Flashcards in Opaque eye 1 &2 Deck (103):
What are a major location of ocular opacities?
corneal (lens opacification accounts for almost all the rest)
What is a very important disease of the cornea?
Name other causes of ocular opacities (other than corneal and lens)
fibrin in AC
vitreal opacities (blood, cells) - uveitis, hypertension
Describe corneal cell basal cells
= transient amplifying cells (TACs)
- capable of mitosis
- TACs come from SCs that reside in limbus
- barrier to FB and tears (i.e. stopping stroma swelling)
What are wing cells?
second layer of epithelium of cornea
- no longer mitotic
- 2-4 layers
What is squamous non-keratinised epithelium for in healing?
slough off with blinking
replenished by cells from below
What are the different types of movement that occur in epithelial wound healing?
When does sliding movement occur in wound healing?
Abrasion = superficial epithelial lesion that doesn't reach basal lamina. Happens quickly
Describe vertical movement in wound healing
first, epithelial cell sliding
then basal cell mitosis
from down up
deals with daily loss of cells
takes 1 week for a cycle
helps to regain the thickness of the layer
Describe centripetal movement in wound healing
from limbus towards center. Affects every layer. For larger epithelial defects. Significance is that pigment proliferation associated with irritation and as part of a scar in corneal disease can migrate centrally, over the pupil
Which dog breeds in particular have a very pigmented limbus? 2
pugs and GSDs
What is healing by sliding?
movement of approximately 1-2mm/day. depends on various factors. limbal SCs act as a barrier to conjunctival overgrowth, conjunctivalisation
What does healing by sliding depend on?
- corneal health
- existence of basal lamina SCs
- existence of a basal lamina (for SCs to adhere to)
- effects of species and age
Why is there superficial pigment deposition with epithelial wound healiong?
Theory - irritants activate melanin production (at lumbus and paralimbal conjunctiva). Pigment deposited in new migrating epithelial cells (centripetal movement over pupil). Severe sometimes - pugs. Other theories too
What is the vascularisation phase of epithelial wound healing?
- angiogenic factors not well understood
- stimulus is inflammation
- vessels can coalesce --> GT
- atrophy over time (once stimulus removed)
- superficial or deep (i.e. stromal) - may aid dx
- travels to the area in need
Name 3 factors aiding epithelial vascularisation in wound healing
nutrients, growth factors and inflammatory cells
structural support for reconstruction/ remodelling
What does epithelial vascularisation indicate?
- lag time of 2-4 days to bud
- then 1mm/2 days
Describe the composition of the corneal stroma
Collagen 1 fibrils arranged in lamellae which travel from limbus to limbus (periodicity of 620A - transparency), united and ordered by GAGs - transparency. Relative state of dehydration: deturgescence - transparency
The mechanism by which the stroma of the cornea remains relatively dehydrated.
Describe keratinocytes in stroma wound healing
- relatively inactive fibrocytes
- low numbers (transparent)
- contribute to lamellar creation and maintenance
- differentiate into fibroblasts and myofibroblasts
- subset are myofibrocytes with pseudopodia with alpha-sm-actin
- cell movement
Outline the chemical interaction moments after injury in the stroma
many different factors (e.g. collagenases and metalloproteases) produced by lacrimal glands, epithelial cells, stromal keratocytes, corneal nerves, leukocytes attracted to wound.
Describe cellular changes in the stroma after injury
- Cellular attraction --> destruction and clean up (monocytes, macrophages, neutrophils, TCs)
- Keratocyte-mediated build up (collagen fibrils and interconnections, IC matrix GAGs but not of correct quantities or types, spatial distribution of fibrils is incorrect at first)
- these 2 factors need to BALANCE otherwise problems
How does a scar form in the stroma?
GAGs not of correct quantities or types and spatial distribution of fibrils is incorrect at first.
What does a stromal defect have to be filled with?
How long does stroma wound healing take?
weeks-months. Depends on injury thus how much remodelling after reconstruction is required.
Which GAGs form in stroma?
Initially hyaluronic acid after injury, its concentration then decreases as other glycoprotein concentrations increase. Ultimately GAG and collagen types similar to original. Fibrillar organisation ensures transparency.
Which animals are better at stroma regeneration?
Cats > dogs
Young > old
What re-establishes corneal curvature?
epithelium via epithelial hyperplasia but initially fascets form (i.e. flat areas) and may remain for life.
