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Respiratory > Equine URT Surgery > Flashcards

Equine URT Surgery Flashcards

1
Q

Primary presenting problems for URT surgery?

A
  • discharge (1)
  • poor performance (2)
  • abnormal resp noise (stridor or stertor) (2)
  • epistaxis (3)
  • abnormal swelling of head/neck
  • cough
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2
Q

How is the URT examined at first?

A
  • examine for nasal discharge, facial symmetry, airflow
  • palpation of nostrils, septum, sinuses, GP, LNs (submandibular and retropharyngeal) larynx, trachea
  • percussion of paranasal sinuses (?)
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3
Q

How is URT examined at work?

A
  • lunge, saddle/harness
  • onset and character of noise
  • exercise intolerance due to unfitness?
  • soundness
  • respiratory pattern and recovery
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4
Q

Which further diagnostics are available for respiratory investigation?

A
  • endoscopy
  • radiography/Ct
  • sinusoscopy
  • bacterial culture and sense (NOT very useful but good to rule out strangles)
  • biopsy for cytology/histo
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5
Q

What is currently performed at the same time of dynamic endoscopy? Why is this test useful?

A
  • dynamic/overgorund endoscopy good for seeing horse in natural work environment
  • treadmill good for standardising fitness tests
  • myopathy assessment carried out concurrently
  • excercising ECG to rule out cardiac issues
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6
Q

(1) How may nasal discharge be characterised? Ddx for each?

A

> character
- serous/mucoid/purulent/necrotic
laterality
- unilateral (sinuses, nasal passage, GP)
- bilateral (lungs, pharynx)
odour
- no odour (LRT, sinusitis, pharyngitis, pouch empyema)
- foul odour (dental disease, neoplasia, necrotising LRT)

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7
Q

5 potential sources of nasal discharge?

A
  • nasal passages
  • paranasal sinus
  • GP
  • pharynx/larynx
  • LRT (see other lecture)
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8
Q

How may source of discharge be determined?

A
  • PE
  • endoscopy (paranasal sinuses, GP, LRT)
  • radiography (sinuses, GPs - look for fluid lines)
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9
Q

Is 1* nasal passage disease common? Potential causes?

A

No

  • bacterial infection (sepotum or turbinates)
  • fungal infection
  • neoplasia
  • FBs
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10
Q

POssibel concurrent signs of nasal discharge d/t nasal passage disease?

A
  • v airflow
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11
Q

How can nasal discharge d/t sinusitis be diagnosed?

A
  • PE: v resonance on percussion, sinus swelling

- endoscopy: draining from nasomaxillary opening

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12
Q

What diagnostics can be sued to examin the sinuses?

A
  • radiography (fluid lines, masses)
  • CT
  • sinus centesis
  • sinoscopy
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13
Q

Causes of sinusitis

A
  • 1* bacterial/fungal infection
  • 1* neoplasia
  • 2* to dental disease (09-11)
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14
Q

POssibel concurrent signs of nasal discharge d/t sinusitis?

A
  • v airflow (not necessarily with bacterial etc.)
  • facial swelling
  • dullness on percussion
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15
Q

Tx of sinusitis

A 
> medical 
- lavage, Abx
* may improve then relapse
> surgical
- sinusoscopy (fenestration of ventral conchal bulla (VCB))
- removing inciting cause 
- flap sinusotomy
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16
Q

which route of entry is advocated for sinus centesis and lavage? which others exist?

A

> concho frontal sinus portal (SinusPortal) best approach in majority of cases

  • eradicates risk of damage to cheek tooth roots in maxillary sinus, and better visability if maxillary sinuses full of crud
  • caudal maxillary SP
  • caudal rostral maxillary SP
  • light indicated rostral maxillary SP
  • rostral rostral maxillary SP
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17
Q

Landmarks for maxillary sinuses?

A
  • facial crest
  • infraorbital foramen
  • canthus of the eye?
  • LOOK UP*
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18
Q

Which bacteria commonly infect the sinuses?

A

1* b haem strep spp.

2* mixed +- plant material

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19
Q

Potential causes of GP disease causing nasal discharge?

