Pneumonia in children (classification, diagnosis). Community-acquired pneumonia in children Community-acquired pneumonia, features of the course in children

Very often, such a serious disease as pneumonia, many people endure on their feet, trying not to end up in a hospital, but not everyone knows how dangerous community-acquired pneumonia is; symptoms in children are associated with severe intoxication, asthenia and insufficient respiratory function. This is a serious blow to health and an opportunity unpleasant consequences for a child. Such a disease must be detected in time and not left unattended.

Lung disease begins to develop in children after an infection that spreads by air and can catch a child on the street, in a kindergarten, preschool or school institution, or in any public place.

Pneumonia most often occurs in the lower sections respiratory system, can be one-sided, but can affect both lungs. Preschoolers and the elderly are especially susceptible to it. Both of these categories have vulnerable immunity and are therefore at risk.

In young children, the bronchi and trachea are much narrower than in adults - because of this, bronchial secretions can be retained, causing congestion, leading to an inflammatory process. In addition, children have underdeveloped respiratory muscles. The disease can occur in acute form and then it takes about a month to completely cure this illness. If the necessary therapy is not taken on time, the disease progresses to chronic form, which significantly aggravates the baby’s condition and threatens complications.

The pathogens that provoke inflammation are pyogenic bacteria - staphylococci, streptococci, as well as Pfeiffer's bacillus (influenza bacillus), Klebsiella from the Enterobacteriaceae family. In addition, other pathogenic microorganisms - mycoplasmas, adenoviruses, chlamydia - can also cause lung damage.

The infection enters the child's body:

• from a carrier of the disease;
• through wounds and abrasions by hematogenous route;
• at open wound breasts;
• when swallowing microbes.

Factors that contribute to this:

• weakened immune system;
• long exposure to cold air, hypothermia;
• insufficient hygiene of the mouth and nasopharynx;
• chronic infection of the respiratory system;
• metabolic disease;
• epidemics in places where children regularly stay.

An aggravating factor can also be the child’s poor diet, the presence of vitamin deficiency, or a deficiency of useful microelements and vitamins. Experiences and stressful situations at home and at school, which can worsen the baby’s well-being, also play an important role.

Video: Pneumonia - School of Dr. Komarovsky

Community-acquired pneumonia: symptoms in children

Pneumonia in children is especially acute due to the fact that the immune system is not yet able to fight pathogenic flora at full strength.

Main signs of the disease:

1. An increase that causes chills, lethargy and weakness in children. Very often it appears against this background headache, aches in joints and muscles. Even the chest hurts in children.
2. An accompanying symptom may be a herpetic rash on the body. Rashes can also appear on a child’s lips.
3. Due to the deterioration of the condition, children refuse to eat. Occasionally, pneumonia is accompanied by stool disorder in infants.
4. The work of the sweat glands is disrupted. Therefore, they intensively synthesize secretion.
5. Since the inflammatory process leads to the formation of an accumulation of pus in the tissues of the bronchi and pulmonary alveoli, it often becomes one of the symptoms. This indicates that the lungs are affected. At first, coughing attacks are dry and unproductive, but over time, mucus secretion appears.
6. Another sign of pneumonia is breathing, which is difficult due to the contents of the bronchi. Wherein pain syndrome in the chest appears when inhaling air.
7. If a complication begins, the child experiences fainting and even loss of consciousness. He is poorly oriented in space and cannot adequately coordinate his movements.

When diagnosed with community-acquired pneumonia, symptoms in children may differ from those in adults. With total, spreading inflammation, diarrhea and a drop in blood pressure are added to the listed manifestations, so the child should be under constant medical supervision.

As for pneumonia without fever, this phenomenon also occurs in children and is dangerous because, in addition to fever, there are no signs of cough. It turns out that identifying the disease correctly can be quite difficult. If a preschooler can somehow explain what hurts, then Small child will not be able to give such information to his parents. This is why out-of-hospital inflammation of the respiratory organs in infants is so dangerous; in some cases, if treatment is delayed, the child may still die.

Adults should remember that pneumonia in a baby can be determined by an unnatural blush on a pale face and typical pinkish-red spots in the cheek area. Breathing in children is accompanied by shortness of breath and a characteristic whistling sound.

When there is a suspicion that the detected pathology is community-acquired pneumonia, treatment in children at home should be carried out in accordance with all the rules and requirements of the pediatrician and under his periodic supervision.

One of the signs of pneumonia is an increase in temperature, which causes chills, lethargy and weakness in children.

Community-acquired pneumonia: treatment in children at home

Before treatment, the doctor must examine the child - blue lips, pallor, changes in respiratory function, cough and other symptoms may prompt the specialist to think about the presence of pneumonia.

Basic examinations that are carried out to clarify the diagnosis:

• X-ray examination of the state of the pulmonary system;
• fiberoptic bronchoscopy is an endoscopic method for diagnosing bronchi;
• blood tests - general and biochemical;
• examination of a sputum sample;
• testing gas exchange in the lungs;
• urine antigen tests;
• serum reaction to foreign proteins using the method of serodiagnosis.

Additionally, computed tomography and magnetic resonance imaging are used, and the polymerase reaction is a method of scanning infectious microorganisms using molecular biology.

In addition, differential diagnosis is carried out to exclude diseases such as tuberculosis, thromboembolism, cancer, and heart failure.

When community-acquired pneumonia is diagnosed, treatment in children at home can be carried out if the inflammation is small and the child is more than three years old. Children under three years of age are required to be admitted to a hospital, since the treatment of the disease is complex and combines different ways impact.

Other indications for hospitalization:

• chronic form of pneumonia;
• circulatory disorders;
• in infants - intrauterine developmental defects;
• risk of complications.

This may include the unfavorable living conditions of a small patient.

If the disease is mild, treatment can be done at home, but this does not replace taking some effective drugs and doctor's instructions.

Home therapy includes:

1. Taking antibiotics is a broad-spectrum drug (Suprax, Summad, Ceftriaxone), which should be selected by the doctor individually after studying laboratory tests. Such drugs should be taken in combination with prebiotics, as they inhibit the intestinal flora of the child’s body and have other side effects.
2. Treatment for the main symptoms involves bronchodilators that can relieve organ spasms (Eufillin, Ephedrine), mucolytics - ACC 100, Bromhexine, to relieve fever - Panadol, Paracetamol, antiallergic drugs - Suprastin, Zyrtec.
3. At home, children can do inhalations using Pulmicort, Berodual, expectorants based on sea water and herbal infusions. Chest massage is helpful.

At home, children can inhale using Pulmicort.

Dads and moms should keep in mind that for some types of community-acquired pneumonia, physical procedures are not advisable, so such activities can only be carried out with the permission of a specialist.

Since community-acquired pneumonia poses a particular threat, symptoms in children should be carefully studied by parents and the children's doctor. From now on, it is advisable to carry out vaccinations in a timely manner and teach children breathing exercises, which is an excellent way to prevent this disease.

All articles undergo mandatory testing by practicing doctors.

Gomzar Anastasia Sergeevna
therapist. More than 20 years of experience Education: Federal State Budgetary Educational Institution of Higher Education Far Eastern State Medical University

Classification of pneumonia in children

Etiology of focal pneumonia

1. Community-acquired: Bacterial agents – 80% (S. pneumoniae, H. influenzae, M. pneumoniae, Staphylococcus spp)., Viral agents – 20% (RS virus, adenovirus, CMV)

2. Nosocomial: Bacterial agents (Gram-negative non-fermenting bacilli, S. pyogenes, P. aeruginosa, S. aureus, Proteus spp., Klebsiella spp.)

3. Pneumonia in immunocompromised individuals: P. carinii, Aspergillum spp., Legionella spp., CMV.

Pathogenesis of pneumonia

1. Primary inflammatory lesion bronchial tree with dysfunction of the mucociliary apparatus and weakening of the lung protection mechanisms - mechanisms of the disorder: Hyperproduction of thick mucus, reducing the lumen of the respiratory tube;, Inability to evacuate the contents of the bronchi to the level of the tracheal bifurcation due to damage to the cilia;, Swelling of the mucous membrane of the bronchi and trachea as a result of inflammation.

2. Inflammatory damage to the respiratory part of the lungs: Impaired function of alveolocytes type I - impaired diffusion of oxygen, Impaired function of alveolocytes type II - impaired synthesis of surfactant

3. Forms of hypoxia: Respiratory (respiratory) - disruption of the gas exchange mechanism., Hypoxemia - deficiency of oxygen in the circulating blood, decrease in the functional activity of respiratory enzymes., Tissue hypoxia - decrease in oxygen concentration below the physiological threshold, anaerobic type of metabolism, accumulation of lactate and other under-oxidized products – metabolic toxicosis (acidosis) – microcirculation disorder: disruption of the functional activity of the central nervous system, myocardium, kidneys, liver, immune system.

Pneumonia is not only damage to the respiratory part of the lungs, but also damage to the lower respiratory tract. Clinical picture pneumonia is characterized by universal syndromes: primary toxic syndrome (fever, decreased appetite, weakness, malaise). Subsequently, the clinic of secondary (metabolic, metabolic) toxicosis joins the primary toxicosis. Sometimes the picture of primary toxicosis is dim, and the clinic of secondary toxicosis (immune inflammation - cytotoxic) comes to the fore. A distinctive feature of secondary toxicosis: there is no temperature reaction. Hypoxia syndrome – shortness of breath and discoloration of the skin. Local functional changes: dullness of pulmonary sound, crepitus, wheezing. CBC: leukocytosis with a shift to the left, increased ESR.

Diagnostic criteria pneumonia in children

• Temperature over 38°C for more than three days
• NPV: up to two months more than 60 per minute, from two years to 1 year more than 50 per minute, from 1 year to 5 years more than 40 per minute. The ratio of heart rate to respiratory rate is 3:1 or 2:1 (normally 4:1)
• Retraction of the compliant areas of the chest (in the absence of bronchial obstruction)
• Local functional symptoms: shortening of percussion sound, crepitus, moist small-caliber rales
• Perioral cyanosis, mucosal cyanosis
• Toxic syndrome
• Change in clinical analysis blood

Versatile Feature childhood: all infectious diseases (including pneumonia) occur atypical. The severity of the infectious process, incl. Pneumonia in young children is caused by additional complications; mortality in this nosology occurs in young children. Difficulty in diagnosis → late treatment → complications.

Community-acquired P in children aged 6 months to 6 years. The main bacterial pathogens of typical P: streptococcus pneumoniae (more than 50%), Haemophilus influenzae (up to 10%). Atypical P at this age are caused by mycoplasmas (10%) and even less often by chlamydia.

Community-acquired patients aged 7 to 15 years are caused by both viruses and bacteria. The main bacterial pathogens of typical P are: pneumococci (40%) and rarely - Haemophilus influenzae and streptococci. Atypical P at this age are most often caused by mycoplasmas (20-40%) and rarely by chlamydia (7-24%).

In children with immunodeficiencies P are caused by: viruses (CMV, herpes, etc.), fungi, pneumocystis.

Classification

By location of infection: community-acquired, hospital-acquired (after 48-72 hours after hospitalization).

Also highlighted:

Aspiration(for diseases accompanied by reflux, dysphagia, in patients with impaired consciousness);

Ventilation– develops in patients on mechanical ventilation: early – in the first 5 days and late – after 5 days of mechanical ventilation;

In newborns: intrauterine (which appeared in the first 72 hours of life), postnatal.

According to clinical and radiological data: focal pneumonia, mono- or polysegmental, focal-confluent, lobar (lobar), interstitial).

By severity: moderate and severe. The severity of pneumonia is determined by the severity clinical manifestations and the presence of complications.

Complications: pulmonary: bulla, abscess, pleurisy, pneumothorax, pyopneumothorax, abscess.

Extrapulmonary complications: DIC syndrome, circulatory failure, infectious-toxic shock.

With the flow: acute (up to 1.5 months), prolonged (1.5-6 months).

Pathogenesis. The pathogenesis of P is based on decreased immunity, often developing as a result of viral diseases. Impaired mucociliary clearance also plays an important role (see “Bronchitis”).

