Brainstem death: Difference between revisions

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The clinical syndrome diagnosed by the prescribed bedside tests was conflated with brain death at that time but, while held to be an irrecoverable premortal state, it was not then confused with death itself.
The clinical syndrome diagnosed by the prescribed bedside tests was conflated with brain death at that time but, while held to be an irrecoverable premortal state, it was not then confused with death itself.
100% chance of death.
==Evolution of diagnostic criteria==
==Evolution of diagnostic criteria==

Revision as of 09:02, 24 November 2010

The brain stem

Brain stem death has been the criterion in use in the United Kingdom for declaring death on neurological grounds since 1979, the diagnostic criteria having been published by the Conference of Medical Royal Colleges in 1976[1] with advice from a sub-committee of the Transplant Advisory Panel.


The criteria were drafted in response to a perceived need for guidance in the management of deeply comatose patients with severe brain damage who were being kept alive by mechanical ventilators but showing no signs of recovery. The Conference sought “to establish diagnostic criteria of such rigour that on their fulfilment the mechanical ventilator can be switched off, in the secure knowledge that there is no possible chance of recovery”. The published criteria – negative responses to bedside tests of some reflexes with pathways through the brain stem and a specified challenge to the brain stem respiratory centre, with caveats about exclusion of endocrine influences, metabolic factors and drug effects - were held to be “sufficient to distinguish between those patients who retain the functional capacity to have a chance of even partial recovery and those where no such possibility exists”. Recognition of that state required the withdrawal of fruitless further artificial support so that death might be allowed to occur, thus “sparing relatives from the further emotional trauma of sterile hope”[1].

The clinical syndrome diagnosed by the prescribed bedside tests was conflated with brain death at that time but, while held to be an irrecoverable premortal state, it was not then confused with death itself.


100% chance of death.

Evolution of diagnostic criteria

In 1979, on the misunderstanding (later admitted) that its criteria diagnosed brain death – “the stage at which all functions of the brain have permanently and irreversibly ceased” – Conference promulgated its conclusion [2] that the identification of its defined syndrome “means that the patient is dead”. This basis for the diagnosis and certification of death enabled the procurement of so-called “cadaveric” organs for transplant from patients with living, functioning, bodies perfused by their still naturally beating hearts[3].

After two further meetings in 1981, Conference issued an easement of its ‘brain death’ – and therefore death – diagnostic protocol, saying : “There may be circumstances in which it is impossible or inappropriate to carry out every one of the tests. The criteria ….. give recommended guidelines rather than rigid rules and it is for the doctors at the bedside to decide when the patient is dead”[4].

Subsequent UK Department of Health Codes of Practice governing the procurement of organs from beating-heart donors[5][6] have required the prior certification of death on essentially similar guidelines.

In 1995, a Working Group of the Medical Royal Colleges[7] formally admitted the inappropriateness of the term ‘brain death’ as a description of the syndrome diagnosed by its criteria. It therefore suggested its replacement by the “more correct” term ‘brain stem death’. But it continued to support the diagnosis of death on those same criteria, although no longer claiming that there is no remaining brain function in patients so certified. Instead, it proposed a new definition of human death, viz. “irreversible loss of the capacity for consciousness, combined with irreversible loss of the capacity to breathe”, which it described as a “clinical state …. equivalent to the death of the individual”. That state was said to be produced by the irreversible cessation of brain stem function (brain stem death). Hence the diagnosis of death should continue on their ‘brain stem death’ criteria, albeit on this novel understanding of what death is – a concept not universally accepted, or even widely discussed.

Implicit in this claim, although never specifically stated or referenced, is the belief that elements of the brain stem are essential for the arousal of consciousness (see below), and that they are irreversibly and irreplaceably out of action when ‘brain stem death’ is diagnosed. Those elements cannot be directly tested. They can be held to be permanently functionless only by implication, i.e. if it can be shown that the whole of the brain stem is certainly dead. The purely bedside tests prescribed for the clinical diagnosis of ‘brain stem death’ lack the power to determine that state[8].

The UK ‘brain stem death’ standard for the diagnosis of death on neurological grounds ignores evidence of persisting life and function in other parts of the brain [6][8][9][10][11] and has never been accepted in the USA – where the irreversible cessation of function of the entire brain, specifically including the brain stem (‘whole brain death’), is required[12]. The US President’s Council on Bioethics has recently described the UK standard as “conceptually suspect” and “clinically dangerous”[13].


