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Nursing Strategies to Prevent Coagulation of the Extracorporeal Circuit
Objectives
This chapter will:
- 1.
Emphasize that clotting in the continuous renal replacement therapy circuit is complex and affected by many factors in the critically ill patient.
- 2.
Explain that anticoagulant agents can prevent or delay clotting but are not the only preventive strategy necessary.
- 3.
Indicate that clotting occurs in either the membrane or the venous air trap chamber and propose how this clot may form.
- 4.
Discuss the need to prevent clotting by ensuring the extracorporeal circuit is not mechanically obstructed and blood flow is maintained.
- 5.
Describe the influence of the access catheter and site, membrane and venous chamber, predilution fluid administration, blood flow setting, and nursing competence on circuit clotting.
The mechanism for blood coagulation in the renal replacement therapy (RRT) extracorporeal circuit (EC) supporting a critically ill patient is complex. Acute renal failure, inflammation with critical illness, and other factors influence the normal roles of key mediators such as thrombin, tissue factor, platelets, and endothelium. A precise explanation of how clotting occurs, or why it does not occur, when blood is being pumped outside the body via plastic tubes is not easily achieved. This also may explain why a wide variation in response to anticoagulation strategies to prevent clotting in the EC can be observed, with time before clotting ranging from only hours to several days with and without anticoagulation, and despite improvements in RRT technology and clinician expertise over the past 20 years.
However, clotting in the EC is inevitable, because this nonbiologic environment places blood under stress, with coagulation occurring at places of high resistance, stasis, and positive or negative pressures with shearing forces. In this respect, the blood is behaving normally. During flow through the EC, cells and plasma separate, cellular aggregation occurs, proteins deposit or build up, and an inflammatory response occurs. This may explain why thrombin generation is increased during continuous hemofiltration by activation of the tissue factor pathway, with this being only one of the many responses causing coagulation. Anticoagulants can be successful in delaying clot formation and make an RRT procedure functional for long periods of time without clotting. However, components of the EC and other influences on the EC are important as adjuncts to the use of anticoagulants and are very important when anticoagulants are not used.
Clotting: Where and How?
The two components of the EC where clotting occurs are the hemofilter (membrane) and the venous bubble trap chamber. Coagulation is not common along the circuit tubing or in the blood pump tubing segment. Additional chambers in the EC for fluid addition, or where smaller tubing enters the main blood path at a T junction, also may be sites of clot formation. However, clot development in these components is not a cause of circuit failure unless the clot formed at these junctions breaks off and embolizes into the main circuit path, obstructing flow into the membrane. This type of EC embolus clotting can obstruct blood flow at entry of blood to the membrane, or at exit of the venous chamber, causing an abrupt cessation to treatment by total blood flow obstruction, with an inability to return the EC blood to the patient. Fig. 169.1 shows a clot obstructing blood flow into a membrane. The picture depicts a membrane autopsy. Immediately after clotting, the membrane is cut in half to reveal the site of the clot obstructing the membrane at blood entry rather than by clotting along the fibers of the membrane, which is a slower progressive process. Fig. 169.2 shows a venous chamber with a large clot formed in the chamber, which can break off from the top section of the chamber and move down to the outlet, thereby causing an acute obstruction.
It is assumed that circuit life data reflect the time before membrane fiber clotting; however, the membrane entry or the venous chamber exit may clot before, and independent of, the membrane fibers. Not only do these events constitute a failure of the circuit but also, in the case of the venous chamber, unless the venous tubing segment can be changed quickly, and this may not be possible in many circuits, blood flow cannot continue, and the circuit volume of blood may not be returned (discarded) to the patient despite the membrane(s) itself being unaffected.
Therefore strategies to prevent clot formation in the EC are aimed at these two components: the membrane and the venous bubble trap. For a more complete understanding of this problem when using continuous RRT (CRRT), this discussion must include all of the EC components and their contribution to circuit clotting at these two sites.
Anticoagulants
Anticoagulant drugs prevent or delay formation of clot in the EC, and many methods are used with variability in the quality of evidence supporting their success and safety. However, the effectiveness of any anticoagulant, or the dose used, may be limited by the component and mechanical design of the EC. This suggests that in addition to an effective anticoagulant drug, or more importantly when no anticoagulation is used in patients at risk of bleeding, other strategies to prevent clot formation in the EC are useful to implement at all times, in every patient treatment.
When clotting does occur in the EC, differentiating between component failure (mechanical obstruction) and anticoagulant failure (dose too low, or poor response) is very important so that the correct remedy is used. For example, prescribing an increase in heparin dose, or changing to a different method may not be appropriate when the cause is mechanical obstruction in the EC.
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