Anterior Seg Disease Flashcards
1
Q
Most common cause of infectious K blindness in developed countries
A
Herpes simples keratitis
HSV-1
2
Q
Most common cause of infectious k blindness in underdeveloped countries
A
Trachoma
3
Q
How is HSV primary infection spread?
A
Via respiratory droplets
4
Q
Primary infection of HSV
A
Uncommon during first 6 months of life due to maternal antibodies
Subclinical or mild fever/upper respiratory tract infection
5
Q
How can you treat primary infections of HSV if they are eye/skin lesions?
A
Topical antiviral ung(ointment)/cream
6
Q
Recurrent Infections of HSV
A
Latent virus within sensory dermatome (trigeminal ganglion) re-activated by various stressors: fever, hormone changes, UV, etc
Virus replicates and moves along sensory nerve to periphery
Recurrence rates vary, but the more you’ve had, the more you’re likely to have again in the future (can be hundreds over a lifetime)
7
Q
HSV epithelial keratitis occurs with what?
A
‘’Active” viral replication (dendritic or geographic)
8
Q
Symptoms of HSV epithelial keratitis
A
Mild/moderate discomfort, redness, photophobia, watering
9
Q
Signs of HSV epithelial keratitis
A
Swollen/opaque epithelial cells —> dendritic ulceration
Decreased K sensation
Ulcer may enlarge to geographic/amoeboid appearance with steroid use
Mild subepithelial haze typical
May see: mild AC rxn, follicular conj., vesicular lid lesions, increased IOP - affecting the outflow of the trabecular meshwork (check non-involved eye first and disinfect)
10
Q
When staining for HSV epithelial keratitis, what stains are used to stain what?
A
NaFl stains the bed of the ulcer
Rose bengal stains the margins of the ulcer
11
Q
HSV dendritic ulcer
A
Branching pattern with end bulbs
Will probably go away on it’s own if no treatment, b/c immune system will catch up with it
12
Q
What can happen if you put a patient on a topical steroid if they have HSV corneal ulceration?
A
It can make it worse and the ulcer can take on the geographic appearance
13
Q
HSV geographic ulcer
A
Occurs due to a patient with HSV being treated with steroids, causing an even larger ulcer than just the dendrites
14
Q
Corneal sensitivity testing checks for what?
A
Pt can lose sensation due to the sensory nerves being affected from HSV
Brushing against the cornea can show if their issue is definitive for the herpes simplex virus instead of bacterial or sometimes viral
15
Q
Diagnosis for HSV epithelial keratitis
A
Clinical (can culture, do PCR, or stain as well)
16
Q
Treatment of HSV epithelial keratitis
A
Most will heal without treatment, but that can increase the pt’s risk of scarring
Anti-viral gel on ung(ointment) 5 x day (typical treatment)
Tablets (for kinds or immunodeficiency pt’s)
Debribement (rub ulcer away)
Aciclovir cream 5 x day for skin vesicles
Antibiotics prophylactically
IOP lowering medications (NOT PROSTAGLANDIN DERIVATIVES)
17
Q
Why do you not want to prescribe the IOP lowering medications, prostaglandin derivatives, to a patient who is suffering from HSV epithelial keratitis?
A
Prostaglandin derivatives are pro-inflammatory; the reason the IOP is elevated is because the trabecular meshwork is inflamed. Using these would just add to the inflammation, and make the IOP worse.
18
Q
Prognosis for HSV epithelial keratitis
A
Virtually all ulcers heal within 2 weeks (but we like to speed this up with topical medications like aciclovir gels/ung to decrease scarring)
Avoid steroids (tobradex = combination of antibiotic and steroid)
Mild subepithelial haze often lingers for weeks after ulcer heals
Persistent haze may increase with each recurrence, eventually compromising vision
19
Q
What response may and HSV stromal keratitis issue represent?
