[Evaluation of ischemic repercussions of intracranial hypertension]

Abstract

The main risk involved in severe intracranial hypertension is, the occurrence of cerebral ischaemia, either locally during herniation or globally as a consequence of reduced cerebral perfusion pressure (CPP). Neurological features of ischaemia occur at a late stage. A continuous monitoring of brain function with EEG or evoked potential techniques, while largely used in the operating room have not been so far fully evaluated in the intensive care setting. Therefore, ischaemic criteria based on the registration of haemodynamic or metabolic data are gaining importance in management of increased intracranial pressure (ICP). Transcranial Doppler of middle cerebral arteries allows at any time the detection of a decrease in brain perfusion. An increased pulsatility index has been repeatedly demonstrated to correlate with decreased CPP. From these reports, the lower limit of autoregulation in brain injured patients appears to be much higher (70 mmHg) than previously estimated (40 mmHg). However, therapies with a cerebral vasoconstrictor impact and associated vasospasm are to be considered for a correct interpretation of Doppler data. Moreover, as a reduced cerebral blood flow is not necessarily insufficient to meet metabolic requirements, a routine insight in cerebral oxygenation and lactate production must be available. Continuous monitoring of jugular blood oxyhaemoglobin saturation (SjO2) measures the reserve of oxygen extraction and a decrease in SjO2 below 50% is considered as to indicate an impending cerebral ischaemia. Indeed, critically reduced CPP under a 70 mmHg limit is reflected by venous desaturation episodes. Increased cerebral lactate production, routinely appraisable by serial measurements of [(a-v) lactate], may afford confirmation of an existing ischaemia. ICP and CPP monitoring remains the basis for intensive care surveillance during the phase of intracranial hypertension, with alarming settled at admitted critical values (ICP = 30 mmHg; CPP = 70 mmHg). As ischaemic threshold for cerebral blood flow may be different in patients and in normal experimental animals, the reliability of these critical values of ICP and CPP is uncertain. Therefore, transcranial Doppler, jugular metabolic monitoring and, as recently available, cortical tissue PO2 monitoring are mandatory for early detection and assessment of ischaemia.