Cornea Flashcards

Question

Can the corneal endothelium regenerate? What happens to the endothelium with age?

Answer 1

No corneal endothelium is not self renewing and number of cells decreases with age

Answer 2

Cells around defect enlarge and slide in to fill the defect - consequence = oedema due to influx of water into stroma

Answer 3

Trigeminal nerve = corneal sensitivity Myelinated fibres pass from trigeminal through anterior stroma in groups termed leashes. As individual nerves leave leashes they maintain a Schwann cell sheath. Penetrate through epithelial basement layer, sheath is lost and naked nerve endings send its terminus up between the cell layers, terminating amongst outer most squamous cells.

Answer 4

300-400 more nerve endings per unit

Answer 5

Oxygen - tear film (+hydration) Limbal blood vessels/aqueous humour = glucose and amino acids

Answer 6

Limbus = junction between corneal and conjunctival epithelia (Anatomically zone also includes Schlemm's cana; and trabecular meshwork but more commonly it is the superficial portion referred to as the limbus. Transitional zone 10-12 layers thick Unlike conjunctival epithelium lacks goblet cells Similar cell-cell and cell-substrate junctions as cornea Basal cells smaller and less columnar than corneal epithelium More mitochondria in basal cells of limbus Smaller area of basal cells with hemidesmosomes - undulation = additional adhesive strength and possibly increased surface area for absorption of nutrients from limbal vasculature. Some of these basal cells hypothesised to be stem cells of the corneal epithelium. Connective tissue below limbal epithelium = more loosely and irregularly arranged than cornea Similar collagen, proteoglycans, soluble glycoproteins as cornea Stroma of limbus = fibroblasts, melanocytes, macrophages, langerhans cells, mast cells, lymphocytes, plasma cells. Blood vessels and lymphatics loop into this region along with bundles of unmyelinated nerves. Connective tissue - large radial folds/ridges (palisades of vogt) house small blood vessels, lymphatics and nerves Crypts of limbal epitheliu, reach down into valley between palisades of vogt and hypothesised that deep housing of basal cells protects stem cell population. Blood supply - anterior ciliary arteries extending from rectus muscles. Drained by venules reversing over same direction.

Answer 7

Yes - stratified squamous epithelium = self renewing Constant state of "healing" Squamous cells shed into tear pool whilst simultaneously being replaced by cells moving centrally from the limbus and anteriorly from the basal layers of the epithelium

Answer 8

Exaggerated version of normal physiological maintenance phase when wound healing. Cellular and subcellular events occurring under influence of extracellular matrix proteins and growth factors. Under normal circumstances epithelial mass does not change X+Y = Z (corneal epithelial cell mass maintenance equation) X = proliferation of basal epithelial cells Y = contribution to cell mass by centripetal movement of peripheral cells z = epithelial cell loss from surface Cell multiplication occurs predominantly at the limbus - limbal stem cells source of multiplying and migrating cells.

Answer 9

Cell elongation + migration, cell proliferation, cell adhesion

Answer 10

3 phases of healing: 1. Cell elongation followed by migration 2. Cellular proliferation 3. Cellular differentiation and adhesion 1st 4-6 hours no appreciable decrease in wound size occurs (may become slightly larger due to necrotic cell removal and rounding off of cells at wound edge) Basal and squamous cells in vicinity show thickening and separation. Within 2hrs all hemidesmosomal attachments between basal cells and basement membrane disappear Demsmosomes between cells remain intact allowing to move as a sheet. Epithelial cells flatten and move across the defect until completely covered - active energy consuming process independent of cell proliferation. Migration = increased synthesis of proteins and glycoproteins with glycogen metabolism being main energy source. Both basal and suprabasal cells participate in migration Flattened epithelial cells filling defect show finger like (filopodia) and coral like (lamellipodia) processes extending onto wound surface - formation of these marks beginning of cell migration. In order to migrate basal cells must release their adhesive junctions and other means of adhesion to allow spreading over the wound. Temporary contacts known as focal contacts formed - actin filament bundles inserting into cell membrane. Fibrin and fibronectin stimulate epithelial cells to release plasminogen activating factor - plasminogen to plasmicn which lyses cell to substrate adhesions allowing cells to advance and form new adhesions. Cycle repeated until migration ceases at wound closure. Normal thickness restored by epithelial proliferation - restore cell numbers and mass. Wave of mitosis generated from periphery - stem cells at limbus produce transient amplifying cells and move from periphery to the wound and continues until wound has healed and normal thickness restored. Wound healing not complete until newly regenerated epithelium has anchored itself to underlying connective tissue. Rapidity with which new hemidesmosimal attachements occur depends on whether basement membrane was intact or not at time of wounding. If was intact new epithelial cells can utilise it and migrate rapidly within 7 days to fill defect forming new strong adhesions. Basement membrane not intact e.g stromal ulcer, normal adhesion may not be for several weeks as a new basement membrane must be constructed by the epithelium and stroma before new adhesions can form.

