A Case of Hyperacute Onset of Vasospasm After Aneurysmal Subarachnoid Hemorrhage and Refractory Vasospasm Treated with Intravenous and Intraventricular Nitric Oxide: A Mini Review.
BACKGROUND
A case of hyperacute vasospasm, indicating a poor prognosis after aneurysmal subarachnoid hemorrhage (SAH), is reported, and a review is presented of the literature addressing use of nitric oxide (NO) donors in cases of refractory vasospasm and recurrent delayed cortical ischemias (DCI).


METHODS
A 65-year-old woman was admitted within 1 hour after aneurysmal SAH (Hunt and Hess grade III, Fisher modified by Frontera grade IV). A hyperacute vasospasm had been confirmed arteriographically, the right middle cerebral artery (MCA) aneurysm was immediately coiled and a standard antivasospastic therapy was started. Within 48 hours, the patient developed cerebral vasospasm with DCI. Because the standard therapy failed to control clinical symptoms and to address severe vasospasm, an individualized rescue treatment with NO donors was initiated. A continuous intravenous molsidomine infusion was started and clinical stabilization was achieved for a week (Hunt and Hess grade I; World Federation of Neurological Surgeons grade I; Glasgow Coma Scale score, 15) after which vasospasm and DCI recurred. During a subsequent DCI, we escalated NO donor therapy by adding intraventricular boluses of sodium nitroprusside (SNP). Over the course of the following 22 days, 7 transient DCIs (Glasgow Coma Scale score, 8) were treated with boluses of SNP during continued molsidomine therapy and each time vasospasm and DCI were completely reversed. Despite initial poor prognosis, the clinical outcome was excellent; at 3, 6, and 12 months follow-up the patient's modified National Institutes of Health-Stroke Scale and modified Rankin Scale scores were 0, with no cognitive deficits.


CONCLUSIONS
The review of the literature suggested that combined intravenous molsidomine with intraventricular SNP treatment reversed refractory, recurrent vasospasm and DCIs probably by addressing the hemoglobin NO sink effect, NO depletion, and decreased NO availability after aneurysmal SAH.
Department of Neurosurgery, Asklepios Klinik St. Georg, Hamburg, Germany. Electronic address: a.ehlert@asklepios.com.
Angelika
A
Ehlert
Department of Neurosurgery, Asklepios Klinik St. Georg, Hamburg, Germany.
Gerd
G
Manthei
Department of Neuroradiology, Asklepios Clinic North, Hamburg, Germany.
Volker
V
Hesselmann
Department of Neuroradiology, Asklepios Clinic, St. Georg, Hamburg, Germany.
Klaus
K
Mathias
Department of Anesthesiology, Asklepios Clinic, St. Georg, Hamburg, Germany.
Berthold
B
Bein
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, Maryland, USA.
Ryszard
R
Pluta
D000368:Aged; D005260:Female; D015600:Glasgow Coma Scale; D023261:Glasgow Outcome Scale; D006801:Humans; D007275:Injections, Intravenous / Q000379:methods; D007276:Injections, Intraventricular / Q000379:methods; D008981:Molsidomine / Q000008:administration & dosage; D009569:Nitric Oxide / Q000008:administration & dosage*; D009599:Nitroprusside / Q000008:administration & dosage; D013345:Subarachnoid Hemorrhage / Q000188:drug therapy*; D016896:Treatment Outcome; D020301:Vasospasm, Intracranial / Q000188:drug therapy*
D009599:Nitroprusside; D009569:Nitric Oxide; D008981:Molsidomine
DCI; Molsidomine; NO donor; SAH; SNP; hyperacute CVS; outcome