Diseases of Sclera

Sclera is posterior 5/6th outer opaque fibrous coat of eyeball with 3 layers:

1. vascular CT: episclera
2. avascular collagen: sclera porper
3. innermost brown: lamina fusca

Whole sclera has an outer tenon’s capsule & in addition covered anteriorly by bulbar conjunctiva.
Schlemm’s canal is the furrow near limbus.
It is thinner at extraocular ms insertions & is sieve-like lamina cribrosa at optic.N exit.
Apertures:

1. anterior limbal- anterior ciliary bv
2. middle- vortex veins
3. posterior- long&short ciliary N&bv

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Episcleritis:

benign recurrent inflmm of episclera & tenon+bulbar conjunctiva.
Etiology:

• usually in young adult [female]
• Associated with immune rxns:
  • rosacea, gout, psoriasis
  • TB, strep toxins

Pathogenesis:

1. episclera: localised lymphocytic infiltration
2. tenon+bulbar conj: edema & hyperaemia

CFs: red, gritty, [mild lacrimation & photophobia]

1. Diffuse: whole scleral inflmm but maximum confined to 1or2 quadrats
2. Nodular: firm, tender, pink-purple nodule 2-3mm form limbus with overlying mobile conjunctiva & surrounding injection

Rx:

• spontaneous regression after 10days-3wks
• protracted course of few days with topical steroids.
• recurrent disease- systemic NSAIDs

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Scleritis

seroius chronic inflmm of sclera proper.
Etiology:

• usually in elderly [40-70 female]
• Associated with:
  1. autoimmune collagen disorders- Rharthritis, PAN,SLE, ankylosing spondylitis, wegner’s granulomatis
  2. metabolic- gout, thyrotoxicosis
  3. scleral infections- Hzoster, staph, strep
  4. Granulomatous diseases- TB, syphilis, leprosy, sarcoidosis
  5. misc- rosacea, bechet’s, VHK syndrome, thermal/chemical burns

Pathogenesis: Granuloma-

1. fibrinoid necrosis
2. infiltration + collagen destruction
3. surrounded by epitheloid giant cells & bv

CFs:

• severe deep pain which radiates to jaw & temple
• local/diffuse redness
• mild to severe lacrimation & photophobia
• occasional visual impairment
• Types:
  

  Anterior non-necrotizing	DIFFUSE INFLMM [commonest]- pink/purple; ≥ 1quadrant NODULAR- 1or2 near limbus; hard elevated purple
  Anterior necrotizing	INFLAMM- localised acute severe; thin transparent ectatic vasculitic infarct; [associated uveitis] SCLEROMALACIA PERFORANS [non-inflmm due to obliteration of arterial supply]- initially yellow sequestrum → dead white → absorbed leaving a punched out sclearal peforation
  Posterior scleritis	CFs of inflmm of associated structures: exudative retinal detachment macular edema proptosis restricted ocular movts
  Complications	sclerosing keratitis, keratolysis complicated cataract secondary glaucoma

Diagnostic investigations:

• TLC, DLC, ESR
• immunological: C3, immune complexes, Rhfactor, LE cells, anti-nuclear antibodies
• syphilitic- VRDL
• gout- uric acid
• TB- mantoux test
• Xrays to rule out foreign body in chest, sacroiliac jt, PNS & orbit

Rx:

1. non-necritizing → topical steroids, systemic NSAIDs
2. necrotizing → oral+topical steroids [CI- subconj inj since scleral perforation], unresponsive cases – mtx,cyclophosphamide

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Blue sclera

Thinning due to

• osteogenesis imperfecta
• Marfan’s, Ehlers Danlos
• Buphthalmos
• high myopia
• healed scleritis

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Staphyloma

Types	localised bulge due to thinned outer fibrous coat	underneath shinning uvea is seen through
Anterior	pseudocornea [scar formed after total sloughing of cornea from organised exudate & eoithelial covering]	plastered prolapsed iris
Intercalary	limbal scar after perforating injury or peripheral corneal ulcer	iris root
Ciliary	thin sclera at 2-3mm from limbus due to perforating inj / scleritis / absolute glaucoma	ciliary body
Equatorial	at vortex vein perforations after scleritis / pathological myopia	choroid
Posterior	thinned sclera behind equatorial after perforating inj / pathological myopia / scleritis	excavation with dipping retinal bv

Glaucoma

ANATOMY:

Pathophysiology revolves around AqH dynamics:

Ciliary body:

AqH production.

Anterior chamber angle

Formed by [ICSTL] iris root, ciliary body anterior, scleral spur, trabecular mesh, Schwalbe’s line[corneal descemet]

Width varies in different individuals

Visualised by Gonioscopic examination [diverts light to angle]

Shaffer’s system of angle width grading:

• 0 0degrees Closed, no structures visible
• 1 10degree chances of closure high [ICSTL]
• 2 20degree possible chances of closure [ICSTL]
• 3 20-35degrees Open angle [ICSTL]
• 4 Wide open [ICSTL]

AqH outflow system:

Trabecular mesh: sieve through which AqH leaves eye

1. UVEAL meshwork – innermost
2. CORNEOSCLERAL meshwork – middle larger portion with elliptical & smaller than uveal openings
3. JUXTACANALICULAR / ENDOTHELIAL meshwork – outermost connecting with Schlemm’s canal & narrowest offerring normal resistance to AqH outflow

Schlemm’s canal:

• oval circumferential channel in scleral sulcus
• inner endothelial cells have giant vacuoles
• Collector channels opn into outer cells

Collector channels / Intrascleral aqueous vessles:

terminate into episcleral veins

2 systems – larger ones terminate directly; smaller ones form intrascleral plexus before terminating

PHYSIOLOGY:

Aq production:

clear watery fluid whicxh maintains IOP & provides substrates & removes metabolites from avascular cornea & lens.

water [99.9], proteins [0.04], Na[144], K[4.5], Cl[110], glucose[6], lactic acid[7.4], aa[5], inositol[0.1

derived from cilliary processes at 2.3 microl/min filling anterior & posterior chambers. Mechanisms: [fluctuates diurnally; passive mechanisms altered by capillary BP, osmotic pressure, IOP; active secretion altered by vasopressin & adenylcyclase]

1. Ultrafiltration of ciliary processes’ stromal capillary plasma & accumulation behind non-pigment epithelium [BaqB].
2. Active secretion of some ions,aa, ascorbic across BaqB into posterior chamber by Na-K-ATPase pump & Carbonic anhydrase.
3. this in-turn causes osmotic diffusion of other plasma constituents into posterior chamber.

Through pupil, AqH flows from posterior to anterior chamber.

AqH drainage from anterior chamber: 2 routes

CONVENTIONAL TRABECULAR OUTFLOW [90%]-

1. giant vacuoles in inner endothelium of Schlemm’s canal trasport AqH from juxtacanalicular to collecting channels by forming intracellular transport channel.
2. 10mm pressure gradient is responsible for unidirectional flow from intraocular trabeculae to intrascleral episcleral veins

Unconventional UVEOSCLERAL outflow:[10%] from ciliary body to suprachoroidal space then into veins of choroid, sclera, ciliary body.

Maintenance of IOP: [10-21 mm]

Local factors:

1. AfH production depends on capillary permeability, osmotic pressure, IOP.
2. resistance offerred at juxtacanalicular /endothelial trabular meshwork.
3. episcleral pressure increases during valsalva & inturn rises IOP
4. in narrow anterior chamber, relative obstruction by iris during pupil dilation rises IOP.

General factors:

1. hereditary, age >40 & greater in females
2. cortisol diurnal fluctuation of 8mm]
3. postural variation & HTN
4. indirectly proportional to plasma osmotic pressure which ris high with mannitol, glycerol, uraemia & low with drinking water provacation tests.
5. general anaesthetics, anti-glaucoma drugs varyIOP. steroids, caffeine, smoking rise IOP & alcohol lowers.

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Glaucoma

gorup of disorders where IOP is raised. above tolerance limit damaging optic.N head leading to irreversible visual defects

Ocular HTN

constantly raised IOP without visual field defects.

Normal/low tension glaucoma

disc cupping +/- visual field defects

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Primary developmental glaucoma

abnormally high IOP due to congenital trabeculodysgenesis causing abscence of angle from flat/concave iris insertion to trabeculum obstructing drainage.

True congenital – if it manifests prior to birth

Infantile – if it manifetss prior to age 3

Juvenile – if it manifests between 3-16 age.

BUPHTHALMOS / Hydrophthalmos – prior to age 3, high IOP even enlarges eyeball.

75% bilateral.

CFs:

1. Lacrimation + photophobia + blepharospasm + eyerubbing – from raised IOP irritating corneal nerves.
2. corneal signs -
   • Corneal edema is frequently the first sign & opacities may occur.
   • Corneal enlargement >13mm with deep anterior chamber [if prior to age 3 , buphthalmos also]
   • Haab’s striae in descemet since it is less elastic than stroma.
3. thin sclera with underlying blue uveal color
4. Iridodonesis
5. flat/subluxated lens due to stretched zonules
6. cupped optic disc
7. moderately high IOP measured with PERKIN’s applanation tonometer [instead of Schiotz since low scleral rigidity in children]

D/D

• corneal trauma/interstitial keratitis/endothelial dystrophy causing corneal edema
• megalocornea
• blocked nasolacrimal duct causing lacrimation
• uveitis, keratitis causing photophobia.
• high IOP from retinoblastoma, prematuruty retinopathy, hyperplastic vitreous, other types of glaucoma.

Rx:

Primarily surgical with prior lowering of IOP with acetazolamide,mannitol, glycerol, beta-blockers.

1. GONIOTOMY
2. Trabeculotomy + trabeculectomy – when corneal clouding prevents gonioscopic examination.

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DEVELOPMENTAL GLAUCOMAS ASSOCIATED WITH SYSTEMIC/OCULAR ANOMALIES

• Iridocorneal dysgenesis – Axenfeld anomaly, Peter’s anomaly, Rieger anomaly.
• Aniridia
• Displaced lens in Marfan, homocystenuria,
• phakomatosis in sturge-weber syndrome, Von recklinghausen’s neurofibromatosis
• Lowe syndrome [oculo-cerebro-renal], microcornea, rubella syndrome.

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Primary open angle glaucoma / Chronic simple [commonest]

↑ IOP due to sclerosed thickenned trabeculae & abscence of giant vacuoles.

Predisposing factors

1. heriditary
2. old age >40yr
3. myopic
4. diabetis, smoking, HTN, thyrotoxicosis

Symptoms:

1. insidious, bilateral, asymtomatic [mild headache/eyeache]
2. after 40% visual field loss – tunnel vision which is progressive & irreversilble.
3. accommodative failure due to pressure on ciliary muscle & nerve.
4. delayed dark adaptation

Signs:

1. Anterior segment [late stage]:sluggish pupillary reflex & corneal haze.
2. IOP [tonometry]:initially exagerrated diurnal variation >8mm. contrary to closed angle glaucoma, falls during evening. In late stages, permanently >21mm.
3. Optic disc: assymetric, progressive changes so recorded [most accurate method: confocal scanning laser topography]. PATHOPHYSIOLOGY: high IOP pushes back lamina cribrosa, mechanically squeezing nerve fibres’ axoplasma + causing vascular ischaemia [no increase in glia = Cavernous optic atrophy]
   • EARLY-
     • vertical oval cup due to superior& inferior loss of neural rim.
     • bilateral assymetry >0.2
     • cup:disc >0.5 [normal=0.3-0.4]
     • splinter hmmrhges at disc margin & pallor areas on disc.
     • atrophied retinal nerve fibre layer [ganglion cells] with red free light.
   • LATE-
     • markedly enlarged cup 0.7-0.9
     • crescentic margin due to notch created from thinning of neural rim.
     • nasal shift in retinal vessels & Bayonetting sign[broken at disc margin; hidden if margin overhangs]
     • Pathognomic: arteriolar pulsations at disc margin when IOP is very high.
     • Lamellar dot sign: slit pores of lamina cribrosa at disc margin.
   • Optic atrophy- head appears white & deeply excavated.
4. Visual field defects:[confrontation test]
   • temporal sup&inf arcuate fibres are most sensitive & macular horizontal fibres are most resistant to glaucomatous damage, hence central vision lost at the end. [central optic fibres are in superficial retina while peripheral fibres in deeper retina.]
   • Natural history of progression:
     1. ISOPTER CONTRACTION- mild total field constriction.
     2. BARING OF BLIND SPOT from central field.
     3. PARACENTRAL SCOTOMA in Bjerrum’s area [above&below blind spot]- earliest clinically significant sign.
     4. SIEDEL’S SCOTOMA- sickel shaped due to joining of blind spot & paracentral.
     5. ARCUATE BJERRUM’S SCOTOMA- extension of siedel’s above&below to reach horizontal line.
     6. RING/DOUBLT ARCUATE SCOTOMA- due to joining of similar arcs.
     7. ROENNE’S CENTRAL NASAL STEP- joining of different arcs forming a right angled defect
     8. PERIPHERAL FIELD DEFECTS- may appear early or late.
     9. ADVANCED DEFECTS- tunnel vision sparing small central & temporal islands. temporal is ultimately left before total blindness.

Ocular associations:

high myopia, fuch’s ED, retinitis pigmentosa, CRVO, retinal detachment.

Diagnosis:

1. Established POAG: cupping/visual field defects with IOP>21mm.
2. Glaucoma suspect / Ocular HTN: IOP>21mm.
   A suspect must be categorised as established case if :
   • IOP>30mm
   • diurnal variation>8mm
   • +Provocation test
   • assymmetry of cups>0.2mm
   • splinter hmrrges near disc.
   • family history
   • DM
   • high myopia
   • Anterior chamber pigment changes
3. NT glaucoma: normal IOP but with cupping+/-visual field defects.
   Etiology- chronic low perfusion makes OPitc.N succeptible to even normal IOP.
   Rx- frustrating

Rx:

1. Good baseline examination – for periodic supervision to prevent further vision loss while lowering IOP.
   • visual acuity, fundus photography, perimetry
   • applanation tonometry, diuranl variation, provocation test
   • slit lamp ex of anterior chamber, goniscopy
   • Nerve fibre layed analyzer – early detection before cup/field changes.
2. Medical therapy to lower IOP- 1st choice topical drug, if ineffective/intolerable shift to 2nd choice drug, if insufficient combination therapy.
   1. beta blockers [↓ AqH secretion]- 1st choice
      Systemic ADRs by absorption through higly vascular nasal mucosa from NLD ∴ CI: asthma, bradycardia
      • timolol, levobunolol [longest action]
      • betaxolol [beta1 selective] – cardiopulmonary case
      • cartiolol – hyperlipidemic
   2. CAinhibitors [dorzolamide - ↓ AqH secretion] – 2nd choice
   3. PG [latanoprost - ↓ uveal outflow] – most used adjuvant but expensive
      low ADRs – ↑ eyelash growth& iris melanin
   4. short-term adjuvants :
      1. acetazolamide [CAinh]
      2. pilocarpine [ciliary spasm opens trabeculae] – CI- older pt with axial lenticular opacities & chronic use in young since myopia&headache.
   5. alpha2 adrenergic [brimonidine- ↓ Aq production] – last resort adjuvant since allergic rxn & tachyphylaxis.
3. Laser trabeculoplasty – shrinking collagen in trab mesh ↑ outflow.
   Indications- noncompliance or failure of medical Rx.
   Complications-
   • transient ↑ IOP if no pretreatment with acetazolamide/pilocarpine
   • inflamm – treat with steroids
   • hmmrg
   • synechiae
   • ↓ accommodation
4. Fistulizing filtration surgery [trabeculectomy]- creates a new ouflow channel from anterior chamber to subconjunctival space.
   Indications- advanced disease or uncontrolled IOP or unavailability of laser trabeculoplasty
   Complications- visual risks

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Primary angle closure glaucoma

↑ IOP due to narrow angle blocking AqH outflow.
Mid-dilated pupil → pupil block → iris bombe [from built up AqH in posterior chamber] → iridocorneal angle closure → transient ↑ IOP → peripheral anterior synechiae causes a chronic ↑ IOP.

Predisposers:

1. Anatomical:
   • hypermetropia, antrerioly placed lens, plateau iris configuration
   • small cornea, small eyeball
   • large lens, large ciliary body
2. General: 50age female, anxiety, familiar, rainy season, SEasian
3. Ppt: dim light, emotional or physical stress, mydriatrics.

