Symptoms of community-acquired pneumonia

Lobar pneumococcal pneumonia is characterized by damage to an entire lobe (or segment) of the lung and the obligatory involvement of the pleura in the inflammatory process.

The second distinctive feature of lobar (croupous) pneumonia is the involvement in the pathogenesis of the disease of an immediate-type hypersensitivity reaction in the respiratory areas of the lungs, which determines the rapid onset of the disease, accompanied by a pronounced violation of vascular permeability. This reaction is based on preliminary sensitization of the macroorganism by antigens of the pathogen - pneumococcus, usually present in the upper respiratory tract. When the pathogen repeatedly enters the respiratory areas of the lung and the allergen comes into contact with mast cells and immunoglobulins located on their surface, an immunoglobulin-antiimmunoglobulin complex is formed, which activates the mast cell. As a result, its degranulation occurs with the release of a large number of inflammatory mediators, which initiates the inflammatory process in the lung,

It should be emphasized that activation of mast cells and 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 "stormy" hyperergic reaction develops, initiating the inflammatory process in the lung.

However, although contact with pneumococcal antigen leads to the formation of immunoglobulins in many patients with pneumococcal pneumonia, the described hyperergic reaction, characteristic of lobar lobar pneumonia, occurred in only a few of them. It is assumed that in these cases, hereditary predisposition plays an important role, including the inheritance of some HLA genes. It is possible that the expression of these genes is combined with an increased ability of B-lymphocytes to secrete immunoglobulins upon contact with antigen.

In lobar pneumonia, inflammation begins in one or more foci and then quickly spreads directly through the lung tissue in the form of an "oil spot", mainly through the interalveolar pores of Kohn. In this case, as a rule, the bronchi are not involved in the inflammatory process (with the exception of the respiratory bronchioles).

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

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

• widespread damage to an entire lobe (or, less commonly, a segment) of the lung with the obligatory involvement of the pleura in the inflammatory process;
• participation in the pathogenesis of pneumonia of the immediate hypersensitivity reaction, which determines the “stormy” hyperergic reaction that initiates the inflammatory process in the lung;
• fibrinous nature of exudate;
• predominant damage to the alveolar tissue and respiratory bronchioles while maintaining complete patency of larger sections of the respiratory tract.

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Course of lobar pneumonia

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

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

The stage of hepatization is characterized by the prevalence of pronounced exudation and emigration of cellular elements participating in inflammation into the inflammatory focus. At this stage, the alveoli are completely filled with fibrinous exudate and lose their airiness. The exudate is rich in fibrin, alveolar epithelial cells, and leukocytes. With pronounced impairment of vascular permeability, a large number of erythrocytes are found in the exudate.

Macroscopically, one or more affected lobes of the lung are enlarged and uniformly compacted (hence the traditional name for this stage - "hepatization"). On a section, 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 foci of "gray hepatization" reflect the predominance of leukocytes, mainly neutrophils, in the exudate. If, in addition to neutrophils and fibrin, a large number of erythrocytes are present in the exudate, the focus of inflammation looks like an area of "red hepatization".

In the past, there was a concept of the obligatory sequential transformation of the areas of "red hepatization" into areas of "gray hepatization". However, it has now been proven that the morphological picture of lobar pneumonia throughout the entire hepatization stage can be represented by both gray and red hepatization areas or a combination of both. In other words, in lobar pneumococcal pneumonia, gray and red hepatization areas can occur simultaneously and are probably not related to the time elapsed from the onset of the disease. Such a motley morphological picture of the lung at the hepatization stage is associated, first of all, with the type of pneumococcus that was the causative agent of the disease, its virulence, and the reactivity of the macroorganism.

In the hepatization stage, fibrinous and fibrinous-purulent deposits are found on the pleura, reflecting the involvement of the pleura in the inflammatory process.

The duration of the hepatization stage usually does not exceed 5-10 days.

The resolution stage is characterized by gradual resorption of inflammatory exudate, increasing disintegration of leukocytes and an increase in the number of macrophages. The alveoli are gradually freed from exudate, slowly restoring their airiness. For some time, the exudate is again located only parietal on the inner surface of the alveoli, and then disappears completely. Edema of the alveolar walls and reduced elasticity of the lung tissue persist for a fairly long time.

