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HI THIS IS A PPT PRESENTATION ON VENOUS THROMBOEMBOLISM BASED ON HARRISONS 18TH EDITION. HOPE IT WILL HELP MY FELLOW COLLEAUGES.

HI THIS IS A PPT PRESENTATION ON VENOUS THROMBOEMBOLISM BASED ON HARRISONS 18TH EDITION. HOPE IT WILL HELP MY FELLOW COLLEAUGES.

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  • Set A1 – Content Slide
  • Recognized risk factors for DVT are generally related to one or more elements of Virchow's triad (stasis, vessel injury, and hypercoagulability), and include surgery, trauma, immobilization, malignancy, use of estrogens, heart or respiratory failure, and smoking.
  • Set A1 – Content Slide
  • Figure 21-5. Chest radiograph showing pulmonary infarct in the right lower lobe. This patient had low-grade fever, hemoptysis, and pleuritic chest pain. The ventilation-perfusion scan was read as high probability for pulmonary embolism. A pleural-based density in the lower lobe with the convexity directed toward the hilum signifies pulmonary infarction. This sign is also known as ?Hampton’s hump.”
  • Figure 21-9. High-probability ventilation-perfusion scan. A and B, Multiple large segmental and subsegmental perfusion defects are seen bilaterally. C, The corresponding ventilation image was normal. The patient was treated for pulmonary embolism.
  • Figure 21-9. High-probability ventilation-perfusion scan. A and B, Multiple large segmental and subsegmental perfusion defects are seen bilaterally. C, The corresponding ventilation image was normal. The patient was treated for pulmonary embolism.
  • Figure 21-11. Pulmonary angiogram showing pulmonary embolism. Access to the pulmonary artery is obtained via transvenous catheter placement. The diagnosis is confirmed by persistent filling defect or abrupt cut-off of flow. Abrupt cut-off of flow to the right and left upper lobe vessels is seen in this patient.
  • Figure 21-22. Complications of anticoagulation. Major bleeding episodes with the use of heparin are much more likely to occur in patients with identifiable risks for bleeding rather than an excessively long activated partial thromboplastin time per se. LMWH does not affect the APTT to a significant degree; therefore, the APTT need not be routinely measured. Many factors influence the prothrombin time during warfarin therapy. Weekly or biweekly measurements are necessary until the prothrombin time stabilizes. Thereafter, monthly measurements of the prothrombin time may be sufficient.
  • Figure 21-22. Complications of anticoagulation. Major bleeding episodes with the use of heparin are much more likely to occur in patients with identifiable risks for bleeding rather than an excessively long activated partial thromboplastin time per se. LMWH does not affect the APTT to a significant degree; therefore, the APTT need not be routinely measured. Many factors influence the prothrombin time during warfarin therapy. Weekly or biweekly measurements are necessary until the prothrombin time stabilizes. Thereafter, monthly measurements of the prothrombin time may be sufficient.
  • Figure 21-22. Complications of anticoagulation. Major bleeding episodes with the use of heparin are much more likely to occur in patients with identifiable risks for bleeding rather than an excessively long activated partial thromboplastin time per se. LMWH does not affect the APTT to a significant degree; therefore, the APTT need not be routinely measured. Many factors influence the prothrombin time during warfarin therapy. Weekly or biweekly measurements are necessary until the prothrombin time stabilizes. Thereafter, monthly measurements of the prothrombin time may be sufficient.
  • Figure 21-22. Complications of anticoagulation. Major bleeding episodes with the use of heparin are much more likely to occur in patients with identifiable risks for bleeding rather than an excessively long activated partial thromboplastin time per se. LMWH does not affect the APTT to a significant degree; therefore, the APTT need not be routinely measured. Many factors influence the prothrombin time during warfarin therapy. Weekly or biweekly measurements are necessary until the prothrombin time stabilizes. Thereafter, monthly measurements of the prothrombin time may be sufficient.
  • Figure 21-18. Important drug interactions with warfarin. The figure includes only a short list of commonly used agents that are known to have clinically significant interactions with warfarin; several other drugs have pharmacokinetic and pharmacodynamic interactions with warfarin. Careful review of medications, alcohol consumption, and dietary factors is mandatory in patients who are on warfarin therapy.
