Purulent-destructive diseases of the lungs and pleura Classification (Mityuk I. I.)

The main nosological forms of infectious destruction of the lungs are abscess and gangrene of the lung. Lung abscess is a purulent melting of lung tissue, delimited from a healthy lung by a pyogenic membrane in the form of a layer of scarring granulation tissue. Lung gangrene is extensive necrosis and ichorous decay of lung tissue.

Frequency. The disease occurs 3-5 times more often than in the general population, among middle-aged men, mainly among alcoholics.

Causes of infectious destruction of the lungs

The causative agents are most often pyogenic bacteria. Among the anaerobes are bacteroides, fusobacteria, and anaerobic gram-negative cocci. Aerobes include Staphylococcus aureus, Streptococcus, Escherichia coli, Klebsiella, Enterobacteriaceae, Legionella, Actinomycetes, etc. Risk factors include alcoholism, neurological disorders (cerebrovascular disorders, swallowing disorders, myasthenia gravis, epilepsy), general anesthesia, surgery on the esophagus and stomach, prolonged vomiting, tumors and foreign bodies in the bronchi, gastroesophageal reflux disease, diabetes mellitus, immunodeficiency states.

The pathogen penetrates into the lung tissue more often bronchogenically (aspiration of the contents of the oropharynx, obstruction of the respiratory tract, bronchopneumonia), less often - hematogenously, lymphogenously or after injury (including closed - bruise, concussion, compression of the chest).

Pathomorphology. A lung abscess is characterized by inflammatory infiltration with the formation of a round cavity, limited from the surrounding tissue by fibrous and granulation tissue. With gangrene of the lung, widespread necrosis is detected with multiple cavities of irregular shape, passing without clear boundaries into the surrounding edematous and leukocyte-infiltrated lung tissue.

Classification. Abscesses can be purulent and gangrenous (an intermediate form between an abscess and widespread gangrene of the lung), acute and chronic (duration of the disease is more than 2 months), primary and secondary (septic embolism or rupture of pleural empyema into the lung), unilateral and bilateral, single and multiple , peripheral and central (root).

Symptoms and causes of infectious lung destruction

During a lung abscess, there are 2 periods: before the breakthrough of pus into the bronchus, when a high temperature with chills, heavy sweats, and a dry cough are observed. Over the affected area, vocal tremor is enhanced, percussion sound is dull, vesicular breathing is weakened, bronchial breathing, dry or moist rales are often heard. After the breakthrough of pus into the bronchus, a coughing attack is observed with a large amount of often foul-smelling sputum (it comes out “full of mouth”), the temperature drops, and overall health improves significantly. The intensity and extent of dullness of percussion sound decrease, and a tympanic tint may appear. Auscultation reveals moist rales of various sizes and bronchial (or its version - amphoric) breathing. In the chronic course of the abscess, the symptoms of intoxication (fever, chills, weakness, sweating, shortness of breath) persist, and a cough with a moderate amount of foul-smelling sputum is bothersome. The terminal phalanges take the shape of “drumsticks”, and the nails - “watch glasses”; signs of right ventricular failure are noted.

With gangrene of the lung, the symptoms of intoxication are more pronounced, there is no appetite, the sputum is putrid in nature and is discharged in large quantities. On auscultation, vesicular breathing is weakened, bronchial breathing and moist rales can be heard.

Diagnosis of infectious lung destruction

Laboratory examination data reveal neutrophilic leukocytosis with a shift to the left, an increase in ESR, and dysproteinemia. In severe cases, anemia and proteinuria are noted. When standing, sputum forms two or three layers.

Microscopy reveals a large number of leukocytes and elastic fibers.

Complications and infectious destruction of the lungs - pleural empyema, pyopneumothorax, sepsis, hemoptysis and pulmonary hemorrhage, adult respiratory distress syndrome.

Diagnosis is based on medical history, clinical, radiological and laboratory examination. To confirm the diagnosis, you can use computed tomography (allows you to accurately determine the localization and extent of the process, assess the involvement of the pleura) and bronchoscopy (helps isolate the pathogen and sanitize the airways).

Forecast. With lung abscesses, the transition to a chronic form is observed in 10-15% of patients, and mortality from complications reaches 10%. Widespread gangrene of the lung is fatal in 40% of cases.

Treatment and prevention of infectious destruction of the lungs

The basis of conservative treatment is antibiotic therapy, which is carried out for a long time (in uncomplicated cases - up to two months), in optimal doses, with bactericidal drugs, preferably intravenously. The choice of drug is determined by the nature of the isolated microflora and its sensitivity to antibacterial agents. Until culture results are obtained, antibacterial, symptomatic and detoxification therapy is carried out according to general principles (see treatment for Mon). In order to improve the drainage function of the bronchi, therapeutic bronchoscopy is indicated. In necessary cases (presence of complications, large abscess or its chronic course, ineffectiveness of antibiotic therapy), surgical treatment is performed.

Prevention. As part of prevention, 3 months after discharge from the hospital, the patient is examined by a pulmonologist at the place of residence and a chest x-ray is performed.

Infectious destruction of the lungs is a severe pathological condition characterized by inflammatory infiltration and subsequent purulent or putrefactive decay (destruction) of lung tissue as a result of exposure to nonspecific infectious pathogens (N.V. Pukhov, 1998). There are three forms of infectious lung destruction: abscess, gangrene and gangrenous lung abscess.

Causes of infectious destruction of the lungs

There are no specific pathogens that cause infectious destruction of the lungs. In 60-65% of patients, the cause of the disease is non-spore-forming obligate anaerobic microorganisms: bacteroides (B.fragilis, B.melaninogenicus); fusobacteria (F.nucleatum, F.necropharum); anaerobic cocci (Peptococcus, Peptostreptococcus), etc. Infectious destructions resulting from aspiration of oropharyngeal mucus are most often caused by fusobacteria, anaerobic cocci and B.melaninogenicus. During aspiration of gastric contents, the most common causative agent of infectious destruction of the lungs is B.fragilis.

