Eye Diseases Notes PDF

Etiology Appearance Image Additional Treatment/ Management RPE Dropout/ Congenital - result of focal loss or - Pale yellow-white - In Macula: excessive - normal benign finding → RPE Dropo...

Etiology Appearance Image Additional Treatment/ Management RPE Dropout/ Congenital - result of focal loss or - Pale yellow-white - In Macula: excessive - normal benign finding → RPE Dropout/ RPE Window diffuse loss of RPE cells - Anywhere in the fundus oxidative stress can cause document & monitor, pt Defect/ RPE atrophy or and therefore loss of - Focal (tiny) size RPE cell dropout education hypotrophy pigment - Round shape - Retinal Pigment Epithelial - if acquired, establish the - Congenital or acquired - Distinct borders Dropout/ RPE atrophy/ reason - Secondary to laser surgery, - Unilateral or bilateral RPE hypotrophy are - observe on Fl angiography RPE degeneration (aging) ACQUIRED and —> HyperFl (constant size or inflammation irreversible, can occur in through all phases) neighbour cells causing large area of atrophy, and their size usually varies RPE Hypertrophy/ - RPE cells may become - black or dark brown, flat Variations: - observe on Fl angiography Congenital hypertrophy of elongated and therefore - Oval/round shape 1. Halo around lesion: may —> HypoFl, stays the RPE (CHRPE) may accumulate more - Single or multiple engraved see greenish-greyish halo constant throughout the pigment RPE cells surrounding representing phases - Congenital - Anywhere in the fundus RPE dropout, slightly less - normal benign finding → - Unilateral or bilateral pigmentation document & monitor, pt - Distinct borders 2. Lacunae (hyperFl): areas education - Evenly pigmented of RPE dropout within the - Size varies lesion, can occur overtime - May contain a “halo” of and can enlarge lighter spots (halo nevi) 3. Bear track: congenital - May contain “lacunae” multiple grouped areas of (hyperFl) (RPE dropout pigmentation, group of 3 within the dark lesion) to 30 individual lesions, - May present in a “bear usually sectorial, variable track” formation (several size (0.1-0.3mm), spots clustered together), unilateral, do not pose a greyer in color and smaller, risk for malignancy will not have lacunae/halo, unilateral CHRPE Mimickers - pigmented fundus lesions - usually bilateral - Hallmark: a life threatening - ask if they any family associated with Familial - Multiple lesions familial cancer (bilateral, history of intestinal cancer Adenoma Polyposis (FAP) - More haphazard multiple quadrants, diff - refer to internist for - Gardner syndrome sub distribution shape/size, irregular additional testing type of FAP - Irregular/ jagged borders pigmentation) - document, monitor, pt - almost 100% of patients - Irregular de-pigmentation - Lesions in the eye are not education with this develop colon on margin—> fish tails or malignant but indicate cancer comma configuration malignancy - Autosomal dominant in the digestive tract condition - 70% of patients w/ FAP will have characteristic lesions in the fundus RPE Hyperplasia - disruption of RPE cells, - irregular shape - may affect VA depending - benign → document, pigment of damaged cell - Flat on location monitor on routine migrates on top of - black/dark brown - Accompany other retinal examination, pt education neighboring cell - Location varies: anywhere changes adjacent to the - determine etiology - acquired from trauma, in fundus, but commonly RPE hyperplasia - Observe on Fl angiography inflammation, degenerative in posterior pole —>HypoFl on angiogram, changes, retinal surgery, age - Distinct margins stays constant throughout related, or laser burns - Size varies the phases - Shape varies - often accompanied with a neighboring area of pigment loss - age-related hyperplasia is typically faint, called “mottling” - may or may not progress Choroidal Nevus - A focal area or areas - oval/round shape - the more asymmetrical in - Observe on Fl angiography composed of dense - Symmetry shape, the greater the risk —>HypoFl on angiogram, choroidal melanocytes - Greenish/grey uniform for malignancy stays constant throughout - can develop from a uveal color - The more non-uniform in the phases tract nevus - Below RPE- vessels run colour, the greater the risk - document & monitor, pt - can be congenital (rarely above for malignancy education observed in young children) - Distinct margins w/ hazy - Red free