MRC III Clinical

Cyklokapron 500mg tablets

Dose

tranexamic acid

- inhibits fibrinolysis

- less gastric upset, lower dose given, less frequent.

500mg tds cyklocapron

Pain relief

Largactil 50mg or 2 ampoules retrobulbar for pain.

Chlopramazine 25mg amp comes as chlorpramazine hcl

Retrobulbar

At 1/2way between limbus and canthus pass posteriorly along floor 10% angled from iris

when the hub is at iris than the needle 4 to 5mm behind globe

Vitamin A deficiency

Fxn

rhodopsin

Conj mucosa integrity

Rpe /srs metabolism

rx Vit A palmitate in oil 6000ug or 200000iu for 2 days (half in kids less than 1 and pregnant mothers) and repeat in 1 month

topical Vit A ointment QIDCF easy Bitots spots=paralimbal spots sivery triangular patch = keratinzied area ,Dec tear BUT loss of retinal pigment unilateral proptosisALL Metastaic neuroblastoma (never primary)Lymphangioma with URTI becomse swelling with conjunctival signs Rhabdoblastoma usually at 7yearsorbital cellulitispseodotumour also kids bilateralmore

anatomypars plana 3 to 4mm from limbus closer on nasal sidefortified dropscephradine or gram positives 1st generationTake a 1gram iv bottle and add 2ml sterile waterAdd 1ml to a 15ml tears naturalle after removing 1ml of tears naturallenow have 500 mg in a bottlefortified gentacin

take Iv gentacin which is 40mg in 2ml ampoue normallyadd to 5ml normal commercial genopticnow have fortified formula

Cephazolin or KefzolTake an IV ampoule that is commercially available as 500mg Add 2ml of sterie waterAdd to 15ml tears naturalle after removing 2ml

subconj doses :gentacin 40mg which is an ampuole of IVkefzol or cephazolin is 125mg or quater ampouleESRman age divided by 2women age plus 10 divided by 2 vallergan preanaesthetic over 2years give 2mg per kgeg 8 kg give 16mgdose 30mg per 5ml forteordinary 7.5mg per 5ml or antihistaminepromethazine phemnergen half teaspoon tdsmakes 2.5 mg per dayml has 1 mgteaspoon is 5 mlvalloron 1drop per year old plus 4 drops qidROP my own understandinguse cyclopentalte 1 % and phenyeprine 1%Typically those born below 1250g or less then 28 weeks.examine them at 6 weeks laterstage one ~~~~ a line between vascularized and avascular retinanormally the eye can't make out the difference.stage two a ridgestage three extraretinal fibrovasvular tissue coming of ridgestage 4 & 5 RD various degreesalso use zones to describe areaszone 1 radius is two times distance from disc to foveazone 2 to orra nasally and to equator temporallyzone 3 remaing crescent temporally superiorly and inferiorly

#CataractspsccHave blurring at nearAnd glare at bright lightLens abnormalitiesEctpoia Lentis= displacement of lens from normal position : causes Marfan weil masheshani homocystinuria hyperlysinaemia sticklers ehler danlos Familial ectopia lentis aniridia sulphate oxidase deficiencyPhacoincision flat against sclera 2mm and then up ________ /_______ /hydropdissection see posterior wavegroove foward phaco power 60% linear and stepped upacceleration

How does Sorbitol cause Cataracts?lens needs glucose and burns it anaerobically and is not very dependent on O2most glucose goe to Glycolysis via hexokinase to G6P providing ATP(only 3% goes to TCA but remember oxidative glycolysis is much more effecient in making ATP5% goes to PPP to make reducing power NADPH which is in turn is used also by aldose reductase to make fructose via sorbitol .This happens only if there is accumulation of glucose.eg in diabetes or galactase def.

Glucose + glucose sucroseGlucose + galactose lactoseGlucose + fructose maltoseglucose~~aldosereductase~~~sorbitol~~aldosereductase~~ fructose

extra glucose becomes sobitol which is and intermediate to fructose via aldose reductase.Sorbitol[as well as fructose]is poorly permeable and will stay in the lens and imbibe water Bottom line Nb;if more glucoseAldose reductose makes sorbitol with nadphAdded knowledge1Pam projects snellen chart to fovea around the cataract2lens interferometer measures variance in space between fringe created by twin sources of monochromatic helium neon laser creating a diffraction fringe patternanatomycapsule 4um at posterior centre14 anterior 17um at equator where zonules are and 22um where capsoluhexis is made( both anterior and posterior) make ccc 1mm less than optic which is 5 or 6mmLammelar = spoke like = zonal opacities of the fetal or nuclear lens that is invariably congenital & often have spokes around em) Diabetic cataracts white punctate or snowflake opacitiesGalactosaemia oil drop cataractTrauma vissius ring after blunt trauma=iris pigment imprinting on anterior capsule dt concussionGalactokinase deficiency Mannsodosis Fabrys Lowes lammelarcongenital lens is small thin disc like (microphakia) & shows posterior lentoglobusrubella dense pearly nucleusmyotonic dystrophy Christmas treeAtopic dermetitis anterior stellatebased on shape:PXE posterior synechie gold chlopramazine Vios ring ~~Posterior subcapsular Myotonic dystrophy DXT~~anterior subcapsular

AACG (glaucfleken) ~~~glue co fleck ken

wilsons miotics pilocaroine will cause catarctamiodarone ~~~cortical

coronary iis a special type ~~~congenital

lammelar always congenital

sutural

Types of Cataracts

Immature only scattered opacities

vs

mature where the cortex is opaque

Intumescent is one that swells as it imbibes water

>>>>secondary pupil block glaucoma

vs

hypermature that is leaking water and hence dangerous! but it itselfis old wrinkled and small

>>>>secondary glaucoma

Morgagnian where the cortex has melted [ nb vacuolation seen histology]and the nucleus has fallen to the back gagged and dead!

#Glaucoma

Cortisol diurnal curve

Peak 6 to 8am

Causes glaucoma same e

Y as steriods

Ie

Dec phagocytosis

Secondary open angle glaucoma

1 Phacolytic or Phacogenic due to leaking hypermature cataract proteins and macrophages in the angle

2RBC glaucoma due to traumatic hyphema

3 angle recession glaucoma due to pigment and destruction of trabecular meshwork after trauma

4Ghost cell glaucoma 2 weeks after vitreous haemorrhage or hyphema

5 Iridocorneal endotheial syndrome

abnormal surface migrates over angle and includes essesntial iris atrophy iris naevus and Chandlers

6 PXE

age > 50 years material all over the body Material is a microfibril with elastin, mucopolysaccharide, and extracellular matrix Exam findings:Usually asymmetric, can look unilateral 50% in 5years bilateral for yrs, severe cases are usually unilateral lens has central disc, intermediate clear zone (brushed off from contact with moving iris), and peripheral granular zone (with radial striations)NB Up to 50% get glaucoma Glaucoma affects the MORE pigmented eye & poorer prognosis, Weak zonular attachments with 10x rate of vitreous loss with cataract extraction.PXE more accelerated galucomatous damageEtiology extracellular matrix synthsis due to lInc TGF beta 1 and mettaloproteinases that is activated by free radicles that appear with dec Vit AVit A

40 to 60 x in Aqueous humour and exreted by ciliary epithelium

Vit c ascrbic acid becomes dehydroascorbarbic acid when oxidized

gluthathione GSSG to GSH reverses this to reform active ascorbc acid (this requires NADPH)

PXF reduced levels AA also absorbs UV

RDA 75mg daily recommended fr AO activty up to3 g

corneal endothelium flakes

iris absent pupillary ruff with white flakes Moth eaten transisllumination defects iris near pupil ,

trabecula meshwork ampaolesi's line (segmental)=pigment along Schwalbe's Line this is causeof glaucoma in more pigmented eye

7 Pigmentary glaucoma

This may occur in 10 % of PDS which consist of mid perphery posterior bow and pigment loss causing Krukenburgs line on endothelium + pupil atrpophy & pigment in furrows Tm pigment & lens both anterior and posterior pigment

Demographics: Myo (especially > -3.00 D), White>>Black (difference in ant. chamber depth) M:F 2:1 Wide diurnal swings in IOP, also assoc. with exercise and accomodation

Exam findings: Krukenberg's spindle on corneal endothelium is nonspecific, seen often in normal women

Iris transillumination spoke wheel deficits in mid-peripheral 1/3 of iris Mechanical contact between zonular packets and iris ( Iris pigment release Pigment stippling on iris over defects, Iridodonesis heterochromia (eye with darker iris is affected) Pigmented TM with concave peripheral iris, Sampaolesi's line Pigment line on posterior lens at vitreal touch Posterior bowing of iris with reverse pupillary block It is called reverse block because the pupil moves back rather than a swollen lens

Rx Pilocarpine good choice to alter anatomy (reverse pupillary block) Try Ocuserts for younger patients (for less miosis) ?Role for thymoxamine/Moxisylate ((-blocker which gives miosis without cyclotropia or decreasing ciliary outflow Consider LPI to decrease concavity and pigment dispersion ALT and Filter both work well myo males middle aged

8 inflammatory glaucoma = glaucomatocylitic crisis =Glaucoma related to inflammatory change in trabecular meshwork Associated with systemic disorder, allergic, or GI (peptic ulcer) diseases Mild inflammation, dilated pupil, high IOP (40-60 mmHg) with corneal edema30-50 years old Unilateral, recurrent attacks, ON usually OK, self limited 1-3 wks Some end up with COAG Open angle: no PAS, no posterior synechiae Some flare, fine KPTx: Prostaglandins are possibly involved ( oral and topical NSAIDsAvoid steroids since patients may be steroid responsive?Apraclonidine in acute attacks

9 Fuch's Heterochromia as a cause of glaucoma (Fuch's Heterochromic Cyclitis) This does not start with a P so lighter one is affected

Sometimes confused with Glaucomacylitic crisis 20-30 yrs old, M=F Most commonly misdiagnosed in Blacks b/c heterochromia less obvious 50% get progressive glaucoma

Exam findings: Unilateral low grade iritis (minimal flare/cell) with fine stellate KP inf. cornea

Severe iris atrophy - lighter iris is pathological( vs PIGMENT & PXE where the darker eye is pathological

10% can be bilateral OPEN angle: NO posterior synechiae, but fine angle vessels

10Trauma

Siderosis (intraocular retention of iron FB or intraocular heme) Chalcosis (retained copper FB - copper gets oxidized) Chemical burns (Alkali and Acid: inital ( IOP, prostaglandin release ( shrinkage of cornea and sclera)

12Aphakic or Pseudophakic Glaucoma

Term discouraged because not due to just one etiology often post op with increased IOP that persists Due to: Distorted anterior chamber angle Viscoelastic (sodium hyaluronate) obstructs TM UGH syndrome (Uveitis/Glaucoma/Hyphema) from inflammatory

reaction to heme Pigment dispersion from PC IOL rubbing on iris Vitreous in AC leading to pupillary block

13Hypothyroidism

May be due to changes in scleral rigidity by inceasing and nence decreasing outflow

Secondary Pupil blocks glaucoma

1Uveal melanoma

2 FB egsilicone oil

3Microspherophakia (Weill-Marchesani syndrome/Lens Induced-loose zonules)

4Phakomorphic (Lens Forward syndrome) Intumescent lens ,dislocated or incacerated

Shallow anterior chamber, ?zonule laxity or post. pressure

5Epithelial Ingrowth/Fibrous Proliferation= fibrous tissue in AC

Epithelial membrane/vascularized fibrous tissue grows into AC through penetrating wound Retrocorneal membrane 2( inflamm or trauma to cornea but Descemet's intact (glaucoma not commonly associated) If unsure, use Argon laser(.2s, 200-500 um, 200-500 mW). If membrane present, blanches tissue white. If iris present, shrinks and hyperpigmentation

6Iridoschisis posterior iris separates and blocks AC

Contrast against pigmentary glaucoma

Older (70's), bilateral, M=F, reactive pupil ?Senile change, post trauma Usually lower half anterior stroma separates from posterior stroma Strands obscure anterior chamber Some have angle closure 'Some have obstruction of TM ( open angle glaucoma (like pigmentary) Glaucoma in 50% as PAS form,

7 Iris Cysts Block AC

Idiopathic, IK (Interstitial Keratitis), Phospholine Iodide8Nanophthalmos

Shallow anterior chamber, narrow angle ( angle closure Uveal effusion ( forward shift of lens-iris diaphragm ( pupillary block actuallly a bit of both pupil block and narrow angle! there last on list

Secondary glaucoma with clinically evident narrow angles1Plateau iris 2PAS 3Neovascular 4ICE{No Pupillary Block} 5 fuchs 6 ppmd

1Plateau iris===Young patient with high iris insertion,

increased IOP with dilation Exam findings: Gonioscopy shows sudden drop off of peripheral iris Deep central anterior chamber, can have pupillary block Tx: Compression gonioscopy can open angle LPI to r/o primary closure, chronic miotics Consider peripheral iridoplasty

2PAS ===Longstanding prior block, flat anterior chamber, uveitis

3Neovascular Demographics: CRVO 1/3, DM 1/3, carotid disease 1/10, RD, melanoma, uveitis Glaucoma develops in 10-20% of rubiosis

3ICEs (Irido-Corneal Endothelial Syndrome)=== Primary CORNEAL endothelial abnormality

Proliferation from abnormal corneal endothelium Contraction of membrane over angle and iris( PAS, correctopia, ectropion uvea Unilateral F middle aged Presents with iris changes, decreased VA from glaucoma or corneal edema, or pain from corneal edema KEY: endothelium has irregular, fine hammered/beaten metal appearance often bilaterally, pleomorphic cells ("ICE cells") Three clinical variations:

Chandelier has frosted glass

Cogan/reese has fingerprints/nodules on iris

1Progressive Iris Atrophy :iris atrophy :

2Chandler's Syndrome Corneal edema :

3Cogan-Reese Syndrome Nodular, pigmented lesions of iris

Ddx Endothelial changes: PPMD (see below) Fuch's endothelial dystrophy Iris holes: Axenfield-Rieger (congenital) Aniridia Iris nodules:Melanoma or Nevi Nodular Inflamm (Sarcoid)5PPMD (Posterior PolyMorphous Dystrophy===Post. cornea with single or groups of blisters/vesicles,Confused with ICE syndrome Demographics: Less than 15% develop glaucoma, nonprogressive Bilateral, familial AD, congenital and asymmetric until adulthoodExam findings:Post. cornea with single or groups of blisters/vesicles, band like lesions with scalloped edges, or islands with endothelial changes at level of Descemet's membrane Few have PAS, corectopia, iris atrophy

5Fuch's Endothelial DystrophyUnclear theory on how guttata are related to IOP Guttata may decrease aqueous outflow? Associated with increased incidence of axial hypermetropia and shallow anterior angle ( increased risk of closed angleOther Glaucomas cilary body 1Malignant Glaucoma (Ciliary Block Glaucoma/Aqueous Misdirection)===Classic definition: acute glaucoma with very shallow central and peripheral anterior chamber in post op patients operated on for angle closure due to Aqueous flow obstruction due to apposition of ciliary processes against equator of lens or anterior hyaloidNB block is very posterior

Posterior pooling of aqueous behind a PVD ( forward displacement of lens-iris or iris-vitreous diaphragm Never has suprachoroidal fluid by ultrasoundDiff Dx: choroidal detachment, suprachoroidal hemorrhage, pupillary block glaucomaRx: Improvement with mydriatics Atropine qid x 5 days, phenylephrine, CAI's,=trusopt apraclonidine, and osmotics may stop 1/2

2Retina iatrogenic = ciliary body swellingOccurs with ciliary body swelling and rotation (ie. after PRP, cryo)

Increased Pv (normal episcleral venous pressure = 8-10 mmHg)Three types:Obstructed venous flow pressure Idiopathic episcleral venous pressure elevation Carotid-Cavernous Sinus Fistula Superior Vena Cava Syndrome Orbital Varix Cavernous Sinus ThrombosisThrombosis ( Acute orbital Ssx, bull neck, may see phlebolith on plain filmsOrbital VarixPosterior dilation of intracranial vessels leads to dilated orbital veins (episcleral and conjunctival) Can be congenital single tortuous vein Kippel-Trenaunay-Weber syndrome Intermittent exophthalmos with head upside down, sneezing, or Valsalva Blurred VA, headache, nausea, and pain( reversal when jugular pressure lowered Blindness from repeated episodes Can have systemic venous abnormalities in buccal mucosa, extremities, and visceraCarotid-Cavernous FistulaHi-Flow (75%)Secondary to trauma (MVA head injury)Pulsating exophthalmosInternal carotid fistula ( surrounding cavernous sinus venous plexus Low-FlowSpontaneous etiologyIndirect or dural connectionMiddle-aged womenMemingeal branch of intracavernous int. carotid a. or ext. carotid a. ( cavernous sincus or adjacent dural vein that connects with the cavernous sinusConjunctival chemosis, episcleral engorgement Bruit with increased with exercise, ocular ischemia Proptosis can increase for weeks CN VI palsy, retrobulbar pain Glaucoma from increased Pv, neovascular from CRVO, or angle

closure

Thyroid Ophthalmopathy Increased proptosis ( orbital congestion 2nry to obstructed venous plexus Increased IOP especially in upgaze 2( fibrosis of inferior rectus

Compressive optic neuropathy commoner in older male,with d.mellitis,more severe orbitopathy.

Retrobulbar Tumors Sturge-Weber Increased IOP 2( to increased episcleral venous pressure 2( to episcleral hemangiomas with AV fistulas

#Sclera &conjuctivaAllergic Conjunctivitis

Seasonal Allergic Conjunctivitis signs/symptoms rapid, lid swelling, chemosis (pale palpebral conjunctiva), itching, mucus, dellen pressure, rhinitis/asthma, episodic symptoms are much greater than signs can sometimes be perennial with multiple overlying allergies dx clinical, Type 1 hypersensitivity only, elevated tear IgE, eosinophils in scraping in chronic cases rx steroids rarely indicated antihistamines systemic and topical are useful topical NSAIDS mast cell stabilizers if chronic condition Vernal (VKC)

common in african males 3 to 30years old often assosiated with allergies chronic lasts for years and is Hs type 4 reaction with allergic eyes and giant papillae chronic stigma are aconcern eg corneal scarring <-- conjunctival neovascularization Tratas spots = clumps of EIO flour dusting of palpable atrophy <-- ptosis histology; fibrinolectin and lamminen deposits on immunhisto studies

Vernal (VKC) bilateral seasonal young (3-25 year old) in warmer climates, M>F FHx of ato allergies usually self limited, average 4-10 years two types: vernal and palpebral signs/symptoms ITCH (worsens in evening, dust, lights, wind, rubbing), clear tears ropy discharge but lids don't get crusted or stick together unless bacterial superinfection giant papilla may cause ptosis limbal involvement more in blacks and can be up to 360 degrees Horner Trantas dots (clumps of degenerated eosinophils), clear elevated cysts SPK, flour dusting of epithelium, intraepithelial cysts, shield ulcers usually upper cornea pseudoarcus, myo astigmatism, associated with keratoconus, rare corneal neovascularization>2 eosinophils/hpf pathognomonic, increased tear histamine eosinophilic products are major cause of corneal epithelial destruction rx lodoxamide 0.1% QID is first line drug topical steroids- pulse rx with exacerbations topical cyclosporine 2% qid can be used as alternative to steroids Atopic (AKC) keratoconjunctivits in patients with atopic dermatitis M>F, teens to 40's, burns out by 40-50 year old, small papilla, milky edema, corneal neovascularization hx of ato eczema (3% of population), similar to vernal findings but no seasonal changes signs/symptoms atopy shiners (bags under eyes from rubbing) symblepharon, foreshortening of inferior fornix, usually lower palpebral conjunctiva affected can mimic OCP in severe cases bilateral cataracts (anterior subcapsular, or posterior polar), 10% of all cases ato dermatitis associated with keratoconus, iritis, cataract RD from pars plana tears or ora dialysis (can have photoreceptor outer segments in anterior chamber which look like cells) pathology increased T helper, macrophages, increased class II HLA similar to OCP and rosacea. more complex than simple mast cell allergic rx. No BM deposition as in OCP rx environmental control is essential systemic antihistamines, nasal cromolyn, topical mast cell stabilizers pulse steroids and cream doxycycline for blepharitis oral and topical cyclosporin (severe cases may need immunosuppression)

Pynguela ==========elastic dgeneration of conjuctiva subepithelial collagen

pterygium ==========elastic generation of conjuctiva subepithelial collagen & corneal collagen

phlyntenosis ========Phlyctenular ulcer = nodular pinkish white limbal elevation with gray crater, can be on conjunctiva caused by type iv hs to staph TB or candida antigen

EKC adenovirus peak 5 to 7 days stage ranges from superficial epithelial keratitis to subepithelial infiltrates (SEI)= immune response to viral antigens on anterior stroma i 80% of casesRx: topical steroids if membranes and SEI's

Pcf viruses 3 4 7 has fever etc ie systemic

Ekc 8 19 localized to eye

HSV

HSV Primary conjunctivitis in children, bilateral, fever, preauricular adenopathy, URI, 3-9 days incubation varied present (mild follicular conjunctivitis to pseudomemb) lid vesicles, ulcerative bleph, 1/2 get small

fleeting corneal dendrites SPK, conjunctival dendrites

HSV Recurrent may be triggered by sunlight, fever, stress, menses, steroids 1 yr 25%, 2 yrs 50% chance of recur one fifth develop stromal keratitis most common infectious cause of corneal blindness in this country blindness from HSV is from recurrent stromal keratitis and/or iritis with the subsequent inflammation and scarring

Clinical tures

1Lids (pseudozoster)

2Rare follicular conjunctivitis

3Epithelial keratitis SPK, dendritic, geographic, marginalshaggy borders, ghost scars of prior dendrites, decreased corneal sensation often with mild stromal edema metaherpetic lesion from poorly healing epithelium, gray thickened heaped up edges usually resolves spontaneously in 3 weeks but treat to decrease the amount of damage RX debride with dry cotton tip applicator limbal lesions antivirals, slower healing diff dx of dendrite contact lens filaments tyrosineamia ca thygsons hzo

4 stromal keratitis: disciform=disc shaped zone of corneal edema presumed immune mediated disease

central corneal edema with fine KPs under edema, mild iridocyclitis, increased IOP, Wessley ring (of infiltrates)

diff dx includes HZO, local bullous keratopathy, EBV virus, connective tissue disease, interstitial keratitis

consider obtaining antiherpes serum antibodies in patients with no hx of herpetic eye disease or when the

diagnosis is in question Rx cycloplegics topical steroids with topical antiviral cover tapered slowly (Pred Forte 8X/day initially tapered down to 2X/day by 2 months) usually self limited in 2-6 months with variable scar

5Stromal keratitis: peripheral atyal, r/o marginal ulcer 6Stromal keratitis: necrotizing presumed etiology from live virus but can be negative on biopsy dense deep stromal infiltrate, multiple cheesy white, necrotic infiltrates no pain, mild iridocyclitis, increased IOP, corneal neovascularization, Rx indolent self limited 2-12 months antivirals with steroids and slow taper (even yrs)

7 Endotheliitis progressive corneal edema with line of KP (looks like PKP rejection, but PKP rejection line is limited to the corneal graft) rx acyclovir 8Uveitis iritis with diffuse iris atrophy multifocal choroiditiscomplications of HSV infection neurotrophic ulcer irregular astigmatism lipid keratopathy corneal perforation

HZO

HZO primary chickenpox rare disciform keratitis SPK limbal pustules lid lesions usually benign, may treat if

involvement

HZO Secondary 2% of adults > 60 year old, pathology: nerve damage, ischemic vasculitis, inflammatory granulomatous rx lid vesicles clear in 3 wks and can result in ptosisconjunctival hyperemia, vesicles following a dermatome, episcleritis

Hutchinson's sign- vesicles on the tip of the nose, indicates involvement of the nasociliary branch of V1

SPK, microdendrites, corneal neovascularization, uveitis, glaucoma, sectoral iris atrophy stromal nummular keratitis, scleritis (nod>diff, limbal can spread to cornea) 1% with optic neuritis, Horner's, EOM palsy (25%) decreased corneal sensitivity leads to neurotrophic ulcers

Rx cycloplegic, Acyclovir 800mg 5x/day x 7 days try to start within 72 hrs

topical steroids for iritis Zovirax 5 times warm compress consider prednisone 60-100 mg po x 3 days if microdissemination, pt may be immunocompromised consider IV steroids, use IV acyclovirHZO Neurological syndromes

postherpetic neuralgia necrotizing angiitis with contralateral hemiplegia and death in 15% wks to months later PML-like syndrome

#CorneaKeratoplasty

Lammelar means partial thickness

most common indication Bullous keratopathy

Tectonic means restotarion of normal antomy in eg dermatocoele or stromal thinning

or therapautic or cosmetic

Surgical procedure

donor o5mm larger to reduce glaucoma flattening and make wound watwer tight

ideal size,7.5mm and the donor should be trephined endothelial up

Lammelar graft

ind'opacities ant 1,3 of stroma

Marginal or localized thinning or descemetocoele or terriens or dellen or limbal dermoidEndotheliumcell density 1400 to 2500cells/mm2critcal no 400-700 cells,mm2

newborn 4000cells/mm2Graft failureEarly dt poor endotheliumLate due to imc50% within 6months vast majority within 1 yearEpithelial linear opacity and later like adenovirus=krachmer spotsMild iritisEndo much more serious since endothelium does not regenerate khoudadoust lineRx topical/systemic steroids

Corneal degenrations Peripheral1dellen ==========easy2moorens=========benign or progressive painful inferior thinning assos trauma or Hepitits C3AI RA melt======= inferior thinning & perforation4Terriens ========quiet superior thinning with pannus rarely perforates5magrinal keratitis *6Rosacea ketatitis*===unknoown cause mostly woman 30 to 50Cf hyperaemia flushing telangiectasia hypertrophic sebacous glands and rhinophyma Rx tetracycline or metronidazole7PhlyCtenosis *mostly in kids and Hs to ag

probaly * = infective

Mooren's

idiopathic unilat painful inferiorly trauma hx, rare perf,more commonly scarring circumferential spread early signs: usually not elevated, small lesions, can be in conjunctiva central edge undermined in stroma, blunt edge peripherally

two types:benign, unilateral, in older, responds to surgery

relentlessly progressive and bilateral in 25%, young NIgerian blacks also ass parasitic infection and abs

25 % of cells in area express MHC hla type IIantigen ie able to present ag to T helper cells there is aslo less tsuppresor cells

Rx: steroid (topical, systemic) lamellar keratoplasty with conjunctival resection, immunosuppressives eg cyclophosphamide and methotraxatecollagenase inhibitors eg acetylkcystine (MUCOmyst 10%) l cystene cyclosprin A topical

check for Hepatitis C Ag and will respond to interferon

steriods may worsen disease sucessfully used cyclosporin 2% topical in olive oil and

oral 10 to 15mg per kg eg 20kg child 100mg bd to load

then 2 to 6 mg maintenence also methotrexate

conjunctival resection to remove inflamatory process

that is TYPE 2 humoral response wiith c fixation and etc it is limbal where 5 times more complement

exists

VII. Management

Most experts would agree on a step-wise approach to the management of Mooren's ulcer, which is outlined as follows:

1. topical Steroids

Initial therapy should include intensive topical program: prednisolone acetate or prednisolone phosphate 1%, hourly, in association with cycloplegics and prophylactic antibiotics.[1, 6] If epithelial healing does not occur within 2 to 3 days, the frequency of topical steroid can be increased to every half hour. Once healing occurs, topical steroids can be tapered slowly over several months. Such management, especially in the unilateral, benign form, has yielded good results.

Oral pulse therapy (Prednisone 60 to 100 mg daily) can be considered when topical therapy is ineffective after 7 to 10 days or in cases where topical steroids may be contraindicated because of precariously deep ulcer or infiltrate.[9] topical tetracycline or medroxyprogesterone can be used for anticollagenolytic properties. Therapeutic soft

contact lens or patching of the eye may be beneficial at this stage. [1]

2. Conjunctival Resection

If the ulcer progresses despite the steroid regimen, conjunctival resection should be performed.[1, 6] Under topical and subconjunctival anesthesia, the conjunctiva is excised to bare sclera, extending at least two clock hours to either side of the peripheral ulcer, and about 4 mm posterior to the corneoscleral limbus and parallel to the ulcer.[8] The overhanging lip of ulcerating cornea may also be removed. Postoperatively, a firm pressure dressing should be used. Multiple resections may be needed. It is thought that the conjunctiva adjacent to the ulcer contain inflammatory cells that may produce antibodies against the cornea and cytokines, which amplify the inflammation and recruit additional inflammatory cells.[23]

Cryotherapy of limbal conjunctiva has been advocated by some surgeons and may have a similar effect.[] Conjunctival resection and thermocoagulation have also been found to give some relief at the site of the ulcers, but recurrence can occur at same or other sites (up to 50%).[]

Keratoepithelioplasty has also been performed in patients with Mooren's ulcer.[] Donor corneal lenticles are sutured onto scleral bed after conjunctival excision. The lenticles form a biological barrier between host cornea and the reepithelializing conjunctiva, and the immune components it may carry. Application of isobutyl cyanoacrylate, a tissue adhesive, may work in the same way but perhaps more simply and without the risk the risk/ of epithelial rejection.

3. Immunosuppressive Chemotherapy

Those cases of bilateral or progressive MU that fail therapeutic steroids and conjunctival resection will require systemic cytotoxic chemotherapy to bring a halt to the progressive corneal destruction.[10] At the Immunology and Uveitis Service at the Massachusetts Eye and Ear Infirmary, we believe that the evidence for the efficacy of systemic immunosuppressive chemotherapy for progressive bilateral MU is quite strong, and that such treatment should be employed sooner rather than later in the care of such patients, before the corneal destruction has become too extensive to need for surgery.

The most commonly used agents are :

-Cyclophosphamide (2 mg/kg/day): degree of fall in WBC is the most reliable indicator of immunosuppression produced by cyclophosphamide

-Methotrexate (7.5 to 15 mg once weekly)

-Azathioprine (2 mg/kg/day)

More recently, oral Cyclosporin A (3-4 mg/kg/day) has been successfully used to treat a case of bilateral MU unresponsive to local therapy with topical corticosteroids, silver nitrate, and conjunctival resection, as well as systemic immunosuppression with corticosteroids, cyclophosphamide, and azathioprine.[12] Cyclosporin A works by suppression of the helper T-cell population and stimulation of the depressed population of suppressor and cytotoxic T cells present in patients with MU.[23]

Adverse effects of these cytotoxic and immunosuppressive medications, such as anemia, alopecia, nausea, nephrotoxicity, and hepatotoxicity, are rare but possible. Therefore, the administering physician must be vigilant about their onset.

topical Cyclosporin A (0.05%) solution has also been tried with "success" in a number of

patients with MU. Local or systemic side effects attributable to topical cyclosporin A were generally not observed.[30]

4. Additional Surgical Procedures

When topical steroids, conjunctival resection, and systemic immunosuppressives have failed in the management of MU, additional surgical procedures may be considered. Superficial lamellar keratectomy has been shown to arrest the inflammatory process and allow healing.[4] Some cases may progress to perforation despite management as just detailed. Small perforations may be treated with application of tissue adhesive and placement of a soft contact lens to provide comfort and to prevent dislodging of the glue. When a perforation is too large for tissue adhesive to seal the leak, some type of patch graft will be necessary, from a small tapered plug of corneal tissue to a penetrating keratoplasty. In case of larger perforations, a partial penetrating keratoplasty may be performed. It should be emphasized that the prognosis of corneal graft in the setting of acute inflammation in patients with MU is very poor.[1, 8]

5. Rehabilitation

Penetrating keratoplasty may be performed once the active ulceration has ceased and the remaining cornea has been completely opacified, even in the face of a thinned and vascularized cornea.[6, 8] In these instances, a 13-mm tectonic corneal graft is first sutured in place with interrupted 10-0 nylon or prolene sutures with the recipient bite extending into the sclera so that the suture will not pull through the thin host cornea and then a 7.5 or 8.0-mm therapeutic graft is placed. In the absence of donor corneas, free lamellar scleral autograft can be used to restore corneal defect, followed by penetrating keratoplasty later.[26]

Because of the immune system's remarkable memory, surgical attempts at rehabilitation in MU should be done only with concurrent immunosuppression, even when the active disease has been arrested, because attempts at penetrating keratoplasty often are associated with recurrence and graft failure. Some authors believe that the risks of recurrence is so great that patients are best served not by any intervention but by maintaining the current status, i.e. the vision provided by their own thinned, scarred cornea.

