4. 3
1.Describe what you think is abnormal in this test
2.What is your diagnosis in this finding?
3.What is your definite treatment in this case?
4.Can this patient undergo phacoemulsification for cataract surgery?
5. Patient underwent endothelial keratoplasty procedure,
this picture reveal an examination in day 1 after surgery
1.Describe finding
2.What is your management?
4
6. 5
1.What happened to this patient?
2.Which are the complications for patient who underwent this operation?
3.What is the most common complication after this operation?
7. 6
1.What is your diagnosis?
2.What are your differential diagnosis?
3.What treatment would you recommend?
4.Would oral acyclovir benefit in preventing development of stromal keratitis?
10. 8
1.What is your diagnosis?
2.What are the risk factors causing this condition?
11. 9
Patient underwent LASIK operation, a few months later he/she began to have a decreased vision
1.What is your diagnosis?
2.What is your management?
14. 1
1.Describe finding on this picture
2.What is your diagnosis?
3.Malignant transformation should be suspected in which appearance?
15. • 1.Describe finding on this picture
• Multiple flat, brown patches of noncystic pigmentation on superficial
conjunctiva
• 2.What is your diagnosis?
• Primary acquired melanosis (PAM)
• 3.Malignant transformation should be suspected in which
appearance?
• Nodularity
• Enlargement
• Increased vascularity
16. Type History Color Appearance Laterality Specific
features
Nevus Longtime presence,
usually from
childhood
Light brown, may
be non-pigmented
during childhood
Slightly raised and
cystic, with well-
defined margins
Mostly
unilateral
Changes
pigmentation
with puberty and
pregnancy
PAM New pigmentation
on ocular surface
Varies from light
brown to darker
brown; rarely non-
pigmented
Flat, diffuse and
noncircumscribed
Unilateral Waxing and
waning of size
and pigmentation
Conjunctival
melanoma
Arises de novo,
from nevus or from
areas of PAM with
atypia
Dark brown in most
cases; can be
amelanotic
Elevated lesion,
thickened, nodular
may be amelanotic or
mixed pigmentation
Unilateral High vascularity
with feeder
vessel
18. Primary Acquired Melanosis
• Acquired melanosis may be
benign, precancerous or cancerous
• Characteristic
• Later in life (30-40 years of age)
• Unilateral
• Almost always Caucasians
• 15-17% of benign PAM will convert to
cancer within 30 years
19. sign
• Sudden development of irregular diffuse, flat, grayish black, brown or
tan bulbar pigmentation
• May extend onto palpebral conjunctiva
• Without cyst**
• Malignant transformation should be suspected with elevation,
nodularity, increased vascularity
20. treatment
• Monitor closely (photo) every 3-6 months
• Refer for biopsy
• Dilated fundus exam to r/o choroidal melanoma
21. PAM without atypia
• Benign proliferation of normal melanocytes confined to the basal
layers of conjunctiva
22. PAM with atypia
• Pre-malignant condition with 50% chance of malignant
transformation within 5 years
• Characterized by melanocytes involving all layers of conjunctiva
24. • 1.What condition could be benefit from using the device?
• Meibomian gland dysfunction
• Dry eye
• Contact lens intolerance
• blepharitis
25.
26.
27.
28.
29.
30.
31.
32.
33. MGD
• Meibomian glands or glandulae
tarsals are large sebaceous glands
which secrete lipids
• Chronic, diffuse abnormality of
the meibomian glands commonly
characterized by terminal duct
obstruction and may result in
alteration of the tear film,
symptoms of eye irritation and
other ocular surface disorders
40. 3
1.Describe what you think is abnormal in this test
2.What is your diagnosis in this finding?
3.What is your definite treatment in this case?
4.Can this patient undergo phacoemulsification for cataract surgery?
