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4/17/2008




   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 
     membrane
   – 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




                                                                           1
4/17/2008




  Cornea: Anatomical & Physiological 
           Considerations
• Descemet’s membrane
   – Breaks result in inflow of aqueous into stroma
   – Capable of self‐healing
• Endothelium
   – Transports 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 painpain,
 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 cornea
          Gr.
          Gr II+ injection
          No flare or cells
          Gr. II+ lid edema
    OS:   NL
 • Pupils NL




                                                             2
4/17/2008




        Attack of the Killer Lampshade
     Assessment:
     • Corneal abrasion secondary to
       trauma
     Plan: pressure patch with:
     • 2 gtt Voltaren
     • 1 gtt Tropicamide 1%
     • 1 gtt Occuflox
     • 400 mg Ibuprofen
     RTC: 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
    – 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 Trauma
                    What Went Wrong On Day 2?
                                   Trauma                Release of bradykinin

                   Release of cell membrane phospholipids

                   Converted by: Phospholipase A




                                 Arachidonic acid


Converted by:         cyclooxygenase            lipoxygenase




                      prostaglandins                 leukotrienes
                  Vasopermeability, Miosis
                                                    Chemotaxis      PMN migration
                  Vasodilation, IOP changes




                                                                                           3
4/17/2008




       Pathogenesis of Inflammation
                               Trauma              Release of bradykinin

           Release of cell membrane phospholipids

                    Converted by Phospholipase A


                               Blocked byy
                                                            Side effects!
                                steroids

                             Arachidonic acid
converted by:       cyclooxygenase           lipoxygenase




                   prostaglandins          leukotrienes
                Vasopermeability, Miosis
                Vasodilation, IOP changes Chemotaxis             PMN migration




           Nonsalicylate NSAIDs
• Used to manage mild to moderate pain
• Compare well with many narcotic
  analgesics in relieving pain
• Effective anti-inflammatory agents- work
            anti inflammatory agents
  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:
        Sensation of pain
        Inflammation
  •   Requires Q 4hr dosing
  •   Should be taken with food
  •   Pediatric syrup available (OK for adults)
  •   Ceiling effect!




                                                                                        4
4/17/2008




Oral Ibuprofen vs. Tylenol No. 4
Cooper, 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
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 Case
A 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
             visit.      then,
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.




                                                        5
4/17/2008




   Your diagnosis of this patient’s
            condition is:

1. Epithelial basement membrane
  dystrophy
2. Recurrent corneal erosion
3. Penetrating corneal injury
4. Fuch’s corneal dystrophy
5. Corneal abrasion
6. Townsend’s syndrome




  Appropriate management of this
       case would include:
 1. Referral to corneal specialist
 2. Hypertonic saline drops and ointment
 3. Bandage contact lens
 4. Topical antibiotic drops
 5. Topical beta blocker or carbonic
      anhydrase inhibitors
 6. All the above except 2




  The most appropriate antibiotic
       for this patient is:

1. Polytrim drops

2. Ciloxan
2 Cilo an ointment

3. Tobramycin drops

4. Tobradex ointment

5. Vigamox drops




                                                  6
4/17/2008




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
                           earlier
 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 prosthesis
 – OS 2 mm area of epithelial ulceration
   OS:                 f    ith li l l ti
   midway between limbus and central
   cornea.
 – Conjunctiva: gr. II+ injection
 – A/C: gr. I+ cells, flare




                                                   7
4/17/2008




       What is your initial plan

 1.   Start topical fluoroquinolone
 2.   Start topical fortified antibiotics;
      Cefazolin & Tobramycin
 3.
 3    Perform corneall scraping and culture
      P f                      i      d    lt
      on agar plates
 4.   Shoot the dogs
 5.   1&3
 6.   2&3




       The One-eyed Wonder
• Assessment: bacterial keratitis
• Plan:
  – Obtain cultures: blood and chocolate
    agar
  – 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




                                                         8
4/17/2008




OK, the guy only has one eye, and
it’s getting worse fast…so what are
           you going to do?
1.   Repeat scraping and culture
2.   Consult lab
3.   Increase dosage frequency
4.   Be patient
5.   Shoot the patient
6.   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 strain
2.   Atypical herpes simplex lesion
3.
3    Fungal ulcer
            l l
4.   Corneal melt
5.   Dog-scratch fever




                                                     9
4/17/2008




        The one-eyed wonder
Day 4
• Ulcerated area increasing in size
• Lab reports fungal growth of Aspergillis
• Plan: start patient on natamycin q 1 hour
Day 5
• Ulcerated area beginning to shrink
• Patient reports improvement in symptoms
• Reduce frequency of drops
Final 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




                                                                 10
4/17/2008




                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 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 conjunctivitis
      p              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?)




