Pulmonary embolism
Pulmonary embolism

Pulmonary embolism

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Virchow’s triad is the aetiological model that describes VTEs.

  1. Endothelial injury
  2. Venous stasis
  3. Hypercoagulability

A pulmonary embolism (PE) is a from of VTE that occurs as a result of thrombus formation within a deep vein of the body (ie. DVT) especially in the lower limbs. The thrombus dislodges and becomes an embolus. This embolus travels to the right side of the heart → pulmonary valve → pulmonary arteries. They obstruct perfusion to the lung tissue and cause strain on the right side of the heart.

It is life-threatening, requiring urgent treatment. If not treated, it can cause right-side heart failure and cardiac arrest.

Pathophysiology

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  • Endothelial injury

Damage to the endothelium of course initiates our coagulation cascade and promotes thrombus formation.

Damage can occur after trauma, surgery, catheterisation.

  • Venous stasis

Poor blood flow and stasis also promotes thrombus formation.

Venous stasis occurs with older age (>40 years), immobility, GA, paralysis, MI, varicose veins, advanced congestive heart failure, advanced COPD.

  • Hypercoagulability

States that increase coagulation include cancer, high-oestrogen (contraceptives, HRT, obesity, pregnancy), IBD, sepsis, thrombophilia (Factor V Leiden and other inherited conditions).

An issue with 1 or more of these 3 factors increases the risk for VTE, most commonly DVT but this then causes PE subsequently.

⚠️ Risk factors

  • Increasing age
  • Immobility
  • Cancer
  • Surgery
  • Pregnancy
  • Oestrogen therapy - oral contraceptive pill, HRT.
  • Previous VTE
  • Inherited thrombophilia - such as Factor V Leiden, prothrombin gene mutation, protein C and S deficiency, antithrombin deficiency, APLAS)

😷 Presentation

⭐️ The most common presentation is shortness of breath.

Other symptoms include:

  1. Tachypnoea
  2. Dyspnoea
  3. Pleuritic chest pain
  4. Tachycardia
  1. Haemoptysis
  2. Fever
  3. Syncope
  4. Haemodynamic instability

Signs of DVT may also be present such as unilateral leg swelling and tenderness.

💡
The “classical” triad for PE is dyspnoea, haemoptysis and pleuritic chest pain. But this only occurs in about 10% of patients. The truth is that PE is tough to diagnose as few patients have this classical presentation due to variability in size of embolus, and location within the pulmonary vessels.
  • Sub-massive PE: there may be signs of right heart strain (such as a raised JVP, parasternal heave, and loud P2)
  • Massive PE: is characterised by hypotension (SBP< 90 mmHg or a drop in SBP of ≥ 40 mmHg for ≥15 minutes) or signs of shock.

🔍 Investigations

🚨
Do not miss!

PE is a do-not-miss diagnosis. One should always suspect PE in a patient with circulatory collapse 1-2 weeks post-surgery.

🦵
Wells score

A Wells score for PE determines the first-line investigation. It calculates the diagnostic possibility of VTE. It needs to be applied AFTER history and physical examination.

Criteria

Features
Points
Clinical signs and symptoms of DVT (leg swelling and pain on palpation)
3
Alternative diagnosis is less likely than PE
3
Tachycardia
1.5
Immobilisation >3 days or surgery within prior 4 weeks
1.5
Previous DVT/PE
1.5
Haemoptysis
1
Malignancy (on treatment or treated in last 6 months)
1

