Definition
A.Acute respiratory distress syndrome (ARDS) is defined by three variables.
1.Bilateral opacities on imaging.
2.Onset within 7 days of a clinical event or worsening respiratory symptoms.
3.Origin of pulmonary edema not fully explained by cardiac failure or volume overload.
B.ARDS is identified as mild, moderate, or severe based on the PF ratio (PaO2/FiO2).
C.Acute lung injury does not exist in the new definition of ARDS.
D.Exclusion of heart failure is not required in the new definition of ARDS.
Incidence
A.It is difficult to obtain an accurate incidence due to variations in the definition used to identify or describe ARDS.
B.An estimated 200,000 cases of ARDS occur each year in the United States.
C.The incidence increases with advancing age.
D.ARDS has not been shown to occur more in one sex than the other.
E.Mortality and morbidity are associated with worsening of the PF ratio.
Pathogenesis
A.An indirect or direct insult causes an inflammatory response and accumulation of pro-inflammatory mediators in the lung microcirculation. Injury occurs to the microvascular endothelium and alveolar epithelium. Endothelium injury leads to capillary permeability and migration of protein-rich fluid into the alveolar space. Due to injury of the alveolar epithelium, pulmonary edema forms and damage occurs to the cells lining the alveoli.
B.Damage to type I and II cells leads to decreased clearance of fluid in the pleural space, increased fluid entry into the alveoli, and decreased surfactant production resulting in decreased alveolar compliance and alveoli collapse.
C.An influx of fibroblasts leads to collagen deposition and possibly fibrosis.
Predisposing Factors
A.Aspiration, including gastric content and drowning.
B.Sepsis.
C.Pneumonia.
D.Massive transfusions.
E.Pancreatitis.
F.Burns.
G.Trauma, including cases with and without pulmonary injury.
H.Underlying interstitial lung disease.
Subjective Data
A.Common complaints/symptoms.
1.Severe dyspnea.
2.Chest discomfort.
3.Tachypnea.
B.Common/typical scenario.
1.Onset is typically 12 to 48 hours after the insult.
2.History shows progressive worsening symptoms.
3.Extrapulmonary complaints may have led to the development of ARDS.
Physical Examination
A.Dyspnea (see Figure 2.1).
B.Tachypnea.
C.Abdominal retractions; obvious respiratory distress.
D.Hypoxia and possibly cyanosis.
E.Tachycardia.
F.Altered mental status, agitation, or confusion.
G.Rales during auscultation.
H.Additional findings that may relate to the underlying etiology of ARDS (e.g., febrile, hypotension, an acute abdomen, or nausea and vomiting seen in pancreatitis).
Diagnostic Tests
A.Chest x-ray (CXR).
1.Patchy infiltrates rapidly evolve and progress to diffuse, bilateral infiltrates.
2.Daily CXRs may be required, especially for patients on mechanical ventilation.
B.Arterial blood gas (ABG).
1.Regular ABGs are required to evaluate management.
2.Development of respiratory acidosis (decreased pH and rising CO2).
3.Hypoxemia is defined by the PF ratio.
a.Less than 300: As mild ARDS.
b.Less than 200: Moderate ARDS.
c.Less than 100: Severe ARDS.
C.Complete blood count (CBC).
1.Evaluate the white blood cell count and platelets.
D.Comprehensive metabolic panel.
1.Evaluate renal and liver function.
FIGURE 2.1 Algorithm for the evaluation of dyspnea.
JVD, jugular venous distention; NT-proBNP, N-Terminal pro brain natriuretic peptide.
2.Magnesium and phosphorus. Strict electrolyte repletion is necessary for cardiac stability and prevention of arrhythmias, especially in the setting of profound tissue hypoxia and/or septic shock, which is often concomitant.
E.Coagulation studies.
1.Prothrombin time and international normalized ratio.
2.Fibrinogen level.
3.Fibrin degradation products.
F.N-Terminal pro brain natriuretic peptide level.
1.This is used to assess for heart failure causing or contributing to the bilateral infiltrates and hypoxemia.
2.It is important for the clinician to note that this value may be elevated secondary to etiologies other than heart failure, such as sepsis and renal failure.
G.Blood cultures.
1.Evaluate infective etiology as a source for ARDS development.
H.Systemic infection markers.
1.Lactic acid. Measure level of end-organ tissue hypoxia and consider trend.
2.Procalcitonin. Consider trend every 24 hours and monitor for effectiveness of treatment of the primarily offending process.
I.Urinalysis and urine culture.
1.Evaluate infective etiology as source for ARDS development.
J.Sputum culture.
1.Evaluate infective etiology as source for ARDS development.
Differential Diagnosis