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Ophthalmology > Opaque eye 1 &2 > Flashcards

Opaque eye 1 &2 Flashcards

1
Q

What are a major location of ocular opacities?

A

corneal (lens opacification accounts for almost all the rest)

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2
Q

What is a very important disease of the cornea?

A

ulcerative keratitis

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3
Q

Name other causes of ocular opacities (other than corneal and lens)

A

hyphema,
hypopion,
fibrin in AC
vitreal opacities (blood, cells) - uveitis, hypertension

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4
Q

Describe corneal cell basal cells

A

= 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)
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5
Q

What are wing cells?

A

second layer of epithelium of cornea

  • no longer mitotic
  • 2-4 layers
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6
Q

What is squamous non-keratinised epithelium for in healing?

A

slough off with blinking

replenished by cells from below

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7
Q

What are the different types of movement that occur in epithelial wound healing?

A

sliding
vertical
centripetal

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8
Q

When does sliding movement occur in wound healing?

A

Abrasion = superficial epithelial lesion that doesn’t reach basal lamina. Happens quickly

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9
Q

Describe vertical movement in wound healing

A 
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
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10
Q

Describe centripetal movement in wound healing

A

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

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11
Q

Which dog breeds in particular have a very pigmented limbus? 2

A

pugs and GSDs

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12
Q

What is healing by sliding?

A

movement of approximately 1-2mm/day. depends on various factors. limbal SCs act as a barrier to conjunctival overgrowth, conjunctivalisation

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13
Q

What does healing by sliding depend on?

A
  • corneal health
  • existence of basal lamina SCs
  • existence of a basal lamina (for SCs to adhere to)
  • effects of species and age
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14
Q

Why is there superficial pigment deposition with epithelial wound healiong?

A

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

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15
Q

What is the vascularisation phase of epithelial wound healing?

A
  • 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
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16
Q

Name 3 factors aiding epithelial vascularisation in wound healing

A

stabilising serum
nutrients, growth factors and inflammatory cells
structural support for reconstruction/ remodelling

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17
Q

What does epithelial vascularisation indicate?

A
  • chronicity
  • lag time of 2-4 days to bud
  • then 1mm/2 days
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18
Q

Describe the composition of the corneal stroma

A

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

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19
Q

Define deturgescence

A

The mechanism by which the stroma of the cornea remains relatively dehydrated.

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20
Q

Describe keratinocytes in stroma wound healing

A
  • 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
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21
Q

Outline the chemical interaction moments after injury in the stroma

A

many different factors (e.g. collagenases and metalloproteases) produced by lacrimal glands, epithelial cells, stromal keratocytes, corneal nerves, leukocytes attracted to wound.

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22
Q

Describe cellular changes in the stroma after injury

A
  • 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
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23
Q

How does a scar form in the stroma?

A

GAGs not of correct quantities or types and spatial distribution of fibrils is incorrect at first.

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24
Q

What does a stromal defect have to be filled with?

A

stroma

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25
Q

How long does stroma wound healing take?

A

weeks-months. Depends on injury thus how much remodelling after reconstruction is required.

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26
Q

Which GAGs form in stroma?

A

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.

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27
Q

Which animals are better at stroma regeneration?

A

Cats > dogs

Young > old

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28
Q

What re-establishes corneal curvature?

A

epithelium via epithelial hyperplasia but initially fascets form (i.e. flat areas) and may remain for life.

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29
Q

Describe normal endothelium of cornea

A
  • 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)
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30
Q

Describe wound healing of endothelium

A
  • Limit to amount of repair (50% cells in this layer exist by time a dog is adult)
  • Polimegathism and pleo/polymorphism occur
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31
Q

What is the point of decompensation of endothelial repair?

A
  • Normally 3000 cells/mm2 (dogs)

- Point for decompensation - variable - usually 800-500 cells/mm2. From this point onward in corneal oedema

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32
Q

Outline how corneal oedema may occur as a result of al repair

A

Damage –> limit to repair –> point of decompensation reached –> corneal oedema

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33
Q

What is the corneal endothelium sensitive to?

A

Intraocular dz - uveitis, glaucoma
drugs
contact (e.g. anterior lens luxation touching endothelium, sx instruments)

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34
Q

What is Primary Endothelial Degeneration?

A

A degenerative process, uncommon

  • hunting breeds especially
  • -> corneal oedema –> blind
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35
Q

What are the main points to consider when dealing with an opaque eye in practice? 2

A
  • superficial/ deep?
  • does tissue KNOW it is ulcerated? (cell to cell communication, corneal sensitisation - desensitisation and brachycephalic factor
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36
Q

Why isn’t cornea often affected by systemic dz?

