Midterm 1 Flashcards
Phlyctenual Keratoconjuctivitis
AKA phlyctenulosis. A nodular inflammation of the peri-limbal tissue. Characterised by the formation of small pinkish circumscribed lesions affected the conjunctiva, limbus, or cornea.
What causes phlyctneular keratoconjunctivitis?
A nonspecific hypersensitive response to diverse antigens. Include staphylcoccus (number one cause in America), TB, and chlamydia.
what are phlyctenules made up of?
Inflammatory products like hisocytes, lymphocytes, plasma cells, and neutrophils. It is subepithelial. The epithelium overlying the phlyctenule is made up of mononuclear phagocytes and neutrophils
Who is phlyctenular keratoconjunctivits most common in?
More common in poor areas, women, and children and young adults. It occurs worldwide
Symptoms of phlyctenular keratoconjuctivitis on the conjunctiva?
Foreign body sensation, ocular discomfort, injection, itching, tearing, discharge (occasionally) Small, raised nodular lesion, pinkish, surrounded by dilated blood vessels. Size may be variable. Usually close to limbus but can occur anywhere on the bulbar conj within the interpalpebral aperture.
Symptoms of phlyctenular keratoconjuctivitis on the cornea?
Also have foreign body sensation, injection, itching, discharge, tearing, AND Pain, photophobia, ciliary spasm, tearing, blurry vision.
Types of phlyctenular keratoconjunctivitis on the conj?
- Within the interpalpebral aperture-when eye is open
2. limbal margin and onto bulbar conj.
How to treat phlyctenular keratoconjuctivitis
Self limiting-can go away by itself. Less symptomatic then the cornea.
Corneal lesions of phlyctenular keratoconjuctivitis
Begins at limbus and migrates onto the cornea. Wedge shaped, white mound at limbus with radial pattern of vascularization. Migrate towards center of cornea as a gray-white superficial ulcer (has a triangle leash of vasculerized pannus) Tend to occur in the inferior aspect of the eye near the lid margin.
Severe corneal lesion of phlyctenular keratoconjuctivitis may result in…
ulcers, scarring, vasculerization, perforation.
Different diagnosis of phlyctenular keratoconjunctivitis?
Inflammed pterygium, pinguecula, nodular episcleritis.
Durezol
Emulsion. Steroid drop. Less dosing but raises IOP by a ton
Lotemax
Steroid drop. Does not raise IOP as much as pred forte. Almost as strong but $$$$
Pred Forte
Steroid Drop
Tobradex
Has tobramyocin (AB) and Dexomethason (steroid) Cheap
Zylet
Has loteprednol (steroid that doesn’t raise IOP as much as dex) and tobramyocin. Very $$$$$$
Treatment for Phlyctenular Keratoconjuctivitis
TB must be ruled out, blepharitis needs to be treated if found.
Treat with topical steroids (Pred forte, durezol, lotemax). Cycloplege for discomfort If there is staining in cornea-limbal area use a combo drug (zylet, tobradex) But never more then 4 times per day. If staphylococcal disease is found then must do lid therapy. Use anti-inflammatory and antibacterial drugs (cyclosporine A). Can also use oral AB. If intestinal parasite, rosacea, chlamydia and HSV are suspected then treat entire system systemically.
Prognosis of phlyctenular keratoconjunctivits
Good if conj. or limbal is treated adequately. Potentially blinding if corneal and not treated correctly.
Exposure Keratopathy
Result from the eye drying due to neurological and or/ mechanical problems. Can be due to incomplete blink, lagophthalmos, ectropion, bell’s palsy, Grave’s Disease.
Objective findings in Exposure keratopathy
PEES (punctate epithelial erosion) in the interpalpebral or inferior cornea. Stains well with NaFl. Conj. injection. In severe causes micropannus, corneal scaring, corneal thinning, filamentary keratitis.
Managing Exposure Keratopathy
Lubrication therapies, mechanical therapies (eyelid taping, lid weights, plastic shields, bandage Cl), tarsorraphy (suture the nasal and temporal canthus shut or the whole eye.
Filamentary Keratitis AKA Corneal Mucous Plaques
Can be chronic, recurrent, and debilitating condition. Occurs on the cornea and is very painful. Small mucus staring that stick to the cornea on one side and are free on the other side. Each blink causes more strands to be pulled off. Aqueous deficient dry eyes can cause corneal irregularities and increased mucin which cause the strands to be built.
What are the strands in filamentary keratitis made of?
Degenerated epithelial cells and mucus. Strands of the filaments attach to the cornea at the apex. Appear as gray sub epithelial opacities. Stains well with rose bengal.
What causes filamentary keratitis?
Most common cause is dry eye syndrome. Also associated with sjogrens, superior limbic keratoconjunctibisis, recurrent corneal erosions, neurotrophic keratopathy, patching, adjacent to surgical wounds. Can be induced or exacerbated by CL wear, ocular surgical procedures, chronic use of ocular and/or systemic medications.
Subjective for filamentary keratitis.
Red eye, Pain (moderate to severe), Foreign body sensation, photophobia
Objective for filamentary keratitis
Mucus strands attached to the cornea, conj. injection, poor tear film, PEE
Treatment for Filamentary Keratitis
Lubrication, punctal occlusion, mucomyst (in inhalers. Smells like rotten eggs), filaments typically resolve in 1-4 days. Treat underlying condition. Debridement of the filament (apply topical anesthetic and remove filaments from their base) Topical steroids, Nsaids. Follow up in 1-4 weeks and if not improved use debridement again, bandage Cl. Lubrication must be used long term.
Thygeson’s Superficial Punctate Keratitis
A chronic, bilateral, recurrent corneal epithelial keratitis. Has exacerbations and remissions. Round conglomerates of distinct granular punctate epithelial lesions. Very small in size. Minimal to no conjunctival involvement (EYE is WHITE). No Stromal inflammation.
What causes Thygeson’s superficial punctate keratitis
Exact etiology is unknown. Most likely due to a typical immune process or an inflammation process. Has a genetic associated with HLA-DR3.
