DISEASES OF ANTERIOR

CHAMBER

-Dr. Rajul Shah

Anterior chamber is an angular space
bounded anteriorly by posterior surface of
the cornea and posteriorly by anterior
surface of the iris and part of ciliary body.

Conjuctiva:-
It is a translucent membrane which covers
the posterior surface of lid and anterior part
of eyeball upto cornea.
-palpabral which covers eyelids
-bulbar which covers eyeball
-fornix which unites two

Function-
1. Tear production
2. O2 to cornea when open
3. Wash of debris
4. Protection of eye
Diseases of conjuctiva-
1. Symptomatic conditions of conjuctiva
2. Inflammation of conjuctiva
3. Degeneration of conjuctiva
4. Cysts and tumor of conjuctiva

Symptomatic conditions of conjuctiva

-hyperemia
-ecchymosis
-xerosis
-chemosis
-pigmentation

Signs-
Redness, discharge, foreign body sensation,
follicles(1.2 mm aggregation),
papillae(hyperplasia of vascular sysytem),
granuloma, subconjuctival
haemorrhage(ecchymosis),
edema(chemosis)
Conjuctivitis:
Inflammation of conjuctiva.
*Infectious:
Bacterial- Staph. aureus and albus, H.
influenza, N. gonorrhoea, N. meningitides,
Strep. Pyogenous, Proteus, Klebsella, E. coli
Viral- Herpes simplex, picornavirus,
adenovirus
Chlamydial
Fungal- aspergillus, candida, nocardia,
actinomyces, rhinosporidium
Parasitic

*Non-infectious:
-allergic
-irritant(physical, foreign body, contact lens
radiation)
-autoimmune
-dry eye
-toxic (chemical and drug)
-idiopathic

#Infectious conjuctivitis:
Acute conjuctivitis: resolving in < 4 weeks
Chronic conjuctivitis: > 4 weeks duration

*Neonatal conjuctivitis(opthalmia
neonatorum)-
Mucoid, mucopurulent or purulent discharge
from one or both eyes in 1st month of life.
It is due to maternal infection acquired at the
time of birth by contaminant in birth
passage.
Causative agents- N. gonorrhoea,
-Chlamydia trachomonas

*Bacterial conjuctivitis:
-Mucopurulent and purulent
-Contagious transmitted by the discharge
-S. aureus is most common agent
-Pathogenicity proportional to coagulase
activity

Clinical features-
Redness, mucus discharge, lids stick to each
other(in morning), severe fiery red eye
Usually severe form is due to N. gonorrhoea-
-moderate to severe pain
-lid edema with copious discharge
-occasional lymphadenopathy(pre auricular
called “hyperacute conjuctivitis” or “acute
blennorrhoea”

Complications-
Rarely corneal ulcers

Diagnosis-
-Bacterial investigations
-Gram stain, giemsa stain and pap stain of
scrapping
Treatment-
1. Tropical drugs-drops of broad spectrum
antibiotics
2. Systemic medication, rarely required-oral
analgesics, antiinflammatory drugs or
antibiotics
3. Supportive management-no bandage of
eye, dark goggles in light, care not to
spread it, clean hands, not to share towel,
handerchief, pillow and fomites
*Chlamydial conjuctivitis:
Mode of transmission- sexual transmission
Common mode through swimming
pool(swimming pool conjuctivitis)
Mother to baby

Clinical- follicular hypertrophy

Investigations-
- immuno-fluorescent using monoclonal
antibodies
-cervical or urethral specimen
-PCR, DNA probe, ELISA

*Viral:
Serous or cleary watery discharge
Follicular conjuctivitis

Epidemic keratoconjuctivitis: adenovirus

*Haemorrhagic conjuctivitis:
picornavirus(coxsackie and entero)
Subconjuctival haemmorhages and
lymphadenopathy

*Chronic infective conjuctivitis:-

Trachoma:
Etiology- chlamydia trachomatis
Predisposing factors-
1. Age-1st few years of life
2. Gender-female
3. Environment-unhyeginic, crowded
4. Source-fingers, towels, flies

Symptoms- irritation, foreign body sensation,

discharge, blurring, severe loss of vision.
Signs- congestion, follicles, papillae
“trachomatous follicle” essential lesion