A

Cornea has no BVs. But still possible.

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37
Q

Outline re-epithelialisation repair

A
  • fast if stroma healthy
  • growth rapid is no dz stops it
  • reanchoring to secure epithelium takes months
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38
Q

Outline stromal reconstruction repair

A
  • 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).
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39
Q

If an opaque eye isn’t healing with your tx plan, what should you consider?

A
  • 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.
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40
Q

3 possible reasons why an opaque eye wound is taking too long to heal

A
  • lack of re-epithelialisation
  • stromal wound deepening
  • stroma is devitalising (melting)
  • ACT - something wrong
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41
Q

What should you do if an opaque eye is taking too long to heal?

A

1 check if you missed something

2 changing topical AB isn’t always answer

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42
Q

What are the diagnostic steps in corneal ulcer dz?

A
  • STT-1

- eyelid exam (S+F, cytology, other factors - brachycephalic?)

43
Q

Why should you refer a corneal ulcer quickly?

A
  • it is only 0.5mm thickness to start

- once collagen break-down advances, sx might be the only option

44
Q

What are the general medical tx options for an opaque eye?

A
  • 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)
45
Q

What is tarsorrhaphy?

A

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

46
Q

Outline a TE/ nictitating membrane flap

A
  • 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.
47
Q

Which ABs can you use for an opaque eye?

A
  • Fusidic acid gel - BID
48
Q

How can you deal with melting in an opaque eye?

A

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

49
Q

How can you help comfort in opaque eye healing?

A
  • 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.
50
Q

How quickly can collagenolysis melt a cornea?

A

within a week

  • don’t wait > 3-5 days to see again
  • exception = SCCEDs
  • if good healing, wait longer till next time
51
Q

T/F: healing is aided by vascular growth

A

True - due to stabilising serum (anticollagenases), GT bed, healing doesn’t depend on it though

52
Q

T/F: > 50% depth (pot-hole appearance) needs to be assessed for reconstructive surgery

A

True

53
Q

Name 2 factors causing collagenolysis

A
  • serin proteases

- MMPs

54
Q

T/F collagenolysis can progress rapidly within hours

A

True - hours to a handful of days

55
Q

Consequence - collagenolysis

A
  • localised disease
  • widespread corneal destruction
  • perforation (either of above)
56
Q

When does Descemetocoele occur?

A

right before a perforation (thus a sx emergency)

57
Q

Describe appearance of Descemetocoele

A
  • 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
58
Q

List primary causes of opaque eye

A 
KCS
SCCEDs
FHV-1
Feline acute bullous keratopathy
Facial nerve paralysis
59
Q

Outline cause of KCS/ dry eye

A
  • evaporative (lipid layer)
  • drug related (affects watery layer of tear)
  • anaesthetics and sedatives (medetomidine)
  • primary, immune-mediated KCS
60
Q

Typical signalment - KCS

A
  • 4-8 years old
  • FS
  • Cockers, Shih-Tzus, KCCS, Westies
  • slowly progressive
61
Q

Outline appearance - KCS

A
  • mucous accumulation
  • hyperaemia
  • +/- vascularisation and pigmentation
  • very mild CS with primary KCS –> early CS may not be detected
62
Q

What are the 2 trends of primary KCS?

A
  • 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
63
Q

T/F: animals always have a complete tear film

A

False - normal animals don’t have a complete tear film until 3 months old

64
Q

What can primary KCS lead to?

A

Central or paracentral ulcers –> perforation in 2-7 days –> collagenolysis (usually centrally)

65
Q

Why does primary KCS lead to perforation?

A
  • diseased cornea (imbalance of destruction/construction)
  • irritant remains (dry)
  • increased thick mucoid discharge (abnormal clearing)
  • changed bacterial flora
  • inflammatory cells in surface
66
Q

Name an early sx option for central ulcers of primary KCS

A

CLCT = corneolimboconjunctival transposition uses clear peripheral cornea, allows for a clearer visual axis for healing than other visual techniques

67
Q

Name an early sx option for peripheral ulcers of primary KCS

A

Conjunctival pedicle graft: slightly faster (than CLCT), doesn’t clear much over time, but not so important as peripheral.

68
Q

Outline medical tx of KCS

A
  • 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)
69
Q

How can an improvement in KCS to Optimmune/immunomodulator be documented?

