Level 2 of 6Must-remember

Pulmonary embolism: recognition, risk stratification and anticoagulation

Assess, manage and stay safe — enough on its own

1 / 10

The card — assess, manage, caution

Assessment— look, ask, measure

Think of it first: pulmonary embolism is the great masquerader, the commonest symptom is nothing more distinctive than unexplained breathlessness, and the diagnosis is made by thinking of it rather than by finding a sign — in every breathless, pleuritic, syncopal or unexplainedly hypoxaemic patient ask (1) is the presentation consistent with PE, (2) are there risk factors, and (3) does an alternative diagnosis explain the whole presentation.
History to ask for: surgery within the previous 4 weeks (especially over 30 minutes' duration, abdominal, pelvic or major lower-limb orthopaedic), immobilisation for more than 3 days, long-distance travel over 4 hours, plaster cast, pregnancy or the puerperium (first 6–12 weeks), combined oral contraceptive or hormone replacement therapy, previous DVT or PE, active malignancy, central venous catheter or PICC line, paralysis, and family history of unprovoked VTE in the young.
Absence of a risk factor never excludes it: a recognised risk factor is present in 80–90% of patients with venous thromboembolism, yet in up to 50% of cases no cause can be established.
Symptoms: dyspnoea, usually of sudden onset; pleuritic chest pain; retrosternal, sometimes crushing pain indistinguishable from infarction in large central emboli; haemoptysis; apprehension or a sense of impending doom; syncope or presyncope; and cough.
Signs: tachypnoea is the most consistent, with tachycardia, low-grade fever, a pleural rub, a raised JVP, a loud pulmonary second sound, a right ventricular heave or gallop, cyanosis, and hypotension in high-risk disease; pulsus paradoxus (a fall in systolic pressure greater than 10 mmHg on inspiration) occurs in massive PE as well as in tamponade and tension pneumothorax.
Examine the legs in every case: measure calf circumferences at a fixed point, conventionally 10 cm below the tibial tuberosity, and record them as numbers — but remember many patients with PE have no leg signs at all because the thrombus has already embolised.
The decision that splits the pathway is haemodynamic instability: systolic blood pressure below 90 mmHg, or a fall in systolic pressure of more than 40 mmHg sustained for more than 15 minutes, not explained by new arrhythmia, hypovolaemia or sepsis.
Other danger signs: syncope, particularly recurrent syncope; cardiac arrest or a peri-arrest state with pulseless electrical activity; metabolic acidosis with a rising lactate (the fingerprint of acute massive PE with circulatory collapse); respiratory rate above 30 breaths per minute; oxygen saturation below 90%; altered mental state; oliguria; cold mottled peripheries; and a raised JVP with clear lung fields in a hypotensive, breathless patient.Not available at your setup — Arterial blood gas. Syncope, respiratory rate, mental state, urine output and cold peripheries are clinical signs — assess them even where oximetry and lactate testing are unavailable.
Score the clinical probability with the two-level Wells score: clinical signs and symptoms of DVT 3.0; an alternative diagnosis less likely than PE 3.0; heart rate above 100 beats/min 1.5; immobilisation more than 3 days or surgery within 4 weeks 1.5; previous DVT or PE 1.5; haemoptysis 1.0; active malignancy 1.0 — a score above 4 means PE likely (image), 4 or less means PE unlikely (D-dimer).
D-dimer is a rule-out test only: sensitivity is at least 95% but specificity is poor; the conventional upper limit is 500 ng/mL, and for patients over 50 with low or intermediate probability use the age-adjusted threshold of age × 10 ng/mL (a 70-year-old's upper limit is 700 ng/mL) — never send one when the Wells score exceeds 4.Not available at your setup — Coagulation (PT/INR).
ECG: often normal and most useful for excluding acute myocardial infarction and pericarditis; commonest findings are sinus tachycardia and T-wave inversion in V1–V4; S1Q3T3 is relatively specific but insensitive; new right bundle branch block occurs with large emboli; a normal ECG never excludes PE.
Chest X-ray and blood gas rarely help and often mislead: normal appearances in an acutely breathless, hypoxaemic patient should raise, not lower, suspicion; the gas typically shows a reduced PaO₂ with a normal or low PaCO₂ and a widened alveolar–arterial gradient but may be entirely normal, and a normal SpO₂ does not exclude PE.Not available at your setup — Arterial blood gas.
Classify by haemodynamic consequence: high-risk (massive) PE, 5–10% of cases, has systemic hypotension; intermediate-risk (submassive), 20–25%, has right ventricular dysfunction and/or raised biomarkers despite a normal blood pressure; low-risk, 65–75%, has normal blood pressure, right ventricle and biomarkers.
Mimics to consider: acute coronary syndrome, pericardial tamponade, aortic dissection, tension pneumothorax, pneumonia, acute heart failure, exacerbation of COPD or asthma, musculoskeletal chest pain, sepsis, and vasovagal syncope (a diagnosis of exclusion only).
The occult PE: where PE occurs alongside overt heart failure or pneumonia, clinical improvement fails to occur despite correct treatment of the concomitant illness — the failure of an expected response is itself the clue.
Age and pregnancy change the picture: the elderly present with syncope, falls, confusion or unexplained deterioration rather than pleuritic pain and their D-dimer is almost always raised by age alone; in pregnancy breathlessness, tachycardia and leg swelling are physiological, so the threshold for objective testing must be low; in children tachycardia and tachypnoea come first and are sustained while hypotension is a late, pre-terminal sign.

