RAPD (relative afferent pupillary defect) : occurs due to unilateral or asymmetrical disease of

retina or optic disc

Fluorescein sodium is used to :

● Stain tear film to investigate dry eye
● Stain tear film for applanation tonometry
● Detect corneal ulcers
● In FFA

OCT : using infrared light to create sliced image of retina

Complications of VEGF injections :

● Raised intraocular pressure
● Vitreous hemorrhage
● Endophthalmitis

Neovascularization of iris seen in :

● Proliferative diabetic retinopathy
● Retinal vascular occlusion

Indications of steroid
● Shield ulcer (Cornea)
● Severe circumcorneal congestion
● Limbal Keratoconjunctivitis

Theme 1

Refractive errors, open angle glaucoma, diabetic retinopathy, retinal dystrophy and
degeneration, cataract

Refractive errors
● Nystagmus and sunken eye indicates bad prognosis
● Retinoscope used for determining refractive error
● Visual acuity does not tells type or magnitude of refractive error
● Distance more than 6 meters is considered infinite in ophthalmology
● Diopters = 1/ focal length (point where light rays converge)
● Eye power 60 D (42 of Cornea and 18 of lens)
● Eyeball length 22.6mm (22 to 24 mm)
● Accommodative reflex
○ Accommodation
○ Pupillary constriction
○ Eye Convergence
● Age 36-40 accommodative amplitude falls below 4 diopters
● Presbyopia
 ○ Usually after age of 40
○ Due to weakness of ciliary muscles
○ Treatment : spectacles, contact lenses or presby LASIK
● Ametropia : light rays from distance are not focused on retina when eye is not
accommodating
● Hypermetropia (long sightedness) : light rays focused behind retina
○ Classification
■ Refractive : Cornea
■ Index : lens
■ Axial : eyeball length
○ Usually present with discomfort on prolonged near task
● Myopia : light is focused in front of retina
○ Classification
■ Refractive
■ Index
■ Axial
○ Pathological myopia : extreme form of axial myopia (-6 diopters or more).
Complication : staphyloma, retinal detachment.
● Anisometropia : difference of refractive error of more than or equal to 1 diopters between
2 eyes. Can lead to anisometropic amblyopia
● Astigmatism : power of cornea at different meridians is different

● Distant vision errors Presentation

○ Gradual painless loss of vision
○ In pre verbal child : wandering gaze, inability to recognise familiar faces, bumping
into furniture
○ Associated symptoms : watering, headache
● Distant vision errors management
○ Spectacles
○ Contact lenses
■ Soft contact lenses
■ Rigid gas permeable : for Keratoconus
○ Laser : PRK, LASIK, LASEK, SMILE
 ● Cyclopentolate is preferred cycloplegic agent as it has stronger action as compared to
tropicamide and shorter duration of action as compared to atropine
● Vision deprivation / sensory amblyopia : occurs due to visually significant Congenital
cataract

Cataract
● Classification (opacification)
○ Immature : red reflex partially obscured
○ Mature : red reflex completely obscured
○ Hyper mature : capsule wrinkles as cortex shrinks
○ Moganian : cortical fibers liquifies and nucleus sinks
● Classification (morphology)
○ Anterior subcapsular : occurs due to
■ Deposition of drugs such as chlorpromazine, amiodarone
■ Trauma or anterior chamber inflammation
○ Posterior subcapsular
■ Occurs due to steroids, in diabetics and due to age
■ Decreased near vision and in brightly lit areas (difficulty in night driving)
○ Cortical
■ Ageing, diabetes
■ Spokes on wheels appearance
■ Produces glares and halos
○ Nuclear
■ Increased density of lens leads to change in colour due to increased
refractive index termed as nuclear sclerosis cataract
■ Increased refractive index increased power of lens so near sight is
improved (second sight)
■ Sunflower cataract occurs as a result of trauma
● Presentation
○ Cataract never causes NPL
○ Children
■ Unilateral : difficult to detect
■ Bilateral : detected early
● Complications
○ Phacomorphic glaucoma : block path between pupil and lens
○ Morgaganian cataract
■ Phacolytic cataract : blocks trabecular meshwork
■ Phacogenic uveitis
○ Amblyopia in pediatric group
■ Vision deprivation preoperatively
■ Anisometropic type postoperatively
● Treatment
○ Pre-op examination
 ■ Ocular : dry eye, amblyopia, corneal scars, retinal disease. If retina is not
visible B scan is performed
■ Systemic : hypertension, Hep B and C, HBA1c and for local anesthesia
ECG
○ Restoring power
■ Aphakic contact lenses and glasses ( magnification and Jack in the box) .
Used in children less than 2 years of age
■ IntraOcular lens : can be placed in anterior chamber (made up of PMMA)
or in posterior chamber (made up of acrylic). Posterior chamber is
preferred. If placed in anterior chamber iridotomy is performed
■ Power of the intraocular lense is calculated by formula power = A-(2.
9*L+.9*K). A is constant, L is the length of the eyeball and K is the power
of the cornea. Length is calculated through A scan
○ Types of surgery
■ Couching
■ Intra capsular cataract extraction
■ Extra capsular cataract extraction
■ Phacoemulsification
○ Painkillers should not be prescribed postoperatively as it may mask early signs of
endophthalmitis
○ Pre-op complications :
■ iris prolapse, posterior capsule rupture.
■ Local anesthesia : ineffective or hemorrhage
○ Post-op
■ Wound leak
■ Corneal edema
■ Posterior capsule opacification(after cataract) : treated by creating
opening in posterior capsule using YAG laser
■ Endophthalmitis

