Lacrimal System Flashcards
1
Q
How can the lacrimal system be divided?
A
Lacrimal secretory system - lacrimal gland, nictitans gland, meibomian glands, conjunctiva/cornea (production of pre-ocular tear film)
Lacrimal excretory system - lacrimal punctae, canaliculi, lacrimal sac, nasolacrimal duct and nasal punctae. (drainage of tears from ocular surface)
2
Q
Where do the orbital lacrimal gland, third eyelid gland, conjunctival goblet cells and meibomian glands originate from embryologically?
A
Surface ectoderm
3
Q
Which species may the Haderian gland be found in and what is it?
A
Rabbits and rodent = accessory lacrimal gland
4
Q
Why are tears essential?
A
Maintain ocular surface health:
Lubricate ocular surface
Flush away debris - allowing for atraumatic eyelid closure
Nutrition to the avascular cornea
Protective anti-microbial proteins (lactoferrins)
Help with refraction - clear vision
5
Q
What is the trilaminar tear film composed of?
A
Lipid, aqueous and mucin
More recent studies show each layer is more intricately mingled
6
Q
How thick is the tear film appoximately?
A
7-10 um (possibly slightly thicker)
7
Q
What portion makes up the majority of the tear film?
A
Majority aqueous
8
Q
How does the tear film usually adhere to the cornea?
A
Corneal epithelial cells have microplicae and microvili which increase surface area of tear binding.
Glycocalyx expressed by the corneal epithelium interact with mucins and promote retention of the tears (wettability)
9
Q
How are the layers of the tear film arranged?
A
Mucin - adherence to cornea
Aqueous - middle, largest portion (antimicrobial proteins within this layer)
Lipid - outside, reduces evaporation and contributes to stability of tear film.
10
Q
Which cells produce mucin?
A
Goblet cells (holocrine) of the conjunctiva, particularly concentrated in lower conjunctival sac - medial/ventral.
Found less commonly in the bulbar conjunctiva.
11
Q
How can mucins be further classified?
A
Membrane bound or secretory
Membrane bound mucins = found on edge of micropilae of surface corneal epithelial cells foriming a dense glycocalyx at epithelial-tear film interface.
Prevents pathogen penetrance and enhances aqueous coherence.
Secretory mucins = help remove debris, hold fluid in place and bind defence molecules.
12
Q
Where is the aqueous layer produced and how much is produced there in terms of %?
A
Lacrimal gland = 70% aqueous tear film
Nictitans/TEL gland = 30% aqueous tear film
Bulk of tear film = aqueous
13
Q
What is aqueous tear film composed of?
A
Water, electrolytes, glucose, urea, surface-active polymers, glycoproteins, tear proteins
Tear proteins = secretory IgA, IgG, IgM, albumin, lysozyme, lactoferrin, lipocalin, epidermal growth factor, transforming growth factor, interleukins
13
Q
Where is the lipid of the tear film produced?
A
Meibomian glands (modified sebaceous glands)
Produce lipid (meibum)
Stabilises tear film and reduces evaporation
14
Q
Where are the meibomian glands located and how many are there per eyelid?
What type of gland are they?
A
Located within tarsal plate of the eyelids
20-40 per eyelid
Holocrine
Lipid meibum transported through a ductule to the orifice at the eyelid margin.
Openings on the eyelid margin form a line often referred to as the grey line.
15
Q
What do the lipids in the meibum consist of?
A
Wax monoesters, sterol esters, triglycerides, free sterols, free fatty acids, polar lipids
16
Q
How are tears distributed across the corneal surface?
A
Distributed by blinking and third eyelid excursions
Corneal drying prevented by ongoing tear production and blinking
17
Q
What is the innervation to the lacrimal and third eyelid glands?
A
Parasympathetic (most important) + small amount sympathetic
Originate PSM nucleus of facial nerve in brainstem- facial nerve to petrous temporal bone to internal acoustic meatus and facial canal then to greater petrosal nerve and deep petrosal nerve to nerve of pterygoid canal synapsing at pterygopalatine ganglion (in the orbit)
Post ganglionic PSM fibres run with zygomatic nerve of trigeminal, branches off and becomes lacrimal nerve
18
Q
Why anatomical factors can affect the distribution of the tear film?