Cornea- keratitis(superficial)
- trachomatous pannus(lymphoid
aggregration and vascularization)
- corneal ulcers
Sequelae- corneal ulcer
- distortion of lid(trachomatous
ptosis, drooping upper lid)

Diagnosis- micro immunofluorescent

- culture(expensive)
Stages I to IV

*Granulomatous conjuctivitis:-
Unilateral with localized granuloma
*Parinaud oculoglandular syndrome:-
Unilateral conjuctivitis associated with
Unilateral lymphadenopathy and fever(with
skin rash) caused by tularemia, TB, mumps,
fungal infection, syphilis.

*Cat-scratch disease:-
H/o being licked and scratched by cat 2 weeks
before symptoms
Treatment supportive- resolve in 4-6 weeks
-topical gentamycin and oral antibiotics
*Tuberculosis of conjuctiva:-
-rare
-young adults
Clinical features- multiple conuctival ulcers
- follicular conjuctivitis
- tuberculoma at the limbus
Investigations- ZN stain-AFB
Bx- langhan’s granuloma
Treatment- excision or
- scrapping and cautery
- systemic antituberculour drugs
*Syphilis:-
-rare
-by oral lesion contact
-primary chancre

*Tularemia:-
Francisella tularensis(deer, cattle, sheep,
squirrel, rabbit)
-by direct skin contact or
-insect vector(ticks and flies)
Clinical features- ulcers and nodules with
lymphadenopathy
- fever, headache

*Fungal conjuctivitis:-
Aspergillous, candida albicans, nocardia,
leptothrix
-follicular conjuctivitis with lymphadenopathy

Treatment- Topical miconazole

#Non-infectious conjuctivitis:

*Allergic conjuctivitis:-
-seasonal allergic or ‘hay fever’ conjuctivitis
-perennial allergic conjuctivitis
-keratoconjuctivitis
-atopic keratoconjuctivitis
-giant papillary conjuctivitis
-contact dermatokeratoconjuctivitis
Etiopathogenesis-
Type- I hypersensitivity reactions to pollens
and other exogenous allergens mediated by
IgE. Sometimes bacterial protein can be
allergen(endogenous)
-fever
-conjuctivitis
-increased IgE level
-itching, redness and watery sectretion
Rx- elimination of allergen
- eye decongestant
- short course of steroid in severe cases

*Immune mediated conjuctivitis:-

Many systemic diseases
Erythema multiforme

*Toxic and chemical conjuctivitis:-

-by type IV hypersensitivity reaction
-many drugs, preservations of drops
Degenerative changes in conjuctiva:
Concretions (lithiaris):-
minute, hard, yellow spots in conjuctiva.
Etiology- collection of epithelial cells and
mucus in depression called Henle glands.
Clinical features- foreign body sensation
- elderly with trachoma
Treatment- Remove with sharp needle
Pinguecula:-
triangular patch on conjuctiva
Etiology- hyaline infiltration and elastotic
degeneration.
Clinical features- elderly, who are exposed to
sunlight, dust, wind etc…
-it is yellow fat-like.(pinguis-fat)
No treatment
Pterygium:-
triangular encroachment of the vascularized
granulation tissue covered by conjuctiva
Etiopathogenesis- degenerative condition of
subconjuctival tissue
Clinical features-frequently follows
pinguecula
-often bilateral, usually on the nasal side
-visual impairment
Treatment- no treatment, removal leads to
scar
Cysts and tumours:-
-dermoid -lymphomas
-papilloma -kaposi’s sarcoma
-granulomata -pigmented tumor
-squamous cell carcinoma -naevi
-basal cell carcinoma -melanosis
-melanoma
Dry eye syndromes:
Xerosis:-
dry, lustreless conjuctiva due to deficiency of
mucin
1. Local ocular effect- conjuctival degeneration
2. General diseases- vitamin A
deficiency(Bitot spot)
Treatment- artificial tears
- mucomimetic drugs
- dark glass
- if vitamin A deficiency- supplementation
Keratoconjuctivitis sicca (Sjogren’s
syndrome)
-due to deficiency of lacrimal secretion
-autoimmune, post menopausal associated
with RA
Lacrimal gland and salivary gland fibrosis and
lymphocyte infiltration.
-dry eye, dry mouth
Dry eye:-
1. Deficiency of tears, sjogren’s syndrome
2. Deficiency of conjuctival mucus
3. Altered corneal surface due to disease \
Treatment- tear supplement
- preservation of natural tear by
occlusion of puncta
Diseases of cornea:
Important because they cause permanent
opacities which diminish visual accuity and
complications lead to complete loss of vision.
Keratitis- inflammation of cornea
Abrasion- loss of epithelium without
inflammation
Ulcer- loss of epithelium without inflammation
of surrounding tissue
Scar- final outcome of inflammation. It is white
and opaque (instead of transparent)
Corneal opacities:-
Nebula- slight opacity
- details of iris can be seen through
opacity
Macula- more dense
- details of iris cannot be seen but
margins of iris and pupils are visible
Leucoma- very dense
- no details of iris and pupils can be
seen
Corneal edema:-
First in epithelium due to fluid collection
between the cells alter refractive conditions.
If edema lasts for long period, epithelium
turns into vesicle-produces pain.
Edema is common in inflammation,
degeneration, glucoma
Hypopyon:-
Collection of pus cells in severe corneal ulcers.
Cornea may be affected by infection, injury,
inflammation, dystrophy, degeneration or
tumour.
Clinical features- decreased vision
- lacrimation
- redness
- photophobia(discomfort on exposure to
bright light)
- foreign body sensation
- pain
- whiteness of cornea

