Abstract

In spite of great success in research severe traumatic brain injury (TBI) remains the most frequent cause for morbidity and mortality in the age < 45 years. The primary lesion emerges at the moment of trauma. Due to several pathophysiological mechanisms secondary lesions occur that enlarge size of contusions significantly. As a consequence of intracranial bleedings and brain edema intracranial pressure (ICP) increases and threaten the patient. Extent of severity (declared in Glasgow Coma Scale Score [GCS]), expansion and type of bleedings (acute and chronic subdural hemorrhage, epidural bleeding, contusion bleedings and intracerebral hemorrhage) determinate operative and conservative therapy as well as intensive care medicine. A specific feature represents frontobasal lesions that, apart of penetrating injuries, are treated interdisciplinary not before ICP is stable, brain edema declining and coagulation sufficient several days after trauma. A persisting rhinoliquorrhoe cause meningitis up to 85 % within 10 years. Patient with GCS < 8 have to be intubated and controlled ventilated. Basic monitoring does not differ from those of other patients treated at the intensive care ward (sufficient breathing [pO (2), pCO (2)], arterial blood pressure, CBC and coagulation parameters, fluid monitoring and nutrition). Additionally, ICP have to be measured and be treated corresponding to the algorithm of ICP treatment. Complementary, oxygen saturation of brain tissue (ptiO (2)), local cerebral blood flow (r-CBF) and cerebral metabolism (micro dialysis) can be measured. Just the combination of the single monitoring parameters gives evidence of the functional condition of the injured brain and relieved planning and performing of the appropriate therapy.

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