Pathophysiology of pneumonia
The structural and functional unit of the lung is the acinus, a terminal bronchiole with alveolar sacs surrounded by pulmonary capillaries. Normally, oxygen diffuses into the blood across the thin alveolocapillary membrane, and carbon dioxide is removed during ventilation.
In pneumonia, inflammation develops in the acinus: alveoli fill with exudate or purulent contents, the membrane thickens, and gas exchange is impaired. A key pathophysiological phenomenon develops—ventilation-perfusion mismatch (V/Q mismatch), leading to hypoxemia.
Routes of infection and risk factors
- Aspiration route—the most frequent. It occurs when pharyngeal, cough, and swallowing reflexes are suppressed (stroke, multiple sclerosis, ALS, opioid use, muscle relaxants on mechanical ventilation, alcohol intoxication). Anaerobic pathogens are typical.
- Inhalation route—pathogen entry via air, especially in crowded conditions (barracks, dormitories, orphanages). It more frequently causes atypical and viral pneumonias.
- Hematogenous route—spread of infection from the bloodstream, typical of intravenous drug use and sepsis.
- Impaired mucociliary clearance—in smokers (squamous metaplasia of the ciliated epithelium), COPD, bronchiectasis, cystic fibrosis (sodium-chloride cotransporter defect).
- Immunodeficiency—in HIV at the AIDS stage (CD4 < 200), CMV, Pneumocystis jirovecii, and other opportunists become active.
Classification
Clinical classification by infection site:
- CAP (Community-Acquired Pneumonia)—pneumonia developing outside a hospital setting. Most often caused by susceptible flora and responsive to amoxicillin.
- HAP (Hospital-Acquired Pneumonia)—nosocomial pneumonia developing 48 hours or more after hospitalization. Multiresistant strains (MRSA, ESBL producers) are typical.
- VAP (Ventilator-Associated Pneumonia)—pneumonia developing in patients on mechanical ventilation for more than 48 hours.
By clinical course, typical and atypical forms are distinguished.
Etiology: typical and atypical pneumonia
Typical pneumonia is caused by Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Klebsiella pneumoniae. Clinically characterized by:
- high fever with rigors (pronounced chills with shaking);
- productive cough with mucopurulent sputum;
- pleuritic chest pain;
- tachypnea, tachycardia, hypoxemia;
- physical signs of consolidation: dullness to percussion, enhanced vocal fremitus, bronchophony, egophony, bronchial breath sounds over the lesion.
Atypical pneumonia is caused by pathogens of the atypical group: Mycoplasma pneumoniae, Chlamydia/Chlamydophila pneumoniae, Legionella pneumophila, as well as viruses (influenza, parainfluenza, RSV, SARS-CoV-2, CMV). Features: low-grade fever, upper respiratory tract symptoms (rhinorrhea, pharyngitis, otalgia), myalgia, headache, bullous myringitis (in mycoplasma), absence of physical signs of consolidation. Legionella is characterized by hyponatremia and elevated liver enzymes.
Diagnostics
Laboratory diagnostics:
- complete blood count—leukocytosis with neutrophilia in bacterial infection, lymphocytosis in viral;
- biochemistry—markers of acute kidney injury (urea, creatinine), liver enzymes, electrolytes;
- respiratory viral panel if viral etiology is suspected.
Chest radiography—the gold standard of diagnostics. Lobar pneumonia involving one or more lobes and bronchopneumonia with multifocal patchy infiltrates are distinguished. On CT, viral pneumonias are characterized by the ground-glass sign, as well as the air bronchogram sign.
Complications
- Parapneumonic effusion—an aseptic accumulation of fluid in the pleural cavity.
- Empyema thoracis—infected pleural effusion.
- Lung abscess—destruction of the parenchyma, most often by anaerobes or S. aureus.
- ARDS—acute respiratory distress syndrome in diffuse alveolar damage.
- Sepsis and multiorgan failure in bacteremia.
Severity assessment and treatment
To determine management tactics, the CURB-65 scale is used: Confusion, Urea > 7 mmol/L, Respiratory rate ≥ 30/min, Blood pressure (SBP < 90 or DBP ≤ 60 mm Hg), age ≥ 65 years—each sign 1 point.
- 0–1 point—outpatient treatment;
- 2 points—hospital admission;
- ≥ 3 points—treatment in the intensive care unit.
Antibiotic therapy is prescribed to all patients with a confirmed diagnosis. According to the 2024 Russian clinical guidelines:
- outpatient without comorbidities—amoxicillin;
- outpatient with comorbidities or recent antibiotic use—amoxicillin/clavulanate, respiratory fluoroquinolones (levofloxacin, moxifloxacin), or oral third-generation cephalosporins;
- in hospital—combination of a beta-lactam (ceftriaxone) with a macrolide or monotherapy with a respiratory fluoroquinolone;
- in the ICU—beta-lactam + macrolide or beta-lactam + respiratory fluoroquinolone;
- at risk for MRSA, P. aeruginosa, or ESBL producers—expanded regimens (carbapenems, vancomycin, linezolid).
Prevention includes pneumococcal and influenza vaccination, smoking cessation, and control of comorbid conditions.
Key points
- The basis of pneumonia pathogenesis is acinar inflammation with the development of V/Q mismatch and hypoxemia.
- The main route of infection is aspiration due to impaired protective reflexes of the medulla oblongata.
- Classification divides pneumonia into CAP, HAP, and VAP; the choice of antibiotic depends on this.
- Atypical pathogens include Mycoplasma, Chlamydia, and Legionella; legionellosis is characterized by hyponatremia and liver involvement.
- The gold standard for diagnosis is chest radiography.
- The CURB-65 scale determines the setting for treatment: outpatient, hospital, or ICU.
- For uncomplicated CAP in patients without risk factors, amoxicillin is effective.
- Main complications: parapneumonic effusion, empyema, abscess, ARDS, sepsis.