Pulmonary Embolism

The answer first

Pulmonary embolism (PE) is the acute obstruction of the pulmonary arterial tree by material embolising from a systemic vein, almost always a deep vein thrombosis (DVT) of the lower limb or pelvis. Together, DVT and PE are venous thromboembolism (VTE) — one disease with two clinical faces. PE is common, lethal, and frequently missed: it kills more inpatients in the developed world than any other preventable cause. [1]

Three decisions determine every PE case, and they must land before the details: [1]

1. How likely is PE right now? Use a structured pre-test probability tool — the Wells score (PE likely greater than 4, PE unlikely 4 or less) or the Revised Geneva score (fully objective). In a clearly low-risk patient, the PERC rule can safely forego testing entirely.
2. Is this patient haemodynamically stable? Shock or sustained hypotension makes this a high-risk (massive) PE — the only category where reperfusion therapy (thrombolysis, embolectomy) is mandatory and immediately life-saving. Everyone else is first anticoagulated.
3. What is the early-death risk? Use sPESI, biomarkers (troponin, BNP), and echo to split the stable group into low (suitable for outpatient or short-stay), intermediate-low, and intermediate-high (admit, monitor for decompensation, consider rescue thrombolysis). [1]

Two facts govern the long view: [1]

• Therapeutic anticoagulation should not wait for imaging when clinical probability is high and there is no contraindication — the risk of the disease exceeds the bleeding risk of a single day of low-molecular-weight heparin.
• Duration of anticoagulation is dictated by provokability, not by the clot itself. Provoked by surgery or a transient risk factor: 3 months. Unprovoked: 3 to 6 months then reassess, often indefinite. Cancer-associated or inherited thrombophilia with recurrent events: indefinite. [1]

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Risk factors — Virchow triad

Every VTE risk factor maps to one of Virchow's three limbs — endothelial injury, venous stasis, or hypercoagulability. Knowing the limb tells you the mechanism and, often, the duration of risk. [1]

DWE high-yield — thrombophilia work-up: Do not test everyone. Test selectively: unprovoked PE in a patient under 50, recurrent VTE, PE in unusual sites (portal/mesenteric/cerebral), family history of VTE, or recurrent fetal loss. Factor V Leiden (the most common inherited thrombophilia) and the prothrombin G20210A mutation are autosomal dominant. Antithrombin, protein C and protein S levels are unreliable during the acute event and on anticoagulation — test at least 2 weeks after stopping therapy. Antiphospholipid syndrome requires a persistently positive lupus anticoagulant or anticardiolipin/beta-2-glycoprotein-I antibody on two occasions at least 12 weeks apart. Finding antiphospholipid syndrome changes management: warfarin (target INR 2 to 3) is preferred over DOACs after the initial period. [1]

Malignancy and PE: Around 10 to 20 percent of patients with an unprovoked PE have an occult cancer diagnosed within a year. A focused malignancy screen (history, examination, basic bloods, age-appropriate screening — colonoscopy, mammography, prostate) is appropriate in every unprovoked PE. Extensive blind CT-PET screening is not routine — it rarely changes outcome and adds harm. [1]

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Pathophysiology — why PE kills

A pulmonary embolus injures through three mechanisms that operate simultaneously: [1]

1. Gas exchange failure (V/Q mismatch and dead space)

The embolised segment is ventilated but not perfused — dead space. Adjacent areas are perfused but under-ventilated because embolised vasoconstrictive mediators (serotonin, thromboxane) redirect flow, creating low V/Q units and shunt. The net result is hypoxaemia with a low PaCO2 (because the patient hyperventilates the remaining lung). Hyperventilation against dead space is why the PaCO2 is low while the patient is still hypoxaemic — a key discriminator from COPD (where CO2 rises). [1]

Two points are under-appreciated: [1]

• The A-a gradient is elevated even when PaO2 looks acceptable, because the measured PaCO2 is lower than expected.
• A paradoxical fall in PaO2 despite oxygen can occur when a patent foramen ovale opens under rising right atrial pressure, producing a right-to-left shunt. [1]

2. Right ventricular pressure overload

The pulmonary circulation is a low-pressure, low-resistance circuit. An embolus suddenly raises pulmonary vascular resistance. The thin-walled RV, built for low afterload, dilates and fails. The sequence is predictable and reversible if caught early: [1]

• RV pressure rises, then RV dilation, then tricuspid regurgitation, then RV failure, then septal shift impairing LV filling, then falling cardiac output, then systemic hypotension, then coronary hypoperfusion of the RV itself — the death spiral of massive PE. [1]

