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Module 15 > Disorders of the Equine Lower Resp Tract 1 > Flashcards

Disorders of the Equine Lower Resp Tract 1 Flashcards

1
Q

how can horses be restrained for endoscopy

A
  1. twitch
  2. stocks
  3. sedation
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2
Q

what sedation can you use for upper airway endoscopy

A

a2 agonist + opioid

detomidine + butorphanol

romifidine + butorphanol

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3
Q

what should you examine in the trachea and bronchi in upper airway endoscopy

A
  1. exessive coughing: suggestive of resp disease
  2. examine carina: may see edema –> suggestive of lower airway inflammation (particularly severe SEA)
  3. examine secretions: may contain food material if dysphagic
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4
Q

what are the two areas where you can get resp cytology

A
  1. tracheal wash
  2. bronchoalveolar lavage
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5
Q

what can resp cytology diagnose

A
  1. inflammatory disorders: infectious/non-infectious
  2. hemorrhage: exercise induced pulmonary hemorrhage (EIPH)
  3. parasitic infections (sometimes)
  4. neoplasia (rarely)
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6
Q

where are secretions collected in a tracheal wash

A

from the distal trachea –> reflects whole of lungs but also trachea

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7
Q

what are the two methods of tracheal wash

A
  1. trans-tracheal (percutaneous)
  2. trans-endoscopic (20ml sterile saline instilled and then retrieved)
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8
Q

what are the two types of catheters used for a trans-endoscopic tracheal wash

A
  1. single lumen: cytology only
  2. triple lumen: cytology + microbiology
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9
Q

how are tracheal wash samples submitted

A

EDTA tube

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10
Q

what is indication of true bacterial infeciton from a tracheal wash

A

increased cell count

increased % degenerate neutrophils

free bacteria

phagocytosed bacteria (intracellular and extracellular)

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11
Q

what is the normal cytology in a tracheal wash

A

macrophages ~70%

lymphocytes ~30%

neutrophils <20%

eosinophils <1%

mast cell <1%

ciliated resp epithelial cells/squamous epithelial cells

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12
Q

what is a normal change to cytology in a horse that has recently travelled

A

tracheal wash neutrophilia

can briefly have up to 50% neutrophils (and rarely even higher) but would expect to then decrease and also have no clinical problems

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13
Q

what is seen here from a tracheal aspirate

A

healthy macrophages

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14
Q

what is seen here from a tracheal aspirate

A

active macrophages surrounded by multiple degenerate neutrophils

possibly caused by infection

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15
Q

what is shown here from a tracheal aspirate

A

multiple eosinophils

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16
Q

what is shown here from a tracheal aspirate

A

ciliated tracheal epithelial cells

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17
Q

how is tracheal wash microbiology done

A

trans-tracheal sample

or

guarded trans-endoscopic sample (triple lumen catheter)

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18
Q

what bacterial can be cultured from a tracheal wash

A

aerobic and anaerobic

fungal?

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19
Q

what do you need to differentiate from a tracheal microbial wash

A
  1. significant isolate vs contaminant
  2. may be non-pathogenic and potentially pathogenic bacteria present in clinically normal horses
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20
Q

what does bronchoalveolar lavage collect

A

respiratory secretions from the peripheral lung (alevoli and distal bronchioles)

not interchangeable with tracheal wash

provides more information –> if diffuse lower resp tract pathology, but may miss focal patholgoy

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21
Q

how is bronchoalveolar lavage (BAL) done

A

blind BAL tube (fogarty)

via endoscope (bronchoscopy)

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22
Q

how is bronchoalveolar lavage done blindly

A

tends to sample right dorsocaudal lobe

via endoscope, after tracheal wash, utilize the catether to deliver lignocaine at the carina

pass sterile BAL tube using sterile gloves

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23
Q

what should you see in the BAL sample

A

it should be foamy –> see the surfactant

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24
Q

what is the normal cytology in a BAL

A

macrophages 40-60%

lymphocytes 20-40%

neutrophils <5%

eosinophils <1%

mast cell <2%

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25
Q

what might you see in a BAL with EIPH

A

hemosiderophages

present up to 6 weeks after a bleed

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26
Q

are BAL samples suitable for microbiology

A

no

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27
Q

what would be consistent with mild/moderate equine asthma from a BAL

A

BALF with neutrophilia (>10%) +/- mast cells (>5%) +/- eosinophils (>5%)

