Lung diseases of various origins have similar symptoms. To conduct microbiological studies and X-rays, time is required, which, unfortunately, the doctor and the patient have very little. In conditions when it is required to make a quick correct decision, the physician's ability to determine the cause of the disease according to clinical and anamnestic data comes to the fore. For this purpose, methods of differential diagnosis have been developed.

First of all, pneumonia is differentiated from:

• tuberculosis;
• pulmonary embolism (TELA);
• tumor lesions;
• allergic reactions to drugs;
• ornithosis;
• allergic pneumonitis;
• sarcoidosis;
• collagenosis.

The health worker begins by examining the patient and asking his or her environment. The goal is to clarify the background on which the disease developed. The presence of concomitant diseases (cancer, tuberculosis, diabetes, HIV, treatment with glucocorticosteroids or cytostatics) is established, living conditions are assessed, contacts with sick people and animals are identified.

At the next stage, the doctor compares the information received about body temperature, chills, the presence of headaches, impaired consciousness, the nature of coughing, shortness of breath, rapid breathing, pain, and the type of sputum. In the differential diagnosis of pneumonia, it is important to consider the age of the patient.

The primary diagnosis and treatment prescription is based on the results of the examination, and only after a blood and sputum test, an X-ray examination, the therapist makes a final conclusion.

Differences between inflammation and other lung diseases

1. Differential diagnosis of pneumonia and tuberculosis

The course of some forms of tuberculosis in the initial stage is very similar to the clinical picture of bacterial pneumonia. However, it should be remembered that the onset of tuberculosis is almost asymptomatic. Patients complain of fatigue, slight malaise (as a result of intoxication), coughing, sweating. At this stage, X-ray examination of the lungs is already obvious. Experienced doctors say: "TB is more visible than heard."

Bacterial pneumonia is characterized by a pronounced onset with chills, fever above 38.5 degrees. The skin of such a patient is dry and hot, and sweating is observed only at the time of the crisis. Sputum with pneumonia - with air bubbles, more viscous than with tuberculosis.

Tuberculosis on an x-ray looks like clear rounded polymorphic foci, more often in the upper lobe. A blood test for pneumonia reveals pronounced leukocytosis, and for tuberculosis - lymphopenia and moderate leukocytosis. Microbiological examination of sputum detects Mycobacterium tuberculosis.

Only 5% of TB patients benefit from broad-spectrum antibiotic treatment. Therefore, if the symptoms of pneumonia in a person last more than 2 weeks, then the diagnosis should be clarified. It's probably tuberculosis. However, broad-spectrum anti-tuberculosis drugs are not recommended for empiric treatment of pneumonia.

1. Differential diagnosis of pneumonia and lung cancer

Cough, sputum, pain and hemoptysis may accompany the germination of metastases in the pleura. Up to this point, lung cancer is asymptomatic, but can be detected on an x-ray. In this case, peripheral cancer is located more often in the anterior upper lobes of the lung, its contours are radiant.

Cancer cells can germinate in other organs or appear in the lungs as metastases. For more details on the differences between acute pneumonia, tuberculosis and lung cancer, see Table 1.

Table 1. Differential diagnosis of pneumonia and tuberculosis.

Differential diagnosis of pneumonia and pulmonary embolism (PE) Prolonged bed rest after surgery, hip fractures, with atrial fibrillation can lead to thrombophlebitis of the lower extremities. The consequence is often pulmonary thromboembolism. In young women, this problem sometimes occurs after taking oral contraceptives.

The characteristic features of TELA, in addition to the background, are:

• cyanosis;
• shortness of breath;
• arterial hypotension;
• tachycardia.

When listening, the doctor detects a pleural friction rub and weakened breathing. X-ray shows a triangular shadow, and perfusion radioisotope scanning shows ischemic "cold" zones. In this case, there is an acute overload of the right side of the heart.

1. Differential diagnosis of pneumonia and eosinophilic infiltrate

When treated with glucocorticosteroids, infiltrates disappear after 10 days.

The nature of the existing inflammation of the lungs will indicate its source. Pneumococcal acute pneumonia is accompanied by chills, fever, headache. If microbes have entered the bloodstream, chills can be severe, especially in children. Elderly people do not have such a reaction.

Bacterial damage to the lungs is characterized by burning pain when breathing in the chest. With a viral and mycoplasmal infection, these symptoms are not observed, but a headache is expressed, a rash is possible.

The nature of sputum:

• bacterial pneumonia - mucopurulent, thick;
• viral and mycoplasmal - a small amount;
• lung abscess - purulent smell;
• pulmonary edema - abundant, frothy, pink;
• lobar pneumonia - rusty;
• bronchoalveolar cancer - salivary;
• bronchiectasis - profuse, purulent, with blood.

Bacterial inflammation of the lungs can be accompanied by liver damage, increased activity of liver enzymes and the level of urea in the blood.

In a blood test, the main indicator of the type of lung infection is the level of leukocytes. Leukocytosis is expressed in bacterial forms of pneumonia (more than 15×10 9 /l), with mycoplasma and viral, the indicator almost does not change.

In children

A number of methods have been developed to make an accurate diagnosis of a pulmonary disease in a child. All of them take into account the age characteristics of patients, the etiology of pneumonia, the factors contributing to its development, the forms of the course of the disease (pathogenesis).

Anatomical and physiological features of the child's body cause a tendency to develop pneumonia at an early age, the possibility of developing into a chronic form and the severity of the course. An equally important role in the development of pneumonia is played by:

• hypothermia;
• poor child care;
• violation of hygiene rules;
• artificial feeding;
• unsanitary living conditions, incl. damp rooms;
• previous infectious diseases.

The most likely pathogen in community-acquired pneumonia in children under 6 months of age are viruses, staphylococci, and gram-negative flora. Later - pneumococcus and H.influenzae type B. In adolescence, streptococcus is added. With a nosocomial infection, the source of infection for both adults and children is likely to be enterobacteria, E. coli, staphylococcus aureus, Proteus, Pseudomonas.

The differential diagnosis of pneumonia in children involves several types of pathology classifications:

• According to the type, focal, segmental, croupous and interstitial acute are distinguished.
• By localization - in the lobe of the lung, in the segment, unilateral and bilateral.
• By type: community and nosocomial, perinatal, ventilator-associated, aspiration, immunodeficiency.
• By severity: mild, moderate and severe with complications. In this case, complications are divided into pulmonary (pleurisy, pneumothorax) and extrapulmonary (cardiovascular insufficiency, infectious-toxic shock, DIC, respiratory distress syndrome).

With all types of pneumonia in children, all the structural elements of the organ are involved in the process, gas exchange becomes difficult, the respiratory rate increases, pulmonary ventilation decreases with an extreme need for oxygen. Pathology can affect the heart, which is forced to compensate for the lack of oxygen with an increased intensity of contractions, followed by dystrophy of the heart muscle.

Oxygen deficiency causes a violation of metabolic processes, acidification of the blood. This is followed by hypoxemia and hypoxia. The cessation of oxygen absorption is externally manifested in the cyanosis of the face (hypoxemia) or earthy gray color (hypoxia). Subsequent profound metabolic disorders can become irreversible and cause death.

The criteria for diagnosing acute pneumonia in children are:

1. On auscultation of the lungs, rapid breathing and an increase in heart rate against the background of apnea, groaning breathing, wheezing, bronchophony.
2. An increase in temperature of more than 38 degrees for at least 3 days.
3. Dry cough, respiratory failure, voice trembling.
4. On x-rays, shadows in the form of lesions, blackouts.
5. A blood test indicates leukocytosis, urine and feces without pathological abnormalities.

See table 2 for signs of respiratory failure.

Table 2. Clinical and laboratory characteristics of respiratory failure in children with acute pneumonia (According to A.F. Tour, A.F. Tarasov, N.P. Shabalov, 1985).

Differential diagnosis of pneumonia and infiltrative pulmonary tuberculosis especially difficult in the localization of pneumonia in the upper lobes and tuberculous lesions in the lower lobes.

Acute onset with high fever is twice as common in pneumonia. For tuberculosis, a gradual or asymptomatic onset of the disease is more indicative. The body temperature rises gradually, with a slight increase by 14-16 o'clock in the afternoon, the patient, as it were, "overcomes".

In the anamnesis, patients with pneumonia are characterized by repeated pneumonia, while patients with tuberculosis are more likely to have long-term colds, pleurisy, treatment with glucocorticoids, and diabetes mellitus; contact with a tuberculosis patient, early tuberculosis; prolonged loss of appetite, weight loss.

Pneumonia is characterized by the rapid development of shortness of breath, cough, chest pain, and with tuberculosis, these symptoms increase gradually and are not so pronounced.

With pneumonia, facial flushing, cyanosis, and herpetic eruptions are noted. These phenomena are not observed in tuberculosis. Patients with tuberculosis are usually pale, they are characterized by profuse night sweats.

With pneumonia, the lower lobes are more often affected, with tuberculosis, the upper lobes. According to the figurative expression of V. Vogralik, non-tuberculous lesions of the lungs are “heavy” - they tend to settle in the lower lobes. Tuberculosis is characterized by "lightness", floating up to the upper sections of the lungs.

Pneumonia is more characteristic of bright physical changes in the respiratory organs, tuberculosis is characterized by poor auscultatory data ("a lot is seen, little is heard").

Leukocytosis with a shift of the leukocyte formula to the left and an increase in ESR is more common in pneumonia, and in tuberculosis - lymphocytosis.

In pneumonia, the sputum is rich in pneumonic flora, while in tuberculosis, the flora is poor, there are individual microbes. The pathognomonic sign of tuberculosis is the detection of Mycobacterium tuberculosis in sputum, especially with repeated findings. The study is carried out multiple times.

Empirical therapy of pneumonia helps differential diagnosis without the use of anti-tuberculosis drugs (rifampicin, streptomycin, kanamycin, amikacin, cycloserine, fluoroquinolones). Usually, in 10-14 days of treatment, pneumonic infiltration undergoes significant positive changes or resolves completely, while with tuberculous infiltration, its resorption occurs within 6-9 months.

