Pulmonary embolism

Last revised by Joshua Yap on 22 Feb 2024

Pulmonary embolism (PE) refers to embolic occlusion of the pulmonary arterial system. The majority of cases result from thrombotic occlusion, and therefore the condition is frequently termed pulmonary thromboembolism, which is what this article mainly covers.

Non-thrombotic pulmonary emboli sources include 30

Classification of a pulmonary embolism may be based upon: 

  • the presence or absence of hemodynamic compromise

  • temporal pattern of occurrence

  • the presence or absence of symptoms

  • the vessel which is occluded

Clinical decision rules, in conjunction with physician gestalt and estimated pretest probability of disease, may serve as a supplement in risk stratification:

  • sinus tachycardia: the most common abnormality

  • right heart strain pattern

    • incomplete or complete right bundle branch block

    • prominent R wave in lead V1

    • right axis deviation

    • T-wave inversion in the right precordial leads +/- the inferior leads is seen in up to 34% of patients and is associated with high pulmonary artery pressures 25

  • SIQIIITIII pattern

The patient may report a history of recent immobilization or surgery, active malignancy, hormone usage, or a previous episode of thromboembolism. The physical exam may reveal suggestive features such as:

  • clinical signs of deep venous thrombosis (DVT)

    • asymmetric pitting lower extremity edema

    • prominent superficial collateral vessels

    • tenderness to palpation along the deep venous system

  • tachycardia

  • dyspnea

  • pleuritic chest pain

  • hemoptysis

D-dimer (ELISA) is commonly used as a screening test in patients with a low and moderate probability clinical assessment, in these patients:

  • normal D-dimer has almost 100% negative predictive value (virtually excludes PE): no further testing is required

  • raised D-dimer is seen with PE but has many other causes and is, therefore, non-specific: it indicates the need for further testing if pulmonary embolism is suspected 4

In patients with a high probability clinical assessment, a D-dimer test is not helpful because a negative D-dimer result does not exclude pulmonary embolism in more than 15%. Patients are treated with anticoagulants while awaiting the outcome of diagnostic tests 4.

Depends to some extent on whether it is acute or chronic. Overall, there is a predilection for the lower lobes.

Chest radiography is neither sensitive nor specific for a pulmonary embolism. It is used to assess differential diagnostic possibilities such as pneumonia and pneumothorax rather than for the direct diagnosis of PE. 

Pleural effusions are associated in 35% of cases (see pleural effusions in pulmonary embolism).

Described chest radiographic signs include:

Sensitivity and specificity of chest x-ray signs 1:

  • Westermark sign

    • sensitivity ~14%, specificity ~92% , PPV: ~38%, NPV: ~76%

  • vascular redistribution

    • sensitivity: ~10% , specificity: ~87% , PPV: ~21%, NPV: ~74%

  • Hampton hump

    • sensitivity: ~22% , specificity: ~82%, PPV: ~29%, NPV: ~76%

  • pleural effusion

    • sensitivity: ~36% , specificity: ~70%, PPV: ~28%, NPV ~76%

  • elevated diaphragm

    • sensitivity: ~20%, specificity: ~85%, PPV: ~30%, NPV: ~76%

Point-of-care ultrasonography is currently not recommended for a haemodynamically stable patient with suspected pulmonary embolism. In the presence of hemodynamic compromise, echocardiography may be of value to assess for the presence of severe right ventricular dysfunction;

  • if absent, another cardiopulmonary derangement is likely responsible

  • if unequivocally present, it can establish the need for emergent treatment

Echocardiographic features which may be suggestive include:

Of note, transesophageal echocardiography has a reported sensitivity of 81% and a specificity of 97% for ruling in acute pulmonary embolism after the detection of right ventricular overload on transthoracic echocardiography 24

Again not recommended as part of first-line work up. 

Cumulative damage from repeated embolic insults is a common cause of chronic thromboembolic pulmonary hypertension, which demonstrates a variable degree of the aforementioned signs, but with significantly higher right ventricular pressures, right ventricular hypertrophy and diastolic dysfunction, and a higher degree of tricuspid regurgitation

CT pulmonary angiography (CTPA) will show filling defects within the pulmonary vasculature with acute pulmonary emboli. When the artery is viewed in its axial plane the central filling defect from the thrombus is surrounded by a thin rim of contrast, which has been called the polo mint sign.

