Pathophysiology of Pediatric Pneumonia
Routes of Infection
- Inhalation of infected droplets — most common route
- Aspiration — oral secretions, feeds, foreign material (kerosene)
- Hematogenous spread — secondary to bacteremia (especially Staph, H. influenzae)
- Contiguous spread — from adjacent infected structures (rare)
Lobar Pneumonia — Pathological Stages
Classically described in pneumococcal lobar pneumonia:
| Stage | Pathology | Duration |
|---|---|---|
| Congestion | Vascular engorgement; serous exudate fills alveoli | Day 1–2 |
| Red hepatization | Alveoli filled with RBCs, neutrophils, fibrin; lung firm, red | Day 3–4 |
| Grey hepatization | RBCs lyse; WBCs and fibrin persist; lung grey, firm | Day 4–8 |
| Resolution | Enzymatic digestion of exudate; normal architecture restored | Day 8+ |
In children, full lobar consolidation is less common than in adults; patchy involvement is more typical.
Bronchopneumonia — Pathological Process
- Bacteria multiply in alveoli → inflammatory exudate
- Scattered areas of consolidation form around bronchi
- Lesions coalesce → lobular → lobar distribution
- Common in: Pneumococcal (later stage), Staphylococcal, H. influenzae infections
Staphylococcal Pneumonia — Unique Mechanism
- Pneumonic process initially diffuse
- Lesions suppurate → bronchoalveolar destruction
- Multiple microabscesses form → erode bronchial wall
- Air enters abscess cavity during inspiration
- Progressive inflation → pneumatoceles (pathognomonic)
- Empyema below 2 years: nearly always staphylococcal
Interstitial Pneumonia — Pathological Process
- Inflammatory cells infiltrate interstitial tissue (around alveoli and bronchioles)
- Alveolar walls thickened; alveolar spaces relatively spared early
- Signs of consolidation are absent or minimal clinically
- Caused by: Viruses (RSV, parainfluenza, adenovirus), Mycoplasma, Streptococcus
Viral Pneumonia — Pathophysiology
- RSV chief cause <6 months; at other ages: parainfluenza, influenza, adenovirus
- Virus infects respiratory epithelium → inflammatory infiltrate in interstitium
- Clinical signs of consolidation absent
- Radiological: perihilar and peribronchial infiltrates
- May predispose to secondary bacterial superinfection (especially Staphylococcal)
Gas Exchange Impairment
| Mechanism | Consequence |
|---|---|
| Alveolar consolidation | V/Q mismatch → hypoxemia |
| Interstitial thickening | Reduced diffusion capacity |
| Airway obstruction (secretions) | Air trapping, atelectasis |
| Extensive disease | Respiratory failure, hypercapnia |
Kerosene (Hydrocarbon) Aspiration Pneumonia
- Kerosene has low viscosity + low surface tension → diffuses rapidly from pharynx to lungs
- Direct chemical toxicity to lung parenchyma
- Milk and alcohol promote GI absorption → CNS toxicity
- Vomiting must NOT be induced (risk of aspiration)
- Gastric lavage is avoided
- Routine antibiotics not indicated (chemical, not infective process primarily)