l6 pulmonary embolism

DR.Bilal Natiq Nuaman,MD C.A.B.M.,F.I.B.M.S.,D.I.M.2016-2017

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Definition● Sudden occlusion of the pulmonary vasculature, which results

in obstruction of the blood flow to the lung parenchyma .● Commonly blood clot (80%)● Fat ● Air ● Amniotic fluid● Placenta ● Parasites ● Septic emboli (from right sided endocarditis) ● Clumped tumor cells (especially choriocarcinoma)

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Epidemiology●PE is the third most common cause of death

Etiology● Pulmonary embolism is most commonly due to a

thrombus (blood clot) originating from Deep Veins of the lower extremities and pelvis.● pelvis (10 – 15%) ● leg (70-80%)

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Pathophysiology● Thrombus-blood clot along the wall of a normal or

slightly damaged blood vessel● Virchow s triad gives the 3 primary influences of a

thrombus formation● Endothelial Injury ● Stasis or turbulent flow● Blood hypercoagulability

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Criteria of diagnosis● Presence of risk factors for PE.●Clinical presentation consistent with PE.● Exclusion of alternative diagnoses .

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● Most important clinically identifiable risk factors for DVT and PE: ●Prior history of DVT or PE●Recent surgery or pregnancy●Prolonged immobilization●Underlying malignancy.

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Classic Triad of pulmonary embolism

Sudden onset of unexplained dyspnea is the most common, and often the only symptom of pulmonary embolism. Pleuritic chest pain and Hemoptysis are present only when infarction has occurred.

1.Dyspnea, 2.Hemoptysis3.Pleuritic chest pain

In reality the triad occurs in <20% of patients

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Classification● Based on clinical presentation and investigations● Treatment of Pulmonary Embolism (PE) are best

understood when classified● Acute Massive PE● Acute Small/Medium PE

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D-dimer● Dimerized plasmin fragment D● Fibrin degradation product● A negative D-dimer result (< 500 U/mL) excluded

PE with a sensitivity of 83.0%● Sensitive but not specific indicator of

thromboembolic disorders● Raised in inflammatory conditions e.g. Pneumonia

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Arterial Blood Gas● Hypoxemia occurs in about 90% of patients with PE● The degree of hypoxemia doesn’t accurately predict

the size of the PE

●PaO2 of <70 mmHg not explained by CXR findings strongly suggest PE

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Chest X-Ray● Use to Rule out other causes● Initial CXR normal in 1/3rd of patients

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Electrocardiograph

● The most common ECG abnormalities are: ● Sinus tachycardia ● Right axis deviation ● Nonspecific ST segment abnormalities (40% of pts)● RBBB

● These findings are not sensitive or specific enough to aid in the diagnosis of PE

●S1Q3T3 pattern is observed in only 20% of patients● ECG pattern is normal in 1/3rd of patients● Exclude: Myocardial Infarction and Pericarditis

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Spiral CT● Contrast material infused ● Spiral chest CT scans are excellent for detecting

pulmonary emboli in the central pulmonary arteries● Does not detect emboli in beyond segmental vessels

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CT Scan

Fig 1. Spiral CT of patient showing large thrombus (arrowed) within the left pulmonary artery

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Doppler Ultra sound● Detection of thrombosis in femoral & popliteal veins

vessels● Primarily or secondarily involved in the majority of

patients with PE● Doppler Ultra sound has a sensitivity and specificity of

95-100%

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Pulmonary Arteriography● “Gold Standard”● Called upon when clinical suspicion of PE is high

and other studies are inconclusive.

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Ventilation/Perfusion Scan● It is based on identifying areas of ventilation without

perfusion (mismatched defects) ● Technetium isotope is given IV to detect areas of non-

perfusion● Labeled xenon is inhaled to demonstrate non-aerated

lung

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Management● General Measures

● ABC’s

● O2 in all PE (if hypoxemia restore to >90%)

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Treatment of acute PE includes immediate anticoagulation with unfractionated heparin (UFH), low molecular weight heparin (LMWH), fondaparinux, or oral rivaroxaban

1-normal renal function:LMWH or fondaparinux are preferred agents because of the ease of subcutaneous administration and their lower rates of thrombocytopenia. 2-renal impairment :intravenous UFH After (5days) of initiation of heparin or fondaparinux, warfarin should be administered. Infusion of heparin or fondaparinux needs to be continued for at least the first 5 days of warfarin therapy until a therapeutic INR of 2 to 3 is reached. 3-advanced renal failureOral rivaroxaban without initial treatment with heparin or fondaparinux.

Medical● Heparin should be stopped when the INR>2 ● Warfarin therapy should be continued

● 3- 6 weeks for patients with identifiable risk factor● 3-6 months for patients with no identifiable risk factor● life for patients with recurrent embolism.

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Thrombolytic therapyIndication- Massive PE manifested by:(1)hypotension or shock or

(2)right ventricular enlargement or dysfunction from massive PE .

types● Streptokinase- ● Urokinase-● Recombinant Tissue Plasminogen activator (r-tPA)-

100mg over 2hr● fastest

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Surgical●Vena caval filter● Percutaneous thrombectomy● Pulmonary embolectomy

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Caval filter● Filter inserted in IVC below

origin of renal vessels● Indications

● Pts with recurrent PE despite adequate anticoagulation

● (prophylacticaly)Pts for whom anticoagulation is contraindications (eg. immediately after surgery)

● Patients with massive PE who survived but in whom recurrent embolism will be invariably fatal 32

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