A
Brachycephalics - lagophthalmos (incomplete blink) - central drying
Imability to blink - e.g facial nerve paralysis
TEL - abnormal shape/function
Eyelids - entropion, trichiasis, ectropion (more evaporation)
19
Q
How do we measure tear production?
A
Schirmer Tear Test
Test strip placed lower eyelid - 1 minute
Measurement of length of wetting
20
Q
What does STT-1 measure? What is the normal value.
A
Volume of tear lake and both basal and reflex tear production (stimulated by the strip against the conjunctiva/cornea)
Normal value = 15mm wetting/min
Values <10mm wetting/min diagnostic for KCS with consistent clinical signs
Readings between 10-15 = equivocal - repeat again periodically in these cases. ?treat if consistent clinical signs.
21
Q
What does STT-2 measure?
A
Local anaesthetic e.g proxymetacaine already applied followed by gentle drying of lower conjunctival sac.
Only measures basal tear production (reflex abolished by local)
Readings approx half of those with STT-1
22
Q
Which breeds are predisposed to KCS and should have STT performed periodically?
A
WHWT, Cavaliers, English/American Cocker Spaniels, English Bulldog, English Bull Terrier, Pekingese, Pug, Shih Tzu, Lhasa Apso, Samoyed, Blood hounds
22
Q
When is it contraindicated/not appropriate to perform the STT?
A
Desmetocoele (restraint/disturbance to eye) risks rupture
23
Which endocrine disease have had an association with KCS also reported?
Hypothyroidism
Diabetes
Hyperadrenocorticism
24
How can we measure the qualitative tear film?
Tear film break up time or Rose Bengal staining
Fluorescein applied followed by enforced blinks to distribute fluorescein evenly
Eyelids then held open and corneal surface observed for signs of break up
Tests ocular mucin component (corneal wettability) and lipid layer (tear film stability and reduction of evaporation)
Normal TFBUT = 15-25 seconds
Less than this suggest tear film quality issue
Rose Bengal = stain uptake not seen in healthy corneas but present when mucus layer of tear film absent
(can be irritant on application so excess should be flushed with saline to avoid discomfort)
25
What is keratoconjunctivitis sicca?
Reduction in tear film production
25
How can we specifically test lipid production from the meibomian glands?
Meibometry - application of test strip against eyelid margin followed by placement of strip into meibometer - numerical reading of lipid level on strip.
Currently experimental only in veterinary species but done in humans
26
List the possible causes of KCS.
Immune mediated (majority of cases)
Congential alacrima
Congenital KCS (in conjunction with ichthysiform dermatosis on Cavaliers)
Neurogenic KCS
Secondary to metabolic diseases - hypothyroidism, diabetes, HAC
Drug induced KCS
Trauma/inflammation to lacrimal gland, orbit or innervation
Infectious - canine distemper
Chronic blepharoconjunctitis
Iatrogenic KCS (removal of TEL gland)
27
What are the clinical signs of KCS?
Tacky mucopurulent ocular discharge - adhered to cornea in strings
Recurrent conjunctivitis +/- corneal ulceration (if present slow to heal)
Conjunctival thickening
Corneal vascularisation (due to lack of nutrition from tear film)
Corneal pigmentation
Corneal fibrosis
Corneal keratinisation
Severe cases = blindness (pigmentation/fibrosis severe)
Non specific signs so often missed/underdiagnosed.
28
What type of infiltrate is seen in dogs with immunogenic KCS?
Lympho-plasmacytic infiltrate associated with acinar fibrosis and atrophy - suggests immunological basis for disease
29
How would you treat immunogenic KCS?
Topical ciclosporin 0.2% (optimmune) - mainstay of therapy, licensed for this indication
Lifelong treatment to suppress immune mediated attack and allow lacrimal recovery.
Treatment started earlier = more effective as less lacrimal tissue permanently damaged
Lag phase - 2-4 weeks but up to 8 weeks before improvement in tear film seen during which false tear products should be applied.
Once lacrimal tissue recovers false tears can often be withdrawn.
Ineffective: - Both off licence
Stronger concentration - 1-2% in corn oil and applied BID (can be irritant topically so some dogs will not tolerate)
Tacrolimus (0.03%) - occasional ocular irritation
(Associated with skin cancer in humans - make aware, lymphoma incidence in mice)
30
What type of drug are ciclosporine and tacrolimus?
