Visual field defects VFD

Normal extent of the visual field

Temporally: 90-100 degrees

Inferior: 70

Nasal: 65

Superior: 50

Minimum field is superiorly and max temporally

Location of blind spot: between 10-20 degree isopters

VFD in POAG

Early

1. Central and para central in bejerrum's area

1st scotoma in glaucoma appears here

2. Seidel scotoma: involves the blind spot with central /para central

3. Roenne's nasal step

4. Arcuate

5. Double arcuate( inferior field involved)

6. Central and temporal island of vision left behind

temporal island of vision stays till last

Baring of blind spot

The whole isopter is contracting and it does not include the blind stop

It is not seen in routine field test

Can be seen in other neurological problems as well and not

pathognomonic of glaucoma

Perimetry

Two types
Kinetic
Static

Kinetic divided into

Central: bejerrum's field used

Peripheral: Listers perimeter

Static
Automated, computerized: pt asked to look for green light while looking at
red light, so basically contrast sensitivity is tested

Humphrey field analyser

Octopus

Are the methods used

Central
Peripheral

Campimetry
Central visual field charting

Central 30 degree tested

Primary angle closure glaucoma

PACG

Risk factors
1. Small eye

2. Shallow anterior chamber

3. Narrow angle

4. Common in females

Maximum closure of angle occurs in a mid dilated pupil

Etiopathogenesis

Pupillary block

Obliteration of angle

C/F

Stage 1: Prodromal stage

Pt is asymptomatic

Stage 2: stage of constant instability

Some part of the angle is blocked and then reopened by itself without
intervention

Stage 3: acute congestive glaucoma

Features:

All 360 degree angle is closed

Pressure rises to 60 degree of Hg, normal is 10-21 mm of Hg

Leading to corneal edema and colored halos

Pain is so much that it leads to nausea and vomiting

Redness, photophobia and blepharospasm

On examination

Stage 4. chronic congestive glaucoma

IOP changes

Fundus involvement

Field defects

Plus

Angle is also closed

Gonioscope used when pupil is constricted

Stage 5. Absolute glaucoma

Total damage

Painful blind eye

Pain is because of increased pressure

Eye described as stony hard

Pt is blind coz total damage of the optic nerve

100% cupping is seen ka Glaucomatous optic atrophy

Cupping

Pale area in center is the cup

Remaining is neuro retinal rim

Thus cup is non neuronal

Normal ratio is less than equal to 0.3

If increases , called cupping

Cupping is always vertical

Macula to cup: papillo macular bundle

Straight fibers these

Superior and nasal radiating fibers from nasal side

Arcuate fibers from top side

Treatment of choice for absolute glaucoma

Cyclocryotherapy

Aim is to relieve the pain

Ciliary processes are damaged 360 degrees, not all destroyed, just done
at regular intervals otherwise shrinkage ka Pthisis bulbi

In atrophic bulbi, dierent layers of eyeball can not be delineated

Thus aqueous is not formed and pressure decreases

Treatment of choice for angle closure glaucoma

Pupillary irodotomy by NDYAG laser

Doc is pilocarpine

Treatment of choice for acute congestive glaucoma

Very high pressure

So iris ischemia

Thus pilocarpine does not work

So use

Mannitol/ Acetazolamide followed by or simultaneous pilocarpine

Secondary glaucoma

Lens induced glaucoma

1. Phacolytic glaucoma( Morgagnian): secondary OAG

2. Phacotoxic, due to trauma, capsular rupture, leakage of protein,

trabecular mesh work blocked

3. Phacoanaphylactic: immune reaction, release of macrophages, engulf

the protein, block the TMW

Q. Lens protein is a sequestered antigen

4. Phacomorphic glaucoma, due to morphology, intumescent cataract

causing pupillary block, touches the iris and blocks

Thus secondary angle closure glaucoma

Pigmentary glaucoma

Pigments released from iris block the TMW

Trans illumination defects

Keratin precipitates aka Krukenburg granules

pseudo exfoliation syndrome

Aka glaucoma capsulare

White dandru like material released from lens capsule and suspensory
ligaments

The same white dandru lines seen on the pupillary border on

examination

most common cause of secondary glaucoma

Malignant glaucoma
Aka Ciliary block glaucoma

Aqueous starts collecting in the vitreous cavity

Happens after intra ocular surgery

Most commonly after Trabeculectomy

Treated by

Atropine

Block opens

If atropine fails

Pars plana vitrectomy done immediately, enter through pars plana

Also called Inverse glaucoma as treated by a Mydriatic

Spherophakia
Also an inverse glaucoma

Neovascular glaucoma
Hypoxia in the retina causes neovascularization

If not treated, hypoxia in the anterior segment leading to Rubeosis Iridis

The vessels grow into the TMW thus an. Open angle glaucoma

initially an OAG but the fibrous tissue in the new vessels contracts and
makes it a closed angle glaucoma