Management— do this, in order

Oxygen first: give enough to reach target saturations of 94–98%, or 88–92% in those at risk of hypercapnic respiratory failure; in the shocked patient begin high and titrate down rather than starting low and climbing.
Access, monitoring and baseline bloods: full blood count; urea, creatinine and electrolytes (they govern both contrast safety and anticoagulant dosing); prothrombin time/INR and APTT before anticoagulation; liver function; group and save; and body weight measured, never estimated.Not available at your setup — Serum electrolytes, Renal function (creatinine/urea), Coagulation (PT/INR), Liver function tests.
Anticoagulate before the scan when PE is likely — anticoagulation is the treatment for PE and mortality falls rapidly once it is commenced; screen first for active bleeding, recent gastrointestinal haemorrhage or peptic ulcer, recent stroke (especially haemorrhagic), recent major, neurological or ocular surgery, head injury, intracranial lesion, uncontrolled severe hypertension, pregnancy, platelet count, INR, APTT, renal function, weight, existing anticoagulant or antiplatelet therapy and known bleeding disorder.Doctor / Nurse
First-line parenteral agent — enoxaparin 1 mg/kg subcutaneously every 12 hours by actual body weight, or 1.5 mg/kg subcutaneously once daily; twice-daily dosing is preferred in the sicker patient and in obesity, and in creatinine clearance below 30 mL/min the dose is 1 mg/kg once daily.Doctor / Nurse
Alternatives if enoxaparin is unavailable: dalteparin 200 units/kg subcutaneously once daily (maximum 18 000 units), which may be split as 100 units/kg 12-hourly where bleeding risk is higher; tinzaparin 175 units/kg subcutaneously once daily; or fondaparinux subcutaneously once daily at 5 mg if under 50 kg, 7.5 mg if 50–100 kg and 10 mg if over 100 kg.Doctor / Nurse
Use unfractionated heparin instead when the patient is haemodynamically unstable (subcutaneous absorption is unreliable in shock), when thrombolysis is being considered, in creatinine clearance below 30 mL/min, at extremes of body weight, or where reversibility is wanted: 80 units/kg intravenous bolus then an infusion at 18 units/kg/hour titrated to an APTT ratio of 1.5–2.5 times control, first APTT at 6 hours, 6 hours after every rate change, then at least daily.Doctor / NurseNot available at your setup — Infusion pump, Coagulation (PT/INR).
Paediatric anticoagulation: enoxaparin 1.5 mg/kg subcutaneously every 12 hours in infants under 2 months and 1 mg/kg subcutaneously every 12 hours in children 2 months and over; unfractionated heparin 75 units/kg intravenous bolus over 10 minutes then 28 units/kg/hour in infants under 1 year and 20 units/kg/hour in children 1 year and over, titrated to an APTT ratio of 1.5–2.5 with the first APTT at 4–6 hours.Doctor / NurseNot available at your setup — Coagulation (PT/INR).
Fluids in small measured boluses only: the failing right ventricle is already distended, so give a deliberate 250–500 mL bolus of 0.9% sodium chloride over 15 minutes (children 10 mL/kg) and reassess after each — if the pressure does not improve or the JVP rises, stop and move to a vasopressor.Doctor / Nurse
Noradrenaline is the vasopressor of choice in obstructive shock: start at 0.05 microgram/kg/minute by infusion pump, titrated against a mean arterial pressure of at least 65 mmHg; dobutamine 2.5–5 micrograms/kg/minute may be added where cardiac output is low but blood pressure is preserved.Doctor / NurseNot available at your setup — Infusion pump.
Analgesia with care: morphine 2 mg intravenously repeated in 2 mg increments to effect with an antiemetic, using 1 mg increments or withholding altogether where blood pressure is marginal; avoid non-steroidal anti-inflammatory drugs in a patient about to be anticoagulated.Doctor / Nurse