The described distinct staging of the inflammatory process in lobar (croupous) pneumonia is currently observed quite rarely, which is associated with changes in the biological properties of the pathogen, as well as the influence of timely prescribed antibacterial therapy on the inflammatory process.

The classic course of lobar (croupous) pneumonia is characterized by a sequential change of 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 the interalveolar walls with decreased elasticity of the lung tissue;
   • parietal location of a relatively small amount of fibrinous exudate,
   • maintaining some airiness of the alveoli in the site of inflammation.
2. Hepatization stage:
   • "tight" filling of the alveoli with fibrinous exudate, compaction of the lung lobe;
   • the presence of both gray and red hepatization areas in the affected lobe;
   • obligatory involvement of the pleura in the inflammatory process.
3. Resolution stage:
   • “dissolution” and resorption of fibrinous exudate, which for some time is located in the alveoli along the walls;
   • gradual restoration of alveolar airiness;
   • long-term swelling of the interalveolar septa and decreased elasticity of the lung tissue.

Interrogation

Questioning of a patient with symptoms suspicious for diffuse pneumonia should include:

1. A comprehensive analysis of the patient's complaints.
2. Assessment of the clinical and epidemiological situation in which pneumonia developed, in particular:
   • possible provoking factors (hypothermia, respiratory viral infections, overwork, alcohol excess, excessive smoking, anesthesia and drug “intoxication”, brain injury or stroke, etc.);
   • long-term stay in an isolated group, in crowded conditions (schools, nursing homes, prisons, etc.);
   • recent travel and hotel stays, including those with air conditioning;
   • possible recent contact with patients with pneumonia, bronchitis, acute respiratory viral infections or “colds”, as well as contact with animals and birds;
   • stay in hospitals, intensive care units;
   • use for diagnostic and therapeutic purposes of endotracheal tube, artificial ventilation, bronchoscopy, etc.;
   • possible recurrent or episodic aspiration of gastric contents, etc.
3. The presence of concomitant chronic diseases (bronchopulmonary, cardiovascular, digestive organs, diabetes, blood diseases, immunodeficiency states, allergic reactions, etc.).
4. The presence of risk factors (age, smoking, alcoholism, drug addiction, etc.).

Stage of the tide

It was shown above that the “hot flash” 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 take a forced position in bed: they lie on their back or on the painful side, pressing with their hands the area of the chest where there is maximum pain. This position somewhat reduces the excursion of the inflamed sheets and relieves the pain.

Consciousness may not be altered, although sometimes various degrees of its impairment are observed. The skin is moist. There is hyperemia of the face and injection of the sclera, often more pronounced on the affected side. Since lobar pneumonia is often accompanied by a viral infection, herpetic eruptions can be found on the lips, wings of the nose and earlobes.

In severe cases and in individuals with concomitant chronic lung or heart diseases, slight cyanosis of the lips, tip of the nose, and earlobes is observed, which is associated with developing respiratory failure and circulatory disorders.

Respiratory system examination

If there is a pronounced pain syndrome, breathing becomes shallow, mainly due to the patient’s desire to reduce the friction of the pleural sheets against each other, which causes pain.

Already at this stage of the disease, it is possible to detect a lag in the affected side of the chest in the act of breathing, although the symmetry of the chest is completely preserved.

Palpation often reveals localized chest pain associated with inflammation of the parietal pleura, as well as a slight increase in vocal fremitus on the affected side. In the projection of the affected lobe of the lung, dullness (shortening) of the percussion sound with a tympanic tint is determined. Dullness of the percussion sound is associated with slight compaction of the lung tissue. The tympanic tint of the percussion sound is due to the preservation of some airiness of the alveoli with a simultaneous significant decrease in the elasticity of the lung tissue. The latter leads to a significant depletion of the timbre coloring of the percussion sound, characteristic of a healthy lung with normal elasticity of the lung tissue. As a result, the pulmonary sound approaches tympanic in its physical characteristics.

During auscultation in the projection of the affected lobe of the lung, two auscultatory phenomena are determined: weakened breathing and crepitation.

