What does a destruction cavity in the lung mean? Acute purulent destructive diseases of the lungs

"Infectious destructive diseases of the lungs"

INFECTIOUS DESTRUCTION OF THE LUNG.

Infectious destruction of the lungs is a severe pathological condition that is characterized by inflammatory infiltration and further purulent or putrefactive decay (destruction) of lung tissue due to the influence of nonspecific infectious pathogens. There are three forms of such destruction: abscess, gangrene and gangrenous lung abscess.

Etiology.

There are no specific causative agents of infectious destruction of the lungs. In 60-65%, the cause of the disease is non-spore-forming obligate anaerobic microorganisms: bacteroides, fusobacteria; anaerobic cocci. Infectious destruction of the lungs, which are caused by aspiration of oropharyngeal mucus, are most often caused by fusobacteria, anaerobic cocci and bacteroides.

In 30-40% of patients they are caused by Staphylococcus aureus, Streptococcus, Klebsiella, Proteus, Pseudomonas aeruginosa, and Enterobacteriaceae.

Factors that contribute to the development of IDL: smoking, chronic bronchitis, bronchial asthma, diabetes mellitus, epidemic influenza, alcoholism, maxillofacial trauma, prolonged exposure to the cold, influenza.

Pathogenesis.

Pathogens of IDL penetrate the lung parenchyma through the respiratory tract, less often hemetogenously, lymphogenously, by spreading from neighboring organs and tissues. Aspiration (microaspiration) of infected mucus and saliva from the nasopharynx, as well as gastric contents, is of great importance. In addition, lung abscesses can occur with closed injuries and penetrating wounds of the chest. With an abscess, a limited inflammatory infiltration with purulent molten lung tissue and the formation of a decay cavity, which is surrounded by a granulation shaft, is first observed.

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 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, widespread necrosis of the lung tissue develops without clear boundaries.

An important pathogenetic factor is also a decrease in the function of general immunity and local bronchopulmonary protection.

Classification.

Etiology (depending on the type of infectious agent).

Aerobic and/or conditionally aerobic flora.
Flora.
Mixed aerobic-anaerobic flora
Non-bacterial pathogens (fungi, simpler ones)

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.

Clinical and morphological form.

Abscesses are purulent.
Gangrenous abscesses
Gangrene of the lungs.

Location within the lungs.

Peripheral.
Central.

Prevalence of the pathological process.

Singles.
Multiple.
One-sided.
Double-sided.
With segment damage.
With the defeat of the share.
With damage to more than one lobe.

The severity of the current.

Light flow.
The course is of moderate severity.
Heavy current.
Extremely severe course.

The presence or absence of complications.

Uncomplicated.
Complicated:

pyopneumothorax, pleural empyema;
pulmonary hemorrhage;
bacteremic shock;
acute respiratory distress syndrome;
sepsis (septicopyemia);
phlegmon of the chest wall;
lesion of the opposite side with primary lesion of one side;
other complications.

The nature of the current.

Spicy.
With a subacute course.
Chronic lung abscesses (chronic gangrene is impossible).

A gangrenous abscess is understood as a form of IDL that is characterized by less common and more predisposed to limiting death of lung tissue than gangrene. In this case, in the process of melting the lung tissue, a cavity is formed with parietal or freely lying tissue sequestration.

^ Lung abscess.

AL is a nonspecific inflammation of the lung tissue, which is accompanied by its disintegration in the form of a limited focus and the formation of one or more purulent-necrotic cavities.

In 10-15% of patients, the process may transition to a chronic form, which can be evidenced only after 2 months. course of the disease.

Clinical picture: before the breakthrough of pus into the bronchus, the following are characteristic: high body temperature, chills, profuse sweats, dry cough with chest pain on the affected side, difficult breathing or shortness of breath due to the inability to take a deep breath or respiratory failure that occurs early. On percussion of the lungs there is an intense shortening of the sound over the lesion; on auscultation, breathing is weakened with a hard tint, sometimes bronchial. Examination: pale skin, sometimes cyanotic blush on the face, more pronounced on the affected side. The patient takes a forced position - on the “sick” side. The pulse quickens and may be arrhythmic. Blood pressure tends to decrease; in extremely severe cases, bacteremic shock may develop with a sharp drop in blood pressure. Heart sounds are muffled.

After a breakthrough into the bronchus: a coughing attack with the release of a large amount of sputum (100-500 ml) - expectoration of sputum “a mouthful”, purulent, often foul-smelling. With good drainage of the abscess, health improves, body temperature decreases, with percussion of the lungs the sound above the lesion is shortened, less often - a tympanic hue due to the presence of air in the void, auscultation - fine bubbling rales; within 6-8 weeks, the symptoms of the abscess disappear. With poor drainage, body temperature remains high, chills, sweats, cough with poor foul-smelling sputum, shortness of breath, symptoms of intoxication, decreased appetite, thickening of the terminal phalanges in the form of “drum sticks” and nails in the form of “hour glass”.

^ Laboratory data.

CBC: leukocytosis, band shift, toxic granularity of leukocytes, significant increase in ESR. After a breakthrough into the bronchus with good drainage - a gradual decrease in changes, with poor drainage and with chronicity - signs of anemia, an increase in ESR.

OAM: moderate albuminuria, cylindrome, microhematuria.

BAC: increased content of sialic acids, seromucoid, fibrin, haptoglobin, α 2 - and γ-globulins, in chronic cases - decreased albumin levels.

General analysis of sputum: purulent sputum with an unpleasant odor, when standing, it is divided into two layers, upon microscopy - leukocytes in large quantities, elastic fibers, crystals of hemetoidin, fatty acids.
X-ray examination: before the breakthrough into the bronchus - infiltration of the lung tissue, after - clearing with a horizontal fluid level.
^ LUNG GANGRENE.

HL is a severe pathological condition, which is characterized by widespread necrosis and ichorous disintegration of the affected lung tissue, which is not prone to limitation and rapid purulent melting.

^ Clinical picture:

General serious condition: hectic body temperature, severe intoxication, weight loss, lack of appetite, shortness of breath, tachycardia.
Chest pain that gets worse with coughing.
When percussing over the affected area, there is a dull sound and pain (Kryukov-Sauerbruch symptom); when pressed with a stethoscope, a cough appears in this area (Kiessling symptom). With the rapid disintegration of necrotic tissue, the dull zone increases, and areas of higher sound appear against its background.
When auscultating, breathing over the affected area is weakened or bronchial.
After a breakthrough into the bronchus, a cough appears with the discharge of foul-smelling, dirty-gray sputum in large quantities (up to 1 liter or more), and moist rales are heard over the affected area.

The course of HF is always difficult; complications often develop, which can lead to death.

^ Laboratory data.

UAC: signs of anemia, leukocytosis, band shift, toxic granularity of leukocytes, significant increase in ESR.

OAM: moderate albuminuria, cylindruria.

TANK: increased content of sialic acids, seromucoid, fibrin, haptoglobin, α 2 - and γ-globulins, transaminases.