Treatment

Pan retinal photocoagulation

Since the main issue is in the retina

Steroid induced glaucoma

Occurs due to deposition of mucopolysaccharides in TMW, OAG

Glaucoma associated with anterior uveitis

Posterior and anterior synechiae can cause CAG

Aqueous cells( inflammatory cells) when they block the TMW, cause OAG

In acute inflammation, there is ciliary shutdown so the pressures are

recorded low in the acute stage

ICE syndrome, OAG

Irido corneo endothelial syndrome

Endothelial cells never proliferate but they do in this condition

Thus a Proliferative endotheliopathy

There are three forms of the disease

1. Progressive iris atrophy: atrophy of iris

2. Cogan Reese syndrome: nodules and nevus in the iris
3. Chandlers syndrome: corneal edema

Treatment of glaucoma

Medical
Laser
Surgery

Medical

Topical
Systemic

Topical drugs
blockers
MOA: decreases formation

Timolol, Betaxolol, levobunolol

Q. CI in asthma

Q. Which is a selective blocker: Betaxolol , thus can be given in asthma

Q. Which anti glaucoma drugs causes naso lacrimal duct obstruction:

timolol

Alpha agonist
MOA: either decreases formation and increases drainage

Epinephrine

Dipivefrine

Brimonidine

Apraclonidine

Q. Alpha agonist CI in HT and heart disease

Q. Selective are brimonidine and apraclonidine

Q. Which causes drowsiness: brimonidine

It is also considered to be a neuro protective drug

It increases the uveo scleral outflow

Miotics

MAO: Miosis and increses the conventional aka trabecular outflow

Pilocarpine

Q. CI in uveitis

Prostaglandin analogues

MAO : increases the Uveoscleral outflow

Latanoprost

Travoprost

Brimatoprost

Q. CI in uveitis

Topical carbonic anhydrase inhibitors

MAO: decreases formation of aqueous

Dorzolamide

Brinzolamide

Q. CI in sulfa allergies as these are sulfonamides

Systemic drugs

1. Carbonic anhydrase inhibitor

Acetazolamide

CI in sulfa allergies

2. Hyper osmotic agents

Mannitol

Glycerol

Isosorbide

Urea

Laser therapy

ACG
Peripheral irodotomy by NDYAG

OAG
Trabeculoplasty thus coagulative laser used

Surgical treatment

Treatment of choice for congenital glaucoma

1. Goniotomy

2. Trabeculectomy

Direct connection between the anterior chamber and sub conjunctival

space

Partial thickness V shaped scleral flap

Cut the trabecular mesh work

Do an iridectomy

Loose sutures to keep the flow

Cover the whole thing with the conjunctival flap

Presence of conjunctival bleb indicates success of surgery

resection of the TMW and making a fistula between the anterior chamber
and sub conjunctival space

to prevent the closure of the fistula

1. Anti mitotic drugs

Mitomycin C

5 FU

2. Aqueous drainage implant

Ahmed glaucoma valve AGV

Molteno implant

express implant made up of stainless steel( rest all are silicone)

3. Trabeculotomy
Schlemm's canal and TMW cut

Cornea

Shape is aspheric, gradually tapering

11-11.75 mm

>13 is megalocornea

<10 is micro cornea

Power: 45-50 D

Index: 1.37

Structure of cornea

5 layers

Uppermost is epithelium

Below is Bowman's membrane

Stroma

Descement's membrane

Endothelium

Physiology

Avascular

Dehydrated as hydration leads to opacification

Aerobic metabolism, O2 by environmental air

Nutrition from aqueous humor

Q. Thus in a contact lens wearer, glucose utilization is hampered

Cornea is surrounded by water on all sides

Main reason for dehydrated state is Pump function and barrier function of
the endothelium

If any problem in this, corneal edema

No of endothelial cells per mm square

In adults: 2500-3000

Children: 3500-5500

Q. Corneal layers which do not regenerate

Endothelium

Bowman's membrane

Endothelial cells compensating morphology by mechanism of

Polymegathism and pleomorphism

Adjacent cells takes over

If the cells decrease below 500 cell/ mm square

Thus edema happens

First stromal edema

Then epithelial edema

Lastly bullae filled with fluid ka Bullous keratopathy

This happened as there was no compensation from the cornea so it is
also ka Corneal Decompensation
Epithelium regenerates from limbal stem cells