41. 1. Describe what you think is abnormal in this test
1. Cell Density = 1763
2. Guttata presentation
3. CV = 44%
2. What is your diagnosis in this finding?
1. Fuchs endothelial dystrophy
3. What is your definite treatment in this case?
1. DMEK
2. DSAEK
3. PKP
4. Can this patient undergo phacoemulsification for cataract surgery?
1. Yes but with caution of using too high energy
42. DDX PPMD
Vesicle-like lesions at the level of Descemet's membrane and endothelium are the hallmark lesions of PPMD.
They appear as transparent cystic lesions surrounded by gray halos and commonly occur in lines or clusters. .
43. Band lesions, sometimes called "snail tracks," are classically horizontal lesions with parallel, scalloped, non-tapering
edges at the level of the posterior cornea. Below are examples of these lesions in 2 separate patients.
DDX PPMD
44. DDX ICE (chandler variant)
Fine hammered silver appearance of posterior cornea
Pleomorphism in size and shape
Dark areas within the cells
Loss of clear hexagonal margins
45. Endothelial cell count
• CD is a measurement of cell density in mm2 and decreases with age.
• A low CD value for a particular age may indicate that the endothelium is depleting faster than
normal.
• CV represents the coefficient, or degree, of variation in the sizes of the
endothelial cells (polymegethism).
• By measuring the variation in size between endothelial cells, the system can measure how
much cell loss is occurring. A CV less than 40 is normal.
• HEX indicates the variability in hexagonal cell shape over time.
• Hexagonality above 50% is suggested to be normal.
46.
47. • Endothelial cell photography is a covered procedure under Medicare
when reasonable and necessary for patients who meet one or more
of the following medical criteria
• slit lamp evidence of endothelial dystrophy (corneal guttata).
• slit lamp evidence of corneal edema (unilateral or bilateral).
• about to undergo a secondary intraocular lens implantation.
• had previous intraocular surgery and require cataract surgery.
• about to undergo a surgical procedure associated with a higher risk to the
corneal endothelium (i.e., phacoemulsification or refractive surgery, with
evidence of posterior polymorphous dystrophy of the cornea or irido-corneal-
endothelium syndrome).
• about to be fitted with extended wear contact lenses after intraocular
surgery.
48.
49. Patient underwent endothelial keratoplasty procedure,
this picture reveal an examination in day 1 after surgery
1.Describe finding
2.What is your management?
4
50. Patient underwent endothelial keratoplasty procedure, this picture
reveal an examination in day 1 after surgery
• 1.Describe finding
• Donor graft dislocation
• 2.What is your management?
• Reposition with bubble injection
52. Pupillary block
• Inadequate intraoperative air
release
• Patient inadvertently leans his or
her head forward
• Pupillary block may occur due to
migration of the air behind the iris
• The acute rise in pressure
produces pain and can exacerbate
underlying glaucoma
• An inferior iridectomy may
prevent pupillary block
53. Dislocation of the donor graft
• Rate of occurrence depend on surgeon’s experience
• 4% with experienced surgeon
• 35-50% with novice surgeon (those who have had fewer than 10 cases)
• Occurs primarily within the first 24 hours
• Occasionally inadvertent trauma from eye rubbing or a sudden blow to the eye
• The dislocation is managed with re-injection of air
54.
