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Pulmonary Embolism & DVT
By Prof. Dr. Abdul Hameed AI Qaseer
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Definition It indicates occlusion of pulmonary artery
by exogenous or endogenous material that travels to the lung through the pulmonary circulation , causing potential spectrum of consequences,
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Introduction Pathophysiology Risk Factors Symptoms Lab Findings
Radiology Findings Treatment Prevention
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Risk Factors for PE and DVT
Immobilization Surgery within the last 3 months Stroke History of venous thromboembolism Malignancy Preexisting respiratory disease Chronic Heart Disease Age >60 Surgery requiring >30mins of anesthesia Recent travel (past 2weeks, >4 hours) Varicose veins Superficial vein thrombosis Central VV catheter/port/pacemaker Additional RF in Women: Obesity BMI >/=29 Heavy smoking (>25cigs/day) Hypertension Pregnancy
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Pathophysiology Dislodgement of a blood clot:
Lower Extremities: 65% to 90% Pelvic venous system Renal venous system Upper Extremity Right Heart
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Symptoms of P.E. Dyspnea(~ 73%) Pleuritic pain ( 66%) Cough ( 37%)
Hemoptysis (blood tinged/streaked/ pure blood) (~ 13%) From PIOPED study .
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Signs of P.E. Tachypnea ( 70%) Rales(51%) Tachycardia ( 30%) Hypoxia
Accentuated pulmonic component of S2 (23%) Fever: T <102 F (39C) (14%) Chest wall tenderness may be the only sign
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Signs in Massive P.E. “Massive PE”: hemodynamic instability with SBP <90 or a drop in baseline SBP by >/=40mmHg Signs as before PLUS: Acute right heart failure Elevated J.V.P. Right-sided S3 Parasternal lift
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P.E. & Leg Symptoms Most patients with P.E. do not have leg symptoms at time of diagnosis Patients with leg symptoms may have asymptomatic P.E.
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Differential diagnosis
Chronic PE Acute minor PE Acute massive PE Chronic occlusion of pulmonary microvasculature ,RHF Occlusion of segmental pulmonary artery--> infarction & sometimes pleural effusion Major homodynamic effects ,reduction in cardiac output ,acute RHF Pathophisology Exertional dyspnea .Late symptoms of pulmonary hypertension or RHF . Pleuritic chest pain ,restricted breathing ,haemoptysis Faintness or collapse ,central chest pain ,apprehension ,severe dyspnea Symptoms May be minimal early in disease .Later RV heave ,loud split P Terminal RHF Tachycardia ,pleural rub ,raised hemidiaphram ,crackles ,effusion ,low-grade fever Major circulatory collapse ,tachycardia ,hypotension. high JVP ,RV gallop rhythm ,split P2 .Severe cyanosis ,low UO Signs Enlarged pulmonary artery trunk ,enlarged heart ,prominent RV Pleuropulmonary opacities ,pleural effusion ,linear shadows ,raised hemidiaphragm Usually normal .May be subtle oligaemia . Chest x-ray RV hypertrophy and strain Sinus tachycardia ,right axis deviation S1Q3T3 ,anterior T wave inversion ,RBBB ECG Exertional reduction in PaO2 or desaturation May be normal or reduced PaCO2 Low PaO2 & low PaCO2 ,Metabolic acidosis Arterial blood gases Other causes of pulmonary hypertension Pneumonia ,pneumothorax ,musculoskeletal chest pain MI ,pericardial tamponade ,aortic dissection Differential diagnosis
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Differential Diagnosis
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WELL`S Clinical prediction rule for Likelihood of PE
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Lab & Radiologic Findings in P.E.
ABG BNP Cardiac Enzymes: Troponin D-dimer ECG Echocardiography CXR Ultrasound with colour Doppler study of leg veins V/Q Scan Spiral CT scanning Angiography
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Lab Findings in P.E. (ABG)
Hypoxemia Hypocapnia (low CO2) Respiratory Alkalosis Massive PE: hypercapnia, mix resp and metabolic acidosis (inc lactic acid) Patients with RA pulse ox readings <95% are at increased risk of in-hospital complications, resp failure, cardiogenic shock, death
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Lab Findings in P.E. (BNP)
BNP (brain natriuretic peptide) Insensitive test{ sensitivity(60%) & specifity (62%)} Patient’s with PE have higher levels than pts without, but not ALL patients with PE have high BNP Prognostic value measure: if BNP >90 pg| ml associated with adverse clinical outcomes (death, CPR, mechanical vent, pressure support, thrombolysis, embolectomy), One meta analysis revealed that BNP > 100 pg\ml or NT- proBNP > 600 pg\l increased mortality rate fold .
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Lab Findings in P.E. (Troponin)
High in 30-50% of pts with large PE
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Lab Findings in P.E. (D- dimer)
Degredation product of fibrin >500 is abnormal Sensitivity: High, 95% of PE pts will be positive Specificity: Low
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Lab Findings in P.E. (cont’d)
ECG 2 Most Common finding on ECG: Nonspecific ST-segment and T-wave changes Sinus Tachycardia Historical abnormality suggestive of PE S1Q3T3 Right ventricular strain New incomplete RBBB
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PE ECG
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PE ECG
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Classic ECG S1,Q3,T3
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S1Q3T3!!!
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RAD Right Atrial Enlargement
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Radiologic Findings in P.E.
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Radiology Findings in P.E. (cont’d)
CXR: Normal Atelectasis and/or pulmonary parenchymal abnormality Pleural Effusion Cardiomegally
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The CXR is read as “ normal” in up to 30% of pats
The CXR is read as “ normal” in up to 30% of pats. With angiographically proven PE (Mayo. 2008). In some series , an elevated hemidiaphragm is the most common finding with acute PE .
