Red Eyes

Anatomy and Physiology

• The conjunctiva is a transparent loose connective tissue that covers
the surface of the eyeball (bulbar conjunctiva) and reflects back upon
itself to form the inner layer of the eyelid (palpebral conjunctiva).
• This tissue firmly adheres to the sclera at the limbus, where it meets
the cornea (corneoscleral limbus).
• The accessory lacrimal glands (Krause and Wolfring), along with
goblet cells, are contained within the conjunctiva and are responsible
for keeping the eye lubricated and allows the eyelids to open and
close easily.
Anatomically, it is divided into the following:
• The palpebral conjunctiva
Starts at the mucocutaneous junction of the lid margins and is firmly
attached to the posterior tarsal plates. The tarsal blood vessels are
vertically orientated.
• The forniceal conjunctiva
Loose and redundant.
• The bulbar conjunctiva
Covers the anterior sclera, continuous with the corneal epithelium at
the limbus.
Blood supply:
• Anterior and Posterior conjunctiva arteries and veins.

Lymphatic Drainage:
• Preauricular and submandibular lymph nodes.

Nerve Supply
It is supplied by two different sets of nerves:
1. Sensory nerves—These are branches of ophthalmic and maxillary division
of the 5th cranial nerve.
2. Sympathetic nerves—These are derived from the sympathetic plexus.
Conjunctiva
1. Acute Conjunctivitis
2. Allergic Conjunctivitis
3. Ophthalmia neonatorum
4. Pterygium
5. Subconjunctiva haemorrhage
6. Dry eyes
7. Subtarsal foreign body
Conjunctivitis = Conjunctival Inflammation
Discharge
• It consists of serous exudate, epithelial debris, mucus and tears.
• Watery—It is present in acute allergic and viral conjunctivitis.
• Mucin—It is seen in spring catarrh and keratoconjunctivitis sicca.
• Mucopurulent—It is present in mild bacterial infection and chlamydial
infection.
• Purulent—It is seen in severe acute bacterial infection.
Conjunctival Reactions
• Hyperaemia—It is seen maximum in the fornices and minimum at the
limbus. It is due to congestion of the conjunctival vessels.
• Oedema and chemosis—It is due to swelling of the conjunctiva as a
result of exudation from capillaries. It is seen maximum in the
fornices and the bulbar conjunctiva as they are lax.
• Follicle—There is lymphoid hyperplasia with a germinal centre. They
are usually multiple, discrete, slightly elevated, round, measuring 0.5-
5 mm in size.
• Papilla—It is a vascular structure invaded by the inflammatory cells.
Diphtherial, β-haemolytic Pneumococcal, streptococcal,
streptococcal conjunctivitis. gonococcal, adenovirus & autoimmune
conjunctivitis
Clinical Presentation
• Itching and burning or a gritty,
• Foreign-body sensation.
• Pus sliding may distort vision (normal visual acuity)
Diagnosis and Treatment
Dx confirmed by:
• Bacteriological examination
• Histological examination of the secretion and scrapings of the
epithelium
• Conjunctival culture

Treatment:
• Antibiotic drops (days)
• Antibiotic ointments (night)
Acute Mucopurulent Conjunctivitis
• It is caused by several organisms such as Staphylococcus,
Streptococcus, Pneumococcus, Haemophilus aegyptius, adenovirus,
etc.
• It is often associated with measles and scarlet fever.
Symptoms
1. There is redness and grittiness (foreign body sensation)
2. Mucopurulent discharge and crusting is present in the fornices and
margins of lids.
3. There is sticking together of lids specially in the morning because of
accumulation of mucous discharge during the night.
4. Coloured halos due to flakes of mucus passing across the cornea may
be present.
Signs
1. Conjunctival congestion is always present. The conjunctiva is fiery
red (pink eye or red eye).
2. Chemosis and subconjunctival hemorrhage may be present.
Treatment
1. Cleanliness—Frequent washing of the eyes with warm saline or clean
water.
2. Control of infection
i. Frequent instillation of appropriate bacteriostatic antibiotic eye drops and
application of eye ointment at bedtime (culture and sensitivity from
conjunctival swab)
ii. Eyes should not be bandaged as this prevents the free exit of secretion and
encourage bacterial growth due to warmth and stasis.
iii. In case of photophobia, dark glasses or an eye shade may be worn.
Prophylaxis
1. Isolation of the patient should be done when possible.
2. Avoid using the patients towel or other fomites.
3. Avoid contact with the infected eye as it is highly contagious.
4. Patient must keep his hands clean by washing them often.
Acute Purulent Conjunctivitis
• In adult
• Caused by gonococcus but same clinical picture may be seen with
Staphylococcus, Streptococcus diphtheriae, Chlamydia oculogenitalis
and in mixed infections.
• Occurs in males commonly on right eyes first.
• Associated infection in the genital area and urethritis
• Incubation period is from a few hours to 3 days.
Symptoms
1. Acute onset with swelling of the lids and conjunctiva.
2. Purulent discharge is present at lid borders, canthi and fornices.
3. Constitutional disturbances including fever.
Signs
1. Marked conjunctival congestion & palpebral conjunctiva is red.
2. Severe chemosis and pus discharge are present.
3. Swollen, red, tense and tender lids.
4. Pseudomembrane over palpebral conjunctiva may be seen rarely.
5. Preauricular lymphadenopathy may be present.
Treatment
1. Frequent washing of the conjunctival sac with warm saline.
2. Instillation of aqueous solution of benzyl penicillin drops (10,000
units per ml) every minute × half an hour. Later it can be continued 4
hourly × 3 days.
3. If allergic to penicillin, ciprofloxacin, tobramycin gentamicin,
tetracycline or any other suitable antibiotics are instilled every few
minutes initially. Later on they are applied four times daily.
4. Atropine is applied if there is corneal involvement and associated
iritis.
Prophylaxis
1. Protect the other eye by protective covering and topical antibiotics.
2. Isolation of the patient should be done.
Allergic Conjunctivitis
• Allergic conjunctivitis is an inflammatory response occurs due o
immunologic responses (major type I hypersensitivity reactions) triggered
by various allergens.