In 30-40% of patients, infectious destruction of the lungs is caused by Staphylococcus aureus, Streptococcus, Klebsiella, Proteus, Pseudomonas aeruginosa, and Enterobacteriaceae. These pathogens most often cause infectious destruction of the lungs, not primarily associated with aspiration of oropharyngeal mucus or gastric contents.

Infectious destruction of the lungs of hematogenous-embolic origin is most often caused by Staphylococcus aureus.

In rare cases, the cause of the disease is non-bacterial pathogens (fungi, protozoa).

Predisposing factors: smoking, chronic bronchitis, bronchial asthma, diabetes mellitus, epidemic influenza, alcoholism, maxillofacial trauma, prolonged exposure to the cold, influenza.

Pathogenesis of infectious destruction of the lungs

The causative agents of infectious destruction of the lungs penetrate the pulmonary parenchyma through the respiratory tract, less often hematogenously, lymphogenously, by spreading from neighboring organs and tissues. In case of transbronchial infection, the source of microflora is the oral cavity and nasopharynx. Aspiration (microaspiration) of infected mucus and saliva from the nasopharynx, as well as gastric contents, plays an important role. In addition, lung abscesses can occur with closed injuries (bruises, compression, concussions) and penetrating wounds of the chest. With an abscess, limited inflammatory infiltration is initially observed with purulent melting of the lung tissue and the formation of a decay cavity surrounded by a granulation shaft.

Subsequently (after 2-3 weeks), a breakthrough of the purulent focus into the bronchus occurs; with good drainage, the walls of the cavity collapse with the formation of a scar or an area of ​​pneumosclerosis.

With gangrene of the lung, after a short period of inflammatory infiltration due to the influence of microflora waste products and vascular thrombosis, extensive necrosis of the lung tissue develops without clear boundaries. In necrotic tissue, many foci of decay are formed, which are partially drained through the bronchus.

The most important pathogenetic factor is also a decrease in the function of general immunity and local bronchopulmonary protection (see “Chronic bronchitis”).

Classification of infectious destruction of the lungs

1. Causes (depending on the type of infectious agent).
   • Aerobic and/or conditionally anaerobic flora.
   • Obligate anaerobic flora.
   • Mixed aerobic-anaerobic flora.
   • Non-bacterial pathogens (fungi, protozoa).
2. Pathogenesis (mechanism of infection).
   • Bronchogenic, including aspiration, post-pneumonic, obstructive.
   • Hematogenous, including embolic.
   • Traumatic.
   • Associated with the direct transfer of suppuration from neighboring organs and tissues.
3. Clinical and morphological form.
   • Abscesses are purulent.
   • Abscesses are gangrenous.
   • Gangrene of the lung.
4. Location within the lungs.
   • Peripheral.
   • Central.
5. Prevalence of the pathological process.
   • Single.
   • Multiple.
   • One-sided.
   • Double-sided.
   • With segment damage.
   • With the defeat of the share.
   • With damage to more than one lobe.
6. The severity of the current.
   • Light flow.
   • The course is of moderate severity.
   • Heavy current.
   • Extremely severe course.
7. The presence or absence of complications.
   • Uncomplicated.
   • Complicated:
     • pyopneumothorax, pleural empyema;
     • pulmonary hemorrhage;
     • bacteremic shock;
     • adult acute respiratory distress syndrome;
     • sepsis (septicopyemia);
     • phlegmon of the chest wall;
     • defeat of the opposite side in a primarily unilateral process;
     • other complications.
8. The nature of the flow (depending on time criteria).
   • Spicy.
   • With a subacute course.
   • Chronic lung abscesses (chronic gangrene is impossible).

Note: a gangrenous abscess is understood as an intermediate form of infectious destruction of the lungs, characterized by less extensive and more prone to delineation than gangrene, necrosis of the lung tissue. In this case, in the process of melting the lung tissue, a cavity is formed with parietal or free-lying tissue sequesters.

– these are complications of bacterial pneumonia that occur with the development of purulent-inflammatory processes in the lung and pleura. Common manifestations of various forms of bacterial destruction of the lungs are symptoms of purulent intoxication and respiratory failure. Diagnosis and differential diagnosis are based on data from chest radiography, ultrasound of the pleural cavity, thoracentesis, laboratory examination of sputum, exudate, and peripheral blood. The basic principles of treatment for bacterial destruction of the lungs include antibiotic therapy, infusion detoxification, sanitation of the bronchi, and, if indicated, puncture and drainage of the pleural cavity, surgical treatment.

ICD-10

J85 J86

General information

Bacterial destruction of the lungs (syn. purulent-destructive pneumonia) is an inflammation of the lung tissue that acquires a purulent-necrotic character and leads to gross morphological changes in the lung parenchyma. Bacterial destruction of the lungs complicates about 10% of pneumonia in children, with a mortality rate of 2–4%. Among adults, purulent-destructive pneumonia is most often recorded in men aged 20-40 years. In approximately 2/3 of cases, the right lung is affected, in 1/3 - the left lung, very rarely (in 1-5% of patients) bilateral bacterial destruction of the lungs develops. Since this condition is always secondary and develops against the background of bacterial pneumonia, the most important task of pulmonology is to find ways to prevent, early diagnosis and optimal treatment of destructive processes in the lungs.

Causes

The most common initiators of destructive pneumonia are staphylococci, viridans streptococci, Proteus, Pseudomonas aeruginosa and Escherichia coli. Among the pathogens, there is an absolute predominance of staphylococcus, which forced staphylococcal destruction of the lungs to be identified as a special etiological subgroup. Less commonly, bacterial destruction of the lungs is caused by Pfeiffer and Friedlander bacilli and pneumococci. In most cases, purulent-necrotic processes begin with microbial associations, simultaneously represented by 2-3 or more types of bacteria.

