Adult Respiratory Distress Syndrome

Adult Respiratory Distress Syndrome (ARDS) is an acute respiratory failure that occurs with acute lung injuries of various etiologies and is characterized by non-cardiogenic pulmonary edema, respiratory disorders and hypoxia.

The syndrome is described by Esbach in 1967 and is named by analogy with the distress syndrome of the newborn, which is caused by a congenital surfactant deficiency. In adult respiratory distress syndrome, surfactant deficiency is secondary. The literature often uses synonyms of adult respiratory distress syndrome: shock lung, non-cardiogenic pulmonary edema.

According to Marini (1993), 150,000 cases of adult respiratory distress syndrome are recorded annually in the United States, or 0.6 per 1,000 population.

[1], [2], [3], [4], [5],

The cause of adult respiratory distress syndrome

The most common causes of adult respiratory distress syndrome are:

• pneumonia (bacterial, viral, fungal, and other etiologies);
• sepsis;
• shock (septic, anaphylactic, etc.), long-lasting and pronounced;
• disseminated intravascular coagulation syndrome (acute and subacute);
• aspiration of vomit, water (when drowning);
• chest injuries and crush syndrome;
• inhalation of irritating and toxic substances: chlorine, oxides of nitrogen, phosgene, ammonia, pure oxygen (oxygen intoxication);
• pulmonary embolism (fatty, air, amniotic fluid);
• massive blood transfusions, in which multiple microthromboembolism develops in the vascular bed of the lungs. This is due to the fact that in canned blood up to 30% of erythrocytes is in the form of microaggregates up to 40 μm in diameter and the lungs, being a kind of filter, retain these microaggregates and pulmonary capillaries are blocked. In addition, serotonin is released from red blood cells, causing pulmonary arteriole spasm and capillaries;
• venous fluid overload (colloid and saline solutions, plasma, plasma substitutes, fat emulsions);
• use of the heart-lung machine (postperfusion respiratory distress syndrome in adults);
• severe metabolic disorders (diabetic keto-acidosis, uremia);
• acute hemorrhagic pancreatonecrosis. In the development of adult respiratory distress syndrome in acute pancreatitis, enzymatic intoxication is of paramount importance, causing a disturbance in the synthesis of surfactant. An especially large role is assigned to the enzyme lecithinase A, which intensively destroys surfactant, which leads to the development of alveolar atelectasis, obliterating alveolitis, predisposes to the development of pneumonia;
• autoimmune diseases - systemic lupus erythematosus, Goodpasture syndrome, etc.;
• long stay at high altitude.

Pathogenesis of adult respiratory distress syndrome

Under the influence of etiological factors in the pulmonary capillaries, interstitial lung tissue accumulates a large number of activated leukocytes and platelets. They are supposed to secrete a large amount of biologically active substances (proteinases, prostaglavdins, toxic oxygen radicals, leukotrienes, etc.) that damage the alveolar epithelium and the vascular endothelium, alter the tone of the bronchial muscles, vascular reactivity, and stimulate the development of fibrosis.

Under the influence of the above biological substances, the endothelium of the lung capillaries and the alveolar epithelium is damaged, the vascular permeability increases sharply, the pulmonary capillaries spasm and the pressure in them increases, there is marked sweating of the plasma and erythrocytes in the alveoli and interstitial lung tissue, pulmonary edema and atelectasis develop. The development of atelectasis also contributes to the secondary decrease in surfactant activity.

As a result of these processes, the main pathophysiological mechanisms develop: alveolar hypoventilation, venous blood shunting to the arterial bed, violation of the correspondence between ventilation and perfusion, disturbance of oxygen and carbon dioxide diffusion.

[6], [7], [8], [9], [10], [11], [12], [13],

Pathomorphology of adult respiratory distress syndrome

Adult respiratory distress syndrome develops over a period of time from several hours to 3 days from the onset of exposure to the etiological factor. There are three pathological phases of adult respiratory distress syndrome: acute, subacute and chronic.

The acute phase of respiratory distress syndrome in adults lasts 2-5 days and is characterized by the development of ingestive, and then alveolar pulmonary edema. The edematous fluid contains protein, red blood cells, leukocytes. Along with edema, a lesion of the pulmonary capillaries and pronounced damage to the alveolar epithelium of types I and II are detected. Damage to type II alveolocytes leads to disruption of the synthesis of surfactant, as a result of which microatelectases develop. With a favorable course of respiratory distress syndrome adults after a few days, the acute phenomena subside, the edematous fluid dissolves. However, such a favorable course of adult respiratory distress syndrome is not always observed. In some patients, adult respiratory distress syndrome enters a subacute and chronic phase.

The subacute phase is characterized by interstitial and broncho-alveolar inflammation.

