Annals of Long Term Care

Author Affiliations: Dr. Jacobs is Professor of Clinical Medicine & Division Chief, Geriatrics, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY.

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Although anticoagulants have been a part of the medical armamentarium for more than 50 years, their use is complex, and new agents and regimens are being added. It is critically important that each facility consider the issues surrounding the use of anticoagulants in LTC settings, as these agents have significant risks and benefits, and are in frequent use. Monitoring of anticoagulants is a frequent area of error and adverse outcomes in the LTC setting. Policies and procedures should address drug administration; bedside monitoring for bleeding by nurses and aides; policy recommendations for the minimum frequency of laboratory monitoring, if required; and administrative systems for obtaining laboratory monitoring in a timely fashion, including obtaining and reporting of laboratory testing results to the facility and to the physicians in a timely manner. (Annals of Long-Term Care: Clinical Care and Aging 2009;17[1]:34-38

Introduction

A recent study of adverse events with warfarin use in long-term care (LTC) residents highlights several important issues for anticoagulant use in nursing homes in general.1 The rate of serious, life-threatening, or fatal events was 2.49 per 100 resident-months, and 57% of these events were considered preventable. Twenty-nine percent of all of the adverse events identified may have been prevented, and most were related to prescribing and monitoring, such as incorrect dosing, a known drug interaction, insufficient monitoring, or a delayed or no response to test results.

Anticoagulants inhibit both venous and arterial thromboses, which is the incipient event in many cardiovascular diseases. They are frequently prescribed for older adults in the acute care and LTC settings. Although anticoagulants have been a part of the medical armamentarium for more than 50 years, their use is complex, and new agents and regimens are being added.

Clot Formation and the Coagulation Pathways

The incidence of both venous and arterial thromboses increases significantly with age.2 Clot formation (and dissolution) is a carefully regulated cascade of events initiated when tissue factor is generated or exposed at a site of injury. In the high-pressure arterial system, atherosclerotic plaque rupture exposes a thrombogenic lipid core to which platelets adhere, activate, and aggregate, to form a platelet plug. Clot formation is further propagated by activation of the coagulation cascade. Venous clots occur in low-flow sites and are predominantly comprised of fibrin, the final product of the coagulation cascade, and red cells, in contrast to the platelet core of arterial clots. Other agents that are used to prevent clotting, but are not anticoagulants, include antiplatelet agents such as aspirin and clopidogrel, and thrombolytic agents.

Clotting or coagulation factors are precursor proteins or proenzymes, which become activated as the cascade proceeds. Classically, the coagulation sequence is separated into the “intrinsic” and “extrinsic” pathways, although this may not be the actual sequence of events in vivo. Both result in a final common pathway in which factor Xa mediates the conversion of prothrombin to thrombin (factor IIa). Factor Xa catalyzes the formation of fibrin from fibrinogen, as well as activating other clotting factors through feedback mechanisms. Fibrin reinforces the platelet plug. Anticoagulant agents used in clinical practice act either indirectly through a plasma cofactor, such as the heparins, or directly interfere with the action of thrombin (IIa).

Heparins, Low-Molecular-Weight Heparins, and Pentasaccharides

Pharmacology

Heparin is found in animal tissue and is composed of a mixture of long chains of glycosaminoglycans.