Search

This review focuses on the potential application of hypothermia in adults suffering traumatic brain injury (TBI). Hypothermia is neuroprotective, reducing the damaging effects of trauma to the brain in a variety of experimental situations, such as brain ischemia and brain injury, but it has failed to demonstrate outcome improvement in a major controlled, randomized trial. The evidence for the use of hypothermia as a protective procedure is scarce and contradictory. However, evidence does suggest that hypothermia is effective in reducing intracranial hypertension after head injury. Since hypothermia has important side effects, further work is necessary before introducing this procedure into clinical practice for TBI.

Following traumatic brain injury, uncontrollable intracranial hypertension remains the most frequent cause of death. Despite general agreement on the deleterious effects of elevated intracranial pressure (ICP), however, the evidence supporting the use of ICP monitoring has recently been questioned. The aim of this review was to evaluate the pros and cons of ICP monitoring and to discuss the hypothetical desirability and feasibility of a trial testing the benefits of ICP monitoring.

Aim: The aim of this study was to evaluate the arterio-venous difference in carbon dioxide tension (DPCO2) and the ratio between DPCO2 and arterio-jugular oxygen difference (AJDO2) as indicators of compensated or uncompensated cerebral hypoperfusion., Methods: Cerebral blood flow (CBF) was reduced stepwise in 6 pigs by inducing intracranial hypertension with consequently cerebral perfusion pressure (CPP) reduction: CBF 100%, 50-60 % of baseline, 20-30% of baseline. Intracranial pressure (ICP), mean arterial pressure (MAP), CPP and CBF (laser-Doppler method) were continuously recorded. Superior sagittal sinus was punctured for the determination of AJDO2 and DPCO2., Results: CBF impairment was accompanied by changes in AJDO2 from 6.03 +/- 1.21 vol% to 7.32 +/- 1.30 vol%, up to 8.07 +/- 1.32 vol% (P < 0.01), in DPCO2 from 12.17 +/- 3.25 mmHg to 16 +/- 4.12 mmHg, up to 26.5 +/- 6.41 mmHg (P < 0.01), and DPCO2/AJDO2 ratio from 2.05 +/- 0.39 to 2.06 +/- 0.72 up to 3.41 +/- 1.09 in the 3 phases (P < 0.05)., Conclusions: When CBF declines AJDO2 increases, indicating greater extraction of O2 to satisfy aerobic metabolism. However, this mechanism can no longer compensate once a critical CBF threshold is reached. DPCO2 rises slowly during moderate CBF reduction because of defective washout; the rise is steeper during marked CBF impairment when anaerobic metabolism takes place. During cerebral hypoperfusion the venous blood gases and acid base variables mirror the degree of cerebral perfusion. In particular the DPCO2, and the DPCO2/ AJDO2 ratio may be useful markers of critical brain hypoperfusion.