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Pulmonary Embolism

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Pulmonary Embolism

Comprehensive exam-ready guide to pulmonary embolism in orthopaedic patients - PERC rule, Wells criteria, CTPA diagnosis, risk stratification (massive/submassive/low-risk), thrombolysis, and prevention

complete
Updated: 2025-12-25
High Yield Overview

PULMONARY EMBOLISM

Wells Score | CTPA Gold Standard | Risk Stratify | Anticoagulate or Thrombolyse

0.5-2%PE incidence after major ortho surgery WITH prophylaxis
30%Mortality if massive PE untreated
95%Sensitivity of CTPA for PE
1-5%Intracranial bleeding risk with thrombolysis

PE RISK STRATIFICATION

Massive (High-Risk)
PatternSustained hypotension (SBP less than 90 mmHg), cardiac arrest, cardiogenic shock
TreatmentThrombolysis or embolectomy + anticoagulation
Submassive (Intermediate)
PatternNormotensive BUT RV dysfunction on echo or elevated troponin/BNP
TreatmentAnticoagulation, consider thrombolysis if deteriorating
Low-Risk
PatternNormotensive, no RV dysfunction, stable vitals
TreatmentAnticoagulation only, may discharge if PESI low risk

Critical Must-Knows

  • Wells score estimates PE probability - guides need for CTPA
  • CTPA is gold standard (95% sensitive) - VQ scan if contrast contraindicated
  • Risk stratification determines treatment: Massive = thrombolysis, Low-risk = anticoagulation only
  • Thrombolysis saves lives in massive PE but 1-5% intracranial bleed risk
  • IVC filters ONLY if anticoagulation absolutely contraindicated - NOT routine

Examiner's Pearls

  • "
    PERC rule: If ALL 8 criteria negative AND low clinical suspicion, PE excluded (no D-dimer needed)
  • "
    Massive PE = hemodynamic instability (SBP less than 90) - thrombolyse immediately
  • "
    D-dimer negative with low Wells score excludes PE (99% NPV)
  • "
    Postop PE is provoked - anticoagulate 3 months, NOT indefinite

Clinical Imaging

Imaging Gallery

3-panel DVT imaging: duplex ultrasound compression test and CT venography after arthroplasty
Click to expand
3-panel DVT imaging: duplex ultrasound compression test and CT venography after arthroplastyCredit: Byun SS et al., Korean J Radiol via Open-i (NIH) - PMC2627179 (CC-BY)
2-panel duplex ultrasound showing DVT in CFV and popliteal vein
Click to expand
2-panel duplex ultrasound showing DVT in CFV and popliteal veinCredit: Nasrin S et al., J Med Case Rep via Open-i (NIH) - PMC4827182 (CC-BY)

Critical Exam Concepts

Massive PE Requires Thrombolysis

Massive PE = sustained hypotension (SBP less than 90 mmHg) or cardiac arrest. This is an emergency. Give alteplase 50-100mg over 2 hours IMMEDIATELY after confirming on CTPA. Mortality 30% if untreated vs 10% with thrombolysis.

IVC Filters are NOT Routine

IVC filters do NOT prevent PE or reduce mortality. Only use if absolute contraindication to anticoagulation (active bleeding, recent neurosurgery). PREPIC trial showed filters increase DVT without reducing PE death.

Risk Stratification Guides Treatment

Massive (high-risk): Thrombolysis. Submassive (intermediate): Anticoagulation, watch for deterioration. Low-risk: Anticoagulation, consider outpatient if PESI low risk. Do NOT thrombolyse submassive routinely.

CTPA is Gold Standard

CTPA has 95% sensitivity and 98% specificity for PE. Direct visualization of thrombus in pulmonary arteries. VQ scan only if contrast contraindicated (renal failure, severe allergy). Wells score determines who gets CTPA.

Quick Decision Guide

Clinical ScenarioWells ScoreNext StepTreatment
Low suspicion (all PERC negative)Not neededNo further testingPE excluded - no D-dimer needed
Moderate suspicion, low Wells (less than 4)0-3 (PE unlikely)D-dimer firstIf negative stop. If positive CTPA
High suspicion, high Wells (4+)4+ (PE likely)Skip D-dimer, go to CTPAIf positive, anticoagulate
Massive PE (SBP less than 90, shock)Not neededCTPA if stable, or empiric thrombolysis if crashingAlteplase 50-100mg over 2h + anticoagulation
Mnemonic

PEACH 3-3-1.5Wells Score for Pulmonary Embolism

P
Prior DVT/PE
1.5 points - previous documented VTE
E
Elevated heart rate
1.5 points - HR greater than 100 bpm
A
Alternative diagnosis unlikely
3 points - PE most likely diagnosis
C
Cancer active
1 point - treatment within 6 months or palliative
H
Hemoptysis
1 point - blood in sputum
3
3 points - Clinical DVT signs
Leg swelling and deep vein tenderness = 3 points
3
3 points - Surgery/immobilization
3 points - surgery or bedridden within 4 weeks
1.5
1.5 points - Heart rate/prior VTE
HR greater than 100 or prior VTE = 1.5 each

Memory Hook:PEACH 3-3-1.5: Score less than 4 = PE unlikely (D-dimer), score 4+ = PE likely (CTPA). Remember Prior DVT, Elevated HR, Alternative unlikely, Cancer, Hemoptysis!

Mnemonic

PERC 8PERC Rule (PE Rule-Out Criteria)

P
Pulse less than 100
Heart rate must be less than 100 bpm
E
Estrogen not used
Not on oral contraceptives or HRT
R
Recent surgery/trauma absent
No surgery or trauma in past 4 weeks
C
Coughing up blood absent
No hemoptysis
8
8 criteria ALL must be negative
Age less than 50, O2 sat 95%+, no prior VTE, no unilateral leg swelling

Memory Hook:If ALL 8 PERC criteria negative AND low clinical suspicion, PE excluded - NO D-dimer needed! Saves unnecessary testing.

Mnemonic

H-R-SMassive vs Submassive vs Low-Risk PE

H
High-risk (Massive)
Hemodynamic instability - SBP less than 90 mmHg, shock, arrest. THROMBOLYSE!
R
Right ventricle dysfunction (Submassive)
Normotensive BUT RV strain on echo or elevated troponin/BNP. Anticoagulate, watch closely
S
Stable (Low-risk)
Normotensive, no RV dysfunction, stable. Anticoagulate, consider outpatient

Memory Hook:H-R-S: High-risk needs thrombolysis, RV dysfunction needs monitoring, Stable can go home!

Overview and Clinical Significance

Why PE is Critical in Orthopaedic Surgery

Pulmonary embolism is the LEADING cause of preventable perioperative death in orthopaedic surgery. THA and TKA have 10-20% PE risk without prophylaxis. With modern prophylaxis, risk is 0.5-2% but still significant. Early recognition and treatment are life-saving.