A 
> GP empyema
- most common 
- bacterial infection of GP often d/t s. equi 
> GP catarrah 
- excessive mucus production by pouch d/t inflammation 
> GP Mycosis 
- concurrent signs likely seen 
> GP neoplasia
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20
Q

POssibel concurrent signs of nasal discharge d/t GP disease?

A
  • swelling at Viborg’s triangle

- other signs of GP myscosis

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21
Q

Diagnosis of GP empyema?

A
  • endoscopy: discharge/fluid accumulation in pouch
  • radiography: fluid line
  • r/o chondroids
  • culture
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22
Q

Tx GP empyema?

A

> medical
- pouch lavage
- Abx (strep equi = penicillin with gelatin and TMPS)
- removal of chondroids if necessary (BEFORE lavage)
surgical [rare nowadays]
- Viborg’s triange approach for drainage
- ventral paramedian (Whitehouse) for chondroid removal [most common]
- dyspnoeic horses may need tracheostomy

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23
Q

What equipment may be used to lavage the GP?

A
  • foley catheter and chambers catheter
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24
Q

(2) what causes abnormal noises in the resp tract?

A

turbulent flow

  • so there must be flow
  • and an obstruction
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25
Q

Where is URT resistance greatest at inspiration and expiration?

A
  • inspiration: URT
  • expiration: lung
    > small v airway diameter -> ^4 increase in airway resistnace!
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26
Q

How may URT noises be characterised? DDx for each?

A 
> constancy
- fixed (mass, chondritis, strictures) 
- dynamic (RLN, DDSP, AEE) 
> quality 
- stridor (narrowed airway: RLN, chondritis, mass, stricture)
- sturtor (tissue vibration: DDSP, nostril problems) 
> phase
- inspiratory (RLN)
- expiratory (DDSP, AEE) 
- both (mass, chondritis)
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27
Q

Potential sites of URT obstruction and which disorders cause these?

A 
> nostrils
- alar fold collapse/alar flutter
- incomplete dilation 
> nasal passages
- septal disease
- small nasal passages
- eruption bumps (tubercula transitoria) 
- mass lesions 
> sinuses (expansile lesions NOT 1* sinusitis)
- cysts
- masses
> nasopharynx
- DDSP 
- postural compression -> nasopharyngeal collapse on flexion
- pharyngeal cysts 
> larynx
- RLN roarers
- epiglottic entrapment 
- arytenoid chondritis
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28
Q

Clinical signs of DDSP?

A
  • “choking down” stopping very suddenly at gallop
  • expiratory stertor
  • mouth breathing (pathognomic)
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29
Q

Diagnosis of DDSP?

A
  • gold standard dynamic endoscopy
  • difficult at rest
  • history
    > resting endoscopy can rule out other disorders
  • assess GPs (inflame/exudate, retropharyngeal lymphadenopathy)
    > DDSP suspected if
  • horse readily displaces with nasal occlusion and doesn’t easily replace
  • marked hypoplasia or deformity of epiglottis
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30
Q

Conservative Tx of DDSP?

A
  • tx concurrent disorders (GP disease as may affect nn. running alongside, LRT disease)
  • minimise poll flexion
  • keep mouth closed (drop noseband, Cornell collar mimics action of TH muscle, tongue tie)
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31
Q

Surgical Tx of DDSP?

A
  • numerous procedures shows aetiology poorly understood
  • Llewelyn procedure (Sternothyroideus myectomy +- staphylectomy (trim edge of palate))
  • Thermal palatoplasty (laser or cautery, stiffens palate to prevent billowing, cheap, effectiveness recently questioned)
  • surgical tension palatoplasty (similar concept to thermal)
  • laryngeal tie-forward, Cornell (placing sutures to mimic function of thyrohyoideus m.)
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32
Q

Which sites may pharyngeal cysts arise? What type of obstruction do these cause?

A
  • subepiglottic (thyroglossal duct)
  • dorsal pharyngeal (craniopharyngeal duct)
  • palatine
    > static obstruction
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33
Q

Clinical signs of pharyngeal cysts in foals and young adults?

A 
> foals 
- dysphagia
- dyspnoea 
> young adults
- poor performance
- respiratory noise
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34
Q

Which muscle is affected with RLN? Pathogenesis?

