Lobar pneumonia: clinical manifestations, diagnostic methods, complications, treatment. Lobar pneumonia, treatment, symptoms, signs

Therefore, the term “lobar” or “lobar” pneumonia more correctly defines the essence of the disease as a peculiar reaction of the body than the name of pneumonia only based on the causative agent ( pneumococcal pneumonia etc.).

At modern methods treatment, lobar pneumonia dramatically changed its course: the classic form, characterized by a fever lasting about a week, gave way to a short illness, often terminated on the 1st-3rd day by a drug crisis.

Causes of lobar pneumonia

Previously, lobar pneumonia was associated exclusively with colds and hypothermia, but then, based on epidemics, it became clear infectious nature illness; With the discovery of pneumococcus, this doctrine was finally strengthened. The development of lobar pneumonia (as well as other infectious diseases) cannot be reduced to the mere presence of pneumococcus in the body and the disease cannot be presented as a direct consequence of local damage to the lung tissue by invading pneumococcus and as a consequence of the humoral effects of pneumococcal toxins on distant organs.

The development of the disease when pneumococci enter the body is possible only with the suppression of neurovascular, phagocytic, immunological reactions, usually as a result of such disease-promoting influences as hypothermia, trauma, nervous shock, previous infections that reduce tissue resistance primarily by disrupting the nervous regulation of body functions . Botkin pointed out that nervous shocks contribute to the onset of the disease.

The main and obligatory cause of lobar pneumonia, as is firmly established, is an infection, usually pneumococcus, which has leading value and in disease prevention.

Susceptibility to lobar pneumonia also depends on the degree of immunity, which is also influenced by the nervous system. Persons free from everyday contact with virulent pneumococcus and therefore not immune to it, when placed in a crowded environment, give rise to severe epidemics of pneumonia, which was clearly observed among French troops during the war of 1914-1917. With increased resistance, the introduction of virulent pneumococcus can only lead to pharyngitis, otitis, etc. or only to carriage.

With a decrease in resistance, already low-virulent types can cause lobar pneumonia, while in young, strong subjects, pneumonia is usually caused only by the first two, virulent types of pneumococcus (in total, about 75 types and subtypes of pneumococcus are known).

Infection in a family or community occurs more often from carriers, as in meningococcal meningitis, or from patients with other pneumococcal diseases. Patients with pneumonia are freed from virulent pneumococcus more quickly than healthy carriers, which partly explains the rarity of nosocomial diseases. Cases of multiple intrafamilial pneumonia are very rare.

Pneumococci higher types represent normal inhabitants of the nasopharynx and cause pneumonia in the form of autoinfection.

More cases are observed in cities during the cold season, from November to May, probably as a result of greater crowding.

Typically young people suffer from typical lobar pneumonia (possibly due to the hyperergic nature of the disease), with men almost 3 times more likely than women. Children and the elderly, if the body is weakened by other diseases, are especially susceptible to secondary pneumonia.

The actual pathogenesis of lobar pneumonia has not been sufficiently studied, in particular, the neuroreflex mechanisms, which mainly determine its clinical signs known to us from the very beginning of the disease, have not been studied.

It is necessary to take into greater account the pathological impulses that arise during inflammatory processes from the receptor fields of the lung tissue, pulmonary vessels, pleura, etc. In particular, the cardiovascular signs of lobar pneumonia, which often have a decisive influence on the outcome of the disease, are due to a large extent to the reflex changes in the activity of the central nervous system, and not just toxic effects. It has been established that the infection penetrates the respiratory tract and penetrates into the lungs through the bronchi (in monkeys, typical lobar pneumonia can be caused by intratracheal injection of very small doses of pneumococcus). In the lungs, bacteria first settle in the lymphatic network, followed by rapid coverage of the entire lobe of the lung with fibrinous effusion, which is characteristic, as is the tendency to end in necrosis, for hyperergic inflammation. Pneumococcus is found in the blood only in a third of cases. Virulent pneumococci are found in the affected lung and in sputum until a critical drop in temperature. Likewise, toxins—type-specific polysaccharides—flood the patient’s blood and are excreted in the urine until the crisis, when there is no free toxin left, not bound by antibodies; pneumococci disappear from sputum, apparently, mainly due to the accumulation of antibacterial antibodies.

In the critical resolution of pneumonia, local acidosis is also important, partly associated with insufficient blood flow into the compacted lung and reaching such an extent that the vital activity of the pneumococcus stops and proteolytic enzymes are activated, destroying fibrin and cellular exudate.

Convalescent serum contains so-called preventive substances, i.e. antibodies which, when administered in combination with lethal dose the same type of pneumococcus into the animal's body, protect it, especially the sensitive white mouse, from disease. In addition, during recovery, type-specific agglutinins and precipitins accumulate.

Very frequent repeated, even multiple, human diseases of lobar pneumonia most often seem to depend on infection with another type of pneumococcus.

Clinical and anatomical periods of lobar pneumonia

Lobar pneumonia is one of the diseases in which it has long been established that the development of the main local physical signs corresponds to the changing anatomical lesions of the organ.

IN early period high tide (the first day of the disease), the affected lobe is full of blood and its elastic properties are already reduced, although the alveoli are still partially passable for air, and the capillaries are passable for blood; upon percussion, some muffling and tympanic tone are detected, as well as (for a short time) crepitating rales (crepitatio indux) or. only weakened breathing in the affected area of ​​the lung.

With the onset of complete compaction in the affected lobe, the air is completely replaced by fibrinous effusion, rich in erythrocytes and peytrophils and containing an admixture epithelial cells. The cut surface is dry, fine-grained, reddish-brown in color, with a reddish thick scraping; pieces of affected tissue sink (red liver). The capillaries are also compressed. Clinical lobar muffling with bronchial breathing, bronchophony, and increased vocal tremors.

Red hepatization gradually (approximately on the 4-5th day) turns into gray and then (on the 6-7th day) resolution occurs. The lung acquires a grayish-white color, the cut surface. becomes more moist, granular plugs appear even more sharply when scraped, and the cloudy liquid accumulates in larger quantities. Pneumococci are in a phagocytosed state. When resolved, the lung becomes softer, the plugs disappear, there is a purulent fluid on the cut, desquamation and regeneration of the epithelium of the alveolar walls.

From the time air passes into the alveoli, which often happens when there are completely hepatized areas nearby, a typical crepitation (crepitatio redux) is heard for a number of days, followed by sonorous subcrepitating rales as it resolves.

The section reveals the trachea and bronchi containing blood-stained viscous sputum, fibrin convolutions in the heart, a moderately enlarged spleen, usually cloudy swelling of the liver and kidneys, purulent complications (pleurisy, pericarditis, meningitis, endocarditis, arthritis).

Symptoms and signs of lobar pneumonia

The incubation period usually lasts 1-2 days, sometimes up to a week; with traumatic pneumonia it is sometimes reduced to several hours (as with experimental intratracheal infection).

Occasionally, prodromes are observed in the form of headache, general malaise, gastrointestinal disorders. In some cases, lobar pneumonia develops after bronchitis, laryngitis, nasopharyngitis, tonsillitis (secondary lobar pneumonia).