• Subclassified into:
1) Seasonal allergic conjunctivitis (SAC)
2) Perennial allergic conjunctivitis (PAC)
3) Atopic keratoconjunctivitis (AKC)
4) Giant papillary conjunctivitis (GPC)
5) Limbal and tarsal vernal keratoconjunctivitis (VKC)
Classification
Vernal - of appropriate to spring
Atopic - denoting a form of allergy or hypersensitivity reaction
Perennial - chronic, year round

Allergic conjunctivitis
• without involvement of the cornea:
• Symptom duration ~24 hours - acute allergic conjunctivitis
• Symptoms occurring during one season - seasonal allergic conjunctivitis (SAC)
• Symptoms occurring throughout all seasons - perennial allergic conjunctivitis (PAC)
• with involvement of the cornea:
• Vernal keratoconjunctivitis (VKC)
• Atopic keratoconjunctivitis (AKC)
Signs and symptoms
1. Itching (prominent)
2. Watery secretion (mucoid)
3. Redness swollen lid
4. Marked congestion with multiple follicles.

Diagnosis: Made by thorough history and careful clinical

observation.
• Personal or family history of atopic disease, such as allergic rhinitis,
bronchial asthma and atopic dermatitis.
Seasonal/Perennial conjunctivitis

• Bilateral conjunctival injection

• Chemosis
• watery discharge (mucous)
Atopic keratoconjunctivits (AKC)

• Bilateral conjunctival injection with associated eczematoid belpharitis,

watery/mucoid discharge, and boggy edema.
• Papillary hypertrophy of superior or inferior tarsal conjunctival can
occur with increased risk for eyelid thickening and scarring.
• Can develop loss of eyelashes, conjunctival scarring, corneal
neovascularization, ulcers or scars, punctate epithelial keratitis and
associated keratoconus anterior/posterior subcapsular cataracts
(severe)
Giant papillary conjunctivitis (GPC)
• The laterality of symptoms is associated with contact lens, suture, or
prostheses wear pattern.
• Have papillary hypertrophy of the superior tarsal conjunctiva.
• In long-standing, (untreated) the papillae will develop white fibrotic
centers.
• In severe cases, patients will have lid swelling and ptosis.

Itching (foreign object sensation)

Eye redness
Excess mucus
Swelling
Vernal keratoconjunctivitis (VKC)

• Bilateral bulbar conjunctival injection with associated watery mucoid

discharge.
• Giant papillary hypertrophy of only the superior tarsal conjunctiva,
resembling “cobblestones”.
• Specific findings that help differentiate VKC from AKC are: limbal
(Horner-Trantas) dots which are small white-yellow chalky
concretions around the corneal limbus; corneal vernal plaques; or
shield (Togby’s) shaped ulcers of the cornea.
Treatment
Seasonal/Perennial Allergic Conjunctivitis
Topical drops
• First line: Over-the-counter antihistamine/vasoconstrictor
agent. drops for allergi
• Second line: Second-generation topical histamine H1-receptor
antagonist.
• Third line: recurrent/persistent - mast-cell stabilizers can be used
Combined medications can also be used: low potency Corticosteroid,
NSAID
Oral antihistamines
Treatment
Vernal/Atopic Keratoconjunctivitis
• Although the disease process is more advanced in both VKC and AKC, the
general treatment similar to of SAC/PAC.
• However, if an acute exacerbation occurs, topical corticosteroids are often
added to reduce inflammation. Another adjunctive therapy is addition of
topical cyclosporin 2%.
• If the VKC or AKC is not responsive to topical therapy, supratarsal injection
of corticosteroid can be considered.

Giant Papillary Conjunctivitis

• Management in GPC is modifying the causative entity.
• Removal or replacement of sutures, rotating the knots, or using a
therapeutic contact lens.
Ophthalmia Neonatorum
• Neonatal conjunctivitis is defined as conjunctival inflammation
occurring within the first 30 days of life
• It is a preventable disease occurring in newborn babies.
Etiology
1. Chemical (ophthalmic silver nitrate)
2. Bacterial (C. trachomatis most common, Neisseria gonnorhea,
S. aureus)
3. Viral HSV)
Incidence
1. It is bilateral usually.
2. It commonly occurs in the newborns due to maternal infection.
Signs and symptoms
C.trachomatis
• Presentation may range from mild hyperemia with scant mucoid
discharge to eyelid swelling, chemosis, and pseudomembrane
formation.
N.gonorrhea
• Presents with acute conjunctivitis, associated with chemosis,
severe lid edema, and mucopurulent discharge.
• Corneal involvement (serious complication):
• Diffuse epithelial edema and ulceration  perforation of the cornea
and endophthalmitis
Treatment
• It is same as for adults. Topical therapy is supplemented by parenteral
penicillin or newer cephalosporin (cefotaxime) for 3-5 days

Prophylaxis
1. Aseptic delivery using gloves and sterile technique.
2. Proper antenatal care and treatment of any vaginal discharge prior to
delivery.
3. Instil penicillin or broad spectrum antibiotic eyedrops immediately
after birth.
Pterygium
• Ocular surface lesion originating in the limbal conjunctiva within the
palpebral fissure with progressive involvement of the cornea.
• The lesion occurs more frequently at the nasal limbus than the
temporal with a characteristic wing-like appearance.
• The etiology is unknown. Associated with a history of increased UV
exposure.
Symptoms
• Though frequently asymptomatic.
• Can become inflamed and cause ocular surface irritation.
• As the lesion progresses vision may be affected by induction of
astigmatism or obscuration of the visual axis.
Signs
• Fibrovascular conjunctival growth within the palpebral fissure extending to
the corneal surface
• Triangular shape with the apex, extending onto the cornea
• A thin translucent membrane or significantly thickened with an elevated
mound of gelatinous material.
• Raised lesion, white to pink in color depending on vascularity
• Ranges from a fine transparent area with very mild elevation, few vessels,
and minimal corneal involvement in the early stages to a thick opaque
vascular growth extending to the visual axis in later stages.
• Pinguecula are often present in the ipsilateral or contralateral eye
• A pigmented epithelial iron line (Stocker’s line) adjacent to a pterygium is
evidence of chronicity.
Diagnosis
made by slit-lamp examination of the typical limbal growth at the
characteristic location within the palpebral fissure. Often clear clinically,
but histopathologic confirmation is performed routinely.
Management
Medical
1. Vasoconstrictor drops
2. Lubricating drops and ointments
Surgery
1. Excision: simple excision or simple conjunctival closure will result in
a recurrence rate as high as 80% and is now considered
unacceptable.
2. Conjunctival Flap/Graft : this is considered the Gold Standard of
care and carries an approximate rate of recurrence of 5-10% with
minimal complications.
 Subconjunctival Haemorrhage (Ecchymosis)
• Rupture of conjunctival blood vessel causes a bright red, sharply delineated
area surrounded by normal looking conjunctiva. Subconjunctival
haemorrhage is common since the conjunctival vessels are loosely
supported.
Etiology
There is rupture of small blood vessels in the conjunctiva due to :
• Minor injury to the eyeball and orbit
• Spontaneous/haemorrhage.
• Severe conjunctivitis due to, e.g. pneumococcus, adenovirus, etc.
• Mechanical straining, e.g. vomiting, whooping cough lifting heavy weight,
etc.
• Bleeding disorder, e.g. purpura, scurvy, leukemia, etc.
• Head injury, e.g. fracture of the base of skull
• Prolonged pressure on thorax and abdomen leads to venous congestion.
Symptom
• Red eye is the most predominant feature.

