Exam #4: Equine Respiratory Pt. 3 Flashcards
DDx? Poor performance, hypophagia, lethargy, history of “flu and URT-like” infections, mild tachypnea, intermittent wheeze with rebreathing bag, intermittent cough and “sore throat” (2)
1) Exercise-induced pulmonary hemorrhage
2) Inflammatory airway disease
Others = post-viral bronchitis/bronchiolitis (based on history) or lymphoid follicle hyperplasia
Dx of non-febrile and poor performance respiratory disease (EIPH, IAD)
- History and PE
- CBC = often WNL
- Endoscopy
- Transendscopic/percutaneous tracheal wash
- Cytology
- Culture & sensitivity
+/- Thoracic rads
What grades of lymphoid hyperplasia is normal in young horses? Abnormal in adults?
Young = normal = grades 1-2 out of 4
Older/adults = chronic and heavy breathing, grades 3-4
Common inciting agent/pathology and risk factors (2) for EIPH
- Inciting agent = strenuous exercise –> extravasation of RBC’s from pulmonary capillaries
- May have been preceded by IAD or previous viral infections
- Risk factors = age, speed of exercise (develops more in older horses with increasing race speeds)
- INTENSITY of exercise is more important than duration
Clinical signs of EIPH
+ Poor athletic performance = most commonly
+/- Dyspnea
+/- Excessive swallowing
+/- Coughing
+ Epistaxis, during or shortly thereafter exercise
Diagnosis of EIPH
- History and PE
- Endoscopy WITHIN 90 MINUTES of race (graded)
- BAL or TTW cytology = see hemosiderophages, RBC’s, erythrocytophagia
- Thoracic radiographs = helps r/o other disease like abscesses, tumors, IAD (interstitial)
Treatment of EIPH
> Reduce pressure in capillaries = furosemide
+/- Enalapril’s efficacy hasn’t been proven in the lungs, NO as a vasodilator
Reduce blood viscosty = pentoxyfylline (ok with EIPH)
Reduce airway obstruction = nares dilator strips
Reduce airway inflammation/bronchoconstriction = bronchodilators, corticosteroids, low allergenic bedding
Rest
+/- Hemostasis promoters (vit-K, estrogens)
+/- Inhibition of platelet aggregation = aspirin
+/- Herbals, etc.
Comparison of age with IAD and RAO
- IAD = occurs at any age
- RAO = primarily mature to older horses that have been previously sensitized to antigens
Comparison of clinical signs at rest with IAD and RAO
- IAD = subtle, poor performance, exercise intolerance, chronic/intermittent coughing, +/- tracheal mucus
- RAO = overt EXPIRATORY effort at rest (heaves), severe exercise intolerance
Where do we sample from for cytology for EIPH, IAD, or RAO for dx? What do we see?
- EIPH = sample trachea with TTW (more localized) = RBC’s, hemosiderophages, erythrocytophagia
- IAD = BAL = mild neutrophilia, lymphocytosis, monocytosis, may see eosinophils or mast cells
- RAO = BAL = most are neutrophils, fewer lymphocytes and monocytes, usually no mast cells or eosinophils
Comparison of response to treatment for IAD and RAO
BOTH improve with corticosteroids, bronchodilators, and environmental change
Comparison of inciting factors for IAD and RAO
- IAD = no systemic infection, but non-infectious agents are important, Ex: aerosolized particles, dust, gases, endotoxins, mite debris, etc.
- RAO = aerosolized allergens and endotoxins from hay and bedding
*BOTH triggered by environmental conditions so it can be hard to differentiate
What do the airways look like and respond like with IAD?
- Lung function and gas exchange is impaired = may see evidence of hypoxemia on bloodwork
- Evidence of airway obstruction
- Hyperreponsive airways = secrete mucus
Non-infectious LRT disease treatment (IAD, RAO)
> Environmental and allergen management
- Use feedstuffs and bedding that are low dust and endotoxin
- Reduce airborne particles and noxious gases
- Ex: paper bedding, soaked hay, pelleted diets
Control airway inflammation = glucocorticoids (inhalation, PO, systemic), mast cell stabilizers
Bronchodilators = clenbuterol, albuterol
*Systemic glucocorticoids risk laminitis