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4/17/2008 1 Complex Corneal Grand Rounds William D. Townsend, OD, FAAO Advanced Eye Care Canyon, TX Adjunct Professor, UHCO Houston, TX INTERACTIVE 1.acting one upon or with the other. 2.of or pertaining to a twoway system of electronic communications, as by means of television or computer: interactive communications between families using twoway cable television. This course will be interactive. Cornea: Anatomical & Physiological Considerations Epithelium Protective function In abrasions, cells “slide” to cover debrided areas Regenerates in 67 days Trauma to basal cells may result in irregular basement membrane Nerve concentration 20x that of dental pulp Bowman’s layerhighly resistant to penetration Anchoring filaments based in stroma Stroma Regular spacing of fibrils results in clarity Hydrophilic Prone to edema Damage is repaired by keratocytes, usually not transparent

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Complex Corneal Grand Rounds

William  D. Townsend, OD, FAAO

Advanced Eye Care          Canyon, TX

Adjunct Professor, UHCO    Houston, TX

INTERACTIVE

1.acting one upon or with the other. 

2.of or pertaining to a two‐way system of electronic communications, as by means of television or computer: interactive communications between families using two‐way cable television.

This course will be interactive.

Cornea: Anatomical & Physiological Considerations

• Epithelium– Protective function– In abrasions, cells “slide” to cover debrided areas– Regenerates in 6‐7 days– Trauma to basal cells may result in irregular basement membranemembrane

– Nerve concentration 20x that of dental pulp• Bowman’s layer‐ highly resistant to penetration

– Anchoring filaments based in stroma• Stroma

– Regular spacing of fibrils results in clarity– Hydrophilic– Prone to edema– Damage is repaired by keratocytes, usually not transparent

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Cornea: Anatomical & Physiological Considerations

• Descemet’s membrane– Breaks result in inflow of aqueous into stroma– Capable of self‐healing

• EndotheliumTransports fluid out of cornea– Transports fluid out of cornea

– 50% of cells lost over a lifetime– Loss of function results in decompensation

• Tear film – Protective functions: lysozyme, other enzymes– Removes potential pathogens

Attack of the Killer Lampshade

A 43 year old female presents with a history of having struck herself in the right eye with a lampshade. She complains of moderate pain complains of moderate pain, photophobia, blurred vision, and lid edema. Her general health history is unremarkable; she takes no systemic medications, and has no known medication allergies.

Attack of the Killer Lampshade

• VA = OD 20/25 OS 20/20• SLE:

OD: Abrasion superior corneaGr II+ injectionGr. II+ injectionNo flare or cellsGr. II+ lid edema

OS: NL• Pupils NL

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Attack of the Killer Lampshade

Assessment:• Corneal abrasion secondary to

traumaPlan: pressure patch with: • 2 gtt Voltaren• 1 gtt Tropicamide 1% • 1 gtt Occuflox• 400 mg IbuprofenRTC: 1 day

Attack of the Killer Lampshade• Day 2: Removed patch in office. • Subjective: Complains of “shooting pains in

OD, eye feels feverish, swollen”• VA = OD 20/30 OS 20/20• SLE:

Corneal abrasion 95% healed– Corneal abrasion 95% healed– A/C: trace cells, flare, decreased injection

• Assessment: The eye looks great, almost healed

• What is wrong with our management of this case?

• Plan: ?

Corneal Abrasion: A Model For TraumaWhat Went Wrong On Day 2?

Release of cell membrane phospholipids

Converted by: Phospholipase A

Trauma Release of bradykinin

Arachidonic acid

cyclooxygenase lipoxygenase

prostaglandins leukotrienesVasopermeability, Miosis

ChemotaxisVasodilation, IOP changes

Converted by:

PMN migration

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Pathogenesis of Inflammation

Blocked by

Release of cell membrane phospholipids

Converted by Phospholipase A

Trauma

Side effects!

Release of bradykinin

Arachidonic acid

ysteroids

cyclooxygenase lipoxygenase

prostaglandins leukotrienesVasopermeability, Miosis

ChemotaxisVasodilation, IOP changes

Side effects!

