2. Preface
• All the best for those sitting the ophthalmology board exam.
• This revision has most of the common cases. It is organized as (with
few exceptions):
• 1st slide: a photo for description
• 2nd slide: Important points about the case to know
4. Table of contents
• Neurophthalmology………………………………………………………………p.5
• Paediatric ophthamology……………………………………………………..p.43
• Cornea and external diseases……………….………………………………p.74
• Refractive surgery complications………………………………………….p.152
• Never miss slide! ……………………………….. ……………………………p.171
6. • 35 year old lady with abrupt
onset of OD visual loss.
7. Optic neuritis
• Young women (77%)
• Retrobulbar optic neuritis (2/3)
• Pain with ocular movement (92%)
• First presentation of MS in 30% of patients. If no plaque seen in MRI (25% chance of
subsequent MS), if one or more (72% chance of subsequent MS).
• Uhthoff phenomenon, pulfrich phenomenon.
• In children, commonly bilateral disease and MRI may mimick optic nerve tumor.
• Tx:
• IV methylpred 1g od for 3 days, then 1mg/kg for 11 days.
• IV hastened the resolution of the symptoms only. IV steroid showed reduction in conversion to MS in
patients with acute optic neuritis in subgroup( MRI lesions 2 or more) at 2yr follow up 16% vs 36% in
untreated group, but this effect disappear after 3 yrs.
• NEVER use oral prednisone as a primary treatment because of increased risk of recurrence found in
ONTT.
8. 55 year old hypertensive man with sudden
loss of vision in the right eye
9. NA-AION
• Due to reduced blood supply to the ONH from short posterior ciliary
arteries.
10. 70 year old women with headache, difficulty
chewing.
11. Arteritic AION
• Features in the previous slides
• Smoking is a risk factor
• Granulomatous necrotizing arteritis
• Temporal headache, jaw claudication, constitutional symptoms, fever, high
ESR.
• Biopsy (within 7-14 days of starting steroids), 2-3cm and if negative, may
biopsy contralateral side.
• Tx:
• Stop smoking
• IV methylpred 1g for 3 days (to prevent affection of the other eye, 90% affects in the next 1-7
days). Then 1mg/kg for 6-12 months tapering according to symptoms and ESR.
• PPI and calcium to overcome steroids side-effects
13. LHON
• Mitochondrial inheritance, affects papillomacular bundle early.
• Presents unilaterally affected but is a bilateral disease
• Maternal (mitochondrial) inheritance. However, associated with x-chromosome
abnormalities as well and thus M:F is about 8:1
• Signs:
• Peripapillary telangiectatic microangiopathy
• Disc hyperaemia
• VF central or cecocentral scotoma
• Tx:
• Idebenone (Raxone(®): electron transport chain anti-oxidant: pervent further visual loss.
• Avoid risk factors of optic neuropathy like vitamin deficiencies, smoking, alcohol.
• Refer to cardiology for conduction defect.
• Gene therapy
• Poor prognosis
14.
15. Papilloedema
The following funduscopic features suggest true acquired disc edema:
• Hyperemia
• microvascular abnormalities on the disc surface such as telangiectasis or
flame hemorrhages
• opacification of the peripapillary retinal NFL
• Pseudopapilloedema:
• Optic disc drusens
• Myelinated NFL
• Hypermetropic small crowded disc
• Chronic papilloedema: Refractile bodies, opacification of the RNFL,
optocilliary shunts.
16. IIH
• Headache, tinnitus, TVOs, dipolopia (6th nerve palsy due to tethering at the dorello canal)
• Characteristic MRI findings of intracranial hypertension include flattening of the globe, enlarged optic
nerve sheaths, partially empty sella, and narrowing of the distal transverse sinus.
• Initially need to exclude SOL and venous sinus thrombosis, then need LP to make diagnosis.
• VF: enlarged blind spot. The average blind spot is 7.5° in diameter, vertically centered 1.5° below the
horizontal meridian and 15 ° temporal to the fovea.
• Children can have IIH. LP opening pressure similar to adults and may be more to 280mmh2o.
• Tx:
• Weight loss
• Exclude causes: vitamin A (>100,000 U/day), lithium, tetracycline, doxycycline, minocycline, OCP, steroids
• Headache: paracetamol, diamox
• VF defects: Diamox, frusemide, topiramate
• Progressive VF defects:
• ON sheath fenestrations: If optic nerve more affected
• CSF diversion procedures (Lumboperitoneal or ventriculoperitoneal): if headaches are more of a problems
• Gastric bypass
17. • What are the 3 types of nystagmus associated with this disease?
18. Arnold Chiari Malformation
• Type 1 is the most common.
• Nystagmus:
• Gaze evoked nystagmus (most common)
• Downbeat nystagmus
• Periodic alternating nystagmus
20. 6th nerve palsy
• Isolated: Mostly ischaemic
• DDx: Duane, mysethenia, restrictive causes,
IIH
• MRI indicated: young, if no vasculopathic
diseases, papilloedema, severe headaches.
• F/U: 6 weeks to 3 months
• Tx:
• Patching, prisms.
• Surgery:
• If forced generation is +ve (Good 80-100%, Fair 50-
80%)): medial rectus recession +/- lateral rectus
resection.
• If forced generation is –ve (< 50%): Vertical muscle
transposition, knapp procedure or best now is
Hammelsheim split tendon with foster
modification.
21. 50 year old with sudden drooping of the lid
and diplopia.
22. Oculomotor nerve palsy
• Diagnostics for isolated third nerve palsy:
• Pupillary involving: Aneurysm until proven otherwise
• Pupillary sparing
• Complete: Ischaemic
• Non-complete: Maybe aneurysm, therefore F/U daily for 5 days for pupillary involvement or otherwise do CTA.
• The pupillomotor fibers of the oculomotor nerve reside superficially in the medial aspect of the nerve
adjacent to the junction of the PCoA and internal carotid artery, a common site for aneurysm formation.
• Pupillary abnormality without involvement of the extraocular muscles is almost always benign.
• The vasculopathic form of oculomotor nerve palsy may produce some efferent pupillary defect in up to 20%
of cases, although the pupillary involvement is generally mild (typically :I mm anisocoria).
• Divisional oculomotor palsy (i.e. only certain muscles are involved) warrant MRI as the divisions of the third
nerve may occur in the cavernous sinus (although typically at the entrance of the superior orbital fissure).
• If pupil-involving and imaging/angiography are negative (Start with CTA and then may consider MRA), an LP
should be considered.