PE Epidemiology

  • Incidence: 60-100 per 100,000 population annually
  • Ortho surgery (with prophylaxis): 0.5-2%
  • THA/TKA (without prophylaxis): 10-20%
  • Peak: Days 3-7 postoperatively
  • Mortality: 2-8% overall, 30% if massive PE untreated
  • Fatal PE: Often first presentation (25% sudden death)

Consequences of PE

  • Massive PE: 30% mortality if untreated, 10% with thrombolysis
  • Submassive PE: 10-15% deterioration to massive
  • Post-PE syndrome: Chronic dyspnea 50% at 1 year
  • Chronic thromboembolic pulmonary hypertension (CTEPH): 2-4%
  • Recurrent VTE: 10-30% over 5 years if inadequately treated

Pathophysiology

Mechanism of Pulmonary Embolism

PE results from venous thrombus (95% from lower limb DVT) embolizing to pulmonary circulation:

1. Thrombus Formation (Virchow's Triad):

  • Venous stasis (immobility, surgery)
  • Endothelial injury (surgical trauma, central lines)
  • Hypercoagulability (inflammatory response, cancer, thrombophilia)

2. Embolization:

  • Thrombus breaks off from DVT (usually proximal leg veins)
  • Travels through IVC and right heart
  • Lodges in pulmonary arteries (lobar, segmental, or subsegmental)

3. Hemodynamic Effects:

  • Small PE: Minimal effect, may be asymptomatic
  • Moderate PE: Ventilation-perfusion mismatch, hypoxia, tachycardia
  • Massive PE: Acute RV failure from sudden afterload increase, cardiogenic shock

4. Gas Exchange Impairment:

  • Dead space ventilation (ventilation without perfusion)
  • Hypoxemia from V/Q mismatch
  • Hyperventilation and hypocapnia (initially)
  • Atelectasis from surfactant depletion

RV Failure in Massive PE

Massive PE causes acute RV failure because the thin-walled RV cannot generate sufficient pressure to overcome sudden increase in pulmonary vascular resistance. RV dilatation impairs LV filling (ventricular interdependence), reducing cardiac output and causing cardiogenic shock.

Orthopaedic Surgery Risk Factors

Why orthopaedic surgery is very high risk for PE:

  • Prolonged immobility: Pre-op, intra-op (anesthesia), post-op
  • Direct vascular trauma: Hip and knee surgery near large veins
  • Bone marrow embolization: Fat and marrow emboli activate coagulation
  • Cement polymerization: Thermal injury, microemboli
  • Tourniquet use: Ischemia-reperfusion injury, endothelial damage
  • Inflammatory response: Massive cytokine release activates coagulation cascade

Risk by Procedure (without prophylaxis):

  • THA: 10-20% symptomatic PE, 0.5-1% fatal PE
  • TKA: 10-20% symptomatic PE, 0.3-0.7% fatal PE
  • Hip fracture surgery: 10-15% PE
  • Spine surgery: 2-5% PE
  • Arthroscopy: Less than 1% PE (but still occurs)

Classification

PE Risk Stratification Classification

Hemodynamic Classification (Primary):

  • Massive (High-Risk): Sustained hypotension (SBP less than 90 mmHg for 15+ minutes), cardiac arrest, or cardiogenic shock
  • Submassive (Intermediate-Risk): Normotensive BUT RV dysfunction on echo/CT OR elevated troponin/BNP
  • Low-Risk: Normotensive, no RV dysfunction, normal biomarkers

Anatomical Classification:

  • Saddle PE: Thrombus at bifurcation of main pulmonary artery
  • Central PE: Main or lobar pulmonary arteries
  • Segmental/Subsegmental PE: Peripheral branches

Temporal Classification:

  • Acute PE: New thrombus, fresh clot
  • Chronic thromboembolic disease: Organized thrombus, may lead to CTEPH

Advanced Classification Considerations

ESC 2019 Classification:

  • Integrates hemodynamics, RV dysfunction markers, and clinical risk scores
  • Guides treatment intensity and monitoring requirements

PESI Score Categories:

  • Class I (less than 65 points): Very low risk, less than 1% 30-day mortality
  • Class II (66-85 points): Low risk
  • Class III (86-105 points): Intermediate risk
  • Class IV (106-125 points): High risk
  • Class V (greater than 125 points): Very high risk, 10-25% 30-day mortality

Exam Viva Point

Classification drives treatment: Massive PE = thrombolysis indicated. Submassive PE = anticoagulation with close monitoring for deterioration. Low-risk PE = anticoagulation, consider outpatient if PESI Class I-II.

PE Classification and Treatment

CategoryKey FeaturesTreatment Approach
MassiveSBP less than 90, shock, arrestThrombolysis + heparin
SubmassiveNormotensive, RV dysfunction or elevated biomarkersAnticoagulation, monitor closely, rescue thrombolysis if deteriorates
Low-RiskNormotensive, no RV dysfunctionAnticoagulation, PESI-guided outpatient if appropriate

Clinical Presentation

PE Presentation is Highly Variable

25% of fatal PE present with sudden death without prior symptoms. Symptoms range from none (incidental finding) to sudden cardiovascular collapse. Maintain high index of suspicion in postoperative orthopaedic patients.

Symptoms (Nonspecific)

SymptomFrequencyClinical Notes
Dyspnea (sudden onset)80-90%Most common - often pleuritic
Pleuritic chest pain50-70%Sharp, worse with inspiration (pleural irritation)
Cough40-50%Dry or productive
Hemoptysis10-20%Blood-streaked sputum (pulmonary infarction)
Syncope10-15%Suggests massive PE with hypotension
Leg pain/swelling30-40%Concurrent DVT

Classic triad (dyspnea, pleuritic pain, hemoptysis) occurs in less than 20% of cases.

Signs

SignFrequencySignificance
Tachypnea (RR greater than 20)70-80%Most sensitive sign
Tachycardia (HR greater than 100)40-60%Compensatory response to hypoxia
Hypoxemia (O2 sat less than 95%)50-70%V/Q mismatch
Hypotension (SBP less than 90)5-10%MASSIVE PE - RV failure
Elevated JVP20-30%RV dysfunction
DVT signs (unilateral leg swelling)30-40%Source of embolus

Clinical Syndromes

Massive (High-Risk) PE

Definition: Sustained hypotension (SBP less than 90 mmHg for 15+ minutes) OR requiring inotropes OR cardiac arrest OR cardiogenic shock.

Clinical Features:

  • Severe dyspnea, often unable to speak
  • Hypotension, cold peripheries
  • Altered mental status (confusion from poor perfusion)
  • Cyanosis
  • Elevated JVP, RV gallop
  • ECG: Sinus tachycardia, S1Q3T3 pattern (25%)

Mortality: 30% if untreated, 10% with thrombolysis.

Management: THROMBOLYSIS (alteplase) + anticoagulation. Surgical embolectomy if thrombolysis contraindicated.

This is a medical emergency requiring immediate action.

Submassive (Intermediate-Risk) PE

Definition: Normotensive (SBP greater than 90 mmHg) BUT evidence of RV dysfunction or myocardial injury.

Criteria for RV dysfunction:

  • Echo: RV dilatation (RV/LV ratio greater than 0.9), RV hypokinesis
  • CT: RV/LV ratio greater than 1.0 on axial images
  • BNP greater than 90 pg/mL or NT-proBNP greater than 500 pg/mL
  • Troponin elevation

Clinical Features:

  • Dyspnea, pleuritic pain
  • Tachycardia, tachypnea
  • Normal blood pressure (key difference from massive)
  • May have elevated JVP, RV heave

Risk: 10-15% will deteriorate to massive PE.

Management: Anticoagulation. Close monitoring for hemodynamic deterioration. Consider thrombolysis if deteriorating (rescue thrombolysis). PEITHO trial showed routine thrombolysis reduces hemodynamic collapse but increases bleeding - NOT routinely recommended.

Low-Risk PE

Definition: Normotensive (SBP greater than 90 mmHg) AND no RV dysfunction AND stable.

Clinical Features:

  • Mild dyspnea or pleuritic pain
  • Normal vital signs (may have mild tachycardia)
  • No RV dysfunction on echo
  • Normal troponin and BNP

Mortality: Less than 1% with anticoagulation.

Management: Anticoagulation only. If PESI score low risk, can be managed outpatient with rivaroxaban or apixaban (oral from day 1).

PESI Score: Pulmonary Embolism Severity Index. Score less than 85 (Class I-II) = low risk, suitable for outpatient management if no other contraindications.

Diagnostic Approach

Clinical Probability Assessment is First Step

Never order CTPA without first assessing pretest probability. Use PERC rule (very low suspicion) or Wells score (low to high suspicion) to determine who needs D-dimer vs CTPA. This reduces unnecessary radiation and contrast exposure.