Answer 11

Stroma cannot heal/remodel until re-epithelialisation complete Fibronectin from tear film deposited onto ulcer bed and basal epithelial cells use fibronectin to make focal adhesions and migrate across the ulcer bed. Once re-epithelialised fibroblasts (keratocytes) from surrounding stroma migrate to wounded area and start to lay down new collagen matrix (type 3) Collagen is not as regularly arranged as the unwounded cornea and this results in opaque scar formation. With time the fibroblasts can remodel the scar tissue and the opacity may reduce in size.

Answer 12

Oedema Pigmentation Vascularisation Fibrosis Cellular infiltration Lipid deposition Calcium deposition Most corneal disease will incorporate a number of these signs.

Answer 13

Blue/grey - corneal oedema Red - neovascularisation White - lipid/calicum/cellular infiltrate Black/Brown - pigmentation Describe location and distribution of this colour change.

Answer 14

Fluid within cornea - due to epithelial or endothelial dysfunction Disruption to regular arrangement of collagen fibrils = opacity

Answer 15

Epithelial dysfunction - corneal ulceration (usually deep = stroma) Endothelial dysfunction - primary (age/breed related) or secondary (intraocular inflammation/uveitis, anterior lens luxation, increased IOP, intraocular mass, intraocular surgery/trauma)

Answer 16

Full ophthalmic exam Fluorescein IOP - tonometry important Consider ocular ultrasound if unable to visualise eye with diffuse severe corneal oedema.

Answer 17

Can get superficial and/or deep vascularisation of the cornea in response to release of angiogenic factors by the injured (anoxic) cornea, infiltrating cells or neoplasms. Try to establish if the blood vessels are superficial or deep.

Answer 18

Chronic corneal disease Melanin - superifical or endothelial Corneal sequestrum in cats = their version of pigmentation.

Answer 19

Fibrosis - from stromal healing - irregular collagen deposition therefore these areas are opaque. Overtime remodelling can occur and regular lamellae arrangement restored reducing opacity. Cellular infiltrate (white/pink) - usually superficial and proliferative. Identification of cell type with corneal cytology (scraping lesion with topical anaesthesia). May consider keratectomy for diagnostic/therapeutic purposes. Lipid deposition (white and SPARKLY, think fat = glistening) - various casues, superficial or deep deposits Cholesterol or triglycerides. Corneal lipid dystrophy Lipid Keratopathy Arcus lipoides corneae Steroid keratopathy Calcium deposition - (white and GRITTY, think mineral) - degenerative condition usually seen in older dogs. Often may have concurrent diseases e.g renal/cardiac disease

Answer 20

Infiltrative e.g cellular, neoplastic, non cellular VS Non infiltrative - congenital/acquired Vs Infectious

Answer 21

Predisposed = GSD, Collies, Greyhounds Usually 3-5 years old at presentation "Red eyes" Corneal lesions start at ventro-lateral limbus and spread out across cornea Vascularisation, infiltration and pigmentation characteristic Conjunctival involvement including TEL common and in some cases may be affected without corneal lesions (plasma cell infiltrate of TEL - plasmoma, loss of pigmentation of TEL) Lesions bilateral generally and may be complicated by lipid deposition Rare to be ulcerated

Answer 22

CSK - often suspected based on presentation/breed however could confirm with biopsy - plasma cells dominate Treatment = topical steroids or ciclosporin (Optimmune = licensed) Most cases respond rapidly to treatment but often prone to relapse once therapy withdrawn - affected dogs require repeat courses of treatment/lifelong therapy Flares ups often associated with high UV Vascularisation and infiltration will decrease with treatment but lipid deposition/pigment often persists. ?Superficial keratectomy if vision severely impaired by pigmentation.

Answer 23

Immune mediated disease White/pink deposits (resembling cottage cheese) in superficial cornea and stroma Can also involve conjunctiva (occasionally just conjunctiva affected - loss of pigmentation of eyelids also) Young - middle aged cats ?possible link to FHV-1

Answer 24

Diagnosis = cytology of corneal scrapings or biopsies Mast cells and eosinophils predominate with occasional mixed inflammatory cells.

Answer 25

Topical steroids or ciclosporin - clinical remission Many cases will have seasonal reoccurence and require repeat treatments. In past megoestrol acetate was used for treatment but s/e (increased risk of mammary neoplasia, appetite increase, weight gain, increased risk diabetes etc) mean it is reserved only for refractory cases.