filter: RPE - monitor 6-12 months after - Common in caucasian edges lesions will look like its first diagnose, if stable, population, >50 years old - Size varies still there (better contrast), monitor yearly - Edges may be blended due choroidal lesions will fade - look for signs of to it being below the RPE away and become invisible malignancy - low grade, spindle shaped, - If lesion appears to be - refer for second opinion if ovular/round melanocyte more elevated, the greater looks suspicious with varying cytoplasmic the risk for malignancy - ultrasound, serial pigmentation - * Drusen will only appear photography - may develop drusen within within choroidal nevus—> the lesion after prolonged one way to distinguish presence (benign/good choroidal nevi from RPE finding) located between hypertrophy ( with RPE &BM or within RPE lacunae) layer - if in the macular area (appears organe/brown due to xanthophyll), can cause photoreceptor degeneration & decreased VA Choroidal Melanoma - most common of all - Large Class 1 = low metastatic - refer to specialist & get posterior ocular - Change in size- growing potential (spindle cells) physical exam to rule out melanomas/intraocular - Elevated Class 2 = high metastatic pot. metastatic tumor malignancies (along w/ - Variation in colour within (epithelioid cells) - biopsy ciliary body) lesion 95% of metastasizing occurs - Treatment based on tumor - geographically, generally - Variable margins in the LIVER size: Small (monitor), seen more in northern - Asymmetrical - spindle cells → smaller, Medium (radioactive hemisphere (people w/ paler - Metamorphopsia tightly packed cells, better therapy-plaque, affects skin) - decreased VA and VF defect prognosis, low mitotic vision but can keep eye), - occurs earlier in Asian - Usually large (>5DD = activity Large (enucleation with or populations greater risk of malignancy) - epithelioid cells → larger, without radioactive therapy - older age population - presence of lipofuscin loosely packed, worse before removal- to kill (45-80) granules (in a linear tract) prognosis, high mitotic extraneous tumorous cells) - risk factors: light eyes/ (looks like drusen - activity (bad!) blonde, ocular melanocytic indicates malignancy! But - Diagnostic testing: Classic Risk Factors: abnormalities (nevi), is also called the “aging “To find small ocular dysplastic nevus syndrome pigment” bc can occur with FAF- fundus autofluorescence melanomas doing imaging” (atypical moles), genetic age) - Lipofuscin will glow T - thickness > 2mm predisposition, monosomy - serous detachment (50% - Low dose intravenous (ultrasound) 3 (prognosis of metastasis is erupt thru Bruch’s radioactive phosphorus F - fluid under retina (serous high towards liver and membrane) uptake test- p32 test RD) (OCT) aggressive tumour - At RPE level: clumps of - Ultrasounds: A scan: S - symptoms: metamorph., behaviour) or trisomy 8 orange pigment tumours have acoustic, photopsias (flashes), VF loss (prognosis of metastasis - could be asymptomatic hallow (low to medium (Snellen acuity) shows aggressive tumor - Collar Button sign → tumor internal reflectivity). B O - orange pigment overlying behaviour) breaks thru Bruch’s, can scan: size, dome shaped, tumor (Fundus AutoFl) - 2 risk factors = 22% chance spread laterally between position and excavation M - margins touching ONH of malignancy RPE & PR layer → can - Button color signs: (ultrasound) - 3RF= 34% lead to retinal detachment ballooning of tumour in DI - diameter > 5mm (fundus - 4 RF = 50% subretinal space as the imaging) melanoma mushrooms out Chorioretinal Scar - secondary inflammation or - well demarcated edges Related findings: - document & monitor infection (toxoplasmosis) - White (scar is in the sclera) - toxoplasmosis : Infection - Check VF and VA loss causing loss of the RPE to bright yellow (scar depth caused by a bacteria - determine etiology layer, part of the sensory is the choroid) lesion transmitted by retina and the choroid surrounded by black/dark unpasteurized milk, - Congenital or acquired brown pigmentation (RPE undercooked hyperplasia), can be meats or cats, Infection will surrounded by RPE dropout transmit through the - Generally oval but could be choroid and can lead to a variable shapes scar, when immune system - Location variable but is weak it can reactivate the generally posterior pole scar if its is caused by this depending on