Sign
• Fresh bright red blood is visible under the conjunctiva.

Course
• i. At first it is bright red in colour (oxyhaemoglobin).
• ii. Subsequently, it looks blackish—red or orange-yellow. This is
• due to the breakdown of oxyhaemoglobin.
• iii. Ultimately it gets absorbed within 2-3 weeks depending on the
amount of haemorrhage.
Treatment
• 1. Assurance is given to the patient that it is not a serious condition
by itself.
• 2. No treatment is required as blood gets absorbed in 1-3 weeks.
• 3. Vitamin C may help in healing process.
• 4. Cold fomentation is given to stop further bleeding.
 Xerosis [Dry eye]

• It is a dry, lustreless condition of the conjunctiva due to the unstable tear

film, exposing the conjunctival and corneal epithelium to evaporation.
• The tear film consists of three layers:
i. Outer lipid layer—It is secreted by the meibomian and Zeis glands. It
retards the evaporation of aqueous layer and lubricates the eyelids.
ii. Middle aqueous layer—It is secreted by the lacrimal and accessory
lacrimal glands. It supplies atmospheric oxygen to cornea, has antibacterial
function and washes away debris.
iii. Inner mucin layer—It is secreted by goblet cells, glands of Henle and
Manz. It makes the corneal surface hydrophilic so that tear film sticks to
cornea.
Etiology
1. Deficiency of tears—It is the most common cause of dry eye.
i. Sjögren’s syndrome (keratoconjunctivitis sicca)
ii. Senile or ideopathic atrophy of the lacrimal gland
2. Deficiency of conjunctival mucus—It occurs due to the scarring of the
conjunctiva resulting in the destruction of goblet cells which secret mucus as in.
i. Trachoma
ii. Vitamin A deficiency
iii. Burns—chemical, thermal, radiation
iv. Stevens-Johnson syndrome
v. Ocular pemphigoid
vi. Erythema multiforme
vii. Drug induced—Sulfonamides, epinephrine, etc.
3. Irregular corneal surface—It results in poor wetting of cornea as in healed
corneal ulcer.
4. Insufficient resurfacing of the cornea—It occurs in lid paralysis (facial nerve
palsy), proptosis and decreased blink rate in very sick and morbid patients.
5. Lipid layer abnormality
i. Chronic blepharitis
ii. Acne rosacea
6. Visual display terminal syndrome (VDTS)
It is seen in contact lens and computer users.
Keratoconjunctivitis Sicca (Sjögren’s Syndrome)
• It is an autoimmune disease which results in the fibrosis of the
lacrimal glands.
• It occurs in women after menopause usually female to male ratio of
9:1.
• It is often associated with rheumatoid arthritis and presence of
antinuclear antibody.
Superficial foreign body (Subtarsal)
• Small foreign bodies such as particles of steel, coal or sand often
impact on the corneal or conjunctival surface.
• They may be washed along the tear film into the lacrimal drainage
system or adhere to the superior tarsal conjunctiva and abrade the
cornea with every blink, when a pathognomonic vertical pattern of
linear corneal abrasions may be seen.
• Occasionally a barbed foreign body, such as an insect or plant
material will become deeply embedded, with resultant substantial
discomfort.

Barbed insect leg embedded

in the subtarsal conjunctiva
Corneal
Clinical features
• Marked ocular grittiness is characteristic.
• Leukocytic infiltration is typically seen around the embedded foreign
body (Fig. 21.27C), and ferrous particles in situ for even a few hours
cause rust staining of the bed of the abrasion (Fig. 21.27D). Mild
secondary uveitis may occur, with associated irritative miosis and
photophobia.
Recently embedded foreign body
with mild surrounding cellular
infiltration

Rust ring after removal of

metallic foreign body
 Cornea

• Transparent, elliptical, smooth shiny surface

• Avascular structure
• Nutrition from Average diameter- 11-
-perilimbal blood vessel 12mm
thickness: 0.52mm
-aqueous humor
(central), 0.67 (peripheral)
-atmospheric air oxygen

• Nerve supply: ophthalmic division of 5th CN

The cornea (Figure 1.5 ) is 0.5 mm thick and comprises:

• The epithelium , an anterior non - keratinized squamous layer,

• Bowman’s membrane- collagen fibril that does not

regenerate when damaged> opacity

• An underlying stroma of collagen fibrils, ground substance

and fibroblasts. The regular packing, small diameter and
narrow separation of the collagen fibrils account for corneal
transparency. This orderly architecture is maintained by
regulating stromal hydration.
• Descemet’s membrane- thin but strong homogenous elastic
membrane that can regenerate
• The endothelium , a monolayer of non - regenerating cells
which actively pump ions and water from the stroma,
controlling corneal hydration and hence transparency.
Function of cornea
• It protects the internal ocular structures.
• Together with the lens, it refracts and focuses light onto the retina.
The junction between the ambient air and the curved surface of the
cornea, covered by its optically smooth tear film, forms a powerful
refractive interface.
Cornea
Keratitis
Corneal ulcer
Abrasion
Foreign body
Bacterial keratitis
Protection of eye
• blinking
• washing away of debris by the flow of tears;
• entrapment of foreign particles by mucus;
• the antibacterial properties of the tears;
• the barrier function of the corneal epithelium ( Neisseria
gonorrhoeae is the only organism that can penetrate the intact
epithelium).
Predisposing causes
• Keratoconjunctivitis sicca (dry eye);
• Breach in the corneal epithelium (e.g. following surgery or
trauma);
• Contact lens wear;
• Prolonged use of topical steroids.
 S and S