^ General sputum analysis: color - dirty gray, when standing, three layers are formed: the top - liquid, foamy, whitish in color, the middle - serous, the bottom - consists of purulent detritus and the remains of lung tissue, which disintegrates; elastic fibers and a large number of neutrophils are also present.

^ X-ray examination.

Before the breakthrough into the bronchus, there is massive infiltration without clear boundaries, which occupies one or two lobes, and sometimes the entire lung.

After a breakthrough into the bronchus, against the background of massive darkening, multiple, often small, irregularly shaped clearings are determined, sometimes with a fluid level.

^ Treatment of suppurative diseases

In the treatment of acute lung abscesses, both conservative and surgical methods are used. Currently, intensive conservative therapy using “minor surgery” techniques is the basis of treatment for most patients with suppurative lung diseases, while surgical interventions are used in the acute period only for special indications, arising mainly in cases of ineffectiveness of conservative therapy or the presence of complications.

Treatment of suppurative lung diseases should be carried out in specialized departments in the following main areas:

^ 1. Maintenance and restoration of general condition and disturbed homeostasis.

The patient should be placed in a well-ventilated room, preferably isolated from other patients. A varied diet high in protein is necessary. Patients should receive vitamins both through food and in dosage forms. The dose of ascorbic acid should be 1-2 g/day, B vitamins are also used. In order to correct impaired water-electrolyte and protein metabolism, reduce intoxication and anemia, infusion therapy is carried out. To maintain energy balance, glucose solutions with the addition of potassium, calcium, and magnesium chlorides are used. To replenish protein losses, protein hydrolysates are used: aminokrovin, hydrolysine, as well as solutions of amino acids. The amount of protein administered parenterally should replenish at least 40-50% of its daily requirement (corresponds to 1 liter of aminokrovin). In cases of severe hypoalbuminemia, albumin infusion is indicated (100 ml - 2 times a week). To improve protein absorption, retabolil is prescribed 1 ml of a 5% solution IM once a week, Nerobolil 25 - 50 mg (1-2 ml) IM once a week. Low molecular weight drugs are used for detoxification:

reopolyglucin (400 ml IV drip) and hemodez (200 - 400 ml IV drip). If fluid excretion is insufficient, it is permissible to force diuresis using furosemide. In case of severe anemia, red blood cell transfusions of 250 - 500 ml are carried out 1-2 times a week. For the purpose of detoxification, hemosorption and plasmapheresis are used in severe patients. To increase nonspecific resistance, extracorporeal ultraviolet irradiation is used. To reduce hypoxemia, oxygen therapy and hyperbaric oxygenation are indicated.

According to indications, symptomatic therapy is used: cardiac glycosides for heart failure, for pain syndrome, analgesics (non-narcotic, do not depress breathing and do not suppress the cough reflex).
^ 2 Ensuring optimal drainage of foci of destruction in the lung (and pleura).

It is necessary to improve the natural separation of decay products of lung tissue through the draining bronchus (expectorants are ineffective in these cases). Eufillin (2.4% solution 10-20 ml IV) helps improve drainage and dilate the bronchi. To reduce the viscosity of sputum, use a 2% solution of potassium iodide or mucolytic drugs (acetylcysteine, bromhexine). Steam inhalations with a 2% solution of sodium bicarbonate are used. To improve the outflow of contents from a purulent focus, postural drainage is recommended. The patient should take a position in which the draining bronchus is directed vertically downwards. For the same purpose, therapeutic bronchoscopy is performed with aspiration of purulent contents from the site of destruction, followed by washing it and administering mucolytics and antibacterial drugs.

^ 3. Suppression of microorganisms - causative agents of the infectious process.

Modern chemotherapy is an important component of treatment and is initially carried out empirically, and subsequently adjusted in accordance with the results of sputum examination, identifying microbes that cause the inflammatory process and determining their sensitivity to the antibiotics used. If identification is difficult, then broad-spectrum drugs are prescribed in fairly large doses. The most effective is intravenous administration of antibacterial agents.

Chemotherapy should begin with amoxicycline (250-500 mg/day), trimethoprim in combination with sulfamethoxazole (up to 800 mg/day), doxycillin (100 mg/day), erythromycin (250-500 mg/day). In the absence of a pronounced clinical effect or the appearance of allergy symptoms, it is recommended to use 2nd and 3rd generation cephalosporins, macrolides (clarithromycin, azithromycin) and quinolones (ofloxacin, diprofloxacin).

For destruction caused by staphylococcus, semi-synthetic penicillins are prescribed: methicillin 4-6 g/day, oxacillin 3-8 g/day with quadruple administration intramuscularly or intravenously. In severe cases of the disease, combinations of gentacymine (240–480 mg/day) and lincomycin (1.8 g/day) are used with quadruple administration intramuscularly or intravenously.

For the treatment of infections caused by Klebsiella pneumonia, it is recommended to combine gentamicin or kanamycin with chloramphenicol (2 g/day) or with tetracycline drugs (morphocycline - 300 mg/day, metacycline - 600 mg/day, doxycycline -200 mg/day day).

If Pseudomonas aeruginosa is detected, gentamicin is prescribed in combination with carbenicillin (4 g/day 4 times IM).
In the presence of predominantly gram-negative flora (Pseudomonas aeruginosa, Escherichia coli, Klebsiella), a long-acting aminoglycoside antibiotic, netromycin, is highly effective. Prescribed 200-400 mg/day IM or IV.

To suppress non-spore-forming anaerobic microflora, metronidazole (Trichopol, Flagyl) is prescribed - 1.5-2 g/day. Large doses of penicillin (20-50 million units/day intravenous drip) in combination with metronidazole actively affect most anaerobic pathogens. Lincomycin and chloramphenicol are effective against almost the entire group of non-spore-forming anaerobes; these drugs replace penicillin in case of intolerance; Lincomycin is prescribed at a dose of 1-1.5 g/day orally in 2-3 doses or up to 2.4 g/day. IM or IV in 2-3 doses.

For viral etiology of the disease, interferon is used in treatment locally in the form of irrigation of the mucous membrane of the nasopharynx and bronchi, as well as inhalations for 5-15 days.

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

Lung abscess is a more or less limited cavity formed 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.

A generic term "destructive pneumonitis" used to refer to the entire group of acute infectious destruction of the lungs.

Destructive pneumonitis - infectious and inflammatory processes in the pulmonary parenchyma occur 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 ways is transcanalicular (transbronchial), since the overwhelming 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, one or another amount of infected fluid, mucus, or 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 ~ this is, 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 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:

purulent lung abscess;
gangrenous lung abscess;
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. By pathogenesis:

bronchogenic:

a) aspiration;

b) post-pneumonic;

c) obstructive;

hematogenous;
traumatic;
of other origins (including the transfer of suppuration from neighboring organs).

4. By localization:

central (hilar) abscess;
peripheral abscess (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 moderate severity;
severe pneumonitis;
extremely severe pneumonitis.

