Ophthalmology Notes

Taken from the Lecture Notes book and Group D6’s summary, complied by Shatha AbuTaha

Table of Contents
Red Eye Lecture ....................................................................................................................................... 2
Retinal Vascular Disease .......................................................................................................................... 7
Retinal detachment ............................................................................................................................... 18
Cataracts ............................................................................................................................................... 23
Eye Trauma ........................................................................................................................................... 31
Refractive errors.................................................................................................................................... 42
Strabismus ............................................................................................................................................ 52
The Orbit ............................................................................................................................................... 62
Glaucoma .............................................................................................................................................. 70

1
Red Eye Lecture
 Red eye is a sign and symptom, not a disease, and it has a wide differential.
 Normally the eye has a strong resistance to the damaging effects of even the most virulent of
microorganisms.
 Resistance is based on a number of factors:
o Normal tear production
o Stable tear film
o Normal blink reflex, full lid closure
o Corneal sensation, intact corneal epithelium
 Allergic Conjunctivitis
o Itchy (prominent), mucoid/watery discharge bilaterally with
papillary lesions on inside of eyelids.
o Acute or Chronic
 the chronic type exhibits the papillary lesions
(cobblestone) like that seen in Vernal
Keratoconjunctivitis (vernal catarrh)
o TREATMENT
 Identify cause
 Cool compresses
 Lubricants without preservative
 Mast cell stabilizers
 Short course of steroids (for 2 weeks, until the mast cell stabilizers start
working)
 Bacterial Conjunctivitis
o Gritty sensation to tender inflamed conjunctiva
o Eye may look beefy red
o No corneal or anterior chamber involvement
o Purulent discharge – eye may be “glued shut”
o Usually starts unilaterally then spreads to
become bilateral
o Treatment
 Antibiotic eye drops / ointment (quick response)
 No eye pad
 Meticulous hygiene (clean out discharge)
 Viral Conjunctivitis (Pink Eye)
o Gritty, watery eye with associated lid swelling
o Recent URI or contact history
o Unilateral or bilateral (usually starts unilateral than
becomes bilateral).
o Common in children

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 o May see a Follicular reaction – dome-shaped elevations in the conjunctiva, represent
lymphoid hypertrophy
 Not always seen especially early on
o May have associated lymphadenopathy
o May develop late keratitis (viral keratoconjunctivitis)
with blurred vision
 Keratitis is usually a delayed immune reaction
(viral antigens in cornea are attacked) after the
original viral infection resolves
 Small opaque spots on cornea, pt complains of
photophobia and blurred vision
 Tx: long-term steroids or wait to see if it will resolve on its own (which may take
years)
o TREATMENT
 Symptomatic, no pad
 Lubricants, cool compresses
 Never steroids – except in keratitis
 Prevent cross infection. May take weeks to settle

3
  Subconjunctival hemorrhage
o Usually localized hemorrhage that appears spontaneously
o Unilateral.
o Pain free. Vision unchanged.
o Not as scary as It looks – anything that causes valsalva
(constipation, vomiting, cough) may cause it
o TREATMENT
 Reassurance - Gradually reabsorbs
 Check BP / anticoagulant levels
 If recurrent, exclude bleeding tendency
 If traumatic and extends backwards may indicate orbital fracture / penetrating
eye injury (PEI) – recall that in the case of trauma, it may conceal beneath it a
ruptured globe.
 Scleritis and Episcleritis
o The episclera is the fibrovascular coat covering the sclera (only on the
globe). Meanwhile, we have bulbar conjunctiva, forniceal conjunctiva, and
palpebral conjunctiva.
o Episcleritis/ Scleritis vs Conjunctivitis:

Episcleritis/ Scleritis Conjunctivitis

Location of maximal redness On the globe on the forniceal and
palpebral conjunctiva
Localization Localized Diffuse
Discharge Minimal or absent Present

o Episcleritis vs. Scleritis

Episcleritis Scleritis
Pain Painless, usually discomfort Painful – severe, deep and
rather than pain continuous
Phenylephrine drop Superficial blood vessels – Deep blood vessels – won’t
(vascoconstictior) will constrict, blanches - constrict – won’t blanch
redness goes away (dx and
tx)
Danger Innocuous and self-limiting Dangerous, 50% of the time
associated with systemic
disease – refer to
rheumatologist
Treatment Lubricant/ Vasoconstrictor Tx systemic disease
+/- minimal short course If none present→ oral
steroids NSAIDs, steroids

4
  Herpes Simplex Keratitis
o Gritty, watery with typical dendritic ulcer (pathognomonic)
o Stains with fluorescein.
o Vision blurred.
o Painful.
o May progress to stromal keratitis –
severe with vascularization → pt may
require a corneal transplant
o TREATMENT
 Anti-viral agents (acyclovir).
 No pad.
 NO STEROIDS – or else the
dendritic ulcer will progress to a
2 Dendritic ulcer 2 Geographic ulcer
geographic ulcer.
 Corneal ulcers
o May be due to bacterial keratitis – urgent, needs antibiotics
o Inflamed, painful eye
o Anesthetic drop and fluorescein staining
o Exclude foreign body - corneal or subtarsal, eye lash irritation
o Look for presence of hypopyon – indicating an intraocular
infection (endophthalmitis)
o Differentiate from abrasion (ulcer deeper, often round)
o Differentiate from dendritic ulcer (Herpes Simplex Virus
infection)
o May be related to contact lens use
o TREATMENT
o Hospital admission, antibiotics
o No eye pad. Use shield prn. (Generally, don’t patch eye infections, may ↑ penetration.)
o If corneal opacification occurs→ may require corneal transplant
o If ocular history indicative ofintraocular foreignbody (IOFB) –CT scan required
 Acute Closed Angle Glaucoma
o Patient presentation:
 Pain (often severe)
 Nausea / headache
 Blurred vision
 Usually unilateral
 Red eye
 Steamy cornea (cloudy)
 Fixed oval semi-dilated pupil
 Elevated intra ocular pressure (IOP) (hard)
 Shallow anterior chamber
o TREATMENT
 Urgent referral to ophthalmologist - aim is to lower
IOP as soon as possible

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  Medication - oral acetazolamide, Glycerol, IV mannitol
 Eye drops to constrict pupil and lower IOP – i.e. Pilocarpine, Iopidine
 Will need bilateral laser – peripheral iris iridotomy
 Acute iritis
o Pain, aching eye, photophobia
o Redness is maximal around the cornea – ciliary flush
o Anterior chamber may appear cloudy from white cells /
flare
o If chronic, may form posterior synechiae – adhesions
between the iris and the lens → when pupil dilates, a part
of it remains stuck, giving us an irregular pupil
o TREATMENT
 Mydriatic eye drops
 Analgesia
 Steroid eye drops-only used after ophthalmic assessment to exclude infection

(End-of-lecture-notes)

 Posterior uveitis
o two types→ chorio-retinitis, and retino-choroiditis
 either started in the choroid and affected the retina, or started in the retina and
then affected the choroid
o if the lesion is central and affects the macula → blurring of vision (scotoma)
o if the lesion is peripheral → pt sees increasing floaters due to associated vitritis
o Painless
o If untreated, may progress to cystoid macular edema

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Retinal Vascular Disease
 Retinal vascular disease may occur by two main pathologies:
o Arterial occlusion→ leads to a pale, ischemic retina beyond the point of occlusion
o Venous occlusion→ leads to congestion, hemorrhage and edema of the retina before
the point of occlusion
 If complete and persistent, may lead to ischemia
 Persistent occlusion→ thinning of the tunica media→ aneurysms, which are leaky and easily
ruptured→ signs of vascular leakage
 The signs of retinal vascular disease result from two changes in the retinal capillary
microcirculation:
o Vascular leakage→ leads to
 transudate (edema)
 hard lipid exudates – formed of lipids, lipoproteins and lipid-containing
macrophages – these are deep and yellow with well-defined margins, mostly
found around microaneurysms
 extravasation (hemorrhage)
o Vascular occlusion→ leads to
 cotton-wool spots – fluffy superficial white lesions with indistinct margins
 the retinal area most susceptible to ischemia is the nerve fiber layer
which contains the axons of ganglion cells
 These spots occur due to obstruction axoplasmic flow→ build - up of
axonal debris in the nerve fiber layer of the retina
 seen close to the optic disc where the nerve fiber layer is thick
 appear white b/c accumulated axoplasmic particles scatter light
 irregular retinal veins
 tortuous vessels
 venous beading
 new vessels
 ischemic retina→ VEGF→ growth of abnormal blood vessels and fibrous
tissue on retina and into the vitreous
 these vessels are:
o insufficient to compensate the wide ischemic area
o more permeable and friable so
 they leak dye leak dye during retinal fluorescein
angiography
 are predisposed to break and bleed → vitreous
hemorrhage
o likely to be fibrosed → retinal detachment
 so our aim in treatment is to prevent new blood vessel formation

7
8
Diabetic Retinopathy
 The most common retinal vascular disorder
 MC in type 1 DM b/c it’s more aggressive and since pts tend to be younger, there is a larger
window of time for development and progression of the disease
o So while younger patients are more likely to develop proliferative disease, older patients
are more likely to develop maculopathy
 Diabetes is associated with the following ocular events:
o Recurrent corneal abrasions and poor wound healing
o Glaucoma
o Cataract – a rare “snowflake cataract” in youth
o Retinopathy
o Extra-ocular muscle palsy – due to microvascular disease in the 3rd, 4th
or 6th cranial nerves (mainly in the 6th)
 Risk factors for development of diabetic retinopathy
o Most important one: duration of diabetes (regardless of tight
control)
o Poor diabetic control
o Coexisting diseases, esp. HTN
o Smoking
o Diabetic nephropathy
o Obesity and hyperlipidemia
o Pregnancy – accelerates the development of retinopathy
 Classification

o
 Pathological changes in retina:

9
 o Non-Proliferative Diabetic Retinopathy (NPDR)
 Development of microaneurysms
 Start temporal to the optic disc (which is on the nasal side of the retina)
 Allow plasma leak into the retina→ evidence of leakage (mentioned
above) like hard exudates, edema and hemorrhages
 ↓ in number of pericytes surrounding the capillary endothelium
 Classification of NPDR according to severity:
 Mild – pathological changes involve one quadrant of the retina→
screening fundoscopy q 1 year
 Moderate – pathological changes between mild and severe – screening
fundoscopy q 6 months
 Severe – pathological changes involve all 4 quadrants of the retina –
screening fundoscopy q 3 months
o Proliferative Diabetic Retinopathy (PDR)
 Evidence of occlusion (mentioned above)
 Capillary non-perfusion (patchy closure of the capillary net)→ areas
of ischemic retina and AV shunts→ VEGF induces new blood vessel
formation
 Differentiate between new vessels and main vessels: new vessels are
thin and look like a spider web around a main vessel
 5-10% of diabetics reach this stage
 Sites of neovascularization:
 At the optic disc→ NVD
 At the iris→ NVI→ leads to neovascular glaucoma
 Elsewhere→ NVE
 Complications of PDR
 Pre-retinal hemorrhage
o Bleeding between retina and vitreous capsule
o Only affects vision if it occurs over the macula
 Vitreous hemorrhage
o Tea-colored hemorrhage within the vitreous
o Prevents visualization of the retina during exam
 Tractional retinal detachment
o Due to a fibrous layer being formed over the retinal
surface→ this layer has contractile properties→
pulls on retina, causing its detachment
 Vascular glaucoma
o One of the worst types of glaucoma
o Due to NVI, prevents drainage of aqueous humor
o Diabetic Maculopathy
 Can occur w/ any stage (NPDR or PDR)
 The most common cause of drop of vision in diabetic patients
 Due to microaneurysms→ edema over the macula
 Start screening via fundoscopy:

10
 o 5 years after the diagnosis in pts w/ DM type 1 – since time of onset is known
o At the time of diagnosis in pts w/ DM type 2 – since time of onset is unknown
 History
o May be asymptomatic, even in the proliferative stage
o Visual acuity may be reduced gradually by a maculopathy or suddenly by a vitreous
hemorrhage
 Treatment:
o Non proliferative/ Pre-proliferative→ tight blood glucose control, control of risk factors
and follow up
o Proliferative retinopathy: neovascularization is an indication to start treatment
 Mainstay is laser PRP: Panretinal laser photocoagulation
 Converts ischemic cells to necrotic cells, halts
VEGF production
 Do not laser the macula, since it’s responsible for
90% of vision
 The peripheral area that we do laser has a lot of
rods and it’s responsible for night vision, so the pt
may complain of ↓ vision at night after surgery
 Permanent and curative
 Anti-VEGF treatment (avastin) as an adjunct
 A temporary treatment + pt requires recurrent injections
o Vitreous hemorrhage
 At presentation→ give anti-VEGF
 Wait a few weeks to allow the hemorrhage to clear
 If it clears→ do PRP
 If it doesn’t clear→ do vitrectomy followed by PRP
o Diabetic maculopathy:
 Mainstay is Anti-VEGF
 Laser is used as adjunct

11
 The signs of diabetic eye disease.
(a) Background diabetic
retinopathy.
(b) Diabetic maculopathy: note
the circinate exudate temporal to
the macula.
(c) Preproliferative retinopathy
with a venous loop.
(d, e) Proliferative retinopathy:
new vessels have formed on the
retina, their presence
demonstrated by leakage of
fluorescein (hyperfluorescence)
on the fluorescein angiogram;
closure of some of the retinal
capillary network is
demonstrated by its failure to fill
with fluorescein.
(f) Advanced diabetic
retinopathy: the
neovascularization has caused a
traction retinal detachment.