• Aberrent regeneration (Eyelid-gaze or pupil-gaze dykinesis) indicated tumor or trauma or congential.
• F/U after 3 months for ischaemic palsy and meanwhile to see internest.
23. • 50 year old man with diplopia on
left gaze and abnormal eye
movement
24. Internal ophthalmoplegia (INO)
• Defect in the MLF.
• DDx: Duane, medial rectus palsy, myasthenia
• Signs: limited adduction with abducting eye nystagmus,
skew deviation.
• WIBINO (Wall eyed) in bilateral INO (pic), most common
cause is demylination similar to unilateral INO.
• WIBINO is associated with upbeat nystagmus and skew
deviation.
• Convergence intact in posterior INO (because in anterior
tract which is caudal is close to the convergence centre;
therefore posterior preserved, anterior absent)
• Causes: MS, stroke, masses.
25. • 50 year old with bilateral repetitive squeezing of the eyes.
26. Essential belpharospam
• Onset between 40-60 years
• Bilateral disease
• Cause: Dysfunction in basal ganglia
• Workup:
• Exclude local ophthalmic cause especially dry eyes, inflammation, photophobia.
• Neuroimaging non-revealing.
• Tx:
• Botox: Treatment of choice
• Neuroleptics
• Tinted glasses
• Surgery: Rarely which includes extirpation of the orbicularis or seventh nerve
ablation.
27. • 70 year old lady with episodic spasms of half of her right face.
28. Hemifacial spasms
• Unilateral
• Cause: seventh nerve root exit zone by an aberrant vessel (normally
vertebrobasilar artery) leading to abnormal motor firing.
• Less than 1% is caused by cerebellopontine tumors, therefore MRI is indicated.
• Tx:
• Botox (repeated every 3 months)
• Carbamazepine, clonazepam, or baclofen may provide improvement in some patients.
• Suboccipital craniectomy with placement of a sponge between the seventh nerve and the
offending blood vessel (microvascular decompression) may be considered for advanced
cases or younger patients. Surgical decompression may offer a cure but carries higher risks
than alternative treatments.
• A rare disorder called spastic paretic (weakness + spasms) of facial muscles can
be caused by pontine tumors.
29. • 50 year old patient came with twitching of multiple muscle areas in
the left side of his face.
30. Facial myokymia
• Unilateral
• fine fascicular muscle movement.
• It is usually the result of a pontine glioma in children and multiple
sclerosis in adults.
• Tx:
• carbamazepine, phenytoin sodium
• Botox
31. 50 year old with sudden onset of facial pain
and weakness.
32. 7th nerve palsy
• Bell’s palsy is a diagnosis of exclusion.
• Bilateral 7th nerve is seen in sarcoidosis at the parotid glands or meningitis
or gullian barre.
• Facial diplegia, ataxia and ophthalmoplegia is seen in miller fisher
syndrome (variant of Gullian barre). A high percentage of patients with
Miller Fisher syndrome have anti-GQlb IgG antibodies in their serum.
• In Melkersson-Rosenthal syndrome, recurrent unilateral or bilateral facial
paralysis is accompanied by chronic facial swelling and lingua plicata
(furrowing of the tongue). Cause unknown.
• Other etiologies include cerebellopontine tumors (can result in
neurotrophic and neuroparalytic keratitis; requires early punctal plugs,
tarsorrhaphy, gold weights or botox) or infectious like lyme’s disease.
34. Pituitary Apoplexy
• Ophthalmic emergency, need to refer to neurosurgery
• Can be from a pre-existing tumor or no tumor after blood loss in
pregnancy (sheehan’s syndrome).
• Classification of pituitary tumors?
• Secretory (75%): Mostly microadnomas
• Chromophobes (50%): Prolactin
• Acidophils (20%): GH
• Basophils (5%): TSH, LH, FSH
• Non-secretory (25%):
• Microadenoma (<10mm)
• Macroadenoma (>10mm)
35. VF in pituitary tumors
• Central (80%)
• Pre-fixed (15%): Chiasm
anterior to pituitary: macular
bitemporal hemianopia (due
to compression of the macular
fibres running in the posterior
chiasm or the optic tract).
• Post-fixed (5%): Chiasm in
posterior to pituitary: RAPD
(due to direct compression of
the optic nerve) + junctional
scotoma.
38. 45 year old lady with mild ptosis which gets
worse in the course of the day.
39. Myasthenia gravis
• Fluctuations
• Must think about it in young with ptosis. Orbicularis is often involved.
• Penicillamine can have MG like effect.
• Diagnostics:
• Rest test: 30 mins of eye close improve the ptosis
• Fatigability test: Looking upwards for 1 min worsens the ptosis
• Ice-pack test: improves ptosis after 2 min
• Ach receptor autoantibodies
• Single muscle fibre EMG
• Tenislon test: Injecting 0.2mg, 0.4mg or edrophonium. Must be under monitor and atropine standby.
• CXR/CT for thymoma and TFT for thyroid dysfunction.
• Tx:
• Surgery for thymoma (considered as the cause of the antibodies).
• If breathing or swallowing difficulty refer urgent to neurology.
• Pyridostigmine
• Steroids: second line but may precipitate respiratory distress therefore patient must be hospitalized.
• Others like azathioprine.
41. Superior oblique palsy
• Congenital: High fusional amplitudes (up to 35PD), asymmetrical face, larger on side of
deviation.
• Unilateral vs bilateral (V pattern, excyclotortion >10*, diplopia with left and right gaze,
chin-down)
• Fusional control weakens over time, resulting in a deviation that becomes manifest in
later life, that is why patient present late in teenage years or adults.
• Good to see old photos
• Tx:
• Hypertropia <15 PD: Graded recession with anteriorization ipsilateral inferior oblique muscle
• Hypertropia >15 PD: Graded recession and anteriorization ipsilateral inferior oblique muscle, and
contralateral inferior rectus recession (if there is a significant hyper in down gaze)
• Extorsion: Treated with Harada-Ito
• Bilateral cases treated with bilateral tuck
42. Head Tilt Test Made Easy (from Kenneth wright)
Because of the complexity of the three-step test, it is difficult to do it in
your mind without a paper and pencil and at least one textbook on
strabismus. A trick that simplifies the three-step test is to consider the
head tilt first. If the hypertropia increases on head tilt to the side of the
hypertropia then an oblique muscle is paretic. A hypertropia that
increases on head tilt to the opposite side of the hypertropia is caused
by a paretic vertical rectus muscle. This quickly narrows the field of
possibilities. For example, a left hypertropia that increases on head tilt
to the left (same side as the hypertropia) indicates a paretic oblique
muscle either LSO or RIO. If the left hypertropia increases in right gaze
it is a paretic LSO. If the left hypertropia increases in left gaze it is a RIO
palsy.