Emboli may be occlusive or non-occlusive, the latter is seen with a thin stream of contrast adjacent to the embolus. Typically the embolus makes an acute angle with the vessel, in contrast to chronic emboli. The affected vessel may also enlarge 9.

Acute pulmonary thromboemboli can rarely be detected on non-contrast chest CT as intraluminal hyperdensities 12.

Dual-energy CT holds much promise for the diagnosis and prognosis of PE. Z effective and iodine maps provide lung perfusion assessment. The use of low monoenergetic reconstructions (low monoE) allows 'iodine boosting' of the pulmonary arteries which are useful during suboptimal contrast opacification thereby preventing the need to repeat undiagnostic scans ref.

In contrast to acute pulmonary embolism, chronic thromboemboli are often complete occlusions or non-occlusive filling defects in the periphery of the affected vessel which form obtuse angles with the vessel wall 9. The thrombus may be calcified.

Features noted with chronic pulmonary emboli include:

  • webs or bands, intimal irregularities 3

  • abrupt narrowing or complete obstruction of the pulmonary arteries 3

  • pouching defects” which are defined as chronic thromboembolism organized in a concave shape that “points” toward the vessel lumen 3

Indirect signs include 7:

  • mosaic perfusion

  • vascular calcification

  • bronchial or systemic collateralisation

It is difficult to obtain technically adequate images for pulmonary embolism patients using MRI. Magnetic resonance pulmonary angiography (MRPA) should be considered only at centers that routinely perform it well and only for patients for whom standard tests are contraindicated. Technically-adequate magnetic resonance angiography has a sensitivity of 78% and a specificity of 99% 13.

A ventilation/perfusion (V/Q) scan will show ventilation-perfusion mismatches. A high probability scan is defined as showing two or more unmatched segmental perfusion defects according to the PIOPED criteria.

Providing cardiopulmonary support is the initial treatment. Anticoagulation is provided in patients without risk of active bleeding. If the emboli are large or there is a large clot burden, thrombolysis is an option. In some cases, embolectomy or placement of vena cava filters is required.

Anticoagulation treatment for subsegmental pulmonary embolism may be driven by considerations on recurrence risk, bleeding risk, and patient's preferences 34.

The right ventricular failure due to pressure overload is considered the primary cause of death in severe PE 14.

Around 80% of emboli resolve at approximately 30 days 20,21. Residual pulmonary obstruction at 6 months after the first episode was shown to be an independent predictor of recurrent venous thromboembolism and/or chronic thromboembolic pulmonary hypertension 28.

It was first reported in the 1850s by the German physician and pathologist Rudolf Virchow 33.

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Cases and figures

  • Figure 1: saddle embolism
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  • Figure 2: blood clots aspirated post vacuum thrombectomy
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  • Case 1: saddle pulmonary emboli
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  • Case 2: saddle embolus
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  • Case 3: adherent to vessel wall
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  • Case 4: with severe right heart strain
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  • Case 5: with lung infarction
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  • Case 6
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  • Case 7a: perfusion defects on spectral CTPA
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  • Case 7b: perfusion defects on spectral CTPA
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  • Case 8
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  • Case 9
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  • Case 10
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  • Case 11
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  • Case 12
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  • Case 13
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  • Case 14
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  • Case 15
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  • Case 16
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  • Case 17
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  • Case 18
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  • Case 19
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  • Case 20: saddle embolus
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  • Case 21: dual-energy
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  • Case 22
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  • Case 23: segmental thrombosis
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  • Case 24: complete occlusion
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  • Case 25
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  • Case 26: chronic PE
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  • Case 27: MRI
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  • Case 28: with infarction
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  • Case 29: Hampton's hump
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  • Case 30
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  • Case 31
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  • Case 32: with right heart strain
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  • Case 33: acute pulmonary embolism
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  • Case 34: suboptimal CTPA saved by spectral low monoE
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  • Case 35: SPECT-CT
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  • Case 36: with right atrial thrombus
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