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Acute Respiratory Distress Syndrome for ABIM

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Acute Respiratory Distress Syndrome (ARDS) for the American Board of Internal Medicine Exam
Acute Respiratory Distress Syndrome (ARDS) is a severe form of acute respiratory failure characterized by non-cardiogenic pulmonary edema and hypoxemia. It is caused by diffuse alveolar damage and can result from various direct or indirect lung insults.
Pathophysiology
ARDS is primarily caused by injury to the alveolar-capillary membrane, leading to increased permeability, fluid accumulation in the alveoli, and impaired gas exchange.
  • Phases of ARDS:
    • Exudative Phase (First 7 Days): Inflammation and alveolar flooding due to increased vascular permeability. Hyaline membrane formation occurs, contributing to impaired oxygen diffusion.
    • Proliferative Phase (7-21 Days): Initiation of lung repair with proliferation of fibroblasts and type II pneumocytes. Alveolar edema resolves, but lung compliance remains low due to fibrosis.
    • Fibrotic Phase (After 3 weeks): Some patients progress to irreversible fibrosis, characterized by diffuse scarring and remodeling of the lung architecture, leading to prolonged ventilatory support.
  • Cytokine Storm: The release of pro-inflammatory cytokines, such as TNF-α, IL-1, and IL-6, leads to widespread inflammation and damage to the alveolar epithelium and endothelium, increasing vascular permeability.
  • Impaired Gas Exchange: Fluid accumulation in the alveoli causes V/Q mismatch and shunting, leading to hypoxemia that is resistant to supplemental oxygen.
Etiology
ARDS can result from various direct and indirect lung insults. These causes are important to identify, as they can guide management.
  • Direct Lung Injury:
    • Pneumonia: Most common cause of ARDS. Bacterial, viral (e.g., COVID-19), or fungal pneumonia can lead to alveolar damage.
    • Aspiration of gastric contents: Aspiration pneumonitis causes chemical injury to the alveoli.
    • Pulmonary contusion: Trauma to the lungs leads to localized inflammation and edema.
    • Inhalational injury: Smoke or toxic gas inhalation can damage the alveoli.
  • Indirect Lung Injury:
    • Sepsis: The most frequent non-pulmonary cause. Systemic inflammation from sepsis can result in ARDS.
    • Pancreatitis: Release of inflammatory mediators can damage distant organs, including the lungs.
    • Trauma: Severe trauma, particularly involving multiple systems, can lead to ARDS due to systemic inflammation.
    • Transfusion-related acute lung injury (TRALI): Occurs after blood transfusion, mediated by recipient antibodies reacting with donor leukocytes.
Diagnostic Criteria (Berlin Definition)
The Berlin criteria are used to diagnose ARDS. Key features include:
  • Timing: ARDS must occur within one week of a known clinical insult or new/worsening respiratory symptoms.
  • Chest Imaging: Bilateral opacities on chest X-ray or CT scan that are not explained by other causes, such as pleural effusion or atelectasis.
Bilateral Opacities in Acute Respiratory Distress Syndrome
  • Origin of Edema: Respiratory failure not fully explained by cardiac failure or fluid overload. Echocardiography is often used to rule out hydrostatic edema.
  • Hypoxemia (PaO2/FiO2 Ratio):
    • Mild ARDS: PaO2/FiO2 200-300 mmHg with PEEP or CPAP ≥ 5 cm H2O.
    • Moderate ARDS: PaO2/FiO2 100-200 mmHg with PEEP ≥ 5 cm H2O.
    • Severe ARDS: PaO2/FiO2 < 100 mmHg with PEEP ≥ 5 cm H2O.
Clinical Presentation
  • Symptoms:
    • Dyspnea: Acute onset of severe shortness of breath.
    • Tachypnea: Rapid breathing due to hypoxemia and lung stiffness.
    • Hypoxemia: Often refractory to oxygen therapy due to intrapulmonary shunting.
    • Accessory muscle use: Suggestive of increased work of breathing.