• pain, usually severe

• purulent discharge;
• ciliary injection;
• visual loss (severe if the visual axis is involved);
• hypopyon – sometimes (a mass of white cells collected in the
anterior chamber; );
• a white corneal opacity which can often be seen with the naked
eye
Management
• Scrapes are taken from the base of ulcer for Gram staining and
culture.
• Dual therapy (e.g. cefuroxime against Gram + positive bacteria and
gentamicin for Gram - negative bacteria)
• Drop gives hourly and reduce in frequency
Acanthamoeba keratitis

• freshwater amoeba
• more common with the increasing use of soft contact lenses
• A painful keratitis with prominent, infiltrated corneal nerves results
• Topical chlorhexidine, polyhexamethylene biguanide (PHMB) and
propamidine
Herpes simplex keratitis
• Type 1 for ocular disease
• Type 2 for genitalia disease can infantile chorioretinitis

• fever;
• vesicular lid lesions;
• follicular conjunctivitis;
• pre - auricular lymphadenopathy.
Couse of disease

Primary • Conjunctivitis
infection

• Virus stay
Heal and latent in
trigeminal
latent ganglion

Reactivate • Virus travels

to corneal
and keratitis epithelium
• Dendritic ulcer- pathognomonic
• Treated with antivirals
• Steroid is contraindicated (inhibit healing by fibrosis and also retard
epithelialization)
Herpes zoster ophthalmicus ( ophthalmic
shingles)
• VZV
• ophthalmic division of the trigeminal nerve is affected

• Unlike HSV, there will be prodromal period with the patient

systemically unwell

• preceded by pain and

• the appearance of vesicles in the distribution of the ophthalmic
division of the trigeminal nerve
Sign:
• lid swelling (which may be bilateral);
• keratitis;
• iritis;
• secondary glaucoma.

• Oral antiviral treatment (acyclovir, famciclovir)

• Topical steroid
• Antibiotics for 2ndary infection
 Fungal keratitis
Uncommon, it should be considered when:
• lack of response to antibacterial therapy in corneal ulceration;
• cases of trauma with vegetable matter;
• cases associated with the prolonged use of steroids.

• The corneal opacity appears fluffy, and satellite lesions may be present.
• Liquid and solid Sabouraud ’s medium is used to grow the fungi. Incubation
may need to be prolonged.
• Treatment requires topical pimaricin (natamycin) 5%.
Corneal Ulcer
• Common: bacteria, protozoa, fungal
• Less common: virus

Predisposing factor
• Epithelial damage (foreign body, misdirected eyelash)
• Virulent organism (pneumococcus, pseudomonas, gonococcus)
• Poor resistance (malnutrition, neuroparalytic keratitis, exposure of cornea
due to proptosis, keratomalacia (Dryness)

• Clinical features
• Red eye, pain, tearing, photophobia, eyelid swelling
Stages of Corneal Ulcer
There are three stages namely;
1. Progressive stage
• There is grey zone of infiltration by polymorphs.
• Localised necrosis and sloughing of sequestrum is present.
• Saucer-shaped ulcer with overhanging edges due to oedema is characteristic.
2. Regressive stage
• The dead material is thrown off and the oedema subsides.
• The floor and edges of the ulcer are smooth and transparent.
3. Healing stage
• Minute superficial vessels grow in from the limbus near the ulcer.
• There is formation of fibrous tissue which fills the gap. The irregular arrangement
of fibrous tissue results in opacity, as the new fibres refract the light irregularly. As
Bowman’s membrane never regenerates, permanent opacity remains if it is
damaged.
Complication of corneal ulcer
1) Opacity
2) Ectatic cicatrix
3) Descemetocele
4) Perforation

endophthalmitis (interior eye) , panophthalmitis, loss of vision, loss of

eye.
Complication- corneal ulcer-opacity due to scarring
Involve Bowman’s Involve half thickness of Full thickness of stroma
capsule and superficial stroma
layer of stroma

• irregular astigmatism
• stops all light which falls upon it
 Cx- cont

Ectatic Cicatrix Descemetocele

Herniation of descement membrane
Thinning of ulcer>
bulging forwards
when IOP
increase
Cx- perforation
• Etiology—Sudden strain due to cough, sneez or spasm of orbicularis
muscle may cause perforation.

• Course—The aqueous gushes out resulting in the collapse of anterior

chamber (IOP = zero). There is forward displacement of iris-lens
diaphragm. The only benefit is that the nutrition of the cornea
improves, pain is relieved and scarring takes place.
Management
Corneal scraping and culture

Control of infection
• Intensive antibiotics to control the infection(Tobramycin, ciprofloxacin, vigamox,
gentamicin, chloramphenicol)
• * use steroid is contraindicated

Dressing
• Irrigation with warm saline to wash away tissue debris, toxin, secretion, organism etc

