Acute Respiratory Distress Syndrome (ARDS)

Johnathan W. Cain, DO
The Operative Review of Surgery. 2023; 1:29-40.  

Table of Contents

General Information

Berlin Criteria 1 Mn

  • Timing: Onset Must Be Within One Week of a Known Clinical Insult or New/Worsening Respiratory Symptoms
  • Chest Imaging: Bilateral Opacities (Not Fully Explained by Effusions, Lobar Collapse, or Nodules)
  • Origin: Respiratory Failure Cannot Be Fully Explained by Cardiac Failure or Fluid Overload
  • Oxygenation: PaO2:FiO2 < 300

Severity 1

  • *Based on PaO2/FiO2 (P:F Ratio)
  • Mild: P:F ≤ 300
  • Moderate: P:F ≤ 200
  • Severe: P:F ≤ 100

Prevalence 3

  • Mild: 30.0%
  • Moderate: 46.6%
  • Severe: 23.4%

Mortality

  • Overall High Mortality (37-43%) 4,5
  • Increases with Disease Severity 3,6
    • Mild: 27-35%
    • Moderate: 32-40%
    • Severe: 45-46%

Causes 7-10

  • Sepsis (31-43%) – Most Common Cause
  • Pneumonia (40-42.3%)
  • Aspiration (8-30%)
  • Trauma (9-17%)
  • Massive Transfusion/Transfusion-Related Acute Lung Injury (TRALI)
  • Pancreatitis
  • Inhalation Injury
  • Cardiothoracic Surgery
  • Medications
  • Drugs
  • Alcohol
  • *Risk Increased by Simultaneous Factors 7

Clinical Features 11,12

  • Dyspnea
  • Tachypnea
  • Tachycardia
  • Altered Mental Status
  • Respiratory Distress

ARDS on Chest X-Ray 2

Phases and Pathophysiology

Starling Equation 13

  • Describes Fluid Movement Between the Vasculature & Interstitium
  • Q = K x [(Pc – Pi) – σ (πc – πi)]
    • Q: Net Transvascular Flow
    • K: Filtration Coefficient of Endothelial Membrane Permeability
    • Pc: Capillary Hydrostatic Pressure
    • Pi: Interstitial Hydrostatic Pressure
    • σ: Reflection Coefficient of the Capillary Barrier
    • πc: Capillary Oncotic Pressure
    • πi: Interstitial Oncotic Pressure
  • Normal Lung Function Prevents Alveolar Edema 14
    • Retained Intravascular Proteins Increase Oncotic Pressure
    • Interstitial Lymphatic Reabsorb Large Volumes of Fluid
    • Tight Junctions Between Alveolar Epithelium Prevent Leakage

Stage 1 (Exudative Phase)

  • Characterized by Diffuse Alveolar Damage (DAD) 15
  • Occurs Over the First 7-10 Days
  • Effects:
    • Lung Injury Causes Release of Proinflammatory Cytokines (TNF, IL-1, IL-6, and IL-8) 16-19
      • Causes Inflammation and Edema
      • Cytokines Recruit Neutrophils Causing Release of Toxic Mediators that Further Damage Capillary/Alveolar Epithelium 20,21
    • Necrosis and Sloughing of Type I Pneumocytes and Capillary Endothelium 22
      • Loss of Tight Junctions that Normally Prevent Fluid Movement 22
    • Increased Vascular Permeability Causes an Inflammatory Exudate (Protein Rich Fluid) to Flood the Alveoli 23
    • Surfactant Inhibition Causes Collapse and Shunting 24
    • Hyaline Membranes Form within the Alveoli 25

Stage 2 (Fibroproliferative Phase)

  • Characterized by Proliferation of Type II Pneumocytes 23
  • Occurs After 7-10 Days
  • Generally Lasts About 14-21 Days
  • Effects:
    • Early Collagen Formation 26,27
    • Interstitial Infiltration of Myofibroblasts with Myointimal Thickening
    • Squamous Metaplasia 28
    • Decreased Compliance 29
  • Effects are Still Reversible

Stage 3 (Fibrotic Phase)

  • Characterized by Interstitial Fibrosis 30-32
  • Not a Universal Outcome Seen in All Patients
  • Associated with Prolonged Mechanical Ventilation and Increased Mortality 30,31

