Emergency Clinical Guide

Pulmonary Embolism (PE)

Wells PE score, CTPA, massive vs submassive PE, thrombolysis, and haemodynamic resuscitation in the GCC critical care setting

Medical Emergency Wells PE Score CTPA Diagnosis Thrombolysis DHA · DOH · SCFHS · QCHP
Overview
Diagnosis
Management
Massive PE
GCC Context
MCQ Practice

🫁 Pulmonary Embolism — Overview

Pulmonary Embolism (PE) occurs when a blood clot (usually from a DVT in the legs or pelvis) travels to and occludes pulmonary arteries, causing haemodynamic compromise and respiratory failure.

PE is a leading cause of preventable hospital death. Massive PE (with haemodynamic instability) has up to 30–50% mortality. Prompt diagnosis and treatment are essential.

Clinical Presentations — Spectrum

CategoryHaemodynamicsFeaturesMortality
Massive PEUnstable: SBP <90 or drop ≥40 mmHg for >15 minShock, syncope, cardiac arrest (PEA)30–50%
Submassive PEStable but RV dysfunction presentElevated troponin/BNP, RV dilation on echo/CT5–15%
Low-risk PEStable, no RV dysfunctionDyspnoea, pleuritic chest pain, haemoptysis<1%

Classic PE Symptoms

  • Dyspnoea — most common symptom (~73%); sudden onset
  • Pleuritic chest pain — sharp, worse on inspiration; indicates peripheral infarction
  • Haemoptysis — blood in sputum; pulmonary infarction
  • Syncope / near-syncope — massive PE; sudden collapse
  • Tachycardia, tachypnoea, hypoxaemia
  • Leg swelling/pain from underlying DVT (~50% of cases)
  • Low-grade fever (infarction)
PE can present as PEA (pulseless electrical activity) arrest. PEA in the absence of obvious reversible causes should prompt consideration of massive PE → empirical thrombolysis during CPR may be lifesaving.

ECG in PE

  • Most common: sinus tachycardia (non-specific but important)
  • S1Q3T3 pattern: deep S wave lead I, Q wave + T wave inversion lead III — classic but only ~20% of PE
  • New right bundle branch block (RBBB) — RV strain
  • T wave inversions V1–V4 — right heart strain pattern
  • New AF — complication of acute PE

🔬 Diagnosis of PE

Wells PE Score

Clinical FeatureScore
Clinical signs/symptoms of DVT (swollen leg, deep vein tenderness)+3
PE is #1 diagnosis OR equally likely as alternative+3
Heart rate >100 bpm+1.5
Immobilisation ≥3 days OR surgery within 4 weeks requiring GA+1.5
Previous documented DVT or PE+1.5
Haemoptysis+1
Active malignancy (treatment within 6 months or palliative)+1
Wells PE ScoreProbabilityPE Prevalence
≥5 (PE likely)High~40–67%
<5 (PE unlikely)Low–moderate~8–12%

Diagnostic Pathway

SituationApproach
HAEMODYNAMICALLY UNSTABLE — massive PE suspectedDo NOT delay for imaging; bedside ECHO (RV dilation = high suspicion); treat immediately; if arrest → empirical thrombolysis
Wells <5 (PE unlikely)D-dimer: if negative = PE excluded; if positive → CTPA
Wells ≥5 (PE likely)Go directly to CTPA — D-dimer is not useful

CTPA — Gold Standard

  • CT Pulmonary Angiogram: definitive investigation for PE
  • Sensitivity ~96–100%, specificity ~98% for segmental PE and above
  • Also identifies alternative diagnoses (pneumonia, aortic dissection, cardiac tamponade)
  • V/Q scan: alternative if CTPA contraindicated (contrast allergy, severe renal impairment, pregnancy)

Additional Investigations — Risk Stratification

  • Troponin: Elevated = RV myocardial injury → higher mortality
  • BNP/NT-proBNP: Elevated = RV pressure overload → worse prognosis
  • Echocardiogram: RV dilation, D-sign (septal flattening), McConnell's sign (RV free wall hypokinesis, preserved apex)
  • ABG: ↓PaO₂ + ↓PaCO₂ + respiratory alkalosis (hyperventilation pattern)
Classic ABG in PE: Hypoxaemia + hypocapnia + respiratory alkalosis. The patient hyperventilates to compensate for hypoxia, blowing off CO₂ and causing alkalosis.

💊 PE Management — Haemodynamically Stable

Immediate Supportive Care

  • High-flow O₂ via non-rebreather mask — target SpO₂ ≥94%
  • IV access × 2; cautious fluids (250–500 mL) if hypotensive — excess fluids worsen RV overload
  • Continuous cardiac monitoring
  • Analgesia for pleuritic pain (NSAIDs or opioids)
Start anticoagulation BEFORE CTPA if clinical probability is high and no contraindication.

