Inflammatory Airway Disease

Question 1

What are the characteristics of IAD

Answer 1

mucoid or mucopurulent exudate in nasopharynx, a non-septic inflammation,

Question 2

What are some possible causes?

Answer 2

dust, molds, pollutants inhaled, but the exact cause is unknown

Question 3

CLinical signs of IAD

Answer 3

poor athletic performance is the big one, but lack of fever, coughing, and maybe EIPH. Often subclinical

Question 4

Dx of IAD is…

Answer 4

TW for culture, BAL to look for Mast cells, PMNs, or eosinophils (>2%, >5%, and >1%), endoscopic exam finding exudate. THis is a R/O disease causing poor performance

Question 5

Treatment for IAD is

Answer 5

Change something in the environment like the possible causes. Some people give corticosteroids but we need to rule out bacterial infection first (TW). THat is important to know before we give bronchodilators as well.
Sodium cromoglycate is good (if mast cells from BAL)
and decrease EIPH

Question 6

Prevalence of IAD

Answer 6

20-65% in race horses, 85% of coughing horses have this

Question 7

Who mainly gets IAD?

Answer 7

young performance horses

Question 8

What does IAD rarely cause?

Answer 8

auscultable pulmonary abnormalities

Question 9

What age does RAO usually hit?

Answer 9

middle to older

Question 10

What is RAO associated with?

Answer 10

stabling and exposure to dust, hay and molds. Summer pastures this is less common

Question 11

What is the etiology of RAO?

Answer 11

respirable organic dust
Hay and bedding - hypersensitivity to dusts or molds in poorly cured hay –> Aspergillus fumigatus and Faenia rectivirgula
pollen on some pastures (SPAOPD)
.

Question 12

What is the pathogenesis?

Answer 12

Inhalation of the agent –> infiltration of neutrophils –> inflammatory change to airways –> edema (acute) –> airway remodelling (chronic) with mucus metaplasia, sm msc hypertrophy, peribronchiolar fibrosis and inflammation –> Mucus accumulation from increased production and viscoelasticity –> bronchospasm –> decreased lung compliance –> increased resistance –> increased work to breathe –> arterial hypoxemia (no hypercapnia)

Question 13

Clinical signs of RAO

Answer 13

chronic spont cough
mucopurulent nasal discharge
accented expiratory effort
heave line
increased resp rate and maybe respiratory distress
adventitious lung sounds (wheezes and crackles)
exercise intolerance
weight loss

Question 14

What is not a clinical sign of RAO

Answer 14

fever

Question 15

Dx of RAO

Answer 15

Hx, C/S,
Wheezes on exp,
crackels in insp and exp
percussion may have expanded lung field
interstitial and bronchiolar pattern on rads
TTW and endoscopy - exudate (not sensitive) and neutrophils with copious mucous
BAL - THis is the most important. Higher than the normal 5-10% neutrophils or up to 25% in stabled horses. There will be increase in mucous and non-degen neutrophils
THe others: arterial blood gas, atropine/glycopyrr test, CBC, chem,

The stupid ones are intradermal skin testing and serum allergen testing

Question 16

Tx of RAO

Answer 16

environmental management!!! - decrease dust, give rest, pasture, soak hay, ventilate
Drugs - corticosteroids (inhaled or systemic)
also bronchodilators

Question 17

What are the corticosteroids we use for RAO?

Answer 17

dexamethasone and prednisolone for systemics

fluticasone, beclomethasone given by nebulizers, aeromasks, or metered dose inhalers

Question 18

WHat are some of the bronchodilators in RAO?

Answer 18

betas - clenbut (ventipulmin), albuterol (proventil), pirbuteral (maxair)
Anticholinergics (atrovent) which is ipratropium
disodium cromoglycate