Ocular Grand Rounds
COPE: 40399-SD
Andrew S. Gurwood, O.D., F.A.A.O., Dipl.
Marc D. Myers, O.D., F.A.A.O.
Course Description: Challenging cases involving the adnexa, anterior and posterior segments
will be presented. The latest diagnostic and ocular management strategies will be discussed.
Course Objectives:
1. Ability to identify and differentiate benign versus malignant skin lesions of the adnexa.
2. Ability to identify the etiology and differentiate and treat acute corneal disease.
3. Discussion of the mechanism of hyphema as well as the management of the diagnosis.
4. Discussion of the etiology as well and the diagnosis and management of acute retinal arterial
occlusion.
Course Outline:
I. Skin Lesion Involving the Adnexa
A. Recognition of suspicious skin lesions
1. Lesion that patient reports as being "new" or only recently noticed
2. An existing lesion that grows in size
3. Any pigmented lesion, especially if it is new or enlarged
4. Pearly telangiectatic nodule
5. Area of diffuse hardening or ulceration
6. Lid notch or retracted area
7. Madarosis
B. The "A-B-C" (D-E) rule
1. Asymmetric shape
2. Borders are irregular
3. Color is mottled, not uniform
4. Diameter of the lesion
5. Elevation of the lesion
C. Squamous cell carcinoma (SCC)
1. Accounts for 9% of eyelid malignancies
a. Fair skin, elderly, excessive UV exposure over the course of a lifetime
b. Younger patients, consider UV sensitivity or immunocompromised
2. Patient symptoms and signs of SCC
a. Symptoms may include pain, burning and numbness
b. The lesion may appear as an indurated, opaque nodule, with or without ulceration
c. Location UL: LL (1.4 : 1.0)
d. Most commonly involves the conjunctiva, cornea, and mucous membranes
e. Lesion may involve lymph glands and/or nerves of the head and neck. Signs of
nerve involvement may include facial paralysis, reduced corneal reflex, and
numbness. The Trigeminal and Facial nerves are commonly involved.
3. SCC and METS
a. Rate of involvement is 1.3% to 21.4%
b. Usually a late development in advanced cases
c. Rate depends on depth of invasion, lesion size, location, histology, etiology, growth
rate, immunosuppression, and perineural invasion.
d. More associated with non-actinically induced lesions
4. Differential diagnoses
a. Premalignancies such as actinic keratosis (AK), KA, and Bowen's disease
b. Other malignancies such as BCC, sebaceous cell carcinoma, and melanoma
II. Acute Corneal Finding
A. Herpes Simplex Virus
1. Differentiate HSV-1 and HSV-2
a. Primary Infection
1). Pathophysiology
a). Route of infection
b). Incubation period
c). Contagiousness
b. Reactivation of HSV-1
1). Environmental factors: UV light, temperature
2). Occurrence Sites
3). Ocular Manifestations:
a). Conjunctivitis
b). Punctate Keratitis
c). Dendritic Keratitis
d). Geographic ulcer
e). Disciform Keratitis
f). Interstitial keratitis
g). Iridocyclitis
h). Retinitis
4). Symptoms
a). Foreign body sensation, irritation
b). Pain
c). Blurry vision
d). Photophobia
e). Tearing
f). Eye redness
B. Herpetic Eye Disease Studies
1. HEDS I
a. The efficacy of topical corticosteroids in treating stromal keratitis in conjunction with
topical trifluridine (SKN).
b. The efficacy of oral acyclovir in treating stromal keratitis in conjunction with topical
corticosteroids and topical trifluridine (SKS).
c. The efficacy of oral acyclovir in treating iridocyclitis in conjunction with topical
corticosteroids and trifluridine (IRT).
2. HEDS II
a. The benefit of early treatment with oral acyclovir in preventing stromal keratitis and
iridocyclitis in patients with ulcerative keratitis (EKT).
b. The benefit of oral acyclovir in preventing recurrent HSV ocular infection (APT).
c. The external factors on the induction of recurrences of HSV ocular diseases (RFS).