PE Diagnostic Algorithm

Step 1Assess Clinical Probability

Very low suspicion AND all PERC criteria negative? PE excluded, stop. Otherwise calculate Wells score for PE.

Step 2A (Low Wells)D-dimer if Wells less than 4

If Wells 0-3 (PE unlikely), check D-dimer. If NEGATIVE - PE excluded (99% NPV). If POSITIVE - proceed to CTPA.

Step 2B (High Wells)CTPA if Wells 4+

If Wells 4+ (PE likely), skip D-dimer and go directly to CTPA. D-dimer has low utility when pretest probability is high.

Step 3CTPA or VQ Scan

CTPA is gold standard (95% sensitive). VQ scan if contrast contraindicated. If positive, risk stratify (massive/submassive/low-risk).

Step 4Risk Stratification

Check BP, echo (RV function), troponin, BNP. Classify as massive (thrombolyse), submassive (anticoagulate + monitor), or low-risk (anticoagulate +/- outpatient).

PERC Rule (PE Rule-Out Criteria)

If ALL 8 criteria are NEGATIVE AND clinical suspicion is LOW, PE is excluded (no D-dimer needed):

  1. Age less than 50 years
  2. Heart rate less than 100 bpm
  3. Oxygen saturation 95% or greater on room air
  4. No hemoptysis
  5. No estrogen use (OCP, HRT)
  6. No prior DVT or PE
  7. No unilateral leg swelling
  8. No surgery or trauma requiring hospitalization in past 4 weeks

Only use PERC if suspicion is LOW. If ANY criterion positive OR suspicion moderate/high, proceed to Wells score.

Wells Score for PE

Clinical FeaturePoints
Clinical signs of DVT (leg swelling + tenderness)+3
Alternative diagnosis less likely than PE+3
Heart rate greater than 100 bpm+1.5
Immobilization (3+ days) or surgery in past 4 weeks+1.5
Previous DVT or PE+1.5
Hemoptysis+1
Active cancer (treatment within 6 months or palliative)+1

Interpretation:

  • Score 0-3: PE unlikely (15% prevalence) - check D-dimer
  • Score 4+: PE likely (40% prevalence) - skip D-dimer, go to CTPA

Investigations

D-dimer Testing

Principle: D-dimer is fibrin degradation product elevated in VTE. High sensitivity (95-98%) but low specificity (40-60%).

When D-dimer is Useful

  • Low Wells score (less than 4)
  • Negative D-dimer = PE excluded
  • High negative predictive value (99%)
  • Avoids unnecessary CTPA (radiation + contrast)

When D-dimer is NOT Useful

  • High Wells score (4+) - go to CTPA
  • Postoperative patients - often elevated
  • Cancer, pregnancy, elderly - often elevated
  • Positive D-dimer does NOT diagnose PE

Interpretation:

  • Negative D-dimer + Low Wells: PE excluded, no CTPA needed
  • Positive D-dimer: Proceed to CTPA (does NOT confirm PE)
  • In postop ortho patients: Often falsely elevated - CTPA may be needed regardless

Age-adjusted D-dimer: In patients over 50, use cutoff of (age x 10) instead of 500 ng/mL to improve specificity.

CT Pulmonary Angiography (Gold Standard)

Technique: IV contrast-enhanced CT timed for pulmonary artery opacification. Direct visualization of thrombus as filling defect.

FeatureValue
Sensitivity95%
Specificity98%
Positive findingFilling defect in pulmonary artery
AdvantagesFast, widely available, visualizes alternative diagnoses
DisadvantagesRadiation, contrast nephropathy, allergic reactions

Findings:

  • Central PE: Thrombus in main or lobar pulmonary arteries (high mortality risk)
  • Segmental/subsegmental PE: Peripheral thrombus (lower risk)
  • RV/LV ratio greater than 1.0: RV dysfunction (submassive PE)
  • Reflux of contrast into IVC: Severe RV dysfunction

Contraindications:

  • Severe renal impairment (CrCl less than 30) - use VQ scan
  • Contrast allergy - use VQ scan or MR angiography
  • Pregnancy - VQ scan preferred (lower fetal radiation)

Ventilation-Perfusion (VQ) Scan

Indication: Alternative to CTPA when contrast contraindicated (renal failure, severe allergy, pregnancy).

Technique:

  • Perfusion: IV radiotracer shows pulmonary blood flow
  • Ventilation: Inhaled radiotracer shows air distribution
  • PE causes: Perfusion defect with normal ventilation (V/Q mismatch)

Interpretation (PIOPED II criteria):

  • Normal: PE excluded
  • High probability: 2+ large mismatched defects - PE very likely (treat)
  • Low probability: Small defects, matched defects
  • Intermediate: Non-diagnostic - need further imaging (CTPA if possible)

Limitations:

  • 30-50% are non-diagnostic (intermediate probability)
  • Less accurate in pre-existing lung disease (COPD, pneumonia)
  • Does not provide anatomic detail

Advantages:

  • No contrast needed
  • Lower radiation than CTPA in pregnancy

Additional Investigations

ECG (non-specific, helps rule out MI):

  • Sinus tachycardia (most common - 70%)
  • S1Q3T3 pattern (S wave lead I, Q wave + inverted T in lead III) - 25% of PE
  • Right bundle branch block (acute RV strain)
  • T wave inversion V1-V4 (RV strain)

Chest X-ray (normal in 30%, helps rule out alternative diagnoses):

  • Westermark sign: Oligemia (decreased vascular markings) distal to embolus
  • Hampton hump: Wedge-shaped pleural-based opacity (pulmonary infarction)
  • Palla sign: Enlarged right descending pulmonary artery

Arterial Blood Gas (non-specific):

  • Hypoxemia (PaO2 less than 80 mmHg)
  • Hypocapnia (PaCO2 less than 35 mmHg) from hyperventilation
  • Respiratory alkalosis
  • A-a gradient elevated

Echocardiography (not diagnostic but assesses RV function):

  • RV dilatation (RV/LV ratio greater than 0.9)
  • RV hypokinesis
  • Tricuspid regurgitation, elevated RV systolic pressure
  • McConnell sign: RV free wall hypokinesis with apical sparing (specific for PE)
  • Rarely: Direct visualization of thrombus in right heart or pulmonary arteries

Biomarkers (risk stratification, not diagnostic):

  • Troponin: Elevated in 30-50% of PE (myocardial strain) - worse prognosis
  • BNP/NT-proBNP: Elevated in RV dysfunction
  • Help stratify submassive PE

Lower Limb Venous Duplex (DVT Source Identification):

  • Not required for PE diagnosis but identifies source
  • Concurrent DVT present in 30-40% of PE patients
  • May guide anticoagulation duration
  • Useful if bilateral leg symptoms or recurrent VTE

Deep Vein Thrombosis Imaging (Source Identification)

95% of PE arises from lower limb DVT. Identifying concurrent DVT confirms the VTE diagnosis and may influence treatment duration.

