Aspects on Mechanisms, Treatment and Outcome in Severe Traumatic Brain Injury
Abstract: Traumatic brain injury (TBI) is a leading cause for mortality and morbidity worldwide. The primary injury has great impact on patient outcome and cannot be cured, but attentive neurointensive care (NIC) may reduce detrimental secondary brain injuries and is the focus of this thesis.Some patients with severe TBI develop dangerously high intracranial pressure (ICP). In paper I, we found that decompressive craniectomy was an efficient last-tier treatment of intracranial hypertension in an escalated management protocol also including barbiturates. Furthermore, the cerebral perfusion pressure (CPP) is a treatment target in TBI to avoid cerebral hypo-/hyperperfusion, but it does not take into account the cerebral blood flow (CBF) pressure autoregulatory status. In paper II, we found that intact CBF pressure autoregulation, particularly day 2 to 5, was significantly associated with favorable outcome and that keeping the absolute CPP close to autoregulatory (CPPopt)- rather than fixed CPP-thresholds correlated more strongly with favorable outcome. In paper III, ICP variability was found to be a predictor of favorable outcome, possibly as it partly reflects better regulation of CBF. TBI treatments ultimately aim to optimize cerebral energy metabolism. In paper IV and V, two physiological variables were separately evaluated in relation to cerebral energy metabolism in TBI, monitored with a microdialysis in the brain. In paper IV, mild hyperventilation (pCO2 4.0-4.5 kPa), a therapy to reduce ICP by cerebral vasoconstriction, was found to be more commonly employed when ICP was high, but tended to improve the CBF pressure autoregulation. There was no association between mild hyperventilation and worse cerebral energy metabolism, indicating that this level was safe and did not induce cerebral ischemia. In paper V, higher arterial glucose was associated with worse CBF pressure autoregulation, cerebral energy metabolic disturbances and worse clinical outcome. This indicates that arterial hyperglycemia could induce secondary brain injuries in TBI.Today, TBI patients are treated according to “one size fits all”-protocols. However, with better understanding of the pathophysiological mechanisms and the effects of TBI treatments by means of multimodality monitoring, we will be able to earlier detect and diagnose different pathological processes and evaluate the effects of treatments. This will help us give more individualized care to reduce secondary brain injuries and improve outcome for these patients.
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