Delayed ischemic neurological deficit (DIND) and delayed cerebral infarction (DCI) are the most important postoperative risk factors for poor outcome after aneurysmal subarachnoid hemorrhage (SAH) . Aneurysmal SAH is associated with a total mortality of estimately 50% including patients who die before admission to a hospital. In spite of new diagnostic tools, modern intensive care therapy and early aneurysm occlusion, the in-hospital mortality has remained at 25%. Experimental and clinical data on the use of various neuroprotective agents and therapeutic measures after aneurysmal subarachnoid hemorrhage (SAH). While calcium antagonists have been used in the past and are still part of the standard treatment regimen in most departments involved in the treatment of SAH, other classes of drugs and various other methods have been tested for their potential to inhibit delayed ischemia after SAH. Early brain damage in the first minutes after rupture of an aneurysm cannot be treated or reversed, as it usually occurs outside hospital walls. Treatment can begin when emergency physicians or paramedics have the first contact with the patient. At first, only general measures of treatment can be undertaken like analgesic therapy, application of oxygen or sometimes intubation and mechanical ventilation. Free radicals are produced after SAH by a decay of leukocytes and by autooxidation of hemoglobin . The degradation of membrane proteins and lipids are the consequence of the free radical activity resulting in a damage of endothelial cells, smooth muscle cells and perivascular neurons.
Thomas Westermaier, Neuroprotective Treatment Strategies for Delayed Cerebral Ischemia after Subarachnoid Hemorrhage â Review of Literature and Future Prospects
Last date updated on June, 2014