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 QID

CF easy Bitots spots=paralimbal spots sivery triangular patch = keratinzied area ,Dec tear
BUT loss of retinal pigment
unilateral proptosis
ALL
Metastaic neuroblastoma (never primary)
Lymphangioma with URTI becomse swelling with conjunctival signs
Rhabdoblastoma usually at 7years
orbital cellulitis
pseodotumour also kids bilateralmore

anatomy
pars plana 3 to 4mm from limbus closer on nasal side
fortified drops
cephradine
or gram positives 1st generation
Take a 1gram iv bottle and add 2ml sterile water
Add 1ml to a 15ml tears naturalle after removing 1ml of tears naturalle
now have 500 mg in a bottle
fortified gentacin

take Iv gentacin which is 40mg in 2ml ampoue normally

add to 5ml normal commercial genoptic
now have fortified formula
Cephazolin or Kefzol
Take an IV ampoule that is commercially available as 500mg
Add 2ml of sterie water
Add to 15ml tears naturalle after removing 2ml

subconj doses :
gentacin 40mg which is an ampuole of IV
kefzol or cephazolin is 125mg or quater ampoule
ESR
man age divided by 2
women age plus 10 divided by 2
vallergan preanaesthetic
over 2years give 2mg per kg
eg 8 kg give 16mg
dose 30mg per 5ml forte
ordinary 7.5mg per 5ml
or
antihistamine
promethazine phemnergen half teaspoon tds
makes 2.5 mg per day
ml has 1 mg
teaspoon is 5 ml
valloron 1drop per year old plus 4 drops qid
ROP my own understanding
use cyclopentalte 1 % and phenyeprine 1%
Typically those born below 1250g or less then 28 weeks.
examine them at 6 weeks later
stage one ~~~~ a line between vascularized and avascular retina
normally the eye can't make out the difference.
stage two a ridge
stage three extraretinal fibrovasvular tissue coming of ridge
stage 4 & 5 RD various degrees
also use zones to describe areas
zone 1 radius is two times distance from disc to fovea
zone 2 to orra nasally and to equator temporally
zone 3 remaing crescent temporally superiorly and inferiorly

#Cataracts
pscc
Have blurring at near
And glare at bright light
Lens abnormalities
Ectpoia Lentis= displacement of lens from normal position : causes Marfan weil masheshani homocystinuria
hyperlysinaemia sticklers ehler danlos Familial ectopia lentis aniridia sulphate oxidase deficiency
Phaco
incision flat against sclera 2mm and then up
________
/
_______ /
hydropdissection see posterior wave
groove 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 O2
most 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 ATP
5% 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 sucrose
Glucose + galactose lactose
Glucose + fructose maltose
glucose~~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 glucose
Aldose reductose makes sorbitol with nadph
Added knowledge
1Pam projects snellen chart to fovea around the cataract
2lens interferometer measures variance in space between fringe created by twin sources of monochromatic
helium neon laser creating a diffraction fringe pattern
anatomy
capsule 4um at posterior centre
14 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 6mm
Lammelar = 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 opacities
Galactosaemia oil drop cataract
Trauma vissius ring after blunt trauma=iris pigment imprinting on anterior capsule dt concussion
Galactokinase deficiency Mannsodosis Fabrys Lowes lammelar
congenital lens is small thin disc like (microphakia) & shows posterior lentoglobus
rubella dense pearly nucleus
myotonic dystrophy Christmas tree
Atopic dermetitis anterior stellate
based 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 damage
Etiology extracellular matrix synthsis due to lInc TGF beta 1 and mettaloproteinases that
is activated by free radicles that appear with dec Vit A
Vit 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 Iodide
8Nanophthalmos
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 adulthood
Exam 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 Dystrophy
Unclear 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 angle
Other 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
hyaloid
NB 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 ultrasound
Diff Dx: choroidal detachment, suprachoroidal hemorrhage, pupillary block glaucoma
Rx: Improvement with mydriatics Atropine qid x 5 days, phenylephrine, CAI's,=trusopt apraclonidine, and osmotics may stop 1/2

2Retina iatrogenic = ciliary body swelling

Occurs 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 Thrombosis
Thrombosis ( Acute orbital Ssx, bull neck, may see phlebolith on plain films
Orbital Varix
Posterior 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 viscera
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

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 &conjuctiva
Allergic 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, marginal
shaggy 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 choroiditis
complications 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 acyclovir
HZO Neurological syndromes
postherpetic neuralgia necrotizing angiitis with contralateral hemiplegia and death in 15% wks to months later PML-like
syndrome

#Cornea
Keratoplasty
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 dermoid
Endothelium
cell density 1400 to 2500cells/mm2
critcal no 400-700 cells,mm2
newborn 4000cells/mm2
Graft failure
Early dt poor endothelium
Late due to imc
50% within 6months
vast majority within 1 year
Epithelial linear opacity and later like adenovirus=krachmer spots
Mild iritis
Endo much more serious since endothelium does not regenerate khoudadoust line
Rx topical/systemic steroids