Signs- loss of transparency with decreased

vision
- congestion surrounding cornea
- loss of smoothness of the surface
- vascularization
- change in shape, thickness and curvature
- nodules or growth on surface
External examination done by
-torch
-magnifying loops
-slit lamps
Surface irregularities by corneal reflex
Measure of curvature by keratometry
Corneal thickness by manual pachymeter,
ultrasonic pachymeter and slit scanning
topography
Inflammation(keratitis):-
1. Exogenous- including organisms present in
conjuctiva
2. Endogenous- immunologic( persist for long
period as cornea is avascular)
- hypersensitivity
- autoimmune
common near margin so marginal keratitis or
marginal corneal ulcers.
3. Contagious spread from ocular tissues:
Conjuctiva to corneal epithelium
Sclera to corneal stroma
Uveal tract to corneal endothelium

Clinically they are divided

~Based on location- superficial
- deep
~Based on nature- infection
- immune
- degenerative
- neoplastic
- traumatic
Infections affecting cornea:
a) Suppurative or non-suppurative
b) Ulcerative or non-ulcerative
c) Bacterial or viral or fungal or parasitic

Superficial involves epithelium

Deep involves stroma as well
• Loss of corneal sensation:-
When damage to corneal nerve as seen in herpes
simplex or herpes zoster and lesion affecting
opthalmic division of trigeminal nerve.

• Infectious keratitis and corneal ulcer:-

Symptoms- pain, lacrimation, photophobia and
diminished vision.
Signs- red eye with loss of vision, conjuctival
and circumcorneal, hazy cornea that stains
with fluorescein dye.
-slit lamp examination and graded according
to size, area of infiltration and depth(mild,
moderate, severe)

Diagnosis- Corneal scrapping

- gram and giemsa stain
- culture and sensitivity
Bacterial ulcers:-
 purulent keratitis
 always exogenous
 Pseudomonas, Staph. aureus
 Pneumococcus
 N. gonorrhoea
 E. coli
Only N. gonorrhoea and C. diptheria can
invade intact epithelium. Most other
bacteria produce ulceration when
epithelium is damaged.
Stages
-progressive stage
-keratouveitis
-hypopyon
-regressive stage
-healing process, cicatrization and corneal
scar
Fungal corneal infection:-
Mycotic or fungal keratitis
-in rural areas
-tropical countries
-immunocompromised person

Organisms- aspergillus, candida albicans

Mode of infection- vegetable matter

injury(thorn, wooden stick)
Symptoms- very mild

Signs- inflammatory ulcers with feathery

margin
- hypopyon
- immune ring around ulcer(Wesseley)
- satellite lesions
- ciliary and conjuctival congestion but
pain, watering and photophobia are less.
Complications of corneal ulcers:

