title: Serum uric acid as a novel marker for uterine atony and post-spinal vasopressor use during cesarean delivery.
abstract: BACKGROUND
  Serum uric acid is a marker for oxidative stress in preeclampsia. Because oxidative stress can result in diminished uterine contractility and impaired vascular relaxation, we hypothesized that an elevated serum uric acid level in women undergoing neuraxial anesthesia for cesarean delivery would be associated with greater uterine atony, as measured by supplemental uterotonic agent use and blood loss, and less hypotension, as measured by total vasopressor use.
  
  
  METHODS
  All records of patients (n=2527) undergoing cesarean delivery in 2009 were reviewed. Serum uric acid was measured within 24h of delivery in 509 patients; data from 345 patients with singleton pregnancies undergoing neuraxial anesthesia were analyzed. Demographic data, medical and obstetric history, anesthetic management and peripartum course were evaluated. ANOVA, Chi-square, and multivariate logistic and linear regression analyses were performed.
  
  
  RESULTS
  Increased serum uric acid correlated positively with preeclampsia and the need for supplemental uterotonic agents (odds ratio 1.53, 95%CI 1.2-2.0, P=0.002), but not blood loss. The presence of preeclampsia also correlated with greater supplemental uterotonic agent use (P=0.01). The correlation between serum uric acid and post-spinal vasopressor use (i.e., none, moderate, and high) was of borderline significance (P=0.05). In patients without diabetes, serum uric acid levels correlated inversely with post-spinal vasopressor use (P=0.04).
  
  
  CONCLUSIONS
  Elevated serum uric acid in parturients undergoing cesarean delivery with neuraxial anesthesia correlated with increased use of supplemental uterotonic agents and decreased use of post-spinal vasopressors. Further validation of this study is required to determine if serum uric acid in parturients can serve as a reliable predictor for higher and lower occurrences of uterine atony and spinal-induced hypotension, respectively.
authors.affiliation: Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
authors.forename: V P
authors.initials: VP
authors.lastname: Kovacheva
authors.forename: M A
authors.initials: MA
authors.lastname: Soens
authors.forename: L C
authors.initials: LC
authors.lastname: Tsen
mesh_terms: D000328:Adult; D000773:Anesthesia, Obstetrical; D015415:Biomarkers / Q000097:blood*; D016063:Blood Loss, Surgical; D002585:Cesarean Section / Q000009:adverse effects*; D005260:Female; D006400:Hematocrit; D006801:Humans; D016014:Linear Models; D018384:Oxidative Stress; D011225:Pre-Eclampsia / Q000097:blood / Q000175:diagnosis; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood / Q000453:epidemiology; D011256:Pregnancy Outcome; D017382:Reactive Oxygen Species / Q000097:blood; D012189:Retrospective Studies; D014527:Uric Acid / Q000097:blood*; D014593:Uterine Inertia / Q000097:blood*; D014662:Vasoconstrictor Agents / Q000009:adverse effects*
chemical_list: D015415:Biomarkers; D017382:Reactive Oxygen Species; D014662:Vasoconstrictor Agents; D014527:Uric Acid