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Deep Venous Thrombosis Ranjith Thampi
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Deep Venous Thrombosis Ranjith Thampi

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Deep Vein Thrombosis is an important and frequently missed out diagnosis that can often lead to sudden death in post operative patients. Did this powerpoint for an O&G seminar. Mainly focusses on DVT …

Deep Vein Thrombosis is an important and frequently missed out diagnosis that can often lead to sudden death in post operative patients. Did this powerpoint for an O&G seminar. Mainly focusses on DVT in OBG and its management and prevention. Kindly leave a comment and let me know what you think.

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  • Process by which liquid blood flowing through the vascular system turns into a solid mass of platelets, cells and fibrin within the blood vessel. A blood clot in a major vein that usually develops in the legs and/or pelvis. DVT and its sequelae, Pulmonary embolism are the leading causes of preventable in-hospital mortality. Types of Puerperal Venous Thrombosis: Phlebothrombosis and Thrombophlebitis. 1 can be superficial or deep(DVT). Initial event being vascular thrombosis. 2 can be suppurative or Non suppurative. Initial event being inflammation of vessel wall.
  • Venous Stasis- Gravid uterus pressure on pelvic veins and also due to decreased venous tone, supine positioning and effects of anaesthesia Hypercoagulable- Increased levels of fibrinogen, factors 7,8,10, increased ability to neutralize heparin, increased platelet count and decreased fibrinolytic activity. There is higher levels of Factors 5,7,10 in first few days after delivery Vascular damage- From excessive vasodilatation, direct injury Infection- acts as a triggering point.
  • Patients should be assessed individually, both considering any existing risk factors for VTE , and their risk of bleeding (i.e may be already at lower risk of DVT). A decision can then be made whether VTE prevention should be offered and, if so, whether this should be pharmacological or mechanical. For patients with increased risk, the balance of risk versus benefits of treatment should be reassessed at regular intervals. For patients in hospital this should be 24 hours after admission or whenever there is a change in the clinical situation. Genetic Risk Factors- Factor V and Prothrombin G20210A mutation have been identified Other Risk factors- Immobilization during prolonged travel, obestiy, smoking, surgery, trauma, oral contraceptive use, postmenopausal HRT. Medical conditions increasing risk- Cancer, APLA.
  • Normal D-dimer level is <500 μ g/mL( ELISA)
  • Low molecular weight heparin (LMWH4) - synthetic alternatives may be more acceptable to patients who want a non-animal based product. Heparin in higher doses inhibits platelet aggregation and prolongs BT.
  • Contraindicated in First Trimester- Teratogenic Also in later stages of pregnancy for fear of fetal bleeding.
  • Warfarin avoided in pregnant patients Mild haemorrhage or markedly elevated INR values- treat with Vit. K Severe bleeding while anticoagulated with warfarin- Treat with FFP or cryoprecipitate Severe Hge with UFH or LMWH- protamine

Transcript

  • 1. DVT PROPHYLAXIS Dr. Ranjith R Thampi CRRI Department of Obstetrics and Gynaecology
  • 2. BackgroundIt is a common, yet preventable perioperativecomplication.Highest risk in critical care and spinal cordinjury patients- 60-80%Post- Ortho Procedures: 40-60%Post-General Surgery/ Obstetric- 15-40%Variable for Urologic Cases
  • 3. Incidence• Incidence of Thrombophlebitis in Antepartum period is 2/1000 pregnancies; of which, Majority(Superficial) is 1.7/1000 pregnancies and DVT is 3.6/1000 pregnancies• In Postpartum period, incidence of superficial thrombophlebitis increases by 7 times(12/1000) and that of DVT by 4-5 times(15/1000)• Thromboembolic complications in pregnancy occur in 2-5/1000 deliveries, where clinical presentation of DVT is found in 0.5-0.7% and PE is found in 0.3%-1.2%.
  • 4. Sites for DVT Ileo-femoral veins (80% cases) Popliteal veins Calf veins(extending proximally in 30% cases) Inferior Vena Cava(rarely)
  • 5. Pathogenesis• Physiologic changes during pregnancy predispose to DVT with a 6-fold increase from non-pregnant state, due to Virchow’s triad, i.e., - Venous Stasis - Altered Blood Coagulability - Vascular damage *Infection All concert together in promoting DVT in low flow areas.