The development of primary bacterial destruction of the lungs is based on the aerogenic or aspiration mechanism of pathogen penetration into the lungs with the development of bacterial pneumonia. Risk factors in this case are acute respiratory viral infections preceding pneumonia, aspiration of the contents of the nasopharynx, oropharynx, and stomach; GERD, fixation of foreign bodies in the bronchi, etc. With secondary metastatic destruction, the hematogenous spread of infection from local purulent foci (in acute osteomyelitis, furunculosis, umbilical sepsis, etc.) plays a leading role.

The development of bacterial destruction of the lungs is facilitated by conditions accompanied by a decrease in the cough reflex, level of consciousness and resistance of the body: nicotine addiction, alcohol abuse, drug addiction, occupational hazards, head injury, hypothermia, epileptic seizures, stroke, coma, previous infections, etc. Often destructive processes in the pulmonary tissues develop as a result of functioning esophageal-bronchial fistulas and lung injury.

Pathogenesis

In its development, bacterial destruction of the lungs goes through three stages: pre-destruction (from 1-2 to 7-14 days), actual destructive changes and outcome. The pre-destruction stage proceeds according to the type of focal confluent pneumonia or purulent lobitis. The second stage is characterized by necrosis and disintegration of the pulmonary parenchyma, followed by rejection of necrotic masses and the formation of an encysted purulent cavity. A favorable outcome of bacterial destruction of the lungs is recovery with the formation of pneumofibrosis or a lung cyst; unfavorable outcomes include complications and death.

Classification

Bacterial destruction of the lungs is classified according to etiology, mechanism of infection, forms of damage, and course. Depending on the type of pathogen, processes caused by aerobic, anaerobic, aerobic-anaerobic flora are distinguished. Some authors, based on the same principle, distinguish between staphylococcal, streptococcal, Proteus, Pseudomonas, and mixed destructions. According to the mechanism of damage, pathological processes are divided into primary (aerogenic - 80%) and secondary (hematogenous - 20%). Among the clinical and radiological forms of bacterial destruction of the lungs, the following are distinguished:

• pre-destruction (acute massive pneumonia and lobitas)
• pulmonary forms (pulmonary bullae and abscesses)
• pulmonary-pleural forms (pyothorax, pneumothorax, pyopneumothorax)
• chronic forms (lung cysts, bronchiectasis, pneumofibrosis, chronic lung abscess, pleural empyema) are the results of acute destruction.

In clinical practice, pulmonary-pleural forms of destruction predominate; pulmonary forms account for only 15-18%. According to the dynamics of the process, the process can be stable, progressive, regressive; uncomplicated and complicated. The course of bacterial destruction of the lungs can be acute, protracted and septic.

Symptoms

The clinical symptoms of destructive pneumonia develop when acute manifestations of pneumonia have already subsided. Thus, against the background of satisfactory health, hyperthermia up to 38-39 o C, chills, weakness, sweating, dry cough, and pain in the chest reappear. Shortness of breath and cyanosis are rapidly increasing; the patient's condition rapidly deteriorates. Usually, in the predestruction stage, there are no specific radiological data, so the patient is diagnosed with pneumonia.

At the same time, a number of clinical signs allow one to suspect the onset of bacterial destruction of the lungs: putrid breath, severe intoxication characteristic of purulent processes (adynamia, tachycardia, temperature peaks up to 39-40 o C, anorexia, etc.). After the abscess breaks into the bronchi, profuse coughing up of purulent, foul-smelling sputum begins. Against this background, there is an improvement in well-being, a decrease in temperature, an increase in activity, the appearance of appetite, etc. If the abscess does not drain, the purulent-septic syndrome persists and progresses.

With pyothorax, the patient's condition worsens gradually. Severe chest pain occurs when breathing, shortness of breath progresses, body temperature rises, mainly in the evenings. Children may develop abdominal syndrome simulating an acute abdomen and neurotoxicosis. Pyopneumothorax, which is a consequence of rupture of lung tissue and breakthrough of a purulent focus into the pleural cavity, can take a rapid clinical course. In this case, a paroxysmal cough, shortness of breath, increasing cyanosis, and tachycardia suddenly occur. Due to sudden collapse of the lung and pleuropulmonary shock, short-term apnea is possible. With limited pyopneumothorax, all symptoms are moderate.

The course of chronic forms of bacterial destruction of the lungs is characterized by signs of purulent intoxication (pale, sallow-gray skin color, malaise, poor appetite, weight loss). Worrying cough with a moderate amount of purulent sputum with a smell, hemoptysis, slight shortness of breath. Mild cyanosis and thickening of the distal phalanges of the fingers are typical.

Complications

Various forms of bacterial destruction of the lungs can be complicated by pulmonary hemorrhage, intrapleural bleeding (hemothorax), and pericarditis. With massive infection and reduced immune reactivity, fulminant sepsis develops, and with a chronic course, amyloidosis of internal organs. Lethal outcomes are mostly caused by acute renal failure and multiple organ failure.

Diagnostics

Blood tests show signs of active inflammation: leukocytosis with a shift to the left, a significant increase in ESR; an increase in the level of sialic acids, haptoglobin, seromucoids, fibrin. Microscopic examination of sputum determines its purulent nature, a large number of leukocytes, the presence of elastic fibers, cholesterol, and fatty acids. The pathogen is identified by bacteriological culture of sputum. Bronchial secretions can be obtained both by coughing and during diagnostic bronchoscopy.

The picture revealed by chest radiography varies depending on the form of bacterial destruction of the lungs. In typical cases, pulmonary destruction is defined as cavities with a horizontal fluid level, around which inflammatory infiltration of the lung tissue spreads. In case of pleural complications, a shift of the mediastinal shadow to the healthy side, the level of fluid in the pleural cavity, and partial or complete collapse of the lung are detected. In this case, it is advisable to supplement the X-ray picture with ultrasound data of the pleural cavity, pleural puncture and examination of exudate. Bacterial destruction of the lungs must be differentiated from the cavitary form of lung cancer, bronchogenic and echinococcal cysts, and cavernous tuberculosis. Pulmonologists, thoracic surgeons, and phthisiatricians should participate in differential diagnostics.

