Ophthalmoology Study Notes comprehensive
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Transcript of Ophthalmoology Study Notes comprehensive
MRC III Clinical
Cyklokapron 500mg tablets
Dose
tranexamic acid
- inhibits fibrinolysis
- less gastric upset, lower dose given, less frequent.
500mg tds cyklocapron
Pain relief
Largactil 50mg or 2 ampoules retrobulbar for pain.
Chlopramazine 25mg amp comes as chlorpramazine hcl
Retrobulbar
At 1/2way between limbus and canthus pass posteriorly along floor 10% angled from iris
when the hub is at iris than the needle 4 to 5mm behind globe
Vitamin A deficiency
Fxn
rhodopsin
Conj mucosa integrity
Rpe /srs metabolism
rx Vit A palmitate in oil 6000ug or 200000iu for 2 days (half in kids less than 1 and pregnant mothers) and repeat in 1 month
topical Vit A ointment QIDCF easy Bitots spots=paralimbal spots sivery triangular patch = keratinzied area ,Dec tear BUT loss of retinal pigment unilateral proptosisALL Metastaic neuroblastoma (never primary)Lymphangioma with URTI becomse swelling with conjunctival signs Rhabdoblastoma usually at 7yearsorbital cellulitispseodotumour also kids bilateralmore
anatomypars plana 3 to 4mm from limbus closer on nasal sidefortified dropscephradine or gram positives 1st generationTake a 1gram iv bottle and add 2ml sterile waterAdd 1ml to a 15ml tears naturalle after removing 1ml of tears naturallenow have 500 mg in a bottlefortified gentacin
take Iv gentacin which is 40mg in 2ml ampoue normallyadd to 5ml normal commercial genopticnow have fortified formula
Cephazolin or KefzolTake an IV ampoule that is commercially available as 500mg Add 2ml of sterie waterAdd to 15ml tears naturalle after removing 2ml
subconj doses :gentacin 40mg which is an ampuole of IVkefzol or cephazolin is 125mg or quater ampouleESRman age divided by 2women age plus 10 divided by 2 vallergan preanaesthetic over 2years give 2mg per kgeg 8 kg give 16mgdose 30mg per 5ml forteordinary 7.5mg per 5ml or antihistaminepromethazine phemnergen half teaspoon tdsmakes 2.5 mg per dayml has 1 mgteaspoon is 5 mlvalloron 1drop per year old plus 4 drops qidROP my own understandinguse cyclopentalte 1 % and phenyeprine 1%Typically those born below 1250g or less then 28 weeks.examine them at 6 weeks laterstage one ~~~~ a line between vascularized and avascular retinanormally the eye can't make out the difference.stage two a ridgestage three extraretinal fibrovasvular tissue coming of ridgestage 4 & 5 RD various degreesalso use zones to describe areaszone 1 radius is two times distance from disc to foveazone 2 to orra nasally and to equator temporallyzone 3 remaing crescent temporally superiorly and inferiorly
#CataractspsccHave blurring at nearAnd glare at bright lightLens abnormalitiesEctpoia Lentis= displacement of lens from normal position : causes Marfan weil masheshani homocystinuria hyperlysinaemia sticklers ehler danlos Familial ectopia lentis aniridia sulphate oxidase deficiencyPhacoincision flat against sclera 2mm and then up ________ /_______ /hydropdissection see posterior wavegroove foward phaco power 60% linear and stepped upacceleration
How does Sorbitol cause Cataracts?lens needs glucose and burns it anaerobically and is not very dependent on O2most glucose goe to Glycolysis via hexokinase to G6P providing ATP(only 3% goes to TCA but remember oxidative glycolysis is much more effecient in making ATP5% goes to PPP to make reducing power NADPH which is in turn is used also by aldose reductase to make fructose via sorbitol .This happens only if there is accumulation of glucose.eg in diabetes or galactase def.
Glucose + glucose sucroseGlucose + galactose lactoseGlucose + fructose maltoseglucose~~aldosereductase~~~sorbitol~~aldosereductase~~ fructose
extra glucose becomes sobitol which is and intermediate to fructose via aldose reductase.Sorbitol[as well as fructose]is poorly permeable and will stay in the lens and imbibe water Bottom line Nb;if more glucoseAldose reductose makes sorbitol with nadphAdded knowledge1Pam projects snellen chart to fovea around the cataract2lens interferometer measures variance in space between fringe created by twin sources of monochromatic helium neon laser creating a diffraction fringe patternanatomycapsule 4um at posterior centre14 anterior 17um at equator where zonules are and 22um where capsoluhexis is made( both anterior and posterior) make ccc 1mm less than optic which is 5 or 6mmLammelar = spoke like = zonal opacities of the fetal or nuclear lens that is invariably congenital & often have spokes around em) Diabetic cataracts white punctate or snowflake opacitiesGalactosaemia oil drop cataractTrauma vissius ring after blunt trauma=iris pigment imprinting on anterior capsule dt concussionGalactokinase deficiency Mannsodosis Fabrys Lowes lammelarcongenital lens is small thin disc like (microphakia) & shows posterior lentoglobusrubella dense pearly nucleusmyotonic dystrophy Christmas treeAtopic dermetitis anterior stellatebased on shape:PXE posterior synechie gold chlopramazine Vios ring ~~Posterior subcapsular Myotonic dystrophy DXT~~anterior subcapsular
AACG (glaucfleken) ~~~glue co fleck ken
wilsons miotics pilocaroine will cause catarctamiodarone ~~~cortical
coronary iis a special type ~~~congenital
lammelar always congenital
sutural
Types of Cataracts
Immature only scattered opacities
vs
mature where the cortex is opaque
Intumescent is one that swells as it imbibes water
>>>>secondary pupil block glaucoma
vs
hypermature that is leaking water and hence dangerous! but it itselfis old wrinkled and small
>>>>secondary glaucoma
Morgagnian where the cortex has melted [ nb vacuolation seen histology]and the nucleus has fallen to the back gagged and dead!
#Glaucoma
Cortisol diurnal curve
Peak 6 to 8am
Causes glaucoma same e
Y as steriods
Ie
Dec phagocytosis
Secondary open angle glaucoma
1 Phacolytic or Phacogenic due to leaking hypermature cataract proteins and macrophages in the angle
2RBC glaucoma due to traumatic hyphema
3 angle recession glaucoma due to pigment and destruction of trabecular meshwork after trauma
4Ghost cell glaucoma 2 weeks after vitreous haemorrhage or hyphema
5 Iridocorneal endotheial syndrome
abnormal surface migrates over angle and includes essesntial iris atrophy iris naevus and Chandlers
6 PXE
age > 50 years material all over the body Material is a microfibril with elastin, mucopolysaccharide, and extracellular matrix Exam findings:Usually asymmetric, can look unilateral 50% in 5years bilateral for yrs, severe cases are usually unilateral lens has central disc, intermediate clear zone (brushed off from contact with moving iris), and peripheral granular zone (with radial striations)NB Up to 50% get glaucoma Glaucoma affects the MORE pigmented eye & poorer prognosis, Weak zonular attachments with 10x rate of vitreous loss with cataract extraction.PXE more accelerated galucomatous damageEtiology extracellular matrix synthsis due to lInc TGF beta 1 and mettaloproteinases that is activated by free radicles that appear with dec Vit AVit A
40 to 60 x in Aqueous humour and exreted by ciliary epithelium
Vit c ascrbic acid becomes dehydroascorbarbic acid when oxidized
gluthathione GSSG to GSH reverses this to reform active ascorbc acid (this requires NADPH)
PXF reduced levels AA also absorbs UV
RDA 75mg daily recommended fr AO activty up to3 g
corneal endothelium flakes
iris absent pupillary ruff with white flakes Moth eaten transisllumination defects iris near pupil ,
trabecula meshwork ampaolesi's line (segmental)=pigment along Schwalbe's Line this is causeof glaucoma in more pigmented eye
7 Pigmentary glaucoma
This may occur in 10 % of PDS which consist of mid perphery posterior bow and pigment loss causing Krukenburgs line on endothelium + pupil atrpophy & pigment in furrows Tm pigment & lens both anterior and posterior pigment
Demographics: Myo (especially > -3.00 D), White>>Black (difference in ant. chamber depth) M:F 2:1 Wide diurnal swings in IOP, also assoc. with exercise and accomodation
Exam findings: Krukenberg's spindle on corneal endothelium is nonspecific, seen often in normal women
Iris transillumination spoke wheel deficits in mid-peripheral 1/3 of iris Mechanical contact between zonular packets and iris ( Iris pigment release Pigment stippling on iris over defects, Iridodonesis heterochromia (eye with darker iris is affected) Pigmented TM with concave peripheral iris, Sampaolesi's line Pigment line on posterior lens at vitreal touch Posterior bowing of iris with reverse pupillary block It is called reverse block because the pupil moves back rather than a swollen lens
Rx Pilocarpine good choice to alter anatomy (reverse pupillary block) Try Ocuserts for younger patients (for less miosis) ?Role for thymoxamine/Moxisylate ((-blocker which gives miosis without cyclotropia or decreasing ciliary outflow Consider LPI to decrease concavity and pigment dispersion ALT and Filter both work well myo males middle aged
8 inflammatory glaucoma = glaucomatocylitic crisis =Glaucoma related to inflammatory change in trabecular meshwork Associated with systemic disorder, allergic, or GI (peptic ulcer) diseases Mild inflammation, dilated pupil, high IOP (40-60 mmHg) with corneal edema30-50 years old Unilateral, recurrent attacks, ON usually OK, self limited 1-3 wks Some end up with COAG Open angle: no PAS, no posterior synechiae Some flare, fine KPTx: Prostaglandins are possibly involved ( oral and topical NSAIDsAvoid steroids since patients may be steroid responsive?Apraclonidine in acute attacks
9 Fuch's Heterochromia as a cause of glaucoma (Fuch's Heterochromic Cyclitis) This does not start with a P so lighter one is affected
Sometimes confused with Glaucomacylitic crisis 20-30 yrs old, M=F Most commonly misdiagnosed in Blacks b/c heterochromia less obvious 50% get progressive glaucoma
Exam findings: Unilateral low grade iritis (minimal flare/cell) with fine stellate KP inf. cornea
Severe iris atrophy - lighter iris is pathological( vs PIGMENT & PXE where the darker eye is pathological
10% can be bilateral OPEN angle: NO posterior synechiae, but fine angle vessels
10Trauma
Siderosis (intraocular retention of iron FB or intraocular heme) Chalcosis (retained copper FB - copper gets oxidized) Chemical burns (Alkali and Acid: inital ( IOP, prostaglandin release ( shrinkage of cornea and sclera)
12Aphakic or Pseudophakic Glaucoma
Term discouraged because not due to just one etiology often post op with increased IOP that persists Due to: Distorted anterior chamber angle Viscoelastic (sodium hyaluronate) obstructs TM UGH syndrome (Uveitis/Glaucoma/Hyphema) from inflammatory
reaction to heme Pigment dispersion from PC IOL rubbing on iris Vitreous in AC leading to pupillary block
13Hypothyroidism
May be due to changes in scleral rigidity by inceasing and nence decreasing outflow
Secondary Pupil blocks glaucoma
1Uveal melanoma
2 FB egsilicone oil
3Microspherophakia (Weill-Marchesani syndrome/Lens Induced-loose zonules)
4Phakomorphic (Lens Forward syndrome) Intumescent lens ,dislocated or incacerated
Shallow anterior chamber, ?zonule laxity or post. pressure
5Epithelial Ingrowth/Fibrous Proliferation= fibrous tissue in AC
Epithelial membrane/vascularized fibrous tissue grows into AC through penetrating wound Retrocorneal membrane 2( inflamm or trauma to cornea but Descemet's intact (glaucoma not commonly associated) If unsure, use Argon laser(.2s, 200-500 um, 200-500 mW). If membrane present, blanches tissue white. If iris present, shrinks and hyperpigmentation
6Iridoschisis posterior iris separates and blocks AC
Contrast against pigmentary glaucoma
Older (70's), bilateral, M=F, reactive pupil ?Senile change, post trauma Usually lower half anterior stroma separates from posterior stroma Strands obscure anterior chamber Some have angle closure 'Some have obstruction of TM ( open angle glaucoma (like pigmentary) Glaucoma in 50% as PAS form,
7 Iris Cysts Block AC
Idiopathic, IK (Interstitial Keratitis), Phospholine Iodide8Nanophthalmos
Shallow anterior chamber, narrow angle ( angle closure Uveal effusion ( forward shift of lens-iris diaphragm ( pupillary block actuallly a bit of both pupil block and narrow angle! there last on list
Secondary glaucoma with clinically evident narrow angles1Plateau iris 2PAS 3Neovascular 4ICE{No Pupillary Block} 5 fuchs 6 ppmd
1Plateau iris===Young patient with high iris insertion,
increased IOP with dilation Exam findings: Gonioscopy shows sudden drop off of peripheral iris Deep central anterior chamber, can have pupillary block Tx: Compression gonioscopy can open angle LPI to r/o primary closure, chronic miotics Consider peripheral iridoplasty
2PAS ===Longstanding prior block, flat anterior chamber, uveitis
3Neovascular Demographics: CRVO 1/3, DM 1/3, carotid disease 1/10, RD, melanoma, uveitis Glaucoma develops in 10-20% of rubiosis
3ICEs (Irido-Corneal Endothelial Syndrome)=== Primary CORNEAL endothelial abnormality
Proliferation from abnormal corneal endothelium Contraction of membrane over angle and iris( PAS, correctopia, ectropion uvea Unilateral F middle aged Presents with iris changes, decreased VA from glaucoma or corneal edema, or pain from corneal edema KEY: endothelium has irregular, fine hammered/beaten metal appearance often bilaterally, pleomorphic cells ("ICE cells") Three clinical variations:
Chandelier has frosted glass
Cogan/reese has fingerprints/nodules on iris
1Progressive Iris Atrophy :iris atrophy :
2Chandler's Syndrome Corneal edema :
3Cogan-Reese Syndrome Nodular, pigmented lesions of iris
Ddx Endothelial changes: PPMD (see below) Fuch's endothelial dystrophy Iris holes: Axenfield-Rieger (congenital) Aniridia Iris nodules:Melanoma or Nevi Nodular Inflamm (Sarcoid)5PPMD (Posterior PolyMorphous Dystrophy===Post. cornea with single or groups of blisters/vesicles,Confused with ICE syndrome Demographics: Less than 15% develop glaucoma, nonprogressive Bilateral, familial AD, congenital and asymmetric until adulthoodExam findings:Post. cornea with single or groups of blisters/vesicles, band like lesions with scalloped edges, or islands with endothelial changes at level of Descemet's membrane Few have PAS, corectopia, iris atrophy
5Fuch's Endothelial DystrophyUnclear theory on how guttata are related to IOP Guttata may decrease aqueous outflow? Associated with increased incidence of axial hypermetropia and shallow anterior angle ( increased risk of closed angleOther Glaucomas cilary body 1Malignant Glaucoma (Ciliary Block Glaucoma/Aqueous Misdirection)===Classic definition: acute glaucoma with very shallow central and peripheral anterior chamber in post op patients operated on for angle closure due to Aqueous flow obstruction due to apposition of ciliary processes against equator of lens or anterior hyaloidNB block is very posterior
Posterior pooling of aqueous behind a PVD ( forward displacement of lens-iris or iris-vitreous diaphragm Never has suprachoroidal fluid by ultrasoundDiff Dx: choroidal detachment, suprachoroidal hemorrhage, pupillary block glaucomaRx: Improvement with mydriatics Atropine qid x 5 days, phenylephrine, CAI's,=trusopt apraclonidine, and osmotics may stop 1/2
2Retina iatrogenic = ciliary body swellingOccurs with ciliary body swelling and rotation (ie. after PRP, cryo)
Increased Pv (normal episcleral venous pressure = 8-10 mmHg)Three types:Obstructed venous flow pressure Idiopathic episcleral venous pressure elevation Carotid-Cavernous Sinus Fistula Superior Vena Cava Syndrome Orbital Varix Cavernous Sinus ThrombosisThrombosis ( Acute orbital Ssx, bull neck, may see phlebolith on plain filmsOrbital VarixPosterior dilation of intracranial vessels leads to dilated orbital veins (episcleral and conjunctival) Can be congenital single tortuous vein Kippel-Trenaunay-Weber syndrome Intermittent exophthalmos with head upside down, sneezing, or Valsalva Blurred VA, headache, nausea, and pain( reversal when jugular pressure lowered Blindness from repeated episodes Can have systemic venous abnormalities in buccal mucosa, extremities, and visceraCarotid-Cavernous FistulaHi-Flow (75%)Secondary to trauma (MVA head injury)Pulsating exophthalmosInternal carotid fistula ( surrounding cavernous sinus venous plexus Low-FlowSpontaneous etiologyIndirect or dural connectionMiddle-aged womenMemingeal branch of intracavernous int. carotid a. or ext. carotid a. ( cavernous sincus or adjacent dural vein that connects with the cavernous sinusConjunctival chemosis, episcleral engorgement Bruit with increased with exercise, ocular ischemia Proptosis can increase for weeks CN VI palsy, retrobulbar pain Glaucoma from increased Pv, neovascular from CRVO, or angle
closure
Thyroid Ophthalmopathy Increased proptosis ( orbital congestion 2nry to obstructed venous plexus Increased IOP especially in upgaze 2( fibrosis of inferior rectus
Compressive optic neuropathy commoner in older male,with d.mellitis,more severe orbitopathy.
Retrobulbar Tumors Sturge-Weber Increased IOP 2( to increased episcleral venous pressure 2( to episcleral hemangiomas with AV fistulas
#Sclera &conjuctivaAllergic Conjunctivitis
Seasonal Allergic Conjunctivitis signs/symptoms rapid, lid swelling, chemosis (pale palpebral conjunctiva), itching, mucus, dellen pressure, rhinitis/asthma, episodic symptoms are much greater than signs can sometimes be perennial with multiple overlying allergies dx clinical, Type 1 hypersensitivity only, elevated tear IgE, eosinophils in scraping in chronic cases rx steroids rarely indicated antihistamines systemic and topical are useful topical NSAIDS mast cell stabilizers if chronic condition Vernal (VKC)
common in african males 3 to 30years old often assosiated with allergies chronic lasts for years and is Hs type 4 reaction with allergic eyes and giant papillae chronic stigma are aconcern eg corneal scarring <-- conjunctival neovascularization Tratas spots = clumps of EIO flour dusting of palpable atrophy <-- ptosis histology; fibrinolectin and lamminen deposits on immunhisto studies
Vernal (VKC) bilateral seasonal young (3-25 year old) in warmer climates, M>F FHx of ato allergies usually self limited, average 4-10 years two types: vernal and palpebral signs/symptoms ITCH (worsens in evening, dust, lights, wind, rubbing), clear tears ropy discharge but lids don't get crusted or stick together unless bacterial superinfection giant papilla may cause ptosis limbal involvement more in blacks and can be up to 360 degrees Horner Trantas dots (clumps of degenerated eosinophils), clear elevated cysts SPK, flour dusting of epithelium, intraepithelial cysts, shield ulcers usually upper cornea pseudoarcus, myo astigmatism, associated with keratoconus, rare corneal neovascularization>2 eosinophils/hpf pathognomonic, increased tear histamine eosinophilic products are major cause of corneal epithelial destruction rx lodoxamide 0.1% QID is first line drug topical steroids- pulse rx with exacerbations topical cyclosporine 2% qid can be used as alternative to steroids Atopic (AKC) keratoconjunctivits in patients with atopic dermatitis M>F, teens to 40's, burns out by 40-50 year old, small papilla, milky edema, corneal neovascularization hx of ato eczema (3% of population), similar to vernal findings but no seasonal changes signs/symptoms atopy shiners (bags under eyes from rubbing) symblepharon, foreshortening of inferior fornix, usually lower palpebral conjunctiva affected can mimic OCP in severe cases bilateral cataracts (anterior subcapsular, or posterior polar), 10% of all cases ato dermatitis associated with keratoconus, iritis, cataract RD from pars plana tears or ora dialysis (can have photoreceptor outer segments in anterior chamber which look like cells) pathology increased T helper, macrophages, increased class II HLA similar to OCP and rosacea. more complex than simple mast cell allergic rx. No BM deposition as in OCP rx environmental control is essential systemic antihistamines, nasal cromolyn, topical mast cell stabilizers pulse steroids and cream doxycycline for blepharitis oral and topical cyclosporin (severe cases may need immunosuppression)
Pynguela ==========elastic dgeneration of conjuctiva subepithelial collagen
pterygium ==========elastic generation of conjuctiva subepithelial collagen & corneal collagen
phlyntenosis ========Phlyctenular ulcer = nodular pinkish white limbal elevation with gray crater, can be on conjunctiva caused by type iv hs to staph TB or candida antigen
EKC adenovirus peak 5 to 7 days stage ranges from superficial epithelial keratitis to subepithelial infiltrates (SEI)= immune response to viral antigens on anterior stroma i 80% of casesRx: topical steroids if membranes and SEI's
Pcf viruses 3 4 7 has fever etc ie systemic
Ekc 8 19 localized to eye
HSV
HSV Primary conjunctivitis in children, bilateral, fever, preauricular adenopathy, URI, 3-9 days incubation varied present (mild follicular conjunctivitis to pseudomemb) lid vesicles, ulcerative bleph, 1/2 get small
fleeting corneal dendrites SPK, conjunctival dendrites
HSV Recurrent may be triggered by sunlight, fever, stress, menses, steroids 1 yr 25%, 2 yrs 50% chance of recur one fifth develop stromal keratitis most common infectious cause of corneal blindness in this country blindness from HSV is from recurrent stromal keratitis and/or iritis with the subsequent inflammation and scarring
Clinical tures
1Lids (pseudozoster)
2Rare follicular conjunctivitis
3Epithelial keratitis SPK, dendritic, geographic, marginalshaggy borders, ghost scars of prior dendrites, decreased corneal sensation often with mild stromal edema metaherpetic lesion from poorly healing epithelium, gray thickened heaped up edges usually resolves spontaneously in 3 weeks but treat to decrease the amount of damage RX debride with dry cotton tip applicator limbal lesions antivirals, slower healing diff dx of dendrite contact lens filaments tyrosineamia ca thygsons hzo
4 stromal keratitis: disciform=disc shaped zone of corneal edema presumed immune mediated disease
central corneal edema with fine KPs under edema, mild iridocyclitis, increased IOP, Wessley ring (of infiltrates)
diff dx includes HZO, local bullous keratopathy, EBV virus, connective tissue disease, interstitial keratitis
consider obtaining antiherpes serum antibodies in patients with no hx of herpetic eye disease or when the
diagnosis is in question Rx cycloplegics topical steroids with topical antiviral cover tapered slowly (Pred Forte 8X/day initially tapered down to 2X/day by 2 months) usually self limited in 2-6 months with variable scar
5Stromal keratitis: peripheral atyal, r/o marginal ulcer 6Stromal keratitis: necrotizing presumed etiology from live virus but can be negative on biopsy dense deep stromal infiltrate, multiple cheesy white, necrotic infiltrates no pain, mild iridocyclitis, increased IOP, corneal neovascularization, Rx indolent self limited 2-12 months antivirals with steroids and slow taper (even yrs)
7 Endotheliitis progressive corneal edema with line of KP (looks like PKP rejection, but PKP rejection line is limited to the corneal graft) rx acyclovir 8Uveitis iritis with diffuse iris atrophy multifocal choroiditiscomplications of HSV infection neurotrophic ulcer irregular astigmatism lipid keratopathy corneal perforation
HZO
HZO primary chickenpox rare disciform keratitis SPK limbal pustules lid lesions usually benign, may treat if
involvement
HZO Secondary 2% of adults > 60 year old, pathology: nerve damage, ischemic vasculitis, inflammatory granulomatous rx lid vesicles clear in 3 wks and can result in ptosisconjunctival hyperemia, vesicles following a dermatome, episcleritis
Hutchinson's sign- vesicles on the tip of the nose, indicates involvement of the nasociliary branch of V1
SPK, microdendrites, corneal neovascularization, uveitis, glaucoma, sectoral iris atrophy stromal nummular keratitis, scleritis (nod>diff, limbal can spread to cornea) 1% with optic neuritis, Horner's, EOM palsy (25%) decreased corneal sensitivity leads to neurotrophic ulcers
Rx cycloplegic, Acyclovir 800mg 5x/day x 7 days try to start within 72 hrs
topical steroids for iritis Zovirax 5 times warm compress consider prednisone 60-100 mg po x 3 days if microdissemination, pt may be immunocompromised consider IV steroids, use IV acyclovirHZO Neurological syndromes
postherpetic neuralgia necrotizing angiitis with contralateral hemiplegia and death in 15% wks to months later PML-like syndrome
#CorneaKeratoplasty
Lammelar means partial thickness
most common indication Bullous keratopathy
Tectonic means restotarion of normal antomy in eg dermatocoele or stromal thinning
or therapautic or cosmetic
Surgical procedure
donor o5mm larger to reduce glaucoma flattening and make wound watwer tight
ideal size,7.5mm and the donor should be trephined endothelial up
Lammelar graft
ind'opacities ant 1,3 of stroma
Marginal or localized thinning or descemetocoele or terriens or dellen or limbal dermoidEndotheliumcell density 1400 to 2500cells/mm2critcal no 400-700 cells,mm2
newborn 4000cells/mm2Graft failureEarly dt poor endotheliumLate due to imc50% within 6months vast majority within 1 yearEpithelial linear opacity and later like adenovirus=krachmer spotsMild iritisEndo much more serious since endothelium does not regenerate khoudadoust lineRx topical/systemic steroids
Corneal degenrations Peripheral1dellen ==========easy2moorens=========benign or progressive painful inferior thinning assos trauma or Hepitits C3AI RA melt======= inferior thinning & perforation4Terriens ========quiet superior thinning with pannus rarely perforates5magrinal keratitis *6Rosacea ketatitis*===unknoown cause mostly woman 30 to 50Cf hyperaemia flushing telangiectasia hypertrophic sebacous glands and rhinophyma Rx tetracycline or metronidazole7PhlyCtenosis *mostly in kids and Hs to ag
probaly * = infective
Mooren's
idiopathic unilat painful inferiorly trauma hx, rare perf,more commonly scarring circumferential spread early signs: usually not elevated, small lesions, can be in conjunctiva central edge undermined in stroma, blunt edge peripherally
two types:benign, unilateral, in older, responds to surgery
relentlessly progressive and bilateral in 25%, young NIgerian blacks also ass parasitic infection and abs
25 % of cells in area express MHC hla type IIantigen ie able to present ag to T helper cells there is aslo less tsuppresor cells
Rx: steroid (topical, systemic) lamellar keratoplasty with conjunctival resection, immunosuppressives eg cyclophosphamide and methotraxatecollagenase inhibitors eg acetylkcystine (MUCOmyst 10%) l cystene cyclosprin A topical
check for Hepatitis C Ag and will respond to interferon
steriods may worsen disease sucessfully used cyclosporin 2% topical in olive oil and
oral 10 to 15mg per kg eg 20kg child 100mg bd to load
then 2 to 6 mg maintenence also methotrexate
conjunctival resection to remove inflamatory process
that is TYPE 2 humoral response wiith c fixation and etc it is limbal where 5 times more complement
exists
VII. Management
Most experts would agree on a step-wise approach to the management of Mooren's ulcer, which is outlined as follows:
1. topical Steroids
Initial therapy should include intensive topical program: prednisolone acetate or prednisolone phosphate 1%, hourly, in association with cycloplegics and prophylactic antibiotics.[1, 6] If epithelial healing does not occur within 2 to 3 days, the frequency of topical steroid can be increased to every half hour. Once healing occurs, topical steroids can be tapered slowly over several months. Such management, especially in the unilateral, benign form, has yielded good results.
Oral pulse therapy (Prednisone 60 to 100 mg daily) can be considered when topical therapy is ineffective after 7 to 10 days or in cases where topical steroids may be contraindicated because of precariously deep ulcer or infiltrate.[9] topical tetracycline or medroxyprogesterone can be used for anticollagenolytic properties. Therapeutic soft
contact lens or patching of the eye may be beneficial at this stage. [1]
2. Conjunctival Resection
If the ulcer progresses despite the steroid regimen, conjunctival resection should be performed.[1, 6] Under topical and subconjunctival anesthesia, the conjunctiva is excised to bare sclera, extending at least two clock hours to either side of the peripheral ulcer, and about 4 mm posterior to the corneoscleral limbus and parallel to the ulcer.[8] The overhanging lip of ulcerating cornea may also be removed. Postoperatively, a firm pressure dressing should be used. Multiple resections may be needed. It is thought that the conjunctiva adjacent to the ulcer contain inflammatory cells that may produce antibodies against the cornea and cytokines, which amplify the inflammation and recruit additional inflammatory cells.[23]
Cryotherapy of limbal conjunctiva has been advocated by some surgeons and may have a similar effect.[] Conjunctival resection and thermocoagulation have also been found to give some relief at the site of the ulcers, but recurrence can occur at same or other sites (up to 50%).[]
Keratoepithelioplasty has also been performed in patients with Mooren's ulcer.[] Donor corneal lenticles are sutured onto scleral bed after conjunctival excision. The lenticles form a biological barrier between host cornea and the reepithelializing conjunctiva, and the immune components it may carry. Application of isobutyl cyanoacrylate, a tissue adhesive, may work in the same way but perhaps more simply and without the risk the risk/ of epithelial rejection.
3. Immunosuppressive Chemotherapy
Those cases of bilateral or progressive MU that fail therapeutic steroids and conjunctival resection will require systemic cytotoxic chemotherapy to bring a halt to the progressive corneal destruction.[10] At the Immunology and Uveitis Service at the Massachusetts Eye and Ear Infirmary, we believe that the evidence for the efficacy of systemic immunosuppressive chemotherapy for progressive bilateral MU is quite strong, and that such treatment should be employed sooner rather than later in the care of such patients, before the corneal destruction has become too extensive to need for surgery.
The most commonly used agents are :
-Cyclophosphamide (2 mg/kg/day): degree of fall in WBC is the most reliable indicator of immunosuppression produced by cyclophosphamide
-Methotrexate (7.5 to 15 mg once weekly)
-Azathioprine (2 mg/kg/day)
More recently, oral Cyclosporin A (3-4 mg/kg/day) has been successfully used to treat a case of bilateral MU unresponsive to local therapy with topical corticosteroids, silver nitrate, and conjunctival resection, as well as systemic immunosuppression with corticosteroids, cyclophosphamide, and azathioprine.[12] Cyclosporin A works by suppression of the helper T-cell population and stimulation of the depressed population of suppressor and cytotoxic T cells present in patients with MU.[23]
Adverse effects of these cytotoxic and immunosuppressive medications, such as anemia, alopecia, nausea, nephrotoxicity, and hepatotoxicity, are rare but possible. Therefore, the administering physician must be vigilant about their onset.
topical Cyclosporin A (0.05%) solution has also been tried with "success" in a number of
patients with MU. Local or systemic side effects attributable to topical cyclosporin A were generally not observed.[30]
4. Additional Surgical Procedures
When topical steroids, conjunctival resection, and systemic immunosuppressives have failed in the management of MU, additional surgical procedures may be considered. Superficial lamellar keratectomy has been shown to arrest the inflammatory process and allow healing.[4] Some cases may progress to perforation despite management as just detailed. Small perforations may be treated with application of tissue adhesive and placement of a soft contact lens to provide comfort and to prevent dislodging of the glue. When a perforation is too large for tissue adhesive to seal the leak, some type of patch graft will be necessary, from a small tapered plug of corneal tissue to a penetrating keratoplasty. In case of larger perforations, a partial penetrating keratoplasty may be performed. It should be emphasized that the prognosis of corneal graft in the setting of acute inflammation in patients with MU is very poor.[1, 8]
5. Rehabilitation
Penetrating keratoplasty may be performed once the active ulceration has ceased and the remaining cornea has been completely opacified, even in the face of a thinned and vascularized cornea.[6, 8] In these instances, a 13-mm tectonic corneal graft is first sutured in place with interrupted 10-0 nylon or prolene sutures with the recipient bite extending into the sclera so that the suture will not pull through the thin host cornea and then a 7.5 or 8.0-mm therapeutic graft is placed. In the absence of donor corneas, free lamellar scleral autograft can be used to restore corneal defect, followed by penetrating keratoplasty later.[26]
Because of the immune system's remarkable memory, surgical attempts at rehabilitation in MU should be done only with concurrent immunosuppression, even when the active disease has been arrested, because attempts at penetrating keratoplasty often are associated with recurrence and graft failure. Some authors believe that the risks of recurrence is so great that patients are best served not by any intervention but by maintaining the current status, i.e. the vision provided by their own thinned, scarred cornea.
