Pulmonary Embolism

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Basics

Pulmonary embolism (PE) is an acute cardiovascular disorder that requires emergent medical attention due to its high early mortality rates. PE causes pulmonary vascular bed obstruction, which results in acute right ventricular failure, a life-threatening condition.

Description

  • PE is the most serious presentation of venous thromboembolism (VTE).
  • Classified based on severity:
    • Low-risk PE: acute and absence of clinical markers of adverse prognosis
    • 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

Case fatality rates vary widely (1–60%); case fatality rate is approximately 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 (including postpartum)
Prevalence
  • Epidemiology is difficult to determine outside of the hospital setting because some patients with PE may remain asymptomatic, the first presentation of PE can be sudden death or diagnosis of PE is incidental.
  • Within hospitalized patients:
    • 17.3% prevalence of PE in hospitalized adults who were admitted for first episode of syncope (between 2012–2014)
    • 2.5–23 per 10,000 patient prevalence of PE in Asian countries (China, India, Japan, Korea, Singapore) (1)

Etiology and Pathophysiology

  • Venous stasis, endothelial damage, and changes in coagulation properties trigger 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.

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

Risk Factors

  • Older age, obesity, prolonged immobilization, surgery, major trauma, joint replacement, spinal cord injury, cancer, hormonal replacement therapy, pregnancy/puerperium, previous thrombosis, antiphospholipid syndrome, genetics
  • Oral contraceptive most frequent risk factor in women.

General Prevention

  • Low VTE risk: early ambulation after surgery, compression stockings, and intermittent pneumatic compression
  • Hip or knee arthroplasty (high VTE risk): 10 or more 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.

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Basics

Pulmonary embolism (PE) is an acute cardiovascular disorder that requires emergent medical attention due to its high early mortality rates. PE causes pulmonary vascular bed obstruction, which results in acute right ventricular failure, a life-threatening condition.

Description

  • PE is the most serious presentation of venous thromboembolism (VTE).
  • Classified based on severity:
    • Low-risk PE: acute and absence of clinical markers of adverse prognosis
    • 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

Case fatality rates vary widely (1–60%); case fatality rate is approximately 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 (including postpartum)
Prevalence
  • Epidemiology is difficult to determine outside of the hospital setting because some patients with PE may remain asymptomatic, the first presentation of PE can be sudden death or diagnosis of PE is incidental.
  • Within hospitalized patients:
    • 17.3% prevalence of PE in hospitalized adults who were admitted for first episode of syncope (between 2012–2014)
    • 2.5–23 per 10,000 patient prevalence of PE in Asian countries (China, India, Japan, Korea, Singapore) (1)

Etiology and Pathophysiology

  • Venous stasis, endothelial damage, and changes in coagulation properties trigger 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.

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

Risk Factors

  • Older age, obesity, prolonged immobilization, surgery, major trauma, joint replacement, spinal cord injury, cancer, hormonal replacement therapy, pregnancy/puerperium, previous thrombosis, antiphospholipid syndrome, genetics
  • Oral contraceptive most frequent risk factor in women.

General Prevention

  • Low VTE risk: early ambulation after surgery, compression stockings, and intermittent pneumatic compression
  • Hip or knee arthroplasty (high VTE risk): 10 or more 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.

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