bubble_chart Overview

Adult respiratory distress syndrome (ARDS) is an acute progressive hypoxic respiratory failure that occurs during the course of various severe diseases, such as shock, trauma, and aspiration. The main pathophysiological changes include diffuse lung injury, increased pulmonary microvascular permeability, and alveolar collapse, leading to increased intrapulmonary blood shunting and ventilation/perfusion mismatch. The primary clinical manifestations are severe and refractory hypoxemia, tachypnea, and respiratory distress.

bubble_chart Etiology

The disease causes of ARDS include pulmonary diseases such as severe infections (including viruses, pneumocystosis), lung trauma, pulmonary embolism (fat, amniotic fluid), aspiration, inhalation of toxic gases (phosgene, smoke), etc.; and extrapulmonary diseases such as severe trauma, sepsis, shock of various causes, acute pancreatitis, DIC, as well as extracorporeal circulation, massive transfusion of stored blood, long-term high-concentration (>70%) oxygen inhalation, etc.

The mechanism of disease in ARDS has not been fully elucidated. During the course of the aforementioned diseases, vasoactive substances such as histamine, serotonin, bradykinin, catecholamines, bacterial toxins, superoxide anions, etc., may be produced and released, causing injury to the pulmonary vascular wall, increasing permeability, or leading to pulmonary capillary microthrombi, pulmonary circulation disorders, or damage to alveolar type II cells, resulting in reduced synthesis of alveolar surfactant, increased alveolar tension, and widespread alveolar collapse. Hypoxia in brain tissue can also cause reflexive pulmonary capillary constriction and increased pulmonary venous pressure, ultimately leading to permeability pulmonary edema, ventilation/perfusion mismatch, intrapulmonary venous shunting, and severe hypoxemia.

In the early stages, lung weight increases, primarily due to increased water content, which can exceed 80% of normal levels. The appearance is dark red or purplish-red, resembling liver-like changes, with significantly reduced alveolar air content. Microscopically, microthrombi formation in small pulmonary vessels and focal hemorrhage can be observed, along with the formation of alveolar hyaline membranes. As the disease progresses, focal hemorrhage gradually resolves, but edema persists, often accompanied by widespread bronchopneumonia and pulmonary interstitial fibrosis. Subsequently, the hyaline membranes gradually absorb, with fibrosis becoming the main pathological change, and alveolar macrophages significantly increasing.

Although the disease causes of ARDS are varied, the pathophysiological changes in the lungs are fundamentally the same, with the following main characteristics:

1. Injury to pulmonary microvascular endothelium and increased permeability, leading to pulmonary interstitial edema followed by alveolar edema;
2. Widespread formation of pulmonary capillary microthrombi with focal hemorrhage, and the release of vasoactive substances causing pulmonary small vessel constriction, increasing intrapulmonary shunting;
3. Damage to alveolar type II cells, reduced surfactant, and increased alveolar recoil leading to generalized alveolar collapse and impaired oxygen diffusion. The consequences of these changes inevitably result in ventilation/perfusion mismatch, intrapulmonary venous shunting, and gas exchange disorders, thereby causing severe progressive hypoxemia.

bubble_chart Diagnosis

1. Have primary diseases that can cause ARDS, such as shock, trauma, aspiration, severe infection, and corresponding manifestations;
2. During the course of the above diseases, sudden progressive respiratory distress occurs, with a respiratory rate >28 breaths/min, gradually worsening cyanosis, usually difficult to improve with conventional oxygen therapy. In the advanced stage, bubbling sounds, tubular breath sounds, and inspiratory crackles can be heard in the lungs;
3. Chest X-ray findings: early stages often show no abnormalities, but as the condition worsens, reticular, patchy, or large areas of increased density shadows may appear, sometimes with air bronchograms visible within the consolidation shadows;
4. Stirred pulse blood gas analysis: when breathing air, PaO₂<8kPa（60mmHg），PaO2/FIO2（吸氧濃度）<300（PaO₂ (calculated in mmHg), PaCO₂ in the early stage <4.67kPa（35mmHg）或正常；
5. can exclude cardiogenic pulmonary edema.

bubble_chart Treatment Measures

The treatment principles for ARDS include correcting hypoxia, overcoming alveolar collapse, improving pulmonary microcirculation, eliminating pulmonary edema, and controlling the primary disease.