PMN migration

converted by:

Nonsalicylate NSAIDs• Used to manage mild to moderate pain• Compare well with many narcotic

analgesics in relieving pain• Effective anti-inflammatory agents- work Effective anti inflammatory agents work

peripherally and centrally• Central nervous system effect reduces

recognition of pain• Antipyrexic- (lower body temperature)• Ceiling effect- dosing above given level

does not further increase pain relief

Ibuprofen• OTC in 200m tablets, capules, gel caps• Rx 400mg, 600 mg, 800 mg• Gel caps give most rapid relief of pain

and inflammation• Acts centrally and peripherally to reduce: • Acts centrally and peripherally to reduce:

Sensation of pain Inflammation

• Requires Q 4hr dosing• Should be taken with food• Pediatric syrup available (OK for adults)• Ceiling effect!

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Oral Ibuprofen vs. Tylenol No. 4Cooper, Steven A. “The relative efficacy of ibuprofen in dental pain” Compend. Cont. Ed. Dent. Vol VII, No 8.

“ Ibuprofen 400 mg was significantly more effective than acetaminophen 300 mg with codeine 60 mg for every analgesic measure (P < .05).”

Lessons from This Case

Ultimately, patients may remember how well you managed or mismanaged their pain rather than mismanaged their pain rather than how you managed their disease. You have a 12 hour window to be a hero or a heel. Always address pain proactively rather than reactively.

A Garden Variety CaseA sixty-seven year old female presents with a history of having been struck in the right eye with the tip of a cactus while working in the garden. The episode occurred four days prior to her visit Since then she has had prior to her visit. Since then, she has had persistent watering and foreign body sensation, but no mucopurulent discharge. She denies any blurring or loss of vision. Her general health history is unremarkable. As a child she suffered a blow to her right eye without any known permanent sequelae.

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Your diagnosis of this patient’s condition is:

1. Epithelial basement membrane dystrophy

2. Recurrent corneal erosion3. Penetrating corneal injury4. Fuch’s corneal dystrophy5. Corneal abrasion6. Townsend’s syndrome

Appropriate management of this case would include:

1. Referral to corneal specialist2. Hypertonic saline drops and ointment3. Bandage contact lens4. Topical antibiotic drops5. Topical beta blocker or carbonic

anhydrase inhibitors6. All the above except 2

The most appropriate antibiotic for this patient is:

1. Polytrim drops

2 Cilo an ointment2. Ciloxan ointment

3. Tobramycin drops

4. Tobradex ointment

5. Vigamox drops

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How We Would Manage This Case in 2008

• Bandage contact lens• Topical Vigamox drops Q 4 hrs• Topical beta blocker Q24 hrs (do

careful medications, health Hx)• Daily monitoring of patient• Emphasize need to report redness,

pain, or blurred vision immediately

The One-eyed Wonder

A 71 year old male presents with pain and photophobia in his left eye. His right eye had been enucleated following trauma years earlier He following trauma years earlier. He initially denied any history of trauma, but later stated he may have scratched his eye playing with his dogs. His hypertension was controlled by medications, and he denied any history of drug allergy.

The One-eyed Wonder

• VA: OD N/A OS 20/30• SLE:

– OD coated prosthesisOS 2 f ith li l l ti – OS: 2 mm area of epithelial ulceration midway between limbus and central cornea.

– Conjunctiva: gr. II+ injection– A/C: gr. I+ cells, flare

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What is your initial plan

1. Start topical fluoroquinolone2. Start topical fortified antibiotics;

Cefazolin & Tobramycin3 P f l i d lt 3. Perform corneal scraping and culture

on agar plates4. Shoot the dogs5. 1 & 36. 2 & 3

The One-eyed Wonder

• Assessment: bacterial keratitis• Plan:

– Obtain cultures: blood and chocolate agaragar

– Start Ciloxan per manufacturer’s recommendations

– Admit to hospital: (patient was from out of town and had no place to stay)