A characteristic sudden onset with stunning chills is observed in 4 out of 5 patients with pneumonia and almost always with the first type of pneumococcus. The patient cannot warm up. He trembles from head to toe, his teeth chatter, his lips are blue, his limbs are icy, although the temperature reaches 40°. Other complaints that come to the fore early include pain in the side and cough. Stitching pain in the side, aggravated by pressure, sneezing, talking, can reach an extreme degree and radiate to the shoulder and stomach.

When listening, a pleural friction noise is detected; fibrinous pleurisy accompanies lobar pneumonia (except central) almost constantly. The pain may disappear the next day or in the coming days; Particularly persistent pain foreshadows pleural empyema. Relieves compression pain chest hand, a compress, an adhesive plaster, as well as separation of the pleura with effusion or air (based on the experience of attempts to treat pneumonia with pneumothorax at one time), as well as injections of novocaine in the febrile period. Complaints of a vague feeling of pressure and heaviness in the chest are also common.

The cough, initially dry, paroxysmal, extremely painful, becomes somewhat easier with the appearance of sputum; it exhausts the patient, disturbs his sleep, burdens the right heart due to increased intrathoracic pressure, worsens respiratory exchange, but, by displacing fibrinous plugs in the bronchi, it prevents atelectasis to a certain extent.

The sputum, initially scanty, foamy, whitish or faintly streaked with blood, contains pneumococci; by the end of the day it becomes rusty from the admixture of blood, viscous, translucent, and later becomes cloudy from the abundance of leukocytes and fibrin. By the time pneumonia resolves, the sputum becomes more liquid and abundant, lemon yellow or saffron in color, it contains fewer red blood cells and leukocytes. Sputum can remain bloody throughout the illness, especially in heart patients and in traumatic pneumonia, when real pulmonary hemorrhages are observed. Sputum is rich in protein, which disappears after a crisis.

The general appearance of the patient is characteristic from the very first days of the disease and already allows, in combination with constant high fever, to assume lobar pneumonia. The doctor sees a seriously ill patient, maintaining a passive position on his back, with shiny eyes, a juicy purple-cyanotic face, with a herpetic rash on the lips, in the corners of the mouth, on the nose, ears, chin, etc.; Such rashes, appearing from the 3rd day of illness, rarely earlier, are characteristic of pneumococcal lesions in general. The skin is hot, dry to the touch, and there is painful shortness of breath. Breathing is shallow, with short inhalations interrupted by pain, with movement of the wings of the nose, in children with an exhaling groan. Later, when the pleural pain subsides and the tightening of the lung develops further, breathing becomes deeper, more difficult, with the participation of auxiliary muscles.

The respiratory rate depends on pain, fever, the severity of lung damage, the degree of intoxication and reaches 25-40-50 or more per minute. The normal ratio of the number of respirations and pulse, equal to 1: 4, with pneumonia increases to 1: 3-1: 2 and even J: 1. In the first days of the disease, the pulse is feverish and galloping.

Cyanosis can be especially sharp at the onset of the disease and decrease with complete hepatization, when blood circulation through the affected lobes drops sharply and, therefore, almost all the blood of the pulmonary circle passes through healthy areas of the lungs and arterializes there, while the blood that previously passed through the affected lobe retained its venous character and thus caused the admixture of significantly undersaturated blood with oxygen to the total arterial blood large circle (central cyanosis). In this case, the percentage of hemoglobin undersaturation with oxygen, which is normally equal to 5 in arterial blood and 25 in venous blood, rises to 15-20-40 in arterial blood and to 50 and higher in venous blood. In addition, pneumococcus has the inherent property of converting hemoglobin into methemoglobin, which is no longer involved in gas exchange.

The affected side of the lungs lags behind in breathing, percussion reveals a muted lobar character, less often complete dullness, depending on the degree of adherence of the hepatic area to the surface of the chest and the massiveness of the inflammatory coverage of the affected lobe or affected lobes.

In addition to bronchial breathing, the hepatized lung intensively conducts voice tremors. At the height of the disease, no wheezing is heard over the affected lobe, but often due to concomitant bronchitis, diffuse bronchitis, mainly dry, wheezing is heard. Particularly characteristic is the crepitus of the resolution period, caused by the passage of air during inspiration through the accumulations thick secretion at the level of the confluence of the terminal bronchus into the alveoli.

X-ray is characterized by a dense homogeneous darkening, often established even before clinical signs of hepatization, usually spreading from the root to the periphery, covering one or another entire lobe. The diaphragm is higher than normal on the affected side. The symptoms of atelectasis are rarely obvious. When resolved over a period of time, a mottled picture remains.

The cardiovascular system is often affected. In severe cases, circulatory failure of central toxic origin develops (as first pointed out by S.P. Botkin), due to paralysis of the vasomotor center, from which animals also die during experimental infection with pneumococcus. Patients are apathetic, their body is covered with cold sweat; there is diffuse ashy pale cyanosis, relaxation of skeletal muscles, collapse of visible veins, low venous pressure, insufficient blood supply to the heart, thread-like pulse that increases simultaneously with a drop in temperature, low systolic and diastolic blood pressure (acute vascular insufficiency); At the same time, other signs of brain poisoning occur—excitement, coma, etc.

Pneumonia often leads to heart failure; the myocardium is damaged as a result of the action of toxins, as well as overload. Turning off the vascular network in the hepatized lung and reducing excursions of the chest and movements of the diaphragm worsen blood circulation in the pulmonary circle, creating increased load, especially for the right heart. The pressure in the pulmonary circle increases, causing an increase in the second sound of the pulmonary artery. The right ventricle expands to the right, heart contractions become more frequent, venous pressure increases, the jugular veins swell, blood flow slows down, as a result of which cyanosis (cardiac) increases, the second pulmonary artery sound becomes weaker, a systolic murmur is heard at the apex; congestive swelling of the liver occurs, diuresis decreases. In the presence of heart disease prior to pneumonia in persons suffering from emphysema and pneumosclerosis, symptoms of right heart failure occur earlier. In those suffering from cardiosclerosis and hypertension, pneumonia can cause left heart failure, in particular, congestive pulmonary edema. Extrasystoles are observed more often in the elderly and, not accompanied by sudden tachycardia, do not necessarily mean a poor prognosis.

Tachycardia, especially increased heart rate, over 120-125, accompanies vascular insufficiency, and myocardial damage, why is it so prognostically important; The easiest way to distinguish between vascular and heart failure is in venous pressure (which falls with vascular failure and rises with heart failure), of course, in combination with other clinical signs of general poisoning or heart damage.

Pneumonia also affects the gastrointestinal tract. intestinal tract. Appetite disappears. From the onset of the disease, there is increased thirst, coated tongue, vomiting - with a rapid rise in temperature due to irritation of the meninges, especially in children and women, from severe cough, not to mention the possible side effects of sulfonamides. The action of the intestines is delayed, in severe cases there is flatulence due to toxic damage intestines and restriction of diaphragm movements. At the height of the fever, worms may be released. Manifestations of pneumococcal sepsis can be meningitis with vomiting, enteritis with diarrhea, and general peritonitis.

The liver can be enlarged and sensitive due to infectious-toxic hepatitis with jaundice (bilious pneumonia, according to the terminology of old authors) or heart failure; with effusion in the pleura, the liver is lowered.

