The Uveal Tract
Anatomical & physiological considerations
The cornea forms the anterior 1/6 of outer coat of globe. It is transparent and avascular. It has the following dimensions:
- Diameters: Vertical 9-11 mm & horizontal 11-12 mm.
- Thickness: 0.8 mm at limbus & 0.5 in centre.
- Radius of curvature of anterior surface is about 7.8 mm.
- Radius of curvature of posterior surface is about 6.2 mm.
- Refractive index = 1.37.
- Refractive power = 42 D.
It consists of the following 5 layers:
- It is stratified squamous non‑keratinizing epithelium. It is formed of 5 - 6 layers, the basal layer is columnar, the intermediate layers polyhedral and superficial layers are flat.
- Epithelial cells rest on basement membrane which is secreted by the basal cells. It is very important to fix the epithelial cells to the underlying layers. When the basement membrane is damaged, recurrent corneal erosion syndrome develops.
2) Bowman’s membrane (10-12 micron):
It is a homogeneous acellular condensation of the anterior stromal lamellae. When it is injured it does not regenerate and a permanent opacity is produced. It ends at limbus.
3) Stroma (substantia propria):
- It forms 90 % of the thickness of the cornea.
- It is formed of C.T. bundles arranged in about 300 layers, the lamellae in each layer are parallel to each other but perpendicular to those in the next layer.
- The collagenous fibrils are very uniform. The distance between each other is less than half the wave length of visible light. This is very important for corneal transparency.
- In-between the corneal lamellae, there are spaces known as lacunae containing cells known as keratocytes.
- The matrix is formed of special types of mucopolysaccharides that are not present in any other tissue in the human body. It can absorb large amounts of water causing corneal edema. Normal hydration of the cornea is maintained by the corneal endothelium.
- It is continuous with the sclera and limbus.
4) Descemet's membrane:
- It is elastic and resists digestion by proteolytic enzymes.
- At the limbus it becomes 2 layers. One of them continues over the trabecular meshwork. The other layer ends by a condensation forming "the anterior ring of Schwalbe".
- It is formed of one layer of flat hexagonal cells arranged in a mosaic pattern.
- It is continuous with endothelium of the trabecular meshwork and anterior surface of the iris.
- It is responsible for the deturgescence of the cornea, so that when it is injured corneal edema occurs.
- It is not capable of mitosis and regeneration. When injured, the healthy cells flatten to cover the area of lost endothelium.
Supplies of the cornea:-
* Nerve supply:
- It is derived from long & short ciliary nerves of nasociliary nerves which are branches of ophthalmic division of trigeminal nerve (see the nerve supply of eyeball). In the cornea the nerve fibers are non myelinated.
* Nutrition of cornea:
The cornea being avascular, derives its nutrition from the following sources:
- Diffusion from Tears: 85% of oxygen is taken through the tear film. During lid closure, oxygen diffuses from upper palpebral conjunctival vessels.
- Glucose and other nutrients diffuse from aqueous humour.
- Diffusion from limbal capillaries.
Cause of corneal transparency:
1. Anatomical factors:
a. Cornea does not contain opaque structures:
- No keratin in the epithelium.
- No blood vessels.
- No myelin sheath around nerve fibers.
b. Regular arrangement of collagenous bundles in the stroma.
c. Smooth anterior surface.
2. Physical factors:
- The spacing between the collagenous fibrils is uniform and less than half the wavelength of visible light (400-700 nm). So that the scattered light rays destroy each other allowing clear vision.
3. Physiological factors (deturgescence of the cornea):
- The corneal lamellae are not fully hydrated. It is an energy consuming function of the endothelium. If the cornea becomes edematous, it will be opaque because the spacing between the collagenous fibrils will be greater than half the wavelength of visible light. Also the corneal epithelium has a role in prevention of corneal edema.
Causes of corneal lustre:
- Healthy intact epithelium.
- Intact tear film.
Classification of corneal diseases
I. Inflammatory (Keratitis).
II. Degenerative diseases.
III. Ectatic corneal conditions.
IV. Miscellaneous subjects.
Causes of keratitis:-
1. Infections by bacteria, viruses, fungi, ....
2. Non infective keratitis as:
- Trauma (mechanical, UV rays or chemical).
- Degenerative as neurotrophic and atheromatous ulcers.