This is why a bedside echocardiogram is the single most useful test in a haemodynamically unstable patient with suspected PE: RV dilation, septal flattening, McConnell sign (akinesia of the RV free wall with preserved apical contraction), and tricuspid annular plane systolic excursion (TAPSE) reduction identify the failing right heart and justify immediate reperfusion. [1]

3. Humoral amplification

Clot-bound platelets release serotonin and thromboxane, which constrict downstream pulmonary arterioles far beyond the mechanical obstruction. This explains why the degree of hypoxaemia and RV strain often exceeds what the angiographic clot burden would predict, and why modest clots in a diseased lung (COPD, heart failure) can cause disproportionate collapse. [1]

Why the S1Q3T3 pattern? Acute RV dilation rotates the heart, changing the electrical axis. Lead I shows a deep S wave (rightward axis), lead III shows a Q wave and inverted T. It is a specific but insensitive sign — its absence never excludes PE, and sinus tachycardia is by far the commonest ECG finding. [1]

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Clinical presentation

The textbook triad of pleuritic chest pain, dyspnoea, and haemoptysis is seen in a minority. Most patients have an isolated symptom — dyspnoea is the commonest (around 80 percent), followed by pleuritic pain and cough. [1]

Massive (high-risk) PE presents as obstructive shock: hypotension (systolic BP less than 90, or a drop of at least 40 from baseline), tachycardia, tachypnoea, cool peripheries, raised JVP, and oliguria. The key discriminator from cardiogenic shock is a raised JVP with clear lung fields — the failing right heart cannot fill the left heart, so the lungs stay dry while systemic pressure collapses. [1]

Submassive (intermediate-risk) PE describes a patient who is normotensive but has right ventricular dysfunction on imaging or myocardial injury (raised troponin/BNP). They look well but are one further clot, one arrhythmia, or one vasoconstrictive surge away from collapse. They need monitoring and a low threshold for rescue thrombolysis. [1]

DWE trap — syncope: Isolated syncope in an older patient with unexplained hypoxaemia is PE until proven otherwise. The classic arrhythmia work-up will miss it. Apply a Wells score, check a D-dimer, and image. [1]

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Clinical assessment tools

The diagnosis of PE is algorithmic, not Gestalt. You must commit to a pre-test probability (PTP) before you order a test, because the interpretation of every test (D-dimer, CTPA, V/Q) depends on the pre-test probability. [1]

Wells score for PE

Two-tier interpretation (preferred, Wells 2001, PMID 11453709): PE unlikely if 4 or less, PE likely if greater than 4. The two-tier version outperforms the older three-tier version in contemporary practice and is what the ESC endorses. [1]

PERC rule (Pulmonary Embolism Rule-out Criteria)

Eight items — all must be negative for the rule to apply: [1]

1. Age less than 50
2. Pulse less than 100
3. O2 saturation at least 95 percent
4. No unilateral leg swelling
5. No haemoptysis
6. No recent surgery or trauma
7. No prior PE or DVT
8. No hormone use (oestrogen) [1]

If the patient is low-risk by clinician gestalt (less than 15 percent) and PERC-negative, no D-dimer and no imaging is required — PE is excluded at the bedside (Kline 2008, PMID 18318689). PERC is the highest-yield tool in a busy ED: it safely avoids thousands of unnecessary D-dimers and the CTPAs they trigger. [1]

Revised Geneva Score

A fully objective alternative to Wells — it has no subjective "PE most likely" item, which is why some clinicians and the French/NICE pathways prefer it (Le Gal 2006, PMID 16461960). [1]

Three-tier: low (0 to 3), intermediate (4 to 10), high (at least 11). Can be dichotomised: unlikely 0 to 3, likely at least 4. [1]

Examiner question — Wells vs Geneva: Wells requires a clinical judgement ("is PE most likely?"); Geneva is fully objective. Both perform similarly when used within a structured D-dimer/imaging pathway. The point is to commit to a rule and use it consistently — the danger is unstructured clinician gestalt, which both over-investigates and misses. [1]

D-dimer and the age-adjusted cutoff

D-dimer is highly sensitive and poorly specific — a negative result excludes PE in a low-probability patient; a positive result means nothing on its own. [1]