Terrien's (NOT an ulcer)

quiet thinning superiorly with fine micropannus can spread 360 degreescommonly in adults >50 year old, M>F, bilateral but more advanced in one eye

steep central wall, mild inflammation later, lipid deposits at edge of pannus, epithelium intact rare perforation Rx: mild steroids chronically to suppress inflammation lamellar or PKP

Marginal corneal melt

autoimmune disease, most commonly rheumatoid arthritis

unilateral, inferiorly, may have infiltrate can have rapid progression stops if epithelium heals

Age related furrow

lucid areas of arcus, no inflammation, vessels, or perforation

Degenerations

Age related changesarcusvogts white limbal girdle = white deposits

cornea farinata = flour like central depositsof lipofuscin, dots, commas in deep stroma anterior to Descemet products of cellular degenerationcrocodile shagreen guttata = collagen on DM seen by specular reflection

hassal-henle bodies

Other usually work related or deposits

sueprficial stroma or subepithelial ike labradeor colorgolden brown = sheroidal degeneration [ due to sunlightwhite ring with iron Coats white ring grey white nodlues = saltmanscreamyy=lipid calcium = bandHistologysuperficial stroma protein or iron1Shephroidal protein in the superficial stroma2Coat's white ring = subepithelial or anterior stromal circular white ring with Fe deposits associated with metallic corneal foreign body3Salzmanns nodular degeneration = elevated gray white elevated subepithelial nodules with fe deposits Bowman's or in space above ie Ca or lipidBand Keratopathy ===deposition of calcium salts in Bowman's4Lipid Keratopathy= yellow between Bowmans and epithelium

1Shephroidal degeneration = occurs as amber deposits of protein in the superficial stroma due to sun exposurebilateral M>F, golden brown spheres in anterior stroma/Bowmans in palpebral zone risk factor age, UV exposure, probably elastotic degeneration of collagen symptoms: decreased visual acuity, FBS, irritation signs: usually not elevated, small lesions, can be in conjunctiva

2Salzmanns nodular degeneration = elevated gray white elevated subepithelial nodules with fe deposits adjacent to previous

corneal conditions but can also be isolated occurs 2ndry to keratitis or tracoma F>M middle age Rx: local excision +/- excimer smoothing3Band Keratopathy ===deposition of calcium salts in Bowman's

commonly associated with: local inflammation: dry eyes, uveitis, long standing whiglaucoma, interstitial keratitis, phthisis ophthalmic medications: pilocarpine systemic disorders: chronic disease, conditions associated with systemic increase in Ca, Phos, mercury such as hyperparathyroidism, excess vit. D ingestion, renal failure, sarcoidosis, milk-alkali syndrome, thiazide, bone mets other causes: gout with urates, discoid lupus erythematosis, tuberous sclerosis

Rx: removal with 3% EDTA, give topical anesthetic then EDTA for 1 min, scrape and sponge until it clears

4Lipid Keratopathy=elevated, nodular, yellow between Bowmans and epithelium occurring in areas of vascularized scars especially surgical

5Coat's white ring = subepithelial or anterior stromal circular white ring with Fe deposits associated with metallic corneal foreign body

Amyloidosis

deposition of noncollagenous protein

subepithelial, salmon color, avascular primary: tend toward mesenchymal deposit secondary: organ deposit

metachromasia crystal violet, flourescent thiaflavine T, birefringence/dichroism Congo Red, +with Siruis Red

primary localized most common form with palpebral conjunctival asymmetry (brown/yellow waxy firm subconj nodules) lattice is special form does NOT affect lids, but can be orbital presenting as VI nerve palsy primary systemicbilateral symmetric yellow or ecchymotic lid papules, light near dissociation vitreous opacities, EOM palsies, proptosis, glaucoma secondary local after chronic inflammation, trichiasis, keratoconus, granular dystrophy salmon to yellow, fleshy, waxy nodular lesion on cornea secondary systemic most common in general medicine and doesn't usually affect eyelids may be purpuric

corneal edemawhenever epithelium disrupted, can stimulate iritis via reflex arc

epithelial

intracellular first

intercellular with microbulla

then subcellular with frank bulla

stomal

all extracellular

factors

imbibition pressure = IOP - swelling pressure (nl 50)

fluid into cornea from IOP, gyclosoaminoglycans's

fluid out of cornea by dehydration, pump

IOP is inverse with swelling pressure

with nl endothelium, high IOP-- epithelial edema

with nl IOP, poor endothelium-- stromal edema

rx

mild

muro 128, hair dryer, control IOP

moderate

soft CL, cycloplegia, PK, conjunctival flap

Corneal Dystrophys

Epithelail dystrophies

3 types

1inger & dots Microcystic or cogans

2Honeycomb or Reis buckler

3bubble paper or Meesmans

1Microcystic or dot finger print or cogans or epithelial basment membrane dystrophy===============thckened BM & cysts with debrismaps- thickening of subepithelial collagen and basement membrane, no flourescein staining dots- cyst like spaces in epithelium containing cellular debris fingerprints- lines in deep epithelium best seen with retroillumination >30 y.o. 10% have corneal abrasions 50% of pts with recurrent corneal abrasions have MDF asymptomatic or present with recurrent erosions, rarely presents with irregular astigmatism Rx: hypertonic saline, debridement with cotton swablubricants, soft contact lens, excimer PTK effective anterior stromal puncturetopical anesthetic, debride areause 23g needle and penetrate anterior stroma up to 1/3 depth may perform even in visual axis but space punctures further apart antibiotic ointment and pressure patchwarn pts about extreme pain afterwards2Reis bucklers ===============progresive dystrophy with grey white deposits at Bowmans & honey comb appearenceReis-Bucker's

D, childhood, gray white opacities at Bowman's layer, becoming more confluent over the yearshistology: destruction of Bowman's layer and accumulation of "rod shaped bodies" replacing Bowman's layerreticulated pattern of scarringpainful recurrent erosions, by 50's marked corneal opacities Rx: excimer PTK, peeling off the superficial accumulated material, recur post PKP

3 Meesmans ===============AD and innoccous with epithelial cysts

AD dystrophy with thick BM, intraepithelial microcysts with peculiar PAS+ substance best seen on retroillumination asymptomatic until 10-20 y.o. when develop recurrent erosions, irritation, small decreased Vano rx necessary differential diagnosis includes cystinosis (metabolic defect resulting in accumulation of refractile cystine crystals, can be seen in peripheral cornea)

Stromal

mnemonic: Marilyn Monroe Always Gets Her Man in LA County.

Macular dystrophy- Mucopolysaccharides stains with Alcian blue GrEY CLOUDS

Granular dystrophy- Hyaline stains with Masson's trichrome stain SNOWFLAKES

Lattice dystrophy- Amyloid stains with Congo red LATTICE

Lattice and granular AD

macular and granular needs grafts corneal

Macular AR, peripheral cornea involved* decreased Va in childhood with diffuse stromal clouding mucopolysaccharides accumulates

type I: error in synthesis of keratan sulfate

type II: can synthesize keratan sulfate but 30% below normal gray white opacities with indefinite margins may involve full thickness of stroma, guttata stains with alcian blue, colloidal iron stain can recur after PKP

Granular = snowflake

AD milky deposits in central cornea, anterior stroma, with intervening clear areas with time,the center of opacities becomes more white;"snowflake" like appearanceaccumulation of hyaline stains with Masson's trichrome stainperiphery may be + for amyloid (ancestry to Avellino, Italy) may recur yrs after PKP often amenable to PTK

Lattice = (Amyloid) childhood, central lines, dots, haze (ground glass) recurrent corneal abrasion, decreased Va by 40 years olddeposits of amyloid stain with congo red, PAS, and Masson's trichrome stain recurrence post PKP common

Central crystalline (Schnyder) =doughnut crystals fat [ cholesterol

Fleck = dandruff uncommon, nonprogressive stromal dystrophy normal Va, no symptoms begins in childhood bilateral but asymmetric gray white dandruff-like opacities to periphery, increased glycosaminoglycans, lipids associated limbal dermoid, keratoconus, central cloudy dystrophy, pseudoxanthoma elasticum, decrease

CCD (central cloudy dystrophy)= clouds bilateral symmetric nonprogessive or very slowly progressive multiple nebulous gray areas with cracks of intervening clea zones normal vision

polymorphic stromal dystrophy = amyloid bilateral symmetric progressive late in lifenormal Va,

associated with systemic amyloidosis

Pre-Descemet farinata pre-Decemet degeneration deep stromal punctate specks above Descemet'sPosterior amorphous stromal dystrophy rare bilateral child with good Va extends to limbus, iris processes, endothelium disrupt focally peripheral variant with clear center CHSD (congenital hereditary stromal dystrophy) flaky feathery anterior central opacity at birth

EndothelialCorneal guttata

thickening and localized excresences of Descemet's membraneresults from abnormal production of collagen by endothelial cells "beaten metal" or "orange peel" appearance do not affect vision but may lead to endothelial dysfunction and corneal edema

Fuchs's dystrophy

AD, F>M, (most common in post menopausal women)It is surprising > common in F and is inherited AD & slightly > conmmon in COAG bilateral and asymmetric, rare in Orientals central guttata first, pigment in endothelium (can have borders)

worse Va in mornings, humid days, increased IOP

Cf endothelial protrberences = guttata and later bulla when stroma thickened by 30% rarely pigmented gutatta can decreased Va (20/60 range)in long standing cases, subepithelial fibrosis, grayish Descemet thickening posterior collagenous layer can obscure all the guttatadiff dx of corneal edema- other endothelial problems, PPMD, disciform keratitis

Rx only if symptomatic, treat as in other causes of corneal edema if considering phacoemulsification check corneal thickness also 5% NS & lower IOP

BCL protects corneal nerves and flattens bulla

Posterior polymorhous dystrophy

innocuous inherited condition with various vessicluar band like or geographic assymitircal opacities .

AD bilateral childhood, progressive, asymmetrypresents as a spectrum of corneal changes that occasionally involve iris and angle endothelial cells act like epithelium, may look like ICE posterior surface with ridges, lines and circles with scalloped edges, stromal edema, iridocorneal adhesionsbest seen in retroillumination

CHED (congenital hereditary endothelial dystrophy)

Type I: AR, most common, no pain or tearing stationary, diffuse, often present at birth associated with nystagmus

Type II: AD, presents at 1-2 year old, painful tearing, progressive, less corneal edema, no nystagmus, cornea blue ground glass, associated with deafness

Other corneal pathology

Keratoconus

severe > 54D nipple oval or globus classification depending on central cone size

CJ scissor retinoscopy

irregular astigmatism where principle merideans no londer at 90'

photokeratoscopy or pacidos disc irregular

slit lamp vogts lines and prominent corneal nerves.

later central thinning scarring fleisher ring acute hydrops

central or paracentral corneal thinning and bulging

sporadic, can be familial (<10% of occur in blood relative)

bilateral but asymmetric

associated with Down's, Leber's, atopy

signs: Vogt's striae,Vogts striae in keratoconus is lines on cornea when compressed

Fleischer ring- iron deposits at the base of the cone, scarring, early astigmatism

Ehler Danlos VI

keratoglobus, spontaneous perforation of globe, blue sclerae

Rx

bcont lens

Patch

Hypertonic saline 5% normal saline

Instruct do not rub eyes

Keratoglobus

thinning greater in periphery near the apex of the protrusion, mild scar, not genetic, connective tissue disorders

associated Ehlers-Danlos type VI

Pterygium ==========elastic generation of conjuctiva subepithelial collagen & corneal collagen

Phlyntenosis ========Phlyctenular ulcer = nodular pinkish white limbal elevation with gray crater, can be on conjunctiva caused by type iv hs to staph TB or candida antigen

Infective Corneal ulcers & KerititisBacterial keratitis

risk factor: + atopy, prior HSV, , bullous keratopathy, OCP, Stevens Johnson syndrome, abnormal lid position

Most common Staph/Pseudomonas are more than 50% of all cultured cases

Virulence Worst are Pseudomonas, Strep (B-hemolytic, pneumoniae)

Penertration direct epithelial penetration by GC, H egypticus, Diptheroids, Listeria

Staphgram positive cocci~~~ulcer is usually localized with distinct borders- may satellite

S. aureaus vs S. epidermidis (coagulase-negative) causes deeper ulcers, more inflammation, hypopyon, and endothelial plaque t

Strep pneumoniae~~~~~ ulcerative keratitis + inflammatory membranes

risk acute or subacute purulent conjunctivitis

Neisseria gonorrhoea~~~ mucopurulent discharge may cause perforation

risk~hyperacute onset most often a progression from conjunctivitis

Moraxella~~~~~~~~~~~peripheral or paracentral infiltrate

risk more chronic, indolent keratitis- in chronically debilitated patients-

special dx consider calcium alginate swab so

Pseudomonas ~~~~~~~perforation

risk contact lens

Haemophilus ~~~no membranes

risk group purulent conjunctivitis and preseptal cellulitis in children

Phlyctenular ulcerpinkish white limbal elevation with gray crater, can be on conjunctiva type IV immune mediated response caused by: staph, TB, Candida, Chlamydia, nematodes, gonococcal antigens, adenovirus early Terrien's can look similarRx: treat the infection if active, topical steroids used to minimize scar formation

Staph Marginal Infiltrates =margial kerartitis

type III immune reactiongray limbal ulcer usually with clear cornea all around, early corneal neovascularizationallergic rx usually to staph at 8/10 and 2/4 o'clockcan progress to ring ulcer, usually spread toward limbus not centrallycan get superinfectedAtopy Wg C UC SLe scleroderma hookworm influenza TB samonella dengue gold poisoning Gc athritisInfectious Crystalline keratopathy===feathery "crystalline" edge, assoc. with chronic steroids, (eg. PKP) due to alpha strep viridens,

poor response to topical therapy biopsy usually for diagnosis rx with concentrated topical bacitracin

Acanthameoba

found in water, existing as a cyst or trophozoite

mimics HSV early, later ring infiltrate, often misdiagnosed as HSV

symptoms: wax and wane with photophobia, FBS, severe pain

signs: first abnormal epithelium (SPK, persist defects, SEI, edema, whorl like patterns, dendritiform lesions)

then central/paracentral stromal infiltrate with satellites, turns into ring

neurokeratitis with cuffing of nerves

preauricular adenopathy

Dx: biopsy , stains (Giemsa, calcofluor white, acridine orange) are faster and better than culture touch material instead of smearing on slides

use spray fixative instead of air drying IFA, calcofluor white, conjugated lectin flourescein stain culture on non-nutrient agar with E. Coli overlay Rx: difficult, often fails, use multidrug approach

antiseptic (PHMB or chlorhexidine) + Brolene 0.1%, neosporin add clotrimazole 1% q15-q1h +/- ketoconazole 200 mg po bid or fluconazole po no steroids once infection in peripheral cornea, poor candidate for graft Acanthamoeba(Every hour for first week and 5 min apartBrolene and Neosprin +ADD Oral ketoconazole + 1% topical Clotrimazole If lack of response or advancing stromal involvement(Tapered after 1 week(Continue 1 year Brolene and Neosprin Other regimesTriple therapy Polyhexamethylene biguanide, which is a cystocidal as well as a trophozoicidal (none of these agents has worked consistently, alone or in combination. Fungal

mostly filamental, Fusarium, Aspergillus >50 %

Candida 10% in older, keratoconjunctivitis sicca,

Dx: stains with calcofluor white, 10% KOH wet mount

Gomori methenamine silver or PAS

culture Sabouraud's and blood agar

Rx: filamentous fungi is now fluconazole with good penetration

second-line drugs include amphotericin B 0.15% (1.5 mg/ml) or imidazoles (miconazole 1% or ketoconazole 1-5%)

first-line for candida is ampho alone or in combination with flucytosine, do not use flucytosine alone because of high resistance

second-line for candida is imidazoles ViralHSVHZOThygesons superficial puctate keratits=rare presumed viral fleeting keratitis=small grey intraepithelial dots with mild subepithelial haze

Fungal Keratitsfilaments parakacinuse ampho B or azole for cystsCf very florrid limbal vasculaization and fluffy discharge

Interstitial keratitis

syphilis Cogan's syndrome =bilateral intersitial keratitis associated with vestibuloauditory symptoms may also involve polyarteritis nodosa,and necrotizing lesions that leads to endocarditis and gastrointestinal hemorrhages

other conditions associated with interstitial keratitis TB leprosy LGV sarcoid HSV IHZO mumps Kaposi's sarcoma

protozoan/helminths lyme disease Hodgkins ncontinentia pigmenti

Steven Johnson

RX topical steroids & oral steroids

Rx Topical Retinoic acid for keratinization

Punctal occlusion & tear supplments

Scleritis

Diffuse anterior scleritis . Erythematous, immovable and tender inflamed nodules Approximately, 20% of cases progress to necrotizing scleritis. Necrotizing anterior scleritis Scleromalacia perforans, rheumatoid arthritis.notable for its absence of symptoms Anterior scleritis is demonstrated in 94% of patients In 15% of the cases, scleritis is the presenting cvd Sex: The female to male ratio is ~ 1.6:1. Pain Severe, constant, deep, boring or pulsating May awaken the patient at night The onset of scleritis is more gradual than the acuteness seen with episcleritis. Both eyes are affected in slightly over one-half the cases. degree of injection, as well as, the presence of a bluish hue, signifying attenuation of the sclera. Prominent findings may include photophobia, tearing without discharge, tenderness of the eye and purplish-red, edematous, engorged blood vessels.

Deeper scleral blood vessels appear darker, follow a radial pattern and do not move when manipulated with a cotton swab.

Phenylephrine application causes blanching of the more superficial episcleral vessels but does not change deeper vessels.

Scleral thinning: the choroid pigment becomes visible as a bluish hue Use of a red-free filter (green light) .

Posterior Scleritis:

Causes: Scleritis coexists with a serious systemic disease in almost one-half of cases.Rheumatoid arthritis occurs almost a one-third

Discoloration depicting scleral thinning

%Pupil Pupi test Rapd is caused by assymetrial pupilomotot response

Horner's syndrome

-miosis, ptosis, anhydrosis, and apparent relative enophthalmos (heterochromia in congenital cases)

-caused by sympathetic lesion (pre or post-ganglionic)

1st order horners occurs in the brain 2nd i the chest or neck and 3rd along the caorotid

First order - CNS lesion caused by stroke or tumor

Second order - caused by cervical disc disease or trauma to C-spine, apical lung tumors (Pancoast syndrome), tumors metastatic to cervical lymph nodes, chest surgery, thoracic aortic aneurysms, trauma to brachial plexus.

Third order - caused by intracranial diseases including migraine (Raeder's syndrome Type II) and cavernous sinus inflammatory (Tolosa-Hunt syndrome), traumatic (carotid-cavernous fistula) and neoplastic (meningioma, metastasis, lymphoma) diseases.

-no dilatation with topical cocaine (4% - 10%) Normally it prevetns NA uptake andtherefore augments NA thatis present

-pre and post-ganglionic Horner's differentiated with Paredrine 1% (hydroxyamphetamine) test

pre-ganglionic dilates

post-ganglionc does not dilate

Works on premise that noradrenaline can be released at iris by hydroxyamphetamine if the ganglion can make it and is ok

--------= 0----------=

it either works or not at ganglion

cocaine works only if there is a supply of noradrenaline and prevents its reuptake----- so it only works if the system is ok.*

#Lacrimal SysytemEpiphora in kids below 1 tear is due to failure of the lower NLd to perforate. This happens at about at latest 1 year so wait ubtil then before probing

In adults it is most commonly due to Chronic Dacrocystitis

Mucucoeles are genrally not operated on as they lead to fistulas or may spread infection

#OpticsRetinoscopy

static Accomodation is suppressed by cycloplegia

& dynamic

Essntials

1lght in the form of a cone or streak is projected using a mirror to illuminate the retina as a Patch.This acts as a secondaey Light source.

The obserever views a central aperture yo view the light emerging from the pupil

Aim is to neutalize the obserevd movement ie when to far point of the eye is reached

#Defintions nanophthalmos = high hypermetropia

red free is done using green light This

Optic disc ishchemia early on and leakage later

Optic Pit

Think where pits are most destructive inferior temporal

Maddox rods

What is Pulfich phenomenon

Hue Farnsworth Munsell 100 hue test chips

#Glaucomasupeior and inferiortemporal arcuate fibres are most sensitive to glaucomatous changes hence 1st defect is Nasal superior extension of blind spot. which is anatomically at about 15' from fixation.

This is( B)jerrms area

Therefore look near blind spot and nasally

2nd defect is a nasal step or temporal wedge.

If you see these look for a paracentral scotoma carefully.

Later constriction occurs nasally temporally and then centrally

Perimetry

Humphrey or Octopus

spot size is 0.43' and duration is 0.1 sec

contrast in decibels

no of targets 25 or 72 or 132

The numeric display is the patients threshold {minumum response}value in decibels

The symbolic is similar except it explains it in 5 grades and relative to normal population for age

The graphic is similar except it explains it in 9 shades of grey

Threshold measures the patients threshold and then compares it to age matches it is quantative

Superthreshold measures spots above threshold ie qualatative and screening.

Its aim is to pick up changes in young people.

Visual threshold

This is luminence seen in 50% of individuals.

We need 10% change to notice difference therefore log scale

fovea sensitivity is 35 db at 20 years & we lose1 db lose per 10 year) hence at 70 years it is 30 db

Visual field

60' nasally 90' temporally 50' superiory 70' inferiorly

Neural rim thickness

ISNT

Grade of angle

Look for

IV~~~~~~~~ciliary body Brown

III ~~~~~~~scleral spur A little sharp just anterior to Ciliary body

II White trabeculum ( which is anttwerir and posterior thicker Baige or greyish nBlue

NB in Argon Trabeculoplasty applie burns to the junction

I ~~~~~~~Scwalbes line only White

0 ~~~~~~~use this word inability to see apex of corneal wedge.

NB I need indentation gonioscopy to differentiate appositional & Synechial angle closure.

# Retinal Detachment Cryopexy takes 2 to3 weeks to from an adhesion freezing cc and RPE right down to outer photoreceptor layer thus closing space VS Laser pexy that is instantanous as the RPE burns and closes space

Exudative Retinal Detachment (ERD)==Occurs when either retinal blood vessels or RPE is damaged, allowing fluid to pass into the subretinal space

Neoplasia and inflammatory dz are leading causes of large ERD

Shifting fluid responding to force of gravity Smooth, bullous appearance

There is no photopsia and not commonly floaters as these will occur only secodary to vitritis and not due to snchisis as often see on RRD

signs smooth and convex or bullous

shifting fluid is the hallmark

look for the cause eg tumour and u won't see a tear!

Idiopathic Coat's ???CSCR Uveal Effusion Syndrome ????Congenital FEVR ???Optic pit Nanophthalmos Postsurgical PRP RD repair Hemorrhagic choroidal detachment Inflammatory Scleritis Orbital pseudotumor HZO CMV retinitis VKH??? SO PIC AMPPE Vascular Toxemia of pregnancy AMD Hypertensive retinopathy Diabetic retinopathy Chronic renal failure Cardiac insufficiency

Hematologic TTP Leukemia Neoplastic

Peripheral Retinal Abnormalities

Landmarks read up anatomy

Long posterior ciliary nerves at 3:00 and 9:00 Short posterior nerves usu. superior and inferior Vortex veins at the equator and near superior & infer rectus ie 12 and 6 o clock

Scleral depression

Depress just posterior to recti insertions, since ora serrata lies just underneath Spiral of Tillaux

Retinal breaks

ARE Any full-thickness defect in the neurosensory retina

Horseshoe tear* ~~~~Strip of retina pulled anteriorly by vitreoretinal traction

Giant retinal tear ~~~~Tear that extends 90o or more circumferentially

Operculated hole~~~~ Traction is sufficient to tear a piece of retina completely free from adjacent retinal surface

Retinal dialysis~~~~~~Break occurring along ora serrata, commonly resulting from blunt trauma (superotemporal quadrant most common if traumatic) Usu. at posterior border of vitreous base

PVD

Vitreous base (VB) - , extending 2mm anterior and 4mm posterior to ora

Vitreous also firmly attached at: Major retinal vessels, Margin of lattice degeneration, sites of chorioretinal scars

Initial event - syneresis =(liquifaction) of central vitreous~~~ Hole develops in posterior vitreous ~~~~ Liquified vitreous passes into subhyaloid space, rapidly separating posterior hyaloid from retina,~~~~ BUT Vitreous gel remains attached at VB Resulting vitreous traction, commonly at posterior margin of VB, may produce retinal break

symptoms: photopsia, floaters = (VH, glial cells from optic disc, aggregated collagen fibers) Weiss ring is glial cells from OD

15% of pts w/ acute, symptomatic PVD have a retinal tear

70% of pts w/ VH assoc. w/ PVD have a retinal tear

2 to 4% of pts w/o VH assoc. w/ PVD have a retinal tear

Prevalence of PVD increases w/: Increased axial length Advanced age Aphakia nflammatory dz Trauma myopia

Macular hole is formed by tnagential traction followed by ap traction that causes PVD but also takes a bit of fovea

complete pvds are therefore not going to cause holes

Traumatic retinal breaks

Traumatic breaks often multiple and commonly found inferotemporal and superonasal

Dialysis most common, usu. at posterior border of VB

Avulsion of VB (anterior vitreous detachment) may be assoc. w/ a dialysis, and is considered pathognomonic of ocular contusion. "Buckle handle" Vitreous may eventually liquify over a tear, subsequently leading to RRD. Clinical presentation of RD usu. delayed

12% immediately 30% in 1 month 50% in 8 months 80% in 24 months

traumatic RD in young pts. usu. show chronicity shallow w/ multiple demarcation lines subretinal deposits & intraretinal cysts Blunt trauma (A/P compression w/ equatorial expansion)

Coup mechanism (adjacent to point of trauma) Contrecoup injury (opposite point of trauma)

Benign Peripheral degenerations =Lesions not predisposing to RD

cobbelstone paving dark tiles small (micrcystic ) honey spread or snowflakes serial or drusen degenerations will not cause slipping

vs

lettuce on the floor or folded or tufts of grass or bays sandor excavations will lead to a fall

Cobblestone (paving stone) degeneration===Small, discrete areas of ischemic atrophy of outer retina

attenuation or absence of CC Loss of RPE and outer retinal layers Adhesion btw remaining retinal layers and Bruch's MB Most common in inferior quadrants, anterior to EQ Appear yellow-white, may be surrounded by rim of hypertrophic RPE Large choroidal vessels may be visible (RPE absent)May be confluent Present in 22% of people >20 y.o.

RPE hyperplasi or RPE hypertrophy Microcystoid === tiny red coloured vesicles Snowflakes ====white scattered dots Honeycomb===fine network perivascular Drusen

Lesions predisposing to RD

Lattice degeneration===discontinnuity of ilm & atrophy of inner retinal layer due to condensed aherent vitreous

6% to 10% of general populatio Bilateral in 1/3 to 1/2 More common in myopes Histopathology:discontinuity of ILM, overlying pocket of liquified vitreous, condensation and adherence of vitreous at lesion margin, atrophy of

retinal inner layers, sclerotic blood vessels Underlying cause in 20% to 30% of all RRD Vitreoretinal tufts=== retinal elevations due to vitreous traction

Small, peripheral retinal elevations caused by focal areas of vitreous or zonular traction Classified as: noncystic retinal tuft, cystic retinal tuft, zonular-traction retinal tuft

Cystic and zonular-traction types more likely to predispose to RD because of firm vitreoretinal adhesion Meridional folds===Folds of redundant retina

Usu. superonasal Most commonly assoc. w/ dentate processes Enclosed ora bays===ora pars plana in retina

Oval islands of pars plana epithelium located just posterior to ora; completely (or almost completely)

circumscribed by peripheral retina Peripheral retinal excavations

May represent atypical lattice

Often aligned w/ meridional folds

Retinal Breaks

tears such as round, atrophic holes, operculated holes, macular holes have a minimal chance of progressing to RD

acute, symptomatic tears carry a considerable risk factors to consider in risk/benefit of Rx: symptoms, residual traction, location of break, phakic status, refractive error, status of fellow eye, family history, presence of subretinal fluid, and follow-up reliability

Rhegmatogenous Retinal Detachment (RRD)

Rhegma: Greek for break

Caused by liquified vitreous passing through retinal break into potential space between sensory retina and RPE

Shafer's sign: small clumps of pigmented cells (tobacco dust) in vitreous or AC Corrugated appearance, undulating w/ eye movements (however, in old RRD the retina may appear smooth and thin) Convex ie balooning

vs

Tractional Retinal Detachment (TRD)

Smooth surface, immobile Concave Rarely extends beyond ora serrata May cause tear leading to RRD

PVR

RPE, glial, and other cells grow on both the inner and outer retinal surfaces and on the vitreous face

Contraction occurs >fixed folds>equatorial traction>detachment of nonpigmented epithelium of pars plana>generalized retinal shrinkage

Causative retinal breaks may reopen, new breaks may occur, or a TRD may develop

PVR Classification

Grade A: vitreous haze, & pigment clusters on inferior retina Grade B: wrinkling or stiffness of inner retinal surface, rolled and irregular edge of retinal break, Grade C P 1-12: posterior to equator. full-thickness folds*, subretinal strands all expressed in number of clock hours Grade C A 1-12: anterior to equator.

#VitreousAsteroid hyalosis=calcium containing phosphoipids in vitreous=White Opacities evenly distributed Assoc. w/ diabetesIncidence 1:200 > 50 y.o. unilateral 75% vision NAD

VS

RARE AND visually significant

cholesterolois (hemophthalmos, synchysis scintillans)=Golden Numerous yellow, white, gold or multicolored cholesterol crystals in vitreous and ACAlmost exclusively s/p accidental or surgical trauma w/ large intraocular hemorrhage PVD common - allows crystals to settle inferiorly very rare most of the time in clinica you will asteriod hyalosis

Diseases of the Vitreous

Tunica vasculosa lentis== Entire hyaloid system, either patent or occluded, may persist from disc to lens None of these remnants is visually significant

Mittendorf's dot (anterior remnant): attached to lens capsule

Bergmeister's papilla (posterior remnant): fibroglial tuft extending into vitreous from optic nerve head margin

Prepapillary vascular loops===Normal retinal vessels that have grown into Bergmeister's papilla before returning to the disc

Usu. < 5 mm in height May supply one or more quadrants of retina 85% arterial, 5% venous Complications: BRAO, amaurosis fugax, VH

Persistent Hyperplastic Primary Vitreous (PHPV)/

Persistent Fetal Vasculature (PFV)=Failure of primary vitreous to regress

Usu. found in otherwise normal, full-term infants of normal birth weight Unilateral 90% Usu. obvious at birth (unlike retinoblastoma)

Anterior form: Hyaloid artery remains White vascularized fibrous membrane present behind lens Associated findings: microphthalmos, shallow AC, long ciliary processes visible around small lens, cataract, secondary angle closure glaucoma Very poor prognosis for useful visual acuityPosterior form: May occur w/ anterior PHPV Microphthalmos may be present, but AC usu. normal and lens usu. clear, without retrolental membrane Stalk of tissue emanates from optic disc toward lens, often running in apex of retinal fold in an inferior quadrant Stalk fans out circumferentially toward anterior retina

DDx: ROP, toxocariasis, FEVR

Hereditary hyaloideoretinopathies with optically empty vitreous===Hallmark is vitreous liquefaction resulting in optically empty cavity except for thin layer of cortical vitreous behind lens, and white avascular membranes adherent to retina

Equatorial and perivascular (radial) lattice ERG may be subnormal

only with ocular manifestations: AD, myopia, strabismus, cataract

Wagner dz - usu. not assoc. w/ RD High myope, post. cortical cataract at puberty, peripheral vitreous veils, strabismus, perivenous radial lattice Jansen dz - high incidence of RD

with assoc. systemic manifestations:

Stickler syndrome (hereditary arthro-ophthalmopathy-Marfanoid variety)

AD High incidence of RD Myopia Open angle glaucoma CataractOrofacial findings: Midfacial flattening Pierre-Robin malformation complex (micrognathia, cleft palate, glossoptosis) Skeletal abnormalities: Joint hyperextensibility/enlargement Arthritis Spondyloepiphyseal dysplasia

Hereditary arthro-ophthalmopathy with stiff joints (Weill-Marchesani-like variety) High incidence of RD Four varieties w/ frank dwarfism: Kniest syndrome RD common Dwarfism, facial abnormalities, joint stiffness, sensorineural deafness Spondyloepiphyseal dysplasia RD less common Congenital dwarfism, normal facies, joint laxity, normal hearing 2 other varieties variable incidence of RD

FEVR with Peripheral fibrovascularization Large syneresis cavities ERM Dragged macula Increased arborization ^ may mimic Coat's May have abnormal platelet aggregation Usu. bilateral Full-term w/ normal respiratory status No peripheral mesenchymal shunt

Amyloidosis==Bilateral vitreous opacification (glass wool appearance) &may cause decreased visual acuity warranting vitrectomy

Spontaneous vitreous hemorrhage

Diabetic retinopathy (39% - 54%) Retinal break w/o RD (12% - 17%) PVD (8% - 12% RRD% - 10%) NV s/p BRVO or CRVO (4% - 10%) Any cause of peripheral NV Congenital retinoschisis Pars planitis

Vitreoretinal interface abnormalitiesEpiretinal membrane (ERM)===PVD may leave cortical vitreous attached to macula, or may cause dehiscience in ILM allowing retinal glial cells to proliferate along retinal surface/posterior cortical vitreous Contracture of ERM > cellophane maculopathy > macular pucker Shallow TRD

Secondary to: retinal vascular occlusions, uveitis, trauma, intraocular surgery, retinal breaks Idiopathic - abnormality of vitreoretinal interface in conjunction w/ PVD > 50 y.o. M=F 20% bilateral CME Traction on vessels > leakage on FA

Vitreomacular traction syndrome

PVD incomplete in maculaVitreous opacities overlying maculaShallow macular detachmentFA: leakage in macula and disc

RD surgery

Silastic sponge through Peitomy excision tenons

#Denerations and Dystrophies of fundus seen mostly at Macula

Nb RPE is drusen etc and causes masking while PR is RP color /night blindnessRPE=bests stagarts&flavimac drusen & AVFMD

photo= RP cone dys csn blindness albipunctus lebers amaurosis

RPE degeneration

diagnosis absence of normal background choriodal flurescence due to pathological rpe

1Bests = egg yolk lesion

AD stage i abnormal stage ii yolk stage iii pseudo hypopyon stage iv scrabbled egg stage v end stage

2Adult foveamacular viteliform dystrophy

3Stargarts macular dystrophy = beaten bronze macular & fundus flavimaculatus= fish tail like spots

4familial drusen

Photoreceptor dystrophy

1RP Spradic most common AD XL AR 1 in 4000 disease of Rods

Cf:bilateral arteriolar attenuation,bony spiculation waxy disc pallor By 30 5% are symtomatic

2Cone dystrophy = bulls eye fundus central ring of atrophy

3Leber amaurosis variable

4Congenital staionery night blindness normal fundus

5Fundus albipunctus = fine yellow spots in fundus NM Remeber seeing apaptient with this

Maculopathies

Anatomy and the eye

Spaces

1 choriocapilaris 2 Bruch3RPE 4outer 1/3 sensory Retina with Photoreceptor (supplied by chriocapilaris) and5inner 2/3 sensory retina that has arterioles and venules

Every patholgy must be explained by AREA

Drusen ARMD~~~~~hyaline between bruchs and RPE( with RPE atrophy and depigmentation)

