Community-acquired pneumonia: diagnosis and differential diagnosis
A.I. Sinopalnikov
The collective term "pneumonia" is usually used to denote a group of acute infectious (mainly bacterial nature) focal lesions of the respiratory parts of the lungs with different degrees of etiology, pathogenesis, morphological characteristics of focal lesions of the respiratory parts of the lungs with the presence of intraalveolar exudation, manifested in varying degrees of febrile reaction, intoxication and detected during physical and radiological studies.
The most widespread classification is taking into account the conditions in which the disease developed, the features of infection of the lung tissue, as well as the immunological reactivity of the organism. Correct consideration of these factors allows predicting the etiology of the disease with a significant degree of probability and, ultimately, choosing an adequate direction for empirical antimicrobial chemotherapy. In accordance with this classification, the following types of pneumonia are distinguished:
a) community-acquired (acquired outside a medical institution) pneumonia (synonyms: home, outpatient);
b) nosocomial (acquired in a medical institution) pneumonia (synonyms: hospital, nosocomial);
Alexander Igorevich Sinopalnikov - Professor, Head of the Department of Pulmonology with a course of phthisiology at the State Institute for Advanced Training of Doctors of the Ministry of Defense of the Russian Federation.
c) aspiration pneumonia;
d) pneumonia in persons with severe immunosuppression (congenital immunodeficiency, HIV infection, iatrogenic immunosuppression).
The most practically significant is the division of pneumonia into community-acquired and nosocomial. It must be emphasized that such a subdivision has nothing to do with the severity of the course of the disease, and the main and only criterion for differentiation is the environment in which pneumonia developed.
The term "community-acquired pneumonia" describes cases of acute illness occurring in community-acquired
conditions, accompanied by symptoms of lower respiratory tract infection (fever, cough with sputum, possibly purulent, chest pain, shortness of breath) and X-ray evidence of “fresh” focal-in-infiltrative changes in the lungs in the absence of an obvious diagnostic alternative.
Diagnostics
The diagnosis of pneumonia is complicated by the fact that there is no specific clinical sign or combination of signs that can be reliably relied on if this diagnosis is suspected. Rather, the absence of any of the nonspecific symptoms or the absence of local stetho-acoustic
These changes in the lungs make the diagnosis of pneumonia less likely.
In general, the key clinical and radiological signs of community-acquired pneumonia (CAP) can be formulated as follows:
Analysis of clinical features and X-ray data allows in some cases to make an assumption about a particular pathogen, but this information is of relative value;
Sudden onset, febrile fever, tremendous chills, pleural chest pains, lobar infiltration are characteristic of Streptococcus pneumoniae (it is often possible to isolate pneumococcus from the blood), partly for Legionella spp., Less often for other pathogens. On the contrary, this picture is absolutely not typical for Mycoplasma pneumoniae and Chlamy-dophila (Chlamydia) pneumoniae;
“Classic” signs of pneumonia (acute febrile onset, chest pains, etc.) may be absent, especially in weak or elderly patients;
Approximately 25% of CAP patients over the age of 65 years have no fever, and leukocytosis is recorded only in 50-70%. In this case, symptoms can be represented by weakness, nausea, anorexia, abdominal pain, intellectual and mental disorders;
Late diagnosis and delay in starting antibiotic therapy lead to a worse prognosis: mortality among patients over 65 reaches 10-25%;
The most common X-ray signs of pneumonia are
Pneumonia should always be suspected if the patient has a fever in combination with complaints of cough, shortness of breath, sputum production and / or chest pain.
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focal blackouts appear in the projection of one or more segments;
In cases of lobar infiltration, the phenomenon of "air bronchogram" is visualized in 33% of patients;
Pleural effusion complicates the course of CAP in 10-25% of cases and is not particularly important in predicting the etiology of the disease;
The formation of cavities of destruction in the lungs is not typical for pneumococcal, mycoplasma and chlamydial pneumonia, but rather testifies in favor of staphylococcal infection, aerobic gram-negative pathogens of the intestinal group and anaerobes;
Reticulo-nodular infiltration in the basal parts of the lungs is characteristic of mycoplasma pneumonia (however, in 20% of cases, it may be accompanied by focal-confluent infiltration in the projection of several segments or even a lobe).
Pneumonia should always be suspected if the patient has a fever in combination with complaints of cough, shortness of breath, sputum production and / or chest pain. Patients suffering from pneumonia often complain of unmotivated weakness, fatigue, and heavy sweating at night.
Information obtained from physical examination of patients with CAP depends on many factors, including the severity of the disease, the prevalence of pneumonic infiltration, age, and the presence of comorbidities. The classical objective signs of pneumonia are the shortening (dullness) of the percussion tone over the affected area of the lung, locally audible bronchial breathing, the focus of sonorous small-bubble wheezing or inspiratory crepitus, increased bronchophonia and vocal tremor. However, in some patients, objective signs of pneumonia may differ from typical ones or be absent altogether (in about 20% of patients).
Chest x-ray
This is the most important diagnostic test. Almost always, the diagnosis of CAP requires the detection of focal infiltrative changes in the lungs in combination with the corresponding symptoms. And although there is an opinion that steto-acoustic signs of focal infiltration usually coincide with radiographic data, numerous studies have shown their low sensitivity and specificity in the diagnosis of pneumonia.
There are several reasons for false negative x-ray results in patients with pneumonia. These include dehydration (however, there is not enough data for this theory), deep neutro-
the development of a localized acute inflammatory reaction in the lung tissue, early stages of the disease (it is believed that pneumonia can be recognized by auscultation one day before the appearance of infiltration on the radiograph) and, finally, cases of pneumonia caused by Pneumocystis carinii in HIV-infected patients (in 10-20% of patients, there are no radiological changes).
Sometimes there are diagnostic problems associated with false positive x-ray results (see below).
The value of chest x-ray is not only in verifying the diagnosis of pneumonia (as a rule, in the presence of appropriate clinical signs), assessing the dynamics of the process and the completeness of recovery. Changes on the radiograph (prevalence of infiltration, presence or absence of pleural effusion, destruction) correspond to the severity of the disease and serve as a kind of “guide” in the choice of antibiotic therapy.
Other studies
A clinical blood test is the standard diagnostic test. Obviously, neither the total number of leukocytes in the peripheral blood, nor the leukocyte formula make it possible to speak with certainty about the potential causative agent of pneumonia. However, leukocytosis of more than 10-12 x 109 / L indicates a high likelihood of bacterial infection, and leukopenia below 3 x 109 / L or leukocytosis above 25 x 109 / L are unfavorable prognostic signs.
Biochemical blood tests, including liver and kidney function tests, and electrolyte analysis are also standard methods of investigation in patients with CAP requiring hospitalization.
In hospitalized patients with CAP, microbiological studies are mandatory: blood cultures twice (before antibiotics are prescribed), in the presence of a productive cough - bacterioscopy of a Gram stained sputum smear and its culture (see below).
In patients with symptoms of respiratory failure due to widespread pneumonic infiltration, massive pleural effusion, the development of pneumonia against the background of chronic obstructive pulmonary disease, it is necessary to determine arterial blood gases. In this case, hypoxemia with a decrease in the pO_ level below 60 mm Hg. Art. prognostically unfavorable and indicates the need to place the patient in the intensive care unit.
In the presence of pleural effusion and conditions for safe pleural puncture (visualization on a laterogram of a freely displaceable fluid with a layer thickness> 1.0 cm), the study of pleural fluid should include counting leukocytes with a leukocyte formula, determining pH, lactate dehydrogenase activity, protein content, staining strokes on Gram and on
The absence or inaccessibility of radiographic confirmation of focal infiltration in the lungs makes the diagnosis of pneumonia inaccurate / uncertain.
Potential causative agents of CAP, depending on the conditions of its occurrence
Conditions of occurrence Possible pathogens
Alcoholism Chronic bronchitis / tobacco smoking Decompensated diabetes mellitus Staying in nursing homes Non-sanitized oral cavity Influenza epidemic Massive aspiration Development of pneumonia on the background of bronchiectasis, cystic fibrosis Intravenous drug addiction Local bronchial obstruction (for example, lung cancer) Contact with air conditioners, humidifiers An outbreak of the disease in a team (schoolchildren, military personnel) S. pneumoniae, anaerobes, aerobic enterobacteria (Klebsiella pneumoniae, etc.) S. pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Legionella spp. S. pneumoniae, Staphylococcus aureus S. pneumoniae, Enterobacteriaceae, H. influenzae, S. aureus, Chlamydophila pneumoniae, anaerobes Anaerobes S. pneumoniae, S. aureus, Streptococcus pyogenes, H. influenzae Anaerobes Pseudomonas aeruginosa, a P. cepacia, S. S. aureus, anaerobes Anaerobes Legionella pneumophila S. pneumoniae, Mycoplasma pneumoniae, Chlamydophila pneumoniae
no Bartlett J.G. Management of Respiratory Tract Infections. Philadelphia, 1999. Mandell L.A. et al. // Clin. Infect. Dis. 2000. V. 31. P 383.
acid-fast bacteria, sowing on aerobes, anaerobes and mycobacteria.
Diagnosing CAP
The diagnosis of CAP is definite if the patient has radiologically confirmed focal infiltration of lung tissue and at least two clinical signs from among the following:
a) acute fever at the onset of the disease (body temperature> 38.0 ° C);
b) cough with phlegm;
c) physical signs (focus of crepitus and / or fine bubbling rales, hard bronchial breathing, shortening of percussion sound);
d) leukocytosis> 10 x 109 / l and / or stab shift (> 10%).
If possible, you should strive for clinical and radiological confirmation of the diagnosis of CAP. In this case, it is necessary to take into account the likelihood of known syndromic diseases / pathological conditions.
The absence or inaccessibility of radiographic confirmation of focal infiltration in the lungs makes the diagnosis of CAP inaccurate / uncertain. In this case, the diagnosis of the disease is based on taking into account the data of the anamnesis, complaints and corresponding local symptoms.
If, when examining a patient with fever, complaints of cough, shortness of breath, sputum and / or chest pain, X-ray examination is unavailable and there are no local stetho-acoustic symptoms, then the assumption of PFS becomes unlikely.
Etiological diagnosis
Obviously, the establishment of the fact of PFS, based on the results of physical and X-ray examinations, can only be equated with a syndromic diagnosis, but it becomes nosological after the identification of the pathogen. Unconditional evidence of the causal role of the microorganism in the development of pneumonia is its isolation from the lung tissue, however, the clinician has to rely on the results of micro-
biological blood tests (positive in 6-10% of cases), pleural fluid, sputum (possible contamination of bronchial secretions when passing through the oropharynx) or immunoserological tests, as well as anamnestic data (table).
