Pulmonary Embolism Study Notes

PULMONARY EMBOLISM

BY DR ODEYEMI A.O.
DEPARTMENT OF MEDICINE, COLLEGE OF HEALTH SCIENCES, OSUN STATE UNIVERSITY
OSUN
3080 LIVING SPRING OF KNOWLEDGE AND CULTURE

OUTLINE

  • Introduction
  • Thrombotic versus non-thrombotic
  • Epidemiology
  • Pathogenesis
  • Aetiology / risk factors
  • Classification of PE
  • Clinical features
  • Investigations
  • Treatment

INTRODUCTION

  • Pulmonary embolism (PE) occurs when a blood clot (thrombus) becomes lodged in a pulmonary artery in the lung, blocking blood flow to the lung.

THROMBOTIC VS NON-THROMBOTIC

  • PE may also be referred to as pulmonary thromboembolism, denoting its thrombotic origin.
  • Non-thrombotic causes of PE include:
    • Fat
    • Amniotic fluid
    • Neoplastic cells
    • Parasites
    • Particulate matter, e.g., cannula tips, cotton.

THROMBOTIC VS NON-THROMBOTIC (CONT'D)

  • Non-thrombotic emboli are typically referred to by their specific aetiologies (e.g., fat embolism, amniotic fluid embolism) rather than being classified generally as PE.

EPIDEMIOLOGY

  • PE is found in 60-80% of patients with deep venous thrombosis (DVT); more than 50% of these patients remain asymptomatic.
  • It is the third most common cause of death in hospitalized patients in the USA, with an estimated 650,000 cases occurring annually.
  • Autopsy studies reveal that about 60% of patients who die in the hospital had PE, with up to 70% of these cases remaining undiagnosed prior to death.

PATHOGENESIS

Virchow’s Triad

  • Endothelial injury

  • Stasis or turbulence of blood flow

  • Hypercoagulable states

  • Thrombosis originates as a platelet nidus on valves in veins, typically in the lower extremities.

  • Further growth involves the accumulation of platelets and fibrin, leading to the formation of a red fibrin thrombus.

PATHOGENESIS (CONT'D)

  • A thrombus may break off and cause PE or it may occlude the vein entirely, resulting in venous thrombosis.
  • The endogenous thrombolytic system partially dissolves the thrombus, which may then become organized and incorporated into the venous wall.

PATHOGENESIS (CONT'D)

  • PE typically arises from thrombi originating in the deep venous system of the lower limbs but may also originate in pelvic, renal, upper extremity veins, or right heart chambers.
  • Large thrombi may lodge at the bifurcation of the main pulmonary artery or its lobar branches, causing hemodynamic compromise.
  • Smaller thrombi usually travel distally, occluding smaller vessels in the lung periphery and are more likely to produce pleuritic chest pain through an inflammatory response adjacent to the parietal pleura.

Additional Information

  • Majority of pulmonary emboli are multiple, with lower lobes more frequently involved than upper lobes.

PATHOGENESIS (CONT'D)

  • Pulmonary artery obstruction and neurohumoral mediators result in increased pulmonary artery pressure and vascular resistance.
  • Increased right ventricular (RV) wall tension leads to RV dilation and dysfunction, with the release of brain natriuretic peptide due to abnormal RV stretch.
  • The interventricular septum bulges into the left ventricle (LV), leading to LV diastolic dysfunction, reducing LV distensibility and impairing LV filling.

Consequences of RV Dysfunction

  • Increased RV wall tension compresses the right coronary artery, reducing myocardial oxygen supply and possibly precipitating ischemia and microinfarction in the RV, indicated by troponin release.
  • Underfilling of the LV may decrease cardiac output and systemic arterial pressure, potentially leading to circulatory collapse and death.

