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Equine Final Year > Equine Asthma > Flashcards

Equine Asthma Flashcards

1
Q

Physical exam of thoracic cavity?

A
  • Review the landmarks of the thoracic cavity
  • Use a systematic approach
  • Examine in several areas
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2
Q

Discuss auscultation at rest and re-breathing?

A

Is there air moving throughout the entire lung field?

Areas of dullness suggesting pleural effusion or pulmonary consolidation/abscessation/masses

Are there any abnormal sounds?

Large airway sounds suggesting consolidation

Wheezes and crackles suggesting airway narrowing, or discharges in airways

Does the horse tolerate and recover from re- breathing rapidly?

Coughing, distress suggesting pleural pain

Is there a tracheal rattle?

Suggesting discharge pooling at the thoracic inlet

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3
Q

Discuss susceptibility to equine respiratory disease?

A

The prevalence of disease (morbidity) varies within different age groups due to

  • immunological factors
  • environmental factors
  • managemental factors
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4
Q

Discuss susceptibility of diff diseases in horses at diff ages?

A

Diseases of foals

  • Infectious causes (bacterial)
  • Congenital abnormality
  • Sepsis, trauma, other

Diseases of weanlings

  • Infectious causes (bacterial/parasite/virus) & contagious

Disease of young adults (young race horse 4-5 yrold)

  • EQUINE ASTHMA SYNDROME
    • May be precipitated by Infectious causes (bacterial and viral and mycoplasma)

Disease of the older/aged/mature horses

  • EQUINE ASTHMA SYNDROME
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5
Q

Discuss diseases of mature horses further?

A

Diseases of mature horses

Infectious causes

  • Lungworm
  • Tuberculosis (occacionalmycobacteria infection) •

Inflammatory disease

  • EQUINE ASMTHA SYNDROME (by far most common)

Thoracic neoplasia (non of these are common)

  • Pulmonary Granular Cell Tumour
  • Cranial Mediastinal Lymphosarcoma
  • Malignant melanoma

Miscellaneous

  • Exercise induced pulmonary heamorrhage(cause poor performance in race horse)
  • Interstitial pneumonia
  • Pulmonary interstitial fibrosis
  • Equine pulmonary nodular fibrosis
  • Granulamotous pneumonia
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6
Q

Discuss equine asthma syndrome?

A

Redefined in 2016 for to encapsulate RAO and IAD

  • Causes chronic cough
  • Excess respiratory mucus production
    • Snotty nose and discharge usually bilateral
  • Poor performance
    • However systemically healthy otherwise may have a snotty nose

Recurrent Airway Obstruction

  • Old/mature horse
  • Chronic

Inflammatory airway disease

  • Any age (typically younger horse condition)
  • Temporary condition if managed appropriately animal will recover

Not a disease continuum (probably)

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7
Q

Compare recurrent airway obstruction and inflammatory airway disease?

A
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8
Q

Compare recurrent airway obstruction and inflammatory airway disease?

A
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9
Q

What is the pathogenesis of RAO?

A

Neutrophilic inflammation

  • Type I (mast cell degranulation)
  • Type III (Immune complex)
  • Type IV (delayed) hypersensitivity
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10
Q

What is the pathogenesis of Inflammatory airway disease (IAD)?

A

IAD

Airway hyper-responsiveness

  • Not allergic response an inflammatory response in response to non-specific stimuli
  • Feature of many inflammatory airway diseases
  • Contributes to airway obstruction
    • airways have an increased sensitivity to excitatory neurotransmitters, inflammatory mediators, and nonspecific irritants such as dusts.
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11
Q

Compare pathogenesis of RAO and IAD?

A
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12
Q

Discuss recurrent airway obstruction?

A

Equine Asthma: RAO

  • Chronic disease
    • poor performance to overt signs of respiratory dysfunction
    • with/without coughing
    • Nasal discharge
    • hypertrophy of the abdominal muscles
  • Exacerbation of other respiratory disease
    • Upper airway collapse egDDSP
    • EIPH
  • housed in poorly ventilated stall in ‘winter’ OR at pasture during summer
  • previous episodes, worsening over the years Nasal discharge worse at onset of exercise
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13
Q

Discuss inflammatory airway disease?

A

Equine Asthma: IAD

  • Non specific inflammatory condition
    • Affects younger horses (primarily)
    • Secondary to airway hyper responsiveness
      • Viral, Bacterial, Toxicological, Irritant
  • Often subclinical –results in only poor performance
    • Difficult to diagnose
    • Chronic cough -variable
  • Lower airway disease with excess mucus but not RAO
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14
Q

Discuss acute recurrent airway obstruction?