The formal rules for the diagnosis of ‘brain stem death’ – then called ‘brain death’ - were first published[1] in 1976. With only minor modifications, they have remained the basis on which death is diagnosed when the patient is identified as a beating-heart organ donor. The most recent revision of the Code of Practice governing that procedure[6] reaffirms the preconditions for its consideration. These are:

  1. There should be no doubt that the patient’s condition - deeply comatose, unresponsive and requiring artificial ventilation - is due to irreversible brain damage of known aetiology.
  2. There should be no evidence that this state is due to depressant drugs.
  3. Primary hypothermia as the cause of unconsciousness must have been excluded, and
  4. Potentially reversible circulatory, metabolic and endocrine disturbances likewise.
  5. Potentially reversible causes of apnoea (dependence on the ventilator), such as muscle relaxants and cervical cord injury, must be excluded.

With these pre-conditions satisfied, the definitive criteria are:

  1. Fixed pupils which do not respond to sharp changes in the intensity of incident light.
  2. No corneal reflex.
  3. Absent oculo-vestibular reflexes – no eye movements following the slow injection of at least 50ml of ice-cold water into each ear in turn (the caloric test).
  4. No response to supraorbital pressure.
  5. No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation.
  6. No observed respiratory effort in response to disconnection of the ventilator for long enough (typically 5 minutes) to ensure elevation of the arterial partial pressure of carbon dioxide to at least 6.0 kPa (6.5 kPa in patients with chronic carbon dioxide retention). Adequate oxygenation is ensured by pre-oxygenation and diffusion oxygenation during the disconnection (so the brain stem respiratory centre is not challenged by the ultimate, anoxic, drive stimulus). It should be noted this is a dangerous - potentially lethal – test[14][15].

Unlike an earlier (1959) protocol for the diagnosis of a stage in the management of comatose patients at which further life-support is fruitless[16], the UK Code of Practice requires no evidence that the brain stem (medullary) centres controlling heart-rate and blood pressure have ceased to function.

Two doctors, of specified status and experience, are required to act together to diagnose death on these criteria and the tests must be repeated after “a short period of time … to allow return of the patient’s arterial blood gases and baseline parameters to the pre-test state”. These criteria for the diagnosis of death are not applicable to infants below the age of two months.

Prognosis and Management

With due regard for the cause of the coma, and the rapidity of its onset, testing for the purpose of diagnosing death on ‘brain stem death’ grounds should be delayed beyond the stage where brain stem reflexes may be absent only temporarily – because the cerebral blood flow is inadequate to support synaptic function although there is still sufficient blood flow to keep brain cells alive[14] and capable of recovery. There has recently been renewed interest in the possibility of neuronal protection during this phase by use of moderate hypothermia[15], and by correction of the neuroendocrine abnormalities commonly seen in this early stage[17].

Published studies of patients meeting the criteria for ’brain stem death’ or ‘whole brain death’ – the American standard which includes ‘brain stem death’ diagnosed by similar means – record the persistence of cardiac function for only a few hours or days if ventilation is continued after diagnosis[18]. However, there have been some very long-term survivals[19] and it is noteworthy that expert management can maintain the bodily functions of pregnant ‘brain dead’ women for long enough to bring them to term[20].

It is unlikely that there will be further studies of survival after diagnosis of ‘brain stem death’, mechanical ventilation and other life-support measures being continued, because the diagnosis is not sought unless it is the intention (a) to use the patient as an organ donor if the criteria are satisfied, or (b) to leave the ventilator disconnected if there is no spontaneous respiratory effort during the (second) apnoea test – the last test of the prescribed series. In both cases the patient dies. The prognosis of imminent death on satisfaction of the ‘brain stem death’ criteria is therefore self-fulfilling.

The official UK prognosis[6] is that, if support is continued after diagnosis, “both adults and children will ultimately suffer cessation of heartbeat … often within a few days, but (it) may take weeks or even months if aggressive support is maintained, although there are no verified reports of patients recovering brain-stem function during this time”.

The management of patients pronounced dead on meeting the ‘brain stem death’ criteria depends upon the reason for diagnosing death on that basis. If the patient is to be used as an organ donor, the ventilator is reconnected and life-support measures are continued, perhaps intensified, with the addition of procedures designed to protect the wanted organs until they can be removed. If it is the intention to allow the patient to die, with as much dignity and as little distress to all concerned as may still be possible, the ventilator is left disconnected on confirmation of the lack of respiratory centre response (the last test). In the second case, the diagnostic procedure may be less rigorous, e.g. omission of the caloric test which could be intensely, and unnecessarily, distressing if there might be any remaining degree of sentience.

