Carrying out auscultation for pneumonia. Causes of pulmonary inflammation
Pneumonia (pneumonia) is a group of different etiologies, pathogenesis and morphological characteristics acute local infectious inflammatory diseases, which are characterized by focal damage to the respiratory sections (alveoli, bronchioles) of the lungs with intra-alveolar exudation, confirmed by physical and x-ray examination, and are accompanied by varying degrees of severity of febrile reaction and intoxication.
The definition emphasizes the acute nature of inflammation, so there is no need to use the term “acute pneumonia” (in the International Classification of Diseases adopted World Organization healthcare, the heading “acute pneumonia” is missing and replaced by the term “pneumonia”).
Depending on the epidemiological situation, the incidence of pneumonia in Russia ranges from 3-5 to 10-14 cases per 1000 population, and in the elderly group it can reach 30-50 cases per 1000 population per year.
Classification
In our country, the classification of acute pneumonia (AP) proposed by E.V. has been used for a long time. Gembitskiy et al. (1983). This is a modification of the classification developed by N.S. Molchanov (1962) and approved by the XV All-Union Congress of Therapists. It contains the following sections.
Etiology:
Bacterial (indicating the pathogen);
Viral (indicating the pathogen);
Ornithosis;
Rickettsial;
Mycoplasma;
Fungal (indicating the species);
Mixed;
Allergic, infectious-allergic;
Unknown etiology.
Pathogenesis:
Primary;
Secondary.
Primary AP is an independent acute inflammatory process of predominantly infectious etiology. Secondary refers to pneumonia that occurs as a complication of other diseases (diseases of the cardiovascular system with circulatory disorders in the pulmonary circulation, chronic diseases kidneys, blood systems, metabolism, infectious diseases, etc.) or developing against the background of chronic respiratory diseases (tumor, bronchiectasis, etc.), etc.
Clinical and morphological characteristics:
Parenchymatous - lobar, focal;
Interstitial.
The division into focal and lobar AP is valid only for pneumococcal pneumonia. Establishing a diagnosis of interstitial pneumonia must be approached with great responsibility. This is due to the fact that interstitial processes in the lung accompany a large group of both pulmonary and extrapulmonary diseases, which can contribute to the overdiagnosis of interstitial pneumonia.
Localization and extent:
One-sided;
Bilateral (indicating the extent of both localizations). Gravity:
Extremely heavy;
Heavy;
Moderate;
Light and abortifacient. Flow:
Lingering.
It was proposed to consider a protracted course of AP in which its complete resolution did not occur within a period of up to 4 weeks, which is not true, since the complete resolution of pneumonia caused by staphylococcus and a number of other pathogens requires a much longer period.
Currently, this classification is not used for a number of reasons described below.
The modern definition of pneumonia emphasizes infectious nature inflammatory process and, thus, excludes from the group of pneumonia pulmonary inflammations of other origins (immune, toxic, allergic, eosinophilic, etc.), for which, in order to avoid terminological confusion, it is advisable to use the term “pneumonitis”.
Inflammatory processes in the lungs caused by obligate bacterial or viral pathogens (causative agents of plague, typhoid fever, measles, rubella, etc.) are considered within the framework of the corresponding nosological forms.
Due to the need for early etiotropic treatment of pneumonia and the impossibility in most cases of timely verification of its causative agent, the European Respiratory Society (1993) proposed a working classification of pneumonia based on the clinical and etiological principle, taking into account the epidemic situation and risk factors.
Community acquired pneumonia.
Hospital acquired (hospital or nosocomial) pneumonia.
Pneumonia in immunodeficiency states.
Aspiration pneumonia.
The presented grouping of clinical forms of pneumonia allows us to identify a certain spectrum of pathogens characteristic of each form of the disease. This makes it possible to make a more targeted empirical choice of antibacterial drugs at the initial stage of treatment of the disease.
The general group did not include atypical pneumonia as a disease caused by atypical pathogens and having an atypical clinical picture. With such pneumonia, there is no alveolar exudation, and therefore there is no main auscultatory sign - moist, ringing, fine-bubble rales. In Russia, the term “atypical pneumonia” was used several years ago to refer to severe acute respiratory syndrome (SARS), caused by a coronavirus and spreading in a certain epidemic situation. The causative agent of acute respiratory syndrome, labeled as SARS-CoV, belongs to the group Coronavirus. Its source is animals (cats, dogs); the disease is transmitted from person to person.
Community-acquired pneumonia is an acute infectious disease of predominantly bacterial etiology, occurring in out-of-hospital conditions, belonging to the most common forms of pneumonia and having the most characteristic clinical picture. As before, pneumonia that occurs in closed youth groups (schoolchildren, students, soldiers) and often has the character of an epidemic outbreak occurs with atypical symptoms.
Hospital-acquired (nosocomial) pneumonia includes those pneumonias that developed within 48-72 hours or more after the patient was admitted to the hospital for another disease. The main reasons leading to the development of nosocomial pneumonia are most often previous operations, artificial ventilation, various endoscopic procedures and previous treatment with broad-spectrum antibiotics.
Pneumonia that develops against the background of an altered immune status occurs in patients with AIDS, people receiving immunosuppressive treatment, patients with systemic diseases, etc. They are classified as pneumonia in immunodeficiency states.
Aspiration pneumonia most often develops in persons suffering from alcoholism and drug addiction, less often - after anesthesia, with depression of consciousness. The role of gastroesophageal reflux in the occurrence of aspiration pneumonia has increased.
Etiology
In community-acquired pneumonia in 80-90% of cases, the causative agents are Streptococcus pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae And Moraxella catarrhalis. Among the most common pathogens of pneumonia, the main one remains Streptococcus pneumoniae(Pneumococcus). In addition, it can be caused Chlamydia psittaci and Klebsiella (Friedlander's bacillus).
Hospital-acquired (nosocomial) pneumonia is characterized by a wide variety of etiological agents, including gram-negative microflora (enterobacteria, Pseudomonas aeruginosa, Acinetobacter), Staphylococcus aureus and anaerobes.
Pneumonia in patients with an immunodeficiency state, in addition to pneumococci and gram-negative bacilli, is often caused by Pneumocystis jiroveci (Pneumocystis carinii), viruses (including cytomegalovirus - a marker of HIV infection), fungi, Nocardia spp. and mycobacteria. If neutropenia is detected in such patients during a blood test, then the pathogens most often are Staphylococcus aureus, Escherichia coli And Pseudomonas aeruginosa, often leading to a septic course of the disease.
Since the main cause of aspiration pneumonia is the penetration of microflora of the oropharynx or stomach into the respiratory tract, the main pathogens are anaerobic bacteria, gram-negative microflora and Staphylococcus aureus.
The main causative agents of atypical pneumonia are Mycoplasma pneumoniae, Chlamydia pneumoniae, Chlamydia psittaci, Legionella pneumophyla And Coxiella burnetti.
During an influenza epidemic, the role of viral-bacterial associations increases (staphylococci are most often found), as well as opportunistic microorganisms. In viral-bacterial pneumonia, respiratory viruses play an etiological role only in initial period disease: the main etiological factor determining the clinical picture, severity and outcome of the disease remains the bacterial microflora.
Pathogenesis
In the pathogenesis of pneumonia, the main role belongs to the influence of an infectious pathogen entering the lungs from the outside. Most often, microflora penetrates into different departments lungs through the bronchi by aspiration (from the nasal or oropharynx) and inhalation routes (together with inhaled air). The bronchogenic route of infection is considered the main route for community-acquired pneumonia.
The pathogen enters the lungs through the hematogenous route in pneumonia that develops as a complication of sepsis and infectious diseases, as well as in pneumonia of thrombotic etiology. Lymphogenic spread
The resolution of infection with the development of the disease is noted only with chest wounds.
There is also an endogenous mechanism for the development of inflammation of the lung tissue, due to the activation of the lung microflora. Its role is especially great in nosocomial pneumonia.
The initial link in the development of pneumonia is the adhesion of microorganisms (Fig. 1-1) to the surface of the epithelial cells of the bronchial tree, which is largely facilitated by the previous dysfunction of the ciliated epithelium and impaired mucociliary clearance. After adhesion, the next stage in the development of inflammation is colonization of epithelial cells by the microorganism. Damage to their membrane promotes intensive production of biologically active substances- cytokines (IL-1, 8, 12, etc.).
Under the influence of cytokines, chemotaxis of macrophages, neutrophils and other effector cells taking part in the local inflammatory reaction occurs. In the development of subsequent stages of inflammation, invasion and intracellular persistence of microorganisms, as well as their production of endo- and exotoxins, play a significant role. These processes lead to inflammation of the alveoli and bronchioles and the development of clinical signs of the disease.
Risk factors play an important role in the development of pneumonia. These include age (elderly people and children), smoking, chronic diseases of the lungs, heart, kidneys and gastrointestinal tract, immunodeficiency conditions, contact with birds,
Rice. 1-1. Pathogenesis of pneumonia
zuna and other animals, travel (trains, stations, planes, hotels), hypothermia and staying in a closed group.
In addition to infectious ones, the development of pneumonia can be facilitated by unfavorable external and internal environment, under the influence of which there is a decrease in the general nonspecific resistance of the body (suppression of phagocytosis, production of bacteriolysins, etc.) and suppression of local defense mechanisms(impaired mucociliary clearance, decreased phagocytic activity of alveolar macrophages and neutrophils, etc.).
In the pathogenesis of nosocomial pneumonia, importance is often attached to the development of immune reactions. Saprophytes and pathogenic microorganisms, becoming antigens, contribute to the production of antibodies, which are fixed primarily on the cells of the mucous membrane respiratory tract. Here the antigen-antibody reaction occurs, which leads to tissue damage and the development of the inflammatory process.
When there are common antigenic determinants of microorganisms and lung tissue, or when the latter is damaged by viruses, microorganisms and toxins, leading to the manifestation of its antigenic properties, autoallergic processes develop. They contribute to a longer existence of pathological changes and a protracted course of the disease. In addition, the protracted course of pneumonia is often caused by associations of microorganisms (see Fig. 1-1).
Clinical painting
The clinical picture consists of a combination of the following main syndromes.
General intoxication syndrome: general weakness, fatigue, headaches and muscle pain, shortness of breath, palpitations, pallor and loss of appetite.
Syndrome of general inflammatory changes: feeling of heat, chills, increased body temperature, changes in acute-phase blood parameters (leukocytosis with a shift in the leukocyte formula to the left, an increase in ESR, concentrations of fibrinogen, a2-globulins and C-reactive protein).
Syndrome of inflammatory changes in the lung tissue (cough, sputum production, shortening of percussion sound), increased voice tremors and bronchophony, changes in the frequency and nature of breathing, the occurrence of moist rales and characteristic x-ray changes.
Syndrome involving other organs and systems (cardiovascular system, gastrointestinal tract, kidneys, nervous system).
The severity of these disorders characterizes the severity of pneumonia (Table 1-1).
The clinical picture of pneumonia depends on a number of reasons and is largely determined by the characteristics of the pathogen and the state of the macroorganism. Thus, in the clinical picture of atypical pneumonia, signs of general intoxication predominate, while the symptoms of bronchopulmonary syndrome fade into the background. Aspiration pneumonia is characterized by the development of purulent
Table 1-1. Determining the severity of pneumonia
destructive processes in the lungs. At different stages of the disease, the clinical picture may change depending on the addition of certain complications.
Complications
All complications of pneumonia are divided into pulmonary and extrapulmonary. Basic pulmonary complications:
Abscess formation;
Pleurisy (para- and metapneumonic), much less often - pleural empyema;
Attachment of the asthmatic component.
In severe cases of pneumonia (viral or massive confluent bacterial pneumonia), conditions are created for the formation of pulmonary edema, the development of acute respiratory failure and distress syndrome.
Extrapulmonary complications:
Infectious-toxic shock with symptoms of acute vascular, acute left ventricular and renal failure, ulceration of the gastrointestinal mucosa and bleeding, as well as the development of disseminated intravascular coagulation (DIC) of blood at the final stage;
Infectious-allergic myocarditis;
Infective endocarditis (IE);
Pericarditis;
Meningitis or meningoencephalitis;
Glomerulonephritis;
Hepatitis.
In addition, with severe lobar pneumonia, the development of intoxication psychoses is possible, and with confluent total pneumonia - acute pulmonary heart disease, disseminated intravascular coagulation syndrome and sepsis.
Required:
Determine the main complaints that suggest pneumonia;
Assess the severity of the patient’s condition;
Suggest the etiology of the disease, taking into account the onset and course of the process.
The main complaints presented by patients: cough, sputum production, chest pain, aggravated by breathing and coughing, shortness of breath, poor general health and increased body temperature.
The cough can be dry (in the initial period of lobar pneumonia, throughout the entire disease with interstitial pneumonia) or with sputum (mucous, mucopurulent, purulent mucous, bloody).
“Rusty” sputum is characteristic of lobar pneumonia, and bloody, viscous sputum is characteristic of pneumonia caused by Klebsiella (Friedlander’s bacillus). Purulent bloody sputum is one of the signs of pneumonia of streptococcal etiology. Viral pneumonia can occur with the release of bloody sputum. Persistent, sometimes paroxysmal cough with a small amount of mucous purulent sputum noted in mycoplasma pneumonia. In addition, they are characterized by a feeling of “soreness” in the throat.
Hemoptysis is one of the characteristic features of pneumonia in pulmonary mycoses. It can also be a sign of pulmonary embolism; in this case, hemoptysis in combination with pain in the side is a sign of infarction pneumonia.
Pain in the side, aggravated by deep breathing and coughing, is characteristic of pneumonia involving the pleura in the pathological process (most often for lobar pneumococcal pneumonia). The development of parapneumonic pleurisy is recorded in half of patients with pneumonia caused by Pfeiffer bacillus, and in 30-80% of patients with diseases of streptococcal etiology. When pneumonia is localized in the lower parts of the lungs and the diaphragmatic pleura is involved in the process, the pain can radiate into the abdominal cavity, resembling the picture acute abdomen. If the upper or lower lingular segment of the left lung is involved in the process, then the pain is localized in the heart area.
In 25% of patients, shortness of breath is one of the main complaints. It is most pronounced in pneumonia that develops against the background of chronic respiratory diseases (chronic bronchitis, bronchiectasis) and heart failure. The severity of shortness of breath increases in parallel with the disturbance in general health (headache, lethargy, delirium, vomiting, etc.).
Symptoms of severe intoxication are most characteristic of psittacosis and mycoplasma pneumonia, often present in staphylococcal, influenza and pneumococcal (lobar) pneumonia, as well as in diseases caused by viral-bacterial associations.
The patient may experience chills and increased body temperature. An acute onset with chills is more typical for bacterial pneumonia, primarily for lobar (pneumococcal) pneumonia. The disease, as a rule, begins suddenly with the onset of stunning chills and fever.
body temperature to febrile. Against the general background of intoxication and febrile temperature, local symptoms are noted.
With viral pneumonia at the onset of the disease, the patient does not give the impression of being seriously ill (except for patients with influenza), since the clinical picture is not yet accompanied by symptoms of pneumonia.
To establish an etiological diagnosis, a correct assessment of the symptoms of the disease at its very beginning is important. Hoarseness or the inability to speak is characteristic of pneumonia caused by the parainfluenza virus (children may even develop false croup). Watery eyes, pain in the eyes (symptoms of conjunctivitis), sore throat when swallowing, copious discharge from the nose (symptoms of nasopharyngitis) without changes in other parts of the respiratory tract are recorded in pneumonia caused by adenovirus. If patients, against the background of mild catarrhal symptoms in the upper respiratory tract, develop bronchitis (often with an asthmatic component) and pneumonia, then it is more likely that their causative agent is the respiratory syncytial virus. This disease is characterized by low body temperature and severe symptoms of intoxication.
When studying your medical history, you should pay attention to concomitant diseases of other organs and systems that may affect the symptoms and course of pneumonia. Thus, patients with various tumor diseases, hematological malignancies, receiving chemotherapy, immunosuppressants and (or) drug addiction are classified as a group in which the development of pneumonia occurs against the background of a sharp change in immune status.
In the occurrence of pneumonia occurring with atypical symptoms, importance is attached to the epidemiological history: contact with birds (domestic or ornamental) - sources Chlamydia psittaci, rodents; travel (for example, Legionella can be found in water in hotel air conditioning systems). Pay attention to group outbreaks of febrile diseases in closely interacting groups.
