title: Primary fibrinolysis during supraceliac aortic clamping.
abstract: OBJECTIVE
  An increased incidence of bleeding complications has been observed after supraceliac aortic clamping (SCC). This study was performed to identify possible hemostatic abnormalities that contribute to this problem.
  
  
  METHODS
  A prospective cohort study over a 3-month period was performed by comparing hemostatic parameters in 10 consecutive patients who required elective SCC with those of eight concurrent randomly selected control subjects who required infrarenal clamping (IRC) for abdominal aortic reconstruction. Measures of coagulation, fibrinolysis, platelet function, temperature, hemodilution, and hepatic function were performed at selected times before, during, and after operation.
  
  
  RESULTS
  Aneurysm size, fibrinogen, D-dimers, prothrombin, partial thromboplastin time, platelet counts, bleeding times, hemodilution, and temperature were comparable in both groups. Patients in the SCC group, however, consistently developed a primary fibrinolytic state within 20 minutes after supraceliac clamping, reflected by significantly decreased euglobulin clot lysis times (ECLT; p < 0.0001), elevated tissue plasminogen activator (t-PA) levels (p < 0.0006), elevated t-PA-to-plasminogen activator inhibitor-1 ratios (p < 0.0001), and reduced alpha 2-antiplasmin levels (p < 0.002). SCC produced hepatocellular injury documented by elevations in both aspartate transaminase (p < 0.0001) and lactate dehydrogenase (p < 0.009).
  
  
  CONCLUSIONS
  SCC rapidly induces a primary fibrinolytic state manifested by increased circulating t-PA, reduced alpha 2-antiplasmin, and increased fibrinolytic activator-to-inhibitor ratios. These effects may be a result of hepatic hypoperfusion caused by SCC leading to insufficient clearance of t-PA. Antifibrinolytic agents may be of benefit if bleeding develops after aortic procedures that require supraceliac clamping.
authors.affiliation: Department of Surgery, University of Rochester Medical Center, NY 14642, USA.
authors.forename: K A
authors.initials: KA
authors.lastname: Illig
authors.forename: R M
authors.initials: RM
authors.lastname: Green
authors.forename: K
authors.initials: K
authors.lastname: Ouriel
authors.forename: P N
authors.initials: PN
authors.lastname: Riggs
authors.forename: S
authors.initials: S
authors.lastname: Bartos
authors.forename: R
authors.initials: R
authors.lastname: Whorf
authors.forename: J A
authors.initials: JA
authors.lastname: DeWeese
authors.forename: A
authors.initials: A
authors.lastname: Chhibber
authors.forename: V J
authors.initials: VJ
authors.lastname: Marder
authors.forename: C W
authors.initials: CW
authors.lastname: Francis
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000933:Antifibrinolytic Agents / Q000032:analysis; D001013:Aorta, Thoracic / Q000502:physiology*; D017544:Aortic Aneurysm, Abdominal / Q000097:blood / Q000601:surgery*; D001219:Aspartate Aminotransferases / Q000097:blood; D015331:Cohort Studies; D003250:Constriction; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D005342:Fibrinolysis; D006801:Humans; D007432:Intraoperative Period; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008099:Liver / Q000378:metabolism; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011446:Prospective Studies; D011897:Random Allocation; D010959:Tissue Plasminogen Activator / Q000097:blood; D000979:alpha-2-Antiplasmin / Q000032:analysis
chemical_list: D000933:Antifibrinolytic Agents; D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; D000979:alpha-2-Antiplasmin; C036309:fibrin fragment D; D005340:Fibrinogen; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D010959:Tissue Plasminogen Activator