RPE and sensory detachment ~~~~clear fluid between bruchs and RPE

RPE and sensory haemoragic detachment~~~ blood

SRNM below RPE grey green to pink slightly elevated lesion

broken into subretial space tranlucent pink white lesion

CSCR serous fluid below separated sensory retina

CMO cysts in sensory retina at outer plexiform layer

causes vascular or non vascular

post surgery trauma

DM CRVO teleangiectasia

lamella hole sensory retina thin

macular hole only RPe left

Myopia atrphophy retina RPE and CC

Fuchs spots = pigmentaion in retina

Macular plucker = peretinal fibrosis and traction

Chroidal folds simple

angoid streaks dark lines deep errated and irregular and termoinate abrubtly ~~cracks in bruchs

Chloroqune toxity choroquine accumulates products in RPE and visible esp at foveola

RP bone spicule perivascular outer 2/3 neurosesory pigmentation Optic disc waxy pallor ~~~ ischemia or hyaline drusen

bests lipofuschin at RPE sensory level space that colasece= yolk

AFVD

1CSR

2CMO

histology intracellular fluid accumulation in mullers cells which is reversable and is seen as large spaces in OPL

it is irreversable if acculation is intracellularly

DDX stage 1 macular hole lamelar hole epiretinal membrane solar retinopathy pattern dystrophy

RRD x linked Retinoshisis difuse mac oedema

causes postop eg ECCE PK iridotomy PRP Cryo buckling RS dystrophies inheited RP AD CMO vascular DM Coats JF telangiectasia choriodal neov radiation CRVO HT Macroaneurysm Ocular ishemic syndrome TX CM Inflam Bechets Sarcoid birdshot PP Vitritis Toxo CMV Meds Epinephrine Nicotinic acid

3Macular hole

Idiopathic macular cyst and hole

6th-8th decades assoc. w/ tangential vitreomacular traction Bilateral 25% - 30% B scan of both eyes since

separation of posterior vitreous face has much better prognosis Gass classification:

Stages of macular holes (new - Gass 1995)

1A) foveolar detachment

1B) foveal detachment

2) early hole (<400 microns)

3) larger hole (>400 microns) +/- operculum

4) full thickness hole with PVD

Outer lamellar hole ~~~~s/p Berlin's, optic pit, sun gazing

Inner lamellar~~~~~~~~~ more common, CME, 20/20 to 20/80, Amsler distort, minimal to no window defect on flourescein angiogram, <1/3 DD

4Myopic maculopathy

5Angoid streaks

causes PEPSI Pagets ehler danos pseodoxanthoma elasstica sickle cell idopathic

6Choroidal folds

7Toxic maculopathy Phenothiazines choloquine tamoxifen canthxanthain

hydroxychloroquine incidence 0.08% vs 1 to 2 % for chloroquine

Related to lysosomal degradation and lipofucin production

Plaquanil (hydroxychloroquine) (>400 mg/day) may have a direct toxic effect on receptors daily dose more important than total dose

Chloroquine >250 mg/day

Cummulative dose more than 200g or 4 years

Contrast did not deterioratw as much as color

ass gene for stargarts dx susceptibility more if gene present

Explains why only some get it

(more toxic) do it within 6 months of

early loss of foveal reflex granularity of macula bulls eye lesion arterial narrowing sheathing and peripheral pigment cornea verticillata poliosis CN VI palsy decreased accommodation decreased corneal sensation blurred VA Paracentral /central scotoma dyschromatopsia

tests ERG increased a, decreased b, normal dark adaptation baseline VA, Amsler, color plates, photos, exam q 6 months HVF central 10 if needed, if decreased by 0.5 log, stop drug do not need red light with HVF since measuring decibels

Phenothiazines~~~ Concentrated in uvea and RPE by binding to melanin granules Mellaril (thioridazine) (>800 mg/day) effects after 3-8 wks. nyctalopia, fine stippling to widespread atrophy of RPE, CC ring/ central scotoma, blurred VA Thorazine (chlorpromazine) lid, conjunctiva, corneal, capsular pigmentation, ASC/PSC, >1200 mg/day of >1 yr., rare pigmentary retinopathy Digitalis~~~toxic dose is cone toxic, therefore colors changes blurred VA, pericentral scotomata, yellow vision Desferroxamine used for hemosiderosis bilateral rapid LOV 1 wk. after last dose, nyctalopia VA returns in 75% by 3-4 months Tamoxifen& canthxanthain >200 mg/day for 1 yr. (>100 gm total)normal dose is 10-20 mg bid inner retinal refractile deposits CME Decreased VA optic neuritis white corneal opacities DDx Crystalline retinopathy may resemble that seen after ingestion of high doses of canthaxanthine (carotenoid used to stimulate tanning) Prolonged methoxyflurane Ax: crystalline maculopathy w/ renal oxalosis/failure Oxalosis primary hyperoxaluria, ethylene glycol abuse, prolonged methoxyflurane anesthesia crystals in RPE Methanol seeing spots to blindness 18-24 hours after ingestion (formic acid toxic) early optic nerve swelling, vein dilation, retinal edema 1-2 month later, optic nerve atrophy, cecocentral scotoma, decreased ERG most of the recovery takes place in one week severity related to acidosis, consider hemodialysis Clofazimine for dapsone-resistant leprosy, HIV+ and MAI bull's eye lesions with window defects and normal Va reported

Age related maculopathy

Choroidal degeneration

1Choroidemia degeneration of choriocapilleris and RPE

fa large chorioidal vessels only seen thru window defect

XLR scalloped RPE and loss of choroid, CC, and RPE starting at equator and moving anterior/posterior. nyctalopia, 4-20 y.o., VF loss peripheral, no spicules but clumping < 20/200 by 50 y.o. ERG abnormal Carriers: can have symptoms, pigment clumping, RPE granularity, ERG and VF normal Abnormal gene codes for a component of rab geranylgeranyl transferaseDDx: high myopia, gyrate atrophy, RP, Bietti's crystalline dystrophy

II Gyrate choroidal degeneration

ARrnithine aminotransferase def., 10X increased ornithine, as early as 8 y.o. scalloped RPE/CC loss, peripheral paving stone, rest of RPE increased pigmentation, myopia, cataracts progressive loss of VA and VF , nyctalopia, abnormal EEG, changes in hair/muscle fibers, ERG abnormal <20/200 by 40 y.o. dietary restriction of arginine, vit. B6

IIICentral aereolar choroidal dystrophy

IVGenralized choroidal atrophy

VCentral areolar pigment epithelial dystrophy CAPED

Vitroreinal degeneration

Sticklers

Retinoschisis

Avre Goldman ===synchysis + Retinoshisis + RD like

Familial vitroretinopathy

#Retinal vascular disorders1DR

2RVO

3RAO

4HR

5Retinopathy in blood disorders iSickle cell iianaemias iiileukaemias ivhyperviscosity vROP

6Retinal telangiectasia 3 Types: Idiopathic juxtafoveolar retinal telangiectasia least severe and presents with

microaneurysms and kinked microvascular channels near fovea. Lebers miliary aneurysms saccular dilations Coats This is the most severe and occurs mostly in young boys and presents with subretinal exudation males frm 18months to 18 years unilateral mostly superior quadrant pathophys bd of inner BR barrier telangiectasia cap closure deposit of macrophage elated lipid gives it typical exudative lok which is different from exudative detachment that may follow

coats response =is massive exudation in any disease

7Retinal artery macroanerysm

#Uveitisidiopathic common

Fuchs iridocyclitis acute onset adult anterior uveitis Intermediate uveitis=pars palnitis juvenile chronic uveitis

Fuchs uvietis syndrome 2% of all one eye and middle age

Cf Mild uveitiswhite KP mild uveitis and no posterior synechie IrisHeterchromia iridis and iris atrophy and enarged pupil and occasional koeppe nodules mild vitritis gonioscopy fine radial twig like neovascularizationn which are probably responsible for haemorrhage noted with paracentesis=amslers, fine membrane or small fine PAS

Amsler's sign =bleeding occurs during cataract extraction and is due to wispy iris vessels which extends from the iris to the trabecular meshwork and do not cause anterior synechiae

Cx secondary glaucoma cataract

Rx topical steriods NO objective improvement.

Iris nodules

Koeppe ===small and on pupil margin common

Busaca opposite!!===large and on whole pupil large central and lss comon

Uveitis grading use a slitbeam 3mm × 1mm

anterior ueitis 1 < 10 cells

2 20

3 50

4 > 50

Idiopathic rare

nemonic singing bird singing serpent sweating ealewhite galucoma patient & multiple retinal vessels white dot

1Birdshot 2serpenginous 3Acute M P3 epitheliopathy 4sympathetic5Punctate inner choroidopathy 6Multifocal choroiditis and panuveitis 7Eales 8Retinal vasculitis 9Glaucomatocyclitic crisis 10idiopathic rareMultiple evanescent whitedot syndrome (also causesoptic atrophy)

the classication may be simplified to the 6 idiopathic inflamatory white dt syndromes

MEWDS young males small white dts

AMPEE ass HLA B7 largers placiod cotton wool like

PIc myopic females small yellow

brdshot moderate creamy middle age with vitritis

Multifocal choroiditis discrete grey yellow

Serpiginous

AMP3e ===deep cream B27 male = female

Serpenginous===

Birdshot===

Multiple evanescent white dot syndrome see optic neurpathy

Punctate inner choriodpathy ===young female myopes small yellow choriodal lesions at posterior pole

Multifocal Chorioditis ===age 20 to 50 multiple grey yellow lesions simialr to sarciod and treatment is similar

Eales===young male peripheral occlusion and neovascularization like sickle cell aneamia

Assosiated with systemic disease eg Sarcoid Bechets Behcets classic triad of hypopyon iritis (short lived, often painless), aphthous oral ulcers, and genital ulcers increased incidence of HLA-B5 or subset B51 may actually cause a panuveitis (included in anterior section because of the classic acute hypopyon iritis)

young males from age 15 to 55 rare in US; more common in Japan, Mediterranean countries

Behcetine skin test: puncture skin intradermally with sterile hypodermic needle( if pustule forms within few minutes, indicates a positive test (rarely done)

systemic generalized occlusive vasculitis of unknown cause recurrent aphthous ulcers up to 1 cm, painful, demarcated mucosal ulcers are deeper and scar nodular genital lesions with central ulceration

skin lesions of erythema nodosum and pseudofolliculitis (pustular vasculitis) pathergy test is not useful in United States can mimic IBD with ulcerative hemorrhages in the GI tract

nondestructive recurrent arthritis- arthralgia in wrists/ankles in 60%

1/4 with CVA, confusional state, meningoencephalitis

ocular initial eye presentation in 25% of men and 10% of women asymmetric bilateral eye disease posterior involvement more common than anterior in men recurrent noncoagulable hypopyon iritis (10%)

common posterior findings of vasculitis ultimately leads to vision loss (sheathing, retinal necrosis, CME, vitritis, serous RD, ischemic optic neuropathy, CRVO) vasculitis tends to be hemorrhagic and involves both arteries and veins

prognosis risk of visual loss is higher in males and higher in patients with skin lesions, arthritis, and/or posterior uveitis

chronic and recurrent over 10 years before burning out

in the U.S., only 25% end up with Va < 20/200

RX

includes oral steroids, chlorambucil and other immunosuppressives

colchicine (pts have increased PMN mobility)=inhibits WBC motility and is ths antiinfamatory dose 0.5mg tds contarindicate din pregnancy

cyclosporine, cyclophosphomideVogt Koyanagi Harada(VKH)

Infectious Syphilis TB AIDS Lyme Leprosy brucellosis

syphilis

most eye involvment is in 2' and 3' stage

iridocylitis rare and only in 4% presents with G or NG uveitis

great mimicker

multifocal chrioditis is most common and later the can bone spiclues like RP

unifocal choroiditis is rarer and usually at macular and peripappilary

Neuroretinitis is independent of chorioditis and causes optic atrophy plus a florrid retinits and perivasculitis

other AR pupil retobulbar neouritis occ palsies VF defects

RX 12 to 24 MU IV for 10 days and 2.4MU IM for 21 days OR 500MG Doxy or Erythr QID for 30 days

Lymes spirochete borrelia burgdoferi via tick ixodes

first stage is a erythema migrans second atge is with eye signs and arthritis and CNS and Myocarditis 3rd stage is chronic arthritis that can be mistaken for RA

eye stage first a conjunctivitis and then a iridocylitis that may become interemdiate and also cause retinal vasculitis VERY rarely choroiditis and stage 3 with orbital myositis KPs and epicleritis (THIS ORDER IS abit strange but indicates chronic low grade nature

Goes front retina and than front again!

Brucella aborticus affects animal workers and causes Gran Uveitis

Parasite Toxo Toxocara

Viral Hzand Hs iris Acute reinal necrosis Congental rubella

Fungal Presummed occulat histplasmosis Candida

assosiated Arhritis Reiters ankylosing spondylitis JCA Psoriasis Reiters triad of urethritis, conjunctivitis, arthritis

85-95% are HLA-B27 positive may have a mucopurulent papillary conjunctivitis severe chronic recurrent acute attacks of iritis (50%) polyarthritis recurrent asymmetric lower extremity migratory polyarthritis sacroiliitis (1/3) nonspecific urethritis often forgotten, prostatic fluid culture negative often after epidemic dysentery or STD from Chlamydia, Ureaplasma, Shigella, Salmonella, and Yersinia other major keratoderma blennorrhagia of hands and feet (looks like pustular psoriasis) circinate balanitis persistent, scaly, erythematous, circumferential rash minor nail bed pitting palatal and tongue aphthous ulcers enteritis plantar fasciitis achilles tendonitis

VKH

albino retarded deaf limping ching for directions===similar to sympathetica ohthalmia Asian or American Indian ancestry between 30 and 50 years of age any patients with pigmentation are at risk bilateral disease unknown etiology, presumed autoimmune with assos deafness

early CSF pleocytosis severe acute bilateral anterior uveitis posterior uveitis with bilateral serous RD dallen fuchs nodules meningeal symptoms temporary deafness or tinnitus (1/3) seizures mono and hemiparesis coma late vitiligo poliosis alopecia perilimbal vitiligo (Sugiura's sign) in>75% sunset glow fundus (depigmented choroid)

get audiogram,, HLA-DR4 lumbar puncture is exactly like sympathetic ophthalmia but involves choriocapillaris

Parasitic Toxoplasmosis T. gondii ~~~25% uveitis in IMC &~~~congenital (1:10,000) 3C's: Convulsions, Ca+2 on x ray, Chorioretinitis most commonly bilateral classic sign of focal exudative retinitis segmental periarteritis

Worms Toxocariasis 1chronic endophthalmitis 2-9 years old white eye, cyclitic membrane, RD, CME, cataract 2localized granuloma 6-14 years old 3peripheral granuloma 6-40 years old can mimic snowbank rarely bilateral atypical treatment steroids if inflammation when worm diesNO benefit to treatment with antiparasitic agents l

Toxoplasmosis and Toxocara cani and actis

Toxoplasmosis is a parasite of cats that can exist in a spore ( egg) encysted or active trophozite form.

Our children become infected by eating contamianted food by cat faeces in our homes and we adults may eat uncooked food of intermediate hosts like beef pork and lamp ie We may get it from other animals too !!!. Our mothers spread it transplacentally

Congential

causing stillbirth early in pregancy and CNS convulsiones etc if late in pregancy.Dx intracranial calcification Most of the time it is mild and subclinical with chorioretinal scars found incidentally when doing eye exam later in life

Acute acqiured systemic

mild with fever LAd plus chrioretinitis mild and encelomeningitis

Onchocerciasis=== Cysticercosis=== subconjunctival "dermoid", vitreal cysts, endophthalmitis

Fungal Candida albicans===string of pearls, multifocal retinitis, may mimic toxoplasmic choroiditis: Histoplasmosis 1POHS===classic triad is punched out peripheral lesions ("histo spots"), peripapillary atrophy, and an asymmetric maculopathy 2endophthalmitis 3solitary granuloma

Viral HSV, HZO done already! Acute retinal necrosis===heavy vitritis, peripheral necrosis, CMV===(total) cataract, multiple peripheral lesions with minimal tissue destruction, optic nerve atrophy, viral inclusion bodies Rubella=== retinal pigmentation iritis, cataracts, glaucoma & vision and ERG generally normal Post Viral

Krills (Acute Retinal Pigment Epitheliitis)===2-4 gray spots with yellow white halos seen in macula ocuring

inyoung adults

HIVHIV retinopathy 1CMV retinitis most common opportunistic "brush fire" = yellow-white margin at the border of burned out atrophic retina fulminant form: posterior pole necrosis indolent form: white retinitis or primary papillitis 2Progressive Outer Retinal Necrosis Syndrome ass zoster 3Toxoplasmosis no prior scars bilateral in 1/3 multifocal vitritis +IgM to T gondii in 6-12% pts +concurrent encephalitis necessary to continue antitoxoplasmic therapy for the life of patient do NOT use corticosteroids due to risk from further immunosuppression 4Pneumocystis carinii choroiditis 5HSV 6Mycobacterial and Gm + 7Kaposi's sarcoma 8molluscum DNA poxvirus 9Cryptococcosis tap with India ink prep 10HZO

end of summary uveitis

Parasitic worms larva causr prolems

Toxoplasmosis

T. gondii ~~~25% uveitis in IMC &~~~congenital (1:10,000)

3C's: Convulsions, Ca+2 on x ray, Chorioretinitis most commonly bilateral

highest risk of infection in first trimester

acquired reactivation in IMC

often subclinical, may have fever, rash, hepatospenomegaly

from cats, raw meats, dusty environments

signs/symptoms

classic sign of focal exudative retinitis adjacent to old scar usually in posterior pole

retinitis = active organisms, all else immune rx (except in AIDS, where pt can have infectious choroiditis)

segmental periarteritis near lesion, o/w diffuse venous sheathing

vitreal precipitates, satellite lesions

punctate outer toxoplasmosis has only small punctate peripheral retinal lesions

50% of population is sero+

ANY positive titer (Ig G) is significant (test in undiluted serum) in a patient with suspicious lesions

atypical deep yellow lesion, massive granuloma>6DD CNV, ERM, RD

RX

rx if Va has decreased > 2 lines because of vitreous cells, macula (within the arcades) or optic nerve threatened (within 1/2 DD), or if immunosuppressed

follow WBC and platelets weekly

in immunocompromised individuals, chronic suppression treatment is needed

Quadruple therapy:

pyrimethamine (Daraprim) 150mg PO load then 25mg PO QD x 1 to 6 weeks

sulfadiazine 4gm load then 1gm QID x 3 to 6 weeks (caution re: kidney stones, Stevens-Johnsons)

clindamycin 300mg PO QID (caution re: pseudomembranous colitis)

prednisone 80mg PO QD or QOD tapered off in 3 weeks

may substitute Bactrim or Septra as alternative to above therapy

if using pyrimethamine (Daraprim), don't use Bactrim or Septra as the sulfa component of the therapy because the trimethoprim interferes with the action of pyrimethamine

add Folinic acid 3gm IM 3x a week or 5mg PO QD if on Daraprim > 1 week as it generally prevents the leukopenia and thrombocytopenia that may result from pyrimethamine treatment

Toxocariasis

worm of cats that may be transmitted to man and other animals byeating ova that hatch in the gut and cause visceral larva migrans

Toxocara canis children and young adults with normal WBC and no systemic eosinophilia 10% with positive serology have it

ova and parasites in stool specimens are negative in ocular toxocariasis

3 recognizable ocular syndromes:

1chronic endophthalmitis 2-9 years old white eye, cyclitic membrane, RD, CME, cataract

2localized granuloma 6-14 years old yellow white 1-2 dd elevated lesion posterior pole stress lines, hard exudates, minimal reaction

3peripheral granuloma 6-40 years old with retinal folds dragged macula, RD, dense vitreous bands can mimic snowbank rarely bilateral

atypical optic neuritis, motile worm, diffuse chorioretinitis conjunctivitis, iris nodules, keratitis

treatment steroids if inflammation when worm diesNO benefit to treatment with antiparasitic agents like thiabendazole may need vitrectomy to clear the media and decrease vitreous traction

Onchocerciasis===iridocyclitis, microfilaria, posterior synechiae, cataracts, peripheral anterior synechiae, glaucoma, choroiditis

Onchocerca volvulus river blindness

Cysticercosis===subconjunctival "dermoid", vitreal cysts, endophthalmitis

Taenia soliumpork tapeworm, intestinal parasite that spreads hematogenously to the eyesubretinal larvae can be destroyed with laser or surgery stool O & P, r/o systemic involvement with CT, LFTs death of larvae ( severe inflammatory reaction surgical removal of vitreous larvae via PPV

Fungal

Candida albicans===string of pearls, multifocal retinitis, may mimic toxoplasmic choroiditis: lesions originate in retina and result in exudation into vitreous

ketoconazole, Amphotericin may add PO flucytosine, fluconazole, rifampin

Histoplasmosis

1POHS===classic triad is punched out peripheral lesions ("histo spots"), peripapillary atrophy, and an asymmetric maculopathy

histo spot teens & macular lesions develop after the second decade NO vitritis CNV occurs commonly

differential includes angioid streaks, choroidal rupture, and idiopathic CNV

don't do skin test, can activate disease

2endophthalmitis

no POHS lesions, disseminated disease

focal retinitis with vitritis, iritis

culture vitreous/aqueous

rx with amphotericin and ketoconazole

3solitary granuloma

chorioretinal location may mimic toxoplasmosis

immune suppressed pts

Viral

HSV, HZO done already!

Acute retinal necrosis===heavy vitritis, peripheral necrosis, vasculitis, RD 70%, in healthy adolescents to older adults after HSV and HZV

2nd eye in 1/4, posterior pole tends to be spared Acyclovir 1500 mg/m2 QD in 3 divided doses x 7-10 days

corticosteroids and immunosuppressives probably contraindicated but corticosteroids probably okay once retinitis and intravitreal inflammation begin to resolve

anticoagulants including heparin and warfarin for 2-3 weeks

post chicken pox (especially adults) with less vision loss, no RD, < 6 clock hrs or retinitis

if the fellow eye is not involved in 3-6 weeks, then it will usually not be affected (but can be involved years later)

CMV===(total) cataract, multiple peripheral lesions with minimal tissue destruction, optic nerve atrophy

Congenital diagnosed with clinical findings, viral inclusion bodies (in urine, saliva and subretinal fluid) and systemic disease findings (fever, pancytopenia, pneumonitis, anemia, HSM)

Rubella=== retinal pigmentation iritis, cataracts, glaucoma & vision and ERG generally normal

congenital: assoc. with MR, congenital heart disease, deafness

Post Viral

Krills (Acute Retinal Pigment Epitheliitis)===rare, young adults, sudden decrease in vision with 2-4 gray spots with yellow white halos seen in macula

with resolution, spots may increase or decrease but halos remain completely resolves over 6-12 wks but residual scars may ( central serous choroidopathy flourescein angiogram: active center spots, halos -

HIV

Approach to HIV

summaryThe most common pathology is due to HIV itself and looks like DM The most common infection is CMV and cuases blindness in 6

months Look for brush border fire at margins of atrpohic scars.ARN necrosis appears after Zoster and is a quiet deep circular necrosis

more common in the periphery Toxoplasmosis typically has densely opaque thick retinitis with smooth borders and minimum

hemorrhage as compared to CMV Since only 5% have prexisting scars it is a primary infection rather then reactivation PNC cuases

choroiditis if diseeminnated HSV HZV severe severe Panuveitis TB retinits,Karposis sarcoma inferoir fornix Molluscum pox

virus more severe Cryptococcu s severe Panuvitis papplits EOM palsy

hiv

conjunctival capillary dilatation, irregular vessel caliber, granular look to blood column keratoconjunctivitis sicca in 15% subconjunctival hemorrhage but r/o Kaposi's sarcoma rapid myopia can occur

HIV retinopathy

most common ocular finding, found in 50 to 70% of cases multiple CWS along vascular arcades microaneurysms, retinal hemorrhages, and optic neuropathy direct endothelial and neuroretinal toxicity, immune complex deposition

1CMV retinitis

most commonly seen opportunistic ocular infection in pts with AIDS: if untreated, it can destroy the retina within 6 months

diagnosis is clinical as serologic tests and viral culture are of limited value as majority of population show evidence of previous exposure

pay special attention to the border areas of lesions since this is where active retinitis occurs"brush fire" appearance is the most diagnostic as yellow-white margin at the border of burned out atrophic retina If optic nerve swollen,then r/o Toxoplasmosis

fulminant form: posterior pole necrosis along arcades

indolent form: white retinitis with dry granular borders without hemorrhage- common in periphery or in treated patients

often with circumferential spread with sparing of posterior pole until late mild vitritis, anterior chamber rx, slow progression, often with areas of scarring

primary papillitis

white disc with hemorrhage and surrounding necrotizing neuroretinitis

Risk for CMV encephalitis CNS symptoms are unlikely to be caused by CMV encephalitis without concurrent retinitis

2Progressive Outer Retinal Necrosis Syndrome ====2/3 deep multifocal retinal lesions (peripheral>macula) progressing in a circumferential fashion sparing the retinal vasculature occuring rarely infection in AIDS pts who present with decreased Va can occur in the absence of, concurrently with or subsequent to a cutaneous zoster infection

minimal anterior and posterior cellshistory of cutaneous zoster

3Toxoplasmosis

it is a parasite of dogs and exists as actively reproducing form trophozoite and quiet tissue cyst bradyzoite and a resistant sporocyst excreted by dog.

man can get by eating meat with bradyzoites eating faecse infested spopzoites & tranplacental trphozoite spread

to distinguish from CMV, toxoplasmosis typically has densely opaque thick retinitis with smooth nongranular borders and minimum hemorrhage

inflammatory reaction in choroid, retina and vitreous is less than in pts with an intact immune system

preexisting scars are only present in 5% of AIDS patients, so probably represents primary infection

no prior scars bilateral in 1/3 multifocal vitritis +IgM to T gondii in 6-12% pts +concurrent encephalitis c/o blurring anterior chamber rx peripheral white retinitis lesions larger in AIDS pts RD tears

can present with diffuse areas of necrosis,

usually respond to pyrimethamine with sulfadiazine, clindamycin, or tetracyclines (caution with bone marrow toxicity)

necessary to continue antitoxoplasmic therapy for the life of patient do NOT use corticosteroids due to risk from further immunosuppression

4Pneumocystis carinii choroiditis

rare but if choroiditis is present, systemic dissemination also present more common when aerosolized pentamidine was Rx of choice for PCP bilateral oval pale multiple choroidal lesions 1-3mm (Arch June 89) minimal inflammation with lesions in posterior pole and periphery slow growth over months with little effect on Va choroiditis tx requires hospitalization for a 3 week regimen of IV trimethoprim (20mg/kg body wt per day) and sulfamethoxazole (100mg/kg body wt per day) or pentamidine (4mg/kg body wt per day). within 3-12 weeks of tx, most of the lesions disappear leaving mild overlying pigmentary changes

5HSV

prolonged course fibrinoid anterior chamber with hypopyon, vitritis, phlebitisyellow white retinitis outside the arcades and gray-white geographic deep retinitis in posterior pole

6Mycobacterial and Gm +

organisms also have been dx as causing retinitis

7Kaposi's sarcoma

inferior fornix most common site but can have orbital mass, lids involved stage 1 and 2 are flat (<3mm height), patchy, and less than 4 months duration stage 3 lesions are nodular and of greater than 4 months duration

8molluscum

DNA poxvirus larger, more rapid, more numerous and more resistant to standard rx

9Cryptococcosis 1/2 of pts with meningitis have ocular problems usually in posterior segment, but can be iris nodule with severe anterior uveitis optic nerve edema, optic nerve atrophy, EOM palsy, VF defects, uveitis perform anterior chamber tap with India ink prep

10HZO increased incidence

Pars Planitisbilateral (80%) young patients association with MS, HLA-DR2

vitreous snowballs (cellular aggregates) +/-inferior snowbanks (fibrovascular exudative changes of the inferior pars plana) in at least 30% snowbank is correlated with more severe disease

CME is major cause of visual loss; others PSC cataracts, preretinal and subretinal neovascular membranes and vitreous hemorrhage other signs of low-grade AC rxn, minimal post synechiae, band keratopathy, retinal phlebitis, KP with local corneal edema, NVD, NVE, retinoschisis, tractional RD NVD often responds to steroids F/A: diffuse peripheral venular leakingaac typically is chronic with remissions and ultimately burns out r/o sarcoid, syphilis, MS (found in up to 5%), Lyme disease (+ anterior chamber rx)

Rx mild cases without macular edema and not bothered by floaters (30%) no treatment is necessary steroids usually treat macular edema with posterior deep sub-Tenon's depot corticosteroids may need 3-4 subtenon's injections if Va less 20/40, then PO chronically after 6 months of steroids, probably irreversible CME immunosuppressives cryotherapyfor severe cases unresponsive to steroids (30%) with significant vitreous haze and CME single freeze thaw of inferior snowbank with contiguous uninvolved retina (1/3 width of snowbank) avg 20 freezes per eyegive posterior subtenon's injection of 40mg depomedrol and topical steroids post op laser may be less traumatic than cryo vitrectomy may be needed to treat severe visual loss caused by dense vitreal veils, hemorrhage or traction

#Fluorescein Angiography FA & other diagnostic modalitiesSlit lamp

Scleral scatter=aim lateral light beam at limbus and is transmitted by TIR in cornea

Retroilumination

Direct ilumination & Lateral ilumination

spectal illumination

FA

Fluoresceincolors white and is seen the periphery of bv as apoosed to Color phtogaphs that show central RBCs ofbv

Rules

Fluoresceine is bound 80% to plasma and can be taken orally

outer blood retinal barrier and major choroidal blood vessels impermeaple but Choriocapillaries allow a liitle across Bruchs into sub RPE space

inner blood retinal barrier impermeable

fluoresceine

triphenymethelene

light emmision ceases when light stops

emits green yellow light

Hb absorbs excited light

excitaion 475nm blue emmision 525nm yellow

photography xenon light source blue light barrier

technique

Normal angiogram

1st choriodal and cilioretinal artery uneven choroidal fluorescence is normal

Methods of examination use 20D in cinics to see slides against light box

Drusen

degree of fluorescence of drusen~~ low lipid content ->susceptable to subretinal neovascullarization usually soft

soft are water loving and cause neovasculiraztion

SRNM=== fibrovascular tissue originating from choriocapilleris thru defects in bruch to sub rpe space to sub retinal space and causing or may cause RPE deytachment

Bruchs membrane defects cause hyperfluorescence as more fluorescene

Variants of normal

1 rection in background fluorescence in a balck person vs increase background fluorescence in albanoid fundus Large cilioretinal artery Artefacts Autofluorescence eg some optic nerve drusen

A Hyperfluorescence

1Leakage implies bd of blood retinal barrier and is characterized by fluid in the sensory retina and spread of hyperfluorescence with INDISTINCT bouderies

2Pooling in below Rpe or subretina space or intrartinal spaces in RPE detachment homogenous appearence and boundaries remain unchanged.eg between RPE and neuroretina in CSR spreading hyperfluorescence,cystic spaces of neuroretina in CMO

3 Staining taken up and retainedeg it is normal for lamina cribiosa sclera and bruchs staining of optic disc is normal as well as sclera after choroidal rupture &scar tissue in discform ARMD

4 Transmission or window defect become apparent when choroid fills and fade as it empties

Hyper fluorescence 4 1RPE atrpohy cause window defects 2 Poolling of dye in sub retinal space 3 leakake of dye into sensory retina 4 staining of tissue due prolonged retention

BHypofluorescence

1 Masking or blockage Melaninn or Haemorrhage & Exudation are the 2 most important causes eg Bests These are usually more profound hypo fluorescence than filling defects

2 Filling defects This is either choirdal or retinal defects

Hypo Fluorescence 3

1Dense RPE causing masking due to pigment (xanthophyll in sensry retina or melanin in RPE) or abnormal deposits {haemorrhage, hard exudates lipofucin } 2 Poor retinal or choroidal blood flow3 Loss of blood vessels (choroidemia or myopia)

PATTERNS

RPE detachment

CP~~~see extent of detachment

AV~~~ increase as dye pools under

LP ~~~well circumscribed and now now increase in fluorescence

Classic SRN

CP~~~cartwheel or lacy specific membrane seen

AV~~~ leak in to subretinal space

LP~~~ late hyperfluorescence as leakage into sensory retina

CSR

AV~~~small spot becomes->smoke stack appearence = vertical filling

LP~~~ umbrella horizontal

CMO

LP~~~flower patel = pooling into cysts that persists

Macula hole

AV~~~punched out RPE window defect

BVO hyperpermeability

AV survivng blood vessels totuous and dilated little capillaries closure

LP increased fluorescence from damaged inner blood retinal barrier

foveal ischaemia

EP details of capillaries bed obscurred by haemorrhage

LP inspite of haemorrhage there is closure of capillaries above FAZ non ishcheamic

DR

BDR mild microaneurysms fluorescent dotshaemorrhage small patches maskingsmall patches non perfusion or leakagewidened inter capillary spaces & capillary dilationcotton wools spots correspond areas of capillary non perfusion

Ishceamic maculopathy nn perfuion related to cotton wools spots

CSMOsee haemorrhage microaneurysms exudates

+ ***Remeber this leakage from perifovealar capillary bed = Petaloid pattern of CMO

Pre proliferative DR Cotton wool spots blotchy haemorrhagethis is subtle but the game is given away by non perfusion of the entire periphery~~~non perfusion

proliferative

florrid neovascularization and peripheral non perfusion

photocoagulaion scars~~~ areas of hypo fluorescencelate

e from disc neovascularization~~~ intense laekag

ARMD

Drusen larger drusen ~~~~~~~~exibit hyperfluorescence and will continue throughout as absorb fluoresceine.

small drusen ~~~~~~~~~~~~~will exibit fluorescence but tend not to absorb and hence loose huper fluorescence

RPE atrophy ~~~window defect

RPE increased pigment ~~~masking

Geographical atrophy =indicates loss of choriocapilleris & RPE~~~~~window defect with notiable large choroidal vessels & no spread beyond bounderies NBGeogrphical atrophy may spare the central fovea and this must not be confused with SRN

dilated parafoveal capilleries & leakage into intraretinal cystic spaces~~~~patteloid pattern

assosiated CMO & SRNM ~~~~~~~~classic pattern of SRNV & later the patteloid pattern with the central bud of the flower diappearing as pooling occurs from SRNM

SRNM has typical ROUND or LACY to COTTONWOOL pattern

EP~~~~discrete neovascular frond under fovea ROUND that become more intense and confluent as dye leaks LACY

LP ~~~extends beyond bounderies as it leaks into SRS COTTONWOOL

Exudative RPE detachment The characteristics are in between geographical atrophy and SRNM

EP~~~there is early masking of choroidal fluorescence and the round distinct margins of the RPE detachment defined.