Anticoagulation — First-Line

DrugRegimenNotes
Rivaroxaban15 mg BD × 21 days → 20 mg ODFirst-line DOAC; with food
Apixaban10 mg BD × 7 days → 5 mg BDPreferred in CKD; no food requirement
Enoxaparin (LMWH)1 mg/kg SC BDCancer-associated PE; pregnancy
UFH infusion80 units/kg bolus → 18 units/kg/hr (aPTT target 60–100s)Massive/submassive PE — rapid reversibility if thrombolysis needed

Duration of Treatment

ScenarioDuration
Provoked PE (surgery, trauma)3 months
First unprovoked PEMinimum 3 months; consider extended/indefinite
Second PE eventIndefinite anticoagulation
Cancer-associated PEDuration of cancer + minimum 3–6 months

Low-Risk PE — Outpatient Management

  • PESI class I–II or sPESI = 0: consider outpatient DOAC with close follow-up within 5 days
  • Criteria: haemodynamically stable, adequate renal function, no significant comorbidity, good social support, can take oral medication
  • Most GCC centres admit PE patients for ≥24 hours minimum for observation

🚨 Massive PE — Emergency Management

Massive PE = SBP <90 mmHg OR fall ≥40 mmHg for >15 min not explained by other cause → ACTIVATE RESUS TEAM

Immediate Resuscitation Steps

  1. Call for help — anaesthetics, ICU, cardiology
  2. 100% oxygen — prepare airway management
  3. IV UFH 80 units/kg bolus immediately
  4. Cautious IV fluid bolus 250–500 mL (avoid excess — worsens RV overload)
  5. Vasopressors (noradrenaline) if SBP <90 despite fluid
  6. Bedside echocardiography — confirm RV dilation, McConnell's sign
  7. CTPA if patient stable enough; if not → treat based on clinical/echo diagnosis

Systemic Thrombolysis — Alteplase

Alteplase dosing for massive PE:
• Standard: 10 mg IV bolus over 1–2 min, then 90 mg over 2 hours (total 100 mg)
• In cardiac arrest: 50 mg IV bolus → continue CPR ≥60–90 minutes
• Restart UFH 2 hours post-alteplase (once aPTT <80 seconds)

Contraindications to Thrombolysis

Absolute Contraindications

  • Prior intracranial haemorrhage (ever)
  • Intracranial structural disease (AVM, tumour)
  • Ischaemic stroke within 3 months
  • Active significant internal bleeding
  • Head trauma within 3 months
  • Suspected aortic dissection

Relative Contraindications (weigh risk/benefit in massive PE)

  • Major surgery within 3 weeks
  • Non-compressible vascular punctures
  • Prolonged CPR (>10 minutes)
  • Pregnancy
  • Active peptic ulcer
  • Severe hypertension (SBP >180)
In PEA cardiac arrest from PE: Thrombolysis takes priority over most relative contraindications. Give alteplase 50 mg bolus and continue CPR for ≥60–90 minutes for clot lysis.

Surgical / Interventional Options

  • Surgical embolectomy: Open removal of clot — when thrombolysis fails or absolutely contraindicated; requires cardiothoracic surgical centre
  • Catheter-directed thrombolysis: Low-dose local thrombolytic via catheter — option for submassive PE; lower systemic bleeding risk
  • ECMO: Bridge to definitive therapy in refractory massive PE — available at major GCC cardiac centres (KFSH, Cleveland Clinic Abu Dhabi, HMC Doha)

🌍 GCC-Specific Context

PE Risk in GCC Populations
  • Obesity (major VTE risk factor) highly prevalent: KSA 35%, Kuwait 38%, Qatar 35%
  • High T2DM prevalence = hypercoagulable state
  • Long-haul air travel common in GCC populations and pilgrims
  • Increasing bariatric and orthopaedic surgical volumes — highest VTE risk surgeries
  • Hajj pilgrims: prolonged immobility during travel + dehydration in heat → significant PE risk; Saudi MOH provides VTE prophylaxis guidance for high-risk pilgrims
  • Construction workers: prolonged standing/sitting in heat + dehydration
PE Management Resources in GCC
  • CTPA available 24/7 at all major GCC tertiary hospitals
  • DOACs (rivaroxaban, apixaban) widely available as first-line treatment
  • Thrombolysis available at all Level 2+ hospitals — cardiac ICU monitoring required
  • Catheter-directed thrombolysis and ECMO at major cardiac centres: KFSH, KAUH, Cleveland Clinic Abu Dhabi, HMC Qatar, Sultan Qaboos University Hospital
  • PE protocols align with ESC and ACCP international guidelines across GCC
SCFHS / DHA / QCHP Exam Focus
  • Massive PE: SBP <90 or drop ≥40 mmHg → haemodynamic instability → thrombolysis (alteplase)
  • PE triad: dyspnoea + chest pain + haemoptysis (only ~20% have all three)
  • ECG: sinus tachycardia (most common); S1Q3T3 pattern (20%)
  • ABG in PE: ↓PaO₂ + ↓PaCO₂ + respiratory alkalosis
  • Wells ≥5 = high probability → CTPA directly (no D-dimer)
  • Wells <5 → D-dimer first; if negative = PE excluded
  • UFH preferred for massive/submassive PE (allows reversal if thrombolysis needed)
  • Alteplase: 10 mg bolus + 90 mg over 2 hours (standard); 50 mg bolus in cardiac arrest
  • PEA arrest → think PE → empirical thrombolysis + CPR ≥60 minutes
  • RV dilation on echo = poor prognosis; McConnell's sign = RV free wall hypokinesis with preserved apex = acute PE

📝 MCQ Practice

1. A 52-year-old woman returns from a 9-hour flight with sudden dyspnoea and right-sided pleuritic chest pain. BP 118/76, HR 108, SpO₂ 91%. Wells PE score is 6.5. What is the MOST appropriate next step?

2. A patient develops PEA cardiac arrest. PE is suspected. CPR is ongoing with no ROSC after 5 minutes. What is the appropriate next step?

3. An ABG on a patient with suspected PE shows: pH 7.49, PaO₂ 8.1 kPa, PaCO₂ 3.2 kPa. How should this be interpreted?

4. A patient is treated with UFH infusion for massive PE. Thrombolysis with alteplase is given. When should UFH be restarted after alteplase infusion ends?