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28
Q

what would stabling or a travelling healthy horse look like with BAL

A

>10% and up to 25% neutrophils with no clinical signs

care with interpretation –> in light of other clinical findings

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29
Q

what is seen with bacterial pneumonia on BAL

A

depending on location of lesion/focal or diffuse may see neutrophilia, degenerate neutrophils, intra or extra cellular bacteria

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30
Q

is hematology and serum biochem useful for equine asthma

A

no its not very useful

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31
Q

what is hematology and serum biochemistry useful for (5)

A
  1. infectious diseases (influenza serology, may be lymphopenia in viral infection)
  2. pneumonia/pleuropneumonia: except left shift neutrophilia, elevated fibrinogen and SAA
  3. parasitism: may be inflammatory response
  4. neoplasia
  5. immunodeficiency syndromes
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32
Q

what does arterial blood gas analyze

A

O2 and CO2

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33
Q

when does hyperpnea start at

A

~ PaO2 <70 mmHg

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34
Q

what sites can arterial blood gas analysis be taken at

A

transverse facial or facial

in foals: great metatarsal artery, brachial artery

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35
Q

what is thoracic ultrasonography useful for (5)

A
  1. peripheral lung disease: abscess, consolidation, comet tails (pleural inflammation/thickening)
  2. pleural disease: pleural effusion
  3. pneumothorax
  4. rib fracture
  5. diaphragmatic hernia (rare)
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36
Q

what is shown here

A

pleural surface (hyperechoic) with parallel artefacts

it slides

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37
Q

what is shown here

A

pleural fluid

atelectasis or consolidation

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38
Q

what is shown here

A

comet tails: pleural inflammation/thickening

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39
Q

what is thoracocentesis useful for

A
  1. total white cell count and protein concentrations
  2. cytological examination
  3. microbiological culture and sensitivity
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40
Q

how is thoracocentesis fluid classified

A
  1. transudate/modified transudate
  2. exudate
  3. hemorrhage
  4. chylous
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41
Q

what are the most common causes of pleural effusion

A
  1. bacterial infection
  2. neoplasia
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42
Q

what are other diagnostic tests that can be used (6)

A
  1. dynamic endoscopy
  2. CT/MRI
  3. lung function testing
  4. lung scintigraphy
  5. mass FNA/biopsy
  6. lung biopsy
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43
Q

what is equine asthma

A

nonseptic lower airway inflammation

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44
Q

how is equine asthma categorized

A

to the presence or absence of resp effort at rest

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45
Q

what is severe equine asthma

A

adult horses with lower airway inflammation and obstruction associated with frequent coughing and increased respiratory effort at rest

46
Q

how can severe equine asthma obstruction reversed by

A

bronchodilators or environmental change

47
Q

what is severe equine asthma prev known as

A

recurrent airway obstruction (ROA)

heaves

chronic obstructive pulmonary disease (COPD)

48
Q

what is mild to moderate equine asthma

A

no infection detected and no increased resp effort at rest

49
Q

what is seen in BAL fluid with mild to moderate equine asthma

A

excess tracheobronchial mucus and/or increased ratio neutrophils, eosinophils and/or mast cells in BAL fluid

50
Q

what would a horse be experiencing with mild to moderate equine asthma

A

any age horse with chronic (>4 weeks) and/or poor performance

51
Q

what is mild to moderate EA prev known as

A

inflammatory airway disease (IAD)

52
Q

what is SEA caused by

A

hypersensitivity response to airborne organic dust

53
Q

what kind of airborne organic dust can cause SEA

A
  1. stabling and/or feeding hay
  2. moulds (fungal spores), bacterial endotoxins (hay/straw baled with high moisture content)
  3. +/- irritants such as ammonia, cold air, dust, etc
54
Q

what is the pathophysiology of SEA (6)

A
  1. non-infectious LRT inflammatory disease (hypersensitivity response)
  2. neutrophil influx into the airways
  3. mucus accumulation
  4. bronchospam
  5. bronchial hyperreactivity
  6. bronchoilitis, bronchiectasis, progressive fibrosis (airway remodelling over time)
55
Q

how are the bronchi innervated (3)