Standard test methods are Gram-stained bacterioscopy and deep-coughing sputum culture. Before starting a microbiological study, it is necessary to stain the smear according to Gram. If there are less than 25 leukocytes and more than 10 epithelial cells in the smear, further examination is impractical (most likely the material is the contents of the oral cavity). The detection in a smear of a significant number of gram-positive or gram-negative microorganisms with typical morphology (gram-positive lanceolate diplococci - S. pneumoniae; clusters of gram-positive cocci in the form of clusters - S. aureus, gram-negative coccobacilli - H. influenzae) can serve as a guide for
the appointment of antibiotic therapy. The diagnostic value of sputum test results can be assessed as high when a potential pathogen is isolated in a concentration of more than 105 CFU / ml (CFU - colony forming units).
Obviously, the interpretation of the results of bacterioscopy and sputum culture should be based on clinical evidence.
Seriously ill patients, including the majority of hospitalized patients, should be cultured twice before starting antibiotic therapy (blood is taken from different places with an interval of at least 10 minutes).
When collecting sputum, the following rules must be observed
1. Sputum is collected before meals, if possible before the start of antibiotic therapy.
2. Before collecting sputum, rinse the mouth thoroughly with boiled water.
3. The patient is instructed to receive the contents of the lower respiratory tract, and not the oronopharynx.
4. Collection of sputum should be done in sterile containers.
5. Duration of storage of samples at room temperature should not exceed 2 hours.
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While it is important to obtain laboratory material prior to antibiotic prescribing, microbiological testing should not delay antibiotic treatment. This is especially true for patients with a severe course of the disease.
Serological diagnostics
infections of Mycoplasma pneumoniae, Chlamydophila (Chlamydia) pneumoniae and Legionella are not considered among the mandatory research methods, because, taking into account the repeated sampling of blood serum in the acute period and during the period of convalescence (a few weeks after the onset of the disease), this is not a clinical, but an epidemiological level diagnostics.
Currently, the enzyme immunoassay for the determination of the specific soluble antigen of Legionella pneumophila (serotype 1) in urine with severe CAP has become widespread abroad. Od-
However, in our country, the use of this expensive method of express diagnostics of legionella infection has not gone beyond the framework of individual clinical centers. Determination of Streptococcus pneumoniae antigen in urine is considered as a promising additional method, however, the available data are insufficient to give unambiguous recommendations.
The polymerase chain reaction (PCR) method is developing very quickly and seems to be promising for the diagnosis of such causative agents of CpD as C. pneumoniae and M. pneumoniae. However, this method cannot yet be recommended for widespread clinical practice.
Fibrobronchoscopy with a quantitative assessment of the microbial contamination of the material obtained (“protected” brush biopsy, bronchoalveolar lavage) or other methods of invasive diagnostics (transtracheal aspiration, transthoracic
biopsy, etc.) are reserved for individual cases: pneumonia in patients with immunosuppression, suspected pulmonary tuberculosis in the absence of productive cough, obstructive pneumonitis in lung cancer or foreign body aspiration, etc.
Unfortunately, due to subjective and objective difficulties: incorrect sampling of material or absence of sputum, errors in conducting a microbiological study, the widespread practice of patients taking antibacterial drugs before going to the doctor (for example, taking even one dose of a potentially effective antibiotic makes it unlikely that a pneumococcal culture is isolated) - in a large number of cases, the causative agent of pneumonia cannot be identified.
Differential diagnostics will be discussed in the next issue of the journal.
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For citation: Yu.K. Novikov Pneumonia: complex and unresolved issues of diagnosis and treatment // BC. 2004. No. 21. S. 1226
Pneumonia is an infectious lesion of the alveoli, accompanied by infiltration of inflammatory cells and exudation of the parenchyma, as a response to the introduction and proliferation of microorganisms, into sterile (normally) parts of the respiratory tract. The pneumonia section does not consider lung lesions in infectious diseases related to other nosological forms: plague, typhoid fever, tularemia, etc. If you follow the above definition for the diagnosis of pneumonia, then none of the diagnostic criteria can be objectively proven. Neither inflammation nor damage to the alveoli. And only by indirect data (determination of the pathogen in sputum or an increase in the titer of antibodies in the blood), one can judge the infectious nature of lung damage. Direct evidence of inflammation in the pulmonary parenchyma and identification of the pathogen is possible only with a morphological study of the material obtained from a biopsy. The symptom complex, including cough with sputum and / or hemoptysis, chest pains usually with coughing and deep breathing, fever and symptoms of intoxication, is not characteristic only of pneumonia, but is detected in a number of other lung diseases. The most common are: - lung cancer; - thrombosis and pulmonary embolism; - pulmonary tuberculosis; - ARVI; - acute and infectious exacerbation of bronchitis; - pleurisy; - bronchiectasis; - acute forms of alveolitis; - pulmonary mycosis; - infectious diseases (typhus, tularemia, infectious hepatitis, etc.). The usual algorithm of clinical thinking provides for the solution (often unconscious) of the following questions when meeting a patient: - is the patient sick; - if sick, what organs and systems are involved in the process; - if the lungs are affected, then what is the nature of the lesion; - if pneumonia, then what is its etiology. Following this algorithm allows you to achieve maximum treatment efficiency. Differential diagnosis plays an important role in this.
Differential diagnosis for pneumonia Clinical and anamnestic criteria
Lungs' cancer
Belonging to a risk group: - men over 40; - smokers; - suffering from chronic bronchitis; - with a history of cancer; - have a family history of cancer. A typical picture of anamnesis, in addition to belonging to a risk group, includes a gradual onset of the disease, when symptoms of intoxication, bronchial obstruction, and tumor spread appear and increase: weakness, increasing fatigue, over time, weight loss, dynamics of the cough syndrome - from dry hacking unproductive cough , cough with mucous or mucopurulent sputum streaked with blood to sputum like "raspberry jelly", hemoptysis, recurrent inflammation in the same areas of the lung, recurrent pleurisy, symptoms of compression of the superior vena cava. Extrapulmonary symptoms of lung cancer: indomitable skin itching, ichthyosis, drum fingers, progressive dementia, myopathic syndrome, Itsenko-Cushing's syndrome. It should be emphasized that despite a thorough clinical examination, it is not possible to identify a gradual onset of the disease and in 65% of cases the onset is regarded as acute - in the form of cancerous pneumonitis, paracancrotic pneumonia, and, in fact, atelectasis-pneumonia in the zone of obstructed bronchus.
Pulmonary tuberculosis
Contact with a patient with tuberculosis. More often, even with a visible acute onset, there is a gradual increase in clinical symptoms. ... Relatively easily tolerated intoxication in comparison with a similar volume of damage to lung tissue of other etiology. ... Scant physical symptoms, inconsistent with significant R-logical changes. ... Dry cough, often mucous than purulent, sputum. ... Isolated pleurisy, especially at a young age.
Infarction pneumonia with pulmonary embolism and pulmonary thrombosis History of lesion of the veins of the lower extremities and pelvis. More often, embologenous thrombosis is localized in the popliteal (20%), iliocaval segments. Veins of the upper extremities (8%) and heart cavities (2%) are less significant as causes of PE. It should be noted that only 40% of venous thrombosis clinic is preceded by PE. The development of the symptom complex of pneumonia (cough, hemoptysis, intoxication) is preceded by shortness of breath and chest pain, the severity of which depends on the caliber of the affected lung vessel. In pulmonary embolism, the presence of an embolism in a large circle should not be confused, since through an open oval window with a changed hemodynamics, emboli enter the large circle.
Pain in pulmonary embolism:
Angina pectoris, infarction with concomitant coronary artery disease; - bursting with increasing pressure in the pulmonary artery; - pleural with the development of infarction pneumonia with pleurisy; - in the right hypochondrium (abdominal) due to acute circulatory failure and stretching of the Glisson capsule of the liver.
Shortness of breath with PE:
Sudden; - not related to physical activity; - uncharacteristic orthopnea position; - shallow breathing.
Hemoptysis with pulmonary embolism:
On the second or third day after the development of infarction pneumonia.
Physical symptoms:
Wheezing, dullness, fever, intoxication, an emphasis of the second tone on the pulmonary artery, swelling of the cervical veins - do not have specific features characteristic only of PE and are late signs. It should be noted that all symptoms associated with increased pressure in the pulmonary artery are found only in massive PE (50% vascular lesions).
Fibrosing alveolitis
The gradual but steady progression of shortness of breath, characteristic of interstitial lesions, does not cause difficulties in terms of differential diagnosis with pneumonia. The acute form (Libov desquamative pneumonia, Haman-Rich syndrome) has no significant clinical differences from bacterial pneumonia. Most often, after unsuccessful antibiotic treatment, the appointment of steroids with a pronounced positive effect suggests, and then using objective examination methods to prove the diagnosis of alveolitis.
For allergic exogenous alveolitis:
There is a connection with the allergen; - the elimination effect is noted; - the positive effect of corticosteroid treatment.
With toxic fibrosing alveolitis:
Communication with a toxic agent (drugs, occupational exposure to toxic substances).
Influenza and ARVI
The main difference from pneumonia is the absence of damage to the lung parenchyma and, accordingly, the absence of local physical symptoms. Cough and intoxication symptoms are not specific. It should be borne in mind that ARVI, influenza are complicated by associated pneumonia. Physical symptoms in this case depend on the size of the pneumonic focus and the depth of its location from the surface of the chest. Often only laboratory and X-ray methods can detect pneumonia (leukocytosis, shift of the formula to the left, increased ESR, infiltrative shadow, bacteriological examination of sputum).
Bronchitis and bronchiectasis
With bronchitis, there is no symptomatology of local lung damage (wet wheezing, dullness, increased vocal tremor). To a lesser extent than in pneumonia, symptoms of intoxication are expressed. Shortness of breath in obstructive bronchitis is a nonspecific symptom, since up to 80% of cases of pneumonia are accompanied by obstructive changes in the FVD. The final diagnosis is established after laboratory and instrumental examination. With dysontogenetic bronchiectasis, the anamnesis is more often traced from childhood. With acquired - anamnesis of pneumonia, tuberculosis. A variety of physical symptoms (wheezing, moist, voiced, small-coarsely blistering, dullness, etc.) depends on the prevalence of the process and the phase of inflammation. Cough, the amount of sputum cannot serve as objective symptoms of the diagnosis.
Hereditary-determined lung diseases
Violation of the main defense mechanisms (mucociliary transport in cystic fibrosis and ciliary insufficiency, immune defense in case of deficiency of immunoglobulin, especially immunoglobulin A, T-cell deficiency, pathology from macrophages) leads to damage to the lungs and bronchi, manifested mainly by the clinic of recurrent inflammation in the bronchopulmonary system (bronchitis, acquired bronchiectasis, pneumonia). And only laboratory and instrumental examination can reveal the root cause of nonspecific clinical symptoms.
