Respiratory dysfunction commonly occurs as a sequela of critical illness in dogs and cats. Early detection of pulmonary compromise
allows early recognition of problems, aggressive management, and therefore increased survival. Apart from frequent and relatively
benign complications such as fluid overload and atelectasis, other pulmonary complications in the critical patient reflect
the lung response to inflammation as part of the Systemic Inflammatory Response Syndrome (SIRS), immunosuppression, and failure
of lung defenses. The complications most commonly seen include the canine acute respiratory distress syndrome, bacterial pneumonia,
and thromboembolic disease.
Canine acute respiratory distress syndrome
The canine acute respiratory distress syndrome (ARDS) is an acute, usually fatal, complication of a number of disease states,
particularly sepsis. In sepsis, a diffuse inflammatory process is triggered by bacterial endotoxin, which results in activation
of an avalanche of diverse inflammatory mediators, including a variety of cytokines, the complement and arachidonic acid cascades,
and cells such as neutrophils and macrophages. This common pathway of inflammation can affect the function of any or all organ
systems in the septic patient. Patients that develop respiratory failure due to ARDS are simply demonstrating a local pulmonary
manifestation of SIRS. Alternatively, ARDS may be triggered by local pulmonary catastrophes such as severe aspiration pneumonia,
pulmonary contusions or smoke inhalation, which can trigger an inflammatory response that may become generalized within the
lung parenchyma. In either case, since the lung has only one way to respond to inflammatory damage, the clinical and histopathologic
findings are very similar.
In dogs with ARDS, the initial stages of the syndrome begin as a diffuse exudative vascular leak syndrome, with infiltration
of neutrophils and macrophages into the lung. These changes are accompanied by effusion of protein-rich fluid into the alveoli,
and clinical evidence of progressive pulmonary edema. As ongoing inflammation is combined with early attempts at repair by
the lung tissue, we begin to see proliferation of Type II pneumocytes, formation of hyaline membranes within alveoli due to
organization of protein-rich fluid and cellular debris, deficiency of surfactant, and collapse and atelectasis of alveoli.
Much later, these changes are followed by interstitial fibrosis as the lung attempts to repair the damaged tissue. The inflammatory
changes in the lung may vary in severity, and are usually unevenly distributed, affecting ventral areas first. At times, the
process is mild and then termed Acute Lung Injury (ALI). In more severely affected animals, the inflammation is profound,
overwhelming, and leads to severe hypoxia (ARDS).
ARDS is recognized clinically by the development of pulmonary edema in an animal with a predisposing cause of an inflammatory
response. Animals that have ARDS are in severe respiratory distress, and are usually cyanotic. Auscultation reveals harsh
lung sounds that rapidly progress to crackles. Dogs may expectorate pink foam, and if intubated, sanguinous fluid may drain
out of the endotracheal tube. Arterial blood gases usually reveal hypoxia and hypocarbia, and metabolic acidosis may be present.
These animals usually have diffuse bilateral pulmonary alveolar infiltrates throughout all lung fields on thoracic radiographs.
Most dogs and cats with ARDS show little response to oxygen supplementation, and remain severely dyspneic. If placed on a
ventilator, the lungs are found to have very poor compliance, and high peak airway pressures may be seen even if the tidal
volume is small. Positive end expiratory pressure is usually required to achieve adequate oxygenation.
Few options are available for definitive management of ARDS and patient care is primarily aimed at treating the underlying
cause and supporting oxygenation. In humans, there is a very high mortality rate, and even those who survive require positive
pressure ventilation for several weeks. Obviously, this is beyond the capability of most veterinarians. Because of the variety
of inflammatory cascades and cells that mediate the inflammatory response in ARDS, specific anti-inflammatory drugs such as
corticosteroids are largely ineffective for treatment, and may cause immunosuppression that can exacerbate sepsis. Advances
such as liquid ventilation, synthetic surfactant therapy, inhaled nitric oxide, and other new drugs, which have begun to be
useful in human medicine, have not yet been evaluated in dogs with naturally occurring disease.