It is classified into groups according to:
1. Site of the pathology (superficial, interstitial or deep).
2. Nature of the pathology (Suppurative or non suppurative).
3. Etiology (infectious, allergic, traumatic, degenerative,...).
These groups are:
A. Superficial keratitis:-
1. Ulcerative (corneal ulcers).
2. Non ulcerative K. as Pannus (superficial corneal inflammation and vascularization).
B. Interstitial keratitis:
1. Suppurative (Interstitial abscess).
2. Non suppurative I.K.:
a. Diffuse I.K. of congenital syphilis (affects all the cornea).
b. Localized I.K. (disciform keratitis): see dendritic corneal ulcer.
C. Deep keratitis:
1. Suppurative: posterior corneal abscess.
2. Non suppurative: Keratitis profunda.
CORNEAL ULCERS (ULCERATIVE K.)
The types of corneal ulcers are:
1. Non infective ulcers:
a. Traumatic ulcers (mechanical, chemical or physical trauma).
b. Degenerative ulcers as:
- ulcer with lagophthalmos.
- neurotrophic ulcer.
- atheromatous ulcer.
c. Hypersensitivity reactions as catarrhal ulcers and phlyctenular ulcers.
d. Autoimmune diseases as Mooren's ulcer and rheumatoid arthritis.
2. Infective ulcers:
a. Bacterial ulcers.
b. Hypopyon corneal ulcer.
c. Dendritic corneal ulcer.
d. Fungal corneal ulcers.
e. Acanthameba corneal ulcer.
NB. Vital stains of the cornea:
1. Fluorescein stain: It stains the corneal stroma green and conjunctival ulcers yellow.
2. Rose bengal stain: It stains the viral infected cells.
3. Double stain: Fluorescein + metheline blue. It is not used now.
Bacterial corneal ulcers
It is a localized suppuration and necrosis of the corneal epithelium and underlying stroma due to invasion by bacteria.
A. The causative organisms:
a. Bacteria that can invade healthy corneal epithelium are gonococcus, diphtheria, hemophilus and listeria.
b. Other bacteria can invade the cornea after damage of the epithelial barrier, such as pneumococcus, pseudomonas, staph and other pyogenic bacteria.
B. The sources of infection:
1. Contaminated trauma as trichiasis, foreign bodies, scratch, badly sterilized contact lenses,...
NB. Extended wear contact lenses predispose to pseudomonas corneal ulcers.
2. The presence of a nearby external infection as blepharitis and dacryocystitis.
C. The predisposing factors:
Unless the organism is very virulent, the resistance of the tissues should be lowered at first. The tissue resistance can be lowered by general and local factors.
1. The general causes include:
- Extremes of age.
- Diabetes mellitus.
- Systemic steroids and immunosuppressive drugs.
2. The local causes include:
- Corneal edema as in cases of absolute glaucoma.
- Corneal dryness as in cases of xerosis and lagophthalmos.
- Corneal anaesthesia.
The ulcer runs in the following three stages:
1. The progressive stage (Unclean ulcer stage):
- The organism becomes adherent to the damaged epithelium releasing its toxins. PNL are attracted to the site of reaction releasing proteolytic enzymes.
- The ulcer has grey unclean appearance with necrotic wall and PNL infiltration around the ulcer.
- If the bacteria overcome the tissue resistance, the ulcer grows in size and depth till it reaches Descemet's membrane. As Descemet's membrane is elastic and can resist perforation for few days, it bulges as a small sac called "Descematocele". Finally perforation occurs.
- The released toxins will irritate the iris leading to toxic iridocyclitis.
2. The regressive ulcer stage (stage of clean ulcer):
- The necrotic material is shed off, so that the ulcer will be larger and more demarcated with regular transparent sloping edges.
3. The stage of healing:
* The epithelium heals by migration to cover the ulcer then regenerates by mitosis.
* The stroma and Bowman’s membrane heal by irregular fibrous scar. So that, once Bowman's membrane is injured, a permanent scar will result. This scar may be dense (leukoma) or faint (nebula). The scar may be vascularized.
1. Diminution of vision if the ulcer is central.
2. Pain:- It is pricky (sharp stitching) in nature and increases with blinking.
- It occurs due to irritation of the nerve endings by movement, toxins and associated uveitis and glaucoma.
- Accompanied by referred frontal and temporal headache through other branches of ophthalmic division of V.
- Reflex lacrimal, photophobia and blepharospasm.