55. Epithelial ingrowth
• May be seen first as a white deposit within the
interface
• May be relatively stable and asymptomatic
• Rare case, may lead to graft failure
• The source of the ingrowth may be host
surface epithelial cells implanted within the
eye during placement of the donor tissue or
donor epithelial cells inadvertently left in place
and implanted following eccentric
trephination beyond the microkeratome
dissection
• Most case can be observed without further
intervention
• In the atypical case that lead to graft failure, a
second DSEK or PK leads to a good prognosis
without recurrent ingrowth
56. Interface problems
• Infections can occur as pathogens pass through vent incision, due to donor
tissue’s contamination or from ocular surface into an interface
• Interface opacification may occur because of retention of fibers, incomplete
removal of Descemet membrane, calcareous deposition and persistent interface
fluid
• Textural interface opacity
• Elongated type (lacy honeycomb pattern of deposits intervening clear zones)
• Punctate type (small discrete deposits)
57. Decreased postoperative VA
• Preexisting basement membrane changes may cause superficial irregularity or
subepithelial fibrosis
• Corneal debridement or superficial keratectomy may be necessary
• Light scattering due to anterior stromal haze
• Alteration of the posterior corneal curvature
58. Progression of cataracts
• Phakic DSEK induces progression
of cataracts
• Narrow anterior chambers
(<3.0mm)
• Combined DSEK and cataract
extraction has been recommended
in patients older then 50 years or
presented with mild to moderate
cataract
59. Primary graft failure
• Rate 3-12%
• Higher rate depend on surgeon’s learning curve
• Lower rate depend on surgeon with more experienced
• Less tissue manipulation
• Less endothelium trauma
60. Corneal graft rejection
• Lower rate than PK
• Average rejection rate of 1-10%
• Lower incidence may be related
to the lack of corneal sutures
• Presented with multiple KP
scattered across the cornea
61. Endothelial cell loss
• Manipulation of tissue
• Microkeratome dissection
• Placement
• Air bubble
• 5-years follow up case series of 95 eyes, mean cell loss was only 53%
comparing to PK with cell loss up to 70%
62. 5
1.What happened to this patient?
2.Which are the complications for patient who underwent this operation?
3.What is the most common complication after this operation?
63. • 1.What happened to this patient?
• Radial keratotomy
• 2.What are the complications for patient who underwent this
operation?
• Undercorrection
• Overcorrection
• Hyperopic shift
• Diurnal fluctuation of RF error
• 3.What is the most common complication after this operation?
• Hyperopic shift
64. Radial keratotomy
• A refractive surgical procedure to
correct myopia that was
developed in 1974 by Svyatoslav
Fyodorov
65. Radial keratotomy
• Incision are made with a diamond
knife
• Penetrate only the superficial
corneal stroma are less effective
than those reaching deep into the
cornea
• Roughly equivalent to 90% of
corneal depth based on thickness
66. Postsurgical healing
• Healing corneal wounds consist of newly
abutting corneal stroma, fibroblastic cells
and irregular fibrous connective tissue
• Closer to the wound surface lies the
epithelial plug
• A bed of the cells that form the normal
corneal epithelium which have fallen into
the wound
• As the cells migrate from the depth of the
plug up to the surface, some die before
reaching it, forming breaches in the
otherwise healthy epithelial layers
• May be prone to infection in late onset
68. Corneal perforations
• Microperforation
• Inferior and temporal cornea
• Incidence of small ruptures in DM is 2-10%
• Macroperforation
• Incidence is 0-0.45%
• Factors contribute to corneal perforations
• Inexperienced with knife blade
• Centripetal incisions
• IOP elevation during incision
• Recutting incisions
• Prolonged corneal dehydration intraoperatively
• Corneal thickness measurement error
• Unexpected movement of the patient
69. Corneal perforation
• Self-sealing perforation are treated with cycloplegia ( to dilate the pupil and
prevent adherence of the iris to the perforation site)
• Topical aqueous suppressants
• Topical ATB
• Ocular shield
• Eye patching is not recommended
• In macroperforation, interrupted 10-0 nylon suture are place to seal the wound
and the eye should be patched if the AC is depth
70.
71. overcorrection
• Risk factors
• Radial incision prolonged to the limbus
• Multiple enhancement procedures
• Peripheral re-deepening operation
• Absence of preoperative cycloplegic refraction
• CL wear postoperatively
• Postoperatively ocular massage
• Can occur immediately after surgery when edema and the effect of
the incisions cause gaping and greater flattening of the cornea
• It usually resolves spontaneously within a few weeks
73. 6
1.What is your diagnosis?
