1
Q
What is the normal corneal hydration %
A
78%
2
Q
What are the corneal dimensions
A
11.5mm vertically
12mm horizontally
3
Q
What is the corneal thickness centrally (normal)
A
540 microns centrally.
Thicker in the periphery
4
Q
What are the different corneal layers and types of cells
A
epithelium- stratified squamous non keratinized epithelium (single layer of columnar basal cells attached by hemidesmosomes to underlying BM, 2-3 strata of wing cells, 2 layers squamous surface cells
Bowman layer- acellular superficial layer of stroma
Stroma - 90% thickness, regularly oriented collagen fibrils spacing maintained by proteoglycan with interspersed modified fibroblasts. Regular arrangement allows for corneal clarity. Stroma scars
DM- fine latticework of collagen fibrils. Anterior banded zone deposited in utero and posterior non banded zone laid down throughout life. Has regenerative potential.
Endothelium- monolayer of polygonal cells. maintains corneal deturgescence by pumping out excess fluid through the stroma
5
Q
What is the density of endothelial corneal cells and at what rate does it reduce
A
3000 cells/ mm squared. Decrease at 0.6% per year
6
Q
What are PEE’s
A
epithelial defects staining with fluorescein and rose Bengal early sign of epithelial compromise.
Superior- vernal disease/chlamydial conjunctivitis, SLK, floppy eyelid
Interpalpebral- dry eye, reduced corneal sensation, UV keratopathy
Inferior- chronic blepharitis, lagophthalmos, eye drop toxicity, self induced, entropion
Diffuse- viral conjunctivitis, drop toxicity
Central- prolonged CL wear
7
Q
What are PEK (punctate epithelial keratitis)
A
granular opalescent swollen epithelial cells with focal intraepithelial infiltrates. Visible unstained but stain well with rose bengal and variable with fluorescein.
Causes are infections: adenoviral, chlamydia, molluscum, early HSK, HZO, thygeson SPK
8
Q
What are subepithelial infiltrates and what causes them
A
tiny subsurface foci of non staining inflammatory infiltrates. causes are severe/ prolonged adenoviral keratoconjunctivitis, herpes zoster keratitis, adult inclusion conjunctivitis, marginal keratitis, rosacea
9
Q
What are superficial punctate keratitis and what causes them
A
non specific term describing any corneal epithelial disturbance of dot like morphology
10
Q
What are the causes of superificial corneal NV
A
feature of chronic ocular surface irritation or hypoxia as in CL wear
11
Q
How to differentiate infective/ sterile infiltrates
A
PEDAL
Pain
Epithelial Defects
Discharge
AC reaction
Location
12
Q
What is corneal melting
A
tissue disintegration in response to enzymatic activity often with mild or no infiltrate eg PUK
13
Q
What is a descemetocoele
A
bubble like herniation of DM into cornea plugging a defect that would otherwise be full thickness
14
Q
At what corneal endothelial cell density is corneal oedema likely to occur
A
> 700 cells/mm squared but unlikely above 1000 cells/mm squared
15
Q
What is corneal topography used for
A
detection and management of corneal ectasia
16
Q
What are some ways to promote epithelial healing
A
reduction of exposure to toxic medications + preservatives
Lubrication, taping lids
antibiotic ointment, BCL, surgical eyelid closure, botox, temporary/permanent lateral tarsorrhaphy, conj (gundersen flap), amniotic membrane patch grafting, tissue adhesive (cyanoacrylate glue) to seal small perforations, corneal cross linking, LSCC, cessation smoking
17
Q
Which bugs can penetrate intact corneal epithelium
A
N gonorrhoea
N meningitidis
Corneybacterium diphtherium
H influenza
18
Q
What type of bacteria is pseudomonas aeruginosa
A
ubiquitous gram negative bacillus (Rod) commensal of GI tract. Aggressive infection causing over 60% CL related keratitis
19
Q
What type of bug is S. Aureus
A
common gram positive and coagulase positive commensal of nares/ skin/ and conjnctiva. Keratitis is focal and fairly well defined white or yellow white infiltrate
20
Q
What are some risk factors for bacterial keratitis
A
cl wear- extended use. corneal epithelial compromise secondary to hypoxia/ minor trauma. Bacterial adherence to lens
Trauma- refractive surgery like LASIK with atypical mycobacteria. Ocular surface disease like herpetic keratitis/ bullous keratopathy, dry eye, chronic blepharitis, trichiasis, entropion, exposure
systemic immunosuppression/ vitamin A deficiency
21
Q
Signs of bacterial keratitis
A
epi defect with infiltrate- significiant circumcorneal injection. stromal oedema, folds in DM, hypopyon, posterior synechiae, KP’s, scleritis can develop in perilimbal infection, endoph rare in absence of perforation. Reduced corneal sensation suggest neurotrophic keratopathy (also in HSK related, long term CL wear)
22
Q
How to investigate bacterial keratitis
A
corneal scraping for:
>2mm ulcers
involve middle- deep stroma, within visual axis, chronic in nature, atypical in appearance
Scraping via disposable scalpel blade 11 or Bard Parker. Margins and base are scraped. Routinely blood, chocolate, sabouraud media used. Brain heart infusion also used.
Conj swabs
CL cases
Gram stain
Culture and sensitivity reports
23
Q
What is blood agar medium used for
A
most bacteria and fungi except neisseria haemophilus and moraxella
24
Q
What is chocolate agar used for
A
fastidious bacteria particularly h influenza, moraxella, neisseria
25
What is sabouraud dextrose agar used for
fungi
26
What is non nutrient e coli used for
Acanthamoeba
27
What is Brain heart infusion used for
difficult to culture organisms like streptococci, meningococci, supports yeast and fungal growth
28
What is cooked meat broth used for
Anaerobic eg P acnes as well as fastidious bacteria
29
What is Lowenstein Jensen used for
Mycobacteria
Nocardia
30
What is Gram stain used for
Bacteria
Fungi
Microsporidia
31
What is Giemsa stain used for
Bacteria
Fungi
Acanthamoeba
Microsporidia
32
What is Calcofluour white used for
Acanthamoeba
Fungi
Microsporidia
33
What is AFB stain like ZN stain used for
Mycobacteria
Nocardia
34
What is Grocott Gomori methenamine silver stain used for
Fungi
Acanthamoeba
Microsporidia
35
What is PAS Stain used for
Fungi
Acanthamoeba
36
Local therapy for bacterial keratitis
antibiotic monotherapy hourly day and night for first 48 hours. Fluoroquinolone. In some areas with resistance, moxiflocacin/ gatifloxacin/ besifloxacin have gram positive activity. Moxifloxacin superior ocular penetration. Antibiotic duotherapy combination of cephalosporin/ aminoglycoside. Subconjunctival abx if poor compliance with topical treatment. Mydriatics, steroids, promote replication of some organisms like fungi/ mycobacteria.