A
  1. symapthetic innervation: B2 adgrenergic receptors (reduced in SEA horses)
  2. parasympathetic: cholinergic (mainly excitatory)
  3. nonadrenergic-noncholinergic innervation: majority of inhibition –> bronchodilation
56
Q

when is SEA typically seen

A

in mature animals (>7 years)

57
Q

what are the clinical signs of SEA (6)

A

variable and can be subtle

  1. mucoid nasal discharge
  2. cough
  3. exercise intolerance
  4. increased resp effort (bronchiolar narrowing, eventually hypertrophy of external abdominal oblique muscles)
  5. nostril flaring
  6. tachypnea
58
Q

how is SEA diagnosed

A
  1. history, clinical signs and physical exam (end expiratory wheezes, early inspiratory crackles)
  2. tracheal endoscopy
  3. tracheal wash
  4. BAL
  5. evidence of obstruction
59
Q

on tracheal wash how would SEA be confirmed

A

neutrophillic inflammation (usually >50%) –> may be degenerate

but no evidence of primary bacterial infection (a culture may identify secondary infection)

60
Q

what would be seen on BAL that would confirm SEA

A

neutrophilic inflammation (usually >25%)

key to diagnosis –> good correlation between differential cell counts and airway obstruction

61
Q

how is evidence of obstruction in SEA measured

A

pulmonary function tests (+/- challenge test ex. buscopan)

can detect obstruction when no visual signs

should acheive bronchodilation and should improve all signs (wheezes, resp effort) and as soon as drug wears off it will be back to the signs

62
Q

what can atropine be used for in SEA horses

A

rescue –> one of treatment of severe resp signs

63
Q

what are the goals of treatment/management in SEA

A
  1. treat airway inflammation
  2. relieve airway obstruction
  3. prevent reoccurrence
64
Q

how is SEA managed/treated

A
  1. environmental management
  2. pharmacological treatment
65
Q

how is SEA environmentally managed (7)

A
  1. 24 hour turnout if possible
  2. low dust housing (pasture, low dust bedding)
  3. low dust feed (haylage, soaked hay, steam hay, pellets)
  4. good ventilation
  5. stable: avoid deep bedding, neighbours managment, groom outside, damp all feeds, don’t muck out with horse in stable
  6. forage/staw store location
  7. muck heap location
66
Q

what pharmacological therapies can be used for SEA

A
  1. systemic
  2. inhalational
67
Q

what are the pros of systemic pharmaceuticals for SEA

A

easy and cheap

68
Q

what are the pros of inhalational pharmaceticals in SEA

A

effacious

deliver high concentrations to airway with reduced risk of side effects

compliance

69
Q

what are the aims of therapy in SEA (7)

A
  1. decrease inflammation
  2. relieve bronchospasm
  3. reduced bronchoconstriction
  4. increased mucociliary clearance
  5. decrease viscosity
  6. stabilize mast cells
  7. suppress immune response
70
Q

what therapy should you focus on when in resp distress with SEA

A
  1. decrease inflammation
  2. relieve bronchospasm
  3. reduce bronchoconstriction
71
Q

what are the mainstay of SEA to control airway inflammation

A

corticosteroids

systemic or inhalational

72
Q

what are systemic corticosteroids used for SEA to reduce airway inflammation

A

prednisolone or dexamethasone

but risk of laminitis

73
Q

what are inhalational corticosteroids used for SEA to reduce airway inflammation

A

metered dose inhaler (MDI) or nebulized

74
Q

do NSAIDs or anti-histamines have an effect on reducing airway inflammation in SEA