The atypical course of pneumonia is characterized by fever, headache and the appearance of a non-productive cough. Damage to the lower sections is preceded by symptoms of pathological changes in the upper respiratory tract: sore throat, loss of voice and cough, which is periodically paroxysmal in nature and disturbs sleep.
Aspiration pneumonia is characterized by a gradual onset, increased body temperature, cough with purulent sputum, the most common lesion of the upper segment of the lower lobe (with aspiration in a semi-sitting position) or posterior sections upper lobe (with aspiration in the supine position) right lung, prolonged course with the development of late purulent complications in the form of a lung abscess or pleural empyema.
If you suspect the development of pneumonia in a patient who is in the hospital for another disease, you should remember the risk factors for the development of nosocomial pneumonia. These include the patient’s stay in intensive care wards or resuscitation departments, artificial ventilation, tracheostomy, bronchoscopic examinations, postoperative period, previous massive antibiotic therapy and septic conditions. This group of patients has concerns
Leaving is extremely difficult. Complications such as pleural empyema and atelectasis often develop.
Aspiration pneumonia occurs in severe alcoholism, epilepsy, in patients in a comatose state, in acute cerebrovascular accident and other neurological diseases, as well as in swallowing disorders, vomiting, etc.
Knowing these options clinical course pneumonia, taking into account the specific gravity of various pathogens for each of them will allow, with a certain degree of probability, to carry out the etiological diagnosis of the disease already at this stage of the diagnostic search.
On first stage of diagnostic search pneumonia can be assumed, but a definitive diagnosis cannot be made, since the main symptom of the disease - the syndrome of inflammatory changes in the lung tissue - can be detected at the second stage, and in some cases - only at the third stage of the diagnostic search. Along with this, in elderly patients or with severe concomitant illness, extrapulmonary symptoms (confusion, disorientation) may come to the fore, which should prompt the doctor to suspect the development of pneumonia at the first stage of the diagnostic search.
The most significant for the diagnosis is the existence of a syndrome of inflammatory changes in the lung tissue, consisting of the following symptoms:
Lagging of the affected side of the chest when breathing;
Shortening of percussion sound in the area of projection of the lesion over a greater or lesser extent;
Changes in the nature of breathing (hard, bronchial, weakened, etc.);
The occurrence of pathological respiratory sounds (moist, ringing, fine-bubble rales and crepitus).
The breathing pattern can change in different ways. In the initial stage of lobar pneumonia, it may be weakened, with prolonged exhalation; in the hepatization phase, along with an increase in dullness of the percussion sound, bronchial breathing is listened to; when the pneumonic focus resolves with a decrease in percussion dullness, breathing becomes harsh. With focal pneumonia there is no such clear dynamics of physical data. The most persistent symptoms of focal pneumonia are hard breathing and moist, ringing, fine-bubble rales. In some cases (for example, with central hilar pneumonia), physical data are presented very poorly, and recognition of the disease is possible only after an X-ray examination.
Mycoplasma pneumonia is characterized by a paucity of physical data. Severe intoxication in combination with a very small number of wheezes (extensive exudation “clogs” the bronchioles and alveoli) is noted in pneumonia caused by Klebsiella pneumonia. For interstitial pneumonia of any etiology, percussion and auscultation data are very scarce.
In a number of cases (with pneumonia that developed against the background of chronic bronchitis, diseases caused by the Pfeiffer bacillus, as well as in the case of
connections to pneumonia of an allergic/asthmatic component) upon auscultation, a lot of bass and treble dry rales, which are not characteristic of inflammatory infiltration syndrome, come to the fore. The most pronounced sensitizing effect is exerted by mold fungi (urticaria, allergic rhinitis, eosinophilic infiltrate, Quincke's edema).
Physical examination helps to detect other pulmonary complications of pneumonia: pleurisy (pleural friction noise or percussion dullness without respiratory sounds) and lung abscess (dullness and sharp weakening of breathing in the first phase, dull tympanitis, amphoric breathing and moist medium-bubble rales in the second phase).
It is possible to determine the concomitant involvement of organs and systems in the pathological process or complications caused by damage to other organs. In severe cases of pneumonia, a decrease in blood pressure is often noted (a sign of vascular and heart failure).
Other symptoms can help establish an etiological diagnosis:
Detection of a small-spotted (as with rubella) rash in combination with lymphadenopathy is characteristic of adenovirus infection;
Local enlargement of the lymph nodes (especially axillary and supraclavicular) allows one to suspect a lung tumor and perifocal pneumonia;
Fungal pneumonia is combined with damage to the mucous membranes, skin and nails;
Hepatolienal syndrome and slight jaundice are characteristic of ornithosis and Cu-rickettsial pneumonia;
For typical lobar (pneumococcal) pneumonia, note characteristic appearance patient (pale face with a feverish blush on the affected side, herpetic rashes, swelling of the wings of the nose when breathing).
The most important is the detection of signs that confirm or reject the existence of pneumonia; clarifying the nature and specificity of the pathogen; indicating the severity of the inflammatory process; clarifying the state of the body’s immunological reactivity; clarifying the degree of involvement of other organs and systems in the process and the development of complications.
The most important method to clarify the existence of pneumonia and the degree of involvement of lung tissue in the process is an X-ray examination of the chest organs. Large-frame fluorography and radiography in two projections, carried out in dynamics, help (taking into account the clinical picture) to diagnose pneumonia.
Sometimes, by the nature of x-ray changes, one can judge with a certain degree of probability about the pathogen that caused the disease. Staphylococcal pneumonia is distinguished by a clear segmentation of lung damage involving several segments (in 60% of cases - bilateral damage). Their characteristic radiological sign is the formation on the 5-7th day from the onset of the disease of multiple cavities in the lungs, such as pneumocele, and subsequently - necrotic cavities containing fluid.
Unlike true abscesses, the configuration and number of cavities change rapidly.
Lobar lesions most often serve as a sign of lobar pneumococcal pneumonia. Homogeneous darkening of the entire lobe or most of it, usually not corresponding to the segmental division of the lung, is also recorded in pneumonia caused by Klebsiella. Most often, lesions are found in the upper lobe of the right lung.
X-ray examination can detect effusion in the pleural cavity, sometimes not determined by physical methods. It is often formed during streptococcal pneumonia, as well as during a disease caused by Pfeiffer's bacillus, localized in the lower lobe, and in two thirds of patients involving more than one lobe.
Focal pneumonia is often characterized by a discrepancy between clinical and radiological data.
X-ray examination data are especially important when detecting a disease with mild auscultatory changes, which is typical for interstitial and hilar pneumonia. In such cases, computed tomography (CT) is recommended to clarify the diagnosis. It is also carried out to diagnose pneumonia that occurs with pronounced clinical signs, but without clear radiological changes. CT scan of the lungs in this situation can detect infiltration of the lung tissue.
If it is necessary to carry out a differential diagnosis of pneumonia with tuberculosis and lung cancer, bronchoscopy is performed.
Bronchography makes it possible to detect decay cavities in the lung tissue, as well as bronchiectasis, around which infiltrative changes occur during exacerbation (the so-called perifocal pneumonia).
Sputum examination helps clarify the etiology of the disease. A large number of eosinophils indicates allergic processes, the presence of atypical cells indicates lung cancer and perifocal pneumonia. Mycobacterium tuberculosis is found in tuberculosis; elastic fibers serve as evidence of the breakdown of lung tissue (cancer, tuberculosis, abscess). In case of mycotic pneumonia, along with the detection of fungi, the absence of pyogenic microflora is noted due to the inhibitory effect of the waste products of the former.
According to bacterioscopy (microscopy of sputum smears stained with Gram), it is possible to determine gram-negative or gram-positive microorganisms living in the bronchi already on the first day of the patient’s hospital stay (this is important to consider when choosing antibiotics).
Bacteriological examination of sputum (bronchial washings) before prescribing antibacterial drugs helps to detect the pathogen and determine its sensitivity to antibiotics. The study of bronchial lavage is especially important in the diagnosis of pneumonia of Pneumocystis etiology.
In the diagnosis of viral and viral-bacterial pneumonia, virological and serological studies are important.
IN last years special meaning attached to the determination of antigens in urine. Antigen detection Streptococcus pneumoniae And Legionella pneumophila provo-
using the urease test. It can be positive even if the patient received antibiotics the day before. When examining patients who are not amenable to conventional treatment, in the case of an atypical course of the disease or the development of severe complications, all complex immunological, virological and serological methods must be used.
The severity of the inflammatory process can be judged by the severity of acute-phase blood parameters and the dynamics of their changes (leukocytosis with a shift in the leukocyte formula, an increase in ESR, increased contentα2-globulins, fibrinogen, CRP, sialic acids). For bacterial pneumonia, neutrophilic leukocytosis with a shift in the leukocyte formula to the left is more typical. ESR is increased, and the degree of its increase is determined by the prevalence and severity of the process. Viral pneumonia is distinguished by leukopenia. With ornithosis pneumonia, a significant increase in ESR is noted. For parainfluenza and adenoviral pneumonia, as a rule, a tendency to leukopenia is characteristic, but the ESR in these cases is not changed.
In severe cases of pneumonia, repeat sputum cultures are performed, the results of which can help determine the etiology of the disease.
Laboratory and instrumental research methods are of additional importance in clarifying the degree of involvement of other organs and systems in the process and the development of complications:
An ECG allows you to assess the condition of the myocardium;
Echocardiography (EchoCG) for complications of IE helps to detect pericardial effusion or bacterial colonies on the heart valves;
Indicators of external respiration function allow us to assess the state of bronchial patency.
Diagnostics
Diagnosis of pneumonia is based on determining the main and additional diagnostic criteria. The main criterion is the syndrome of local inflammatory infiltration of lung tissue (clinical and radiological data). Additional criteria include:
Syndrome of general inflammatory changes;
Intoxication syndrome;
Syndrome of involvement of other organs and systems;
Existence of risk factors.
A major role in establishing an etiological diagnosis belongs to a correct assessment of the epidemiological situation in combination with the clinical picture of the disease and X-ray data. Help in this case is provided by the results of bacterioscopy, which should be performed on the first day of the disease and interpreted taking into account clinical data.
The etiological affiliation of pneumonia, in which the properties of the pathogen are not fully expressed and there is no characteristic clinical and radiological picture, is established according to bacteriological, virological and serological study during treatment. Even using a wide range of microbiological studies, it is possible to determine the etiology of the disease in hardly half of the cases.
The wording of the expanded clinical diagnosis includes:
Conditions of occurrence (clinical and etiological classification);
Etiology (if established);
Localization and prevalence;
The severity of the current;
Presence of complications;
The flow phase (height, resolution, convalescence). Treatment
The principles of treating a patient with pneumonia are presented in Table. 1-2. Table 1-2. Principles of treating a patient with pneumonia
The treatment measures carried out are listed below.
Therapeutic regimen and rational nutrition.
Drug treatment:
Etiotropic;
Pathogenetic;
Symptomatic.
Physiotherapeutic effects.
Dispensary observation.
Therapeutic regimen and balanced nutrition
Patients with pneumonia must be hospitalized. Indications for it include the patient’s age over 65 years with any degree of severity of the disease, the existence of serious concomitant diseases and (or) signs of impairment of the vital functions of the body, as well as the lack of adequate care at home. In other cases, you can organize a hospital at home. Bed rest is mandatory during the entire period of fever and intoxication. At the same time, the patient needs plenty of fluids, a diet rich in vitamins and proteins.
Drug treatment
Carried out using medicines, affecting the pathogen (etiotropic therapy), various links in pathogenesis, individual signs of the disease (hypoxia, fever, cough, etc.) and developed complications
opinions. The main method of treating pneumonia is antibacterial therapy, which is prescribed empirically until the results of a bacteriological study are obtained. Its results become known 2-3 days after collecting the material and in most cases do not have a significant impact on treatment tactics (Table 1-3).
Table 1-3. Dosage regimen of antibacterial drugs (during empirical antibacterial therapy)
End of table. 1-3
* On the first day, a double dose of 0.5 g is prescribed.
Etiotropic treatment of pneumonia. Antibacterial drugs are used, when prescribing which three basic conditions must be met:
Start treatment as early as possible, without waiting for the isolation and identification of the pathogen, focusing in the choice of dosage regimen on the features of the clinical picture and radiographic data;
Prescribing drugs in sufficient doses and at such intervals that a therapeutic concentration of the drug is created and maintained in the blood and lung tissue;
Monitoring the effectiveness of treatment using clinical observation and, if possible, bacteriological examination.
Of all antibacterial agents, the most effective are antibiotics, which are chosen taking into account the characteristics of the possible pathogen and the patient’s tolerability of the drug. For gram-positive microflora, it is preferable to prescribe semisynthetic penicillins and cephalosporins; for gram-negative microflora, fluoroquinolones, aminoglycosides and imipenem (imipenem + cilastatin) are preferable. Patients with viral-bacterial association should be prescribed broad-spectrum antibiotics in combination with semisynthetic and protected penicillins.
A subjective response to antibiotics is usually noted within 3-4 days from the start of treatment. Objective response includes assessment of fever, symptoms, laboratory values, and radiographic changes. The average dynamics of these parameters is presented in table. 1-4.
The effectiveness of antibiotics is assessed after 2-3 days. If there is no clinical effect from using the drug for three days, it should be replaced with another, focusing, if possible, on the sensitivity of the isolated microflora. Despite high efficiency, at
Table 1-4. Average rate of resolution of clinical and laboratory signs for uncomplicated community-acquired pneumonia
long-term antibacterial therapy, the antibacterial agent is replaced with another after 10-12 days.
Treatment of community-acquired pneumonia
Patients can be treated both in outpatient and inpatient conditions. When conducting antibacterial therapy on an outpatient basis, two groups of patients are distinguished:
Group I - age less than 60 years, no concomitant diseases;
Group II - age over 60 years and (or) concomitant diseases.
As a rule, the duration of antibacterial therapy is 7-10 days.
Conducting antibacterial therapy in patients of group I
The drugs of choice are amoxicillin (0.5-1.0 g orally 3 times a day) or amoxicillin + clavulanic acid (0.625 g orally 3 times a day). Alternative drugs - macrolides: clarithromycin (orally 0.5 g 2 times a day), roxithromycin (orally 0.15 g 2 times a day), azithromycin (orally 0.5 g 1 time a day), spiramycin (orally 1.5 million IU 3 times a day). If an atypical pathogen is suspected, macrolides are considered the drugs of choice, and respiratory fluoroquinolones (oral levofloxacin at a dose of 0.5 g once a day or moxifloxacin at a dose of 0.4 g once a day) can be alternative drugs.
Conducting antibacterial therapy in patients of group II
The drugs of choice are amoxicillin + clavulanic acid (0.625 g orally 3 times a day or 1.0 g 2 times a day), cefuroxime (0.5 g orally 2 times a day). Alternative drugs: levofloxacin (0.5 g orally once a day), moxifloxacin (0.4 g orally once a day) or ceftriaxone (intramuscular 1.0-2.0 g once a day).
Macrolides should be preferred in case of intolerance p-lactam antibiotics and pneumonia, presumably caused Mycoplasma pneumoniae And Chlamydia pneumoniae. The indication for parenteral administration of drugs is the impossibility of taking them orally.
Antibacterial therapy in hospital settings
Drug treatment in hospital depends on the severity of pneumonia.
Treatment of mild to moderate pneumonia. Drugs of choice: amoxicillin + clavulanic acid (intravenous 1.2 g 3 times a day), ampicillin (intravenous or intramuscular 1.0-2.0 g 4 times a day), benzylpenicillin (intravenous 2 million units 4-6 once a day), cefotaxime (intravenously or intramuscularly 1.0-2.0 g 2-3 times a day), ceftriaxone (intravenously or intramuscularly 1.0-2.0 g 1 time a day), cefuroxime (intravenously or intramuscularly 0.75 g 3 times a day). Alternative drugs: levofloxacin (intravenously at a dose of 0.5 g once a day) or moxifloxacin (intravenously at a dose of 0.4 g once a day).
After 3-4 days of treatment, when a clinical effect is achieved (normalization of body temperature, reduction in the severity of intoxication and other symptoms of the disease), one should switch from parenteral administration of drugs to oral administration. The total duration of treatment is 7-10 days.