Urine is saturated, of high specific gravity, rich in urobilin, nitrogenous waste, but contains almost no table salt, retained during pneumonia in pulmonary exudate and in the skin; Chlorides are not retained in the blood. The amount of urine decreases, especially in severe cases, which is also important for treatment with sulfonamides. In almost half of the cases there is slight albuminuria, some hyaline cylinders in the sediment (febrile albuminuria due to turbid swelling or fatty degeneration of the tubules), rarely more severe kidney damage with azotemia. The crisis is accompanied by the release of large amounts of urine and table salt (postcritical polyuria and polychloruria).

The blood reacts from the first day with significant neutrophilic leukocytosis, reaching 15,000-25,000, and in young, strong individuals even up to 50,000-70,000; eosinophils disappear, the percentage of neutrophils rises to 90-95 with a sharp shift to the left, supranucleus, to 20-40; Young neutrophils and even myelocytes are often found in the blood. Leukocytosis lasts another 1-2 or even more days after the crisis, when eosinophils also appear in the blood. In severe cases, as well as in debilitated individuals, there is no leukocytosis; sometimes the number of leukocytes drops even below normal. Red blood suffers significantly only during complications. ROE is accelerated, except in cases of severe cyanosis, which inhibits the erythrocyte sedimentation rate. Plasma is rich in globulins, especially fibrinogen, corresponding to the richness of pneumonic exudate in fibrin.

From the nervous system, complaints of severe headache are usually noted from the first hours of illness. Initial vomiting and insomnia are common already during the prodrome. Due to intoxication of the nervous system - sweats, flatulence, coma. Delusional phenomena on the 4-6th day of illness, quiet muttering or manic delirium, also indicating persistent plethora of the brain, are prognostically difficult. Patients must be under constant close supervision, as they can jump out of the window, etc. In alcoholics, even after the fever has subsided, hallucinations may remain for a long time. A post-critical state of confusion is also observed with cardiac and vasomotor weakness. It occurs as a result of sudden stagnation or anemia of brain tissue and occurs with great prostration, insomnia, hallucinations, whirlwind of thoughts, delusions of persecution, poisoning.

Prognosis of lobar pneumonia

Lobar pneumonia is a serious disease that previously had a mortality rate of 12-15% or more. Pneumonia is especially dangerous for children and the elderly, for patients with chronic failure blood circulation, for those suffering from emphysema, alcoholics, for patients with malignant tumors, diabetes, cirrhosis of the liver and for infections such as typhoid and typhus, malaria, influenza in the postpartum and postoperative period. In the Soviet Union, unlike the United States, a significant reduction in mortality from lobar pneumonia was achieved thanks to the successes of socialist healthcare (early hospitalization, timely rational treatment, etc.). The average hospital mortality rate during treatment with sulfonamide drugs and penicillin is below 4%; among young healthy individuals it is no more than 1% and is caused almost exclusively by virulent pathogens.

Women generally get sick somewhat more severely; pregnant women often experience miscarriage, which has an especially unfavorable prognosis in the first 2-3 days of illness. At the same time, the outcome in chronic pneumonia observed less frequently in women.

Pneumonia caused by pneumococcus III is more severe (although they often affect older people), Friedlander forms and forms caused by hemolytic streptococcus. Intrafamilial pneumonia is sometimes observed, which apparently depends on the particular virulence of the infection. Repeated pneumonia in the same patient is usually somewhat milder.

The following clinical signs are prognostically unfavorable: tachycardia (over 125 pulses per minute in an adult), absence of a leukocyte reaction when neutrophils shift to the left, abundance of pneumococci in the sputum, agitation or adynamia, stupor, severe cyanosis, heart failure with a gallop rhythm, pulmonary edema, venous And arterial hypotension, severe jaundice, intestinal flatulence, anuria.

Temporary disability in uncomplicated cases and with early treatment may be limited to 15-20 days.

Prevention of lobar pneumonia

Isolating patients and keeping them in bright, sunny rooms (pneumococci quickly die in the light) can limit the incidence of infection and the number of bacilli carriers. Propylene glycol and oil treatment of the room are tested for the same purpose. To prevent the disease, it is important to avoid crowding, especially in winter, and hypothermia.

Specific vaccination with capsular polysaccharides is promising, but not widespread. Immunity from vaccination lasts about six months. Systematic prophylaxis of collectives with sulfonamides and penicillin is not advisable, since pneumococcus may acquire a certain degree of resistance, limiting the specific treatment of cases of pneumonia in the future.

Treatment of lobar pneumonia

Treatment consists of prescribing general regime and the use of specific means.

Proper care remains of great importance to this day. A patient with pneumonia is placed in a spacious, bright, well-ventilated room, placed on a bed with a fairly firm mattress, which is comfortable for the patient and facilitates his examination and maintenance, saving his strength. Cool air improves sleep and deepens breathing movements. The patient is provided with a sippy cup and is asked to frequently drink water, cranberry juice, lemonade with added alkalis, for example, potassium tartrate - a total of at least 3 liters of liquid per day, ensuring a diuresis of at least 1.5 liters (especially when treated with sulfonamides).

There is no need to insist on eating while the patient has no appetite, if, as usual, the illness lasts only a few days. At the height of the disease, liquid and semi-liquid food is given - a strong broth, with which some tonic substances and table salt are introduced, milk (with tea, coffee, in the form of kefir, curdled milk, etc.), jelly, jelly, soft-boiled eggs or raw broth, porridge, etc.

At feeling better the patient can be given an apple, chewing of which increases the secretion of saliva, helps cleanse the teeth, minced meat cutlet, bread. To prevent mixed lung infections and, in particular, complications of gangrene (fusospirillosis), be sure to wipe the oral cavity with a swab containing hydrogen peroxide.

Herpetic blisters and ulcerations are lubricated with zinc ointment. The intestines are cleansed with a regular enema, and for persistent constipation, hypertonic salt enemas are used. It is recommended to avoid laxatives. A gas outlet tube is used against intestinal bloating.

In cases of agitation and severe headache, wiping the body with a sponge and putting ice on the head are prescribed. Specific treatment (sulfonamides, penicillin) is started as early as possible.

Sulfonamides [sulfidine (sulfapyridine), sulfazine (sulfadiazine), norsulfazole (sulfathiazole), sulfazole] have fast action for pneumonia caused by any type of pneumococcus, Friedlander's bacillus and streptococcus, subject to long-term maintenance of a sufficient concentration in the blood of the free (non-acetylated) drug - usually 5-7-10 mg%, and for septic pneumonia 10-15 mg% - not only until the symptoms disappear pneumonia, but before the body produces protective antibodies, when the cessation specific treatment already threatens the return of the disease.

According to a widely accepted treatment regimen, 7.0 sulfidine is given on the 1st day, 6.0 on the 2nd, 4.0 on the 3rd and 4th, and 2.0 on the 5th day; start with 2.0 on the first day of treatment and then give a daily dose in 6-4 doses.

It is more advisable, however, to use higher doses - on the 1st day of treatment - 10.0 with the first dose of 4.0; In this way, it is possible to quickly interrupt the pneumonic process, and the lack of action speaks more definitely against lobar pneumonia.

