title: Red blood cell transfusion increases cerebral oxygen delivery in anemic patients with subarachnoid hemorrhage.
abstract: OBJECTIVE
  Anemia is common after subarachnoid hemorrhage and may exacerbate the reduction in oxygen delivery (DO(2)) underlying delayed cerebral ischemia. The association between lower hemoglobin and worse outcome, including more cerebral infarcts, supports a role for red blood cell transfusion to correct anemia. However, the cerebral response to transfusion remains uncertain, because higher hemoglobin may increase viscosity and further impair cerebral blood flow (CBF) in the setting of vasospasm.
  
  
  METHODS
  Eight patients with aneurysmal subarachnoid hemorrhage and hemoglobin <10 g/dL were studied with (15)O-positron emission tomography before and after transfusion of 1 U red blood cells. Paired t tests were used to analyze the change in global and regional CBF, oxygen extraction fraction, and oxygen metabolism after transfusion. DO(2) was calculated from CBF and arterial oxygen content. CBF, oxygen metabolism, and DO(2) are reported in mL/100 g/min.
  
  
  RESULTS
  Transfusion resulted in a 15% rise in hemoglobin (8.7+/-0.8 to 10.0+/-1.0 g/dL) and arterial oxygen content (11.8+/-1.0 to 13.6+/-1.1 mL/dL; both P<0.001). Global CBF remained stable (40.5+/-8.1 to 41.6+/-9.9), resulting in an 18% rise in DO(2) from 4.8+/-1.1 to 5.7+/-1.4 (P=0.017). This was associated with a fall in oxygen extraction fraction from 0.49+/-0.11 to 0.41+/-0.11 (P=0.11) and stable oxygen metabolism. Rise in DO(2) was greater (28%) in regions with oligemia (low DO(2) and oxygen extraction fraction > or =0.5) at baseline but was attenuated (10%) within territories exhibiting angiographic vasospasm, where CBF fell 7%.
  
  
  CONCLUSIONS
  Transfusion of red blood cells to anemic patients with subarachnoid hemorrhage resulted in a significant rise in cerebral DO(2) without lowering global CBF. This was associated with reduced oxygen extraction fraction, which may improve tolerance of vulnerable brain regions to further impairments of CBF. Further studies are needed to confirm the benefit of transfusion on delayed cerebral ischemia and balance this against potential systemic and cerebral risks.
authors.affiliation: Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA. dharr@neuro.wustl.edu
authors.forename: Rajat
authors.initials: R
authors.lastname: Dhar
authors.forename: Allyson R
authors.initials: AR
authors.lastname: Zazulia
authors.forename: Tom O
authors.initials: TO
authors.lastname: Videen
authors.forename: Gregory J
authors.initials: GJ
authors.lastname: Zipfel
authors.forename: Colin P
authors.initials: CP
authors.lastname: Derdeyn
authors.forename: Michael N
authors.initials: MN
authors.lastname: Diringer
mesh_terms: D000740:Anemia / Q000150:complications / Q000378:metabolism / Q000628:therapy*; D001783:Blood Flow Velocity; D002545:Brain Ischemia / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D017707:Erythrocyte Transfusion; D005260:Female; D006801:Humans; D008875:Middle Aged; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption; D049268:Positron-Emission Tomography; D012307:Risk Factors; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000378:metabolism / Q000628:therapy*; D020301:Vasospasm, Intracranial / Q000378:metabolism / Q000628:therapy
chemical_list: D010100:Oxygen