Treatment of severe pneumonia. Drugs of choice: a combination of clarithromycin (0.5 g intravenously 2 times a day), or spiramycin (1.5 million IU intravenously 3 times a day), or erythromycin (orally 0.5-1.0 g 4 times a day). day) with amoxicillin + clavulanic acid (intravenous 1.0-2.0 g 3 times a day) or cefepime (intravenous 1.0-2.0 g 2 times a day), or cefotaxime (intravenous 1.0 -2.0 g 2-3 times a day), or ceftriaxone (intravenously at a dose of 1.0-2.0 g 1 time a day). Alternative medicines: a combination of levofloxacin (intravenously at a dose of 0.5 g 1-2 times a day), or moxifloxacin (intravenously at a dose of 0.4 g once a day), or ofloxacin (intravenously at a dose of 0.4 g 2 times a day ), or ciprofloxacin (intravenously at 0.2-0.4 g 2 times a day) with cefotaxime (intravenously at 1.0-2.0 g 2-3 times a day) or ceftriaxone (intravenously at a dose of 1.0- 2.0 g 1 time per day).
Parenterally, the drugs are administered for 7-10 days. The total duration of treatment is 14-21 days.
Treatment of nosocomial pneumonia
When treating, it should be taken into account that often the causative agents of the disease are multidrug-resistant gram-negative bacteria (including Pseudomonas aeruginosa), staphylococci, and anaerobes. Treatment of nosocomial pneumonia with antibacterial agents depends on the presence or absence of associated risk factors. The duration of use of antibacterial drugs is determined individually. In the treatment of nosocomial (nosocomial) pneumonia, taking into account the most common pathogens (Pseudomonas aeruginosa, Staphylococcus aureus), the first place is taken by cephalosporins of the III-IV generation, resistant to the action of p-lactamases, fluoroquinolones and imipenem.
Antibacterial treatment of nosocomial pneumonia occurring in patients without associated risk factors
Drugs of choice: amoxicillin + clavulanic acid (intravenous 1.2 g 3 times a day), cefotaxime (intravenous or intramuscular 1.0-2.0 g 2-3 times a day), ceftriaxone (intravenous or intramuscular in
dose 1.0-2.0 g 1 time per day), cefuroxime (intravenously or intramuscularly 0.75 g 3 times per day). Alternative medicines: levofloxacin (intravenously at a dose of 0.5 g once a day), moxifloxacin (intravenously at a dose of 0.4 g once a day), a combination of cefepime (intravenously 1.0-2.0 g twice a day). day) with amikacin (intravenously at a dose of 15-20 mg/kg once a day) or gentamicin (intravenously at a dose of 3-5 mg/kg once a day).
Antibacterial treatment of nosocomial pneumonia occurring in patients with associated factors risk
Drugs of choice: imipenem (0.5 g intravenously 3-4 times a day), or ceftazidime (1-2 g intravenously 2-3 times a day), or cefepime (1.0-2.0 g
2 times a day), or meropenem (0.5 g intravenously 3-4 times a day) in combination with amikacin (intravenously at a dose of 15-20 mg/kg 1 time per day) or vancomycin (1.0 g intravenously 2 times a day). Alternative therapeutic agents: aztreonam (intravenously or intramuscularly at 0.5-2.0 g 2-3 times a day), or levofloxacin (intravenously at a dose of 0.5 g once a day), or moxifloxacin (intravenously at a dose of 0. 4 g 1 time per day), or a combination of amikacin (intravenously at a dose of 15-20 mg/kg 1 time per day) with piperacillin + tazobactam (intravenous 4.5 g 3 times per day) or with ticarcillin + clavulanic acid (intravenous 3.2 g 3 times a day). Instead of amikacin, gentamicin can be used (intravenous 3-5 mg/kg body weight once a day).
Treatment of aspiration pneumonia
Aspiration pneumonia is almost always caused by anaerobic and (or) gram-negative microflora, which requires the administration of aminoglycosides, protected penicillins in combination with metronidazole and carbapenems. Drugs of choice: amoxicillin + clavulanic acid (1.2 g intravenously
3 times a day, or benzylpenicillin (2 million units intravenously 4-6 times a day) in combination with metronidazole (0.5 g intravenously 3 times a day). Alternative medicines: imipenem (0.5 g intravenously 3-4 times a day) or meropenem (0.5 g intravenously 3-4 times a day). Intravenous administration of clindamycin (0.3-0.9 g 3 times a day) has a good effect. The duration of antibacterial therapy for aspiration pneumonia is determined individually.
Treatment of pneumonia in immunodeficiency states
Treatment of pneumonia in combination with severe immune defects should be carried out only in a hospital setting. In patients with immunodeficiency conditions, the choice of antibacterial therapy largely depends on the origin of the pathogen. The most common regimen is the administration of aminoglycosides in combination with modern cephalosporins. In AIDS patients with the development of pneumonia caused by Pneumocystis carinii, The accepted treatment regimen is parenteral administration of pentamidine, cotrimoxazole and septrim. Treatment of Pneumocystis pneumonia is carried out with cotrimoxazole (intravenously at a dose of 20 mg/kg per day in 3-4 doses). Duration of treatment - 21 days.
At poor tolerance antibiotics and high sensitivity isolated microflora to nitrofurans, furaltadone is prescribed (0.1 g orally
4 times a day), furazidin (intravenous drip of 300-500 ml of 0.1% solution per day; 3-5 infusions per course). If antibiotics are ineffective, you can
Successful use of quinoxaline derivatives (hydroxymethylquinoxaline dioxide).
To prevent candidiasis (especially with massive and long-term antibacterial therapy), the use of nystatin and levorin (orally 500 thousand units 4 times a day) is recommended.
For pneumonia of fungal etiology, antifungal agents are prescribed: amphotericin B, itraconazole, ketoconazole, fluconazole, etc.
Pathogenetic treatment of pneumonia. To restore nonspecific resistance in severe and prolonged pneumonia, immunomodulatory agents (interferon preparations, azoximer bromide, thymus extract) are used.
For staphylococcal pneumonia, passive immunization with staphylococcal toxoid is carried out.
To restore bronchial patency, bronchodilators and agents that dilute bronchial secretions are used (ingestion of acetylcysteine, ambroxol, bromhexine, hot alkaline drink). Bronchodilators are preferably administered by inhalation: adrenomimetic (fenoterol, salbutamol) and anticholinergic drugs (ipratropium bromide, orally - theophylline).
In cases of prolonged pneumonia, the restoration of bronchial drainage using bronchoscopic sanitation sometimes plays a decisive role.
To restore the body's nonspecific resistance, vitamins A, C, E, group B, biogenic stimulants and adaptogenic agents (aloe, tincture of ginseng and schisandra, liquid extract of Eleutherococcus) are prescribed.
For patients who may have a viral etiology, administration of human immunoglobulin anti-influenza and antiviral drugs (riboverine, ganciclovir, etc.) is recommended. On an outpatient basis, inhalations of phytoncides are used (garlic and/or onion juice, prepared ex temporae, in isotonic sodium chloride solution).
Symptomatic treatment of pneumonia. For a non-productive dry cough, antitussives are prescribed (codeine, prenoxdiazine, glaucine, butamirate + guaifenesin, butamirate, etc.); for difficult sputum discharge - expectorants (thermopsis herb infusion, marshmallow root, etc.) and mucolytic drugs (marshmallow herb extract, ambroxol, acetylcysteine). In case of poor tolerance to high body temperature, antipyretics (metamizole sodium, acetylsalicylic acid) are indicated. Patients with concomitant pathological changes in the cardiovascular system (especially the elderly), as well as in severe cases of the disease, are prescribed injections of camphor, procaine + sulfocamphoric acid.
The presence of shortness of breath and cyanosis is an indication for oxygen therapy. In case of severe intoxication and destruction pulmonary infiltrate detoxification treatment is carried out (intravenous administration of dextran [average molecular weight 30,000-40,000], hemodez* and other solutions).
Intravenous administration of glucocorticoids is recommended for patients with severe pneumonia, severe intoxication and infectious-toxic shock.
Physiotherapeutic impact
When treating patients with pneumonia, distracting procedures are used (cupping, mustard plasters, mustard wraps), which are carried out from the first days of illness at a low body temperature. After a decrease in body temperature, diathermy, inductothermy, microwave, UHF, etc. are prescribed to eliminate inflammatory changes. Chest massage and physiotherapy(physical therapy).
Aerosol therapy using bronchodilator mixtures alone or in combination with various antibacterial drugs is used in the resolution stage.
Dispensary observation
Recovery criteria:
Good health and general condition of the patient;
Persistent normalization of body temperature;
Elimination of clinical, laboratory and radiological signs of pneumonia.
Forecast
Pneumonia is one of those diseases that, as a rule, ends in complete recovery. The outcome of pneumonia largely depends on the prevalence of the inflammatory process, the existence or absence of complications, the start date and usefulness of antibiotic therapy, the condition of the body and other reasons.
All patients with a widespread inflammatory process, a prolonged course of pneumonia, impaired functions of external respiration and the immune system, as well as complicated pneumonia should be sent to rehabilitation departments for follow-up treatment and restoration of morphological and functional parameters.
The period of medical examination for patients who have had pneumonia without complications can be 6 months, in all other cases - at least a year.
Prevention
Preventive measures are aimed at carrying out general sanitary and hygienic measures (working hours, combating dust, gas pollution, overheating and hypothermia, ventilation of premises, isolation of sick people, etc.). Personal prevention includes hardening the body, physical education and tourism, good nutrition and sanitation of foci of infection. Timely and correct treatment of acute respiratory diseases and other anti-epidemic measures are of great importance.
Prevention of pneumonia is especially important in patients suffering from chronic pulmonary diseases. They consider it mandatory to carry out influenza vaccination, and, if possible, to immunize with a vaccine to prevent pneumococcal infections.
Strict adherence to the regimen and other doctor’s instructions is necessary for diseases that may be complicated by pneumonia (myocardial infarction, stroke, condition after surgical intervention and etc.).
In 3% of cases, chronicity of the inflammatory process is noted. Chronic pneumonia or chronic pneumonia(CP) - chronic damage to the parenchyma and interstitial lung tissue, developing at the site of unresolved pneumonia, limited to a segment (segments) or lobe (lobes) and clinically manifested by repeated outbreaks of the inflammatory process in the affected part of the lung. The morphological substrate of CP is pneumosclerosis and (or) carnification of the lung tissue, as well as irreversible changes in the bronchial tree such as local bronchitis, often with deformation and the development of bronchiectasis in the future. Due to the widespread and successful use of antibacterial drugs for the treatment of infectious processes of the lower respiratory tract, CP is currently rarely recorded.
The existence of CP is not recognized by all researchers, but it is identified by pathologists and a number of clinical doctors (Putov N.V., Silvestrov V.P.).
Classification. Currently, there is no classification of CP that would satisfy all the requirements. The classification of CP officially adopted in 1972 led to overdiagnosis of this disease and practically replaced all other forms of so-called chronic respiratory diseases of the lungs, in particular chronic bronchitis, bronchiectasis and chronic obstructive pulmonary disease.
Currently, the main criterion for the transition of protracted pneumonia to chronic pneumonia - the duration of the disease is 8 weeks - has been rejected (Silvestrov V.P., 1974). Only the absence of positive x-ray dynamics, despite long-term and intensive treatment, and most importantly, the existence of repeated outbreaks of the inflammatory process in the same area of the lung, allows us to talk about the transition of prolonged pneumonia into a chronic form.
Etiology. CP is an inflammatory disease of infectious origin, so its etiology corresponds to that of pneumonia. Although there is no microorganism that causes the chronic course of pneumonia, varying degrees of importance of various pathogens in the transition of an acute inflammatory process to a chronic one have been proven.
Most often, the causative agents of the inflammatory process in CP are associations of nonbacterial (viruses, mycoplasmas) and bacterial (mainly pneumococci and Haemophilus influenzae) agents.
The role of viral infection is especially great in the transition of an acute inflammatory process to a chronic one.
Pneumonia, in the occurrence of which viruses play a leading role, leading to destructive processes, ends with the formation of fibrotic changes in the lungs.
The influenza virus damages the bronchial wall with the development of drainage and ventilation disorders, causes inflammatory changes in the interstitial tissue, which are relatively persistent and prone to slow reverse development.
The influenza virus is a conductor of autoinfection, creating a favorable background for the manifestation of the pathogenic properties of diverse opportunistic and saprophytic microflora.
A possible reason for the chronicity of the process is a defect in the development of lung tissue in the area acute inflammation, promoting relapse of the inflammatory process, and colonization of the pathogen.
Pathogenesis. The immediate causes that determine the transition of an acute inflammatory process to a chronic one have not been sufficiently studied. The following facts are considered undoubted.
In the occurrence of repeated outbreaks of infection in a previously affected area of the lung, remaining changes play a role, causing local disruption of the drainage function of the bronchi. In some cases, the determining factor in the pathogenesis of CP is concomitant chronic bronchitis, which greatly complicates the drainage and aeration function of the bronchi in the zone of acute inflammation.
A focal infection present in the patient’s body can serve as a constant source of autoinfection and sensitization of the body, expressed in increased sensitivity bronchopulmonary system to various microorganisms, viruses and their metabolic products.
The prerequisites for the formation of CP are all conditions (intoxication including viral, alcohol, smoking, hypothermia, overwork, old age, etc.) that suppress general reactivity and contribute to changes in the immune status of the body and local immunity bronchopulmonary system. These changes are expressed in a decrease in the activity of alveolar macrophages and leukocytes, weakening of phagocytosis, deficiency of secretory IgA and a decrease in the concentration of bacteriolysins.
In CP, the development of autoimmune processes has been noted. Antipulmonary antibodies have pulmonary cytotoxic properties, which results in inflammation of the interstitial tissue.
As a result of the influence of all these factors, the inflammatory process in pneumonia (Fig. 1-2) is not completely eliminated. Areas of carnification remain, which subsequently serve as a site for recurrence of the inflammatory process.
The process is not limited to the lung parenchyma, but moves to the interstitial tissue, bronchi and blood vessels. In connection with this, the morphological substrate of CP is considered to be an inflammatory-sclerotic process (pneumosclerosis), leading to a decrease in the volume of the affected part of the lung and its cicatricial wrinkling. In areas of the bronchial tree corresponding to the affected area, the phenomena of local bronchitis develop, which in the future can acquire a deforming character with the subsequent development of bronchiectasis.
The process never becomes diffuse, therefore the severity of functional disorders of the respiratory and circulatory system in the pulmonary circulation is insignificant. In this regard, the development of respiratory (pulmonary) failure and cor pulmonale, even with extensive foci of CP, is rarely recorded.
Rice. 1-2. Pathogenesis of chronic pneumonia
Clinical picture. The following main syndromes are characteristic of CP:
Inflammatory infiltration;
Local pneumosclerosis.
Broncho-obstructive syndrome and respiratory failure syndrome are optional signs that can occur at different stages of the disease.
There are three degrees of activity of the inflammatory process:
I degree - minimal signs;
II degree - moderate signs of exacerbation;
III degree - clinical, radiological and laboratory indicators of exacerbation are clearly expressed.
Depending on the predominance of a particular syndrome, CP occurs in two main forms - interstitial and bronchiectasis.
The interstitial form of CP is characterized by a predominance of changes in the form of focal pneumosclerosis (N.V. Putov, 1984). This is the most common form of CP. In the bronchiectasis form, along with focal pneumosclerosis, there are also bronchiectasis (CP with bronchiectasis). This form is not recognized by all doctors (N.R. Paleev, 1985).
N.V. Putov, in addition to the interstitial one, also identifies a carnifying form of CP (with a predominance of carnification of the alveoli). With this form of CP, patients, as a rule, do not complain, and radiographically there may be intense, fairly clearly defined shadows, which must be differentiated from signs of a peripheral tumor.
Interstitial form of chronic pneumonia. At the first stage of the diagnostic search The following complaints can be found:
Cough, in the vast majority of cases - with the release of a small amount of sputum, sometimes - hemoptysis;
Chest pain on the affected side;
Shortness of breath on exertion;
Increased body temperature;
Phenomena of asthenia (weakness, headache, sweating, loss of appetite and body weight).
Complaints are most vivid and numerous with severe exacerbation. The amount of sputum increases, it becomes purulent. After the addition of broncho-obstructive syndrome, along with the productive one, a persistent paroxysmal cough with difficult sputum production occurs.
In CP without bronchiectasis, the occurrence of hemoptysis always indicates the activity of the process and, as a rule, is slightly expressed. Hemoptysis is usually noted in the bronchiectasis form of CP, since it is one of the generally recognized symptoms of bronchiectasis.
In case of exacerbation of the process, chest pain often occurs or intensifies on the side of the inflammatory process: a constant feeling of heaviness (most often at the angle of the scapula) is disturbing. A nagging stabbing pain may intensify with breathing (involvement of the pleura in the process). Body temperature is often subfebrile, rarely febrile. An exacerbation is accompanied by sudden sweating, severe weakness and loss of appetite.
