ICH affects approximately 65,000 individuals in the United States and has higher rates of morbidity and mortality than do ischemic strokes of similar volume. Despite the advances in critical care management, treatment is usually supportive and the prognosis of these patients continues to be poor (85,86), perhaps due to the lack of a consensus for the appropriate management of ICH.
Development of new treatments is required to prevent deterioration of neurologic function after ICH. Potential therapies include prevention of hematoma expansion and limitation of secondary neuronal injury. Although a recent study suggests that the administration of recombinant activated factor VII reduces the growth of hemorrhage, reducing mortality and improving functional outcome, additional data is required to determine safety in patients at risk for thromboembolic disease (87).
The toxic effect of blood and blood products is well known; it induces BBB breakdown and edema formation after ICH. The effect of hematoma evacuation has been studied, and randomized trials have been conducted, but they failed to show clear benefit. A defined indication and more accurate timing for surgical intervention are needed.
At the cellular level, the development of therapies that reduce cerebral edema and neuronal damage may require a better understanding of the pathophysiologic sequence and mediators that produce secondary injuries. Possible therapeutic options for the future include the development of new neuroprotective agents or therapies that would inhibit inflammation, apoptosis, MMPs, or excitatory amino acids.
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