Guide staff members to better management of patients receiving antithrombotic medications.
Abstract: Review necessary management techniques regarding safe use of anticoagulant therapy.
There's been an upsurge in the market of new pharmacologie agents released for the treatment of thromboembolic disorders. While these medications may have similar names and indications, their usefulness varies greatly. In fact, the safety and efficacy of these drugs hinges on individual patient situations.
Drug response monitoring proves crucial to treatment success and is inherent in the nursing role. Failure to adhere to protocols and properly monitor results may yield poor patient outcomes, increased lengths of stay, and unnecessary laboratory testing. Higher patient acuity levels necessitate that you and your staff members remain vigilant in monitoring and administering these medications to avoid errors.
To help staff best understand anticoagulant drug actions, facilitate their familiarity with Virchow's triad, platelet function, and the clotting cascade. Virchow's triad consists of three conditions: venous stasis, vascular damage, and a hypercoagulable state, which predisposes an individual to hypercoagulability or thrombosis.
Venous stasis is associated with prolonged periods of immobility, cancer, pregnancy, obesity, and vascular access device usage. As a result, the patient is at increased risk for thrombotic or embolie events. Atherosclerosis, vasculitis, infection, surgery, vascular access device usage, or deep vein thrombosis can produce injuries to the vascular endothelium, initiating the intrinsic clotting pathway.
Hypercoagulability is associated with abnormalities in the activation or deactivation of the clotting cascade. Antifhrombin Uf deficiency, cancer, diabetes, pregnancy, and the use of estrogen or progestin are among the etiologies of these inherited or acquired abnormalities.
Patients can be at risk for developing a thrombus in a narrowed coronary artery or from plaque rupture (vascular damage). Platelets respond to vascular injury by adhering to the injured site and activating the clotting cascade, which results in further platelet aggregation and clot formation. In addition, many of the reactions in the clotting cascade occur on the surface of the platelets. The activation of the clotting cascade may be through the intrinsic or extrinsic pathway. The intrinsic pathway is initiated when the endothelium is damaged or blood comes into contact with collagen, which occurs with every venipuncture and catheter insertion. The extrinsic pathway is initiated when tissue injury occurs. Factor VII is activated and binds with calcium to activate factor X and begin the common pathway of the clotting cascade.1
* Platelet inhibitors: The most common platelet inhibitor is aspirin (ASA). It works by inhibiting the production of thromboxane A2 by blocking the enzyme cyclooxygenase-thus, platelets don't adhere to each other. ASA doses range from 81 mg to 325 mg per day to achieve the desired effect. ASA is indicated to reduce the risk of stroke, myocardial infarction (MI), unstable angina, and other ischémie events. Recent studies find that combination therapies using ASA with other platelet inhibitors and anticoagulants can be safely administered when monitored closely.2'3
Clopidogrel (Plavix) and ticlopidine (Ticlid) are also classified as platelet inhibitors. Unlike ASA, they achieve therapeutic effect by blocking adenosine diphosphate (ADP) from binding to its receptors. For patients who can't take aspirin or warfarin for anticoagulation, clopidogrel or ticlopidine are suitable alternatives.4 Note, though, that ticlopidine is associated with agranulocytosis and thrombocytopenia, so monitor your patients closely.
Glycoprotein lib/Ilia (GP Ilb/IIIa) inhibitors are another group of platelet inhibitors, which include abciximab (ReoPro), eptifibatide (Integrelin), and tirofiban (Aggrastat). The glycoproteins located on the surface of the platelets serve as a receptor for fibrinogen. The GP Ilb/IIIa inhibitors bind to the GP Ilb/IIIa receptors and inhibit platelet aggregation. These medications are administered only through an intravenous (I.V.) route.
All are indicated in acute coronary syndrome and before and during percutaneous interventions. While abciximab isn't considered reversible, stopping the infusion can reverse the effects of eptifibatide and tirofiban. Abciximab can inhibit platelet aggregation for up to 36 hours.5
* Anticoagulants: Anticoagulants prevent thrombus formation by inhibiting several coagulation enzymes. Unfractionated heparin (UFH) works specifically by increasing the formation of antithrombin III-thrombin complex; it deactivates thrombin and prevents conversion of fibrinogen to fibrin. Heparin's other demonstrated properties include the suppression of smooth muscle proliferation, enhancement of antibody production, lowering of triglycerides, and protection against endothelial injury.6
UFH is administered subcutaneousIy or intravenously. Base doses on body weight, age, and renal function. Laboratory monitoring is necessary with I.V. administration. Dosing is guided by the activated partial thromboplastin time (aPTT). A desired therapeutic range of the aPTT is 2 to 2.5 times the control.7 Heparin induced thrombocytopenia (HIT) may occur in up to 5% of patients,8 so monitor the patient's platelet level.
