Pathophysiology
P-II-16. Respiratory disease, Case 3
呼吸器疾患 症例3
Case III — 33-year-old female, rather shattered, has fever, dyspnea, allergic airway disease in her medical history
Medical history:
33 years old, previous hospitalisation due to asthma, adheres to maintained antiasthmatic treatment, does not smoke, works as a kindergarten teacher.
Complaints:
Feels shattered, 39 °C fever, cough without discharge, pain on the right side of the chest (sharp, in connection with breathing, moving), mild dyspnea.
Physical examination:
Faint wheezing at the end of expiration over both lungs, RR: 115/78, P: 98/min.
Findings:
- PaO2: 65 mmHg, PaCO2: 30 mmHg, pH: 7.48, BE: -3.0 mmol/l
- CRP: 300 mg/l
- Procalcitonin: 1.5 ug/l (normal)
- ions normal
- General bacterial culture from sputum: negative
Chest X-ray: Right perihilar infiltrate (before and after treatment).
ECG: negative.
Treatment and new findings:
- Amoxicillin-clavulanic acid + clarithromycin, oral
- Daily 120 mg, then 80 mg systemic steroid, IV
- Inhaled short-acting β2 agonist, 6x daily
As there is no decrease in CRP after 3 days, modification to:
- ceftazidim + clarithromycin IV antibiotic treatment (antipseudomonal effect as well).
Within 1 week fever breaks, radiological findings improve, CRP: 12 mg/l. Pulmonary function test shows no remaining obstructive ventilation disorder.
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| 39 °C fever; “cough without discharge”; CRP 300 mg/l | Acute lower respiratory tract infection with a strong inflammatory response |
| “Right perihilar infiltrate” on chest X-ray | Radiographic consolidation → confirms pneumonia |
| “pain on the right side of the chest (sharp, in connection with breathing)” | Pleuritic chest pain from inflammation of the pleura overlying the infected lung |
| Procalcitonin 1.5 (normal range stated); sputum culture negative | No clear typical bacterial signal → atypical organism considered |
| PaO2 65, pCO2 30, pH 7.48 | Mild hypoxaemia with respiratory alkalosis from hyperventilation |
| “no remaining obstructive ventilation disorder” after recovery | Her background asthma is not the cause here → the event was an acute infection that fully resolved |
| Faint end-expiratory wheeze; kindergarten teacher | Mild bronchial reactivity; occupational exposure to respiratory pathogens |
Key Points
- Diagnosis: Community-acquired pneumonia (with a pleuritic component) in a patient with background asthma.
- Supporting features: Fever, cough, very high CRP, and a perihilar infiltrate that resolves with antibiotics.
- Pleuritic pain: Sharp, breathing-related chest pain indicates pleural involvement.
- Organism clue: Negative culture and need for broader/antipseudomonal cover suggest an atypical/resistant pathogen.
- Key distinction: Normal post-recovery spirometry shows the illness was infective, not an asthma exacerbation.
一問一答
▶How do you interpret pH 7.48, pCO2 30, PaO2 65 in this patient?
Mild hypoxaemia with respiratory alkalosis from compensatory hyperventilation.
▶Why do a negative sputum culture and need for broader cover suggest an atypical pathogen?
Atypical organisms (e.g. Mycoplasma, Chlamydophila, Legionella) don't grow on routine cultures and require macrolide/broader therapy.
▶Why does this patient have sharp, breathing-related (pleuritic) chest pain?
Inflammation of the pleura overlying the infected lung causes pain that worsens with breathing and movement.
▶What chest X-ray finding confirms pneumonia in this patient?
A right perihilar infiltrate (consolidation).
▶What is the diagnosis in an asthmatic woman with fever, cough, pleuritic chest pain, very high CRP, and a perihilar infiltrate?
Community-acquired pneumonia (with a pleuritic component).
▶Why does normal post-recovery spirometry show this was not an asthma exacerbation?
No residual obstruction means the illness was an infection that fully resolved, not bronchospasm from asthma.
▶What does a CRP of 300 mg/L indicate here?
A very strong systemic inflammatory response to the acute infection.
▶Why is mild hypoxaemia common in pneumonia?
Alveolar consolidation/exudate creates ventilation-perfusion mismatch and impairs oxygen uptake.
▶Why might a kindergarten teacher be at higher exposure risk for respiratory infections?
Close contact with many young children increases exposure to respiratory pathogens.
▶Why was systemic steroid added to this asthmatic patient's pneumonia treatment?
To control airway inflammation/bronchial reactivity in the setting of background asthma.
▶Why was therapy escalated to antipseudomonal antibiotics after 3 days?
Failure of CRP to fall suggested a resistant organism, prompting broader (antipseudomonal) cover.
▶Why is falling CRP and improving radiology used to judge treatment response?
They objectively show resolving inflammation and infection.
▶What is the difference between typical and atypical pneumonia?
Typical (e.g. pneumococcal) causes lobar consolidation with productive cough; atypical causes more diffuse/interstitial patterns with dry cough and extrapulmonary symptoms.
▶Why is a dry (non-productive) cough notable in this case?
It can point toward an atypical/viral pathogen rather than a classic bacterial lobar pneumonia.
▶What is the most common bacterial cause of community-acquired pneumonia overall?
Streptococcus pneumoniae (pneumococcus).
▶Why does fever raise respiratory rate and contribute to respiratory alkalosis?
Fever and hypoxaemia stimulate ventilation, lowering pCO2 and raising pH.
▶What is a pleural effusion or empyema as a complication of pneumonia?
Fluid (or infected pus) collecting in the pleural space adjacent to the pneumonia.
▶Why does the end-expiratory wheeze occur in this asthmatic with pneumonia?
Underlying bronchial hyperreactivity causes mild airway narrowing, heard as wheeze.
▶Why are inhaled short-acting β2-agonists given 6x daily here?
To relieve bronchospasm and keep the airways open during the acute illness.
▶Why is procalcitonin useful in pneumonia management?
It helps distinguish bacterial infection (elevated) from viral/atypical causes and can guide antibiotic decisions.