Describe normal endothelium of cornea
-One cell layer, very sensitive cells and the hexagonal cells form a chicken wire pattern. Important because contains intercellular Na/K ATPase pumps in between endothelial cells which pump fluid back into AC.
- Natural barrier between cells (strong IC junctions, epithelial layer too)
Describe wound healing of endothelium
- Limit to amount of repair (50% cells in this layer exist by time a dog is adult)
- Polimegathism and pleo/polymorphism occur
What is the point of decompensation of endothelial repair?
- Normally 3000 cells/mm2 (dogs)
- Point for decompensation - variable - usually 800-500 cells/mm2. From this point onward in corneal oedema
Outline how corneal oedema may occur as a result of al repair
Damage --> limit to repair --> point of decompensation reached --> corneal oedema
What is the corneal endothelium sensitive to?
Intraocular dz - uveitis, glaucoma
contact (e.g. anterior lens luxation touching endothelium, sx instruments)
What is Primary Endothelial Degeneration?
A degenerative process, uncommon
- hunting breeds especially
--> corneal oedema --> blind
What are the main points to consider when dealing with an opaque eye in practice? 2
- superficial/ deep?
- does tissue KNOW it is ulcerated? (cell to cell communication, corneal sensitisation - desensitisation and brachycephalic factor
Why isn't cornea often affected by systemic dz?
Cornea has no BVs. But still possible.
Outline re-epithelialisation repair
- fast if stroma healthy
- growth rapid is no dz stops it
- reanchoring to secure epithelium takes months
Outline stromal reconstruction repair
- starts immediately
- takes longer to complete (vs. re-epithelialisation)
- if unstable --> melting/collagenolysis due to excessive inflammation (continued irritation, secondary infxn, once melting starts v difficult to control).
If an opaque eye isn't healing with your tx plan, what should you consider?
- tear film problem (quantitative or qualitative
- eyelid and TE faults or problems blinking
- repair process (brachycephalic effect, secondary infxn, melting)
- EXCEPTIONS are primary corneal problems but these are rare.
3 possible reasons why an opaque eye wound is taking too long to heal
- lack of re-epithelialisation
- stromal wound deepening
- stroma is devitalising (melting)
- ACT - something wrong
What should you do if an opaque eye is taking too long to heal?
1 check if you missed something
2 changing topical AB isn't always answer
What are the diagnostic steps in corneal ulcer dz?
- eyelid exam (S+F, cytology, other factors - brachycephalic?)
Why should you refer a corneal ulcer quickly?
- it is only 0.5mm thickness to start
- once collagen break-down advances, sx might be the only option
What are the general medical tx options for an opaque eye?
- corneal protection (Elizabethan collar)
- AB for prophylaxis
- Atropine (comfort) --> mydriasis, relaxation of CB (cicloplegia), BUT it dries the eye a little
- Ciclosporin (tx for KCS, doesn't interfere with stromal/ epithelial healing
- NEVER STEROIDS AND MOST NSAID drops (--> enhance collagenolysis, slow healing)
What is tarsorrhaphy?
Sx technique for corneal protection: horizontal mattress suture through eyelids, use stents made of IV tubes to protect eyelids, +/- bandage lens, sturues engages the holding layer (tarsal plate). Generally preffered to a TE/nictitating membrane flap
Outline a TE/ nictitating membrane flap
- may be helpful for corneal protection
BUT not recommended over a bandage lens and tarsorrhaphy. Offers no additional protection than a bandage lens, suturing damages conjunctiva close to cornea, doesn't allow exit of debris or easy penetration of medication, cannot evaluate eye under it at all.
Which ABs can you use for an opaque eye?
- Fusidic acid gel - BID
How can you deal with melting in an opaque eye?
Can be prevented, less so reduced, very hard to stop:
- serum eyedrops (contain antiproteases), frequent application, re-evalisate every 4-6 hrs, supports epithelial healing in various ulcer scenarios
How can you help comfort in opaque eye healing?
- Atropine (mydriatic-cycloplegic, long-acting): BID for 1-2 d in smallies, longer in horses, causes temporary dryness and gut stasis, Tropicamide is a short-term alternative.
- Preservative-free viscous tears, long-term reassess.
