Fig. 1.
Neuromonitoring during severe intracranial hypertension in two traumatic brain-injured patients. On the left, ICP rises to 70 mm Hg over a period of 12 h and PRx was not significantly impaired prior to the increase in mean ICP. In addition, although PBTO2 decreased with increasing ICP, it did not reach severely hypoxic values even during the maximal mean ICP (PBTO2 ~ 20 mm Hg at ICP 60 mm Hg). On the right, ICP rises dramatically from below 20 mm Hg to over 60 mm Hg in the space of 10 h. This increase in ICP was associated with a fall in CPP, and brain tissue oxygenation. In this case, PRx was disturbed (> 0.25) even in the first 3 h, while ICP was under 20 mm Hg. Despite large increases in ICP over the last 5 h, pulse amplitude of ICP (yellow) shows little change. These two cases illustrate that refractory intracranial hypertension may have different neuromonitoring phenotypes. ICP intracranial pressure; AMP pulse amplitude of ICP; MAP mean arterial pressure; CPP cerebral perfusion pressure; PBTO2 brain tissue oxygenation; PRx pressure reactivity index; RAP index of cerebrospinal compensatory reserve