Symptoms of croupous pneumonia

Shared pneumococcal pneumonia is characterized by the defeat of a whole lobe (or lung segment) of the lung and mandatory involvement in the inflammatory process of the pleura.

The second distinctive feature of lobar pneumonia is participation in the pathogenesis of the immediate reaction hypersensitivity reaction in the respiratory zone of the lungs, which determines the rapid onset of the disease, accompanied by a pronounced impairment of vascular permeability. This reaction is based on the preliminary sensitization of the macroorganism by the pathogen antigens-pneumococci, as a rule, present in the upper respiratory tract. When the pathogen again enters the respiratory sections of the lung and contacts the allergen with mast cells and immunoglobulins located on their surface, an immunoglobulin-antiimmunoglobulin complex is formed that activates the mast cell. As a result, it degranulates with the release of a large number of inflammatory mediators, which initiates an inflammatory process in the lung,

It should be emphasized that the activation of the mast cell and the release of inflammatory mediators can also occur under the influence of physical factors (cold, excessive physical exertion, "cold" in the form of acute respiratory viral infection, etc.). If by this time the respiratory sections of the lungs are colonized by Streptococcus pneumoniae, a "violent" hyperergic reaction develops, initiating the inflammatory process in the lung.

However, despite the fact that contact with the pneumococcal antigen leads to the formation of immunoglobulins in many patients with pneumococcal pneumonia, the described hyperergic reaction, characteristic of lobar croup pneumonia, occurs in only a few of them. It is assumed that in these cases an important role is played by hereditary predisposition, including the inheritance of some NLA genes. It is not excluded that the expression of these genes is combined with the increased ability of B-lymphocytes to secrete immunoglobulins upon contact with the antigen.

In croupous pneumonia, inflammation begins in one or more foci, and then spreads rapidly through the pulmonary tissue in the form of an "oil stain", mainly through the interalveolar pores of Kona. In this case, as a rule, bronchi are not involved in the inflammatory process (with the exception of respiratory bronchioles).

The third important feature of lobar pneumonia is the fibrinous nature of the exudate caused by a pronounced impairment of the vascular wall permeability associated with immunocomplex damage to the microcirculatory vascular bed of the pulmonary parenchyma. An additional damaging factor is the pneumococcal isolated hyaluronidase and hemolysins. Fibrinogen, upon contact with damaged lung tissues, is converted into fibrin, which forms the basis for the formation of a specific fibrin film that "lined" the surface of alveolar sacs and, apparently, respiratory bronchioles, without affecting larger bronchi. The film is easily removed, resembling that of diphtheria "croup". Hence the old name of lobar pneumonia - croupous pneumonia - a term that is not currently used in scientific medical literature, although it is often used in Russian medical practice.

Important distinctive features of share (croup) pneumonia, which largely determine the clinical picture of the disease, are:

• widespread defeat of the whole lobe (or less commonly - segment) of the lung with mandatory involvement in the inflammatory process of the pleura;
• participation in the pathogenesis of pneumonia of an immediate type of hypersensitivity reaction, which determines a "violent" hyperergic reaction initiating the inflammatory process in the lung;
• fibrinous character of exudate;
• the primary lesion of alveolar tissue and respiratory bronchioles with the preservation of the full patency of larger respiratory tract.

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

The course of lobar pneumonia

The classical course of lobar pneumonia is characterized by the stage of development of morphological changes in the lungs.

The tidal stage is characterized by a sharp hyperemia of the lung tissue, a violation of microcirculation and vascular permeability. Rapidly developing edema of the alveolar walls, accompanied by a decrease in the elasticity of the lung tissue. A small amount of exudate, which begins to fill the alveoli, for some time is located near the wall, as if "lining" their inner surface. The alveoli themselves still retain their airiness. Usually, at the end of this stage, it is possible to identify the involvement of the pleura in the inflammatory process. The duration of the tide stage does not exceed 1-2 days.