etiology organism - Variable ion size but generally approx >1DD in size - outer retina damage → scotoma (especially if in macular region) - inner retinal vessels still intact - damage to choroidal blood stream if spread to choriocapillaris Retinal Hole - loss of sensory retina from - Well defined area - Causes/etiology: variable, - document & monitor size the ILM to PR layer - Round I.e: vascular insufficiency and location, pt education - RPE, choroid, - Red coloration - determine etiology choriocapillaris and Bruch’s - can be as large as 1-2DD - Diagnose associated membrane are intact - VA & Amsler affected if in findings - Weak anatomical macular region - Refer for treatment attachment between sensory - location : macular (thin and depending on etiology retina and RPE is susceptible to holes), - If macular- symptoms are - the hole is a focal area of peripheral retina (equator to much more likely (VA and tissue loss thru the sensory ora serrata), vitrea base amsler will be affected) retina most prone to formation of and surgery may be retina hole required Microaneurysms - Loss of intramural pericytes - Red Complications: - Monitor for complications - Weakening of the capillary - Very small in size 1. Dot and blot hems (intra- such as dot/blot walls (out pouching) (50-100um) retina hemorrhages hemorrhages and hard - Proliferation of endothelial - Perfectly round 2. Hard exudates exudates cells in the capillary beds - Distinct margins - Observe Fl angiography—> - Layering of basement Capillary changes in early HyperFl- only present in membrane causes increased Diabetic retinopathy late AV phase, takes time permeability of the larger 1. Capillary microaneurysms for FL to reach the edge of molecules 2. Pericyte deficient the vessel and pool, size is - Lumen of microaneurysm capillaries- non perfused constant underneath, in may occlude leading to retina venous phase, edges might hypoxia to the inner layers 3. Degenerated capillaries not be as distinct due to of the retina 4. Occluded capillaries possible leakage - Originates in the INL Earliest finding in diabetic patients (nasal to ONH) Dot and blot Hemorrhages - Dot blot hemorrhages are a - Small in size Earliest place to find dot and - resolves very slowly (Intra-retina hemorrhage) remnant of a burst - Generally round blot hemorrhages is nasal to - Observe on Fl angiography microaneurysm - Fuzzy edges the ONH in diabetic patients —> HypoFl - Originate in INL but found - Multiple across retina - Treat diabetes in OPL (cystic spaces) - Do not obscure larger retinal blood vessels - Secondary to vascular disease causing stasis and congestion Hard Exudates - Leakage of fluid from - Yellow/waxy Findings if exudates are close - treat diabetes microaneurysms; secondary - Irregular shape to macula to partial occlusion of - Refractile (shiny) 1. Macular edema capillary beds - Unilateral or bilateral (thickening of macular - Fluids can leak out of - Random dispersion area) microaneurysms→ - Exudates will be lipid/ 2. OPL cystic spaces are macrophages come to protein in substance fluid filled absorb this fluid but leave - Accompanied by micro 3. Vision will most likely be deposits of hard exudates in aneurysms, dot and blot affected the OPL, originates form hems INL If further out in retina—> - Circinate ring around leaky retinal edema micro aneurysms - Remain for a long time Found in diabetic patients Intraretinal Microvascular - associated with ischemia - Faint, flat and tortuous in Found in diabetic patients - address the etiology Abnormalities (IRMA) and non-perfused (hypoxia) shape - Observe on Fl angiogarphy areas of the inner retina and - Remnants of the capillaries —> HypoFl- leakage will INL remaining appear more occur in late AV phase, it - Originates in the INL but dilated takes time for FL to reach can spread up into the NFL - Might be surrounded by the capillary ends and leak - Significant precursor for other ischemic changes like - Treat diabetes retinal neovascularization micro aneurysms, dot and blot hems, hard exudates, cotton wool spots) Venous Beading - Not very common, occurs - The venous columns will IRMA + Venous Beading = - treat diabetes when diabetic retinopathy is dilate, then constrict, then predictor for severe dilate, then constrict (and so neovascularization of retina - Focal areas of constriction on) causing structural bc of increased hypoxia & dilation weakness