A
Either an immune-mediated response or an “active” viral replication (within stroma)
20
Q
Symptoms of HSV stromal keratitis
A
Blurring of vision (due to some opacification
21
Q
Signs of HSV stromal keratitis
A
Infiltration of stroma (usually without accompanying dendritic ulceration) that may be diffuse or focal
Anterior chamber reaction with KP’s (penetrating keratoplasty) underlying area of infiltration
Stromal (interstitial) scarring (opacification), thinning, and vascularization may ensue
22
Q
Treatment for HSV stromal keratitis
A
Topical steroids with antiviral cover (often oral)
Best managed by a corneal specialist
23
Q
Appearance of mild HSV stromal keratitis
A
Eye is red
Don’t stain b/c epithelium is intact
Do cross-section, an notice place in stroma (focal stromal infiltration) where it has a grayish color
24
Q
Appearance of marked HSV stromal keratitis
A
Graying through the stroma, coving part of vision
Has neovascularization
Will affect vision
Can lead to scarring
25
Appearance of significant scarring from HSV stromal keratitis
White circular opacification-like spot right on the center of the pupil, located within the stroma of the cornea
Significant scar due to stromal herpetic simplex
Very common cause of vision loss
26
Disciform endotheliitis (or disciform keratitis)
Frequent form of recurrent HSV keratitis thought to be an immune reaction rather than infection of the endothelial cells
27
Symptoms of disciform endotheliitis (keratitis)
Gradual blurring of vision with “haloes around lights”
28
Signs of disciform endotheliitis (keratitis)
Central zone of stromal edema in a circular (disc-like) pattern
Underlying KP’s
Surrounding immune (Wessely) ring of deep stromal haze
29
History of disciform endotheliitis (keratitis)
Don’t always have clear history of prior HSV epithelial ulcer, but decreasing corneal sensitivity may assist diagnosis
30
Treatment of disciform endotheliitis (keratitis)
Topical steroids with antiviral cover
31
Outcome for vision in patients with disciform endotheliitis (keratitis)
Visual loss is usually reversible with steroid drops (since the edema can be treated, the vision can come back)
32
Appearance of HSV disciform keratitis
Won’t stain b/c no topical viral infiltration present
Disc-like, typically in the center, due to endothelialitis
Large circular white opacification in the cornea
33
Associated condition with HSV keratitis
Neurotrophic keratopathy
| Iriddocyclitis
34
What treatment can make HSV keratitis worse?
Antiviral drops b/c it is not an active viral disease
35
Treatment for neurotrophic keratopathy
Lubricants, etc. with judicious use of steroids for any inflammatory component
36
Decompensation of epithelium due to loss of sensation
Neurotrophic keratitis
37
Issues arising from neurotrophic keratopathy
Corneal hypoesthesia or complete anesthesia from damage to corneal nerves, possibly leading to persistent non-healing corneal epithelial defects (stromal scarring, corneal perforation, or secondary bacterial infection)
38
Issues arising from iridocyclitis
May present without signs of active keratitis
Acute trabeculitis may result in an acute rise in IOP
Uveitis associated with HSV mandates a thorough fundoscopic exam to exclude concomitant acute retinal necrosis
39
Treatment for iridocyclitis
Steroids (and often oral antiviral cover)
| Must differentiate from IOP spike due to steroid treatment
40
Prophylaxis for HSV keratitis
Cuts recurrence rate of epithelial/stromal keratitis in half
Indicated for frequent, severe recurrences or monocular patients
Common regimen is 400 mg oral aciclovir bid x years
41
Complications of HSV keratitis
```
Secondary infections (most often bacterial)
Glaucoma (due to trabeculitis or chronic steroid use, both causing an increase in IOP)
```
42
What is sometimes the end result for HSV keratitis?
Keratoplasty
- recurrent HSV keratitis common
- rejection common
43
Herpes zoster ophthalmicus (HZO)
Shingles involving the ophthalmic division of trigeminal (CN V) nerve
Reactivation when immunity fades
Follows initial infection (HSV) of chickenpox
44
Hutchinson’s sign
In HZO, if pt presents with nose rash involved, the eye will likely be involved as well
45
How is the cornea affected by HZO?
```
Direct infection (epithelial keratitis)
Secondary infection (stroma, endothelium)
Nerve damage (hypo-aesthesia which may lead to neurotrophic keratopathy)
```
46
Typical age of patient’s to get HZO
50-60’s (when immunity fades from the chickenpox virus)
47
How does singles present?
Prodrome (fever, malaise, HA) for 3-5 days
| Painful rash respecting midline —> vesicles, crust/heal over weeks —> scarring/depigmentation
48
Diagnosis of shingles
Clinical, aided by PCR, microscopy, etc.
