Subarachnoid hemorrhage (SAH) is a clinical phenomenon caused by the abrupt rupture and bleeding of blood vessels at the surface or base of the brain, which can occur for a number of reasons. As a result, the subarachnoid membrane receives direct blood flow. SAH is a debilitating neurological disorder with high morbidity and mortality. Despite advancements in medicine and surgical care, patients who survive their first bleeding event are at high risk for secondary sequelae, including delayed cerebral ischemia (DCI) and cerebral vasospasm (CV)
CV denotes a temporary, self-resolving constriction of the intracranial arteries that occurs several days after an SAH. This phenomenon is closely linked to clinical deterioration resulting from DCI, affecting up to 30% to 40% of patients. DCI is a significant clinical event that typically manifests 3 to 14 days after the initial bleeding and is characterized by subsequent neurological deterioration. These complications can lead to poor functional outcomes and long-term disability
Subarachnoid hemorrhage is classified into aneurysmal subarachnoid hemorrhage (aSAH) and Traumatic SAH (tSAH). TSAH has been described as an adverse prognostic factor leading to progressive neurological deterioration and increased morbidity and mortality. Traumatic subarachnoid hemorrhage is caused by head injuries from events like falls, motor vehicle crashes, and blows to the head, which damage blood vessels within the skull. The injury itself is the primary cause, leading to the brain being hit against the skull and tearing these blood vessels
Patients aged between eighteen to sixty five years Diagnosed with tSAH on Head Computed Tomography(CT)within 24 hours of trauma.
Both Genders are included Indication for endovascular or microsurgical treatment plan
Aneurysmal or spontaneous SAH Sever hepatic dysfunction.
Known hypersensitivity to magnesium sulfate
Renal disease with glomerular filtration rate<15 ml/min.
pregnancy
Parallel
Magnesium Sulfate 10 MG/ML
DrugAs a rule, MgSO4 will be given(for group A) within 24 hours after establishing a diagnosis of tSAH. The protocol will include MgSO4 10% application with a loading dose of 50 mg/kg body weight over 1 hour. The infusion rate (20-40 mmol) per hour will depend on blood pressure with a target mean arterial pressure of 65 mm Hg. Thereafter, patients will receive a continuous application of 81 mmol/ 24 hours for a maximum of 7 days. Target Serum Magnesium Levels Serum magnesium levels will be monitored daily during the infusion period. The target therapeutic range for serum magnesium will be between 2.0-2.5 mmol/L. If the serum magnesium level exceeds the upper limit (2.5 mmol/L), the infusion rate will be reduced, and the patient will be closely monitored for signs of magnesium toxicity, such as hypotension, bradycardia, respiratory depression, or reflexes loss. In the event of severe hyper-magnesemia, calcium gluconate will be administered as an antidote.
To evaluate the effect of early intravenous magnesium sulfate on the incidence and severity of cerebral vasospasm in patients with traumatic subarachnoid hemorrhage assessed by cerebral blood flow velocity measured Through Transcranial Doppler
To evaluate the effect of early intravenous magnesium sulfate on the incidence and severity of cerebral vasospasm in patients with traumatic subarachnoid hemorrhage assessed by cerebral blood flow velocity measured Through Transcranial Doppler
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