Answer 26

Breeds = Shetland Sheepdog, Minature Dachshunds Multiple pin point fluorescein +ve punctate corneal opacities Treatment = topical steroids (only time steroids are indicated when fluorescein +ve)

Answer 27

Corneal neoplasia alone very rare Squamous cell carcinomas - can occur at limbus and reported in cats, also dogs associated with chronic keratitis Limbal/epibulbar melanoma - slow growing benign tumour in dogs, darkly pigmented breeds e.g Labradors/GSD Surgical resection tx of choice and can be followed with Strontium 90 radiation therapy. Larger lesions may need reconstructive techniques e.g corneo-scleral transposition. Cryotherapy/laser photoablation also options. Haemagioma/haemangiosarcoma - reported at limbus and on cornea.

Answer 28

Dystrophy = implies inherited Lipidosis = inheritance unproven

Answer 29

Lipid = sparkly appearance Breeds = Cavalier King Charles, Rough Collies, Shetland Sheepdogs, Afghan Hounds, Beagle, Boxer, Husky, GSD, Samoyed Lipid deposition in corneal stroma of both eyes Not a systemic disease although systemic factors can influence NOT ASSOCIATED WITH VASCULARISATION Condition usually seen in young adults (occasionally as puppies) Bilateral and reasonably symmetrical (one eye may be affected in advance of the other) Opacity usually central/paracentral and typically crystalline sparkling appearance. Integrity of epithelium confirmed with lack of fluorescein uptake. No associated inflammation and opacity once formed remains static. Occasionally will regress and occasionally progress in which case low grade inflammatory response may follow on. In bitches sometimes associated with oestrus, pregnancy and lactation.

Answer 30

Cholesterol = main type of lipid - free and esterified form with lesser quantities of free fatty acids and phospholipids

Answer 31

Main defect = with keratocytes of stroma Accumulates large amounts of lipid before dying in situ - crystalline cholesterol associated with death and necrosis of the keratocytes. Changes restricted to anterior third of the corneal stroma

Answer 32

Majority of cases - no treatment required Only if opacity becomes progressive and dense is further investigation required to establish lipid and lipoprotein profile and determine if systemic treatment can be used to modify evolution of corneal opacity.

Answer 33

Can occur in one or both corneas VASCULARISATION = KEY FEATURE Vascularisation may precede or follow lipid deposition Some affected animals (not all) - plasma hyperlipoproteinemia Usually associated with anterior segment inflammation, localised corneal disease, previous corneal/ocular insult (including surgery) Many accompany systemic disturbance of lipoprotein metabolism Often smaller lipoproteins (HDL cholesterol) which are raised in lipid keratopathy.

Answer 34

Characteristic histopath report Lipid accumulation and death of stromal fibroblasts. + other lipid filled foam cells in progressive lesions (macrophage derived) Considerable quantities extracellular crystalline lipid (free and esterified cholesterol) and non crystalline lipid may accumulate in affected corneas associated with cell death. Corneal neovascularisation always present and vessels may be the source for direct stromal lipid deposition as well as affording entry for haematogenous macrophages.

Answer 35

Lipid/lipoprotein profile - check for systemic abnormalities as some animals present with systemic hyperlipoproteinemia If systemic abnormalities identified then treat these to restore normolipoproteinemia Local ocular disease should be identified and treated Keratectomy if desired should only be performed once normolipoproteinemic and underlying local factors bought under control. Suitably medical treatment/dietary modification (avoid high fat diets) some lesions will regress but lipid removal is always a much slower process than lipid deposition. Can be associated with topical steroid use = especially long term cases.

Answer 36

Signalment Ophthalmic history Biochemistry (T4 etc) Lipid/lipoprotein profile

Answer 37

Bilateral condition in dogs PERIPHERAL corneal lipid deposition Excessive plasma lipoproteins - almost always associated with hyperlipoproteinemia - larger sized lipoproteins (triglycerides) result in arcus Opacity peripheral and within corneal stroma, particularly superficial stroma Short time frame opacities become vascularised but blood vessels are delicate in comparison with those seen in lipid keratopathy. Accumulates more densely in warmest parts of cornea Often secondary conditions leading to hyperlipoproteinemia e.g hypothyrodism If underlying reason for hyperlipoproteinemia not addressed then more generalised lipid deposition results (then histopath more commonly resembles lipid keratopathy)

Answer 38

Treatment = depends on primary (rare) or secondary hyperlipoproteinaemia No specific tx for primary - dietary modification can be tried Specific tx for any underlying causes e.g thyroid replacement therapy in hypothyroidism.

Answer 39

Occasionally can get ulceration in areas of lipid depositon and can be slow to heal May also be indicated if causing considerable vision issues (make sure normolipoproteinemic first if going to perform)

Answer 40

Old dogs (often >14yrs) Associated with systemic disease (renal, cardiac etc - "end of life sign", not a good prognostic sign") GRITTY rather than sparkling appearance

Answer 41

Can be associated with recurrent ulceration/discomfort EDTA Contact lenses - analgesic barrier Pain relief If very ulcerated - topical AB cover, sometimes diamond burr/keratectomy performed.