                                                                     11
4/17/2008




 Lessons from One Eyed Wonder
• Think of the worst case scenario when
  dealing with corneal conditions
• If in doubt, culture ulcers
• Gi special consideration t one-
  Give       i l      id   ti  to
  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
 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 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)




                                                     12
4/17/2008




        Mr. 20/20 (with help)
            Your diagnosis is:
 1. Recurrent corneal erosion
    secondary to trauma
 2. Diffuse bacterial keratitis
 3. Chemical keratitis secondary to
    BACL preserved drops
 4. Post traumatic DLK
 5. 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
     w/ hypertonic drops QID
3.   Start Vigamox 1 drop every three hrs.
4.   Start Pred Forte every hour
5.   Start gin & tonic every 30 minutes




        And the diagnosis is:
                Here’s a hint!


Yes, Sahib, there is
something in your
eye…… and it could
           d       ld
be sand!




                                                    13
4/17/2008




     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
    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 DLK
 • Epithelial damage, reduced pH
   postulated to initiate this condition
Aldave AJ, Hollander DA, Abbott RL. Late onset
traumatic flap dislocation and diffuse lamellar
inflammation after laser in situ keratomileusis. Cornea
August 2002




   Lessons from 20/20 with Help
                Post Traumatic DLK

 • Inform LASIK patients that even moderate
   trauma can lead to complications years out
 • 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




                                                                14
4/17/2008




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




                                                             15
4/17/2008




                  Syncope
• Cardiac                  • Situational
• Tachydysrythmia          • Cough
• Bradydysrythmia          • Defecation
• Myocardial               • Micturation
  ischemia




         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
    Increased h
             d heart rate, cardiac output, blood
                    t t       di     t t bl d
    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




                                                         16
4/17/2008




          Managing Syncope
• ABC’s of life support plus
• Airway cleared?
• Breathing?
• 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 p
       p                  patient at all times
• 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
  certified
     tifi d
• Ambu-bag or CPR screen available at all
  times
  Engel G. “Psychologic stress, vasodepressor
  (vasovagal) syncope, and sudden death”.
  Ann Internal Med 1978; 89:p 43-412




                                                         17
4/17/2008




               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
                           vision.
 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 Mission
 Donaldson 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%




                                                           18
4/17/2008




             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
• 49% have chalazia
    %            i
• 85% have conjunctival injection




             Ocular Rosacea
• 2 primary etiologic components;
  vascular and inflammatory
• Ocular signs & symptoms may precede
  cutaneous changes in 20% of patients
• Pathophysiology unknown; theories
  – Type IV hypersensitivity reaction
  – Demodex mites initiate inflammation
  – Helicobacter pylori has been implicated




                Man of Steel
 A 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
 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?




                                                            19
4/17/2008




           Man of Steel: Examination
         VA: OD = 20/20, OS = 20/20
     Pupils: PERRLA PANA: negative OU
• SLE: OD                     • SLE: OS
• Cornea: 1 x 1 mm            • All findings nl
  foreign body w/
  surrounding area of
  rust, necrosis
  rust
• Conj: generalized
  injection, > local to fb
• AC: gr . flare, tr. cells
• Lids: tr edema
• Tears: 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.   Spud
2.   Bent needle
3.   Forceps
4.   Alger brush
5.   Micro chain saw
6.   1,2, 3, and 4 are appropriate




                                                        20
4/17/2008




 The best post op management
    scheme would include:
 1. Tobradex ung, homatropine, and
    Acular
 2. Vigamox gtt, tropicamide, and
    bandage 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 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
     • No MRI on suspected metallic foreign body
     • CT or X-Ray OK
• All vegetative FB carry a risk for fungal
  keratitis




