2019

OPHTHALMOLOGY

OM SUBHAM PRAHARAJ
 ERRORS OF REFRACTION AND ACCOMMODATION

HYPERMETROPIA/HYPEROPIA/LONG-SIGHTEDNESS
• Definition: the refractive state of the eye wherein parallel rays of light coming from infinity are focused behind
the retina with accommodation being at rest
• Etiology:
1) Axial hypermetropia
➢ mc
➢ axial shortening of eyeball
➢ 1 mm shortening of the AP diameter → +3D
➢ may be developmental or pathological
2) Curvatural hypermetropia
➢ curvature of cornea, lens or both is flatter than the normal
➢ 1 mm increase in radius of curvature → +6D
➢ may be developmental or pathological
3) Index hypermetropia
➢ decrease in refractive index of the lens in old age due to cortical sclerosis
4) Positional hypermetropia
➢ posteriorly placed crystalline lens
5) Absence of crystalline lens
➢ leads to aphakia
• Clinical types:
A. Simple/developmental/physiological
1) Developmental axial
2) Developmental curvatural
B. Non-physiological
1) Congenital
➢ Microphthalmos
➢ Nanophthalmos
➢ Microcornea
➢ Congenital posterior subluxation of lens
➢ Congenital aphakia
2) Acquired
a) Senile
➢ Index – acquired cortical sclerosis in old age
➢ Curvatural – decreased curvature of the outer lens fibers
b) Positional – posterior subluxation of lens
c) Aphakia – congenital or acquired absence of lens
d) Consecutive – surgically overcorrected myopia
e) Acquired axial – forward displacement of the retina: RD, CSR, orbital tumors
f) Acquired curvatural – post-traumatic or post-inflammatory corneal flattening
g) Pseudophakic – implantation of an underpowered IOL
C. Functional – paralysis of accommodation: 3rd nerve paralysis, internal ophthalmoplegia
• Components: Total hypermetropia = latent + manifest
Total hypermetropia - total amount of refractive error estimated after complete cycloplegia with atropine
1) Latent - amount of hypermetropia which is normally corrected by the inherent tone of ciliary muscle
2) Manifest - remaining portion of total hypermetropia, which is not corrected by the ciliary tone
a) Facultative - part which can be corrected by the patient’s accommodative effort
b) Absolute - residual part of manifest hypermetropia which cannot be corrected by the patient’s
accommodative efforts
• Symptoms:
1) Asymptomatic – refractive error corrected by mild accommodative effort
2) Asthenopic symptoms
➢ tiredness of eyes, frontal or frontotemporal headache, watering, mild photophobia
➢ d/t sustained accommodative efforts
➢ a/w near work and increase towards evening
3) Defective vision with asthenopic symptoms – more for near than distance
4) Defective vision only – marked for near and distance
• Signs:
1) Size of eyeball – small
2) Cornea – smaller than the normal
3) Anterior chamber – shallow
4) Retinoscopy and autorefractometry – hypermetropic refractive error
5) Fundus examination – small optic disc, pseudopapillitis, shot silk appearance
6) A-scan USG – short AP length of the eyeball
• Grading-
1) Low: <+2D
2) Moderate: +2 to +5D.
3) High: >+5D
• Complications-
1) Recurrent styes, blepharitis or chalazia
2) Accommodative convergent squint
3) Amblyopia
4) Primary narrow angle glaucoma
• Treatment
A. Optical treatment: principle – to prescribe convex lenses, so that light rays are brought to focus on the retina
a) Spectacles
b) Contact lenses
B. Surgical treatment
1) Cornea based procedures
a) Thermal laser keratoplasty (TLK)
b) Hyperopic photorefractive keratectomy (PRK)
c) Hyperopic LASIK
d) Conductive keratoplasty (CK)
2) Lens based procedures
a) Phakic refractive lens (PRL) or implantable contact lens (ICL)
b) Refractive lens exchange (RLE)

APHAKIA
• Definition: a condition in which the lens is absent from the pupillary area
• Causes:
1) Congenital absence of lens
2) Surgical aphakia
3) Aphakia due to absorption of lens matter
4) Traumatic extrusion of lens from the eye
5) Posterior dislocation of lens in vitreous
• Optical changes
➢ Hypermetropia of high degree.
➢ Total power of eye is reduced to about +44D (normal: 60D)
➢ Anterior focal point becomes 23.2 mm in front of the cornea (normal: 15.7 mm).
 ➢ Posterior focal point is about 31 mm behind the cornea
➢ Accommodation lost fully
• Symptoms
➢ Defective vision – for both far and near
➢ Erythropsia and cyanopsia – d/t excessive entry of UV and IR rays
• Signs
➢ Anterior chamber: deeper than normal
➢ Iridodonesis
➢ Pupil: jet black
➢ Purkinje’s image test: 2 images (normal: 4 images)
➢ Fundus examination: hypermetropic small disc
➢ Retinoscopy and autorefractometry: high hypermetropia
• Treatment
1) Spectacles
➢ Disadvantages-
a) Image magnified by 30% → diplopia in uniocular aphakia
b) spherical and chromatic aberrations of thick lenses
c) Field of vision limited
d) Prismatic effect of thick glasses
e) Roving ring scotoma (Jack in the box phenomenon)
f) Cosmetic blemish
2) Contact lens
➢ Advantages-
a) Less magnification of image
b) Elimination of aberrations and prismatic effect of thick glasses
c) Wider and better field of vision
d) Cosmetically more acceptable
e) Better suited for uniocular aphakia
➢ Disadvantages-
a) more cost
b) cumbersome to wear
c) corneal complications
3) IOL implantation
a) Primary – done during cataract surgery
b) Secondary – done in aphakic patients
4) Refractive corneal surgery
a) Keratophakia: lenticule prepared from the donor cornea is placed b/w the lamellae of patient’s cornea
b) Epikeratophakia: lenticule prepared from the donor cornea is stitched over the surface of cornea after
removing the epithelium
c) Hyperopic LASIK

MYOPIA/SHORT-SIGHTEDNESS
• Definition: a type of refractive error in which parallel rays of light coming from infinity are focused in front of the
retina when accommodation is at rest
• Etiological classification
1) Axial myopia – increase in AP length of the eyeball
2) Curvatural myopia – increased curvature of the cornea, lens or both
3) Positional myopia – anterior placement of crystalline lens in the eye.
4) Index myopia – increase in the refractive index of crystalline lens a/w nuclear sclerosis
5) Myopia due to excessive accommodation – in patients with spasm of accommodation
• Grading
1) Low: <-3D
2) Moderate: -3 to -6D
3) High: >-6D
• Clinical varieties
1) Congenital
2) Simple/developmental
3) Pathological/degenerative
4) Acquired/secondary
• Treatment
1) Optical treatment
➢ minimum acceptance providing maximum vision should be prescribed, undercorrection is always better
➢ concave lenses – spectacles and contact lenses
2) Surgical treatment
A. Cornea based procedures
a) Radial keratotomy (RK)
➢ making deep radial incisions in the peripheral part of cornea
b) Laser ablation corneal procedures
i) Photorefractive keratectomy (PRK)
➢ a central optical zone of anterior corneal stroma is photoablated using excimer laser
ii) Laser in-situ keratomileusis (LASIK)
➢ flap of 130–160 micron thickness of anterior corneal tissue raised using femtosecond laser →
midstromal tissue ablated directly with an excimer laser beam
➢ refractive surgery of choice for myopia of up to -8D
➢ Patient selection criteria-
▪ Patients >20 years of age
▪ Motivated patient
▪ Absence of corneal pathology
c) Refractive lenticule extraction (ReLEx) / All-Femtolaser-Vision-Correction /
SMILE (small incision lenticular extraction)
➢ a lenticule of corneal stroma is extracted with femtosecond laser
d) Intercorneal ring (ICR) implantation
➢ into the peripheral cornea at approximately 2/3 stromal depth → vaulting effect
➢ advantage: reversible
e) Orthokeratology
➢ non-surgical reversible method of molding the cornea with overnight wear of unique rigid gas
permeable contact lenses
➢ advantage: can be used in patients <18 years of age
B. Lens based procedures
a) Refractive lens exchange: Fucala’s operation
➢ recommended for myopia of more than 12D
b) Phakic refractive lens (PRL) or implantable contact lens (ICL)
➢ for myopia of more than 12D
3) General measures
➢ Balanced diet rich in vitamins and proteins.
➢ Early management of associated debilitating disease
➢ Visual hygiene, proper posture and adequate illumination
➢ Avoidance of outdoor sports and strenuous activities
4) Low vision aids
5) Prophylaxis: genetic counselling
SIMPLE/DEVELOPMENTAL/SCHOOL MYOPIA
• mc variety
• physiological error not a/w any disease of the eye
• Prevalence = 20–40% of population, rise occurs at school going age (8-12 years)
• Etiology: normal biological variation in the development of eye
1) Axial type - physiological variation in length of eyeball or a/w precocious neurological growth during
childhood
2) Curvatural type - underdevelopment of the eyeball
3) Genetics
• Symptoms
➢ Short-sightedness
➢ Asthenopia
➢ Half shutting of the eyes
• Signs
➢ Eyeballs: prominent
➢ Anterior chamber: deeper than normal
➢ Pupils: large
➢ Magnitude of refractive error: low to moderate (<-6D)
• Diagnosis: by refraction

PATHOLOGICAL/DEGENERATIVE/PROGRESSIVE MYOPIA
• Definition: a rapidly progressive error which starts in childhood and results in high myopia
• Etiology: a rapid axial growth of the eyeball which is outside the normal biological variations of development

• Symptoms
1) Defective vision
2) Muscae volitantes
➢ Floating black opacities in front of the eyes
➢ d/t degenerated liquified vitreous
3) Night blindness
• Signs
1) Eyeballs: prominent
2) Cornea: large
3) Anterior chamber: deep
4) Pupils: large, react sluggishly to light
5) Fundus examination
a) Optic disc: large and pale
➢ myopic crescent – at temporal edge
➢ peripapillary crescent – encircling the disc
➢ super-traction crescent – on the nasal side
b) Degenerative changes in retina and choroid
 ➢ Chorioretinal atrophic patches
➢ Foster-Fuchs’ spot
➢ Cystoid degeneration
➢ Lattice degeneration and snail track lesions +/- retinal holes/tears
➢ Total retinal atrophy
c) Posterior staphyloma: due to ectasia of sclera at posterior pole
d) Degenerative changes in vitreous
➢ Liquefaction
➢ vitreous opacities
➢ posterior vitreous detachment (PVD)
6) Visual fields: contraction
7) ERG: subnormal
• Complications
➢ Retinal detachment
➢ Complicated cataract
➢ Vitreous haemorrhage
➢ Choroidal haemorrhage
➢ Strabismus fixus convergence

STURM’S CONOID
• Definition: configuration of rays refracted through a toric surface

• Shape of bundle of the light rays-

➢ Point A → horizontal oval or an oblate ellipse
➢ Point B = 1st focus → horizontal line
➢ Point C → horizontal oval
➢ Point D = circle of least diffusion
➢ Point E → vertical oval
➢ Point F = 2nd focus → vertical line
➢ Beyond F → vertical oval or prolate ellipse
• Focal interval of Sturm: distance b/w the two foci (B and F)
ACCOMMODATION
• Definition: a unique mechanism of our eyes by which we can even focus the diverging rays coming from a near
object on the retina in a bid to see clearly
• Mechanism: von Helmholtz’s capsular theory → accommodation is achieved by change in the shape of lens
➢ When the eye is at rest (unaccommodated): ciliary ring is large and keeps the zonules tense → lens is kept
compressed (flat) by the capsule
➢ Contraction of the ciliary muscle → ciliary ring shortens → releases zonular tension on the lens capsule →
elastic capsule acts unrestrained to deform the lens substance → lens becomes more convex or conoidal

PRESBYOPIA
• Definition: a condition of physiological insufficiency of accommodation leading to a progressive fall in near vision
• Pathophysiology:
➢ in an emmetropic eye far point is infinity and near point varies with age (7 cm at the age of 10 years, 25 cm
at the age of 40 years and 33 cm at the age of 45 years)
➢ we usually keep the book at about 25 cm, so we can read comfortably up to the age of 40 years
➢ After the age of 40 years, near point of accommodation recedes beyond normal reading or working range
➢ This condition of failing near vision is due to age-related decrease in the amplitude of accommodation or
increase in punctum proximum
• Causes
A. Age-related
1) Changes in the lens
➢ Decrease in the elasticity of lens capsule
➢ Progressive increase in size and hardness of lens substance
2) Decline in ciliary muscle power
B. Premature
➢ Uncorrected hypermetropia
➢ Premature sclerosis of the crystalline lens
➢ Chronic simple glaucoma
• Symptoms
1) Difficulty in near vision
2) Asthenopia
3) Intermittent diplopia
• Treatment
1) Optical treatment
➢ prescription of appropriate convex glasses for near work
➢ The weakest convex lens with which an individual can see clearly at the near point should be prescribed
2) Surgical treatment
A. Cornea based procedures
a) Monovision LASIK
b) Monovision conductive keratoplasty (CK)
c) Presbyopic bifocal LASIK or LASIK-PARM (Presbyopia Avalos Rozakis Method)
B. Lens based procedures
a) Multifocal or accommodating IOL implantation
b) Monovision with intraocular lenses
C. Sclera based procedures
a) Anterior ciliary sclerotomy (ACS)
b) Scleral spacing procedures and scleral ablation
c) Scleral expansion
 DISEASES OF CONJUNCTIVA

