Symptoms of bronchopneumonia

Symptoms and outcomes of focal pneumonia differ from the described bittern of clinical manifestations of lobar (lobar) inflammation of the lung, which is largely due to the peculiarities of the pathogenesis and morphological changes of both clinical and morphological variants of pneumonia.

[1], [2], [3], [4],

Clinical features

First, with focal pneumonia, the inflammatory process is usually limited to a lobule or lung segment. Often, pneumonic lesions may merge, capturing a larger portion of the lobe of the lung or even the whole lobe. In these cases, they speak of confluent focal pneumonia. It is characteristic that, unlike lobar (croupous) pneumonia, the pleura is involved in the inflammatory process only with superficial localization or confluent focal pneumonia.

Secondly, in contrast to the lobar (croupous) pneumonia, focal pneumonia, as a rule, is not accompanied by immediate-type hypersensitivity; more typical are normergicheskie and hyperergic reactions of the body. This feature probably determines a less violent, gradual formation of the inflammatory focus and a much smaller violation of vascular permeability than with croupous inflammation.

Thirdly, due to less severe violations of vascular permeability in the inflammatory focus, the exudate in focal pneumonia contains only a small amount of fibrin and in most cases is in the nature of a serous or mucopurulent exudate. For the same reason, there are no conditions for a massive release of red blood cells into the lumen of the alveoli.

Fourth, focal pneumonia almost always has the character of bronchopneumonia, in which the bronchial mucosa (bronchitis) is first involved in the inflammatory process, only after this the inflammation passes to the lung parenchyma and pneumonia is formed. This is another important feature: with focal pneumonia, a significant amount of serous or mucopurulent exudate is found directly in the lumen of the airways, which contributes to more or less pronounced violations of bronchial permeability both at the level of respiratory bronchioles and at the level of larger bronchi.

Finally, fifthly, the relatively slow spread of inflammation within the affected segment leads to the fact that certain parts of it are at different stages of the inflammatory process. While in one group of alveoli only hyperemia and edema of the interalveolar walls are revealed (the stage of hyperemia), other groups of alveoli are already completely filled with exudate (stage of hepatitis). Such a motley morphological picture of the focus of inflammation with uneven compaction of the lung tissue, which is very characteristic of bronchopneumonia, is complemented by the presence of micro-tectonic sites caused by impaired permeability of the predominantly small bronchi. Thus, focal pneumonia as a whole is not characterized by the staging of inflammation, detected in some patients with lobar (lobar) pneumonia.

The clinical and morphological variant of focal pneumonia is distinguished by the following pathogenetic and morphological features:

1. Relatively small length of the inflammatory focus, exciting one or several lobules or a segment of the lung. The exception is drain pneumonia, which captures significant portions of the lobe of the lung or even the whole lobe.
2. Focal pneumonia is accompanied by a normergic or hyperergic reaction of the body, which determines the slower formation of the inflammatory focus and moderate violation of vascular permeability.
3. Serous or mucopurulent character of exudate.
4. Involvement in the inflammatory process of the bronchi (bronchitis), which is accompanied by impaired patency of both small and (more rarely) larger bronchi.
5. The absence of a clear phasic inflammatory process, characteristic of lobar pneumonia.

These features of the pathogenesis largely determine the clinical manifestations of focal pneumonia (bronchopneumonia). Nevertheless, it should be remembered that the biological properties of pathogens of pneumonia and some other factors also have a significant impact on the clinical picture of this disease.

[5], [6], [7], [8],

Questioning

In contrast to lobar (lobar) pneumonia, the onset of bronchopneumonia is more gradual and extended in time. Often, focal pneumonia occurs as a complication of acute respiratory viral infection, acute or acute exacerbation of chronic bronchitis. For several days, the patient noted an increase in body temperature to 38.0-38.5 ° C, runny nose, lacrimation, cough with separation of mucous or mucopurulent sputum, malaise and general weakness, which is regarded as a manifestation of acute tracheobronchitis or ARVI.

Against this background, it is very difficult to establish the beginning of bronchopneumonia. Nevertheless, the ineffectiveness of the therapy carried out over several days, the increase in intoxication, the appearance of dyspnea and tachycardia, or the new “wave” of body temperature rise suggest the onset of focal pneumonia.

The patient's cough and separation of mucopurulent or purulent sputum increases, body temperature rises to 38.0-39.0 ° C (rarely higher), weakness increases, headache worsens appetite.

Chest pain associated with involvement in the inflammatory process of the pleura (dry pleurisy), appear only in some patients with superficial location of the center or the presence of confluent focal pneumonia. However, even in these cases, pleural pain usually does not reach such an intensity, which is observed in lobar (lobar) pneumonia. The pain increases or appears with deep breathing; its localization corresponds to the defeat of certain areas of the parietal pleura. In some cases (with the defeat of the diaphragmatic pleura), abdominal pain associated with breathing may occur.

