Diseases of the parenchymal lung tissue present a unique clinical problem. With impaired gas exchange and hyoxemia rapid diagnosis
and treatment is essential. The real issue is that common diseases may look the same but have very different treatments. These
diseases include pulmonary edema and pneumonia. With edema, treatments are aimed at clearing excess lung water with diuretics
while with pneumonia, hydration is necessary to mobilize the inflammatory debris blocking the airways. We will review both
to highlight the clinical differences while reviewing the treatment options for each.
Noncardiogenic pulmonary edema occurs occasionally in dogs and cats secondary to electric cord bites, sepsis, following near
drowning or choking, snake bites, uremia, smoke inhalation, upper airway obstruction, and the adult respiratory distress syndrome
Most dogs and cats that chew on electric cords are presented with acute onset of dyspnea and oral burns that may or may not
be associated with dysphagia or ptyalism. The syndrome occurs most commonly in young dogs and cats. Tonioclonic muscle activity
is common in dogs immediately following contact with an electric cord. Pulmonary edema develops rapidly, generally within
hours. Common physical examination abnormalities include oral burns, dyspnea, and pulmonary crackles. Thoracic radiographs
show mixed interstitial and alveolar patterns that are most prominent in the dorsal portions of the caudal lung lobes. The
pathogenesis of edema is thought to be increased pulmonary capillary hydrostatic pressure and increased alveolar-capillary
permeability. Increased pulmonary capillary hydrostatic pressure is likely due to a centrally mediated burst of sympathetic
activity that causes constriction of resistance and capacitance vessels leading to a shift of blood from the splanchnic viscera
into the circulation. This ultimately results in overcirculation of the pulmonary vasculature. Increased pulmonary capillary
hydrostatic pressure is made worse by increased peripheral vascular resistance; pulmonary venous pressures increase as the
left ventricle pumps against increased outflow resistance. Treatment includes administration of diuretics, oxygen (mask, nasal
insufflation or cage), morphine, corticosteroids or positive end expiratory pressure ventilation. Morphine can be an excellent
drug; at low doses it sedates dyspneic animals while drawing excess fluid from the lungs via splanchnic vasodilatation. Survival
rates are approximately 60%.
The clinical signs and physical examination abnormalities associated with near drowning, smoke inhalation, and snake bite
are similar to those with electric cord bites with the exception of oral burns. Historical findings confirm near drowning
and smoke inhalation. Puncture wounds, and a swollen face or extremities may be found on animals with snakebite. The primary
pathogenesis of dyspnea associated with near drowning is dilution of pulmonary surfactant with resultant alveolar collapse.
Salt-water inhalation increases the diffusion of water from the interstitium into the alveoli. Increased alveolar-capillary
permeability may also occur.
Pulmonary edema occasionally develops secondary to upper airway obstruction in dogs. Laryngeal and pharyngeal diseases are
most common. Inspiratory and expiratory stridor, dyspnea, crackles, and cyanosis are common physical examination abnormalities.
Mixed interstitial and alveolar lung infiltrates are detected in the perihilar and dorsocaudal lung fields. Treatment can
include administration of oxygen, diuretics and glucocorticoids, as well as tracheostomy if needed. Edema is primarily related
to decreased intrathoracic pressure resulting in decreased interstitial hydrostatic pressure and hypoxia resulting in increased
alveolar capillary permeability.
Adult respiratory distress syndrome (ARDS) results from a variety of pulmonary insults and can be thought of as organ failure
of the lung. The clinical criteria for a diagnosis of ARDS include normal pulmonary capillary wedge pressure (noncardiogenic
pulmonary edema), decreased pulmonary compliance, diffuse lung infiltrates on thoracic radiographs, and hypoxemia due to ventilation-perfusion
mismatch. The primary pathogenesis of edema is increased alveolar capillary permeability. Primary lung diseases associated
with the development of ARDS include aspiration, pulmonary contusion, inhalation of noxious gases, oxygen toxicity and a variety
of infectious diseases. Secondary lung diseases associated with the development of ARDS include gram-negative sepsis, trauma
(not just chest trauma), pancreatitis, parvovirus enteritis, transfusion reactions and toxins. Removal of the primary causes
and administration of oxygen support preferable with positive end expiratory pressure are the principle treatments. The prognosis