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Deep Vein Thrombosis - DVT

Deep vein thrombosis

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Deep Vein Thrombosis - DVT

  1. 1. How to learn DVT Prophylaxis like a Pro …. Areej Abu Hanieh 1
  2. 2. Epidemiology  occurrence of DVT is 10%–80% Precise incidence in the critically ill population is challenging because of inconsistencies in patient populations, different diagnosis strategies.  Rate of DVT , In the absence of prophylaxis: 30% in medical-surgical patients, 50%–60% in trauma patients, up to 80% in orthopedic surgical patients, and 20%–50% in neurosurgical patients 2
  3. 3. Risk Factors  Malignancy,  previous VTE  Immobility  known thrombophilia  recent (1 month or less) surgery or  Trauma  older age (70 years or older)  heart or respiratory failure  sepsis, obesity (body mass index of 30 kg/m2 or more),  pregnancy  erythropoiesis-stimulating agents with hemoglobin of 12 g/dL or more  hormonal therapy,  recent transfusions of concentrated clotting factors,  central venous lines,  long distance travel 3
  4. 4. Types of Prophylaxis  Primary prophylaxis — Primary prophylaxis, the preferred method for VTE prevention, is carried out using either drugs (eg, heparin) or mechanical methods (eg, intermittent pneumatic compression boots) that are effective for preventing deep vein thrombosis (DVT).  Secondary prophylaxis — Secondary prevention involves the early detection and treatment of subclinical venous thrombosis by screening medical patients with objective tests that are sensitive for the presence of DVT. However, it is not commonly used as the efficacy of available screening methods (eg, contrast venography, venous ultrasound, MRI venography) is not well established, used in pregnant women that has high risk for thrombosis. 4
  5. 5. DVT Scoring  There is multiple scoring systems , but in avarage :  Score < 4 is low risk  Score > 4 is high risk 5
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  7. 7. Non pharmacological Treatments  Intermittent pneumatic compression (IPC)  graduated compression stockings (GCS)  venous foot pumps (VFP) 7
  8. 8.  Low risk patient , acute medical illness and who are without obvious risk factors for VTE (eg, young patients admitted for a 12 hour observation following an episode of syncope from hypoglycemia),pharmacological treatments is not recommended .  Moderate risk patient , an acute medical illness, who have at least one risk factor for VTE and do not have an increased risk of bleeding, we recommend the use of pharmacologic thromboprophylaxis rather than mechanical methods or no prophylaxis.  High risk patient , (eg, critically-ill, cancer, stroke) and at low risk of bleeding, we recommend the use of pharmacologic thromboprophylaxis rather than mechanical methods or both . 8
  9. 9. VTE prevention for non- orthopedic surgery 9
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  11. 11. Heparin-induced thrombocytopenia  HIT is a severe, immune-mediated reaction potentially leading to life- threatening complications such as myocardial infarction, skin necrosis, stroke, and VTE. 11
  12. 12. Frequency of HIT  Higher in patients receiving unfractionated heparin compared with low-molecular-weight heparin .  Higher risk in cardiac or orthopedic surgical patients receiving unfractionated heparin (15%) than in medical patients (0.1%–1%). 12
  13. 13.  Alternative causes of thrombocytopenia in critically ill patients include extracorporeal devices like dyalisis , intra-aortic balloon pumps, sepsis, disseminated intravascular coagulation caused by sepsis , bleeding, and medications. 13
  14. 14. Diagnosis of HIT  Suspected when a patient has a decrease in absolute platelet count to less than 150,000/mm3 or a relative decrease of at least 50% from baseline, skin lesions at injection sites, or systemic reactions after intravenous boluses.  Typical onset is 5–10 days after heparin exposure, though onset can be delayed and occur up to 3 weeks after therapy cessation .  Recent heparin exposure may result in rapid- onset HIT, occurring within hours after rechallenge. 14