Answer 42

Dermoids - usually located at the limbus, slow growing, sometimes pigmented and may be asymptomatic if hairless. Superficial keratectomy = tx of choice. Breed predisposition GSD, St Bernard (increasingly seeing in French Bulldogs) Micro and megalocornea - both rare, no other associated ocular abnormalities. Bilateral and non progressive. Persistent pupillary membranes - may sometimes attach to posterior cornea, localised or more generalised opacities at point of contact (originate from iris collarette (anterior synechiae = pupillary margin)) Keratoconus and keratoglobus - keratoconus = bilateral thinning of central cornea (may also be associated with lenticonus). Keratoglobus = limbal to limbal cornea thinning such that cornea protrudes. Lysosomal storage disease - specific enzyme deficiencies lead to accumulation of abnomal products within cell lysozymes and the disorders are classified depending on substrate that accumulates. Neurological signs predominate but can have ocular signs - retinal changes, blindness, corneal clouding.

Answer 43

Dystrophy = primary inherited conditions Occurs in number of pedigree dogs although exact inheritance pattern unknown Most common breeds affected = Springer Spaniel, Chihuahua, Boston Terrier Endothelial numbers sufficient but function is impaired. Affected dogs late middle age (8-13 yrs) May also be seen in older dogs due to endothelial loss (endothelial degeneration if not suspected hereditary - reduced number of cells to pump water away from stroma) Occasionally seen in DSH's but rare.

Answer 44

Stromal oedema Non painful condition but severity of oedema can affect vision Bilateral condition (although one eye often affected before the other) Progressive Corneal profile can alter with time - keratoconus/keratoglobus Can develop bullous keratopathy secondary to the oedema then painful with the ulcerations - non healing ulcers. Vascularisation and corneal decompensation develop in more advanced cases.

Answer 45

No specific treatment Therapy aims to reduce corneal oedema and its effect on cornea Hyperosmotic solutions - glycerol and sodium chloride can be used to draw fluid from the cornea but do often cause irritation. Contact lenses = analgesia in painful ulcerated cases Systemic analgesia if ulcerated ?Thermal keratoplasty - post op fibrosis squeezes fluid out and prevents further fluid entry. Corneal opacity may increase after this procedure so not a method for restoring vision. Used in cases where medical therapy failed and desire is to prevent recurring painful non healing ulceration.

Answer 46

Manx cats - simple autosomal recessive

Answer 47

Slowly progressive corneal dystrophy causing stromal opacity with/without associated vascularisation. Labador Retrievers around 5yrs of age DNA test now available (carbohydrate sulfotransferase gene 6 mutation)

Answer 48

Cranial nerve V - trigeminal (neurotrophic) or Cranial Nerve VII - facial (neuroparalytic palsy) will result in keratitis due to loss of a blink reflex - drying and dessication of the ocular surface as not spreading tear film. Also factor in brachycephalic dogs as protrusion of glove leading to incomplete blink and tear film spreading with drying of central cornea.

Answer 49

Only seen in the cat Breed predisposition - Persians, Birmans and Burmese but can be seen in any breed Cornea's response to chronic damage and irritation Associated with FHV-1 infection Other causes = entropion, KCS, chronic exposure keratitis May be an inherited problem such as a stromal dystrophy or may be associated with brachycephalic syndrome similar to seen in dogs (lagophthalmos and central corneal drying) Thorough ocular examination indicated to identify any concurrent ocular disease. Deep brown staining deep within stroma to start with. As progresses darkens and increases in area and extends into anterior stroma eventually breaching epithelium. No issues for cat whilst in stroma but once ulceration occurs with breaching of the epithelium considerable ocular discomfort. Chronic cases may be accompanied by oedema and vascularisation. Some sequestra will slough spontaneously but can be very long painful process. Condition is usually unilateral but other eye may become affected at later date if pedigree cause.

Answer 50

Determine underlying cause if present and correct (e.g entropion) Superficial keratectomy = tx of choice for removing lesion and can be followed up with supporting graft and contact lens for comfort. Topical tear replacement useful in some cases Recurrence possible and sometimes will reoccur even underneath graft.