1. Keratectasia:-
Superficial ulcers heal with scarring.
Deep ulcers- loss of tissue and thinning at ulcer
site so bulge under normal IOP- ‘ectatic
cicatrix’

• 2. Keratocele or descemetocele:-
Herniation of descemet’s membrane through
ulcer
3. Perforation:- by coughing, sneezing,
straining at stool
4. Secondary glucoma:-
5. Anterior capsular catract:-
6. Spontaneous expulsion of lens and vitreous
7. Intraocular haemorrhage

Treatment- control infection

- symptomatic relief
- cleanliness, heat, rest and
protection
Viral infections of cornea:-
Herpes zoster, adenovirus, chlamydia
trachomatis
Clinical features- multiple superficial
erosions
- superficial punctuate
keratitis

Treatment- topical and systemic antiviral

Parasitic infestation of cornea:-
 Acanthamoebic keratitis
 due to soft lens wearing(saline solution
used)
 swimming or bathing in contaminated
water.
Severe ocular pain
Treatment- topical treatment
Helminthic infection:-
Onchocerciasis- snow flake corneal opacities

• Immune mediated diseases:-

o Phlyctenular keratitis: following conjuctival
affection
 allergic reaction to endogenous, commonly
tuberculoprotein
o Acne rosacea: elderly women, ocular
irritability and lacrimation, conjuctivitis
+small corneal ulcers
Marginal ulcers(near limbus):-
 old age, immune reactions to toxin to staphy.
resting in conjuctiva or lid.
Treatment- antibiotics, hot fermentation lid
massage and clearing.

• Chronic serpiginous ulcers(rodent ulcers):-

 rare degenerative, starting at margin and
spreading circumferentially.
 autoimmune lysis of epithelium
 severe and persistent neuralgic pain and
 small grey ulcers
Treatment- difficult as ischemia is underlying
cause.
• Intestitial keratitis:-
Stromal inflammation
Possible causes- measles, typhoid, syphilis,
TB
Cogan syndrome- keratitis+ deafness(young)
Syphilis
Corneal dystrophies:-
-non inflammatory, herediatry corneal
disorder characterized by bilateral, non
vascularized corneal opacities.
-Epithelial and subepithelial
dystrophies(adult)
-Bowman layer dystrophies- autosomal
dominant
- childhood,
recurrent corneal dystrophies
-Stromal corneal dystrophies- bilateral, at
puberty, affect central cornea
-Endothelial dystrophies- in elderly, stromal
edema

• Degenerative changes:-
-non herediatory and unilateral
1) Primary degeneration
2) Secondary degeneration
3) Infiltration associated with metabolic
disturbances
Ectatic conditions:-
o Keratoconus(conical cornea):
Etiology- congenital weakness of cornea but
manifests after puberty
- or secondary to trauma

Signs- centrally thin

- visual impairment
- conical cornea(Munsen sign)
Treatment- initially specs but contact lens are
more benificial
o Keratoglobus:
-congenital
-spherical protusion of whole cornea, bilateral
-familial and herediatory

• Miscellaneous conditions:-
o Vitamin A deficiency and keratomalacia:
-developing countries
-early in life, bilateral
-dull, insensitive, hazy and yellow infiltrate
lastly necrosis
-no inflammation
-severely affected kids cannot close the eye,
cornea is exposed and secondary bacterial
infection.
Treatment- 3 doses of vitamin A, 1st on
admission, 2nd on 24 hrs and 3rd at 2nd week.

o Exposure keratopathy:
In eye insufficiently covered by
lid(logophthalmos)
o Neurotrophic keratopathy:
Trigeminal nerve paralysis

o Neuroparalytic:
Bell’s palsy, leprosy
Sclera
Three parts- episclera, sclera proper and
lamina fusca
Inflammation:-
Superficial- episcleritis
Deep- scleritis
o Episcleritis:
Etiopathology- after allergic to endogenous
toxins
-collagenous diseases(RA)
Clinical features- young female, redness, mild
pain in one or both eyes, no discharge.
1)Simple or diffuse episcleritis- diffuse redness
of one or both the eyes.
2)Nodular episcleritis- circumscribed nodule,
hard, tender and immobile
-composed of lymphocytes
-no pain, only discomfort
o Scleritis:
-usually bilateral
-associated with RA, polyarteritis nodosa,
SLE, ankylosing spondylitis, wegner’s
granulomatosis