Clinical course	CFs	Diagnosis	Rx
Latent Glaucoma / Prodromal phase transient(seconds) ↑ IOP due to ppt factors	blurred vision, colored halos, mild headache corneal edema, shallow anterior chamber, narrow angle	colored halos around bright lights due to corneal edema [D/D: acute purulent conjunctivitis [discharge] & immature cataract [Fincham's test segmented halos when viewed thr stenopic slit] Gonioscopy -grade 1or 2 Slit-lamp grading against conreal thickness Provocation tests – darkroom [1hr & awake for dilated pupil], mydriatric test + → succeptible to spontaneous closure - → doesn’t rule out closure so warn for symptoms	pre-operative pilocarpine + both eyes : iridectomy / laser iridotomy
Intermittent Glaucoma / Constant instabaility phase recurrent (min-hrs) regular ↑ IOP followed by bright light/sleep induced miosis	impaired vision, colored halos, eyeache/ frontal headache dilated pupil corneal edema, shallow anterior chamber, narrow angle	similar to above	similar to above
Acute congestive/angle closure Glaucoma sudden total angle closure causing high ↑ IOP for days	sudden severe pain [with vomiting, prostration] rapid progressive vision impairment redness lacrimation, photophobia edema of lids, conj, cornea very shallow anterior chamber, total angle closure pupil is mid-dilated : vertically oval, fixed optic disc : edema, hyperaemia fellow eye : shallow anterior chamber, narrow angle	D/D: acute red eye: conjunctivitis, iridocyclitis secondary acute congestive glaucomas: neovascular, phacomorphic, glaucomatocyclitic	temporary emergency medical therapy: stat analgesic [pethidine] injection topical drugs to lower IOP: initially [mild drugs since iris is ischaemic]- hyperosmotics[mannitol, glycerol], acetazolamide later- pilocarpine, beta blockers inflmm- steroid drops synechiae causing <50%angle closure- iridectomy / laser iridotomy to bypass pupil block >50% synechiae or uncontrolled IOP- fistualization filtration surgery [trabeculectomy] prophylactic surgery on fellow eye
Chronic closed angle Glaucoma constant ↑ IOP due to extensive peripheral anterior synechiae formed from intermittent or gradual[creeping] angle closure	permanently red & painful except in creeping[white, painless] visual field defects similar to POAG ↓ visual acuity gonioscopy: angle closure due to peripheral anterior synechiae optic disc cupping	D/D of creeping synechiae: POAG	for synechiae: ↓ IOP with medical therapy + filtration surgery prohylactic surgery in fellow eye
Absolute Glaucoma due to untreated chronic phase	completely blind painful eye perilimbal red-blue zone due to dilated anterior ciliary veins; later caput medusae initial corneal insensitivity → later hazy, bullous keratopathy / filamentous keratitis very shallow anterior chamber atrophic iris pupil : dilated, fixed, green disc atrophy stony hard eyeball due to high IOP	-	for pain- destroy ciliary ganglion with retrobulbar alcohol inj lower IOP- destroy secretory ciliary epithelium with cyclocryotherapy / diathermy/ photocoagulation failed conservativeRx / malignant progression- enucleation
Complications	corneal ulcer staphyloma from bulged out atrophic sclera from high IOP atrophic bulbi from ciliary body degeneration	-	-

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Scondary glaucomas

Phacogenic glaucomas	MOA	Rx
Phacomorphic [angle/pupil block]	altered lens morphology intumescent [swollen] anterior subluxated / dislocated spherophakia	medical to ↓ IOP & lens extraction surgery
Phacolytic	morgagnian hypermature cataractous lens leaks fine white protein thr lens capsule → phagocytosed by macrophages → clog trabe mesh	medical therapy to ↓ IOP & lens extraction surgery
Lens particle	disloged lens particles after trauma → clog trabe mesh	medical therapy to ↓ IOP & apsirate lens particle
Phacogenic uveitis	lens induced uveitis → lens particles & inflm cells clog trabe mesh	medical therapy to ↓ IOP uveitis- steroids & cycloplegics aspirate lens particles
Phacoanaphylaxis	fulminating inflm from antibody attacks to lens protein	medical to ↓ IOP steroids

Inflammatory glaucomas Glaucomas associated with uveitis	MOA & CFs	Rx
Acute anterior uveitis	clogged trabe mesh from inflm cells exudate turbid AqH edema ↑ IOP	steroids, cycloplegics & ↓ IOP with medical therapy
Post-inflmmatory	pupil block from annular synechiae or iris bombe angle closure from organization of inflmm debris	synechiae prophylaxis – steroids&cycloplegics &darrIOP with medical therapy [CI-miotics] pupil block – iridectomy angle closure – trabeculectomy
Specific HTNisve uveitis syndromes	Fuch’s uveitis syndrome Glaucomatocyclitic crisis	-

Pigmentary glaucoma [young myopic male]	pigment shedding from mechanical rubbing of iris & zonules → clog trabe mesh krukenberg’s spindle on posterior cornea zonules lens SAMPAOLESI’s line [inferior schwalbe's line] Pathognomic: iris shows radial slits in mid-periphery on trans-illumination	Rx: similar to POAG

Neovascular intractable glaucoma 3 stgaes: rubeosis iridis pretrabecular neovascular membrane → open angle glaucoma goniosynechiae [contacture of neovasc membrane] → zipper angle closure glaucoma	Etiology: retinal ischaemia in D.retinopathy CRVO, CRAO Sickle cell retinopathy Eale’s disease Intraocular – chronic inflm, tumor R.detachment	Rx: curb neovasc → Pan-retinal photocoagulation ↓ intractableIOP with Artificial drainage shunt [seton valve implant]

Intraocular tumors [MalignantMelanoma (iris, choroid, ciliary body) Retinoblastoma]	tumor cell invasion or clogging of trabe mesh neovasculariztn of angle vortex venous stasis from obstruction anterior subluxation of iris	Rx: enucleation

Pseudo-exfoliative / Glaucoma capsulare	amorphous grey dandruff like material deposition on: anterior lens posterior iris zonules ciliary processes	Rx: similar to POAG

Glaucomas-in-aphakia	conditions: poat-operative ↑ IOP due to hyphaema, inflm, chymotrypsin, vitreous in anterior chamber angle closure due to flat anterior chamber pupil block from anterior synechiae / vitreous herniation pre-existing POAG steroids for post-operative cataract post-operative epithelial ingrowth into trabe mesh aphakic malignant glaucoma

Steroid induced glaucoma [topical/systemic]	inn a genetically determined[40%] patient may cause mucopolysaccharides deposition in trabe mesh	Rx: monitoring IOP while steroid use discontinue steroids & treat glaucoma with timolol filtration surgery if glaucoma is intractable after 1mos

Traumatic glaucoma	blunt/perforating injury causes the following conditions which ↑ IOP: uveitis hmmrg ruptured lens anterior synechiae adherent leucoma epithelial/fibrous ingrowth trabe disruption & fibrosis causing angle recession	Rx: ↓ IOP with medical therapy treat the causative conditions

Malignant glaucoma / Ciliary block glaucoma [rare early post-operative complication of any intraocular surgery esp PACG - peripheral iredectomy / trabeculectomy]	Ciliary block of AqH flow at: cilio-lenticular in phakic cilio-vitreal in aphakic which causes AqH to collect posteriorly as vitreous pockets & ↑ IOP: persistent flat anterior chamber negative Seidel’s test unresponsive to miotics	Rx: atropine to dilate ciliary ring acetazolamide & timolol to ↓ AqH production i.v mannitol to shrink vitreous posterior sclerotomy if unresponsive to medical Rx for 5days aspirate fluid from vitreous inject air into anterior chamber

Intraocular hmmrges [hyphaema, vitreous]

types of glaucoma: Red cell glaucoma – trabe clogged by RBCs in fresh massive traumatic hyphaema [after few days corneal blood staining occurs] Hemolytic glaucoma – trabe clogged by macrophages with lysed RBC Ghost cell glaucoma [vitreous hmmrg in aphakia]- after 2wks RBCs turn khaki colored ghost cells which clog trabe Hemosiderin glaucoma [rare]- sclerosis induced by iron from trabe’s endothelial cells’ phagocytosed Hb.

Iridocorneal endothelial syndromes progressive iris atrophy [iris hole] chandler’s syndrome [corneal edema] cogan reese syndrome [iris pigmented lesions]	usually seen in a middle aged female with abnormal corneal endothelium → proliferates forming a membrane in angle → contraction causes synechiael angle closure glaucoma

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Surgical procedures for glaucoma:

1. Peripheral Iridectomy- Rx+prophylaxis for PACG
2. Fistulization guarded filtering surgery – trabeculectomy [partial thickness fistula] – [post-operative complications: hyphaema, iritis, endophthalmitis, cataract]
   1. POAG
   2. >50% synechiae in PACG
   3. congenital&dev glaucomas where trabeculotomy&goniotomy fail
   4. secondary glaucoma
3. Antimetabolites[fluprpuracil,mitomycinC] + trabeculectomy:
   1. previous failed fistula
   2. glaucoma in aphakia
   3. some secondary glaucomas [inflmm,trauma]
   4. >3yr medical Rx for glaucoma
4. Artificial drainage shunt [seton's valve implant] – neovascular glaucoma, glaucoma with aniridia, intractable primary/secondary glaucomas
5. Cyclocryotherapy – destroy secretory ciliary epithelium in Absolute glaucomas.

Diseases of Conjunctiva

DISEASES OF CONJUNCTIVA

ANATOMY

CONJUCTIVA:

translucent mucous membrane posterior to eyelids & anterior to eyeballs.

3 parts:

PALPEBRAL

Marginal- from lid margin to sulcus subtarsalis

Tarsal- firmly adherent & highly vascular; whole upper tarsal plate & half of lower tarsal; yellow streaks of tarsal glands.

Orbital- loosely between tarsal plate and fornix.

BULBAR

loose over epislera & tenon’s capsule (anterior to sclera)

limbal conjunctiva- 3mm ridge around cornea firmly adherent to episclera & tenon.

FORNIX

circular cul-de-sac joining bulbar & palpebral, broken at the medial caruncle & plica semilunaris.

structure: 3 layers

EPITHELIUM

Marginal & Limbal have 5layered str sq.

Tarsal has 2layered cylindrical & flat.

Fornix & Bulbar have 3layered cylindrical, polyhedral & cuboidal.

ADENOID/LYMPHOID

fine CTreticulum with lymphocytes

most dev at fornix

dev after 3mos of birth, so no follicular rxn in infants.

FIBROUS

thick with c&e fibres, bv & nerves; blends with tenon’s in bulbar region.

thin in tarsal region.

Glands: 2types

MUCIN SECRETORY GLANDS:

epithelial goblet

tarsal henle crypts

limbal manz

ACCESSORY LACRIMAL GLANDS:

Krause (fornix: upper 42 & lower 8),

Wolfring (upper superior tarsus & lower inferior tarsus)

PLICA SEMILUNARIS in medial canthus: pink crescent conjunctival fold with concave lateral border.[atavistic nictitating membrane].
CARUNCLE medial to plica: small oval pink mass covered with str sq & contains sweat glands, sebaceous gl & hair follicles.

ARTERIES:

Marginal palpebral arcade

Peripheral palpebral arcade

Anterior ciliary artery

Palpebra & fornix by peripheral & marginal arcades

Bulbar & pericorneal plexus by posterior conj[peripheral arcade] & ant conj[ant ciliary]

LYMPHATICS

Preauricular -lateral

Submandibular -medial

NERVES

Long ciliary nerve supplies cornea

rest supplied by lacrimal, infra & supra trochlear, supraorbital, frontal.

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INFLAMMATORY DISEASES

= hyperaemia + discharge.

INFECTIVE commonest [inspite protection from low temp due to air exposure, lids, tears flush, lysozymes, Igs.]

BACTERIAL CONJUNCTIVITIS

common in developing countries & epidemics during monsoon.
PREDISPOSERS- hot dry, unhygienic, flies.
CAUSE-

1. Staph aureus most common
2. Staph epidermidis [innocuous]
3. Strep pneum [acute with subconjunctival petechiae]
4. Strep pyo(hemolyticus) [virulent- pseudomembranous]
5. Pseudomonas pyocyanea [virulent- invades cornea]
6. H.inf [mucopurul red eye epidemics in tropics]
7. Neiseria mening [mucopurul conj]
8. Moraxella lacunate [angular conj]

MODE

EXOGENOUS air,water, flies, fingers, towels.

LOCAL from lids, lacrimal sac, nasopharynx; innocuous organism

ENDOGENOUS[rare] blood e.g. neisseria

PATHOLOGY [more marked in purulent than in mucopurulent]

Vasodilation- congestion of conj bv

Cellular exudation of macrophages into substansia propria & conj sac

Edematous epithelium- superficial desq, basal prolifertn, increased goblet cells

Discharge- tears, mucus, infl cells, fibrin, bacteria [severe infection even causes RBC diapedesis

CLINICAL TYPES

Acute- catarrhal/mucopurul, purul, membranous, pseudomembranous

Chronic- catarrhal, angular

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Acute mucopurulent/catarrhal conj most common acute bacterial conj; generally accompanies measles & scarlet fever.

Cause

Staph

Strep

H.inf

Signs & Symptoms

Conjunctival congestion other than circumcorneal zone[fiery red eye]& chemosis -Foreign body sensation due to vasodil.

Flakes in fornices, canthi, lid margins & matted cilia with yellow crusts -mucopurulent discharge, sticking lid margins after sleep, colored halos due to prismatic effect on cornea.

[Petechiae if Strep.pneum.]

Course – 10-15 days or passes to less intense Chr catarrhal conj.

Rx

Topical broad spectrum antibiotics : chloramphenicol, gentamycin, framycetin [unresponsive cases cipro]

1-2/day Irrigation with sterile warm saline [CI: but freq eyewash removes lysozyme]

Dark goggles for photophobia [CI: bandaging rises temp promoting bacteria]

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Acute purulent/ Hyperacute conjunctivitis predominat in adult males.

acute purulent conj of adults

ophthalmia neonatorum in newborn

Acute purulent conj of adults

CAUSE

Gonococci – commonest & usually associated with urethritis/arthritis.

Staph aureus

Strep pneum

COURSE

3 stages

INFILTRATION: initial 5 days of painful bright red velvety chemosed conj, swollen lids, watery discharge, enlarged preauricular LN.

BLENORRHOEA: purulent copiuos trickling discharge,lids swelling incr.

SLOW HEALING: all symptoms decrease except conj remain chemosed.

Rx:

imp to give systemic antibiotics for 5days[norfloxacin/cefoxitim], followed by 7days of doxycycline/erythromycin.

topical bacitracin/erythro every 2hrs for 3days then 5times/day for 7days

irrigation with sterile saline every hr to remove debris.

[if cornea involved - topical atropine]

Ophthalmia neonatorum:

bilateral conj inflm in less than 30day infant.

MODE

BEFORE BIRTH – infected liquor amnii with ruptured membranes.

DURING BIRTH(common) – face presentation / with forceps.

AFTER BIRTH – contamination from lochia or during first bath.

CAUSE

chemicals [Incubation period 5hrs]-silver nitrate, prophylactic antibiotics.

genital gonococcal infection [Incubation period 2-3 days]

Staph aureus, Strep pneum, Strep hemolyticus.[Incubation period 4-5 days]

D to K Chlamydia trachomatis [neonatal inclusion conj][Incubation period 5-14 dys]

Herpes simplex2 (rare)[Incubation period 5-7 days]

SIGNS & SYMPTOMS:

pain [hyperaemia, chemosis]

discharge- purulent in gonococci, others mucoid/mucopurulent.

swollen lids

[herpes simplx - corneal superficial punctate keratitis, mild papillary]

Rx:

PROPHYLAXIS:

1. antenatal- genital inf in mother.
2. natal most common so imp]- aseptic delivery, throrough cleansing & drying of neonatal’s closed lids.
3. postnatal- immediately after birth topical tetracyline/erythr/silver nitrate; if mother has gonococcal inf: single inj of ceftriaxone

CURE:

1. chemical cause – self limiting condition.
2. gonococcal inf – topical [saline irrigation, bacitracin 4times/day, cornea involv needs atropine]; systemic [7days of cipro/ceftriaxone/cefotaxime]
3. other bacterial inf with topical broad spectrum antibiotics for 2wks
4. neonatal inclusion conj with topical tetracyline/erythr for 3wks 7 the implied chlamydia colonization of upper resp tract with systemic erythr qid 3wks
5. herpes simplex is self-limiting & topical anti-virals prevent recurrences.

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Acute membranous conjunctivitis rare in unimmunised 2-8yr chidren [violent inflm of conj; membrane=fibrinous exudate in palpebral conj[surface as well in substance] which undergoes coag necrosis & sloughing & granulation]

CAUSE

Corynebact diphth [typically]

virulent Strp hemolyticus

Course

febrile; 3 stages.

INFILTRATION: pain, red chemosed & firmly adherent grey-yellow membrane on conj, enlarged preauricular LN.