Low-molecular-weight heparins (LMWH) such as enoxaparin (Lovenox) and dalteparin sodium (Fragmin) accelerate formation of antithrombin EIthrombin complex-and deactivate thrombin, preventing conversion of fibrinogen to fibrin. These LMWHs have better diffusion than UFH following subcutaneous injection, requiring less frequent dosing and less laboratory monitoring. Advantages of LMWH are decreased risk of HIT and less osteopenia.9'10 These drugs are administered subcutaneously; the dose is adjusted based on body weight and indication. Because of different manufacturing processes, instruct staff not to substitute one LMWH for another.
LMWHs are indicated for the prevention and treatment of deep vein thrombosis. Enoxaparin has been used off-label for the prevention of thrombi in patients with artificial valves and those who are pregnant. Following clinical studies, the manufacturers of enoxaparin have added warnings to the label to stop this practice.11
The cost of LMWHs may be offset by the fact that laboratory monitoring isn't necessary. Also, because patients are taught to self-administer these drugs, lengths of stay often decrease, further offsetting the higher cost of these drugs.
Warfarin (Coumadin) is an oral anticoagulant that works by blocking the synthesis of factors II (prothrombin), VIIx IX, and X, as well as proteins C and S. Indications for warfarin are numerous.
Continued anticoagulation with warfarin depends on patient condition and desired outcomes. Measure warfarin's therapeutic effectiveness by monitoring the International Normalized Ratio (INR). The therapeutic range of INR is 2.0 to 3.0-with a goal of 2.5-for most conditions; for patients with mechanical heart valves, an INR of 2.5 to 3.5 is desirable.12
Derived from hirudin, which binds with thrombin, direct thrombin inhibitors are the most recent medications to become available for anticoagulation.13 The following direct thrombin inhibitors are available for I.V. administration: lepirudin (Refludan), Argatroban, and bivalirudin (Angiomax).
The Food and Drug Administration (PDA) has approved Argatroban and lepirudin for use in patients with HIT. The PDA has also approved bivalirudin given in conjunction with aspirin for use with patients with unstable angina undergoing percutaneous transluminal coronary angioplasty. These drugs produce a predictable and reversible anticoagulant effect. Adjust infusion rates based on aPTT. You may monitor the effectiveness of bivalirudin by using activated clotting times.14
* Fibrinolytics: Used to dissolve clots and reestablish blood flow to the tissues, fibrinolytics are used in acute MI, to prevent further neurologic deficits in nonhemorrhagic strokes, and to treat thrombi in acute peripheral arterial occlusion and in pulmonary embolism. Fibrinolytics are most effective when administered within the first few hours of symptom onset. Usage helps reduce mortality during the first 30 days after an ML15
Because hemorrhage is a risk for patients, these medications aren't indicated for patients with gastrointestinal bleeding, recent surgery or trauma. Be sure to establish baseline hemoglobin, hematocrit, platelet counts, and bleeding times. Select follow-up laboratory monitoring according to the adjuvant anticoagulant medications.16
Alteplase (Activase) has FDA approval for catheter clearance. Reteplase (Retavase) has also been used. Note that streptokinase has warnings against it for this purpose.
Work the process
Providing your staff with the appropriate and most up-to-date information about anticoagulant medications is one step in assuring safe medication administration. Consider multidisciplinary collaboration to develop flow sheets to monitor dosages and laboratory findings.
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2. Ambrose, J., and Martinez, E.: "A new paradigm for plaque stabilization," Circulation. 105(16):2000-2004, 2002.
3. Mines, S.: "Recent strides in antithrombotic therapy," Patient Care. 34(15):2022, 25-26, 28, 35, 2002.
5. DiDomenico, R.: "New antithrombotics for the intensive care unit setting: GPIIb/llla inhibitors, low molecular weight heparins, and direct thrombin inhibitors," Critical Care Nursing Quarterly. 22(4): 61-74, 2000.
7. Navuluri, R.: "Understanding hemostasis: An overview of the process," American Journal of Nursing. 101(9):24B-24C, 2002.
8. DiDomenico, R.: loc cit.
10. Gylys, K.: "Pharmacology," Journal of Cardiovascular Nursing. 15(4): 91-95, 2001.
11. Aventis Pharmaceuticals: Safety Alert: Lovenox, 2002.
12. Karen, A.: Nursing Drug Guide. Philadelphia: Lippincott Williams & Wilkins, 2002.
13. Blann, A., Landray, M., and Lip, G.: "An Overview of Antithrombotic Therapy," British Medical Journal. 325(7367): 762765, 2002.
14. long, L., and Mendez, M.: "Therapeutic considerations in the management of patients with heparin induced thrombocytopenia," Progress in Cardiovascular Nursing. 17(3):142-147, 2002.
15. Blann, A., Landray, M., and Lip, G.: loc cit.
By Paige Wimberley, RN-CS, MSN, and Nonie Wiggins, CCRN, MSN
About the authors
Paige Wimberley and Nonie Wiggins are assistant professors of nursing at Arkansas State University, Jonesboro, Ark.
Copyright Springhouse Corporation Feb 2004
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