The stage of curation (hepatization) is characterized by the predominance of pronounced exudation and emigration to the inflammatory focus of cellular elements involved in inflammation. In this stage, the alveoli are completely filled with fibrinous exudate, and lose their airiness. Exudate is rich in fibrin, alveolar epithelial cells and leukocytes. At the expressed infringement of a vascular permeability in an exudate the considerable quantity of erythrocytes is found out.

Macroscopically, one or more lesions of the lung are enlarged and uniformly compacted (hence the traditional name for this stage is "curing", or "hepatitis"). On the cut, the surface of the lung tissue can be of different colors - from dirty gray to dark red - depending on the severity of vascular permeability disorders. The centers of "gray curing" reflect the prevalence of leukocytes in the exudate, mainly neutrophils. If in Exudate, in addition to peytrophils and fibrin, there is a large number of red blood cells, the focus of inflammation looks like a site of "red curing".

In the past, there was an idea of the mandatory sequential transformation of the areas of "red custody" in the areas of "gray custody". However, it has now been proved that the morphological pattern of lobar pneumonia throughout the entire stage of custody can be represented by gray foci, hack and red regions, or by a combination of both. In other words, with lobar pneumococcal pneumonia, foci of gray and red opacification can occur simultaneously and probably are not related to the time elapsed since the onset of the disease. Such a variegated morphological picture of the lung in the stage of curing is connected, first of all, with the type of pneumococcus, which was the causative agent of the disease, its virulence, and also with the reactivity of the macroorganism.

In the stage of curation of the pleura, fibrinous and fibrinous-purulent overlays are found that reflect the involvement of the pleura in the inflammatory process.

The duration of the treatment phase usually does not exceed 5-10 days.

The resolution stage is characterized by a gradual resolution of the inflammatory exudate, an increase in the breakdown of leukocytes, and an increase in the number of macrophages. Alveoli are gradually released from exudate, slowly restoring its airiness. For some time, exudate re-located only pristenochno on the inner surface of the alveoli, and then disappears completely. Suffice for a long time, the edema of the walls of the alveoli and the reduced elasticity of the lung tissue remain.

The described distinct staging of the inflammatory process in case of lobar pneumonia is presently observed very rarely, which is associated with a change in the biological properties of the pathogen, as well as the effect of the timely prescribed antibacterial therapy on inflammation.

The classic course of lobar pneumonia is characterized by a successive change in the three stages of the inflammatory process, the morphological manifestations of which underlie the entire clinical picture of the disease:

1. Stage of the tide:
   • inflammatory hyperemia and edema of interalveolar walls with a decrease in the elasticity of the lung tissue;
   • the parietal location of a relatively small amount of fibrinous exudate,
   • preservation of some airiness of the alveoli in the focus of inflammation.
2. The stage of curation (hepatitis):
   • "Tight" filling of alveoli with fibrinous exudate, consolidation of the lobe of the lung;
   • presence in the affected portion of the sites of both gray and red curing;
   • mandatory involvement in the inflammatory process of the pleura.
3. Resolution stage:
   • "Dissolution" and resorption of fibrinous exudate, which for some time is located in the alveoli pristenochno;
   • gradual restoration of airiness of alveoli;
   • long-lasting puffiness of the interalveolar septa and reduced elasticity of the lung tissue.

Resolve

The patient's questioning with the presence of symptoms suspicious of spilling pneumonia should include:

1. An exhaustive analysis of the patient's complaints.
2. Evaluation of the clinical and epidemiological situation in which pneumonia has developed, in particular:
   • Possible provoking factors (hypothermia, respiratory viral infections, overfatigue, alcoholic excesses, excessive smoking, anesthesia and narcotic "intoxication", cerebral trauma or stroke, etc.);
   • long stay in an isolated team, in conditions of crowding (school institutions, nursing homes, prisons and so on);
   • recent trips and accommodation in hotels, including air-conditioned;
   • possible recent contacts with patients with pneumonia, bronchitis, ARVI or "colds", as well as contact with animals, birds;
   • stay in hospitals, intensive care units;
   • application for the diagnosis and treatment of endotracheal tube, mechanical ventilation, bronchoscopy, etc .;
   • possible recurrent or episodic aspiration of gastric contents, and the like.
3. Presence of concomitant chronic diseases (bronchopulmonary, cardiovascular, digestive organs, diabetes, blood diseases, immunodeficiency states, allergic reactions, etc.).
4. Presence of risk factors (age, smoking, alcoholism, drug addiction, etc.).

