discussions in
anterior segment disease
ALAN G. KABAT, OD, FAAO
MEMPHIS, TN
JOSEPH SOWKA, OD, FAAO ANDREW GURWOOD, OD, FAAO
FT. LAUDERDALE, FL PHILADELPHIA, PA
Course Description: Case presentations provide a springboard for in-depth discussion of several challenging anterior segment conditions. Emphasis is placed on understanding the presentation, pathophysiology and management of the various clinical entities.
Learning Objectives/Outcomes: At the conclusion of this course, the attendee will be able to:
1. Identify the pathophysiology, clinical presentation and management of bacterial keratitis;
2. Identify the pathophysiology, clinical presentation and management of dacryoadenitis;
3. Identify the pathophysiology, clinical presentation and management of corneal laceration;
4. Identify the pathophysiology, clinical presentation and management of uveitis, as well as the essential laboratory work up;
5. Identify the pathophysiology, clinical presentation and management of herpes simplex keratitis;
6. Identify the pathophysiology, clinical presentation and management of recurrent corneal erosion.
BACTERIAL KERATITIS
· Breakdown of corneal defenses (dry eyes, corneal trauma, corneal hypoxia, etc.)
· Introduction of pathogen (corneal abrasion mismanagement, contact lenses, etc.)
· Proliferation of organisms and release of toxins and proteolytic enzymes
· Antigen-antibody reaction
· Stromal edema (splitting of stromal collagen lamellae sheets)
· Cellular transudation and emigration
· Infiltration
· Phagocytosis of organisms with proteolytic enzyme release and stromal lysis
· Antigenic neutralization (hopefully)
· Cicatrization (fibroblastic proliferation of scar tissue)
· Visual loss
Clinical Picture of Bacterial Keratitis
· Pain, photophobia, lacrimation
· Profound conjunctival and episcleral injection
· Involvement of innocent bystanding tissue
· Anterior chamber reaction
· Possible (sterile) hypopyon
· Focal infiltrate with overlying epithelial staining and breakdown
· The spectrum of clinical findings is broad (from an initially mild, often misdiagnosed presentation of S. aureus to the exaggerated presentation of Pseudomonas)
- Any staining infiltrate should be presumed to be an infectious ulcer until proven otherwise
Management of Bacterial Keratitis
· Cultures and sensitivity studies
· Broad spectrum antibiosis: Fluoroquinolones
1. Ciprofloxacin (Ciloxan) ii gtt Q15min X 6hrs, then ii gtt Q 30min X 18 hrs.
2. Ocuflox Q30 minutes while awake, and then BID at night is as effective as fortified antibiotics.
3. Levofloxacin (Quixin)?
4. New alternatives- fourth generation fluoroquinolones: Vigamox/ Moxeza (moxafloxacin); Zymar/ Zymaxid (gatifloxacin) – Q1H
· Equal gram (-) coverage, greater gram (+) coverage than earlier generation fluoroquinolones
5. Newest options: Besivance (besifloxacin), Moxeza (moxifloxacin), Zymaxid (gatifloxacin)
· Cycloplegics (scopolamine 0.25% TID or atropine 1% BID) - decreases blood-aqueous barrier breakdown
· Corticosteroids (reduces inflammation by constricting blood vessel walls and reducing vessel wall permeability. Also blocks prostaglandin formation and release and stabilizes lysosomal membranes).
· Use corticosteroids only if step 1 is successfully completed (clinical impressions vs. microbiologic study results).
DACRYOADENITIS
· Inflammation of the lacrimal gland
· Usually seen in younger adults
· May be acute or chronic:
o Acute form presents with greater pain, redness & symptomology; usually infectious in nature (bacterial or viral)
o Chronic form is more common; usually inflammatory & due to underlying systemic autoimmune disease (e.g. sarcoidosis, Sjögren's syndrome, systemic lupus erythematosus, Wegener's granulomatosus)
· Acute Dacryoadenitis -
o Typically unilateral
o Ocular redness, tearing, & swelling of the upper lid
o Painful proptosis & ophthalmoparesis
o May have associated preauricular lymphadenopathy & fever
· Chronic Dacryoadenitis -
o Usually bilateral
o S-shaped swelling to outer ⅓ of the eyelid
o Pain is variable
o Swollen lacrimal gland is often evident on lid retraction
· Dacryoadenitis: Diagnostic management
o Orbital CT or MRI
o Laboratory studies
o CBC with differential
o Serology based on history & associated symptoms (e.g. ACE, FTA-ABS, RPR, PPD with anergy panel)
o Transcutaneous, transeptal biopsy should be performed in recalcitrant cases of dacryoadenitis or when a malignant process is suspected
· Dacryoadenitis: Therapeutic Management
o Acute - warrants systemic antibiotics
§ Amoxicillin (250-500 mg po q8h)
§ Cephalexin (250-500 mg po q6h)
§ In more severe cases, hospitalization with IV antibiotics may be necessary
o Chronic dacryoadenitis may be managed with a course of systemic steroids
§ Typical therapy involves 80-100 mg of oral prednisone daily for 1-2 weeks, followed by slow taper.
PENETRATING INJURY: CORNEAL LACERATION
· Excessive PAIN, decreased vision
· Deeper than abrasion; may be smaller, linear
· + Seidel’s sign; additionally, may see hyphema, A/C rxn, flattened A/C (relative), air bubbles in A/C
· Iris prolapse possible
· IOP is low -- DO NOT perform tonometry!