Background of Thygeson’s superficial punctate keratitis
Chronic course with exacerbations and remissions. Last year to decades. No gender predilection. No age predilection. Usually bilateral but can be unilateral. Does NOT respond to AB
Subjective thygeson’s superficial punctate keratitis
FB sensation, photophobia, blurry vision (if on center of cornea), Tearing, redness, dryness, Eye is usually white and quiet. Patient may be asymptomatic.
Objective thygeson’s superficial punctate keratitis
Multiple epithelial lesions that are gray-white, coarse, granular, raised, and vary in size. Epithelial lesions more numerous centrally. Variable straining with NaFl. Slightly raised. Lesions can move around and come and go. Have an average of 20 but vary from 1-50. Can also have sub epithelial opacities caused by edema. Corneal sensitivity may be reduced but never absent. During inactive stage lesions can disappear or appear as flat, gray, stellate shaped sub epithelial opacities that do not stain with NaFl. Some opacities are permanent.
How to manage mild cases of thygeson’s keratitis
Artificial tears, ointment qhs, counsel regarding chronic nature of disease.
How to manage moderate to severe cases of thygeson’s keratitis
Mild topical steroids (Pred mild, FML, Alrex). Cyclosporine A can be use that don’t respond to steroids. Therapeutic bandage CL to increase comfort.
Follow up with Thygeson’s Keratitis
Weekly during exacerbation, 3-6 months during remission. If on steroids IOP must be checked every 3 months. Visual prognosis is usually really good. Pt. Live to be productive.
Dysgenesis
You are born with this disease. Congenitial malformation. May have a hereditary pattern. May be isolated or as part of systemic pattern.
Dystrophy
Generally a hereditary pattern. Generally bilateral. Tend to be predispose the centrl cornea. May become more pronounced with age but age is not the primary cause
Degeneration
No developmental or hereditary pattern. Unilateral or bilateral. May be a manifestation of age. Usually starts in peripheral cornea and may ultimately involve the central cornea. Inflammatory process may be involved early in the process. Systemic disease may be associated with the degenerations.
Age related and Common Corneal Degenerations
Pinguecula, limble girdle of vogt, arcus, hassal-henle bodies, crocodile shagreen
Local and systemic conditions, less common Corneal degenerations
Pterygium, Amyloid degeneration, Band Keratopathy, Salzmann’s nodular, Terrien’s marginal, pellucid marginal
Arcus
Patients are normally asymptomatic. Very common. More common in African Americans. Bilateral white band in mid-periphery. Gradual onset (inferior and superior and then fills). Cholosterol/lipid deposition at Bowman’s. Often hereditary factors. Caused by hyperlipidemia/high cholesterol. Normally if over 40-50. If under 40 consider other factors (CV disease self or family, CV risk factors). Referral if under 40. Follow up annual if no risk factors
Limbal Girdle of Vogt
Usually nasal temporal. Patient is asymptomatic, 45+, and may be higher in women. It is a bilateral, narrow band of white crystalline like opacity in the nasal and temporal limbus area, caused by degeneration of collagen fibers and is not vascularized. There are two types…1. associated with early band keratopathy-see clear zne between limbus and opacity line 2. simply peripheral corneal finding-no clear zone. Do nothing for type 2 and treat band keratopathy for type 1.
Dellen
Patient will be asymptomatic and it can occur at any age. It is focal peripheral thinning near the limbus. Epithelium endothelium are okay but stroma has eroded. Surrounded tissue may be clear or hazy. Occurs due to poor wetting or next to conjunctival mass. Treat with lubrication and therapeutic SCL.
Hassall-Henle Bodies
Peripheral Guttata. Patient will be asymptomatic. Small round thickenings of descement’s membrane with overlying endothelial displacement in peripheral cornea. Normal chang with aging but may see with associated corneal edema. No treatment
Pellucid Marginal Degeneration
Usually asymptomatic until Vas decrease. Bilateral, inferior corneal thinning. Causes central cornea to bulge out above the thinning zone creating irregular ATR astigmatism. Looks like birds kissing. More common in early adults even though degeneration. Hydrops and scaring can occur with progression. Treat by correcting astigmatism with gas permeable CL, keratoplasty if necessary.
Terrien’s Marginal Degneration
Very rare but must worse then Pellucid (Terrien’s is a terror). Thining goes all around limbus and creeps toward pupil. Patient feels this and has decreased VA. Rare, any age, usually bilateral but asymmetric. Marginal stromal thinning, opacification, and superficial neovascularization. Begins as superior nasally marginal opacification (looks like arcs). Lucid zone between thinning and limbus. Central edge may have a yellow border of lipid. Distortion of cornea with irregular astigmatism. Minor trauma can cause rupture. Treat with steroids (comfort) and keratoplasty or LV as necessary.
Idiopathic Marginal Furrow degneration
Bilateral thinning seen in or adjacent to arcs. Epithelium is intact. No neovascularation. VA’s not normally affected.
Associated with Systemic Disease Marginal Furrow Degeneration
Ring ulcer seen with Acute Rheumatoid Arthritis, systemic lupus erythematous, leukemia, polyarteritis nodosa, TB. Treat the underlying systemic cause.
Mooren’s Ulcer
Very worse of thinning conditions. M more affected. Older pt=unilateral and responds to Tx. Younger pt=bilateral and difficult to manage. Painful with photophobia. Nigerian have severe form. Begins with marginal infiltrate–>chronic, serpiginous limbal ulceration. 3-12 moth course with remissions. Mild trauma can perforate globe. Has adjacent conj injections. Etiology is unclear. Responds poorly and steroids may speed up perforation. Refer to corneal specialist and conj. excision/corneal reconstruction.
Posterior Crocodile Shagreen
Asymptomatic. Bilateral. Small, gray polygonal crocodile skin patches of various sizes at descement’s membrane. No treatment.
Amyloid Degeneration
Degeneration in the area of Bowman’s and epithelium. Secondary to long standing disease. There is a fleshy mass with a nodular surface. Salmon to yellow white. Cornea may be vascularized. Treat by primary cause prevention, keratectomy, corneal transplant.