Treatment with late onset can be carried out in a shorter period of time - 4, 3 or even 2 days, using only 15.0-20.0 of the drug, since the body is already approaching biological recovery.

If the drug is thrown away by vomiting, immediately repeat the same dose; intravenous administration (preferably 5-10% solution of the sodium salt of norsulfazole and sulfazine) is used in patients who are in unconscious or in case of the most severe septic infection, with complications of meningitis, switching as soon as possible to giving the drug orally. In severe cases, sulfazine is recommended at a dose of 4.0 intravenously and then 3.0 every 6 hours orally. Norsulfazole is preferably prescribed for staphylococcal pneumonia.

The total dose in some cases of wandering, recurrent, septic pneumonia has to be increased to 35.0-40.0 per patient. In general, if the weekly treatment fails, there is no benefit in continuing sulfonamide therapy.

Sulfidine, like other sulfonamide drugs, turns out to be ineffective in rare cases of acquired sulfonamide resistance of pneumococci (with prevention carried out before the disease or treatment with small doses of sulfonamides).

Sulfonamides are not very effective against pneumococcal meningitis and viral pneumonia and have no effect on tuberculosis pneumonia.

When used on any day of an uncomplicated pneumonic process, these sulfonamide drugs critically break the fever within about a day and toxic effect pneumococci with improvement of all subjective symptoms of the disease; the already formed pneumonic infiltrate resolves at normal speed. If the infiltrate has not yet developed, the anatomical process may also be interrupted. The effect of sulfonamides does not depend on the presence of excess polysaccharide toxins. Sulfonamides do not inhibit the formation of protective antibodies.

Each dose of sulfidine and other sulfonamides must be taken with a glass of water and soda to ensure sufficient diuresis (at least 1.5 l) and prevent dysuric phenomena.

To prevent crystalluria, it is necessary to maintain an alkaline urine reaction (pH not lower than 7.5), which requires about 10.0-15.0 soda per day or an appropriate amount of Borjomi, sodium citrate or lactic acid.

Avoid exposure to ultraviolet rays to avoid severe dermatitis; the prohibition of sulfuric acid salts (laxatives) is not justified. Daily observation by a doctor is required; in this condition, treatment can be carried out at home.

Sulfonamides are contraindicated in case of individual intolerance known from history or revealed at the beginning of treatment in the form of dermatitis, leukopenia, paradoxical drug fever. In patients with severe kidney damage (low concentration function, azotemia), it is permissible to prescribe smaller doses, no more than 4.0 per day, which, however, ensures the required concentration of the drug in the blood due to poor excretion by the kidneys.

Leukopenia as a consequence of severe pneumonia, and not medication, makes it possible and even necessary treatment large doses of sulfonamides (however, severe pneumonia is more correctly treated from the very beginning with penicillin). The appearance of dysuria, hematuria, and anuria due to the formation of sulfonamide stones requires urgent cessation of treatment and increased fluid administration. During the period of treatment with sulfonamides, it is advisable to repeatedly, even every day, count leukocytes and, if possible, determine the concentration of the free drug in the blood, as well as conduct careful daily monitoring of drug tolerability, and test urine for crystals of sulfonamides and their derivatives.

Penicillin is used intramuscularly at an average dose of 200,000-250,000 and up to 800,000 units per day for toxic and septic pneumonia in elderly, weakened, dehydrated patients, for leukopenia, meningitis, empyema, as well as for revealed intolerance or invalidity of sulfonamides (if fever does not subsides within 2 days of treatment with sulfonamides), with pneumonia caused by hemolytic streptococcus (sometimes sulfonamide-resistant) and staphylococcus. Penicillin is a more effective remedy against pneumonia than sulfonamides.

Penicillin has no effect on pneumonia caused by influenza bacillus and Friedlander's pneumonia, which responds well to treatment with streptomycin (intramuscular and intratracheal).

Treatment with a type-specific serum in a large dose intravenously is rarely used due to the complexity and indifference of this method, although in principle immunotherapy is superior to chemotherapy, since, by neutralizing polysaccharides, the serum immediately stops intoxication. It is necessary to determine the type of pneumococcus in the patient, to have the appropriate serum available (horse or, better, rabbit serum, preferably freed from excess protein); treatment should be carried out no later than the 3-4th day of illness and, in order to ensure the necessary excess of antibodies, warmed serum should be slowly administered intravenously at 50,000-200,000 units or more, sometimes repeatedly.

To prevent anaphylaxis, start with a test and desensitizing dose of 1 ml; persons suffering from serum sickness, asthma, or idiosyncrasy to medications should not be administered serum due to the risk of fatal anaphylaxis; hypersensitivity can be determined by test injection of diluted serum intradermally (nettle blister!) or into the conjunctiva.

An anaphylactic reaction is expressed by chest tightness, shortness of breath similar to an asthmatic attack, facial redness and cyanosis. An injection of adrenaline (repeated if necessary) or atropine, which should always be available, eliminates these symptoms, except in the most severe cases, which can result in death.

Less dangerous is protein fever, accompanied by chills and sweat, which can be alleviated and often prevented with salicylates, morphine, novocaine administered intravenously, pyramidon, wine, and serum sickness, which manifests itself after 1-2 weeks with the usual symptoms (fever, skin rashes, general increase in lymphatic nodes, joint pain), against which diphenhydramine, novocaine, salicylates, pyramidon, calcium salts are used.

Treatment of pneumonia with novocaine intradermal infiltration of the area of ​​​​the corresponding skin segments (in the shape of a rhombus with a center on the upper thoracic vertebrae) according to Speransky’s method can have a beneficial trophic effect on the affected lung. In cases of hypoxemia, cardiovascular failure, etc., pathogenetic and symptomatic treatment. Oxygen treatment is carried out either through a nasal catheter, or by applying a special mask, or by placing the patient in an oxygen tent. With weak respiratory movements, cyanosis, atelectasis, 5-10% carbon dioxide is added to oxygen.

Cardiovascular drugs are used that simultaneously stimulate the central nervous system, such as camphor, caffeine, strychnine; the latter, in case of severe vascular insufficiency, is used subcutaneously in a maximum amount of 2 mg per dose and 5 mg per day (higher doses are also recommended). In case of severe collapse, injection of adrenaline or ephedrine, lobeline (to excite the respiratory center), ether (for the purpose of reflex excitation of the center), inhalation of carbon dioxide (also an irritant of the respiratory and vasomotor, in particular, venomotor center), as well as saline solution under the skin is indicated. , even blood transfusions, wine, especially quickly absorbed champagne; Simple remedies such as rubbing the skin, hot bottles and mustard plaster on the feet, hot drinks, and fresh air are also beneficial. In case of failure of the heart itself, foxglove is indicated, especially when atrial fibrillation, or strophanthus preparations; bloodletting (300-400 ml), especially with threatening pulmonary edema; circular cups on the chest, morphine. Intravenous administration of glucose is used for heart failure (excess glucose can overload the heart!), and for vascular weakness, and as a general neutralizing agent, sometimes together with small doses of insulin.

For persistent cough, pain in the side, use dry cups, mustard plasters, codeine (Godeini phosphorici 0.015-0.03 per dose; morphine is contraindicated for atelectasis, as well as for flatulence and distension of the bladder), rubbing in irritating ointments, a warm compress that fixes the chest cage and limiting pulmonary excursions.

