Acute pneumonia is an acute disease that unites a group of inflammatory, more often infectious, processes in the lungs with various etiologies, pathogenesis and morphological characteristics, with a primary lesion of their respiratory departments.
In the structure of morbidity, it occupies a significant place – 16 cases per 100,000 population per year.
CLASSIFICATION (O.V. Korovina, 1978).
· By etiology:
· bacterial (with indication of the causative agent)
· viral (with indication of the causative agent)
· mycoplasma and rickettsiosis (with indication of the causative agent)
· due to physical and chemical factors
· unspecified etiology
· By pathogenesis:
· By clinical and morphological characteristics
· By length:
· Bilateral (with segments indicated)
· By severity: Extremely heavy, Severe, Moderate, Light
· Flow: Acute, prolonged.
The most common causative agent of acute pneumonia is pneumococcus.
Other microorganisms that cause pneumonia can be staphylococci, streptococci, E. coli, Friedlander diplobacterium, enterococcus, protea, Pseudomonas aeruginosa, respiratory viruses, mycoplasmas, chlamydia, fungi.
Predisposing factors are exposure to various chemical and physical irritants (toxic substances entering the respiratory tract, smoking, hypothermia, injuries).
For secondary pneumonia:
· CCC diseases with NK according to the ICC
· chronic kidney diseases
· blood and lymph nodes diseases , immunodeficiencies
· respiratory diseases: swelling, bronchiectasis, etc.
The pathogen enters the lungs in three ways: hematogenous, lymphogenous and bronchogenic.
· The hematogenous route of infection is usually observed with sepsis and with infectious diseases.
· Lymphogenous infection spreads through wounds to the chest.
· Most often, microflora penetrates into the respiratory departments through the bronchi.
The occurrence of acute pneumonia, the features of its course and the outcome largely depend on the state of the mechanisms of nonspecific protection of the bronchi and lungs, which prevent microbes from entering the respiratory tract and lungs. These include:
· impaired mucociliary clearance
· defects in the surfactant system of the lungs
· insufficient phagocytic activity of neutrophils and alveolar macrophages
· changes in local and general immunity
· impaired bronchial patency
· impaired mobility of the chest and diaphragm
· decreased cough reflex.
The pathogenesis of croupous and focal pneumonia is different.
· Focal is an expression of a normal and hypoergic reaction of an organism to an infectious agent, while croupous is considered as a manifestation of a hyperergic reaction
. Sensitization to various microorganisms is present in both croupous and focal pneumonia, but the level of specific immunity in patients with croupous pneumonia is higher, which is associated with more significant antigenic irritation and immune defense.
· When analyzing the state of the T- and B-systems of immunity, certain changes were identified associated with the characteristics of the course of the disease. Their smallest changes are observed in patients with a favorable course of focal pneumonia. In cases of a protracted course, the content of T cells, their functional activity and the amount of immunoglobulins in the blood serum decrease. In patients with croupous pneumonia, there is a decrease in the number of T cells, an increase in B cells, and an increase in the content of immunoglobulins.
· Focal pneumonia is localized more often in the posterior regions of the lungs and is usually combined with damage to the bronchial tree (bronchopneumonia). The inflammatory process encompasses lobules or groups of lobules within one or more segments.
· Depending on the size of the foci, small-focal, large-focal and confluent pneumonias are distinguished. When draining the process may take a segment, several segments, part or all of the share.
· Macroscopically, a mottled picture is observed: individual pneumonic foci alternate with areas of normal lung tissue, atelectasis.
· During histological examination in the central, dense part of the lesion, the alveoli and bronchioles were performed with exudate containing leukocytes and an admixture of fibrin. On the periphery, the focus is surrounded by a zone of microbial edema with multiplying microorganisms.
· Croupous pneumonia captures the entire lobe or segment of the lung.
· The pathoanatomical picture differs in stages:
· The stage of the tide lasts from 12 hours to 3 days and is characterized by hyperemia of the lung tissue, impaired patency of the capillaries with an increase in inflammatory edema. In edematous fluid, a large number of microorganisms are determined.