Coat’s white Ring
Caused by foreign body. Asymptomatic. Granualar whitish oval ring in the cornea. May contain iron. Though to be lipid in nature. No treatment.
Band Keratopathy
Asymptomatic early on but later stages have a decrease in VA. May have recurrent corneal erosions in late stages. Calcium deposits within the inerpalpebral fissure. White to yellow deposits at Bowman’s and anterior stroma. May be secondary to ocular inflammation or systemic diseases (chronic anterior uveitis, prolonged glaucoma, phthisis bulb, hypercalcemia condition: sarcoid, Vitamin D toxicity, hyperparathyroid, Metastic carcinoma of the bones, gout, lupus JRA). Treat the primary cause and ocular lubrication, chelating agents, scape off. Can grow back.
Bullous Keratopathy
Acute and painful. Caused by long term prolonged corneal edema. Bubbling of the cornea, break down and reform and will eventually scar. Treat with anti edema meds (steroids and sodium chloride), therapeutic CLs early on, Late stages that is poor prognosis. LV.
Salzmann’s Nodular Degeneration
Usually asymptomatic and may be more common in F. Non-inflammatory multiple bluish white nodules usually at the mid periphery. Bilateral. Vision depends on location. Related to previous inflammation (especially phlyctenular disease). Treatment: asymptomatic monitor 3-6 months, with epithelial break down therapeutic CLS, antibiotic, Keratoplasty, LV as necessary.
Xerophthalmia and Keratomalacia
Degneration of the cornea due to drying. Both related to vitamin A deficiency either by malnutrition or failure to absorb it. Treat with vitamin A supplement and ocular changes may reverse
Xerophthalmia
Keratinization of the epithelium. Atrophy of conjunctival goblet cells. Corneal edema. Neovascularization.
Keratomalacia
Acute corneal tissue liquefaction. Both may see Bitot’s spots.
Kruckenberg’s Spindle
Pigment deposition on the back of the cornea. From the iris and carried by the aqueous. Brownish in color and vertical spindle shaped pigment deposition on posterior cornea. Inferior 1/3 to 1/2. Suggests old uveitis or pigment dispersion syndrome.
Vortex Keratopathy
Greyish or golden epithelial deposits. Appear in a swirl pattern from a point below the pupil. Occur in patient with fairy disease and in patient being treated with amiodarone, hydroxycholorquine, indomethacin, tamoxifene.
Arlt’s Triangle
Brownish in color. Triangular shaped pigment at the 6 o’clock position in endothelium. Usually caused by old uveitis
Brawny Cornea
Brownish in color. Edematous haze in epithelium. Caused by EBMD(epethilal basement membrane drystoph), RCE
Ferry’s Ring
Orangish brown in color. Ferric deposition around a surgical filtration bleb. No pathological indication
Fleisher Ring
Orangish in color. Ferric deposition at the base of keratoconic cone. Indicates keratoconus
Goar’s Line
Brownish in color. Pigment granules forming a horizontal line on the inferior cornea. Inidicates pigmentary glaucoma.
Hemosiderosis
Reddish brown color. Blood staining the endothelium in the anterior chamber. Caused by hyphema or intracorneal bleeding.
Hudson-Stahli Line
Orangish brown in door. Deposition at Bowman’s. Area of upper and lower lid junction. More in males and ore come with age. Seen as a faint segmental or continuous line or a line with surrounding white opacity. A frequent site of RCE.
Kaiser-Fleischer Ring
Orangish in color. Posterior cornea-anterior angle. Best seen in gonioscopy. Copper deposition. Suggests wilson’s hepaticolenticular disease. Wilson’s disease is liver cirrhosis, basal ganglia degeneration, due to decreased ceruloplasmin with copper deposition into organs.
Keratic Precipitates
White or pigmented WBC in endo. Endothelial surface. Caused by trauma or uveitis.
Keratomelanocytosis
Pigmented spokes radiating out into the cornea from the limbus. Most in heavily pigmented ppl. Most frequent at 4 and 8 o’clock. Caused by truma, infection, focal toxic inflammation of staph.
Salmon Patch
Orangish in color. Discoloration of midstream (intersitial keratitis). Caused by syphilic keratitis. Has a haze due to scare and vascularization
Sampoalesi’s Line
Pigment granuels at Schwalbe’s line. Suggests pigmentary glaucoma
Stocker’s line
Orangish brown in color. Ferric deposition at pterygium leading edge.
ICE Syndrome (Iiridocorneal endothelial syndrome)
Typically unilateral and in F. Consists of three overlapping disorders with most mild at start (chandler syndrome, cogan-reese syndrome, progressive Iris Atrophy) The common link between the three forms in abnormal corneal endo. Endo. can proliferate and migrate into the angle and onto the iris. Migration causes glaucoma. Will see corectopia (malposition of the pupil), Pseduopolycoria (multiple pupils), iris atrophy. Corneal endo. abnormalities such as a hammered appearance and cornea edema.
Chandler Syndrome
Causes ICE. Severe corneal changes. Corneal Edema moderate to severe. Iris is normal or has mild atrophy. Normal to high IOP. Correctopia mild to sever. 5% glaucoma
Cogan-Reese Syndrome
Diffuse nevi, iris surface is matted looking, 50% have iris atrophy. Usually high IOP. Mild to moderate corneal edema. Moderate to severe correctopia. 50% glaucoma
Progressive Iris Atrophy
Severe iris changes. Iris stromal atrophy, iris hole formation. Pupil displacement towards area of synechiae. Usually high IOP, mild to moderate corneal edema, correctopia is moderate to severe. Glaucoma in 37%
Cornea Plana
Char. by a severe decrease in corneal curvature. Shallow anterior chamber. Usually associated with other anterior segment abnormalities.
Microcornea
Condition where the adult corneal diameter is
Megalocornea
Non-progressive, symmetric, inheritied condition. The adult cornea diameter is >13 mm. Usually X-linked recessive. M more frequently affected. High myopia and astigmatism. Must make sure they do not have congenital glaucoma.