Answer 51

Breeds - WHWT, toy poodles, springer/cocker spaniels, Shih Tzu, Lhaso Apso etc Middle aged dogs Presenting signs = mucoid to mucopurulent discharge, often adhered to cornea. Intermittent conjunctivitis. Corneal vascularisation and pigment deposition, non healing corneal ulcerations, melting ulceration Diagnosis = STT (<10, 10-15 early KCS) and compatible clinical signs Tx - ciclosporin 0.02% (optimmune) - licensed, false tear preparations Off licence - 1-2% ciclosporin in corn oil, tacrolimus 0.03% (protopic), +/- topical steroids +/- topical antibiotics

Answer 52

Smooth rounded superficial corneal lesions when corneal epithelium seeds into superficial stroma. Some congenital, others acquired post trauma/surgery (possibly complication of grid keratectomy if go too deep). Non painful Fluorescein -ve and variable size Tx = surgical excision

Answer 53

Acute FHV = conjunctivitis + corneal involvement as has tropism for corneal epithelium URT signs also see as tropism for respiratory epithelium "Cat flu" stage Corneal involvement often ulceration (sometimes severe) Chronic/carrier status Symblepharon (adhesions) Dendritic ulceration/non healing ulcers Stromal keratitis Dry eye Conjunctivitis

Answer 54

Severe infections = stem cells at limbus damaged by FHV-1 therefore unable to maintain normal corneal epithelium In response conjunctiva grows across the cornea to resurface it and adhesions are formed. If extensive conjunctival growth can cause blindness. Surgical removal can be attempted but symblepharon usually reoccurs (again due to damage of limbal stem cell population important for normal corneal maintenance)

Answer 55

Usually diagnosed based on clinical signs and hx. PCR (although care with interpretation) - many cats exposed Serology not useful as vaccination commonplace

Answer 56

Symptomatic therapy and support with nursing care Antibiotics if secondary bacterial infection Anivirals = severe disease False tear preparations

Answer 57

Recurrent conjunctivitis = antivirals Dendritic ulcers = antivirals (+ topical prophylactic AB's, analgesia) Non healing ulcers - antivirals +/- debridement +/- superficial keratectomy Stromal keratitis (often autoimmune type behaviour) - antivirals + corticosteroids or ciclosporin (need some kind of immunosuppression to clear)

Answer 58

Fungal contamination of corneal wounds Should always be considered in keratitis cases refractory to treatment Ulcerative disease = most common presentation Cases often have hx of previous topical and/or steroid treatment Characteristic white (frosty/icing sugar) appearance to the stroma/ulcer surface Often small amount of vascularisation Very painful ulceration Not usually brachycephalics, often working type dogs out in countryside

Answer 59

Hx/clinical presentation Cytology - presence of fungal hyphae Histology +/- culture PCR

Answer 60

Medical antifungals: Voriconazole - IV solution made up and frozen in 1ml syringes - use 1 syringe per day as drop 6x daily Clotrimazole (canesten cream) - well tolerated in eye Surgical - superficial keratectomy often combined with conjunctival pedicle graft.

Answer 61

Superficial ulceration = should heal within 7 days, if does not then need to look for underlying cause.

Answer 62

Prophylactic AB cover - e.g chloramphenicol/fusidic acid + Analgesia (e.g systemic NSAID)

Answer 63

Duration Depth - superficial, deep (stromal), desmetocoele, rupture - use slit beam + fluorescein to help determine Is it infected? - Melting corneal ulcer = gelatinous edges/infiltrate Any other complicating factors - KCS, entropion, distichiasis, ectopic cilia etc

Answer 64

Also known as SCCED (spontaneous chronic corneal epithelial defect), recurrent epithelial erosion, Boxer ulcer etc SUPERFICIAL corneal ulcer that fails to heal within usual 7 day time frame Not infected May be associated with localised oedema +/- vascularisation (often associated with chronicity) Painful Often significant epiphora Characteristic fluorescein staining pattern = irregular, under running/lifting of ulcer edges Middle aged dogs (does not occur in young dogs! Generally >7yrs old although brachys can sometimes be a bit younger) Condition may reoccur in same eye repeatedly or occur in other eye. In some individuals = exuberant production of granulation tissue protruding from corneal surface.

Answer 65

Boxers, Staffordshire Bull Terriers, Corgis, WHWT, Boston Terriers

Answer 66

Defect in basement membrane formation and epithelial basal cell adhesion (corneal epithelial dystrophy) via hemidesmososmes that anchor the basal corneal eptihelial cells in place. Poor healing response = chronic ulceration Hx = superficial corneal ulceration unresponsive to usual intervention.