· In the next stage of red hepatization, lasting from 1 to 3 days, due to diapedesis of blood cells (mainly erythrocytes) and the effusion of plasma proteins (primarily fibrin) into the alveoli and small bronchi, the affected area becomes airless, dense, red.
· In the stage of gray hepatization lasting from 2 to 6 days, the lung in the section has a grayish-yellow color, the alveoli are filled with a large number of neutrophils in which phagocytized microbes are detected by microscopy.
· The last stage of resolution is manifested by the gradual dissolution of fibrin. There is desquamation of the alveolar epithelium, filling the alveoli with macrophages that phagocytize neutrophils containing microbes. The duration of the stage depends on the prevalence of the process, the therapy, the reactivity of the body, the virulence of the pathogen.
Focal pneumonia of complaint
· for cough: dry or with sputum (mucous, mucopurulent, purulent), its amount is variable,
· Manifestations of general intoxication: general weakness, headache, fever, chills.
· With large focal discharge pneumonia, shortness of breath is possible
Anamnesis of the disease:
· Onset of focal pneumonia:
· acute – with an increase in body temperature
· gradual against the background of acute respiratory disease or bronchitis.
· Provoking factors:
· Acute respiratory infections, bronchitis
· Inhalation of toxic substances
· OVERALL INSPECTION:
· Dyspnea when several segments are affected
· Lip cyanosis
· RESPIRATORY SYSTEM – the clinical data correspond to the picture of focal pulmonary compaction syndrome:
· dullness of percussion sound when the size of the pneumonic focus is not less than 4 cm in diameter and is close to the surface of the chest
· Weakened vesicular or hard breathing
· sonorous wet small bubbling rales
· When examining other pathology systems is not detected
LARGE PNEUMONIA (PLEUROPNEUMONIA)
begins, as a rule, sharply, suddenly, with tremendous chills.
· pain in the side, aggravated by deep breathing, due to involvement of the pleura;
· gradually (as the lobe is removed from the breath), increasing shortness of breath
· headache, severe malaise. Symptoms of general intoxication can be so pronounced that the patient has an arousal, sometimes delirium.
· From 2-3 days sputum begins to separate, first sparse, viscous, then its amount increases and it acquires a brown-red tint (“rusty” sputum).
· In the first days of the disease, when examined, hyperemia of the cheeks is observed
· often mainly on the affected side, swelling of the wings of the nose when breathing
· herpetic eruptions on the lips
CARDIOVASCULAR SYSTEM: it is often noted –
· the right border of relative cardiac dullness may shift outward (due to an increase in the right ventricle)
· an accent of II tone appears on the pulmonary artery (due to increased pressure in the pulmonary circulation).
Increased (sometimes up to 3O-4O per minute) shallow breathing is noted.
· Symptoms of lobar compaction of the lung tissue, corresponding to the stage of the pathological process.
· At high tide
· blunt-tympanic percussion sound
· weakened vesicular breathing
· In the midst stage, which combines the pathological stages of red and gray hepatitis
· increased voice trembling
· dull percussion sound
· decreased mobility of the lower pulmonary margin
· bronchial breathing
· positive bronchophony.
· At the stage of resolution
· a blunt-tympanic percussion sound turning into a clear pulmonary
· weakened vesicular breathing
· moist finely bubbly sonorous rales
Examination of the digestive system does not reveal specific symptoms for pneumonia.
The duration of the febrile period, the duration and severity of the subjective and objective manifestations of acute pneumonia are very variable and depend on the type of pathogen, the reactivity of the patient, and the adequacy of the treatment.
Body temperature, having reached high figures in a few hours, can remain at this level for several days, after which it decreases critically (in 12-24 hours) or lytically (in 2-3 days).
· abscess formation (the appearance of a cavity syndrome in the lung)
· para- and metapneumonic pleurisy (first manifested by pleural friction noise, and as fluid accumulates in the pleural cavity)
· acute respiratory failure
· asthmatic component attachment
· infectious toxic shock
· infectious allergic myocarditis, pericarditis, endocarditis
· meningitis and meningoencephalitis
· intoxication psychoses
ADDITIONAL METHODS OF RESEARCH
· In peripheral blood, it is noted:
· neutrophilic leukocytosis
· with croupous pneumonia, a shift of the leukocyte formula to the left to metamyelocytes and myelocytes is possible, usually only a stab shift.