– RTC x 1 day

The One-eyed Wonder

• Day 2• All findings stable to slightly worse• Cultures show no growth after 24 hrs• Day 3• All findings stable with slight

enlargement of ulcerated area• Lab reports no growth

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OK, the guy only has one eye, and it’s getting worse fast…so what are

you going to do? 1. Repeat scraping and culture2. Consult lab3. Increase dosage frequency 4. Be patient5. Shoot the patient6. Shoot yourself

The one-eyed wonder

• Day 3- it was worse, believe me…..• A personal visit to the microbiology

lab: culture showed a small colony on one of the plates; lab staff refers to it p ;as “contamination”

• I refer to it as, “my last hope”• Plan: re-streak “contaminants” on to

additional Sabouraud's agar plates

Your final shot at this case

1. Resistant bacterial strain2. Atypical herpes simplex lesion3 l l3. Fungal ulcer4. Corneal melt5. Dog-scratch fever

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The one-eyed wonderDay 4• Ulcerated area increasing in size• Lab reports fungal growth of Aspergillis• Plan: start patient on natamycin q 1 hourDay 5Day 5• Ulcerated area beginning to shrink• Patient reports improvement in symptoms• Reduce frequency of dropsFinal Outcome• Best corrected VA = 20/30: small scar OS

Wong TY et al “Risk factors and clinical outcomes between fungal and bacterial keratitis: a comparative study”. CLAO 1997; 23 (5), p 275-81

Compared relationship of fungal and bacterial keratitis with respect to:

• Trauma • Contact lens wear• Findings: in a five year period,

– 103 cases of infectious keratitis managed; – Cases definitely identifiable as fungal or bacterial

included– All others excluded

Wong TY et al 29 of 103 eyes met criteria for fungal keratitis

• Males/females = 3.8/1• 27% had satellite lesions• 21% had perforation• 55% had Hx of trauma• 7% wore contact lens• 24 % were using topical steroids

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Wong TY et al 51 of 103 eyes met criteria for bacterial

keratitis

• Males/females = 1.8/1• 0% had satellite lesions• 4% had perforation• 31% had Hx of trauma• 31% wore contact lenses• 31% were using topical steroids

Wong TY et al Conclusions

• Trauma a significant risk factor for fungal keratitis

• Contact lens wear a significant risk factor for bacterial keratitisbacterial keratitis

• Use of steroids significantly increases risk for keratitis of either kind

• Satellite lesions highly suggestive of fungal keratitis

• Perforation 5x more likely in fungal keratitis

Townsend, W. “A question of culture”. Contact Lens Spectrum; April 1998

• Monocular individuals with infectious keratitis• Large ulcerative lesions impinging on the visual axis• Pediatric ulcerative keratitis, highly purulent keratitis,

suspected Haemophilus conjunctivitisp p j• Chronic lesions that fail to respond in • Bilateral corneal ulceration ( almost exclusively in

immuno-compromised patients)• Suspected chlamydial infection (use DNA probe w/

PCR sensitivity and selectivity)• Possible fungal or amoebic infection (biopsy

needed?)

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Lessons from One Eyed Wonder

• Think of the worst case scenario when dealing with corneal conditions

• If in doubt, culture ulcersGi i l id ti t • Give special consideration to one-eyed individuals with potential disease

• Do not trust labs; they can let you down at exactly the wrong moment

• Remember fungal keratitis as a possible etiology in corneal disease

With all this refractive surgery being done…….

Mr. 20/20 (with help)A 22 y/o Hispanic male who underwent LASIK two years ago presents with LASIK two years ago presents with blurring in his right eye. He was struck in right eye by his daughter’s fingernail. He wants to know why he is blurry, but has minimal pain.

Mr. 20/20 (with help)• VA: OD 20/30 OS 20/20• SLE:

– OD • Trace injection• Anterior stromal hazeAnterior stromal haze• Anterior chamber clear NOFC• Tr. stain w/ NaFL

– OS- all findings unremarkable• TA OD 17 mm Hg OS 16 mm Hg• Meds: artificial tears OD for discomfort

(patient did not bring with him)

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Mr. 20/20 (with help)Your diagnosis is:

1. Recurrent corneal erosion secondary to trauma

2. Diffuse bacterial keratitis3. Chemical keratitis secondary to

BACL preserved drops4. Post traumatic DLK5. Posner-Slossman Syndrome

Your initial treatment would be..