Duplex ultrasound demonstrating deep vein thrombosis
Click to expand
Duplex ultrasound scan demonstrating acute deep vein thrombosis (DVT) in a patient who subsequently developed pulmonary embolism: (a) Right common femoral vein (CFV) showing absent color flow signal - a non-compressible vein with absent flow is diagnostic of DVT, (b) Right popliteal vein (PopV) also showing absent flow. The extent of DVT (proximal vs distal) has prognostic significance - proximal DVT (above knee) has higher risk of embolization to the pulmonary circulation.Credit: Nasrin S et al., J Med Case Rep - PMC4827182 (CC-BY)
Multimodal DVT imaging after orthopaedic surgery
Click to expand
Deep vein thrombosis diagnosed after simultaneous left total hip and knee arthroplasty: (A-B) Duplex sonography demonstrating calf vein DVT - without compression (A) the vein is visible, with compression (B) the vein fails to collapse (non-compressible = positive for DVT), (C) Coronal CT venography confirming thrombus in the calf veins (arrows). CT venography is increasingly performed combined with CTPA as a single contrast injection can image both pulmonary arteries and leg veins.Credit: Byun SS et al., Korean J Radiol - PMC2627179 (CC-BY)

Compression Ultrasound Technique:

  • Gold standard for DVT diagnosis - sensitivity 95%, specificity 96%
  • Two-point compression: common femoral and popliteal veins
  • Non-compressible vein = DVT (thrombus prevents collapse)
  • Color Doppler shows absent or reduced flow

Risk Stratification

Risk Stratification Determines Treatment

ALL confirmed PE patients must be risk stratified to determine if they need thrombolysis (massive), close monitoring (submassive), or standard anticoagulation (low-risk). This is NOT just for prognosis - it directly impacts treatment decisions.

PE Risk Stratification

CategoryHemodynamicsRV DysfunctionBiomarkersMortalityTreatment
Massive (High-Risk)SBP less than 90 mmHg or shock or arrestUsually presentUsually elevated30% untreatedTHROMBOLYSIS + anticoagulation
Submassive (Intermediate)SBP greater than 90 mmHg (normotensive)Present (echo or CT)Troponin or BNP elevated10-15% deteriorationAnticoagulation + close monitoring, rescue thrombolysis if deteriorates
Low-RiskSBP greater than 90 mmHg (stable)AbsentNormalLess than 1%Anticoagulation, consider outpatient if PESI low

Assessing RV Dysfunction (for Submassive PE)

Echocardiography:

  • RV dilatation: RV/LV diameter ratio greater than 0.9 (apical 4-chamber view)
  • RV hypokinesis
  • McConnell sign (RV free wall hypokinesis with apical sparing)

CT:

  • RV/LV diameter ratio greater than 1.0 on axial images

Biomarkers:

  • BNP greater than 90 pg/mL or NT-proBNP greater than 500 pg/mL
  • Troponin I greater than 0.4 ng/mL

If ANY of the above present with normotensive patient = submassive PE.

Management Algorithm

Start Anticoagulation Immediately

Once PE is diagnosed (or strongly suspected while awaiting CTPA), start anticoagulation immediately. Delays increase mortality. Choice of agent depends on hemodynamic status, bleeding risk, and renal function.

Anticoagulant Options for PE

AgentAdvantagesDisadvantagesAustralian Context
Rivaroxaban/Apixaban (DOACs)Oral from day 1, no monitoring, no LMWH lead-inCost, renal impairment, limited reversalPBS approved, first-line
LMWH + WarfarinCheap, reversible, familiarLMWH injections, INR monitoring, drug interactionsTraditional approach, still used
IV Unfractionated HeparinReversible (short half-life), can use in renal failureIV access needed, monitoring (aPTT), HIT riskUsed in massive PE, perioperatively
LMWH aloneNo monitoring, predictableInjections, expensive long-termCancer-associated PE

Direct Oral Anticoagulants (First-Line for Stable PE)

Rivaroxaban:

  • 15mg BD for 21 days, then 20mg daily
  • No LMWH lead-in needed
  • Reduce to 15mg daily if CrCl 30-50
  • Avoid if CrCl less than 30

Apixaban:

  • 10mg BD for 7 days, then 5mg BD
  • No LMWH lead-in needed
  • Reduce to 2.5mg BD if 2 of: age greater than 80, weight less than 60kg, creatinine greater than 133
  • Avoid if CrCl less than 30

Advantages: Oral from day 1, predictable, no monitoring, easier than warfarin, similar efficacy, lower bleeding risk.

Use for: Low-risk and submassive PE (after ruling out need for thrombolysis).

Do NOT use for: Massive PE (use IV heparin initially), CrCl less than 30, active bleeding, mechanical valve, antiphospholipid syndrome.

Unfractionated Heparin (Massive PE or High Bleeding Risk)

Indication: Massive PE, perioperative period, renal failure (CrCl less than 30), high bleeding risk (need reversibility).

Protocol:

  • Bolus: 80 units/kg IV (max 10,000 units)
  • Infusion: 18 units/kg/hour (max 1,800 units/hour)
  • Target aPTT: 1.5-2.5 times control (60-80 seconds)
  • Check aPTT every 6 hours until stable, then daily

Advantages: Short half-life (reversible with protamine), can use in renal failure.

Disadvantages: IV access required, frequent monitoring, heparin-induced thrombocytopenia (HIT) risk 1-5%.

LMWH (Alternative to UFH)

Enoxaparin: 1mg/kg SC every 12 hours OR 1.5mg/kg daily Dalteparin: 200 units/kg SC daily (max 18,000 units)

Advantages: SC administration, no monitoring, lower HIT risk. Disadvantages: Cannot use if CrCl less than 30 (accumulation).

Warfarin + LMWH Bridging (if DOAC contraindicated)

Warfarin Initiation

LMWH + WarfarinDay 1-5

Start LMWH (enoxaparin 1mg/kg BD) AND warfarin 5-10mg daily. Check baseline INR.

INR MonitoringDay 3-7

Check INR daily. Adjust warfarin to target INR 2-3. Continue LMWH until INR greater than 2 for 2 consecutive days.

Stop LMWHDay 5-10

Once INR therapeutic (2-3) for 2 days, stop LMWH. Continue warfarin long-term with regular INR monitoring.

Monitoring: INR weekly until stable, then monthly.

Why not first-line: More complicated than DOACs, requires monitoring, many drug and food interactions.

Treatment Duration

VTE TypeDurationRationale
Provoked (surgery)3 monthsTransient risk factor removed, low recurrence risk (1-3% annually)
Unprovoked first3-6 months minimumAssess bleeding vs recurrence risk. May extend if low bleeding risk
Recurrent unprovokedIndefiniteHigh recurrence risk (15% annually if stopped)
Active cancerIndefinite (while active)Ongoing hypercoagulable state, high recurrence

Post-Surgical PE is Provoked

PE occurring after orthopaedic surgery is PROVOKED (transient risk factor). Treat for 3 months only. Lower recurrence risk (1-3% annually) vs unprovoked PE. Do NOT anticoagulate indefinitely.

Thrombolysis for Massive PE

Thrombolysis Saves Lives in Massive PE

Massive PE has 30% mortality if treated with anticoagulation alone vs 10% with thrombolysis. If patient has sustained hypotension (SBP less than 90 mmHg) or cardiogenic shock, give alteplase 50-100mg IV over 2 hours IMMEDIATELY after confirming PE on CTPA.

Indications for Thrombolysis

Absolute indication (Massive PE):

  • Sustained hypotension (SBP less than 90 mmHg for 15+ minutes) AND confirmed PE
  • Cardiac arrest due to PE
  • Cardiogenic shock

Relative indication (Submassive PE - controversial):

  • Normotensive BUT severe RV dysfunction AND deteriorating clinically
  • PEITHO trial showed routine thrombolysis in submassive PE reduces hemodynamic collapse (2% vs 5%) but increases major bleeding (11% vs 2%) and stroke (2% vs 0.2%)
  • Current recommendation: Anticoagulation for submassive, rescue thrombolysis only if deteriorates

Thrombolytic Agents

AgentDoseNotes
Alteplase (tPA)100mg IV over 2 hours OR 50mg bolus (if arrest)First-line, most evidence
Tenecteplase30-50mg IV bolus (weight-based)Single bolus, easier administration
Streptokinase1.5 million units over 2 hoursRarely used (antigenic, allergic reactions)

Give heparin concurrently (bolus + infusion as per protocol).

