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Brainstem or entire brain-based declaration of death: is there a difference?
  1. Panayiotis N Varelas
  1. Correspondence to Dr Panayiotis N Varelas, Departments of Neurology and Neurosurgery, Henry Ford Hospital, K-11, 2799 West Grand Blvd, Detroit MI 48202, USA; varelas{at}neuro.hfh.edu

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In this issue of Practical Neurology, Cameron et al, review in detail the confirmation of brainstem death process in the UK. The diagnosis of non-cardiorespiratory death is defined as irreversible cessation of all brainstem function, and, with certain caveats as described in the Academy of Medical Royal Colleges1; this is considered to be death. The assessment is based on: (1) the identification of a cause for irreversible brainstem function loss, (2) exclusion of potential confounders, (3) testing of brainstem reflexes as a proxy for residual brainstem function and (4) completion of the apnoea test. In cases where there is any doubt about the diagnosis or parts of the evaluation cannot be completed, ancillary tests are also performed.

In the USA, the definition is that the entire brain function should have irreversibly ceased rather than just that of the brainstem. In most states, brain death is determined according to ‘accepted medical standards’, which downstream translates practically to following the American Academy of Neurology (AAN) guidelines2 in most hospital policies. These describe a pretty similar approach to the one followed in the UK, with few procedural differences beyond the entire brain death versus brainstem death divide: in the UK, two physicians who are both present and observing each other, perform sequentially the brainstem death testing, with the apnoea tested twice. Within most US state laws, a single examination with one apnoea test is sufficient. Temperature should be >34°C in the UK, 36°C (again per AAN guidelines). Specific serum electrolyte and glucose concentrations that preclude testing in the UK are mentioned, but not in the AAN guidelines. In the UK, there is no absolute PaCO2 level of 8 kPa (60 mm Hg) to be reached during apnoea. Rather the process is: (1) to disconnect the patient from the ventilator after reducing the minute ventilation and reaching a starting PaCO2 level of 6 kPa (45 mm Hg); (2) to observe the patient for 5 min for signs of ventilatory effort and (3) to recheck arterial blood gases to prove that a 0.5 kPa (3.75 mm Hg) rise has occurred.

Beyond these procedural differences, which are also encountered across the New World among states and hospitals,3 questions arise: do the different approaches produce different outcomes? Is one better than the other at excluding false positives, that is, at avoiding declaring somebody dead who is not? To answer this question, one needs to have a deeper understanding of how the entire brain, or the brainstem, irreversibly ceases functioning.

There are three different ways in which the brainstem may cease functioning. The first is when a supratentorial lesion or injury is so severe and widespread that it gradually leads to transtentorial herniation with compression of the upper brainstem, followed eventually by complete rostrocaudal herniation and medullary function loss, including breathing. These are patients with massive strokes, cerebral oedema or severe trauma. There is no question that in the end they have lost both supratentorial and infratentorial function and will meet both US and UK criteria.

The second way is when both supratentorial brain and brainstem irreversibly lose function at the same time, as after cardiac arrest, without necessarily developing massive cerebral oedema and central herniation. Again there should be a transatlantic agreement for those cases too.

There is a small minority of patients, however, who have a massive primary injury to the brainstem, for example, from basilar artery thrombosis or large brainstem or cerebellar bleed. These patients clinically meet brain death criteria and could be pronounced as such in the UK. In the USA, though, they do not. Although in deep coma, they do retain blood flow and even electroencephalographic activity, which may arguably be surrogate markers of potential residual consciousness in specific cases, though importantly this has never been proven. This leaves the question whether patients with this type of brainstem injury might regain function or consciousness of some type? In an eloquent paper in Brain,4 Eelco Wijdicks, the leading brain death expert of our time, discussed the history of the transatlantic divide and the unsuccessful search to identify patients who fulfilled brainstem death but who survived. He concluded there was no difference in clinical practice despite the differing conceptual backgrounds. It remains possible, in theory, with modern intensive care unit support that some patients with primary brainstem destruction might recover despite fulfilling criteria for brainstem death, even though there are no such cases reported to date. A prospective study in the USA using a registry to collect all these rare, but very important patients, could answer this question; this in turn would allow the development of common diagnostic standard and standardised international code of practice.

References

Footnotes

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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