2.What are your differential diagnosis?
3.What treatment would you recommend?
4.Would oral acyclovir benefit in preventing development of stromal keratitis?
74. • 1.What is your diagnosis?
• Herpes simplex keratitis with dendritic lesions and terminal bulbs
• 2.What are your differential diagnosis?
• Herpes zoster keratitis
• Healing recurrent erosion
• Soft CL wear
• 3.What treatment would you recommend?
• Trifluorothymidine 1% (Viroptic) 9 times per day.
• Alternatively, 3% vidarabine ointment (Vira A) may be used 5 times a day.
• The patient should be examined about 48 hours after starting treatment to evaluate therapeutic
efficacy
• 4.Would oral acyclovir benefit in preventing development of stromal keratitis?
• NO
• According to HEDS, oral acyclovir not significant prevent HSV epithelial keratitis from developing
stromal keratitis and irits
78. HEDS study results
• Stromal keratitis : topical steroid was significantly decrease stromal inflammation and
shortened duration of stromal keratitis
• Stromal keratitis : oral acyclovir has no benefit if add on topical trifluridine and topical
steroid
• HSV iritis : oral acyclovir 400mg x 5times/day for 10 weeks may be in benefit but non
significant result due to low number of subject
• Oral acyclovir is not significant in preventing HSV epithelial keratitis from developing
stromal keratitis and iritis
• Low dose acyclovir 400mg oral bid for 12 months significant decrease recurrent rate of
HSV infection 50%
• No result confirm trigger factor for recurrent HSV infection (stress, sunlight, systemic
infection, men, CL wear, eye injury)
80. • 1.Describe finding
• Khodadoust line
• Donor graft edema and haziness
• 2.What is your management?
• Corticosteroid eyedrops in the mainstay of therapy
• As often as every 15 minutes to 2 hours depending on the severity of the
episodes
82. Epithelial rejection
• Immune response may be directed entirely at the donor epithelium
• Lymphocytes cause an elevated, linear epithelial ridge that advances
centripetally
• Rate of 10% of patient experiencing rejection
• Seen in 1-13 months
83. Subepithelial rejection
• May cause no symptoms
• May accompany with AC reaction
• Subepithelial infiltrates can best be seen with broad, tangential light
• If treated, leave no sequelae
84. Stromal rejection
• Not common
• Stromal infiltrates
• Neovascularization
• Typically noninfiltrative keratolysis
within the graft-host interface not
extending into the peripheral recipient
stroma
• If prolonged, stroma can become
necrotic
85. Endothelial rejection
• Most common form
• 8-37%
• Most serious form of corneal
transplant rejection
• Leading to loss of a significant
number of endothelial cells which
results in graft failure
• Presented with fine KP, corneal
edema, khodadoust line, AC reaction
• Patient have symptoms of corneal
edema such as photophobia,
redness, irritation, halos around
lights ang foggy vision
86. Treatment
• Topical steroids is the mainstay of therapy
• Dexamethasone 0.1% or prednisolone 1.0% are used q 15 min up to 2 hours
depending on the severity of episode
• Difluprednate ophthalmic emulsion 0.05% can also be used with less frequency in
dosage
• Close follow up
• Monitor increased IOP
• Topical steroids oinment may be used on occasion
• Periocular injection of corticosteroids for severe rejection episodes or
noncompliant patients
• In fulminant case, systemic corticosteroids may be used orally or intravenously
87. 8
1.What is your diagnosis?
2.What are the risk factors causing this condition?
88. • 1.What is your diagnosis?
• Spheroidal degeneration
• Climatic droplet keratopathy
• 2.What are the risk factors causing this condition?
