Pulmonary embolism recognition and risk stratification

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Pulmonary embolism commonly produces sudden breathlessness, pleuritic chest pain, tachycardia, haemoptysis, syncope or unexplained hypoxaemia, but presentations range from incidental clot to obstructive shock. Embolic obstruction and vasoconstriction raise pulmonary vascular resistance. The acutely pressure-loaded right ventricle dilates, increases wall stress and oxygen demand, and may fail; left-ventricular filling then falls, causing hypotension and systemic hypoperfusion. Symptoms and routine observations are therefore interpreted as a pattern, while immediately excluding other lethal causes such as acute coronary syndrome, aortic dissection, tension pneumothorax and sepsis.

Two different questions must remain separate. In non-pregnant adults, diagnostic probability asks how likely PE is before definitive imaging and determines PERC, D-dimer or CTPA use; pregnancy and the puerperium require a separate objective-testing pathway. Prognostic stratification starts once PE is confirmed or strongly suspected and asks how likely early deterioration or death is. Haemodynamic instability defines the emergency group. In stable, non-pregnant adults with PE, clinical scores such as PESI or simplified PESI, right-ventricular findings, biomarkers, oxygen requirement, bleeding risk and comorbidity refine disposition. PESI and simplified PESI were not derived for pregnancy and should not be used there. A low numerical score is necessary but insufficient for discharge: reliable medication access, cognition, social support, direct clinical contact and a follow-up plan are also required.

Key points

Assess haemodynamic stability before calculating any diagnostic or outpatient score: shock or persistent hypotension places the patient in the emergency high-risk branch.
In non-pregnant adults with low overall clinical suspicion and a feasible alternative diagnosis, consider PERC; otherwise use two-level Wells: above 4 needs immediate CTPA, while 4 or less needs D-dimer, with interim therapeutic anticoagulation whenever the indicated test is delayed.
Only physiologically low-risk patients should enter outpatient assessment, using a validated prognostic tool plus bleeding, comorbidity, social and follow-up checks.
In a non-pregnant adult, for Wells more than 4 arrange CTPA immediately where possible; for Wells 4 or less, use D-dimer before imaging.
In a non-pregnant adult, a low clinical impression can support PERC use when alternative diagnoses are feasible, but PERC is not a severity score and NICE notes it is unvalidated in COVID-19.
A positive troponin or right-ventricular dysfunction increases concern in a stable patient, yet neither alone is a NICE indication for routine systemic thrombolysis.
V/Q SPECT or planar scanning is an alternative when iodinated contrast allergy, creatinine clearance below 30 mL/min or irradiation risk makes CTPA unsuitable.
Negative imaging should prompt reconsideration of alternative diagnoses and, when DVT remains suspected, proximal leg-vein ultrasound rather than false reassurance.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Thromboembolic source

Most pulmonary emboli arise from venous thrombus in the lower limbs or pelvis. Stasis, endothelial injury and hypercoagulability interact after surgery, immobility, cancer, pregnancy, oestrogen exposure or previous VTE.

Provoked and unprovoked events

A major transient factor suggests time-limited exposure, whereas active cancer, persistent inflammatory disease or no identifiable trigger changes recurrence assessment and later anticoagulation decisions.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Pulmonary vascular obstruction
Mechanical obstruction plus mediator-driven vasoconstriction abruptly raises pulmonary vascular resistance, increasing right-ventricular afterload and impairing forward flow.
2
Right-ventricular failure
Acute pressure overload dilates the thin-walled right ventricle, increases wall tension and may cause ischaemia, tricuspid regurgitation and interventricular septal shift.
3
Systemic hypoperfusion
Reduced right-sided output lowers left-ventricular preload and cardiac output; hypotension then worsens coronary perfusion, creating a destructive cycle of RV ischaemia and shock.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Compatible symptoms and context

New dyspnoea, pleuritic pain, tachycardia, haemoptysis, syncope or unexplained desaturation gains weight when combined with recent surgery, immobility, active cancer, previous VTE, pregnancy or oestrogen exposure.

Haemodynamic instabilityRed flag

Persistent hypotension, shock, cardiac arrest, cool peripheries, confusion, oliguria or elevated lactate reflects inadequate output from acute right-ventricular pressure overload and mandates emergency escalation.

Right-ventricular stress without shock

Tachycardia, raised jugular venous pressure, right-heart strain on imaging or elevated cardiac biomarkers may identify a stable patient at increased risk who needs observation for decompensation.

Low-risk phenotype

Normal blood pressure, acceptable oxygenation, low validated prognostic score, low bleeding risk and no major comorbidity may support outpatient care only when practical and follow-up criteria are satisfied.