Contraindications to Thrombolysis

Contraindications

AbsoluteRelative
Active bleedingRecent minor bleeding (less than 10 days)
Intracranial hemorrhage (ever)Recent major surgery (10-14 days)
Ischemic stroke within 3 monthsIschemic stroke greater than 3 months ago
Neurosurgery or head trauma within 3 monthsMajor trauma
Brain tumor, arteriovenous malformationCPR greater than 10 minutes
Pregnancy, first week postpartum
Uncontrolled hypertension (SBP greater than 180)

If absolute contraindication: Consider surgical embolectomy or catheter-directed thrombolysis.

Complications of Thrombolysis

ComplicationIncidenceManagement
Major bleeding10-15%Stop thrombolytic, transfuse, consider reversal (cryoprecipitate, TXA)
Intracranial hemorrhage1-5%STOP thrombolytic, reverse, neurosurgical consultation
Minor bleeding20-30%Local pressure, monitor
Allergic reaction (streptokinase)5-10%Antihistamines, steroids, switch to alteplase

Intracranial hemorrhage is the most feared complication - occurs in 1-5%. Risk higher in elderly, uncontrolled HTN, prior stroke.

Management Algorithm

📊 Management Algorithm
Pulmonary Embolism Management Algorithm
Click to expand

Management Summary

Immediate Management (All PE):

  • Oxygen supplementation to maintain SpO2 greater than 94%
  • IV access and cardiac monitoring
  • Assess hemodynamic status and risk stratify

Treatment by Risk Category:

  • Massive PE: Thrombolysis (alteplase 100mg over 2 hours) + heparin anticoagulation
  • Submassive PE: Anticoagulation + close monitoring, rescue thrombolysis if deterioration
  • Low-Risk PE: Anticoagulation alone, consider outpatient with PESI Class I-II

Anticoagulation Selection:

  • DOACs (rivaroxaban, apixaban): First-line for stable PE
  • LMWH: Perioperative patients, cancer, renal impairment
  • UFH infusion: Massive PE (easily reversible)

Advanced Management Considerations

Treatment Duration:

  • Provoked PE (post-surgery): 3 months
  • First unprovoked PE: 3-6 months, consider extended if low bleeding risk
  • Recurrent unprovoked PE: Indefinite
  • Cancer-associated PE: Indefinite while cancer active

Escalation Options:

  • Catheter-directed thrombolysis: Lower bleeding risk than systemic
  • Surgical embolectomy: Contraindication to thrombolysis
  • ECMO: Bridge therapy in refractory shock

Exam Viva Point

Post-surgical PE is provoked: Duration is 3 months only. Recurrence risk is low (1-3% annually) after stopping anticoagulation. Do NOT anticoagulate indefinitely for provoked PE.

Anticoagulation Duration

VTE TypeDurationRecurrence Risk After Stopping
Provoked (surgery)3 months1-3% annual
First unprovoked3-6 months minimum10-15% annual if stopped
Recurrent unprovokedIndefinite30%+ if stopped
Cancer-associatedIndefinite while activeVery high

Surgical and Interventional Options

Surgical Pulmonary Embolectomy

Indication: Massive PE with absolute contraindication to thrombolysis OR failed thrombolysis.

Procedure:

  • Median sternotomy
  • Cardiopulmonary bypass
  • Direct removal of thrombus from pulmonary arteries via pulmonary arteriotomy

Outcomes:

  • Mortality 30-50% (very sick patients)
  • Success depends on speed of intervention
  • Reserved for last resort

Availability: Only at tertiary cardiac surgery centers.

Catheter-Directed Thrombolysis or Thrombectomy

Techniques:

  • Catheter-directed thrombolysis: Local delivery of tPA via catheter into pulmonary arteries (lower systemic dose, less bleeding)
  • Catheter thrombectomy: Mechanical extraction of thrombus (AngioVac, FlowTriever devices)

Indications:

  • Massive PE with high bleeding risk (relative contraindication to systemic thrombolysis)
  • Submassive PE deteriorating despite anticoagulation

Advantages: Lower thrombolytic dose, less bleeding than systemic tPA.

Disadvantages: Requires interventional radiology expertise, not widely available.

Evidence: Emerging modality, limited RCT data. Case series show promise.

Extracorporeal Membrane Oxygenation (ECMO)

Indication: Massive PE with cardiac arrest or refractory shock as bridge to definitive therapy (thrombolysis or embolectomy).

Role: Temporary cardiopulmonary support while clot resolves.

Outcomes: Case series show survival 30-50% in PE arrest patients.

Availability: Only at ECMO-capable centers.

IVC Filters - Evidence and Indications

IVC Filters Do NOT Prevent PE Death

The PREPIC trial clearly showed IVC filters do NOT reduce PE mortality. They prevent recurrent PE in the first 2 weeks but INCREASE the risk of DVT long-term. Only use if absolute contraindication to anticoagulation.

Indications for IVC Filter

Absolute indications (very narrow):

  • Acute VTE with absolute contraindication to anticoagulation (active bleeding, recent intracranial hemorrhage, recent neurosurgery)
  • Recurrent VTE despite therapeutic anticoagulation (documented compliance + therapeutic levels)

Relative indications (controversial, generally NOT recommended):

  • Free-floating IVC or iliofemoral thrombus (no good evidence)
  • Very limited cardiopulmonary reserve where any PE would be fatal (debated)

NOT indicated:

  • Primary prophylaxis in high-risk patients (ortho surgery, trauma) - use chemical prophylaxis instead
  • PE with contraindication to thrombolysis (can still anticoagulate)

Evidence Against Routine IVC Filters

PREPIC Trial (1998):

  • RCT of IVC filter + anticoagulation vs anticoagulation alone in DVT patients
  • Filter group: Lower PE at 12 days (1.1% vs 4.8%)
  • BUT: Increased DVT at 2 years (21% vs 12%)
  • NO difference in mortality at 2 years or 8 years

Implication: Filters prevent early PE but cause more DVT. Net benefit is ZERO. Only use if cannot anticoagulate at all.

Types of IVC Filters

TypeIndicationNotes
Retrievable (removable)Temporary contraindication to anticoagulationShould be removed within 2-4 weeks once anticoagulation starts
PermanentPermanent contraindication to anticoagulationRarely needed

Always use retrievable filters and set removal date. Many are left in permanently by mistake.

VTE Prophylaxis in Orthopaedic Surgery

VTE Prophylaxis is Mandatory

All orthopaedic surgery patients require VTE prophylaxis unless absolute contraindication. The goal is to reduce VTE risk from 10-20% to 0.5-2%. Use mechanical (TED stockings, intermittent pneumatic compression) PLUS chemical prophylaxis (LMWH, fondaparinux, rivaroxaban, or aspirin).

Risk Assessment

High-risk procedures (require extended prophylaxis):

  • Total hip arthroplasty (THA): 28-35 days
  • Total knee arthroplasty (TKA): 10-14 days
  • Hip fracture surgery: 28-35 days
  • Spine surgery (multilevel, malignancy): 10-14 days

Moderate-risk procedures:

  • Arthroscopy: 7-10 days if other risk factors (age greater than 40, obesity, prior VTE)
  • Upper limb surgery: Generally low risk, prophylaxis only if additional risk factors

Prophylaxis Options

AgentDoseDurationAustralian Context
Enoxaparin (LMWH)40mg SC daily (20mg if weight less than 50kg or CrCl less than 30)28-35d THA, 10-14d TKAPBS approved, widely used
Rivaroxaban10mg PO daily28-35d THA, 10-14d TKAPBS approved, oral convenience
Apixaban2.5mg PO BD28-35d THA, 10-14d TKAPBS approved, oral
Fondaparinux2.5mg SC daily28-35dPBS approved, synthetic pentasaccharide
Aspirin100mg PO daily28-35d (after initial LMWH)Cheaper, ASA trial showed non-inferiority after initial LMWH
WarfarinTarget INR 2-3Rarely used nowReplaced by DOACs

Mechanical prophylaxis:

  • TED stockings (graduated compression stockings)
  • Intermittent pneumatic compression (IPC) devices
  • Early mobilization

Use BOTH mechanical AND chemical unless contraindication.