Thrombolyse acute massive PE with haemodynamic instability: alteplase 100 mg intravenously over 2 hours, commonly given as 10 mg over 1–2 minutes followed by 90 mg over 2 hours; in cardiac arrest or peri-arrest use the accelerated regimen of 0.6 mg/kg over 15 minutes to a maximum of 50 mg, and where thrombolysis is given during arrest continue cardiopulmonary resuscitation for at least 60–90 minutes before abandonment.DoctorNot available at your setup — Infusion pump.
Around thrombolysis: withhold the unfractionated heparin infusion during alteplase and restart it, without a bolus, once the APTT falls below twice control; paediatric thrombolysis is weight-based and should be directed by a paediatric haematologist.DoctorNot available at your setup — Coagulation (PT/INR).
Continuation — choose and record one of three strategies: (1) parenteral drug overlapped with warfarin 5 mg once daily titrated to INR 2.0–3.0 (target 2.5), continuing the parenteral agent a minimum of 5 days and until two sequential INR values at least a day apart are in range; (2) LMWH for 5 days then a straight switch to dabigatran 150 mg orally twice daily or edoxaban 60 mg orally once daily (30 mg once daily if creatinine clearance 15–50 mL/min, weight 60 kg or less, or with certain P-glycoprotein inhibitors); (3) oral monotherapy from the outset with rivaroxaban 15 mg orally twice daily for 21 days then 20 mg once daily (taken with food), or apixaban 10 mg orally twice daily for 7 days then 5 mg twice daily.Doctor
Continue anticoagulation for a minimum of 3 months in every patient with proximal DVT or PE; the acute phase lasts 5–10 days, the maintenance phase a minimum of 3 months, and the long-term phase beyond that.
Where CT is unavailable and the patient is shocked: bedside echocardiography looking for right ventricular dysfunction or overload becomes the decision-making test — RV dilatation in a shocked, hypoxaemic patient with clear lungs and a compatible history is sufficient grounds to treat for PE; where neither test is achievable in a dying patient, make the diagnosis clinically and document the reasoning, because absence of imaging is not a reason to withhold treatment.Not available at your setup — CT scan, Ultrasound. Where neither CT nor echocardiography is achievable in a dying patient, make the diagnosis clinically and document the reasoning.
If the patient bleeds: stop the drug, secure access, resuscitate, group and cross-match, apply direct pressure, consider tranexamic acid where the source is amenable, and reverse — protamine sulphate 1 mg per 100 units of heparin given in the preceding hour to a maximum of 50 mg by slow intravenous injection for unfractionated heparin (partial reversal only for LMWH); vitamin K 5–10 mg intravenously plus four-factor prothrombin complex concentrate (typically 25–50 units/kg) or fresh frozen plasma for warfarin; idarucizumab 5 g intravenously over 5 minutes for dabigatran; andexanet alfa or four-factor prothrombin complex concentrate for apixaban, edoxaban and rivaroxaban.Doctor / NurseNot available at your setup — Blood & blood products.
Airway support is uniquely hazardous here: induction agents drop systemic pressure and positive-pressure ventilation raises intrathoracic pressure and reduces venous return, either of which can convert a shocked patient with massive PE into a cardiac arrest within a minute — if intubation is unavoidable, an experienced operator should do it with vasopressor support already running, using low tidal volumes and the lowest airway pressures that ventilate.DoctorNot available at your setup — Endotracheal intubation kit, Mechanical ventilator.