In the remission stage, complaints are few. The most common symptom is a cough with scanty mucopurulent sputum.
On first stage of diagnostic search It is considered important to establish a correct diagnosis to detect a connection between these complaints and previously suffered pneumonia (often a protracted course), untimely initiation and insufficiently complete treatment. In the absence of clear instructions for previous illness it is necessary to establish whether there have been previously frequently recurring acute respiratory diseases. Repeated inflammation of the same area of lung tissue can be noted.
In the anamnesis of patients with CP there are no indications of pneumoconiosis, tuberculosis, sarcoidosis and other diseases accompanied by similar clinical signs (their existence in the anamnesis requires a revision of the diagnostic concept).
On the second stage of the diagnostic search it is necessary to determine the syndromes of local pneumosclerosis and inflammatory infiltration, which can be characterized by the following clinical symptoms:
Delay in breathing and (or) retraction of the affected side of the chest (pronounced with significant involvement of lung tissue in the process);
Dullness or shortening of percussion sound;
Moist, ringing, fine-bubble rales over the lesion, caused by local focal pneumosclerosis.
If the pleura is involved in the process, then a pleural friction noise is heard. With broncho-obstructive syndrome, prolongation of exhalation and dry wheezing are noted. The latter also occur when an asthmatic (allergic) component is added to CP, the development of which is one of the main and serious complications diseases at present. The development of respiratory failure is accompanied by shortness of breath at rest, cyanosis and tachycardia. Outside of exacerbation of CP, clinical signs are scarce: moist, silent, fine-bubble rales are heard in a limited area.
On third stage of diagnostic search perform instrumental and laboratory studies that allow:
Make a final diagnosis of CP based on radiological signs of local (segmental or lobar) pneumosclerosis, endoscopic signs of local bronchitis, and exclusion of diseases with a similar clinical picture;
Determine the degree of activity of the inflammatory process;
Determine and (or) clarify the severity of complications.
X-ray examination is of decisive importance in the diagnosis of CP and its exacerbations. With a pronounced exacerbation of the process, inflammation of the infiltrative and (or) peribronchial type is noted. The infiltrative type is characterized by focal darkening against the background of variously expressed interstitial changes (pneumosclerosis) and adhesive pleurisy (interlobar, paramediastinal adhesions, fusion of the costophrenic sinuses). The peribronchial type is characterized by changes around the segmental bronchi in the form of concentric couplings or cords parallel to the bronchus in combination with signs of focal pneumosclerosis (heaviness and deformation of the pulmonary pattern, a decrease in the volume of the affected area of the lung). There is no characteristic localization of the inflammatory process in CP.
Since the clinical picture is similar to CP in the chronic focal form of pulmonary tuberculosis, chronic abscess and bronchogenic tumors, radiological methods become crucial for differential diagnosis. X-ray examination in combination with data from the first and second stages of the diagnostic search also makes it possible to exclude thoracic sarcoidosis and Hamman-Rich syndrome. The results are of decisive importance in carrying out differential diagnosis
Bronchography is performed before surgery to clarify the nature and extent of bronchial damage.
Bronchoscopic examination data significantly helps:
In establishing the final diagnosis of CP, since local purulent or catarrhal endobronchitis is a bronchoscopic marker of the disease;
In the exclusion (detection) of bronchogenic cancer, manifesting a clinical picture similar to CP;
In assessing the degree of activity of the inflammatory process (by the severity of hyperemia and swelling of the mucous membrane, the nature and amount of secretion in the bronchi).
All patients with CP undergo a study of external respiratory function (spirometry). Its results help to detect and assess the severity of broncho-obstructive syndrome and respiratory failure. In uncomplicated CP, restrictive disorders are usually identified.
The detection of a large number of neutrophils during sputum microscopy indicates the activity of the inflammatory process: the detection of eosinophils is characteristic of the development of an allergic (asthmatic) component, complicating the course of CP; determination of Mycobacterium tuberculosis and elastic fibers forces us to reconsider the previously assumed diagnosis of CP.
Bacteriological examination of sputum helps determine the type of microflora. A high concentration of microorganisms (more than 106 in 1 μl) reliably indicates its pathogenicity. When sputum is cultured, the sensitivity of microflora to antibiotics is also determined.
The role of clinical and biochemical blood tests in assessing the activity of the inflammatory process is insignificant. The results obtained do not sufficiently reflect the degree of inflammation. Changes in acute-phase indicators (increased ESR, leukocytosis with a shift in the leukocyte formula to the left, increased fibrinogen, α2-globulins, CRP) are noted only with severe inflammation. If the process is less active, all of these indicators may be normal. Exacerbation of the pathological process in these cases is diagnosed based on a combination of clinical picture data, the results of X-ray examination and bronchoscopy, as well as sputum analysis.
Bronchiectasis form of chronic pneumonia. This form is distinguished based on a number of features of the clinical picture.
On first stage of diagnostic search A number of diagnostic clinical signs are noted.
The originality of complaints and the degree of their severity:
A large amount of sputum secreted (up to 200 ml per day), coming out “full of mouth” and sometimes acquiring a putrefactive character (hemoptysis is often noted);
When sputum production is delayed, the body temperature becomes febrile;
Patients are concerned about severe weight loss (carcinophobia often develops), lack of appetite and significant severity of symptoms of intoxication.
The active inflammatory process occurs continuously or with frequent exacerbations. This is explained by a more dramatic severity of morphological changes in the focus of chronic inflammation with a significant disruption of the drainage function of the regional bronchi, as well as more pronounced disturbances in general and immunological reactivity.
Less effective conservative therapy.
On the second stage of the diagnostic search a typical clinical picture is observed.
Distinct severity of clinical symptoms: loss of body weight, change in the shape of nails (they take on the appearance of watch glasses) and deformation of the fingers according to the type drumsticks. Physical changes detected during examination of the respiratory organs are also more pronounced and persistent. You can listen to not only small but also medium bubble rales. During percussion, it is possible to determine local shortening of the percussion sound.
Complications are detected: pulmonary hemorrhage, spontaneous pneumothorax, signs of cor pulmonale.
On third stage of diagnostic search The most important information for diagnosis is provided by x-ray examination of patients.
Plain radiographs show gross focal deformation of the pulmonary pattern and cystic clearings. A volumetric decrease in a lobe or segment of the lung is possible with a shift of the mediastinum towards the lesion.
CT scan can identify areas of carnification, thin-walled cavities and cylindrical expansion of the draining bronchus.
Bronchograms reveal pathological changes in the regional bronchi, specify the segmental localization of the process and the type of bronchiectasis (cylindrical, fusiform, saccular).
Complications of HP:
Broncho-obstructive syndrome;
Respiratory failure;
Chronic cor pulmonale;
Formation of an allergic (asthmatic) component;
Pulmonary hemorrhage;
Spontaneous pneumothorax.
Diagnostics. When establishing a diagnosis of CP, the following are taken into account:
A clear connection between the onset of the disease and previous pneumonia (less often with acute respiratory infection, including influenza);
Repeated inflammation of the same area of lung tissue within one segment or lobe of the lung (focal nature of the pulmonary process), physical signs of focal inflammation and pneumosclerosis (depending on the phase of the process) and nonspecific signs of inflammation (according to laboratory research methods);
X-ray (including CT) signs of focal pneumosclerosis, the existence of deforming bronchitis, pleural adhesions and local bronchiectasis;
Bronchoscopic picture of local purulent or catarrhal bronchitis;
The absence of other chronic respiratory diseases of the lungs, as well as tuberculosis, pneumoconiosis, sarcoidosis, Hamman-Rich syndrome, which determine the long-term existence of pulmonary tissue compaction syndrome, as well as the development of bronchiectasis.
When formulating a diagnosis of “chronic pneumonia”, you should reflect:
Clinical and morphological form of pneumonia (interstitial CP or CP with bronchiectasis);
Localization of the process (shares and segments);
The phase of the process (exacerbation, remission), while during exacerbation the degree of activity of the process is indicated;
Complications.
Treatment. In the acute phase, treatment includes:
Measures aimed at eliminating the exacerbation of the inflammatory process (antibacterial therapy);
Pathogenetic therapy (restoration of bronchial patency; prescription of drugs that increase the body's resistance);
Treatment of complications.
In principle, the treatment corresponds to that for AP, but has some peculiarities.
When carrying out antibacterial therapy, the characteristics of the pathogen should be taken into account. The course of antibiotic treatment for CP is extended, preference is given to parenteral route introduction.
With the development of bronchiectasis, it is advisable to administer antibiotics locally through a bronchoscope after sanitizing the bronchi and washing them with hydroxymethylquinoxaline dioxide. If necessary (expressed general signs inflammation, high degree of activity of purulent endobronchitis) the same drugs are additionally administered parenterally.
The use of this method of drug delivery through a nebulizer opens up the possibility of inhalation therapy using a combination of the antibiotic thiamphenicol glycinate acetylcysteinate at a dose of 250 mg with the mucolytic ambroxol.
In case of severe relapse caused by staphylococcus, Pseudomonas aeruginosa and other pathogens, passive specific immunotherapy with hyperimmune plasma and γ-globulin should be performed.
During exacerbation of the disease and during the recovery stage, the use of immunomodulatory drugs is recommended: thymus extract, azoximer bromide, glucosaminyl muramyl dipeptide. Oral and parenteral administration of vitamin preparations and a complete diet rich in proteins and vitamins are necessary. In cases of weight loss and prolonged intoxication, anabolic steroids are prescribed (intramuscular administration of nandronol 2 ml once a week).
An important part of treatment is taking measures aimed at restoring or improving bronchial obstruction.
To improve the drainage function of the bronchi, expectorants and mucolytics are prescribed, sanitary bronchoscopy is performed, postural drainage and special exercises are used in a complex of breathing exercises.
In order to eliminate bronchospasm, long-acting theophylline preparations and inhaled bronchodilators (β2-agonists and m-anticholinergics or their combination - berodual) are prescribed. If the effect of therapeutic measures is insufficient, complex treatment includes intra-
tracheal administration of hydrocortisone at a dose of 25 mg and other glucocorticoids. For the asthmatic component, treatment is supplemented with the prescription of inhaled glucocorticoid drugs in the form of metered-dose inhalers.
In the phase of subsiding exacerbation It is recommended to take anti-inflammatory drugs (meloxicam, fenspiride) and biogenic stimulants (aloe, Chinese lemongrass, etc.). The use of antibiotics for active endobronchitis is limited to local administration (through a bronchoscope, inhalation). During this period, breathing exercises, chest massage and physiotherapeutic procedures (UHF therapy, diathermy, inductothermy, electrophoresis of calcium chloride, potassium iodide, etc.) become important.
Treatment of CP in remission involves a set of measures aimed at preventing exacerbation, i.e. secondary prevention measures. The patient should stop smoking and constantly practice breathing exercises. He needs rational employment, sanatorium treatment and observation in the pulmonology office of the clinic. A course of treatment with weakened vaccines is recommended: bronchomunal, ribomunil and bronchovaxone.
Forecast. In most cases, the prognosis is favorable for life, but patients require long-term follow-up and periodic treatment.
Prevention. The main preventive measures are prevention, early diagnosis, timely and rational treatment of pneumonia.
– acute lesion lungs of an infectious-inflammatory nature, which involves all the structural elements of the lung tissue, mainly the alveoli and interstitial tissue of the lungs. The clinical picture of pneumonia is characterized by fever, weakness, sweating, chest pain, shortness of breath, cough with sputum (mucous, purulent, “rusty”). Pneumonia is diagnosed based on auscultation patterns and chest x-ray data. IN acute period treatment includes antibiotic therapy, detoxification therapy, immunostimulation; taking mucolytics, expectorants, antihistamines; after the cessation of fever - physiotherapy, exercise therapy.
Among the extrapulmonary complications of pneumonia, acute cardiopulmonary failure, endocarditis, myocarditis, meningitis and meningoencephalitis, glomerulonephritis, infectious-toxic shock, anemia, psychosis, etc. often develop.
Diagnosis of pneumonia
When diagnosing pneumonia, several problems are solved at once: differential diagnosis of inflammation with other pulmonary processes, clarification of the etiology and severity (complications) of pneumonia. Pneumonia in a patient should be suspected based on symptomatic signs: rapid development of fever and intoxication, cough.
Physical examination reveals compaction of the lung tissue (based on percussion dullness of pulmonary sound and increased bronchophony), a characteristic auscultatory pattern - focal, moist, fine-bubbly, sonorous rales or crepitus. Echocardiography and ultrasound of the pleural cavity sometimes detect pleural effusion.
As a rule, the diagnosis of pneumonia is confirmed after a chest x-ray. With any type of pneumonia, the process most often affects the lower lobes of the lung. X-rays of pneumonia may reveal the following changes:
- parenchymal (focal or diffuse darkening of various localization and extent);
- interstitial (the pulmonary pattern is enhanced due to perivascular and peribronchial infiltration).
X-rays for pneumonia are usually taken at the onset of the disease and after 3-4 weeks to monitor the resolution of inflammation and exclude other pathologies (usually bronchogenic lung cancer). Changes in the general blood test during pneumonia are characterized by leukocytosis from 15 to 30 109/l, a band shift in the leukocyte formula from 6 to 30%, an increase in ESR to 30-50 mm/h. A general urinalysis may reveal proteinuria and, less commonly, microhematuria. Sputum analysis for pneumonia allows you to identify the pathogen and determine its sensitivity to antibiotics.
Treatment of pneumonia
Patients with pneumonia are usually hospitalized in the general medical department or the pulmonology department. For the period of fever and intoxication it is prescribed bed rest, plenty of warm drinks, high-calorie, vitamin-rich food. For severe symptoms of respiratory failure, patients with pneumonia are prescribed oxygen inhalation.
Antibacterial therapy is the mainstay in the treatment of pneumonia. Antibiotics should be prescribed as early as possible, without waiting for the pathogen to be identified. The choice of antibiotic is carried out by a doctor; no self-medication is acceptable! For community-acquired pneumonia, penicillins (amoxicillin with clavulanic acid, ampicillin, etc.), macrolides (spiramycin, roxithromycin), cephalosporins (cefazolin, etc.) are more often prescribed. The choice of method of antibiotic administration is determined by the severity of the pneumonia. For the treatment of nosocomial pneumonia, penicillins, cephalosporins, fluoroquinolones (ciprofloxacin, ofloxacin, etc.), carbapenems (imipenem), aminoglycosides (gentamicin) are used. If the pathogen is unknown, a combination antibiotic therapy of 2-3 drugs is prescribed. The course of treatment can last from 7-10 to 14 days, it is possible to change the antibiotic.
For pneumonia, detoxification therapy, immunostimulation, and the prescription of antipyretics, expectorants, mucolytics, and antihistamines are indicated. After the cessation of fever and intoxication, the regimen is expanded and physiotherapy is prescribed (electrophoresis with calcium chloride, potassium iodide, hyaluronidase, UHF, massage, inhalations) and exercise therapy to stimulate resolution of the inflammatory focus.
Treatment of pneumonia is carried out until the patient’s complete recovery, which is determined by the normalization of condition and well-being, physical, radiological and laboratory parameters. With frequent repeated pneumonia in the same localization, the issue of surgical intervention is decided.
Prognosis for pneumonia
In pneumonia, the prognosis is determined by a number of factors: the virulence of the pathogen, the age of the patient, underlying diseases, immune reactivity, and the adequacy of treatment. Complicated variants of the course of pneumonia, immunodeficiency states, and resistance of pathogens to antibiotic therapy are unfavorable in terms of prognosis. Pneumonia in children under 1 year of age caused by staphylococcus, Pseudomonas aeruginosa, and Klebsiella is especially dangerous: the mortality rate for them ranges from 10 to 30%.
With timely and adequate treatment measures, pneumonia ends in recovery. Depending on the types of changes in the lung tissue, the following outcomes of pneumonia can be observed:
- complete restoration of the lung tissue structure - 70%;
- formation of an area of local pneumosclerosis - 20%;
- formation of a site of local carnification – 7%;
- reduction of a segment or share in size – 2%;
- shrinkage of a segment or lobe – 1%.
Prevention of pneumonia
Measures to prevent the development of pneumonia include hardening the body, maintaining immunity, eliminating the factor of hypothermia, sanitizing chronic infectious foci of the nasopharynx, combating dust, stopping smoking and alcohol abuse. In weakened bedridden patients, in order to prevent pneumonia, it is advisable to carry out breathing and therapeutic exercises, massage, and prescribe antiplatelet agents (pentoxifylline, heparin).
