FRCA Notes

Pulmonary Embolism

The curriculum asks us to understand 'anticoagulant and thrombolytic prophylaxis and therapy, including management of pulmonary embolus', 'disorders of the pulmonary circulation - venous' and finally ' the causes, detection and management of pulmonary embolus'.

Resources

  • Pulmonary embolism is part of the spectrum of venous thromboembolic diseases
    • 30% of those with proven PE have co-existing DVT
    • 50% of those with DVT had (often silent) PE

  • The incidence is 60-70/10,000
  • There is an up to 30% recurrence rate
  • Treated 30-day mortality is up to 5 - 10%
  • Genetic predisposition, typically some coagulopathy such as:
    • Factor V Leiden
    • Protein C deficiency
    • Antithrombin III deficiency
    • Antiphospholipid syndrome

  • Hormone status e.g. use of oral contraceptive pills, pregnancy

  • Virchow's triad
    1. Immobility e.g. spinal injury, prolonged surgery, trauma e.g. #NOF, other lower limb fracture
    2. Inflammatory state e.g. surgery, malignancy, burns, trauma
    3. Impaired blood flow e.g. smoking, obesity, heart failure

Dead space

  • The lung tissue distal to the embolus is ventilated but not perfused → intra-pulmonary dead space
  • This should cause hypercarbia, but the presence of tachypnoea means PCO2 is rarely significantly raised

Shunt

  • The area of the lung which is no longer perfused is at risk of pulmonary infarct, though often remains oxygenated due to oxygen supply via the bronchial circulation
    • Arterial blood from the bronchial artery supplies the lung tissue
    • This drains into the bronchial veins and then into the pulmonary veins
    • Flow through this pathway increases in PE → intra-pulmonary physiological shunt and hypoxia
      • In patients with a PFO there may be paradoxical RA - to - LA shunt, which exacerbates the existing hypoxia
    • This is exacerbated by alveolar collapse

Pulmonary hypertension and ventricular failure

  • The presence of emboli reduces the cross-sectional area of the pulmonary arterial bed
    • There is release of vasoconstricting inflammatory mediators e.g. TXA2, serotonin
    • Furthermore, the hypoxia of the affected lung units induces hypoxic pulmonary vasoconstriction
    • This raises pulmonary artery pressure i.e. causes a degree of pulmonary hypertension
    • There is thus reduced RV cardiac output via the Frank-Starling mechanism

  • The impaired RV cardiac output leads to RV dilatation
    • The RV becomes 'D' shaped rather than crescent shaped
    • It leads to bulging of the interventricular septum, compromising LV function (reduced volume, poorer compliance, reduced preload) and causing reduced CO

  • The AHA Guidelines stratify PE by 'massiveness'
Category Frequency Haemodynamic state RV function Management
Massive 5% Unstable ± cardiac arrest Dysfunction Thrombolysis
Sub-massive 25% Stable Dysfunction Anticoagulation ± thrombolysis if deteriorating
Non-massive 70% Stable Normal function Anticoagulation

  • Pulmonary embolism is sometimes referred to as 'the great pretender', as its array of non-specific respiratory, cardiac and constitutional signs mimic other major pathology

Symptoms

  • Asymptomatic, bar the presence of predisposing factors

  • Dyspnoea
  • Chest pain - typically due to distal pleural irritation from pulmonary infarction
  • (Pre-)syncope
  • Haemoptysis

Signs

  • Haemodynamic instability
  • Tachypnoea
  • Hypoxaemia
  • Slight pyrexia

Clinical scoring tools

  • The PERC rule is a useful exclusion tool in patients with a low pre-test probability for PE
  • The modified Wells' Criteria can be used to stratify patients to further investigations (i.e. D-dimer or CTPA)

Bloods

  • D-dimer
    • High negative predictive value therefore used to exclude PE
    • Not validated in pregnancy
    • Raised by a number of other pathological states

  • Biomarkers of right heart strain may be used to risk stratify patients:
    • Troponin: poor specificity but if raised is a poor prognostic marker
    • BNP

Simple tests

  • ECG
    • The most common feature in PE is sinus tachycardia (40%)
    • There may be signs of right heart strain:
      • AF
      • RVH
      • RAD
      • RBBB
      • T-wave inversion in V1-4
      • 'S1Q3T3' is present in <20%

  • CXR
    • Not a diagnostic tool for PE but may have been performed for investigation of the dyspnoeic patient
    • Signs in PE include:
      • Hypovascularity (Westermark's sign)
      • Peripheral wedge-shaped infarct (Hampton's hump)

  • Doppler ultrasound of the leg veins
    • High sensitivity and specificity for detecting DVT in patients with leg symptoms

  • Transthoracic echocardiography
    • Is the best imaging option for massive PE as haemodynamic instability often precludes CTPA
    • Should be performed for patients with non-massive PE with evidence of right heart strain on ECG
    • Provides detailed information about RA pressures, RV dysfunction and RA enlargement
    • A normal TTE does not exclude PE

More complex imaging

  • V/Q scan (lung scintigraphy)
    • Often inconclusive
    • Largely superseded by CTPA

  • CTPA
    • Contrast-enhanced scan performed rapidly to:
      • Avoid movement artifact due to respiratory and cardiac pulsation
      • Reduce radiation exposure e.g. in pregnancy
    • Filling defects in the pulmonary vasculature are diagnostic
    • Sensitivity 83%, specificity 96% (NEJM, 2006)

  • MR pulmonary angiography
    • Benefits from lack of ionising radiation and reduce nephrotoxicity from Gadolinium (vs. iodinated) contrast
    • Suffers from less diagnostic accuracy than CTPA and less widely available

  • Invasive pulmonary angiography is reserved for patients with pulmonary hypertension awaiting pulmonary endarterectomy

Thrombolysis

  • Recombinant t-PA e.g. alteplase 0.9mg/kg (max 90mg) with 10% over 2 mins then 90% over subsequent 1hr
  • Numerous contra-indications:
Absolute Relative
Previous intra-cranial bleed at any time Concurrent anticoagulant use
Stroke within last 6 months Invasive/surgical procedure within 2 weeks
Closed head or facial trauma within 3 months Prolonged CPR
Suspected aortic dissection Pregnancy
HTN >180/100mmHg Controlled but severe hypertension
Known cerebrovascular lesion inc. AVM, aneurysm or tumour Active peptic ulcer
Thrombocytopaenia or known coagulopathy Diabetic or haemorrhagic retinopathy
Pericardial effusion
Septic embolus

Anticoagulation

  • Can choose from either:
    1. DOAC e.g. rivaroxaban, apixaban
    2. Treatment dose LMWH for 5 days, then dabigatran/edoxaban/warfarin

  • Initial treatment duration is 3-6 months, after which one can consider:
    • Stopping if provoked PE
    • Continuing if unprovoked PE

  • Bleeding complications are often minor and the risk of major bleeding is often outweighed by the benefits of anticoagulant therapy, but can use scoring systems such as HAS-BLED to inform decision making

IVC filters

  • In theory prevent lower limb emboli reaching pulmonary circulation
  • May only provide benefit in the initial post-insertion period; complications such as post-thrombotic syndrome and recurrent VTE are more frequent

Surgical

  • Catheter - directed clot retrieval
  • Surgical embolectomy