Risk
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Recent data estimates the incidence at 190,000 cases per year in USA. True incidence is unknown due to difficulty in defining the disease and making the diagnosis.
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Represents 10.4% of all ICU admissions and 23.4% of pts requiring mechanical ventilation per a recent 2016 publication.
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Mortality rates vary from 25% to 40%. Mortality rate is strongly influenced by associated conditions (e.g., higher when associated with sepsis, liver disease, and advanced age; lower with trauma, transfusion-related lung injury, drug overdose, or other reversible conditions).
Perioperative Risks
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Increased risk of sudden and profound hypoxia secondary to loss of alveolar recruitment
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Worsening resp status due to effects of anesthesia and surgery
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Difficult balance between maintaining adequate intravascular volume and avoiding pulm edema and right heart strain leading to decreased oxygenation and ventilation
Perioperative Risks
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Increased risk of sudden and profound hypoxia secondary to loss of alveolar recruitment
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Worsening resp status due to effects of anesthesia and surgery
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Difficult balance between maintaining adequate intravascular volume and avoiding pulm edema and right heart strain leading to decreased oxygenation and ventilation
Overview
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Berlin definition of ARDS (published in 2012) requires each of the following criteria:
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Timing—onset within 1 week of a known clinical insult or new or worsening resp symptoms.
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Chest imaging (CXR or CT)—bilateral opacities; not fully explained by effusions, lobar/lung collapse, or nodules.
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Origin of edema—resp failure not fully explained by cardiac failure or fluid overload, need objective assessment (ECHO) to exclude cardiogenic pulm edema.
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Oxygenation:
Mild—PaO 2 /FiO 2 200 to 300 mm Hg with PEEP or CPAP ≥ 5 cm H 2 O.
Mod—PaO 2 /FiO 2 100 to 200 mm Hg with PEEP ≥ 5 cm H 2 O.
Severe PaO 2 /FiO 2 ≤ 100 mm Hg with PEEP ≥ 5 cm H 2 O.
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Though classically defined by severe hypoxia, also can be associated with profound hypercarbia due to elevated alveolar dead space.
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Associated with low pulm compliance and lung volumes (due to alveolar edema and atelectasis) and, in certain pts, with abnormally low chest wall compliance.
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Most deaths are from sepsis or multisystem organ failure (more rarely from refractory hypoxemia or hypercarbia).
Etiology
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Direct or indirect lung injury leading to acute inflammatory alveolar damage characterized by increased microvascular permeability with interstitial and alveolar edema and often progressing to fibrosis.
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Precipitants include aspiration, pneumonia, sepsis, massive transfusion, pancreatitis, trauma, ischemia-reperfusion, drugs and alcohol, CNS injury, air embolism, cardiopulmonary bypass, genetic predisposition.
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Mechanical ventilation may worsen lung injury through alveolar overdistention and shear forces from cyclic opening and closing of collapsed alveoli (ventilator-associated lung injury).