SPECIAL SELECTED TOPICS- RESPIRATORY SYSTEM DISORDERS-SSTRSDO-QAA 004

1. What is Adult Respiratory Distress Syndrome (ARDS)?

Acute Respiratory Distress Syndrome (ARDS) is a severe form of acute diffuse lung injury characterized by rapidly developing respiratory failure. It results from widespread damage to the alveolar-capillary membrane. Increased vascular permeability causes leakage of protein-rich fluid into alveoli.

Surfactant is lost, resulting in diffuse alveolar collapse. Patients develop severe hypoxemia that is resistant to oxygen therapy. Bilateral pulmonary infiltrates are seen on chest imaging without evidence of left heart failure.

Histologically, diffuse alveolar damage with hyaline membrane formation is characteristic. Mechanical ventilation is often required. Mortality remains high despite advances in intensive care.

2. Which conditions are associated with the development of ARDS?

ARDS commonly develops after severe systemic or pulmonary insults. Sepsis is the leading cause worldwide. Severe bacterial or viral pneumonia frequently precipitates ARDS. Aspiration of gastric contents causes direct alveolar injury.

Major trauma, burns, and multiple fractures may trigger inflammatory lung damage. Acute pancreatitis releases inflammatory mediators that injure pulmonary capillaries. Massive blood transfusion may produce transfusion-related acute lung injury.

Inhalation of toxic gases, smoke, or chemicals damages alveolar epithelium. Drug overdose and near-drowning are additional causes. All these conditions initiate diffuse inflammatory injury of the alveolar-capillary membrane.

3. What are the pathologic features of ARDS?

The hallmark of ARDS is diffuse alveolar damage affecting both lungs. Grossly, the lungs are heavy, firm, congested, and edematous. Microscopically, capillary congestion and interstitial edema are prominent.

Necrosis of type I pneumocytes occurs early in the disease. Protein-rich edema fluid fills alveolar spaces. Hyaline membranes composed of fibrin and necrotic cellular debris line the alveoli. Inflammatory cells infiltrate the interstitium and alveolar walls.

Type II pneumocyte hyperplasia develops during the repair phase. Fibrosis may occur in prolonged disease. These pathological changes severely impair pulmsonary oxygen exchange.

4. Describe the pathogenesis of ARDS.

ARDS begins with injury to alveolar epithelial cells and pulmonary capillary endothelial cells. Activated neutrophils release cytokines, proteases, and reactive oxygen species that amplify tissue damage. Endothelial injury increases vascular permeability, allowing protein-rich fluid to enter alveoli.

Type I pneumocyte destruction impairs the alveolar barrier. Loss of surfactant from damaged type II pneumocytes causes widespread alveolar collapse. Hyaline membranes form from fibrin-rich exudate and necrotic epithelial cells.

Lung compliance decreases markedly, making ventilation difficult. Severe ventilation-perfusion mismatch produces refractory hypoxemia. Persistent inflammation promotes fibrosis in some patients.

The combined effects result in acute respiratory failure requiring intensive supportive care.

5. What is the clinical course of ARDS?

ARDS usually begins within 24–72 hours after a severe pulmonary or systemic insult. Patients develop rapidly progressive dyspnea, tachypnea, and severe hypoxemia. Oxygen saturation remains low despite supplemental oxygen due to diffuse alveolar damage. Chest radiographs show bilateral diffuse pulmonary infiltrates.

Most patients require intensive care and mechanical ventilation with lung-protective strategies. Complications include ventilator-associated pneumonia, barotrauma, and multiorgan failure. The exudative phase is followed by a proliferative repair phase, and some patients progress to pulmonary fibrosis.

Mortality remains approximately 30–40%, depending on the underlying cause and severity. Survivors often regain satisfactory lung function, although some have persistent restrictive defects. Early recognition and supportive management improve outcomes.

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DR.C.GANESAN M.D

PROFESSOR OF MEDICINE