Equine URT Surgery Flashcards
Primary presenting problems for URT surgery?
- discharge (1)
- poor performance (2)
- abnormal resp noise (stridor or stertor) (2)
- epistaxis (3)
- abnormal swelling of head/neck
- cough
How is the URT examined at first?
- examine for nasal discharge, facial symmetry, airflow
- palpation of nostrils, septum, sinuses, GP, LNs (submandibular and retropharyngeal) larynx, trachea
- percussion of paranasal sinuses (?)
How is URT examined at work?
- lunge, saddle/harness
- onset and character of noise
- exercise intolerance due to unfitness?
- soundness
- respiratory pattern and recovery
Which further diagnostics are available for respiratory investigation?
- endoscopy
- radiography/Ct
- sinusoscopy
- bacterial culture and sense (NOT very useful but good to rule out strangles)
- biopsy for cytology/histo
What is currently performed at the same time of dynamic endoscopy? Why is this test useful?
- 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
(1) How may nasal discharge be characterised? Ddx for each?
> 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)
5 potential sources of nasal discharge?
- nasal passages
- paranasal sinus
- GP
- pharynx/larynx
- LRT (see other lecture)
How may source of discharge be determined?
- PE
- endoscopy (paranasal sinuses, GP, LRT)
- radiography (sinuses, GPs - look for fluid lines)
Is 1* nasal passage disease common? Potential causes?
No
- bacterial infection (sepotum or turbinates)
- fungal infection
- neoplasia
- FBs
POssibel concurrent signs of nasal discharge d/t nasal passage disease?
- v airflow
How can nasal discharge d/t sinusitis be diagnosed?
- PE: v resonance on percussion, sinus swelling
- endoscopy: draining from nasomaxillary opening
What diagnostics can be sued to examin the sinuses?
- radiography (fluid lines, masses)
- CT
- sinus centesis
- sinoscopy
Causes of sinusitis
- 1* bacterial/fungal infection
- 1* neoplasia
- 2* to dental disease (09-11)
POssibel concurrent signs of nasal discharge d/t sinusitis?
- v airflow (not necessarily with bacterial etc.)
- facial swelling
- dullness on percussion
Tx of sinusitis
> medical - lavage, Abx * may improve then relapse > surgical - sinusoscopy (fenestration of ventral conchal bulla (VCB)) - removing inciting cause - flap sinusotomy
which route of entry is advocated for sinus centesis and lavage? which others exist?
> 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
Landmarks for maxillary sinuses?
- facial crest
- infraorbital foramen
- canthus of the eye?
- LOOK UP*
Which bacteria commonly infect the sinuses?
1* b haem strep spp.
2* mixed +- plant material
Potential causes of GP disease causing nasal discharge?
> 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
POssibel concurrent signs of nasal discharge d/t GP disease?
- swelling at Viborg’s triangle
- other signs of GP myscosis
Diagnosis of GP empyema?
- endoscopy: discharge/fluid accumulation in pouch
- radiography: fluid line
- r/o chondroids
- culture
Tx GP empyema?
> 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
What equipment may be used to lavage the GP?
- foley catheter and chambers catheter
(2) what causes abnormal noises in the resp tract?
turbulent flow
- so there must be flow
- and an obstruction
Where is URT resistance greatest at inspiration and expiration?
- inspiration: URT
- expiration: lung
> small v airway diameter -> ^4 increase in airway resistnace!
How may URT noises be characterised? DDx for each?
> 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)
Potential sites of URT obstruction and which disorders cause these?
> 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
Clinical signs of DDSP?
- “choking down” stopping very suddenly at gallop
- expiratory stertor
- mouth breathing (pathognomic)
Diagnosis of DDSP?
- 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
Conservative Tx of DDSP?
- 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)
Surgical Tx of DDSP?
- 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.)
Which sites may pharyngeal cysts arise? What type of obstruction do these cause?
- subepiglottic (thyroglossal duct)
- dorsal pharyngeal (craniopharyngeal duct)
- palatine
> static obstruction
Clinical signs of pharyngeal cysts in foals and young adults?
> foals - dysphagia - dyspnoea > young adults - poor performance - respiratory noise
Which muscle is affected with RLN? Pathogenesis?
- degenerative axonopathy
- left side
- most common in large horses
- impaired function of cricoarytenoideus dorsalis (CAD) muscle (1* abductor of arytenoid cartilages)
Which vessels do the leftand right bracnhes of RLN wrap around?
- left : aortic arch
- ricght: subclavian
Clinical signs of RLN?
- asymptomatic at rest/low level exercise
- inspiratory stridor with mod-marked exercise
- impaired athletic performance at high levels
What causes the roaring associated with RLN?
- vocal coards would be tightened by abduction of arytenoids, instead lie lax in the resp tract, leaving laryngeal ventricles open -> roaring
How may RLN br graded?
- in resting, unsedated horses
2. at exercise (not always possible)
Outline gradingsystem for RLN horses at rest
- synchronous full abduction of both arytenoids
- asynchronous movement of L arytenoid, but FULL abduction induced by nasal occlusion
- asynchronous movement of L arytenoid that cannot be induced by nasal occlusion/saline in airway
- marked asymmetry at rest, no substantial movementof L arytenoid
Outline grading system of RLN at exercise
A: full abduction
B: not fully abducted but held at normal resting position
C: dynamic collapse (neg pressure in airway sucks cartilage across)
How does resting and excercising grade relate?
- ALl grade 1 and 2 horses will be A
- All grade 4 horses will be C
> Grade 3 horses variable so require endoscopy
Treatment of laryngeal dysfunction to varying degrees?