LP ~~~lesion becomes intensely fluorescent without loosing borders. The above may be complicated by SRNM hence irregalr fillingor increase pigment hence maskingor tears of RPE presenting as window defects

Bests

yellow dome~~~~~~~masking at macula

pseudohypopyon =yellow exudate accumulates inferiorly~~~~~~~~~~window defect and masking inferiorly

SRNM & RPE atrophy or fibrosis~~~~~~~~~~~~~~~~~easy!

Adult fovemacular viteeliform dystrophy

yellow exudate ~~~~~masking

atrophy~~~~~~~~~~~window defect

ring of parafoveal RPE atrophy~~~~~ window defect

Stargardts & Fundus Flavimaculatus= fundus with yellow flecks

Pale flecks at level of RPE usually with atrophy of macular

atrophy~~~macular window defect

flecks may be ~~~~hyperfluorescent or hypofluorescent

Rest of Fundus RPE with lipofuchcin deposits~~~masking or silent retina

Macular holes

1st & 2nd stage ~~~~~~~non specific

Full thickness hole causing RPE atrophy + small amounts drusen~~~~~~~~~~~~~~~~patchy central window defect

Epiretinal membranes=pucker=cellophane=prerinal fibrosis

disc vessels straightened and dragged centrally~~~ same!

irregular capillary leakage ~~~~~~~~~~~~~~~~~~~same!

Choroidal folds

crests & troughs ~~~~~~same

Indocyanine green

low fluorescence and difficult to image

longer wavlength absorbtion and excitation (805nm & 835nm) that is less absorbed by RPE and therefore greater visibility of choroid.

completely plasma bound therefore will not leak out of vessles it useful to look at the choroid in SRMN in ARMD.

BUT normal FA is needed to assess leakage in SRMN iofARMD.

Scanning Laser Ophthalmoscope

Revolution because it reqiures low irradiance and small aperture because it uses sensitive light detectors and they is high collimation of beam

requires only 70uW/cm of irradiance vs 5000 of normal camera

Can use fluoresciene & ICG

3d digital construction possible , less scatter less light needed

Only real disadvantage is that it it monochromatic

Amsler

q1 do you see the central black spot q2 corners q3 interuptions in small squares q4 are thelines straight q5 see anything else q6 where do you see distotrions

Lasers

ND-Yag

Laser capsulotomy

power per puncture 1 to 2.5 millijoules

Apraclodipine 1%->Contact lens enlarges cone angle of the beam & diameter of focus is smaller and easier-->aiming beam should be less than 30' with the viaual axis to avoid astigmatism

PI

Settings 4 to 8 mJ depending on color with 2 to 3 bursts per shot and 3 to 4 shots

USE 3 shots of 6mj is average ( 2 bursts)

technique 1% apraclonidine and pilocarpine 2% to achieve miosis-->upper tempporal and find a crypt-->special contact lens-->apply apraclonidine 1% again

laser are uV since they need gh energy

Eximer laser

Argon Fluoride at UV 193nm breaks hydrocarbon bonds

SE superficial stromal scarring

NB 535nm is green 496nm is blue 570nm is red

UV is blue invisible blue light

Shirmers

gently dry eye

-->5mm folded & keep for 5 minutes -->Normal wetting is 15 mm -->Less than 6mm is abnormal->Obvioulsy anaethetict will reduce tearing slightly

Tear substitutes

3 types

a Cellulose derivitives eg tears naturalle

b Polyvinyl alcohol based

and

c mucomimitics

lacrilube petroloeum mineral oil

Mucoloytic agents 5% acetylycysteine useful for mucous paques ans filaments

used 4× daily

In RPE detachments fluid is accumulated between Bruchs and the RPE not deeper

Drug Safe choroamphenicol can cause Optic neuropathy

TC Intracranial Hypertension

Sticklers is an AD that is most common CT dyspasia disease

Retinochisis is common in Hypermetropes

x linked type is assosiated with Cystoid Macular Oedema

Punctal probing soft stop indicates canalicili blocked.

hard stop indicates NLD blocked.

%NeurologyAION

inferior altitudinal defects are commonest

Post chiasmal lesions

The more anterior the more likely the macular is split ie as we get towards the occpital lobe there is less separation

temporal cresent indicates occipital lesion

Tersons

Intrarerinal Hx

ILM hx

Defined as vitreous hx in the presence of intracraial or subarachniod haemorage often due to aneurysm rupture

DDx hypertesive Anaemic Valsalva NAI Purtchers IPCV

skew deviation = one eye is above the other ie vertical difference

due to RMLF ofcajal near cnIII eg parinauds

Optic discs

optociliary shunts imply chronic inflamation shunts between retina and ciliary

Dural shunts are shunts that are small and communicate with with the Cavernous sinus.

This is similar to Caratocavernous sinus except that there will be no pulsation and the vessels on the conjunctiva will be snaky

Reflexes

Rapd 3 reasons wh it my diasppear

vermiform reflexes

whorl pupil

oscilating pupilmargin

%Tumours & PathologyOrbital inflamation masses

Wegen Granulomaosis

Fibrinous

affects orbit sinus and lung

disease ofsmall blood vessels

c ANCA antibodies

Chonic diopathic orbital infmation or Pseudortumour

painless proptosis that must e dfferentiated frm low grade lymphoma

Fungal Phycomycosis and Sprgilosis whis differs in that it causes a granulomatous inflamtion

Tumurs can arise frmo pericyte = large stag horn spaces and often recurs cavernous lymph cappliery

Inherited retinal dystrophies

There are 2 types

those withsyndromes and tose without

Ushers

Bad Bil Dell

Ref Some

Atalipoprtienaeis

Kern Sayer

Pathology 34 slides

Pyogenic granuloma arise from

Cavernous haemangioma mst e diffrenrtiated from vaices and av anomlies that haveno rndothelail ce'lls

Dermoid oriinates from

periguim elastosis is prominent

Moluscum contagiosum looks quite typical

holesteo clefts and ganu'oma ocus after bleeding

mason trichrome macula dydtrophy

ptterigem is defined by resence of e'astin

BCCpalisadin

chalazion granolama

AACG

look for rubosis ans PAS

cyclocryodoid urns if used willcase TM pigmenation

Endophthalmitis

recognise a Neutruphil

sqamos a and aanthamoeba lok very smilar

look for keratiniztion since this is a clue to origin

B ha s fleise ? whorls

FED thikened DM and guttatae

Acqiued melanosis

macula dystrophy or granular mason trichrome

choiooiodal melanoma

sebaceous gland ca often the presence of fat in the cells helps with iagnosis and look for mucin spreads pagetiod in nature

Onchocerciasis

Rx Inovaedtin ecreases parasite load

transmitted black flyMeningioma PathPsammona bodiesage 40 - 50 females > malesDiffuse caused sinus thrombosis

Uveal Melanoma

most common 1' tumour of eye and oculurdermal melanosis inc risk

most commnly at 60

Dx remember phosphorus 32 uptake radioactive phosphorus emits b irradiation picked up by geiger counter which can differentiate from haemangima color doppler differentiate from haemarhage

rx

radioactive plaques containing ý emitting isotopes cobalt & iodine

cyclon generated charged particles

hist epilthleoid worst

also spindle a and b with prominent nucleolus

prognosis

size anterior worse due to late pick up epitleiod worse diffuse growing worse highly pigmented worse older than 65

CB melanoma

ddx medulepithlioma cysts leimyoma cystic adenoma

PR cells have no potential for malignacy only hyperplasia as in Toxoplama scars,etc

hamatoma of the retina and RPE as well as blood can appear black

UM that are : ~~~2mm in size ~~~raised ~~~contain lipufuchcin ~~~or have SRF are dangerous

Rx Plague radiotherapy 106 RU 125 I or cyclotron delivered helium or proton particles Brachy therapy

Drusen is often assosiated and appears white NB The may not be black. All white masses are assumed to be secondaies

AI patholgy classification

TypeI disorders Hayfever

Type II Ocular cicatricial pempigoid

paek onse at 70 years and 0 will have systemic signs including pharyngeal strictures blisters onscalp ans limbs assosiated in 6% with AIlike SLEPAN CF Loss of plica and caruncle and retcular fibrosis of tarsal conjunctiva

RX Injection of Mitimycin Moderate Dapsone Sulpyramide Severe Cyclophoamide steroids

Type III Marginal Keratitis,

Rheumatiod Melt RXMild topical steriods Moderate Mehtotrexate Severes Cyclophosamide ad oral cteriods

Type IV Atopic KC and Vernal KC

5 stypes according to corneal changes

PEE

microerosions

plague

subepithelial scariing

pseudogerontoxon

#PaedetricsApproach to Aniridia

1 in 100 000

have macula (hypoplasia) Lens(cataract subluxation microphakia) glaucoma (40%) and Corneal(pannus hazy)

involvment

3 types 1 85% AD incomplete penetrance and only eye involvement 2/3 hae normal parents 2 sporadic 11p deletion with Wilms and Urinary disorder and MR( with MR we call it =Millers) 3 very rare AR with cerebellar and brain anomalies on CT but normal macular=Gillespies

Approach to blindness

Secondary nystagmus only starts at 2 to 4 months

Pupli respones is there from 31 weeks gestation but is difficult to see in infants because of smll pupils

VA new born 20/1000 but 1 month already 20/600 4months 2/200 and 1 year 20/50

by 3 years atleast 20/40 and needs to be evaluated if more than 1 line diffrence in snellen

at 6 weeks fixates and follows

Most babies with blindness will have a detectable clinical cause

approach

WITH NYSTAGMUS the nystagmus is seaching if severe eg optic nerve involvment and pendular if some fixation eg foveal hypoplasia

SEARCHING1 LCA(normal fudus becomes pigmented evetually) 2

Optic nerve hypoplasia often ass 1 sagital midline defects and hyppit & can be reversed with rx 2aHydraenceph ancep 3 drugs quinine anti convulsives 4 maternal diabetes

PENDULAR

3 OC or O ablinism

4 Juvenile Retinichisis

5 Achromatopsia =cone dystrophy

6 CSNB

No Nystagmus ( breakup into normal and abnormal clinical findings

1 Refractive errors 2 Cortical blindness sec to perinatal asphyxia with developmental or seizures 3 Ocular motorapraxia =failure to elicit saccades on command but may be present by reflex. The child is thought to be blind because of lack of response esp in first few months when horizontal head jerks not yet developed NB patient can see but we don know! usually congenital but can be aquired 4Delayed Visual maturation DVM usually catch up by 6 months commoner in prems and babies with other ocular abnormality

VA teste preferencial looking

hundreds an d thousands at least 6/24

DUANES cant abduct and retracts on adduction

BROWNS cant elevate on adduction

Duanes

paplapral fissue widens in abduction and narrows on addcution.

Cause congenital cocontracture of LR and MR

20% Bilateral associations:Deafness Speech disorder congenital defects (Pseudo Duanes is an acqiured restrictive codition due to adhesion of any muscle)

Browns=so contracture ie does not allow io to work!

No elevation in adduction and Normal elvation in abduction

May widen p.fissure on adduction=opposite to duanes

other features v pattern cause congnital and 10% bilateral

due to SO trochlear trauma or inflammation

RA & trauma can cause Browns

Sqiunts

examination corneal light reflex

pupil border is 30 diopters or 15 degrees [ 1 degree is 2 diopters and limbus 45 1mm pupil is 9 diopters

cover uncover used to find heterotropia

alternate cover uncover: 2seconds covered and then qiukly uncover and look at the same eye

used to pick up heterophoria

Infantile esotropia

Congenital Esoptropia is assos IO overacttion and A pattern or DVD Left side is more common so they will look tothe Left onset after 2 years disturbance of downwad movement and disturbamce ofvergence

Assessment

Look for amblyopia , the squint A or V cyloplegic refraction and reinoscopy.

when? 1st 6 months

look for the nystagmus and if it dampens on convergence it is an entity called nystagmus blockage syndrome.

Rx usually at 2 years old and recess both MRAim alighmnet to within 10 D

complications 1 Overcorrection 2 A pattern due to IO overaction which will become bilateral within 6 months! 3 DVD which is characterized by updrift with excyclodeviation UNDER cover which will normalize after mostly bilateral but can be unilateral

Rx SR recession +- Faden procedure (Find out!!! 4 Amblyopia in 40%! 5 accomodative problem suspect if start to reconverge Accomodative esotropia Synoptophore is best for cylodeviations DVD is characterized by updrift with excyclodeviation 12 oclock at 9 o clock UNDER cover which will normalize after

Forced duction test

DIFFERENTIATE restrictive FROM neurological

Method

Amethocaine

Grasp insertion of muscle and move in direction of action

compare with normal side

Positive IF diificult to move ie entrapment or fibrosis

Negative if freely mobile

Kid scataracts

prpeller Fabrys

presenileNeurofibromotis typeII

lammelar or nulear Rubellas

#Phacomatoses

Von REck

Cafe a lait neurofibroma skin brain skull neurofibroma

eye~~~orbital ne

durofibroma gliomas

Sturge webers

port wine along 5th nerve capillary haem

eye~~~choriodal haemangioma and glaucoma scleral haemangioma

Tuber sclerosis Bournvilles

Brain stem glioma face sebacous adenoma butterfly astrocytoma

eye~~~optic gliomas mullberry optic disc retina nodules

Von Hippel laundau

brain haemagniomas assos with RCC

eye~~~retinal haemangiomas and large feeders can bleed and RD

Congenital Anomalies

megalo=l diameter >13mm, X-linked

r/o glaucoma, increased risk factor for ectopia,??? cataract, glaucoma rarely associated with renal cell cancer, r/o congenital glaucoma nl endothelial density F carriers may have slightly larger

micro =l diameter <10mm, hyperopes (because is flat) AD>AR20% with angle closure glaucoma, usually eye nl

r/o nanophthalmos, microphthlamos, trisomy 13, Ehlers Danlos, dwarfism, fetal alcohol syndrome

Anterior segment dysgenesis=a broad spectrum of developmental anomalies invloving migration of the mesenchyme of neural crest origin

main defects localized to angle

eg schalbes line displaced anteriorly or gysgenisis or embryotoxin posterior defects in descements

iris processes iris atrophy iris adhesions iris stromal opacities

lens absent

axenfelds ~~~~angle anomalies

reigers ~~~~~~with iris involvment

peters~~~~~~~with corneal involvment +/- lens in type 2

Axenfeld anomaly-Reiger syndrome:

Axenfeld thickened, centrally displace schwalbe's line posterior embryotoxin plus prominent iris processes

Rieger's anomaly: posterior embryotoxin, = detached descements membraneand prominent scwelbes lime

prominent iris processes, plus iris stroma atrophy

Peters

clearing of leukoma with waiting, glaucoma

Type 1- unilateral defect in descemet's membrane, central l stromal opacity, nl lens and no systemic involvement

Type 2- bilateral lens involved, bilateral, often glaucoma

r/o von Hippel's internal l ulcer (no lens abnormality) and local posterior keratoconus (endothelium/descemet present). Neither are assoc. with iris adhesion.

Haab's striae=breaks in DM horizontal on buphthalmos

associated with congenital glaucoma * striae are horizontal opposed to striae associated with forceps injury during delivery, which are vertical

Congenital opacities

facets, nebula, macula, leukoma

l keloid probably from intrauterine trauma

sclero =peripheral sclera-like opacification of the results from defect in mesenchymal migrationbilateral, often with systemic and other ocular problems nonprogressive, sporadic, AR (more severe) or AD

#Orbit/Plastics LidsEntopian

Cautery thru skin below lashes

Transverse lid everting sutures

Weis procedure

full thickness horizontal id split and everting sutues

Fox procedure base down conjunctival and tarsal excision

shorten lower retractors

Upper lid split anterior lamellar with lid split

1Make a lid crease cut and separate under OO to lashes

2split lid at grey line

3 Pull up anterior lamellae to get adequte eversion

4 Pass 3 6 0 vicryl thru skin and OO 1to2mm above lashes and attach 3 to 4 mm superiorly to Tarsus ad back to skin and tie outside

Pearls aim for overcorrection ie pull the anterior lammelle high

Ectopian

Ziegler Cautery puctures 5mm below puctum

Medial Conjunctoplasty excise diamond piece of tissue 8mm long parallel to canaliculisand 4mm high

Lazy T in addition to above a full thickness trapezoid excision adjacent base up

Bick procedure Larger trapezoid excision at lateral canthus that may be combined with z plasty

Ptosis

types Neurogenic Muscular Aponeurotic(=skin crease is high or absent )and mechanical

CF

measure interpalpable fissure, torch lite to lid margin levator function while excluding frontalis and look at lid crease distance to margin

Palpebral fissure normally 27-30 mm long, 8-10 wide

Normal LPS can raise upper lid 15 mm, frontalis adds 2 mm

THis in clinical language!!

1 Marginal reflex distance(MRD)which normally is 4.to 4. mm 2mm or less severe 3mmmoderate 4mm normal

2 Vertical fissure height normal M 7 to 10mmf 8 to 12

3 upper lid excursion place thunb on brow to negate Frontalis normal levation from straight is 12mm poor is 5mm

4 upper lid crease measure in down gaze distance from margin to crease female 10mm male 8mm

low crease means ABnormal Levator function

x Fasanella Servat procedure fascinate!

excision of uppet border of tarsus with lower border of MUllers and overlying conjunctiva.

Indications

good levator function eg horners and othe mild ptosis with no apeuneurotic defects

Levator resection

mderate to severe ptosis

Frontalis bow suspension using a sling of fascia lata to attach tarsus to frontalis

severe ptosis

Tolosa Hunt==grnulomatous inflammation of cavernous sinus

CF recurs & remits vs

Pseutotumour==non specific orbital inflammation usually 20 to 50 years old

CF variable course including progresive fibrosis or frozen orbit

Bilateral involvement occurs more commonly in kids and if in adults think about sytemic diseases like TB S WG PAN SS Waldestroms If the sinuses are involved it is unlikely Pseudotumour so remember it is an orbital inflammation.Rx oral steroids ie prednisolone 60-80 mg daily DXT and cyclophosamide may be bilateral in kids Dx is often response to steriods DDx Lym/Leu Thyriod Orbtal cellulitis

FBC shows leucocytosis and biopsy shoes PMNs plus Eiosinophils

Orbital Myosis

Bacterial & Fungal

Thyroid dsease

examination

no specs

Optic nerve compression va color ishahara optic pallor posterior folds external compression lid lag look down lid retraction

lid retraction or proptosis causes scleral show

exophthalmometre lateral canthus to lateral canthus

if difference > 2 usually 16

ocular motility diplopia pain and fatique

exposure

sensation

superior limbal conjunctivitis sign look for PEE using rose bengal

conjunctivitis

injection along recti gowers

#To be filed MIscellanous just to readFundoscopy

HT arterioles straighter

CRVO more tortuose

Women higher risk cad if pronounced ht retinopathy

Inner or commonly called superficial haemorages are flame shaped

Choriodal infarcts present as Elschings spots l!ook for em

Lenticular Astigmatism

PDSKrukenbergs spindle occurs in Pigment dispersion syndrme not pimentary galucoma necessarily commener in myopes

Rhabdosarcoma extra conal growth therefore non axial proptosis not familial

Pseudotumour = T= TUMOUR T= TENDON

develop lymphiod hyperplasia in 20% and the muscle tendon is characteristicly involved in contrast to Dysthyroid eye disease which is not thyroid is a non tender! Disease

DED inferior rectus most common

Vogts limbal girdle is a degenartion

SLE does not cause any corneal melts

Keratoconus

Munsons sign lower eyelid protruberence

Fleisher rings inferiorly

Refsums is caused by Excess Phytanic acid

Astroocytosis is assoiated gyrate atrophy

Tersons is Intraocular haemorage secondary to subarachnoid haemorrhage

Keratoconus Hydrops is stable and never ruptures

Conjunctivitis

Pemphigoid not pemphigus causes cicatrisation

foster kennedy is IC mass causing optic atrpohy and paploedema in other eye

Krypton

less scattering, less absorption by blood, & yellow pigments (lens, foveal xanthophyll)

better uptake for choroidal tumors, blue iris

more choroidal uptake causes more pain, decrease accommodation, choroidal edema/hemorrhage

not good for acute hemorrhage during PRP, microaneurysms, blond fundi

really hits receptors, RPE, choroid

higher power needed for same lesions as argon

Rodenstock lens

minifies image, increases spot size

absorbs more energy than Goldman lens, so increase power

note: toward periphery, spots vrbecome smaller and relative power increases

fundus landmarks

Ciliary Artery

Paired long posteror ciliary pierce sclera in front of circle if Zinn and travel in suprachoriod space to ciliary body to form Major Ciliary circle at 3 and 9 oclockShort posterior Ciliary artery 10 -20 pierce sclera about Optic nerve Circle of Zinn supplies Optic nerve head lanmina and preamina

anterior ciliary pierce at muscle insertions

congenitaldefects

extra skin inlids canthus or cloed lids or coloboma

Ankyloble===fusion of lids

Blepharophimosis===congenital tetrad syndrome : epicanthus inversus, telecanthus, blepharoptosis and phimosis

Crytophthalmos===Skin covers all ocular structures

Distichiasis =extra row of lashes

Ectropion usually with Down's or blepharophimosis variation with total bilateral eversion of upper lids in newborns with marked chemosis and prolapse of conjunctiva

Entropion rare, by defn is isolated

Epiblepharon, most commonly asians r/o frank entropion

Epicanthus rare at birth but up to 20% by 2 yo

palpebralis (simple) equal, most common inversus - below, often with other abnormalities tarsalis - above, asians supraciliaris - from eyebrow

Euryblepharon===horizontally widened PF with anterior and downward placed lateral canthus and ectropion laterally

Eyelid Colomboma=== full thickness isolated defect in upper lid at inner 1/3 junction 20% are bilateral

===lower lid at lateral 1/3 often with systemic syndromes, especially AD Treacher Collins lower lid often partial thickness with adjacent margin deformities such as trichi

ERG

terms proximal is nearest photoreceptor

Mass response evoked from entire retina

Types:

Scotopic (rod response; dark-adapted) Dim white flash below cone threshold ( rods = 1000x more sens. to light than cones)

Maximal combined response (dark-adapted) Bright flash > max stimulation of rods and cones

Oscillatory potentials Result of feedback interactions among integrative cells of proximal retina ie near photreceptor

Photopic (cone response; light-adapted) 30 Hz flicker cone response (8Hz = practical limit of rods) Focal ERG Dx organic dz in macula

Bright flash ERG Ascertain retinal function in eyes w/ opaque media

Pattern ERG Correlates w/ integrity of optic nerve Info. about ganglioncells and their retinal interactions ie distal retina

waves

a wave negative wave; photoreceptor potential

b wave positive wave; Muller & bipolar cells oscillations in ascending b wave disappear in ischemia, CSNB

theoretically, ischemic retina would show increased b-wave implicit times and Log K

c wave late +, correlated with RPE, EOG hyperpolarization of apical RPE

x wave bump on b wave in dark adap. bright flash = a wave diagnosis infarcted retina would correlate with b/a wave amplitude ratio and Rmax inversion of b/a ratio or delay in 30 Hz flicker response bodes poorly in CRVO

early siderosis has paradoxical larger ERG responses than normal, which in later stages become subnormal

Electrophysiology

EOGRPE and PR interactions30' lateral excursions

Standing potential and light sensitive potentialArden index refers to lisht peak to dark peak and is normaly 170%RP~~~~~~decrease amplitude in light sensitive potentialPERGN35 P50N95Macular Dz P50 Decreased optic Neuropathy N95 Decreased

VEPERGtest of perpheral retina & distal to GangliaA PR which is supplied ChoriodGlaucoma is disease of optic nerve and ganglion cells so ERG is normal

EOGCompares amplitude from dark and light adapted readings

Arden ratio = largest potential in light/largest potential in dark x 100 (normal > 1.85)

Useful in Best's dz, hydroxychloroquine toxicity STARGARTDS

VEP

N1P1N2P2 to confirm optic neuropathy, albinism

Also used for VA in children, malingering

Ultrasound (U/S)PVD due to trauma/hemorrhage can be differentiated from RD by no attachments to optic nerve, irregular in thickness, cannot be traced to ora, and the amplitude is lower except when beam is perpendicular

new VH can be acoustically clear

asteroid is highly reflective, fills the vitreous which is usually retracted from retina

choroidal detachments are convex, rarely go posterior to vortex veins, and may be anterior to ora

metal/glass FB give shadowing, easier to see with lowering the gain

BB's give comet trail appearance

#NeurologyI. Neuro-ophthalmologic examination II Neuroimaging III Visual pathwaysIV pupil responses VOptic disc disorders including papiloedema & atrophy VI ocuular motility VIInystagmus VIII facial nerve palsies IX Headaches

I. Neuro-ophthalmologic examination

Tests

Photostress recovery test -helps in differentiating visual loss due to optic nerve disease or maculopathy. -bright light is shone for 10 sec at a distance of 2-3 cm. -record time it takes for patient to be able to recover and read at his/her best acuity (or next larger line) on Snellen chart. -recovery time prolonged in maculopathy (90-180 sec) but normal in optic nerve disease (less than 60 sec). -valid only for patients with visual acuity of 20/80 or better.

Spatial contrast sensitivity

-measures contrast threshold using gratings of various sizes and background -elevated contrast threshold may be seen despite visual acuity of 20/20 in diseases such as cataracts, glaucoma, macular lesions, optic neuropathies, and cerebral diseases.

Visual field testing

Confrontation testing

-crude but easy method of quickly assessing visual field

-should usually be followed by more sensitive tests such as Goldman perimetry or tangent screen testing if patient is capable (confrontation may be the only test some patients can respond to reliably).

Tangent screen

-evaluates the central 30° field

-may be useful in identifying small scotoma not detected by bowl perimetry

Bowl Perimetry

Goldmann perimeter

-useful for evaluating both central and peripheral fields.

-utilizes static and kinetic testing

-manual and operator dependent

Automated bowl perimeters

-evaluates only the central field (30° or 60°)

-utilizes static testing

-standardized with statistical evaluation of data

-may be difficult for some patients

Visually evoked cortical potentials (VECP)

-records electrical signals in the cortex generated by stimulation of the retina with light.

-a measure of macular visual function because of the disproportionately large representation of the fovea in the occipital cortex.

-p100 wave - positive deflection that occurs at 100 msec after the stimulus is most reliable parameter to measure.

latency increased in disorders with demyelination as a component of pathology including multiple sclerosis, optic nerve compression, infiltration or toxicity.

amplitutde may be decreased in all conditions that reduce visual acuity.

Gaze and Ocular motility

Nine cardinal positionsRotational testing -involves vestibulo-ocular reflex-useful for infants and comatose patients

Parks-Bielschowsky 3 step test

SO4eye is deviated up and worse when looking nasally or when tilting head to ipsilateral side

In congenital so4 will have and ncreased abnormal vertical fusional convergence of 10 to 15 while in aqiured it is only 3 ie eye cant move up and converge

test for hypertropia

Step 1: Determine eye with hypertropia at primary gaze

Step 2: Hypertropia increases at lateral gaze ipsilateral

( eye in abduction where rectus muscles are primary vertical deviators)vs

( eye in adduction where oblique muscles are primary vertical deviators)

Step 3: Hypertropia increases on head tilt

ispsilateral to hypertropic eye - oblique muscle

contralateral to hypertropic eye - rectus muscle

Maddox rod testing

-for evaluation of tropias and cyclodeviations

-right eye covered with Maddox rod and cylinder aligned in same direction of deviation. (This avoids confusion over the pattern that results from reversing which eye has the rod).

-uncovered eye fixates on light

-red line appears separate from white light when latent (phoria) or manifest (tropia) ocular deviation exists. (Maddox rod brings out latent deviations by eliminating fusion).

-axis and size of deviation determined by rotation of Maddox rod and correction with prism

Alternate prism cover testing

-cover-uncover test used initially to distinguish tropia from phoria

-eyes are covered alternately as patient fixates on a target

-test positive if each uncovered eye move to re-fixate on target

-axis and degree of deviation determined by position and power of prism necessary to halt eye movement.

II. Neuro-imaging

B. Computed tomography (CT scan)-

-provides excellent detail of bony architecture and sites of bleeding (hemorrhage/hematoma)

C. Magnetic Resonance Imaging (MRI)

shows demyelinating changes not visible in CT

-poor in evaluating bony architecture or acute bleeding

T1 - spin lattice time t 1water is dark black one time is a drink!!

(time required for 63% of protons to realign with the magnetic field)

-CSF and vitreous appear dark (high water content) and white matter white (high fat content)

-orbital lesions generally are dark on T1 except blood, melanin, and mucus

T2 - spin-spin relaxation time fat is dark

(time required for 63% of protons to relax while spinning with the plane perpendicular to the magnetic field)

-image opposite to that of T1

MRI diagnosis

1 Optic neuritis~~gadolium enhances optic nerve in optic neuritis due to inflamatory response and permeability

2 MS

III. Visual systemA. Visual pathway

Retinocortical pathway

retina --> ON --> optic chiasm (decussation of nasal retinal fibers)--> optic tract --> LGB --> optic radiations --> occipital cortex

B. Visual fields

1. Nerve fiber bundle defects (unilateral scotomas)a. papillomacular bundle

central scotoma centrocecal scotoma paracentral scotoma

b. arcuate nerve fiber bundle Bjerrum scotoma Seidel scotoma Rhonne scotoma Nasal step

c. nasal nerve fiber bundles Wedge shaped scotomas at temporal visual field

2. Optic nerve -unilateral

-scotoma always extends from the blind spot -respects the nasal horizontal meridian

3. Optic chiasm bitem.poral hemianopia respecting vertical meridian

4. Optic tract contra.lateral homonymous hemianopia

-respects vertical midline (all homonymous visual field defects do) incongruous

5. Lateral geniculate body -rare

congruous homonymous hemianopia homonymous horizontal sectoranopia

6.Optic radiations

a. Meye.r's loop (temporal lobe)-pie in the sky field defect, contralateral homonymous upper quadrantanopia

b. Parietal lobe inferior homonymous quadrantanopia/ hemianopia

7. Occipital lobe (visual cortex)

incongruous respects vertical midline hemianopic paracentral scotoma

-lesion at posterior segment(tip) of occipital lobe

-etiology blunt trauma or severe hypotension (watershed area)

-homonymous hemianopia with macular sparing

due to du,al blood suply (post. cerebral and middle cerebral a.) with occlusion of post. cerebral.

- homonymous hemianopia with macular splitting

-more common

-bilateral homonymous hemianopia with macular sparing

-produceconstricted visual field

C. Disorders of visual integration

Alexia

-inability to read despite normal vision~~~~ angular gyrus dominant parietal lobe

-agraphia =inability toWrite~~~~~~~~~~~~~~~~~ angular gyrus

Visual neglect===patien ignores one side of visual space~~~~~ dominant parietal lobe

Agnosia===inability to recognize objects by sight~~~~~~~v2

Prosopagnosia===inability to recognize face~~~~~~~~~~~~v2

Cerebral achromatopsia===color blindness in one hemifield~~~~~~~~~~~~~v1

Visual hallucinations=== temporal lobe

Palinopsia===abnormal perseveration of visual images~~~ right hemisphere occipito-parietal convexity

IV. Pupillary disorders

A. Pupillary light reflex pathway

photoreceptors --> retinal ganglion cell axons --> reflex relay in tectum ->pretectal nucleus --> pretecto-oculomotor tract --> bilat. Edinger Westphal nuclei --> CN III --> ciliary ganglion --> iris sphincter & ciliary body

B. Afferent pupillary defect

-elicited by swinging flashlight test-normal pupillary response is constriction followed by slight redilation -abnormal response is decreased or absent constriction with redilation or redilation that is larger than when light is swung to other eye. indicator of optic nerve disease which causes light to appear dimmer in the affected eye than in the opposite eye. also seen in extensive retinal disease (eg. large RD), brunescent cataract, and some amblyopes (up to 0.6 log unit density defect)

C. Anisocoria

approach to aniscoria

exclude physiological and CNII then do tests for aidies and horners

most of tome it will be physiological

Definition - unequal pupillary size

1. Physiologic most common cause of anisocoria pupillary size difference less than 1 mm and varies from day to day

2. Third nerve palsy

I anisocoria (mydriasis) associated with ptosis and ocular motility disturbance ~~~~~~~~~~~~~~~~~~~~~seen in intracranial aneurysms (ICA/Post. comm. a.)