Stage of the tide

It was shown above that the "tide" stage is characterized by a significant increase in body temperature (up to 39-40 ° C and higher), accompanied by chills, increasing symptoms of intoxication, chest pain associated with breathing with the appearance of a dry, sometimes painful cough.

Inspection

Patients often occupy a forced position in bed, lie on their backs or on their sore sides, pressing their hands with a section of the chest in which there is maximum pain. This situation somewhat reduces the excursion of sore leaflets and relieves pain.

Consciousness can not be changed, although sometimes different degrees of its violation are observed. Skin wet. There is a hyperemia of the face and an injection of sclera, often more pronounced on the side of the lesion. Since lobar inflammation of the lung is often accompanied by a viral infection on the lips, wings of the nose and ear lobes, herpetic eruptions can be detected.

In severe cases and in patients with concomitant chronic diseases of the lungs or heart there is a small cyanosis of the lips, the tip of the nose, earlobes, which is associated with the developing respiratory insufficiency and circulatory disorders.

Examination of the respiratory system

If there is severe pain, breathing becomes superficial, mainly because of the patient's desire to reduce the friction of the pleural sheets against each other, causing pain.

Already in this stage of the disease it is possible to identify the lag of the diseased side of the chest in the act of breathing, although the symmetry of the thorax is completely preserved

When palpation is often determined by the local tenderness of the chest, associated with inflammation of the parietal pleura, as well as a slight increase in vocal jitter on the side of the lesion. In the projection of the affected lobe of the lung, blunting (shortening) of the percussion sound with a tamponic shade is determined. Dullness of percussion sound is associated with a small compaction of lung tissue. The timbre of the percussion sound is due to the preservation of some airiness of the alveoli, while a significant decrease in the elasticity of the lung tissue. The latter leads to a substantial depletion of the timbre of percussion sound, characteristic of a healthy lung with normal elasticity of the lung tissue. As a result, the pulmonary sound by the physical characteristics approaches the tympanic.

In auscultation, two auscultatory phenomena are defined in the projection of the affected lung fraction: weakened breathing and crepitation.

It was shown above that in the initial stage of lobar pneumonia (the "tidal" stage) the alveoli only partially retain their airiness, and the inner surface of their walls, as well as the walls of the respiratory bronchioles, lining the viscous fibrinous exudate, and the alveolar walls themselves are edematic and rigid.

During most of the inspiration, the alveoli and, possibly, the respiratory bronchioles are in a collapsed state, which resembles the picture of multiple micro-telelectases, the appearance of which in the projection of the affected lobe of the lung and explains the auscultatory phenomenon of weakening of breathing. It is clear that a much higher gradient of pressure in the pleural cavity and upper respiratory tracts is required to straighten the adherent walls of the alveoli than in the norm. This pressure gradient is reached only towards the end of the inspiration. During this period, the walls of the alveoli containing the exudate dissolve, and a specific sound arises that is commonly called crepitacio index (initial crepitation).

Crepitation is very similar to wet fine bubbling rales (fine cracles), but differs in that it occurs only at the height of a deep inspiration and does not change when you cough.

It should also be remembered that crepitation can also occur in other pathological conditions, which are also characterized by a decrease in the airiness of the alveoli and the violation of the patency of the respiratory bronchioles that are (together with the alveoli) during the first half of the inspiration in the asleep state. This situation occurs with compression atelectasis, lung infarction, pneumonitis and other diseases.

The most characteristic physical signs of the initial stage of lobar (croupous) pneumonia (tidal stage) are:

• weakened vesicular breathing in the projection of the affected lobe of the lung, accompanied by crepitatio index;
• in the same projection - dullness of percussion sound with tympanic shade (less constant sign).

[5]

The stage of custody

The stage of "curation" (the height of the disease) is characterized by the persistence of high fever, symptoms of intoxication, the appearance of a cough with the separation of "rusty" and mucopurulent sputum, an increase in signs of respiratory failure, and in some cases - cardiac and vascular insufficiency.