                                                         21
4/17/2008




     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
                   spud
    Brush*
•   Broad spectrum antibiotic in office (ung vs
    gtts)
•   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 (
                    p       (1564-1616)  )
    – 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
  aminoglycosides
• 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




                                                             22
4/17/2008




                    Coding




                    Curly Sue
    A sixteen year old female student
    presents to your office. She had
    been curling her hair when the
    cu g o s pped a d
    curling iron slipped and 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: Examination
            VA: OD = 20/20 OS = 20/20
                 Pupils PERRLA
         SLE: OD                 SLE: OS
• All findings nl     • Cornea: central area of
                        burned epithelium w/
                        loss strands of tissue
                            damage epithelial
                        only
                      • Conj: gr. II+ injection
                      • Tears: epiphora
                      • AC: gr. I+ flare, no cells
                      • Lids: nl




                                                           23
4/17/2008




       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.
• 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
              unremarkable
  known medication allergies. There is
  no previous history of eye trauma.




                                                                   24
4/17/2008




          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 days
•OOne week later: Patient complains of
            kl t    P ti t        l i f
  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, edema
                         folds
  – Gr. II+ conjunctival injection
• Plan
  – Repeat treatment, but use bandage
    contact lens in addition to hyperosmotics
    and antibiotic.




                                                             25
4/17/2008




    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 sleep
• Ti
  Tissue may be torn from basement
               b t    f   b        t
  membrane during REM of on
  awakening
• Physiologic edema (nocturnal)
  contributes to develop of recurrent
  erosions




                                                             26
4/17/2008




     Recurrent Corneal Erosion
• Signs and symptoms
    – Sudden onset pain upon awakening
    – Photophobia, lacrimation, injection
    – Loosened epithelial tissue, underlying
                          tissue
      stromal edema
    – Epithelial cysts
    – Brawny edema (actually not edema but
      focal concentration of inflammatory cells)
    – Stromal dystrophy in fellow eye




     Recurrent Corneal Erosion
       Management: Initial Presentation
• Debride all loosened tissue
• Voltaren or Nevanac
• Cycloplegia (
    y    p g (Homatropine 2.5 % or 5%)
                           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 Erosion
    Management: 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




                                                         27
4/17/2008




    Recurrent Corneal Erosion
      Management: Subsequent Erosions
• Bandage CL for chronically recurrent cases
• Treat concurrently w/ antibiotic (low
  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
  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
•LLaser depth set for 5 um
          d th t f
• “Swirling motion” to reduce change in
  refractive error
• Incidence of recurrent erosions after
  PTK is very low




                                                       28
4/17/2008




            Make a big splash!
  A forty-two year old male presents
  to your office for evaluation with
  a history of having splashed a
  cleaning chemical iinto hi right
   l    i     h    i l t his i ht
  eye. His eyes were irrigated with
  water and he was rushed to your
  office. His health and eye history
  are unremarkable.




            Make a Big Splash
 SLE:
 • OD:
      – Cornea: diffuse superficial punctate
        keratitis 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, solvent
  –   Base
  –   Acid
  –   Any solids
• Estimated time of injury
• Was there immediate irrigation
• Estimate chemical temperature: hot is
  worse




                                                          29
4/17/2008




           Chemical Burns
        Solvents 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 Burns
         Solvents and Detergents
                Treatment
• Irrigation followed by topical antibiotic
  (avoid aminoglycosides)
• 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 Burns
             Acids and Bases


• Acids- (sulfurous, hydrochloric,
  phosphoric, sulfuric
  phosphoric sulfuric, nitric)
• Epithelial tissue acts as protein buffer;
  damage minimized unless pH is < 2.5.
• Greatest damage from sulfurous acid.