37
What did the SCUT trial (steroids for corneal ulcers trial) find
no eventual benefit in most cases but severe cases (CF/ large ulcers central 4mm cornea) tended to do better. A positive culture result was an inclusion crtierion and steroids introduced after 48 hours moxifloxacin
38
What cover does fluoroquinolone have against streptococcus
limited effectivity
39
When are systemic antibiotics indicated for bacterial keratitis
Potential for systemic involvement- get micro/ ID advise.
N meningitidis- iM ben pen/ cef/oral cipro indicated. H influenza with pO Augmentin. N gonorrheoea third gen cephalosporin
Severe corneal thinning- threatened or actual perforation ciprofloxacin for antibacterial activitiy, tetracycline for anticollagenase effect
Scleral involvement PO/IV treatment
40
How to manage apparent treatment failure of bacterial keratitis (no improvement in 24-48 hours of treatment)
review antibiotic regime. No need to change initial therapy if favourable response even if cultures show resistance. If still no improvement after further 48 hours, suspend treatment for 24 hours then rescrape with inoculation on broader media. Cultures negative, then corneal biopsy for histology and culture. Consider collagen cross linking (PACK- CXL) if corneal melt/ bacterial resistance. Excisional keratopalasty/ PK/ deep lamellar for incipient or actual perforation
41
What is the visual rehab like after bacterial keratitis
Keratoplasty for dense residual corneal scarring
rigid CL for irregular astigmatism introduced 3 months after re-epithelialization
Cataract surgery due to lens opacity from severe inflammation
Prognosis depends on size/ location/ depth/ aetiology of ulcer
42
Which 2 main fungi cause keratitis
Yeasts like Candida- ovoid unicellular organisms reproduce by budding
Filamentous Fungi (Fusarium/ Aspergillus)- multicellular organisms produce tubular projections called hyphae. Keratitis more aggressive
43
What are some predisposing factors to fungal keratitis
chronic ocular surface disease
long term topical steroid use
CL wear
Systemic immunosuppression
Diabetes
Filamentary kertatits- associated with trauma with plant material/ gardening
44
What are the symptoms and signs of candida/ filamentous keratitis
Gradual pain onset
grittiness, photophobia, blurry vision, watery discharge. Candida- yellow white densely suppurative infiltrate
Filamentous keratitis- grey or yellow white stromal infiltrate with indistinct fluffy margins, progressive infiltration with satelite lesions, feathery branch like extensions may develop, rapid progression with necrosis and thinning. Endoph
45
What kind of lab investigations are useful in fungal keratitis
staining with KOH direct microscopic evaluation
Gram + Giemsa stain 50% accurate
Other stains PAS/ Calcoflour white, methenamine silver
Culture- corneal scrapes on Sabouraud agar, scrape from the BASE.
PCR of specimen upto 90% sensitive. Corneal biopsy if no improvement in 3-4 days. 2-3mm block taken. AC tap and
Confocal
46
Where do filamentous fungi proliferate in the cornea
just anterior to DM so a deep stromal specimen corneal biopsy may be required
47
How is fungal keratitis treated
Admit, remove epithelium over lesion. Topical antifungals for 48 hours then reduce.
Candida- amphotericin B 0.15%, econazole 1%, voriconazole 1/2%
Filamentous fungi natamycin 5% or econazole 1%
Natamycin used in mycotic keratitis
Broad spectrum antibiotic prevent coinfection, cycloplegia, subconj fluconazole, systemic antifungals (Vori 400mg PO BD), Tetracyclines for MMP effect, Perforation, Superficial keratectomy, Therapeutic keratoplasty, AC washout
48
What is Microsporidia keratitis
obligate intracellular single celled parasites thought to be protozoa but NOW reclassified as fungi. Rarely cause infection in immunocompetent. In AIDS more common. Enteritis is commonest infection in humans causing keratoconjunctivitis
49
How to make a diagnosis of Microsporidia keratitis
Bilateral chronic diffuse PEK
Unilateral slow progressive deep stromal keratitis may rarely affect immunocompetent patients, Biopsy shows spores and intracellular parasites. PCR of scrapes low sensitivity.
50
How is Microsporidia keratitis treated
Medical therapy of epithelial disease with fumagilin. HAART for AIDS may help. Stromal disease treat with fumagillin + oral albendazole 400mg PO OD for 2 weeks repeated 2 weeks later with a second course. Monitor for hepatic toxicity. Keratoplasty may be indicated but infection can recur in graft periphery.
51
What are the features of HSV virus
Enveloped cuboidal capsule. Linear ds- DNA genome. 2 subtypes HSV1, HSV2
52
What is the rate of ocular recurrence in HSV keratitis
10% after one episode at 1 year
50% at 10 years
53
What are the risk factors for severe disease in HSK keratitis
atopic eye disease
childhood
immunodeficiency
malnutrition
measles
malaria
54
How can Rose Bengal differentiate HSK from atypical recurrent corneal abrasion
Virus laden cells at the margin of ulcer stain with Rose Bengal compared to other conditions
55
What investigations can be used to detect HSV keratitis and what do they show
PCR / Immunocytochemistry available.
Giemsa stain shows multinucleated giant cells
HSV serological titres rise on primary infection but can be used to confirm previous viral exposure in cases of stromal disease when diagnosis is in doubt
56
What are the differentials for HSV keratitis
HZO keratitis, healing corneal abrasion, acanthamoeba keratitis, epithelial rejection in corneal graft, tyrosinaemia type 2, epithelial defects of soft contact lenses, toxic keratopathy secondary to topical medication.
57
What common preservative in contact lens solution and dry eye products can cause dendritiform keratopathy
polyquadernium 1
58
How is HSV keratitis treated
Topical- aciclovir 3% ointment/ ganciclovir 0.15% gel 5x/day for 10 days. Trifulridine alternative but 9x/day use until epithelium closed. Drugs are non toxic even when used for upto 60 days. 99% ulcers heal in 2 weeks
Debridement- resistant cases. epithelium removed 2mm beyond ulcer edge
Signs of treatment toxicity- epithelial whorling, follicular conjunctivitis.
PO aciclovir 400mg 5x/day for 10 days for immunodeficient patients. Interferon monotherapy. Skin lesions treated with aciclovir cream 5x/day for cold sores. Cycloplegia for comfort
59
Which glaucoma drops should be avoided in HSK keratitis
prostaglandin analogues
60
What is the aetiology of disciform keratitis (endothelitis)
unclear
may be result of active HSK of keratocytes or endothelium or a hypersensitivity reaction to viral antigen in the cornea
61
What are the clinical features of disciform keratitis
blurry vision gradual onset. discomfort redness milder. central zone of stromal oedema with overlying epithelial oedema. Large KP's, DM folds, Wesely immune ring of deep stromal haze deposition of viral antigen and host complexes, IOP may be elevated, reduced corneal sensation, healed lesions faint stromal/ subepithelial opacifiation. Recurrence causes worsening subepithelial/ stromal scarring.
