Fighting complications of acute pneumonia

Treatment of infectious-toxic shock

According to Z. Abovskaya (1987), infectious-toxic shock develops in 10% of patients with acute pneumonia and in 11.9% of cases can lead to death. It is observed in patients with the most severe course of the disease, often with legionellosis etiology. The leading mechanism is acute toxic vascular insufficiency with progressive decrease in venous return of blood, disorganization of microcirculation, accompanied by development of metabolic acidosis, DIC syndrome, multiple organ lesions.

The shock unfolds at the height of intoxication, preceded by a fever of a hectic type, chills. With infectious-toxic shock there is a redistribution of blood in the vascular bed and a violation of adequate tissue perfusion. The development of shock is due to bacterial, less often viral intoxication.

When organizing treatment in the event of an infectious-toxic shock, you should remember about its three stages.

• Stage I begins with chills, body temperature rises sharply, nausea, vomiting, diarrhea, headache, anxiety and shortness of breath often occur. The blood pressure is normal or slightly reduced, perhaps even a slight increase (the stage of "warm hypertension").
• II stage is characterized by pallor of the skin with acrocyanosomes, dyspnea, tachycardia, oliguria, arterial hypotension (the stage of "warm hypotension").
• Stage III is different in that patients are in a sore or coma, oliguria is sharply expressed, the skin is pale, cold, blood pressure is sharply reduced, it can not be determined (the stage of "cold hypotension").

With infectious-toxic shock, the following treatment measures are carried out.

Restoration of the volume of circulating blood (intravascular volume)

Catheterization of the subclavian vein is performed, central venous pressure (CVP) is measured and an intravenous infusion of rheopolyglucin is given at a rate of 10 ml per 1 kg of mass at a rate of 15-20 ml per minute.

Reopoliglyukin (dextran-40, reomacrodex) is a 10% solution of partially hydrolysed dextran with a molecular weight of 30,000-40,000. The drug also has anti-aggregation effect, improves microcirculation, restores transcapillary blood flow. The circulation time in the blood is 4-6 hours. In severe shock, especially in its late phase, treatment begins with the jet injection of reopolyglucin in combination with polyglucin.

Polyglucin is a 6% solution of the mid-molecular fraction of partially hydrolysed dextran with a molecular weight of 60,000 (close to the molecular weight of albumin). Polyglukin slowly penetrates through the vascular walls and when introduced into the bloodstream, it circulates for a long time in it (up to several days).

In addition to synthetic colloids, intravenous infusion of 100-150 ml of 25% albumin solution is also used. Due to a relatively higher increase in oncotic pressure than with the use of plasma, albumin actively attracts the intercellular fluid into the bloodstream (1 ml of 25% solution of albumin attracts about 20 ml of intravascular fluid). In the absence of albumin, intravenous plasma can be used.

Along with infusions of colloidal blood substitutes, albumin, plasma, intravenous drip infusion of crystalloid plasma substitutes - isotonic sodium chloride solution, Ringer's solution, 5-10% glucose solution. With intravenous administration of crystalloid solutions, they are only partially retained in the vascular bed, mainly moving to interstitial spaces, which can create excess water and sodium in them.

Thus, the recovery of the circulating blood volume is advisable to begin with the introduction of rheopolyglucin, combining it with polyglucin, using albumin preparations, connecting further crystalloid solutions.

Infusion of plasma substitutes is carried out under the control of CVP and hourly recording of diuresis. The total amount of fluid administered intravenously for infectious-toxic shock should not exceed 25-30 ml / kg per day. Infusion of plasma substitutes stops when the CVP is raised to the optimal level, the pulse appears on the peripheral arteries, the systolic blood pressure is raised to 90-110 mm Hg. Art.

In the late stage of infectious-toxic shock, when refractory to intravenous administration of plasma-replaceable fluids, intra-arterial administration of 800 ml of polyglucin is indicated.

Normalization of vascular tone and blood pressure

When replenishing the volume of circulating blood, blood pressure can rise up to full normalization.

In the case of the severity of arterial hypotension, refractoriness to the measures taken, it is necessary to inject intravenously dopamine. To do this, 40 mg of the drug is dissolved in 200 ml of 5% glucose solution (a concentration of 200 μg / ml is obtained), administered intravenously at a rate of 2-3 μg / kg per minute (i.e., 15-17 drops per minute) and gradually increased the rate of administration under the control of arterial pressure and pulse rate. To normalize blood pressure, sometimes you need to increase the infusion rate to 20-30 or more drops per minute.