45. Infantile esotropia
• Uncommon in the first 3 months of life and if it happens likely to persist.
• Exotropia by contrast is common. Exotropia is more commonly controlled by the high convergence
amplitudes (up to 30PS) and in contrary the esotropia are unlikely controlled due to poor divergence
amplitudes (6-8PD)
• Triad of motor abnormalities:
• IOOA with V pattern
• DVD
• Latent nystagmus: Bilateral jerky nystagmus towards the fixing eye manifests when one eye is occluded
• The mild abduction deficit on version movement can be tested with dolls eye movement (it will disappear; if
persisting test with OKN if saccades are present then it is likely a tight muscle secondary to infantile
esotropia). Differentiate from pseudo-esodeviation (epicanthal folds, Narrow IPD, -ve angle kappa)..
• Tx:
• Treat between 6 months and 2 years. At least 2 consecutive visits are required (1 month apart) with stable angles (early
management superior sensory outcome but higher number of procedures required).
• Alignment can be treated before amblyopia. Patching for amblyopia may be initiated before surgery and end point is
alternate esotropia.
• Aim for some peripheral fusion and Monofixation syndrome (small angle esotropia) is a favorable outcome (central
suppression, peripheral fusion and microtropia). Angle needs to be < 10PD.
46. DVD
• Tx:
• If IOOA, recession + anteriorization
• If no IOOA, superior rectus fadenization or less often recession (associated
with hypotropia).
48. Accommodative esotropia
• Manifests normally after 6 months. If in the first 6 months likely to be infantile esotropia.
• non-Refractive or high AC/A ratio: a quick test is to measure deviation at distance and then at near 0.33m . If
at near more than 15PD (accommodates 3D and thus with AC will be 15PD for AC/A ratio of 5).
• Refractive gets worse until 5-7 years before getting better
• Partially accommodative can be treated surgically
• High AC/A ratio can be treated with executive or flat topped bifocals and then weaned off at 10 years.
• When correcting hyperopia, power can be decreased after full correction to aid the emmotropization
process (however, esophoria should be <10 to allow the divergence amplitude to work and does not disrupt
binocular fusion).
• Acquired non-accommodative commitment esotropia
• (DIVERGENCE PARESIS PATTERN):
• In children usually secondary: Look for Arnold chairi malformation or potine tumors, trauma or high ICP. Thought to have central loss of
fusion (6th nerve palsy, but paresis still is not evident).
• In adults (>50 years) usually primary: resolves spontaneously after several months.
• Tx: bi-lateral resection
• Basic type (esotropia similar at distance and near):
• Usually after acquired cause such as hyphaema, ptosis ….etc
50. Exotropia
• Exotropia is more commonly controlled by the high convergence
amplitudes (up to 30PS) and in contrary the esotropia are unlikely
controlled due to poor divergence amplitudes (6-8PD)
• Risk factors for exotropia include maternal smoking during pregnancy,
premature birth, family history of strabismus, and uncorrected refractive
errors.
• Types: As with esotropias, can be primary or secondary.
• Primary is either constant (mostly infantile and basic, often associated with CNS
abnormalities) or
• Intermittent (which is also variable with near and more with distance). Intermittent is
the most common type. If near is worse, think about convergence insufficiency (no
distance exo) or convergence weakness (near exo worse than distance exo).
51. •Intermittent: Can occur in the first year of life. Worse with far vision (therefore parents might not notice it early) mostly noticed during fatigue.
oTrue distance exotropia with normal AC/A is rare.
oThe difference is usually due to tenacious proximal fusion, a slow-to-dissipate fusion mechanism at near (fusional convergence), but it may also be due to a high
accommodative convergence/ accommodation (AC/ A) ratio; however, a high AC/ A ratio occurs much less commonly in exotropia than in esotropia. To differentiate between
the two use extended cover test (45mins) and then +3 lens. The difference for pseudo divergence excess is within 10PD.
Control of exotropia is important:
History: Poor control = dissociates when fully awake, and if > 1/2 of the day, or if dissociates does not become straight (duration) + progression )if worsening)
Examination: assess stereopsis, spontaneous breaking, angle of deviation, If exotropic on initial obervation, or if dissociates after 30s. Then check grades of re-fixation as above
table.
Surgery is done after 4 years of age to avoid the consecutive esotropia.
Surgical correction for pseudo divergence excess (neutrilize after patch test, they become the same) is based on
distance PD. However if true divergence excess based on mean of distance and near.
True divergence excess is usually due to high AC/C ratio. Therefore after surgery, they might need + lenses because the
high AC/A ratio persists.
52. Nystagmus
• Nystagmus arises from imbalances in the vestibulo-ocular or gaze-holding system; it may
also arise in the smooth pursuit, optokinetic, or rarely the vergence system.
• Must have slow phase (abnormal movement). If no slow phase, called intrusions or
oscillations.
• The most common cause of sea-saw nystagmus is craniopharyngioma.
• Can be:
• Congenital (Jerky most common) or acquired
• Jerky or pendular
• Congenital:
• Jerky, abolishes with sleep, horizontal, no oscillopsia.
• Must exclude organic diseases or the eye
• Can be idiopathic motor nystagmus (diagnosis of exclusion), or latent nystagmus or spasmus nutans
(head nodding, pendular disconjugate can be uniocular nystagmus and torticollis - Must do MRI to
exclude parasellar glioma – self resolves after 2 years).
• If null point: either to use prisms or surgery on all muscles opposite to the null point from primary
position. (Kestenbaum procedure)
• Acquired: see table opposite, vestibular nystagmus is very important.
• Tx:
• Treat underlying cause
• Beclofen in PAN
• Kestenbaum procedure
53.
54. Monocular elevation syndrome
• Restriction in both adduction and abduction
• Ptosis or psuedoptosis (50% / 50%). Pseudoptosis because of the common sheath between superior rectus and lavator muscle.