Complications

  • Impaired Gas Exchange & Hypoxemia 33
    • Primarily Due to a Ventilation-Perfusion Mismatch Due to Physiologic Shunting and Increased Dead Space 33
    • The Most Common Long-Term Defect in Recovered Patients is Decreased Diffusion Capacity 34
  • Decreased Lung Compliance 29
  • Barotrauma 35
  • Pulmonary Hypertension Due to Hypoxic Vasoconstriction, Vascular Compression Due to Positive Airway Pressure Ventilation, Airway Collapse, Parenchymal Destruction, and Hypercarbia 36

Diagnosis

Diagnosis 37

  • Clinical Diagnosis Based on the Berlin Criteria 1
  • Evaluation Should Focus on Identifying ARDS and the Underlying Cause
  • Laboratory Testing is Nonspecific
  • Imaging Includes CXR or CT
  • Exclude Acute Cardiogenic Pulmonary Edema by Clinical Evaluation, BNP, and/or Echocardiogram 38,39

Berlin Criteria 1 Mn

  • Timing: Onset Must Be Within One Week of a Known Clinical Insult or New/Worsening Respiratory Symptoms
  • Chest Imaging: Bilateral Opacities (Not Fully Explained by Effusions, Lobar Collapse, or Nodules)
  • Origin: Respiratory Failure Cannot Be Fully Explained by Cardiac Failure or Fluid Overload
  • Oxygenation: PaO2:FiO2 < 300

Severity 1

  • *Based on PaO2/FiO2 (P:F Ratio)
  • Mild: P:F ≤ 300
  • Moderate: P:F ≤ 200
  • Severe: P:F ≤ 100

Lung Injury Prediction Score (LIPS) 40

  • Scoring System to Evaluate the Risk for Developing ARDS
  • Features: 40
    • Predisposing Conditions:
      • Shock (+2 Points)
      • Aspiration (+2 Points)
      • Sepsis (+1 Points)
      • Pneumonia (+1.5 Points)
    • High-Risk Surgery:
      • Orthopedic Spine (+1 Points)
      • Acute Abdomen (+2 Points)
      • Cardiac (+2.5 Points)
      • Aortic Vascular (+3.5 Points)
      • Emergency Surgery (+1.5 Points)
    • High-Risk Trauma:
      • Traumatic Brain Injury (+2 Points)
      • Smoke Inhalation (+2 Points)
      • Near Drowning (+2 Points)
      • Lung Contusion (+1.5 Points)
      • Multiple Fractures (+1.5 Points)
    • Risk Modifiers:
      • Alcohol Abuse (+1 Points)
      • Obesity (BMI > 30) (+1 Points)
      • Hypoalbuminemia (+1 Points)
      • Chemotherapy (+1 Points)
      • FiO2 > 0.35 (> 4 L/min) (+2 Points)
      • Tachypnea (RR > 30) (+1.5 Points)
      • SpO2 < 95% (+1 Points)
      • Acidosis (pH < 7.35) (+1.5 Points)
      • Diabetes (Only if Sepsis) (-1 Points)
  • Interpretation: 41
    • Score ≤ 4: Low Risk of Developing ARDS
      • Negative Predictive Value 97% ­– Better at Defining Patients at Low Risk than Defining Patients at High Risk 41
    • Score > 4: High Risk of Developing ARDS
      • Sensitivity 69%, Specificity 78% 41

Treatment

Primary Treatment

  • Primarily Supportive Care 42
    • Treat Underlying Pathology
    • Nutritional Support 43
    • General Critical Care Managements (VTE Prophylaxis, Hemodynamic Monitoring, Stress Ulcer Prophylaxis)
    • Manage Patient-Ventilator Dyssynchrony
  • Lung Protective Ventilation 44
  • Conservative Fluid Management 45-47
    • Goal CVP < 4 mmHg or PAOP < 8 mmHg 45
    • May Require Diuretics as Long as the Patient is Hemodynamically Stable
    • Liberal Fluid Management Has a Higher Risk for Pulmonary Edema
    • Improves Ventilator-Free Days and ICU-Free Days 45
    • No Clear Mortality Benefit 45
    • Possibly an Increased Risk for Cognitive Impairment (Not Clear) 48

