Respiratory Distress Syndrome, Acute (ARDS)

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Basics

Description

  • Acute respiratory distress syndrome (ARDS) is defined as the onset of acute hypoxemia within 7 days of a known clinical insult or new or worsening respiratory symptoms with bilateral opacities (patchy, diffuse, or homogenous) consistent with pulmonary edema on imaging. This respiratory failure is not explained by cardiac failure or fluid overload, and no evidence of left atrial hypertension is present.
  • Severity of ARDS depends on oxygenation of the blood. It is measured with a ratio of partial pressure of arterial oxygen (PaO2) to fraction of inspired oxygen (FiO2) at a positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) of at least 5 cm H2O.
    • Mild: 200 mm Hg < PaO2/FiO2 ≤300 mm Hg
    • Moderate: 100 mm Hg < PaO2/FiO2 ≤200 mm Hg
    • Severe: PaO2/FiO2 ≤100 mm Hg
  • Synonym(s): acute lung injury; increased-permeability pulmonary edema; noncardiac pulmonary edema
  • Systems affected: pulmonary, cardiovascular

Epidemiology

Incidence
  • Incidence of ARDS is highly variable and under-recognized.
  • Highest incidence rate is in United States of 78.9/100,000 person-years.

Etiology and Pathophysiology

  • ARDS is a response to alveolar injury, which can be direct or indirect, that produces diffuse alveolar damage.
    • Direct
      • Aspiration of gastric contents
      • Pneumonia (bacterial, viral, fungal, or opportunistic infections)
      • Air, fat, or amniotic fluid emboli
      • Near drowning
      • Pulmonary contusion
      • Inhalation injury
    • Indirect
      • Sepsis (nonpulmonary source)
      • Shock
      • Transfusion
      • Major burn injury
      • Nonthoracic trauma
      • Drug overdose
      • Pancreatitis, severe
      • Cardiopulmonary bypass
      • Reperfusion edema after lung transplant or embolectomy
      • Eclampsia
  • Progression of the diffuse alveolar damage in ARDS is divided into three phases.
    • Exudative phase: The initial highly inflammatory phase when alveolar macrophages are activated due to lung injury, leading to complement activation, release of pro-inflammatory mediators, and activation of neutrophils. This causes epithelial–endothelial barrier disruption leading to intra-alveolar and extra-alveolar flooding with fluid, and is followed by hyaline membrane formation leading to alveolar collapse.
    • Fibroproliferative phase: characterized by fibroblasts, myofibroblasts, and alveolar epithelial cell (ACE) II mediated repair. Formation of new matrix, differentiation into ACE I, and formation of cellular junctions begin which leads to expression of aquaporin and ion channels, aiding in the reabsorption of fluid.
    • Fibrotic phase: Not every patient progresses to this phase; is related to prolonged mechanical ventilation and associated with increased mortality.

General Prevention

Good ICU practices like low tidal volumes in all mechanically ventilated patients, early resuscitation and antibiotics for sepsis, restrictive use of blood products, and intensivist involvement may help prevent nosocomial ARDS.

Commonly Associated Conditions

  • Pneumonia, sepsis, and aspiration of gastric contents lead to 85% of ARDS cases, with sepsis being the most common cause.
  • Other causes include:
    • Trauma
    • Burns
    • Cardiothoracic surgery
    • Pancreatitis
    • Inhalational injuries and near drowning
    • Transfusion-related acute lung injury (TRALI)
    • Shock
    • Medication toxicity

-- To view the remaining sections of this topic, please or --

Basics

Description

  • Acute respiratory distress syndrome (ARDS) is defined as the onset of acute hypoxemia within 7 days of a known clinical insult or new or worsening respiratory symptoms with bilateral opacities (patchy, diffuse, or homogenous) consistent with pulmonary edema on imaging. This respiratory failure is not explained by cardiac failure or fluid overload, and no evidence of left atrial hypertension is present.
  • Severity of ARDS depends on oxygenation of the blood. It is measured with a ratio of partial pressure of arterial oxygen (PaO2) to fraction of inspired oxygen (FiO2) at a positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) of at least 5 cm H2O.
    • Mild: 200 mm Hg < PaO2/FiO2 ≤300 mm Hg
    • Moderate: 100 mm Hg < PaO2/FiO2 ≤200 mm Hg
    • Severe: PaO2/FiO2 ≤100 mm Hg
  • Synonym(s): acute lung injury; increased-permeability pulmonary edema; noncardiac pulmonary edema
  • Systems affected: pulmonary, cardiovascular

Epidemiology

Incidence
  • Incidence of ARDS is highly variable and under-recognized.
  • Highest incidence rate is in United States of 78.9/100,000 person-years.

Etiology and Pathophysiology

  • ARDS is a response to alveolar injury, which can be direct or indirect, that produces diffuse alveolar damage.
    • Direct
      • Aspiration of gastric contents
      • Pneumonia (bacterial, viral, fungal, or opportunistic infections)
      • Air, fat, or amniotic fluid emboli
      • Near drowning
      • Pulmonary contusion
      • Inhalation injury
    • Indirect
      • Sepsis (nonpulmonary source)
      • Shock
      • Transfusion
      • Major burn injury
      • Nonthoracic trauma
      • Drug overdose
      • Pancreatitis, severe
      • Cardiopulmonary bypass
      • Reperfusion edema after lung transplant or embolectomy
      • Eclampsia
  • Progression of the diffuse alveolar damage in ARDS is divided into three phases.
    • Exudative phase: The initial highly inflammatory phase when alveolar macrophages are activated due to lung injury, leading to complement activation, release of pro-inflammatory mediators, and activation of neutrophils. This causes epithelial–endothelial barrier disruption leading to intra-alveolar and extra-alveolar flooding with fluid, and is followed by hyaline membrane formation leading to alveolar collapse.
    • Fibroproliferative phase: characterized by fibroblasts, myofibroblasts, and alveolar epithelial cell (ACE) II mediated repair. Formation of new matrix, differentiation into ACE I, and formation of cellular junctions begin which leads to expression of aquaporin and ion channels, aiding in the reabsorption of fluid.
    • Fibrotic phase: Not every patient progresses to this phase; is related to prolonged mechanical ventilation and associated with increased mortality.

General Prevention

Good ICU practices like low tidal volumes in all mechanically ventilated patients, early resuscitation and antibiotics for sepsis, restrictive use of blood products, and intensivist involvement may help prevent nosocomial ARDS.

Commonly Associated Conditions

  • Pneumonia, sepsis, and aspiration of gastric contents lead to 85% of ARDS cases, with sepsis being the most common cause.
  • Other causes include:
    • Trauma
    • Burns
    • Cardiothoracic surgery
    • Pancreatitis
    • Inhalational injuries and near drowning
    • Transfusion-related acute lung injury (TRALI)
    • Shock
    • Medication toxicity

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