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Pulmonary Thromboembolism (PE)

Etiology

  • Most common origins of pulmonary emboli are systemic veins
    • Pelvic and abdominal veins
    • Femoral veins
    • Axillary veins
  • Clots in veins form due to combination of
    • Sluggish blood flow
    • Local injury/compression of vein
    • Hypercoagulable state
  • Emboli can also occur from a tumour, fat (long bone fracture), amniotic fluid, foreign body

Risk factors

  • Oestrogen therapy + hormonal replacement therapy
  • Pelvis surgery or fracture
  • Malignancy
  • Myeloproliferative disorders
  • MI/stroke
  • Age
  • BMI >30
  • Varicose veins
  • Immobility
  • Pregnancy

Pathophysiology

  • Following PE, lung tissue is ventilated but not perfused (V/Q mismatch)
    • Produces an intrapulmonary dead space
    • Results in impaired gas exchange
  • After few hours, the non-perfused lung no longer produces surfactant
    • Alveolar collapse → exacerbates hypoxemia
  • Main haemodynamic consequence of PE
    • ↓in cross-sectional area of pulmonary arterial bed → ↑pulmonary arterial pressure + ↑RV afterload → ↓CO
    • RV ischemia – shown by rise in troponin + creatinine kinase
  • Distal embolisation – leads to alveolar haemorrhage, haemoptysis, pleuritic effusion

Clinical Features

  • Sudden onset unexplained dyspnoea
  • Pleuritic chest pain, haemoptysis – when infarction has occurred
  • Tachypnea, fever
  • Pleural rub, coarse crackles
  • Hypotension with tachycardia – BAD prognosis

Diagnosis

  • Clinical status at presentation is divided into ‘high risk’ and ‘not high risk’ – based on presence of shock or hypotension
    • If pts are ‘not high risk’ then probability of PE is determined using Wells rule (see table)
  • CXR – atelectasis; wedge-shaped pulmonary infarct
  • ECG – sinus TC; RA dilation; RAD; RBBB
  • ABGs – can be normal or show hypoxaemia
  • ↑Troponins
  • D-dimer – negative test EXCLUDES PE
  • Radionuclide V/Q scanning   – with 99mTc scintigraphy
    • Shows underperfused areas with normal ventilation
  • USS of veins to demonstrate clots
  • CT angiogram
  • Echo – to show RV dysfunction
  • Use Geneva score if Hemodynamically stable

Treatment

Acute management

  • High flow oxygen
  • Anticoagulant – LMWH or fondaparinux
    • LMWH (5 days) > rivaoxaban/dabigatran > warfarin
  • IV fluids + Inotropic agents – to improve pumping of right heart
  • Thrombolysis – to improve pulmonary perfusion
    • Indicated in every pt presenting with acute massive PE and cardiogenic shock
    • Streptokinase
  • Surgical embolectomy
  • LMWH (5 days) > rivaoxaban/dabigatran > warfarin

Prevention of further emboli

  • Prophylactic anticoagulation
    • Warfarin (Vit K antagonist) – for 3-6 months, INR 2-3
    • Dabigatran (direct thrombin inhibitor); rivaroxaban + apixaban (Xa inhibitor) – safer than warfarin
    • LMWH heparin – for pts with cancer/pregnant
  • Vena cava filter in femoral vein

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