PULMONARY EMBOLISM Jan Tomis 2018 Pulmonary embolism Obstruction

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PULMONARY EMBOLISM Jan Tomis, 2018

PULMONARY EMBOLISM Jan Tomis, 2018

Pulmonary embolism § § § Obstruction of (branches) pulmonary arteries with embolus (less commonly

Pulmonary embolism § § § Obstruction of (branches) pulmonary arteries with embolus (less commonly with other material – tumour, air, foreign bodies, fat Acute pulmonary embolism → obstruction of pulmonary arteries → ↑ pulmonary vascular resistence → pulmonary artery pressure → acute right ventricule failure → ↓ CO → shock potentially fatal Acute/subacute/chronic (CTEPH) presentation

Pulmonary embolism In most cases (99%) venous tromboembolism – other forms (fat, foreign body,

Pulmonary embolism In most cases (99%) venous tromboembolism – other forms (fat, foreign body, air embolism are very rare) Origin of emboli in proximal lower extremity veins – iliac, femoral, popliteal Other sources are rare (upper extremity veins, renal vein) Virchow triad - venous stasis, endothelial injury, and a hypercoagulable state

Epidemiology Incidence circa 50 -100 cases per 100000 a year 300000 deaths anually in

Epidemiology Incidence circa 50 -100 cases per 100000 a year 300000 deaths anually in Europe 1 year mortality after pulmonary embolism estimated at 10 -13%

Symptoms Wide range of symptoms – asymptomatic patiets (incident finding on CT) v. s.

Symptoms Wide range of symptoms – asymptomatic patiets (incident finding on CT) v. s. hemodynamic shock (SUDDEN ONSET) DYSPNOE!!!! Chest pain - pleuritic (with periferal emboli and infarction) v. s. stenocardia (central emboli with RV ischemia) Shock, syncope, hypotension Hemoptysis, palpitations, caught

Risk factors Inherited – hypercoagulation (FV Leiden, prothrombin mutation, factor C and S deficiency)

Risk factors Inherited – hypercoagulation (FV Leiden, prothrombin mutation, factor C and S deficiency) Acquired – recent surgery, trauma, initiation of hormonet herapy, active cancer, obesity, heavy cigarette smoking, older age, generally any severe internal comorbidity (heart failure, COPD, pneumonia, infection, dehydration …. )

Pathophysiology

Pathophysiology

Diagnosis- stable patients

Diagnosis- stable patients

Diagnosis – D - dimer D-dimer – product of fibrinolysis – not specific, however

Diagnosis – D - dimer D-dimer – product of fibrinolysis – not specific, however negative result safely rule out pulmonary embolism (99, 5 % negative predictive value) Random positive result DOES NOT mean pulmonary embolism – elevation od D dimer level in many clinicalsituation (infection, sepsis, trombosis, cancer, heart failure, myocardial infarction, pregnancy… )

Diagnosis – CT pulmonary angiography Gold standard of diagnosis Shows absence of contrast filling

Diagnosis – CT pulmonary angiography Gold standard of diagnosis Shows absence of contrast filling of affected pulmonary artery branches

Predictive scores

Predictive scores

Predictive scores

Predictive scores

Diagnosis- unstable patients

Diagnosis- unstable patients

Diagnosis - echocardiography Right ventricule dilation and systolic dysfunction Pulmonary hypertension Intracardiac trombi D

Diagnosis - echocardiography Right ventricule dilation and systolic dysfunction Pulmonary hypertension Intracardiac trombi D shape (of left ventricle) Mc. Connell sign Normal echocardiographic finding does not rule out pulmonary embolism per se, but makes a pulmonary embolism as a cause of hemodynamic instability highly improbable Differential diagnosis of other causes of cardiogenic shock

Classification The clinical severity of pulmonary embolism does not strictly correlate to mass of

Classification The clinical severity of pulmonary embolism does not strictly correlate to mass of pulmonary emboli – small embolisationmight cause hemodynamic compromise inpatient with severe preexisting cardiopulmonary morbidity

Classification

Classification

Classification

Classification

Therapy- non high-risk PE Oxygen, antikoagulant therapy LMWH Preparát Dávkování Enoxaparine 1. 0 mg/

Therapy- non high-risk PE Oxygen, antikoagulant therapy LMWH Preparát Dávkování Enoxaparine 1. 0 mg/ kg 2 x / day 1. 5 mg/ kg 1 x Nadroparine 86 IU/ kg 2 x Dalteparine 100 IU/ kg 2 x 200 IU/ kg 1 x 5 mg (t. h. < 50 kg) 1 x Fondaparinux 7, 5 mg (t. h 50 -100 kg) 10 mg (t. h. >100 kg) 3 months in provoked pulmonary embolism, at least three months in unprovoked (usually 6 months), permanent anticoagulation in recurrent PE or in hereditary thrombogenic mutations Venous filters?

NOAC Drug Dosing Pretreatment Dabigatran 150 mg 2 x / day After 5 -10

NOAC Drug Dosing Pretreatment Dabigatran 150 mg 2 x / day After 5 -10 day LMWH Apixaban 10 mg 2 x / day for 7 days, than 5 mg 2 x /day No pretreatment with LMWH Rivaroxaban 15 mg 2 x / day for 21 No pretreatment days, than 20 mg 1 x /day with LMWH Edoxaban 60 mg 1 x/ day VKA in severe renal function impairement After 5 day LMWH

Therapy- high – risk PE Oxygen, inotropes, vasopressors, arteficial pulmonary ventilation, ECMO… Anticoagulant therpay

Therapy- high – risk PE Oxygen, inotropes, vasopressors, arteficial pulmonary ventilation, ECMO… Anticoagulant therpay – Heparine – 80 IU/kg bolus, 18 IU/kg/h continous administration Trombolysis: Preparát Dávkování rt. PA (alteplase, Actilyse) 100 mg in 2 hours 0, 6 mg/kg in 15 minutes In thrombolysis contraindiation, consider surgical thrombectomy (high risk procedure, no experiences in most hospitals … extremely rare), selective thrombolysism catheter thrombectomy/aspiration, ECMO

CTEPH Rare consequence of PE (5/1000000). 80% patients have clinical history of VTE, risk

CTEPH Rare consequence of PE (5/1000000). 80% patients have clinical history of VTE, risk factors – inadequate anticoagulation, recurent PE, high embolic burden, Lupus anticoagulans, hig level FVIII. Fibrotic organisation of emboli PAMP > 25 mm Hg after 3 months of anticoagulant therapy , PCW < 15 mm Hg and at least one segmental perfusion defect at ventilation perfusion scintigraphy

CTEPH Treatment of choice – pulmonary endarterectomy NYHA II-IV. Oxygen therapy, diuretics, permanent anticoagulation

CTEPH Treatment of choice – pulmonary endarterectomy NYHA II-IV. Oxygen therapy, diuretics, permanent anticoagulation No sufficient evidence of benefic of caval filter implantation