DISEASES OF THE CORNEA AND SCLERA..ppreset

Medicine

1. DISEASES OF THE CORNEA AND SCLERA.
Cornea is clear, circular transparent portion of the external coat
of the eyeball.
It is avascular structure.
SOURCE OF NUTRITION.
Prelimbal plexus of blood vessels.
Aqueous humor.
Tears.
Palphebral conjunctiva when the lids are closed.
Disease of the cornea is called keratitis – inflammation of the
cornea.

2. MODES OF INFECTIONS.
EXOGENOUS.
•Virulent organism if present in the conjunctiva may affect the
cornea.
FROM OCULAR TISSUES.
•Due to anatomical continuity, inflammation of the conjunctiva,
sclera, uveal track may affect the cornea.
ENDOGENOUS
•It is rare due to avascularity of the cornea.
•It is typically of allergic rather than metastatic in nature.

3. CORNEAL ULCERS OR PURULENT KERATITS.
ETIOLOGY
Its nearly always exogenous due to pyogenic organisms which
invade the cornea from out side.
Bacilli only that can invade the normal epithelium are;
•Gonorrhea- gonococci.
•Diphtheria- C –diphtheria.
Other bacteria are capable of producing ulceration when the
epithelium is intact like pneumococcus.

4. SOURCE OF INFECTIONS.
Injury with puddy husks.
Thorns.
Contact lens.
Locally as conjunctivitis.
Chronic dacryocystitis.
FACTORS THAT ENHENCE CORNEAL ULCER
OCCURRENCE.
•Reduction of general resistance of the host.
•Diminished corneal epithelial resistance.
•Aged individuals
•Alcoholic subjects.
•Xerosis and keratomalacia.

5. OTHER PREDISPOSING FACTORS
Corneal anesthesia as in;
•Leprosy.
•Neuroparalytic keratitis.
•Absolute glaucoma.
Lagophthalmos.
CAUSATIVE ORGANISMS.
BACTERIA.
•Pseudomonas pyocyanea
•Pneumococcus.
•Gonococcus.
•C- diphtheria, staphylococcus coagulase, streptococcus,
moraxella etc.

6. Pseudomonas pyocynea infection of the cornea is rapid,
progressive and severe which results in total destruction of the
eye.
FUNGI.
•Candida albican.
•Norcandla.
•Aspergillum fumigate.
Fungal infection of the cornea is seen in;
•Indiscriminate use and abuse of antibiotic and steroids.
•Trauma or injury with woods, sticks and puddy husks.
•So superadded infection with fungi becomes commoner.

7. VIRUSES.
•Herpes simplex.
•Herpes zoster,
PARASITE.
•Acanthameoba.
STAGES OF CORNEAL ULCER.
PROGRESSIVE STAGE.
A localized necrosis in the most anterior part of the cornea.
Sequestrum is then cast off leaving a saucer shape ulcer.
Surrounding area packed with leucocytes appearing as a gray
zone of filtration.

8. REGRESSIVE STAGE.
Polymorphornucleus leucocytes forms as a secondary defense.
Leucocytes exert their digestive functions.
CICATRIZATION STAGE.
Ulcer filled with fibrous tissue derived partly from corneal
corpuscles and growing endothelial edge.
Scar formed is not transparent and parallel as in corneal stroma
Corneal opacity (Nebula, macula and leucoma) are formed.
Sometimes a depression known as facet is developed.
If the ulcer is superficial, involves only the epithelium, no scar
will be left, but if it is deeper, scar will be left.

9. SYMPTOMS OF CORNEAL ULCER.
oPain because of exposure of fibrils of the trigeminal
nerve.
oRedness and watering due to reflex sensory
stimulation.
oBlepharospasm, forceful closure of the eyelid due to
corneal irritation.
•This reflex can be abolished by instilling local
anesthetic in the eye.
•1% atropine is used to treat corneal ulcer
photophobia.
oHeadache and blurred vision;
•Edema of the eyelids.
•Conjunctival and cillary congestion.
•Ulcer starts as a dull grayish infiltration of a localized
area of the cornea.

10. •Typical ulcer is formed as the superficial layers are
cast.
•Ulcer is surrounded by grayish infiltrations.
oHypopyon.
•Is collection of pus in the anterior chamber.
•There is violent iritis, small pupil and cloudy aqueous.
•Toxins secreted by the bacteria diffuse through the
cornea into the anterior chamber.
•Has an irritative effect on the iris and cillary body
vessels.
•Leucocytes as a result of irritations are poured into the
aqueous and aggregate to the bottom of the anterior
chamber.
•Hypopyon may be so small and scarcely visible, may
reach half the iris or may fill the whole anterior
chamber.