• Can be due to:
• Restriction
• positive forced duction on elevation
• normal elevation force generation and elevation saccadic velocity (no muscle paralysis)
• often an extra or deeper lower eyelid fold on attempted upgaze
• poor or absent Bell phenomenon
• elevator muscle innervational deficit
• free forced duction on elevation
• reduced elevation force generation and saccadic velocity
• preservation of Bell phenomenon (indicating a supranuclear cause) in many cases
• Combination
• positive forced duction on elevation
• reduced elevation force generation and saccadic velocity
• Tx:
• If restriction originating from below the eye is present, the inferior rectus muscle should be recessed, using an adjustable suture if possible.
• If there is no restriction, the medial and lateral rectus muscles can be transposed toward the superior rectus muscle (Knapp procedure).
• Alternatively, the surgeon can recess the ipsilateral inferior rectus and either recess the contralateral superior rectus muscle or resect the ipsilateral
superior rectus muscle.
• Ptosis surgery should be deferred until the vertical deviation has been corrected and the pseudoptosis component removed.
55.
56. Brown syndrome
• Abnormal superior oblique tendon/trochlea complex
• Cause: trauma, inflammation, congenital.
• Tx:
• Observation if straight in primary gaze
• Treat underlying condition
• Massage
• Tenotomy nasal to superior rectus
• Spacer
58. Duane retraction syndrome
• Cause is agenesis of the 6th nerve nucleus
• Treatment (Duane retraction syndrome): Normally these patients have
good stereopsis.
1) Treatment of amblyopia: Normally due to anisometropia
2) Deviation in primary position (along with abnormal head posture): For
DRS 1, medial rectus recession (if >20PD, bimedial rectus recession). DRS
2, lateral rectus recession.
3) Upshoot or downshoot: This is normally caused by abnormal strong firing
of the lateral rectus innervation (leash phenomenon). Y split procedure
of the lateral rectus or faden suture.
4) Retraction of the globe: Recession of all horizontal muscles in both eyes
(but with different amplitudes, medial less).
60. • DDx of oil droplet sign:
• Keratoconus: The anterior cone
• Galactosemia: The influx of water changes the refractive error of the lens and
thus appears as oil droplet (not a true cataract)
• Posterior lenticonus: Sporadic isolated disease
62. Optic nerve hypoplasia
• Visual acuity may range from 20/20 to no light perception.
• Cause: Drugs (phenytoin, LSD) or DM (more of segmental hypoplasia)
• Because visual acuity depends only on the degree of papillomacular nerve fiber bundle
hypoplasia, it does not necessarily correlate with the overall size of the disc.
• the outer ring itself corresponds with the abnormal extension of the retina and pigment
epithelium over the outer portion of the lamina cribrosa; and the inner ring corresponds to the
hypoplastic optic nerve
• septo-optic dysplasia (de Morsier syndrome) describes the constellation of optic nerve
hypoplasia, absence of the septum pellucidum, and partial or complete agenesis of the corpus
callosum, absence of the pituitary infundibulum with or without posterior pituitary ectopia
• Tx:
• Correct any refractive error and amblyopia.
• Endocrinology consultation. Most common deficiency is growth hormone followed by TSH (neonatal
jaundice). If Corticotrophin releasing hormone is absent, can result in sudden death from hypoglycemia.
66. Morning glory (see flower) syndrome
• Unilateral and typically female, same spectrum as coloboma and can
have serous RD similar to pit.
• Central funnel shaped excavation
• Core of glial tissue with radiating vessels.
• Visual acuity ranges from 20/20 to no light perception
• Complications: Serous RD
• Associations: Exclude myomyo (therefore MRI) and PHACEs
67. Diffrenciate true bitemporal superior
quadrantinopia from tilted disc syndrome
• Features of tilted disc syndrome:
• Titlted discs on fundoscopy
• VF defect does not respect vertical line
• VF disappears with refractive correction (usually myopia)
• Associated with oblique astigmatism which might be lenticular.
68. Congenital corneal anomalies
• Microcornea: AD, associated with other anomalies
• Macrocornea: Most common is X-linked recessive
• Cornea plana: AR
69. Corneal dystrophies
• CHED AR (previously CHED2) : appears at birth, nystagmus, non-
progressive
• CHED AD (CHED 1): presents later at 2 years, same entity as PPMD.
Now eliminated from the IC3D
• PPMD: AD, can be unilateral, can be glaucoma in 1/3 of cases, snail
track, multilayered endothelium.
70. Notes on metabolic diseases
1) Lysosomal storage diseases are a group of disorders resulting from defects in the
lysosomal enzymes either to breakdown lipids (diseases called
(gangliosidosis/sphinolipidosis) or glycoproteins called (mucopolysaccharides).
• Cherry red spot: Results from opacification of the RNFL due to accumulation of the
sphingolipids. Seen gangliosidosis or sphinolipidosis resulting in neurodegeneration.
• Examples: Tay-sach (more common in ashkenzie jews), neiman pick, gauchers, farber (all
autosomal recessive) and fabry’s disease (x-linked recessive- no cherry red spot though).
• Corneal opacification: Results from progressive opacification of the corneal due to
accumulation of mucopolysaccarides.
• Examples: Hurler syndrome, Schie (autosomal recessive), Hunter (less corneal clouding, x-linked
recessive).
2) Corneal crystals: Seen in defective metabolism of cysteine. Crystals deposited in the
cornea and retina. Oral cysteamine has been shown to alleviate the systemic problems but
not the corneal crystal deposition. Topical cysteamine eyedrops can prevent or reverse
painful crystalline keratopathy.
72. ROP
• Know:
• Risk factors
• Screening guidelines
• Zones, stages, plus and rush disease
• Cryo-ROP, ETROP (type 1 and type 2, tx with laser), Beat-ROP studies (tx with
anti-VEGF; advantages include better VF, less myopia).
• When to stop screening
73. Most common manifestation of congenital
infections
• Rubella: Pigmentary retinopathy
• CMV and toxo: chorioretinitis
• Microphthalmia: CMV, Rubella
• Syphilis: Interstitial keratitis
76. Bacterial keratitis
• Most common microbial keratitis.
• All keratitis should be treated initially as bacterial unless another organism
is cultured otherwise or patient is not improving.
• Neisseria gonorrhoeae, Neisseria meningitidis, Corynebacterium
diphtheriae and Hemophilus influenzae are able to penetrate a healthy
corneal epithelium, usually in association with severe conjunctivitis.
• Bacterial keratitis associated with conjunctivitis (thus a lot of discharge) are
H.influenza, pneumococcus and Neisseria gonorrhea.
• Infective keratitis have are normally central and the epithelial defect is
larger than the infiltration (immune keratitis: epithelial defect is smaller
than infiltration).
•
77.