It was shown above that in the initial stage of lobar pneumonia (the “flood” stage), the alveoli only partially retain their airiness, and the inner surface of their walls, as well as the walls of the respiratory bronchioles, is lined with viscous fibrinous exudate, and the walls of the alveoli themselves are edematous 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 microatelectases, the appearance of which in the projection of the affected lobe of the lung explains the auscultatory phenomenon of weakening of breathing. It is clear that to straighten the stuck together walls of the alveoli, a much higher pressure gradient in the pleural cavity and upper respiratory tract is required than in the norm. Such a pressure gradient is achieved only by the end of inspiration. During this period, the walls of the alveoli containing exudate come apart, and a specific sound occurs, which is usually called crepitation (crepitacio index - initial crepitation).

Crepitation is very similar to fine cradle cap, but differs in that it occurs only at the height of a deep breath and does not change when coughing.

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 obstruction of the patency of the respiratory bronchioles, which are (together with the alveoli) in a collapsed state during the first half of inspiration. This situation occurs in compression atelectasis, pulmonary infarction, pneumonitis and other diseases.

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

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

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Hepatization stage

The stage of "hepatization" (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 failure.

During examination, for several days from the onset of the disease, the patient may remain in a forced position on the affected side, associated with the involvement of the pleura in the inflammatory process (dry pleurisy), as well as hyperemia of the face and injection of the sclera on the affected side. In severe cases of the disease, cyanosis increases, caused by progressive ventilatory respiratory failure.

Respiratory system examination

Breathing is frequent (up to 25-30 or more per 1 min) and shallow. With a significant extent of inflammation affecting two or more lobes of the lung, attention is drawn to the presence of not only tachypnea, but also severe difficulty breathing, in particular dyspnea of an inspiratory nature, participation of accessory muscles in breathing, distension of the wings of the nose during breathing, etc.

A distinct lag in the act of breathing of the diseased half of the chest is also noted. At this stage of the disease, vocal tremor and bronchophony are increased on the diseased side.

Percussion reveals a marked dullness of the percussion sound over the affected area, which does not, however, reach the level of an absolutely dull (femoral) sound, the appearance of which in a patient with lobar pneumonia indicates the formation of exudative pleurisy.

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

Against the background of increasing signs of intoxication, the heart rate increases to 110 12 per 1 min. A functional systolic murmur can be heard at the apex, and in some cases, arrhythmia.

In the 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 hepatization stage are:

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

Resolution stage

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

All pathological data are revealed in the stage of hepatization during percussion and auscultation gradually regress. A kind of "clarification" of the dull percussion sound occurs. Dullness again, as in the first stage, initially acquires a tympanic shade, and then a clear pulmonary sound is restored.

During auscultation, the bronchial tone of breathing weakens, which is associated with a decrease in the compaction of the lung tissue. Due to the gradual absorption of the exudate, the airiness of the alveoli is partially restored. The exudate is located parietal. Therefore, just as in the first stage of the disease, weakened breathing is determined over the affected area of the lung for some time. At the end of inhalation, the alveoli and respiratory bronchioles "unstick" again, which is the cause of crepitation (crepitacio reduх - final crepitation). Unlike the first stage, crepitacio reduх becomes sonorous.

As the exudate is removed and the swelling of the alveolar walls disappears, the elasticity and airiness of the lung tissue is restored, vesicular breathing begins to be detected again over the lungs, and crepitation disappears.

The most characteristic physical signs of the resolution stage are

• dullness of percussion sound with a tympanic tint, which is gradually replaced by a clear pulmonary sound;
• weakened vesicular breathing, which turns into vesicular breathing;
• the appearance of crepitacio reduх with the subsequent disappearance of this auscultatory phenomenon.

It should be emphasized that the described clear staging of clinical manifestations of lobar (croupous) pneumonia is currently observed relatively rarely. In this regard, laboratory and radiological signs of the disease are of particular importance for diagnosis.

Patient's complaints of lobar pneumonia

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

1. general intoxication and
2. bronchopulmonary.

The first of these includes fever, chills, headache, general and muscular weakness, fatigue, and the second group includes chest pain, cough, shortness of breath, sputum production, etc.

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Fever

Lobar pneumonia in most cases begins acutely, with a sudden increase in body temperature to 39-40 ° C and higher and chest pain. According to the apt expression of A. L. Myasnikov, a patient with lobar pneumonia remembers the day and hour when the disease began. The increase in body temperature is usually preceded by a stunning chill lasting 3 hours. Subsequently, a high fever (38.1-39 ° C) of a constant nature (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. Constant fever can last 7-10 days, but with adequate antibacterial therapy this period is usually reduced to 3-4 days.