Terrien's (NOT an ulcer)
quiet thinning superiorly with fine micropannus can spread 360 degreescommonly in adults >50 year old, M>F, bilateral but more advanced in one eye
steep central wall, mild inflammation later, lipid deposits at edge of pannus, epithelium intact rare perforation Rx: mild steroids chronically to suppress inflammation lamellar or PKP
Marginal corneal melt
autoimmune disease, most commonly rheumatoid arthritis
unilateral, inferiorly, may have infiltrate can have rapid progression stops if epithelium heals
Age related furrow
lucid areas of arcus, no inflammation, vessels, or perforation
Degenerations
Age related changesarcusvogts white limbal girdle = white deposits
cornea farinata = flour like central depositsof lipofuscin, dots, commas in deep stroma anterior to Descemet products of cellular degenerationcrocodile shagreen guttata = collagen on DM seen by specular reflection
hassal-henle bodies
Other usually work related or deposits
sueprficial stroma or subepithelial ike labradeor colorgolden brown = sheroidal degeneration [ due to sunlightwhite ring with iron Coats white ring grey white nodlues = saltmanscreamyy=lipid calcium = bandHistologysuperficial stroma protein or iron1Shephroidal protein in the superficial stroma2Coat's white ring = subepithelial or anterior stromal circular white ring with Fe deposits associated with metallic corneal foreign body3Salzmanns nodular degeneration = elevated gray white elevated subepithelial nodules with fe deposits Bowman's or in space above ie Ca or lipidBand Keratopathy ===deposition of calcium salts in Bowman's4Lipid Keratopathy= yellow between Bowmans and epithelium
1Shephroidal degeneration = occurs as amber deposits of protein in the superficial stroma due to sun exposurebilateral M>F, golden brown spheres in anterior stroma/Bowmans in palpebral zone risk factor age, UV exposure, probably elastotic degeneration of collagen symptoms: decreased visual acuity, FBS, irritation signs: usually not elevated, small lesions, can be in conjunctiva
2Salzmanns nodular degeneration = elevated gray white elevated subepithelial nodules with fe deposits adjacent to previous
corneal conditions but can also be isolated occurs 2ndry to keratitis or tracoma F>M middle age Rx: local excision +/- excimer smoothing3Band Keratopathy ===deposition of calcium salts in Bowman's
commonly associated with: local inflammation: dry eyes, uveitis, long standing whiglaucoma, interstitial keratitis, phthisis ophthalmic medications: pilocarpine systemic disorders: chronic disease, conditions associated with systemic increase in Ca, Phos, mercury such as hyperparathyroidism, excess vit. D ingestion, renal failure, sarcoidosis, milk-alkali syndrome, thiazide, bone mets other causes: gout with urates, discoid lupus erythematosis, tuberous sclerosis
Rx: removal with 3% EDTA, give topical anesthetic then EDTA for 1 min, scrape and sponge until it clears
4Lipid Keratopathy=elevated, nodular, yellow between Bowmans and epithelium occurring in areas of vascularized scars especially surgical
5Coat's white ring = subepithelial or anterior stromal circular white ring with Fe deposits associated with metallic corneal foreign body
Amyloidosis
deposition of noncollagenous protein
subepithelial, salmon color, avascular primary: tend toward mesenchymal deposit secondary: organ deposit
metachromasia crystal violet, flourescent thiaflavine T, birefringence/dichroism Congo Red, +with Siruis Red
primary localized most common form with palpebral conjunctival asymmetry (brown/yellow waxy firm subconj nodules) lattice is special form does NOT affect lids, but can be orbital presenting as VI nerve palsy primary systemicbilateral symmetric yellow or ecchymotic lid papules, light near dissociation vitreous opacities, EOM palsies, proptosis, glaucoma secondary local after chronic inflammation, trichiasis, keratoconus, granular dystrophy salmon to yellow, fleshy, waxy nodular lesion on cornea secondary systemic most common in general medicine and doesn't usually affect eyelids may be purpuric
corneal edemawhenever epithelium disrupted, can stimulate iritis via reflex arc
epithelial
intracellular first
intercellular with microbulla
then subcellular with frank bulla
stomal
all extracellular
factors
imbibition pressure = IOP - swelling pressure (nl 50)
fluid into cornea from IOP, gyclosoaminoglycans's
fluid out of cornea by dehydration, pump
IOP is inverse with swelling pressure
with nl endothelium, high IOP-- epithelial edema
with nl IOP, poor endothelium-- stromal edema
rx
mild
muro 128, hair dryer, control IOP
moderate
soft CL, cycloplegia, PK, conjunctival flap
Corneal Dystrophys
Epithelail dystrophies
3 types
1inger & dots Microcystic or cogans
2Honeycomb or Reis buckler
3bubble paper or Meesmans
1Microcystic or dot finger print or cogans or epithelial basment membrane dystrophy===============thckened BM & cysts with debrismaps- thickening of subepithelial collagen and basement membrane, no flourescein staining dots- cyst like spaces in epithelium containing cellular debris fingerprints- lines in deep epithelium best seen with retroillumination >30 y.o. 10% have corneal abrasions 50% of pts with recurrent corneal abrasions have MDF asymptomatic or present with recurrent erosions, rarely presents with irregular astigmatism Rx: hypertonic saline, debridement with cotton swablubricants, soft contact lens, excimer PTK effective anterior stromal puncturetopical anesthetic, debride areause 23g needle and penetrate anterior stroma up to 1/3 depth may perform even in visual axis but space punctures further apart antibiotic ointment and pressure patchwarn pts about extreme pain afterwards2Reis bucklers ===============progresive dystrophy with grey white deposits at Bowmans & honey comb appearenceReis-Bucker's
D, childhood, gray white opacities at Bowman's layer, becoming more confluent over the yearshistology: destruction of Bowman's layer and accumulation of "rod shaped bodies" replacing Bowman's layerreticulated pattern of scarringpainful recurrent erosions, by 50's marked corneal opacities Rx: excimer PTK, peeling off the superficial accumulated material, recur post PKP
3 Meesmans ===============AD and innoccous with epithelial cysts
AD dystrophy with thick BM, intraepithelial microcysts with peculiar PAS+ substance best seen on retroillumination asymptomatic until 10-20 y.o. when develop recurrent erosions, irritation, small decreased Vano rx necessary differential diagnosis includes cystinosis (metabolic defect resulting in accumulation of refractile cystine crystals, can be seen in peripheral cornea)
Stromal
mnemonic: Marilyn Monroe Always Gets Her Man in LA County.
Macular dystrophy- Mucopolysaccharides stains with Alcian blue GrEY CLOUDS
Granular dystrophy- Hyaline stains with Masson's trichrome stain SNOWFLAKES
Lattice dystrophy- Amyloid stains with Congo red LATTICE
Lattice and granular AD
macular and granular needs grafts corneal
Macular AR, peripheral cornea involved* decreased Va in childhood with diffuse stromal clouding mucopolysaccharides accumulates
type I: error in synthesis of keratan sulfate
type II: can synthesize keratan sulfate but 30% below normal gray white opacities with indefinite margins may involve full thickness of stroma, guttata stains with alcian blue, colloidal iron stain can recur after PKP
Granular = snowflake
AD milky deposits in central cornea, anterior stroma, with intervening clear areas with time,the center of opacities becomes more white;"snowflake" like appearanceaccumulation of hyaline stains with Masson's trichrome stainperiphery may be + for amyloid (ancestry to Avellino, Italy) may recur yrs after PKP often amenable to PTK
Lattice = (Amyloid) childhood, central lines, dots, haze (ground glass) recurrent corneal abrasion, decreased Va by 40 years olddeposits of amyloid stain with congo red, PAS, and Masson's trichrome stain recurrence post PKP common
Central crystalline (Schnyder) =doughnut crystals fat [ cholesterol
Fleck = dandruff uncommon, nonprogressive stromal dystrophy normal Va, no symptoms begins in childhood bilateral but asymmetric gray white dandruff-like opacities to periphery, increased glycosaminoglycans, lipids associated limbal dermoid, keratoconus, central cloudy dystrophy, pseudoxanthoma elasticum, decrease
CCD (central cloudy dystrophy)= clouds bilateral symmetric nonprogessive or very slowly progressive multiple nebulous gray areas with cracks of intervening clea zones normal vision
polymorphic stromal dystrophy = amyloid bilateral symmetric progressive late in lifenormal Va,
associated with systemic amyloidosis
Pre-Descemet farinata pre-Decemet degeneration deep stromal punctate specks above Descemet'sPosterior amorphous stromal dystrophy rare bilateral child with good Va extends to limbus, iris processes, endothelium disrupt focally peripheral variant with clear center CHSD (congenital hereditary stromal dystrophy) flaky feathery anterior central opacity at birth
EndothelialCorneal guttata
thickening and localized excresences of Descemet's membraneresults from abnormal production of collagen by endothelial cells "beaten metal" or "orange peel" appearance do not affect vision but may lead to endothelial dysfunction and corneal edema
Fuchs's dystrophy
AD, F>M, (most common in post menopausal women)It is surprising > common in F and is inherited AD & slightly > conmmon in COAG bilateral and asymmetric, rare in Orientals central guttata first, pigment in endothelium (can have borders)
worse Va in mornings, humid days, increased IOP
Cf endothelial protrberences = guttata and later bulla when stroma thickened by 30% rarely pigmented gutatta can decreased Va (20/60 range)in long standing cases, subepithelial fibrosis, grayish Descemet thickening posterior collagenous layer can obscure all the guttatadiff dx of corneal edema- other endothelial problems, PPMD, disciform keratitis
Rx only if symptomatic, treat as in other causes of corneal edema if considering phacoemulsification check corneal thickness also 5% NS & lower IOP
BCL protects corneal nerves and flattens bulla
Posterior polymorhous dystrophy
innocuous inherited condition with various vessicluar band like or geographic assymitircal opacities .
AD bilateral childhood, progressive, asymmetrypresents as a spectrum of corneal changes that occasionally involve iris and angle endothelial cells act like epithelium, may look like ICE posterior surface with ridges, lines and circles with scalloped edges, stromal edema, iridocorneal adhesionsbest seen in retroillumination
CHED (congenital hereditary endothelial dystrophy)
Type I: AR, most common, no pain or tearing stationary, diffuse, often present at birth associated with nystagmus
Type II: AD, presents at 1-2 year old, painful tearing, progressive, less corneal edema, no nystagmus, cornea blue ground glass, associated with deafness
Other corneal pathology
Keratoconus
severe > 54D nipple oval or globus classification depending on central cone size
CJ scissor retinoscopy
irregular astigmatism where principle merideans no londer at 90'
photokeratoscopy or pacidos disc irregular
slit lamp vogts lines and prominent corneal nerves.
later central thinning scarring fleisher ring acute hydrops
central or paracentral corneal thinning and bulging
sporadic, can be familial (<10% of occur in blood relative)
bilateral but asymmetric
associated with Down's, Leber's, atopy
signs: Vogt's striae,Vogts striae in keratoconus is lines on cornea when compressed
Fleischer ring- iron deposits at the base of the cone, scarring, early astigmatism
Ehler Danlos VI
keratoglobus, spontaneous perforation of globe, blue sclerae
Rx
bcont lens
Patch
Hypertonic saline 5% normal saline
Instruct do not rub eyes
Keratoglobus
thinning greater in periphery near the apex of the protrusion, mild scar, not genetic, connective tissue disorders
associated Ehlers-Danlos type VI
Pterygium ==========elastic generation of conjuctiva subepithelial collagen & corneal collagen
Phlyntenosis ========Phlyctenular ulcer = nodular pinkish white limbal elevation with gray crater, can be on conjunctiva caused by type iv hs to staph TB or candida antigen
Infective Corneal ulcers & KerititisBacterial keratitis
risk factor: + atopy, prior HSV, , bullous keratopathy, OCP, Stevens Johnson syndrome, abnormal lid position
Most common Staph/Pseudomonas are more than 50% of all cultured cases
Virulence Worst are Pseudomonas, Strep (B-hemolytic, pneumoniae)
Penertration direct epithelial penetration by GC, H egypticus, Diptheroids, Listeria
Staphgram positive cocci~~~ulcer is usually localized with distinct borders- may satellite
S. aureaus vs S. epidermidis (coagulase-negative) causes deeper ulcers, more inflammation, hypopyon, and endothelial plaque t
Strep pneumoniae~~~~~ ulcerative keratitis + inflammatory membranes
risk acute or subacute purulent conjunctivitis
Neisseria gonorrhoea~~~ mucopurulent discharge may cause perforation
risk~hyperacute onset most often a progression from conjunctivitis
Moraxella~~~~~~~~~~~peripheral or paracentral infiltrate
risk more chronic, indolent keratitis- in chronically debilitated patients-
special dx consider calcium alginate swab so
Pseudomonas ~~~~~~~perforation
risk contact lens
Haemophilus ~~~no membranes
risk group purulent conjunctivitis and preseptal cellulitis in children
Phlyctenular ulcerpinkish white limbal elevation with gray crater, can be on conjunctiva type IV immune mediated response caused by: staph, TB, Candida, Chlamydia, nematodes, gonococcal antigens, adenovirus early Terrien's can look similarRx: treat the infection if active, topical steroids used to minimize scar formation
Staph Marginal Infiltrates =margial kerartitis
type III immune reactiongray limbal ulcer usually with clear cornea all around, early corneal neovascularizationallergic rx usually to staph at 8/10 and 2/4 o'clockcan progress to ring ulcer, usually spread toward limbus not centrallycan get superinfectedAtopy Wg C UC SLe scleroderma hookworm influenza TB samonella dengue gold poisoning Gc athritisInfectious Crystalline keratopathy===feathery "crystalline" edge, assoc. with chronic steroids, (eg. PKP) due to alpha strep viridens,
poor response to topical therapy biopsy usually for diagnosis rx with concentrated topical bacitracin
Acanthameoba
found in water, existing as a cyst or trophozoite
mimics HSV early, later ring infiltrate, often misdiagnosed as HSV
symptoms: wax and wane with photophobia, FBS, severe pain
signs: first abnormal epithelium (SPK, persist defects, SEI, edema, whorl like patterns, dendritiform lesions)
then central/paracentral stromal infiltrate with satellites, turns into ring
neurokeratitis with cuffing of nerves
preauricular adenopathy
Dx: biopsy , stains (Giemsa, calcofluor white, acridine orange) are faster and better than culture touch material instead of smearing on slides
use spray fixative instead of air drying IFA, calcofluor white, conjugated lectin flourescein stain culture on non-nutrient agar with E. Coli overlay Rx: difficult, often fails, use multidrug approach
antiseptic (PHMB or chlorhexidine) + Brolene 0.1%, neosporin add clotrimazole 1% q15-q1h +/- ketoconazole 200 mg po bid or fluconazole po no steroids once infection in peripheral cornea, poor candidate for graft Acanthamoeba(Every hour for first week and 5 min apartBrolene and Neosprin +ADD Oral ketoconazole + 1% topical Clotrimazole If lack of response or advancing stromal involvement(Tapered after 1 week(Continue 1 year Brolene and Neosprin Other regimesTriple therapy Polyhexamethylene biguanide, which is a cystocidal as well as a trophozoicidal (none of these agents has worked consistently, alone or in combination. Fungal
mostly filamental, Fusarium, Aspergillus >50 %
Candida 10% in older, keratoconjunctivitis sicca,
Dx: stains with calcofluor white, 10% KOH wet mount
Gomori methenamine silver or PAS
culture Sabouraud's and blood agar
Rx: filamentous fungi is now fluconazole with good penetration
second-line drugs include amphotericin B 0.15% (1.5 mg/ml) or imidazoles (miconazole 1% or ketoconazole 1-5%)
first-line for candida is ampho alone or in combination with flucytosine, do not use flucytosine alone because of high resistance
second-line for candida is imidazoles ViralHSVHZOThygesons superficial puctate keratits=rare presumed viral fleeting keratitis=small grey intraepithelial dots with mild subepithelial haze
Fungal Keratitsfilaments parakacinuse ampho B or azole for cystsCf very florrid limbal vasculaization and fluffy discharge
Interstitial keratitis
syphilis Cogan's syndrome =bilateral intersitial keratitis associated with vestibuloauditory symptoms may also involve polyarteritis nodosa,and necrotizing lesions that leads to endocarditis and gastrointestinal hemorrhages
other conditions associated with interstitial keratitis TB leprosy LGV sarcoid HSV IHZO mumps Kaposi's sarcoma
protozoan/helminths lyme disease Hodgkins ncontinentia pigmenti
Steven Johnson
RX topical steroids & oral steroids
Rx Topical Retinoic acid for keratinization
Punctal occlusion & tear supplments
Scleritis
Diffuse anterior scleritis . Erythematous, immovable and tender inflamed nodules Approximately, 20% of cases progress to necrotizing scleritis. Necrotizing anterior scleritis Scleromalacia perforans, rheumatoid arthritis.notable for its absence of symptoms Anterior scleritis is demonstrated in 94% of patients In 15% of the cases, scleritis is the presenting cvd Sex: The female to male ratio is ~ 1.6:1. Pain Severe, constant, deep, boring or pulsating May awaken the patient at night The onset of scleritis is more gradual than the acuteness seen with episcleritis. Both eyes are affected in slightly over one-half the cases. degree of injection, as well as, the presence of a bluish hue, signifying attenuation of the sclera. Prominent findings may include photophobia, tearing without discharge, tenderness of the eye and purplish-red, edematous, engorged blood vessels.
Deeper scleral blood vessels appear darker, follow a radial pattern and do not move when manipulated with a cotton swab.
Phenylephrine application causes blanching of the more superficial episcleral vessels but does not change deeper vessels.
Scleral thinning: the choroid pigment becomes visible as a bluish hue Use of a red-free filter (green light) .
Posterior Scleritis:
Causes: Scleritis coexists with a serious systemic disease in almost one-half of cases.Rheumatoid arthritis occurs almost a one-third
Discoloration depicting scleral thinning
%Pupil Pupi test Rapd is caused by assymetrial pupilomotot response
Horner's syndrome
-miosis, ptosis, anhydrosis, and apparent relative enophthalmos (heterochromia in congenital cases)
-caused by sympathetic lesion (pre or post-ganglionic)
1st order horners occurs in the brain 2nd i the chest or neck and 3rd along the caorotid
First order - CNS lesion caused by stroke or tumor
Second order - caused by cervical disc disease or trauma to C-spine, apical lung tumors (Pancoast syndrome), tumors metastatic to cervical lymph nodes, chest surgery, thoracic aortic aneurysms, trauma to brachial plexus.
Third order - caused by intracranial diseases including migraine (Raeder's syndrome Type II) and cavernous sinus inflammatory (Tolosa-Hunt syndrome), traumatic (carotid-cavernous fistula) and neoplastic (meningioma, metastasis, lymphoma) diseases.
-no dilatation with topical cocaine (4% - 10%) Normally it prevetns NA uptake andtherefore augments NA thatis present
-pre and post-ganglionic Horner's differentiated with Paredrine 1% (hydroxyamphetamine) test
pre-ganglionic dilates
post-ganglionc does not dilate
Works on premise that noradrenaline can be released at iris by hydroxyamphetamine if the ganglion can make it and is ok
--------= 0----------=
it either works or not at ganglion
cocaine works only if there is a supply of noradrenaline and prevents its reuptake----- so it only works if the system is ok.*
#Lacrimal SysytemEpiphora in kids below 1 tear is due to failure of the lower NLd to perforate. This happens at about at latest 1 year so wait ubtil then before probing
In adults it is most commonly due to Chronic Dacrocystitis
Mucucoeles are genrally not operated on as they lead to fistulas or may spread infection
#OpticsRetinoscopy
static Accomodation is suppressed by cycloplegia
& dynamic
Essntials
1lght in the form of a cone or streak is projected using a mirror to illuminate the retina as a Patch.This acts as a secondaey Light source.
The obserever views a central aperture yo view the light emerging from the pupil
Aim is to neutalize the obserevd movement ie when to far point of the eye is reached
#Defintions nanophthalmos = high hypermetropia
red free is done using green light This
Optic disc ishchemia early on and leakage later
Optic Pit
Think where pits are most destructive inferior temporal
Maddox rods
What is Pulfich phenomenon
Hue Farnsworth Munsell 100 hue test chips
#Glaucomasupeior and inferiortemporal arcuate fibres are most sensitive to glaucomatous changes hence 1st defect is Nasal superior extension of blind spot. which is anatomically at about 15' from fixation.
This is( B)jerrms area
Therefore look near blind spot and nasally
2nd defect is a nasal step or temporal wedge.
If you see these look for a paracentral scotoma carefully.
Later constriction occurs nasally temporally and then centrally
Perimetry
Humphrey or Octopus
spot size is 0.43' and duration is 0.1 sec
contrast in decibels
no of targets 25 or 72 or 132
The numeric display is the patients threshold {minumum response}value in decibels
The symbolic is similar except it explains it in 5 grades and relative to normal population for age
The graphic is similar except it explains it in 9 shades of grey
Threshold measures the patients threshold and then compares it to age matches it is quantative
Superthreshold measures spots above threshold ie qualatative and screening.
Its aim is to pick up changes in young people.
Visual threshold
This is luminence seen in 50% of individuals.
We need 10% change to notice difference therefore log scale
fovea sensitivity is 35 db at 20 years & we lose1 db lose per 10 year) hence at 70 years it is 30 db
Visual field
60' nasally 90' temporally 50' superiory 70' inferiorly
Neural rim thickness
ISNT
Grade of angle
Look for
IV~~~~~~~~ciliary body Brown
III ~~~~~~~scleral spur A little sharp just anterior to Ciliary body
II White trabeculum ( which is anttwerir and posterior thicker Baige or greyish nBlue
NB in Argon Trabeculoplasty applie burns to the junction
I ~~~~~~~Scwalbes line only White
0 ~~~~~~~use this word inability to see apex of corneal wedge.
NB I need indentation gonioscopy to differentiate appositional & Synechial angle closure.
# Retinal Detachment Cryopexy takes 2 to3 weeks to from an adhesion freezing cc and RPE right down to outer photoreceptor layer thus closing space VS Laser pexy that is instantanous as the RPE burns and closes space
Exudative Retinal Detachment (ERD)==Occurs when either retinal blood vessels or RPE is damaged, allowing fluid to pass into the subretinal space
Neoplasia and inflammatory dz are leading causes of large ERD
Shifting fluid responding to force of gravity Smooth, bullous appearance
There is no photopsia and not commonly floaters as these will occur only secodary to vitritis and not due to snchisis as often see on RRD
signs smooth and convex or bullous
shifting fluid is the hallmark
look for the cause eg tumour and u won't see a tear!
Idiopathic Coat's ???CSCR Uveal Effusion Syndrome ????Congenital FEVR ???Optic pit Nanophthalmos Postsurgical PRP RD repair Hemorrhagic choroidal detachment Inflammatory Scleritis Orbital pseudotumor HZO CMV retinitis VKH??? SO PIC AMPPE Vascular Toxemia of pregnancy AMD Hypertensive retinopathy Diabetic retinopathy Chronic renal failure Cardiac insufficiency
Hematologic TTP Leukemia Neoplastic
Peripheral Retinal Abnormalities
Landmarks read up anatomy
Long posterior ciliary nerves at 3:00 and 9:00 Short posterior nerves usu. superior and inferior Vortex veins at the equator and near superior & infer rectus ie 12 and 6 o clock
Scleral depression
Depress just posterior to recti insertions, since ora serrata lies just underneath Spiral of Tillaux
Retinal breaks
ARE Any full-thickness defect in the neurosensory retina
Horseshoe tear* ~~~~Strip of retina pulled anteriorly by vitreoretinal traction
Giant retinal tear ~~~~Tear that extends 90o or more circumferentially
Operculated hole~~~~ Traction is sufficient to tear a piece of retina completely free from adjacent retinal surface
Retinal dialysis~~~~~~Break occurring along ora serrata, commonly resulting from blunt trauma (superotemporal quadrant most common if traumatic) Usu. at posterior border of vitreous base
PVD
Vitreous base (VB) - , extending 2mm anterior and 4mm posterior to ora
Vitreous also firmly attached at: Major retinal vessels, Margin of lattice degeneration, sites of chorioretinal scars
Initial event - syneresis =(liquifaction) of central vitreous~~~ Hole develops in posterior vitreous ~~~~ Liquified vitreous passes into subhyaloid space, rapidly separating posterior hyaloid from retina,~~~~ BUT Vitreous gel remains attached at VB Resulting vitreous traction, commonly at posterior margin of VB, may produce retinal break
symptoms: photopsia, floaters = (VH, glial cells from optic disc, aggregated collagen fibers) Weiss ring is glial cells from OD
15% of pts w/ acute, symptomatic PVD have a retinal tear
70% of pts w/ VH assoc. w/ PVD have a retinal tear
2 to 4% of pts w/o VH assoc. w/ PVD have a retinal tear
Prevalence of PVD increases w/: Increased axial length Advanced age Aphakia nflammatory dz Trauma myopia
Macular hole is formed by tnagential traction followed by ap traction that causes PVD but also takes a bit of fovea
complete pvds are therefore not going to cause holes
Traumatic retinal breaks
Traumatic breaks often multiple and commonly found inferotemporal and superonasal
Dialysis most common, usu. at posterior border of VB
Avulsion of VB (anterior vitreous detachment) may be assoc. w/ a dialysis, and is considered pathognomonic of ocular contusion. "Buckle handle" Vitreous may eventually liquify over a tear, subsequently leading to RRD. Clinical presentation of RD usu. delayed
12% immediately 30% in 1 month 50% in 8 months 80% in 24 months
traumatic RD in young pts. usu. show chronicity shallow w/ multiple demarcation lines subretinal deposits & intraretinal cysts Blunt trauma (A/P compression w/ equatorial expansion)
Coup mechanism (adjacent to point of trauma) Contrecoup injury (opposite point of trauma)
Benign Peripheral degenerations =Lesions not predisposing to RD
cobbelstone paving dark tiles small (micrcystic ) honey spread or snowflakes serial or drusen degenerations will not cause slipping
vs
lettuce on the floor or folded or tufts of grass or bays sandor excavations will lead to a fall
Cobblestone (paving stone) degeneration===Small, discrete areas of ischemic atrophy of outer retina
attenuation or absence of CC Loss of RPE and outer retinal layers Adhesion btw remaining retinal layers and Bruch's MB Most common in inferior quadrants, anterior to EQ Appear yellow-white, may be surrounded by rim of hypertrophic RPE Large choroidal vessels may be visible (RPE absent)May be confluent Present in 22% of people >20 y.o.
RPE hyperplasi or RPE hypertrophy Microcystoid === tiny red coloured vesicles Snowflakes ====white scattered dots Honeycomb===fine network perivascular Drusen
Lesions predisposing to RD
Lattice degeneration===discontinnuity of ilm & atrophy of inner retinal layer due to condensed aherent vitreous
6% to 10% of general populatio Bilateral in 1/3 to 1/2 More common in myopes Histopathology:discontinuity of ILM, overlying pocket of liquified vitreous, condensation and adherence of vitreous at lesion margin, atrophy of
retinal inner layers, sclerotic blood vessels Underlying cause in 20% to 30% of all RRD Vitreoretinal tufts=== retinal elevations due to vitreous traction
Small, peripheral retinal elevations caused by focal areas of vitreous or zonular traction Classified as: noncystic retinal tuft, cystic retinal tuft, zonular-traction retinal tuft
Cystic and zonular-traction types more likely to predispose to RD because of firm vitreoretinal adhesion Meridional folds===Folds of redundant retina
Usu. superonasal Most commonly assoc. w/ dentate processes Enclosed ora bays===ora pars plana in retina
Oval islands of pars plana epithelium located just posterior to ora; completely (or almost completely)
circumscribed by peripheral retina Peripheral retinal excavations
May represent atypical lattice
Often aligned w/ meridional folds
Retinal Breaks
tears such as round, atrophic holes, operculated holes, macular holes have a minimal chance of progressing to RD
acute, symptomatic tears carry a considerable risk factors to consider in risk/benefit of Rx: symptoms, residual traction, location of break, phakic status, refractive error, status of fellow eye, family history, presence of subretinal fluid, and follow-up reliability
Rhegmatogenous Retinal Detachment (RRD)
Rhegma: Greek for break
Caused by liquified vitreous passing through retinal break into potential space between sensory retina and RPE
Shafer's sign: small clumps of pigmented cells (tobacco dust) in vitreous or AC Corrugated appearance, undulating w/ eye movements (however, in old RRD the retina may appear smooth and thin) Convex ie balooning
vs
Tractional Retinal Detachment (TRD)
Smooth surface, immobile Concave Rarely extends beyond ora serrata May cause tear leading to RRD
PVR
RPE, glial, and other cells grow on both the inner and outer retinal surfaces and on the vitreous face
Contraction occurs >fixed folds>equatorial traction>detachment of nonpigmented epithelium of pars plana>generalized retinal shrinkage
Causative retinal breaks may reopen, new breaks may occur, or a TRD may develop
PVR Classification
Grade A: vitreous haze, & pigment clusters on inferior retina Grade B: wrinkling or stiffness of inner retinal surface, rolled and irregular edge of retinal break, Grade C P 1-12: posterior to equator. full-thickness folds*, subretinal strands all expressed in number of clock hours Grade C A 1-12: anterior to equator.