Calcineurin inhibitors
Activation of T cell receptor = rise in intracellular calcium which via calmodulin activates calcineurin. Calcineurin = regulates activation and subsequent nuclear translocation of nuclear factor of activated T cells (NF-AT) which increases activity of genes coding for IL-2 and related cytokines.
Calcineurin inhibitors prevent T cell production of specific inflammatory cytokines thereby reducing immune mediated inflammation (T cell lymphocyte mediated disease) within lacrimal gland.
Suppresses lacrimal acinar and conjunctival cell apoptosis, thereby restoring more normal tear film production (quantitatively and qualitatively)
31
How else might ciclosporine improve tear film quality not just quantity?
Improves conjunctival mucin secretion by stimulating goblet cells - may contribute to therapeutic effect on KCS
Direct lacrimal stimulant effect also reported and mediated by increased neurotransmitter release
32
When might topical antibiotics be required for KCS patients?
More prone to secondary bacterial infections/conjunctivitis
May be required until tear film returned to normal.
Normal flora of conjunctiva disrupted with KCS - bacterial culture/sensitivity may be indicated.
33
Why can we see neurogenic KCS?
Due to way lacrimal gland innervated
Lacrimal gland = parasympathetic innervation mainly (small amount sympathetic)
Originate from parasympathetic nucleus of facial nerve within brainstem, run with facial nerve via petrous temporal bone, internal acoustic meatus and facial canal. Then join greater petrosal nerve and deep petrosal nerve (sympathetic) to form the nerve of pterygoid canal. Fibres synapse at pterygopalatine fossa in pterygopalpatine ganglion.
Post ganglionic fibres then join the zygomatic nerve (branch of trigeminal) and finally branch off as the lacrimal nerve to reach lacrimal gland.
Due to intimate contact with peripheral vestibular system and middle ear disease processes such as otitis can affect facial nerve function and therefore tear production.
34
Why may we see Horner's syndrome with neurogenic KCS?
Can sometimes see Horners + KCS
Sympathetic innervation also passes in close contact to structures of inner/middle ear - disease of these structures may see Horner's + KCS
35
How do patients with neurogenic KCS present?
Ipsilateral dry eye + nose (xeromycteria)
Innervation to lateral nasal gland (parasympathetic control via facial nerve) shares the same pre-ganglionic fibres proximal to the pterygopalatine fossa.
Occurs if lesion proximal to pterygopalatine fossa.
36
What STT reading do patients with neurogenic KCS usually have?
<5mm/wetting (often 0)
Whilst other eye often normal.
36
How may you work up a case of neurogenic KCS further?
Neurological examination - involvement of other cranial nerves
PE including aural examination
Diagnostic imaging if suspicious of underlying cause - (CT bony structures e.g tympanic bullae, or MRI)
36
What causes of neurogenic KCS are there?
Idiopathic (majority of cases)
Middle ear disease - otitis interna/media
Skull trauma
Facial nerve damage/lesion (neoplasia)
37
How would you treat neurogenic KCS?
Treat underlying cause if detected
(Otitis media - prolonged course antibiotic 6-8 weeks)
(Inflammation petrous temporal bone - NSAIDS)
Trauma - facial nerve damage may/may not resolve with time
Frequent application of topical tear film replacement (may need hourly to begin with!)
DO NOT RESPOND TO CICLOSPORIN/TACROLIMUS
PILOCARPINE = given orally as very irritant when applied topically and not well tolerated.
Due to denervation hypersensitivity using pilocarpine works as PARASYMPATHOMIMETIC
Oral = 1 drop 2% pilocarpine per 10kg 2-3x daily
Dose increased by 1 drop increments at each dosing until signs of systemic toxicity (hypersalivation, vomiting, diarrhoea, cardiac arrhythmia) then dose lowered to previous highest dose tolerated.
Topical pilocarpine = 0.1-0.25% in saline - may cause blepharospasm, miosis and conjunctival hyperaemia
38
Which drugs may induce KCS?