II anisocoria that is isolated~~~~~~~~~may be seen with uncal herniation or basal meningitis

III anisocoria during eye movement ~~~seen in aberrent regeneration of CN III

3. Traumatic/surgical 4. Pharmacologic

5. Adie's tonic pupil===characterized by poor constriction to light and brisk response to near

caused by post-ganglionic parasympathetic lesion -80% initially unilateral and more common in females (70%) supersensitivity to diluted pilocarpine (0.05% - 0.1%)-Holmes-Adie syndrome if diminished deep tendon reflex and orhtostatic hypotension also present

6. Horner's syndrome

see section on pupil

D. Light -near dissociation

Retinocortical pathway

retina --> ON --> optic chiasm (decussation of nasal retinal fibers)--> optic tract --> LGB --> optic radiations --> occipital

cortex->Visual calcarine cortex -> superior colliculus->

Pupillary light reflex pathway

photoreceptors --> retinal ganglion cell axons --> reflex relay in tectum -->pretectal nucleus --> pretecto-oculomotor track Bypassing MLF --> bilat. Edinger Westphal nuclei --> CN III --> ciliary ganglion --> iris sphincter & ciliary body

ConVergence

Visual calcarine cortex -> superior colliculus-> pretectal nucleus ->pretecto-oculomotor track Bypassing MLF --> bilat. Edinger Westphal nuclei --> CN III --interneuron CN VI

The difference lies in short circiut in Brain stem. Hence Brain stem lesions preferentially affect pupil reflex rather then accomodation

Keep in mind Supranuclear inputs Visual calcarine cortex to superior colliculus Non-visual frontal eye field or vestibular system (semicircular canals)

Gaze centers Horizontal CN VI / pontine paramedian reticular formation (PPRF) PONS Vertical rostral interstitial nucleus of the MLF (RiMLF) (interstitial nucleus of Cajal) MIDBRAIN

Argyll-Robertson======= pupil poor light response but react to near by small irregular pupils

lesion reflex relay in tectum

Adie's tonic pupil pupil===characterized by poor constriction to light and strong response to near

-lesion caused by post-ganglionic parasympathetic nerve fibre damage mechanism is uncertain but there may be a separate abberent regenerating nerve fibre for near vision in addition to a defective nerve fibre for lightmaking 2 separate tracts to the ciliary muscle 80% initially unilateral and more common in females (70%) supersensitivity to diluted pilocarpine (0.05% - 0.1%)-Holmes-Adie syndrome if diminished deep tendon reflex and orhtostatic hypotension also present

Parinaud syndrome===poor light response and intact near response associated with verical gaze paresis,mid position pupils with nystagmus, and lid retraction with scleral show above limbus;convergence-retraction (of globe)

lesion: reflex relay in tectum =[pupil site ]+ RiMLF=(vertical gaze centre)

The retraction is of lid upwards and the globe inward because the eye cant look up so it tries to to stimulate levator and hence lid/globe

And it tries to converge

V. Optic nerve disordersBlood supply: Optic nerve head: retinal arterioles or cilioretinal artery branches Prelaminar and lamina cribosa: posterior ciliary arteries; terminal arteries with watershed zone Intraorbital: intraneural branches of central retinal artery, multiple recurrent pial branches Intracanalicular: ophthalmic artery Intracranial: internal carotid and ophthalmic artery

A. Optic disc edema

1Features

narrowing of cup with relative preservation of cup depth, obscuring underlying disc margin, retinal (Paton's lines)/choroidal fold

2. Papiledema v. papillopathy

Papilledema ===due to raised intracranial pressure bilateral, MOSTLY

Papillopathy ===due to optic nerve disease (eg. inflammatory & vascular) severe decrease in visual acuity and/or visual field loss

3. Pseudotumor cerebri BIH

-etiology unknown but can occur in COPD, radical neck dissection, corticosteroid use or withdrawal, with elevated levels of Vit. A (renal failure), tetracycline, lithium, and nalidixic acid. initial treatment is weight loss followed by use of Diamox or Lasix to reduce intracranial pressure.

4. Optic neuritis===subacute loss of vision in contrast to sudden vision loss in ischaemic optic neuropathy usually affects young women 2/3 of cases show normal optic disc (retrobulbar neuritis) 1/3 show optic disc swelling (papillitis) MRI shows gadolinium enhancement of the optic nerve and often foci of demyelination in the CNS. Presence of >2 plaques increses risk of developing clinically definite MS within 2 years (up to 39%). 50% of recovered patients may develop transient decrease in vision after exercise or elevation of body temperature (Uhthoff's ootoff!! phenomenon). -long-term risk of developing MS is greater than 60%

-recommended treatment from the Optic Neuritis Treatment Trial (ONTT) study is IV methylprednisolone (250 mg qid x 3d) followed by oral prednisone (1mg/kg/day x 11 days) which hastened visual recovery (slightly) and reduced rate of development of MS within 2 years in patients with 2 or more demyelinating foci. -ddx central serous retinopathy big blind spot syndrome multiple evanescent white dot syndrome anterior ischemic optic neuropathysyphilitic optic neuritis postviral optic neuritis Leber hereditary optic neuropathy (mitochondrial gene mutations) toxic/ nutritional optic neuropathy malignant optic glioma

5. Ischemic optic neuropathy

A. Arteritic===narrowing and thrombosis of posterior ciliary artery supplying aminar and relamnar oDdue to temporal arteritis (a.k.a. giant cell arteritis) treatment is prednisone 60-120 mg/day or IV methylprednisolone.

B. Non-arteritic===idiopathic ischemia of optic nerve assoc. with HTN (50%) and DM (25%); presumed atherosclerosis as basis. -no effective medical or surgical therapy -clinical course shows partial recovery of vision of 3 or more lines within 6 months in 43% of cases.-recurrence rare but involvement of contralateral eye occurs in 25% by 3 years and up to 50% by 10 years.

C. Posterior ischemis optic neuropathy===ischemic damage to retrobulbar optic nerve-often bilateral and simultaneous -rare condition which occurs in setting of severe hypotension or anemia (eg. massive bleeding) or vasculitis (Hayreh)

6. Multiple evanescent white dot syndrome===idiopathic disorder which presents as acute unilateral loss of vision (mild to severe)affects young individuals, females more than males, in association with flu symptoms {see uveitis}

CF blurring of optic disc, and characteristic small white dots (100-200 µm) at level of RPE located perifoveally. Mild sheathing, cells in vitreous, macular granularity, and flame hemorrhages may also be present on fundoscopic exam. fluorescein angiogram shows early hyperfluorescence of the dots with late staining and mild leakage. ERG shows depressed a and b waves on acute sage of the disease but normalizes with visual recoveryclinical course self-limited and visual recovery usually achieved by 8 weeks.

7. Infiltrative optic neuropathy

8. Diabetic papillopathy===occurs in juvenilie insulin-dependent DM no ischemia on fluorescein angiography clinical course shows full visual recovery in 3 months to a year.

9. Dysthyroid optic neuropathy

10. Papillophlebitis (Big blind spot syndrome)=== as mild decrease in vision (unilateral) in young healthy adults clinical course self-limited with full recovery by 1 year.

11. Miscellaneous causes

uveitis, central retinal vein occlusion, malignant HTN, and hypotony

12. Pseudopapilledema

Optic nerve drusen===deposits of calcium, mucopolysaccharides, hemosiderin and amino acids in the optic nerve head often autofluorese usually bilateral (75-80%) and occurs predominantly in caucasians -inherited as autosomal dominant may be associated with retinitis pigmentosa no ????Paton's lines.

Tilted optic disc===one side displaced posteriorly and the other anteriorly. crescent on side of disc depression retinal vessels are directed obliquely -seen in high myopic patients

Optic nerve hypoplasia===unilateral or bilateral small disc has double ring sign (concentric choroidal-retinal pigment changes)etiology unknown but increased incidence in children of mothers taking LSD, anti-seizure medications, quinine, and ETOH abuse.-may be associated with intracranial tumors and endocrine abnormalities.

B. Optic atrophy

1.Compressive

a. Optic nerve glioma ===most common cause of orbital tumors in children (20%) 50% intraorbital and 50% intracranial 10-50% have neurofibromatoses b.Malignant optic glioma (glioblastoma multiforme)===rare form of optic nerve glioma seen primarily in adults c.Optic nerve meningioma -represents 5% of orbital tumors snail tract sign MRI -more common in women than men (3:1) CF usual + remember opticociliary shunt vessels may increase in size during pregnancy not surgically resectable but may respond to radiation therapy

d. Pituitary adenoma

-pituitary apoplexy (infarction) presents as acute loss of vision with headache and diplopia, unilateral or bilateral 3rd, 4th, or 6th cranial nerve palsy,

e. Craniopharyngioma===tumor arising from Rathke's pouch which impinges on the optic chiasm

5% of intracranial neoplasms bimodal peak of occurrence (< 20 y.o. and 50-70 y.o.) presents with visual loss, headache, growth disturbance, obesity, somnolence, or diabetes insipidus may have accompanying psychiatric problems CT shows solid or cystic tumor with calcification

f. Miscellaneous empty sella syndrome Sheehan's syndrome

2.Toxic/ Nutritional

-toxic methanol, lead, ehambutol, chloramphenicol, rifampin, and amiodarone (amiodarone controversial is due to toxic effect of the drug v. AION in high risk patients).

nutritional deficiency :thiamine and vitamin B12

3.Hereditary/Congenital

a. Leber's optic neuropathy===caused by point mutation in mitochondrial gene coding for NADH mode of transmisssion is mother to sons with daughters being carriers of the gene occurs predominantly in 10-30 y.o. males special CF. Venous tortuosity remains indefinitely as a marker but not present in all. avoid use of tobacco and alcohol which may trigger optic neuropathy females may be affected usually milder

b. Kjer dominant optic atrophy===autosomal dominant disorder causing progressive loss of vision onset 5 - 10 years of age

c. Optic nerve dysplasia

optic nerve coloboma====incomplete closure of fetal fissure

-exam shows large excavation of the disc inferiorly

vs

morning glory disc=======rare dysplastic also coloboma of the optic disc appears as a funnel shaped excavation of the disc surrounded by pigmented ring of chorioretinal atrophy usually unilateral and more common in females (2:1)

optic pit==============round or oval pit in optic disc which appears darker than surrounding disc tisssue assoc. with macular edema (50% )

other Barrens 3 types juvenile infantile and at birth juvenile least affected also have retinal pigmentation like RP and other eye features that are more prominent in juvenile type. lipfuscon deposits in neurons PAS + lysosyme storage defect mitichhondrial cause other features neurological eg hypotony MR epilepsy etc Hist vacuolated lymphocytes and PAS + neorons even peripheral

4.Traumatic optic neuropathy

VI. Ocular motility disordersA.CN III1. Nucleus located in the midbrain at level of superior colliculusinnervates contralateral SR, ispsilateral MR, IR, and IO, and bilateral levator palpebrae muscles. Edinger-Westphal nucleus innervates ipsilateral pupil

-lesions are rare and would

cause~~~ bilateral ptosis and paresis of contralateral SR and ipsilateral MR, IR, and IO. Usually also some ipsilateral SR weakness from involvement of fibers passing through involved nucleus from the other side.

2. Fascicle courses ventrally through the red nucleus and exits through the medial portion of the cerebral peduncles

lesions are usually of vascular or metastatic etiology

- causes 4 types of syndromes a. Nothnagel superior cerebellar peduncle~~ cerebellar ataxia b. Benedikt lesion red nucleus and medial lemniscus~~contralateral loss of sensation, brain stem uncontrolled movements (rubral tremor,hemichorea, athetosis, and ballismus)c. Claude ~~ combined d. Weber cerebral peduncle~~~contralateral spastic paralysis

Nonagel=cerebellum

Benedict=loss sensation[ml]/uncontrolled mvment[red nuc]

Claude=cerebellum/basal ganglia/ml

Weber=peduncle spastic paralysis

3. Subarachnoid course

-susceptible to injury by uncal herniation clivas ridge syndrome ie compression against here or post. comm. a. aneurysm nb this is anterior to circle of willis meningeal infiltrative (inflammatory and neoplastic) results in ~~~CN III palsy with pupillary involvement

4. Cavernous sinus

CN III susceptible to injury from carotid-cavernous sinus fistula, aneurysms, tumors,inflammatory (Tolosa Hunt syndrome=inflamation idiopathic of cavernous sinus) and infectious processes:

-results in~~~ CN III palsy as well as involvement of other cranial nerves (IV, V, VI)

5. Orbit -CN III divides into superior division -innervates SR and laevator palpebrae inferior division -innervates IR, MR, IO, iris sphincter, ciliary muscle

6. Isolated third nerve palsy with sparing of pupils due to ischemia of CN III seen in DM, HTN or just old age -occurs in older patients (> 40 y.o.) -self-limited and resolves in 12 weeks vasoasorum obitertaed

7. Aberrent regeneration of CN III:nb the 111 rd cn supplies itself incorrectly

results in :Pseudo von Grafe sign =lid retraction with downgaze -due to innervation of levator palpebrae by IR fibers Inverse Duane's syndrome=lid retraction with adduction-due to innervation of levator palpebrae by MR fibers Pseudo-Argyll-Robertson pupil=light-near dissociation due to innervation of pupillary sphincter by MR fibers Pupillary constriction on downgaze due to innervation of pupillary sphincter by IR fibers

B.CN IV

1. Nucleus -located at periaqueductal gray matter of midbrain -innervates contralateral superior oblique

lesion produces hypertropia causing vertical diplopia as well as ex-cyclotorsion (12:00 position toward the ear)

-ipsilateral Horner's syndrome may also be present due to adjacent descending sympathetic fibers in dorsal midbrain

-etiology includes hemorrhage, infarction, demyelination and trauma/surgery

2. Fascicle courses dorsocaudally and decussates at anterior medullary velum prior to exiting at level of inferior colliculus-susceptible to injury by compression (eg. severe head trauma or pinealoma) resulting in bilateral CN IV palsy

-Bielschowsky test may be negative and requires double Maddox rod test for diagnosis (>10° of excyclotorsion)

3.Subarachnoid course

-long intracranial course traversing dorsal to ventral along the tentorial edge

-highly susceptible to injury from neurosurgery and head trauma

-lesion produces ipsilateral CN IV palsy (or bilateral if anterior medullary velum involved)

4.Cavernous sinus

-located in lateral wall below CN III and above CN V

-lesion produces multiple CN palsy (III, IV, V, VI) and Horner's syndrome

5. Orbit

-enters via the superior orbital fissure to innervate the SO muscle

-CN IV can be affected in orbital apex syndrome

6. Congenital CN IV palsy

-represents 29% - 67% of fourth nerve palsy

-seen most commonly in children but can decompensate later and may present in adults (50-70 y.o.)

-exam shows large vertical fusion amplitude (>3D)

-old photographs showing head tilt help make diagnosis

C. CN VI

1.Nucleus located at the floor of the fourth ventricle below facial colliculus (fibers if CN VII loop over nucleus of CN VI) contains motor neurons that innervate LR but also interneurons that project ot contralateral MR subnucleus via medial longitudinal fasciculus (MLF)

-lesion results in conjugate horizontal gaze palsy

-a Duane's syndrome=congenital absence of abduscens nucleus LR innervated by branches of CN III leads to defective abduction & stimulate CN III when abducting wil also raise the eye and widen fissure ( relativeand narrowing of palpebral fissure from globe retraction with adduction) usually does not complain of diplopia b Mobius syndrome= congenital absence of abduscens and facial nuclei -may also involve CN IX and XII nuclei

2. Fascicle courses ventrally and laterally to exit at the pontomedullary junction

-lesion usually affects other nearby structures :Millard-Gubler sybdrome~~involvement of the pyramidal tract~~-ipsilateral CN VI palsy with contralateral hemiplegia Foville's syndrome~~involvement of CN VII nucleus/fasciculus, spinal tract of CN V, and sympathetic fibers~~horizontal conjugate gaze palsy, facial weakness and numbness, and Horner's syndrome

3. Subarachnoid course courses upward along the clivus and is susceptible to injury by tumors, basal skull fracture, trauma, raised intracranial pressure ("false-localizing CN VI palsy")

4. Petrous pyramid -CN VI passes through Dorello's canal which is bounded by the petrous bone and petroclinoid ligament

-susceptible to injury from petrous bone fracture, tumors, and infectious/inflammatory processes of the middle ear

-Gradenigo syndrome~~~ ipsilateral CN VI palsy, with decreased hearing, facial pain and facial paralysis due to abscess formation in petrous apex following otitis media ie involves CN five to eight

-Pseudo-Gradenigo syndrome~~similar symptoms as Gradenigo's syndrome but due to nasopharyngeal CA or cerebellopontine angle tumors

5. Cavernous sinus -accompanied by post-ganglionic sympathetic fibers

-lesion produces multiple CN palsy (III, IV, V, VI) and Horner's syndrome

6. Orbit enters via the superior orbital fissure to innervate the LR lesion can be involved in orbital apex syndrome

7. Isolated CN VI palsy

- post viral -seen commonly in young patients (<15 y.o.) -neoplasm more common in younger than older patients need to R/O with neuroimaging study

-ischemic mononeuropathy seen in older patients (>55 y.o.) esp. with DM and HTN -self-limited with recovery occuring by 6-8 weeks

D. Multiple cranial nerve palsy

1. Cavernous sinus syndrome ===lesion in the cavernous sinus causes painful ophthalmoplegia, facial numbness, and Horner's syndrome

cavernous sinus is a dural venous sinus which contains the internalcarotid a., CN III, CN IV, CN V, CN VI, and oculosympathetic fibers -various etiology a. internal carotid artery aneurysm b. carotid-cavernous fistula c. cavernous sinus thrombosis d. neoplasm e. inflammation (Tolosa-Hunt syndrome)

2. Orbital apex syndrome=== crowding of intraorbital contents due to tumor, inflammation, infection, or edema from trauma which causes injury to CN II, CN III, CN IV, CN V 1,2, and CN VI

3. Myasthenia gravis

-ptosis is asymmetric and worsens after prolonged upward gaze. Manual elevation of more ptotic lid results in greater ptosis of the fromer less ptotic lid due to Hering's law.

-diagnostic tests

a. Tensilon test -test dose of 2 mg edrophonium chloride (Tensilon) is injected followed by 8 mg slowly injected starting 1 minute later -positive test if ptosis and ocular motility improves -common side effects include diaphoresis, lacrimation, abdominal cramping, nausea, vomiting, salivation, syncope rare but serious complications include bradycardia and respiratory arrestantidote is atropine sulfate (but symptoms are usually over by the time this can be administered) b Sleep test patient rests and closes eyes for 30 minutes -positive

test if ptosis and ocular motility~~~ improves after rest period c.Ice pack test ice pack is placed over closed eyes for ptosis ~~~ improves after 2 minutes because neuromuscular transmission is enhanced in the cold

4.Multiple sclerosis

increasing prevelence further fro equator

affects primarily young adults (25-40 y.o.) and women greater than men (2:1) may present as myriad of neuro-opthalmologic deficits but commonly manifests as optic neuritis,bilateral INO, CN VI or CN VIII palsy, and nystagmus

75% womea nd 35% man with ON will develop MS in 15 years

On ocurs in 70% of MS and is icreased if winter onset HLA dr2 & Uhtoffs phenomenon

CF easy eg decreased VA and color

Px 75% recover in 4 weeks to 6/9 or better but have residual decreased colr and contrast sensitivity

Other motility disorders

INO invoving MLF most common

1 cant adduct (with contralateral eye manifesting uncertainty in sympathy and hence 2nystagmating

3 but normal convergence

explantion horizontal gaze PPcentre near CN 6 and MLF crosses here

Rx steroids ie methylprednislone 250mg IV qid for 3 days with oral Pred 1mg per kg for 11 days speeds recovery

interferon

case with retrochiasmal clinical features ie quadrantanopia

common to have MRI plaques in this area but rare t have clinical features

Dx Visually evoked cortical potentials (VECP)

-records electrical signals in the cortex generated by stimulation of the retina with light.

-a measure of macular visual function because of the disproportionately large representation of the fovea in the occipital cortex.

-p100 wave - positive deflection that occurs at 100 msec after the stimulus is most reliable parameter to measure.

latency increased in disorders with demyelination as a component of pathology including multiple sclerosis, optic nerve compression, infiltration or toxicity.

ON imunomodulatory drugs ABC

avonex IF beta 1a

Betaseron IF beta1b

Copaxone glatramer acetate

have been shown to reduce reurrence rate in MS by 44%

Diagnosis of plaques 2 or more white matter abnormalities on t2 weighted MRI

ONTT summary High dose IV follwed by oral accelerated recovery but no long term benfit to vision

it aslo delayed defintite MS during 2 years but not after 3

5. Thyroid ophthalmopathy

6. Chronic progressive external ophthalmoplegia- === etiology is mitochondrial abnormality in extraocular muscles -usually presents as bilateral asymmetric ptosis before adolescence which progresses to external opthalmoplegia rare diplopia due to symmetric nature may have weakness of orbicularis, facial muscles, arms legs, and chewing serum CK may be elevated EM shows ragged red fibers seen on H&E to be abnormal aggregates of malformed mitochondria

7. Botulism===cholinergic blockade due to botulinum toxin that blocks aCh at NMJ and Para -may be acquired from food, wound infection or birth ocular findings include ophthalmoplegia, ptosis, and dilated poorly reactive pupils systemic symptoms are nausea vomiting, and generalized weakness

Botox 100 units type A avaialablr use 5 u for strabismus and 25u for ocular spasm or plastic surgery

Toxity

Give botulinim antitoxoid im 50000u type a and balso type e 5000u

E. Supranuclear gaze palsy

Gaze centers

Horizontal CN VI / pontine paramedian reticular formation (PPRF)

Vertical rostral interstitial nucleus of the MLF (RiMLF)

(interstitial nucleus of Cajal) near CN III

Supranuclear inputs

Visual calcarine cortex = sensory superior colliculus

Non-visual frontal eye field = motor

vestibular system (semicircular canals)

Horizontal gaze disorders

1there is no lateral gaze -----------------------------------HGP

lesion opposite gaze if supranulear or at ipsilateral gaze centre PPRF

2on lateral gaze medial rectus cannot move------------------INO

ipsilateral MLF

3or on lateral gaze medial rectus cannot move and lateral gaze to other side there is no gaze ----------------------------------------1 & 1/2

Rostal ipsilateral PPRF & MLF

4or both medial rectus cannot move ----------------------------WEBINO

rostral MLF lesion with involvement of CNIII nucleus

1 Unilateral horizontal gaze palsy

-lesion of CN VI nucleus and/or PPRF or supranuclear pathways from contralateral cerebral hemisphere

2.Internuclear ophthalmoplegia (INO)===results in inability to adduct the eye ipsilateral to the lesioned MLF with nystagmus of contralateral abducting eye

-lesion in MLF disconnecting ipsilateral CN III, medial rectus subnucleus from contralateral CN VI / PPRF -usually orthophoria in primary gaze

MS, vertebrobasilar insufficiency, AVM, tumors, and inflammatory diseases (INO is thought to be uncommon from brainstem vascular disease since there is collateral flow to the dorsal brainstem from long circumferential vessels and most lacunes occur in the ventral brainstem in the distribution of the short penetrating arteries medially.)

3 One and a half syndrome

-lesion of CN VI nucleus / PPRF and ipsilateral MLF

-ipsilateral conjugate gaze palsy

-contralateral INO

4.WEBINO===walleyed bilateral INO===exotropia in primary gaze with inability to adduct either eye past midline

lesion at rostral MLF lesion with involvement of CNIII nucleus

5. Fisher syndrome===variant of Guillain-Barre that involves only brainstem and cranial nerves that results in unilateral or bilateral ophthalmoplegia with ataxia and areflexia

self-limited and usually follows a viral illness CSF examination shows elevated protein but no pleocytosis

Vertical gaze disorders 1. Tonic deviation ===upward oculogyric crises occurs in post-encephalitic Parkinsons's disease can also be seen in comatose patients -tonic upgaze indicates bilateral cerebral/cerebellar lesions -tonic down gazeindicates bilateral thalamic bleed or infarct tonic downgaze can also occur in metabolic encephalopathy 2.Parinaud's syndrome===lesion in dorsal midbrain characterized by supranuclear paresis of vertical gaze with intact vestibular-ocular reflexes ptosis light-near pupillary dissociation skew deviation convergence retraction nystagmus etiologies congenital aqueductal stenosis pinealoma head trauma vascular formation long standing multiple sclerosis basilar CVA 3.Progressive supranuclear palsy===progressive conjugate paresis of gaze which presents initially as decreased downgaze associated with progressive dementia and death usually in 5 years-has OKN "drift sign",normal Doll's eye, and normal Bell's response4Downgaze palsy===rarely isolated lesion in RiMLF rostral to CNIII and dorsomedial to red nucleus 5.Skew deviation===lesion in internuclear connections involved in vertical gazeproduces ipsilateral hypotropia in lower brainstem lesionipsilateral hypertropia in pontine and midbrain lesions

VII: Facial nerve

Motor root: muscles of facial expression in four groups of nuclei, upper face receives corticobulbar input from both cerebral hemispheres, lower face only from opposite hemisphere, motor fibers wrap around VI nucleus to form facial colliculus

Sensory root: special visceral afferent for taste, general somatic afferent for sensation from external auditory meatus and retroauricular skin, general visceral afferent for preganglionic parasympathetic to lacrimal, submaxillary and sublingual glands

Pathway

precentral motor cortex (frontal lobe) -->corticobulbar tract -->*CN VII nucleus -->CN VII nerve --> facial muscles

*CN VII nucleus receives bilateral input for upper face but only contralateral input for lower face innervation

1. UMN facial palsy===results in contralateral weakness of lower two thirds of face with sparing of forehead &eyelid closure usually only mildly affected

2. Facial nerve palsy===results in ipsilateral weakness of both upper and lower portions of the face & impairs closure of the eyelids and results in exposure keratopathy Causes

1. cerebellopontine angle tumor (eg. acoustic neuroma) associated with hyperacusis, decreased taste, and involvement of CN V, VI, or VIII 2 Ramsay-Hunt syndrome===herpes zoster in CN VII and CN VIII & diagnosed by finding by vesicles in external auditory canal,

typanic membrane or external ear pinna less chance for recovery compared with Bell's palsy 3 Bell's palsy === unknown but thought

to be auto-immune, viral induced inflammation or ischemic injury may be associated with decreased tearing, taste and dysacusis, and usually pain behind the mandible 84% show spontaneous recovery, but aberrent regeneration may be present (eg. crocodile tears) CN 7 parotid lacrimal closes eyelid expression and taste to poserior tongue

Latest

Bells is viral HSK

Rx prednisolone 80mg per day tapered over 10 days quickly with oral ACYCLOVIR 800mg 5times for 10 days

Esp poor px ie

Old/dec taste/hyperarcus/full palsy

Ocrocodile tears = 7 nerve fibres going to the lacrimal gland rather then parotid when stimuated for taste by the reflex action of taste of the 7 CN greater petrosal nerve normally goes to lacrimal but chordae tympani to submax/man nerve goes to lactmal glan

to treatment is oral corticosteroids to reduce nerve edema and consequent damage 4. trauma/surgery 5. sarcoidosis often bilateral Heerfordt's syndrome of "uveoparotid fever" combines uveitis, fever, parotid swelling and CN VII palsy 6. Lyme disease 7 Leprosy

3. Essential blepharospasm===bilateral episodic contraction of orbicularis oculi

4. Hemifacial spasm===unilateral episodic clonic spasm of the face

5. Facial myokymia===unilateral fibrillation of facial muscles

Phakomatoses

NFtype 1 ~~~~ 2 or more of following:

6 or more CAL,ON glioma intertrigo freckling ,2 or more lisch nodules=iris hamartoma,distinctive osseaous lesions immediate family member, 2 or more neurofibrommas

Type II 1 of following

bilateral Acoustic neuromas

What is a harmatoma:non malignant normal tissue in an inappropiate site

Tuberous sclerosis{ bournville)

Stagnent mulberry like tumour AStrocyte hamartoma of retina or optic nerve that does not cause RD or have feeder blood vessels but may calcify

Critical features Adenoma sebacum= butterflydistribution red papules nad brain astrocyto

Scleral scatter pick up corneal opacities uses total internal reflection

specular illumination aim microcope at angle that biseects light ray that is incident and its reflection and look at diffuse illumination used to see endothelium

Childhood

VA is checked by preferrential looking acuity cards

or The Catford drum

or by STYCAR lettere E test

or Sheridan Gardiner chartor pictures

& the kay picture chart

Hertel thyroid

Hirshprings test estimates anle of heterotropia by corneal

ihght reflex

Angle kappa is the angle between the visual axis and anatomiical axis

normally fovea just temporaal to optical axis and hencc e corneaal reflex just nasal we are slight EXOTROPIA

this is normal and +

TumoursConjunctival tx

Choristioma === tx normal tissue in abnormal location. include dermoid and lipidermoid

dermoid ===skin like tiisuecinsisting of dermis likeconnective tissue and covered by epidermis containing tissue appendage lke hair glands etc etc

lipidermoid ===adipose tissue and dermis like connective tissue and occur in subconjunctica as movable yellow masses esp at limbus or canthus

LASER

ALT

1% Apraclondine

spot size 50um duration 0.1 sec initial power 700mW

Increase stepwise increments of 200mW use 25 burns in one mirror

spot must be round NOT oval

aim at jxn posteroir pigmented and ant white TM

Drugs

Mannitol

1 to 2 g per Kg of body weight

or 5 to 10 mls per Kg of Commercially available solution (20% solution in water

speed of admin not more than 60 drpos per minute acts in 30 minute and lasts for 6 houts

Augmentin 12g tds ivi or kids 5kg 120mg ivi td

ampuoes 1.2g or 6mg vials

%SurgeryGlaucoma Filtarion Sx ComplicationsShallow ACGrade I perpheral iris cornea touchGrade II Entire iris in contact with corneaGrade III Lens Cornea touch

%Diabetes MellitisPDRRxInitially 2000-3000 burns in more then 1 session since a single session has an increased risk of bleedingThe spot size depends on the contact lens usedGoldmann uses 500um but panfundoscopic uses 300-500 um the durartion is .1 to .05 secondsPower is a gentle burnFollow up 4 - 8 weeksMay increase in increments 50 mW until a grey white burn is achievedFlat NVE with fibrous tissue treated 500um medium intensity burnssevere NVd need 5000 or more burns

CSMORetinal thickening within 500um of centre of FAZHard exudates within 500un of FAZ WITH associated retinal thickeningRetinal thickening 1500um in diameter within 1500um of FAZ

%Social OphthalmologyChildhood Blindness

Trachoma rx zithromycin T one a year

Protocol

aacg

500mg ivi diamox or oral

+g timoptol

g predsol

after 1hr pilocarpine 4 3 drops sta a nd then qid

recheckiop after 30 min

if still high 50% glycerol 1g per kgor 20 mannitol 1 to2 g per kg over 45 minute

CRAO

hollenhorst palque=embolus of cholesterol frm carotid artery= bright refractile plaque at bifarcation of arteriole

Diamox 500mg Po stat

timoptol 025% BD

Alkali burns

Vit C

chor

maxidex

cyclo

V. Endophthalmitis

post operative 75%, trauma 5-20%, endogenous 5%

gram+ >60% Staph. epi> Staph. aureus, Streptococci, Bacillus, P acnes, actinomycetesgram- 25% Pseudomonas, H. flu, Proteus, Klebsiella, Serratiafungal 15% Candida most common, Fusarium

Postoperative postoperative rate for cataract surgery is 0.1 to 0.4% virtually all cases are inoculated at time of surgery acute 1 to 14 days after surgery mild have less pain, vision better than 20/400, and present later Staph.

epidermidis is most commonly recovered organism severe usually 1-4 days later marked pain, vitritis, vision worse than 20/400 fundal details are not visible Staph aureus, Streptococci, and gram negative organisms chronic 2 weeks or later after surgery gradual symptoms, good vision, minimal pain, hypopyon, and mild vitritis S. epidermidis most

commonly within 6 weeks fungal usually within 6 months and most commonly Candida P. acnes can occur 2 months to 2 years white plaque with P. acnes and residual lens material found

inside capsular bag there have been reports of endophthalmitis following YAG capsulotomy EVS- Endophthalmitis Vitrectomy Study no benefit in final visual acuity from systemic antibiotics patients with initial Va of HM or better

Posttraumaticposttraumatic rate is 2.4 to 8% in urban areas and up to 20% to rural settings

Bacillus can be recovered in up to 1/3 of these cases and causes a rapid severe infection

Bleb relatedbleb associated is 1 0 yrs, >75% yield + culture, usually bleb intact and organisms penetrate conjunctiva

Streptococci 1/2, H. flu 1/4, P. acnes, Moraxella, Pseudo. cepacia, Fusarium

Vision correlates with virulence of organism and often is poor

Endogenousinfection usually begins in retina with focal chorioretinitis

later, it will breakthrough into the vitreous with vitreal masses overlying the original sites

Candida

often debilitated without ocular complaints

chorioretinitis with multiple chorioretinal white lesions <250 um often in posterior pole

up to 10% of pts with candidemia will develop such lesions

endophthalmitis leading to "headlight in the fog"

nonspecific signs seen with candidemia include retinal hemorrhages, Roth spots, CWS, rare hypopyon, iritis

amphotericin B, vitrectomy, f/u with fluconazole

Klebsiella

endogenous with 90% ending up with Va of CF

1/4 with no known primary site of infection

can happen even when patients are on appropriate therapy

pts at risk are diabetics with liver disease or UTI or in any patient with liver abscess

Diagnosisaqueous: 25-30 gauge needle through the limbus into AC and withdrawing a 0.1ml sample

vitreous: 23-gauge 1 inch needle passed through pars plana 3.5mm posterior to the limbus into anterior vitreous to obtain 0.2ml of undiluted vitreous or do pars plana vitrectomy using tubing set that connects to 10mm collection syringe

inoculate directly onto culture media: blood (aerobic and anaerobic), Sabouraud's agar, chocolate agar, and thioglycollate broth.

in cases of chronic postoperative endophthalmitis, the lab should hold anaerobic cultures for 2 weeks because P. acnes may take that long to grow

RX Gentamicin 100-200 mcg/Amikacin 400 mcg and Vancomycin 1000 mcg

gentamicin and clindamycin 450-1000 mcg (good for P, acne, B fragilis)