A

ACUTE & SEVERE RESPIRATORY DISTRESS

  • Usually only RAO that has acute response
  • increased respiratory effort (expiratory)
  • double expiratory effort / dyspnea(biphasic respiration becomes more obvious in horses with RAO)

Usually seen in horses previously diagnosed and treated

  • Treatment failure
  • Environmental challenge
  • Secondary infection
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15
Q

What can be seen on this tracheal endoscopy?

A

Tracheal endoscopy.

RAO

Evidence of inflammation and lots of mucopus.

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16
Q

Diagnostics test indications and reasons?

A

Indications

  • Horses that relapse
  • Do not respond to therapy
  • Do not respond to management change

Reasons

  • Confirm diagnosis
  • Rule out bacterial component
  • Rule out parasitic disease
  • Tracheal wash (endoscopic)
  • Trans-tracheal wash
  • Trans-endoscopic wash
  • Bronchoalvealor lavage (often most appropriate)
17
Q

Compare diagnostic tests for RAO and IAD?

A
18
Q

Considerations for cytology?

A
  • Use cytology to rule out pharyngeal contamination
    • Look for presence of squames if there no point culturing sample
    • Extracellular bacteria
  • Correlate bacterial growth with clinical signs
    • Contaminants
      • Pseudomonas, Bordatella etc
19
Q

Discuss therapeutic strategies for equine asthma?

A
20
Q

Discuss management for RAO and IAD?

A
21
Q

Discuss environmental control further?

A

Turn out if feasbile& signs are not evident at pasture

  • rarely that simple

Conversely some pasture-associated cases may respond to stabling

Usually takes up to 4 weeks to resolve clinical signs

  • Longer with chronic disease
22
Q

What things can we look at in the stable environment to improve equine asthma?

A

Bedding:

  • Change to shavings / paper
  • avoid deep litter

Feed

  • From the ground to aid drainage
  • haylage(high dry matter silage)
  • chopped dried alfalfa
  • cubed / pelleted diets
  • Soaking/steaming hay

Ventilation

  • top door open all the time, vent (0.3m 2 )
  • Net across bottom door and leave it open

Location of stable

  • other stables with hay/straw, feed stores & manure piles
  • Don’t muck out/groom horse in stable
23
Q

Discuss beta-agonists (clenbuterol bronchodilators)?

A

Faster onset improvement

  • Compared with corticosteroids

Must be combined with environmental control otherwise they increase penetration of allergens into airway via dilated bronchioles

Bronchodilatory and mucocillary effects

Sweating and tachycardia –usually IV

Side effects short lived

0.8ug/kg PO

Receptor downregulation

  • May result in treatment failure and recurrence of clinical signs down the line

ClenbutoralB2 agonist by activating the sympathetic nervous system

24
Q

Discuss mucolytic agents?

A

Limited evidence of benefit

  • May help with early management of severe disease
  • Used where significant mucus on tracheal cytology
  • Widely used in human COPD
    • Improved respiratory function (subjective)
    • Modest reduction in acute exacerbations
    • Reduced numbers of disability and hospitilisation
      • Advised under NICE guidelines
25
Q

Describe preventative strategies for equine asthma?

A

Allergen hyposensitisation

  • Some improvement in 60%
  • Expensive
  • Requires steroid free period –skin testing

Mast cell stabilizers

  • Limited evidence
26
Q

Discuss mast cell stabilisers?

A

Mast Cell Stabilizers

Only useful for horses IN REMISSION/not showing clinical signs

  • Prevent disease

Sodium cromoglycate

Nedocromilsodium

  • Inhibit degranulation
  • Prevent release of inflammatory mediators
    • Histamine
    • Leukotrienes
    • Cytokines

Also stabilizes

Neutrophils, eosinophils and macrophages

27
Q

Discuss Sodium cromoglycate?

A
  • Dose = 80 –200 mg via nebulization
  • Treatment of mast cell rich IAD in young racehorses
  • Use before an event and get up 20 days of protection
  • Most effective BEFORE challenge
    • Not a replacement for steroids and bronchodilators
    • Reduces histamine content in equine mast cells
  • Useful for Pasture associated RAO
28
Q

Discuss nebulised bronchodilators?

A

Have rapid onset of effect

Reduced some of the systemic effects

  • But still detectable in blood so still have detectable levels and cant compete

Direct effects if poor absorption

29
Q

Discuss efficacy of inhaled therapy?

