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Premium member Presentation Transcript VENOUS THROMBOEMBOLISM: VENOUS THROMBOEMBOLISM Ubaidur Rahaman Senior Resident, CCM, SGPGIMS Lucknow, IndiaSlide 2: Virchow’s triad stasis Coagulation activation Vascular injury >90% of PE- thrombi arise from deep veins of leg clinically important PE- thrombi arise from popliteal or more proximal deep veins of leg Clinical manifestation of PE size, site and number of thrombi + cardiorespiratory reserve of patient Recurrence of VTE is more with ileofemoral vein thrombosis than popliteal vein thrombosisdiagnosis: diagnosis Clinical presentation PE confirmed PE excluded Symptoms Dyspnoea 80% 59% Chest pain-pleuritic 52% 43% Chest pain- substernal 12% 8% Cough 20% 25% Hemoptysis 11% 7% Syncope 19% 11% Signs Tachypnoea(>20/min) 70% 68% Tachycardia( >100/min) 26% 23% Signs of DVT 15% 10% Fever (>38C) 7% 17% Cyanosis 11% 9%Slide 4: CXR plate like atelectasis Elevation of hemidiaphram Pleural effusion ABG- ↓PaO2, ↑A-aO2 EKG- signs of RV strain , RBBB Non specific Helpful in exclusion of other causes Usually found in massive PE Can be caused by other causes Normal in upto 20% patientsD- dimer: D- dimer degradation product of cross linked fibrin Elevated in presence of acute clot formation simultaneous activation of coagulation and fibrinolysis But fibrin is also produced in inflammation, necrosis, malignancy, dissection of aorta, aging high negative predictive value, low positive predictive valueDVT: DVT Detection of DVT in proven PE venography – 70% compression USG – 50% Compression USG Sensitivity-90%, specificity-95% for proximal DVT Not sensitive for isolated calf vein thrombosis Negative result-Should be repeated after 1 week COMPRESSION USG ** back up procedure to avoid false positive results with SDCT Patients with contraindication to dye or irradiation **GUIDELINES ON THE DIAGNOSIS AND MANAGEMENT OF ACUTE PULMONARY EMBOLISM- EHJ 2008Slide 7: Objectively documented DVT 50% suffer PE, many are asymptomatic Angiographically documented PE 50-70% have detectable DVT clinically suspected PE >50%-diagnosis not confirmed by investigation Objective test for diagnosis of PE V/Q scan Pulmonary angiography Spiral CT- chest MR angiography costly Invasive Radiation Mobilization of patient 2 D echocardiography ≥40% of vascular bed obtstruction to produce detectable features of RV overload TEE more valuable than TTE Coexistent cardiorespiratory disease Not useful in hemodaynamically stable patientsSlide 8: Clinical signs, symptoms and routine investigation do not help in confirmation or exclusion of PE Help in increasing the index of suspicionSlide 9: Suspected PE which patient should be mobilized for costly, invasive/ radiation exposure investigation Clinical probability of PE Low- 9% prevalence of PE Intermediate-30% prevalence of PE High-68% prevalence of PE Clinical prediction rule Based on history, sign and symptomsCLINICAL PREDICTION RULE WELLS score : CLINICAL PREDICTION RULE WELLS score predisposing factors: Previous documented DVT or PE 1.5 Recent immobilization ≥ 3 days or major surgery in last 4 weeks 1.5 Active cancer- receiving treatment or treated in last 6 months or palliative care 1 Clinical sign/ symptoms: Clinical signs and symptoms of DVT 3 HR >100 1.5 hemoptysis 1 Alternate clinical diagnosis less likely than VTE 3 2 level > 4- -------- likely PE 0-4-------- unlikely PE 3 level 0-1--------------- low 2-6---- intermediate ≥7--------------- high CLINICAL PROBABILITYWELLS SCORE clinical prediction rule: WELLS SCORE clinical prediction rule More than10,000 patients studied <1% develop VTE within 90 days of evaluation Prevalence of PE- 20% Clinical probability- PE unlikely D-dimer- negative No treatment with anticoagulants Clinical probability- PE likely Clinical probability- PE unlikely but D- dimer- positiveRisk stratification according to expected PE related early mortality risk GUIDELINES ON THE DIAGNOSIS AND MANAGEMENT OF ACUTE PULMONARY EMBOLISM- EHJ 2008: Risk stratification according to expected PE related early mortality risk GUIDELINES ON THE DIAGNOSIS AND MANAGEMENT OF ACUTE PULMONARY EMBOLISM - EHJ 2008 MORTALITY RISK RISK MARKERS POTENTIAL TREATMENT IMPLICATIONS Shock or hypotension RV dysfunction Myocardial injury HIGH > 15% + + a + a Thrombolysis or Embolectomy NON- HIGH INTERMEDIATE 3-15% - + + Hospital admission - + - - - + LOW <1% - - - Early discharge or Home treatment a in the presence of shock or hypotension it is not necessary to confirm presence of RV dysfunction/ myocardial injury to classify as high risk PE related mortality risk.Principle markers use for risk stratification: Principle markers