Brain tissue pO(2)-monitoring in comatose patients: Implications for therapy

Monitoring of brain tissue partial pressure of O-2 (ti-pO(2)) is a promising new technique that allows early detection of impending cerebral ischemia in brain-injured patients. The purpose of this study was to investigate the effects of standard therapeutic interventions used in the treatment of intracranial hypertension in comatose patients on cerebral oxygenation. In the neurosurgical intensive care unit ti-pO(2), arterial blood pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and jugular bulb oxygen saturation (SjvO(2)) were prospectively studied (0.1 Hz acquisition ratel in 23 comatose patients (21 with severe traumatic brain injury, 2 with intracerebral hematoma) during various treatment modalities: elevation of CPP with dopamine (n = 35), lowering of the head in = 22), induced arterial hypocapnia (n = 13), mannitol infusion (n = 16), and decompressive craniotomy (n = 1). Ischemic episodes ('IE'= ti-pO(2) < 10 mmHg for > 15 min) within the first week after the insult were always associated with unfavorable neurological outcome. Elevation oi CPP from 32 +/- 2 to 67 +/- 4 mmHg significantly improved ti-pO(2) by 62% (13 +/- 2 to 21 +/- 1 mmHg) and reduced ICP indicating intact cerebral autoregulation. Further raising CPP from 68 +/- 2 to 84 +/- 2 mmHg did not alter ti-pO(2). Mannitol-induced ICP reduction from 23 +/- 7 to 16 +/- 2 mmHg did not affect ti-pO(2), nor did lowering of the head from 30 degrees to 0 degrees. Hyperventilation from an endtidal pCO(2) of 29 +/- 3 to 21 +/- 3 mmHg normalized ICP and CPP, but significantly reduced ti-pO(2) from 31 +/- 2 to 14 +/- 13 mmHg. Decompressive craniotomy in a 15-year old patient with refractory intracranial hypertension instantly restored ti-pO(2). Based on the present data, our understanding of many interventions previously believed to improve brain oxygenation might have to be re-evaluated. A CPP > 60 mmHg emerges as the most important factor determining sufficient brain tissue pO(2). Any intervention used to further elevate CPP does not improve ti-pO(2), to the contrary, hyperventilation even bears the risk of inducing brain ischemia.