Pulmonary Embolism

Descriptive text is not available for this image BASICS

Pulmonary embolism (PE) is an acute cardiovascular disorder that causes pulmonary vascular bed obstruction, which may result in acute right ventricular failure.

DESCRIPTION

  • PE is the most serious presentation of venous thromboembolism (VTE).
  • Classified based on severity:
    • Low-risk PE: no evidence of end organ damage or hemodynamic instability
    • Submassive PE: no systemic hypotension, but there is either myocardial necrosis (elevated troponin) or right ventricle (RV) dysfunction (RV dilation or systolic dysfunction on echocardiography [echo], RV/LV ratio >1 on computed tomography [CT], elevation of B-type natriuretic peptide [BNP] or N-terminal pro-BNP, or consistent electrocardiogram [ECG] changes)
    • Massive PE: hemodynamic instability with sustained hypotension; pulselessness; or persistent bradycardia, cardiogenic shock, acute manifesting RV failure

EPIDEMIOLOGY

Third leading cause of vascular death (after MI and stroke); case fatality rates vary (1–60%); ~11% at 2 weeks

Incidence

  • Approximately 30 to 80/100,000, with higher incidence in African Americans and lower in Asians; >100,000 cases annually in the United States
  • Incidence increases with age, most occurring at 60 to 70 years of age.
  • 250,000 hospitalizations per year in the United States, 10–60% in hospitalized patients (highest risk for orthopedic and cancer patients; 1:1,000 pregnancies)

Prevalence

Within hospitalized patients: 17.3% prevalence of PE in hospitalized adults who were admitted for first episode of syncope (between 2012 and 2014) (1)

ETIOLOGY AND PATHOPHYSIOLOGY

  • Venous stasis, endothelial damage, and changes in coagulation properties generates thrombus formation.
  • Thrombus causes increased pulmonary vascular resistance, impaired gas exchange, and decreased pulmonary compliance. RV failure due to pressure overload is usually the primary cause of death.
  • The most common source (85%) of PE is proximal lower extremity deep vein thrombosis (DVT).

Genetics

  • Factor V Leiden: most common thrombophilia; >5.5% in Caucasians; 2.2% in Hispanics; 1.2% in African Americans, 0.5% in Asians; associated with 20% of VTE
  • Prothrombin G20210A: 3% of Caucasians; rare in African Americans, Asians, and Native Americans; 6% in patients with VTE
  • Rarely, deficiencies in protein C, S, and antithrombin

RISK FACTORS

  • Older age, obesity, prolonged immobilization, surgery (total hip and knee arthroplasty, hip fracture cancer), major trauma, joint replacement, spinal cord injury, active cancer, hormonal replacement therapy, pregnancy/puerperium, previous thrombosis, antiphospholipid syndrome, genetics
  • Oral contraceptive is the most frequent risk factor in women.

GENERAL PREVENTION

  • Low VTE risk: early ambulation after surgery, compression stockings, and intermittent pneumatic compression
  • Use of thromboprophylaxis in COVID-19 infection is not commonly done but may be considered in those at high risk (prior VTE, recent surgery, limb immobilization, recent trauma, etc.)
  • Hip or knee arthroplasty (high VTE risk): ≥10 days prophylaxis with low–molecular-weight heparin (LMWH), fondaparinux, apixaban, dabigatran, rivaroxaban, or low-dose unfractionated heparin (UFH)
  • Spinal cord injury, hip fracture surgery, and trauma surgery (high VTE risk): 28 to 35 days with LMWH, fondaparinux, UFH, or vitamin K antagonists (VKA)
  • Long-distance travel (>8 hours): hydration, walking, avoidance of constrictive clothing and frequent calf exercises, compression stockings below knee
  • Patients with factor V Leiden; prothrombin G20210A with no previous thrombosis do not need prophylaxis.

COMMONLY ASSOCIATED CONDITIONS

COVID-19 infection, cancer, sepsis, illnesses leading to hospitalizations, surgery

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