Red flags requiring action

Systolic hypotension, obstructive shock, syncope with ongoing compromise, or cardiac arrest requires an emergency PE pathway.
Severe or escalating hypoxaemia, altered consciousness, cold peripheries, oliguria or rising lactate indicates impaired right-heart output.
Active major bleeding, recent intracranial disease or recent major surgery materially changes anticoagulation and reperfusion choices.
Pregnancy, severe renal impairment or contrast allergy changes imaging selection but must not permit diagnostic drift or dangerous delay.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Two-level PE Wells score and D-dimerFirst step
Why
Select the NICE pre-test probability branch in non-pregnant adults before definitive thoracic imaging.
Interpretation and limitations
More than 4 means PE likely and triggers immediate imaging; 4 or less means PE unlikely and triggers D-dimer, with positive results proceeding to imaging.
02
CT pulmonary angiography
Why
Demonstrate intraluminal pulmonary arterial thrombus and assess alternative thoracic disease.
Interpretation and limitations
A positive scan confirms PE. If negative despite suspected DVT, arrange proximal leg-vein ultrasound; always reconsider alternative diagnoses and image quality.
03
V/Q SPECT or planar scan
Why
Provide an alternative when iodinated contrast or radiation considerations make CTPA unsuitable.
Interpretation and limitations
Use when contrast allergy, severe renal impairment or high irradiation risk applies; interpret probability with the chest radiograph and clinical context.
04
ECG, chest radiograph and basic blood tests
Why
Assess physiological impact, mimics, bleeding risk and suitability for anticoagulation.
Interpretation and limitations
Findings such as sinus tachycardia or right-heart strain support severity assessment but are not diagnostic; check FBC, renal and hepatic function, PT and APTT without delaying indicated interim anticoagulation.
05
Echocardiography and cardiac biomarkers
Why
Assess right-ventricular dysfunction and myocardial injury in confirmed or strongly suspected PE.
Interpretation and limitations
RV dysfunction or elevated troponin refines risk in stable PE and supports monitored care; it does not alone justify routine systemic thrombolysis under NICE guidance.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Acute coronary syndrome

Central pressure, diaphoresis and dynamic ECG or troponin change may overlap with PE; coronary-territory findings and targeted imaging guide urgent parallel assessment.

Aortic dissection

Abrupt tearing pain, pulse or neurological deficit and a new aortic regurgitation murmur demand an aortic imaging strategy and alter anticoagulation safety.

Pneumonia or sepsis

Fever, focal crackles and infiltrate suggest infection, although pulmonary infarction can also cause fever and opacity; integrate cultures, imaging and haemodynamic pattern.

Pneumothorax or pericardial tamponade

Unilateral absent breath sounds or distended neck veins with muffled heart sounds may identify another immediately reversible obstructive cause of shock.

Additional chapter-specific clues

Alternative lethal diagnoses

Tearing pain or pulse deficit, dynamic ischaemic ECG change, unilateral absent breath sounds, fever with shock, or focal neurological catastrophe should redirect or broaden urgent testing.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Emergency pathwayUnstable suspected or confirmed PEFirst stepShock, persistent hypotension, cardiac arrest or rapidly worsening organ perfusion is present.

1Start monitored ABC resuscitation, summon senior critical-care and PE expertise, establish vascular access and avoid excessive fluid loading that may worsen right-ventricular distension.
2Obtain the fastest safe confirmation and right-heart assessment, begin continuous UFH for confirmed unstable PE when not contraindicated, and assess systemic thrombolysis immediately against bleeding hazards.
3EscalationIf thrombolysis is contraindicated or fails and expertise exists, escalate urgently for catheter-based treatment or surgical embolectomy rather than persisting with ineffective support.
4After stabilisation, document reperfusion response, bleeding, end-organ recovery and the long-term anticoagulation plan.

02Diagnostic pathwayStable non-pregnant adult with suspected PEPE is clinically suspected in a non-pregnant adult without haemodynamic instability.

1If overall suspicion is low and other diagnoses are feasible, consider PERC; otherwise calculate the two-level PE Wells score.
2For Wells above 4 obtain immediate CTPA, using suitable V/Q imaging for specified contrast, renal or irradiation concerns; give interim therapeutic anticoagulation if imaging cannot be immediate.
3For Wells 4 or less obtain D-dimer within 4 hours if possible, anticoagulating in the interim when delayed; image only if D-dimer is positive.
4Act on imaging, stop interim anticoagulation when PE is excluded unless it has another indication, and give explicit safety-net advice.

03Disposition pathwayConfirmed stable PE risk assessment in a non-pregnant adultPE is confirmed in a non-pregnant adult who remains normotensive without shock.