Venous loops (Abrubt - Platelets are stickier than - Triggers neovascularization curving near non-perfused normal in hyperglycemia - Can also present with retina, Venous caliber - Adhere to the abnormal venous loops change bc of change in basement membrane & blood flow, Not as severe as damaged cell wall venous beading) - Abnormal aggregation of platelets cause focal capillary occlusion & focal areas of ischemia - Can be congenital or acquired - Originates and found in Significant predictor for NFL proliferative diabetic retinopathy Retinal Neovascularization - Whole retina is hypoxic - appears very fragile & lacy Complications: - observe on Fl angiography- - Occurs secondary to retinal - Caliber (diameter) of 1. Hemorrhages- Since the due to the loose junctions of ischemia or hypoxia vessels narrower than new blood vessels are the new blood vessels, the (decreased O2) which leads normal fragile, have looser Fluorescein will seep out to to a signal of Vascular - lack of pericytes leads to no junctions, have no retinal surrounding tissue and Endothelial Growth Factor directionality (tortuous) barriers, no pericytes and cause a bright white effect- (VEGF) to be released → - association w/ preretinal or the basement membrane HyperFl (size and shape causes existing blood vitreous hemorrhage endothelial cells are changes based on vessels to ‘grow’ more - can affect VA if in posterior abnormal → the blood neovascularization size blood vessels pole vessels can break and throughout the phases and - Advanced glycosylation - NVD = neo at disc (within cause hemorrhages (Pre- continues into venous end-product (AGE) → 1DD) retinal hemorrhages or phase, florid) formed when glycosylated - NVE = neo elsewhere vitreal hemorrhages) - refer to retina specialist for tissue can’t dissociate - Contraction of vitreous gel 2. Tractional retinal treatment glucose → promotes PKC pulls on fibrovascular tuft, detachment- Due to the - no physical exertion to (Protein Kinase C pathway causing retinal traction and growth of new blood avoid rupturing of vessels up regulates vascular possible hemorrhage vessels, a scaffolding - Tractional retinal endothelial growth factor - AGE tissue alteration support system will form, detachment is one of the (VEGF)) results in high cholesterol overtime this supporting leading causes of blindness -VEGF promotes neo. = (LDL), leading to membrane becomes more in diabetics in bad! atherosclerosis (which can observable (white/thread- underdeveloped countries - Precursor to pre-retinal lead to HTN), thickening of like tissue) of fibro- hemorrhages that are BM, oxidative stress vascular nature, the located between the NFL + formation of this ILM or the ILM + Vitreous fibrovascular tuft or’tree’ 1. New blood vessel is not a good signal it formation creates traction on the 2. Proliferation of retina, lifting up creating existing blood vessels separation between but with a thin caliber sensory retina and RPE ( HypoFl (blood creates arcades wispy, feathery (blood - Patients with ONH disease barrier blocking intensity of - Could be associated with spreads horizontally) choroidal flush to our view, systemic disease affecting - Could slightly curved stays constant throughout arterial based diseases (follow the contour of the the phases) (HTN, renal disease, NFL) glaucoma, ONH disease) Cotton Wool Spot - hypoxia secondary to - White or greyish - CWS (opaque) + flame - observe with Fl vascular diseases such as - Feathery edge hemorrhage—> angiography—> HypoFl on HTN, diabetes, or renal - Opaque to translucent hypertension, renal disease, angiogram because the NFL diseases - obscures the view of the or Vascular dyscrasia is above the RPE and will - Also known as “soft larger retinal blood vessels - CWS (translucent) with dot/ block the choroidal exudates” (at the same plane) blot hem, micro aneurysm, hyperfluorescent flush - Located in the NFL - Usually within 3DD of hard exudates, and IRMA beneath, stays constant (follows the contour of ONH in NFL diabetes tends to be throughout the phases NFL) associated with diabetes - Occlusion of terminal retinal arterioles leading to - will never be any focal areas of inflammation CWS in the foveal avascular in NFL (not leaky materials zone as the NFL does NOT as in hard exudates) extend in the macular region White Centered - associated with systemic - yellow/white centre - address etiology Hemorrhage