Keratoglobus
Resembles megalocornea. Cornea is thin especially in the periphery. Sometimes classified with the dystrophies. Extremely rare. Presents bilateral. Must avoid trauma so a rupture does not occur.
Posterior Keratoconus
NOT related to anterior keratoconus. Indentation of the posterior cornea. Variable degrees of central stromal hazing. Anterior surface is normal. Acuity is usually near normal. Usually unilateral and non-progressive. Treat with a cornea transplant.
Peter’s Anomaly
Rare but serious developmental anomaly. Glaucoma in 50-70%. Can have micro cornea, micropthalmos, coloboma, iris dysgenesis. The lens sticks to the cornea. Congenital central corneal opacification. Peripheral cornea usually remains clear. Posterior stroma, descemet’s and endothelium is abnormal. Common to have iris strands attached to the opacity. Common to have keratolenticular apposition.
Posterior Embryotoxon
Anterior displacement of Schwalbe’s line. Ring may be partial or complete. Usually the greatest at 3-9 position. Can be seen with slit lamp but better with gonioscopy. Monitor IOP’s annually. Glaucoma risk is low if this is all that is present.
Axenfeld’s Anomaly or Syndrome
Posterior embryotoxin PLUS iris strands that run across AC attach to Schwalbe’s line. May see iris abnormalities. Prominent iris sphincter. Increased risk of glaucoma. Anomaly=IOPs normal Syndrome=Elevated IOPs
Rieger’s Anomaly or Syndrome
All of Axenfeld’s plus iris hypoplasia. Has corectopia (pupil distortion) and may see corneal defects of strabismus. Increased risk of glaucoma. Anomaly=involved only the eye
Syndrome=involves systemic findings as well. Primarily facial (hypoplasia esp. teeth)
Treatment for Corneal segment dysgeneses
Determine structures affected and refer to pediatric ophthalmologist. Determine if there is associated findings. Determine risk of secondary glaucoma. Determine the significance to visual performance, etc.
Corneal Dystrophies
No consensus for precise definition. Most are autosomal dominant. No associated systemic diseases or ocular diseases. Usually onset is early in life with variable progression. Bilateral but may or may not be symmetrical. Generally slow progression. Most involve a single layer and tend to be central. Usually observed during second decade. Treat acute complication and enhance visual function.
Corneal Dystrophies IC3D Categories on genotype
C1: Well defined, gene mapped and ID. Specific mutations known
C2: Well defined, mapped to 1 or more specific chrome. loci, but genes remain to be ID
C3: well defined, not yet mapped to a chromosomal locus
C4: suspected new or previously documented. Evidence as distinct entity not yet convincing.
Corneal Dystrophies IC3D Categories on phenotype
Epithelial and sub epithelial, bowman’s layer, stromal, descemet’s membrane/endothelium
Epithelial Basement Membrane Dystrophy AKA map dot fingerprint Subjective
Epithelium attached to bowman’s by hemidesomes and these are defective. When patients open their eyes they rip their epithelium off. Can be from Mild to severe. Mild is asymptomatic and may have short lived irritation in the morning when waking up. Moderate has morning syndrome or chronic corneal irritation that may wake them up. Transient visual fluctuation. Mild to moderate photophobia or glare. Severe has a history of recurrent spontaneous corneal erosions. Reduction in VA.
Epithelial Basement Membrane Dystrophy Objective
Best seen in high mag and retro illumination. May be subtle. May see TBUT that is instantaneous (epithelial irregularities) Has maps, dots, fingerprints
EBMD Maps
Gray patches with sharp margins. Geographic lines or patterns. Lines or edges become more pronounced with age and recurrence of erosion. Average sized 1-3 mm. NaFl break up over map area.
EBMD Dots
Discreat grayish to clear spots. Round, ameboid or comma shaped. May be clustered. usually
EBMD fingerprints
Large patterns centrally. Swirled refractive lines. May originate out of a single point (Mares tail) and is clear to gray.
EBMD Symptoms
Most common complication is spontaneous epithelial erosions. Peeling off of large piece of epithelium as the patient blinks or opens eyes when awakening. Pain tearing, photophobia, perilimbal injection, sensation when in morning. Usually recurrent: increases to infection and over scarring and vision.
EBMD Treatment if Asymptomatic
If Asymptomatic: advise and educate. Follow up routine and PRN
EBMD if mild symptoms
If mild symptoms: use hypertonic 5% NaCl at night and lubrication.
EBMD if moderate symptoms
If Moderate: Use hypertonic solution, ointment, high water content SCL, prophylactic AB, homatropine, diclofenac. Lid hygiene. Follow up PRN 3 months if with CLs. Always continue therapy with hyper tonics for several weeks after symptoms have stopped.
EBMD if Severe symptoms
If severe: instill anesthetic and deride loose epithelium. Therapeutic SCL wear, continue with hypertonic saline, prophylactic AB, Anterior stromal puncture (use bent tipped gauge needle to puncture bowman’s and into ant. stroma in diffuse pattern. Refer to corneal specialist for other surgical options: lamellar keratectomy or photo therapeutic keratectomy. Closely watch during the acute phase. Acute phase usually lasts 6-12 months.
Prognosis for EBMD
Most retain good vision-usually no less than 20/50. Educate patient that there is no cure and recurrent in nature.
Meesman’s Juvenile Epithelial Dystrophy
Intraepithelial cysts or vesicles (best seen with indirect retro). Onset 1-2 years. Extends to the limbus. Results in irregular astigmatism (any visual reduction is slight). May have epithelial erosions after 40. Treat the symptoms. Follow up routinely. Have an excellent prognosis.
Bowman’s Layer Dystrophies
Reis-Buckler’s Dystrophy and Anterior Mosaic Dystrophy
Reis-Buckler’s Dystrophy
Gray white irregular opaque pattern in bowman. Creates a fish net pattern. Painful RCE. Cause anterior stroma opacification. usually by age 20-30 VAs drop. Treat with erosion treatment, low vision aids, ketaoplasty. Prognosis is guarded. REMEMBER: Pirate Reis has buckles and is on bow and throws out his fish net. (:
Anterior Mosaic Dystophy
Gray polygonal opacities of bowman. Vision usually not affected. Unclear whether a true dystrophy or age related. Not as bad as Reis and normally just monitor.
