Etiology and pathogenesis
The primary causative agent of the disease is the pneumococcus (Streptococcus pneumoniae), which accounts for over 90% of cases. The disease can also be caused by the Friedländer's bacillus and other microorganisms. The route of infection transmission is airborne droplet.
The development is based on a type I hypersensitivity reaction in the alveoli and alveolar ducts. The early stages are explained by two theories:
- Aspiration theory — microorganisms from the upper respiratory tract enter the alveoli under the influence of triggering factors (e.g., hypothermia), causing a hyperergic reaction.
- Hematogenous-immune complex theory — the pathogen penetrates the bloodstream and parenchyma via the lymphoid tissue of the nasopharynx, after which it is secondarily seeded via the bloodstream, damaging the microvasculature.
Stages of morphological changes
The classic course of the pathological process includes 4 stages:
- Stage of congestion (inflammatory edema) — first 24 hours. Characterized by marked capillary congestion, interstitial edema, and fluid exudate containing microbes, which rapidly spreads through the pores of Kohn.
- Stage of red hepatization — day 2. The lobe becomes dense and airless, resembling liver tissue. A mass of erythrocytes and fibrin strands accumulates in the alveolar lumens.
- Stage of gray hepatization — days 4–6. The dark lung tissue is filled with a vast number of polymorphonuclear leukocytes and macrophages phagocytosing microbes.
- Stage of resolution — occurs on days 9–11. Enzymatic lysis of fibrin by leukocytes and evacuation of exudate via lymphatic drainage and sputum take place.
Complications and outcomes
Complications of lobar pneumonia are divided into pulmonary and extrapulmonary. They develop against the background of decreased immunity and a deficiency of defense cells.
- Pulmonary complications: carnification of the lung (organization of exudate and its replacement by connective tissue due to lymphostasis), acute abscess, gangrene, and empyema of the pleura, as well as life-threatening respiratory distress syndrome.
- Extrapulmonary complications: associated with bacteremia (found in 30% of cases). Lymphogenous dissemination (purulent mediastinitis, pericarditis) or hematogenous dissemination (purulent meningitis, metastatic brain abscesses, ulcerative endocarditis involving the tricuspid valve) is possible.
Outcome: in most cases favorable with complete recovery, although adhesions may remain on the pleura. Death results from acute cor pulmonale/heart failure or purulent complications.
Briefly: answers to topical questions
What macroscopic changes of the lung are observed in the stage of gray hepatization?
In the stage of gray hepatization, the affected lobe of the lung is macroscopically enlarged, heavy, dense, and completely airless. On cross-section, the surface of the lung tissue acquires a characteristic gray color and a granular appearance. The visceral pleura is thickened, appears cloudy, and is covered with pronounced fibrinous deposits.
How does lobar pneumonia differ from bronchopneumonia?
Croupous pneumonia differs from bronchopneumonia in the extent of the lesion and the nature of the process.
| Sign | Lobar Pneumonia | Bronchopneumonia |
|---|---|---|
| Nature of the lesion | Lobar pneumonia: an entire lobe of the lung is affected | Focal nature of the lesion |
| Pleural involvement | Involvement of the visceral pleura is characteristic; hence the synonym "pleuropneumonia" is used | This sign is not specified for bronchopneumonia in the sources |
| Propagation | Sources indicate involvement of the respiratory divisions of the lungs and intra-alveolar exudation | Spreads bronchogenically |
| Status | Independent nosological entity | Focal form of pneumonia |
What microscopic signs are characteristic of pulmonary carnification?
Pulmonary carnification is microscopically characterized by the replacement of intra-alveolar exudate with connective tissue. During this process, the following changes are observed:
- Alveolar lumina — instead of fibrinous masses and cellular exudate, maturing and then mature fibrous connective tissue is found.
- Alveolar septa — thickened and sclerosed.
- Acinus architectonics — disrupted, air-containing spaces are sharply reduced or absent.
The four stages of croupous pneumonia are easy to remember by their physical state: Edema (congestion) $ ightarrow$ Blood (red hepatization) $ ightarrow$ Gray leukocytes (gray hepatization) $ ightarrow$ Resorption (resolution).
Class and exam questions
Why is croupous pneumonia called lobar pneumonia or pleuropneumonia?
The name "lobar" reflects the morphology of the process, in which an entire lobe of the lung is affected. The term "pleuropneumonia" is used because the visceral pleura is invariably involved in the inflammation.
What is pulmonary carnification and why does it occur?
Carnification is a pulmonary complication in which fibrinous exudate is invaded by connective tissue (organization). This occurs due to impaired lymph outflow and lymphostasis.
Which pneumococcal serotypes are the most virulent?
Types 1, 2, 5, 7, 12, and 14 possess the highest virulence and are capable of affecting initially healthy individuals.
What else to study on this topic
- Pneumococcal serotyping and characteristics of their virulence in adults and children
- Comparison of the aspiration and hematogenous-immune complex theories of pathogenesis
- Cytological composition of the exudate at different stages of inflammation
- Modern pathomorphosis of croupous pneumonia and abortive forms
- The role of bacterial enzymes (hyaluronidase, leukocidin) in the development of stages
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