11. COMPLICATIONS AND SEQUELE OF CORNEAL
ULCER.
Corneal scar, nebula, macula and leucoma.
Secondary glaucoma due to associated hypopyon and
irridicyclitis.
Protrusion and descemetocele of the descemet’s
membrane.
Perforation of the corneal ulcer much greater in
hypopyon due to;
•Virulence of the organism.
•Resistance of the host is lost.
•Inflammation occurs at three level, superficial, deep
layer and some diffuse in endothelium and
descemet’s.
•Fungal corneal ulcer if not well treated.

12. Purulent irridocyclitis, enophthalmos, panophthalmos may
occur.
Phthisis bulbi, the eyeball is small , shrunken, sightless, soft
and has lost its size.
INVESTIGATION
Corneal scrapings- under anesthesia, the edge and base of the
ulcers are scrapped, material obtained are prepared fore direct
smear and culture.
DIRECT SMEAR.
Gram stain- identifies 60- 70% bacterial infections.
Potassium hydroxide 10% mount- used to visualized filaments.

13. Giemsa stain – identifies cellular response and inclusion
bodies.
Gomori methamine silver stain – identifies 90% of fungal
infections.
Culture and sensitivity inoculation into blood agar
TREATMENT OF UNCOMPLICATED CORNEAL ULCER.
GENERAL.
Alleviate patient’s immune and nutritional status;
•Diet rich in nutrients.
•Fresh air.
•Vitamin A and C.
•Encourage personal hygiene.

14. Treatment of preexisting local conditions.
Dacryocystitis; irrigate lacrimal sac and then DCR.
Lagophthalmos and corneal anesthesia – tarsorrhapy.
FB on the cornea should be removed.
Trichiasis and entropion should be corrected.
 LOCAL.
Broad spectrum antibiotics;
Ciprofloxacin eye drops, first line and is effective against
pseudomonas and pneumococcus.
Amino glycosides (gentamycine and tobramycine) gentamycine
subconjunctival 20mg daily till the hypopyon resolves.

15. TREATMENT OF FUNGAL CORNEAL ULCER.
This is often difficult because of ;
•Poor penetration of the antifungal agents.
•Late presentation of patients.
•Low spectrum of antifungal agents.
Natamycin 5% eye drop best for ulcers – effective against
candida,Aspergilum and Fusarum.
Amphotericin B 0.2% ointment – effective against candida.
Ketaconazole 1% topical against filament fungi, p.o 200mg bd.
Atropine 1% eye drop or ointment – actions,
•Dilates pupil, increase flow of fresh aqueous rich in nutrients
and antibodies.
•Rest pupil (iris and cilliary body).
•Dilates limbal vessels thereby promotion of nutrition to cornea.

16. Hot compress.
Green or dark glasses if there is discharge.
Analgesics – panadol, asprine, diclofenac tablets.
Corticosteroids if infection is controlled.
ACANTHAMEOBA KERATITIS.
Is caused by a free living protozoa found in water and
soil.
It is a rare condition.
RISK FACTORS.
Trauma.
Contact lens wearer.

17. CLINICAL FEATURES.
Severe pain.
Redness and tearing.
Photophobia.
Epithelial irregularity with dendritic pattern.
LATE STAGE.
Paracentral ring infiltrates.
Perineural radial keratitis – severe pain.
Stromal abscess.
Associated scleritis.

18. COMPLICATIONS.
Descemetocele.
Perforation.
Scleritis.
TREATMENT.
Corneal scrapings for examination.
Neomycin eye drops 3 hourly.
Topical ketaconazole or oral miconazole 200mg BD.
Propamidine and dibromopropamidine isethionate 1% eye
drops.
Epithelial debridement is essential.

19. MORREN’S RODENT ULCER.
Is a superficial ulcer of a degenerative type occurring in elderly
people.
It is painful and progressive characteristically.
CHARACTERISTICS OF THE ULCER.
•Localized at the limbal region.
•Crusty overhanging edges.
•Vascularization of the base.
FORMS OF THE ULCER.
•Benign and unilateral found in older males.
•Is a bilateral ulceration that tends to progress and found in
younger patients.

20. CLINICAL FEATURES.
Severe neuralgia (face and head).
Redness.
Photophobia.
Whitish overhanging edge of ulcer.
Base becomes vascularized.