diseases such as leukemia, surrounded by flame diabetes, shaking baby - There are many different syndrome “centers” including a - Also called “Roth spots” if Cotton Wool Spot, fibrin associated with conditions thrombosis, white blood that cause sub-acute cells, and fibrin surrounding bacterial endocarditis a flame hemorrhage Collaterals - occurs when retinal hypoxia - Tortuous ( maintain - DOES NOT occur in - Observe Fl angiography—> is present directionality) diabetic patients HypoFl- vessels have tight - Pre-existing vessels net - Can have multiple in one junctions so Fl does not work area leak out-vessel lights up) - Drain blood around an area - Tight junctions in their wall - These are good! of retinal compromise - Shunt is usually vein to - Indicates shunting of blood vein (can be artery to vein, from one vessels to another artery to artery- least self healing collaterals common) shunt blood around an occluded artery or vein Macroaneurysms - Rare - Usually surrounded by - address etiology - Visible circinate exudates - Indicates pretty severe HTN - Associated with vascular - Large diseases (more in HTN) - Significant ballooning of - More commonly seen in vessel (isolated artery) females - Noticeable (cane seen with - More common in older Direct O’scope patients >50 years old - Swollen/ elevated Drusen - indicated a dysfunction in - Pale/dull yellowish Note: NOT associated with - address etiology the RPE layer and - Dull generally, not refractile presence of microaneurysm, - Observe Fl angiography—> associated with reduced in early stages dot/blot, etc HyperFl- picks up the vascular perfusion from the - Distinct borders stain, stays constant choriocapillaris causing - Typically bilateral, Dropout (light yellow) vs throughout the phases and degeneration of RPE cells, symmetrical Drusen (more depth, more fades away in late venous resulting in failure to - Round pigment) phase phagocytose PR waste - Small: 125 microns 2. Find CRV (can be affected) (involves RPE + BM) superior/inferior)- thick - Peripheral retinal - Number of drusen vary BV coming off ONH degeneration- Far periphery between eye 3. Diameter of CRV as soon (b/w equator and ora - Can affect VA if in macula as it leaves the ONH serrata) (age-related - Not uniform macular region bounces into the retina and finding) - Could also see RPE the width is equal to dropout/hyperplasia 125um - Hard (nodular): smaller, more defined, round, signifies localized RPE dysfunction, 63um in diameter - Soft: larger, indistinct borders, round, between RPE and Bruch’s membrane, has more pathological implication, risk factor for neovascularization originating from the choroid (CNV), larger than 63um - Can grow (change shape and size) over time Choroidal Neovascular - An abnormal formation of - found in posterior pole: Factors that may cause CNV - address etiology Membrane (CNVM or CNV new blood vessels macular area most prone to formation - Immediate referral to retina formation) (neovascularization) from CVN formation 1. Arteriosclerosis–or the specialist the Choroid up into the - can lead to subretinal or narrowing of the lumen - Anti-VEGF RPE and/or sensory retina sub-RPE hemorrhage or causing decreased blood - Observe in Fl angiography - Age-related serous detachment (fluid- flow–can be due to —> HyperFl - Most common reason for filled) genetics, environmental CNVM formation is Drusen (UV), or human behavior - Complications : (stress, smoking) Hemorrhages (Sub-RPE 2. Imbalance of promotors/ Hemorrhage, Sensory inhibitors- Usually, we Retinal Hemorrhage (sub have a system where retinal hemorrhage), Serous promotors and inhibitors Fluid Accumulation leading are equally balanced but in to Serous Detachment (Sub- CNV formation, RPE Serous Detachment or promotors like hypoxia Sensory Retinal Serous and VEGF outweigh the Detachment) inhibitors leading to ocular angiogenesis 3. Due to the thickening and calcification of Bruch’s membrane, it becomes brittle and can break. Neovascularization from the Choroid can now penetrate through Bruch’s membrane and reach further up into the RPE and sensory retina. Sub-Retinal Hemorrhage - Brighter red (because - Sub-retinal hemorrhage is - long time to resolve (Sensory retina) above the RPE layer, not formed from a CNVM that - Causes permanent scotoma pigment blocking it) is right beside or below the (longer fluid sits there, - Loose junctions b/w RPE