A

A positive change in at least 3 of:

  • mucous production
  • redness
  • comfort
  • keratitis
  • (tear readings)
70
Q

Aetiology - Feline Corneal Sequestrum

A

Spontaneous

71
Q

Signalment - Feline Corneal Sequestrum

A

Any breed with predisposition - Persians, Himalayans
Uni or bilateral
- possible in dogs too

72
Q

Appearance - feline corneal sequestrum

A
  • 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
73
Q

Sx - Feline Corneal Sequestrum

A

Remove the piece of dead black tissue via keratectomy

74
Q

When does a Feline Corneal Sequestrum become painful?

A

From when the epithelium starts to detach

75
Q

What is the nature of a Feline Corneal Sequestrum pigment?

A

Controversial, possibly pigment (melanin), iron, porphyrins

76
Q

Etiology - Feline Corneal Sequestrum

A

IDIOPATHIC:
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

77
Q

Tx - Feline Corneal Sequestrum

A
  • 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
78
Q

Recurrence rate of Feline Corneal Sequestrum post-sx

A

Relatively high recurrence rate - lower if removed completely, constant BV supply long term (through graft)

79
Q

Post-op supportive medical tx for Feline Corneal Sequestrum

A
  • 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.
80
Q

Define SCCED

A

Spontaneous Chronic Corneal Epithelial Defects (aka Boxer ulcers, indolent ulcers, non healing ulcers). Possibly in cats but not studied extensively.

81
Q

2 main features of canine SCCEDs

A
  • loose epithelial edges

- under-running of fluorescein dye with a pulsed saline test to confirm this

82
Q

Other possible features of SCCEDs

A

+/- corneal oedema
+/- ocular pain
+/- vascularisation
Always rule out other causes of ulcer (KCS

83
Q

What may SCCED be associated with?

A

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
84
Q

Canine tx - SCCED

A
  • Debridement
  • Grid keratotomy/ Superficial scrape
  • Keratectomy
85
Q

Feline tx - SCCED

A
  • Debridement
  • Grid keratotomy/superficial scrape
  • keratectomy
    RISK OF SEQUESTRUM with debridement and superficial scrape so CONTRAINDICATED IN CATS.
86
Q

Outline mechanical debridement of SCCED

A

Removed all loose epithelium and hyaline plaque follow with superficial grid scraping/superficial scraping (NOT cats) done gently. Always buster collar!

87
Q

Describe the superficial grid scrape

A 
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
88
Q

What is a new tx for SCCED?

A

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)

89
Q

Medical tx - SCCED

A

Topical AB - chloramphenicol 3x/day
Consider serum eye drops
Protective collar always

90
Q

When should you re-evaluate SCCED?

A
  • 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
91
Q

Where does FHV-1 live?

A

trigeminal ganglion and corneal tissue, usually infected in kittenhood. recrudesces with stress

92
Q

What is FHV-1 associated with in kittens?

A
  • symblepharon.

- corneal ulcerative dz can be severe

93
Q

What ulcer type does FHV-1 cause?

A

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).

94
Q

What do many vets use to tx FHV-1 but has virtually no study efficacy?

A

IFN and L-lysine

  • IFN –> possible decreased severity of CS and decreased CPE
  • L-lysine: interferes with viral replication and reduces viral shedding
95
Q

Tx - FHV-1

A
  • 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)
96
Q

Aetiology - feline acute bullous keratopathy

A
  • unknown
97
Q

What is feline acute bullous keratopathy?

A

Acute development of corneal oedema (cornea becomes soft, risk of melting/perforation v high). REQUIRES RAPID REFERRAL. Worse if bilateral (unknown why)

98
Q

Tx - feline acute bullous keratopathy

A
  • REFERRAL

- not well described – many options and no best option ID

99
Q

Aetiologies - facial nerve (FN) paralysis - V IMPORTANT TO LEARN

A
  • 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
100
Q

What may cause loss of blink that is usually temporary?

A

systemic ABs and/or myringotomy and topical ear meds

- CATS

101
Q

When may FN paralysis be permanent

A

70% ECA

40-70% TECA/LBO - nowadays should be less

102
Q

Tx - FN paralysis

A
  • Tarsorrphaphy for 1-2 months (horizontal mattress suture)
  • Protective collar
  • Topical AB (fucithalmic BID-TID)
  • preservative-free, viscous tear (Cellusvisc)
103
Q

What can FN paralysis lead to?

A

Interpalpebral fissue ulceration: superficial but can deepen/melt (imbalance), sequestrum formation possible

Ophthalmology (14 decks)

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