Diabetic retinopathy
● Progressive dysfunction of retinal microvasculature due to hyperglycemia resulting in
damage to neural retina
● Investigations
○ General : HBA1c, blood sugar, blood pressure
○ Eye : OCT, FFA
● Non proliferative :
○ Absence of micro aneurysms rule out diabetic retinopathy
○ FFA differentiates micro aneurysms from hemorrhage. Micro aneurysms appear
white whereas hemorrhage has dark appearance
○ micro aneurysms; blot, flame, dot hemorrhage,
○ Macular edema (petaloid pattern in FFA) , hard exudates(macrophages take up
plasma lipids of macular edema) .
 ○ Cotton wool spots (have fuzzy margin whereas hard exudates have sharply
defined margin) . Once they appear NPDR is termed as advanced.
○ Presentation : bilateral relatively symmetrical Gradual loss of vision
○ Treatment : Anti VEGF(aflibercept) , steroids(triamcinolone acetate) and
laser(seals micro aneurysms)
● Proliferative :
○ neovascularization (hallmark) leading to hemorrhage (vitreous, retinal,
subhyaloid).
■ Can occur at optic disc (NVD)
■ Can occur elsewhere (NVE)
○ Presentation : Sudden painless loss of vision in addition to Gradual painless loss
of vision can also occur
○ Treatment
■ laser(gold standard). Peripheral retina is destroyed (pan retinal). Results
in loss of Peripheral and night vision.
■ Anti VEGF injection
○ Complications : retinal detachment, neovascular Glaucoma

Retinal dystrophy and degeneration

● Bruch's membrane is boundary between choroid main retina
● Age related macular degeneration
○ Bilateral slowly Progressive disorder of macula affecting elderly featuring loss of
central vision
○ Outer 4 layers of retina supplied by choroidal capillaries whereas inner 6 layers
supplied by central retinal vessels. Watershed zone between 2 is inner nuclear
layer
○ Dry :
■ drusen : deposit of lipids, ameloids, cellular components and complement
factors in Bruch's membrane in the macular region. Soft drusen
Pathological whereas hard drusen physiological
■ Metamorphopsia : drusen causes misalignment of photoreceptors leading
to distorted image perception by retina. Lead to central scotoma
■ geographical atrophy : atrophy of RPE followed by atrophy of
photoreceptors and choroidal vasculature in macula
■ Presentation : gradual painless loss of vision, Metamorphopsia and
central scotoma
■ Investigations : OCT, amsler's grid
■ Treatment : progression can be slowed by weight loss, diet improvement,
cessation of smoking, antioxidant and zinc therapy. Low vision aids
○ Wet :
■ neovascularization due to VEGF release by Outer 4 retinal layers
supplied by choroid.
■ leading to bleeding and Scar formation.
■ Presentation: sudden painless loss of vision
 ■ Management : VEGF injections and low vision aids

● Retinitis pigmentosa
○ A group of genetically determined retinal dystrophy affecting photoreceptors and
retinal pigmented epithelium. Photoreceptors die prematurely
○ In most variants rods are affected first
○ Most have X linked inheritance
○ Classical Presentation
■ Gradual painless loss of vision
■ Pigment hypertrophy resembling bony spicules
■ Pale waxy optic disc
■ Attenuated blood vessels
○ Treatment : counselling, low vision aids, vitamin A

Open angle glaucoma

● Progressive optic nerve neuropathy with characteristic visual field defect and IOP as
significant risk factor
● Causes irreversible blindness
● Glaucoma triad
○ Raised intraocular pressure
○ Optic disc cupping (initially it is vertical and later on spreads horizontally)
○ Visual field defects
● Measuring intraOcular pressure
○ Digital method
○ Contact method : shiortz , goldmann applanation tonometry (gold standard)
○ Non contact : air puff
○ Glaucoma can occur at high or normal intraocular pressure. Conversely it is also
possible to have high intraocular pressure and no Glaucoma
● Cupping
○ Superior and inferior arcuate fibers are first affected due to their dense packing
○ Retinal nerve fiber loss :
■ mechanical compression due to pressure
■ Ischemia due to retinal vasculature dysregulation
○ Normal Cup / Disc ratio : 0.3 - 0.4
○ Monitoring
■ Visual
■ Photograph : can see progression over time
■ OCT : objective and sensitive
○ Physiological blind spot is present in inferior temporal field (superior nasal retina)
○ While testing visual field scotoma in inferior temporal field is present in superior
nasal retina
○ Initial Peripheral vision is affected leading to tunnel vision