For flatulence, a gas outlet tube, 0.5-1 ml of pituicrine under the skin (recipe No. 246), injections of prostigmine methyl sulfate - 1 ml of 0.5°/oo solution are also recommended.

In case of nervous excitement, apply ice to the head and wet wrapping. For the delirium of alcoholics, stimulants. For delirium tremens, alcohol, spinal puncture, and methenamine are prescribed. For post-critical delirium, sedatives (bromides, luminal, even scopolamine).

Many other means are also recommended (for example, intravenous administration hypertonic solution table salt, which is advantageous to combine with penicillin therapy due to the retarding effect of salt on the release of penicillin). With delayed resolution, pulmonary diathermy, autohemotherapy, blood transfusion.

For pneumococcal meningitis, sulfazine orally and intravenously (5.0 in an alkaline solution), maintaining its concentration in the blood at 10-15 mg%; At the same time, penicillin is administered intramuscularly and also intralumbarally through a lumbar puncture (since penicillin passes into the cerebrospinal fluid worse than sulfidine). Combined treatment with sulfonamides and penicillin is also carried out for septic pneumonia.

Lobar pneumonia, which is also commonly called lobar pneumonia, thanks to antibacterial drugs, is now much less common than in the middle of the last century. However, if this disease nevertheless overtakes a person, then its course is quite severe, and the consequences, if the treatment regimen is not followed, can even be fatal.

The very name “lobar pneumonia” corresponds to the characteristics of pneumonia. Croup or fibrin film are grayish-colored formations that cover inflamed areas of lung tissue. The main component of these films is the substance fibrin.

The disease can occur after severe cooling of the patient’s body, close contact with an already sick person, as well as a long stay of the person in the hospital, especially in the intensive care unit.

Typically, lobar pneumonia covers an entire lobe of the organ.

The lining of the lung, called the pleura, also becomes inflamed. It is important to note that it is the inflammation of the latter that causes pain symptoms. The fact is that it is in the pleura that pain receptors are located.

The onset of the disease is usually abrupt and aggressive, since the interaction of lung tissue with the microorganism that is its causative agent is partly reminiscent of an allergic reaction. The causative agent of lobar pneumonia - Streptococcus pneumoniae– normally located in the upper respiratory tract person, that is, in contact with the body of a potential patient.

Streptococcus pneumoniae

This causes the body to become sensitive to it. Later, when the microbe comes into contact with the respiratory parts of the lung, a reaction resembling an allergic one occurs. There is a rapid and severe inflammation lungs. In this case, the lesion, as a rule, does not affect the bronchi, but only affects the lung tissue itself.
If lobar pneumonia proceeds in a typical manner, then from the onset of the disease until the patient’s recovery, several stages can be distinguished:

1. Tide stage;
2. Hepatization stage;
3. Resolution stage.

The flushing stage occurs during the process of inflammation itself. The blood flow in the microvessels of the lung is disrupted, the walls of the respiratory sacs thicken and fill with blood, and the flexibility of the organ tissue decreases. In this case, the so-called exudate is released into the respiratory sacs from the vessels: blood plasma and inflammatory cells. The exudate seems to line the respiratory sac from the inside and is adjacent to its walls. The airiness of the lung and its ability to take part in breathing also decreases. And by the end of the hot flash stage, the inflammatory process affects the pleura, which is usually confirmed by symptoms of pain and limitation of respiratory movements of the chest from the inflamed lung. The duration of the stage, as a rule, does not exceed 48 hours.

The hepatization stage is characterized by complete filling of the respiratory sacs with exudate. The airiness of the affected lobe of the lung is completely lost.

The affected lobe in this case resembles the lobe of the liver, so the process is called hepatization.

During the resolution stage, the exudate gradually resolves, and the lung tissue restores its airiness, flexibility and ability to take part in the respiratory act.

Signs of the disease in its different stages

Symptoms of lobar pneumonia during different stages inflammatory process somewhat different.

The onset of the disease is usually characterized by high fever: a rise in temperature to 39-40 degrees or higher,

and severe pain in the chest, which becomes stronger during the breathing movement. This indicates inflammation of the pleura - pleurisy. The fever usually lasts about a week. And if the patient is quickly prescribed adequate antibacterial therapy, then the symptoms decrease within 3-4 days from the onset of the disease.

On the first day of illness, a dry cough may occur, which usually begins when the patient tries to take a deep breath.

After a couple of days, the cough is usually accompanied by sputum, which may have a rusty color due to the presence of blood cells in it. This indicates the beginning of the hepatization stage.

In addition to fever, cough and pain, lobar pneumonia is characterized by shortness of breath. This means that the patient's breathing is difficult, he begins to breathe more often and less deeply. The patient also usually notes general weakness, headache, sweating and a feeling of malaise.

These symptoms reflect intoxication, that is, the toxic effect of the pathogenic bacterium on the patient’s body.

Listening to the lungs is usually characterized by a weakening of the respiratory sound, as well as crepitus in the first and last stages of the disease. Crepitation is a sound similar to the creaking of snow under a shoe. This sound occurs at the end of inhalation.

In the second stage, listening to the lungs will give so-called pathological bronchial breathing. This means that the breathing sounds are a bit like the sounds you hear if you start listening for breathing in the neck area. Crepitation is not audible. A pleural friction rub may be heard, which is similar to crepitus, but can be heard not only when the patient inhales, but also when the patient exhales.

Laboratory and instrumental data important for diagnosing the disease

Leukocytosis will be detected in the blood of a patient diagnosed with lobar pneumonia. This means that the number of white blood cells will exceed normal value, since the latter take an active part in inflammation. The rate of sedimentation of erythrocytes - red blood cells - to the bottom of the tube will also be increased. In addition, C-reactive protein may appear in the blood. This substance is normally absent, and can appear only when any tissue in the body is destroyed. In this case, the disease has a destructive effect mainly on lung tissue.

An important and highly reliable study is chest radiography. X-rays are performed in frontal and lateral projections. This means that the rays are passed through the patient's chest twice: first from the front and then from the side of the patient.

Sites white on the radiograph are called areas of shading. Possible pneumonia will be indicated by darkening of part of the lung.

In the case of lobar pneumonia, the darkening extends to the entire lobe of the organ.

You can also examine the patient’s sputum when it appears in order to culture it on a nutrient medium in a microbiological laboratory. This will allow you to accurately determine the causative agent of the disease in a given patient and select adequate antibacterial therapy for him. The choice of therapy is made by adding specific antibiotics to the pathogen culture

and subsequent dynamic observation of the microorganism’s reaction to them.

Therapeutic measures

Treatment of lobar pneumonia begins with choosing the correct antibacterial therapy. Most often, aminopenicillin antibiotics, which include amoxicillin, are suitable for lobar pneumonia.

You can also use macrolides, which include clarithromycin.

If the course of the disease is particularly severe, the so-called “respiratory” fluoroquinolones should be taken into account.

These include levofloxacin and moxifloxacin. The latter are suitable as “heavy artillery”.

You should not start therapy with them.

