Acute respiratory distress syndrome (ARDS) is an extremely severe manifestation of respiratory insufficiency, accompanied by the development of non-cardiogenic pulmonary edema, respiratory disorders and hypoxia. Despite the variety of factors leading to ARDS, it is based on damage to the pulmonary structures that cause the failure of oxygen transport to the lungs. Other names for respiratory distress syndrome are “shock”, “wet”, “traumatic” lung.
J80 Respiratory disorder [distress] syndrome in an adult.
Acute respiratory distress syndrome causes
The mechanism triggering the development of respiratory distress syndrome is the embolization of small vessels of the lungs by blood micro-clots, particles of damaged tissues, fat droplets against the background of toxic biologically active substances formed in the tissues — kinins, prostaglandins, etc. Microembolization of pulmonary vessels develops as a result of direct or indirect effects of various damaging factors on the capillary-alveolar membrane of pulmonary acinuses.
Aspiration of blood, vomit and water, inhalation of smoke and toxic substances, contusion of the lungs, rib fracture, rupture of the diaphragm, overdose of narcotic drugs have a direct damaging effect. Indirect, indirect damage to capillary-alveolar membranes is caused by activation and aggregation of shaped blood elements in bacterial and viral pneumonia, sepsis, burns, combined injuries and traumatic shock, accompanied by massive blood loss, pancreatitis, autoimmune processes, electrotrauma, eclampsia, etc.
Increased membrane permeability to protein and fluid causes swelling of interstitial and alveolar tissues, decreased extensibility and gas exchange function of the lungs. These processes lead to the development of hypoxemia, hypercapnia and acute respiratory failure. Respiratory distress syndrome can develop for several hours or days from the moment of exposure to the damaging factor. During ARDS , three pathomorphological phases of ARDS are distinguished:
- Acute phase (up to 2-5 days) – interstitial and alveolar pulmonary edema, damage to the capillaries of the lungs and the epithelium of the alveoli, the development of microatelectases. In the case of a favorable course of respiratory distress syndrome, after a few days, the severity of the phenomena subsides, the transudate resolves; otherwise, a transition to a subacute or chronic course is possible.
- The subacute phase is the development of bronchoalveolar and interstitial inflammation.
- The chronic phase corresponds to the development of fibrosing alveolitis. There is a thickening and flattening of capillary-alveolar membranes, the growth of connective tissue in them, the formation of microthrombosis and desolation of the vascular bed. The outcome of the chronic phase of respiratory distress syndrome is the development of pulmonary hypertension and chronic respiratory failure. Pronounced alveolar fibrosis may occur after 2-3 weeks.
Acute respiratory distress syndrome symptoms
The development of respiratory distress syndrome in adults is characterized by a sequential change of stages, reflecting pathological changes in the lungs and a typical picture of acute respiratory failure.
I (stage of damage) – the first 6 hours from the time of exposure to the stress factor. Complaints, as a rule, are absent, clinical and radiological changes are not determined.
II (stage of imaginary well–being) – from 6 to 12 hours from the time of exposure to the stress factor. Increasing shortness of breath, cyanosis, tachycardia, tachypnea (increased breathing more than 20 per minute), patient anxiety, cough with foamy sputum and streaks of blood develop. Shortness of breath and cyanosis are not stopped by oxygen inhalations, the oxygen content in the blood is steadily falling. Auscultation in the lungs – wheezing, crepitation; radiological signs correspond to diffuse interstitial edema.
III (stage of respiratory failure) – 12-24 hours after exposure to a stressful factor. Bubbling breathing with the release of foamy pink sputum, increasing hypoxemia and hypercapnia, shallow breathing, an increase in central venous and a decrease in blood pressure. Moist, multiple wheezes of various calibers are heard all over the surface of the lungs. Radiographs determine the fusion of focal shadows. At this stage, the formation of hyaline membranes occurs, filling of the alveoli with fibrin, exudate, decaying blood cells, damage to the endothelium of capillaries with the formation of hemorrhages and microelectases.
