Heparin – Lovenox - Coumadin Charnelle Lee, RN, MSN

Heparin Anticoagulant Does not dissolve clots Interrupts the clotting process Helps the body stop the size of the clot from increasing Takes 6 weeks for an existing clot to dissolve Of course this is dependant on the size and patient condition

Heparin Antidote Heparin® Antidote Protamine Sulfate Protamine sulfate is a heparin antidote that works against the anti-coagulating effects of heparin by binding to the drug and making it ineffective. Originally derived from the sperm of salmon, protamine sulfate can only effectively counteract heparin if 1mg of protamine sulfate is administered for every 100 IU of active heparin received. It's important to note that Vitamin K, which is effective at promoting blood clotting, is not an effective heparin antidote, as Vitamin K cannot stop heparin from working (like protamine sulfate does).

Protamine Sulfate Unfortunately, using protamine sulfate to stop the effects of heparin can have its own complications, including: constricting the lung's airways (bronchoconstriction) dramatically increasing or decreasing blood pressure severe allergic reaction, characterized by facial or tongue swelling, breathing difficulties and/or skin rash promoting anti-coagulation (if large enough doses are administered)

Side Effects Abdominal or stomach pain or swelling Back pain or backaches Bleeding from the gums when brushing teeth Blood in the urine Constipation Coughing up blood Dizziness Headaches, severe or continuing Heavy bleeding or oozing from cuts or wounds Joint pain, stiffness, or swelling Menstrual bleeding, unexpected or unusually heavy Unexplained bruising or purplish areas on the skin Unexplained nosebleeds Vomiting of blood or material that looks like coffee grounds

Heparin-Induced hrombocytopenia (HIT) Description – Two distinct types Type I HIT – Most common type – Non-autoimmune condition – Transient, often resolves spontaneously Type II HIT – Less common, more severe

Etiology of Type II HIT Immune-mediated response to the administration of heparin – Observed in 3% to 5% of patients treated with unfractionated heparin – Also occurs after exposure to low– molecular-weight heparin (less common) Characterized by severe thrombocytopenia during heparin therapy Onset 5 to 14 days after first exposure to heparin, can be within hours of re-exposure to heparin Mortality rates as high as 30%

Pathophysiology of Type II HIT Thrombocytopenia related to formation of heparin-antibody complexes – Release of platelet factor 4 (PF4) PF 4 attracts heparin molecules forming immunogenic complexes that adhere to platelet and endothelia surfaces Activation of platelets stimulates release of thrombin and formation of platelet clumps

Pathophysiology of Type II HIT FIGURE 27-2 Pathophysiology of heparin-induced thrombocytopenia. First, heparin binds to platelet factor 4 (PF4), forming a highly reactive antigenic complex on the surface of platelets. Susceptible patients then develop an antibody (IgG) to the heparin/PF4 antigenic complex. Once produced, the IgG then activates the platelets via their Fc receptors. Thrombocytopenia develops as the reticuloendothelial system consumes activated platelets, platelet microaggregates, and IgG- coated platelets. (Courtesy GlaxoSmithKline, Philadelphia, Pa.)

Assessment and Diagnosis of Type II HIT Clinical manifestations – Related to formation of thrombi and vessel occlusion – Most thrombotic events are venous Deep vein thrombosis, pulmonary embolism, limb ischemia, thrombotic stroke, and myocardial infarction (Continued)

Assessment and Diagnosis of Type II HIT (Continued) Laboratory findings – Key indicator is platelet count Platelet count <50,000/mm 3 Sudden drop of 30% to 50% from patient’s baseline platelet count – Assays to assist in confirming diagnosis Heparin-induced platelet aggregation Serotonin release assay

Medical Management of Type II HIT Early identification is critical to managing effects of Type II HIT Focus of medical management revolves around: – Identification of Type II HIT – Discontinuation of heparin therapy – Alternative form of anticoagulation if needed

Heparin® Induced Thrombocytopenia Treatment The typical treatment for heparin induced thrombocytopenia involves: discontinuing use of the heparin drug taking lepirudin, another anti-coagulant medication In most cases, this combination of factors will prevent new clotting as patients work towards living a healthier lifestyle. As with many conditions, heparin induced thrombocytopenia will have the best prognosis the earlier the condition is diagnosed and treated.

Nursing Management of Type II HIT Nursing priorities in the management of the patient with HIT are focused toward: – Ensuring that all heparin is discontinued. – Maintaining surveillance for complications. – Providing comfort and emotional support.