Rest and protection

• 1% of atropine to paralyze ciliary muscle. To prevent spasm
• Pad and bandage to prevent eye movement and also protect from dust or irritant.
Treatment (Non-healing corneal ulcer)
1. Cauterization—The chemical cautery acts as an antiseptic.
i. Pure carbolic acid—It acts both as an antiseptic and caustic.
ii. Trichloracetic acid 10-20%
iii. Silver nitrate 1%. It is a mild antiseptic.
2. Paracentesis—Aqueous is released slowly by making an opening in the
lower temporal quadrant of cornea. It improves the nutrition of the cornea
by bringing in fresh aqueous. It prevents complications of spontaneous
perforation which usually occurs in the centre of the cornea involving the
visual axis.
3. Conjunctival flap—The non-healing ulcer may be covered with the
conjunctival flap.
4. Therapeutic keratoplasty—Full thickness graft is applied to enhance
healing and to prevent perforation.
5. Tarsorrhaphy—It is done in cases of neuroparalytic ulcers and exposure
keratitis.
6. Treat the underlying cause which is responsible for non-healing ulcer.
TREATMENT OF IMPENDING PERFORATION (DESCEMETOCELE)
1. Rest—Preferably bed-rest is advised.
2. Pressure pad and bandage—By applying extra pad and tight bandage over
the eye, support is given to the cornea.
3. Intraocular pressure is kept low by giving oral acetazolamide.
4. Paracentesis may be done to prevent central perforation.
5. Straining factors are avoided, e.g. coughing, sneezing or straining at
passing stool.
6. Therapeutic full thickness or penetrating keratoplasty is done as the last
resort.
TREATMENT OF CORNEAL ABSCESS
• There is a localised collection of pus in the corneal stroma. The
epithelium is usually intact and therefore the fluorescein staining is
negative. The clinical features are similar to corneal ulcer.
Treatment
1. Evacuation of pus is done first by a sterile autoclaved fine needle or
knife before starting the topical antibiotic treatment as for corneal
ulcer.
2. Cauterization done by chemical (carbolic acid) cautery is also
effective.
TREATMENT OF PERFORATED CORNEAL ULCER
1. Immediate—It depends on the site and size of perforation.
1. If perforation is small in the pupillary area and there is no prolapse of iris:
i. Rest in bed is advised.
ii. Atropine and antibiotic ointment are applied.
iii. Pressure pad and bandage helps in sealing perforation.
2. Tissue adhesives, e.g. isobutyl cyanoacrylate may be used.
3. Soft contact lens helps in the healing process.
4. Conjunctival flap covers the perforation site and aids healing.
5. Therapeutic penetrating keratoplasty may be done as a final resort.

Conjunctival flap
Foreign body object
Clinical features
• Marked ocular grittiness
• Pain, red eye
• Photophobia
• Tearing

• Leukocytic infiltration is typically seen around the embedded foreign

body
• ferrous particles in situ (rust staining)
 Management
• be carefully examined for intraocular foreign body.
• dilation of the pupil to allow a good view of the lens and retina

• A radiograph of the orbits, with the eyes looking up and then down, or
a CT scan, may also be indicated if an intraocular foreign body is
suspected

• Small, rotating burr- for metal, iron, rusting ring.

• Subtarsal objects can often be swept away with a cotton - wool bud
from the everted lid.
• The patient is then treated as for an abrasion
 Corneal abrasion
• Loss of surface epithelial of cornea

• Causes
• Injury ( fingers, fingernails, paper, mascara brushes, self-inflicted rubbing )
• Blowing dust, sand, or debris
• Extended contact lens wear
• Ocular foreign bodies embedded under an eyelid
• Iatrogenic - Unconscious patients, accidental injury by health care workers, improper
eyelid patching in patients with Bell palsy, and other neuropathies in which the eyelid
cannot be closed voluntarily
• Corneal foreign bodies - Objects difficult to see ( small glass fragments)
• Slit lamp examination with fluorescein to diagnose a
corneal abrasion in ambulatory patients; without the
magnification of the slit lamp, small abrasions can be
missed.
• If ocular penetration with a retained foreign body is
suspected, such as in a high-velocity injury (lawn mower,
string trimmer, hammering metal), then an ocular CT
scan, ocular MRI
• Tx : heal with time, Prophylactic topical antibiotic
Episcleritis
 EPISCLERITIS
• Benign recurrent inflammation of the episclera, involving the
overlying Tenon's capsule but not the underlying sclera.
• It typically affects young adults, being twice as common in women
than men.
 Etiology & Pathology
• Etiology- Exact etiology is not known.
It is found in association with gout,
rosacea and psoriasis. It has also been
considered a hypersensitivity reaction
to endogenous tubercular or
streptococcal toxins.

• Pathology- Localised lymphocytic

infiltration of episcleral tissue
associated with oedema and
congestion of overlying Tenon's
capsule and conjunctiva
Clinical Picture
• Symptoms: redness, mild ocular discomfort described as gritty,
burning or foreign body sensation
• Signs
• On examination two clinical types of episcleritis diffuse (simple)
and nodular.
• In diffuse episcleritis, although whole eye maybe involved to
some extent, the maximum inflammation is confined to one or
two quadrants
• In nodular episcleritis, a pink or purple flat nodule surrounded
by injection is seen, usually 2-3mm away from limbus is firm,
tender and the overlying conjunctiva moves freely.
Clinical course
• Episcleritis runs a limited course of 10 days to 3 weeks and resolves
spontaneously. However, recurrences are common and tend to
occur in bouts
Treatment
• usually self - limiting
• As symptoms are tiresome, topical corticosteroid eyedrops
instilled 2-3 hourly
• Cold compresses applied to the closed lids may offer symptomatic
relief from ocular discomfort.
• In rare, severe or recurrent disease, systemic NSAIDs may be
required.
• ibuprofen (2000 mg TID)
• indomethacin (25 mg three times a day)
• oxyphenbutazone
SCLERITIS
• Scleritis refers to a chronic inflammation of the sclera proper.
• More severe condition than episcleritis which may cause visual
impairment
• Incidence is much less than that of episcleritis.
• It usually occurs in elderly patients (40-70 years) involving females
more than the males.
Etiology 50% asso. connective tissue disease
• Autoimmune collagen disorders, especially rheumatoid
arthritis (most common), polyarteritis nodosa, SLE.
• Metabolic disorders like gout and thyrotoxicosis
• Some infections, particularly herpes zoster ophthalmicus,
chronic staphylococcal and streptococcal infection
• Granulomatous diseases like tuberculosis, syphilis, sarcoidosis,
leprosy
• Miscellaneous conditions like irradiation, chemical burns
• Idiopathic
 Anterior ( 98%) Posterior ( 2%)

Non-necrotising ( 85%)
Necrotising ( 13% )
• Diffuse
• With inflammation
• Nodular
• Without Inflammation
• ( Scleromalacia perforans )
Symptoms

• Patients complain of moderate to severe pain

which is deep and boring in character and often
wakes the patient early in the morning .
• Ocular pain radiates to the jaw and temple.
• It is associated with localised or diffuse redness,
mild to severe photophobia and lacrimation.
• Occasionally there occurs diminution of vision.
 Signs
• Non-necrotizing anterior diffuse scleritis
 commonest variety
 widespread involving a quadrant or more of the anterior sclera.
 The involved area is raised and salmon pink to purple in colour

• Non-necrotizing anterior nodular scleritis

 one or two hard, purplish elevated scleral nodules, usually situated near the
limbus
 Sometimes, the nodules are arranged in a ring around the limbus (annular
scleritis).