Anterior Stromal Dystrophies
Granular dystrophy, lattice dystrophy, crystalline dystrophy
Granular Dystrophy
Usually acquire before age 10. Round, oval, discrete white spots. Tend to increase in number and coalesce. VA’s gradually drop (usually no worse then 20/200 by age 60). Treat with keratoplasty (can recur), LV. Prognosis is good/guarded.
Lattice Dystrophy
Anterior stromal refractive lines. May see dots flakes, and stellate opacities between the lines. Early pt. have good vision. Tend to thicken and creates stromal haze. Can have RCE. Treat RCE, keratoplasty by age 40, LV aids. Prognosis is guarded.
Crystalline Dystrophy
Crystals form a ring during the 1-2 decade. Crystals are white to yellow or may be polychromic. Crystals contain cholesterol. Patient usually develop corneal arcs by age 30-40. VA’s usually not affected. Associated with hypercholesterolemia. May see Xanthelasma (fat deposits in upper lid). Refer for CV work up. Prognosis is good but ocular findings do not reverse.
Phototherapeutic Keratectomy
Useful for epithelial and anterior stromal corneal dystrophies. Less invasive then PKP.
Macular Dystrophy
Full thickness Stromal. Stroma is invaded by mucopolysaccharide material (Sugar). Diffuse corneal clouding by age 5-9. Increases in density. VA’s drop. Can be autosomal recessive or extend to periphery. Fix with keratoplasty or LV aids/lenses.
What is Keratoconus/ what causes it?
Thinning and bulging. with a loss of symmetrical curvature of the cornea in the central and pericentral areas. Central corneal thickness Keratocyte a ptosis–>secondary stromal thinning and corneal ectasia or that it is due to allergies, eye rubbing, and UV/free radicals.
Subjective Keratoconus
Slow changes in VA. Usually start age 15-25. Progressive for 5-6 years. Tends to stabilize (younger=more likely for transplant). Possible history of asthmas and allergies. There may also be hereditary etiology or environmental. Mostly asymptomatic except glare, photophobia, or diplopia (can be monocular)
Keratoconus Objective
Frequent RX changes, reduced VA’s. Scissor reflex on retinoscopy and oil drop reflex with direct. Steeper K’s and distortions (CLs give better VA’s). Munson’s sign-pouching out of cornea when looking down. Fleisher’s ring-brownish-orange ferrous ring at the base of the cone. Vogt’s Striae: Vertical lines or thickening at posterior surface (cat scratches). Can have posterior corneal breaks or hydrous (descemet’s membrane splits) They are very painful, edema, results in scarring.
Treating Keratoconus
No specific treatment if no symptoms. Spectalces for reduced Vas early on. CLs (RGP) Anti-edema drugs, Keratoplasty and LV as necessary. Looking at putting riboflavin on cornea and blasting with light to prevent progression. Follow up in 6-12 months. More frequent if complications.
Endothelial Dystrophies
Fuch’s Endothelial Dystrophy. Congenital Hereditary Dystrophy. Posterior Polymorphous Dystrophy.
Fuch’s Endothelial Dystrophy about and objective
Fs, symptomatic 50-60, multilayer involvement. Gutta formation (posterior to descemet’s) Starts age 20-30 and increases. More guttata after age 40. May see endothelial pigmentary dusting. CCT high >600.
Vision loss with Fuch’s
Endothelial cells overlying the guttata enlarge and are functionally disrupted. Disrupts the pump mechanism. Causes edema of stroma and epithelium. Stromal edema causes striae and thickening. Epithelial edema causes epithelial micro cyst, wet ground glass-like, bullae formation.
Complications with Fuch’s
VA’s drop in late stages. Photophobia and glare (edema). Edema causes fluctuating VA. Acute bullae can cause painful erosions. Cataracts appear earlier, POAG earlier.
Treatment for Fuch’s
Hypertonic solution day and ointment at night. Hot air (hair dryer), SCL for bullae. Use RXN in AM as symptoms more commong. Dilation (open the pupil around the central clouding. Can use parasympatholytic to add cycloplegia (sympathomimetic will not). Low vision lenses. Keratoplasty for visual rehabilitation.
Congenital Hereditary Endothelial Dystrophy
There are 2 forms (both similar to Fuch’s but early onset): 1. Recessive form-has nystagmus and congenital. 2. Dominant form-no nystagmus and onset 1-2 decade. Rare or absent endothelial cells. Increased thickness of corneal mass. Diffuse edema and thickening of descents. Results in Vas drop, can lead to blindness, epithelial bullae and erosions. Treat with NaCL, LV aids, lenses, keratoplasty, results often poor.
Posterior Polymorphous Dystrophy
Rare innocuous and symptomatic: the endothelium has epithelial characteristics. The endothelium has multiple layers. Objective: vesicular pattern, endo. band like lesions, geographic pattern. Asymmetrical findings. Inheritance usually AD 25-50. May be associated with Alpert’s syndrome, keratoconus. Vesicles on epithelium my rupture and form bullae. Can have photophobia, FB sensation, decr. VA. Treat with artificial tears, hypertonic saline drops, temporary bandage CLs, recurrent corneal erosion treatment, secondary glaucoma treatment, rarely corneal surgical treatment.
Corneal Pannus
Asymptomatic (decreased VA if central). Superficial vascular invasion with fibrous tissue bed. Usually chronic result of inflammatory response. Caused by staph, rosacea, CL overwear, phlyctenule, chlamydia, HSV, chemical burn, trauma, Superior limbic keratoconjunctivitis, chlamydia. Treat underlying cause, discontinue CL wear, document size and extent, topical vasoconstrictors may reduce redness. Follw up 1-2 weeks if progressing and monitor once stable.