X-ray signs, systematized by A.I. Borokhov and L.G. Dukov (1977) and presented in the form of a table:

X-ray differences between pneumonia and tuberculous infiltrate

Table 3

It is also necessary to carry out differential diagnosis with the following diseases:

Lungs' cancer.

Lung infarction.

Pulmonary edema.

Eosinophilic infiltrate.

ICD codes - 10

J 13- J 18

The purpose of the lecture is based on the knowledge gained, make a diagnosis of pneumonia, make a differential diagnosis with other lung diseases, formulate a diagnosis and prescribe a personalized treatment for a specific patient with pneumonia.

Lecture plan

Clinical case

Definition of pneumonia

Epidemiology of pneumonia

Etiology, pathogenesis, pathomorphology of community-acquired pneumonia

Etiology, pathogenesis, pathomorphology of nosocomial pneumonia

Clinic of pneumonia

Complications of pneumonia

Differential diagnosis of pneumonia

Classification of pneumonia

Treatment of pneumonia

Prognosis, prevention of pneumonia

Patient P., 64 years old,

complained of cough with a small amount of yellowish-green sputum, fever up to 38.3ºС, pain in the right side of the chest that occurs when coughing and taking a deep breath, general weakness, shortness of breath with moderate exercise, sweating and headache. He fell ill acutely 3 days ago, after hypothermia. When contacting the clinic at the place of residence, the doctor prescribed gentamicin 80 mg / m 2 times a day, mukaltin 3 tablets a day, aspirin. During treatment, no significant positive dynamics was noted.

The patient is a former soldier, currently retired, working as a watchman. Smokes for 22 years 1.5 - 2 packs of cigarettes a day. Periodically (2-3 times a year) after hypothermia or ARVI, a cough with yellow-green sputum is noted; in the last 2 years, shortness of breath has appeared with moderate physical exertion.

On examination: the state of moderate severity, the skin is clean, moderate humidity, there is hyperemia of the skin of the face. Body temperature - 39.1ºС. The subcutaneous fat layer is moderately developed, there are no edema, peripheral lymph nodes are not enlarged. HR at rest -30 per minute. The chest is emphysematous; on examination, the lagging of the right half of the chest during breathing attracts attention. During percussion of the lungs against the background of a box sound, a dull area is determined on the right below the angle of the scapula, in the same area there is an increase in voice trembling. During auscultation, scattered dry buzzing rales are heard, on the right below the angle of the scapula there is a crepitus zone. Heart sounds are muffled, there are no murmurs. Heart rate - 105 per minute, blood pressure - 110/65 mm Hg. The abdomen is soft, painless, accessible to palpation in all departments. The liver and spleen are not enlarged. There are no dysuric disorders.

Blood test: hemoglobin - 15.6 g/l; erythrocytes - 5.1x10.12 .; hematocrit - 43%; leukocytes - 14.4x10.9; mailbox - 12%; s / i - 62%; lymphocytes - 18%; eosinophils - 2%; monocytes - 6%; platelets - 238x10.9; ESR - 28 mm/h Biochemical blood test: serum creatinine 112 µmol/l, biochemical liver parameters without deviations from the norm. Pulse oximetry revealed a decrease in blood oxygen saturation:Sao2 94%. Sputum analysis: the character is mucopurulent, leukocytes densely cover the field of view; eosinophils, Kurshman's spirals, Charcot-Leiden crystals, BC - absent; gram-positive diplococci are determined. Spirometry revealed a decrease in FEV1 to 65% of the expected value (a sign of bronchial obstruction). X-ray of the chest cavity in two projections: the area of ​​darkening (infiltration) of the lung tissue is determined in the lower lobe of the right lung (segments 6,9,10), pulmonary emphysema, increased lung pattern due to the interstitial component.

Thus, the patient has symptoms of acute lower respiratory disease and a history of recurrent respiratory syndromes (cough and shortness of breath). It is necessary to solve the following tasks: diagnostic - to establish the nosological form of the underlying and concomitant disease and therapeutic - to prescribe treatment in accordance with the established diagnosis.

Definition of pneumonia

Pneumonia - a group of acute infectious diseases of different etiology, pathogenesis, morphological characteristics (mainly bacterial), characterized by focal lesions of the respiratory sections of the lungs with the obligatory presence of intraalveolar exudation; the development of an inflammatory reaction in the lung tissue is a consequence of a violation of the protective mechanisms of the macroorganism against the background of a massive impact of microorganisms with increased virulence.

Community acquired pneumonia (CAP) - an acute illness that occurred in a community setting or later than 4 weeks after discharge from the hospital, or was diagnosed within the first 48 hours from the moment of hospitalization, or developed in a patient who was not in nursing homes / long-term care units for more than 14 days, accompanied by symptoms of infection lower respiratory tract (fever, cough, sputum, chest pain, shortness of breath), radiological signs of fresh focal infiltrative changes in the lungs in the absence of a diagnostic alternative.

Nosocomial pneumonia (NP) (hospital, nosocomial) - a disease characterized by the appearance on the radiograph of "fresh" focal infiltrative changes in the lungs 48 hours or more after hospitalization, in combination with clinical data confirming the infectious nature (a new wave of fever, purulent sputum or purulent discharge of the tracheobronchial tree, leukocytosis, etc.), with the exclusion of infections that were in the incubation period of NP at the time of admission of the patient to the hospital.

Health Care Associated Pneumonia

This category includes pneumonia in people in nursing homes or other long-term care facilities. According to the conditions of occurrence, they can be attributed to community-acquired, but they, as a rule, differ from the latter in the composition of pathogens and the profile of their antibiotic resistance.

Epidemiology of pneumonia

According to the WHO, CAP ranks 4th in the structure of causes of death. According to official statistics in Russia in 1999, 440,049 (3.9%) cases of CAP were registered among people over the age of 18. In 2003, in all age groups, the incidence of CAP was 4.1%. It is assumed that these figures do not reflect the true incidence of CAP in Russia, which, according to calculations, is 14-15%, and the total number of patients annually exceeds 1.5 million people. In the United States, 5-6 million cases of CAP are diagnosed annually, of which more than 1 million require hospitalization. Despite advances in antimicrobial therapy, the mortality rate from pneumonia did not decrease significantly. Of the number of patients hospitalized for CAP, more than 60 thousand people die. According to the Ministry of Health of the Russian Federation, in 2003 in our country from pneumonia 44,438 people died, which is 31 cases per 100,000 population.

NP occupies 13-18% of all nosocomial infections and is the most common infection in the ICU (more than 45%). Ventilator-associated pneumonia (VAP) develops in 9-27% of intubated patients.

Attributable mortality (directly related to NP) ranges from 10 to 50%.

Etiology, pathogenesis, pathomorphology of CAP

Etiology of CAP

community-acquired pneumonia as an independent nosological form, it is an infectious disease, the main morphological substrate of which is exudative inflammation in the respiratory sections of the lungs without lung tissue necrosis. The etiology of CAP is directly related to the normal microflora that colonizes the upper respiratory tract. Of the numerous microorganisms, only a few have pneumotropism and increased virulence and are capable of causing an inflammatory reaction when they enter the lower respiratory tract.

According to the frequency of etiological significance among the causative agents of CAP, S. pneumoniaiae (30-50%); M. Pneumoniae, C. pneumoniae, legionela determined with a frequency of 8 to 30%, rarer pathogens. (H. influenzae, S. aureands, Klebsiellaand other enterobacteria found in 3-5%. Microorganisms that inhabit the upper respiratory tract and are not the causes of CAP are: Streptococcus viridans, Staphylococcus epidermidis, Enterococcus, Neisseria, Candida. Often in adult patients with CAP, mixed or co-infection is detected, for example, a combination of pneumococcal etiology of the disease and the simultaneous detection of serological signs of active mycoplasmal or chlamydial infections. Respiratory viruses do not often cause direct damage to the respiratory portions of the lungs. Viral respiratory infections, primarily epidemic influenza, are considered to be the leading risk factor for CAP. CAP may be associated with new, previously unknown pathogens that cause outbreaks. The causative agents of CAP identified in recent years include SARS-associated coronovirus, avian influenza virus (H5N1), swine influenza virus (H1N1) and metapneumovirus.

It is necessary to distinguish pathological interstitial changes in the lung tissue caused by viruses from bacterial pneumonia itself, since the approach to the treatment of these two conditions is fundamentally different. The etiological structure of CAP may vary depending on the age of the patients, the severity of the disease, and the presence of concomitant diseases. From a practical point of view, it is advisable to single out groups of patients with CAP and probable pathogens.

Non-severe CAP in individuals without concomitant diseases who have not taken antimicrobial drugs in the last 3 months.

Likely causative agents : S pneumoniae, M. Pneumoniae, C. pneumoniae, H. influenzae.

mild CAP in patients with comorbidities ( COPD, diabetes mellitus, congestive heart failure, cerebrovascular diseases, diffuse diseases of the liver, kidneys with impaired function, chronic alcoholism, etc.) and/or who have taken antimicrobials in the last 3 months.

Likely causative agents : S. pneumoniae, H. influenzae, C. pneumoniae, S. aureus, Enterobacteriaceae. Treatment is possible on an outpatient basis (from a medical standpoint).

VP of non-severe flow, ltreatment in hospitals (department of general profile).

Likely causative agents : S. pneumoniae, H. influenzae, C. pneumoniae, M. Rneumoniae, S. aureus, Enterobacteriaceae.

Severe VP, inpatient treatment (ICU).

Likely causative agents : S. pneumoniae, Legionella, S. aureus, Enterobacteriaceae.

CAP risk factors:

hypothermia;

intoxication;

gas or dust that irritates the respiratory tract;

• contact with air conditioning systems;

  flu epidemics;

  unsanitized oral cavity;

  outbreak in a closed team;

  addiction.

In patient A.

the symptoms that were the reason for the appeal developed acutely in out-of-hospital conditions. There are risk factors for pneumonia - a long history of smoking with a smoker index of about 20 years, signs of pathology predisposing to the development of pneumonia - repeated episodes of coughing and shortness of breath, a tendency to "cold" diseases.