7. Presence of complications:

uncomplicated;
complicated:

a) pyopneumothorax or pleural empyema;

b) bleeding;

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

d) phlegmon of the chest;

e) bacteremic shock;

f) respiratory distress syndrome;

g) sepsis;

h) other secondary processes.

8. By the nature of the flow:

spicy;
subacute (protracted);
chronic abscess:

a) in the 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:

the period of abscess formation until pus breaks through the bronchial tree;
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). Cough, usually dry "y. 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 illness.

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.

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

Middle layer 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.

Surface the 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.

TREATMENT

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 is effective 1,5- 2g per day.

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.

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.

A.A. Tatur Doctor of Medical Sciences,
professor of the 1st department
surgical diseases of BSMU,
head of Minsk city
center for thoracic surgery
M.N. Popov, head surgical
thoracic purulent department

Bacterial destruction of the lungs are severe pathological conditions characterized by inflammatory infiltration and subsequent purulent or putrefactive decay (destruction) of lung tissue. Clinically bacterial destruction of the lungs(BDL) manifest as an acute abscess (simple, gangrenous) or gangrene. Depending on the state of the patient’s body’s defenses, the pathogenicity of the microflora, the ratio of damaging and restorative processes in the lungs, either the delimitation of necrotic areas or the progressive spread of purulent-putrefactive melting of the lung tissue occurs.

Under acute simple lung abscess It is generally accepted to understand the destruction of lung tissue within one segment with the formation of a purulent cavity surrounded by inflammatory infiltration of lung tissue. Gangrenous abscess - this is, as a rule, a decomposition of a section of necrotic lung tissue limited, as a rule, to a lobe of the lung, with a tendency to be rejected into the lumen of the abscess of necrotic masses (sequestra) and delimited from unaffected areas. Therefore, a gangrenous abscess is also called limited gangrene. Lung gangrene in contrast to a gangrenous abscess, it is a progressive putrefactive destruction of the lung, which has a tendency to spread to the entire lung and parietal pleura, which always causes an extremely difficult general condition of the patient.

BDL occurs more often (60%) at the age of 20-40 years, and in men 4 times more often than in women. This is explained by men’s more frequent abuse of alcohol, long-term smoking, drug addiction, greater susceptibility to hypothermia, as well as occupational hazards. Often these are people suffering from chronic alcoholism and having no fixed place of residence. In 2/3 of patients, the right lung is affected, in 1/3 – in the left. Rarely (1-5%) bilateral BDL is possible. The high incidence of damage to the right lung is due to its anatomical features: the wide right main bronchus is a continuation of the trachea, which allows infected material to enter the right lung during inhalation (aspiration). Damage to the lower lobes of the lungs is observed in 80% of patients.

Causes of development and pathogenesis

BDL are most often caused by staphylococci and putrefactive (Escherichia coli, Pseudomonas aeruginosa, Proteus) microbes. Various anaerobic, i.e. pathogens living in an environment without access to oxygen are found in 75-10% of patients with BDL. It is characteristic that 3/4 of patients suffer from ARVI or influenza before destructive pneumonitis. Undoubtedly, a viral infection is a provoking factor in the development of BDL due to damage to the bronchial mucosa with disruption of their drainage function, weakening of cellular and humoral immunity and the creation of an additional nutrient substrate for microorganisms. According to WHO, during periods of influenza epidemic, the number of deaths associated with lung abscesses increases 2.5 times. Depending on the routes of penetration of microorganisms into the lung tissue, BDL are divided into bronchogenic (75-80%), traumatic (5-10%) and hematogenous (1-10%).

Today it has been proven that the occurrence of BDL is always determined by the combination and interaction of three main factors, the sequence of which is quite arbitrary. This:

acute inflammation pulmonary parenchyma, i.e. pneumonia, most often of aspiration origin
blockage of the lumen of the bronchus or bronchi with the development obstructive atelectasis, i.e. airless non-aerated area of the lung
decreased blood supply to the lung tissue, which means its increasing hypoxia in the area of inflammation.

These factors interact and enhance each other’s effects, and soon after the onset of the disease it is no longer possible to determine which of them played the trigger role.

The main mechanism for the development of BDL is aspiration and subsequent fixation in the bronchi of foreign bodies (pieces of food), infected contents of the oral cavity, nasopharynx, and stomach in conditions of reduced or absent drainage function and cough reflex. Prolonged blockage of the bronchial lumen leads to atelectasis, in the zone of which, against the background of decreased blood flow and an immunodeficiency state, favorable conditions are created for the vital activity of aerobic and then anaerobic microorganisms, the development of purulent inflammation, necrosis and subsequent melting of the corresponding part of the lung.

The development of BDL is facilitated by conditions that significantly reduce the level of consciousness, reflexes and reactivity of the body: acute and chronic alcohol intoxication, anesthesia, drug addiction, severe brain injuries, comatose states, cerebrovascular accident, gastroesophageal reflux disease. Favorable background conditions that contribute to the development of BDL include chronic obstructive pulmonary diseases, diabetes mellitus, and old age.

Confirmation of the leading role of the aspiration mechanism in the development of abscess or gangrene of the lungs is the generally accepted facts of the predominant development of the disease in persons who abuse alcohol (aspiration of vomit), as well as the frequent localization of the pathological process in the posterior segments of the lung, most often the right. Lung abscesses can occur due to stenosis or fusion of the lumen of the bronchus, blockage or compression by a benign or malignant tumor, in the presence of functioning esophageal-respiratory fistulas. Cases of lung abscesses are described, the cause of which was gastrointestinal, colonic, biliary and pancreatic cystobronchial fistulas, i.e. pathological communications of the lumen of the bronchi with the stomach, colon, bile ducts, and pancreatic cyst. Acute hematogenous abscesses develop during sepsis and are often diagnosed in “syringe drug addicts.”

BDL is a staged process. The stage of atelectasis-pneumonia or pre-destruction, lasting from 2-3 days to 1-2 weeks, passes into the stage of destruction, i.e. necrosis and disintegration of necrotic tissue. Subsequently, necrotic areas are rejected with the formation of a purulent cavity delimited from healthy lung tissue. The closed period gives way to an open period, when the pus-filled cavity breaks into the lumen of the bronchus. The final stage of BDL is the stage of outcomes: favorable with recovery (pneumofibrosis, lung cyst) and unfavorable (complications, chronic abscess, death).

Clinical picture.

The clinical course according to the dynamics of the process can be progressive, stable and regressive, uncomplicated and complicated by pyopnevothorax, purulent pleurisy, hemoptysis or pulmonary hemorrhage, sepsis.

