Numerous studies report that increased ICP aggravates cerebral ischaemia ( 6– 9). Moreover, impaired cerebral microvascular system is responsible for secondary brain damage. Severe TBI contributes to reduced cerebrovascular reserve, affecting normal cerebral perfusion pressure (CPP 50–70 mmHg) and cerebral blood flow. TBI initiates a series of pathophysiological pathways that are responsible for systemic complications and decreased survival rate. Secondary brain lesions are represented by impaired cerebral blood flow, energy flow (glucose availability, mitochondrial dysfunction) or tissue oxygenation (hypoxia/ischaemia, impaired oxygen regulation, impaired microcirculation) ( 3– 5). TBI can cause cerebral lesions directly or indirectly because of side-effects and complications of post-traumatic brain injury. Severe polytrauma cases are often accompanied by traumatic brain injury (TBI). The most common as well as the most significant injuries found in patients with trauma are head, spinal, thoracic, abdominal, pelvic, extremity and soft tissue injuries ( 2– 5). Trauma patient requires complex therapeutic management because of multiple and severe injuries or because of their association with post-traumatic complications ( 1).