When examined for several days from the onset of the disease, the patient's forced position on the affected side may be retained due to involvement of the pleura in the inflammatory process (dry pleurisy), as well as flushing of the face and injection of the sclera on the side of the lesion. With a severe course of the disease, cyanosis increases due to progressive ventilation respiratory failure.

Examination of the respiratory system

Respiration is frequent (up to 25-30 or more per 1 min) and superficial. With a considerable extent of the inflammation affecting two or more lobes, the presence of not only tachypnea, but also a pronounced difficulty in breathing, in particular inspiratory dyspnea, participation in the respiration of the auxiliary musculature, swelling with the breathing of the wings of the nose, etc., attracts attention.

There is also a distinct lag in the act of breathing of the patient's half of the chest. At this stage of the disease, vocal tremor and bronchophonia are strengthened on the diseased side.

With percussion, pronounced dullness of the percussion sound above the lesion area is noted, not reaching, however, to the degree of absolutely dull (femoral) sound, the appearance of which in the patient with lobar pneumonia indicates the formation of exudative pleurisy.

During the height of the disease, above the projection of the affected lung, abnormal bronchial respiration is heard, due to the compaction of the lung tissue while maintaining the patency of the airways. For backward reasons, crepitation is not heard, since the alveoli are completely filled with fibrinous exudate and airiness is lost. Often, for several days, the noise of friction of the pleura continues to be heard over the affected area, which subsequently disappears.

Against the background of increasing signs of intoxication, the heart rate increases to 110 12 per 1 min. At the top, functional systolic noise can be heard, in some cases, arrhythmia.

In uncomplicated course of lobar pneumonia, the duration of the peak period of the disease usually does not exceed 7-10 days, after which the resolution stage begins.

The most characteristic physical signs of the stage of custody are:

• pathological bronchial breathing in the projection of the affected lobe of the lung and the noise of friction of the pleura;
• pronounced blunting of percussion sound.

Stage of resolution

The stage of resolution in cases of uncomplicated course of the disease is characterized by a decrease in body temperature (lytic or, in more rare cases, a critical decrease in all manifestations of general toxication syndrome and respiratory failure, cessation of coughing.

All pathological findings are revealed in the stage of curing with percussion and auscultation gradually regress. There is a kind of "enlightenment" of blunted percussion sound. Dulling again, like in the first stage, acquires at first a tympanic hue, and then a clear pulmonary sound is restored.

At auscultation, the bronchial shade of respiration weakens, which is associated with a decrease in the compaction of lung tissue. Due to the gradual dissolution of the exudate, the airiness of the alveoli is partially restored. The exudate is located near the wall. Therefore, just as in the first stage of the disease, weakened breathing is determined over the affected part of the lung for some time. At the end of the inhalation, the "breaking" of the alveoli and respiratory bronchioles again occurs, which is the cause of crepitation (crepitacio redux - the ultimate crepitation). Unlike the first stage crepitacio redux becomes sonorous.

As the removal of the exudate and the disappearance of edema of the alveolar walls, the elasticity and airiness of the lung tissue are restored, vesicular breathing begins to be determined over the lungs, crepitation disappears.

The most characteristic physical signs of the resolution stage are

• dullness of percussion sound with a tympanic tinge, which is gradually replaced with a clear pulmonary sound;
• weakened vesicular breathing, which passes into vesicular breathing;
• the appearance of reduptio redux, with the subsequent disappearance of this auscultatory phenomenon.

It should be emphasized that the described precise staging of clinical manifestations of lobar (croupous) pneumonia is presently relatively rare. In this connection, laboratory and radiographic signs of the disease acquire special significance for diagnosis.

Complaints of the patient for shared pneumonia

All early symptoms of developing lobar pneumonia can be divided into two groups:

1. generalintoxication and
2. bronchopulmonary.

The first of these includes fever, chills, headache, general and muscle weakness, weakness, to the second group - pain in the chest, cough, shortness of breath, separation of sputum, etc.

