Acute Respiratory Distress Syndrome (ARDS) PDF

Acute Respiratory Distress Syndrome (ARDS) De nition: Clinical syndrome characterized by: Severe dyspnea of rapid onset Hypoxemia Diffuse pulmonary in ltrates leading to respiratory...

Acute Respiratory Distress Syndrome (ARDS) De nition: Clinical syndrome characterized by: Severe dyspnea of rapid onset Hypoxemia Diffuse pulmonary in ltrates leading to respiratory failure Causes of ARDS: Can be caused by direct lung injury (e.g., toxic inhalation) Can be caused by indirect lung injury (e.g., sepsis) Incidence and Epidemiology: Annual incidence estimated to be as high as 60 cases per 100,000 population before COVID-19 pandemic Approximately 10% of all ICU admissions involve patients with ARDS Classi cation and Severity: De ned by three categories based on the degrees of hypoxemia (mild, moderate, severe) Associated with mortality risk and duration of mechanical ventilation in survivors Etiology: Most cases (>80%) caused by: Pneumonia and sepsis (~40-60%) Aspiration of gastric contents, trauma, multiple transfusions, and drug overdose Speci c conditions in trauma patients include pulmonary contusion, multiple bone fractures, and chest wall trauma/ ail chest Risk Factors: Older age Chronic alcohol abuse Pancreatitis Severity of critical illness Trauma patients with higher Acute Physiology and Chronic Health Evaluation (APACHE) II scores (≥16) have increased risk fi fi fi fi fi fl  Clinical Course and Pathophysiology of ARDS Phases of ARDS 1. Exudative Phase Pathophysiology: Injury to alveolar capillary endothelial cells and type I pneumocytes (alveolar epithelial cells) Loss of alveolar barrier function, leading to uid and protein-rich edema in interstitial and alveolar spaces Increased proin ammatory cytokines (e.g., IL-1, IL-8, TNF-α) and lipid mediators (e.g., leukotriene B4) Recruitment of leukocytes, especially neutrophils, into pulmonary spaces Formation of hyaline membrane whorls due to aggregated plasma proteins, cellular debris, and dysfunctional surfactant Early pulmonary vascular injury with microthrombi and brocellular proliferation Clinical Features: Predominant alveolar edema in dependent lung regions with reduced aeration Large lung sections collapse, decreasing lung compliance Intrapulmonary shunting and hypoxemia develop, increasing work of breathing and dyspnea Hypercapnia from increased pulmonary dead space Radiographic Findings: Chest X-ray shows opacities consistent with pulmonary edema involving at least three-quarters of lung elds Non-speci c ndings resembling cardiogenic pulmonary edema but without cardiomegaly or pleural effusions Differential Diagnosis: Consider cardiogenic pulmonary edema, bilateral pneumonia, alveolar hemorrhage, and other interstitial lung diseases 2. Proliferative Phase Duration: Typically from day 7 to day 21 Clinical Course: Many patients recover, are liberated from mechanical ventilation Persistent dyspnea, tachypnea, and hypoxemia in some Early signs of pulmonary brosis may develop Histologically, resolution begins with organization of alveolar exudates, shift from neutrophil- to lymphocyte- predominant in ltrates Type II pneumocyte proliferation and surfactant synthesis contribute to repair 3. Fibrotic Phase Outcome: Occurs in some patients 3–4 weeks post-injury Pathological Features: Conversion of edema and exudates to extensive alveolar-duct and interstitial brosis Emphysema-like changes with large bullae due to disruption of acinar architecture Intimal broproliferation in pulmonary microcirculation leads to vascular occlusion and pulmonary hypertension Increased risk of pneumothorax, reduced lung compliance, and pulmonary dead space Lung biopsy showing brosis is associated with higher mortality risk fi fi fi fi fl fi fi fl fi fi fi  Treatment of Acute Respiratory Distress Syndrome (ARDS) General Principles Recognition and Treatment: Identify and treat underlying medical and surgical disorders (e.g., pneumonia, sepsis, aspiration, trauma) Minimize unnecessary procedures and their complications Implement standardized “bundled care” approaches in ICU, including prophylaxis against complications like venous thromboembolism, gastrointestinal bleeding, aspiration, prolonged mechanical ventilation, and central venous catheter infections Promptly recognize and manage nosocomial infections Ensure adequate nutrition via enteral route when feasible Management of Mechanical Ventilation Minimizing Ventilator-Induced Lung Injury: Mechanisms include volutrauma (alveolar overdistention) and atelectrauma (alveolar collapse) Optimal Ventilation Strategy: Use low tidal volume ventilation (6 mL/kg of predicted body weight) to reduce volutrauma and barotrauma Target lower airway pressures (plateau pressure ≤30 cm H2O) to further mitigate lung injury Signi cant mortality bene t observed with low tidal volume ventilation compared to conventional approaches Prevention of Alveolar Collapse with Positive End-Expiratory Pressure (PEEP): Adjust PEEP to maintain adequate oxygenation without causing alveolar overdistention Various methods to determine optimal PEEP: Use PEEP-FiO2 tables from ARDS Network trials Generate static pressure-volume curves to set PEEP just above lower in ection point Consider measuring esophageal pressures for estimating transpulmonary pressure in patients with stiff chest wall Recent trials have shown no clear bene t of routine esophageal pressure-guided PEEP titration over empirical high PEEP-FiO2 titration Prone Positioning: Improved arterial oxygenation observed without initial mortality bene t in previous trials Signi cant reduction in 28-day mortality demonstrated in severe ARDS (Pao2/Fio2 75 years signi cantly increases mortality risk to ~60%). Presence of sepsis in older patients (>60 years) triples mortality risk. Preexisting organ dysfunction (e.g., chronic liver disease, chronic alcohol abuse, chronic immunosuppression) increases mortality risk. Direct lung injury (e.g., pneumonia, aspiration) doubles mortality risk compared to indirect causes. Surgical and trauma-related ARDS without direct lung injury generally have better survival rates. Severity and Mortality Increasing severity of ARDS (as per Berlin de nition) correlates with higher mortality rates. Parameters like high PEEP (≥10 cm H2O), low respiratory system compliance (≤40 mL/cm H2O), extensive alveolar in ltrates on chest radiography, and high dead space volume (≥10 L/min) do not signi cantly predict mortality beyond severity classi cation. Functional Recovery in ARDS Survivors Respiratory Function Majority of ARDS survivors regain near-normal lung function within 6 months. One year post-extubation, over one-third have normal spirometry and diffusion capacity. Remaining patients typically exhibit mild pulmonary function abnormalities. Poor recovery associated with low static respiratory compliance, high PEEP requirements, prolonged mechanical ventilation, and severe lung injury scores. Long-term Physical and Psychological Impacts Despite pulmonary function recovery, many survivors experience exercise limitations and decreased physical quality of life. Psychological issues are common, including depression and posttraumatic stress disorder among patients and caregivers. Long-term follow-up and support are crucial for managing these aspects of recovery. fi fi fi fi fi