AETIOLOGY / RISK FACTORS

  • Risk factors can be classified using Virchow’s triad:

Stasis

  • Causes include:
    • Paralysed limb
    • Congestive heart failure (CHF)
    • Being bedbound or ‘bedfast’
    • Pregnant uterus
    • Long trips or flights

Primary Hypercoagulable States

  • Conditions include:
    • Hematopathies
    • Deficiencies in antithrombin III, protein C & protein S
    • Antiphospholipid antibodies
    • Factor V Leiden mutation
    • Prothrombin 20210A mutation
    • Hyperhomocysteinemia

Secondary Hypercoagulable States

  • Contributing factors include:
    • Smoking
    • Pregnancy
    • Use of contraceptives
    • Malignancy
    • Nephrotic syndrome

Endothelial Injury

  • Steps leading to endothelial injury:
    • Surgical procedures
    • Trauma

CLASSIFICATION

Massive PE

  • Accounts for 5-10% of PE cases, involving extensive thrombosis affecting at least 50% of the pulmonary vasculature.
  • Symptoms include dyspnea, syncope, hypotension, and cyanosis.
  • Patients may present in cardiogenic shock, potentially leading to multisystem organ failure.

Submassive PE

  • Constitutes 20-25% of patients.
  • Characterized by RV dysfunction but with normal systemic arterial pressure.
  • The presence of right heart failure and elevated cardiac biomarkers indicates a high risk of clinical deterioration.

Low-Risk PE

  • Represents about 65-75% of PE cases.
  • These patients generally have an excellent prognosis.

DIAGNOSIS

  • PE is often termed “the Great Masquerader” due to the nonspecific nature of symptoms and signs.
  • Most common symptom: unexplained breathlessness.
  • Other symptoms include:
    • Unexplained syncope

CLINICAL FEATURES OF DVT

  • Majority are silent, necessitating a highly suspicious clinical approach.
  • May often be asymptomatic.
  • Vague non-specific features such as:
    • Localized pain
    • Swelling and tenderness in the affected limb
    • Marked physical findings such as phlegmasia cerulea dolens indicative of extensive underlying ilio-femoral process.

CLINICAL FEATURES OF PE

  • Multi-system manifestations affecting:
    • Respiratory system
    • Cardiovascular system
    • Lower limbs

Characteristics Influencing PE Presentation

  • The type (acute vs chronic)
  • Characteristics of pulmonary vessels:
    • Size
    • Number
    • Location

CLINICAL FEATURES OF PE: RESPIRATORY

  • Symptoms include:
    • Breathlessness
    • Chest pain
    • Cough
    • Hemoptysis
    • Tachypnea
    • Cyanosis
    • Pleural rub
    • Rhonchi
    • Crackles

CLINICAL FEATURES OF PE: CARDIOVASCULAR

  • Symptoms include:
    • Tachycardia
    • Raised jugular venous pressure (JVP)
    • Prominent “a” wave
    • Sternal heave
    • Accentuated S2 (P2) and splitting
    • Additional sounds: s3, s4
    • Tricuspid regurgitation
    • Evidence of shock

CLINICAL FEATURES: LOWER LIMBS (Evidence of DVT)

  • Indicators include:
    • Calf discomfort
    • Oedema
    • Superficial vein distension
    • Palpable cords in superficial thrombophlebitis
    • Phlegmasia alba dolens (venous occlusion with associated arterial compromise)
    • Homans’ sign (pain or resistance on passive dorsi-flexion of the ankle)

INVESTIGATIONS

Aims

  • Detection of pulmonary embolus (PE)
  • Assess effects of PE
  • Detect deep vein thrombosis (DVT)
  • General investigations for safety
  • Rule out differential diagnoses

INVESTIGATIONS: PE

Arterial Blood Gases

  • Findings:
    • Low PaO2
    • Low PCO2

Blood Tests

  • Indicators may include:
    • Leukocytosis
    • High erythrocyte sedimentation rate (ESR)
    • High lactate dehydrogenase (LDH)
    • Elevated D-dimer levels

INVESTIGATIONS: PE (CONT'D)

  • Quantitative plasma D-dimer ELISA:
    • Elevates in the presence of DVT or PE due to breakdown of fibrin by plasmin.
    • Sensitivity is >80% for DVT (including isolated calf DVT) and >95% for PE.
    • A normal D-dimer is a useful rule out test.
    • However, D-dimer assays lack specificity as levels can be elevated in hospitalized patients.