78. 60 year old post trauma with vegetative
matter
79. Fungal keratitis
• Risk factors: Trauma, steroid use
• Organisms:
• In diseased eyes: candida is more common
• In non-diseased eyes: fusarium or aspergillus
• Signs: Feathery margins, satellite lesions, endothelial plaques, infective
hypopyon.
• Treatment:
• First line is polyenes (fungicidal), natamycin for filamentous, amphotericin B for non-
filamentous. Voriconazole is an azole which is fungistatis for both filamentous and non-
filamentous.
• Systemic fluconazole or itaconazole are used in deep ulcers and because the hypopyon is
infective.
• Non-responsive: revisit the (diagnosis, cultures, sensitivities), rescrape, take
biopsy, and last is therapeutic keratoplasty.
81. Acanthamoeba keratitis
• Risk factors: swimming with CL, cleaning CL with tap water
• Symptoms more than signs due to radial perineuritis.
• Signs (early to late): Punctate epitheliopathy, pseudodandrite, radial
perineuritis, ring ulcer.
• Stain: Chalcoflour stain, Culture: Non-nutrient agar with E.Coli.
• Diagnosis can be augmented by confocal microscopy to look for cysts.
• Tx:
• Biguanide (cystacidal; either PHMB or chlorhexidine) +
• Diamidine (doe not affect cysts): like propamidine (prolene) +/-
• Oral anti-fungal (e.g. itraconazole, voriconazole)
82. ).
Figure 3.1.1. Alkali burn.
Increased IOP, second- and third-degree burns of the surrounding skin, and loca
83. • Alkaline burn (most common ammonia) more common than acid (hydrochloric or sulphuric acid). Hydrofloric acid acts like alkaline.
• Alkali penetrate (saponification), acid surface damage (coagulative necrosis and denatures protein and precipitate on surface).
• Grading by Hughes (modified by ropper hall seen above), Dua classification involves limbal stem cells and conjunctival ulceration).
• General principles of management (phases of injury):
• Immediate phase: irrigation and assessment
• Acute phase (week 1): Decrease the chance of infection and further injury by inhibiting collagenases as well as acute IOP rise
• Early reparative phase (weeks 2-3): promote healing
• Late reparative phase (> 3 weeks0: Treat surgically symplepharon, corneal scarring.
• IOP rises:
• Acute: Especially alkali burns, penetrates to the stroma of the cornea leads to damage and loss of the proteoglycans and thus collagen shrinkage which distorts the
globe at the trabecular meshwork).
• Intermediate: Uveitis due to breakdown of the blood aqueous barrier.
• Late: Trabecular meshwork damage
• Tx: copious wash (double evertion of lid), epithelial debridement, tetracycline ointment qid, cycloplegia, preservative free lubrications, steroids (anti-
collagenases), citrate (to chelate ca need for neutrophils to degranulate to reduce collagenases), ascorbic acid (to replenish the AC stores due to
impaired secretion from the damaged ciliary body and due to the increased demand used in the healing of cornea), N-acetylcestine (optional
anticollagenase), Systemic doxy also optional.
• Options of amniotic membrane, BCL and serum eyedrops are optional.
• Borate-buffered saline and amphoteric solutions were found to be most effective in reducing aqueous humor pH after an alkali burn. Normal saline
and tap water were found to be intermediately effective, and phos- phate buffered saline and lactated Ringer’s were found to have the least effective
buffering capacity
• Steroids should be reduced after 1 week, to promote healing. To use medroxyprogesterone if prolonged steroids is needed as it does not hinder
healing.
• Surgery: amniotic membrane, tarsorrhaphy, tenoplasty, limbal stem cells transplantation, corneal grafting including keratoplasty.
Table 13-1 The Hughes Classification of Ocular Alkali Burns
Grade I Grade II Grade Ill Grade IV
Corneal epithelial Corneal epithelial Total corneal epithelial Opaque cornea
defect without defect with stromal defect, with stromal obscuring view
limbal ischemia haze and ischemia haze obscuring iris of iris or pupil;
affecting less than details and ischemia ischemia of greater
one-third of the affecting one-third than one-half of the
limbus to one-half of the limbus
limbus
84. 25 year old admitted to ICU with skin
breakdown
85. SJS
• Erythema multiforme minor or major (SJS) or severe form TEN
• Cause: drugs (sulphonamides) or infectious (mycoplasma)
• Signs
• Acute phase: Conjunctival congestion, chemosis, discharge, epithelial defects
• Cicatricial phase: symblepharon, short fornicies, trichisis, entropion/ectropion
and lagophthalmos, loss of stem cells, corneal scarring and
conjunctivalization.
• Treatment:
• Acute phase: artificial tears, weak steroid, topical antibiotic, lysis of
membranes, amniotic membrane within 2 weeks
• Cicatricial phase: surgery, stem cell transplantation, keratoprosthesis.
86. Limbal Stem cell transplantation
• Can be autogenic,
allogenic (from
related donor or
cadaveric) or
cultivated (CLET,
SLET or COMET)
• Also can be
keratolimbal (for
bilateral disease) or
conjunctival.
87. • 45 yr old with eye discomfort
Meibomian gland dropout increases with age in normal
subjects,43
not necessarily in response to the presence of
obstructive MGD. Obata has suggested that gland dropout also
occurs as an age-related atrophic process.78
It is hypothesized
that measurable dropout is a feature of MGD and increases
with MGD severity. Loss may be proximal (at the attached
border of the lid), central, or distal (at the free margin of the
paste-like material (Figs. 6–8). These qualities have been incor-
porated into various grading schemes.75,96,97
Alternatively, the
FIGURE 5. Photographic montage of the lower lid viewed by transil-
lumination meibography. There is extensive meibomian gland dropout
in a patient with meibomian gland dysfunction (courtesy of N. Yokoi).
FIGURE 7. Meibomian gland dysfunction: expression of opaque
meibum (courtesy of D. Korb).
2012 Tomlinson et al. IOVS, Special Issue 2011, Vol. 52, No. 4
88. • Dry eyes can be due to aqueous deficiency or evaporative
• Evaporative is more common.
• Inspissated: Thickened, heavy blocked glands
• Symptoms: Discomfort, irritation, FB sensation, momentary blurring of vision.
• Assessment:
• Inspection: Roseacea, eyelid notching, ectropion, lagophthalmos with poor bells
• Lids for hyperaemia and MGD: try expressing meibum and assess the color and thickness of it. Retroillumination to assess MG dropout (above photo). Lid scarring.