● Congenital
 ○ Primary : trabecular meshwork
○ Secondary : Ocular or systemic
○ Presentation : poor vision, increased IOP, cupping, buphthalmos
○ Treatment : medial management, goniotomy, trabeculotomy and trabeculectomy
● Juvenile
○ Raised IOP
○ MYOC gene
○ Rapidly progressive
● Primary open angle glaucoma
○ Raised IOP
○ MYOC gene, myopia risk factor
○ Inherent abnormality in trabecular meshwork
○ Diagnosis : OCT, visual field, intraocular pressure
● Secondary open angle glaucoma
○ Raised IOP
○ Defect in trabecular meshwork as result of identifiable secondary cause
○ Etiology
■ Inflammation
■ Deposition in anterior chamber
■ Pigmentary : rubbing of iris (krukenberg spindle, transillumination defect)
■ Steroids : increased expression of Extracellular matrix
■ Pseudoexfoliative : amyloid deposition
■ Trauma, intraocular
hemorrhage
● Ocular hypertension
○ Not glaucoma
○ Visual field, OCT done every 2 year
● Normal /low tension glaucoma
○ Behaves live primary open angle glaucoma but with normal IOP
○ Occurs due to vascular dysregulation
● Presentation Acquired glaucoma
○ Gradual painless loss of vision
○ Usually bilateral
○ Inability to see coming cars
○ Bumping into people
○ Signs
■ Raised IOP
■ RNFL : OCT
■ Cupping
■ Visual field defects
○ Signs and symptoms of cause in secondary form
○ RAPD in unilateral case
● Treatment
 ○ Medical : prostaglandin analog (first choice, cause vasodilation in iris and ciliary
body resulting in increased absorption ), Beta blockers, alpha agonist, carbonic
anhydrase inhibitors, pilocarpine
○ Laser trabeculoplasty : holes created in trabecular meshwork
○ Trabeculectomy
○ Minimally / micro invasive glaucoma surgery : stent insertion

Theme 2

Conjunctivitis (painless) , keratitis, angle closure glaucoma, uveitis

Conjunctivitis
● Acute (allergic)
○ Perennial : through year with exacerbations
○ Seasonal
○ Presentation : Itching (sine qua non), congestion, mucoid discharge,
photophobia, papillae
○ Management : mast cell stabilizers, decongestants, Antihistamine, Lubricants
and cool packs
● Chronic (allergic)
○ Vernal-keratoConjunctivitis
■ Palpebral type : cobblestone papillae only on upper lid
■ Limbal : Homer Trantas dots
■ Mixed : both
■ Corneal ulcers due to rubbing
■ Presentation : same as acute form. Gradual weakness also may be
present
■ Management : same as acute form. Tacrolimus and cyclosporine also
used
○ Giant papillary Conjunctivitis
■ Occurs due to chronic irritation to contact lenses, sutures, prosthesis
○ atrophic
■ Associated with asthma and atopic dermatitis
■ Presentation similar to Vernal keratoConjunctivitis
● Keratoconus
○ Bilateral Progressive inferior corneal steepening resulting in thinning of cornea
○ causes : Conjunctivitis, down syndrome, marfan syndrome, retinitis pigmentosa
○ Presentation : gradual painless loss of vision. Chronic itchy eye or other
manifestation of cause. Frequent changes in spectacle prescription
○ Signs : munson sign (notching of eyelid) , rizzuti sign (arrow head like reflection),
oil droplet sign (charleaux sign), scissor reflex
○ Investigations : Galilei scan( current gold standard investigation) orb scan, penta
scan
 ○ Treatment : spectacles, soft contact lenses, rigid contact lenses, corneal Cross
linking with riboflavin, intracorneal ring insertion, Keratoplasty
● Viral Conjunctivitis (adenovirus)
○ Follicular
■ Presentation : red watery eye
■ Signs : conjunctival congestion, watery eye, Follicular lymphoid reaction,
pre auricular lymphadenopathy
■ Management : supportive
○ Pharyngoconjunctival fever
■ Presentation : signs of Follicular Conjunctivitis, fever and pharyngitis
■ Management : supportive
○ Epidemic keratoConjunctivitis :
■ Most severe form
■ Signs : those of Follicular Conjunctivitis, conjunctival hemorrhage, corneal
ulcers
■ Treatment : supportive, steroids for corneal ulcers
● Papillae are red in colour whereas lymphatic Follicles are white in colour
● Acute Bacterial Conjunctivitis :
○ Etiology : Staph Aureus, Staph Pneumoniae, Hemophilius influenzae
○ Presentation : foreign body sensation, irritation, sticky and red eyes
○ Signs : conjunctival congestion, papillae formation, muco purulent discharge, tear
film disruption
○ Management : lid hygiene, tropical antibiotics, supportive
● Hyperacute bacterial Conjunctivitis
○ Etiology : Neisseria
○ Transmission : birth canal, contact with genital
○ Presentation :copious eye discharge, may lead to keratitis
○ Management : ceftriaxone
● Chronic bacterial Conjunctivitis :
○ Etiology : Chlamydia Trachomatis
○ Presentation : red sticky eye, Arlt line, Herbert's pit, Trichiasis, entropion
○ Management : tetracycline ointment (neonates prophylaxis), azithromycin
(elderly) Erythromycin (neonates)