49
Treatment for shingles
```
Oral antivirals (ex. 800 mg aciclovir 5x daily for 5-7 days)
Prompt treatment (within 72 hours) decreases the severity/duration and likelihood of post-herpetic neuralgia and late ocular complications (x 50%)
IV antivirals for severe presentations or immunodeficient pt’s
Contagious - can spread chickenpox (avoid those pregnant or immunodeficient)
```
50
Skin reactivation of VZV infection
Shingles
51
If there is a singles rash on the abdomen, does it still equal HZO?
No; the eyes won’t be affected
52
If there is a shingles rash on the face, including Hutchinson’s sign, can this equal HZO?
```
Yes! Is still shingles, but this zoster has the subset of shingles
CN 5 (ophthalmic branch)
```
53
Half of pt’s with HZO develop what soon after the rash?
Dendritic epithelial ulcerations (smaller/finer than with HSV and usually self-resolve) = pseudodendrites - don’t have end bulbs an don’t stain quite as well
54
What are some ocular inflammation issues that can occur with HZO?
```
Stromal (interstitial) keratitis
Anterior uveitis common (can elevate IOP)
Disciform keratitis (left often with HSV)
Posterior uveitis = PRN (posterior retinal necrosis)/ARN (acute retinal necrosis), so must do DFE (dilated fundus exam)
```
55
HZO infection that can show pseudodendrites
HZO epithelial keratitis
56
HZO infection that is the leading form of blindness in this country, causing scarring, is what kind of infection?
HZO stromal (interstitial) keratitis
57
Infections that cause interstitial keratitis
```
Syphilis
Herpetic viruses (more common in simplex than zoster)
```
58
Non-infectious things that can cause interestitial keratitis
Sarcoidosis
59
Non-viral things that can cause interstitial keratitis
Tuberculosis
60
If pt’s acquire interstitial keratitis at birth, what are the side-effects?
Lesion is in the stroma, leading to lots of inflammation and neovascularization in the cornea
61
What is HZO?
Shingles with ocular involvement
62
What are some potential issues of HZO?
Neurotrophic keratitis (half) - not typically severe
Scleritis, if chronic, can lead to patchy atrophy
Lid scarring —> ptosis, exposure (incomplete closure), trichiasis
Post-herpetic neuralgia = pain long after rash heals
63
Post-herpetic neuralgia is most commonly associated with what?
HZO
Pain greater than a month after the shingles rash heals
More likely with increased age (over 70)
Can be very sever and best dealt with by a pain specialst
64
Can you give HZO pt’s a vaccine?
Once you acquire the virus, you can’t eradicate the organism, but you can give them a booster to decrease their likelihood of developing the reactivation of shingles later on.
Doesn’t treat shingles, but helps to avoid shingles in the first place.
65
CASE:
22 yo, CL wearer, suspected to have acanthomoeba; descemet’s membrane shows folds = edema (swelling); you notice circular graying of the cornea. What do you do?
What do you suspect?
Stain to see if it’s in the stroma or the epithelium
This is disciform scarring (edema) - will reabsorb and vision should better
Treatment with steroid drops (prednisone QID)
66
CASE:
44 yo, has been taking medications; after staining the eye with sodium fluorescein, you notice multiple large lesions on the surface of the cornea very well.
What layer of the cornea is likely involved?
What lesion do you think this could be?
What do you think this could be caused by?
Most likely the epithelium
Geographic ulcerations, caused by taking steroid medications after already having corneal involvement of herpes (dendritic ulcers)
Herpes simplex virus
67
CASE:
On SLE, you notice some type of elevated, mounted up, raised looking bubbles that don’t really have the appearance of an ulcerations on a pt’s cornea that don’t stain real well; pt has no history of red eye; this is noticed a few days after a pt has come down with a rash on their face.
What do you think it could be?
What would you do to treat it?
Epithelial involvement of zoster reactivation
They are probably already on aciclovir for the rash, and you probably don’t want to give them any topical drops b/c it won’t help.
68
CASE:
75 yo develops redness, tearing, light sensitivity, and blurred vision in the right eye (20/400); looks like there may be an ulceration in his central vision, with some neovascularization around the outer edge of the cornea; he has a history of recurrent corneal simplex keratitis, with his last episode being about 6 months ago; he has substantial denervation due to constant recurrence, and he’s on topical antivirals for treatment.