A
  • degenerative axonopathy
  • left side
  • most common in large horses
  • impaired function of cricoarytenoideus dorsalis (CAD) muscle (1* abductor of arytenoid cartilages)
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35
Q

Which vessels do the leftand right bracnhes of RLN wrap around?

A
  • left : aortic arch

- ricght: subclavian

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36
Q

Clinical signs of RLN?

A
  • asymptomatic at rest/low level exercise
  • inspiratory stridor with mod-marked exercise
  • impaired athletic performance at high levels
37
Q

What causes the roaring associated with RLN?

A
  • vocal coards would be tightened by abduction of arytenoids, instead lie lax in the resp tract, leaving laryngeal ventricles open -> roaring
38
Q

How may RLN br graded?

A
  1. in resting, unsedated horses

2. at exercise (not always possible)

39
Q

Outline gradingsystem for RLN horses at rest

A
  1. synchronous full abduction of both arytenoids
  2. asynchronous movement of L arytenoid, but FULL abduction induced by nasal occlusion
  3. asynchronous movement of L arytenoid that cannot be induced by nasal occlusion/saline in airway
  4. marked asymmetry at rest, no substantial movementof L arytenoid
40
Q

Outline grading system of RLN at exercise

A

A: full abduction
B: not fully abducted but held at normal resting position
C: dynamic collapse (neg pressure in airway sucks cartilage across)

41
Q

How does resting and excercising grade relate?

A
  • ALl grade 1 and 2 horses will be A
  • All grade 4 horses will be C
    > Grade 3 horses variable so require endoscopy
42
Q

Treatment of laryngeal dysfunction to varying degrees?

A
  • 1 and 2: monitor, no tx required
  • 3A (asynchronous at rest but fine at exercise): no tx required
  • 3B ventriculocordectomy +- laryngoplasty (plaryngeal prosthesis/’tie back’) depending on level
  • 3C treat as Grade 4
  • 4: dependant on level of performance
    > high: laryngoplasty ‘tieback’ to improve performance +- ventriculocordectomy to remove noise
    > low: ventriculocordectomy to remove noise
  • newer tx: CAD reinnervation by nerve anastomosis/nerve:muscle pedicle grafting (not viable in racing industry as takes too long)
43
Q

Potential complications of a tieback surgery?

A
  • cant collapse during swallowing (other side will usually compensate) -> cough after eating (10%)
  • aspiration pneumonia (1% cases)
  • suture sinus (1%)
  • lack of improvement 30% cases
44
Q

What does laryngeal tieback procedure effectively do?

A

Replace CAD muscle

45
Q

What is AEE? Which horses are predisposed?

A

Epiglottic entrapment in subepiglottic mucosa and aryepiglottic folds

  • most common in horses with epiglottic hypoplasia or deformity
  • may be intermittent
46
Q

CLinical signs of AEE?

A
  • poor performnance
  • expiratory stridor
  • may be asymptomatic
47
Q

Where does the aryepiglottic tissue lie normally?

A

under epiglottis and round sides over top of corniculate processes to make “button hole” that epiglottis pokes through

48
Q

How does epiglottic entrapment appear endoscopically?

A
  • no BVs
  • smooth edges
    > as covered in membrane|!
  • ulceration may be seen
49
Q

Tx of AEE (epiglottic entrapment)

A

> midline division of entrapping tissue

  • laryngotomy
  • transendoscopic laser
  • bistoury hook
50
Q

Complications of epiglottic entrapment AEE surgery?

A
  • re-entrapment 5-40%
  • laceration of soft palate or epiglottis
  • DDSP 10% (initial problem may have been protective of DDSP)
51
Q

What is arytenoid chondritis and which disease may it mimic? Clinical signs?

A
  • chronic infection of arytenoid cartilage body
    -> thickened cartilages and intraliuminal grnaulations
    > clinical signs
  • inspiratory stridor in intense work (aymptomatic at rest)
  • mimics RLN (look for ulceration and swelling of arytenoid body, lateral to corniculate processes to differentiate)
  • more stable obstruction than RLN
52
Q

Aetiology of arytenoid chondritis?

A
  • unknown
  • may follow laryngitis
  • can be experimentally induced by denuding arytenoid mucosa but only in some cases not always
53
Q

Tx arytenoid chondritis?