#VitreousAsteroid hyalosis=calcium containing phosphoipids in vitreous=White Opacities evenly distributed Assoc. w/ diabetesIncidence 1:200 > 50 y.o. unilateral 75% vision NAD
VS
RARE AND visually significant
cholesterolois (hemophthalmos, synchysis scintillans)=Golden Numerous yellow, white, gold or multicolored cholesterol crystals in vitreous and ACAlmost exclusively s/p accidental or surgical trauma w/ large intraocular hemorrhage PVD common - allows crystals to settle inferiorly very rare most of the time in clinica you will asteriod hyalosis
Diseases of the Vitreous
Tunica vasculosa lentis== Entire hyaloid system, either patent or occluded, may persist from disc to lens None of these remnants is visually significant
Mittendorf's dot (anterior remnant): attached to lens capsule
Bergmeister's papilla (posterior remnant): fibroglial tuft extending into vitreous from optic nerve head margin
Prepapillary vascular loops===Normal retinal vessels that have grown into Bergmeister's papilla before returning to the disc
Usu. < 5 mm in height May supply one or more quadrants of retina 85% arterial, 5% venous Complications: BRAO, amaurosis fugax, VH
Persistent Hyperplastic Primary Vitreous (PHPV)/
Persistent Fetal Vasculature (PFV)=Failure of primary vitreous to regress
Usu. found in otherwise normal, full-term infants of normal birth weight Unilateral 90% Usu. obvious at birth (unlike retinoblastoma)
Anterior form: Hyaloid artery remains White vascularized fibrous membrane present behind lens Associated findings: microphthalmos, shallow AC, long ciliary processes visible around small lens, cataract, secondary angle closure glaucoma Very poor prognosis for useful visual acuityPosterior form: May occur w/ anterior PHPV Microphthalmos may be present, but AC usu. normal and lens usu. clear, without retrolental membrane Stalk of tissue emanates from optic disc toward lens, often running in apex of retinal fold in an inferior quadrant Stalk fans out circumferentially toward anterior retina
DDx: ROP, toxocariasis, FEVR
Hereditary hyaloideoretinopathies with optically empty vitreous===Hallmark is vitreous liquefaction resulting in optically empty cavity except for thin layer of cortical vitreous behind lens, and white avascular membranes adherent to retina
Equatorial and perivascular (radial) lattice ERG may be subnormal
only with ocular manifestations: AD, myopia, strabismus, cataract
Wagner dz - usu. not assoc. w/ RD High myope, post. cortical cataract at puberty, peripheral vitreous veils, strabismus, perivenous radial lattice Jansen dz - high incidence of RD
with assoc. systemic manifestations:
Stickler syndrome (hereditary arthro-ophthalmopathy-Marfanoid variety)
AD High incidence of RD Myopia Open angle glaucoma CataractOrofacial findings: Midfacial flattening Pierre-Robin malformation complex (micrognathia, cleft palate, glossoptosis) Skeletal abnormalities: Joint hyperextensibility/enlargement Arthritis Spondyloepiphyseal dysplasia
Hereditary arthro-ophthalmopathy with stiff joints (Weill-Marchesani-like variety) High incidence of RD Four varieties w/ frank dwarfism: Kniest syndrome RD common Dwarfism, facial abnormalities, joint stiffness, sensorineural deafness Spondyloepiphyseal dysplasia RD less common Congenital dwarfism, normal facies, joint laxity, normal hearing 2 other varieties variable incidence of RD
FEVR with Peripheral fibrovascularization Large syneresis cavities ERM Dragged macula Increased arborization ^ may mimic Coat's May have abnormal platelet aggregation Usu. bilateral Full-term w/ normal respiratory status No peripheral mesenchymal shunt
Amyloidosis==Bilateral vitreous opacification (glass wool appearance) &may cause decreased visual acuity warranting vitrectomy
Spontaneous vitreous hemorrhage
Diabetic retinopathy (39% - 54%) Retinal break w/o RD (12% - 17%) PVD (8% - 12% RRD% - 10%) NV s/p BRVO or CRVO (4% - 10%) Any cause of peripheral NV Congenital retinoschisis Pars planitis
Vitreoretinal interface abnormalitiesEpiretinal membrane (ERM)===PVD may leave cortical vitreous attached to macula, or may cause dehiscience in ILM allowing retinal glial cells to proliferate along retinal surface/posterior cortical vitreous Contracture of ERM > cellophane maculopathy > macular pucker Shallow TRD
Secondary to: retinal vascular occlusions, uveitis, trauma, intraocular surgery, retinal breaks Idiopathic - abnormality of vitreoretinal interface in conjunction w/ PVD > 50 y.o. M=F 20% bilateral CME Traction on vessels > leakage on FA
Vitreomacular traction syndrome
PVD incomplete in maculaVitreous opacities overlying maculaShallow macular detachmentFA: leakage in macula and disc
RD surgery
Silastic sponge through Peitomy excision tenons
#Denerations and Dystrophies of fundus seen mostly at Macula
Nb RPE is drusen etc and causes masking while PR is RP color /night blindnessRPE=bests stagarts&flavimac drusen & AVFMD
photo= RP cone dys csn blindness albipunctus lebers amaurosis
RPE degeneration
diagnosis absence of normal background choriodal flurescence due to pathological rpe
1Bests = egg yolk lesion
AD stage i abnormal stage ii yolk stage iii pseudo hypopyon stage iv scrabbled egg stage v end stage
2Adult foveamacular viteliform dystrophy
3Stargarts macular dystrophy = beaten bronze macular & fundus flavimaculatus= fish tail like spots
4familial drusen
Photoreceptor dystrophy
1RP Spradic most common AD XL AR 1 in 4000 disease of Rods
Cf:bilateral arteriolar attenuation,bony spiculation waxy disc pallor By 30 5% are symtomatic
2Cone dystrophy = bulls eye fundus central ring of atrophy
3Leber amaurosis variable
4Congenital staionery night blindness normal fundus
5Fundus albipunctus = fine yellow spots in fundus NM Remeber seeing apaptient with this
Maculopathies
Anatomy and the eye
Spaces
1 choriocapilaris 2 Bruch3RPE 4outer 1/3 sensory Retina with Photoreceptor (supplied by chriocapilaris) and5inner 2/3 sensory retina that has arterioles and venules
Every patholgy must be explained by AREA
Drusen ARMD~~~~~hyaline between bruchs and RPE( with RPE atrophy and depigmentation)
RPE and sensory detachment ~~~~clear fluid between bruchs and RPE
RPE and sensory haemoragic detachment~~~ blood
SRNM below RPE grey green to pink slightly elevated lesion
broken into subretial space tranlucent pink white lesion
CSCR serous fluid below separated sensory retina
CMO cysts in sensory retina at outer plexiform layer
causes vascular or non vascular
post surgery trauma
DM CRVO teleangiectasia
lamella hole sensory retina thin
macular hole only RPe left
Myopia atrphophy retina RPE and CC
Fuchs spots = pigmentaion in retina
Macular plucker = peretinal fibrosis and traction
Chroidal folds simple
angoid streaks dark lines deep errated and irregular and termoinate abrubtly ~~cracks in bruchs
Chloroqune toxity choroquine accumulates products in RPE and visible esp at foveola
RP bone spicule perivascular outer 2/3 neurosesory pigmentation Optic disc waxy pallor ~~~ ischemia or hyaline drusen
bests lipofuschin at RPE sensory level space that colasece= yolk
AFVD
1CSR
2CMO
histology intracellular fluid accumulation in mullers cells which is reversable and is seen as large spaces in OPL
it is irreversable if acculation is intracellularly
DDX stage 1 macular hole lamelar hole epiretinal membrane solar retinopathy pattern dystrophy
RRD x linked Retinoshisis difuse mac oedema
causes postop eg ECCE PK iridotomy PRP Cryo buckling RS dystrophies inheited RP AD CMO vascular DM Coats JF telangiectasia choriodal neov radiation CRVO HT Macroaneurysm Ocular ishemic syndrome TX CM Inflam Bechets Sarcoid birdshot PP Vitritis Toxo CMV Meds Epinephrine Nicotinic acid
3Macular hole
Idiopathic macular cyst and hole
6th-8th decades assoc. w/ tangential vitreomacular traction Bilateral 25% - 30% B scan of both eyes since
separation of posterior vitreous face has much better prognosis Gass classification:
Stages of macular holes (new - Gass 1995)
1A) foveolar detachment
1B) foveal detachment
2) early hole (<400 microns)
3) larger hole (>400 microns) +/- operculum
4) full thickness hole with PVD
Outer lamellar hole ~~~~s/p Berlin's, optic pit, sun gazing
Inner lamellar~~~~~~~~~ more common, CME, 20/20 to 20/80, Amsler distort, minimal to no window defect on flourescein angiogram, <1/3 DD
4Myopic maculopathy
5Angoid streaks
causes PEPSI Pagets ehler danos pseodoxanthoma elasstica sickle cell idopathic
6Choroidal folds
7Toxic maculopathy Phenothiazines choloquine tamoxifen canthxanthain
hydroxychloroquine incidence 0.08% vs 1 to 2 % for chloroquine
Related to lysosomal degradation and lipofucin production
Plaquanil (hydroxychloroquine) (>400 mg/day) may have a direct toxic effect on receptors daily dose more important than total dose
Chloroquine >250 mg/day
Cummulative dose more than 200g or 4 years
Contrast did not deterioratw as much as color
ass gene for stargarts dx susceptibility more if gene present
Explains why only some get it
(more toxic) do it within 6 months of
early loss of foveal reflex granularity of macula bulls eye lesion arterial narrowing sheathing and peripheral pigment cornea verticillata poliosis CN VI palsy decreased accommodation decreased corneal sensation blurred VA Paracentral /central scotoma dyschromatopsia
tests ERG increased a, decreased b, normal dark adaptation baseline VA, Amsler, color plates, photos, exam q 6 months HVF central 10 if needed, if decreased by 0.5 log, stop drug do not need red light with HVF since measuring decibels
Phenothiazines~~~ Concentrated in uvea and RPE by binding to melanin granules Mellaril (thioridazine) (>800 mg/day) effects after 3-8 wks. nyctalopia, fine stippling to widespread atrophy of RPE, CC ring/ central scotoma, blurred VA Thorazine (chlorpromazine) lid, conjunctiva, corneal, capsular pigmentation, ASC/PSC, >1200 mg/day of >1 yr., rare pigmentary retinopathy Digitalis~~~toxic dose is cone toxic, therefore colors changes blurred VA, pericentral scotomata, yellow vision Desferroxamine used for hemosiderosis bilateral rapid LOV 1 wk. after last dose, nyctalopia VA returns in 75% by 3-4 months Tamoxifen& canthxanthain >200 mg/day for 1 yr. (>100 gm total)normal dose is 10-20 mg bid inner retinal refractile deposits CME Decreased VA optic neuritis white corneal opacities DDx Crystalline retinopathy may resemble that seen after ingestion of high doses of canthaxanthine (carotenoid used to stimulate tanning) Prolonged methoxyflurane Ax: crystalline maculopathy w/ renal oxalosis/failure Oxalosis primary hyperoxaluria, ethylene glycol abuse, prolonged methoxyflurane anesthesia crystals in RPE Methanol seeing spots to blindness 18-24 hours after ingestion (formic acid toxic) early optic nerve swelling, vein dilation, retinal edema 1-2 month later, optic nerve atrophy, cecocentral scotoma, decreased ERG most of the recovery takes place in one week severity related to acidosis, consider hemodialysis Clofazimine for dapsone-resistant leprosy, HIV+ and MAI bull's eye lesions with window defects and normal Va reported
Age related maculopathy
Choroidal degeneration
1Choroidemia degeneration of choriocapilleris and RPE
fa large chorioidal vessels only seen thru window defect
XLR scalloped RPE and loss of choroid, CC, and RPE starting at equator and moving anterior/posterior. nyctalopia, 4-20 y.o., VF loss peripheral, no spicules but clumping < 20/200 by 50 y.o. ERG abnormal Carriers: can have symptoms, pigment clumping, RPE granularity, ERG and VF normal Abnormal gene codes for a component of rab geranylgeranyl transferaseDDx: high myopia, gyrate atrophy, RP, Bietti's crystalline dystrophy
II Gyrate choroidal degeneration
ARrnithine aminotransferase def., 10X increased ornithine, as early as 8 y.o. scalloped RPE/CC loss, peripheral paving stone, rest of RPE increased pigmentation, myopia, cataracts progressive loss of VA and VF , nyctalopia, abnormal EEG, changes in hair/muscle fibers, ERG abnormal <20/200 by 40 y.o. dietary restriction of arginine, vit. B6
IIICentral aereolar choroidal dystrophy
IVGenralized choroidal atrophy
VCentral areolar pigment epithelial dystrophy CAPED
Vitroreinal degeneration
Sticklers
Retinoschisis
Avre Goldman ===synchysis + Retinoshisis + RD like
Familial vitroretinopathy
#Retinal vascular disorders1DR
2RVO
3RAO
4HR
5Retinopathy in blood disorders iSickle cell iianaemias iiileukaemias ivhyperviscosity vROP
6Retinal telangiectasia 3 Types: Idiopathic juxtafoveolar retinal telangiectasia least severe and presents with
microaneurysms and kinked microvascular channels near fovea. Lebers miliary aneurysms saccular dilations Coats This is the most severe and occurs mostly in young boys and presents with subretinal exudation males frm 18months to 18 years unilateral mostly superior quadrant pathophys bd of inner BR barrier telangiectasia cap closure deposit of macrophage elated lipid gives it typical exudative lok which is different from exudative detachment that may follow
coats response =is massive exudation in any disease
7Retinal artery macroanerysm
#Uveitisidiopathic common
Fuchs iridocyclitis acute onset adult anterior uveitis Intermediate uveitis=pars palnitis juvenile chronic uveitis
Fuchs uvietis syndrome 2% of all one eye and middle age
Cf Mild uveitiswhite KP mild uveitis and no posterior synechie IrisHeterchromia iridis and iris atrophy and enarged pupil and occasional koeppe nodules mild vitritis gonioscopy fine radial twig like neovascularizationn which are probably responsible for haemorrhage noted with paracentesis=amslers, fine membrane or small fine PAS
Amsler's sign =bleeding occurs during cataract extraction and is due to wispy iris vessels which extends from the iris to the trabecular meshwork and do not cause anterior synechiae
Cx secondary glaucoma cataract
Rx topical steriods NO objective improvement.
Iris nodules
Koeppe ===small and on pupil margin common
Busaca opposite!!===large and on whole pupil large central and lss comon
Uveitis grading use a slitbeam 3mm × 1mm
anterior ueitis 1 < 10 cells
2 20
3 50
4 > 50
Idiopathic rare
nemonic singing bird singing serpent sweating ealewhite galucoma patient & multiple retinal vessels white dot
1Birdshot 2serpenginous 3Acute M P3 epitheliopathy 4sympathetic5Punctate inner choroidopathy 6Multifocal choroiditis and panuveitis 7Eales 8Retinal vasculitis 9Glaucomatocyclitic crisis 10idiopathic rareMultiple evanescent whitedot syndrome (also causesoptic atrophy)
the classication may be simplified to the 6 idiopathic inflamatory white dt syndromes
MEWDS young males small white dts
AMPEE ass HLA B7 largers placiod cotton wool like
PIc myopic females small yellow
brdshot moderate creamy middle age with vitritis
Multifocal choroiditis discrete grey yellow
Serpiginous
AMP3e ===deep cream B27 male = female
Serpenginous===
Birdshot===
Multiple evanescent white dot syndrome see optic neurpathy
Punctate inner choriodpathy ===young female myopes small yellow choriodal lesions at posterior pole
Multifocal Chorioditis ===age 20 to 50 multiple grey yellow lesions simialr to sarciod and treatment is similar
Eales===young male peripheral occlusion and neovascularization like sickle cell aneamia
Assosiated with systemic disease eg Sarcoid Bechets Behcets classic triad of hypopyon iritis (short lived, often painless), aphthous oral ulcers, and genital ulcers increased incidence of HLA-B5 or subset B51 may actually cause a panuveitis (included in anterior section because of the classic acute hypopyon iritis)
young males from age 15 to 55 rare in US; more common in Japan, Mediterranean countries
Behcetine skin test: puncture skin intradermally with sterile hypodermic needle( if pustule forms within few minutes, indicates a positive test (rarely done)
systemic generalized occlusive vasculitis of unknown cause recurrent aphthous ulcers up to 1 cm, painful, demarcated mucosal ulcers are deeper and scar nodular genital lesions with central ulceration
skin lesions of erythema nodosum and pseudofolliculitis (pustular vasculitis) pathergy test is not useful in United States can mimic IBD with ulcerative hemorrhages in the GI tract
nondestructive recurrent arthritis- arthralgia in wrists/ankles in 60%
1/4 with CVA, confusional state, meningoencephalitis
ocular initial eye presentation in 25% of men and 10% of women asymmetric bilateral eye disease posterior involvement more common than anterior in men recurrent noncoagulable hypopyon iritis (10%)
common posterior findings of vasculitis ultimately leads to vision loss (sheathing, retinal necrosis, CME, vitritis, serous RD, ischemic optic neuropathy, CRVO) vasculitis tends to be hemorrhagic and involves both arteries and veins
prognosis risk of visual loss is higher in males and higher in patients with skin lesions, arthritis, and/or posterior uveitis
chronic and recurrent over 10 years before burning out
in the U.S., only 25% end up with Va < 20/200
RX
includes oral steroids, chlorambucil and other immunosuppressives
colchicine (pts have increased PMN mobility)=inhibits WBC motility and is ths antiinfamatory dose 0.5mg tds contarindicate din pregnancy
cyclosporine, cyclophosphomideVogt Koyanagi Harada(VKH)
Infectious Syphilis TB AIDS Lyme Leprosy brucellosis
syphilis
most eye involvment is in 2' and 3' stage
iridocylitis rare and only in 4% presents with G or NG uveitis
great mimicker
multifocal chrioditis is most common and later the can bone spiclues like RP
unifocal choroiditis is rarer and usually at macular and peripappilary
Neuroretinitis is independent of chorioditis and causes optic atrophy plus a florrid retinits and perivasculitis
other AR pupil retobulbar neouritis occ palsies VF defects
RX 12 to 24 MU IV for 10 days and 2.4MU IM for 21 days OR 500MG Doxy or Erythr QID for 30 days
Lymes spirochete borrelia burgdoferi via tick ixodes
first stage is a erythema migrans second atge is with eye signs and arthritis and CNS and Myocarditis 3rd stage is chronic arthritis that can be mistaken for RA
eye stage first a conjunctivitis and then a iridocylitis that may become interemdiate and also cause retinal vasculitis VERY rarely choroiditis and stage 3 with orbital myositis KPs and epicleritis (THIS ORDER IS abit strange but indicates chronic low grade nature
Goes front retina and than front again!
Brucella aborticus affects animal workers and causes Gran Uveitis
Parasite Toxo Toxocara
Viral Hzand Hs iris Acute reinal necrosis Congental rubella
Fungal Presummed occulat histplasmosis Candida
assosiated Arhritis Reiters ankylosing spondylitis JCA Psoriasis Reiters triad of urethritis, conjunctivitis, arthritis
85-95% are HLA-B27 positive may have a mucopurulent papillary conjunctivitis severe chronic recurrent acute attacks of iritis (50%) polyarthritis recurrent asymmetric lower extremity migratory polyarthritis sacroiliitis (1/3) nonspecific urethritis often forgotten, prostatic fluid culture negative often after epidemic dysentery or STD from Chlamydia, Ureaplasma, Shigella, Salmonella, and Yersinia other major keratoderma blennorrhagia of hands and feet (looks like pustular psoriasis) circinate balanitis persistent, scaly, erythematous, circumferential rash minor nail bed pitting palatal and tongue aphthous ulcers enteritis plantar fasciitis achilles tendonitis
VKH
albino retarded deaf limping ching for directions===similar to sympathetica ohthalmia Asian or American Indian ancestry between 30 and 50 years of age any patients with pigmentation are at risk bilateral disease unknown etiology, presumed autoimmune with assos deafness
early CSF pleocytosis severe acute bilateral anterior uveitis posterior uveitis with bilateral serous RD dallen fuchs nodules meningeal symptoms temporary deafness or tinnitus (1/3) seizures mono and hemiparesis coma late vitiligo poliosis alopecia perilimbal vitiligo (Sugiura's sign) in>75% sunset glow fundus (depigmented choroid)
get audiogram,, HLA-DR4 lumbar puncture is exactly like sympathetic ophthalmia but involves choriocapillaris
Parasitic Toxoplasmosis T. gondii ~~~25% uveitis in IMC &~~~congenital (1:10,000) 3C's: Convulsions, Ca+2 on x ray, Chorioretinitis most commonly bilateral classic sign of focal exudative retinitis segmental periarteritis
Worms Toxocariasis 1chronic endophthalmitis 2-9 years old white eye, cyclitic membrane, RD, CME, cataract 2localized granuloma 6-14 years old 3peripheral granuloma 6-40 years old can mimic snowbank rarely bilateral atypical treatment steroids if inflammation when worm diesNO benefit to treatment with antiparasitic agents l
Toxoplasmosis and Toxocara cani and actis
Toxoplasmosis is a parasite of cats that can exist in a spore ( egg) encysted or active trophozite form.
Our children become infected by eating contamianted food by cat faeces in our homes and we adults may eat uncooked food of intermediate hosts like beef pork and lamp ie We may get it from other animals too !!!. Our mothers spread it transplacentally
Congential
causing stillbirth early in pregancy and CNS convulsiones etc if late in pregancy.Dx intracranial calcification Most of the time it is mild and subclinical with chorioretinal scars found incidentally when doing eye exam later in life
Acute acqiured systemic
mild with fever LAd plus chrioretinitis mild and encelomeningitis
Onchocerciasis=== Cysticercosis=== subconjunctival "dermoid", vitreal cysts, endophthalmitis
Fungal Candida albicans===string of pearls, multifocal retinitis, may mimic toxoplasmic choroiditis: Histoplasmosis 1POHS===classic triad is punched out peripheral lesions ("histo spots"), peripapillary atrophy, and an asymmetric maculopathy 2endophthalmitis 3solitary granuloma
Viral HSV, HZO done already! Acute retinal necrosis===heavy vitritis, peripheral necrosis, CMV===(total) cataract, multiple peripheral lesions with minimal tissue destruction, optic nerve atrophy, viral inclusion bodies Rubella=== retinal pigmentation iritis, cataracts, glaucoma & vision and ERG generally normal Post Viral
Krills (Acute Retinal Pigment Epitheliitis)===2-4 gray spots with yellow white halos seen in macula ocuring
inyoung adults
HIVHIV retinopathy 1CMV retinitis most common opportunistic "brush fire" = yellow-white margin at the border of burned out atrophic retina fulminant form: posterior pole necrosis indolent form: white retinitis or primary papillitis 2Progressive Outer Retinal Necrosis Syndrome ass zoster 3Toxoplasmosis no prior scars bilateral in 1/3 multifocal vitritis +IgM to T gondii in 6-12% pts +concurrent encephalitis necessary to continue antitoxoplasmic therapy for the life of patient do NOT use corticosteroids due to risk from further immunosuppression 4Pneumocystis carinii choroiditis 5HSV 6Mycobacterial and Gm + 7Kaposi's sarcoma 8molluscum DNA poxvirus 9Cryptococcosis tap with India ink prep 10HZO
end of summary uveitis
Parasitic worms larva causr prolems
Toxoplasmosis
T. gondii ~~~25% uveitis in IMC &~~~congenital (1:10,000)
3C's: Convulsions, Ca+2 on x ray, Chorioretinitis most commonly bilateral
highest risk of infection in first trimester
acquired reactivation in IMC
often subclinical, may have fever, rash, hepatospenomegaly
from cats, raw meats, dusty environments
signs/symptoms
classic sign of focal exudative retinitis adjacent to old scar usually in posterior pole
retinitis = active organisms, all else immune rx (except in AIDS, where pt can have infectious choroiditis)
segmental periarteritis near lesion, o/w diffuse venous sheathing
vitreal precipitates, satellite lesions
punctate outer toxoplasmosis has only small punctate peripheral retinal lesions
50% of population is sero+
ANY positive titer (Ig G) is significant (test in undiluted serum) in a patient with suspicious lesions
atypical deep yellow lesion, massive granuloma>6DD CNV, ERM, RD
RX
rx if Va has decreased > 2 lines because of vitreous cells, macula (within the arcades) or optic nerve threatened (within 1/2 DD), or if immunosuppressed
follow WBC and platelets weekly
in immunocompromised individuals, chronic suppression treatment is needed
Quadruple therapy:
pyrimethamine (Daraprim) 150mg PO load then 25mg PO QD x 1 to 6 weeks
sulfadiazine 4gm load then 1gm QID x 3 to 6 weeks (caution re: kidney stones, Stevens-Johnsons)
clindamycin 300mg PO QID (caution re: pseudomembranous colitis)
prednisone 80mg PO QD or QOD tapered off in 3 weeks
may substitute Bactrim or Septra as alternative to above therapy
if using pyrimethamine (Daraprim), don't use Bactrim or Septra as the sulfa component of the therapy because the trimethoprim interferes with the action of pyrimethamine
add Folinic acid 3gm IM 3x a week or 5mg PO QD if on Daraprim > 1 week as it generally prevents the leukopenia and thrombocytopenia that may result from pyrimethamine treatment
Toxocariasis
worm of cats that may be transmitted to man and other animals byeating ova that hatch in the gut and cause visceral larva migrans
Toxocara canis children and young adults with normal WBC and no systemic eosinophilia 10% with positive serology have it
ova and parasites in stool specimens are negative in ocular toxocariasis
3 recognizable ocular syndromes:
1chronic endophthalmitis 2-9 years old white eye, cyclitic membrane, RD, CME, cataract
2localized granuloma 6-14 years old yellow white 1-2 dd elevated lesion posterior pole stress lines, hard exudates, minimal reaction
3peripheral granuloma 6-40 years old with retinal folds dragged macula, RD, dense vitreous bands can mimic snowbank rarely bilateral
atypical optic neuritis, motile worm, diffuse chorioretinitis conjunctivitis, iris nodules, keratitis
treatment steroids if inflammation when worm diesNO benefit to treatment with antiparasitic agents like thiabendazole may need vitrectomy to clear the media and decrease vitreous traction
Onchocerciasis===iridocyclitis, microfilaria, posterior synechiae, cataracts, peripheral anterior synechiae, glaucoma, choroiditis
Onchocerca volvulus river blindness
Cysticercosis===subconjunctival "dermoid", vitreal cysts, endophthalmitis
Taenia soliumpork tapeworm, intestinal parasite that spreads hematogenously to the eyesubretinal larvae can be destroyed with laser or surgery stool O & P, r/o systemic involvement with CT, LFTs death of larvae ( severe inflammatory reaction surgical removal of vitreous larvae via PPV
Fungal
Candida albicans===string of pearls, multifocal retinitis, may mimic toxoplasmic choroiditis: lesions originate in retina and result in exudation into vitreous
ketoconazole, Amphotericin may add PO flucytosine, fluconazole, rifampin
Histoplasmosis
1POHS===classic triad is punched out peripheral lesions ("histo spots"), peripapillary atrophy, and an asymmetric maculopathy
histo spot teens & macular lesions develop after the second decade NO vitritis CNV occurs commonly
differential includes angioid streaks, choroidal rupture, and idiopathic CNV
don't do skin test, can activate disease
2endophthalmitis
no POHS lesions, disseminated disease
focal retinitis with vitritis, iritis
culture vitreous/aqueous
rx with amphotericin and ketoconazole
3solitary granuloma
chorioretinal location may mimic toxoplasmosis
immune suppressed pts
Viral
HSV, HZO done already!
Acute retinal necrosis===heavy vitritis, peripheral necrosis, vasculitis, RD 70%, in healthy adolescents to older adults after HSV and HZV
2nd eye in 1/4, posterior pole tends to be spared Acyclovir 1500 mg/m2 QD in 3 divided doses x 7-10 days
corticosteroids and immunosuppressives probably contraindicated but corticosteroids probably okay once retinitis and intravitreal inflammation begin to resolve
anticoagulants including heparin and warfarin for 2-3 weeks
post chicken pox (especially adults) with less vision loss, no RD, < 6 clock hrs or retinitis
if the fellow eye is not involved in 3-6 weeks, then it will usually not be affected (but can be involved years later)
CMV===(total) cataract, multiple peripheral lesions with minimal tissue destruction, optic nerve atrophy
Congenital diagnosed with clinical findings, viral inclusion bodies (in urine, saliva and subretinal fluid) and systemic disease findings (fever, pancytopenia, pneumonitis, anemia, HSM)
Rubella=== retinal pigmentation iritis, cataracts, glaucoma & vision and ERG generally normal
congenital: assoc. with MR, congenital heart disease, deafness
Post Viral
Krills (Acute Retinal Pigment Epitheliitis)===rare, young adults, sudden decrease in vision with 2-4 gray spots with yellow white halos seen in macula
with resolution, spots may increase or decrease but halos remain completely resolves over 6-12 wks but residual scars may ( central serous choroidopathy flourescein angiogram: active center spots, halos -
HIV
Approach to HIV
summaryThe most common pathology is due to HIV itself and looks like DM The most common infection is CMV and cuases blindness in 6
months Look for brush border fire at margins of atrpohic scars.ARN necrosis appears after Zoster and is a quiet deep circular necrosis
more common in the periphery Toxoplasmosis typically has densely opaque thick retinitis with smooth borders and minimum
hemorrhage as compared to CMV Since only 5% have prexisting scars it is a primary infection rather then reactivation PNC cuases
choroiditis if diseeminnated HSV HZV severe severe Panuveitis TB retinits,Karposis sarcoma inferoir fornix Molluscum pox
virus more severe Cryptococcu s severe Panuvitis papplits EOM palsy
hiv
conjunctival capillary dilatation, irregular vessel caliber, granular look to blood column keratoconjunctivitis sicca in 15% subconjunctival hemorrhage but r/o Kaposi's sarcoma rapid myopia can occur
HIV retinopathy
most common ocular finding, found in 50 to 70% of cases multiple CWS along vascular arcades microaneurysms, retinal hemorrhages, and optic neuropathy direct endothelial and neuroretinal toxicity, immune complex deposition
1CMV retinitis
most commonly seen opportunistic ocular infection in pts with AIDS: if untreated, it can destroy the retina within 6 months
diagnosis is clinical as serologic tests and viral culture are of limited value as majority of population show evidence of previous exposure
pay special attention to the border areas of lesions since this is where active retinitis occurs"brush fire" appearance is the most diagnostic as yellow-white margin at the border of burned out atrophic retina If optic nerve swollen,then r/o Toxoplasmosis
fulminant form: posterior pole necrosis along arcades
indolent form: white retinitis with dry granular borders without hemorrhage- common in periphery or in treated patients
often with circumferential spread with sparing of posterior pole until late mild vitritis, anterior chamber rx, slow progression, often with areas of scarring
primary papillitis
white disc with hemorrhage and surrounding necrotizing neuroretinitis
Risk for CMV encephalitis CNS symptoms are unlikely to be caused by CMV encephalitis without concurrent retinitis
2Progressive Outer Retinal Necrosis Syndrome ====2/3 deep multifocal retinal lesions (peripheral>macula) progressing in a circumferential fashion sparing the retinal vasculature occuring rarely infection in AIDS pts who present with decreased Va can occur in the absence of, concurrently with or subsequent to a cutaneous zoster infection
minimal anterior and posterior cellshistory of cutaneous zoster
3Toxoplasmosis
it is a parasite of dogs and exists as actively reproducing form trophozoite and quiet tissue cyst bradyzoite and a resistant sporocyst excreted by dog.
man can get by eating meat with bradyzoites eating faecse infested spopzoites & tranplacental trphozoite spread
to distinguish from CMV, toxoplasmosis typically has densely opaque thick retinitis with smooth nongranular borders and minimum hemorrhage
inflammatory reaction in choroid, retina and vitreous is less than in pts with an intact immune system
preexisting scars are only present in 5% of AIDS patients, so probably represents primary infection
no prior scars bilateral in 1/3 multifocal vitritis +IgM to T gondii in 6-12% pts +concurrent encephalitis c/o blurring anterior chamber rx peripheral white retinitis lesions larger in AIDS pts RD tears
can present with diffuse areas of necrosis,
usually respond to pyrimethamine with sulfadiazine, clindamycin, or tetracyclines (caution with bone marrow toxicity)
necessary to continue antitoxoplasmic therapy for the life of patient do NOT use corticosteroids due to risk from further immunosuppression
4Pneumocystis carinii choroiditis
rare but if choroiditis is present, systemic dissemination also present more common when aerosolized pentamidine was Rx of choice for PCP bilateral oval pale multiple choroidal lesions 1-3mm (Arch June 89) minimal inflammation with lesions in posterior pole and periphery slow growth over months with little effect on Va choroiditis tx requires hospitalization for a 3 week regimen of IV trimethoprim (20mg/kg body wt per day) and sulfamethoxazole (100mg/kg body wt per day) or pentamidine (4mg/kg body wt per day). within 3-12 weeks of tx, most of the lesions disappear leaving mild overlying pigmentary changes
5HSV
prolonged course fibrinoid anterior chamber with hypopyon, vitritis, phlebitisyellow white retinitis outside the arcades and gray-white geographic deep retinitis in posterior pole
6Mycobacterial and Gm +
organisms also have been dx as causing retinitis
7Kaposi's sarcoma
inferior fornix most common site but can have orbital mass, lids involved stage 1 and 2 are flat (<3mm height), patchy, and less than 4 months duration stage 3 lesions are nodular and of greater than 4 months duration
8molluscum
DNA poxvirus larger, more rapid, more numerous and more resistant to standard rx
9Cryptococcosis 1/2 of pts with meningitis have ocular problems usually in posterior segment, but can be iris nodule with severe anterior uveitis optic nerve edema, optic nerve atrophy, EOM palsy, VF defects, uveitis perform anterior chamber tap with India ink prep
10HZO increased incidence
Pars Planitisbilateral (80%) young patients association with MS, HLA-DR2
vitreous snowballs (cellular aggregates) +/-inferior snowbanks (fibrovascular exudative changes of the inferior pars plana) in at least 30% snowbank is correlated with more severe disease
CME is major cause of visual loss; others PSC cataracts, preretinal and subretinal neovascular membranes and vitreous hemorrhage other signs of low-grade AC rxn, minimal post synechiae, band keratopathy, retinal phlebitis, KP with local corneal edema, NVD, NVE, retinoschisis, tractional RD NVD often responds to steroids F/A: diffuse peripheral venular leakingaac typically is chronic with remissions and ultimately burns out r/o sarcoid, syphilis, MS (found in up to 5%), Lyme disease (+ anterior chamber rx)
Rx mild cases without macular edema and not bothered by floaters (30%) no treatment is necessary steroids usually treat macular edema with posterior deep sub-Tenon's depot corticosteroids may need 3-4 subtenon's injections if Va less 20/40, then PO chronically after 6 months of steroids, probably irreversible CME immunosuppressives cryotherapyfor severe cases unresponsive to steroids (30%) with significant vitreous haze and CME single freeze thaw of inferior snowbank with contiguous uninvolved retina (1/3 width of snowbank) avg 20 freezes per eyegive posterior subtenon's injection of 40mg depomedrol and topical steroids post op laser may be less traumatic than cryo vitrectomy may be needed to treat severe visual loss caused by dense vitreal veils, hemorrhage or traction
#Fluorescein Angiography FA & other diagnostic modalitiesSlit lamp
Scleral scatter=aim lateral light beam at limbus and is transmitted by TIR in cornea
Retroilumination
Direct ilumination & Lateral ilumination
spectal illumination
FA
Fluoresceincolors white and is seen the periphery of bv as apoosed to Color phtogaphs that show central RBCs ofbv
Rules
Fluoresceine is bound 80% to plasma and can be taken orally
outer blood retinal barrier and major choroidal blood vessels impermeaple but Choriocapillaries allow a liitle across Bruchs into sub RPE space
inner blood retinal barrier impermeable
fluoresceine
triphenymethelene
light emmision ceases when light stops
emits green yellow light
Hb absorbs excited light
excitaion 475nm blue emmision 525nm yellow
photography xenon light source blue light barrier
technique
Normal angiogram
1st choriodal and cilioretinal artery uneven choroidal fluorescence is normal
Methods of examination use 20D in cinics to see slides against light box
Drusen
degree of fluorescence of drusen~~ low lipid content ->susceptable to subretinal neovascullarization usually soft
soft are water loving and cause neovasculiraztion
SRNM=== fibrovascular tissue originating from choriocapilleris thru defects in bruch to sub rpe space to sub retinal space and causing or may cause RPE deytachment
Bruchs membrane defects cause hyperfluorescence as more fluorescene
Variants of normal
1 rection in background fluorescence in a balck person vs increase background fluorescence in albanoid fundus Large cilioretinal artery Artefacts Autofluorescence eg some optic nerve drusen
A Hyperfluorescence
1Leakage implies bd of blood retinal barrier and is characterized by fluid in the sensory retina and spread of hyperfluorescence with INDISTINCT bouderies
2Pooling in below Rpe or subretina space or intrartinal spaces in RPE detachment homogenous appearence and boundaries remain unchanged.eg between RPE and neuroretina in CSR spreading hyperfluorescence,cystic spaces of neuroretina in CMO
3 Staining taken up and retainedeg it is normal for lamina cribiosa sclera and bruchs staining of optic disc is normal as well as sclera after choroidal rupture &scar tissue in discform ARMD
4 Transmission or window defect become apparent when choroid fills and fade as it empties
Hyper fluorescence 4 1RPE atrpohy cause window defects 2 Poolling of dye in sub retinal space 3 leakake of dye into sensory retina 4 staining of tissue due prolonged retention
BHypofluorescence
1 Masking or blockage Melaninn or Haemorrhage & Exudation are the 2 most important causes eg Bests These are usually more profound hypo fluorescence than filling defects
2 Filling defects This is either choirdal or retinal defects
Hypo Fluorescence 3
1Dense RPE causing masking due to pigment (xanthophyll in sensry retina or melanin in RPE) or abnormal deposits {haemorrhage, hard exudates lipofucin } 2 Poor retinal or choroidal blood flow3 Loss of blood vessels (choroidemia or myopia)
PATTERNS
RPE detachment
CP~~~see extent of detachment
AV~~~ increase as dye pools under
LP ~~~well circumscribed and now now increase in fluorescence
Classic SRN
CP~~~cartwheel or lacy specific membrane seen
AV~~~ leak in to subretinal space
LP~~~ late hyperfluorescence as leakage into sensory retina
CSR
AV~~~small spot becomes->smoke stack appearence = vertical filling
LP~~~ umbrella horizontal
CMO
LP~~~flower patel = pooling into cysts that persists
Macula hole
AV~~~punched out RPE window defect
BVO hyperpermeability
AV survivng blood vessels totuous and dilated little capillaries closure
LP increased fluorescence from damaged inner blood retinal barrier
foveal ischaemia
EP details of capillaries bed obscurred by haemorrhage
LP inspite of haemorrhage there is closure of capillaries above FAZ non ishcheamic
DR
BDR mild microaneurysms fluorescent dotshaemorrhage small patches maskingsmall patches non perfusion or leakagewidened inter capillary spaces & capillary dilationcotton wools spots correspond areas of capillary non perfusion
Ishceamic maculopathy nn perfuion related to cotton wools spots
CSMOsee haemorrhage microaneurysms exudates
+ ***Remeber this leakage from perifovealar capillary bed = Petaloid pattern of CMO
Pre proliferative DR Cotton wool spots blotchy haemorrhagethis is subtle but the game is given away by non perfusion of the entire periphery~~~non perfusion
proliferative
florrid neovascularization and peripheral non perfusion
photocoagulaion scars~~~ areas of hypo fluorescencelate
e from disc neovascularization~~~ intense laekag
ARMD
Drusen larger drusen ~~~~~~~~exibit hyperfluorescence and will continue throughout as absorb fluoresceine.
small drusen ~~~~~~~~~~~~~will exibit fluorescence but tend not to absorb and hence loose huper fluorescence
RPE atrophy ~~~window defect
RPE increased pigment ~~~masking
Geographical atrophy =indicates loss of choriocapilleris & RPE~~~~~window defect with notiable large choroidal vessels & no spread beyond bounderies NBGeogrphical atrophy may spare the central fovea and this must not be confused with SRN
dilated parafoveal capilleries & leakage into intraretinal cystic spaces~~~~patteloid pattern
assosiated CMO & SRNM ~~~~~~~~classic pattern of SRNV & later the patteloid pattern with the central bud of the flower diappearing as pooling occurs from SRNM
SRNM has typical ROUND or LACY to COTTONWOOL pattern
EP~~~~discrete neovascular frond under fovea ROUND that become more intense and confluent as dye leaks LACY
LP ~~~extends beyond bounderies as it leaks into SRS COTTONWOOL
Exudative RPE detachment The characteristics are in between geographical atrophy and SRNM
EP~~~there is early masking of choroidal fluorescence and the round distinct margins of the RPE detachment defined.