Objective examination data
Pulmonary tuberculosis
X-ray Depending on the form of tuberculosis - focal shadow, infiltration, infiltration with decay, cavernous tuberculosis - a path to the root and an increase in root lymph nodes, old foci (petrification), with localization more often in I-III and VI segments, are characteristic. Tomography, including computer Clarification of the number, size of cavities, their walls, bronchial patency, the state of the lymph nodes of the root and mediastinum. Sputum analysis - lymphocytes, erythrocytes (with hemoptysis) Microscopy - tubercle bacilli Sputum culture - tubercle bacilli FBS - scars, fistulas, tubercles with damage to the bronchi Biopsy - tuberculous (caseous) granuloma Blood test Anemia - severe forms, leukocytosis, lymphocytosis, increased ESR Biochemical blood test Dysproteinemia, hypoalbuminemia in severe forms, hypoproteinemia Analysis of urine Nonspecific changes - protein, leukocytes In case of kidney damage, sowing of a tubercle bacillus. Lungs' cancerX-ray Decrease in airiness of lung tissue, atelectasis, infiltrates, focal formations. Tomography, including computer Narrowing of the bronchus or its complete obstruction, enlargement of the lymph nodes of the root. FBS - narrowing of the bronchus, plus tissue Lavage - atypical cells Biopsy - tumor tissue, cells Ultrasound - search for metastases or the main tumor, if metastases in the lungs (liver, kidneys, pancreas) Isotope research - search for metastases (liver bone) or tumors, if metastases in the lungs. Fibrosing aulveolitesX-ray Dissemination in the middle and lower sections, "frosted glass", interstitial fibrosis, "cellular lung" CT scan - clarification of pathology FBS - nonspecific inflammatory changes Lavage - neutrophilia - ELISA, lymphocytosis - EAA Biopsy - desquamation, exudation (alveolitis), bronchiolitis, arteritis - ELISA, granulomas with EAA, arteritis with TFA, thickening of the basement membrane, body test - restrictive changes, impaired diffusion. Immunology An increase in IgG - ELISA, an increase in rheumatoid factor - ELISA, an increase in anti-pulmonary antibodies - ELISA, an increase in IgE - EAA, an increase in mucin antigen.
Congenital pathology
X-ray see bronchitis Immunology IgA or other Ig deficiency, T cell deficiency, macrophage deficiency Sweat analysis - increase in chlorides Genetic research - identification of the gene for cystic fibrosis.
SARS and flu
X-ray - ENT norm - laryngitis, pharyngitis, rhinitis Sputum analysis - neutrophils, columnar epithelium Blood test - lymphocytosis.
Bronchiectasis
X-ray Strengthening, deformation of the pulmonary pattern, depending on the prevalence. Cellularity of the pulmonary pattern in the later stages. Tomography Expansion and deformation of the bronchi (saccular, cylindrical) FBS - indirect signs of bronchiectasis and bronchitis Lavage - macrophages, neutrophils, bacteria Sputum - the same sputum culture - pneumotropic pathogens, more often Gr + and Gr - flora, in credits> 10 CFU / ml Bronchography - saccular bronchiectasis, cylindrical Blood test - nonspecific inflammation Blood chemistry - depending on the severity and duration: hypoproteinemia, hypoalbuminemia, dysgammaglobulinemia. Analysis of urine - nonspecific changes With prolonged course - changes for amyloidosis of the nephrotic syndrome.
Bronchitis
X-ray Strengthening the pulmonary pattern Tomography - too FBS - hyperemia, swelling of the mucous membrane, sputum. Diffuse lesion. Lavage - neutrophils, macrophages Biopsy - metaplasia in chronic bronchitis Sputum culture - non-specific counting CFU / ml of non-specific flora Sputum analysis - macrophages, neutrophils Serology - increased titers of antibodies to pneumotropic pathogens FVD - obstructive type Immunology - various variants of immunological, secondary insufficiency.
TELA
Roentgenogram Non-specific infiltrative shadows Tomogram Does not provide additional information for the diagnosis of PE FBS - contraindicated ECG - symptoms of overload with massive PE (more than 50% of the vessels) SI QIII (neg.) T in V 1 V 2 Perfusion lung scan Focal decrease in isotope accumulation - 100% reliability of the diagnosis in the absence of changes in the R-gram. 15% errors in cancer, tuberculosis, abscess. Angiopulmonography Vascular filling defect, vessel breakage or depletion, delay in filling phases are signs of Westermark. Doppler ultrasonography of veins Search for embologenous thrombosis Phlebography - the same Blood test Anemia with massive lesions, leukocytosis, left shift, increased ESR Blood chemistry Bilirubinemia with massive lesion Analysis of urine Nonspecific changes, protein, leukocytes, oligo-anuria - in shock.
Clinical criteria for pneumonia
Patients complain: - cough dry or with phlegm, hemoptysis, chest pain; - fever above 38 °, intoxication. Physical data Crepitation, small bubbling rales, dullness of percussion sound, increased vocal tremor. Objective diagnostic criteria To determine the diagnosis, the following studies are prescribed: - X-ray of the chest organs in two projections is shown with an incomplete set of clinical symptoms; - microbiological examination: Gram smear staining, sputum culture with quantitative determination of CFU / ml and antibiotic sensitivity; - clinical blood test. The listed methods are sufficient for the diagnosis of pneumonia at the outpatient stage and with an uncomplicated typical course of pneumonia in a hospital.
Additional research methods
X-ray tomography, computed tomography are prescribed in case of damage to the upper lobes, lymph nodes, mediastinum, decrease in the volume of the lobe, suspicion of abscess formation with ineffectiveness of adequate antibiotic therapy. Microbiological examination of sputum, pleural fluid, urine and blood, including mycological examination, is advisable in case of continued febrile state, suspected sepsis, tuberculosis, superinfection, AIDS. Serological research - determination of antibodies to fungi, mycoplasma, chlamydia and legionella, cytomegalovirus - is indicated for an atypical course of pneumonia in the risk group in alcoholics, drug addicts, with immunodeficiency (including AIDS), in the elderly. A biochemical blood test is prescribed for severe pneumonia with manifestations of renal, hepatic failure, in patients with chronic diseases, decompensation of diabetes mellitus. Cyto- and histological studies are carried out in the risk group for lung cancer in smokers after 40 years, in patients with chronic bronchitis and a cancer family history. Bronchological examination: diagnostic bronchoscopy is performed in the absence of the effect of adequate therapy for pneumonia, if lung cancer is suspected in the risk group, the presence of a foreign body, including aspiration in patients with loss of consciousness, if necessary, biopsy. Therapeutic bronchoscopy is performed during abscess formation to ensure drainage. Ultrasound examination of the heart and abdominal organs is carried out with suspicion of sepsis, bacterial endocarditis. Pulmonary isotope scanning and pulmonary angiography are indicated for suspected pulmonary embolism (PE). Additional methods included in the examination plan, in fact, allow for differential diagnosis and are carried out in a hospital, where the patient is hospitalized depending on the severity of the condition and / or with an atypical course of the disease that requires a diagnostic search.
Determining the severity of pneumonia is one of the key points when making a diagnosis and is in the first place before the doctor after determining the nosological form. Subsequent actions (determination of indications for hospitalization, in which department) depend on the severity of the condition.
Hospitalization criteria
Hospitalization of patients with pneumonia is indicated in the presence of the following factors: - age over 70 years; - concomitant chronic diseases (chronic obstructive pulmonary disease, congestive heart failure, chronic hepatitis, chronic nephritis, diabetes mellitus, alcoholism or substance abuse, immunodeficiency); - ineffective outpatient treatment for three days; - confusion or decreased consciousness; - possible aspiration; - the number of breaths is more than 30 per minute; - unstable hemodynamics; - septic shock; - infectious metastases; - multi-lobe lesion; - exudative pleurisy; - abscess formation; - leukopenia less than 4000 / ml or leukocytosis more than 20,000; - anemia: hemoglobin less than 9 g / ml; - renal failure (urea more than 7 mmol); - social indications.
Indications for intensive care- Respiratory failure - PO2 / FiO2<250 (<200 при ХОБЛ), признаки утомления диафрагмы, необходимость в механической вентиляции; - Недостаточность кровообращения - шок (систолическое АД<90 мм рт.ст., диастолическое АД<60 мм рт.ст.), необходимость введения вазоконстрикторов чаще, чем через 4 часа, диурез < 20 мл/ч; - Острая почечная недостаточность и необходимость диализа; - Синдром диссеминированного внутрисосудистого свертывания; - Менингит; - Кома.
Antibacterial therapy
Lactam antibiotics
Most? -lactam drugs concentration in the lung parenchyma is less than in the blood. Almost all drugs enter the sputum at a concentration much lower than in the bronchial mucosa. Moreover, many causative agents of respiratory diseases ( H. influenzae, Moraxella catarrhalis, Streptococcus spp.) are located precisely in the lumen of the bronchi or in the mucous membrane, therefore, large doses of drugs are required for successful treatment. Uh? -lactam drugs concentration in the liquid covering the epithelium of the lower respiratory tract, more than in sputum, bronchial secretions. However, after concentration? β-lactam drug will exceed the MIC of the pathogen, a further increase in concentration is meaningless, since the effectiveness of these drugs depends mainly on the time during which the concentration of the antibiotic exceeds the MIC. ? β-lactam drugs in high doses retain their effectiveness against pneumococci with intermediate sensitivity, in contrast to macrolides and fluoroquinolones.
Macrolides Macrolides are highly lipophilic, which ensures their high concentration in the tissues and fluids of the respiratory tract. Due to their high diffusion capacity, they accumulate better in the lung tissue, reaching higher concentrations there than in plasma.
Azithromycin (Hemomycin) has approximately the same properties, while its concentration in serum is usually difficult to determine, and in the lung tissue it remains at a very high level for 48-96 hours after a single administration. In general, the concentration of new macrolides in the bronchial mucosa is 5-30 times higher than the serum concentration. Macrolides penetrate better into the epithelial cells than into the liquid on the surface of the epithelium. Azithromycin, after a single oral administration at a dose of 500 mg, reaches a concentration in the epithelium lining fluid that is 17.5 times greater than the MIC90 for S. Pneumoniae... To combat intracellular pathogens ( Legionella spp., C. pneumoniae) of particular importance is the concentration that antibacterial agents reach in alveolar macrophages. While highly ionized? β-lactam drugs practically do not penetrate intracellularly, macrolides are able to accumulate in macrophages at a concentration that is many times higher than their concentration in the extracellular space.
Fluoroquinolones Fluoroquinolones accumulate in the bronchial mucosa at approximately the same concentration as in plasma. The concentration of fluoroquinolones in the epithelial fluid is very high. The effectiveness of drugs in this group is determined by both the duration of action and the concentration. Since the mid-90s, respiratory fluoroquinolones (levofloxacin, sparfloxacin) have taken a firm place in antibiotic selection algorithms (ABP) based on the principles of evidence-based medicine (recommendations of the Society for Infectious Diseases, USA, 1998; guidelines of the American Thoracic Society, 2001; recommendations of the British Thoracic Society, 2001) But along with this, it must be stated that the cost of respiratory fluoroquinolones is significantly higher than the cost of ABPs used in routine practice. In addition, the ban on the use of drugs of this group for the treatment of children and pregnant women remains.