                                                     30
4/17/2008




           Chemical Burns
             Acids and Bases

             Alkalis (bases)
• Greatest damage if pH is > 11.5
•P d
  Produce far more tissue damage than
            f        ti    d          th
  acids of similar concentration tissue
  damage
  – Calcium hydroxide (lime)
  – Sodium hydroxide (lye)
  – Ammonium hydroxide (ammonia) *




           Chemical Burns
             Acids and Bases

                   Alkalis
• React with lipids to form soaps, saponify
  fats- damage cell membranes and
  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 Burns
             Mild to Moderate

• Cornea- SPK to focal epithelial loss
• Limbus & conjunctiva- injection, but no
  areas of focal ischemia
• Anterior chamber- clear or minimal
  iris/flare
• IOP- normal or near normal
• Skin- mild to 1st or 2nd degree burns




                                                    31
4/17/2008




 Classification of Chemical Burns
             Moderate 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 Burns
               Mild 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 and check fornices for solid particles,
  Irrigate    d h kf        i    f   lid   ti l
  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 Burns
             Moderate 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




                                                           32
4/17/2008




             Conclusion

• Never before has there been a time
  when optometrists were so well
  prepared or positioned to manage
  trauma.
• Take advantage of our expanded
  scope and superb education by
  providing your patients with the kind
  of trauma management they want
  and deserve.




