CLINICAL RESPIRATORY CARE
ACUTE RESPIRATORY DISTRESS SYNDROME by Bill Wojciechowski, MS, RRT
he expression acute respiratory distress syndrome (ARDS) emerged from the American-European Consensus Conference on
ARDS in 1994. Previous to that date, the designation adult respira- tory distress syndrome, introduced by Ashbaugh in 1967, was used to describe this condition. Before 1967, ARDS was described by nu- merous terms which included: Da Nang lung, white lung syndrome, pump lung, shock lung, wet lung, stiff lung syndrome, adult hyaline membrane disease, & adult respiratory insufficiency. In addition to renaming ARDS in 1994, the American-European
Consensus Conference on ARDS standardized the definition of this syndrome and established clinical criteria used to differentiate ARDS from acute lung injury (ALI). The criteria used to define ARDS and ALI are listed below.
Clinical Criteria Used to Differentiate ARDS from ALI
Criteria Defining ARDS • onset: acute • oxygenation: PaO2/FIO2 < 200 • chest radiography: bilateral pulmonary infiltrates • hemodynamic monitoring: pulmonary capillary wedge pressure <18 torr, or absence of left atrial hypertension.
Criteria Defining ALI
• onset: acute • oxygenation: PaO2/FIO2 < 300 • chest radiography: bilateral pulmonary infiltrates • hemodynamic monitoring: pulmonary capillary wedge pressure <18 torr, or absence of left atrial hypertension. Interestingly, the response among patients to injury varies. Some
patients develop ARDS and others ALI. Still, others demonstrate no signs and symptoms. Despite the attention received by ARDS over the years, a dismal
clinical outcome continues to be associated with this syndrome. Al- though its pathophysiology has been extensively studied and re- searched, mortality rates remain high, i.e., around 50% to 60%. Relatively recent mechanical ventilation strategies such as permissive hypercapnia and the use of low tidal volumes have somewhat im- proved the prognosis.
Epidemiology According to the American Lung Association, the incidence of
ARDS ranges between 1.5 and 75 per 100,000 persons each year in the United States. According to the American-European Consensus Conference on ARDS, approximately 150,000 people in the United States develop ARDS every year. In light of the high mortality rate associated with ARDS, the ac-
tual survivability depends on multiple factors. These factors include predisposing conditions, severity of illness, age, comorbid condi-
tions, and, in patients with trauma, severity of the underlying pul- monary injury.
Etiology Acute respiratory distress syndrome is not a disease per se.
ARDS is a syndrome, encompassing a complex array of signs and symptoms. It can also be viewed as a life-threatening complica- tion of some other disease or condition. ARDS is a medical emergency that has multiple causes. The
conditions producing ARDS are often classified into two cate- gories: direct lung (pulmonary) injury and indirect lung (nonpul- monary) injury. Causes of ARDS resulting from direct lung injury include the following conditions: pneumonia, aspiration of gastric contents, pulmonary contusion, fat embolism, smoke/chemical inhalation, near-drowning, and re-perfusion pulmonary edema. The lungs are the primary site of injury for these conditions Conditions that cause ARDS from indirect lung injury in-
clude: sepsis, burns, acute pancreatitis, drug overdose, multiple trauma, cardiopulmonary bypass, and multiple blood transfu- sions. These disparate causes share a commonality in their rela- tionship with ARDS. They all produce acute inflammation of the alveolar-capillary membrane despite a site other than the lungs being the primary location of injury. Among the causes of ARDS, sepsis is the most common.
However, other factors such as blood transfusions, advanced age, and cigarette smoking increase the risk of developing ARDS.
Pathophysiology The primary abnormality in ARDS is the disruption of the
alveolar-capillary membrane. The breakdown of this barrier results in alveolar and pulmonary capillary permeability. This increased permeability leads to pulmonary interstitial and alveolar edema. This protein-rich fluid floods the alveoli. Neutrophils and macrophages are summoned to the site of
the pulmonary capillary endothelium. There these scavengers cells release cytokines (interleukins and tumor necrosis factor), oxygen radicals, arachidonic acid metabolites (leukotrienes and prostaglandins), and proteolytic enzymes (elastase and collage- nase). These mediators produce an inflammatory response and are responsible for damage to the alveolar epithelium and the cap- illary endothelium, resulting in increased alveolar-capillary per- meability. As a consequence to the cellular damage and the alveolar
flooding, pulmonary surfactant is inactivated. The sequel to the inactivation of pulmonary surfactant is an increase in the surface tension within the alveoli. This development causes alveolar col- lapse, capillary shunting, a decreased functional residual capacity, decreased lung compliance, and an in-
continued on page 8 Focus Journal Fall 2011 7
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