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  • Pressure Is Only Part of the Story In Traumatic Brain Injured Patients; Focal Cerebral Blood Flow Goes To Zero In Some Patients With Adequate Cerebral Perfusion Pressure

    Final Number:
    169

    Authors:
    George Chovanes MD, FACS, FAANS; Rafael M Richards MD

    Study Design:
    Other

    Subject Category:

    Meeting: Congress of Neurological Surgeons 2013 Annual Meeting

    Introduction: The pathophysiology of traumatic brain injury (TBI) is still not clearly understood. Recently, a decompressive craniectomy trial (1) and a trial of intracranial pressure (ICP) treatment with ICP monitoring vs. no monitoring (2) failed to support the concept that increases in ICP are exclusively responsible for TBI mortality and morbidity. To analyze the role ICP, cerebral perfusion pressure (CPP= BP-ICP), and cerebral blood flow (CBF) play in head injury, we monitored brain injured patients' ICP, blood pressure (BP), CPP, and focal cerebral blood flow (fCBF), recording the real-time data for computer analysis.

    Methods: 20 patients with severe brain injury were monitored with recordings of ICP, BP, CPP, and fCBF every minute.17 patients had severe closed TBI, 1 gunshot wound, and 2 intracerebral hemorrhages. 13 patients lived (GCS 3-9, average 5), 7 died (GCS 3-7, average 5). Of the 7 patients who died, 5 had technically adequate recordings before and as death supervened. Graphs were prepared of time vs. CPP, ICP and fCBF and reviewed for the time course of fCBF deterioration vs. CPP elevation. If CPP obviously and substantially decreased before fCBF decreased, that was termed a pressure death. However, if CPP stayed adequate and fCBF still decreased to zero, that was termed a non-pressure death.

    Results: Three patients had a pressure death (Fig 1), and two patients had a non-pressure death (Fig 2).

    Conclusions: This may be the first real-time documentation of non-CPP dependent brain death as expressed by fCBF. There are pathologic processes in the injured brain that do not directly involve increases in ICP and decreases in CPP. Heretofore clinical treatment efforts in brain injury have focused on ICP: other mechanisms are also extant and should be further investigated so as to more successfully treat brain injury.

    Patient Care: It will increase awareness that intracranial pressure increases are only one pathophysiologic process involved with traumatic brain injury, and hence treatment has to address other factors as well.

    Learning Objectives: By the conclusion of this session, participants should be able to 1)Describe the limitations of an exclusive focus on intracranial pressure in traumatic brain injury 2) Discuss in small groups what other factors could be operative 3) Tentatively identify how those putative other factors could be treated to improve the prognosis of traumatic brain injury.

    References: 1. Decompressive Craniectomy in Diffuse Traumatic Brain Injury, Coooper, DJ et al, NEJM 2011; 364:1493-1502 2. A Trial of Intracranial-Pressure Monitoring in Traumatic Brain Injury, Chestnut, RM et al, NEJM 2012; 367:2471-2481

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