Cornea Flashcards
interstitial keratitis
presentation:
etiology:
trx:
presentation: non ulcerating inflammation of corneal stromal
– red, painful, photophobic, excessive lacrimation
– unil or bil
–stroma neovascularization
– AC rx : cells/flare
etiology: 2’ to immune rxn caused by exposure to infectious agents that trigger deployment of T-cells to stroma.
– Herpes simplex (unilateral)
– congenital syphilis (most common)
–Lyme disease
trx: IF HERP. SIMPL
– topical steroid q1-6hours
–cyclopegic
– valtrex 1 gram p.o tid
– recovery, the stromal bv become non-perfused or look like ghost vessels
congenital syphilis
Hutchinson triad(HID)
interstitial keratitis
peg shaped incisors
deafness
dilated exam: optic atrophy, salt/pepper fundus
interstitial keratitis: inflamm. of cornea cause blurry vision & pain
pt w/ interstitial keratitis due to lyme disease
– symptoms :
– definitive diagnostis
– fatigue, HA, fever
DEFINITIVE diagnostic: red rash w/ bull’s eye at site of infection
lyme disease trx
oral doxycycline in early lyme disease
syphilis trx
IV aqueous crystallin PCN G
corneal defect that frequently occurs in response to a previous corneal abrasion due to something organic (fingernail or tree branch)
recurrent corneal abrasion
explain RCE
initial abrasion heals but short time after, pt experiences another episode w/o incident.
– happens 1st thing in AM/
-eyelids stick to new unstable epithelium and cause it to tear when eyes open
ideal way to treat RCE
erythromycin ointment qid, PF ATs q2hours + BCL
– monitor every 1-2 days until corneal defect healed
hyperosmotic drops or ATS 6-8 weeks post to ensure hemidesmisomes form properly
in the event of an RCE, w/ no pt improvement.
clinical exam reveals corneal defect w/ loose epithelium & areas of heaping around edges. What is best course of action? explain procedure
corneal debridement
- anesthetize cornea
- use cellulose sponge & forcepts to remove loose epithelium
giving medical advice to pt over the phone requires what 2 actions?
document date, time, and specific instructions (OTC meds recommended to buy)
– call pt in 1-2 days to make sure they got correct product and f/u
marginal keratitis/staphylococcal hypersensitivity keratitis
clinical presentation
- sterile marginal infiltrates superior or inferiorly (lid margins rest on corneal surface)
- single or multiple infiltrates concentric to limbus
- local conjunctival hyperemia
- epithelial defects overlying lesion but smaller than infiltrate
- AC usually quiet
- anterior blepharitis (flakes on lashes)
pt symptoms for marginal keratitis
etiology
photophobia, pain, localized conjunctival redness, chronic eyelid crusting, fb sensation, ocular dryness
etiology: staphyloccal aureus bacteria on eyelid margins
how does clinical presentation of phlyctenule differ from marginal keratitis
corneal phlyctenule is small, white nodule found at the limbus.
- assoc w/ ulceration of corneal epithelium
- lesion can travel to central cornea, leaving corneal scar, neovascularization
presentation of bacterial corneal ulcer
- severe redness, pain, photophobia, decreased VA, discharge
- focal white opacity in corneal stroma + epithelial defect that stains with fluorescein
corneal dellen symptoms/signs
- mild irritation and fb sensation
- SLE: corneal thinning at limbus adjacent to conjunctival or corneal elevation
- sodium fluorescein pooling in the area
thygeson superficial punctate keratitis
chronic bilateral condition
- fb sensation, tearing, photophobia
- macro-punctate gray-white corneal epithelial opacities that are slightly elevated
- stain centrally
treatment for marginal keratitis
–address blepharitis: warm compress, eyelid hygiene
-fluoroquinolone antibiotic qid or bacitracin, erythromycin
- mod to severe case: low dose topical steroid: loteprednol 0.2% to 0.5% or prednisolone 0.25% qid or combo such as Tobradex.
DONT USE STEROID ALONE
-add systemic tetracyline (doxycline) if symptoms continue
- topical restasis/cyclosporine for long term control of ocular inflammation
resolves on its own if left alone for several weeks. self limiting
hallmark signs of keratoconus
-central/paracentral stromal thinning
- apical corneal protrusion
- irregular astigmatism
- scissor reflex on retinoscopy
SLE: - munson sign- bulging of Lower lid
- iron deposits at base of cone -epithelium -kayser ring
-vertical deep striae in corneal stroma(disappears w/ external pressure)
- rupture of descemet, leading to aqueous into cornea–> hydrop
describe keratometry finding for keratoconus
- steep K value >48D or >54D in severe case
- corneal pachy shows progressive corneal thining corresponding to area of conical protrusion
difference in clinical presentation & topography of keratoconus and pellucid marginal corneal degeneration
PMD protrudes superior to area of corneal thinning
hallmark sign: kissing birds patten on topography
keratoglobus is defined as
corneal thinning over the entire cornea; ectasia is generalized
Terrient marginal degeneration
- peripheral corneal thinning or extensive areas of cornea
- degeneration starts superiorly, thin stroma
- anterior stromal opacities
- clear region between opacities and limbus
*note optical section
forme fruste keratoconus topography reveals:
topography displays central or paracentral irregular astigmatism
- pt asymptomatic
best candidates for corneal CXL
- 35 YO and younger
- moderate keratoconus, max K power <65D
- corneal thickness >400micron
- 20/30 or worse VA
standard protocol for corneal CXL requires minimum corneal thickness of ____ after removal of corneal epitheal in order to prevent endothelial damage
standard protocol for corneal CXL requires minimum corneal thickness of 400um after removal of corneal epitheal in order to prevent endothelial damage
contraindications to CXL
prior hx of herpetic infections (to avoid viral reactivation)
- concurrent infection
- severe corneal scarring/opacity
- hx of poor wound healing, severe ocular surface disease
- hx of autoimmune disorders
it pt NEEDS cxl w/ hx of herpetic infections, pre & postoperative prophylactic oral acyclovir can be considered
epithelial ingrowth
epidemiology:
happens days to weeks post LASIK and seen on flap edge interface.
- ingrowth due to proliferation of surface epithelial cells into the corneal flap interface
- possibly due to interruption- epithelial cells wont migrate as long as they are surrounded by other epith cells. lasers can disrupt
- risk factors: older pt, EBMD, RCE hx, eye rubbers, diabetic pt, LASIK, over manipulation of flap
diffuse lamellar keratitis/sands of sahara
2-5 days post LASIK
- little to no conj injection
- hyperopic shift w/ astigmatism
- SLE : diffuse inflammatory infiltrates across periphery of surgical interface but not in stroma or in the flap
-central corneal hazy
TRX: topical steroids every hour
- if infiltrates are severely condensed, flay need to be lifted and interface debrided
- stromal melt could happen if not detected & treated early
difference between microbial keratisis & diffuse lamellar keratitis
infections cause redness, include some discharge. cant trx infection with steroid
pt will note irritation/discomfort
treating epithelial ingrowth post LASIK
if epith ingrowth is small and only in periphery of flap: monitor in 2-3 weeks to make sure VA is unchages and ingrowth stays in that location
mild ingrowth can spontaneously resolve
if change in VA and progression, refer to surgeon to re-lift flap and remove aberrant cells
topical ophthalmic meds used 1 week post LASIK
ATs
topical steroid gtts
topical antibiotic
