Early Intravenous Magnesium Sulfate and Its Impact on Cerebral Vasospasm in Traumatic Subarachnoid Hemorrhage

NCT ID: NCT07252505

Last Updated: 2025-11-26

Basic Information

• Recruitment Status: NOT_YET_RECRUITING
• Clinical Phase: EARLY_PHASE1
• Total Enrollment: 50 participants
• Study Classification: INTERVENTIONAL
• Study Start Date: 2025-11-30
• Study Completion Date: 2027-10-31

Brief Summary

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

Detailed Description

Magnesium is a noncompetitive calcium antagonist with several important vascular and potentially neuro-protective effects. For instance, magnesium can lead to vasodilatation by blocking the voltage-dependent calcium channel and decreasing glutamate release and block the influx of calcium ions, inhibiting blood vessel contraction and preventing CV.In addition, magnesium also attenuates the effect of various potent vasoconstrictors, such as endothelin 1, and blocks the formation of reactive oxygen species These potentially helpful effects of magnesium on vasodilation and consequent neuro-protection has led some investigators to study the ability of magnesium to prevent of cerebral vasospasm and delayed cerebral ischemia after subarachnoid hemorrhage (SAH). Limited data exist for tSAH. Early intravenous Magnesium Sulfate (MgSO₄)application within 24 hours after diagnosis may prevent or attenuate vasospasm and improve neurological recovery and outcome

Conditions

Trauma and Emergency Care

Study Design

• Allocation Method: RANDOMIZED
• Intervention Model: PARALLEL
• Primary Study Purpose: TREATMENT
• Blinding Strategy: SINGLE

Study Groups

Group A: patients will be given magnesium sulfate (MgSO4) with infusion rate (20- 40 mmol) per hour.

will be given magnesium sulfate (MgSO4) with infusion rate (20- 40 mmol)

Group Type: PLACEBO_COMPARATOR

Magnesium Sulfate 10 MG/ML

Intervention Type: DRUG

As 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.

Group B: will be given normal saline (placebo group).

will be given normal saline (placebo group).

Group Type: NO_INTERVENTION

No interventions assigned to this group

Interventions

Magnesium Sulfate 10 MG/ML

As 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.

Intervention Type: DRUG

Other Intervention Names

MgSo4

Eligibility Criteria

Inclusion Criteria

• 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

Exclusion Criteria

• Aneurysmal or spontaneous SAH Sever hepatic dysfunction.
• Known hypersensitivity to magnesium sulfate
• Renal disease with glomerular filtration rate<15 ml/min.
• pregnancy

• Minimum Eligible Age: 18 Years
• Maximum Eligible Age: 65 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: No

Sponsors

Assiut University

OTHER

Sponsor Role: lead

Responsible Party

Zeinab Salah El-Dein Quashty Aly

Emergency Medicine assistant lecturer

Responsibility Role: PRINCIPAL_INVESTIGATOR

Principal Investigators

Zeinab Quashty, MD

Role: PRINCIPAL_INVESTIGATOR

Assisstant lecturer

Central Contacts

Zeinab Quashty, MD

Role: CONTACT

zeinabsalah404@gmail.com

0021143751762

Fatma Abd El-Aal, Professor

Role: CONTACT

fatmaabdelal@aun.edu.eg

0021113221317

Other Identifiers

Magnesium Sulfate

Identifier Type: -

Identifier Source: org_study_id