Acute lung injury and acute respiratory distress syndrome (ARDS) are challenging and frequently lethal respiratory disorders encountered in veterinary medicine. These disorders have been recognized since the late 1960s in human medicine1 but have only recently been defined in the veterinary community.2 While you may not commonly encounter these conditions in general practice, it is important to be familiar with them as complications of critical illness. Early recognition of acute lung injury and ARDS is essential in helping you make the best treatment decisions, which may include early referral, since affected animals usually require 24-hour critical care.
Acute lung injury and ARDS are severe disturbances in respiration that result in hypoxemia, tachypnea, dyspnea, and death in about 50% of affected people.3 ARDS is the more severe form of acute lung injury; it has a specific and more severe level of hypoxemia.
Acute lung injury and ARDS are always considered to be secondary to a primary respiratory disease or systemic disorder (Table 1).2,3 The most common causes in dogs are thought to be bacterial or aspiration pneumonia, sepsis, or shock.4 Critical illness can be complicated by multiple organ dysfunction syndrome, causing multiple organ failure including pulmonary failure or acute lung injury and ARDS. Acute lung injury and ARDS are suspected to occur in cats based on pathologic findings at necropsy examination in septic cats, but these disorders are less understood in this species.5 Clinically, acute lung injury and ARDS are not commonly appreciated in cats.
Table 1: Known Risk Factors for Acute Lung Injury and ARDS*
The primary insult that results in acute lung injury and ARDS produces systemic and respiratory tissue inflammation with ensuing release of macrophages, neutrophils, and inflammatory cytokines. These cells and cytokines directly damage the epithelial integrity of type I pneumocytes, which are the primary cell type that line alveoli and are involved in gas exchange. The endothelial lining of blood capillaries in the lung tissue is also directly damaged, allowing for increased permeability.3,6,7 The damage to these two cell layers and subsequent increased permeability result in extravasation of a high-protein fluid (edema) into lung parenchyma and alveolar spaces. Pulmonary edema causes poor oxygen exchange in the lungs, decreased lung compliance, and increased ventilation-perfusion (V/Q) mismatch; in acute lung injury and ARDS, this edema is considered noncardiogenic.3,6,7
Three phases of acute lung injury and ARDS have been identified in people (see boxed text titled "Phases of acute lung injury and ARDS").
Phases of acute lung injury and ARDS