• Actinic exposure
• Dust and wind exposure
90. Spheroidal degeneration
• Translucent, golden brown, spheroid-like deposits in the
subepithelium, bowman layer, or superficial stroma
• Have many names
• Climatic droplet keratopathy
• Bietti nodular dystrophy
• Labrador keratopathy
91. • Primary spheroidal degeneration
• Bilateral and initially located in the nasal and temporal cornea
• May extend to conjunctiva
• Unrelated to other ocular disease
• Secondary spheroidal degeneration
• Ocular injury, Ocular inflammation
• All cases show extracellular, proteinaceous, hyaline deposits with elastotic
degeneration
• Combined factors : genetic predisposition, actinic exposure, age,
environmental trauma (dust and wind)
Spheroidal degeneration
92. treatment
• Lubrication is recommended to address uneven layering of the tear
film over affected area
• Central involvement requires superficial keratectomy or
Phototherapeutic keratectomy using excimer laser
93. 9
Patient underwent LASIK operation, a few months later he/she began to have a decreased vision
1.What is your diagnosis?
2.What is your management?
94. • Patient underwent LASIK operation, a few months later he/she began
to have a decreased vision
• 1.What is your diagnosis?
• Epithelial ingrowth
• 2.What is your management?
• lifting the flap and scraping the epithelial cells from the stromal bed and
undersurface of the flap, typically followed by placed of a bandage contact
lens.
95. Epithelial ingrowth
• Ingrowth of epithelium into the corneal flap interface is a relatively uncommon
complication of LASIK.
• The incidence of visually significant epithelial ingrowth is about 1% in primary cases and
2% on enhancement cases in microkeratome-assisted flap creation.
• The incidence may be less with femtosecond-assisted flap creation.
• Ingrowth of these cells into the corneal stromal interface is usually asymptomatic,
however, these cells may lead to decreased vision due to irregular corneal astigmatism,
direct intrusion of cells into the visual axis, or lead to melting of the overlying flap.
Treatment is generally needed in instances where there is decreased vision or threat for
a flap melt.
96. Signs
• Nests of cells at flap interface, usually
close to the edge of the flap
• Fibrosis in area of longstanding
epithelial ingrowth
• White plaque of cells in flap interface
• Irregular astigmatism
• Fluorescein staining at border of flap
where cellular invasion may originate
98. Probst/Machat grading
• Grade 1: thin ingrowth, 1-2 cells thick, limited to within 2 mm of flap edge, transparent,
difficult to detect, well-delineated white line along advancing edge, no associated flap
changes, nonprogressive. (No treatment required)
• Grade 2: thicker ingrowth, discrete cells evident within nest, at least 2 mm from flap
edge, individual cells translucent, easily seen on slit lamp, no demarcation line along
nest, corneal flap edge rolled or grey, no flap edge melting or erosion, usually
progressive. (Requires non-urgent treatment within 2-3 weeks)
• Grade 3: pronounced ingrowth, several cells thick, greater than 2 mm from flap edge,
ingrowth areas appear opaque, obvious on slit lamp, white geographic areas of necrotic
epithelial cells without a demarcation line, corneal flap margins rolled with thickened
white-greyish appearance. Progression results in large areas of flap melting from
collagenase release from necrotic epithelium. Confluent haze develops peripheral to the
flap edge as flap pulls away, leaving exposed stromal bed in contact with surface
epithelium. (Urgent treatment required with close follow-up due to frequent
recurrences)
100. General treatment
• Grade 1 ingrowth may be observed.
• Grades 2 and 3 require treatment.
• Treatment involves removing the invading epithelial cells from the
interface and achieving closure of the flap edge to prevent recurrent
invasion of epithelium into the flap stromal interface space.
101. Medical therapy
• Topical antibiotics and steroids are given postoperatively as per
routine after LASIK surgery.
• A bandage contact lens may be placed to improve comfort.
• Glasses and contact lenses may be used to improve vision at least
until the patient is treated surgically.
102. Surgery
• Surgery should be considered as per the Probst/Machat grading criteria.