  15. 15. Laboratory testing  GTI-PF4 (Genetic Testing Institute, Waukesha, WI) and ID-PaGIA.  Antibody present if sample from patient binds to the heparin-PF4–coated wells.  High sensitivity (greater than 90%) and low to moderate specificity  (a) Clinically insignificant HIT antibodies are often detected among patients who have received heparin 5–100 days earlier.  (b) Detects a range of immunoglobulin IgA and IgM antibodies that are not pathogenic. 15
  16. 16. Functional assays  Heparin-induced platelet aggregation (HIPA) and C14 serotonin release assay.  Detect platelet activation in the presence of heparin, Patient serum is mixed with washed platelets from healthy volunteers and low and high concentrations of heparin. In the presence of HIT antibodies, platelets are activated in low concentrations of heparin and detected using radioactive serotonin (serotonin release assay) or visually (HIPA).  It is high sensitivity and specificity but not always available and expensive . 16
  17. 17. Treatment of HIT  Immediately discontinue all sources of heparin, and initiate an alternative non-heparin anticoagulant.  Parenteral direct thrombin inhibitors (bivalirudin , Dabigatran) are the agents of choice for anticoagulation in acute HIT because they have no cross-reactivity with heparin.  Some studies support the use of the factor Xa inhibitor fondaparinux for the treatment of HIT, though there are reports of fondaparinux-induced HIT.  Parenteral direct thrombin inhibitors are associated with a higher rate of major bleeding complications than is unfractionated heparin 17
  18. 18.  Initiate warfarin once the platelet count has recovered and is within normal limits (at least 150,000/ mm3 ) and after at least 5 days of therapy with an alternative anticoagulant. Alternatively, conservative warfarin dosing may begin once the platelet count is recovering. If a patient is receiving warfarin at the time of HIT diagnosis, reversing with vitamin K is recommended. 18
  19. 19.  Argatroban dosing in the critically ill population :  i. Mean dose in critically ill patients was 0.24 ± 0.16 mcg/kg/minute and 0.22 ± 0.15 mcg/kg/ minute in critically ill patients with multiple organ dysfunction.  ii. In patients with severe liver impairment, consider 0.5 mcg/kg/minute.  iii. Target aPTT is 1.5–3 times baseline.  f. Bivalirudin dosing in the critically ill population  i. Dose reduced to 0.05–0.1 mg/kg/hour, depending on renal function and bleeding risks  ii. Target aPTT is 1.5–2.5 times baseline. 19
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  21. 21. Duration of Prophylaxis  VTE prophylaxis should ideally continue until the patient is ambulatory or discharged from the hospital.  Thromboprophylaxis is typically not administered in chronically immobilized patients residing at home or in a nursing home. 21
  22. 22. In Critically ill patients TIPS  Routine screening for VTE with ultrasonography is not recommended.  Dosing frequency of low-dose unfractionated heparin (twice vs. thrice daily).  The bioavailability of subcutaneously administered drugs is reduced in critically ill patients with the concomitant use of vasoactive drugs or the presence of edema, thereby potentially providing a reduced effect. 22
  23. 23.  Patients at high risk of bleeding with a moderate to high risk of VTE may be considered for mechanical VTE prophylaxis; however, pharmacologic prophylaxis should be reassessed when the bleeding risk is no longer present.  An inverse relationship between body weight and anti-factor Xa (anti-Xa) concentration may exist in patients with obesity; however, the risk of VTE and optimal anti-Xa concentrations to achieve is unclear !! 23
  24. 24. Oral Anticoagulants for VTE Prophylaxis  No studies to date of critically ill ICU patients with direct thrombin inhibitors (dabigatran) or factor Xa inhibitors (rivaroxaban, apixaban, edoxaban)  Rivaroxaban is noninferior to standard treatments in other settings such as orthopedic surgery.  Rivaroxaban 10 mg orally once daily was compared with enoxaparin 40 mg subcutaneously daily for 10 days, increased bleeding rates occurred in the rivaroxaban group.  Low-molecular-weight heparin is preferred to vitamin K antagonists such as warfarin for prophylaxis; however, it may be used in patients who refuse injections. 24