· There is an acceleration of ESR
· at the beginning of croupous pneumonia aneosinophilia is often detected.
· A biochemical blood test reveals positive “acute phase” reactions, they are much more pronounced with croupous pneumonia: an increase in the content of fibrinogen, sialic acids, globulins (the amount of albumin decreases, the reaction to C-reactive protein becomes sharply positive
· In urinalysis during a febrile period can be detected (which is a consequence of the effect of infectious toxins on the renal parenchyma): a small amount of protein, cylinders, single red blood cells,
· Sputum of patients with focal pneumonia contains:
· a large number of leukocytes
· desquamated epithelium of the respiratory tract
· with croupous red blood cells are often found
· Bacteriological research sputum to determine the pathogen and its sensitivity to antibacterial agents.
· with focal pneumonia, areas of darkening of medium or low intensity, often with uneven contours, are detected
· With croupous pneumonia:
· in the tide and there is an increase in the pulmonary pattern of the affected area, expansion of the root of the lung
· Later – homogeneous dimming of the whole lobe or segment
· At the stage of resolution, the dimming becomes spotty.
· With extensive focal focal or croupous pneumonia, disorders of the function of external respiration of a restrictive type develop:
· decreased lung capacity (VC)
· maximum lung ventilation (MVL)
· increased minute respiratory volume (MOD).
diagnostic criteria for pneumonia are:
· detection of signs of lung tissue compaction in combination with the acute onset of the disease
· the most important sign is the X-ray picture of the infiltrative changes in the lungs
· For focal pneumonia, the only physical sign may be the presence of sonorous, moist, small bubbling rales in a small area of the chest.
The formulation of a detailed clinical diagnosis.
Example 1. Primary bacterial (staphylococcal) focal pneumonia in the lower lobe of the left lung, prolonged course, lung abscess.
Example 2. Primary bacterial (pneumococcal) croupous lower lobe right-sided pneumonia, acute. Acute respiratory failure.
Differential diagnosis is carried out with diseases that occur with an increase in body temperature, cough and sputum production. The most important differential diagnostic sign of acute pneumonia is the x-ray picture.
· Croupous pneumonia differentiates primarily with focal pneumonia, from which it is distinguished:
· staged flow
· signs of
lobar compaction of the lung · x-ray picture of a homogeneous lobar or segmental infiltration.
· Pneumonia differs from exacerbation of chronic bronchitis:
· more severe course
· greater severity of symptoms of general intoxication
· sonorous sound of wheezing.
· Croupous pneumonia involving the diaphragmatic pleura in the process can be accompanied by abdominal pain and simulate a disease of the abdominal organs. The difference is the mandatory for pneumonia signs of a syndrome of compaction of the lung tissue and the absence of symptoms inherent in diseases of the digestive system.
· The presence of severe pain in the chest with pneumonia, a decrease in blood pressure necessitates differentiating it with myocardial infarction. It matters:
· a different nature of the pain syndrome
· another location – as a rule, pain in the side, and not behind the sternum;
· The relationship of pain with deep breathing;
· Usually stitching, not compressive or compressive in nature
· The absence of signs of a heart attack in an electrocardiogram with pneumonia is important
· Treatment of acute pneumonia should be carried out in a hospital.
An easily digestible, high-calorie diet with a high content of vitamins is prescribed.
· Etiopatogenetichesky therapy involves:
· effects on pathogen (antibiotics, sulfa drugs)
· elimination intoxication (gemodez, reopoligljukin)
· immunocorrection (pirogenal, interferon, levamisole)
· expectorants (thermopsis, 3% potassium iodide solution mukaltin)
· bronchodilators (aminophylline)
· With the development of heart failure, cardiac glycosides are prescribed, and in the presence of vascular insufficiency, camphor, sulfocamphocaine.
· To accelerate the resorption of inflammatory infiltration, physiotherapeutic treatment is prescribed (electrophoresis of calcium chloride, UHF, microwave therapy, physiotherapy exercises).
The criterion for treating acute pneumonia is the elimination of clinical, laboratory, radiological signs of the disease.