  • Figure 21-26. Various inferior vena caval filters. A, Greenfield filter; B, Titanium Greenfield filter; C, Simon-Nitinol filter; D, LGM or Vena Tech filter; E, Amplatz filter; F, Bird’s Nest filter; G, Günther filter. Surgical interruption of the inferior vena cava was first practiced more than 100 years ago. The practice is percutaneous insertion of a filter device in the inferior vena cava under fluoroscopy to prevent pulmonary embolism. (Adapted from Becker et al.[38].)
  • Methods that have been explored for DVT prophylaxis include general measures such as the use of aspirin or mechanical prevention with graduated compression stockings (GCS) or intermittent pneumatic compression (IPC) devices. Anticoagulants commonly used include unfractionated heparin (UFH) (usually given as 5000 units 2 or 3 times daily), low-molecular-weight heparins (LMWH) (usually enoxaparin or dalteparin), or vitamin K antagonists (most commonly warfarin, but also including acenocoumarol, phenindione, and dicoumarol), and fondaparinux (a selective factor Xa inhibitor).

Dr.sudhanshu Dr.sudhanshu Presentation Transcript

    • “ If medicine is to fulfill her great task, then she must enter the political and social life. Do we not always find the diseases of the populace traceable to defects in society? In my listing, "CROWD DISEASES" or "ARTIFICIAL DISEASES" caused by poverty included typhus, scurvy, TB, leprosy, cholera, relapsing fever, and mental illness. If disease is an expression of individual life under unfavorable circumstances, then epidemics must be indicative of mass disturbances.”
    • “ Since disease so often results from poverty, the physicians are the natural attorneys of the poor, and the social problems should largely be solved by them. THE MEDICAL REFORM OF WHICH I often spoke WAS A REFORM OF SCIENCE AND SOCIETY. I urged that people treat criminal justice, education, unemployment, and occupational safety as if they are medical problems rather than political ones. Your era is beginning to do this.”
    • “ I have only one other suggestion for medical school teaching. Don't leave all mention of the social causes of disease to the social workers and statisticians. Lung cancer and emphysema are caused when ignorant children are lured into a deadly addiction. Endocarditis is caused by the cycle of poverty and lawlessness from which young people seek relief through IV drugs. Alcoholic cirrhosis is caused by frustrations that drive people to drink. Prematurity is caused by educational and economic barriers that prevent the poor from obtaining prenatal care. Urinary tract infections result when secretaries are forbidden to take unscheduled bathroom breaks, or when people are so accustomed to soda pop that they will not drink adequate water. Reasonable people can differ about solutions, but the underlying pathology is as much society's problem as it is the individual's.”
    • RUDOLF VIRCHOW
    • 13.10 1821 – 05.09.1902
  • Dr.Sudhanshu Mishra Co-Ordinator; Dr.R.A.Manghani HOD Medicine I&B VENOUS THROMBOEMBOLISM
  • Venous Thromboembolic Disease
    • Venous thrombosis - ~ 5 million pts yearly
        • Most caused by inadequate prophylaxis in hospitalized pts
    • 10 % suffer pulmonary embolism ~ 500,000
    • ~ 1% of all hospitalized pts have PE
    • Contributes to 6 % of all hospital deaths
    • ~ 125,000 deaths annually from PE
        • 3rd most common cardiovascular cause of death (MI, CVA)
        • Most deaths occur early – PREVENTION IS KEY !!
    • Diagnosis of PE made in < 30% when contributes to death; < 10% if incidental
  • Virchow’s Triad Factors Contributing to Venous Thrombosis Altered Blood Flow (Stasis) Blood Coagulability Vessel Wall Damage
  • Risk Factors for DVT
    • Stasis
      • Surgery, trauma, immobility, paresis
      • Increasing age
      • Pregnancy and postpartum
      • Heart or respiratory failure
      • Obesity
    • Vessel Injury
      • Previous DVT
      • Smoking
      • Varicose veins
      • Central venous catheterization
    • Hypercoagulability
      • Increasing age
      • Malignancy
      • Cancer therapy
      • Estrogen therapy
        • (OCP or HRT)
      • Acute medical illness
      • Inflammatory bowel disease
      • Nephrotic syndrome
      • Myeloproliferative disorders
      • Paroxysmal nocturnal hemoglobinuria
      • Inherited or acquired thrombophilia
  • Hereditary conditions associates with DVT and PE
    • Most of the hereditary factors for clotting disorders is due to certain SNPs with relatively high frequencies in the general population.