Currently, the following main mechanisms for the development of P are distinguished:

Microaspiration of oropharyngeal secretions;

Inhalation of aerosol containing microorganisms;

Hematogenous spread of microorganisms from an extra-local source of infection;

Direct spread of infection from neighboring affected organs.

SIADH syndrome*

Rice. 1.8.Scheme of the pathogenesis of pneumonia

* SIADH – antidiuretic hormone stimulation syndrome.

Factors predisposing to microaspiration are:

Age up to 6 months;

Encephalopathy;

Dysphagia (regurgitation, vomiting, gastroesophageal reflux);

Bronchial obstruction syndrome;

The mechanism of violation of protective barriers (probe, intubation, tracheomalacia, repeated vomiting with intestinal paresis, severe illnesses;

Development of a critical condition due to the underlying disease;

Malformations of the heart, lungs;

Neuromuscular blockade.

Research. ABOUT general blood and urine analysis, chest x-ray. According to indications: culture of sputum for flora (includingM. pneumoniae, andU. urealyticumin newborns), study of CBS indicators, determination of chlamydia in saliva and other biological fluids, spirogram, express diagnosis of viral antigens using the immunofluorescence method, determination of antibody titer to chlamydia and mycoplasma.

Outpatient studies , Order of the Ministry of Health of the Russian Federation No. 263: complete blood count, chest x-ray. According to indications: microbiological examination of sputum (includingM. pneumoniae, andU. urealyticumin newborns), serological tests for infections and viruses, lung tomography.

History, clinic. In approximately half of children, the development of P is preceded by ARI. The most characteristic signs of P are: body temperature more than 38 0 C for 3 days or more, shortness of breath, retraction of the compliant areas of the chest, cough, intoxication.

Febrile fever an important sign of P. Temperature below 38 0 C with 95% high probability indicates against P - except for atypical ones. The absence of fever in a child older than 6 months casts doubt on the presence of P. Without the use of antibiotics, the fever lasts more than three days.

Dyspnea The more extensive the lung damage is, the more often it is detected (20-60%). Cyanosis is a very rare sign of respiratory failure.

Intoxication syndrome: poor appetite, agitation or apathy, sleep disturbance, tearfulness, pallor, tachycardia.

Respiratory catarrhal syndrome: runny nose, cough, conjunctivitis, etc. The features of its manifestations depend on the etiology of the previous ARI (occurs in 40-50% of cases).

Aucultative-percussion changes: a change in percussion sound is detected the more often, the larger the zone of pneumonic infiltration (with lobar processes - in 75%).

Weakened breathing, local hard breathing, bronchial breathing over the infiltration zone - 70%, local fine rales - less than 50%, scattered wet rales - 25%, scattered dry rales - 10%.

Attention! In 20-30% of patients with P there are no local percussion and auscultation changes. The absence of local changes in the patient's lungs does not exclude the presence of P.

Depending on the etiology and clinical manifestations of P conditionally divided into typical and atypical.

Table 1.24. Signs of typical and atypical community-acquired pneumonia in children in the first months of life(V.K. Tatochenko, 2006)

Complications(see “classification of pneumonia”).

Features of the clinic P of various etiologies

Pneumococcal pneumonia.Krupoznaya P in older children it is characterized by a temperature of 40 0 ​​C and higher, chills. There may be a cough with rusty sputum. Herpetic rashes, redness of the cheek on the affected side, pain in the chest. Possible disorder of consciousness (delirium, fears). When examining the lungs, local percussion symptoms (shortening) are revealed; auscultatory (decreased breathing, bronchophony, intermittent crepitating rales) changes.

X-ray examination often reveals unilateral, both lobar and focal (including spherical) shadows or darkening of 1-2 segments. The blood test shows leukocytosis above 15-20×10 9 /l with a shift of the blood formula to the left, an increase in ESR to 20-40 mm/h and higher.

Pneumococcal P in young children occur with a small volume of infiltrate, with moderate toxicosis. There is often no shortness of breath. With massive infiltrates, the pleura is involved in the process (syn- and metapneumonic pleurisy). Sometimes pyopneumothorax and intrapulmonary thin-walled cavities (bullas) develop. In blood tests, leukocytosis is observed above 15-20×10 9 /l with a shift in the blood count to the left, an increase in ESR to 20-40 mm/h and higher.

Staphylococcal pneumonia are more often formed in children in the first months of life, as well as in patients with immunodeficiencies. During nosocomial infection, staphylococci cause P, especially in children who have received penicillin. The presence of a previous ARI is characteristic.

When examining the lungs, a shortening of the percussion sound, local changes in breathing, scattered wet and dry rales (a sign of purulent bronchitis) are revealed. Such patients often develop severe pneumonic toxicosis, shortness of breath, cough, and groaning breathing. During pleural puncture in cases of pleurisy, creamy pus can be detected.

X-ray examination initially reveals a vaguely limited infiltrate, which quickly increases in size; signs of pleurisy; air cavities (sometimes with a liquid level). A blood test often reveals leukocytosis above 25×10 9 /l, an increase in ESR above 30-40 mm/h.

Streptococcal pneumonia Children aged 2-7 years are affected. Characterized by an acute onset, febrile temperature, toxicosis. When examining the lungs, there are often no clear percussion signs and a small amount of wheezing. On the part of the heart, atrioventricular block may develop.

X-ray examination reveals multiple round foci of infiltration in different phases (from infiltration to abscess), enlargement of the hilar lymph nodes; pronounced interstitial component of inflammation (scattered small foci, often with cavities). Bilateral pleurisy with liquid pus is often detected. An increase in ASL-O titers can be detected in the blood.

Pneumonia caused by Haemophilus influenzae Children under 5 years old are sick. This etiology of P is characterized by an acute onset, febrile temperature, and toxicosis.

X-ray examination reveals foci of infiltration, sometimes pleural effusion of a hemorrhagic nature.

Blood tests show normal white blood cell count and ESR. Antibiotics such as penicillin are ineffective.

Mycoplasma pneumonia more often observed in school-age children. The incidence is seasonal, with the number of patients increasing every 4-5 years.

The clinical picture is characterized by a persistent cough, heat in a relatively mild condition. Many children have a gradual onset of the disease, with scant catarrhal manifestations.

When examining the lungs, scattered fine bubbling rales, often asymmetrical, are heard.

X-ray examination reveals inhomogeneous infiltration of both lungs, often asymmetrical.

Blood tests reveal the absence of leukocytosis, normal or moderately elevated ESR.

Chlamydial pneumonia typical for children in the first 6 months of life. The mother has a history of genital discharge during pregnancy or erosion. In children in the first month of life, conjunctivitis is possible. The temperature is usually normal. A growing cough is characteristic (whooping cough-like, without recurrence).

When examining the lungs, shortness of breath is detected without clinical signs of bronchial obstruction. During auscultation, scattered moist rales are heard in the lungs.

X-ray examination reveals swelling and intensification of the pulmonary pattern, many small foci (reminiscent of the picture of miliary tuberculosis).

Blood tests often reveal severe leukocytosis (above 20-30×10 9 /l) and eosinophilia (above 5%).

Viral pneumonia can develop with a severe form of influenza (clinic of hemorrhagic pulmonary infarction), adenoviral infection, MS infection, parainfluenza. The clinic of these Ps is difficult to distinguish from the clinic of bronchitis.

The diagnosis of viral P is justified when an X-ray reveals inhomogeneous pneumonic infiltration without clear contours, in the absence of changes in the blood characteristic of bacterial P.

Diagnosis. When diagnosing P take into account: violation general condition, increased body temperature (fever for more than three days), cough, shortness of breath of varying severity and characteristic physical manifestations (local disturbances in breathing and percussion sound). Radiological confirmation is based on the identification of focal or infiltrative changes on the radiograph.

At the stage of diagnosis verification, it is allowed to make a diagnosis of acute P only based on clinical signs. It should be remembered that small (less than 1-2 cm in diameter), scattered foci of infiltration, as a rule, are not detected by X-ray examination of the lungs. In this case, great importance is attached to changes in the dynamics of the blood - acceleration of ESR, neutrophilic leukocytosis with a shift to the left.

Laboratory research

With P, the most characteristic are the following hematological changes: leukocytosis above 10×10 9 /l – detected in 50% of patients. High leukocytosis is characteristic of destructive P, P, caused by chlamydia trachomatis. P with a low number of leukocytes is observed during the isolation of mycoplasma and Haemophilus influenzae. P is characterized by an ESR above 20 mm/h. The absence of hematological changes does not allow us to exclude P.

X-ray examination. Homogeneous shadow (polysegmental, lobar focal) is characteristic of bacterial P; heavy, inhomogeneous shadows – for atypical P (mycoplasma). It is very difficult to judge its etiology by the shape of the pneumonic shadow.

Disseminated process in infants it is characteristic of chlamydia or pneumocystis; in older children - for streptococcal etiology P.

Focal-confluent dense shadows with a bulging border are characteristic of destructive P; in the presence of a concave border, they speak of the presence of an atelectatic component.

Radical darkening – reaction of the roots to ARI or tuberculous bronchoadenitis. The diagnosis of “hilar pneumonia” is inappropriate.

X-ray monitoring is indicated only for massive and complicated lesions, as well as in the absence of treatment effect.

For uncomplicated P, a repeat radiograph is performed in cases of complete clinical effect no earlier than 3-4 weeks (since the resorption of the pneumonic infiltrate occurs precisely during this period).

The presence of bronchial obstruction with a high degree of probability excludes the typical etiology of P. These manifestations are possible with atypical P and nosocomial infection.

An important place in the diagnosis of P belongs to the determination of the etiological agent (causative agent) by bacterioscopy and culture of sputum and bronchial lavages. Detection of a bacterial agent from the upper respiratory tract does not necessarily indicate that it is the causative agent of P.

Start of inspection:

T 0 > 38 0 > 3 days

and/or shortness of breath and/or

chest indrawing (without obstruction)

Asymmetry of moist rales

Local symptoms:

shortening of percussion sound

and/or

decreased or bronchial breathing

and/or

local wheezing

Signs of toxicosis

X-ray or initiation of treatment

Rice. 1.9.Diagnostic algorithm for pneumonia(according to V.K. Tatochenko, 2006)

Blood cultures for sterility reveal the pathogen in 10-20% of cases, and in the presence of pleurisy in 40%.

Semi-quantitative cultures of tracheal sputum give good results for pneumococci, but not for Haemophilus influenzae and staphylococci.

Isolation of atypical pathogens from the respiratory tract indicates the presence of infection or carrier, however, does not necessarily indicate its role in the development of P.

There is no increase in antibody titers to pneumotropic microorganisms diagnostic value due to the phenomenon of polyclonal activation of the immune system. To confirm the role of atypical flora, the detection of IgM class antibodies is important, however, this occurs only in the second or third week of the disease.

In everyday practice, etiological diagnostic methods are recommended only for cases refractory to treatment, as well as for nosocomial infection.

All children with acute respiratory infections and cough are classified as having (V.K. Tatochenko, 2006):

Probably severe P if at least one of the following symptoms is present, regardless of the temperature level:

Increased breathing rate in the absence of obstruction;

Retraction of intercostal spaces in the absence of obstruction;

Moaning, grunting breath;

Cyanosis of the nasolabial triangle;

Signs of toxicosis (sick appearance, refusal to eat and drink, drowsiness, impaired consciousness, severe pallor at elevated temperature).

Probably having P - in the absence of the signs specified in paragraph 1, in the presence of at least one of the following symptoms:

– temperature > 38 0 C for more than 3 days;

Local physical signs of pneumonia;

Asymmetry of wheezing, especially in the presence of conjunctivitis and other symptoms of mycoplasma infection.

In cases where P develops against the background of various other diseases of the lungs, heart, blood, after injuries, wounds, poisoning, etc. a diagnosis of secondary P is established: infarction-pneumonia, hypostatic, congestive P, aspiration, etc.