• Use the high-sensitivity assay (quantitative ELISA or immunoturbidimetric).
• Standard cutoff: 500 micrograms/L FEU (fibrinogen-equivalent units).
• Age-adjusted cutoff (ADJUST-PE, PMID 24643601): for patients over 50, use age multiplied by 10 micrograms/L (e.g., a 75-year-old uses 750). This safely increases the proportion of older patients in whom PE can be excluded without CTPA, from around 15 percent to around 30 percent.
• Never rely on a negative D-dimer in a high-probability patient — go straight to imaging. [1]

DWE trap: Ordering a D-dimer in a high-probability patient is a category error. A negative D-dimer does not have a low enough likelihood ratio to exclude PE when the pre-test probability is high. If Wells is "PE likely," image. [1]

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Investigations

CTPA — first-line in most adults

Computed tomography pulmonary angiography is the diagnostic standard. It directly visualises the clot, stratifies burden, and finds alternative diagnoses (pneumonia, dissection, malignancy). [1]

Strengths: high sensitivity and specificity for segmental and larger clots; fast; widely available; rules in and rules out. [1]

Limitations and pitfalls: [1]

• Overdiagnosis of isolated subsegmental PE — a consequence of ever-improving scanner resolution. A tiny subsegmental clot in a low-risk patient may not need anticoagulation; clinical judgement and follow-up imaging are reasonable.
• Contrast nephropathy — caution when eGFR is less than 30 to 45; consider V/Q or renal-dose strategies.
• Radiation — relevant in pregnancy and young patients.
• Incidental findings — pulmonary nodules, adrenal adenomas, and other "red herrings" drive follow-up and anxiety. Use a structured reporting pathway. [1]

V/Q scan — preferred when CTPA is unsuitable

Ventilation-perfusion scanning is the modality of choice in: renal impairment, contrast allergy, pregnancy (lower radiation to mother and fetus than CTPA), and follow-up of a known PE (where chronic change confounds CTPA). Its weakness is that around a quarter of patients with a pre-existing cardiopulmonary disease have an "intermediate" (non-diagnostic) result, which forces a CTPA anyway. A normal perfusion scan excludes PE; a high-probability scan confirms it. [1]

Lower limb compression ultrasound

Around half of patients with PE have a concurrent DVT. A positive leg ultrasound in a patient with suspected PE confirms VTE and supports treatment if CTPA is contraindicated. A negative leg ultrasound does not exclude PE. [1]

ECG

Rarely diagnostic. Common findings: sinus tachycardia (most common), anterior T-wave inversion (V1 to V3 or V4), right axis deviation, S1Q3T3, new right bundle branch block, new atrial fibrillation or flutter. The ECG's main job in PE is to exclude STEMI and arrhythmia as the cause of collapse. [1]

Arterial blood gas

Hypoxaemia with respiratory alkalosis (low PaCO2) and an elevated A-a gradient. A normal PaO2 never excludes PE — around 15 percent of confirmed PEs have PaO2 over 80 mmHg. The ABG's main role is in the unwell, hypoxaemic, or ventilated patient to assess severity and guide support. [1]

Biomarkers and echo in the unstable patient

When the patient is too unstable to leave the department for CTPA, a bedside echocardiogram demonstrating acute RV dilation and dysfunction, in the right clinical context, is sufficient to justify thrombolysis or embolectomy without confirmatory imaging. Troponin and BNP/NT-proBNP quantify the myocardial strain and, with echo, drive the intermediate-risk stratification. Lactate reflects tissue hypoperfusion and is a marker of severity. [1]

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Risk stratification

The 2019 ESC guideline stratifies PE into four strata that integrate clinical, imaging, and biomarker data — because a stable-looking patient can be hiding a failing right heart. [1]

PESI and sPESI

The Pulmonary Embolism Severity Index (PESI) uses 11 routinely-available variables to stratify 30-day mortality into five classes (Aujesky 2005, PMID 16020800). The simplified PESI (sPESI) keeps only six binary variables — any score of at least 1 means the patient is not low-risk and should not be considered for outpatient treatment (Jimenez 2010, PMID 20696966): [1]

A sPESI of 0 plus a negative troponin and an echo showing no RV dysfunction identifies a genuinely low-risk patient in whom home or short-stay anticoagulation is safe. This is the single most important disposition decision in modern PE care. [1]

What the trials mean for reperfusion in intermediate-risk PE

• MAPPET-3 (2002, PMID 12374874): alteplase plus heparin versus heparin alone in submassive PE reduced the need for escalation (intubation, catecholamines, rescue thrombolysis) — established that lysis can prevent deterioration.
• PEITHO (2014, PMID 24716681): single-bolus tenecteplase in intermediate-risk PE reduced the composite of death or decompensation but significantly increased major bleeding and haemorrhagic stroke (around 2 percent intracranial haemorrhage). [1]

