Hypervolemic hemodilution (H-H) therapy for neurological deficit due to delayed cerebral vasospasm has been shown to be effective. The purpose of the present study was to monitor the hemorrheological and hemodynamic states (Ht, RBC-aggregation, cardiac output (CO), cardiac index (CI), pulmonary capillary wedge pressure (PCWP), serum albumin, a2-macroglobulin (a2-MG), circulating blood volume (CirBV) and cerebral blood flow (CBF) with patients with aneurysmal SAH and to assess how H-H therapy improved these factors during cerebral vasospasm.
We studied 50 patients who underwent early clipping surgery for aneurysmal SAH at our institution between January 1994 and December 1994. Twenty-one (42%) patients developed clinical vasospasm. The Ht of the patients with vasospasm was decreased significantly from 37.7% to 31.6% by H-H therapy. The RBC aggregation rate increased during day 4-6 and was significantly reduced by the therapy. The serum albumin decreased and a2-MG increased at the same periods. CirBV data showed that the patients tend to be hypovolemic a few days after ictus, and that the patients receiving H-H therapy became normovolemic to hypervolemic. CO (4.7±0.4) and CI (3.1±0.3) at the onset of vasospasm, increased significantly to 6.8±1.1 and 4.1±0.5 respectively after H-H therapy. At the onset of vasospasm, the CBF (44.7±1.2 ml/100g/min) on the side of surgery was significantly lower than that on the contra-lateral side. During H-H therapy the CBF increased to 56.6±3.2 ml/100g/min.
After H-H therapy, 15 patients (71.5%) had good recovery, 4 (19.0%) had moderate disability, 2 (9.5%) had severe disability. Death and vegetative state were not present. Severe disability from clinical vasospasm occurred in 4% of all patients with SAH.
Our study showed that H-H therapy including albumin decreased the Ht and RBC aggregability and increased CirBV and CO, consequently increased CBF. We conclude that the improvement of hemorrheological and hemodynamic parameters by H-H therapy effectively reversed progressive neurological deterioration due to cerebral vasospasm.