• Anterior necrotizing scleritis with inflammation

 an acute severe form of scleritis
 intense localised inflammation with areas of infarction due to vasculitis
 The affected necrosed area is thinned out and sclera becomes transparent and
ectatic with uveal tissue shining through it
 Signs
• Anterior necrotizing scleritis without inflammation (scleromalacia
perforans)
 Elderly females usually suffering from long-standing RA.
 yellowish patch of melting sclera (due to obliteration of arterial supply) which
often together with the overlying episclera and conjunctiva completely
separates from the surrounding normal sclera
 This sequestrum of sclera becomes dead white in colour, which eventually
absorbs leaving behind it a large punched out area of thin sclera through which
the uveal tissue shines

• Posterior scleritis
 inflammation involving the sclera behind the equator
 characterised by features of associated inflammation of adjacent structures,
which include: exudative retinal detachment, macular oedema, proptosis and
limitation of ocular movements
Investigations
• TLC, DLC and ESR
• Serum levels of complement (C3), immune complexes,
rheumatoid factor, antinuclear antibodies and L.E cells
for an immunological survey.
• FTA - ABS, VDRL for syphilis.
• Serum uric acid for gout.
• Urine analysis.
• Mantoux test.
• X-rays of chest, paranasal sinuses, sacroiliac joint and
orbit to rule out foreign body especially in patients with
nodular scleritis
 Treatment

Non-necrotising scleritis
• Topical steroid eyedrops,
• Systemic indomethacin
Necrotising Scleritis
• Topical steroid
• Immuno-suppresive agents: Methotrexate / cyclophos-phamide
 Anterior Chamber

• Hyphema
• Acute primary angle-closure
glaucoma
Anterior Chamber
• Hyphema = Collection of blood in the
anterior chamber
• conjunctival or scleral vessels due to minor
ocular trauma or otherwise.
Treatment.
• Most hyphemas absorb spontaneously and thus
need no treatment.
• Sometimes hyphaema may be large and associated
with rise in IOP. In such cases, IOP should be lowered
by acetazolamide and hyperosmotic agents.
• If the blood does not get absorbed in a week’s time,
then a paracentesis should be done to drain the
blood.
Acute primary angle-closure glaucoma
• An attack of acute primary angle closure glaucoma
occurs due to a sudden total angle closure leading
to severe rise in IOP.
• It usually does not terminate of its own and thus if
not treated lasts for many days
• Symptoms
• Pain. Typically acute attack is characterised by sudden onset of very
severe pain in the eye which radiates along the branches of 5th
nerve.
• Nausea, vomiting and prostrations are frequently associated with
pain.
• Rapidly progressive impairment of vision, redness, photophobia
and lacrimation develop in all cases.
• Past history. About 5 percent patients give history of typical
previous intermittent attacks of subacute angle-closure glaucoma.
Signs (Fig. 9.19)
• Lids may be oedematous
• Conjunctiva is chemosed and congested(both conjunctival and
ciliary vessels are congested)
• Cornea becomes oedematous and insensitive
• Anterior chamber is very shallow. Aqueous flare or cells may be
seen in anterior chamber
• Angle of anterior chamber is completely closed as seen on
gonioscopy (shaffer grade 0)
• Iris may be discoloured
• Pupil is semidilated, vertically oval and fixed. It is non-reactive
to both light and accommodation
• IOP is markedly elevated, usually between 40 and 70 mm of Hg,
• Optic disc is oedematous and hyperaemic
 Management
Treatment
• Medical therapy as emergency to prepare for surgical therapy.
• Systemic hyperosmotic agent Iv mannitol > reduce IOP
• Acetazolamide
• Pilocarpine eyedrops (started after the IOP is bit lower)
• Analgesics and anti-emetics
• Corticosteroid eyedrops (reduce the inflammation)

• Surgical
• Peripheral iridotomy (Re-establishes communication between
posterior and anterior chamber)
• Filtration surgery.
• Clear lens extraction
Anterior uveitis—It can be divided as follows:
• Iritis—The inflammation mainly affects the iris.
• Iridocyclitis—Iris and pars plicata part of the ciliary body are involved equally.
• Cyclitis—Pars plicata part of the ciliary body is affected predominantly.
Acute anterior uveitis (AAU) is the most common presentation, of
which HLA-B27-related and idiopathic forms make up the largest
proportion.
Chronic anterior uveitis (CAU) is less common than AAU. It is more
commonly bilateral, and associated systemic disease is more likely.
Symptoms

1.rapid onset of unilateral pain

2.Photophobia
3.redness
4.watery discharge,
5.Blurring of vision is related to severity.
SIGNS of anterior uveitis