2. Ciliary injection: deep red injection of the circumcorneal 4 mm zone due to dilatation of the anterior ciliary vessels. It does not move with the movement of the conjunctiva.
3. Cornea: the site of the ulcer becomes:
- Opaque (edema & infiltration)
- Positive fluorescein stain: 2 % eye drops is instilled and wash the excess. The ulcer will be stained green when illuminated by cobalt blue illumination.
4. Signs of iritis:
- Miosis, aqueous flare & cells. If hypopyon develops (with highly virulent organisms as pneumococcus and pseudomonas), it will be called "hypopyon corneal ulcer".
5. Decreased visual acuity.
A. Complications of the active non perforated corneal ulcer:
1. Toxic iridocyclitis.
2. Secondary OAG.
B. Complications of perforated ulcer:
1. Loss of Ac leading to formation of PAS.
2. Complications of sudden drop of IOP.
4. Iris prolapse.
5. Complications of small central perforations.
C. Permanent complications after healing of the ulcer:
II. Secondary ACG.
A. Complications of the non perforated ulcer:
1. Iridocyclitis: Occurs due to diffusion of bacterial toxins into the anterior chamber, not the bacteria itself (sterile anterior chamber reaction). It may be severe with formation of hypopyon.
2. Secondary glaucoma (Due to iridocyclitis especially with hypopyon formation):
* It is secondary OAG due to clocking of the trabecular meshwork by fibrin and cells.
* Rise of IOP is diagnosed by digital tonometry (other tonometers are contraindicated for fear of perforation).
* Secondary glaucoma will be complicated by:
- Delayed healing of the ulcer.
- Easy perforation.
* It is treated medically by diamox till spontaneous absorption of exudates.
NB. SST can not be done during the activity of the corneal ulcer. Also pilocarpine can not be used.
* It is the bulge of Descemet's membrane that occurs when the ulcer is very deep (Descemet's membrane resists perforation for a short time).
* It appears as a small translucent bleb surrounded by the greyish ulcer.
* It differs from the perforated ulcer in that the Anterior chamber. is not lost, IOP is not soft, and the pupil is regular and rounded.
* It does not occur in children (thin Descemet’s membrane) & hypopyon ulcers (destroyed Descemet’s membrane).
* It is treated immediately by tight bandage of bandage contact lens, then cyano-acrylate (a tissue adhesive material) is applied.
B. Complications of perforated corneal ulcer:
Complications vary according to the site and size of perforation. So that the following complications can occur:
Loss of the anterior chamber will lead to contact between the iris root and the angle causing PAS which will lead to secondary chronic angle closure glaucoma after healing of the ulcer.
2. Complications of sudden drop of IOP (concussion of the eye):
1. The lens may be subluxated, dislocated or even expelled outside.
2. Macular edema & disc edema.
3. Choroidal hemorrhage that may be severe enough to expel the whole ocular structures to the outside (expulsive choroidal hemorrhage).
4. Iris prolapse:-
It occurs due to perforation of paracentral and peripheral ulcers.
- It is beneficial because:
a. The iris blocks the perforation causing rapid formation of the anterior chamber.
b. The iris is vascular providing rapid healing.
- Its disadvantage is that the iris will be permanently tented to the ulcer forming leukoma adherent.
5. Complications of small central corneal perforations:-
a. Anterior polar cataract.
b. Central leukoma non adherent.
c. Corneal fistula:
- It occurs due to repeated dislodgement of the fibrin plug. Finally epithelialization of the wall of the ulcer occurs. So that the perforation will never close. Not only, but also the repeated loss of anterior chamber causes marked PAS. So that severe secondary angle closure glaucoma develops after treatment of the condition by keratoplasty.
C. Permanent complications that remain after healing of the ulcer:
I. Corneal scars:
The scars may be:
a. Nebula due to healing of superficial ulcer. It leads irregular astigmatism if central. It is treated by any of the following methods:
- Photo-therapeutic keratectomy (PTK) using excimer laser.
- Rigid gas permeable contact lens.
- Optical keratoplasty.
b. Leukoma non adherent due to healing of either a deep non perforated ulcer or a perforated central ulcer. It is treated by penetrating keratoplasty if the scar is central. If the eye is amblyopic, a coloured contact lens is used for cosmetic rehabilitation.
c. Leukoma adherent due to healing of a perforated paracentral ulcer with iris prolapse.
d. Partial or total anterior staphyloma:
- It occurs as a final outcome of large corneal perforations where most of the iris prolapses and becomes covered by fibrin. This fibrin will be organized into fibrous tissue.