Treatment of bacterial destruction of the lungs

Depending on the form and course of bacterial destruction of the lungs, its treatment can be conservative or surgical with mandatory hospitalization in a pulmonology hospital or thoracic surgery department. A conservative approach is possible for well-draining uncomplicated lung abscesses and acute pleural empyema.

Regardless of the tactics for managing the pathology, massive antibacterial, detoxification and immunostimulating therapy is carried out. Antibiotics (carbapenems, fluoroquinolones, cephalosporins, aminoglycosides) are administered intravenously, as well as endobronchially (during sanitation bronchoscopy) and intrapleurally (during therapeutic punctures or flow-wash drainage of the pleural cavity). In addition to infusion detoxification, extracorporeal methods (ILBI, UVB, plasmapheresis, hemosorption) are widely used in the treatment of bacterial destruction of the lungs. Immunocorrective therapy involves the administration of gamma globulins, hyperimmune plasma, immunomodulators, etc. In the subsiding phase of inflammation, drug therapy is supplemented by methods of functional rehabilitation (physiotherapy, exercise therapy).

Among the surgical methods of treatment for inadequate emptying of the abscess in the lung, pneumotomy (open drainage) is used, sometimes resection interventions (lobectomy, bilobectomy) or pneumonectomy. Chronic pleural empyema may require thoracoplasty or pleurectomy with lung decortication.

Prognosis and prevention

About a quarter of cases of bronchial destruction of the lungs end with complete recovery; In half of the patients, clinical recovery is achieved with preservation of residual radiological changes. Chronicity of the disease occurs in 15-20% of cases. 5-10% of cases are fatal. The basis for preventing the development of bacterial destruction of the lungs is timely antibiotic therapy for bacterial pneumonia and purulent extrapulmonary processes, clinical and radiological monitoring of cure, and increased attention to patients at risk for the development of destructive processes in the lungs. At the stage of primary prevention, it is important to promote a healthy lifestyle and combat alcoholism and drug addiction.

Pneumonia is one of the most common diseases of mankind. And this is not strange, because due to physiological and anatomical characteristics, a person is poorly protected from pathologies of this type. Pneumonia occurs more often in cold and wet periods of the year, when there are all conditions for the development of the pathogen, and the human body is significantly weakened.

Due to the high severity of its course, pneumonia often leads to severe complications and is a very dangerous condition for humans. Rational treatment is the only way to save the patient’s life.

Inflammation can be caused by a large number of pathogens and harmful factors, but most often it is caused by streptococcus bacteria.

Acute purulent destructive pneumonia is a severe form of pneumonia, which is caused by a huge range of microorganisms and is characterized by destructive changes in the lung tissue.

The process begins acutely and often causes severe complications. Most often occurs in young children. Destructive pneumonia in children occurs quite often and accounts for 8-12% of the number of childhood pneumonias.

The pathology requires urgent hospitalization, correct diagnosis and adequate treatment. Otherwise, the patient faces serious consequences, including death.

Etiology of the disease in children

Risk factors for the development of pneumonia are:

• prematurity;
• previous prolonged acute respiratory viral infections;
• congenital and acquired immunodeficiencies;
• taking glucocortecosteroids;
• damage during the birth process;
• asphyxia with placental fluid;
• septicemia and septicopyemia;
• inadequate antibiotic therapy;
• poor living conditions.

All sorts of microorganisms can be the direct causative agents of destructive lung disease, but the most common culprit of the disease is a pathogenic strain of staphylococcus. You can often find whole “assortments” of pathogens, when, for example, staphylococcus causes the onset of the disease, and other microorganisms take advantage of the decrease in the body’s protective functions and aggravate the process.

In addition to staphylococcus, the following are important in the etiology of pneumonia:

• Boulevard Proteus;
• pseudomonas;
• enterobacteria;
• Klebsiella;
• flu;
• parainfluenza;
• adenoviruses.

Features in adults

The etiological causes and factors of purulent-destructive pneumonia in adults are practically no different from those in children. In addition to the risk factors listed in pediatric etiology, in adults several more acquired pathologies are added:

• human acquired immunodeficiency syndrome;
• hepatitis groups A, B, C;
• diabetes mellitus type 1 and 2;
• sepsis;
• alcoholism;
• smoking;
• addiction;
• unfavorable working conditions and occupational hazards.

The causative agents of inflammation are the same as in children.

The pathogenetic mechanisms of inflammation development are very simple and banal. The infectious agent penetrates into the lung tissue at the site of damaged mucous membrane (respiratory route of infection), through contaminated blood in septic conditions (hematogenous route of infection), as well as through lymph.

After the pathogen enters the lung tissue, it begins to rapidly multiply. As microorganisms multiply, small cavities filled with air (bulae) or encapsular abscesses (abscesses) develop. In the case of cavities located near the visceral pleura and their rupture into the pleural cavity, the possibility of developing pleural empyema, dry pleurisy or pneumothorax arises.

In rare cases, ulcers are located near large vessels. Having melted the vessel wall, microorganisms enter the blood, causing sepsis.

Classification

• Bronchogenic form: the route of infection is the respiratory tract. Occurs in 4/5 cases of the disease and is the primary independent form of the disease. During diagnosis, local damage to the lung tissue is most often noted.
• Hematogenous form: the route of infection is infected blood, for example, in sepsis. In children, the cause of secondary destructive inflammation may be neonatal phlegmon. When diagnosed, generalized damage to the lung tissue is most often noted.

According to the development of bronchopneumonia, the following stages of the process are distinguished:

• Stage of acute destructive pneumonia (intrapulmonary form);
• Stage of contact purulent-inflammatory process (pulmonary-pleural form). It is characterized by the transmission of infection from the lung tissue to the pleura and pleural cavity by contact.

As a separate option, there is a mediastinal form of destruction.

When diagnosing pneumonia, you must immediately determine whether it is primary or secondary.