SUPPURATION:symptoms decr with sloughing of membrane & copious purulent discharge.

CICATRISATION: healing by epithelialisation which may cause triciasis & xerosis[symblepharon].

Rx:

TOPICAL

1. pencillin drops every 1/2hr.
2. antidpth serum every 1hr.
3. broad spectrum antibiotic before bedtime.
4. [corna invlv -atropine]

SYSTEMIC

1. stat antidpth serum i.m.inj
2. i.m. inj of crystalline Pn 2times daily for 10days.

Symblepharon prevention-

apply contact shell or sweeping fornices with a oint smeared glass rod.

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Acute Pseudo membranous conjunctivitis ~mucopurulent conj + fornices&palpebral conj has thin yellow white pseudomembrane can be easily peeled off leaving intact conjunctiva.

Cause

Bacteria: low virulent C.dipth, staph, strep, H.inf.

viral: H.simplex, adenovirus.

chemicals: acids, NH3, lime, silver nitrate, coppur sulfate.

---

Chronic catarrhal conjunctivitis:mild catarrhal inflm.

Cause

Predisposing: chronic exposure to dust/smoke/chemicals, local trichiasis/concretions/foreign body/seborrhoeic scales, eye strain[refractive errors/phorias/convergence insufficiency], insomnia, alcohol, metabolic disorders.

Staph aureus is commonest cause, Gm- bacteria: Proteus mirabilis, K.pneum, E.coli, Moraxella lacunata.

contact/air/contamination, untreated acute mucopurulent conj, from chronic dacryocystitis/rhinitis/Upper RT inf.

Signs & symptoms:

mild

burning & grittiness[paillary hypertrophy in palpebral] esp in evening, red[posterior conj bv] sticky conj, mucoid discharge esp in canthi, intermittent lacrimation, hot dry congested lid margins, tired & sleepy eyes.

Rx:

TOPICAL- chloramphenicol/gentamycin 3/day for 2wks.

symtomatic relief – zinc boric acid drops.

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Angular conjunctivitis / Diplobacillary conj -type of chr conj mild inflm confined to angles of lids & conj + macerated skin.

Cause

Predisposing: chronic exposure to dust/smoke/chemicals, local trichiasis/concretions/foreign body/seborrhoeic scales, eye strain[refractive errors/phorias/convergence insufficiency], insomnia, alcohol, metabolic disorders

Moraxella axenfeld is commonest cause- spread from nasal cavity to eyes by contaminated fingers; its proteolytic enzyme collects in angles & macerates epithelium of conj.lids,skin followed by vascular & cellular responses of mild chronic inflm

Signs & symptoms

angles [conj,lids,excoriated skin]- redness, dirty white foamy mucopurulent discharge, irritation.

Rx

prophylactic therapy for nasal infs.

cure: topical oxytetracycline 3times daily for 14 days, zincoxide for maceration.

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CHLAMYDIAL CONJUNCTIVITIS

intracellular, sensitive to antibiotics; PLT group

Trachoma chr keratoconj with mixed follicular 7 papillary response; leading cause of preventable blindness after cataract.

Etiology:

Chlamydia trachomatis – epitheliotropic, HP intracytoplasmic inclusion bodies, 11serotypes-

• A-C cause hyperendemic/blinding trachoma with secondary bacterial infection, hypoendemic trachoma without secondary infection.
• D-K cause paratrachoma/oculogenital trachoma which is predominantly seen in urban areas & spreads from genitals. it includes adult inclusion conjunctivitis & ophthalmia neonatorum.

Predisposers: early childhood, females, jews, dry dusty weather [common in outdoor workers], unhygenic,flies.

superimposed bacterial inf discharge intensifies spread; modes- air, water, contamination from flies/fingers/fomites.

Course-

Insidious[subacute] onset [incubation 5-21 days]; in endemic regions acute infection in first decade of life & becomes inactive in second decade & sequelae start in 4th/5th decade.

pure disease is symptomless [mild foreign body sensation & occassional lacrimation, scant mucoid discharge & slight sticky lids.

typical acute mucopurulent conjunctivitis symptoms only with secondary bacterial inf which in early stages is indistinguishable [trachoma dubium]

1. upper palpebral conjunctival signs – esp at tarsus & fornix shows hyperaemia [Incipient stage], follicles & papillae [Florid stage], scarring [Cicatrization stage], concretions [Sequelae due to mucus&epithelial debris in henle glands].
   sometimes follicles are seen even in lower fornix, caruncle, & pathognomically on bulabr conjunctiva.
   Follicles are scattered lymphocyte aggregations in adenoid layer. histiocytes& multinucleated leber cells are seen centrally while proliferating lymphocytes, bv are in the periphery. Differentiated from other follicular conjunctivitis by presence of Leber cells & necrosis.
   Papillae are red, flat topped raised areas giving a velvety appearance with central dilated blood vessels & surrounding lymphocytes covered by epithelial hypertrophy.
2. Corneal signs – upper part shows superficial epithelial keratitis & pannus, limbus shows herbert follicles & healed herbert pits, end stage shows corneal opacity which may encroach pupil area causing visual impairment.
3. Sequelae -
   lids- trichiasis, entropion, tylosis, ptosis, madarosis, ankyloblepahron.
   conjunctiva- concretions, pseudocyst, xerosis, symblepharon.
   cornea- opacity, ectasia, xerosis, total pannus [blindness]
   chronic dacryocystitis
   secondary glaucoma
4. the only complication – corneal ulcer from concretions / trichiasis + secondary bacterial infection.

WHO classification-

1. Trachomatous inflammation follicular – ≥ 5 follicles on upper tarsal conjunctiva; visible deep tarsal bv thr follicles&papillae.
2. Trachomatous inflammation intense – thickenned upper tarsal conjunctiva
3. Trachomatous scarring – white sheets in tarsal conjunctiva
4. Trachomatous trichiasis – atleast 1 eyelash rubs eyeball
5. Corneal opacity – atleast encroaching the pupil margin

Diagnosis-

• giemsa smear shows lymphocytes, leber cells, inclusion bodies.
• isolation by yolksac inoculation & tissue culture.
• serotyping for TRIC agents[A-K].

D/D:

adenoviral epidemic KC [follicles on lower conj , unlike trachoma no papillae or panus]
spring catarrh [large cobblestone papillae, ropy discharge, but unlike trachoma no acidic tears / papillae / pannus]

Rx:

topical or systemic antibiotics in mild cases

• tetracycline / erythromycin / sulfacetamide drops 3/day fro 6wks.
• tetracycline / erythromycin doxycycline tabs for 4wks or single dose arithromycin.
• cimbined topical 7 systemic in severe cases.

Sequalae-

• concretions – reomove with hypodermic needle
• trichiasis – remove with epilation / electrolysis / cryolysis
• entropion – surgical
• xerosis – artificial tears

Adult inclusion conjunctivitis

Cuase – genital contamination [male urethritis, female cervicitis] from D-K chlamydia
CFs-

• mucopurulent discharge, foreign body sensation, mild photophobia.
• conjunctival hyperaemia esp fornices.
• follicles in lower conjunctiva.
• superficial keratitis in upper cornea.
• pre-auricular lymphadenopathy.

Rx: systemic + topical antibiotics [since asymptomatic venereal disease]

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Viral KC- serous, hmmrg, follicular

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Follicular conjunctivitis-

1. Acute catarrhal [lower conjunctiva]
   • adult inclusion
   • adenoviral epidemic KC
   • pharygoconjunctival fever
   • newcastle conjunctivitis
   • acute herpetic conjunctivits
2. mild Chronic catarrhal [lower conjunctiva]
3. specific conjunctivitis with follicles like trachoma.

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Allergic conjunctivitis

conjunctiva is 10 more sensitive than skin to allergens.
It is either delayed CMI or immediate HMI.

Simple allergic conjunctivitis:

Etiology:

non-specific

1. hay fever- due to pollen & fur; associated allergic rhinitis.
2. seasonal [common] – due to pollen.
3. perennial [uncommon] – due to dust mites.

Pathogenesis:

• vascular response – sudden extreme vasodilation, exudation.
• cellular response – eosinophils, plasma cells, histamine releasing mast cells.
• conjunctival tissue response – mild papillae, boggy due to ↑ CT

CFs: acute / subacute

• intense itch & burn
• watery discharge
• mild photophobia
• conj – hyperaemia, chemosis, mild papillae
• swollen lids

Diagnosis:

eosinophils in conj tissue & no infection

Rx:

• avoid allergen
• vasoconstr- adr, eohedrine, naphazoline
• recurrent cases – cromoglycate
• severe / nonresponsive – steroids

Vernal KC / Spring catarrh:

Etiology:

due to external allergens; family history of other atopic diseases [hay, asthma, eczema]
Predisposers:

• 4-20 age boys
• periodically in summer in warm humid tropics

Pathology:

• papillae in upper tarsal conjunctiva due to epithelial hyperplasia; subepithelial projections from papillae
• adenoid infiltration
• vascular – dilation, exudation, proliferation

CFs: bilateral

• intense itch & burn
• ropy discharge
• mild photophobia
• heavy lids
• upper tarsal conjunctiva – cobblestone papillae; cauliflower like giant papillae in severe cases
• bulbar conjunctiva – dusky red trinagular hyperaemia on either side, gelatinous limbal membrane + white tranta’s spots
• Keratopathy -
  • upper cornea shows punctate keratitis or shallow transverse ulcer.
  • plaques due to deposition of altered exudates on macroerosions
  • subepithelial ring scar
  • cupid bow pseudogerontoxon

Rx: recurrent but self-limiting; regresses after 5-10yrs

• dark goggles, cold compresses / climate
• topical steroids [medrysone; + monitor IOP for induced glaucoma], naphazoline, cormoglycate, acetic acid [neutralize alkaline tears], cyclosporine in severe/nonresponsive cases
• systemic aspirin[anitPG] & anti-H; seveere/nonresponsive case-steroids
• giant papillae – supratarsal inj of long acting steroid /cryo/ beta-radiation /surgery
• keratopahty- high dose steroids, keratectomy

Atopic KC:

History:

young adult male + atopic dermatitis

CFs:

• itch, sore, dry
• mucoid discharge
• photophobia / blurring
• chronically inflamed lid margins
• tarsal conj – fine papillae, milky, hypaeraemia, scar
• lower cornea – punctate, vascularztn, thinning, plaques
• [keratoconus, atopic cataract]

Rx: recurrent diseae, regresses after age 50

frustrating [cromoglycate, steroids, artificail tears] ; treat dermatitis & lids.

Giant papillary conjnctivitis:

Etiology:

due to tears leaching the rough surface of a foreign body [lens,sutures]

CFs:

• itch
• stringy discharge
• ↓ wearing of lens
• 1mm papillae with hyperaemia in upper tarsus

Rx:

resolves after 1mos of foreign body removal; cromoglycate to hasten resolution.

Phlyctenular KC: [D/D for bulabr conjunctival nodule: episcleritis, scleritis, FBgranuloma]

Etiology:

delayed CMI to endogenous microbial proteins [TB, staph, moraxella, parasites]

Predisposers- 3-15 age female, malnourishment, poor hygiene

Pathological stages:

• nodule – due to exudative infiltrate into deep conjunctiva; [neutrophylls at centre, peripheral lymphocytes, surrounded by bv dilation+proliferation
• ulceration - at apex, mast cells & plasma cells
• granulation of floor
• healing with minimal scarring

CFs: few, mild

discomfort, watering

secondary mucopurulent conjunctivitis

bulbar conjunctival nodule near limbus

• simple [common] – 1or2 pink-white nodules + hyperaemia + apex ulcerates&epithelializes
• necrotizing – pustular conj due to very large nodule+ulcer
• miliary – multiple nodules

Keratitis

• ulcerative-
  1. sacrofulous – shallow marginal perpendicular to limbus, heals without scarring
  2. fascicular – with parallel leash of bv; heals with band opacity
  3. miliary – multiple small ulcers
• diffuse infiltrative – central infiltration & rich vasculrztn around limbus

Rx: recurrent; self-limiting in 10days

• topical steroids, antibiotics for secondary inf
• corneal lesion – atropine 1% ointment OD
• treat the cause – TB, sepsis, parasite
• high protein diet

Contact dermoconjunctivits:

Etiology:

delayed CMI to drugs [atropine, penicillin, neomycin/genta/sofra]

CFs:

conj esp lower- hyperaemia, papillae
cutaneous eczema of lids & face

Diagnosis:

eosinophylls in conjunctiva

+skin test for allergen

Rx:

discontinue the drug

topical steroids – eyedrops & skin oint

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Degenerative conditions: due to exposure to sun,dust,wind

Pinguecula:

on bulbar conj near limbus – avascular yellow-white triangular patch due to collagen degeneration&hyaline deposition.

Pterygium:

Etiology:

• usually seen in elderly male
• subconjunctival degeneration & hyperplasia as vascular granulation triangular fold encroaching & destroying cornea in interpalpebral area often nasal.
  1. Progressive- fleshy with cap
  2. Regressive- atrophic, less vascular, without cap

Complications- infection, cystic degenertion, neoplasia

D/D: pseudopterygium from chemical burns = chemosed bulbar conjunctiva adherent to corneal ulcer.

Rx:

• surgery – cosmetic, progressive from, hindered ocular movts causing diploplia
• recurrent cases
  1. transplant to lower fornix
  2. beta-radiation
  3. anti-mitotic drugs
  4. excise with sclera or mm graft
  5. recalcitrant cases – excise + lamellar keratectomy/plasty

Concretions:

• seen in elders or scarring trachoma
• upper conj – yellow-white hard raised areas due to mucus-epithelial debris in henle loops
• may cause corneal abrasion
• Rx: removal with hypodermic needle

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Conjunctival symptoms:

simple Hyperaemia: [not associated with disease]

1. Transient -
   1. irritation from cilia, dust, fumes, wind, light, cold/heat, rubbing
   2. reflex from eyestrain, inflm in neighbouring structures
   3. acute febrile conditions
2. chronic – smokers, alcoholics, dusty ill-ventilated rooms, prolonged exposure to heat, rosacea, insomnia

CFs:

gritty, heavy, tired eyes

mild watering & mucus

hyperaemic fornix

Rx:

topical decongestant[adr] & astringent[Zn-Boric acid]

Chemosis/ conj edema causes:

1. Inflm – conjunctivitis, corneal ulcer, fulminant iridocyclitis, end/pan ophthalmitis, stye, dacrocystitis, meibomitis, cellulitis, tenonitis
2. obstruction to blood/lymph by tumor, cyst, exophthalmos, CSthrombosis, acute glaucoma, surgical damage
3. systemic – severe anaemia, nephrotic syndrome, CHF, angioneurotic edema, urticaria

Ecchymosis:

• defined bright-red flat small/extensive hmrrg
• causes;
  ‘
  1. trauma
  2. inflm – pneumococcal, leptospirus, picorna virus
  3. sudden venous congestion of head causes capillary rupture – whooping cough, epilepsy, jugular vein strangulation, crush inj to thorax/abdomen
  4. spontaneous rupture dut to ATH, HTN, DM, anomalies like aneurysm, varicosity, telangectasia, blood disorders
  5. acute febrile conditions
  6. rare vicarious due to menstruation
• Rx: assurance since absorbed within 21days [severe cases some pigmentation may be left] ; cold compress in early stages & later hot

Xerosis: dry lustreless conjunctiva

1. Parenchymatous – after cicatrization
   • interstitial conjnctivitis – trachoma, diphtheria, pemphygoid, SJsyndrome, thermal, chemical, radiation
   • prollonged exposure to air – proptosis, facial palsy, ectropion, coma, lagophthalmos due to symblepharon
2. Epithelial – usually in children due to ↓ vitA = XEROPHTHALMIA where conj is thick, wrinkled,pigmented.

Rx:artificial tears.

Diseases of Lacrimal apparatus

Anatomy:

Main Lacrimal gland: [serous acinus glands like salivary]

1. ORBITAL part:
   • superior surface is in contact with outer orbital plate of frontal bone.
   • inferior surface is separated from Palpebral part by levator palpebrae superioris.
2. PALPEBRAL part: smaller part continous posteriorly with the larger Orbital part.
3. Ducts of lacrimal gland [10-12] pass downwards to open in lateral part of superior fornix [1or2 in inferior fornix]

Nerve supply:

1. Sensory: trigeminal-ophth-lacrimal.N
2. Sympathetic: cervical carotid plexus.
3. Secretomotor [parasympathetic]: superior salivary nucleus.

Accessory Lacrimal gland:

1. KRAUSE -beneath superior[42] & inferior[6-8] palpebral conjunctiva.
2. WOLFRING -extremes of superior&inferior tarsus.

