Pneumonia — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mrs Asha Patel, 72 years old. ^[1]

Presenting complaint: Three-day history of fever, rigors, productive cough with rust-coloured sputum, progressive dyspnoea, and confusion. Found drowsy and breathless at home by her daughter. Brought to ED by ambulance. ^[1]

Past history:

• COPD diagnosed 8 years ago — FEV1 55% predicted (GOLD 2, moderate), Group E (two exacerbations last year). Still smoking 15 cigarettes/day (40 pack-year total)
• Type 2 diabetes (HbA1c 72 mmol/mol) on metformin and empagliflozin
• Hypertension
• Osteoporosis (wrist fracture 2 years ago)
• Cholecystectomy 10 years ago
• Lives with her husband, independent in activities of daily living ^[1]

Current medications:

• Tiotropium 18 mcg inhaled daily
• Salmeterol/fluticasone 50/500 one puff BID
• Salbutamol PRN
• Metformin 1 g BID
• Empagliflozin 10 mg daily
• Perindopril 5 mg daily
• Alendronate 70 mg weekly ^[1]

Examination findings (trainee elicits):

• Drowsy, confused (GCS 13 — disoriented to time and place)
• Respiratory rate 34/min, using accessory muscles
• Blood pressure 82/54 mmHg, heart rate 124/min, temperature 39.2 degrees C
• SpO2 86% on room air, improving to 94% on 8 L/min via simple face mask
• Right base: dullness to percussion, bronchial breath sounds, coarse crackles, increased vocal resonance
• Reduced right side chest expansion
• No rash, no peripheral stigmata of endocarditis, no meningismus ^[1]

Investigations:

• WBC 22.4 x 10^9/L (neutrophilia), CRP 280 mg/L
• Urea 11.5 mmol/L, creatinine 130 micromol/L (baseline 80)
• Sodium 130 mmol/L, glucose 14.2 mmol/L
• ALT 65 U/L, albumin 28 g/L
• Lactate 3.2 mmol/L
• ABG on 8 L/min: pH 7.32, PaCO2 34 mmHg (4.5 kPa), PaO2 62 mmHg (8.3 kPa), HCO3 22 mmol/L
• CXR: right middle and lower lobe consolidation with a right pleural effusion (25 mm on lateral decubitus)
• Blood cultures: Streptococcus pneumoniae (penicillin-sensitive) after 14 hours
• Pneumococcal urinary antigen: positive ^[1]

Candidate's structured presentation (model)

Opening statement: ^[1]

'Mrs Patel is a 72-year-old retired teacher and 40 pack-year smoker who presents with a 3-day history of fever, rigors, and rusty sputum, progressing to confusion and shock. She has COPD (GOLD 3, Group E) and type 2 diabetes. ^[1]

On arrival she was confused, tachypnoeic at 34, hypotensive at 82/54, febrile at 39.2, and hypoxic with a PaO2 of 62 on supplemental oxygen. Her CXR shows right middle and lower lobe consolidation with a parapneumonic effusion. Her blood cultures grew penicillin-sensitive Streptococcus pneumoniae. ^[1]

Her CURB-65 is 5, her PSI is class V, and she meets the IDSA/ATS major criteria for severe CAP with septic shock. Her SMART-COP is 10 (2 for hypotension, 1 each for multilobar involvement, low albumin, tachypnoea and confusion, 2 each for hypoxaemia and acidosis). ^{[1] [2] [4]}

Her main problems are:

1. Severe bacteraemic pneumococcal CAP with septic shock — immediate threat to life
2. A right parapneumonic effusion requiring diagnostic thoracentesis and likely drainage
3. Acute kidney injury (creatinine 130 from baseline 80) secondary to sepsis and hypoperfusion
4. COPD and type 2 diabetes complicating her management and prognosis
5. Hyperglycaemia (glucose 14.2) exacerbated by sepsis and steroids
6. Ongoing smoking — a critical modifiable risk factor
7. Osteoporosis and functional decline requiring rehabilitation planning' ^[1]

Investigation summary: ^[1]

'Her blood gas shows a type 1 respiratory failure with a metabolic acidosis — the low pH and low bicarbonate with an elevated lactate of 3.2 reflect septic shock with tissue hypoperfusion, and she is compensating with a low PaCO2. Her hyponatraemia (130) is consistent with SIADH from pneumonia. Her acute kidney injury is pre-renal from hypoperfusion and will require careful fluid management. Her blood cultures confirm bacteraemic pneumococcal CAP — penicillin-sensitive — which allows de-escalation but mandates a search for metastatic infection. Her CXR shows multilobar consolidation, a minor severity criterion, and a pleural effusion requiring thoracentesis.' ^[1]

