Complications of Pneumonia

General classification of complications

Depending on the scale and localization of the pathological process, all complications are traditionally divided into two broad groups: local and systemic.

Pulmonary complications include pathologies developing directly in the airways, lung parenchyma, and pleura. Among them, lesions of the pleural layers (dry or exudative parapneumonic pleurisy, as well as purulent pleural empyema) are the most common. A separate subgroup consists of destructive processes—lung abscess and gangrene. The development of pyopneumothorax and pronounced bronchoobstructive syndrome is also possible. It is important to distinguish acute conditions from outcomes: thus, pulmonary carnification, which represents the overgrowth of unresolved exudate by connective tissue, is not an acute complication, but a pathological outcome of pneumonia.

Extrapulmonary complications are caused by the entry of infection into the bloodstream and a massive release of inflammatory mediators. This group includes infectious-toxic shock, sepsis, and septic shock. Acute respiratory distress syndrome (ARDS) is an extremely severe variant of the systemic reaction. Hematogenous dissemination of microorganisms can lead to the involvement of other systems with the development of meningitis, endocarditis, myocarditis, or pericarditis. In addition, DIC syndrome, multiorgan failure, and decompensation of concomitant chronic conditions (diabetes mellitus, chronic heart failure, COPD) frequently arise against the background of severe intoxication.

A special place is occupied by acute respiratory failure — this condition can be regarded in two ways: both as a severe local consequence of excluding lung tissue from gas exchange, and as a systemic complication of the inflammatory process.

Temporal criteria of development

According to the timing of the formation of pathological processes, pulmonary complications are classified into two categories:

• Early complications. They occur in the acute period of the disease, at the peak of the inflammatory reaction. These include the development of infectious-toxic shock, acute respiratory failure, and parapneumonic pleurisy. If the inflammatory focus is located subpleurally, fibrin deposits rapidly form on the pleura, leading to the appearance of a characteristic clinical sign—pleural friction rub.
• Late complications. They form during the resolution stage of pneumonia or during its protracted course. This group includes purulent processes (abscess formation, pleural empyema), the formation of bronchiectasis, and pulmonary carnification.

Pathogenesis and types of lung abscess

Lung abscess is the formation of a clearly demarcated rounded cavity in the lung parenchyma filled with purulent contents (as opposed to phlegmon, which is a diffuse purulent inflammation).

Postpneumonic abscess formation, particularly characteristic of lobar pneumonia, occurs as a result of the complex interaction of several factors. The key link in the pathogenesis is the excessive activity of proteolytic enzymes released by neutrophils. If the elimination of the primary pathogen is insufficient and the general resistance of the body is reduced, secondary pyogenic microflora actively joins the process. Abscess formation is promoted by conditions that impair the quality of phagocytosis and the processes of proteolytic resolution of exudate: senile age, immunodeficiencies, chronic alcoholism, and diabetes mellitus.

According to the etiopathogenetic mechanism, the following groups of abscesses are distinguished:

1. Postpneumonic — a direct complication of acute pneumonias (including suppuration of a pulmonary infarction zone).
2. Bronchogenic (aspiration) — a consequence of foreign masses entering the airways with the development of abscessing pneumonia.
3. Hematogenous (metastatic) — the result of bacteria being carried by the bloodstream from a distant primary focus.
4. Traumatic — occur due to contusions or penetrating wounds of the chest cavity.
5. Contact — form upon the spread of purulent melting from neighboring organs (for example, in subphrenic abscess).

Chronification of the process and causes of mortality

In cases where acute destructive complications (such as acute abscess) or processes of exudate organization (carnification) are not resolved, the pneumoniogenic mechanism of chronification is triggered. The result is the development of a chronic abscess or chronic pneumonia. These conditions are characterized by a pronounced restrictive component—a persistent decrease in the volume of functioning lung tissue due to extensive proliferation of fibrous structures.

The development of complications drastically worsens the prognosis of the disease. A fatal outcome in severe pneumonias is most often caused by a complex of factors. Firstly, this is the exclusion of a significant volume of the lung from adequate gas exchange. Secondly, it is the progression of concurrent purulent complications that lead to massive systemic intoxication and the development of acute cardiopulmonary failure.

Class and exam questions

What else to study on this topic

• Pathogenesis of the development of acute respiratory distress syndrome (ARDS).
• Mechanisms of formation of cardiopulmonary failure in extensive inflammatory processes.
• Infectious-toxic shock: hemodynamic and microcirculatory disorders.
• Morphogenesis and pathological anatomy of the stages of lobar pneumonia.
• Bronchoobstructive syndrome as a complication of inflammatory diseases of the respiratory tract.

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