1. D/C present drop & start non-preserved hypotonic artificial tears

2. Debride corneal epithelium and apply bandage lens and start Zymar BID along bandage lens and start Zymar BID along w/ hypertonic drops QID

3. Start Vigamox 1 drop every three hrs.4. Start Pred Forte every hour5. Start gin & tonic every 30 minutes

And the diagnosis is:Here’s a hint!

Yes, Sahib, there is something in your

d it ld eye…… and it could be sand!

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Diffuse lamellar keratitis (DLK)AKA Sands of the Sahara

• Usually occurs within 1-4 days of procedure

• Inflammatory cells (mononuclear cells and granulocytes) in the LASIK flap interface

• Keratocyte activation and altered • Keratocyte activation and altered extracellular matrix can lead to irreversible scarring

• Risk factors include– Use of certain microkeratomes– Lower corneal endothelial cell density– Larger palpebral fissure

• Treatment is aggressive regimen of topical steroids

Post-traumatic Diffuse Lamellar Keratitis (DLK)

• Can occur months or years after procedure

• Onset is rapid, signs same as conventional DLKconventional DLK

• Epithelial damage, reduced pH postulated to initiate this condition

Aldave AJ, Hollander DA, Abbott RL. Late onsettraumatic flap dislocation and diffuse lamellar inflammation after laser in situ keratomileusis. Cornea August 2002

Lessons from 20/20 with HelpPost Traumatic DLK

• Inform LASIK patients that even moderate trauma can lead to complications years outTell your LASIK patients to report any eye • Tell your LASIK patients to report any eye trauma, no matter how trivial immediately

• If the patient shows signs of DLK, attack this condition very aggressively; start steroids every hour

• Inform the refractive surgeon of your findings, disposition STAT

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Macho Man?

• VA = 20/20 OU• SLE: OD:

– Heavily rusted foreign body 3 mm from the visual axis

– Gr. II+ cells, flare, Gr. II+ injection• You anesthetize the eye and attempt to

remove the foreign body. The patient mumbles that he feels he is about to collapse, and faints in your arms.

• Diagnosis and management?

Syncope• Definition: “Transient loss of

consciousness and postural done due to inadequate cerebral flow with prompt recovery without resuscitative measures ”measures.

• Etiology: May be due to a variety of processes– Vasomotor– Cardiac– Situational

Syncope

• Vasomotor• Postural (orthostatic) hypotension• (Reduction of > 20 mm Hg upon

t di )standing)• Anaphylaxis• Hemorrhage• Hypovolemia (dehydration)• Neurocardiogenic (vasovagal)*

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Syncope

•• CardiacCardiac•• TachydysrythmiaTachydysrythmia•• BradydysrythmiaBradydysrythmia

•• SituationalSituational•• CoughCough•• DefecationDefecation

•• Myocardial Myocardial ischemiaischemia

•• MicturationMicturation

Vasovagal Syncope

• 25% more common in females, 48% of all individuals report experiencing at some time

• Most common cause of fainting in healthy individuals

• Cerebral blood flow of 55 ml/100 gm of brain tissue required for adequate perfusion

• When blood flow drops below 20 ml/ 100 gm, reduced perfusion causes loss of consciousness

Managing Syncope• Vasovagal syncope results from an altered

or abnormal “fight or flight” response• Initial phase occurs when danger, threat

perceived (esp. Pain)I d h t t di t t bl d – Increased heart rate, cardiac output, blood pressure, systemic resistance

• Second phase occurs when “nothing happens” after the initial response– Rapidly reduced heart rate, cardiac output,

blood pressure,peripheral resistance accompanying vasodilation, pooling in extremities