Differential diagnosis They are used with various diseases of both the respiratory system and other infectious diseases. The pronounced predominance of signs of intoxication, especially at the onset of the disease, makes it necessary to differentiate the diagnosis with such infectious diseases as typhus, tonsillitis, etc., the primary manifestation of which is general intoxication. It is necessary to remember pulmonary tuberculosis, especially in cases where X-ray examination reveals a round or oval infiltrate with clear contours in the upper lobes of the lungs against the background of petrification. At the same time, Mycobacterium tuberculosis can be detected in sputum and in washing water from the bronchi.

The presence of respiratory catarrhal manifestations requires exclusion ARI, bronchitis(see table 1.19) .

If pronounced infiltrative changes appear in the lungs, it should be excluded exudative pleurisy and tumors, for which further instrumental (x-ray, bronchological) and laboratory examination is necessary.

In case of prolonged course of P, it should be differentiated from congestion in the lungs of cardiac origin, with malignant neoplasms of the lungs, especially in cases where there is bronchial obstruction.

Table 1.24. Differential diagnosis of pneumonia

Treatment.Treatment objectives: sanitation of the pathogen, relief of respiratory failure, treatment of changes that have developed in various organs and systems (toxicosis, cardiovascular failure, impairment of CBS, etc.).

Treatment scheme. Mandatory for P is the prescription of antibiotics and oxygen therapy (for DN II-III degrees).

Auxiliary treatment: routine points, nutritional recommendations, symptomatic (syndromic) treatment.

children in the first six months of life; complicated P; signs of hypoxia or severe dehydration; the presence of severe concomitant pathology; lack of effect from initial antibiotic therapy within 36-48 hours; hospitalization for social reasons.

Principles antibacterial therapy pneumonia

Initial antibiotic therapy is prescribed empirically (without isolating the pathogen) immediately after diagnosis or if there is a suspicion of P.

The prescribed antibacterial drug must be effective against all the most likely pathogens of P. When choosing a drug, it is necessary to rely on all available data regarding the possible etiology of the disease (bacteriological monitoring for a given region, guidelines etc.).

The patient's previous antibacterial therapy significantly changes the patient's microbial landscape, which must be taken into account when prescribing treatment (see below).

Indications for replacement antibacterial drug is the lack of effect of treatment (see below).

When isolating a pathogen from a patient, prescribing an antibiotic should be based on the type of pathogen and/or the results of a study of the pathogen's sensitivity to antibiotics.

Table 1.25.Choosing a starting drug for community-acquired pneumonia in children(Guidelines for pneumonia, 2009)

* Modern macrolides: azithromycin, clarithromycin, midecamycin, roxithromycin, spiramycin.

Table 1.26. Initial therapy for nosocomial pneumonia ( VC. Tatochenko, 2009)

For community-acquired P, the starting drugs are penicillins because the main pathogens of P (pneumococcus, Haemophilus influenzae) remain sensitive to them.

In case of nosocomial infections, it is necessary to determine the microflora and its sensitivity to antibiotics.

In children receiving treatment on an outpatient basis, injectable forms of antibiotics should not be used.

For severe P, antibiotics should be administered intravenously.

Combinations of antibiotics should be used when the etiology of the disease is unclear or in severe cases of P.

After obtaining the effect of parenteral administration of antibiotics, you should switch to their oral forms (stepped method of treatment).

It is necessary to observe the most optimal timing of treatment for P (see below).

Antibacterial therapy does not require accompanying treatment with antihistamines and antifungals.

On an outpatient basis, I do not use gentamicin to treat P.

Sensitivity of bacterial pathogens to antibiotics. Currently, pneumococci remain sensitive to penicillin. Their sensitivity to gentamicin is almost absent, and to biseptol - reduced.

Haemophilus influenzae : sensitive to amoxicillin, cephalosporins of ΙΙ-ΙV generations.

Staphylococcus aureus: Sensitivity to oxacillin, protected penicillins, lincosamide, macrolides, and aminoglycosides was preserved.

Chlamydia and mycoplasma : highly sensitive to macrolides, tetracyclines.

Full treatment effect : a drop in body temperature below 37.5 0 C after 24-48 hours for uncomplicated and after 3-4 days for complicated P, against the background of improved general condition and appetite, decreased shortness of breath. During this period, radiological changes do not increase or decrease.

Partial effect: preservation of febrile body temperature after the above periods with a decrease in the severity of toxicosis, shortness of breath, improved appetite and the absence of negative x-ray dynamics. It is usually observed with destructive P and/or with metapneumonic pleurisy. No antibiotic change is required.

No effect: persistence of fever with deterioration of general condition and/or increase in pathological changes in the lungs or pleural cavity (increase in the volume of effusion or its cytosis). With chlamydia and pneumocystosis, an increase in shortness of breath and hypoxemia is noted. Lack of effect requires changing the antibiotic.

Duration of initial antibacterial therapy.

Indications for switching to alternative drugs are the lack of clinical effect from the first-choice drug within 36-48 hours for mild and 48-72 hours for severe P, as well as the development of serious adverse drug reactions.

The duration of antibacterial therapy should be sufficient to suppress the vital activity of the pathogen. With an adequate choice of antibiotic, 6-7 days are enough for this. It is believed that antibacterial treatment should be continued for another 2-3 days after the onset of the effect of the treatment. Pneumococcal Ps (6-7 days) respond best to treatment, while Ps caused by Haemophilus influenzae (10-14 days) are worse. The longest treatment period for destructive P is several weeks.

Table 1.27. Stepped antibacterial therapy for pneumonia in children

Treatment of respiratory failure includes the following main components:

1. Restoration of airway patency. 2. Oxygen inhalation. 3. Ventilation. 4. Improved sputum drainage. 5. Correction of associated disorders.

At I degree DN There is no need for oxygen therapy. It is enough to ventilate the premises, keep the child on the verandas and in the corridors.

At DN II oxygen therapy is indicated. When carrying it out, the following provisions must be taken into account: 1. The oxygen concentration in the oxygen-air mixture must be minimally sufficient. 2. Oxygen should be supplied to a sick child warm and hydrated. 3. Oxygen therapy regimens depend on the method of oxygen delivery to the patient, the severity of respiratory failure, the presence and nature of complications.

Improving sputum drainage includes the use of: mucolytics (Erespal, Lazolvan, etc.), the use of mechanical removal of sputum (sanitation of the upper respiratory tract, sanitation of the trachea in the presence of an endotracheal tube).

Correction of associated disorders includes: a) elimination of acute heart failure (fluid volume limitation, cardiac glycosides, diuretics, dopamine with a cardiotonic effect), b) elimination of dehydration (see infusion therapy P), c) restoration of adequate functioning of the microcirculation system, improvement of rheological properties blood and its transport function (dopamine at a dose of 1-3 mcg/kg/min, nicotinic acid 0.5-1 ml intravenously once; Cavinton 1 mg/kg intravenously drip); d) impact on blood coagulation properties (use of heparin for hypercoagulation at a dose of 50-100 IU/kg/day intravenously evenly).

Hydration during P should be carried out carefully and preferably orally. The volume of daily fluid in children with P should be less than the MSF (daily maintenance fluid), but not less than 700-1000 ml.

Indications for testing infusion therapy : severe exicosis, collapse, microcirculation disorders, threat of development of disseminated intravascular coagulation syndrome. The volume of intravenously administered fluid should not exceed 20-30 ml/kg/day. In the composition of infusion media, colloidal solutions should make up 1/3 of the total volume.

The administration of protease inhibitors (contrical, Trasylol, gordox) is indicated only in the first three days of the disease, because then they are not effective.

Outcomes. P – a serious disease, the outcomes of which depend on: the age of the child, the etiology of P, living conditions, the presence of background pathology (prematurity, malnutrition, anemia, diseases nervous system and etc.). Some children with P develop pulmonary and extrapulmonary complications. In Russia, 50-70% of all deaths from P are associated with hospital-acquired pneumonia. Mortality from community-acquired diseases depends on untimely hospitalization and inadequate treatment.

Prevention It includes the prevention of acute respiratory infections, influenza, adherence to a regime of rest and rest, a balanced diet, physical exercise, systematic ventilation of premises, and sufficient time in the fresh air.

Much attention should be paid to the timely identification and elimination of exogenous and endogenous risk factors for the development of P.

An important role should be given to nonspecific prevention, which increases the body's resistance to adverse environmental factors, in particular to hypothermia. This is facilitated by hardening and active physical education, balanced nutrition.

To prevent nosocomial infections, it is necessary to change approaches to hospitalization of children with ARI and eliminate the unjustified prophylactic use of antibiotics.

One of the effective preventive measures is vaccination. Vaccination against influenza reduces not only the incidence of influenza, but also mortality, primarily from influenza and P.

The use of a vaccine against infection caused by H. influenzae type B (in Russian Federation The Act-Hib vaccine is registered), in children in the first months of life it reduces the incidence of severe P of this etiology by 80% and the incidence of all severe P by 22-26%.

The polysaccharide pneumococcal vaccine (the Pneumo-23 vaccine is registered in the Russian Federation) is immunogenic only in children over 2 years of age; in adults, its effectiveness is 83% against “vaccine” serotypes, 74% against all serotypes of pneumococcus, and in children - 94% against invasive forms of pneumococcal infection. The use of this vaccine is recommended for children at risk of severe pneumococcal infection (with congenital asplenia or a removed spleen; with neutropenia; with a deficiency of complement components; suffering from chronic liquorrhea).

Questions for the exam. Acute pneumonia. Etiology. Pathogenesis. Classification. Community-acquired and nosocomial pneumonia. Clinical picture. Severity criteria. Diagnostics. X-ray signs. Flow. Indications for hospitalization of patients with acute pneumonia. Treatment. Features of antibacterial therapy intra- and community-acquired pneumonia. Outcomes. Prevention.

PULMONARY COMPLICATIONS OF PNEUMONIA

According to the current classification of pneumonia, pulmonary complications include: bullae, abscess, pleurisy, pneumothorax, pyopneumothorax.

At the same time, to designate the listed pathological conditions in practice, the concepts of “acute bacterial destruction of the lungs” (ABLD), “acute destructive pneumonia” (ADP), etc. are often used.

Etiology

Classification. Of the many proposed classifications of bacterial destruction of the lungs, the most acceptable is the following:

I. Acute bacterial destruction.

By genesis - primary (aerobronchogenic), secondary (hematogenous).

According to clinical and radiological forms:

destruction with intrapulmonary complications:

a) abscesses;

destruction with pleural complications:

a) pyothorax (mantle-shaped, total (pleural empyema), limited;

b) pyopneumothorax and pneumothorax (tense, non-tense, limited).

According to the flow - acute, protracted, septic.

II. Chronic forms (outcomes of acute destruction):

chronic abscess, chronic pleural empyema, acquired pleural cysts.

Destructive pneumonia most often manifests itself as bullae, pyopneumothorax, abscess, and pyothorax.

Pathogenesis of destructive pneumonia

Rice. 1.10.Scheme of the pathogenesis of destructive pneumonia

Research(See Parapneumonic Effusion and Empyema).

History, clinic

1. Bulls – thin-walled air cavities that develop at different stages of the pneumonic process. Bullae are identified exclusively radiographically and have different sizes and shapes that can change quickly (bulla play) . There is often no pus in these cavities, which leads to a favorable clinical picture. By the time the bullae form, patients stop having a fever, appetite improves, and the peripheral blood picture normalizes. Respiratory disorders, as a rule, are not observed. In most cases, bullae disappear on their own over time.

2. Lung abscess characterized by febrile temperature, manifestations of respiratory failure, intoxication (pallor of the skin with a marbled pattern, lethargy, drowsiness). The physical picture is represented by a decrease in respiratory excursions on the affected side, a shortening of the percussion sound in the projection of the affected lobe. Since in the presence of a lung abscess, reactive pleurisy is usually pronounced, the data from auscultation and percussion may correspond to the picture of pyothorax (see below). Diagnosis of a lung abscess in the infiltration phase is difficult. In the phase of a formed abscess, the diagnosis is radiological.

3. Pneumothorax. Pneumothorax is based on rupture of the lung or parietal bulla. There are latent and tension pneumothoraxes. The history reveals various bronchopulmonary pathologies. With tension pneumothorax, the clinical picture develops suddenly and is characterized by shortness of breath, anxiety, swelling of the affected half of the chest, and cyanosis. In some cases, cough and manifestations of vascular collapse appear. An objective examination reveals severe tympanitis and sharply weakened breathing on the affected side, a lag of the affected half of the chest in the act of breathing, and a displacement of the mediastinal organs to the healthy side.