• Assess the tear lake, and hyperaemia, scarring or neovascularization of cornea.
• Investigations:
• Osmolality: a screening tool for both aqueous deficiency and evaporative dry eyes
• Schirmer test: Tests aqueous production
• Basic secretion (with anaesthesia): <5mm in 5 mins abnormal
• Schirmer I (without anaesthesia): <10mm in 5 mins abnormal
• Schirmer II (includes irritation of the nasal mucosa as well)
• TFBUT: Test mucinous layer (Dark spot < 10s)
• Lassimine green (better than rose bangal) : Any epitheliopathy in cornea and conjunctiva, tests for devitalized cells which lost their mucinous layer.
• Impressin cytology: To count goblet cell number
• Treatment (according to the cause):
• MGD: Open blocked ducts, worm compress, lid hygiene and massage, tetracycline or doxycycline ( to reduce MMP)
• Aqueous deficiency: Tear supplements and punctal plugs
• Mucinous layer: Systane
• Others: Steroids, cyclosporine to reduce the inflammation, no evidence for omega 3
Meibomian gland dropout increases with age in
subjects,43
not necessarily in response to the pres
obstructive MGD. Obata has suggested that gland drop
occurs as an age-related atrophic process.78
It is hypot
that measurable dropout is a feature of MGD and in
with MGD severity. Loss may be proximal (at the a
border of the lid), central, or distal (at the free margin
lid) or may involve the whole gland. Extensive dro
associated with increasing evaporative water loss fr
eye.86,87,90
It will be important in the future to
whether total loss of meibomian gland mass and/or nu
affected glands and/or site of dropout (e.g., proxima
distal) has the greatest effect on the other meibomian
including clinical lid characteristics, size of the margin
reservoir, spread and integrity of the lipid film, lipid c
tion, and the evaporation rate. No study to correlate t
tion of dropout with the presence of plugging or the e
ibility or quality of expressed lipid has yet been condu
could be anticipated that distal dropout, close to the
would have the most profound functional effect a
correlate most closely with a diagnosis of MGD. It
unclear whether lipid composition would be altered
gland with partial dropout.
FIGURE 5. Photographic montage of the lower lid viewed b
lumination meibography. There is extensive meibomian gland
in a patient with meibomian gland dysfunction (courtesy of N
89. • The main ingredient of artificial tears are hydrogel polymers, so called
because of their ability to retain water. The following hydrogels have been
used in artificial tear substitutes: hydroxypropyl methylcellulose, carboxy
methylcellulose, polyvinyl alcohol, Carbopol, polyvinylpyrrolidone,
polyethylene glycol, dextran, hyaluronic acid, or carbomer 940 (polyacrylic
acid).
• Systane: Hydrogel exists as monomers in a borate-containing solution in
the dispensing bottle. After instillation to the patient’s eye, contact of
hydrogel with the patient’s tear, which is at a different pH, causes the
hydrogel to cross-link with borate to create a more viscous and elastic
matrix with an increased duration of effect compared with th other eye
drops.
91. Ophthalmia neonatorum
Timing
• Chemical irritation: first few days.
• Gonococcal: first week.
• Staphylococci and other bacteria: end of the first week.
• HSV: 1–2 weeks. (systemic vesicles).
• Chlamydia: 1–3 weeks. (systemic features of pneumonitis and otitis media)
Tx:
• Erythromycin elixir 50 mg/kg/day orally in four divided doses for 14 days, plus
erythromycin ointment q.i.d. (for chlamydia)
• Cefotaxime 100mg/kg single dose (for gonococcus)
• Others: bactericin, tobramycin, gentamicin or moxiflox.
92.
93. Cicatricial conjunctivitis
• Causes:
• OCP
• SJS
• Chemical burn
• Trochoma.
• OCP: mucous membrane disease in old women, type II hypersensitivity
reaction, immunhisto shows antibody attached to basement membrane.
Symptoms of dysphagia. Stages shown in table. Tx dapsone for mild to
moderate disease, other immune modulators, cyclophosphamide reserved
for severe cases.
• EM/SJS/TEN: most commonly secondary to Sulphur meds or allopurinol.
95. Interstitial keratitis
• Usually a retrospective term used for corneal scar with
vascularization.
• Immune mediated keratitis on a quiet eye
• Associated with syphilis, Herpes, EBV, measles…
• First associated with syphilis. Congenital infections are usually
bilateral associated with red eye.
97. HSV dendritic ulcer
• Represents HSV active viral replication similar to necrotizing stromal
keratitis.
• Dendrites with end-bulbs. Stains well with flurecein.
• Can start as PEEs, then becomes dendritic and then geographical.
• DDx
• Varicella virus epithelial keratitis: can be as part of herpes zoster ophthalmicus, no
end-bulbs, stains more with Rose-Bengal
• Tx:
• The dendrites may be debrided.
• Acyclovir eye ointment 5/day for 14 days, tapered quickly
• Cycloplegia
99. Disciform keratitis
• A type of non-necrotizing stromal keratitis, sometimes referred to
endotheliitis.
• Represents an immune reaction rather than active replication.
• Tx:
• Prophylactic oral dose acyclovir 400mg bid (or valcyclovir 500mg od)
• Predforte tapered slowly over weeks.
• Cycloplegia.
103. Corneal ectasia
• PMD (beer-belly): protrusion is above the thinning point. Varient of keratoconus, but presents
later. pellucid, meaning clear, to describe this thinning disorder. These corneas are generally
clear and avascular, with no iron ring,infiltrate, or lipid deposition.
• Keratoglobus: If congenital usually associated with Ehler danlos or brittle cornea syndrome. If
acquired, variant of KC.
107. PAM
• Light skinned individuals, unilateral, may progress to melanoma if
with atypia as shown in the second picture.
• PAM with atypia progresses to conjunctival melanoma in 36%-75% of
cases. High risk if > 3 clock hours.
• Conjunctival melanoma arises from PAM with atypia in 70%.
• BAM: racial melanosis, bilateral, dark complexion individuals.
108.
109. Lymphoproliferative conjunctival lesions
• Salmon pink colour
• Reactive hyperplasia Vs lymphoma: Need biopsy
• 1/3 have systemic lymphoma
• Percentage of systemic lymphoma: eyelids 67% > orbit (35%) >
conjunctiva(20%);
• Tx:
• External beam radiotherapy if localized
• If with systemic lymphoma, need chemotherapy.
110.
111. OSSN
• Spectrum of dysplasia, CIN, carcinoma in
situ and invasive SCC.