      • Types
        • Factor V Leiden (G1691A)
        • Prothrombin G20210A
      • Features
        • These prothrombotic SNPs are found in almost half of all cases of idiopathic thromboembolism
        • high gene frequency
        • low disease expression
  • APPROACH TO DVT
    • History
    • Physical examination
    • Probability scoring
    • Blood test
    • Imaging study
  • Symptoms
    • For patients with DVT most common history is a cramp in the lower calf that persists for several days and becomes more uncomfortable as time progresses.
    • For patients who have PE most common history is unexplained breathlessness.
  • Clinical Signs of DVT
    • Unilateral edema
    • Leg tenderness
    • Redness, hotness
    • Bluish discoloration
    • Absent or decrease pulse
  •  
  • Surgical Emergencies
    • Phlegmasia cerulea dolens
    • Leg is cyanotic from massive ileofemoral venous obstruction. The leg is usually markedly edematous, painful, and cyanotic. Petechiae are often present.
    • Phlegmasia alba dolens
    • Painful white inflammation was originally used to describe massive ileofemoral venous thrombosis and associated arterial spasm. The affected extremity is often pale with poor or even absent distal pulses
  • Phlegmasia cerulea dolens
  • Pulmonary Embolism
    • Unexplained shortness of breath
    • Chest pain or palpitations
    • Anxiety and/or sweating
    • Coughing up blood
    • Fatigue and/or fainting
  • Differential Diagnosis
    • DVT
    • Ruptured Baker's cyst
    •    Cellulitis
    •   Postphlebitic syndrome/venous insufficiency
    • PE
    •    Pneumonia, asthma, chronic obstructive pulmonary disease
    • Congestive heart failure
    •     Pleurisy: &quot;viral syndrome,&quot; costochondritis, musculoskeletal discomfort
    • Rib fracture, pneumothorax
    • Acute coronary syndrome
    • Anxiety
    • Pericarditis
    •    
  • Physical examination
    • Homans' test : Dorsiflexion of foot elicits pain in posterior calf. Warning : it must be noted that it is of little diagnostic value and is theoretically dangerous because of the possibility of dislodgement of loose clot.
    • Pratt's sign : Squeezing of posterior calf elicits pain.
  • Signs or symptoms observed in patients with thromboembolism Study Stein et al., % (n= 117) Anderson et al., % (n= 131) Pulmonary embolism Dyspnea 73 77 Tachypnea 70 70 Chest pain 66 55 Cough 37 — Tachycardia 30 43 Cyanosis 1 18 Hemoptysis 13 13 Wheezing 9 — Hypotension — 10
  • Signs or symptoms observed in patients with thromboembolism Study Stein et al., % (n= 117) Anderson et al., % (n= 131) Pulmonary Embolism Syncope — 10 Elevated jugular venous pulse — 8 Temperature >38.5°C 7 — S-3 gallop 3 5 Pleural friction rub 3 2
  • Signs or symptoms observed in patients with thromboembolism Study Stein et al., % (n= 117) Anderson et al., % (n= 131) Deep vein thrombosis Swelling 28 88 * Pain 26 56 Tenderness — 55 Warmth — 42 Redness — 34 Homan ’ s sign 4 13 Palpable cord — 6
  • Score (Wells Score) Clinical Parameter Score +1 Active cancer (treatment ongoing, or within 6 mo or palliative) +1 Paralysis or recent plaster immobilization of the lower extremities +1 Recently bedridden for >3 d or major surgery <4 wk +1 Localized tenderness along the distribution of the deep venous system +1 Calf swelling >3 cm compared with the asymptomatic leg +1 Pitting edema (greater in the symptomatic leg) +1 Previous DVT documented +1 Collateral superficial veins (nonvaricose) -2 Alternative diagnosis (as likely or greater than that of DVT)
  • Wells Score Total of Above Score > 3 High probability 1 or 2 Moderate probability < 0 Low probability
  • BLOOD TESTS
    • D-Dimer ELISA :-
    • D-dimer antibodies account for their high sensitivity for venous thrombo embolism.