Pre-anaeshetic and anaesthetic agents - reduce tears for 24hrs at least (associated with duration, >2hrs = longer)
Anti-cholinergics - atropine
(Ocular lubrication for all anaesthetised patients and continued in at risk breeds e.g brachys for at least 48hrs)
Atropine (used for uveitis management) - can be prolonged
Important to measure tear production before application - may exacerbate disease e.g if ulcer due to KCS
Systemic sulphomaides (sulfasalazine, trimethoprim-sulphonamide, sulfadiazine) - acute onset KCS. T cell mediated response to proteins haptenated by oxidative sulfonamide metabolites may be responsible. Prolonged systemic use = permanent severe KCS following complete atrophy of the glands.
Etodolac (NSAID)
39
How would you treat drug induced KCS?
Withdrawal of drug
Chronic administration - tear film may never recover
False tear preparations (e.g post anaesthetic)
If cannot give false tears 1-2hrs and chronic lacrimal adenitis and damage consider parotid duct transposition.
40
Which breeds has congenital KCS been reported in?
Yorkshire terriers
Cocker Spaniels
Cavalier King Charles
41
What mechanism do we think causes congenital KCS?
Congential alacrima - congenital lacrimal gland agenesis or hypoplasia or possible central/peripheral neuropathy
Congenital absence of tear production
42
How do congenital KCS cases usually present?
Often unilateral but can be bilateral
First few weeks/months of life
STT often <0
Blepharospasm
Tacky discharge
Vascularisation and pigmentation of cornea
Very quickly progressive
43
Describe congenital KCS with ichthyosiform dermatosis. Which breed does it occur in?
Cavaliers
Born with rough curly coat
After eyelid opening KCS apparent with frequent bouts of secondary bacterial conjunctivitis and sometimes corneal ulceration
Scurfy sparse coat with hyperkeratinisation of pads and abnormal nail growth
Mechanism for KCS not really understood - quantative and qualitative deficiency
Genetic mutation responsible can now be screened for
44
How would you treat congenital KCS?
Frequent false tear application (most owners unable to apply drops every 1-2hrs every day as required however)
Parotid duct transposition in severely affected cases
CKCS with dermatosis - variable response to lacrostimulants e.g ciclosporin
45
What is the normal STT for a cat? When is KCS diagnosed?
10-15mm wetting/min = normal
KCS diagnosed values <5mm in combination with consistent clinical signs
46
What is the normal TFBUT in cats?
12-21 seconds
47
What is the most common cause of KCS in cats?
Secondary to herpesvirus
FHV-1 = tropism for conjunctival epithelium
Cytopathic effect = conjunctival swelling (obstructing lacrimal ductules from orbital lacrimal gland and third eyelid gland) and conjunctival ulceration.
Symblepharon formation - adhesions between conjunctival epithelium or cornea (when corneal ulceration also present)
48
How would you treat KCS in cats?
Address underlying FHV-a
Topical and/or systemic antivirals
Supportive care
Prevention of adhesions - cotton tip swab under local anaesthetic
Can get re-establishment of tear production when swelling subsides
Permanent occlusion of lacrimal ductules - parotid duct transposition could be considered.
49
How can qualitative tear deficiencies occur in cats?
Associated with ulcerative keratitis, meibominanitis or lipogranulomatous conjunctivitis
50
When may KCS be associated with radiation?
Eye/orbit included in field of radiation e.g for nasal tumour
Poorly responsive to lacrimal stimulation and treatment largely replacement therapy.
Irradiation may also cause cataracts and retinal degenerationso enucleation may be opted rather than prolonged intensive medication if eye is blind.
51
How may trauma cause a KCS?
How would you treat?
Trauma or inflammation of the lacrimal gland may result in KCS
Orbital trauma (e.g RTA), cellulitis
Typically poor response to lacrimostimulant drugs
Aim treatment at reducing inflammation associated with primary disease
Supportive care - tear replacements
Damage can sometimes be severe/permanent - long term tear replacement or parotid duct transpositon,
52
What is iatrogenic KCS?
Removal of TEL gland, often performed in breeds already predisposed to dry eye (e.g Bulldogs) - severe lifelong KCS
53
What is the prognosis for KCS?
Depends on underlying cause.
Immunogenic - very good, especially if caught early
Left untreated - grave for vision due to increasing vascularisation, pigmentation and keratinisation. Ulceration common and slow to heal. Risk of perforation.
Poorer prognosis = neurogenic non responsive, iatrogenic, trauma, congenital, chronic drug induced
Parotid duct transposition required in many of those cases
54
When is a parotid duct transpositon (PDT) indicated? What is this procedure.
