Pulmonary Embolism

Other Names

• Pulmonary Embolism (PE)

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Background

• This page refers to pulmonary embolism (PE), a form of venous thromboembolism (VTE) that is common and sometimes fatal

History

• Rudolph Virchow defined the pathophysiology of pulmonary embolism while investigating Cruveilhier's doctrine
  • Virchow realized that a venous thrombus can break loose from its origin, travel through the blood stream, and involve the vessels of other organs
• In 1872, Trendelenburg, a noted German surgeon and founder of the German Surgical Society, realized the sudden mortality associated with this condition while reviewing the deaths of 9 patients from pulmonary embolism at the hospital at Leipzig

Epidemiology

• The overall incidence is higher in males compared with females
• Incidence
  • Estimates of the incidence of pulmonary embolism (PE) in the general population have increased following the introduction of D-dimer testing and computed tomographic pulmonary angiography in the 1990s
• Mortality
  • In the United States, PE accounts for approximately 100,000 annual deaths
  • Deaths from diagnosed PE have been declining with one study reporting deaths from PE that decreased between 1979-1998, from 191 to 94 per million

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Pathophysiology

Prominent left pulmonary artery seems to end abruptly just downstream of the left hilum suggesting acute VTE, also termed 'Westermark Sign'

• General
  • Refers to obstruction of the pulmonary artery vasculature material (eg, thrombus, tumor, air, or fat) that originated elsewhere in the body
  • Typically, this is due to a deep vein thrombosis which embolizes to the right side of the heart and becomes lodged in the pulmonary arteries
• The pathogenesis of pulmonary embolism (PE) is similar to that which underlies the generation of thrombus (Virchow's triad): venous stasis, endothelial injury, and a hypercoagulable state
• Most emboli are thought to arise from lower extremity proximal veins (iliac, femoral, and popliteal) where the thrombus will travel to the pulmonary vasculature and can cause pulmonary infarction, hypoxia, or hemodynamic compromise
• Virchow's triad consists of
  • Stasis of blood
  • Venous injury
  • State of hypercoagulability

Associated Conditions

• Deep Vein Thrombosis

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Risk Factors

• Inherited:
  • Factor 5 Leiden
  • Prothrombin gene mutation
• Acquired:
  • Recent surgery
  • Trauma
  • Immobilization
  • Initiation of hormone therapy
  • Active cancer
  • Obesity
  • Heavy cigarette smoking

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Differential Diagnosis

• Acute coronary syndrome
• Aortic Dissection
• Cardiac Tamponade
• Myocarditis
• Pericarditis
• Pneumothorax
• Esophageal Perforation
• Pneumonia
• Asthma
• Bronchitis
• Panic attack

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Clinical Features

• History
  • Dyspnea (most common)
  • Chest pain (classically pleuritic)
  • Cough
  • Symptoms of DVT
  • Hemoptysis
  • Shock
  • Arrythmia
  • Syncope
• Physical Exam
• Special Tests

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Evaluation

Chest CT showing large saddle embolism in axial cut

Ekg showing the classic S1Q3T3 findings.

Laboratory

• D-dimer Level
  • High sensitivity, low specificity
  • Can use wells score, PERC, years criteria to help risk stratify

Electrocardiogram

• EKG
  • Most common finding is sinus tachycardia
  • New RBBB, T wave inversions, ST elevations or depressions
• Classic S1Q3T3
  • Deep S wave in Lead I: ≥1.5 mm
  • Q wave in Lead III: ≥1.5 mm
  • T wave inversion in Lead III
  • Neither sensitive nor specific

Radiographs

• Standard Chest Radiograph
  • Pulmonary infarction
  • Westermark sign

CT

• CTA of the chest
  • Best diagnostic imaging modality

Nuclear Medicine

• V/Q scan in select patients
  • Typically those with contrast allergy can not receive a CTA

Ultrasound

• DVT Ultrasound
  • In select patients, DVT ultrasound in the setting of signs of symptoms of PE
  • Not standard practice

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Classification

• Low Risk:
  • Normotensive
  • No RV dysfunction
  • Normal biomarkers
• Intermediate Risk (Submassive):
  • Normotensive
  • RV strain (on CT or TTE) categorized as RV dilation, RV dysfunction, BNP> 90 pg/mL, proBNP >500 pg/mL
  • Myocardial Necrosis: Troponin I>0.4 ng/mL, Troponin T >0.1 ng/mL
  • EKG findings of new RBBB, anteroseptal T wave inversions, or anteroseptal ST elevations/depressions
• High Risk (Massive):
  • Hypotension (SBP<90 for >15 min)
  • Obstructive Shock requiring vasopressors
  • Pulselessness

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Management

Nonoperative

• Supplemental oxygen (maintain O2 saturation >90%)
• Hemodynamic support (IVF and vasopressors)
• Anticoagulation:
  • Low risk PE: DOAC or non DOAC and clinical surveillance
  • Intermediate risk PE: DOAC or non DOAC and catheter directed thrombolysis or mechanical thrombectomy
  • High risk PE: thrombolysis or catheter directed thrombolysis

Operative

• Catheter directed thrombolysis if not candidate for systemic thrombolysis

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Rehab and Return to Play

Return to Play/ Work

• Stepwise resumption of noncontact athletic participation has been proposed beginning as early as 3 weeks after VTE, and full return to noncontact activity can be achieved while the athlete remains anticoagulated
• Once initial anticoagulation therapy is completed, risk of recurrent VTE is <1/6000 per day and of fatal recurrent VTE <1/100,000 per day (absolute risks are very low)
• Athletes do not necessarily need to be prevented from competing in contact sports while being anticoagulated. With DOACs now available, after obtaining PK/PD data for a specific athlete, an individualized treatment plan can be developed to allow for participation with only a small increase in risk

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Complications and Prognosis

Prognosis

• Asymptomatic or lower risk PE patients tend to have favorable prognosis
• Moderate and/or high risk PE patients tend to have variable prognosis
• If left untreated, mortality rates up to 30% compared with 2-11% in those treated with anticoagulation

Complications

• Pulmonary infarction
• Hypoxic respiratory failure
• Hemodynamic collapse
• Cerebrovascular accident
• Pulmonary Hypertension (if long standing subsegmental PE)

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See Also

• Cardiology Main
• Pulmonology Main
• Vascular Main

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