                                                33

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CORNEA

  • 1. 4/17/2008 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  membrane – 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 1
  • 2. 4/17/2008 Cornea: Anatomical & Physiological  Considerations • Descemet’s membrane – Breaks result in inflow of aqueous into stroma – Capable of self‐healing • Endothelium – Transports 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 painpain, 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 cornea Gr. Gr II+ injection No flare or cells Gr. II+ lid edema OS: NL • Pupils NL 2
  • 3. 4/17/2008 Attack of the Killer Lampshade Assessment: • Corneal abrasion secondary to trauma Plan: pressure patch with: • 2 gtt Voltaren • 1 gtt Tropicamide 1% • 1 gtt Occuflox • 400 mg Ibuprofen RTC: 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 – 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 Trauma What Went Wrong On Day 2? Trauma Release of bradykinin Release of cell membrane phospholipids Converted by: Phospholipase A Arachidonic acid Converted by: cyclooxygenase lipoxygenase prostaglandins leukotrienes Vasopermeability, Miosis Chemotaxis PMN migration Vasodilation, IOP changes 3
  • 4. 4/17/2008 Pathogenesis of Inflammation Trauma Release of bradykinin Release of cell membrane phospholipids Converted by Phospholipase A Blocked byy Side effects! steroids Arachidonic acid converted by: cyclooxygenase lipoxygenase prostaglandins leukotrienes Vasopermeability, Miosis Vasodilation, IOP changes Chemotaxis PMN migration Nonsalicylate NSAIDs • Used to manage mild to moderate pain • Compare well with many narcotic analgesics in relieving pain • Effective anti-inflammatory agents- work anti inflammatory agents 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: Sensation of pain Inflammation • Requires Q 4hr dosing • Should be taken with food • Pediatric syrup available (OK for adults) • Ceiling effect! 4
  • 5. 4/17/2008 Oral Ibuprofen vs. Tylenol No. 4 Cooper, 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 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 Case A 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 visit. then, 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. 5
  • 6. 4/17/2008 Your diagnosis of this patient’s condition is: 1. Epithelial basement membrane dystrophy 2. Recurrent corneal erosion 3. Penetrating corneal injury 4. Fuch’s corneal dystrophy 5. Corneal abrasion 6. Townsend’s syndrome Appropriate management of this case would include: 1. Referral to corneal specialist 2. Hypertonic saline drops and ointment 3. Bandage contact lens 4. Topical antibiotic drops 5. Topical beta blocker or carbonic anhydrase inhibitors 6. All the above except 2 The most appropriate antibiotic for this patient is: 1. Polytrim drops 2. Ciloxan 2 Cilo an ointment 3. Tobramycin drops 4. Tobradex ointment 5. Vigamox drops 6
  • 7. 4/17/2008 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 earlier 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 prosthesis – OS 2 mm area of epithelial ulceration OS: f ith li l l ti midway between limbus and central cornea. – Conjunctiva: gr. II+ injection – A/C: gr. I+ cells, flare 7
  • 8. 4/17/2008 What is your initial plan 1. Start topical fluoroquinolone 2. Start topical fortified antibiotics; Cefazolin & Tobramycin 3. 3 Perform corneall scraping and culture P f i d lt on agar plates 4. Shoot the dogs 5. 1&3 6. 2&3 The One-eyed Wonder • Assessment: bacterial keratitis • Plan: – Obtain cultures: blood and chocolate agar – 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 8
  • 9. 4/17/2008 OK, the guy only has one eye, and it’s getting worse fast…so what are you going to do? 1. Repeat scraping and culture 2. Consult lab 3. Increase dosage frequency 4. Be patient 5. Shoot the patient 6. 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 strain 2. Atypical herpes simplex lesion 3. 3 Fungal ulcer l l 4. Corneal melt 5. Dog-scratch fever 9
  • 10. 4/17/2008 The one-eyed wonder Day 4 • Ulcerated area increasing in size • Lab reports fungal growth of Aspergillis • Plan: start patient on natamycin q 1 hour Day 5 • Ulcerated area beginning to shrink • Patient reports improvement in symptoms • Reduce frequency of drops Final 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 10
  • 11. 4/17/2008 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 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 conjunctivitis p 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?) 11
  • 12. 4/17/2008 Lessons from One Eyed Wonder • Think of the worst case scenario when dealing with corneal conditions • If in doubt, culture ulcers • Gi special consideration t one- Give i l id ti to 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 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 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) 12
  • 13. 4/17/2008 Mr. 20/20 (with help) Your diagnosis is: 1. Recurrent corneal erosion secondary to trauma 2. Diffuse bacterial keratitis 3. Chemical keratitis secondary to BACL preserved drops 4. Post traumatic DLK 5. 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 w/ hypertonic drops QID 3. Start Vigamox 1 drop every three hrs. 4. Start Pred Forte every hour 5. Start gin & tonic every 30 minutes And the diagnosis is: Here’s a hint! Yes, Sahib, there is something in your eye…… and it could d ld be sand! 13
  • 14. 4/17/2008 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 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 DLK • Epithelial damage, reduced pH postulated to initiate this condition Aldave AJ, Hollander DA, Abbott RL. Late onset traumatic flap dislocation and diffuse lamellar inflammation after laser in situ keratomileusis. Cornea August 2002 Lessons from 20/20 with Help Post Traumatic DLK • Inform LASIK patients that even moderate trauma can lead to complications years out • 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 14
  • 15. 4/17/2008 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 standing) t di ) • Anaphylaxis • Hemorrhage • Hypovolemia (dehydration) • Neurocardiogenic (vasovagal)* 15
  • 16. 4/17/2008 Syncope • Cardiac • Situational • Tachydysrythmia • Cough • Bradydysrythmia • Defecation • Myocardial • Micturation ischemia 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 Increased h d heart rate, cardiac output, blood t t di t t bl d 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 16
  • 17. 4/17/2008 Managing Syncope • ABC’s of life support plus • Airway cleared? • Breathing? • 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 p p patient at all times • 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 certified tifi d • Ambu-bag or CPR screen available at all times Engel G. “Psychologic stress, vasodepressor (vasovagal) syncope, and sudden death”. Ann Internal Med 1978; 89:p 43-412 17