Net lesson: prophylactic thrombolysis in intermediate-high PE is not routine — the bleeding cost is too high. Standard care is anticoagulation plus close monitoring, with rescue thrombolysis reserved for the patient who actually decompensates (a fall in blood pressure). [1]

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Management

Immediate (first hour)

1. ABCs. High-flow oxygen to correct hypoxaemia. Vascular access. Continuous cardiac monitoring.
2. Analgesia for pleuritic pain — paracetamol first; avoid NSAIDs (bleeding risk once anticoagulated). Opioids for severe pain in small doses (caution: vasodilation can worsen hypotension).
3. Haemodynamic support in shock: cautious IV fluids (250 mL boluses — too much worsens RV failure), noradrenaline for vasoplegia, dobutamine if low cardiac output with adequate pressure.
4. Therapeutic anticoagulation immediately if PE is suspected and there is no contraindication — do not wait for imaging in a high-probability patient. A single dose of LMWH is safe while the work-up proceeds. [1]

Anticoagulation — the cornerstone

Unless the patient is bleeding, every PE is anticoagulated from the moment of suspicion or diagnosis. Three drug families: [1]

Parenteral: [1]

• LMWH (enoxaparin 1 mg/kg subcutaneously twice daily, or 1.5 mg/kg once daily) — standard initial therapy; preferred in cancer, pregnancy, and severe renal impairment adjusted appropriately. Rapid, predictable, no monitoring.
• Unfractionated heparin (IV bolus then infusion, weight-based, APTT-monitored) — preferred when rapid reversibility is needed (high bleeding risk, planned thrombolysis/embolectomy, extreme obesity, severe renal failure with eGFR less than 30).
• Fondaparinux — once-daily pentasaccharide; an option when heparin-induced thrombocytopenia is a concern. [1]

Direct oral anticoagulants (DOACs) — first-line for most stable adults: [1]

Apixaban and rivaroxaban are the most convenient because they are oral from day one — no LMWH lead-in, no INR monitoring. Both showed non-inferior efficacy and less major bleeding than warfarin. [1]

Dose reduction triggers for DOACs (know at least one drug cold):

• Apixaban 2.5 mg twice daily (instead of 5 mg) if any two of: age at least 80, body weight at most 60 kg, creatinine at least 133 micromol/L.
• Edoxaban 30 mg once daily (instead of 60) if CrCl 30 to 50 mL/min, weight at most 60 kg, or concomitant strong P-gp inhibitors. [1]

Warfarin is now third-line for most patients but remains preferred in: antiphospholipid syndrome (DOACs had worse outcomes in TRAPS), severe renal failure (some patients), mechanical heart valves, and pregnancy (teratogenic — never in pregnancy). If warfarin is used, bridge with LMWH for at least 5 days and until INR is at least 2.0 for 24 hours. [1]

Duration — provokability decides

Examiner question — why indefinite for unprovoked? Because the annual recurrence after stopping is around 10 percent (versus around 1 to 3 percent for provoked), and recurrence is often fatal. The decision is recurrence risk versus bleeding risk — use HAS-BLED or similar to quantify the latter and discuss with the patient. [1]

Thrombolysis for massive (high-risk) PE

Massive PE is the only situation in which thrombolysis is unequivocally indicated — it is life-saving. The patient is hypotensive or shocked. [1]

• Alteplase (tPA) 100 mg IV over 2 hours is the standard regimen (the "100 mg over 2 hours" PE protocol). Continue heparin at reduced rate or hold per local protocol during infusion.
• In cardiac arrest, a 50 mg IV bolus of alteplase may be given once and CPR continued — do not delay lysis for confirmatory imaging if PE is the most likely cause. [1]

Absolute contraindications to thrombolysis: haemorrhagic stroke or stroke of unknown origin at any time, ischaemic stroke in the last 6 months, intracranial neoplasm, major surgery or trauma in the last 3 weeks, active bleeding. Relative contraindications include recent GI bleed, uncontrolled hypertension (over 180/110), pregnancy, recent puncture of a non-compressible vessel. When thrombolysis is contraindicated or has failed, surgical embolectomy or catheter-directed thrombolysis/thrombectomy (ULTRAS, OPTALYSE) are the rescue options. [1]