1. Primary form. Thus, in the case of the bronchogenic form, the damage to the lung tissue will be localized, unilateral, most often located within one lobe. Symptoms make themselves felt already on the first or second day after the onset of the disease.

The patient's body temperature rises sharply, performance decreases, headache, nausea, vomiting, myalgia, joint pain appear, and the dry cough that appears relatively quickly turns into a mucous, mucopurulent, purulent cough. Hemoptysis occurs less frequently.

By percussion it is possible to hear dullness of sound in the area where the abscess is localized.

Auscultation reveals weakened vesicular breathing.

According to X-ray data, it is possible to determine the exact location of the pathological process, thanks to the massive amount of infiltrate and exudate. The image will show rounded zones that differ in the naivety of the liquid. If the fluid level is clearly visible, you can accurately say that the abscess is naive. When there is a cavity, but there is no fluid level, a bulla can be suspected.

In the blood, neutrophilic leukocytosis predominates with a shift in the leukocyte formula to the left. SOE increases significantly.

1. Secondary form. Develops against the background of other infections. Therefore, the importance of history prevails over the primary form. The clinic depends on the primary disease, but has several common characteristics.

With the progression of the secondary form of destruction, the phenomena of respiratory and cardiovascular failure most often develop. In addition to high fever, weakness, myalgia, nausea and vomiting, the patient experiences acrocyanosis, pallor, loss of consciousness, and shortness of breath.

X-rays show multiple chaotically located small cavities in both lungs, which contain air or pus.

If the abscess ruptures into the pleural cavity, the clinical picture rapidly worsens. Signs of inflammation of the pleura and pyopneumothorax appear: pain when breathing, shallow breathing, increased shortness of breath, a dull sound to percussion in the nooks of the pleura, displacement of the mediastinal organs.

The liquid level is determined using the X-ray method.

Children suffer inflammation much more severely than adults, so destructive pneumonia in children often causes complications.

Differential diagnosis must be carried out from other forms of pneumonia, polycystic pulmonary disease, and lung gangrene.

In the case of the primary form of the disease, First of all, it is necessary to get rid of the intoxication syndrome. For this purpose, the parenteral route of administration of rheopolyglucin preparations and potassium-sparing diuretics is used. 10-20% glucose and contrical are also administered. The patient is prescribed multivitamin complexes and antihistamines (diphenhydramine, diazepam).

Antibiotics are used as etiotropic therapy. It is very important to choose the appropriate antibiotic to which the pathogen is most sensitive. To do this, you need to wait for the results of the bacterial analysis and sensitivity test.

When using broad-spectrum antibiotics, if the results of bacterial analysis are not yet available, and treatment must be started immediately, the patient should be prescribed a course of eubiotics to prevent possible dysbacteriosis.

The course of antibiotic treatment lasts as the symptoms of the disease disappear, on average 1-2 weeks. But there are cases when purulent-destructive pneumonia goes away, but cavities with pus (abscesses) remain. In this case, the course of antibiotic therapy must be continued until the abscesses completely disappear.

As part of complex therapy, the patient is prescribed aminophylline to improve blood circulation and ventilation of the lungs, and immunoglobulins to stimulate the immune system.

In case of secondary form it is necessary to simultaneously get rid of the original source of infection and treat the destructive pneumonia caused by it. Treatment depends on the initial infection and is considered individually.

If cardiovascular failure develops, it is necessary to prescribe treatment with cardiac drugs: digitoxin, corglycone, strophanthin. Anticoagulants are used to prevent thrombosis.

If the patient develops pyopneumothorax, drainage of the pleural cavity is indicated. In this case, it is necessary to thoroughly clean the cavity from pus and rinse with antiseptics and antibiotics.

There are three main clinical and morphological forms: abscess, gangrenous abscess and lung gangrene.

A lung abscess is a more or less limited cavity that forms as a result of purulent melting of the pulmonary parenchyma.

Lung gangrene is a much more severe pathological condition, characterized by extensive necrosis and ichorous disintegration of the affected lung tissue, not prone to clear demarcation and rapid purulent melting.

There is also an intermediate form of infectious destruction of the lungs, in which necrosis and purulent-ichorous decay are less common, and in the process of its delimitation, a cavity is formed containing slowly melting and tearing off sequesters of the lung tissue. This form of suppuration is called gangrenous lung abscess.

The general term “destructive pneumonitis” is used to refer to the entire group of acute infectious destruction of the lungs.

Destructive pneumonitis is an infectious and inflammatory process in the pulmonary parenchyma that occurs atypically, characterized by irreversible damage (necrosis, tissue destruction) of the lung tissue.

ETIOLOGY. Currently, it is generally accepted that there is no clear difference in the etiology of purulent and gangrenous processes in the lung tissue. For patients with aspiration genesis of the disease, when any form of destruction is possible, anaerobic etiology is most typical. At the same time, destruction resulting from aspiration of oropharyngeal mucus is more often caused by fusobacteria, anaerobic cocci and B. Melaninogenicus, while with aspiration from the underlying parts of the gastrointestinal tract, a process associated with B. fragilis often occurs. At the same time, with pneumonitis of other origins, the causative agents are often aerobes and facultative anaerobes (Klebsiella, Pseudomonas aeruginosa, Proteus, Staphylococcus aureus, etc.).

In tropical and subtropical countries, protozoa play a significant role in the etiology of lung abscess: Entamoeba hystolytica is of greatest practical importance. Cases of lung abscess caused by fungi, in particular actinomycetes, have been described.

The question of the importance of respiratory viruses in the etiology of destructive pneumonitis has not been studied at all. The studies have convincingly shown that in many cases, viral infection has an active influence on the course and sometimes on the outcome of destructive pneumonitis. Virological studies revealed the presence of an active viral infection in half of the patients suffering from abscess and gangrene of the lungs.

PATHOGENESIS. In the overwhelming majority of cases, microorganisms that are causative agents of destructive pneumonitis enter the pulmonary parenchyma through the airways, and much less often - hematogenously. Suppuration is possible as a result of direct infection of the lung with penetrating injuries. Rarely, suppuration spreads to the lungs from neighboring organs and tissues, continuitatem, and also lymphogenously.