TRACHOMA / EGYPTIAN OPHTHALMIA

• chronic keratoconjunctivitis affecting the superficial epithelium of conjunctiva and cornea
simultaneously
• characterised by a mixed follicular and papillary response of conjunctival tissue
• Etiology
A. Causative organism: Chlamydia trachomatis
▪ Epitheliotropic
▪ produces intracytoplasmic inclusion bodies → HP bodies (Halberstaedter Prowazek bodies)
▪ Serotypes A, B, Ba and C → hyperendemic (blinding) trachoma
Serotypes D to K (except I) → inclusion conjunctivitis (oculogenital chlamydial disease)
B. Predisposing factors
1) Age: infancy and early childhood
2) Sex: females > males
3) Race: mc = Jews
4) Climate: mc = dry and dusty weather
5) Socioeconomic status: mc = poor classes
6) Environmental factors: exposure to dust, smoke, irritants, sunlight
C. Source of infection: mc = conjunctival discharge of the affected person
D. Modes of infection
1) Direct spread
2) Vector transmission
3) Material transfer
• Prevalence: worldwide
• Clinical features
A. Phase of active trachoma
▪ mc = childhood
▪ due to active chlamydial infection
▪ Incubation period = 5-22 days
▪ Onset = insidious (subacute)
▪ Symptoms
➢ In the absence of secondary infection
✓ mild foreign body sensation
✓ occasional lacrimation
✓ slight stickiness of the lids
✓ scanty mucoid discharge
➢ In the presence of secondary bacterial infection
✓ Discomfort, foreign body, grittiness, blurring and redness
✓ Photophobia
✓ Sticking together of lid margins
▪ Signs
a) Conjunctival signs
1) Congestion of upper tarsal and forniceal conjunctiva
2) Conjunctival follicles
➢ mc = upper tarsal conjunctiva and fornix
 ➢ formed d/t scattered aggregation of lymphocytes and other cells in the adenoid layer
➢ Central part → mononuclear histiocytes, lymphocytes and large multinucleated cells
(Leber cells)
➢ Cortical part → lymphocytes showing active proliferation
➢ Most peripheral part → blood vessels
➢ Later stages → signs of necrosis
➢ Presence of Leber cells and signs of necrosis differentiate trachoma follicles from
follicles of other forms of follicular conjunctivitis.
3) Papillary hyperplasia
➢ reddish, flat topped raised areas which give red and velvety appearance to the tarsal
conjunctiva
➢ consists of central core of numerous dilated blood vessels surrounded by
lymphocytes and covered by hypertrophic epithelium
b) Corneal signs
1) Herbert follicles: present in the limbal area
2) Progressive pannus
➢ infiltration of cornea is ahead of vascularization
➢ vessels are superficial and lie between epithelium and Bowman’s membrane
B. Phase of cicatricial trachoma
▪ manifests in middle age
▪ due to continued mild grade chronic inflammation
▪ chronic immune response consisting of cell-mediated delayed hypersensitivity (Type IV)
reaction to the intermittent presence of chlamydial antigen
▪ end stage of cicatricial trachoma = sequelae of trachoma
▪ Signs
a) Conjunctival signs
1) Conjunctival scarring
➢ Arlt’s line = linear scar present in the sulcus subtarsalis
2) Concretions
➢ hard looking whitish deposits
➢ formed due to accumulation of dead epithelial cells and inspissated mucus in the
depressions (glands of Henle)
3) Pseudocyst
4) Xerosis
5) Symblepharon
b) Corneal signs
1) Regressive pannus (pannus siccus): vessels extend a short distance beyond the area of
infiltration
2) Herbert pits: oval or circular pitted scars, left after healing of Herbert follicles in the
limbal area
3) Corneal opacity: end result of trachomatous corneal lesions
4) corneal ectasia
5) corneal xerosis
6) total corneal pannus
c) Lid signs
1) trichiasis
2) entropion
3) tylosis
 4) ptosis
5) madarosis
6) ankyloblepharon
d) Lacrimal apparatus sequelae
1) Chronic dacryocystitis
2) chronic dacryoadenitis
• Grading of trachoma
A. McCallan’s classification
1) Stage I: incipient trachoma or stage of infiltration
hyperemia of palpebral conjunctiva and immature follicles
2) Stage II: established trachoma or stage of florid infiltration
mature follicles, papillae and progressive corneal pannus.
3) Stage III: cicatrising trachoma or stage of scarring
obvious scarring of palpebral conjunctiva.
4) Stage IV: healed trachoma or stage of sequelae
B. WHO classification
1) TF: Trachomatous inflammation-follicular
➢ stage of active trachoma with predominantly follicular inflammation
➢ at least five or more follicles must be present on the upper tarsal conjunctiva
➢ deep tarsal vessels should be visible through the follicles and papillae
2) TI: Trachomatous inflammation intense
➢ pronounced inflammatory thickening of the upper tarsal conjunctiva obscures more than
half of the normal deep tarsal vessels
3) TS: Trachomatous scarring
➢ scarring in the tarsal conjunctiva
4) TT: Trachomatous trichiasis
➢ at least one eyelash rubs the eyeball
5) CO: Corneal opacity
➢ easily visible corneal opacity is present over the pupil
➢ corneal scarring is so dense that at least part of pupil margin is blurred when seen through
the opacity
• Complication: corneal ulcer
• Diagnosis
A. Clinical diagnosis: Clinical grading
B. Laboratory diagnosis
1) Conjunctival cytology: Giemsa-stained smears → predominantly polymorphonuclear reaction
with presence of plasma cells and Leber cells
2) Detection of inclusion bodies
3) ELISA for chlamydial antigens
4) PCR
5) Isolation of Chlamydia
➢ yolk-sac inoculation method
➢ tissue culture technique: Standard single-passage McCoy cell culture
6) Serotyping of TRIC agents
➢ Micro-immunofluorescence (micro-IF) method
➢ Direct monoclonal fluorescent antibody microscopy
• Differential diagnosis
1) Trachoma with follicular hypertrophy → EKC
 ➢ Distribution of follicles:
Trachoma → upper palpebral conjunctiva and upper fornix
EKC → lower palpebral conjunctiva and lower fornix
2) Trachoma with papillary hypertrophy → VKC
➢ VKC: Papillae large in size, typical cobble-stone arrangement
➢ pH of tears: Trachoma → acidic, VKC → alkaline
➢ VKC: ropy discharge
• Management
A. Treatment of active trachoma
1) Topical therapy regimes
▪ Tetracycline (1%) or erythromycin (1%) eye ointment
▪ Sulfacetamide (20%) eye drops + tetracycline (1%) eye ointment
2) Systemic therapy regimes
▪ Azithromycin 250 mg OD × 4 days
▪ Tetracycline/erythromycin
▪ Doxycycline
3) Combined topical and systemic therapy regime
Tetracycline (1%) or erythromycin eye ointment + oral azithromycin
preferred when the ocular infection is severe (TI) or when there is associated genital infection
B. Treatment of trachoma sequelae
C. Prophylaxis for trachoma infection and blindness
SAFE strategy
S: Surgery (Tertiary prevention)
A: Antibiotic use (Secondary prevention)
F: Facial hygiene (Primary prevention)
E: Environmental changes (Primordial prevention)

EPIDEMIC KERATOCONJUNCTIVITIS (EKC)

• a type of acute follicular conjunctivitis a/w superficial punctate keratitis
occurs in epidemics
• Etiology: adenoviruses type 8 and 19
markedly contagious
patients infectious for up to 11 days after onset
• Symptoms
➢ Redness and watering
➢ Ocular discomfort and foreign body sensation
➢ Photophobia
• Signs
➢ Eyelids swollen
➢ Conjunctival signs
▪ Hyperemia
▪ Chemosis
▪ Follicles: lower fornix and palpebral conjunctiva
➢ Corneal involvement
▪ Epithelial microcystic diffuse fine non-staining lesions
▪ Superficial punctate keratitis (SPK)
 ➢ Pre-auricular lymphadenopathy
• Differential diagnosis
1) Pharyngoconjunctival fever
2) Acute haemorrhagic conjunctivitis
3) Herpes simplex virus conjunctivitis
4) Trachoma
• Diagnosis
➢ Typical clinical features
➢ Conjunctival cytology: Giemsa stain → mononuclear cells
➢ PCR
➢ Point-of-care immunochromatography test
➢ Viral cultures
• Treatment
1) Supportive treatment
a) Cold compresses and sun glasses: to decrease glare
b) Decongestant and lubricant tear drops: to decrease discomfort
2) Topical antibiotics: to prevent superadded bacterial infections
3) Prevention of spread of infection to the contacts
a) Frequent handwashing
b) Relative isolation of infected individual
c) Avoiding eye rubbing and common use of towel or handkerchief sharing
d) Disinfection of ophthalmic instruments and clinical surfaces after examination of a patient

OPHTHALMIA NEONATORUM
• bilateral inflammation of the conjunctiva occurring in an infant, less than 30 days old
any discharge or even watering from the eyes in the first week of life should arouse suspicion of
ophthalmia neonatorum
• Etiology
➢ Source and mode of infection
1) Before birth → through infected liquor amnii
2) During birth (mc) → from infected birth canal
3) After birth
▪ during first bath of newborn
▪ from soiled clothes or fingers with infected lochia.
➢ Causative agents
1) Chemical conjunctivitis
▪ mcc = silver nitrate
▪ prophylactic antibiotics
2) Gonococcal infection
3) Other bacterial infections
▪ Staphylococcus aureus
▪ Streptococcus haemolyticus
▪ Streptococcus pneumoniae
4) Neonatal inclusion conjunctivitis
▪ serotypes D to K of Chlamydia trachomatis
▪ mcc in developed countries
 5) Herpes simplex ophthalmia neonatorum
▪ herpes simplex-II virus
▪ rare
• Symptoms and signs
1) Pain and tenderness in the eyeball
2) Conjunctival discharge
➢ purulent in gonococcal infection
➢ mucopurulent in other bacterial infections and neonatal inclusion conjunctivitis
3) Lids → swollen
4) Conjunctiva → hyperemia and chemosis
• Complications
1) corneal ulceration
2) corneal opacification
3) staphyloma formation
• Treatment
A. Prophylaxis
1) Antenatal measures
➢ thorough care of mother
➢ treatment of genital infections
2) Natal measures
➢ Deliveries should be conducted under hygienic conditions taking all aseptic measures
➢ The newborn baby’s closed lids should be thoroughly cleansed and dried
3) Postnatal measures
➢ Povidone-iodine 2.5% solution
➢ 1% tetracycline ointment or 0.5% erythromycin ointment: into the eyes of the babies
immediately after birth
➢ Single injection of ceftriaxone: to infants born to mothers with untreated gonococcal
infection
B. Curative treatment
1) Chemical ophthalmia neonatorum: self-limiting
2) Gonococcal ophthalmia neonatorum
a) Topical therapy
➢ Saline lavage: hourly till the discharge eliminated
➢ Bacitracin eye ointment: 4 times/day
➢ Atropine sulphate ointment: if cornea is involved
b) Systemic therapy: 7 days
➢ Ceftriaxone
➢ Cefotaxime
➢ Ciprofloxacin
➢ Crystalline benzyl penicillin G
3) Other bacterial ophthalmia neonatorum
➢ broad-spectrum antibiotic drops and ointments: 2 weeks
4) Neonatal inclusion conjunctivitis
➢ topical tetracycline 1% or erythromycin 0.5% eye ointment
➢ oral erythromycin
5) Herpes simplex conjunctivitis
➢ self-limiting
➢ High dose iv acyclovir → suspected systemic herpes infection
VERNAL KERATOCONJUNCTIVITIS (VKC) OR SPRING CATARRH
• recurrent, bilateral, interstitial, self-limiting, allergic inflammation of the conjunctiva having a periodic
seasonal incidence
• Etiopathogenesis: Th2 lymphocyte alteration → exaggerated IgE response to allergens
➢ Age and sex: 4–20 years; boys > girls
➢ Season: summer
➢ Climate: tropics
• Pathology
➢ Conjunctival epithelium: hyperplasia
➢ Adenoid layer: marked cellular infiltration
➢ Fibrous layer: proliferation
➢ Conjunctival vessels: proliferation, increased permeability and vasodilation
• Symptoms
➢ Marked burning and itching sensation: intolerable
➢ Photophobia
➢ Lacrimation
➢ stringy (ropy) discharge
➢ heaviness of lids
• Signs
1) Palpebral form
➢ hard, flat topped, papillae arranged in a cobble-stone or pavement stone fashion
➢ upper tarsal conjunctiva of both eyes involved
➢ conjunctival hyperemia
➢ white ropy discharge
2) Bulbar limbal form
➢ Dusky red triangular congestion of bulbar conjunctiva in palpebral area
➢ Gelatinous thickened accumulation of tissue around the limbus
➢ Horner-Tranta’s spots: discrete whitish raised dots along the limbus
3) Mixed form: combined features of both palpebral and bulbar forms
• Vernal keratopathy
➢ primary or secondary due to extension of limbal lesions
➢ more frequent with palpebral form
➢ lesions
1) Punctate epithelial keratitis
▪ involves upper cornea
▪ lesions stain with rose bengal and fluorescein dye
2) Ulcerative vernal keratitis (shield ulceration)
▪ shallow transverse ulcer in upper part of cornea
▪ due to epithelial macroerosions
3) Vernal corneal plaques: due to coating of bare areas of epithelial macroerosions with a
layer of altered exudates
4) Subepithelial scarring: ring scar
5) Pseudogerontoxon: in recurrent limbal disease → classical cupid’s bow outline
• Clinical course: self-limiting, burns out spontaneously after 5–10 years
• Differential diagnosis: trachoma with predominant papillary hypertrophy
• Treatment
 A. Topical anti-inflammatory therapy
1) Topical steroids: Medrysone and fluorometholone
➢ use should be minimized → cause steroid induced glaucoma
monitoring of intraocular pressure very important during steroid therapy
➢ 4 hourly for 2 days followed by 4 times a day for 2 weeks
2) Mast cell stabilizers: sodium cromoglycate drops
3) Dual action antihistamines and mast cell stabilizers: azelastine, olopatadine and ketotifen
4) NSAIDs eye drops: ketorolac and diclofenac
5) Immune-modulators
➢ topical cyclosporine: steroid-sparing agent or when steroids ineffective, inadequate
➢ Tacrolimus ointment: refractory cases
B. Artificial tears: carboxymethyl cellulose
C. Topical mucolytics: acetyl cysteine
D. Systemic therapy
1) Oral antihistaminics: relief from itching in severe cases
2) Oral steroids: for advanced, very severe, non-responsive cases
E. Treatment of large papillae
1) Supratarsal injection of long acting steroid
2) Cryo application
3) Surgical excision
F. General measures
1) Dark goggles
2) Cold compresses
3) Change of place from hot to cold area
G. Treatment of vernal keratopathy
1) Punctate epithelial keratitis: instillation of steroids increased
2) Large vernal plaque: surgical excision → superficial keratectomy
3) Severe shield ulcer: surgical treatment → debridement, superficial keratectomy, excimer laser
therapeutic keratectomy and amniotic membrane transplantation