Latent pneumothorax is very difficult to detect clinically due to the small amount of air in the pleural cavity.

4. Pyopneumothorax is the result of a breakthrough of air from the lung into the pleural cavity affected by empyema. There are tense and hidden variants of pyopneumothorax.

Tension pyopneumothorax clinically manifested by cardiorespiratory disaster. Main symptoms: chest pain, dyspnea, severe respiratory failure, cyanosis, tachycardia, thready pulse, decreased blood pressure, fever, severe intoxication. The affected half of the chest is swollen, breathing over it is either sharply weakened or absent. On percussion there is a dull sound above the pus. Above the accumulation of air - tympanitis. The boundaries of the heart are shifted to the healthy side.

Hidden pyopneumothorax manifested by a picture of purulent pleurisy and the appearance of air in the pleural cavity (see below).

Diagnosis

Bulls diagnosed solely by the results of x-ray examination (thin-walled air cavity of various sizes and shapes) .

Pneumothorax. Tension pneumothorax is diagnosed on the basis of characteristic clinical manifestations and is confirmed by the results of an x-ray examination, in which The presence of air in the pleural cavity, the absence of a pulmonary pattern, a collapsed lung to varying degrees, and a displacement of the mediastinal organs to the healthy side are detected. Limited pneumothorax is detected only by the results of an x-ray examination (a small amount of air in the pleural cavity).

Lung abscess. This form of pulmonary destruction can have several options: an abscess filled with pus (not communicating with the bronchial tree), an abscess with a fluid level (when the abscess cavity is drained through the bronchus). X-ray examination reveals a cavity with a level of pus and a pronounced pyogenic membrane.

Pyopneumothorax. The diagnosis of tension pyopneumothorax is established on the basis of the described characteristic clinical picture and is confirmed by the results of an x-ray examination, which reveals darkening of the costophrenic sinus and the level of fluid above which there is air. The lung is collapsed. The mediastinum is shifted to the healthy side. The diagnosis of latent (non-tension) pyopneumothorax is radiological.

In blood test All forms of destructive pneumonia are characterized by a decrease in hemoglobin and red blood cells, leukocytosis with a shift of the neutrophil formula to the left, and a high ESR.

Differential diagnosis

Lung abscess. It is difficult to differentiate the infiltrative phase of an abscess from a pneumonic infiltrate on an x-ray, however, the roundness of the forms and more intense darkening in the center make it possible to speak with greater confidence about abscess formation. An abscess with a fluid level should be differentiated from a suppurating congenital lung cyst.

Pneumothorax differentiated with large air cavities (bullas), lobar emphysema, diaphragmatic hernia.

Pyopneumothorax must be differentiated from pneumothorax.

Bulls differentiate with congenital and acquired cysts, limited pneumothorax, cystic hypoplasia of the lung.

Treatment,treatment objectives: decompression (with tension in the pleural cavity), relief of inflammatory changes in the pleura and lungs; eradication of the pathogen.

Treatment scheme. Mandatory treatment: antibacterial therapy, combating intoxication, treatment of respiratory failure, ensuring effective bronchial drainage (mucolytics, drainage position, vibration massage), drainage of the pleural cavity in the mode of active aspiration (with tension in the pleural cavity).

Auxiliary treatment: surgical treatment, diet therapy, regimen, sanitation bronchoscopy, immunoreplacement therapy, enzyme therapy, vitamin therapy.

Indications for hospitalization: all children with complications of pneumonia are subject to hospitalization.

For treatment details, see the section “Parapneumonic effusion and empyema.”

Parapneumonic effusion and empyema.Parapneumonic (sypneumonic) pleurisy is pleurisy that occurs simultaneously with pneumonia. Metapneumonic pleurisy called pleurisy, which developed against the background of the reverse development of pneumonia. Immunopathological processes take part in the development of metapneumonic pleurisy.

Empyema – purulent inflammation of the pleura.

Epidemiology. Parapneumonic effusion and empyema occur with an incidence of 3.3 per 100,000 children. Parapneumonic effusion and empyema are more common in boys than in girls, and newborns and young children are more often affected. The disease occurs more often in winter and spring, which is probably due to its infectious nature.

Predisposing factors: immunodeficiencies, aspiration, conditions after surgery and trauma.

In a healthy child, pleural effusion usually occurs secondary to acute bacterial pneumonia and less commonly as a result of chronic infections such as pulmonary tuberculosis.

Etiology. It has been established that empyema is caused by viral-bacterial associations, the viral components of which are most often influenza viruses, parainfluenza viruses and adenoviruses.

Among the bacteria, the most commonly isolated are Staphylococcus aureus, pneumococcus, Haemophilus influenzae, pyogenic streptococcus and Klebsiella pneumoniae. In a third of children, empyema is caused by anaerobes, including bacteroides, anaerobic bacilli and Fusobacterium. The frequency of pathogen isolation in pleural effusion is about 17%. Even when using the latest molecular methods, the etiological factor is detected only in 75% of cases.

Pathogenesis. Infection affecting an adjacent lung or vascular tissue and activates immune defense and inflammation of the pleura. Increasing vascular permeability allows cells involved in the inflammatory process (neutrophils, lymphocytes and eosinophils) to migrate into the pleural cavity. A number of cytokines take part in the process, such as interleukin-1 (IL1), IL-6, IL-8, TNF-α, PAF (platelet activating factor), produced by the mesothelium that limits the pleural cavity. The result is exudative stage pleural effusion. A clear fluid with a small number of leukocytes accumulates in the pleural cavity (simple parapneumonic effusion).

Second stage of pleurisy fibrinous-purulent. Fibrin deposition begins in the pleural cavity, which leads to the development of septa and limited cavities. The number of white blood cells increases, the fluid thickens (complicated parapneumonic effusion), which ultimately leads to the formation of pus (empyema).

Third stage - organization - fibroblasts infiltrate the pleural cavity, the thin intrapleural membrane is reorganized into a thick and inelastic one. These dense pleural membranes can lead to immobility of the lung, impaired lung function, and a permanent cavity that is potentially open to infection. In this case, spontaneous healing or the development of chronic empyema may occur.

Research. See “Pneumonia”. Initial examination for suspected pleural effusion includes: chest x-ray, ultrasound of the chest, bacteriological blood test (including anaerobic flora), sputum culture (if possible), ASLO, complete blood count with counting erythrocytes, leukocytes and leukoformula, blood electrolytes, total serum protein, C-reactive protein (according to indications).

History, blade. There are two options for the onset of the disease. First option: The child has classic symptoms of pneumonia. When pleural effusion appears, these symptoms intensify. Chest pain may occur, the child takes a forced position on the affected side.

A child with parapneumonic effusion or empyema usually exhibits a typical picture of pneumonia (cough, local auscultatory and percussion changes, malaise, loss of appetite), although a more severe condition than usual is possible, and sometimes pleural chest pain appears. Inflammation in the lower lobes of the lungs may be accompanied by abdominal pain. Characterized by fever, severe intoxication, and signs of respiratory failure.

During an objective examination, pleural effusion is diagnosed by a unilateral dull sound upon percussion, weakened (absent) breathing and scoliosis. Cyanosis may also appear due to an imbalance in the ventilation-perfusion ratio. Effusion is often visible on a chest x-ray.

Second option possible in children who have been diagnosed with pneumonia, but have not received the usual treatment for this case. If the child continues to have a fever or his condition does not improve within 48 hours after starting treatment for pneumonia, reassessment of the condition is necessary, taking into account the possible development of complications. By the time of recovery, examination of the patient will necessarily reveal weakening of breathing and dullness of percussion sound over the affected area; this is due to thickening of the pleura and should not be a cause for concern.

Diagnosis. In children who have already been diagnosed with pneumonia, severe fever and the absence of positive dynamics within 48 hours after the start of antibiotic therapy may be a signal of the possibility of effusion into the pleural cavity.

Laboratory research

darkening of the costophrenic angle is detected - this is early sign the appearance of pleural effusion, the fluid level may be ascending to the lateral wall of the chest in the anteroposterior projection. If the image is taken in the supine position (in small children), the fluid appears as a homogeneous darkening of the entire lung. It is impossible to differentiate between empyema and pleural effusion based on radiographic results alone. The X-ray picture returns to normal by 3-6 months.

Ultrasound can also reveal the presence of fluid in the pleural cavity. Although ultrasound cannot confirm the presence of infection, it nevertheless allows one to assess the size of the effusion and differentiate between free and encysted fluid (its echogenicity is assessed). Also, with the help of ultrasound, thinning of the pleura is detected, secondary and tuberculous effusions are differentiated (for example, the presence of small nodules on the surface of the pleura). In some difficult cases, CT is indicated.

General blood analysis does not allow identifying differences in children with bacterial and viral etiology of the disease. The most common findings are leukocytosis, a shift in the blood count to the left, and an increase in ESR.

Examination of pleural fluid. It is necessary to culture the pleural fluid and perform a cytological examination. If lymphocytes are present in the fluid, it is necessary to exclude tuberculosis and malignant neoplasms. Parapneumonic pleural effusion is accompanied by the appearance of polymorphonuclear leukocytes. The predominance of lymphocytes should be alarming regarding tuberculosis or malignant neoplasms.

Treatment,treatment objectives: relief of inflammatory changes in the pleura and lungs; pathogen eradication; evacuation of contents from the pleural cavity.

Treatment scheme. Mandatory treatment: therapeutic and diagnostic pleural puncture, antibacterial therapy, infusion therapy, antipyretics.

Auxiliary treatment: regimen, diet, immunocorrective therapy, anti-inflammatory therapy, oxygen therapy, intrapleural fibrinolytic therapy.

Indications for hospitalization. All children with suspected pleural diseases should be hospitalized.

Initial activities.

Intravenous fluids are indicated if the child is dehydrated or is unable or unwilling to drink. The basis of detoxification therapy is controlled infusion hemodelution. The main components of infusion therapy: colloids (infucol, reamberin), crystalloids (10-15 ml/kg body weight), glucose solutions.

Antibiotic therapy. Initial therapy is prescribed empirically. In all cases, antibiotics must be administered intravenously. In children with weakened immune systems, drugs with a broad spectrum of action are prescribed. Intravenous antibiotics are continued until the child's body temperature drops or until the drainage is removed. Oral medications such as co-amoxiclav (60-90 mg/kg daily in 3 doses IV or orally) are then prescribed for a period of 1-4 weeks or longer if symptoms of the disease remain.

Rice. 1.11. Algorithm for diagnosis and treatment of pleural infection in children

Differential diagnosis

Table 1.28.Differentialdiagnosis of pleurisy

The dose of antibiotics should not be excessive to avoid pleural penetration. For pleurisy due to community-acquired pneumonia, the following are prescribed: Cefuroxime, Co-amoxiclav, Penicillin, Amoxicillin, Clindamycin. For allergic reactions to penicillin, clindamycin is prescribed.

It has been established that analgesics (analgin 50% 0.1 ml per year of life) and antipyretics (ibuclin 20-40 mg/kg/day in several doses) contribute to a more rapid relief of the manifestations of pleurisy.

Immunocorrective therapy. Indications for use: young children, severe disease, pronounced clinical and laboratory manifestations of secondary immunological deficiency. Prescribed: immunoglobulins for intravenous administration, transfusion of hyperimmune antistaphylococcal or other plasma (10 ml/kg body weight).

Intrapleural fibrinolytic therapy shortens hospitalization and is recommended for use in cases of complicated pleural effusions (thick fluid or encysted fluid) or empyema. Fibrinolytics can lyse fibrin bridges in encysted empyemas and open lymphatic pores. For this purpose, Urokinase is used abroad.

Physiotherapy does not have a positive effect in this pathology.

For anti-inflammatory purposes Vobemzym is indicated (1 tablet per 6 kg of body weight/day 30 minutes before meals for 1 month), and antipyretics for fever.