The most important of these pathways is the transcanalicular (transbronchial) one, since the vast majority of destructive pneumonitis is associated with it.

The progression of infection from the proximal to the distal parts of the airways can occur as a result of two mechanisms:

Inhalation (aerogenic), when pathogens move towards the respiratory sections in the flow of inhaled air;

Aspiration, when during inhalation a certain amount of infected fluid, mucus, and foreign bodies is aspirated from the oral cavity and nasopharynx.

The most important factor contributing to the aspiration of infected material are conditions in which the swallowing, nasopharyngeal and cough reflexes are temporarily or permanently impaired (mask inhalation anesthesia, deep alcohol intoxication, unconsciousness associated with traumatic brain injury or acute cerebrovascular accidents, epileptic seizure, electric shock used in the treatment of certain mental illnesses, etc.).

Alcohol abuse is of greatest importance. Such patients often experience advanced caries, periodontal disease, and gingivitis. During deep alcoholic intoxication, regurgitation of gastric contents often occurs with aspiration of mucus and vomit. Chronic alcohol intoxication “inhibits humoral and cellular immunity, suppresses the mechanism of cleansing the bronchial tree and thereby not only contributes to the onset of the disease, but also leaves an extremely unfavorable imprint on its entire course.

The likelihood of aspiration of infected material is also increased by various forms of esophageal pathology (cardiospasm, achalasia, cicatricial strictures, hiatal hernia), which contribute to regurgitation and the entry of mucus, food particles, and gastric contents into the bronchi.

Along with aspiration, the inhalation route is also considered, in which pathogens enter the lung along with the inhaled air.

Pathogenetic significance during aspiration is not only the fact of penetration of microorganisms into the small branches of the bronchial tree, but also the obstruction of these branches by infected material with disruption of their drainage function and the development of atelectasis, contributing to the occurrence of an infectious-necrotic process.

Hematogenous lung abscesses are, as a rule, a manifestation or complication of sepsis (septicopyemia) of various origins. The source of infected material can be blood clots in the veins of the lower extremities and pelvis, blood clots in phlebitis associated with long-term infusion therapy, blood clots in small veins surrounding osteomyelitic and other purulent foci. The infected material, together with the blood flow, enters the small branches of the pulmonary artery, precapillaries and capillaries and, obstructing them, gives rise to an infectious process with subsequent abscess formation and breakthrough of pus through the bronchial tree. Hematogenous abscesses are characterized by multiplicity and usually subpleural, often lower lobe, localization.

Abscesses of mild traumatic origin, associated mainly with blind gunshot wounds, are well known. The pathogens enter the lung tissue through the chest wall along with the wounding projectile. Such abscesses develop around foreign bodies and intrapulmonary hematomas, which play a major role in the pathogenesis of suppuration.

Direct spread of the suppurative-destructive process from neighboring tissues and organs per continuitatem is observed relatively rarely. Sometimes it is possible for subphrenic abscesses and liver ulcers to break through the diaphragm into the lung tissue.

Lymphogenic invasions of pathogens into the lung tissue do not have any significant significance in the pathogenesis of destructive pneumonitis.

The respiratory organs are equipped with very advanced anti-infective defense mechanisms. These include the mucociliary clearance system, the alveolar macrophage system, and various classes of immunoglobulins found in bronchial secretions. To implement the infectious-necrotic process in the lung, it is necessary to influence additional pathogenetic factors that suppress the general and local anti-infective defense systems of the macroorganism. Such factors are: various forms of local changes in bronchial patency, sharply disrupting the mucociliary clearance system and the drainage function of the bronchi, promoting the accumulation of mucus and the development of infection distal to the site of bronchial obstruction.

The most important pathogenetic factor contributing to the development of destructive pneumonitis is respiratory viruses, which sharply suppress local defense mechanisms and the general immunological reactivity of the patient. During periods of influenza A epidemic, the number of deaths associated with lung abscesses increases approximately 2.5 times.

Under the influence of a viral lesion, inflammatory edema, infiltration, necrobiotic and necrotic changes occur in the integumentary epithelium of the bronchi and alveoli, resulting in a sharp disruption of the function of the ciliated epithelium and mucopillar clearance. Along with this, cellular immunity is sharply disrupted, the phagocytic ability of neutrophils and macrophages decreases, the number of T- and B-lymphocytes decreases, the concentration of endogenous interferon drops, natural antibody-dependent killer activity is inhibited, and the synthesis of protective immunoglobulins by B-lymphocytes is disrupted.

Of the bad habits, in addition to alcoholism, smoking plays a significant role in pathogenesis - an important exogenous factor in the development of chronic bronchitis, which disrupts the mechanism of local anti-infective defense of the bronchial tree (restructuring of the bronchial mucosa with the replacement of ciliary cells with mucous ones, hypertrophy of the mucous glands, impaired bronchial obstruction, etc. .). In the vast majority of patients, both factors act in combination, mutually reinforcing each other.

A decrease in the general immunological reactivity of the body is often caused by severe general diseases. The most important is diabetes mellitus - a universal factor that promotes necrosis and suppuration. Diseases such as leukemia, radiation sickness, exhaustion and other conditions associated with suppression of protective mechanisms also contribute to infectious destruction of the lungs. The occurrence of destructive pneumonitis can be facilitated by massive therapy with corticosteroids, which reduces the resistance of patients to pyogenic infection.

CLASSIFICATION OF DESTRUCTIVE PNEUMONITIS

(asbcesses and gangrene of the lungs) ; (N.V. Putov, Yu.N. Levashov, 1989)

1. According to clinical and morphological features:

Lung abscess is purulent;

Lung abscess, gangrenous;

Gangrene of the lung.

2. By etiology:

Pneumonitis caused by anaerobic infection;

Shievmonitis caused by mixed microflora;

Non-bacterial pneumonitis (caused by protozoa, fungi, etc.).

