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PULMONARY EMBOLISM DR. M. A. SOFI MD; FRCP; FRCPEDIN; FRCSEDIN.

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Presentation on theme: "PULMONARY EMBOLISM DR. M. A. SOFI MD; FRCP; FRCPEDIN; FRCSEDIN."— Presentation transcript:

1 PULMONARY EMBOLISM DR. M. A. SOFI MD; FRCP; FRCPEDIN; FRCSEDIN

2 PULMONARY EMBOLISM  PE is the most common preventable cause of death in hospitalized patients  600,000 deaths/year  80% of pulmonary emboli occur without prior warning signs or symptoms  2/3 of deaths due to pulmonary emboli occur within 30 minutes of embolization  Death due to massive PE is often immediate  Diagnosis can be difficult  Early treatment is highly effective

3 Pulmonary embolism is a medical emergency. It may present with very few clinical signs and/or symptoms, making it easy to miss, and a high index of suspicion is warranted. Pulmonary Embolism : Epidemiology The incidence of venous thromboembolism (VTE) varies from 1-1.5 per 1,000 person-years. Pulmonary embolism (PE) results from obstruction within the pulmonary arterial tree. The emboli can be caused by: Thrombosis - accounts for the majority of cases and has usually arisen from a distant vein and travelled to the lungs via the venous system. Fat - following long bone fracture or orthopaedic surgery. Amniotic fluid. Air - following neck vein cannulation or bronchial trauma

4 NATURAL HISTORY OF VTE 40-50% of pts with DVT develop PE, often “silent” PE presents 3-7 days after DVT  Fatal within 1 hour after onset of respiratory symptoms in 10%  Shock/persistent hypotension in 5-10% (up to 50% of patients with RV dysfunction) Most fatalities occur in untreated pts Perfusion defects completely resolve in 75% of all patients (who survive)

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6 Inherited Risk Factors Family History (+) Acquired risk factor (+) Prior deep venous thrombosis Inherited Risk Factors (2)  Antithrombin III deficiency  Protein C deficiency  Protein S deficiency  Protein C resistance (Factor V Leiden)  Hyperhomocystinemia  Abnormal fibrinogen  Abnormal fibrinolytic system RISK FACTORS

7 Acquired Risk Factors  surgery or trauma of pelvis/lower extremities  immobilization  surgery with >30 min general anesthesia  local tissue trauma and vessel destruction  pregnancy especialy in the perpuriam Acquired Risk Factors (II)  Age > 40  Malignancy  Obesity  Heart Failure  After cesarian section  Estrogen therpy  Myocardial infarction RISK FACTORS

8 Acquired Risk factors (III)  Prior DVT  Nephrotic Syndrome  Antiphospholipid Syndrome  PNH  Waldenström Macroglobinemia Symptoms  Chest pain  Pleuritic pain  Dyspnea  Cough  Hemoptysis  Syncope RISK FACTORS

9 Standard tests:  ECG  Chest radiograph  Arterial blood gases  Echocardiography  Imaging venous thrombus  Imaging pulmonary emboli Standard tests:  Leucocytosis  ESR increases  D-Dimer increases  Low---- Exclusion of PE Laboratory Tests

10 Chest Radiography  Usually nonspesific  Not sensitive or specific  Proximal, large segmental artery  Multiple small segmental artery Chest Radiography (II)  Atelectasis  Elevation of the hemidiaphragm  Pleural efusion  Dilatation of the main branches of PA  Paranchymal densities (in the lower lung fields, pleural based)  Zones of oligemia Laboratory Tests

11 DIAGNOSIS: ECG Usually non-specific ST/T waves changes Tachycardia RV strain patterns suggest severe PE  Inverted T waves V1-V4  QR in V1  Incomplete RBBB  S1Q3T3

12 S1Q3T3 AND T WAVE CHANGES

13 Arterial Blood Gases Acute PaCO2 decreases Massive PaO2 decreases Submassive Normal / Near normal Echocardiograph y  Shows emboli in main pulmonary arteries, but not in lober and segmentaL arteries  Dilated hypokinetic RV  Distorsion of the interventricular septum in diastole  Tricuspid regurgitation associated with increase in systolic pressure in pulmonary artery Laboratory Tests

14 Perfusion (-) and Ventilation (+) PE Perfusion (N) and Clinical sym and signs (N) PE excluded Low probability PVLS and low probability of clinical sym and signs PE excluded High probability PVLS and high probability of clinical symp and signs Anticoagulation Ventilation-Perfusion Lung Scan It remains the first line investigation of possible PE. It should be performed in all clinically stable patients. A Ventilation Perfusion scan is most useful when the result category is one of normal, low or high probability.

15 Deep Vein Thrombosis  90% of PE originates from DVT (popliteal or proximal leg veins)  leg pain or swelling  Homan’s sign  signs of infection in subcutaneous veins Deep Vein Thrombosis  Phlebography  Doppler Laboratory Tests

16 Deep Vein Thrombosis

17 PERFUSION/VENTILATION LUNG SCAN

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19 This algorithm allowed for a management decision in 98% of patients presenting with symptoms suggestive of PE

20  Direct visualization of emboli.  Both parenchymal and mediastinal structures can be evaluated.  Offers differential diagnosis in 2/3 of cases with a negative scan. BUT…  Dye load and large radiation dose  Optimally used when incorporated into a validated diagnostic decision tree SPIRAL CT

21 Clinical Probability of acute PE High Probability (80-100%) Risk factors (+) Dyspnea Tachypnea Chest pain Radiology (+) PaO2 decreases P (A-a)O2 increases Intermediate Probability (20-79%) Low Probability (1-19%) Risk Factors (-) Clinical and laboratory findings can be explained Treatment  To prevent death  To reduce morbidity  To prevent pulmonary hypertension  Progresing due to thromboemboli

22 Anticoagulation 1.Unfractioned heparin 2.LMWH 3.Thrombolysis 4.Embolectomy Prognosis Mortality rate – 30% Depends on associated pathology Resolution – 5 days 36% 2 weeks 52% 3 months 73% Pulmonary hypertension recurrent microemboli (rare) TREATMENT

23 Unfractioned Heparin IV 5000 U bolus + 30-35 000 U/kg aPTT- twice the control value Thrombocytopenia Early: thrombocyte aggregation slight, reveresible, no need to stop Late: antibodies against thrombocytes arterial and venous thromboemboli Osteopenia LMWH  long acting  less binding to plasma protein  greater bioavailibity  no need monitoring TREATMENT

24 Thrombolysis Massive pulmonery emboli with hemodynamic instability Streptokinase Urokinase t-PA **serious bleeding Secondary prevention UFH + oral anticoagulan (6 months) LMWH SC + oral anticoagulan (6 months ) LMWH (pregnancy) Recurrance / unknown origin / permanantly increased risk (throughout life) TREATMENT

25 CATHETER EMBOLECTOMY & FRAGMENTATION An alternative in high-risk PE patients when thrombolysis is absolutely contraindicated or has failed


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