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Management of complications of acute pneumonia

 
, medical expert
Last reviewed: 06.07.2025
 
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Treatment of infectious toxic shock

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

Shock develops at the height of intoxication, preceded by hectic fever and chills. In 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 caused by bacterial, less often viral intoxication.

When organizing treatment measures in case of infectious toxic shock, one should remember its three stages.

  • Stage I begins with chills, a sharp increase in body temperature, nausea, vomiting, diarrhea, headache, anxiety and shortness of breath often occur. Blood pressure is normal or slightly reduced, perhaps even a slight increase (the "warm hypertension" stage).
  • Stage II is characterized by pallor of the skin with acrocyanosis, shortness of breath, tachycardia, oliguria, arterial hypotension (the “warm hypotension” stage).
  • Stage III is characterized by the fact that patients are in a stupor or coma, oliguria is pronounced, the skin is pale, cold, blood pressure is sharply reduced and may not be detectable (the “cold hypotension” stage).

In case of infectious toxic shock, the following treatment measures are carried out.

Restoration of circulating blood volume (intravascular volume)

The subclavian vein is catheterized, central venous pressure (CVP) is measured, and intravenous jet infusion of rheopolyglucin is prescribed at a rate of 10 ml per 1 kg of body weight at a rate of 15-20 ml per minute.

Rheopolyglucin (dextran-40, rheomacrodex) is a 10% solution of partially hydrolyzed dextran with a molecular weight of 30,000-40,000. The drug also has an antiaggregatory effect, improves microcirculation, and 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 a jet injection of rheopolyglucin in combination with polyglucin.

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

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

Along with infusions of colloid blood substitutes, albumin, plasma, intravenous drip infusion of crystalloid plasma substitutes is performed - isotonic sodium chloride solution, Ringer's solution, 5-10% glucose solution. When crystalloid solutions are administered intravenously, they are only partially retained in the vascular bed, mainly moving into the interstitial spaces, which can create an excess of water and sodium in them.

Thus, it is advisable to begin the restoration of circulating blood volume with the introduction of rheopolyglucin, combining it with polyglucin, using albumin preparations, and then adding crystalloid solutions.

Infusion of plasma substitutes is performed under the control of central venous pressure and hourly diuresis monitoring. The total amount of fluid administered intravenously in infectious toxic shock should not exceed 25-30 ml/kg per day. Infusion of plasma substitutes is stopped when central venous pressure increases to the optimal level, a pulse appears in the peripheral arteries, and systolic blood pressure increases to 90-110 mm Hg.

In the late stage of infectious toxic shock with refractoriness to intravenous administration of plasma-substituting fluids, intra-arterial administration of 800 ml of polyglucin is indicated.

Normalization of vascular tone and blood pressure

When the volume of circulating blood is replenished, arterial pressure can increase to the point of complete normalization.

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

Along with increasing blood pressure, the drug dilates the renal vessels, improves blood circulation in them, and enhances the contractility of the myocardium by stimulating beta1 receptors.

In addition, in case of deep arterial hypotension, intravenous administration of 120-240 mg of prednisolone is recommended. Subsequently, if necessary, prednisolone administration is repeated at intervals of 2-4 hours.

In the absence of dopamine and persistent deep arterial hypotension, one can try to administer norepinephrine intravenously by drip (1 ml of 0.2% solution in 250 ml of 5% glucose solution) at an initial rate of 20-40 drops per minute.

However, the administration of norepinephrine is less preferable compared to dopamine due to the pronounced vasoconstrictive effect of norepinephrine and the deterioration of the microcirculation system.

Increased contractility of the myocardium

Increasing the contractility of the myocardium in infectious toxic shock is important. For this purpose, intravenous drip administration of dopamine at a rate of up to 10 mcg/kg per minute is recommended, as well as intravenous slow administration (over 3-5 min) of 0.3 ml of 0.05% strophanthin solution in 20 ml of 40% glucose solution or isotonic sodium chloride solution.

Oxygen therapy

Oxygen therapy is performed by inhaling humidified oxygen through nasal catheters.

Use of proteolytic enzyme inhibitors

Proteolytic enzyme inhibitors block kallikrein, a blood and tissue enzyme that catalyzes the formation of kinins from their precursors. Kinins (bradykinin, kallidin) are polypeptides that act as shock mediators. They cause capillary dilation, increased permeability, and decreased peripheral resistance, causing a drop in blood pressure. The kallikrein-kinin system is linked to the blood coagulation and anticoagulation systems via the Hageman factor and general inhibitors and determines the state of microcirculation.

In the treatment of infectious toxic shock, intravenous drip administration of 100,000-200,000 IU of trasylol or 50,000-100,000 IU of contrical in 300-500 ml of 5% glucose solution is recommended, primarily in the early phase of shock.