· Management
o Photodocument (if possible for clinicolegal purposes)
o MINIMAL manipulation of the globe!
o Avoid topical medications!
o Shield the eye but DO NOT PATCH!
o N.P.O.
o Refer IMMEDIATELY for surgical repair
ANTERIOR UVEITIS
· Associated factors
o An inflammation of the iris and ciliary body
o May result from direct trauma to the eye (most often)
o May occur as a result of inflammation of other ocular structures (e.g., keratitis, scleritis)
o May be associated with underlying systemic disease (including but not limited to):
§ ankylosing spondylitis
§ Behçet’s disease
§ inflammatory bowel disease
§ juvenile rheumatoid arthritis
§ Reiter’s syndrome
§ sarcoidosis
§ syphilis
§ tuberculosis
§ Lyme disease
o Improper management may result in secondary, inflammatory glaucoma
o
· Signs and Symptoms
o Signs:
§ Variable redness
§ Ptosis or blepharospasm (due to discomfort)
§ Tearing
§ Visual acuity normal to mildly reduced
- 20/40 or better in most cases
- More difficulty with near / accommodative tasks
o Symptoms:
§ Deep, dull “achy” pain in affected eye and orbit
§ Extreme photophobia
§ “Hazy” vision
§
· Biomicroscopic evaluation
o Mild lid congestion (pseudoptosis); palpebral conjunctiva is unaffected
o Circumlimbal “flush” , i.e., injection of the episclera and conjunctiva concentrated around the cornea
o Mild corneal edema
o Keratic precipitates in chronic conditions (“granulomatous”)
o Anterior chamber “cells & flare” **
§ “cells” = white blood cells liberated from uveal blood vessels
§ “flare” = proteinaceous by-products of inflammation
o Posterior or (less commonly) anterior synechia
o Iris nodules
o Altered intraocular pressure
§ Initially reduced because of secretory hypotony
§ Inflammatory by-products clog the trabecular meshwork, inducing IOP elevation
§ May range from 30 to 80 mmHg in extreme cases
· Management
o 2 primary goals:
1. immobilize the iris & ciliary body to decrease pain and prevent exacerbation
2. quell the inflammatory response to prevent ocular sequelae
o STRONG topical cycloplegics
§ Choice of drug dependent upon severity of reaction, iris color, and presumed patient compliance
§ Best choices include
- ¼% scopolamine
- 1% atropine
o Topical corticosteroids
§ Must be deeply penetrating and efficacious
§ Must be given FREQUENTLY, particularly during early stages of treatment
§ Drug choices include:
- difluprednate **
- prednisolone acetate
- loteprednol ?
o Address synechiae using 1% atropine + 10% phenylephrine topically
o Elevated IOP should be addressed using standard topical antiglaucoma therapy:
§ b-blockers (e.g., TimopticÒ, BetopticÒ)
§ CAIs (e.g., TrusoptÒ)
§ Prostaglandin analogs (e.g., XalatanÒ) offer no clinical benefit
§ Miotics (e.g., pilocarpine) are ABSOLUTELY CONTRAINDICATED
o In recurrent cases (i.e., two or more similar presentations), a thorough medical evaluation to ascertain underlying etiology is indicated
§ CXR
§ Sacroiliac joint films
§ Serology:
- CBC with differential
- ESR
- ANA
- HLA-B27
- RF
- ACE
- FTA-ABS
- Lyme titer
Herpes Simplex Keratitis
· Pathophysiology:
- Initial infection by herpes simplex virus occurs in childhood (hand to eye, mouth to eye)
- After initial infection, virus enters a dormant phase in cell ganglia
§ "Trigger factors" induce reactivation of viral replication throughout the patient's life; include: fever, emotional stress, exposure to UV radiation, menstruation, trauma, immunosuppression
§ About half of all infected patients experience re-activation within 5 years
§ Most commonly ocular manifestion is dendritic epithelial keratitis
§ More severe presentations can manifest as geographic epithelial keratitis
· Clinical presentation - dendritic keratitis:
- Branching epithelial ulcer; may begin as nondescript punctate epitheliopathy
- Stains centrally with NaFl, peripherally with rose bengal or lissamine green ("terminal end-bulbs")
- Associated conjunctival injection, edema; uveitis possible
- Recurrent attacks lead to corneal hypoesthesia, i.e. diminished corneal sensitivity
§ (+) Cotton-wisp test
§ Patients may be far less symptomatic than predicted by ocular appearance
· Management:
- Herpes virus cannot be eradicated; management efforts are aimed at suppression and amelioration of symptoms
- Historical tandard of care in U.S. is topical trifluridine 1% q2h - 9 times daily, tapered to q3-4h as ulcer shows signs of closure; maintain at QID for at least 7-10 days.
- More recent option is ganciclovir 0.15% ophthalmic gel 5 times daily until resolution, then reduced to TID for 7 days
- Oral acyclovir may be used in patients who lack dexterity or compliance with topicals (400 mg po five times daily)
- Corticosteroids are absolutely contraindicated in active epithelial infection
- Herpetic Eye Disease Study (HEDS) 1998: Acyclovir 400 mg po BID X 12 months may reduce rate of recurrence by as much as 50%
RECURRENT CORNEAL EROSION
· History, History, History
- History of Corneal Abrasion
- Previous episodes of RCE
- Pain on awakening
· A breakdown of the epithelial layer of the cornea due to a breach in the integrity of the basement membrane
· Common Etiologies:
- Corneal dystrophy (e.g. granular dystrophy)
- Trauma; often follows improperly treated corneal abrasion
· Can present as a small epithelial defect or as a large abrasion
· Treatment
- Bandage SCL
§ Pressure patching in rare instances
- Prophylactic ntibiotic
- Cycloplegic
- Artificial Tears and Hypertonic agents
- Anterior Stromal Puncture (ASP)
- Oral doxycycline + topical steroids
- Amniotic membrane… ?