TREATMENT.
Snipping of the overhanging edge with scissors then cauterized
with 10 or 20% trichloroacetic acid.
Cryoapplication to the edge of the ulcer.
Excision of 4-7mm of adjacent conjunctiva.
Bandage soft contact lens.
Lamellar keratoplasty.

21. Local corticosteroids.
Antibiotics for super infections.
VIRAL KERATITIS.
Viruses play an important role in infection of the eye e.g;
•Herpes simplex virus.
•Adenovirus.
•Molluscum contagiosum.
•Herpes zoster etc.

22. HERPES SIMPLES KERATITIS.
Primary infection occurs in infancy or early childhood as;
•Sub clinical infection in person with high antibody titer.
•Vesicles on the lid, lid margin and lips usually unilateral.
•Acute follicular keratoconjunctivitis with enlarged periauricle
lymph nodes.
After primary infection, the virus becomes symbiotic and
harmless at the site of original infection (trigeminal ganglion).
Recurrence is triggered by; malaria, corneal FB, URTI, flue,
trauma, physical and emotional stress etc.
Recurrent diseases may occur as one of a combination of the
following;
•Epithelial infectious ulcers.
•Epithelial trophic ulcer.

23. •Stromal interstitial keratitis.
•Stromal immune disc form keratitis.
•Iridocyclitis.
EPITHELIAL KERATITIS.
Dendritic or geographical ulceration of the cornea is caused by
live virus.
The viruses are present in the intra and extra cellular location –
basal epithelium.
Use of corticosteroid in epithelial infection increases the
ulceration and prolong infectious phase.
Debridement of the involved area and normal epithelium is
performed under slit lamp with a sterile cotton applicator.

24. ANTIVIRAL CHEMOTHERAPY
Zovirax 3% ointment 5 times daily – Best.
Trifluridine 1% eye drops.
Vidarabine 3% eye drops.
IDU 0.5%
EFFECTS OF PROLONG USE OF ANTIVIRAL AGENTS.
Toxic punctate keratitis.
Retardation of epithelial healing.
Superficial stromal opacification.
Follicular conjunctivitis.
Punctal occlusion.

25. DISCIFORM KERATITIS.
Is a delayed hypersensitivity reaction to herpes simplex virus.
It may cause focal bullous, edema and generalized epithelial
changes.
Disciform keratitis is a sub acute none suppurative disc like
lesion usually localized at the center of the cornea – mid
stroma.
Disciform keratitis is a gray disc edema of the epithelium, striae
keratitis and fine keratic precipitate.
Striae keratitis is wrinkling or stretching of the descemet’s
membrane.

26. CLINICAL FEATURES.
Stromal edema.
Striae keratitis.
Fine keratic precipitate.
Vision is completely compromised.
No pain and redness.
Vascularization is absent but seen in chronic cases.
Commonly seen in HSV keratitis but also in HZV, mumps,
chemical keratitis etc.
Stromal opacification seen under slit lamp.
TREAMENT.
Debridement of epithelium and antiviral agent started before
two days of steroids.

27. Steroid should be reduced if ulcer progress.
ANTIVIRAL PREPARATIONS.
Acyclovir 3% ointment.
Triflorothymidine.
IDU.
HERPES ZOSTER OPHTTHALMICUS.
Varicella zoster affects various ocular tissues including; eyelids,
conjunctiva, cornea, uvea, sclera, retina. Optic nerve, EOM etc.
The corneal involvement were;
•Punctate keratitis.
•Early pseudo dendrites.
•Anterior keratouvietis.
•Stromal keratitis.

28. SIGNS AND SYMPTOMS.
Punctate keratitis with or without skin eruption.
Corneal plagues.
Disc form keratitis with or without iridicyclitis.
Sclerokeratitis.
Pseudo dendrites.
TREATMENT.
Early treatment with Acyclovir 400 – 500 mg 5 times daily.
Corticosteroid for keratitis if intraocular inflammations are
present and active phase of corneal ulcer is controlled, use with
great caution.
Antibiotic topically.

29. PHLYECTENULITIS.
Is a nodular accumulation of inflammatory cells mostly located
in the limbal area.
It is associated to delay hypersensitivity reaction to microbial
antigens.
ETIOLOGY.
Hypersensitive reaction to staphylococcal antigens.
Chronic blepharitis.
Chlamydia.
Fungi.
Parasites.

