Diseases of the parenchymal lung tissue present a unique clinical problem. With impaired gas exchange and hyoxemia rapid diagnosis and treatment is essential.
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 (ARDS).
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 is guarded.
Pneumonia is inflammation of the lung parenchyma; bronchopneumonia is pneumonia that has begun in the terminal bronchioles. Bacterial pneumonia in dogs is rarely a primary disease. Occasionally, Bordetella bronchiseptica or Mycoplasma spp. can induce pneumonia in dogs and cats due to their adverse affects on mucociliary function. Most cases of bacterial bronchopneumonia are secondary to immunosuppressive diseases or previous inflammatory insults including viral infection, aspiration, and irritant inhalation. Owners should be carefully questioned concerning potential exposure to other animals and clinical signs associated with immunosuppressive diseases or aspiration.
Most animals with bacterial pneumonia will be clinically ill. Common complaints include depression, anorexia, dyspnea, productive, moist cough with a terminal retch, and exercise intolerance. Some animals with pneumonia will present only with cough. Physical examination findings commonly include fever, crackles and wheezes, and muffled lung sounds in cases with consolidated or abscessed lung lobes. Many dogs will have increased tracheal sounds, a tracheal cough, and pharyngeal inflammation due to transport of inflammatory cells up the mucociliary apparatus to the mouth.
The initial diagnostic plan for animals with suspected bacterial pneumonia should include a CBC, biochemical panel, urinalysis, and thoracic radiographs. Cats should be screened for FeLV and FIV infection. Neutrophilic leucocytosis with or without a left-shift is common but not present in all cases. Monocytosis is common in chronic pneumonia. Assessment of the biochemical panel and urinalysis will often detect underlying immunosuppressive diseases. Clinically dyspneic animals should have an arterial blood gas analysis to assess oxygenation and ventilation and provide a baseline value to monitor therapy.
Thoracic radiographs usually reveal a mixed alveolar, bronchial, and interstitial pattern. Aspiration pneumonia generally has radiographic lesions that are most pronounced in the right middle lung lobe. Animals with opacity of the right middle lung lobe should be evaluated for esophageal and gastrointestinal disease or respiratory stridor. Esophageal diseases leading to regurgitation and aspiration may be evident on evaluation of thoracic radiographs. Laryngeal paralysis, characterized by inspiratory stridor can predispose dogs to aspiration.
Following documentation of pulmonary disease on thoracic radiographs, a TTW for cytology, aerobic bacterial and Mycoplasma culture, and antibiotic susceptibility testing should be performed. Transthoracic aspiration of consolidated lung lobes should be considered for anaerobic culture and antibiotic susceptibility testing. Bronchoscopy for brush cytology, biopsy, and bronchoalveolar lavage is sometimes required especially in larger animals and dogs with ciliary dyskinesia.
The combination of increased numbers of neutrophils and macrophages on cytologic assessment of secretions obtained by the tracheal wash and positive bacterial culture confirms the diagnosis of bacterial pneumonia. Bacterial culture is commonly positive in healthy animals and so the presence of bacteria without inflammatory cells does not document pneumonia.
Following correction of underlying conditions, the most important treatment of bacterial pneumonia hydration. The mucociliary apparatus functions best in a well-hydrated animal and is essential for the clearance of infection. Affected animals should receive parenteral fluid therapy until able to maintain hydration orally. Airway hydration can be accentuated by nebulization or by placing the animal in a closed bathroom while running hot water through the shower.
Common bacterial isolates include Bordetella bronchiseptica, Pasteurella multocida, Klebsiella spp., Streptococcus spp., and Escherichia coli.
In 2005, researchers at the University of Florida and Cornel University reported outbreaks of canine influenza virus, which causes an acute respiratory infection, had been identified in dogs in shelters, humane societies, boarding facilities and veterinary clinics in Florida and North along the East Coast. Since that time infection has been identified in other racing Greyhounds and intensively housed dogs around the United States. Further research has demonstrated that this virus is a mutation of the equine influenza virus that is able to infect dogs and is transmissible between dogs. This highly contagious virus causes a clinical syndrome that mimics "kennel cough." Canine influenza virus infections are can easily be mistaken for infections caused by the Bordetella bronchiseptica/parainfluenza virus complex.
As a brand new pathogen, all dogs, regardless of breed or age, are susceptible to infection and have no naturally acquired or vaccine-induced immunity. Virtually 100 percent of exposed dogs become infected. Nearly 80 percent have clinical signs. There are two general clinical syndromes – the milder syndrome and a more severe pneumonia syndrome. The milder disease syndrome occurs in most dogs.
In the milder disease, the most common clinical sign is a cough that persists for 10 to 21 days despite therapy with antibiotics and cough suppressants. Most dogs have a soft, moist cough, while others have a dry cough similar to that induced by Bordetella bronchiseptica/parainfluenza virus infection. Many dogs have purulent nasal discharge and a low-grade fever. The nasal discharge likely represents a secondary bacterial infection that quickly resolves with treatment with a broad-spectrum, bactericidal antibiotic.
Some dogs develop a more severe disease with clinical signs of pneumonia, such as a high fever (104F to 106F ) and increased respiratory rate and effort. Thoracic radiographs may show consolidation of lung lobes. Dogs with pneumonia often have a secondary bacterial infection and have responded best to a combination of broad-spectrum, bactericidal antibiotics and maintenance of hydration with intravenous fluid therapy. Fatal cases have been reported, but the fatality rate so far is low, at 1 percent to 5 percent.
The incubation period is two to five days after exposure before clinical signs appear. Infected dogs may shed virus for seven to 10 days from the initial day of clinical signs. Nearly 20 percent of infected dogs will not display clinical signs and become the silent shedders and spreaders of the infection.
Currently there is no vaccine for canine influenza virus. This virus is spread by aerosolized respiratory secretions, contaminated inanimate objects and even by people moving back and forth between infected and uninfected dogs. This is an enveloped virus that is most likely killed by routine disinfectants, such as quaternary ammoniums and 10 percent bleach.
Because the virus is highly contagious and all dogs are susceptible to infection, veterinarians, boarding facilities, shelters and pet stores should use isolation protocols for all dogs that have a "kennel cough."