- 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)
Potential complications of a tieback surgery?
- 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
What does laryngeal tieback procedure effectively do?
Replace CAD muscle
What is AEE? Which horses are predisposed?
Epiglottic entrapment in subepiglottic mucosa and aryepiglottic folds
- most common in horses with epiglottic hypoplasia or deformity
- may be intermittent
CLinical signs of AEE?
- poor performnance
- expiratory stridor
- may be asymptomatic
Where does the aryepiglottic tissue lie normally?
under epiglottis and round sides over top of corniculate processes to make “button hole” that epiglottis pokes through
How does epiglottic entrapment appear endoscopically?
- no BVs
- smooth edges
> as covered in membrane|! - ulceration may be seen
Tx of AEE (epiglottic entrapment)
> midline division of entrapping tissue
- laryngotomy
- transendoscopic laser
- bistoury hook
Complications of epiglottic entrapment AEE surgery?
- re-entrapment 5-40%
- laceration of soft palate or epiglottis
- DDSP 10% (initial problem may have been protective of DDSP)
What is arytenoid chondritis and which disease may it mimic? Clinical signs?
- 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
Aetiology of arytenoid chondritis?
- unknown
- may follow laryngitis
- can be experimentally induced by denuding arytenoid mucosa but only in some cases not always
Tx arytenoid chondritis?
- 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)
Which obstructions can only be diagnosed on dynamic endoscopy?
- DDSP (will always replace when swallowing)
- nasopharyngeal collapse (fat ponies flexing)
- epigl;ottic retroversion
- axial deviation aryepiglottic folds
- intermittent epiglottic entrapment
Which conditions can only be diagnosed at exercise?
> dynamic obstructions
- DDSP
- nasopharyngeal collapse (fat horses flexing)
- epiglottic retroversion
- axial deviation aryepiglottic folds
- intermittent epiglottic entrapemnt
What 1* problems may cause respiratory obstruction 2*?
- inflammation affecting muscles (muscle needed to stabilise all structures of the larynx!!)
- lymphoid hyperplasia commonly seen on endoscopy esp young racehorses
How may epistaxis be described or refined?
> 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)
What diagnositcs can be used to determine hte source of epistaxis?
> endoscopy - paranasal sinuses - gutternal pouches - LRT > radiography - sinuses - GPs
What is PEH?
> 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
HIstology of PEH
- capsule respiratory mucosa and fibrous tissue
- stroma blood, fibrous tissue, macrophages, giant cells, haemosiderocytes (suggests repeated bouts of local haemnorrhage)
Clinical signs and commonly affected horses for PEH?
- 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)
What is seen on endoscopy with PEH?
- smooth greenish-black/reddish-brwonb mass
- may reveal nothing or just blood exiting nasomaxillary opening
What is visable on radiographs with eithmoidal haematoma?
- 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!!
How is diagnosis of ethmoidal haematoma confirmed?
- 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
Ddx of ethnmoidal haematoma?
- neopplasia
- fungal infection
- trauma
Why may tx of PEH be risky?
Lesion lies close to cribiform plate
Conventional tx of ethmoidal haematoma? Prognosis?
- radical excision via a maxillary/frontonasal bone flap
- under standing sedation (profuse haemorrhage occours under GA)
> majority no recurrence
What less conventional txs are available for ethmoidal haematoma? Pros and cons?
> 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)
Aetiology of GP mycosis?
- 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
Clinicla signs of GP mycosis?
- 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
Why can the internal carotid a. not be ligated if ruptured?
joins circle of willis so will back bleed from brain
DIagnosis of GP mycosis?
> endoscopy
- blood xiting pharyngeal opening of pouch
- direct visualisation of mycotic lesion
radiography
- fluid line in pouch
- osteitis of stylohyoid bone
Tx of GP mycosis?
> 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)
Are fungi 1* pathogens?
NO opportunistic, will invade due ot damage or destruction of commensals by antibiotics etc.
Presentation of fungal sinusitis?
Nasal discharge or epistaxis
Aetiology of fungal sinusitis
Unknown
Diagnosis and Tx of fungal sinusitis? What should be avoided?
- 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
Clinical signs of Atheroma?
- sebaceous cyst in nasal diverticulum
- noticed shortly after birth
- grow through first couple of years
- may be unilateral or bilateral
- cosmetic not obstructive
Tx of atheroma?
> surgical excision en toto
- via nostril or incision
drainage and chemical ablation of secretory lining (ensure complete removal!)
Aetiology of sinus swellings?
- 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)
Clinical presentation of sinus cysts??
- 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
Tx of sinus cysts? prognosis?
- breakdown of cyst wall via flap sinusotomy
- prognosis for work guarded
Most common sinus neoplasm?
- squamous cell carcinoma often originating in theh oral cavity
- sarcomas also reeported
Clinical sings of sinus neoplasia?
- facial swelling
- old horse
- v airflow on affected side
- epiphora (due to occlusion of nasolacrimal duct)
Tx sinus neoplasia? Prognosis?
- Excision via flap sinusotomy
- laser obliteration
> Prognosisvery poor
What is GP tympany?
> congenital
- neonates formation of pharyngeal opening of pouch
acquired
- older foals, yearlings
- swelling involving pharyngeal opening of pouch
Clinical signs of GP tympany?
- tympanic (drumlike) swelling of parotid region
- unilateral or bilateral
- dysphagia and respiratory distress if severe
Tx GP tympany?
- 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)