[6], [7]

Fever

In most cases, lobar pneumonia begins acutely, with a sudden rise in body temperature to 39-40 ° C and higher and pain in the chest. Myasnikov, sick with croupous pneumonia, remembers the day and the hour when the disease began. The rise in body temperature is usually preceded by a tremendous chill, lasting 3 hours. Further high fever (38.1-39 ° C) of a constant character (febris continua) is established with small daily fluctuations in body temperature not exceeding 0.5-1.0 ° C, which is very typical for the uncomplicated course of pneumococcal pneumonia. The constant fever can last 7-10 days, but against the background of adequate antibiotic therapy this period is usually reduced to 3-4 days.

If the swings of body temperature exceed 1-2 ° C (laxative, hectic) within a day and are accompanied by chills or scrotaling with each new rise in body temperature, one should think about possible purulent-destructive and septic complications-abscessing of pneumonia, development of pleural empyema, sepsis and etc.

In uncomplicated course of lobar pneumonia, the febrile period ends with a lytic (gradual) or (rarely) critical (sudden) drop in body temperature. A critical drop in temperature may be accompanied by symptoms of acute vascular insufficiency.

Among the most important factors determining the nature of the temperature response in pneumonia, today include inflammatory mediators (prostaglandins, leukotrienes, cytokines, a significant increase in which is observed during the height of the inflammatory process in the lungs, and affects the functional state of the thermoregulatory centers.

Thus, the temperature response as a whole not bad reflects the nature and dynamics of the inflammatory process in the lung, as well as the effectiveness of antibiotic and anti-inflammatory therapy. Nevertheless, it should be remembered that the normalization of body temperature does not in itself mean the completion of the pathological process in the lung. Moreover, in some cases, the lack of a temperature response in the formation of lobar pneumonia, especially in elderly and senile patients or weakened patients suffering from severe concomitant diseases. Can have a serious prognostic value, indicating a sharp decrease in the reactivity of the body.

[8], [9], [10]

Chest pain

The second earliest and most characteristic sign of the onset of lobar pneumonia, indicating the involvement of the lower part of the parietal pleura adjacent to the diaphragm, in which a dense network of pain receptors is concentrated, is involved in the inflammatory process.

The most characteristic signs of pleural pain is the acute intense nature of pain in the chest, arising and / or amplifying at the height of a deep inspiration. Usually the pain is strictly localized - and the patient can accurately indicate the place of maximum pain. Pain, as a rule, increases when the patient is bent to the healthy side, since this position increases the friction of the inflamed pleura sheets against each other with deep breathing. When a pain syndrome occurs, the patients often breathe superficially, instinctively trying to avoid irritation of the painful receptors of the pleura.

It should be remembered that with lesions of the diaphragmatic pleura, intense acute pains can be localized in various parts of the abdomen, simulating a clinical picture of such diseases as acute cholecystitis, stomach ulcer or 12-intestinal ulcer and even acute appendicitis; pain in the left side with pneumonia can simulate acute pancreatitis. In these cases, the presence of high fever and general toxication syndrome further complicates clinical diagnosis. Nevertheless, a careful analysis of the nature of the pain in the abdominal area and, first of all, a clear connection of pain with breathing in most cases allows one to suspect the patient's having pleuropneumonia and conduct an appropriate diagnostic search.

With pleuropneumonia, acute chest pain associated with breathing usually lasts 2-3 days and then disappears. Nevertheless, the increased sensitivity of the skin in the area of the affected pleura may persist for a long time, even after the completion of the inflammatory process, increasing with hypothermia, after physical exertion, when respiratory diseases occur, and so on. Such increased pain sensitivity of the pleura can be detected by palpation of the corresponding sections of the thorax. At the same time, the patient himself with deep breathing often feels a kind of discomfort in this area, although it does not characterize him as intense pain.

In uncomplicated course of lobar pleural pneumonia, chest pain lasts no more than 2-4 days and has the character of typical pleural pain, which is characterized by:

• acute intense character;
• clearly localized pain;
• the occurrence or intensification of pain at the height of a deep inspiration;
• Increased pain when bending the patient to a healthy side.