62
How to manage disciform keratitis
topical steroid with antiviral cover QDS. Once improved, reduce frequency of drops over not less than 4 weeks. IOP control essential + cycloplegia. If ED present, keep steroid use low as possible for effect with more frequent antiviral cover
PO steroids sometimes used. Topical ciclosporin 0.05% useful if epithelial ulceration and tapering of steroids needed. DND reported successful to address CoNV
63
What causes necrotizing stromal keratitis
active viral replication within the stroma though immune mediated inflammation likely plays a significant role
64
What is neurotrophic keratopathy and what are signs and treatment
failure of re- epithelialization from corneal anaesthesia, exacerbated by factors like drug toxicity
Signs- non healing ED, stroma gray and opaque, secondary bacterial + fungal infection may occur.
Treat same as that for persistent ED. Topical steroid to control inflammatory component kept to minimum
65
What is herpetic iridocyclitis
can occur without corneal inflammation. IOP elevation common due to trabeculitis. Steroid induced IOP rise common. Patchy iris atrophy may provide a clue and transillumination may demonstrate subtle lesions. Aqueous sampling for PCR is diagnostic. Treat with topical steroids, adjunctive oral acyclovir may be given
66
What are some prophylactic considerations for recurrent HSK
Long term oral aciclovir reduces recurrence rate of epithelial + stromal keratitis by 50%. Good for patients with frequent debilitating recurrences if bilateral/ only eye. PO Aciclovir 400mg BD for 12 months. Can lead to aciclovir resistant cases HSV1. Check periodic renal function
Oral valaciclovir 500mg PO OD. Less frequent dosing better tolerated
Topical not great due to epithelial toxicity. Vaccines under ix
67
What are some complications of HSK keratitits
secondary infection with bacteria
glaucoma secondary to inflammation/ chronic steroid use. Corneal thinning. Stromal vascularization/ lipid keratopathy. Topical aganirsen helps to reduce CoNV. Cataracts and iris atrophy
68
What are the mechanisms for ocular involvement in HZO
Direct viral invasion lead to conjunctivitis + epithelial keratitis
Secondary inflammation + occlusive vasculitis, scleritis, episcleritis, keratitis, uveitis optic neuritis, CN palsy. Reactivation causes necrosis and inflammation in affected sensory ganglia causing corneal anaesthesia
69
What are the predictive factors for ocular involvement in HZO
Hutchinson sign- vesicles on skin supplied by external nasal nerve branch of nasociliary nerve. May NOT be predictive. Rash in distribution of lower part of forehead (Supratrochlear nerve) more predictive. Age- HZO occurs in 6-7th decade. Older have more severe signs
AIDS have severe disease early indicator of HIV.
70
What is Zoster sine herpete
shingles without a rash may be more common than previously thought
71
What are the treatment options for HZO V1
PO Antiviral within 72 hours of rash onset reduces severity and duration of acute episode and post herpetic neuralgia. Reduce ophthalmic complication risk by 50%. Aciclovir 800mg 5x/day for 7-10 days. DONT USE WITH 5-FU
IV aciclovir 5-10mg/kg TDS for severe disease. Systemic steroids controversial but useful for neurological complications. AVOID in immunocompromised patients
72
How can HZO be prevented
Vaccines approved for 50 years and above
1) Zoster vaccine live attenuated live virus with limitation in efficacy lost within 10 years
2) Recombinant zoster vaccine needs 2 injections + 10% incidence of local/ acute systemic reaction
73
How to treat the ophthalmic manifestations of acute HZO
Acute epithelial keratitis develops within 2 days of rash- topical antiviral
conjunctivitis- treatment not required if cornea ok but can use topical abx/ antiviral cover.
Episcleritis- spontaneuous resolution +/- NSAID
Scleritis uncommon but can develop end of the first week. Treat with flurbiprofen 100mg TDS. PO steroid + antiviral cover for severe involvement
Nummular keratitis - mild topical steroid
stromal keratitis topical steroid slow taper
Disciform keratitis (immune mediated endothelitis)- topical steroid
AAU- steroid, Posterior uveitis- retinal necrosis - ARN can be caused by VZV. Monitor IOP and also cranial nerve palsy
74
Which cranial nerve is usually affected in HZO
3rd most common, 4th and 6th nerve recovers within 6 months.
Optic neuritis rare
CNS manifestations rare- encephalitis, cranial arteritis, GBS
75
What are the signs of chronic eye disease in HZO ocular involving
Neurotrophic keratopathy- 50% mild and settles. Scleritis patchy scleral atrophy, staphyloma formation rare. Mucous plaque keratitis topical steroid + NAC. Lipid degeneration- severe nummular / disciform keratitis. Lipid filled granulomas, subconjunctival scarring, eyelid scarring causing ptosis/ cicatricial entropion
76
How to manage post herpetic neuralgia
Develops in upto 75% patients over 70 years.
Local: cold compress, topical capsaicin 0.075%, lidocaine 5% patches
Systemic: simple analgesia, stronger analgesia codieine, TCA amitryptilline, Carbamazepine, Gabapentin
77
What is interstitial keratitis and what causes it
inflammation of corneal stroma without primary epi/endothelium. Inflammation thought due to immune mediated process triggered by antigen. Causes are syphilis, HSV, VZV, TB, Lyme, Cogan syndrome
78
What are some features of congenital syphilis
early- failure to thrive, maculopapular rash, mucosal ulcers, rhagades. Late- sensorineural deafness, saddle shaped nose deformity, sabre tibiae, bulldog jaw, Hutchinson teeth, clutton joints
Ocular- AAU, Interstitial keratitis, dislocated lens, cataract, optic atrophy, salt pepper pigmentary retinopathy, Arygll Robertson pupil
79
What are the signs and symptoms of syphilitic IK
Presentation follows IK, aged 5-25. Initial symptoms AAU, bilateral in 80%, profound drop in VA, Limbitis with deep stromal vascularization, salmon patch appearance, granulomatous AAU, Cornea clears and vessels non perfused ghost vessels, if cornea gets inflamed later vessels refill and bleed into stroma, healed stage- ghost vessels, feathery deep stromal scar, thinning, astigmatism, BK
80
How is syphilitic IK treated
Topical steroids +cycloplegics + systemic therapy under GUM specialist
81
What is Cogan syndrome
rare systemic autoimmune vasculitis characterized by intraocular inflammation + vestibuloauditory dysfunction developing within months of each other. Occurs in young adults with both sexes affected equally.
82
How is Cogan syndrome diagnosed
Ocular + inner ear symptoms separated by months- years.
1) Vestibuloauditory symptoms -deafness, tinnitus, vertigo
2) Ocular symptoms- redness/ pain/ photophobia/ blurry vision
3) Ocular signs- corneal involvement faint bilateral peripheral anterior stromal opacities
83
How to investigate Cogan syndrome
ESR/ CRP/ WCC all elevated.
Antibodies to inner ear antigens may be detectable
MRI shows inner ear/ other abnormalities
84
How is Cogan syndrome treated
Topical steroids for keratitis
Systemic steroids if vestibuloauditory symptoms 1-2mg/kg prednisolone to prevent hearing loss. Systemic steroids for scleritis/ retinal vasculitis
85
What kind of organism is Acanthamoeba
ubiquitous free-living protozoa commonly
found in soil, fresh or brackish water and the upper respiratory
tract. The cystic form is highly resilient.