Metabolically most active is endothelium

Epithelium is involved in bullous keratopathy

Ulcer
Breach in the continuity of the epithelium

Organism that can penetrate intact cornea

GDHL

Gonorrhea

Diphtheria

Hemophilus

Listeria

Investigation

1. Keratometry

Only the central corneal surface is measured

2. Corneal topography
Corneal curvature of whole cornea

3. Pachymetry
Thickness of cornea

Center: 0.5-0.6 mm

Limbus: 1 mm

4. Specular microscopy
To examine the endothelial cells

5. Aesthesiometer
To see the corneal sensation

6. Microbiological investigation:
Staining

Culture

Keratitis
Inflammation of the cornea

Presenting symptoms:

Pain

Redness

Photophobia

Blepharospasm

Discharge

Redness
3 types

Ciliary congestion

Circumciliary congestion:

Conjunctival congestion: only conjunctival vessels involved

Ciliary congestion seen in keratitis

Bacterial keratitis

Same presenting features

O/E

Fluorescein stain positive ulcer

Hypopyon: pus in anterior chamber, always sterile in bacterial etiology

Localized ulcer heals and forms opacity

Perforating Corneal ulcer: iris seals the ulcer ka Leucoma adherens

Sloughing corneal ulcer: pseudo cornea composed of inflammatory

exudates present as normal cornea gone, virulent organism

Q. Hypopyon corneal ulcer: seen with pneumococcus

Q. Ulcer of pneumococcus also ka Ulcus Serpens

Treatment of bacterial keratitis

1. Antibiotic eye drops

Broad spectrum/ culture sensitivity

If fails

Go for fortified antibiotic eye drops

Cefazoline concentrated at 50 mg/ ml plus gentamicin at 15 mg/ ml

2. Antibiotic ointment at night

3. Atropine for managing associated uveitis

4. Oral anti inflammatory drugs

5. Oral vitamin A and C

Management of a non healing ulcer

1. Debridement: removing the necrotic tissue from the periphery of ulcer

2. Chemical cautery: trichloroacetic acid TCA

It acts as a local anesthetic

3. Conjunctival flapping: as the movement of lids prevents healing

Management of impending perforation

1. Decrease the IOP, start anti glaucoma drugs

2. Sino acrylate glue at the area of thinning

3. Bandage contact lens BCL, it's a soft CL with high water content

Types of CL

1. Soft

2. Semi soft aka rigid gas permeable lenses

Fungal keratitis aka Keratomycosis

Q. How does one acquire

Trauma by vegetative or organic matter this more common in farmers

Q. Signs are more than symptoms in Keratomycosis

Q. Most common fungus: aspergillus Fumigatus

Next best is Fusarium

Q. Most common fungus infecting lids in India

Candida Albicans

Dermatophytes

O/E

Ulcer has a dry and rough look

Projecting hyphae

Unsterile hypopyon

Satellite nodules seen

investigations of Keratomycosis

Staining
1. KOH smear

2. Gomori's methamine silver stain

Culture
1. Saboraud's agar

2. Brain heart infusion broth

Treatment

Doc for fungal keratitis

Natamycin

Others

Nystatin eye ointment

Fluconazole

Viral keratitis

Q. Herpes simplex> herpes zoster

Q. Pathognomonic feature of viral keratitis : decreased corneal sensations

Other causes of decreased corneal sensations

Leprosy

DM

Pthisis bulbi

Section of trigeminal nerve

Chronic degenerative conditions of cornea

Herpes simplex keratitis

C/F are same 5 features

Endothelitis involves central disc like edema: Disciform keratitis

treatment
3% acyclovir ointment given 5 times a day

Only other ointment in ophthal is tetracycline 1%

In any infective ulcer/ keratitis

Two rules that are to be followed

Steroids CI

No pad and bandage

Only exception

But if the pt presents with only Disciform keratitis, steroids can be given
under antiviral cover

Herpes zoster ophthalmicus

Skin involvement

Eye involvement

Trigeminal neuralgia

Hutchison's rule

If the tip of the nose is involved, eye will be involved, happens due to
involvement of naso ciliary nerve

CF are the same

epithelium
Superficial punctate ulcer

Pseudo or micro dendrites seen, not dendritic ulcer

Stroma
Involves superficial stroma and are circular lesions called Nummular
keratitis

