Intravascular volume after aneurysmal subarachnoid hemorrhage

Intravascular volume after aneurysmal subarachnoid hemorrhage A subarachnoid hemorrhage (SAH) from a ruptured cerebral aneurysm is a devastating disorder with an often poor prognosis. The occurrence of delayed cerebral ischemia (DCI) is one of the most important factors determining outcome in patients who have survived the first hours after the hemorrhage. Hypotension and hypovolemia have been associated with an increased risk for DCI after SAH. The aim of the research presented in this thesis was to study the relation between the presumed and the actual condition of the systemic circulation and thereby find a way to improve hemodynamic management after aneurysmal SAH. In a prospective observational study in 50 patients, we assessed the effectiveness of fluid balance guided fluid therapy (current standard therapy) in maintaining normovolemia. Circulating blood volume (CBV) was measured with pulse dye densitometry (PDD) on alternating days during the first two weeks after SAH. We found that hypo- and hypervolemia occurred frequently but found no association between CBV and the daily fluid balance or between CBV and a cumulative fluid balance, adjusted for insensible loss through perspiration and respiration. In a next study on 43 patients, we asked ICU- and Medium Care Unit nurses to predict the present volume status as hypo-, normo- or hypervolemic. They could base their assessments on all usually available hemodynamic data. These assessments were compared with the actual CBV, that was measured daily during the first ten days after SAH. The results showed that deviations from normovolemia occurred frequently but that most instances were not recognized as such, which resulted in a very low sensitivity of the predictions. In a prospective controlled study in 102 patients with recent SAH we compared fluid management guided by daily measurements of CBV to conventional fluid balance guided fluid therapy, during the first 10 days after SAH. In the intervention group, with fluid management guided by CBV, fewer measurements were in the severe hypovolemic range (6.7% versus 17.1%) and a smaller part of patients had measurements indicating severe hypovolemia (39% versus 54%). Pulmonary edema (PED) after SAH is often seen as a sign of hypervolemia and treated as such with diuretics, inotropics and a reduction in fluid intake. We prospectively studied CBV, fluid balance and cardiac index and compared it between patients who did or did not develop PED. The results showed that patients developing PED had actually a lower mean CBV than those without PED and had CBV measurements in the hypovolemic range. Patients with PED after SAH must be considered as hypovolemic and measures taken to counteract the pulmonary edema must be balanced against the risk of worsening hypovolemia. Results from the studies in this thesis show that a normal volume status after SAH is not easy to achieve or to maintain. A probable cause is that SAH results in multiple organ dysfunctions and a systemic inflammatory response syndrome (SIRS). A coordinated multidisciplinary approach of the SAH patient would be appropriate, in research as well as in patient care.