Farid Salih1, Tobias Finger2, Peter Vajkoczy2, Stefan Wolf2. 1. Department of Neurology, Charité-Universitätsmedizin, Augustenburger Platz 1, 13353 Berlin, Germany. Electronic address: farid.salih@charite.de. 2. Department of Neurosurgery, Charité-Universitätsmedizin, Augustenburger Platz 1, 13353 Berlin, Germany.
Abstract
PURPOSE: Patients who received decompressive craniectomy (DC) are usually not regarded to qualify for brain death (BD) as intracranial pressure (ICP) is not assumed to reach levels critical enough to cause cerebral perfusion failure. Here we investigated the incidence of BD after DC and analyzed the pathophysiological mechanisms. MATERIALS AND METHODS: We searched our chart records of patients with DC for individuals who developed BD (2010-2016). We then analyzed the course of ICP and cerebral perfusion pressure (CPP) prior to BD and results from radiological tests that aim at demonstrating loss of cerebral perfusion in BD. RESULTS: BD was diagnosed in 12 of 164 (incidence 7.3%) patients (age=16-70years; male=7; mean longitudinal diameter: 136.2mm). Mean latency between DC and BD was 69.4h. Immediately after DC, mean ICP was 30.0mmHg (standard deviation±24.7mmHg), CPP was 56.8mmHg (±28.1). In the course to BD, ICP increased to 95.8mmHg (±16.1), CPP decreased to -9.9mmHg (±11.2). In patients in whom radiological methods were performed (n=5) loss of cerebral perfusion was demonstrated. CONCLUSIONS: Our study evidences that DC does not exclude BD. Even after DC, BD is preceded by a severely reduced CPP, supporting loss of cerebral perfusion as a critical step in BD pathophysiology.
PURPOSE:Patients who received decompressive craniectomy (DC) are usually not regarded to qualify for brain death (BD) as intracranial pressure (ICP) is not assumed to reach levels critical enough to cause cerebral perfusion failure. Here we investigated the incidence of BD after DC and analyzed the pathophysiological mechanisms. MATERIALS AND METHODS: We searched our chart records of patients with DC for individuals who developed BD (2010-2016). We then analyzed the course of ICP and cerebral perfusion pressure (CPP) prior to BD and results from radiological tests that aim at demonstrating loss of cerebral perfusion in BD. RESULTS: BD was diagnosed in 12 of 164 (incidence 7.3%) patients (age=16-70years; male=7; mean longitudinal diameter: 136.2mm). Mean latency between DC and BD was 69.4h. Immediately after DC, mean ICP was 30.0mmHg (standard deviation±24.7mmHg), CPP was 56.8mmHg (±28.1). In the course to BD, ICP increased to 95.8mmHg (±16.1), CPP decreased to -9.9mmHg (±11.2). In patients in whom radiological methods were performed (n=5) loss of cerebral perfusion was demonstrated. CONCLUSIONS: Our study evidences that DC does not exclude BD. Even after DC, BD is preceded by a severely reduced CPP, supporting loss of cerebral perfusion as a critical step in BD pathophysiology.
Authors: Marta Fedriga; Andras Czigler; Nathalie Nasr; Frederick A Zeiler; Soojin Park; Joseph Donnelly; Vasilios Papaioannou; Shirin K Frisvold; Stephan Wolf; Frank Rasulo; Marek Sykora; Peter Smielewski; Marek Czosnyka Journal: J Neurotrauma Date: 2021-01-12 Impact factor: 4.869