A

Mask based systems

  • 6-14% delivery (CFC vsHFA)
  • Remains on external nares

Spacer based devices

  • 8% delivery to lung
  • Must align to nares
  • Horse can move away
30
Q

Discuss Parasympatholytics?

A

Inhibit main bronchoconstriction pathway

  • Vago-vagal effects
    • Will induce vagal long term GI dismotilityso horses get colic. Only ever use in acute crisis.
  • Systemic side effects limit use
    • Reserve for respiratory distress
    • Atropine
31
Q

Discuss Ipratropium Bromide?

A

Inhaled parasympatholytic

Nonselective muscarinic antagonist

Like atropine

  • Also inhibits cough

Little systemic uptake

Short duration of action (4-6 hours)

  • Dose :
    • Nubuliser2-3 μg/kg
    • Dry powder inhaler 200 μg/100 kg; 2400 μghorse
    • MDI 180 –360 μg/500 kg horse
  • Onset 15 –30 min
  • Duration of action 4 –6 hours
  • Does not improve exercise performance
32
Q

Discuss inhaled beta2 agonists?

A
  • Β2 agonists are highly effective
    • But efficacy studies cannot be compared
    • Different methods of administration
  • Albuterol(450-900 ugq 4-6d)
    • Rapid onset (5 mins) short duration (1 hour)
    • Rescue therapy
  • Salmeterol(210mcg q 12hrs)
    • Slower onset (30 mins), longer duration (6 hours)
    • Given 30 mins before exercise
33
Q

Discuss use of systemic corticosteroids?

A

Systemic corticosteroids

  • Usually 1 week lag between onset of treatment and clinical response (can combine with bronchodilators)
  • Requires at least 2 weeks of therapy
  • Must be combined with environmental improvement
    • Reduced cell accumulation and activation
    • Reduced vascular change
    • Reduce bronchoconstriction by blocking inflammation
  • Dexamethasone: 0.05 to 0.1mg/kg IV/PO Every 48 hours (more effective than pred)
  • Prednisolone: 0.5-1 mg/kg PO q 24hrs (licensed formulation)
34
Q

Discuss corticosteroid side effects?

A

SIDE EFFECTS

SUPPRESSION OF ADRENAL FUNCTION

  • q2-4 day administration

IMMUNOSUPRESSION

  • used with concurrent ABX in specific cases egLAI

LAMINITIS

  • Small risk horses that get it are already at risk of laminitis (obese, equine metabolic syndrome)
  • Product?
  • Dose?
  • Predisposing conditions
    • Cushings, laminitic tendency
    • Severe systemic illness?
35
Q

Discuss inhaled corticosteroids?

A

Reduced risk of laminitis even further if concerned

Local administration

  • Adrenal suppression
  • Detectable plasma concentrations
  • Reduced systemic side effects

Rapid onset of effects

  • 24 hours after admin

Taper dose to minimal effective

  • Occasionally to every other day

Variable response between individuals

May require systemic corticosteroids initially

  • 2-4 weeks loading dose
36
Q

Discuss inhaled steroid therapy?

A

Beclomethasone -by aerosol (500ug)

Cheaper to use

Improved clinical score after 10 days

More rapid response with higher doses

  • 1320ug BID –within 3 days
  • Longer for pulmonary resistance to improve (10days)

Fluticasone> beclomethasone>flunisolide

Potency in relation to dexamethasone

  • Flunisolide= 1.9
  • Triamcinolone = 2.0
  • Beclomethasone= 13.5
  • Fluticasone= 18.0
37
Q

Why does therapy fail?

A

Wrong diagnosis

  • Horses have pre-existing secondary infection
  • Other inflammatory conditions
  • Other lung conditions

Not combined with environmental control

Beta Receptor down-regulation

  • Occurs after 2-4 weeks
  • May result in treatment failure and recurrence of clinical signs
  • Can be offset by combination with corticosteroid

Data sheet: ‘Treatment should be continued for as long as necessary’

38
Q

What are the reasons for treatment failure?

A

Differential diagnosis

  • Bronchopneumonia: Fever, depression
  • Viral infection: Fever, lethargy, depression
  • EIPH • Lungworm
  • Neoplasia
    *
39
Q

How are relapsing cases managed?

A
  • Rule out secondary bacteria
  • Tracheal wash / BALF cytology
    • Intracellular bacteria, neutrophilic inflammation
    • Neutrophil degeneration
  • Transtracheal culture
    • Must be combined with cytology
  • Care when interpreting bacterial culture
    • Is pathogen likely?
    • Does pathogen fit with clinical presentation

Equine Final Year (102 decks)

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