Why catheter-directed over systemic? It delivers the lytic directly into the clot at a fraction of the systemic dose (around 20 to 25 mg alteplase over 12 to 24 hours), reducing systemic bleeding while achieving local clot lysis. It needs an interventional team and is for intermediate-high or selected massive PE in centres with capability. [1]

IVC filters

Retrievable inferior vena cava filters have one indication: acute VTE with an absolute contraindication to anticoagulation (active bleeding, imminent surgery), or recurrent PE despite adequate anticoagulation. They do not improve survival, they do not prevent DVT, and they carry their own thrombotic risk. Every retrievable filter must have a removal plan — many are never removed and become a source of new thrombosis. [1]

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Chronic thromboembolic pulmonary hypertension (CTEPH)

CTEPH is the chronic sequel of PE — organised, fibrotic thrombus fails to resolve and occludes the pulmonary arterial bed, producing pulmonary hypertension and progressive right heart failure. It is underdiagnosed and curable. [1]

• Incidence: around 0.4 to 4 percent of patients after a symptomatic PE (Pengo 2004, PMID 15163775). Higher after recurrent or central PE.
• When to suspect: any patient with persistent or new dyspnoea at 3 to 6 months after PE, especially with exertional presyncope or oedema.
• Diagnostic pathway: echocardiogram (raised RVSP), then V/Q scan (the screening test of choice — a normal V/Q effectively excludes CTEPH), then right heart catheterisation and pulmonary angiography to define anatomy.
• Treatment:
  • Pulmonary endarterectomy (PEA) — the potentially curative operation for operable (proximal) disease. Done in specialist centres.
  • Balloon pulmonary angioplasty (BPA) — for non-operable or residual disease; staged procedures.
  • Riociguat (soluble guanylate cyclase stimulator) — medical therapy for inoperable or persistent CTEPH.
  • Lifelong anticoagulation for all. [1]

DCE trap: A patient returns 6 months after a "recovered" PE with breathlessness. Do not label it deconditioning or anxiety. Order an echo and a V/Q scan — CTEPH is treatable, and the cost of missing it is right heart failure. [1]

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Special situations

Pregnancy

PE is a leading cause of maternal death. Key rules: [1]

• Diagnosis: V/Q preferred over CTPA (lower radiation to mother and fetus, especially in the first and second trimester). If CT is needed, the dose is acceptable.
• D-dimer is physiologically raised in pregnancy and less useful — but a negative high-sensitivity D-dimer still excludes PE in a low-probability patient.
• Treatment: weight-adjusted LMWH (enoxaparin) throughout pregnancy and for 6 weeks postpartum (minimum 3 months total). Never warfarin (teratogenic in weeks 6 to 12; fetal bleeding near term). Never DOACs (limited safety data).
• Thrombolysis is used for massive PE in pregnancy when life-saving; rt-PA does not cross the placenta in significant amounts.
• Anticoagulation around delivery: plan an elective induction with LMWH withheld 24 hours beforehand; resume postpartum. Bridging to warfarin is safe postpartum and breastfeeding. [1]

Malignancy

Cancer-associated thrombosis (CAT) is common and high-risk. LMWH was historically first-line (the CLOT trial). Now, rivaroxaban and edoxaban are non-inferior and oral — they are first-line for most CAT, with LMWH reserved for upper GI / urological cancers where bleeding risk from DOACs is higher (SELECT-D showed more upper GI bleeds with rivaroxaban in upper GI cancer). Therapy continues while cancer is active. [1]

Renal failure

• eGFR at least 30: apixaban, rivaroxaban, dose-adjusted LMWH all usable.
• eGFR less than 30: apixaban is the best-evidenced DOAC (no renal dose adjustment needed at 5 mg twice daily, though caution and monitoring); rivaroxaban and dabigatran should be avoided. Unfractionated heparin infusion is the safest parenteral option and is dialysis-filterable. Warfarin remains a valid option.
• Dialysis: apixaban 2.5 mg twice daily or warfarin; avoid dabigatran (predominantly renal clearance). [1]

Heparin-induced thrombocytopenia (HIT)

A falling platelet count (greater than 50 percent drop) 5 to 14 days after starting heparin, with new or worsening thrombosis, is HIT — a prothrombotic immune adverse effect, not a bleeding one. Stop all heparin (including flushes), confirm with a serotonin-release assay or ELISA, and switch to a non-heparin anticoagulant (argatroban, danaparoid, fondaparinux, or a DOAC). Do not give platelet transfusions. [1]

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DCE long-case approach

Opening statement (SASPOP)