What do you think this could be?
How do you treat this patient?
Neurotrophic epithelial keratitis
Stop all drops/medications immediately (no preservatives -artificial tears); may need to go to amniotic membrane or flap or graft to heal this up; need to treat with lubrication before they develop secondary bacterial corneal infections; send pt to specialist
69
What does meta-herpetic mean?
Associated with herpes, but non-healing epithelial ulcerations
70
Corneal sensitivity testing has two methods. One is the qualitative method and the other is the quantitative method. Describe the qualitative method.
If they feel it much more on one eye than the other, you know there is corneal desensitization on one eye = corneal hypo-asthesia
Herpetic diseases are most common cause of this
71
Corneal sensitivity testing has two methods. One is the qualitative method and the other is the quantitative method. Describe the quantitative method.
Thin filament you touch to the eye; keep shortening the filament until they feel it (more resistance the shorter it gets)
Helps to decide the magnitude of sensitivity loss
72
What test do you use to rule out HSV keratitis?
Corneal sensitivity test
73
How can you use rigid dental floss to test for corneal sensitivity, which checks for HSV keratitis?
First, touch the unaffected eye with the floss. The pt can grad the sensitivity on a scale of 1-10.
Then, touch the other eye and see if they sensitivity is low or non-existent.
74
61 yo femal pt presents with itchy eyes, dryness, and occasional burning. She has seen other doctors and gets improvement for 2-4 weeks, but no resolution. She has previously used lid scrubs and tobradex. The location of her itchiness is more at the lash margin. You don’t notice any discharge or grittiness, but there is a clear sleeve around the base of the lashes.
What do you think this pt has?
How do you treat them?
```
Demodex blepharitis (if the pt presented with itchiness in the nasocanthal corner of the eye, then you would suspect allergies)
Tx: Tea tree oil
```
75
57 yo female pt presents with itching and irritated eye lids, occurring over 2 years on and off. She has tried numerous OTC products with no relief. You notice dandruff/flaking/scales in the lashes, with nothing at the base, and suspect it’s coming from the skin instead.
What do you think is the issue wit this patient?
How do you treat this pt?
Seborrheic dermatitis
| Tx: tramcinolone dermatological prep (steroid cream) and can use OcuSoft lid scrub plus
76
Pt presents with frothy tear film.
| What do you suspect immediately?
MGD = most common cause of evaporative dry eye
77
Pt is a CL wearer, who has dry eye. What is the key to treat their dry eye?
Treat the underlying MGD (meibomian gland deficiency)/DED (dry eye deficiency)
78
You stain a pt’s eye with NaFL dye who you suspect might have dry eye. Corneal staining indicates what?
Late indicator of disease
79
How do you treat a pt with neurotrophic dry eye (someone with shingles)?
It’s good to use punctal occlusion first to treat the dry eye
80
What is known as the top level of dry eye management?
Scleral lenses
81
Acanthamoeba keratitis
Ubiquitous Protozoa of soil, water, and URT (upper respiratory tract)
82
Disease often associated with CL’s rinsed with tap water in the USA?
Keratitis (acanthamoeba keratitis)
83
Symptoms of acanthamoeba keratitis
Blurred vision
| Discomfort/pain —> clinical picture (helps differentiate from HSV)
84
Signs of acanthamoeba keratitis
Grayish irregular K surface —> infiltrates
Slowly progressive stromal opacification/vascularization
Corneal melt may occur at any stage
85
Different types of infiltrates found in acanthamoeba keratitis
Perineural = ‘radial keratoneuritis’ virtually pathognomonic
| Focal/diffuse anterior stromal gradually coalesce and enlarge - often forming ring abscess
86
Whiteish (WBC’s) around the corneal nerve that’s pathognomonic for acanthamoeba keratitis
Radial keratoneuritis
87
Diagnosis of acanthamoeba keratitis
Difficult and often delayed
Consider whenever there’s limited response to antibiotics
Stains and/or cultures - of corneal scrapes
PCR and in vivo confocal microscopy
Biopsy
88
Treatment for acanthamoeba keratitis
The earlier the better!!!