hemorrhage on the fundus. worse damage it makes) Hemorrhages between the & PR means the blood The blood is not always - Observe in Fl angiography RPE Layer & Photoreceptor spreads more laterally and pooled on top of the CNVM —> HypoFl (stays constant layer. Due to leaks in blood is not confined throughout the phases) vessels from the CNVM - Larger in size (occupies more surface area) Secondary to degenerative - Not as elevated because of processes or inflammatory lateral spread of blood process, breaks in Bruch’s and - Shape: irregular because RPE there are no tight borders to confine it - Location: posterior pole & macula - Able to see the retinal vessels above it while looking at the fundus - Is underneath the major retinal vessels Sub-Retinal/Sensory Retinal - Lateral spread, - Sub-retinal serous - Observe in Fl angiography Serous Detachment - less confined detachment can occur at the —> HyperFl - less elevated because of same time as a sub-retinal If fluid leaks from the blood loose junctions hemorrhage vessels and gets trapped - Larger between the layers. Fluid can - irregular borders separate the 2 layer which leads to a serous detachment Serous Detachments are not always associated with CNVM, other things can cause it. Metamorphopsia results from this. Sub-RPE hemorrhage - Deep red/brown, almost - long time to resolve- scar black in color (below - Observe in Fl angiography Hemorrhage b/w RPE & pigmented RPE layer) —> HypoFl (stays constant Bruch’s. Bruch’s can be - CNVM grey/green & throughout the phases) weakened because of drusen. opaque - Permanent scotoma Secondary to degenerative - Smaller in size (compact) as process/inflammatory break in blood is more confined Bruch’s because of tight junctions it doesn't spread laterally, more elevated because of vertical spread - Distinct borders - Round - Location: posterior pole & macula Sub-RPE Serous Detachment - fluid is more confined - Sub-RPE Serous - Observe in Fl angiography - defined borders Detachment can occur at —> HyperFl Fluid leaks from the blood - round same time as Sub-RPE vessels and get trapped - Less lateral spread, more Hemorrhage between the RPE & bruch’s elevated layer Serous Detachments are not always associated with CNVM, other things can cause it. Metamorphopsia results from this. Glaucoma - chronic, progressive optic - No single sign that is 100% - (low CSF linked to neuropathy specific to glaucoma! glaucoma) - Compromise of the neuron- - generalized enlargement of retinal rim tissue cup, C/D ratio of 0.6 or - Factors to diagnose larger glaucoma (IOP, Slit lamp, - barred circumlinear vessels Optic never evaluation, (inside the cup - not on visual field, gonioscopy, rim), sloping cups- may OCT, patchymetry need 3D to tell if bared or unbared) - bean pot enlargement - Bayoneting of blood vessels - vertical cup elongation (C/ D >0.2 vertically than horizon.) - IST/IS rule (inf>sup>temp - thinning rims) - notching (focal loss of GC typically sup/inf temporal), produces scotomas in Bjerrum’s area respecting horizontal meridian - Rim involement- thinning of rim ST/IT - asymmetric C/D between eyes (difference of ≥0.2 significant) - distorted lamina dots (ovular) - NFL dropout (loss of white haze) - drance hemorrhage (flame- shape usually within one disc from disc margin and inferior) - PPA (focal or 360- mottled, alpha zone abuts the optic nerve, beta zone is farthest away) - blood vessels shift nasally - acquired optic pit (rare) Disc Edema - primarily raised intracranial - indistinct/elevated disc Address cause... see each pressure (papilledema) margins category of disc edema to - infiltration/inflammation of - edema of NFL follow the nerve itself (neuritis) - hyperemia, venous - problem w/ blood supply engorgement (ischemic optic neuropathy) - flame-shaped hemorrhages at or near the disc - ant. extension of ONH - retinal (Paton) folds, choroidal folds (outer layers of the retina buckle) - absence of physiological cup - macular star (cat scratch), hard exudates form along Henle’s Fibers - Dilated veins Papilledema - increased ICP - typically bilateral (can be Causes of unilateral - if you see bilateral disc (200mmH2O, 20-25mmHg) unilateral if one eye has papilledema: edema, assume papilledema - blockage of CSF flow, not severe optic atrophy) 1. Congenital variation in the until proven otherwise as overproduction - indistinct disc margins subarachnoid