1. To correct hypoxia and overcome alveolar collapse, oxygen therapy alone is often ineffective. Mechanical ventilation with positive end-expiratory pressure (PEEP) can significantly improve outcomes. PEEP involves connecting a plastic tube from the ventilator's outlet to a water-sealed bottle, with the tube submerged 3–5 cm underwater (gradually increasing to 10 cmH₂O or 0.98 kPa). Since positive pressure is maintained throughout the respiratory cycle, PEEP helps prevent small airway and alveolar collapse, promotes the reopening of atelectatic alveoli, reduces pulmonary shunting, and thereby increases PaO2. Recently, high-frequency jet ventilation has been proposed as an alternative, as it can generate a spontaneous PEEP effect without requiring tracheal intubation or tracheostomy. This method can also deliver high-concentration oxygen and may have some therapeutic benefits for ARDS.
2. **Improving pulmonary microcirculation** Pulmonary microcirculatory dysfunction can result from small pulmonary vein spasms, microthrombi, or disseminated intravascular coagulation (DIC). Although opinions vary, corticosteroids are commonly used in early stages to inhibit the release of vasoactive substances, thereby relieving bronchial and pulmonary vascular spasms, reducing pulmonary embolism and inflammatory responses, preventing protease release, protecting lung tissue, promoting surfactant synthesis and secretion, maintaining alveolar membrane stability, and inhibiting pulmonary fibrosis. Early high-dose administration is recommended (e.g., hydrocortisone 200–300 mg/day or dexamethasone 20–30 mg/day via intravenous drip), with gradual tapering to minimize adverse effects. Heparin may be used in cases of hypercoagulability to prevent DIC, but caution is required in patients with bleeding tendencies. Other agents like 654-2, scopolamine, phentolamine, papaverine, and low-molecular-weight dextran can also improve microcirculation and may be selected as appropriate.
3. **Eliminating pulmonary edema** ARDS involves interstitial and varying degrees of alveolar edema, necessitating fluid restriction, especially intravenous infusion, to prevent worsening edema. Early administration of salt-free albumin combined with rapid-acting diuretics may facilitate fluid removal from the lungs. However, as vascular permeability increases significantly in later stages, albumin may become less effective due to elevated interstitial osmotic pressure. In such cases, potent diuretics should be prioritized, with attention to electrolyte balance.
4. **Aggressive treatment of the primary disease** Bingben is essential, as secondary pulmonary infections are common and require prompt identification and management.

bubble_chart Prognosis

The mortality rate of ARDS patients is very high, often exceeding 50%, but early detection and timely treatment may improve the prognosis.

bubble_chart Prevention

1. For patients prone to ARDS due to shock, severe trauma, infection, etc., vigilance for the onset of this condition should be maintained throughout the course of the illness. For certain severe diseases, especially in patients with impaired consciousness, enhanced nursing care is necessary to prevent aspiration, shock, and other complications to avert the occurrence of ARDS.
2. During the course of the aforementioned diseases, if there is a tendency for the respiratory rate to increase (>20 breaths/min), the possibility of ARDS should be considered, and close monitoring of the patient's condition is advisable. If the respiratory rate progressively accelerates, even if it has not yet reached 28 breaths/min, or if PaO₂ is >8 kPa but PaO₂/FiO₂ shows a progressive decline, the case should be classified as highly suspicious, and early intervention should be initiated to prevent progression to the more challenging classic ARDS.

bubble_chart Differentiation

The key points for differentiation from cardiogenic pulmonary edema are: left heart failure is evidenced by cardiac disease, often presenting with pink frothy sputum, difficulty lying flat, basal lung crackles, a butterfly-shaped shadow on chest X-ray, elevated pulmonary wedge pressure, and responsiveness to cardiac glycosides and diuretics. In contrast, ARDS patients show no evidence of cardiac disease, have widespread lung crackles (sometimes with inspiratory crackles or tubular breath sounds), normal or reduced pulmonary wedge pressure, and no response to cardiac glycosides or diuretics. Additionally, differentiation from bronchopneumonia may sometimes be necessary.