Retinal Vein Occlusion

 Ocular blood supply:

12
  The central retinal artery and vein enter the globe through the optic nerve.
 The central retinal artery then branches off into sup-temporal, inf-temporal, sup-nasal and inf-
nasal branches.
o with each artery, there is a vein that goes with it
 Pathogenesis:
o Retinal vein occlusion may result from:
 In young patients: Virchow’s Triad:
 Hypercoagulability (factor V Leiden, Protein C/S deficiency,
homocystinuria, nephrotic syndrome, OCPs, pregnancy, etc.)
 Endothelial injury (vasculitis)
 Hemodynamic changes (stasis, turbulence)
 ↑ IOP
 In elderly patients: HTN → arteriosclerosis of arteries→ compression of a branch
retinal vein at the crossing point of an arteriole and a vein
 Uncontrolled HTN is the most important risk factor for its development
o Types of RVO:
 Non-ischemic retinal vein occlusion→ 75% of the time
 Ischemic retinal vein occlusion→ VEGF release→ new blood vessels → ↑ risk of
vitreous hemorrhage and rubeotic (neovascular) glaucoma
 History:
o Sudden partial/ complete loss of vision, though less acute than that of arterial occlusion
o If CRVO→ all quadrants affected→ significant ↓ of vision
o If branch RVO→ symptomatic if the macula is involved

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  Signs:
o Marked hemorrhage
o Tortuous and swollen veins
o Swollen optic disc
 Investigation:
o Vascular and hematological workup to exclude ↑
blood viscosity
 Treatment:
o In the case of non-ischemic RVO:
 Treat the underlying cause and control the
risk factors 3 Superior branch RVO
o In the case of ischemic RVO:
 Laser
 Anti-VEGF
 Prognosis: if macula is affected, usually does not improve

Retinal Artery Occlusion

 Pathogenesis:
o Usually embolic in origin, either
 Fibrin-platelet emboli from diseased
carotid arteries
 Cholesterol emboli from diseased
carotid arteries
 Calcific emboli from diseased heart
valves
 History
o Sudden painless loss of all or part of vision
o Pt may have history of amaurosis fugax→
fleeting loss of vision as the emboli pass
through the retinal circulation 4 Inferior branch retinal artery occlusion
 Signs:
o Swollen white edematous retina
o A bright yellow, reflective cholesterol
embolus may be seen occluding an arterial
branch point
o Cherry-red spot on fovea (because the
choroid may be seen through the thin retina
of the fovea)
 Not pathognomonic – also occurs in
Tay-Sachs, Neimann-Pick…
5 Cholesterol emboli sparkle when viewed w/ a
o After several weeks→ pale atrophic disk direct ophthalmoscope
with attenuated arterioles
 Investigation:

14
 o Vascular workup and Doppler ultrasound to search for carotid artery disease (may
require carotid endarterectomy) and cardiac workup (Echo) to search for cardiac disease
– 5 year survival rate of pts ↓ by 50% after retinal artery occlusion
 Treatment:
o Only worthwhile within the first 24 hours of obstruction (the
golden period is within 1.5-4 hours), afterwards vision loss
becomes irreversible because necrosis starts.
o Aimed at dilating the arteriole to permit the embolus to pass
more distally and limit the damage:
 Acetazolamide→ to ↓ IOP
 Ocular massage
 Paracentesis→ needle inserted into anterior chamber
to release aqueous and ↓ IOP rapidly
 Rebreathe into a paper bag→ ↑ CO2→ vasodilation
 Prognosis: usually severe unrecoverable vision loss

Retinopathy of Prematurity

 A common but preventable vascular retinopathy→ causes 1/5 child blindness

 Pathogenesis:
o Premature birth→ initial failure of normal retinal vascularization
 At 16 weeks→ blood vessels reach the optic disc
 At 22 weeks→ blood vessels reach the macula
 At 36 weeks→ blood vessels reach the nasal periphery
 At 40 weeks→ blood vessels reach the temporal periphery
o Usually, blood vessel development w/in the avascular area occurs normally

15
 o Area of avascular retina senses ischemia→ VEGF production→ aggressive new vessel
formation → extend into the vitreous → RD or vitreous hemorrhage
 Risk factors:
o Gestational age less than 32 weeks
o Birth-weight below 1500 g
o Exposure to supplemental oxygen
o Unstable clinical course: apnea, sepsis, blood transfusion, IVH, RDS, BPD, NEC, anemia,
hydrocephalus
 Stages:
o 1) demarcation line separates vascular and avascular retina
o 2) demarcation ridge separates vascular and avascular retina
o 3) new blood vessel formation in the ridge
o 4) partial tractional RD
o 5) complete tractional RD
 Signs
o New vessels
o Retinal hemorrhages
o ↑ tortuosity and dilation of retinal vessels
o Potentially blindness from vitreous hemorrhage or RD
 Screening is indicated when:
o Gestational age less than 32 weeks
o Birth-weight below 1500 g
o Unstable clinical course
 Screen at 4-6 weeks post-delivery or at 31 weeks chronological age, whichever is
later
 Treatment
o Treat stage 3 and up
o Applying cryotherapy or laser to the avascular retina

Age-Related Macular Degeneration

 The commonest cause of irreversible vision loss in the developed world.
 Pathogenesis:
o The retina is composed of 10 layers:
 9 layers forming the neurosensory retina
 Retinal Pigment Epithelium (RPE)→ single layer of cuboidal cells, contain
melanin, separate the neurosensory retina from the choroid.
o RPE normally removes and processes the used discs of the photoreceptor outer
segments.
o With time, undigested lipid products (lipofuschin) accumulate in the RPE
o Excess material is transferred to Bruch’s membrane, impairing its diffusional properties.
o Extracellular deposits form between the RPE and Bruch’s membrane, seen on the
ophthalmoscope as discrete, sub-retinal yellow lesions called drüsen.
 Collections of drusen→ age-related maculopathy (vision is still normal)
o Dry/ non-exudative macular degeneration:

16
  More common (90%)
 RPE shows degenerative changes
 ↓ in vision
o Wet/ exudative macular degeneration:
 Less common (10%)
 VEGF stimulates formation of a sub-retinal neovascular membrane
 Leads to hemorrhage into the sub-retinal space and vision loss
 Risk factors: old, white, blue-eyed smoker in the sun
o Age
o White race
o Smoking
o Excessive UV light exposure
o Blue eyes
 Symptoms:
o Gradual ↓ of vision
o Blurred central vision
o Metamorphopsia (distorted vision) caused by a
disturbance in photoreceptor arrangement
 Micropsia→ ↓ in object size
 Macropsia→ ↑ in object size
o Scotoma (loss of central visual field)
 Occurs if photoreceptors
are covered by blood or
destroyed
 Signs:
o Absent foveal reflex
o Drusen
o Areas of hyper/hypopigmentation
o In wed MD→ sub-retinal or pre-
retinal hemorrhages
 Investigation:
o Fluorescein angiogram→
delineate the position of the sub -
retinal neovascular membrane.
 Treatment:
o Dry MD:
 Antioxidants
 Zinc
 Quit smoking
 Use magnifiers/ CCTV
when necessary
o Wet MD:
 Anti-VEGF injection

17
Retinal detachment
 Separation of the RPE and neuroretina with accumulation of
fluid in the subretinal space. Posterior Vitreous
 It’s an ophthalmic emergency requiring urgent diagnosis and
treatment Detachment
Pathogenesis Tears in the retina are MC
 Between the neuroretina and the RPE is a potential space that associated with the onset of a
corresponds to the cavity of the embryonic optic vesicle. These posterior vitreous detachment.
two tissues are loosely attached and may become separated in
With aging, the vitreous undergoes
three possible scenarios:
degenerative changes over the age
o Rhegmatogenous RD→ a tear occurs in the retina,
of 60 (earlier in myopes)
allowing liquefied vitreous to gain entry into the sub-
retinal space Vitreous is liquefied and fragments
 The vitreous is surrounded by a hyaloid of condensed vitreous are formed,
membrane that separates it from the lens casting shadows on the retina and
anteriorly and the retina posteriorly giving rise to the symptom of
 This hyaloid membrane is loosely attached to vitreous ‘floaters’ – spots that
the retina obscure vision only slightly and
 As the gel separates from the retina, the move when the eyes move,
traction it exerts becomes more localized and reflecting the fluid nature of the
thus greater→ tears in the retina and vitreous)
subsequent RD
Posterior vitreous detachment
 Risk is ↑ in high myopes and patients with
occurs when the vitreous gel
an underlying peripheral weakness in the
collapses and separates from
retina (lattice degeneration).
points of retinal attachment, giving
o Traction RD→ the retina is pulled off by contracting
rise to acute symptoms of
fibrous tissue on the retinal surface
photopsia (flashing lights) due to
o Exudative RD→ fluid accumulates in the sub-retinal
traction on the peripheral retina
space as a result of an exudative process (retinal
and a shower of floaters
tumors, pre-eclampsia…)
representing either condensations
 In RD the retina loses nutrition→ loss of function→ drop of
within the collapsed vitreous or a
vision
vitreous hemorrhage

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Rhegmatogenous RD
 The most common type of RD
 Risk factors for rhegmatogenous RD:
o High myopia (↑ axial length)
o History of RD in the fellow
eye
o History of cataract surgery,
especially if it was
accompanied by vitreous
loss
o Eye trauma
o Family history or familial
conditions, like Ehlers-
Danlos or Marfan syndrome
o Inflammation: CMV, HSV or
herpes zoster infection
 Symptoms:
o Preceded by symptoms of
posterior vitreous
detachment (floaters and flashing lights)
o A progressive visual field defect described as a “shadow or curtain falling over their
vision”
o If the macula is detached→ marked fall in visual acuity.
o If a superior detachment is present→ rapid progression
 Signs:
o Detached retina
 Visible on ophthalmoscopy as a floating, diaphanous
corrugated opaque membrane which partly obscures
choroidal vascular detail
 It looks opaque due to fluid accumulation under the retina.
o Tear in the retina
 Looks reddish pink because of underlying choroidal vessels
o Debris in the vitreous, either
 Blood (vitreous hemorrhage)
 The free-floating lid
(operculum) of a retinal hole
 Management: urgent surgery
o The earlier the intervention, the better
the results.
o The main principle is to:
 Close the causative break in the
retina

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  ↑ the strength of attachment between the surrounding retina and RPE by
cyroprobe or laser, which induces inflammation in the area and prevents re-
detachment.
o This is achieved by 2 main surgical techniques:
 The external (conventional) approach (Buckling)
 Non-invasive
 The accumulated sub-retinal fluid is drained
by sclerostomy (piercing the sclera and
choroid with a needle)
 The break is closed by indenting the sclera
with an externally located strip of silicone
sponge (or plomb) sutured to the globe
 This relieves the vitreous traction on the
retinal hole and apposes the RPE to the
retina.
 The internal approach (vitreoretinal surgery)
 Invasive
 Vitrectomy: the vitreous is removed with a
microsurgical cutter introduced into the
vitreous cavity through the pars plana.
o This relieves the vitreous traction
on the break.
o The vitreous will be replaced slowly
with aqueous humor
 Sub-retinal fluid is drained through the
causative retinal break itself
 Laser or cryotherapy is applied to the
surrounding retina → adhesions to prevent
re-detachment
 Tamponade: a material with ↑ surface
tension is used to hold the retina in place,
closing the hole from inside and preventing
further passage of fluid from the leak. This may be either:
o An inert fluoro-carbon gas bubble which is absorbed slowly
 The pt has to maintain a particular head posture for a
few days to ensure the bubble covers the retinal break
continuously
 Air travel must be avoided due to the risk of gas
expansion at ↓ barometric pressure (can cause
glaucoma)
o Silicone oil, which stays as long as we need, but needs to be
removed later.

20
  This has a ↑ success rate but affects normal eye physiology: can ↑ risk
of cataracts, and if there are any small holes that you miss there may be
re-detachment.
o Retinal tears unassociated with sub-retinal fluid are treated prophylactically to prevent
RD
o Always make sure to check the peripheral retina in the fellow eye, as tears may be
present there as well.
 Prognosis:
o If the macula is attached and the surgery is successful→ outlook for vision is excellent.
o If the macula is detached for more than 24 hours prior to surgery, the previous visual
acuity will probably not recover completely.
o If the surgery is complicated and the retina is not successfully attached, fibrotic changes
may occur in the vitreous (proliferative vitreoretinopathy PVR) which may cause traction
on the retina and further RD
o Worse prognosis in younger patients, syndromic patients and post-trauma.

