Acute Respiratory Distress Syndrome (ARDS)

Background

• Acute respiratory distress syndrome (ARDS) is a clinical syndrome of diffuse lung injury characterized by acute onset with hypoxemia and bilateral radiographic infiltrates and without left atrial hypertension.
• The 2012 Berlin definition (replacing the prior 1994 American-European Consensus Conference definition) of acute respiratory distress syndrome consists of:
  • onset within 1 week of a known clinical insult or new or worsening respiratory symptoms
  • bilateral opacities not fully explained by effusions, lobar/lung collapse, or nodules on chest x-ray or computed tomography
  • respiratory failure not fully explained by a cardiac failure or fluid overload (in the absence of risk factors for ARDS, an objective assessment such as echocardiography is required to exclude these causes of hydrostatic edema)
  • impaired oxygenation status:
    • mild ARDS is defined as a PaO₂/FiO₂ > 200 mm Hg but ≤ 300 mm Hg with positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥ 5 cm H₂O
    • moderate ARDS is defined as PaO₂/FiO₂ > 100 mm Hg but ≤ 200 mm Hg with PEEP ≥ 5 cm H₂O
    • severe ARDS is defined as PaO₂/FiO₂ ≤ 100 mm Hg with PEEP ≥ 5 cm H₂O
  • The mortality of ARDS varies with its severity:
    • mild is associated with 27% mortality
    • moderate is associated with 32% mortality
    • severe is associated with 45% mortality
• ARDS can be caused by direct lung injury or indirectly by inflammatory processes focused in other organs:
  • The most common causes of direct lung injury leading to ARDS are pneumonia and aspiration of gastric contents.
  • The most common causes of indirect lung injury leading to ARDS are nonpulmonary sepsis, severe trauma, and large amounts of blood transfused over a short period of time (> 8 units/24 hours, termed transfusion related acute lung injury [TRALI]).

Evaluation

• Perform a complete blood count (CBC) with differential to evaluate for possible sepsis or infection as the underlying cause.
• Perform an arterial blood gas (ABG) to calculate the PaO₂/ FiO₂ (per Berlin Definition checked on positive end-expiratory pressure [PEEP] ≥ 5 cm H₂O) to classify acute respiratory distress syndrome as mild, moderate, or severe.
• Obtain a chest x-ray and consider a chest computed tomography (CT) to evaluate for pulmonary infiltrates.
• Obtain an echocardiogram and brain natriuretic peptide level to evaluate for cardiogenic causes of the pulmonary infiltrates.
• Consider a bronchoscopy and bronchoalveolar lavage if other causes suspected if patient not showing improvement, or (in extremely select cases) an open lung biopsy, to help determine the underlying cause if the patient is clinically stable enough to tolerate the procedure.

Management

• Treat the underlying cause (such as pneumonia or shock) if it is known as well as associated complications (such as renal failure or disseminated intravascular coagulaltion).
• Mechanical ventilation supports gas exchange while waiting for the illness to resolve and is the mainstay of supported care.
  • Barotrauma and oxygen toxicity from mechanical ventilation can contribute to lung injury so the goal should be to maintain adequate rather than "normal" gas exchange to minimize any lung injury.
  • The standard ARDSNet protocol for mechanical ventilation for patients with acute respiratory distress syndrome (ARDS) states:
    • set the initial tidal volume to 8 mL/kg predicted body weight and reduce the tidal volume by 1 mL/kg at ≤ 2-hour intervals until the tidal volume is 6 mL/kg predicted body weight
    • set the initial respiratory rate to the approximate baseline minute ventilation (not more than 35 breaths per minute)
    • adjust the tidal volume (with goal ≤ 6 mL/kg predicted body weight) and respiratory rate to achieve a pH goal of 7.3-7.45 and plateau pressure goal of ≤ 30 cm H₂O
    • adjust fraction of inspired oxygen (FIO2) to maintain PaO₂ 55-80 mm Hg (SpO₂ 88%-95%)
    • consider using the incremental fraction of inspired oxygen (FiO₂/positive end-expiratory pressure [PEEP] combinations) to achieve the oxygenation goal
  • Use prone positioning for > 12 hours/day early after initiation of ventilation in patients with severe ARDS; consider ≥ 16 hours/day, especially in patients with severe hypoxemia (such as requiring FiO₂ > 60%) despite high PEEPs and tidal volumes ≤ 8 mL/kg.
  • Utilize PEEP to maintain oxygenation and to prevent trauma caused by atlectasis. Use the lowest PEEP that allows reduction of FiO₂ to ≤ 60%.
  • Consider using higher PEEP in select patients for lung recruitment, which can potentially reduce mortality and reduce the duration of mechanical ventilation. Higher PEEP strategies are likely to be most beneficial in those with severe ARDS, and those who have lung recruitability. Importantly, higher PEEP is associated with decreased venous return, reduced cardiac output and resulting hypotension.
  • The optimal ventilator settings may require heavy sedation and even neuromuscular blockade if sedation and analgesics do not achieve patient-ventilator synchrony.
• Use conservative fluid management in patients with ARDS to reduce the need for mechanical ventilation and shorten the duration of intensive care unit (ICU) stay..
• Corticosteroids have conflicting evidence regarding their effect on mortality in adults with ARDS.
  • Their benefit may depend on the underlying etiology.
    • There is no significant difference in mortality in patients with unselected ARDS or sepsis-related ARDS.
    • The evidence suggests increased mortality in ARDS associated with influenza.
    • The evidence suggests decreased mortality in postoperative ARDS.
  • Use may be considered in early moderate to severe ARDS with partial pressure of oxygen in arterial blood (PaO₂) to fraction of inspired oxygen (FiO₂) of < 200 and within 14 days.
• Consider using extracorporeal membrane oxygenation (ECMO) to improve survival in a patient with severe respiratory failure that is not responsive to above management.