Pulmonary embolism case study
The case
Patient: A 58‑year‑old male, Mr A, presents to the emergency department with sudden onset shortness of breath.
Presenting complaint:
- Dyspnoea at rest for 3 hours, progressively worsening.
- Pleuritic chest pain on the left side, sharp, aggravated by deep inspiration.
- Light‑headedness and a single episode of near‑syncope while walking to the bathroom.
History of present illness:
- Symptoms began abruptly while the patient was watching television.
- No prior similar episodes.
- No recent trauma, surgery, or prolonged immobilisation.
- Denies cough, fever, wheeze, or haemoptysis.
Past medical history:
- Hypertension for 10 years, on amlodipine 5 mg daily.
- Type 2 diabetes mellitus, on metformin 500 mg twice daily.
- Obesity (BMI = 32 kg/m²).
Social history:
- Former smoker, 20 pack‑years, quit 5 years ago.
- Works as a sales manager; recent business trip involved a 12‑hour flight 4 days ago.
- No regular alcohol intake.
Family history:
- Father died of myocardial infarction at 62 years.
- Mother has osteoarthritis.
Examination:
| Parameter | Value |
|---|---|
| General | Alert, mildly diaphoretic, in mild respiratory distress |
| Vitals | BP 138/84 mm Hg, HR 112 bpm, RR 28 /min, SpO₂ 88 % on room air, Temp 36.8 °C |
| Cardiovascular | Regular rhythm, no murmurs, jugular venous pressure mildly raised |
| Respiratory | Decreased breath sounds at left lower zone, pleural friction rub, no wheeze |
| Extremities | No oedema, calf tenderness on left posterior calf, Homan’s sign positive |
| Skin | No cyanosis, no petechiae |
Initial investigations:
| Test | Result |
|---|---|
| CBC | Hb 13.2 g/dL, WBC 9.8 × 10⁹/L, Platelets 210 × 10⁹/L |
| Electrolytes & renal panel | Na 138 mmol/L, K 4.2 mmol/L, Creatinine 1.0 mg/dL |
| Cardiac enzymes | Troponin‑I 0.04 ng/mL (reference < 0.03 ng/mL) |
| D‑dimer | 2.1 µg/mL FEU (reference < 0.5 µg/mL) |
| ABG (room air) | pH 7.46, PaO₂ 58 mm Hg, PaCO₂ 30 mm Hg, HCO₃⁻ 22 mmol/L, SaO₂ 88 % |
| ECG | Sinus tachycardia, S1Q3T3 pattern, right‑axis deviation |
| CXR | Westermark sign (oligemia) in left lung field, no infiltrates |
| Lower‑limb Doppler US | Acute thrombus in left popliteal vein (non‑compressible) |
| CT pulmonary angiography (CTPA) | Filling defects in the segmental branches of the left lower lobe pulmonary artery and subsegmental branches of the right lower lobe |
The patient is diagnosed with acute pulmonary embolism (PE) with right‑ventricular (RV) strain.
Questions
- What is the most likely diagnosis and which clinical and investigation findings support it?
- Using the ESC 2022 risk stratification algorithm, into which risk category does this patient fall and why?
- What are the immediate management steps for this patient, including anticoagulation and reperfusion options?
- Which further investigations are indicated to identify underlying aetiology and to assess prognosis?
- Discuss the potential short‑term and long‑term complications of pulmonary embolism and their preventive strategies.
Answers
1. Diagnosis and supporting findings
Diagnosis: Acute pulmonary embolism (PE).
Key supporting elements:
| Category | Findings |
|---|---|
| Clinical presentation | Sudden dyspnoea at rest, pleuritic chest pain, tachypnoea, hypoxaemia, recent long‑haul travel (Virchow’s triad: stasis), calf tenderness with Homan’s sign suggesting deep‑vein thrombosis (DVT). |
| Risk factors | Recent 12‑hour flight (immobility), obesity, hypertension, diabetes, prior smoking – all increase venous thrombo‑embolism (VTE) risk. |
| Vital signs | Tachycardia (HR > 100 bpm), tachypnoea (RR > 20/min), SpO₂ < 90 % – typical for PE. |
| Laboratory | Elevated D‑dimer (> 0.5 µg/mL) – high sensitivity for VTE; mild troponin rise indicating myocardial strain. |
| ECG | Sinus tachycardia, S1Q3T3 pattern, right‑axis deviation – classic but not specific signs of acute RV overload. |
| Imaging | CTPA shows intraluminal filling defects in segmental/subsegmental pulmonary arteries – gold‑standard confirmation. |
| Adjunctive | Lower‑limb Doppler confirming DVT provides a source for emboli, strengthening the diagnosis. |
Together, the acute onset, risk profile, objective evidence of RV strain (troponin, ECG), and definitive CTPA findings fulfill the diagnostic criteria for PE.