use for risk stratification Clinical markers Shock or hypotension a Markers of RV dysfunction ECHO- RV dialatation, hypokinesia or pressure overload SPIRAL CT- RV dialatation PA catheter- increased pressures Biochemical- elevated BNP, pro BNP Markers of myocardial injury Elevated Trop T, Trop I a SBP<90 or drop of ≥ 40 from baseline for >15 min, if not caused by new onset arrhythmia, hypovolemia or sepsis GUIDELINES ON THE DIAGNOSIS AND MANAGEMENT OF ACUTE PULMONARY EMBOLISM- EHJ 2008Diagnostic algorithm for suspected HIGH RISK PE: Diagnostic algorithm for suspected HIGH RISK PE CT Immediately available ECHO RV overload MD-CTPA NO or patient unstable to be transported YES NO YES No other test available or patient unstable Consider thrombolysis or embolectomy Search for other causes Search for other causes NEGATIVE POSITIVE CT available or Patient stabilizes GUIDELINES ON THE DIAGNOSIS AND MANAGEMENT OF ACUTE PULMONARY EMBOLISM- EHJ 2008 Surgical embolectomy- where thrombolysis is contraindicated or failed Percutaneous catheter embolectomy or fragmentation- alternate to surgical embolectomyDiagnostic algorithm for suspected non-HIGH RISK PE: Diagnostic algorithm for suspected non-HIGH RISK PE ASSESS CLINICAL PROBABILITY Clinical prediction rule score D-dimer MD-CTPA Low/ intermediate probability or PE unlikely High probability or PE likely Negative positive No treatment or investigate further Treatment antithrombosis Search for other causes positive negative MD-CTPA negative Positive Treatment antithrombosis No treatment GUIDELINES ON THE DIAGNOSIS AND MANAGEMENT OF ACUTE PULMONARY EMBOLISM- EHJ 2008 Compression USGanticoagulation: anticoagulation Start without delay, awaiting definitive diagnostic confirmation Drugs Unfractionated heparin, LMWH, anti Xa- fondaparinux, vit K antagonist High risk PE- unfractionated heparin LMWH was not included in study for safety Non high risk PE- LMWH, fondaparinux except when renal failure- CLcr<30 or high risk of bleeding- unfractionated heparin Vit K antagonist- warfarin start simultaneouly with heparin, stop heparin only after INR is 2-3 for 2 consecutive daysHEPARIN UNFRACTIONATED: HEPARIN UNFRACTIONATED Efficacy depends on achieving therapeutic level within first 24 hours Failure associated with 23.3% recurrent VTE Dose- 80 U/kg iv stat, then 18 U/kg/hr Dose titrated according to normogram aPTT Q4h- modify dose accordingly- achieve target within 24 hour Once target achieved – aPTT Q24hHeparin Normogram: Heparin Normogram aPTT ( sec) Dose modification <35 ( < 1.2 times control) 80 U/kg bolus, ↑ infusion rate by 4 U/kg/hr 35-45 ( 1.2-1.5 times control) 40 U/kg bolus, ↑ infusion rate by 2 U/kg/hr 46-70 ( 1.5-2.3 times control) No change 71-90 ( 2.3- 3.0 times control) ↓ infusion rate by 2 U/kg/hr >90 ( > 3 times control) Stop infusion for 1 hr, then ↓ infusion rate by 3 U/kg/hrVit K antagonist WARFARIN: Vit K antagonist WARFARIN Inhibits vit K dependent gamma corboxylation of factors Clotting facors- II, VII, IX, X Anticoagulant factors- protein C, protein S Decreased levels of protein C, protein S – procoagulant activity Combined with heparin for first 5 days Factor VII has shortest T 1/2- 6 hours Anticoagulant activity starts in 6 hours, but full effect takes 36-72 hours Target INR- 2-3 Start simultaneously with heparin 5 mg PO OD – titrate according to INR Stop Heparin once INR is 2-3 for 2 consecutive daysVit K antagonist WARFARIN: Vit K antagonist WARFARIN vit K bioavailabity Diet Drugs Antimicrobials- gut flora producing vit K Interaction with warfarin Protein binding Metabolism 3. Increase potency for causing bleeding- antiplateletsWARFARIN OVERANTICOAGULATION: WARFARIN OVERANTICOAGULATION INR 3-5 -------- hold dose of that day INR ≥5 – 7.5-- hold dose of that day + vit K 1 mg ivi stat INR ≥7.5-10----hold dose of that day + vit K 2 mg ivi stat INR ≥10 --------hold dose of that day + vit K 3 mg ivi stat If active bleeding – fresh frozen plasma- 10-15ml/kg bw demonstrable reduction in INR- 6-8 hours correction on INR-----------------12-24 hours Half life of vit K < warfarin– repeat dose may be required Antagonist- vit KHemodynamic support: Hemodynamic support Volume challenge modest and cautious Ionotropes and vasodialators Iv- isoprenaline- added advantage of pulmonary vasodialatation Iv- Dobutamine, noradrenaline, adrenaline Iv- Levosimenden- ionodialator Oral/ iv- Sildenafil Inhaled- NO, PGI2Respiratory support: Respiratory support Mechanical ventilation high ITP may further aggravate RV afterload and failure Low PEEP Lung protective ventilationSlide 24: Thank you Not everything that counts can be counted. 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