Symptoms of bronchopneumonia

The symptoms and outcomes of focal pneumonia differ from the clinical manifestations of lobar (croupous) pneumonia described above, which is largely due to the peculiarities of the pathogenesis and morphological changes of both clinical and morphological variants of pneumonia.

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Clinical features

Firstly, with focal pneumonia, the inflammatory process is usually limited to a lobe or segment of the lung. Often, pneumonic foci can merge, capturing a more significant part of the lung lobe or even the entire 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, unlike lobar (croupous) pneumonia, focal pneumonia is usually not accompanied by immediate hypersensitivity; normergic and hyperergic reactions of the body are more typical. This feature probably determines the less violent, gradual formation of the inflammatory focus and a significantly smaller violation of vascular permeability than with lobar inflammation.

Thirdly, due to the lesser severity of vascular permeability disorders in the inflammation focus, the exudate in focal pneumonia contains only a small amount of fibrin and in most cases has the character of serous or mucopurulent exudate. For the same reason, there are no conditions for a massive release of erythrocytes into the lumen of the alveoli.

Fourthly, focal pneumonia almost always has the character of bronchopneumonia, in which the inflammatory process initially involves the bronchial mucosa (bronchitis), only after which the inflammation passes to the lung parenchyma and pneumonia is formed. Hence another important feature: in focal pneumonia, a significant amount of serous or mucopurulent exudate is contained directly in the lumen of the airways, which contributes to more or less pronounced disturbances of bronchial patency both at the level of the respiratory bronchioles and at the level of larger bronchi.

Finally, fifthly, the relatively slow spread of inflammation within the affected segment results in its individual areas being at different stages of the inflammatory process. While one group of alveoli shows only hyperemia and edema of the interalveolar walls (hyperemia stage), other groups of alveoli are already completely filled with exudate (hepatization stage). Such a motley morphological picture of the inflammation focus with uneven compaction of the lung tissue, which is very characteristic of bronchopneumonia, is supplemented by the presence of areas of microatelectasis caused by obstruction of mainly small bronchi. Thus, focal pneumonia as a whole is not characterized by the staging of inflammation found in some patients with lobar (croupous) pneumonia.

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

1. A relatively small extent of the inflammatory focus, capturing 1 or several lobes or a segment of the lung. The exception is confluent pneumonia, capturing significant parts of the lung lobe or even the entire lobe.
2. Focal pneumonia is accompanied by a normergic or hyperergic reaction of the body, which determines a slower formation of the inflammatory focus and a moderate violation of vascular permeability.
3. Serous or mucopurulent nature of the exudate.
4. Involvement of the bronchi in the inflammatory process (bronchitis), which is accompanied by obstruction of both small and (less commonly) larger bronchi.
5. The absence of clear staging of the inflammatory process, characteristic of lobar pneumonia.

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

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Interrogation

Unlike lobar pneumonia, the onset of bronchopneumonia is more gradual and prolonged. Often, focal pneumonia occurs as a complication of acute respiratory viral infection, acute or exacerbation of chronic bronchitis. Over the course of several days, the patient notes an increase in body temperature to 38.0-38.5°C, runny nose, lacrimation, cough with mucous or mucopurulent sputum, malaise and general weakness, which is regarded as a manifestation of acute tracheobronchitis or acute respiratory viral infection.

Against this background, it is very difficult to establish the onset of bronchopneumonia. However, the ineffectiveness of therapy conducted over several days, the increase in intoxication, the appearance of shortness of breath and tachycardia, or a new "wave" of increased body temperature make us assume the occurrence of focal pneumonia.

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

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

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Physical examination

During examination, hyperemia of the cheeks, possibly slight cyanosis of the lips, and increased moisture of the skin are determined. Sometimes significant pallor of the skin is noted, which is explained by severe intoxication and a reflex increase in the tone of the peripheral vessels.

