• Clinical science
  • Clinician

Pulmonary embolism

Summary

Pulmonary embolism (PE) is the obstruction of one or more pulmonary arteries by solid, liquid, or gaseous masses. In most cases, the embolism is caused by blood thrombi, which arise from the deep vein system in the legs or pelvis (deep vein thrombosis) and embolize to the lungs via the inferior vena cava. Risk factors include immobility, inherited hypercoagulability disorders, pregnancy, and recent surgery. The clinical presentation is variable and, depending on the extent of vessel obstruction, can range from asymptomatic to cardiogenic shock. Symptoms are often nonspecific, including chest pain, coughing, dyspnea, and tachycardia. The diagnosis of PE is based primarily on the clinical findings and is confirmed by the detection of an embolism in CT pulmonary angiography (CTPA). Arterial blood gas analysis typically shows evidence of respiratory alkalosis with low partial oxygen pressure, low partial carbon dioxide pressure, and elevated pH. Another commonly performed test is the measurement of D-dimer levels, which can rule out PE if negative. Anticoagulation with heparin is initiated to prevent further thromboembolisms as well as to promote the gradual dissolution of the embolism and the underlying thrombosis. In massive PE with shock, the thrombus is resolved with thrombolytic agents or thrombectomy.

Epidemiology

  • Accounts for ∼ 100,000 deaths in the US per year.
  • Incidence rises with age.
  • Sex: >

References:[1]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

references:[1][2]

Pathophysiology


References:[3][1]

Clinical features

Consider PE as a differential diagnosis in recurring or progressive dyspnea of uncertain etiology!

References:[4]

Pretest probability of pulmonary embolism

There are several externally validated decision tools that can be used to assess the pretest probability of PE. These include the original Wells score and modified Wells score, revised Geneva score, and pulmonary embolism rule-out criteria (PERC). None of these scoring systems have been found to have greater levels of accuracy than the others. [5][6]

Wells criteria for pulmonary embolism [7]

The Wells score is a diagnostic algorithm for assessing the probability of PE and has been validated in inpatient and outpatient settings. Note that a different version is used for determining the probability of DVT (see Wells criteria for DVT).

Wells criteria for PE [8][9]
Criteria Points
Clinical symptoms of DVT 3
PE more likely than other diagnoses 3
Previous PE/DVT 1.5
Tachycardia (Heart rate > 100/min) 1.5
Surgery or immobilization in the past 4 weeks 1.5

Hemoptysis

1
Malignancy 1
Original Wells score (clinical probability) [8]

Modified Wells score (clinical probability) [9]

  • Total score ≤ 4: PE unlikely (8%)
  • Total score > 4: PE likely (34%)

Revised Geneva score [10]

The revised Geneva score utilizes objective clinical variables. It has been externally validated and was initially studied in emergency department outpatients.

Revised Geneva score [8]
Criteria Points
Age > 65 years 1
Prior history of DVT or PE 3
Recent surgery or fracture of the lower limbs 2
Personal history of cancer 2
Unilateral lower limb pain 3
Hemoptysis 2
Heart rate 75–94/min 3
Heart rate ≥ 95/min 5
Pain on palpation of lower limb and unilateral edema 4

Clinical pretest probability

Pulmonary embolism rule-out criteria (PERC) [6][11][12]

PERC is only used for patients who have a low pretest probability of PE based on either their Wells score for pulmonary embolism or revised Geneva score.

Pulmonary embolism rule-out criteria (PERC)
Criteria Points
Age > 50 years 1
Heart rate > 100/min 1
Oxygen saturation < 95% 1
Hemoptysis 1
Estrogen use 1
Prior history of DVT or PE 1
Recent surgery or trauma in the past 4 weeks 1
Unilateral lower limb edema 1

Clinical pretest probability

  • Total score 0: pretest probability < 1%; no further testing needed
  • Total score ≥ 1: PE is not ruled out; further testing needed

PERC should only be used in patients with a low pretest probability of PE.

Diagnostics

Diagnostic approach [13][6]

  1. Assess for hemodynamic stability.
    • Stable patients: systolic BP > 90 mm Hg
    • Unstable patients: systolic BP < 90 mm Hg for > 15 minutes, evidence of shock, or BP drop > 40 mm Hg for > 15 minutes
  2. Assess the pretest probability of PE.
  3. Obtain other laboratory studies or imaging as needed.

Laboratory studies [6]

D-dimer levels [6]

  • Indication: pretest probability of PE is either low and does not meet PERC OR is intermediate
  • Findings
    • Normal levels: < 500 ng/mL
    • If ≥ 500 ng/mL: Further testing is required (see below).
    • If the patient is > 50 years of age, adjust for age: age x 10 ng/mL = cut off value in ng/mL
  • Additional considerations

Normal D-dimer values can usually rule out PE or DVT in patients with unremarkable history and physical examination! A positive D-dimer is nonspecific, since it may be elevated in any situation where there is increased fibrinolysis.