3. According to pathogenesis:

Bronchogenic:

A) aspiration;

B) post-pneumonic;

B) obstructive;

Hematogenous;

Traumatic;

Other origins (including the transfer of suppuration from neighboring organs).

4. By localization:

Abscess central (hilar);

Abscess is peripheral (cortical, subpleural).

5. By prevalence:

Single abscess;

Multiple abscess, including:

A) one-sided;

B) bilateral.

6. According to the severity of the current:

Mild pneumonitis;

Pneumonitis with a course of moderate severity;

Severe pneumonitis;

Pneumonitis with an extremely severe course.

7. Presence of complications:

Uncomplicated;

Complicated:

A) pyopneumothorax or pleural empyema;

B) bleeding;

B) damage to the opposite lung in a primary unilateral process;

D) phlegmon of the chest;

D) bacteremic shock;

E) respiratory distress syndrome;

G) sepsis;

H) other secondary processes.

8. By the nature of the flow:

Spicy;

Subacute (protracted);

Chronic abscess:

A) in remission phase;

B) in the acute phase.

SAMPLE FORMULATION OF DIAGNOSIS

I". Chronic post-pneumonic purulent abscess of the upper lobe of the right lung, with a moderate course, in the acute phase. 2. Acute hematogenous-embolic pneumonitis, single, central (hilar), with an extremely severe course, respiratory failure degree II.

CLINICAL AND DIAGNOSTICS OF DESTRUCTIVE PNEUMONITIS

Among patients with abscess and gangrene of the lungs, middle-aged men predominate. This is explained by the fact that men more often abuse alcohol, smoke and work in hazardous occupational conditions that disrupt the protective mechanisms of the bronchi and lungs. Persons of working age are most often affected.

The disease rarely develops against the background of complete health. More often it is preceded by alcohol intoxication with exposure to cold air, sometimes alcoholic delirium, complications of anesthesia, unconsciousness associated with traumatic brain injury, severe epileptic seizure after eating, trauma to the maxillofacial area, diseases of the esophagus, severe tonsillitis and pharyngitis. , diseases of teeth, gums, etc.

In the clinical picture of acute purulent abscess, two periods are distinguished:

1. the period of abscess formation until the pus breaks through the bronchial tree;

2. the period after the abscess breaks into the bronchus, but these periods are not always clearly defined.

The first period lasts from several days to 2-3 weeks (on average about 7-10 days). More often, the disease begins acutely with general malaise, chills, increased body temperature to 39°C and above, and acute chest pain that increases with deep inspiration. The localization of pain usually corresponds to the side and location of the lesion. With destruction affecting the basal segments, pain often irradiates to the body (phrenicus symptom). A cough, usually dry and painful, is noted already in the first days, but sometimes it is absent. Shortness of breath is observed in most patients from the first days of the disease.

In some cases, the disease appears vaguely expressed, sharp pain and shortness of breath may be absent, and the temperature remains low-grade. This course may depend on the characteristics of the etiology of the disease or a violation of the immunological reactivity of patients.

On examination, in typical cases there is pallor and moderate cyanosis of the skin and mucous membranes, sometimes a cyanotic blush, more pronounced on the affected side. Shortness of breath up to 30 or more breaths per minute (tachypnea). The pulse is increased, tachycardia often does not correspond to the temperature. Blood pressure is normal or tends to decrease. In very severe cases of the disease, arterial hypotension is possible due to bacteremic shock.

When examining the chest, there is a lag in breathing on the affected side; on palpation, there is pain in the intercostal spaces above the destruction zone (Kryukov's symptom), as well as skin hyperesthesia in this area.

Physical findings at the first stage of the disease are similar to massive, confluent pneumonia. Upon percussion over the affected area, a pronounced dullness of the percussion sound is determined. On auscultation, bronchial or weakened breathing is heard. There may be no wheezing at first; sometimes it appears finely bubbling, sometimes dry. A pleural friction rub is often heard above the area of ​​dullness.

X-ray examination during this period of the disease reveals massive infiltration of the lung tissue, usually localized in the posterior segments, most often of the right lung. In the surrounding tissue, there is an increase in the interstitial component of the pulmonary pattern. The roots of both lungs are increased in volume and have an unclear structure.

The X-ray picture resembles massive polysegmental or lobar pneumonia. Probable signs of a destructive process at this early stage are convex interlobar boundaries of shading, indicating an increase in the volume of the affected lobe or group of segments, as well as the appearance of even denser foci against the background of shading, sometimes acquiring a rounded shape.

The transition to the second period of the disease is determined not so much by the onset of necrosis and purulent (ichorous) melting of lung tissue, but by the breakthrough of decay products into the bronchus.

Classically, the patient suddenly develops a paroxysmal cough with the discharge of a “mouth full” of copious sputum, the amount of which in a short time can reach 100 ml or more (sometimes more than 1 liter).

Purulent or ichorous sputum sometimes, immediately after the lesion has broken through into the bronchus, contains a larger or smaller admixture of blood. With anaerobic microflora, a foul odor is noted. When settling, the sputum is divided into 3 layers.

The lower one - yellow-white, grayish or brown - is a thick pus, containing in some cases crumbly tissue detritus, sometimes semi-melted scraps of lung tissue, the so-called Dietrich plugs, etc.

The middle layer is serous, is a viscous turbid liquid and mainly consists of saliva, which should be taken into account “when assessing the true amount of sputum itself.

The surface layer consists of foamy mucus mixed with pus.

The change in the condition of patients after the beginning of emptying of the cavities of destruction depends primarily on the rate and completeness of rejection of the necrotic substrate. Feeling better, temperature drops, intoxication decreases or disappears, appetite appears, and the amount of sputum gradually decreases.

The physical picture with such dynamics changes rapidly and the intensity of dullness decreases. Occasionally, tympanitis is found at the site of the former dullness, corresponding to a developing cavity. Large and medium bubble moist rales, bronchial and rarely amphoric breathing are heard.