Features of the treatment of metapneumonic pleurisy. If there are signs of pneumonia progression, antibacterial therapy should be replaced. The use of ibuprofen or indomethacin is indicated, the use of which shortens the febrile period. In the absence of signs of destruction, glucocorticoids can be used.

The patient is treated together with a pediatric surgeon. Surgery indicated if the empyema is at the stage of organization, and if its symptoms are reliable. If the patient has a large effusion or the child is in unsatisfactory condition (respiratory distress syndrome and insufficient oxygenation), it is recommended to immediately transfer the child for further treatment to the surgical (intensive care) department.

Conservative treatment of pleural infection consists of antibiotic therapy alone or in combination with simple drainage. Many small parapneumonic effusions respond to antibiotic therapy without the need for further intervention. An effusion that compresses the lung and impairs its function in a feverish child requires drainage or consideration of the possibility of early surgical intervention. Ultrasound is used to monitor the placement of drainage or thoracentesis. The drainage is blocked if more than 10 ml/kg of fluid is extracted. There is no final clarity on the question of the appropriate volume of evacuated liquid. In adults, it is considered that the drainage should be closed for 1 hour if 10 ml/kg of fluid is removed. In adults, as well as in older children and adolescents, more than 1.5 liters of fluid should not be evacuated at a time, or the drainage rate should not exceed 500 ml/hour.

Outcomes. The prognosis for children who have had empyema is usually favorable. Studies have shown that, despite differences in treatment approaches, most children recover completely and their lung function returns to normal.

Questions for the exam. Pulmonary complications of pneumonia.

Features of development, clinical picture, radiological

changes during pulmonary destruction. Diagnosis. Differential

diagnosis. Features of the treatment of pulmonary destruction. Outcomes.

INFECTIOUS TOXICOSIS (IT)– a special syndrome that develops as a result of an infectious process and is characterized by phase changes in the central nervous system, peripheral circulatory disorders, organ, electrolyte and metabolic changes.

Neurotoxicosis – a special reaction of the body to an infectious disease. The leading manifestations of neurotoxicosis are neurological disorders and peripheral circulatory disorders. There are no obvious signs of dehydration.

Risk factors development of IT: premature babies, a history of seizures and other perinatal lesions of the nervous system, artificial feeding, suffered several weeks before this ARI disease, early age.

Etiology. IT most often develops with influenza, adenovirus infection, and parainfluenza. Less often - with pneumonia, sepsis, meningitis, encephalitis.

Pathogenesis

Rice. 1.12. Scheme of the pathogenesis of infectious toxicosis

Classification. There are three degrees of severity of toxicosis (Table 1.29).

Table 1.29.Severity of toxicosis

Research. General blood and urine analysis, blood electrolytes, CBS indicators, coagulogram, ECG, EchoCG, studies aimed at identifying pathologies of the kidneys, liver, adrenal glands, etc.

History, clinic. IT development is always preceded by some infection. The IT clinic consists of several syndromes (see Fig. 1.13).

Neurological disorders

Fig 1.13. Clinical manifestations of infectious toxicosis

Depending on the leading syndrome, various variants of IT are distinguished: infectious-toxic shock, Reye's syndrome, hemolytic-uremic syndrome, Waterhouse-Friderichsen syndrome, hyperthermic syndrome.

Table 1.30.Classification of peripheral circulatory disorders(Papayan A.V. et al., 1979)

Table 1.31.Classification of neurological disorders in toxicosis(according to Papayan. A.V. and Tsybulkin E.K., 1979)

Table 1.32. Modified Glasgow Scale for Young Children

Diagnosis IT is based on identifying the main manifestations of this syndrome: neurological disorders and microcirculation disorders.

Laboratory research in case of IT, they are necessary to identify organ lesions and determine their functional state.

Differential diagnosis IT is carried out with neuroinfections, encephalitic reactions, sepsis, and the course of infectious diseases.

Tab. 1.33.Differential diagnosis infectious toxicosis (Baranov A.A., co-author, 1997)

Treatment,treatment objectives: treatment of the underlying disease, normalization of peripheral circulatory disorders, elimination of hypersympathicotonia, elimination of hypoxia, relief of neurological disorders, treatment of IT syndromes, treatment of multiple organ failure.

Treatment regimen: Mandatory treatment: elimination of hypersympathicotonia, normalization of microcirculation and hemodynamics, relief of manifestations of multiple organ failure, correction of CBS and electrolyte disturbances, therapy for the disease that caused the development of IT.

Auxiliary treatment: diet, elimination of toxins, prevention of disseminated intravascular coagulation syndrome, maintaining metabolic energy supply, treatment of IT syndromes.

Diet at IT is carried out according to the principles set out in the section “Pneumonia”.

Indications for hospitalization: all children with IT should be hospitalized.

IT 1st degree

The intensive stage of treatment solves the following problems: carrying out a neurovegetative blockade, maintaining the energy supply of metabolism, normalizing microcirculation and hemodynamics, eliminating toxins.

1. Neurovegetative blockade: pipolfen 2.5% solution 0.15 ml/kg body weight intramuscularly or intravenously every 6-8 hours.

2. Correction of hemocirculatory disorders.

a) effect on vascular tone: papaverine 2% solution, 1-2 mg/year of life intramuscularly or intravenously. Subsequently, aminophylline 2.4% solution, 6 mg/kg body weight, is administered intravenously every 6 hours in a glucose solution.

b) impact on vascular permeability and stabilization of cell membranes: ascorbic acid 5% solution, 1 ml intravenously once.

3. Improving the rheological properties of blood: trental 10 mg/kg body weight intravenously.

4. Correction of water and electrolyte disorders. The daily amount of fluid for stage 1 IT is prescribed in the volume of FFS (daily fluid intake). The main route of fluid administration is oral. The following solutions are used for oral administration: Oralit, rehydron, citroglucosalan.

5. Correction of respiratory failure.

6. Normalization of metabolism in brain neurons: piracetam 20% solution 50-100 mg/kg body weight intravenously in glucose solution 3-4 times a day.

7. Elimination of endo- and exotoxins: smecta, polyphepan.

8. Treatment of syndromes characteristic of stage I IT:

a) hyperthermic syndrome: paracetamol 10-15 mg/kg per dose; physical cooling. If there is no effect from antipyretics, lytic mixtures are used, including diphenhydramine, pipolfen, papaverine, analgin.

b) convulsive syndrome: 0.5% solution of seduxen in a single dose of 0.3-0.5 mg/kg (but not more than 10 mg per administration); 20% sodium hydroxybutyrate solution at 50-100 mg/kg; 25% solution of magnesium sulfate 0.2 ml/kg intramuscularly. If there is no effect, hexenal 5% solution is prescribed at 3-5 mg/kg intramuscularly.

9. Treatment of the disease in which IT syndrome has developed.

Infectious toxicosis ΙΙ degree

The intensive stage of treatment solves the following problems: carrying out a neurovegetative blockade, maintaining the energy supply of metabolism, normalizing microcirculation and hemodynamics, eliminating toxins.

1. Neurovegetative blockade - droperidol 0.25% solution, 0.05-0.1 ml/kg body weight intravenously, only after elimination of hypovolemia. The drug is administered every 8-10 hours.

2. Correction of hemocirculatory disorders: pentamine 5% solution 0.05-0.1 mg/year intravenously, once (contraindicated in case of hypovolemia). Then a 2.4% solution of aminophylline is administered at 4-6 mg/kg body weight intravenously in a glucose solution every 6 hours.

3. Effect on vascular permeability and stabilization of cell membranes: prednisolone 1-10 mg/kg/day intravenously every 4 hours.

4. Improving the rheological and coagulation properties of blood: a nicotinic acid 0.5-1.0 ml intravenously, once; Cavinton 1 mg/kg body weight intravenously; heparin (if signs of hypercoagulation are detected) 50-200 IU/kg body weight per day intravenously, evenly; fresh frozen plasma 5-8 ml/kg body weight intravenously, drip, once. To prevent disseminated intravascular coagulation syndrome, chirantil 0.5% solution is also used at a dose of 2-3 mg/kg/day intravenously.

5. Correction of input-electrolyte and metabolic disorders. The daily volume of fluid is reduced by 25% of the FLP. Approximately half of the calculated volume is administered orally, the rest of the fluid is administered intravenously. The choice of blood replacement solutions is determined by the clinical manifestations of toxicosis (cerebral edema, heart failure, etc.). Potassium chloride solutions (4-7.5-10%) should be included in the infusion media. The amount of potassium administered is calculated using the Aberdeen nomogram. The calculated amount of potassium is administered only dropwise, evenly throughout the day. Calcium preparations (calcium chloride, calcium gluconate) are prescribed at the rate of 0.25-0.15 ml/kg/day.

6. Correction of respiratory failure: oxygen therapy.

8. Elimination of exo- and endotoxins: a) Lasix 1-3 mg/kg per day intravenously; b) albumin 10%, 10 ml/kg body weight intravenously.

9. To reduce the activity of lysosomal enzymes, proteolytic enzymes are indicated: trasylol and contrical (intravenous drip at a dose of 500 IU/kg per 50-100 ml of 5% glucose solution).

10. Treatment of syndromes developing with toxicosis of the ΙΙ degree: hyperthermic syndrome, convulsive syndrome, heart failure. In case of heart failure, intravenous cardiac glycosides are indicated (0.05% strophanthin solution or 0.06% corglicon solution, 0.1-0.2 ml 1-2 times a day).

10. Treatment of a disease in which infectious toxicosis syndrome has developed.

Infectious toxicosis ΙΙΙ degree

Reanimation stage solves the following problems: stabilization of central hemodynamics, replenishment of blood volume, early artificial ventilation, correction of life-threatening syndrome.

1. Correction of hemocirculatory disorders, normalization of systemic hemodynamics: prednisolone 5-10 mg/kg body weight intravenously at the same time.

3. Dopamine. At a dose of 2-5 mcg/kg/min, the drug normalizes microcirculation disorders and has a diuretic effect. At a dose of 6-9 mcg/kg/min, dopamine has an inotropic effect (cardiostimulating effect). At doses above 10 mcg/kg/min, dopamine increases blood pressure. Dopamine is diluted with 5% glucose solution or saline to a total volume of 100 ml. In this case, the administration parameter of 1 ml/hour corresponds to the drug administration rate of 1 mcg/kg/min.

Intensive stage treatment solves the following problems: carrying out a neurovegetative blockade, maintaining the energy supply of metabolism, normalizing microcirculation and hemodynamics, eliminating toxins.

1. Neurovegetative blockade (shallow): droperidol 0.25% solution 0.05 ml/kg body weight intravenously, only after elimination of hypovolemia. The drug is administered every 8-10 hours.

2. Impact on vascular tone: aminophylline 2.4% solution, 4-6 mg/kg body weight intravenously every 6 hours.

3. Improving the rheological and coagulation properties of blood: Cavinton 1 mg/kg body weight intravenously.

4. Heparin (for hypercoagulation) 50-100 IU/kg body per day intravenously, evenly.

5. Correction of water and electrolyte disorders. The daily volume of fluid is reduced by 50% of the FLP. The entire calculated volume of fluid is administered intravenously. Potassium chloride solutions (4-7.5-10% solutions) should be included in the infusion media. The amount of potassium administered is calculated using the Aberdeen nomogram. The calculated amount of potassium is administered only dropwise, evenly throughout the day. Calcium preparations (calcium chloride, calcium gluconate) are prescribed at the rate of 0.25-0.15 ml/kg/day. The choice of blood replacement solutions is determined by the clinical manifestations of toxicosis (cerebral edema, heart failure, etc.).

6. Treatment of syndromes developing with toxicosis of the ΙΙΙ degree: infectious-toxic shock, acute heart failure.

7. Normalization of metabolism in brain neurons: piracetam 20% solution 50-100 mg/kg body weight intravenously in glucose solution 3-4 times a day.

8. Elimination of exo- and endotoxins: a) Lasix 1-3 mg/kg per day intravenously; b) albumin 10%, 10 ml/kg body weight intravenously, c) plasmapheresis according to the scheme.