Caution— what harms

Never let a test delay the first dose of anticoagulant in a patient in whom PE is likely, and where a quantitative D-dimer cannot be obtained within about four hours, or the scan will be delayed, anticoagulate in the interim rather than wait.
Never send a D-dimer when the Wells score exceeds 4 — a negative result in a high-probability patient is a trap; and remember the age-adjusted threshold applies to PE only, not to suspected acute DVT.
Do not over-fill the right ventricle: over-filling pushes the septum further into the left ventricle, reduces LV filling and lowers cardiac output — fluid is given in 250–500 mL boluses over 15 minutes with reassessment after each, not as a fixed litre.
A normal chest X-ray, a normal ECG, a normal oxygen saturation and a normal blood gas each fail to exclude PE — a normal film in an acutely breathless, hypoxaemic patient should raise suspicion.
A raised troponin here means right ventricular microinfarction, not a coronary event — it must not trigger reflexive dual antiplatelet loading in a patient about to be anticoagulated.
Thrombolysis carries a 2% risk of intracranial haemorrhage and a higher risk of major bleeding than anticoagulation, so screen carefully for haemorrhage risk; its role in intermediate-risk PE remains contested and is not routine.
Never stop the heparin on the day warfarin is started: warfarin needs at least 5 days to become effective, so continue the parenteral drug for a minimum of 5 days and until the INR is 2.0 or above on 2 consecutive days.
Dabigatran and edoxaban must be preceded by 5–10 days of parenteral anticoagulation — given as the first drug they leave the patient inadequately treated.
The higher initial DOAC dose is not optional: a patient started on rivaroxaban 20 mg once daily from day 1, instead of 15 mg twice daily for 21 days, is under-treated; apixaban must begin at 10 mg twice daily for 7 days.
Weight must be measured, not guessed — a guessed weight is the commonest cause of low-molecular-weight heparin under- or over-dosing.
Warfarin is teratogenic and DOACs cross the placenta: LMWH is the treatment of choice throughout pregnancy, and a woman who conceives on warfarin should be switched by the 6th week (embryopathy occurs between the 6th and 12th weeks).
Anticoagulants prevent thrombus extension and recurrence but do not dissolve clot — the patient may feel no better in the first hour, and this is not a reason to escalate towards thrombolysis.
Do not reach for an inferior vena cava filter: filters do not reduce the risk of recurrent PE compared with anticoagulation alone, are independently associated with increased DVT, and can migrate or embolise; retrievable devices are preferred and should be removed as soon as anticoagulation is safely established.
Remember the emboli anticoagulation does not treat: septic emboli from tricuspid or pulmonary valve endocarditis, tumour emboli (classically choriocarcinoma), fat after long-bone or pelvic fracture, air, amniotic fluid at delivery, and cement or bony fragments after joint replacement.

Refer / escalate

Escalate or transfer immediately if there is haemodynamic instability (systolic below 90 mmHg or a sustained fall of more than 40 mmHg for more than 15 minutes), syncope, cardiac arrest or peri-arrest pulseless electrical activity, metabolic acidosis with rising lactate, oxygen saturation below 90% or respiratory rate above 30/min, right ventricular dysfunction with a raised troponin, a high PESI class, active bleeding on treatment, or where thrombolysis, catheter-directed therapy, embolectomy or ECMO is being considered.

The card — assess, manage, caution

Pulmonary embolism: recognition, risk stratification and anticoagulation — Level 1: CorePrevious Pulmonary embolism: recognition, risk stratification and anticoagulation — Level 3: Core practiceNext

Read the full lesson free

Create a free account to unlock every page, the level exams, and progress tracking.