A
  • sharp/laser excision of intraluminal protruberences
  • partial/complete removal of affected arytenoid cartitlage
  • Abx cannot fully cure as cartilage misshapen but may help (also remember poor blood supply to cartilage)
54
Q

Which obstructions can only be diagnosed on dynamic endoscopy?

A
  • DDSP (will always replace when swallowing)
  • nasopharyngeal collapse (fat ponies flexing)
  • epigl;ottic retroversion
  • axial deviation aryepiglottic folds
  • intermittent epiglottic entrapment
55
Q

Which conditions can only be diagnosed at exercise?

A

> dynamic obstructions

  • DDSP
  • nasopharyngeal collapse (fat horses flexing)
  • epiglottic retroversion
  • axial deviation aryepiglottic folds
  • intermittent epiglottic entrapemnt
56
Q

What 1* problems may cause respiratory obstruction 2*?

A
  • inflammation affecting muscles (muscle needed to stabilise all structures of the larynx!!)
  • lymphoid hyperplasia commonly seen on endoscopy esp young racehorses
57
Q

How may epistaxis be described or refined?

A

> laterality
- Unilateral (nasal passages, sinuses or GP affected)
- Bilateral (LRT)
association with work
- Excercise-induced (EIPH)
- Resting (GP mycosis, ethmoid haematoma, fungal sinusitis)
QUantity
- modest (EIPH, ethmoid haematoma, fungal sinusitis)
- profuse (GP mycosis -> BV rupture)

58
Q

What diagnositcs can be used to determine hte source of epistaxis?

A 
> endoscopy 
- paranasal sinuses
- gutternal pouches
- LRT 
> radiography
- sinuses
- GPs
59
Q

What is PEH?

A

> progressive ethmoidal haematoma

  • progressively enlarging, non-neoplastic mass
  • originates in ethmoid turbinates (sphenopalatine sinus near ethmoid labyrinth)
  • may expand to occupy nasal passages, ,maxillary and frontal sinuses or nasopharynx
60
Q

HIstology of PEH

A
  • capsule respiratory mucosa and fibrous tissue
  • stroma blood, fibrous tissue, macrophages, giant cells, haemosiderocytes (suggests repeated bouts of local haemnorrhage)
61
Q

Clinical signs and commonly affected horses for PEH?

A
  • middle aged (6+) horses as needs time to grow to appropriate size
  • spontaneous epistaxis most common presenting complaint (small volume)
  • can be bilateral (15-30% cases)
62
Q

What is seen on endoscopy with PEH?

A
  • smooth greenish-black/reddish-brwonb mass

- may reveal nothing or just blood exiting nasomaxillary opening

63
Q

What is visable on radiographs with eithmoidal haematoma?

A
  • definition of size and shade of haematoma
  • smnooth, well circumscribed mass rostral to ehtmoid labyrinth
  • in advanced cases, soft tissue density fully occupies maxillary and frontal sinuses and-or nasal passages
    > CT better!!
64
Q

How is diagnosis of ethmoidal haematoma confirmed?

A
  • nasal lesions (CAN biopsy with uterine biopsy forceps under endoscopic guidance, but will break capsule and interfere with tx)
  • sinus lesions (biopsy via sinus centesis or sinoscopy)
    q
65
Q

Ddx of ethnmoidal haematoma?

A
  • neopplasia
  • fungal infection
  • trauma
66
Q

Why may tx of PEH be risky?

A

Lesion lies close to cribiform plate

67
Q

Conventional tx of ethmoidal haematoma? Prognosis?

A
  • radical excision via a maxillary/frontonasal bone flap
  • under standing sedation (profuse haemorrhage occours under GA)
    > majority no recurrence
68
Q

What less conventional txs are available for ethmoidal haematoma? Pros and cons?

A

> transendoscopic laser
- thermally destroys mass lesions
- pros: standing, avoids flap sinusotomy
- cons: equipment $$ need multiple tx as only superficial 5mm of mass detroyed
intralesional formalin
- transendoscopic injection with 4% formalin
- pros: standing, low cost
- cons: repeat txs needed
* neither of these shuld be used if communication with cribiform plate seen)

69
Q

Aetiology of GP mycosis?