9. Treatment of a disease in which infectious toxicosis syndrome has developed.

Questions for the exam. Primary infectious toxicosis. Causes. Pathogenesis. Clinical syndromes. Diagnostics. Differential diagnosis. Treatment. Indications and features of infusion therapy. Correction of cardiovascular disorders and respiratory failure.

CHRONIC NON-SPECIFIC BRONCHOPULMONARY DISEASES (CNPD) are a chronic inflammatory process based on irreversible morphological changes in the form of bronchial deformation and pneumosclerosis in one or more segments, bronchiectasis and accompanied by relapses of inflammation in the bronchi or lung tissue.

Etiology. The formation of CNBLZ is carried out by: atelectasis of various origins, including congenital; aspiration of foreign bodies, chronic aspiration of food. An unfavorable outcome of the process is facilitated by early age, concomitant diseases, late started and incorrect treatment. Endogenous factors include congenital microdefects of bronchial structures, immunodeficiency, and ciliary dysfunction.

Pathogenesis CNBLZ is not well developed. Infection occupies a central place in the pathogenesis of CNBL. As a result of the development and persistence of the inflammatory process, damage to the ciliary epithelium of the bronchi, hyperplasia of goblet cells, and destruction of the ciliated epithelium develop.

The consequence of long-term inflammatory changes is the formation of irreversible dilatations of the bronchi with pronounced structural changes in their walls and functional inferiority.

The function of the bronchi suffers - a violation of mucociliary clearance, often accompanied by bronchial obstruction.

Rice. 1.14. Scheme of the pathogenesis of CNBLZ

There is a relationship between the etiological factors of chronic pulmonary disease, inflammation and bronchial obstruction (“vicious circle”, Fig. 1.15).

Rice. 1.15. « Vicious circle" in chronic pulmonary disease(Sereda E.V., 2002)

Classification

Chronic lung pathology in children includes:

Infectious and inflammatory lung diseases;

Congenital malformations of the bronchopulmonary system;

Hereditary lung diseases;

Lung lesions in other hereditary diseases;

Allergic lung diseases.

Infectious and inflammatory diseases of the lungs are represented by: chronic bronchitis, bronchiectasis.

Chronic bronchitis (CB)– chronic widespread inflammatory lesion of the bronchi.

CB is currently considered as an independent nosological entity. Primary bronchitis is a chronic widespread inflammatory lesion of the bronchi, occurring with repeated exacerbations. ICD-10 distinguishes: simple, mucopurulent, unspecified chronic disease. CB can also be secondary (a syndrome associated with the underlying pathology).

Bronchiectasis (BEB) is an acquired chronic inflammatory disease of the bronchopulmonary system, characterized by a purulent-inflammatory process in dilated deformed bronchi with infiltrative and sclerotic changes in the peribronchial space.

EBD is an independent nosological form. The term “bronchiectasis” refers to irreversible dilation of the bronchi, which can be localized or cover entire sections of the bronchial tree. Any form of bronchiectasis is associated with a bacterial infection. The main role in the appearance of bronchiectasis is played by damage to the bronchial wall by infection. EBD, as a separate nosological form, should be distinguished from bronchiectasis that develops in other diseases. These include: congenital anomalies of the bronchopulmonary system, Williams-Campbell syndrome, tracheobronchomegaly, cystic fibrosis, primary immunodeficiencies, primary ciliary dyskinesia, Kartagener syndrome, alpha-1-antitrypsin deficiency, Ehlers-Danlos syndrome, Marfan syndrome.

Malformations of the bronchopulmonary system presented lung malformations: pulmonary agenesis, pulmonary aplasia, pulmonary sequestration, pulmonary cysts, pulmonary hypoplasia.

Common malformations of the wall of the trachea and bronchi include: tracheobronchomegaly, tracheobronchomalacia, Williams-Campbell syndrome, bronchiolectatic emphysema.

Limited malformations of the wall of the trachea and bronchi represented by: congenital stenoses, congenital lobar emphysema, diverticula of the trachea and bronchi, accessory bronchi; defects of individual bronchi; tracheobronchoesophageal fistulas.

Research:general blood and urine analysis, sputum culture for flora and cytological examination of sputum, biochemical blood test (generally accepted tests), blood gas test, spirogram(children over 5 years old); test with a bronchodilator; X-ray of the chest organs, bronchoscopy (with analysis of bronchial contents), examination of stool for worm eggs. According to indications: determination of immunoglobulins in the blood, radiography of the paranasal sinuses, ECHO-CG, Mantoux test, sweat test, pneumoscintigraphy, bronchography, biopsy of the bronchial mucosa with examination of the ciliated epithelium, CT, NMR, angiopulmonography, analysis for ά 1-antitrypsin, sweat analysis for chlorides.

History, clinic. In the anamnesis, children with CNBLD include repeated pneumonia of one localization, severe pneumonia of the staphylococcal type, a protracted course of segmental pneumonia, especially in early age; indications of congenital malformations of the bronchopulmonary system, bronchial foreign body, atelectasis in premature infants, immunodeficiency state, bronchopulmonary dysplasia after mechanical ventilation, mucociliary insufficiency, severe whooping cough and measles. Fever, growth retardation, insufficient weight gain, and limitation of physical activity may be detected.

Characteristic complaints are persistent cough, more often in the morning, at night, with sputum discharge (including in the absence of ARI). The amount of sputum can vary from small (20-50 ml per day) to 100-150 ml; in the presence of bronchiectasis, the sputum can be mucopurulent or purulent.

Symptom complex of chronic intoxication,hypoxia- rapid fatigue, decreased performance, impaired concentration, weakened memory, pallor, shadows under the eyes, there may be signs of dystrophy, the presence of “drumsticks”, “watch glasses”, asymmetrical deformation of the chest.

Bronchopulmonary syndrome: a shortening of the sound during percussion of a local nature or a mosaic pattern is detected. On auscultation against the background of hard breathing, there is the presence of persistent local different-sized wet and dry rales of different timbres.

CB is characterized by the presence of a prolonged cough with sputum, constant auscultation of moist and dry rales over the lungs.

BEB is characterized by a cough with a large amount of purulent sputum. There is a delay in children's physical development. Various variants of chest deformation are often identified. Respiratory failure, drumsticks, and watch glasses are typical of varying degrees of severity. Characterized by harsh breathing, moist rales of various sizes, crackling rales such as “machine gun crackling,” and distant rales.

Diagnosis

Diagnosis HB is established on the basis of the clinic and confirmed using bronchoscopy, spirography, bronchography, computed tomography. In this case, all other causes of the formation of chronic bronchopulmonary pathology should be excluded.

Primary chronic disease diagnosed in the presence of cough with sputum, constant wheezing for 3 months or more. There must be at least 3 exacerbations throughout the year. The total duration of the disease is 2 years or more. It is necessary to exclude diseases occurring with secondary bronchitis , which is a component of chronic diseases of the lungs and bronchi (cystic fibrosis, primary ciliary dyskinesia, malformations of the bronchopulmonary system, etc.).

Diagnosis of EBD is established taking into account the clinic’s assessment. In addition to the actual documentation of the presence of bronchiectasis (bronchoscopy, bronchography, CT), X-ray examination reveals deformation of the pulmonary pattern, peribronchial compactions, cellular pulmonary pattern, ring-shaped shadows, displacement of mediastinal organs. It is necessary to make a differential diagnosis between EBD itself and bronchiectasis, as a manifestation of the underlying pathology.

Laboratory research

General blood analysis- during exacerbation of chronic pulmonary disease, neutrophilic leukocytosis and an increase in ESR are recorded.

During X-ray examination in CB it is detected : strengthening and deformation of the pulmonary pattern without local pneumosclerosis.

Bronchoscopy for chronic disease- a picture of simple, mucopurulent endobronchitis. In CB there is deformation of the bronchi varying degrees severity and prevalence. In primary chronic disease, changes are detected in the mucous and submucosal layer of the bronchi with hyperplasia of the glands.

Bronchoscopy with BEB, it reveals various types of bronchiectasis, bronchial deformation and inflammatory changes.

Bronchography with CB, it detects deformation of the walls of the bronchi, their retraction and bulging, curvature and bareness of the bronchial trunks. In this case, local pneumosclerosis is not detected. An important point is that the transformation of CB into bronchiectasis does not occur.

Bronchography with BEB - deformation of the bronchial tree, expansion of the distal sections of the bronchi, the presence of cylindrical and saccular bronchiectasis.

Spirography- dysfunction of external respiration of a restrictive, obstructive or mixed nature.

Sputum analysis- the presence of neutrophils, macrophages, bacteria (usually gram-negative flora, resistant to antibiotics).

Bacteriological research sputum- most often isolated are Haemophilus influenzae, β-hemolytic streptococcus, pneumococcus, different types Staphylococci are often identified as mycoplasmas, both independently and in association with other microorganisms.

Differential diagnosis must be carried out with: tuberculosis; hereditary bronchopulmonary pathology; congenital anomalies of the bronchopulmonary system; lung lesions in systemic diseases; recurrent bronchitis.

Tab. 1.34 Differential diagnosis of chronic bronchitis

Treatment,treatment objectives: relief (reduction of intensity) of inflammatory manifestations, prolongation of the period of remission, improvement of the patient’s quality of life, prevention of disease progression and the formation of complications.

Treatment scheme. Mandatory with CNBLD are: antibacterial therapy, mucolytic therapy, positional drainage, vibration chest massage, anti-inflammatory treatment, exercise therapy.

Auxiliary treatment: regimen, diet, treatment of broncho-obstructive syndrome, physiotherapy, therapeutic bronchoscopy, mucoregulators, herbal medicine, endobronchial administration of antibiotics, surgical treatment.

Indications for hospitalization: severe exacerbations of chronic pulmonary disease, complicated course of the disease, the presence of severe background pathology, the need for in-depth examination, hospitalization for social reasons.

In case of exacerbation of EBD, chronic disease, bed or semi-bed rest, a diet with an increased amount of protein (meat, cottage cheese) and fats (butter, fish oil) are prescribed.

Antibacterial therapy for CP and BEB it is used in all cases of exacerbations of the disease.

Indications for antibacterial therapy in the treatment of CB:

exacerbation of chronic disease or its high activity beyond exacerbation;

development of pneumonia or exacerbation of a pulmonary focus of infection;

addition of mycoplasma or chlamydial infection;

with symptoms suspicious of a bacterial infection;

when an extrapulmonary focus of a bacterial process occurs (sinusitis, otitis media, etc.).

Table 1.35.Mucolytic drugs in the treatment of chronic pulmonary disease

Antibacterial therapy is based on the results of culture of the pathogen from sputum. If culture results are negative, treatment is carried out taking into account the most likely causative agent of the disease. Antibiotic therapy can be started with protected penicillins, cephalosporins, aminoglycosides. For mild exacerbations, oral administration of drugs is possible (see also “Treatment of pneumonia”). If treatment is insufficiently effective, therapeutic bronchoscopy and endotracheal administration of antibiotics are indicated.

An important place in the treatment of exacerbations of CB and EBD is occupied by postural drainage, which is carried out 3-4 times a day for 10-15 minutes before meals.

Mucolytic therapy for CNBLD, it is aimed at liquefying and removing sputum. For these purposes, the use of mucolytics is recommended (Table 1.35).

Treatment of bronchial obstruction syndrome with CNBLD presents a difficult problem. When carrying out this treatment, preference should be given to long-acting drugs, which include long-acting β 2 agonists (Foradil, etc.).

Physiotherapy for CNBLD includes UHF, microwave therapy, drug electrophoresis. For catarrhal manifestations in the lungs, obstruction, hypoventilation, electrophoresis with platiphylline is used. For severe cough - electrophoresis with 0.1% dionine solution. During the period of subsidence of inflammatory changes, inductothermy or ultrasound therapy is prescribed.

Sanatorium treatment consolidates the results of exacerbation therapy, improves preoperative preparation and rehabilitation after surgery and includes: exercise therapy, outdoor games, walks, sports exercises.

From funds herbal medicine used: St. John's wort, chamomile flowers, wild rosemary herb, etc.

The use of positional drainage, vibration massage of the chest, and exercise therapy is indicated.