Severe permanent KCS non responsive to medications
Patient cannot be maintained with topical tear preparations
Relocation of the parotid salivary duct and papilla from the oral cavity to the lower conjunctival sac - requires magnification (surgical loupes)
55
What are the 2 techniques for a PDT?
1. Open method - skin incision over lateral face and parotid duct identified and dissected back to parotid gland.
Papilla cannulated with suture
Facial nerve and vein identified and care taken not to injure during dissection.
Tract bluntly dissected to conjunctival sac and sac opened to allow papilla to be sutured without tension 8/0 to 9/0 polyglactin 910
2. Closed method - dissecting parotid duct back to gland via oral mucosal incision
More difficult due to poor visualisation of structures but avoids facial incision
Papilla sutured to ventral conjunctival sac
56
What complications are associated with a PDT?
Failure of PDT - traction, sectioning or trauma to transposed duct
Sialolith formation in duct - may require surgical removal/massage from duct
Sialadentiis
Overflow of saliva onto face and secondary blephairitis, dermatitis and staining
Calcium deposits on the cornea (from saliva) causing keratitis and discomfort.
57
Which diseases can cause a disruption to the tear film quality.
Meibomianitis (inflammation of meibomian glands)
Goblet cell dysfunction
Poor tear film distribution (Lagophthalmos)
Lacrimal gland neoplasia
Third eyelid gland neoplasia
58
What type of neoplasia can be seen of the lacrimal gland?
Adenocarcinomas/adenoma
59
Where does the nasolacrimal system originate from embyrologically?
Surface ectoderm
Ectodermal cells within nasolacrimal groove (furrow between lateral nasal fold and maxillary process) sink into the mesenchyme below forming a cord. Cord of cells grows towards eyes and nose with ocular end forming two buds near medial canthus that become the upper and lower canaliculi and punctae. Cord canalises to become a duct patent at birth.
60
What type of epithelial cells line the nasolacrimal duct?
Pseudostratified columnar epithelium
61
Where do the punctae of the nasolacrimal system sit?
Upper and lower punctae
3-7mm from medial canthus at junction between eyelid margin and palpebral conjunctiva approximately where meibomian glands end.
Oval to slit like appearance.
62
Where do the punctae lead to?
Lead to canaliculi 4-7mm in length which join together at lacrimal sac (usually very small in dog/cats)
63
Where does the lacrimal sac sit?
Lacrima sac sits in depression of lacrimal bone (lacrimal fossa)
64
Where does the nasolacrimal duct travel from the lacrimal sac?
From lacrimal sac nasolacrimal duct starts and exits through lacrimal bone (where it is slightly constricted - important in foreign body retention)
Nasolacrimal duct then runs through a canal in the maxilla below the nasal mucosa on the medial aspect of the maxilla.
Nasolacrimal duct terminates at nasal punctum located on ventrolateral floor of the nasal vestibule approx 1cm caudal to the external nares.
Approx 50% dogs (often brachys) and cats have accessory opening in the oral mucosa of the hard palate at level of upper canine teeth. (Jones test - check mouth too!)
65
How are tears drained?
Normal = majority via nasolacrimal system
Tear evaporation also plays a role in tear loss.
Majority drained via lower lacrimal punctum and canaliculus via capillary action and siphon effect.
66
What is the tear lake? Which breeds tend to have a shallow tear lake?
Tear lake/lacrimal lake = collection of tears, ventrally below lower eyelid
Height of tear lake varies with breed.
Brachycephalics = shallow lake as shallow orbit and tight eyelid apposition.
67
How is the nasolacrimal system set up in the rabbit?
Only single lacrimal punctum - located medial ventral conjunctival sac
Do not have specific lacrimal sac but rather a region of dilated nasolacrimal duct .
Nasolacrimal duct follows torturous path to the nasal ostium located in ventrolateral nasal vestibule
Duct runs in close proximity to the caudal cheek teeth and incisors (why dental disease often results in dacryocystitis in rabbits...)
68
How does blinking help with nasolacrimal drainage?
Blink - eyelid compresses lacrimal sac and pushes tears into nasolacrimal duct, creates negative pressure as the sac reopens which consequently draws more tears into the canaliculus and lacrimal sac.