"This is Mrs Chen, a 62-year-old office manager who presented three days ago with acute pleuritic chest pain, dyspnoea, and a single episode of presyncope. CTPA confirmed a saddle embolus with right ventricular dilation. She has an unprovoked PE (Wells 7.5, PE likely), sPESI 2 (pulse 116, saturation 88 percent) — intermediate-high risk. [1]

Her main problems are:

1. Unprovoked PE, intermediate-high risk, on therapeutic apixaban — needs monitoring for decompensation
2. Right ventricular strain (echo: RV dilation, septal flattening; troponin mildly elevated)
3. Active ovarian cancer (diagnosed last month) — cancer-associated thrombosis, indefinite anticoagulation
4. Obesity (BMI 36) — mechanical and pharmacokinetic relevance
5. Ongoing investigation for the ovarian primary — surgical and oncology planning" [1]

Integrated management plan

1. Anticoagulation: Apixaban 10 mg twice daily for 7 days then 5 mg twice daily. In cancer-associated thrombosis, apixaban is acceptable; if upper GI tract involvement or bleeding, switch to LMWH. Indefinite duration while cancer is active. [1]2. Monitoring (intermediate-high): Continuous cardiac monitoring, serial observations, daily troponin and BNP, repeat echo at 48 to 72 hours. Have a rescue thrombolysis plan ready — give alteplase 100 mg over 2 hours if she becomes hypotensive.
2. Malignancy: Liaise with oncology and gynaecology for staging and treatment; ensure she is on appropriate thromboprophylaxis during any surgery.
3. Mobility and prophylaxis: Early mobilisation as tolerated; compression stockings for the affected leg if DVT confirmed.
4. Discharge planning: Education on apixaban (adherence, bleeding signs), action plan for worsening breathlessness, thrombosis clinic follow-up at 2 to 4 weeks and 3 months, repeat imaging only if symptoms recur.
5. Screening: Reassess for inherited thrombophilia only if cancer therapy finishes and the question of indefinite therapy remains; in active cancer the cancer is the explanation. [1]

DCE examiner probing questions you must anticipate:

• "Why not thrombolyse her now?" — She is normotensive; PEITHO showed prophylactic lysis in intermediate-high PE adds bleeding (around 2 percent intracranial) without a mortality benefit. Anticoagulate and monitor; rescue-lyse if she decompensates.
• "Why apixaban over LMWH?" — Oral, convenient, non-inferior, less major bleeding than warfarin; the SELECT-D caveats apply to upper GI cancers, and ovarian cancer is not in that high-bleed group.
• "When would you screen her family?" — If she has a first-degree relative with VTE, or if she has a second unprovoked event — test for factor V Leiden, prothrombin mutation, antithrombin, protein C/S, and antiphospholipid antibodies.
• "She wants to know if she can fly." — No long-haul flights until at least 2 weeks stable on anticoagulation; then compression stockings, hydration, calf exercises, and continue her usual apixaban. [1]

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DCE short-case approach

Instruction: "Examine this patient's cardiovascular system." (Three months after a large PE, now on apixaban.) [1]

Systematic routine

1. End of bed: Tachypnoea, oxygen tubing or pulse oximeter, breathlessness at rest or on talking, cachexia or obesity, sallow complexion (chronic illness).
2. Hands: Clubbing (if present, reconsider — PE alone does not club; consider CTEPH with bronchiectasis or coexisting lung disease), peripheral cyanosis, bruising (anticoagulation). Pulse — rate (tachycardia persists), rhythm (AF is a complication of RV dilation). Respiratory rate.
3. Face: Conjunctival pallor, central cyanosis, plethoric facies.
4. Neck: JVP — elevated in pulmonary hypertension or right heart failure. Assess the waveform (prominent V wave of tricuspid regurgitation). Trachea central.
5. Precordial inspection: RV heave at the lower left sternal edge (parasternal). Apex displaced laterally only if RV dilation is severe.
6. Palpation: RV heave, palpable P2 (pulmonary hypertension), thrills (rare).
7. Auscultation: Loud pulmonary component of S2 (P2) — the single most important sign of pulmonary hypertension. An ejection systolic murmur at the upper left sternal edge (flow across the pulmonary valve). A pansystolic murmur at the lower left sternal edge, louder on inspiration (tricuspid regurgitation). A right-sided S3 in RV failure. Listen for a pleural rub if recent infarction.
8. Lungs: Usually clear. Pleural effusion (unilateral, small-to-moderate) or crackles of infarction in the acute phase.
9. Abdomen: Hepatomegaly with a pulsatile liver in severe tricuspid regurgitation; ascites in advanced right heart failure.
10. Legs: Asymmetry, calf tenderness, pitting oedema, evidence of the source DVT (post-thrombotic syndrome — brown discolouration, medial malleolar ulceration). [1]