LACRIMAL PASSAGES:

1. Puncta: opening on papilla of each lid near inner canthus, dipping into lacus lacrimalis [tear collection]
2. Canaliculi: from each puncta a short vertical part right angles with long horz part to converge to open into lacrimal sac.
3. Lacrimal sac: [fundus, body, neck] in lacrimal fossa of medial orbital wall [lacrimal bone, maxilla frontal process]
4. Nasolacrimal duct: [15-18mm] laterally down&backwards in the bony canal formed by maxilla & inferior turbinate, upper part is narrowest; one of its important valve is HASNER which prevents reflux from lower nose.

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Tear film

apart from washing away debris/noxious irritants & providing oxygen to cornea, has 3 layers:

1. outer lipid layer- Meibomian, Zeis, Moll secretion; air-tear interface that lubricates [facilitating movts] eyelids, retains shape & retards evaporation of tears.
2. bulky Aqueous layer- Lacrimal glands’ antibacterial [lysozyme,betalysin,lactoferrin] alkaline/saltish[solutes] watery secretion.
3. thin inner Mucus layer- conjunctival mucin secretory glands’ [goblet, henle, manz] secretion which by its hydrophilic nature keeps cornea & conjunctiva moist.

Tears are continously secreted by lacrimal glands. Basal secretion from accessory glands; Reflex secretion due to sensations[dry epithelium,broken tears] from cornea&conj from Main lacrimal glands; Hyperlacrimation due to irritants.

Elimination of tears by downward&medial flow towards lacus lacrimalis is due to:

1. orbicularis pump mechanism due to its insertion on lacrimal sac creates a negative syphoning pressure due to fundus distension & lower part compression.
2. orbicularis relaxation refills lower part from the fundus.
3. Hence, despite patency, atonia of lacrimal sac causes EPIPHORA.

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DRY EYE: deficiency / abnormality of tear film.

Etiology:

KCS [&darr water]	congenital alacrimia paralytic hyposecretion Sjorgen, RileyDay syndromes
&darr mucin	xerophthalmia [&darr vitA] conjunctival scarring – StevensJohnson, trachoma, pemphigoid, chemicals, radiation.
&darr lipids [rare]	congenital anhydrotic ectodermal dysplasia meibomian abscence – chronic meibomitis, chr blepharitis
&darr blinking	Bell’s plasy, nocturnal lagophthalmos, pterygium, ectropion, exposure keratitis, dellen, symblepharon
Corneal epeithelial abnormality affects tear film stability.

CFs:

• sandy sensation, itch, sore
• unresponsive to eyedrops
• particulate matter, stringy mucus
• lustreless
  • conjunctiva – xerosis, bitot spots, absent marginal tear strip.
  • cornea – punctate epithelial erosions & filaments

TEAR FILM tests:

Break up time	fluorescein is introduced & examined under cobalt blue slit-lamp while the patient is asked to keep blinking	corneal dry spot appearance normal=15-35sec, in unstable tear film <10sec
Schirmer 1	whatman41 filter paper in lower fornix & patient is asked to look up for 5min	[>15mm normal] in severe KCS <5mm.
Rosebengal staining		A pattern = confluent [severe KCS] B pattern = extensive staining [moderate KCS] C pattern = fine punctate stains in interpalpebral area [mild KCS]

Rx:

• artificial tears – cellulose, polyvinyl alcohol.
• &darr evaporation – cool temp, high humidity, glasses, bandage contact lens
• &darr drainage – punctal occlusion with collagen implants, cyanacrylate tissue adherent, electrocautrztn, argon laser, surgery
• &darr viscosity – mucolytic acetylcysteine
• retinoids, NSAIDs, steroids

Sjogren’s syndrome

autoimmune multi-sysytem chronic inflm [focal infiltrate + destruction of lacrimal gland = KCS]

• primary +xerostomia
• secondary +Rharthritis

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Watering eye:

Etiology:

1. Hyperlacrimation -
   1. Primary – direct stimulation, early Lgland tumor/cyst, parasympathomimetics
   2. Reflex – irritation to sensory br of trigeminal.N
      • eyelids – meibomitis, stye, entropion
      • conjunctivitis
      • corneal abrasion, ulcer, keratitis
      • scleritis, episcleritis
      • uveitis
      • acute glaucomas
      • end, pan ophthalmitis
      • orbital cellulitis
   3. Central – emotional, hysterical, voluntary
2. Epiphora -
   1. atonia causing lacrimal pump failure [weak orbicularis]
   2. mechanical obstruction to lacrimal passages
      • punctal obstruction – senile lax eversion, chr conj/blepharitis, ectropion, congenital abscence, foreign body/cicatrial closure, prolonged Rx with idoxuridine pilocarpine causes stenosis.
      • canalicular obstruction – foreign body, strictures from inflm[actinomyces] / trauma.
      • lacrimal sac – congenital folds, traumatic strictures, tumor, stones, atonia, dacryocystitis, TB, syphilis.
      • NLD obstruction – congenital non-canalization, imperforated valves, inflm/traumatic strictures, tumor, bone disease.

Evaluation:

diffuse illumination under magnification	reflex hypersecretion causes, punctal obstruction, Lsac swelling
Regurgitation test [press over Lsac]	mucopurulent discharge thr punctum in chr dacryocystitis
Flourescein dye disappearance	retention of dye in conjsacs is due to obstruction to passages
Lacrimal syringing with N.saline into lower punctum under topical anaesthesia 4%xylocain	partial obstruction requires more pressure while syringing for free passage into nose reflux from the same lower punctum indicates lower canalicular obstruction if on repeating the syringing thr upper punctum also causes reflux from opposite lower punctum, then it indicates common canalicular obstruction reflux thr opposite upper punctum indicates NLD/ Lsac obstruction.
Jones dye [flourescein into conjsac, 5min & cotton bud at NLD end]	positive dye stain indicates primary hyperlacrimation negative unstaining indicates epiphora on syringing gives positive stain, then it indicates partial obstruction causing the retained dye in Lsac. still negative unstaining indicates pump failure.
Dacryocystography [Xrays after radioopaque dianosil.condray280 into Lsac]	obstruction extent, fistulae, diverticulae, stone, tumor
Non-invasive Scintillography with radioactive tracer [sulphur, technitium] to visualize passages with gamma camera

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Dacryocystitis: [Lsac inflm]

Congenital dacryocystitis:

etiology:	symptoms:	complications:
NLD obstruction [membranous(mostly at hasner), epithelial debris, non-canlization, bony occlusion] + infection [staph, strep, pneum]	mild chronic inflm epiphora after 7days copious mucopurulent discharge positive regurgitation test [swelling]	recurrent conjunctivitis chronic dacryocystitis abscess, fistulae

Rx:

1. age <8wks : antibiotic drops + massage[hydrostaticP] to open membranous occlusion
2. >2mos: irrigation &uarr HydraulicP
3. >4mos: bowmann’s probe, if unsuccessful silicone intubation of NLD for 6mos.
4. >4yrs: DCR surgery

Adult dacryocystitis:

Chronic [more common]	Acute
Etiology: chronic NLD obstruction &darr mild infection of conjunctiva, nose, sinuses.	acute exacerbation of chronic disesa or direct extension of infection from neighbouring structures
predisposers: 40-60 age, narrow NLD [females, heriditary], poor hygiene. stasis causes- narrow bony canal, partial canalization, mem folds foreign body, polyp, hypertrophied concha, tumor, DNS hyperlacrimation inflmmatory epithelial debris & mucus plugs stenosis from atrophic rhinitis organisms – staph, strep, pneum, pseudomonas, [granulomatous]
Stages:	Stages:
chronic catarrhal - mild inflm of Lsac [red inner canthus] NLD obstruction epiphora- regurgitation test shows clear fluid [few mucoid flakes]	cellulitis- red hot painful firm swelling epiphora constitutional – fever, malaise
mucocoele- swelling just below inner canthus epiphora – regurgitation test shows mucoid discharge [negative regurgitation test is seen in ENCYSTED mucocoele(large fluctuant swelling) due to obstruction of opening of canaliculi into Lsac. Rx: conjunctivocystorhinostomy.	Abscess- canalicular obstruction causes pus to burst Lsac's ant wall forming a fluctuant PERICYSTIC swelling which due to gravity&ligament opens below&out.
Pyocoele- red swelling, epiphora, conjunctivitis regurgitation test shows purulent discharge.	fistula discharging spontaneously.
chronic fibrotic sac- thickenned mucosa from repeated infection [dacryocystography shows a small sac with mucosal folds]
complications: chronic intractable conjunctivitis lower lid ectropion, skin maceration, eczaema corneal abrasions, hypoyon ulcer surgery on unresolved infection causes endophthalmitis, ∴ prior syringing is essentisl.	complications: conjunctivitis lid abscess corneal ulcer facial cellulitis, osteomyelitis, ethmoiditis cavernous sinus thrombosis septecaemia
Rx: recent cases require SYRINGING + topical antibiotics later DCR is essential [DCT indications: aga60, fibrotic Lsac, granulomatous infection, tumor, atrophic rhinitis	Rx: topical&systemic antibiotics for cellulitis abscess requires draining & later DCT/DCR end stage requires fistulectomy with DCT/DCR

DCR:

• general anaesthesia
• skin incision medial to canthus
• expose MPligament & antLcrest
• dissect Lsac
• expose thick oink nasal mucosa
• prepare lacrimal & nasal H-flaps
• suture nasal with lacrimal flaps.

DCT – Lsac is removed & infected NLD parts are curettaged.

Diseases of Vitreous

Vhumor is present in posterior 4/5ths of eyeball cavity

• transparent jelly serving optical function, stabilizing the globe volume, supplies nutrients to lens & retina
• made of collagen fibrils & hyaluronic acid

Synchysis / Liquefaction

• absence of fibrillar structure + presence of pockets of liquefaction [coarse material moving freely]
• causes -
  1. degenerations – senile, myopic, retinitis pigmentosa.
  2. post-inflmm [uveitis]
  3. trauma, thermal, radiation

Vitreous hmmrrg

etiology

• retinal breaks from PVD
• retinal vascular disorders
• necrosis in retinoblastoma
• trauma
• bv erosion in uveitis

CFs- sudden dev of

1. floaters – if small hmmrrg [black shadows in red pupil reflex]
2. painless vision loss – if massive hmmrrg [no red pupil reflex]

Diagnosis – ultrasonography with Bscan.
FATE-

1. complete absorption in 4-8wks.
2. Organization with yellow-white debris in recurrent cases.
3. synchisis, khakhi cell glaucoma, retinitis proliferans, tractional retinal detachment.

Rx-

1. conservative to let blood settle down – bedrest, head elevation, bilateral eye patches
2. treat the cause
3. vitrectomy if no absorption after 3mos.

Pars plana Vitrectomy indications:

1. endophthalmitis
2. V.hmmrrg
3. proliferative retinopathy – DM,ROP,Eale’s, retinitis proliferans
4. complicated retinal detachment [giant tears, large anterior dialysis, traction bands]
5. to remove foreign body/ nucleus / IOL fallen into vitreous.
6. persistant hyperplastic primary vitreous.

Diseases of Retina

ANATOMY:

Innermost, delicate, transparent, purple red[rods], highly developed tissue of eye. 3 regions:

1. OPTIC DISC:
   • pink, defined circle of d=1.5mm
   • nasal to posterior pole
   • physiologic cup is the central depression where retinal bv emerge.
   • all retinal layers except nerves[which enter lamina cribrosa] terminate.
2. MACULA / YELLOW SPOT:
   • 5.5mm dark area at posterior pole.
   • central depression =1.5mm is fovea with shiny foveola which is the most sensitive part of retina & is 2discs temporal + 1mm inferior.
3. ORA SERRATA: firmly attached to vitreous & choroid.

FOVEA has only tightly packed cones [no rods] & other layers are thin. Cone axons are obliquely arranged in HENLE’s outer plexiform.
FOVEOLA has only cones & its nuclei without any other layers.

Blood supply	Layers
Choroidal bv [supply outer 4 layers]	Pigment epithelium [firmly adherent to choroid's BRUCH] Photoreceptor processes Fenestrated external LM Outer nuclear [rods&cones]
Central Retinal bv emerges from cup, devides into 4 end arteries [superior -nasal&temporal, inferior -nasal&temporal] [supply inner 6 layers]	Outer plexifrom Inner nuclear [Bipolar(1st order neurons), Horz, Amacrine] Inner plexiform Ganglion(2nd order neurons) Nerve fibre /stratum opticum [ganglion cells axons pass thr lamina cribrosa to form Optic.N] Internal LM

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Congenital disorders:

COLOBOMA

embryonic fissure closure failure

minor defect presents as inferior crescent

major defect usually presents as inferonasal

DRUSEN

waxy pea-like refractile bodies [initially deep underneath presenting as pseudo-papilloedema]

HYPOPLASIA

small disc with yellow double ring sign.

associated with maternal use during pregnancy- alcohol,DM, drugs.

MEDULLATED / MYELINATED nerve fibres

fetahery margined white patch around optic disc

due to myelination beyond cribrosa

enlarge the blind spot

disappear in demyelinating disorders

PERSISTANT HYALOID ARTERY

Bergmester’s papilla projecting from optic disc

Vascular loop running in vitreous

Mittendorf dot attached to posterior lens capsule [associated posterior polar cataract]

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Inflammatory disorders of retina

• retinitis
• retinal-vasculitis can be primary[EALE's] or secondary to uveitis
• chorio-retinitis
• neuro-retinitis

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Vascular disordes of retina

Retinal artery occlusion

ETIOLOGY

• thrombosis, embolism
• vasculitis [PAnodosa, scleroderma]
• angiospasm [amaurosis]
• raised IOP [acute angle closure glaucoma, in tight encirclage in retinal detachment surgery

CFs

obstruction at the level of cribrosa [CRAO] or at bifurcation [br.A occlusion causing symtoms distally]

symptom- painless sudden vision loss

signs-

• absent direct pupil light reflex
• narrowed retinal arteries but normal veins with cattle track segmented appearance.
• initially milky edematous retina & wks later atrophies.
• cherry red spot in macula due to shinning of vascular choroid thr thin retina

Rx -unsatisfactory due to life of retina<6hrs. Emergency management:

• lower IOP with mannitol, massage, paracentasis.
• vasodil, CO2 for relieving angiospasm
• anticoag for thrombi
• steroids for vasculitis

Retinal vein occlusion

more common than artery occlusions

affects elders>50

ETIOLOGY

• sclerotic retinal artery pressure
• increased blood viscousity
• periphlebitis
• raised IOP in open angle glaucoma
• local causes like orbital cellulitis, cavernous sinus thrombosis.

Non-ischaemic CRVO venous stasis retinopathy [most common]	Ischaemic CRVO Haemorrhagic retinopathy
mild vision loss mild congestion peripheral superficial flame hmrrg mild papilledema	sudden marked vision loss massive congestion massive hmrrg giving splashed tomato appearnace to whole fundus papilledema, soft exudate macula is involved
Late symptoms: sheathing of veins & collaterals partially absorbed hmrrg moderate cases show chronic cystoid macular edema which causes permanent vision loss. [Rx-steroids]	Late symptoms: marked sheathing of veins & collaterals neovascularization macula shows pigmentary changes & chronic cystoid edema
Rx: 50% cases resolve spontaneously	Rx: photocoagulation to prevent neovascular glaucoma

Hypertensive retinopathy

Pathogenesis – fundus changes due to systemic hypertension

1. retinal arteriolar vasoconstriction – related to severity of sysHTN. Occurs in young & affected by involutional sclerosis in old.
2. arteriosclerosis [wall thickening / narrow lumen causes arteriolar light reflex & A-V nipping] – related to duration of sysHTN. Occurs in old due to involutionary sclerosis.
3. Increased vascular permeability [superficial hmrrg, exudates (reversible soft=cotton-wool spots; lipid hard with macular star), focal edema] – due to hypoxia.

Grading -

1	mild general arteriolar attennuation + tortousity with broadening of arteriolar light [silver-wiring]& vein concealment.
2	marked general arteriolar vasoconstriction with A-V nipping [Salu's sign]
3	in addition to Grade2 changes: arteriolar copper wiring distal veins banking [Bonnet sign] vein tappering on either side of A-Vcrossing [Gunn sign] flame hmrrg, cotton-wool spots, hard exudates.
4	Grade3 changes + papilledema

Clinical types:

SysHTN with Senile/involutionary sclerosis	old age augmented arteriosclerotic retinopathy
SysHTN without sclerosis	young with short duration HTN pale staright constricted arterioles with acute angled branching [tortous]
SysHTN with compensatory nehrosclerosis	young with prolonged HTN proliferation & fobrosis of arteriolar media adbanced changes – albuminuric/renal retinopathy
Malignant HTN / Non-compensated nephrosclerosis	young with prolonged HTN papilledema marked areteiolar narrowing flame hmrrg, cotton wool spots.