PHLYCTENULAR KERATOCONJUNCTIVITIS / MICROBIAL ALLERGIC

CONJUNCTIVITIS
• nodular allergic response of the conjunctival and corneal epithelium to some endogenous allergens
• worldwide distribution
• incidence higher in developing countries
• Etiology: delayed hypersensitivity (Type IV-cell mediated) response to endogenous microbial proteins
A. Causative allergens
1) Tuberculous proteins
2) Staphylococcus proteins
3) proteins of Moraxella Axenfeld bacillus and certain parasites
B. Predisposing factors
1) Age: 3–15 years
2) Girls > boys
3) undernourished children
4) Overcrowded and unhygienic conditions
• Pathology
 1) Stage of nodule formation
➢ exudation and infiltration of leucocytes into the deeper layers of conjunctiva → nodule
formation
➢ central cells: PMNL; peripheral cells: lymphocytes
➢ neighbouring blood vessels dilate and their endothelium proliferates
2) Stage of ulceration
➢ necrosis at apex of nodule → ulcer formed
➢ Leucocytic infiltration ↑ with plasma cells and mast cells
3) Stage of granulation: floor of the ulcer covered by granulation tissue
4) Stage of healing
• Symptoms
➢ discomfort in the eye
➢ irritation
➢ reflex watering
➢ associated mucopurulent conjunctivitis due to secondary bacterial infection
• Signs: 3 forms
1) Simple (mc): pinkish white nodule surrounded by hyperemia on bulbar conjunctiva near limbus
2) Necrotizing: very large phlycten with necrosis and ulceration → severe pustular conjunctivitis
3) Miliary: multiple phlyctens
• Phlyctenular keratitis
1) Ulcerative: 3 forms
a) Sacrofulous ulcer
➢ shallow marginal ulcer formed due to breakdown of small limbal phlycten
➢ no clear space between the ulcer and the limbus
➢ long axis frequently perpendicular to limbus.
b) Fascicular ulcer
➢ has a prominent parallel leash of blood vessels
➢ superficial
➢ leaves behind a band-shaped superficial opacity after healing
c) Miliary ulcer: multiple small ulcers
2) Diffuse: central infiltration of cornea with characteristic rich vascularization from the periphery, all
around the limbus
• Clinical course: self-limiting, disappears in 8–10 days
• Differential diagnosis
➢ Episcleritis
➢ Scleritis
➢ conjunctival foreign body granuloma
• Management
1) Local therapy
a) Topical steroids: dexamethasone or betamethasone
b) Antibiotic drops and ointment: for associated secondary infection
c) Atropine (1%) eye ointment: when cornea involved
2) Specific therapy: search and eradicate causative conditions
3) General measures
➢ high protein diet
➢ vitamins A, C and D
PTERYGIUM
• a wing-shaped fold of conjunctiva encroaching upon the cornea from either side within the
interpalpebral fissure
• Etiology: prolonged effect of environmental factors such as exposure to sun (ultraviolet rays), dry heat,
high wind and abundance of dust
• Pathology
➢ degenerative and hyperplastic condition of conjunctiva
➢ subconjunctival tissue undergoes elastotic degeneration and proliferates as vascularised
granulation tissue under the epithelium → encroaches the cornea
➢ corneal epithelium, Bowman’s layer and superficial stroma destroyed
• Demography
➢ Old age
➢ Males > females
➢ mc on nasal side
• Symptoms
➢ Cosmetic intolerance
➢ Foreign body sensation and irritation
➢ Defective vision: when it encroaches the pupillary area or due to corneal astigmatism induced by
fibrosis
➢ Diplopia: due to limitation of ocular movements
• Signs: a triangular fold of conjunctiva encroaching on the cornea in the area of palpebral aperture
usually on the nasal side
• Parts
➢ Head: Apical part present on the cornea
➢ Neck: Constricted part present in the limbal area
➢ Body: Scleral part, extending between limbus and canthus
➢ Cap: Semilunar whitish infiltrate present just in front of the head
• Types
1) Progressive
➢ thick, fleshy and vascular
➢ cap present = Fuch’s spots / islets of Vogt
2) Regressive
➢ thin, atrophic, attenuated with very little vascularity
➢ no cap
➢ deposition of iron: Stocker’s line
• Complications
➢ Cystic degeneration and infection
➢ Neoplastic change
• Differential diagnosis: Pseudopterygium → a fold of bulbar conjunctiva attached to the cornea. It is
formed due to adhesions of chemosed bulbar conjunctiva to the marginal corneal ulcer; occurs
following chemical burns of the eye
• Treatment: Surgical excision
 DISEASES OF CORNEA

BACTERIAL CORNEAL ULCER

• Definition: discontinuation in normal epithelial surface of cornea a/w necrosis of the surrounding
corneal tissue pathologically characterised by edema and cellular infiltration
• Etiology: 2 factors-
1) Corneal epithelial damage: by-
a) Corneal abrasion - foreign body, misdirected cilia, concretions and trauma
b) Epithelial drying - xerosis and exposure keratitis.
c) Epithelial necrosis - keratomalacia.
d) Desquamation of epithelial cells - bullous keratopathy.
e) Trophic changes - neuroparalytic keratitis
2) Infection of the eroded area
➢ Neisseria gonorrhoeae, Corynebacterium diphtheriae & Neisseria meningitidis invade intact
epithelium
• Sources of infection
1) Exogenous infection
a) From conjunctival sac
b) From lacrimal sac
c) infected foreign bodies
d) infected vegetative material
e) waterborne or airborne infections
2) From the ocular tissue
a) From conjunctiva to corneal epithelium
b) From sclera to corneal stroma
c) From uveal tract to corneal endothelium
• Causative organisms: Staphylococci, Pseudomonas, Streptococcus pneumonia, Enterobacteriaceae,
Neisseria
• Pathogenesis
A. Pathology of localised corneal ulcer
1) Stage of progressive infiltration:
➢ infiltration of PMNL and lymphocytes into the epithelium from the peripheral circulation
and the underlying stroma
2) Stage of active ulceration
➢ results from necrosis and sloughing of the epithelium, Bowman’s membrane and stroma
➢ walls of the active ulcer project due to swelling of the lamellae by the imbibition of fluid and
the packing of masses of leucocytes between them
➢ Hyperaemia of circumcorneal network of vessels → accumulation of purulent exudates on
cornea
➢ vascular congestion of the iris & ciliary body and iritis
➢ lateral extension → diffuse superficial ulceration; deeper penetration → Descemetocele
formation
3) Stage of regression
➢ induced by the natural host defence mechanisms and the treatment
 ➢ A line of demarcation develops around the ulcer, which consists of leucocytes that
neutralize and eventually phagocytose the offending organisms and necrotic cellular debris
4) Stage of cicatrization
➢ healing continues by progressive epithelization
➢ fibrous tissue is laid down partly by the corneal fibroblasts and partly by the endothelial
cells of the new vessels
➢ Scars:
▪ Nebula – ulcers involving Bowman’s membrane and few superficial stromal lamellae
▪ Macula – ulcers involving upto one-third of corneal stroma
▪ Leucoma – ulcers involving more than one-third of corneal stroma
B. Pathology of perforated corneal ulcer
➢ ulcerative process deepens and reaches up to Descemet’s membrane → formation of
Descemetocele
➢ any exertion on the part of patient at this stage will perforate the corneal ulcer
➢ immediately after perforation, the aqueous escapes, IOP falls and the iris-lens diaphragm moves
forward
➢ When the perforation is small and opposite to iris tissue, healing by cicatrization proceeds
rapidly → adherent leucoma
C. Pathology of sloughing corneal ulcer and formation of anterior staphyloma
➢ infecting agent highly virulent and body resistance very low → whole cornea sloughs and total
prolapse of iris → false cornea → pseudocornea → anterior staphyloma
• Clinical features
A. Purulent corneal ulcer without hypopyon
➢ Symptoms
1) Pain and foreign body sensation
2) Watering
3) Photophobia
4) Blurred vision
5) Redness of eyes
➢ Signs
1) Swelling of lids
2) Blepharospasm
3) Conjunctiva chemosed, hyperaemia and ciliary congestion
4) Corneal ulcer
▪ starts as an epithelial defect a/w greyish-white circumscribed infiltrate (early stage)
▪ oval-shaped yellowish-white area
▪ margins swollen and over hanging
▪ floor covered by necrotic material
▪ stromal edema present
B. Hypopyon corneal ulcer / Ulcus serpens
➢ Causative organism: Pneumococcus
➢ Source of infection: chronic dacryocystitis
➢ Factors predisposing to development of hypopyon: high virulence of the infecting organism and
low resistance of the tissues
➢ Mechanism of development of hypopyon: severe iritis → outpouring of leucocytes from the
vessels → cells gravitate to the bottom of the anterior chamber → sterile hypopyon
➢ Symptoms: same as above
➢ Signs
 ▪ a greyish white or yellowish disc-shaped ulcer occurring near the centre of cornea
▪ tendency of the ulcer to creep over the cornea in a serpiginous fashion
▪ Violent iridocyclitis
▪ Hypopyon increases in size very rapidly → secondary glaucoma
▪ Ulcer spreads rapidly → early perforation
• Complications
1) Toxic iridocyclitis
2) Secondary glaucoma
3) Descemetocele
4) Perforation of corneal ulcer
5) Corneal scarring
• Management
A. Clinical evaluation
1) Thorough history taking
2) General physical examination
3) Ocular examination
a) Diffuse light examination
b) Biomicroscopic examination after staining of corneal ulcer with fluorescein dye
B. Laboratory investigations
1) Routine laboratory investigations
2) Microbiological investigations
a) Gram and Giemsa stained smears
b) Culture on blood agar
C. Treatment
➢ Treatment of uncomplicated corneal ulcer
1) Specific treatment: Topical antibiotics
a) Fortified Cefazoline 5%
b) Fortified tobramycin 1.3% or fortified vancomycin 5% or fluoroquinolones
2) Nonspecific treatment
a) Cycloplegic drugs: 1% atropine
b) Systemic NSAIDs: paracetamol and ibuprofen
c) Vitamins (A, B-complex and C)
3) Physical and general measures
a) Hot fomentation
b) Dark goggles
c) Rest, good diet and fresh air
➢ Treatment of non-healing corneal ulcer
1) Removal of any known cause of non-healing ulcer
a) Local causes: raised IOP, concretions, misdirected cilia, impacted foreign body,
dacryocystitis, inadequate therapy, wrong diagnosis, lagophthalmos and excessive
vascularization of ulcer
b) Systemic causes: DM, severe anemia, malnutrition, chronic debilitating diseases and
patients on systemic steroids
2) Mechanical debridement of ulcer
3) Cauterization of the ulcer
4) Bandage soft contact lens
5) Peritomy
➢ Treatment of impending perforation
 1) No strain
2) Pressure bandage
3) Lowering of IOP
4) Tissue adhesive glue: cyanoacrylate
5) Bandage soft contact lens
6) Conjunctival flap
7) Amniotic membrane transplantation
8) Penetrating therapeutic keratoplasty (tectonic graft)
➢ Treatment of perforated corneal ulcer: urgent tectonic keratoplasty

MYCOTIC CORNEAL ULCER

• Fungi involved: Aspergillus (mc), Candida and Fusarium
• Modes of infection
1) Injury by vegetative material
2) Injury by animal tail
3) Immunosuppressed patients
• Role of antibiotics and steroids
➢ Antibiotics disturb the symbiosis between bacteria and fungi
➢ steroids make the fungi facultative pathogens
• Clinical features
➢ Symptoms: same as above
➢ Signs
▪ Corneal ulcer: dry-looking, greyish white, with elevated rolled out margins
▪ Delicate feathery finger-like extensions
▪ sterile immune ring: yellow line of demarcation
▪ hypopyon: big, not sterile
▪ Endothelial plaque: composed of fibrin and leucocytes
▪ Corneal vascularization: conspicuously absent
• Diagnosis
➢ Typical clinical manifestations a/w h/o injury by vegetative material
➢ Chronic ulcer worsening in spite of most efficient treatment
➢ Laboratory investigations: examination of wet KOH, Calcofluor white, Gram’s and Giemsa-stained
films for fungal hyphae and culture on SDA
➢ Confocal microscopic examination
➢ PCR
• Treatment
A. Specific treatment
1) Topical antifungal eyedrops
➢ Aspergillus, Fusarium: Natamycin+AmphotericinB+Fluconazole/Miconazole/Voriconazole
eyedrops
➢ Candida: Nystatin eye ointment
2) Intracameral and intracorneal/intrastromal administration of voriconazole: intraocular
extension
3) Systemic antifungal drugs: severe cases
B. Non-specific treatment: same as above
C. Therapeutic penetrating keratoplasty: non-responsive cases
HERPES ZOSTER OPHTHALMICUS
• Definition: an acute infection of Gasserian ganglion of the 5th cranial nerve by the varicella-zoster
virus in immunocompromised individuals
• Pathogenesis: infection contracted in childhood, manifests as chickenpox and the child develops
immunity → virus remains dormant in the sensory ganglion of trigeminal nerve → with depressed
cellular immunity, the virus reactivates, replicates and travels down along the branches of the
ophthalmic division of the fifth nerve to produce cutaneous and ocular lesions.
• Clinical Features
➢ Nerves involved: frontal > lacrimal > nasociliary
➢ Ocular complications in 50% cases
➢ Hutchinson’s rule = ocular involvement is frequent if the side or tip of nose presents vesicles
(cutaneous involvement of nasociliary nerve)
➢ Lesions are strictly limited to one side of the midline of head
➢ Clinical phases
A. Acute phase lesions
1) General features: fever, malaise and severe neuralgic pain along the course of the affected
nerve which diminishes with the subsidence of eruptive phase (3weeks)
2) Cutaneous lesions
▪ in the area of distribution of the involved nerve
▪ skin becomes red and edematous → vesicle formation → pustules → crusting ulcers →
permanent pitted scars
3) Ocular lesions
a) Conjunctivitis
b) Zoster keratitis
▪ Fine/coarse punctate epithelial keratitis
▪ Microdendritic epithelial ulcers: peripheral, stellate, tapered ends
▪ Nummular keratitis: characterised by anterior stromal infiltrates
▪ Disciform keratitis
c) Episcleritis and scleritis
d) Iridocyclitis
B. Chronic phase lesions
1) Post-herpetic neuralgia
▪ persistence of pain even after subsidence of eruptive phase of zoster
▪ mild to moderate in intensity, worsens at night, aggravated by touch and heat
▪ anaesthesia dolorosa: anaesthesia of the affected skin a/w post-herpetic neuralgia
2) Lid lesions: ptosis, trichiasis, entropion and notching
3) Conjunctival lesions: chronic mucous secreting conjunctivitis
4) Corneal lesions
a) Neuroparalytic ulceration
b) Exposure keratitis
c) Mucous plaque keratitis
5) Scleritis and Uveitis
C. Relapsing phase lesions
• Treatment
A. Systemic therapy
1) Oral antiviral drugs: acyclovir and valaciclovir
2) Analgesics: combination of mephenamic acid and paracetamol or pentazocine
 3) Systemic steroids
4) Cimetidine
5) Amitriptyline
B. Local therapy for skin lesions: Antibiotic-corticosteroid skin ointment or lotions
C. Local therapy for ocular lesions
1) Topical steroid eyedrops
2) Cycloplegics: atropine/cyclopentolate
3) Topical acyclovir 3% eye ointment
D. Surgical treatment
1) Lateral tarsorrhaphy
2) Amniotic membrane transplantation (AMT) or conjunctival flap

KERATOCONUS / CONICAL CORNEA

• non-inflammatory bilateral (85%) ectatic condition of cornea in its axial part
• starts at puberty and progresses slowly
• Etiopathogenesis: defective synthesis of mucopolysaccharide and collagen tissue → progressive
thinning and ectasia
• Symptoms: defective vision due to progressive myopia and irregular astigmatism
• Signs
1) Window reflex: distorted
2) Placido disc examination: irregularity of the circles
3) Slit-lamp examination:
➢ thinning and ectasia of central cornea
➢ opacity at the apex
➢ Fleischer’s ring at the base of cone
➢ folds in Descemet’s and Bowman’s membranes
➢ Vogt lines which disappear with external pressure on the globe
4) Retinoscopy: yawning reflex (scissor reflex) and irregular astigmatism
5) Distant direct ophthalmoscopy: oil droplet reflex
6) Munson’s sign: +ve
7) Keratometry: increased
➢ Mild: 45-48D
➢ Moderate: 48-54D
➢ Severe: >54D
8) Corneal topography (most sensitive method): Forme fruste → earliest subclinical form
• Morphological classification
1) Nipple cone: <5 mm
2) Oval cone: 5–6 mm
3) Globus cone: >6 mm
• Complication: acute hydrops
• Treatment
1) Spectacle correction
2) Contact lenses (rigid gas permeable)
3) Intacs (intracorneal ring segments)
4) Corneal collagen cross linking with riboflavin (CXL or C3R) and UV-A rays
5) Keratoplasty: Deep anterior lamellar keratoplasty (DALK) or penetrating keratoplasty (PK)
 DISEASES OF SCLERA

