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Hypertensive, hypervolemic, hemodilutional therapy for aneurysmal subarachnoid hemorrhage. Is it efficacious? Yes
1Department of Neurosurgery, Mount Sinai School of Medicine, New York, New York, USA.
Insights
Cerebral vasospasm after subarachnoid hemorrhage (SAH) reduces cerebral blood flow (CBF). Induced hypertension, hypervolemia, and hemodilution (HHH) therapy may restore blood flow and improve neurological deficits.
Area of Science:
- Neurology
- Neurosurgery
- Critical Care Medicine
Background:
- Aneurysmal subarachnoid hemorrhage (SAH) frequently leads to cerebral vasospasm, a major cause of mortality and disability.
- Cerebral blood flow (CBF) is often reduced post-SAH, correlating inversely with clinical severity.
- Hypotension and hypovolemia can worsen reduced CBF, leading to critical hypoperfusion.
Purpose of the Study:
- To review the evidence supporting the use of induced hypertension, hypervolemia, and hemodilution (HHH) therapy in managing cerebral vasospasm following SAH.
- To highlight the potential benefits of HHH therapy in restoring blood flow to ischemic areas and preventing neurological deficits.
Main Methods:
- Review of existing literature and clinical evidence regarding HHH therapy.
- Analysis of the challenges in conducting prospective, randomized trials of HHH therapy, such as blinding difficulties.
Main Results:
- Strong evidence suggests HHH therapy can reverse delayed neurological deficits by improving perfusion in ischemic regions.
- Prophylactic HHH therapy may decrease the incidence and severity of delayed ischemic deficits (DID).
Conclusions:
- HHH therapy is a crucial intervention for managing cerebral vasospasm post-SAH.
- While prospective randomized trials are lacking, existing evidence supports the efficacy of HHH therapy in improving patient outcomes.
Abstract:
Vasospasm is an important contributor to death and disability after aneurysmal SAH. CBF is decreased after SAH and correlates inversely with the severity of the clinical grade. It is necessary to avoid hypotension and hypovolemia, which can exacerbate an already reduced CBF, resulting in critically low perfusion. There have been no human, prospective, randomized trials of HHH therapy. This is attributable, perhaps, to the fact that such trials are difficult to blind. Nevertheless, there is strong evidence that HHH therapy can reverse the delayed onset of profound neurologic deficits by restoring blood flow to ischemic regions, and its prophylactic use can reduce the incidence and severity of DID.