LP ~~~lesion becomes intensely fluorescent without loosing borders. The above may be complicated by SRNM hence irregalr fillingor increase pigment hence maskingor tears of RPE presenting as window defects
Bests
yellow dome~~~~~~~masking at macula
pseudohypopyon =yellow exudate accumulates inferiorly~~~~~~~~~~window defect and masking inferiorly
SRNM & RPE atrophy or fibrosis~~~~~~~~~~~~~~~~~easy!
Adult fovemacular viteeliform dystrophy
yellow exudate ~~~~~masking
atrophy~~~~~~~~~~~window defect
ring of parafoveal RPE atrophy~~~~~ window defect
Stargardts & Fundus Flavimaculatus= fundus with yellow flecks
Pale flecks at level of RPE usually with atrophy of macular
atrophy~~~macular window defect
flecks may be ~~~~hyperfluorescent or hypofluorescent
Rest of Fundus RPE with lipofuchcin deposits~~~masking or silent retina
Macular holes
1st & 2nd stage ~~~~~~~non specific
Full thickness hole causing RPE atrophy + small amounts drusen~~~~~~~~~~~~~~~~patchy central window defect
Epiretinal membranes=pucker=cellophane=prerinal fibrosis
disc vessels straightened and dragged centrally~~~ same!
irregular capillary leakage ~~~~~~~~~~~~~~~~~~~same!
Choroidal folds
crests & troughs ~~~~~~same
Indocyanine green
low fluorescence and difficult to image
longer wavlength absorbtion and excitation (805nm & 835nm) that is less absorbed by RPE and therefore greater visibility of choroid.
completely plasma bound therefore will not leak out of vessles it useful to look at the choroid in SRMN in ARMD.
BUT normal FA is needed to assess leakage in SRMN iofARMD.
Scanning Laser Ophthalmoscope
Revolution because it reqiures low irradiance and small aperture because it uses sensitive light detectors and they is high collimation of beam
requires only 70uW/cm of irradiance vs 5000 of normal camera
Can use fluoresciene & ICG
3d digital construction possible , less scatter less light needed
Only real disadvantage is that it it monochromatic
Amsler
q1 do you see the central black spot q2 corners q3 interuptions in small squares q4 are thelines straight q5 see anything else q6 where do you see distotrions
Lasers
ND-Yag
Laser capsulotomy
power per puncture 1 to 2.5 millijoules
Apraclodipine 1%->Contact lens enlarges cone angle of the beam & diameter of focus is smaller and easier-->aiming beam should be less than 30' with the viaual axis to avoid astigmatism
PI
Settings 4 to 8 mJ depending on color with 2 to 3 bursts per shot and 3 to 4 shots
USE 3 shots of 6mj is average ( 2 bursts)
technique 1% apraclonidine and pilocarpine 2% to achieve miosis-->upper tempporal and find a crypt-->special contact lens-->apply apraclonidine 1% again
laser are uV since they need gh energy
Eximer laser
Argon Fluoride at UV 193nm breaks hydrocarbon bonds
SE superficial stromal scarring
NB 535nm is green 496nm is blue 570nm is red
UV is blue invisible blue light
Shirmers
gently dry eye
-->5mm folded & keep for 5 minutes -->Normal wetting is 15 mm -->Less than 6mm is abnormal->Obvioulsy anaethetict will reduce tearing slightly
Tear substitutes
3 types
a Cellulose derivitives eg tears naturalle
b Polyvinyl alcohol based
and
c mucomimitics
lacrilube petroloeum mineral oil
Mucoloytic agents 5% acetylycysteine useful for mucous paques ans filaments
used 4× daily
In RPE detachments fluid is accumulated between Bruchs and the RPE not deeper
Drug Safe choroamphenicol can cause Optic neuropathy
TC Intracranial Hypertension
Sticklers is an AD that is most common CT dyspasia disease
Retinochisis is common in Hypermetropes
x linked type is assosiated with Cystoid Macular Oedema
Punctal probing soft stop indicates canalicili blocked.
hard stop indicates NLD blocked.
%NeurologyAION
inferior altitudinal defects are commonest
Post chiasmal lesions
The more anterior the more likely the macular is split ie as we get towards the occpital lobe there is less separation
temporal cresent indicates occipital lesion
Tersons
Intrarerinal Hx
ILM hx
Defined as vitreous hx in the presence of intracraial or subarachniod haemorage often due to aneurysm rupture
DDx hypertesive Anaemic Valsalva NAI Purtchers IPCV
skew deviation = one eye is above the other ie vertical difference
due to RMLF ofcajal near cnIII eg parinauds
Optic discs
optociliary shunts imply chronic inflamation shunts between retina and ciliary
Dural shunts are shunts that are small and communicate with with the Cavernous sinus.
This is similar to Caratocavernous sinus except that there will be no pulsation and the vessels on the conjunctiva will be snaky
Reflexes
Rapd 3 reasons wh it my diasppear
vermiform reflexes
whorl pupil
oscilating pupilmargin
%Tumours & PathologyOrbital inflamation masses
Wegen Granulomaosis
Fibrinous
affects orbit sinus and lung
disease ofsmall blood vessels
c ANCA antibodies
Chonic diopathic orbital infmation or Pseudortumour
painless proptosis that must e dfferentiated frm low grade lymphoma
Fungal Phycomycosis and Sprgilosis whis differs in that it causes a granulomatous inflamtion
Tumurs can arise frmo pericyte = large stag horn spaces and often recurs cavernous lymph cappliery
Inherited retinal dystrophies
There are 2 types
those withsyndromes and tose without
Ushers
Bad Bil Dell
Ref Some
Atalipoprtienaeis
Kern Sayer
Pathology 34 slides
Pyogenic granuloma arise from
Cavernous haemangioma mst e diffrenrtiated from vaices and av anomlies that haveno rndothelail ce'lls
Dermoid oriinates from
periguim elastosis is prominent
Moluscum contagiosum looks quite typical
holesteo clefts and ganu'oma ocus after bleeding
mason trichrome macula dydtrophy
ptterigem is defined by resence of e'astin
BCCpalisadin
chalazion granolama
AACG
look for rubosis ans PAS
cyclocryodoid urns if used willcase TM pigmenation
Endophthalmitis
recognise a Neutruphil
sqamos a and aanthamoeba lok very smilar
look for keratiniztion since this is a clue to origin
B ha s fleise ? whorls
FED thikened DM and guttatae
Acqiued melanosis
macula dystrophy or granular mason trichrome
choiooiodal melanoma
sebaceous gland ca often the presence of fat in the cells helps with iagnosis and look for mucin spreads pagetiod in nature
Onchocerciasis
Rx Inovaedtin ecreases parasite load
transmitted black flyMeningioma PathPsammona bodiesage 40 - 50 females > malesDiffuse caused sinus thrombosis
Uveal Melanoma
most common 1' tumour of eye and oculurdermal melanosis inc risk
most commnly at 60
Dx remember phosphorus 32 uptake radioactive phosphorus emits b irradiation picked up by geiger counter which can differentiate from haemangima color doppler differentiate from haemarhage
rx
radioactive plaques containing ý emitting isotopes cobalt & iodine
cyclon generated charged particles
hist epilthleoid worst
also spindle a and b with prominent nucleolus
prognosis
size anterior worse due to late pick up epitleiod worse diffuse growing worse highly pigmented worse older than 65
CB melanoma
ddx medulepithlioma cysts leimyoma cystic adenoma
PR cells have no potential for malignacy only hyperplasia as in Toxoplama scars,etc
hamatoma of the retina and RPE as well as blood can appear black
UM that are : ~~~2mm in size ~~~raised ~~~contain lipufuchcin ~~~or have SRF are dangerous
Rx Plague radiotherapy 106 RU 125 I or cyclotron delivered helium or proton particles Brachy therapy
Drusen is often assosiated and appears white NB The may not be black. All white masses are assumed to be secondaies
AI patholgy classification
TypeI disorders Hayfever
Type II Ocular cicatricial pempigoid
paek onse at 70 years and 0 will have systemic signs including pharyngeal strictures blisters onscalp ans limbs assosiated in 6% with AIlike SLEPAN CF Loss of plica and caruncle and retcular fibrosis of tarsal conjunctiva
RX Injection of Mitimycin Moderate Dapsone Sulpyramide Severe Cyclophoamide steroids
Type III Marginal Keratitis,
Rheumatiod Melt RXMild topical steriods Moderate Mehtotrexate Severes Cyclophosamide ad oral cteriods
Type IV Atopic KC and Vernal KC
5 stypes according to corneal changes
PEE
microerosions
plague
subepithelial scariing
pseudogerontoxon
#PaedetricsApproach to Aniridia
1 in 100 000
have macula (hypoplasia) Lens(cataract subluxation microphakia) glaucoma (40%) and Corneal(pannus hazy)
involvment
3 types 1 85% AD incomplete penetrance and only eye involvement 2/3 hae normal parents 2 sporadic 11p deletion with Wilms and Urinary disorder and MR( with MR we call it =Millers) 3 very rare AR with cerebellar and brain anomalies on CT but normal macular=Gillespies
Approach to blindness
Secondary nystagmus only starts at 2 to 4 months
Pupli respones is there from 31 weeks gestation but is difficult to see in infants because of smll pupils
VA new born 20/1000 but 1 month already 20/600 4months 2/200 and 1 year 20/50
by 3 years atleast 20/40 and needs to be evaluated if more than 1 line diffrence in snellen
at 6 weeks fixates and follows
Most babies with blindness will have a detectable clinical cause
approach
WITH NYSTAGMUS the nystagmus is seaching if severe eg optic nerve involvment and pendular if some fixation eg foveal hypoplasia
SEARCHING1 LCA(normal fudus becomes pigmented evetually) 2
Optic nerve hypoplasia often ass 1 sagital midline defects and hyppit & can be reversed with rx 2aHydraenceph ancep 3 drugs quinine anti convulsives 4 maternal diabetes
PENDULAR
3 OC or O ablinism
4 Juvenile Retinichisis
5 Achromatopsia =cone dystrophy
6 CSNB
No Nystagmus ( breakup into normal and abnormal clinical findings
1 Refractive errors 2 Cortical blindness sec to perinatal asphyxia with developmental or seizures 3 Ocular motorapraxia =failure to elicit saccades on command but may be present by reflex. The child is thought to be blind because of lack of response esp in first few months when horizontal head jerks not yet developed NB patient can see but we don know! usually congenital but can be aquired 4Delayed Visual maturation DVM usually catch up by 6 months commoner in prems and babies with other ocular abnormality
VA teste preferencial looking
hundreds an d thousands at least 6/24
DUANES cant abduct and retracts on adduction
BROWNS cant elevate on adduction
Duanes
paplapral fissue widens in abduction and narrows on addcution.
Cause congenital cocontracture of LR and MR
20% Bilateral associations:Deafness Speech disorder congenital defects (Pseudo Duanes is an acqiured restrictive codition due to adhesion of any muscle)
Browns=so contracture ie does not allow io to work!
No elevation in adduction and Normal elvation in abduction
May widen p.fissure on adduction=opposite to duanes
other features v pattern cause congnital and 10% bilateral
due to SO trochlear trauma or inflammation
RA & trauma can cause Browns
Sqiunts
examination corneal light reflex
pupil border is 30 diopters or 15 degrees [ 1 degree is 2 diopters and limbus 45 1mm pupil is 9 diopters
cover uncover used to find heterotropia
alternate cover uncover: 2seconds covered and then qiukly uncover and look at the same eye
used to pick up heterophoria
Infantile esotropia
Congenital Esoptropia is assos IO overacttion and A pattern or DVD Left side is more common so they will look tothe Left onset after 2 years disturbance of downwad movement and disturbamce ofvergence
Assessment
Look for amblyopia , the squint A or V cyloplegic refraction and reinoscopy.
when? 1st 6 months
look for the nystagmus and if it dampens on convergence it is an entity called nystagmus blockage syndrome.
Rx usually at 2 years old and recess both MRAim alighmnet to within 10 D
complications 1 Overcorrection 2 A pattern due to IO overaction which will become bilateral within 6 months! 3 DVD which is characterized by updrift with excyclodeviation UNDER cover which will normalize after mostly bilateral but can be unilateral
Rx SR recession +- Faden procedure (Find out!!! 4 Amblyopia in 40%! 5 accomodative problem suspect if start to reconverge Accomodative esotropia Synoptophore is best for cylodeviations DVD is characterized by updrift with excyclodeviation 12 oclock at 9 o clock UNDER cover which will normalize after
Forced duction test
DIFFERENTIATE restrictive FROM neurological
Method
Amethocaine
Grasp insertion of muscle and move in direction of action
compare with normal side
Positive IF diificult to move ie entrapment or fibrosis
Negative if freely mobile
Kid scataracts
prpeller Fabrys
presenileNeurofibromotis typeII
lammelar or nulear Rubellas
#Phacomatoses
Von REck
Cafe a lait neurofibroma skin brain skull neurofibroma
eye~~~orbital ne
durofibroma gliomas
Sturge webers
port wine along 5th nerve capillary haem
eye~~~choriodal haemangioma and glaucoma scleral haemangioma
Tuber sclerosis Bournvilles
Brain stem glioma face sebacous adenoma butterfly astrocytoma
eye~~~optic gliomas mullberry optic disc retina nodules
Von Hippel laundau
brain haemagniomas assos with RCC
eye~~~retinal haemangiomas and large feeders can bleed and RD
Congenital Anomalies
megalo=l diameter >13mm, X-linked
r/o glaucoma, increased risk factor for ectopia,??? cataract, glaucoma rarely associated with renal cell cancer, r/o congenital glaucoma nl endothelial density F carriers may have slightly larger
micro =l diameter <10mm, hyperopes (because is flat) AD>AR20% with angle closure glaucoma, usually eye nl
r/o nanophthalmos, microphthlamos, trisomy 13, Ehlers Danlos, dwarfism, fetal alcohol syndrome
Anterior segment dysgenesis=a broad spectrum of developmental anomalies invloving migration of the mesenchyme of neural crest origin
main defects localized to angle
eg schalbes line displaced anteriorly or gysgenisis or embryotoxin posterior defects in descements
iris processes iris atrophy iris adhesions iris stromal opacities
lens absent
axenfelds ~~~~angle anomalies
reigers ~~~~~~with iris involvment
peters~~~~~~~with corneal involvment +/- lens in type 2
Axenfeld anomaly-Reiger syndrome:
Axenfeld thickened, centrally displace schwalbe's line posterior embryotoxin plus prominent iris processes
Rieger's anomaly: posterior embryotoxin, = detached descements membraneand prominent scwelbes lime
prominent iris processes, plus iris stroma atrophy
Peters
clearing of leukoma with waiting, glaucoma
Type 1- unilateral defect in descemet's membrane, central l stromal opacity, nl lens and no systemic involvement
Type 2- bilateral lens involved, bilateral, often glaucoma
r/o von Hippel's internal l ulcer (no lens abnormality) and local posterior keratoconus (endothelium/descemet present). Neither are assoc. with iris adhesion.
Haab's striae=breaks in DM horizontal on buphthalmos
associated with congenital glaucoma * striae are horizontal opposed to striae associated with forceps injury during delivery, which are vertical
Congenital opacities
facets, nebula, macula, leukoma
l keloid probably from intrauterine trauma
sclero =peripheral sclera-like opacification of the results from defect in mesenchymal migrationbilateral, often with systemic and other ocular problems nonprogressive, sporadic, AR (more severe) or AD
#Orbit/Plastics LidsEntopian
Cautery thru skin below lashes
Transverse lid everting sutures
Weis procedure
full thickness horizontal id split and everting sutues
Fox procedure base down conjunctival and tarsal excision
shorten lower retractors
Upper lid split anterior lamellar with lid split
1Make a lid crease cut and separate under OO to lashes
2split lid at grey line
3 Pull up anterior lamellae to get adequte eversion
4 Pass 3 6 0 vicryl thru skin and OO 1to2mm above lashes and attach 3 to 4 mm superiorly to Tarsus ad back to skin and tie outside
Pearls aim for overcorrection ie pull the anterior lammelle high
Ectopian
Ziegler Cautery puctures 5mm below puctum
Medial Conjunctoplasty excise diamond piece of tissue 8mm long parallel to canaliculisand 4mm high
Lazy T in addition to above a full thickness trapezoid excision adjacent base up
Bick procedure Larger trapezoid excision at lateral canthus that may be combined with z plasty
Ptosis
types Neurogenic Muscular Aponeurotic(=skin crease is high or absent )and mechanical
CF
measure interpalpable fissure, torch lite to lid margin levator function while excluding frontalis and look at lid crease distance to margin
Palpebral fissure normally 27-30 mm long, 8-10 wide
Normal LPS can raise upper lid 15 mm, frontalis adds 2 mm
THis in clinical language!!
1 Marginal reflex distance(MRD)which normally is 4.to 4. mm 2mm or less severe 3mmmoderate 4mm normal
2 Vertical fissure height normal M 7 to 10mmf 8 to 12
3 upper lid excursion place thunb on brow to negate Frontalis normal levation from straight is 12mm poor is 5mm
4 upper lid crease measure in down gaze distance from margin to crease female 10mm male 8mm
low crease means ABnormal Levator function
x Fasanella Servat procedure fascinate!
excision of uppet border of tarsus with lower border of MUllers and overlying conjunctiva.
Indications
good levator function eg horners and othe mild ptosis with no apeuneurotic defects
Levator resection
mderate to severe ptosis
Frontalis bow suspension using a sling of fascia lata to attach tarsus to frontalis
severe ptosis
Tolosa Hunt==grnulomatous inflammation of cavernous sinus
CF recurs & remits vs
Pseutotumour==non specific orbital inflammation usually 20 to 50 years old
CF variable course including progresive fibrosis or frozen orbit
Bilateral involvement occurs more commonly in kids and if in adults think about sytemic diseases like TB S WG PAN SS Waldestroms If the sinuses are involved it is unlikely Pseudotumour so remember it is an orbital inflammation.Rx oral steroids ie prednisolone 60-80 mg daily DXT and cyclophosamide may be bilateral in kids Dx is often response to steriods DDx Lym/Leu Thyriod Orbtal cellulitis
FBC shows leucocytosis and biopsy shoes PMNs plus Eiosinophils
Orbital Myosis
Bacterial & Fungal
Thyroid dsease
examination
no specs
Optic nerve compression va color ishahara optic pallor posterior folds external compression lid lag look down lid retraction
lid retraction or proptosis causes scleral show
exophthalmometre lateral canthus to lateral canthus
if difference > 2 usually 16
ocular motility diplopia pain and fatique
exposure
sensation
superior limbal conjunctivitis sign look for PEE using rose bengal
conjunctivitis
injection along recti gowers
#To be filed MIscellanous just to readFundoscopy
HT arterioles straighter
CRVO more tortuose
Women higher risk cad if pronounced ht retinopathy
Inner or commonly called superficial haemorages are flame shaped
Choriodal infarcts present as Elschings spots l!ook for em
Lenticular Astigmatism
PDSKrukenbergs spindle occurs in Pigment dispersion syndrme not pimentary galucoma necessarily commener in myopes
Rhabdosarcoma extra conal growth therefore non axial proptosis not familial
Pseudotumour = T= TUMOUR T= TENDON
develop lymphiod hyperplasia in 20% and the muscle tendon is characteristicly involved in contrast to Dysthyroid eye disease which is not thyroid is a non tender! Disease
DED inferior rectus most common
Vogts limbal girdle is a degenartion
SLE does not cause any corneal melts
Keratoconus
Munsons sign lower eyelid protruberence
Fleisher rings inferiorly
Refsums is caused by Excess Phytanic acid
Astroocytosis is assoiated gyrate atrophy
Tersons is Intraocular haemorage secondary to subarachnoid haemorrhage
Keratoconus Hydrops is stable and never ruptures
Conjunctivitis
Pemphigoid not pemphigus causes cicatrisation
foster kennedy is IC mass causing optic atrpohy and paploedema in other eye
Krypton
less scattering, less absorption by blood, & yellow pigments (lens, foveal xanthophyll)
better uptake for choroidal tumors, blue iris
more choroidal uptake causes more pain, decrease accommodation, choroidal edema/hemorrhage
not good for acute hemorrhage during PRP, microaneurysms, blond fundi
really hits receptors, RPE, choroid
higher power needed for same lesions as argon
Rodenstock lens
minifies image, increases spot size
absorbs more energy than Goldman lens, so increase power
note: toward periphery, spots vrbecome smaller and relative power increases
fundus landmarks
Ciliary Artery
Paired long posteror ciliary pierce sclera in front of circle if Zinn and travel in suprachoriod space to ciliary body to form Major Ciliary circle at 3 and 9 oclockShort posterior Ciliary artery 10 -20 pierce sclera about Optic nerve Circle of Zinn supplies Optic nerve head lanmina and preamina
anterior ciliary pierce at muscle insertions
congenitaldefects
extra skin inlids canthus or cloed lids or coloboma
Ankyloble===fusion of lids
Blepharophimosis===congenital tetrad syndrome : epicanthus inversus, telecanthus, blepharoptosis and phimosis
Crytophthalmos===Skin covers all ocular structures
Distichiasis =extra row of lashes
Ectropion usually with Down's or blepharophimosis variation with total bilateral eversion of upper lids in newborns with marked chemosis and prolapse of conjunctiva
Entropion rare, by defn is isolated
Epiblepharon, most commonly asians r/o frank entropion
Epicanthus rare at birth but up to 20% by 2 yo
palpebralis (simple) equal, most common inversus - below, often with other abnormalities tarsalis - above, asians supraciliaris - from eyebrow
Euryblepharon===horizontally widened PF with anterior and downward placed lateral canthus and ectropion laterally
Eyelid Colomboma=== full thickness isolated defect in upper lid at inner 1/3 junction 20% are bilateral
===lower lid at lateral 1/3 often with systemic syndromes, especially AD Treacher Collins lower lid often partial thickness with adjacent margin deformities such as trichi
ERG
terms proximal is nearest photoreceptor
Mass response evoked from entire retina
Types:
Scotopic (rod response; dark-adapted) Dim white flash below cone threshold ( rods = 1000x more sens. to light than cones)
Maximal combined response (dark-adapted) Bright flash > max stimulation of rods and cones
Oscillatory potentials Result of feedback interactions among integrative cells of proximal retina ie near photreceptor
Photopic (cone response; light-adapted) 30 Hz flicker cone response (8Hz = practical limit of rods) Focal ERG Dx organic dz in macula
Bright flash ERG Ascertain retinal function in eyes w/ opaque media
Pattern ERG Correlates w/ integrity of optic nerve Info. about ganglioncells and their retinal interactions ie distal retina
waves
a wave negative wave; photoreceptor potential
b wave positive wave; Muller & bipolar cells oscillations in ascending b wave disappear in ischemia, CSNB
theoretically, ischemic retina would show increased b-wave implicit times and Log K
c wave late +, correlated with RPE, EOG hyperpolarization of apical RPE
x wave bump on b wave in dark adap. bright flash = a wave diagnosis infarcted retina would correlate with b/a wave amplitude ratio and Rmax inversion of b/a ratio or delay in 30 Hz flicker response bodes poorly in CRVO
early siderosis has paradoxical larger ERG responses than normal, which in later stages become subnormal
Electrophysiology
EOGRPE and PR interactions30' lateral excursions
Standing potential and light sensitive potentialArden index refers to lisht peak to dark peak and is normaly 170%RP~~~~~~decrease amplitude in light sensitive potentialPERGN35 P50N95Macular Dz P50 Decreased optic Neuropathy N95 Decreased
VEPERGtest of perpheral retina & distal to GangliaA PR which is supplied ChoriodGlaucoma is disease of optic nerve and ganglion cells so ERG is normal
EOGCompares amplitude from dark and light adapted readings
Arden ratio = largest potential in light/largest potential in dark x 100 (normal > 1.85)
Useful in Best's dz, hydroxychloroquine toxicity STARGARTDS
VEP
N1P1N2P2 to confirm optic neuropathy, albinism
Also used for VA in children, malingering
Ultrasound (U/S)PVD due to trauma/hemorrhage can be differentiated from RD by no attachments to optic nerve, irregular in thickness, cannot be traced to ora, and the amplitude is lower except when beam is perpendicular
new VH can be acoustically clear
asteroid is highly reflective, fills the vitreous which is usually retracted from retina
choroidal detachments are convex, rarely go posterior to vortex veins, and may be anterior to ora
metal/glass FB give shadowing, easier to see with lowering the gain
BB's give comet trail appearance
#NeurologyI. Neuro-ophthalmologic examination II Neuroimaging III Visual pathwaysIV pupil responses VOptic disc disorders including papiloedema & atrophy VI ocuular motility VIInystagmus VIII facial nerve palsies IX Headaches
I. Neuro-ophthalmologic examination
Tests
Photostress recovery test -helps in differentiating visual loss due to optic nerve disease or maculopathy. -bright light is shone for 10 sec at a distance of 2-3 cm. -record time it takes for patient to be able to recover and read at his/her best acuity (or next larger line) on Snellen chart. -recovery time prolonged in maculopathy (90-180 sec) but normal in optic nerve disease (less than 60 sec). -valid only for patients with visual acuity of 20/80 or better.
Spatial contrast sensitivity
-measures contrast threshold using gratings of various sizes and background -elevated contrast threshold may be seen despite visual acuity of 20/20 in diseases such as cataracts, glaucoma, macular lesions, optic neuropathies, and cerebral diseases.
Visual field testing
Confrontation testing
-crude but easy method of quickly assessing visual field
-should usually be followed by more sensitive tests such as Goldman perimetry or tangent screen testing if patient is capable (confrontation may be the only test some patients can respond to reliably).
Tangent screen
-evaluates the central 30° field
-may be useful in identifying small scotoma not detected by bowl perimetry
Bowl Perimetry
Goldmann perimeter
-useful for evaluating both central and peripheral fields.
-utilizes static and kinetic testing
-manual and operator dependent
Automated bowl perimeters
-evaluates only the central field (30° or 60°)
-utilizes static testing
-standardized with statistical evaluation of data
-may be difficult for some patients
Visually evoked cortical potentials (VECP)
-records electrical signals in the cortex generated by stimulation of the retina with light.
-a measure of macular visual function because of the disproportionately large representation of the fovea in the occipital cortex.
-p100 wave - positive deflection that occurs at 100 msec after the stimulus is most reliable parameter to measure.
latency increased in disorders with demyelination as a component of pathology including multiple sclerosis, optic nerve compression, infiltration or toxicity.
amplitutde may be decreased in all conditions that reduce visual acuity.
Gaze and Ocular motility
Nine cardinal positionsRotational testing -involves vestibulo-ocular reflex-useful for infants and comatose patients
Parks-Bielschowsky 3 step test
SO4eye is deviated up and worse when looking nasally or when tilting head to ipsilateral side
In congenital so4 will have and ncreased abnormal vertical fusional convergence of 10 to 15 while in aqiured it is only 3 ie eye cant move up and converge
test for hypertropia
Step 1: Determine eye with hypertropia at primary gaze
Step 2: Hypertropia increases at lateral gaze ipsilateral
( eye in abduction where rectus muscles are primary vertical deviators)vs
( eye in adduction where oblique muscles are primary vertical deviators)
Step 3: Hypertropia increases on head tilt
ispsilateral to hypertropic eye - oblique muscle
contralateral to hypertropic eye - rectus muscle
Maddox rod testing
-for evaluation of tropias and cyclodeviations
-right eye covered with Maddox rod and cylinder aligned in same direction of deviation. (This avoids confusion over the pattern that results from reversing which eye has the rod).
-uncovered eye fixates on light
-red line appears separate from white light when latent (phoria) or manifest (tropia) ocular deviation exists. (Maddox rod brings out latent deviations by eliminating fusion).
-axis and size of deviation determined by rotation of Maddox rod and correction with prism
Alternate prism cover testing
-cover-uncover test used initially to distinguish tropia from phoria
-eyes are covered alternately as patient fixates on a target
-test positive if each uncovered eye move to re-fixate on target
-axis and degree of deviation determined by position and power of prism necessary to halt eye movement.
II. Neuro-imaging
B. Computed tomography (CT scan)-
-provides excellent detail of bony architecture and sites of bleeding (hemorrhage/hematoma)
C. Magnetic Resonance Imaging (MRI)
shows demyelinating changes not visible in CT
-poor in evaluating bony architecture or acute bleeding
T1 - spin lattice time t 1water is dark black one time is a drink!!
(time required for 63% of protons to realign with the magnetic field)
-CSF and vitreous appear dark (high water content) and white matter white (high fat content)
-orbital lesions generally are dark on T1 except blood, melanin, and mucus
T2 - spin-spin relaxation time fat is dark
(time required for 63% of protons to relax while spinning with the plane perpendicular to the magnetic field)
-image opposite to that of T1
MRI diagnosis
1 Optic neuritis~~gadolium enhances optic nerve in optic neuritis due to inflamatory response and permeability
2 MS
III. Visual systemA. Visual pathway
Retinocortical pathway
retina --> ON --> optic chiasm (decussation of nasal retinal fibers)--> optic tract --> LGB --> optic radiations --> occipital cortex
B. Visual fields
1. Nerve fiber bundle defects (unilateral scotomas)a. papillomacular bundle
central scotoma centrocecal scotoma paracentral scotoma
b. arcuate nerve fiber bundle Bjerrum scotoma Seidel scotoma Rhonne scotoma Nasal step
c. nasal nerve fiber bundles Wedge shaped scotomas at temporal visual field
2. Optic nerve -unilateral
-scotoma always extends from the blind spot -respects the nasal horizontal meridian
3. Optic chiasm bitem.poral hemianopia respecting vertical meridian
4. Optic tract contra.lateral homonymous hemianopia
-respects vertical midline (all homonymous visual field defects do) incongruous
5. Lateral geniculate body -rare
congruous homonymous hemianopia homonymous horizontal sectoranopia
6.Optic radiations
a. Meye.r's loop (temporal lobe)-pie in the sky field defect, contralateral homonymous upper quadrantanopia
b. Parietal lobe inferior homonymous quadrantanopia/ hemianopia
7. Occipital lobe (visual cortex)
incongruous respects vertical midline hemianopic paracentral scotoma
-lesion at posterior segment(tip) of occipital lobe
-etiology blunt trauma or severe hypotension (watershed area)
-homonymous hemianopia with macular sparing
due to du,al blood suply (post. cerebral and middle cerebral a.) with occlusion of post. cerebral.
- homonymous hemianopia with macular splitting
-more common
-bilateral homonymous hemianopia with macular sparing
-produceconstricted visual field
C. Disorders of visual integration
Alexia
-inability to read despite normal vision~~~~ angular gyrus dominant parietal lobe
-agraphia =inability toWrite~~~~~~~~~~~~~~~~~ angular gyrus
Visual neglect===patien ignores one side of visual space~~~~~ dominant parietal lobe
Agnosia===inability to recognize objects by sight~~~~~~~v2
Prosopagnosia===inability to recognize face~~~~~~~~~~~~v2
Cerebral achromatopsia===color blindness in one hemifield~~~~~~~~~~~~~v1
Visual hallucinations=== temporal lobe
Palinopsia===abnormal perseveration of visual images~~~ right hemisphere occipito-parietal convexity
IV. Pupillary disorders
A. Pupillary light reflex pathway
photoreceptors --> retinal ganglion cell axons --> reflex relay in tectum ->pretectal nucleus --> pretecto-oculomotor tract --> bilat. Edinger Westphal nuclei --> CN III --> ciliary ganglion --> iris sphincter & ciliary body
B. Afferent pupillary defect
-elicited by swinging flashlight test-normal pupillary response is constriction followed by slight redilation -abnormal response is decreased or absent constriction with redilation or redilation that is larger than when light is swung to other eye. indicator of optic nerve disease which causes light to appear dimmer in the affected eye than in the opposite eye. also seen in extensive retinal disease (eg. large RD), brunescent cataract, and some amblyopes (up to 0.6 log unit density defect)
C. Anisocoria
approach to aniscoria
exclude physiological and CNII then do tests for aidies and horners
most of tome it will be physiological
Definition - unequal pupillary size
1. Physiologic most common cause of anisocoria pupillary size difference less than 1 mm and varies from day to day
2. Third nerve palsy
I anisocoria (mydriasis) associated with ptosis and ocular motility disturbance ~~~~~~~~~~~~~~~~~~~~~seen in intracranial aneurysms (ICA/Post. comm. a.)