Aminoglycosides Aminoglycosides show approximately the same tissue and plasma concentrations. When comparing the concentration of gentamicin in bronchial secretions on a biological model with intramuscular multiple, intramuscular single and intravenous bolus administration, the concentration of gentamicin in the bronchi reached the MIC level only with intravenous bolus administration. Aminoglycosides slowly accumulate in macrophages (ribosomes), but at the same time it loses its activity. In the study of vancomycin, it was shown that this antibiotic in the liquid covering the epithelium of the lower respiratory tract reaches the MIC90 value for the majority of Gy + - pathogens of respiratory infections. When conducting empirical antibiotic therapy, it seems rational to use combinations of drugs, which enhances the antimicrobial effect and allows you to fight a wider range of potential pathogens. It should be noted that the existing opinion about the inadmissibility of combining drugs with bacteriostatic and bactericidal action has been revised in relation to combinations of macrolides with cephalosporins. Tables 1-3 show the approach to the choice of antibiotic in various clinical situations, depending on the age and condition of the patient, the severity of pneumonia.
Literature
1. Chuchalin A.G. Pneumonia. - M., 2002.
2. A pragmatice guidlines for the managemant of community acquired
pneumonia in adults (in Process Citation). Clin. Inf. Dis. - 2000.
- Vol.31. - P.347.
3. Bartlett J. Management of Respiratory Tract Infections. -
Lippincott W. et Wilkins, 2001.
4. Brevis R.A.L. Lecture notes on respiratory diseases. - Blackwell
scientific publications, 1985.
5. Empiric Treatment of Community-acquired Pneumonia: ATS and IDSA
Guidelines American Thorac. Soc. - 2001.
6. Fein A. et al. Diagnosis and management of pneumonia and other
respiratory infections. - Professional Communications inc., 1999.
7. Inglis T.J.J. Clinical Microbiology. - Churchil Livingston, 1997.
8. Management of adult community-acquired lower respiratory tract
infections. Erohtan Study on Community Acquired Pneumonia (ESOCAP)
committee / Chairmen: Huchon G., Woodhead M. - 1999.
9. Mandel L.A. Community-acquired pneumonia. Etiology, epidemiology
and treatment. Chest. - 1995. - Vol.81. - P. 357.
10. Pneumonia. Ed. by A. Torres and M. Woodhead. - Eropian Respiratory
Monograph., 1997
11.Pulmonary Differential Diagnosis. Harold Zaskon. W.B.Saunders,
2000.
12. Bartlett JG, Gorbach SL, Tally FP, et al. Bacteriology and treatment
of primary lung abscess. Am Rev Respir Dis. 1974; 109: 510-518.
13. Huxley EJ, Viroslav J, Gray WR, et al. Pharyngeal aspiration in
normal adults and patients with depressed consciousness. Am J Med.
1978;64:564-568.
14. Driks MR, Craven DE, Celli BR, et al. Nosocomial pneumonia in
intubated patients given sucralfate as compared with antacids or histamine
type 2 blockers. N Engl J Med. 1987; 317: 1376-1382.
15. Tryba M. Risk of acute stress bleeding and nosocomial pneumonia
in ventilated intensive care unit patients: Sucralfate versus
antacids. Am J Med. 1987; 83 (Suppl 3B): 117-124.
16. Bartlett JG, Finegold SM. Anaerobic infections of the lung and
pleural space. Am Rev Respir Dis. 1974; 110: 56-77.
17. Finegold SM. Anaerobic Bacteria in Human Disease. New York:
Academic Press; 1977.
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Medicine (Baltimore). 1972; 51: 413-450.
Differential diagnosis of pneumonia and infiltrative pulmonary tuberculosis especially difficult with localization of pneumonia in the upper lobes and tuberculous lesions in the lower lobes.
Acute onset with high fever is twice as common in pneumonia. For tuberculosis, a gradual or asymptomatic onset of the disease is more indicative. The body temperature rises gradually, with a slight increase by 14-16 o'clock in the afternoon, the patient seems to be "overcoming".
The history of patients with pneumonia is characterized by repeated pneumonia, while patients with tuberculosis often have long-term colds, pleurisy, treatment with glucocorticoids, diabetes mellitus; contact with a tuberculosis patient, early tuberculosis; prolonged loss of appetite, weight loss.
Pneumonia is characterized by the rapid development of shortness of breath, cough, chest pain, and with tuberculosis, these symptoms increase gradually and are not so pronounced.
With pneumonia, facial flushing, cyanosis, and herpetic eruptions are noted. These phenomena are not observed in tuberculosis. Patients with tuberculosis are usually pale, they are characterized by profuse night sweats.
With pneumonia, the lower lobes are more often affected, with tuberculosis, the upper ones. According to the figurative expression of V. Vogralik, non-tuberculous lesions of the lungs are "heavy" - they tend to settle in the lower lobes. Tuberculosis is distinguished by its "lightness", float to the upper parts of the lungs.
For pneumonia, bright physical changes on the part of the respiratory system are more characteristic;
Leukocytosis with a shift of the leukocyte formula to the left and an increase in ESR is more common in pneumonia, and in tuberculosis - lymphocytosis.
In pneumonia, sputum is rich in pneumonic flora, while in tuberculosis, the flora is scarce, there are individual microbes. A pathognomonic sign of tuberculosis is the detection of mycobacterium tuberculosis in sputum, especially with repeated finds. The research is carried out many times.
Empiric therapy of pneumonia without the use of anti-tuberculosis drugs (rifampicin, streptomycin, kanamycin, amikacin, cycloserine, fluoroquinolones) helps the differential diagnosis. Usually, within 10-14 days of treatment, pneumonic infiltration undergoes significant positive changes or resolves completely, while with tuberculous infiltration, its resorption occurs within 6-9 months.
Radiological signs systematized by A.I. Borokhov and L.G. Dukov (1977) and presented in the form of a table:
X-ray differences between pneumonia and tuberculous infiltrate
Table 3
|
Signs |
Tuberculous infiltrate |
Pneumonia |
|
Preferential localization |
Upper lobe |
Lower lobe |
|
Rounded |
Wrong |
|
|
Blurry |
||
|
Shadow intensity |
Expressed | |
|
Seeding foci |
Characteristic (fresh soft shadows) |
Absent |
|
General background of pulmonary pattern |
Not changed | |
|
Path to the root of the lung |
Is characteristic |
Absent or poorly expressed |
|
Enlargement of the roots of the lungs |
Missing |
Characteristically, often bilateral |
|
Resorption dynamics |
6-9 months or more or lung tissue decay |
1-3 weeks |
It is also necessary to carry out differential diagnostics with the following diseases:
Lungs' cancer.
Lung infarction.
Pulmonary edema.
Eosinophilic infiltrate.
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Classification of pneumonia, causes, treatment
1. Classification
2. Etiology (reasons)
3. Lobar (lobar pneumonia)
4. Focal (bronchopneumonia)
5. Diagnosis of pneumonia
6. Differential diagnosis
7. Complications
8. Treatment of uncomplicated pneumonia
1. Classification of pneumonia
Pneumonia is an acute infectious and inflammatory disease, with focal lesions of the respiratory parts of the lungs, intraalveolar exudation, severe febrile reaction and intoxication.
1. Community-acquired pneumonia. It develops at home and is the most common form of pneumonia. Its causative agents are more often - pneumococci, streptococci, Haemophilus influenzae and other gram-positive microorganisms.
2. Nosocomial pneumonia (synonyms: hospital, nosocomial). It develops during the patient's stay in the hospital for another disease, but not earlier than 48-72 hours after hospitalization or 48 hours after discharge from the hospital.
3. Aspiration pneumonia occurs in patients with impaired consciousness (stroke, eclampsia, traumatic brain injury), as well as in the aspiration of food, vomit, foreign bodies, in violation of the cough reflex.
4. Pneumonia in persons with severe immunity defects (congenital immunodeficiency, HIV infection).
According to the clinical and morphological course of pneumonia:
1. Lobar (croupous) pneumonia is characterized by damage to an entire lobe (less often a segment) of the lung with involvement in the inflammatory process of the pleura;
1.acute onset with severe clinical manifestations
2.fibrinous nature of exudate
3. damage to alveolar tissue and respiratory bronchioles while maintaining airway patency
4.staging in the development of inflammation
2. Focal pneumonia (bronchopneumonia) is characterized by damage to a lobule or segment of the lung;
1. gradual onset and less pronounced clinical manifestations;
2. serous or mucopurulent nature of the exudate;
3. impaired airway patency;
4. there is no staging in the development of inflammation.
The severity of pneumonia is determined by the severity of clinical manifestations, and according to this they are distinguished:
1. Mild severity
Body temperature up to 38 ° C, respiratory rate (RR) up to 25 per minute, heart rate (HR) up to 90 per minute, mild intoxication and cyanosis, no complications or decompensation of concomitant diseases.
2. Moderate severity
Body temperature - 38-39 ° C, NPV 25-30 per minute, heart rate 90-100 per minute, a tendency to arterial hypotension, moderate intoxication and cyanosis, the presence of complications (pleurisy), decompensation of concomitant diseases is not expressed.
3. Severe severity
Body temperature above 39 ° C, NPV> 30 per minute, heart rate> 100 per minute, pronounced intoxication and cyanosis, blood pressure syst.<90 мм рт. ст, АД диаст. <60 мм рт.ст., наличие осложнений (эмпиема, инфекционно-токсический шок, токсический отек легких и др.), выраженная декомпенсация сопутствующих заболеваний.
2. Etiology(causespneumonia)
The etiology of pneumonia is associated with a typical microflora colonizing the upper respiratory tract, but only a few of them with increased virulence are capable of causing an inflammatory reaction when they enter the lower respiratory tract.
Typical bacterial pathogens:
Pneumococci Streptococcus pneumoniae
Haemophilus influenzae
Rare bacterial pathogens
Staphylococcus aureus Staphylococcus aureus;
Klebsiella and Escherichia coli Klebsiella pneumoniae, Escherichiacoli and other members of the Enterobacteriaceae family;
Pseudomonas aeruginosa Pseudomonas aeruginosa.
Atypical bacterial pathogens:
Mycoplasma Mycoplasma pneumoniae
Chlamydia Chlamydia pneumoniae;
Legionella Legionella pneumophila
Thus, the etiology of pneumonia is associated with the microflora of the upper respiratory tract, the composition of which depends on the environment in which the person is, his age and general health. Predisposing factors for pneumonia are children, old and old age, background bronchopulmonary diseases (bronchitis, bronchial asthma, COPD, etc.), pathology of ENT organs, previous pneumonia, smoking, etc. Contributing factors of pneumonia include exposure to cold, chest trauma, anesthesia, alcohol intoxication, drug addiction, surgery, etc.
Pathogenesis
There are four pathogenetic mechanisms that determine the development of pneumonia:
1. Aspiration of the contents of the oropharynx is the main route of infection of the respiratory parts of the lungs, and hence the main pathogenetic mechanism of the development of pneumonia.
