Why and when to manage intracranial hypertension
The detrimental effects of intracranial hypertension (HICP, high intracranial pressure) are well documented [1, 2]. HICP can cause secondary brain injury and death, and therefore, intracranial pressure (ICP) elevations should be aggressively treated.
HICP has been classically defined as an ICP > 20 mmHg, and this threshold has been considered the trigger for treatment . Recent BTF guidelines have moved this threshold to 22 mmHg , grounded on a single-centre, retrospective study. This modification is trivial . As for many other treatment options in intensive care, a single threshold is debatable. In fact, recent evidence suggests that not a single value but the time spent over the threshold and its intensity, the so-called ICP dose, is more important . Moreover, Guiza demonstrated that not only higher values but also prolonged exposure to values below the classical threshold are associated with negative outcomes . In addition, if cerebral perfusion pressure (CPP, i.e. MAP-ICP) is critically low (< 50 mmHg), ICP is no longer a predictor for poor outcome and lower ICP values might be barely tolerated. On the contrary, ICP insults in the range 18–23 mmHg can be tolerated for a longer duration at higher CPPs. In my practice, the ICP alarm is set at 20 mmHg and low CPP alarm at 55 mmHg. This is a warning signal for nurses at the bedside. Before starting any treatments for high ICP, I consider both the intensity and duration of HICP. I am flexible with thresholds putting them in the clinical contest, considering also CPP. Short-lasting, low-intensity episodes (low ICP dose with normal CPP) are observed and not treated. On the contrary, higher ICP doses, progressively rising trends, or/and HICP impacting CPP require prompt treatment.