space; if the this is sight- or even life- - Relative increase in venous - VA & pupils good, unless space terminates threatening! pressure at the level of the long standing, (-) RAPD retrolaminarly, no swelling - Emergency—> refer to lamina cribosa, or - fields usually full, but will be apparent neurologist, need a CBC prelaminar, leads to enlarged blind spot 2. Atrophied disks may also (complete blood count) & papilledema - Capillary dilation show reduced signs of SED rate in addition to - axoplasmic stasis (blockage - headache upon waking, edema imaging (MRI/CT scan) of axoplasmic flow is a coughing, weight-lifting, 3. Past optic nerve issues: - If Grade 4 Hypertension—> major factor in overall straining, laying down such as unilateral trauma refer to internist increase in tissue volume - nausea/vomiting, lethargy, or unilateral ischemic immediately (seen in young and appears mostly 6th nerve palsy (CNS optic neuropathy- the pts with kidney problems) retrograde) lesions) papilledema may present - focus on lowering CSF - main cause of increased - transient obscuration as unilateral or pressure ICP: pseudotumor cerebri (vision blackouts) asymmetric in appearance - Acute papilledema—> (aka idiopathic intracranial - pulsatile tinnitus (hear MRI/MRV of brain + orbits hypertension - IIH) blood pulsing in vessels) within 24 hours (need to - tumor, space-occupying - loss of spontaneous venous rule out venous sinus lesion, venous thrombosis, pulsation (SVP) if had thrombosis, aneurysm, or severe HT, Vit A. or lead before- indicates that the IP inter cranial mass) toxicity rises - If MRI is clean—> do - retinal/choroidal folds lumbar puncture to - if chronic → pale disc due determine CSF pressure and to axonal loss, optociliary chemistry (LP is performed shunt vessels (collateral after MRI) vessels), decreased VA & color vision, field loss, lipid exudates on ONH (appear as refractile bodies) Pseudotumor Cerebri - idiopathic increase in - headaches - if the papilledema - if MRI comes back negative intracranial pressure - neck pain continues, pt is at risk for & no problem w/ CSF on - usually occurs in young - diplopia (6th nerve palsy) developing optic atrophy lumbar puncture → (20-40yo) obese females - pulsatile tinnitus and blindness pseudotumor cerebri (ICP is - more prone if taking: Vit. A, - nausea greater than 200nm of water tetracycline, doxycycline, - asymptomatic or greater than 15mm of steroids - flattening of posterior sclera mercury) - Type of papilledema (back of eye) - weight loss - Venous tortuosity of optic - Reduce levels of salt in diet nerve - Treat sleep apnea - Increase dilation of the - Diamox (metallic taste) optic sheaths - Topamax (antiseizure drug, - Empty sella turcica inhibits carbonic anhydrase - Intraocular protrusion of the activity) prelaminar optic nerve - Lasix - Bilateral or unilateral; dura - steroids venous sinus stenosis - surgical: CSF shunting - Octreotide (injection that suppresses growth hormone) Foster Kennedy Syndrome - rare -optic atrophy in 1 eye - lesion compression & (secondary to lesion papilledema compression), disc edema in - usually in pts w/ frontal the other (secondary to lobe/olfactory tumors papilledema) Optic Neuritis - second to glaucoma as the - sense of darkening and loss Signs of demyelination - if you suspect ON, get a most common optic of color intensity in the - sensation of electrical good history (signs of neuropathy affected eye especially for shocks in the arms and legs demyelination) - Most cases of ON are G/R when the head is flexed to - MRI of head and orbits associated with - RAPD if unilateral the chest—> L’Hermitte within 1 week unless demyelinating conditions - Vision is decreased 20/20- - Reduction in visual known diagnosis of MS - 2 main etiologies: primary to 20/70 (usually decreases function associated with an - if focal defects are shown inflammation- progressively between increase in body on MRI—> intravenous demyelinating disease (e.g. - May report flashing lights temperature—> Uhthoff steroids can delay the onset Multiple sclerosis) or or phosphenes of signs/symptoms of MS) infiltration - No typical visual field Post Optic Neuritis Attack - If MRI shows at least one - Mean age 32 defect - mild red desaturation locus of demyelinating - Female 77% - Some temporal pallor of the plaques—> future - Highest incidence in optic nerve development of MS within populations