Corneal degenrations Peripheral

1dellen ==========easy
2moorens=========benign or progressive painful inferior thinning assos trauma or Hepitits C
3AI RA melt======= inferior thinning & perforation
4Terriens ========quiet superior thinning with pannus rarely perforates
5magrinal keratitis *
6Rosacea ketatitis*===unknoown cause mostly woman 30 to 50
Cf hyperaemia flushing telangiectasia hypertrophic sebacous glands and rhinophyma Rx tetracycline or
metronidazole
7PhlyCtenosis *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 changes
arcus
vogts white limbal girdle = white deposits
cornea farinata = flour like central depositsof lipofuscin, dots, commas in deep stroma anterior to Descemet products
of cellular degeneration
crocodile shagreen guttata = collagen on DM seen by specular reflection
hassal-henle bodies
Other usually work related or deposits
sueprficial stroma or subepithelial ike labradeor color
golden brown = sheroidal degeneration [ due to sunlight
white ring with iron Coats white ring grey white nodlues = saltmans
creamyy=lipid
calcium = band
Histology
superficial stroma protein or iron
1Shephroidal protein in the superficial stroma
2Coat's white ring = subepithelial or anterior stromal circular white ring with Fe deposits associated with metallic
corneal foreign body
3Salzmanns nodular degeneration = elevated gray white elevated subepithelial nodules with fe deposits
Bowman's or in space above ie Ca or lipid
Band Keratopathy ===deposition of calcium salts in Bowman's
4Lipid Keratopathy= yellow between Bowmans and epithelium

1Shephroidal degeneration = occurs as amber deposits of protein in the superficial stroma due to sun exposure
bilateral 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
smoothing
3Band 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 edema
whenever 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 debris
maps- 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 afterwards
2Reis bucklers
===============progresive dystrophy with grey white deposits at Bowmans & honey comb
appearence
Reis-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's
Posterior 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

Endothelial
Corneal 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 & Kerititis

Bacterial 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 ulcer
pinkish 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 reaction
gray limbal ulcer usually with clear cornea all around, early corneal neovascularization
allergic rx usually to staph at 8/10 and 2/4 o'clock
can progress to ring ulcer, usually spread toward limbus not centrally
can get superinfected
Atopy Wg C UC SLe scleroderma hookworm influenza TB samonella dengue gold poisoning Gc athritis
Infectious 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 apart
Brolene 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 regimes
Triple 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
Viral
HSV
HZO
Thygesons superficial puctate keratits=rare presumed viral fleeting keratitis=small grey intraepithelial dots with
mild subepithelial haze

Fungal Keratits
filaments parakacin
use ampho B or azole for cysts
Cf 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 Sysytem
Epiphora 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
#Optics
Retinoscopy
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
#Glaucoma
supeior 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.

#Vitreous
Asteroid 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 abnormalities

Epiretinal 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 blindness
RPE=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 disorders

1DR
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

#Uveitis
idiopathic 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

WormsToxocariasis 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
summary
The 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 Cryptococcus 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 Planitis
bilateral (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 modalities

Slit 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.
%Neurology
AION
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 & Pathology

Orbital 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 fly
Meningioma
Path
Psammona bodies
age 40 - 50 females > males
Diffuse
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

#Paedetrics
Approach 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 Lids
Entopian
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 read
Fundoscopy
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 oclock
Short 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
EOG
RPE and PR interactions
30' lateral excursions

Standing potential and light sensitive potential

Arden index refers to lisht peak to dark peak and is normaly 170%
RP~~~~~~decrease amplitude in light sensitive potential
PERG
N35
P50
N95
Macular Dz P50 Decreased
optic Neuropathy N95 Decreased

VEP
ERG
test of perpheral retina & distal to Ganglia
A PR which is supplied Choriod
Glaucoma is disease of optic nerve and ganglion cells so ERG is normal

EOG
Compares 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

#Neurology
I. 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
SO4
eye 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 system
A. 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 disorders

Blood 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 disorders
A.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
NF
type 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 +
Tumours
Conjunctival 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

%Surgery
Glaucoma Filtarion Sx Complications
Shallow AC
Grade I perpheral iris cornea touch
Grade II Entire iris in contact with cornea
Grade III Lens Cornea touch

%Diabetes Mellitis
PDR
Rx
Initially 2000-3000 burns in more then 1 session since a single session has an increased risk of bleeding
The spot size depends on the contact lens used
Goldmann uses 500um but
panfundoscopic uses 300-500 um
the durartion is .1 to .05 seconds
Power is a gentle burn
Follow up 4 - 8 weeks
May increase in increments 50 mW until a grey white burn is achieved
Flat NVE with fibrous tissue treated 500um medium intensity burns
severe NVd need 5000 or more burns