CAP pathogenesis

In 70% of healthy people, microorganisms colonize the oropharynx. These are pneumococci, influenza bacillus, staphylococcus aureus. Microaspiration of oropharyngeal secretion under physiological conditions is also observed in healthy individuals, mainly during sleep. Anti-infective protection of the lower respiratory tract is carried out by protective mechanisms: mechanical (aerodynamic filtration, anatomical branching of the bronchi, epiglottis, coughing, sneezing, oscillation of the cilia of the cylindrical epithelium), mechanisms of specific and nonspecific immunity. Thanks to these systems, the elimination of infected secretions from the lower respiratory tract is ensured and their sterility is ensured. The development of pneumonia can be promoted, firstly, by a decrease in the effectiveness of the protective mechanisms of the macroorganism, and secondly, by the massive dose and / or virulence of the pathogen.

The main pathogenic mechanisms development of the EaP are:

aspiration of the secret of the nasopharynx, containing potential pathogens of pneumonia;

inhalation of an aerosol containing microorganisms;

hematogenous and lymphogenous spread of infection from an extrapulmonary focus (sepsis, tricuspid valve endocarditis, thrombophlebitis);

direct spread of infection from neighboring organs (liver abscess, etc.);

infection with penetrating wounds of the chest.

Aspiration of oropharyngeal secretions

When the mechanisms of "self-purification" of the tracheobronchial tree are damaged, for example, during a viral respiratory infection, when the function of the ciliated epithelium is disturbed and the phagocytic activity of alveolar macrophages decreases, favorable conditions are created for the development of pneumonia .

Aspiration b a large amount of contents from the oropharynx and / or stomach may be accompanied by the development of three syndromes, depending on the nature of the aspirate: chemical pneumonitis (hydrochloric acid aspiration - Mendelssohn's syndrome), mechanical obstruction, aspiration pneumonia, which develops when a bacterial infection is attached to mechanical obstruction and chemical pneumonitis . Factors contributing to aspiration: depression of consciousness, gastroesophageal reflux, repeated vomiting, anesthesia of the nasopharynx, mechanical violation of protective barriers.

Inhalation of an aerosol containing microorganisms

This mechanism of development of pneumonia plays a major role in the infection of the lower respiratory tract with obligate pathogens, such as legionella.

The condition favoring the multiplication of microflora in the lower respiratory tract is the excessive formation of mucus, which protects microbes from the effects of protective factors and promotes colonization. When exposed to risk factors (hypothermia, respiratory viral infection, etc.) and violation of protective mechanisms

protective barriers on the way from the nasopharynx to the alveoli are overcome, the pathogen enters the respiratory sections of the lungs and the inflammatory process begins in the form of a small focus.

Pathomorphology of VP

The inflammatory process develops in the respiratory sections of the lungs - a set of anatomical structures of the lung located distally to the terminal bronchioles, which are directly involved in gas exchange. These include respiratory bronchioles, alveolar sacs, alveolar ducts, and alveoli proper. In addition to air-containing spaces, the respiratory part of the lung includes the walls of bronchioles, acini and alveoli, i.e. interstitial structures, in which an infectious process can also develop. Exudative inflammation in the respiratory part of the lung determines the main radiological sign of pneumonia - a local decrease in the airiness of the lung tissue ("darkening", "reducing the transparency of the lung field", "seal", "infiltration"). The localization of the pneumonic focus is often unilateral, in the lower lobes or in the axillary subsegments of the upper lobes, the spread of infiltration occurs within one or two bronchopulmonary segments. Such localization of infiltrative changes reflects the main pathogenetic mechanism for the development of CAP - aspiration or inhalation of pathogenic pathogens into the lungs with air through the respiratory tract. Bilateral changes are more typical for pulmonary edema, interstitial lung diseases, metastases of malignant tumors in the lungs, hematogenous and lymphogenous infection of the lungs in sepsis.

There are clinical and morphological differences in CAP, depending on the pathogen.

pneumococcal pneumonia

For pneumonia caused by endotoxin-producing pathogens(pneumococcus, Haemophilus influenzae, Klebsiella), the process begins, as a rule, with a toxic lesion of the alveolocapillary membrane, leading to bacterial edema. Pneumococci types I-III can cause both sporadic and epidemic cases of the disease in organized groups due to infection from bacteriocarriers. Pneumococcus penetrates into the lung tissue and into the vascular bed, in 25% of patients in the first hours of the disease it is sown from the blood. The pathomorphological picture in pneumococcal pneumonia types I-III is characterized as croupous or pleuropneumonia, in the classical version, proceeding in three stages: the stage of bacterial edema, the stage of hepatization and the stage of resolution. In the first stage, under the action of endotoxin, released during the death of pneumococci, and enzymes (hemolysins, hyaluronidase), the alveolocapillary membrane is damaged, vascular permeability increases, plasma sweating occurs and a large amount of edematous fluid is formed, which spreads like an oil stain, from the alveolus to the alveolus through the pores of Kohn. and through the bronchi. Pneumococci are located on the periphery of the edema, in the center a non-microbial zone of fibrinous and purulent exudate is formed. Depending on the reactivity of the organism, the prevalence of the process is segmental, polysegmental, lobar, subtotal. The second stage usually begins on the 3rd - 4th day from the onset of the disease and is characterized by diapedesis of erythrocytes, leukocyte infiltration and massive fibrin loss, as a result of which the exudate in the alveoli turns from liquid into a dense, resembling liver tissue in density (hepatization or hepatization stage). The duration of this stage is from 5 to 7 days, sometimes longer, after which the stage of resolution of pneumonia begins. At this stage, the exudate is resorbed with the participation of the fibrinolytic system of the lung and proteolytic enzymes of neutrophils. A mandatory component of pneumococcal pneumonia is fibrinous pleurisy. Perhaps the accession of purulent bronchitis.

Pneumococci of other strains cause the development focal pneumonia(bronchopneumonia). The inflammatory process, which primarily occurs in the bronchi, passes to the lung parenchyma, spreading along the bronchi. In the lung tissue, foci of red and red-gray color are formed, histologically, serous exudative inflammation with plethora and leukocyte infiltration of the lung tissue is detected.

Pneumococcal pneumonia is characterized by the absence of lung tissue destruction and almost complete restoration of its structure.

Staphylococcal pneumonia

For pneumonia caused by exotoxin-producing flora(staphylococcus, streptococcus), the process begins with the development of focal purulent inflammation with purulent fusion of lung tissue in its center. As a rule, staphylococcal pneumonia develops with influenza A, in which the protective mechanisms of the respiratory tract are damaged. Staphylococcus forms an exotoxin, produces enzymes - lecithinase, phosphatase, hemolysins, coagulase, which cause the rapid development of lung tissue destruction. Histologically, staphylococcal pneumonia is characterized by limited foci of leukocyte infiltration, with obligatory purulent fusion of lung tissue in the center of these foci.

A variant of staphylococcal pneumonia is hematogenous pneumonia with sepsis.

streptococcal pneumonia, like staphylococcal, develops after (or against the background of) influenza and other respiratory viral infections. Often complicated by pleural effusion and abscess formation.

Friedlander's pneumonia

Pneumonia caused by Friedlander's bacillus (Klebsiela pneumonia) often develops against the background of an immunodeficiency state in patients with diabetes mellitus, alcoholism, the elderly, and in patients taking immunosuppressants. According to the morphological symptoms, Friedlander's pneumonia resembles croupous, the development of hemorrhagic necrosis with the collapse of the lung tissue against the background of areas of bacterial confluent edema is characteristic. The causes of disintegration are multiple thromboses of small vessels in the area of ​​inflammation.

Mycoplasma pneumonia.

Mycoplasma, ornithosis, some viral pneumonia begins with an inflammatory lesion of the interstitial lung tissue.

Mycoplasma pneumonia (Mycoplasma pneumonia) is very virulent, epidemic outbreaks of infection are possible. At the onset of the disease, the clinical picture is characteristic of an acute respiratory viral infection, with inflammatory interstitial edema developing in the lungs. With the development of pneumonia, cellular infiltration of the lung parenchyma joins, the pneumonic focus is similar to pneumococcal pneumonia. Resorption of pneumonia is delayed up to 2-3 weeks.

Haemophilus pneumonia

Pneumonia caused by Haemophilus influenzae in adults is rarely an independent disease, more often it develops as a secondary pneumonia in patients with chronic bronchitis. According to the morphological picture, it is similar to focal pneumococcal pneumonia.

legionella pneumonia

Pneumonia is caused by the gram-negative endotoxin-forming bacterium Legionella pneumophila. Legionella multiplies rapidly in a warm and humid environment; air conditioners and heating mains are probable sources of infection. According to the clinical and morphological picture, legionella pneumonia resembles severe mycoplasmal pneumonia.

Pneumonia in viral diseases.

Influenza pneumonia due to the cytopathogenic effect of the virus, the epithelium of the respiratory tract begins with hemorrhagic tracheobronchitis with rapid progression of the disease when the bacterial flora, more often staphylococcal, is added. Respiratory viral infection (influenza viruses A, B, adenovirus infection, respiratory syncytial virus infection, parainfluenza infection) is considered as a risk factor for pneumonia, the virus is a kind of "conductor" of a bacterial infection. The role of respiratory viruses in the occurrence of pneumonia is to suppress local immunity in the respiratory tract, in particular, damage to the epithelium, impaired bronchial secretion, suppression of the activity of neutrophils and lymphocytes with impaired immunoglobulin synthesis. Due to these reasons, the bacterial flora is activated, which determines the development of pneumonia. Pneumonia in influenza A and B is considered as a complication of influenza infection, it develops more often in persons with concomitant diseases and in pregnant women. A viral lesion is characterized by the development of bilateral interstitial pulmonary edema without signs of consolidation, often considered as acute respiratory distress syndrome (ARDS). Virological examination reveals a high titer influenza virus, bacteriological examination of sputum often does not reveal pathogenic bacterial flora. The pathomorphological picture is characterized by hemorrhagic tracheobronchitis, hemorrhagic pneumonia, the formation of hyaline membranes on the surface of the alveoli, a significant number of leukocytes in the alveoli. Bacterial pneumonia develops after a short (1-4 days) improvement in the condition, infiltration foci are detected in the lungs, pneumococci, staphylococci, Haemophilus influenzae are detected in sputum. The main difference between influenza pneumonia and secondary bacterial pneumonia is the ineffectiveness of antibiotic therapy in the first case and the effect of antibiotics in the second.