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

Percussion over the lesion reveals a dull percussion sound, although if the inflammatory focus is small in size or deep in location, percussion of the lungs is uninformative.

Auscultation of the lungs is of the greatest diagnostic value. Most often, a pronounced weakening of breathing is determined over the affected area, caused by a violation of bronchial patency and the presence of multiple microatelectases in the inflammation focus. As a result, sound vibrations formed when air passes through the glottis, along the trachea and (partially) the main bronchi, do not reach the surface of the chest, creating the effect of weakening breathing. The presence of bronchial patency disorders explains the fact that even with confluent focal bronchopneumonia, pathological bronchial breathing is not heard as often as with lobar (croupous) pneumonia.

In rare cases, when bronchopneumonia has developed against the background of chronic obstructive bronchitis, and the inflammation site is located deep, harsh breathing can be heard during auscultation, caused by narrowing of the bronchi located outside the pneumonic site.

The most striking and reliable auscultatory sign of focal bronchopneumonia is the detection of fine-bubble moist sonorous (consonant) wheezing. They are heard locally over the area of inflammation and are caused by the presence of inflammatory exudate in the airways. Fine-bubble moist sonorous wheezing is heard mainly throughout the entire inhalation.

Finally, in some cases, when the pleural sheets are involved in the inflammatory process, pleural friction noise can be heard.

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

Comparative characteristics of lobar (croupous) and focal pneumonia

Signs	Lobar (croupous) pneumonia	Focal bronchopneumonia
Features of pathogenesis
The extent of the lesion	Share, segment	One or more lobules, segment; multiple foci of inflammation are possible
Spread of inflammation	Directly along the alveolar tissue (Kohn's pores)	Inflammation of the bronchi "spreads" to the lung parenchyma
Immediate hypersensitivity reaction in the respiratory zone of the lungs	Characteristic	Not typical
Involvement of the bronchi in the inflammatory process	Not typical	Typical
Airway patency	Not violated	Violated, microatelectasis may occur
Involvement of the pleura in the inflammatory process	Always	Only with superficial localization of the inflammation focus or with confluent pneumonia
Stages of development of morphological changes	Characteristic	Not typical
Nature of exudate	Fibrinous	Mucopurulent, serous
Clinical features
Onset of the disease	Acute, sudden onset of chills, fever and chest pain	Gradually, after a period of acute respiratory viral infection, acute tracheobronchitis or exacerbation of chronic bronchitis
Chest pain ("pleural")	Characteristic	Rarely, only with superficial localization of the inflammation focus or with confluent pneumonia
Cough	At first dry, then with the separation of "rusty" sputum	From the very beginning, productive, with the separation of mucopurulent sputum
Symptoms of intoxication	Expressed	Less common and less pronounced
Dyspnea	Characteristic	Possible, but less common
Dullness of percussion sound	In the hepatization stage, there is a pronounced dullness of sound	Expressed to a lesser degree, sometimes absent
Breathing pattern during auscultation	In the stage of influx and stage of resolution - weakened vesicular, in the stage of hepatization - bronchial	Often weakened breathing throughout the illness
Adverse respiratory sounds	In the stage of influx and the stage of resolution - crepitation, in the stage of hepatization - pleural friction noise	Wet, fine-bubble, sonorous wheezing
The appearance of bronchophony	Typical	Not typical

The most significant clinical signs that allow one to distinguish focal bronchopneumonia from lobar (croupous) pneumonia are:

• 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" chest pain;
• cough with the separation of mucopurulent sputum;
• absence of bronchial breathing in most cases;
• the presence of moist, fine-bubble, sonorous wheezing.

It should be added that the signs listed in the table, which allow us to distinguish between the two clinical and morphological variants of pneumonia, refer to the typical classical course of these diseases, which is currently not always observed. This is especially true for cases of severe hospital pneumonia or pneumonia that has developed in weakened patients and elderly and senile individuals.

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