• Circumciliary congestion
Anterior chamber: aqueous flare
Sign of anterior chamber:
Keratic precipitates on corneal endothelium
Sign of anterior chamber:
Hypophon & hyphema
white cells collected to form a fluid level in the inferior anterior chamber.
Iris sign:
Posterior synechiae
adhesion or attachment of iris to the adjacent structures
> give the pupil an irregular appearance
Iris nodules
Koeppe’s nodules are situated at the pupillary border and
may initiate posterior synechia.
Busacca’s nodules situated near the collarette are large but
less common than the Koeppe’s nodules.
1. Haematological investigations
• TLC and DLC to have a general information about inflammatory response of
body.
• ESR to ascertain existence of any chronic inflammatory condition in the body.
• Blood sugar levels to rule out diabetes mellitus.
• Blood uric acid in patients suspected of having gout.
• Serological tests for syphilis, toxoplasmosis, and histoplasmosis.
• Tests for antinuclear antibodies, Rh factor, LE cells, C-reactive proteins and
antistreptolysin
2. Urine examination for WBCs, pus cells, RBC and culture to rule out urinary
tract infections.
3. Stool examination for cyst and ova to rule out parasitic infestations.
4. Radiological investigations include X-rays of chest, paranasal sinuses,
sacroiliac joints and lumbar spine.
5. Skin tests. These include tuberculin test, Kveim’s test and toxoplasmin test.
Management
1. Atropine
2. Heat application
3. Cortocosteroid
4. Analgesic
5. Antibiotic
Vitreous, Eyelids & Orbit
Ruth
Vitreous
• The vitreous is a clear gel occupying two-thirds of the globe.
• It is 98% water. The remainder is gel-forming hyaluronic acid traversed by a fine
collagen network. There is a few cells.
• It is firmly attached anteriorly to the peripheral retina, pars plana and around the
optic disc, and less firmly to the macula and retinal vessels.
• It has a nutritive and supportive role.
• Collapse of the vitreous gel (vitreous detachment), which is common in later life,
puts traction on points of attachment and may occasionally lead to a peripheral
retinal break or hole, where the vitreous pulls off a flap of the under- lying retina
Vitreous humour
Endopthalmitis
• Endogenous results from the distant spread of organism from distant source of
infection (eg. Endocarditis)
• Blood borne organisms permeate the blood ocular barrier by direct invasion or
changes in vascular endothelial
• May be subtle as white nodules on the lens capsule, iris retina or choroid. Or
globe full of all ocular tissues – purple tea exudate
• Exogenous direct inoculation of an organism from outside as complication of
ocular surgery, foreign bodies, blunt or penetrating ocular trauma
Endopthalmitis
Endopthalmitis
• Bacterial endophthalmitis usually presents acutely with pain, redness, lid swelling,
and decreased visual acuity. Also, some bacteria (eg, Propionibacterium acnes)
may cause chronic inflammation with mild symptoms.
• This organism is typical skin flora and usually is inoculated at the time of
intraocular surgery.
• Fungal endophthalmitis may present with an indolent course over days to weeks.
Symptoms are often blurred vision, pain, and decreased visual acuity.
• A history of penetrating injury with a plant substance or soil-contaminated foreign
body may often be elicited.
• Individuals with candidal infection may present with high fever, followed several
days later by ocular symptoms.
• Persistent fever of unknown origin (FUO) may be associated with an occult
retinochoroidal fungal infiltrate.
Endopthalmitis
Symptoms may include the following:Visual symptoms in any hospitalized
patient or patient taking immunosuppressive therapy
• Visual loss
• Eye pain and irritation
• Headache
• Photophobia
• Ocular discharge
• Intense ocular and periocular inflammation
• Injected eye
• *search for chronic uveitis*
Endopthalmitis
Endogenous endophthalmitis
at risk for developing endogenous endophthalmitis usually have
comorbidities that predispose them to infection. Fungi infection>bacterial
diabetes mellitus, chronic renal failure, cardiac valvular disorders, systemic
lupus erythematosus, AIDS, leukemia, gastrointestinal malignancies,
neutropenia, lymphoma, alcoholic hepatitis, and bone marrow
transplantation.
ComplicationsComplications of endophthalmitis may include the
following:Impairment of vision
Complete loss of vision, Loss of eye architecture, Enucleation
 Disease of the vitreous causing red eyes
• Vitreous haemorrhage
• Abnormal vessels prone to bleeding, normal vessels ruptured under stress,
extension of blood from an adjacent source.
• Present as preretinal (subhyaloid) or intragel haemorrhage (anterior, middle,
posterior, or whole vitreous body)
• Painless unilateral floater (small haemorrhage)/visual loss(massive
haemorrhage), vision is worse in the morning, hx of trauma or surgery
• Indirect ophthalmoscope with sclera depression, gonioscopy, slit lamp
• Complete absorption (4-8weeks), Organization of haemorrhage (forming yellow-
white debris), complication (vitreous liquefaction, khaki cell glaucoma), retinitis
proliferans
• Bed rest, head elevation, bilateral eye patches, vitrectomy by pars plana route
(3months later)
The eyelids (tarsal plates)
• offer mechanical protection to the anterior globe
• spread the tear film over the conjunctiva and cornea with each blink;
• contain the meibomian oil glands, which provide the lipid component of the tear
film
• through closure and blinking prevent drying of the eyes
• Contain the puncta through which the tears flow into the lacrimal drainage
system.
The eyelids (tarsal plates)
They comprise:
• an anterior layer of skin
• The orbicularis muscle, innervated by the seventh nerve
• A tough collagenous layer (the tarsal plate) which houses the oil glands
• An epithelial lining, the tarsal conjunctiva, which is reflected onto the globevia
the fornices.
• Contraction of the peripheral fibres of the orbicularis muscle results in a
protective, forced eye closure, while that of the inner, palpebral muscle results in
the blink.
The eyelid
 • Entropion
• This is an inturning of the lid margin and lashes,
Eyelid diseases causing red eye
usually of the lower lid, towards the globe.
• It may occur if the patient looks downwards or be
induced by forced lid closure.
• The inturned lashes abrade the cornea and cause
marked irritation of the eye. The eye may be red.
• Short-term treatment includes the application of
lubricants to the eye or taping of the lid to turn the
lashes away from the globe. The condition can be
alleviated for a period by the injection of
botulinum toxin into the palpebral part of the
orbicularis muscle of the lower lid, or cured
permanently by surgery.
 • Ectropion
Eyelid diseases causing red eye
• there is an eversion of the lid away from the globe
• Usual causes include:• age-related orbicularis muscle
laxity; • scarring of the periorbital skin;• seventh nerve
palsy.
• The malposition of the lids everts the puncta and
prevents drainage of the tears, leading to epiphora. It
also exposes the conjunctiva and lower globe to
dehydration.
• Ectropion causes an irritable eye. Surgical treatment is
again an effective treatment.
Eyelid diseases causing red eye
Blepharitis
• This is a very common, chronic inflammation of the lid
• In anterior blepharitis inflammation is concentrated in the lash line and
accompanied by squamous debris around the eyelashes.
• The conjunctiva becomes injected. Can associated with a chronic staphylococcal
infection.
• In severe disease the cornea is affected (blepharokeratitis). Small infiltrates or
ulcers may form in the peripheral cornea (marginal keratitis) due to an immune
complex response to staphylococcal exotoxins.
• In posterior blepharitis (or meibomian gland dysfunction) the meibomian glands
are usually obstructed by squamous debris.
• The two forms may occur independently.
Eyelid diseasesSymptoms:
causing red eye
• tired, itchy, sore eyes, worse in the morning;
• crusting of the lid margins in anterior blepharitis and
redness in both.
Signs
• In anterior blepharitis there may be:
• redness and scaling of the lid margins; some lash bases
may be ulcerated – a sign of staphylococcal infection
• debris in the form of a collarette around the eyelashes
(cylindrical dan- druff). This may indicate an infestation
of the lash roots by Demodex folliculorum.
• a reduction in the number of eyelashes.
Blepharitis
Eyelid diseasesIn posterior
causing redthere
blepharitis eyemay be:
• obstruction and plugging of the meibomian orifices
• thickened, cloudy, expressed meibomian secretions
• injection of the lid margin and conjunctiva
• tear film abnormalities and punctate keratitis.
• Both forms of blepharitis are strongly associated with
seborrhoeic dermatitis, atopic eczema and acne rosacea.
• In rosacea there is hyperaemia and telangiectasia of the
facial skin and a rhinophyma (a bulbous irregular swelling
of the nose with hypertrophy of the sebaceous glands).
Eyelid diseasesIn posterior
causing redthere
blepharitis eyemay be:
• obstruction and plugging of the meibomian orifices
• thickened, cloudy, expressed meibomian secretions
• injection of the lid margin and conjunctiva
• tear film abnormalities and punctate keratitis.
• Both forms of blepharitis are strongly associated with
seborrhoeic dermatitis, atopic eczema and acne rosacea.
• In rosacea there is hyperaemia and telangiectasia of the
facial skin and a rhinophyma (a bulbous irregular swelling
of the nose with hypertrophy of the sebaceous glands).
Eyelid diseasesTreatment
causing red eye
• difficult and long-term for these chronic conditions.
• For anterior blepharitis, lid toilet with a cotton bud
wetted with bicarbonate solution or diluted baby
shampoo helps to remove squamous debris from the lash
line.
• Topical steroids can reduce inflammation but must be
used infrequently, to avoid steroid complications.
• Staphylococcal lid disease may also require therapy with
topical antibiotics (e.g. fusidic acid gel), and occasionally
with systemic antibiotics.
• Demodex infestation responds to the application of‘tea
tree oil’.
Eyelid diseasesTreatment
causing red eye
• For meibomian gland dysfunction, abnormal secretions
can be expressed bylid massage after hot bathing through
the closed lids.
• If this treatment fails, then there may be a place for
topical azithromycin drops.
• Alternatively, meibomian gland function can be improved
by short courses of oral tetracycline.
• Where meibomian gland obstruction is extensive, the
absence of an oily layer on the tear film can induce an
evaporative dry eye, which requires treatment with
artificial tears.
• Prognosis is chronic in blepharitis.
 • Preseptal cellulitis
• A preseptal cellulitis involves lid structures alone
Eyelid diseases causing red eye
• It presents with periorbital inflammation and
swelling but not the other ocular features of orbital
cellulitis.
• Eye movement is not impaired.
• An orbital mucocoele arises from accumulated
secretions within any of the paranasal sinuses
when natural drainage of the sinus is blocked.
Surgical excision may be required.
Eyelid diseases causing red eye
Trichiasis
• Common condition in which aberrant eyelashes are
directed back- wards towards the globe. It is distinct
from entropion.
• The lashes rub against the cornea and cause irritation
and abrasion. It may result from any cicatricial process.
• In developing countries, trachoma is an important
cause and trichiasis is an important basis for the
associated blindness.
Eyelid diseases causing
Lagophthalmos
completely.
red
is the eye
inability to close the eyelids

