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Controversies about irreversible loss of brain functions and cerebral perfusion in brain death

We would like to thank the authors of the letters of Rady and Verheijde and Revuelto-Rey et al. for their interest and for sharing their thoughts. It is readily apparent that Drs Rady and Verheijde have major reservations about the concept of brain death [1]. They cite a few publications that, at first glance, seem to support this view. However, the neurophysiological data of Facco et al. [2] were obtained from a group of patients not all of whom were brain dead: some of the patients were under barbiturates – a fact that, e.g. under German recommendations, would be incompatible with examination for brain death. First, brain death is defined as the irreversible loss of all brain functions. Cerebral circulation arrest results in brain death. On the other hand, a minimally preserved cerebral perfusion does not challenge the concept of brain death. This has been shown previously in brain death, e.g. in patients who underwent hemicraniectomy [3]. Secondly, assessment of the cessation of intracranial circulation relies on intraarterial angiography, which probably has limited sensitivity in detecting very small amounts of blood entering the brain vasculature. Thirdly, at the time brain death was determined some of our patients showed a positive cerebral perfusion pressure (CPP) [4]. However, we are unable to define exactly the point in time at which brain death had occurred in our patients, nor do we have any information about intracranial pressure (ICP) and CPP at that time. It is possible that CPP could have been zero or even negative previously at the time when brain death occurred. Our data do not demonstrate evidence for secondary insults as postulated [4]. Our results showed a clear correlation between ICP and mean arterial pressure (MAP) during apnoea testing [4]. During apnoea testing pCO2 continuously increased until reaching a pCO2 of at least 60 mmHg. In contrast curves of ICP values were very variable. Figures for ICP, CPP and MAP of every single brain death examination can be seen as Supporting Information in the online version of our article. Therefore, it is unlikely that cerebral vasodilatation due to increasing pCO2 values leading to increased ICP occurs in brain dead patients, as suggested by Revuelto-Rey et al. [5]. Changes in the diameter of cerebral vessels have never been observed in studies using angiography or Doppler ultrasound. Furthermore, increase of ICP leads to the breakdown of the blood– brain barrier and cerebral autoregulation, resulting in an effect of MAP on ICP long before brain death occurs. In brain dead patients with cerebral circulation arrest there might be a direct effect of MAP on the intravasal cerebral blood column. In summary, we strongly reject the hypothesis that apnoea testing may lead to further cerebral damage.