Along with the increase in arterial pressure, the drug dilates the blood vessels of the kidneys, improves blood circulation in them, enhances the contractile ability of the myocardium, stimulating beta-1 receptors.

In addition, with deep arterial hypotension, intravenous administration of 120-240 mg of prednisolone is recommended. In the future, if necessary, repeated introduction of prednisolone at intervals of 2-4 h.

In the absence of dopamine and the preservation of deep hypotension, you can try to inject intravenously drip norepinephrine (1 ml of 0.2% solution in 250 ml of 5% glucose solution) with an initial rate of 20-40 drops per minute.

However, the administration of norepinephrine is less preferred than dopmin in connection with the pronounced vasoconstrictive effect of norepinephrine and the deterioration of the microcirculation system.

Increased myocardial contractility

An increase in myocardial contractility in infectious-toxic shock is important. For this purpose, an intravenous drip of dopamine is recommended at a rate of up to 10 μg / kg per minute, as well as intravenous slow administration (within 3-5 minutes) of 0.3 ml of 0.05% solution of strophanthin in 20 ml of 40% glucose solution or isotonic sodium chloride solution.

Oxygen therapy

Oxygenotherapy is performed by inhalation of moistened oxygen through nasal catheters.

The use of inhibitors of proteolytic enzymes

Inhibitors of proteolytic enzymes block kallikrein, a blood and tissue enzyme that catalyzes the formation of kinins from their precursors. Kininy (bradykinin, kallidin) are polypeptides that are the mediators of shock. They cause the expansion of capillaries, increase their permeability, reduce peripheral resistance, causing a drop in blood pressure. Kallikrein-kinin system through Hageman factor and general inhibitors is associated with coagulating and anticoagulating systems of blood and determines the state of microcirculation.

In the treatment of infectious-toxic shock, an intravenous drip injection of 100,000-200,000 ED of trachylol or 50,000-100,000 units of ED is required in 300-500 ml of 5% glucose solution, mainly in the early phase of shock.

Correction of metabolic acidosis

Correction of metabolic acidosis is carried out under the control of blood pH, deficiency of buffer bases. Introduced intravenously drip from 200 to 400 ml per day 4% sodium bicarbonate solution.

Treatment of "shock lung"

If a picture of the "shock lung" appears, intubation should be performed and artificial ventilation of the lungs with positive exhalation pressure should be started.

Treatment of acute respiratory failure

Acute respiratory failure (ODN) is a severe complication of acute pneumonia. There are 3 degrees of acute respiratory failure.

I degree of acute respiratory failure. It is characterized by complaints about a feeling of lack of air, anxiety, euphoria. Skin moist, pale, with light acrocyanosis. Increases shortness of breath - 25-30 breaths per minute, moderately increases blood pressure. RaO _{2 is} reduced to 70 mm Hg. St, Razo ₂ - up to 35 mm Hg. Art. And below.

II degree of acute respiratory failure. The patient is excited, nonsense, hallucinations. There are profuse sweat, cyanosis (sometimes with hyperemia), pronounced dyspnea (number of breaths per minute 35-40), tachycardia, arterial hypertension. RaO _{2 is} reduced to 60 mm Hg. Art.

III degree of acute respiratory failure. Coma comes with clonic and tonic cramps, pupils are wide, cyanosis is pronounced, breathing is superficial, frequent (more than 40 per minute), before the heart stops breathing becomes rare. Blood pressure is sharply reduced. PaO _{2 is} less than 50 mm Hg. , RaCO _{2 was} increased to 100 mm Hg. Art.

Acute respiratory failure is caused by a decrease in lung perfusion, which is facilitated by:

• shutdown of most of the lungs from ventilation;
• increasing aggregation of blood elements;
• release of vasoactive mediators: serotonin is released during platelet aggregation and causes spasm of postcapillary (venular) sphincters; histamine, bradykinin, catecholamines cause vaso- and bronchoconstriction, a change in the permeability of the alveolar-capillary membrane;
• relaxation in future arteriolar sphincters and preservation of spasm of venular sphincters, which causes stagnation of blood in the lungs;
• an increase in hypoxia and lactic acidosis;
• violation of the permeability of the vascular wall and hydrostatic pressure due to stagnation of blood contributes to the release of fluid from the vascular bed into the interstitial space, the fluid accumulates in the lungs;
• due to perivascular edema and a decrease in perfusion, the production of the surfactant decreases, the alveoli decrease;
• interstitial fluid compresses terminal bronchioles, which further reduces pulmonary volumes.

Acute respiratory failure complicates the course of croupous pneumonia, focal focal, viral-bacterial, often legionellosis and other types of pneumonia.