1Use a validated prognostic tool such as PESI, simplified PESI or an established outpatient exclusion rule, while separately reviewing RV imaging and biomarkers.
2Exclude outpatient treatment when oxygen needs, active bleeding, high bleeding risk, severe pain, major comorbidity or likely deterioration requires admission.
3Confirm cognition, adherence, medication supply, home support, transport, direct thrombosis-team contact and out-of-hours access before discharge.
4Arrange an explicit monitoring and follow-up plan and explain symptoms of recurrent VTE, bleeding and chronic thromboembolic disease.

04Pregnancy pathwaySuspected PE in pregnancy or the puerperiumSymptoms or signs suggest PE during pregnancy or the puerperium; generic NG158 PERC, Wells and D-dimer rules are not applied.

1Arrange expeditious objective testing under the local multidisciplinary pregnancy protocol and give therapeutic LMWH until VTE is excluded unless anticoagulation is strongly contraindicated.
2Obtain ECG and chest radiography; when DVT symptoms or signs are present, perform bilateral compression duplex ultrasound and continue VTE treatment without further chest imaging if DVT is confirmed.
3Without DVT symptoms or signs, perform V/Q imaging or CTPA; prefer CTPA when the chest radiograph is abnormal and involve the woman in discussion of the small, differing maternal and fetal radiation risks.
4AlternativeIf V/Q imaging or CTPA is normal but clinical suspicion remains, continue anticoagulation and arrange alternative or repeat testing until PE is definitively excluded.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Obstructive shock

Progressive RV failure causes hypotension, tissue hypoperfusion, cardiac arrest and high early mortality; deterioration can occur after an initially stable presentation.

Pulmonary infarction

Peripheral emboli may produce pleuritic pain, haemoptysis, fever and wedge-shaped opacity, sometimes with a reactive pleural effusion.

Recurrent venous thromboembolism

Recurrence may reflect interrupted treatment, non-adherence, malignancy, persistent risk factors or treatment failure and demands structured reassessment.

Chronic thromboembolic disease

Persistent organised obstruction can lead to exercise limitation, pulmonary hypertension and progressive right-heart dysfunction, requiring specialist investigation after unresolved symptoms.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

During acute assessment trend blood pressure, heart rate, respiratory rate, oxygen saturation, mental state, urine output and lactate rather than relying on one normal observation set.
For stable PE with RV dysfunction or myocardial injury, monitor closely for new hypotension, rising oxygen need, syncope, oliguria or lactate elevation that should trigger rescue reassessment.
Before and during anticoagulation review full blood count, renal and hepatic function, PT, APTT, bleeding, drug interactions and adherence; act on baseline results within 24 hours when interim treatment was started.
Outpatients need written warning signs, a named expert contact, out-of-hours access and a scheduled clinical review that confirms symptoms, treatment tolerance and continuing suitability.
At follow-up ask about persistent dyspnoea, exercise limitation, syncope and functional decline; investigate unresolved symptoms for recurrent PE, chronic thromboembolic pulmonary hypertension or another cause.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Probability is not prognosis

In non-pregnant adults, Wells and PERC govern whether to test for PE. PESI, simplified PESI, haemodynamics, RV findings and biomarkers address outcome risk. Substituting one domain for the other creates both missed diagnoses and unsafe discharges.

PERC has a narrow entry point

In non-pregnant adults, PERC is considered only after overall clinical suspicion is low and plausible alternative diagnoses exist. Applying it after moderate or high suspicion, or treating it as proof of no PE, misuses the rule.

Pregnancy uses a separate objective-testing pathway

NICE NG158 excludes pregnancy, and PESI or simplified PESI should not be used to select pregnant patients for outpatient care. Follow a local obstetric VTE protocol: investigate expeditiously, use leg duplex when DVT features coexist, select V/Q imaging or CTPA according to chest radiography and local expertise, and continue anticoagulation until PE is objectively excluded unless strongly contraindicated.

Incidental PE still needs assessment

An incidentally reported embolus requires confirmation of image quality, anatomical extent, symptoms, bleeding risk and provoking factors. Physiological stability and the validity of the radiology finding guide urgency and treatment planning.

Outpatient care is a service

A low prognostic score does not create safe ambulatory care by itself. Medication availability, education, rapid advice, review capacity and a route back to hospital are active components of treatment.

11Common pitfallsFrequent interpretation and management errors.

01
Using a negative D-dimer after a high Wells score to avoid imaging undermines the probability-led pathway.
02
Calling RV dysfunction “massive PE” in a normotensive patient confuses anatomical or imaging findings with haemodynamic high risk.
03
Offering routine systemic thrombolysis to a stable patient with RV strain ignores NICE guidance and exposes the patient to major bleeding.
04
Discharging on the basis of simplified PESI alone overlooks oxygen need, bleeding risk, severe pain, comorbidity and social feasibility.
05
Interpreting tachycardia, S1Q3T3 or raised troponin as diagnostic proof forgets that none is specific for pulmonary embolism.

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