Neurointensive care of subarachnoid hemorrhage : Clinical and neurochemical aspects

Sammanfattning: Neurointensive care (NIC) has gained terrain in the treatment of patients with various acute cerebral conditions. It is based on the concept that an unfavorable clinical outcome, to a certain extent, results from all secondary ischemic insults sustained by the brain during the acute phase of the disease. This thesis covers a clinical longitudinal study of the consequences of the introduction of NIC for overall management and outcome of 873 patients with aneurysmal subarachnoid hemorrhage (SAH) over a 12-year period, and neurochemical phenomena monitored by intracerebral microdialysis (MD) in a subgroup of patients with serious SAH.Progressive awareness of the emergency nature of the disease with faster referral, increasing patient age and severity of neurological condition emerged with time. Management was characterized by a more aggressive approach with greater use of computerized tomography, angiography, artificial ventilation, ventriculostomy, pharmacological and surgical treatment in a NIC unit. The most striking results were a gradual reduction in mortality rate and improved clinical outcome, particularly in patients with Hunt and Hess Grades I to II SAH, and in those with intraventricular hemorrhage. The frequency of "talk and die" patients (conscious on admission who eventually died) also decreased dramatically. A pattern of focal ischemic perturbation with zero levels of glucose, increased lactate/pyruvate (L/P) ratios and glutamate concentrations was identified. Furthermore a presumably global cerebral hypermetabolism strongly associated with a good outcome was found. The detection of this favorable prognostic metabolic pattern may become a new important indication for MD in NIC. Different neurochemical profiles in neurologically similar patients may result from early events after the SAH. Therefore further implementation of ultra-early resuscitative measures and treatment may enhance the brain's capacity to react and cope with the extreme metabolic demands elicited by the SAH and thus promote neurological restoration.