Keratitis
● Infectious form involves central cornea whereas Autoimmune involved limbus
● Etiology
○ Bacterial : Staphylococcal Aureus, Streptococcus Pneumoniae, Neisseria,
Pseudomonas. Occurs due contact wear followed by trauma
○ Fungi : fusarium, aspergillus, candida. Trauma with concurrent contamination
with plant material
○ Viral : secondary infection due to reactivation. Caused by HSV, HZV
○ Acanthamoeba : contamination contact lenses solutions and bathing water
● Presentation
 ○ Symptoms : red watery eye, blurred vision, pain and photophobia, history of
inciting event
○ Signs : circumcorneal congestion, ulceration, infiltration, constricted pupil
○ Hypopyon, pannus / corneal vascularization late features. Pannus involves only
limbus whereas vascularization extends beyond limbus
○ Viral keratitis : dendritic ulcer, disciform corneal edema(steroids given as
treatment) , Herpes zoster ophthalmicus, post herpetic neuralgia
○ Acanthosis : ring infiltration / abscess, pain out of proportion to clinical sign
● Management
○ Anti Fungal and anti amebic treatment not started until diagnosed
○ Bacterial : moxifloxacin (+ and -), tobramycin (-), cefazolin(+), vancomycin(+)
○ Fungal : fluconazole and amphotericin b
○ Viral : acyclovir
○ Acanthamoeba : chlorhexidine
○ Grades of corneal Scar density :
■ Nebular : faint
■ Macular : dense Scar with clear spaces in between
■ Lecucomal : dense Scar with no spaces in between
○ Visual rehabilitation : Keratoplasty
● Infectious keratitis complications : descemetocele, corneal perforation, extrusion of
contents, endophthalmitis
○ Descemetocele : thinning of cornea leads to its out pocketing. Grafts (amniotic
member, tectonic (Cornea)) used
○ Tarsorrhaphy may also be done

Angle closure glaucoma

● Closure of anterior chamber angle by forward displacement of iris
● Classification
○ Primary : due to small eyeball
○ Secondary : due to Pathological conditions affecting eye e.g anterior Uveitis
● Examination technique
○ Digital tonometry
○ Gonioscopy
○ Perpendicular illumination
● Grading (schafer system)
○ Grade 4 : normal. All structures visible
○ Grade 3 : ciliary body not visible
○ Grade 2 : scleral spur not visible (angle closure suspect)
○ Grade 1 : Trabecular meshwork not visible. Aqueous humor not drained
○ Grade 0 : Schwalbe's line not visible. Angle closure and angle closure glaucoma.
AC is shallowest.
● Risk factors : hypermetropia (more than +5), age (lens thickness increases), female
● Primary angle closure suspect : hypermetropia more than or equal to +5. IOP normal.
Anterior chamber is shallow.
● Acute primary angle closure
○ Raised IOP. Less than or equal to Grade 1 in more than 3 quadrants.
○ Pupillary block : precipitating factors allow lens and iris to oppose blocking
movement of aqueous humor. This lead to collection of aqueous humor behind
iris leading to if forward displacement forming iris bombe
○ Angle crowding : as pupil dilates iris begins to crowd angle impeding aqueous
flow
○ presentation :
■ Red painful eye, photophobia, blurry vision, vomiting
■ Hazy Cornea, mid dilated non reacting pupil (due to ischemia),
circumcorneal congestion
○ Management :
■ Break acute attack : decrease IOP to reverse iris ischemia. Pull iris away
from angle. Mannitol / glycerol, pilocarpine, timolol, apraclonidine carbonic
anhydrase inhibitors, steroids. Protagonist analogs contraindicated
■ Prevent future attacks. Peripheral iridotomy(performed on upper quadrant
to prevent diplopia). Trabeculotomy
● Intermittent primary angle closure: it attack of acute primary angle that resolves
spontaneously
○ Signs
■ Glaucomflecken
■ Iris atrophy
● Primary angle closure glaucoma: angle closure with glaucmatous otic disc and visual
field defect. Gonioscopicaly grade 0 in more than 3 quadrant
○ Repeated attacks of intermittent angle closure can lead to formation of Peripheral
anterior synechiae (adhesion of iris to corneal periphery) leading to primary angle
closure glaucoma
○ Presentation : Propensity to bump into people and inability to see coming cars.
History of recurrent attacks of intermittent angle closure glaucoma. Gradual
relativly painless loss of vision, Red eye
○ Signs : Glaucomflecken, iris atrophy. Raised IOP, glaucomatous optic nerve
changes, visual field defect
○ Management :
■ Medical management not very successful
■ Surgical : trabeculotomy, glaucoma drainage device, ciliary body
destruction
● Mid dilated non reacting pupil differentiates Acute primary angle closure from acute
anterior Uveitis
● Acute secondary angle closure : pupil is not mid dilated
● Acute secondary angle closure. Gonioscopicaly grade 1 or less in more than 3 quadrant.
○ causes
■ Push : Phacomorphic glaucoma, Acute anterior Uveitis (formation of
posterior synechiae)
 ■ Pull : Neovascularization of iris (clot formation due to bleeding), Acute
anterior Uveitis (formation of Peripheral anterior synechiae)
○ Presentation : red painful eye, headache, vomiting
○ Signs : increased IOP, circumcorneal congestion, hard, tender eye, hazy cornea,
signs of underlying condition.
○ Management : break acute attack (same drugs that are used in primary form
except pilocarpine ) , treat underlying condition
● Secondary angle closure glaucoma : glaucomatous optic disc cupping and visual field
defect. Gonioscopicaly grade 0 or 1 in more than or equal to 3 quadrant
○ Symptoms : relatively painless loss of vision, Minimally red eye. Visual acuity
affected due to underlying condition. Propensity to bump into people and inability
to see coming cars
○ Signs : decreased VA, glaucomatous disc changes, visual field defect. Signs of
underlying condition.
○ Management :
■ Medical management not very successful
■ Surgical management same as that of primary angle closure glaucoma
● Surgical management
○ Trabeculectomy : passage is created through sclera to allow aqueous to drain
outside the eye. Fluid form bleb outside eye where it is slowly absorbed by
conjuctiva. Peripheral iridotomy is performed to prevent iris from blocking
passage.
■ Complications : over filtration, under filtration and blebitis

