Q What are some pulmonary complications in dogs that I might see in my practice?
A Dr. Lesley G. King at the 2004 Western Veterinary Conference in Las Vegas gave a lecture on pulmonary complications of critical
illness in dogs. Some relevant points in this lecture are provided below.
Canine acute respiratory distress syndrome
Canine acute respiratory distress syndrome (ARDS) is an acute, usually fatal, complication of a number of disease states.
In sepsis, a diffuse inflammatory process is triggered by bacterial endo-toxin that 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 dog. Alternatively, ARDS can be triggered by local pulmonary catastrophes, such as severe aspiration pneumonia,
pulmonary contusions or smoke inhalation. In either case, because 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, 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 occur. Much later,
these changes are followed by interstitial fibrosis as the lung attempts to repair the damaged parenchymal tissue. The inflammatory
changes in the lung can vary in severity and are usually unevenly distributed, often affecting the ventral areas first. At
times, the process is mild and then termed acute lung injury. In more severely affected dogs, the inflammation is profound,
overwhelming and leads to severe hypoxia.
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 might expectorate pink foam, and if intubated, sanguineus fluid can drain out
of the endotracheal tube. Arterial blood gases usually reveal hypoxia and hypocarbia, and metabolic acidosis can be present.
These animals usually have diffuse bilateral pulmonary alveolar infiltrates throughout all lung fields on thoracic radiographs.
Most dogs 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 can be seen even if the tidal volume is small.
Positive end expiratory pressure usually is required to achieve adequate oxygenation.
Few options are available for definitive management of ARDS, and supportive care is primarily aimed at treating the underlying
cause and supporting oxygenation. Because of the variety of inflammatory cascades and cells that mediate the inflammatory
response in ARDS, specific anti-inflammatory drugs, such as corticosteroids, largely are ineffective for treatment and can
cause immunosuppression that can exacerbate sepsis. Advances such as liquid ventilation, synthetic surfactant therapy and
inhaled nitric oxide have yet to be evaluated in dogs with naturally occurring disease.
Bacterial pneumonia is another common complication in dogs. The protective reflex of laryngeal closure to prevent tracheobronchial
aspiration, and the normal cough reflex that forcefully expels material from the airway when tracheobronchial aspiration occurs
are compromised by muscle/nerve weakness, sedation or intubation. In these situations, the pharynx rapidly becomes colonized
with pathogenic gram-negative bacteria that can then easily invade the tracheobronchial airway. The cleansing action of the
mucociliary blanket is compromised by intubation and inhalation of dry, cold air. Further, bronchus-associated lymphoid tissue
and alveolar macrophages can have decreased function as a result of malnutrition and protein catabolism.
Aspiration of gastrointestinal tract contents is perhaps the most common means by which bacterial pneumonia occurs in these
dogs. Initial chemical damage to the lung is rapidly followed by bacterial multiplication. Any vomiting or regurgitating dog
is a candidate for aspiration pneumonia, especially if combined with laryngeal abnormalities. However, aspiration pneumonia
is not always associated with episodes of overt vomiting or regurgitation. "Silent aspiration" can occur in weak or semi-conscious
animals (for example, extubated dogs recovering from anesthesia). In these dogs, aspiration of gastrointestinal contents can
occur without overt vomition and without obvious coughing or distress.