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Analysis of coagulation changes associated with supraceliac aortic crossclamping using thromboelastography
P V Anagnostopoulos1, A D Shepard, I I Pipinos
1Division of Vascular Surgery, Department of Surgery, Henry Ford Hospital, Detroit, Michigan 48202, USA.
The Journal of Surgical Research
|May 23, 2001
Summary
Supraceliac aortic cross-clamping (AXC) increases clotting during the procedure but does not cause fibrinolysis. Post-clamping, reduced clot formation speed and fibrinogen levels suggest clotting factor consumption.
Area of Science:
- Cardiovascular Surgery
- Hematology
- Surgical Physiology
Background:
- The causes of coagulation changes during supraceliac (SC) aortic cross-clamping (AXC) are debated, with both fibrinolysis and clotting factor consumption proposed.
- Thromboelastography (TEG) was used to dynamically assess coagulation and fibrinolysis by measuring thrombus viscoelastic properties.
Purpose of the Study:
- To investigate the etiology of coagulation alterations during SC AXC.
- To differentiate between fibrinolysis and clotting factor consumption as causes of these changes.
Main Methods:
- Eight pigs underwent 30 minutes of SC AXC, with five controls undergoing infrarenal (IR) AXC.
- Blood samples were collected pre-AXC, pre-unclamping, and at 5 and 60 minutes post-unclamping.
- TEG and standard coagulation tests (PT, PTT, fibrinogen, platelets) were performed; TEG parameters included fibrinolytic index, R value, K value, and alpha angle.
Main Results:
- No significant difference in fibrinolysis was observed between SC and IR groups.
- SC AXC showed increased intrinsic coagulation activity (lower R value) during clamping compared to IR AXC.
- Post-unclamping, SC AXC exhibited decreased clot formation speed (higher K, lower alpha angle) and lower fibrinogen levels compared to IR AXC.
Conclusions:
- Thirty minutes of SC AXC does not induce fibrinolysis.
- Coagulation changes observed are characterized by increased clotting during SC AXC, followed by impaired clot formation and reduced fibrinogen post-procedure.
- These findings support clotting factor consumption as the primary mechanism behind SC AXC-induced coagulation alterations.