Uveitis
● Uveal tract : includes iris, ciliary body and choroid
● Uveitis : inflammation of whole or part of Uveal tract
● Anterior uveitis (Acute) :
○ Presentation : sudden painful loss of vision, photophobia, usually one eye
involved. Symptoms of underlying cause
○ Signs : irregularly miosed pupils, circumcorneal congestion, keratitis precipitates,
arlt triangles, hazy cornea. Anterior and posterior synechiae. Can cause Raised
IOP due to synechiae formation
● Anterior uveitis (chronic) :
○ Presentation : less pain, photophobia, minimal circumcorneal congestion mutton
fat / granulomatous, IOP high
● Treatment anterior Uveitis
○ Pain : relieve spasm, treat intraocular pressure
○ Inflammation : steroids, MTX, azithroprim, cyclosporine
○ Treat underlying condition
● Complication of anterior Uveitis : cataract (steroids), Glaucoma (Raised IOP) , macular
edema (cystoid in appearance on FFA and OCT)
● Intermediate uveitis:
○ Presentation : painless loss of vision
 ○ Floaters, painless loss of vision
○ Management : Idiopathic (steroids), treat Infectious cause, treat multiple sclerosis
● Posterior uveitis :
○ Presentation (acquired) : painless loss of vision. toxoplasmosis leads to headlight
in fog appearance of retina, Chronic cases present as punched out Scar
○ Presentation (Congenital) : retinal Scar, poor Central vision

Category Common Etiologies Disease Entity

Acute Anterior Uveitis • Idiopathic/ Unknown ● Iritis

• Seronegative (RF-ive) ● Iridocyclitis
spondyloarthropathies ● Anterior Cyclitis
• Ankylosing
spondylitis (AS)
• Psoriatic arthritis
(PsA)
• Inflammatory bowel
disease (IBD) &
associated arthritis
• Reactive arthritis
(formerly Reiter
syndrome; ReA)
• Behçet’s syndrome
• Phacogenic Uveitis

Chronic Anterior Uveitis • Idiopathic/ Unknown • Iritis

• Juvenile idiopathic arthritis (JIA) • Iridocyclitis
< 16 years age esp. ♀ • Anterior Cyclitis
• Sarcoidosis
• Syphilis
• Tuberculosis

Intermediate Uveitis • Idiopathic/ Unknown ● Posterior Cyclitis

• Sarcoidosis ● Hyalitis (Vitritis)
• Multiple Sclerosis

Posterior Uveitis • Idiopathic/ Unknown ● Choroiditis

• Sarcoidosis ● Chorioretinitis
• Syphilis ● Retinitis
• Tuberculosis
• Toxoplasmosis

Pan Uveitis • Idiopathic/ Unknown

• Sarcoidosis
• Syphilis
• Tuberculosis
• Toxoplasmosis

Trauma
● Blowout fracture : damage to eyeball
○ periorbital ecchymosis and edema, subconjunctival hemorrhage, enophthalmos,
vertical diplopia, dystopia and lower eyelid anesthesia (intra orbital nerve
damage).
○ Levator function differentiates between exophthalmos and ptosis
 ● Eyeball : Black Eye, subconjunctival hemorrhage (if posterior border of hemorrhage is
visible then hemorrhage is due to conjunctival vessels other wise it is due to orbital
vessels), hyphema and iridodialysis (can cause glaucoma) , cataract (sunflower), lens
subluxation, vitreous hemorrhage, pre retinal hemorrhage, retinal detachment (RAPD+)
and optic nerve avulsion (RAPD+). Always open eye to see extent of damage
● Surface trauma :
○ Lids : tears, foreign body
○ Cornea : UV light (electric arc welding), foreign body
○ Management Lids : repair. Ensure lacrimal system continuity. Foreign body
removed with 1cc syringe
○ Management Cornea : Lubricants. Removal of foreign body (1cc syringe)
● Penetrating injury : only creates an entry wound and remains in organ
● Perforating injury : creates an exit wound in addition to entry wound implying that FB is in
outside organ
● Evisceration : removal of contents of the eye leaving sclera intact. Used to prevent
sympathetic ophthalmitis(due to exposure of choroidal / Uveal antigens . Not to be used
for malignancy
● Enucleation : removal of complete eye ball. For malignancy or infections confined to the
eyeball.
● Exenteration : removal of all the contents of orbit including muscles, skin, bone lacrimal
gland system. For malignancy or that extends beyond the confines of the eyeball
affecting muscles, adnexa etc.
● Chemical injury :
○ Alkali : Penetrating
○ Acid : less penetration
○ Treatment : copious irrigation
● Phthisis bulbi : severe trauma leads to ciliary body shut down. Over time the eye ball
shrinks and is no longer functional.