Saike, McNichol and Campbell (1974) identify four consecutive stages of treatment for acute respiratory failure in acute pneumonia:

1. Suppression of infection and restoration of tracheobronchial permeability by drainage of the respiratory tract and the introduction of active bronchodilators.
2. Adequate oxygen therapy.
3. Stimulation of respiration.
4. Endotracheal intubation or tracheostomy, transition to artificial ventilation.

Suppression of infection and restoration of tracheobronchial passableness

With the development of acute respiratory failure in patients with acute pneumonia, intensive antibacterial therapy should be continued, since suppression of the infectious inflammatory process in the lungs naturally improves perfusion and gas exchange in the lungs.

It is necessary to continue intravenous injection of active bronchodilators. The most commonly used euphyllin is drip (10-20 ml of 2.4% solution in 150 ml of isotonic sodium chloride solution).

For the purpose of drainage of the bronchi, it is advisable to intravenously administer 10 ml of a 10% solution of sodium iodide (active expectorant), ambroxol 15-30 mg intravenously (the drug stimulates the production of surfactant, dilutes sputum, facilitates its withdrawal), at the initial stages of acute respiratory failure, inhalations can be used expectorants. Mucosolvinum is also used - 2 ml of 5% solution intramuscularly 2 times a day.

In the absence of the effect of the above measures, a medical bronchoscopy is performed with washing the tracheobronchial tree, which makes it possible to eliminate bronchial congestion with purulent or mucopurulent secretions.

Adequate oxygen therapy

Adequate oxygen therapy is the most important method of treatment of acute respiratory failure in acute pneumonia. The decrease in PaO _{2 is} below 50 mm Hg. Art. Threatening the life of the patient, so raising RaO ₂ above this critical level is the goal of oxygen therapy. However, an increase in PaO _{2 of} more than 80 mm Hg should be avoided . St, as it does not increase the oxygen content in the blood, but creates the danger of its toxic effect.

A common method in the complex therapy of respiratory failure is oxygen therapy with moistened oxygen through nasal catheters or special masks.

Μ. Μ. Tarasyuk (1989) recommends that oxygen be passed through Bobrov's apparatus filled with warm decoctions of expectorants (thyme, plantain, coltsfoot, sage) with the addition of muco-and bronchodilator drugs. In the absence of herbs, Bobrov's apparatus can be filled with a 1% solution of sodium bicarbonate, warm mineral water. Oxygen is supplied in a mixture with air 1: 1 at a rate of 5-6 l / min.

In recent years, in the treatment of patients with severe pneumonia, the method of oxygen therapy with a constant positive airway pressure is used. The essence of the method is that the patient exhales air through a device that creates pressure on the exhalation. For spontaneous breathing with continuous positive pressure breathing apparatus is used, "I of Nimbus- ^".

This method leads to an increase in alveolar pressure and expansion of the asleep alveoli, prevents the expiratory closure of the airways. As a consequence, ventilation improves, the diffusion surface of the lungs increases, pulmonary shunting decreases and oxygenation of the blood improves.

In recent years, hyperbaric oxygenation has been used in the pressure chamber at a pressure of 1.6-2 atm. Conduct daily for 1-3 sessions lasting 40-60 minutes. The method leads to an increase in the oxygen capacity of the blood.

Oxygen therapy is advisable to combine with the use of antihypoxants (reducing brain hypoxia): sodium oxybutyrate intravenously, cytochrome C intravenously, etc.

Stimulation of respiration

Although Sikes and co-authors consider the use of respiratory analeptics to be justified and necessary for acute respiratory failure, most authors exclude these drugs from the arsenal of methods for treating acute respiratory failure.

The most justified use of drugs that stimulate the respiratory center when it is oppressed, which is observed, as a rule, at the most severe degrees of acute respiratory failure, in a coma, when a decrease in the rhythm of respiration may indicate an approaching lethal outcome.

The most known respiratory stimulant is cordiamin, which is administered intravenously in an amount of 4 ml with the threat of stopping breathing.

Transfer to artificial ventilation

Indications for transfer to artificial ventilation (ventilator): marked agitation or loss of consciousness, change in pupil size, increasing cyanosis, active participation in respiration of the auxiliary musculature against hypoventilation, respiratory rate more than 35 per minute, PaCO ₂ more than 60 mm Hg. , PaO ₂ less than 60 mm Hg. The pH is less than 7.2.

The most effective ventilation with positive pressure at the end of expiration up to 3-8 cm of water. Art.