The widespread and not always justified use of antibiotics, especially broad-spectrum antibiotics, has led to the selection of resistant strains and the development of antibiotic resistance. Viruses are also capable of causing inflammatory changes in the lungs, affecting the tracheobronchial tree, creating conditions for the penetration of pneumotropic bacterial agents into the respiratory sections of the lungs.
The main route of infection is airborne penetration of pathogens or aspiration of secretions containing microorganisms from the upper respiratory tract.
Less common is the hematogenous spread of pathogens (endocarditis of the tricuspid valve, septic thrombophlebitis of the pelvic veins) and the direct spread of infection from neighboring tissues (liver abscess) or infection from penetrating wounds of the chest.
CLINICAL PICTURE AND CLASSIFICATION.
Depending on the conditions of occurrence, clinical course, state of the patient’s immunological reactivity, the following types are distinguished:
Community-based (home, outpatient)
Hospital (nosocomial, in-hospital)
Aspiration
Against the background of immunodeficiency conditions
This classification is used to justify empirical therapy. Detailing P taking into account risk factors (chronic alcohol intoxication, against the background of COPD, viral infections, malignant and systemic diseases, chronic renal failure, previous antibiotic therapy, etc.), allows us to take into account the entire range of possible pathogens and increases the targeting of the starting
The clinical picture of P is determined both by the characteristics of the pathogen and the condition of the patient and consists of extrapulmonary symptoms and signs of damage to the lungs and bronchi.
Clinical symptoms of pneumonia.
1) Bronchopulmonary: shortness of breath, sputum production, sometimes dullness of percussion sound, weakening of vesicular or bronchial breathing, crepitus, pleural friction noise;
2) Extrapulmonary: hypotension, weakness, tachycardia, sweating, confusion, acute psychosis, meningeal symptoms, decompensation of chronic diseases
In patients with chronic alcohol intoxication or severe concomitant diseases (congestive heart failure, cerebral infarction, etc.) or in the elderly, extrapulmonary symptoms may prevail over bronchopulmonary ones.
When P is localized in the lower parts of the lungs and when the diaphragmatic pleura is involved in the process (with lobar pneumonia - pleuropneumonia), the pain can radiate to the abdominal cavity, simulating the picture of an acute abdomen.
In some cases, pleuropneumonia must be differentiated from pulmonary infarction, which is also characterized by the sudden onset of pain, often hemoptysis, and suffocation. However, at the onset of the disease, the presence of high temperature and intoxication are not pathognomonic. In these patients, it is possible to identify possible sources of thromboembolism (thrombophlebitis of the lower extremities, heart disease, post-infarction cardiosclerosis). When recording an ECG, symptoms of right heart overload are revealed (right bundle branch block, sign S I-Q III. ).
In case of spontaneous acute development of pain syndrome can be combined with increasing respiratory failure (tension spontaneous pneumothorax). Percussion reveals tympanitis, weakening of breathing, sometimes an increase in volume and limitation of respiratory excursions of the corresponding half of the chest.
Complications of P are pleurisy, abscess formation, pyopneumothorax and pleural empyema, adult respiratory distress syndrome, infectious-toxic shock, broncho-obstructive syndrome, vascular insufficiency. In severe cases with severe intoxication, in weakened patients, the development of sepsis, infective endocarditis, myocardial and kidney damage is possible.
Lobar pneumonia obligately associated with pneumococcal infection, is one of the most severe forms of P. It is characterized by: acute onset of the disease with tremendous chills, cough, chest pain when breathing, rusty sputum, distinct percussion and auscultation changes in the lungs, a critical drop in body temperature; the development of hypotension, acute vascular insufficiency, respiratory distress syndrome in adults, infectious-toxic shock is possible.
With staphylococcal infections, which are more common during influenza epidemics, severe intoxication and purulent complications develop.
In the elderly and in people with alcohol dependence, they are often caused by gram-negative flora, in particular Klebsiella pneumoniae. With these Ps, extensive damage to the lung tissue with destruction, purulent complications, and intoxication is observed.
LIST OF QUESTIONS FOR A PATIENT WITH PNEUMONIA.
1) Time of onset of the disease.
2) Presence of risk factors aggravating the course of P
Chronic diseases bad habits etc.
3) Finding out the epidemiological history.
Identifying signs of a possible infectious disease.
4) Duration and nature of the temperature increase.
5) The presence of cough, sputum, its nature, hemoptysis.
6) The presence of pain in the chest, its connection with breathing, coughing
7) Is there shortness of breath, attacks of suffocation?
DIAGNOSTIC CRITERIA FOR PNEUMONIA.
1. The patient’s complaints of cough, sputum production, chest pain, shortness of breath
2. Acute onset of the disease
3. Changes during percussion (dullness of percussion sound) and auscultation (weakening of vesicular breathing, bronchial breathing, crepitus, pleural friction noise) of the lungs, manifestations of broncho-obstruction
4. Increase in temperature
5. Symptoms of intoxication
When examining a patient, it is necessary to measure temperature, respiratory rate, blood pressure, heart rate; palpate the abdomen to identify symptoms of decompensation of concomitant diseases.
If you suspect AMI, PE, in old age, with concomitant atherosclerosis, it is necessary to conduct an ECG study.
Detection of pneumonic infiltration during radiographic examination confirms the diagnosis of P.
Data from laboratory tests (peripheral blood analysis, biochemical studies), determination of blood gas composition are important for assessing the severity of the patient’s condition and choosing therapy.
Cytological examination of sputum makes it possible to clarify the nature of the inflammatory process and its severity.
Bacteriological examination of sputum, bronchial contents, and blood is important for the correction of antibacterial therapy, especially in severe cases of P.
Clinical example. Patient V., 44 years old, called the SS and NMP team due to the sudden onset of chills, an increase in temperature to 38.5, sharp pain in the right side, aggravated by breathing and movement. History of alcohol abuse.
He was hospitalized with a diagnosis of acute cholecystitis. During examination in the emergency department, surgical pathology was excluded, but dullness of percussion sound on the right in the lower parts of the lungs was revealed, as well as increased breathing and bronchophony there. The emergency department doctor suspected pneumonia. X-ray examination confirmed the diagnosis of lower lobe prolateral pleuropneumonia. Thus, in this case, in a patient with right-sided pleuropneumonia, pleural pain radiated to right hypochondrium and imitated the picture.
For a doctor of SUI, the division of P according to severity is of great importance, which makes it possible to identify patients who require hospitalization and intensive care at the prehospital stage. The main clinical criteria for the severity of the disease are the degree of respiratory failure, the severity of intoxication, the presence of complications, and decompensation of concomitant diseases.
Criteria for severe pneumonia (Niederman et al., 1993).
1. Respiratory rate > 30 per minute.
2. Temperature above 38.5 C
3. Extrapulmonary foci of infection
4. Impaired consciousness
5. The need for artificial ventilation of the lungs
6. State of shock (SBP less than 90 mmHg or DBP less than 60 mmHg)
7. The need to use vasopressors for more than 4 hours.
8. Diuresis< 20 мл/ч или проявления острой почечной недостаточности.
Patients with risk factors for complications and fatal outcome, are also subject to hospitalization.
Risk factors that increase the likelihood of complications and mortality from pneumonia (Niederman et al., 1993).
1. Chronic obstructive pulmonary diseases
2. Diabetes mellitus
3. Chronic renal failure
4. Left ventricular heart failure
5. Chronic liver failure
6. Hospitalizations during the previous year.
7. Swallowing problems
8. Violation of higher nervous functions
9. Splenectomy
10.Alcoholism
11. Nutritional depletion
12.Age over 65 years
Patients with P of moderate and severe course, with a complicated course, in the presence of risk factors, are subject to hospitalization. A number of patients at the prehospital stage may develop symptoms that require correction by a doctor of SUI.
ALGORITHM OF DOCTOR'S TACTICS SYNMP IN PNEUMONIA
Arterial hypotension in patients with lobar P (pleuropneumonia) occurs due to a generalized decrease in the tone of the smooth muscles of the walls of arterioles and small arteries and a decrease in total peripheral resistance. According to some authors, the reason for this is the immediate response of the vascular wall during an anaphylactic reaction of a sensitized organism to the breakdown products of pneumococcus, which in this case act not as toxins, but as antigens.. Patients with lobar P should be hospitalized in therapeutic departments in a lying position. Before hospitalization, you should not start antibacterial therapy or prescribe antipyretic or analgesic drugs, as this can lead to a drop in blood pressure, which is especially dangerous when transporting the patient.
To ensure maintenance of SBP at 100 mmHg. fluids are administered (iv drip isotonic solutions of sodium chloride, dextrose, dextran 40 in a total volume of 500 - 1000 ml).
Acute respiratory failure - respiratory distress syndrome adults (ADSV). ARDS often develops in sepsis, bacterial shock, and in patients with immunodeficiency (chronic alcohol intoxication, neutropenia, drug addiction, HIV infection). In response to infection, a local inflammatory reaction develops, leading to vasodilation, increased permeability of the vascular wall, release of a number of cellular components (lysosomal enzymes, vasoactive amines, prostaglandins), and the complement system is activated, attracting neutrophils into the pulmonary microcirculation. Granulocytes and mononuclear cells accumulate at the site of injury and form a conglomerate with local fibroblasts and endothelial cells. Adhesion of neutrophils to the endothelium stimulates the release of toxic substances that damage it. As a result of damage to the endothelium of the pulmonary capillaries, pulmonary edema develops, clinically manifested by severe shortness of breath and severe hypoxemia, resistant to oxygen therapy, which causes an increased need for oxygen. Patients require mechanical ventilation. Diuretics are ineffective for pulmonary edema in patients with ARDS. IV administration of furosemide can improve gas exchange without reducing the degree of pulmonary edema, which may be explained by the redistribution of pulmonary blood flow (increasing it in well-ventilated areas of the lungs).
The main goal of therapy in the treatment of respiratory failure is to maintain tissue oxygenation. In ARDS, oxygen consumption in the periphery is directly proportional to its delivery. For arterial hypotension and decreased cardiac output, intravenous infusion of dobutamine is indicated at a dose of 5 - 10 mcg/kg min.
Peripheral vasodilators worsen pulmonary hypoxemia by increasing intrapulmonary shunting. Arterial hemoglobin oxygen saturation is maintained above 90%, which is sufficient to maintain oxygen delivery to peripheral tissues. Currently, it is considered unproven that the use of glucocorticosteroids in high doses reduces the inflammatory process in the lungs. In the same time high doses glucocorticosteroids increase the risk of developing secondary infection.
Infectious - toxic shock can complicate the course of lobar (pleuropneumonia), staphylococcal P., occurs in P. caused by gram-negative flora and in patients with risk factors. Treatment at the prehospital stage consists of infusion therapy and dobutamine administration. For more details, see the corresponding section.
Broncho-obstructive syndrome - see the corresponding section.
Pleural pain sometimes they are so severe that they require the administration of analgesics. The most rational use of drugs from the NSAID group (paracetamol 0.5 g per os, ibuprofen - 0.2 g per os ; aspirin 0.5 - 1.0 g. per os or parenterally in the form of lysine monoacetylsalicylate 2.0 g; diclofenac - 0.075 g per os or parenterally intramuscularly deep into the gluteal muscle 0.075 g). Analgin, which is still widely used as an analgesic, much more often causes serious undesirable effects (acute anaphylaxis, inhibition of hematopoiesis) and therefore cannot be recommended for use.
In patients with lobar P (pleuropneumonia), the administration of analgesics can provoke hypotension and it is better to refrain from their use at the prehospital stage.
PARACETAMOL. The maximum concentration in the blood is reached 0.5-2 hours after administration, the duration of action is 3-4 hours.
Indications for use are mild to moderate pain, temperature above 38 C.
For liver and kidney diseases, chronic alcohol intoxication, the drug should be used with caution.
Contraindications include a history of hypersensitivity reactions to the drug.
Undesirable effects (rarely develop): cytopenia, liver damage (less commonly, kidney damage) in case of overdose, especially when drinking alcohol. With prolonged use, the development of acute pancreatitis is possible.
When used in combination with prokinetics and long-term joint use with indirect anticoagulants, it is possible to enhance the effect of prokinetics and anticoagulants.
Doses: adults are prescribed 0.5-1.0 g orally every 4 to 6 hours, the maximum daily dose is 4 g.
ASPIRIN (). The maximum concentration in the blood is achieved 2 hours after administration. Duration of action 4 hours.
Indications: mild to moderate pain, temperature above 38 C
In case of asthma, a history of allergic reactions, liver and kidney diseases, dehydration, during pregnancy and in elderly patients, the drug should be used with caution.
In children under 12 years of age, nursing mothers, with peptic ulcers, hemophilia, hypersensitivity to aspirin and other NSAIDs, severe renal and liver failure, and in the 3rd trimester of pregnancy, the use of aspirin is contraindicated.
Undesirable effects include gastrointestinal dyspepsia, bronchospasm, and skin reactions. With long-term use, ulcerogenic effects, increased bleeding time, thrombocytopenia, and hypersensitivity reactions are possible.
When combined with other NSAIDs and glucocorticosteroids, the risk of developing undesirable effects increases; with anticoagulants, the risk of bleeding increases. Combined use with cytostatics and antiepileptic drugs increases the toxicity of these drugs.
Doses: adults - 0.25 - 1.0 g every 4 - 6 hours, maximum dose 4 g / day.
Lysine monoacetylsalicylate is an aspirin derivative for parenteral administration. Surpasses it in the speed of development and strength of the analgesic effect. Single dose 2 g, maximum - up to 10 g per day. Adverse reactions - similar to action aspirin.
The maximum concentration in the blood develops 1-2 hours after oral administration, analgesic and antipyretic effects last up to 8 hours. prescribed for mild to moderate pain, temperature above 38 C
Contraindications are hypersensitivity to NSAIDs, severe renal and liver failure, and the third trimester of pregnancy.
Undesirable effects: gastrointestinal dyspepsia, hypersensitivity reactions, bronchospasm; cytopenias, autoimmune syndromes, with a course of treatment, ulcerogenic effects, worsening renal and liver failure, headache, dizziness, hearing loss, orientation, photosensitivity, rarely papillary necrosis, aseptic meningitis.
Combined use with other NSAIDs and glucocorticosteroids increases the risk of developing undesirable effects. When combined with fluoroquinolones, it is possible to develop a convulsive syndrome. When combined with diuretics, ACE inhibitors, beta blockers, there is a decrease in the therapeutic effect of these drugs and an increase in the risk of side effects. When combined with cytostatics, antiepileptic drugs, lithium drugs, their effects increase; when combined with anticoagulants, the risk of hemorrhagic complications increases; when combined with cardiac glycosides, NSAIDs can increase their plasma concentration.
DICLOFENAC. The maximum concentration in the blood develops after 0.5 - 2 hours. after oral administration and after 10 - 30 minutes. after intramuscular injection.
Indications - see above
Contraindications: see above, as well as exacerbation of chronic intestinal diseases, porphyria.
Interactions: typical for drugs of the NSAID group (see above).
Doses: 75 - 150 mg / day in two - three doses orally, 75 mg intramuscularly deep into the gluteal muscle.
Timely initiation of antibiotic therapy has a decisive influence on the course of P and its outcome. When a patient is admitted to a hospital, the choice of antibiotic is made taking into account the above clinical features.
ANTIBIOTIC THERAPY FOR PNEUMONIA.
|
Clinical situation |
Most common pathogens |
First line antibiotics |
|
P non-severe course in patients under 60 years of age with a clear medical history |
S. pneumoniae M. pneumoniae, H. influenzae |
Aminopenicillins, macrolides |
|
P in patients 60 years of age and older and/or with concomitant pathology |
S. pneumoniae H. influenzae Enterobacteriaceae |
Amoxicillin - Clavulanate (+ aminoglycosides), II generation cephalosporins (+ aminoglycosides) |
|
P severe course |
S. pneumoniae Enterobacteriaceae Staphylococcus aureus, Spp. |
(+aminoglycosides, oxacillin), Macrolides fluoroquinolones |
|
P in immunocompromised patients |
Enterobacteriaceae Pseudomonas spp., S. pneumoniae Staphylococcus aureus, mushrooms |
Fluoroquinolones (+ aminoglycosides, vancomycin), antipseudomonas cephalosporins III generation (antipseudomonas penicillins) + aminoglycosides, vancomycin, amphotericin, diflucan |
|
Aspiration P |
S. pneumoniae Staphylococcus, Enterobacteriaceae anaerobes |
III generation cephalosporins (+aminoglycoside), amoxicillin - clavulanate + aminoglycoside, fluoroquinolones, metronidazole |
Most foreign pulmonology schools characterize pneumonia as “an acute respiratory disease with focal signs and radiographically established darkening, which was previously absent, and there are no other known reasons for its appearance." In domestic practical pulmonology, it is allowed to make a diagnosis of "pneumonia" without characteristic radiological changes ("X-ray negative pneumonia") based on obvious clinical manifestations of the disease.