- Finally the cornea will be replaced by a thin scar lined by atrophic iris, with total loss of the angle leading to severe secondary ACG.
- Finally the scar (pseudo cornea) will bulge because of the IOP. It appears as bluish ectatic lobulated mass (staphyloma = bulge of the outer coat lined by middle coat).
- If the eye is blind and painful, enucleation can be done followed by artificial eye fixation.
The complications of corneal scars may be:
1. Defective vision leading to amblyopia:
* If unilateral, squint occurs.
* If the scar is bilateral in early childhood it will lead to nystagmus (for example; ulcers secondary to ophthalmia neonatorum or keratomalacia ulcer).
NB. The 2-4-6 rule:
- Bilateral lesions before the age of 2 years always cause nystagmus.
- Bilateral lesions after the age of 6 years never cause nystagmus.
- Bilateral lesions between 2 and 6 years may cause nystagmus.
2. Ectasia of the scar: If the iris is adherent to the ectatic scar, it will be called “staphyloma”.
NB. Scar ectasia is usually caused by secondary glaucoma. So that scar ectasia is more common after healing of a perforated ulcers (more PAS).
3. Cosmetic disfigurement.
4. Atheromatous corneal ulcer: Atheromatous degeneration may occur in the old standing leukoma. This leads to desquamation of the degenerated scar and secondary infection. This type of ulcers is resistant and rapidly progressive due to the poor vitality of the scar tissue. It commonly perforates the cornea leading to endophthalmitis.
II. Permanent secondary ACG:
* It occurs due to PAS, so that it is more common after healing of perforated ulcers.
- Persistent pain and ciliary congestion.
- PAS involving most of the angle.
- Persistent elevation of IOP leading to glaucomatous cupping.
1. Scar ectasia.
2. Failure of keratoplasty that would be done for a scar. So that SST should be done before keratoplasty.
3. Post-glaucomatous optic atrophy.
- If seeing we do SST after medical control of IOP.
- If blind and painful we do ..., ..., ... .
Treatment of corneal ulcers:-
Treatment will be classified into the following items:
A. Treatment of uncomplicated cases.
B. Treatment of resistant cases.
C. Treatment of complications and perforation.
A. Treatment of uncomplicated cases:-
Scraping of the ulcer is done to provide material for culture and to remove necrotic tissue to allow better penetration of antibiotics.
It is a muscarinic receptor blocker.
Its values in treatment are:-
- Dilates the pupil to prevent posterior synaechia.
- Relaxation of ciliary body spasm leading to decreasing pain and increasing blood supply of ciliary body.
Dose and preparations:
- Atropine drops 1% are given to adults 3 times / day.
- 1% Ointment is given to children because it has less systemic absorption and less incidence of systemic toxicity.
i. Atropine allergy with conjunctival redness, edema and follicle formation. It is treated by shifting to another cycloplegic as cyclopentolate 1 %.
ii. Systemic toxicity can occur in children causing hallucination, hyperthermia and flushing. It is treated by cold fomentations.
iii. Rise of IOP: Do not stop atropine, but add timolol and diamox.
2. Local antibiotics:-
We take a specimen for culture and sensitivity, then start with broad spectrum antibiotics. After the results of the culture are obtained shift to the proper antibiotic. Antibiotics are given in the form of fortified (highly concentrated) eye drops. Antibiotic ointments are used at bed time.
It is very important because:-
- It relieves the patient from pain caused by lid movements.
- Prevents continuous removal of healing epithelium by lid movement.
It is contraindicated if there is discharge or chronic dacryocystitis.
4. Hot fomentations and analgesics.
The ulcer usually heals in 1-2 weeks if treatment is successful. During healing pain becomes less and the ulcer decreases in size. Finally the ulcer is not stained with fluorescein.
B. Treatment of resistant ulcers:-
The causes of resistance are:
- Misdiagnosed of the organism as fungi and acanthameba.
- Bad choice of antibiotics.
- High resistance of the organism.
- Incomplient patient.
1. Reculture: Antibiotics are stopped for 3 days, then fungal and bacterial cultures are taken.
2. Proper antibiotics are given by frequent instillation of highly concentrated drops. Also subconjunctival injections can be given.