Cough is the third characteristic sign of pleuropneumonia. As you know, cough occurs when the receptors of the vagus nerve and the upper laryngeal nerve are irritated, located in the pharynx, larynx, trachea, large bronchi and in the pleura. The pathological process, localized only in the parenchyma of the lung or in the small bronchi, is not accompanied by a cough until the sputum enters the larger bronchi.

At the very beginning of the disease (in the 1-2 days of the disease) cough is dry, without separation of sputum. It is associated with involvement in the inflammatory process of the pleura and increased sensitivity of cough receptors. Dry cough often appears with a deep breath, simultaneously with the appearance or intensification of the pain described above in the chest.

After 1-2 days from the onset of the disease, the cough acquires a different character. By this time, the process of exudation begins to grow, and a small amount of viscous fibrinous exudate appears in the alveoli, and then in the terminal and larger bronchi, which contains a large number of leukocytes and, quite often, erythrocytes. As a result, a cough is accompanied by the release of a small amount of sputum "rusty" color, which reflects the formation in the inflamed lobe of the light areas of "red curing" of lung tissue.

Occasionally, with more pronounced impairment of vascular permeability in the inflammatory focus, sputum or even blood clots may appear in the sputum. In uncomplicated course of lobar pneumonia, uninvited "hemoptysis" or separation of "rusty" sputum continues for a relatively short time (no more than 2-3 days). In the future, sputum usually acquires a mucous or muco-purulent character and is separated in a small amount.

Longer separation of bloody sputum causes differential diagnosis of pleuropneumonia with such diseases and syndromes as tuberculosis, lung cancer, infarct pneumonia, bronchiectatic disease, lung abscess, hemorrhagic tracheobronchitis, and others.

In patients with lobar pneumonia, a dry (reflex) cough associated with involvement in the inflammatory process of the pleura appears in the first 1-2 days from the onset of the disease. During the next 2-3 days, a small amount of sputum appears, often "rusty" in color, and in rare cases - veins and clots of blood in the sputum.

[11], [12], [13], [14]

Dyspnea

A constant sign of lobar inflammation, although its severity largely depends on the severity of the course of the disease, the stage of the inflammatory process, and the presence of concomitant diseases of the bronchopulmonary and cardiovascular system.

In any case, dyspnea with lobar pneumonia is a manifestation of respiratory failure due to three main causes:

• switching off part of the pulmonary parenchyma from pulmonary ventilation;
• increased rigidity of the lungs, which hinders breathing and limits the ventilation of the lungs;
• a decrease in ventilation-perfusion ratios in the affected lung, causing a right-left-handed discharge of venous blood and even the formation of a venous alveolar shunt.

For obvious reasons, the greatest manifestation of dyspnea reaches the stage of custody. In some cases, usually in young patients who do not have concomitant diseases of the lungs and heart, respiratory failure is manifested only by a slight feeling of lack of air and tachypnea arising from physical exertion.

In severe pneumonia, especially in elderly patients, as well as in persons with concomitant diseases of the bronchi, lungs and cardiovascular system, acute respiratory failure may occur. A significant increase in respiratory movements, not only during physical exertion, but also at rest, is accompanied by a painful sense of lack of air and objective signs of respiratory failure - diffuse "gray" cyanosis, participation in respiratory support muscles, tachycardia, etc.

The respiratory rate in a patient with pneumonia to 24 in 1 min or more is regarded as a severe course of pneumonia requiring hospitalization in the ICU.

[15], [16], [17]

General Intoxication Syndrome

It was mentioned above that one of the main clinical signs of lobar pneumonia is a significant increase in body temperature, accompanied by other manifestations of general toxicity syndrome, general weakness, malaise, sweating, headache, confusion (delirium, hallucinations and even loss of consciousness).

Often there are also disorders of the function of other organs and systems: a sharp decrease in appetite, heaviness in the epigastric region, unstable stool, flatulence, myalgia, arthralgia, arrhythmia, cardiac and vascular insufficiency.