2. Inhalation of microbial aerosol
3. Hematogenous spread of the pathogen from the extrapulmonary focus of infection (tricuspid endocarditis, septic endocarditis of the pelvic veins)
4. Direct spread of the pathogen from neighboring affected organs (liver abscess, mediastinitis) or as a result of infection with penetrating chest wounds
Symptomscommunity-acquiredpneumonia
The clinical manifestations of community-acquired pneumonia depend on the etiology of the process, the patient's age, the severity of the disease, and the presence of concomitant pathology. The most significant causative agents of pneumonia are:
Pneumococcal pneumonia
The most common causative agent of community-acquired pneumonia for all age groups is pneumococcus (30-50% of cases). Pneumococcal pneumonia manifests itself usually in two classic variants: lobar (lobar) pneumonia and focal (bronchopneumonia).
The disease usually begins acutely with fever, chills, cough with scanty sputum, often with severe pleural pain. At first, the cough is unproductive, however, soon there is a typical "rusty" sputum, sometimes mixed with blood.
On physical examination, there is a dullness of the pulmonary sound, bronchial breathing, crepitus, moist fine bubbling rales, pleural friction noise.
The most common complications are parapneumonic pleurisy, acute respiratory and vascular insufficiency.
Streptococcal pneumonia
The causative agent is β-hemolytic streptococcus, and the disease often develops after a viral infection (measles, influenza, etc.), has a severe course and is often complicated by sepsis. It is characterized by high fever with large daily fluctuations, repeated chills and sweats, stitching pain in the side of the affected side, streaks of blood appear in the sputum. In a febrile period, polyarthralgias are often noted.
Typical complications of this pneumonia are exudative pleurisy (70% of patients) and abscess formation. Mortality reaches 54%.
Staphylococcal pneumonia
Caused by Staphylococcus aureus, it is often associated with influenza A and B epidemics and other respiratory viral infections.
This pathogen is characterized by a peribronchial lesion with the development of a single or multiple lung abscesses.
The disease begins acutely, proceeds with pronounced symptoms of intoxication, fever, repeated chills, shortness of breath, cough with purulent sputum. Pneumonia is usually multifocal, the development of new foci, as a rule, is accompanied by another rise in temperature and chills. With subpleural localization of the abscess, it can drain into the pleural cavity with the formation of pyopneumothorax.
Viral pneumonia
It is more often caused by influenza A and B viruses, parainfluenza, adenoviruses. Pneumonia is characterized by pathogenetic features - the inflammatory process begins with pronounced edema of the mucous membrane of the bronchi, peribronchial space and alveoli, and is also complicated by the development of thrombosis, necrosis and bleeding. The disease begins with fever, chills, myalgia, conjunctivitis, sore throat, and dry cough. With the development of pneumonia, shortness of breath, separation of purulent-hemorrhagic sputum join the usual symptoms of influenza. Confusion of consciousness up to delirium often develops. Primary viral pneumonia from the 3-5th day from the onset of the disease becomes viral-bacterial. Auscultation in the lungs is characterized by alternation of foci of hard or weakened breathing, dry wheezing with foci of crepitus, moist wheezing.
Also observed:
Haemophilus Daddy Pneumonia
Klebsiella pneumonia (Friedlander pneumonia)
Mycoplasma pneumonia
Hemorrhagic pneumonia.
Physicalmethodsdiagnostics
Suspicion of pneumonia should arise if the patient has a fever in combination with complaints of cough, shortness of breath, sputum production and / or chest pain. At the same time, an atypical onset of pneumonia is possible, when the patient complains of unmotivated weakness, fatigue, and heavy sweating at night. In elderly patients with concomitant pathology, in drug addicts, against the background of alcohol intoxication, extrapulmonary symptoms (drowsiness, confusion, anxiety, disturbed sleep and wakefulness cycle, impaired appetite, nausea, vomiting, signs of decompensation of chronic diseases of internal organs) often prevail over bronchopulmonary.
3.Kruse(dolepneumonia)
Symptoms
The information obtained during the physical examination of the patient depends on the severity of the disease, the prevalence of the inflammation focus, age, concomitant diseases and, above all, on the morphological stage of development of lobar pneumonia.
The tide stage (1-2 days) is characterized by a sharp chill, high body temperature (39-40 ° C), shortness of breath, increasing symptoms of intoxication, chest pain associated with breathing, the appearance of a dry, painful cough. On examination, the patient lies on his back or sore side, pressing his hands on the area of the chest where the pain is most pronounced. This position somewhat reduces chest excursion and pain. The skin is hot, on the cheeks a febrile blush, acrocyanosis, redness of the sclera of the eyes, more on the affected side. If lobar inflammation of the lung is accompanied by a viral infection, then herpetic eruptions are noted on the lips, wings of the nose and earlobes. In severe pneumonia, cyanosis of the lips, tip of the nose, and earlobes is noted, which is associated with an increase in respiratory failure and impaired hemodynamics.
There is a lag of the sore side of the chest in the act of breathing, although the symmetry of the chest is still preserved. On palpation, local soreness of the chest is determined, associated with inflammation of the parietal pleura, a slight increase in voice tremor and bronchophonia on the affected side due to compaction of the lung tissue. With percussion - there is a dullness (shortening) of the percussion sound with a tympanic shade.
With auscultation - in the projection of the affected lobe of the lung, weakened vesicular breathing and crepitus are heard. In the initial stage of lobar pneumonia, the alveoli only partially retain their airiness, the inner surface of their walls and bronchioles is lined with viscous fibrinous (inflammatory) exudate, and the walls themselves are edematous and rigid. During most of the inhalation, the alveoli and bronchioles are in a collapsed state, which explains the weakening of vesicular respiration. To straighten the adhered walls of the alveoli, a higher pressure gradient in the pleural cavity and upper respiratory tract is required than normal, and this is achieved only by the end of inspiration. During this period, the walls of the alveoli containing exudate break apart, and a specific sound occurs - initial crepitation (crepitatioindux). In sound, it resembles wet fine bubbling rales, but differs in that it occurs only at the height of a deep breath and does not change when coughing.
The stage of hepatization (5-10 days - the height of the disease) is characterized by the persistence of high fever, symptoms of intoxication, the appearance of a cough with the separation of "rusty" and mucopurulent sputum, an increase in signs of respiratory and sometimes cardiovascular insufficiency. On examination, for several days from the onset of the disease, the patient's forced position on the sore side, associated with the involvement of the pleura in the inflammatory process, as well as facial hyperemia and reddening of the sclera on the affected side, may persist. With a severe degree of pneumonia, cyanosis increases, due to an increase in ventilation respiratory failure. Breathing is frequent (25-30 or more in 1 minute) and shallow. When two or more lobes of the lung are involved in the process - tachypnea, dyspnea of the inspiratory type (exhalation is difficult), participation in the act of breathing of auxiliary muscles, swelling of the wings of the nose, etc. The lag in the act of breathing of the sick half of the chest is clearly noted. Vocal tremor and bronchophonia are enhanced on the affected side. With percussion - a pronounced dullness of the percussion sound over the affected area. On auscultation, weakened vesicular breathing is replaced by hard, bronchial breathing, crepitus is not heard. For several days, a pleural friction noise is heard over the affected area.
The stage of resolution (from the 10th day) with an uncomplicated course of pneumonia is characterized by a decrease in body temperature, a decrease in symptoms of general intoxication, cough, and respiratory failure. With percussion - dullness of the percussion sound with a tympanic tone, which is gradually replaced by a clear pulmonary sound. On auscultation - weakened vesicular respiration and at the end of inhalation, when the alveoli and bronchioles are "separated", the final crepitus (crepitatioredux) is heard. As the exudate is removed from the alveoli and the edema of their walls disappears, the elasticity and airiness of the lung tissue is restored, vesicular breathing is heard over the lungs, crepitus disappears.
4. Focal(bronchopneumonia)
Symptoms
It has a less acute and prolonged onset. It often arises as a complication of a previous acute respiratory viral infection, acute or exacerbation of chronic bronchitis. Within several days, the patient notes an increase in body temperature to 37.5-38.5 ° C, runny nose, malaise, weakness, cough with mucous or mucopurulent sputum. Against this background, it is difficult to diagnose bronchopneumonia, but the lack of effect of treatment, an increase in intoxication, the appearance of shortness of breath, tachycardia speaks in favor of focal pneumonia. Gradually, the patient's cough and the separation of mucopurulent or purulent sputum intensify, weakness, headache increase, appetite decreases, body temperature rises to 38-39 ° C. On examination, hyperemia of the cheeks, cyanosis of the lips are determined, the skin is moist. Sometimes pallor of the skin is noted, which is explained by severe intoxication and a reflex increase in the tone of peripheral vessels. The chest on the side of the lesion lags only slightly behind in the act of breathing. With percussion, a dullness of the percussion sound is noted above the lesion, but with a small focus of inflammation or its deep location, lung percussion is not informative. On auscultation, a pronounced weakening of vesicular breathing is heard over the affected area, due to a violation of bronchial patency and the presence of a multitude of microatelectasis in the focus of inflammation. The most reliable auscultatory sign of focal pneumonia is listening to sonorous moist fine bubbling rales over the affected area throughout the entire inhalation. These wheezing is due to the presence of an inflammatory exudate in the airways. When involved in the inflammatory process of the pleura, a pleural friction noise is heard.
Thus, the most significant clinical signs that distinguish focal bronchopneumonia from lobar (lobar) pneumonia are:
· Gradual onset of the disease, developing, as a rule, against the background of acute respiratory viral infections or exacerbation of chronic bronchitis.
· Cough with discharge of mucopurulent sputum.
· Absence of acute pleural chest pain.
· Lack of bronchial breathing.
· The presence of moist sonorous fine bubbling rales.
5. Diagnosticspneumonia
Based on patient complaints, history data and physical examination methods.
In a general blood test, leukocytosis is detected, blood biochemistry can determine an increase in liver enzymes, creatinine, urea, changes in the electrolyte composition. Microscopic examination of sputum and blood serology make it possible to verify the causative agent of pneumonia.
Instrumental methods: X-ray examination of the lungs in two projections. Evaluate the presence of infiltration, pleural effusion, destruction cavities, the nature of darkening: focal, confluent, segmental, lobar or total.
6. Differentialdiagnosticspneumonia
etiology pathogenesis diagnosis pneumonia
The main nosologies requiring differential diagnosis with pneumonia are the following:
Acute respiratory viral infections (ARVI)
· Intercostal neuralgia
· Pulmonary tuberculosis
Acute diseases of the abdominal organs
Acute myocardial infarction
Acute respiratory viral infections
The absence of seasonality in pneumonia (which is more typical for ARVI), the presence of a fever superior to that in ARVI, the results of a physical examination obtained with careful percussion and auscultation - shortening of the percussion sound, foci of crepitus and / or moist fine bubbling rales.