Pneumocystis pneumonia

A group of microorganisms united under the name Pneumocystis carinii refers to yeast-like fungi. The results of serological studies show that the majority of people had an asymptomatic pneumocystis infection in the first years of life, antibodies to pneumocysts are present in more than 90% of adults. The main route of infection is person-to-person transmission. People with a normal immune system are not permanent carriers of pneumocystis, pneumocystis pneumonia is a disease of patients with an immunodeficiency state, characterized by impaired cellular and humoral immunity. The infection rarely spreads beyond the lungs, due to the low virulence of the pathogen. Pneumocystis pneumonia has three pathological stages of development. The first stage is characterized by the penetration of the pathogen into the lungs and its attachment to the fibronectin of the walls of the alveoli. In the second stage, desquamation of the alveolar epithelium and an increase in the number of cysts in alveolar macrophages occur. In this stage, clinical symptoms of pneumonia appear. The third (final) stage is an alveolitis, with intense desquamation of alveolocytes, mono- or plasmacytic infiltration of the interstitium, a large number of pneumocysts in alveolar macrophages and the lumen of the alveoli. As the disease progresses, trophozoites and detritus, accumulating in the alveoli, lead to their complete obliteration, the surfactant synthesis is disturbed, which leads to a decrease in the surface tension of the alveoli, a decrease in lung elasticity and ventilation-perfusion disorders. Clinical conditions associated with pneumocystis pneumonia: HIV infection, immunosuppressive therapy, old age, etc.

Cytomegalovirus pneumonia

Cytomegalovirus (CMV) is a herpesvirus. CMV is a typical representative of opportunistic infections that appear only in primary or secondary immunodeficiency. In 72-94% of the adult population of the Russian Federation, specific antibodies are detected in the blood, which means the presence of the virus itself in the body. In immunocompetent individuals, primary CMV infection is asymptomatic or with mild mononucleosis-like syndrome. Like all herpesviruses, CMV remains latent in the human body after primary infection, and severe disease can develop in immunological disorders as a result of activation of the latent virus or re-infection. The risk group includes HIV-infected patients, patients after organ transplantation, cancer patients, pregnant women, people receiving immunosuppressive therapy, etc. The condition for CMV reactivation is a violation in the cellular link of immunity, primarily CD + 4-lymphocyte-helpers.

Etiology, pathogenesis, pathomorphology of nosocomial pneumonia

Etiology of NK

Most NP has a polymicrobial etiology and is caused by gram (-) bacteria (Klebsiella pneumoniae, Pseudomonas aeruginosa, Acinetobacter spp. and Gram (+) cocci (Staphylococcus aureus). Anaerobes, viruses and fungi are rare causative agents of NP; in NP patients without immunodeficiency conditions, no have etiological significance such pathogens as C. albicans, Streptococcus viridans, Enterococcus spp, coagulase-negative staphylococci.

Risk factors for NP:

elderly age;

unconscious state;

aspiration;

emergency intubation;

prolonged (more than 48 hours) IVL;

probe feeding;

horizontal position;

surgical intervention, especially on the organs of the chest and abdominal cavity and anesthesia;

acute respiratory distress syndrome;

bronchoscopy in ventilated patients

the use of a number of drugs - sedatives, antacids, H2-blockers

NK pathogenesis

A prerequisite for the development of NP is to overcome the protective mechanisms of the lower respiratory tract. The primary route of entry of bacteria into the lower respiratory tract is the aspiration of oropharyngeal secretions containing potential NP pathogens, as well as secretions containing microorganisms from the endotracheal tube.

Colonization of the oropharynx by Streptococcus pneumoniae, Haemophilus influenzae, anaerobes is typical for many healthy people. On the contrary, the colonization of gram (-) flora, first of all. Pseudomonas aeruginosa, Acinetobacter is rare in normal conditions, but increases with length of hospital stay and severity of illness . The frequency of aspiration increases with impaired consciousness, swallowing disorders, decreased gag reflex, slowed gastric emptying, impaired motility of the gastrointestinal tract. Rarer pathogenetic mechanisms for the development of NP include: inhalation of a microbial aerosol, direct penetration of the pathogen into the respiratory tract, hematogenous spread of microbes from infected venous catheters, translocation of non-sterile contents of the esophagus / stomach.

Under normal conditions, the stomach is sterile, colonization of the stomach can develop with achlorhydria, malnutrition and starvation, enteral nutrition, and taking drugs that reduce the acidity of gastric juice. During mechanical ventilation, the presence of an endotracheal tube in the airways violates the protective mechanisms: it blocks mucociliary transport, violates the integrity of the epithelium, and promotes colonization of the oropharynx by nosocomial microflora, followed by its penetration into the lungs. On the surface of the endotracheal tube, biofilm formation is possible, followed by the formation of emboli in the distal respiratory tract. The source of baterial contamination is the skin of the patient himself, the hands of the staff. Biofilm enhances the accumulation of bacteria, increases resistance to antimicrobial therapy. Aspiration is facilitated by the horizontal position of the patient on the back, enteral nutrition.

Clinic of pneumonia

Community-Acquired Pneumonia Clinic

Patient's complaints

Pneumonia should be suspected if the patient has a fever associated with cough, dyspnea, sputum production, and/or chest pain. The clinical picture of pneumonia depends on the pathogen, however, based on the symptoms of pneumonia, it is not possible to speak with certainty about the probable etiology. The age of the patient, the presence of concomitant diseases also affect the clinical manifestations of the disease. Such characteristic symptoms of pneumonia as an acute onset of the disease with fever, chest pain, cough may be absent, especially in debilitated patients and the elderly. In a number of elderly patients, clinical symptoms are manifested by weakness, impaired consciousness, and symptoms of dyspepsia. Often, community-acquired pneumonia “debuts” with symptoms of exacerbation of concomitant diseases, for example, heart failure.

In the considered clinical case

and alobe the patient for fever, cough with sputum, shortness of breath are characteristic of acute inflammatory (taking into account the severity of development, most likely infectious) diseases of the lower respiratory tract. Severe intoxication, chest pain associated with breathing is characteristic of lung tissue damage and suggests pneumonia. History data (long-term smoking, periodic cough with sputum, dyspnea) suggest that the patient has chronic obstructive pulmonary disease (COPD), which, along with the patient's age of 64 years, may be a risk factor for developing pneumonia. In this case, hypothermia is the provoking factor.

Medical history

The clinical picture of pneumonia consists of two groups of symptoms: pulmonary (respiratory) and extrapulmonary (general).

Typical pneumococcal pneumonia characterized by an acute febrile state (body temperature above 38%), the presence of cough with sputum, chest pain, shortness of breath.

croupous inflammation, the frequency of which has increased again in recent years, is characterized by the most severe course. Usually, the onset of the disease is associated with hypothermia. Pneumococcal pneumonia in typical cases is characterized by stages of the course. Clinical symptoms and physical signs are dynamic and depend on the period of the course of pneumonia.

Initial period(1-2 days) has an acute character: sudden onset of pain in the chest associated with breathing, severe chills, followed by an increase in temperature to febrile numbers, dry cough (cough), general weakness, weakness. Over the next day, the cough intensifies, viscous rusty sputum is separated. Objective data: on examination, the patient's face is haggard, swelling of the wings of the nose during breathing is often noted, herpes on the lips, wings of the nose; there is a lag in breathing of the chest on the side of the lesion, the patient, as it were, spares it because of the pain, holding it with his hand.

On palpation over the affected area, an increase in voice trembling is determined. With percussion of the lungs, a dull-tympanic sound is revealed due to inflammatory edema with air still remaining in the alveoli. During auscultation, weakened vesicular respiration is determined due to a decrease in the elasticity of the alveoli impregnated with inflammatory exudate, and crepitus (introductory-indux), which occurs at the height of inspiration, when the alveoli, stuck together during exhalation, when filled with air, disintegrate, creating a characteristic sound. Pneumonia can be recognized on auscultation even before the appearance of a pulmonary infiltrate on an x-ray. This period of time is about 24 hours.

peak period(1-3 days) is characterized by constant fever up to 39 - 40 degrees C with daily fluctuations within one degree. The decrease in temperature occurs under the influence of adequate treatment, usually within 1-3 days, which is accompanied by a decrease in the symptoms of intoxication: headache, fatigue, weakness. On physical examination during the peak period, a dull sound is determined in the affected area, since the lung is airless, and bronchial breathing .

Permission period lasts up to 3-4 weeks, during which there is a normalization of temperature, the disappearance of symptoms of intoxication, a decrease in cough and sputum, which acquires a mucous character, the disappearance of pain in the chest. On physical examination during this period, a dull - tympanic sound, weakened vesicular breathing, sonorous crepitus (redux) is again detected above the affected area.

Bronchopneumonia (focal) occurs more frequently in the outpatient setting. According to the conditions of occurrence, two “scenarios” are possible: the occurrence of pneumonia after SARS or as a complication of bronchitis. Clinical manifestations in focal pneumonia are also characterized by an acute onset, but less pronounced fever, intoxication, and the absence of a cyclical disease. The severity of pneumonia, as well as physical data, depends on the prevalence of the process. On examination, a lag in breathing of the chest on the side of the lesion can be determined. On palpation, there is an increase in voice trembling and bronchophony. With percussion over the foci of infiltration, areas of a shortened percussion tone are determined. Auscultation revealed hard breathing, dry and wet rales. The severity of these symptoms is determined by the localization of the foci.

Physical examination of patient A, 64 years old

lung tissue compaction syndrome is detected: lag of half of the chest during breathing, increased voice trembling, shortening of percussion sound. Crepitus is due to the accumulation of fibrinous exudate in the alveoli, and it can be assumed that the compaction of the lung tissue is a consequence of inflammatory infiltration. Thus, in the presence of characteristic complaints of cough, shortness of breath and chest pain and the results of an objective examination of the patient, a preliminary diagnosis of pneumonia with localization in the lower lobe on the right is quite likely. There are objective signs of diffuse lesions of the bronchi - dry scattered buzzing rales, signs of emphysema. A long history of smoking, chronic cough, and dyspnoea prior to the onset of the present illness suggest that the patient has a concomitant disease, chronic obstructive pulmonary disease (COPD). In this case, COPD, as a risk factor, increases the likelihood of a diagnosis of pneumonia.