EPISCLERITIS
• benign recurrent inflammation of the episclera involving the overlying Tenon’s capsule
• young adults
• twice as common in women than men
• Etiology:
1) Idiopathic
2) Systemic diseases: gout, rosacea, psoriasis and connective tissue diseases.
3) Hypersensitivity reaction to endogenous tubercular or streptococcal toxins
4) Infectious episcleritis: herpes zoster virus, syphilis, Lyme disease and tuberculosis
• Pathology: localised lymphocytic infiltration of episcleral tissue associated with edema and congestion
of overlying Tenon’s capsule and conjunctiva
• Types:
1) Simple
2) Nodular
• Symptoms:
➢ redness
➢ mild ocular discomfort
• Signs:
1) Simple
➢ sectorial inflammation of episclera
➢ engorged episcleral vessels run in radial direction beneath the conjunctiva
2) Nodular
➢ pink or purple flat nodule surrounded by injection
➢ situated 2–3 mm away from the limbus
➢ firm, tender and can be moved separately from the sclera
• Clinical course: limited course → 10 days to 3 weeks, resolves spontaneously, recurrences common
• Differential diagnosis
1) Simple → conjunctivitis
2) Nodular
➢ pinguecula
➢ foreign body in bulbar conjunctiva
➢ scleritis
• Treatment
1) Topical NSAIDs: ketorolac
2) Topical mild corticosteroid eyedrops: fluorometholone or loteprednol
3) Topical artificial tears: carboxy methyl cellulose
4) Cold compresses
5) NSAIDs: flurbiprofen, indomethacin
 DISEASES OF UVEAL TRACT

ANTERIOR UVEITIS
• Definition: inflammation of the uveal tissue from iris up to pars plicata of ciliary body
• Etiology: Duke Elder’s classification
1) Infective
➢ Modes-
a) Exogenous
b) Secondary
c) Endogenous
➢ Types-
a) Bacterial
b) Viral
c) Fungal
d) Parasitic
e) Rickettsial
2) Immune-related
a) Microbial allergy
b) Anaphylactic
c) Atopic
d) Autoimmune
e) HLA-associated
3) Toxic
a) Endotoxins
b) Endocular toxins
c) Exogenous toxins
4) Traumatic
a) Direct mechanical effects
b) Irritative effects of blood products
c) Microbial invasion,
d) Chemical effects of retained intraocular FBs
e) Sympathetic ophthalmia in the other eye
5) a/w noninfective systemic diseases
a) Sarcoidosis
b) Collagen related diseases
c) Metabolic diseases
d) Disease of the CNS
e) Diseases of skin
6) Idiopathic
a) Specific
b) Non-specific
• Pathology
1) Suppurative
➢ exogenous infection by pyogenic organisms
➢ outpouring of purulent exudate and infiltration by PMNL
➢ whole uveal tissue thickened and necrotic
➢ cavities of eye filled with pus
2) Non-suppurative
a) Non-granulomatous
➢ either due to physical and toxic insult to tissue or as a result of hypersensitivity reactions
 ➢ marked dilatation and ↑permeability of vessels, breakdown of blood aqueous barrier with an
outpouring of fibrinous exudate and infiltration by lymphocytes, plasma cells and macrophages
➢ inflammation: diffuse
➢ iris waterlogged, oedematous, muddy with blurring of crypts and furrows → mobility reduced
➢ pupil small in size
➢ aqueous flare and deposition of fine KPs at the back of cornea
➢ posterior synechiae formation
➢ cyclitic membrane formation
b) Granulomatous
➢ chronic inflammation of proliferative nature in response to an irritant FB
➢ infiltration with lymphocytes, plasma cells and mononuclear cells → epithelioid and giant cells →
aggregate into nodules
➢ mutton fat KPs
➢ necrosis in the adjacent structures → reparative process → fibrosis and gliosis of the involved area
• Symptoms
1) Pain
➢ dominant symptom
➢ dull aching throbbing sensation
➢ worse at night
➢ referred along the distribution of branches of 5th nerve
2) Redness
➢ active hyperaemia of anterior ciliary vessels → circumcorneal congestion
3) Photophobia and blepharospasm
➢ due to a reflex b/w sensory fibres of 5th nerve and motor fibres of 7th nerve
4) Lacrimation
➢ result of lacrimatory reflex mediated by 5th nerve and secretomotor fibres of the 7th nerve
5) Defective vision
➢ Factors responsible-
▪ induced myopia
▪ corneal haze
▪ aqueous turbidity
▪ pupillary block
▪ complicated cataract
▪ vitreous haze
▪ cyclitic membrane
▪ macular edema
▪ papillitis
▪ secondary glaucoma
• Signs-
A. Lid edema: mild
B. Circumcorneal congestion: marked
C. Corneal signs
1) Corneal edema
➢ due to toxic endothelitis
2) Keratic precipitates
➢ proteinaceous cellular deposits occurring at the back of cornea
➢ arranged in a triangular fashion occupying the centre and inferior part of cornea
➢ Types-
a) Mutton fat KPs
▪ occur in granulomatous iridocyclitis
▪ composed of epithelioid cells and macrophages
b) Small and medium (granular) KPs
▪ pathognomic of non-granulomatous uveitis
 ▪ composed of lymphocytes
c) Fine/stellate KPs
▪ cover entire corneal endothelium → endothelial dusting
▪ seen in Fuch’s heterochromic iridocyclitis, herpetic iritis and CMV retinitis
d) Old KPs
▪ sign of healed uveitis
3) Posterior corneal opacity
D. Anterior chamber signs
1) Aqueous cells
➢ early feature
➢ counted in an oblique slit-lamp beam
➢ Grading-
– = < 1 cells
± = 1–5 cells
+1 = 6–15 cells
+2 = l 6–25 cells
+3 = 26–50 cells
+4 = >50 cells
2) Aqueous flare
➢ due to leakage of protein particles into the aqueous humour from damaged blood vessels
➢ demonstrated on the slit-lamp examination
➢ marked in non-granulomatous uveitis
➢ Grading-
0 = no aqueous flare.
+1 = faint
+2 = moderate flare
+3 = marked flare
+4 = intense flare
3) Hypopyon: sterile pus in the anterior chamber
➢ Dense immobile hypopyon – slow to absorb, seen in HLA-B27 acute anterior uveitis
➢ Hypopyon in Behcet’s syndrome – quick to absorb
➢ Haemorrhagic hypopyon – a/w herpetic infection, trauma and rubeosis iridis
4) Changes in depth and shape
5) Changes in the angle
➢ observed with gonioscopic examination
E. Iris signs
1) Loss of normal pattern: due to edema and waterlogging of iris
2) Changes in iris colour: muddy in colour
3) Iris nodules
➢ occur in granulomatous uveitis
➢ Types-
a) Koeppe’s nodules: situated at the pupillary border
b) Busacca’s nodules: situated near the collarette
4) Posterior synechiae
➢ adhesions b/w posterior surface of iris & anterior capsule of crystalline lens or anterior hyaloid face
➢ formed d/t organisation of fibrin-rich exudates
➢ Types-
a) Segmental
▪ adhesion of iris to the lens at some points
b) Annular/ring
▪ 360° adhesions of pupillary margin to anterior capsule of lens
▪ prevent the circulation of aqueous humour from posterior chamber to anterior chamber
(seclusio pupillae) → aqueous collects behind the iris and pushes it anteriorly → iris-bombe
 c) Total
▪ due to plastering of total posterior surface of iris with the anterior capsule of lens
▪ formed in acute plastic type of uveitis
▪ results in deepening of anterior chamber
5) Rubeosis iridis
➢ neovascularisation of iris
➢ seen in Fuch’s heterochromic iridocyclitis
F. Pupillary signs
1) Narrow pupil: due to irritation of sphincter pupillae by toxins
2) Irregular pupil shape
➢ results from segmental posterior synechiae formation
➢ dilatation of pupil with mydriatics at this stage → festooned pupil
3) Ectropion pupillae
➢ eversion of pupillary margin
➢ due to contraction of fibrinous exudate on the anterior surface of the iris
4) Pupillary reaction: sluggish
5) Occlusio pupillae: due to organisation of the exudates across the entire pupillary area
G. Changes in the lens
1) Pigment dispersal
2) Exudates
3) Complicated cataract
H. Changes in the vitreous and retina
1) Exudates and inflammatory cells
2) CME

• Complications
1) Complicated cataract
2) Secondary glaucoma
a) Early: exudates and inflammatory cells in the anterior chamber → clogging of trabecular meshwork
b) Late/post-inflammatory: result of pupil block
3) Cyclitic membrane: due to organisation of exudates present behind the lens
4) Choroiditis
5) Retinal complications: CME, macular scar, macular hole, ERM, exudative RD, retinal scars
6) Papillitis
7) Band-shaped keratopathy
8) Phthisis bulbi
a) Stage of atrophic bulbi without shrinkage: d/t continued inflammation and loss of nutritional support
➢ shape of globe maintained
➢ vision completely lost
➢ lens cataractous
➢ IOP raised
b) Stage of atrophic bulbi with shrinkage: d/t continued ciliary body dysfunction
➢ IOP lowered
➢ cornea edematous and vascularised
➢ anterior chamber collapsed
➢ eyeball smaller and square shaped
c) Atrophic bulbi with disorganization: d/t continued disorganization of ciliary body
➢ IOP markedly lowered
➢ size of eyeball markedly decreased

• Differential diagnosis:
 1) Acute red eye → acute congestive glaucoma and acute conjunctivitis
Feature Acute conjunctivitis Acute iridocyclitis Acute congestive glaucoma
1. Onset gradual gradual sudden
2. Pain mild moderate severe
3. Discharge mucopurulent watery watery
4. Coloured halos +/- - +
5. Vision good slightly impaired markedly impaired
6. Congestion superficial conjunctival deep ciliary deep ciliary
7. Tenderness - marked marked
8. Pupil normal small and irregular large and vertically oval
9. Media clear hazy hazy
10. Anterior chamber normal deep very shallow
11. Iris normal muddy edematous
12. IOP normal normal raised
13. Constitutional symptoms - little prostration, vomiting

2) Granulomatous versus non-granulomatous uveitis

Feature Granulomatous Non-granulomatous
1. Onset insidious acute
2. Pain minimal marked
3. Photophobia slight marked
4. Ciliary congestion minimal marked
5. KPs mutton fat small
6. Aqueous flare mild marked
7. Iris nodules + -
8. Posterior synechiae thick and broad based thin and tenuous
9. Fundus nodular lesions diffuse involvement

• Treatment:
A. Nonspecific treatment
1) Local therapy
a) Cycloplegic drugs:
➢ 1% atropine sulfate eye ointment or drops, mydricain subconjunctival inj.
➢ MOA-
▪ gives comfort and rest to the eye by relieving spasm of iris sphincter and ciliary muscle
▪ prevents the formation of synechiae
▪ reduces exudation by decreasing hyperaemia and vascular permeability
▪ increases blood supply to anterior uvea
b) Corticosteroids
➢ Preparations: dexamethasone, betamethasone, hydrocortisone, prednisolone
➢ MOA: anti-inflammatory, anti-allergic, anti-fibrotic
c) Broad spectrum antibiotic drops
2) Systemic therapy
a) Corticosteroids: prednisolone
➢ acute disease – daily therapy regime
➢ absence of acute disease – alternate day therapy regime
b) NSAIDs
c) Immunosuppressive drugs – in cases of failure of NSAIDs
3) Physical measures
a) Hot fomentation
b) Dark goggles
B. Specific treatment of the cause
C. Treatment of complications
ENDOPHTHALMITIS
• Definition: an inflammation of the inner structures of the eyeball (uveal tissue and retina) a/w pouring of
exudates in vitreous cavity, anterior chamber and posterior chamber
• Etiology:
A. Infective
➢ Modes of infection-
1) Exogenous infections
2) Endogenous/metastatic
3) Secondary infections from surrounding structures
➢ Causative organisms-
1) Bacterial: S. aureus, S. epidermidis
2) Fungal: Aspergillus, Fusarium, Candida
B. Non-infective
➢ inflammation of inner structures of eyeball caused by certain toxins/toxic substances
➢ Situations-
1) Post-operative sterile endophthalmitis
2) Post-traumatic sterile endophthalmitis
3) Phacoanaphylactic endophthalmitis
4) Intraocular tumour necrosis
• Source of infection
1) patient’s own periocular bacterial flora
2) contaminated solutions and instruments
3) environmental flora
• Onset
1) Acute – bacterial
2) Delayed – fungi, Propionibacterium acne
• Symptoms
➢ severe ocular pain
➢ redness
➢ lacrimation
➢ photophobia
➢ loss of vision
• Signs
1) Lids: red and swollen.
2) Conjunctiva: chemosis and marked circumcorneal congestion.
3) Cornea: edematous, cloudy and ring infiltration
4) Edges of wound: yellow and necrotic
5) Anterior chamber: hypopyon
6) Iris: oedematous and muddy.
7) Pupil: yellow reflex
8) Vitreous exudation → amaurotic cat’s-eye reflex
9) IOP: early stage – raised, severe cases – lowered
• Treatment
A. Antibiotic therapy
1) Intravitreal antibiotics and diagnostic tap
➢ transconjunctivally under topical anaesthesia from the area of pars plana
➢ vitreous tap is made using 23-gauge needle followed by the intravitreal injection
➢ 1st choice: vancomycin + ceftazidime
2) Topical concentrated antibiotics
➢ vancomycin/cefazoline + amikacin/tobramycin
3) Systemic antibiotics
 ➢ iv ciprofloxacin
➢ vancomycin + ceftazidime
➢ cefazoline + amikacin
B. Steroid therapy
➢ after 24 to 48 hours of control of infection by intensive antibiotic therapy
➢ intravitreal injection of dexamethasone or topical dexamethasone or systemic prednisolone
C. Supportive therapy
1) Cycloplegics: 1% atropine or 2% homatropine eyedrops
2) Antiglaucoma drugs: acetazolamide, timolol
D. Vitrectomy
➢ performed if patient does not improve with the above intensive therapy for 48-72 hours or when the
patient presents with severe infection with visual acuity reduced to hand movement close to face
 DISEASES OF LENS