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Managing Syncope

• ABC’s of life support plus• Airway cleared?• Breathing?• Cardiovascular function• Cardiovascular function• Pupillary reflexes intact• Trendlenberg position: tilt your exam

chair back or recline patient in supine position and position legs higher than head

Managing Syncope

• Waft ammonia spirits (smelling salts)• Cool moistened towel on forehead• Keep someone with patient at all timesp p• If total loss of pulse and blood pressure,

0.4 mg atropine subcutaneous

Managing Syncope: Preparation

• Keep ammonia spirits (smelling salts) in every exam room, CL delivery room

• Identify patients with Hx of syncope• Teach your staff basic CPR or have them

tifi dcertified• Ambu-bag or CPR screen available at all

timesEngel G. “Psychologic stress, vasodepressor (vasovagal) syncope, and sudden death”. Ann Internal Med 1978; 89:p 43-412

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On a Mission

During a medical mission to Mexico, we encountered a 19 year old Hispanic male with a history of progressively diminishing vision He also progressively diminishing vision. He also has a history of a chronic skin condition. The patient complains of photophobia and glare. He has never been treated for his ocular or dermal condition.

On a Mission• VA s

– OD 10/120 OS 10/100– Pinhole no improvement

• External,, papules and pustules, and– Generalized erythema, telangiectasias– Multiple papules concentrated in the

glabellar and malar area– Rhinophyma

• SLE– Bilateral corneal pannus radiating from

the inferior limbus

Man on a MissionDonaldson KE, Karp CL, Dunbar MT. Evaluation and Treatment of Children With Ocular Rosacea. Cornea 2007 Volume 26, Number 1,

• Rosacea affects @ 10% of the adult population

• Pediatric rosacea grossly under recognized– Dermatologic changes are often not

present in children• Demographics: Hispanic 60%,

Caucasian 25%, Black 15%

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Ocular Rosacea• Donaldson KE, Karp CL, Dunbar MT. Evaluation and

Treatment of Children With Ocular Rosacea. Cornea 2007 Volume 26, Number 1,

• 95% have meibomian gland disease% i• 49% have chalazia

• 85% have conjunctival injection

Ocular Rosacea

• 2 primary etiologic components; vascular and inflammatory

• Ocular signs & symptoms may precede cutaneous changes in 20% of patientscutaneous changes in 20% of patients

• Pathophysiology unknown; theories– Type IV hypersensitivity reaction– Demodex mites initiate inflammation– Helicobacter pylori has been implicated

Man of SteelA forty-one year old male presents to your office with a history of foreign body sensation OD for the past 24 hours. He works as a welder and frequently grinds iron and steel, often frequently grinds iron and steel, often with high velocity particles being spun off the work surface. He cannot specifically pinpoint the time the sensation began. His wife noted a brown spot on the OD cornea. Additional Hx?

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Man of Steel: ExaminationVA: OD = 20/20, OS = 20/20

Pupils: PERRLA PANA: negative OU•• SLE: ODSLE: OD•• Cornea: 1 x 1 mm Cornea: 1 x 1 mm

foreign body w/ foreign body w/ surrounding area of surrounding area of rust necrosisrust necrosis

•• SLE: OSSLE: OS•• All findings nlAll findings nl

rust, necrosisrust, necrosis•• Conj: generalized Conj: generalized

injection, > local to fbinjection, > local to fb•• AC: gr . flare, tr. cellsAC: gr . flare, tr. cells•• Lids: tr edemaLids: tr edema•• Tears: epiphoraTears: epiphora

All of the following are appropriate except

1. X-ray of orbits for retro-bulbar foreign body

2. Refer to another practitioner for FB removal

3. MRI of orbits for retro-bulbar foreign body

4. Removal of foreign body with sterile spud or needle

5. All the above are appropriate

Your car payment is overdue. You decide to remove the foreign body. Which instrument

is most appropriate?