    • D-dimer level may be elevated in any medical condition where clots form. D-dimer level is elevated in trauma, recent surgery, hemorrhage, cancer, and sepsis.
    • The D-dimer assays have low specificity for DVT; therefore, they should only be used to rule out DVT, not to confirm the diagnosis of DVT
    • D-dimer results should be used as follows :
      • A negative D-dimer assay result rules out DVT in patients with low-to-moderate risk and a Wells DVT score less than 2.
      • All patients with a positive D-dimer assay result and all patients with a moderate-to-high risk of DVT (Wells DVT score > 2) require a diagnostic study.
  • Elevated Cardiac Biomarkers
    • Serum troponin and plasma heart-type fatty acid–binding protein levels increase because of RV microinfarction.
    • Myocardial stretch results in elevation of brain natriuretic peptide or NT-pro-brain natriuretic peptide.
    • Elevated cardiac biomarkers predict an increase in major complications and mortality from PE
  • ECG Changes S1 Q3 T3 Pattern
  • T-wave inversion
  • Rt. Ventricular Strain
  • CXR Findings
    • A normal or nearly normal chest x-ray often occurs in PE.
    • Well-established abnormalities include focal oligemia (Westermark's sign), a peripheral wedged-shaped density above the diaphragm (Hampton's hump), and an enlarged right descending pulmonary artery (Palla's sign).
  • Chest Radiograph
  • Echocardiography
    • Transthoracic echocardiography rarely images thrombus directly.
    • The best-known indirect sign of PE on transthoracic echocardiography is McConnell's sign : hypokinesis of the RV free wall with normal motion of the RV apex.
    • Transesophageal echocardiography can identify saddle, right main, or left main PE.
  • Noninvasive Imaging Modalities
    • Venous Ultrasonography
    • Criteria for Establishing the Diagnosis of Acute DVT
    • Lack of vein compressibility (principal criterion)
    • Vein does not &quot;wink&quot; when gently compressed in cross-section
    • Failure to appose walls of vein due to passive distention
    • Direct Visualization of Thrombus  
    • Homogeneous and Low echogenicity
    • Abnormal Doppler Flow Dynamics  
    • Normal response: calf compression augments Doppler flow signal and confirms vein patency proximal and distal to Doppler
    • Abnormal response: flow blunted rather than augmented with calf compression
    •  
  • Chest CT
    • Computed tomography of the chest with intravenous contrast is the principal imaging test for the diagnosis of PE.
    • Multidetector-row spiral CT acquires all chest images with 1 mm of resolution during a short breath hold. This generation of CT scanners can image small peripheral emboli.
  • Spiral CT
  • Before After
  • Lung Scanning
    • Lung scanning has become a second-line diagnostic test for PE, used mostly for patients who cannot tolerate intravenous contrast.
    • Small particulate aggregates of albumin labeled with a gamma-emitting radionuclide are injected intravenously and are trapped in the pulmonary capillary bed.
    • The perfusion scan defect indicates absent or decreased blood flow, possibly due to PE. Ventilation scans, obtained with a radiolabeled inhaled gas such as xenon or krypton, improve the specificity of the perfusion scan.
  • High-probability ventilation-perfusion scan
  • High-probability ventilation-perfusion scan
  • Magnetic Resonance (MR) Contrast-Enhanced
    • When ultrasound is equivocal, MR venography with gadolinium contrast is an excellent imaging modality to diagnose DVT. MR imaging should be considered for suspected VTE patients with renal insufficiency or contrast dye allergy.
    • MR pulmonary angiography may detect large proximal PE but is not reliable for smaller segmental and subsegmental PE.
  • MRA with contrast
  • MRA Real Time
  • Invasive Diagnostic Modalities
    • Pulmonary Angiography
    • Chest CT with contrast has virtually replaced invasive pulmonary angiography as a diagnostic test.
    • Invasive catheter-based diagnostic testing is reserved for patients with technically unsatisfactory chest CTs and those in whom an interventional procedure such as catheter-directed thrombolysis or embolectomy is planned.
    • A definitive diagnosis of PE depends on visualization of an intraluminal filling defect in more than one projection.