located at - Mild RAPD next 15 years is about 72%, higher latitudes no such lesions risk= 25%, - Adult optic neuritis: - women are 3x more likely overall clinically definite unilateral, retrobulbar optic to develop MS MS developed in 50% of neuritis, associated with ONTT patients in 15 years pain on eye movements, - OCT detects thinning of most often idiopathic, high NFL in most patients with portability of recurrent ON inflammatory - If pt is diagnosed with MS demyelinating events in the (Fingolimod- Gilenya- oral CNS and a Dx of MS capsule- typically get - Paediatric optic neuritis: macular edema → bilateral, Papillitis, important to monitor), associated with headache, baseline OCTS, color vision most often post-infectious and OCTs are important for or post immunization, low regular exams probability of recurrent - Usually recovery of vision demyelinating events and a & edema begins to decrease Dx of MS within 1-4wks (but no recovery of vision within 5wks for atypical) Papillitis - pain on eye movement - vision will improve - refer to PCP or neuro, - unilateral for adults uncover etiology of - intraocular form in which - Bilateral for kids infection, may need MRI disc swelling is observed - More common in children post viral and usually vision is significantly decreased Retrobulbar neuritis - pain on eye movement - refer to neuro- - Unilateral ophthalmologist for MRI - involves the orbital portion - Nerve looks normal within a week to rule out of the optic nerve MS lesions - View with O’scope= normal - IV steroids optic nerve - 65% of ON cases - demyelinating diseases (MS), mainly in adults < 50 yo, more common in women & caucasians Atypical Optic Neuritis - less than 12 or older than 50 Neuromyelitis (aka Devic - Blood test: CBC, ESR years old Disease) (measurement of - demyelination is not the (immunocompromised) inflammation in blood), etiology - Severe vision loss (i.r. NPL) - An inflammatory CNS autoantibodies, Lyme - Result of infections, post - Bilateral reduction in vision disorder that is associated - Chest X-Ray infection responses, (no recovery of vision with aquaporin-4 - MRI inflammations within 5 weeks) immunoglobulin G (AQP4- - Lumbar puncture - Post or active: viral - Absence of pain on eye IgG) conditions, rubeola, movements - More common in Asia and mumps, mono, Lyme, - Cells in the vitreous West Indies herpes zoster, paranasal - The spinal cord and eyes sinusitis, sarcoidosis, are more affected, this tease systemic lupus, COVID, is rare ulcerative colitis, symphilis, - Serum NMO antibody dengue, and Chikungunya testing is positive in 70% - Vision loss is usually more for pts diagnosed with this severe disease Neuroretinitis - papillitis with retinitis, - doxycycline 100mg 2x/day macular star (hard exudates for 1 month - Papillitis with a retinitis - looks like firework) causing macular star composed of hard exudates - Least common form of optic neuritis - Frequently associated with viral infection, cat scratch fever - Other potential infectious and inflammatory causes of neuroretinitis include: Lyme disease, sarcoidosis, symphilis, toxoplasmosis, tuberculosis, and viruses - Cat scratch is diagnosed with high IgG antibodies to B.henselae Anterior Ischemic optic - another cause of disc edema - pale disc edema neuropathy (AION) - acute ischemia of the front - Acute decrease in vision (anterior) part of the optic - Starts unilaterally nerve which is supplied mainly by the posterior ciliary arteries leading to infarction of the nerve fiber bundles Arteritic anterior iscehmic - Vision 20/100—>NPL, - Doppler ultrasound of Order Hematologocial testing: optic neuropathy (AAION) sudden loss especially at temporal artery: if there is aka Temporal Arteritis night, progresses for more no dark halo sign, a 1. Erythrocyte sedimentation than 1-2 days diagnosis of TA cannot be rate (ESR)- how many - 5-10% of cases - Central/inferior field loss supported mm blood fall in one hour, - Also called giant cell - Rarely will vision improve high sed rate arteritis, temporal arteritis, - Cupping normal in fellow - Sed Rate Norms cranial arteritis, and eye Men → Age/2 granulomatous arteritis - RAPD if monocular Women → (Age + 10)/2 - Systemic inflammatory - Sed rate and C-reactive 2. C-Reactive protein (CRP)- vasculitis of unknown protein usually elevated normal C-reactive protein etiology that affects - Weight loss, low grade is