· Intercostal neuralgia
The misdiagnosis of "intercostal neuralgia" is one of the most common causes of underdiagnosis of pneumonia. For the correct diagnosis of pneumonia, it is important to take into account the peculiarities of the pain syndrome: if with pneumonia, pain is usually associated with breathing and coughing, then with intercostal neuralgia, it increases with turns of the body, movements of the hands. Palpation of the chest reveals areas of cutaneous hyperalgesia.
· Pulmonary tuberculosis
To verify the diagnosis of tuberculosis, it is necessary, first of all, to use well-known diagnostic methods, such as anamnestic data (the patient has a history of tuberculosis of any localization, information about past diseases, such as exudative pleurisy, prolonged subfebrile condition of unclear genesis, unexplained malaise at night, profuse sweating weight loss, prolonged cough with hemoptysis). Such physical data as the localization of pathological percussion sounds and auscultatory data in the upper parts of the lungs are of diagnostic value.
The leading role in the diagnosis of tuberculosis belongs to X-ray research methods, incl. CT, MRI, microbiological research.
Lung cancer, lung metastases
Anamnestic data (smoking, working with carcinogenic substances such as heavy metals, chemical dyes, radioactive substances, etc.) are of great importance in the diagnosis of lung cancer. In the clinical picture of lung cancer, there is a persistent cough, a change in the timbre of the voice, the appearance of blood in sputum, weight loss, lack of appetite, weakness, chest pain. Final verification of the diagnosis is possible on the basis of sputum examination for atypical cells, pleural exudate, tomography and / or CT of the lungs, diagnostic bronchoscopy with biopsy of the bronchial mucosa.
Congestive heart failure
In patients with left ventricular failure, which is a complication of ischemic heart disease, arterial hypertension, heart disease, cardiomyopathy, asthma attacks, as a rule, occur at night. Patients wake up from a painful hacking cough and a feeling of suffocation. At the same time, bilateral moist rales are heard, mainly over the lower parts of the lungs. A simple technique allows differentiating the origin of wheezing: the patient is offered to lie on his side and auscultation is repeated after 2-3 minutes. If at the same time the number of wheezing decreases over the overlying parts of the lungs and, on the contrary, increases over the underlying ones, then with a greater degree of probability these wheezes are due to congestive heart failure. In acute pulmonary pathology, ECG is noted - signs: P-pulmonale (overload of the right atrium); right bundle branch block; high R waves in the right chest leads. Acute diseases of the abdominal organs. When pneumonia is localized in the lower parts of the lungs, the pain syndrome often spreads to the upper abdomen. The severity of abdominal pain, sometimes combined with other gastrointestinal disorders (nausea, vomiting, dyspepsia), often causes misdiagnosis in patients with pneumonia, acute diseases of the abdominal organs (cholecystitis, perforated ulcer, acute pancreatitis, impaired intestinal motility). In such cases, the diagnosis of pneumonia is helped by the absence of abdominal muscle tension and symptoms of peritoneal irritation in patients.
Acute cerebrovascular accident (ACVI)
Symptoms of CNS depression - drowsiness, lethargy, confusion, up to stupor, developed in severe pneumonia, can cause an erroneous diagnosis of stroke and hospitalization of patients in the neurological department. At the same time, when examining such patients, as a rule, there are no symptoms characteristic of stroke, such as paresis, paralysis, pathological reflexes, and the reaction of the pupils is not disturbed.
Acute myocardial infarction
With left-sided localization of pneumonia, especially in patients with involvement in the inflammatory process of the pleura, the development of severe pain syndrome is possible, which can lead to an erroneous diagnosis of "Acute myocardial infarction". To differentiate pleural pain, it is important to assess its relationship with breathing: pleural pain increases with inspiration. To reduce pain, patients often assume a forced position on their side, on the affected side, which reduces the depth of breathing. In addition, the genesis of coronary pain is usually confirmed by characteristic changes in the electrocardiogram.
Pulmonary embolism (PE)
The acute onset of the disease, observed in particular with pneumococcal pneumonia, is also characteristic of thromboembolism in the pulmonary artery system (PE): shortness of breath, dyspnea, cyanosis, pleural pain, tachycardia and arterial hypotension up to collapse. However, along with severe shortness of breath and cyanosis in pulmonary embolism, swelling and pulsation of the cervical veins are observed, the borders of the heart are displaced outward from the right edge of the sternum, pulsation often appears in the epigastric region, accent and bifurcation of the II tone above the pulmonary artery, and gallop rhythm. Symptoms of right ventricular failure appear - the liver enlarges, its palpation becomes painful. ECG - signs of overload: right atrium: P - pulmonale in leads II, III, AVF; right ventricle: McGin-White sign or SI-QIII syndrome.
7. Complicationspneumonia
Diagnostic and therapeutic tactics of managing patients with community-acquired pneumonia is determined by the presence or absence of complications. Common complications include:
Acute respiratory failure
Pleurisy
Broncho-obstructive syndrome
Acute vascular insufficiency (collapse)
Acute respiratory distress syndrome (noncardiogenic pulmonary edema)
Infectious toxic shock
Sharprespiratoryfailure(ONE)
This is one of the main manifestations of the severity of pneumonia and can develop from the first hours after the onset of the disease in 60-85% of patients with severe pneumonia, and more than half of them need artificial ventilation. The severe course of pneumonia is accompanied by the development of a predominantly parenchymal (hypoxemic) form of respiratory failure. The clinical picture of ARF is characterized by a rapid increase in symptoms and the involvement of vital organs in the pathological process - the central nervous system, heart, kidneys, gastrointestinal tract, liver and the lungs themselves. Shortness of breath is one of the first clinical signs, while rapid breathing (tachypnea) is accompanied by an increasing sensation of respiratory discomfort (dyspnea). As ARF increases, a pronounced tension of the respiratory muscles is noticeable, which is fraught with fatigue and the development of hypercapnia. The increase in arterial hypoxemia is accompanied by the development of diffuse cyanosis, reflecting a rapid increase in the content of unsaturated hemoglobin in the blood. In severe cases, with SaO2 values<90%, цианоз приобретает сероватый оттенок. Кожа при этом становится холодной, часто покрывается липким потом. При тяжелой дыхательной недостаточности важно оценить динамику выраженности цианоза под влиянием оксигенотерапии - отсутствие изменений свидетельствует о паренхиматозном характере ОДН, в основе которой лежат выраженные вентиляционно-перфузионные расстройства. Отрицательная реакция на ингаляцию кислорода указывает на необходимость перевода больного, на искусственную вентиляцию легких (ИВЛ). ОДН на начальных стадиях сопровождается тахикардией, отражающей компенсаторную интенсификацию кровообращения. С развитием декомпенсации и дыхательного ацидоза нередко развивается брадикардия - весьма неблагоприятный признак, сопровождающийся высоким риском летального исхода. При тяжелой дыхательной недостаточности нарастает гипоксия ЦНС. Больные становятся беспокойными, возбужденными, а по мере прогрессирования ОДН развивается угнетение сознания и кома.
Treatment. It is necessary to ensure normal gas exchange in the lungs with the achievement of Sa02 above 90%, and PaO2> 70-75 mm Hg. and normalization of cardiac output and hemodynamics. To improve oxygenation, oxygen is inhaled, and if the effectiveness of oxygen therapy is insufficient, respiratory support in the ventilator mode is indicated. In order to normalize hemodynamics, infusion therapy is carried out with the addition of glucocorticoid hormones and vasopressor amines (dopamine).
Pleurisy
Pleurisy is one of the most frequent complications of community-acquired pneumonia and more than 40% of pneumonia is accompanied by pleural effusion, and with massive accumulation of fluid, it becomes of leading importance in the clinic of the disease. The onset of the disease is characterized by the appearance of acute intense chest pain associated with breathing. Shortness of breath often takes on the character of suffocation. In the early stages of fluid accumulation, there may be a paroxysmal dry ("pleural") cough. On examination - restriction of respiratory movements, the intercostal spaces are wider, the lag of the affected half of the chest in the act of breathing. With percussion - above the zone of effusion, the percussion sound is shortened, and the upper border of dullness has a characteristic form of an arched curve (Damoiseau's line), weakening of voice tremor. On auscultation - weakened vesicular breathing. With a significant amount of fluid in the lower parts of the pleural cavity, respiratory noises are not carried out, and in the upper (in the zone of lung collapse) breathing sometimes takes on a bronchial character. With percussion, signs of displacement of the mediastinum in the opposite direction can be detected, which is confirmed by a change in the boundaries of cardiac dullness.
Treatment. For relief of pleural pain and inflammation, non-steroidal anti-inflammatory drugs are indicated, in particular, lornoxicam.
Broncho-obstructivesyndrome
This syndrome is typical for patients with community-acquired pneumonia, which developed against the background of chronic obstructive pulmonary disease (COPD).
The main symptoms of broncho-obstructive syndrome:
· Cough - persistent or worsening periodically, usually productive;
Shortness of breath, the severity of which depends on the severity of the pneumonia and the severity of bronchial obstruction.
On auscultation, dry wheezing rales are heard over the entire surface of the lungs against the background of an elongated exhalation. Moist wheezing, as a rule, is limited to the area of inflammatory infiltration. The severity of bronchial obstruction is detected when assessing exhalation, which is much longer than inhalation, as well as using expiratory tests. The study of the function of external respiration, in particular, a simple technique of peak flowmetry, allows you to determine the severity of obstructive ventilation disorders.
Treatment. An effective drug for eliminating broncho-obstructive syndrome in patients with pneumonia is the combined drug Berodual. Berodual can be used both in the form of metered aerosols and in the form of solutions through a nebulizer - in a dose of 1-2 ml (20-40 drops) in a dilution of sodium chloride 0.9% - 3 ml. Patients in whom edema of the bronchial mucosa prevails in the pathogenesis of broncho-obstructive syndrome, which is especially characteristic of COPD, a good result is achieved by combination therapy through a nebulizer: 20-25 drops of berodual in combination with a corticosteroid budesonide (pulmicort) at a starting dose of 0.25-0.5 mg ... In the absence or insufficient effectiveness of inhaled drugs, it is possible to use theophyllines, in particular, intravenous administration of 5-10 ml of 2.4% aminophylline solution slowly, as well as intravenous injections of prednisolone 60-120 mg. It is advisable to evaluate all the noted measures to eliminate bronchial obstruction by dynamic control of the peak flowmetry results. Oxygen therapy has a positive effect on lung function and hemodynamics of the pulmonary circulation (increased pressure in the pulmonary artery decreases), however, patients with COPD need to be careful, because inhalation of high concentrations of oxygen in the inhaled air is fraught with the development of hypercapnic coma and respiratory arrest. In such patients, the recommended oxygen concentration in the inhaled air is 28-30%. The result of oxygen therapy is assessed by pulse oximetry. It is necessary to achieve an increase in Sa02 of more than 92%.