Theme 3

Ocular surface anomalies, lid malposition

Ocular surface anomalies :

● Conjunctival degeneration : associated with environmental exposure and dry conditions.
UV exposure leads to degeneration of conjunctival collagen. Include pinguecula and
pterygium
● Pinguecula : yellow colored thickening of bulbar conjunctiva. Bilateral
● Pterygium : conjunctival fibrovascular growth that extends to Cornea. Presents as slow
growing mass causing irritation, watering and decreased visual acuity(Astigmatism or by
covering Visual axis) . If inflamed it causes congestion.
● Pseudo pterygium can be lifted off conjunctiva whereas pterygium can not be lifted
● Arcus senilis and arcus juvenilis : arcus juvenilis starts before age of 40. warrants
investigation.
 ● Anterior blepharitis (chronic) :
○ Types : Staphylococcal, Seborrhoeic.
○ Staphylococcal : hard scales at base of lashes
○ Seborrhoeic : greasy and oily scales at base with crusting of lashes
○ Tear film breakup time (TFBT) : instability of tear film if TFBT is less than 10
seconds
○ Complications : chalazion, hordeolum
● Posterior blepharitis (chronic) :
○ Types : meibomianitis, age related meibomian gland dysfunction
○ Worse in morning
○ Signs : capped meibomian glands
○ Complications : chalazion, hordeolum
● Benign lid swelling
○ Risk factors : dry eye, Anterior or posterior blepharitis and demodex infestation
○ Chalazion : sterile lipogranulomatous inflammation of gland of zeis and
meibomian gland. Occurs due to retention of gland secretions. If infected it is
termed as internal hordeolum.
○ Hordeolum : acute pyogenic inflammation of one or more eyelid structures.
Prolonged infection may cause pre septal or orbital cellulitis.
Two types
■ Internal : involves meibomian glands
■ External (stye) : involves glands of zeis, moll or eyelashes
● Malignant swelling
○ Recurrent chalazion should be biopsied to rule out carcinoma
○ Basal cell carcinoma : UV exposure cause. Extensive local spreading but very
low risk of metastasis. Types
■ Nodular
■ Nodulo ulcerative
■ Sclerosing
○ Squamous cell carcinoma : UV exposure cause. Has metastatic potential. Types
■ Nodular
■ Ulcerative
■ plaque like

Lid malposition
● Levator palpebrae superioris (CN 3) and muller muscle (superior cervical ganglion) only
present in superior lid.
● Insertion of Levator palpebrae superioris form lid crease and in its malformation lid
crease is absent
● Ectropion (mostly lower lid)
○ Outward turning of eyelid
○ Presents a red, watery eye with foreign body sensation. Severe cases may also
have corneal ulcers
● Entropion (mostly lower eyelid)
 ○ Inwards turning of eyelid
○ Presents with red, watery eye with foreign body sensation
○ Associated with trichiasis
● Trichiasis vs distichiasis
○ Trichiasis : associated with Ectropion but may also occur in isolation
○ Distichiasis : congenital or acquired condition in which extra eyelashes emerge
from the meibomian gland. May have no affect or may cause corneal scarring
● Blepharoptosis
○ Drooping of eyelid
○ Congenital
■ Congenital horner syndrome : heterochromia, mild ptosis, anisocoria
■ Levator palpebrae superioris malformation : absent lid crease
■ Complications : amblyopia
○ Acquired :
■ Acquired horner syndrome : heterochromia is not seen
■ Levator palpebrae superioris dishescence : lid crease is absent
○ Compensatory mechanism
■ Raised brow on affected eye
■ Raised resting point of eyelid on normal side

Lacrimal drainage system and dry eye

● Epiphora : excessive watering due to abnormal drainage system
● Lacrimation : excessive watering due to excessive tear production
● Lacrimal pump component
○ Orbicularis oculi
○ Valves that allow one way flow
● Regurgitation test : nasolacrimal duct is blocked so on pressing sac tears flow back onto
eye
● Dye test : fluorescence dye is instilled into eye. If lacrimal pump is functioning no
significant dye should be left in eye showing that defect is in nasolacrimal duct
● Congenital nasolacrimal duct blockage :
○ + Regurgitation test + fluorescence test.
○ Treatment : lacrimal probing + syringing, lacrimal intubation,
dacryo-cysto-rhinostomy
● Lacrimal pump failure
○ - Regurgitation test - fluorescence test
○ Treatment : lacrimal bypass tube. Allow drainage of tears from eyes to nasal
cavity bypassing lacrimal pump and lacrimal sac
● Acquired nasolacrimal duct blockage
○ + Regurgitation test
○ Treatment : lacrimal probing and syringing (also used for diagnosis),
dacryo-cysto-rhinostomy
● Acute dacryocystitis
○ Painful swelling, red sticky eye
 ○ Complications : periorbital and orbital cellulitis,Chronic dacryocystitis
○ Treatment : antibiotics
● Chronic dacryocystitis
○ Presentation : painless swelling, red sticky eye
○ Fibrosis leads to blockage of ducts
○ Complications : mucocele, pyocele and fistula formation
○ Treatment : dacryo-cysto-rhinostomy
● Dry eye
○ Tear film components :
■ Lipid : meibomian gland
■ Water : lacrimal gland
■ Mucin : goblet gland of conjunctiva
○ Aqueous deficient dry eye (decreased production by lacrimal gland) :
■ sjogren syndrome
■ Non sjogren syndrome
○ Evaporative dry eye (extrinsic) :
■ Decreased Lipid production
■ Disorder of blinking (increased exposure)
○ Evaporative dry eye (intrinsic)
■ Vitamin A deficiency : bitot spot
○ Schimmer test normal : 15 to 20 mm
○ Tear film breakup time normal more than or equal to 10 s
○ Complications
■ Filamentary strands: composed of degenerated epithelial cells and mucus
■ Corneal erosion, ulceration, scars