The disease begins suddenly: against the background of apparent well-being, chills, an increase in body temperature to 38-39 o C, malaise, and dull pain in the chest occur. Often the patient can accurately indicate the date and even hours when the first symptoms of the disease appeared. The general condition of the patient quickly becomes serious. Rapid breathing, redness of the skin of the face, and a dry cough appear. In blood tests, the number of leukocytes sharply increases and the ESR accelerates. On radiographs in the initial stage of the disease, inflammatory infiltration of the lung tissue without clear boundaries is determined. During the closed period, if the patient seeks medical help, the disease is usually interpreted as pneumonia, since it does not yet have specific features. An important early sign of the onset of lung destruction is the appearance of bad breath when breathing. An abscess that has already formed in the lung, but has not yet drained into the bronchus, is manifested by signs of severe purulent intoxication: increasing weakness, adynamia, sweating, lack of appetite, the appearance and increase of anemia, increased leukocytosis, tachycardia, high temperature up to 39-40 o C. When the parietal pleura is involved in the inflammatory process and dry or exudative pleurisy develops, pain in the chest increases significantly, especially with deep breathing. In typical cases, the first phase of purulent-necrotic melting of the lung lasts from 3 to 10 days, and then the abscess breaks into the bronchi. The leading clinical symptom of the open period is copious discharge of purulent sputum, the first portions of which usually contain an admixture of blood. In cases of gangrenous abscess formation, up to 500 ml of purulent sputum or even more can be released immediately when coughing. When standing in a vessel, the sputum is divided into three layers. Detritus (necrotic lung tissue) accumulates at the bottom, above it there is a layer of turbid liquid (pus), and foamy mucus is located on the surface. Microscopic examination of sputum reveals large quantities of leukocytes, elastic fibers, cholesterol, fatty acids and a variety of microflora. After the abscess begins to empty through the draining bronchus, the patient’s condition immediately improves: body temperature decreases, appetite appears, and activity increases. An X-ray examination in the open period against the background of inflammatory infiltration of the lung tissue clearly identifies an abscess cavity with a horizontal fluid level.

The further course of BDL is usually determined by the conditions of drainage of the pulmonary abscess into the bronchus. With adequate drainage, the amount of purulent sputum gradually decreases, it first becomes mucopurulent, then mucous. If the course of the disease is favorable, a week after the abscess ruptures, sputum production may stop completely, but this outcome is not often observed. A decrease in the amount of sputum with a simultaneous increase in temperature and the appearance of signs of intoxication indicates a deterioration in bronchial drainage, the formation of additional sequestration and the accumulation of purulent contents in the decay cavity of the lung. At lung gangrene the symptoms are much more severe. Anemia, signs of severe purulent intoxication, pulmonary-cardiac, and often multiple organ failure are rapidly increasing.

The most serious complications of BDL are pulmonary hemorrhage, breakthrough of abscess and air into the free pleural cavity - pyopneumothorax and aspiration damage to the opposite lung. The incidence of pyopneumothorax in BDL is 60-80%. Other complications (sepsis, pneumonia, pericarditis, acute renal failure) occur less frequently. Pulmonary bleeding from small to profuse, which actually threatens the patient’s life, due to arrosion of the pulmonary and bronchial vessels, occurs in 10% of patients with abscesses and in 30-50% of patients with pulmonary gangrene. With pulmonary hemorrhage, the patient may die if prompt assistance is not provided to him. But not from blood loss, but from asphyxia, i.e. suffocation, and for this it is enough for only 200-250 ml of blood to quickly enter the tracheobronchial tree.

Diagnostics

The diagnosis of BDL is made on the basis of clinical and radiological data. In typical cases, radiographs clearly show one or more cavities of destruction, most often with a horizontal level of fluid and inflammatory infiltration of the lung tissue around the abscess. Differential diagnosis of BDL is carried out with a cavitary form of lung cancer, cavernous tuberculosis, suppurating bronchogenic and echinococcal cysts, limited pleural empyema based on an assessment of clinical data and the results of X-ray (x-ray, polyposition fluoroscopy, computed tomography), fibrobronchoscopy, histological and bacteriological studies.

Treatment.

Patients with simple, well-draining, uncomplicated lung abscesses generally do not require surgical expertise and can be successfully treated in pulmonary departments. Patients with limited and widespread gangrene of the lungs, multiple, bilateral, as well as blocked and inadequately draining abscesses into the bronchus should be treated in specialized thoracic surgical departments.

The basis of treatment is the maintenance and restoration of the general condition of the patient’s body, antibacterial, detoxification and immunostimulating therapy, measures that promote the constant drainage of purulent cavities in the lungs. Broad-spectrum antibiotics, taking into account the sensitivity of microorganisms to them, are administered only intravenously or through a special catheter inserted directly into the pulmonary artery on the BDL side. For the purpose of detoxification in the most severely ill patients, extracorporeal methods are effective: hemosorption, exchange plasmapheresis, ultraviolet and laser irradiation of blood, which are quite widely used today. To correct the immune status, hyperimmune plasma, gamma globulins, immunomodulators (diucifon, thymalin, immunofan), staphylococcal toxoid, lycopid, etc. are used.

Adequate emptying of the abscess is ensured by the use of the so-called postural drainage, those. drainage of the abscess depending on its location in the lung by choosing a “draining” body position, in which the bronchus is directed vertically downwards. This technique with maximum expectoration of sputum is repeated 8-10 times a day. The patient regularly undergoes therapeutic fibrobronchoscopy with irrigation of the purulent cavity with solutions of antiseptics and enzymes. If using the listed methods it is not possible to restore bronchial drainage and empty the abscess naturally through the bronchi, it is considered that the abscess is blocked, and the treatment tactics are changed. In such cases, it is performed under local anesthesia. thoracopneocentesis with the introduction of a drainage tube into the cavity of the abscess, which is connected to the vacuum aspiration system. If there are large sequesters in the abscess cavity, it is effective videoabscessoscopy using a thoracoscope, allowing them to be fragmented and removed.

Of the surgical treatment methods, the simplest is pneumotomy, in which, after resection of sections of one or two ribs in the projection of the purulent cavity, the latter is opened and drained with gauze swabs. This forced palliative operation is performed only for health reasons if the complex treatment is ineffective. Radical, but very traumatic, operations involving the removal of a lobe or two lobes for acute lung abscesses, unlike chronic ones, are resorted to extremely rarely, mainly only in case of life-threatening profuse pulmonary hemorrhages. Removal of the lung is absolutely justified only in case of progressive gangrene of the lungs and is performed after 7-10 days of intensive preoperative preparation, aimed at reducing intoxication, correcting gas exchange and cardiac disorders, hydroionic disorders, protein deficiency, and maintaining energy balance.

The most common outcome (35-50%) of conservative treatment of acute lung abscesses is the formation of a so-called dry residual cavity at the site of the abscess, which is accompanied by clinical recovery. In most patients, it later either scars or is asymptomatic. Patients with a dry residual cavity should be under medical supervision. Only in 5-10% of patients, 2-3 months after treatment of an acute, usually gangrenous, abscess, it can become chronic with periods of exacerbations and remissions. Chronic lung abscesses cannot be treated conservatively, and therefore they are treated only surgically as planned. Complete recovery, characterized by scarring of the cavity, is observed in 20-40% of patients. Rapid elimination of the cavity is possible with small (less than 6 cm) initial sizes of necrosis and destruction of lung tissue. The mortality rate of patients with acute lung abscesses is 5-10%. Due to the provision of accessible specialized thoracic surgical care, mortality among patients with pulmonary gangrene has been reduced, but it still remains very high and amounts to 35-40%.