AGE-RELATED/SENILE CATARACT
• mc type of acquired cataract
• bilateral
• Forms-
1) Cortical/soft cataract
a) Cuneiform (70%)
b) Cupuliform / posterior subcapsular (5%)
2) Nuclear/hard cataract (25%)
• Risk factors
1) Age: >50 years
2) Sex: females > males
3) Heredity
4) UV radiations
5) Dietary factors: Diet deficient in certain proteins, amino acids, vitamins and essential elements
6) Dehydrational crisis
7) Smoking
➢ causes accumulation of pigmented molecules: 3-hydroxykynurenine & chromophores → yellowing
➢ Cyanates in smoke causes carbamylation and protein denaturation.
• Mechanism of loss of transparency
➢ Cortical-
▪ ↓levels in the crystalline lens of total proteins, amino acids and potassium
▪ ↑conc. of sodium and marked hydration of the lens
▪ coagulation of lens proteins
➢ Nuclear-
▪ intensification of the age-related nuclear sclerosis
▪ dehydration and compaction of the nucleus
▪ ↑conc. of water insoluble proteins
• Stages of maturation:
A. Cortical type-
1) Stage of lamellar separation
➢ earliest change
➢ demarcation of cortical fibres due to their separation by fluid
➢ demonstrated by slit-lamp examination only
➢ reversible
2) Stage of incipient cataract
a) Cuneiform-
➢ wedge-shaped opacities with clear areas in between
➢ extend from equator towards centre
➢ can only be demonstrated after dilatation of the pupil
➢ first seen in the lower nasal quadrant
➢ present both in anterior and posterior cortex, slowly progress towards the pupil
➢ oblique illumination: radial spoke-like pattern of greyish white opacities
➢ DDO: opacities appear as dark lines against the red fundal glow
➢ visual disturbances noted at a comparatively late stage
b) Cupuliform-
➢ saucer-shaped opacity
➢ develops just below the capsule - in the central part of posterior cortex, extends outwards
➢ early loss of visual acuity
 3) Immature senile cataract (ISC)
➢ opacification progresses further
➢ cuneiform or cupuliform patterns can be recognised till the advanced stage of ISC
➢ lens appears greyish white
➢ iris shadow visible
➢ lens swollen due to continued hydration: intumescent cataract
➢ anterior chamber shallow
4) Mature senile cataract (MSC)
➢ opacification complete
➢ lens pearly white: ripe cataract
5) Hypermature senile cataract (HMSC)
a) Morgagnian type
➢ whole cortex liquefies
➢ lens converted into a bag of milky fluid
➢ small brownish nucleus settles at the bottom
b) Sclerotic type
➢ cortex disintegrated
➢ lens shrunken due to leakage of water
➢ anterior capsule wrinkled and thickened due to proliferation of anterior cells
➢ anterior chamber deep; iridodonesis
B. Nuclear type-
➢ progressive nuclear sclerotic process → lens inelastic and hard, ↓accommodation
➢ begin centrally and spread slowly peripherally
➢ nucleus pigmented: amber, brown (cataracta brunescens), black (cataracta nigra), reddish (cataracta
rubra)
• Symptoms
1) Glare: earliest visual disturbance
2) Uniocular polyopia
3) Coloured halos
4) Stationary black spots in front of eyes
5) Image blur, distortion of images and misty vision
6) Deterioration of vision:
➢ Cuneiform – delayed visual loss, patients see better when pupil is contracted
➢ Cupuliform – early visual loss, patients see better when pupil is dilated
➢ Nuclear - distant vision deteriorates due to progressive index myopia
• Signs:

Examination Nuclear cataract ISC MSC HMSC (M) HMSC (S)

1. Visual acuity 6/9 to PL+ 6/9 to CF+ HM+ to PL+ PL+ PL+
2. Colour of lens Amber, brown, Greyish white Pearly Milky white Dirty white
black or red white
3. Iris shadow Not seen Seen Not seen Not seen Not seen
4. DDO with Central dark area Multiple dark No red No red glow No red glow
dilated pupil against red fundal areas against glow milky white pupil dirty white pupil
glow red fundal glow white pupil
Areas of Complete Milky white Shrunken
5. Slit-lamp Nuclear opacity normal with cataractous cortex with cataractous lens
examination clear cortex cataractous cortex sunken brownish with thickened
cortex nucleus anterior capsule

• Differential diagnosis:
➢ ISC → nuclear sclerosis
➢ MSC → leukocoria
• Complications:
1) Phacoanaphylactic uveitis
2) Lens-induced glaucoma
a) Phacomorphic glaucoma
b) Phacolytic glaucoma
c) Phacotopic glaucoma
3) Subluxation/dislocation of lens
• Management
A. Non-surgical measures
1) Treatment of cause of cataract
➢ Adequate control of DM
➢ Removal of cataractogenic drugs
➢ Removal of irradiation
➢ Early and adequate treatment of ocular diseases
2) Measures to delay progression
➢ Topical preparations containing iodide salts of calcium and potassium
➢ Vitamin E and aspirin
3) Measures to improve vision in the presence of incipient and immature cataract
➢ Prescription of glasses
➢ Adjustment of illumination
➢ Use of dark goggles
➢ Mydriatics
B. Surgical management
➢ Indications
1) Visual improvement
2) Medical indications
a) Lens-induced glaucoma,
b) Phacoanaphylactic endophthalmitis
c) Retinal diseases like diabetic retinopathy or retinal detachment
3) Cosmetic indication
➢ Preoperative medications and preparations
1) Consent
2) Scrub bath, care of hair and marking of the eye
3) Preoperative antibiotics and disinfectants
a) Topical antibiotics: 4th generation FQ
b) Povidone-iodine (10%) solution
4) IOP lowering: must for conventional ECCE
5) Mydriasis
a) Topical tropicamide/cyclopentolate + phenylephrine
b) Topical NSAIDs
➢ Types and choice of surgical techniques
1) Intracapsular cataract extraction (ICCE)
2) Extracapsular cataract extraction (ECCE)
▪ major portion of anterior capsule with epithelium, nucleus and cortex removed leaving behind
intact posterior capsule
▪ surgery of choice
▪ Contraindications: markedly subluxated or dislocated lens
▪ Different techniques
a) Conventional ECCE
b) Manual small incision cataract surgery (SICS)
c) Phacoemulsification
LAMELLAR/ZONULAR CATARACT
• Definition: developmental cataract in which the opacity occupies a discrete zone in the lens
• mc type of congenital cataract presenting with visual impairment
• Etiology:
1) Genetic pattern – familial AD variety
2) Environmental form – a/w:
➢ vitamin D deficiency
➢ hypocalcemia
➢ maternal rubella infection b/w 7th and 8th week of gestation
• Characteristic features:
➢ occurs in a zone of foetal nucleus
➢ small linear opacities like spokes of a wheel (riders): seen towards the equator
➢ usually b/l
➢ causes severe visual defects

CORONARY CATARACT
• occurs about puberty
• involves either the adolescent nucleus or deeper layer of the cortex
• opacities hundreds in no. and have a regular radial distribution in the periphery of lens encircling the central axis
(corona of club-shaped opacities)
• vision usually unaffected

DIABETIC/SNOWFLAKE/SNOWSTORM CATARACT
• occurs in young adults
• cause: osmotic over hydration of the lens d/t accumulation of sorbitol
• large no. of fluid vacuoles underneath anterior and posterior capsules → bilateral snowflake-like white opacities
in the cortex
• resolve spontaneously or mature within a few days

COMPLICATED CATARACT
• opacification of the lens secondary to some other intraocular disease
• Etiology: any condition in which ocular circulation is disturbed or in which inflammatory toxins are formed
1) Inflammatory conditions: uveal inflammations, hypopyon corneal ulcer and endophthalmitis
mcc = anterior uveitis
2) Degenerative conditions: retinitis pigmentosa and myopic chorioretinal degeneration.
3) Retinal detachment
4) Glaucoma (primary or secondary)
5) Intraocular tumours: retinoblastoma, melanoma
• Clinical features-
➢ breadcrumb appearance
➢ polychromatic luster: appearance of iridescent coloured particles of reds, greens and blue (rainbow
cataract)
➢ diffuse yellow-haze: in the cortex
➢ deposition of calcium
AFTER/SECONDARY CATARACT
• Definition: opacity which persists or develops after extracapsular lens extraction
• Causes:
1) Residual opaque lens matter - imprisoned between the remains of the anterior and posterior capsule
surrounded by fibrin or blood
2) Proliferative type - develop from the left out anterior epithelial cells in the capsular bag
• Clinical types:
1) Posterior capsule opacification (PCO)
2) Dense membranous after cataract
3) Soemmering’s ring
4) Elschnig’s pearls
• Treatment:
1) PCO & Elschnig’s pearls – YAG-laser capsulotomy or discission with cystitome or Zeigler’s knife
2) Dense membranous after cataract – surgical membranectomy
3) Soemmering’s ring – no treatment
 GLAUCOMA

AQUEOUS HUMOUR
• Functions
➢ maintenance of a proper IOP
➢ metabolic and nutritional role – provides substrates and removes metabolites from avascular cornea & lens
➢ maintains optical transparency
➢ clears blood, macrophages, remnants of lens matter and products of inflammation from anterior chamber
• Formation: derived from plasma within the capillary network of ciliary processes
1) Ultrafiltration: most of the plasma substances pass out from the capillary wall and loose connective tissue →
dialysate accumulates behind the pigmented and nonpigmented epithelium of ciliary processes
2) Secretion: dialysate from plasma transported into pigment epithelium → paired Na+/ H+ and Cl-/HCO3-
antiports actively transport Na+ and Cl- from the stroma into the cells
3) Diffusion: Active transport of substances across non-pigmented ciliary epithelium → osmotic gradient →
movement of other plasma constituents into the posterior chamber → Schlemm’s canal
• Drainage:

CONGENITAL/DEVELOPMENTAL GLAUCOMA
• Definition: a group of diverse disorders in which abnormal high IOP results due to developmental abnormalities
of the angle of anterior chamber obstructing the drainage of aqueous humour
• Pathogenesis: death of retinal ganglion cells → progressive optic neuropathy → characteristic optic disc
appearance and specific visual field defects
• Etiological factors of RGC death-
A. Primary insults
1) Raised IOP (Mechanical theory)
2) Pressure independent factors (Vascular insufficiency theory)
a) Failure of autoregulatory mechanism of blood flow
b) Vasospasm – migranous headache and Raynaud’s phenomenon
c) Systemic hypotension
 d) acute blood loss and abnormal coagulability profile
B. Secondary insults (Excitotoxicity theory):
RGCs death due to primary insults
↓
release of toxic factors – glutamate, oxygen-free radicals, NO
↓
neuronal degeneration
• Types-
A. Primary developmental/congenital glaucoma
➢ Definition: abnormally high IOP which results due to developmental anomaly of the angle of the anterior
chamber, not a/w any other ocular or systemic anomaly
➢ Types-
1) Newborn or true congenital
▪ 55% cases
▪ IOP raised during IUL and child is born with ocular enlargement
2) Infantile
▪ 40% cases
▪ IOP raised before 3 years
3) Juvenile
▪ 5% cases
▪ IOP raised after 3 years but before adulthood
➢ Pathogenesis:
▪ maldevelopment of trabeculum from neural crest derived cells (trabeculodysgenesis)
▪ characterized by absence of the angle recess with iris having a flat or concave direct insertion into
the surface of trabeculum
➢ Clinical features
1) Lacrimation, photophobia and blepharospasm
2) Corneal signs
a) Corneal edema
b) Corneal enlargement
c) Tears and breaks in Descemet’s membrane (Haab’s striae)
3) Sclera: thin, blue
4) Anterior chamber: deep
5) Iris: iridodonesis and atrophic patches
6) Lens: flat
7) Optic disc: cupping and atrophy
8) IOP: raised
9) Axial myopia
➢ Differential diagnosis
1) Cloudy cornea – trauma
2) Large cornea - megalocornea, sclerocornea and high myopia
3) Lacrimation – corneal abrasion, corneal dystrophy
4) Photophobia – keratitis, uveitis
5) Raised IOP - retinoblastoma, ROP, PHPV, traumatic glaucoma and secondary congenital glaucoma
➢ Treatment
1) Medical treatment: hyperosmotic agents, acetazolamide and beta-blockers to lower IOP
2) Surgical treatment
a) Incisional angle surgery
▪ Goniotomy
▪ Trabeculotomy
b) Filtration surgery
▪ Trabeculectomy with antimetabolites
▪ Combined trabeculotomy and trabeculectomy with antimetabolites
 c) Glaucoma drainage devices (GDD)

B. Developmental glaucoma with associated congenital ocular anomalies

1) Glaucoma a/w iridodysgenesis
a) a/w aniridia
b) a/w familial iris hypoplasia
c) a/w congenital ectropion uvea
d) a/w congenital microcornea
e) a/w congenital nanophthalmos
2) Glaucoma a/w iridocorneal dysgenesis
a) Posterior embryotoxon
b) Axenfeld-Rieger syndrome
c) Peter’s anomaly
d) Combined Reiger’s syndrome and Peters anomaly

C. Developmental glaucoma with associated systemic anomalies

1) a/w chromosomal disorders
2) a/w ectopia lentis syndromes
3) a/w phakomatosis
4) a/w metabolic syndromes

PRIMARY OPEN-ANGLE OR CHRONIC SIMPLE GLAUCOMA

• Characteristics
1) Slowly progressive raised intraocular pressure (>21 mm Hg)
2) Open normal appearing anterior chamber angle
3) Characteristic optic disc cupping
4) Specific visual field defects
• Predisposing and risk factors
1) IOP
2) Family history (Heredity)
➢ Myocilin C (MYOC)
➢ Optineurin (OPTN)
➢ WD repeat domain 36 (WDR 36)
3) Age: increasing
4) Race: black>white
5) Myopes
6) Central corneal thickness (CCT): thinner
7) Diabetics
8) Cigarette smoking
9) High BP: diastolic perfusion pressure of <55 mm Hg
10) Thyrotoxicosis
• Pathogenesis of rise in IOP:
Thickening and sclerosis of trabecular meshwork with faulty collagen tissue
Narrowing of intertrabecular spaces
Deposition of amorphous material in the juxtacanalicular space
Collapse of Schlemm’s canal and absence of giant vacuoles in the cells lining it
↓↓↓↓
trabecular meshwork stiffening and apposition of Schlemm’s canal wall
↓↓
failure of aqueous outflow pump mechanism
 ↓
reduced aqueous outflow facility
↓
rise in IOP
• Pathogenesis of optic neuropathy: described above
• Epidemiology:
Ethnic group POAG PACG
Europeans, Africans and Hispanics 5 1
Mongolian 1 3
Urban Chinese 1 2
Indian 1 1