Retinopathy in PIH:

PIH= HTN, proteinuria, anasarca

retinal changes seen if >160/100

CFs:

nasal arteiolar narrowing, later generalised.

hypoxia from severe persistant spasm causes cotton-wool spots & superficial hmrrg

continued pregnancy causes rapid progression to retinal edema & exudation may be with macular star[discrete hard lipid deposits in macular edema] or flat macular detachment.

Management:

pre-organic changes are reversible after delivery.

terminate pregnancy with hypoxic retinopathy to prevent permanent visual loss.

Diabetic retinopathy

Pre-disposers:

• DM duration irrespective of blood glucose levels – 90% dev after 30yrs, 50% after 10yrs.
• females, pregnancy accelarates.
• hereditary esp for PDR
• HTN

Pathogenesis:

DM causes micro-vascular occlusion by:

• thickening BM
• endothelial damage
• RBC changes & making Plts sticky

occlusion in retinal bv causes retinal ischaemia signs-

• microaneurysms
• hmmrrges
• edema
• hard exudates
• A-V shunts
• neovasclrztn

Clinical types:

1. NPDR:
   • macular microaneurysms [VERY MILD NPDR]
   • hmmrges – deep dot & blot/infarcts , superficial flame
   • hard exudates – waxy yellow-white patches arranged in clumps or circinate pattern.
   • [above 3 signs inMILD NPDR (1,2quadrants); MODERATE NPDR (2,3quadrants)]
   • edema
   • [inaddition to above signs, the following are seen in any 1 in SEVERE NPDR & >2 in VERY SEVERE NPDR]
     • cotton-wool spots [>8mm risk of PDR]
     • venous beading, loops, dilatation
     • AV shunts
2. D.maculopathy: affects vision when there is clinically significant macular edema [due to increased permeability] which meets atleast 1criteria
   1. edema within 500microns from foveola
   2. hard exudates within 500microns from foveola
   3. =/>1disc edema, part of which is within 1disc of foveola

   Flourescein angiography TYPES:

   1. Focal exudative (focal leak) : microaneurysms, hmrrges, macular edema, hard exudates (circinate).
   2. Diffuse exudative (diffuse leak) : diffuse edema, few hard exudates.
   3. Ischaemic (early changes- enlarged foveal avascular zone & capillary dropouts, adv changes- blocked precapillary arterioles) : marked visual loss, microaneurysms, hmrrges, mild macular edema, few hard exudates.
   4. Mixed {ischaemic + exudative}
3. PDR: common in juvenile onset DM.
   • very severe NPDR
   • neovasculrztn [esp temporal - NVD, NVE] – high risk PDR if
     • NVD <1/4disc +/- VH/PRH
     • NVD 1/4 + VH/PRH
     • NVE >1/2 + VH/PRH
   • adv – fibrovascular epiretinal membrane around noevascl due to CT condensation.
4. ADED : due to uncontrolled PDR
   • VH
   • Tractional RD
   • neovascl Glaucoma

Diagnosis:

urine ex, blood glucose levels, fundus flourescein angiography[neovascl, leak, non-pefusion]

Rx:

• strict blood glucose control
• HTN control
• yearly screening [modNPDR -6mos; severeNPDR -3mos; non-high riskPDR -2mos]
• photocoagulation (CI in ischaemic) -
  • panretinal – high risk PDR
  • grid – diffuse macular edema
  • focal – focal exudative Mculopathy
• pars plana vitrctomy – epiretinal membrane,ADED [VH, RD]

Retinopathy of prematurity [ROP]

Etiology-

premature infants[<1.3kg] exposed to high[>30%] oxygen conc in first 5-10wks of life.

Pathogenesis-

bilateral proliferative retinopathy – obliteration followed by neovascl & retrolental fibroplasia.

CFs – 5stages	Rx
1 – demarcation line between vascular & avascular retina.	spontaneous regression in 80-90%cases.
2 – line acquires volume to form a ridge	spontaneous regression in 80-90%cases
3 – extra-retinal fibrovascular proliferation into vitreous	cryo/laser
4 – subtotal retinal detachment from exudate from incompetent bv or fibrous tissue traction a- not involving macula b- involves macula	a- buckling b- vitrectomy
5 – total retinal detachment [funnel]	vitrectomy
3 retinal zones with optic disc as centre:	circle with r= 2times disc-macula distance; severe due to peripheral avascularity inbetween zone when circle is drawn with r=disc-nasal oraserrata. remaining temporal arc outside zone2.
PLUS disease	zone1 with torous dilated bv
RUSH	PLUS + iris neovasclrtn
THRESHOLD	PLUS in 5continous or 8discontinous clock hrs.

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Common retinal dystrophy – RETINITIS PIGMENTOSA

• primary / hereditery – appears in childhood, insidiously progresses to blindness by middle-age.
• pigmentary [rods>cones]
• bilaterally equal
• males

CFs:

symptoms-

• early charecteristic is NIGHT-BLINDNESS due to degeneration of rods.
• increased threshold for dark adaptation.
• tunnel vision n late stage finally lending in blindness.

signs-

• perivacular pigmentary changes resembling bone corpuscles -initially equatorial, later ant&post
• narrow arterioles
• adv – pale waxy disc, optic atrophy.
• Visual field – anular scotoma initially corresponding to eq, later ant&post.
• early ERG changes.

Rx: unsatisfactory.

management with low vision aids

check regression with vasodil, placental extracts, rectus transpltn, light exclusion therapy, vitAE.

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MACULAR DISORDERS

Photoretinitis / solar / eclipse burn

etiology-

IR rays of bright sunlight [or by directly watching sun during eclipse] gets absorbed by pigment eoithelium causing foveola burn.

CFs-

persisting negative after-image of sun progressing later to positive scotoma & metamorphopsia

late sign – macular hole [kidney shaped pigmented spot with yellow-white fovea] & surrounding mottled pigmentation.

Prognosis – guarded since some visual acuity loss mostly persists.

Central serous retinopathy

spontaneous detachment of neurosensory retina in macula due to fluid collection from pigEpi defect.

CFs-

• sudden painless vision loss, positive scotoma, metamorphopsia, micropsia.
• mild macular elevation demarcated by circular ring reflex. Distorted foveal reflex.
• self-resolution after 3wk-1yr may leave small areas of atrophy & pigment changes.

Dignosis- flourescein angiography pattern

• Ink blot – later increass in sige.
• smoke stack – later expands as mushroom cloud.

Rx-

• spontaneous resolution within 3wks-1yr in 80%cases.
• laser photocoagulation – when marked vision loss >4mos, recurrent with vision loss, permanet vision loss in other eye due to CSR.

Cystoid macular edema

fluid collection in henle’s outer plexiform layer around foveola due to innerBRB capillary leak, associated with many disorders:

• post-operative complication of cataract extraction,keratoplasty
• retinal vascular disorders & dystrophies
• uveitis
• adrenaline drops

CFs-

• moderate vision loss
• honey-comb appearance of macula
• flower-petal appearance of macula with flourescein.

Rx-

prophylaxis with anit-PG drops, steroids may help.

Age-related Macular degeneration

bilateral senile macular degeneration

leading cause of blindness in developed countries in age>65yrs.

NON-EXUDATIVE / DRY	EXUDATIVE / WET / NEOVASCULAR
90% ARMD mild visual loss	10%ARMD rapidly progressive marked vision
drusens [colloid bodies] – small discrete yellow-white elevated spots. geographic – pale atrophied pigEpi& irregular / clustered pigmentation.	choroidal neovasc hmmrrgic retinal detachment disciform scarring macular degeneration
Rx is not effective.	Rx : photocoagulation for extrafoveal choroidal neovascl to prevent further vision loss.

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Retinal detachment

neurosensory layer separation from pigEpi in retina.

Primary / Rhegmatogenous

prdisposers: senile posterior viteous detachment peripheral retinal degenerations aphakia myopia trauma

cause retinal tears

causes rapid degeneration of sub-retinal vitreous which sweeps in & separates layers.

CFs-

prodromal symtoms – dark spots, photopsia.

localised visual field loss usually in upper temporal, which progresses to total loss when macula gets involved or sudden painless vision loss due to large central detachment.

signs-

• grey pupil reflex
• raised retina with oscillating folds or funnel shaped total detachment.
• red breaks in upper temporal- round / horseshoe / slit / large anterior dialysis

scotomas & ERG changes

Diagnosis- ultrasonography esf if media is hazy

Rx-

• seal breaks with photo/cryo-coagulation to produce asceptic sclerochoroid.
• scleral buckling/encirclage to reattach retina to sclerochoroid.

Complications in log-standing cases-

• proliferative vireo-retinopathy
• complicated cataract
• uveitis
• phthisis bulbi

Secondary RDs:

Exudative / solid

etiology -retina is pushed away by fliud/neoplasm

• systemic causes – PIH, renal HTN, blood dyscrasias, PAnodosa.
• ocular causes- neop[lasms, inflm & vascular disorders, sudden hypotony from perforation.

CFs- smooth, convex

• shifting fluid withh gravity
• fixed on tumor +/- pigment/neovascl.

Rx- spontaneouly regresses after fluid absorption or tumor enucleation.

Tractional

etiology - vitreo-retinal traction band contraction

• post-traumatic scar
• proliferative diabetic retinopathy, eale's proliferative retinopathy
• post-hmmrgic retinitis proliferans, sickle cell retinopathy
• ROP

CFs-

• vitro-retinal bands with causative lesion
• concave detached area.

Rx- buckling + vitrectomy for bands & internal tamponade.

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Retinoblastoma

most common intraocular tumor of childhood.

congenital neurosensory tumor due to malignant proliferation of retinoblasts [small round cells with large nuclei] which can be

• undifferentiated
• well-differntiated – Flexner-wintersteiner rosette, Homer-wright rosette
• lesion may also show necrosis & calcification.

noticed at age 1-2yrs

unilateral[sporadic cases - 94%], bilateral [familial cases]

4stages:

1. QUIESCENT [lasts 6mos-1yr]-
   • leucoria/amaurotic cat’s eye reflex.
   • convergent squint
   • nystagmus in bilateral cases
   • early tumor growth before leucoria
     • endophytic into vitreous – polyploid, white/pink, cottege cheese like if calcification.
     • exophytic separating retina from choroid.
2. Glaucomatous-
   • severe pain
   • hazy cornea
   • conj redness
   • watering
   • apparent proptosis, raised IOP.
   • masquerading as iridocyclitis.
3. Extraocular extension- rapid fungation into extraocular tissues 7 globe bursts usually at limbus & there is marked proptosis.
4. Metastasis to preauricularLN, contigousspread to opticN & brain, thr blood to bones.

Diagnosis -

• ophthalmoscopy [anaesthesia+mydriasis]
• IOP measurement
• corenal diameter
• Xrays can detect calcification
• raised LDH in AqH
• ultrasonography

Rx-

• early 1stage [<10mm, OpticN uninvolved] – radiotherapy, photocoagulation, cryotherapy.
• late 1 & 2 stages – enucleation & radio+chemo for nerve involvement.
• 3&4 stages – debulking + radio&chemotherapy.
• poor prognosis if nerve & choroid involvement, undifferentiated tumor cells. Hence enucleation before extraocular extension.
• spontaneous regression from necrosis & calcification

D/D of leucoria[yellow-white pupil reflex] causes [PSEUDOGLIOMA] apart from Retinoblastoma:

• congenital cataract
• inflm deposits[uveitis] in vitreous
• toxocara endophthalmitis
• choroid coloboma
• ROP
• exudative retinopathy of coats
• persistant hyperplastic primary vitreous.

DISEASES OF LENS

ANATOMY:

unequally biconvex , transparent, avascular, crystalline.

diameter = 9-10mm; thick = 3.5[birth] 5[adult]

Power = 15D, Accommodation = 15D[birth], 7D[25 age], 1D[50age].

RI = 1.39

STRUCTURE:

1. Capsule – thicker anteriorly.
2. Anterior epithelium – cuboidal [posterior epithelium is absent since used up in filling developmental lens vesicle.
3. Lens fibres - formed from elongation of equatorial epithelial cels & arranged compactly as NUCLEUS [oldest fibres in b layers: Embryonic fibres[meet arount Ysutures], Fetal , Infantile, Adult] & young CORTEX.
4. Ciliary zonules – position lens & exert ciliary ms action.

Cortical METABOLISM:

being avascular depends on aqH chemical exchange for growth & active transport.

anaerobic glycolysis [80%], HMPshunt [15%], oxidative Kreb [little], Sorbital only in cataractproduction in DM & Galactosemia.

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CATARACT

opacification of lens fibres due to :

1. growth disturbance – CONGENITAL [central involving Embryonic / Foetal nucleus] & DEVELOPMENTAL [peripheral : infantile / adult nucleus , deep cortex, capsule]
2. degenerative from either water & electrolyte imbalance or denatured protein -ACQUIRED [Senile, Traumatic, Complicated, Metabolic, Toxic (steroids, myotics, Cu, Fe), with diseases of skin/bone/down's syndrome]

morphologically: polar, capsular, subcapsular, cortical, supranuclear, nuclear.

Etiology:

1. Dominant inheritance
2. Maternal factors – malnutrition; rubella,toxoplasmosis,CMV; steroids; radiation.
3. Foetal factors – anoxia, hypoglycemia, malnutrition, trauma, Down’s
4. 50% idiopathic.

Clinical types:

Congenital – delayed dev of anterior chamber
Acquired – contact with cornea

Clinical type of cataract	Opacity	Etiology	Vision defect
Pulverulenta /Embryonic nuclear	central round powdery	dominant inheritance
Zonular / Lamellar / Foetal nuclear (most common 50%)	ring with riders	dominant inheritance, Vit D, rubella	SEVERE.
Sutural	punctate opacities around Y sutures.
Anterior polar	plaque / pyramid / reduplicated	amterior pole (capsule +/- subcapsular)
Posterior polar (common)	circumscribed circular opacity at posterior pole	incomplete hyalloid bv regression (persistant posterior vascular capsule)
Coronary (common)	radially arranged club shaped opacities at periphery	DEVLOPMENTAL cataract involving adolescent nucleus or deep cortex
Punctate / Blue dot / cerulea	peripheral round blue dots	DEVELOPMENTAL cataract involving adolescent nucleus or deep cortex	diminished vision if associated with CORONARY cataract
Total congenital soft (common)	uni/bilateral soft / liquefied white nuclear cataract which is progressive	dominant inheritance, rubella
Congenital membranous (misdiagnosed as congenital aphakia)	thin membranous or fine transparent capsule	total or partial absorption of congenital cataract.

Rx:

• ignore if cataract is small
• iridectomy or mydriatic to improve vision in incomplete central cataract.
• remove in few wks after birth if complete cataract
• Surgical procedures – Intracapsular capsular cataract extraction [antrior capsulotomy, phacoemulcification, posterior chamber IOL implantation]
• Aphakia in child <5yr corrected with extended wear contact lens & in child with age >5yr corrected with posterior chamber IOL.

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SENILE CATARACT

age related degeneration in >50yr age & usually unequally bilateral.

Factors influencing onset & maturation:

1. genes
2. UVrays
3. diet – proteins, Vit E C riboflavin , essential elements
4. severe dehydration

CORTICAL / SOFT cataract	NUCLEAR / HARD cataract
PATHOGENESIS: diminished active transport causing decrease in proteins & [K]+ but increase in [Na]+&water which denatures colloid into soft lens.	PATHOGENESIS & MATURATION: increased sclerosis causing dehydration-compaction & increased insoluble proteins which make the lens hard progressing from centre to periphery except for a cortical rim.
MATURATION STAGES
Reversible lamellar separation of cortex due to fluid	hard lens is inelastic leading to decrease in accommodation / increased myopia & obstructing light.
INCEPIENT cataract has small early opacities with clear areas inbetween. 2 types: CUNEIFROM [70%]- peripheral & radially arranged wedge opacities initially in inferior nasal [late vision loss] CUPULIFORM [5%] – posterior subcapsular cataract causing early vision loss due to axial rays obstruction.	25% common
IMMATURE cataract is irregularly diffuse opacity of both nucleus & cortex but with inbetween clear cortex [thus iris shadow] still visible. INTUMESCENT cataract sometimes forms due to continued hydration & swelling up of lens with water clefts in cortex. [shallow anterior chamber]	Grey opacity or pigmented [brown, black, red]
MATURE / RIPE cataract is a complete pearly white opacification of lens.
Hypermature: MORGAGNIAN – milky liquefication of cortex & brown nucleus settles at bottom. SCLEROTIC – disintegration of cortex + water leakage causes the lens to shrink & the capsule is wrinkled+thickened.