Controversial aspects

The stated purpose for the promulgation, in 1976, of official criteria[1] for the diagnosis of ‘brain stem death’ – confused with brain death at that time – was to aid the identification of a stage in the management of comatose, mortally brain damaged, ventilator dependent, patients at which it is pointless and unkind to continue life-support measures (particularly mechanical ventilation) which could then be seen as thwarting and prolonging the dying process. Those formal guidelines for the diagnosis of a clinical syndrome to which an inevitably fatal prognosis attached – death within a few hours or days, whatever was done – were welcomed as providing a consensus basis for discontinuation of otiose therapy. They could also have offered protection against litigation, although this was never a serious threat in the UK[21].

It may be that, after unwarranted and ultimately unsuccessful attempts to put those criteria to a different use, viz. the diagnosis of death for transplant purposes, they will find their proper place as prognostic guidelines once again.

There was no sound scientific or philosophical basis for the equation of ‘brain stem death’ with death in 1979[22][23][24]. It clearly confused a prognosis of death with death itself. It assumed the acceptance of brain death as human death – still a highly controversial issue[10][11][13] – and implicitly claimed that its simple bedside tests could, unaided by the more sensitive diagnostic techniques available even then, reliably establish the permanent cessation of all brain functions. The speciousness of that claim was admitted[25] by one of the protagonists of the ‘brain stem death’ criterion in 1985 and Conference finally abandoned it[7] in 1995. Since that time there has been no formal basis for the diagnosis of brain death in the UK[24].

Having failed to establish ‘brain stem death’ as a valid basis for the diagnosis of death on that false premise, Conference “suggested” a novel redefinition of death based on the supposedly quintessential functions of the brain stem, viz. permanent loss of the capacity for consciousness and of the ability to breathe[7]. That definition of human death remains the basis upon which the ‘brain stem death’ syndrome is equated with death in the UK today[6]. It is not accepted in the USA[13]. It is not unequivocally satisfied by the clinical criteria for ‘brain stem death’ as originally and more recently specified[8].


Sound scientific support is lacking for the claim that the specified purely bedside tests have the power to diagnose true and total death of the brain stem[8], the necessary condition for the assumption of permanent loss of the intrinsically untestable consciousness-arousal function of those elements of the reticular formation which lie within the brain stem (there are elements also within the higher brain). Knowledge of this arousal system is based upon the findings from animal experiments[26][27][28] as illuminated by pathological studies in man[29]. The current neurological consensus is that the arousal of consciousness depends upon reticular components which reside in the midbrain, diencephalon and pons[30][31]. It is said that the midbrain reticular formation may be viewed as a driving centre for the higher structures, loss of which produces a state in which the cortex appears (on the basis of electroencephalographic studies) to be awaiting the command or ability to function. The rôle of diencephalic (higher brain) involvement is stated to be uncertain and we are reminded that the arousal system is best regarded as a physiological rather than a precise anatomical entity[30]. There should, perhaps, also be a caveat about possible arousal mechanisms involving the first and second cranial nerves (serving sight and smell) which are not tested when diagnosing ‘brain stem death’ but which were described in cats in 1935 and 1938[26]. There is also concern about the permanence of consciousness loss, based on studies in cats, dogs and monkeys which recovered consciousness days or weeks after being rendered comatose by brain stem ablation and on human studies of brain stem stroke raising thoughts about the “plasticity” of the nervous system[29]. Other theories of consciousness place more stress on the thalamocortical system[32]. Perhaps the most objective statement to be made is that consciousness is not currently understood. That being so, proper caution must be exercised in accepting a diagnosis of its permanent loss before all cerebral blood flow has permanently ceased.


The ability to breathe spontaneously depends upon functioning elements in the medulla – the ‘respiratory centre’. In establishing a diagnosis of ‘brain stem death’ this centre is challenged with the strong stimulus offered by an unusually high concentration of carbon dioxide in the arterial blood. But it is not challenged by the more powerful drive stimulus provided by anoxia – although the effect of that ultimate stimulus is sometimes seen after final disconnection of the ventilator in the form of agonal gasps.


Neither requirement of the UK Health Department’s Code of Practice basis for the equation of ‘brain stem death’ with death is satisfied by its current diagnostic protocol[6]. And in terms of its ability to diagnose de facto brain stem death it falls far short. No testing of testable brain stem functions such as oesophageal and cardiovascular regulation is specified. There is published evidence[33][34][35] strongly suggestive of the persistence of brain stem blood pressure control in organ donors.