IV (terminal stage) – metabolic acidosis, hypoxemia and hypercapnia are not eliminated by extremely large volumes of intensive therapy and ventilation. False-positive X-ray dynamics (the appearance of foci of enlightenment) is caused by the proliferation of connective tissue replacing the lung parenchyma. In this terminal period of respiratory distress syndrome, multiple organ failure develops, characterized by:
- arterial hypotension, pronounced tachycardia, atrial fibrillation, ventricular tachycardia;
- hyperbilirubinemia, hyperfermentemia, hypoalbuminemia, hypocholesterolemia;
- DIC syndrome, leukopenia, thrombocytopenia ;
- increased urea and creatinine, oliguria;
- gastrointestinal and pulmonary bleeding;
- depression of consciousness, coma.
During the relief of respiratory distress syndrome, complications in the form of lung barotrauma, bacterial pneumonia, the development of DIC syndrome, left ventricular heart failure are possible. Manifestations of barotrauma developing as a result of hardware ventilation of the lungs are subcutaneous emphysema, pneumothorax, pneumomediastinum. The increased risk of developing barotrauma in patients with respiratory distress syndrome is due to overgrowth of the alveoli with a decrease in the elasticity of the lung tissue.
Acute left ventricular insufficiency (or cardiogenic pulmonary edema) in ARDS is caused by stagnation of blood circulation in the small circle. DIC syndrome (disseminated intravascular coagulation syndrome) develops with sepsis, pancreatic necrosis and other damaging factors and is expressed in multiple organ damage to various systems.
Respiratory distress syndrome is a critical condition and requires an emergency assessment of the patient’s condition. Early objective manifestations of ARDS are increasing shortness of breath, tachycardia and cyanosis. The auscultative picture of the lungs changes according to the stages of respiratory distress syndrome: from hard “amphoric” breathing to bubbling wet wheezing and the symptom of a “mute” (“silent”) lung in the terminal stage.
A characteristic indicator of the blood gas composition in ARDS is RaO2 below 50 mmHg (hypoxemia), despite the ongoing oxygen therapy (with FiO2 more than > 60%.), an increase in hypercapnia. In patients with ARDS, severe respiratory insufficiency and hypoxemia persist even with inhalations of a highly concentrated oxygen mixture.
Biochemical parameters of venous blood are characterized by hypoalbuminemia, an increase in clotting factors, an increase in transaminases and bilirubin. Lung x-ray reveals diffuse multiple shadows on the periphery (a symptom of a “snowstorm”), a decrease in the transparency of the lung tissue, pleural effusion is usually absent.
Indicators of the function of external respiration indicate a decrease in all respiratory volumes and static stretching of the lung tissue less than 5 ml / mm of water. Measuring the pressure in the pulmonary artery with a Swan–Ganz catheter shows its “jamming” at a level of less than 15 mm Hg. Respiratory distress syndrome should be distinguished from cardiogenic pulmonary edema, pneumonia, PE.
Acute respiratory distress syndrome treatment
Treatment of respiratory distress syndrome is carried out in the intensive care unit and intensive care unit. Measures for the relief of ARDS include:
- elimination of the stress damaging factor;
- correction of hypoxemia and acute respiratory failure;
- treatment of multiple organ disorders.
At the first stage of treatment of respiratory distress syndrome, direct damaging factors of the lungs are eliminated, massive antibacterial therapy is prescribed for bacterial pneumonia, sepsis, and appropriate treatment of burns and injuries is carried out. To eliminate hypoxia, an adequate oxygen therapy regimen is selected with dynamic control of blood gases (with maintenance of PO2 of at least 60 mmHg). Oxygen supply can be carried out through a mask or a nasal catheter, with ineffective oxygenation, a ventilator is indicated (at a BH of 30 per minute).
To prevent the development of DIC syndrome, acetylsalicylic acid, dipyridamole and rheopolyglucin, heparin are prescribed. Despite interstitial and alveolar edema, infusion therapy is performed to improve organ nutrition, normalize diuresis and maintain blood pressure levels. The effectiveness of treatment of respiratory distress syndrome depends on its timeliness: it is successful only in the early stages of this condition before the onset of irreversible lesions of the lung tissue.
Prognosis and prevention
Mortality in the III stage of respiratory distress syndrome is about 80%, in the terminal stage, corresponding to multiple organ failure, usually all patients die. With a favorable outcome, lung function can almost completely recover after the relief of ARDS, but long-term maintenance therapy is more often required.
There are no specific preventive measures for respiratory distress syndrome. One should beware of the effects of stress damaging factors leading to the development of ARDS.
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