Infectious pulmonary destructions: causes, symptoms, diagnosis, treatment

Infectious destruction of the lungs are severe pathological conditions characterized by inflammatory infiltration and subsequent purulent or putrefactive decay (destruction) of the lung tissue as a result of exposure to non-specific infectious agents (N. V. Pukhov, 1998). Three forms of infectious destruction of the lungs are distinguished: abscess, gangrene, and gangrenous lung abscess.

Causes of infectious destruction of the lungs

There are no specific pathogens of infectious destruction of the lungs. In 60-65% of patients, the cause of the disease is non-spore-forming obligate anaerobic microorganisms: bacteroids (B.fragilis, B.melaninogenicus); fusobacteria (F.nucleatum, F.necropharum); anaerobic cocci (Peptococcus, Peptostreptococcus), etc. Infectious destructions that occur as a result of aspiration of oropharyngeal mucus are most often caused by fusobacteria, anaerobic cocci and B.melaninogenicus. In case of aspiration of gastric contents, the most common pathogen of infectious destruction of the lungs is B.fragilis.

In 30-40% of patients, infectious destruction of the lungs is caused by Staphylococcus aureus, Streptococcus, Klebsiella, Proteus, Pseudomonas aeruginosa, and Enterobacteria. The named pathogens most often cause infectious destruction of the lungs, not primarily associated with aspiration of oropharyngeal mucus or gastric contents.

Infectious destruction of the lungs of hematogenous-embolic origin is most often caused by Staphylococcus aureus.

In rare cases, the disease is caused by non-bacterial pathogens (fungi, protozoa).

Predisposing factors: smoking, chronic bronchitis, bronchial asthma, diabetes, epidemic flu, alcoholism, maxillofacial trauma, prolonged exposure to cold, flu.

Pathogenesis of infectious destruction of the lungs

The causative agents of infectious destruction of the lungs penetrate the lung parenchyma through the respiratory tract, less often hematogenously, lymphogenously, by spreading from adjacent organs and tissues. In transbronchial infection, the source of microflora is the oral cavity and nasopharynx. Aspiration (microaspiration) of infected mucus and saliva from the nasopharynx, as well as gastric contents, plays a major role. In addition, lung abscesses can occur with closed injuries (bruises, compression, concussion) and penetrating wounds of the chest. With an abscess, limited inflammatory infiltration with purulent melting of the lung tissue and the formation of a cavity of decay surrounded by a granulation ridge is initially observed.

Subsequently (after 2-3 weeks) a breakthrough of the purulent focus into the bronchus occurs; with good drainage, the walls of the cavity collapse with the formation of a scar or an area of pneumosclerosis.

In gangrene of the lung, after a short period of inflammatory infiltration, due to the impact of microflora waste products and vascular thrombosis, extensive necrosis of the lung tissue without clear boundaries develops. In the necrotic tissue, many foci of decay are formed, which are partially drained through the bronchus.

Another important pathogenetic factor is the decrease in the function of general immunity and local bronchopulmonary protection (see “ Chronic bronchitis ”).

Classification of infectious destructions of the lungs

1. Causes (depending on the type of infectious agent).
   • Aerobic and/or conditionally anaerobic flora.
   • Obligately anaerobic flora.
   • Mixed aerobic-anaerobic flora.
   • Non-bacterial pathogens (fungi, protozoa).
2. Pathogenesis (mechanism of infection).
   • Bronchogenic, including aspiration, postpneumonic, obstructive.
   • Hematogenous, including embolic.
   • Traumatic.
   • Associated with the direct transfer of suppuration from adjacent organs and tissues.
3. Clinical and morphological form.
   • Abscesses are purulent.
   • Gangrenous abscesses.
   • Gangrene of the lung.
4. Location within the lung.
   • Peripheral.
   • Central.
5. Prevalence of the pathological process.
   • Single.
   • Multiple.
   • One-sided.
   • Double-sided.
   • With segment damage.
   • With the defeat of the share.
   • With damage to more than one lobe.
6. Severity of the current.
   • Light flow.
   • Moderate severity.
   • Severe course.
   • Extremely severe course.
7. Presence or absence of complications.
   • Uncomplicated.
   • Complicated:
     • pyopneumothorax, pleural empyema;
     • pulmonary hemorrhage;
     • bacteremic shock;
     • acute adult respiratory distress syndrome;
     • sepsis (septicopyemia);
     • phlegmon of the chest wall;
     • defeat of the opposite side in a primarily unilateral process;
     • other complications.
8. Nature of the flow (depending on time criteria).
   • Sharp.
   • With a subacute course.
   • Chronic lung abscesses (chronic course of gangrene is impossible).

Note: Gangrenous abscess is an intermediate form of infectious destruction of the lungs, characterized by less extensive and more prone to delimitation than gangrene, necrosis of the lung tissue. In this case, in the process of melting the lung tissue, a cavity with parietal or freely lying tissue sequesters is formed.

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