2. ESC 2022 risk stratification
The European Society of Cardiology (ESC) 2022 guideline classifies acute PE into high‑risk (massive), intermediate‑high, intermediate‑low, and low‑risk based on haemodynamic status, RV dysfunction, and myocardial injury.
Step‑wise assessment for this patient:
Haemodynamic stability:
- BP 138/84 mm Hg (systolic ≥ 90 mm Hg) → stable → not high‑risk.
RV dysfunction:
- Echocardiography (not yet performed) would likely show RV dilatation; however, surrogate markers are present:
- ECG S1Q3T3, right‑axis deviation.
- Troponin‑I mildly elevated (0.04 ng/mL).
- CTPA may show RV/LV diameter ratio > 0.9 (not reported but probable).
- Echocardiography (not yet performed) would likely show RV dilatation; however, surrogate markers are present:
Myocardial injury:
- Troponin‑I above the upper limit of normal → positive.
Risk category:
- Intermediate‑high risk (stable haemodynamics + both RV dysfunction and myocardial injury).
Rationale: The patient meets the ESC criteria for intermediate‑high risk because he is haemodynamically stable but has evidence of RV strain (ECG, probable imaging) and a positive cardiac biomarker. This categorisation guides the need for close monitoring and consideration of early reperfusion if deterioration occurs.
3. Immediate management
A. Initial stabilisation
| Action | Details |
|---|---|
| Oxygen therapy | Target SpO₂ ≥ 94 % (or 90 % in COPD). Administer via nasal cannula or face mask; consider high‑flow if needed. |
| Analgesia | Low‑dose morphine (2‑4 mg IV) for severe pleuritic pain and to reduce respiratory drive, if not contraindicated. |
| Fluid management | Avoid aggressive IV fluids; maintain euvolemia to prevent RV overload. |
B. Anticoagulation (first‑line)
- Choice: Low‑molecular‑weight heparin (LMWH) – enoxaparin 1 mg/kg subcutaneously every 12 h (adjust for renal function; CrCl > 30 mL/min).
- Alternative (if renal impairment or contraindication): Unfractionated heparin (UFH) bolus 80 U/kg IV followed by infusion targeting aPTT 1.5–2.5 × control.
- Rationale: Immediate anticoagulation reduces clot propagation and mortality; LMWH preferred per ACCP 2023 guideline (Grade 1A).
C. Reperfusion considerations
Indication: High‑risk (massive) PE or clinical deterioration (hypotension, shock, persistent hypoxaemia).
Current status: Patient is intermediate‑high risk, haemodynamically stable. Routine systemic thrombolysis is not indicated.
Potential options if deterioration occurs:
- Systemic thrombolysis – alteplase 100 mg IV over 2 h (or 0.6 mg/kg, max 50 mg).
- Catheter‑directed thrombolysis – lower dose (e.g., 10‑20 mg alteplase) for patients at higher bleeding risk.
- Surgical embolectomy – reserved for contraindication to thrombolysis or massive clot burden.
D. Monitoring
- Admit to a monitored unit (step‑down or ICU).
- Continuous ECG, pulse oximetry, and frequent vitals (q15‑30 min initially).
- Serial troponin and BNP/NT‑proBNP every 6‑12 h to detect worsening RV strain.
- Repeat echocardiography within 24 h to assess RV size/function.
E. Transition to oral anticoagulation
- After 5‑7 days of LMWH (or UFH), switch to a direct oral anticoagulant (DOAC) – e.g., rivaroxaban 15 mg PO twice daily for 21 days, then 20 mg once daily.
- Duration: minimum 3 months; extended therapy considered if unprovoked or persistent risk factors.
F. Ancillary measures
- Compression stockings for DVT prophylaxis in the contralateral limb.
- Early ambulation as tolerated.
4. Further investigations
| Investigation | Purpose | Expected findings / interpretation |
|---|---|---|
| Transthoracic echocardiography (TTE) | Assess RV size, systolic function (TAPSE, RV free‑wall strain), pulmonary artery pressure, and presence of McConnell’s sign. | RV dilatation (RV/LV > 0.9), reduced TAPSE < 16 mm, elevated PASP > 30 mm Hg – confirms RV strain. |
| Repeat CTPA or ventilation‑perfusion (V/Q) scan (if CTPA limited) | Evaluate clot burden, monitor resolution. | Decrease in filling defects on follow‑up imaging after 3 months. |
| Thrombophilia screen (if unprovoked or recurrent) | Identify inherited/acquired hypercoagulable states (e.g., Factor V Leiden, antiphospholipid antibodies). | Positive result may dictate indefinite anticoagulation. |
| Cancer screening (age > 50, unprovoked PE) | Rule out occult malignancy (CT abdomen/pelvis, colonoscopy, PSA). | Detect underlying neoplasm that may be the embolic source. |
| Pulmonary function tests (PFTs) & 6‑minute walk test (after acute phase) | Baseline for long‑term functional assessment, especially if chronic thrombo‑embolic pulmonary hypertension (CTEPH) suspected. | Reduced DLCO, limited distance on 6‑MWT may indicate residual impairment. |
| Blood gas analysis (repeat) | Monitor oxygenation and acid‑base status during therapy. | Improvement in PaO₂ and normalization of pH. |
These investigations help refine prognosis, guide duration of anticoagulation, and detect underlying causes that may necessitate specific treatment (e.g., cancer therapy, lifelong anticoagulation for thrombophilia).