  • 6. Risk Factors
  • 7. Risk Factors
  • 8. THECOAGULATION CASCADE
  • 9. Coagulation mechanism
  • 10. INTRINSICPATHWAY XIIa XII XIa XI IXa IX VIIIa VIII X Xa Va V PROTHROMBIN THROMBIN FIBRINOGEN FIBRIN
  • 11. EXTRINSIC PATHWAY XIIa XIITissue Factor XIa XIfrom damagedendothelium VIIa VII IXa IX VIIIa VIII X Xa Va V PROTHROMBIN THROMBI N FIBRINOGEN FIBRIN
  • 12. Anticoagulants andThrombolytics XIIa XIITissue Factor XIa XIfrom damagedendothelium VIIa VII IXa IX VIIIa VIII X Xa Va V PROTHROMBIN THROMBIN FIBRINOGEN FIBRIN Degradation PLASMINOGEN Plasmin
  • 13. FACT(Researched)– Type A blood is associated with lower levels of antithrombin III and higher levels of factor VIII than type O blood.– Women of reproductive age with type A blood are 4 times as likely to develop DVT.– This association of risk with blood type A does not extend to older men or to women past reproductive age
  • 14. Clinical Features• Tenderness occurs in 75% confined to the calf muscles or over the course of the deep veins in the thigh.• Warmth or erythema of skin can be present over the area of thrombosis.• Clinical signs and symptoms of pulmonary embolism as the primary manifestation occur in 10% of patients with confirmed DVT.• The pain and tenderness associated with DVT does not usually correlate with the size, location, or extent of the thrombus
  • 15. Clinical Features• Many patients are asymptomatic• Pedal Edema, principally unilateral, is the most specific symptom• Leg pain (50%, )• Pain can occur on dorsiflexion of the foot (Homans sign).
  • 16. Signs of DVT• Tenderness• Warmth or erythema of skin Can be present• Clinical signs and symptoms of pulmonary embolism as the primary manifestation occur in 10% of patients with confirmed DVT• Moses’ sign- tenderness elicited by squeezing or pressing firmly on sole of foot or calf
  • 17. Phlegmasia cerulea dolens Patients may have variable discoloration of the lower extremity. The most common abnormal hue is reddish purple from venous engorgement and obstruction. In rare cases, the leg is cyanotic from massive ileofemoral venous obstruction. This ischemic form of venous occlusion was originally described as phlegmasia cerulea dolens or painful blue inflammation.
  • 18. The leg is usually markedly edematous, painful, and cyanotic. Petechiae are often present
  • 19. Differential Diagnosis• Abcesses• Baker’s cyst• Cellulitis• Musculoskeletal Injury• Venous stasis
  • 20. INVESTIGATIONS• D-dimer• Contrast Venography• Duplex ultrasonography• Impedance plethysmography• MRI• Nuclear Medicine Imaging Studies
  • 21. D-dimerRecent interest has focussed on the use of D-dimer in the diagnostic approach to Deep Vein ThrombosisD-dimer has high sensitivity but low specificity D-Dimer levels remain elevated in DVT for about 7 days.
  • 22. Venous Thromboembolism suspected
  • 23. Contrast VenographyFor many reasons, including allergicreactions, contrast-induced Deep VeinThrombosis noninvasive studies haveessentially replaced venography as theinitial diagnostic test of choice.
  • 24. Duplex ultrasonographySensitivity of duplex ultrasonography forproximal vein Deep Vein Thrombosis is97% but only 73% for calf vein Deep VeinThrombosis.
  • 25. Impedance PlethysmographyPlethysmography is derived from theGreek word meaning "to increase."This procedure is based on recordingchanges in blood volume of an extremity,which are directly related to venousoutflow.
  • 26. MRI• MRI is the diagnostic test of choice for suspected iliac vein or inferior vena caval thrombosis.• In suspected calf vein thrombosis, MRI is more sensitive than any other noninvasive study. Nuclear ImagingNuclear medicine studies with I125-labeled fibrinogen are not recommended now. Radioactive isotope incorporates into a growing thrombus, this test can distinguish new clot from an old clot
  • 27. Management: All Patients• Avoid dehydration unless there is a specific clinical reason.• Encourage early mobilisation.• Aspirin or antiplatelet agents should not be considered adequate prophylaxis.• Consider temporary IVC filters for patients at a very high risk of VTE (eg active malignancy or previous VTE event) if there are contra-indications to pharmacological and mechanical prophylaxis. These are devices which can be inserted into the inferior vena cava to prevent the development of a pulmonary embolus.
