Transcranial Doppler for brain death after decompressive craniectomy: persistence of cerebral blood flow with flat EEG

Dear Editor, Brain death (BD) diagnosis is made based upon clinical criteria—unresponsive coma with absence of brainstem reflexes and persistent apnea—and upon neurophysiologic observation of persistent ‘‘flat EEG.’’ Cerebral circulatory arrest (CCA) must also be assessed with ‘‘ancillary tests,’’ e.g. conventional angiography, transcranial Doppler (TCD), and other neuroimaging techniques, in infants younger than 12 months, when EEG flattening may be related to sedative treatment, and in BD of uncertain origin [1]. CCA may indeed happen both when intracranial pressure (ICP) overrides mean arterial blood pressure (MAP) as well as in diseases affecting cerebral tissue at a cellular level, with ICP not exceeding MAP. TCD is a sensitive, specific, and noninvasive technique to detect CCA in BD by identifying specific patterns [2]. However, it may lead to false-negative results in cases of skull defects (decompressive craniectomy, external drains, and in infants), because in these cases the increase in ICP may partially be compensated for. For these reasons, we recently described the TCD modifications of the CCA patterns in infants with BD, confirming that CCA detection for BD confirmation should be done cautiously in these cases [3]. Here we describe the different TCD findings observed in two adults with BD who were subjected to decompressive craniectomy. Case 1 was a female, 62 years old, with intracerebral right temporo-parietal hemorrhage, middle cerebral artery aneurism rupture. She underwent large right frontotemporal craniectomy and presented with unresponsive coma and flat EEG (Fig. 1). TCD, performed under stable hemodynamic conditions (BP 140/70 mmHg), showed the typical CCA pattern. Short compression of the dural expansion induced a further reduction of the signal, promptly returning to the basal conditions at the end of compression (Fig. 1). Case 2 was female, 56 years old, with a small deep right basal ganglia hemorrhage and aneurysm of the right intracranial internal carotid artery. She was treated with an endovascular procedure. Following sedation withdrawal, 2 days after the procedure, she was conscious but agitated and uncooperative, and she was again sedated. TCD performed under stable hemodynamic conditions (BP 150/ 100 mmHg) (Fig. 2a) showed a very high-resistive pattern with diastolic reduction in both the middle cerebral arteries and expression of elevated ICP, confirmed by invasive