Surgical treatment It is recommended in the presence of a well-demarcated area of ​​pneumosclerosis with bronchiectasis, as well as (palliative surgery) in case of extensive manifestations that negatively affect the development of the child. In severe bilateral processes, removal of the most affected segments reduces the degree of intoxication and promotes the physical development of the child.

Outcomes. The prognosis for chronic pulmonary disease depends on the type of disease and the prevalence of bronchopulmonary changes . The most favorable prognosis for CB. Improvement in the condition and course of the disease is observed in adolescence.

The prognosis for BEB is more serious than for CB. Improvement with age is observed in only 1/3 of patients. However, the disease does not progress either. There is no complete recovery even after surgery.

The most serious prognosis is for cystic hypoplasia of the lung. During observation, clinical manifestations of the disease persist.

Prevention CNBLZ includes the whole range of measures used for acute pneumonia (improvement of living conditions, rational nutrition, hardening, treatment of background pathology, etc.). A special place is occupied by the use of pneumococcal vaccines. Timely removal is important foreign bodies, early recognition and treatment of atelectasis.

Questions for the exam. Chronical bronchitis. Bronchiectasis. Etiology. Pathogenesis. Clinical picture. Diagnostics. Indications for bronchological examination. Bronchological research methods: bronchoscopy, bronchography. Non-invasive research methods: X-ray examination of the lungs, computed tomography (CT), nuclear magnetic resonance imaging (NMRI). Radioisotope research methods. Differential diagnosis. Treatment . Non-drug treatment methods. Indications for surgical treatment. Outcomes. Prevention.

Currently pneumonia in children is an urgent medical and social problem. The epidemiology of pneumonia at the present stage is characterized by a tendency to increase morbidity and mortality throughout the world.
Pneumonia is an acute infectious and inflammatory disease of the lung parenchyma, which is characterized by infiltrative changes in the lung tissue and respiratory failure.

Acute pneumonia in children manifests itself infectious lesion alveoli, which is accompanied by inflammatory infiltration of the parenchyma (neutrophils, macrophages, lymphocytes, etc.), as well as exudation, water-electrolyte and other metabolic disorders with pathological changes in all organs and systems of the child’s body.

Classification.

Origin:

• Community-acquired (outpatient) – acute pneumonia that occurs in a child in normal home conditions;
• Nosocomial (hospital-acquired) – pneumonia that develops after 48 hours of a child’s hospital stay, provided there is no infection at the time the patient is admitted to the hospital or within 48 hours after discharge;
• Ventilation – pneumonia, develops in patients who undergo artificial pulmonary ventilation (ALV). Depending on the time of development, there are: early (occurs for the first time on the 4th day of mechanical ventilation) and late (after 4 days of mechanical ventilation);
• Intrauterine pneumonia (congenital) – pneumonia that occurs for the first time within 72 hours of a child’s life;
• Aspiration pneumonia occurs in patients after an episode of massive aspiration or in patients who have risk factors for developing aspiration.

For clinical and radiological form:

• Focal – a variant of the course in which inflammatory infiltrates on an x-ray look like small foci;
• Segmental (mono-polysegmental) – infiltrative shadow coincides with the anatomical boundaries of the segment (or segments);
• Lobar (lobar) - inflammatory damage to the lung tissue in the area of ​​one lobe of the lungs;
• Interstitial – lung damage with predominance pathological process in interstitial tissue.

According to the degree of severity -I,II,III,IV,V degree.

• I degree -<50 балов, риск летальности — 0,1, амбулаторное лечение;
• II degree – 51-70 points, risk of mortality – 0.6, outpatient treatment;
• III degree – 71-90 points, risk of mortality – 2.8, hospitalization;
• IV degree – 91-130 points, risk of mortality – 8.2, hospitalization;
• V degree - >130 points, risk of mortality - 29.2, hospitalization;

Points are calculated according to the severity index:

• Age:
  < 6 мес – (+25);
  > 6 months -3 years – (+15);
  3-15 years – (+10).
• Accompanying illnesses:
  — birth defects hearts – (+30);
  — malnutrition – (+10);
  — immunodeficiency states – (+10);
  — impaired consciousness – (+20);
  — shortness of breath – (+20);
  — cyanosis – (+15);
  — chest pain – (+20);
  — toxic encephalopathy – (+30);
  - body temperature more than 39 or less than 36 - (+15).
• Laboratory data:
  — leukocytosis – (+20);
  — leukopenia – (+10);
  — anemia – (+10);
  — pH< 7,35 – (+30);
  — BUN >11 mmol/l – (+20);
  —Hct<30% — (+10);
  — SaO2<90% — (+20);
  — KVP – (+20);
  — multilobar infiltration on a radiograph – (+15);
  — infectious-toxic shock – (+40);
  — pleural exudate – (+30);
  — destruction – (+50).

For the degree of respiratory failure (RF) - I, II, III.

For complications:

• Uncomplicated;
• Complicated:
  — ;
  — cardio-respiratory;
  - circulatory;
  - pulmonary complications (destruction, abscess, pleurisy, pneumothorax);
  - extrapulmonary complications (osteomyelitis, otitis media, meningitis, pyelonephritis).

By localization:

• One-sided: left-sided, right-sided, indicate segment (you) or share;
• Two-way: specify the segment(s) or share.

Behind the current:

• Acute (up to 6 weeks);
• Protracted (from 6 weeks to 8 months).

Etiology.

Etiological structure of community-acquired pneumonia depending on age:

• 0 – 6 months – E.coli, S.agalactiae, L.monocytogenes, S.aureus, C.trachomatis, viruses;
• 6 months – 5 years – S.pneumoniae (70-88%), H.influenzae type b (up to 10%), M.pneumoniae (15%), C.pneumoniae (3-7%), viruses;
• Over 6 years - S. pneumoniae (35-40%), M. Pneumonia (23-44), C. Pneumoniae (15-30%), H. influenzae type b - rare.

Clinical diagnosis.

Clinical symptoms of community-acquired pneumonia:

• Acute onset;
• more than 3 days;
• Severe intoxication syndrome;
• Cough with sputum production.

During examination, you should pay attention to the phenomena of respiratory failure - shortness of breath, cyanosis, participation of auxiliary muscles in the act of breathing, tachycardia.

Degrees of respiratory failure:

• I degree – shortness of breath during physical activity. Oral cyanosis, which worsens with anxiety. P/D = 2.5:1. The gas composition changed slightly (SaO2 decreased by up to 90%);
• II degree – shortness of breath at rest, constant. Permanent cyanosis of the face and hands. Blood pressure is increased. Tachycardia.
  P/D = 2-1.5:1. SaO2 is 70-85%. Respiratory or metabolic acidosis;
• III degree – severe shortness of breath (respiratory rate above 150% of normal). Generalized cyanosis. Blood pressure is reduced. SaO2 below 70%. Decompensated mixed acidosis.

Physical signs of compaction of lung tissue:

• Palpation - retraction of the chest, increased vocal tremors;
• Percussion – local shortening of percussion sound;
• Auscultation - weakened breathing, local crepitus or asymmetry of moist, sonorous rales during auscultation.

Clinical picture of atypical community-acquired pneumonia:

• Gradual onset;
• The intoxication syndrome is slightly expressed;
• Dry cough;
• The presence of nonspecific respiratory symptoms: mild dyspnea, dry wheezing;
• Lack of response to pre-treatment with β-lactams.

Laboratory research methods:

General blood analysis.

The likelihood of community-acquired pneumonia of bacterial etiology is quite high in the presence of leukocytosis (especially above 20x10 9 /l), neutrophilia and accelerated ESR, especially if this is associated with a fever above 39C.
In atypical pneumonia: lymphocytosis, eosinophilia, accelerated ESR.
Determination of indicators of the acute phase of inflammation: an increase in the level of CRP, procalcitonin, sialic acids is not so much diagnostic as it can be an indicator of the effectiveness of treatment.

Instrumental research methods:

• .
  Should be performed in all children with suspected pneumonia and hypoxemia. The presence of hypoxemia should be the basis for making a decision for hospitalization of the patient, further diagnostic testing and the amount of treatment;
• X-ray of the chest organs.
  Characteristic are infiltrative changes, focal or segmental, against the background of an intensified pulmonary pattern with a compacted root due to edematous hilar lymph nodes.
  Children with clinical signs of pneumonia are recommended to have a chest x-ray when:
  — clinical results are ambiguous;
  - there are suspicions of complications, such as pleural effusion;
  - long-term pneumonia that does not respond to antimicrobial drugs.
  Chest radiography is not necessary for uncomplicated community-acquired pneumonia, when treatment is carried out on an outpatient basis.
  X-ray of the chest organs in two projections (posterior-anterior and lateral) should be performed in patients:
  — with hypoxemia;
  - significant respiratory distress;
  - if you suspect a complicated course of pneumonia.

Something to remember! Falsely negative results for the diagnosis of pneumonia are observed in the early stages of the disease, dehydration, neutropenia, and also in pneumonia caused by Pneumocystis carini. In these cases it is necessary to repeat X-ray examination in 24 hours.
It should be noted that the results of x-ray examination cannot be used to determine the etiological factor of pneumonia.
Repeated chest X-ray should be performed only if there is no positive dynamics within 48-72 hours of antibacterial therapy, as well as if complications are suspected.
Repeated chest radiography should be performed 4-6 weeks after pneumonia in patients with recurrent pneumonia, as well as in cases of suspected anatomical abnormalities or foreign body aspiration.

Etiological diagnosis:

• Gram staining of sputum or bronchial exudate and bacteriological culture (culture of material from the nose is not informative);
• Immunofluorescence methods (some viruses);
• Serological research methods (complement fixation reaction, RFGA);
• Diagnostic pleural puncture with culture of the contents for flora (for pleural effusion);
• A tuberculin skin test is carried out according to indications in children who are in contact with a patient with tuberculosis;
• Bacteriological blood culture for sterility in outpatients is carried out according to indications, while in hospitalized patients it is mandatory;
• Urine antigen tests are not recommended for diagnosing pneumococcal pneumonia in children due to the possibility of a false-positive result.

General indications for hospitalization of patients for pneumonia:

• Complicated course of the disease;
• DN - II–III, unstable hemodynamics;
• Unfavorable premorbid background;
• Chronic diseases accompanying pneumonia;
• Unfavorable social and living conditions;
• Ineffectiveness of therapy after 24-36 hours.

Indications for hospitalization in young children:

• Sao2<92%, цианоз;
• Respiratory rate >70 per minute;
• Labored breathing;
• Intermittent apnea, distant wheezing;
• Refusal to feed.

Indications for hospitalization in older children:

• Sao2<92%, цианоз;
• Respiratory rate >50 per minute;
• Labored breathing;
• Distant wheezing;
• Signs of dehydration.

Treatment of pneumonia will be outlined in the next article.

Literature: V.G. Maydannik E.O. Yemchinska. “Clinical findings from the diagnosis and treatment of drug-induced pneumonia in children.” Kiev – 2013.

Community-acquired pneumonia is an inflammatory change in the lungs that occurs outside the walls of a medical institution. In comparison with the nosocomial form, for this type of disease there is a special list of pathogens, symptoms and treatment tactics. Right-sided, left-sided, upper lobe, lower lobe, focal, segmental - high-quality diagnostics will help identify and treat these forms. Classifications will help you select treatment for the disease: clinical and according to ICD 10.

The etiology of community-acquired pneumonia is caused by bacterial infection of the respiratory tract. In 20% of cases in children, the disease is caused by pneumococcus (streptococcus pneumonia). In adults, right-sided lower lobe inflammation, caused by mixed flora, is more common.

Common pathogens of community-acquired pneumonia:

• Mycoplasma pneumoniae;
• Chlamydia pneumoniae;
• Klebsiella pneumoniae;
• Haemophilus influenzae;
• Escherichia coli;
• Staphylococcus. aureus;
• Streptococcus pyogenes;
• Chlamydia psittaci;
• Coxiella burnetii;
• Legionella pneumophila.

The etiology of the disease affects treatment. The use of antibiotics in the early stages of the disease can prevent respiratory failure and death. To prescribe adequate drugs, it is important to determine the causative agent of the disease.