86
What are symptoms and signs of acanthamoeba keratitis
blurry vision, pain often severe and disproportionate to findings. Early disease- epithelial surface irregular and greyish, pseudodendrites, limbitis with focal or diffuse anterior stromal infiltrates, characteristic perineural infiltrates pathognomonic
Ring infiltrate, scleritis can form, progressive stromal opacification and vascularization. Corneal melt when stromal disease. Melt develops at peripheral of infiltrate
87
What investigations can one do for Acanthamoeba keratitis
staining of corneal scrapes with PAS/ calcofluor white (fluorescent dye with affinity for amoebic cysts and fungi). Gram and Giemsa stain also demonstrate cysts. Culture, Non nutrient agar with Ecoli which trophozoites consume. Immunohistochemistry, PCR, in vivo confocal microscopy. Corneal biopsy may be necessary for diagnosis
88
How is Acanthamoeba keratitis treated
Early- maintain high index of suspiscion treat early if limited response to antibacterial therapy.
Debridement of epithelium helpful and facilitiate eye drop penetration
Topical amoebicides: Acanthamoeba cysts resistant to most agents. Some only active against trophozoite stage:
PHMB 0.02% and Chlorhexidine 0.02% kill trophozoites and cysticidal
Hexamidine/ Propamidine (Brolene). Former more activity. Voriconazole less toxic to ocular surface and first line effective. A clear response takes 2 weeks.
Avoid topical steroid
Pain control- NSAID
Corneal cross linking PACK - CXL for severe cases. Therapeutic keratoplasty for resistant cases. Late scarring PKP.
89
What is marginal keratitis
caused by a hypersensitivity
reaction against staphylococcal exotoxins and cell wall proteins with deposition of antigen–antibody complexes in the peripheral cornea with a secondary lymphocytic infiltration.
90
What are the symptoms and signs of marginal keratitis
mild discomfort, redness, lacrimation. Chronic blepharitis typical. Inferior PEE's early manifestation. Subepithelial marginal infiltrates separated from limbus by clear zone. Epi defect smaller than infiltrate. Little to no AC reaction even with smaller infiltrates.
91
How is marginal keratitis treated
Weak topical steroid FML/ Pred 0.5% instilled QDS for 1-2 weeks sometimes combined with topical antibiotic. PO tetracycline course avoid in children and breastfeeding mothers in pregnancy
92
What is phlyctenulosis
self limiting disease but can rarely be severe. high income countries more likeely due to presumed delayed hypersensitivity reaction to staphylococcal antigen sometimes rosacea associated. Low income country associated with TB/ helminthic infestation.
93
Signs/ symptoms of phlyctenulosis
photophobia
lacrimation
blepharospasm
small white limbal/ conj nodule with intense hyperaemia. Limbal phlycten may extend onto cornea. Spontaneous resolution within 2-3 weeks. Healed lesion leaves triangular limbal based scar + superificial CoNV
TB ix only in endemic areas
94
How is phlyctenulosis treated
topical steroid- short course accelarates healing given with topical antibiotic
95
What are the signs of Rosacea ocular
non specific irritation and lacrimation. lid signs margin telangiectasia, posterior blepharitis with recurrent meibomian cyst formation
conj hyperaemia, bulbar. Rarely cicatricial conjunctivitis, conj granulomas, phlyctenulosis.Corneal inferior PEE's, peripheral vascularisation in inflamed eye, marginal keratitis, focal/ diffuse corneal thinning in severe cases inferior cornea
96
How is ocular Rosacea treated
lubricants, hot compress, lid hygiene, topical fusidic acid, erythromycin, azithromycin to lid margins at bedtime for 4 weeks. Steroids for exacerbations.
Systemic therapy: tetracyclines for altering MG function lower fatty acid production and reduce lid flora. Have MMP inhibition so prevent thinning.
Retinoids helpful but contraindicated in pregnancy
97
What are some causes of peripheral corneal thinning
PUK with systemic autoimmune disease
Marginal keratitis
Mooren ulcer
Terrien Marginal Degeneration
Dellen
Ocular Rosacea
Furrow degeneration
Pellucid Marginal degeneration
98
What is a Mooren ulcer
rare autoimmune disease progressive circumferential peripheral stromal ulceration with late central spread. Host reaction to calgranulin C. A normal hidden antigen in corneal keratocytes
99
What are the two forms of Mooren ulcer
1) Affects older patients one eye, respond well to medical therapy
2) More aggressive need systemic immunosuppression. Carries poor prognosis may be bilateral with severe pain in younger patients including widespread reports in south Asian men.
100
What are the signs/ symptoms of Mooren ulcer
pain prominent may be severe. Peripheral ulceration involving superficial one third of stroma with variable epithelial loss. Several foci may be present and coalesce. Undermined and infiltrated leading edge CHARACTERISTIC. Limbitis may be present but not scleritis which distinguishes from systemic disease associated PUK. Progressive circumferential and central stromal thinning. Vascularization involving bed of ulcer upto leading edge but not beyond. Healing has thinning/ vascularization and scarring
101
What are the complications of Mooren ulcer
severe astigmatism
perforation
secondary bacterial infection
cataract
glaucoma
102
How is Mooren ulcer treated
Topical steroid hourly, combined with topical antibiotic. Topical ciclosporin upto 2% but may take weeks to exert effect. Tacrolimus 0.1% effective at refractive cases. Adjunctive artificial tears, collagenase inhibitors like NAC 10-20%, Conjunctival resection: excise necrotic tissue. should extend 4mm back from limbus and 2mm beyond circumferential margins. Systemic immunosuppression needed like rituximab, Systemic collagenase like doxycycline, lamella keratectomy dissect central island remove stimulus for further inflammation, perforations managed, keratoplasty once inflammation settled
103
What is PUK associated with systemic autoimmune disease
Severe peripheral corneal infiltration, ulceration, or thinning unexplained by ocular disease should prompt investigation for systemic collagen vascular disorder. Mechanism is immune complex deposition in peripheral cornea/ episcleral and conjunctival capillary occlusion with secondary cytokine release and inflammatory cell recruitment, upregulation of collagenases and reduced inhibitor activity. Associated with RA, GPA, Polyartertis nodosa, SLE, Crohns
104
What are the clinical features of PUK associated with systemic autoimmune disease
crescenteric ulceration with epi defect, thinning and stromal infiltration at the limbus. Spread circumferential and occasionally central. In contrast to Mooren ulcer extension to sclera may occur. Limbitis/episcleritis/ scleritis present. Advanced disease may result in contact lens cornea. Rheumatoid paracentral ulcerative keratitis (PCUK) with punched out more centrally located lesion with little infiltrate in quiet eye
105
How to treat PUK associated with systemic autoimmune disease
systemic steroids, immunosuppressive therapy, biological blockers for long term management. topical preservative free lubricants, topical antibiotics, oral tetracycline, topical steroids worsen thinning so avoided, conj excision if medical treatment ineffective
106
What is Terrien Marginal Degeneration
uncommon idiopathic thinning of peripheral cornea in young adult to elderly patients. some cases associated with episcleritis/ scleritis. 75% affected patients male/ bilateral/ but asymmetrical
107
What are some signs and symptoms of Terrien Marginal Degeneration
asymptomatic with gradual visual deterioration due to astigmatism. Occasional episodic pain and inflammation. Fine yellow white refractive stromal opacities with mild superficial vascularization superiorly spread circumferentially separated from limbus by clear zone. Slow peripheral thinning results in peripheral gutter outer slope shelves gradually central part rises sharply. Band of lipid present at central edge. Perforation rare.
