Page 2 of 32

PA25.1-2 | Pneumonia & Lung Abscess — SDL Guide (Part 2)

Bronchopneumonia — Patchy Consolidation

A four-panel diagram shows bronchopneumonia as bilateral patchy peribronchial lower-lobe consolidation with microscopic suppurative bronchiolitis and comparison to uniform lobar pneumonia. — **Panel A:** Bilateral lungs showing patchy grey-yellow consolidation, lower-lobe predominance, posterior gravity-dependent distribution, peribronchial foci, and intervening normal lung.. **Panel B:** Magnified gross lung slice showing lobular peribronchial consolidation patches around bronchioles with relatively normal or haemorrhagic lung between foci.. **Panel C:** Microscopic view of suppurative bronchiolitis with bronchiole and adjacent alveoli filled by neutrophilic exudate, less fibrin, and compensatory emphysema in nearby alveoli.. **Panel D:** Comparison of lobar pneumonia with uniform whole-lobe consolidation versus bronchopneumonia with bilateral patchy lower-lobe consolidation..

Bronchopneumonia (lobular pneumonia) is the other major anatomical pattern of acute bacterial pneumonia. It is more common than lobar pneumonia at the extremes of age (infants, elderly) and in hospitalised, debilitated, or post-surgical patients.

Macroscopic features
- Multiple foci of grey-yellow consolidation (2–4 cm patches), typically bilateral and predominantly in the lower lobes and posterior segments (gravity-dependent distribution).
- Foci are centred on bronchioles ('peribronchial' consolidation). Between foci, lung may be relatively normal or haemorrhagic.

Microscopic features
- Suppurative bronchiolitis: bronchiole and surrounding alveoli are filled with a neutrophilic exudate.
- Fibrin formation is less prominent than in lobar pneumonia.
- Adjacent alveoli may show compensatory emphysema.
- No stage-by-stage progression (lobe is not uniformly involved).

Causative organisms: secondary/mixed flora — Staphylococcus aureus, Streptococcus pyogenes, H. influenzae, Klebsiella, Pseudomonas, anaerobes. Also follows viral pneumonias (influenza superinfection).

Comparison with lobar pneumonia

Feature	Lobar	Bronchopneumonia
Distribution	Entire lobe	Bilateral, patchy, lower lobes
Exudate centre	Alveoli	Bronchiole + surrounding alveoli
Fibrin	Abundant	Scanty
Stages	4 classic stages	None
Common age	Young adults	Infants, elderly, debilitated
Primary agent	S. pneumoniae	Mixed; secondary
Prognosis	Better (with Rx)	Worse (underlying disease)

Side-by-side low-power histology comparison showing uniform alveolar fibrinous exudate in lobar pneumonia versus patchy peribronchiolar suppurative exudate in bronchopneumonia. — **Panel A:** Lobar pneumonia: uniformly consolidated alveoli, fibrin meshwork, neutrophils, alveolar septa, residual air spaces, same low-power magnification scale bar, CXR homogeneous lobar opacity with air bronchograms.. **Panel B:** Bronchopneumonia: bronchiole, peribronchiolar suppurative exudate, patchy consolidation, surrounding normal aerated alveoli, same low-power magnification scale bar, CXR patchy bilateral lower-zone opacities..

CLINICAL PEARL

Clinical-radiological correlation: In lobar pneumonia, the entire lobe consolidates → chest X-ray shows a homogeneous opacity with air bronchograms (air-filled bronchi visible within the dense lobe). In bronchopneumonia, scattered foci of consolidation produce patchy bilateral opacities without a lobar distribution — sometimes called 'bilateral lower-zone haziness'. This difference is diagnostically important: if the CXR shows bilateral patchy shadowing in a 70-year-old who just had hip surgery, you should think bronchopneumonia (nosocomial, mixed flora, gram-negatives), not pneumococcal lobar pneumonia.

Complications of Pneumonia

A multi-panel medical diagram showing the major complications of bacterial pneumonia, including lung abscess, empyema, pleuritis, carnification, bacteraemia, respiratory failure, and ARDS. — **Panel A:** Consolidated right lower lobe, bacterial pneumonia, pleural spread, cavity formation, bloodstream spread, organisation/fibrosis, gas-exchange failure. **Panel B:** Lung abscess, thick-walled cavity, central liquefactive necrosis, pus, surrounding consolidation, aspiration pneumonia, S. aureus, Klebsiella, anaerobes. **Panel C:** Visceral pleura, parietal pleura, pleural cavity, pus in pleural space, empyema thoracis, fibrinous pleuritis, pleuritic chest pain, reduced breath sounds. **Panel D:** Organising fibrin, granulation tissue, collagen scar, obliterated alveoli, shrunken dark fleshy lobe, carnification, permanent loss of function. **Panel E:** Pulmonary veins, systemic circulation, bacteraemia, septicaemia, endocarditis, meningitis, septic arthritis, osteomyelitis. **Panel F:** Bilateral consolidation, ventilation-perfusion mismatch, type I respiratory failure, low PaO2, normal/low PaCO2, ARDS, diffuse alveolar damage, hyaline membranes.