Sharpvascularfailure(collapse)
Patients complain of severe headache, general weakness, dizziness, aggravated by a change in body position. In the supine position, a decrease in systolic blood pressure to a level of less than 90 mm Hg is usually determined. Art. or a decrease in the usual systolic blood pressure for the patient by more than 40 mm Hg. Art., and diastolic blood pressure less than 60 mm Hg. Art. Such patients may experience severe fainting when trying to sit or stand. Vascular insufficiency in pneumonia is caused by dilatation of peripheral vessels and a decrease in BCC due to the transfer of fluid from the vascular bed to the extracellular space. Emergency care for arterial hypotension begins with giving the patient a position with a lowered head and a raised leg end. With severe pneumonia and arterial hypotension (BP<90/60 мм рт.ст.) необходимо восполнение потери жидкости: у больных с лихорадкой при повышении температуры тела на 1°С количество жидкости в организме уменьшается на 500 мл /сутки.
Treatment. Jet intravenous drip injection of 0.9% sodium chloride solution 400 ml or 5% glucose solution 400 ml. Antipyretic drugs should not be prescribed until blood pressure normalizes, as this can lead to aggravation of arterial hypotension. With persisting arterial hypotension - but only after replenishing the BCC, the use of vasopressor amines is indicated until systolic blood pressure reaches 90 - 100 mm Hg. Art .: Dilute 200 mg of dopamine in 400 ml of 0.9% sodium chloride solution or 5% glucose solution and inject intravenously drip at 5-10 μg / kg per minute. The drip infusion should not be stopped abruptly; a gradual decrease in the rate of administration is necessary. To eliminate increased permeability of the vascular endothelium, glucocorticoid hormones are used - prednisolone in an initial dose of 60-90 mg (up to 300 mg) intravenously.
Spicyrespiratorydistress syndrome(ARDS,noncardiogenicedemalungs)
ARDS most often develops within the first 1–3 days after the onset of pneumonia. In the acute exudative phase of ARDS, the patient is worried about excruciating shortness of breath, dry cough, discomfort in the chest, palpitations. After a while, shortness of breath increases and turns into dyspnea. If the exudate enters the alveoli (alveolar pulmonary edema), suffocation increases, a cough appears with a frothy sputum, sometimes pinkish in color. On examination, the patient is agitated, takes a forced semi-sitting position (orthopnea). Diffuse, gray cyanosis appears and rapidly grows due to progressive impairment of oxygenation in the lungs. The skin is moist, the body temperature is elevated. Breathing, regardless of the genesis of ARDS, is speeded up, auxiliary muscles are involved in the act of breathing, for example, retraction of the intercostal spaces and supraclavicular fossae during inhalation, inflation of the wings of the nose. With percussion, there is a slight shortening of the percussion sound in the posterior-lower parts of the chest. On auscultation, in the same place, against the background of weakened breathing, crepitus is heard symmetrically on both sides, and then a large number of moist finely - and medium-sized bubbling rales, which spread to the entire surface of the chest. In contrast to the auscultatory manifestations of pneumonia, wheezing in ARDS is heard diffusely on symmetrical areas of the lungs on both sides. In severe cases of alveolar pulmonary edema, noisy breathing and large bubbling, moist rales can be heard from a distance (bubbling breathing). Deaf heart sounds, heart rate 110-120 in 1 min. Blood pressure is lowered, pulse is rapid, may be arrhythmic, low filling. In the terminal stage of acute respiratory distress syndrome, signs of multiple organ failure may appear due to the effect of systemic inflammation on the internal organs, and the functions of the kidneys, liver, and brain are impaired. Pulmonary edema that develops in pneumonia is a noncardiogenic pulmonary edema. In this case, transcapillary filtration increases not due to an increase in hydrostatic pressure, but mainly due to increased vascular permeability. The accumulated fluid and protein in the interstitial tissue enter the alveoli, which leads to an increasing deterioration in the diffusion of oxygen and carbon dioxide. As a result, patients develop signs of acute respiratory distress syndrome. The main clinical manifestations of pulmonary edema in pneumonia are cough and shortness of breath. In contrast to cardiogenic pulmonary edema, shortness of breath in patients with ARDS develops into a feeling of suffocation.
On auscultation, moist rales are heard over the entire surface of the lungs, oxygen saturation drops sharply (Sa02< 90%), нарастает артериальная гипотензия. Интенсивная терапия направлена на нормализацию повышенной проницаемости альвеоло-капиллярной мембраны и улучшение газообмена. Для устранения высокой проницаемости стенки капилляров легких и блокирования мембраноповреждающих факторов воспаления (интерлейкины, фактор некроза опухоли и др.) применяют глюкокортикоидные гормоны - преднизолон внутривенно болюсно 90-120 мг (до 300 мг) или метилпреднизолон из расчета 0,5-1 мг/кг (суточная доза 10-20 мг/кг массы тела).
An important element of the pathogenetic therapy of ARDS is adequate oxygen therapy, which begins with the inhalation of 100% humidified oxygen through a nasal catheter 6-10 L / min. In the absence of an effect and an increase in hypoxemia, it is necessary to transfer the patient to artificial ventilation. At present, it is considered inappropriate to increase oxygen delivery to tissues in patients with acute respiratory distress syndrome using inotropic amines (dopamine). The exception is cases where there are signs of heart failure, and a decrease in cardiac output is associated not with the development of hypovolemia, but with a decrease in the contractility of the heart muscle.
Infectious toxicshock
The number of patients with severe pneumonia complicated by infectious-toxic shock can reach 10%. Most often, infectious-toxic shock is caused by gram-negative flora, while the mortality rate reaches 90%. The so-called "cold" or "pale" shock develops, which is based on the high permeability of the vascular wall, and a massive release of the liquid part of the blood into the interstitial space with a sharp decrease in the BCC. The second component of "cold" shock is widespread peripheral vasospasm. Clinically, this type of shock is characterized by an extremely serious condition with impaired consciousness, pallor of the skin, a threadlike pulse and a decrease in blood pressure below critical values. In one third of patients, shock is the result of exposure to gram-positive flora, with a mortality rate of 50-60%. Such patients develop a so-called "warm shock" with peripheral vasodilation, blood deposition and decreased venous return to the heart. Clinically, this variant of shock is also manifested by arterial hypotension, however, the skin is warm, dry, cyanotic. Thus, as a result of the effect of pneumonia pathogens on the vascular system, hypovolemic shock develops, characterized by a decrease in BCC, cardiac output, CVP (pressure in the right atrium) and filling pressure of the left ventricle. In severe cases, if the toxic effect of microorganisms continues, hypoxia of organs and tissues, aggravated by respiratory failure and hypoxemia, leads to the development of fatal microcirculation disorders, metabolic acidosis, disseminated intravascular coagulation syndrome and a sharp impairment of vascular permeability and function of peripheral organs.
On examination - a sharp pallor of the skin and visible mucous membranes, acrocyanosis, the skin is moist and cold. When examining patients, characteristic signs of shock are revealed:
Tachypnea;
Increasing hypoxemia (Sa02< 90%);
Tachycardia> 120 beats per minute, threadlike pulse;
Reduction of systolic blood pressure to 90 mm Hg. Art. and below;
Significant decrease in pulse blood pressure (up to 15-20 mm Hg);
Deafness of heart sounds;
Oliguria.
In severe cases, it is possible to develop stupor and even coma. Cold, moist, pale skin takes on an earthy gray hue, which is an indicator of severe peripheral circulatory disorders. Body temperature drops below 36 ° C, shortness of breath increases, NPV increases to 30-35 per minute. Pulse threadlike, frequent, sometimes arrhythmic. Heart sounds are muffled. Systolic blood pressure is not higher than 60-50 mm Hg. Art. or not defined at all. Intensive care is a complex of urgent measures, the algorithm of which depends on the type and severity of shock. First of all, it is important to start antibacterial therapy in a timely manner, using drugs with the widest spectrum of action - ceftriaxone 1.0 g. intravenously diluted with 10 ml of 0.9% sodium chloride solution. Due to the high frequency of hypoxemic respiratory failure, patients with infectious toxic shock usually need respiratory support - non-invasive mechanical ventilation with oxygen therapy, and with the development of tachypnea (NPV above 30 / min), tracheal intubation and mechanical ventilation should be planned. In order to block the systemic inflammatory reaction, glucocorticoid hormones are used - prednisolone at the rate of 2-5 mg / kg of body weight intravenously. Infusion therapy involves the intravenous administration of saline solutions such as chlosalt, acesol, trisol 400 ml intravenously with dopamine 200 mg under the control of blood pressure. Free radical oxidation of lipids and proteins, expressed in infectious-toxic shock, requires an increase in antioxidant protection. For this purpose, it is recommended to administer ascorbic acid at the rate of 0.3 ml of 5% solution per 10 kg of body weight intravenously.
8. Treatmentuncomplicatedpneumonia
Uncomplicated community-acquired pneumonia can be treated on an outpatient basis, under the supervision of polyclinic doctors. However, in recent years, patients with any form of pneumonia are trying to be hospitalized in a hospital.
Bed rest is necessary in the first days of the disease, diet therapy is easily digestible, with a sufficient amount of vitamins and free fluid, restriction of carbohydrates. Antipyretic drugs are prescribed with a significant increase in temperature, which violates the general condition of the patient. At a body temperature of up to 38 ° in patients without severe concomitant pathology, the appointment of antipyretics is not justified. With concomitant bronchitis - the appointment of expectorants, bronchodilators. Breathing exercises.
Etiotropic therapy consists of antibiotic therapy. Amoxiclav or antibiotics from the macrolide and cephalosporin groups are prescribed. The duration of treatment is usually 10-14 days.
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Pneumonia as a group of infectious diseases, the main morphological substrate of which is inflammatory exudate in the respiratory parts of the lungs. Types of pneumonia and their distinguishing features, clinical symptoms and X-ray picture.
Lung diseases of various origins have similar symptoms. It takes time to carry out microbiological examinations and X-ray images, which, unfortunately, is very short for the doctor and the patient. In conditions when it is required to make a quick correct decision, the physician's ability to determine the cause of the disease from clinical and anamnestic data comes to the fore. For this purpose, methods of differential diagnosis have been developed.
First of all, pneumonia is differentiated from:
- tuberculosis;
- pulmonary embolism (PE);
- tumor lesions;
- allergic reactions to medications;
- psittacosis;
- allergic pneumonitis;
- sarcoidosis;
- collagenosis.
The health care provider begins by examining the patient and interviewing his environment. The goal is to find out the background against which the disease has developed. The presence of concomitant diseases (cancer, tuberculosis, diabetes, HIV, treatment with glucocorticosteroids or cytostatics) is established, living conditions are assessed, contacts with sick people and animals are identified.
At the next stage, the doctor compares the information received about body temperature, chills, the presence of headaches, impaired consciousness, the nature of the cough, shortness of breath, rapid breathing, pain, the type of phlegm. In the differential diagnosis of pneumonia, it is important to take into account the patient's age.