Correction of metabolic acidosis

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

Treatment of "shock lung"

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

Treatment of acute respiratory failure

Acute respiratory failure (ARF) is the most severe complication of acute pneumonia. There are 3 degrees of acute respiratory failure.

I degree of acute respiratory failure. Characterized by complaints of a feeling of lack of air, anxiety, euphoria. The skin is moist, pale, with mild acrocyanosis. Dyspnea increases - 25-30 breaths per minute, arterial pressure increases moderately. PaO 2 is reduced to 70 mm Hg, PaCO 2 - to 35 mm Hg and below.

II degree of acute respiratory failure. The patient experiences agitation, delirium, hallucinations. Profuse sweating, cyanosis (sometimes with hyperemia), severe dyspnea (35-40 breaths per minute), tachycardia, arterial hypertension appear. PaO2 is reduced to 60 mm Hg.

III degree of acute respiratory failure. Coma with clonic and tonic convulsions occurs, pupils are dilated, cyanosis is pronounced, breathing is shallow, frequent (more than 40 per minute), before cardiac arrest breathing becomes rare. Blood pressure is sharply reduced. PaO 2 is less than 50 mm Hg, PaCO 2 is increased to 100 mm Hg.

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

  • exclusion of a large part of the lungs from ventilation;
  • increased aggregation of formed elements of the blood;
  • release of vasoactive mediators: serotonin is released during platelet aggregation and causes spasm of the postcapillary (venular) sphincters; histamine, bradykinin, catecholamines cause vaso- and bronchoconstriction, changes in the permeability of the alveolar-capillary membrane;
  • subsequent relaxation of the arteriolar sphincters and maintenance of spasm of the venular sphincters, which causes blood stagnation in the lungs;
  • increasing hypoxia and lactic acidosis;
  • impaired permeability of the vascular wall and hydrostatic pressure due to blood stagnation contributes to the release of fluid from the vascular bed into the interstitial space, and fluid accumulates in the lungs;
  • as a result of perivascular edema and decreased perfusion, surfactant production decreases and the alveoli collapse;
  • interstitial fluid compresses the terminal bronchioles, which further reduces lung volumes.

Acute respiratory failure complicates the course of lobar pneumonia, confluent focal, viral-bacterial, often legionella and other types of pneumonia.

Sykes, McNichol and Campbell (1974) identified four sequential stages in the treatment of acute respiratory failure in acute pneumonia:

  1. Suppression of infection and restoration of tracheobronchial patency by drainage of the airways and administration of active bronchodilators.
  2. Adequate oxygen therapy.
  3. Stimulation of breathing.
  4. Endotracheal intubation or tracheostomy, transition to artificial ventilation.

Suppression of infection and restoration of tracheobronchial patency

If acute respiratory failure develops in a patient with acute pneumonia, intensive antibacterial therapy should be continued, since suppression of the infectious and inflammatory process in the lungs will naturally improve perfusion and gas exchange in the lungs.

It is necessary to continue intravenous administration of active bronchodilators. Most often, euphyllin is used by drip (10-20 ml of 2.4% solution in 150 ml of isotonic sodium chloride solution).

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

If the above measures are ineffective, a therapeutic bronchoscopy is performed with lavage of the tracheobronchial tree, which allows eliminating the blockage of the bronchi with purulent or mucopurulent secretions.

Adequate oxygen therapy

Adequate oxygen therapy is the most important method of treating acute respiratory failure in acute pneumonia. A decrease in PaO 2 below 50 mm Hg is life-threatening for the patient, so increasing PaO 2 above this critical level is the goal of oxygen therapy. However, an increase in PaO2 above 80 mm Hg should be avoided, since this does not increase the oxygen content in the blood, but creates a risk of its toxic effect.

A generally accepted method in the complex treatment of respiratory failure is oxygen therapy with humidified oxygen through nasal catheters or special masks.

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

In recent years, the method of oxygen therapy with constant positive pressure in the respiratory tract has been used to treat patients with severe pneumonia. The essence of the method is that the patient exhales air through a device that creates pressure on exhalation. For spontaneous breathing with constant positive pressure on exhalation, the Nimbus-I device is used.

This method increases alveolar pressure and straightens collapsed alveoli, prevents expiratory closure of the airways. As a result, ventilation improves, the diffusion surface of the lungs increases, pulmonary shunting decreases, and blood oxygenation improves.

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

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

Stimulation of breathing

Although Saike et al. consider the use of respiratory analeptics to be justified and necessary in acute respiratory failure, most authors exclude these drugs from the arsenal of methods for treating acute respiratory failure.

The most justified use of drugs is that stimulate the respiratory center when it is depressed, which is usually observed in the most severe degrees of acute respiratory failure, in a comatose state, when a decrease in the respiratory rate may indicate an approaching death.