Tractional RD
 The second MC type of RD
 Path:
o This may be seen in proliferative
diabetic retinopathy, ischemic CRVO,
ROP, sickle cell retinopathy or
proliferative vitreoretinopathy.
o Advanced microangiopathy→
thickening of the posterior hyaloid
membrane and formation of tractional
membranes
o The neuroretina is pulled away from the
pigment epithelium by contracting
fibrous tissue which has grown on the
retinal surface.
 Patient presentation:
o Gradual ↓ in vision (subacute)
o No flashes or floaters because it is not preceded by vitreous detachment
 Treatment:
o Vitreoretinal surgery with excision of the tractional membranes, followed by silicone oil
tamponade to flatten the retina and retain its normal contour.
o However, removal of tractional membranes won’t restore normal vision, since the retina
is already ischemic

21
Exudative RD

 Rare, less than 1% of all RD

 Occurs suddenly
 Fluid accumulates in the sub-retinal space as a result of an exudative process, separating the
RPE and neuroretina
 Causes:
o Inflammatory conditions
 Uveitis
 Retinitis
 Scleritis
 Retinitis, viral or bacterial
o Infiltrative tumors
 Leukemia/ Lymphoma
 Choroidal melanoma or hemangioma
o Fluid overload
 Liver disease, pre-eclampsia, protein-losing enteropathy
 Treatment:
o Treat the underlying cause
o Surgery is contraindicated

22
Cataracts
 Cataracts → any light-scattering opacity within the lens (regardless of its effect on vision or
location on lens)
 The MCC of treatable blindness in the world
 RFs for age-related cataracts
o Smoking
o UV radiation
o ↑ blood sugar
o Ocular conditions
 Classification according to cause:
o Primary
 Age-related cataract
 Systemic disease
 Diabetes and other metabolic disorders (galactosemia, hypocalcemia,
Fabry disease, neurofibromatosis)
 Congenital rubella
 Myotonic dystrophy
 Syndromes like Down’s and Lowe’s
 Atopic dermatitis
 Congenital
 X-radiation
 Drugs (steroids, chlorpromazine, amiodarone, mitoics)
o Secondary – due to ocular conditions:
 High myopia
 Uveitis – either due to the disease itself (inflammation) or due to its treatment
(steroid eye drops)
 Steroid eye drops
 Acute closed angle glaucoma
 Trauma
 Intraocular tumor
 Classification according to morphology:
o Nuclear → appears yellow to brown
o Cortical → appears w/ radial spoke-like
opacities
6 cortical cataract 7 nuclear cataract
o Anterior subcapsular

23
 o Posterior subcapsular → like steroid-induced cataracts
o Polar→ in the central posterior part of the lens
 The more anterior the site of the cataract is, the less likely it is to affect vision, and
vice versa.
o A posterior subcapsular cataract is more likely to affect vision because of its
position→ affects the nodal point (the point where rays converge during
8 posterior subcapsular
refraction), so any opacification here leads to significant scattering of light,
therefore symptoms appear early and are aggravated my miosis (↑ passage of light
through the nodal point)
o A cortical cataract may reach advanced stages with little effect on vision due to its
position on the periphery rather than the nodal point, so the center of the lens is still
relatively normal. (However, mydriasis will cause glare and haloes around lights,
affecting quality rather than acuity).
 Classification according to maturity
o Immature – lens is partially opaque
 Iris shadow (which represents some clear cortex) is visible on slit
lamp exam
 Looks like a black crescent
 Due to the presence of a clear interval between the iris and
lens opacity
 Wedge-shaped opacities seen at the periphery of the lens
 Relatively ok vision
o Mature – lens is completely opaque (ripe)
 No iris shadow or fundus details visible on slit lamp exam
 Severe ↓ in vision (just hand movement or light perception)
 May progress to phacolytic glaucoma phacomorphic
o Hyper-mature – shrunken cataract with a wrinkled anterior capsule
 due to liquefaction of the anterior cortex and leakage of water out of
the lens
 May progress to phacolytic glaucoma
o Morgagnian cataract – a hyper-mature cataract but with the nucleus sunken
inferiorly due to cortex liquefaction
 The anterior cortex usually provides support to the nucleus –
liquefaction results in downwards displacement

24
  Calcium deposits may be seen on the lens capsule

9 iris shadow in immature cataract

 Symptoms:
o Painless progressive loss of vision
o Glare
o In some instances a change in refraction
 Nuclear cataract→ myopic shift (second sight – the pt no longer needs their
reading glasses)
 Cortical cataract→ hyperopic shift
o In infants→ may cause amblyopia (failure of visual maturation)
 Signs:
o ↓ visual acuity for both near and distance vision, especially when test is
carried out in bright light as a result of glare and loss of contrast
o Black red reflex seen on ophthalmoscope
o Slit lamp exam identifies the exact site of the opacity
o Examine ocular adnexia and treat any abnormalities before surgical
intervention
 like if the pt has uveitis, you can’t do surgery until uveitis is controlled for 3-6
months
 if pt has RAPD (Relative Afferent Pupillary Defect) this indicates optic nerve
disease, so surgery probably won’t do the pt much good
 Pathology: - not fully understood (so just read this who cares)
o The lens is mostly water and protein fibers.
o Opacity occurs when the lens protein (crystallins) clump together
o The ability of the lens to refract light is ↓ → ↓ visual acuity
o Chemical modification of the lens causes it to thicken and harden
o Diabetes and cataracts:
 early DM→ hyperglycemia→ ↑ glucose in the aqueous and vitreous that
surround the lens→ ↑ glucose in the lens→ blurred vision and a myopic shift
(↑ refractive power) (whereas hypoglycemia may cause hyperopia)
 this is reversible
 later DM→ sustained hyperglycemia→ ↑ glucose in the lens → glucose is
converted to sorbitol via aldose reductase (the polyol pathway)→ sorbitol has
significant osmotic effects and is water insoluble → influx of fluid into lens→
overhydration of lens fibers→ lens opacity

25
  this is irreversible
 Cataracts may lead to three types of glaucoma:
o Phacomorphic glaucoma – closed angle
 Lens tumescence due to cataract→ blocks the iridocoroneal angle by a forward
push of the iris
o Phacolytic glaucoma – open angle
 Proteins diffuse from the lens capsule of a mature or hyper-mature cataract to
the angle→ obstruct the trabecular meshwork
o Phacoantigenic glaucoma – open angle
 IgG binds to lens particles→ immune complex formation → this leads to a
granulomatous reaction causing increased IOP secondary to blocking the
trabecular meshwork.
 Treatment may start with temporary measures like glasses and improving the lighting in the pt’s
room
o Definitive treatment is surgical – should be a joint decision between the patient and the
doctor
o Indications for surgery:
 Optical causes: cataract affects pt’s lifestyle and ability to do daily activities ,
glare, patient needs to pass an eye test for their driver’s license, aniseikonia (a
defect of binocular vision in which the two retinal images of an object differ in
size)
 Medical causes: to monitor retinal disease (like if the patient has diabetic
retinopathy/ ARMD/ RD and you need to see fundus details)
o Intra-capsular cataract extraction (ICCE)
 Remove the entire lens in its capsule
 IOL is placed in the anterior chamber
or in its proper place via scleral
fixation
 Placement in anterior
chamber may lead to:
o Hyphema
o Uveitis
o Corneal injury 10 ICCE
o Closed angle
glaucoma
 Only done in Marfan and homocystinuria w/ dislocated lens (because it’s no use
keeping the capsule if it’s dislocated as well)
o Extra-capsular cataract extraction (ECCE)
 The lens capsule is left in place to hold the IOL, while the cataract is removed

26
  Method:
 A wide incision is made in the limbus
 A circular disk of the anterior capsule is removed
 A cannula is placed under the anterior capsule and
fluid is injected to separate the lens nucleus from the
cortex
 The hard nucleus of the lens is removed through the
incision by expression (pressure on the eye) and
residual material is aspirated with a cannula
 IOL is implanted into the remains of the capsule
 The incision is the sutured
 Indications:
 Very hard, dense nucleus (stage 4)
o If you were to use phaco, the U/S waves
would cause thermal damage to the
corneal endothelium→ corneal edema →
may progress to Pseudophakic bullous
keratopathy (the MCC of corneal
transplant)
 Pseudoexfoliation syndrome
o Zonules are weak→ when phaco moves the lens, the zonlues
may detach from the ciliary body and you may drop the nucleus
 Low endothelial count (corneal dystrophy)
o Because you can’t afford to lose any corneal endothelial cells to
U/S induced thermal damage
 Complications:
 Sutures may lead to corneal astigmatism
 Loose sutures may ↑ risk of infection
o Phacoemulsification (Phaco)
 Usually the preferred method of cataract removal
 Method:
 A small, self-sealing incision is made in the cornea or anterior sclera
 A circular disk of anterior capsule is removed
 A cannula is placed under the anterior capsule and fluid is injected to
separate the lens nucleus from the cortex
 The phacoemulsification probe is introduced through the small incision,
and shaves away the nucleus via ultrasound.
 The remaining soft lens matter is aspirated, leaving only the posterior
capsule and the peripheral part of the anterior capsule.
 IOL is injected through a special introducer into the remains of the
capsule
 No sutures necessary
o Femtosecond laser

27
  Similar to phaco, except that the corneal wound, capsular wound and nuclear
damage are all done by laser
 Advantages:
 Corneal wound and capsular wound are more precise
 No ultrasound waves necessary (↓ risk or corneal damage in hard
cataract)
 Disadvantages:
 Expensive and new (not widely available)
 The optical power of the IOL is determined prior to surgery via:
o Ultrasound→ measures the length of the eye
o Keratometry→ measures the curvature of the cornea and thus its optical power
 The IOL should provide emmetropia (good distance acuity without glasses)
 Post-op, the patient will be given:
o A short course of steroids
o Antibiotic drops
o Reading glasses – since they can no longer accommodate. (Not needed if the pt got
multifocal IOL)
 Complications of cataract surgery:
o Anesthesia complications (complications of retrobulbar injection)
 Can damage blood vessels→ retrobulbar hemorrhage
 Can damage muscles → fibrosis and paralysis
 Can damage the globe itself
o Vitreous loss
 Posterior capsule damage→ vitreous gel comes forward into the anterior
chamber→ risk for glaucoma or may cause retinal traction
 Do vitrectomy and defer IOL to secondary procedure
o Iris prolapse
 The iris may protrude through the surgical incision in the immediate
post-op period.
 Appears as a dark area at the incision site w/ a distorted pupil
 Requires prompt surgical repair
o Argentinian flag sign
 During capsulotomy, a radial anterior capsular tear occurs through a 11 Iris prolapse
trypan blue stained anterior lens capsule.
 After the tear has propagated equatorially, what is left is a light blue
torn anterior capsule with a central white cataract protruding from
the capsule. (looks like an Argentinian flag)
 Occurs if the cataract is very mature with ↑IOP
o Endophthalmitis
 Rare but serious – an ophthalmologic emergency
 Patients present within a few days of surgery with

28
  A painful red eye
 ↓ visual acuity
 Hypopyon (WBCs in the anterior chamber
 Requires urgent sampling of the aqueous and vitreous for
microbiological analysis and intravitreal, broad-spectrum,
antibiotic injection at the time of sampling.
o Cystoid macular edema
 May occur especially if surgery was accompanied by vitreous loss or followed by
inflammation.
 Treat with topical NSAIDs and steroid
o Retinal detachment
 May occur if there was associated vitreous loss
o Opacification of the posterior capsule

 In 20% of patients, residual epithelial cells (normally just behind the anterior
capsule) migrate across the surface of the posterior capsule to form an opaque
scar
 Patient complains of blurry vision and glare.
 Treat with YAG capsulotomy.
o Suture breakage
o Pseudophakic bullous keratopathy (PBK)
 Only with phacoemulsification
 Ultrasound waves cause mechanical and thermal
damage to the corneal endothelium, which
governs fluid and solute transport across the
posterior surface of the cornea and maintains the
cornea in the slightly dehydrated state that is
required for optical transparency.
 Loss of corneal endothelial cells → irreversible corneal edema.
 MCC of corneal transplant
o Astigmatism
 Due to sutures (↓ by postop removal)
o Suprachoroidal hemorrhage

29
  Due to sudden decompression of choroidal blood vessels→ bleeding between
choroid and retina→ retina pushed forwards
 Requires immediate repair
 ↑ risk in the elderly, glaucoma, high myopia, and atherosclerosis/ HTN.

Congenital cataract
 Obstruct vision and hence may lead to amblyopia, squint and nystagmus.
 If bilateral→ urgent surgery and fitting of contact lenses to correct the aphakia
 If unilateral→ management is controversial.
o Results of surgery are disappointing
o Amblyopia develops despite adequate optical correction with a contact lens
 Why use contacts and not an IOL from the beginning? Because the eye becomes
increasingly myopic as the child grows, making the choice of lens implant power
difficult. Also there is a ↑ risk of subsequent glaucoma

Change in lens shape

 The curvature of the anterior part of the lens may be increased centrally ( anterior lenticonus )
in Alport’s syndrome

Ectopia lentis
 Weakness of the zonules→ lens displacement.
o Lens becomes more rounded→ eye becomes more myopic
 Seen in Marfan syndrome (upwards displacement of the lens), homocystinuria (downwards
displacement of the lens) and trauma.
 The irregular myopia can be corrected optically, although sometimes an aphakic correction may
be required if the lens is substantially displaced from the visual axis
 Surgical removal may be indicated, especially if the displaced lens caused a secondary glaucoma.