In conclusion, I would like to emphasize that the treatment of BDL is complex and lengthy, and despite the use of the most modern medications and effective surgical interventions, it is not always successful. Its development, like many other life-threatening diseases, is always easier to prevent than to treat. Prevention of BDL is associated with the implementation of broad measures aimed at promoting a healthy lifestyle, combating influenza, alcoholism, drug addiction, improving working and living conditions, observing personal hygiene rules, early diagnosis and adequate treatment of patients with community-acquired and hospital-acquired pneumonia.

PURULENT - DESTRUCTIVE DISEASES

LUNGS

Purulent destructive diseases of the lungs include acute abscesses, gangrene and chronic lung abscesses.

LUNG GANGRENE - purulent - putrefactive necrosis of a significant area (lobe or more) of lung tissue without clear demarcation, with a tendency to spread and accompanying extremely severe general intoxication.

GANGRENOUS ABSCESS - purulent - putrefactive necrosis of a section of lung tissue with sequestration and a tendency to delineation.

LUNG ABSCESS is an area of purulent or putrefactive decay within a segment (rarely more), with destruction cavities filled with pus and surrounded by a zone of perifocal inflammation.

M:F = 8:1, most common between the ages of 30 and 50 years. In Western countries there is no such problem - in France, for example, in 1988. 8 people got sick.

CLASSIFICATION

I. Abscesses A) pathogenesis aspiration embolic post-traumatic septic

B) acute chronic course

B) localization central peripheral

D) complications empyema bleeding pyopneumothorax without complications

II. Gangrenous abscesses

III. Gangrene of the lung

REASONS FOR DEVELOPMENT:

Bronchial obstruction

Acute infectious process of parenchyma

Impaired blood flow and necrosis of parenchyma

Most often, purulent-destructive lung diseases develop in weakened people with a history of disturbances of consciousness of various origins.

Chronic alcoholism and severe drug addiction are characterized by decreased immunity, cough reflex, bone marrow granulocyte reserve, and suppressed phagocytosis.

The percentage of alcoholics among patients with OGDD does not decrease below 50%. All patients with lung gangrene have caries in advanced stages, since carious processes change the ratio of aerobes and anaerobes in the oral cavity and increase the possibility of aspiration of anaerobic flora.

The most severe cases of HDLD occur in asthmatics against the background of long-term use of hormones, which increases the body’s sensitivity to infection, increases the resistance of microflora to asthma, reduces inflammatory reactions, immunity, and fibroblast proliferation.

ETIOLOGY

Over the past 30 years, there has been a change in flora from pneumococcus and streptococcus through staphylococcus flora to anaerobic and gram-negative associations. In recent years, mushrooms and mixed forms of associations have begun to play an increasing role.

10 years ago - staphylococcus 69%, now: staphylococci - 15 - 20%, gram-negative (coliform, SGP, proteus) - 40%, obligate non-spore-forming anaerobes - 55 - 75%. Friedlander's bacillus is the most severe pneumonia with severe sequestration (0.5 - 4%). In 57%, the flora is multiresistant to antibiotics.

During influenza epidemics, the frequency of staphylococcal processes increases. All of these microorganisms are non-pathogenic with normal protective mechanisms in the lungs.

WAYS OF DEVELOPMENT OF OGDZL.

1. As a consequence of PNEUMONIA - from 63 to 95%, abscesses - from focal, gangrene - from lobar due to hyperergic inflammation.

Reasons for the transition of pneumonia to an abscess:

Untimely incorrect treatment

Severe extrapulmonary pathology

Immune suppression

Localization of inflammation.

Up to 43% of pneumonias are complicated by gastrointestinal tract diseases.

Pathogenesis.

Infection - inflammation - obstruction of small bronchi - atelectasis - progressive inflammation - edema - microcirculation stasis - necrosis in an airless inflamed area with vascular thrombosis - purulent - putrefactive decay.

2. ASPIRATION MECHANISM.

It begins with obstruction of the small bronchi. The inflammatory process develops secondary. Aspiration abscesses form quickly, within 8-14 days. More often they form on the right in the lower sections, as well as in the posterior apical and upper lower lobe segments, if a person lies on his back or on his side.

3.HEMATOGENOUS - EMBOLIC MECHANISM 0.8 - 1% (up to 9%)

Against the background of pulmonary infarction. Mortality - 36%.

Causes: septic endocarditis, thrombophlebitis of the veins of the lower extremities and pelvis, phlebitis after catheterization of veins, abscesses of various locations.

The presence of a heart attack is not the cause of abscess formation, and the heart attack itself resolves quickly due to abundant collaterals. Destruction develops with bronchogenic infection.

PA ligation does not cause infarction, while PV thrombosis leads to hemorrhagic infarction.

4. OBTURATORY SUPUPERATION OF THE PULMONAS - HDPL, caused by blockage of the bronchus by a foreign body, tumor, bronchial stenosis, postoperative dislocation (0.3%). Cancerous abscesses are now extremely rare (0.4%). The middle lobe is most often affected.

5. POST-TRAUMATIC ABSCESSES and gangrene are divided into two groups:

a) non-penetrating damage to the main body (bruises, compression)

b) penetrating damage to the HA.

This kind of purulent destruction develops when large bronchi are damaged.

In the clinic, with a closed chest injury, GDD developed in 0.5%. With penetrating wounds, GDSL are also rare; according to the Second World War, no more than 2% in open pneumothorax and 0.47% in all chest wounds. Empyema and bronchial fistulas occurred more often.

Abscesses from gunshot wounds can develop months or even years after the injury.

CLINIC AND DIAGNOSTICS.

There are three types of abscess formation:

I - against the background of favorable dynamics of pneumonia, a crisis occurs on days 12-20 with the formation of an abscess.

II - prolonged course of pneumonia with unsuccessful treatment with the formation of an abscess on 20 - 30 days, gradual deterioration.

III - lightning-fast course, the formation of an abscess from the first days; with aspiration, an abscess is formed already on the 5th - 10th day.

Clinic BEFORE abscess drainage:

hectic fever, chills, heavy sweats, cough, dry or with slight discharge of mucopurulent sputum, pain on the affected side, physically - a picture of massive pneumonia, leukocytosis with a pronounced shift of the formula to the left

Suppurative lung diseases or acute infectious destruction of the lungs– a pathological process characterized by inflammatory infiltration and subsequent purulent or putrefactive decay (destruction) of lung tissue as a result of exposure to nonspecific pathogenic microorganisms (specific destructions include tuberculous caseous pneumonia, syphilitic gumma, etc.). Depending on the nature of destruction, lung abscess, gangrene and gangrenous abscess are distinguished.

Lung abscess– localized purulent melting of the lung tissue with the formation of a purulent cavity limited by the pyogenic membrane. In the practice of a therapist, lung abscesses are more common, occurring as “abscess pneumonia” with the formation of small purulent cavities in the area of the pneumonic focus, merging with each other.