Amphotericin B 5 mcg (repeat injections if needed)

alternatives include Ceftriaxone 2,000 mcg, Imipenem, Ciprofloxacin

place 10 cc of fluid from vitrectomy canister into blood culture bottles, aerobic and anaerobic

ceftazimne comes in 1g

dilute with 5ml and take out 1ml we have 200 mg~~~~~NEED 2 millgrams

mix with 10 ml water now 1ml will have have 20 mg

NOW take 0.1ml and inject it and you have 2mg

ciloxin find out but subconj justtake out of bottle

gentacin

come in 40mg packed in 2ml solution

add 1 ml water and take out 1ml

so that each ml has 20mg

add 10ml water so each ml has 2mg

INJECT NOW 0.1ml whichh is .2mg or 200ug which is required

gentamycin comes in80 milligrams in 2ml so 1ml is40 milligrams ~~~~~

GENERAL GUIDELINES FOR TREATMENT OF ALLERGIC CONJUNCTIVITIS

antihistamines levocabastine- 0.05% QID for up to 2 weeks, potent H1 receptor antagonist

mast cell stabilizer lodoxamide- 0.1%, gives some symptomatic relief within two to three days, has some effect on stabilizing eosinophils or cromolyn 4%

nonsteroidal anti-inflammatory acular- 1 drop QID

oral antihistamines (such as claritin 10mg QD)

Uveitis Work Up Guidelineswork up if: bilateral recurrent severe retinal or choroidal involvement

work up of acute iridocyclitis

history is paramount HLA-B27 Angiotensin Converting Enzyme (ACE) often high in kids may be low if patient is on ACE inhibitors elevated in sarcoid but not specific lysozyme CXR FTA-ABS or MHA-TP ?lyme titers

work up of chronic iridocyclitis ANA in childrenACE LysozymeCXRTB Sarcoid HLA-B27 if indicated by histor PPD often not helpful uveitis in North America is rarely secondary to TB may need INH if pt requires oral steroids ?lyme titers

work up of sclerouveitis RF ANA FTA-ABS CXR Sarcoid TB Wegeners ANCA C-ANCA: Wegeners P-ANCA: less specific

Bacterial keraritis

Staph & Strep Pmeumonia oval yellow white stromal suppuration

Pseudomonas sharp ulcerartion mucupurulant exudate and ground glass adacent stroma

E cloi shallow ulcers and ring shaped stromal infiltrates =(corneal rings)

Rx cefuroxime

ciprofloxacin

gentamycin

ciprofloxin 750mg BD

Gram +~~~~~~~~~ cefuroxime like augmentin cover =zinnat ciprofloxacin(= covers MRSA and Pseudomonas that is resistant to genatmycin but poor cover of S Pneumnia)

zovirex 5 times 800mg for 7 days

Gram - ~~~~~~~~~~gentamycin

macular grid 150 burns 0.08 s or 30 mw

0.05 sec

50 um

diclofenac 50mg tds

Crani facial synotosis

craniofacial stenoses

AD synotosis of sutures of thes skull

Crouzens=shallow orbits hence exposure

Aperts shallow

Lateral trachlear collins

antimongoliod slunt rotated orbit

what is velox ? maxidexlike steroid

fresnal prsims

schisi much mre red than normal

congenital retinischisis

CN REvision

CN1 optic 11 olfactory 111 optic iv troclear abducen

v triegeminal mastication sensation face

vii expression cry salivate submax subman taste ant 1/3feels about ear invoves ENT OPhthalmologist and CHEFS

ix salivate taste post 2/3 vagus talk

x1 shrug shoulders

x11 move tongue

CN 6

excycloversion 12 o clock at 2 o clock and elevation

hence verical diplopia and head tilt to opposite side

CN 4 easy

CN 3

PRP 20 um 025 to 03 seconds

036 watts

Retinoblastoma1:20,000 births, becoming more common 6% with FH, 25% have genetic mutation 13q14 with low esterase D levels 1-3 y.o.,nerospecific amulase

present older when unilateral 70% are unilateral with 30% bilateral 1/5 of unilateral on presentation get 2nd eye affected later the differential dx of inflammation is the most difficult leukocoria most common

strabismus inflammation (pseudohypopyon) Ca2+ vitreous seeding normal size globe glaucoma hyphema heterochromia fixed pupil serous RD with dilated vessels

signs different for endophytic/exophytic

metastasis late with spinal cord, bone, skull, lymph nodes, abdomen

assositedpineal gland trilateral tumor with very poor prognosis

up to 50% with secondary cancers especially osteogenic sarcoma, fibrosarcoma, rhabdomyosarcoma many years later

Genetic risk

history determine if germline or somatic germline in multiplex and multifocal cases simplex disease with unifocal RB has 12% risk for germline mutation remember carrier status due to 80% penetrance unaffected parents with one child mutifocal RB have 6% risk for second child examine family for regressed retinocytoma Molecular genetic analysis can find the specific gene mutation using Southern blotting RFLP's to do linkage studies

Diffuse infiltrating RB (1%) likely to be missed occurs later (6 y.o.), unilateral, grows slower

RXchemo etoposide VP16 carboplatin vincristine and cyclosprina result in remarkable regression chemoreduction is given every 4 weeks for 6 cycles until conservative rx possible

it is also used in advanced rx like bilateral cases metastic or intracranial spread

It may be stopped after enucleation is done

Enucleation aim to obtain longest possible Optic nerve studies say it is curative if longer than 5mm so aim for 10 to 15mm in all cases so use a Curved scissor as a tip and ask for it in theatre

also cryptherpy for preeqiutorial tx

Exudative RD covex and

external episceral plaque radiation used in relatively large but localized tumour with or without vitreous seeding use isotopes iodine 125 or ruthenium 106 that target a dose of 40gy to the tumour apex a metal layer on the outer surface of the plague shields emission in other directions

external beam radiation use a linear accelaor 40 to 50 GY given to eye and orbit used when optic disc is involved and photocoaguation is not indicated here there is rapid regression and two scenarios common with or without calcification it is not useful for vitreous seeding because of hypoxia of vitreous

at doses used and the gamma radiaon does not cause major problems like neovascular glaucoma but onlu PSCC which can be dealt with at 6 months later

NB electron beam therapy in contrast is more severe in cloatral damage and other cancers

laser therapy now popular is a diode laser= wavelength in UV spectrum that causes transpuppilary hyperthermia used thru operating micriscope and duration is 1 to 15 minutes exposure

photocoagulation small tumours less than 7mm aim to cut blood supply

CT, MRI: look for calcification, pineal gland U/S: A scan with high internal reflectivity and echo spikes from calcification, B scan with orbital shadowing bone scan, bone marrow, lumbar puncture as needed with massive tumor, enucleation may be primary procedur external beam radiation, Episcleral plaque, Photocoagulation, cryotherapy systemic chemotherapy regression TI cottage cheese TII fish flesh TIII combo of above TIV white sclera 5 yr survival >90%, poorer with metastasis

Histology

Flexner Wintersteiner rosettes -an attempt to make photoreceptors with clear lumen fleurette with outer segs of photoreceptors Homer Wright rosette- lumen with neurofibrillary material, also in medulloblastoma, neuroblastoma pseudorosette-tumor around necrosis viable tumor around vessels with areas of necrosis

Why add cyclodporin?

it switches off p glycoproten that pumps out vincristine etopisife and carboplatin

Coover uncover diiosiateyes that are kept together bybinoculat single vision. and masks a deviation.

focal 50 um spot

0.06 W

.015 secs

Stabismus

V. Vertical Deviation

1DVD 2SO palsy 3Double elevator palsy = cniii palsy no sr or ir action4Brown's syndrome 5Primary SO overaction 6Congenital fibrosis syndrome 7CPEO 8Myotonic dystrophy 9Oculopharyngeal dystrophy 10Skew deviation 11Misc.

1DVD=updrift of nonfixating eye especially with cover -uncover

deviated eye often aBDucts and EXtorts and almost bounces back into position (like SO palsy only abduction rather than elevation)

asymmetrical, spontaneous or with occlusion equal deviation in gazes

etiology unknown, almost always bilateral Usually NO hyPOtropia when hyPERtropic eye fixates Herring's law does NOT apply associated with latent nystagmus, congenital EX measure with base down prism under occluder often becomes evident after EX surgery natural history with resolution in 15-25% diff dx- IO overaction, hypertropia 2SO palsy=Most common cause of vertical diplopia with excyclo and elevation

Longstanding palsies with contraction of IO and vertical concomitance pay careful attention to versions for the diagnosis when fixating with paretic eye, can mimic a SR palsy of opposite side especially in ABDuction (inhibitional paresis of the contralateral antagonist), ptosis Three Step Test

1patient prefers head tilt to OPPosite side with chin depression to minimize diplopia 2 HyPERtropia IPSIlaterally with elevation on ADDuction 3 + Bielschowsky test: head tilt to IPSIlateral side with increased HYPER Do Biechowsky head tilt supine and standing. Often, acute acquired IVth nerve will have normal exam in supine position and hyperdeviation in standing.

Cyclotorsion often worse in downgaze

double maddox rod often less than the true tropia due to sensory adaptation

pay attention only to the net torsion between the eyes

fundus exam gives the true cyclotropia

Congenital long standing head tilt amblyopia uncommon, may indicate absent SO facial asymmetry with affected side being more full can decompensate at later age often with subtle complaints of intermittant diplopia, asthenopia, neck ache with reading no torsion on Maddox rod secondary to sensory compensation may have mild decrease in stereo forced ductions in OR show laxity and it is loose upon inspection

Acquired traumatic, CVA, sinusitis, tumor complain of tilting of objects discrete hx of onset can measure torsion with Maddox rod usually < 20pd of hyperopia in primary ischemic causes usually are in older patients with

5-10 pd of hypertropia forced ductions in OR reveal normal SO of both sides Bilateral uncommon,associated with trauma V-pattern ET downgaze often with chin down posture Double Maddox rod > 10-15 degrees excylotorsion Head tilt shows either alternating hypertropia or is reduced to very little or none can be masked

IVBrown's syndrome

Clinically io palsy =congenital, tenosynovitis, IO abnormalities Decreased elevation on ADDuc usually DEPr on ADDuc + forced duction V[ ie contracture restriction io action] V pattern, straight in primary bilateral in 1/10 r/o IO paresis

acquired watch and wait often resolves trochlear bursiti JRA adult RA sinusitis/surgery blepharoplasty mets orbital surgery SLE post partum scleroderma

there is true muscular overcontraction, so tenotomy does not produce secondary SO palsy be careful if patients have fusion

III. Esotropia

1Congenital Esotropia 2Accomodative ET 3Incomitant ET 4Duane's syndrome 5Mobius syndrome 6Convergence spasm

1Congenital ESotropia=congenital absence of motor fusion characteristics large with V = up out icycloversionOASO with A = down out and excycloversion DVD latent nystagmus asymmetric OKN

Rx treat amblyopia and trial of glasses if > +3.00 surgery by 18 months to achieve single binocular vision (>90%) if surgery after 2 yo, < 1/2 have binocularity Diff Dx accomodative ET Duane's T1 Mobius syndrome neurological abnormalities nystagmus blockage bilateral abducens palsy sensory ET{Nystagmus blockage= manifest congenital nystagmus dampened by convergence both eyes are crossed and face turn may be seen eyes straighten under general anesthesia} variable angles, but nystagmus often disappears with convergence

2Accomodative ES =6 months to 7 yrs, avg 2.5 yrs, +FH

starts intermittent, precipitating illness, trauma amblyopia frequent no diplopia since suppression or ARC

1Refractive=+3.00 - +10.00 D, avg +4.00 hyperopia increases till age 7, then decreases & deviation same distance and near, 20 - 30 pd If delayed RX, may not respond If > +5.00 D, can get bilateral ammetropic amblyopia RX patch amblyopia, full time Rx repeat refraction 2 months post glasses since ciliary relaxation if overcorrected post surgery, try over minus therapy

High AC/A= moves easily without focusing!! & need gasses if near 10pd > than distance is a rough clinical measurement usually

hyperopic (+2.25 D avg, but can be myopic or +10.00) MUST BE ACCOMODATING TO GET FULL EXcan get nonaccommodative EX measurement normal AC/A 4:1 ie 4 diopters convergence per change inpower Gradient method: (ES near with +3.00 lens - ES n) /3 (dioptric distance) Heterophoria method: (PD (cm) + Es near - ES distance)/ D (of near)

RX: +3.00 large flattop bifocals with the segment splitting the pupils bring target close to child and if they reflexively assume chin up posture, then they are using bifocals Diff dx nonaccomodative (stress, cyclic) paralytic sensory deprivation divergence insufficency (ET > dist than near) Spasm of convergence

3Incomitant ES MR restriction thyroid, blowout, post op forced ductions are useful guide to surgical planning VI nerve paresis often with head turn for fusion common in children Check neurological exam, trauma, CT, MRI patch, fresnel prisms, botulinum for diplopia short term Post XT surgery usually improves spontaneously RX prisms, miotics, full CRx, p atch, surgery

Surgery

chances for consecutive exotropia increase with anisometropia, high hyperopia, amblyopia, or cerebral palsy Tablesmay do symmetrical surgery of weakening MR or strengthening LR by same amount OU in adults with >45pd of esotropia, consider three or four muscle surgery to avoid limitation of ductions Note that these are a starting point and should be continuously monitoredrecess-resect may weaken MR and strengthen LR of same eye by reading across table used if one eye has much better vision not as good for large deviations

ET angle (pd)

recess MR in mm

resect LR in mm

<15

3-5 (only one)

15

3.0

4

20

3.5

5

25

4.0

6

30

4.5

7

35

5.0

8

40

5.5

9

50

6.0

10

>60

7

10

4Duane's syndrome= no VI nerve nucleus innervation of LR by III nerve

sporadic usually, but AD in 1/10 F > M, OS > OD (slightly) usually unilateral children rarely complain, present usually with head turn adults complain of asthenopia, intermittant diplopia, and vague discomfort ocular decreased ABduction variable loss of ADduction +/- upshoots and downshoots on adduction paresis of convergence uveal colobomas crocodile tears amblyopia On ADd, PF narrows, globe retracts secondary to activation of LR systemic decreased hearing Wildervanck syndrome deafness, Klippel Feil anomaly (web neck), and Duane's syndrome F>>M Types most commonly, patients have TI Duanes with ES in primary and minimal enophthalmos/leash, willhavegood stereo,the less ES in primary position, the greater the enophthalmos TI: decreased ABd, straight to ET in primary, bilateral 20% TII: XT in primary and limit ADD( this is a funny Duanes) TIII: decreased ABD and ADD

5Mobius syndrome=no abduction mask facies and gaze palsies due to VI, VII nerve palsies, abn PPRF moby dick never looked outwards!

some can also have III, IV, V, IX, X, and XII may have variety of motility disturbances inclding limitation of adduction that improves with convergence fissure changes vertical muscle involvement mask like facies sporadic, although rare AD varients have been reported systemic Poland's anomaly (absent pectoralis muscle) limb, chest, and tongue defects micrognathia, small mouth, hypodontia 15% have MR

7Convergence Spasm= Intermittent ES, miosis, and myopia (accommodation)

Symptoms include headache, asthenopia, diplopia, photophobia May appear to have bilateral VI th nerve palsies, but will have miosis with abduction Functional vs organic (posterior fossa, vestibulopathy, pituitary tumors, diffuse metabolic disease, MS, and trauma) Baclofen has been tried in MS

IV. Exotropia

1Basic 2Divergence excess3convergenceinsufficiency4PseudoXT

1Basic same at distance and near

2Divergence excess =distance > near by 15 pd due tohigh AC/A = easy mobility and poor focus check post occlusion (break fusion) simulated excess if becomes basic with +3.00D after patching for one hour most do not become ET at near post op if straight at distance

3Convergence insufficiency exotropia of near is 15dp more than exotrpoia when checking in distance near point of convergence (NPC) is remote{ or more easlly very close toeye that itis hidden!!! low AC/A does not converge but accomodates blurred near vision often only with exophoria traumatic often resolve within one year (up to 2/3) remaining are difficult to treat usually prisms, orthoptics are ineffective Rxpencil pushups reading or TV with BO prism to increase convergence amplitudes chronically, can treat with BI prism often have significant overcorrection early on, especially with bimedial resections a recess/resect procedure provides some incomitance so the patient can fuse without diplopia

4Pseudo EX + angle kappa cornea nasal fovealateralROP dragged macula Toxacara telecanthus Duanes TII incomitant

How do they present

1Exophoria

NPC near point of convergence may be remote, asthenopia if controlled by accommodative convergencemost commonly a ~~~problem with convergence insufficiency NOT treatable by surgery, use convergence exercises

2Intermitant XT =most idiopathic, +FH, F>M usually starts around age 2 close one eye in bright sunlight ARC V pattern ,only 1/4 improve or are stable often complain about diplopia when driving or moving must measure with accommodative target bilateral temporal hemiretinal suppression

progressive with decrease tonic convergence, developed suppression, decreased accommodation, and orbital divergence with age most are pseudo-divergence excess, so patch 45min or check with +3.00d rx give f3

4Consecutive XT must check adduction to see if MR has slipped

Surgery

wait until 2 1/2 to 4 year old to promote fusion if in lateral gaze measures10 pd < straight, then decrease recession by 1mm/muscle

BLRR should aim for 10 - 20 pd of ET early on resect/recess should aim for a few pd overcorrected early on for long standing cases, need to release contracted conjunctiva and Tenon's

Tables may do symmetrical surgery of weakening LR or strengthening MR of both eyes may weaken LR and strengthen MR of same eye by reading across table at larger angles, may prefer to do four muscle surgery with the numbers in parenthesis

XT angle (pd)

recess LR in mm

resect MR in mm

15

4

3

20

5

4

25

6

5

30

7

6

35

7.5

6.5

40

8

7

50

9 (6)

7 (5)

60

10 (7)

8 (6)

70

11 (7.5)

9 (6.5)

80

12 (8)

10 (7)

consecutive ETusually resolve with time may patch, prisms, full plus glasses, phospholine iodide rare to have persistance, especially when ductions are full if incomitant, after a resect/recess, may require reoperation

ICE

iris naevus EIA syndrome= iris atrophy with PAS pulling iris to one sideand ectrpian uvea Chandlers syndrome=chandlers is in between atrophy and naevus having a bit of bith

the common denominater is glaucoma and corneal endothelial abnormalies

age and sex : ONE eye of middle aged women

notes

Pars planitis risk of MS sarcoid and syphiilis

ARC and suppression

children supress vision to protect aganist diplopia

suppression eliminates central diplopia and creates a small scotoma with ET= esotrpia and a hemiretinal with XT

ARC eliminates peripheral diplopia use bagolini lenses to test

Tests for Central scotoma Diplopia & Steropsis

Central scotoma Tests

1use 4pd BO test (no movement in in eye that has no fixation and is amblopic 2Bagolini lenses(eye with hemiretinal scotoa picked up since glasses close dissociate fields 3 Worth 4 dot ( 4 dots seen at near but lose 1 as dots are moved back in ambyopic macular )

Diplopia tests

A red glass in front of the eye means all light will be filtered out except red which will go thru.

1Red filter red filter over one eye, do they see a pink/red/white fixation light or double? 2prism neutralization if sees double

with prism neutralization ie straight , then patient has ARC 3 W4D )can test strength of fusion by darkening the room and increasing the dissociation (up close, normal periphery, back off at 1/3 -1 meter will show scotoma and pt will see only 3 dotsdots are separated by 6 degrees at 1/3 m, and 1.25 degrees at 6 m, and 12 degrees at 1/6 m NB alternating suppression can be confused with diplopia

W4D explained. put on green red glasses and look at screen with 2 green lights one red light and 1 white light that has obvioulsy both green and red eminiting (one red and 2 green is used to differntiate the eyes

by convention red in front R and green in front L

look for normal binocular fusion 2ARC 3 Lor R suppression 4diplopia 5 Alternating supression

if 4 normal binocular

if there is a manifest squint and 4 dots ARC

if 3 green and 2 red DIPLOPIA

if 3 green only R supp

if 2 red only L suppresion

Addedknowledge

VA is 300 to 400um spacing of photorecepter at fovea this equates to one minute of arc or 60sec nb the small Es of 6/6 subtend 1minute at each arm

Steropsis Testing Normal bifoveal fixation is 20-50 arc seconds & 80-3000 arc seconds is normal peripheral fusio When testing you

must have adequate illumination to test properly since it is a peripheral phenomenon You can use the 1Titmus Fly is 3000 arc seconds>>>>> or 50 minutes or just under a degree or animals 400-200-100 arc seconds or circles 800-400-200-140-100-80-60-50-40 arc seconds [10 minute s to about one It has monocular clues and as a check rotate 90 deg,to lose

stereopsis so if patient can see smallest circle foveal fixation is intact2Randot better positive testing equals high grade stereopsis

Normal phorias adults at 6m have 2 pd Esophria & at 30cm have 6 pd Exophoria while children at 6m have ahigher 8

pd Esophria & at 1/3 m have a higher 8 pd Exophoria Angle Kappa fovea in relation to centre of cornea usually cornea is a bit nasal to fovea is normal + kappa an abnormal angle kappa is different than eccentric fixation because the fovea is still usedpositive= normal, nasalnegative= abnormal, temporal

Fusional amplitudeshorizontal convergence D 14pd N 38pd divergence D 6pd N16pdvertical2.5pd

Bruckner testdirect ophthalmoscope at arms length, full brightness perform Hirschberg's, then compare brightness of red reflex assess fixation or

nd red relex brighter in esotropic eye

hypoaccomodationasymmetric red reflexes are due to strabismus, anisometropia, anisocoria, posterior pole abn/media opacities

1 Amblyopia 2% of population with neutral density filter, the difference between the eyes diminish crowding phenomenon eccentric fixation can be found with dense amblyopia Causes

1Strabismic 2Refractive imeridiona l >+3.00 ii ametropic usually >+5.00give correct Rx may take a long time for vision to

get better--be patient 3anisometropia very common >1.5 D difference in hyperope, >2 D in myopes children with better initial

vision will do better anisekonia doesn't occur with correct rx very small incidence of ET developing while patching 3Organic often a functional componant is also present deprivation (amblyopia ex anopsia) media opacity such as cataract or corneal opacity structural eg, optic atrophy, macular scar small APD, abnormal PERG 4Occlusion less than 10%usually reversible with cessation of patch or

brief patching of other eye 5Monofixation syndrome <8 pd of strabismus (cover/uncover or simultaneous prism and cover) and 1/3 have no deviation alt cover > cover-uncover, prism and cover anisometropia common small macular scotoma (debate about ARC and suppression) usually good binocular vision, NRC,andabnstereoacuity (<60%) may have HARC (cover test normal), macular lesion most have amblyopia

terms

phtysical eye

correctopiaembrytoxin

Esterman binocular 80 degrees left right

70 to 80 degrees up and down

stimulus III size

backgrouund 31.5 ASB

intensity 10 DB time about 5 mins for entire test

DVLA regulations: guidlines

PRP

100um 0.05 sec 240mW about 2000

Drugs

cefuroxine

elixir

vexol

Cross Cylinder

cyliders are marked

estimate cyl axis Retinoscopy

Use .25 cross cylinder to start

Correct Axis first

1correct axis by lining handle white dots and move

increment 10 degrees towards the type of cylinder eg if + green positive may move towards thsi line many times

2 correct power

then do power line up with color line does not matter which one either be plus .25 or a minus .25

thne change cylinder power in trial frame

use rings wernhoff rings to test aqouityneeds 6 / 12 at least

before cross cyl have em look green red lights

which better

green refracted less he is more myopic

get them onto green add to get em to green

green red diff 0.25

then do cross cylinder thren remove extra minus

use rins only if up to 6 12

if worse us e cross cys with appropaite target

Back verteb distance usuallt 12 to 15mm

messuer lens to lid

use conversion disc

with minmus lens clooser to eye weaker lens that is add some plus

if plus add some

use for more then to 5diopters

Vocabulary artuafactual

Laser

Argon laser

laser tube is filled wiith argon gas under pressure. A current causes argon molecules to emit blue grreen

light that is delivered via fibre optical cable to the slit lamp

spot sizes vary from 50 to 1000 mciirons --usually use 200u-500u time is 01 sec

Red light emitted from Krypton may also be useful

Xanthophyl in mature cataract and macuular & HB absorb blue green light.~~~~therefore avoid Hx CF zone and BV.

Most of BG light absored by RPE therefore burnconfined to outer retina therefore moderate burn is useds anything more burns all tissue

blue green light is scattered more than red by media and this is a great disa dva

white tissue like OD fibrosis hard exudates cR atrpothy refllect BG ~~~~ no effect

Pigmentation absord ~~~~~ risk of burns

Energy density ~~ size [ duartion

S S P T

200um macula 500 paeriphery

small spots genarlly not necessary

tiime 01 to 0,2 sec

Macula moore xanthophull more pigmented Rpe therefore no laser inside FAZ risk of spread

hhere red krytpon with less absorbtion is better

NB

FAZ vessesl more susceptible loose glail suuport so easy separeted and ~~~~CMO

Lasers

Most are water or air cooled

Xenon not used due to larges spot sixe and poor heat control

Histology

laser destorys RPe and and deep tissue bruchs not ruptuterd

Technigue

1ideal burn yellow in light pigmneted

and grey in dark pigmented

2 make perimeter and then fill centre

watt is joule per sec = power

energy is joule

OpeartionTurn on the air pump

wait 1,2 minute then turn on switch

sit down

adjust power to 200 mw {0,2 watts and sppot to 500um= 0.2 jouels per sec or 200mj per sec

beam will lihgt up dustparticles in a dark room

place aper at site if intensity increase chsnges fromb lut ogreen

duration of burn 01 sec

observersmust wear yellow filter glasses as obbserver has built in laser

Wave length of laser

Argon ~~~~~~488 to 514 B G

Krypton ~~~~~647 red

Diode ~~~~~~800 IR

Nd Yag ~~~~~1064 IR

CO2 ~~~~~~~10600 IR

Trabeculectomy

CL

Single mirror goni lens

Abraham or wise iridotomy lens PI

Goldmenaa style 3 mirror

Panretinal

Modes of laser operation

1Continoues wave~~~~ thermal damage

2Pulsed~~~ thermal

3Q switched extremeely shrot durartion eg nanoseconds= cold ~~~~ photdisrution~~~~ capsutomy iridectomy

4A mode locked train of extremly short (pico) photdisruption capsultomy iredectomy

5fundamental orrMulti mode ==

Fundamnetal===one type of wave therefore no divergence and small spot high power ~~~used in capsultomy and irodectomy

Multimode many waves in different direction s~~~~ calcified membranes and heavy tasks

books

Practical ophthalmic surgery

willshaw livinstone chirchill

drugs

Timoptol LA .25% .5 %

Cosopt 2% trusopt .5% Timoptol

Entropian

Everting sutures Double armed 4/0 catgut are passed thru full thickness eylid from conj side just below the inferior tarsal plate and tied in the eyelid skin at aslightly higher level

Weiss horizontal incision below inferior tasua plate

1bouble armed 4/0 catgut passed from conj side thru con and skin just below insicion

2they then pass thru pretarsal orbcullaris on upper side and tied on skin 2 to3 mm below eyelashes

3 close skin with silk

Cyclocryo

4mm probe temp -60 to -80 'C

8 applicationss over 2 quadrants 2.05 mm from limbus for 60 seconds

Trans screla Nd Yag

free running or thermal mode 20 millsec pulses of 1064 nm (ir) light

sclera is penetrated

techniigue

2mm from limbus 20 applications over 180'

Tanponades

Silicon oil demethyl siloxine colorless sg 1 refrective index 1.004 viscsity abot 12000 cps

Gas tamponade

sulfur hexafluride SF6 used as 20% mixtxture with air as total sF6 with expand dangerously when the bubble enters blood nitrogen

gas is loost very qiuckly therefore top up after op

time usually 1 to 2 hours

anterior eye

SR

LR 6.9

MR 5.5

sr 7.7ir 6.6

OS temporal 7 to 8

OS nasal 6 to 7 less saceon side of nse

ora serat to equator 6 to 8mm

equator to macula 18 to 20mm

vortex veins either side of SR &IR 6to mm behind eutor

IR 5 to 6 bbehind ewutor

at 1 5 7 11 ocock

starbismus pearls

obliues move eye towards the nose so test for overactivty and underactivty

the eye forms ie optic al axis of a 22.5 or 23^ axis with the orbital axis

normal fusional vergence is 15D for far and 25D for ear and is decreased with fatiaqe It helps to keep eyes keep eyes straight

Examination

Hirshbergs states a light relex 15 degrees or 30D if at pupil margin and 45 degrees or 45D at limbus

also for pseudostabismus ie wide nasal bridge oe broad epicantal folds or close set eyes

psedoexo can be de to shortening of tempeal canthusk

Understanding angle kappa

we should expect the fea to be at the optical axis as we se the fovea to look straigt ahead but it actually is a little temporal

alternate cover with prism cover for 2 seconds and place apex of prism in direction of deviation

use a base out small pris power to detect binocular single vision eg 4 diopters

place prism in front of eye and check for coective movement if it is present then thr person is fusing and u have sucessflly boken it

maddox wing dissociates eyes and measures heterophoria

maddox rod remeber that when cylinders are horizontal they convert a wit dot into a vertical line

chilkdhood esotropia

pearls more likely t have dvd if nystagmus present

kids normally +1.5 dioptor hyperopes

IO overaction occurs most common at 2years and becomes bilateral

DVD excyclo and updrift ( ie eye is bells and away when covered!!)

appears after years f surgery faden is procedure dne fr csmesis

ambyopia 40%

Jenson transposition split the lateral rectus and SR & IR in 2 leaving attachment and the suture corners with non absorbalbes

RD colors

colors blue ~~~~~~~~detatched

red ~~~~~~~~~~~~~4~attached

brown ~~~~~~~~~~~~choriod

black ~~~~~~~~~~~~~~pigment

greem ~~~~~~~~~~~~media opacities

yellow~~~~~~~~~~~~ chorioretinal exudates

3mirrro=r only unside down

lense 20D magnification 2.3 times fiels 40 '

28D 1.5 but larger field 60'

14D larger field

90D SMALL FIELD AND

90 d 2/3 magnifation mltiplied by slit lamp mag

Explants may be sponge tyre starp sixes 3 4 5 7.5 mm diameter

instruments St martins is toothed forceps

the eye focuse green ight

red is not deviated therefore seen best in myopic eyes myopes drift towads red

duochrome test should get emto green

Tarsorraphy

epithelium excisedfrom lid margins posterior to ge0y linelatereal U L lids

40 nylon or sik passesd as a matress from skin of upper lid thru raw trasal margin and out of skin of lower tru tubing and back again to be tied on skin upper tru tubing

ectropian

full thickness lid resection

lazy t

do full thickness lid resection 4mm lateral topctuma

resect a diamond 2 triangles of conE & taral plate with 2 apices vertival below puctum

appose apices and close with fullthickness 40 catgut

suture full thickness lid resection

Lee medial catho

plasty for ectropian and eveted puncta

2 lacrimal probe sinserted fr safety

lid is splitinto 2 medial to pucta into anterior skin and posterior lammela

suture abooveupper canaliculis andbelow lwwr cana

when tied the puctu is inverted again

Axial Globe Displacement:=mass w/in muscle cone ~~~~~cavernous hemangioma glioma meningioma mets avm

vs

Superior Globe Displ: ~~~~~~~max sinus tumor

vs

Down + Medial Globe Displ: ~~~~~dermoid cysts lac gland tumor

vs

Down + Lateral Globe Displ: ~~~~ frontoethmoidal mucocoele abscess (subperiosteal) osteoma sinus ca

Pulsation

w/o Bruits: neurofibromatosis meningoencephaloceles post op ie s/p removal orb roof

vs

w/ Bruit: c-c fistula dural av fistula orbital av fistula

Keratometer

measure curcature of central 3mm radius of curvature nomally is 7.8mm

priciple object is placed so that image is at f2= 2nd focal point which is half way to c or radius of curvature

therefore r which is 7.8mm approximately is image size divided by object size multiplied by 2 u or distance of of bject from cornea which is standard and known

O/I = distance of object / distance of image ( 1/2 R or F2 or normally 3.9mm or 4 mm

object size × imagedistance or 1/2 radius = image size × object distance

IN all U is constant

In JAVAL shiotz mires one object size is varied to obtain a standard image size

VS

In Helm hortz object is fixed and and the image size is adjusted.

Helm hortz

2 mires in a lantern with colored window

space between mies is the object size

image is formed by refection by cornea

but viewing telescope has quartz prism to splits each latern image into 2 at at fixed angle therefore getting images to touch makes them the right size and image can be used as correct just like Applantion tonometer!!!

made so thateach step is one diopter

an additon i the HAAG Strey Javal schiotz incorparte a horizontal line to faciliate vertical allignment

Slit lamp

1Bliue cobaltfilter

3Green red free

scattering is greates when short wavelength used therefore use to see vitreous

Aplanation tonometer

appied to cornea with sfficient force to PRODUCE a STANDARD area of contact = booyles law = to flatten a sphere the area yoy flatten is drportional to pressure important

not so important!!!we use 3.06 where conveniatlysurface tension and corneal rigiditycancel out

head of prism 2 prisms kissing at tips ie base out

as we look tru ton head wesee prism splitting 2 half circles by moving images latrally likeanyprism does

Galeilien telescope

concave={diverging} eye piece and convex={condensing }objective sepatrated by differebce in foca lenth

produces erect magnified image

REDUCED EYE AS PER LISTINGA single princple point and a single nodal pointused

Refractingpower uesed 58.6 D

all distances from cornea

princple point 1.35

nodal point 7.08

first fovcal point -15.7

2nd focal point 24.13

NBcorresponding focal lenth = -17.05 and 22.28

Drwingi objects deviated at princple line and go tru nodal point

Far point is thatpoint in arelaexed eye the image falls on the retina

Maddox rods

diisosiate the eyes so they see disimar objects and allows muscle imbalance to become manifest.