Clinical features of CAP of mycoplasmal etiology. The fever does not reach a high degree of severity. Symptoms of respiratory tract damage are characteristic: cough (the most common symptom), shortness of breath (a rare symptom), symptoms of pharyngitis. With percussion of the lungs, changes are often not detected; during auscultation, unexpressed wheezing is determined - dry or wet finely bubbling. Extrapulmonary manifestations of mycoplasmal infection: inflammation of the eardrum (pain in the ear), asymptomatic sinusitis, hemolysis with increased titers of cold agglutinins, catarrhal pancreatitis, catarrhal meningitis, meningoencephalitis, neuropathy, cerebral ataxia; maculo-papular skin lesions, erythema multiforme, myocarditis (not often), glomerulonephritis (not often), myalgia, arthralgia (without a picture of true arthritis). X-ray data of the lungs: increased lung pattern,

focal infiltrates, discoid atelectasis, enlargement of the lymph nodes of the roots of the lung, pleurisy. Laboratory data: hemolytic anemia with reticulocytosis, thrombocytosis as a response to anemia, in the cerebrospinal fluid is determined l protein immunocytosis. Etiological diagnostics: determination of antimycoplasmal antibodies IgM, IgG in the blood serum, which are detected by the immunological method) from the 7-9th day of the disease in a titer of more than 1:32 or, with an increase in dynamics by 4 times. and determination of antigens - mycoplasma DNA within one week from the onset of the disease.

Clinical features of CAP of chlamydial etiology

Pulmonary symptoms: cough dry or with light sputum, chest pain, moderate dry whistling or moist rales.

Extrapulmonary symptoms: intoxication of varying severity, hoarseness, often angina, meningoencephalitis, Guillain-Barre syndrome, reactive arthritis, myocarditis. X-ray data of the lungs: increased lung pattern or local subsegmental infiltration. Laboratory findings: normal blood count. Etiological diagnosis: detection of antibodies by the method RSK, antigen determination by methods ELISA, PCR .

Clinical features of CAP of legionella etiology

Pulmonary symptoms: cough (41-92%), shortness of breath (25-62%), chest pain (13-35%). Extrapulmonary symptoms: fever (42 - 97%, temperature above 38.8 degrees C), headache, myalgia and arthralgia, diarrhea, nausea / vomiting, neurological symptoms, impaired consciousness, kidney and liver dysfunction. X-ray data: infiltrative shadows with a tendency to merge, increased lung pattern, exudative pleurisy. Laboratory data: leukocytosis with a shift to the left, increased ESR, relative lymphopenia, thrombocytopenia; hematuria, proteinuria, hyponatremia, hypophosphatemia. Etiological diagnosis: seeding on selective media, determination of antigen in urine or sputum, determination of antibodies in the blood (initial increase by 2 times or 4 times by the 2nd week of illness, simultaneous increase in IgM and IgG), polymerase chain reaction, sputum staining according to Gram (neutrophilia and gram-negative rods). A feature of the treatment is the lack of effect from beta-lactams and aminoglycosides.

Clinical features of CAP caused by Friedlander's bacillus(Klebsiella pneumoniae)

Extensive damage to the lung tissue (lobar, subtotal), mucus-like nature of sputum, the possibility of developing infarct-like necrosis of the lung, a tendency to purulent complications (abscess, pleural empyema).

Clinical features of pneumocystis pneumonia in HIV-infected patients The presence of diseases caused by opportunistic pathogens, pulmonary and extrapulmonary tuberculosis, stomatitis caused by Candida albicans, widespread perineal ulcers (activation of the herpes simplex virus).

Instrumental and laboratory diagnosis of pneumonia

Radiation diagnosis of pneumonia

X-ray examination of patients with suspected or known pneumonia is aimed at detecting signs of an inflammatory process in the lung tissue and possible complications, and assessing their dynamics under the influence of the treatment. The study begins with a survey radiography of the chest cavity in the anterior and lateral projections. The use of fluoroscopy is limited to clinical situations in which it is necessary to differentiate between changes in the lungs and accumulations of fluid in the pleural cavity. In certain clinical situations - a differential diagnosis, a prolonged course of pneumonia, etc., the appointment of computed tomography is justified. Ultrasound is used to assess the condition of the pleura and pleural cavity with fluid accumulation.

The main radiological sign of pneumonia is a local decrease in the airiness of the lung tissue (“shading”, “darkening”, “seal”, “infiltration”) due to the filling of the inflammatory exudate of the respiratory sections of the lung, as a result of which the lung tissue becomes airless (alveolar type of infiltration). The interstitial type of infiltration of the lung tissue of a reticular (mesh) or peribronchovascular (stringy) nature occurs due to the filling of the interalveolar spaces with inflammatory exudate. The thickening of the interalveolar septa is accompanied by a decrease in the volume of the alveoli while maintaining their airiness, while creating a radiological phenomenon of translucency or "frosted glass". The localization of infiltrative changes reflects the main pathogenetic mechanism for the development of pneumonia - aspiration or inhalation of pathogenic pathogens through the respiratory tract. Infiltration more often extends to one or two segments, is localized mainly in the lower lobes of the lungs (S IX, S X) and axillary subsegments of the upper lobes (SII, S ax-II, III), more often has unilateral and right-sided localization. With pleuropneumonia, the area of ​​lung tissue compaction has a homogeneous structure, is adjacent to the visceral pleura with a wide base, its intensity gradually decreases towards the root, the interlobar pleura is concave towards the compacted area, the volume of the lobe is not changed or reduced, air gaps of large bronchi are visible in the infiltration zone ( symptom of air bronchography). Changes in the pulmonary pattern without infiltration of the lung tissue occur in other diseases, more often as a result of pulmonary circulation disorders in response to intoxication and an imbalance in the extravascular fluid in the lung, but in themselves are not signs of pneumonia, including interstitial. Bronchopneumonia is characterized by the presence in the lung of an infiltration zone of a heterogeneous structure, consisting of numerous polymorphic, centrilobular foci with fuzzy contours, often merging with each other. This type of infiltration is based on the transition of the inflammatory process from small intralobular bronchi to lung tissue. Pneumonic foci can range in size from miliary (1-3 mm) to large (8-10 mm). Bronchial gaps can be traced in some foci, in others the structure is more homogeneous, since small bronchi are obstructed by inflammatory exudate. The zone of focal infiltration extends to one or more segments, a lobe or several segments of neighboring lobes. A control X-ray examination with a favorable clinical course of pneumonia should be carried out two weeks after the start of treatment, the basis for radiography in these cases is the identification of central cancer and tuberculosis occurring under the guise of pneumonia. The reverse development of inflammation is associated with the liquefaction of the exudate and its excretion through the respiratory tract and lymphatic vessels. At the same time, there is a decrease in the intensity of the shadow of infiltration up to its complete disappearance. The process of resolving pneumonia may not be completed completely, while in the alveoli and pulmonary interstitium, areas of carnification are formed due to the organization of inflammatory exudate, or areas of pneumosclerosis due to excessive proliferation of connective tissue elements.

X-ray data of the chest cavity of patient A, 64 years old

The diagnosis of pneumonia is confirmed by a chest X-ray.

Foci of inflammatory infiltration are localized in the lower lobe of the right lung and are combined with expansion of the lung root and increased pulmonary pattern.

Example. X-ray of the lungs of a patient with massive (total) pneumonia.

Noticeably total darkening of the left lung field, which has a heterogeneous character. The size of the affected half of the chest is not changed, there is no mediastinal displacement.

A negative chest x-ray may not completely rule out the diagnosis of CAP when the clinical likelihood is high. In some cases, at the time of diagnosis of CAP, the focus of pneumonic infiltration is not visualized.

Laboratory diagnosis of pneumonia

Clinical blood test

A high probability of a bacterial infection is indicated by leukocytosis (> 10x10 9 / l) and / or a stab shift (> 10%); leukopenia (<3х10.9) или лейкоцитоз >25x10.9 are indicators of an unfavorable prognosis.

Biochemical blood tests

Increasing C - reactive protein> 50 mg / l reflects the systemic nature of the inflammatory process, observed in patients with severe pneumococcal or legionella pneumonia. Level procalcitonin correlates with the severity of pneumonia and may be predictive of poor outcome. Functional studies of the liver, kidneys may indicate the involvement of these organs, which is of prognostic value, and also affects the choice and regimen of antibiotic therapy.

Determination of arterial blood gases

In patients with extensive pneumonic infiltration, in the presence of complications, the development of pneumonia against the background of COPD, with oxygen saturation of less than 90%, the determination of arterial blood gases is indicated. Hypoxemia with pO2 below 69 mm Hg. is an indication for oxygen therapy.

Etiological diagnosis of pneumonia

Microbiological diagnostics. Identification of the causative agent of pneumonia is the optimal condition for the appointment of adequate antibiotic therapy. However, due to the complexity and duration of the microbiological study, on the one hand, and the need for an immediate start of treatment, on the other hand, antibiotic therapy is prescribed empirically, based on clinical and pathogenetic features in each case. An accessible and fast research method is bacterioscopy with sputum smear staining according to Gram. Identification of a large number of gram-positive or gram-negative microorganisms can serve as a guideline for the choice of antibiotic therapy. The grounds for conducting a microbiological study are:

hospitalization in the ICU;

unsuccessful previous antibiotic therapy for this disease;

the presence of complications: destruction or abscesses of lung tissue, pleural effusion;

the presence of a comorbid background: COPD, CHF, chronic alcohol intoxication, etc.

Patients with severe pneumonia require serological diagnostics infections caused by "atypical" pathogens, as well as the determination of L. pneumophila and Streptococcus pneumoniae antigens in the urine. Intubated patients require endotracheal aspirate sampling. Patients with severe pneumonia should take venous blood samples for culture before starting antibiotic therapy (2 samples from two different veins).

