Case studies · Medicine · 23 October 2026

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:

History of present illness:

Past medical history:

Social history:

Family history:

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

  1. What is the most likely diagnosis and which clinical and investigation findings support it?
  2. Using the ESC 2022 risk stratification algorithm, into which risk category does this patient fall and why?
  3. What are the immediate management steps for this patient, including anticoagulation and reperfusion options?
  4. Which further investigations are indicated to identify underlying aetiology and to assess prognosis?
  5. 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:

  1. Haemodynamic stability:

    • BP 138/84 mm Hg (systolic ≥ 90 mm Hg) → stable → not high‑risk.
  2. 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).
  3. Myocardial injury:

    • Troponin‑I above the upper limit of normal → positive.

Risk category:

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)

C. Reperfusion considerations

D. Monitoring

E. Transition to oral anticoagulation

F. Ancillary measures


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


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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