30. EPIDEMIOLOGY.
It is predominately in tuberculosis endemic area.
Has higher incidence (60 – 70%) among younger girls.
SYMPTOMS.
Photophobia.
Tearing.
FB sensation.
SIGNS.
Solitary nodules 1- 4mm located within inter palphebral space.
Corneal vascularization due to infiltrates which accompany the
phylectenules towards the center of the cornea.

31. TREATMENT.
Treat blepharitis if associated.
Topical corticosteroid on short course – prednisolone acetate.
COMPLICATION.
Corneal scar is limbal base of triangular shape.

EXPOSURE KERATITIS.
Is corneal surface desiccation (ulceration) due to malfunction or
malposition of the eyelids.
Cause of corneal ulceration is mainly dryness.

32. ETIOLOGY.
Lagophthalmos due to malfunction of the orbicularis oculi
muscles – seventh nerve palsy.
Malposition of the eyelids e.g. ectropion, cicatricial diseases,
burns etc,
Exophthalmos.
Idiopathic inability to close the eyelids during sleep, infrequent
blinking.
SYMPTOMS AND SIGNS.
Burning sensation.
Eye irritations and redness.
Photophobia.
Superficial punctate keratitis – most exposed part.

33. Contn.
The lower ⅓ and inner palphebral opening is affected.
If cornea is exposed for longer period then frank ulceration and
corneal neovascularzation and scarring occur.
TREATMENT.
Prevention of corneal dryness by;
•Ointment – topically.
•Artificial tears.
•Prevention of evaporation – use sunglasses.
Antibiotic for keratitis.
Additional treatment;
•Eyelid tapping – moist chamber.
•Tarsohrraphy.

34. ROSACEA KERATITIS.
Is a hyperemic disease of the skin.
It primarily affects middle third skin of the face.
It involves the skin of the forehead above the nose, nose and
cheek.
It is characterized by erythema, talangiectasia papules and
hypertrophy of sebaceous gland.
In advanced cases, rhinophema occurs, rhinophema is
hypertrophy of the nose with increased vascularity, increased
size of sebaceous glands.
Blepharoconjunctivitis is common and characterized by
thickening of the lid margin, redness and talangiectasia.
Chalazion are mostly associated with rosecea keratitis.

35. SIGNS AND SYMPTOMS.
Conjunctivitis associated with rosecea is diffuse hyperemia.
Rosecea may be associated with meibominitis and keratitis.
Severe photophobia and FB sensation.
Stromal and sub epithelial abscess.
TREATMENT
Topical corticosteroids for iridicyclitis and keratitis.
Doxycycline caps 100mg BD for 2 – 3 weeks.
Systemic tetracycline 500mg QIDs for 2 – 3 wks.

36. CORNEAL BLOOD STAINING.
Blood staining of the corneal stroma is almost always
associated with trauma – blunt trauma to the globe with
hyphema.
There is high IOP though it is seen with low and normal IOP.
Initially, there is evidence of mild to moderate edema of the
cornea.
The cornea takes a bronze coloration, that is characteristic of
corneal blood staining.
CAUSE.
Breakdown products of the blood are deposited in corneal
stroma.
How these breakdown products are transported into the cornea
is not known.

37. CONTN.
It’s believed to have been possible when the endothelium is
compromised before blood staining can occur.
COURSE.
Once blood staining is present, it remains for months.
Clearing of blood staining starts from periphery towards the
centre.
Severe blood staining is known to take one year or more.
In some severe trauma, fibrosis due to prolonged staining and
edema in the cornea causes permanent scarring.
TREATMENT.
Adults with minimum hyphema less than ⅓ of AC requires
hospitalization or quiet rest.

38. CONTN.
Daily examination of IOP for detection of rebleeding.
Allow patient for quiet ambulatory and bilateral patch.
Atropine 1% eye drops to prevent contraction of cilliary body
and pupil.
Corticosteroid not helpful in traumatic corneal blood staining.
Rebleeding occurs in nearly ⅓of patients with trauma
within 3 -5 days before 7 day of post trauma.
Rebleeding is common in blacks than in white patients.
More severe than original hemorrhage and the prognosis for;
reduced vision, corneal blood staining and secondary glaucoma
is worse.
If corneal endothelium is unhealthy, then corneal blood staining
can occur with normal IOP.

39. CONTN.
Elevated IOP is managed by Acetazolamide 250mg QIDs.
Glycerin in juice 12 hourly.
In 5 – 10% of the patients, to prevent secondary glaucoma,
optic atrophy and periphery synechea formation, surgical
intervention is mandatory.
Optic nerve damage is expected with IOP of 50mmhg or more
for at least five days or 35mmhg for one week.