Despite the apparent simplicity of treating pathology in children, in practice doctors face serious difficulties.

The pathogenesis of pathological changes in lung tissue depends on the type of bacterial agent and the mechanism of action of its toxins. For example, Pseudomonas aeruginosa provokes the development of purulent foci in the pulmonary parenchyma, which cause an increase in temperature and cause death if treatment is inadequate or delayed.

Community-acquired pneumonia occurs differently in children and the elderly, people with strong and weakened immune systems.

If the disease is caused by pneumococcus (S.pneumoniae), in most patients, when the immune system is strengthened, the body independently copes with the bacterial agent. Under the guise of antibacterial drugs, cure occurs in 7-10 days.

In older people, pneumococcus causes long-term and protracted right-sided lower lobe pneumonia with relapses. The pathogenesis of severe disease is due to the weakness of local protective factors of the respiratory tract (lack of alveolar macrophages, chronic bronchitis).

Chlamydial community-acquired pneumonia, provoked by Chlamydia pneumoniae (prevalence rate from 10 to 15%), has a tendency to frequent relapses and a chronic course. It is poorly corrected by antibacterial agents.

The etiology of the disease is determined not only by bacterial agents. Community-acquired pneumonia in winter is caused by viruses - coronavirus, influenza, Hantavirus, RS virus. The classic course of such pneumonia does not exceed 14 days. Antibacterial treatment has no effect on viruses, but doctors prescribe medications to prevent the addition of a bacterial infection.

When selecting treatment, we must not forget about the possibility of a mixed infection, when other bacterial pathogens are added to one pathological agent.

How does the causative agent of community-acquired pneumonia enter the respiratory tract:

• Aerosol (airborne) route - inhalation of air with microbes;
• Aspiration - entry into the respiratory tract of microbes that populate the nasopharynx through vomiting or swallowing stomach contents;
• With blood (hematogenous) – in the presence of infections in organs;
• Contact – from neighboring organs if there is inflammation in them (pancreatic abscess).

Some microorganisms detected by bacterial culture do not cause inflammation of the upper respiratory tract. Their detection only indicates contamination of the oropharynx - Candida spp., Neisseriaspp., Enterococcus spp.

Considering the difficulty of determining the etiological factor of the disease, we propose to divide all patients into categories based on the cause of pneumonia by age, symptoms and pathogens (see Table No. 1).

Pathogenesis of inflammation of the alveolar acini

Mycoplasma and chlamydia community-acquired pneumonia make up the majority of cases of pneumonia in children. According to ICD 10, these forms of the disease are classified as a separate category, and therefore require the prescription of special medications.

The bacteria Chlamidia pneumoniae and Mycoplasma pneumoniae cause up to 30% of cases of inflammatory changes in the pulmonary alveoli in children. In old age, the frequency of their detection is insignificant.

Under the influence of these microorganisms, left-sided lower lobe inflammatory changes are observed in women of reproductive age. These forms of the disease are chronic and characterized by frequent relapses. Only timely diagnosis of chlamydia, mycoplasma and legionella will prevent chronicity of the pathological process.

We draw the attention of readers: pneumococcus and Haemophilus influenzae (Afanasyev-Pfeiffer) cause complications such as purulent otitis media, pleurisy, and meningitis. In combination with Moraxella (Branhamella) catarrhalis, streptococcus pneumoniae leads to the development of purulent complications. Without adequate treatment, it is difficult to expect that inflammation of the lung tissue caused by these bacterial agents will go away on its own.

Clinical classification of pneumonia:

• aspiration;
• home;
• outpatient;
• in persons with defects in the immune system.

The aspiration form in adults occurs due to ingestion of gastric contents during vomiting. Its diagnosis is not difficult, since patients with this pathology are admitted to the intensive care unit due to respiratory failure.

In people with pathology of the defense system, a mixed infection (a combination of several bacterial agents) is observed.

Classification according to ICD 10 (international classification 10 revision):

• viral (J12);
• streptococcal (J13);
• Haemophilus influenzae (J14);
• unclassified bacterial (J15);
• unclassified non-bacterial (J16);
• pneumonia in illness (J17);
• without specifying the pathogen (J18).

Taking into account the above types of classification (clinical and according to the ICD), doctors formulate a diagnosis of “community-acquired pneumonia”. It also includes the following characteristics of pneumonia:

1. Clinical and morphological form (lobar, focal);
2. X-ray picture (lower lobe, segmental, total);
3. Course (mild, moderate, severe);
4. Presence/absence of respiratory failure.

Example of diagnosis: Community-acquired left-sided lower lobe pneumonia of mild severity, DN 0 (J17).

Symptoms of inflammation or how people get infected at home

Community-acquired pneumonia in children is more acute. This happens as a result of an unformed immune system. Symptoms of pneumonia are indicative (classical), so doctors show medical university students patients with pneumonia, mostly children.

The main symptoms of pneumonia:

• Cough;
• Temperature increase;
• Sputum separation;
• Pain in the chest;
• Weakness;
• Heavy sweating at night.

It should be understood that community-acquired polysegmental pneumonia manifests itself more acutely than focal pneumonia, regardless of whether it occurs in children or adults. This form requires immediate treatment, as it quickly leads to respiratory failure.

When examining patients with suspected pneumonia, the therapist auscultates (using a phonendoscope) determines the following symptoms:

• Shortening of percussion sound;
• Bronchial breathing;
• Voice tremors and increased bronchophony;
• Fine bubbling rales.

The signs described above are not indicative. Diagnosis of the disease is based on identifying not the entire list of pathological syndromes. It is enough to find 2-3 signs in the patient and send him for a chest x-ray.

The causative agents of community-acquired pneumonia cause an excellent clinical picture, so radiography is used to identify foci of inflammation of the lung tissue and assess the dynamics of treatment.

Differential diagnosis is carried out at the initial stages of the disease if inflammation of the pulmonary alveoli is suspected. The pathology is compared with the following diseases:

• Tuberculosis of the lungs. To distinguish it from bacterial inflammation, it is necessary to take sputum smears for the presence of Mycobacterium tuberculosis according to Ziehl-Nelson;
• Malignant neoplasms (adenoma, lymphoma, metastases, primary cancer);
• Diseases associated with pathology of the immune system (pneumonitis, lupus nephritis, granulomatosis, bronchiolitis obliterans, allergic aspergillosis);
• Pulmonary infarction and pulmonary embolism;
• Other diseases (focal pneumopathy, sarcoidosis, aspiration, congestive heart failure).

Differential diagnosis should also take into account the use of medications by a person, the presence of blood eosinophilia, and helminthic infestations.

It should be understood that community-acquired left-sided lower lobe pneumonia differs in symptoms from right-sided pneumonia. Signs of the disease differ in children and adults.

If the image shows upper lobe pneumonia, the radiologist will most likely send the person for a consultation with a phthisiatrician, since this localization is specific for mycobacteria.

High-quality diagnostics is based on many specific signs of pathological changes in the body. Among them, X-ray diagnostics of the lungs is important. It allows you to establish not only the morphological forms of the disease (focal, segmental, polysegmental), but also to identify the presence or absence of complications.

Treatment of pneumonia requires taking into account the causative agent of the disease, as well as its sensitivity to the action of antibacterial drugs.

Ideally, it is necessary to identify the antibiotic sensitivity of the pathogen in each individual patient. For these purposes, bacteriological culture of sputum is done on nutrient media. After the colonies of the microorganism grow, plates with several antibiotics are placed next to them. Where the bacterial culture stops growing, its sensitivity to the drug is noted.

An antibiotic sensitivity test in children is the highest quality method for successful treatment of the disease. It is rarely used in the treatment of pneumonia. This is due to the fact that the culture of microorganisms grows on a nutrient medium for about 2 weeks. Without adequate therapy during this period, the patient will die from respiratory failure. To prevent this from happening, empirical antibiotic therapy is carried out in the initial stages. Within 2 weeks it leads to the cure of the disease, so the rationality of the antibiotic sensitivity test disappears.

Pneumonia in children requires hospitalization regardless of the form of the disease (focal, polysegmental, right-sided, left-sided, lower lobe, upper lobe). In adults, mild symptoms of the disease are treated on an outpatient basis. In children, due to the likelihood of rapid development of complications, they are placed in a hospital at the first signs of inflammation of the lung tissue.

Therapy at home

Outpatient treatment of inflammation of the lung tissue includes the following procedures:

1. All patients are divided into 2 groups: up to 55 years without concomitant pathology and after this age;
2. The first group of patients is prescribed a combination regimen using amoxicillin (0.5 grams 3 times a day), levofloxacin (0.5 grams 3 times), azithromycin (0.25 grams 1 time a day);
3. The second group needs to treat concomitant diseases. Of the antibacterial drugs, parenteral agents are of primary importance: penicillins (1.2 grams 2 times a day), amoxicillin (1.2 grams 3 times a day), cefuroxime (0.75 grams 3 times), azithromycin (1 time 0. 25 grams), levofloxacin (0.5 grams 1 time)

The average duration of the above treatment is 10-14 days. The timing may be shifted if preliminary diagnosis did not reveal the presence of complications or concomitant diseases, and at the treatment stage they aggravated the clinical course of the disease.

Additional symptoms can worsen the treatment time for pneumonia in children:

• Respiratory failure (more than 20 respiratory acts per minute);
• Severe blood leukocytosis (increased number of white blood cells);
• Weak dynamics of treatment on x-ray.

The unidentified etiology of the disease reduces the healing time of the disease, which complicates the correct selection of medications.

Inpatient treatment of pneumonia in children

In small children, inpatient treatment is prescribed depending on the severity of the pathology. To assess the child’s condition, the following diagnostics are carried out:

• X-ray of the chest organs in 2 projections (in children over 10 years of age). Radiologists prefer to perform only one image of the lungs (in direct projection) for preschoolers in the absence of moderate and severe disease;
• Sputum microscopy by Gram;
• Determination of antibiotic sensitivity of microorganisms;
• Taking blood for bacteriological examination.

Inpatient therapy in children is carried out mainly with parenteral antibacterial agents according to the following scheme:

• Penicillins 2 million units about 5 times a day;
• Ampicillin – 1-2 grams 4-6 times;
• Ceftriaxone – 1-2 grams 1 time;
• In severe cases, doctors add clarithromycin or fluoroquinolones.

The duration of treatment for inflammation of the pulmonary parenchyma in children is 7-10 days. In severe cases of the disease, they extend to 14 days. If community-acquired left-sided lower lobe pneumonia in a child is provoked by an atypical infection (chlamydia, mycoplasma, legionella), the time frame for getting rid of the pathology can increase to 21 days.

Antibiotic therapy in both adults and children is stopped if the following symptoms are present:

• Persistent low-grade fever (temperature up to 38 degrees). Drug fever;
• Residual changes on the radiograph;
• Weak cough;
• Increased erythrocyte sedimentation rate;
• Sweating and weakness.

How are preventive measures carried out?

Prevention of inflammatory changes in the lungs includes the following measures:

• Good nutrition;
• Normalization of work and rest;
• Hardening;
• Sanitation of foci of infection;
• Physical education and sports classes;
• Treatment of colds;
• Vaccination of long-term and frequently ill children;
• Quitting bad habits (alcohol, smoking, drugs);
• Healthy lifestyle.

Who should get vaccinated?

People over 55 years of age, older people, and those with chronic respiratory and heart diseases should be vaccinated against pneumonia pathogens.

Right lower lobe pneumonia often occurs in the following groups of people:

• With human immunodeficiency virus;
• Diabetes mellitus;
• Hemoglobinopathies;
• Kidney diseases.

If children and adolescents from 10 months to 18 years of age experience right- or left-sided inflammatory changes in the lungs several times a year, it is rational to administer a vaccine. It will allow the body to adapt to common pathogens.

The optimal time to vaccinate before a flu epidemic is in November.

In conclusion, we note that even focal inflammation of the alveolar acini is a dangerous condition leading to respiratory failure. Its timely detection and treatment can save lives.

Symptoms of lung disease cannot be ignored. If they appear, consult a doctor immediately. If he recommends radiography, you should not refuse it.

High-quality prevention can prevent irreversible changes in lung tissue!