II anisocoria that is isolated~~~~~~~~~may be seen with uncal herniation or basal meningitis
III anisocoria during eye movement ~~~seen in aberrent regeneration of CN III
3. Traumatic/surgical 4. Pharmacologic
5. Adie's tonic pupil===characterized by poor constriction to light and brisk response to near
caused by post-ganglionic parasympathetic lesion -80% initially unilateral and more common in females (70%) supersensitivity to diluted pilocarpine (0.05% - 0.1%)-Holmes-Adie syndrome if diminished deep tendon reflex and orhtostatic hypotension also present
6. Horner's syndrome
see section on pupil
D. Light -near dissociation
Retinocortical pathway
retina --> ON --> optic chiasm (decussation of nasal retinal fibers)--> optic tract --> LGB --> optic radiations --> occipital
cortex->Visual calcarine cortex -> superior colliculus->
Pupillary light reflex pathway
photoreceptors --> retinal ganglion cell axons --> reflex relay in tectum -->pretectal nucleus --> pretecto-oculomotor track Bypassing MLF --> bilat. Edinger Westphal nuclei --> CN III --> ciliary ganglion --> iris sphincter & ciliary body
ConVergence
Visual calcarine cortex -> superior colliculus-> pretectal nucleus ->pretecto-oculomotor track Bypassing MLF --> bilat. Edinger Westphal nuclei --> CN III --interneuron CN VI
The difference lies in short circiut in Brain stem. Hence Brain stem lesions preferentially affect pupil reflex rather then accomodation
Keep in mind Supranuclear inputs Visual calcarine cortex to superior colliculus Non-visual frontal eye field or vestibular system (semicircular canals)
Gaze centers Horizontal CN VI / pontine paramedian reticular formation (PPRF) PONS Vertical rostral interstitial nucleus of the MLF (RiMLF) (interstitial nucleus of Cajal) MIDBRAIN
Argyll-Robertson======= pupil poor light response but react to near by small irregular pupils
lesion reflex relay in tectum
Adie's tonic pupil pupil===characterized by poor constriction to light and strong response to near
-lesion caused by post-ganglionic parasympathetic nerve fibre damage mechanism is uncertain but there may be a separate abberent regenerating nerve fibre for near vision in addition to a defective nerve fibre for lightmaking 2 separate tracts to the ciliary muscle 80% initially unilateral and more common in females (70%) supersensitivity to diluted pilocarpine (0.05% - 0.1%)-Holmes-Adie syndrome if diminished deep tendon reflex and orhtostatic hypotension also present
Parinaud syndrome===poor light response and intact near response associated with verical gaze paresis,mid position pupils with nystagmus, and lid retraction with scleral show above limbus;convergence-retraction (of globe)
lesion: reflex relay in tectum =[pupil site ]+ RiMLF=(vertical gaze centre)
The retraction is of lid upwards and the globe inward because the eye cant look up so it tries to to stimulate levator and hence lid/globe
And it tries to converge
V. Optic nerve disordersBlood supply: Optic nerve head: retinal arterioles or cilioretinal artery branches Prelaminar and lamina cribosa: posterior ciliary arteries; terminal arteries with watershed zone Intraorbital: intraneural branches of central retinal artery, multiple recurrent pial branches Intracanalicular: ophthalmic artery Intracranial: internal carotid and ophthalmic artery
A. Optic disc edema
1Features
narrowing of cup with relative preservation of cup depth, obscuring underlying disc margin, retinal (Paton's lines)/choroidal fold
2. Papiledema v. papillopathy
Papilledema ===due to raised intracranial pressure bilateral, MOSTLY
Papillopathy ===due to optic nerve disease (eg. inflammatory & vascular) severe decrease in visual acuity and/or visual field loss
3. Pseudotumor cerebri BIH
-etiology unknown but can occur in COPD, radical neck dissection, corticosteroid use or withdrawal, with elevated levels of Vit. A (renal failure), tetracycline, lithium, and nalidixic acid. initial treatment is weight loss followed by use of Diamox or Lasix to reduce intracranial pressure.
4. Optic neuritis===subacute loss of vision in contrast to sudden vision loss in ischaemic optic neuropathy usually affects young women 2/3 of cases show normal optic disc (retrobulbar neuritis) 1/3 show optic disc swelling (papillitis) MRI shows gadolinium enhancement of the optic nerve and often foci of demyelination in the CNS. Presence of >2 plaques increses risk of developing clinically definite MS within 2 years (up to 39%). 50% of recovered patients may develop transient decrease in vision after exercise or elevation of body temperature (Uhthoff's ootoff!! phenomenon). -long-term risk of developing MS is greater than 60%
-recommended treatment from the Optic Neuritis Treatment Trial (ONTT) study is IV methylprednisolone (250 mg qid x 3d) followed by oral prednisone (1mg/kg/day x 11 days) which hastened visual recovery (slightly) and reduced rate of development of MS within 2 years in patients with 2 or more demyelinating foci. -ddx central serous retinopathy big blind spot syndrome multiple evanescent white dot syndrome anterior ischemic optic neuropathysyphilitic optic neuritis postviral optic neuritis Leber hereditary optic neuropathy (mitochondrial gene mutations) toxic/ nutritional optic neuropathy malignant optic glioma
5. Ischemic optic neuropathy
A. Arteritic===narrowing and thrombosis of posterior ciliary artery supplying aminar and relamnar oDdue to temporal arteritis (a.k.a. giant cell arteritis) treatment is prednisone 60-120 mg/day or IV methylprednisolone.
B. Non-arteritic===idiopathic ischemia of optic nerve assoc. with HTN (50%) and DM (25%); presumed atherosclerosis as basis. -no effective medical or surgical therapy -clinical course shows partial recovery of vision of 3 or more lines within 6 months in 43% of cases.-recurrence rare but involvement of contralateral eye occurs in 25% by 3 years and up to 50% by 10 years.
C. Posterior ischemis optic neuropathy===ischemic damage to retrobulbar optic nerve-often bilateral and simultaneous -rare condition which occurs in setting of severe hypotension or anemia (eg. massive bleeding) or vasculitis (Hayreh)
6. Multiple evanescent white dot syndrome===idiopathic disorder which presents as acute unilateral loss of vision (mild to severe)affects young individuals, females more than males, in association with flu symptoms {see uveitis}
CF blurring of optic disc, and characteristic small white dots (100-200 µm) at level of RPE located perifoveally. Mild sheathing, cells in vitreous, macular granularity, and flame hemorrhages may also be present on fundoscopic exam. fluorescein angiogram shows early hyperfluorescence of the dots with late staining and mild leakage. ERG shows depressed a and b waves on acute sage of the disease but normalizes with visual recoveryclinical course self-limited and visual recovery usually achieved by 8 weeks.
7. Infiltrative optic neuropathy
8. Diabetic papillopathy===occurs in juvenilie insulin-dependent DM no ischemia on fluorescein angiography clinical course shows full visual recovery in 3 months to a year.
9. Dysthyroid optic neuropathy
10. Papillophlebitis (Big blind spot syndrome)=== as mild decrease in vision (unilateral) in young healthy adults clinical course self-limited with full recovery by 1 year.
11. Miscellaneous causes
uveitis, central retinal vein occlusion, malignant HTN, and hypotony
12. Pseudopapilledema
Optic nerve drusen===deposits of calcium, mucopolysaccharides, hemosiderin and amino acids in the optic nerve head often autofluorese usually bilateral (75-80%) and occurs predominantly in caucasians -inherited as autosomal dominant may be associated with retinitis pigmentosa no ????Paton's lines.
Tilted optic disc===one side displaced posteriorly and the other anteriorly. crescent on side of disc depression retinal vessels are directed obliquely -seen in high myopic patients
Optic nerve hypoplasia===unilateral or bilateral small disc has double ring sign (concentric choroidal-retinal pigment changes)etiology unknown but increased incidence in children of mothers taking LSD, anti-seizure medications, quinine, and ETOH abuse.-may be associated with intracranial tumors and endocrine abnormalities.
B. Optic atrophy
1.Compressive
a. Optic nerve glioma ===most common cause of orbital tumors in children (20%) 50% intraorbital and 50% intracranial 10-50% have neurofibromatoses b.Malignant optic glioma (glioblastoma multiforme)===rare form of optic nerve glioma seen primarily in adults c.Optic nerve meningioma -represents 5% of orbital tumors snail tract sign MRI -more common in women than men (3:1) CF usual + remember opticociliary shunt vessels may increase in size during pregnancy not surgically resectable but may respond to radiation therapy
d. Pituitary adenoma
-pituitary apoplexy (infarction) presents as acute loss of vision with headache and diplopia, unilateral or bilateral 3rd, 4th, or 6th cranial nerve palsy,
e. Craniopharyngioma===tumor arising from Rathke's pouch which impinges on the optic chiasm
5% of intracranial neoplasms bimodal peak of occurrence (< 20 y.o. and 50-70 y.o.) presents with visual loss, headache, growth disturbance, obesity, somnolence, or diabetes insipidus may have accompanying psychiatric problems CT shows solid or cystic tumor with calcification
f. Miscellaneous empty sella syndrome Sheehan's syndrome
2.Toxic/ Nutritional
-toxic methanol, lead, ehambutol, chloramphenicol, rifampin, and amiodarone (amiodarone controversial is due to toxic effect of the drug v. AION in high risk patients).
nutritional deficiency :thiamine and vitamin B12
3.Hereditary/Congenital
a. Leber's optic neuropathy===caused by point mutation in mitochondrial gene coding for NADH mode of transmisssion is mother to sons with daughters being carriers of the gene occurs predominantly in 10-30 y.o. males special CF. Venous tortuosity remains indefinitely as a marker but not present in all. avoid use of tobacco and alcohol which may trigger optic neuropathy females may be affected usually milder
b. Kjer dominant optic atrophy===autosomal dominant disorder causing progressive loss of vision onset 5 - 10 years of age
c. Optic nerve dysplasia
optic nerve coloboma====incomplete closure of fetal fissure
-exam shows large excavation of the disc inferiorly
vs
morning glory disc=======rare dysplastic also coloboma of the optic disc appears as a funnel shaped excavation of the disc surrounded by pigmented ring of chorioretinal atrophy usually unilateral and more common in females (2:1)
optic pit==============round or oval pit in optic disc which appears darker than surrounding disc tisssue assoc. with macular edema (50% )
other Barrens 3 types juvenile infantile and at birth juvenile least affected also have retinal pigmentation like RP and other eye features that are more prominent in juvenile type. lipfuscon deposits in neurons PAS + lysosyme storage defect mitichhondrial cause other features neurological eg hypotony MR epilepsy etc Hist vacuolated lymphocytes and PAS + neorons even peripheral
4.Traumatic optic neuropathy
VI. Ocular motility disordersA.CN III1. Nucleus located in the midbrain at level of superior colliculusinnervates contralateral SR, ispsilateral MR, IR, and IO, and bilateral levator palpebrae muscles. Edinger-Westphal nucleus innervates ipsilateral pupil
-lesions are rare and would
cause~~~ bilateral ptosis and paresis of contralateral SR and ipsilateral MR, IR, and IO. Usually also some ipsilateral SR weakness from involvement of fibers passing through involved nucleus from the other side.
2. Fascicle courses ventrally through the red nucleus and exits through the medial portion of the cerebral peduncles
lesions are usually of vascular or metastatic etiology
- causes 4 types of syndromes a. Nothnagel superior cerebellar peduncle~~ cerebellar ataxia b. Benedikt lesion red nucleus and medial lemniscus~~contralateral loss of sensation, brain stem uncontrolled movements (rubral tremor,hemichorea, athetosis, and ballismus)c. Claude ~~ combined d. Weber cerebral peduncle~~~contralateral spastic paralysis
Nonagel=cerebellum
Benedict=loss sensation[ml]/uncontrolled mvment[red nuc]
Claude=cerebellum/basal ganglia/ml
Weber=peduncle spastic paralysis
3. Subarachnoid course
-susceptible to injury by uncal herniation clivas ridge syndrome ie compression against here or post. comm. a. aneurysm nb this is anterior to circle of willis meningeal infiltrative (inflammatory and neoplastic) results in ~~~CN III palsy with pupillary involvement
4. Cavernous sinus
CN III susceptible to injury from carotid-cavernous sinus fistula, aneurysms, tumors,inflammatory (Tolosa Hunt syndrome=inflamation idiopathic of cavernous sinus) and infectious processes:
-results in~~~ CN III palsy as well as involvement of other cranial nerves (IV, V, VI)
5. Orbit -CN III divides into superior division -innervates SR and laevator palpebrae inferior division -innervates IR, MR, IO, iris sphincter, ciliary muscle
6. Isolated third nerve palsy with sparing of pupils due to ischemia of CN III seen in DM, HTN or just old age -occurs in older patients (> 40 y.o.) -self-limited and resolves in 12 weeks vasoasorum obitertaed
7. Aberrent regeneration of CN III:nb the 111 rd cn supplies itself incorrectly
results in :Pseudo von Grafe sign =lid retraction with downgaze -due to innervation of levator palpebrae by IR fibers Inverse Duane's syndrome=lid retraction with adduction-due to innervation of levator palpebrae by MR fibers Pseudo-Argyll-Robertson pupil=light-near dissociation due to innervation of pupillary sphincter by MR fibers Pupillary constriction on downgaze due to innervation of pupillary sphincter by IR fibers
B.CN IV
1. Nucleus -located at periaqueductal gray matter of midbrain -innervates contralateral superior oblique
lesion produces hypertropia causing vertical diplopia as well as ex-cyclotorsion (12:00 position toward the ear)
-ipsilateral Horner's syndrome may also be present due to adjacent descending sympathetic fibers in dorsal midbrain
-etiology includes hemorrhage, infarction, demyelination and trauma/surgery
2. Fascicle courses dorsocaudally and decussates at anterior medullary velum prior to exiting at level of inferior colliculus-susceptible to injury by compression (eg. severe head trauma or pinealoma) resulting in bilateral CN IV palsy
-Bielschowsky test may be negative and requires double Maddox rod test for diagnosis (>10° of excyclotorsion)
3.Subarachnoid course
-long intracranial course traversing dorsal to ventral along the tentorial edge
-highly susceptible to injury from neurosurgery and head trauma
-lesion produces ipsilateral CN IV palsy (or bilateral if anterior medullary velum involved)
4.Cavernous sinus
-located in lateral wall below CN III and above CN V
-lesion produces multiple CN palsy (III, IV, V, VI) and Horner's syndrome
5. Orbit
-enters via the superior orbital fissure to innervate the SO muscle
-CN IV can be affected in orbital apex syndrome
6. Congenital CN IV palsy
-represents 29% - 67% of fourth nerve palsy
-seen most commonly in children but can decompensate later and may present in adults (50-70 y.o.)
-exam shows large vertical fusion amplitude (>3D)
-old photographs showing head tilt help make diagnosis
C. CN VI
1.Nucleus located at the floor of the fourth ventricle below facial colliculus (fibers if CN VII loop over nucleus of CN VI) contains motor neurons that innervate LR but also interneurons that project ot contralateral MR subnucleus via medial longitudinal fasciculus (MLF)
-lesion results in conjugate horizontal gaze palsy
-a Duane's syndrome=congenital absence of abduscens nucleus LR innervated by branches of CN III leads to defective abduction & stimulate CN III when abducting wil also raise the eye and widen fissure ( relativeand narrowing of palpebral fissure from globe retraction with adduction) usually does not complain of diplopia b Mobius syndrome= congenital absence of abduscens and facial nuclei -may also involve CN IX and XII nuclei
2. Fascicle courses ventrally and laterally to exit at the pontomedullary junction
-lesion usually affects other nearby structures :Millard-Gubler sybdrome~~involvement of the pyramidal tract~~-ipsilateral CN VI palsy with contralateral hemiplegia Foville's syndrome~~involvement of CN VII nucleus/fasciculus, spinal tract of CN V, and sympathetic fibers~~horizontal conjugate gaze palsy, facial weakness and numbness, and Horner's syndrome
3. Subarachnoid course courses upward along the clivus and is susceptible to injury by tumors, basal skull fracture, trauma, raised intracranial pressure ("false-localizing CN VI palsy")
4. Petrous pyramid -CN VI passes through Dorello's canal which is bounded by the petrous bone and petroclinoid ligament
-susceptible to injury from petrous bone fracture, tumors, and infectious/inflammatory processes of the middle ear
-Gradenigo syndrome~~~ ipsilateral CN VI palsy, with decreased hearing, facial pain and facial paralysis due to abscess formation in petrous apex following otitis media ie involves CN five to eight
-Pseudo-Gradenigo syndrome~~similar symptoms as Gradenigo's syndrome but due to nasopharyngeal CA or cerebellopontine angle tumors
5. Cavernous sinus -accompanied by post-ganglionic sympathetic fibers
-lesion produces multiple CN palsy (III, IV, V, VI) and Horner's syndrome
6. Orbit enters via the superior orbital fissure to innervate the LR lesion can be involved in orbital apex syndrome
7. Isolated CN VI palsy
- post viral -seen commonly in young patients (<15 y.o.) -neoplasm more common in younger than older patients need to R/O with neuroimaging study
-ischemic mononeuropathy seen in older patients (>55 y.o.) esp. with DM and HTN -self-limited with recovery occuring by 6-8 weeks
D. Multiple cranial nerve palsy
1. Cavernous sinus syndrome ===lesion in the cavernous sinus causes painful ophthalmoplegia, facial numbness, and Horner's syndrome
cavernous sinus is a dural venous sinus which contains the internalcarotid a., CN III, CN IV, CN V, CN VI, and oculosympathetic fibers -various etiology a. internal carotid artery aneurysm b. carotid-cavernous fistula c. cavernous sinus thrombosis d. neoplasm e. inflammation (Tolosa-Hunt syndrome)
2. Orbital apex syndrome=== crowding of intraorbital contents due to tumor, inflammation, infection, or edema from trauma which causes injury to CN II, CN III, CN IV, CN V 1,2, and CN VI
3. Myasthenia gravis
-ptosis is asymmetric and worsens after prolonged upward gaze. Manual elevation of more ptotic lid results in greater ptosis of the fromer less ptotic lid due to Hering's law.
-diagnostic tests
a. Tensilon test -test dose of 2 mg edrophonium chloride (Tensilon) is injected followed by 8 mg slowly injected starting 1 minute later -positive test if ptosis and ocular motility improves -common side effects include diaphoresis, lacrimation, abdominal cramping, nausea, vomiting, salivation, syncope rare but serious complications include bradycardia and respiratory arrestantidote is atropine sulfate (but symptoms are usually over by the time this can be administered) b Sleep test patient rests and closes eyes for 30 minutes -positive
test if ptosis and ocular motility~~~ improves after rest period c.Ice pack test ice pack is placed over closed eyes for ptosis ~~~ improves after 2 minutes because neuromuscular transmission is enhanced in the cold
4.Multiple sclerosis
increasing prevelence further fro equator
affects primarily young adults (25-40 y.o.) and women greater than men (2:1) may present as myriad of neuro-opthalmologic deficits but commonly manifests as optic neuritis,bilateral INO, CN VI or CN VIII palsy, and nystagmus
75% womea nd 35% man with ON will develop MS in 15 years
On ocurs in 70% of MS and is icreased if winter onset HLA dr2 & Uhtoffs phenomenon
CF easy eg decreased VA and color
Px 75% recover in 4 weeks to 6/9 or better but have residual decreased colr and contrast sensitivity
Other motility disorders
INO invoving MLF most common
1 cant adduct (with contralateral eye manifesting uncertainty in sympathy and hence 2nystagmating
3 but normal convergence
explantion horizontal gaze PPcentre near CN 6 and MLF crosses here
Rx steroids ie methylprednislone 250mg IV qid for 3 days with oral Pred 1mg per kg for 11 days speeds recovery
interferon
case with retrochiasmal clinical features ie quadrantanopia
common to have MRI plaques in this area but rare t have clinical features
Dx Visually evoked cortical potentials (VECP)
-records electrical signals in the cortex generated by stimulation of the retina with light.
-a measure of macular visual function because of the disproportionately large representation of the fovea in the occipital cortex.
-p100 wave - positive deflection that occurs at 100 msec after the stimulus is most reliable parameter to measure.
latency increased in disorders with demyelination as a component of pathology including multiple sclerosis, optic nerve compression, infiltration or toxicity.
ON imunomodulatory drugs ABC
avonex IF beta 1a
Betaseron IF beta1b
Copaxone glatramer acetate
have been shown to reduce reurrence rate in MS by 44%
Diagnosis of plaques 2 or more white matter abnormalities on t2 weighted MRI
ONTT summary High dose IV follwed by oral accelerated recovery but no long term benfit to vision
it aslo delayed defintite MS during 2 years but not after 3
5. Thyroid ophthalmopathy
6. Chronic progressive external ophthalmoplegia- === etiology is mitochondrial abnormality in extraocular muscles -usually presents as bilateral asymmetric ptosis before adolescence which progresses to external opthalmoplegia rare diplopia due to symmetric nature may have weakness of orbicularis, facial muscles, arms legs, and chewing serum CK may be elevated EM shows ragged red fibers seen on H&E to be abnormal aggregates of malformed mitochondria
7. Botulism===cholinergic blockade due to botulinum toxin that blocks aCh at NMJ and Para -may be acquired from food, wound infection or birth ocular findings include ophthalmoplegia, ptosis, and dilated poorly reactive pupils systemic symptoms are nausea vomiting, and generalized weakness
Botox 100 units type A avaialablr use 5 u for strabismus and 25u for ocular spasm or plastic surgery
Toxity
Give botulinim antitoxoid im 50000u type a and balso type e 5000u
E. Supranuclear gaze palsy
Gaze centers
Horizontal CN VI / pontine paramedian reticular formation (PPRF)
Vertical rostral interstitial nucleus of the MLF (RiMLF)
(interstitial nucleus of Cajal) near CN III
Supranuclear inputs
Visual calcarine cortex = sensory superior colliculus
Non-visual frontal eye field = motor
vestibular system (semicircular canals)
Horizontal gaze disorders
1there is no lateral gaze -----------------------------------HGP
lesion opposite gaze if supranulear or at ipsilateral gaze centre PPRF
2on lateral gaze medial rectus cannot move------------------INO
ipsilateral MLF
3or on lateral gaze medial rectus cannot move and lateral gaze to other side there is no gaze ----------------------------------------1 & 1/2
Rostal ipsilateral PPRF & MLF
4or both medial rectus cannot move ----------------------------WEBINO
rostral MLF lesion with involvement of CNIII nucleus
1 Unilateral horizontal gaze palsy
-lesion of CN VI nucleus and/or PPRF or supranuclear pathways from contralateral cerebral hemisphere
2.Internuclear ophthalmoplegia (INO)===results in inability to adduct the eye ipsilateral to the lesioned MLF with nystagmus of contralateral abducting eye
-lesion in MLF disconnecting ipsilateral CN III, medial rectus subnucleus from contralateral CN VI / PPRF -usually orthophoria in primary gaze
MS, vertebrobasilar insufficiency, AVM, tumors, and inflammatory diseases (INO is thought to be uncommon from brainstem vascular disease since there is collateral flow to the dorsal brainstem from long circumferential vessels and most lacunes occur in the ventral brainstem in the distribution of the short penetrating arteries medially.)
3 One and a half syndrome
-lesion of CN VI nucleus / PPRF and ipsilateral MLF
-ipsilateral conjugate gaze palsy
-contralateral INO
4.WEBINO===walleyed bilateral INO===exotropia in primary gaze with inability to adduct either eye past midline
lesion at rostral MLF lesion with involvement of CNIII nucleus
5. Fisher syndrome===variant of Guillain-Barre that involves only brainstem and cranial nerves that results in unilateral or bilateral ophthalmoplegia with ataxia and areflexia
self-limited and usually follows a viral illness CSF examination shows elevated protein but no pleocytosis
Vertical gaze disorders 1. Tonic deviation ===upward oculogyric crises occurs in post-encephalitic Parkinsons's disease can also be seen in comatose patients -tonic upgaze indicates bilateral cerebral/cerebellar lesions -tonic down gazeindicates bilateral thalamic bleed or infarct tonic downgaze can also occur in metabolic encephalopathy 2.Parinaud's syndrome===lesion in dorsal midbrain characterized by supranuclear paresis of vertical gaze with intact vestibular-ocular reflexes ptosis light-near pupillary dissociation skew deviation convergence retraction nystagmus etiologies congenital aqueductal stenosis pinealoma head trauma vascular formation long standing multiple sclerosis basilar CVA 3.Progressive supranuclear palsy===progressive conjugate paresis of gaze which presents initially as decreased downgaze associated with progressive dementia and death usually in 5 years-has OKN "drift sign",normal Doll's eye, and normal Bell's response4Downgaze palsy===rarely isolated lesion in RiMLF rostral to CNIII and dorsomedial to red nucleus 5.Skew deviation===lesion in internuclear connections involved in vertical gazeproduces ipsilateral hypotropia in lower brainstem lesionipsilateral hypertropia in pontine and midbrain lesions
VII: Facial nerve
Motor root: muscles of facial expression in four groups of nuclei, upper face receives corticobulbar input from both cerebral hemispheres, lower face only from opposite hemisphere, motor fibers wrap around VI nucleus to form facial colliculus
Sensory root: special visceral afferent for taste, general somatic afferent for sensation from external auditory meatus and retroauricular skin, general visceral afferent for preganglionic parasympathetic to lacrimal, submaxillary and sublingual glands
Pathway
precentral motor cortex (frontal lobe) -->corticobulbar tract -->*CN VII nucleus -->CN VII nerve --> facial muscles
*CN VII nucleus receives bilateral input for upper face but only contralateral input for lower face innervation
1. UMN facial palsy===results in contralateral weakness of lower two thirds of face with sparing of forehead &eyelid closure usually only mildly affected
2. Facial nerve palsy===results in ipsilateral weakness of both upper and lower portions of the face & impairs closure of the eyelids and results in exposure keratopathy Causes
1. cerebellopontine angle tumor (eg. acoustic neuroma) associated with hyperacusis, decreased taste, and involvement of CN V, VI, or VIII 2 Ramsay-Hunt syndrome===herpes zoster in CN VII and CN VIII & diagnosed by finding by vesicles in external auditory canal,
typanic membrane or external ear pinna less chance for recovery compared with Bell's palsy 3 Bell's palsy === unknown but thought
to be auto-immune, viral induced inflammation or ischemic injury may be associated with decreased tearing, taste and dysacusis, and usually pain behind the mandible 84% show spontaneous recovery, but aberrent regeneration may be present (eg. crocodile tears) CN 7 parotid lacrimal closes eyelid expression and taste to poserior tongue
Latest
Bells is viral HSK
Rx prednisolone 80mg per day tapered over 10 days quickly with oral ACYCLOVIR 800mg 5times for 10 days
Esp poor px ie
Old/dec taste/hyperarcus/full palsy
Ocrocodile tears = 7 nerve fibres going to the lacrimal gland rather then parotid when stimuated for taste by the reflex action of taste of the 7 CN greater petrosal nerve normally goes to lacrimal but chordae tympani to submax/man nerve goes to lactmal glan
to treatment is oral corticosteroids to reduce nerve edema and consequent damage 4. trauma/surgery 5. sarcoidosis often bilateral Heerfordt's syndrome of "uveoparotid fever" combines uveitis, fever, parotid swelling and CN VII palsy 6. Lyme disease 7 Leprosy
3. Essential blepharospasm===bilateral episodic contraction of orbicularis oculi
4. Hemifacial spasm===unilateral episodic clonic spasm of the face
5. Facial myokymia===unilateral fibrillation of facial muscles
Phakomatoses
NFtype 1 ~~~~ 2 or more of following:
6 or more CAL,ON glioma intertrigo freckling ,2 or more lisch nodules=iris hamartoma,distinctive osseaous lesions immediate family member, 2 or more neurofibrommas
Type II 1 of following
bilateral Acoustic neuromas
What is a harmatoma:non malignant normal tissue in an inappropiate site
Tuberous sclerosis{ bournville)
Stagnent mulberry like tumour AStrocyte hamartoma of retina or optic nerve that does not cause RD or have feeder blood vessels but may calcify
Critical features Adenoma sebacum= butterflydistribution red papules nad brain astrocyto
Scleral scatter pick up corneal opacities uses total internal reflection
specular illumination aim microcope at angle that biseects light ray that is incident and its reflection and look at diffuse illumination used to see endothelium
Childhood
VA is checked by preferrential looking acuity cards
or The Catford drum
or by STYCAR lettere E test
or Sheridan Gardiner chartor pictures
& the kay picture chart
Hertel thyroid
Hirshprings test estimates anle of heterotropia by corneal
ihght reflex
Angle kappa is the angle between the visual axis and anatomiical axis
normally fovea just temporaal to optical axis and hencc e corneaal reflex just nasal we are slight EXOTROPIA
this is normal and +
TumoursConjunctival tx
Choristioma === tx normal tissue in abnormal location. include dermoid and lipidermoid
dermoid ===skin like tiisuecinsisting of dermis likeconnective tissue and covered by epidermis containing tissue appendage lke hair glands etc etc
lipidermoid ===adipose tissue and dermis like connective tissue and occur in subconjunctica as movable yellow masses esp at limbus or canthus
LASER
ALT
1% Apraclondine
spot size 50um duration 0.1 sec initial power 700mW
Increase stepwise increments of 200mW use 25 burns in one mirror
spot must be round NOT oval
aim at jxn posteroir pigmented and ant white TM
Drugs
Mannitol
1 to 2 g per Kg of body weight
or 5 to 10 mls per Kg of Commercially available solution (20% solution in water
speed of admin not more than 60 drpos per minute acts in 30 minute and lasts for 6 houts
Augmentin 12g tds ivi or kids 5kg 120mg ivi td
ampuoes 1.2g or 6mg vials
%SurgeryGlaucoma Filtarion Sx ComplicationsShallow ACGrade I perpheral iris cornea touchGrade II Entire iris in contact with corneaGrade III Lens Cornea touch
%Diabetes MellitisPDRRxInitially 2000-3000 burns in more then 1 session since a single session has an increased risk of bleedingThe spot size depends on the contact lens usedGoldmann uses 500um but panfundoscopic uses 300-500 um the durartion is .1 to .05 secondsPower is a gentle burnFollow up 4 - 8 weeksMay increase in increments 50 mW until a grey white burn is achievedFlat NVE with fibrous tissue treated 500um medium intensity burnssevere NVd need 5000 or more burns
CSMORetinal thickening within 500um of centre of FAZHard exudates within 500un of FAZ WITH associated retinal thickeningRetinal thickening 1500um in diameter within 1500um of FAZ
%Social OphthalmologyChildhood Blindness
Trachoma rx zithromycin T one a year
Protocol
aacg
500mg ivi diamox or oral
+g timoptol
g predsol
after 1hr pilocarpine 4 3 drops sta a nd then qid
recheckiop after 30 min
if still high 50% glycerol 1g per kgor 20 mannitol 1 to2 g per kg over 45 minute
CRAO
hollenhorst palque=embolus of cholesterol frm carotid artery= bright refractile plaque at bifarcation of arteriole
Diamox 500mg Po stat
timoptol 025% BD
Alkali burns
Vit C
chor
maxidex
cyclo
V. Endophthalmitis
post operative 75%, trauma 5-20%, endogenous 5%
gram+ >60% Staph. epi> Staph. aureus, Streptococci, Bacillus, P acnes, actinomycetesgram- 25% Pseudomonas, H. flu, Proteus, Klebsiella, Serratiafungal 15% Candida most common, Fusarium
Postoperative postoperative rate for cataract surgery is 0.1 to 0.4% virtually all cases are inoculated at time of surgery acute 1 to 14 days after surgery mild have less pain, vision better than 20/400, and present later Staph.
epidermidis is most commonly recovered organism severe usually 1-4 days later marked pain, vitritis, vision worse than 20/400 fundal details are not visible Staph aureus, Streptococci, and gram negative organisms chronic 2 weeks or later after surgery gradual symptoms, good vision, minimal pain, hypopyon, and mild vitritis S. epidermidis most
commonly within 6 weeks fungal usually within 6 months and most commonly Candida P. acnes can occur 2 months to 2 years white plaque with P. acnes and residual lens material found
inside capsular bag there have been reports of endophthalmitis following YAG capsulotomy EVS- Endophthalmitis Vitrectomy Study no benefit in final visual acuity from systemic antibiotics patients with initial Va of HM or better
Posttraumaticposttraumatic rate is 2.4 to 8% in urban areas and up to 20% to rural settings
Bacillus can be recovered in up to 1/3 of these cases and causes a rapid severe infection
Bleb relatedbleb associated is 1 0 yrs, >75% yield + culture, usually bleb intact and organisms penetrate conjunctiva
Streptococci 1/2, H. flu 1/4, P. acnes, Moraxella, Pseudo. cepacia, Fusarium
Vision correlates with virulence of organism and often is poor
Endogenousinfection usually begins in retina with focal chorioretinitis
later, it will breakthrough into the vitreous with vitreal masses overlying the original sites
Candida
often debilitated without ocular complaints
chorioretinitis with multiple chorioretinal white lesions <250 um often in posterior pole
up to 10% of pts with candidemia will develop such lesions
endophthalmitis leading to "headlight in the fog"
nonspecific signs seen with candidemia include retinal hemorrhages, Roth spots, CWS, rare hypopyon, iritis
amphotericin B, vitrectomy, f/u with fluconazole
Klebsiella
endogenous with 90% ending up with Va of CF
1/4 with no known primary site of infection
can happen even when patients are on appropriate therapy
pts at risk are diabetics with liver disease or UTI or in any patient with liver abscess
Diagnosisaqueous: 25-30 gauge needle through the limbus into AC and withdrawing a 0.1ml sample
vitreous: 23-gauge 1 inch needle passed through pars plana 3.5mm posterior to the limbus into anterior vitreous to obtain 0.2ml of undiluted vitreous or do pars plana vitrectomy using tubing set that connects to 10mm collection syringe
inoculate directly onto culture media: blood (aerobic and anaerobic), Sabouraud's agar, chocolate agar, and thioglycollate broth.