Endothelial

Disciform keratitis

Uveitis

Cranial nerve palsies

Most common 3rd

Least common 4th

Also 6th

Although most commonly nerve involved in zoster is frontal

Treatment

Topical treatment is same as simplex

Along with that, oral acyclovir given, 800mg tablet/5 times a day

Ideally antivirals should not continue for more than 14 days

If present , will lead to

Metaherpetic keratitis

Due to toxicity of anti virals

Stop the drug and start lubricating eye drops

Acanthamoeba keratitis

Rare

Seen in soft CL users washing lenses in tap water

Most common infection after CL use: pseudomonas

While soft CL users are more prone to develop Acanthamoeba keratitis

C/F

Same 5 feature

But pain is disproportionately much more due to perineural invasion

O/E

Ring lesion

Or

May present as

Pseudo dendrites

Or

Reticular pattern

Investigation

Staining
Calcoflour white

Acridine orange

Lactophenol blue

Culture
Q. Non nutrient agar with E. Coli

Treatment

First line is , doc is

1. PHMB: polyhexamethylene Biguanides

Others

2. Propamidine isithionate

3. Neomycin

Interstitial keratitis

Only stromal keratitis, no involvement of epithelium and endothelium

Causes
Syphilis

Leprosy

TB

Sarcoidosis

Cogan syndrome: interstitial keratitis with deafness

Q. Salmon patch is seen in syphilis interstitial keratitis

Keratoconus

Ectatic dystrophy of cornea

Ectasia is protrusion

Dystrophy is idiopathic spontaneous change with no inflammatory

component

There is a conical protrusion

Genetic disease

Slowly progressive in nature

keratoconus will have myopia and irregular astigmatism

Leading to diminution of vision

O/E

Flescher's ring

Iron deposition in epithelium

Keyser fleischer ring in Descement's membrane in Wilson's disease

V shaped deformity on the lower lid on downward gaze: Munson sign

Corneal topography: irregular astigmatism

On retinoscopy:

Scissors reflex seen due to irregular cornea

Q. Prominent corneal nerves seen due to thinning of cornea and not

thickening of nerves

Q. Vogt's triad

Haab's striae: seen in buphthalmos

Total cornea involved and stretched

Causes of thickening of the nerves

Leprosy

NF-1

Treatment

Spects usually ineective

Always a rigid gas permeable CL used

If nothing works

Penetrating keratoplasty

Keratoplasty
Aka corneal transplantation

Replacement of diseased cornea by the donor cornea

Q. Where do we get donor cornea: cadaveric eyes

Should be taken in 6 hours but can be extended to 12 hours

Q. Storage media: MK medium: Mc Carry Kauman medium

Short term storage: for 48 hours, kept in Moist chamber

Intermediate term storage: MK medium, 4 days

Long term storage: either for 30 days: organ culture

Indefinite time: cryopreservation

Two types of keratoplasty

Penetrating: full thickness

Lamellar: partial thickness
Also of two types

DALK: deep anterior lamellar keratoplasty

DELK: deep endothelial lamellar keratoplasty aka Descement's membrane

stripping

Q. Endothelial cell loss in this procedure is 20-25%

Corneal degeneration

1. Age related
Arcus senilis

Round opacity on cornea on old age, found at limbus

Lucid interval of Vogt: the clear cornea in between

Due to lipid deposition in stroma

2. Band shaped keratopathy

Calcium deposition on the cornea in a band

most commonly

Idiopathic

Others

Chronic uveitis in children suering from JRA

Pthisis bulbi

Hypercalcemia, thus also a feature of sarcoidosis

Treatment
Q. Chelation by EDTA

Calcium is deposited just under the epithelium but above the Bowman's
membrane

Corneal dystrophies

Epithelial
Will present with Recurrent erosions

Treated by pad and bandage with antibiotic ointment

Or

Keratoplasty

Eg.

A. Microcystic aka fingerprint aka Mapdot

B. Meesman's dystrophy

C. Reis Buckler dystrophy

Stromal
Diminution of vision

Treated by keratoplasty

Eg

Granular

Macular

Lattice

Endothelial
Present with corneal edema

Treated by

First line

Hypertonic saline eye drops

If doesn't work: keratoplasty

Eg

Fuchs endothelial dystrophy

Posterior polymorphus dystrophy

Q. Most common type of corneal dystrophy: microcystic

Q. Least common type: macular

Q. Which is asso with mucopolysaccharidoses: macular

Q. Which is AR: macular

Q. Most common stromal dystrophy: lattice

Q. Which is asso with Amyloidosis: lattice

Q. Corneal dystrophies are primary and bilateral

Corneal opacities

Stroma has to be involved for an opacity

1. Nebular corneal opacity: little stroma involved, faint white

2. Macular: more stroma involved, white

3. Leucoma: full thickness, dense white

Q. Nebular diminishes the vision most coz they refract light and aect the
rest of the cornea as well while others just obstruct light