General weakness is one of the most important manifestations of general intestinal toxicity syndrome and in many cases has prognostic value, to a certain extent reflecting the dynamics of the inflammatory process in the lungs. With shared (croupous) pneumonia, general weakness occurs from the first hours of the disease and, rapidly growing, reaches a maximum in 1-2 days.

In severe cases, adynamia appears. Any physical activity causes a painful sense of weakness. Patients with difficulty can raise their hands, sit in bed, even open their eyes. Such severe adynamia is usually accompanied by a pronounced increase in respiration (more than 30 in 1 min), tachycardia (heart rate - 100-120 per 1 min), a decrease in systolic and diastolic blood pressure and, as a rule, has a serious prognostic significance, indicating the attachment of a pronounced respiratory and cardiovascular insufficiency.

In this regard, it is important to remember that any increase in body temperature by 1C in patients who have no signs of intoxication or a decrease in the function of the cardiovascular system, is accompanied by an increase in heart rate of only 10-12 beats per minute. Therefore, the appearance of tachycardia and tachypnea in a patient with lobar pneumonia on a background of normal or slightly elevated body temperature indicates a pronounced intoxication and has a particularly unfavorable prognostic value.

With less severe intoxication in patients with pneumonia, there are signs of hypodynamia. They can get out of bed, go to the toilet, try to do some work around the house, for example, to make a bed, cook food etc., causes a feeling of weakness and tachycardia.

Often in patients with longitudinal pneumonia for a long time, even after normalizing body temperature and reducing the physical and radiological signs of the pathological process in the lungs, a pronounced asthenic syndrome is retained. Performing the usual physical exertion in the past (walking along the street, traveling in transport, cleaning an apartment, etc.) causes rapid fatigue, weakness, a desire to relax. This symptomatology indicates the presence of latent intoxication in patients with pneumonia, including recalcalsents, which must be taken into account when prescribing individual rehabilitation programs for patients.

The dynamics of the described manifestations of general weakness in a patient with pneumonia can serve as an important additional criterion for the effectiveness of the therapy and regress of the inflammatory process in the lungs. For example, a relatively rapid decrease in overall weakness shortly after normalization of body temperature and a reduction in the fiscal and radiological signs of pneumonia indicate a favorable course of the disease. Conversely, rapid re-growth of general weakness in later terms of the disease or even in the period of convalescence indicates possible formation of purulent-destructive and other complications. Pneumonia, for example exudative pleurisy, pericarditis, hyperinfection, and the like.

Sweating

It also belongs to the number of persistent clinical signs of general toxicosis syndrome in patients with pneumonia. In most cases, sweating has a clear connection with the temperature response and is most pronounced with a decrease in body temperature, especially when its critical incidence.

In other cases, excessive sweating, together with asthenic syndrome and subfebrile condition, is observed for a long time after the transferred pneumonia, indicating insufficient resolution of the inflammatory process.

Disturbances of consciousness, which develop in some patients with lobar pneumonia, are also often associated with general toxication syndrome and indicate the severity of the inflammatory process. Most often they develop in elderly and senile patients, especially with concomitant vascular or other genesis of chronic encephalopathy. In these cases, mental disorders can reach the degree of cerebral coma that simulates the development of ONMC. However, in the clinical picture of the disease, general cerebral neurological symptoms predominate, associated with general intoxication and brain edema.

Another variant of the disturbance of consciousness is delirium and hallucinations, which usually appear on the background of a significant and rapid increase in body temperature at the very beginning of the disease.

The general intestinal syndrome in patients with lobar pneumonia is of great diagnostic and prognostic value, reflecting to a certain extent the severity of the inflammatory process in the lungs. It includes the following clinical manifestations:

• fever with chills;
• general weakness, lack of exercise, or adynamia;
• severe sweating;
• disorders of consciousness (delirium, hallucinations, signs of encephalopathy, cerebral coma with cerebral neurological symptoms);
• violations of the function of other organs and systems (cardiovascular system, gastrointestinal tract, liver and kidneys, the system of endocrine organs, etc.).

Physical examination

The results of a physical investigation of a patient with lobar (pneumatic) pneumonia depend, first of all, on the stage of the development of the disease, the severity of pneumonia and the presence of these or other complications.