5. Complications and prevention
| Complication | Pathophysiology | Clinical features | Prevention / Management |
|---|---|---|---|
| Hemodynamic collapse (massive PE) | Sudden obstruction → RV failure → systemic hypotension. | Syncope, shock, SBP < 90 mm Hg, oliguria. | Early risk stratification, prompt thrombolysis or catheter‑directed therapy in high‑risk patients. |
| Right‑ventricular failure (sub‑massive) | Persistent pressure overload → RV dilatation, interventricular septal shift. | Elevated JVP, peripheral oedema, hepatomegaly, low cardiac output. | Adequate anticoagulation, careful fluid balance, consider reperfusion if deterioration. |
| Chronic thrombo‑embolic pulmonary hypertension (CTEPH) | Incomplete resolution → organised fibrotic obstruction of pulmonary arteries. | Dyspnoea on exertion months after PE, exercise intolerance, echo shows RV hypertrophy. | Early anticoagulation, follow‑up imaging at 3‑6 months, referral for pulmonary endarterectomy if CTEPH confirmed. |
| Recurrent VTE | New emboli from residual DVT or new thrombus formation. | Re‑appearance of dyspnoea, chest pain, leg swelling. | Continue anticoagulation for appropriate duration, address reversible risk factors (weight, mobility), consider IVC filter only if anticoagulation contraindicated. |
| Bleeding (major or clinically relevant non‑major) | Anticoagulant therapy → mucosal or intracranial bleeding. | Haematemesis, melena, drop in Hb > 2 g/dL, intracranial signs. | Use DOACs with lower bleeding risk, dose adjust for renal function, monitor for drug interactions, educate patient on signs of bleeding. |
| Post‑PE syndrome | Persistent dyspnoea, reduced exercise capacity despite normal imaging. | Fatigue, anxiety, reduced QoL. | Pulmonary rehabilitation, psychosocial support, optimize anticoagulation, treat comorbidities (e.g., obesity). |
Preventive strategies focus on prompt diagnosis, risk‑adjusted anticoagulation, early mobilisation, and addressing modifiable risk factors (weight loss, smoking cessation). In selected high‑risk patients, mechanical prophylaxis (intermittent pneumatic compression) may be added during hospital stay.
Key learning points
- Sudden dyspnoea, pleuritic chest pain, and risk factors (immobility, obesity) should raise suspicion for PE.
- D‑dimer is highly sensitive but not specific; a markedly elevated value (> 0.5 µg/mL) warrants imaging in low‑intermediate pre‑test probability.
- CTPA remains the gold standard for confirming PE; lower‑limb Doppler identifies the thrombus source.
- ESC 2022 risk stratification separates patients into haemodynamic (high‑risk) and RV‑function/biomarker‑based (intermediate) categories, guiding intensity of monitoring and reperfusion decisions.
- Initial anticoagulation with LMWH (or UFH) should be started immediately; DOACs are preferred for long‑term therapy per ACCP 2023.
- Systemic thrombolysis is reserved for haemodynamically unstable patients; catheter‑directed therapy offers a lower bleeding risk alternative.
- Follow‑up imaging and assessment for underlying thrombophilia or occult malignancy are essential for secondary prevention.
- Long‑term complications include CTEPH, recurrent VTE, and post‑PE syndrome; early rehabilitation and risk‑factor modification reduce morbidity.
Practice MCQs
1. A 58‑year‑old man with acute PE is haemodynamically stable but has a troponin rise and RV dilatation on echo. According to ESC 2022, he belongs to which risk category?
A. Low‑risk
B. Intermediate‑low risk
C. Intermediate‑high risk
D. High‑risk
Answer: C — The presence of both RV dysfunction and myocardial injury in a haemodynamically stable patient classifies him as intermediate‑high risk.
2. Which of the following is the preferred initial anticoagulant for a patient with acute PE and normal renal function?
A. Unfractionated heparin infusion
B. Enoxaparin (LMWH) subcutaneously
C. Warfarin loading dose
D. Aspirin
Answer: B — LMWH (enoxaparin 1 mg/kg SC q12 h) is recommended as first‑line anticoagulation in acute PE with normal renal function (ACCP 2023, Grade 1A).
3. A patient with confirmed PE develops hypotension (SBP = 80 mm Hg) and signs of shock. The most appropriate immediate reperfusion therapy is:
A. Start high‑dose intravenous steroids
B. Systemic thrombolysis with alteplase 100 mg IV over 2 h
C. Immediate surgical embolectomy without thrombolysis
D. Increase LMWH dose to therapeutic level only
Answer: B — In high‑
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