Conjunctiva

Conjunctivitis

Same 5 CF

But redness would be Conjunctival congestion

Discharge will depend on etiology

Bacterial: purulent

Chlamydial: muco purulent

Viral and allergic: watery discharge

Pathology
Two types

Follicular reaction: aggregation of lymphoid cells

Papillary reaction: epithelial hyperplasia

Treatment
Bacterial: Abx

Chlamydia: Abx

Viral: Abx

Allergic: anti allergic/ steroids

Membranous conjunctivitis

All the CF plus a membrane which is dicult to peel and bleeds on

peeling

Caused by C. Diphtheria

Pseudo membranous conjunctivitis

Will not bleed on peeling

Rest all same

Etiology: mild diphtheria infection

Severe adenovirus infection

Streptococcus hemolyticus

Angular conjunctivitis

Conjunctivitis involving the two canthii with excoriation of skin

Q. Cause: Moraxella axenfeld, Also Moraxella Lacunata

S. Aureus

Treatment

1. Abx eye drops

2. Zinc oxide( inhibits the proteolytic enzymes)

Hemorrhagic conjunctivitis

All the features with sub conjunctival hemorrhages

Causes

Bacterial: Hemophilus and pneumococcus

viral: entero virus 70 , adenovirus, coxsackie 24, echovirus 34

Causes of sub conjunctival hemorrhages

Trauma

Hemorrhagic conjunctivitis

Hypertension

Bleeding diasthesis

Pertussis: whooping cough

Trachoma

Chronic conjunctivitis of children, 0-9 years

Chlamydia trachomatis

Q. Strain A, B, Ba and C

Q. D and K cause adult inclusion conjunctivitis aka swimming pool

conjunctivitis

C/F
Itching

Watering

O/E

Follicles on the upper palpebral conjunctiva or on the upper limbus called

Herbert follicles

Later linear scarring happens: Arlt's line

Scarring of Herbert follicles is called Herbert pits

WHO classification of trachoma

FISTO
Stage 1: >=5 follicles in the upper palpebral conjunctiva

Stage 2: inflammation, itching and irritation

Stage 3: scarring

Stage 4: Trichiasis

Stage 5: corneal opacity

Q. Complication of trachoma: only corneal ulcer

Pathology
One infection where both follicular and papillary reaction

HP bodies: intracytoplasmic inclusion bodies: Halbersteidter Prowasek

Community ophthalmology

SAFE strategy
WHO program to control trachoma in a community

Surgery: only Trichiasis surgery

Antibiotics: oral azithromycin(easy compliance, 1gm in adult and 20 mg

in children) or topical tetracycline(1%)

Facial hygiene

Environmental cleaning

Criteria for starting SAFE

Prevalence of trachoma follicles in age 2-9

If prevalence more than 10%, start

If between 5-10: only F and E done

Doc for blanket therapy in trachoma: Azithromycin

Q. Trachoma is included in the Program Vision 2020

Treatment
Doc is azithromycin

Vision 2020
WHO program to prevent blindness

5 diseases

Cataract

Trachoma

Onchocerciasis

Childhood blindness

Refractive errors

Diseases in India : onchocerciasis removed and 3 more added

Diabetic retinopathy

Glaucoma

Corneal blindness

Allergic conjunctivitis

1. Phlyctenular keratoconjunctivitis
Type 4 HS reaction
Q. Allergy towards endogenous Ag

1. S. Aureus

2. TB

C/F

Itching and watering

O/E

Phlycten: nodule at the limbus

Conjunctival congestion

Later involves cornea leading to Fascicular ulcer

It later extends as ring ulcer

treatment
1. Both Mast cell stabilizers and anti histaminic properties

Olapatadine

Epimastine

2. Na cromoglycate

3. If nothing works, mild steroids

Vernal keratoconjunctivitis aka springcatarrh

Disease of summers

Q. Exogenous allergy

Male children mostly

Q. No follicular reaction, only papillary reaction

C/F

I/ W

Ropy discharge: fibrin threads in the discharge

O/E

Papillary hyperplasia on the upper palpebral conjunctiva and upper

limbus

Q. This is ka cobblestone appearance

Central dots at limbus papilla: Horner Tranta spots, these are eosinophils

On the cornea, white opacity called Cupid's bow aka pseudo Gerontoxon
as Gerontoxon is arcus senilis
Q. Maxwell lym sign: eosinophilia in ropy discharge

Q. Type 1 HS reaction

Treatment

Same as phlyctenular