Lung gangrene– massive necrosis and putrefactive decay of lung tissue, not prone to delineation.

Gangrenous abscess characterized by less extensive and more prone to delimitation than with gangrene of the lung, putrefactive decay of the lung tissue with the formation of a purulent cavity with parietal or free-lying tissue sequestration.

Epidemiology. There are no sufficiently complete data on the frequency of infectious destruction of the lungs either in domestic or foreign literature. In developed Western countries, the incidence of lung destruction has decreased significantly and there are isolated cases. In Russia, this problem remains very relevant. Thus, according to A.G. Chuchalin (2002), in 1999, over 40 thousand patients with purulent pulmonary diseases were registered in Russian medical institutions, which is a very unfavorable indicator. The mortality rate for lung abscess reaches 20%, and for gangrene – 40% or more.

Etiology. For a long time, the main causative agent of acute infectious destruction of the lungs was considered Staphylococcus aureus(due to the frequent entry into the sputum of a sick staphylococcus, saprophytic in the nasopharynx). In recent years, the leading etiological role of staphylococcus has been established only in post-pneumonic and hematogenous-embolic lung abscesses during sepsis.

The causative agents of aspiration lung abscesses are gram-negative microorganisms(Pseudomonas aeruginosa, Klebsiella pneumoniae (Friedlander's bacillus), Proteus, Escherichia coli) and anaerobes(bacteroides, fusobacteria, anaerobic cocci). Lung gangrene is usually caused by an association of microorganisms, among which anaerobic microflora is necessarily present. Anaerobes are saprophytes of the oral cavity; with its pathology (pulpitis, periodontal disease), the content of anaerobes increases many times over.

Pathogenesis. The most common route of infection of the lung bronchogenic, including aerogenic (inhalation)– when pathogenic flora enters the respiratory sections with air flow and aspiration– during aspiration of infected mucus, saliva, vomit, blood from the nasopharynx. Aspiration is promoted by deep alcoholic intoxication, unconscious states associated with traumatic brain injury, acute cerebrovascular accident, epileptic seizure or anesthesia, hiatal hernia and other pathology of the esophagus. Infected material causes obstruction of the bronchi with the development of atelectasis of the lung tissue, which creates favorable conditions for the life of anaerobic flora.

Aspiration of foreign bodies (dentures, buttons, seeds and others) with the addition of a secondary infection is possible. When acidic gastric contents regurgitate and enter the bronchi (Mendelssohn syndrome), chemical damage to the pulmonary parenchyma occurs, followed by infection.

Less common are hematogenous, lymphogenous and traumatic routes of infection. Hematogenous lung abscesses develop, as a rule, during sepsis as a result of embolism of infected material into the vessels of the pulmonary artery. The source of emboli can be infected blood clots in the veins of the lower extremities and pelvis, vegetations on the tricuspid valve due to infective endocarditis in injection drug users, etc. Possible bronchogenic infection of pulmonary infarctions that develop as a result of pulmonary embolism with primarily sterile blood clots.

In the pathogenesis of infectious destruction of the lungs, the pathogenic properties of microorganisms and the patient’s anti-infective defense mechanisms interact. Most pathogens of destruction are not capable of adhesion on cells of normal bronchial epithelium due to the perfect system of local bronchopulmonary protection - mucociliary clearance, humoral protective factors produced in the alveoli and bronchi (lysozyme, complement, interferon), alveolar surfactant, phagocytic activity of macrophages, broncho-associated lymphoid tissue.

The development of destructive processes is facilitated by the suppression of general and local reactivity as a result of exposure of the patient to various infectious and non-infectious factors. These include:

1. Respiratory viral infections, causing necrosis of the bronchial epithelium and suppression of local immunity, which promotes the activation of opportunistic microorganisms, Staphylococcus aureus, etc.

2. Pneumococcal pneumonia, promoting secondary contamination of the affected lung tissue with pyogenic microorganisms.

3. Chronic bronchitis, including those associated with smoking, which disrupts the mechanisms of anti-infective defense and the drainage function of the bronchi.

4. Bronchiectasis, being a source of infection of the lung parenchyma.

5. Therapy with glucocorticosteroids, having an immunosuppressive effect.

6. Diabetes mellitus, AIDS and other immunodeficiency conditions, reducing the patient's defense mechanisms

7. Alcohol abuse, which plays a special role due to the high probability of aspiration of vomit during alcohol intoxication, decreased general and local reactivity of the body, high contamination of the oral cavity with anaerobic flora due to poor dental care, and the presence of chronic bronchitis smoker

8. Hypothermia.

In the presence of etiological, provoking and predisposing factors, infectious necrosis of the lung tissue develops, followed by purulent or putrefactive melting under the influence of exotoxins of microorganisms. In lung gangrene, microthrombosis of the pulmonary vessels in the affected area plays an important pathogenetic role, making it difficult to form granulation tissue to demarcate the necrosis zone.

Pathological anatomy. With a lung abscess, in the center of the pneumonic infiltrate, purulent melting of the lung tissue occurs with the formation of an abscess cavity containing purulent detritus, and in the stage of drainage of the cavity - pus and air. The cavity is separated from viable lung tissue by a pyogenic membrane. As the process resolves, the abscess cavity is cleared of pus and shrinks or remains an air cyst of the lung.

With gangrene of the lung, massive putrefactive necrosis develops, without clear boundaries, passing into the surrounding edematous lung tissue. The gangrenous lung is a grayish-green mass with multiple decay cavities containing foul-smelling fluid. The appearance of a pyogenic membrane around necrosis indicates the transformation of lung gangrene into a gangrenous abscess.

Classification. In clinical practice, the classification of acute infectious destruction of the lungs according to N.V. Putov (2000) is most widespread.

By pathogenesis:

Postpneumonic

Aspiration

Hematogenous - embolic

Traumatic

Suppuration of pulmonary infarction

By clinic:

Peripheral lung abscesses

Central lung abscesses:

a) single, b) multiple

Lung gangrene

By severity:

Mild degree

Extremely severe

According to the nature of the flow:

Subacute

Chronic

Complications:

Respiratory failure

Infectious-toxic shock

Respiratory distress syndrome

Pulmonary hemorrhage

Pyopneumothorax

Empyema of the pleura

Septicopyemia

Damage to the opposite lung in a primarily unilateral process

Phlegmon of the chest

Amyloidosis of internal organs

Pulmonary heart

Clinic. Infectious destruction of the lungs more often develops in men of working age who abuse alcohol. The disease is often preceded by hypothermia in a state of alcohol intoxication (in 50–75% of cases).

IN clinical picture of lung abscess Traditionally, two periods are distinguished:

1. The period of abscess formation before the breakdown of decay products into the bronchus.

2. The period after the abscess breaks into the bronchus.

Lung abscess usually has an acute onset. In the first period clinical findings are consistent with severe pneumonia. Fever, chills, severe sweating, dry cough, chest pain on the affected side, and shortness of breath are observed. Upon examination, mild acrocyanosis and lag of the affected half of the chest in the act of breathing are revealed. There is a dullness of percussion sound, bronchial or hard vesicular breathing, against which dry and fine moist rales are heard, and sometimes crepitus and pleural friction noise.