Debribement - facilitates gtt penetration
Topical amoebicides (initially hourly, then dec., can take weeks to clear, and often continued for months)
Pain control (oral NSAIDs) - ibuprofen
Adjunctive low-dose steroids IF necessary
May require PK (penetrating keratoplasty) for resistance, late scarring, or perforation
89
Do we try to treat or prescribe for acanthamoeba keratitis?
No; it’s difficult to treat, so get a corneal specialist to do it
90
Onchocerciasis keratitis
River blindness
Transmitted by black fly bite and worm transmitted to the cornea
The body kills the worm, and then bacterial infection if what causes so many issues into the cornea (hypersensitivity reaction)
Found mainly in equatorial Africa (fast moving rivers)
91
Marginal keratitis
Hypersensitivity to staphylococcal exotoxins and cell wall proteins
92
What kind of infiltration does marginal keratitis have?
Lymphocytic infiltration, not infectious
93
Signs of marginal keratitis
Peripheral ‘marginal’ K infiltrates (outer margins)
Adjacent conjunctival hyperemia
Typically only a small, in any, overlying epithelial defect
Multiple infiltrates may coalesce/enlarge circumferentially (crescent shape around the cornea)
94
Symptoms of marginal keratitis
No pusy/ropey discharge
Mild discomfort
Redness
Tearing
95
Treatment for marginal keratitis
Often self-resolving over week
Occasionally with residual superficial scarring/pannus (vascularization)
**Treat any associated blepharitis
Sometimes a weak topical steroid +/- antibiotic given QID x 1-2 weeks
96
Phlyctenular keratitis
Nodular inflammation of cornea resulting from hypersensitivity reaction to a foreign antigen/bacteria (staph aureus, mycobacterium tuberculosis, etc.)
97
Symptoms of phlyctenular keratitis
Photophobia
Lacrimation
Blepharospasm
98
Who commonly gets phlyctenular keratitis?
Primarily in children from 6 months to 16 years old
99
Signs of phlyctenular keratitis
White limbal nodule, that may extend further onto cornea, with associated intense local conjunctival hyperemia
100
Disease that is less common, but more severe than marginal keratitis
Phlyctenular keratitis
101
Treatment for phlyctenular keratitis
Usually spontaneously resolve over weeks - often with scar, superficial vascularization and thinning
Can lead to ulceration
102
What two things do you want to decrease when treating phlyctenular keratitis?
Inflammatory response (generally topical steroids +/- antibiotic)
Source of antigens
(Treat blepharitis or underlying infection - TB, chlamydia, etc.)
** not infectious
103
Pt’s are generally more bothered by this more than marginal keratitits
Phlyctenular keratitis
104
Rosacea
Common chronic condition of sun-exposed skin (face. And neck) characterized by telangiectasia (vessels that have always been there but not evident until swelling), papule/pustule formation, rhinophyma (nose gets bulbous/large on tip = meaty) and facial flushing
105
Rosacea is a multifactorial etiology that involves defects where?
In the body’s immune response to pathogens (skin/GI) and vasoregulatory process
106
Rosacea that is common and has eye involvement
Ocular rosacea
107
Ocular rosacea includes what structures?
Lids - marginal telangiectasia and MGD
Conjunctiva - inflammation
Cornea
108
What kind of things do you find with corneal involvement with ocular rosacea?
Punctate epithelial erosions inferiorly
Peripheral vascularization
Marginal keratitis (one of many causes)
Thinning which can progress to perforation
Scarring/vascularization may eventually develop
109
Appearance of dermatological rosacea
Common facial pattern with papules and pustules; bilateral and symmetrical; chronic and long-term; can’t really cure
110
Appearance of ocular rosacea
Pannus = blood vessels growing superiors into the cornea from the sclera
Cornea is becoming involved (thinned)
Potential opacification of cornea
111
Management of ocular rosacea
Directed toward symptomatic control and disease prevention (avoid flare triggers) rather than cure
112
When treating ocular rosacea, what kind of approach can be undertaken?
Stepwise approach
113
In the stepwise approach to treat ocular rosacea, what is the first step?
Lid hygiene and artificial tears
114
In the stepwise approach to treat ocular rosacea, what is the second step?
Anti-inflammatory medications (low dose doxycycline = controlled release form) - oral tetracyclines most common and effective regimen
Lower ones than used for antibiotic effect
115
What does treating ocular rosacea with low-dose anti-inflammatories do for MGD treatment?
