Intra-abdominal adhesion formation is a common and potentially life-threatening complication of abdominal surgery in horses.1–4 Foals reportedly develop postoperative adhesions more often than adult horses do, negatively affecting postoperative outcome.5–9 Existing estimates of the risk of postoperative adhesion formation might be inaccurate because a noninvasive method for adhesion detection does not exist; however, the reported incidence of intra-abdominal adhesions following abdominal surgery in adult horses is 1.5% to 7%10–12 and in foals is 8% to 33%.6–9 Adhesion formation is secondary to surgical trauma, intra-abdominal inflammation, and the ensuing abdominal repair process that involves fibrin deposition and fibroblast migration concurrent with fibrinolysis.
The usual balance of several coagulation factors is altered in horses with acute gastrointestinal disease,13–15 resulting in an excess of procoagulant factors overwhelming the anticoagulant response.16 Therefore, adhesion development within the abdomen following abdominal surgery has been attributed to insufficient fibrinolysis.17,18 When fibrinolysis is delayed or impaired, fibrin persists and serves as a scaffold for the migration of fibroblasts and adhesion development.17
Differences in risks of adhesion formation might be explained through differences in amounts of 4 proteins involved in hemostasis: fibrinogen, plasminogen, antiplasmin, and D-dimer.19,20 Fibrinogen, a soluble plasma glycoprotein transformed via coagulation to insoluble fibrin, acts as the matrix for adhesion development and maturation. Plasminogen, a proenzyme activated by tPA or urokinase plasminogen activator, is the major fibrinolytic protease that degrades fibrinous adhesions in the abdominal space. Antiplasmin, a serpin inhibitor, is a major negative regulator of fibrinolysis that acts by forming an irreversible complex with free (non–fibrin-bound) plasmin.21,22 D-dimer is the terminal degradation fragment released by plasmin-mediated proteolysis of cross-linked fibrin.16 The concentration or activity of these 4 proteins can therefore be used to characterize conditions favoring fibrin deposition (eg, high fibrinogen or high antiplasmin inhibitory activity) or indicators of impaired fibrinolysis (eg, low plasminogen activity or low D-dimer concentration).
The purpose of the study reported here was to compare indices of hemostasis between adult horses and foals to identify differences that might explain the apparent increased risk of postoperative abdominal adhesion formation in foals versus adult horses. We hypothesized that if foals with colic had an inherent propensity to form postoperative adhesions, a relative imbalance would be detected in ≥ 1 of these hemostatic analytes in foals, compared with analyte values in adult horses evaluated similarly.
Plasminogen activator inhibitor
Tissue plasminogen activator
Vacutainer, Becton-Dickinson Co, Franklin Lakes, NJ.
STACompact, Diagnostica Stago, Parsippany, NJ.
Fibrinogen, Diagnostica Stago, Parsippany, NJ.
STAchrom Plasminogen, Diagnostica Stago, Parsippany, NJ.
STAchrom Antiplasmin, Diagnostica Stago, Parsippany, NJ.
Unicalibrator, Diagnostica Stago, Parsippany, NJ.
HemosIL, D-dimer Calibrator, Instrumentation Laboratory, Bedford, Mass.
Statistix 9, Analytical Software, Tallahassee, Fla.
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