About Ptergium
Wing shaped fibrous growth from the interpalpebral conjunctiva onto the cornea. Can result from pinguecula. Can have no symptoms, possible reduced VA, irritation, dry gritty eyes, and can become inflamed with progression. Related to sun/wind/dust exposure. High in latino populations. Can induce irregular astigmatism and distort cornea. Can decrease VAs.
Ptergium Treatment
Protect eyes, artificial tears, topical vasoconstrictor, Topical NSAID, topical mild steroid if inflamed, corneal surgical removal if near visual axis. Follow up 1-2 weeks if treating topically and 1 week if using steroid.
About Intersitial Keratitis
Stroma is not normal. Usually unilateral but may become bilateral. Redness, pain, mild to severe decreased VA. Acute form appears in 1-2 decade. Chronic signs of old IK persist through life. Acute can occur 5-15 years after systemic infection. Congential can present at age 15.
Causes of Intersitial Keratitis
Congential syphilis (usually both eyes affected), Acquired syphilis (unilateral) TB (unilateral) Cogan’s syndrome (hearing loss), leprosy, HSV, lyme disease
Triad of findings with IK
- Stomal infiltration-stromal haze and edema toward center of cornea
- Stromal thinning-most apparent in chronic forms
- Neovascularization-usually superior 180 degree and deep stroma. No blood in chronic inactive form.
Can also see thickened nerve, flesh nodules on iris, Iritis, conjunctivitis. Will see salt and pepper dystrophy and optic atrophy.
Leutic (congenital syphilis related) signs of IK
Saddle nose bridge as well as Hutchinson’s Triad (notched incisor teeth, deafness, IK)
Detecting IK
Can run lab tests as well as what you see under slit and dilated funds exam.
Treating Acute IK
Cycloplegic, topical steroid, glaucoma meds for elevated IOP, Treat underlying disease
Treating Chronic IK
Corneal transplant if central scaring and amblyopia. Refere to specialist.
Recurrent Corneal Erosion about
Epithelial not held strongly to stroma (damage to epithelial BM or bowman’s). EBM repair after 2-3 months. Epithelium is easily loosened.
Causes of RCE
Injury, Iatrogenic (surgeries), Corneal dystrophies (EBMB, Meesman’s, Reis-buckler, Lattice, graunular, macular, Fuch’s) and Diabetes.
Subjective RCE
Recent history of injury. Acute pain upon awakening. Sandy irritation. Lid spasms, photophobia, may have reduced Vas
Objective RCE
Localized roughening of corneal epithelium. Fluorescein dye may lightly outline area. Possible dots, fingerprint, or map like epithelial patterns. Underlying stromal edema may be present. Anterior chamber reaction may be present.
Treatment for RCE
Cycloplegic for comfort, Therapeutic bandage CL, AB drops, Topical steroid if uveitis, sunglasses for photphobia, topical sodium chloride drops, aritical tears. Corneal epithelium debridement. Anterior stromal puncture. Phototherapeutic Keratectomy.
Epithelium
Squamous cells on surface. Basals layer is below the basement membrane.
Disrupted epithelium heals in…
2-3 days if BM not damaged
6-8 days if BM is damaged
Damaging Bowman’s layer causes…
scars. There is no regeneration.
Superficial Punctate Keratitis (SPK)
Describes superficial punctate corneal epithelial disruption. Can be punctuate epithelial erosion or punt ate epithelial keratopathy.
Punctate Epithelial Erosions (PEEs) or Superfical Punctate Keratitis (SPKs)
Focal areas of epithelial disruption or lesion. Slight depressed. Will stain well with NaFL, rose bengal, and lissamine green. Bacterial origin is usually associated with bleph. Distrubution seen in a variety of patterns. Will have FB sensation, redness, tearing, photophobia.
Punctate Epithelial Keratopathy (PEK)
Grayish white opacities in the epithelium. Accumulation of epithelial cells that are surrounded by a focal inflammatory infiltrate. Seen without staining. Stains poorly with NaFl but well with rose bengal and lissamine green.
What do you expect when you see diffuse SPKs
Bacterial conjunctivitis, adenoviral conjunctivitis, medicamentoasa (reaction to medication), allergic conjunctivisi, severe dry eye syndrome
Upper 1/3 SPKs
Superior limbic keratoconjunctivitis, vernal keratoconjunctivitis, trachoma
Lower 2/3 SPKs
Staph bleph, ectropian, entropion, lagophthalmos, exposure keratopathy
Interpalpebral SPK
Keratoconjunctivitis sicca, expsoure keratophaty, UV keratopathy
Linear SPK
abrasion, triachiasis, entropian, FB
Sectoral SPK
Triachiasis, trauma
Diffuse SPK staining vs. confluent, vs focal
Focal is the deepest and will result in the most likely scaring
What organisms can cause Superficial Bacterial Keratitis
Staphy, Strep, Haemophilus
Signs and symptoms of Staph. Keratitis
Gram pos. Staph aureus is the most common ocular pathogen. Usually associated with acute or chronic staph bleph or blepharoconjunctivisis. Exotons from staph cause a band of punctate epithelial keratitis across inferior cornea.
Phlyctenulosis from Staph.
Associated signs: crusts and collarets around lashes, conj. hyperemia and papillae, mucus discharge, lids sticking in AM. Symptoms: FB sensation, photophobia, tearing, redness. Treat associated bleph. or conj with warm compress, scrubs, massage, meiobomian expression. Can apply AB ointment (bacitracin, erythromycin, polysproin) or AB drop (gentamicin, tobramycin, polytrim)
Besivance
A unique fluoroquinolone. Has longer ocular residence and decreased resistance as ocular.
Treating Superficial bacterial keratitis from staph
Use topical antibodic therapy that is broad spectrum (azithromycin) Must continue 14 days, artificial tears,
Superficial Bacterial Keratitis caused by Streph
Gram positive cocci. Signs: Diffuse punctate keratitis. Acute conjunctivitis, pseudomembrane formation, mucous discharge, URI or otis media. Symptoms include FB sensation, photophobia, tearing, redness.