Molecular biological methods causative agents of pneumonia Mycoplasma pneumoniae, Chlamydophila. pneumoniae, Legionella pneumophila difficult to diagnose using traditional methods. For their identification, molecular biological methods are used, the most acceptable method among all currently existing methods for rapid diagnostics is the polymerase chain reaction (PCR). Indications for its implementation in pneumonia may be a severe course of the disease, the ineffectiveness of initial antibiotic therapy, and the epidemiological situation.

Examination of the pleural fluid

In the presence of pleural effusion, a study of the pleural fluid is indicated with a count of leukocytes and a leukocyte formula, determination of pH, LDH activity, protein content, bacterioscopy of a smear, and cultural examination.

Invasive diagnostic methods.

Diagnostic fibrobronchoscopy with microbiological, cytological examination of bronchial contents, biopsy, bronchoalveolar lavage is indicated if differential diagnosis with tuberculosis, bronchogenic cancer and other diseases is necessary.

The volume of instrumental and laboratory examination of a patient with EP is decided individually.

Diagnostic minimum examination in outpatients should include, in addition to the history and physical examination, studies to decide on the severity of treatment and the need for hospitalization. These include a chest x-ray and a complete blood count. Routine microbiological diagnosis of CAP on an outpatient basis does not significantly affect the choice of an antibacterial drug.

Diagnostic minimum examination in hospitalized patients should include studies to establish the diagnosis of CAP, the severity and decide on the place of treatment (therapeutic department or ICU). These include:

X-ray of the chest organs;

General blood analysis;

Biochemical blood test (glucose, creatinine, electrolytes, liver enzymes);

Microbiological diagnostics: microscopy of sputum smear, Gram-stained, bacteriological examination of sputum with isolation of the pathogen and determination of sensitivity to antibiotics, bacteriological examination of blood.

Additional methods in severe patients: pulse oximetry, blood gas studies, cytological, biochemical and microbiological examination of pleural fluid in the presence of pleurisy.

Laboratory data of patient A, 64 years old,

confirm the presence of acute inflammation (leukocytosis with a shift of the formula to the left, an increase in ESR, mucopurulent sputum with a high content of leukocytes and cocci). The detection of Gram-positive diplococci in sputum suggests a pneumococcal etiology of the disease. Biochemical indicators do not have deviations from normal values. Pulse oximetry revealed a decrease in oxygen saturation to 95%, one hundred indicates respiratory failure of the 1st degree. Spirography revealed signs of bronchial obstruction - a decrease in FEV1 to 65% of the proper value.

Diagnostic criteria for pneumonia

The main task that the doctor solves when a patient with symptoms of a lower respiratory tract infection contacts him is to confirm or exclude pneumonia as a disease, the outcome of which depends on the correct and timely prescribed treatment. . The "gold standard" for diagnosing pneumonia would be to identify the potential pathogen from the site of infection. However, in practice, such a diagnostic approach, which involves invasive manipulations, is not possible. In this regard, an alternative is a combined diagnostic approach, including taking into account clinical symptoms, radiological, microbiological and laboratory signs, as well as the effectiveness of antibiotic therapy.

Suspicion of pneumonia should arise if the patient has the following syndromes:

syndrome of general inflammatory changes: acute onset with fever to febrile numbers, chills, severe sweating at night, weakness, loss of appetite, headaches and muscle pain; acute phase blood counts (increased PSA);

lower respiratory tract syndrome cough with sputum, shortness of breath, chest pain;

lung injury syndrome: over the affected area of ​​\u200b\u200bthe lung, local increase in voice trembling and bronchophony, shortening of percussion sound, focus of crepitus (indux, redux) or sonorous fine bubbling rales, bronchial breathing.

pulmonary infiltrate syndrome, previously not determined., with x-ray examination; Nosological diagnosis is confirmed by the definition of the pathogen.

certain The diagnosis of CAP is when the patient has:

Radiologically confirmed focal infiltration of the lung tissue and,

At least two of the following clinical signs:

(a) acute fever at the onset of the disease (temperature > 38.0 °C; (b) cough with sputum);

(c) physical signs: focus of crepitus and/or small bubbling rales, hard, bronchial breathing, shortening of percussion sound;

(d) leukocytosis >10.9/L and/or stab shift >10%.

inaccurate/undefined The diagnosis of CAP may be made in the absence or inaccessibility of radiological confirmation of focal infiltration in the lungs. In this case, the diagnosis is based on taking into account the epidemiological history, complaints and relevant local symptoms.

Unlikely diagnosis of CAP is considered if, when examining a patient with fever, complaints of cough, shortness of breath, sputum production and / or chest pain, an x-ray examination is not available and there are no local symptoms

The diagnosis of pneumonia is nosological after the pathogen has been identified. To establish the etiology, a bacterioscopy of a Gram-stained sputum smear and a cultural study of sputum are performed, such a study is mandatory in a hospital and optional in an outpatient setting.

CAP diagnostic criteria

Clinical diagnosispatient A. 64 years old

is formulated on the basis of diagnostic criteria: clinical acute fever at the onset of the disease > 38.0 gr.С; cough with phlegm; local physical signs of inflammation of the lung tissue - increased voice trembling, shortening of percussion sound, focus of crepitus in the subscapular region on the right), radiological (focal infiltration of the lung tissue in the lower lobe on the right andS8,9,10); laboratory (leukocytosis with stab sdaig and accelerated ESR).

The occurrence of the disease at home indicates community-acquired pneumonia.

When sowing sputum, pneumococcus was isolated in a diagnostic titer of 10.7 degrees, which determines the nosological diagnosis.

Diagnosis of concomitant disease - COPD can be made on the basis of characteristic criteria: risk factor (smoking), clinical symptoms - long-term cough with sputum, shortness of breath, objective signs of bronchial obstruction and pulmonary emphysema (dry scattered wheezing, boxed sound on lung percussion). Confirmation of the diagnosis of COPD are radiological signs of emphysema and the presence of obstructive ventilation disorders (decrease in FEV1 to 65% of the proper value). The number of exacerbations more than 2 per year and the average degree of ventilation impairment allow us to refer the patient to the high-risk group C.

Complications of CAP

In severe pneumonia, complications may develop - pulmonary and extrapulmonary.

Complications of pneumonia

Pulmonary:

pleurisy

acute purulent destruction of lung tissue.

Extrapulmonary:

infectious-toxic shock;

acute respiratory failure;

acute cor pulmonale;

secondary bacteremia;;

acute respiratory distress syndrome;

infectious-toxic lesions of other organs: pericarditis, myocarditis, nephritis, etc.

sepsis

Acute purulent destruction of the lung

Pneumonia is the cause of acute suppurative processes in the lung in 92% of cases. Clinical and morphological forms of acute purulent destruction of the lung are acute abscess, focal purulent-necrotic destruction of the lung, gangrene of the lung.

Acute abscess purulent-necrotic lesion of the lung with bacterial and / or autolytic proteolysis of necrosis as it forms with the formation of a single (or multiple) cavity (cavities) of decay with demarcation from viable lung tissue. Abscess pneumonia - acute suppurative process, the main feature of which is the occurrence of small purulent foci in the areas of inflammation.

Focal purulent-necrotic destruction of the lung characterized by the formation of multiple purulent-necrotic foci of bacterial or autolytic proteolysis without clear demarcation from viable lung tissue.

Gangrene of the lung rapidly progressive purulent-putrefactive necrosis of the lung without delimitation.

Acute purulent-destructive processes of the lung may be complicated by pyopneumothorax, pleural empyema, bleeding, phlegmon of the chest wall, as well as extrapulmonary complications: sepsis, DIC, etc.

Factors predisposing to the development of a purulent-destructive process: respiratory viral infection, alcoholism, immunodeficiency states, traumatic brain injury, etc. Etiological factors in the development of purulent lung destruction can be staphylococci, streptococci, Pseudomonas aeruginosa, Klebsiella, enterobacteria, fungi (aspergillus) , mycoplasmas. In the etiology of acute infectious destruction of the lungs, the role of non-spore-forming anaerobes has been established: bacteroids, fusobacteria and anaerobic cocci, which usually saprophyte in the oral cavity, especially in people with dental caries, pulpitis, periodontitis, etc. The development of acute purulent-destructive processes in the lungs is not completely studied. In pneumococcal pneumonia, a purulent-destructive process develops as a result of secondary invasion by opportunistic microorganisms in the zone of edema and infiltration of the lung tissue. Viral damage to the eithelium of the lower respiratory tract creates conditions for invasion into the lung tissue of opportunistic flora located in the respiratory tract. In the case of aspiration, bronchial obstruction by a tumor or a foreign body, anaerobic flora may be attached, which causes putrefactive processes in the lung. The ways of penetration of microbial agents into the lung are different: endobronchial, hematogenous, traumatic

Pathogenesis of purulent-destructive processes in the lungs.

In response to the invasion of microorganisms and tissue damage around the foci of inflammation and destruction, the phenomenon of disseminated blockade of microcirculation occurs (local or organ syndrome of disseminated intravascular coagulation - DIC - syndrome). The blockade of microcirculation around the lesion is a natural and early protective reaction that provides separation from healthy tissues and prevents the spread of bacterial flora, toxins, pro-inflammatory mediators, and tissue destruction products throughout the body. Massive microthrombosis of vessels with fibrin clots and aggregates of blood cells with the development of sludge captures areas of the lung tissue far from the lesion, this is accompanied by a violation of microcirculation, which leads to inefficient respiration, hypoxia, and disruption of repair processes in the lung tissue. The blockade of microcirculation around the lesion and destruction of the lung tissue prevents the entry of drugs, in particular antibiotics, into the lesion, which contributes to the formation of antibiotic resistance. A widespread microthrombotic reaction with an unfavorable course often captures not only areas adjacent to the foci of inflammation, but also spreads to far-located tissues and organs. At the same time, microcirculatory disorders develop, leading to dysfunction of many organs: the central nervous system, kidneys, liver, gastrointestinal tract. Due to the decrease in the barrier function of the intestinal mucosa, it becomes permeable to the intestinal microflora, which leads to the development of secondary endogenous sepsis with the formation of foci of infection in various tissues and organs.