How quickly can collagenolysis melt a cornea?
within a week
- don't wait > 3-5 days to see again
- exception = SCCEDs
- if good healing, wait longer till next time
T/F: healing is aided by vascular growth
True - due to stabilising serum (anticollagenases), GT bed, healing doesn't depend on it though
T/F: > 50% depth (pot-hole appearance) needs to be assessed for reconstructive surgery
Name 2 factors causing collagenolysis
- serin proteases
T/F collagenolysis can progress rapidly within hours
True - hours to a handful of days
Consequence - collagenolysis
- localised disease
- widespread corneal destruction
- perforation (either of above)
When does Descemetocoele occur?
right before a perforation (thus a sx emergency)
Describe appearance of Descemetocoele
- partial bulging of Descemet's membrane
- doesn't uptake fluorescein (wall of oedematous stroma around it does)
- clear center (as no stroma to have oedema), may appear black as seeing pupil below
List primary causes of opaque eye
Feline acute bullous keratopathy
Facial nerve paralysis
Outline cause of KCS/ dry eye
- evaporative (lipid layer)
- drug related (affects watery layer of tear)
- anaesthetics and sedatives (medetomidine)
- primary, immune-mediated KCS
Typical signalment - KCS
- 4-8 years old
- Cockers, Shih-Tzus, KCCS, Westies
- slowly progressive
Outline appearance - KCS
- mucous accumulation
- +/- vascularisation and pigmentation
- very mild CS with primary KCS --> early CS may not be detected
What are the 2 trends of primary KCS?
- TREND A: biphasic age distribution, 0-females, entire, ulcerative keratitis (50-72%), may rapidly perforate!
- TREND B: 5 years of age, females> males, lower incidence of ulcerative keratitis (4-22%), most superficial
T/F: animals always have a complete tear film
False - normal animals don't have a complete tear film until 3 months old
What can primary KCS lead to?
Central or paracentral ulcers --> perforation in 2-7 days --> collagenolysis (usually centrally)
Why does primary KCS lead to perforation?
- diseased cornea (imbalance of destruction/construction)
- irritant remains (dry)
- increased thick mucoid discharge (abnormal clearing)
- changed bacterial flora
- inflammatory cells in surface
Name an early sx option for central ulcers of primary KCS
CLCT = corneolimboconjunctival transposition uses clear peripheral cornea, allows for a clearer visual axis for healing than other visual techniques
Name an early sx option for peripheral ulcers of primary KCS
Conjunctival pedicle graft: slightly faster (than CLCT), doesn't clear much over time, but not so important as peripheral.
Outline medical tx of KCS
- Topical ciclosporin (doesn't interfere with corneal healing)
- preservative-free viscous tears, long-term, reassess
- topical AB (chloramphenicol, BS, good penetration, 10-14 days, rarely need other stronger/different cover, do C+S if worried)
- serum eyedrops (4x / day)
- Optimmune = ciclosporin (or other immunomodulators - Tacrolimus), expensive, usually for life, at least 2 months (takes 4-6 wks to work)
How can an improvement in KCS to Optimmune/immunomodulator be documented?
A positive change in at least 3 of:
- mucous production
- (tear readings)
Aetiology - Feline Corneal Sequestrum
Signalment - Feline Corneal Sequestrum
Any breed with predisposition - Persians, Himalayans
Uni or bilateral
- possible in dogs too
Appearance - feline corneal sequestrum
- tan to black discolouration of the superficial stroma,
- localisation varies with cause (typically central to parancentral, central usually, otherwise where there is irritation)
- progresses over a wide variety and variable time --> darker plaque, neovascularisation, ulceration around plaque, mild to very painful
Sx - Feline Corneal Sequestrum
Remove the piece of dead black tissue via keratectomy
When does a Feline Corneal Sequestrum become painful?
From when the epithelium starts to detach
What is the nature of a Feline Corneal Sequestrum pigment?
Controversial, possibly pigment (melanin), iron, porphyrins
Etiology - Feline Corneal Sequestrum
associated with corneal trauma
medial lower eyelid entropion
- Effect of tear film stability and goblet cell function
- lower corneal sensitivity (effect on tear film and blink rate)
- lipid abnormalities and possible dissecation
- role of FHV-1
Tx - Feline Corneal Sequestrum
- Superficial keratectomy +/- bandage lens +/ tarorrphaphy
OR superficial keratectomy and grafting (conjunctival pedicle, corneoconjunctival pedicle, biosist)
- a CLCT offers transparency
- Medial lower eyelid entropion correction if necessary
Recurrence rate of Feline Corneal Sequestrum post-sx
Relatively high recurrence rate - lower if removed completely, constant BV supply long term (through graft)
Post-op supportive medical tx for Feline Corneal Sequestrum
- Topical AB until re-epithelialisation
- Preservative-free viscous tear preparation (Celluvisc 1%), used long-term? recurrence still possible despite grafting and complete recurrence and complete removal, clipping of pedicle of conjunctival graft not recommended.