    • Secondary signs of PE include abrupt occlusion (&quot;cut-off&quot;) of vessels, segmental oligemia or avascularity, a prolonged arterial phase with slow filling, and tortuous, tapering peripheral vessels.
    • Contrast Phlebography
    • Venous ultrasonography has virtually replaced contrast phlebography as the diagnostic test for suspected DVT
  • Pulmonary angiogram
  • Pulmonary Angiogram
  • Management of DVT
    • Non-pharmacological
    • These include lifestyle changes like
    • Avoid smoking
    • Eating a healthy balanced diet
    • Getting regular exercise and
    • Maintaining a healthy weight or losing weight if patient obese
    • Leg Raising:This reduces the pressure in the calf veins
  • Travelling
    • Drink enough amount of water
    • Avoid taking sleeping pills as it can cause immobility
    • Perform simple leg exercises, such as regularly flexing ankles
    • Take occasional short walks when possible
    • Wear elastic compression stockings
  • ANTICOAGULANTS
    • Anticoagulation is the foundation for successful treatment of DVT and PE
    • Immediately effective anticoagulation is initiated with a parenteral drug: unfractionated heparin (UFH), low-molecular-weight heparin (LMWH), or fondaparinux.
    • Parenteral agents are continued as a transition or &quot;bridge&quot; to stable, long-term anticoagulation with Warfarin.Since it requires 5–7 days to achieve a therapeutic effect. During that period, one should overlap the parenteral and oral agents.
    • However, anticoagulants do not directly dissolve thrombus that already exists.
  • Unfractionated Heparin
    • MOA is by binding to and accelerating the activity of antithrombin, thus preventing additional thrombus formation and permitting endogenous fibrinolytic mechanisms to lyse clot that already has formed.
    • UFH is dosed to achieve a target activated partial thromboplastin time (aPTT) that is 2–3 times the upper limit of the laboratory normal.
    • For UFH, a typical intravenous bolus is 5000–10,000 units followed by a continuous infusion of 1000–1500 U/h
    • ADVANTAGE
    • The major advantage of UFH is its short half-life. This is especially useful if the patient may undergo an invasive procedure such as embolectomy
    • DISADVANTAGE
    • Major disadvantage of UFH is that achieving the target aPTT is empirical and may require repeated blood sampling and heparin dose adjustment every 4–6 hours.
    • Furthermore, patients are at risk of developing heparin-induced thrombocytopenia
  • Low-Molecular-Weight Heparins
    • These fragments of UFH exhibit less binding to plasma proteins and endothelial cells and consequently have greater bioavailability, a more predictable dose response, and a longer half-life than does UFH.
    • No monitoring or dose adjustment is needed unless the patient is markedly obese or has chronic kidney disease.
    • 2 commonly used LMWH preparations are enoxaparin and dalteparin.
    • Enoxaparin is approved as a bridge to warfarin for VTE.
    • Dalteparin is also approved as monotherapy without warfarin for symptomatic VTE patients with cancer in a dose of 200 U/kg once daily for 30 days, followed by 150 U/kg once daily for months 2–6.
  • Fondaparinux
    • Fondaparinux, an anti-Xa pentasaccharide, is administered as a once-daily subcutaneous injection in a prefilled syringe to treat DVT and PE as a &quot;bridge&quot; to warfarin.
    • No laboratory monitoring is required.
    • Patients weighing <50 kg receive 5 mg, patients weighing 50–100 kg receive 7.5 mg, and patients weighing >100 kg receive 10 mg.
    • Fondaparinux is synthesized in a laboratory and, unlike LMWH or UFH, is not derived from animal products
    • It does not cause heparin-induced thrombocytopenia.
    • The dose must be adjusted downward for patients with renal dysfunction because the kidneys metabolize the drug.
  • Warfarin
    • This vitamin K antagonist prevents carboxylation activation of coagulation factors II, VII, IX, and X.
    • The full effect of warfarin requires at least 5 days even if the prothrombin time, used for monitoring, becomes elevated more rapidly.
    • If warfarin is initiated as monotherapy during an acute thrombotic illness, a paradoxical exacerbation of hypercoagulability can increase the likelihood of thrombosis rather than prevent it.
    • Overlapping UFH, LMWH, or fondaparinux with warfarin for at least 5 days can counteract the early procoagulant effect of unopposed warfarin.