40. OCULAR SURFACE BURN.
Major ocular burns are ocular emergencies.
Potentially blinding ocular injuries are from;
Thermal burns (Accident associated with fire works, explosions,
steam and boiling water).
Chemical burns ( Occur due to acids or alkaline).
ALKALINE AGENTS (Sodium hydroxide, calcium hydroxide)
Have hydrophilic and lipophilic properties.
Penetrates cell membranes causing extensive damage to
ocular surface.
Severe alkaline burn melts the cornea, access the intraocular
structures.
It causes irreversible damage and blindness.

41. CONTN.
ACIDIC AGENT (Sulphuric acid and hydrochloric acid).
Acid solution causes less damage than alkaline.
Many corneal protein bind to acid acting as buffer.
Acid binds to collagen causing fibril shrinkage that would act as
barrier preventing further penetration of the acid.

42. CONTN.
DIFFERENCE BETWEEN ALKALIN AND ACID BURN.
ALKALINE. ACID.
Disrupt or break normal
barrier of the cornea by
saponifying the lipids of the
corneal epithelium & gain
access to AC.
Coagulates protein & form a
barrier which prevent deep
penetration into the AC.
Severe intraocular
complications of uvietis,
cataract & glaucoma.
Complications limited to the
lids, conjunctiva & cornea.
PH is high, more ocular
penetration & damage.
PH is low, less penetrations
and damage.

43. CONTN.
CLINICAL PRESENTATIONS.
MILD.
Conjunctival hyperemia.
Chemosis.
Sub conjunctival hemorrhage.
No perilimbal ischemia.
With or without corneal haziness.
Patchy loss of corneal epithelium.
AC flares and cell +1.
Normal IOP and clear lens.
MODERATE.
Periocular dermal injury.

44. CONTN.
Blanching of perilimbal conjunctiva and episcleral vessels.
Corneal edema.
Corneal epithelium denuded.
AC reaction present cells +3 but may not be seen due to
edema.
Lens may be affected resulting to cataract.
MANAGEMENT OF CHEMICAL BURN.
IMMEDIATE MANAGEMENT.
Irrigate with copious water under tap.
Debridement of the particulate to avoid contact of the cornea
with chemical.
Broad spectrum antibiotic ointment.
Refer to a centre for a better management.

45. CONTN.
INTERMEDIATE MANAGEMENT.
This is aimed at preventing several complications.
Corticosteroids because of uvietis for the first and third week, it
should be stopped in the second week to promote formation of
collagen.
Vitamin C to promote healing.
Mydriatics and cycloplegic to a rest the excursion of the eye.
Collagenase inhibitor like 20% Acetylcystein drops to initiate
epithelial regeneration and migration.
Artificial tear.
Corneal graft is considered after when the cornea is
repopulated with limbus derived epithelial cells.

46. CORNEAL DYSTROPHIES.
KERATOCONUS (ECTATIC CORNEAL DYSTOPHIES)
Is a disorder characterized by conical ectasia (bulging) of the
central cornea with thinning and scarring resulting in painless
progressive loss of vision.
CAUSE – Idiopathic.
FINDINGS.
Vertical striae may be seen in the posterior stroma with axial
thinning of the cornea and increased axial corneal curvature.
Reticulate scarring of bowman’s membrane appears.
Breaks in endothelium and descemet’s membrane results in
gross edema of the stroma (corneal hydrops).
Stromal corneal nerves will be visible & fibrillary lines seen.

47. CONTN.
FEATURES OF KERATOCONUS.
Striae keratitis.
Hydrops (sub epithelial bullae).
Decreased vision.
Photophobia.
Itching sensations.
TREATMENT.
Best is corneal transplantation.
Correct refractive error by spectacles.
Steroids for itching sensations.

48. OCULAR ANOMALIES ASSOCIATED WITH
KERATOCONUS.
Blue sclera.
Ectopia lentis.
Anaridia.
Cataract.
Retinitis pigmentosa.
Optic atrophy.

49. FUCH’S ENDOTHELIAL DYSTROPHY (Bullous
Keratopathy)
Is a progressive condition characterized by increasing corneal
thickening due to edema.
CAUSES.
Inheritance.
Failure of the endothelium membrane to pump water and
bicarbonate out of the cornea i.e. low endothelial cell count.
OCCURRENCE.
 More commonly diagnosed in women of fifth and sixth decade
of life.

