Disorders of the Equine Lower Resp Tract 1 Flashcards
1
Q
how can horses be restrained for endoscopy
A
- twitch
- stocks
- sedation
2
Q
what sedation can you use for upper airway endoscopy
A
a2 agonist + opioid
detomidine + butorphanol
romifidine + butorphanol
3
Q
what should you examine in the trachea and bronchi in upper airway endoscopy
A
- exessive coughing: suggestive of resp disease
- examine carina: may see edema –> suggestive of lower airway inflammation (particularly severe SEA)
- examine secretions: may contain food material if dysphagic
4
Q
what are the two areas where you can get resp cytology
A
- tracheal wash
- bronchoalveolar lavage
5
Q
what can resp cytology diagnose
A
- inflammatory disorders: infectious/non-infectious
- hemorrhage: exercise induced pulmonary hemorrhage (EIPH)
- parasitic infections (sometimes)
- neoplasia (rarely)
6
Q
where are secretions collected in a tracheal wash
A
from the distal trachea –> reflects whole of lungs but also trachea
7
Q
what are the two methods of tracheal wash
A
- trans-tracheal (percutaneous)
- trans-endoscopic (20ml sterile saline instilled and then retrieved)
8
Q
what are the two types of catheters used for a trans-endoscopic tracheal wash
A
- single lumen: cytology only
- triple lumen: cytology + microbiology
9
Q
how are tracheal wash samples submitted
A
EDTA tube
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)
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
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
13
Q
what is seen here from a tracheal aspirate
A
healthy macrophages
14
Q
what is seen here from a tracheal aspirate
A
active macrophages surrounded by multiple degenerate neutrophils
possibly caused by infection
15
Q
what is shown here from a tracheal aspirate
A
multiple eosinophils
16
Q
what is shown here from a tracheal aspirate
A
ciliated tracheal epithelial cells
17
Q
how is tracheal wash microbiology done
A
trans-tracheal sample
or
guarded trans-endoscopic sample (triple lumen catheter)
18
Q
what bacterial can be cultured from a tracheal wash
A
aerobic and anaerobic
fungal?
19
Q
what do you need to differentiate from a tracheal microbial wash
A
- significant isolate vs contaminant
- may be non-pathogenic and potentially pathogenic bacteria present in clinically normal horses
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
21
Q
how is bronchoalveolar lavage (BAL) done
A
blind BAL tube (fogarty)
via endoscope (bronchoscopy)
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
23
Q
what should you see in the BAL sample
A
it should be foamy –> see the surfactant
24
Q
what is the normal cytology in a BAL
A
macrophages 40-60%
lymphocytes 20-40%
neutrophils <5%
eosinophils <1%
mast cell <2%
25
what might you see in a BAL with EIPH
hemosiderophages
present up to 6 weeks after a bleed
26
are BAL samples suitable for microbiology
no
27
what would be consistent with mild/moderate equine asthma from a BAL
BALF with neutrophilia (\>10%) +/- mast cells (\>5%) +/- eosinophils (\>5%)
28
what would stabling or a travelling healthy horse look like with BAL
\>10% and up to 25% neutrophils with no clinical signs
care with interpretation --\> in light of other clinical findings
29
what is seen with bacterial pneumonia on BAL
depending on location of lesion/focal or diffuse may see neutrophilia, degenerate neutrophils, intra or extra cellular bacteria
30
is hematology and serum biochem useful for equine asthma
no its not very useful
31
what is hematology and serum biochemistry useful for (5)
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
32
what does arterial blood gas analyze
O2 and CO2
33
when does hyperpnea start at
~ PaO2 \<70 mmHg
34
what sites can arterial blood gas analysis be taken at
transverse facial or facial
in foals: great metatarsal artery, brachial artery
35
what is thoracic ultrasonography useful for (5)
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)
36
what is shown here
pleural surface (hyperechoic) with parallel artefacts
it slides
37
what is shown here
pleural fluid
atelectasis or consolidation
38
what is shown here
comet tails: pleural inflammation/thickening
39
what is thoracocentesis useful for
1. total white cell count and protein concentrations
2. cytological examination
3. microbiological culture and sensitivity
40
how is thoracocentesis fluid classified
1. transudate/modified transudate
2. exudate
3. hemorrhage
4. chylous
41
what are the most common causes of pleural effusion
1. bacterial infection
2. neoplasia
42
what are other diagnostic tests that can be used (6)
1. dynamic endoscopy
2. CT/MRI
3. lung function testing
4. lung scintigraphy
5. mass FNA/biopsy
6. lung biopsy
43
what is equine asthma
nonseptic lower airway inflammation
44
how is equine asthma categorized
to the presence or absence of resp effort at rest
45
what is severe equine asthma
adult horses with lower airway inflammation and obstruction associated with frequent coughing and **increased respiratory effort at rest**
46
how can severe equine asthma obstruction reversed by
bronchodilators or environmental change
47
what is severe equine asthma prev known as
recurrent airway obstruction (ROA)
heaves
chronic obstructive pulmonary disease (COPD)
48
what is mild to moderate equine asthma
no infection detected and **no increased resp effort at rest**
49
what is seen in BAL fluid with mild to moderate equine asthma
excess tracheobronchial mucus and/or increased ratio neutrophils, eosinophils and/or mast cells in BAL fluid
50
what would a horse be experiencing with mild to moderate equine asthma
any age horse with chronic (\>4 weeks) and/or poor performance
51
what is mild to moderate EA prev known as
inflammatory airway disease (IAD)
52
what is SEA caused by
hypersensitivity response to airborne organic dust
53
what kind of airborne organic dust can cause SEA
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
what is the pathophysiology of SEA (6)
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
how are the bronchi innervated (3)
1. symapthetic innervation: B2 adgrenergic receptors (reduced in SEA horses)