30
Eye Trauma

 Orbital injury classification:

o Open injury→ full thickness injury of the fibrous capsule (cornea or sclera)
 Laceration→ out-in injury with a sharp object, well-demarcated, so the site of
injury is the same as the site of trauma
 Ruptured globe→ blunt trauma leads to ↑ IOP and in-out trauma, so the globe
ruptures at its weakest points (away from the site of trauma):
 At sites of muscle insertion
 At sites of old operations
 Around vessel/ optic nerve entry points
 At the limbus
 Intra-ocular foreign body
 Perforating→ w/ only an entrance site
 Penetrating→ w/ an entry and exit site
o Closed injury→ partial thickness injury of the fibrous capsule (cornea or sclera)
 Like extraocular foreign body, partial laceration, etc.
 Forms of injury include:

31
 o Foreign bodies
o Blunt trauma
o Penetrating trauma
o Chemical and radiation injury
 History is important (obviously)
o Usually non-specific, buy may provide some important clues
o Note the mechanism of trauma
o Pt uses hammer and chisel and presents w/ a tell -tale subconjunctival hemorrhage→
suspect scleral penetration and a retained foreign body
 Examination:
o Visual acuity
 The most important factor to examine
 Usually, good visual acuity at presentation = good prognosis and vice versa
o Ocular motility
 Look for restriction of movement
 Upwards restriction, for example, indicates inferior rectus muscle
entrapment in inferior wall fractures
 Orbital injury
o The orbit is pyramidal in shape with a roof, floor, medial wall and lateral wall.
 The MC damaged walls: inferior→ medial→ superior→ lateral (which is rarely
fractured)
 The weakest wall is the medial wall but it’s protected by the nose
 The strongest wall is the lateral wall
 The MC site of injury is the infero-lateral quadrant of the orbit because it is the
most exposed one

32
 o Damage to the orbit itself (a blow-out
fracture) is suspected if the pt presents
with:
 Surgical emphysema→ indicates a
fractured sinus
 Paresthesia below the orbital
rim→ indicates infraorbital nerve
damage (the MC injured nerve in
blow-out fractures involving the
floor of the orbit
 Enophthalmos – eye recession
into the orbit
 Not easily seen acutely
b/c of edema pushing the
eye outwards, so it usually
appears when edema
resolves
 The patient may even
present with exophthalmos is the case of retrobulbar bleeding
 Limitation of eye movements, particularly on upgaze and downgaze, due to
trapping of the inferior rectus muscle by CT septa caught in the fracture site in
the inferior orbital floor
 Diplopia→ may be due to a) muscle/ nerve paralysis or b) surrounding edema/
muscular tethering

33
  Differentiate between a and b via passively moving the eye with forceps
under anesthesia
o If the eye moves freely→ problem is due to muscle or nerve
paralysis
o If the eye doesn’t move freely→ problem is due to restriction of
movement
o Do a CT scan whenever a blow-out fracture is suspected to delineate the bony/ soft
tissue injury
o Treatment:
 If at presentation there is evidence of muscle entrapment or nerve paralysis→
immediate surgical intervention, because if it persists it may lead to muscle
fibrosis or nerve ischemia
 If not→ conservative treatment (analgesics, prophylactic antibiotics, cold
compresses) for 2-4 weeks then re-evaluate the patient when edema has
settled. Do surgery if:
 Enophthalmos is cosmetically unacceptable
 Eye movements are significantly limited
 Eyelid injury
o Evaluate: is it blunt or penetrating? Is there ptosis? Is there a
laceration?
o If the lid margin is cut at the medial canthus, it’s important to
determine if either of the lacrimal canaliculi is severed. This will
cause epiphora (watery eyes) if untreated
o Before suturing a laceration (especially if it’s near a punctum) be
sure to probe for the adjacent lacrimal duct to avoid accidentally
suturing it shut.
 Conjunctival injury
o Chemosis→ edema of the conjunctiva
 Appears swollen and pale
 Blood vessels become more pronounced
 May be due to:
 Direct trauma
 Retrobulbar compression preventing venous drainage
o Laceration
 Usually heals rapidly, except when it is > 12mm, in which case it requires
surgical repair
o Subconjunctival hemorrhage
 Hemorrhage between the conjunctiva and Tenson’s capsule
 May be benign or indicate underlying pathology (like scleral perforation):
 If it presents alone without any other symptoms/ alarming
history→ observation
 If it presents w/ scleral hemorrhage, foreign body, ↓ visual acuity or
other symptoms→ indication for surgical exploration
o Chemical injury

34
  White and ischemic conjunctiva with a hazy cornea
 Corneal healing may be impaired if damage occurred to epithelial stem
cells at the limbus

 Corneal Injury
o Classification:
 Open→ full thickness or partial thickness
 Full thickness injury usually self-seals w/ no need for suturing (because
of the spherical shape of the cornea)
 Closed→ abrasion or a foreign body
 An abrasion is loss of the epithelial layer of the cornea (with a part of
Bowman’s layer) – although painful they tend to heal rapidly
o Recall the cornea has 5 layers: epithelium, Bowman’s layer,
stroma, Descemet’s membrane, endothelum
o Differentiate between open and closed injury with Seidel’s test
 Used to assess the presence of anterior chamber
leakage into the cornea
 Concentrated fluorescein is dark orange but turns
bright green under blue light after dilution
 This indicates aqueous leakage, which is diluting the
green dye.
 If you see pooling of green→ closed injury→ Seidel -
 If you can see fluorescein streaming/ dilution/ gushing
→ open injury→ Seidel +)
o Lacerations, abrasions and foreign bodies
 Fluorescein instillation will identify the extent of an abrasion and may
identify a leak of aqueous through a penetrating wound

12 corneal foreign body

35
  If fine, staining, vertical, linear corneal abrasions are seen,
suspect a subtarsal foreign body
 The upper lid must be everted to expose the underside
of the lid, and identify and remove the foreign body
o Management of abrasions/ foreign body:
 Remove corneal FB with a needle under topical anesthesia
 Remove subtarsal FB with a cotton bud from an everted lid
 Give:
 Antibiotic ointment→ because the cornea is avascular and has ↓
immunity and ↑ risk of infection which is difficult to treat if it occurs
 Cyclopentolate (cycloplegic agent) → relives pain caused by spasm of
the ciliary muscle
 Do NOT give steroids because they halt the inflammatory reaction which
induces the healing process (in general, only given in chemical and radiation
trauma)
o Electromagnetic radiation damage
 Due to unprotected exposure to UV light (arc lamp, snow reflection)
 Pt: severe acute onset ocular pain, 6 hours after exposure to the radiation.
 The cornea shows diffuse epithelial edema and punctate erosions
 Resolves within 24-48 hours.
 The anterior chamber
o Iritis
 The eye is connected to the systemic
circulation via the “vascular layer” which
consists of the:
 Iris – which has a major arterial circle
at its root and a minor arterial circle
2mm away from the pupillary border
 Ciliary body
 Choroid
 Therefore, the “source of inflammation” in the
anterior chamber is the iris (provides a source of inflammatory mediators that
↑ the permeability of iris vessels)
 Trauma→ ↑ pressure on the iris→ shedding of pigment + breaking the blood-
aqueous barrier→ inflammatory
reaction
 Hypopyon→ a collection of pus (WBCs)
in the anterior chamber (w/ a fluid
level)
 Hyphema→ a collection of blood (RBCs)
in the anterior chamber (w/ a fluid
level)
 The MC complication of hyphema is ↑ IOP, especially if there is a
secondary bleed, due to:

36
 o Accumulation of empty, red cell ‘ ghosts ’ in the trabecular
meshwork
o Damage to the drainage angle itself (angle recession)
 Clears more slowly after trauma in patients with sickle cell disease b/c
the hypoxic and acidic environment within the anterior chamber
precipitates sickling, and sickling retards red cell removal via the
trabecular meshwork.
 Management of hyphema:
o Rest→ ↓ the risk of re-bleeding (which is ↑ in the first 5-6
days) – admit pediatric patients to make sure they rest, while
adults can be treated at home
o Steroid drops→ ↓ the risk of re-bleeding
o Mydriatic drops, to:
 ↓ the risk of re-bleeding
 Prevent recurrent dilation and narrowing
of the pupil→ thus preventing
compression of blood vessels→ ↓ RBC/
WBC leakage into the anterior chamber
 ↓ the surface available for adhesions
(synechiae)
 Anterior synechiae→ btw the
13Posterior synechia showing part
cornea and iris of iris adherent to the lens
 Posterior synechiae→ btw the iris
and lens
o Direct trauma to the iris
 The pupil has two muscles:
 Sphincter pupillae centrally
 Dilator pupillae peripherally
 Damage of the sphincter pupillae muscle forms a
V-shaped tear in the iris (avoid mydritic agents)
 Iridodialysis→ separation of the iris from its
insertion into the ciliary body
 Produces a D-shaped pupil and polycoria
(more than one pupillary opening)
 Aniridia→ complete separation of the iris

37
  Traumatic mydriasis→ fixed dilation of the pupil as a result of blunt trauma

16 sphincter pupillae trauma 16 aniridia

16 iridodialysis

 Ciliary body
o Ciliary muscle spasm
 Trauma→ ciliary muscle spasm→ ↑ accomodation→ temporary
myopia
o Hypotony
 The ciliary body usually produces aqueous humor
 Trauma may lead to ciliary shutdown (no aqueous humor
production)→ ↓IOP
o Angle-recession glaucoma
 Due to traumatic separation of the layers of the ciliary body
(longitudinal and oblique)
 Damage to the drainage angle →↑IOP
 The Lens
o There are two important parameters for the lens:
 Structure: clear or cataract (may or may not be visually significant)
 Location:
 Dislocation→ due to tearing of all zonules, the lens is displaced from the
normal visual axis
o Suggested by iridodonesis (fluttering of the iris diaphragm on
eye movement)
 Subluxation→ due to tearing some zonules, the lens is found
in its place but is unstable
 Both are treated with surgery and replacement w/ a new lens
o Traumatic cataract:
 Trauma may cause any type of cataract, (but MC is posterior
subcapsular)
 May be due to
 Blunt trauma→ develops slowly due to micropunctures
within the capsule (may be transient, according to book)
 Penetrating trauma→ develops rapidly due to capsule
rupture
 The posterior chamber
o Must be evaluated after trauma by:

38
  Slit lamp
 Ultrasound if there is an opacity preventing visualization (like hyphema, cataract
or corneal edema)
o Examine the vitreous – is it attached or detached? Is there hemorrhage or not?
 In the case of vitreous hemorrhage the patient will report seeing “floaters”
 You must exclude retinal damage
in these patients
 If not associated with other
alarming symptoms or conditions
requiring emergent surgery, you
may observe the patient for a few
weeks→ if it hasn’t resolved,
proceed to vitrectomy
 The optic nerve
o Assess for optic nerve damage by:
 Checking for a RAPD (relative
afferent pupillary defect)
 Examining brightness sensitivity
(shine a bright light and compare
between both eyes, ↓ sensitivity
in the bad eye)
 Checking for red desaturation (pt sees a washed-out red in their bad eye)
 Assessing color vision
 Assessing the visual field - central scotoma or arcuate scotoma may indicate
optic nerve damage
o The patient may develop traumatic optic neuropathy, with optic nerve atrophy only
seen 3-6 weeks after injury
o Give these pts pulses of IV steroids
 The retina
o Commotio retina
 Traumatic retinopathy (contusion) secondary to direct or indirect trauma to the
globe.
 Retinopathy may be present at areas of scleral impact (coup) and or distant sites
(contrecoup) including the macula
 MC site damaged is the supero-nasal retina

39
  Signs:
 white patches on the retina
due to swelling and edema of
ganglion cells
 areas of hemorrhage
 cherry red fovea (when
there’s macular involvement)
 Prognosis is excellent→ vision returns
to normal within 4-6 weeks
 But it’s a RF for:
 Retinal detachment – especially if there were micropunctures in the
retina
 Granulation due to excessive healing – if this occurs in the macula there
is a risk for permanent loss of vision
o Retinal tears
 Treated by retinopexy via cryotherapy or laser around the tear to induce
healing→ promotes adhesion between the retina and underlying tissue
o Retinal detachment
 Intra-ocular foreign body
o A special cause of penetrating trauma
o Siderosis oculi
 Retained, iron - containing foreign bodies in
the vitreous
 Leads to diffusion of Fe+2 ions throughout the
globe
 Free radicals are produced by the Fenton
reaction
 The patient presents with:
 Progressive degeneration of the retina
 Heterochromia
 Fixed mydriasis
 Cataracts
 Irreversible blindness (if the FB is not removed at the time of injury) due
to degeneration of photoreceptors
 Events of this kind emphasize the need to wear protective goggles when using
metal hammers or hammering on metal.