[9], [10], [11], [12]

Physical examination

On examination, the hyperemia of the cheeks is determined, perhaps a slight cyanosis of the lips, an increased humidity of the skin. Sometimes there is a significant pallor of the skin, which is explained by severe intoxication and reflex increase in the tone of peripheral vessels.

When examining the chest lag in the act of breathing on the affected side is detected only in some patients, mainly in persons with confluent focal pneumonia.

With percussion over the lesion, a dull percussion sound is detected, although with a small extent of the inflammatory focus or a deep location of it, the percussion of the lungs is uninformative.

The greatest diagnostic value is auscultation of the lungs. Most often, a marked weakening of respiration is determined over the lesion area, due to a violation of bronchial patency and the presence of multiple microatelectases in the focus of inflammation. As a result, the sound vibrations generated by the passage of air through the glottis through the trachea and (partially) the main bronchi do not reach the surface of the chest, creating the effect of weakening breathing. The presence of violations of the bronchial patency explains the fact that even with confluent focal bronchopneumonia, pathological bronchial respiration is not heard as often as with lobar (lobar) pneumonia.

In rare cases, when bronchopneumonia has developed against the background of chronic obstructive bronchitis, and the center of inflammation is located deeply, during auscultation, you can listen to hard breathing caused by a narrowing of the bronchi located outside the pneumonic focus.

The most striking and reliable auscultatory sign of focal bronchopneumonia is the definition of finely moist moist sonorous (consonant) wheezing. They are heard locally over the area of inflammation and are due to the presence of inflammatory exudate in the airways. Small, moist, sonorous wheezes are heard mainly throughout the entire inhalation.

Finally, in some cases, when pleural leaflets are involved in the inflammatory process, you can hear the pleural friction noise.

The most significant differences between the two clinical and morphological variants of pneumonia: lobar (lobar) and focal pneumonia (bronchopneumonia).

Comparative characteristics of lobar (lobar) and focal pneumonia

Signs of	Lobar (lobar) pneumonia	Focal bronchopneumonia
Features of pathogenesis
Lesion volume	Share segment	One or more segments, segment; possible multiple foci of inflammation
Spread of inflammation	Directly on the alveolar tissue (pore Kona)	Inflammation of the bronchi "moves" to the lung parenchyma
Immediate-type hypersensitivity reaction in the respiratory areas of the lungs	Is characteristic	Not typical
Involvement in the inflammatory process of the bronchi	Not typical	Characteristic
Airway	Not broken	Disrupted; microatelectasis possible
Involvement in the inflammatory process of the pleura	Is always	Only with superficial localization of the source of inflammation or with confluent pneumonia.
Stage development of morphological changes	Is characteristic	Not typical
The nature of the exudate	Fibrinous	Mucopurulent, serous
Clinical features
Onset of the disease	Acute, sudden with chills, fever and chest pain	Gradual, after a period of SARS, acute tracheobronchitis or exacerbation of chronic bronchitis
Chest pain ("pleural")	Is characteristic	Rarely, only with superficial localization of the center of inflammation or with confluent pneumonia.
Cough	Dry at first, then with rusty sputum	From the outset, productive, with the separation of mucopurulent sputum
Symptoms of intoxication	Expressed	Less common and less pronounced
Dyspnea	Is characteristic	Possible, but less common
Dull percussion sound	In the gapping stage, pronounced dullness of sound	Expressed to a lesser extent, sometimes absent
Type of breathing during auscultation	At the stage of tide and resolution stage - weakened vesicular, in the stage of hepatization - bronchial	More often weakened breathing throughout the course of the disease.
Adverse respiratory noise	At the tide stage and the resolution stage - crepitus, at the gapping stage - pleural friction noise	Wet fine bubble resounding wheezing
Appearance of bronchophony	Characteristic	Not typical

The most significant clinical signs that allow differences, focal bronchopneumonia from lobar (lobar) pneumonia are:

• the gradual onset of the disease, developing, as a rule, against the background of acute respiratory viral infections, acute tracheobronchitis or exacerbation of chronic bronchitis;
• absence in most cases of acute "pleural" pain in the chest;
• cough with mucopurulent sputum;
• the absence in most cases of bronchial respiration;
• the presence of moist fine bubbling wheezing.

It should be added that the signs listed in the table, allowing to distinguish two clinical and morphological variants of pneumonia, relate to the typical classical course of these diseases, which is now far from always observed. This is especially true for cases of severe hospital pneumonia or pneumonia that have developed in debilitated patients and elderly people.

[13], [14]