Timing of Prophylaxis

First dose:

  • LMWH/fondaparinux: 12 hours post-op (NOT pre-op if neuraxial anesthesia planned - epidural hematoma risk)
  • Rivaroxaban/apixaban: 6-10 hours post-op (once hemostasis achieved)
  • Aspirin: Post-op day 1

Neuraxial anesthesia (spinal/epidural) considerations:

  • LMWH given pre-op requires 12-24 hour gap before neuraxial
  • LMWH given post-op requires 12 hour gap before catheter removal
  • DOACs require 24 hour gap before neuraxial

Contraindications to Chemical Prophylaxis

Absolute:

  • Active bleeding
  • Severe bleeding risk (e.g., bleeding peptic ulcer, recent intracranial hemorrhage)
  • HIT with thrombosis (cannot use heparin-based agents)

Relative:

  • Recent neurosurgery or ophthalmologic surgery (balance risk vs benefit)
  • Platelets less than 50,000 (relative, depends on bleeding risk)
  • Severe renal impairment (avoid LMWH/fondaparinux, use UFH or reduce dose)

If contraindication: Use mechanical prophylaxis alone, consider IVC filter if very high risk (NOT routinely recommended).

Complications and Long-Term Sequelae

Acute Complications of PE

ComplicationIncidenceManagement
Death (massive PE)10-30%Thrombolysis reduces to 10%
Cardiogenic shock5-10%Thrombolysis, inotropes, consider ECMO
Cardiac arrest2-5%CPR, thrombolysis, consider ECMO
Recurrent PE5-10% if inadequate anticoagulationEnsure therapeutic anticoagulation, consider IVC filter if recurrent despite therapy
Bleeding from anticoagulation1-3% major bleed annuallyReversal agents, transfusion

Chronic Complications

Chronic Thromboembolic Pulmonary Hypertension (CTEPH):

  • Incidence: 2-4% of PE survivors
  • Pathophysiology: Unresolved thrombus causes chronic pulmonary artery obstruction and pulmonary hypertension
  • Presentation: Progressive dyspnea, exercise intolerance, right heart failure
  • Diagnosis: RV systolic pressure greater than 25 mmHg on echo, confirmed by right heart catheterization + V/Q scan showing perfusion defects
  • Treatment: Pulmonary thromboendarterectomy (surgical removal of organized thrombus) OR balloon pulmonary angioplasty OR pulmonary vasodilators (sildenafil, riociguat)
  • Screen for CTEPH if persistent dyspnea 3-6 months post-PE

Post-PE Syndrome:

  • Chronic dyspnea without pulmonary hypertension
  • Incidence: 50% at 1 year
  • Cause: Deconditioning, anxiety, subclinical RV dysfunction
  • Management: Pulmonary rehabilitation, exercise training

Recurrent VTE:

  • 10% first year (unprovoked), 1-3% annual (provoked)
  • Prevention: Appropriate duration anticoagulation
  • Risk factors for recurrence: Unprovoked PE, residual thrombus, thrombophilia, cancer

Postoperative Care

Post-PE Monitoring

Inpatient Monitoring by Severity:

  • Massive PE: ICU admission, continuous monitoring
  • Submassive PE: HDU/step-down for 24-48 hours
  • Low-risk PE: Ward care or outpatient if PESI Class I-II

Clinical Monitoring:

  • Vital signs every 4-6 hours
  • Oxygen saturation target greater than 94%
  • Watch for deterioration (dropping BP, worsening dyspnea)

Anticoagulation Monitoring:

  • DOACs: No routine monitoring required
  • Warfarin: INR target 2-3, weekly until stable
  • LMWH: Anti-Xa levels if renal impairment or extreme weight

Advanced Post-PE Follow-Up

Outpatient Follow-Up Schedule:

  • 2-4 weeks: Clinic review, compliance check
  • 3 months: Assess symptoms, decide anticoagulation duration
  • 6 months: If persistent dyspnea, screen for CTEPH

CTEPH Screening:

  • Suspect if persistent dyspnea 3+ months post-PE
  • Echo for pulmonary hypertension
  • V/Q scan for perfusion defects
  • Right heart catheterization to confirm

Exam Viva Point

CTEPH screening: Chronic thromboembolic pulmonary hypertension affects 2-4% of PE survivors. If patient remains dyspneic at 3-6 months, screen with echo and V/Q scan. CTEPH is treatable with pulmonary thromboendarterectomy.

Follow-Up Protocol

TimepointAssessmentAction
2-4 weeksCompliance, bleedingAdjust anticoagulation if needed
3 monthsSymptoms, decision pointStop if provoked, continue if unprovoked
6 monthsPersistent symptomsScreen for CTEPH

Outcomes

PE Outcomes Summary

Short-Term Mortality:

  • Massive PE untreated: 30%
  • Massive PE with thrombolysis: 10%
  • Submassive PE: 3-15%
  • Low-risk PE: Less than 1%

Recurrence Rates:

  • Provoked PE (post-surgery): 1-3% annual after stopping anticoagulation
  • Unprovoked PE: 10-15% annual if anticoagulation stopped

Long-Term Sequelae:

  • CTEPH: 2-4% of PE survivors
  • Post-PE syndrome: 50% have persistent dyspnea at 1 year
  • Bleeding from anticoagulation: 1-3% major bleed annually

Advanced Outcome Considerations

Prognostic Factors:

  • Favorable: Provoked PE, young age, no RV dysfunction, low PESI
  • Unfavorable: Massive PE, cancer, recurrent VTE, elevated troponin

Treatment Outcome Data:

  • Thrombolysis in massive PE: Absolute mortality reduction 20%
  • DOACs vs warfarin: Similar efficacy, lower bleeding with DOACs
  • Extended anticoagulation: Reduces recurrence but increases bleeding

Exam Viva Point

Provoked vs unprovoked outcomes: Provoked PE (post-surgery) has excellent prognosis with 1-3% annual recurrence after 3 months anticoagulation. Unprovoked PE has much higher recurrence (10-15% annually) - consider extended anticoagulation.

Outcome by PE Type

PE Type30-Day MortalityAnnual Recurrence After Stopping
Massive (treated)10%Depends on anticoagulation
Submassive3-15%As per provoked vs unprovoked
Low-riskLess than 1%1-3% provoked, 10-15% unprovoked

Evidence Base

PEITHO Trial - Thrombolysis in Submassive PE

1
Meyer et al. • NEJM (2014)
Key Findings:
  • RCT of 1006 patients with submassive PE (normotensive + RV dysfunction)
  • Tenecteplase vs placebo (both groups received heparin)
  • Thrombolysis reduced hemodynamic decompensation (2.6% vs 5.6%, p=0.015)
  • BUT increased major bleeding (11.5% vs 2.4%) and stroke (2.4% vs 0.2%)
  • No mortality difference at 30 days
Clinical Implication: Routine thrombolysis NOT recommended for submassive PE due to high bleeding risk. Reserve for patients deteriorating despite anticoagulation (rescue thrombolysis).

PREPIC Trial - IVC Filters in DVT

1
Decousus et al. • Circulation (1998)
Key Findings:
  • RCT of 400 DVT patients: IVC filter + anticoagulation vs anticoagulation alone
  • Filter reduced early PE (1.1% vs 4.8% at 12 days)
  • BUT increased DVT at 2 years (20.8% vs 11.6%)
  • NO difference in mortality at 2 years (16.9% vs 15.6%)
  • 8-year follow-up confirmed no mortality benefit
Clinical Implication: IVC filters do NOT reduce PE mortality and cause more DVT. Only use if absolute contraindication to anticoagulation.