40
  Sympathetic ophthalmia
(also called spared eye
injury)
o Diffuse bilateral
uveitis of both eyes
after trauma to one
eye
o May develop within
days and up to
several years
o Due to destruction
of choroid→
pigment release→ antibody formation→ autoimmune uveitis
o So w/ extensive eye injury, remove the damaged eye so you don't lose the other.)
 Chemical Injury
o Either alkaline or acidic
o Alkaline damage is worse because while acid leads to coagulative necrosis (which
prevents further penetration), alkali lead to liquefactive necrosis (↑ penetration and ↑
damage)
o The prognosis is worst when there is corneal injury
o The patient presents with:
 History of chemical injury
 Blurred, hazy vision
 White and ischemic conjunctiva
 Congested limbus
 Burns on skin around the eye
o Classification of chemical ocular injury:
 Grade 1: no limbal ischemia,
clear cornea→ good prognosis
 Grade 2: limbal ischemia < 1/3
of the circumference, clear
cornea→ good prognosis
 Grade 3: limbal ischemia btw
1/3 – ½ the circumference, hazy
cornea→ middling prognosis
 Grade 4: limbal ischemia > ½ the
circumference or total corneal
opacification→ worst prognosis
→ requires amniotic membrane/
limbus transplant
o Treatment:
 Irrigation

41
  Under running water, 2L or for 15 minutes, be sure to irrigate the
subtarsal groove
 Steroid drops
 Dilating drops
 Vitamin C
 Tetracyclines due to their anticollagenase activity

Refractive errors
(Honestly, this lecture should have come first)

 For the eye to generate accurate visual information,

light must be correctly focused on the retina. The
focus must be adjustable to allow equally clear vision
of near and distant objects
o The air/tear interface at the cornea is
responsible for 2/3 of the focusing power of
the eye – 40 diopters
o The lens is responsible for the remaining 1/3 –
20 diopters
 These two converge the rays of light because
o The refracting surfaces of the cornea and lens
are spherically convex
o The cornea has a higher refractive index than
air; the lens has a higher refractive index than
the aqueous and vitreous humors that surround it.
 The velocity of light is reduced in a dense medium so that light is refracted
towards the normal.
 Emmetropia→ when parallel rays of light from a distant object (6m and beyond) are brought to
a focus on the retina w/ the eye at rest (no accommodation) → can see sharply in the distance
without accommodation
 Ammetropia→ parallel rays of light are not focused on the retina w/ the eye at rest: may be
divided into myopia, hyperopia and astigmatism.
 Diagnosis of refractive errors may be
done by:
o Pinhole glasses
 Light rays that are
perpendicular to the lens
to not refract but go
straight ahead.
 If visual acuity improves
with this test, that
means the patient has a
refractive error
o Auto Refractor (AutoRef)

42
  The autorefractor can determine when a patient's eye properly focuses an
image.
 It calculates the refraction of the eye, sphere, cylinder and axis.
o Retinoscope
o Phoropter
 Myopia (short-sightedness)
o The optical power of the eye is too high
o Parallel rays of light are brought to a focus in front of the retina.
o Causes of myopia:
 Axial→ due to an elongated globe
 Refractive→ the optical power is higher than normal, due to:
 Excessive curvature of the cornea (like keratoconus)
 Excessive curvature of the lens (like lenticonus)
 ↑ refractive index of the lens (like nuclear cataracts)
o Requires diverging (negative, concave) lenses for image correction
o Types of myopia:
 Benign myopia→ starts in school-aged children, stable in adulthood
 Pathological (progressive and malignant) myopia→ increases rapidly each year,
associated w/ vitreous opacity and chorio-retinal damage
 Congenital (infantile) myopia→ present at birth, persists through infancy.
 Usually myopia > 10 diopters
 Increases slowly each year
 Pseudomyopia→ blurry vision due to ciliary muscle spasm
o Pathological causes of myopia:
 Keratoconus
 Nuclear cataract
 DM (hyperglycemia→ ↑ glucose in the lens)
 Marfan syndrome
o High myopia (6 diopters and up) ↑ the risk of
the following changes:
 Deep anterior chamber
 Atrophy of the ciliary muscle
 Premature vitreous collapse and
opacification
 Fundus changes:
 Loss of RPE pigment and RPE
atrophy at the macula
 Large tilted optic disc
17 Elongated eyeball with posterior staphylomas
 White crescent on the
temporal side
 Posterior staphyloma (bulging of the posterior surface of the globe)

43
  Chorio-retinal degeneration (formation of retinal holes and lattice
degeneration ↑ the risk of retinal detachment)

o Complications of myopia:
 Open-angle glaucoma (deep anterior chamber)
 Cataract
 Retinal detachment
 Macular degeneration
 Amblyopia - occurs if the pt is young and has anisometropia – difference in the
refractive power between both eyes
 The younger the pt, the more they’re able to handle anisometropia
 However, if this occurs in a young child and they suppress the blurry
image from the worse eye → amblyopia
 Hyperopia (hypermetropia) (far-sightedness)
o The optical power of the eye is too low
o Parallel rays of light converge towards a point behind the retina
o Causes of hypermetropia:
 Axial→ the globe is too short
 Refractive→ the optical power is too low due to:
 ↓ curvature of the cornea
 ↓ curvature of the lens
 ↓ refractive index of the lens (like in cortical cataract)
o When examining a hyperopic patient, administer cycloplegic drops to induce ciliary
muscle relaxation and exclude accommodation to measure the true visual acuity.
 Since these pts usually have ciliary spasm, when you prescribe glasses, prescribe
them weaker than the pt really needs (or else vision blurs)→ tx their manifest
hyperopia, not their latent one.

44
 o Most hyperopic patients are able to accommodate by a few diopters – however,
accommodation for long periods of time leads to ciliary muscle spasm, eye fatigue,
headache and ophthalmoplegia
o We’re all born with certain degree of hypermetropia (around 2-3 D), which decreases as
your eye grows and gets longer and with signals from accommodation
(Emmetropization)
 However, if a kid has a lot of screen time from a young age, the eye
accommodates a lot→ so the eye “thinks” it has really ↑↑↑ hypermetropia→
so it reacts by ↑↑ the axial length of the eye→ this leads to the kid developing
myopia by the time they reach middle school.
o Morphologic changes in hypermetropia:
 Shallow anterior chamber
 Pseudo-optic neuritis (indistinct cup margin, no physiologic cup)
o Complications of hypermetropia:
 closed angle glaucoma due to shallow anterior chamber
o Requires converging (positive, convex) lenses for image correction
 Astigmatism
o The optical power of the cornea in different
planes is not equal.
o Parallel rays of light passing through these
different planes are brought to different
points of focus.
 These points may be behind, in front
of, or on the retina.
 The steepest and flattest meridians
of the eye are called principal
meridians
o Instead of being spherical, the cornea is more
similar to an American football
o The patient’s main complaint here is persistent
blurry vision regardless of distance
 Most people have some degree of
astigmatism but it is usually mild and
tolerated so there’s no need for glasses
o Pathological causes of astigmatism:
 Corneal: post-surgical, traumatic, infectious
 Lid masses which exert external pressure on the cornea
o The curvature of the cornea may be measured with a keratometer.
o Types of astigmatism – regular vs. irregular astigmatism
 Regular astigmatism→ the principal meridians are perpendicular to each other
 With the rule astigmatism→ seen in kids, the vertical meridian is the
steepest

45
  Against the rule astigmatism→ seen in the elderly, the horizontal
meridian is the steepest

 Oblique astigmatism→ the steepest curve lies between 120-150 D and

30-60 D
 Irregular astigmatism→ the principal meridians are not perpendicular to each
other
 Can’t be fixed with glasses, requires contact lenses
o Types of astigmatism: Simple vs. Compound astigmatism
 Simple myopic astigmatism
 Light comes to two focal points: one
before the retina, and one on the
retina
 Requires cylindrical lenses for vision
correction
 Simple hyperopic astigmatism
 Light comes to two focal points: one
behind the retina, and one on the
retina
 Requires cylindrical lenses for vision
correction
 Compound myopic astigmatism
 Light comes to two focal points, both
of which are before the retina but at
two different locations before the
retina.
 Requires sphero-cylindrical lenses for vision correction
 Compound hyperopic astigmatism
 Light comes to two focal points both of which would be in a virtual
location behind the retina but at different virtual locations behind the
retina.
 Requires sphero-cylindrical lenses for vision correction
 Mixed astigmatism
 Light rays come to two focal points, one of which is before the retina
and the other of which is behind the retina
 Requires sphero-cylindrical lenses for vision correction

46
 o Cylindrical lenses are required to correct for the non-spherical shape of the cornea in
simple astigmatism→ they affect just one meridian, fixing it while maintaining the other
in its correct position
o Spherocylindrical (toric) lenses are required in compound astigmatism
 the spherical portion works on both meridians and turns the astigmatism from
compound to simple
 the cylindrical portion fixes the remaining meridian

Accommodation and presbyopia

 Accommodation (the Helmholtz theory): when an object is brought nearer to the eye→ ciliary
muscle contraction→ relaxes zonular tension on lens equator → lens becomes more spherical→
↑ lens power→ focus on image is maintained.
o the accommodation reflex is also accompanied by converging of the eyes and miosis
 The degree of accommodation needed depends on how far/near the object you’re looking at is:
o Diopters = 1/ distance of the object (in meters)
o To see an object 0.25 m away, you need 1/0.25 = 4 diopters of accommodation (a lot)
o To see an object 4 m away, you need ¼ = 0.25 diopters of accommodation (a little)
 Children have a greater ability to accommodate than adults:
o A 1 year old may accommodate 20 degrees of hyperopia
o A 20 year old may accommodate 10 degrees of hyperopia
o A 40-45 year old may accommodate only 1-2 degrees of hyperopia
 Presbyopia: pathological ↓ ability to accommodate with age (especially after age 40) due to
age-related loss of elasticity of the lens capsule
o Due to deposits of insoluble proteins in the lens w/ age → ↓ elasticity→ ↓
o Leads to difficulty w/ near vision (b/c rays from near objects are divergent are require
accommodation)
o Occurs earlier in hypermetropes than in myopes
 Spectacle options for presbyopia:
o Separate pairs of glasses for near and far
vision (reading glasses)
o Bifocal lenses→ near correction is added
to the lower segment of the distance lens
o Varifocal lenses→ the power of the lens
gradually changes from the distance
correction (in the upper part) to the near
correction (in the lower part). This
provides sharper middle - distance vision.

Optical correction after cataract extraction

 Aphakia→ after cataract extraction, the eye is rendered highly
hypermetropic (b/c no lens). This can be corrected by:
o The insertion of an intra-ocular lens (IOL)
 An eye w/ an IOL is termed pseudophakic
 Placed at the site of the natural lens
 Yields the best optical results

47
  Can’t change shape, so they can’t accommodate, however
 Hinged lenses with some accommodation are available
 Multifocal IOLs are available (however because of ↓ contrast and glare,
they’re not for everybody
o Contact lenses
 Produce slight magnification of the retinal image (110%) (not of visual
significance)
 Insertion, removal and cleaning can be difficult for elderly patients
o Aphakic spectacles
 Powerful positive lenses which magnify the retinal image by about 133%,
causing the patient to misjudge distances
 Cannot be used to correct one eye alone if the other eye is phakic or
pseudophakic b/c of the disparity in image size between the two corrected eyes
(aniseikonia) → causes dizziness and diplopia
 May distort images due to the thickness of the lens

Contact lenses and spectacles

 Contact lenses are either soft or rigid
Rigid lenses Soft lenses
Comfort Uncomfortable Better tolerated physically
Gas permeability Greater Less
Risk of corneal damage by Less Greater
hypoxia
Ease of cleaning Easier, so ↓ risk of infection Harder, so ↑ risk of infection
Correction of astigmatism Can Only if toric *?
Proteinaceous debris Less likely, so ↓ risk of More likely, so ↑ risk of
adhering to lens allergic conjunctivitis allergic conjunctivitis
 Daily disposable contact lenses are available as well
 Thin, soft contact lenses without a refractive function may also be used as ocular bandages, e.g.
in the treatment of some corneal diseases such as a persistent epithelial defect.
 Glasses vs contact lenses
Glasses Contact lenses
Cosmetic Disliked Preferred
Quality of vision Poor quality of vision, Better quality of vision
especially at high degrees
due to ↑ magnification or
minimization of image size
(2% per 1 D)
Risk of corneal hypoxia None All contacts cause a degree of
hypoxia, may lead to corneal
vascularization
Risk of infection, dryness or No risk ↑ risk (require careful daily
allergy cleaning and disinfection)
 Contact lenses are indicated (rather than glasses) in:
o Irregular corneal astigmatism

48
 o High anisometropia
o Corneal disease
 Contraindications to contact lens use:
o History of atopy
o Dry eyes
o Previous glaucoma filtration surgery
o Inability to handle/ cope with lenses

Refractive surgery
 Can be lens-based surgery or cornea-based surgery
 In lens-based surgery, an implantable contact lens (ICL) is implanted
in front of the natural lens
o Pros:
 Preserves accommodation
 Can correct high degrees
o Cons:
 May cause over/under correction
 ↑ risk of infection
 ↑ risk of ↑ IOP
 In cornea-based surgery, an excimer laser is used to ablate a
superficial layer of corneal stroma→ modifies the shape of the
cornea→ alters its refractive function by re-shaping it.
o Myopia is corrected by flattening the cornea (results of these pts are usually better)
o Hyperopia is corrected by steepening the cornea

 Photorefractive Keratectomy (PRK)

o The corneal epithelium is removed
o The laser is applied to the corneal surface
o The cornea is resurfaced in a few days (epithelium regenerates peripheral to central)
o Patients report discomfort for a few days→ ↓ w/ bandage contacts and NSAIDs.
 LASIK: Laser-Assisted in Situ Keratomileusis

49
 o A rapidly moving automated blade removes a hinged, partial-thickness flap of cornea
stroma (the epithelium remains intact)
o The laser is applied to the stromal bed
o The flap is then restored
o Instantaneous improvement with minimal discomfort
LASIK PRK
Healing Occurs within 24 hours Occurs within a week
When is visual acuity 6/6 the next day Blurry vision within the first
achieved? week, then improves. The
final results are appreciated
within 1-3 months
Pain after surgery No pain Mild to severe pain (usually
severe)

 How to choose between LASIK and PRK?

