Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
1. Why does venous thrombosis happen ? 2. What are the risk factors ? 3. How do we prevent it ? 4. How do we treat it ? 5. Are there special considerations for cancer patients ? 6. Scattered pointless NZ photos. • • 10% of DVT embolise to lungs PE associated with 5-10% hospital deaths Age ( Over 70 -) Sex , M:F 1.2:1 Hospitalization - Medical and surgical Cancer ( x 20) Immobilization Drugs (OCP – 3,HRT-2) Pregnancy (6-8) Travel (2) Pregnancy x 6-8 1 postpartum period -20 2 HRT and OCP x 2 ( Depends on oestrogen content <50ug low risk )3 1.T&H 2010 Feb;103(2):306-11. Epub 2009 Nov 2.Obst Gynae . 2011 Mar;117(3):691-703 3. J OBST GYN Can . 2010 Dec;32(12):1192-7 Antithrombin deficiency Protein C Protein S Factor V Leiden / APC resistance Prothrombin 20210A mutation Increased factor II, VIII, IX, XI 9.7 fold Marked in first year MGUS x 3.5 Increased by IMIDs Most hospitalized patients with cancer require thromboprophylaxis throughout hospitalization ● Thromboprophylaxis is not routinely recommended for ambulatory patients with cancer; it may be considered for very select high-risk patients ● Assess using Khorana score but most inpatient cancer patients need VTE prophylaxis. Myeloma , immobilised patients Myeloma on IMIDs Lymphoma , large intra-abdominal mass A meta-analysis of 11 studies found an increased risk of deep vein thrombosis for PICCs (odds ratio [OR] 2.55, 95% CI 1.54-4.23); there were no pulmonary embolism events Risk factors for DVT associated with PICC catheter placement include prior DVT, recent surgery, and cancer The rate of symptomatic venous thrombosis is 2-5% ACCP- Routine prophylactic systemic anticoagulation is not recommended for patients with indwelling central venous catheters It may be reasonable to administer prophylactic anticoagulation in high–risk patients when the perceived risk of thrombosis outweighs the risk of bleeding Uncomplicated venous thrombosis anticoagulate Line can be kept in Duration depends on line remaining in place Once line removed continue for 2-6 weeks. Treat with LMWH LMWH and warfarin Dabigatran Rivaroxaban Apixiban Edoxaban Can initiate warfarin first day with LMWH Adjust starting warfarin to patient Ensure good communication to warfarin team Ensure follow up Target 2.5 INR Monitor Narrow therapeutic index High bleeding risk Many drugs interact with it Cumbersome to start and stop fractionation from UFH MW 4,000-6,500 daltons bioavailability 90% t ½ 4-12 hours function - accelerates inhibition of Xa > lla Simple, safe and effective A meta-analyses (seven RCTs; 1908 patients with cancer), reported that compared to VKAs, LMW heparin reduced the rate of recurrent VTE (hazard ratio [HR], 0.47; 95% CI 0.32-0.71), a benefit that occurred without a survival advantage. The CLOT trial was a multicenter, international, randomized trial of 672 cancer patients with acute VTE that compared six months of treatment with warfarin with the LMW heparin, dalteparin. Dalteparin was associated with a significant reduction in the rate of recurrent VTE at six months (9 versus 17 percent; HR, 0.48, 95% CI 0.30-0.77). There were no significant differences in the rates of major bleeding (6 versus 4 percent), any bleeding (14 versus 19 percent), or overall mortality (39 versus 41 percent). Six months of treatment with LMWH Consider dose reduction to 75% after 4 weeks Extend duration if persistent cancer If recurrence on treatment consider 25% dose increase Avoid IVC filters if possible And now into the future and beyond Direct thrombin inhibitor – Dabigatran Direct Xa inhibitors – Rivaroxaban - Apixiban - Edoxaban Effective As effective as enoxaparin for primary prevention of VTE in patients undergoing total hip or knee replacement1 As effective at treating VTE as warfarin As effective at preventing CVA in atrial fibrillation. Dabigatran is better at preventing stroke Safe Reduced Cerebral bleeds by 60% Reduced major bleeds by 30% No liver toxicity observed2 Fast onset and offset of action 3 Cmax achieved in 2 hours Half-life: 12–17 hours4 Predictable anticoagulant effect 3 No routine coagulation monitoring required No clinically meaningful drug–food effects4 Low potential for cytochrome P450-related drug interactions3 Cmax = maximum concentration; VTE = venous thromboembolism 1. Wolowacz SE et al. Thromb Haemost 2009;101:77–85; 2. Ezekowitz MD et al. Am Heart J 2009:157: 805–10.e2; 3. Stangier J. Clin Pharmacokinet 2008;47:285–95; 4. Pradaxa™ Product Monograph No accurate monitoring test Compliance Expensive No reversing agent Higher GI bleeding risk In one meta-analysis of six studies that included 1132 patients with DVT and cancer, compared with conventional therapy (heparin plus warfarin) similar rates of VTE recurrence (4 versus 6 percent; odds ratio [OR], 0.63; 95% CI, 0.37-1.10) and major bleeding (OR, 0.77; 95% CI, 0.41-1.44) were reported in those taking DOACs [42]. Not enough evidence with DOACs in cancer Be pragmatic DVT nurse specialist All VTE patients are seen by coagulation team at outset Reviewed at 3 months and decision on duration made in thrombosis clinic Standard of treatment is DOAC New VTE nurse specialist to investigate and treat PE Expand role of warfarin nurses in Nenagh and Ennis to manage DVT to provide a regional standard service 1. Venous thrombosis is multifactorial 2. Cancer is a major risk factor for VTE 3. Routine prophylaxis is not recommended outside of hospital but required in hospital 4. PICCs are associated with significant thrombosis rates 5. Venous thrombosis in cancer should be treated with LMWH at present but DOACs maybe on the way 6. VTE in non- cancer patients should be treated with DOACs 7. Hopefully the future lies with Nurse specialist management of VTE