In addition to therapy, the action of which is directed directly at the pathogen, you can also use non-drug methods treatments that will help improve sputum discharge, that is, increase the drainage function of the bronchi. For this purpose, you can use chest massage, as well as breathing exercises.

In addition, you can use drugs - mucolytics, which increase sputum discharge. These include acetylcysteine, bromhexine or ambroxol.

Possible complications

Complications of lobar pneumonia are usually caused by incorrect selection of antibacterial drugs and incorrect treatment, as well as the initial serious condition of the patient who has pneumonia and the severe characteristics of the causative agent of pneumonia in a particular patient. For example, pneumonia in weakened intensive care patients is often caused by Pseudomonas aeruginosa, which is insensitive to antibacterial drugs.

All complications of lobar pneumonia can be divided into pulmonary and extrapulmonary complications.

Of the pulmonary complications, acute respiratory failure is the most dangerous.

It usually occurs if the patient is sick with severe pneumonia, and is most often caused by the exclusion of an entire lobe of the lung from performing the respiratory function. A predisposing factor may be a preliminary decrease in the functioning of the lungs as a whole: with many years of smoking or constant inhalation of harmful substances by the patient, at work, for example.

Sepsis should be recognized as the most severe extrapulmonary complication. Sepsis is usually called the spread of an infection, that is, a causative microorganism, through the bloodstream from the main inflammatory focus throughout the body.

This course of events is not natural for the human body, since such a generalization of the process contradicts the main function of inflammation: delimiting. Therefore, sepsis is usually very severe and often, without massive antibiotic therapy or if it is not started in a timely manner, can lead to death.

Warning

If a person experiences symptoms similar to those of lobar pneumonia, he should definitely consult a doctor!

You cannot prescribe treatment for yourself!

This can lead to serious complications!

Acute lobar pneumonia is a lung disease accompanied by massive bilateral inflammatory damage to the lung tissue with severe intoxication syndrome and secondary changes in internal organs.

Without timely combined treatment, the pathology quickly leads to human death due to respiratory, cardiovascular failure and cerebral hypoxia.

Pathogenesis of lobar form

The cause of lobar pneumonia in most cases is a bacterium called Friendler's bacillus. However, bilateral pneumonia can also be caused by typical pathogens(staphylococcus, streptococcus, pneumococcus) against the background of reduced immunity.

In this pathology, the inflammatory process occurs not locally, but simultaneously in several areas of one or both lungs. In this case, the infiltrate not only accumulates in the alveoli, but also bronchial edema occurs due to immediate hypersensitivity reactions (IHT). They appear due to the similarity of pathogen antigens with certain bronchial proteins.

Thus, the pathogenesis of lobar pneumonia is due to the direct proliferation of Friendler's bacillus in the wall of the alveoli and the occurrence of allergic reactions in the respiratory tract.

It should be understood that the main causative agent of lobar pneumonia is highly toxic due to its ability to quickly destroy tissue. Because of this, the disease progresses rapidly.

The disease is also characterized by a specific x-ray picture, accompanied by the presence of many small shadows in both lungs, which represent inflammatory infiltrates.

Symptoms of lobar pneumonia can be classified into 2 categories:

1. Bronchopulmonary;
2. Intoxicating.

Bronchopulmonary symptoms in bilateral pneumonia:

• Cough;
• "Rusty" sputum;
• Increased respiratory rate (tachypnea) and shortness of breath;
• Chest pain.

Cough against the background of bilateral pneumonia is caused by irritation of the receptors of the upper laryngeal and vagus nerves. They are localized in the larynx, pharynx, large bronchi and pleura.

It should be understood that the accumulation of sputum in the small bronchi does not lead to the appearance of cough impulses, since in this part of the respiratory tract there are no specific receptors responsible for their occurrence. Only when the inflammatory fluid rises higher will a cough appear.

Such anatomical feature lung plays a negative role for early diagnosis of the disease. By doing x-rays at the beginning of the disease, it is clearly visible that there is an inflammatory infiltrate in the alveoli, but the objective condition of the person remains unchanged.

Only a few hours after the pathogen begins to multiply in the respiratory tract, like a “bolt from the blue”, all the symptoms of the pathology strike the person simultaneously.

On the first day of illness, the cough is dry. No sputum production is observed. On day 2, the patient may observe a “rusty” discharge, which is caused by the presence of red blood cells due to damage to blood vessels by bacterial toxins. At the same time, the person’s condition sharply worsens due to intoxication syndromes.

If at this stage a macropreparation is prepared from lung tissue, then it will be possible to observe the red color of the lung tissue in the affected area. This phenomenon is caused by hemorrhages in the alveolar acini.

The respiratory rate on the 3rd day of illness can reach 40 respiratory movements per minute. At the same time, tachycardia (increased heart rate) and severe shortness of breath are observed, which does not allow a person to climb even the first floor of the stairs.

A specific feature of lobar pneumonia is the accumulation of fibrinous exudate in the bronchial cavity. It is represented not only by infiltrative fluid, but by the presence of a protein of the blood coagulation system - fibrin. This protein causes a specific morphological type of the disease - hepatization, since the structure of such tissue resembles the liver.

Chest pain appears when inflammatory changes in the pleural layers join the pathological process. Often, against the background of pathology, there is an accumulation of fluid in the projection of the costophrenic sinus ( exudative pleurisy).

Clinical stages and complications of the disease

The stages of acute lobar pneumonia are distinguished depending on the morphological changes in the lungs:

• Red liver;
• Gray hepatization (hepatization);
• Permissions.

Red liver– the first stage of lobar pneumonia. It is observed during the appearance of “rusty” sputum.

Gray Heat formed when there is accumulation in the lumen of the alveoli large quantities fibrin, which complicates the process of gas exchange between red blood cells and external air. Macropreparation, which is made from lung tissue at this stage pathological process, will show that the alveoli are filled with dense gray contents.

Permission– resorption of infiltrates in the alveoli and exudates in the bronchial wall.

During the red hepatic stage, a person often experiences hemoptysis when affected large number vessels. This phenomenon lasts for several days, and then the sputum becomes mucopurulent or purulent in nature.

If symptoms persist for a week, it is necessary to exclude lung diseases such as tuberculosis, abscess, and hemorrhagic tracheobronchitis.

In an uncomplicated course of the pathology, the process ends with a critical or lytic (gradual) decrease in temperature and disappearance pathological symptoms. However, lobar pneumonia is rarely completely cured within a month, although lung films do not show infiltrative shadows.

Complications of lobar pneumonia in children are very often observed, which increase the likelihood of bronchial asthma or relapse of the disease after some time.

Friendler's bacillus is prone to chronicity, so when the immune system is weakened, it can again provoke inflammatory changes in the lungs. As a result, even with slight increase For patients with previous lobar pneumonia, doctors prescribe a second course of antibiotic therapy to prevent relapse of the disease.

In conclusion, I would like to note that the high level of modern medicine has reduced mortality from lobar pneumonia, but it remains quite high. This indicator is largely due to the late presentation of patients for qualified medical care.

Principles of treatment

Treatment of acute lobar pneumonia is carried out either in a pulmonology hospital or in intensive care wards. It requires correction of metabolism, intravenous antibiotic therapy, artificial ventilation lungs, as well as normalization of the functioning of other organs and systems.