The initial diagnosis and prescription of treatment is based on the results of the examination, and only after the analysis of blood and sputum, an X-ray examination, the therapist makes a final conclusion.
Differences between inflammation and other lung diseases
- Differential diagnosis of pneumonia and tuberculosis
The course of some forms of tuberculosis in the initial stage is very similar to the clinical picture of bacterial pneumonia. However, it should be remembered that the onset of tuberculosis is almost asymptomatic. Patients complain of fatigue, slight malaise (as a result of intoxication), coughing, sweating. At this stage, on x-ray examination, lung damage is already evident. Experienced doctors say: "Tuberculosis is more visible than heard."
Bacterial pneumonia is characterized by a pronounced onset with chills, an increase in temperature above 38.5 degrees. The skin of such a patient is dry and hot, and perspiration is observed only at the time of the crisis. Sputum with pneumonia - with air bubbles, more viscous than with tuberculosis.
Tuberculosis on an X-ray image looks like clear, rounded polymorphic foci, more often in the upper lobe. A blood test for pneumonia reveals pronounced leukocytosis, and for tuberculosis - lymphopenia and moderate leukocytosis. Microbiological examination of sputum reveals mycobacterium tuberculosis.
Only 5% of TB patients benefit from treatment with broad-spectrum antibiotics. Therefore, if the symptoms of pneumonia in a person persist for more than 2 weeks, then the diagnosis should be clarified. This is probably tuberculosis. At the same time, in empiric therapy of pneumonia, it is not recommended to prescribe broad-spectrum anti-tuberculosis drugs.
- Differential diagnosis of pneumonia and lung cancer
Cough, phlegm, pain and hemoptysis can accompany the growth of metastases in the pleura. Until this point, lung cancer is asymptomatic, but it can be detected on an x-ray. In this case, peripheral cancer is located more often in the anterior upper lobes of the lung, its contours are radiant.
Cancer cells can invade other organs or appear in the lungs as metastases. For more details on the differences between acute pneumonia, tuberculosis and lung cancer, see Table 1.
Table 1. Differential diagnosis of pneumonia and tuberculosis.
| Sign | Focal pneumonia | Peripheral lung cancer | Tuberculosis |
|---|---|---|---|
| Age | At any age, but more often in people under 50 | More often in people over 50 | At any age |
| Floor | Equally often in men and women | More common in male smokers | More often in men |
| Onset of the disease | Usually acute with fever | May be imperceptible or as the temperature rises | Acute, subacute with few symptoms |
| Cough | In the beginning it may not be | Often absent | Dry or coughing |
| Dyspnea | With a large lesion of the lung tissue | May be absent | With extensive damage to the lung tissue |
| Hemoptysis | Rarely | Rarely | Often |
| Chest pain | Occur when the pleura is involved | Possible | More often absent |
| Intoxication | Not expressed | Often not expressed | Pronounced, progressing continuously |
| Physical data | Expressed brightly: the nature of breathing changes and moist wheezing appears | Little or no | Little or no |
| Laboratory data | Leukocytosis, an increase in ESR, which decrease after the resolution of pneumonia | Moderate increase in ESR with a normal number of leukocytes | Usually ESR and leukocyte count do not change |
| X-ray data | Sharply expressed, the lower lobes are more often affected, the focal shadows are homogeneous, the borders are vague, increased pulmonary pattern, an increase in the roots of the lung | Initially, the tumor shadow is low-intensity with indistinct contours and "antennae" | Localization is more often in the upper lobe, the foci are polymorphic, have different ages with clear contours, there may be a "path" to the root and foci of seeding |
| Antibiotic effect | Expressed, reverse development of the process after 9-12 days | There is no or false positive dynamics, but changes during X-ray examination persist | Missing; radiological changes persist for a long time |
Differential diagnosis of pneumonia and pulmonary embolism (PE) Prolonged bed rest after surgery, hip fractures, with atrial fibrillation can lead to thrombophlebitis of the lower extremities. The consequence is often pulmonary thromboembolism. In young women, this problem sometimes occurs after taking oral contraceptives.
The characteristic features of PE, in addition to the background, are:
- cyanosis;
- shortness of breath;
- arterial hypotension;
- tachycardia.
When listening, the doctor detects a pleural friction noise and a weakening of breathing. X-rays show a triangular shadow, and perfusion radioisotope scans show ischemic "cold" zones. In this case, there is an acute overload of the right heart.
- Differential diagnosis of pneumonia and eosinophilic infiltrate
When treated with glucocorticosteroids, infiltrates disappear after 10 days.
The nature of the pneumonia present will indicate its source. Pneumococcal acute pneumonia is accompanied by chills, high fever, headache. If germs enter the bloodstream, chills can be severe, especially in children. Elderly people do not have such a reaction.
For bacterial damage to the lungs, burning pains when breathing in the chest are characteristic. With a viral and mycoplasma infection, these symptoms are not observed, but a headache is expressed, a rash is possible.
The nature of the sputum:
- bacterial pneumonia - mucopurulent, thick;
- viral and mycoplasma - a small amount;
- lung abscess - purulent odor;
- pulmonary edema - profuse, frothy, pink;
- lobar pneumonia - rusty;
- bronchoalveolar cancer - salivary;
- bronchiectasis - profuse, purulent, with blood.
Bacterial pneumonia can be accompanied by liver damage, increased activity of liver enzymes and increased blood urea levels.
In a blood test, the main indicator of the type of lung infection is the level of leukocytes. Leukocytosis is expressed in bacterial forms of pneumonia (more than 15 × 10 9 / l), with mycoplasma and viral, the indicator is almost unchanged.
In children
A number of techniques have been developed to make an accurate diagnosis of a pulmonary disease in a child. All of them take into account the age characteristics of patients, the etiology of pneumonia, factors contributing to its development, the forms of the course of the disease (pathogenesis).
Anatomical and physiological features of the child's body determine the tendency to develop pneumonia at an early age, the possibility of developing into a chronic form and the severity of the course. An equally important role in the development of pneumonia is played by:
- hypothermia;
- poor child care;
- violation of hygiene rules;
- artificial feeding;
- unsanitary living conditions, incl. damp rooms;
- previously transferred infectious diseases.
The most likely pathogen for community-acquired pneumonia in children under 6 months of age are viruses, staphylococci and gram-negative flora. Later - pneumococcus and H. influenzae type B. In adolescence, streptococcus is added. In case of nosocomial infection, the source of infection for both adults and children is likely to be enterobacteria, E. coli, staphylococcus aureus, proteus, pseudomonas.
The differential diagnosis of pneumonia in children involves several types of classifications of pathology:
- By type, focal, segmental, croupous and interstitial acute are distinguished.
- By localization - in the lobe of the lung, in the segment, unilateral and bilateral.
- By type: community-acquired and nosocomial, perinatal, ventilator-associated, aspiration, immunodeficiency.
- By severity: mild, moderate and severe with complications. In this case, complications are divided into pulmonary (pleurisy, pneumothorax) and extrapulmonary (cardiovascular failure, infectious toxic shock, disseminated intravascular coagulation syndrome, respiratory distress syndrome).
With all types of pneumonia in children, all the structural elements of the organ are involved in the process, gas exchange is hampered, the respiratory rate increases, pulmonary ventilation decreases with extreme need for oxygen. Pathology can affect the heart, which is forced to compensate for the lack of oxygen by increased intensity of contractions, followed by dystrophy of the heart muscle.
Oxygen deficiency causes metabolic disorders, blood acidification. Further, hypoxemia and hypoxia are observed. Cessation of oxygen assimilation externally manifests itself in a cyanosis of the face (hypoxemia) or an earthy gray color (hypoxia). Subsequent profound metabolic disorders can become irreversible and cause death.
The criteria for the diagnosis of acute pneumonia in children are:
- With auscultation of the lungs, rapid breathing and an increase in heart rate against the background of apnea, moaning breathing pattern, blistering rales, bronchophonia.
- An increase in temperature of more than 38 degrees for at least 3 days.
- Dry cough, respiratory distress, voice tremors.
- On X-ray images, shadows in the form of lesions, darkening.
- A blood test indicates leukocytosis, urine and feces without pathological abnormalities.
The signs of respiratory failure can be found in Table 2.
Table 2. Clinical and laboratory characteristics of respiratory failure in children with acute pneumonia (According to AF Tur, AF Tarasov, NP Shabalov, 1985).
| DN step | Clinical characteristics | External respiration indicators | Blood gas composition, acid-base state (CBS) |
|---|---|---|---|
| I | Dyspnea at rest is absent. Perioral cyanosis, intermittent, aggravated by anxiety. Pallor of the face, blood pressure - normal, less often - moderately increased. Ps: RR = 3.5-2.5: 1, tachycardia. Behavior unchanged, sometimes anxiety | MO (respiratory minute volume) is increased, RD (respiratory reserve) is decreased. VC (vital capacity of the lungs), DE (respiratory equivalent) increase in OD (breathing volume) slightly decreased | The gas composition of the blood at rest is unchanged or the blood oxygen saturation is moderately reduced (by 10%; pO2 = 8.67-10.00 kPa, however, when breathing oxygen, it approaches the norm.Hypercapnia (РСО2 is higher than 4.67 kPa or РСО2 is normal There are no natural changes in the CBS. Increase in the content of carbon dioxide in the blood. |
| II | Shortness of breath at rest, breathing with the participation of accessory muscles, retraction of the intercostal spaces and the suprasternal fossa. Ps: RR = 2-1.5: 1, tachycardia. Perioral cyanosis of extremities, permanent, does not disappear when breathing oxygen, but is absent in the oxygen tent. Generalized pallor of the nail bed. Blood pressure is increased. Behavior: lethargy, weakness, decreased muscle tone. | MOD increased. VC is reduced by more than 25-30%. RD and AP are reduced to 50% or less. DE is significantly increased, which indicates a pronounced decrease in oxygen utilization in the lungs. | Oxygen saturation of the blood is 70-85% (pO2 = 7.33-8.53 kPa. Hypercapnia (PCO2 greater than 6.0 kPa; blood pH - 7.34-7.25 (acidosis); base deficiency (BE) is increased. Plasma bicarbonate level is determined by the nature of acidosis.CBS depends on the state of hemodynamics |
| III | Dyspnea is expressed (respiratory rate is more than 150% of the norm), irregular breathing, periodically bradypnoe, paradoxical breathing. Decrease or absence of respiratory noises on inspiration, blood pressure is reduced. Generalized cyanosis. Cyanosis of the lips, mucous membranes does not disappear when breathing oxygen. Generalized pallor, marbling. Behavior: lethargy, depressed consciousness, decreased skeletal muscle tone, coma, convulsions. | MOD is reduced, VC and AP are reduced by more than 50%, RD = 0 | Blood oxygen saturation - less than 70% (pO2 below 5.33 kPa; decompensated acidosis (pH less than 7.2) BE greater than 6-8; hypercapnia (РСО2, more than 9.87 kPa), bicarbonate and buffer levels bases (BE) lowered |
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