Pulmonary embolism Pulmonology Refresher Course 27 May 2011
Pulmonary embolism Pulmonology Refresher Course 27 May 2011 Dr. JM Nel Department of Critical Care
Incidence n Pulmonary embolism (PE) – In 1% of patients admitted to hospital – Accounts for 5% of in hospital deaths – Common mode of death § Cancer § Stroke – Most common cause of death in pregnancy
Etiology n Majority (75%) § Propagation of lower limb DVT n Other (rare) § § § Amniotic fluid Placenta Air Fat Tumour Septic emboli (from endocarditis affecting tricupid or pulmonary valves)
Risk factors n Surgery – Major abdominal/ pelvic surgery – Hip/ knee surgery – Post- operative intensive care n Obstetrics n Cardiorespiratory disease n Lower limb problems n Malignant disease n Miscellaneous – Pregnancy/ puerperium – – – COPD Congestive cardiac failure Other disabling disease – Fracture – Varicose veins – Stroke/ spinal injury – Abdominal pelvic – Advanced/ metastatic – Concurrent chemotherapy – – – Increasing age Previous proven VTE Immobility Thrombotic disorders Trauma
Clinical features n Clinical features vary DIFFICULT DIAGNOSIS
Clinical features ASK 3 QUESTIONS – Is the presentation consistent with PE ? – Does the patient have risk factors for PE ? – Is there another diagnosis that can explain the patients presentation ?
Clinical features n Clinical features – Acute massive PE – Submassive PE – Acute small/ medium PE
Acute massive PE n Symptoms § Collapse § Central chest pain § Severe dyspnoea n Signs § Major circulatory collapse – – – Tachycardia Hypotension Increased JVP Loud P 2 Parasternal heave RV gallop rhythm § Severe cyanosis
Acute small/medium PE n Symptoms § § § Pleuritic chest pain Restricted breathing Haemoptysis n Signs § § § § Tachycardia Pleural rub Raised hemidiaphragm Crackles Effusion Low- grade fever Normal BP
Submassive PE WHAT’S THAT ? ? ?
Submassive PE n Massive PE § RV Strain/dilatation § Low BP n Submassive PE § RV Strain/dilatation § Normal BP
Investigations n CXR n Heart sonar n ECG n Other biomarkers n Arterial blood gas n Imaging n D- dimer
Investigations: Chest x- ray n High index of suspicion if normal CXR – Acute dyspnoec and hypoxemic patient n Exclude differential diagnoses § Heart failure § Pneumonia § Pneumothorax
Investigations: Chest x- ray n Radiographic appearances – Pleural effusion – Pulmonary opacities – Oligaemia of lung field – Wedge shaped opacity – Enlarged pulmonary artery – Horizontal linear opacities – Elevated hemidiaphragm
Investigations: Chest x- ray n Acute massive PE § Usually normal § Oligaemia n Acute small/ medium PE § Pleuropulmonary opacities § Pleural effusion § Linear shadows § Raised hemidiaphragm
Investigations: ECG n Common but non- specific n Most common n Exclude other differential diagnoses – Sinus tachycardia – Acute myocardial infarction – Pericarditis
Investigations: ECG n Massive/Submassive PE – Acute cor pulmonale § § § n S 1 Q 3 T- wave inversion RBBB P-wave pulmonale Right axis Small/ medium PE § Sinus tachycardia
Investigations: A- blood gas n Typical A- blood gas § Low Pa. O 2 § Normal or low Pa. CO 2
Investigations: D- dimer n Degradation product n Positive D- dimer – High negative predictive value – Screening test for PE – ELISA based D-dimer superior sensitivity n Other causes for elevation § § § § Myocardial infarction Pneumonia/Infection Sepsis Pregnancy Malignancy Hospitalised patients Elderly Trauma
Investigations: Heart sonar n Massive/Submassive PE § Acute dilatation of the right heart § Pulmonary hypertension § Thrombus can be seen LOOK FOR: RV DYSFUNCTION • RV enlargement • Hypokinesis of free wall • Leftward septal shift • PHT
Investigations: Other biomarkers n Cardiac troponin Detects myocardial injury § Risk stratification § Elevated in massive PE – 6 -12 hours after symptoms n Pro-BNP Detects myocardial dysfunction § Increases with ventricular stretching § But also elevated in other causes of PHT/congestive heart failure
Investigations: Other biomarkers Normal levels: • Low risk of death/complications Increased levels: • Cannot predict early death • RISK ASSESSMENT • Do not dictate need for early thrombolysis
Investigations: Imaging n V/Q scans – If normal § Excludes PE – If underlying chronic cardiopulmonary pathology (COPD, congestive cardiac failure) § Majority of scan indeterminate
Investigations: Imaging n CT pulmonary angiography – Difficult to detect small peripheral emboli n Duplex doppler of legs – DVT in leg n Pulmonary angiography – Gold standard
Management n General measures n Anticoagulation n Thrombolytic n Caval filters therapy
Management: General n Oxygen for hyoxaemic patients – Keep arterial oxygen saturation > 90% n Analgesics – Opiates § Careful in hypotensive patients n Avoid diuretics and vasodilators n Treat hypotension – IVI fluids – Inotropic agents of limited value
Confirmed PE ECHO RV dysfunction NO YES Hemodynamically Stable ? Low risk Non-massive PE YES Anticoagulate UFH LMWH Submassive PE Anticoagulate NO Massive PE Thrombolysis if no contra-indication
Management: Anticoagulation n Start immediately – High or intermediate probability of PE n Low molecular weight heparin sc – – – – Clexane Give according to weight Reduces mortality in PE Reduces the propagation of clot and risk of further emboli Give at least 5 days Start Warfarin Stop Clexane when INR is >2
Management: Anticoagulation n Duration of Warfarin therapy – If underlying prothrombotic risk or previous emboli § For life – If identifiable and reversible risk factor § 3 Months – If idiopathic § 6 Months
Management: Thrombolytic therapy n Acute massive pulmonary embolism – Patient shocked – Improves outcome n If normal BP – Unsure if advantage above heparin n High risk of intracranial haemorrhage – Screen patient for haemorrhagic risk
Management: Caval filters n Filter inserted in inferior vena cava § Below origin of renal vessels n Indications § Recurrent PE despite adequate anticoagulation § Contraindication to anticoagulation
Prognosis n Lowest recurrence after operation n If right ventricular dysfunction § Risk of cardiogenic shock § Increased risk of death n If pulmonary hypertension and right ventricular dysfunction after 6 weeks § Increased risk to develop right heart failure over next 5 years
Pulmonary Embolism: Case Studies
Pulmonary embolism n Case Presentation 1: – 64 year old male – Previous hip surgery 20 days ago – Sudden dyspnoea – Pleuritic chest pain – Hypoxic – BP 130/80 – Clinically DVT
Pulmonary embolism DIFFERENTIAL DIAGNOSIS § Pulmonary embolism § Pneumonia § Pneumothorax § Musculoskeletal chest pain
Pulmonary embolism ASK 3 QUESTIONS – Is the presentation consistent with PE ? – Does the patient have risk factors for PE ? – Is there another diagnosis that can explain the patients presentation ?