Answer 67

Success rate of healing within 2 weeks - aim of therapy to disturb basement membrane Eye should be prepped with 1:50 povidone iodine before any of these procedures performed. Cotton bud debridement (63% first attempt, Grid keratotomy = 85% (combined with cotton bud debridement) Diamond burr (90% success rate) Superficial keratectomy (near 100% success rate) - referral, requires operating microscope, keratectomy knife/beaver blade. (Phenol cautery - often not performed now due to H+S, 1 drop on cotton bud following debridment, rub ulcer bed then flushed with sterile water)

Answer 68

Analgesia = systemic NSAID Atropine = prevent ciliary body spasm, additional analgesia Contact lens = added comfort Topical AB cover (prophylactic) e.g chloramphenicol QID (Occasionally may use systemic AB's if concerned preparations slowing down healing) +/- temporary tarsorrhaphy (may help keep contact lens in place)

Answer 69

Repeated trauma - Hairs (ectopic cilia, trichiasis, distichia, entropion), Foreign bodies (check under TEL, conjunctival fornix etc) KCS Oedema - all causes Infiltrates - lipid/calcium Immune mediated - CSK (Pannus), punctate keratitis SCCED

Answer 70

Cytology from edge of ulcer and if indicated swabs for C+S

Answer 71

Cotton bud debridement = ok Superficial keratectomy = ok Should never perform grid keratotomy, diamond burr or phenol cautery - all associated with corneal sequestrum formation Often viral related - consider use of antivirals, contact lens etc

Answer 72

Infected corneal ulcer - rapidly progressive Occur when excessive production of proteases and collagenases - produced by pathogenic organisms, stromal keratocytes and inflammatory cells. Effect = liquidification of stromal collagen and melting appearance to cornea. Protease/collagenases normal part of stromal remodelling/homeostasis but when upregulated lead to disastrous loss of stromal integrity.

Answer 73

Pseudomonas and B-haemolytic streps (Will sometimes see sterile melts in some brachycephalics and patients with dry eye)

Answer 74

EMERGENCY - NEED TO STABILISE STROMA QUICKLY to prevent loss of stromal integrity and risk of rupture/perforation Hospitalise - need intensive medical therapy and monitoring of ulcer progression Cytology + Culture and sensitivity Topical broad spectrum antibiotics q 1-2hrs (use cytology to help with choice whilst await C+S - rods = ofloxacin, cocci - chloramphenicol) Anti-collagenase therapy - serum = most effective choice q1-2 hourly (consider EDTA, plasma, tetracyclines also) Systemic NSAIDs for analgesia +/- Atropine (but beware effect decreased tear production, so may not be sensible choice if suspect borderline KCS for example) +/- Opioids if additional analgesia required +/- Corneal cross linking +/- Surgery CONTRAINDICATED = steroids (avoid systemically too = immunosuppression), contact lenses (trap bacteria), third eyelid flaps (inability to visualise ulcer/trap bacteria/reduce effectiveness of therapy penetrating)

Answer 75

Formation of chemical bridges between protein residues and/or other molecules Cross links formed by chemical reactions initiated by heat, pressure or radiation. Normal enzymatic cross linking occurs as part of remodelling of collagen - improve biomechanical stability of cornea. In veterinary medicine as part of therapy for melting corneal ulcers.

Answer 76

Riboflavin (Vit B2) acts as photosensitiser when exposed to UV light at a peak of 370nm Free radicals generated Formation of covalent cross links on surface of collagen fibrils and within protein network surrounding collagen (up to depth 300um) Cross links = increase corneal biomechanical and biochemical stability Direct increase in corneal stiffness Reduction of enzymatic collagenolysis (steric hinderance of collagenase binding sites to collagen molecules) Free radicals damage DNA and RNA leading to cell apoptosis of microbes + riboflavin intercalates with microbes nucleic acids inhibiting replication. Should reduce healing time, increase patient comfort and reduce hospitalisation time and need for surgery. May also improve visual outcome with less scarring.

Answer 77

Copious flushing with saline or water (water actually preferred in these situations, greater osmotic potential to draw out) Assess pH (acids less destructive than alkalis - alkalis greater corneal penetration) Use pH of tear to guide flushing - aim for pH 7 Post flushing = lubrication, topical AB, NSAID for analgesia +/- atropine Anticollagenases may be required Scarring = probable complication Very severe scarring - can get symblepharon formation - damage to limbus

Answer 78

Magnification - operating microscope preferred

Answer 79

Lateral canthotomy - can provide exposure to surgical site Stabilisation of globe position - neuromuscular blockade to maintain central eye position (or consider scleral stay suture/artery forceps

Answer 80

8/0 - 10/0 vicryl

Answer 81

Correct placement important = ensure watertight seal and prevent leakage of aqueous, good post operative function and satisfactory appearance. Needle (spatula) should enter cornea as near to perpendicular as possible. Penetrate 2/3rds corneal thickness Pass through opposite side of wound at same depth as first side Needle should emerge as near to perpendicular as possible and equidistant from wound compared to other side. Once tied - accurate apposition and a watertight seal.