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

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

Among the most important factors that determine the nature of the temperature reaction in pneumonia, at present, are inflammatory mediators (prostaglandins, leukotrienes, cytokines, a significant increase of which, observed during the height of the inflammatory process in the lungs, affects the functional state of the thermoregulatory centers.

Thus, the temperature reaction as a whole reflects well the nature and dynamics of the inflammatory process in the lung, as well as the effectiveness of the antibacterial and anti-inflammatory therapy. However, it should be remembered that the normalization of body temperature in itself does not mean the end of the pathological process in the lung. Moreover, in some cases, the absence of a temperature reaction during the formation of lobar pneumonia, especially in elderly and senile people or weakened patients suffering from severe concomitant diseases. It can have serious prognostic significance, indicating a sharp decrease in the body's reactivity.

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Chest pain

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

The most characteristic signs of pleural pain are acute, intense pain in the chest that occurs and/or intensifies at the height of a deep breath. Usually, the pain is strictly localized - and the patient can accurately indicate the location of the maximum pain. The pain usually intensifies when the patient bends toward the healthy side, since this position increases the friction of the inflamed pleural sheets against each other during deep breathing. When pain occurs, patients often breathe shallowly, instinctively trying to avoid irritation of the pleural pain receptors.

It should be remembered that when the diaphragmatic pleura is affected, intense acute pain can be localized in various parts of the abdomen, simulating the clinical picture of such diseases as acute cholecystitis, gastric ulcer or duodenal 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 intoxication syndrome further complicates clinical diagnosis. Nevertheless, a thorough analysis of the nature of pain in the abdomen and, first of all, a clear connection between pain and breathing in most cases allows us to suspect the presence of pleuropneumonia in the patient and conduct an appropriate diagnostic search.

In pleuropneumonia, acute chest pain associated with breathing usually persists for 2-3 days and then disappears. However, increased sensitivity of the skin in the area of the affected pleura may persist for quite a long time, even after the end of the inflammatory process, increasing with hypothermia, after physical exertion, with the occurrence of respiratory diseases, etc. Such increased pain sensitivity of the pleura can be detected by palpation of the corresponding areas of the chest. At the same time, the patient himself often feels a kind of discomfort in this area when breathing deeply, although he does not characterize it as intense pain.

In uncomplicated cases of lobar pleuropneumonia, chest pain lasts no more than 2-4 days and is typical of pleural pain, which is characterized by:

• acute intense character;
• clearly localized pain;
• occurrence or increase of pain at the height of deep inhalation;
• increased pain when the patient bends towards the healthy side.

Cough is the third characteristic symptom of pleuropneumonia. As is known, cough occurs when the receptors of the vagus nerve and the superior laryngeal nerve located in the pharynx, larynx, trachea, large bronchi and pleura are irritated. The pathological process, localized only in the lung parenchyma or in small bronchi, is not accompanied by cough until sputum gets into larger bronchi.

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

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

Occasionally, with a more pronounced impairment of vascular permeability in the inflammation focus, streaks or even blood clots may appear in the sputum. In uncomplicated lobar pneumonia, scant "hemoptysis" or separation of "rusty" sputum continues for a relatively short time (no more than 2-3 days). Subsequently, the sputum usually acquires a mucous or mucopurulent character and is separated in small quantities.

A longer separation of bloody sputum requires differential diagnosis of pleuropneumonia with such diseases and syndromes as tuberculosis, lung cancer, infarction pneumonia, bronchiectasis, lung abscess, hemorrhagic tracheobronchitis, etc.

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

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Dyspnea

A constant sign of lobar pneumonia, although its severity largely depends on the severity of the disease, the stage of the inflammatory process, as well as the presence of concomitant diseases of the bronchopulmonary and cardiovascular systems.

In any case, shortness of breath with lobar pneumonia is a manifestation of respiratory failure caused by three main reasons:

• exclusion of part of the lung parenchyma from pulmonary ventilation;
• increased rigidity of the lungs, which makes breathing difficult and limits ventilation of the lungs;
• a decrease in ventilation-perfusion relations in the affected lung, causing a right-to-left cardiac shunt of venous blood and even the formation of a venous alveolar shunt.