Successful treatment of any pathology is impossible without a complete examination. A number of diseases require a comparative analysis in order to more accurately clarify the picture. In this sense, the differential diagnosis of pneumonia is necessary in order to exclude similar symptoms, and ultimately determine the only correct diagnosis and prescribe a therapeutic course. The technique allows you to avoid incorrect treatment and incorrect dosages of drugs, prevents the occurrence of complications and side effects associated with erroneous examination, which is especially important for diseases in children. Detailed information about pneumonia is

Diagnostic methods

The process of differential testing of pathologies is carried out according to the dropout scheme, that is, at first the symptoms are grouped, then they are excluded in small groups until the real clinical picture is formed. Diagnostics is carried out in several stages:

• Primary data are summed up under the general syndrome, on their basis a list of possible pathologies is formed
• The symptoms, general condition of the patient, changes in his state of health are studied in detail and a schedule is drawn up, taking into account various factors
• According to the list, a comparative analysis is carried out, including the clinical picture, accompanying signs and their features. Another graph of similar and different values ​​is drawn up
• The symptoms are compared, and their belonging to the original disease is clarified.
• The specialist finds third-party signs that are not related to this pathology
• Diseases are excluded, the clinic of which does not fit into the overall picture
• Based on the final information, a diagnosis is established and treatment is prescribed.

As for the general examination methods, in this case they are identical to traditional analyzes and tests of the patient:

• Listening to the patient's complaints, taking an anamnesis, checking the medical record for past pathologies
• Auscultation and percussion
• General inspection
• Biochemical tests
• radiograph
• Electrocardiogram
• Ultrasound procedure
• Magnetic resonance and computed tomography
• Bronchoscopy
• Spirometry.

The collected and analyzed history allows you to get a reliable picture, including the causes of the disease in children and adults, often recurring symptoms. The doctor also detects other disorders in the body. The initial examination does not provide complete data, since the assessment of the patient's own well-being is almost always subjective. Young children cannot tell where it hurts at all.

Differentiation of pneumonia

Pathologies of the respiratory system have the same clinical picture, especially in the early stages of development. Many analyzes and tests take time to complete, and in the case of an acute course, every minute counts, especially for children. Often patients turn to doctors when the processes become threatening.

Inflammation of the lungs that is difficult to treat may turn out to be tuberculosis or mask oncological pathologies. In addition, there is some similarity of symptoms with heart failure, thromboembolism, vasculitis. First of all, differentiation is established between different types of pneumonia in children and adults. Visual data of symptoms and causes are shown in the table:

Since most of the symptoms have a similar picture, the main principle of diagnosis is bacterial culture. When collecting an anamnesis, the doctor must necessarily reflect the following points:

• Etiological factors
• Presence of underlying pathologies
• The prevalence and features of foci of pneumonia
• Severity
• development stage
• Possible complications and risks of their occurrence.

In each case, the type of pathogen is indicated. If such data are not available or it takes time to obtain them, the reasons, available results of radiographs, bronchoscopy and spirometry are described. In case of lack of information, an empirical treatment regimen should be prescribed, which is corrected in the course of supplementing the diagnosis.

If there is an underlying disease, the pediatrician or therapist describes its symptoms, course features and effects on the patient's condition. Therapy is based on the specifics of the interaction and combination of different drugs and antibiotics. This fact is most important, since associated pneumonia can become protracted or lead to irreversible consequences.

Differentiation from other diseases

When examining a patient, the doctor faces two tasks. The first is the limitation of pulmonary inflammation from other diseases of the respiratory system. The second is the definition of extrapulmonary pathologies by symptoms from the respiratory system. Each such principle has specific distinguishing features:

with tuberculosis

The most common mistakes are made when comparing these two diseases. According to studies, infection with mycobacteria is complicated by influenza or pneumonia. The exacerbation of tuberculosis is similar to the manifestations of pneumonia - it is a dry cough, pallor of the skin, subfebrile temperature.

Sometimes the inflammatory process is accompanied by positive tuberculin tests, which further complicates the diagnosis. However, differentiation plays an important role, since most of the methods of physiotherapy that are used for pneumonia are unacceptable for tuberculosis. The formation of infiltrates may be accompanied by nonspecific changes - hyperemia, hyperreaction, lymphostasis. This creates fertile ground for the attachment of viruses to mycobacteria.

When analyzing the patient's condition, the main question arises - how does developing catarrh affect the course of already existing tuberculosis. Usually the clinical picture during the formation of cavities and caseous formations is similar. In both cases, an acute onset is detected, cough with pain, sputum with bloody discharge. X-ray examination shows that the affected area is enlarged, there are characteristic changes.

The difference lies in a number of factors: with tuberculosis, the shadows are heterogeneous and compacted, the areas of enlightenment coincide with the seeded foci. Therapeutic regimens that are effective for pneumonia do not give results for more than three days. In sputum, a massive spread of mycobacteria is found. Also, the restriction allows you to determine the biochemical test. With tuberculosis, an increase in leukocyte elements is found in the blood, which are lowered in pneumonia.

With bronchitis

Pathology most often begins to develop as a result of respiratory viral infections or simultaneously with them. The main symptom is bouts of coughing, first dry, then with sputum. Temperature rises are short-term, it rises within 2-3 days, then remains within subfebrile indicators. On percussion, the sound does not change; on auscultation, wheezing is observed. The pulmonary pattern is enhanced, but there is no infiltration.

When differentiating pneumonia and bronchitis, there are two main mistakes: when the first disease is interpreted as an exacerbation of the second. In addition, patients with pneumonia who smoke may have a characteristic pattern of chronic smoker bronchitis. In most cases, pulmonary inflammation is more severe. It has a predominantly bacteriological nature, while bronchitis is pulmonary. Difficulty arises when the origin of both pathologies is the same, but in such cases confirmation will be based on additional examinations.

With the flu

Misdiagnosis when compared with respiratory pathologies is not uncommon. During a pandemic, it is especially difficult to limit lung inflammation and influenza. It is necessary, first of all, to take into account the specifics of the clinical picture:

• Respiratory lesions begin acutely, the temperature is high, a runny nose joins, the cough is dry, the sputum is transparent, non-viscous. Sore throat, redness of the eyes, swollen face.
• With the flu, the patient complains of pain in the joints and aches, severe weakness, fever with high temperatures. Initially absent catarrhal symptoms appear after 3-4 days.
• Pneumonia can develop both slowly and suddenly. The patient suffers from shortness of breath, loses appetite, loses weight dramatically. The cough is frequent, the discharge is viscous, have purulent or bloody inclusions. There is pain in the chest area.

Often, pulmonary inflammation is a complication after influenza or respiratory infections. In this case, they can develop as a result of a direct viral infection or due to the penetration of bacteria as a secondary factor. Examination reveals thickening of tissues, foci of infiltration, separate areas with destruction.

With pleurisy

A massive inflammatory lesion of the respiratory system resembles pleural changes, especially when both processes occur in the lower lobar areas. Painful sensations in the chest are characteristic of both pathologies. Some patients complain of discomfort during coughing. But there are a number of symptoms that have cardinal differences. Exudative pleurisy is characterized by a special feature - the sound of friction of the pleura during breathing.

After the first stage of development with a specific clinical picture, the following series of symptoms occurs. This is a sharper pain than with pneumonia, which is aggravated by bending and turning. The temperature is normal or slightly elevated, the cough is dry, sputum is poorly separated. A radiograph is considered the most reliable examination technique, but with an effusion volume of less than 300 ml, confirmation by puncture is mandatory, which helps not only to determine the amount of fluid, but also its composition. The same method is suitable for differentiation with pneumonia. To a coma of that data of the biochemical analysis matter.

With atelectasis

Lung damage with tissue collapse and impaired gas exchange can also have similar symptoms with pneumonia. Shortness of breath, cyanosis, shortness of breath. Chest pain is associated with impaired gas exchange. In the curled area, a favorable environment for the development of infection is formed. The etiological factors of atelectasis are blockages and compressions associated with trauma, aspiration, destructive tissue changes, and surfactant deficiency. This is the main difference from pneumonia.

The initial clinical picture is identical: with atelectasis, cyanosis, shortness of breath, but cough are also observed. Usually dry. With the deterioration of the condition and the development of respiratory failure, the risk of death increases. The temperature rises. If, against the background of a collapse of the lung, an infection is connected. This indicates the onset of pneumonia with abscess formation. In this case, intoxication and sputum join, often with bloody patches due to vascular damage and increased pressure in the pulmonary circulation.

with cancer

The initial manifestations of oncological formations do not differ from the inflammatory process in the lungs. A few years ago, misdiagnosis was 70%. If pneumonia is suspected, the doctor will prescribe antibiotics. If the drugs do not bring results after a two-week intake, it is urgent to examine the patient for the development of malignant neoplasms. Differentiation consists in early diagnosis, since in cancer the signs are scarce at first, only in the later stages are pronounced.

When metastasis begins and the tumor grows into the pleural tissues, the clinical picture becomes clear. The patient develops pain, sputum with blood clots is present in the cough. Especially clearly allows you to see the progression of the pathology of the x-ray. Later there are characteristic pains in the joints, especially at night. With all open signs, the temperature rarely rises, it remains subfebrile throughout the disease.

with other pathologies

It is often necessary to distinguish between pulmonary inflammation and dysfunctions of the heart and blood vessels, which lead to congestion in the respiratory system and proliferation of connective tissue. Like pneumonia, hepostasis is accompanied by shortness of breath, wheezing and sounds during percussion. Since hypothermia is characteristic of heart failure, the patient's condition gradually worsens.

In collagenoses and rheumatoid arthritis, the person also suffers from similar symptoms. At the same time, the data of auscultation and X-ray examination are identical - enhanced pulmonary shadows, the presence of infiltrates. The difference is that antibacterial therapy for collagenosis is ineffective, but when taking glucocorticosteroids, there is a positive trend. In addition, sputum is practically absent, there are no changes in the position of the diaphragm, atelectasis is bilateral.

In a heart attack, the lungs are affected due to thrombosis that affects the adjacent arteries. Pathology develops after phlebitis of the lower extremities, varicose veins. In addition, people with impaired myocardial function, vasculitis, and ischemia are susceptible to the disease. The main symptom is pain syndrome, aggravated by turning the torso, coughing, sneezing, laughing. Many patients develop a serous pleural lesion against the background of a heart attack.