  • 18. 4/17/2008 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 vision. 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 Mission Donaldson 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% 18
  • 19. 4/17/2008 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 • 49% have chalazia % i • 85% have conjunctival injection Ocular Rosacea • 2 primary etiologic components; vascular and inflammatory • Ocular signs & symptoms may precede cutaneous changes in 20% of patients • Pathophysiology unknown; theories – Type IV hypersensitivity reaction – Demodex mites initiate inflammation – Helicobacter pylori has been implicated Man of Steel A 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 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? 19
  • 20. 4/17/2008 Man of Steel: Examination VA: OD = 20/20, OS = 20/20 Pupils: PERRLA PANA: negative OU • SLE: OD • SLE: OS • Cornea: 1 x 1 mm • All findings nl foreign body w/ surrounding area of rust, necrosis rust • Conj: generalized injection, > local to fb • AC: gr . flare, tr. cells • Lids: tr edema • Tears: 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. Spud 2. Bent needle 3. Forceps 4. Alger brush 5. Micro chain saw 6. 1,2, 3, and 4 are appropriate 20
  • 21. 4/17/2008 The best post op management scheme would include: 1. Tobradex ung, homatropine, and Acular 2. Vigamox gtt, tropicamide, and bandage 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 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 • No MRI on suspected metallic foreign body • CT or X-Ray OK • All vegetative FB carry a risk for fungal keratitis 21
  • 22. 4/17/2008 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 spud Brush* • Broad spectrum antibiotic in office (ung vs gtts) • 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 ( p (1564-1616) ) – 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 aminoglycosides • 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 22
  • 23. 4/17/2008 Coding Curly Sue A sixteen year old female student presents to your office. She had been curling her hair when the cu g o s pped a d curling iron slipped and 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: Examination VA: OD = 20/20 OS = 20/20 Pupils PERRLA SLE: OD SLE: OS • All findings nl • Cornea: central area of burned epithelium w/ loss strands of tissue damage epithelial only • Conj: gr. II+ injection • Tears: epiphora • AC: gr. I+ flare, no cells • Lids: nl 23
  • 24. 4/17/2008 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. • 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 unremarkable known medication allergies. There is no previous history of eye trauma. 24
  • 25. 4/17/2008 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 days •OOne week later: Patient complains of kl t P ti t l i f 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, edema folds – Gr. II+ conjunctival injection • Plan – Repeat treatment, but use bandage contact lens in addition to hyperosmotics and antibiotic. 25
  • 26. 4/17/2008 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 sleep • Ti Tissue may be torn from basement b t f b t membrane during REM of on awakening • Physiologic edema (nocturnal) contributes to develop of recurrent erosions 26
  • 27. 4/17/2008 Recurrent Corneal Erosion • Signs and symptoms – Sudden onset pain upon awakening – Photophobia, lacrimation, injection – Loosened epithelial tissue, underlying tissue stromal edema – Epithelial cysts – Brawny edema (actually not edema but focal concentration of inflammatory cells) – Stromal dystrophy in fellow eye Recurrent Corneal Erosion Management: Initial Presentation • Debride all loosened tissue • Voltaren or Nevanac • Cycloplegia ( y p g (Homatropine 2.5 % or 5%) 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 Erosion Management: 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 27
  • 28. 4/17/2008 Recurrent Corneal Erosion Management: Subsequent Erosions • Bandage CL for chronically recurrent cases • Treat concurrently w/ antibiotic (low 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 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 •LLaser depth set for 5 um d th t f • “Swirling motion” to reduce change in refractive error • Incidence of recurrent erosions after PTK is very low 28
  • 29. 4/17/2008 Make a big splash! A forty-two year old male presents to your office for evaluation with a history of having splashed a cleaning chemical iinto hi right l i h i l t his i ht eye. His eyes were irrigated with water and he was rushed to your office. His health and eye history are unremarkable. Make a Big Splash SLE: • OD: – Cornea: diffuse superficial punctate keratitis 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, solvent – Base – Acid – Any solids • Estimated time of injury • Was there immediate irrigation • Estimate chemical temperature: hot is worse 29
  • 30. 4/17/2008 Chemical Burns Solvents 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 Burns Solvents and Detergents Treatment • Irrigation followed by topical antibiotic (avoid aminoglycosides) • 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 Burns Acids and Bases • Acids- (sulfurous, hydrochloric, phosphoric, sulfuric phosphoric sulfuric, nitric) • Epithelial tissue acts as protein buffer; damage minimized unless pH is < 2.5. • Greatest damage from sulfurous acid. 30
  • 31. 4/17/2008 Chemical Burns Acids and Bases Alkalis (bases) • Greatest damage if pH is > 11.5 •P d Produce far more tissue damage than f ti d th acids of similar concentration tissue damage – Calcium hydroxide (lime) – Sodium hydroxide (lye) – Ammonium hydroxide (ammonia) * Chemical Burns Acids and Bases Alkalis • React with lipids to form soaps, saponify fats- damage cell membranes and 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 Burns Mild to Moderate • Cornea- SPK to focal epithelial loss • Limbus & conjunctiva- injection, but no areas of focal ischemia • Anterior chamber- clear or minimal iris/flare • IOP- normal or near normal • Skin- mild to 1st or 2nd degree burns 31
  • 32. 4/17/2008 Classification of Chemical Burns Moderate 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 Burns Mild 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 and check fornices for solid particles, Irrigate d h kf i f lid ti l 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 Burns Moderate 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 32
  • 33. 4/17/2008 Conclusion • Never before has there been a time when optometrists were so well prepared or positioned to manage trauma. • Take advantage of our expanded scope and superb education by providing your patients with the kind of trauma management they want and deserve. 33