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Update in Standard of Care for Venous Thromboembolism from the June 2012 Supplement to CHEST and 2017 AC Forum

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Update in Standard of Care for Venous Thromboembolism from the June 2012 Supplement to CHEST and 2017 AC Forum Update in Standard of Care for Venous Thromboembolism from the June 2012 supplement to CHEST and 2017 AC Forum Sharyl Magnuson, MD Adjunct Faculty, Pacific University School for PA Studies former Associate Medical Director, Lovelace Clinical Thrombosis Center Member THSNA Disclosures • Nothing to disclose from pharmaceutical sources of income. • I have been an Investigator on many Pharmaceutical sponsored Clinical trials, last more than 7 years ago. • I have been a promotional speaker in the past for Xarelto, last more than 2 years ago. Scope of the Problem • “On average, one American dies of a blood clot every 6 minutes” 100,000/year. National Blood Clot Alliance • The precise number of people affected by DVT/PE is unknown, although as many as 900,000 people could be affected (1 to 2 per 1,000) each year in the United States. • Estimates suggest that 60,000-100,000 Americans die of DVT/PE (also called venous thromboembolism). • 10 to 30% of people will die within one month of Clot diagnosis. • Sudden death is the first symptom in about one-quarter (25%) of people who have a PE. • Among people who have had a DVT, one-half will have long-term complications (post-thrombotic syndrome) such as swelling, pain, discoloration, and scaling in the affected limb. • One-third (about 33%) of people with DVT/PE will have a recurrence within 10 years. • Cdc.gov Best Resource • MAQI2 version 1.7, the Michigan Anticoagulation Quality Improvement Initiative, a consortium of AC clinics and experts across MI, produced this 65pg Quick Reference using updated review literature. http://anticoagulationtoolkit.org/sites/default /files/toolkit_pdfs/toolkitfull.pdf • Free. Also, you should have a direct, downloadable link through this conference with my favorite Dental AC advice publications included as well. Available anti-coagulants Heparins Unfractionated Heparin = UFH Low Molecular weight Heparins = LMWH Pentasaccharide (Fondaparinux) Vitamin K antagonists (VKA) Warfarin = Coumadin In Europe, Macumal and some others, all same effect on INR DOAC’s Dabigatran , Rivaroxaban, Apixaban, Edoxaban, with Betrixaban Investgational (targeting Fac XI & XII) Established Anticoagulants XII XIIa I N WARF VIIIa T R XIa XI EXTRINSIC IX I N WARF IXa UFH S LMWH I C TF VIIa WARF Xa II Va X WARF IIa FIBRINOGEN FIBRIN A. Spyropoulos Our old friend, Warfarin • Wisconsin Alumni Research Foundation + the “arin” to relate it to coumarin. Why something + warfarin is needed to initiate VTE therapy. Warfarin is a competative inhibitor of Vit K, inhibits carboxylation reactions required for synthesis of factor II, VII, IX, & X, all pro -thrombotic. Also inhibits production of anti-thrombotic proteins, Proteins C & S. Kitchens, Alving, & Kessler; Consultative Hemostasis& Thrombosis; 2nd edition; pg 449 Approx 1/2-Life of Vit K-Dependent Factor/pro- & Anti-coagulants • Factor or Anticoagulant Half-Life • Factor VII (pro) 6 hours (INR) • Factor IX “ 24 hours • Factor X “ 36 hours • Factor II (Thrombin) “ 50 hours • Protein C (anti) 8 hours • Protein S “ 30 hours Table Compiled from data from Goodman and Gillman’s The Pharmacological Basis of Therapeutics, 1996 Fall of Vit K Dependent Factors with the start of Warfarin Fac VII, inversely impacts INR. Vit K dep factors K dep Vit Prot C, hypercoagulable when low. Thrombin, drop has most meaningful impact on anticoagulation. [Danger Zone] days Warfarin induced skin. necrosis. Due to acquired Prot C deficiency with early Warfarin tx. Early drop of Prot C, late fall of Fac II (Thrombin) in setting of thrombogenic milieu is cause of this adverse event of Warf initiation. Can also cause clot extension, embolism, infarction. In Afib patients with active atrial clots, can lead to clot growth with friable new clot and increased embolic risk, stroke and arterial emboli. It takes 5-10 days off Warfarin for the system to reset to Warfarin naive, requiring new initiation bridge. Initial Unbalanced Fall of Vit K dependent factors PT is prolonged by decreases in factor VII, one of the earliest factors to fall, especially if warfarin is “loaded”. This may also cause an early profound drop in Protein C levels, producing an unfavorable balance of anti- vs pro- thrombotic effects. When in the setting of an active clot, the preponderance of pro-thrombotic influences is particularly dangerous. Kitchens, pg 449. Choosing A Safe Initial Bridging Agent Initial Bridge Choices LMWH: Can be monitored with Factor Xa levels. Must monitor Platelets 5-10 days into treatment (small risk of HIT compared w UFH). Partial reversal w Protamine. Dalteparin (Fragmin): 200 units/kg/day SC, max 18,000 units/dose. Dosing nomogram wt based in insert. QD dosing. Proph dosing, 5000 units SQ qd Metabolism, liver; CYP450. T1/2 3-5hrs, 6-7 in renal impairment. In severe renal impairment (CrCl < 30), test anti-Xa levels after 3-4 doses, target 0.5-1.5 IU/ml. Adjust accordingly. Half dose with platelet counts 50-100K. Don’t use if Plt < 50K. Arch Intern Med. 2012;172(22):1713-1718. Published online November 5, 2012. doi 10.1001/2013.jamainternmed.369 LMWH cont. Enoxaparin (Lovenox): 1mg/kg/bid SC (or 1.5mg/kg/qd, equally safe and effective). 