CSMO
Retinal thickening within 500um of centre of FAZ
Hard exudates within 500un of FAZ WITH associated retinal thickening
Retinal thickening 1500um in diameter within 1500um of FAZ

%Social Ophthalmology
Childhood 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, actinomycetes
gram- 25% Pseudomonas, H. flu, Proteus, Klebsiella, Serratia
fungal 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

Posttraumatic
posttraumatic 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 related
bleb 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

Endogenous
infection 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

Diagnosis
aqueous: 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 Guidelines

work 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

Retinoblastoma
1:20,000 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 N16pdvertical
2.5pd
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 imeridional >+3.00 iiametropic 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

SSPT
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
Opeartion
Turn 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 LISTING
A 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

Cataracts
1/3 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
Retinoblastoma
ost 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

ROP
85% 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 1.5kg

screen at after 6 weeks

stages 1 to 5
look every 2 weeks
if stage 111 see em every week
threshold stage 3 5 clock hours continous or 8 clokcs with + disease
white kline 1
ridgge 2
stage3 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 space
in 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 questions

1Discuss 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 afterwards
2Reis bucklers
progresive dystrophy with grey white deposits at Bowmans & honey comb appearence
Reis-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 fundi
True 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 strabismus
Oculocutaneous 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 syndrome
Oculocutaneous albinism w/ platelet defect
Easy bleeding/bruising
Usu. Puerto Rican
Hair bulb incubated with tyrosine
Will produce pigmentation if has tyrosinase
Kids more than 4
albinoid
Telecanthus and epicanthus which is extra skin fold over medial canthus repair
Hypertelorism
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
MRI
spectroscopy checks for abnormal neurometabolites and normal metabolites eg choline peak indicates
membrane turnover and therefre a neoplasmic peak
surgery
amniomic membrane for conjunctival grafts good substrtae for cell migration
Clinical tests
Brightness acuity tester measres glare and cmpares to tinted glasses sunglasses and
antireflectives
PAM Potrntial aquity meter quantitve m acular health assessment standardized to Snellens
Equivlent phaco time eg 10 sconds at 20% power is 2 seconds EPT
Posterior lammelae keratoplasty
A deep ,stromal pocket made thru 9mm scleral incision
Rhabdomyosarcoma
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 anmalies
Mrning 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

Cyclocryotherapy
ciliary 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 quide
MG 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 pictures
Bulls 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 nuclei
Remember IIIrd and VIth nuclei have ipsilateral innervation, whereas the IVth nerve
nucleus has contralateral innervation it decussates near inf colliculis
Physiology

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 verner
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
W4D:
far: 1.25 degrees(1 degree is 60 min or 3600 sec)
near (33 cm): 6 degrees
In 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 20
Reduced eye al 22.6
anteriorfocal point 17mm from cornea
posterior focal point 22.6 mm from cornea to retina
Nodal point 5.6 mmfrom cornea
Avearage Index ofeye 1.33 ie as water
Anterior and posteror focal points differ Because the media on each side of refractive media is
different ie air and waterOptimal pupil1.2mm
contrast= imax - imin/ imax +imin
The refractive error of an eye is the dioptwric quivalent of the far point
Focal 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 hereditory
A) Bilateral
1) 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 hereditory

1) sporadic: 80%
2) ocular abnormalities: 10% (PHPV)
3) traumatic: 10% (beware child abuse)
Phaco
Micro surg alcon acurus
30% phaco power 90mm hg pressure
250 vacuum
New 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
shape
Instruments in micro phaco:
1mm diamond knife with 7 depth settings up tp 6mm
Sideport fixation knife 0.8mm
23 gauge capsulorrhexis
Irrigating chopper with karate
23 gauge bimanual irrigating aspirating handpieces

Phaco
Micro surg alcon acurus
30% phaco power 90mm hg pressure
250 vacuum
New 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
shape
Instruments in micro phaco:
1mm diamond knife with 7 depth settings up tp 6mm
Sideport fixation knife 0.8mm
23 gauge capsulorrhexis
Irrigating chopper with karate
23 gauge bimanual irrigating aspirating handpieces
Radial sponge Rd
Find the hole
Cut 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 lineux
Cryo around hole
?nd suture dirrction is radial and sponge goes thru loops and trim anyeriorly

Nysyagmus and strabismus

Congenital
Two causes of cogenital nystagmus
1 Sensory or pendular and 2 motor or jerk
Exam look for anormalous head postions
Look for best VA this may be at near as convergence may improve nystagmus
Motor is due to conjugate motor centre defects and is pendularNystagmus as per kai tut
Surgery for motor nystagmus with good visioneg the eye null point lateral gaze and head turn to right
According to anderson besselbaum protocol do 8 mm 5 mm 6mm 7 mm suregery to move eye to the right
Modify to get better results
Ie 20% increase for 20D and 40% increase for 45D
You 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