• Symptoms
1) Asymptomatic
2) Headache and eye ache
3) Scotoma
4) Difficulty in reading and close work – frequent changes in presbyopic glasses
5) Delayed dark adaptation
6) Significant loss of vision and blindness – end result
• Signs-
A. Anterior segment signs
1) pupil reflex: sluggish
2) CCT: low (<555 μm)
B. IOP changes
➢ initial stages: exaggeration of the normal diurnal variation → Diurnal variation test
➢ Patterns-
▪ Morning rise in IOP – 20% of cases
▪ Afternoon rise in IOP – 25% of cases
▪ Biphasic rise in IOP – 55% of cases
➢ A variation in IOP of over 5 mm Hg (Schiotz) is suspicious and over 8 mm of Hg is diagnostic
➢ later stages: IOP permanently raised above 21 mm of Hg
C. Optic disc changes
a) Early glaucomatous changes
1) Vertically oval cup
2) Asymmetry of the cups
3) Large cup
4) Splinter haemorrhages
5) Pallor areas
6) Atrophy of RNFL
b) Advanced glaucomatous changes
1) Marked cupping
2) Thinning of neuroretinal rim
➢ crescentic shadow adjacent to the disc margin
➢ notching of the rim specially up to disc margin is pathognomic
3) Nasal shifting of retinal vessels – Bayonetting sign
4) Pulsations of the retinal arterioles – pathognomic sign
5) Lamellar dot sign
c) Glaucomatous optic atrophy
1) all the neural tissue of the disc destroyed
2) optic nerve head: white and deeply excavated
D. Visual field defects – appear only after about 40% of axons have been damaged
1) Isopter contraction
 2) Baring of blind spot
3) Paracentral scotoma
4) Seidel’s scotoma
5) Arcuate or Bjerrum’s scotoma
6) Ring or double arcuate scotoma
7) Roenne’s central nasal step
8) Roenne’s peripheral nasal step
9) Advanced glaucomatous field defects
➢ tubular vision and a temporal island of vision left
➢ temporal island of vision is more resistant and is lost in the end → no light perception
• Investigations-
1) Applanation tonometry
2) CCT measurement
3) Diurnal variation test
4) Gonioscopy
5) Documentation of optic disc changes
6) Slit-lamp examination of anterior segment
7) Perimetry
8) Nerve fibre layer analyzer (NFLA)
9) Provocative tests: in border-line cases → Water drinking test
• Management-
A. Medical therapy
1) Single drug therapy
a) PG analogues
➢ increases the uveo-scleral outflow of aqueous
➢ drug of first choice
➢ preparations: Latanoprost, Travoprost, Bimatoprost, Unoprostone
b) Topical beta-blockers
➢ drug of choice in poor and average income patients
➢ reduces the aqueous secretion
➢ Preparations:
▪ Timolol maleate – non-selective beta-blocker; not used in patients having associated
bronchial asthma and heart blocks
▪ Betaxolol – selective beta-1 blocker; preferred as initial therapy in patients with asthma and
other pulmonary problems
▪ Levobunolol – longest acting
▪ Carteolol – best choice in patients with having associated hyperlipidemias or atherosclerotic
cardiovascular disease
c) Adrenergic drugs
➢ Epinephrine hydrochloride and dipivefrin hydrochloride – increases aqueous outflow
➢ Brimonidine – decreases aqueous production and increases uveo-scleral outflow
d) Topical carbonic anhydrase inhibitors
➢ Dorzolamide or Brinzolamide – decreases aqueous production
e) Pilocarpine: contracts longitudinal muscle of ciliary body → opens spaces in trabecular meshwork →
increases aqueous outflow
2) Combination topical therapy: one drug which decreases aqueous production + one drug which increases
aqueous outflow
3) Oral carbonic anhydrase inhibitors – Acetazolamide and methazolamide
4) Hyperosmotic agents – mannitol
➢ for patients with very high IOP (>30 mm Hg)
5) Neuroprotective agents
 B. Laser trabeculoplasty
1) Argon (ALT) or Diode laser trabeculoplasty (DLT)
➢ increases outflow facility
➢ Treatment regime – 50 spots on the anterior half of the trabecular meshwork over 180°
➢ Complications-
▪ Transient acute rise of IOP
▪ Transient inflammation
2) Selective laser trabeculoplasty (SLT)
➢ based on the principle of selective photothermolysis
➢ targets selectively pigmented trabecular meshwork (TM)
C. Surgical therapy: Filtration operations-
1) External filtration surgery
a) Free-filtering operations
b) Guarded filtering surgery – trabeculectomy
c) Non-penetrating filtration surgery
➢ Deep sclerectomy
➢ Viscocanalostomy
2) Internal filtration surgery
a) Canaloplasty
b) Trabectome
c) iStent

PRIMARY ANGLE-CLOSURE GLAUCOMA

• Epidemiology: described above
• Predisposing risk factors
A. Demographic risk factors
1) Age – mc in 6th and 7th decades of life
2) Gender – M:F = 1:3
3) Race – mc in South-East Asians, Chinese and Eskimos
B. Anatomical and ocular risk factors
1) Hypermetropic eyes
2) Eyes in which iris-lens diaphragm is placed anteriorly
3) Eyes with narrow angle of anterior chamber
4) Plateau iris configuration
5) Heredity
• Pathomechanisms of rise in IOP
1) Pupillary block mechanism: precipitating factors-
a) Physiological mydriasis
b) Pharmacological mydriasis
c) Pharmacological miosis
d) Valsalva maneuver
2) Plateau iris configuration and syndrome: anterior chamber angle is closed by a pushing mechanism because
of the anterior positioned ciliary processes displacing the peripheral iris anteriorly
3) Phacomorphic mechanism: abnormal lens contributes by either causing pupillary block or by pushing the
peripheral iris forward into the angle structures
• Pathogenesis: gradual synechial closure of the angle of anterior chamber
• Clinical features-
A. Subacute PACG
➢ unilateral transient blurring of vision
➢ coloured halos around light, headache, browache and eyeache on the affected side
 ➢ self-termination of the attack
➢ irido-trabecular contact noted on gonioscopy in >270° angle
➢ IOP elevated and/or PAS
➢ Optic disc: glaucomatous cupping
➢ Visual field defects
B. Acute PACG
➢ Pain
➢ Nausea, vomiting and prostrations
➢ Rapidly progressive impairment of vision, redness, photophobia and lacrimation
➢ Conjunctiva: chemosed and congested
➢ Cornea: edematous and insensitive
➢ Anterior chamber: very shallow
➢ Angle of anterior chamber: completely closed
➢ Pupil: semi-dilated, vertically oval and fixed; non-reactive to both light and accommodation
➢ IOP: markedly elevated
➢ Optic disc: edematous and hyperemic; glaucomatous cupping
➢ Visual field defects
➢ Fellow eye: shallow anterior chamber and occludable angle
C. Chronic PACG
➢ IOP: constantly raised
➢ Eyeball: white and painless
➢ Optic disc: glaucomatous cupping
➢ Visual field defects
➢ Gonioscopy: >270° of angle closure + PAS
• Diagnosis
1) Irido-trabecular contact is noted on gonioscopy in greater than 270° of angle
2) PAS formed
3) IOP elevated
4) Optic disc: glaucomatous damage
5) Visual fields: typical glaucomatous defects
• Treatment
1) Laser iridotomy +/- medical therapy
2) Trabeculectomy (filtration surgery)
3) Prophylactic laser iridotomy in fellow eye

ABSOLUTE PRIMARY ANGLE-CLOSURE GLAUCOMA

• PACG, if untreated, gradually passes into the final phase of absolute glaucoma
• Clinical features-
➢ Painful blind eye
➢ Perilimbal reddish blue zone
➢ Caput medusae
➢ Cornea: insensitive → hazy
➢ Anterior chamber: very shallow
➢ Iris: atrophic
➢ Pupil: fixed and dilated; gives a greenish hue.
➢ Optic disc: glaucomatous optic atrophy
➢ IOP: high
➢ Eyeball: stony hard
• Management-
1) Retrobulbar alcohol injection: to relieve pain; destroys the ciliary ganglion
 2) Destruction of secretory ciliary epithelium: to lower the IOP by cyclocryotherapy or cyclodiathermy or
cyclophotocoagulation
3) Enucleation of eyeball
• Complications-
➢ Corneal ulceration
➢ Staphyloma formation – ciliary/equatorial
➢ Atrophic bulbi

LENS-INDUCED/PHACOGENIC GLAUCOMAS
Classification-

A. Lens-induced secondary angle closure glaucoma

1) Phacomorphic glaucoma
2) Phacotopic glaucoma
B. Lens-induced secondary open angle glaucoma
1) Phacolytic glaucoma
2) Lens particle glaucoma
3) Phacoanaphylactic glaucoma

1) Phacomorphic Glaucoma
• Causes-
➢ Intumescent lens
➢ Anterior subluxation or dislocation of the lens and spherophakia → Phacotopic glaucoma
• Pathogenesis: secondary acute angle closure glaucoma
• Clinical presentation-
➢ same as acute PACG
➢ lens: always cataractous and swollen
• Treatment-
➢ Medical treatment: iv mannitol, systemic acetazolamide and topical beta-blockers
➢ Laser iridotomy
➢ Cataract extraction with implantation of PCIOL
2) Phacolytic Glaucoma (Lens Protein Glaucoma)
• Pathogenesis
➢ secondary open angle glaucoma
➢ trabecular meshwork is clogged by the lens proteins, macrophages which have phagocytosed the lens
proteins, and inflammatory debris
➢ leakage of the lens proteins occurs through an intact capsule in the hypermature (Morgagnian)
cataractous lens
• Clinical features
➢ Features of acute congestive glaucoma
➢ Anterior chamber: deep
➢ Aqueous contains fine white protein particles → settle down as pseudohypopyon
➢ Anterior chamber angle: open on gonioscopy
• Management
➢ Medical therapy – to lower IOP
➢ Extraction of the hypermature cataractous lens with PCIOL implantation
3) Lens Particle Glaucoma
• Pathogenesis
➢ secondary open angle glaucoma
➢ trabecular meshwork blocked by the lens particles floating in the aqueous humour
 • Clinical features
➢ Features of acute congestive glaucoma
➢ Lens particles in anterior chamber
• Management
➢ Medical therapy – to lower IOP
➢ Irrigation-aspiration of the lens particles from the anterior chamber
4) Phacoantigenic Glaucoma
• Pathogenesis
➢ secondary open angle glaucoma → trabecular meshwork clogged by both inflammatory cells and the
lens particles
➢ fulminating acute inflammatory reaction due to antigen-antibody reaction
➢ preceding disruption of lens capsule by extracapsular cataract extraction, penetrating injury, or leak of
proteins from the capsule
➢ distinguishing feature - latent period
➢ IOP raised due to inflammatory reaction of the uveal tissue excited by the lens matter
➢ Typical finding - granulomatous inflammation in the involved eye after it undergoes surgical trauma
• Management
➢ Medical therapy – to lower IOP
➢ Irrigation-aspiration of the lens particles from the anterior chamber

NEOVASCULAR GLAUCOMA (NVG)

• Definition: an intractable glaucoma which results due to formation of neovascular membrane involving the angle
of anterior chamber
• Etiology-
➢ a/w rubeosis iridis
➢ develops following retinal ischemia in-
▪ PDR
▪ CRVO
▪ Sickle-cell retinopathy
▪ Eales’ disease
• Clinical profile: 3 stages-
1) Pre-glaucomatous stage (stage of rubeosis iridis)
2) Open-angle glaucoma stage – due to formation of a pretrabecular neovascular membrane; and
3) Secondary angle closure glaucoma – due to goniosynechiae resulting from contracture of the neovascular
membrane (zipper angle closure)
• Treatment
➢ Panretinal photocoagulation
➢ Glaucoma drainage device
 DISEASES OF VITREOUS

MUSCAE VOLITANTES
• physiological opacities
• residues of primitive hyaloid vasculature
• fine dots and filaments, which drift in and out of the visual field against a bright background

VITREOUS HEMORRHAGE
• occurs from the retinal vessels
• Causes
1) Retinal tear, PVD and RD
2) Trauma to eye: blunt, perforating
3) Inflammatory diseases: acute chorioretinitis, Eales’ disease, uveitis
4) Vascular disorders: hypertensive retinopathy, CRVO
5) Metabolic diseases: diabetic retinopathy
6) Exudative ARMD: high CNVM
7) Blood dyscrasias: retinopathy of anemia, leukemia, polycythemia and sickle-cell retinopathy
8) Bleeding disorders: purpura, hemophilia and scurvy
9) Neoplasms: retinoblastoma and malignant melanoma of choroid
10) Coat’s disease, radiation retinopathy, retinal capillary aneurysm
• Types
1) Anterior
2) Mid
3) Posterior
4) Total
• Symptoms
➢ Small: floaters of sudden onset
➢ Massive: sudden painless loss of vision
• Signs
➢ Distant direct ophthalmoscopy
▪ Small: black shadows against the red glow
▪ Large: no red glow
➢ Direct and indirect ophthalmoscopy
▪ Small: blood in the vitreous cavity
▪ Large: non-visualization of fundus
➢ Slit-lamp examination: reddish mass in the vitreous
• Fate
1) Complete absorption
2) Organization of haemorrhage with formation of a yellowish-white debris
3) Complications: vitreous liquefaction, degeneration and khaki cell glaucoma
4) Retinitis proliferans
• Treatment
1) Conservative treatment: bed rest and elevation of patient’s head
2) Treatment of the cause
3) Pars plana vitrectomy
 NEURO-OPHTHALMOLOGY

OPTIC NEURITIS
• inflammatory and demyelinating disorders of the optic nerve
• Etiology
1) Idiopathic
2) Hereditary optic neuritis = Leber’s disease
3) Demyelinating disorders (mc)
➢ multiple sclerosis
➢ neuromyelitis optica (Devic’s disease)
➢ diffuse periaxial encephalitis of Schilder
4) Parainfectious optic neuritis
➢ Measles
➢ mumps
➢ chickenpox
➢ whooping cough
➢ glandular fever
5) Infectious optic neuritis
➢ acute ethmoiditis
➢ cat scratch fever
➢ syphilis
➢ tuberculosis
➢ Lyme disease
➢ cryptococcal meningitis in patients with AIDS
6) Autoimmune disorders
➢ Sarcoidosis
➢ SLE
➢ polyarteritis nodosa
➢ GBS
➢ Wegener’s granulomatosis
7) Toxic optic neuritis
➢ Tobacco amblyopia
➢ Ethyl alcohol amblyopia
➢ Methyl alcohol amblyopia
➢ Quinine amblyopia
➢ Ethambutol amblyopia
• Types
A. Anatomical
1) Papillitis: involvement of the optic disc
2) Neuroretinitis: combined involvement of optic disc and surrounding retina in the macular area
3) Retrobulbar neuritis: involvement of optic nerve behind the eyeball
B. Etiological
1) Typical: associated with demyelination
2) Atypical: associated with causes other than demyelination disorders
• Symptoms
➢ Visual loss: monocular sudden, progressive and profound
➢ Dark adaptation: lowered
➢ Visual obscuration in bright light
➢ Impairment of colour vision
➢ Movement and sound-induced phosphenes
➢ Uhthoff’s symptom: Episodic transient obscuration of vision on exertion and on exposure to heat,
which recovers on resting or moving away from the heat
➢ Pulfrich’s phenomenon: Depth perception for moving object impaired
➢ mild dull eyeache
• Signs
➢ Visual acuity: reduced markedly
➢ Colour vision: severely impaired (red desaturation)
➢ Pupil: ill-sustained constriction to light
Diagnostic sign: Marcus Gunn pupil → relative afferent pupillary defect (RAPD)
detected by the swinging flash light test
➢ Ophthalmoscopic features
a) Papillitis
▪ hyperaemia of the disc and blurring of the margins
▪ Disc edematous and physiological cup obliterated
▪ Retinal veins congested and tortuous
▪ Splinter haemorrhages and fine exudates
b) Neuroretinitis
▪ Papillitis a/w macular star formation
c) Retrobulbar neuritis
▪ Fundus normal
▪ neither the ophthalmologist nor the patient sees anything
➢ Visual field changes: central or centrocaecal scotoma
➢ Contrast sensitivity: impaired
➢ Visually evoked response (VER): reduced amplitude and delay in the transmission time
➢ FFA: mild-moderate leak in early phase → increases with time
• Differential diagnosis
➢ Papillitis
▪ Papilloedema
▪ ischemic optic neuropathy
▪ anterior orbital compressive neuropathy
▪ pseudopapilloedema
➢ Acute retrobulbar neuritis
▪ Malingering
▪ hysterical blindness
▪ cortical blindness
▪ indirect optic neuropathy
• Evolution: 2-5 days
• Recovery: 4-6 weeks
• Complications
1) primary optic atrophy
2) postneuritic optic atrophy
• Treatment
 1) Treatment of the causes
2) Corticosteroid therapy: to shorten the period of visual loss
Brain MRI scan: lesions supportive of multiple sclerosis → iv methylprednisolone 1 gm daily for 3
days followed by oral prednisolone 1 mg/kg/day for 11 days
taper prednisolone over 4 days
3) Interferon therapy