The incidence of acute pneumonia remains high: in the group of nonspecific lung diseases it accounts for 29.3% of cases, and in the structure of general morbidity it averages 0.33%.
ETIOLOGY AND PATHOGENESIS
The classification provides for the division of pneumonia.
By etiology (by factor of occurrence):
bacterial (indicating the pathogen);
viral;
mycoplasma and rickettsial;
allergic;
caused by physical and chemical factors;
mixed;
unspecified etiology.
By pathogenesis (by development mechanism):
primary;
secondary.
According to morphological characteristics:
lobar (lobar, fibrinous);
focal (lobular, bronchopneumonia).
With the flow:
acute;
protracted.
Clinically significant is the division of pneumonia into community-acquired and nosocomial (hospital-acquired, nosocomial). This division of pneumonia has nothing to do with the severity of their course. The main and only criterion for differentiation is the environment in which pneumonia developed.
To date, a large number of pathogens of pneumonia are known: bacteria, viruses, rickettsia, fungi, mycoplasma, legionella, chlamydia, protozoa.
Pneumococcus remains the most common causative agent of community-acquired pneumonia. Mycoplasmas and chlamydia often occur in young and middle-aged people (up to 20-30%), and their role in the occurrence of the disease in older patients age groups less significant (1-3%).
Legionella is a rare causative agent of community-acquired pneumonia, but Legionella pneumonia ranks second (after pneumococcal) in terms of mortality. Haemophilus influenzae more often causes pneumonia in smokers, as well as against the background of chronic bronchitis. Escherichia coli and Klebsiella pneumoniae (less commonly other members of the Enterobacteriaceae family) are found, as a rule, in patients with risk factors (diabetes mellitus, congestive heart failure, etc.). The likelihood of staphylococcal pneumonia (Staphylococcus aureus) increases in older people or in people who have had the flu.
Nosocomial (nosocomial) pneumonia is pneumonia that develops in a patient no earlier than 48 hours after hospitalization and was not in the incubation period.
The occurrence of nosocomial pneumonia is dominated by gram-negative microflora of the Enterobacteriaceae family - Pseudomonas aerogynosis (Pseudomonas aeruginosa).
There is a special type of nosocomial pneumonia - ventilator-associated pneumonia (VAP), associated with the length of time the patient remains on mechanical ventilation.
With the so-called early VAP (development in the first 4 days of being on mechanical ventilation), the most likely pathogens are streptococcus, Haemophilus influenzae and Staphylococcus aureus and other representatives normal microflora oral cavity. The development of late VAP (more than 4 days on mechanical ventilation) is associated with Pseudomonas aeruginosa, Acinetobacter, and representatives of the Enterobacteriaceae family.
Mycoplasma and viral pneumonia are characterized predominantly by interstitial changes, when edema and infiltrative-proliferative changes are noted in the interalveolar and interlobular septa, peribronchial and perivascular tissue. These changes can hardly be attributed to the concept of “pneumonia”, since they are not a process in the respiratory part of the lungs.
Predisposing factors to the development of pneumonia are acute and chronic diseases of the respiratory system, heart (congestive heart failure), kidneys, gastrointestinal tract; various types of immune imbalance, hypothermia, stress, smoking, alcoholism, drug addiction, chest injuries. In addition to the above, risk factors for the development of pneumonia include age (children, elderly people), contact with birds, rodents, and other animals; professional factors (frequent train travel, hotel stays, etc.).
The age factor plays a special role due to the high mortality rate of pneumonia (about 10% for pneumococcal and 70% for pneumonia caused by gram-negative flora) in older people. Concomitant diseases that occur in most patients over 60 years of age (for example, chronic bronchitis, coronary heart disease, hypertension, diabetes mellitus) affect the severity of pneumonia and the possibility of pharmacological correction. The most aggressive risk factor is long-term smoking, accompanied by the formation of mucociliary insufficiency and colonization of pathogenic microflora in the airways.
According to the mechanism of development, primary (bronchogenic) and secondary (metastatic) pneumonia are distinguished. With bronchogenic spread of infection, the process in the lungs is predominantly unilateral in nature with polysegmental lung damage, rapid fusion of foci of infiltration, and frequent pleural complications (pneumothorax, pyopneumothorax). The process is, as a rule, unilateral in nature, localized around the bronchi and clearly associated with them (panbronchitis with extensive damage to the bronchi, leukocyte infiltration and destruction of the walls).
The development of pneumonia is directly dependent on the state of the macroorganism (primarily its immunological reactivity) and the aggressive properties of the microbial pathogen.
From these positions, lobar pneumonia is considered as a result of a hyperergic reaction, and focal pneumonia is considered as a manifestation of normo- or hyperergic reactions of the macroorganism to an infectious agent. There is another point of view, according to which lobar pneumonia is caused by more pathogenic strains of pneumococci.
Microorganisms can enter the lungs in various ways: bronchogenic (through the bronchi), hematogenous and lymphogenous (from the blood and lymph). Hematogenous entry occurs with sepsis and general infectious diseases, and lymphogenous entry occurs with chest injuries. But the main route of infection is bronchogenic (inhalation and aspiration). Naturally, the condition of the respiratory tract is of great importance. Violation of them leads to obstruction of the bronchial tree and contributes to the development of an infectious process in the respiratory sections. A decrease in the activity of protective factors of the respiratory system is facilitated by smoking and inhalation of toxic or irritating substances, circulatory disorders in cardiovascular diseases, chronic debilitating diseases (alcoholism, diabetes mellitus, etc.). Factors predisposing to the development of acute pneumonia may be hypothermia, physical and mental stress.
With lobar pneumonia, the pathogens enter directly into the alveoli, exerting a sharp toxic effect on them. As a result of local irritation, serous inflammatory edema develops with increased proliferation of microorganisms located along the periphery of the edema. The process spreads by spreading edematous fluid from the affected alveoli into the adjacent interalveolar pores of Kohn. Characteristic is the rapid formation of effusion, the high content of fibrin in it, which significantly complicates phagocytosis (absorption and digestion) by neutrophils and ensures massive damage to the lung tissue (at least a segment, often an entire lobe of the lung). Lobar pneumonia is characterized by minor damage to the bronchi, which remain patent.
With focal pneumonia in the area of inflammation under the influence of a microbial exotoxin, fast education the focus of necrosis and limiting the area of inflammation from the surrounding tissue. In most cases, the initial inflammatory process develops in the bronchi. The lesions are small in size, occupying an acinus or lobule, but sometimes merge to form larger lesions and can occupy an entire lobe.
Acute pneumonia is often an independent disease - primary pneumonia, but even more often as a complication of other pathological processes (diseases of the cardiovascular system, tumors, infectious diseases, injuries, bronchopulmonary diseases, chronic bronchitis, bronchial asthma, etc.) - secondary pneumonia.
Pneumonia is considered protracted if the normalization of clinical and indicators is delayed for more than 4 weeks. The reasons for the protracted course of pneumonia are different. The most common of them:
untimely initiation and (or) inadequate treatment, which may be due to the patient’s late presentation for medical care, incorrect diagnosis, drug intolerance, early cessation of antibacterial therapy, insufficient use of the entire arsenal of therapeutic measures (including non-drug treatment methods);
the presence of chronic respiratory diseases (especially obstructive);
chronic diseases of other organs and systems;
various chronic intoxication(including production ones).
CLINICAL PICTURE
Acute pneumonia
The clinical picture of acute pneumonia consists of common symptoms, independent of the causal structure of the disease, and clinical manifestations determined by the nature of the pathogen.
General clinical manifestations are expressed by a number of syndromes:
intoxication: weakness, increased fatigue, headaches and muscle pain, loss of appetite, etc.;
inflammatory changes: fever with a feeling of heat or chills, cough with sputum, signs of infiltrative changes in the lungs (percussion (by tapping), auscultation (by listening), radiological, laboratory);
involvement of other organs and systems (cardiovascular, nervous, kidney, etc.).
The main clinical manifestations of pneumonia are cough with sputum, chest pain, shortness of breath and fever; in elderly patients, disorders of consciousness and delirium are possible. Percussion (tapping) of the lungs reveals local pain and shortening of the sound. Listening allows you to listen for crepitus, dry and moist rales, as well as changes in the nature of breathing (weakened, vesicular, bronchial). X-ray examination determines infiltrative changes in the lung tissue.
Clinical options Acute pneumonia is largely determined by the type of pathogen.
Lobar pneumonia
Lobar pneumonia is the “classic form” of acute pneumonia. It is characterized by damage to a lobe or even whole lung with mandatory involvement of the pleura in the process (pleuropneumonia). It is caused by pneumococci types I, II, III, and much less frequently by Friedlander's bacillus, a capsular form of Escherichia coli.
The disease begins acutely (the patient can indicate the hour of onset of the disease) with tremendous chills and an increase in temperature to 39-40°C. Almost simultaneously with this, chest pain appears, associated with breathing, and then with coughing. The cough develops later (during the day), at first it is dry or with difficult to separate viscous sputum; in some patients (1 out of 5-7 patients) the sputum may take on a “rusty” character. The duration of separation of such sputum usually does not exceed 4-6 days.
On examination, the condition is serious, shortness of breath at rest, feverish flush of the cheeks, more pronounced on the affected side, cyanosis of the nasolabial triangle, herpetic rashes on the lips and wings of the nose. There is a lag in breathing on the affected side; sometimes patients take a forced position on the affected side with the head end raised. The lag in breathing on the affected side is associated with the involvement of the pleura in the process.
Already from the first day of the disease, during percussion there is a shortening of the percussion sound over the affected area (in the first hours there may be, on the contrary, tympanitis), which later turns into a dull sound.
The tympanic tone of the sound is caused by a decrease in the elasticity of the lung tissue, a decrease in the tone of the alveoli, and swelling of the interalveolar spaces. When the alveoli are filled with exudate and the lung tissue thickens, the percussion sound becomes dull, and vocal tremors increase.
The auscultatory picture in the lungs also depends on the nature of the morphological changes in the lungs: in the stage of hot flashes, a weakening of breathing is first noted and initial crepitus can be heard, with a pleural reaction - pleural friction noise. In the stage of hepatization (thickening of the lungs due to pronounced exudation into the alveoli), bronchial breathing and ringing moist rales of various sizes are heard. As the process resolves and the exudate resolves, secondary crepitus appears, breathing becomes harsh, weakened, and then vesicular.
The X-ray picture of lobar pneumonia is characterized by a homogeneous darkening of the lung tissue with a clear contour limited to a lobe or segment; there is an expansion of the shadow of the lung root on the affected side. The resolution process takes 2-3 weeks.
Febrile fever with lobar pneumonia occurs from the first hours of the disease and is often ongoing; The duration of the febrile period is on average 3-6 days.
Lobar pneumonia most often occurs in the right lung; damage to both lungs is relatively rare.
For the modern course of lobar pneumonia, a lobar process is uncharacteristic; 1-3 segments are most often affected, along with high temperature Cases with slightly elevated temperature are not uncommon.
Focal pneumonia
The disease is often preceded by an acute viral infection of the upper respiratory tract. The inflammatory process in most cases begins in the bronchi with subsequent transition to the alveolar tissue. Therefore, early symptoms of focal pneumonia are fever, sometimes with chills, and cough. The cough may be dry at first, and after 1-2 days with mucopurulent sputum. The onset of the disease is acute, but more often gradual, with the appearance of catarrhal changes in the upper respiratory tract, cough, weakness, shortness of breath, then mild pain in the chest.
Fever with focal pneumonia is usually of the wrong type, lasting from 3-5 to 10 days or more. The decrease in temperature is usually gradual, often with a long period of low-grade fever in the evenings.
Objective signs depend on the distribution and depth of inflammatory changes in the lungs. Most patients experience a shortening of the percussion sound over the affected area, increased vocal tremors or bronchophony.
Some authors consider shortening of the percussion sound over the root of the lung on the affected side to be an early symptom of focal pneumonia, which is associated with inflammatory infiltration of the root.
During auscultation, harsh breathing is heard, sometimes weakening of breathing, moist small and medium-bubble rales in a limited area, often in combination with dry rales. Only dry wheezing can indicate pneumonia if it is heard in a limited area.
The X-ray picture of focal pneumonia is distinguished by the diversity of changes in the lungs - areas of infiltration alternate with areas of unchanged lung tissue or areas of compensatory swelling of the lung tissue. There may be single, often large, foci, as well as small multiple or confluent foci of infiltration. In the infiltration zones there is a change in the interstitial peribronchial and perivascular tissue in the form of stringy and cellular changes with fuzzy outlines. The roots of the lungs are expanded, infiltrated with a slight increase in lymph nodes.
Focal pneumonia develops more often in the lower lobes, more on the right, with predominant damage to the basal segments. Often there is a bilateral localization of the process. The clinical manifestations of focal pneumonia are largely determined by the type of pathogen.
Pneumococcal pneumonia is characterized by an acute onset with high temperature (39-40°C), severe intoxication, a significant increase in neutrophilic leukocytosis in the blood, and a severe course. Drugs penicillin series within 1-2 days in most patients they cause a decrease in temperature and intoxication.
Klebsiella pneumoniae is caused by gram-negative capsular bacteria. The disease often develops in weakened patients, alcoholics and the elderly. Along the way, it can be acute and protracted (“creeping” - with a slow development of the process). Typical acute pneumonia begins with chills, but the temperature rarely reaches 39°C, severe general weakness, severe shortness of breath, and adynamia are noted. The cough is persistent, painful, with difficult to clear, very viscous, often bloody (or contains streaks of blood) sputum, often with the smell of burnt meat. There is almost always pleural pain, fibrinous or exudative pleurisy. Sputum contains a large number of capsule sticks. The process is often localized in the upper lobe or is polylobar in nature. Inflammatory infiltrates merge and quickly form a vast lesion with a picture of hepatization, as in lobar pneumonia.
Radiologically, the shadow of the affected lobe is sharply marked, its volume is increased; already on the first day of illness, decay and melting of lung tissue with the formation of cavities or thin-walled cysts is possible. The formation of an acute abscess often ends in the first 3-4 days of illness.
Tapping often reveals dullness consistent with a lobar lesion. When listening, bronchial breathing and a small amount of wheezing are detected, since the bronchi and alveoli are filled with viscous mucus.
A decrease in blood pressure, hemorrhages on the skin and mucous membranes are possible, digestive disorders and scleral icterus often occur. When examining blood, leukopenia with monocytosis and a shift of the leukocyte formula to the left is more often observed; Leukocytosis appears in most cases with purulent complications. Even with proper treatment, the course of Klebsiella pneumonia differs in duration and frequency of complications.
Staphylococcal pneumonia. The disease is characterized by a high tendency of the pneumonic focus to abscess formation and the formation of cavities. The mortality rate for staphylococcal pneumonia in adults reaches 37%. Most often, staphylococcal pneumonia occurs against or after influenza.
Metastatic (secondary) staphylococcal pneumonia develops with hematogenous introduction (through the bloodstream) of infection from a purulent focus (abscess, endometritis, etc.). At the beginning of the disease, subpleurally located multiple infiltrates are detected in the lungs, which subsequently disintegrate with the formation of cavities and bullae of varying sizes, but there is not a large amount of sputum. The defeat is usually bilateral.
Clinical and radiologically, the following forms of staphylococcal pneumonia are distinguished: staphylococcal infiltrate of the lung, staphylococcal destruction (destruction) of the lung (pulmonary form - abscess and bullous, and pulmonary-pleural).
Staphylococcal pneumonia is characterized by an acute onset with high fever, often with chills, cough (dry or with mucopurulent sputum), and chest pain. Sometimes a typhoid-like onset is observed with high fever (up to 41°C), severe symptoms of intoxication, meningeal symptoms, and confusion. The severity of staphylococcal pneumonia does not always correspond to the size of the lung lesion.