NB the eye is deviating opposite to the line seen

Focal point is only a point thru which light travels and it is half radius

vs

Far point and Near point

Surgical procedures

Punctal stenosis 3 snip insert scissors vertically down make 2 cuts outward follow up with one horizontal cut out triangle

A & v Patterns managment

A as we go up the eyes go in A esotropia

V as we go down the eyes go inV esotopia

or exotropia V or a

The common deviation is INWARD or outward

RX 1 vertcal rectus transpalnation

May get V or A exotropiapull inwards ~~~~ trnspalnt nasally

in esotria V or A vertical rectus tranplanted temporally 7mm 2 Horizontal recess rescet

MR naturally convergers strongly on downgaze

& LR naturaly diverges on upgaze This either one produces V patterns when they overact

RX weaken these

A patterns due to underaction muscles RX therefore strengthen

usually move 5mm may also adjut height to reduce pattern

eg A esotrpoia recess MR and elevate

V esotrpia recess MR and move down A exotrpoia recess LR abd move down V exotppia LR reecss andmve up

3OBliquesSo overaction{ relative IO underaction)~~~~~ A pattern mostly in exodeviationmore than 20D weakening egtenotomy ---IO overaction ~~~~V pattern mostly esodeviatyion

RX strengthen SO by

Anatomy

sleral thickness temporally not thicker then 1mm

nasally 1.5mm

macula 1.5mm

very thin bemeath tendons ie .0.3 mm!

Surgical instruments eyelid conjunctica Bard parker knife chalzion forceps and curette graefe muscle hook ptosis forceps? Snellen entropian forceps lod forceps jaeger lid plate caliper needle holder suturing forceps stevens tenotomy scissors blunt or sharp Westcott tennotomy scissors lester fixation forceps straight or curved tissue forceps seerine clamp to hold loose ends in squint surgery

corneal instruments corneal scissirs bonn tissue forceps suturomng forceps

Lens diamond tooke corneal knife barrquer iris scissors capsule forceps iris retracter and espressor lens loop synechie spatula iris spatula troutman cannula gills forceps

Defintions

Dermatochalasis=older persons skin of yelid becomes relaxed redundent due to atrpohy of subcutaneous tiisue

culture media

Acanthamoeba culture on non-nutrient agar with E. Coli overlay

blood agar

chocilate haemolysed blood

fungal??

viral??

Blindness Certification

VA lwss than 3/60

partial 6 /60 to 3 / 60

Mysrilate 0.5ml + Betnesol.0.5 .ml subconjunctival injection for Uveitis

hydrocortisone 0.5% is a weak steroid cream andse thisfor skineczema others 1%&2% mayalso use

Drugs and prblems

amiodarone coritca catarct

Nrmal parmaete

corneal diameter

5. Leukocoria

Cataracts1/3 genetic, 1/3 diseases, 1/3 idiopathicn monocular are not metabolic or genetic capsule forms in 5th week and limits entry of organisms opacities >3mm are visually significant

Anterior

polar 1/3 are bilateral abnormal separation of lens from surface ectoderm 90% sporadic pyramidal 2 mm projecting cone with surrounding cortical opacity cones can be fibrotic and touch to fragment bilateral and sporadic subcapsular idiopathic, trauma, often acquired lenticonus Alports X linked dominant Difficult capsulorhexis Chronic steroid use may present with PSC cataracts ===hereditary nephritis sensorineural deafness PPMD whitish dots in macular and mid periphery Central

Nuclear in general, congenital origin either the embryonic or fetal nucleus

usually non-progressive bilateral are often AD inherited Sutural or

Lamellar acquired usually after 6 months progressive hypoglycemia and galactosemia can cause lamellar pattern Posterior

Posterior lenticonus looks like PSC, bowl like central outpouching unilateral, progressive at surgery, post capsule often thin wispy and difficult to peel off opacity

PHPV

posterior capsular

associated with Down's syndrome

Oil Drop cataract

associated with galatosemia

Lowe's

XLR

systemic hypotonia hyporeflexia mental retardation Aminoaciduria metabolic acidosis growth retardation renal failure

often with early death

ocular most commonly small thick opaque bilateral cataracts pupils can be very miotic with lens adhesions female carriers have white punctate opacities throughout their lenses glaucoma in 50% by age 6 but can be early on corneal keloids

Hallerman Streif

Labs

especially to exclude Lowe's, galactosemia

consider TORCHS titers even in unilateral cases

Urine

reducing substances, aminoacids, blood/protein

copper, sediment

Blood

Ca+2/phos, glaucoma, amino acids, TORCHS serology, others

PHPV wide spectrum of presentation congenital, non hereditary, usually unilateral not associated with other defects except cataracts retinoblastoma is rarely found in microphthalmic eyes

elongated ciliary processes microphthalmos shallow anterior chamber radial iris vessels retinal detachment retrolental plaque intraocular hemorrhage angle closure glaucoma

US/CT very diagnostic

natural history of untreated eyes with moderately severe disease is progressive shallowing of anterior chamber, cataract formation, and angle closure glaucoma

Pseudogliomas

benign neoplasm

astrocytic harmartoma

can mimic RB, involvement of disc, multifocal, bilateral

usually with tuberous sclerosis, rarely with neurofibromatosis

little postnatal growth

von Hippel angioma

medulloepithelioma

uveitis

nematode endophthalmitis

usually older boys, inflammation more

inactive lesions show more changes than RB (cataract, synechiae, etc)

ELISA + 90% with 1:8 dil

retinitis, old VH

Non-rhegmatogenous retinal detachment

Coats'

usually older boys age 8-10 years old

anomalous grapelike clusters of leaking blood vessels

serous RD with dilated vessels can look like retinoblastoma

aneurysmal dilation can look like angioma, but no feeder vessels

about one half of untreated patients will progress

treatment includes laser and cryotherapy

retinal dysplasia

juvenile retinoschisis

Misc

retinal hemorrhage

retinal folds

colobomas

Retinoblastomaost comon eye tumur in kids initiall detected n one eye but becmes bilateral in 1/3 of cases

avareage age starts is 18monhs bt there is a late pesentain at 3months

inheritence

only 6% will have a family history and then it is AD with incompete penetrence

Therefre 94% sporadic 25% germinal and 75% somatic

1:20,000 births, becoming more common

6% with FH, 25% have genetic mutation 13q14 with low esterase D levels

1-3 y.o., present older when unilateral

70% are unilateral with 30% bilateral

1/5 of unilateral on presentation get 2nd eye affected later

the differential dx of inflammation is the most difficult

leukocoria most common

strabismus

inflammation (pseudohypopyon)

Ca2+

vitreous seeding

normal size globe

glaucoma

hyphema

heterochromia

fixed pupil

serous RD with dilated vessels

signs different for endophytic/exophytic

metastasis late with spinal cord, bone, skull, lymph nodes, abdomen

pineal gland trilateral tumor with very poor prognosis

up to 50% with secondary cancers especially osteogenic sarcoma, fibrosarcoma, rhabdomyosarcoma many years later

Genetic risk

history

determine if germline or somatic

germline in multiplex and multifocal cases

simplex disease with unifocal RB has 12% risk for germline mutation

remember carrier status due to 80% penetrance

unaffected parents with one child mutifocal RB have 6% risk for second child

examine family for regressed retinocytoma

Molecular genetic analysis

can find the specific gene mutation using Southern blotting

RFLP's to do linkage studies

Diffuse infiltrating RB

(1%) likely to be missed

occurs later (6 y.o.), unilateral, grows slower

RX

CT, MRI: look for calcification, pineal gland

U/S: A scan with high internal reflectivity and echo spikes from calcification, B scan with orbital shadowing

bone scan, bone marrow, lumbar puncture as needed

with massive tumor, enucleation may be primary procedure

external beam radiation, Episcleral plaque, Photocoagulation, cryotherapy

systemic chemotherapy

regression

TI cottage cheese

TII fish flesh

TIII combo of above

TIV white sclera

5 yr survival >90%, poorer with metastasis

Histology

Flexner Wintersteiner rosettes -an attempt to make photoreceptors with clear lumen

fleurette with outer segs of photoreceptors

Homer Wright rosette- lumen with neurofibrillary material, also in medulloblastoma, neuroblastoma

pseudorosette-tumor around necrosis

viable tumor around vessels with areas of necrosis

Rx chemotherpy

VP vincistine and ?? evry 4 weeks for 6 cyclesa

usually regresses after 2nd treatet

enucluation best results with 15mm or more of optic nerve resection so aim for this as sprewad is via optic nerve

Radiotherapy

ROP85% of ROP is transient disease with spontaneous regression

examine all children born under 32 weeks or weighing less than 1,500 gm

CRYO-ROP study had 6% of children <1251 gm reach threshold, 20% prethreshold, 60% have some ROP

Risk factors include <750 gm, PCA of <28 wks, O2 > 3wks, black < white

initial exam at a post-conceptual age of 32 weeks

long term risks include

pseudostrabismus myopia

PAS and glaucoma RD

cataract microphthlamia

phthisis

classification

stage 1 line

stage 2 ridge

stage 3 neovascularization

stage 4 partial RD

stage 5 total RD

plus disease is retinal tortuosity and dilation, pupil rigidity, vitreous haze

plus disease with ROP Zone I = rush disease, exam q48 hrs

rx

decreases the risks of a bad outcome by 50%

treat for 5 continuous clock hours or 8 total clock hrs of Stage 3 plus disease

cryotherapy or indirect laser

Anti Fungals amphotericin B 0.15% (1.5 mg/ml) or imidazoles (miconazole 1% or ketoconazole 1-5%)

Fungizole Amphotericin B

2 ml water with 1 ampuole

take 2ml tears naturlae out of bottle and add 2ml Fungizole to 13ml tears naturalle

Daktaris Miconazole

take 7ml out of Tn and add 7ml of Daktarin ampoule

SporonaxItraconazole

dissolve 1 capsule 100mg in 5ml water

Take 5ml out of 15ml BSS and add

Natycin 5% drops

ROP screen less then 1.5kgscreen at after 6 weeks

stages 1 to 5look every 2 weeks if stage 111 see em every weekthreshold stage 3 5 clock hours continous or 8 clokcs with + diseasewhite kline 1ridgge 2stage3 fibrovascular

Marginal corneal pathology

Terriens ussually one eye and not so painful

Moorens bilateral and painful

A AND V PATTERNS

Any of the foregoing types of strabismus may exhibit a change in horizontal deviation in upward and downward gaze.

If the deviation is more exotropic or less esotropic in upward gaze, the change is referred to as a V pattern

( if the deviation is more exotropic or less esotropic in downward gaze, the change is called an A pattern. By consensus, the change from up- to downgaze must be at least 15 PDs in a V pattern and at least 10 PDs in an A pattern, although a difference of 20 PDs or more for each is more likely to be clinically significant. A or V pattern occurs in from 15 to 25% of patients with horizontal strabismus

Although there is no clear understanding of why A or V patterns develop,they are frequently associated with imbalance of the oblique muscles-A patterns with overaction of the superior oblique muscles and corresponding underaction of the inferior obliques, V patterns with overaction of the inferior oblique muscles and corresponding underaction of the superior obliques ( The oblique muscle imbalance does not appear to be due to paresis of the underacting muscles, because there is no change in vertical alignment with head tilt (Bielschowsky head tilt test) as one would expect with an oblique muscle palsy. Nevertheless, there is a torsional change in eye position consistent with the oblique muscle imbalance. This torsion is evident on funduscopy and demonstrable by

heterotopia of the blind spots on visual-field testing.67 Weakening of the overacting oblique muscles collapses the A or V pattern, making the deviation more comitant in up- and downgaze.66 There is relatively little change in the primary position alignment with bilateral inferior or superior oblique weakening procedures alone,68, 69 so additional horizontal muscle surgery must be done to correct a significant deviation in the primary position.

There are a few special conditions in which oblique muscle imbalance similar to that seen in V patterns seems to be related to an abnormality of orbital anatomy. Patients with craniofacial dysostosis of the Crouzon or the Apert type frequently have overaction of the inferior oblique muscles and V-pattern deviations (Fig. 309-8).70, 71 Likewise, children with unilateral coronal synostosis and plagiocephaly frequently have hypertropia of the eye on the affected side with overaction of the inferior oblique muscle and underaction of the ipsilateral superior oblique (Fig. 309-9). The latter has been attributed to a change in the anatomy of the superior orbit and the position of the trochlea.

Rarely, patients with A or V pattern do not have obvious oblique muscle imbalance. In these patients, the change in horizontal deviation in upward and downward gaze can be neutralized by shifting the attachment of the horizontal rectus muscles up or down. This is often done at the time these muscles are recessed or resected to correct the associated horizontal strabismus.63, 75, 76 The insertions of the horizontal recti are moved upward or downward in the direction in which one wishes to weaken their horizontal action. A similar effect can be obtained by monocular vertical displacement of the horizontal recti, moving one muscle up and its antagonist down according to the principle of displacing the muscle in the direction in which one wishes to weaken its horizontal action. Displacements of the horizontal recti are not effective in reducing A and V patterns if oblique muscle imbalance is present. For reasons that are not clear, surgical weakening of the inferior oblique muscle does not cause torsional symptoms, whereas tenotomy of the superior oblique muscle does induce a symptomatic torsional change.77 Because adults have difficulty adjusting to changes in cyclotorsion, superior oblique weakening for A patterns in adults is not advisable.

MICROTROPIA

But less than 10 seconds abnormal

norma shirmers is 15mm and slightly less with topical anaesthetic

rose bengal affinty dead degenerate cells and mucous

tear substitites

celluluse polyvinyl alcohol mucomemetics

Argon iridotomy

Abraham lens that magnifies periphery

drop pilocarpine

8 large low power circle of shots 200um 200mw and 0.1 sec

follow by high power burns 50um 1000mw .2 secons

site two thirds distance from puppliery margin

kids vallergen forte 2mg per kg

drpos .5% tropicamide

dormicon inject drops into nose beyond neonatal period

visual aquity chart equivalents

Close to 1 is better

20 , 400 6/120 decimel .05

20/200 6/60 .10

20/80 6/24 .25

20/60 6/18 .33

20/40 6/12 .5

20/30 6/9 .67

20/25 6/7.5 .8

20/20 6/6 1

20/15 6/4.5 1.33

20/10 6/3 2

Cornea approach

Age relatedchanges crocldile shegreen guttata farinnata arcus vogts limble girdle

work related Think about the salt mines in Austria

band sheroidal saltzmans lipid

sheroidal amber stromal granule

saltzmans is a stromal soft nodule often with iron that lifts epithelium

surface

cogans map dot fingerprintreis bucklers

meesmans bubble paper intraeipthelial cysts

granular abnormal collagen hyaline

macular abnormal keraten sulpahte mucopolysacharides

lattice abnormal deposits of amyoid that form a network

typew one accurs at 10years and type 2 in middlwe age and assosiated Genearalized amyoidosis

Granular

type 1 occurs 10year small discrete spots or granulea

ulcers

marginal keratitis

rosacea

terriens clear zone and thinning

mostly middle age males usually superior cornea

moorens caused by limbal vasculitis and ishchama and collagenases relased by adjacent conjunctiva

young people with good immune systems develop the progressive form while in the old it is innocuous

although it is virulent it rarely perforates

AI kerititis

dellen is a localized thinning caused by ppressure and dehydration for eg had contact lenses

Phlenctenolosis

psedogema vcv

gonioscopy

scwalbes isa nopaque line

trabeculummwhitish non functional and greyish translucent functional layer.

pigmentation is rare and ifit is it is inferior

sclems canal

slightly darkerline in inferior trabeculum

blood in canal

caridocabv fistula svc syndrome turge weber

and ocular hupotony cause blood incanal

iris processes vs anteripor synechia

anterior synechiae are broader

iris processes in kids and disappear

4 see cilairy body 40%

3 see scleral spur impossiple to close 30%

2 see tabeculae meshwork minor risk of closusure 20%

1 scwelbes 10% closure risk high

childhood glaucomas

nos and facts

adultcornea mean horizontal diameter 11.8mm aznd kids 10mm

most incrase occurs n first year

if greater than 12mm in kids less than 1year and any diameter morethan 13mm is of cconcern

posterior embryotoxin is a prominenent scwalbes line

pterygium

advancement graft

or swiing

most imp limbus conjunctiva

ac a ratio is the amount convergence measured in prism diopters per change in dioper poer change in accomodation

eg4 prism diaopter means move 4 prism dioptetrs and change power 1 diptor

high causes esotrpia or convergence when we try to focus near we overdo convergence

a nd low divergewnce

thyroid disease

infewrior rectus affected most then lateral rectus

focal laser garankuwa

setting on green as it is less speading

start 0.1watts and increase

jan usess 0.3 watts

ptosis

normal cornea is 11mm height and normally 2mm is covered

so measure exposed cornea and write ir down

eg 6 mm this means 3mm ptosis

grade 2mm mild

3mm moderate

4mm severe

remember for stabisms surgery.

MALEfor A and V pattern move muscle in direction you want to weaken it

medial rectus towards apex and lateral rectus towards empty spacein leatr ressection 6mm resection will lift eye 1mm

ddx acute blindness ie optic neurtis

central serous retinopathy big blind spot syndrome

multiple evanescent white dot syndrome anterior ischemic optic neuropathy

syphilitic optic neuritis postviral optic neuritis

Leber hereditary optic neuropathy (mitochondrial gene mutations) toxic/ nutritional optic neuropathy

malignant optic glioma

FINAL EXAM questions1Discuss cavernous sinus syndrome with regard to cinical findings and pathology

Cavernous sinus is a dural venous sinus which contains the internalcarotid a., CN III, CN IV, CN V, CN VI, and osympathetic fibers -various etiology

a. internal carotid artery aneurysm

b. carotid-cavernous fistula due to trauma and pulsating proptosis and bruit

c. cavernous sinus thrombosis

d. neoplasm eg haemangioma with axial displacement

e. inflammation (Tolosa-Hunt syndrome)

clinically

1Glaucoma due to increased veonous pressure eg cavernous sinus thrombosis or carotocavernous fistula 2 horners Third order 3 nerve palsies

detailed discussion

Carotid-Cavernous Fistula

Hi-Flow (75%)Secondary to trauma (MVA head injury)Pulsating exophthalmosInternal carotid fistula ( surrounding cavernous sinus venous plexus Low-FlowSpontaneous etiologyIndirect or dural connectionMiddle-aged womenMemingeal branch of intracavernous int. carotid a. or ext. carotid a. ( cavernous sincus or adjacent dural vein that connects with the cavernous sinus

Conjunctival chemosis, episcleral engorgement Bruit with increased with exercise, ocular ischemia Proptosis can increase for weeks CN VI palsy, retrobulbar pain Glaucoma from increased Pv, neovascular from CRVO, or angle closure

Blepharospasm

3 Discuss glaucomatocylitic crisis

=Glaucoma related to inflammatory change in trabecular meshwork

Associated with systemic disorder, allergic, or (peptic ulcer)

age30-50 years old

clinically Mild inflammation, dilated pupil, high IOP (40-60 mmHg) with corneal edema Unilateral, recurrent attacks, ON usually OK, self limited 1-3 wks Some end up with COAG Open angle: no PAS, no posterior synechiae Some flare, fine KP

Tx: Prostaglandins are possibly involved ( oral and topical NSAIDsAvoid steroids since patients may be steroid responsive?Apraclonidine in acute attacks

Discuss pathology of ophthalmic lesions occuring in the Phacomatoses

approach are phacomatoses because they are congenital and have some eye involvement+ skin & neural tissue

present with haemangiomas (sturge webers and hippal lindau) and gliomas (von recklinghausen & tuber sclerosis)in the retina & optic nerve

(G)Von REck eye~~~orbital gliomas Cafe a lait neurofibroma skin brain skull neurofibroma

(G)Tuber sclerosis Bournvilles eye~~~optic gliomas mullberry optic disc retina nodulesBrain stem glioma face sebacous adenoma butterfly astrocytosis

(HA)Sturge webbers eye~~~choriodal haemangioma and glaucoma port wine along 5th nerve capillary haem

(HA)Von Hippel laundau eye~~~retinal haemangimas and large feeders can bleed and RD brain haemagniomas assos with RCC

Discuss recurrent corneal erosions

causes FB allergy and Epithelial dystrophies

Epithelail dystrophies

3 types

1inger & dots Microcystic or cogans

2Honeycomb or Reis buckler

3bubble paper or Meesmans

1Microcystic pathology: thckened BM & Epithelial cysts with debris

age >30 y.o & 10% have corneal abrasions

50% of pts with recurrent corneal abrasions have MDF cf :asymptomatic or present with recurrent erosions, rarely presents with irregular astigmatism Rx: hypertonic saline, debridement with cotton swablubricants, soft contact lens, excimer PTK effective anterior stromal puncturetopical anesthetic, debride areause 23g needle and penetrate anterior stroma up to 1/3 depth may perform even in visual axis but space punctures further apart antibiotic ointment and pressure patchwarn pts about extreme pain afterwards2Reis bucklers progresive dystrophy with grey white deposits at Bowmans & honey comb appearenceReis-Bucker's

D, childhood, gray white opacities at Bowman's layer, becoming more confluent over the yearshistology: destruction of Bowman's layer and accumulation of "rod shaped bodies" replacing Bowman's layerreticulated pattern of scarringpainful recurrent erosions, by 50's marked corneal opacities Rx: excimer PTK, peeling off the superficial accumulated material, recur post PKP

3 Meesmans ===============AD and innoccous with epithelial cysts

AD dystrophy with thick BM, intraepithelial microcysts with peculiar PAS+ substance best seen on retroillumination asymptomatic until 10-20 y.o. when develop recurrent erosions, irritation, small decreased Vano rx necessary differential diagnosis includes cystinosis (metabolic defect resulting in accumulation of refractile cystine crystals, can be seen in peripheral cornea)

cornea data

horizontal diameter 11.75mm

vertical 10.55mm

radius curvature flatter anterior 7.8 and rounder posterior 6.5

thickness centre .058 and periphery 1.1

IOL power measurment

Anaomy

axial length 22.6mm

raduis of curvature 7.5 to 7.9 7.5mm =45 diopters

emmetropia 18 diopter.

1.25 diopter for every measured diopter change in prescribtion

errors

.1mm axial length is .25 diopter

.1 mm radius of curvature is .50 diopters

ie 1mm axial length is 2.5 D &

7.5 to 8.5 keratometry is 5D

ac length .1mm is .05 to .25 diopter

across cylinder has for example +.25 at 180^ and - .25 at 90^

spherical equvalent is sphere plus half cylinder

power of lens is 1/ focal length in metres

surgical procedures

strabismus occlusion

one week for every year of life

asdf'

Or use atropine 1% in good eye once every week.

Local anaesthesia

subtenons

take 2ml 10% lidnocaine and 2ml 0.5% marcaine and insert in a syinge

make inscion medialy 1cm below limbus

It is better to do it medially avoid inferior oblique .

take rod blunt neede and directto apexand inject

Classification

Nonproliferative Diabetic Retinopathy (NPDR)

Microaneurysms (MA)

Dot and blot intraretinal hemorrhages (DBH)

Retinal edema

Hard exudates

Venous beading

Intraretinal microvascular anomalies (IRMA)

NFL infarcts (cotton wool spots)

Arteriolar abnormalities

Focal areas of capillary nonperfusion

vision loss in NPDR due to macular ischemia (capillary closure) and macular edema (increased intraretinal vascular permeability)

Severe NPDR

Characterized by any one of the following (ETDRS, 4:2:1 rule)

Diffuse intraretinal hemorrhages and MA in 4 quadrants

Venous beading in 2 quadrants

IRMA in 1 quadrant

think of emma and her beads and bleeding!

Very severe NPDR

Any 2 of the above 3 characteristics

Proliferative diabetic retinopathy (PDR)

Extraretinal fibrovascular proliferation extends beyond the ILM

New vessels evolve in 3 stages:

1) Fine new vessels w/ minimal fibrous tissue

2) Increased size/extent of new vessels w/ increased fibrous component

3) Regression of new vessels w/ residual fibrovascular proliferation along posterior hyaloid

Tractional complications

Partial PVD

Traction on NV

Preretinal or vitreous hemorrhage

Macular heterotopia

Retinal detachment (RD)

Retinal breaks

Rhegmatogenous RD

Chronic RD>further retinal ischemia>rubeosis>NVG

Clinical trials in diabetic retinopathy

Diabetic Retinopathy Study (DRS)

Randomized, prospective clinical trial evaluating panretinal photocoagulation Rx to one eye of pts. w/ clear media and advanced NPDR or PDR in both eyes

Primary outcome measurement was severe visual loss (SVL), defined as visual acuity less than 5/200 on 2 consecutive f/u visits 4 months apart

Demonstrated 50% or greater reduction in the rates of SVL in eyes Rx'd w/PRP vs. untreated control eyes during a f/u of up to 5 yrs.

High-risk PDR defined:

Mild NVD (1/4 to 1/3 disc area) w/ vitreous hemorrhage (VH)

Moderate to severe NVD w/ or w/o VH

Moderate (1/2 disc area) of neovascularization elsewhere (NVE) w/ VH

High-risk PDR also defined by 3 of the following 4:

Vitreous or preretinal hemorrhage

NV

NV on or near optic disc

Moderate to severe extent of NV

Complications of Argon laser PRP

Decreased visual acuity by 1 or more lines (11%)

Visual field loss (5%)

Early Treatment Diabetic Retinopathy Study (ETDRS)

Randomized, prospective study evaluating photocoagulation and aspirin Rx in pts. w/ less than high-risk PDR

Primary outcome measurement outcome was moderate visual loss (MVL) comparing baseline w/ f/u visual acuities. MVL defined as doubling of visual angle (e.g. a drop from 20/40 to 20/80), a drop of 15 or more letters on ETDRS vision charts, or a drop of 3 or more lines of Snellen equivalent

Clinically significant macular edema (CSME) defined as:

1) Retinal edema at or within 500 u of the macular center

2) Hard exudates at or within 500 u of the macular center if associated w/ adjacent retinal thickening

3) Zone of retinal thickening larger than 1 disc area if located within 1 DD of the macular center

3 central findings:

1) focal laser Rx for CSME resulted in a 50% or greater reduction in MVL

2) PRP not recommended for mild or moderate NPDR, but is recommended for severe NPDR and should not be delayed when high-risk characteristics appear

3) Aspirin (650 mg per day) did not alter the rates of progression of diabetic retinopathy, had no effect on visual acuity outcomes, and did not show any ocular benefits. i.e. no benefits/no contraindications

Diabetic Retinopathy Vitrectomy Study (DRVS)

Randomized, prospective clinical trial investigating the benefit of early (1-6 mos. After onset of VH) vs. late (at 1 year) for eyes w/ severe VH and visual loss (<5/200)

Outcome measurements: % of eyes w/ 10/20 or 10/50 visual acuity on standardized charts at 2 and 4 yr. f/u

Early vitrectomy was beneficial in Type 1 diabetics, but not in Type 2 or mixed diabetics

Diabetes Control and Complications Trial (DCCT)

Randomized, prospective clinical trial to study the connection between glycemic control and retinal, renal, and neurologic complications in Type 1 diabetics

Findings:

Intensive insulin therapy can delay the onset and slow the progression of diabetic retinopathy, nephropathy, and neuropathy in Type I diabetics

pts. w/ baseline mild or moderate NPDR showed worsening of retinopathy during first year.

Intensive control group had increased risk of hypoglycemic episodes and increased risk of weight gain

Not applicable to Type 2 diabetics or prepubescent pts.

Ischaemic maculopathy trial

Dec sys bp by 10mmhg and dias by 5 mmhg reduces risk of losing 1/2 visual angle at 10 years by half!

Ie BP greatest risk in Ischaemic maculopathy

Possible indications for pars plana vitrectomy (PPV) in diabetics

Dense, nonclearing VH

Tractional RD involving macula

Combined TRD and rhegmatogenous RD

Severe progressive fibrovascular proliferation (fp)

Anterior hyaloidal fp

Ghost cell glaucoma

Dense premacular hemorrhage

Laser Therapy

Laser Rx generally recommended for CSME and high-risk PDR

Risk factors for poor visual acuity despite laser Rx

Diffuse macular edema

Ischemic maculopathy

Hard exudates in fovea

Marked cystoid edema (CME)

Potential side effects of PRP

Decreased night vision, color vision, and/or peripheral vision

Loss of 1 to 2 lines of visual acuity

Loss of accommodation

Glare

Photopsia

Aggravation of macular edema

Choroidals

Mydriasis

VH

Retinal holes

RD

Lens and iris burns

ERM

foveal burn

small spots cool quickly, large spots have high temps centrally

power density = power x time

media opacities

% increase in power needed

corneal 5-30% especially for stromal

flare/cell 10-35%

cataract 10-50%

vitreal 10-35%

Krypton

less scattering, less absorption by blood, yellow pigments (lens, foveal xanthophyll)

better uptake for choroidal tumors, blue iris

more choroidal uptake causes more pain, decrease

not good for acute hemorrhage during PRP, microaneurysms, blond fundi

really hits receptors, RPE, choroid

higher power needed for same lesions as argon

Rodenstock lens

minifies image, increases spot size

absorbs more energy than Goldman lens, so increase power

note: toward periphery, spots become smaller and relative power increases

Diabetes pearls

IRMA intraretitinal microvascular abnormalities are red in color and resenble focal areas of flat neovascularization

The 3 clues that they are not neovascularization are intraretinal and not raised secondly do not leak profusely on FA and thirdly do not cross major blood vessels.

AS they due to ischamia they appear adjacent to areas of neovascuaization

PDR is defined as extraretinal fibroproliferation beyond inrenal limiting layer

Severe BDR or NPDR is defined as IRMA in 1 quadrant

or venous beading in 2 quadrants or difuuse intarretinal hx(d & B) abd MA in all 4 quadrants

Very severes NPDR is defined as 2 or more of above~~~~~~45% chance to progress to PdR in 1 year vs 15% for above

intravitreaal antibiotics

gentamycin Lid anatomy & landmarks for sugery

Splitting the eyelid

When getting tarsal plate and conjuntival remember that the tasrsus is 1cm tall and is crescent shaped vs 5mm for inferior tarsus

the grey line is between the lashes and the meiobomian glands and is an avascular sulcus and splits into anterior lamella with skin Obicularis and posterior lammella with tarsal plate septum and conjuntiiva.

Chalazion is inflamation of meibomian glands and is on conjuntical side so make a slit thru conjunctival surface

Lymph drainage lateral superficial parotid

medial submandibular

Sensory supply to the eyelid

nerves lacrimal suraorbital and subra troclear all V1

infraorbital V1 and infratrochlear V2

When blocking look for the obvois notches and block these

Incisions to orbit

SUbBrow

lid crease

subcilial incision

superior nasal rim

external ethmoidectomy incision for lynch procedure

inferior llid sulcus oincision

The Medial wall is important in DcR

Summary

4 bones anterior to psoterior

Frontal process of Maxilary Lactrimal Ehhtmoid and Small part of body of sphenoid

We cut into Maxillary bone in DCR

lacrimal groove is anterior and only invoves frontal process of maxillary and lacrimal and is bounded by crests that kind of protect it. I was confused with remembering the crests but they are easy as anterior crest is maxillary

Surgery

endocapsular flexible pmma roings reforms capsular zonuar barrier

ARMD zinc and antioxidants in AREDS study

Vetoporfin for PDT =Visudyne predominantly for classic CNV in AMD pathological Myopia and OHS

Phaco News

Blue circles dimensions in the retina gauge range of pseudo accomodation in implanted IOLs

Surgery pearls Ferrero ring for Keratoconus

1mm wide incisions are made on the periphery on the steepest axis. to 7mm from optical zone The correct depth and tunnels made with a Suarez spreader and Ferreo double spacula

Neurology pearls

Surgical instrument pearls

Fixation rings to fixate globe when performing paracentesis

RGP lens new presbyopic lens combines shereical lens for distance

multifocal for intermediate distance and bifocal properties for near

Endothelial cell loss as seen by specular microscopy deends on nuclear density visco type solution

low weight and dispersive viscoelastic

Idiopathic polypoidal choroidal vasclpoathy

=dilated choriodal vessels inpolyp like configeration with no DRUsen( vs ARMD)

more common in blacks misdiagnosed exudative AMD

RX as for AMD and presents

Plastic surgery

frontalis suspension

incisions 2mm above lash line and just above eyebrow line to create a trapizoid

if levator fxn less than 2mm

use wright needle and place fascia between posterior aponeurosis and tasus nb dont pierce tarsal plate so becareful when doing surgery

placement of eyelid

in congenital ptosis at superior limbus

Drugs

cyclosprin 10 to 15 mg per kg in a twice daily diveded dose and manitainence of2 to 6mg per kg

same dose on kids

no need to do blood evels if not transplant pateint easliy reachws toxic levels do baseline u&E and LFTS

good because IMC with no bone marrow suppresion

inhibits IL2 is MOA

uses severe psoriasis and G vs host rejection

causes inc K cholesterol UA hirsitism gingivial hyperpasia

HT tremor + nephro and hepatooxixcity

CTR

uses zonular dyalysis prevents capsul fornix from being aspirated and fluid from

other uses PXF Marfans weil Marchasani syndrome pateints silicone iol tamponade and subseqeunt progressive zonular atrphy

Indian people weak zonules

Weil Marsesani opposte of Marfans mesodemal hyerplasia inferior lens dislocation AD

Albinism

tyrosine positive have better prognosis because melanin is made but not sequestrated by melanocytes compared to tyrosine -

ocular is just a paucity of melanocytes and hence has the best prognosis

macular hypplasia leads to nystagmus and photophobia is due to light bouncing around

two special types one in OCULAR & one in OCA tyrosine +

check haemtalogist if recurrent infections ass with ocular type type that has chadeck higashi

if blleding subtype of tyr + OCA =hamansky PUDLAK

no increased risk of Malignant melanoma only skin cancer

OC albinism that is severe Tyrosine + or less severe - 2 Xllink or AR ocular that has normal mothers of x linked

Oculacutaneous albinism

2 syndromes asso are chedick higashi with infections and hemanssky pudlaf with platelet dysfunction and bruisng

AR affetcing eyes and skin

Pathophysiology

melanin madein melanosome and ratelimiting step is Tyrosinase which copper containing

tyrosinase levels absent as used in the hairbulb tesecopper normal

MSH normal tyrosine levels normal and normal no melanocytes

CF foveal hypoplasia hypopigmetation of fundus and iris and secondary problems like myopia nystagmus dec VA photophobia dec binocularity ans stereopsis

PLUS systemic features that are obvious and we see em a lot in RSA

DDX ocular albinsm affects only eyes xlinked giant melanosomes

Albinism

2 clinical patterns; both may have photophobia, iris transillumination, hypopigmented fundiTrue albinism:

hypoplastic fovea, no foveal pit, no yellow macula lutea pigment; may also have abnormal retinogeniculostriate projections (temporal fibers may decussate) perhaps accounting for high rate of strabismusOculocutaneous albinism (eyes and skin affected)

Reduction in amount of primary melanin in melanosomes

AR

Tyrosinase positive (some degree of pigmentation)

Tyrosinase negative (total lack of pigment)Ocular albinism (only eyes affected)

Reduction in number of melanosytes

XL

2 potentially lethal forms of albinism:

Chediak-Higashi syndrome Oculocutaneous albinism w/ extreme susceptibility to infxn.Hermansky-Pudlak syndromeOculocutaneous albinism w/ platelet defectEasy bleeding/bruisingUsu. Puerto RicanHair bulb incubated with tyrosine Will produce pigmentation if has tyrosinaseKids more than 4albinoidTelecanthus and epicanthus which is extra skin fold over medial canthus repairHypertelorism Make a Y mark and then a Z at 60^ and 45^Medial palpapral ligamnet lies above nasolacrimal sac so dont dissect too deep!It is under orbicularis so remove this and fat. Angular vein from the facial crosses MPL infront of it about 8mm medial to the medial canthusMRIspectroscopy checks for abnormal neurometabolites and normal metabolites eg choline peak indicates membrane turnover and therefre a neoplasmic peaksurgeryamniomic membrane for conjunctival grafts good substrtae for cell migrationClinical testsBrightness acuity tester measres glare and cmpares to tinted glasses sunglasses and antireflectives PAM Potrntial aquity meter quantitve m acular health assessment standardized to SnellensEquivlent phaco time eg 10 sconds at 20% power is 2 seconds EPTPosterior lammelae keratoplastyA deep ,stromal pocket made thru 9mm scleral incisionRhabdomyosarcoma mostcomon paediatric malignancy

10% of all Rhabdo start in orbit vs 25% in head and neck

trunk is rare

ageis 7years and superiornasal orbit rapid growth

histolgy embronal is mostcommon ( superiornasal)followed by alveolar inferior orbit and has worst prognosis

botyriod ocurin subconjunctiva and pleomorhic which is weel difeentiated havebest prognosis

Rxchemo vincristine and actinomycin for 1 year plusorbital radaition 450 to 00 ads

90% survival rate rarely haveto exenterate

Fundus dydtrophies

RPE dystrpohies 4 common types

1 Bests yellow dots = lipofuschin in space between sensory retina and RPE which may coalsce to form egg yolk FA blocked choroidal flurescence

This may absorb completely or break up to look like sscrabbled egg

It may eventually form a hypertrohic scar or atrophic scar or vasculized scar with CNV

2 Adult foveomacular vittiform dystrophy

small yellow subfovbeal deposit = as bests but smaller and less progression and more localized

3 Stargarts & Fundus Flavimaculatis

Stargarts

oval lesion snail slime or bronze beaten 1.5 disc diameter = degenerative changes in RPE and SRS

Fundus flavimaculatis

yeelow white spots usually piscform or oval in shape and spread to periphery from macula= Lipofuschin or other waste product at RPE level

FA early on these lipfuchin causes blockage of backgrond choroidal flurescene and if RPE is atrphic there is a window defect

4 Familial Dominantdrusen

PHOTORECEPTOR dystrophies

1RP Bony spicule pigmentation beging in midperiphery arteriolar attenuation and waxy disc pallor=loss of photoreceptor esp rods and subsequint RPE damage manifesting by pigment absorbtion

2Cone dystrophy

Bulls eye lesion which is yellow ring of atrophy with normal red centre at fovea = loss of cones at fovea and also loss of RPE sparring the foveala where the cones and RPE are more resilient.

