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Lung-nontumor

Other non-neoplastic disease

Infarct / pulmonary emboli


Reviewers: Elliot Weisenberg, M.D. (see Reviewers page)
Revised: 19 December 2011, last major update December 2011
Copyright: (c) 2003-2011, PathologyOutlines.com, Inc.

Clinical features
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● 50,000+ deaths / year in US due to pulmonary emboli (major cause of death in 10% of adults dying acutely in hospitals)
● 95% of emboli are from deep leg veins; often in immobilized individuals; also central venous lines may cause right atrial thrombi
● Occlusions usually embolic, not thrombotic, as pulmonary vasculature is low pressure, uncommonly occurs with pulmonary hypertension
● Autopsy studies show incidence in general population of 1%, including 30% of patients with severe burns or trauma
● Large emboli cause sudden death by (a) lodging in major branches of pulmonary arteries or at bifurcations, causing electromechanical dissociation with rhythm but no pulse or (b) acute cor pulmonale (dilation of right side of heart) due to local increased resistance to blood flow, pulmonary hypertension and right sided failure
● Other risk factors are trauma, hypercoagulable states, protein C/S deficiency, lupus anti-coagulant, Factor V Leiden mutation, prothrombin mutation, carcinoma and Trousseauís syndrome, oral contraceptives, heart failure, pregnancy and older age
● Small infarcts usually have minimal symptoms; if bronchial circulation is inadequate (so reduced collateral circulation), then have shortness of breath, tachycardia, pain, fever, cough, hemoptysis, fibrinous pleuritis or friction rub
● If cardiovascular function is adequate, bronchial artery may compensate for pulmonary emboli, leading to hemorrhage without infarction; lungs can recover from hemorrhage but not from infarction
● Emboli cause infarction only when circulation is already inadequate, so rare in young
Fat emboli: due to long bone fracture or CPR
Amniotic fluid emboli: rare pregnancy complication, with squames in vessels
Hypercoagulable states: either primary (deficiency of antithrombin III or protein C, lupus anticoagulant, Factor V Leiden mutation, prothrombin mutation, defective fibrinolysis) or secondary (obesity, surgery, cancer, estrogen and pregnancy)

Diagnosis
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● Although other tests may be more sensitive, D-dimer testing is an excellent validated screening test for thromboembolic disease; a negative result essentially rules out pulmonary embolism
CT angiography: Very sensitive and specific, fast and readily available imaging study to rule in or rule out pulmonary embolism; has essentially replaced conventional angiography
Chest Xray: wedge shaped infarct after 12-36 hours; may simulate carcinoma
Nuclear scan: macroaggregates of labeled albumin with perfusion lung scanning; angiography most definitive diagnostic test

Gross description
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● Wedge shaped, hemorrhagic parenchyma and fibrinous pleural exudate; eventually scars

Gross images
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Thromboemboli in pulmonary artery


Saddle embolus


Hemorrhagic infarct


Organizing infarct


Fibrous band

Micro description
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● Neutrophils present if septic emboli

Micro images
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Thromboemboli


Small thromboemboli


With recanalization

   
Left-fat emboli; right-amniotic fluid emboli

Virtual slides
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Infarct due to septic emboli


Hemorrhagic infarct


Thromboemboli

End of Lung-nontumor > Other non-neoplastic disease > Infarct / pulmonary emboli


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