|Title:||Can Cerebral Hypoperfusion after Sympathetic Used to Diagnose Brain Death ? A Retrospective Traumatic Brain Injury Patients||Authors:||CHAI, CHUNG LIANG
|Keywords:||brain death;sympathetic storm;irreversible apneic coma;traumatic brain injury||Issue Date:||2008||Journal Volume:||v.64||Journal Issue:||697||Start page/Pages:||-||Source:||JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE||Abstract:||
Background: The aim of this study was to identify the precise time of occurrence of irreversible coma from brain stem dysfunction that precedes brain death. Sympathetic storm, which is a cardiovascular hyperdynamic state manifested by brain stem ischemia, is known to be related to brain stem failure in animal models. We studied sympathetic storm in the clinical setting and compared the clinical findings observed before and after sympathetic storm to identify the precise time of occurrence of irreversible apneic coma. Methods: We conducted a retrospective study of 15 comatose traumatic brain injury adult patients at the National Taiwan University Hospital's Neurosurgical Intensive Care Unit. Data on arterial blood pressure, heart rate, intracranial pressure, and clinical findings such as cerebral blood flow pattern, Glasgow Coma Scale, brain stem reflexes, utilizations of catecholamines, and occurrence of central diabetes insipidus throughout the course in the intensive care unit were collected retrospectively from medical records. Results: Prolonged uncorrectable cerebral hypoperfusion was found after a characteristic irreversible apneic coma-associated sympathetic storm (IACASS) in all 15 patients. A mean cerebral perfusion pressure of 11.9 mm Hg + /- 10.3 mm Hg and 13 mm Hg +/- 3.5 mm Hg remained at 12 hours and 24 hours, respectively, after IACASS. Differences in clinical findings before and after IACASS that were statistically significant were cerebral circulation pattern( p = 0.0455), Glasgow Coma Scale (p = 0.0143), brain stem reflexes (p = 0.0143), utilization of catecholamines (p = 0. 0254), and occurrence of central diabetes insipidus (p = 0. 00468). Conclusions: Coma might have become irreversible immediately after IACASS because the prolonged duration of cerebral hypoperfusion could have caused irreversible cerebral tissue injury. Our study provides some preliminary findings suggesting that IACASS may be a predictor of impending brain death. A prospective study is the next step to understanding whether this phenomenon can be applied clinically to diagnose irreversible apneic coma.
|Appears in Collections:||醫學系|
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