Superficial bacterial keratitis caused by strep
Treat associated conjunctivitis. Antibiotic ointment (bacitracin, erythromycin, polysporin) AB drops (polytrim) Fluroquinolones (besivance)
Superficial bacterial Keratitis caused by Haemophilus
Gram negative. Signs: diffuse punctate keratisis. Associated with acute conjunctivitis (possible petechial hemorrhages), mucus discharge, matted eyes, associated URI or otitis media.
Superficial bacterial Keratitis caused by Haemophilus Treatment
Treat associated conjunctivitis. AB ointment (polysporin), Treat with polytrim, amino glycosides, fluroquinolones.
Treatment of Superficial bacterial keratitis with ointment
polysporin, bacitracin, erythromycin
Treatment of superficial bacterial keratitis with solution
Polytrim q3h, aminoglycosides, fluroquinolones. Treat for 7-14 days. Most topical ABS can eradicate most bacterial infections if used frequently enough.
Corneal Infiltrates AKA Corneal infiltrative events (CIE) General info.
An antibody-antigen reaction or hypoxia (not due to corneal infection). More common than infections. Variable staining with NaFl. Includes intraepithelial keratitis and sub epithelial keratitis. Usually from chronic conjunctivitis but can also be seen with acute. Associated with CL wear. Common in adults.
Corneal Infiltrative types
Marginal, Multiple and diffuse, sub epithelial but no stroma (will get scaring), with stromal involvement (will get scars)
CLARE
Contact lens related red eye
CLPU
Contact lens peripheral ulcer
Corneal infiltrates signs
Single or multiple. Separated from the limbus by a clear area. Size is variable. Overlying epithelium is usually intact (if an epithelial defect it is smaller then the infiltrate). Stain to see if overlying epithelium is intact. Will have pain (mild to moderate), tearing, photophobia, FB sensation. Most likely no anterior chamber rxn.
Treatment of Corneal infiltrates
Treat source of conjunctivitis (blepharitis. Warm compresses, lid scrubs, antibiotics) Discontinue CL wear or change solution. Steroid if certain there is no infection. (Lotemax, Pred forte, FML, Durezol *=strong) If epithelial break is present use (Tobradex or zylet) and homatropine if symptoms severe.
Corneal Ulcers
An infection compromise in the epithelium with the underlying stroma infiltrated. Epithelial edges are usually distinct with an indicting underlying stromal border. Corneal edema surrounds area involved. In adults caused by CL overwear and trauma. In kids caused by systemic illness and trauma. Must treat quickly and aggressively.
Risk Factors for Ulcers
Extending wear of CL, poor tear film, uncontrolled staph. bleph, smoking, swimming with CL, under 22 years, M
How to diagnose Ulcers
P: Pain E: Epithelial Defects D: discharge A: Anterior chamber rxn L: Location-central
Infiltrate will be no to all and location is peripheral.
Bacterial Corneal Ulcer
Bacteria needs a disrupted epithelial layer before they can cause ulceration. Most common are staphy, strep, and pseudo. People are more predisposed if they have corneal trauma, tear film abnormalities, corneal degenerations, diabetes, immune disorders, use of immunosuppresive meds. A lab workout may be needed to be done to ID the organism.
Symptoms of bacteria corneal ulcer
Decreased VA, photophobia, pain, redness, swelling of the lids, purulent discharge, Lid and conj inflam, hyperemia, mod to severe edema, stormal infiltration, corneal edema surrounding ulcer, destruction of corneal tissue. Severe AC reaction, Hypopyon, Synechiae, Elevated IOP
Bacterial corneal ulcer caused by Staph
Gram pos, yellow-white infiltrated central ulcer, round or oval, distinct borders, usually minimal anterior chamber reaction. pt. not in as much pain as you expect with an ulcer.
Bacterial corneal ulcer caused by strep
Gram pos, round or oval, grey-yellow ulcer, Spreads centrally. Leading edge may be shaggy or indistinct, marked hypopyon is common. Resistant strains common.
Bacterial Corneal Ulcer caused by Pseudomonas
Gram neg. Associated with trauma due to contacts. Centrally located. Gray infiltrate. Yellow-green discharge. Ulcer is more profuse (progresses rapidly to involve the entire cornea). Greenish mucopuruelent discharge often adhere to ulcer site. Usually associated with severe anterior chamber reaction and hypopyon formation is common. Resistant strains are common and appear worse in 24 hours. If untreated the cornea usually perforated in 24-48 hours.
Treating Bacterial Corneal Ulcer
Photo-documentation, detailed degram with size, location, neovascularization, depth of hypopyon if present, depth of ulcer. Discontinue CL wear. Use broad spectrum AB until the organisms is IDed. Can use mono therapy with fluoroquinoles, combo. therapy with cefazolin and tobramycin, or combo. therapy with fluroquinolones and AB. Use homatropine to relieve discomfort. If no response with fluroquinolones hourly ad generic polytrim hourly. Use steroid if necessary and ulcer is threatening visual axis. Should not be used until progressive improve of ulcer is seen for 2-3 days and organism has been IDed. Subconj. injections can be used if compliance with topical is a problem. Systemic treatment indicated for cornea-scleral ulcers, perforated ulcers, post perforating injury ulcers, infection caused by Bacteria known to require systemic therapy.
SCUT
Steroid Corneal Ulcer Treatment. Found steroids were effective but some dr. still scared of it.
Ulcer vs. infilatrate epidemiology
Rare vs. common
Ulcer vs. infilatrate etiology
Infection vs. inflammatory
Ulcer vs. infilatrate degree of pain
Moderate to severe vs. none to mild
Ulcer vs. infilatrate location
Tend to be central but can be peripheral (will move more central) vs. tend to be more peripheral but can be central
Ulcer vs. infiltrate number of lesions
1 vs multiple
Ulcer vs. infilatrate A/C reaction
Usually present vs. rarely present
Ulcer vs. infilatrate conj. injection
diffuse vs. sectoral
Ulcer vs. infilatrate tears
Debris in tears vs. clear or watery
Ulcer vs. infilatrate therapy
AB (steroids after healing maybe) vs. steroid or combo
Ulcer vs. infilatrate NaFl staining
Yes vs. yes or no.
