COPD — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Robert Hayes, 70 years old. [1]

Presenting complaint: Four-day history of worsening dyspnoea, increased yellow-green sputum, and increasing drowsiness. Brought to ED by his wife. Over the past 6 months he has become breathless dressing (mMRC 4) and has had three hospital admissions for exacerbations. [1]

Past history:

• Severe COPD diagnosed 12 years ago — 50 pack-year smoker, still smoking 10/day
• Cor pulmonale diagnosed 2 years ago
• Osteoporosis — left wrist fracture 18 months ago
• Depression — diagnosed 3 years ago
• Hypertension
• Appendicectomy age 25 [1]

Current medications:

• Tiotropium 18 mcg daily
• Salmeterol/fluticasone 50/500 BID
• Salbutamol MDI PRN
• Frusemide 40 mg daily
• Sertraline 50 mg daily
• Alendronate 70 mg weekly
• Amlodipine 5 mg daily [1]

Examination findings (trainee elicits):

• Thin, cachectic; breathless at rest, using accessory muscles, pursed-lip breathing, tripod position
• Central cyanosis; no clubbing; fine tremor
• Temperature 37.9 C, HR 110 (sinus), BP 135/85, RR 28/min
• Barrel chest, hyper-resonant to percussion, globally reduced breath sounds with prolonged expiration and expiratory wheeze
• JVP elevated 4 cm; RV heave; loud P2; soft pansystolic murmur at LLSB louder on inspiration (tricuspid regurgitation)
• Pitting oedema to mid-shin bilaterally [1]

Investigations:

• ABG on 28% Venturi: pH 7.27, PaCO2 75 mmHg (10.0 kPa), PaO2 56 mmHg, HCO3 32 mmol/L
• FBE: Hb 168, haematocrit 0.54, WCC 13.2, eosinophils 0.08 x 10^9/L
• CRP 68 mg/L
• CXR: hyperinflation, flattened diaphragms, no consolidation, enlarged pulmonary arteries, clear lung fields
• ECG: sinus tachycardia, right axis deviation, tall R in V1, p-pulmonale
• Echo (from recent admission): dilated RV, estimated PASP 52 mmHg, preserved LV function
• Spirometry (recent): FEV1 1.0 L (32% predicted), FEV1/FVC 0.48
• Blood cultures sent [1]

Candidate's structured presentation (model)

Opening statement: [1]

"Mr Hayes is a 70-year-old retired boilermaker and current smoker who presents with an acute exacerbation of COPD complicated by acute-on-chronic hypercapnic respiratory failure. He has severe COPD (GOLD 3, Group E — three admissions this year), cor pulmonale, osteoporosis, and depression. [1]

His main problems are:

1. Acute exacerbation of COPD with acute-on-chronic type 2 respiratory failure (pH 7.27, PaCO2 75) requiring non-invasive ventilation
2. Severe COPD (GOLD 3) with a frequent-exacerbator phenotype and likely inappropriate ICS use (eosinophils 0.08)
3. Cor pulmonale with pulmonary hypertension (PASP 52, RV dilatation, peripheral oedema)
4. Osteoporosis (prior fracture, on alendronate)
5. Depression
6. Ongoing tobacco dependence — critical given the fire risk with any future home oxygen
7. Polycythaemia (haematocrit 0.54) from chronic hypoxaemia" [1]

Investigation summary: [1]

"His blood gas confirms acute-on-chronic hypercapnic respiratory failure — the low pH of 7.27 indicates an acute decompensation on top of his chronically elevated bicarbonate of 32 (renal compensation for chronic CO2 retention). His CXR excludes pneumonia and pneumothorax. His ECG shows right axis deviation, p-pulmonale, and tall R in V1, consistent with right ventricular hypertrophy from pulmonary hypertension. His echo confirms cor pulmonale. His polycythaemia reflects chronic hypoxaemia. His low eosinophils predict poor ICS responsiveness and pneumonia risk." [1]

Management plan: [1]

1. Immediate:

   • Controlled oxygen (28% Venturi, target SpO2 88-92%) — never high-flow
   • NIV (BiPAP): IPAP 10-12 titrating up, EPAP 4-5; this is the mortality-reducing, first-line intervention for his hypercapnic respiratory failure (Plant et al., Lancet 2000)
   • Nebulised salbutamol 5 mg + ipratropium 500 mcg every 4-6 hours
   • Prednisone 40 mg orally daily for 5 days (REDUCE trial)
   • Amoxicillin-clavulanate 875/125 mg BID for 5 days — Anthonisen Type 1 with purulent sputum and raised CRP
   • Monitor ABG at 1-2 hours; escalate to ICU if NIV fails (pH less than 7.25 despite optimised NIV) [1]

2. Medium-term (once stabilised):

   • Pulmonary rehabilitation within 4 weeks of discharge
   • Reassess inhaled therapy: consider ICS withdrawal (switch to LAMA/LABA) given low eosinophils and pneumonia risk
   • Assess for LTOT (ABG in stable state at 4-6 weeks; if PaO2 less than 55, prescribe at least 15 h/day — NOTT mortality benefit)
   • Assess for domiciliary NIV if chronic daytime hypercapnia persists
   • Smoking cessation: intensive counselling + varenicline (mandatory before LTOT) [1]

3. Comorbidity management:

   • Cor pulmonale: continue frusemide; oxygen is primary therapy for pulmonary hypertension
   • Osteoporosis: continue alendronate; DEXA; minimise oral steroid courses
   • Depression: continue sertraline
   • Vaccinations: influenza, pneumococcal, COVID-19
   • Polycythaemia: will improve with oxygen therapy [1]