  1. ^ a b c d Conference of Medical Royal Colleges and their Faculties in the UK. Diagnosis of brain death. British Medical Journal 1976;2:1187-8
  2. ^ Conference of Medical Royal Colleges and their Faculties in the UK. Memorandum on the diagnosis of death. British Medical Journal 1979;1:332
  3. ^ Cadaveric organs for transplantation - a Code of Practice including the diagnosis of brain death. UK Department of Health, February 1983
  4. ^ Robson JG. Brain death (in Cadaveric organs for transplantation, above, pp.38-9)
  5. ^ A Code of Practice for the diagnosis of brain stem death. UK Department of Health, March 1998
  6. ^ a b c d e f A Code of Practice for the Diagnosis and Confirmation of Death. Academy of Medical Royal Colleges (70 Wimpole Street, London, W1G 8AX), October 2008
  7. ^ a b c Conference of Medical Royal Colleges and their Faculties in the UK. Criteria for the diagnosis of brain stem death. Journal of the Royal College of Physicians of London 1995;29:381-2
  8. ^ a b c d Evans DW, Hill DJ. The brain stems of organ donors are not dead. Catholic Medical Quarterly 1989;40:113-121
  9. ^ Hill DJ. Brain death . A United Kingdom anaesthetist’s view. In Finis Vitae. Is brain death still life? Ed. De Mattei R. 2006 (see below), 147-59
  10. ^ a b Beyond brain death - the case against brain based criteria for human death. Eds. Potts M, Byrne PA, Nilges RG. Kluwer Academic Publishers, Dordrecht, 2000
  11. ^ a b Finis vitae - is brain death still life? Ed. de Mattei R. National Research Council of Italy, Rubbettino Editore, 88049 Soveria Mannelli (Catanzaro), 2006
  12. ^ Guidelines for the determination of death. Report of the medical consultants on the diagnosis of death to the President’s Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioural Research. JAMA 1981;246:2184-86
  13. ^ a b c Controversies in the Determination of Death : a White Paper by the President's Council on Bioethics. Washington, DC December 2008.
  14. ^ a b Coimbra CG. Implications of ischemic penumbra for the diagnosis of brain death. Brazilian Journal of Medical and Biological Research 1999;32:1479-87
  15. ^ a b Coimbra CG. The apnoea test – a bedside lethal ‘disaster’ to avoid a legal ‘disaster’ in the operating room. In Finis Vitae – is brain death still life? pp.113-145
  16. ^ Mollaret P, Goulon M. Le coma dépassé. Revue Neurologique 1959;101:3-15
  17. ^ Coimbra CG. Hypopituitarism in brain death. In preparation
  18. ^ Pallis C, Harley DH. ABC of brain stem death. BMJ Publishing Group, 1996, p.30
  19. ^ Shewmon DA. ‘Brain body’ disconnection : implications for the theoretical basis of ‘brain death’. In Finis Vitae – is brain death still life? pp. 211-250
  20. ^ Powner DJ, Bernstein IM. Extended somatic support for pregnant women after brain death. Crit Care Med 2003;31:1241-49
  21. ^ Skegg PDG. Law, ethics, and medicine. Studies in medical law. OUP (New York), 1984
  22. ^ Evans DW, Lum LC. Cardiac transplantation. Lancet 1980;1:933-4
  23. ^ Evans DW, Lum LC. Brain death. Lancet 1980;2:1022
  24. ^ a b Evans DW. The demise of ‘brain death’ in Britain. In Beyond brain death – the case against brain based criteria for human death pp. 139-158
  25. ^ Pallis C. Defining death. BMJ 1985;291:666
  26. ^ a b Moruzzi G, Magoun HW. Brain stem reticular formation and activation of the EEG. Electroencephalog Clin neurophysiol 1949;1:455-73
  27. ^ Ward AA. The relationship between the bulbar-reticular suppressor region and the EEG. Clin Neurophysiol 1949;1:120
  28. ^ Lindsley DB et al. Effect upon the EEG of acute injury to the brain stem activating system. EEG Clin Neurophysiol 1949;1:475-8627
  29. ^ a b Parvizi J, Damasio AR. Neuroanatomical correlates of brainstem coma. Brain 2003;126:1524-36
  30. ^ a b Textbook of clinical neurology, 2nd Edn. Ed. Goetz CG. Elsevier Science, 2003
  31. ^ Bleck TP. In Textbook of clinical neurology, 3rd Edn. Ed. Goetz CG. Elsevier Science, 2007
  32. ^ Tononi G. An information integration theory of consciousness. BMC Neuroscience 2004;5:42
  33. ^ Hall GM et al. Hypothalamic-pituitary function in the ‘brain dead’ patient. Lancet 1980;2:1259
  34. ^ Wetzel RC et al. Hemodynamic responses in brain dead organ donor patients. Anesthesia and Analgesia 1985;64:125-8
  35. ^ Pennefather SH, Dark JH, Bullock RE. Haemodynamic responses to surgery in brain-dead organ donors. Anaesthesia 1993;48:1034-38