Spontaneous Chronic Corneal Epithelial Defects (aka Boxer ulcers, indolent ulcers, non healing ulcers). Possibly in cats but not studied extensively.
2 main features of canine SCCEDs
- loose epithelial edges
- under-running of fluorescein dye with a pulsed saline test to confirm this
Other possible features of SCCEDs
+/- corneal oedema
+/- ocular pain
Always rule out other causes of ulcer (KCS
What may SCCED be associated with?
Hx of minor trauma but are NOT traumatic in origin but spontaneous
- Problems ID in dogs include:
- anterior stroma
- PAS+ and acellular zone with a hyaline membrane which interferes with epithelial adherence to stroma
- NOT a basement membrane dystrophy
Canine tx - SCCED
- Grid keratotomy/ Superficial scrape
Feline tx - SCCED
- Grid keratotomy/superficial scrape
RISK OF SEQUESTRUM with debridement and superficial scrape so CONTRAINDICATED IN CATS.
Outline mechanical debridement of SCCED
Removed all loose epithelium and hyaline plaque follow with superficial grid scraping/superficial scraping (NOT cats) done gently. Always buster collar!
Describe the superficial grid scrape
2nd part of tx for canine SCCED
- 2mm+ apart
1-2mm into healthy corneal epithelium
remain VERY superficial
(remember corneal thickness is 0.5mm)
you should NOT be able to see the grid that you make
What is a new tx for SCCED?
Diamond Burring --> removes epithelium and supposedly the hyaline membrane, always under sedation/GA (reported not to cause distress). Must be used with a bandage lens (improves comfort) with a tarsorrphaphy to help lens stay in place (not necessary in cats)
Medical tx - SCCED
Topical AB - chloramphenicol 3x/day
Consider serum eye drops
Protective collar always
When should you re-evaluate SCCED?
- every 2 weeks
- remove tarsorrphaphy and bandage lens on 1st re-visit
- May need to debride (topical anaesthesia, caution in cats = sequestrum), may need to repeat part of scrape in dogs, may or may not replace lens
Where does FHV-1 live?
trigeminal ganglion and corneal tissue, usually infected in kittenhood. recrudesces with stress
What is FHV-1 associated with in kittens?
- corneal ulcerative dz can be severe
What ulcer type does FHV-1 cause?
Early 'dendritic' ulcer (i.e. dendrite shape as virus spreads through epithelial cells) but this matures and becomes circular (then known as a geographic ulcer and these are seen most commonly).
What do many vets use to tx FHV-1 but has virtually no study efficacy?
IFN and L-lysine
- IFN --> possible decreased severity of CS and decreased CPE
- L-lysine: interferes with viral replication and reduces viral shedding
Tx - FHV-1
- IFN and ly-lysine (little evidence base)
- Antivirals (better option) - target rapilcation so static rather than cidal so needs to be frequently applied. E.g. idoxuridine OR TFT (trifluorothymidine) OR cidofovir (cytosine mimicking pyrimidine analogue to reduce CS severity/shedding)
- Pen-Gan and A-ciclovir: but toxic orally (liver, kidney, BM), they are adenosine/guanosisne-mimicking purine analogue
- Famcylovir is safe orally (pemciclovir is the active metabolite)
Aetiology - feline acute bullous keratopathy
What is feline acute bullous keratopathy?
Acute development of corneal oedema (cornea becomes soft, risk of melting/perforation v high). REQUIRES RAPID REFERRAL. Worse if bilateral (unknown why)
Tx - feline acute bullous keratopathy
- not well described -- many options and no best option ID
Aetiologies - facial nerve (FN) paralysis - V IMPORTANT TO LEARN
- Viral (flu, calici, FHV-1)
- OM (tympanic bulla)
- Ear canal avulsion = ECA (trauma)
- severe OE (low risk of FN paralysis in cats)
- ear canal neoplasia
- TECA with LBO
- idiopathic (some might be immune-mediated_
- part of a polyneuropathy
What may cause loss of blink that is usually temporary?
systemic ABs and/or myringotomy and topical ear meds
When may FN paralysis be permanent
40-70% TECA/LBO - nowadays should be less
Tx - FN paralysis
- Tarsorrphaphy for 1-2 months (horizontal mattress suture)
- Protective collar
- Topical AB (fucithalmic BID-TID)
- preservative-free, viscous tear (Cellusvisc)