EINSTEIN PE Trial - Rivaroxaban vs Warfarin

1
Buller et al. • NEJM (2012)
Key Findings:
  • RCT of 4832 patients with acute PE
  • Rivaroxaban (15mg BD x21d then 20mg daily) vs LMWH + warfarin
  • Non-inferior for recurrent VTE (2.1% vs 1.8%)
  • Similar major bleeding (1.1% vs 2.2%)
  • Oral from day 1 without LMWH bridging
Clinical Implication: Rivaroxaban is effective and safe for PE treatment without LMWH lead-in, making it first-line.

ACCP Guidelines - Antithrombotic Therapy for VTE

1
Kearon et al. • Chest (2016)
Key Findings:
  • DOACs recommended over warfarin for non-cancer PE (Grade 2B)
  • Thrombolysis recommended for massive PE (Grade 2B)
  • Thrombolysis NOT routinely recommended for submassive PE (Grade 2C)
  • Provoked PE: 3 months anticoagulation (Grade 1B)
  • IVC filters only if contraindication to anticoagulation (Grade 1B)
Clinical Implication: Evidence-based guidelines support DOAC as first-line, thrombolysis for massive PE only, and limited use of IVC filters.

Exam Viva Scenarios

Practice these scenarios to excel in your viva examination

VIVA SCENARIOStandard

Scenario 1: Post-THA PE Suspected (~2-3 min)

EXAMINER

"A 70-year-old woman develops sudden onset dyspnea and pleuritic chest pain on day 5 after total hip arthroplasty. Vitals: BP 130/80, HR 110, RR 24, SpO2 92% on room air. How would you assess and manage?"

EXCEPTIONAL ANSWER
This patient has signs concerning for pulmonary embolism postoperatively. My approach: First, stabilize - apply oxygen to maintain SpO2 greater than 94%, establish IV access, and ECG to rule out MI. Second, assess clinical probability using Wells score for PE: she scores at least 4.5 points (surgery within 4 weeks 1.5 points, HR greater than 100 bpm 1.5 points, alternative diagnosis less likely 3 points if PE most likely). With Wells 4+ (PE likely), I would skip D-dimer and proceed directly to CTPA. While awaiting CTPA, I would start empiric anticoagulation with LMWH (enoxaparin 1mg/kg BD) or unfractionated heparin infusion unless contraindication. Third, if CTPA confirms PE, I would risk stratify: check BP (looking for hypotension SBP less than 90 indicating massive PE), echocardiography for RV function, troponin and BNP. Fourth, treatment depends on risk stratification. If massive PE (hypotension), I would give thrombolysis (alteplase 100mg over 2 hours). If submassive (normotensive but RV dysfunction), I would anticoagulate and monitor closely, reserving thrombolysis for deterioration. If low-risk (stable, no RV dysfunction), I would switch to a DOAC (rivaroxaban 15mg BD for 21 days then 20mg daily). Fifth, this is provoked PE (post-surgery), so anticoagulation duration is 3 months. Counsel about bleeding risk and compliance.
KEY POINTS TO SCORE
Wells score 4+ = PE likely, skip D-dimer, go to CTPA
Start empiric anticoagulation while awaiting CTPA
Risk stratify ALL PE patients (massive/submassive/low-risk)
Massive PE (SBP less than 90) = thrombolysis immediately
Provoked PE = 3 months anticoagulation
COMMON TRAPS
✗Ordering D-dimer with high Wells score - wastes time
✗Waiting for CTPA before starting anticoagulation if high suspicion
✗Not risk stratifying - treatment depends on massive vs submassive vs low-risk
✗Thrombolysing all PEs - only massive PE has clear indication
LIKELY FOLLOW-UPS
"What if her BP drops to 80/50 mmHg?"
"What are contraindications to thrombolysis?"
"Would you place an IVC filter?"
VIVA SCENARIOChallenging

Scenario 2: Massive PE Decision-Making (~3-4 min)

EXAMINER

"A 65-year-old man collapses 3 days after hip fracture surgery. On arrival to ED, BP 75/40, HR 130, RR 30, SpO2 85% on high-flow oxygen. CTPA shows large bilateral PE with RV/LV ratio of 1.5. He had neurosurgery for subdural hematoma 6 weeks ago. What is your management?"

EXCEPTIONAL ANSWER
This is a massive PE with cardiogenic shock - a life-threatening emergency. The key decision is whether to thrombolyse given his recent neurosurgery. First, immediate resuscitation: IV fluids cautiously (avoiding overload which worsens RV function), inotropes (noradrenaline) to maintain perfusion, high-flow oxygen, prepare for intubation if deteriorates further. Start unfractionated heparin bolus (80 units/kg) and infusion (18 units/kg/hour) immediately. Second, this is massive PE (sustained hypotension SBP less than 90 mmHg) with RV dysfunction on CT (RV/LV ratio greater than 1.0). Mortality is 30% with anticoagulation alone vs 10% with thrombolysis. The standard treatment would be immediate thrombolysis with alteplase 100mg over 2 hours. However, he has neurosurgery 6 weeks ago, which is a RELATIVE contraindication (absolute contraindication is within 3 months for intracranial surgery). Third, I would urgently contact neurosurgery to discuss risk vs benefit. If they confirm he has healed well and no ongoing intracranial pathology, I would consider thrombolysis as the benefit (saving his life from massive PE) likely outweighs the 1-5% risk of intracranial hemorrhage. If neurosurgery advises against thrombolysis, alternatives include: surgical pulmonary embolectomy (if cardiac surgery available and patient stable enough for transfer), catheter-directed thrombolysis or thrombectomy (lower systemic dose), or ECMO as bridge if available. Fourth, I would NOT place an IVC filter - the PREPIC trial showed filters do not reduce mortality, and he needs anticoagulation anyway. Fifth, ongoing care: ICU monitoring, continue heparin infusion, monitor for bleeding if thrombolysed, echo to assess RV recovery. Once stabilized, transition to DOAC for 3 months (provoked PE).
KEY POINTS TO SCORE
Massive PE (SBP less than 90) needs thrombolysis - mortality benefit clear
Recent neurosurgery (6 weeks) is RELATIVE contraindication (absolute is less than 3 months)
Discuss risk/benefit with neurosurgery - may still thrombolyse if benefit greater than risk
Alternatives if absolute contraindication: surgical embolectomy, catheter-directed therapy, ECMO
IVC filters do NOT reduce mortality - PREPIC trial
COMMON TRAPS
✗Avoiding thrombolysis automatically due to neurosurgery - 6 weeks is relative contraindication, assess individually
✗Not knowing alternative treatments if thrombolysis contraindicated
✗Placing IVC filter thinking it will help - filters do NOT reduce PE mortality
✗Fluid overloading the patient - can worsen RV function
LIKELY FOLLOW-UPS
"What are absolute contraindications to thrombolysis?"
"What is the dose of alteplase for PE?"
"What is the evidence for IVC filters?"
VIVA SCENARIOStandard

Scenario 3: Submassive PE and VTE Prophylaxis (~3-4 min)

EXAMINER

"A 55-year-old woman has confirmed PE on CTPA 1 week after TKA. She is normotensive (BP 125/75) but echo shows RV/LV ratio 1.1 and troponin is elevated. She was on rivaroxaban 10mg daily for prophylaxis but admits she stopped taking it 3 days ago. How do you manage? Also, what prophylaxis protocol should have been used?"