1. Spud2. Bent needle3. Forceps4. Alger brush5. Micro chain saw6. 1,2, 3, and 4 are appropriate

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The best post op management scheme would include:

1. Tobradex ung, homatropine, and Acular

2. Vigamox gtt, tropicamide, and bandage CLbandage CL

3. Tobradex gtt, homatropine and Voltaren

4. Vigamox gtt, homatropine, and bandage CL

5. Beer and an old Elvis Presley movie

Non-Penetrating Corneal Foreign Bodies

• Etiology: particulate matter that penetrates the corneal surface

• Speed of impact, type of material and causative factors important in Hxcausative factors important in Hx

• Signs & Symptoms: variable depending on material; Fe foreign bodies tend to be more symptomatic

• Pain, FB sensation, photophobia, epiphora

Non-Penetrating Corneal Foreign Bodies

• Differential– Intraocular FB– Foreign body embedded in lid

Intra orbital foreign body – Intra-orbital foreign body • No MRI on suspected metallic foreign body• CT or X-Ray OK

• All vegetative FB carry a risk for fungal keratitis

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Non-Penetrating Ferrous Corneal Foreign Bodies: Management

• Topical anesthetic• NSAID gtts• Cycloplegia (not mydriasis)• Remove w/ your favorite weapon

Remove rust w/ spud needle or *Alger • Remove rust w/ spud, needle or *Alger Brush*

• Broad spectrum antibiotic in office (ung vsgtts)

• Bandage Cl as indicated• Non-preserved antibiotic gtt x 5-7 days• Cover pseudomonas, fungal infection late

Managing the visual axis foreign body

• Refer – The better part of valor is discretion, in the

which better part I have saved my life. William Shakespeare (1564-1616) p ( )

– OR….• Warn the patient that VA may be

decreased no matter how well the procedure goes and document it!

Managing the visual axis foreign body

• Remove all foreign material leaving the “cleanest” possible surface (remove all rust)

• Start fluoroquinolone- no aminoglycosidesaminoglycosides

• Add steroid when lesion is non-staining• Taper steroid over a period of weeks

– Remember, steroids work by inhibiting protein synthesis!

• Document all conversations, warnings

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Coding

Curly SueA sixteen year old female student presents to your office. She had been curling her hair when the curling iron slipped and passed cu g o s pped a d passed across her cornea. Interestingly, her pain is not reported as being terribly severe. She also complains of blurred vision. She has no known allergies to medications.

Curly Sue: ExaminationVA: OD = 20/20 OS = 20/20

Pupils PERRLASLE: ODSLE: OD

•• All findings All findings nlnlSLE: OSSLE: OS

•• Cornea: central area of Cornea: central area of burned epithelium w/ burned epithelium w/ loss strands of tissueloss strands of tissue

damage epithelial damage epithelial onlyonly

•• Conj: gr. II+ injectionConj: gr. II+ injection•• Tears: Tears: epiphoraepiphora•• AC: gr. I+ flare, no cellsAC: gr. I+ flare, no cells•• Lids: Lids: nlnl

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Thermal Corneal Burns• Etiology• Any direct flame, high temperature object,

material• Common causes:

– Curling irons, cigarettes, welding slag, hot liquids, very bad luck

• Differential– Chemical burns– Old scar– Metaherpetic lesion

Thermal Corneal Burns: Management

• Topical anesthetic• Topical NSAID pre-debridement• Debride all damaged epithelium: Kimura spatula,

Wick sponge• Cycloplegia: 2% - 5% homatropine sol.Cycloplegia: 2% 5% homatropine sol.• Broad spectrum antibiotic w/ good activity against

P. aeruginosa• Bandage CL• Follow patient daily until re-epithelialized• Continue antibiotic drops minimum 5 days• Refer if damage extends deeper than epithelium

Eroding Relationships

A 34 year old male presents to your office with a finger nail injury to the right cornea. His ocular and general health are unremarkable He has no health are unremarkable. He has no known medication allergies. There is no previous history of eye trauma.

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Eroding Relationships

• VA: OD 20/40 OS 20/20• SLE

– OS: NL– OD: Corneal abrasion: lesion is 3 mm x 5 mm,

loose edges, stromal folds, diffuse edema• Plan:

– Proparacaine– Debride edges of lesion to remove loose tissue– Pressure patch with antibiotic ung, NSAID– Recheck one day

Eroding

• Follow-up: The patient appeared to recover nicely from the injury.