A
  • fungal infection (Aspergillus spp. normally)
  • roof of medial compartment near articulation of stylohyoid bone with temporal bone
  • lesion can be localised or spread ropstrally/laterally/axially into opposite pouch
  • clinical signs liekly due to injury of adjacent pouch structures
70
Q

Clinicla signs of GP mycosis?

A
  • epistaxis (internal carotid/external/maxillary aa.)
  • dysphagia (cranial nn. IX, X)
  • nasal discharge (mucosa irritated)
  • Horner’s syndrome (sympathetic trunk)
    > Bear these in mind when treating major bleed as these signs wont go away by themselves
71
Q

Why can the internal carotid a. not be ligated if ruptured?

A

joins circle of willis so will back bleed from brain

72
Q

DIagnosis of GP mycosis?

A

> endoscopy
- blood xiting pharyngeal opening of pouch
- direct visualisation of mycotic lesion
radiography
- fluid line in pouch
- osteitis of stylohyoid bone

73
Q

Tx of GP mycosis?

A

> epistaxis
- ligate, balloon occlude or coil BOTH SIDES of affected vessel
mycotic lesion
- systemic antifungals
- topical antifungals/antiseptics
supportive care
(mycotic lesion generally resolves if vessel ligated)

74
Q

Are fungi 1* pathogens?

A

NO opportunistic, will invade due ot damage or destruction of commensals by antibiotics etc.

75
Q

Presentation of fungal sinusitis?

A

Nasal discharge or epistaxis

76
Q

Aetiology of fungal sinusitis

A

Unknown

77
Q

Diagnosis and Tx of fungal sinusitis? What should be avoided?

A
  • sinoscopy
  • TX: sinus lavage with DMSO or topical antifungals (time dependant activity so not v. effective)
  • debridement surgically if severe
  • avoid Abx or irritant lavages, don’t interfere too much after initial tx
78
Q

Clinical signs of Atheroma?

A
  • sebaceous cyst in nasal diverticulum
  • noticed shortly after birth
  • grow through first couple of years
  • may be unilateral or bilateral
  • cosmetic not obstructive
79
Q

Tx of atheroma?

A

> surgical excision en toto
- via nostril or incision
drainage and chemical ablation of secretory lining (ensure complete removal!)

80
Q

Aetiology of sinus swellings?

A
  • sinus cysts
  • neoplasia
  • PEH
  • obstruction of nasomaxillary orifice
  • NB: dental disease = common cause of sinusITIS but NOT sinus swelling (will rupture easily and drain into mouth/out of nose)
81
Q

Clinical presentation of sinus cysts??

A
  • 1-2yo
  • facial swelling
  • also seen in mature horses (not clear whether this is congenital)
  • concurrent signs: v airflow on affected side
  • nasal discharge, epiphora
    > cystic dysplasia of sinus mucosa
82
Q

Tx of sinus cysts? prognosis?

A
  • breakdown of cyst wall via flap sinusotomy

- prognosis for work guarded

83
Q

Most common sinus neoplasm?

A
  • squamous cell carcinoma often originating in theh oral cavity
  • sarcomas also reeported
84
Q

Clinical sings of sinus neoplasia?

A
  • facial swelling
  • old horse
  • v airflow on affected side
  • epiphora (due to occlusion of nasolacrimal duct)
85
Q

Tx sinus neoplasia? Prognosis?

A
  • Excision via flap sinusotomy
  • laser obliteration
    > Prognosisvery poor
86
Q

What is GP tympany?

A

> congenital
- neonates formation of pharyngeal opening of pouch
acquired
- older foals, yearlings
- swelling involving pharyngeal opening of pouch

87
Q

Clinical signs of GP tympany?

A
  • tympanic (drumlike) swelling of parotid region
  • unilateral or bilateral
  • dysphagia and respiratory distress if severe
88
Q

Tx GP tympany?

A
  • unilateral: fenestration of median septum via Viborg’s triangle approach or transendoscopic laser or electroscalpel
  • bilateral: fenestration of median septum plus resection of lateral lamina or auditory tube (-> allow drainage into nasopharynx)

Respiratory (18 decks)

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