Most cases of bacterial pneumonia resolve without sequelae with appropriate antibiotic therapy. However, several clinically important complications can occur:

Lung abscess: failure of resolution with central liquefactive necrosis → cavity formation. Particularly follows aspiration pneumonia, necrotising organisms (S. aureus, Klebsiella, anaerobes). Discussed in detail in the next section.

Empyema thoracis (pyothorax): extension of infection across the visceral pleura → pus in the pleural cavity. Presents with systemic sepsis + dullness to percussion + reduced breath sounds. Requires chest drainage (intercostal tube or VATS decortication).

Organisation and fibrosis (carnification): failure of fibrinolysis → fibrin organises into granulation tissue → collagenous scar replaces alveoli. Lobe becomes solid, dark, and shrunken ('fleshy' — carnification from carnis, flesh). Permanent loss of that lung segment's function.

Bacteraemia and septicaemia: organisms enter pulmonary veins → systemic circulation → sepsis syndrome. Can seed heart valves (endocarditis), meninges (meningitis), joints (septic arthritis), or bones (osteomyelitis).

Respiratory failure: bilateral extensive consolidation → ventilation–perfusion mismatch → type I respiratory failure (low PaO₂, normal/low PaCO₂). In severe cases: ARDS (diffuse alveolar damage superimposed).

Pleuritis: fibrinous pleuritis over the involved lobe causes the classic pleuritic chest pain (sharp, worse on inspiration). Pleural rub on auscultation. Usually resolves with pneumonia.

SELF-CHECK

A 55-year-old alcoholic is treated for right lower-lobe pneumonia but continues to spike fever despite two weeks of antibiotics. Repeat CT chest shows a thick-walled cavity in the right lower lobe with an air-fluid level. Which complication of pneumonia has most likely developed?

A. Empyema thoracis

B. Carnification (organisation)

C. Lung abscess

D. Respiratory failure

Reveal Answer

Answer: C. Lung abscess

A thick-walled cavity with an air-fluid level on CT, persisting after pneumonia treatment in an alcoholic (who is at high risk for aspiration), is the classic presentation of a lung abscess. Empyema is pleural (not intrapulmonary) and appears as a D-shaped pleural fluid collection, not an intrapulmonary cavity. Carnification produces a solid, not cavitary, lobe. Respiratory failure would not produce a localised cavity.

Lung Abscess — Aetiology and Pathogenesis

Medical diagram explaining lung abscess pathogenesis through aspiration, post-pneumonic necrosis, bronchial obstruction, and haematogenous spread, with a central cavitary abscess overview. — **Panel A:** Anterior lung cutaway, trachea, right main bronchus, left main bronchus, wider vertical right main bronchus, cavitary lung abscess, pus, necrotic tissue, inflamed lung parenchyma. **Panel B:** Aspiration pathway, oropharyngeal anaerobes, gastric acid, dependent right lung segments, posterior segment of right upper lobe, superior segment of right lower lobe, right middle lobe, basal lower lobe segments. **Panel C:** Post-pneumonic abscesses, bronchopneumonia pattern, multiple small abscess cavities, Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa, anaerobes. **Panel D:** Bronchial obstruction, bronchogenic carcinoma, foreign body, mucus plug, obstructive atelectasis, retained secretions, distal infection, abscess distal to obstruction. **Panel E:** Haematogenous spread, septic emboli, pulmonary arteries, distant septic focus, multiple peripheral abscesses.

A lung abscess is a localised area of suppurative necrosis within the lung parenchyma, resulting in a cavity containing pus and necrotic tissue.

Aetiology — the four main mechanisms

1. Aspiration (commonest, ~60%)
- Predisposing states: altered consciousness (alcoholism, general anaesthesia, epilepsy, drug overdose, stroke), dysphagia (neurological disease, oesophageal disease), dental sepsis.
- Aspirated material: oropharyngeal bacteria (predominantly anaerobes — Bacteroides fragilis, Fusobacterium nucleatum, peptostreptococci) + gastric acid (chemical injury → secondary infection).
- Location: right lung > left lung (wider, more vertical right main bronchus); in supine patients — posterior segment of right upper lobe or superior segment of right lower lobe (these are the dependent segments in the supine position); in upright/semi-upright — right middle lobe or lower lobe basal segments).

2. Post-pneumonic (secondary to pneumonia)
- Necrotising organisms: Staphylococcus aureus (especially in children and post-influenza adults), Klebsiella pneumoniae (Type III — thick capsule, 'mucoid' colonies), Pseudomonas aeruginosa, anaerobes.
- Multiple small abscesses in bronchopneumonia pattern.

3. Bronchial obstruction
- Tumour (bronchogenic carcinoma — most important in adults >40), foreign body aspiration (especially in children), mucus plug.
- Mechanism: obstructive atelectasis → retained secretions → infection → abscess distal to obstruction.
- Clinical rule: any lung abscess in an adult >40 must prompt bronchoscopy to exclude carcinoma.

4. Septic emboli (haematogenous)
- Source: right-sided infective endocarditis (tricuspid valve), septic thrombophlebitis, IV drug users.
- Pattern: multiple, bilateral, peripheral abscesses.