Equine LRT Disorders Flashcards

1
Q
  1. Main thing to look for on endoscopy of LRT?
  2. Other things to assess for on endoscopy.
A
  1. Mucus.
  2. Blood.
    Sensitivity of trachea.
    Structural abnormalities.
    FB.
    Thickening of the carina (blunting = oedema and remodelling).
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2
Q
  1. How does mucus accumulation occur?
  2. Mucus when disease present.
A
  1. Imbalance of secretion and clearance.
  2. Composition change - thickened so airway obstruction.
    Colour and opacity changes.
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3
Q
  1. How can cytology of TW and BAL samples indicate severity of disease?
  2. Why is cytology on TW samples more difficult?
A
  1. Based on proportions of inflammatory cells.
    - some labs give percentages of the cells that are present.
    - other labs will give categories and estimates of numbers for TW e.g. +, ++, +++, -.
  2. Cells more likely degenerate and trapped in mucus.
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4
Q
  1. Normal cells in TW cytology.
  2. What about TW cytology in disease?
A
  1. Epithelial cells.
    Macrophages.
    <20% neutrophils.
    <1% eosinophils.
    <1% mast cells.
  2. Neutrophilia.
    Occasionally eosinophilia and mast cell response.
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5
Q
  1. BAL cytology normal findings.
  2. Most common inflammatory response in horses.
A
  1. Macrophages (~60%; 40-80).
    Lymphocytes (~35%; 20-50).
    Neutrophils (<5%).
    Mast cells (<2%).
    Eosinophils (<1%).
  2. Neutrophilia - irrespective of if infectious or non-infectious.
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6
Q

TW culture.

A

Normal bacterial flora of conducting airways.
True infection - pure growth of single organism.
Impaired mucociliary clearance.
- inflammatory/allergic.
Contamination during the procedure.
- e.g. pseudomonas due to poor cleaning of endoscope.

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7
Q
  1. What is equine asthma.
A
  1. Umbrella term.
    LRT disease resulting from airway inflammation.
    Resulting from small airway obstruction caused by an immune-mediated hypersensitivity to inhaled particles in more severe cases.
    Most common non-infectious respiratory disease.
    Most common cause of coughing in adult stabled horses.
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8
Q

Equine asthma pathogenesis.

A

Airway inflammation leads to airway obstruction due to:
- Bronchospasm (smooth muscle contraction).
- Mucus accumulation.
- Airway wall changes cased by oedema, inflammation and remodelling (severe and chronic). .

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9
Q
  1. Prevalence of mild to moderate equine asthma.
  2. Mild to moderate equine asthma age of horses affected.
  3. Severe equine asthma age of horses affected?
  4. Prevalence of severe equine asthma.
A
  1. > 70%.
  2. Any age.
  3. Middle aged-older (av. 9yo onset).
  4. 10-15%.
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10
Q

Mild to moderate asthma clinical signs.

A

Often subtle.
Poor performance/lack of energy.
Prolonged recovery from exercise.
Cough (~30%).
Nasal discharge (serous-mucoid - most commonly just post exercise).
No increased respiratory effort.
Not systemically ill, not off-colour.

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11
Q

Severe equine asthma clinical signs.

A

Chronic presentation more common than acute.
Coughing.
Tachypnoea/dyspnoea.
Exercise intolerance.
Nasal discharge.
Nostril flaring.
Heave line (increased abdominal expiratory effort).

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12
Q
  1. What is heard on auscultation of horses presenting w/ asthma?
  2. What can be done to make respiratory auscultation easier?
A
  1. Abnormal breath sounds e.g. expiratory wheezes, crackles.
  2. Rebreathing bag - makes auscultation more sensitive as makes horse breathe much more deeply.
    - DO NOT USE IN ACUTELY DYSPNOEIC!
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13
Q

Dx of equine asthma.

A

CE.

Not w/ blood tests.

Endoscopy - increased tracheal mucus.
- blunting of carina in severe cases.

TW/BAL - neutrophilic inflammation (increases w/ severity of disease)
– DO NOT PERFORM IN ACUTELY DYSPNOEIC PATIENTS.
– less commonly mixed inflammatory response (eosinophils, mast cells).

Trial treat bronchodilator - IV Buscopan, Clenbuterol or atropine.

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14
Q

Mild to moderate equine asthma Tx.

A

Aim to decrease environmental dust and control airway inflammation.
- Environmental management.
- Corticosteroids – control inflammation.

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15
Q
  1. Advantages of inhalation and nebuliser therapy.
  2. Disadvantages of inhalation and nebuliser therapy.
A
  1. High local conc. in airways.
    Rapid onset action.
    Reduced total dosage.
    Decrease risk of side effects.
    Reduced detection time in competition horses.
  2. Poor access to restricted airway.
    - may be more advantageous to start w/ oral meds and transfer to inhaled once condition more stable.
    Lack of patient/owner compliance.
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16
Q

Tx of acute severe asthma?

A

Remove from stable.
Administer bronchodilator for immediate relief of airway obstruction:
- IV Buscopan.
- IV Clenbuterol (side effects sweating, tachycardia).
- IV atropine (side effect ileus).
Corticosteroids - reduce inflammation:
- IV dexamethasone (care - laminitis).