The chronic phase of adult respiratory distress syndrome is the phase of development of fibrosing alveolitis. In the alveolar-capillary basement membrane connective tissue grows, the membrane dramatically thickens, flattens. There is a pronounced proliferation of fibroblasts and enhanced collagen synthesis (its amount increases by 2-3 times). Severe interstitial fibrosis can form within 2-3 weeks. In the chronic phase, there are also changes in the vascular bed of the lungs - the desolation of blood vessels, the development of microthrombosis. Ultimately, chronic pulmonary hypertension and chronic respiratory failure develop.

[14], [15], [16], [17], [18],

Symptoms of adult respiratory distress syndrome

In the clinical picture of adult respiratory distress syndrome, it is customary to distinguish 4 periods. Period - the latent or the period of the etiological factor. It lasts about 24 hours after exposure to the etiological factor. In this period, pathogenetic and pathophysiological changes occur, but they have no clinical and radiological manifestations. However, tachypnea is often observed (the number of breaths is more than 20 per minute).

II period - the initial changes, develops in 1-2 days from the onset of the etiological factor. The main clinical symptoms of this period are moderately severe shortness of breath, tachycardia. With auscultation of the lungs, hard vesicular breathing and scattered dry rales can be determined.

On radiographs of the lungs there is an increase in vascular pattern, mainly in the peripheral regions. These changes indicate the beginning of interstitial pulmonary edema.

Examination of the blood gas composition either does not give abnormalities or reveals a moderate decrease in PaO2.

The III period - the developed or the period of the expressed clinical manifestations, is characterized by the expressed symptomatology of acute respiratory failure. Severe dyspnea appears, auxiliary muscles are involved in breathing, swelling of the wings of the nose and intercostal spaces are clearly visible, pronounced diffuse cyanosis is observed. With auscultation of the heart, tachycardia and deafness of the heart tones attract attention, blood pressure is significantly reduced.

When percussion of the lungs is determined by dulling the percussion sound, more in the lower back areas, auscultatory - hard breathing, dry rales can be heard. The appearance of moist rales and crepitations indicates the appearance of fluid in the alveoli (alveolar pulmonary edema of varying severity).

On the radiograph of the lungs is determined by pronounced interstitial pulmonary edema, as well as bilateral infiltrative shadows of irregular cloud-like shape, merging with the roots of the lungs and with each other. Very often, focal shadows appear in the marginal regions of the middle and lower lobes against the background of an enhanced vascular pattern.

Characteristic of this period is a significant drop in PaO2 (less than 50 mmHg, despite the inhalation of oxygen).

The IV period is terminal, it is characterized by a pronounced progression of respiratory failure, the development of severe arterial hypoxemia and hypercapnia, metabolic acidosis, the formation of acute pulmonary heart due to increasing pulmonary hypertension.

The main clinical symptoms of this period are:

• severe dyspnea and cyanosis;
• profuse sweating;
• tachycardia, deafness of heart tones, often a variety of arrhythmias;
• a sharp drop in blood pressure until collapse;
• cough with pink sputum;
• a large number of moist rales of different sizes in the lungs, copious crepitus (signs of alveolar edema of the lungs);
• development of signs of increasing pulmonary hypertension and acute pulmonary heart syndrome (splitting and accent II of the pulmonary artery; ECG signs - high pointed teeth P in leads II, III, avF, V1-2, marked deviation of the electrical axis of the heart to the right; radiographic signs of increase pressure in the pulmonary artery, bulging its cone);
• development of multiple organ failure (impaired renal function, as manifested by oligoanuria, proteinuria, cylindruria, microhematuria, increased blood levels of urea, creatinine; impaired liver function in the form of mild jaundice, a significant increase in blood levels of alanine aminotransferase, fructose-1-phosphatal-dolase, lactate dehydrogenase; dysfunction of the brain in the form of lethargy, headaches, dizziness, there may be clinical signs of impaired cerebral circulation).

The study of the gas composition of the blood reveals deep arterial hypoxemia, hypercapnia, the study of acid-base balance - metabolic acidosis.

[19], [20], [21], [22],

Diagnosis of adult respiratory distress syndrome

In 1990, Fisher and Foex proposed the following diagnostic criteria for adult respiratory distress syndrome:

• respiratory failure (severe shortness of breath);
• a lot of work of breathing, increasing chest stiffness;
• clinical picture of increasing pulmonary edema;
• typical X-ray picture (increased pulmonary pattern, interstitial pulmonary edema);
• arterial hypoxemia (usually PaO2 is less than 50 mmHg) and hypercapnia;
• hypertension in the pulmonary circulation (pressure in the pulmonary artery is more than 30/15 mm Hg);
• normal pulmonary artery wedge pressure (<15mmHg). The definition of this criterion is important for the differentiation of adult respiratory distress syndrome from cardiogenic pulmonary edema, which is characterized by an increase in the pressure of pulmonary artery wedging;
• arterial pH is less than 7.3.

Adult Respiratory Distress Syndrome Screening Program

1. General analysis of blood, urine.
2. EKG.
3. Radiography of the lungs.
4. The study of acid-base balance.
5. Study of blood gas composition: determination of PaO2, PaCO2.

[23], [24], [25],