DESCRIPTION

• Acute respiratory distress syndrome (ARDS) is a diffuse inflammatory form of lung injury. It is defined as the onset of acute hypoxemia after at least 6 hours and up to 7 days after the onset of a known clinical insult. This is not a primary diagnosis, rather it is triggered by other primary diagnoses such as sepsis, trauma, pancreatitis. ARDS presents as new or worsening respiratory symptoms with bilateral alviolar infiltrates on imaging.
• The severity of ARDS is defined by the extent of hypoxia present, measured by the PF ratio, which is the ratio of partial pressure of arterial oxygen (PaO₂) to the fraction of inspired oxygen (FiO₂).
  • Mild distress corresponds with a ratio of 200 mm Hg < PaO₂/FiO₂ ≤300 mm Hg
  • Moderate distress corresponds with a ratio of 100 mm Hg < PaO₂/FiO₂ ≤200 mm Hg
  • Severe distress corresponds with a ratio of PaO₂/FiO₂ ≤100 mm Hg
• Synonym(s): acute lung injury; increased-permeability pulmonary edema; noncardiac pulmonary edema
• Systems affected: pulmonary, cardiovascular

EPIDEMIOLOGY

ETIOLOGY AND PATHOPHYSIOLOGY

• ARDS is a response to direct or indirect alveolar injury leading to diffuse alveolar damage.
  • Direct
    • Pneumonia (bacterial, viral, fungal, or opportunistic)
    • Aspiration of gastric contents
    • Near drowning
    • Pulmonary contusion
    • Inhalation injury
  • Indirect
    • Sepsis (nonpulmonary)
    • Shock
    • Transfusion-related acute lung injury (TRALI)
    • Major burn injury
    • Nonthoracic trauma
    • Drug overdose
    • Cardiopulmonary bypass
    • Reperfusion edema after lung transplant or embolectomy
• The 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. This is followed by hyaline membrane formation leading to alveolar collapse.
  • Proliferative phase—the second 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 begins which leads to expression of aquaporin and ion channels, aiding in the reabsorption of fluid.
  • Fibrotic phase—the final phase, not experience by every patient, is characterized by prolonged mechanical ventilation and associated with increased mortality.

RISK FACTORS

• Patients that are low-risk may be identified by a lung injury prevention score; however, this score is less accurate in high risk patients.
• There are several risk factors that predispose patients to developing ARDS. These include advanced age, female sex, smoking, alcohol use, aortic or cardiovascular surgeries, and traumatic brain injury.
• Increased levels of markers of systemic inflammation have been associated with adverse outcomes.

GENERAL PREVENTION

To date, there has been no effective strategy proven to prevent developing ARDS; however, measures can be taken to mitigate risk factors. Early lung protective ventilation and sepsis management have both been shown to improve clinical outcomes in ARDS.

COMMONLY ASSOCIATED CONDITIONS

• Pneumonia, sepsis, and aspiration of gastric contents cause 85% of ARDS cases in the medical ICU setting.
• Other causes can include:
  • Trauma
  • Burns
  • Cardiothoracic surgery
  • Pancreatitis
  • Inhalational injuries and near drownings
  • TRALI
  • Shock
  • Medication toxicity