Cellulitis
● Pathogenesis
○ Contiguous : from sinuses
○ Direct : from lid infections, dacryocystitis, trauma, insects bite and pre septal
cellulitis (orbital cellulitis)
○ Hematogenous : dental infections
● Organisms : Staphylococcal Aureus, Staph epidermidis and streptococcus Pneumoniae
● Preseptal cellulitis
○ Infection of skin subcutaneous tissue of lid and surrounding tissue in front of
orbital septum
● Orbital cellulitis
○ Infection of soft tissue behind orbital septum
○ Differentiating signs and symptoms :
■ Fever
■ Decreased vision
■ Proptosis
■ Reduced Ocular movement and pain
■ Decreased visual acuity with red saturation
 ■ RAPD
■ CT scan in orbital cellulitis show inflammatory mass behind eye ball
whereas in pre septal cellulitis it is in front of eyeball

Theme 4

Retinal vascular occlusion, optic neuritis, retinal detachment

Retinal vascular occlusion

● Inner 6 layers supplied by Central retinal artery
● Outer 4 layers supplied by choroidal vasculature
● In 25 % population cilio retinal artery is present which supplies blood to fovea
● Investigations
○ FFA
○ OCT
● Arterial occlusion (White infarct) :
○ 2 types
■ Cental (usually due to thrombosis)
■ Branch (usually due to emboli)
○ Presentation
■ Sudden painless loss of vision
■ Flickering sight (amaurosis fugas)
■ Pale retina
■ Cherry red spot in fovea
■ Box carrying effect in arteries
○ Complications
■ Retinal and iris neovascularization
○ Presence of cilio retinal artery preserves visual acuity in event of artery occlusion
● Venous occlusion
○ Cental
■ Ischemic : severe loss of vision( less than 6/60) due to ischemia
■ Nonischemic : moderator loss of vision due to edema
○ Branch
■ Loss of vision may occur due to edema
○ RAPD positive in ischemic type
○ Retina is congested : battlefield, sunset or stormy sea appearance of fundus
○ Complications
■ Retinal and iris neovascularization
■ 100 day glaucoma : neovascular Glaucoma

Optic neuritis
● Classification
○ Papillitis
○ Retro bulbar optic neuritis
 ○ Neuro retinitis
● Etiology
○ Autoimmune : multiple sclerosis, sarcoidosis
○ Infectious
● Presentation
○ Sudden painless loss of vision
○ Decreased visual acuity
○ Red desaturation
○ RAPD
○ Retro bulbar pain
○ Papillitis
■ Indistinct optic disc margin
■ Cup not visible
■ Congested margin
○ Retro bulbar optic neuritis
■ Optic disc appears normal
● Investigations
○ MRI
○ CSF analysis ( for multiple sclerosis )
○ Lhermitte's sign (multiple sclerosis)
○ Uhthoff's sign
● Oral prednisolone never prescribed alone as it increases risk of recurrence
● Rapid recovery of vision but colour vision and contrast remain affected

Optic disc atrophy

● Death of axon of ganglion cells that comprises optic nerve resulting in pale optic disc in
fundoscopy
● Occur due to various causes such as
○ Optic neuritis
○ Glaucoma

Papilledema
● Swelling of optic disc (Papillitis is inflammation not swelling)
● Occur due to increased intracranial pressure
● Does not cause loss of vision in acute phase
● Disc margin in both Papilledema and Papillitis are blurry but in Papilledema congestion
is less

Retinal detachment
● Separation of neural layers of retina from underlying retinal pigmented epithelium
● Rhegmatogenous
○ Retinal detachment due to break in retina in presence of liquefied vitreous
 ○ Pathogenesis : age related, traumatic, Pathological myopia (more than or equal -
6), lattice degeneration (genetic) and connective tissue disorder. Detachment
occurs only if fluid moves between neural layer and pigmented epithelium
○ Presentation
■ Pre break : flashes
■ Break : Floaters (blood and pigment)
■ Detachment : patient complaints of curtain coming in front of eye.
Sudden painless loss of vision. Visual acuity is affected if fovea is
involved. Leukocoria (White pupillary reflex). RAPD
○ Management
■ Pre break : observation. Patient education
■ Break : prophylactic sealing
■ Detachment : scleral buckling, pars plana vitrectomy, pneumatic
retinopexy
● Tractional detachment
○ Occurs due to formation of bands between retina and vitreous
○ Risk factors : vitreous hemorrhage and inflammation, proliferative diabetic
retinopathy, retinal neovascularization, trauma
○ Presentation
■ Pre detachment : flashes
■ Post detachment : same as in Rhegmatogenous except leukocoria
○ Management
■ Relieve traction
■ Treat underlying condition
● Exudative
○ Due to accumulation of fluid beneath neural layer
○ Association
■ Malignant hypertension
■ Pre-eclampsia, eclampsia
○ Presentation :
■ Sudden painless loss of vision
■ Shifting visual loss
■ RAPD
○ Treatment : manage underlying condition

