Sir: I suggest that in their recent publication “Limitations of computed tomographic angiography in the diagnosis of brain death”, Quesnel et al. make a profound discovery [1]. They report that of 21 adults with brain death (BD) diagnosed by accepted clinical tests and confirmatory electroencephalogram, computed tomographic angiography (CT-a) confirmed BD in only 11 patients (52.4%; 95% CI 30.4–73.6) [1]. Similarly, Leclerc et al. found 7/15 (46%) of clinically brain-dead patients had blood flow in the major branches of the circle of Willis by CT-a [2]. Perhaps more telling, Combes et al. found that 13/43 (30%) of clinically brain-dead patients with absent conventional angiographic brain blood flow had persistent cerebral perfusion by CT-a [3]. The interpretation offered for these findings is that CT-a is not appropriate to confirm BD because of a lack of sensitivity for BD. This interpretation is problematic. A more obvious interpretation would be that current clinical and ancillary tests for BD are not specific. In other words, when a patient is declared brain-dead by currently accepted clinical tests, supplemented by electroencephalogram or angiography if required, it is still uncertain that their entire brain is dead. Other findings support this as the more likely explanation for the CT-a findings. For example, not all brain functions are lost when BD is declared. It is known that, in patients correctly diagnosed with BD, there is lack of diabetes insipidus in 50%; electroencephalogram activity, brainstem-evoked potential activity, brain blood flow, and lack of pathologic destruction of brain in 5–20%; and in some cases respiratory activity at a PaCO2 > 60 mmHg [4]. In one study, five of nine patients without clinical BD had no brain blood flow on radionuclide angiography (but did not undergo CT-a) [5]. Another report documents a case of BD with absent angiographic brain blood flow, but with radionuclide brain blood flow [6]. Alternative explanations offered, such as cerebral reperfusion after intracranial pressure falls, decompressing cranial fractures or shunts, extracranial herniation of intracranial vessels, and jugular vein reflux [7], are unlikely to explain the high proportion of brain-dead patients with early CT-a multiple arterial brain blood flow. Moreover, the suggestion that “intracranial pressure may be insufficient to completely stop cerebral perfusion” is likely correct [1]. This explanation however, does not solve the dilemma. Complete circulatory arrest to the brain due to absent cerebral perfusion pressure is the purported pathophysiology of BD, accounting for the suggestion that all critical functions of the brain are irreversibly absent when BD is diagnosed. The findings from CT-a suggest otherwise. References
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