Blinking covers the eye with a thin layer of tear fluid,

thereby promoting a moist environment
The tears also flush out foreign bodies and wash
them away.
The main cause is facial nerve paralysis (paralytic
lagophthalmos), but it also occurs after trauma or
surgery (cicatricial lagophthalmos) or during sleep
(nocturnal lagophthalmos).
Ointments can be applied to the cornea once at bedtime or throughout
the day in cases of severe corneal exposure. Moisture goggles also
may be used.
Lagopthalmos
Lagopthalmos
Eyelid diseases causing
Tarsorrhaphy. ared eye
temporary tarsorrhaphy achieves
narrowing of the interpalpebral fissure.
Gold weight implantation. Gold weights can be
implanted into the upper eyelid to treat paralytic
lagophthalmos. This procedure enhances eyelid
closure in a gravity-dependent fashion.
Upper eyelid retraction and levator recession.
Recession of the upper eyelid retractors (levator and
Müller’s muscles)
Lower eyelid tightening and elevation. Laxity of
the lower eyelid may occur in conditions such as
facial nerve palsy and floppy eyelid syndrome.
The orbit
The eye lies within the bony orbit, which has the shape of a four-sided pyramid.
At its posterior apex is the optic canal, which transmits the optic nerve to the
chiasm, tract and lateral geniculate body.
The superior and inferior orbital fissures allow the passage of blood vessels and
cranial nerves which supply orbital structures.
The lacrimal gland lies anteriorly in the supe- rolateral aspect of the orbit.
On the anterior medial wall lies the fossa for the lacrimal sac.
The orbit
Orbital disease causing red eye
• Orbital cellulitis
• Orbital cellulitis is a serious condition which can cause blindness and may spread
to cause a brain abscess.
• The infection often arises from an adjacent ethmoid sinus, reflecting that the
medial wall of the orbit is extremely thin.
• The commonest causative organisms are Staphylococcus and Streptococcus.
• The patient presents with:• a painful, proptosed eye;• conjunctival injection;•
periorbital inflammation and swelling; • reduced eye movements;• possible
visual loss;• systemic illness and pyrexia.
 • An MRI or CT scan is helpful in diagnosis and in
Orbital disease causing red eye
planning treatment. The condition usually responds to
intravenous broad-spectrum antibiotics, but it may be
necessary to drain an abscess or decompress the orbit,
particularly if the optic nerve is compromised.
• Optic nerve function must be watched closely, checking
acuity, monitoring colour vision and testing for a
relative afferent pupillary defect. Orbital
decompression is usually performed with the help of an
ear, nose and throat (ENT) specialist.
 Orbital diseases resulting red eye
• Inflammatory disease
• The orbit may be involved in various inflammatory disorders, including
sarcoidosis and orbital pseudotumour, a non-specific lymphofibroblastic disorder.
• Diagnosis of such conditions is difficult. The presence of other systemic signs of
sarcoidosis may be helpful.
• If an orbital pseudotumour is suspected it may be necessary to biopsy the tissue
to differentiate the lesion from a lymphoma.