For thin corneas PRK
For ↑ grade refractive errors LASIK
For ↓ grade refractive errors PRK
For patients with dry eyes PRK
For patients with ↑ risk of trauma (athletes) PRK
o Otherwise, according to patient preference
 LASEK: Laser-Assisted Subepithelial Keratomileusis
o Creates only an epithelial flap, leaving a thicker stroma
o Good for those with a thin cornea
o Takes longer to heal than with LASIK
 Small Incision Lenticule Extraction (SMILE)
o Uses a single femtosecond laser referenced to the corneal surface to cleave a thin
lenticule from the corneal stroma for manual extraction
o Better healing than LASIK (no flap necessary)
o Used for grades 3 and up.
 Complications of refractive surgery:
o Over/under correction
o Infections (rare, but aggressive if they do occur)

Keratoconus
 Thinning of the center of the cornea, leading to an ectatic, conical
corneal shape
o Due to a failure of adhesion between the collagen fibrils of
the stroma, responsible for its mechanical strength. Thinning
is due to an unravelling process.
o Causes marked myopia and irregular astigmatism
o Usually sporadic but may occasionally be inherited
o Painless
o Bilateral

50
 o Progressive
 The patient presents with blurred vision, progressive myopia and progressive astigmatism
 Diagnosis by keratometer/ pentacam topography
 Signs:
o Munson’s sign: bulging of the eyelid on
downgaze, a sign of advanced keratoconus
o Fleischer ring: ring around the cornea
o Vogut striae: formed at the site of bulging due
to stretching of the cornea
o Corneal scarring: due to corneal edema 19 Fleischer ring + Vogut’s striae + 19 Munson's sign
o Oil-droplet reflex: on distant direct stromal scarring at the apex
ophthalmoscopy, the central and peripheral
areas of cornea are separated by shadows

 Management:
o Cross-linking of stromal collagen
 By exposing the stroma to UVA 20 Oil Droplet Reflex
radiation in the presence of riboflavin
 the generation of free radicals results in cross-linking and inhibits progression of
the disease
o Contact lenses
 The contact lens arches over the irregularly shaped cornea to
provide a new, optically perfect anterior surface which
restores the optics of the eye
o Corneal ring
 Supports the cornea
o Frequent changing of glasses 21 corneal ring
 But when irregular astigmatism develops, glasses become
useless
o Corneal transplant – in severe cases
 Keratoglobus: same process as keratoconus, but it affects the entire
cornea instead of just the center
 Pellucid marginal degeneration: same process as keratoconus, but it
affects the periphery of the cornea instead of the center

22 Pellucid Marginal Degeneration

51
Strabismus
Anatomy and physiology

 Muscles of the orbit: 6 extraocular muscles + levator palpebrae superioris

Muscle Primary action Secondary action Tertiary action Testing postion

Lateral rectus Abduction - - Abduction
Medial rectus Adduction - - Adduction
Superior rectus Elevation Intorsion Adduction Up and out
Inferior rectus Depression Extorsion Adduction Down and out
Superior oblique Intorsion Depression Abduction Down and in
Inferior oblique Extorsion Elevation Abduction Up and in

 Eye mobility:
o One eye→ -duction (supraduction, infraduction, abduction, adduction…)
o Both eyes→ -version (dextroversion, levoversion, dextroelevation, levoelevation…)
allow conjugate and unconjugated eye movements
 Yoke muscles: contralaterally paired extraocular muscles that work
synergistically to direct the gaze in a given direction for conjugate eye
movement
o Like contraction of the right lateral rectus with the left medial rectus
in order to look to the right
 When you want to examine the extraocular muslces, the patient is asked to
look in the 9 diagnostic positions of gaze.

52
  Start by examining one eye at a time, then both eyes.
 Smooth pursuit: the speed with which the eyes follow a moving target
 Saccades: the rapid movements required to take up a new position of gaze
o Both are controlled by higher cortical centers which influence the brainstem nuclei

Strabismus
 Anatomical axis: a straight line that goes from the posterior pole to the center of the cornea,
dividing the eye in two
 Visual axis: the straight line that extends from the viewed object through the center of the pupil
to the fovea
o Normally the visual axes of both eyes meet and intersect at the object of interest
o Eye movements are coordinated so that the retinal images of an object fall on
corresponding points of each retina.
 Angle of Kappa: the angle between the visual axis and the anatomical axis, usually around 5
degrees
 Strabismus is a misalignment of the visual axes of the two eyes.

 Binocular single vision: a state of simultaneous vision, achieved by the coordinated use of both
eyes, so that separate and slightly dissimilar images arising in each eye are appreciated as a
single image by the process of fusion.
 Stereopsis: perception of depth and 3D structure obtained because each eye views an object
from a different angle
o Development requires that eye movements and visual alignment are coordinated in the
first 5 years of life.
 Advantages of stereopsis and binocular single vision:
o ↑ the field of vision and eliminate the blind spot (since
the blind spot of one eye falls in the seeing field of the
other)
o Provide binocular acuity, which is greater than
monocular acuity
o Stereopsis provides depth perception and elimination
of distance
 In strabismus, the visual axes of both eyes are not aligned, so
binocular single vision is not possible, leading to:
o Diplopia: one object is seen to be in two different places

53
 o Visual confusion: two separate and different objects appear to be at the same point.
o In children with strabismus, the image in the squinting
eye is suppressed, thus:
 No diplopia
 However, strabismic amblyopia develops if this is
prolonged and constant during the sensitive
period of visual development (the first 5 years)
and thus causes a reduced visual acuity in the
squinting eye.
 If the child alternates the squinting eye,
they will not develop amblyopia since a
focused image always falls on one or
other retina. However, they will not
develop stereopsis.
 The direction of deviation in strabismus may be:
o Eso- nasal horizontal deviation
o Exo- temporal horizontal deviation
o Hyper- superior vertical deviation
o Hypo- inferior vertical deviation
 Classifications of squint include concomitant vs. incomitant,
congenital vs. acquired, manifest vs. latent, alternating vs.
monocular squint.
 Concomitant (non-paretic) squint vs. Incomitant squint

Concomitant Incomitant
Angle of deviation Constant regardless of the Varies as the patient changes their gaze
gaze position or the fixating position or the fixating eye
eye
Movements of Full without restriction There is under-action of one or more eye
both eyes muscles due to paralytic causes (a nerve
palsy, extraocular muscles paresis) or
restrictive causes (like tethering of the
globe in blow out # or Graves’ disease)
 CN6 palsy→ failure of eye abduction
 CN4 palsy→ defective depression of the eye when attempted in adduction
o Patient has diplopia when going downstairs or reading
 CN3 palsy→ ptosis, down and out eye, + a dilated pupil if there is autonomic involvement
 Etiology of concomitant squint:
o In an otherwise “normal child” with normal eyes – due to an abnormality in central
coordination of eye movements
o Associated with refractive error or ocular disease:
 Refractive error
 MCC
 Prevents formation of a clear image on the retina

54
  If the refractive error is dissimilar in the two eyes (anisometropia) one
retinal image will be blurred
 Increased accommodative effort in a child w/ equal hyperopia in both eyes
 Increased accommodative effort is required or focus on both distant
and particularly near objects
 However, there is a link (synkinesis) between accommodation and
convergence, so this ↑ accommodation is accompanied by ↑
convergence and ultimately a convergent squint in one eye.
 Eye opacities
 Blurring/ preventing the formation of the retinal image
 Like cataracts or corneal opacities
 Abnormalities of the retina
 Inadequate info is transmitted to the visual cortex
 Congenital vs. Acquired squint:
o Congenital→ squint develops within 6 months of life
o Acquired→ squint develops after 6 months of life
 Manifest vs. Latent squint:
o Latent squint→ heterophoria:
 The patient’s eyes appear normal most of the time, and the squint only arises
under certain conditions (like CNS depression, fever, fatigue, post-trauma,
daydreaming).
 Fusional control is usually present
 The squint is not manifested before testing or after testing, but is visible during
testing.
o Manifest squint→ heterotropia, either:
 Intermittent: comes and goes, so that it is not manifested before testing, but is
present both during and after testing.
 Fusional control is present part of the time
 Constant: present at all times, so fusional control is not present
o A squint may progress from latent to intermittent to constant
o May be expressed as:
E→ esophoria ET→ esotropia
X→ exophoria XT→ exotropia
RH→ right hyperphoria RHT→ right hypertropia
LH→ left hyperphoria LHT→ left hypertropia
RHO→ right hypophoria RHOT→ right hypotropia
LHO→ left hypophoria LHOT→ left hypotropia
Intermittent tropia → (T)
E"→ problem in near vision

 Alternating vs. Monocular squint:

o Monocular squint: abnormal alignment of one eye (right or left), so the patient is a
monocular fixator

55
 o Alternating squint: spontaneous alternation of the squint between the right and left
eyes.
 Pseudostrabismus: the false appearance of eye misalignment (looks like a convergent squint)
o May be due to:
 Prominent epicanthal folds (like in
Asian kids)
 Wide nasal bridge
 Narrow interpalpebral fissure
 Very large/ small angle of Kappa

Examination of a child with strabismus

 Always start with history and physical exam.
o Rule out (or rule in) life-threatening conditions,
amblyopia
 Inspect for abnormal head posture: head tilt to the
right or left/ chin elevation or depression/ face turn to
the right or left
o In horizontal strabismus (like in abducens
palsy) → face turn to compensate the defect
o In vertical strabismus→ chin elevation or
depression
o In oblique strabismus (like in CN 4 palsy)→
contralateral head tilt to compensate their
oblique diplopia
 Inspect for torticollis – which may be due to:
o Muscular causes (like SCM fibrosis)
o Ocular causes, which include:
 Oblique dysfunction, especially an inferior oblique muscle problem
 AV pattern strabismus
 Nystagmus with a null point (which is the direction of gaze at which the
nystagmus has the smallest amplitude. The patient always tries to look through
this point for better vision)
o In muscular torticollis, the patient may present with:
 Palpable induration of the SCM
 Painful limitation of neck movement
 Asymmetric facial expression/ bones
 Persistence of torticollis during sleep
 Persistence of torticollis when the patient is asked to close their eyes and the
neck is passively manipulated
o In ocular torticollis, the patient may present with:
 Facial symmetry and free and painless neck movement with no limitations
 Torticollis that disappears when asleep
 Torticollis that disappears when the patient is asked to close their eyes and the
neck is passively manipulated
 Examination of a strabismus patient must include examination of:

56
 o Vision (visual acuity)
o Motility (detect any abnormalities in eye movement)
o Type and angle of strabismus (with tests of squint)
o Stereopsis and binocular single vision with special 3D pictures and a synoptophore,
respectively.
o Determination of any refractive errors after cyclopentolate drops
o Detailed eye exam, including fundus view, after cyclopentolate drops.
 Tests of squint:
o Bruckner test
 Use an ophthalmoscope to see the red reflex (from the
retina)→ it appears darker in the normal eye, and lighter
(↑ light reflex) in the squinting eye
 Good for rough estimation
o Hirschberg test
 Also uses an
ophthalmoscope – sit
33cm away from the
patient and shine the
light on both eyes at
once
 Good for uncooperative
patients and poor
fixators
 Asses the corneal light
reflex in both eyes to
test eye alignment
 If the abnormal
corneal reflex appears temporally, that means the eye is deviated
nasally, and vice versa
 If the reflex is deviated inferiorly that means the eye is superiorly
deviated and vice versa
 It can also be used to determine the angle of deviation:
 Under mesopic light (light that is midway between photopic and
scotopic) the pupil is 4mm in diameter, w/out pupillary constriction or
dilation
 Normally, in orthotropia, the corneal reflex should be in the middle of
the pupil
 Each 1 mm deviation from the center = 7 degrees of strabismus
 Every degree of strabismus = 2 prism diopters
 If the reflex is at the pupillary margin it’s 2 mm away from the center→
angle of deviation is 28 prism diopters
 If the reflex is between the pupillary margin and the limbus (mid-iris)→
angle of deviation is 30 prism diopters
 If the reflex is at the limbus→ angle of deviation is 45 prism diopters

57
 o Krimsky test
 To do this test you need a source of light
and a prism bar
 The apex of the prism should be
directed towards the side of
deviation (not towards the
deviating eye)
 The prism should be placed upon
the fixating eye
 The power of the prism is increased
gradually until the corneal reflexes are
symmetrical (the reflex in the affected eye
appears centrally) → neutralization of the
angle of deviation
 Then the angle of deviation is quantified by
determining how much prism is required to
center the reflex.
 Like for example, you need 50 prism diopters to neutralize the deviation

o Cover test
 To detect manifest squint (-tropia) of the uncovered
eye
 The fixating eye is completely covered for a few
seconds
 If the other eye has been maintaining fixation
it should not move
 If it moves outwards to take up fixation an
esotropia is present.
 If it moves inwards to take up fixation an
exotropia is present
 This test reveals the re-fixational movement as the
squinting eye is forced to see via its fovea

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 o Uncover test
 To detect latent squint (-phoria) of the covered
eye
 This test interrupts binocular fusion (inhibits
bifoveal visual stimulation) to reveal a tendency of
the visual pathways to drift apart which is
corrected by unconscious effort
 Cover one eye and then quickly look under
the cover
 If the eye deviates when covered and then
quickly returns to its position when
uncovered (the covered eye shows a
refixation movement once binocular
conditions are restored)→ latent squint
 The eyes will be straight before and after
this test, squint is only revealed during
testing.

o Alternate cover test

 This test will allow the full deviation to be
measured as it will bring out any phoria that is
present in addition to the tropia determined on
single cover testing by suspending binocular
fusion.
 This test involves covering one eye and holding the
occluder for several seconds to suspend fusion,
then shifting the occluder to the other eye and
rapidly alternating back and forth without
allowing the patient to become binocular
 The eye under the occluder is observed as the
23The alternate cover test.
Top: Exotropia, left eye
occluder is removed and placed over the fellow eye in order to determine the
fixating. Middle and bottom: direction of deviation.
Both eyes move each time  If there is an outward, or lateral, refixation in the nasal to temporal direction –
the cover alternates from 1
eye to the other.
this represents an eso deviation.
 If there is an inward, or medial, refixation in a temporal to nasal fashion – this
represents an exo deviation.