50. FINDINGS.
A progressive condition characterized by increasing corneal
thickening due to edema.
As the stromal edema increases, epithelial edema occurs.
Fluid collection in the epithelium causes blisters or bullea
(bullous keratopathy).
COMPLICATIONS AS A RESULT OF INCREASING EDEMA
AND WHEN IT BECOMES CHRONIC.
Vascularization of the cornea.
Vision is decreased.
Endothelial cell count becomes low.
Severe pain due to rupture of the bullae.

51. IMPORTANT FEATURES.
Gutae – drops.
Stromal thickening.
Sub epithelial edema.
Epithelial bullae.
TREATMENT.
Lamellar keratotomy – ULA.
Treat glaucoma – Diamox 250mg QIDs.
Ointment topically to prevent desiccation and breakage of the
epithelium.
Corneal transplantation.
5% sodium chloride 4 – 6hrly drops topically.

52. EPISCLERITIS.
Is inflammation which is limited to the superficial sclera and
episclera.

CAUSES AND OR PREDISPOSING FACTORS.
Gout arthritis.
Rheumatoid arthritis.
Gynecological infection.
OCCURRENCE.
Predominantly seen in women than in men.

53. SYMPTOMS.
Ocular discomfort.
Little or no pain.
Redness – pinkish and localized.
Tearing.
SIGNS.
Nodular – commonest inflammation and localized.
Diffused hyperemia of the conjunctiva.
SIGNS ON RECURRENCE.
Pinkish red nodule 2 -5mm in size located temporary.
Nodule surrounded by a patch of hyperemia of conjunctiva.
Blood vessels course over the nodule.

54. Is tender to touch and never ulcerates.
TREATMENT.
Hydrocortisone 1% ointment or drops tds.
Hot fomentation.
Treat the cause – septic foci.
Anti inflammatory e.g. Ibrufen tablets 200mg tds, Aspirin 600mg
tds, Diclofenac 50mg tds.
SCLERITIS.
Is severe inflammation of the deeper portion of the sclera.

55. CONTN.
ETIOLOGY
Common in women as in; menstruation – exciting,
gynecological sepsis.
Associated with collagen diseases such as gout arthritis,
rheumatoid arthritis etc.
Exogenous infections from conjunctiva after trauma, operation
for retinal detachment and squint.
Allergy due to tuberculosis or streptococcus.
Syphilis.
Leprosy.
Toxic reaction to drugs like sulphonomide.

56. SYMPTOMS.
Marked pain radiating to neighboring structures.
Tearing.
Photophobia.
SIGNS.
Diffused redness.
Nodular dark red or violet patches adjacent to the cornea.
Inflammation may extend to the equator or surround the limbus
forming anular scleritis.
No ulceration but much absorption, sclera becomes thinned, a
dark purple cicatrix forming.

57. A scar occasionally too weak to withstand the IOP leading to
scleral staphyloma formation.
In necrotizing scleritis, eye is inflamed and very painful, sclera
is destroyed.
Scleromalacia perforance – soft degenerated sclera may
disappear leaving hole.
COMPLICATIONS.
Cornea sclerosing keratitis.
Scleral staphyloma.
Iridicyclitis.
Secondary glaucoma.
Posterior scleritis.

58. TREATMENT.
Hydrocortisone 1% eye drops or ointment tds.
Atropine 1% for keratitis and iridocyclitis.
Hot fomentation.
SYSTEMIC.
Treat the cause – septic foci.
Anti inflammatory drugs.
Corticosteroids for necrotizing scleritis and posterior scleritis.

59. STAPHYLOMA.
Is ectasia or bulging or protrusion of the outer protective layer
of the eye either cornea or sclera.
There is incarceration of the uveal tissue such as iris, cilliary
body and choroids.
ANTERIOR STAPHYLOMA.
Is protrusion of the cornea with incarceration of the iris.
CAUSES.
Perforated corneal ulcer.
Perforating corneal injury.

60. INTERCALLARY OR PSEUDOCALLARY STAPHYYLOMA.
Is ectasia of the sclera with incarceration of the root of iris.

CAUSES.
Absolute glaucoma.
Recurrent scleritis.
Perforating injury to the sclera.
CILLIARY STAPHYLOMA.
Is ectasia of the sclera with incarceration of the choroids.
CAUSE – As above.

61. EQUATORIAL STAPHYLOMA.
Is incarceration of the choroids.
TREATMENT.
Correct refractive error with spherical concave lens, contact
lens.
Enucleation if there is absolute glaucoma.
THE END