Pulmonary embolism WHAT NOW ? ? ?
Pulmonary embolism n CXR – Exclude differential diagnoses § Heart failure § Pneumonia § Pneumothorax n High index of suspicion if normal CXR – Acute dyspnoeac and hypoxaemic patient
Pulmonary embolism n ECG – Exclude other differential diagnoses § Acute myocardial infarction § Pericarditis n Most common – Sinus tachycardia
Pulmonary embolism n Arterial n Low bloodgas Pa. O 2
Pulmonary embolism n D- dimer n POSITIVE
Pulmonary embolism n Heartsonar n Massive/Submassive PE – Acute dilatation of the right heart – Pulmonary hypertension – Thrombus can be seen n NORMAL n Alternative diagnoses – – – Left ventricular failure Aortic dissection Pericardial tamponade
Pulmonary embolism n Duplex n DVT doppler of legs in leg
Pulmonary embolism n V/Q scan n PULMONARY EMBOLISM
Pulmonary embolism: Management n General measures – Oxygen for all hyoxaemic patients § Keep arterial oxygen saturation > 90% n Anticoagulation – Clexane 80 mg bd sc § Give at least 5 days – Warfarin – Stop Clexane when INR is > 2
Pulmonary embolism: Management n n HOW LONG DO I TREAT THIS PATIENT WITH WARFARIN ? ? ? 3 Months n Duration of Warfarin therapy – If underlying prothrombotic risk or previous emboli § For life – If identifiable and reversible risk factor § 3 Months – If idiopathic § 6 Months
Pulmonary embolism n Case Presentation 2: – 28 year old lady – Oral contraceptives – 10 hour flight – Sudden dyspnoea – BP 90/40 – Loud P 2/ Increased JVP – Hypoxic
Pulmonary embolism DIFFERENTIAL DIAGNOSIS § Massive pulmonary embolism § Myocardial infarction § Pericardial tamponade § Aortic dissection
Pulmonary embolism n CXR n NORMAL
Pulmonary embolism n ECG – S 1 Q 3 T 3 – RBBB n Arterial bloodgas – Low Pa. O 2 n D- dimer – POSITIVE
Pulmonary embolism n Heartsonar – Right ventricular dilatation – Increased pulmonary pressure
Pulmonary embolism n CT pulmonary angiography MASSIVE PULMONARY EMBOLISM
Pulmonary embolism: Management n General measures § Oxygen for all hypoxaemic patients – Keep arterial oxygen saturation > 90% § Treat hypotension with IVI fluids n. Thrombolytic § RV dilatation § Low BP therapy
Pulmonary embolism: Management n Complications of thrombolytic therapy § Intracranial haemorrhage § Haemorrhage at other sites § Anaphylaxis
Pulmonary embolism n Case Presentation 3: – 28 year old lady – Oral contraceptives – 10 hour flight – Sudden dyspnae – BP 130/80 – Loud P 2/ Increased JVP – Hypoxic
Pulmonary embolism n CXR n NORMAL
Pulmonary embolism n ECG – S 1 Q 3 T 3 – RBBB n Arterial bloodgas – Low Pa. O 2 n D- dimer – POSITIVE
Pulmonary embolism n Heartsonar – Right ventricular dilatation – Increased pulmonary pressure
Pulmonary embolism n CT pulmonary angiography PULMONARY EMBOLISM
Pulmonary embolism n Patient has normal BP n Patient has RV strain SUBMASSIVE PULMONARY EMBOLISM
Confirmed PE ECHO RV dysfunction NO YES Hemodynamically Stable ? Low risk Non-massive PE YES Anticoagulate UFH LMWH Submassive PE Anticoagulate NO Massive PE Thrombolysis if no contra-indication
Thrombolytic therapy n Associated with rapid resolution of radiographic abnormality n No reduction in – In submassive PE mortality !!!
Thrombolytic therapy n Indicated only in hemodynamically unstable patients !!! – SBP < 90 mm. Hg or drop of 40 mm. Hg for at least 15 minutes – Best if given in 48 hours, still benefit after 14 days (if still symptomatic) n All must be followed by therapeutic anticoagulation
Submassive PE n To thrombolise or not to thrombolise THAT REMAINS THE QUESTION !!!
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