• Plan: Muro 128 ung hs x 60 daysO k l t P ti t l i f • One week later: Patient complains of pain, blurring on awakening. Has been using meds, but had forgotten to use them the previous night.

Eroding

• SLE: OD– Epithelium in original area of abrasion has

detached from underlying tissue– Underlying stromal folds edemaUnderlying stromal folds, edema– Gr. II+ conjunctival injection

• Plan– Repeat treatment, but use bandage

contact lens in addition to hyperosmotics and antibiotic.

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Recurrent Corneal Erosion

• Etiology: Painful loosening of epithelium secondary to corneal dystrophy or trauma

• Anatomy– Epithelium bonded to underlying tissue by p y g y

hemidesmosomes and intermediate filaments– Hemidesmosomes anchored to stroma by

anchoring filaments and anchoring plaques– Ripping or shearing injuries damage the

ultrastructural connection between epithelium and underlying tissue (finger nail injuries and paper cuts are the worst)

Corneal Erosion: A Model For Management of Bad Ocular Pain

• 30 day rule- hemidesmisomes• 60 day rule- anchoring filaments

Recurrent Corneal Erosion• Once damage from trauma or

dystrophy occur, epithelium becomes less firmly attached and may adhere to tarsal conjunctiva during sleepTi b t f b t • Tissue may be torn from basement membrane during REM of on awakening

• Physiologic edema (nocturnal) contributes to develop of recurrent erosions

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Recurrent Corneal Erosion

• Signs and symptoms– Sudden onset pain upon awakening– Photophobia, lacrimation, injection

Loosened epithelial tissue underlying – Loosened epithelial tissue, underlying stromal edema

– Epithelial cysts– Brawny edema (actually not edema but

focal concentration of inflammatory cells)– Stromal dystrophy in fellow eye

Recurrent Corneal ErosionManagement: Initial Presentation

• Debride all loosened tissue• Voltaren or Nevanac• Cycloplegia (Homatropine 2.5 % or 5%)y p g ( p )• Vigamox or Zymar solution QID• After re-epithelialized, Muro 128 ung hs for a

minimum of 6 weeks• Bandage contact lens as indicated

(unpreserved antibiotic)• Pressure patch only as a last resort

Recurrent Corneal ErosionManagement: Subsequent Presentations

• Lubrication/ hypertonics ( ung and gtts)• Massage lids prior to opening eyes after

awakening (6 weeks minimum)• Epithelial debridement- remove all loose

tissue w/ Kimura spatula• Use NSAIDs and cycloplegics to control pain• Bandage CL or pressure patch until

epithelialized• Treat with conventional methods after

stable

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Recurrent Corneal Erosion

Management: Subsequent Erosions • Bandage CL for chronically recurrent cases• Treat concurrently w/ antibiotic (low

toxicity = Polytrim)toxicity Polytrim)• Watch closely for signs of keratitis and

change lenses regularly in office (hygeine)• Continue CL therapy for at least 3 months• Educate patient RE dangers of keratitis and

need to report any signs or symptoms

Recurrent Corneal Erosion Stromal Micropuncture

• Perform when conventional treatments fail• Perform at slit lamp- (KEEP PATIENT’S

FOREHEAD FORWARD) avoid vitreous puncture

• Use bent 25 ga needle (can purchase from Use bent 25 ga needle (can purchase from Look, Inc) or bend 0.15 mm from tip away from bevel

• Puncture should penetrate epithelium and penetrate 5% to 10% of Bowman’s layer.

• Can be done in area that is already debrided

• Minimal scarring , but avoid doing on visual axis

Recurrent Corneal Erosion

Excimer Laser Phototherapeutic Keratectomy (PTK)

• Initial studies show excellent results L d th t f 5 • Laser depth set for 5 um

• “Swirling motion” to reduce change in refractive error

• Incidence of recurrent erosions after PTK is very low

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Make a big splash!