Additional testing

Imaging

CT pulmonary angiography (CTPA)

Ventilation/perfusion scintigraphy (V/Q scan) [19]

  • Indications: an alternative to CT pulmonary angiography in patients with renal insufficiency and/or contrast allergy
  • Procedure
    • A chest radiograph must be obtained prior to a V/Q scan to correlate findings.
    • Radioactive agents (e.g., TC-99m) are inhaled and administered intravenously.
    • The distribution of these agents in the alveoli and pulmonary arteries is registered via gamma cameras.
    • Perfusion scintigraphy is usually performed first, followed by ventilation scintigraphy.
  • Findings [20]

Echocardiography [21]

  • Indication: to detect signs of right atrial pressure (RAP)
    • Rapid presumptive diagnostic tool in hemodynamically unstable patients
    • Prognostic tool in a hemodynamically stable patient
  • Supportive findings
  • Additional considerations: Evidence of new right heart strain supports a presumptive diagnosis of PE. However, ECHO findings are not as specific as other diagnostic modalities. [18]

Lower-extremity duplex ultrasound

  • Indications [13][6]
    • Symptoms of deep venous thrombosis and pulmonary embolism
    • Contraindications to CTPA (e.g., contrast allergy and renal insufficiency)
    • Pregnant women
  • Supportive findings [19]
    • Hypoechoic material in the lumen of veins: may be occlusive or nonocclusive
    • Venous lumens do not collapse under compression.
  • Additional considerations
    • Low sensitivity for the diagnosis of probable PE
    • A negative ultrasound may not be sufficient to rule out PE. [22][23]

Chest x-ray [19]

Pulmonary angiography [19]

  • Definition: an invasive radiological procedure performed with contrast dye to visualize the pulmonary vasculature
  • Indications
    • To guide the planning of concomitant endovascular treatment [19]
    • Suspicion for PE is high despite negative findings. [18]
  • Procedure
  • Supportive findings: intraluminal filling defects in pulmonary arteries
  • Additional considerations: not commonly used because it is more invasive and harder to perform than CTPA

Magnetic resonance pulmonary angiography [24]

  • Indications: when standard imaging (CTPA or V/Q scan) cannot be performed
  • Supportive findings [19]
  • Additional considerations: high risk for technically inadequate imaging and poor sensitivity.

Additional diagnostics

Electrocardiography (ECG) [25]

Identifying the underlying cause

Treatment

Approach

  1. Stabilize the patient and provide supportive care.
    • Pulseless patient with suspected PE: Start ACLS and consider administration of thrombolytics (e.g., tPA ). [32][33].
  2. Assess bleeding risk (see risk factors for bleeding in patients with VTE).
  3. Consider empiric parenteral anticoagulation while awaiting a definitive diagnosis.
  4. Risk stratify the patient based on prognostic models (see risk stratification of pulmonary embolism).
  5. Consult pulmonary embolism response team (PERT), if available. [34]
  6. Initiate therapy based on risk stratification and bleeding risk.

Supportive care

Hypervolemia can be harmful if right ventricle strain is present.

Assessment of bleeding risk

There are currently no scoring systems with sufficient prediction outcomes for the bleeding risk from anticoagulant therapy in patients with PE. The HAS-BLED score is sometimes used but it was designed and validated for anticoagulant therapy in patients with atrial fibrillation. See risk factors for bleeding in patients with VTE. [36]

Empiric parenteral anticoagulation for pulmonary embolism

  • Indications: consider starting empiric anticoagulation in patients awaiting a definitive diagnosis, depending on the risk of bleeding, the pretest probability of PE, and the expected timing of the diagnostic study [33][35]
    • Low probability of PE and diagnostic study is expected to be delayed > 24 hours [33]
    • Intermediate probability of PE and diagnostic study is expected to be delayed > 4 hours [33]
    • High probability of PE
  • Absolute contraindication: high bleeding risk
  • Choice of medication [33][35]
    • Stable patients: LMWH [33]
    • Unstable patients or patients with renal insufficiency: UFH [37]

An absolute contraindication for empiric anticoagulation is a high risk of bleeding (e.g., recent surgery, hemorrhagic stroke, active bleeding)!

Risk stratification of pulmonary embolism

Risk categories based on the risk of adverse outcomes [38][39]

Pulmonary Embolism Severity Index (PESI) and simplified PESI (sPESI) [40][41]

The Pulmonary Embolism Severity Index stratifies the risk of mortality or adverse outcomes and is used to assist in decisions on inpatient vs. outpatient management.

