Exposure to artificial surface devices (ASD)

Patients undergoing cardiac surgery display a shift in balance from hypercoagulability to hypocoagulability and back to hypercoagulability. In cases where patients who become recipients of artificial surface devices such as valves, artificial hearts, and heart assist devices, hypercoagulability is further enhanced post surgery. The reason for this is that continuous exposing of blood to artificial surfaces and the accompanying flow turbulence almost invariably leads to activated platelets (white clot), often with activation of the intrinsic and/or extrinsic system, resulting in the formation of thrombi (red clot). Gross thrombotic deposits may impede the function of the artificial organ, and thrombotic deposits may fragment and be swept downstream to distal organs, potentially causing stroke, DVT, etc.

To prevent these ischemic events, an anticoagulation regimen needs to be initiated once a patient's vascular recovery post surgery is achieved, and then closely monitored to achieve and maintain the delicate balance between the anticoagulated and the prothrombotic states.

Haemoscope has developed a specific protocol to monitor hemostasis in recipients of ASD that has been tested with various heart assist devices and has proven its utility. The ASD protocol has been described and submitted for publication in the details of a case study for one particular heart assist device.

In brief, the protocol to monitor patients intra- and post-ASD procedures consists of four phases:


 
Phase Objective Rationale
1. Pre- and intra operative Prevent clot formation Achieve artificial surface patency
2. Post protamine / short-term ICU Enhance clot formation Achieve vascular recovery
3. Long-term ICU Prevent clot formation and bleeding Achieve balanced hemostasis
4. Discharge Balanced hemostasis Maintain balanced hemostasis
 

Case study
43 yo female with non-active cancer, poor liver function, and recent DVT. Balloon pump 2 days prior to VAD insertion. Bridge to transplantation (heart).

 
Phase I.(Prevent clot formation) Baseline. Patient hemostasis is prothrombotic, which may be due to the presence of cancer and the balloon pump surfaces two days prior to surgery. The patient was heavily anticoagulated and the VAD was successfully inserted with full artificial surface patency. Phase I Baseline
Phase II. (Achieve vascular recovery) 1st and 2nd hour short-term ICU. Patient bleeding from suture wounds, CT output is 220 cc first hour, 330 cc second hour; TEG® analysis indicates possible von Willebrand factor deficiency; patient treated with FFP. Bleeding stopped. CTD output gradually diminished to 30-60cc, indicative of vascular recovery and readiness for Phase III. Phase II Post protamine Phase II Vascular Recovery
Phase III. (Achieve balanced hemostasis) CTD 15 cc/hr. Vascular system is restored, leading to closed system. Patient normal hemostasis is achieved. Phase III shifts from enhancing clot formation to anticoagulation to prevent an ischemic event due to continuous exposure of the blood to ASD surface. To achieve the delicate balance of hemostasis, both enzymatic and platelet anticoagulation must be considered. In this case 300 U/hr heparin and 81mg ASA was given. This increased the R value. Platelet inhibition due to ASA is evidenced by a reduction in MA, as measured by the new TEG® ASA platelet inhibition assay. Phase III
Before anticoagulation
Phase III
New TEG ASA platelet inhibition assay
Phase III
After anticoagulation with 300 U/ml of heparin
Phase IV. (Maintaining balanced hemostasis). Once balanced hemostasis is achieved, anticoagulation is changed from heparin to Coumadin at 5 mg qd. Balanced hemostasis was maintained until heart transplantation. Had the platelet inhibition assay shown aspirin resistance, platelet anticoagulation would have shifted to Plavix or Persantine, or both, depending on TEG MA value. Phase IV Balanced hemostasis
 
References

Copeland JG, Tsau PH, Arabia FA, Xie, T. Correlation of Clinical Embolic Events with Coagulability in a Patient with a Total Artificial Heart. J Heart Lung Transplant 1995;14:990-8.

Case report showing strong correlation between embolic events and thrombelastography results during TAH bridge to transplantation.

Szefner J. Control of Bleeding in Total Artificial Heart Implants. In Pifarre R (ed) Management of Bleeding in Cardiovascular Surgery. Hanley & Belfus, Inc. 2000, Philadelphia PA.



Coronary Artery Bypass Graft (CABG)
Liver transplantation
Exposure to artificial surface devices (ASD)
Percutaneous Coronary Angioplasty (PTCA)
Disseminated Intravascular Coagulation (DIC)



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