Theme 4 Ocular Deviations

Thyroid eye disease, Retinoblastoma

Thyroid eye disease

● Refers to eye disease associated with any type of Thyroid disease
● Involves muscles and fat while sparing tendons
● Thyrotropin receptor antibodies activate T cells and lead to deposition of extracellular
matrix
 ● Presentation
○ Symptoms
■ Lid, soft tissue : foreign body sensation, tearing, photophobia
■ Proptosis onwards : pain, redness, diplopia, decreased vision
○ Only systemic signs
○ Only lid signs (due to muller muscle)
■ Eyelid retraction (Dalrymple sign)
■ Lid lag (von graefe sign)
○ Soft tissue signs
■ Conjunctival chemosis
■ Swollen eyelid
■ Superior limbic keratoConjunctivitis
○ Proptosis
○ Extra Ocular muscle restriction : inferior rectus mostly commonly affected which
result in restricted upwards gaze
○ Corneal opacity : reversible sight loss
○ Sight loss :
■ Permanent loss due to nerve compression
■ Visual field defects
■ RAPD
■ Red desaturation
■ Optic atrophy

STAGE MANAGEMENT PRINCIPLES

ANY STAGE Manage any underlying thyroid dysfunction
No-Signs Patient Education. Supportive: Lubricants if required by patient
Only Lid Signs Supportive: Lubricants, Beta-blockers (lower sympathetic flow to
Muller’s Muscle)
Tarsorrhaphy (if signs/ symptoms of early exposure keratopathy appear:
corneal erosions)
Soft tissue Signs Supportive: Lubricants ± Beta-blockers (if lid retraction and/or lag
persists in spite of lid edema), Tarsorrhaphy (if signs/ symptoms of early
exposure keratopathy appear)
Proptosis Supportive: Lubricants, patching or other eye protection
Advanced proptosis (causing optic nerve compression):
Oral or IV (severe cases) Steroid ± Radiotherapy
Orbital surgery (decompression) if non-responsive
EOM Restriction Oral or IV Steroids to reduce inflammation
Orbital surgery (decompression) to reduce proptosis
 If restriction persists and causing diplopia than muscle surgery ONCE
disease has stabilized
Corneal Opacity Tarsorrhaphy
Consider Keratoplasty –After disease has stabilized
Sight Loss Save other eye

Retinoblastoma
● Primary Malignant neoplasms arising from retinoblasts
● Generally sporadic (unilateral). Can also be genetic (bilateral). Genetically autosomal
dominant inheritance
● Presentation
○ Leukocoria
○ Deviations of eye
○ Watering
○ Raised intraocular pressure
○ Fundus examination : white mases
○ Metastasis
● Differentials of leukocoria
○ Persistent fetal vasculature
○ Coats disease : abnormal dilated telangiectatic vasculature. Large aneurysms
○ Retinopathy of prematurity : due to unmonitored oxygen supply
○ Cataract
○ Rhegmatogenous retinal detachment

Squint
● Strabismus : eyes do not maintain orthophoric alignment with each other
● Orthophoria : normal state in which both eyes are aligned with each other
● Binoculars single vision : 2 types of fusion occur
○ Motor fusion (allows you to see 3D)
○ Sensory fusion
● Loss of binocular single vision leads to
○ Confusion
○ Diplopia
○ Compensatory mechanism
■ Suppression scotoma (immediate)
■ Strabismic amblyopia : if age is less than 12
● Phoria (latent Strabismus) : occurs when eye is covered
● Tropia (manifest Strabismus) : 2 types
○ Non paralytic : pathology in Sensory fusion
○ Paralytic : pathology in motor fusion
● Esotropia : inwards
○ Accommodative : in latent hypermetropes
 ○ Non accommodative :
■ Primary : fault in programming of Sensory fusion
■ Secondary
○ Presentation : parents complain that child has deviated eye
○ Management accommodative :
■ Spectacles and patching
■ Surgical correction if some Strabismus remains after spectacles
○ Management non accommodative
■ Primary : surgery
■ Secondary : manage underlying cause + patching
● Exotropia : Outwards
○ Primary : due to faulty programming of Sensory fusion
■ Convergence insufficiency
■ Divergence excess
○ Secondary
○ Presentation : parents complain that their child has a deviated eye. Starts as
exophoria and later develops into Exotropia
○ Management
■ Spectacles and patching
■ Surgical correction
■ Management of underlying cause in secondary form
● Paralytic Squint : Deviation of eye secondary to paralysis of ExtraOcular muscle
○ Congenital :
■ head tilts
○ Acquired :
■ diplopia
■ Head turn
○ Management (Congenital)
■ Observation
■ Prism : creates visual anomalies (rainbow effect)
■ Surgery
○ Management (Acquired)
■ Observation
■ Surgery
○ Surgical correction
■ Esotropia : medial rectus is weaken and lateral rectus is strengthened
■ Exotropia : medial rectus is strengthened and lateral rectus weaken
■ Surgery on medial rectus : 1cm = 2 degree correction
■ Surgery on lateral rectus : 1 cm = 1 degree correction