Clinical Features of Acute Respiratory Distress Syndrome (ARDS)
Acute Respiratory Distress Syndrome (ARDS) is characterized by severe dyspnea, tachypnea, and unremitting hypoxemia, with bilateral pulmonary infiltrates on chest imaging and non-cardiogenic pulmonary edema developing within one week of a known clinical insult. 1
Diagnostic Criteria
ARDS is diagnosed based on the following criteria:
- Onset within one week of a known insult or new/worsening respiratory symptoms
- Bilateral pulmonary opacities on chest radiography not explained by effusions, collapse, or nodules
- Respiratory failure not explained by cardiac failure or fluid overload
- Profound hypoxemia classified by PaO₂/FiO₂ ratio:
- Mild: 201-300 mmHg
- Moderate: 101-200 mmHg
- Severe: ≤100 mmHg 1
Clinical Manifestations
Respiratory Features
- Severe dyspnea and respiratory distress
- Tachypnea (>30 breaths/minute)
- Increased work of breathing
- Refractory hypoxemia despite oxygen therapy
- Decreased lung compliance
- Increased airway resistance (bronchoconstriction)
- Increased physiological dead-space ventilation 2
Radiographic Findings
- Bilateral infiltrates that may be diffuse, peripheral, and interstitial
- Infiltrates may be asymmetric or patchy
- Standard chest radiographs poorly predict severity of oxygenation defect or clinical outcome 2
Systemic Features
- Altered mental status may be present
- Extrapulmonary organ failure may complicate respiratory dysfunction
- Purple-black facial complexion in severe cases
- Cold limbs with cold sweating in critical cases 2
Pathophysiological Phases
ARDS progresses through distinct phases:
Early Exudative Phase (Days 1-5):
- Interstitial swelling
- Proteinaceous alveolar edema
- Hemorrhage and fibrin deposition
- Hyaline membrane formation
- Neutrophilic infiltration 2
Fibroproliferative Phase (Days 6-10):
- Alveolar edema resolution
- Decreased hyaline membrane prominence
- Mononuclear cell infiltration
- Fibroblast proliferation
- New collagen deposition 2
Fibrotic Phase (After 10 Days):
- Interstitial fibrosis
- Obliteration of vascular bed
- Persistent high minute ventilatory requirements
- Increased dead-space ventilation 2
Hemodynamic Features
- Increased pulmonary artery pressure
- Mildly to moderately elevated pulmonary vascular resistance
- Pulmonary hypertension due to:
- Hypoxic vasoconstriction
- Vasoactive mediators (thromboxane, endothelin)
- Intravascular obstruction
- Perivascular edema
- Later fibrotic obliteration of vascular bed 2
Severity Assessment
The American Thoracic Society recommends classifying ARDS severity based on the PaO₂/FiO₂ ratio:
- Mild: 201-300 mmHg
- Moderate: 101-200 mmHg
- Severe: ≤100 mmHg 1
The Lung Injury Score (LIS) can also assess disease severity:
- LIS score >3.5: correlates with 18% survival rate
- LIS score <1.1: correlates with 66% survival rate 1
Clinical Course and Prognosis
- Natural history dominated by the inciting event rather than the lung injury itself
- Death from refractory respiratory failure is unusual
- Most common cause of death is multiple organ failure or recurrent sepsis
- In-hospital mortality for severe ARDS ranges from 46% to 60%
- Survivors are at risk for diminished functional capacity, mental illness, and decreased quality of life 2, 3
Common Pitfalls in ARDS Diagnosis
- Failing to differentiate ARDS from cardiogenic pulmonary edema
- Overlooking the underlying cause (most commonly pneumonia or sepsis)
- Delaying diagnosis by waiting for all classic radiographic findings
- Misinterpreting radiographic findings, which may be asymmetric or patchy
- Not recognizing ARDS early when patients present with severe dyspnea, tachypnea, and hypoxemia before meeting all criteria 2, 3
Early recognition of ARDS clinical features and prompt implementation of appropriate management strategies are crucial for improving outcomes in this life-threatening condition.