title: Diagnostic blood loss from phlebotomy and hospital-acquired anemia during acute myocardial infarction.
abstract: BACKGROUND
  Hospital-acquired anemia (HAA) during acute myocardial infarction (AMI) is associated with higher mortality and worse health status and often develops in the absence of recognized bleeding. The extent to which diagnostic phlebotomy, a modifiable process of care, contributes to HAA is unknown.
  
  
  METHODS
  We studied 17,676 patients with AMI from 57 US hospitals included in a contemporary AMI database from January 1, 2000, through December 31, 2008, who were not anemic at admission but developed moderate to severe HAA (in which the hemoglobin level declined from normal to <11 g/dL), a degree of HAA that has been shown to be prognostically important. Patients' total diagnostic blood loss was calculated by multiplying the number and types of blood tubes drawn by the standard volume for each tube type. Hierarchical modified Poisson regression was used to test the association between phlebotomy and moderate to severe HAA, after adjusting for site and potential confounders.
  
  
  RESULTS
  Moderate to severe HAA developed in 3551 patients (20%). The mean (SD) phlebotomy volume was higher in patients with HAA (173.8 [139.3] mL) vs those without HAA (83.5 [52.0 mL]; P < .001). There was significant variation in the mean diagnostic blood loss across hospitals (moderate to severe HAA: range, 119.1-246.0 mL; mild HAA or no HAA: 53.0-110.1 mL). For every 50 mL of blood drawn, the risk of moderate to severe HAA increased by 18% (relative risk [RR], 1.18; 95% confidence interval [CI], 1.13-1.22), which was only modestly attenuated after multivariable adjustment (RR, 1.15; 95% CI, 1.12-1.18).
  
  
  CONCLUSIONS
  Blood loss from greater use of phlebotomy is independently associated with the development of HAA. These findings suggest that HAA may be preventable by implementing strategies to limit blood loss from laboratory testing.
authors.affiliation: Department of Internal Medicine, Division of Cardiovascular Disease, Saint Luke's Mid America Heart and Vascular Institute, Kansas City, MO 64111, USA.
authors.forename: Adam C
authors.initials: AC
authors.lastname: Salisbury
authors.forename: Kimberly J
authors.initials: KJ
authors.lastname: Reid
authors.forename: Karen P
authors.initials: KP
authors.lastname: Alexander
authors.forename: Frederick A
authors.initials: FA
authors.lastname: Masoudi
authors.forename: Sue-Min
authors.initials: SM
authors.lastname: Lai
authors.forename: Paul S
authors.initials: PS
authors.lastname: Chan
authors.forename: Richard G
authors.initials: RG
authors.lastname: Bach
authors.forename: Tracy Y
authors.initials: TY
authors.lastname: Wang
authors.forename: John A
authors.initials: JA
authors.lastname: Spertus
authors.forename: Mikhail
authors.initials: M
authors.lastname: Kosiborod
mesh_terms: D000368:Aged; D000740:Anemia / Q000097:blood / Q000209:etiology*; D005260:Female; D006454:Hemoglobins / Q000378:metabolism; D006470:Hemorrhage / Q000097:blood / Q000209:etiology*; D017052:Hospital Mortality / Q000639:trends; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications* / Q000401:mortality; D018962:Phlebotomy / Q000009:adverse effects*; D012189:Retrospective Studies; D012307:Risk Factors; D015996:Survival Rate / Q000639:trends
chemical_list: D006454:Hemoglobins