A

no

75
Q

what is aerohippus

A

an inhaler

a spacer chamber

for MDI only

76
Q

what is flexineb

A

MDI

nebulize: steroids, antimicrobials, acetylcysteine, saline, etc

77
Q

what are the functions of inhaled corticosteroids in SEA

A
  1. decreased airway reactivity
  2. improved pulmonary function
78
Q

what is fluticasone propionate

A

most potent inhalant corticosteroids

longest pulmonary residence time

causes least adrenal suppression

benefit noted 24-48 hours

1000-2500 ug/450 kg BID or SID

79
Q

what is beclomethasone dipropionate

A

longer term control of airway inflammation

cheaper

500-3750 ug/450kg horse BID or SID

80
Q

what is aservo equihaler

A

ciclesonide

inactive prodrug –> low affinity of glucocorticoid receptors

enzyme activiation in lungs –> high affinity for glucocorticoid receptors

good safety profile

81
Q

what are the functions of bronchodilators

A

relief in lower airway obstruction

82
Q

what are bronchodilators used in combo with

A

in combo with dust control and corticosteroids (improve deposition of inhaled corticosteroids)

83
Q

are bronchodilators rapid or slow onset

A

rapid –> rescue treatment

84
Q

are corticosteroids rapid or delayed onset

A

delayed

there is a lag period

85
Q

what are the two types of bronchodilators

A
  1. B2 adrenergic agonists
  2. anticholinergics
86
Q

what is the smooth muscle tone in the bronchi mostly

A

mainly parasympathetic

87
Q

what is the B2 adnergic receptors innervated by

A

sympathetic innervation

88
Q

do B2 adrenergic agonists have a anti-inflammatory effect

A

yes they might

89
Q

what is clenbuterol

A

B2 adnergic agonist

90
Q

how is clenbuterol administered

A

IV

oral

91
Q

when giving oral clenbuterol what do you need to do

A

exceed recommended dose rate (0.8ug/kg)

because in severe resp distress there is reduced B2 adrenergic receptors

stepwise increase over time, as drug induces down regulation of B2 over time

–> prevented by corticosteroids

92
Q

what are the side effects of clenbuterol

A

sweating/mild colic

affects uterus –> can interfere with parturition

93
Q

what are inhaled bronchodilators

A
  1. salbutamol (albuterol)
  2. salmeterol
94
Q

what is the difference in salbutamol and salmeterol

A

slabutamol is short acting –> rescue

salmeterol: longer term control

95
Q

what is salbutamol used for

A

emergency relief or rescue drug

increase corticosteroid deposition

<4x/week unless together with corticosteroid

96
Q

what is salmeterol used for

A

longer term control of SEA

duration 6-8 hours

use with corticosteroid

97
Q

how long is the duration of salmeterol

A

duration 6-8 hours

98
Q

what should salmeterol be used with and what are the benefits of this

A

use with corticosteroid

anti-inflammatory effect

reduce smooth muscle proliferation

improved mucociliary clearance

improved pulmonary function?

99
Q

what are examples of anticholinergic bronchodilators

A
  1. ipratropium
  2. atropine
  3. buscopan
100
Q

what is ipratropium

A

inhaled anticholinergic

longer action than B2

101
Q

what is atropine

A

anticholinergic bronchodilator

systemic

102
Q

when is atropine used in SEA

A

immediate resuce when in severe resp distress

103
Q

what are the side effects of atropine

A

side effects on GI tract (prolonged reduction in intestinal motility)

cannot repeate dose

104
Q

what is buscopan used for

A

diagnostic for SEA

rescue

normally used to aid rectal exam/spasmodic colic

105
Q

what is buscopan

A

systemic anticholinergic

106
Q

when would antibiotics be indicated in SEA

A

if secondary infection with bacteria involved

107
Q

what other medications can be used in SEA

A
  1. mucolytics
  2. expectorants
  3. mast cell stabilizers: inhalational sodium cromoglycate
108
Q

how can SEA be conservatively managed

A

where less than desirable environment/feeding practice can be easily identified

change environment/feeding –> turn out

no treatment, or just oral clenbuterol

reserve further investigation for non-response

109
Q

for high performance horses how is SEA treated

A

futher investigation (cytology)

oral clenbuterol for two weeks or inhaled B2 agonist, combined with longer term inhaled, or systemic, corticosteroids

110
Q

what is summer pasture associated SEA

A

clinically indistinguishable from SEA

similar signalment, clinical signs

some may have both SEA and SPA-SEA

111
Q

what triggers SPA-SEA

A

different aeroallergens

seen at pasture

allergy to flower/crop/trees/grass pollens and moulds

seen in summer/autumn when plants/trees are flowering

Module 15 (27 decks)

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