Treatment of pathology is carried out under constant monitoring of the level of blood gases - oxygen and carbon dioxide using special equipment. At the slightest change in these indicators in a negative direction, doctors administer oxygen inhalations.

Antibacterial therapy of the disease is carried out according to a combined scheme using several pharmaceutical groups of antibiotics simultaneously.

Despite their efforts, resuscitators often fail to save the patient’s life. This could have been avoided if the person had sought qualified help on time. One should not hope for an independent favorable outcome of the pathology, since the causative agent of the disease is highly toxic. It will quickly cause severe intoxication and brain hypoxia.

The content of the article

This is an acute infectious-allergic disease characterized by inflammatory damage to the lung tissue with accumulation of exudate rich in fibrin in the alveoli, and a typical cyclical course of both pathomorphological and clinical manifestations.
IN last years lobar pneumonia is less common in children. This may be due to the fact that during the period of widespread use of antibiotics, mainly penicillin, pneumococcus apparently lost its virulent properties and gave way to pathogenic staphylococcus and gram-negative flora. Croupous pneumonia mainly affects children of preschool and school age, rarely at the age of 1 - 3 years and, as an exception, in the first year of life.

Etiology of lobar pneumonia

Pathogenesis of lobar pneumonia

Pathomorphology of lobar pneumonia

Clinic of lobar pneumonia

Complications of lobar pneumonia

Diagnosis of lobar pneumonia

Differential diagnosis of lobar pneumonia

Croupous pneumonia (pneumonia crouposa) is an acute infectious disease. The process involves the entire lobe and pleura corresponding to the affected area of ​​the lung. Therefore, lobar pneumonia is otherwise called lobar (lobar) pneumonia, as well as pleuropneumonia. Men get sick more often, mainly in autumn and spring

Etiology and pathogenesis. The causative agents are various bacteria, most often streptococci, staphylococci, pneumococci, E. coli, etc. The disease is preceded by physical overexertion, a decrease in the body's resistance, caused by various factors, including intoxication, etc. Anatomical changes successively go through the following stages: a) hyperemia, b) red hepatitis, c) gray hepatitis and d) resolution. In the first stage, liquid serous exudate accumulates in the alveoli; in the second stage, the alveoli are filled with red blood cells and fibrin, which coagulates and turns the affected lung lobe the dense liver tissue is red in color, which is why this stage is called the “red hepatization” stage. In the third stage, leukocytes penetrate into the alveoli, which give the inflammatory focus a gray color, hence the name “gray hepatization.” In the fourth stage, the process is resolved - the exudate is absorbed and partially expectorated. The periods during which the successive changes in stages occur are very individual, especially in connection with new methods of treatment with antibiotics and chemotherapy. However, the entire process is generally completed within 10-12 days.

Symptomatology. The disease most often begins with stunning chills, followed by fever and an increase in temperature to 39-40°. Patients complain of severe headache, dry cough, and pain in the side. On the second day of the disease, rusty sputum and a rash on the lips and wings of the nose (herpes labialis et nasalis) appear. The appearance of patients is very characteristic: a puffy face, shiny eyes, blush on the cheek corresponding to the sore side, the skin is dry and hot, breathing is frequent (up to 30-40 per minute) and shallow, restless sleep, sometimes patients are delirious.

During percussion in the first stage in the area of ​​the pneumonic focus, the percussion sound is dull, has a tympanic tint, and upon auscultation, crepitation indux is observed. In the stages of red and gray hepatization, upon percussion, a dull sound is detected over the diseased area and bronchial breathing is heard there. During the period of resolution, the percussion sound again becomes dull with a tympanic tinge and crepitatio redux is again heard on inspiration.

Changes in the heart and vascular system are observed. With a sharp weakening of the heart, the pulse quickens, becomes incomplete - soft, sometimes arrhythmic, swelling appears in the periphery, the liver enlarges, and the neck veins swell. With toxic damage to the vasomotor center, collapse develops - the pulse quickens, blood pressure decreases, the body becomes deathly pale, and the temperature drops below normal. Sometimes vomiting, loss of appetite, constipation, and bloating appear. Lobar pneumonia almost always causes dramatic changes in the central nervous system. Patients often complain of headaches, irritability, insomnia, sometimes they become delusional, try to leave, jump out of the window, get out of bed, or go on a rampage. Delusional phenomena are especially often observed in persons who abuse alcohol.

To recognize lobar pneumonia, the condition of the blood is important. Neutrophilic leukocytosis with a shift to the left is observed. The number of leukocytes reaches 15,000-20,000 per 1 mm 3, neutrophils make up up to 80-90% of all leukocytes, ROE (erythrocyte sedimentation reaction! accelerates and lasts for another 10-15 days after a persistent drop in temperature. On the part of the urinary organs, a decrease in the amount of urine is noted, the appearance in the urine of protein, red blood cells, an increase in the amount of nitrogenous substances (urea, uric acid) due to increased cellular breakdown and a sharp decrease in table salt, which is retained in the alveoli and tissues.

X-ray examination reveals darkening, which disappears upon recovery.

Atypical forms of lobar pneumonia are observed in weakened individuals. The process is very difficult for them, despite a slight increase in temperature. Sometimes pneumonia ends in 2-3 days (the so-called ragged forms), however, there are also forms when the disease becomes protracted and (the process moves from one lobe to another, from one lung to another - wandering pneumonia. Croupous pneumonia can accompanied by complications - pulmonary suppuration, pleurisy, pericarditis and peritonitis.

Viral pneumonia develops during an epidemic. The incubation period is 1-2 weeks, the onset of the disease is gradual, the temperature does not exceed 39° and drops lytically after 3-5 days. Patients complain of feeling exhausted, headaches, dry cough and chest pain. Sometimes in the lungs one can notice dullness of percussion sound with a tympanic tint and fine wheezing at the height of inspiration, and radiographically - a homogeneous shadow. From the blood side, leukopenia, netrophilia with a shift to the left, and monocytosis are observed. The disease sometimes ends within 1-3 days, in rare cases - at a later date.

Aspiration pneumonia develops in people who are unconscious due to craniofacial wounds, diabetic coma, azotemic uremia, poisoning, intoxication, etc. In these cases, food particles, liquid, mucus, foreign bodies are not thrown out by a cough impulse due to a decrease in reflex excitability of the bronchial mucosa. They penetrate the respiratory tract, clog the bronchi and cause collapse (atelectasis) of the lung, and then pneumonia in the collapsed area. Aspiration pneumonia, which occurs when infected material enters the respiratory tract, is especially dangerous due to the possible putrefactive decay of the lung.

Congestive pneumonia. It is observed in people with heart disease and in patients bedridden for a long time. With this form of pneumonia, foci of dullness in the lower lobes of the lungs, bronchial breathing and crepitus are noted.

Prevention and treatment. Patients are placed in a bright and well-ventilated room. The rooms should be bright and face the sunny side, the head end of the bed should be slightly raised to facilitate the patient's breathing. Silence must be maintained in the room. The patient should receive at least 1500-2000 ml of fluid per day. Food should be liquid or semi-liquid, digestible and high in calories (crackers, milk, yogurt, jelly, jelly, cream, soft-boiled eggs, fruit juices, cereals, chicken cutlets, etc.). It is necessary to wipe the tongue and mucous membrane of the oral cavity with a swab moistened with hydrogen peroxide. Herpetiform blisters should be lubricated with zinc ointment or methylene blue. For constipation, a cleansing enema is given, and for intestinal bloating, a gas outlet tube is given. Patients who are in an excited state, with a sharp headache, should wipe their body with a damp sponge, and if their consciousness is darkened, put ice on their head. In such cases, constant supervision of medical personnel (separate post) is required.