Presentation template

"I examined Mrs Chen's cardiovascular system. She is comfortable at rest on room air with a respiratory rate of 18. She has no clubbing and is afebrile. The pulse is 88 and regular. The JVP is elevated 4 cm with a prominent V wave. [1]

On palpation there is a right ventricular heave at the lower left sternal edge. The pulmonary component of the second heart sound is loud and palpable. There is a pansystolic murmur at the lower left sternal edge that is louder on inspiration, consistent with tricuspid regurgitation. The chest is clear. There is pitting oedema to the mid-shin bilaterally and a healed varicose-eczema pattern on the left medial malleolus. [1]

In summary, these findings are consistent with pulmonary hypertension and right heart strain, most likely post-pulmonary-embolism, complicated by tricuspid regurgitation and a history of deep vein thrombosis in the left leg." [1]

Examiner: "Why is P2 loud?" — Elevated pulmonary artery pressure closes the pulmonary valve more forcefully, producing an accentuated P2. Combined with an RV heave and elevated JVP, this is pulmonary hypertension with right heart involvement — in her case, likely early CTEPH after a large PE, and warrants a V/Q scan and echocardiographic estimation of RV systolic pressure. [1]

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Key DWE MCQ patterns

1. Wells score threshold: "PE likely" if greater than 4; "PE unlikely" if 4 or less. The two-tier version is preferred.
2. PERC rule: all eight items must be negative, and clinician gestalt must be low, to avoid any testing. PERC is not for high-risk patients.
3. Age-adjusted D-dimer: age multiplied by 10 micrograms/L for age over 50; doubles the exclusion rate in the elderly.
4. Anticoagulate before imaging if PE is likely and there is no contraindication.
5. DOAC monotherapy: apixaban (10 mg twice daily for 7 days then 5 mg twice daily) and rivaroxaban (15 mg twice daily for 3 weeks then 20 mg once daily) need no LMWH lead-in. Dabigatran and edoxaban do. [1]6. Thrombolysis for massive PE: alteplase 100 mg over 2 hours is the only unequivocal reperfusion indication. Not for routine intermediate-high PE (PEITHO).
6. Duration: provoked — 3 months; unprovoked — indefinite (or 3 to 6 months then reassess); cancer-associated — indefinite; antiphospholipid syndrome — indefinite (warfarin).
7. Pregnancy: LMWH throughout, no warfarin, no DOACs; V/Q over CTPA for diagnosis.
8. CTEPH incidence: around 0.4 to 4 percent after PE; screen with V/Q scan at 3 to 6 months if symptomatic; pulmonary endarterectomy is curative.
9. HIT: falling platelets on heparin with new thrombosis — stop all heparin, switch to argatroban/fondaparinux/DOAC, confirm with serotonin-release assay.
10. Apixaban dose reduction: any two of age at least 80, weight at most 60 kg, creatinine at least 133 micromol/L — drop to 2.5 mg twice daily.
11. JVP up, lungs clear, hypotensive = obstructive shock from massive PE, not cardiogenic. Echocardiogram confirms RV failure; thrombolyse. [1]

