Systemic Anticoagulation Considerations in Critically Ill with Chronic Kidney Disease

Abstract

Background: Hemostasis is the process that maintains the integrity of a closed, high-pressure circulatory system after vascular damage. Vessel-wall injury and the extravasation of blood from the circulation rapidly initiate events in the vessel wall and in blood that seal the breach. Circulating platelets are recruited to the site of injury, where they become a major component of the developing thrombus; blood coagulation, initiated by tissue factor, culminates in the generation of thrombin and fibrin. In general, the presence of CKD is not a reason to avoid pharmacological thromboprophylaxis when indicated. Prophylaxis using low-dose unfractionated heparin (UFH) at 5,000 units subcutaneously 3 times daily does not require any dose modifications in CKD. Aims: The aim of this essay is to adjust use of anticoagulation in critically ill patient with chronic kidney disease. Conclusion: The mechanisms for increased coagulation are multifactorial. Patients with CKD are known to have increased levels of procoagulant factors. Simultaneously, decreases in endogenous anticoagulants and fibrinolytic activity might occur. Commonly used medications, such as erythropoietin stimulating agents, can also increase the risk of thromboembolism. HIT is an adverse immune mediated drug reaction that is associated with a high risk of venous and arterial thrombosis. Risk factors for HIT include duration and type of heparin exposure, patient population, severity of trauma, and gender. Although thrombocytopenia is the most common presenting feature of HIT, in up to 25% of patients with HIT the development of thrombosis precedes the development of thrombocytopenia. The first step in the treatment of HIT is discontinuation of all forms of heparin and LMWH.