Sudden attacks of shortness of breath, up to suffocation, are characteristic of thromboembolism. Diagnosis and differentiation is based on a preliminary examination of thrombophlebitis, diseases associated with vascular lesions. The blockage is not related to bacterial etiology, the pathogen may act as a subsequent factor, as in the area. Closed by a thrombus, microcirculation is disturbed, which creates conditions for the penetration and growth of pathogens. For such patients, isotope scanning of the respiratory organs and angiopulmonography of the system are performed.

For a visual comparison of the principles of differentiation, you can use the table, which displays the characteristic signs and causes of the four main pathologies:

Differential diagnosis is a technique necessary to distinguish between several types of pathologies with the same symptoms. It plays an important role in determining therapeutic regimens, especially in cases where bacteria are able to show resistance. Thanks to such methods of examination, it became possible for early detection of not only pneumonia, but also tuberculosis, atelectasis, cancer, and empyema. The techniques are aimed at accelerating recovery, improving the condition of patients with irreversible disorders and preventing death for people at risk.

- This is a pulmonary infection that developed two or more days after the patient was admitted to the hospital, in the absence of signs of the disease at the time of hospitalization. Manifestations of nosocomial pneumonia are similar to those in other forms of pneumonia: fever, cough with sputum, tachypnea, leukocytosis, infiltrative changes in the lungs, etc., but may be mild, erased. The diagnosis is based on clinical, physical, radiological and laboratory criteria. Treatment of nosocomial pneumonia includes adequate antibiotic therapy, sanitation of the respiratory tract (lavage, inhalations, physiotherapy), infusion therapy.

ICD-10

J18 Pneumonia without specification of the causative agent

General information

Hospital-acquired (nosocomial, hospital-acquired) pneumonia is an infection of the lower respiratory tract acquired in a hospital, the signs of which develop no earlier than 48 hours after the patient is admitted to a medical institution. Nosocomial pneumonia is one of the three most common nosocomial infections, second in prevalence only to wound infections and urinary tract infections. Nosocomial pneumonia develops in 0.5-1% of patients undergoing treatment in hospitals, and in patients of intensive care units and intensive care units it occurs 5-10 times more often. Mortality in nosocomial pneumonia is extremely high - from 10-20% to 70-80% (depending on the type of pathogen and the severity of the patient's background condition).

The reasons

The main role in the etiology of nosocomial bacterial pneumonia belongs to gram-negative flora (Pseudomonas aeruginosa, Klebsiella, Escherichia coli, Proteus, serrations, etc.) - these bacteria are found in the secretion of the respiratory tract in 50-70% of cases. In 15-30% of patients, the leading pathogen is methicillin-resistant Staphylococcus aureus. Due to various adaptive mechanisms, these bacteria develop resistance to most known antibacterial agents. Anaerobes (bacteriodes, fusobacteria, etc.) are the etiological agents of 10-30% of nosocomial pneumonia. Approximately 4% of patients develop legionella pneumonia, which usually occurs as mass outbreaks in hospitals, caused by legionella contamination of air conditioning and water systems.

Significantly less frequently than bacterial pneumonia, nosocomial infections of the lower respiratory tract caused by viruses are diagnosed. Among the causative agents of nosocomial viral pneumonia, the leading role belongs to influenza viruses A and B, RS-virus, in patients with weakened immunity - to cytomegalovirus.

General risk factors for infectious complications in the respiratory tract are prolonged hospitalization, hypokinesia, uncontrolled antibiotic therapy, advanced and senile age. The severity of the patient's condition, due to concomitant COPD, postoperative period, trauma, blood loss, shock, immunosuppression, coma, etc., is essential. Medical manipulations can contribute to the colonization of the lower respiratory tract by microbial flora: endotracheal intubation and reintubation, tracheostomy, bronchoscopy, bronchography, etc. The main routes of entry of pathogenic microflora into the respiratory tract are aspiration of the secret of the oronasopharynx or stomach contents, hematogenous spread of infection from distant foci.

Ventilator-associated pneumonia occurs in ventilated patients; at the same time, every day spent on mechanical breathing increases the risk of developing nosocomial pneumonia by 1%. Postoperative, or congestive pneumonia, develops in immobilized patients who have undergone severe surgical interventions, mainly on the chest and abdominal cavity. In this case, the background for the development of a pulmonary infection is a violation of the drainage function of the bronchi and hypoventilation. The aspiration mechanism of the occurrence of nosocomial pneumonia is typical for patients with cerebrovascular disorders who have impaired cough and swallowing reflexes; in this case, the pathogenic effect is exerted not only by infectious agents, but also by the aggressive nature of the gastric aspirate.

Classification

According to the timing of the occurrence of nosocomial infection is divided into early and late. Early is nosocomial pneumonia that occurs in the first 5 days after admission to the hospital. As a rule, it is caused by pathogens that were present in the patient's body even before hospitalization (St. aureus, St. pneumoniae, H. influenzae, and other representatives of the microflora of the upper respiratory tract). Typically, these pathogens are sensitive to traditional antibiotics, and the pneumonia itself proceeds more favorably.

Late nosocomial pneumonia manifests itself after 5 or more days of inpatient treatment. Its development is due to the actual hospital strains (methicillin-resistant St. aureus, Acinetobacter spp., P. aeruginosa, Enterobacteriaceae, etc.), which exhibit highly virulent properties and polyresistance to antimicrobial drugs. The course and prognosis of late nosocomial pneumonia is very serious.

Taking into account the causative factors, 3 forms of nosocomial respiratory tract infection are distinguished:

• postoperative or congestive pneumonia

At the same time, quite often, various forms overlap each other, further aggravating the course of nosocomial pneumonia and increasing the risk of death.

Symptoms of nosocomial pneumonia

A feature of the course of nosocomial pneumonia is the erasure of symptoms, which makes it difficult to recognize a pulmonary infection. First of all, this is due to the general severity of the condition of patients associated with the underlying disease, surgery, advanced age, coma, etc.

However, in some cases, nosocomial pneumonia can be suspected on the basis of clinical findings: a new episode of fever, an increase in the amount of sputum / tracheal aspirate, or a change in their nature (viscosity, color, odor, etc.). Patients may complain of the appearance or intensification of cough, shortness of breath, chest pain. In patients who are in a severe or unconscious state, attention should be paid to hyperthermia, increased heart rate, tachycardia, signs of hypoxemia. The criteria for a severe infectious process in the lungs are signs of severe respiratory (RR> 30/min.) And cardiovascular insufficiency (HR> 125/min., BP

Diagnostics

A complete diagnostic examination for suspected nosocomial pneumonia is based on a combination of clinical, physical, instrumental (lung x-ray, chest CT scan), laboratory methods (OAC, biochemical and gas composition of blood, sputum culture).

To make an appropriate diagnosis, pulmonologists are guided by the recommended criteria, which include: fever above 38.3 ° C, increased bronchial secretion, purulent nature of sputum or bronchial secretions, cough, tachypnea, bronchial breathing, moist rales, inspiratory crepitus. The fact of nosocomial pneumonia is confirmed by radiological signs (the appearance of fresh infiltrates in the lung tissue) and laboratory data (leukocytosis> 12.0 x 10 9 /l, stab shift> 10%, arterial hypoxemia Pa02

In order to verify the likely pathogens of nosocomial pneumonia and determine antibiotic sensitivity, a microbiological study of the secret of the tracheobronchial tree is performed. For this, not only samples of freely coughed up sputum are used, but also tracheal aspirate, bronchial washings. Along with cultural isolation of the pathogen, PCR research is widely used.

Treatment of nosocomial pneumonia

The complexity of the treatment of nosocomial pneumonia lies in the polyresistance of pathogens to antimicrobials and the severity of the general condition of patients. In almost all cases, the initial antibiotic therapy is empirical, i.e., begins even before the microbiological identification of the pathogen. After establishing the etiology of nosocomial pneumonia, the drug can be replaced with a more effective one in relation to the identified microorganism.

The drugs of choice for nosocomial pneumonia caused by E. Coli and K. pneumoniae are III-IV generation cephalosporins, inhibitor-protected penicillins, and fluoroquinolones. Pseudomonas aeruginosa is sensitive to the combination of III-IV generation cephalosporins (or carbapenems) with aminoglycosides. If hospital strains are represented by St. aureus, cefazolin, oxacillin, amoxicillin with clavulanic acid, etc. are required. For the treatment of pulmonary aspergillosis, voriconazole or caspofungin is used.

In the initial period, the intravenous route of administration of the drug is preferable; in the future, with positive dynamics, it is possible to switch to intramuscular injections or oral administration. The duration of antibiotic therapy in patients with nosocomial pneumonia is 14-21 days. Evaluation of the effectiveness of etiotropic therapy is carried out according to the dynamics of clinical, laboratory and radiological parameters.

In addition to systemic antibiotic therapy, with nosocomial pneumonia, important attention is paid to the sanitation of the respiratory tract: bronchoalveolar lavage, inhalation therapy, tracheal aspiration. Patients are shown an active motor regime: frequent change of position and sitting down in bed, exercise therapy, breathing exercises, etc. Additionally, detoxification and symptomatic therapy is carried out (infusion of solutions, administration and administration of bronchodilators, mucolytics, antipyretic drugs). For the prevention of deep vein thrombosis, heparin or wearing compression stockings is prescribed; in order to prevent stress ulcers of the stomach, H2-blockers, proton pump inhibitors are used. In patients with severe septic manifestations, intravenous immunoglobulins may be indicated.

Forecast and prevention

Clinical outcomes of nosocomial pneumonia include resolution, improvement, treatment failure, relapse, and death. Nosocomial pneumonia is the main cause of death in the structure of nosocomial infections. This is due to the complexity of its timely diagnosis, especially in elderly, debilitated patients, patients in a coma.

Prevention of nosocomial pneumonia is based on a complex of medical and epidemiological measures: treatment of concomitant foci of infection, compliance with the sanitary and hygienic regimen and infection control in healthcare facilities, prevention of the transfer of pathogens by medical staff during endoscopic manipulations. Early postoperative activation of patients, stimulation of sputum expectoration is extremely important; seriously ill patients need an adequate toilet of the oropharynx, constant aspiration of the tracheal secretion.