4. Prognosis and advance care planning:

   • Calculate BODE score to prognosticate
   • Discuss goals of care, ceiling of treatment, and advance care directive [1]

Examiner discussion questions

Q: "His PaCO2 is 75 with pH 7.27 on NIV settings of IPAP 12, EPAP 4. The repeat gas at 1 hour shows pH 7.29, PaCO2 68. What do you do?" [1]

"He is improving — the pH has risen and PaCO2 has fallen, confirming NIV is working. I would increase the IPAP by 2 cmH2O to 14, which increases tidal volume and further reduces PaCO2, and recheck the ABG at 1-2 hours. The goal is to normalise the pH toward 7.35 while keeping SpO2 88-92%. As long as the trend is improving and he is comfortable, I would continue NIV and wean gradually over 24-72 hours as the exacerbation resolves. I would only intubate if he deteriorated despite optimised NIV." [1]

Q: "Would you give him a theophylline infusion?" [1]

"No. Intravenous aminophylline/theophylline is not recommended in acute COPD exacerbation. It has marginal bronchodilator efficacy compared with nebulised beta-agonists and anticholinergics, and a narrow therapeutic window with significant toxicity — nausea, seizures, and cardiac arrhythmias, especially in a patient who is already tachycardic. The GOLD and NICE guidelines advise against routine theophylline use in exacerbations." [1]

Q: "He wants to go home and keep smoking. How do you counsel him about home oxygen?" [1]

"This is a safety-critical issue. Home oxygen therapy and active smoking are an unacceptable combination — oxygen supports combustion and creates a serious fire and explosion risk. I would not prescribe LTOT until he has a credible smoking cessation plan in place. I would counsel him directly: the fire risk is real and has caused fatalities; smoking is accelerating his disease and will almost certainly lead to further admissions; and the two interventions that improve survival in COPD are smoking cessation and oxygen, but they cannot safely coexist. I would offer varenicline and intensive behavioural support, and revisit oxygen once he has stopped or has a clear plan to stop." [1]

Q: "What is the significance of his polycythaemia (haematocrit 0.54)?" [1]

"Secondary polycythaemia is a predictable response to chronic hypoxaemia — the kidney increases erythropoietin production to improve oxygen carriage. In COPD it is a marker of severe chronic hypoxia and is itself one of the criteria for LTOT (haematocrit greater than 0.55 in the presence of PaO2 55-59 mmHg qualifies for oxygen). It increases blood viscosity and the risk of thromboembolism. The treatment is not venesection unless symptomatic — the correct treatment is long-term oxygen therapy, which corrects the hypoxaemic stimulus and the haematocrit falls over weeks." [1]

DCE Short Case — Respiratory Examination

Instruction

"Examine this patient's respiratory system. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates

• Thin, cachectic body habitus (emphysema phenotype, systemic inflammation)
• Pursed-lip breathing, accessory muscle use, tripod position (dynamic hyperinflation, mechanical disadvantage)
• Barrel chest with increased AP diameter
• Reduced cricosternal distance (hyperinflation)
• Hyper-resonance to percussion bilaterally (air trapping)
• Globally reduced breath sounds with prolonged expiration and expiratory wheeze
• Cor pulmonale signs: elevated JVP, RV heave, loud P2, tricuspid regurgitation murmur (louder on inspiration — Carvallo's sign), peripheral oedema
• Central cyanosis (hypoxaemia); no clubbing (important negative — confirms no coexisting malignancy/bronchiectasis/fibrosis)
• Fine tremor (beta-agonist effect) [1]

Presentation template

"I examined Mr Jones's respiratory system. He is a thin, cachectic man who is breathless at rest, using accessory muscles with pursed-lip breathing in a tripod position. There is central cyanosis but no clubbing. He has a fine tremor. The respiratory rate is 24 per minute. [1]

The chest is barrel-shaped with increased anteroposterior diameter. Cricosternal distance is reduced. Chest expansion is diminished and symmetrical at 3 cm. The percussion note is hyper-resonant throughout. On auscultation, breath sounds are globally reduced with a prolonged expiratory phase and widespread expiratory polyphonic wheeze. [1]

The JVP is elevated 4 cm with a prominent V wave. There is a right ventricular heave. The pulmonary component of the second heart sound is loud. There is a pansystolic murmur at the lower left sternal edge, louder on inspiration, consistent with tricuspid regurgitation. There is pitting oedema to the mid-shin bilaterally. [1]

In summary, these findings are consistent with severe chronic obstructive pulmonary disease with hyperinflation, complicated by cor pulmonale secondary to pulmonary hypertension." [1]

Discussion template

1. Summarise findings → "severe COPD with hyperinflation and cor pulmonale."
2. Differential from signs → "The combination of hyperinflation, wheeze, and cor pulmonale is most consistent with COPD. I would distinguish this from: asthma (younger age, atopy, fully reversible obstruction); bronchiectasis (clubbing, daily purulent sputum, crackles); interstitial lung disease (fine Velcro crackles, clubbing, restrictive spirometry); and cardiac failure (basal crackles, gallop, displaced apex, no hyper-resonance)."
3. Key negative finding → "The absence of clubbing is important — clubbing is not a feature of uncomplicated COPD. Its presence would prompt investigation for lung cancer, bronchiectasis, or pulmonary fibrosis."
4. Investigations → "Post-bronchodilator spirometry to confirm obstruction (FEV1/FVC less than 0.70) and grade severity; CXR; ABG to assess for type 2 respiratory failure; echo to evaluate pulmonary hypertension and RV function; alpha-1-antitrypsin level; BODE index for prognostication."
5. Management → "Smoking cessation, bronchodilator therapy (LAMA/LABA), pulmonary rehabilitation, assess for LTOT, vaccination, treat comorbidities." [1]