40% renal excretion. T1/2 4.5-7 hrs Must adjust for CrCl less than 30 to 1mg/kg/day. Doesn’t remove well with Dialysis. Accumulates in renal impaired patients even at the 40mg SQ QD prophylactic dose. Choice of Initial Bridging Agent cont. Fondaparinux(Arixtra): 3 tiered daily dosing. 5mg SC if wt < 50kg, 7.5mg SC if wt 50-100 kg, and 10mg SC if wt > 100kg. Excreted mainly in urine. T1/2 17-21 hrs. No good reversal agents. Synthetic. Almost no HIT risk. UFH or Heparin: Mention only to discourage use in the treatment of outpatient VTE. Can be used easily IV. Less easily SQ weight based. No pre-prepared single use syringes other than the 5000 U Proph dose, must be drawn up by patient for treatment dosing. Direct-Acting Oral Anticoagulants DOACs • NOAC----”no anticoagulant” That’s a real problem. Happened several times in interpretation of hospital orders. • TSOAC----Thought to be a bit obscure. Target specific is correct, but TS is hard to say. • DOAC is easy and clear, D stands for Direct- Acting or Directed. Now the DOAC’s Directed Oral AntiCoagulants • Factor Xa inhibitors: – Share mixed clearance, renal and hepatic, to variable degrees. – All to be avoided in severe Hepatic failure. – All need to be used carefully in renal insufficiency. – Clarithromycin/Erythromycin, -azole antifungals, and HIV protease inhibitors---all lead to increased drug levels. – CYP3A4 inducers that cause measurable decreased levels: rifampicin, carbamazepine, phenobarbatol, St. John’s Wort. Fac Xa inhibitors • Rivaroxaban (Xarelto) and Apixaban (Eliquis) – Both can be started alone to treat VTE. – Both use larger starting dose in setting of active VTE. –Rivaroxaban: – Starter pack, 21 days of 15mg bid and 9 days of 20mg qd taken with the evening meal. – 36% excreted unchanged in urine. – 2/3 of dose is metabolized through various pathways: CYP450, P-gp transport. – Normal PT/INR means no sig Rivaroxaban levels. !!!Rivaroxaban is the only Fac Xa inhibitor that can use the INR this way to test residual drug presence!!!! Riva & Apixa –Apixaban: – Downloadable calendar to remind patients to take (2) 5mg tabs BID for 7d, then 5mg BID. – Cleared 25% total dose in feces & urine, CYP metabolism main pathway. – Biggest mistake is under-dosing. Patients have increased risk of VTE events or strokes if dose too low. Assess risk accurately. • 2.5 mg twice daily is recommended for patients with at least 2 of the following characteristics: • age ≥80 years • body weight ≤60 kg • serum creatinine ≥1.5 mg/dL More Xa inhibitors • Edoxaban (Savaysa): – requires a 7d pretreatment of LMWH or UFH before starting tx. – Less than 10% dose metabolized via any pathway, very few interactions. • P-gp inducers, rifampin, can lower drug level. • Some P-gp inhiitors can raise levels, requiring dose reduction from 60mg qd to 30mg qd. • 50% excreted unchanged in urine. • Reduce dose to 30mg qd for CrCl 15-50 ml/min. • Betrixaban just released for post hospitalization VTE prophylaxis. – Not yet approved for VTE tx. No reversal agents yet for Fac Xa Inhibitors Direct Thrombin inhibitor, Dabigatran (Pradaxa) • No overall improved safety over warfarin, but decreased Intra-Cranial Hemorrhage. (ICH) • Requires 5-10 days parenteral AC prior to starting. Then BID dosing. (A function of the study design) • Induces number and activity of Thrombin receptors on platelets. May be reason cessation leads to increased thrombosis. • GI upset common non-bleeding side effect. • Dronedarone and Ketakonazole co-use lead to sig increase in levels. Dabigatran Cont. • 80% renally cleared. • The rest, hepatic, so not advised in severe liver failure. (you will see this only in pkg insert fine print). • HemoDialysis removes 62% of circulating Dabigatran in 2hrs. • aPTT or TCT (Thrombin Clotting Time) testing measures residual Dabigatran effect. • Praxbind is available antidote. Safety & Monitoring of DOACs See MAQI pg 52 • Assess labs: – Just post initiation: H/H and ? in 1 month and 3 months – Q 6 months Renal function if CrCl 30-60 ml/min* or if on dabigatran and >75 years or fragile – Q 3 months Renal function if CrCl 15-30 ml/min* – As needed If clinically indicated for conditions that may impact renal or hepatic function. DOAC Safety and Monitoring cont. • With each visit Assess: – Compliance: Educate, monitor adherence, Stress non- compliance concerns. Riva with food. Dabi in package, ect. – Thromboembolism: TIA, Stroke, VTE, art emb, PE. – Bleeding: Remember, increased GI. Investigate per normal screening stool, uterine, and urine bleeding protocols. If benign and minor, treat to mitigate and encourage continuation. – Side effects: Usually minor bleeding. GI upset on Dabi.
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