  • Warfarin Dosing
    • In an average-size adult, warfarin usually is initiated in a dose of 5 mg. Doses of 7.5 or 10 mg can be used in obese or large-framed young patients who are otherwise healthy.
    • Patients who are malnourished or who have received prolonged courses of antibiotics are probably deficient in vitamin K and should receive smaller initial doses of warfarin, such as 2.5 mg.
    • The Prothrombin time is standardized by calculating the International normalized ratio (INR), which assesses the anticoagulant effect of warfarin (Chap. 58). The target INR is usually 2.5, with a range of 2.0–3.0.
    • The warfarin dose is titrated to achieve the target INR.
    • Proper dosing is difficult because hundreds of drug-drug and drug-food interactions affect warfarin metabolism.
    • Variables such as increasing age and comorbidities such as systemic illness reduce the required warfarin dose
  • Novel Anticoagulants
    • Novel oral anticoagulants are administered in a fixed dose, establish effective anticoagulation within hours of administration, require no laboratory coagulation monitoring, and have few of the drug-drug or drug-food interactions that make warfarin so difficult to dose.
    • Rivaroxaban , a factor Xa inhibitor, and Dabigatran , a direct thrombin inhibitor, are approved in Canada and Europe for prevention of VTE after total hip and total knee replacement.
    • Because of these drugs' rapid onset of action and relatively short half-life compared with warfarin, &quot;bridging&quot; with a parenteral anticoagulant is not required.
  • Complications of Anticoagulants
    • The most serious adverse effect of anticoagulation is hemorrhage . For life-threatening or intracranial hemorrhage due to heparin or LMWH, protamine sulfate can be administered.
    • Major bleeding from warfarin is best managed with prothrombin complex concentrate. With non-life threatening bleeding in a patient who can tolerate large volume, fresh-frozen plasma can be used. For minor bleeding or to manage an excessively high INR in the absence of bleeding, oral vitamin K may be administered.
    • Heparin-induced thrombocytopenia (HIT) and osteopenia are far less common with LMWH than with UFH. Thrombosis due to HIT should be managed with a direct thrombin inhibitor: Argatroban for patients with renal insufficiency and Lepirudin for patients with hepatic failure. In the setting of percutaneous coronary intervention, one should administer bivalirudin.
    • During pregnancy, warfarin should be avoided if possible because of warfarin embryopathy, which is most common with exposure during the sixth through twelfth week of gestation. However, women can take warfarin postpartum and breast-feed safely. Warfarin can also be administered safely during the second trimester.
  • Complications of anticoagulation Complication Management Heparin Bleeding Stop heparin infusion. For severe bleeding, the anticoagulant effect of heparin can be reversed with intravenous protamine sulfate 1 mg/100 units of heparin bolus or 0.5 mg for the number of units given by constant infusion over the past hour; provide supportive care including transfusion and clot evacuation from closed body cavities as needed.
  • Complications of anticoagulation Complication Management Heparin Heparin-induced osteoporosis (therapy >1 mo) LMWHs may have lower propensity to cause osteoporosis as compared with unfractionated heparin; consider LMWH if prolonged heparin therapy is necessary.
  • Complications of anticoagulation Complication Management Heparin Heparin-induced thrombocytopenia and thrombosis Carefully monitor platelet count during therapy. Stop-heparin for platelet counts <75,000. Replace heparin with direct inhibitors of thrombin-like desirudin if necessary. These agents do not cause heparin-induced thrombocytopenia. Avoid platelet transfusion because of the risk for thrombosis.
  • Complications of anticoagulation Complication Management Warfarin Bleeding Stop therapy. Administer vitamin K and fresh-frozen plasma for severe bleeding; provide supportive care including transfusion and clot evacuation from closed body cavities as needed Skin necrosis (rare) Supportive care. Teratogenicity Do not use in pregnancy or in patients planning to become pregnant.