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Chest Radiography
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What’s This??? Hampton’s Hump
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How About This??? Westermark's Sign: an abrupt tapering of a vessel caused by pulmonary thromboembolic obstruction. This CXR shows enlargement of the left hilum accompanied by left lung hyperlucency, indicating oligemia (Westermark's sign).
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PE Chest x-ray
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Radiology Findings in P.E. (cont’d)
Lower Extremity Ultrasounds If DVT found then treatment is same if patient has a P.E. Disadvantage: If negative, patients with PE may be missed If false positive (3%), unnecessary intervention
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Radiology Findings in P.E. (cont’d)
CT Pulmonary Angiography (CT-PA) Widely used Institution dependent Sensitivity (83%) Specificity (96%): if negative, very low likelihood that pt has P.E.
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Figure 19. 58 CT pulmonary angiogram
Figure CT pulmonary angiogram. The arrow points to a saddle embolism in the bifurcation of the pulmonary artery. Downloaded from: StudentConsult (on 18 November :58 AM) © 2005 Elsevier
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Radiology Findings in P.E. (cont’d)
Pulmonary Angiogram Gold Standard Not easily accessible Radiologist dependent
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Pulmonary Angiography
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Radiology Findings in P.E. (cont’d)
Echocardiogram Increased Right Ventricle Size Decreased Right Ventricular Function Tricuspid Regurgitation Rarely: RV thrombus Regional wall motion abnormalities that spare the right ventricle apex (McConnell’s Sign)
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Deep Vein Thrombosis Diagnosis
Compression ultrasonography of femoral & popliteal veins, sensitive for proximal vein thrombosis but less sensitive for calf vein thrombosis Impedance plethysmography Contrast venography Radionuclide venography
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Contrast Venography Showing Ilio-femoral DVT
Left leg Right leg
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Inter-iliac collaterals
Radionuclide venography showing chronic iliofemoral DVT Inter-iliac collaterals
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Treatment of P.E. Respiratory Support: Oxygen, intubation
Hemodynamic Support: IVF, vasopressors Anticoagulation Thrombolysis IVC Filter
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Anticoagulation Start during resuscitation phase itself
If suspicion high, start emperic anticoagulation Evaluate patient for absolute contraindication (i.e.: active bleeding)
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Anticoagulation-1 Bed rest is not recommended for DVT unless substantial pain & swelling PE diagnosed, in patient therapy with initial bed rest for 24 to 48 hrs : often recommended
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Anticoagulation-2 APE (+):IV anticoagulation with LMW heparin , or standard, UF heparin should be initiated unless contraindicated Not thrombolytic, but decreasing the thromboembolic burden If the suspicion of PE is high, parenteral anticoagulation should be considered even before imaging
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Anticoagulation-3 Warfarin can be initiated on day 1 of therapy
SC LMWH or weight-based UFH IV should be administered for at least 5 days until INR=2.0 to 3.0 for 2 consecutive days With standard heparin, a PTT checked Q6h until it is =1.5 to 2.5 X control Achieving a therapeutic a PTT within 24 hours ,reduce the risk of recurrence
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Anticoagulation-4 VTE require long-term anticoagulation to prevent extension & recurrence Documented VTE with transient risk factors should treat 3 to 6 months, but more extended treatment is appropriate when significant risk factors persist, idiopathic or previous episodes of VTE D-dimer levels may help guide decisions about the duration of therapy
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Management LMWH Prepared by depolymerization of unfractionated heparin
MW ,000 (Mean 1,500-5,000) Better bioavailability S/C once or twice daily dose Longer half-life More predictable dose response Less risk of adverse bleeding events
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Management Complications of heparin / LMWH
Major bleeding - 5% (less with LMWH) Osteoporosis – heparin > 1 month during pregnancy Thrombocytopenia - 3% ( platelet count < 100,000 cells/ mm3)
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Management Oral vitamin K antagonist (Warfarin) – started within 24 hours of heparin therapy INR maintained between Heparin is discontinued when warfarin has been given for 4 days and INR is > 2.0 for two consecutive days Oral anticoagulants are continued for 3 months or longer
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Thrombolysis Considered once P.E. diagnosed
If chosen, hold anticoagulation during thrombolysis infusion, then resumed Associated with higher incidence of major hemorrhage Indications: persistent hypotension, severe hypoxemia, large perfusion defects, right ventricular dysfunction, free floating right ventricular thrombus, paten foramen ovale Activase or streptokinase
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Complications of Thrombolytic Therapy
The most devastating complication :ICH retroperitoneal & GI bleeding & bleeding from surgical wounds or sites of recent invasive procedures Contraindications : intracranial, spinal, or ocular surgery or disease, recent major surgery or other invasive procedures, active or recent major bleeding, pregnancy, & clinically obvious risks of bleeding
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IVC Filter Indication: Also:
Absolute contraindication to anticoagulation (i.e. active bleeding) Recurrent PE during adequate anticoagulation Complication of anticoagulation (severe bleeding) Also: Pts with poor cardiopulmonary reserve Recurrent P.E. will be fatal Patient’s who have had embolectomy Prophylaxis against P.E. in select patients (malignancy)
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Management IVC Filter Simon Nitinol IVC Filter, Nickle & Titanium - MRI compatible
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Embolectomy Surgical or catheter Indication:
Those who present severe enough to warrant thrombolysis In those where thrombolysis is contraindicated or fails
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