59
 o Alternate cover test with prism
 The most accurate test to detect the angle of deviation
 More accurate than Krimsky because while this test detects both
tropias and phorias, Krimsky only detects tropias because we don’t
break fusion
 Put the prism on the deviated (non-fixating) eye
 Direct the apex towards the side of deviation
 Neutralize the deviation with a prism of the correct power.
 Perform the alternate cover test until there is no longer a
shift in fixation in either eye. This is when the deviation has
been truly neutralized. 24The prism alternate cover
test. Top: The exotropia is
neutralized with a prism of
the correct power. Middle
Management: and bottom: The eyes do not
move as the cover alternates
 Any significant refractive error is first corrected with glasses from one eye to the other.

 If amblyopia is present and the vision does not

improve with glasses the better-seeing eye is
patched for limited periods of time to stimulate
visual development and promote an improvement of
visual acuity in the amblyopic eye.
 If squint still hasn’t resolved after these two steps,
surgery is indicated
o The principle of surgery is to realign the eyes
by:
 Recession: moving the muscle
insertion backwards, weakening its
action
 Resection: removing a segment of
the muscle at its insertion to
strengthen its action.

Scenarios:

 A patient has alternating esotropia (50 prism

diopters) and +6 hypermetropia in both eyes.
o Start management with glasses
o Have the patient come for follow-up after 1-2 months to evaluate both the patient’s
vision and the angle of strabismus while they are wearing their glasses
o If the patient’s vision is 6/6 with their glasses on→ no amblyopia
 If at follow-up the patient’s vision is still not 6/6 with their glasses, this patient
has amblyopia and requires patching of their normal eye
 If at a later follow-up, vision becomes 6/6 with glasses→ their amblyopia has
been fixed.

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 o If the patient’s eyes are ortho with glasses and eso without them we call this full
accommodative esotropia
 When you fixed their hypermetropia you fixed their squint has well
o Here the management is only glasses
o Follow up the patient regularly, and when they’re 18 do refractive surgery to fix their
hypermetropia
 A patient has alternating esotropia (50 prism diopters) and +6 hypermetropia in both eyes.
o You started management with glasses, but at follow-up 2 months later, the patient has
30 prism diopters of esotropia with their glasses on, and 50 prism diopters of esotropia
without their glasses.
o This patient has partially accommodative esotropia
 Only partially accommodative means that there is a non-accommodative
element (muscle) that requires surgery
 So management involves glasses to fix 20 prism diopters and surgery to fix the
remaining 30 prism diopters
 After surgery, the patient will be ortho with their glasses on and exo
(consecutive exotropia) without their glasses
 A patient has alternating esotropia (50 prism diopters) and +6 hypermetropia in both eyes
o You started management with glasses, but at follow-up 2 months later, while vision is
6/6, the angle of deviation with and without glasses has remained the same.
o This patient has non-accommodative esotropia
 Their strabismus is not due to hypermetropia
 Requires surgical management.
 A 6 months-old infant has alternating esotropia (crossing eyes) and +1
hypermetropia in both eyes.
o You started management with glasses, but at follow up 2 months later,
there has been no improvement, in neither the esotropia nor in the
refractive error
o This patient has congenital/ infantile esotropia
 Appears at birth or within the first 6 months of
life
 The infant’s refractive error is within the normal
physiological limits
 A moderate to large angle esotropia with angle
of deviation typically greater than 30 prism
diopters.
 The infant has crossing eyes – uses their
left eye to look right, and their right eye
to look left
 40% of cases are associated with amblyopia
 Associated conditions include dissociated vertical deviation (a condition in
which one eye drifts upward), nystagmus and inferior oblique overaction (eye
is elevated in adduction, both horizontally and in upgaze)
 Treat with surgery (between 6 months and 2 years of age)

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  A 5 year old patient with no known refractive errors develops esotropia suddenly.
o This patient has acute-onset esotropia/ late-onset esotropia
 This patient should have a full neurological exam (rule out neuro disease, life-
threatening conditions…) including a cranial nerves exam and extraocular
muscle motility
 Check for papilledema→ would indicate ↑IOP
 If the patient is found to have a refractive error, this could mean that though
the eye had been accommodating fine before, the patient has been exposed to
a stress that lead to disruption of their accommodation→ the squint appeared.

The Orbit
Anatomy:

 The orbit is pyramidal in shape, with an apex posteriorly and a base anteriorly.
 Protects and stabilizes the globe
 It’s 30-35 mm in diameter, and 30 cm3 in volume
 Borders of the orbit:
o Lateral→ greater wing of the sphenoid + the zygomatic bone
o Medial→ the body of the sphenoid + the maxillary, lacrimal, and ethmoid bones

62
 o Floor→ the zygomatic, maxillary and palatine bones
o Roof→ the lesser wing of the sphenoid + the frontal bone
 The weakest area in the orbit is the postero-medial part of the floor because it has the inferior
orbital groove, which gives way to the infra-orbital foramen.
o The infra-orbital nerve (a branch of V2) emerges through the infra-orbital foramen
 The thinnest part of the orbit is the lamina papyracea (the ethmoidal portion of the medial wall)
o It is paper-thin and separates the ethmoid sinus from the orbit.
o Orbital cellulitis may occur when bacterial infection spreads from the ethmoid sinus
through this thin wall into the orbit
 The MC fractured wall of the orbit is the floor (trauma→ ↑IOP→ blow-out fracture) which may
lead to:
o Paresthesia due to infraorbital nerve compression
o Diplopia due to inferior rectus muscle restriction
o Enophthalmos when orbital contents are displaced into an adjacent sinus
 The lateral walls of the right and left orbits are
perpendicular to each other
 The medial walls of the right and left orbits are parallel to
each other
 The angle between the medial and lateral walls of the orbit
is 45°
 The orbital axis is the line from the center of the optic
foramen (apex of orbit) extending anteriorly, laterally, and
inferiorly to the middle of the orbital opening.
 The orbital axes are separated by 45°

 Pathways into the orbit:

63
 o Optic canal
 Transmits the optic nerve and the ophthalmic artery
o Superior orbital fissure
 Between the lesser and greater wings of the sphenoid
 Transmits in its upper half:
 LFT: Lacrimal (V1), Frontal (V1) and Trochlear nerves
 The superior ophthalmic vein
 Transmits in its lower half:
 The oculomotor nerve
 The nasociliary nerve (V1)
o Inferior orbital fissure
 Transmits the maxillary nerve, the zygomatic nerve and the inferior ophthalmic
vein
 Proptosis (Exophthalmos)
o A protrusion of the eye caused by a space-occupying lesion
o Differentiate it from pseudo-proptosis which may be caused
by:
 Contralateral ptosis
 Contralateral enophthalmos
 Ipsilateral lid retraction 25 buphthalmos

 Ipsilateral large globe like buphthalmos (enlargement

of the eyeball, usually indicates the presence of
infantile glaucoma
o Can be measured with an exophthalmometer– a difference
greater than 3mm between the eyes is significant
o Causes of true proptosis:
 Axial: If the eye is displaced directly forwards, it
suggests an intra-conal lesion
 The “cone” refers to the muscle cone of extra-ocular recti muscles from
the annulus of zinn.
 Like an optic nerve sheath meningioma
 Non-Axial: If the eye is displaced to one side, it suggests an
extra-conal lesion
 Like a tumor of the lacrimal gland displacing the globe
infranasally
 Or like a tumor of the lacrimal sac displacing the globe
supero-temporally
o The MCC of proptosis overall is thyroid disease
o The MCC of unilateral proptosis is thyroid disease
o The MCC of bilateral proptosis is thyroid disease
o The MCC of pulsatile proptosis is caroticocavernous fistula
o Visual acuity may be decreased by
 optic nerve compression→ requires emergency lateral canthotomy to
relieve pressure 26 lateral canthotomy

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  exposure keratopathy→ in severe proptosis, when the cornea is no longer
protected by the lids and tear film
 distortion of the macula→ due to compression of the globe by a posterior
space-occupying lesion
o A transient proptosis induced by
valsalva is a sign of orbital varices
o A slow-onset proptosis suggests a
benign tumor, whereas rapid onset is
seen in inflammatory disorders,
malignant tumors and
caroticocavernous fistula

 Enophthalmos
o Backwards displacement of the globe

o True enophthalmos is caused by:

 A blow-out fracture
 Sclerosing diseases
 Post-radiation
 Phthisis bulbi (a shrunken, non-functional eye.)
o Pseudo-enophthalmos is caused by:
 Small size of the globe (like axial hypermetropia, prosthetic eye)
 Ptosis (Horner syndrome)

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  Contralateral lid retraction
 Infective disorders of the eye include orbital cellulitis, pre-septal
cellulitis and orbital mucocele
o Orbital mucocele arises from accumulated secretions within
any of the paranasal sinuses when natural drainage of the
sinus is blocked.
o Pre-septal cellulitis is inflammation and edema anterior to
the orbital septum
o Orbital cellulitis is inflammation both anterior and posterior
to the septum
o They may be caused by sinusitis (usually ethmoid), sepsis,
trauma or insect bites.
 The MCC of pre-septal cellulitis is dacryocystitis
o The MC causative organisms are Staph and Strep

Pre-septal cellulitis Orbital cellulitis

Extent of involvement Skin only (anterior lid The entire orbit
inflammation)
Systemic illness and pyrexia Absent Present
Conjunctival erythema Absent Present
Restriction of eye Absent Present
movement
Optic nerve function Normal Compression of optic nerve→ RAPD, ↓
visual acuity and color vision impairment
Proptosis Absent Present (Axial) and painful
WBC, ESR, CRP Mildly elevated Markedly elevated
Management Outpatient oral antibiotics Admission, IV broad-spectrum antibiotics,
+/- surgery to drain any abscesses (if
present) and orbital decompression (if
the optic nerve is compromised

 In the case of orbital cellulitis, you must

o Order a CT scan→ to rule out a sub-periosteal abscess that would require subsequent
drainage
o Order an ENT consult (to manage their sinusitis)
o Do frequent eye exams (q6hrs) to check for optic nerve involvement

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 27 preseptal
cellulitis

 Binocular diplopia
o Occurs when only one eye is fixated on a target, thus the image in the second eye does
not fall upon the fovea
o May be due to:
 Muscle involvement: the eye appears to be tethered, so that eye movement is
restricted in a direction away from the field of action of the affected muscle
 Like myositis, Graves’ disease
 Nerve involvement: diplopia occurs during gaze into the field of action of the
muscle (paralytic squint)
 Like palsy of the right lateral rectus produces diplopia in the right
horizontal gaze
o Differentiate between the two via forced duction testing
 Assesses passive movement of the globe
 Apply topical anesthesia to the globe
 The eye is then moved with forceps
 No resistance→ nerve involvement (muscle
paralysis
 Resistance→ mechanical restriction of movement
(muscle involvement)
o The MCC of ophthalmoplegia is thyroid eye disease
o The MC muscles affected by thyroid eye disease are the
inferior and medial recti.
 Orbital pseudotumor (Idiopathic orbital inflammatory disease)
o A marginated, mass-like enhancing soft tissue involving any
area of the orbit
o Occurs MC in females between 20 and 40
o CT scan shows mild orbital inflammation
o Definitive diagnosis is by biopsy
o Treatment: steroids.

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  Caroticocavernous sinus fistula

o The superior and inferior ophthalmic veins drain into the cavernous sinus
o Contents of the cavernous sinus: CN3, CN4. V1, V2, CN6, the internal carotid artery and
the carotid plexus (sympathetic fibers)
o Path: a fistula (usually due to trauma) forms between the internal carotid artery and the
cavernous sinus→ ↑ intravascular pressure in the orbital veins
o Patient presentation:
 Proptosis
 Engorged conjunctival veins
 Pulsatile tinnitus
 Bruit over the eye
 ↓ eye movements
 ↑ IOP
o Management: embolizing and thrombosing the affected vascular segment
 Capillary hemangiomas
o Another vascular lesion, may present on the eyelid of infants
o May cause sufficient ptosis to cause amblyopia.
o Most undergo spontaneous resolution within the first 5 years of life
o Treatment is indicated if size/ position obstructs the visual axis (↑ risk of
amblyopia)
 With local injections of steroids/ propranolol
 Orbital tumors:
o Lacrimal gland tumor
 If malignant, poor prognosis
 If benign, complete excision is indicated to prevent malignant transformation
o Optic nerve glioma
 Associated with neurofibromatosis type 1
 If slow growing may require no intervention
o Meningioma

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  Rare
 If arising in the middle cranial fossa, may spread through the optic canal into the
orbit
 Monitor over time, may require radiotherapy
o Lymphoma
 If localized→ radiotherapy is indicated
 If widespread→ chemotherapy is indicated
o Rhabdomyosarcoma
 The MC orbital tumor in children
 Rapidly growing and malignant
 Chemotherapy is effective of the disease is localized to the orbit
 Dermoid cysts
o Path: congenital lesions, due to continued growth of ectodermal tissue
beneath the surface
o Patient: a mass at the medial/ lateral aspect of the superior orbit
o Some may be attached deeply by a stalk , so a CT may be necessary before
surgery
o Treatment: surgical excision, both for cosmetic reasons and to avoid traumatic rupture,
which may cause scarring
 Graves’ disease
o MC in females than males
o Smoking is a RF for thyroid eye disease
o Path: TSH receptor antibody-mediated disease
 Activated T cells release cytokines (TNFa,
IFN-y) which activate fibroblasts (along
with TRab to a lesser degree), causing
increased secretions of
glycosaminoglycans
 GAG deposition leads to osmotic muscle
swelling, muscle inflammation, and
increased adipocyte count → eyes being
pushed out
 Dysfunction of extraocular muscles causes restricted extraocular movements
and diplopia
o Stages:
 Acute: proptosis, pain, redness, lid retraction
 Fibrotic
o Management:
 Lubricants (to prevent exposure keratopathy)
 If the optic nerve is compressed→ ↑ dose steroids
 Surgical decompression is indicated if the patient doesn’t respond to steroids