For obvious reasons, dyspnea reaches its greatest severity in the hepatization stage. In some cases, usually in young patients who do not suffer from concomitant lung and heart diseases, respiratory failure manifests itself only as a slight feeling of shortness of breath and tachypnea that occurs during physical exertion.

In severe cases of pneumonia, especially in elderly patients, as well as in individuals 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 feeling of shortness of breath and objective signs of respiratory failure - diffuse "gray" cyanosis, participation of accessory muscles in breathing, tachycardia, etc.

An increase in respiratory rate in a patient with pneumonia to 24 per 1 min or more is considered a severe course of pneumonia, requiring hospitalization in the intensive care unit.

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General intoxication syndrome

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

Disorders of the function of other organs and systems are also often observed: 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 intoxication syndrome and in many cases has prognostic significance, to a certain extent reflecting the dynamics of the inflammatory process in the lungs. In lobar (croupous) pneumonia, general weakness occurs from the first hours of the disease and, rapidly increasing, reaches its maximum degree in 1-2 days.

In severe cases, adynamia occurs. Any physical activity causes a painful feeling of weakness. Patients can hardly raise their arm, sit up in bed, or even open their eyes. Such severe adynamia is usually accompanied by a pronounced increase in respiratory rate (more than 30 per 1 min), tachycardia (HR - 100-120 per 1 min), a decrease in systolic and diastolic blood pressure and, as a rule, has a serious prognostic value, indicating the addition of severe respiratory and cardiovascular insufficiency.

In this regard, it is important to remember that any increase in body temperature by 1C in patients who do not have signs of intoxication or decreased cardiovascular function is accompanied by an increase in heart rate of only 10-12 beats per minute. Therefore, the occurrence of tachycardia and tachypnea in a patient with lobar pneumonia against the background of normal or slightly elevated body temperature indicates severe intoxication and has a particularly unfavorable prognostic value.

With less severe intoxication, patients with pneumonia show signs of hypodynamia. They can get out of bed, go to the toilet, and attempts to do any housework, such as changing the bed, preparing food, etc., cause a feeling of weakness and tachycardia.

Often, patients with lobar pneumonia have a pronounced asthenic syndrome for a long time, even after the body temperature has normalized and physical and radiographic signs of the pathological process in the lungs have decreased. Performing physical activities that were usual in the past (moving along the street, traveling in transport, cleaning the apartment, etc.) causes rapid fatigue, weakness, and a desire to rest. Such symptoms indicate the presence of latent intoxication in patients with pneumonia, including recuperators, which must be taken into account when prescribing individual rehabilitation programs to 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 regression of the inflammatory process in the lungs. For example, a relatively rapid decrease in general weakness soon after normalization of body temperature and a decrease in fiscal and radiographic signs of pneumonia indicate a favorable course of the disease. On the contrary, a rapid repeated increase in general weakness at later stages of the disease or even in the recovery period indicates the possible formation of purulent-destructive and other complications of pneumonia, such as exudative pleurisy, pericarditis, hyperinfection, etc.

Sweating

It is also one of the constant clinical signs of general intoxication syndrome in patients with pneumonia. In most cases, sweating has a clear connection with the temperature reaction and is most pronounced when the body temperature decreases, especially when it falls critically.

In other cases, increased sweating along with asthenic syndrome and subfebrile temperature is observed for a long time after pneumonia, indicating insufficient resolution of the inflammatory process.

Impaired consciousness, developing in some patients with lobar pneumonia, is also often associated with general intoxication syndrome and indicates the severity of the inflammatory process. Most often, they develop in elderly and senile patients, especially with concomitant vascular or other chronic encephalopathy. In these cases, impaired consciousness can reach the level of cerebral coma, simulating the development of stroke. However, the clinical picture of the disease is dominated by general cerebral neurological symptoms associated with general intoxication and cerebral edema.

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

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

• fever with chills;
• general weakness, hypodynamia or adynamia;
• profuse sweating;
• disturbances of consciousness (delirium, hallucinations, signs of encephalopathy, cerebral coma with general cerebral neurological symptoms);
• dysfunction of other organs and systems (cardiovascular system, gastrointestinal tract, liver and kidneys, endocrine system, etc.).

Physical examination

The results of a physical examination of a patient with lobar pneumonia depend, first of all, on the stage of development of the disease, the severity of pneumonia and the presence of certain complications.