General blood analysis reveals neutrophilic leukocytosis up to 18-20 thousand with a shift of the leukoformula to the left to young forms, toxic granularity of neutrophils (+++), an increase in ESR up to 40-50 mm/hour. At biochemical blood test an increased content of α 2 - and γ - globulins, fibrinogen, seromucoids, C-reactive protein is determined. Possible proteinuria due to toxic kidney damage. By microscopy sputum leukocytes are detected, and upon bacteriological examination - various types of bacteria.

X-ray of the chest organs reveals intense infiltrative darkening of varying extent, reminiscent of confluent focal, segmental or lobar pneumonia. The lesion's border is convex towards the healthy lobe, as well as the appearance of denser foci against the background of darkening. Most often, the abscess is localized in the posterior segment of the upper lobe (S 2) and in the apical segment (S 6) of the lower lobe.

The prescribed antibacterial treatment has no effect. Purulent-resorptive fever persists, intoxication increases. In the 2nd week from the onset of the disease, when purulent melting of the bronchial wall passing through the site of destruction begins, the patient’s sputum acquires a fetid odor, which is also felt when the patient breathes. An unpleasant odor emanating from a patient with a lung abscess is felt upon entering the ward.

At this time, radiologically, against the background of infiltration of the lung tissue, areas of clearing of the lung tissue (zones of decay) associated with the accumulation of gas produced by anaerobic microflora are revealed.

Second period The disease begins with the breakthrough of pulmonary decay products into the bronchus. The patient suddenly develops a paroxysmal cough with the discharge of copious foul-smelling sputum (0.5 liters or more), often “a mouthful.” The sputum is purulent, often mixed with blood. When settling, it is divided into three layers: the lower one is thick, grayish in color, contains pus and elastic fibers; medium – cloudy, viscous, consists of saliva; the upper one is foamy, mucous, mixed with pus.

After the abscess breaks through, if the abscess is well drained, the patient’s condition quickly improves - body temperature decreases, appetite appears, and the amount of sputum decreases. The area of percussion dullness decreases. With superficially located abscesses, a tympanic percussion sound appears, and sometimes amphoric breathing. The number of moist rales when opening an abscess increases and then quickly decreases.

X-ray in the second period of lung abscess, the clearing of the lung tissue takes on a rounded shape with a horizontal level of liquid, which, with good drainage, is determined at the bottom of the cavity. The infiltration zone decreases to the size of an abscess.

At fiberoptic bronchoscopy endobronchitis is determined, thick pus comes from the lumen of the draining bronchus. Blood tests are gradually improving.

Subsequently, infiltration of the abscess walls decreases, the fluid level disappears, and the cavity itself decreases and becomes obliterated (complete recovery) or turns into a thin-walled cyst (clinical recovery). With a favorable course of the disease, complete recovery occurs after 1–3 months in 25–40% of patients.

With poor drainage of the abscess cavity, hectic fever with chills, sweating, and lack of appetite persist. For several weeks or months, despite treatment, patients continue to produce copious purulent sputum. Rapid exhaustion develops. The complexion becomes earthy gray, the fingers take on the shape of “drumsticks”, the nails – “watch glasses”.

X-ray Against the background of persistent infiltration, a large cavity with a high level of fluid is determined. At laboratory research anemia, hypoproteinemia (due to loss of protein in sputum and impaired protein synthesis in the liver), proteinuria are detected. Amyloidosis of internal organs develops. This condition is interpreted as chronic lung abscess and is usually treated surgically.

Lung gangrene clinic has a very severe course. The periods of illness, unlike lung abscess, are not pronounced. The leading syndromes are putrefactive intoxication and acute respiratory failure. The fever is hectic in nature, accompanied by debilitating chills and severe sweating. Disturbing cough with the release of foul putrefactive sputum mixed with blood and pain in the chest. The foul odor emanating from a patient with pulmonary gangrene is felt already upon entering the department.

Over the affected lung, dullness of percussion sound is determined. Very quickly, against the background of dullness, areas of tympanitis appear due to the formation of multiple foci of decay. On auscultation, breathing is weakened or bronchial, and moist rales are heard. Over the affected area, there is pain in the intercostal spaces (Kryukov-Sauerbruch symptom); when pressed with a stethoscope, a cough appears (Kiessling symptom), which indicates involvement of the pleura in the process.

X-ray a massive infiltration of lung tissue without clear boundaries is determined, occupying 1-2 lobes or the entire lung, with the appearance of multiple merging cavities of irregular shape against its background.

Blood tests are characterized by pronounced changes in the leukoformula (shift to the left to young, metamyelocytes, etc.), anemia, hypoproteinemia. The development of DIC syndrome is characteristic. Putrid sputum contains sequesters of lung tissue (Dietrich's plugs), blood.

Widespread gangrene in more than 40% of patients leads to early mortality (on the 5th – 7th day of illness) due to increasing intoxication and the development of severe complications.

Complications of abscess and gangrene of the lungs:

1. Infectious-toxic shock develops in the acute period with a massive entry into the blood of infectious microorganisms and their toxins. It manifests itself as acute vascular, respiratory, cardiac, renal failure and the development of disseminated intravascular coagulation. Death from shock occurs in more than 50% of cases.

2. Acute respiratory distress syndrome(shock lung, non-cardiogenic pulmonary edema) develops with infectious-toxic shock or in the absence of severe disorders of central hemodynamics. It is based on microcirculation disorders in the area of the alveolo-capillary membrane, associated with exposure to infectious toxins and biologically active, endogenous inflammatory mediators. The permeability of pulmonary capillaries sharply increases, which leads to interstitial and alveolar pulmonary edema.

3. Pyopneumothorax and pleural empyema develop in more than 20% of patients due to a breakthrough of a pulmonary abscess into the pleural cavity. The patient suddenly feels sharp pain in the chest and increased shortness of breath. The amount of sputum decreases. The pleural cavity communicates with the external environment through the focus of destruction and the bronchial tree. The lung partially or completely collapses. The patient's condition sharply worsens with the formation of a valve mechanism in the area of bronchopleural communication and the development of tension pyopneumothorax.

When examining the patient, cyanosis, increased breathing, and a forced sitting position in bed are determined. By percussion, tympanitis is determined over the upper parts of the affected lung, and in the lower parts there is dullness of sound with a horizontal upper border. Breath sounds disappear. Radiologically, against the background of a compressed lung, air and liquid are detected in the pleural cavity.

With intense pyopneumothorax against the background of increasing shortness of breath (up to 40 breaths per minute or more) and cyanosis, a rapid increase in the volume of the neck, face, and chest occurs. By palpation in the area of swelling, crepitus associated with subcutaneous emphysema is determined. Emphysema can spread to the lower body and mediastinal tissue with severe hemodynamic impairment.

