Pneumonia

Pneumonia – acute inflammatory lung disease with obligatory alveoli involment and exudative formation in them.

Classification

1. Acceding to the particularities of infection:

• nonhospital pneumonia;

• pneumonia in outpatients;

• pneumonia in innnpatients;

• intrahospital pneumonia;

• asperities pneumonia;

• pneumonia at severe immunodeficiency persons.

The category of the patients with nonhospital pneumonia:

1 category – pneumonia in patients without associated pathology and other modified factor;

2 category – pneumonia in patients with associated pathology and/or other modified factor;

3 category – pneumonia that needs hospitalization (without intensive treatment);

4 category – severe pneumonia that needs intensive treatment (reanimation).

3. The groups with intrahospital pneumonia:

1 group (A) – patients with mild or moderate pneumonia severity (without risk factors) that develops in different period of hospitalization or grave pneumonia with early manifestation (less than 5 days of hospitalization);

2 group (B) – patients with slight or moderate pneumonia severity (with specific risk factors) that develops in different period of hospitalization or grave pneumonia with early manifestation (less than 5 days of hospitalization);

3 group (C) – patients with grave in presence risk factors) or pneumonia with late manifestation (more than 5 days of hospitalization).

Nonhospital pneumonia means pneumonia that develops outside from hospital (in conditions of life).

Intrahospital pneumonia means pneumonia that develops in first 48-72 hours after hospitalization in condition of reject infectious in incubation period on the moment of admission to the hospital.

The main risk factors:

• smoking;

• taking of alcohol;

• chronic left ventricular heart failure;

• chronic obstructive pulmonary disease;

• influence of toxic ecologic and professional factors;

• innate defects of bronchopulmonary system;

• chronic infection in nosepharynx;

• the state of immunodeficiency and treatment with immune depressants;

• the status after operation;

• general exhaustion;

• long confinement to bed;

• old age.

The main pathogenic links:

- entrancing of the pathologic agent to the pulmonary tissue;

- impaired local bronchopulmonary resistance;

- development of the local inflammatory process and its overspreading in lung tissue;

- sensebilization advance to infectious agents and input of proinflammatory reactions;

- impaired microcirculation;

- activation of oxidative stress and proteolysis in lung tissue;

- antibody and immune complexes formation.

Acute lobar pneumonia

All authors who studied the etiology of acute lobar pneumonia (pleuropneumonia, croupous pneumonia), discovered Frenkel pneumococci (mostly types I and II, less frequently types III and IV) in about 95 per cent of cases. Fridlaender diplobacillus, streptococcus, staphylococcus, etc. are found less frequently.

Acute lobar pneumonia occurs mostly after severe overcooling. The main portal of infection is bronchogenic, less frequently lymphogenic and haematogenic. Congestion in the lungs in cardiac failure, chronic and acute diseases of the upper airways, avitaminosis, overstrain and other factors promote the onset of pneumonia. Acute lobar pneumonia is relatively frequent in patients who had pneumonia in their past history (it recurs in 30- 40 per cent of cases which is another evidence of the hyperergic character of the disease).

Pathological anatomy: Four stages are distinguished in the course of acute lobar pneumonia. The stage of congestion is characterized by acute hyperemia of the lung tissue, exudation, obstruction of capillary patency, and stasis of the blood. It lasts from 12 hours to 3 days. The stage of red hepatization continues from 1 to 3 days. The alveoli are filled with plasma rich in fibrinogen and erythrocytes. The stage of grey hepatization is characterized by cessation of erythrocyte diapedesis; the erythrocytes contained in the exudate decompose and their hemoglobin converts into haemosiderin. The alveoli (containing fibrin) become filled with leucocytes. The lungs become grey. The stage lasts from 2 to 6 days. The last stage is resolution. Fibrin is liquefied by proteolytic enzymes and exudate is gradually resorbed.

Clinical features

The onset of the disease. Typical acute lobar pneumonia begins abruptly with shaking chills, severe headache, and fever, to 39-40°C. The chills usually persist for 1-3 hours, then pain appears in the affected side; sometimes it may arise below the costal arch in the abdomen to simulate acute appendicitis, hepatic colics, etc. (this usually occurs in inflammation of the lower lobe of the lung, when the diaphragmal pleura becomes involved in the process). Cough is first dry and in 1-2 days dusty sputum is expectorated.

Objective examination: the patient's general condition is grave. General examination shows hyperemia of the cheeks, more pronounced on the affected side, dyspnea, cyanosis, often herpes on the lips and nose; the affected side of the chest lags behind in the respiratory act. Vocal fremitus is slightly exaggerated over the affected lobe. Sounds over the lungs are quite varied and depend on the distribution of the process, the stage of the disease, and other factors. At the onset of the disease, shortened percussion sound can be heard over the affected lobe, often with tympanic effect because liquid and air are simultaneously contained in the alveoli; the vesicular breathing is decreased while bronchophony is increasing; the so-called initial crepitation (crepitus indux) is present.

The height of the disease (classified by pathologists as the red and grey hepatization stages) is characterized by the grave general condition. It can be explained not only by the size of the affected area of the lung which thus does not take part in respiration but also by general toxicosis. Respiration is accelerated and superficial (30-40 per min) and tachycardia (100-200 beats per min) is characteristic. Dullness is heard over the affected lobe of the lung; bronchial respiration is revealed by auscultation. Vocal fremitus and bronchophony are exaggerated. Vocal fremitus is in some cases either absent or enfeebled (in combination with pleurisy with effusion, and also in massive acute lobar pneumonia, in which the inflammatory exudate fills large bronchi); bronchial breathing is inaudible. Before the antibiotic era, the patient with acute lobar pneumonia would often develop vascular failure with a marked drop in the arterial pressure due to toxic sis. Vascular collapse is attended by general asthenia, drop of temperature, increased dyspnea, cyanosis and accelerated small pulse. The nervous system is also affected (sleep is deranged; hallucinations and delirium are possible, especially in alcoholic patients). The heart, liver, kidneys and other organs are also affected. Fever persists for 9-11 days if antibiotics are not given. The temperature then drops abruptly during 12-24 hours or lytically during more than 2-3 days. Resolution stage. The exudate thins, air again fills the alveoli to decrease dullness of the percussion sound, tympany increases, and bronchial breathing lessens. Crepitation is heard again (crepitus redux) because the alveolar walls separate as air fills them. Moist rales are heard. Exaggerated vocal fremitus, then bronchophony, and finally bronchial breathing disappear.