Management plan: ^[1]

1. Immediate (first hour):

   • Sepsis Six: high-flow oxygen (target SpO2 94-98%, checking ABG at 30 min for CO2 retention given COPD — narrow to 88-92% if needed), blood cultures, IV antibiotics within the hour, 30 mL/kg crystalloid, lactate, urine output monitoring
   • Piperacillin-tazobactam 4.5 g IV TDS plus azithromycin 500 mg IV daily — broad enough for pneumococcus and atypicals, with anti-pseudomonal breadth given COPD. De-escalate to ceftriaxone or benzylpenicillin once sensitivities confirmed
   • Noradrenaline via central line if fluid-refractory shock (she is likely to need this given her BP and lactate)
   • ICU admission for septic shock ^[1]

2. Corticosteroids:

   • Prednisone 50 mg daily for 7 days (or hydrocortisone 200 mg/day IV) for severe CAP per the Blum and Siemieniuk evidence — reduced mortality, mechanical ventilation, and ARDS. ^[3]
   • Monitor blood glucose closely — she has diabetes and steroids will worsen hyperglycaemia — insulin sliding scale may be needed ^[1]

3. Parapneumonic effusion:

   • Pleural ultrasound to characterise the 25 mm effusion
   • Diagnostic thoracentesis: send for pH, protein, LDH, glucose, cell count, Gram stain, culture
   • Chest drain if pH under 7.2 or frank pus; consider intrapleural tPA/DNase if loculated ^[1]

4. Renal and metabolic:

   • Hold metformin and empagliflozin during acute illness (AKI and risk of euglycaemic ketoacidosis respectively)
   • Insulin sliding scale for hyperglycaemia
   • Monitor renal function and electrolytes; correct electrolyte disturbances ^[1]

5. COPD:

   • Continue inhaled bronchodilators (nebulised during acute illness)
   • The corticosteroids for her CAP will also treat any COPD component ^[1]

6. Prevention and follow-up:

   • Smoking cessation counselling and pharmacotherapy (varenicline or NRT)
   • Pneumococcal conjugate and influenza vaccination before discharge
   • Repeat CXR at 6 weeks to confirm resolution and exclude underlying lesion (critical in a 40 pack-year smoker)
   • Pulmonary rehabilitation and functional recovery assessment ^[1]

Examiner discussion questions

Q: 'She has a COPD exacerbation on top of her pneumonia. Would you give systemic corticosteroids for the COPD separately?' ^[1]

'No — the corticosteroids I am already giving for severe CAP (prednisone 50 mg daily for 7 days) will cover both the pneumonia and any COPD component. Giving additional steroids would increase the risk of adverse effects, particularly hyperglycaemia in this diabetic patient, without additional benefit. The Blum regimen of prednisone 50 mg for 7 days is actually similar to or higher than the standard COPD exacerbation steroid course (prednisone 40 mg for 5 days per the REDUCE trial), so there is no need to add more.' ^[1]

Q: 'Her repeat CXR at 6 weeks still shows some consolidation. Is this a concern?' ^[1]

'Some radiographic resolution lag is normal — CXR resolution typically takes 4-12 weeks, and elderly patients, smokers, and those with multilobar disease resolve more slowly. However, persistent consolidation beyond 6-8 weeks, or a non-resolving pneumonia, mandates investigation for an underlying cause — particularly bronchial obstruction from lung cancer, which is a real concern in a 40 pack-year smoker. I would arrange a CT chest with contrast to characterise the persistent consolidation, look for a mass or hilar lymphadenopathy, and consider bronchoscopy if there is any suggestion of obstruction. I would also exclude tuberculosis and atypical infections if the picture is atypical. The key message is that non-resolution is a red flag, especially in a smoker, and lung cancer must be actively excluded.' ^[1]

Q: 'Her pneumococcal urinary antigen is positive. What is the clinical significance?' ^[1]

'The pneumococcal urinary antigen detects the C-polysaccharide cell wall antigen common to all pneumococcal serotypes. It is highly specific (over 90%) and reasonably sensitive (70-80%) in adults with bacteraemic pneumococcal pneumonia. In this case it corroborates the blood culture result, confirming pneumococcal CAP. Its main clinical value is in patients who have already received antibiotics — the blood cultures may be sterilised but the urinary antigen persists, allowing aetiological diagnosis. It does not change my management here, since the blood cultures already gave the organism and sensitivities, but it supports a confident diagnosis and would have been useful if the cultures had been negative.' ^[1]