108
How to treat Terrien Marginal Degeneration
Safety spectacles if thinning significant
Contact lenses for astigmatism- scleral or soft lenses with rigid gas permeable piggybacking
Surgery- crescenteric/ annular excision of gutter with lamellar or full thickness transplant- reasonable results arrests progression
109
What is Neurotrophic keratopathy
Loss of trigeminal innervation to the cornea resulting in partial/ complete anaesthesia. Results in intracellular oedema, exfoliation, loss of goblet cells, epithelial breakdown with persistent ulceration.
110
What are the stages of neurotrophic keratopathy
reduced corneal sensation
stage 1: interpalpebral epithelial irregularity and staining, oedema and tiny focal defects. stage 2: larger persistent epithelial defects with rolled and thickened edges assuming punched out config with underlying stromal oedema. stage 3: stromal melting with minimal discomfort, perforation can occur with 2 infection
111
What is the treatment of neurotrophic keratopathy
discontinuation of potentially toxic medication. Non preserved lubricants . Anticollagenase agents like NAC/ tetracycline ointment or systemic tabs. Cenegermin 0.002% topical recombinant human nerve growth factor. instilled 6x/day for 2 months. increases corneal nerve density.
Protection of ocular surface by taping of lids, botox, tarsorrhaphy, amniotic membrane patch. Perforation dealt with, Corneal neurotization from supratrochlear nerve with sural nerve graft
112
What is exposure keratopathy and what are some causes
result of incomplete lid closure lagophthalmos with drying of cornea despite normal tear production. Neuroparalytic like facial nerve palsy, reduced muscle tone in parkinsonism, mechanical like lid scarring, eczematous skin tightening, post blepharoplasty and proptosis.
113
What are the signs and symptoms of exposure keratopathy
symptoms same as dry eye. Signs: mild punctate epithelial changes inferior 1/3rd cornea with nocturnal lagophthalmos. Epithelial breakdown. Stromal melt leading to perforation. Inferior fibrovascular change with Salzmann degeneration overtime. Secondary infection
114
How to treat exposure keratopathy
Reversible:
Artificial tears during day, ointment at night, taping lid closed at night, BCL management of proptosis by orbital decompression if necessary, temporary tarsorrhaphy
Permanent:
Permanent tarsorrhaphy, gold weight upper lid insertion for facial nerve palsy, permanent central tarsorrhaphy, amniotic membrane graft/ conj flap
115
What is Thygeson SPK
uncommon idiopathic bilateral condition characterized by exacerbations and remissions. Commin in young adulthood
116
Symptoms and signs of Thygeson SPK
recurrent attacks irritation, photophobia, blurry vision, watering. Signs: granular coarse elevated greyish epithelial lesions staining with fluorescein, involve central cornea. Mild subepithelial haze may be present, little or no conj hyperaemia, anterior stromal scarring can occur. Ddx is post adenoviral keratitis
117
What is the treatment for Thygeson SPK
Lubricants in mild cases
Low dose steroid drops BD with gradual tapering to once weekly instillation.
Ciclosporin 0.05% if steroid response inadequate or alternative in longer term therapy. Contact lenses if steroids ineffective/ contraindicated.
PTK short term relief but recurrence likely
118
What is filamentary keratopathy
Common condition causing considerable discomfort. Loose area of epithelium acts as focus of mucus deposition and cellular debris
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What are some causes of filamentary keratopathy
aqueous deficiency (KCS)
Excessive CL wear
Corneal epithelial instability (RCES/ Corneal graft/ cataract surgery/ refractive surgery/ drug toxicity)
SLK
Bullous keratopathy
Neurotrophic keratopathy
Prolonged/ frequent eye closure
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What is the treatment for filamentary keratitis
treat underlying cause
change medication topical to unpreserved
mechanical filament removal give short term relief
mucolytics 5%/ 10% NAC
NSAID like diclofenac
Hypertonic saline 5% drops
BCL protect cornea from shearing lid action
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What is RCES and some causes?
Abnormally weak attachment between basal cells of corneal epithelium and BM. Minor trauma like eyelid/ cornea interaction during sleep can precipitate detachment. Erosions may be due to previous trauma/ previous corneal surgery/ with corneal dystrophies
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What are some symptoms and signs of RCES
Pain photophobia, redness in the morning. Usually prior history of corneal abrasion.
Signs: epithelial defect may not be present as they may heal but extent of loose epithelium may be seen and rapid TBUT, infiltrate not present though greyish sloughed rolled epithelium may be seen, Epithelial basement membrane disturbance like microcysts/ punctate/ linear fingerprint opacities present.
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What is the treatment for RCES
Acute: Antibiotic ointment QDS, Pressure patching not helpful/ impairs healing. BCL may improve comfort but not improve healing. Antibiotic drops over ointment should be used. Debridgement of heaped/ scrolled areas of epi with sterile cellulose sponge may improve comfort allow healing from edges of defect. Topical diclofenac 0.1% improves pain. Hypertonic saline 5% QDS improves epithelial adhesion,.
Recurrent: topical lubricant gel, PO doxycyline, topical steroid may be helpful. both inhibit MMP, long term BCL wear, simple epithelial debridement followed by bowman layer smoothing with diamond burr/excimer laser. Anterior stromal puncture for localised areas off visual axis.
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What is Xerophthalmia
Spectrum of oculardisease caused by inadequate vitamin A intake.
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What are the symptoms and signs of Xerophthalmia
Nyctalopia
Discomfort
Vision loss
Xerosis dryness of conjunctiva in interpalpebral zone with goblet cell loss, squamous metaplasia and keratinization. Bitot spots are triangular patches of foamy keratinized epithelium caused by corynebacterium xerosis.
Lustreless corneal appearance due to secondary xerosis, bilateral PEE in interpalpebral zones, Keratinization, sterile corneal melting causing perforation.
Retinopathy: yellowish peripheral dots in advanced cases cause decreased ERG amplitude
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How is Xerophthalmia treated
Keratomalacia indicator of very severe vitamin A deficiency. Treated as medical emergency due to risk of death particularly in infants
Systemic oral (oil based 200000 IU) or IM (aqueous based 100000 IU) Vitamin A for keratomalacia.