3Lebers amaurosis

Intravitreal injections

air saline silicon oil expanding gases or perflurocarbones

1air is used in hypotony posterior breaks radial retinal tears called pneumatic retinopexy

air is absorbed by 5th day adding 30% sulfur hexafluride lasts twice as long as it takes up nitrogen as air is absorbed

2 longer acting gases expanding gases egPerfluropropane c3f8 and PFethane c2f8

3silicon iol is better in PVR where the retina is immobile

4 Perflurocarbons are clear heavy liquids twice SG water low viscosity allows easy injection

infantile eso

if nystaagmus dampenson convergenge= nystagmus blockage syndrome

To pick up normal fxning LR rotate the child ordolls head manourvre

Occlusion

1 week for every year of age

never more than 6 months not beneficial after that

could do 1 to2 hours daily over a longer peroid

yunger do better

atrpoine therapy to cause blur in the good eye for mild amblyopia in hypermetropia

pleotics in kids pover 9 years where fovea is shielded and parafoveal retina temporarily blinded with bright light forcing fixation with lazy fovea

do surgery in 1 month even ifamblyopic if glasses have made no improvement

the eyelid

tarsus is 1omm in heigt and is con tinous with septum

the lvetaor apounourosis attaches to the superior tarsus and pierces the septum it also attches to skin to form the skin fold which is a great landmark

most anatomy is behind septum ie fat which is a good landmark as it separates aponourisi from septum superorly before piercing septum

this fat can be resected as it may herinite thru septum if it is cut

the aponourisi is much broader than the levator muscle aand it has horns attached to the medial and lateralpalpabral ligaments

deviations DVD IOO A&V is signifiant if more than 15 diopters

DVD is excyclodeviation and updrift when an eye js covered

RX sperior rectus recession +- Faden procedure

usually bilateral and follows eso surgery and rx indicated when cosmeticaly apparent

NYstagmus is jerk or pendular

jerk is gaze induced or gaze parlytic and describe it in terms of the fast phase

Nystagmus may be physiological motor imbalance or ocular

Ocular is pendular and horizontal and generally all kids who lose central vision before 2 develo it

occasionally abnormal head posture may be adopted todecerasew nystagmus

OCT optical coherence tomography

10um of retina can be studied

normal macular 165um thick in CMO we see a central cyst thickening to 450um and loss of foveal depression

Eximer is excited dimmer we get when inert argon acts with Fl to releases UV light 597nm that causes thermal controlled damage

News

corneal prosthesis ookp osteo odonto keratoprosthesis

Wavefront analysis is another way to do corneal topography uses ray aberations of mirrors and lenses using Hartmann screen which is a metal sheet with holes and or lenses

Intraocular lens

aphakic glassesmagnification ~30% contact lens ~10% IOL only 4%

less magnification the more posterior the lens but postop correction is complicated as a normal galelian telescope is a iol with a spectacle in the front

for each diopter of glasses at 12mm magnication is 2%

therefore leave people a bit myopic so a minus lens of 1diopter will minify by 2% so canceling the iol effect

normally > 5% anisikonia= diffrence in size is untolerable

There are 3reasonsto make a person myopic by 1 to 1.5dioter ie put a stronger lens

1 Less magnification almost to zero

2better tolerated than hyperopia

3 allow some function at near without glasses

ie use more powerful lensesrather than less

P is = A constan(118 or 113 for AC lense) t + -2.5 × axial lenth in mm + -0.9 keratometry in diopters

eg P = 118 -2.5 × 22.6 - .9 × 44 = 118 -100 = 18dioters

a is generally 118 or 114 for anterior chambers lens

ie anterior chamber lens are less powerful(nb the more anterior the less powerful the lens needs to be ,this can be seen in practice as we never prescribe 22 diopter glasses eg iol is 1.25 glasses prescribtion

when working out axis the 3 oclock position is 0 12 oclock is 90 and 9 oclock is 180 by convention

with the rule astigmatism tighter or more powerful curve is vertical

Tablets 25 and 5 mg ugs Imuran = azathioprine becomes mercaptopurine and blocks DNA synthesis used in rgan trasnplant SLE RA and Chronic active epatitis Tablets 25 qnd 50u mg use also in graves ophthalmia

Endonasla holmium DCR

diode newer laser

surgery

sling ptosis repair

done hen no levator function

use 20 goretex

start at lid 5mm above margin nad dont g thru tarsus

make 2 slings as a pentagon the central brow one above 1cm above brow in centre and make the knots here

aim is to raise to limbus at end remeber to leave knots lng as yu can adjust after suture

Telecanthus and epicanthus which is extra skin fold over medial canthus repair

Make a Y mark and then a Z at 60^ and 45^

Medial palpapral ligamnet lies above nasolacrimal sac so dont dissect too deep!

It is under orbicularis so remove this and fat. Angular vein from the facial crosses MPL infront of it about 8mm medial to the medial canthus

z plastiy is used to stretch a scar closed by releasing tissue sideways at 60' and than tranpose

This is very easy as you make space and suture

MRI

spectroscopy checks for abnormal neurometabolites and normal metabolites eg choline peak indicates membrane turnover and therefre a neoplasmic peak

Tumours

Harmatoma is tissue normally found at asite but in excess eg optic nerve glioma there is normally glial tissue but here there is excess growth

Choristoma

It is a tumour of normal tissue usually fat or C/T covered by epidermis of skin in an unusual site eg limbus

these are the pictures we have

Plastic surgery

Entropian

choice of procedure

assess for horizontal lid laxity

u may use simple suture repair which lasts only 18months

a more perment procedure is the Weiss which corrects most involutional entropian

If significant lid laxity exists (check this pulling lower lid and if it does not spring back after a blink it is severe a quick spring return is normal and a s low return is mild or check by moving lid dowmwards and if the posterior lid margin is more than 10mm from cornea

do sutures if you cant a bedside procedure where u use 4 o absorbable vicryl=catgut that is double armed

start on conjunctival side 2mm below lower tasrus and aim obliguely upwards to exit on skin just below eye lases about 2. 4 mm below............. now tie the 2 arms on skin

NB for less severe entropian you dont have to be that oblique ie be more horizontal ie from lower tarsus border to slightly higher outside skin

2 Weiss procedure

Make an stab incision 4 to 5 mm inferior to lashes ie thru tarsus and extend with scissors full thickness remember to protect withlid guard u may be 5 mm inferior laterally

Inspect the lower edge of incision from inside u hace conjunctiva lower lid retractors = white sheet of tissue , obicularis and skin

Place 3 double armed 4/0 absorbable sutures thru conjunctiva and lower lid retractors 2mm below cut edge

Pass the suture into Orbicularis anterior to Tarsus in the upper wound edge to emerge 2mm inferior to lashes

Tie the sutures to achieve slight overcorrection

Remenber to close skin with 6/0 silk and remove in 1 week

U may remove the everting sutures at 10 days if thee is marked overcorrection.

Anterior lid split as per collins

Make a curvilinear line

incise at crease deepen to tarsal plate and inferiorly

2mm abve lashes make a double loop and thru top of tarsus and tie at lashes

remove redundant skin and clse as blepharplasty

congenital optic disc anmaliesMrning glory syndrome is unilateral large evacuated disc with glial tissue and hyaloid remnents and is a colobma

blood vessels arive as a spoke around nerve which is the give away pattern

Coloboma

Drusen

tilted

Pit darker area in disc

hypoplasia midline structures double ring sign

myleinated

aicardies large colboma x linked males

Cyclocryotherapyciliary body ttemp declines in the first 2 to 30 seconds

can achieve IOP reduction in 60% of time when using temp of -80 degrees celcius for 60 seconds

probe tip of 2.5mm is used and 1 to 1.5mm from limbus

limit to one hemisphere at first sitting

Treatment of uveitis

Azathioprine Imuran

converted to mercaptopurine

dose of utoimmune use is 1 to 2 mg per kg that is the stable dose

aailable in 25 and 50mg tablets

baseline U&E FBC & LFTS every 2 weeks for 2 months

Contraindicated in pregnancy and with allopurinol(for gout) rifapicin(TB and warfarin

guidlines to watch and stop:

wcc less then 4

Neut less than 2

platelets less tha 150

AST ALT more than 3 times

o r serious ulcers or bleeding

Methotrexate

dose 7.5mg orally weekly

give with folinic acid

reti

Phaco

piezoelectric handpiece frequecy 24 to 56 000 hz and average bore is 18 gauge the purple is smaaler and the blue larger

nb the larger the no the smaller the gauge

waardenbergs syndrome

heterochromia premature greying hair loss hearind loss due t endolymphatic hypdrops (ELH)

wide inne corners of eyes broad nasal bridge virtiligo eyebrows that grow together sevee pms hirshprungs spinal disorders

Prisms

Eye moves towars the base

presbyopia is caused by this progressive growth crowding the ciliary body. If his theory is correct, the progression of presbyopia should be halted if lens growth is arrested, and it should be reversed if the diameter of the ciliary body is enlarged. With this in mind, the scleral expansion surgery was developed

Goldmann 3 mirror

cetral aprt central 30' posterior pole

equtorial mirror oblong and largest 30' to equator

peripheral mirror square and intermediate in size and square shape equtoria to ora

goni dome shaped angle

look for rd in upper temporal

Corneal Pachymetry arule central corneal thickness more than 600um indicates endothelial dysfxn and oedema ~~~~indicate postop risk

specular microscopy normal more than 2400cells per mm2 abnormal less than 1000

polymegathhism (enlarged) or pleomorphism ~~~~indicate postop risk

canthal tendon laxity

pull the medial or lateral canthus away and any movement more than 1mm indicates Medial or lateral canthal tendon laxity

Lid laxity horizontal pull the lid away from the eye quick snap indicates normal

slow return mild

incomplete return even after a blink severe laxity

ARMD,Prostrare cancer lycopene 10mg daily

Malignant Melaoma Studies states mosts lesions are not Malignant Melanoma

melanomas may be melntic or amelanotic

THey include

Neavus

Melanocytoma pimented benign lesion of the optic disc histologically form of neavus with heavily pimented cells

Bilateral diffuse uveal melanocytic prolif(BDUMP) paraneoplastic syndrome multiple

Metastaic cutaneous melanoma

RPE related

Congential hypertrpohy of RPE well circunscribed darkly pigmented often ass vascular anormalies no malignant potential

Tumours of RPE very rare and can include adenocx

ReactiveHyperpasia of RPE to trauma or injury

Combined hamatoma of retina and RPE

eg juxtapapillary have glial tisse as well

Non Pigmented

1' choriodal tumuors

Choriodal haemangioma raised reddish brown patch (VS in Sturge webber it is diffuse red )

Choriod osteoma in yug healthy females exclude Bscan highly reflective mass when reduce senstivity to exclude all tissue

2' choriodal neoplasms

most common intraocular malignacy

eye is although not a favoured site

Non neoplastic non pigmented

Presumed aquired retinal heamangioma

Age related choriodal neovascularization

easy will have some degree if bleeding and discform

Inflammatory lesins

Posterior scleritis

TB

and choriod is most frequent site Breast cx cream yellow other cx pale

Contact lenses

Base curve post curve ~8.1 to fit snug on cornea

cornea 0.5mm centrally and 0.7mm periphery

abrasion healing 4 days

peripheral flatter creating asheric

radius of curvature of apex is 7.5 to 7.9mm

Correction of astigmatism

increase power (shorter radius) ~~~put a tight suture and do wedge resection

decrease power ~~~~~~~~~~~~~~make transverse cut or relaxing incisions

remember surgery changes power reciprocally in 2 merideans

Transverse cuts about 90% deep 2 to 4mm long ~~~change power by 1 to 2 D

Relaxing incision about 3 clock hours and 90% deep ~~~~~~~~~~~~~~~1 to 10 D

Ruiz proocedure trapeziod with 2 radial and 2 to4 enclosed transverse

wedge resection 20 diopters

change due to age incison depth healing process and elasticity ( = youngs modulus ie stress / strain

ptosis a quideMG fatiuability o sustantained upgaze is simpsons test

cogans lid twitch sign overshoot of lid when rapid fixation from dowgaze

ice for 2 mintes er ptotic eye improves ptosis

CNIII palsy

what is webers or benedicts or norhnagel

aberent regeneation = adduction on upgaze or consriction of pupil on laeral gaze or elevation of lid on downgazeeg meningioma or aneurysm means longstanding and infarct unlikely

levator dehiscence

high skin crease and levator function ok

causes

incolutional=senile

trauma to SR complex in Cataract Sx

blepharochalasis=idio recurrent non piting oedema of upper lid

Marcus gunn jaw winking

open mouth or move jaw corrects ptosis

cause misdirected trigeminal nerve into levator muscle and hence synkinetic elevation when pterygiod is stimulated

Plexiform neuroma

Blepharophimposis

horners

Aproach to Clinical picturesBulls eye(is a Fluroscene defintion) is due to cetrally normal pigmented fovea surrounded by full ring of depeigmented RPE which is seen as transmission defect on FA Chloroquine binds to melanin in RPE and later causes atrophy

Causes cone dystrophy chlorquine and synthetic antimalarial Stargarts where there is a widespread RPE epithilopathy with lipofuscin Benign concentric anular ddytrophy where Rods and cones and later RPE atrophy 20 to 30% of RP

Macular Star = lipid rich exudation in outer plexiform layer that ppts in a stellate pattern as fliud is absorbed

Causes Capillary angiomas HT Lebers Idiopathic stellate retinopathy Pappilitis /pappiloedema as leakage of bv to optic nerve

Macular cherry red spot=non oedemaous retina at fovea

Group of inherited metablic diseases accumulate sphingolipids in ganglion cells causeing them to become white in contrast to fovea NB the late stage is optic and NFL atrophy

1Tay sachs Ganglisideroses type 1 AR and in infants and die by 2 years so we will not see in adults

2 Nieman pick A B C D with severe to no CNS involvment Group D presents late so you may see in adults and will end up with CNS involvment

others one type with hypotoactivty etc and sialososi with myoclonic jerks in contrast

White spots at fundus

Approach to choroiditis and retinitis

choroidits usually milder and causes blurring with only mild vitreous infamation

HALLMARK yellow grey subretinal lesions

if non inflamatory it is POHS that may dev SRNM

If inflammatory and focal it is TB sarciod toxocara or norcadia

if mutifocal it is white dot syndrome and if less 50 years old MEWDS AMPEE GHPC or mutfocal choroiditis BUT if more than 50 Birdshot and you can do something like steriods and cyclosprin

if diffuse it is SO or VKH

Retinitis

HALLMARK Retinitis whitish opacification with haemorrhage exudation and vitritis As the retina is vascular usually a vascultis

Remember to check vasculitis if it is occlusive haemorrhagic or occlusive . It may also be primary and cause a secondary retinitis

1Subacute is Toxoplasma or Candida (which starts in the choroid )

2Acute multifocal is Bechets that has a serious vascultis assosiated

3 suuden peripheral progressive is ARN

4 Diffuse progressive CMV and syphitic

5 Oclusive vasculitis has sheathing haemorrhage exudation and is differentiated into inflammatory or non inflammatory

Approach to CWS

infarct of nerve fibre layer ass with blood vessel ie superficial

ischaemic whitening

location

A macular epiretinal membrane

B vein 1 beeding~~~ DM

2 dilation ~~~Ocular ischaemic syndrome

C artrery 1spasm PET 2 nicking Chronic HT

Dgeneralized with1infection~~~AIDs septicemia or Bact Endocaditis with2 heart dx anaemia or atheroma with CVD SLE

Approach Sheathing

vessel walls usaully transparent we only see blood

occlusion of blood resluts in Ghost vessel

It may be inflamatory or occlusive with resultant exudation

fuzzy iregular cuffing of BV

1perpappilary Hyaloid remnant developmental

2After pappilitis

#Approach to Neuro

Phacomatoses

Sturge weber is also called encepholtrigeminal angiomatosises and is only one without hereditory basis Neavus flamus=angiona of 1st and 2nd branch of CNV The cause of mental ahndicap and epilepsy is P/Temporal meningela angioma that is common and on Ct it is calcified

the eyes:

Tram track on skull xray

Dt calcification of haemangioma

60% have Glacouma and Buphthalmos and 40% the glacouma occurs after 2 years due to angle anomalies or raised episcleral pressure due to episcleral haemangioma.

40% have a diffuse choriodal unilateral haemangioma

others iris CB or episcleral haemangioma

Tuberous sclerosis Bournvilles or epiloia Auto dominenthave adenoma sebacum that is angiofibrima in butterfly distribution that progresses CAL spots firous plaques skin tags ash leaf spots=hypomelnotic spots CNS slow growing astrocyte hamartoma usually parventricularly that cause epilepsy and hydrocephalus

visceral subungal and heart rhabdomyoma and kidney angiomyolipoma

The Eye

50% have retinal astrocytomas and commnly hypopigmented irsi spots and hypopigmented fundus rare.

Van hippel lindau AD haemangioma of Cerebellum oR MO is most common also cysts pof kidey and liver with phaeochromcytoma

The eye usually bilateral optic nerve and retina cap haemangiomas that are multiple but you cannot predict a brain or kidney lesion

Ataxia telangiectasi AR progressive cerebelar ataxia and MR in adolecence with skin telangiectasia of ear lips face

The eye bulbar telangiectasia at about 5 years old and ocluar motilty problems

Six nerve palsy

Think about the nerve itself that is associated with the PONS and the acoustic nerve and facial nerve as well as the tip of petrous bone

acoustic neuroma compresses this and vth nerve

base of skull raised icp nasopharyngeal cx

Retinal detachent sx with JO

there was an inferior RD

step 1 full peritomy done

and 6 silk isolated all 4 muscles remember to go under with bunt part of needle while holding tip

step 2 slide under IR silicon tire 9mm width

step 3 slide silicon band 2.5mm under rest of muscles and tru groove in tire

step 4 take silicon sleeve and ask assistant to open to width1.65

thread band thru and leave excess long

put a suture posterior to tire in direction with band and continue matress anterior . tie this

now insert yellow needle to drain fluid and robe with canailiculus probe

step 4 pull band taut gauging by iop and indentation

cut excess band

doe cryo with indirect

close

scleral buckle KI James themba

do 360 perimetry

use one loop hoding needle at tip to expose muscles use 6 0 silk and attach to misquito

thread silicon tire 9mm beginning at 6 o clock and thru all muscles (it is aloop so cut it first)

step 3 thread band the same way 7.6 mm width dont woory about getting it in the groove

step 4 use utility and toothe to get it in grrove

step 5 at 7 or 8 oclock where they will meet insert matress posterior to sleeve and then anterrior and tie.

this is your holding suture

step 6 ask assistant to open slleve and put both ends thru while pulling tight dont worry about which is ontop or below

step 7 put 3 more matress sutures at 3 9 and 6

step 8 drain fluid with a green needle at 4 points

step 9 at pars plana at 2 and 10 drain fliud u can use a 15 degree knife

insert fliud exchange syringe and then air syringe insert air or sf6 t

flatten retina

Mustard jumping man for epicanthus

remeber that u try to get skin more away from eye"X Tris" I

‹

>----- ‹

1Mark the site of of the intented canthus

2Pull the epicanthal folds medially to a point and mark this NB this is where the z plasty is going to be. Make a 60^ z and a 45^ z

3 cut with blade and retrarct flaps with suture

4 now do the telecanthus by exposing subcutaneous fat and then OO and fat to EXPOSE MCL you will see periosteum at side of nose . dont cut angular vein beware.

5cut MCL but dont damage underlying Lacrimal appartus

6 pass 4 o silk double armed from posterior to anterior thru MCL near medial canthus

7 pass thru insertion and periostium from posterior to anterior and tie

8Transpose flaps and it may be necessary to trim to neaten

close PPV sites 6 silk

close conj

Anatomy of neuroretina

inner nuclear layer is where bipolar amacrine and horizontal cells lie

inner and ouert plexiform layer is on either side of this and is the landmarks xanthophyl here and source of herdingers brushes on plane polarized light.

the capillary arcade is in the inner nerve layer

look for the superficial nerve fibre layer and the outer nuclear usually ass with a fixation cause detachment ass with rpe

PPV how to do

Do perimetry and make sure 9 to 4 o clock open

4mm from limbus at 4 o clock put a suture going foward and one 2 mm in front going backward . that is a matress

pierce with PPv spear or use 15 degree for a start aim to apex watch to see tip insert flow port and dont on until all instruments in

repeat at 2 and 10 oclock and put light and vitrector

do vitrectomy in anterior vitreous and than put ontact lens and do posterior vitreous

close after vitrecting ports

Thing to ask

Vitrector pack cassette and bag

infusion port

the pack will have 3 ports that light on and fit

remember to prime outside the eye

remeber to focus when the contact lens is on so you will need all four limbs go to high mag

Rx glaucoma latanoprost travaprost

Lumigan brimoprost se hyperaemia so use at night also increased risk of CMO and uveitis if already susceptible grows lashes and darkens eyes

corneal thickness less than 550um increased risk of glaucoma because it means thinning due to glaucoma

ocular hypertension study

Refractive sx

keraromeleusis= greek for hornlike cornea and smileusis = carving

LASIKtechnique

speculum and mark epithelium with lammela surgery epithelial marker then put pneumatic suction ring to fixate and increase IOP and create a track for keratome

before putting on microkeartome ensure IOP is >65mm with Barraquer tonometer.

put on the microkeratome that is loaded in dove tailed grooves of suction ring with foot padel

stop vacuum and remove suction ring

Laser ablation

make sure patient of perpendicular to laser and raise flap fold out of ablation field .prior to ablation wipedry fliud that may accumulate with a single motion sponge

as laser comes to hinge cover with a blunt instrument to prevent ablation of flap

Reposition flap usung a blunt instrument after irrigating

check appostion

Examining squints

Va fixation central light reflex

C unC with light

What is surg limbus?

2mm band with postpr vrslrlsu

N lebn e omn n hebsadps ht e hebsadslrlsu

RBCLCOYLma aetl ugcllmu aft \ cea et y4md aaetssscn y2m ceooy

Op

Coeotrfa

F sMmC5ui yyiieaaou hti luiae n rvnsdasnhdsi ioi hs

Oe2mt 0prm n hn5gprm ntnapiain o e asol oi oeihlu v iiyi hc lsfbolss yooydmgsedtlu n i oyadds s02t . Gprm

l e M40o . ieo n dblcdamiehon eaa ntph tabri lkhiwncmtms

What is gradenigo

Gradenigo syndrome ie involves CN five to eight

~~~ ipsilateral CN VI palsy, with decreased hearing, facial pain and facial paralysis due to abscess formation in petrous apex following otitis me

-Pseudo-Gradenigo but due to nasopharyngeal CA or cerebellopontine angle tumors

Disc is 5 degrees

Color vision fields

central 4 degrees: no blue; red & green only=fovea

4 to 20-30 degrees: trichromat=macula

30-70 degrees: dichromat (red-green blind)=equator

> 70 degrees: monochromat=peripheral

Color vision terminology

R-G-B

protan: red: erythro

deutan: green: chloro

tritan: blue: cyano

anomalous: sees 3 colors but not at same wavelengths as normals

anopia: sees 2 colors (missing pigment)

Optimal Wavelengths

1) blue cone: 450 nm

2) green cone: 550 nm

3) red cone: 580 nm

4) rods: blue-green= 500nm

Entoptic Phenomena 8 phenomenon 4 from reina and 4 from rest

wbc bv macula pigment and nfl and one from retina vitreous and lens and pupil each

Bv/wbc/nfl/xanthophyl absorbtion of polarized light

3) Purkinje figures: images of retinal blood vessels with bright or angled light

5) blue field entoptic phenomenon (flying spots): represent passing of WBC in blood vessels- can be used to determine size of FAZ

6) blue arcs of retina : NFL - shine rectangle on retina

7) Haidinger's brushes radiating from the point of fixation due with plane polarized blue light: due to variations of absortion of light by xanthophyll in Henle's layer outer plexiform - may be affected in macular edema before obvious edema

1) lens: radiating lines in star due to suture lines

2) phosphenes (flashes): vitreous pulling on retina

4) floaters: vitreous collagen, syneresis casting shadow

8) Styles-Crawford effect: parallel rays of light are more effective in stimulating cones; rays from edge of pupil which hit retina obliquely are less sensitive than those thru center of pupil

Ct scan

Look at turbinates superior

Is anterior and inferior is big baloon at back

Ehtmoid is anterior and spheniod posterior

Dont let maxillary fool you as it is next to ethmoid

It is not an ethmoid wall erosion bt the maxillary

Macula

5.5 mm in diam. (3.5 mm or 18^ degrees of visual angle) centered 4 mm temp and 0.8 mm inf. to center of optic disc

Fovea:

concave central retinal depression 1.5 mm in diam. (1 DD or 5^ degrees)

Foveola:

0.35 mm in diam. - FAZ

Umbo (clivus): central concavity of foveola floor / light reflex

Neurosensory retinal thickness

0.23 mm - papillomacular bundle near optic nerve

0.11 mm - ora serrata

0.10 mm - foveola

Retinal circulation

CRA supplies inner retina incl. inner 1/3 of INL

Choriocapillaris (CC) supplies outer 2/3 of INL to RPE

Bruch's Membrane

Layers (inner to outer)

BM of RPE

Inner collagenous zone

Elastin layer

Outer collagenous zone

BM of CC endothelium

if the TM cannot be seen easily, the patient moves his eye in the direction of the gonioscopic mirror to open the angle and improve visibility.

Latersl tarorrhaphy

05mm deep incision with knife over meibomion glands for 1 to 1.5 cm perpendicular to margin

2 grasp with forceps and cut .nb: this is posterior lid margin and avoid anterior lammela and lashes as this will lead to entropian

Use 6 o nylon thru debrided tarsus and posterior lid margin

Begin and end at lateral side threading from raw cut side

Tie qiute tight as nylon has elasticity

CN nucleiRemember IIIrd and VIth nuclei have ipsilateral innervation, whereas the IVth nerve nucleus has contralateral innervation it decussates near inf colliculisPhysiology

Vicryl causes greatest inflammatory response prism diopter is the no of cm drviation at 100cm a ray of light id deviated eg 40 prism diopters moves image 40 cm down at 100 cm deviatipn is towards the base of the prism eg place the apex in the direction of squint so light ray going on will be away from apex towards base use this info in squints

But when you look into a prism the image we see is displaced to the apex ie the common teaching if somebody sees something higher help him with a prism with the apex in the direction downward that is to correct the higher image VA is 300 to 400um spacing of photorecepter at fovea this equates 8 seconds of arc vernerone minute of arc or 60sec nb the small Es of 6/6 subtend 1minute at each armSteropsis Testing Normal bifoveal fixation is 20-50 arc seconds & 80-3000 arc seconds is normal peripheral fusio When testing you must have adequate illumination to test properly since it is a peripheral phenomenon

W4D: far: 1.25 degrees(1 degree is 60 min or 3600 sec)near (33 cm): 6 degreesIn mavula amblyopia image 4 dots seen at near but lose 1 as dots are moved back in ambyopic macular )

At 33 cm goldmann vf spot is .43 degree this is minified 20 times at retina since second focal point is 17mm behind nodal point so 330\17 is 20Reduced eye al 22.6anteriorfocal point 17mm from corneaposterior focal point 22.6 mm from cornea to retinaNodal point 5.6 mmfrom corneaAvearage Index ofeye 1.33 ie as waterAnterior and posteror focal points differ Because the media on each side of refractive media is different ie air and waterOptimal pupil1.2mmcontrast= imax - imin/ imax +iminThe refractive error of an eye is the dioptwric quivalent of the far pointFocal length is the reciprocal ofthe diopteric power of the eye.Ie 1\ 1.7cm *100 = 58 approx 45 + 20

Congenital cataracts(if bilateral most likely unknown and second hereditoryA) Bilateral1) sporadic (60%)2) heriditary without syst. Assoc. (30%)3) with syst. disease: 5%4) with TORCHS: 3%5) with other ocular abnormalities: 2%

B) Unilateral( if unilateral unlikely to be hereditory1) sporadic: 80%2) ocular abnormalities: 10% (PHPV)3) traumatic: 10% (beware child abuse)Phaco Micro surg alcon acurus30% phaco power 90mm hg pressure 250 vacuumNew iols implant thru 1.6mm this is mics microinvasion sx healon 5 2.3% na hyaluronate

Modified wavefront algorithm aims for prolate cornea or -0.46 aspheric factor to compensate for spherical abberation ie dont flatten but keep the shape done by increasing optical zone ad hence preserving corneal shapeInstruments in micro phaco:1mm diamond knife with 7 depth settings up tp 6mmSideport fixation knife 0.8mm 23 gauge capsulorrhexis Irrigating chopper with karate23 gauge bimanual irrigating aspirating handpieces

Phaco Micro surg alcon acurus30% phaco power 90mm hg pressure 250 vacuumNew iols implant thru 1.6mm this is mics microinvasion sx healon 5 2.3% na hyaluronate

Modified wavefront algorithm aims for prolate cornea or -0.46 asheric factor to compensate for spherical abberation ie dont flatten but keep the shape done by increasing optical zone ad hence preserving corneal shapeInstruments in micro phaco:1mm diamond knife with 7 depth settings up tp 6mmSideport fixation knife 0.8mm 23 gauge capsulorrhexis Irrigating chopper with karate23 gauge bimanual irrigating aspirating handpiecesRadial sponge RdFind the holeCut sponge and put radially 2 scleral sutures in a matress one ant and one post in radial direction but nb dont have go anterior to spiral of lineuxCryo around hole?nd suture dirrction is radial and sponge goes thru loops and trim anyeriorly

Nysyagmus and strabismusCongenitalTwo causes of cogenital nystagmus1 Sensory or pendular and 2 motor or jerk Exam look for anormalous head postionsLook for best VA this may be at near as convergence may improve nystagmusMotor is due to conjugate motor centre defects and is pendularNystagmus as per kai tutSurgery for motor nystagmus with good visioneg the eye null point lateral gaze and head turn to rightAccording to anderson besselbaum protocol do 8 mm 5 mm 6mm 7 mm suregery to move eye to the rightModify to get better resultsIe 20% increase for 20D and 40% increase for 45DYou may do the same for chin up or down

Remember to move eye away from to null point ie tofard abnormal head posture which is what is being treated