  • 28. Choice of prophylaxis: MechanicalSeveral methods are available:•Graduated compression stockings are effective in decreasing the risk of DVT,either alone or in combination with pharmacological prophylaxis in high-riskpatients. Thigh-length graduated compression/anti-embolism stockings can beused unless contra-indicated (eg in patients with established peripheral arterialdisease or diabetic neuropathy). They should be used routinely for surgicalinpatients. If thigh-length stockings are not appropriate (for reasons of fit orcompliance) knee-length stockings may be used instead.•Stocking compression profile should be equivalent to the Sigel profile (a pressureprofile for elastic stockings) and approximately: 18 mm Hg at the ankle 14 mm Hg at the mid-calf 8 mm Hg at the upper thigh•Staff trained in the use of compression stockings should show the patient how towear them correctly, monitor their use and provide assistance when needed.•Patients should be encouraged to wear stockings from admission until they returnto their normal level of mobility.•Intermittent pneumatic compression or foot impulse devices may be usedinstead of, or as well as, graduated compression stockings while patients are inhospital.
  • 29. Choice of prophylaxis: PharmacologicalChoice depends on co-morbidities (e.g renal failure), a patients wishes andlocal policies. Options include: Anticoagulants, Both oral and parenteral.Oral- WarfarinParenteral: UFH LMWH Pentasaccharide(Fondaparinux)Two new agents, dabigatran and rivaroxaban, have recently been licensedfor use in orthopaedic thromboprophylaxis.-Patients with high risk and those having orthopaedic surgery should beoffered LMWH. Fondaparinux is an effective and safe alternative.-Consideration should be given to the risks and benefits of stopping pre-existing anticoagulation or antiplatelet therapy before surgery.-Pharmacological prophylaxis may need to be stopped if regional anaesthesiais employed to minimise the risk of haematoma (the timing depending on thetype of anticoagulant and the type of procedure)
  • 30. Oral Anticoagulant- WarfarinDose- starts from 5 mg PO daily. Acts by inhibiting Vit. K reductase enzyme, thereby depleting Vit. K-dependent clotting factors II, VII, IX and X. Good oral absorption but requires 4-5 days to achieve full anticoagulant effect Combine with parenteral till INR reaches atleast 2.0 Monitor INR twice weekly for first 2 weeks, then weekly for 2 weeks, then less frequently.
  • 31. Recommended INR?Recommended INR for various indications are as follows-Prophylaxis of DVT 2 - 2.5Treatment of DVT  2 - 3Recurrent VTE, MI, prosthetic heart valve disease  3 - 3.5
  • 32. Parenteral- UFHDerived from porcine intestinal mucosa Promotes Anti-Thrombin mechanism and inactivates Thrombin and Factor Xa DVT Prophylaxis dose 5,000 U SC Q8-12H aPTT monitoring not needed Therapeutic Dosing i/v Bolus (80U/Kg) + i/v continuous infusion (18U/Kg/hr) Safe in patients with Renal Dysfunction
  • 33. Parenteral- LMWH ENOXAPARIN, TINZAPARIN, DALTEPARINProduced by chemical or enzymatic cleavage of UFH Inactivates factor Xa to a greater extent than Thrombin. Minimally prolongs the aPTT Factor Xa monitoring is required in Renal dysfunction, Obesity and Pregnancy DVT Prophylaxis dose Enoxaparin 40 mg SC once daily for 8-12days Drug of choice in pregnant women requiring longterm anticoagulation for thrombosis and in those with mechanical heart valves
  • 34. Parenteral- LMWH• ENOXAPARIN 1 mg/Kg SC Q12H• TINZAPARIN 175 IU/Kg SC daily• DALTEPARIN 200 IU/Kg SC dailyDrug of choice in cancer patients and in those with failed oral anticoagulation.
  • 35. • The dose and frequency is controlled by aPTT measurement which is kept at 50-80 sec or 1.5-2.5 times the patient’s pretreatment value. If this test is not available whole blood clotting time should be measured and kept at 2 times the normal value.• After a constant maintenance infusion of 18 U/kg is initiated, the aPTT is checked 6 hours after the bolus and adjusted accordingly. .• The aPTT is repeated every 6 hours until 2 successive aPTTs are therapeutic. Thereafter, the aPTT is monitored every 24 hours as well as the hematocrit and platelet count.