Local treatment: intense lubrication, topical retinoic acid, manage perforation
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What is the WHO grading of Xerophthalmia
XN: Night blindness
X1: Conj xerosis X1A with Bitot spots X1B
X2: Conj Xerosis
X3: Corneal ulceration, <1/3rd (X3A), >1/3rd (X3B)
XS: Corneal scar
XF: Xerophthalmic fundus
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What is keratoconus and when does i present
Progressive disorder of central/ paracentral corneal stromal thinning with apical protrusion and irregular astigmatism.
Presents in teens/ twenties in one eye. 50% fellow eye will progress to KC in 16 years.
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What is mild/moderate and severe KC
Mild <48D
Moderate 48-54D
Severe >54D
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What are some risk factors for KC
allergy
asthma
eczema
persistent eye rubbing
Down syndrome
Ehlers Danlos
Marfan
Osteogenesis Imperfecta
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What are the signs and symptoms of KC
Unilateral visual impairment due to progressive myopia and astigmatism. Can present with hydrops
Oil droplet reflex
Retinoscopy scissoring reflex. Fine vertical deep stromal stress lines Vogt striae which disappear with globe pressure. Epithelial iron deposits with cobalt blue filter may surround base of cone (Fleischer ring)
Progressive corneal protrusion with thinning max at the apex
bulging of lower lid in downgaze (munson)
Acute hydrops: rupture of DM sudden influx of aqueous into cornea. Break heals in 6-10 weeks oedema clears with stromal scarring. Steep Keratometry readings, Corneal topography shows bow tie appearance.
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How is KC treated
Eye rubbing avoided
Spectacles/ soft CL sufficient in early cases. If marked thinning, consider safety spectacles over contact lenses. Rigid contact lenses scleral for high astigmatism degrees
Collagen cross linking using riboflavin drops to photosensitize the eye followed by UV-A exposure to stabilise cornea if progression. CXL successful in >90% cases and even reverse ectasia. Intracorneal ring segment implantation using laser/ mechanical channel. Keratoplasty PK or anterior deep lamellar DALK in severe disease. History of hydrops contraindication to DALK. LASIK contraindicated
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What is Pellucid Marginal Degeneration
rare progressive peripheral corneal thinning disorder involving inferior cornea. Usually adulthood presentation
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What are the symptoms and signs of pellucid marginal degeneration
slow progressive blurring due to astigmatism
bilateral slow progressive crescentic 1-2mm band of inferior corneal thinning extending from 4-8 o clock 1mm from the limbus. Epithelium intact and cornea above the thinned area shows ectasia and appears flattened. Compared to KC, Fleischer rings and Vogt striae dont occur, hydrops rare.
Corneal topography shows butterfly pattern with severe astigmatism and diffuse steepening of inferior cornea
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How is pellucid marginal degeneration treated
early cases managed with spectacles and Contact lenses. Surgical options not ideal. Large eccentric PK, thermocauterization, crescenteric lamella keratoplasty, wedge resection of diseased tissue, epikeratoplasty and intracorneal ring segment implant. Results of collagen CXL are encouraging
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What is Keratoglobus
Rare condition seen at birth when differential diagnosis is congenital glaucoma and megalocornea. In contrast to KC, cornea develops globular rather than conical ectasia associated with generalised thinning. Acute hydrops rare but cornea prone to rupture on mild trauma. Corneal topography shows generalised steepening. CL wear unsatisfactory. Protect eye from trauma
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What are some epithelial corneal dystrophies
Cogan (epithelial BM dystrophy)
Meesman Epithelial Dystrophy
Gelatinuous drop like corneal dystrophy
Lisch epithelial corneal dystrophy
Subepithelial mucinous corneal dystrophy
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What are some Bowman layer/ anterior stromal dystrophies
Reis Bucklers corneal dystrophy
Thiel Behnke corneal dystrophy
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What are some Stromal corneal dystrophies
Lattice corneal dystrophy TGFB1 type
Lattice corneal dystrophy, gelsolin type
Granular corneal dystrophy, type 1 (Classic)
Granular corneal dystrophy (type 2)
Macula corneal dystrophy
Schnyder corneal dystrophy
Francois central cloudy dystrophy
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What are some DM and endothelial dystrophies
Fuchs
Posterior polymorphous corneal dystrophy
Congenital hereditary endothelial dystrophy
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Features of cogan dystrophy
considered degenerative rather than inherited. Sporadic. Histology shows thickening of BM with deposition of fibrillary protein between BM and bowman layer. Basal epithelial cell hemidesmosomes are deficient. Occurs in 2nd decade, 10% RCES. Lesions seen by retroillumination. Dot like microcystic epithelial lesions, subepithelial map like patters surrounded by faint haze, whorled fingerprint like lines, bleb like subepithelial pebbled glass pattern. Treat similar to RCES
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Features of Meesmann epithelial dystrophy
Rare non progressive abnormality of corneal epithelial metabolism. Inheritance AD. Histology shows irregular thickening of epithelial BM and intraepithelial cysts. Asymptomatic/ mild RCES/ blur. Signs: myriad tiny intraepithelial cysts of uniform size but variable density maximal centrally and extend toward but not reach limbus. Cornea thinned and sensation reduced. Treat with lubricants
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What are the features of Reis Bucklers corneal dystrophy
may be categorized as anterior variant of granular corneal stromal dystrophy GCD type 3 also known as corneal basement dystrophy I (CBD1). Inheritance AD, affected gene TGFB1. Histology: replacement of Bowman layer by connective tissue bands. Symptoms: severe RCES in childhood. Grey white geographic subepithelial opacities most dense centrally increasing in density with age to form a reticular pattern. Treatment directed towards RCES. Excimer keratectomy is good
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Features of Thiel Benhke corneal dystrophy
Honeycombed shaped corneal dystrophy + corneal basement dystrophy type 2 (CBD 2). Less severe features than Reis Buckler. Inheritance AD, gene TFB1, histology shows bowman layer curly fibres on EM, RCES in childhood, subepithelial opacities less individually defined than granular dystrophy type lesions seen in Reis Buckler. Develop in a network of tiny rings or honeycomb like morphology involving central cornea. Treatment not necessary
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Features of Lattice corneal dystrophy TGFB1 type
Classic form of lattice dystrophy.