  • Important drug interactions with warfarin Drugs that decrease warfarin requirement Drugs that increase warfarin requirement Phenylbutazone Barbiturates Metronidazole Carbamazepine Trimethoprim-sulfamethoxazole Rifampin Amiodarone Penicillin Second- and third-generation cephalosporins Griseofulvin Clofibrate Cholestyramine Erythromycin Anabolic steroids Thyroxine
  • Various inferior vena caval filters
  • Inferior Vena Caval Filters
    • The two principal indications for insertion of an IVC filter are
    • (1) Active bleeding that precludes anticoagulation
    • (2) Recurrent venous thrombosis despite intensive anticoagulation
    • It is not useful in PE as the filter itself may fail by permitting the passage of small- to medium-size clots. Large thrombi may embolize to the pulmonary arteries via collateral veins that develop.
    • Paradoxically, by providing a nidus for clot formation, filters double the DVT rate over the ensuing 2 years after placement.
  • Fibrinolysis
    • Successful fibrinolytic therapy rapidly reverses right heart failure and may result in a lower rate of death and recurrent PE by
    • (1) dissolving much of the anatomically obstructing pulmonary arterial thrombus
    • (2) preventing the continued release of serotonin and other neurohumoral factors that exacerbate pulmonary hypertension
    • (3) lysing much of the source of the thrombus in the pelvic or deep leg veins, thereby decreasing the likelihood of recurrent PE.
    • The preferred fibrinolytic regimen is 100 mg of recombinant tissue plasminogen activator (tPA) administered as a continuous peripheral intravenous infusion over 2 hours. Patients appear to respond to fibrinolysis for up to 14 days after the PE has occurred.
    • Contraindications to fibrinolysis include intracranial disease, recent surgery, and trauma. The overall major bleeding rate is about 10%, including a 1–3% risk of intracranial hemorrhage.
    • The only FDA-approved indication for PE fibrinolysis is massive PE
  • Surgical Options
    • Pulmonary Embolectomy :
    • The risk of intracranial hemorrhage with fibrinolysis has prompted a renaissance of surgical embolectomy. More prompt referral before the onset of irreversible cardiogenic shock and multisystem organ failure and improved surgical technique have resulted in a high survival rate. A possible alternative to open surgical embolectomy is catheter embolectomy. P
    • Pulmonary Thromboendarterectomy :
    • Chronic thromboembolic pulmonary hypertension occurs in 2–4% of acute PE patients. Therefore, PE patients who have initial pulmonary hypertension (usually diagnosed with Doppler echocardiography) should be followed up at about 6 weeks with a repeat echocardiogram to determine whether pulmonary arterial pressure has normalized. Patients impaired by dyspnea due to chronic thromboembolic pulmonary hypertension should be considered for pulmonary thromboendarterectomy, which, if successful, can markedly reduce, and at times even cure, pulmonary hypertension. The operation requires median sternotomy, cardiopulmonary bypass, deep hypothermia, and periods of hypothermic circulatory arrest. The mortality rate at experienced centers is approximately 5%.
  • Post Phelibitic Syndrome
    • It occurs in 15% of patients with deep vein thrombosis (DVT). It presents with leg oedema, pain, nocturnal cramping, venous claudication, skin pigmentation, dermatitis and ulceration on the medial aspect of lower leg.
    • Daily use of below-knee 30- to 40-mmHg vascular compression stockings will halve the rate of developing postphlebitic syndrome. These stockings should be prescribed as soon as DVT is diagnosed and should be fitted carefully to maximize their benefit. When patients are in bed, the stockings need not be worn.
  • HITTS
    • Clinicopathologic Syndrome :
        • Unexplained  50% decrease in platelets (even if absolute total > 150)
        • Positive test for Heparin antibodies
            • Activation assay (more relevant but more difficult)
            • Antigen assay
    • Types :
      • Type I
        • begins early (few hours) after starting heparin
        • typically benign with plts usually staying > 100K. No Rx needed.
      • Type II
        • begins several days into treatment (unless previously sensitized)
        • High risk for thrombotic complications. Requires Rx .
  • Methods of DVT Prophylaxis
    • Mobilization
    • Graduated compression stockings
    • Intermittent pneumatic compression
    • Aspirin
    • Unfractionated heparin 5000 s.c TDS
    • Low-molecular weight heparins
      • Enoxaparin(0.4cc), Dalteparin(5000 U daily)
    • Vitamin K antagonists
      • Warfarin, acenocoumarol, phenindione, & dicoumarol
    • Fondaparinux (Factor Xa inhibitor)
    • THANK YOU