INVESTIGATIONS: PE (CONT'D)

Causes of Elevated D-dimer include:

  • Myocardial infarction
  • Pneumonia
  • Sepsis
  • Cancer
  • Postoperative state
  • Pregnancy clinical states (second or third trimester)

INVESTIGATIONS: PE (CONT'D)

ECG Findings

  • Indicators might show:
    • Tachycardia
    • S1Q3T3 (large S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III)
    • T wave inversion in right ventricular leads V1-V4
    • New or transient right bundle branch block (RBBB)
    • P-pulmonale (tall peaked P waves)
    • Arrhythmias, e.g., atrial fibrillation.

INVESTIGATIONS: CHEST X-RAY

  • X-ray findings are usually normal or nearly normal, but established abnormalities include:
    • Focal oligemia (Westermark’s sign)
    • Hampton’s hump: a peripheral wedged-shaped density at the pleural base
    • Palla’s sign: enlarged right descending pulmonary artery.

INVESTIGATIONS: CHEST CT SCAN

  • CT of the chest with IV contrast is the principal imaging test for diagnosing PE.

INVESTIGATIONS: VENTILATION / PERFUSION SCAN

  • This serves as a second-line diagnostic test for PE, particularly for patients who cannot tolerate IV contrast.
  • Procedure:
    • Small particulate aggregates of albumin labeled with a gamma-emitting radionuclide are injected intravenously and become trapped in the pulmonary capillary bed.
    • A defect in the perfusion scan indicates decreased or absent blood flow, possibly due to PE.

INVESTIGATIONS: VENTILATION / PERFUSION SCAN (CONT'D)

  • Ventilation scans involve inhalation of a radiolabeled gas (e.g., xenon or krypton).
  • These scans improve specificity by showing non-ventilated lung areas, possibly indicating perfusion defects for reasons other than acute PE (e.g., asthma, COPD).

INVESTIGATIONS OF PE: IMAGING TECHNIQUES

  • Echocardiography:
    • Shows diastolic and systolic bowing of the interventricular septum (IVS) into the left ventricle due to right ventricular volume and pressure overload.
    • Demonstrates right ventricular hypokinesis.
  • Other imaging techniques include:
    • Spiral CT
    • MRI

TREATMENT

Aims

  • Provide supportive care
  • Prevent further thrombosis/embolism
  • Deliver specific treatment
  • Implement prophylaxis

TREATMENT (CONT'D)

Algorithm for PE Management

  • Risk stratification:
    • Normotension:
    • Anticoagulation alone
    • Hypotension:
    • If normal RV: Secondary prevention
    • If RV hypokinesis:
      • Anticoagulation + thrombolysis or IVC filter
      • Embolectomy (catheter/surgical)

ANTICOAGULATION

Strategies include:

  1. Parenteral anticoagulation:
    • Unfractionated heparin (UFH), low-molecular-weight heparin (LMWH), or fondaparinux bridged to warfarin.
  2. Switch parenteral therapy to a novel oral anticoagulant like dabigatran (direct thrombin inhibitor) or edoxaban (anti-Xa agent) after 5 days.
  3. Oral anticoagulation monotherapy:
    • RivaroXaban or apixaBan (both anti-Xa agents).

IVC FILTERS: INDICATIONS

  • Active bleeding that precludes anticoagulation.
  • Recurrent venous thrombosis despite intensive anticoagulation.
  • Prevention of recurrent PE in patients with right heart failure who are not candidates for fibrinolysis.
  • Prophylaxis in cases of extremely high risk.

MANAGEMENT OF MASSIVE PE

  • In patients presenting with massive PE and hypotension, infuse IV fluids (N/S 500 mL).
  • Consider additional IV fluids (extreme caution advised).
  • Dopamine and dobutamine are first-line inotropic agents in treating PE-related shock.

FIBRINOLYSIS

  • Administer recombinant tissue plasminogen activator (tPA) for fibrinolysis.
  • Contraindications include:
    • Intracranial disease
    • Recent surgery
    • Trauma
  • Major side effect: bleeding.
  • Screen patients carefully for contraindications to minimize bleeding risks before fibrinolytic therapy.

THANK YOU

OSUN STATE UNIVERSITY
3080 LIVING SPRING OF KNOWLEDGE AND CULTURE