Pulmonary Embolism
Clinical
- may be asymptomatic
- SOB, cough +/- haemotypsis
- pleuritic chest pain
- associated leg pain/swelling, signs of DVT
- massive PE - central cyanosis, altered/LOC, collapse or shock
- tachypnoea, tachycardia, hypotension
- elevated JVP, parasternal heave, loud P2
- Fever is common in PE and can occur in ≥25% patients
- clinical categorisation to direct Mx:
- massive (high risk)- shock, persistent brady or asystole
- sub-massive (intermediate risk) - evidence of RV dysfunction but no signs of shock
- low risk - no evidence of RV dysfunction or shock
Investigations
- ECG - often normal
- sinus tachycardia
- signs of R heart strain -SI, QIII, TIII (probably <10%), non-specific ST changes or TWI in anterior leads, right axis deviation, S wave (I and aVL) > 1.5mm, Q in III and aVF, P pulmonale & RBBB
- ABG - hypoxia. Repeat after exercising may enhance diagnostic workup. Resp alkalosis. Metabolic acidosis if shock
- CXR - only to rule out other pathology
- CTPA - may not pick up smaller emboli
- PCT may be useful as usually raised in bacterial infections but not PE
Management
- Low molecular weight heparin (LMWH)
- Fondaparinux.
- Unfractionated heparin.
- Oral anticoagulants: Warfarin, apixaban, or rivaroxaban. CUH DOACs for VTE
- LMWH followed by an oral anticoagulant (dabigatran or edoxaban)
- Thrombolysis - only for massive. Debate continues about their place in sub-massive
- plasminogen activators - fibrin specific rt-PA or non selective agents - streptokinase, urokinase
- IVC filters and embolectomy
| Streptokinase | Urokinase | Alteplase | Reteplase | Tenecteplase | |
|---|---|---|---|---|---|
| activate systemic plasminogen, which is not part of the clot matrix hydrolyses fibrin of thromboemboli, causing clot lysis | preferentially activate plasminogen on clot surface. Classified as fibrin specific |
||||
| Generation | 1st | 1st | 2nd | 3rd | 3rd |
| Clot-specific? | No | No | Yes | Yes | Yes |
| Half-life (mins) | 12 | 7–20 | 4–10 | 11–19 | 15–24 |
Risk factors investigation
if no obvious cause of embolic disease is found, hypercoagulation investigation should follow:
- Antithrombin III deficiency
- Protein C or protein S deficiency
- Lupus anticoagulant
- Homocystinuria
- Occult neoplasm
- Connective tissue disorders
Wells criteria
| Wells criteria for PE | |
|---|---|
| clinical signs and symptoms of DVT | 3 |
| alternative diagnosis is less likely than PE | 3 |
| HR >100 | 1.5 |
| immobilisation ≥3 consecutive days or surgery in the previous 4/52 | 1.5 |
| previous objectively diagnosed PE or DVT | 1.5 |
| haemoptysis | 1 |
| malignancy (on Rx, or in last 6/12 or palliative) | 1 |
| 0-1: low risk 2-6: moderate risk >6: high risk |
|
PESI (Pulmonary Embolism Severity Index)score
| Age | Age in years |
|---|---|
| Male sex | 10 |
| Cancer | 30 |
| Heart Failure | 10 |
| Chronic lung disease | 10 |
| Pulse ≥ 110/min | 20 |
| sBP < 100 mm Hg | 30 |
| RR ≥ 30/min | 20 |
| Temperature < 36°C | 20 |
| Altered mental status | 60 |
| PaO2 sat < 90% (+/-O2 Rx) | 20 |
Risk and Mx strategy:
| score | ||
|---|---|---|
| ≤ 65 | Class I, Very Low Risk | discharge on oral anti-coag |
| 66-85 | Class II, Low Risk | discharge on oral anti-coag |
| 86-105 | Class III, Intermediate Risk | potential for decompensation probable admission for Ix and monitoring |
| 106-125 | Class IV, High Risk | admission |
| > 125 | Class V, Very High Risk | admission |