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Glaucoma
 Glaucoma refers to a group of diseases
causing optic neuropathy,
accompanied frequently but not
invariably by raised ocular pressure on
the optic nerve head. Axon loss→
visual field defects and a loss of visual
acuity
 The optic nerve is formed by axons
arising from the retinal ganglion cell
layer
 It passes out of the eye through the
cribriform plate (lamina cribrosa) of
the sclera, a sieve-like porous
structure with fibrous septae
separating the fibers of the optic
nerve
o This lamina is structurally
weaker than the thicker and
denser sclera, making it
more sensitive to changes in
IOP.
o It reacts to ↑ IOP through
posterior displacement→
deformation of its pores and
pinching or transmitted
nerve fibers and blood
vessels.
 The optic disc is the point where
ganglion cell axons exit the eye to
form the optic nerve
 General (non-ocular) risk factors for
glaucoma:
o Aging
o Family history
o HTN
o Migraines
o Race
 Africans are at ↑ risk for open angle glaucoma
 Asians are at ↑ risk for closed angle glaucoma (due to their small eyes→ narrow
anterior segment→ narrow iridocorneal angle)

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Pathophysiology
 IOP is determined by a balance between production
and removal of aqueous humor
 Aqueous produced by ciliary epithelium and then is
actively secreted into the posterior chamber via a
combination of active transport and ultrafiltration
o Aqueous then passes through the pupil→
anterior chamber→ trabecular meshwork→
canal of Schlemm→ episcleral veins→
bloodstream (the conventional pathway)
o 4% of aqueous drains across the ciliary body
and muscle into the supra-choroidal space→
venous circulation (the uveoscleral pathway)
 Normal IOP is between 11 – 21 mmHg
 ↑ IOP damages the optic nerve via:
o Mechanical damage to the axons (compression and interruption of axoplasmic flow)
o Ischemia of the nerve axons by ↓ blood flow at the nerve head

Classification of glaucoma
 Primary glaucoma
o Chronic open angle
 ↑ outflow resistance due to structural
changes in the trabecular meshwork
o Acute and chronic closed angle
 ↑ outflow resistance due to the peripheral
iris blocking the trabecular meshwork
 Congenital glaucoma
o Primary or Secondary (like in aniridia, sturge-weber,
retinoblastoma or congenital rubella syndrome)
 Secondary glaucoma
o Open angle or closed angle
o Secondary to trauma, surgery, uveitis, steroids, ↑
episcleral venous pressure… etc.
 Normal tension/ low tension glaucoma
o Visual field loss and optic disc cupping
o But with normal IOP
o The optic nerve head in this case is either:
 Unusually susceptible to IOP
 Has intrinsically ↓ blood flow
o Hard to treat, try ↓ IOP if progressive visual loss occurs
 Ocular hypertension
o ↑ IOP without visual field loss or optic disc cupping
o 1% of these patients per year will subsequently develop glaucoma

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Pathogenesis
Primary open angle glaucoma
 Aqueous outflow obstruction due to
o Thickening of the trabecular lamellae
o ↓ in the number of lining trabecular cells
o ↑ extracellular material in the trabecular meshwork spaces
 On gonioscopy (which views the iridocorneal angle) the trabecular meshwork appears normal
while functionally offering ↑ resistance
 Myopia is a risk factor (wide iridocorneal angle)

Closed angle glaucoma

 Relative pupil block: contact between the pupil margin and the lens offers a resistance to
aqueous flow from the posterior into the anterior chamber (physiologic)
o Thus there is a pressure drop between the posterior and the
anterior chamber
 Pupil dilation→ peripheral iris is bunched up at the angle→ ↑
pressure gradient→ iris bowed forward→ closes the drainage angle→
↑IOP
o This peripheral iris contact leads to adhesions called
peripheral anterior synechiae (PAS) which consolidate the
obstruction.

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 o Stagnant circulation of aqueous deprives the whole cornea of nutrition and the posterior
cornea of its oxygen supply→ failure of the endothelial pumping function→ corneal
edema and clouding→ profound fall in vision.
 Occurs in small eyes with small anterior chambers (often hypermetropic)
 A full-blown attack may be preceded by subacute episodes of angle closure w/ transient ↑ IOP,
headaches and rainbow haloes around bright lights due to corneal epithelial edema→
diffraction

Secondary glaucoma
 May be open angle, secondary to trabecular meshwork obstruction by
o RBCs→ hyphema following blunt trauma
o WBCs→ uveitis
o Iris pigment→ pigment dispersion syndrome
o Material produced by the epithelium of the lens, iris and ciliary body→
pseudoexfoliative glaucoma
o Steroid-induced glaucoma (↑ meshwork resistance)
o Angle recession→ blunt trauma damages the drainage angle 28 Sturge – Weber Syndrome
o ↑ episcleral venous pressure, due to:
 Caroticocavernous sinus fistula
 Sturge – Weber syndrome
 May be closed angle, due to
o Neovascular glaucoma (rubeosis iridis)
 The second most common type of glaucoma
 w/ proliferative diabetic retinopathy or CRVO
 abnormal iris blood vessels obstruct the angle 29 pigment dispersion syndrome
o Large choroidal melanoma
o Phacomorphic glaucoma→ cataract swelling
o Uveitis→ iris adheres to the trabecular meshwork
 Secondary glaucoma is rarer than
primary glaucoma and is usually
symptomless. It is important to treat
any underlying cause.
 In difficult cases, it may be necessary
to selectively ablate the ciliary
process to ↓ aqueous production.

Congenital glaucoma
 The exact etiology remains uncertain
- may be due to:
o Developmentally abnormal
iridocorneal angle is covered
with a membrane, which increases the outflow resistance.
o Failure of separation of the iris from the cornea
o Abnormal insertion of the ciliary muscles into the trabecular meshworl
o Absence of Schlemm’s canal.

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  80% w/in the first 6 months of life, 80% in males and 80% bilateral.
 May present at birth or within the first year
 DDx of congenital glaucoma:
o Megalocornea
 No corneal edema/ Haab’s striae/ disc cupping
and normal IOP
o Birth trauma/ metabolic disorders
 The patient may present with:
o Buphthalmos –
 ↑ corneal diameter (>12 mm)
 enlargement of the globe
 progressive myopia
o Blepharospasm (contraction of orbicularis oculi)
o Excessive tearing
o Photophobia
o Cloudy cornea
o Splits in Descemet’s membrane (Haab’s striae)
o Streteched, blue sclera (uvea shines through)
o Deep anterior chamber, due to:
 Enlargement of the globe
 Posterior displacement of the lens 30 Haab striae
o Late cases may present with optic disc cupping and atrophy
 Treatment: usually surgical (medical treatment would only be used temporarily)
o If the corneal diameter is 13 mm or less:
 With a clear cornea: Goniotomy
 An incision is made into the trabecular meshwork to ↑ aqueous
drainage
 With a hazy cornea: Trabeculotomy
 A direct passage between Schlemm’s canal and the anterior chamber is
created
o If the corneal diameter is greater than 13 mm→ external fistulizing operation

Chronic open angle glaucoma

 MC type of glaucoma, prevalence increases with age, and affects males and females equally
 History:
o Symptoms depend on the rate at which IOP rises, and since IOP rises slowly, it is
symptomless until a visual deficit arises or the diagnosis is made by chance
o Screen those with risk factors every year after the age of 40.
 Patient presentation:
o White eye and clear cornea
o ↑ IOP
o Visual field defect
o Cupped optic disc

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  Examination includes checking:
o IOP with a tonometer Measurement of IOP
 Normal pressure is between 11-21
mmHg
 In chronic open angle glaucoma it’s  Applanation tonometry is based on the
typically 22-40 mmHg Imbert-Fick principle, which states that the
 In closed angle glaucoma it rises pressure inside a sphere equals the force
above 60 necessary to flatten its surface divided by
o Corneal thickness with a pachymeter the area of flattening.
 Measured value of IOP must be  In clinic, we measure the force necessary to
adjusted according to corneal flatten a 3.06mm2 area of the cornea.
thickness  IOP measurement depends on the surface
o The iridocorneal angle with gonioscopy area and the rigidity of the tissue
 To confirm that an open angle is  ↑ Rigidity (↑ thickness of the central
present cornea) will ↑ IOP and vice versa.
o The optic disc and cup:disc ratio  Thus, we must measure corneal thickness
 The optic cup is the pale, cup-like area before IOP measurement to avoid false
in the center of the optic disc, and it readings
represents an area devoid of nerve  (After LASIK /PRK→ thinner cornea)
fibers
 The normal cup:disc ratio is between
0.2-0.4
 In chronic glaucoma, axons leaving the optic
disc die, so
 The central cup expands
 The neuro-retinal rim is thinner
 So the vertical cup:disc ratio becomes greater
than 0.4 and the cup deepens
 Notching of the neuro-retinal rim indicates
focal axon loss
 In advanced stages you may see small white
dots representing the lamina cribrosa
o The thickness of different parts of
the retina with Optical coherence
tomography (OCT)
 You may see ↓ thickness
of the nerve fiber layer
around the optic disc
 Good for follow-up of
patients to monitor the
progression of their disease
o Visual field loss with perimetry
 To establish the presence of islands of field loss (scotomata)
and monitor the progression of optic nerve damage

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  A significant proportion of optic nerve fibers is lost before the field loss
becomes apparent
 A “nasal step” visual field defect is commonly an early sign of glaucoma
 This may progress to an arcuate scotoma and, eventually, tunnel vision, where
only a small, central island of vision is left.

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  Treatment → aimed at ↓ IOP
o Medical treatment
 Topical prostaglandin analogues - Latanoprost, travaprost,
 First line treatment
 ↑ aqueous humor passage through the
uveoscleral pathway
 Side effects:
o Hyperpigmentation of the iris and
31 iris hyperpigmentation
periocular skin
o Conjunctival hyperemia and stinging
o Lengthening and darkening of the eyelashes
o Rarely, macular edema and uveitis
 Topical Beta-Blockers –timolol, carteolol
 ↓ aqueous humor secretion

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  Side effects:
o Exacerbate asthma
o Hypotension, bradycardia and heart block
 Parasympathomimetics – pilocarpine
 ↑ outflow of aqueous humor
 Side effects:
o Visual blurring
o Darkening of the visual world
due to pupillary constriction
o May induce myopia or RD
 Carbonic anhydrase inhibitors
 Topicals: dorzolamide, brinzolamide
 Systemic: acetazolamide
 ↓ aqueous humor secretion
 Side effects:
o Renal stones
o Tingling limbs, depression
 Mannitol (not mentioned in the book)
o Laser trabeculoplasty
 Laser the trabecular meshwork to ↓ IOP via
improving aqueous outflow
 Whilst effective initially, the IOP may slowly
increase
o Surgical treatment – Trabeculectomy
 Surgery in indicated when medical treatment
fails, with lack of patient compliance or when
↑ side effects of medication make them
intolerable
 Trabeculectomy involves creating a fistula
between the anterior chamber and the
subconjunctival space to ↓ IOP
 Complications of surgery include:
 Failure to adequately ↓ IOP
 Excessively ↓ IOP (hypotony) which may cause macular edema
 Intraocular infection
 Accelerated cataract development
 Shallowing of the anterior chamber in the immediate post-op period→
risking damage to the lens and cornea
 Topical meds, especially sympathomimetics, may ↓ the success of surgery by ↑
subconjunctival scarring→ non -functional drainage channel
 ↓ the risk of this w/ antimetabolite drugs like mitomycin and 5-FU
 The notes mention iridectomy instead (mentioned later)

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Primary angle-closure glaucoma
 MC in females and in hypermetropic individuals with a narrow anterior segment (and hence a
narrow anterior chamber and iridocorneal angle).
 May be precipitated by the use of mydriatic drugs, spending time in a dark place or iris bombe.
 Iris bombe: a condition in which there is apposition of the iris to the lens or anterior vitreous,
preventing aqueous from flowing from the posterior to the anterior chamber.
o The pressure in the posterior chamber rises, resulting in anterior bowing of the
peripheral iris and obstruction of the trabecular meshwork.
o This may result in an acute attack of angle closure glaucoma.
 History:
o Abrupt onset
o Photophobia and eye pain secondary
to ischemic tissue damage
o Watery eyes
o Loss of vision
o Nausea and abdominal pain
 Examination:
o ↓ visual acuity
o Red eye (ciliary flush)
o Cloudy cornea
o Pupil oval, fixed and dilated
 Treatment: (urgent)
o IV and oral acetazolamide
o Topical beta blocker
o Topical pilocarpine
o Subsequent iridotomy or iridectomy
 A small hole is made in the peripheral iris to
prevent further attacks
 Done via YAG laser or surgically
 If pressure has been raised for some days, peripheral anterior
32 Iridotomy
synechiae occur, damaging the iridocorneal angle and requiring
further measures to ↓ IOP
 It patients with cataracts, lens extraction with implantation of an IOL may help open the
iridocorneal angle

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