4. Pulmonary hemorrhage– when coughing up 50 ml of blood or more per day. It is usually preceded by hemoptysis (blood mixed with sputum). The cause of bleeding is usually arrosion of the branches of the pulmonary artery in the area of destruction. With excessive blood loss, hypovolemic shock quickly develops.

5. Sepsis with septicopyemia manifested by severe hectic fever, enlarged spleen, and seeding of pathogens from the blood. Hematogenous purulent metastases occur in the brain, kidneys, pericardium and other organs and tissues

6. Bronchogenic spread of a primarily unilateral destructive process to the opposite side occurs in weakened patients and patients who violate the treatment regimen.

Differential diagnosis carried out with the following diseases :

1. With infiltrative pulmonary tuberculosis in the phase of decay and formation caverns, which is characterized by less pronounced intoxication and torpid course. The sputum is mucopurulent without a foul odor, in a daily amount of no more than 100 ml. Physical data are often sparse.

X-ray signs of pulmonary tuberculosis are much more pronounced in accordance with the old rule of phthisiatricians - “little is heard, but much is seen.” Segmental or polysegmental darkening of an inhomogeneous nature is determined mainly in the upper lobes of the lungs with small foci of “dropout” in adjacent segments due to bronchogenic dissemination of the process. Formed cavities are revealed in the form of thin-walled cavities without a liquid level.

By microscopy of sputum or in bronchial washings by flotation, mycobacteria can be detected. Diagnosis is helped by anamnestic data on contact with tuberculosis patients and the lack of dynamics from trial treatment with broad-spectrum antibiotics.

2. With a cavitary form of peripheral lung cancer, which develops more often in men over 50 who smoke heavily. The onset of the disease is imperceptible. Rare cough with scanty sputum. Physical data are not expressed, except in cases of development of perifocal pneumonia. Sometimes the diagnosis becomes an x-ray finding - during the examination, a cavity with thick tuberous walls without a fluid level is revealed, which is mistakenly mistaken for a lung abscess. Computed tomography of the lungs and bronchoscopy help clarify the diagnosis.

3. With metastatic lung cancer, which represents multiple homogeneous rounded shadows across all lung fields. Tumors of the genital organs, kidneys, stomach, liver, and bones most often metastasize to the lungs.

With a diaphragmatic hernia, which manifests itself as a thin-walled formation above the diaphragm, often with a horizontal fluid level, without any clinical manifestations of lung destruction. X-ray examination of the gastrointestinal tract with a contrast agent easily reveals that part of the stomach or splenic angle of the colon enters the pleural cavity through the hernial orifice.

Treatment of infectious lung destruction should be carried out in specialized departments of thoracic surgery using conservative, bronchoscopic and surgical methods. Conservative treatment includes three mandatory components:

2. Optimal drainage of destruction cavities.

3. Detoxification and restorative treatment, specific immunotherapy.

1. Antibacterial therapy is carried out until clinical and radiological recovery of patients, often for 1.5 – 3 months. It is of decisive importance in the initial period of the disease. Antibiotics are administered intramuscularly or intravenously, in severe cases - into the subclavian vein through a catheter. At the first stage of treatment, the choice of antibacterial agents is carried out empirically; after microbiological identification of the pathogen, treatment is adjusted. Parenteral antibacterial therapy is carried out until a clinical effect is achieved (decrease in fever, decrease in cough and shortness of breath, decrease in leukocytosis), after which a transition to oral administration of drugs is possible.

The prescribed antibiotics must be sufficiently effective against the main pathogens of destruction - staphylococcus, gram-negative and anaerobic microflora .

At staphylococcal destructions lung drugs, the first line of treatment is the “protected” β-lactamase inhibitor amoxicillin/clavunate ( amoxiclav– 1.2 g intravenously 3 times a day) and cephalosporins of the II and IV generations ( cefuroxime– 0.75–1.5 g 3–4 times a day and cefepime– 0.5–1 g 2 times a day). III generation cephalosporins (cefotaxime, ceftriaxone, ceftazidime) are less active against gram-positive staphylococci. Can also be used oxacillin at the maximum permissible dose, divided into 3 to 4 administrations per day. Lincosamides are also effective antistaphylococcal drugs ( lincomycin, clindamycin– 0.3 – 0.6 g intramuscularly or intravenously 2 times a day) and “respiratory” fluoroquinolones – levofloxacin ( tavanik-– 0.5 g intravenously 1–2 times a day) and moxifloxacin ( avelox).

Combination therapy is usually carried out, combining the above drugs with aminoglycosides ( gentamicin, amikacin) or metronidazole (metragil– 0.5 g intravenously 3 times a day).

If treatment is ineffective, reserve antibiotics – carbapenems ( tienam– 0.5 g intravenously 3 – 4 times a day) or vancomycin(1 g intravenously 2 times a day), highly active against all penicillin-resistant strains of staphylococci.

In the treatment of infectious destruction of the lungs, caused by gram-negative microflora,“protected” aminopenicillins, cephalosporins of II–IV generations, “respiratory” fluoroquinolones are prescribed, in severe cases - in combination with aminoglycosides of II and III generations (gentamicin, amikacin, tobramycin). If there is no effect, monotherapy with carbapenems is indicated.

For aspiration abscesses and gangrene of the lungs, antibacterial drugs with high activity against anaerobic microflora. At the first stage of treatment, preference is given to clindamycin(intravenously 0.3 - 0.9 g 3 times a day with a transition to oral administration of 0.3 g 4 times a day for 4 weeks). Less effective lincomycin, prescribed in the same dose. To influence anaerobes, metronidazole 0.5 g intravenously 3 times a day can also be prescribed.

Considering the predominantly combined etiology of infectious destruction of the lungs, the above drugs, as a rule, are prescribed in combination with “protected” aminopenicillins, cephalosporins of II–IV generations, “respiratory” fluoroquinolones and aminoglycosides, which have a wide spectrum of action against most gram-negative pathogens and staphylococcus.

Carbapenems have high activity against anaerobes ( tienam), which can be prescribed as monotherapy or in combination with aminoglycosides.

2. Drainage of destruction cavities is carried out in accordance with the fundamental principle of purulent surgery - “Where there is pus, empty it.” For optimal drainage of purulent lung cavities, the following measures are carried out:

Postural drainage (the patient assumes a body position in which the draining bronchus is directed vertically downward, at least 8–10 times a day, while performing maximum coughing);

Therapeutic bronchoscopy with washing of the draining bronchus and cavity with antiseptics;

Long-term catheterization of the trachea and draining bronchus using microtracheostomy for sanitation of the bronchial tree;

Transthoracic puncture of a peripherally located abscess and its drainage for subsequent sanitation of the purulent cavity.

Better separation of purulent sputum is facilitated by taking mucolytics ( potassium iodide, bromhexine, mucaltin, acetylcysteine, ambroxol) and bronchodilators, as well as vibration massage of the chest.

If pleural empyema or pyopneumothorax develops, repeated pleural punctures are performed to remove purulent contents and air or a drainage tube is installed.