Control of hypertension and prophylaxis against vasospasm in cases of subarachnoid hemorrhage: a preliminary report. Effect of hypervolemic therapy on cerebral blood flow after subarachnoid hemorrhage : a randomized controlled trial. Prophylactic hyperdynamic postoperative fluid therapy after aneurysmal subarachnoid hemorrhage: a clinical, prospective, randomized, controlled study.
Thirty hypertensive patients with subarachnoid hemorrhage were divided randomly into two groups. The treated group was begun on preliminary volume expansion, and control of hypertension was carried out using vasodilators and centrally acting drugs. The control group was treated in the classical manner for hypertension, with a diuretic as the foundation for therapy. The incidence of clinical vasospasm was compared to that of angiographic spasm. The incidence of preoperative vasospasm in the treated group was 20%, as compared to 60% in the untreated group (P less than 0.01). Of the treated group, 87% survived to operation, whereas only 53% of the control group survived to operation (P less than 0.01). Cerebral blood flow (CBF) is reduced after subarachnoid hemorrhage (SAH), and symptomatic vasospasm is a major cause of morbidity and mortality. Volume expansion has been reported to increase CBF after SAH, but CBF values in hypervolemic (HV) and normovolemic (NV) subjects have never been directly compared.
                On the day after aneurysm clipping, we randomly assigned 82 patients to receive HV or NV fluid management until SAH day 14. In addition to 80 mL/h of isotonic crystalloid, 250 mL of 5% albumin solution was given every 2 hours to maintain normal (NV group, n=41) or elevated (HV group, n=41) cardiac filling pressures. CBF ((133)xenon clearance) was measured before randomization and approximately every 3 days thereafter (mean, 4.5 studies per patient).
                HV patients received significantly more fluid and had higher pulmonary artery diastolic and central venous pressures than NV patients, but there was no effect on net fluid balance or on blood volume measured on the third postoperative day. There was no difference in mean global CBF during the treatment period between HV and NV patients (P=0.55, random-effects model). Symptomatic vasospasm occurred in 20% of patients in each group and was associated with reduced minimum regional CBF values (P=0.04). However, there was also no difference in minimum regional CBF between the 2 treatment groups.
                HV therapy resulted in increased cardiac filling pressures and fluid intake but did not increase CBF or blood volume compared with NV therapy. Although careful fluid management to avoid hypovolemia may reduce the risk of delayed cerebral ischemia after SAH, prophylactic HV therapy is unlikely to confer an additional benefit. To investigate the role of prophylactic hyperdynamic postoperative fluid therapy in preventing delayed ischemic neurological deficits attributable to cerebral vasospasm.
                We designed a prospected, randomized, controlled study and included 32 patients with subarachnoid hemorrhage. Sixteen patients received hypervolemic hypertensive hemodilution fluid therapy; the other 16 patients received normovolemic fluid therapy. All patients were monitored for at least 12 days, with clinical assessments, transcranial Doppler recordings, single-photon emission computed tomographic (SPECT) scanning, and routine computed tomographic scanning. For fluid balance monitoring, a number of blood samples were obtained on a daily basis and continuous central venous pressure and mean arterial blood pressure measurements were performed for both groups. All patients received intravenous nimodipine infusions between Day 1 and Day 12. End points of this study were clinical outcomes, clinically evident and transcranial Doppler sonography-evident vasospasm, SPECT findings, complications, and costs. Clinical examinations (using the Glasgow Outcome Scale) performed 1 year after discharge, together with neuropsychological assessments and SPECT scanning, were the basis for the evaluation of clinical outcomes.
                No differences were observed between the two groups with respect to cerebral vasospasm (as observed clinically or on transcranial Doppler recordings). When regional cerebral blood flow was evaluated by means of SPECT analysis performed on Day 12 after subarachnoid hemorrhage, no differences were revealed. One-year clinical follow-up assessments (with the Glasgow Outcome Scale), including SPECT findings and neuropsychological function results, did not demonstrate any significant group differences. Costs were higher and complications were more frequent for the hyperdynamic therapy group.
                Neither early nor late outcome measures revealed any significant differences between the two subarachnoid hemorrhage treatment models.