Symptoms:

1. earliest symptom – Glare [intolerance to bright light]
2. other early symtoms – Blurring & polyopia due to variable RI.
3. Colored halos due to refraction thr water in lens.
4. Black spots.
5. Slow painless progression of vision loss to end light perception only
   1. early in Cupiliform [day blindness]
   2. late in Cuneiform [night blindness]
   3. second sight in Nuclear [increased near vision]

Signs:

1. Visual acuity
2. Oblique ight beam on pupil -
   1. in immature cataract [clear cortex still seen] a crescentic pupillary iris margin is seen on grey opacity of lens [absent if lens is completely trasparent or opaque]
   2. reveals color of lens in pupillary area.
3. Distant direct ophthalmoscopy shows a black shadow of partial cataract on red fundal reflex.
4. Slit lamp examination in a mydriatic eye shows morphology of opacity.

Non-surgical Rx:

1. treating cause of acquired cataract – DM, uveitis, steroids, miotics, radiation
2. Delay progression with [I]- salts, vitE, aspirin
3. Improve vision in Incipient & Immature cataract by
   1. correcting refraction
   2. varying illumination [bright for peripheral opacity; dull /dark goggles for central]
   3. mydriatic [phenylepherine, tropicamide] for Cupuliform axial cataract

Surgical Rx:

Indications for surgery:

1. visual acuity < 6/36
2. lens induced glaucoma, phacoanaphylactic endophthalmitis, Dretinopathy, Retinal detachment
3. cosmetic reason for black pupil

Pre-operative evaluation:

1. no DM, HTN, cardiac disease, obstructive lung disease, infection in gums/UT
2. no local infection in conj, meibom, bleph, lacrimal
3. Intact retinal function
   • positive light perception
   • negative Marcus Gunn pupillary response due to defective afferrent pathway
   • positive for Projected rays for peripheral retina function
   • 2 light discrimation [2" apart & 2ft far] for macular function
   • positive perception of distant bright light as red line with Maddox rod
   • color perception for optic.N
   • ectopic visualization – point light on closed eyelids perceived as black retinal bv
   • Objective tests – laser interferometry, ultrasonic, ERG, EOG, VER, Indirect ophthalmoscopy
4. Slit lamp examination of anterior segment for KPs, corneal endothelium condition
5. measure IOP

Pre-operative medication:

1. Endophthalmitis prophylaxis – topical tobramycin [QD 3days], i.m Gentamycin [night & morning before]
2. lower IOP – stat acetazolamide/mannitol/glycerol
3. dilate pupil – anti-PG drops [indomethacine, flubriprofen TD 1day + evry 30min 2hrs before] , mydriatic [tropicamide, phenylephrine every 10min for 1hr]]

Surgery : done under local anaesthesia.

INTRACAPSULAR CATARACT EXTRACTION	EXTRACAPSULAR CATARACT EXTRACTION
removal of cataract with capsule	removal of cataract but leaving behind intact posterior capsule
Indications: zonule rupture due to marked subluxated & dislocated lens >50 age with weak zonules when microsurgery / trained surgeon unavailably [developing countries]	Indications: posterior chamber IOL implantation high myopia & degenerated vitreous <40age with strong zonules H/O vitreous prolapse , aphakic retinal detachment
Contra-indications: <40age with strong zonules	Contra-indications ruptured zonules in subluxated & dislocated lens
Complications: endophthalmitis cystoid macular edema retinal detachment vitreous herniation into anterior chamber, pipillary block, touch syndrome	Complications: posterior capsule opacification

ECCE:

1. down gaze fixed with superior rectus bridle suture
2. conjunctival flap to expose limbus
3. heat cautery for haemostasis
4. limbal partial thickness groove [10-2 O'] with razor blade knife
5. anterior capsulotomy
   • can-opener technique – 360. radial cuts with cystitome
   • linear / envelope – only 10-2 incision
   • capsulorrhexis – torn circularly
6. Removal of anterior capsule with Kelman-Mc Pherson forceps
7. Corneo-scleral section [10-2] with enlarging scissors
8. Hydro-dissection with balanced salt soln to separate anterior capsule from lens
9. Removal of nucleus with pressure-counterpressure or irrigating wire vectis loop
10. Cortex aspiration with 2way irrigating aspirating canula
11. Close incision with 5-7 interrupted sutures
12. Conj flap reposited with 2sutures
13. subconj inj of dexamethosone & gentamycin
14. patching with pad & bandage

Phacoemulsification:

1. 3mm corneo-scleral section which is self-sealing.
2. anterior capsulotomy with capsulorrhexis
3. hydro-dissection [separate anterior capsule] & hydro-delineation [separate nucleus]
4. phaco-emulsification with ultrasonic vibrator using divide into 4quadrants & conquer rule.
5. cortex aspiration

IOL implantation:

IOL power is calculated with biometer of A-scan ultrasound machine.

Indications – [PRIMARY] unilateral catarcat removal in developing countries, [SECONDARY] correcting aphakia

foldable IOL is made of silicone / acrylic

most commonly used is Posterior chamber modified C loop IOL [central optic + superior&inferior haptics]- horizontally placed behind iris supported in posterior capsular bag

post-operative complications are high for anterior chamber IOL[in front of iris supported in angle] & iris supported IOL [fixed on iris with sutures,loops, claws].

Post-operative measurs:

3hrs still on back without oral intake

diclofenac inj if mod-severe pain

next morning check for complications after removing bandage

cyclopentolate+antibiotic+steroid oint for 3days

tinted glass + antibiotic-steroid drops for tapered from 4 to 1 times/day for 2wks each

after 6wks remove sutures

after 8wks final spectacles

COMPLICATIONS:

Preoperative	Mangement
anxiety	diazepam at bedtime
nausea/gatritis from acetazolamide, glycerol	antacids, omission of cause
allergic/irritative conjunctivitis from topical antibiotics	withdraw cause potpone surgery for 2days
corneal abrasion from tonometry	antibiotic patching 1day postpone surgery for 2days
retrobulbar local anaesthesia may cause retrobulbar haemorrage oculocardiac reflex perforation subconj haemorrgae posterior dislocation during massage due to degenerated zonules with hypermature cataract	pilocarpine + immediate pressure bandage + surgery posponed 1wk atropine i.v prevent by peribulbar blunt-needle anaesthesia minor so ignore removed by vitrectomy only if it causes uveitis/glaucoma
Operative	Management
superior rectus laceraton from bridle suture	ignore
excessive bleeding from conj flap or incision into anterior chamber	cautery
irregular incision from blunt instruments causes coaptation of wound
sharp instrument during anterior chamder entry may injure cornea, iris, lens	gentle handling with hypotony
vitreous loss due to posterior capsule rupture[most serious complication]	prevent with preoperative hyperosmotic [mannitol, glycerol], lower IOP [acetazolamide, massage], better anaesthesia. minimise external pressure by gentle handling during surgery. fleringa ring in myopic to prevent scleral collapse anterior hyaloid face rupture form unavoidable high IOP can be prevented by posterior sclerotomy with vireous drainage from pars plana. after vitreous loss, partial anterior vitrectomy for clearance from anterior chamber & preventing post-operative complications [updrawn pupil, iris prolapse, touch syndrome]
choroidal haemorrhage [most serious complication]in HTN, arteriosclerosis. occurs immediately / postoperatively [gaping followed by expulsion of lens, citreous, retina, uvea, blood.	drain blood with equatorial sclerotomy; most times eye is lost requiring evisceration.
Early postoperative	Management
hyphaema from minor trauma	if spontaneously not absorbed & causes IOP rise, acetazolamide , mannitol, glycerol ; after a wk Paracentesis.
Iiris prolapse from inadequate suturing	if small & early, reposited & sutured. if large & late, abscission & suturing.
Striate keratopathy [mild corneal edema + descemet folds] due to endothelial damage	if spontaneouslt does not disappear n a wk, hypertonic saline + steroids. penetrating keratoplasty for bullous keratopathy.
flat anterior chamber [rare] due to woundleak >associated hypotony diagnosed with SEIDEL’s test [fluorescein into lower fornix + blink ---> incision seen as diluted AqH in slit-lamp cobalt blue. ciliochoroidal detachment [brown convex mass] pupil block due to vitreous bulge leads to iris bombe —> peripheral anterior synechiae —> angle closure glaucoma	pressure bandage + acetazolamide. If persisting, air is injected in anterior chamber + resuture wound. pressure bandage + acetazolamide. If persisting, suprachoroidal drainage + inject air into anterior chamber. initially with mydriatic +hyperosmotic + acetazolamide. later bypass by peripheral iridectomy.
Bacterial endophthamitis [most dreaded, incidence <0.5] from contamination with flora. ‘[pain, diminished vision, lid edema, conj chemosis, circumciliary congestion, corneal edema, pupil exudates, hypopyon, diminished red reflex]	emergency – frill evisceration to prevent intracranial spread.
Late post-operative [after wks,yrs]	Management
Cystoid macular edema [significant only if dimished vision, diagnosis: fundoscopy - honeycomb pattern of cycstic loculi fluoroscein angiography - flower petal pattern due to perifoveal capillaries dye leak.	Prophylaxis pre& post-operative anti-PGs [indometh, flurbip]
Retinal detachment
Conj epithelial ingrowth
Vitreous touch syndrome [corneal edema -->bullous keratopahty] [IRVINE GASS syndrome = triad of vitreous touch, bullous keratopathy, cystoid macular edema]
Fibrous downgrowth due to imperfect wound apposition —> glaucoma, anterior segment disorganisation, phthisis bulbi.
After cataract = secondary opacification after catarcat lens extraction due to residual opaque lens matter thickened posterior capsule dense membranous Soemmering’s ring between capsules Elschnig’s pearls along posterior capsule as clusters of vacuolated epithelial cells	capsulotomy membranectomy If central posterior capsule is clean, no treatment is required. capsulotomy
Glaucoma in aphakia
IOL related	Management
high with ACIOL & ISIOL: cystoid macular edema, corneal damage, glaucoma, uveitis
Malpositioned IOL : subluxated – sunset, sunrise syndromes. dislocation into vitreous – lost lens syndrome small IOL placed vertically – windshield wiper syndrome
Toxic lens syndrome [uveitis] from sterilizing agent or implanted lens material itself

Diseases of Cornea

Applied Anatomy:

• anterior 1/6th eyeball’s fibrous coat.
• 5layers:
  1. Str-sq-E
  2. Bowmann’s layer [condensed collagen]
  3. Stroma [0.5mm] – has collagen lamellae [arraged parallel to adj lamellae & perpendicular to alt layers], proteoglycans, macrophages
  4. Descemet’s membrane -strong & very resistant to chemicals/ trauma/ pathological changes, can regenerate, peripherally ends as Schwalbe’s line at anterior limit of trabecular meshwork.
  5. Endothelium – hexagonal cells giving mosaic appearance, lost with age [but only after 75% loss, affects active pump function]
• thickness = 0.52 [centre] – 0.7[periphery]
• anterior elliptical surface’ s horizontal diameter in adult / by 2yrs = 11.7mm; at birth = 10mm.
• central area of 5sqmm is powerful refraction surface = 45D [3/4th total 60D of eye]
• refracting medium is due to transparency maintaimed by stromal lamellar arrangement, avscularity & dehydration from barrier effect [endo & epithelium] & active [HCO3-]pump. This requires metabolic energy [in epithelium is 10times that in endothelium] from glucose [through aqH & perilimbal bv] & oxygen [active epithelial uptake from air]
• avascular with only anterior ciliary.N innervation; subconjunctiva overlapping peripheral cornea has anterior ciliary bv loops invading about 1mm

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Congenital anomalies:

CLOUDY:

D/D: [STUMPED] sclerosis, tears in descemet, ulcer, metabolic, posterior corneal defect, endothelial dystrophy, dermoid.

Megalocornea: [often associated with Marfan's]

diameter at birth = adult 11.7 or at 2yr >13mm.

D/D: buphophthalmos [IOP raised & cloudy due to Haab's striae in descemet], Keratoglobus [normal diameter but protruded]

Microcornea:

<10mm

Cornea plana:

flat & results in high astigmatism [<45D]

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Corneal inflammations: KERATITIS

• edema
• infiltrate
• congestion

Classification:

Morphological:

Ulcerative:

1. central; peripheral
2. purulent [bacterial,fungal]; non-pur [chlamydial, viral, allergic]
3. simple; hypopyon
4. superficial, deep, perforated
5. non; sloughing

Non-ulcerative:

1. superficial – diffuse; punctate
2. deep – nonsup [interstitial, discifrom, sclerosing, keratitis profunda]; suppurative [meatstatic abscess- central; posterior]

Etiological:

1. Infective – bacterial, viral, fungal, chlamydial, protozoal, spirochaetal
2. Allergic – phlyctenular, vernal, atopic
3. Trophic – exposure, neuroparalytic
4. skin disease associated
5. collagen vascular disorder associated
6. Traumatic – mechanical, chemical, thermal
7. idiopathic – Mooren’s, superior limbic keratoconj, Thygeson superficial puctate keratitis

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Bacterial corneal ulcer:

Etiology:

1. Epithelial damage: abrasion [foreign body, cilia, concretion, trauma], dryness [xerosis, exposure], trophic [neuroparalytic], necrosis [keratomalacia], desquamation [edema]
2. Infection: [rare endogenous since avascular], exogenous sources like conj, sclera, uvea, lacrimal sac, foreign body, water, air.
3. Organisms: staph, strep, pseud, Ecoli, Pr, Kl, virulent ones like Neisseria & Coryne even thr intact epithelium.

Pathology:

Localised ulcer:

1. Progressive infiltration – into epithelium from circulation.
2. Ulceration -
   1. grey swelled [infiltration & exudation] walls & floor of ulcer.
   2. necrosis & sloughing of epi, Bowman’s, stroma.
   3. circumcorneal hyperaemia – leading to purulent exudates on cornea.
   4. toxic congestion of iris & ciliary body – leading to exudation into anterior chamber [hypopyon]

   extension leading to diffuse superficial ulceration or deeper penetration to desmetocele / perforation.

3. Regression – induced by treatment / immunity, line of demarcation around ulcer with WBC phagocytosing organisms & necrotic debris, results in initial enlargement of ulcer & superficial vascularization that boosts immune response causing healing.
4. Cicatrization – progressive permanent epithelialization & underneath fibrosis thickens stroma & pushes up epithelium. Scarring does’nt occur if only epithelium is involved, but with other layers, opacities form [NEBULA -Bowmann,few lamellae; MACULA -1/3rd stroma; LEUCOMA ->1/2 stroma]

Perforated ulcer:

• deeper upto descemet which is tough so bulges as desmetocele
• perforates on exertion resulting in aqH escape & fall in IOP & iris [lens diaphragm] falls forward & plugs the perforation [if small & opposite] & healed by cicatrization = ADHERANT LEUCOMA

Sloughing ulcer:

• with virulent organism or low immunity.
• complete cornea except for the rim sloughs & total iris prolapse occurs
• iris inflames & exudates cover iris & block pupil, this organizes to thin fibrous layer over which corneal/conj epithelium grows & forms PSEUDOCORNEA.
• this thin false cornea with the plastered iris behind, due to IOP bulges forward = ECTATIC CICATRIX = ANTERIOR STAPHYLOMA which is lobulated due to scar bands & blackened with iris tissue.

Symptoms & signs:

depend on virulence of organism & host immunity.

1. Pain – due to swollen lids, blepharospasm & toxic effect on nerves.
2. reflex hyperlacrimation
3. Photophobia -ambient light intolerance to nerves.
4. redness due to ciliary congestion, conjunctival hyperaemia & chemosis.
5. Blurred vision – due to corneal haze [rough yellow white ulcerative areas]
   1. staph – oval & opaque
   2. Pseudomonas – irregular with green pus & ground glass surrounding
   3. enterobacteriae – shallow with grey pus & diffuse opacity & ring corneal infiltrates may be present due to endotoxins.
6. muddy iris & small pupil due to toxin induced waterlogged iritis
7. hypopyon corneal ulcer shows marked clinical features. It is more common in old debilitated & alcoholic & esp with pneumococci & Pseudomonas pyocyanea, other pyogens. Mechanism – when toxin induced iritis[sterile] is severe, there is outpouring of infiltrate from bv & gravitate into anterior chamber. When ulcer heals, it gets absorbed
   • Ulcus serpens is characteristic hypopyon caused by Pneumococcus. It is a grey/yellow disc near corneal centre, with one edge cicatrized & other edge shows infiltration along which serpiginous spread over cornea occurs.