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References

[1] Wells PS, et al. Excluding PE at the bedside without diagnostic imaging. Ann Intern Med 2001. Established the two-tier Wells (PE likely vs unlikely) plus D-dimer algorithm that halves diagnostic imaging while keeping the miss rate below 1 percent. [2] Le Gal G, et al. Revised Geneva score. Ann Intern Med 2006. A fully objective alternative to the Wells score; three-tier risk stratification; comparable diagnostic performance. [3] Kline JA, et al. PERC rule. J Thromb Haemost 2008. Prospective multicentre validation — low-gestalt-probability and PERC-negative patients have a PE rate below 2 percent and can be discharged without testing. [4] Righini M, et al. ADJUST-PE. JAMA 2014. Age-adjusted D-dimer (age multiplied by 10 for age over 50) safely excludes PE in an additional 15 to 20 percent of elderly patients without imaging. [5] Aujesky D, et al. PESI. Am J Respir Crit Care Med 2005. The 11-variable severity index stratifying 30-day mortality into five classes; Classes I to II identify low-risk patients for outpatient treatment. [6] Jimenez D, et al. sPESI. Arch Intern Med 2010. The six-variable simplification; any score at least 1 means not low-risk; the standard disposition tool in modern PE pathways. [7] Goldhaber SZ, et al. ICOPER. Lancet 1999. The registry that defined the natural history — 3-month mortality around 17 percent; age, cancer, heart failure, and COPD predicted death. [8] Konstantinides S, et al. MAPPET-3. NEJM 2002. Alteplase plus heparin versus heparin alone in submassive PE reduced the need for escalation — the first evidence that lysis can prevent deterioration. [9] Meyer G, et al. PEITHO. NEJM 2014. Tenecteplase in intermediate-risk PE reduced death or decompensation but doubled major bleeding and caused around 2 percent intracranial haemorrhage — the trial that ended routine prophylactic lysis in intermediate-high PE. [10] Buller HR, et al. EINSTEIN-PE. NEJM 2012. Oral rivaroxaban (15 mg twice daily for 3 weeks then 20 mg once daily) non-inferior to enoxaparin/warfarin with less major bleeding. [11] Agnelli G, et al. AMPLIFY. NEJM 2013. Oral apixaban (10 mg twice daily for 7 days then 5 mg twice daily) non-inferior to conventional therapy with significantly less major bleeding. [12] Schulman S, et al. RE-COVER. NEJM 2009. Dabigatran 150 mg twice daily after 5 to 10 days of parenteral therapy non-inferior to warfarin for acute VTE. [13] Buller HR, et al. Hokusai-VTE. NEJM 2013. Edoxaban 60 mg once daily after heparin lead-in non-inferior to warfarin with less clinically relevant bleeding; dose-reduced to 30 mg for CrCl 30 to 50 or weight at most 60 kg. [14] Pengo V, et al. CTEPH incidence. NEJM 2004. Cumulative incidence of symptomatic CTEPH around 3.8 percent at 2 years after a symptomatic PE; prior PE, idiopathic PE, larger perfusion defect, and younger age were risk factors.

ESC/ERS 2019 Acute PE Guidelines; NICE NG158; ASH 2020 VTE Guidelines; CHEST 2021 Antithrombotic Therapy for VTE; Therapeutic Guidelines (Australia). [1]

References

1. [1]Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer Ann Intern Med, 2001.PMID 11453709
2. [2]Le Gal G, Righini M, Roy PM, et al. Prediction of pulmonary embolism in the emergency department: the revised Geneva score Ann Intern Med, 2006.PMID 16461960
3. [3]Kline JA, Courtney DM, Kabrhel C, et al. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria J Thromb Haemost, 2008.PMID 18318689
4. [4]Righini M, Van Es J, Den Exter PL, et al. Age-adjusted D-dimer cutoff levels to rule out pulmonary embolism: the ADJUST-PE study JAMA, 2014.PMID 24643601
5. [5]Aujesky D, Obrosky DS, Stone RA, et al. Derivation and validation of a prognostic model for pulmonary embolism Am J Respir Crit Care Med, 2005.PMID 16020800
6. [6]Jimenez D, Aujesky D, Moores L, et al. Simplification of the pulmonary embolism severity index for prognostication in patients with acute symptomatic pulmonary embolism Arch Intern Med, 2010.PMID 20696966
7. [7]Goldhaber SZ, Visani L, De Rosa M Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER) Lancet, 1999.PMID 10227218
8. [8]Konstantinides S, Geibel A, Heusel G, et al. Heparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolism N Engl J Med, 2002.PMID 12374874
9. [9]Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism N Engl J Med, 2014.PMID 24716681
10. [10]Buller HR, Prins MH, Lensin AW, et al. Oral rivaroxaban for the treatment of symptomatic pulmonary embolism N Engl J Med, 2012.PMID 22449293
11. [11]Agnelli G, Buller HR, Cohen A, et al. Oral apixaban for the treatment of acute venous thromboembolism N Engl J Med, 2013.PMID 23808982
12. [12]Schulman S, Kearon C, Kakkar AK, et al. Dabigatran versus warfarin in the treatment of acute venous thromboembolism N Engl J Med, 2009.PMID 19966341
13. [13]Buller HR, Decousus H, Grosso MA, et al. Edoxaban versus warfarin for the treatment of symptomatic venous thromboembolism N Engl J Med, 2013.PMID 23991658
14. [14]Pengo V, Lensing AW, Prandoni P, et al. Incidence of chronic thromboembolic pulmonary hypertension after pulmonary embolism N Engl J Med, 2004.PMID 15163775