How dead is a brain dead patient?

The conceptual argument behind brain death (a patient on the intensive care with catastrophic brain damage on mechanical ventilation) is to diagnose irreversible failure of the brain as a functional unit, i.e. ‘death’ as the ‘brain as a whole’ and not, as is conceptual in brain death, to diagnose the biological ‘death of the whole brain’. For the concept of brainstem death electrocerebral silence or insignificant residual electrocortical activity, as measured with an electroencephalography (EEG), as well as other confirmatory tests such as brain angiography, are irrelevant, as they are not for the concept of ‘whole brain death’. In brainstem death the structure that allows the brain to function as a unit, the brainstem is paramount, because consciousness and the hope to regain it are non-existent without an intact brainstem. The value of the EEG to confirm brain death remains a controversial issue, even in countries in which whole-brain death is mandatory for the diagnosis of brain death. We should realize that, even in the conceptual idea of whole brain death, the whole brain cannot be proven to be dead as assessed by any confirmatory test. Preserved hypothalamic function, in patients in apneic coma with a destroyed brain stem and electrocerebral silence, is present in approximately 25 percent of the cases. Even in ‘whole brain death’ the dead brainstem and the electrosilent cortex should be seen as a ‘pars pro toto’. So, why is the EEG of importance in the process of brain death determination? The EEG measures only activity of a small portion of cortical neurons. It is estimated that only ten percent of the cortical neurons are represented by EEG recordings. Therefore the assumption that the whole cortex is dead is unfunded and unproven.  Electroencephalographic activity after brainstem death and apnea is described in several cases. The neurologist Grigg reviewed the literature in 1987 and identified 24 cases of continuous electrocortical activity after brainstem death with apnea, additionally they themselves were able to add eleven new cases to this series. In patients with secondary brainstem death due to catastrophic supratentorial brain injury and in patients with primary catastrophical brainstem lesions, residual EEG activity is often recorded. Others found that in patients in deep apneic coma and brainstem death, residual activity is measured for as long as 48 hours.  Plum and Posner, in their landmark book ‘The diagnosis of stupor and coma’ state that “The EEG is particularly helpful in the evaluation of absence of cerebral hemisphere function, and it’s probably imperative to provide objective, very viable support to clinical appraisals when organ transplantation is being considered (in less demanding situations, however, it is doubtful that the experienced physician needs the EEG to tell him when the brain is dead)”.

Why is this residual electrocerebral activity of importance for the individual patient? When all known confounders (hypothermia, metabolic disturbances, drug intoxication, severe hypotension) are ruled out, and the patient is in a deep apneic coma with observable brainstem death, such an individual is not aware of him self or his environment and shall never be again. The residual EEG activity is, in these cases, nothing more than residual activity in a small part of the cerebral cortex above a dead brainstem. One may be more worried about the ‘alive’ hypothalamus than the residual electrocortical activity, as neuropathologic examination of brains from brain dead organ donors have showed widespread areas of normal to near-normal neuronal areas. Consequently, brain death is not, and should not be, synonymous with complete neuronal death of the entire brain. Paramount to all of these remarks is the fact that a functional brain stem is a condition sine qua non for consciousness and therefore that a totally destructed brain stem, as in brain stem death, is not compatible with an intact consciousness nor with even the slightest chance of regaining consciousness ever again.

Patients with the same clinical condition as in these cases, for example in the United Kingdom, are declared brainstem dead and organ donation can be performed. Apparently a patient can be dead in one country, but still alive in another, under the same circumstances.

As reasoned, the state of whole brain death is not equal with complete neuronal death, and a flat EEG may only serve to assure the physician, not to confirm whole brain death, because no confirmatory test exists with the ability to confirm complete neuronal death. Furthermore, it is reassuring that no single case report exists of a brainstem dead patient regaining consciousness. Residual electrocortical activity and insignificant flow observed in CT angiography have no meaning for prognosis and harm doing. These patients are as ‘dead’ as we think brain dead patients are.

It is noticeable that, in spite of the fact that in basilar artery occulusion only infarction of the posterior brain circulation is expected, sparing the anterior circulation including the cortex involved does not lead to persistent cortical activity. The fact that in spite of intact anterior flow to a part of the cerebral cortex, electrocortical silence did eventually occur in these cases of brainstem death supports our suggestion that EEG has no prognostic significance. Possible explanations for the cessation of electroencephalographic activity detected by EEG may involve obstruction hydrocephalus by swelling of the infarcted brainstem or cerebellum and the fact that the destruction of the ascending reticular activating system results in loss of cortical activity.

The world expert on brain death, professor Eelco Wijdicks states that ‘Confirmatory tests for brain death are residua from the earlier days of refining a clinical entity, now known as brain death. These ancillary tests are not accurate, not conclusive, not pertinent, and not warranted’. Brain death is a clinical state, unique for intensive care medicine, in which the patient is in a deep apneic coma with a clear cause and has no brainstem reflexes in the absence of confounders as intoxication, metabolic disturbances and hypothermia. We reason that this delay is unnecessary and gives rise to substantial financial and psychological burden, and may affect the quality of procured organs.

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