In the case of an extremely severe but reversible pulmonary pathology and the absence of the effect of ventilation, extracorporeal membrane oxygenation of the blood is used using membrane oxidants ("artificial lungs"). The device is an oxygenator equipped with a complex system of selective semipermeable membranes through which oxygen diffuses into the blood, ensuring its oxygenation.

Treatment of pulmonary edema

Pulmonary edema occurs as a result of sweating the liquid part of the blood from the capillaries of the small circle and accumulating it first in the pulmonary interstitium, and later in the alveoli. When alveolar edema develops, the alveolar collapses and collapses. Normally, the alveoli are covered from the inside with a surfactant, which reduces the surface tension of the alveoli, stabilizes their structure. With the development of edema, the surfactant is washed away from the alveoli, which leads to their collapse. In addition, the transition of the surfactant to the bleeding liquid makes foam bubbles that block the passage of gases through the alveolar membrane stable, and hypoxemia is aggravated.

Pulmonary edema in a patient with acute pneumonia may be due to pneumonia itself, an inflammatory process in the lung tissue, in which a number of vasoactive substances are released that sharply increase vascular permeability (hypertoxicosis with pulmonary edema). Under these conditions, an intensive permeation of the liquid into the alveoli occurs through the highly permeable wall of the lung capillaries. This is especially true for pneumonia that occurs with severe influenza.

Lung edema can be caused by acute left ventricular failure due to the development of diffuse myocarditis in a patient with acute pneumonia.

The phase of interstitial pulmonary edema is characterized by an increase in dyspnea, cyanosis, compression in the chest, a feeling of lack of air, anxiety.

With the transition of the pulmonary edema to the alveolar phase, orthopnea appears, pronounced cyanosis, the patient is covered with a cold sweat. The patient is disturbed by a strong cough with the separation of a large amount of foamy pink sputum, blood pressure drops, the pulse is threadlike, many wet wheezes are audible in the lungs. Tones of the heart are deaf, often heard the rhythm of the canter.

The main medical measures for pulmonary edema:

• reduction of venous return of blood to the heart: a semi-sitting position of the patient with his legs down; imposing tourniquets, compressing the veins of the limbs; in the absence of arterial hypotension - intravenous drip of nitroglycerin (2 ml of 1% solution in 200 ml of 5% glucose at a rate of 10-20 drops per minute under the control of blood pressure); intravenous rapid-acting diuretic - 60-80 mg furosemide (Lasix);
• neuroleptanalgesia. It removes psychomotor agitation, reduces dyspnea: 1 ml of 0.005% solution of fentanyl analgesic is injected intravenously and 1 ml of 0.25% solution of neuroperptic droperidol in 10 ml of isotonic sodium chloride solution under the control of arterial pressure (it is possible to reduce it);
• reduction of pricing in the airways. To this end, "inhalation of oxygen passed through 70% alcohol or 10% alcohol solution of antifosilane;
• decrease in pressure in a small circle of blood circulation. This is achieved by the use of nitroglycerin intravenously, and by the addition of 10 ml of 2.4% euphyllin solution in 10 ml of isotonic sodium chloride solution under the control of arterial pressure to the vein;
• a decrease in alveolar-capillary permeability is introduced intravenously with 90-120 mg of prednisolone, in the absence of effect, the administration can be repeated after 2-4 hours;

The ventilator with increased resistance at the outlet is produced when the above measures do not give an effect, i.e. With the most severe course of pulmonary edema. During ventilation, the foam is also removed from the respiratory tract by means of an electric pump.

Treatment of ICE-syndrome

Treatment of DIC-syndrome should be carried out taking into account coagulation indicators.

At the stage of hypercoagulation, 10,000 units of heparin are injected intravenously, and then 500-1000 units every hour. Treatment is also carried out with freshly frozen plasma, it is administered after warming up to 37 C intravenously strontically in an amount of 600-800 ml, and then 300-400 ml every 6-8 h.

With each transfusion, 2500 U of heparin should be injected into the vial to activate the antithrombin III introduced with the plasma. In the following days 400 to 800 ml of plasma are injected into the knocks.

Widely used inhibitors of proteolytic enzymes, they inhibit the activity of kallikrein-kinin system, as well as excessive fibrinolytic activity. The inhibitor of proteolysis of trasylol is intravenously dripped in large doses - up to 80,000-100,000 units per day, 3-4 times a day.

In the phase of hypercoagulation, antiplatelet agents are also used: curantyl 100-300 mg 3 times a day, aspirin 0.160-0.3 g once a day.

With the development of acute hemostasis deficiency, an intravenous jet infusion of freshly frozen plasma, inhibitors of proteolysis, heparin and antiaggregants are canceled.

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