Improves meibomian gland secretions by decreasing bacterial lipase
Protects cornea from perforation by inhibiting collagenase (big part of corneal thinning - inhibiting helps stop perforation)
116
In the stepwise approach to treat ocular rosacea, what is the last step?
Late surgical intervention if required
117
Mooren’s ulcer
A rare poorly understood condition characterized by peripheral stromal ulceration that progresses circumferentially
118
Location of Mooren’s ulcer
Focal (non-systemic) autoimmune disorder isolated to the eye
119
Two forms of Mooren’s ulcer
```
Older patients (usually one eye)
Younger patients (may be both eyes and more aggressive)
```
120
Symptoms of Mooren’s ulcer
Pain
Photophobia
Blurred vision
121
Signs of Mooren’s ulcer
Peripheral
Principally stromal
Ulceration
122
Diagnosis of Mooren’s ulcer
Clinical and by exclusion of ocular infection or associated systemic autoimmune disorder
Seems to be associated with certain HLA alleles
123
Treatment of Mooren’s ulcer
Corneal specialist
| Frequent topical steroid gtts —> other immunosuppressants and collagenase inhibitors —> surgery
124
PUK
Peripheral ulcerative keratitis
125
PUK associated with systemic disease
May present before/after systemic autoimmune symptoms
126
Systemic diseases commonly associated with PUK
RA > Wegener’s granulomatosis, polyarteritis nodosa, SLE, etc.
127
Signs of PUK associated with systemic disease
Crescent shaped destructive lesion of the juxtalimbal corneal stroma
Usually with neighboring scleritis (unlike Mooren’s ulcer)
128
Diagnosis of PUK associated with systemic disease
Based on history and physical exam
129
Treatment for PUK associated with systemic disease
Goals are to minimize inflammation, prevent superinfection, and promote healing of the ulcer
Systemic immunosuppession often required to control ocular inflammation (rheumatology consult)
Surgery may be necessary (corneal specialist)
130
Terrien’s marginal degeneration
Uncommon idiopathic from of peripheral thinning (degeneration?) of the cornea
Slowly progressive and non-inflammatory
Unilateral or asymmetrically bilateral
131
Who usually gets terrien’s marginal degeneration?
Young adults onward
132
Symptoms of terrien’s marginal degeneration
```
Often none (discomfort uncommon)
Gradual blur may develop due to astigmatism
```
133
Signs of terrien’s marginal degeneration
Results in peripheral gutter, but rarely perforated
| Associate with superficial corneal vascularization, opacification and lipid deposition
134
Since terrien’s marginal degeneration is not inflammatory, what won’t you see?
Infiltrates (WBC’s)
135
Diagnosis of terrien’s marginal degeneration
Primarily clinical, based on history and slit lamp exam of the eye
Differential from other peripheral corneal thinning disorders
Collagen vascular diseases should be excluded
136
What are some peripheral corneal thinning disorders that must be differentiated from terrien’s marginal degeneration
Lack of inflammation or epithelial defect
Linear deposition of lipid
Slow progressive course
137
Treatment of terrien’s marginal degeneration
```
Protective eyewear (as indicated)
Contact lenses (for irregular astigmatism
Surgery only when impending/actual perforation
```
138
Peripheral ulceration/inflammation due to focal autoimmune rxn; usually treated wth frequent steroid drops initially
Mooren’s ulcer
139
Severe peripheral ulceration/thinning, often with associated scleritis; usually requires systemic (oral/IV) steroids
PUK associated with systemic disease
140
Slowly progressive peripheral thinning without ulceration/inflammation; generally does not require treatment
Terrien’s marginal degeneration
141
Neurotrophic keratopathy
Epithelial breakdown and persistent ulceration may occur with loss of trigeminal innervation from any cause
142
Diagnosis of neurotrophic keratopathy
Corneal sensation reduce
Non-healing epithelial defects tend to have thickened/rolled edges
Progressive stromal melting with minimal discomfort
143
Treatment for neurotrophic keratopathy
If possible, discontinue all drops except non-preserved artificial tears
Perforation is a concern, so anti-collagenase meds sometimes used
Consult corneal specialist: may require tarsorrhaphy, BOTOX, keratoplasty
144
Technique where they sew the upper lid to the lower lid for treatment of the cornea
Tarsorrhaphy
145
Exposure keratopathy results from what?