17
Q
  1. What is the more common indication for use of Buscopan?
A
  1. Colic.
18
Q

Tx of chronic severe asthma?

A

Environmental management to reduce allergen exposure.
Corticosteroids reduce inflammation:
Prevent tolerance to B2.
- e.g. oral prednisolone.
- e.g. inhaled cicelsonide, fluticasone.
- side effect laminitis.
Bronchodilators relieves obstruction:
- B2 agonists.
- oral Clenbuterol (Ventipulmin).
- inhaled/nebulised salbutamol/salmeterol/clenbuterol.
- not used alone, adjunct only.
Mucus clearance drugs:
- e.g. Bisolvon (bromhexine), dembrexine (sputolosin), clenbuterol (ventipulmin).
- inhaled saline and inhaled acetylcisteine used in performance horses.
- little evidence but mucus production will resolve w/ improvements in airway inflammation – down-regulation of goblet cells.

19
Q

Environmental risk factors for equine asthma.

A

Stabling v field - stabling normal horse will cause airway inflammation.
Reduced ventilation e.g. closing barn doors increases dust by 25-30%.
Mucking out - 19x respirable particles.
Mucking out next door - 9x respirable particles.
Hay net - 6x respirable particles compared to feeding from floor.

20
Q

Environmental management.

A

Turn out where possible.
Minimise dust in stable by:
- change stable – away from hay store, minimal foot traffic.
- low-dust bedding.
- optimise ventilation.
- remove horse from stable to muck out or sweep.
- Thorough clean – remove all dust and cobwebs and power hose floor to decrease ammonia.
- hose down yard/alleys.
- manage adjacent stables the same.

21
Q

Feeding asthmatic horses.

A

Dry hay the worst.
Soaked/steamed hay good as long as fed when wet.
Steamed better than soaked as bacteria/mould increases w/ soaking.
Haylage is good.

22
Q
  1. SPAOPD stand for?
  2. What is SPAOPD.
  3. When does SPAOPD occur?
  4. Tx?
A
  1. Summer pasture associated obstructive pulmonary disease.
  2. Similar to severe asthma but trigger is pasture environment.
    - likely due to hypersensitivity to environmental allergens like pollen/mould.
  3. Late spring to early summer.
  4. As for asthma except horse should be removed from pasture.
23
Q
  1. EIPH stand for?
  2. % horses found to have blood in trachea after racing.
  3. Origin?
A
  1. Exercise induced pulmonary haemorrhage.
  2. 75%.
  3. Haemorrhage originates from caudo-dorsal lung lobes.
24
Q
  1. EIPH main aetiology.
  2. Other contributing factors to EIPH?
A
  1. Stress failure of pulmonary capillaries.
    - high pulmonary intracapillary pressure and negative inspiratory pressures w/in airways leads to rupture of the capillary wall.
  2. Poss. association between lower airway inflammation and EIPH.
    Upper airway obstruction (e.g. RLN) may exacerbate EIPH.
    Associated w/ AF.
25
Q

EIPH clinical signs.

A

Epistaxis.
Reduced exercise tolerance (probably due to volume of haemorrhage).
Prolonged post-exercise recovery.

26
Q

EIPH Dx.

A

Endoscopy - blood in trachea.
TW/BAL - RBCs and haemosiderin-laden in less obvious cases.
Thoracic radiographs - caudo-dorsal lung field opacity (not used often clinically).

27
Q

EIPH Tx.

A

Eliminate any potential underlying cause (asthma, URT obstruction, AF).
Attempt to reduce severity.
USA not UK - frusemide (Lasix).
Nasal dilator strips (UK eventing, not racing).
Immunomodulators - airway inflammation.

28
Q

Bacterial pneumonia/pleuropneumonia in horses.

A

Needs a predisposing event that suppresses pulmonary immunity - very rarely primary disease.
Bacterial pathogens invade LRT - mixed infections common.

29
Q

Predisposing events for bacterial pneumonia/pleuropneumonia.

A

Inhalation of feed material
- e.g. choke/dysphagia.
Airway FB.
GA.
Stress/long distance travel (shipping fever) - restricted from lowering head so reduced mucociliary clearance.
Post viral infection.
Penetrating trauma.

30
Q

Bacterial pneumonia/pleural pneumonia clinical signs.

A

Fever, depression, lethargy, cough, nasal discharge.
Pleural effusion.
- Pleural pain (pleurodynia, endotoxaemia.
– Rapid shallow breathing.
–> Severity dept. on vol pleural effusion and extent of pulmonary consolidation.
—> Lack of breath sounds ventrally and abnormal sounds dorsally on auscultation.

31
Q

Bacterial (pleuro)pneumonia Dx.

A

Blood sample: High WBC and fibrinogen.
Bacterial culture of pleural fluid and TW/BAL samples.
Thoracic US.
Thoracic radiography.
Thoracocentesis.

32
Q

Bacterial (pleuro)pneumonia Tx.

A

Broad spectrum ABX.
Supportive care - NSAIDs, fluid therapy, nutritional support.
Thoracocentesis and drainage.