Interpretation

  • 🥇 A score <4 suggests that PE is unlikely → perform D-dimer
    • If D-dimer is positive → perform CTPA
  • 🥇 A score >4 suggests that PE is likely → perform CT pulmonary angiogram (CTPA) and give interim oral anticoagulation in the form of DOACs such as apixaban and rivaroxaban.
    • If CTPA is positive → definitive PE diagnosis established. ✅
    • If CTPA is negative → consider proximal leg vein USS if DVT is suspected.
    • If patient is haemodynamically unstable for CTPA → POCUS echocardiography (point of care US echocardiography).
    • If patient has renal impairment then CTPA is contraindicated as contrast agents are nephrotoxic → V/Q scan. This entails using radioactive isotopes and a camera to compare ventilation with the perfusion of the lungs. The isotopes are inhaled to fill the lungs and a picture is taken to demonstrate ventilation. A contrast with isotopes is then injected and a picture is taken to demonstrate perfusion. The pictures are then compared. A PE causes a perfusion deficit y but not a ventilation deficit.
🔪
Other investigations to consider:
  • FBC - to establish baseline values.
  • Clotting profile - if the patient is at risk of bleeding, then we cannot commence anticoagulation.
  • U&Es - renal function needs to be assessed before CTPA.
  • CXR - to exclude other diagnosis (should be normal in PE). However we may see certain signs, such as:
    • Fleischer sign - enlarged pulmonary artery.
    • Hampton’s hump - peripheral wedge shaped opacity.
    • Westermark’s sign - regional hypovolaemia
      • Fleischer sign
      Fleischer sign
      Hampton’s hump
      Hampton’s hump
      Westermark’s sign
      Westermark’s sign
  • ECG - may be normal. It is not diagnostic of PE but can support diagnosis and rule out other causes.
    • It may show sinus tachycardia and:
      • S1Q3T3
      • Large S wave in lead 1
      • Large Q wave in lead 3
      • Inverted T wave in lead 3
  • ABG - PE patients often have a respiratory alkalosis. This is because they have a high respiratory rate → low CO2 → alkalosis. The other main cause of respIratory alkalosis is hyperventilation syndrome. The difference is that with PE there is low pO2 + alkalosis while in hyperventilation syndrome there is high pO2 + alkalosis.
🚫
Pulmonary embolism rule-out criteria (PERC):

This may be used when there is a low pre-test probability (<15%) and you do not want to perform any investigations but still would like to reassure that is is not PE. All variables must receive a no to be negative. Failing the PERC also does not force the clinician to order tests. Passing the PERC test reduces probability to <2

Criteria
No
Yes
Age >50
0
1
HR >100
0
1
SpO2 <95% on room air
0
1
Unilateral leg swelling
0
1
Haemoptysis
0
1
Recent surgery or trauma
0
1
Prior PE or DVT
0
1
Hormone use
0
1

🧰 Management

🫁
Suspected PE in haemodynamically unstable (SBP <90mmHg) ± hypoxic patient:
  1. Oxygen - high-concentration O2 if SpO2 <90%.
  2. Fluid resuscitation - if SBP <90 and JVP not raised.
  3. DOAC - if diagnosis will be delayed.
    1. Apixaban
    2. Rivaroxaban
📉
Confirmed PE in haemodynamically unstable patient:
  1. Unfractionated heparin (standard heparin)
  2. Thrombolysis (alteplase) - remember, haemodynamic instability (such as shock) is the only indication for thrombolysis in PE. There is a risk of cerebral haemorrhage (2%) when using thrombolytic agents and therefore we should not be frivolous in its use.

Switch to DOAC after thrombolysis.

🚨
Absolute contraindications to thrombolysis:
  • History of spontaneous intracerebral haemorrhage
  • Ischaemic stroke within last 6 months
  • CNS damage, neoplasm or AV malformation
  • Major trauma, surgery, head injury within last 1 month
  • GI bleeding within last 1 month
  • Bleeding disorder
  • Aortic dissection
  • Non-compressible punctures within last 24 hours - such as liver biopsy or lumbar puncture.
⚠️
Relative contraindications to thrombolysis:
  • Chronic oral anticoagulant usage
  • Pregnancy or <1 week postnatally
  • Refractory hypertension (systolic BP >180mmHg and/or diastolic BP >110mmHg).
  • TIA within last 6 months
  • Advanced liver disease
  • Infective endocarditis
  • Active peptic ulcer
  • Prolonged or traumatic CPR
〰️
Confirmed PE in haemodynamically stable patient:
  1. Oral anticoagulation + risk assessment (PESI - discussed below) to determine if patient is safe to be managed as an outpatient.

Choice of anticoagulation:

  • 1st line - DOAC
    • Apixaban or rivaroxaban
  • Active cancer - DOAC
    • Edoxaban this time
  • If DOACs are not appropriate: LMWH (such as enoxaparin) followed by dabigatran/edoxaban/warfarin
  • Pregnant - LMWH
    • Enoxaparin
  • If sever renal impairment - LMWH/UFH followed by warfarin
  • If antiphospholipid syndrome - LMWH followed by warfarin

Patients should stay on coagulants for 3 months after which:

  • VTE was provoked (i.e. surgery) → stop COAG.
  • VTE was unprovoked (no clear factor) continue COAG for 3 months (low risk of bleeding).

Pulmonary embolism severity index (PESI) score:

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0 to 65 Points:
Class I Very low risk
66 to 85 Points:
Class II Low risk
86 to 105 Points:
Class III Intermediate risk
106 to 125 Points:
Class IV High risk
126 to 380 Points:
Class V Very high risk