الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Aneurysmal subarachnoid hemorrhage (SAH) is a worldwide health burden with high fatality and permanent disability rates.
Subarachnoid hemorrhage most commonly presents as a severe headache most often described by the patient as “This is the worst headache of my life. An SAH headache is most often associated with nausea, vomiting, neck rigidity, and photophobia.
There are many complications to SAH including Neurogenic Pulmonary Edema, myocardic complications and vasospasm.
Angiographic vasospasm-induced ischemia has been regarded as a target for therapeutic management of DCI, therefore a deep understanding of the Pathogenesis of Cerebral Vasospasm Following Aneurysmal Subarachnoid Hemorrhage is a mandatory in dealing with Delayed Cerebral Ischemia.
The severity of SAH is clinically assessed and graded using either the Hunt and Hess classification or the World Federation of Neurosurgeons Scale (WFNS).
The ultimate goal in the treatment of cerebral vasospasm after subarachnoid hemorrhage is to avoid DIND (Delayed ischemic neurological deficit) by reducing ICP, optimizing the rate of cerebral oxygen demand, and improving cerebral blood flow. Given these goals, early aneurysm treatment and ventriculostomy placement for patients with elevated intracranial pressure is a necessity. Early aneurysm treatment allows the treatment team to be more aggressive with further vasospasm treatment over the course of care.
During the period between April 2017 and May 2018, 120 patients presented with SAH due to a ruptured intracranial aneurysm to the neurosurgery department of Alexandria University Hospital. Among them 30 patients were fitting the criteria and had findings compatible with symptomatic cerebral vasospasm. Therefore, these patients underwent cerebral angiography for intra-arterial nimodipine treatment.
Informed consent was taken from every patient. Detailed history, complete neurological examinations were obtained from patients. Neuroimaging was obtained according to the situation.
In the neurosurgical intensive care unit, standard medical management included preventive, well-monitored hypertensive, hypervolemic, and hemodilution (triple-H) therapy maximized to the point of elevating systolic arterial pressure to 150 –170 mm Hg. Triple-H therapy was implemented upon admission. All patients received intravenous nimodipine (Nimotop, Bayer AG, Leverkusen, Germany) with a dose of 2 mg of nimodipine per hour by means of continuous infusion beginning when the diagnosis of aneurysmal SAH was established. This treatment was continued until the 21st day in patients developing vasospasm. The drug was temporarily suspended only if refractory hypotension developed.
Arterial blood pressure, central venous pressures were measured continuously in all patients.
Thirty endovascular treatments were performed in 30 patients (10 female, 20 male) aged 40– 63 years. Patients experienced symptomatic vasospasm from day 4 through day 15 after SAH (mean number of days after SAH, 7.3 days).
Vasospasm was assessed subjectively by two consultant’s neurosurgeons. Spasm was graded as mild when arterial narrowing was 25%, moderate when 25– 50% constriction was present and severe when narrowing was 50%.