Respiratory distress cats can present a therapeutic dilemma. These small patients can be so severely compromised that diagnostics
and treatment can stress them to the point of respiratory and cardiac arrest. A diagnosis should not come at the expense of
the patient. An induction chamber or oxygen cage can be valuable to give the cat added oxygen while the clinician can observe
the patient in an attempt to localize the problem. The purpose of this talk will be to review some of the following causes
of respiratory distress in cats using videos of actual case examples.
Cats in distress will require more oxygen than one that is calm. This creates a vicious cycle as cats get more anxious they
require more oxygen and become more distressed. Mild sedation can be life saving by allowing the anxious dyspneic cat to breathe
Restraint for catheterization, radiographs and physical examination may have to wait until the patient is relaxed and breathing
easier. In the case of pleural effusion or pneumothorax, a thoracocentesis can provide a diagnosis at the same time it is
providing the life-saving treatment.
Try to determine the nature of the problem first with observation. A rapid shallow respiratory pattern suggests restrictive
disease while a slow deep inspiratory pattern is seen with airway obstruction. With the restrictive pattern, auscultation
can help differentiate pleural space disease (pneumothorax, hydrothorax) from parenchymal diseases (pneumonia, pulmonary edema).
Cats presenting with upper and lower respiratory signs should have a thoracic radiograph. Bronchial patterns develop as the
peribronchiolar tissues become inflamed. Interstitial patterns develop with thickening of the fibrous structures of the lung.
Alveolar patterns characterized by "Air bronchograms" are caused by fluid accumulation in the alveoli. Thoracic and cervical
radiographs can be used to diagnose collapsing trachea, tracheal or laryngeal foreign bodies, and tracheal or laryngeal masses.
Airway dynamics can be assessed by taking inspiratory and expiratory views of the trachea or through the use of fluoroscopy.
Transoral Tracheal Wash
Transoral tracheal wash (transtracheal wash, TTW) is one of the most useful techniques for the diagnosis of diseases of the
respiratory system. The TTW can be easily performed in most cats in about 15 minutes. The TTW should be performed following
assessment of the thoracic radiographs and is indicated for all coughing cats with interstitial, bronchial, or alveolar lung
patterns that are not suspected to be due to cardiogenic disease or coagulopathy. The goal of the TTW is to collect fluids
from the trachea, bronchi and lower airways for cytology, culture, and antibiotic susceptibility.
Noncardiogenic pulmonary edema occurs occasionally in 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 (ARDS).
Because the lungs are considered the "shock organ" in cats, any hypotensive event can result in alveolar flooding and edema.
Most cats that bite electric cords are presented with acute onset of dyspnea and oral burns, which 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, which 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 peripheral vascular resistance increases
pulmonary capillary hydrostatic pressure and pulmonary venous pressures increase as the left ventricle pumps against increased
outflow resistance. Treatment includes administration of diuretics, oxygen (mask, nasal insulation 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.
The clinical signs and physical examination abnormalities associated with near drowning, smoke inhalation, and snakebite 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. Treatment is similar to electric cord bite. Administration of bronchodilators may also aid in the treatment
of some cases. Smoke inhalation causes dyspnea by inducing carbon monoxide poisoning and damage to respiratory tissues by
heat and noxious gasses. Laryngeal spasm, loss of ciliary function, decreased surfactant activity, bronchospasm, increased
alveolar-capillary permeability, impaired phagocytosis, and sloughing of airway mucosa frequently occur. Bronchial patterns
occur first with interstitial and alveolar edema developing later if edema develops. Treatment is similar to electric cord
bite and near drowning.