The most well-known respiratory stimulant in our country is cordiamine, which is administered intravenously in an amount of 4 ml when there is a risk of respiratory arrest.

Transfer to artificial ventilation

Indications for transfer to artificial lung ventilation (ALV): severe agitation or loss of consciousness, change in pupil size, increasing cyanosis, active participation of accessory muscles in respiration against the background of hypoventilation, respiratory rate more than 35 per minute, PaCO2 more than 60 mm Hg, PaO2 less than 60 mm Hg, pH less than 7.2.

The most effective is artificial ventilation with positive end-expiratory pressure up to 3-8 cm H2O.

In cases of extremely severe but reversible pulmonary pathology and the absence of effect from artificial ventilation, extracorporeal membrane oxygenation of blood is used using membrane oxidizers ("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 the liquid portion of the blood oozing out of the capillaries of the pulmonary circulation and its accumulation first in the pulmonary interstitium and then in the alveoli. With the development of alveolar edema, the alveoli collapse. Normally, the alveoli are covered from the inside with surfactant, which reduces the surface tension of the alveoli and stabilizes their structure. With the development of edema, the surfactant is washed out of the alveoli, which leads to their collapse. In addition, the transition of surfactant into the oozing liquid makes foam bubbles stable, blocking the passage of gases through the alveolar membrane, hypoxemia worsens.

Pulmonary edema in a patient with acute pneumonia may be caused by pneumonia itself, an inflammatory process in the lung tissue, which releases a number of vasoactive substances that sharply increase vascular permeability (hypertoxicosis with pulmonary edema). Under these conditions, intense fluid leaks into the alveoli through the highly permeable wall of the pulmonary capillaries. This is especially characteristic of pneumonia that occurs with severe influenza.

Pulmonary edema may 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 increasing shortness of breath, cyanosis, a feeling of compression in the chest, a feeling of shortness of breath, and anxiety.

When pulmonary edema passes into the alveolar phase, orthopnea, pronounced cyanosis appear, the patient is covered in cold sweat. The patient is bothered by a strong cough with the separation of a large amount of foamy pink sputum, arterial pressure drops, the pulse is threadlike, many moist rales are heard in the lungs. Heart sounds are muffled, a gallop rhythm is often heard.

The main treatment measures for pulmonary edema:

  • reduction of venous return of blood to the heart: a semi-sitting position of the patient with legs down; application of tourniquets that compress the veins of the extremities; in the absence of arterial hypotension - intravenous drip administration 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 arterial pressure); intravenous administration of fast-acting diuretics - 60-80 mg of furosemide (lasix);
  • neuroleptanalgesia. It relieves psychomotor agitation and reduces dyspnea: 1 ml of a 0.005% solution of the analgesic fentanyl and 1 ml of a 0.25% solution of the neuroleptic droperidol in 10 ml of isotonic sodium chloride solution are administered intravenously under the control of arterial pressure (it may decrease);
  • reduction of formation of oxygen in the respiratory tract. For this purpose, "inhalation of oxygen passed through 70% alcohol or 10% alcohol solution of antifomsilane is used;
  • reduction of pressure in the pulmonary circulation. This is achieved by using nitroglycerin intravenously, as well as by intravenous administration of 10 ml of a 2.4% solution of euphyllin in 10 ml of isotonic sodium chloride solution under the control of arterial pressure;
  • to reduce alveolar-capillary permeability, 90-120 mg of prednisolone is administered intravenously; if there is no effect, the administration can be repeated after 2-4 hours;

ALV with increased resistance at the outlet is performed when the above measures do not produce an effect, i.e. in the most severe course of pulmonary edema. During ALV, foam is also removed from the respiratory tract using an electric suction pump.

Treatment of DIC syndrome

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

At the hypercoagulation stage, 10,000 IU of heparin is administered intravenously, and then 500-1000 IU every hour. Treatment with fresh frozen plasma is also carried out, it is administered after warming to 37 C intravenously by jet in the amount of 600-800 ml, and then 300-400 ml every 6-8 hours.

With each transfusion, 2500 U of heparin should be added to the vial to activate the antithrombin III introduced with the plasma. In the following days, 400 to 800 ml of plasma is administered per day.

Inhibitors of proteolytic enzymes are widely used; they inhibit the activity of the kallikrein-kinin system, as well as excessive fibrinolytic activity. The proteolysis inhibitor trasylol is administered intravenously by drip in large doses - up to 80,000-100,000 U 3-4 times a day.

In the hypercoagulation phase, antiplatelet agents are also used: curantil 100-300 mg 3 times a day, aspirin 0.160-0.3 g 1 time per day.

In the event of acute hemostasis failure, intravenous jet infusion of fresh frozen plasma and proteolysis inhibitors is performed, and heparin and antiplatelet agents are discontinued.

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