• The general treatment for removing epithelial ingrowth is lifting the flap and scraping the
epithelial cells from the stromal bed and undersurface of the flap, typically followed by
placed of a bandage contact lens.
• The recurrence rate of lifting and scraping the cells alone has been reported to be as high
as 44%.
• Adjuvant treatments such as ethanol, mitomycin, phototherapeutinc keratectomy (PTK)
have been described for recurrent epithelial ingrowth, however, these may cause
adverse effects.
• Suturing the flap after removal of the epithelial cells to create a tight apposition
between the flap and the stromal bed has been shown to reduce the recurrence rate
without the adverse effects of the listed adjunctive treatments.
103. Surgery
• Adjunctive gluing of the flap after epithelial debribement in recurrent
ingrowth cases to improve flap adhesion to the stromal bed has also been
reported to have favorable outcomes.
• Additionally, Nd:YAG laser is another method used to destroy epithelial
cells. This option may be especially useful when cells are encroaching the
visual axis.
• There are also reports of using amniotic membrane as an adjuvant therapy
for the prevention of epithelial in-growth in patients who require
placement of sutures in the visual axis. The membrane has intrinsic
elasticity and if sutured tightly to the episclera, it can serve as a gentle
pressure patch over the flap.
105. • 1.Describe finding
• Glasslike branching lines in the stroma
• 2.What is your diagnosis?
• Lattice corneal dystrophy
• 3.What is the usual presentation for this condition?
• Recurrent corneal epithelial erosion usually start at 4th decade of life, leading
to progressive scarring and visual loss
109. pathology
• Amyloid deposits concentrated most heavily in the anterior stroma
• May accumulate in the subepithelial area, giving rise to poor
epithelial-stromal adhesion
• Epithelial atrophy and disruption, with degeneration of basal
epithelial cells and focal thinning or absence of the bowman layer
increase progressively with age
• Eosinophilic layer between epithelial basement membrane and
bowman layer develops
110. Amyloid stains rose to orange-red with
congo red dye and metachromatically
with crystal violet dye
111. Clinical finding
• Glasslike branching lines in the
stroma
• Refractile lines, central and
subepithelial ovoid white dots, and
diffuse anterior stromal haze appear
early in life
• Lattice lines, are best seen against a
red reflex or with retro-illumination
• Recurrent epithelial erosions occur
often
• Stromal haze and epithelial surface
irregularity may decrease vision
112. • Recurrent erosions are managed with therapeutic contact lenses,
superficial keratectomy, or PTK
• Sever cases of lattice dystrophy with vision loss are treated with DALK
or PK
• Recurrence may occur in corneal graft
• More recurrence rate comparing to granular or macular dystrophy
treatment
MGD is a highly complex disease condition that is associated with or caused by several host, microbial, hormonal, metabolic and environmental factors. The pathways involved in the pathophysiology of MGD proposed by the 2011 International Workshop on Meibomian Gland Dysfunction are shown in Figure 4.[4][17]A comprehensive double vicious circle which takes DED and MGD pathophysiologies into consideration has been proposed recently.[17] As depicted in the Figure 4, obstruction due to increased viscosity of meibum or hyperkeratinization Meibomian gland ductal system leads to decreased secretion of meibum affecting the tear film’s stability leading to dry eyes. A number factors such as aging process, alterations in sex hormones and the expression of their receptors, nutritional status, reduced blinking of eyes, medications and infections and disease conditions such as seborrheic dermatitis influence physical and functional status of Meibomian glands leading to loss of function, morphologic changes, atrophy and gland drop out.[16][13][18][19]Significant alterations in the expression of 400 genes have been reported in meibomian glands in MGD.[20] Furthermore, these changes also impact the composition of meibum leading to instability of tear film.[21][22][23][24]Staph aureus incidence was higher and Coagulase negative staphylococcus, Corynebacterium and streptococci incidence was lower in patients with mild and moderate to severe disease in lid margin swabs after gland expression.[