in cases of chronic postoperative endophthalmitis, the lab should hold anaerobic cultures for 2 weeks because P. acnes may take that long to grow
RX Gentamicin 100-200 mcg/Amikacin 400 mcg and Vancomycin 1000 mcg
gentamicin and clindamycin 450-1000 mcg (good for P, acne, B fragilis)
Amphotericin B 5 mcg (repeat injections if needed)
alternatives include Ceftriaxone 2,000 mcg, Imipenem, Ciprofloxacin
place 10 cc of fluid from vitrectomy canister into blood culture bottles, aerobic and anaerobic
ceftazimne comes in 1g
dilute with 5ml and take out 1ml we have 200 mg~~~~~NEED 2 millgrams
mix with 10 ml water now 1ml will have have 20 mg
NOW take 0.1ml and inject it and you have 2mg
ciloxin find out but subconj justtake out of bottle
gentacin
come in 40mg packed in 2ml solution
add 1 ml water and take out 1ml
so that each ml has 20mg
add 10ml water so each ml has 2mg
INJECT NOW 0.1ml whichh is .2mg or 200ug which is required
gentamycin comes in80 milligrams in 2ml so 1ml is40 milligrams ~~~~~
GENERAL GUIDELINES FOR TREATMENT OF ALLERGIC CONJUNCTIVITIS
antihistamines levocabastine- 0.05% QID for up to 2 weeks, potent H1 receptor antagonist
mast cell stabilizer lodoxamide- 0.1%, gives some symptomatic relief within two to three days, has some effect on stabilizing eosinophils or cromolyn 4%
nonsteroidal anti-inflammatory acular- 1 drop QID
oral antihistamines (such as claritin 10mg QD)
Uveitis Work Up Guidelineswork up if: bilateral recurrent severe retinal or choroidal involvement
work up of acute iridocyclitis
history is paramount HLA-B27 Angiotensin Converting Enzyme (ACE) often high in kids may be low if patient is on ACE inhibitors elevated in sarcoid but not specific lysozyme CXR FTA-ABS or MHA-TP ?lyme titers
work up of chronic iridocyclitis ANA in childrenACE LysozymeCXRTB Sarcoid HLA-B27 if indicated by histor PPD often not helpful uveitis in North America is rarely secondary to TB may need INH if pt requires oral steroids ?lyme titers
work up of sclerouveitis RF ANA FTA-ABS CXR Sarcoid TB Wegeners ANCA C-ANCA: Wegeners P-ANCA: less specific
Bacterial keraritis
Staph & Strep Pmeumonia oval yellow white stromal suppuration
Pseudomonas sharp ulcerartion mucupurulant exudate and ground glass adacent stroma
E cloi shallow ulcers and ring shaped stromal infiltrates =(corneal rings)
Rx cefuroxime
ciprofloxacin
gentamycin
ciprofloxin 750mg BD
Gram +~~~~~~~~~ cefuroxime like augmentin cover =zinnat ciprofloxacin(= covers MRSA and Pseudomonas that is resistant to genatmycin but poor cover of S Pneumnia)
zovirex 5 times 800mg for 7 days
Gram - ~~~~~~~~~~gentamycin
macular grid 150 burns 0.08 s or 30 mw
0.05 sec
50 um
diclofenac 50mg tds
Crani facial synotosis
craniofacial stenoses
AD synotosis of sutures of thes skull
Crouzens=shallow orbits hence exposure
Aperts shallow
Lateral trachlear collins
antimongoliod slunt rotated orbit
what is velox ? maxidexlike steroid
fresnal prsims
schisi much mre red than normal
congenital retinischisis
CN REvision
CN1 optic 11 olfactory 111 optic iv troclear abducen
v triegeminal mastication sensation face
vii expression cry salivate submax subman taste ant 1/3feels about ear invoves ENT OPhthalmologist and CHEFS
ix salivate taste post 2/3 vagus talk
x1 shrug shoulders
x11 move tongue
CN 6
excycloversion 12 o clock at 2 o clock and elevation
hence verical diplopia and head tilt to opposite side
CN 4 easy
CN 3
PRP 20 um 025 to 03 seconds
036 watts
Retinoblastoma1:20,000 births, becoming more common 6% with FH, 25% have genetic mutation 13q14 with low esterase D levels 1-3 y.o.,nerospecific amulase
present older when unilateral 70% are unilateral with 30% bilateral 1/5 of unilateral on presentation get 2nd eye affected later the differential dx of inflammation is the most difficult leukocoria most common
strabismus inflammation (pseudohypopyon) Ca2+ vitreous seeding normal size globe glaucoma hyphema heterochromia fixed pupil serous RD with dilated vessels
signs different for endophytic/exophytic
metastasis late with spinal cord, bone, skull, lymph nodes, abdomen
assositedpineal gland trilateral tumor with very poor prognosis
up to 50% with secondary cancers especially osteogenic sarcoma, fibrosarcoma, rhabdomyosarcoma many years later
Genetic risk
history determine if germline or somatic germline in multiplex and multifocal cases simplex disease with unifocal RB has 12% risk for germline mutation remember carrier status due to 80% penetrance unaffected parents with one child mutifocal RB have 6% risk for second child examine family for regressed retinocytoma Molecular genetic analysis can find the specific gene mutation using Southern blotting RFLP's to do linkage studies
Diffuse infiltrating RB (1%) likely to be missed occurs later (6 y.o.), unilateral, grows slower
RXchemo etoposide VP16 carboplatin vincristine and cyclosprina result in remarkable regression chemoreduction is given every 4 weeks for 6 cycles until conservative rx possible
it is also used in advanced rx like bilateral cases metastic or intracranial spread
It may be stopped after enucleation is done
Enucleation aim to obtain longest possible Optic nerve studies say it is curative if longer than 5mm so aim for 10 to 15mm in all cases so use a Curved scissor as a tip and ask for it in theatre
also cryptherpy for preeqiutorial tx
Exudative RD covex and
external episceral plaque radiation used in relatively large but localized tumour with or without vitreous seeding use isotopes iodine 125 or ruthenium 106 that target a dose of 40gy to the tumour apex a metal layer on the outer surface of the plague shields emission in other directions
external beam radiation use a linear accelaor 40 to 50 GY given to eye and orbit used when optic disc is involved and photocoaguation is not indicated here there is rapid regression and two scenarios common with or without calcification it is not useful for vitreous seeding because of hypoxia of vitreous
at doses used and the gamma radiaon does not cause major problems like neovascular glaucoma but onlu PSCC which can be dealt with at 6 months later
NB electron beam therapy in contrast is more severe in cloatral damage and other cancers
laser therapy now popular is a diode laser= wavelength in UV spectrum that causes transpuppilary hyperthermia used thru operating micriscope and duration is 1 to 15 minutes exposure
photocoagulation small tumours less than 7mm aim to cut blood supply
CT, MRI: look for calcification, pineal gland U/S: A scan with high internal reflectivity and echo spikes from calcification, B scan with orbital shadowing bone scan, bone marrow, lumbar puncture as needed with massive tumor, enucleation may be primary procedur external beam radiation, Episcleral plaque, Photocoagulation, cryotherapy systemic chemotherapy regression TI cottage cheese TII fish flesh TIII combo of above TIV white sclera 5 yr survival >90%, poorer with metastasis
Histology
Flexner Wintersteiner rosettes -an attempt to make photoreceptors with clear lumen fleurette with outer segs of photoreceptors Homer Wright rosette- lumen with neurofibrillary material, also in medulloblastoma, neuroblastoma pseudorosette-tumor around necrosis viable tumor around vessels with areas of necrosis
Why add cyclodporin?
it switches off p glycoproten that pumps out vincristine etopisife and carboplatin
Coover uncover diiosiateyes that are kept together bybinoculat single vision. and masks a deviation.
focal 50 um spot
0.06 W
.015 secs
Stabismus
V. Vertical Deviation
1DVD 2SO palsy 3Double elevator palsy = cniii palsy no sr or ir action4Brown's syndrome 5Primary SO overaction 6Congenital fibrosis syndrome 7CPEO 8Myotonic dystrophy 9Oculopharyngeal dystrophy 10Skew deviation 11Misc.
1DVD=updrift of nonfixating eye especially with cover -uncover
deviated eye often aBDucts and EXtorts and almost bounces back into position (like SO palsy only abduction rather than elevation)
asymmetrical, spontaneous or with occlusion equal deviation in gazes
etiology unknown, almost always bilateral Usually NO hyPOtropia when hyPERtropic eye fixates Herring's law does NOT apply associated with latent nystagmus, congenital EX measure with base down prism under occluder often becomes evident after EX surgery natural history with resolution in 15-25% diff dx- IO overaction, hypertropia 2SO palsy=Most common cause of vertical diplopia with excyclo and elevation
Longstanding palsies with contraction of IO and vertical concomitance pay careful attention to versions for the diagnosis when fixating with paretic eye, can mimic a SR palsy of opposite side especially in ABDuction (inhibitional paresis of the contralateral antagonist), ptosis Three Step Test
1patient prefers head tilt to OPPosite side with chin depression to minimize diplopia 2 HyPERtropia IPSIlaterally with elevation on ADDuction 3 + Bielschowsky test: head tilt to IPSIlateral side with increased HYPER Do Biechowsky head tilt supine and standing. Often, acute acquired IVth nerve will have normal exam in supine position and hyperdeviation in standing.
Cyclotorsion often worse in downgaze
double maddox rod often less than the true tropia due to sensory adaptation
pay attention only to the net torsion between the eyes
fundus exam gives the true cyclotropia
Congenital long standing head tilt amblyopia uncommon, may indicate absent SO facial asymmetry with affected side being more full can decompensate at later age often with subtle complaints of intermittant diplopia, asthenopia, neck ache with reading no torsion on Maddox rod secondary to sensory compensation may have mild decrease in stereo forced ductions in OR show laxity and it is loose upon inspection
Acquired traumatic, CVA, sinusitis, tumor complain of tilting of objects discrete hx of onset can measure torsion with Maddox rod usually < 20pd of hyperopia in primary ischemic causes usually are in older patients with
5-10 pd of hypertropia forced ductions in OR reveal normal SO of both sides Bilateral uncommon,associated with trauma V-pattern ET downgaze often with chin down posture Double Maddox rod > 10-15 degrees excylotorsion Head tilt shows either alternating hypertropia or is reduced to very little or none can be masked
IVBrown's syndrome
Clinically io palsy =congenital, tenosynovitis, IO abnormalities Decreased elevation on ADDuc usually DEPr on ADDuc + forced duction V[ ie contracture restriction io action] V pattern, straight in primary bilateral in 1/10 r/o IO paresis
acquired watch and wait often resolves trochlear bursiti JRA adult RA sinusitis/surgery blepharoplasty mets orbital surgery SLE post partum scleroderma
there is true muscular overcontraction, so tenotomy does not produce secondary SO palsy be careful if patients have fusion
III. Esotropia
1Congenital Esotropia 2Accomodative ET 3Incomitant ET 4Duane's syndrome 5Mobius syndrome 6Convergence spasm
1Congenital ESotropia=congenital absence of motor fusion characteristics large with V = up out icycloversionOASO with A = down out and excycloversion DVD latent nystagmus asymmetric OKN
Rx treat amblyopia and trial of glasses if > +3.00 surgery by 18 months to achieve single binocular vision (>90%) if surgery after 2 yo, < 1/2 have binocularity Diff Dx accomodative ET Duane's T1 Mobius syndrome neurological abnormalities nystagmus blockage bilateral abducens palsy sensory ET{Nystagmus blockage= manifest congenital nystagmus dampened by convergence both eyes are crossed and face turn may be seen eyes straighten under general anesthesia} variable angles, but nystagmus often disappears with convergence
2Accomodative ES =6 months to 7 yrs, avg 2.5 yrs, +FH
starts intermittent, precipitating illness, trauma amblyopia frequent no diplopia since suppression or ARC
1Refractive=+3.00 - +10.00 D, avg +4.00 hyperopia increases till age 7, then decreases & deviation same distance and near, 20 - 30 pd If delayed RX, may not respond If > +5.00 D, can get bilateral ammetropic amblyopia RX patch amblyopia, full time Rx repeat refraction 2 months post glasses since ciliary relaxation if overcorrected post surgery, try over minus therapy
High AC/A= moves easily without focusing!! & need gasses if near 10pd > than distance is a rough clinical measurement usually
hyperopic (+2.25 D avg, but can be myopic or +10.00) MUST BE ACCOMODATING TO GET FULL EXcan get nonaccommodative EX measurement normal AC/A 4:1 ie 4 diopters convergence per change inpower Gradient method: (ES near with +3.00 lens - ES n) /3 (dioptric distance) Heterophoria method: (PD (cm) + Es near - ES distance)/ D (of near)
RX: +3.00 large flattop bifocals with the segment splitting the pupils bring target close to child and if they reflexively assume chin up posture, then they are using bifocals Diff dx nonaccomodative (stress, cyclic) paralytic sensory deprivation divergence insufficency (ET > dist than near) Spasm of convergence
3Incomitant ES MR restriction thyroid, blowout, post op forced ductions are useful guide to surgical planning VI nerve paresis often with head turn for fusion common in children Check neurological exam, trauma, CT, MRI patch, fresnel prisms, botulinum for diplopia short term Post XT surgery usually improves spontaneously RX prisms, miotics, full CRx, p atch, surgery
Surgery
chances for consecutive exotropia increase with anisometropia, high hyperopia, amblyopia, or cerebral palsy Tablesmay do symmetrical surgery of weakening MR or strengthening LR by same amount OU in adults with >45pd of esotropia, consider three or four muscle surgery to avoid limitation of ductions Note that these are a starting point and should be continuously monitoredrecess-resect may weaken MR and strengthen LR of same eye by reading across table used if one eye has much better vision not as good for large deviations
ET angle (pd)
recess MR in mm
resect LR in mm
<15
3-5 (only one)
15
3.0
4
20
3.5
5
25
4.0
6
30
4.5
7
35
5.0
8
40
5.5
9
50
6.0
10
>60
7
10
4Duane's syndrome= no VI nerve nucleus innervation of LR by III nerve
sporadic usually, but AD in 1/10 F > M, OS > OD (slightly) usually unilateral children rarely complain, present usually with head turn adults complain of asthenopia, intermittant diplopia, and vague discomfort ocular decreased ABduction variable loss of ADduction +/- upshoots and downshoots on adduction paresis of convergence uveal colobomas crocodile tears amblyopia On ADd, PF narrows, globe retracts secondary to activation of LR systemic decreased hearing Wildervanck syndrome deafness, Klippel Feil anomaly (web neck), and Duane's syndrome F>>M Types most commonly, patients have TI Duanes with ES in primary and minimal enophthalmos/leash, willhavegood stereo,the less ES in primary position, the greater the enophthalmos TI: decreased ABd, straight to ET in primary, bilateral 20% TII: XT in primary and limit ADD( this is a funny Duanes) TIII: decreased ABD and ADD
5Mobius syndrome=no abduction mask facies and gaze palsies due to VI, VII nerve palsies, abn PPRF moby dick never looked outwards!
some can also have III, IV, V, IX, X, and XII may have variety of motility disturbances inclding limitation of adduction that improves with convergence fissure changes vertical muscle involvement mask like facies sporadic, although rare AD varients have been reported systemic Poland's anomaly (absent pectoralis muscle) limb, chest, and tongue defects micrognathia, small mouth, hypodontia 15% have MR
7Convergence Spasm= Intermittent ES, miosis, and myopia (accommodation)
Symptoms include headache, asthenopia, diplopia, photophobia May appear to have bilateral VI th nerve palsies, but will have miosis with abduction Functional vs organic (posterior fossa, vestibulopathy, pituitary tumors, diffuse metabolic disease, MS, and trauma) Baclofen has been tried in MS
IV. Exotropia
1Basic 2Divergence excess3convergenceinsufficiency4PseudoXT
1Basic same at distance and near
2Divergence excess =distance > near by 15 pd due tohigh AC/A = easy mobility and poor focus check post occlusion (break fusion) simulated excess if becomes basic with +3.00D after patching for one hour most do not become ET at near post op if straight at distance
3Convergence insufficiency exotropia of near is 15dp more than exotrpoia when checking in distance near point of convergence (NPC) is remote{ or more easlly very close toeye that itis hidden!!! low AC/A does not converge but accomodates blurred near vision often only with exophoria traumatic often resolve within one year (up to 2/3) remaining are difficult to treat usually prisms, orthoptics are ineffective Rxpencil pushups reading or TV with BO prism to increase convergence amplitudes chronically, can treat with BI prism often have significant overcorrection early on, especially with bimedial resections a recess/resect procedure provides some incomitance so the patient can fuse without diplopia
4Pseudo EX + angle kappa cornea nasal fovealateralROP dragged macula Toxacara telecanthus Duanes TII incomitant
How do they present
1Exophoria
NPC near point of convergence may be remote, asthenopia if controlled by accommodative convergencemost commonly a ~~~problem with convergence insufficiency NOT treatable by surgery, use convergence exercises
2Intermitant XT =most idiopathic, +FH, F>M usually starts around age 2 close one eye in bright sunlight ARC V pattern ,only 1/4 improve or are stable often complain about diplopia when driving or moving must measure with accommodative target bilateral temporal hemiretinal suppression
progressive with decrease tonic convergence, developed suppression, decreased accommodation, and orbital divergence with age most are pseudo-divergence excess, so patch 45min or check with +3.00d rx give f3
4Consecutive XT must check adduction to see if MR has slipped
Surgery
wait until 2 1/2 to 4 year old to promote fusion if in lateral gaze measures10 pd < straight, then decrease recession by 1mm/muscle
BLRR should aim for 10 - 20 pd of ET early on resect/recess should aim for a few pd overcorrected early on for long standing cases, need to release contracted conjunctiva and Tenon's
Tables may do symmetrical surgery of weakening LR or strengthening MR of both eyes may weaken LR and strengthen MR of same eye by reading across table at larger angles, may prefer to do four muscle surgery with the numbers in parenthesis
XT angle (pd)
recess LR in mm
resect MR in mm
15
4
3
20
5
4
25
6
5
30
7
6
35
7.5
6.5
40
8
7
50
9 (6)
7 (5)
60
10 (7)
8 (6)
70
11 (7.5)
9 (6.5)
80
12 (8)
10 (7)
consecutive ETusually resolve with time may patch, prisms, full plus glasses, phospholine iodide rare to have persistance, especially when ductions are full if incomitant, after a resect/recess, may require reoperation
ICE
iris naevus EIA syndrome= iris atrophy with PAS pulling iris to one sideand ectrpian uvea Chandlers syndrome=chandlers is in between atrophy and naevus having a bit of bith
the common denominater is glaucoma and corneal endothelial abnormalies
age and sex : ONE eye of middle aged women
notes
Pars planitis risk of MS sarcoid and syphiilis
ARC and suppression
children supress vision to protect aganist diplopia
suppression eliminates central diplopia and creates a small scotoma with ET= esotrpia and a hemiretinal with XT
ARC eliminates peripheral diplopia use bagolini lenses to test
Tests for Central scotoma Diplopia & Steropsis
Central scotoma Tests
1use 4pd BO test (no movement in in eye that has no fixation and is amblopic 2Bagolini lenses(eye with hemiretinal scotoa picked up since glasses close dissociate fields 3 Worth 4 dot ( 4 dots seen at near but lose 1 as dots are moved back in ambyopic macular )
Diplopia tests
A red glass in front of the eye means all light will be filtered out except red which will go thru.
1Red filter red filter over one eye, do they see a pink/red/white fixation light or double? 2prism neutralization if sees double
with prism neutralization ie straight , then patient has ARC 3 W4D )can test strength of fusion by darkening the room and increasing the dissociation (up close, normal periphery, back off at 1/3 -1 meter will show scotoma and pt will see only 3 dotsdots are separated by 6 degrees at 1/3 m, and 1.25 degrees at 6 m, and 12 degrees at 1/6 m NB alternating suppression can be confused with diplopia
W4D explained. put on green red glasses and look at screen with 2 green lights one red light and 1 white light that has obvioulsy both green and red eminiting (one red and 2 green is used to differntiate the eyes
by convention red in front R and green in front L
look for normal binocular fusion 2ARC 3 Lor R suppression 4diplopia 5 Alternating supression
if 4 normal binocular
if there is a manifest squint and 4 dots ARC
if 3 green and 2 red DIPLOPIA
if 3 green only R supp
if 2 red only L suppresion
Addedknowledge
VA is 300 to 400um spacing of photorecepter at fovea this equates to one minute of arc or 60sec nb the small Es of 6/6 subtend 1minute at each arm
Steropsis Testing Normal bifoveal fixation is 20-50 arc seconds & 80-3000 arc seconds is normal peripheral fusio When testing you
must have adequate illumination to test properly since it is a peripheral phenomenon You can use the 1Titmus Fly is 3000 arc seconds>>>>> or 50 minutes or just under a degree or animals 400-200-100 arc seconds or circles 800-400-200-140-100-80-60-50-40 arc seconds [10 minute s to about one It has monocular clues and as a check rotate 90 deg,to lose
stereopsis so if patient can see smallest circle foveal fixation is intact2Randot better positive testing equals high grade stereopsis
Normal phorias adults at 6m have 2 pd Esophria & at 30cm have 6 pd Exophoria while children at 6m have ahigher 8
pd Esophria & at 1/3 m have a higher 8 pd Exophoria Angle Kappa fovea in relation to centre of cornea usually cornea is a bit nasal to fovea is normal + kappa an abnormal angle kappa is different than eccentric fixation because the fovea is still usedpositive= normal, nasalnegative= abnormal, temporal
Fusional amplitudeshorizontal convergence D 14pd N 38pd divergence D 6pd N16pdvertical2.5pd
Bruckner testdirect ophthalmoscope at arms length, full brightness perform Hirschberg's, then compare brightness of red reflex assess fixation or
nd red relex brighter in esotropic eye
hypoaccomodationasymmetric red reflexes are due to strabismus, anisometropia, anisocoria, posterior pole abn/media opacities
1 Amblyopia 2% of population with neutral density filter, the difference between the eyes diminish crowding phenomenon eccentric fixation can be found with dense amblyopia Causes
1Strabismic 2Refractive imeridiona l >+3.00 ii ametropic usually >+5.00give correct Rx may take a long time for vision to
get better--be patient 3anisometropia very common >1.5 D difference in hyperope, >2 D in myopes children with better initial
vision will do better anisekonia doesn't occur with correct rx very small incidence of ET developing while patching 3Organic often a functional componant is also present deprivation (amblyopia ex anopsia) media opacity such as cataract or corneal opacity structural eg, optic atrophy, macular scar small APD, abnormal PERG 4Occlusion less than 10%usually reversible with cessation of patch or
brief patching of other eye 5Monofixation syndrome <8 pd of strabismus (cover/uncover or simultaneous prism and cover) and 1/3 have no deviation alt cover > cover-uncover, prism and cover anisometropia common small macular scotoma (debate about ARC and suppression) usually good binocular vision, NRC,andabnstereoacuity (<60%) may have HARC (cover test normal), macular lesion most have amblyopia
terms
phtysical eye
correctopiaembrytoxin
Esterman binocular 80 degrees left right
70 to 80 degrees up and down
stimulus III size
backgrouund 31.5 ASB
intensity 10 DB time about 5 mins for entire test
DVLA regulations: guidlines
PRP
100um 0.05 sec 240mW about 2000
Drugs
cefuroxine
elixir
vexol
Cross Cylinder
cyliders are marked
estimate cyl axis Retinoscopy
Use .25 cross cylinder to start
Correct Axis first
1correct axis by lining handle white dots and move
increment 10 degrees towards the type of cylinder eg if + green positive may move towards thsi line many times
2 correct power
then do power line up with color line does not matter which one either be plus .25 or a minus .25
thne change cylinder power in trial frame
use rings wernhoff rings to test aqouityneeds 6 / 12 at least
before cross cyl have em look green red lights
which better
green refracted less he is more myopic
get them onto green add to get em to green
green red diff 0.25
then do cross cylinder thren remove extra minus
use rins only if up to 6 12
if worse us e cross cys with appropaite target
Back verteb distance usuallt 12 to 15mm
messuer lens to lid
use conversion disc
with minmus lens clooser to eye weaker lens that is add some plus
if plus add some
use for more then to 5diopters
Vocabulary artuafactual
Laser
Argon laser
laser tube is filled wiith argon gas under pressure. A current causes argon molecules to emit blue grreen
light that is delivered via fibre optical cable to the slit lamp
spot sizes vary from 50 to 1000 mciirons --usually use 200u-500u time is 01 sec
Red light emitted from Krypton may also be useful
Xanthophyl in mature cataract and macuular & HB absorb blue green light.~~~~therefore avoid Hx CF zone and BV.
Most of BG light absored by RPE therefore burnconfined to outer retina therefore moderate burn is useds anything more burns all tissue
blue green light is scattered more than red by media and this is a great disa dva
white tissue like OD fibrosis hard exudates cR atrpothy refllect BG ~~~~ no effect
Pigmentation absord ~~~~~ risk of burns
Energy density ~~ size [ duartion
S S P T
200um macula 500 paeriphery
small spots genarlly not necessary
tiime 01 to 0,2 sec
Macula moore xanthophull more pigmented Rpe therefore no laser inside FAZ risk of spread
hhere red krytpon with less absorbtion is better
NB
FAZ vessesl more susceptible loose glail suuport so easy separeted and ~~~~CMO
Lasers
Most are water or air cooled
Xenon not used due to larges spot sixe and poor heat control
Histology
laser destorys RPe and and deep tissue bruchs not ruptuterd
Technigue
1ideal burn yellow in light pigmneted
and grey in dark pigmented
2 make perimeter and then fill centre
watt is joule per sec = power
energy is joule
OpeartionTurn on the air pump
wait 1,2 minute then turn on switch
sit down
adjust power to 200 mw {0,2 watts and sppot to 500um= 0.2 jouels per sec or 200mj per sec
beam will lihgt up dustparticles in a dark room
place aper at site if intensity increase chsnges fromb lut ogreen
duration of burn 01 sec
observersmust wear yellow filter glasses as obbserver has built in laser
Wave length of laser
Argon ~~~~~~488 to 514 B G
Krypton ~~~~~647 red
Diode ~~~~~~800 IR
Nd Yag ~~~~~1064 IR
CO2 ~~~~~~~10600 IR
Trabeculectomy
CL
Single mirror goni lens
Abraham or wise iridotomy lens PI
Goldmenaa style 3 mirror
Panretinal
Modes of laser operation
1Continoues wave~~~~ thermal damage
2Pulsed~~~ thermal
3Q switched extremeely shrot durartion eg nanoseconds= cold ~~~~ photdisrution~~~~ capsutomy iridectomy
4A mode locked train of extremly short (pico) photdisruption capsultomy iredectomy
5fundamental orrMulti mode ==
Fundamnetal===one type of wave therefore no divergence and small spot high power ~~~used in capsultomy and irodectomy
Multimode many waves in different direction s~~~~ calcified membranes and heavy tasks
books
Practical ophthalmic surgery
willshaw livinstone chirchill
drugs
Timoptol LA .25% .5 %
Cosopt 2% trusopt .5% Timoptol
Entropian
Everting sutures Double armed 4/0 catgut are passed thru full thickness eylid from conj side just below the inferior tarsal plate and tied in the eyelid skin at aslightly higher level
Weiss horizontal incision below inferior tasua plate
1bouble armed 4/0 catgut passed from conj side thru con and skin just below insicion
2they then pass thru pretarsal orbcullaris on upper side and tied on skin 2 to3 mm below eyelashes
3 close skin with silk
Cyclocryo
4mm probe temp -60 to -80 'C
8 applicationss over 2 quadrants 2.05 mm from limbus for 60 seconds
Trans screla Nd Yag
free running or thermal mode 20 millsec pulses of 1064 nm (ir) light
sclera is penetrated
techniigue
2mm from limbus 20 applications over 180'
Tanponades
Silicon oil demethyl siloxine colorless sg 1 refrective index 1.004 viscsity abot 12000 cps
Gas tamponade
sulfur hexafluride SF6 used as 20% mixtxture with air as total sF6 with expand dangerously when the bubble enters blood nitrogen
gas is loost very qiuckly therefore top up after op
time usually 1 to 2 hours
anterior eye
SR
LR 6.9
MR 5.5
sr 7.7ir 6.6
OS temporal 7 to 8
OS nasal 6 to 7 less saceon side of nse
ora serat to equator 6 to 8mm
equator to macula 18 to 20mm
vortex veins either side of SR &IR 6to mm behind eutor
IR 5 to 6 bbehind ewutor
at 1 5 7 11 ocock
starbismus pearls
obliues move eye towards the nose so test for overactivty and underactivty
the eye forms ie optic al axis of a 22.5 or 23^ axis with the orbital axis
normal fusional vergence is 15D for far and 25D for ear and is decreased with fatiaqe It helps to keep eyes keep eyes straight
Examination
Hirshbergs states a light relex 15 degrees or 30D if at pupil margin and 45 degrees or 45D at limbus
also for pseudostabismus ie wide nasal bridge oe broad epicantal folds or close set eyes
psedoexo can be de to shortening of tempeal canthusk
Understanding angle kappa
we should expect the fea to be at the optical axis as we se the fovea to look straigt ahead but it actually is a little temporal
alternate cover with prism cover for 2 seconds and place apex of prism in direction of deviation
use a base out small pris power to detect binocular single vision eg 4 diopters
place prism in front of eye and check for coective movement if it is present then thr person is fusing and u have sucessflly boken it
maddox wing dissociates eyes and measures heterophoria
maddox rod remeber that when cylinders are horizontal they convert a wit dot into a vertical line
chilkdhood esotropia
pearls more likely t have dvd if nystagmus present
kids normally +1.5 dioptor hyperopes
IO overaction occurs most common at 2years and becomes bilateral
DVD excyclo and updrift ( ie eye is bells and away when covered!!)
appears after years f surgery faden is procedure dne fr csmesis
ambyopia 40%
Jenson transposition split the lateral rectus and SR & IR in 2 leaving attachment and the suture corners with non absorbalbes
RD colors
colors blue ~~~~~~~~detatched
red ~~~~~~~~~~~~~4~attached
brown ~~~~~~~~~~~~choriod
black ~~~~~~~~~~~~~~pigment
greem ~~~~~~~~~~~~media opacities
yellow~~~~~~~~~~~~ chorioretinal exudates
3mirrro=r only unside down
lense 20D magnification 2.3 times fiels 40 '
28D 1.5 but larger field 60'
14D larger field
90D SMALL FIELD AND
90 d 2/3 magnifation mltiplied by slit lamp mag
Explants may be sponge tyre starp sixes 3 4 5 7.5 mm diameter
instruments St martins is toothed forceps
the eye focuse green ight
red is not deviated therefore seen best in myopic eyes myopes drift towads red
duochrome test should get emto green
Tarsorraphy
epithelium excisedfrom lid margins posterior to ge0y linelatereal U L lids
40 nylon or sik passesd as a matress from skin of upper lid thru raw trasal margin and out of skin of lower tru tubing and back again to be tied on skin upper tru tubing
ectropian
full thickness lid resection
lazy t
do full thickness lid resection 4mm lateral topctuma
resect a diamond 2 triangles of conE & taral plate with 2 apices vertival below puctum
appose apices and close with fullthickness 40 catgut
suture full thickness lid resection
Lee medial catho
plasty for ectropian and eveted puncta
2 lacrimal probe sinserted fr safety
lid is splitinto 2 medial to pucta into anterior skin and posterior lammela
suture abooveupper canaliculis andbelow lwwr cana
when tied the puctu is inverted again
Axial Globe Displacement:=mass w/in muscle cone ~~~~~cavernous hemangioma glioma meningioma mets avm
vs
Superior Globe Displ: ~~~~~~~max sinus tumor
vs
Down + Medial Globe Displ: ~~~~~dermoid cysts lac gland tumor
vs
Down + Lateral Globe Displ: ~~~~ frontoethmoidal mucocoele abscess (subperiosteal) osteoma sinus ca
Pulsation
w/o Bruits: neurofibromatosis meningoencephaloceles post op ie s/p removal orb roof
vs
w/ Bruit: c-c fistula dural av fistula orbital av fistula
Keratometer
measure curcature of central 3mm radius of curvature nomally is 7.8mm
priciple object is placed so that image is at f2= 2nd focal point which is half way to c or radius of curvature
therefore r which is 7.8mm approximately is image size divided by object size multiplied by 2 u or distance of of bject from cornea which is standard and known
O/I = distance of object / distance of image ( 1/2 R or F2 or normally 3.9mm or 4 mm
object size × imagedistance or 1/2 radius = image size × object distance
IN all U is constant
In JAVAL shiotz mires one object size is varied to obtain a standard image size
VS
In Helm hortz object is fixed and and the image size is adjusted.
Helm hortz
2 mires in a lantern with colored window
space between mies is the object size
image is formed by refection by cornea
but viewing telescope has quartz prism to splits each latern image into 2 at at fixed angle therefore getting images to touch makes them the right size and image can be used as correct just like Applantion tonometer!!!
made so thateach step is one diopter
an additon i the HAAG Strey Javal schiotz incorparte a horizontal line to faciliate vertical allignment
Slit lamp
1Bliue cobaltfilter
3Green red free
scattering is greates when short wavelength used therefore use to see vitreous
Aplanation tonometer
appied to cornea with sfficient force to PRODUCE a STANDARD area of contact = booyles law = to flatten a sphere the area yoy flatten is drportional to pressure important
not so important!!!we use 3.06 where conveniatlysurface tension and corneal rigiditycancel out
head of prism 2 prisms kissing at tips ie base out
as we look tru ton head wesee prism splitting 2 half circles by moving images latrally likeanyprism does
Galeilien telescope
concave={diverging} eye piece and convex={condensing }objective sepatrated by differebce in foca lenth
produces erect magnified image
REDUCED EYE AS PER LISTINGA single princple point and a single nodal pointused
Refractingpower uesed 58.6 D
all distances from cornea
princple point 1.35
nodal point 7.08
first fovcal point -15.7
2nd focal point 24.13
NBcorresponding focal lenth = -17.05 and 22.28
Drwingi objects deviated at princple line and go tru nodal point
Far point is thatpoint in arelaexed eye the image falls on the retina
Maddox rods
diisosiate the eyes so they see disimar objects and allows muscle imbalance to become manifest.