3. Therapeutic contact lenses are helpful in some cases.
4. Conjunctivoplasty to cover the cornea with a flap of conjunctiva. As the conjunctiva is vascular, healing will occur. The conjunctival will remain adherent to the scar forming a “pseudo-pterygium”.
5. Therapeutic keratoplasty is done if the above measures fail.
NB. Carbolic acid cauterization is an old method of treatment. It can be used if there are no other facilities.
C. Treatment of complications:-
1. Secondary glaucoma:-
a. Glaucoma in active ulcer:
It is controlled medically by adding diamox to the treatment (mention the mechanism, dose and side effects in brief).
NB. During activity of the ulcer, we can not use pilocarpine and we can not do SST.
b. Permanent glaucoma after healing of the ulcer:-
- If the eye is seeing, we do SST after complete cessation of inflammation.
- If the eye is blind and painful, we do either cyclocryo, retrobulbar alcohol injection or enucleation with artificial eye fixation.
3. Treatment of perforated corneal ulcers:-
Atropine, systemic and subconjunctival antibiotics + the following treatment:
a. Hospitalization, rest in bed and bilateral bandage.
b. Closure of the perforation by one of the following methods:
- If it is closed by a prolapsed iris, never reposit it.
- Tight bandage.
- Bandage contact lens.
- Cyano-acrylate (tissue adhesive material) if the perforation is small.
- Keratoplasty is needed especially if the perforation is large.
c. Systemic antibiotics are given as a prophylaxis against endophthalmitis.
NB. If endophthalmitis and expulsive hemorrhage are treated by evisceration and systemic antibiotics.
4. treatment of corneal scars:-
a. Central nebula:-
b. Leukoma adherent or non adherent in a seeing eye:
We do penetrating keratoplasty (PKP).
NB. Visual iridectomy (not done now):
- It is indicated in cases of leukoma non adherent only if vision improves by mydriasis.
- It should be nasal at the site of visual axis and down behind the exposed part of cornea.
- It should be small to avoid dazzling.
c. Cosmetic treatment of scars in a blind eye:
i. Cosmetic coloured contact lens.
ii. Cosmetic keratoplasty.
iii. Tattooing (obsolete).
Hypoyon corneal ulcer
It is a primary infective disc shaped paracentral corneal ulcer characterized by severe iridocyclitis with the formation of hypopyon.
A. Predisposing factors:-
B. Causative organism:-
- The typical hypopyon ulcer caused by pneumococcus (80%).
- Atypical hypopyon ulcers can be caused by either:
* Morax axenfield bacillus (10%).
* 10% by staph, pseudomonas, fungi, and other organisms.
C. Source of infection:-
Exogenous (See before).
This ulcer is more common in old age and diabetics.
Pain, redness and drop of vision (See before).
- Lid edema and blepharospasm.
- Conjunctiva shows ciliary injection (mention).
* Paracentral discoid ulcer with loss of transparency and lustre and positive fluorescein staining (mention).
* The ulcer has 2 edges:-
- The central edge is progressive. It is concave and undermined.
- The peripheral edge is the healing edge. It is convex, scarred and vascular.
* The ulcer is deep with posterior abscess formation. So that it commonly perforates and descematocele is never formed.
- Hypopyon which is sterile pus in anterior chamber. It is formed of fibrin and inflammatory cells produced by the severe toxic iridocyclitis.
- Secondary glaucoma is very common.
- Vision. is usually severely affected because the ulcer is near the central area.
The main differences between typical and atypical hypopyon ulcers are:-
As above, but note that:-
A. Before perforation, descematocele can not develop because of the early destruction of Descemet's membrane by the posterior abscess.
B. Small central perforation is not common because the ulcer is usually large and paracentral.
C. After healing, nebula is not a common complication because the ulcer is deep.
Hypopyon corneal ulcer is treated as the ordinary bacterial ulcer (mention in details), but as it is deep and dangerous, from the beginning of treatment we start by:
1. Subconjunctival antibiotics (mention).
2. Carbolic acid cautery (mention).
3. Treatment of secondary glaucoma (mention).
Dendritic corneal ulcer
It is a primary corneal ulcer caused by Herpes simplex virus type I. It is dendritic in shape (linear and branched).
