Acute respiratory distress syndrome

Direct injuries to lungs Indirect injuries
Pneumonia Sepsis
• Gastric contents
• Near-drowning
• Hydrocarbons/solvents
Severe trauma
• Multiple fractures
• Head injury
• Burns
Smoke or toxic gas inhalation Pancreatitis
Pulmonary contusion Multiple blood transfusions
• Thromboembolism
• Fat embolism
• Amniotic fluid embolism
Oxygen toxicity
Reperfusion pulmonary edema
Drug toxicity
• Salicylates
• Hydrochlorothiazide
• Opiates
• Amiodarone
• Cyclosporine
• Tricyclic antidepressants
• Chemotherapeutic agents
Cardiopulmonary bypass
High-altitude exposure


Classic presentation

  • This condition typically manifests in one of two ways:

    • Shortly after the patient’s initial presentation, as in someone who has just sustained a major insult – such as significant smoke inhalation in a fire or near-drowning
    • Several days after admission, in severely ill patients whose initial presentation was more indolent – such as a patient with urosepsis.

  • In the acute, exudative phase of ARDS, damage to the lungs causes fluid to leak across the alveolar-capillary basement membrane, causing alveolar edema and subsequent hypoxemia.

    • As a result of alveolar edema, surfactant activity is significantly compromised and lung compliance decreases

  • The acute phase of ARDS can progress to a fibrotic phase, in which case patients will exhibit continued hypoxemia, increasing dead space, pulmonary hypertension, and even greater loss of lung compliance.
  • Pulmonary edema in ARDS is heterogeneous and leads to atelectatic or consolidated areas of lung interspersed with relatively unaffected regions, creating areas of intrapulmonary shunt, which results in hypoxemia that does not improve with oxygen administration alone.

Critical presentation

  • As pulmonary edema accumulates in the initial exudative phase of the disease, patients will become dyspneic and will demonstrate increased work of breathing.
  • Due to worsening lung compliance, tidal volumes will decrease and respiratory rate will increase. Patients will become progressively hypoxemic due to both worsening V/Q mismatch and shunt physiology.
  • As above, patients may present to the ED in hypoxemic respiratory failure due to a rapidly progressive etiology, or they may present late.
  • Patients may deteriorate rapidly during their ED course despite appropriate therapy.

Diagnosis and evaluation

  • The diagnosis of ARDS is made clinically based on a standardized definition:

    • The syndrome must develop within one week of a known clinical insult or worsening pulmonary symptoms.
    • Chest imaging demonstrates bilateral opacities not fully explained by lobar collapse, nodules, or effusions.
    • The respiratory failure is not fully explained by cardiac failure or volume overload. If a known risk factor for ARDS is not present, objective assessment such as echocardiography should be obtained to rule out hydrostatic edema.
    • The PaO2/FiO2 ratio is <300 on at least 5 cmH2O of positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP).

ARDS degree PaO2/FiO2 ratio
Mild 200–300
Moderate 100–200
Severe <100

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Feb 17, 2017 | Posted by in CRITICAL CARE | Comments Off on Acute respiratory distress syndrome

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