  • Physical Exam:
    • Diffuse crackles: Present on auscultation due to fluid in the alveoli.
    • Cyanosis: Secondary to severe hypoxemia.
    • Respiratory distress: Use of accessory muscles and labored breathing.
Diagnostic Workup
  • Imaging:
    • Chest X-ray: Shows bilateral, diffuse alveolar infiltrates, often described as a "white-out" pattern.
    • CT Scan: May be used for further evaluation of lung parenchyma; findings include bilateral ground-glass opacities and consolidation.
  • Laboratory Studies:
    • ABG (Arterial Blood Gas): Shows hypoxemia with a low PaO2/FiO2 ratio and respiratory alkalosis early on. As ARDS progresses, hypercapnia may develop.
    • Complete Blood Count and Cultures: Evaluate for infection or sepsis as underlying causes.
  • Cardiac Evaluation:
    • Echocardiogram: Used to exclude cardiogenic causes of pulmonary edema (e.g., heart failure).
Management
Ventilatory Support
The cornerstone of ARDS management is mechanical ventilation with lung-protective strategies.
  • Low Tidal Volume Ventilation: Tidal volumes of 4-6 mL/kg of predicted body weight to prevent ventilator-induced lung injury (VILI).
    • Rationale: Reduces overdistension of alveoli and barotrauma.
  • PEEP (Positive End-Expiratory Pressure): Applied to prevent alveolar collapse during expiration and improve oxygenation.
    • Rationale: PEEP keeps alveoli open, improving gas exchange and reducing the need for high oxygen concentrations.
  • Permissive Hypercapnia: Allowing higher levels of CO2 (PaCO2 50-70 mmHg) to avoid barotrauma associated with high ventilatory pressures.
  • Prone Positioning: Improves ventilation-perfusion matching and oxygenation by recruiting more lung units in the dorsal areas.
    • Indicated for moderate to severe ARDS with PaO2/FiO2 < 150 mmHg.
  • Neuromuscular Blockade: Used for patients with severe ARDS to reduce oxygen consumption, improve ventilator synchrony, and minimize patient movement.
Adjunctive Therapies
  • Fluid Management: Conservative fluid management strategies are recommended to prevent worsening pulmonary edema.
    • Diuretics: Used to optimize fluid balance and reduce lung water content, improving oxygenation.
  • Corticosteroids: May be used in late-phase ARDS with fibrosis or in cases associated with COVID-19 or pneumonia, although their routine use remains controversial.
  • Extracorporeal Membrane Oxygenation (ECMO): Considered for patients with severe, refractory hypoxemia who do not respond to conventional therapies.
Complications
ARDS carries a high risk of complications, particularly related to mechanical ventilation.
  • Ventilator-associated pneumonia (VAP): Increased risk due to prolonged mechanical ventilation and endotracheal intubation.
  • Barotrauma: Includes pneumothorax or pneumomediastinum from high ventilatory pressures.
  • Multiorgan Failure: Often seen in severe ARDS, especially in patients with underlying sepsis.
Prognosis
Mortality rates for ARDS vary by severity:
  • Mild ARDS: 30-40% mortality.
  • Severe ARDS: Up to 50-60% mortality.
Survivors may experience long-term complications such as pulmonary fibrosis, decreased exercise tolerance, and psychological issues, including post-traumatic stress disorder (PTSD).
Key Points
  • ARDS is characterized by acute onset of hypoxemia and bilateral pulmonary infiltrates due to non-cardiogenic pulmonary edema.
  • The Berlin criteria are used to classify ARDS severity based on PaO2/FiO2 ratio and PEEP requirements.
  • Management focuses on lung-protective mechanical ventilation (low tidal volume, PEEP) and supportive care, with prone positioning and ECMO reserved for severe cases.
  • Identification and treatment of the underlying cause are critical for improving outcomes, with sepsis and pneumonia being the most common triggers.
  • Complications include ventilator-associated pneumonia, barotrauma, and multiorgan failure, leading to significant morbidity and mortality.

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