Nej Mr a 0907731

Review Article

Acute Pulmonary EmbolismGiancarlo Agnelli, M.D., and Cecilia Becattini, M.D., Ph.D.

N Engl J Med Volume 363(3):266-274 July 15, 2010

Introduction: Pulmonary embolism should be suspected in all patients who present with new or worsening dyspnea, chest pain, or sustained hypotension without a clear alternative cause. Disease spectrum from asymptomatic DVT to massive pulmonary embolism causing immediate death.

About 79% of patients with pulmonary embolism have evidence of legs DVT. Pulmonary embolism occurs in up to 50% of patients with proximal DVT Pulmonary infarction is not usually present due to the dual circulation arising from the pulmonary and bronchial arteries.

Pathophysiology Anatomical obstruction cause compromised physiology Release of vasoactive and bronchoactive agents lead to deleterious ventilationperfusion matching RV afterload increases, RV wall tension rises and lead to dilatation, dysfunction, and ischemia of the RV Death results from RV failure

Pathophysiology of Pulmonary Embolism

Tapson V. N Engl J Med 2008;358:1037-1052

Clinical manifestation Tachypnea and tachycardia-- Common but nonspecific Pleuritic chest pain and hemoptysis -- Frequent in pulmonary infarction ( smaller, more peripheral emboli, and may with pleural rub). Leg pain, warmth, or swelling-- Symptoms of DVT Elevated neck veins, a loud P2, a right-sided gallop, and RV lift Pulmonary hypertension All signs and symptoms are neither sensitive nor specific.. Clinical symptoms didnt correlate with disease severity

The possibility of massive pulmonary embolism should be considered in pts with sudden onset of near syncope or syncope, hypotension, extreme hypoxemia, electromechanical dissociation or cardiac arrest.

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Risk factors Virchow's triad describes the three broad categories of factors that are thought to contribute to thrombosis. 1.Hypercoagulability 2.Hemodynamic change (stasis, turbulence) 3.Endothelial injury / dysfunction It is named for German physician Rudolf Virchow (1821-1902).

Risk Factors for Venous Thromboembolism


Risk factors - Hereditary Antithrombin deficiency Protein C/S deficiency Factor V Leiden mutation Activated protein C resistance without factor V Leiden

C Prothrombin gene mutation Dysfibrinogenemia Plasminogen deficiency

Factor V: coagulation factor five V Factor V Leiden protein C6 5% . >> . >>

Risk factors- acquired Antiphospholipid antibody syndrome Oral contraceptives Hormone-replacement therapy Chemotherapy

Obesity Central venous catheterization Immobilizer or cast Reduced mobility

Antiphospholipid antibody syndrome 1.thrombosis, DVT 2. 3. 4.Lupus endocarditis ( triad)

Risk factors- acquired Advanced age Cancer Acute medical illness Major surgery

Trauma Spinal cord injury Pregnancy and postpartum period Polycythemia vera

Polycythemia vera 786070% 310

: 1. : 2. factor V LeidenC C 3. (Hyperhomocysteinemia) B6B12

: 1. factor V Leiden(12~40%) prothrombin G 20210A mutation(6~18%), (10~20%) 2. Protein CSantithrombin III5~15%() 50%protein S antiphospholipid antibody10~20% 3. 10~20%mucin-secreting adenocarcinoma, brain tumor, acute promyelocytic leukemia myeloproliferative disorders 4. 50% 5.

: 1. Protein Cprotein S AT III 2. Antiphospholipid AbLupus anticoagulant anticardiolipin Ab

EKG * large : Rt heart strain or acute cor pulmonale * the classic signs: S1Q3T3 (up to 20%) * The most commonly: sinus tachycardia(8-69%), Rt axis deviation , RBBB.

signs

Image study Ventilationperfusion scanning Contrast-enhanced CT Magnetic resonance imaging (MRI) Standard pulmonary arteriography

Imaging for detecting DVT Echocardiography

Clinical Prediction Scores for Suspected Acute Pulmonary Embolism


Chest radiograph shows bilateral pleural effusion and long linear bands of atelectasis (Fleischner lines) (arrows).

EMBOLISM WITHOUT INFARCTION (90%) 1. normal chest (25%) 2. platelike atelactasis 3. Westermark sign 4. Knuckle sign : abrupt tapering of an occluded vessel distally

5. local widening of artery by impacted embolus 6. segmental / lobar consolidation 7. pleural effusion

EMBOLISM WITH INFARCTION (10%) 1. wedge-shaped consolidation (50%) 2. may cavitate 3. Hampton hump: a shallow wedge-shaped opacity in the periphery of the lung with its base against the pleural surface 4. pleural effusion (50%) 5. no air-bronchogram 6. melting sign" : regression of consolidation from periphery to center, appears within days to weeks 7. Fleischner lines : long line shadows (fibrotic scar) from invagination of pleura at the base of the collapse resulting in pseudofissure 8. platelike atelactasis (25%) 9. cardiomegaly / CHF (20%) 10. elevated hemidiaphragm (20%)

Contrast-Enhanced CT Angiograms Showing Acute Pulmonary Embolism


Spiral CT of patient showing large thrombus (arrowed) within the left pulmonary artery

Diagnostic Approach to Suspected Acute Pulmonary Embolism


Diagnostic Workup for Pulmonary Embolism

Agnelli G, Becattini C. N Engl J Med 2010;363:266-274 Agnelli G, Becattini C. N Engl J Med 2010;363:266-274

Clinical Management of Confirmed Acute Pulmonary Embolism


Right Ventricular Dilatation

Agnelli G, Becattini C. N Engl J Med 2010;363:266-274

Treatment of Acute Pulmonary Embolism


Treatment of Acute Pulmonary Embolism


Treatment options anticoagulants : also described as "blood thinners," these medications decrease the ability of the blood to clot. Examples of anticoagulants include warfarin (Coumadin) and heparin. fibrinolytic therapy - also called "clot busters," these medications are given intravenously (IV) to break down the clot.

vena cava filter - a small metal device placed in the vena cava (the large blood vessel that returns blood from the body to the heart) may be used to prevent clots from traveling to the lung. These filters are generally used in patients who cannot receive anticoagulation treatment (for medical reasons), who develop additional clots even with anticoagulation treatment, or who develop bleeding complications from anticoagulation.

Treatment options pulmonary embolectomy - surgical removal of a pulmonary embolism. This procedure is generally performed only in severe situations in which the PE is very large, the patient either cannot receive anticoagulation and/or thrombolytic therapy due to other medical considerations or has not responded adequately to those treatments, and the patient's condition is unstable. percutaneous thrombectomy - insertion of a catheter (long, thin, hollow tube) to the site of the embolism, using X-ray guidance. Once the catheter is in place, the catheter is used to break up the embolism, extract it (pull it out), or dissolve it by injecting thrombolytic medication.

Prevention Non-invasive mechanical measures Mechanical measures to prevent DVT include: compression stockings (elastic stockings that squeeze or compress the veins and prevent blood from flowing backward) pneumatic compression devices (sleeves on the legs that are connected to a machine that provides alternating pressure on the legs) getting up and moving as soon as possible after surgery or illness, as movement can help to prevent clots from forming by stimulating blood circulation

PreventionMedication: Anticoagulants, such as heparin and warfarin, are often given prophylactically to prevent DVT.

Motality untreated PE is said to be 26%

Thank you for your attention

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Nej Mr a 0907731