A forty-two year old male presents to your office for evaluation with a history of having splashed a

l i h i l i t hi i ht cleaning chemical into his right eye. His eyes were irrigated with water and he was rushed to your office. His health and eye history are unremarkable.

Make a Big SplashSLE:• OD:

– Cornea: diffuse superficial punctate keratitis with partial loss of epitheliumkeratitis with partial loss of epithelium

– Conjunctiva: gr. II+ injection, chemosis– Limbus: injection, no blanching– Iris: details visible but hazy– A/C: gr. I+ cells, flare

• OS: nl

Chemical Burns• Identify agent (Your staff should tell the

patient or contact to bring it with them)• Identify makeup of agent (1- 800 hotline)

– Detergent, solventBase– Base

– Acid– Any solids

• Estimated time of injury• Was there immediate irrigation• Estimate chemical temperature: hot is

worse

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Chemical BurnsSolvents and Detergents

Solvents - gasoline, alcohol, acetone, cleaners

Detergents- BACl, dish washing detergent, laundering detergents

• Degrade proteins and emulsify lipids, leads to epithelial dessication, keratitis

• Painful, but usually self limiting• Greatest risk is for secondary bacterial

infection

Chemical BurnsSolvents and Detergents

Treatment• Irrigation followed by topical antibiotic

(avoid aminoglycosides)• Patch only in severe cases with Patch only in severe cases with

ointment• If uveitis present, cycloplegia, topical

NSAID (avoid steroids if at all possible)• Contact lens wearers should D/C

contact lenses until corneas are clear

Chemical BurnsAcids and Bases

• Acids- (sulfurous, hydrochloric, phosphoric sulfuric nitric)phosphoric, sulfuric, nitric)

• Epithelial tissue acts as protein buffer; damage minimized unless pH is < 2.5.

• Greatest damage from sulfurous acid.

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Chemical BurnsAcids and Bases

Alkalis (bases)• Greatest damage if pH is > 11.5

P d f ti d th • Produce far more tissue damage than acids of similar concentration tissue damage– Calcium hydroxide (lime) – Sodium hydroxide (lye) – Ammonium hydroxide (ammonia) *

Chemical BurnsAcids and Bases

Alkalis• React with lipids to form soaps, saponify

fats- damage cell membranes and enhances penetration of underlying enhances penetration of underlying tissue

• Protein buffering system not effective against alkaline substances

• Even after the substance has been neutralized, the immune response is source of damage

Classification of Chemical BurnsMild to Moderate

• Cornea- SPK to focal epithelial loss• Limbus & conjunctiva- injection, but no

areas of focal ischemiaareas of focal ischemia• Anterior chamber- clear or minimal

iris/flare• IOP- normal or near normal• Skin- mild to 1st or 2nd degree burns

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Classification of Chemical BurnsModerate to Severe

• Cornea- edema with some obscuration of iris details: entire epithelium may slough leaving a non-staining surface

• Limbus & conjunctiva- chemosis and perilimbal blanching

• Anterior chamber- moderate to severe reaction

• IOP- elevated • Skin- 2nd degree or 3rd degree burns

Treatment of Acid & Alkali BurnsMild to Moderate

• Irrigation with saline for minimum of 30 minutes • Check pH with litmus paper• Do not use acids to neutralize bases or vice

versa. I i t d h k f i f lid ti l • Irrigate and check fornices for solid particles, necrotic conjunctiva with concentrated chemical

• Cycloplegia (scopolamine, homatropine)• Topical antibiotic ointment (erythromycin,

polysporin)• Control IOP with oral (Diamox, Neptazane)

and/or topical (Timolol, Alphagan)

Treatment of Acid & Alkali BurnsModerate to Severe

• Irrigation with saline for minimum of 30 minutes

• Check pH with litmus paper• Patch w/ topical antibiotic after

neutralized• Refer to anterior segment specialist

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Conclusion

• Never before has there been a time when optometrists were so well prepared or positioned to manage ttrauma.

• Take advantage of our expanded scope and superb education by providing your patients with the kind of trauma management they want and deserve.