Pseudoperistalsis within nasolacrimal duct then moves tears to nasal punctum.
69
What clinical signs do we see with nasolacrimal system blockages?
Ocular discharge (varying from epiphora to profuse mucopurulent discharge)
Conjunctivitis + hyperaemia may also sometimes be present
Pressure at medial canthus may cause purulent material to be expelled from lower lacrimal punctum
70
What may we consider doing with ocular discharge?
Consider cytology +/- C+S
Help assess for any bacterial population and choose appropriate antibiotic
71
How can we assess the patency of the nasolacrimal duct?
Patency = Jones Test
Fluorescein applied to tear film
Ipsilateral nares observed for appearance of fluorescein (can take up to 10 mins)
Can get false negatives due to accessory openings - look at pharynx with cobalt blue light (especially brachy/cats)
Can also assess patency with nasolacrimal flushing
72
How would you perform nasolacrimal flushing?
Topical anaesthesia - proxymetacaine
Upper lacrimal punctum and canaliculus catheterised using nasolacrimal cannula or IV catheter (22-24G)
Flushed with saline
Should result in fluid passage out through lower lacrimal punctum (via sac and lower canaliculus)
Occlusion of lower punctum with fingertip should result in fluid passage through the nasolacrimal duct to the nasal punctum.
Tipping nose downwards encourages flow out through nares rather than posteriorally into nasal cavity
Accessory openings - may observe swallowing when fluid passes into mouth or nasopharynx.
If undertake flushing under GA do no forget to pack the nasopharynx to avoid aspiration of flushing saline.
73
How could you retrograde flush the nasolacrimal system?
Not easy
Requires GA + magnification and good lighting
Grasp alar cartilage of nares and pull laterally
Nasal punctum approx 1cm caudal to nares and ventrolateral (usually at junction of pigmentation)
Use nasolacrimal catheter/IV catheter
74
When may radiography be used to assess the nasolacrimal system?
Plain skull radiographs (lateral, intraoral, dorsoventral) under GA
Assess abnormalities in surrounding tissues e.g nasal sinues, maxillary dental arcades) - often other clinical signs suggestive of disease within these structures
Can use contrast dacryocystorhinography to look for nasolacrimal obstructions also.
75
How is contrast dacryocystorhinography performed?
Contrast medium into NL system (done under GA)
Pharynx packed and lower lacrimal duct catheterised
Iodinated contrast solution injected into nasolacrimal system
Placement of swab at nares to collect any contrast material rather than allowing it to enter nasal cavity or onto x-ray plate and obscure detail.
May get some contrast in oral cavity if accessory openings
Do not use too much contrast = 1ml often plenty
76
What can contrast dacryocystorhinography show?
Obstructions within NL system = prevent contrast from following identifying site of obstruction
Cysts connected to NL system - outlined by pooled contrast material
Dilations of lacrimal sac (secondary to obstruction)
Injection of contrast material percutaneously into cysts that are isolated from NL systme but are causing secondary obstruction (e.g seperated canaliculops or dacryops) has been descrived to identify extent of cyst and confirm separation.
77
What may bony lysis detected on radiography indicate?
Osteomyeltis
Neoplastic erosion of maxilla or lacrimal bone (most commonly neoplasia originating from nasal cavity and secondarily involving NL system)
78
How can the whole nasolacrimal system be cannulated?
Sialastic tubing or suture material either anterograde or retrograde if required
79
Which is more useful for investigation of NL disease - CT or MRI?
CT as more bony resolution
80
How can CT be used for investigation of nasolacrimal disease?
Normal CT = assessment of local structures e.g nasal cavity, maxilla (assessment of osteolysis - neoplasia/infection)
Contrast CT dacryocystorhinography - iodinated contrast material injected as for x-rays
Technical difficulties associated with overfilling of NL system with contrast and subsequent contrast leakage into nasal cavity causing reduced quality images.
Contrast can detect - obstructions, dilation of the lacrimal sac or cystic dilatations (pooling of contrast material)
81
How may the NL system be surgically investigated?
E.g if suspect FB in lacrimal sac
Opening up lacrimal sac to investigate (pull 3rd eyelid across and go through conjunctiva)
Undertaken if evidence of abnormality proximally.
82
What is inflammation of the lacrimal canaliculi and sac referred to as?