PAPILLOEDEMA
• Bilateral non-inflammatory passive swelling of optic disc a/w increased intracranial pressure
• Causes
1) Congenital conditions
➢ aqueductal stenosis
➢ craniosynostosis
2) Intracranial space-occupying lesions (ICSOLs)
➢ brain tumours
➢ brain abscess
➢ tuberculoma
➢ gumma
➢ subdural haematoma
➢ aneurysms
3) Intracranial infections
➢ meningitis
➢ encephalitis
4) Intracranial haemorrhages
➢ Cerebral hemorrhage
➢ subarachnoid hemorrhage
5) Obstruction of CSF absorption via arachnoid villi
6) Tumours of spinal cord
7) Idiopathic intracranial hypertension (IIH) = pseudotumour cerebri
8) Systemic conditions
➢ malignant hypertension
➢ pregnancy induced hypertension (PIH)
➢ cardiopulmonary insufficiency
➢ blood dyscrasias
➢ nephritis
9) Diffuse cerebral edema from blunt head trauma
10) Cerebral venous sinus thrombosis
• Unilateral papilloedema
1) Foster-Kennedy syndrome
➢ a/w olfactory or sphenoidal meningiomata and frontal lobe tumours
➢ pressure optic atrophy on the side of lesion
papilloedema on the other side (due to raised intracranial pressure)
2) Pseudo-Foster-Kennedy syndrome
▪ raised intracranial pressure (due to any cause)
a pre-existing optic atrophy (due to any cause) on the other side
• Pathogenesis: Hayreh’s theory

↑ ICP, malignant htn & orbital lesions ocular hypotony

↓ ↓
↑ Tissue pressure within retrolaminar region ↓ Tissue pressure within the prelaminar area
↓
alteration in the pressure gradient across the lamina cribrosa
↓
stasis of axoplasm in the prelaminar region of optic disc
↓
axonal swelling
↓
venous congestion
↓
extracellular edema
• Clinical features
A. General features
▪ Headache
▪ Nausea
▪ projectile vomiting
▪ diplopia
B. Ocular features
1) Early (incipient) papilloedema
➢ Symptoms: absent
➢ Visual acuity: normal
➢ Pupillary reactions: normal
➢ Ophthalmoscopic features
▪ Obscuration of the disc margins: nasal → superior → inferior → temporal
▪ Blurring of peripapillary nerve fibre layer
▪ Absence of spontaneous venous pulsation at the disc
▪ Mild hyperaemia of the disc
▪ Splinter haemorrhages in the peripapillary region
➢ Visual fields: normal
2) Established (fully developed) papilloedema
➢ Symptoms: amaurosis fugax in one or both eyes after standing
➢ Visual acuity: normal
➢ Pupillary reactions: normal
➢ Ophthalmoscopic features
▪ Apparent optic disc edema
▪ Physiological cup of the optic disc obliterated
▪ Disc markedly hyperemic and blurring of the margin present all around
▪ Multiple cotton wool spots and superficial haemorrhages
▪ Veins become tortuous and engorged
advanced cases: disc enlarged and elevated → vessels bend sharply over its margins
indirect ophthalmoscopy: definitive parallax
▪ Paton’s lines: circumferential greyish white folds due to separation of nerve fibres by
the edema
➢ Visual fields: enlargement of blind spot
 3) Chronic or long-standing (vintage) papilloedema
➢ Visual acuity: variably reduced
➢ Pupillary reactions: normal
➢ Ophthalmoscopic features
▪ Acute haemorrhages and cotton wool spots resolve
▪ peripapillary edema resorbed
▪ optic disc → dome of a champagne cork appearance
▪ corpora amylacea on disc surface
➢ Visual fields
▪ enlarged blind spot
▪ beginning of constriction
4) Atrophic papilloedema
➢ Visual acuity: severely impaired
➢ Pupillary reactions: light reflex impaired
➢ Ophthalmoscopic features
▪ Atrophy of neurons and gliosis → greyish white discolouration and pallor of the disc
▪ Prominence of the disc ↓
▪ Retinal arterioles narrowed
veins less congested
whitish sheathing around the vessels
➢ Visual fields: Concentric contraction of peripheral fields
• Differential diagnosis: Pseudopapilloedema
➢ Optic disc drusen
➢ Hypermetropia
➢ Persistent hyaloid tissue
• Treatment
➢ immediate hospitalization
➢ urgent neuroimaging: CT scan or MRI with a gadolinium enhancement
➢ cerebral decompression
➢ treatment of causative disease
 DISORDERS OF EYELIDS

BACTERIAL BLEPHARITIS / CHRONIC ANTERIOR BLEPHARITIS / ULCERATIVE BLEPHARITIS

• chronic infection of the anterior part of the lid margin
• Causative organisms - coagulase positive Staphylococci
• Symptoms
➢ chronic irritation, itching, lacrimation, gluing of cilia, photophobia
➢ characteristically worse in the morning
➢ remissions and exacerbations common
• Signs
➢ Yellow crusts - at the root of cilia which glue them together
➢ Small ulcers - bleed easily, seen on removing the crusts.
➢ Red, thickened lid margins - seen with dilated blood vessels (rosettes).
➢ Mild papillary conjunctivitis
• Complications and sequelae
➢ Lash abnormalities
➢ Tylosis
➢ Eversion of punctum → epiphora
➢ Eczema of skin and ectropion
➢ Recurrent styes
➢ Marginal keratitis
➢ Tear film instability
➢ Secondary inflammatory and mechanical changes in the conjunctiva and cornea
• Treatment
1) Lid hygiene
➢ Warm compresses
➢ Crust removal and lid margin cleaning
2) Antibiotics
➢ Eye ointment - immediately after removal of the crusts
➢ Eye drops - daily
➢ Oral antibiotics – unresponsive cases
3) Topical steroids - fluorometholone
4) Ocular lubricants - artificial tear drops

EXTERNAL HORDEOLUM / STYE

• acute suppurative inflammation of lash follicle and its associated glands of Zeis or Moll
• Predisposing factors
➢ Age - more common in children and young adults, patients with eye strain
➢ habitual rubbing of the eyes or fingering of the lids and nose, chronic blepharitis and DM
➢ metabolic factors, chronic debility, excessive intake of carbohydrates and alcohol
• Causative organism - staphylococcus aureus
• Symptoms - acute pain, swelling of lid, watering and photophobia
• Signs
1) Stage of cellulitis - localised, firm, red, tender swelling at the lid margin a/w marked edema
2) Stage of abscess formation - a visible pus point on the lid margin in relation to the affected cilia
• Treatment
➢ Hot compresses
 ➢ Evacuation of the pus - by epilating the involved cilia
➢ Antibiotic eye drops and eye ointment
➢ Systemic NSAIDs
➢ Systemic antibiotics
➢ Surgical incision - for a large abscess

CHALAZION / TARSAL OR MEIBOMIAN CYST

• chronic non-infective lipogranulomatous inflammation of the meibomian gland
• commonest of all lid lumps
• Predisposing factors
➢ Age - more common in children and young adults, patients with eye strain
➢ habitual rubbing of the eyes or fingering of the lids and nose, chronic blepharitis and DM
➢ metabolic factors, chronic debility, excessive intake of carbohydrates and alcohol
• Pathogenesis:
mild grade infection of the meibomian gland by organisms of very low virulence
↓
proliferation of the epithelium and infiltration of the walls of the ducts → blocked
↓
retention of sebum in the gland → enlargement
↓
non-infective lipogranulomatous inflammation of the blocked meibomian glands
• Symptoms: painless swelling in the eyelid, heaviness, blurred vision, watering
• Signs
➢ Nodule - away from the lid margin; firm to hard and nontender on palpation
Upper lid involved more commonly than the lower lid
➢ Reddish purple area - on the palpebral conjunctiva
• Complications
➢ Slow increase in size
➢ Fungating mass of granulation tissue
➢ Secondary infection → hordeolum internum
➢ Calcification
➢ Malignant change → sebaceous cell carcinoma
• Treatment
1) Conservative treatment: hot fomentation, topical antibiotic eyedrops and oral NSAIDs
2) Intralesional injection of long-acting steroid – triamcinolone
3) Incision and curettage:
Surface anaesthesia by xylocaine drops
↓
Incision by sharp blade
↓
Contents curetted out with chalazion scoop
↓
Carbolic acid cautery → neutralization with methylated spirit
↓
Patching of eye
↓
Postoperative treatment
4) Diathermy – for marginal chalazion
5) Oral tetracycline – prophylaxis in recurrent chalazia
ENTROPION
• inward rolling and rotation of the lid margin toward globe
• Etiological types
1) Congenital entropion
a) Lower eyelid congenital entropion - improper development of the lower lid retractors
b) Upper eyelid congenital entropion - secondary to mechanical effects of microphthalmos
2) Cicatricial entropion - cicatricial contraction of the palpebral conjunctiva
Common causes are trachoma, membranous conjunctivitis, chemical burns, pemphigus and Stevens-Johnson
syndrome
3) Senile (involutional) entropion
➢ common occurrence
➢ affects only the lower lid in elder people
➢ Etiological factors
▪ Horizontal lid laxity
▪ Vertical lid instability
▪ Over-riding of pretarsal orbicularis
▪ Laxity of orbital septum a/w prolapse of orbital fat into the lower lid
4) Mechanical entropion - lack of support provided by the globe to the lids
• Symptoms - foreign body sensation, irritation, lacrimation and photophobia
• Signs
1) Inturning of lid margins
a) Grade I - only the posterior lid border inrolled
b) Grade II - inturning up to the inter-marginal strip
c) Grade III - whole lid margin inturned
2) scarring of palpebral conjunctiva in cicatricial entropion, horizontal lid laxity in involutional entropion
• Treatment
1) Congenital entropion - Hotz procedure
2) Cicatricial entropion
a) Anterior lamellar resection - to correct mild degree
b) Tarsal wedge resection - corrects moderate degree of entropion a/w atrophic tarsus
c) Modified Ketssey’s operation (Transposition of tarsoconjunctival wedge)
to treat mild to moderate amount
d) Posterior lamellar graft – for severe entropion with upper eyelid retraction
3) Senile entropion
a) Transverse everting suture - offer temporary cure (upto 18 months)
b) Wies operation (Transverse lid split and everting sutures)
for long term cure in patients with little horizontal laxity
c) Jones operation (Plication of lower lid retractors) - in severe cases or when recurrence occurs
d) Quickert procedure - in patients having associated marked horizontal lid laxity

PTOSIS
• Definition: abnormal drooping of the upper eyelid
• Clinico-etiological types
A. Congenital ptosis
➢ Etiology: a/w congenital weakness (maldevelopment) of the levator palpebrae superioris (LPS)
➢ Characteristic features
▪ Drooping of one or both upper lids
▪ Lid crease is either diminished or absent
▪ Lid lag on downgaze
 ➢ Forms
1) Simple congenital ptosis
2) Congenital ptosis a/w weakness of superior rectus muscle
3) Blepharophimosis syndrome
congenital ptosis, blepharophimosis, telecanthus and epicanthus inversus
4) Congenital synkinetic ptosis (Marcus Gunn jaw-winking ptosis)
retraction of the ptotic lid with jaw movements, i.e., with stimulation of ipsilateral pterygoid muscle
B. Acquired ptosis
1) Neurogenic ptosis: caused by innervational defects
➢ 3rd nerve palsy
➢ Horner’s syndrome
➢ Ophthalmoplegic migraine
➢ Multiple sclerosis
2) Myogenic ptosis: acquired disorders of the LPS muscle or of the myoneural junction
3) Aponeurotic ptosis: due to defects of the levator aponeurosis
➢ Involutional (senile) ptosis
➢ Postoperative ptosis
➢ Ptosis due to aponeurotic weakness a/w blepharochalasis
➢ Traumatic dehiscence or disinsertion of the aponeurosis.
4) Mechanical ptosis
➢ due to excessive weight on the upper lid → lid tumours, multiple chalazia and lid edema
➢ due to scarring (cicatricial ptosis) → ocular pemphigoid and trachoma
• Treatment
A. Treatment of Congenital ptosis
Severe ptosis → surgery should be performed at the earliest
Mild and moderate ptosis → surgery should be delayed until the age of 34 years
1) Tarso-conjunctivo-Mullerectomy (Fasanella-Servat operation): for mild ptosis and good levator function
2) Levator resection
➢ for moderate and severe grades of ptosis
➢ contraindicated in patients having severe ptosis with poor levator function
➢ Amount of levator resection required
▪ Moderate ptosis
✓ Good function: 16–17 mm (minimal)
✓ Fair function: 18–22 mm (moderate)
✓ Poor function: 23–24 mm (maximum)
▪ Severe ptosis with fair levator function: 23–24 mm (maximum)
➢ Techniques
a) Conjunctival approach (Blaskowics’ operation)
b) Skin approach (Everbusch’s operation)
3) Frontalis sling operation (Brow suspension)
➢ For severe ptosis with no levator function
➢ Best material for sling: fascia lata
B. Treatment of acquired ptosis
➢ Treat the underlying cause
➢ Conservative treatment
➢ Surgical procedures
 DISEASES OF LACRIMAL APPARATUS

EPIPHORA
• Causes
1) Physiological cause
➢ lacrimal pump failure
➢ atonia of sac
2) Mechanical obstruction
a) Punctal causes
➢ Eversion of lower punctum
➢ Punctal obstruction
b) Causes in the canaliculi – foreign body, trauma, idiopathic fibrosis and canaliculitis (mcc =
actinomyces)
c) Causes in the lacrimal sac – congenital mucous membrane folds, traumatic strictures,
dacryocystitis, TB, syphilis, dacryolithiasis and tumours
d) Causes in the nasolacrimal duct
➢ Congenital causes - noncanalization, partial canalization or imperforated membranous
valves
➢ Acquired causes - traumatic strictures, inflammatory strictures, idiopathic stenosis, tumours
and diseases of the surrounding bones
• Clinical evaluation
1) Ocular examination with diffuse illumination using magnification
2) Regurgitation test: reflux of mucopurulent discharge → chronic dacryocystitis with obstruction at
lower end of sac or NLD
3) Fluorescein dye disappearance test (FDDT): prolonged retention of dye in conjunctival sac →
inadequate drainage
4) Lacrimal syringing test
➢ free passage of saline through lacrimal passages into the nose → no mechanical obstruction
➢ saline passes with considerable pressure on the syringe → partial obstruction
➢ no fluid passes into nose → obstruction
5) Jones dye tests
a) Jones primary test (Jones test I)
➢ Positive test → primary hypersecretion
➢ Negative test → partial obstruction or lacrimal pump failure
b) Jones secondary test (Jones test II)
➢ Positive test → partial obstruction
➢ Negative test → lacrimal pump failure
6) Dacryocystography
➢ radiopaque material → lipiodol, pentopaque, dianosil or condray-280
➢ modified technique → subtraction macrodacryocystography
7) Radionucleotide dacryocystography (lacrimal scintillography)
➢ radioactive tracer → sulphur colloid or technetium
➢ visualised with an Anger gamma camera
DACRYOCYSTITIS