Complications:

1. Toxic iridocyclitis – due to absorption of toxins in anterior chamber from purulent corneal ulcer.
2. Secondary glaucoma – from fibrinous exudates blocking the angle.
3. Descemetocele – usually due to virulent organism; associated with severe pain & is an impending perforation.
4. Perforation of corneal ulcer – sudden strain like cough,sneeze, orbicularis ms spasm bursts impending perforation & relieves pain with oozing aqueous. Sequelae:
   • Iris prolapse – to plug the perforation.
   • Subluxation / anterior dislocation of lens – due to sudden stretching & rupture of zonules.
   • Anterior capsular cataract – due to lens coming in contact with the lens through pupil.
   • Corneal fistula – when iris plug is not formed, aqueous leaks through fistula continously.
   • Secondary infection leading to uveitis, endophthalmitis, panophthalmitis.
   • Vitreous or choroidal haemorrage due to sudden lowering of IOP.
   • Corneal scarring from healed ulcer causes permanent visual impairment [nebula, macula, leucoma, ectatic cicatrix / kerectasia, adherent leucoma / anterior staphyloma.

Management:

Ocular examination:

gross lesions in diffuse light.

regurgitation & syringing of lacrimal sac.

biomicroscopic examination of ulcer with fluorescein dye.

scraping the ulcer base & margins with kimura spatula / 20G hypodermic needle for Gram, Giemsa, KOH, Calcofluor white, blood agar, SDagar.

Rx:

Uncomplicated corneal ulcer: urgent eradication of infection since vision threatening.

Specific treatment:

1. Local broad spectrum antibiotics -
   • topical drops of fortified gentamycin+cephazoline every 1hr for first few days then diluted drops & every 2hr.
   • ointment at night.
   • for sloughing ulcer - subconjunctival injection of gentamycin+cephazoline daily for 5days.
2. Systemic antibiotics for fulminating perforation.

Non-specific treatment:

1. Cycloplegics - to prevent ciliary spasm pain, posterior synechia & relieve anterior ciliary.A [increase antibodies & reduce exudation]
2. Systemic NSAIDs
3. Vit A,B,C for hastening healing.

General measures:

1. Hot fomentation
2. Goggles from strong light
3. Bandage if no acute conjunctivitis & copius discharge.

Non-healing corneal ulcer:

removal of know causes:

1. Local causes – raised IOP, concretions, misdirected cilia, foreign body, dacryocystitis, lagophthalmos, vascularization, inadequate therapy, wrong diagnosis.
2. Systemic causes – DM, anaemia, malnutrition, chronic diseases, systemic steroids.

Debridement: scraping necrosed debis from ulcer floor to hasten healing

Cauterisation

Peritomy : for excessive vascularization

Impending perforation: prevent perforation & its complications.

Strict bed rest – avoid sneezing, coughing, straining during stool.

Pressure bandage for external support.

Lowering IOP with acetazolamide, mannitol, glycerol, timolol, paracentesis.

Tissue adhesive glue like cynoacrylate.

Conjunctival flap, bandage soft contact lens for corneal support.

keratoplasty [tectonic graft]

Perforated corneal ulcer:

Tissue adhesive glue like cynoacrylate.

Conjunctival flap, bandage soft contact lens for corneal support.

best is an urgent keratoplasty [tectonic graft]

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MYCOTIC CORNEAL ULCER

Etiology:

Common causative fungi: Aspergillus, Cnadida, Fusarium

Infection mode: injury from vegetative matter or animal tail, systemic / local (eye diseases) immunosuppression.

Catalysts: antibiotics (disturb symbiosis between bacteria & fungi), steroids (fungi shift from symbiosis to facultative saprophytes).

Clinical features:

Symptoms are similar to central corneal ulcer but are less marked & with indolent course : pain, redness, watering, photophobia, blurred vision.

Typical signs of ulcer: dry grey rolled out margins with stromal feather like extensions. Usually a big hypopyon is present which is non-sterile since fungi penetrate anterior chamber without penetration. Yellow immune ring & Satellite lesions may be present.

Lab Diagnosis: KOH, Calcoflour, Gram. Giemsa for fungal hyphae & Sabourauds agar culture.

Rx:

Anti-fungals

Non-specific: cycloplegics, NSAIDs, vit A B C, dry hot fomentation, dark goggles, bandage.

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VIRAL CORNEAL ULCERS

Viruses tend to affect epithelium of conjunctiva & cornea, hence VIRAL KERATOCONJUNCTIVITIS.

Herpes simplex : extremely common

Etiology:

1. HSV – DNA virus. Man is the only host. Epitheliotropic, but may become neurotropic
2. HSV1 causes infection above waist through close contact like kissing.
3. HSV2 causes infection below waist(genitals), ocular infection in neonates during parturition of infected mother.

Clinical features:

Primary herpes:

self-limiting disease of childhood but latent in trigeminal ganglion.

1. periorbital skin lesions : vesicular
2. acute follicular conjunctivitis
3. epithelial keratitis – punctate or diffuse

Recurrent herpes

Periodic reactivation of latent infection usually with UV rays, fever,chr diseases, exhaustion, trauma,mestrual stress, immunosupression.

Epithelial keratitis:

pain, lacrimation, photophobia.

• 1. punctate epithelial keratitis
  2. Debdritic ulcer – linear branching with knobbed ends; diminshed corneal sensations; flourescein stains floor & rose bengal stains viruses at margin.
  3. Geographical ulcer – amoeboid; hastened formation by steroid use in dendritic ulcer.
  4. Rx:
     1. Antivirals for 7days (idoxuridine, triflurothymidine, vidarabine, acyclovir)
     2. If resistance / allergy to antivirals / non-compliance : Mechanical debridement with cotton : involved & surrounding area.

  Stromal keratitis:

  1. Disciform :
     • focal disc like patch of edema due to delayed hypersensitivity ot virus; accompanying iritis, KPs, dimished corneal sensations.
     • mild pain, watering, marked vision loss.
     • Rx: diluted steroid drops 5times/day, Antivirals 2times/day [if with epithelial keratitis, use 5days before steroid use.
  2. Diffuse :
     • invasion + necrosis + blotchy white infiltrates under ulcer + [iritis + KPs + stromal vascularization
     • pain, redness, photophobia
     • Rx: similar to disciform but unsatisfactory; Keratoplasty in quiet eye.
  • due to mechanical healing problem of previous herpetic ulcer.
  • indolent linear / oval epithelial defect.
  • Rx: to promote healing - artificial tears, soft contact lens, lateral tarsorrhaphy.

Sterile trophic / Meta-herpetic

Iridocyclitis

Herpes zoster : Gasserian ganglion[5th.N] infection

Etiology:

• Varicella zoster – DNA virus. neurotropic.
• childhood infection leaves latent virus in sensory ganglion of trigeminal which gets reactivated in old age / decreased cell-mediated immunity to travel down ophthalmic N divs.

CFs:

• unilateral side of head with frontal.N div affected more than lacrimal or naso-ciliary.N
• 50% cases show ocular manifestations esp if (cutaneous involvement of naso-ciliary.N) side/tip of nose presents vesicles [HUTCHINSON'S rule]
• General symptoms: sudden fever, malaise, characteristic neuralgia.
• after 3days & for 3wks, periorbital skin lesions : red & edematous –> vesicles –> pustules –>ulcer crusts –> pitted scars.
• severe neuralgia & anaesthesia diminish after eruptive phase. If persistant called post-herpetic neuralgia & anaesthesia dolorosa.
• Ocular lesions after eruptive subsidence & as 2 or more of:
  1. Conjunctivitis [most common]- mucopurulent with petechiae, acute follicular with lymphadenopathy.
  2. Keratitis [40% , may precede neuralgia/eruptions]-
     1. puctate epi
     2. MICROdendritic ulcer [peripheral stellate]
     3. Nummular [33%] – multiple tiny granular deposits with stromal hazy halo
     4. Disciform [50%] – always preceded by nummular.
     5. Neuroparalytic ulcers – from Gasserian destruction.
     6. Exposure keratitis – due to facial palsy.
  3. Scleritis, episcleritis [50%]
  4. Iridocyclitis [+hypopyon/hyphaema]
  5. Phthisis bulbi – from necrosis / vasculitic ischaemia.
  6. Secondary Glaucoma – from trabeculitis / synechia.
• Neurological: motor.N [3,4,6,7] palsy, optic neuritis, encephalitis in severe cses.

Rx: vigorous to prevent scarring, post-herpitic neuralgia, devastating complications.

• NSAIDs for initial 2wks [pethidine if severe pain]
• systemic acyclovir 5daily/10days – started with rash appearrance.
• steroid+antibiotic skin ointment 3times/day
• systemic steroids – for neuro complications [post-herpetic neuralgia, palsy, neuritis]. CI- in old age.
• cemitidine – for pruritis
• amytriptyline
• Keratitis, Iridocyclitis, Scleritis – topical steroid, acyclovir, cycloplegics.
• Glaucoma – timolol, acetazolamide.
• Neuroparalytic ulcer – lateral tarsorrhaphy
• visual rehabilitation of scarring – keratoplasty

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Allergic keratitis

-phlyctenular, vernal, atopic.

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TROPHIC CORNEAL ULCER

due to epithelial metabolic disturbance.

Neuroparalytic keratitis:

Pathogenesis:

due to corneal sensory.N [5th] paralysis causing antidromic corneal reflex disturbances leading to epithelial metabolites accumulation –> edema, exfoliation, ulceration.

Congenital causes:

dysautotomia, pain insensitivity

Acquired causes:

Alcohol block / electrocoagulation / external tumor pressure / injury / leprosy, syphilis, Hsimplex, Hzoster destruction of Gasserian ganglion

sensory root section of trigeminal.N for neuralgia

CFs: [relapses are common]

loss of corneal sensations

marked ciliary congestion

interpalpebral punctate epithelial erosions & ulceration

Rx: [slow healing]

antibiotic + atropine ointment

lateral tarsorrhaphy for relapses + artificial tears

Exposure keratitis

Causes for lagophthalmus:

Extreme proptosis, facial palsy, severe ectropion, symblepharon, deep coma, during sleep

Pathogenesis:

interpalpebral dry epithelium –> dessication —>cast off —>invasion.

CFs:

punctate epithelial keratitis, necrosis, ulceration, vascularization. [bacterial superinfection - deep ulcer, perforation]

Rx:

artificial tears, soft contact lens for moderate exposure, bandage during sleep, treat cause of exposure or in untreatable cases tarsorrhaphy

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Idiopathic corneal ulcers

Mooren’s ulcer / Rodent / Chronic serpiginous

Etiology:

degenerative due to vasculitic ischaemea, conjunctival collagenase, autoantibodies.

CFs:

BENIGN – unilateral, indolent, in old age

VIRULENT – bilateral, rapidly progressive with scleral involvement, in young age

• symptoms – severe pain, photophobia, lacrimation, defective vision
• signs – initial grey patchy infiltrates on peripheral cornea which coalesce to form superficial ulcer over whole cornea with white overhanging edge & vascularized base.

Rx: unsatisfactory

topical steroids, conjunctival excision & recession, topical collagenase inhibitors, immunosupressants, soft contact lens for pain, graft.

Non-ulcerative : SUPERFICIAL PUCTATE KERATITIS

multiple spotty lesions [puctate erosions, punctate keratitis, filamentary keratitis] in epithelium, Bowmann’s & superficial lamellae.

some Causes:

• Viral – Hsimplex, Hzoster, adeno
• chlamydial
• staph toxin
• Trophic keratitis
• allergic[vernal] or irritative[idoxuridine]
• skin disorders like acnerosacea & pemphegoid
• Keratoconjunctivitis sicca
• Idiopathic – thygeson’s, theodore’s
• photoophthalmitis

CFs:

pain, photophobia, lacrimation, conjunctivitis

Rx: symtomatic

topical steroids, artificial tears, treat cause.

PHOTO-OPHTHALMIA

cause:

UV rays, short circuit, welding, snow

CFs:

latency 5hrs. multiple epithelial erosions. burn, lacrimation, photophobia, blepharospasm, palpebra conjunctival swelling, retrotarsal folds

Rx:

Crooker’s glass, cold compresses, antibiotic bandage.

Non-ulcerative Non-suppurative Deep keratitis : INTERSTITIAL KERATITIS

inflammation of stroma without primary involvement of epithelium or endothelium : causes – syphilis, TB, leprosy, sarcoidosis, malaria, trypanosomiasis, COGAN’s syndrome [interstitial keratitis, tinnitus, vertigo, deafness]

Syphilitic / leutic interstitial keratitis

hypersensitive inflammation to new little invasion after foetal treponema exposure

90% congenital (manifests after 5-15yrs)- bilateral ; acquiredc – unilateral.

Tuberculous interstitial keratitis

unilateral & sectorial usually lower cornea.

CFs:

• late manifestation or part of HUtchinson’s triad [I.keratitis, H.teeth, vestibular deafness]
• PROGRESSIVE stage [2wks]- deep stroma & endothelial edema, pain,lacrimation, photophobia, circumcorneal injection, diffuse corneal haze
• FLORID stage [2mos]- deep vascularization [salmon patch appearance due to corneal haze], Epulit at limbus from heaping of superficial vascularization & conjunctiva.
• REGRESSION stage [1-2yrs]- inflm resolves slowly from periphery due to vascular invasion, leaving behind some opacities & ghost vessels.

Rx:

1. LOCAL- topical steroids & cycloplegics
2. SYSTEMIC- penicillin for syphilis, anti-tubercular drugs for TB.

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CORNEAL DEGENERATIONS

Age related degenerations:

1. Arcus senilis
2. Vogt’s white limbal girdle
3. Hassal-Henle bodies

Pathological degenerations:

1. Lipoid keratopathy / Fatty degeneration
2. Band keratopathy / Calcific degeneration
3. Salzmann’s nodular degeneration
4. Furrow degeneration / senile marginal degeneration
5. Keratotorus / Pellucid marginal degeneration
6. Terrien’s marginal degeneration

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CORNEA DYSTROPHIES

Anterior dystrophies:

1. Epithelial basement membrane dystrophy
2. Reis-Buckler dystrophy
3. Meesman’s dystrophy / Juvenile epithelial dystrophy
4. Stocker-Holt dystrophy

Stromal dystrophies:

1. Granular dystrophy / Groenouw 1
2. Macular dystrophy / Groenouw 2
3. Lattice dystrophy
4. Schnyder’s crystalline dystrophy

Posterior dystrophies:

1. Cornea guttata
2. Fuchs epithelial-endothelial dystrophy
3. Posterior polymorphous dystrophy
4. Congenital heriditary endothelial dystrophy [CHED]

Ectatic dystrophies:

1. Keratoconus
2. keratoglobus

Diseases of Uveal tract

APPLIED ANATOMY

UVEA is middle vascular coat of eyeball & from anterior it is divided to 3 as IRIS, CILIARY BODY, CHOROID.

IRIS

• thin circular disc peripherally attached to ciliary body & with a 4mm aperture PUPIL to regulate light reaching retina.
• anterior surface has a zig-zag line COLLARETTE which divides ciliary & pupillary zones.
• ciliary zone has radial streaks due to radial bv & 2rows of crypts.
• pupillary zone is smooth.
• 1st layer: Anterior limiting layer – has melanocytes & fibroblasts. It is thin in blue iris & thick in brown iris.
• 2nd layer: Stroma – has sphincter & dilator pupillae muscles, bv, nerves, WBC, fibroblasts.
• 3rd layer: Anterior Epithelial layer – continuation of pigment epithelial layer of ciliary body.
• 4th layer: Posterior Epithelial layer – continuation of nonpigment epithelial layer of ciliary body & peripherally forms PIGMENT FRILL of pupil.

CILIARY BODY

• aneriorly forms angle of chambers & has iris attachment.
• outer side is adjacent to sclera with suprachoroidal space inbetween.
• inner side is PARS PLICATA (finger-like Ciliary process) 2mm anteriorly & smooth PARS PLANA 4mm posteriorly.
• 5 layers: Supraciliary lamina (pigmented collagen), Stroma (ciliary muscle, bv,N, collagen, pigment cells), Pigment epithelium, Nonpigment epithelium, Internal limiting membrane.
• Ciliary process is the site of aqueous production.
• Ciliary muscle occupies outer part of ciliary body with parasym supply from short ciliary.N & it is a nonstriated ms with 3 parts: longitudinal & radial help in aqueous outflow, circular helps in accommodation.

CHOROID

• extends from optic disc to ora serrata.
• 1st layer: Suprachoroidal lamina – pigmented collagen. Outer space between it & sclera contains long & short Posterior ciliary bv & N.
• 2nd layer: Stroma – main bulk is formed by bv arranged in 3layers. It also has collagen, elastin, reticulum, pigment cells, plasma cells.
• 3rd layer: BRUCH’s membrane / basal lamina.