• Arises close to limbus, thought to be
limbal dysplasia.
• Risk factors: sun, HPV, HIV, xeroderma
pigmentosa.
• 3 types as seen opposite.
• Tx:
• Excisional biopsy if < 3 clock hours. If > clock
hours, incisional biopsy; if invasive
chemoreduction then surgery; if non-invasive
topical chemotherapy..
• IFN alpha 2b to easiest to use for topical
chemo.
112. • Rose bengal to delineate
the extent of the lesion.
115. DystrophyDegeneration
Often centrally locatedOpacity often eccentric or
peripherally located
Bilateral & symmetricUni/or Bilateral, may be
asymmetric
Presents early in life,
hereditary
Presents later in life,
associated with aging
Progression usually slowProgression variable: very
slow or rapid
AvascularPossible vascular changes
Rare associationLocal or systemic disease
commonly associated Samer Al Suwailem,
BSC 2015
116. Exceptions:
oNon-hereditary: EBMD
oUnilateral: PPCD (However PPCD is mostly bilateral)
oSystemic: MCD, LCD2, Schnyder corneal dystrophy
oMap to same gene (TGFB1), but diff. phenotypes
oYoung except: EBMD, Fuchs
oDoes not recur in grafts: PPCD, Fuchs
oHighest rate of graft recurrence: Reis-Buckler
oAutosomal dominant except (GMC3):
o Gelatinous
o Macular
o Nystagmus associated CHED
o Type 3 lattice
120. Epithelial basement membrane dystrophy
• A.k.a map dot, cogans, anterior basement…
• The most common dystrophy BUT
Thought to be degenerative
- Map lines: subepithelial connective tissue
- Microcysts: white, putty-like dots (degenerated
epithelial cells trapped in abnormal epithelium)
- Fingerprints: parallel lines of basement membrane
separating tongues of reduplicated epithelium
• 10% with the dystrophy get erosions, 50% with
erosions have the dystrophy
• Missing hemidesmosomes
• Diabetes leads to dysfunctional hemidesmosomes and
thickenings of basement membrane.
121. Meesmann (Juvenile hereditary epithelial
dystrophy
• Early onset in life
• RCE, photophobia
• Central Bubble-like blebs or
cysts (interpalpebral) clear in
retroillumination & grey in
direct illumination
• Histo: epithelial cells
contain cysts of PAS-positive
material (peculiar substance);
thickened epithelial
basement membrane
122. Gelatinous
• AR (rare)
• 1st decade
• Droplike (sub epithelial amyloidosis,
primary familiar amyloidosis)
• Histo: Absence of Bowman’s layers
and replacement with subepithelial
amyloidosis.
• Interpalpebral Band keratopathy / or
Mulberry nodules which stain with
flourescein
124. Reis-Bucklers’ (Corneal Dystrophy of
Bowman’s Membrane Type I)
• AD, TGFBI
• Early in life
• Absence of basement
membrane and replaced with
connective tissue staining with
masson trichrome.
• Clinically: Coarse geographical
opacities.
127. Stroma
• Four corneal dystrophies, linked to
TGFBI gene (AD), Chromosome 5q,
including:
• Reis-Bückler
• Granular,
• Lattice
• Avellino
• located on chromosome 5q31
codes for keratoepithelin, a
protein secreted by corneal
epithelium. This protein acts as an
adhesion protein and is present in
normal stroma. Accumulates
when mutated in stroma.
130. Lattice
• TGFBI
• Three types
• Type II associated with
systemic amyloidosis
• Congo RED
• Hyaline lines clinically
• Most common stromal
dystrophy worldwide
• Most common stromal
dystrophy with recurrent
corneal erosion.
131. Granular
• TGFBI
• Intervening stroma
• Hyaline deposits
• Tx:
• PTK is not recommended as it
may lead to more scarring.
132. Others
• Schnyder, associated with High lipids/cholesterol. Control of
dyslipidaemia will not affect the prognosis of the disease.
134. Guttata
• Central (Guttata): Focal excresences
in Decemets membrane (Excess
collagen)
• Periphery (normal degnerative
change with age) called Hassel
Henle bodies.
• Polymegathism, polymorphism
135. Fuchs Endothelial dystrophy
Beaten Bronze
• AD
• Morning blurring of vision
• Cause pseuodphakic bullous keratopathy
• Can be early onset of late onset
• Most common in postmenopausal women
• Beware surgery if <1000/mm2 or if CCT >640um.
136. Posterior polymorphous corneal dystrophy
(PPCD)
• AD
• Early in life
• Endothelium behaves like
epithelium with multiple
layers and can migrate to
angle (glaucoma 15%).
• Clinically broad-bands with
scalloped edges.
• DDx: Congential glaucoma,
ICE/anterior segment
dysgensis.
137. Congenital Hereditary Endothelial Dystrophy (CHED)
• DDX: Clouding of cornea
in newborns with
nystagmus (AR CHED,
previously CHED 2).
• CHED 1 is AD
• Early onset
139. Which one is not inherited in AD manner?
• Macular
• Reis-Buckler
• Granular
• Fuch’s
√
140. Which one of these is not correctly matched
to its tissue stain?
• Macula-Alcian blue
• Granular-Congo red
• Lattice-Congo red
• Avellino- Congo red
√
148. Scleritis
• Infectious (rare) or non-infectious
• 50% associated with systemic diseases
• Classified as:
• Anterior: Diffuse, nodular, necrotizing with or without inflammation
• Posterior: Usually idiopathic.
• Causes:
• Non-infectious:Rheumatoid, Wagners, gout, SLE, sarcoidosis, trauma, post surgery
• Infectious: pseudomonas, Herpes, TB, nocardia.
• Tx:
• Diffuse or nodules: NSAIDs then steroids
• Necrotizing: Systemic steroids
• Posterior: NSAIDs then steroids
• Avoid periocular steroids in necrotizing scleritis.
149. Wagner's disease
• Systemic vasculitis affecting small veins and arteries
• Classically affects sinuses, respiratory system, glomeronephritis, others
(skin, CNS).
• 50% of patients will have ophthalmic problems, including orbital disease
(spread from adjacent paranasal sinuses), scleritis, PUK, uveitis and rarely
retinitis/optic neuritis.
• Diagnosis: Tissue biopsy, C-ANCA directed against proteinase 3 (sensitivity
95%).
• Tx:
• Cyclophosphomide (side effects bone marrow suppression and hemorrhagic cystitis,
sterility) and steroids
• Therefore, needs urinalysis and CBC on routine basis.