Lung Protective Ventilation

  • Definition: Ventilation with Low Tidal Volumes to Reduce Alveolar Overdistention & Barotrauma
    • Based Largely on ARDSnet Protocols 44
  • Improves Mortality for ARDS of All Severities 49-53
  • Ventilation (Tidal Volume/Respiratory Rate)
    • Initial Tidal Volume: 8 ml/kg x Ideal Body Weight (General Standard) 44
    • Decrease Tidal Volume 1 ml/kg Every 1-2 Hours 44
    • Goal Tidal Volume: 4-6 ml/kg x Ideal Body Weight 44
    • Initial Respiratory Rate Should Approximate Baseline Minute Ventilation (Not > 35 bpm) 44
    • Adjust Tidal Volume & Respiratory Rate for Goal Plateau Pressure ≤ 30 cm H2O 44
  • Oxygenation (PEEP/FiO2)
    • Oxygenation Goals: PaO2 55-80 mmHg or SpO2 88-95% 44
    • Adjust PEEP to Required FiO2
    • Initially Recommended to Start with Lower-PEEP Strategy 44
FiO20.30.40.50.60.70.80.91.0
PEEP55-88-101010-141414-1818-24
    • Consider High-PEEP Strategy if Refractory 44
FiO20.30.40.50.6-0.70.8-0.91.0
PEEP5-1414-1616-18202222-24
  • Complications:
    • Permissive Hypercapnia
      • Respiratory Acidosis Allowed to Maintain Low Tidal Volumes
      • Anticipated and Generally Well Tolerated 54,55
      • pH Goal: 7.30-7.45 44
        • If pH < 7.30: Increase Rate (Maximum 35 bpm) 44
        • If pH Remains < 7.15: Can Increase Tidal Volume in 1 ml/kg Increments Until pH > 7.15 44
      • PaCO2 Goal Not Well Defined
    • Patient-Ventilator Dyssynchrony

Adjuncts

  • Systemic Glucocorticoids (Steroids)
    • Indicated for Moderate-Severe ARDS Refractory to Standard Treatments
      • Generally Only Used if Early in the Disease Course (< 13-14 Days)
      • May Also Use Steroids if Otherwise Indicated for Other Underlying Conditions
    • Associated with Improved Mortality and Ventilator-Free Days 56-58
    • Initiation 13-14 Days After Onset was Associated with Increased Mortality 59-61
    • Dosing: Dexamethasone IV 20 mg Once Daily x5 Days, Then Reduce to 10 mg Daily for Another 5 Days – Based on DEXA-ARDS Study
      • *Dexamethasone is a Pure Glucocorticoid (Anti-Inflammatory Effects) without Mineralocorticoid Side Effects (Sodium Retention/Volume Overload)
  • Inhaled Pulmonary Vasodilators (Nitric Oxide/Prostacyclin)
    • Improves Oxygenation for Severe ARDS with Refractory Hypoxemia 62-65
    • No Proven Morbidity or Mortality Benefit 66
    • *See Ventilator Management
  • Paralysis/Neuromuscular Blockade
    • Generally Reserved Only for Severe ARDS with Refractory Hypoxemia
    • Early Short-Term (48 Hour) Paralytics May Improve Mortality in Severe ARDS (Debated with Conflicting Results) 67,68
  • Prone Positioning
    • Indicated for Severe ARDS with Refractory Hypoxemia 69
      • May Also Consider as a Bridge to ECMO
    • Associated with Improved Mortality for Severe ARDS 69,70
    • *See Ventilator Management
  • Extracorporeal Membrane Oxygenation (ECMO)
    • Considered for Acute Severe Pulmonary Failure that is Potentially Reversible & Unresponsive or Conventional Measures
    • Associated with Improved Mortality for Severe ARDS 71
    • *See Mechanical Circulatory Support
  • Alternative Modes of Ventilation:

Mnemonics

Berlin Criteria for ARDS

  • “ABC-3”
  • Acute Onset (< 7 Days)
  • Bilateral Opacities
  • CHF Not Fully Explained
  • P:F < 300

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