Dacryocystitis
83
What are the classical clinical signs of dacryocystitis
Mucoid to mucopurulent ocular discharge emanating from lacrimal punctae
Discharge can be sometimes be massaged from lacrimal sac out of lower lacrimal punctae = pathognomic for dacryocystitis
Conjunctival hyperaemia of ventral conjunctival sac
Secondary blepharitis - possibly draining fistula formation ventral to medial canthus
84
What are the causes of dacryocystitis?
Trauma - RTA, cat fight laceration, surgical incision
Obstructions:
Congenital agenesis (part or all of NL system)
Foreign bodies (grass seeds = most common)
Inflammatory material within canaliculi, lacrimal sac or NL duct
Cystic expansions adjacent to or within NL system
Adjacent neoplastic expansion or abscesses (e.g tooth root)
85
What is atresia of the lacrimal system?
Failure of the system to fully canalise = congenital condition
Most common = punctal atresia
Absence of upper punctum = usually asymptomatic
Absence of lower punctum = epiphora in affected puppies
86
How would you diagnose and treat punctal atresia?
Flushing of saline in upper punctum may result in bulging of conjunctiva overlying the lower canaliculus which can then subsequently be incised and a punctum reformed.
Mucosal site of the punctum is usually thin walled and devoid of blood vessels making surgery bloodless and less prone to secondary stricture formation.
Topical antibiotic-corticosteroid prep usually used for 7 days after
87
How may canaliculi/NL duct atresia be treated?
Less common then punctal atresia but harder to correct.
Creation of communication between NL that is present and nasal cavity (conjunctival rhinostomy), maxillary sinus (conjunctival maxillary sinusotomy) or oral cavity (conjunctival buccostomy) have all been described.
Placement of indwelling sialastic tubing for 3-6 weeks to promote continued patency and reduce post op stricture formation + topical corticosteroid-antibiotic treatment.
88
What is a micropunctum?
Abnormally small punctum - congenital
Epiphora or mucopurulent ocular discharge
Enlargement of small punctae - 1-2-3 snip method
? possibly place catheter for 3 weeks post op with topical corticosteroid+AB medication for 3-4x daily
89
How can a malpositioned lower lacrimal punctum be adressed?
Congenital abnormality
Resulting epiphora if lower punctum, upper punctum usually asymptomatic.
Malpositioning due to anatomy (esp brachycephalics)
Lower medial canthal entropion can position the lower punctum ventrally and limit normal drainage.
Caruncular trichiasis also encountered in these breeds and promotes wicking of tears onto medial canthus compounding epiphora.
Concurrent tight medial canthal ligaments can compress punctum and canaliculus further limiting damage.
Surgical treatment - correct medial entropion (modified Hotz Celsus) + caruncular trichiasis (excision) can help reduce/eliminate epiphora.
Medial canthoplasty as a treatment for medial entropion and caruncular trichiasis may also address tight canthal ligaments.
90
What are canaliculops?
Cysts of the canaliculi which either become separated from the canaliculus or retain communication with the NL system
Both can cause obstructions to tear drainage
Cystic swellings may cause distinct swellings palpable over the facial bones.
Surgical excision curative but careful reconstruction of canaliculus with catheterisation for period of 3-4 weeks and topical AB + Corticosteroid tx indicated to prevent stricture formation.
91
How are cysts of the nasolacrimal duct managed?
Rare but can cause recurrent inflammation with epiphora/mucopurulent discharge
Surgical excision but requires removal of section of maxilla to reach duct (possibly can do endoscopically)
Entire cyst should be removed or marsupialised to the nasal cavity or maxillary sinus
92
What type of cysts of the nasolacrimal system are there?
Canaliculops
Nasolacrimal duct cysts
Maxillary bone cysts
Dacryops (cysts of lacrimal gland ductule tissue)
93
What are dacryops? Which breeds are reported to have had them?
How would you diagnose?
How would you distinguish dacryops from canaliculops.
Cysts of lacrimal gland ductule tissue
Reported Labrador/Bassett Hounds
Ectopic lacrimal tissue with cyst formation most commonly occurs at medial canthus and well defined mass palpable.
Secondary obstruction to canaliculops may result in epiphora.