In the infiltrative form, the process is localized in one, or less often two, segments; X-rays reveal focal infiltrative changes in the lungs, sometimes of a confluent nature.
The pulmonary abscess form of staphylococcal destruction is characterized by the formation of single or multiple abscesses in the lung. The disease is severe, with severe intoxication, respiratory failure, hectic fever, and purulent sputum production up to 200-300 ml per day. There is a very high number of leukocytes in the blood, a sharp increase in ESR. X-rays reveal multiple cavities against the background of infiltration, often with fluid levels.
These are, as a rule, thin-walled cavities with rapidly changing shape and size - bullae. The formation of bullae is explained by the absorption of air into the alveoli during inflammation of the terminal bronchioles and its retention on exhalation due to the formation of the valve mechanism. Restoring the patency of the bronchioles leads to the collapse of the bullae, and prolonged disruption of patency can lead to the development of inflammation with true abscess formation.
Isolation of the pulmonary-pleural form is associated with the presence of pleural complications in almost every third patient with staphylococcal pneumonia.
The course of staphylococcal pneumonia is different - lightning fast, acute and protracted. Fulminant forms manifest themselves as infectious-toxic (septic) shock with rapidly increasing intoxication, cardiovascular and respiratory failure. Death occurs within 3-5 days. Most patients have an acute course, lasting up to 2 months. The protracted course is characterized by sluggish dynamics for 2-4 months, but with proper treatment it ends with recovery. The chronic course of staphylococcal pneumonia ends with the formation of a chronic abscess or pleural empyema. This outcome occurs especially often when inflammation is localized in the lower lobe and when the drainage function of the bronchi is impaired, which is especially typical for chronic obstructive bronchitis.
Streptococcal pneumonia also occurs mainly during epidemic outbreaks of respiratory diseases and can develop as a complication of chronic nonspecific lung diseases. The disease usually begins acutely with chills, sometimes a series of chills, fever, cough, initially dry, then with sputum; the sputum may be streaked with blood. Shortness of breath, symptoms of intoxication, and cyanosis are noted. In 50-70% of cases, pleurisy occurs and pleural empyema often develops. With streptococcal infection, necrosis of the lung tissue develops early in the lesions, so purulent sputum appears early, and a lung abscess can form. X-rays reveal multiple inflammatory foci of medium and large sizes, most often in both lungs, prone to fusion and disintegration with the formation of thin-walled cavities (as with staphylococcal destruction). In the blood - hyperleukocytosis, shift to the left to myelocytes.
Colipneumonia is caused by a gram-negative bacilli from the group of enterobacteriaceae. The disease develops in patients with diabetes, alcoholics, cancer, circulatory disorders, renal failure, and in patients weakened by other infectious diseases. Pneumonia often begins gradually and is localized mainly in the lower lobes. Sometimes the disease develops acutely, even lightning fast, and its first symptom may be collapse. Radiographs reveal confluent foci of infiltration, and sometimes abscess cavities.
The cause of the disease may be special capsule forms that have more high ability to infection. The clinical picture and course of acute pneumonia resembles the classic forms of lobar pneumonia caused by pneumococci, but more often both lungs are affected.
Viral pneumonia as an independent disease is rare and can be detected only in the first 1-3 days of illness; in later periods, inflammation of the lung tissue is associated with the addition of a bacterial infection and should be considered as viral-bacterial. For independent viral infection The respiratory apparatus is characterized by interstitial changes, viral-bacterial pneumonia occurs in the form of a focal inflammatory process.
The clinical symptoms of viral-bacterial pneumonia consist of the picture of viral infection and manifestations of bacterial pneumonia.
Influenza pneumonia is characterized by a predominance of signs of toxicosis: high fever, severe headache, pain in the eyeballs, aches throughout the body, general weakness, weakness, dizziness, nausea, vomiting, impaired consciousness and even delirium. From the 1st day of illness there are signs of damage to the upper respiratory tract: nasal congestion, runny nose, dry paroxysmal, sometimes painful cough, chest pain. Lung damage is often hemorrhagic in nature, which is associated with the toxic effect of a viral infection on the vessels of the lung.
The addition of a bacterial infection causes a deterioration in the patient’s condition: the appearance of a second wave of fever is very typical, clear clinical signs of pneumonia appear, tachypnea (rapid breathing) develops, signs of bronchial obstruction, and respiratory failure increases.
How a special form of influenza pneumonia is distinguished hemorrhagic pneumonia, ending in the death of patients on days 2-3 of illness. From the first day of illness, serous-hemorrhagic sputum appears, a high temperature is noted, shortness of breath and cyanosis quickly increase. The shortness of breath in most patients does not correspond to the size of the lung damage. This is associated with widespread bronchitis (even bronchiolitis) and severe impairments in the diffusion capacity of the alveolar-capillary membrane as a result of its hemorrhagic edema. X-ray examination reveals focal, segmental or lobar uneven infiltration of the lung tissue against the background of strengthening, deformation, and reticulation of the pulmonary pattern.
Parainfluenza pneumonia initially occurs as an acute respiratory disease. Parainfluenza is characterized by minor intoxication and elevated temperature. With the addition of pneumonia, the temperature rises to 38-39°C, and manifestations of intoxication increase. With parainfluenza, the involvement of the larynx in the process is very typical; Laryngitis may be the leading symptom of upper respiratory tract damage. Respiratory syncytial virus infection in adults is often complicated by pneumonia. With the addition of pneumonia there are obvious signs bronchitis with impaired bronchial obstruction, the temperature rises to febrile, and the symptoms of intoxication increase.
Adenovirus infection is characterized by a picture of nasopharyngitis, conjunctivitis, generalized lymphadenopathy is often observed, and there may be a finely spotted rubella-like rash. The temperature is usually elevated, intoxication is moderate. The addition of pneumonia is accompanied by an increase in temperature and increased symptoms of intoxication.
Ornithosis pneumonia is characterized by an acute onset, high fever (39-40°C), severe symptoms of intoxication, and absence of damage to the upper respiratory tract. Signs of lung damage appear on the 2-5th day from the onset of the disease. Typically there is a discrepancy between high fever, clear toxicosis and mild changes in the lungs. By the end of the first week, in most patients the liver and spleen are enlarged. During the recovery period, relapses of the disease are possible (after 7-12 days of normal temperature), and later myocarditis. The disease occurs with leukopenia and a significant increase in ESR. To diagnose the disease, identifying contact with birds is important. X-ray examination reveals interstitial changes, expansion of the roots of the lungs, small foci (2-3 mm) and cloud-like foci of infiltration in the middle and lower pulmonary fields.
Mycoplasma pneumonia is caused by a special pathogen that has the properties of bacteria and viruses, and is often referred to as primary atypical pneumonia. It is characterized by headaches, muscle pain, weakness, repeated chills at elevated temperatures, and moderate symptoms of nasopharyngitis. X-ray examination reveals interstitial changes and heterogeneous inhomogeneous infiltrates in the lungs without clear boundaries.
Today, “atypical pneumonia” includes diseases caused by intracellular microorganisms (mycoplasma, legionella, chlamydia, rickettsia). These pathogens are not detected by routine bacteriological examination of sputum and are insensitive to antibiotics widely used for empirical treatment of pneumonia: penicillins, cephalosporins and aminoglycosides. Atypical pneumonia without any specific symptoms, should be assumed if therapy with penicillins, cephalosporins and (or) aminoglycosides is ineffective within 2-3 days from the start of treatment (fever persists, the patient’s condition worsens). The likelihood of such a pathology increases sharply among people who have arrived from trips abroad to hot countries, who have been in contact with animals, birds, or who have communicated with patients with SARS. Definition atypical pathogens is possible only in specialized laboratories that carry out serotyping, and only at relatively late stages of the disease, which is valuable, first of all, from an epidemiological point of view. The constantly increasing frequency of atypical variants of the course requires a detailed study of the supporting diagnostic signs of pneumonia depending on the cause of occurrence. Thus, epidemiological data indicate the prevalence of mycoplasma pneumonia in childhood, adolescence, and young adulthood. Epidemic outbreaks are recorded in “closed” communities and are seasonal (autumn-winter).
Atypical pneumonia may debut with damage to the upper respiratory tract (pharyngitis, tracheitis), often accompanied by conjunctivitis, lymphadenopathy. Occasionally, a skin rash of a papular-vesicular nature is detected. There is a tendency towards hypotension; Characterized by sonorous fine-bubbling moist rales, as well as enlargement of the liver and spleen. X-ray examination documents the presence of inhomogeneous infiltration, mainly in the lower lobes of the lungs, the resolution of which occurs very slowly (over a month, even if adequate therapy). An increase in the level of leukocytes is not always detected; more constant acceleration of ESR. Characterized by a dynamic increase in the titer of Cold hemagglutinins, a positive Coombs test, and signs of hemolysis.
The risk of Legionella pneumonia is highest among people engaged in construction, excavation work, working in air-conditioned rooms for long periods of time, or using humidifiers. There are epidemic outbreaks with a sharp rise in body temperature. The onset of the disease is acute, accompanied by shortness of breath, dry cough, pleural pain, cyanosis, transient diarrhea, impaired consciousness, pain in muscles and joints. During the examination, bradycardia (decreased heart rate), moist rales, and pleural friction noise are recorded; evidence of toxic kidney damage is the appearance of protein and a small number of blood cells in the urine. Lobar infiltration on a radiograph persists for a long time after the elimination of clinical signs of inflammation. The hemogram is characterized by relative or absolute lymphopenia against the background of moderate leukocytosis with a shift to the left, a significant acceleration of ESR - up to 50 mm/hour. Frequent complications of Legionella pneumonia are destruction of the parenchyma, parapneumonic exudative pleurisy, and sometimes spontaneous pneumothorax. Chlamydia affects individuals who have had professional or household contact with poultry; epidemic outbreaks are familial in nature or associated with professional activities. The acute onset of the disease and the severity of the intoxication syndrome do not correspond to the modest acoustic findings and the volume of the lesion respiratory system determined by X-ray examination. Bradycardia is characteristic. X-ray is determined by focal or focal-confluent infiltration of the lung tissue. A general blood test reveals leukopenia, band shift, and a sharp acceleration of ESR.
DIAGNOSTICS
Early diagnosis is very important, as it ensures timely initiation of treatment and avoids complications. The basis for correct diagnosis is a well-collected and correctly analyzed anamnesis. Diagnosis is not difficult in the acute onset of the disease, accompanied by fever, signs of intoxication, a corresponding clinical picture: cough, chest pain associated with breathing and coughing, the presence of mucopurulent sputum, distinct radiological changes in the lungs - infiltration of the lung tissue. Tapping reveals varying degrees of shortening of the sound (up to femoral dullness) over the area of inflammation of the lung tissue. When listening, weakening of breathing or, conversely, bronchial breathing (with lobar pneumonia) can be detected; dry and moist, usually sonorous wheezing, and, if the pleura is affected, pleural friction noise can be heard in a limited area. In the same zone, increased vocal tremors, or bronchophony, are detected.
When examining peripheral blood, in most cases an increase in the number of neutrophilic leukocytes is observed. In the leukocyte formula, a shift to the left to young leukocytes and even myelocytes is possible; in severe cases, toxic granularity of the cytoplasm of neutrophils, lymphopenia and eosinopenia are observed. With pneumonia, changes occur in the protein composition of the blood: the content of gamma globulins increases, the content of C-reactive protein and sialic acids increases, especially at the height of the disease (the first 2-4 days of illness).
An important place in the diagnosis of acute pneumonia belongs to the examination of sputum. Bacterioscopy of a sputum smear (Gram-stained) allows in most cases to immediately make an etiological diagnosis. Microscopic examination of sputum determines its nature (mucous, purulent, bloody), the presence of microbial flora and its type (in particular, to identify Mycobacterium tuberculosis using Ziehl-Neelsen staining), atypical cells, elastic fibers and other impurities. Studying the sensitivity of microbial flora to antibiotics makes it possible not only to establish the cause of the disease, but also to select the most effective antimicrobial drug. It should be remembered that the concentration of bacteria 106 microbial bodies in 1 ml of sputum is diagnostically significant, i.e., not only qualitative, but also quantitative bacteriological examination of sputum is necessary.
More difficult questions diagnostics are resolved when clinical symptoms are mild, blurred, or the course of the disease is atypical.
It is necessary to point out that 1/3 of patients have no radiological signs of inflammation of the lung tissue, and diagnosis is based on the history and clinical picture of the disease.
In elderly and old age acute pneumonia occurs 2 times more often than before the age of 40 years. Their pneumonia progresses sluggishly, with mild symptoms. The main manifestations of the disease in old people are increasing and severe weakness, shortness of breath, and sweating. As a rule, there is no fever (or a slight increase in temperature is observed), consciousness is often disturbed (disorientation, sometimes deep prostration), and nausea and vomiting are often observed. In old people, the X-ray picture is poor (usually changes in interstitial tissue, weakly expressed foci of infiltration due to emphysema). The pathological process very often involves the kidneys, protein, casts and a small amount of blood appear in the urine. In old people, there is a slow reverse development of inflammatory changes in the lungs (up to 4-5 weeks). The reasons for this course of the disease are disturbances in the drainage function of the bronchi, the development of atelectasis due to blockage of small bronchi, a decrease in the activity of phagocytosis, a decrease in the synthesis of secretory immunoglobulins, and the frequent presence of circulatory failure and hypovitaminosis in people of older age groups.
It seems appropriate to list the indications for hospitalization for community-acquired pneumonia from the American Thoracic Association:
age over 65 years; - presence of one of the concomitant diseases:
chronic obstructive pulmonary diseases, including bronchiectasis, pulmonary fibrosis;
diabetes;
chronic renal failure;
chronic heart failure;
chronic liver diseases of various origins;
previous hospitalization before the onset of pneumonia with a frequency of at least one per year;
suspicion of penetration of stomach contents into the lungs;
disturbances in mental status;
condition after removal of the spleen;
chronic alcohol consumption.
Some physical factors are important (respiratory rate - more than 30 per minute; systolic blood pressure - less than 90 mm Hg, diastolic - less than 60 mm Hg; body temperature more than 38.8 ° C; extrapulmonary pathology - septic arthritis, meningitis, etc.; confusion) and laboratory data (the number of leukocytes is less than 4 g/l, or more than 30 g/l, or neutrophils - less than 1 g/l; hematocrit - less than 30% or hemoglobin - less than 90 g/l; creatinine - more than 1.2 mg/dl or uric acid - more than 20 mg/dl (7 mmol/l); sepsis, metabolic acidosis, thrombocytopenia.
DIFFERENTIAL DIAGNOSIS
Many lung diseases can have symptoms similar to pneumonia. Thus, with the infiltrative-pneumonic form of tuberculosis, there is a great similarity of clinical and radiological symptoms with pneumonia. However, in the first case, patients have fewer complaints, often do not feel sick, and changes in the lungs are an accidental finding by radiologists. Tuberculosis infiltrate has clearer contours, round or oval shape; Often a symptom of a “path” going to the root of the lung is visible, the presence of dense calcifications. Tuberculous changes are localized primarily in the second or sixth segments, and pneumonia is determined in the basal segments and in the root zone.
Pneumonia is often diagnosed in patients with lung cancer, especially since so-called paracancrosis pneumonia very often develops, the symptoms of which decrease and sometimes disappear under the influence of antibacterial therapy. You should always remember the possibility lung cancer in persons over 50 years of age, especially in long-term smokers, with prolonged pneumonia, and also with hemoptysis.
It should be borne in mind that under the mask of acute pneumonia, exacerbations of a number of chronic bronchopulmonary processes may be hidden: bronchiectasis, chronic abscess, lung cysts.
Under the guise of acute pneumonia, diseases can occur that cause compression of the bronchi by enlarged lymph nodes, followed by atelectasis and the development of pneumonia. This may be due to lymphogranulomatosis, tuberculosis of the lymph nodes. In such a situation, tomographic examination and lymph node biopsy are highly informative.
COMPLICATIONS
Complications of acute pneumonia may be associated with the respiratory system or manifest as disorders of other organs and systems.
Acute respiratory failure is an acute respiratory disorder with insufficient oxygen supply to tissues and, as a rule, with impaired removal of carbon dioxide. In the mechanisms of development of acute respiratory failure, the reduction of the respiratory surface of the lungs is of utmost importance, especially if it is combined with the preservation of blood flow through non-ventilated areas of the lung. Factors contributing to the development of respiratory failure may be impaired bronchial obstruction (especially with bronchopneumonia) and slower alveolar-capillary diffusion (as a result of damage to the interstitial interalveolar tissue). Respiratory failure manifests itself with severe shortness of breath and cyanosis. Acute respiratory failure requires urgent measures, including restoration of bronchial patency, oxygen therapy, and normalization of blood gas composition.