A. Congenital Dacryocystitis / Dacryocystitis Neonatorum

• Definition: inflammation of the lacrimal sac occurring in newborn infants
• Etiology
➢ follows stasis of secretions in the lacrimal sac due to congenital blockage in NLD
➢ Causes
▪ Membranous occlusion’ at its lower end near the valve of Hasner (mcc)
▪ epithelial debris
▪ membranous occlusion at its upper end near lacrimal sac
▪ complete noncanalization
▪ bony occlusion
➢ bacteria associated - Staphylococci, Pneumococci and Streptococci
• Clinical features
➢ Epiphora
▪ develops after 7 days of birth
▪ followed by copious mucopurulent discharge from the eyes
➢ Regurgitation test: positive
➢ Swelling on the sac area
• Differential diagnosis
➢ Ophthalmia neonatorum
➢ Congenital glaucoma
• Complications
➢ recurrent conjunctivitis
➢ acute or chronic dacryocystitis
➢ lacrimal abscess
➢ fistulae formation
• Treatment
a) Massage over the lacrimal sac area
b) topical antibiotics
c) Lacrimal syringing with normal saline & antibiotic solution: if condition not cured upto age of 3
months
d) Probing of NLD with Bowman’s probe: if condition not cured up by the age of 6 months
e) Balloon catheter dilation
f) Intubation with silicone tube: kept in NLD for 6 months
g) Dacryocystorhinostomy (DCR) operation: after 4 years
B. Adult Dacryocystitis

1) Chronic Dacryocystitis
• Etiology: vicious cycle of stasis and mild infection of long duration
❖ Predisposing factors
➢ Age: between 40 and 60 years
➢ Sex: females (80%)
➢ Race: Whites
➢ Heredity
➢ Low socioeconomic group
➢ Poor personal hygiene
❖ Factors responsible for stasis of tears in lacrimal sac
➢ Anatomical factors: narrow bony canal, partial canalization of membranous NLD and
excessive membranous folds in NLD
➢ Foreign bodies in the sac
➢ Excessive lacrimation
➢ Mild grade inflammation of lacrimal sac
➢ Obstruction of lower end of NLD: polyps, hypertrophied inferior concha, DNS, tumours
and atrophic rhinitis
❖ Source of infection: conjunctiva, nasal cavity or paranasal sinuses
❖ Causative organisms: Staphylococci, Pneumococci, Streptococci and Pseudomonas
pyocyanea
• Clinical features
a) Stage of chronic catarrhal dacryocystitis
➢ Watering eye: only symptom
➢ syringing → clear fluid or few fibrinous mucoid flakes
➢ Dacryocystography → block in NLD
b) Stage of lacrimal mucocele
➢ constant epiphora a/w a swelling just below the inner canthus
➢ Regurgitation test → milky or gelatinous mucoid fluid from the lower punctum
➢ Dacryocystography → a distended sac with blockage in NLD
➢ continued chronic infection → opening of both canaliculi into the sac blocked → large
fluctuant swelling seen at the inner canthus → encysted mucocele; negative
regurgitation test
c) Stage of chronic suppurative dacryocystitis
➢ epiphora, recurrent conjunctivitis, swelling at the inner canthus
➢ Regurgitation test → frank purulent discharge from the lower punctum
➢ Encysted mucocele → encysted pyocoele
d) Stage of chronic fibrotic sac
➢ small fibrotic sac a/w persistent epiphora and discharge
➢ Dacryocystography → a very small sac with irregular folds in the mucosa
• Complications
➢ Chronic intractable conjunctivitis
➢ Ectropion of lower lid
➢ corneal ulceration
➢ endophthalmitis
 • Treatment
a) Conservative treatment: by probing and lacrimal syringing
b) Balloon catheter dilation / balloon dacryocystoplasty
c) Dacryocystorhinostomy (DCR): operation of choice
d) Dacryocystectomy (DCT): performed only when DCR is contraindicated
Indications-
➢ < 4 years or > 60 years
➢ shrunken and fibrosed sac
➢ TB, syphilis, leprosy or mycotic infections of sac
➢ Tumours of sac
➢ Gross nasal diseases
➢ unskilled surgeon
e) Conjunctivodacryocystorhinostomy (CDCR): in blocked canaliculi

2) Acute Dacryocystitis
• Etiology:
➢ develops-
a) as an acute exacerbation of chronic dacryocystitis
b) as an acute peridacryocystitis due to direct involvement from the neighbouring infected
structures
➢ Causative organisms: Streptococcus haemolyticus, Pneumococcus and Staphylococcus
• Clinical features
a) Stage of cellulitis
➢ painful swelling a/w epiphora, fever and malaise
➢ redness and edema spread to lids and cheek
➢ treatment → resolution
b) Stage of lacrimal abscess
➢ continued inflammation → occlusion of canaliculi → pericystic swelling → lacrimal
abscess
➢ abscess points below and to the outer side of sac
c) Stage of fistula formation
➢ lacrimal abscess left unattended → discharges spontaneously → external fistula below
medial palpebral ligament
• Complications
➢ Acute conjunctivitis
➢ Corneal abrasion
➢ Lid abscess
➢ Osteomyelitis of lacrimal bone
➢ Orbital cellulitis
➢ Facial cellulitis and acute ethmoiditis
• Treatment
a) During cellulitis stage
➢ Systemic and topical antibiotics
➢ systemic anti-inflammatory analgesic drugs
➢ hot fomentation
b) During stage of lacrimal abscess: drained with a small incision
c) Treatment of external lacrimal fistula: fistulectomy + DCT/DCR
 OCULAR INJURIES

PENETRATING AND PERFORATING INJURIES

• Penetrating injury: a single full-thickness wound of the eyewall caused by a sharp object
Perforating injury: two full-thickness wounds of the eyewall caused by a sharp object or missile
• Modes of injury
1) Trauma by sharp and pointed instruments
2) Trauma by foreign bodies travelling at very high speed
• Mechanisms of damage
1) Mechanical effects of the trauma or physical changes
➢ depend upon the size, velocity, type, route of entry and the site up to which a foreign body has
travelled
➢ Foreign bodies >2 mm cause extensive damage
➢ Traumatic lesions produced by intraocular foreign bodies
▪ Corneal and scleral perforation, hyphaema, iris hole
▪ Rupture of the lens and traumatic cataract
▪ Vitreous haemorrhage and/or degeneration
▪ Choroidal perforation, haemorrhage and inflammation
▪ Retinal hole, haemorrhages, edema and detachment
➢ Locations of IOFB
▪ Anterior chamber: sinks at the bottom
✓ Magnetic → removed with a hand-held electromagnet
✓ Non-magnetic → picked up with toothless forceps
▪ Iris: entangled in the stroma → removed by sector iridectomy
▪ Lens: on the anterior surface or inside the lens → managed by ECCE with IOL implantation
▪ Vitreous cavity

✓ Pars plana sclerotomy → hand-held electromagnet

✓ Three-pore pars plana vitrectomy → vitreous forceps
▪ Retina, choroid and sclera: through corneal and scleral perforation
▪ Trapdoor scleral flap → choroidal bed treated with diathermy → choroid incised →
forceps
▪ Orbital cavity
2) Introduction of infection: results in ring abscess of the cornea, sloughing of the cornea, purulent
iridocyclitis, endophthalmitis or panophthalmitis
 3) Post-traumatic iridocyclitis: most dangerous complication of a perforating injury
• Traumatic lesions with management
1) Wounds of the conjunctiva: A wound of more than 3 mm should be sutured
2) Wounds of the cornea
a) Uncomplicated: margins swell up and lead to automatic sealing and restoration of the anterior
chamber
➢ small central wound → pad and bandage with atropine and antibiotic ointments
➢ large wound (more than 2 mm) → sutured
b) Complicated: a/w prolapse of iris, lens matter or vitreous
➢ a/w iris prolapse → sutured meticulously after abscising the iris
➢ a/w lens injury and vitreous loss → lensectomy and anterior vitrectomy
3) Wounds of the sclera: a/w corneal wounds → first suture at the limbus
4) Wounds of the lens
➢ Extensive lens ruptures with vitreous loss → lensectomy and anterior vitrectomy
➢ Small wounds in the anterior capsule → seal → traumatic cataract
5) A severely wounded eye: excision

SYMPATHETIC OPHTHALMITIS
• serious bilateral granulomatous panuveitis which follows a penetrating ocular trauma
• injured eye = exciting eye, fellow eye which also develops uveitis = sympathizing eye
• Etiology
➢ follows a penetrating injury
➢ wounds in the ciliary region (dangerous zone)
➢ wounds with incarceration of the iris, ciliary body or lens capsule
➢ children > adults
➢ does not occur when actual suppuration develops in the injured eye
• Pathogenesis: allergic theory → uveal pigment acts as an allergen and excites plastic uveitis in the
sound eye
• Pathology: characteristic of granulomatous uveitis
➢ Nodular aggregation of lymphocytes, plasma cells, epitheloid cells and giant cells scattered
throughout the uveal tract.
➢ Dalen-Fuchs’ nodules: formed due to proliferation of the pigment epithelium a/w invasion by the
lymphocytes and epitheloid cells.
➢ Sympathetic perivasculitis in retina
• Clinical features
A. Exciting (injured) eye: ciliary congestion, lacrimation and tenderness
B. Sympathizing (sound) eye: involved after 4–8 weeks of injury in the other eye; manifests as acute
plastic iridocyclitis
1) Prodromal stage
➢ Symptoms
▪ Photophobia
▪ transient indistinctness of near objects
➢ Signs
▪ retrolental flare and cell
▪ keratic precipitates
▪ ciliary congestion
▪ tenderness of the globe
 ▪ fine vitreous haze
▪ disc edema
2) Fully-developed stage
➢ Symptoms
▪ Pain
▪ Photophobia
▪ Redness
▪ Lacrimation
▪ ↓ vision
➢ Signs
▪ Lid edema
▪ Circumcorneal congestion
▪ Corneal signs
a) Corneal edema
b) Keratic precipitates: mutton fat KPs
▪ Anterior chamber signs
a) Aqueous cells
b) Hypopyon: sterile
c) Changes in depth and shape of anterior chamber
d) Changes in the angle of anterior chamber: due to cellular deposits
▪ Iris signs
a) Loss of normal pattern: due to edema and waterlogging
b) Changes in iris colour: muddy
c) Iris nodules: Koeppe’s and Busacca’s
d) Posterior synechiae: segmental, annular or total
▪ Pupillary signs
a) Narrow pupil
b) Irregular pupil shape
c) Ectropion pupillae
d) Pupillary reaction sluggish
e) Occlusio pupillae
▪ Changes in the lens
a) Pigment dispersal
b) Exudates
▪ Changes in the vitreous and retina: Exudates and inflammatory cells
• Treatment
A. Prophylaxis
1) Early excision of the injured eye: best when there is no chance of saving useful vision
2) When there is hope of saving useful vision
a) A meticulous repair of the wound using microsurgical technique
b) Immediate expectant treatment: topical and systemic steroids, antibiotics, topical atropine
c) Excision: When the uveitis is not controlled after 2 weeks of expectant treatment
B. Treatment when sympathetic ophthalmitis has already supervened
1) Early excision of the injured eye: when injured eye has no useful vision and sympathizing eye in
prodromal stage
2) Conservative treatment
a) Corticosteroids: systemic, periocular injections and topical drops
b) Atropine
c) Immunosuppressant drugs: severe cases
 SYSTEMIC OPHTHALMOLOGY

XEROPHTHALMIA
• covers all the ocular manifestations of vitamin A deficiency, including the structural
changes affecting the conjunctiva, cornea and retina, and the biophysical disorders of
retinal rods and cones functions
• Etiology
➢ dietary deficiency of vitamin A
➢ defective absorption of vitamin A from the gut
➢ accompanied by protein-energy malnutrition (PEM) and infections
• WHO classification
XN: Night blindness
X1A: Conjunctival xerosis
X1B: Bitot’s spots
X2: Corneal xerosis
X3A: Corneal ulceration/keratomalacia affecting less than one-third corneal surface
X3B: Corneal ulceration/keratomalacia affecting more than one-third corneal surface
XS: Corneal scar due to xerophthalmia
XF: Xerophthalmic fundus
• Clinical features
1) XN: earliest symptom
2) X1A:
➢ one or more patches of dry, lustreless, nonwettable conjunctiva
➢ ‘emerging like sand banks at receding tide’ when the child ceases to cry
➢ Situation - interpalpebral area of temporal and nasal quadrants
➢ a/w conjunctival thickening, wrinkling and pigmentation
3) X1B:
➢ raised, silvery white, foamy, triangular patch of keratinized epithelium
➢ situation - bulbar conjunctiva in the interpalpebral area
➢ bilateral
➢ temporal
4) X2:
➢ earliest change in cornea: punctate keratopathy → lower nasal quadrant
➢ haziness
➢ granular pebbly dryness
➢ lustreless
5) X3A and X3B: Stromal defects in the late stage due to colliquative necrosis
 a) Small ulcers: peripheral, circular, with steep margins and sharply demarcated;
heal under therapy
b) Large ulcers: central; result in blindness
6) XS: due to healing of stromal defects
7) XF: typical seed-like, raised, whitish lesions scattered uniformly over the part of the
fundus at the level of optic disc
• Treatment
1) Local ocular therapy
➢ conjunctival xerosis: artificial tears → hydroxypropyl methyl cellulose,
hypromellose)
➢ keratomalacia: full-fledged treatment of bacterial corneal ulcer
2) Vitamin A therapy
a) All patients above the age of 1 year (except women of reproductive age):
➢ 200,000 IU orally or 100,000 IU by i.m. injection
➢ given immediately on diagnosis and repeated the following day and 4 weeks
later
b) Children under the age of 1 year and children of any age who weigh less than 8 kg:
➢ 100,000 IU orally or 50,000 IU by i.m. injection
c) Women of reproductive age:
➢ For XN, X1A, X1B → 10,000 IU daily for 2 weeks
➢ For X2, X3, XS, XF → 200,000 IU orally on diagnosis and repeated the following
day and 4 weeks later
3) Treatment of underlying conditions
• Prophylaxis
1) Short-term approach: vitamin A supplements under Child Survival and Safe
Motherhood (CSSM)
a) 1st dose (1 lakh IU) - at 9 months of age
b) 2nd dose (2 lakh IU) - at 18 months of age
c) 3rd dose (2 lakh IU) - at 2 years of age
2) Medium-term approach: food fortification with vitamin A
3) Long-term approach:
➢ promotion of adequate intake of vitamin A rich foods → green leafy vegetables,
papaya and drumsticks
➢ Nutritional health education in the curriculum of school children