Incomplete lid closure (lagophthalmos) due to many causes
146
Examples of causes for exposure keratopathy
Facial nerve palsy (CN 7) - Bell’s Palsy
Parkinsonism (overall loss of muscle tone)
Proptosis
Post-blepharoplasty (cosmetic surgery)
147
Symptoms of exposure keratopathy that help in diagnosis
Dry eye (burning, grittiness, FB sensation, etc.)
148
Signs of exposure keratopathy
Punctate epithelial changes (pin pricks of areas with staining that we don’t pick up easily without staining) - preferentially across inferior 1/3 of cornea, which may progress to ulceration, second degree infection, scarring
Potentially with permanent vision loss
149
Treatment of exposure keratopathy
Depends on severity and whether recovery anticipated
150
If exposure keratopathy is reversible, what is the treatment?
Lubricants (Day and night)
Lid taping
BCL (bandage contact lens)
Etc.
151
If not reversible exposure keratopathy, what is the treatment?
Surgically covered via tarsorrhaphy, conjunctival flap, etc.
152
Proptosis appearance
Eyes are bulging forward
Lag ophthalmitis
Looks like the patient is surprise or shocked and raising their eyebrows, but they aren’t
153
Thyroid eye disease
Orbital fat (EOM) become infiltrated and swell up; space in bony orbit is full, and it pushes the eyes forward
154
Appearance of exposure keratopathy
When stained, the inferior portion of the cornea looks like it has multiple different tiny ulcerations, all filling with dye
155
Thygeson’s SPK
Idiopathic, bilateral, disorder, characterized by the episodic appearance of corneal opacities causing irritation/blur
156
Who usually gets thygeson’s SPK?
Onset commonly in young adulthood, but can arise at any age and last (on and off) for decades
157
Symptoms of thygeson’s SPK
Recurrent bouts of irritation
Photophobia
Tearing
Blurred vision
158
Signs of thygeson’s SPK
Multiple small, slightly elevate grayish epithelial irruption across the central cornea - with little if any associated conjunctival injection
159
Management of thygeson’s SPK
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Lubricants (mild cases)
Topical steroids (low potently fluorometholone with prolonged taper)
EW bandage CL (symptomatic relief)
```
160
Does thygeson’s SPK typically cause permanent damage?
Disease tends to wax and wane (flares up and comes and goes) over many years, before eventually disappearing without clinical sequelae (with no permanent damage)
161
Recurrent corneal erosion syndrome
Epithelial erosions caused by abnormal attachment to underlying basement membrane
162
What is recurrent corneal erosion syndrome typically associated with?
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Prior trauma (unilateral) or
Certain corneal dystrophies (bilateral)
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163
Symptoms of recurrent corneal erosion syndrome
Significant pain
Photophobia
Tearing
Difficulty keeping eye open
164
Signs of recurrent corneal erosion syndrome
Epithelial defect not always evident at exam
| Basement membrane irregularities include: microcysts, swirls, etc.
165
Management of recurrent corneal erosion syndrome
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Lubricants
Prophylactic antibiotics (if epithelium compromised)
Oral or topical NSAIDs for pain relief (if needed) (topical = diclofenac)
Bandage CL (symptoms in select cases)
Procedures for frequent recurrent cases
```
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Recent studies have shown that what drugs reduce the frequency of recurrent corneal erosion?
Combination of doxycycline 50 mg bid and a topical corticosteroid (such as prednisolone acetate 1%, or fluorometholone 0.1%) bid or tid x 3 weeks
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Procedures for frequent recurrent corneal erosion syndrome cases include:
Anterior stromal puncture
Diamond blur polishing
PTK (phototherapeutic keratoplasty)
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Filamentary keratopathy
Common uncomfortable condition in which strands of mucus and cellular debris attach to epithelial surface
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Causes of filamentary keratopathy
Aqueous deficient dry eye
SLK (superior limbic keratitis - sometimes related to thyroid eye disese - Superior margin filaments)
RCE (Recurrent corneal erosion)
Toxicity to various eye drops
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Symptoms of filamentary keratopathy
FB sensation
| Sometimes with photophobia
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Treatment of filamentary keratopathy
Elimination of underlying cause
Removal of filaments provides immediate (but temporary) relief to some extent
Acetylcysteine (mucolytic) drops break up mucus strands/plaques on eye and lessen formation
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What stain works best on filamentary keratopathy?