NB the eye is deviating opposite to the line seen
Focal point is only a point thru which light travels and it is half radius
vs
Far point and Near point
Surgical procedures
Punctal stenosis 3 snip insert scissors vertically down make 2 cuts outward follow up with one horizontal cut out triangle
A & v Patterns managment
A as we go up the eyes go in A esotropia
V as we go down the eyes go inV esotopia
or exotropia V or a
The common deviation is INWARD or outward
RX 1 vertcal rectus transpalnation
May get V or A exotropiapull inwards ~~~~ trnspalnt nasally
in esotria V or A vertical rectus tranplanted temporally 7mm 2 Horizontal recess rescet
MR naturally convergers strongly on downgaze
& LR naturaly diverges on upgaze This either one produces V patterns when they overact
RX weaken these
A patterns due to underaction muscles RX therefore strengthen
usually move 5mm may also adjut height to reduce pattern
eg A esotrpoia recess MR and elevate
V esotrpia recess MR and move down A exotrpoia recess LR abd move down V exotppia LR reecss andmve up
3OBliquesSo overaction{ relative IO underaction)~~~~~ A pattern mostly in exodeviationmore than 20D weakening egtenotomy ---IO overaction ~~~~V pattern mostly esodeviatyion
RX strengthen SO by
Anatomy
sleral thickness temporally not thicker then 1mm
nasally 1.5mm
macula 1.5mm
very thin bemeath tendons ie .0.3 mm!
Surgical instruments eyelid conjunctica Bard parker knife chalzion forceps and curette graefe muscle hook ptosis forceps? Snellen entropian forceps lod forceps jaeger lid plate caliper needle holder suturing forceps stevens tenotomy scissors blunt or sharp Westcott tennotomy scissors lester fixation forceps straight or curved tissue forceps seerine clamp to hold loose ends in squint surgery
corneal instruments corneal scissirs bonn tissue forceps suturomng forceps
Lens diamond tooke corneal knife barrquer iris scissors capsule forceps iris retracter and espressor lens loop synechie spatula iris spatula troutman cannula gills forceps
Defintions
Dermatochalasis=older persons skin of yelid becomes relaxed redundent due to atrpohy of subcutaneous tiisue
culture media
Acanthamoeba culture on non-nutrient agar with E. Coli overlay
blood agar
chocilate haemolysed blood
fungal??
viral??
Blindness Certification
VA lwss than 3/60
partial 6 /60 to 3 / 60
Mysrilate 0.5ml + Betnesol.0.5 .ml subconjunctival injection for Uveitis
hydrocortisone 0.5% is a weak steroid cream andse thisfor skineczema others 1%&2% mayalso use
Drugs and prblems
amiodarone coritca catarct
Nrmal parmaete
corneal diameter
5. Leukocoria
Cataracts1/3 genetic, 1/3 diseases, 1/3 idiopathicn monocular are not metabolic or genetic capsule forms in 5th week and limits entry of organisms opacities >3mm are visually significant
Anterior
polar 1/3 are bilateral abnormal separation of lens from surface ectoderm 90% sporadic pyramidal 2 mm projecting cone with surrounding cortical opacity cones can be fibrotic and touch to fragment bilateral and sporadic subcapsular idiopathic, trauma, often acquired lenticonus Alports X linked dominant Difficult capsulorhexis Chronic steroid use may present with PSC cataracts ===hereditary nephritis sensorineural deafness PPMD whitish dots in macular and mid periphery Central
Nuclear in general, congenital origin either the embryonic or fetal nucleus
usually non-progressive bilateral are often AD inherited Sutural or
Lamellar acquired usually after 6 months progressive hypoglycemia and galactosemia can cause lamellar pattern Posterior
Posterior lenticonus looks like PSC, bowl like central outpouching unilateral, progressive at surgery, post capsule often thin wispy and difficult to peel off opacity
PHPV
posterior capsular
associated with Down's syndrome
Oil Drop cataract
associated with galatosemia
Lowe's
XLR
systemic hypotonia hyporeflexia mental retardation Aminoaciduria metabolic acidosis growth retardation renal failure
often with early death
ocular most commonly small thick opaque bilateral cataracts pupils can be very miotic with lens adhesions female carriers have white punctate opacities throughout their lenses glaucoma in 50% by age 6 but can be early on corneal keloids
Hallerman Streif
Labs
especially to exclude Lowe's, galactosemia
consider TORCHS titers even in unilateral cases
Urine
reducing substances, aminoacids, blood/protein
copper, sediment
Blood
Ca+2/phos, glaucoma, amino acids, TORCHS serology, others
PHPV wide spectrum of presentation congenital, non hereditary, usually unilateral not associated with other defects except cataracts retinoblastoma is rarely found in microphthalmic eyes
elongated ciliary processes microphthalmos shallow anterior chamber radial iris vessels retinal detachment retrolental plaque intraocular hemorrhage angle closure glaucoma
US/CT very diagnostic
natural history of untreated eyes with moderately severe disease is progressive shallowing of anterior chamber, cataract formation, and angle closure glaucoma
Pseudogliomas
benign neoplasm
astrocytic harmartoma
can mimic RB, involvement of disc, multifocal, bilateral
usually with tuberous sclerosis, rarely with neurofibromatosis
little postnatal growth
von Hippel angioma
medulloepithelioma
uveitis
nematode endophthalmitis
usually older boys, inflammation more
inactive lesions show more changes than RB (cataract, synechiae, etc)
ELISA + 90% with 1:8 dil
retinitis, old VH
Non-rhegmatogenous retinal detachment
Coats'
usually older boys age 8-10 years old
anomalous grapelike clusters of leaking blood vessels
serous RD with dilated vessels can look like retinoblastoma
aneurysmal dilation can look like angioma, but no feeder vessels
about one half of untreated patients will progress
treatment includes laser and cryotherapy
retinal dysplasia
juvenile retinoschisis
Misc
retinal hemorrhage
retinal folds
colobomas
Retinoblastomaost comon eye tumur in kids initiall detected n one eye but becmes bilateral in 1/3 of cases
avareage age starts is 18monhs bt there is a late pesentain at 3months
inheritence
only 6% will have a family history and then it is AD with incompete penetrence
Therefre 94% sporadic 25% germinal and 75% somatic
1:20,000 births, becoming more common
6% with FH, 25% have genetic mutation 13q14 with low esterase D levels
1-3 y.o., present older when unilateral
70% are unilateral with 30% bilateral
1/5 of unilateral on presentation get 2nd eye affected later
the differential dx of inflammation is the most difficult
leukocoria most common
strabismus
inflammation (pseudohypopyon)
Ca2+
vitreous seeding
normal size globe
glaucoma
hyphema
heterochromia
fixed pupil
serous RD with dilated vessels
signs different for endophytic/exophytic
metastasis late with spinal cord, bone, skull, lymph nodes, abdomen
pineal gland trilateral tumor with very poor prognosis
up to 50% with secondary cancers especially osteogenic sarcoma, fibrosarcoma, rhabdomyosarcoma many years later
Genetic risk
history
determine if germline or somatic
germline in multiplex and multifocal cases
simplex disease with unifocal RB has 12% risk for germline mutation
remember carrier status due to 80% penetrance
unaffected parents with one child mutifocal RB have 6% risk for second child
examine family for regressed retinocytoma
Molecular genetic analysis
can find the specific gene mutation using Southern blotting
RFLP's to do linkage studies
Diffuse infiltrating RB
(1%) likely to be missed
occurs later (6 y.o.), unilateral, grows slower
RX
CT, MRI: look for calcification, pineal gland
U/S: A scan with high internal reflectivity and echo spikes from calcification, B scan with orbital shadowing
bone scan, bone marrow, lumbar puncture as needed
with massive tumor, enucleation may be primary procedure
external beam radiation, Episcleral plaque, Photocoagulation, cryotherapy
systemic chemotherapy
regression
TI cottage cheese
TII fish flesh
TIII combo of above
TIV white sclera
5 yr survival >90%, poorer with metastasis
Histology
Flexner Wintersteiner rosettes -an attempt to make photoreceptors with clear lumen
fleurette with outer segs of photoreceptors
Homer Wright rosette- lumen with neurofibrillary material, also in medulloblastoma, neuroblastoma
pseudorosette-tumor around necrosis
viable tumor around vessels with areas of necrosis
Rx chemotherpy
VP vincistine and ?? evry 4 weeks for 6 cyclesa
usually regresses after 2nd treatet
enucluation best results with 15mm or more of optic nerve resection so aim for this as sprewad is via optic nerve
Radiotherapy
ROP85% of ROP is transient disease with spontaneous regression
examine all children born under 32 weeks or weighing less than 1,500 gm
CRYO-ROP study had 6% of children <1251 gm reach threshold, 20% prethreshold, 60% have some ROP
Risk factors include <750 gm, PCA of <28 wks, O2 > 3wks, black < white
initial exam at a post-conceptual age of 32 weeks
long term risks include
pseudostrabismus myopia
PAS and glaucoma RD
cataract microphthlamia
phthisis
classification
stage 1 line
stage 2 ridge
stage 3 neovascularization
stage 4 partial RD
stage 5 total RD
plus disease is retinal tortuosity and dilation, pupil rigidity, vitreous haze
plus disease with ROP Zone I = rush disease, exam q48 hrs
rx
decreases the risks of a bad outcome by 50%
treat for 5 continuous clock hours or 8 total clock hrs of Stage 3 plus disease
cryotherapy or indirect laser
Anti Fungals amphotericin B 0.15% (1.5 mg/ml) or imidazoles (miconazole 1% or ketoconazole 1-5%)
Fungizole Amphotericin B
2 ml water with 1 ampuole
take 2ml tears naturlae out of bottle and add 2ml Fungizole to 13ml tears naturalle
Daktaris Miconazole
take 7ml out of Tn and add 7ml of Daktarin ampoule
SporonaxItraconazole
dissolve 1 capsule 100mg in 5ml water
Take 5ml out of 15ml BSS and add
Natycin 5% drops
ROP screen less then 1.5kgscreen at after 6 weeks
stages 1 to 5look every 2 weeks if stage 111 see em every weekthreshold stage 3 5 clock hours continous or 8 clokcs with + diseasewhite kline 1ridgge 2stage3 fibrovascular
Marginal corneal pathology
Terriens ussually one eye and not so painful
Moorens bilateral and painful
A AND V PATTERNS
Any of the foregoing types of strabismus may exhibit a change in horizontal deviation in upward and downward gaze.
If the deviation is more exotropic or less esotropic in upward gaze, the change is referred to as a V pattern
( if the deviation is more exotropic or less esotropic in downward gaze, the change is called an A pattern. By consensus, the change from up- to downgaze must be at least 15 PDs in a V pattern and at least 10 PDs in an A pattern, although a difference of 20 PDs or more for each is more likely to be clinically significant. A or V pattern occurs in from 15 to 25% of patients with horizontal strabismus
Although there is no clear understanding of why A or V patterns develop,they are frequently associated with imbalance of the oblique muscles-A patterns with overaction of the superior oblique muscles and corresponding underaction of the inferior obliques, V patterns with overaction of the inferior oblique muscles and corresponding underaction of the superior obliques ( The oblique muscle imbalance does not appear to be due to paresis of the underacting muscles, because there is no change in vertical alignment with head tilt (Bielschowsky head tilt test) as one would expect with an oblique muscle palsy. Nevertheless, there is a torsional change in eye position consistent with the oblique muscle imbalance. This torsion is evident on funduscopy and demonstrable by
heterotopia of the blind spots on visual-field testing.67 Weakening of the overacting oblique muscles collapses the A or V pattern, making the deviation more comitant in up- and downgaze.66 There is relatively little change in the primary position alignment with bilateral inferior or superior oblique weakening procedures alone,68, 69 so additional horizontal muscle surgery must be done to correct a significant deviation in the primary position.
There are a few special conditions in which oblique muscle imbalance similar to that seen in V patterns seems to be related to an abnormality of orbital anatomy. Patients with craniofacial dysostosis of the Crouzon or the Apert type frequently have overaction of the inferior oblique muscles and V-pattern deviations (Fig. 309-8).70, 71 Likewise, children with unilateral coronal synostosis and plagiocephaly frequently have hypertropia of the eye on the affected side with overaction of the inferior oblique muscle and underaction of the ipsilateral superior oblique (Fig. 309-9). The latter has been attributed to a change in the anatomy of the superior orbit and the position of the trochlea.
Rarely, patients with A or V pattern do not have obvious oblique muscle imbalance. In these patients, the change in horizontal deviation in upward and downward gaze can be neutralized by shifting the attachment of the horizontal rectus muscles up or down. This is often done at the time these muscles are recessed or resected to correct the associated horizontal strabismus.63, 75, 76 The insertions of the horizontal recti are moved upward or downward in the direction in which one wishes to weaken their horizontal action. A similar effect can be obtained by monocular vertical displacement of the horizontal recti, moving one muscle up and its antagonist down according to the principle of displacing the muscle in the direction in which one wishes to weaken its horizontal action. Displacements of the horizontal recti are not effective in reducing A and V patterns if oblique muscle imbalance is present. For reasons that are not clear, surgical weakening of the inferior oblique muscle does not cause torsional symptoms, whereas tenotomy of the superior oblique muscle does induce a symptomatic torsional change.77 Because adults have difficulty adjusting to changes in cyclotorsion, superior oblique weakening for A patterns in adults is not advisable.
MICROTROPIA
But less than 10 seconds abnormal
norma shirmers is 15mm and slightly less with topical anaesthetic
rose bengal affinty dead degenerate cells and mucous
tear substitites
celluluse polyvinyl alcohol mucomemetics
Argon iridotomy
Abraham lens that magnifies periphery
drop pilocarpine
8 large low power circle of shots 200um 200mw and 0.1 sec
follow by high power burns 50um 1000mw .2 secons
site two thirds distance from puppliery margin
kids vallergen forte 2mg per kg
drpos .5% tropicamide
dormicon inject drops into nose beyond neonatal period
visual aquity chart equivalents
Close to 1 is better
20 , 400 6/120 decimel .05
20/200 6/60 .10
20/80 6/24 .25
20/60 6/18 .33
20/40 6/12 .5
20/30 6/9 .67
20/25 6/7.5 .8
20/20 6/6 1
20/15 6/4.5 1.33
20/10 6/3 2
Cornea approach
Age relatedchanges crocldile shegreen guttata farinnata arcus vogts limble girdle
work related Think about the salt mines in Austria
band sheroidal saltzmans lipid
sheroidal amber stromal granule
saltzmans is a stromal soft nodule often with iron that lifts epithelium
surface
cogans map dot fingerprintreis bucklers
meesmans bubble paper intraeipthelial cysts
granular abnormal collagen hyaline
macular abnormal keraten sulpahte mucopolysacharides
lattice abnormal deposits of amyoid that form a network
typew one accurs at 10years and type 2 in middlwe age and assosiated Genearalized amyoidosis
Granular
type 1 occurs 10year small discrete spots or granulea
ulcers
marginal keratitis
rosacea
terriens clear zone and thinning
mostly middle age males usually superior cornea
moorens caused by limbal vasculitis and ishchama and collagenases relased by adjacent conjunctiva
young people with good immune systems develop the progressive form while in the old it is innocuous
although it is virulent it rarely perforates
AI kerititis
dellen is a localized thinning caused by ppressure and dehydration for eg had contact lenses
Phlenctenolosis
psedogema vcv
gonioscopy
scwalbes isa nopaque line
trabeculummwhitish non functional and greyish translucent functional layer.
pigmentation is rare and ifit is it is inferior
sclems canal
slightly darkerline in inferior trabeculum
blood in canal
caridocabv fistula svc syndrome turge weber
and ocular hupotony cause blood incanal
iris processes vs anteripor synechia
anterior synechiae are broader
iris processes in kids and disappear
4 see cilairy body 40%
3 see scleral spur impossiple to close 30%
2 see tabeculae meshwork minor risk of closusure 20%
1 scwelbes 10% closure risk high
childhood glaucomas
nos and facts
adultcornea mean horizontal diameter 11.8mm aznd kids 10mm
most incrase occurs n first year
if greater than 12mm in kids less than 1year and any diameter morethan 13mm is of cconcern
posterior embryotoxin is a prominenent scwalbes line
pterygium
advancement graft
or swiing
most imp limbus conjunctiva
ac a ratio is the amount convergence measured in prism diopters per change in dioper poer change in accomodation
eg4 prism diaopter means move 4 prism dioptetrs and change power 1 diptor
high causes esotrpia or convergence when we try to focus near we overdo convergence
a nd low divergewnce
thyroid disease
infewrior rectus affected most then lateral rectus
focal laser garankuwa
setting on green as it is less speading
start 0.1watts and increase
jan usess 0.3 watts
ptosis
normal cornea is 11mm height and normally 2mm is covered
so measure exposed cornea and write ir down
eg 6 mm this means 3mm ptosis
grade 2mm mild
3mm moderate
4mm severe
remember for stabisms surgery.
MALEfor A and V pattern move muscle in direction you want to weaken it
medial rectus towards apex and lateral rectus towards empty spacein leatr ressection 6mm resection will lift eye 1mm
ddx acute blindness ie optic neurtis
central serous retinopathy big blind spot syndrome
multiple evanescent white dot syndrome anterior ischemic optic neuropathy
syphilitic optic neuritis postviral optic neuritis
Leber hereditary optic neuropathy (mitochondrial gene mutations) toxic/ nutritional optic neuropathy
malignant optic glioma
FINAL EXAM questions1Discuss cavernous sinus syndrome with regard to cinical findings and pathology
Cavernous sinus is a dural venous sinus which contains the internalcarotid a., CN III, CN IV, CN V, CN VI, and osympathetic fibers -various etiology
a. internal carotid artery aneurysm
b. carotid-cavernous fistula due to trauma and pulsating proptosis and bruit
c. cavernous sinus thrombosis
d. neoplasm eg haemangioma with axial displacement
e. inflammation (Tolosa-Hunt syndrome)
clinically
1Glaucoma due to increased veonous pressure eg cavernous sinus thrombosis or carotocavernous fistula 2 horners Third order 3 nerve palsies
detailed discussion
Carotid-Cavernous Fistula
Hi-Flow (75%)Secondary to trauma (MVA head injury)Pulsating exophthalmosInternal carotid fistula ( surrounding cavernous sinus venous plexus Low-FlowSpontaneous etiologyIndirect or dural connectionMiddle-aged womenMemingeal branch of intracavernous int. carotid a. or ext. carotid a. ( cavernous sincus or adjacent dural vein that connects with the cavernous sinus
Conjunctival chemosis, episcleral engorgement Bruit with increased with exercise, ocular ischemia Proptosis can increase for weeks CN VI palsy, retrobulbar pain Glaucoma from increased Pv, neovascular from CRVO, or angle closure
Blepharospasm
3 Discuss glaucomatocylitic crisis
=Glaucoma related to inflammatory change in trabecular meshwork
Associated with systemic disorder, allergic, or (peptic ulcer)
age30-50 years old
clinically Mild inflammation, dilated pupil, high IOP (40-60 mmHg) with corneal edema Unilateral, recurrent attacks, ON usually OK, self limited 1-3 wks Some end up with COAG Open angle: no PAS, no posterior synechiae Some flare, fine KP
Tx: Prostaglandins are possibly involved ( oral and topical NSAIDsAvoid steroids since patients may be steroid responsive?Apraclonidine in acute attacks
Discuss pathology of ophthalmic lesions occuring in the Phacomatoses
approach are phacomatoses because they are congenital and have some eye involvement+ skin & neural tissue
present with haemangiomas (sturge webers and hippal lindau) and gliomas (von recklinghausen & tuber sclerosis)in the retina & optic nerve
(G)Von REck eye~~~orbital gliomas Cafe a lait neurofibroma skin brain skull neurofibroma
(G)Tuber sclerosis Bournvilles eye~~~optic gliomas mullberry optic disc retina nodulesBrain stem glioma face sebacous adenoma butterfly astrocytosis
(HA)Sturge webbers eye~~~choriodal haemangioma and glaucoma port wine along 5th nerve capillary haem
(HA)Von Hippel laundau eye~~~retinal haemangimas and large feeders can bleed and RD brain haemagniomas assos with RCC
Discuss recurrent corneal erosions
causes FB allergy and Epithelial dystrophies
Epithelail dystrophies
3 types
1inger & dots Microcystic or cogans
2Honeycomb or Reis buckler
3bubble paper or Meesmans
1Microcystic pathology: thckened BM & Epithelial cysts with debris
age >30 y.o & 10% have corneal abrasions
50% of pts with recurrent corneal abrasions have MDF cf :asymptomatic or present with recurrent erosions, rarely presents with irregular astigmatism Rx: hypertonic saline, debridement with cotton swablubricants, soft contact lens, excimer PTK effective anterior stromal puncturetopical anesthetic, debride areause 23g needle and penetrate anterior stroma up to 1/3 depth may perform even in visual axis but space punctures further apart antibiotic ointment and pressure patchwarn pts about extreme pain afterwards2Reis bucklers progresive dystrophy with grey white deposits at Bowmans & honey comb appearenceReis-Bucker's
D, childhood, gray white opacities at Bowman's layer, becoming more confluent over the yearshistology: destruction of Bowman's layer and accumulation of "rod shaped bodies" replacing Bowman's layerreticulated pattern of scarringpainful recurrent erosions, by 50's marked corneal opacities Rx: excimer PTK, peeling off the superficial accumulated material, recur post PKP
3 Meesmans ===============AD and innoccous with epithelial cysts
AD dystrophy with thick BM, intraepithelial microcysts with peculiar PAS+ substance best seen on retroillumination asymptomatic until 10-20 y.o. when develop recurrent erosions, irritation, small decreased Vano rx necessary differential diagnosis includes cystinosis (metabolic defect resulting in accumulation of refractile cystine crystals, can be seen in peripheral cornea)
cornea data
horizontal diameter 11.75mm
vertical 10.55mm
radius curvature flatter anterior 7.8 and rounder posterior 6.5
thickness centre .058 and periphery 1.1
IOL power measurment
Anaomy
axial length 22.6mm
raduis of curvature 7.5 to 7.9 7.5mm =45 diopters
emmetropia 18 diopter.
1.25 diopter for every measured diopter change in prescribtion
errors
.1mm axial length is .25 diopter
.1 mm radius of curvature is .50 diopters
ie 1mm axial length is 2.5 D &
7.5 to 8.5 keratometry is 5D
ac length .1mm is .05 to .25 diopter
across cylinder has for example +.25 at 180^ and - .25 at 90^
spherical equvalent is sphere plus half cylinder
power of lens is 1/ focal length in metres
surgical procedures
strabismus occlusion
one week for every year of life
asdf'
Or use atropine 1% in good eye once every week.
Local anaesthesia
subtenons
take 2ml 10% lidnocaine and 2ml 0.5% marcaine and insert in a syinge
make inscion medialy 1cm below limbus
It is better to do it medially avoid inferior oblique .
take rod blunt neede and directto apexand inject
Classification
Nonproliferative Diabetic Retinopathy (NPDR)
Microaneurysms (MA)
Dot and blot intraretinal hemorrhages (DBH)
Retinal edema
Hard exudates
Venous beading
Intraretinal microvascular anomalies (IRMA)
NFL infarcts (cotton wool spots)
Arteriolar abnormalities
Focal areas of capillary nonperfusion
vision loss in NPDR due to macular ischemia (capillary closure) and macular edema (increased intraretinal vascular permeability)
Severe NPDR
Characterized by any one of the following (ETDRS, 4:2:1 rule)
Diffuse intraretinal hemorrhages and MA in 4 quadrants
Venous beading in 2 quadrants
IRMA in 1 quadrant
think of emma and her beads and bleeding!
Very severe NPDR
Any 2 of the above 3 characteristics
Proliferative diabetic retinopathy (PDR)
Extraretinal fibrovascular proliferation extends beyond the ILM
New vessels evolve in 3 stages:
1) Fine new vessels w/ minimal fibrous tissue
2) Increased size/extent of new vessels w/ increased fibrous component
3) Regression of new vessels w/ residual fibrovascular proliferation along posterior hyaloid
Tractional complications
Partial PVD
Traction on NV
Preretinal or vitreous hemorrhage
Macular heterotopia
Retinal detachment (RD)
Retinal breaks
Rhegmatogenous RD
Chronic RD>further retinal ischemia>rubeosis>NVG
Clinical trials in diabetic retinopathy
Diabetic Retinopathy Study (DRS)
Randomized, prospective clinical trial evaluating panretinal photocoagulation Rx to one eye of pts. w/ clear media and advanced NPDR or PDR in both eyes
Primary outcome measurement was severe visual loss (SVL), defined as visual acuity less than 5/200 on 2 consecutive f/u visits 4 months apart
Demonstrated 50% or greater reduction in the rates of SVL in eyes Rx'd w/PRP vs. untreated control eyes during a f/u of up to 5 yrs.
High-risk PDR defined:
Mild NVD (1/4 to 1/3 disc area) w/ vitreous hemorrhage (VH)
Moderate to severe NVD w/ or w/o VH
Moderate (1/2 disc area) of neovascularization elsewhere (NVE) w/ VH
High-risk PDR also defined by 3 of the following 4:
Vitreous or preretinal hemorrhage
NV
NV on or near optic disc
Moderate to severe extent of NV
Complications of Argon laser PRP
Decreased visual acuity by 1 or more lines (11%)
Visual field loss (5%)
Early Treatment Diabetic Retinopathy Study (ETDRS)
Randomized, prospective study evaluating photocoagulation and aspirin Rx in pts. w/ less than high-risk PDR
Primary outcome measurement outcome was moderate visual loss (MVL) comparing baseline w/ f/u visual acuities. MVL defined as doubling of visual angle (e.g. a drop from 20/40 to 20/80), a drop of 15 or more letters on ETDRS vision charts, or a drop of 3 or more lines of Snellen equivalent
Clinically significant macular edema (CSME) defined as:
1) Retinal edema at or within 500 u of the macular center
2) Hard exudates at or within 500 u of the macular center if associated w/ adjacent retinal thickening
3) Zone of retinal thickening larger than 1 disc area if located within 1 DD of the macular center
3 central findings:
1) focal laser Rx for CSME resulted in a 50% or greater reduction in MVL
2) PRP not recommended for mild or moderate NPDR, but is recommended for severe NPDR and should not be delayed when high-risk characteristics appear
3) Aspirin (650 mg per day) did not alter the rates of progression of diabetic retinopathy, had no effect on visual acuity outcomes, and did not show any ocular benefits. i.e. no benefits/no contraindications
Diabetic Retinopathy Vitrectomy Study (DRVS)
Randomized, prospective clinical trial investigating the benefit of early (1-6 mos. After onset of VH) vs. late (at 1 year) for eyes w/ severe VH and visual loss (<5/200)
Outcome measurements: % of eyes w/ 10/20 or 10/50 visual acuity on standardized charts at 2 and 4 yr. f/u
Early vitrectomy was beneficial in Type 1 diabetics, but not in Type 2 or mixed diabetics
Diabetes Control and Complications Trial (DCCT)
Randomized, prospective clinical trial to study the connection between glycemic control and retinal, renal, and neurologic complications in Type 1 diabetics
Findings:
Intensive insulin therapy can delay the onset and slow the progression of diabetic retinopathy, nephropathy, and neuropathy in Type I diabetics
pts. w/ baseline mild or moderate NPDR showed worsening of retinopathy during first year.
Intensive control group had increased risk of hypoglycemic episodes and increased risk of weight gain
Not applicable to Type 2 diabetics or prepubescent pts.
Ischaemic maculopathy trial
Dec sys bp by 10mmhg and dias by 5 mmhg reduces risk of losing 1/2 visual angle at 10 years by half!
Ie BP greatest risk in Ischaemic maculopathy
Possible indications for pars plana vitrectomy (PPV) in diabetics
Dense, nonclearing VH
Tractional RD involving macula
Combined TRD and rhegmatogenous RD
Severe progressive fibrovascular proliferation (fp)
Anterior hyaloidal fp
Ghost cell glaucoma
Dense premacular hemorrhage
Laser Therapy
Laser Rx generally recommended for CSME and high-risk PDR
Risk factors for poor visual acuity despite laser Rx
Diffuse macular edema
Ischemic maculopathy
Hard exudates in fovea
Marked cystoid edema (CME)
Potential side effects of PRP
Decreased night vision, color vision, and/or peripheral vision
Loss of 1 to 2 lines of visual acuity
Loss of accommodation
Glare
Photopsia
Aggravation of macular edema
Choroidals
Mydriasis
VH
Retinal holes
RD
Lens and iris burns
ERM
foveal burn
small spots cool quickly, large spots have high temps centrally
power density = power x time
media opacities
% increase in power needed
corneal 5-30% especially for stromal
flare/cell 10-35%
cataract 10-50%
vitreal 10-35%
Krypton
less scattering, less absorption by blood, yellow pigments (lens, foveal xanthophyll)
better uptake for choroidal tumors, blue iris
more choroidal uptake causes more pain, decrease
not good for acute hemorrhage during PRP, microaneurysms, blond fundi
really hits receptors, RPE, choroid
higher power needed for same lesions as argon
Rodenstock lens
minifies image, increases spot size
absorbs more energy than Goldman lens, so increase power
note: toward periphery, spots become smaller and relative power increases
Diabetes pearls
IRMA intraretitinal microvascular abnormalities are red in color and resenble focal areas of flat neovascularization
The 3 clues that they are not neovascularization are intraretinal and not raised secondly do not leak profusely on FA and thirdly do not cross major blood vessels.
AS they due to ischamia they appear adjacent to areas of neovascuaization
PDR is defined as extraretinal fibroproliferation beyond inrenal limiting layer
Severe BDR or NPDR is defined as IRMA in 1 quadrant
or venous beading in 2 quadrants or difuuse intarretinal hx(d & B) abd MA in all 4 quadrants
Very severes NPDR is defined as 2 or more of above~~~~~~45% chance to progress to PdR in 1 year vs 15% for above
intravitreaal antibiotics
gentamycin Lid anatomy & landmarks for sugery
Splitting the eyelid
When getting tarsal plate and conjuntival remember that the tasrsus is 1cm tall and is crescent shaped vs 5mm for inferior tarsus
the grey line is between the lashes and the meiobomian glands and is an avascular sulcus and splits into anterior lamella with skin Obicularis and posterior lammella with tarsal plate septum and conjuntiiva.
Chalazion is inflamation of meibomian glands and is on conjuntical side so make a slit thru conjunctival surface
Lymph drainage lateral superficial parotid
medial submandibular
Sensory supply to the eyelid
nerves lacrimal suraorbital and subra troclear all V1
infraorbital V1 and infratrochlear V2
When blocking look for the obvois notches and block these
Incisions to orbit
SUbBrow
lid crease
subcilial incision
superior nasal rim
external ethmoidectomy incision for lynch procedure
inferior llid sulcus oincision
The Medial wall is important in DcR
Summary
4 bones anterior to psoterior
Frontal process of Maxilary Lactrimal Ehhtmoid and Small part of body of sphenoid
We cut into Maxillary bone in DCR
lacrimal groove is anterior and only invoves frontal process of maxillary and lacrimal and is bounded by crests that kind of protect it. I was confused with remembering the crests but they are easy as anterior crest is maxillary
Surgery
endocapsular flexible pmma roings reforms capsular zonuar barrier
ARMD zinc and antioxidants in AREDS study
Vetoporfin for PDT =Visudyne predominantly for classic CNV in AMD pathological Myopia and OHS
Phaco News
Blue circles dimensions in the retina gauge range of pseudo accomodation in implanted IOLs
Surgery pearls Ferrero ring for Keratoconus
1mm wide incisions are made on the periphery on the steepest axis. to 7mm from optical zone The correct depth and tunnels made with a Suarez spreader and Ferreo double spacula
Neurology pearls
Surgical instrument pearls
Fixation rings to fixate globe when performing paracentesis
RGP lens new presbyopic lens combines shereical lens for distance
multifocal for intermediate distance and bifocal properties for near
Endothelial cell loss as seen by specular microscopy deends on nuclear density visco type solution
low weight and dispersive viscoelastic
Idiopathic polypoidal choroidal vasclpoathy
=dilated choriodal vessels inpolyp like configeration with no DRUsen( vs ARMD)
more common in blacks misdiagnosed exudative AMD
RX as for AMD and presents
Plastic surgery
frontalis suspension
incisions 2mm above lash line and just above eyebrow line to create a trapizoid
if levator fxn less than 2mm
use wright needle and place fascia between posterior aponeurosis and tasus nb dont pierce tarsal plate so becareful when doing surgery
placement of eyelid
in congenital ptosis at superior limbus
Drugs
cyclosprin 10 to 15 mg per kg in a twice daily diveded dose and manitainence of2 to 6mg per kg
same dose on kids
no need to do blood evels if not transplant pateint easliy reachws toxic levels do baseline u&E and LFTS
good because IMC with no bone marrow suppresion
inhibits IL2 is MOA
uses severe psoriasis and G vs host rejection
causes inc K cholesterol UA hirsitism gingivial hyperpasia
HT tremor + nephro and hepatooxixcity
CTR
uses zonular dyalysis prevents capsul fornix from being aspirated and fluid from
other uses PXF Marfans weil Marchasani syndrome pateints silicone iol tamponade and subseqeunt progressive zonular atrphy
Indian people weak zonules
Weil Marsesani opposte of Marfans mesodemal hyerplasia inferior lens dislocation AD
Albinism
tyrosine positive have better prognosis because melanin is made but not sequestrated by melanocytes compared to tyrosine -
ocular is just a paucity of melanocytes and hence has the best prognosis
macular hypplasia leads to nystagmus and photophobia is due to light bouncing around
two special types one in OCULAR & one in OCA tyrosine +
check haemtalogist if recurrent infections ass with ocular type type that has chadeck higashi
if blleding subtype of tyr + OCA =hamansky PUDLAK
no increased risk of Malignant melanoma only skin cancer
OC albinism that is severe Tyrosine + or less severe - 2 Xllink or AR ocular that has normal mothers of x linked
Oculacutaneous albinism
2 syndromes asso are chedick higashi with infections and hemanssky pudlaf with platelet dysfunction and bruisng
AR affetcing eyes and skin
Pathophysiology
melanin madein melanosome and ratelimiting step is Tyrosinase which copper containing
tyrosinase levels absent as used in the hairbulb tesecopper normal
MSH normal tyrosine levels normal and normal no melanocytes
CF foveal hypoplasia hypopigmetation of fundus and iris and secondary problems like myopia nystagmus dec VA photophobia dec binocularity ans stereopsis
PLUS systemic features that are obvious and we see em a lot in RSA
DDX ocular albinsm affects only eyes xlinked giant melanosomes
Albinism
2 clinical patterns; both may have photophobia, iris transillumination, hypopigmented fundiTrue albinism:
hypoplastic fovea, no foveal pit, no yellow macula lutea pigment; may also have abnormal retinogeniculostriate projections (temporal fibers may decussate) perhaps accounting for high rate of strabismusOculocutaneous albinism (eyes and skin affected)
Reduction in amount of primary melanin in melanosomes
AR
Tyrosinase positive (some degree of pigmentation)
Tyrosinase negative (total lack of pigment)Ocular albinism (only eyes affected)
Reduction in number of melanosytes
XL
2 potentially lethal forms of albinism:
Chediak-Higashi syndrome Oculocutaneous albinism w/ extreme susceptibility to infxn.Hermansky-Pudlak syndromeOculocutaneous albinism w/ platelet defectEasy bleeding/bruisingUsu. Puerto RicanHair bulb incubated with tyrosine Will produce pigmentation if has tyrosinaseKids more than 4albinoidTelecanthus and epicanthus which is extra skin fold over medial canthus repairHypertelorism Make a Y mark and then a Z at 60^ and 45^Medial palpapral ligamnet lies above nasolacrimal sac so dont dissect too deep!It is under orbicularis so remove this and fat. Angular vein from the facial crosses MPL infront of it about 8mm medial to the medial canthusMRIspectroscopy checks for abnormal neurometabolites and normal metabolites eg choline peak indicates membrane turnover and therefre a neoplasmic peaksurgeryamniomic membrane for conjunctival grafts good substrtae for cell migrationClinical testsBrightness acuity tester measres glare and cmpares to tinted glasses sunglasses and antireflectives PAM Potrntial aquity meter quantitve m acular health assessment standardized to SnellensEquivlent phaco time eg 10 sconds at 20% power is 2 seconds EPTPosterior lammelae keratoplastyA deep ,stromal pocket made thru 9mm scleral incisionRhabdomyosarcoma mostcomon paediatric malignancy
10% of all Rhabdo start in orbit vs 25% in head and neck
trunk is rare
ageis 7years and superiornasal orbit rapid growth
histolgy embronal is mostcommon ( superiornasal)followed by alveolar inferior orbit and has worst prognosis
botyriod ocurin subconjunctiva and pleomorhic which is weel difeentiated havebest prognosis
Rxchemo vincristine and actinomycin for 1 year plusorbital radaition 450 to 00 ads
90% survival rate rarely haveto exenterate
Fundus dydtrophies
RPE dystrpohies 4 common types
1 Bests yellow dots = lipofuschin in space between sensory retina and RPE which may coalsce to form egg yolk FA blocked choroidal flurescence
This may absorb completely or break up to look like sscrabbled egg
It may eventually form a hypertrohic scar or atrophic scar or vasculized scar with CNV
2 Adult foveomacular vittiform dystrophy
small yellow subfovbeal deposit = as bests but smaller and less progression and more localized
3 Stargarts & Fundus Flavimaculatis
Stargarts
oval lesion snail slime or bronze beaten 1.5 disc diameter = degenerative changes in RPE and SRS
Fundus flavimaculatis
yeelow white spots usually piscform or oval in shape and spread to periphery from macula= Lipofuschin or other waste product at RPE level
FA early on these lipfuchin causes blockage of backgrond choroidal flurescene and if RPE is atrphic there is a window defect
4 Familial Dominantdrusen
PHOTORECEPTOR dystrophies
1RP Bony spicule pigmentation beging in midperiphery arteriolar attenuation and waxy disc pallor=loss of photoreceptor esp rods and subsequint RPE damage manifesting by pigment absorbtion
2Cone dystrophy
Bulls eye lesion which is yellow ring of atrophy with normal red centre at fovea = loss of cones at fovea and also loss of RPE sparring the foveala where the cones and RPE are more resilient.