BLOOD SUPPLY:
Arterial supply by 3:

1. Short posterior ciliary.A – 2trunks from Ophthalmic.A pierce sclera around optic.N & segmentally supply choroid.
2. Long posterior ciliary.A – nasal & temporal br pierce sclera on medial & lateral sides of optic.N & reach ciliary body(iris root) through suprachoroidal space to anastomose(CIRCULUS ARTERIOSUS MAJOR) with Anterior ciliary.A to supply ciliary body. Radial br from this anastomosis anastomose at pupil margin to from CIRCULUS ARTERIOSUS MINOR.
3. Anterior ciliary.A – arises from muscular(recti) branches of Ophthalmic.A & pass anteriorly in episclera to supply sclera,conj & pierces limbus to enter ciliary body CIRCULUS ARTERIOSUS MAJOR.

Venous drainage is through VORTEX veins –>Ophthalmic.V –> Cavernous sinus.

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Congenital anomalies:

 

Heterochromia of Iris

H.iridium if one iris color differs from the other iris

H.iridis if one sector of iris differs from the remainder.

D/D acquired : heterochromic cyclitis, siderosis, malignant melanoma.

Corectopia

eccentric pupil [normal pupil is slightly nasal]

Polycoria

more than one pupil

Aniridia / Iridremia

abscence of iris [may be associated with glaucoma due to angle naomalies]

Persistant pupillary membrane

remnants of lens with pigmented stellate shreds from iris

they either float in anterior chamber or are attached to anterior surface of lens.

Coloboma of uvea

absence of iris, ciliary body or choroid.

TYpical – seen in inferionasal quadrant due to defective embryonic fissure closure.

complete coloboma extends from pupil to optic.N & causes corresponding indentation of lens.

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UVEITIS

 

inflm of uvea is always assosiated with some inflm of adjacent retina, vitreous, sclera, cornea.

Anatomical classification:

1. ANTERIOR UVEITIS – iris to pars plicata [iritis, iridocyclitis, anterior cyclitis]
2. INTERMEDIATE UVEITIS – pars plana & peripheral retina
3. POSTERIOR UVEITIS – chrioretinitis

Clinical classification:

acute is <6wks & symtomatic; chronic is insidious & asymtomatic (diagnosed from defective vision).

ETIOLOGICAL CLASSIFICATION:

Infective uveitis:

microbial invasion of uvea -

Exogenous	perforation by injury, corneal ulcer, intraocular surgery. suppurative starts as acute iridocyclitis & turns into endophthalmitis.
Endogenous /Metastatic	rarely through blood from caries, septicaemia.
Secondary	extension of infection from adjacent conjunctivitis, keratitis, scleritis, retinitis, orbital cellulitis, orbital thrombophlebitis.

Bacterial	granulomatous -tubercular, leprotic, syphilitic, brucellosis pyogenic – strep, staph, gonococci
Viral	H.simplex, H.zoster
Fungal (rare)	histoplasmosis, aspergiloosis…
Parasitic	toxoplasm …
Rickettsial	typhus

Allergic uveitis:

commom

Microbial	tubercular lesion in lungs / lymph nodes. streptococcal infection in teeth, paranasal sinuses, tonsils, prostrate, genitals.
Anaphylactic	serum sickness, angioneurotic edema.
Atopic	airborne pollen, cat dander, chicken feather, house dust, egg albumin.
Autoimmune	Rh arthritis, SLE, Reiter’s Phacoanaphylactic endophthalmitis, sympathetic ophthalmitis.
HLA associated	ankylosing spondylitis, Reiter’s, Behcet’s, VKH.

Toxic uveitis:

Endotoxins	pneumococcal/gonococcal conjunctivitis fungal corneal ulcer
Endocular	blind eyes, retinal detachment, intraocular haemorrages, intraocular tumors, phacotoxic.
Exogenous	chemicals, drugs [miotics, cytotoxic]

Traumatic uveitis:

mechanisms:

• mechanical effect
• intraocular haemorrage
• microbial invasion
• foreign body chemical effect
• sympathetic ophthalmia in other eye

Noninfective systemic diseases:

• sarcoidosis
• collagen diseases – polyarteritis nodosa, SLE, Rharthritis
• Metabolic – DM, gout
• CNS – sclerosis
• Skin – psoriasis, pemphigus, erythema nodosum, lichen planus.

Idiopathic:

pars planitis, sympathetic ophthalmitis, Fuch’s heterochromic iridocyclitis.

PATHOLOGICAL CLASSIFICATION:

Exaggerated inflm due to extreme vascularity & looseness of uvea.

Types: suppurative, nonsuppurative [granulomatous & nongranulomatous]

Suppurative uveitis	usually part of endophthalmitis/panophthalmitis. Cause: exogenous pyogens – staph, strep, pneum, gonococci, pseudomonas. whole uvea is thickened by infiltrate & necrotic. eye cavities get filled with pus.
Nongranulomatous uveitis [predominantly iris & C.body]	acute / chronic with diffuse inflm & marked symtoms:pain, photophobia, ciliary congestion (redness). Cause: Traumatic, Toxic, Allergic. marked bv dilatation & outpouring of infiltrate & fibrinous exudate. waterlogged Iris – muddy, edematous (blurred crypts), constricted pupil marked aqueous flare – exudate & infiltrate poured into anterior chamber fine granular KPs at the back of cornea. posterior synechiae (thin & tenous) – adhesions due to organised exudate between iris & lens. in severe inflm, cyclitic membrane, behind lens, due to exudate from ciliary processes. after healing, pin-point necrosis or atrophy. Chronic cases show scarring.
Granulomatous uveitis	insidious with minimal symtoms chronic inflm with the infiltrate[lymphocytes, plasma cells] transforming to epitheloid & giant cells & aggregating into nodules. Cause: foreign body, haemorrage, necrotic tissue, nonpyogenic & non-virulent organisms Iris nodules – Koeppe’s nodules near pupillary border or less common Busacca’s nodules near colleratte. [these nodules may initiate posterior synechia (thick & broad)] large mutton fat KPs at the back of cornea. necrosis in adjacent areas leads to fibrosis of involved area

Transitional forms: Autoimmune phacoanaphylactic endophthalmitis & sympathetic ophthalmia showing granulomatous pathology. Infective/suppurative uveitis by leptospirae showing nongranulomatous pathology.

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ANTERIOR UVEITIS / IRIDOCYCLITIS
symptoms & signs:

 

1. dominating symptom is a marked tenderness, moderate pain referred along 5th nerve first div towards forehead
2. deeper violish red circumcorneal congestion of ant ciliary bv
3. photophobia: irritation of 5th nerve sensory fibres
4. blepharospasm: 7th nerve motor fibres supplying orbicularis oculi
5. watery exudation: lacrimatory reflux by 7th nerve secretomotor & 5th nerve sensory
6. slightly impaired vision: ciliary spasm induced myopia, corneal edema & KPs, pupillary block due to exudates, vitreous haze, macular edema
7. mild lid edema
8. Corneal signs:

Corneal edema from toxic endothelitis
Posterior corneal opacity in chronic cases
KPs: protein-WBC deposits occupying central & inferior parts of the back of cornea
Mutton fat KPs	few but large greasy composed of macrophages ; granulomatous cause
Granular KPs	many small dirty white composed of lymphocytes; nongranulomatous cause
Red KPs	seen in haemorragic uveitis
Old KPs	shrunken faded pigmented KPs of Healed uveitis

9. Anterior chamber signs:

Aqueous cells	+ =6-10 cells
Aqueous flare	Brownian movts/ Tyndall phenomenon of suspended protein particles that leaked into aqueos from bv; marked in nongranulomatous uveitis
Hypopyon	sterile pus which settled down
Hyphaema	Haemorragic uveitis
changes in depth, shape, angle	Synechia formation

10. Iris signs:

loss of crypts pattern	due to exudate in acute phase atrophy in chronic phase & in Fuch’s heterochromic iridocyclitis
color changes: muddy hyper & depigmented	active phase healed stage
Iris nodules: Koeppe’s Busacca’s	common; small; at pupillary border large; near colleratte
Posterior synechia: segmental- causes irregular pupil annular/ring- cause seclusio pupillae, leading to Iris bombe & acute glaucoma total- deepens anterior chamber, seen in acute plastic uveitis	adhesions due to organized fibrin-rich exudation between iris & lens
Neovascularization [rubeosis iridis]	seen in some chronic cases

11. Pupillary signs:

from segmental posterior synechia; atropine dilatation shows a Festooned pupil

Small pupil	toxic irritation of sphincter pupillae & mecahnicallly by iris edema
Irregular
Ectropion/evertion of margin	due to contraction of fibrinous exudate on anterior surface of iris
diminished pupillary reaction	due to iris edema & hyperaemia
occlusio pupillae	due to organization acroos entire pupil

12. Lens changes:

Pigment dispersal on anterior capsule

exudate deposits over lens

complicated cataract – polychromatic luster & breadcrumb like early posterior subcapsular opacities

13. Anterior Vitreous changes:

inflm cells & flare [protein -tyndall effect]

COMPLICATIONS & SEQUELAE:

1. copmplicated cataract- polychromatic lustre, breadcrumb posterior subcapsular opacities, pigment left after temporary iris adhesion
2. secondary glaucoma- early [during inflm phase due to clogging of trabeculae], late [postinflmm pupil block from ring synechiae or occlusio pupillae
3. cyclitic membrane due to fibrin exudate behind lens
4. choroiditis in chronic cases
5. Retinal complicationscystoid macular edema & macular degeneration, exudative retinal traction detachment
6. Papillitis [optic disc inflm]
7. Band shaped keratopathy [calcific degeneration in chronic cases]
8. Phthisis bulbi: end stage of chronic uveitis; disorganised ciliary body due to recti pressure & aq production is lost making the eye a soft small atrphic globe.
9. Hypotony [low pressure]- temporary from acute ciliary body inflm; permanent [leading to vision loss] from chronic inflm & cyclitic membrane traction on ciliary body.

INVESTIGATIONS:

1. Haematological: TLC & DLC about inflm response, ESR for chronic inflm, serology for syphilis, toxoplasmosis, histoplasmosis.
2. X-rays for sarcoidosis & TB.

NON-SPECIFIC TREATMENT:

Local therapy:

1. Mydriatric cycloplegic drugs- [MOA- relieves sphincter & ciliary muscle spasm, prevents & breaks synechiae, reduces exudation by decreasing vascular permeability, antibodies are reached & toxins absorbed by relieving ciliary bv pressure] For mild inflm, short acting tpical drugs like cyclopentolate is used (2-3 times/day), long acting subconjunctival inj (continued for another 2-3wks) of homatropine & atropine are used if synechiae are already formed
2. Corticosteroids (prednisolone, dexamethasone, betamethasone, floromethalone)- reduce inflm & fibrotic destruction, use in allergic uveitis. (topical drops 4-6 times/day, ointment before bedtime, subconjunctival inj 1-2 times/day) [ADR- cataract, glaucoma; wt gain, peptic ulcer, osteoporosis, HTN, DM]

Systemic therapy:

1. Corticosteroids (prednisolone, dexa, beta, i.v methylprednisolone, periocular triamcinolone inj]- definite use in nongranulomatous cause due to Ag-Ab rxn. Daily for atleast 2wks in marked inflm, alternate day in non-acute cases & taperad completely in 6-8wks.
2. Immunosupressors (cyclophosphamide, chlorambucil, azathioprim, MTX) (anti Tcell cyclosporin & tacrolimus when resistant to cytotoxic agents)- last resort ot prevent blindness like in severe cases: Behcet syndrome, sympathetic ophthalmia, pars planitis, VHK syndrome.

Physical:

1. Hot fomentation – pain, circulation
2. Dark goggles – photophobia, lacrimation, blepharospasm

Specific treatment of cause:

1. antitubercular drugs
2. Pn for syphilis
3. Sulfa+pyrimth for toxopl
4. Broad antibiotics for masked infection in nongranulomatous cause

Treatment of complications:

1. early inflm glaucoma- timolol, acetazolamide for lowering IOP
2. late post-inflm glaucoma- iridectomy for ring synechiae
3. complicated cataract- lens extraction if no KPs
4. retinal traction detachment- vitrectomy
5. phthisis bulbi- enucleation

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POSTERIOR UVEITIS / CHORIORETINITIS

 

Suppurative	always occurs as a part of endophthalmitis
Nonsuppurative 3 Types:	GRANULOMATOUS or nongranulomatous grey white lesion due to exudation & infiltration hiding the red choroidal bv.
DIFFUSE	spreading lesion involving most choroid syphilitic, tuberculosis
DISSEMINATED	multiple & scattered over greater part of choroid In many cases cause is obscure
FOCAL: (location) Central Juxtacaecal / Juxtapapillary Anterior peripheral Equatorial	-Involves macular area, typical in toxopl, hitopl, TB, syphilis, visceral larva migrans. -Adjoins optic disc, like Jensen’s choroiditis in young people -Multiple & in peripheral choroid, often syphilitic.

SYMPTOMS & SIGNS: painless without external signs except for a few KPs from cyclitis. It is characterised by visual symptoms esp in a central lesion than in a peripheral lesion.

1. Blurring – mild due to vitreous haze, severe if central choroiditis
2. Photopsia – irritation(inflm) to rods-cones is interpreted by brain as flashes
3. Black floaters – large exudative clumps in vitreous
4. Metamorphopsia – raised retinal contour distorts images
5. Micropsia – due to separation of visual cells
6. Macropsia -due to crowding of visual cells
7. Positive scotoma – from the fixed lesion
8. Vitreous OPACITIES – fine, coarse, stringy, snowball
9. PATCH – In active phase, grey white raised lesion with ill-defined margins, deeper to retinal bv & hiding choroidal bv; retina is edematous. In healed stage, the lesion shows atrophic choroid with sharp margins & black peripheral clumps (D/D: degenerative conditions like pathological myopia & retinitis pigmentosa.)

Complications: inflm extension to anterior uvea, complicated cataract, vitreous degenration, macular edama, periphlebitis retinae, retinal detachment.

Non-specific Rx:

1. Corticosteroids: topical & systemic; Acute phase – posterior sub-tenon inj.
2. Immunosupressors

Specific Rx: for toxopl, TB, syphilis…

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PURULENT UVEITIS & ENDOPHTHALMITIS

 

direct pyogenic invasion first affecting anterior or posterior uvea, then progressing to retina & vitreous, resulting in purulent endophthalmitis.

Cause: staph, strep, pseudomonas, E’coli, proteus.

Exogenous spread	perforation by injury, corneal ulcer, intraocular operations
Endogenous spread	through blood from caries, septicaemia
Secondary extension	from orbital cellulitis, thrombophlebitis, corneal ulcer

Symptoms & signs of endophthalmitis:

1. severe ocular pain
2. marked vision loss
3. redness, lacrimation, photophobia
4. Lids – red & swollen
5. Conjunctiva – chemosed & circumcorneal congestion
6. Cornea – ring infiltration
7. Anterior chamber – Hypopyon, may completely fill.
8. Iris – muddy
9. Pupil – yellow reflex due to purulent exudation
10. In exogenous, margins get necrotic yellow
11. In endogenous, posterior uvea is first involved & yellow white mass is seen [AMAUROTIC CAT'S EYE REFLEX]
12. Initial rise inIOP till cilliary body is destroyed.

Rx: early is the hallmark

Topical Rx:

1. 2 concentrated antibiotic drops every 30min – amikacin/trobramycin + vancomycin/cefazoline
2. Dexamethasone QID
3. Cycloplegics QID – atropine/homatropine

Subconjunctival inj of 2 antibiotics every 12hrs

Diagnostic tap & intravitreal inj – in pars plana region (4-5mm from limbus), if no improvement, repeat after 48hrs considering culture report

Systemic Rx:

1. i.v antibiotics – amikacin+cefazoline QID for7-10days/ ciprofloxacin BD for 2-4days
2. oral corticosteroids – after 24hrs of antibiotics

VITRECTOMY – after ’48-72hrs of medical Rx’ to remove bacteria, toxins, enzymes.

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PANOPHTHALMITIS

 

purulent inflm of whole eyeball; begins as anterior/posterior uveitis & through a short stage of endophthalmitis.

Symptoms & signs:

1. severe ocular pain
2. COMPLETE vision loss; no perception of vision
3. marked redness
4. profuse watering & purulent discharge
5. constitutional: fever & malaise
6. Proptosed eye with limiting & painful ocular movts
7. Lids – red & swollen
8. Conjunctiva – chemosed, ciliary & circumcorneal comgestion.
9. Cornea – edematous
10. Anterior chamber – full of pus
11. marked rise in IOP
12. limbal perforation leads to fall in IOP

Rx: little hope in saving the eye; emergency pain & toxaemia

1. antiinflm & analgesics
2. broad spectrum antibiotics
3. Frill evisceration to avoid intracranial dissemination