Adenovirus Background
Non-enveloped DNA virus. Has different serotypes. Related to the common cold virus. High contagious. Frequent cause of infectious conjunctivitis (AKA pink eye) Patient may have cold symptoms or no symptoms.
Viral Shedding
Occurs by budding (use host cell membrane as envelop), apoptosis (host cell death, macrophages absorb), Exocytosis (host cell vacuoles expels visions). Released from a body part to another, real eased from body into the environment.
Adenovirus History
Notice a rapid onset (1 day), may or may not have lid edema, water discharge (rare stringy mucous), may have been around kids/pool. May be in 1 or both eyes. usually mild to no visual bold. Cold/flu or stress recently. Palpable pre auricular lymph node, pink to red injection, Follicular conjunctivitis, SEIs (sub epithelial infiltrates).
Adenovirus rule of 8
Rule of 8: caused by adenovirus 8, 8 day latency from exposure to onset of symptoms, symptoms usually last 8 days.
Rule of 8: first 8 days conjunctivitis with mild SPk. Next 8 days deep epithelial lesions, Next 8 days infiltrates may form.
EKC with sub epithelial infiltrates
Classic EKC corneal finding. Multiple round white lesions. May or may not stain with fluorescein days. Highly contagious. Seen in Adenovirus (virus spreads all across cornea)
Symptoms of Adenovirus
- EKC with sub epithelial infiltrates 2. bulbar hyperemia and subconjunctival hemorrhages (SCHs are usually small patches throughout conj. Watery eye. Heme resolves in 1-2 weeks) 3. Follicular Conjunctivitis (with small mucous strand mid conj) 4. Pseudomembrane (fibrinous inflammatory secretion from conj. cells. May or may not be firmly adherent to conj.)
What to do about psuedomembrane?
Remove it. use cotton swab or forceps. Rarely true membrane. It may bleed.
How to confirm adenovirus?
RPS test. Takes 10 minutes.
Treatments of Adenovirus
- Original: none
- Paliative: articial tears, cool compress, rest
- Off label treatment: AB/Steroid combo. Reduce risk of super infection and scarring
- Topical cidofovir-not available
- 5% betadine-need prop and NSAIDs
- Zirgan-treats Herpetic keratitis and may be able to treat this too.
Molluscum Contagiosum
Viral infection of skin and mucous membranes. Spreads through skin to skin contact. Contagious till the bumps are gone (6 months). Pt. usually asymptomatic. Chronic keratoconjunctivitis with Eyelid lesions. Biopsy to confirm. Bacterial superinfection. Can last week to years. Flesh colored and umbiculated.
Molluscum Contagiosum Tx
Lesion destruction by cryotherapy, laser treatment, Astringent, tea tree oil, benzoyl periodized, immunosuppresents, salicylic acid.
Syphilis is caused by what?
Organism is treponma pallidum. Spiral shaped parasite.
Congential syphilis
Pt. has intersitial keratitis, notched teeth, deafness
Acquired syphilis
The great mimicker.
Primary Syphilis
Chancre (erythemotous papule) at inoculation site. Lesion 4 weeks after initial infection and heals in 1-2 months.
Secondary Syphilis
Generalized maculopapular or pustular rash, and lymphadenopathy. Appears 4-10 weeks after initial manifestation. Lesion on palms, soles. Fever/HA/joint pain. 10% ocular involved
Latent Syphilis
Early and late forms. Within and beyond 1 year post infection.
Tertiary Syphilis
Benign: granulomas of skin/ mucous membrane chroid, CB, Iris. Cardiovascular, neurosphillis
Quaternary
Aggressive neurosphillis, necrotizing encephalitis in patients with AIDS
Syphilis Ocular Manifestations
Intersitial Keratitis, episcleritis, scleritis, iritis, iris papules, secondary cataract, chorioretinitis, papillitis/neuritis, retinal vasculitis, exudative retinal detachment.
Syphilis related history
History of sexual transmission, IV drug use, Transplacental transmission (congenital), accident contact with infected lesion, blood transfusions
Syphilitic Intersitial Keratitis About
Nonulcerative and nonsuppurative diffuse of local inflammation of corneal stroma. Inflammation may be either direct result of infectious process or secondary to immunological response to a specific foreign antigen (more common), Characterized by cellular infiltration of stroma. In general no primary involvement of corneal epithelium or endothelium. May form stromal neo is untreated.
Congential Syphilis causing Syphilit Keratitis
90%. Commonly appears age 6-12. Corneal edema and infiltrates present. Have lacrimation and photophobia. Corneal stromal vascularization. May get cornea pink ‘salmon patch’ look. Generally begins unilaterally. Becomes bilateral in 90% of cases.
Hutchinson’s Triad for Congenital syphilis
Intersitial keratitis, teeth abnormalities, deafness
Acquired syphilis causing sphilitic Keratitis
10%. Active IK shows stromal inflammation (especially peripheral cornea) Marginal infiltrates of anterior stroma may be present, when inflammation subsides, corneal scarring appears. Evidence of stromal neovascularization just anterior to descemet’s membrane may be present.
Syphilitis Intersitial Keratitis Work up
VDRL-allows you to monitor treatment. There are many other tests
Tests for Syphilis
- Dark field immunofluorescence microscopy
- Electron microscopy
- Ganzfeld electroretinogram
- Indocyanine green angiography
Treatment Syphilis
- Penicillin IV q4h 10-14 days-standard
- Penicillin intramsuclarrly with probenecide
- Following above two treatments-benzathine penicillin IM for 3 weeks
- If allergic to penicillin then doxycyline, erythromycin, tetracycline
5.
Treatment for ocular syphilis
- Topical broad spectrum AB (Erythromycin)
- Topical steroids if uveitis/stromal involvement and fungal infections rules out
- Copious preservative free tears
- cyclopeic agent.
