VA Eye Clinic Grand Rounds
Andrew B Mick, OD, FAAO
San Francisco VA Medical Center
UC Berkeley School of Optometry
UCSF Department of Ophthalmology
Floppy eyelid syndrome (FES) / obstructive sleep apnea syndrome (OSAS)
A. Clinical features of FES
1. Middle aged obese men
2. Rubbery tarsal plate and elastic feeling of upper lid
3. Dramatic upper lid eversion with minimal lateral traction
4. Symptoms/signs worse in the morning
5. Affected side corresponds to the side the patient preferentially sleeps
(pillow everts upper lid)
6. Marked papillary conjunctivitis
7. Superficial punctate keratitis (universal)
8. Corneal scarring and neovascularization in severe cases
9. Blepharoptosis
10. Upper lid lash ptosis
B. Obstructive sleep apnea syndrome (OSAHA)
1. Disorder defined by the stoppage of breathing during sleep
2. Results from obstruction of upper airway during sleep
3. Found in 3-7% of men and 2-5% of women in US
4. Found in 41% of people with BMI over 28 and 78% of morbidly obese
5. Diagnosed by a sleep study and presence of characteristic comorbidities
a) Excessive daytime sleepiness
b) Insomnia
c) Impaired cognition
d) Mood disorders
e) Hypertension
f) Ischemic heart disease
g) Stroke
6. FES is found in 5-25% of patients with OSAS overall, but increases to
40% in severe OSAS
7. All patients diagnosed with FES should be evaluated for OSAS
C. Treatment for FES
1. Eye shields to prevent lid eversion
2. Blepharoplasty
Narrow angles in your practice: What to do?
A. Primary angle closure suspects (PACS)
1. Less than 90% of pigmented trabecular meshwork visible without
indentation
2. No peripheral anterior synechiae
3. IOP not elevated
B. Primary angle closure (PAC)
1. Less than 90% of pigmented trabecular meshwork visible without
indentation
2. Peripheral anterior synechiae OR elevated IOP
3. No glaucomatous optic neuropathy
C. Primary angle closure glaucoma (PACG)
1. Less than 90% of pigmented trabecular meshwork visible without
indentation
2. Peripheral anterior synechiae OR elevated IOP
3. Characteristic glaucomatous optic neuropathy
D. Primary angle closure (mechanistic classification)
1. Pupillary block
2. Plateau Iris Configuration
3. Phacomorphic
E. Secondary angle closure
1. Anything but the three causes of primary angle closure
2. Push or pull mechanisms
F. What is unique about PACS eyes?
1. Narrow anterior chamber angle
2. Thick lens
3. Anterior position of the lens
4. Sclera relatively thick
5. Small corneal diameter
G. Risk of PACS converting to PAC or PACG (evidence from high risk
populations)
1. ~6% will have acute PAC attacks (3-5 years)
2. ~13% will develop chronic peripheral anterior synechiae (3-5 years)
3. ~20% overall risk of progressing from PACS (3-5 years)
H. Risk factors for progression from PACS
1. Family history of PAC/G
2. Fellow eyes of PAC/G
3. Eskimo > Chinese/Southeast Asian > Caucasian / Black / Hispanic
I. Dynamic factors that influence static anatomy and result in progression
1. Pupil dilation to light / drugs
2. Decrease in cross sectional area of iris with pupil dilation
3. Irido-lenticular channel dynamics
4. Forward movement of lens in response to changes in uveal
swelling
5. Meds that trigger angle closure affect pupil or uveal swelling
J. Complications of LPI
1. Common: Transient elevation in IOP and mild AC inflammation
2. Uncommon: Lens damage, Corneal Damage, Hyphema, Retinal
K. How much does LPI reduce the risk of PACS progressing?
1. Significantly when main mechanism is pupillary block (Majority)
2. Less successful with plateau iris and phacomorphic components
3. Less likely once IOP is elevated or synechiae have formed
4. Time to refer is when patients are identified as PACS!!
L. Treatments when LPI fails to stop progression
1. Argon laser peripheral iridoplasty
2. Early cataract surgery
3. Topical medications for when angles are open / stable and IOP high
Brimonidine Induced Anterior Uveitis
A. Unifying clinical features
1. Acute, granulomatous anterior uveitis
2. Onset 12-15 months after starting brimondine
3. Preceded by conjunctivitis
4. Often associated with an increase in intraocular pressure
5. Resolution with discontinuation of brimonidine with topical steroid
6. All had uveitic recurrence within 3 weeks of rechallenge with brimondine
B. Direct mechanism:
1. Drug gains entry into the eye
2. Occurs within 24-48 hours
3. Usually drug is applied topically or intracamerally
C. Indirect mechanism:
1. Drug or protein bound drug triggers antibody production
2. Immune complexes deposit in uveal tract
3. Reaction can occur weeks or months after initial exposure
4. Explains delayed reaction
5. Explains incidence as drug often discontinued after initial conjunctivitis
Ocular surface squamous cell neoplasia (OSSN)
A. Definitions
1. Bowman’s layer is the key barrier
2. Conjunctival intraepithelial neoplasia (CIN), above Bowman’s
3. Invasive squamous cell carcinoma (SCC), penetrated Bowmans
B. Epidemiology
1. Average age 65 years
2. More common in Caucasians
3. More common in skin cancer patients
C. Clinical Signs
1. Often associated with existing pinguecula and/or pterygia
2. Most common in interpalpebral space
3. Corneal involvement in 50% of cases
4. Stains with rose bengal
5. Nodular gelatinous 50%
6. Flat leukoplakic 41%
7. Superficial diffuse 9%
D. Clinical symptoms
1. Red eye 68%
2. Ocular irritation 57%
3. Asymptomatic 10%
4. Rarely cause decreased VA
E. Established risk factors
1. Increased sun exposure
2. Human papillomavirus
3. HIV seropositivity
4. Increased p53 tumor suppressor expression
F. Treatment for OSSN
1. Excision
2. Excision and cryotherapy
3. Topical mitomycin C
4. Topical interferon
5. Excision with topical therapies
6. Enucleation
Peripheral Exudative Hemorrhagic Chorioretinopathy
A. AKA: Extramacular disciform lesion, peripheral choroidal neovascularization
1. Demographics
a) Females > Males
b) Increased age
c) Caucasian ethnicity
d) More common macular degeneration patients
C. Clinical Characteristics
1. Average size 3-9 mm
2. Peripheral pigment epithelial detachment
3. Hemorrhage most common feature
4. Associated subretinal exudation and fluid common
5. Most common inferior- temporal and temporal
6. Rarely bilateral and nasal
7. Histopathology shows breaks in Bruchs/RPE barrio (CNVM?)
8. Vision affected by extension to macular areas or breakthrough vitreous
heme
9. Late changes include chorioretinal atrophy and scarring
D. Management
1. Smaller lesions can be monitored
2. Treat to central macula should be referred for treatment (Avastin/Laser)
3. Rule out choroidal neoplastic disease in large lesions