Rose bengal
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Xerophthalmia
Refers to the constellation of ocular signs and symptoms associated with Vitamin A deficiency (as a late manifestation of such)
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What is xerophthalmia usually associated with?
Malnutrition, but can occur due to malabsorption and metabolic abnormalities
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The World Health Organization (WHO) estimated that about how many children have Vitamine A deficiency and how many have xerophthalmia?
254 million have vitamine A deficiency
| 2.8 million have xerophthalmia
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The most common cause of childhood blindness
Xerophthalmia
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Where is the most likely place you’ll find someone with vitamin A deficiency and xerophthalmia?
Children from South and South East Asia
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Why is vitamin A important for the eye?
Maintains the integrity and proliferation of the epithelium of the conjunctiva and cornea (deficiency can cause conjunctival and corneal xerosis = dryness, corneal ulcers, keratomalacia, and corneal scarring)
Precursor to rhodopsin (rods are much more sensitive to vitamin A deficiency than cones, such that defective vision in dim light (nyctalopia) occurs first
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Nyctalopia
Defective vision in dim light
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Systemic treatment for xerophthalmia
Vitamin A supplementation (oral or injection initially)
| -underlying diseases such as liver disease an inflammatory bowel disease must also be managed in non-dietary cases
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Ocular treatment for xerophthalmia
Intense lubrication (while guarding against perforation)
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Bitot spots are specific to what condition?
Xerophthalmia
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Keratoconus
Progressive thinning and anterior protrusion of a portion of the paracentral cornea
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What is keratoconus associated with?
Various connective tissue disorders and eye rubbing
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Presentation of keratoconus usually occurs when?
During teens/20’s unilaterally, becoming bilateral over time
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Symptoms of keratoconus
Blurred vision due to irregular astigmatism - sometimes with CL intolerance
If descemet’s membrane ruptures (acute hydrops) —> pain, photophobia, decreased vision
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If descemet’s membrane ruptures, what is this known as? If in keratoconus, what symptoms will they have?
Acute hydrops
| Pain, photophobia, decreased vision
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Signs of keratoconus
“Oil droplet” reflex with ophthalmoscopy
“Scissoring” reflex with retinoscopy
Vogt striae = vertical stress lines in deep stroma
Fleischer’s ring = epithelial iron deposition at base of “cone” best seen with cobalt filter
“Cone” observable from side or against lower lid upon downgaze (Munson sign)
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Confirmation/quantification of keratoconus
Keratometry - steep readings, often upwards of 50 D
| Corneal topography - demonstrates contours of anterior protrusion
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Treatment of keratoconus
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Avoid eye rubbing
Use protective eyewear
Specialty CL fitting (RGPs, sometimes scleral)
Corneal cross-linking
Intracorneal implants (Intax)
Keratoplasty (often DALK)
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What is contraindicated in pt’s with keratoconus?
LASIK (refractive surgery candidates) b/c cornea is already so thin
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Topography appearance of keratoconus
Deep red lower/inferiorly, and paracentrally (this is where the cone is)
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Acute hydrops with keratoconus
Sudden significant stromal edema due to a tear in descemet’s membrane
-may occur with any corneal ectasia/thinning (either spontaneously or with trivial trauma)
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Symptoms of acute hydrops with keratoconus
Sudden onset pain and photophobia with decreased BCVA
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Signs of acute hydrops with keratoconus
Severe corneal edema
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Prognosis for acute hydrops with keratoconus
Most cases of acute corneal hydrops spontaneously resolve over 2-4 months, with resolution of edema, but often with variable degrees of scarring
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Two different types of management for acute hydrops associated with keratoconus
Conservative treatment
| Surgery
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Conservative treatment for acute hydrops associated with keratoconus
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Cycloplegia
Hydronic saline
Topical antibiotic for prophylaxis
Bandage CL
Anti-glaucoma medications
Corticosteroids or non-steroidal anti-inflammatory agents
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Surgery management for acute hydrops associated with keratoconus
Injection of anterior chamber air or gas may accelerate recovery; reduce scarring
Penetrating keratoplasty if indicated (for underlying ecstatic disorder or scarring)