2. parasympathetic: cholinergic (mainly excitatory)
3. nonadrenergic-noncholinergic innervation: majority of inhibition --\> bronchodilation
56
when is SEA typically seen
in mature animals (\>7 years)
57
what are the clinical signs of SEA (6)
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
how is SEA diagnosed
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
on tracheal wash how would SEA be confirmed
neutrophillic inflammation (usually \>50%) --\> may be degenerate
but no evidence of primary bacterial infection (a culture may identify secondary infection)
60
what would be seen on BAL that would confirm SEA
neutrophilic inflammation (usually \>25%)
key to diagnosis --\> good correlation between differential cell counts and airway obstruction
61
how is evidence of obstruction in SEA measured
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
what can atropine be used for in SEA horses
rescue --\> one of treatment of severe resp signs
63
what are the goals of treatment/management in SEA
1. treat airway inflammation
2. relieve airway obstruction
3. prevent reoccurrence
64
how is SEA managed/treated
1. environmental management
2. pharmacological treatment
65
how is SEA environmentally managed (7)
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
what pharmacological therapies can be used for SEA
1. systemic
2. inhalational
67
what are the pros of systemic pharmaceuticals for SEA
easy and cheap
68
what are the pros of inhalational pharmaceticals in SEA
effacious
deliver high concentrations to airway with reduced risk of side effects
compliance
69
what are the aims of therapy in SEA (7)
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
what therapy should you focus on when in resp distress with SEA
1. decrease inflammation
2. relieve bronchospasm
3. reduce bronchoconstriction
71
what are the mainstay of SEA to control airway inflammation
corticosteroids
systemic or inhalational
72
what are systemic corticosteroids used for SEA to reduce airway inflammation
prednisolone or dexamethasone
but risk of laminitis
73
what are inhalational corticosteroids used for SEA to reduce airway inflammation
metered dose inhaler (MDI) or nebulized
74
do NSAIDs or anti-histamines have an effect on reducing airway inflammation in SEA
no
75
what is aerohippus
an inhaler
a spacer chamber
for MDI only
76
what is flexineb
MDI
nebulize: steroids, antimicrobials, acetylcysteine, saline, etc
77
what are the functions of inhaled corticosteroids in SEA
1. decreased airway reactivity
2. improved pulmonary function
78
what is fluticasone propionate
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
what is beclomethasone dipropionate
longer term control of airway inflammation
cheaper
500-3750 ug/450kg horse BID or SID
80
what is aservo equihaler
ciclesonide
inactive prodrug --\> low affinity of glucocorticoid receptors
enzyme activiation in lungs --\> high affinity for glucocorticoid receptors
good safety profile
81
what are the functions of bronchodilators
relief in lower airway obstruction
82
what are bronchodilators used in combo with
in combo with dust control and corticosteroids (improve deposition of inhaled corticosteroids)
83
are bronchodilators rapid or slow onset
rapid --\> rescue treatment
84
are corticosteroids rapid or delayed onset
delayed
there is a lag period
85
what are the two types of bronchodilators
1. B2 adrenergic agonists
2. anticholinergics
86
what is the smooth muscle tone in the bronchi mostly
mainly parasympathetic
87
what is the B2 adnergic receptors innervated by
sympathetic innervation
88
do B2 adrenergic agonists have a anti-inflammatory effect
yes they might
89
what is clenbuterol
B2 adnergic agonist
90
how is clenbuterol administered
IV
oral
91
when giving oral clenbuterol what do you need to do
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
what are the side effects of clenbuterol
sweating/mild colic
affects uterus --\> can interfere with parturition
93
what are inhaled bronchodilators
1. salbutamol (albuterol)
2. salmeterol
94
what is the difference in salbutamol and salmeterol
slabutamol is short acting --\> rescue
salmeterol: longer term control
95
what is salbutamol used for
emergency relief or rescue drug
increase corticosteroid deposition
\<4x/week unless together with corticosteroid
96
what is salmeterol used for
longer term control of SEA
duration 6-8 hours
use with corticosteroid
97
how long is the duration of salmeterol
duration 6-8 hours
98
what should salmeterol be used with and what are the benefits of this
use with corticosteroid
anti-inflammatory effect
reduce smooth muscle proliferation
improved mucociliary clearance
improved pulmonary function?
99
what are examples of anticholinergic bronchodilators
1. ipratropium
2. atropine
3. buscopan
100
what is ipratropium
inhaled anticholinergic
longer action than B2
101
what is atropine
anticholinergic bronchodilator
systemic
102
when is atropine used in SEA
immediate resuce when in severe resp distress
103
what are the side effects of atropine
side effects on GI tract (prolonged reduction in intestinal motility)
cannot repeate dose
104
what is buscopan used for
diagnostic for SEA
rescue
normally used to aid rectal exam/spasmodic colic
105
what is buscopan
systemic anticholinergic
106
when would antibiotics be indicated in SEA
if secondary infection with bacteria involved
107
what other medications can be used in SEA
1. mucolytics
2. expectorants
3. mast cell stabilizers: inhalational sodium cromoglycate
108
how can SEA be conservatively managed
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
for high performance horses how is SEA treated
futher investigation (cytology)
oral clenbuterol for two weeks or inhaled B2 agonist, combined with longer term inhaled, or systemic, corticosteroids
110
what is summer pasture associated SEA
clinically indistinguishable from SEA
similar signalment, clinical signs
some may have both SEA and SPA-SEA
111
what triggers SPA-SEA
different aeroallergens
seen at pasture
allergy to flower/crop/trees/grass pollens and moulds
seen in summer/autumn when plants/trees are flowering