Symptoms- pain, redness, watering,

discharge, bluish discolouration

Signs- in nodular scleritis, one or more

nodules.
o Posterior scleritis:
-may be extension of anterior scleritis
-or occurs as inflammation of posterior sclera
Clinical features- decrease vision
with/without pain, restricted ocular
movement

o Specific inflammatory disease associated

with scleritis:
*Collagen vascular disease: RA
*Infections: - TB
- suppurative bacterial infections
pseudomonas
- staphyloma
- weakening of eye ball
Tumors:-
o Choriostoma(benign):
Presence of normal tissue at abnormal site.
o Malignant:
Secondary involvement by retinoblastoma
malignant melanoma
lacrimal gland tumors

Congenital abnormalities:-
o Blue sclera: (may be seen in families with
osteogenesis imperfecta) associated with
frequent bone fractures and deafness.

 Uveal tract:
-iris is responsible for metabolism of anterior
segment.
-it is affected by vascular, immune and
infectious disease.

• Granulomatous iridocyclitis:-
Keratin precipitates in cornea and iris
• Granulomatous uveitis:-
Type IV hypersensitivity
• Non granulomatous uveitis:-
Etiopathogenesis of uveitis-
• Inflammatory: - infection
- immunologic
a) Infective exogenous infection
-through perforating wound or ulcer
-acute suppurative iridocyclitis
b) Secondary infection
-from ocular tissues like cornea, sclera or retina
c) Endogenous infection
-from other organ to eye by bloodstream
Eg. TB, syphilis, gonorrhoea, influenza in
iridocyclitis
d) Immune related inflammation

Clinical features-
• Anterior uveitis: hyperemia
• Iritis: -leads to pupil contraction, swollen
iris with impaired movement
-extravasated fluid causes irritation of muscle
and sphincter overcome the action of dilator
muscle and contraction of pupil.
-increase IOP
-repeated attacks of iris leads to atrophy of
iris
-iritis is mistaken as acute glucoma
(Treatment of both is opposite)

Cyclitis:-
-iridocyclitis(chronic)
-extremely chronic disease
-decrease vision with few physical signs
Treatment- In anterior uveitis,
-dilatation of pupil
-relaxation of ciliary muscles
-control of inflammation
-immunosuppression in some cases

Panopthalmitis:-
whole eye involved by inflammation.
In deep injury, vitreous is first
affected(endopthalmitis)
Specific type of uveitis:-

• Bacterial uveitis:
1) TB
2) leprosy
3) brucellosis
4) syphilis
5) viral uveitis (cytomegalo, herpes, rubela,
HIV, EB, influenza)
Acute retinal necrosis(ARN) severe viral
infection in AIDS, immunocompromised or
immunosupressive treatment.
6) fungal- coccidiodides, Histoplasma
capsulatum
7) parasitic
8) onchocerciasis
9) immunological uveitis
-anykylosing spondylitis
-juvenile chronic arthritis
10) uveitis associated with vitiliogo, poliosis
and deafness (Vogt-koyanagi-harada
syndrome)

Vascular disease:-
Neovascularisation in diabetic retinopathy or
central retinal vein obstruction.

Degenerative disease:-
-essential atrophy of iris(loss of vision)
-pigment dispersion syndrome
-secondary choroidal degeneration
-primary choroidal degeneration
-essential atrophy of choroid
-age related macular degeneration(ARMD)

Congenital abnormalities:-
-both iris are of different colour
(heterochromia iridium) or parts of same
iris (heterochromia iridis)
-brown patches(benign melanomata)
-nasal side displaced pupil (correctopia)
-holes in iris other than pupil (polycoria)
-absent iris (aniridia)
-albinism (pink iris) (tyrosinase deficiency)
decrease photophobia, defective vision