EXCEPTIONAL ANSWER
This is submassive PE (normotensive but RV dysfunction on echo and elevated troponin). First, immediate management: start therapeutic anticoagulation immediately. Since she is hemodynamically stable, I would use rivaroxaban 15mg BD for 21 days then 20mg daily (or apixaban 10mg BD for 7 days then 5mg BD). Check renal function first - if CrCl less than 30, use LMWH plus warfarin instead. Do NOT thrombolyse routinely - the PEITHO trial showed thrombolysis in submassive PE reduces hemodynamic decompensation (2.6% vs 5.6%) but increases major bleeding (11.5% vs 2.4%) and stroke (2.4% vs 0.2%) with no mortality benefit. Reserve thrombolysis for rescue if she deteriorates (BP drops, worsening hypoxia). Second, close monitoring in HDU/ICU for 24-48 hours to detect deterioration early. Repeat echo if clinical worsening. Third, duration: this is provoked PE (post-TKA), so treat for 3 months. Counsel about importance of compliance (this PE occurred because she stopped prophylaxis). Fourth, regarding prophylaxis protocol: for TKA, the standard is rivaroxaban 10mg daily (or enoxaparin 40mg SC daily) for 10-14 days starting 6-10 hours post-op. She should have continued until day 10-14, not stopped at day 4. The ACCP guidelines recommend 10-14 days for TKA (shorter than THA which requires 28-35 days). Additionally, mechanical prophylaxis (TED stockings, intermittent pneumatic compression) should have been used intra-op and post-op. Fifth, education: reinforce that VTE prophylaxis compliance is critical, and stopping early dramatically increases risk (this case proves it).
KEY POINTS TO SCORE
Submassive PE = normotensive + RV dysfunction/elevated biomarkers
Anticoagulate, do NOT routinely thrombolyse (PEITHO trial - more bleeding, no mortality benefit)
Close monitoring for deterioration, rescue thrombolysis if deteriorates
Provoked PE = 3 months anticoagulation
TKA prophylaxis: rivaroxaban 10mg daily OR enoxaparin 40mg daily for 10-14 days
COMMON TRAPS
✗Thrombolysing submassive PE routinely - only if deteriorating
✗Not knowing PEITHO trial results
✗Not counseling about prophylaxis compliance - major preventable error in this case
✗Treating for 6-12 months - 3 months sufficient for provoked PE
LIKELY FOLLOW-UPS
"What is the PEITHO trial and what did it show?"
"When would you consider catheter-directed therapy?"
"What is the difference in prophylaxis duration for THA vs TKA?"

MCQ Practice Points

Wells Score Interpretation

Q: A patient has Wells score of 2 for PE. What is the next step? A: D-dimer. Wells less than 4 = PE unlikely, check D-dimer. If negative, PE excluded. If positive, CTPA.

Massive vs Submassive PE

Q: What defines massive PE? A: Sustained hypotension (SBP less than 90 mmHg for 15+ minutes) OR cardiac arrest OR cardiogenic shock. Massive PE requires thrombolysis. Submassive PE is normotensive BUT has RV dysfunction.

Thrombolysis Indication

Q: What is the indication for thrombolysis in PE? A: Massive PE (hemodynamic instability). PEITHO trial showed NO benefit for routine thrombolysis in submassive PE, only increased bleeding.

IVC Filter Evidence

Q: What did the PREPIC trial show about IVC filters? A: Filters reduce early PE but increase DVT and do NOT reduce mortality. Only use if absolute contraindication to anticoagulation.

Australian Context

Australian Practice Considerations

PBS Anticoagulants:

  • Rivaroxaban 10mg: PBS listed for VTE prophylaxis post-arthroplasty
  • Rivaroxaban 15mg/20mg: PBS listed for VTE treatment
  • Apixaban 2.5mg/5mg: PBS listed for prophylaxis and treatment
  • Enoxaparin: PBS listed for prophylaxis and treatment

VTE Prophylaxis Guidelines:

  • Follow NHMRC VTE Prevention Guidelines
  • THA: 28-35 days prophylaxis
  • TKA: 10-14 days prophylaxis
  • Hip fracture surgery: 28-35 days

Thrombolysis Availability:

  • Alteplase and tenecteplase available in major EDs
  • Catheter-directed therapy: Major tertiary centers only

Advanced Australian Context

Imaging Access:

  • CTPA: Available 24/7 at metropolitan hospitals
  • Rural/regional: May require retrieval for massive PE
  • Teleradiology supports after-hours reporting

Interventional Resources:

  • Catheter-directed thrombolysis: Sydney, Melbourne, Brisbane, Perth, Adelaide tertiary centers
  • Surgical embolectomy: Cardiac surgery centers only
  • ECMO: Major tertiary hospitals

Quality Indicators:

  • AOANJRR tracks VTE rates post-arthroplasty
  • ACHS clinical indicators for VTE prophylaxis compliance

Exam Viva Point

Australian VTE prophylaxis: PBS provides rebates for rivaroxaban and apixaban for VTE prophylaxis post-arthroplasty. NHMRC guidelines recommend mechanical plus pharmacological prophylaxis. Duration differs: THA 28-35 days, TKA 10-14 days.

PBS VTE Medications

MedicationIndicationPBS Status
Rivaroxaban 10mgVTE prophylaxis post-THA/TKAPBS listed
Rivaroxaban 15/20mgVTE treatmentPBS listed
Apixaban 2.5/5mgProphylaxis and treatmentPBS listed
EnoxaparinProphylaxis and treatmentPBS listed

PULMONARY EMBOLISM

High-Yield Exam Summary

Wells Score for PE (PEACH 3-3-1.5)

  • •Prior DVT/PE +1.5, Elevated HR (greater than 100) +1.5
  • •Alternative diagnosis unlikely +3, Cancer active +1, Hemoptysis +1
  • •Clinical DVT signs +3, Surgery/immobilization (4 weeks) +1.5
  • •Score less than 4 = PE unlikely (D-dimer), score 4+ = PE likely (CTPA)

Diagnostic Algorithm

  • •PERC rule: If ALL 8 negative + low suspicion, PE excluded (no D-dimer)
  • •Low Wells (less than 4): D-dimer - if negative stop, if positive CTPA
  • •High Wells (4+): Skip D-dimer, go to CTPA
  • •CTPA gold standard (95% sensitive), VQ scan if contrast contraindicated

Risk Stratification

  • •Massive (High-Risk): SBP less than 90 or shock or arrest � THROMBOLYSE
  • •Submassive (Intermediate): Normotensive BUT RV dysfunction (echo/CT) or elevated troponin/BNP � Anticoagulate + monitor
  • •Low-Risk: Normotensive, no RV dysfunction � Anticoagulate, consider outpatient if PESI low
  • •RV dysfunction: RV/LV ratio greater than 0.9 (echo) or greater than 1.0 (CT)

Treatment - Anticoagulation

  • •First-line: DOACs (rivaroxaban 15mg BD x21d then 20mg OR apixaban 10mg BD x7d then 5mg BD)
  • •No LMWH lead-in with rivaroxaban/apixaban
  • •Massive PE: IV heparin initially (UFH bolus 80 units/kg, infusion 18 units/kg/h)
  • •Duration: Provoked (surgery) = 3 months, Unprovoked = 3-6 months minimum

Thrombolysis

  • •Indication: Massive PE ONLY (SBP less than 90 or shock)
  • •Agent: Alteplase 100mg IV over 2h (or 50mg bolus if arrest)
  • •Reduces mortality from 30% to 10% in massive PE
  • •Complications: Major bleed 10-15%, intracranial hemorrhage 1-5%
  • •PEITHO trial: Do NOT routinely thrombolyse submassive PE (more bleeding, no mortality benefit)

IVC Filters and VTE Prophylaxis

  • •IVC filter ONLY if absolute contraindication to anticoagulation (NOT routine)
  • •PREPIC trial: Filters reduce early PE but increase DVT, NO mortality benefit
  • •THA prophylaxis: Rivaroxaban 10mg daily OR enoxaparin 40mg daily for 28-35 days
  • •TKA prophylaxis: Rivaroxaban 10mg daily OR enoxaparin 40mg daily for 10-14 days
Quick Stats
Reading Time143 min
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