Intracranial hypertension and cerebral ischemia after severe traumatic brain injury

Abstract

<jats:p>Arterial hypotension and intracranial hypertension are detrimental to the injured brain. Although artificial elevation of cerebral perfusion pressure (CPP) has been advocated as a means to maintain an adequate cerebral blood flow (CBF), the optimal CPP for the treatment of severe traumatic brain injury (TBI) remains unclear. In addition, CBF evolves significantly over time after TBI, and CBF may vary considerably in patient to patient. For these reasons, a more useful approach may be to consider the optimal CPP in an individual patient at any given time, rather than having an arbitrary goal applied uniformly to all patients. Important information for optimizing CBF is provided by monitoring intracranial pressure in combination with assessment of the adequacy of CBF by using global indicators (for example, jugular oximetry), supplemented when appropriate by local data, such as brain tissue oxygen tension.</jats:p>

Assessment of critical thresholds for cerebral perfusion pressure by performing bedside monitoring of cerebral energy metabolism

“…This threshold varies among different patients and different areas of the brain, and the penumbral zones surrounding focal brain lesions appear to be the most sensitive. 15,33,41 Thus, the optimal treatment protocol for patients with severe traumatic brain lesions and increased ICP probably differs among patients. In an individual patient, the preservation of normal cerebral energy metabolism within areas at risk during a decrease in CPP can be guaranteed by performing intracerebral microdialysis and bedside biochemical analyses.…”

“…15 Based on these experiences, it might seem logical both to restore circulating blood volume and to use vasopressors liberally to achieve a further increase in CPP. This idea has gained additional support from the (previously) generally accepted hypothesis that a pharmacologically induced increase in MABP effectively decreases ICP.…”

Biomarkers for the Diagnosis, Prognosis, and Evaluation of Treatment Efficacy for Traumatic Brain Injury

“…118 Elevated ICP can lead to further brain tissue damage via cerebral hypoperfusion, secondary ischemia, and brain tissue herniation, and may eventually result in death. 119 In a prospective study comparing the levels of C-tau between severe TBI and neurologic and non-neurologic controls, Zemlan et al 37 reported that serum C-tau levels could be used to differentiate those TBI patients with an ICP Ͻ30 mmHg from those with an ICP Ͼ30 mmHg. The serum levels of GFAP and S100B have also been proposed as markers capable of differentiating between TBI patients based on their ICP status.…”

Cerebral Blood Flow in Experimental and Clinical Neurotrauma: Quantitative Assessment

“…The most probable reason for it could be the reverse effect of changed levels of vasoactive agents due to impairment of cerebral autoregulation, or expressed production of vasoconstrictors. Clinical studies show the presence of vasospasm on days 7-9 (Hlatky et al, Robertson, 2003;Voulgaris et al, 2005) and it shows increased blood flow in the main arteries of the brain, Willis circle, whenever the microcirculation in cerebral cortex could be different and altered due to local conditions. Being an influent factor in outcomes of TBI, cortical perfusion is not the determinant of increased vulnerability of immature to neurotrauma.…”

“…Correlation between impaired flow and GCS and outcome on admission, was founded in another study in 121 patients with TBI (Chan et al, 1992). Experimental TBI investigations show reduced response of CBF to endogenous vasodilators as nitric oxide (NO) (Cherian et al, 2004;Hlatky et al, 2003). There are several investigations on Cerebral Blood Flow (CBF) in TBI.…”