Intracranial pressure and cerebral perfusion pressure in patients developing brain death

• Published in: Journal of critical care Vol. 34; pp. 1 - 6
• Main Authors: Salih, Farid, MD, Holtkamp, Martin, MD, Brandt, Stephan A., MD, Hoffmann, Olaf, MD, Masuhr, Florian, MD, Schreiber, Stephan, MD, Weissinger, Florian, MD, Vajkoczy, Peter, MD, Wolf, Stefan, MD
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.08.2016; Elsevier Limited
• Subjects: Adolescent; Adult; Aged; Biomarkers; Blood; Blood Pressure - physiology; Brain - blood supply; Brain death; Brain Death - physiopathology; Brain Injuries - physiopathology; Cerebral perfusion pressure; Cerebrovascular Circulation - physiology; Coma; Critical Care; Critical closing pressure; Disease; Electroencephalography; Female; Glasgow Coma Scale; Humans; Intensive care; Intracranial pressure; Intracranial Pressure - physiology; Male; Middle Aged; Physiology; Predictive Value of Tests; Retrospective Studies; Traumatic brain injury; Young Adult; critical closing pressure; intracranial pressure; Brain death; cerebral perfusion pressure; Critical closing pressure; Intracranial pressure; Cerebral perfusion pressure
• ISSN: 0883-9441; 1557-8615
• DOI: 10.1016/j.jcrc.2016.03.009

Abstract Purpose We investigated whether a critical rise of intracranial pressure (ICP) leading to a loss of cerebral perfusion pressure (CPP) could serve as a surrogate marker of brain death (BD). Materials and Methods We retrospectively analyzed ICP and CPP of patients in whom BD was diagnosed (n = 32, 16–79 years). ICP and CPP were recorded using parenchymal (n = 27) and ventricular probes (n = 5). Data was analyzed from admission until BD was diagnosed. Results ICP was severely elevated (mean ± SD, 95.5 ± 9.8 mmHg) in all patients when BD was diagnosed. In 28 patients, CPP was negative at the time of diagnosis (− 8.2 ± 6.5 mmHg). In four patients (12.5%), CPP was reduced but not negative. In these patients, minimal CPP was 4–18 mmHg. In one patient, loss of CPP occurred 4 hours before apnea completed the BD syndrome. Conclusions BD was universally preceded by a severe reduction of CPP, supporting loss of cerebral perfusion as a critical step in BD development. Our data shows that a negative CPP is neither sufficient nor a prerequisite to diagnose BD. In BD cases with positive CPP we speculate that arterial blood pressure dropped below a critical closing pressure, thereby causing cessation of cerebral blood flow.