Contrast dacryocystorhinography - demonstrates swelling separate from NL system and flushing usually possible to the nasal punctum
Ultrasonography can reveal thin walled cystic structure - aspiration of fluid may reveal inflammatory cells but usually absence of bacteria.
CT and MRI can help with surgical planning and confirm isolation of the cyst from the NL system.
Histology - single to double cell layered cuboidal non ciliated epithelium with some areas flattening to squamous cell type.
Distinguish from canaliculops by immunohistochemisty for smooth muscle actin (SMA) +ve = dacryops
Surgical excision curative
Risk iatrogenic laceration of lower canaliculus - require apposition to fix if occurs with magnification and catheterisation of canaliculus post op to prevent stricture formation.
94
What is the most common foreign body to cause obstructions to NL system in dogs? Where do they usually migrate to?
Grass awns/plant material
Usually migrate to lacrimal punctae with barbs preventing backwards movement, can become lodged in canaliculus with tip visible at punctum or more commonly become retained in lacrimal sac.
Another site of retention if entrance of nasolacrimal bony canal where duct is at its narrowest.
95
How can we treat foreign bodies within the NL system?
Flushing may be able to dislodge FB to punctum in some cases but incision into lacrimal sac or nasolacrimal duct often required
If reaches bony nasolacrimal canal then becomes more tricky as maxillary bone needs to be removed to access.
Post op stent/sialastic tubing placement to allow healing and prevent strictures - removed 3-4 weeks later
AB-Corticosteroid tx topically until stent removal
96
What complications can be seen with foreign bodies within NL system?
Secondary granuloma formation within lacrimal sac/canaliculi
Stricture formation following granulation tissue healing of nasolacrimal laceration - close apposition of tissues not achieved, sutures placed into NL system mucosa.
Closure of NL duct defect (after removal of FB) described using an overlay of porcine small intestinal submucosa to prevent re-epithelialisation.
97
How should lacerations of the NL system (e.g post RTA) be approached?
Careful re-apposition to prevent long term epiphora and obstruction.
Upper punctum/canaliculus = no effect
Lower = epiphora
Appose surrounding tissues accurately without direct suturing of canaliculus to prevent stricture.
Operating microscope for visualisation
Flushing can help identify site of laceration
Damage of NL duct within lacrimal/maxilla bone will require apposition of bony fragments and removal of small fragments that may form sequestra.
Indwelling catheter 4-6 weeks to encourage re-epithelialisation of the duct and maintain patency.
98
What conditions can cause obstruction of the feline lacrimal excretory system?
Symblepharon (FHV-1 infection) - obstruct lacrimal punctae/canaliculi, results in epiphora (most common cause NL obstruction in cats)
Atresia (more commonly upper punctum, occasionally lower)
Conformation - brachycephalics may result in epiphora due to lacrimal punctal malpositioning with medial entropion, trichiasis from medial entropion wicking tears onto lower eyelid and tight medial canthal ligaments compressing lower canaliculus.
Dacryocystitis - can be associated with rhinitis and dental disease.
99
Describe the anatomy of the lacrimal system in the rabbit.
Single ventral lacrimal punctum - medioventral conjunctival sac
Does not have recognisable lacrimal sac (just dilated proximal NLD)
Nasolacrimal duct torturous path - nasal ostium to ventrolateral nasal vestibule
Close proximity of NLD to cheek teeth proximally and incisors distally
100
What is dacryocystitis commonly associated with in rabbits?
Dental disease - secondary obstruction of NLD
Coupled with bacterial infection - staph, pastuerella main isolates. Steptococcus, moraxlla and bodetella also reported.
101
What type of discharge is classically associated with dacryocystitis in rabbits. What other clinical signs are often seen?
White casesous to profuse creamy discharge that can be milked from lacrimal punctum by eyelid massage.
Often conjunctival hyperaemia, thickening, occasional secondary keratitis
Periocular scald/dermatitis
102
How can we locate the area of obstruction of the NLD in rabbits?
Skull radiography + contrast dacryocystorhinography |
(assessment of teeth also!)
103
How do we treat dacryocystitis in rabbits?
Nasolacrimal flushing in combination with topical antibiotic cover
Management of periocular scald - bathing and keeping clean
Tackle underlying issues - dentistry, husbandry to prevent ongoing issue
(Oral antibiotics, NSAIDs and dental surgery may be required)