3Lebers amaurosis
Intravitreal injections
air saline silicon oil expanding gases or perflurocarbones
1air is used in hypotony posterior breaks radial retinal tears called pneumatic retinopexy
air is absorbed by 5th day adding 30% sulfur hexafluride lasts twice as long as it takes up nitrogen as air is absorbed
2 longer acting gases expanding gases egPerfluropropane c3f8 and PFethane c2f8
3silicon iol is better in PVR where the retina is immobile
4 Perflurocarbons are clear heavy liquids twice SG water low viscosity allows easy injection
infantile eso
if nystaagmus dampenson convergenge= nystagmus blockage syndrome
To pick up normal fxning LR rotate the child ordolls head manourvre
Occlusion
1 week for every year of age
never more than 6 months not beneficial after that
could do 1 to2 hours daily over a longer peroid
yunger do better
atrpoine therapy to cause blur in the good eye for mild amblyopia in hypermetropia
pleotics in kids pover 9 years where fovea is shielded and parafoveal retina temporarily blinded with bright light forcing fixation with lazy fovea
do surgery in 1 month even ifamblyopic if glasses have made no improvement
the eyelid
tarsus is 1omm in heigt and is con tinous with septum
the lvetaor apounourosis attaches to the superior tarsus and pierces the septum it also attches to skin to form the skin fold which is a great landmark
most anatomy is behind septum ie fat which is a good landmark as it separates aponourisi from septum superorly before piercing septum
this fat can be resected as it may herinite thru septum if it is cut
the aponourisi is much broader than the levator muscle aand it has horns attached to the medial and lateralpalpabral ligaments
deviations DVD IOO A&V is signifiant if more than 15 diopters
DVD is excyclodeviation and updrift when an eye js covered
RX sperior rectus recession +- Faden procedure
usually bilateral and follows eso surgery and rx indicated when cosmeticaly apparent
NYstagmus is jerk or pendular
jerk is gaze induced or gaze parlytic and describe it in terms of the fast phase
Nystagmus may be physiological motor imbalance or ocular
Ocular is pendular and horizontal and generally all kids who lose central vision before 2 develo it
occasionally abnormal head posture may be adopted todecerasew nystagmus
OCT optical coherence tomography
10um of retina can be studied
normal macular 165um thick in CMO we see a central cyst thickening to 450um and loss of foveal depression
Eximer is excited dimmer we get when inert argon acts with Fl to releases UV light 597nm that causes thermal controlled damage
News
corneal prosthesis ookp osteo odonto keratoprosthesis
Wavefront analysis is another way to do corneal topography uses ray aberations of mirrors and lenses using Hartmann screen which is a metal sheet with holes and or lenses
Intraocular lens
aphakic glassesmagnification ~30% contact lens ~10% IOL only 4%
less magnification the more posterior the lens but postop correction is complicated as a normal galelian telescope is a iol with a spectacle in the front
for each diopter of glasses at 12mm magnication is 2%
therefore leave people a bit myopic so a minus lens of 1diopter will minify by 2% so canceling the iol effect
normally > 5% anisikonia= diffrence in size is untolerable
There are 3reasonsto make a person myopic by 1 to 1.5dioter ie put a stronger lens
1 Less magnification almost to zero
2better tolerated than hyperopia
3 allow some function at near without glasses
ie use more powerful lensesrather than less
P is = A constan(118 or 113 for AC lense) t + -2.5 × axial lenth in mm + -0.9 keratometry in diopters
eg P = 118 -2.5 × 22.6 - .9 × 44 = 118 -100 = 18dioters
a is generally 118 or 114 for anterior chambers lens
ie anterior chamber lens are less powerful(nb the more anterior the less powerful the lens needs to be ,this can be seen in practice as we never prescribe 22 diopter glasses eg iol is 1.25 glasses prescribtion
when working out axis the 3 oclock position is 0 12 oclock is 90 and 9 oclock is 180 by convention
with the rule astigmatism tighter or more powerful curve is vertical
Tablets 25 and 5 mg ugs Imuran = azathioprine becomes mercaptopurine and blocks DNA synthesis used in rgan trasnplant SLE RA and Chronic active epatitis Tablets 25 qnd 50u mg use also in graves ophthalmia
Endonasla holmium DCR
diode newer laser
surgery
sling ptosis repair
done hen no levator function
use 20 goretex
start at lid 5mm above margin nad dont g thru tarsus
make 2 slings as a pentagon the central brow one above 1cm above brow in centre and make the knots here
aim is to raise to limbus at end remeber to leave knots lng as yu can adjust after suture
Telecanthus and epicanthus which is extra skin fold over medial canthus repair
Make a Y mark and then a Z at 60^ and 45^
Medial palpapral ligamnet lies above nasolacrimal sac so dont dissect too deep!
It is under orbicularis so remove this and fat. Angular vein from the facial crosses MPL infront of it about 8mm medial to the medial canthus
z plastiy is used to stretch a scar closed by releasing tissue sideways at 60' and than tranpose
This is very easy as you make space and suture
MRI
spectroscopy checks for abnormal neurometabolites and normal metabolites eg choline peak indicates membrane turnover and therefre a neoplasmic peak
Tumours
Harmatoma is tissue normally found at asite but in excess eg optic nerve glioma there is normally glial tissue but here there is excess growth
Choristoma
It is a tumour of normal tissue usually fat or C/T covered by epidermis of skin in an unusual site eg limbus
these are the pictures we have
Plastic surgery
Entropian
choice of procedure
assess for horizontal lid laxity
u may use simple suture repair which lasts only 18months
a more perment procedure is the Weiss which corrects most involutional entropian
If significant lid laxity exists (check this pulling lower lid and if it does not spring back after a blink it is severe a quick spring return is normal and a s low return is mild or check by moving lid dowmwards and if the posterior lid margin is more than 10mm from cornea
do sutures if you cant a bedside procedure where u use 4 o absorbable vicryl=catgut that is double armed
start on conjunctival side 2mm below lower tasrus and aim obliguely upwards to exit on skin just below eye lases about 2. 4 mm below............. now tie the 2 arms on skin
NB for less severe entropian you dont have to be that oblique ie be more horizontal ie from lower tarsus border to slightly higher outside skin
2 Weiss procedure
Make an stab incision 4 to 5 mm inferior to lashes ie thru tarsus and extend with scissors full thickness remember to protect withlid guard u may be 5 mm inferior laterally
Inspect the lower edge of incision from inside u hace conjunctiva lower lid retractors = white sheet of tissue , obicularis and skin
Place 3 double armed 4/0 absorbable sutures thru conjunctiva and lower lid retractors 2mm below cut edge
Pass the suture into Orbicularis anterior to Tarsus in the upper wound edge to emerge 2mm inferior to lashes
Tie the sutures to achieve slight overcorrection
Remenber to close skin with 6/0 silk and remove in 1 week
U may remove the everting sutures at 10 days if thee is marked overcorrection.
Anterior lid split as per collins
Make a curvilinear line
incise at crease deepen to tarsal plate and inferiorly
2mm abve lashes make a double loop and thru top of tarsus and tie at lashes
remove redundant skin and clse as blepharplasty
congenital optic disc anmaliesMrning glory syndrome is unilateral large evacuated disc with glial tissue and hyaloid remnents and is a colobma
blood vessels arive as a spoke around nerve which is the give away pattern
Coloboma
Drusen
tilted
Pit darker area in disc
hypoplasia midline structures double ring sign
myleinated
aicardies large colboma x linked males
Cyclocryotherapyciliary body ttemp declines in the first 2 to 30 seconds
can achieve IOP reduction in 60% of time when using temp of -80 degrees celcius for 60 seconds
probe tip of 2.5mm is used and 1 to 1.5mm from limbus
limit to one hemisphere at first sitting
Treatment of uveitis
Azathioprine Imuran
converted to mercaptopurine
dose of utoimmune use is 1 to 2 mg per kg that is the stable dose
aailable in 25 and 50mg tablets
baseline U&E FBC & LFTS every 2 weeks for 2 months
Contraindicated in pregnancy and with allopurinol(for gout) rifapicin(TB and warfarin
guidlines to watch and stop:
wcc less then 4
Neut less than 2
platelets less tha 150
AST ALT more than 3 times
o r serious ulcers or bleeding
Methotrexate
dose 7.5mg orally weekly
give with folinic acid
reti
Phaco
piezoelectric handpiece frequecy 24 to 56 000 hz and average bore is 18 gauge the purple is smaaler and the blue larger
nb the larger the no the smaller the gauge
waardenbergs syndrome
heterochromia premature greying hair loss hearind loss due t endolymphatic hypdrops (ELH)
wide inne corners of eyes broad nasal bridge virtiligo eyebrows that grow together sevee pms hirshprungs spinal disorders
Prisms
Eye moves towars the base
presbyopia is caused by this progressive growth crowding the ciliary body. If his theory is correct, the progression of presbyopia should be halted if lens growth is arrested, and it should be reversed if the diameter of the ciliary body is enlarged. With this in mind, the scleral expansion surgery was developed
Goldmann 3 mirror
cetral aprt central 30' posterior pole
equtorial mirror oblong and largest 30' to equator
peripheral mirror square and intermediate in size and square shape equtoria to ora
goni dome shaped angle
look for rd in upper temporal
Corneal Pachymetry arule central corneal thickness more than 600um indicates endothelial dysfxn and oedema ~~~~indicate postop risk
specular microscopy normal more than 2400cells per mm2 abnormal less than 1000
polymegathhism (enlarged) or pleomorphism ~~~~indicate postop risk
canthal tendon laxity
pull the medial or lateral canthus away and any movement more than 1mm indicates Medial or lateral canthal tendon laxity
Lid laxity horizontal pull the lid away from the eye quick snap indicates normal
slow return mild
incomplete return even after a blink severe laxity
ARMD,Prostrare cancer lycopene 10mg daily
Malignant Melaoma Studies states mosts lesions are not Malignant Melanoma
melanomas may be melntic or amelanotic
THey include
Neavus
Melanocytoma pimented benign lesion of the optic disc histologically form of neavus with heavily pimented cells
Bilateral diffuse uveal melanocytic prolif(BDUMP) paraneoplastic syndrome multiple
Metastaic cutaneous melanoma
RPE related
Congential hypertrpohy of RPE well circunscribed darkly pigmented often ass vascular anormalies no malignant potential
Tumours of RPE very rare and can include adenocx
ReactiveHyperpasia of RPE to trauma or injury
Combined hamatoma of retina and RPE
eg juxtapapillary have glial tisse as well
Non Pigmented
1' choriodal tumuors
Choriodal haemangioma raised reddish brown patch (VS in Sturge webber it is diffuse red )
Choriod osteoma in yug healthy females exclude Bscan highly reflective mass when reduce senstivity to exclude all tissue
2' choriodal neoplasms
most common intraocular malignacy
eye is although not a favoured site
Non neoplastic non pigmented
Presumed aquired retinal heamangioma
Age related choriodal neovascularization
easy will have some degree if bleeding and discform
Inflammatory lesins
Posterior scleritis
TB
and choriod is most frequent site Breast cx cream yellow other cx pale
Contact lenses
Base curve post curve ~8.1 to fit snug on cornea
cornea 0.5mm centrally and 0.7mm periphery
abrasion healing 4 days
peripheral flatter creating asheric
radius of curvature of apex is 7.5 to 7.9mm
Correction of astigmatism
increase power (shorter radius) ~~~put a tight suture and do wedge resection
decrease power ~~~~~~~~~~~~~~make transverse cut or relaxing incisions
remember surgery changes power reciprocally in 2 merideans
Transverse cuts about 90% deep 2 to 4mm long ~~~change power by 1 to 2 D
Relaxing incision about 3 clock hours and 90% deep ~~~~~~~~~~~~~~~1 to 10 D
Ruiz proocedure trapeziod with 2 radial and 2 to4 enclosed transverse
wedge resection 20 diopters
change due to age incison depth healing process and elasticity ( = youngs modulus ie stress / strain
ptosis a quideMG fatiuability o sustantained upgaze is simpsons test
cogans lid twitch sign overshoot of lid when rapid fixation from dowgaze
ice for 2 mintes er ptotic eye improves ptosis
CNIII palsy
what is webers or benedicts or norhnagel
aberent regeneation = adduction on upgaze or consriction of pupil on laeral gaze or elevation of lid on downgazeeg meningioma or aneurysm means longstanding and infarct unlikely
levator dehiscence
high skin crease and levator function ok
causes
incolutional=senile
trauma to SR complex in Cataract Sx
blepharochalasis=idio recurrent non piting oedema of upper lid
Marcus gunn jaw winking
open mouth or move jaw corrects ptosis
cause misdirected trigeminal nerve into levator muscle and hence synkinetic elevation when pterygiod is stimulated
Plexiform neuroma
Blepharophimposis
horners
Aproach to Clinical picturesBulls eye(is a Fluroscene defintion) is due to cetrally normal pigmented fovea surrounded by full ring of depeigmented RPE which is seen as transmission defect on FA Chloroquine binds to melanin in RPE and later causes atrophy
Causes cone dystrophy chlorquine and synthetic antimalarial Stargarts where there is a widespread RPE epithilopathy with lipofuscin Benign concentric anular ddytrophy where Rods and cones and later RPE atrophy 20 to 30% of RP
Macular Star = lipid rich exudation in outer plexiform layer that ppts in a stellate pattern as fliud is absorbed
Causes Capillary angiomas HT Lebers Idiopathic stellate retinopathy Pappilitis /pappiloedema as leakage of bv to optic nerve
Macular cherry red spot=non oedemaous retina at fovea
Group of inherited metablic diseases accumulate sphingolipids in ganglion cells causeing them to become white in contrast to fovea NB the late stage is optic and NFL atrophy
1Tay sachs Ganglisideroses type 1 AR and in infants and die by 2 years so we will not see in adults
2 Nieman pick A B C D with severe to no CNS involvment Group D presents late so you may see in adults and will end up with CNS involvment
others one type with hypotoactivty etc and sialososi with myoclonic jerks in contrast
White spots at fundus
Approach to choroiditis and retinitis
choroidits usually milder and causes blurring with only mild vitreous infamation
HALLMARK yellow grey subretinal lesions
if non inflamatory it is POHS that may dev SRNM
If inflammatory and focal it is TB sarciod toxocara or norcadia
if mutifocal it is white dot syndrome and if less 50 years old MEWDS AMPEE GHPC or mutfocal choroiditis BUT if more than 50 Birdshot and you can do something like steriods and cyclosprin
if diffuse it is SO or VKH
Retinitis
HALLMARK Retinitis whitish opacification with haemorrhage exudation and vitritis As the retina is vascular usually a vascultis
Remember to check vasculitis if it is occlusive haemorrhagic or occlusive . It may also be primary and cause a secondary retinitis
1Subacute is Toxoplasma or Candida (which starts in the choroid )
2Acute multifocal is Bechets that has a serious vascultis assosiated
3 suuden peripheral progressive is ARN
4 Diffuse progressive CMV and syphitic
5 Oclusive vasculitis has sheathing haemorrhage exudation and is differentiated into inflammatory or non inflammatory
Approach to CWS
infarct of nerve fibre layer ass with blood vessel ie superficial
ischaemic whitening
location
A macular epiretinal membrane
B vein 1 beeding~~~ DM
2 dilation ~~~Ocular ischaemic syndrome
C artrery 1spasm PET 2 nicking Chronic HT
Dgeneralized with1infection~~~AIDs septicemia or Bact Endocaditis with2 heart dx anaemia or atheroma with CVD SLE
Approach Sheathing
vessel walls usaully transparent we only see blood
occlusion of blood resluts in Ghost vessel
It may be inflamatory or occlusive with resultant exudation
fuzzy iregular cuffing of BV
1perpappilary Hyaloid remnant developmental
2After pappilitis
#Approach to Neuro
Phacomatoses
Sturge weber is also called encepholtrigeminal angiomatosises and is only one without hereditory basis Neavus flamus=angiona of 1st and 2nd branch of CNV The cause of mental ahndicap and epilepsy is P/Temporal meningela angioma that is common and on Ct it is calcified
the eyes:
Tram track on skull xray
Dt calcification of haemangioma
60% have Glacouma and Buphthalmos and 40% the glacouma occurs after 2 years due to angle anomalies or raised episcleral pressure due to episcleral haemangioma.
40% have a diffuse choriodal unilateral haemangioma
others iris CB or episcleral haemangioma
Tuberous sclerosis Bournvilles or epiloia Auto dominenthave adenoma sebacum that is angiofibrima in butterfly distribution that progresses CAL spots firous plaques skin tags ash leaf spots=hypomelnotic spots CNS slow growing astrocyte hamartoma usually parventricularly that cause epilepsy and hydrocephalus
visceral subungal and heart rhabdomyoma and kidney angiomyolipoma
The Eye
50% have retinal astrocytomas and commnly hypopigmented irsi spots and hypopigmented fundus rare.
Van hippel lindau AD haemangioma of Cerebellum oR MO is most common also cysts pof kidey and liver with phaeochromcytoma
The eye usually bilateral optic nerve and retina cap haemangiomas that are multiple but you cannot predict a brain or kidney lesion
Ataxia telangiectasi AR progressive cerebelar ataxia and MR in adolecence with skin telangiectasia of ear lips face
The eye bulbar telangiectasia at about 5 years old and ocluar motilty problems
Six nerve palsy
Think about the nerve itself that is associated with the PONS and the acoustic nerve and facial nerve as well as the tip of petrous bone
acoustic neuroma compresses this and vth nerve
base of skull raised icp nasopharyngeal cx
Retinal detachent sx with JO
there was an inferior RD
step 1 full peritomy done
and 6 silk isolated all 4 muscles remember to go under with bunt part of needle while holding tip
step 2 slide under IR silicon tire 9mm width
step 3 slide silicon band 2.5mm under rest of muscles and tru groove in tire
step 4 take silicon sleeve and ask assistant to open to width1.65
thread band thru and leave excess long
put a suture posterior to tire in direction with band and continue matress anterior . tie this
now insert yellow needle to drain fluid and robe with canailiculus probe
step 4 pull band taut gauging by iop and indentation
cut excess band
doe cryo with indirect
close
scleral buckle KI James themba
do 360 perimetry
use one loop hoding needle at tip to expose muscles use 6 0 silk and attach to misquito
thread silicon tire 9mm beginning at 6 o clock and thru all muscles (it is aloop so cut it first)
step 3 thread band the same way 7.6 mm width dont woory about getting it in the groove
step 4 use utility and toothe to get it in grrove
step 5 at 7 or 8 oclock where they will meet insert matress posterior to sleeve and then anterrior and tie.
this is your holding suture
step 6 ask assistant to open slleve and put both ends thru while pulling tight dont worry about which is ontop or below
step 7 put 3 more matress sutures at 3 9 and 6
step 8 drain fluid with a green needle at 4 points
step 9 at pars plana at 2 and 10 drain fliud u can use a 15 degree knife
insert fliud exchange syringe and then air syringe insert air or sf6 t
flatten retina
Mustard jumping man for epicanthus
remeber that u try to get skin more away from eye"X Tris" I
‹
>----- ‹
1Mark the site of of the intented canthus
2Pull the epicanthal folds medially to a point and mark this NB this is where the z plasty is going to be. Make a 60^ z and a 45^ z
3 cut with blade and retrarct flaps with suture
4 now do the telecanthus by exposing subcutaneous fat and then OO and fat to EXPOSE MCL you will see periosteum at side of nose . dont cut angular vein beware.
5cut MCL but dont damage underlying Lacrimal appartus
6 pass 4 o silk double armed from posterior to anterior thru MCL near medial canthus
7 pass thru insertion and periostium from posterior to anterior and tie
8Transpose flaps and it may be necessary to trim to neaten
close PPV sites 6 silk
close conj
Anatomy of neuroretina
inner nuclear layer is where bipolar amacrine and horizontal cells lie
inner and ouert plexiform layer is on either side of this and is the landmarks xanthophyl here and source of herdingers brushes on plane polarized light.
the capillary arcade is in the inner nerve layer
look for the superficial nerve fibre layer and the outer nuclear usually ass with a fixation cause detachment ass with rpe
PPV how to do
Do perimetry and make sure 9 to 4 o clock open
4mm from limbus at 4 o clock put a suture going foward and one 2 mm in front going backward . that is a matress
pierce with PPv spear or use 15 degree for a start aim to apex watch to see tip insert flow port and dont on until all instruments in
repeat at 2 and 10 oclock and put light and vitrector
do vitrectomy in anterior vitreous and than put ontact lens and do posterior vitreous
close after vitrecting ports
Thing to ask
Vitrector pack cassette and bag
infusion port
the pack will have 3 ports that light on and fit
remember to prime outside the eye
remeber to focus when the contact lens is on so you will need all four limbs go to high mag
Rx glaucoma latanoprost travaprost
Lumigan brimoprost se hyperaemia so use at night also increased risk of CMO and uveitis if already susceptible grows lashes and darkens eyes
corneal thickness less than 550um increased risk of glaucoma because it means thinning due to glaucoma
ocular hypertension study
Refractive sx
keraromeleusis= greek for hornlike cornea and smileusis = carving
LASIKtechnique
speculum and mark epithelium with lammela surgery epithelial marker then put pneumatic suction ring to fixate and increase IOP and create a track for keratome
before putting on microkeartome ensure IOP is >65mm with Barraquer tonometer.
put on the microkeratome that is loaded in dove tailed grooves of suction ring with foot padel
stop vacuum and remove suction ring
Laser ablation
make sure patient of perpendicular to laser and raise flap fold out of ablation field .prior to ablation wipedry fliud that may accumulate with a single motion sponge
as laser comes to hinge cover with a blunt instrument to prevent ablation of flap
Reposition flap usung a blunt instrument after irrigating
check appostion
Examining squints
Va fixation central light reflex
C unC with light
What is surg limbus?
2mm band with postpr vrslrlsu
N lebn e omn n hebsadps ht e hebsadslrlsu
RBCLCOYLma aetl ugcllmu aft \ cea et y4md aaetssscn y2m ceooy
Op
Coeotrfa
F sMmC5ui yyiieaaou hti luiae n rvnsdasnhdsi ioi hs
Oe2mt 0prm n hn5gprm ntnapiain o e asol oi oeihlu v iiyi hc lsfbolss yooydmgsedtlu n i oyadds s02t . Gprm
l e M40o . ieo n dblcdamiehon eaa ntph tabri lkhiwncmtms
What is gradenigo
Gradenigo syndrome ie involves CN five to eight
~~~ ipsilateral CN VI palsy, with decreased hearing, facial pain and facial paralysis due to abscess formation in petrous apex following otitis me
-Pseudo-Gradenigo but due to nasopharyngeal CA or cerebellopontine angle tumors
Disc is 5 degrees
Color vision fields
central 4 degrees: no blue; red & green only=fovea
4 to 20-30 degrees: trichromat=macula
30-70 degrees: dichromat (red-green blind)=equator
> 70 degrees: monochromat=peripheral
Color vision terminology
R-G-B
protan: red: erythro
deutan: green: chloro
tritan: blue: cyano
anomalous: sees 3 colors but not at same wavelengths as normals
anopia: sees 2 colors (missing pigment)
Optimal Wavelengths
1) blue cone: 450 nm
2) green cone: 550 nm
3) red cone: 580 nm
4) rods: blue-green= 500nm
Entoptic Phenomena 8 phenomenon 4 from reina and 4 from rest
wbc bv macula pigment and nfl and one from retina vitreous and lens and pupil each
Bv/wbc/nfl/xanthophyl absorbtion of polarized light
3) Purkinje figures: images of retinal blood vessels with bright or angled light
5) blue field entoptic phenomenon (flying spots): represent passing of WBC in blood vessels- can be used to determine size of FAZ
6) blue arcs of retina : NFL - shine rectangle on retina
7) Haidinger's brushes radiating from the point of fixation due with plane polarized blue light: due to variations of absortion of light by xanthophyll in Henle's layer outer plexiform - may be affected in macular edema before obvious edema
1) lens: radiating lines in star due to suture lines
2) phosphenes (flashes): vitreous pulling on retina
4) floaters: vitreous collagen, syneresis casting shadow
8) Styles-Crawford effect: parallel rays of light are more effective in stimulating cones; rays from edge of pupil which hit retina obliquely are less sensitive than those thru center of pupil
Ct scan
Look at turbinates superior
Is anterior and inferior is big baloon at back
Ehtmoid is anterior and spheniod posterior
Dont let maxillary fool you as it is next to ethmoid
It is not an ethmoid wall erosion bt the maxillary
Macula
5.5 mm in diam. (3.5 mm or 18^ degrees of visual angle) centered 4 mm temp and 0.8 mm inf. to center of optic disc
Fovea:
concave central retinal depression 1.5 mm in diam. (1 DD or 5^ degrees)
Foveola:
0.35 mm in diam. - FAZ
Umbo (clivus): central concavity of foveola floor / light reflex
Neurosensory retinal thickness
0.23 mm - papillomacular bundle near optic nerve
0.11 mm - ora serrata
0.10 mm - foveola
Retinal circulation
CRA supplies inner retina incl. inner 1/3 of INL
Choriocapillaris (CC) supplies outer 2/3 of INL to RPE
Bruch's Membrane
Layers (inner to outer)
BM of RPE
Inner collagenous zone
Elastin layer
Outer collagenous zone
BM of CC endothelium
if the TM cannot be seen easily, the patient moves his eye in the direction of the gonioscopic mirror to open the angle and improve visibility.
Latersl tarorrhaphy
05mm deep incision with knife over meibomion glands for 1 to 1.5 cm perpendicular to margin
2 grasp with forceps and cut .nb: this is posterior lid margin and avoid anterior lammela and lashes as this will lead to entropian
Use 6 o nylon thru debrided tarsus and posterior lid margin
Begin and end at lateral side threading from raw cut side
Tie qiute tight as nylon has elasticity
CN nucleiRemember IIIrd and VIth nuclei have ipsilateral innervation, whereas the IVth nerve nucleus has contralateral innervation it decussates near inf colliculisPhysiology
Vicryl causes greatest inflammatory response prism diopter is the no of cm drviation at 100cm a ray of light id deviated eg 40 prism diopters moves image 40 cm down at 100 cm deviatipn is towards the base of the prism eg place the apex in the direction of squint so light ray going on will be away from apex towards base use this info in squints
But when you look into a prism the image we see is displaced to the apex ie the common teaching if somebody sees something higher help him with a prism with the apex in the direction downward that is to correct the higher image VA is 300 to 400um spacing of photorecepter at fovea this equates 8 seconds of arc vernerone minute of arc or 60sec nb the small Es of 6/6 subtend 1minute at each armSteropsis Testing Normal bifoveal fixation is 20-50 arc seconds & 80-3000 arc seconds is normal peripheral fusio When testing you must have adequate illumination to test properly since it is a peripheral phenomenon
W4D: far: 1.25 degrees(1 degree is 60 min or 3600 sec)near (33 cm): 6 degreesIn mavula amblyopia image 4 dots seen at near but lose 1 as dots are moved back in ambyopic macular )
At 33 cm goldmann vf spot is .43 degree this is minified 20 times at retina since second focal point is 17mm behind nodal point so 330\17 is 20Reduced eye al 22.6anteriorfocal point 17mm from corneaposterior focal point 22.6 mm from cornea to retinaNodal point 5.6 mmfrom corneaAvearage Index ofeye 1.33 ie as waterAnterior and posteror focal points differ Because the media on each side of refractive media is different ie air and waterOptimal pupil1.2mmcontrast= imax - imin/ imax +iminThe refractive error of an eye is the dioptwric quivalent of the far pointFocal length is the reciprocal ofthe diopteric power of the eye.Ie 1\ 1.7cm *100 = 58 approx 45 + 20
Congenital cataracts(if bilateral most likely unknown and second hereditoryA) Bilateral1) sporadic (60%)2) heriditary without syst. Assoc. (30%)3) with syst. disease: 5%4) with TORCHS: 3%5) with other ocular abnormalities: 2%
B) Unilateral( if unilateral unlikely to be hereditory1) sporadic: 80%2) ocular abnormalities: 10% (PHPV)3) traumatic: 10% (beware child abuse)Phaco Micro surg alcon acurus30% phaco power 90mm hg pressure 250 vacuumNew iols implant thru 1.6mm this is mics microinvasion sx healon 5 2.3% na hyaluronate
Modified wavefront algorithm aims for prolate cornea or -0.46 aspheric factor to compensate for spherical abberation ie dont flatten but keep the shape done by increasing optical zone ad hence preserving corneal shapeInstruments in micro phaco:1mm diamond knife with 7 depth settings up tp 6mmSideport fixation knife 0.8mm 23 gauge capsulorrhexis Irrigating chopper with karate23 gauge bimanual irrigating aspirating handpieces
Phaco Micro surg alcon acurus30% phaco power 90mm hg pressure 250 vacuumNew iols implant thru 1.6mm this is mics microinvasion sx healon 5 2.3% na hyaluronate
Modified wavefront algorithm aims for prolate cornea or -0.46 asheric factor to compensate for spherical abberation ie dont flatten but keep the shape done by increasing optical zone ad hence preserving corneal shapeInstruments in micro phaco:1mm diamond knife with 7 depth settings up tp 6mmSideport fixation knife 0.8mm 23 gauge capsulorrhexis Irrigating chopper with karate23 gauge bimanual irrigating aspirating handpiecesRadial sponge RdFind the holeCut sponge and put radially 2 scleral sutures in a matress one ant and one post in radial direction but nb dont have go anterior to spiral of lineuxCryo around hole?nd suture dirrction is radial and sponge goes thru loops and trim anyeriorly
Nysyagmus and strabismusCongenitalTwo causes of cogenital nystagmus1 Sensory or pendular and 2 motor or jerk Exam look for anormalous head postionsLook for best VA this may be at near as convergence may improve nystagmusMotor is due to conjugate motor centre defects and is pendularNystagmus as per kai tutSurgery for motor nystagmus with good visioneg the eye null point lateral gaze and head turn to rightAccording to anderson besselbaum protocol do 8 mm 5 mm 6mm 7 mm suregery to move eye to the rightModify to get better resultsIe 20% increase for 20D and 40% increase for 45DYou may do the same for chin up or down
Remember to move eye away from to null point ie tofard abnormal head posture which is what is being treated