Among medications, sulfonamides are prescribed (norsulfazole, sulfadimezin) according to the following scheme: the first day 7 g - 1 g every 4 hours, the second day 6 g, the third, fourth and fifth days 4 g per day. A total of 25 g per course of treatment. To avoid the formation of sulfonamide kidney stones, you should take the medicine with Borjomi or soda water. Antibiotics are prescribed penicillin at 800,000 units per day, streptomycin, tetracycline, etc. For coughs, codeine, mustard plasters and chest cups are prescribed. When cardiac activity is weakened, camphor and caffeine are given; in case of collapse, strophanthin with glucose, mesatone, and oxygen are given intravenously. Bed rest is observed throughout the febrile period. You can start working 3-4 weeks after the temperature has normalized.

Prevention of pneumonia consists of timely treatment of diseases that lead to pneumonia (measles, typhus) and the fight against factors predisposing to it (intoxication, cold, overwork). Prevention of aspiration and congestive pneumonia is achieved proper care for patients: oral care, breathing exercises, correct regimen.

PLEURITIS

Etiology and pathogenesis. Pleurisy or inflammation of the pleural layers is most often observed with pulmonary tuberculosis, pneumonia, chest injuries, rheumatism, diseases of the mediastinal organs if the process moves to the pleura. Pleurisy can be dry and exudative. With exudative pleurisy, inflammatory fluid of a serous, hemorrhagic, purulent and putrefactive nature accumulates in the pleural cavity. With pleurisy, adhesions can form between the pleural layers, sometimes between the pleura and the diaphragm. The fluid accumulated in the pleural cavity can be inflammatory (exudate) or non-inflammatory (transudate). In the latter, the protein content does not exceed 2.5%, the specific gravity is not higher than 1.015, the sediment is very scanty and does not contain erythrocytes or leukocytes, while the specific gravity of the exudate reaches 1.020, and protein - 3% or more.

Symptomatology. Dry pleurisy is characterized by the appearance of limited pain in the chest, which intensifies with a deep breath, dry cough and low-grade fever. There is a lag in breathing and limited mobility of the lungs on the affected side, pleural friction noise, often in the mid-axillary line. Dry pleurisy can end within a few days, but there are cases with a longer course, which is especially typical for tuberculosis of the lungs and lymph nodes.

Exudative pleurisy. At the onset of the disease, the symptoms are the same as with dry pleurisy. Subsequently, as fluid accumulates in the pleural cavity, the pleural layers separate and the pain disappears. At the same time, new symptoms appear - high fever, ear cough with scanty sputum, breathing becomes frequent and shallow, signs of heart failure develop if the exudate is significant. There is a noticeable protrusion of the affected side of the chest and its lag during breathing. The intercostal spaces are smoothed. During percussion, there is a dullness of the percussion sound; when listening, there is no respiratory noise on the painful side, bronchophony and vocal tremor over the effusion, where the lung compressed by exudate is located, are enhanced.

On X-ray examination, there is a shadow of varying sizes depending on the size of the effusion. With significant effusions, displacement of the mediastinal organs is observed. In order to clarify the diagnosis, they resort to a test pleural puncture using a twenty-gram syringe with a needle with a length of at least 7 cm and a diameter of at least 1 mm. The puncture is performed in the eighth or ninth intercostal space along the posterior axillary line. The patient is seated on a chair. The patient raises his hand on the affected side and places it on his head, this makes the injection easier, as the intercostal spaces expand. The syringe is held in the hand like a pen, and the needle is inserted along the upper edge of the underlying rib. After suctioning out 5-10 ml of effusion, the needle is quickly removed from the pleural cavity, and the puncture site is clamped with sterile cotton wool and then with a piece of gauze with collodion. The resulting liquid is sent to the laboratory for testing.

The course of effusion pleurisy is longer than dry pleurisy. Usually after 1-2 weeks the temperature begins to decrease, but sometimes the fever lasts 4 weeks or more (with tuberculosis). Pneumonic, rheumatic pleurisy ends safely in a relatively short time. Cancerous pleurisy does not resolve and its outcome is associated with the underlying disease. After pleurisy, adhesions occur with limited mobility of the lungs on the affected side, sometimes complete infection of the pleural cavity and retraction of the chest.

Treatment consists of bed rest, cough suppression with codeine, heroin. Further treatment depends on the etiology of pleurisy; for tuberculous pleurisy, streptomycin, ftivazid, PAS are prescribed; for rheumatic pleurisy, salicylates are prescribed 1 g 5 times a day. Calcium chloride (5% solution, 1 tablespoon 3 times a day), hypothiazide, novuritis are used as a diuretic; for desensitization - prednisone, prednisolone 5 mg 3 times a day. In order to accelerate the absorption of exudate, quartz irradiation and solux are used, and to prevent the formation of adhesions, breathing exercises are used. Good nutrition with plenty of vitamins is also of great importance. For large effusions, fluid is pumped out using a Potena apparatus, but no more than 1 liter at a time. The pumping puncture is performed similarly to the test puncture. Before pumping, camphor and cordiamine are prescribed to maintain cardiac activity. If coughing, dizziness, or tinnitus occur, pumping is stopped.

Pothen's apparatus (Fig. 1) is a graduated vessel with a capacity of 1 liter. Two rubber tubes are attached to it. One of them contains a needle for suction, and the other is connected to a pump that discharges the device, with the help of which air is pumped out of the device and the valve at the end of the discharge tube is closed.

Purulent pleurisy. Purulent pleurisy develops due to the penetration of pyogenic microbes into the pleural cavity from various purulent foci in the body. Purulent pleurisy also develops with tuberculosis, when mycobacteria enter from the cavity. Sometimes serous pleurisy turns purulent.

Symptomatology. Purulent pleurisy is very difficult. The temperature reaches 40° and then drops to normal levels with heavy sweat, which is very exhausting for the patient. The data from an external examination of the chest, percussion, and auscultation are the same as for effusion pleurisy. However, in contrast to effusion pleurisy, geytrophilic leukocytosis (up to 25,000-30,000 in 1 mm 3) with a shift to the left, a significant acceleration of ROE, anemia, and weight loss are observed. At the same time, the cardiovascular system also suffers greatly. The pulse becomes frequent, sometimes arrhythmic. In rare cases, self-healing is observed when pus from the pleural cavity is opened into the bronchus and coughed up in the form of a creamy mass. Purulent pleurisy can cause amyloidosis of the kidneys with disruption of their functions.

Treatment is carried out by systematically pumping out pus from the pleural cavity using the Poten apparatus, followed by the introduction of antibiotics into the cavity. At the same time, subcutaneous injections of penicillin 1,000,000 units and streptomycin from 0.5 to 1 g per day are prescribed. If there is no effect from conservative treatment, surgical intervention is resorted to.