Answer 82

Cellulose sponge - leakage of aqueous when press around edges of wound Siedel test with fluorescein

Answer 83

Double overhand throw (surgeons knot) followed by 2-3 single throws in alternate directions

Answer 84

Simple interrupted - many situations, breakage of one knot does not affect whole line like continuous patterns. Main disadvantage = slower to place, more uneven spread of tension and more knots placed as potential irritants. Continuous - repairing limbal incisions/performing penetrating keratoplasties, potentially clean lacerations also. Adv - speed, fewer knots, ability to spread tension evenly Disadvantage - one knot to hold whole length Cruciate - reduce no of knots used, can bury knot within wound Mattress sutures - usually reserved for areas with marked corneal tension or if cornea holding sutures poorly.

Answer 85

"Glue" - ophthalmic hexabond (N-butyl cyanoacrylate) Can be used to seal small corneal defects e.g small partial lacerations, pin point desmetocoeles and small diameter stromal ulcers. Contraindicated - infection/perforations Epithelium able to grow under plug and plug spontaneously extruded Additional N-acetyl group stops exothermic reaction Instantly polymerises in contact with fluid - cornea dry before application (canned air to facilitate) Adhesive painted on layer by layer 30G needle Plug should not exceed normal corneal surface

Answer 86

Porcine submucosal collagen (A-cell and others) Amniotic membrane (Omnigen) Can be used in multiple layers and for particularly deep/unstable defects. Amniotic membrane also has anti-inflammatory properties and useful in ocular surface re-construction.

Answer 87

Deep/large stromal ulcers (>50% corneal depth) Desmetocoeles Perforated corneal ulcers (with and without iris prolapse)

Answer 88

Additional support for weakened cornea No risk of rejection as from host animal Contain blood vessels and lymphatics which offer significant antimicrobial (bacteria, virus, fungi) and antiprotease (including anticollagenase) effects. Leukocytes, antibodies, serum and alpha-2 macroglobulin (anticollagenase factor) immediately placed onto corneal bed. Conjunctival blood vessels- systemic antibiotics able to reach ulcer site at higher levels. Fibrovascular/deeper layers of conjunctival transplant = fibroblasts and collagen to begin rebuilding the stroma.

Answer 89

Result in varying degrees of corneal scarring/impinge on visual axis Anticipated scarring can be reduced using post operative corticosteroids once ulcer healing is completed.

Answer 90

1. Lateral canthotomy and eyelid speculum placed to improve exposure Ulcer bed to be prepared if needed - debrided and devitalised tissue removed and adherent epithelium. 2. Bulbar conjunctiva - incision made 1-2mm from limbus 3. Incision extended 90-120 degrees around eye following curvature of limbus 4. Conjunctiva freed with gentle blunt dissection (ideal flap semi-transparent) 5. Conjunctiva then pulled down over ulcer (advancement flap) or by making second incision parallel to first and transecting one end of flap rotating into place (pedicle graft) Pedicle grafting preferred for larger defects (other variations hood flaps, bridge grafts, 360 flaps) 6. Pedicle grafts - trimmed to fit the defect 7. Sutured into place simple interrupted pattern - at least 4x sutures (cardinal sutures) to secure to cornea, base of pedicle secured onto limbus at least x2 sutures (Pg 211 BSAVA book for diagram)

Answer 91

Easier to perform - less technical (may be option if referral not possible) Magnification still required

Answer 92

Deep stromal ulcers (>50% depth) Desmetocoeles Feline corneal sequestra (Infectious keratitis - use should be delayed until infectious process has been resolved)

Answer 93

Transplant of adjacent normal cornea and attached bulbar conjunctiva into corneal wound or keratectomy site. 1. Lateral canthotomy to increase exposure and eyelid speculum. Neuromuscular blockade to keep eye central. 2. Recipeint ulcer/keratectomy site should be prepared by removal of any diseased tissue. Edge of ulcer "squared off" 3. 2x slightly diverging corneal incisions are made with no 64 Beaver blade and extended to limbus 4. Pedicle of anterior stroma (50% depth) and epithelium separated from deeper stroma to the limbus with a corneal lamellar dissector 5. Once limbus traversed with blade the conjunctival (or occasionally scleral if performing corneoscleral transposition) portion of graft is mobilised with small tenotomy scissors Conjunctival portion of graft should be wider than recipient site to allow for graft shrinkage. 6. Edges of graft sutured into place (simple interrupted or continuous pattern) Consider temporary tarsorrhaphy for post op period to provide tamponade to graft bed, prevent blinking and reduce exposure. Corneal portion of graft should clear within first few weeks post op whilst conjunctival portion takes several months to clear. Limbal region opposed to axial cornea will always be apparent. (Pg 211 BSAVA book for diagram)

Answer 94

Central visual axis remains clear and so vision not impaired.

Answer 95

Not routinely performed in veterinary patients. Frozen/preserved corneas - tectonic graft composed of "correct" type of collagen

Answer 96

Usually heal without primary repair May tidy wound with trimming off loose pieces of epithelium under local anaesthetic - may enhance healing.

