Craniocerebral trauma--new pathophysiological and therapeutic viewpoints. 1: Management of the acute phase

Abstract

As there is only few evidence-based knowledge in the treatment of head trauma, the aim of this work was to demonstrate the close relationship between pathophysiology and clinical treatment modalities during the primary phase of head trauma. Review article. Cerebral hypoxia represents the main source of secondary brain injury. Depending on severity and duration, there results an irreversible brain damage. Under clinical conditions, the continuous monitoring of cerebral perfusion pressure (CPP) allows an estimation of the risk for cerebral hypoxia and the beginning of causal therapy. The priority of treatment lies in normalization of arterial O2 and increase in cerebral blood flow (CBF). In case of unchanged autoregulation of CBF, a decrease of CPP is followed by vasodilation with increase of cerebral blood volume (CBV) and a increase of CPP leads to a decrease of CBV by vasoconstriction. The usual shift of autoregulation on the right side after trauma requires CPP-values > 70 mmHg in the initial posttraumatic phase as there exists the most probable risk of hypoxia. The therapy of elevated ICP > 20 mmHg is oriented on CPP. A decrease in ICP under load of CPP has to be avoided. Beyond it, there is a need of origin of ICP-increase. The priority of initial treatment after head trauma lies in the individual optimization of CBF by maintenance of adequate CPP and cerebrovascular resistance. Afterwards, there will be performed a goal-directed treatment being based on the differentiation of the varying subgroups of head trauma and their related pathophysiology, what leads to the required treatment strategy. For this reason, it is necessary to put in the traditional treatment option by means of the multimodal monitoring as soon as possible.