X-ray, against the background of a decreasing infiltrate, a cavity, usually round in shape, with a fairly even internal contour and a horizontal level of fluid, begins to be determined. With good drainage, the level is determined at the bottom of the cavity and then disappears completely. Subsequently, the infiltration resolves, and the cavity becomes deformed, decreases in size and, finally, ceases to be defined.

GANGRENOUS ABCCESS and especially gangrene of the lung are clinically different from purulent abscesses in that they are more severe and have a less favorable outcome.

In most cases, the temperature becomes hectic in nature, and intoxication quickly increases. Severe chest pain on the affected side, aggravated by coughing. The percussion picture often changes quickly. The dull zone increases. Auscultatory breathing is weakened or becomes bronchial.

Radiologically, against the background of massive shading, multiple, often small, irregularly shaped clearings are determined.

DIFFERENTIAL DIAGNOSIS

Differential diagnosis of destructive pneumonitis is carried out - with infiltrative tuberculosis in the phase of decay and cavity formation, with a cavitary form of peripheral lung cancer, with suppurating lung cysts.

The X-ray picture of tuberculosis is characterized by great stability. The cavities that form usually contain little or no fluid. An important radiological sign of tuberculosis is the presence of so-called dropout foci around the disintegrating infiltrate or emerging cavity, i.e. small round or irregularly shaped shadows measuring 0.5-1.5 cm, resulting from bronchogenic dissemination of the process. Sometimes lesions appear in the opposite lung.

Diagnosis ex juvantibus is essential; this takes into account the lack of clinical and radiological dynamics as a result of a course of intensive anti-inflammatory therapy.

The differential diagnosis of an abscess and the cavitary form of peripheral lung cancer is of great practical importance.

The X-ray picture of cancer differs significantly from changes in a lung abscess. The external contour of the cavity wall in cancer, in contrast to an abscess, is quite clear, sometimes has a slightly lumpy shape. There is no inflammatory infiltration. The thickness of the cavity wall varies, but on average, it is greater than with a lung abscess. The internal contour of the wall, unlike an abscess, is uneven. The cavity inside the tumor node either does not contain liquid or its amount is minimal. Sometimes other radiological symptoms of cancer are detected (enlargement of the hilar or paratracheal lymph nodes, the appearance of effusion).

The differential diagnosis of destructive pneumonitis and central lung cancer or other tumor complicated by an obstructive abscess is successfully carried out using bronchoscopy.

Suppurating congenital lung cysts are relatively rare. X-rays reveal an extremely thin-walled round or oval cavity with a horizontal fluid level, but without pronounced inflammatory infiltration in the circumference.

COMPLICATIONS. The most common and very severe complication is pleural empyema or pyopneumothorax, subcutaneous and intermuscular emphysema, mediastinal emphysema, bleeding, distress syndrome, sepsis, bacteremic shock.

First of all, careful patient care is required. It is best to isolate him from other patients. A varied, nutritious diet containing large amounts of protein and vitamins is necessary (the dose of vitamin C should be at least 1-2 grams per day).

Use of antibacterial therapy. The most effective is intravenous administration of antibiotics. For most aerobic and conditionally aerobic pathogens, broad-spectrum drugs are used in large doses. For staphylococcal etiology, semisynthetic penicillins that are resistant to the action of penicillinase are indicated: methicillin 4-6 g per day, oxacillin 3-8 g per day with 4-fold intramuscular or intravenous administration. For gram-negative microflora, broad-spectrum antibiotics are also recommended. If the etiological factor is Klebsiella, a combination with chloramphenicol (2g per day) is recommended. For the treatment of infections caused by Pseudomonas aeruginosa, gentamicin is effective in combination with carbenicillin (4 g per day intramuscularly) or doxycycline (0.1-0.2 g per day orally once).

For the treatment of infections caused by non-spore-forming anaerobic microorganisms, the use of metronidazole 1.5-2 g per day is effective.

If respiratory viruses are involved in the etiology of destructive pneumonitis, antiviral therapy (interferon, human immunoglobulin, ribonuclease, deoxyribonuclease) is indicated.

Treatment to restore and stimulate the body’s immunological defense factors. Antistaphylococcal gamma-lobulin, immunoglobulins, immunomodulators (levomizole, diucifon, T-activin, timolin, pentoxyl, methyluracil) are used.

To correct disturbances in water-electrolyte and protein balance and reduce intoxication, massive infusion therapy is carried out: 5% glucose solution, hemodez, Ringer's solution, protein hydrolysates (aminocrovin, hydrolysin), 10% human albumin, rheopolyglucin.

In recent years, hemosorption and plasmapheresis have been used in the most severely ill patients.

To combat hypoxemia, oxygen therapy is used, and hyperbaric oxygen therapy may be used. Symptomatic therapy may be used. For heart failure - cardiac glycosides, for pain syndrome - analgesics, for insomnia - sleeping pills.

To facilitate outflow from a purulent focus, the use of postural drainage is recommended. Intravenous administration of 10-20 ml of a 2.4% aminophylline solution is used, mucolytics - acetylcysteine, bromhexine, etc.; inhalation with 2% sodium bicarbonate solution.

OUTCOME OF DESTRUCTIVE PNEUMONITIS

4 types of outcomes are considered:

1. Complete recovery with healing of the destruction cavity and persistent disappearance of signs of pulmonary disease (25-40%).

2. Clinical recovery, when a persistent thin-walled cavity remains at the site of the destruction site (35-50%).

3. Formation of chronic abscess (15-20%).

4. Fatal outcome (5-10%).

PREVENTION OF DESTRUCTIVE PNEUMONITIS

Since most destructive pneumonitis is of aspiration origin, the following are extremely important in prevention: the fight against alcohol abuse, careful care for patients who are unconscious or suffering from swallowing disorders.

A very significant measure of secondary prevention is the earliest and most intensive treatment of massive inflammatory infiltrates in the lung tissue, usually interpreted as “drain” or “lobar” pneumonia.