150. • 40 year old with eye pain after waking up from sleep
151. Recurrent corneal erosion syndrome
• Defective adhesion complexes/hemidesmsomes of epithelium to basement
membrane.
• Causes:
• Primary: Epithelial and stromal dystrophies
• Secondary: Abrading trauma, HSV, band keratopathy, CDK
• Typically occurs after waking up from sleep as the epithelium swells up and
shearing forces of the eyelids sloughs the epithelium; thus the use of muro125.
• Tx:
• Lubrication + BCL
• Treat any blepharitis, MMP inhibitors
• Punctal blugs
• Surgery: Anterior stromal puncture (non-central), diamond burr, alcohol delamination, PTK.
154. Central toxic keratopathy
• Can be post LASIK or PRK
• Related to enzymic degradation of
keratocytes without inflammation.
• Does not progress
• Does not respond to steroids
• OCT shows full thickness scar
• Resolves over 1-2 years resulting in
scar with hyperopia.
236
155. 6 weeks post PRK
CHAPTER 6: Photoablation: Complications and
A 8
Figure 6-8 Corneal haze after PRK. A, Severe haze 5 months after P
is characteristic of PRK-induced haze. B, Haze has improved to a mod
postoperatively. {Courtesy of Roger F Steinert, MD.!
156. Post PRK haze
• Results from Wound healing consequence, keratocytes producing increased glycosaminoglycans
(seen in pic).
• Risk factors:
• Greater amounts of correction
• Smaller ablation zones
• Post enhancement
• Can occur 6-12 months after PRK.
• Associated with myopic shifts
• It gradually resolves, may take up to 6 months.
• Prevention:
• MMC, vitamin c, proper case selection
• Tx:
• Prolonged steroids/cyclosporin with observation.
• If does not resolve in 6-12 months, a superficial keratectomy or phototherapeutic keratectomy (PTK) may be
performed with adjunct use of MMC.
158. Diffuse lamellar keratitis (AKA sands of Sahara
syndrome).
• Inflammatory
• Must differentiate from infectious
opposite.
• Inciting factors include foreign material
on the surface of the microkeratome
blade or motor, Meibomian gland
secretions, povidone-iodine solution
(from the preoperative skin preparation),
marking ink.
• 3% of those undergoing LASIK.
• Early. Occurs within days of treatment.
• Tx: As per stage opposite.
Stage 1
Peripheral faint
white blood
cells; granular
appearance
Stage 2
Central scattered
white blood cells;
granular
appearance
Stage 3
Central dense
white blood
cells in visual
axis
Stage 4
Permanent
scarring or
stromal melting;
flap wrinkling
Frequent topical steroids
Flap lifting and irrigation + intensive
topical steroids +/- systemic steroids
116 • Refractive Surgery
LASIKinfectious keratitis
It is important to differentiate sterile interface inflammation from potentially devastating
infectious inflammation. Increased pain and decreased vision are the primary indicators
of infection. However, postoperative eye pain is common, so it is difficult for patients to
distinguish between normal and abnormal eye pain. Moreover, because corneal nerves
are severed during flap creation, corneal sensation may be reduced, along with the subjec-
tive symptom of pain that usually accompanies infection. Infection after LASIK is usually
associated with redness, photophobia, and decreased vision. Several distinct features can
help distinguish between DLK and infectious keratitis (Table 6-3). DLK is usually vis-
ible within 24 hours of surgery and typically begins at the periphery of the flap. There
is usually a gradient of inflammation, with the inflammation being most intense at the
periphery and diminishing toward the center of the cornea. In general, the inflammatory
reaction in DLK is diffusely distributed but localized and confined to the area of the flap
interface; it does not extend far beyond the edge of the flap (Fig 6-13). In contrast, post-
LASIK infectious keratitis usually begins 2-3 days after surgery and involves a more focal
inflammatory reaction that is not confined to the lamellar interface. An anterior chamber
reaction may further help differentiate between an infectious and a sterile process. The
inflammatory reaction can extend up into the flap, deeper into the stromal bed, and even
beyond the confines ofthe flap.
Table 6-3 Diffuse Lamellar Keratitis vs Infectious Keratitis
Diffuse Lamellar Keratitis
Usually visible within first 24 hours
Typically begins at flap periphery
More intense inflammation at periphery
decreasing toward center
Inflammation primarily confined to interface
Diffuse inflammation
Minimal to no anterior chamber reaction
Flap melts can occur
Infectious Keratitis
Usual onset at least 2-3 days postoperatively
Can occur anywhere under flap
Inflammation extends above and below
interface, and beyond flap edge
Focal inflammation around infection
Mild to moderate anterior chamber reaction
Flap melts can occur
Modified with permission from Culbertson WW. Surface ablation and LASIK patients share similar
infection potential. Refractive Eyecare. September 2006:12.
Figure 6-13 DLK is differentiated from infec-
tious keratitis by the confinement of the infil-
trate to the interface alone in DLK. !Reproduced
with permission from Culbertson WW Surface ablation and
LASIK patients share similar infection potential. Refractive
Eyecare. September 2006:12.)
DLK Infectious
keratitis
159. NOTE on: Atypical mycobacteria
• Used to be the most common organisms to cause post LASIK infectious keratitis.
• However, prophylactic 4th generation fluoroquinolone decreased the incidence.
• Two most common organisms?
• M. chelonae (2/3 of cases)
• M. fortuitum (1/3 of cases)
• How to diagnose the organisms early?
• Ziehl-Neelson acid-fast stain is the primary method used to detect acid-fast organisms.
• Treatment?
• 4th generation fluoroquinolone
• Amikacin
• Oral clarithromycin
161. Decentered ablation
• Astigmatism post refractive surgery:
• Decentered ablation
• Ectasia
• Decentered ablation results from:
• Large angle kappa
• Wrong registration of pupil by machine (more
common after PRK, no suction cup). Ablation
must be 0.5mm more than mesopic pupil.
• Loss of fixation by patient.
• Decentration leads to comma aberration.
Wavefront Science
Fig. 2.15
Fig. 2.16
163. Pressure-induced stromal keratopathy (PISK)
• IOP will be falsely low due to fluid under the flap
• Tx:
• Rapid cessation of steroids
• Antiglaucoma medications
167. Epithelial ingrowth
• Risk factors:
• Epithelial defect
• Repeated flap lifting
• Flap dehiscence.
• Treat if centrally involving only, with flap lifting and scraping and then
applying glue or suturing the edge.