  • 36. Parenteral- FONDAPARINUX• Synthetic pentasaccharide structurally similar to Heparin• Selective Factor Xa Inhibitor• Monitoring of factor Xa levels similar to LMWH (renal dysfunction)• Dosing FONDAPARINUX 7.5 mg SC daily
  • 37. Selective Indirect Factor XaXIIa inhibition Tissue factor XIa VIIa IXa Xa × Antithrombin Fondaparinux Factor II (prothrombin) Fibrinogen Fibrin clot
  • 38. Indications of warfarin1. Prophylaxis and/or treatment of venous thrombosis and its extension, and pulmonary embolism.2. Prophylaxis and/or treatment of the thromboembolic complications associated with atrial fibrillation and/or cardiac valve replacement.3. To reduced the risk of death, recurrent myocardial infarction, and thromboembolic events such as stroke or systemic embolization after myocardial infarction.
  • 39. Heparin: Mechanism of ActionAccelerates antithrombin III activity Antithrombin III (Heparin)Factor X Factor IXa Ca2+, PL Factor VIIIa Factor Xa Prothrombin Thrombin Factor Va Ca2+, PL
  • 40. Heparin Side Effects• Bleeding• Osteoporosis (inhibits osteoblasts, activates osteoclasts) – > 3 mths, > 20,000 units qd• Thrombocytopenia • Type I HIT • Type II HIT (3-5%)• Skins lesions- urticaria, papules, necrosis• Hypoaldosteronism, hyperkalemia
  • 41. Heparin Contraindications• Bleeding disorders, HIT.• Severe hypertension, threatened abortion, piles• SABE, large malignancies, Tuberculosis’• Ocular and neurosurgery, LP• Chronic alcoholics, cirrhosis, renal failure
  • 42. BUT…What if treatment with anti- coagulant is contraindicated??? IVC filter.
  • 43. These pulmonary emboli removed at autopsy look like casts of the deep veins of the leg where they originated.
  • 44. VTE & PregnancyPre-pregnancy counselling and a management plan should be offered to all womenwho are at high risk of VTE. All pregnant women should have their risk factorsassessed and documented.This assessment should be repeated if there is a hospital admission for any reasonor if complications develop. Thrombophilia should be excluded in women with aprevious non oestrogen-related VTE which has been provoked by a minor risk factor.Prophylaxis should begin as soon as possible in pregnancy.LMWH is the prophylaxis of choice, being safer and equally effective as UFH.Any woman with three or more persistent or recurrent risk factors identified should beconsidered for antenatal prophylaxis.LMWH should not be given routinely to women who have had one previous VTEevent providing this is non oestrogen-related and they have no other risk factors butthey should be monitored closely.
  • 45. VTE & PregnancyWomen should be offered prophylaxis antenatally if:They have a history of recurrent DVTAn unprovoked, oestrogen-related or pregnancy-related VTEA previous VTE and a first-degree relative with a history of DVT or provendiagnosis of thrombophiliaWomen with asymptomatic inherited or acquired thrombophilia should bemonitored closely antenatally but should be referred to a local expert if:They have antithrombin deficiencyThe have more than one thrombophilic defect (including homozygosity forfactor V Leiden)They have additional risk factorsWomen given LMWH should not have any more LMWH injections if theyhave vaginal bleeding or go into labour.
  • 46. After deliveryMobilisation should be encouraged during and after labourFluid intake should be encouragedWomen with two or more risk-persisting risk factors should be consideredfor LMWH for 7 days postnatally.Women with three or more such factors should be given graduatedcompression stockings as well as LMWHWomen with BMI>40kg/m2 should be considered for LMWH prophylaxisfor 7 days postnatallyThe decision to initiate LMWH at the time of discharge for women who havehad emergency or elective LSCS and duration of treatment will depend onwhat risk factors are present (age, weight, co-morbidities, family history ofthrombophilia)
  • 47. After deliveryWomen who have had a VTE before the current pregnancy should beconsidered for LMWH for six weeks postnatally.If they are receiving LMWH before pregnancy, preventive doses of LMWHshould be given until 6 weeks postpartum. A postnatal risk assessmentshould then be made.Patients on long-term warfarin can recommence this when the risk ofhaemorrhage is lowBreast-feeding is no contra-indication to either warfarin or LMWHRepeated risk assessments for VTE should be carried out if womendevelop intercurrent problems, or they require surgery or readmission forany reason in the puerperiumFor women with additional risk factors lasting >7 days postpartum –eg: wound infection, prolonged admission - thromboprophylaxis should becontinued for up to six weeks or until the risk factors have resolved