A pleural reaction often occurs in acute pneumonia, especially with a subpleural location of the inflammatory process, and, as a rule, does not require special treatment. Pleural effusion with an increase in the area of dullness of percussion sound and weakening of breathing, increasing restrictive respiratory failure requires pleural puncture. Pleurisy that develops in the later stages of pneumonia (metapneumonic pleurisy) often leads to the formation of pleural empyema.
Infectious-toxic shock is associated with bacterial or viral intoxication: there is a violation of vasomotor regulation with paresis of venous vessels, the deposition of blood in them and a sharp decrease in the volume of circulating blood, a progressive disorder of microcirculation and the development of morphological damage to vital organs. A feature of infectious-toxic shock is the early development of DIC syndrome.
Other complications of acute pneumonia may be acute cor pulmonale, acute cardiac and vascular failure, myocarditis, pericarditis, bacterial endocarditis, meningitis, hepatitis, acute psychosis, etc.
TREATMENT
Treatment of acute pneumonia should be early and comprehensive. It is preferable to carry out it in stationary conditions. In any case, bed rest is necessary for the period of high fever and gentle rest for the entire period of rising temperature.
Early initiation of treatment prevents the development of complications and the transition of the process to protracted or chronic.
The complex of treatment for acute pneumonia includes:
fight against infection and intoxication;
restoration of bronchial patency;
normalization of immunological reactivity and activation protective forces body;
acceleration of regenerative processes, treatment of complications.
Have great importance proper nutrition and care for a patient with acute pneumonia, which include: a spacious room with good ventilation and lighting, fresh cool air, oral care and plenty of drinking up to 2.5-3 liters per day (fruit drinks, liquid fruit, vegetable, berry juices ); a diet with sufficient protein, fat, carbohydrates, vitamins; regulation of intestinal function (prunes, boiled beets with vegetable oil on an empty stomach, kefir, yogurt or laxatives, cleansing enemas).
Antibacterial therapy plays a leading role in the treatment of acute pneumonia. To select an effective antibacterial agent, it is necessary to decipher the etiological structure of pneumonia. But the results of bacteriological examination of sputum become known late. Therefore, etiological diagnosis is based on the characteristics of the clinical picture of the disease, as well as bacterioscopy data of a sputum smear taken before treatment. In this case, it is possible to determine the type of microbial flora - cocci, rods, its cultural properties - relation to Gram staining.
The basic principles of antibacterial therapy are:
choosing the most active and less toxic drug;
determination of optimal doses and methods of administration;
timely start and sufficient course.
When carrying out antibacterial treatment, monotherapy (treatment with one drug) is preferable. The combined use of antibiotics is justified in severe cases of the disease, in mixed infections, in the absence of effect from sufficient doses of antibacterial monotherapy, in long-term disease, and also when it is necessary to reduce the toxic effect of antibiotics. Doses of antibiotics must be optimal and sufficient, since low doses lead to the selection of resistant microbial mutants and a decrease in the clinical effect. This provision remains valid and in combination antibacterial therapy it is necessary to use full therapeutic doses of the components.
Treatment of acute pneumonia is best started with the prescription of bactericidal antibiotics. If there is a need for combined antibacterial therapy, then it is rational to combine bactericidal drugs with bactericidal drugs, bacteriostatics with bacteriostatics. Optimally selected antibacterial therapy produces a clinical effect within 2-3 days. The lack of effect after 48 hours dictates the need to either increase the dose of the antibiotic, or change the route of administration, or change the drug. But one should caution against frequent, especially unjustified, changes in antibiotics. Intravenous use of antibiotics leads to the development of phlebitis, so if the condition improves, you should switch to another route of administration. The duration of antibacterial therapy is determined by the temperature reaction; the administration of antibiotics continues for 4-5 days after the temperature normalizes. Often 10-14 days of treatment are sufficient; if long-term use of the antibiotic is necessary, replacement should be made every 10 days.
Since in most cases pneumonia is pneumococcal in nature, it is advisable to start antibacterial therapy with penicillin or its semisynthetic derivatives. To obtain a therapeutic effect, a single dose of at least 300 thousand units is required. The choice of dose and method of administration are carried out taking into account the severity of the disease. For mild cases, 1.2-1.5 million units of benzylpenicillin per day are prescribed, for moderate cases - 3-5 million units per day, for severe cases - 15-20 million units per day or more.
For staphylococcal pneumonia, benzyl penicillin also retains its importance, but intravenous administration is preferable, which can be combined with intramuscular administration. If penicillin is ineffective, you should switch to semisynthetic penicillins - ampicillin, carbenicillin or penicillinase-resistant ones - methicillin (4.0-12.0), oxacillin (4.0-6.0), dicloxacillin (2.0-4.0) per day.
Streptococcal pneumonia is well treated with benzylpenicillin.
The reserve drugs in all cases are cephalosporins: ceporin, cephalexin, cefamezin (kefzol), and erythromycin.
The main drugs for the treatment of Klebsiella pneumonia are aminoglycosides, mostly gentamicin (40-80 mg 2-3 times a day), reserve drugs - erythromycin, tetracyclines, chloramphenicol.
For pneumonia caused by Escherichia coli, Proteus, Pseudomonas aeruginosa, semisynthetic penicillins, aminoglycosides, and chloramphenicol are effective. Erythromycin works best against mycoplasma and legionella. For mycoplasma pneumonia, tetracycline and lincomycin are somewhat less effective.
When treating patients with community-acquired pneumonia, a differentiated approach to the choice of antimicrobial drugs should be taken into account, taking into account age, severity of the condition, the presence of concomitant diseases, location of the patient (at home, in the general ward of a hospital, in the intensive care unit (ICU), previous antimicrobial therapy, use of glucocorticoids, etc.
Prognostically, the rapid initiation of antimicrobial therapy, no later than 4 hours after diagnosis, is very important.
When choosing antimicrobial drugs for a patient with nosocomial pneumonia, the nature of the department in which he is located (general profile or ICU), the use of mechanical ventilation and the time of development of VAP are taken into account. Empirical therapy is planned based on local data on the sensitivity of likely pathogens. Sputum examination is mandatory, and it is desirable to obtain material invasive methods with quantitative assessment of results, and blood cultures.
In the treatment of outpatient forms of community-acquired pneumonia, preference should be given to antimicrobial drugs for oral administration. However, for severe infections, antimicrobial drugs must be administered intravenously. In the latter case, step therapy is also highly effective, which involves switching from intravenous administration to oral administration. The transition should be made when the course of the disease stabilizes or the clinical picture improves (on average 2-3 days from the start of treatment).
For uncomplicated community-acquired pneumonia, antibiotic therapy can be completed once stable normalization of body temperature is achieved. The duration of treatment is usually 7-10 days.
If there are clinical and/or epidemiological data on mycoplasma, chlamydial or legionella pneumonia, the duration of antibacterial therapy should be longer due to the risk of relapse of infection - 2-3 weeks.
The duration of use of antimicrobial drugs for complicated community-acquired pneumonia and nosocomial pneumonia is determined individually.
In any case, the persistence of individual clinical, laboratory and/or radiological signs is not an absolute indication for continuation of antibacterial therapy or its modification. In most cases, these signs resolve spontaneously over time.
For mild cases of pneumonia, antibacterial drugs such as sulfonamides (short and long-acting), their derivatives (biseptol, sulfatone), as well as nitrofurans, have not lost their importance. Their distinctive feature is good permeability through biological filters.
Drug treatment of acute pneumonia, along with etiotropic (antibacterial) therapy, includes pathogenetic and symptomatic treatment:
detoxification and anti-inflammatory drugs;
bronchodilators and expectorants;
cardiovascular;
immunomodulators;
oxygen therapy.
For detoxification, synthetic plasma-substituting solutions (hemodez, rheopolyglucin), protein hydrolysates, 200-400 ml intravenous drips 1-2 times a day, are used.
To eliminate edema, improve microcirculation and ventilation of the lungs, anti-inflammatory drugs are used (acetylsalicylic acid 0.5 g 2-3 times a day, less often - non-steroidal anti-inflammatory drugs: indomethacin, brufen, voltaren). But their immunosuppressive effect and their reduction in the effectiveness of phagocytosis dictate the need for long-term use and strict justification for prescription. With a sluggish course of the disease, especially in combination with bronchospastic syndrome, it is possible to use short courses of small doses of glucocorticoids (prednisolone 10-15 mg per day for 3-5-7 days).
To improve the drainage function of the bronchi and restore bronchial patency, the use of bronchodilators (aminophylline, theophedrine, euspiran, asthmapent, etc.) and expectorants is indicated. At the onset of the disease, with a strong non-productive cough, it is advisable to prescribe antitussive drugs (codeine, libexin).
In the complex treatment of pneumonia, an important role is played by the normalization of immune defense mechanisms and nonspecific reactivity of the body (thymalin, T-activin, prodigiosan, gamma globulin, aloe extract, FiBS, etc.).
In severe cases of acute pneumonia (lobar, staphylococcal), as well as in the elderly, there is always a tendency to develop acute vascular and heart failure. In these cases, it is impossible to do without cardiovascular drugs. In case of high fever and severe intoxication, it is necessary to prescribe vascular agents (caffeine, cordiamine, camphor, sulfocamphocaine), and when signs of heart failure appear and in elderly patients, it is necessary to prescribe cardiac glycosides (corglikon, strophanthin, lanicor) parenterally. If signs of pulmonary edema appear, diuretics (Lasix intravenously or furosemide orally) must be added to treatment. At all stages of treatment of acute pneumonia, especially at the onset of the disease, active oxygen therapy is indicated.
From the first days of the disease, a prescription is necessary non-drug methods treatment. They allow you to accelerate the resorption of inflammatory changes, reduce intoxication, improve ventilation of the lungs and blood circulation in them. In the initial period of the disease - with high fever - only methods of distraction therapy can be used: cold compresses on the head, mustard wraps. When the temperature drops below 38°C, jars and mustard plasters can be used. Physical methods are an important factor in treatment. They are not prescribed for in serious condition, severe intoxication, signs of heart failure, hemoptysis, temperature above 38°C. During the period of active inflammatory process (exudation and swelling of lung tissue, impaired capillary circulation) good effect applies an ultra-high frequency (UHF) electric field to the area of inflammation, ultraviolet irradiation of the chest with erythemal doses of quartz (3-5 procedures). From the 7-10th day of illness, during the period of resorption of infiltration in the lungs, it is preferable to prescribe microwaves (microwave therapy), electromagnetic waves decimeter range, inductothermy. During this period, electrophoresis with calcium, magnesium, iodine, etc. ions is effective. In case of prolonged pneumonia, during the period of residual inflammatory changes, especially against the background of impaired drainage function of the bronchi, it is preferable to prescribe amplipulse therapy, thermal procedures (paraffin, ozokerite, mud), as well as ultrasound. In the same situation, the use of chest massage and aeroionotherapy is effective.
The complex of therapeutic measures in the early stages of the disease should include breathing exercises, which help improve the drainage function of the bronchi and reduce the formation of pleural adhesions. At the same time, medication is also prescribed physical culture, especially in older people.
In respect of rehabilitation activities A desirable step in the treatment of acute pneumonia is Spa treatment. It should be carried out mainly in local sanatoriums, but climatic resorts in low-mountain conditions, in forest zones, and on the southern coast of Crimea can also be used. Mountain resorts are located mainly in the Caucasus, Kyrgyzstan, and Altai Territory. Steppe resorts are located in the Orenburg region, Bashkiria, Kazakhstan and Western Siberia (Abastumani, Teberda, Dombay, Borovoe, etc.).
Persons who have suffered acute pneumonia with clinical and radiological signs of recovery are subject to mandatory clinical observation for at least six months.
In case of prolonged pneumonia, clinical observation should be carried out for 12 months. During this period, secondary prevention measures are carried out: the prescription of bronchodilators and expectorants (especially with concomitant bronchitis), treatment of foci of chronic infection, as well as a set of primary prevention measures: the fight against smoking and alcohol abuse, hardening.
All persons who have suffered acute pneumonia should be employed through the CEC, especially under unfavorable working conditions. In case of uncomplicated course of the disease, employment is carried out for a period of up to 2-3 months, and in case of protracted course - up to 6 months. It provides for exemption from work in conditions of increased dust, heavy physical activity, sudden changes in temperature in the production area, as well as from work outside in the cold season.
The clinical picture of pneumonia consists of 4 main syndromes:
- Intoxication syndrome - weakness, weakness, headache and muscle pain, palpitations, pallor, loss of appetite.
- Syndrome of general inflammatory changes - fever, chills, inflammation indicators in laboratory tests(increased ESR, leukocytosis).
- Syndrome of inflammatory changes in lung tissue– shortness of breath, cough, sputum production, change in respiratory rate, wheezing in the lungs, x-ray changes.
- Syndrome involving other organs and systems - cardiovascular, nervous, digestive, etc.
The severity of each syndrome depends on the type of pathogen, the form of the disease, and the reactivity of the body.
Symptoms of pneumonia
Lobar pneumonia has an acute onset. High temperature with chills, weakness and weakness - these are the first complaints of the patient. Then a cough is added to them: initially dry, reflexive, then with the release of “rusty” sputum; pain in the chest on the affected side, aggravated by coughing. The patient's condition is serious. Upon examination, a feverish flush is revealed, more pronounced on the side of the affected lung. Noteworthy are herpetic rashes on the lips, chin, and wings of the nose. The lips are often cyanotic. Breathing is shallow and rapid, and on the affected side the chest is slightly behind in the act of breathing.
An examination of the lungs gives a characteristic picture: in the initial stage, harsh breathing with prolonged exhalation and crepitus are heard. Later, bronchial breathing and moist fine bubbling rales appear. A pleural friction rub may appear.
From the cardiovascular system, rapid heartbeat, decreased blood pressure, and muffled heart sounds are detected.
Laboratory tests reveal sudden inflammatory changes in the blood picture. Protein often appears in the urine.
X-ray examination in the initial phase reveals an increase in the pulmonary pattern in the affected segment, in place of which intense darkening soon appears. Gradually, during the healing process, the size and intensity of the darkening decreases, and the root of the lung can remain expanded for a long time even after recovery.
Focal pneumonia Unlike lobar, it begins gradually, unnoticeably. Focal pneumonia is usually preceded by a viral infection in the upper respiratory tract. Symptoms of intoxication are not so pronounced: the temperature rises within 38-39 degrees, there is some weakness, headache, and shortness of breath. The main complaint is cough with mucopurulent sputum.
If the focus of pneumonia is small, then the clinical picture is blurred and mild. With large lesions and confluent pneumonia, shortness of breath, cyanosis, and chest pain are expressed.
On auscultation, moist fine bubbling rales are heard over the site of the lesion.
X-ray reveals inflammatory infiltrates in 1 or several segments of the lung. Confluent lesions appear in the form of spotty darkening.
Clinical picture, course of pneumonia
The clinical course of pneumonia may vary depending on the pathogen.
Pneumococcal pneumonia characterized by a detailed picture of lobar pneumonia.
Staphylococcal and streptococcal pneumonia, as a rule, one-sided, characterized by a severe course with high fever, cough with purulent sputum. The rapid development of purulent complications is characteristic: lung abscesses, pleurisy, pyothorax, sepsis.
Coli pneumonia develops most often due to aspiration of vomit. Clinically manifested by damage to both lungs. As a rule, this is confluent pneumonia. Radiographs clearly show confluent lesions. Escherichia coli is cultured in the sputum.
Viral pneumonia preceded by symptoms of viral infection of the upper respiratory tract (rhinitis, laryngotracheitis). The leading role in the clinic is occupied by general inflammatory and intoxication syndromes. Unlike bacterial pneumonia, viral pneumonia is characterized by leukopenia in a general blood test.
Diagnosis of pneumonia
Diagnosis of pneumonia is based on 5 generally accepted clinical signs.
- Acute onset of the disease with a rise in temperature above 38 degrees.
- The appearance or intensification of cough with the release of mucopurulent, purulent or hemorrhagic sputum.
- The appearance of local dullness of pulmonary sound during percussion. And auscultated bronchial breathing, crepitus, moist rales, pleural friction noise.
- Neutrophilic leukocytosis in a general blood test (in the case of viral pneumonia - leukopenia).
- X-ray shows inflammatory infiltrates in the lungs.
