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Thrombotic complications resulting from hypercoagulable states in chronic hemodialysis vascular access
C J LeSar1, H W Merrick, M R Smith
1Department of Surgery, Medical College of Ohio, Toledo 43614-2598, USA.
Insights
Hypercoagulable states are a significant cause of PTFE graft thrombosis in dialysis patients. Early diagnosis and warfarin therapy (INR 2.7-3.0) can reduce graft thrombosis and associated morbidity.
Area of Science:
- Nephrology
- Vascular Surgery
- Hematology
Background:
- Vascular access complications cause significant morbidity and cost in dialysis patients.
- Graft anastomosis stenosis and antiphospholipid antibodies are known risk factors for thrombosis.
- The role of broader hypercoagulable states in PTFE graft thrombosis requires further investigation.
Purpose of the Study:
- To determine the frequency of hypercoagulable states in dialysis patients with recurrent PTFE graft thrombosis.
- To evaluate the impact of hypercoagulability on graft thrombosis and the effectiveness of warfarin therapy.
Main Methods:
- Retrospective case series of 34 end-stage renal disease patients undergoing 91 PTFE graft operations.
- Evaluation for anastomotic stenosis and comprehensive hypercoagulable state testing.
- Consideration of warfarin therapy for patients with documented hypercoagulable states.
Main Results:
- 64.7% of patients experienced thrombotic complications.
- 85.7% of tested patients had underlying hypercoagulable states.
- Hypercoagulability was the sole identifiable cause for 41.8% of thrombotic events.
- Warfarin therapy (INR 2.7-3.0) reduced thrombosis rates from 4.0 to 1.2 events per year.
Conclusions:
- Hypercoagulability is a major factor in PTFE graft thrombosis, particularly in patients with multiple thromboses or nonanatomic causes.
- Antiphospholipid antibodies and deficiencies in Protein C, Protein S, and Antithrombin III are prevalent.
- Diagnostic evaluation for hypercoagulability is recommended for dialysis patients with PTFE graft thrombosis.
- Warfarin therapy, with INR maintained at 2.7-3.0, is effective in reducing graft thrombosis and morbidity.
Background:
Vascular access-related complications are an important cause of morbidity, and they account for 14% to 17% of dialysis patients' hospitalizations with an annual cost in the United States of approximately $1 billion. Previous studies have related the major predisposing factor of thrombotic complications to stenosis of the graft anastomosis. Several recent reports suggest that antiphospholipid antibodies may cause frequent thrombotic complications. The broad spectrum of diseases that cause hypercoagulable states has not been correlated with frequent PTFE graft thrombosis.
Study Design:
A retrospective case series study was performed to determine the frequency of hypercoagulable states in dialysis patients who had repeated thrombotic complications of their PTFE grafts. Between May 1996 and June 1998, 91 operations were performed on 34 patients with end-stage renal disease. All arteriovenous fistulas were created with PTFE grafts and placed by a single surgeon. All patients were evaluated at operation for anastomotic stenosis, and the majority of patients were studied for hypercoagulable states. Patients with a documented hypercoagulable state were considered for warfarin therapy.
Results:
Twenty-two individuals (64.7%) developed 67 thrombotic complications. Twelve of the 14 patients tested (85.7%) were shown to have hypercoagulable states of various causes and degrees. Thirteen patients developed multiple thrombotic complications, 11 (81.8%) were tested and proved to be hypercoagulable. Thirty-eight of the thrombotic complications had nonanatomic causes and 28 (41.8%) had hypercoagulability as the only determinable cause. Ten of the 12 hypercoagulable patients (83.3%) were relegated to intermediate to high-intensity warfarin therapy to reduce the incidence of thrombotic events. Hypercoagulable patients not receiving warfarin had a thrombosis rate of 4.0 events per year; patients on warfarin had a rate of 1.2 events per year. Twenty-three thrombotic events occurred in the anticoagulated group all with an International Normalized Ratio (INR) less than 2.7. This incidence of vascular access thrombosis may be prevented when patients are maintained at an optimal INR of 2.7-3.0.
Conclusions:
Hypercoagulability has been a major etiologic factor in PTFE graft thrombosis. Hypercoagulable states are often found in patients with multiple graft thromboses and in patients with nonanatomic causes for thrombosis. Antiphospholipid antibodies are prevalent in the patients with PTFE graft thrombosis, as well as abnormalities in the Protein-C, Protein-S, and Antithrombin III systems. PTFE graft thrombosis has been a frequent cause of morbidity in patients on hemodialysis, and diagnostic evaluation should include a hypercoagulability profile. Based on our data, warfarin therapy should be instituted when hypercoagulable states are found, unless otherwise contraindicated, and INR maintained at 2.7-3.0 to decrease morbidity and frequency of graft thrombosis.