C. Treatment
1. Topical
2. Systemic – treatment vs. preventative care
III. Hyphema
A. History
1. Define the problem
2. Symptoms
3. Timing of injury
4. Recurrence
5. Other factors (underlying issues, history of surgery, history involving contact lenses)
B. Examination
1. External assessment
a. The globe (position, conjunctiva [edema, laceration])
b. The adnexa (blink rate, lid position, skin color, visible discharge)
c. Palpation / percussion of the adnexa
2. Visual acuity
3. E.O.M.s.
a. Cover test
b. Versions
c. Ductions
4. Pupil testing
5. Confrontational visual fields
6. Biomicroscopy
a. Lids, lashes, tear film
1). Nasolacrimal duct interruption
b. Conjunctiva
1). Laceration
2). Subconjunctival hemorrhage
c. Cornea
d. Anterior chamber
1). Cells and flare
2). Bleeding
a). Grade of hyphema
b). Corneal blood staining
3). Foreign body trail
4). Gonioscopy
e. Iris
1). Position (need for gonioscopy and timing), shape, stability, color
2). Synechiae (posterior, peripheral)
3). Rubeosis (underlying cause)
4). Transillumination defects
5). Ectropion uvea
6). Iridiodialysis/angle recession
f. Lens
1). Voisius ring
2). Dislocation, subluxation
3). Cataract formation
g. Posterior segment (vitreous, retina, nerve)
C. The base management of hyphema
1. Cycloplegia
2. Antibiotic (topical and oral)
3. Lubrication
4. Antiinflammation (topical and oral)
5. Analgesia (topical and oral)
G. Other elements of hyphema management
1. IOP control (topical and oral)
a. Hemolytic glaucoma
b. Ghost cell glaucoma
c. Hemosiderosic glaucoma
d. Late traumatic glaucoma
e. Topical IOP control
1) Beta blockers
2) Alpha adernergics
3) Topical carbonic anhydrase inhibitors (CAI)
4) Oral CAI
5) Surgical modialities
2. Supportive
a. Cold compress
b. Stool softener
c. Nasal spray
d. Rest, inactivity
3. Lab testing for clotting abnormalities (Sickle cell, Von Willibrands, hemophilia, anemia)
4. If rubeosis is present….underlying cause
5. Surgical modalities
a. Wash out
b. Enucleation considerations
c. Trabeculectomy/seton
IV. Retinal Artery Occlusion
A. Associated anatomy.
B. Anatomy of an embolis.
1. Thrombus.
2. Cholesterol (Hollenhorst plaque)
3. Calcific
C. Central retinal artery occlusion (CRAO), branch retinal artery occlusion (BRAO)
1. On the continuum of ischemic optic neuropathy (ION)
a. Nonarteritic – embolic
b. Arteritic – Giant cell arteritis (GCA)
2. Ocular management
a. Retinal autoregulation.
1). Carbogen, increased intake of carbon dioxide
2). "Mashing the eye"
b. Decreasing the IOP
1). Phamaceuticals.
a). Timoptic
b). Iopidine
c). Diamox
d). Hyperosmotics
2). Parecentisis
3. Systemic management.
a. Morbididty and mortality
1). Increased mortality from 27% to 56% over 9 yrs.
2). Decreased life expectancy to 5.5 years from 15.4 yrs.
3). 3% per year increased risk of stroke
b. Lab testing
1). Complete blood count (CBC w diff and platelets)
2). Erythrocyte sedimentation rate (ESR)
3). General inflammatory C – reactive protein (CRP)
4). Prothrombin time (PT), activated partial thromboplastin time (aPTT)
5). Lipid Panel
6). Two–D echocardiogram, transesophogeal echocardiogram
7). Carotid doppler
8). BP
D. Arteritic AION – GCA
1. Anatomy
2. Lab testing
a). ESR (erythrocyte sedimentation rate)
b). CRP (C-reactive protein)
c). Temporal artery biopsy
3. Systemic Management
a). IV Methylprednisolone
b). Oral steroids