Inheritance AD gene TGFB1
Histology: amyloid stain with congo red and green birefringence with polarizing filter. Symptoms recurrent erosions at end of first decade in classic form. Signs: refractile anterior stromal dots, coalescing into fine filamentous lattice spreads gradually spares periphery. Corneal sensation reduced. Stromal haze may progress. Treatment by PK/ DALK. Can recur
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Features of Lattice corneal dystrophy gelsolin type
Also known as LCD 2, Meretoja syndroma. Systemic condition rather than a true corneal dystrophy. Inheritance aD, gene GSN. Histology shows amyloid deposition in corneal stroma. Ocular irritation and late impairment of vision, erosions rare. Sparse stromal lattice lines spread centrally from periphery, corneal sensation impaired. Systemic features like progressive cranial and peripheral neuropathy, mask like facies, autonomic features. Homozygous disease rare but severe. Keratoplasty may be needed
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Features of Granular corneal dystrophy type 1 classifc
Inheritance AD Gene TFB1. Homozygous disease more severe featurs. Amorphous hyaline deposits staining bright red with Masson trichrome. Glare and photophobia. With blurring as progression occurs. RCES uncommon. Discrete white central anterior stromal deposits resembling sugar granules/ breadcrumbs or glass splinters separated by clear stroma. Gradual increase in number and size of deposits with deeper and outward spread sparing limbus. Gradual confluence and diffuse haze leads to visual impairment. Corneal sensation impaired. Treat by PK/ DALK. Superficial recurrences need excimer laser keratectomy
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Features of granular corneal dystrophy (type 2)
Also known as Avelino and combined granular lattice dystrophy.
Inheritance AD, Gene TFB1. Histology shows both hyaline and amyloid. Symptoms recurrent erosions mild, visual impairment late features. Signs present by end of first decade. Fine superficial opacities progress to form stellate or annular lesions associated with deeper linear opacities. Treatment not required. Corneal trauma accelarates progression. Refractive surgery contraindicated
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Features of Macula corneal dystrophy
Ineritance AR CHST6 gene, common in ICELAND.
Histology: aggregations of GAG intra and extracellularly stain with Alcian Blue and colloidal iron. Early visual deterioration (end of 1st decade), RCES common. Signs: dense but poorly delineated greyish white spots centrally in anterior stroma and peripherally in posterior stroma. No clear delineation between opacities which may be elevated. Eventual involvement of full thickness stroma extending to limbus no clear zone. Thinning occurs early, reduced sensation. Treat with PK, recurrence common
150
Features of Schnyder corneal dystrophy
disorder of corneal lipid metabolism associated with dyslipidaemia in some patients. Use of crystalline not in name as crystals NOT a feature. Inheritance AD, Gene UBIAD1, Histology, phospholipid and cholesterol deposits, symptoms visual impairment and glare. Signs central haze is an early feature, progressing to more widespread full thickness involvement over time. Subepithelial crystalline opacities in 50%, prominent corneal arcus typical and progresses centrally leading to haze. Treat by excimer keratectomy or PKP
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Features of Francois central corneal cloudy dystrophy
Not certain if this is a dystrophy. Clinically look like crocodile shagreen degeneration. Inheritance AD, No symptoms, cloudy greyish polygonal or rounded posterior stromal opacities most prominent centrally, No treatment required
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Features of Fuch's endothelial dystrophy
most inherited sporadically. commonly in women, bilateral. Mutation in COL8A2 gene and TCF4 gene in others. Worsening blur in morning due to corneal oedema. onset in middle age or later. Signs corneal guttata irregular warts or excresences on DM secreted by abnormal endothelial cells.Epithelial oedema in late cases with microcysts and bullae and discomfort. Rupture of bullae cause pain due to exposed nerve fibres. Subepithelial scar and peripheral vascularization in longstanding cases.
Treat by 5% Nacl,hair dryer for corneal dehydration, cycloplegia, antibiotic and BCL for ruptured bullae. Posterior lamella keratoplasty DMEK/DSAEK/ PK. Rho kinase inhibitors with prior transcorneal endothelial cryotherapy stimulates endothelial cell proliferation improve function
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At what preop corneal thickness is corneal oedema likely to occur in post op phaco
630-640 microns
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What are the features of PPCD
3 forms. PPCD1-3. Associations with iris abnormalities, glaucoma, Alport syndrome. Pathology is metaplasia of endothelial cells. Inheritance AD, Gene VSX-1 in PPCD-1/2. PPCD2 caused by mutations in COL8A2 and PPCD 3 by ZEB1 mutation. No symptoms with incidental diagnosis. Subtle vesicular band like or diffuse endothelial lesions.
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What are the features of CHED
Rare dystrophy focal or diffuse thickening of DM and endothelial degeneration. CHED2 more common more severe form than CHED1. Associated with late onset deafness (Harboyan syndrome)
CHED1- AD gene locus on chromosome 20, CHED1 may be similar to PPCD.
CHED2 is AR, gene SLC4A11
Photophobia watering common in CHED 1 not CHED 2. Signs are corneal clouding and thickening, neonatal in CHED2 and develop in 1-2 years in CHED1. Visual impairment varible and VA may be better than corneal appearance. Nystagmus more common in CHED2. Treat with lamella/ PKP
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What is Vogt limbal girdle and what is the difference between type 1 and 2
innocuous condition present in 60% individuals over 40 years. mainly women. white crescenteric limbal bands composed of chalk like flecks centred at 9 and or 3 o clock more nasally. May be irregular extensions. T1- variant of band keratopathy featuring swiss cheese hole pattern . Type 2: more prevalent and distinguished by absence of holes and juxtalimbal clear zone. Histological changes similar to pingecula and pterygium
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What is crododile shagreen degeneration
asymptomatic greyish white polygonal stromal opacities separated by clear spaces. involve anterior 2/3rd stroma but can be found more posterior. Can be indistinguishable from Francois central cloudy dystrophy
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What is lipid keratopathy
Primary is rare- spontaneously occurs. Yellow or white crystalline stromal deposits cholesterol, fat, phospholipid. not associated with vascularization. Secondary lipid keratopathy more common associated with previous ocular injury/ disease with corneal vascularization. Commonest cause herpes simplex/ herpes zoster keratitis. Treatment aimed at medical control of underlying inflammatory disease. Other options are photocoagulation or needle cautery of feeder vessels. PKP in advanced but quiescent disease.
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Features of band keratopathy
age related calcium deposition in Bowman, epithelial BM and anterior stroma. Causes are ocular. chronic AU (children JIA), glaucoma, phthisis, silicone oil in AC, chronic corneal oedema and chronic keratitis. Age related. Metabolic due to hypercalcaemia, hyperparathyroidisim, viramin D toxicity, milk- alkali syndrome, sarcoid, end stage renal disease, Paget disease, multiple myeloma. Signs: peripheral interpalpebral calcification with clear cornea separating band from limbus. Treat with chelation mild cases.
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How is chelation for band keratopathy done
treatment indicated if vision threatened, eye uncomfortable. Corneal epithelium and solid calcium layer scaped off with forces and scalpel blade No. 15. Cornea then rubbed with cotton tipped applicator in EDTA until all calcium removed. 15-20 mins given for chelation to occur. Re-epithelialization takes many days. Other ways excimer laser, diamond burr, lamella keratoplasty
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Features of spheroidal corneal degeneration
labrador keratopathy. Occurs in men whose working lives spent outdoors. UV exposure a factor. Histology: proteinaceous deposits in the anterior stroma replace bowman layer. Protect against uv damage with sunglasses, superficial keratectomy, lamella keratoplasty
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Features of Salzmann nodular degeneration
nodules of hyaline tissue located anterior to Bowman layer. Occur in any form of chronic corneal irritation or inflammation like trachoma/ dry eye/ chronic blepharitis/ chronic allergic keratoconjunctivitis. Treat with lubrication with control cause, removal via manual superficial keratectomy - lesion can be peeled away and surface flattened with diamond burr. Adjunct MMC reduce recurrence rate.