Answer 97

If any risk perforated as will irritate intraocular structures

Answer 98

Often covered by coagulated aqueous Fresh injuries iris should be repositioned into anterior chamber Iris contaminated/devitalised then can be excised (but care as may bleed profusely) Anterior chamber can be reformed using balanced salt solution/air bubble. As lacerations which involve iris prolapse are often large these corneal defects are often supported with additional conjunctival flap.

Answer 99

Full thickness vs partial thickness Full thickness further divided: With/without iris prolapse With/without lens involvement With/without loss of intraocular contents

Answer 100

Seal wound without incarceration of uveal tissue Anterior chamber re-established

Answer 101

Dogs = more marked uveal inflammation than cats following corneal lacerations and repair Age - less than 1 year = greater chance of glaucoma/phthisis bulbi

Answer 102

Cause of injury - cat claw/wood etc produce more intensive post operative uveitis than metal Iris prolapse >24hrs (exposed iris often has to be excised - more intense post op uveitis + risk of intraocular haemorrhage Axial or central lacerations - more adverse effect on restoration of vision and increased chance of lens involvement Additional ocular involvement - iris prolapse, laceration of anterior lens capsule, loss of lens/vitreous, intraocular haemorrhage, lacerations of sclera - decrease prognosis for restoration of vision Enucleation/evisceration with intrascleral prosthesis = option for eyes with large lacerations, loss of intraocular contents and no realistic prospect for vision

Answer 103

If anterior lens capsule torn then often need to perform concurrent lendectomy to prevent severe intraocular inflammation/ongoing uveitis Cats - discuss risk of post traumatic sarcoma formation - associated with ocular trauma particularly to lens

Answer 104

Superficial - can often be removed with surgical spear or foreign body spud

Answer 105

Should never use forceps to try and grab - easy to inadvertently push FB further into eye

Answer 106

Embedded in stroma (penetrating - one entry wound) - no fibrin Protruding into anterior chamber (perforating - entry and exit wound) - fibrin in anterior chamber or on cornea, pupil often misshapen (dyscoria) Typically splinters, thorns and other plant material.

Answer 107

Siedel test

Answer 108

Anaesthetise Best to have operating microscope/magnification at hand in case becomes perforating Option 1: Undermine around foreign body and grasp from side or dislodge and lift out with foreign body spud Option 2: Use needle to lance object, perpendicular to line of penetration and then gently pull out in opposite direction

Answer 109

Removal more challenging if penetrates anterior chamber Surgical removal either via anterior cornea or posterior cornea from anterior chamber If removal from outside then horizontal mattress suture across corneal defect before removal can make easier to sew up post removal/reduce loss of AH.

Answer 110

Generally good prognosis Infection of site is rare Some scarring expected Longer term problems if damaged lens capsule = phacoclastic uveitis (poor prognosis)

Answer 111

Atropine 1% - pupil dilation, prevent ciliary spasm NSAID - analgesia Topical prophylactic broad spectrum AB cover ?possibly systemic AB cover if concerns infection

Answer 112

Corneal sequestrum removal Dermoid removal Symblepharon (but high rate reoccurence) Chronic superficial keratitis Pigmentary keratitis Chronic/recurrent corneal erosions (SCCEDS) Corneal superficial dystrophies Corneal or limbal neoplasia Superficial foreign bodies Post keratectomy if still superficial - defect left to heal and medically managed as would corneal ulceration Deep keratectomy = may be necessary to repair defect - CCT or conjunctival pedicle graft/flap. (Extends deeper than 1/2 to 2/3rd stromal depth)

Answer 113

Only disease area within epithelial and anterior stromal layers should be excised Normal dog/cat cornea = 0.5-0.6mm, up to 1mm thick in disease No 64 Beaver blade or fixed depth lamellar knife to perform procedure Desired depth estimate with slit lamp prior to surgery and should be sufficient to remove diseased cornea Edge of section grasped with corneal forceps (colibri forceps) Dissection plane within stroma same parallel lamellae depth throughout. Blade held tangential to corneal stroma to prevent progressively deeper dissection. Dissected stroma then removed and any remaining tags of stroma cut with scissors. Contact lens useful post op - relieve discomfort and allow close observation of wound healing process if they fit properly.

Answer 114

Atropine 1% - prevent reflex uveitis, improve comfort Topical AB's - prophylactic (e.g chloramphenicol QID), infected/melting (use cytology + C/S to guide) Systemic antibiosis Analgesia - NSAID systemically +/- opioid Contact lenses for comfort (not if infected/melting) Inflammation - NSAID/steroids (care if ulceration with steroids - contraindicated whilst fluorescein +ve) N.B intraocular involvement - drops rather than ointment.