum in 1983 made additional recommendations about the timing of the clinical tests and who should perform them. It also confirmed that there may be circumstances in which it is impossible or inappropriate to carry out every one of the tests and it is for the doctor at the bedside to decide when the patient is dead.

Simultaneously to the guidance being issued in the UK, other countries were formalising practice. In the USA, the 1981 Report to the President’s Commission confirmed the requirement for the irreversible cessation of brain and brainstem functions to diagnose death.5 Because death of the whole brain is diagnosed in the USA, this report recommended that confirmatory tests be used to support the clinical diagnosis and reduce the required time of observation.

CRITERIA FOR THE DIAGNOSIS OF BRAIN DEATH

Common to the determination of brain death in the UK and USA is the confirmation of the absence of clinical function of the brainstem, i.e. loss of consciousness, unresponsiveness, coma and loss of brainstem reflexes, including the capacity to breathe. The UK criteria form the basis of the clinical diagnosis of brain death in other countries and will be used as an exemplar of clinical testing. The diagnostic algorithm has three sequential but interdependent steps. Certain preconditions and exclusions must be fulfilled before clinical tests of brainstem function are performed.9

PRECONDITIONS

• The patient should be in apnoeic coma, i.e. unresponsive and dependent on mechanical ventilation.
• The patient’s condition must be due to structural brain damage that is consistent with the diagnosis of brainstem death.
• The underlying disorder that has led to this state must be established.

In all cases a cranial computed tomography (CT) scan and full neurological examination are essential. Establishing the causative diagnosis is relatively straightforward in the case of head injury or intracranial haemorrhage but may take longer in coma arising from hypoxia or other causes.

EXCLUSIONS

Reversible causes of coma must be excluded. These include:

• Alcohol intoxication or drug overdose. Drug history must be reviewed and, in case of any doubt, a toxicology screen obtained.
• The effects of therapeutic depressant drugs. Narcotics, hypnotics and tranquillisers are likely to have been administered in the period leading up to brain death. These can have lengthy and unpredictable elimination times, particularly in critically ill patients. The drug’s type, dose, pharmacokinetics, half-life and the presence of organ dysfunction are all factors that contribute to duration of effect. Adequate time must be allowed for the residual sedative effects of these drugs to be excluded and, in the absence of organ dysfunction, a period of 3–4 times the half-life of the drug is recommended. Most commonly used drugs are cleared within 10–12 hours. Measurement of plasma concentration of active drug or metabolite will indicate whether drug levels are below the usual therapeutic range. However, plasma concentration does not always correlate with therapeutic effect in critically ill brain-injured patients. The use of specific pharmacological antagonists may be used in certain circumstances.
• Residual action of neuromuscular-blocking agents. This must be excluded by confirmation of the absence of deep tendon reflexes or lack of response to peripheral nerve stimulation.
• Hypothermia. Extreme hypothermia (< 28°C) invariably results in depressed brainstem reflexes but higher temperatures (32–34°C) can also have effects on conscious level. Core temperature should be > 35°C prior to testing brainstem reflexes.
• Metabolic and endocrine disturbances. There must be no profound abnormality of serum urea and electrolytes, acid–base status or blood glucose.

• Serum sodium values < 115 mmol/l and > 160 mmol/l should be corrected prior to testing brainstem reflexes. Diabetes insipidus (DI) is a regular sequela of brain death and significant hypernatraemia is common. The 1998 UK Code of Practice allows differentiation between abnormalities which arise as a consequence of brainstem failure (e.g. hypernatraemia due to DI) from causative abnormalities of endocrine or biochemical function.9
• Blood glucose should be between 2 and 20 mmol/l.
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