Laboratory monitoring: platelet count Check PLT count daily to detect heparin induced thrombocytopenia (HIT) If count drops 30-50%, consider HIT, withdraw heparin, start alternative anticoagulant, order confirmatory test for HIT Overdose of UFH Stop heparin and monitor PTT. Heparin half-life is approximately 30 minutes. If bleeding is severe, consider protamine sulfate (1 mg/100 units heparin) FFP does not reverse heparin effect

DTI’s Direct Thrombin Inhibitors (DTIs): Argatroban and Lepirudin DTI indications Substitute for heparin when HIT is suspected or confirmed. Even when HIT's only manifestation is thrombocytopenia and heparin is stopped, risk of thrombosis in subsequent 30 days approaches 50% unless alternative anticoagulant is used. DTI dosages Lepirudin: 0.4 mg/kg slowly IV, then 0.15 mg/kg continuous infusion for 2-10 days depending on indication Argatroban: 2 µg/kg/min IV DTI half-lives Lepirudin: 20 minutes Argatroban: minutes

Laboratory monitoring of DTIs PTT is used to prevent bleeding or thrombosis Lepirudin: collect blood four (4) hours after initial dosage, adjust dosage to PTT x mean of reference interval Argatroban: collect blood two (2) hours after initial dosage, adjust dosage to PTT x mean of reference interval Lepirudin accumulates in kidney failure Argatroban accumulates in liver failure Do not start in patients with PTT longer than 2.5 x mean of reference interval In HIT, warfarin may be introduced when platelet count starts to increase but DTIs should be continued until platelet count normalizes. After 4-5 days of warfarin, if platelet count is normal and PT is therapeutic, stop DTI for a few hours and recheck INR. If between 2-3, it is safe to discontinue DTI. [top]

Coumadin Warfarin (Coumadin  ) Indications for warfarin Treatment of arterial and venous thrombosis to prevent clot propagation Prevention of thromboembolic disease in thrombophilia, atrial fibrillation, mechanical heart valves, and high-risk surgery Mechanism of action for warfarin Prevents the vitamin K dependent gamma-carboxylation of factors II, VII, IX, and X, proteins C and S, slowing thrombin production Dosage of warfarin 5-10 mg/day with no loading dose. Must be monitored due to unpredictable half- life. Affected by many drugs and dietary variation Requires 2-7 days to reach therapeutic levels. To achieve immediate anticoagulation, begin with heparin

Laboratory monitoring: The INR PT generates the international normalized ratio (INR) by this formula: INR = (Patient PT/MRI PT) ISI Where… PT = prothrombin time in seconds MRI = geometric mean of reference interval ISI = international sensitivity index supplied by reagent manufacturer Target INRs Post-myocardial infarction, most therapy and prophylaxis: INR Mechanical heart valves: INR Laboratory monitoring sequence Daily until INR is therapeutic twice at least 24 hours apart Twice a week for 2 weeks, then once a month until therapy is complete

Minor bleeding Warfarin dosage INR Decrease, look for site INR Stop drug, reinstitute at lower dose INR 5-8 Stop drug, give 2.5 mg K PO or 1 mg SQ INR 5-8, thrombotic risk high Stop drug, do not give K INR > 8 · Stop drug, give 5 mg K PO or 2-5 SQ · Consider 10 mL/kg FFP or 25 U/kg PCCs (p. 36)

Managing warfarin overdose No bleeding Warfarin dosage INR Decrease, do not stop drug INR 5-8 Decrease, consider 1 mg K PO INR 5-8, bleeding risk high Decrease, give mg K PO or1 mg SQ INR > 8 Stop drug, give mg K PO or 2-3 mg SQ INR > 8, bleeding risk high · Stop drug, give 5 mg K PO or 3-5 mg SQ · Consider 10 mL/kg FFP or 25 U/kg PCCs (p. 36)

Major bleeding Warfarin dosage INR Stop drug, give 5 mg SQ K or IV, repeat as necessary, look for bleeding site INR · Stop drug, give 5-10 mg K SQ or IV, repeat · Consider mL/kg FFP or U/kg PCCs (p. 36) INR 5-8 · Stop drug, give 5-10 mg K SQ or IV, repeat · Give 15 mL/kg FFP or U/kg PCCs (p. 36) INR >8 · Stop drug, give10 mg K SQ or IV, repeat 6h · Give 15 mL/kg FFP or U/kg

Antidotes Heparin – Coumadin- – 1 – 2

LMWH What is Lovenox? Lovenox is an anticoagulant (blood thinner) that prevents the formation of blood clots. Lovenox is used to treat or prevent a type of blood clot called deep vein thrombosis (DVT), which can lead to blood clots in the lungs (pulmonary embolism). A DVT can occur after certain types of surgery, or in people who are bed- ridden due to a prolonged illness. Lovenox is also used to prevent blood vessel complications in people with certain types of angina (chest pain) or heart attack. Lovenox may also be used for other purposes not listed in this medication guide

Difference between Heparin and Lovenox Lovenox is a brand name for the prescription medication enoxaparin, which, like heparin, is prescribed for the treatment of blood clots. Lovenox is actually derived from heparin and has molecules with a lighter weight than its parent drug. Read more at Suite101: Lovenox vs. Heparin: Differences Between Anticoagulant Medications | Suite101.com heparin-a193192#ixzz1RomQ8fcpLovenox vs. Heparin: Differences Between Anticoagulant Medications | Suite101.com heparin-a193192#ixzz1RomQ8fcp