Introduction #
Feline asthma is a common respiratory condition in cats characterized by lower airway inflammation, bronchoconstriction, and excessive mucus production. It shares some pathophysiological features with human asthma, making it both a clinically important veterinary condition and a minor model for human disease. This chronic respiratory disorder affects approximately 1-5% of the domestic cat population, with certain breeds showing increased susceptibility, particularly Siamese and Himalayan cats.
Pathophysiology #
Feline asthma is primarily an allergic inflammatory disease of the lower airways. The pathophysiology involves three key components: airway inflammation, airway hyperresponsiveness, and airway remodeling. The immunological basis of feline asthma centers on a type I hypersensitivity reaction with significant involvement of T-helper 2 (Th2) lymphocytes. These cells release cytokines (particularly IL-4, IL-5, and IL-13) that stimulate IgE production by B cells and recruit eosinophils to the airways.
When a sensitized cat encounters an allergen, it triggers crosslinking of IgE receptors on mast cells, leading to degranulation and release of inflammatory mediators including histamine, leukotrienes, and prostaglandins. These substances induce acute bronchoconstriction, edema, and mucus hypersecretion. Common allergens include dust mites, pollens, molds, and various household irritants.
Airway remodeling occurs with chronic inflammation, featuring goblet cell hyperplasia, subepithelial fibrosis, smooth muscle hypertrophy, and angiogenesis. These structural changes reduce airway compliance and contribute to the chronic, progressive nature of the disease.
Neurogenic mechanisms also play a role, with stimulation of afferent sensory nerve endings in airways activating parasympathetic reflexes that further exacerbate bronchoconstriction through muscarinic receptors on airway smooth muscle cells.
Clinical Presentation #
Feline asthma presents with several characteristic clinical signs that may vary in severity. The hallmark symptom is expiratory wheezing, often accompanied by coughing that is frequently described as “hacking” or mistaken for hairball attempts. Tachypnea and respiratory distress may be evident, particularly during acute exacerbations. Affected cats often assume a characteristic hunched posture with neck extended and abdominal breathing pattern during severe episodes.
The clinical course is typically characterized by episodic exacerbations interspersed with periods of minimal or absent clinical signs. Triggering factors for these episodes include exposure to aeroallergens, exercise, stress, and respiratory infections. In severe cases, cyanosis may be present, indicating significant hypoxemia.
Physical examination findings during acute episodes include audible wheezes, prolonged expiratory phase, and increased bronchovesicular sounds upon thoracic auscultation. Thoracic radiography typically reveals a bronchointerstitial pattern with peribronchial infiltrates and, in some cases, air trapping leading to lung hyperinflation and flattened diaphragm.
Diagnosis typically involves a combination of clinical history, physical examination, radiographic findings, bronchoscopy, bronchoalveolar lavage (showing increased eosinophil count), and exclusion of other respiratory conditions such as heartworm disease, lungworm infection, and respiratory neoplasia.
Clinical Management During Anesthesia #
Anesthetizing cats with asthma presents significant challenges due to their compromised respiratory function and potential for intraoperative bronchoconstriction. Preoperative assessment is crucial and should include thorough evaluation of respiratory status, radiography, and potentially arterial blood gas analysis to assess the severity of the condition.
Premedication should be carefully selected to minimize respiratory depression. Anticholinergics like atropine or glycopyrrolate may help reduce airway secretions and prevent vagally-mediated bronchoconstriction.
Induction agents should be selected for their bronchodilatory properties. Propofol and ketamine are generally considered advantageous, with ketamine providing bronchodilation through sympathomimetic effects. Conversely, thiopental should be avoided due to its potential to trigger histamine release and induce bronchoconstriction.
Endotracheal intubation should be performed with care to avoid airway irritation that could trigger bronchospasm. Pre-oxygenation prior to induction is advisable, and equipment for emergency intubation should be readily available. Once intubated, maintaining adequate ventilation is critical, with attention to preventing air trapping by allowing sufficient expiratory time if mechanical ventilation is employed.
Inhalational anesthetics, particularly isoflurane and sevoflurane, are preferred for maintenance due to their bronchodilatory properties. However, cold inspired gases may initially increase secreations and may potentiate bronchoconstriction.
Regional anesthetic techniques are beneficial when appropriate for the surgical procedure, as they reduce the requirement for general anesthesia and associated respiratory complications. Opioid selection should be cautious, with preference for those less likely to cause histamine release (fentanyl, hydromorphone) over morphine.
Emergency drugs for managing acute bronchospasm during anesthesia should be readily available, including short-acting beta-2 agonists (albuterol/salbutamol) and injectable bronchodilators (terbutaline).
Prognosis #
The long-term prognosis for cats with asthma varies significantly based on several factors including disease severity, response to therapy, and owner compliance with treatment protocols. With appropriate management, most cats with mild to moderate asthma can maintain a good quality of life with minimal clinical signs.
Factors associated with poorer prognosis include severe airway remodeling, frequent acute exacerbations requiring emergency intervention, and concurrent conditions such as obesity or cardiac disease. Approximately 15-20% of cases may progress to more severe disease despite optimal therapy.
Long-term therapeutic management typically involves a combination of environmental modification to reduce allergen exposure, corticosteroids (inhaled or systemic), and bronchodilators. Novel approaches including immunotherapy and leukotriene modifiers show promise in managing cases refractory to conventional therapy.
The impact of feline asthma on lifespan is variable, but with appropriate management, most cats can achieve a normal life expectancy. However, severe, untreated asthma can lead to life-threatening respiratory compromise and status asthmaticus, which carries a guarded prognosis even with intensive care.
References #
- Reinero CR. Advances in the understanding of pathogenesis, and diagnostics and therapeutics for feline allergic asthma. Vet J. 2011;190(1):28-33.
- Trzil JE, Reinero CR. Update on feline asthma. Vet Clin North Am Small Anim Pract. 2014;44(1):91-105.
- Cocayne CG, Reinero CR. Feline respiratory disease: what is the role for mycoplasma infections? J Feline Med Surg. 2020;22(11):1064-1073.
- Nafe LA, DeClue AE, Lee-Fowler TM, et al. Evaluation of biomarkers in bronchoalveolar lavage fluid for discrimination between feline asthma and chronic bronchitis. J Vet Intern Med. 2010;24(5):1022-1030.
- Lee-Fowler TM, Cohn LA. Feline respiratory disease: what is the role for Mycoplasma species? J Feline Med Surg. 2015;17(5):425-431.
- Padrid P. Feline asthma: diagnosis and treatment. Vet Clin North Am Small Anim Pract. 2000;30(6):1279-1293.
- Galler A, Shibly S, Bilek A, Hirt RA. Inhaled budesonide therapy in cats with naturally occurring chronic bronchial disease. J Small Anim Pract. 2013;54(5):238-243.
- Johnson LR. Clinical canine and feline respiratory medicine. Wiley-Blackwell; 2010.
- Reinero CR, DeClue AE, Rabinowitz P. Asthma in humans and cats: is there a common sensitivity to aeroallergens in shared environments? Environ Res. 2009;109(5):634-640.
- Byers CG, Dhupa N. Feline bronchial asthma: pathophysiology and diagnosis. Compend Contin Educ Pract Vet. 2005;27(6):418-425.