PESI and sPESI
Criteria Points
PESI [40] sPESI [41]
Age 1 per year 1 if > 80 years
History of cancer 30 1
Systolic blood pressure < 100 mm Hg 30 1
Heart rate ≥ 110/min 20 1
O2 saturation on room air < 90% 20 1
Heart failure 10 1
Chronic lung disease 10
Altered mental status 60 Not considered
Temperature < 96.8°F (< 37°C) 20
Respiratory rate ≥ 30/min 20
Sex

Male: 10

Female: 0

PESI interpretation (30-day mortality rate, inpatient mortality) [40]

  • < 66 points: class I, very low risk (0–1.6%, ≤ 1.1%)
  • 66–85 points: class II, low risk (1.7–3.5%, ≤ 1.9%)
  • 86–105 points: class III, intermediate risk (3.2–7.1%, ≤ 4.7%)
  • 106–125 points: class IV, high risk (4.0–11.4%, ≤ 7.0%)
  • > 125 points: class V, very high risk (10.0–23.9%, ≤ 17.2%)

sPESI interpretation (30-day mortality) [41]

  • 0 points: low risk (1%)
  • ≥ 1 point: high risk (10.9%)

Treatment of massive pulmonary embolism

Initiate directed therapy based on bleeding risk and the presence of any contraindications to thrombolytic therapy in massive pulmonary embolism.

Thrombolytic therapy in pulmonary embolism

Systemic thrombolysis [37]

Catheter-directed thrombolysis [37]

Contraindications to thrombolysis

Contraindications to thrombolytic therapy in massive pulmonary embolism [37]
Absolute contraindications
Relative contraindications

Embolectomy in pulmonary embolism [33]

  • Indication: : treatment of last resort when thrombolysis is contraindicated or unsuccessful
  • Procedure: surgical or catheter-based thrombus removal

Treatment of nonmassive pulmonary embolism and submassive pulmonary embolism

Initiate directed therapy based on the bleeding risk from anticoagulant therapy in pulmonary embolism.

Anticoagulation for pulmonary embolism [33][37][39][44]

Specific populations [37]

  • Recurrent VTE
    • Assess for true recurrence, medication compliance, and underlying malignancy.
    • If on VKA or DOAC, switch to LMWH at least temporarily (usually at least for 1 month).
    • If there is a recurrence while on LMWH, increase the dose by one-quarter to one-third.
  • Subsegmental PE
    • If there is a low risk for recurrence , anticoagulation is not necessary.
    • Otherwise, initiate anticoagulation.
    • Ultrasound of lower extremities to rule out proximal DVT.
  • Low-risk PE based on risk stratification (see risk stratification of pulmonary embolism)
    • Patients with adequate home circumstances may be treated at home or discharged early (after 5 days of treatment).

Risk factors for bleeding during anticoagulant therapy in patients with VTE

The following risk factors apply to both patients with PE and/or DVT: [37]

Interpretation: bleeding risk categorization [37]

Risk category

Total risk of major bleeding
Anticoagulation 0–3 months Anticoagulation after first 3 months
Low (0 risk factors) 1.6% 0.8%/year
Moderate (1 risk factor) 3.2% 1.6%/year
High (≥ 2 risk factors) 12.8% ≥ 6.5%/year

Acute management checklist

Initial management

  • Hemodynamic support in patients with hypotension
  • Supplemental oxygen as needed
  • Analgesics
  • Consult Pulmonary Embolism Response Team (PERT). [34]

Nonmassive and submassive pulmonary embolism

  • Assess bleeding risk and consider empiric parenteral anticoagulation while awaiting definitive diagnosis.
  • If bleeding risk is low to moderate, start anticoagulation (see anticoagulation for pulmonary embolism).
  • If bleeding risk is high, consider IVC filter placement.
  • Consider continuous pulse oximetry and/or continuous telemetry.
  • In select patients with very low-risk PE (e.g., sPESI = 0): Consider outpatient therapy.
  • In patients with subsegmental PE with low risk of recurrent VTE: Consider clinical surveillance only.

Massive pulmonary embolism

Pulseless patient with suspected PE

  • Start ACLS.
  • Consider administration of reduced dose of tPA.

Complications

References:[1][45]

We list the most important complications. The selection is not exhaustive.

Differential diagnoses

Pathology

  • Purpose: distinguish cause of embolism (see Etiology above)
  • Histological findings: Thrombus might show Lines of Zahn ;
    • Alternating layers of platelets mixed with fibrin (light pink layers) and red blood cells (dark red layers)
    • Only appear premortally (help distinguish a premortal thrombus from a postmortem one)

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last updated 07/10/2020
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