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What are some examples of Metabolic Keratopathy
cystinosis
mucopolysaccharidoses
wilson disease
Lecithin cholesterol acyltransferase deficiency (LCAT)
Immunoprotein deposition
Tyrosinaemia type 2
Fabry disease
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Features of cystinosis
rare AR gene CTNS lysosomal storage disorder-deposition of cystine crystals leading to paediatric renal failure. Non nephropathic and intermediate forms can occur.Keratopathy in first year with progressive crystal deposition in cornea. Systemic tx with cysteamine given in drop form to reverse corneal crystal formation
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Features of Mucopolysaccharidoses
MPS lysosomal storage disorder enzyme dysfunction for breakdown of GAG's. Inheritance AR. Facial coarseness, skeletal anomalies, heart disease, learning difficulties, keratopathy is Punctate corneal opacification, diffuse stromal haze. Other ocular features are pigmentary retinopathy and optic atrophy
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Features of Wilson disease
Hepatolenticular degeneration rare condition with widespread deposition of copper in tissues. Deficiency of caeruloplasmin, major copper carrying blood protein. Presents with liver disease, basal ganglia dysfunction/ psych disturbances. Kayser Fleischer ring present in 95% cases- brownish yellow zone of fine copper dust in DM peripherally. Treat with penicillamine. Anterior capsular sunflower cataract is seen
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Features of LCAT deficiency
disorder of lipoprotein metabolism with complete an partial forms both AR (Gene LCAT). Keratopathy has numerous minute greyish dots throughout the stroma in periphery like arcus configuration
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Features of tyrosinaemia type 2
very rare AR disease (gene TAT). Enzyme deficiency leads to elevated plasma tyrosine levels. Ocular involvement may be the presenting feature. Painful plantar and palmar hyperkeratotic lesions and variable CNS involvement seen. Bilateral pseudodendritic keratitis with crystalline edges in childhood cause photophobia redness.
169
Features of Fabry disease
X linked lysosomal storage disorder- deficiency of enzyme alpha galactosidase A leads to abnormal tissue accumulation of glycolipid. All males develop the condition and some heterozygous females.
170
What are some optic therapeutic uses for contact lenses
Irregular astigmatism with keratoconus corrected by rigid contact lenses after spectacles failed and before corneal graft necessary
Superficial corneal irregularitis neutralized by rigid contact lenses. Anisometropia where binocular vision cannot be achieved by spectacles due to anisekonia
171
What are some 'promotion of epithelial healing' therapeutic uses for contact lenses
persistent epithelial defects often heal if corneal epithelium isprotected by constant rubbing of lids allowing hemidesmosomal attachment to basement membrane
RCES associated with BM dystrophy require long term CL wear to reduce recurrence rate.
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What are some 'pain relief' therapeutic uses for contact lenses
Bullous keratopathy with soft BCL. Protect exposed corneal nerve endings from shearing forces of lids when blinking. Lens may flatten bullae into fine epithelial cysts
Filamentary keratopathy
Others like Thygeson SPK, Trichiasis corneal protection
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What are some 'preservation of corneal integrity' therapeutic uses for contact lenses
Descemetocoele temporarily capped with tight fitting large diameter soft or scleral lens prevent perforation encourage healing.
Splinting and apposition of edges of small corneal wound achieved by contact lens. Larger perforations sealed with glue + BCL
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Complications of contact lens wear
Mechanical and hypoxic keratitis- insufficient oxygen transmission through CL. SPK 3-9 o clock, Tight lens syndrome, Acute hypoxia epithelial microcysts, necrosis and endothelial blebs, chronic hypoxia-> vascularization, treat by refitting with thinner lens, gas permeable rigid lens, modifying lens fit to increase movement, reduce lens wear time
Immune response hypersensitivity keratitis
Toxic keratitis
Suppurative keratitis
Contact lens associated GPC
175
What is microcornea and what are some associations with this condition
normal neonatal diameter 10mm, adult 12mm reached by age 2. This is rare autosomal dominant unilateral/bilateral condition in which corneal horizontal diameter is 10mm or less over age 2 or <9mm in newborn. Cornea steep on keratometry.
Associated with glaucoma, congenital cataract, leukoma, persistent fetal vasculature, coloboma, optic nerve hypoplasia, anirida, nanophthalmos
176
What is Microphthalmos and what are the associations
Entire eye small. AL- 2 sd below mean for age. Nanophthalmos is an eye structurally normal apart from short length.
Associated with coloboma/ orbital cyst/ range of other ocular abnormalities. 50% have systemic probkems. Environmental causes are fetal alcohol syndrome/ intrauterine infections
177
What is nanophthalmos
entire eye small axial length <20mm. Both eyes affected. Ocular associations glaucoma (especially angle closure), hypermetropia, ametropia, amblyopia, strabismus. Childhood management of refractive error and amblyopia are critical.Glaucoma surgery leads to aqueous misdirection and choroidal effusion. Best option is IOL implant.
178
What is Anophthalmos
complete absence of any globe structure though microphthalmic remnant or cyst may be present. Associated with absence of extraocular muscles, short conjunctival sac, microblepharon. Same causative factors as microphthalmos
179
What is Megalocornea
rare bilateral non progressive condition. X linked recessive. 90% male. Adult horizontal corneal diameter 13mm or more. Deep AC. High myopia/ astigmatism but normal corrected VA. lens may sublux due to zonule stretching. PDS may occur.
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What is cornea plana
rare bilateral condition with corneal flattening more than normal. Radius of curvature larger. Reduction in refractive power resulting in high hypermetropia. 2 forms cornea plana 1 dominant inheritance CNA1 milder than cornea plana 2 recessively inherited CNA2
181
What is sclerocornea
rare bilateral condition may be associated with cornea plana. sporadic cases common but milder form inherited as AD and more severe form AR. Peripheral corneal opacification with no visible border between sclera and cornea confers appearance of reduced corneal diameter in mild- moderate disease. Occasionally whole cornea involved
182
What is posterior keratoconus
Sporadic condition
unilateral non progressive increase in corneal curvature posterior surface. Anterior surface and VA normal because of similar refractive indices of cornea and aqueous humour. Can be generalised or localised
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Part 2
flashcards
Decks in class (20)
# Cards
-
Exam Techniques68
-
Eyelids183
-
Lacrimal Drainage System41
-
Orbit167
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Dry Eye34
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Conjunctiva80
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Cornea183
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Corneal and Refractive Surgery49
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Episclera and Sclera35
-
Lens101
-
Glaucoma236
-
Uveitis191
-
Retinal Vascular Disease147
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Acquired Macula Disorders163
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Inherited Retinal Degenerations127
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Retinal Detachment99
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Vitreous Opacities10
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Strabismus201
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Neuro-ophthalmology352
-
Ocular Tumours164