It is caused by Herpes simplex virus (a large DNA virus) type I which is responsible for infection above the waste. The primary infection occurs in early childhood leading to follicular conjunctivitis (not dendritic ulcer) that heals usually without residual damage. The virus becomes dormant in the trigeminal ganglion waiting for drop of the immunity to cause recurrences. The recurrent attacks are dangerous for vision because central corneal opacities are common.
Precipitating factors of recurrence = Causes of drop immunity:-
- Exposure to cold, so that recurrences are more common in winter.
- Fevers as influenza, common cold, ....
- Local or systemic steroids.
- Immunosuppressive drugs.
Symptoms (it is usually recurrent):
- Marked drop of vision is common because the ulcer is commonly central.
- Pain is usually mild because of corneal hyposthesia.
- Ciliary injection (See before).
- Cornea: The ulcer runs in 2 stages; infiltration and ulceration:
* Early stages: there is punctate and stellate epithelial keratitis with positive rose bengal stain. The infected cells did not shed yet, so that the fluorescein stain is negative in this stage.
* Stage of ulceration: It is characterized by:
- The ulcer is superficial and dendritic shape (linear and branched). The branches end by knobs
- Loss of lustre and transparency in the area of ulcer.
- The ulcer is stained by fluorescein 2% due to shedding of the infected epithelial cells and its edges (infected epithelium) are stained by rose bengal.
- Corneal hyposthesia as diagnosed by weak blink response on touching the cornea by a sterile piece of cotton.
Complications of dendritic ulcer:-
1. Recurrences always in the same eye.
2. Iridocyclitis that may be severe.
3. Secondary glaucoma due to iridocyclitis.
4. Disciform keratitis due to invasion of stroma by viral antigen, not due to stromal infection. It may occur several months after healing of the ulcer.
- If peripheral and not affecting vision steroids are not indicated.
- If it is central local steroids under umbrella of zovirax should be given to avoid corneal scarring and vascularization.
5. Amoeboid (geographical) ulcer formation: Here most of the corneal epithelium is infected due to marked weakness of immunity or local steroids. The ulcer will be large and amoebic in shape.
6. Keratitis metaherpetica: There is shedding of the epithelium at the site of the previous ulcer due to improper healing, not due a recurrence. There will be positive fluorescein staining, but rose bengal staining is negative (why). It is treated by:
- Bandage or bandage contact lens.
- Vitamin A and local lubricant preparations as regepithel eye ointment.
7. Neurotrophic ulcer due to destruction of corneal sensation. It is deep and perforating.
8. Corneal scars: Nebula is the commonest type of scars because the ulcer is superficial. However, deeper scars can sometimes occur.
I. Treatment of uncomplicated ulcer:
1. Local antiviral drugs.
2. Atropine (See before).
3. Prophylactic antibiotics in small doses to prevent secondary infection.
The local antiviral drugs:
Mechanism of action:
They are local antimetabolites. They are structurally similar to the nitrogenous bases necessary for viral DNA synthesis. So that they interfere with DNA synthesis by competitive inhibition with these bases.
They are toxic to the corneal epithelium causing epithelial erosions and delayed healing of the ulcer especially on long term treatment.
Examples of antiviral drugs:
1. Trifluorothimidine (TFT) 1 % eye drops.
2. Adenine arabinoside (Ara A): 3 % eye ointment.
3. Acycloguanosine (Zovirax = Acyclovir): 3 % eye ointment. It has 2 advantages:
a. It penetrates into the substantia propria of the cornea.
b. It is absorbed only by the infected cells not by the healthy cells. So that its toxicity is minimal and accordingly it can be given for long time as in cases of disciform keratitis.
II. Treatment of resistant dendritic ulcer:-
Beside the above treatment the following is added:
1. Debrdiment by wiping the ulcer by a sterile cotton tipped applicator to remove the infected cells. It has 2 very helpful advantages:
- Protects the adjacent cells from infection.
- Removes the antigen which causes disciform keratitis.
a. Chemical cautery by 7% iodine in absolute alcohol (superficial effect).
b. Cryo at - 50 degrees for 5 seconds.
3. Therapeutic lamellar keratoplasty may be needed.
III. Treatment of complications:-
1. Treatment of secondary glaucoma (See before).
2. Treatment on disciform keratitis (See before).
3. Treatment of keratitis metaherpetica (See before).
4. Treatment of nebula (See before).
HERPES ZOSTER OPHTHALMICUS
It is a common infection caused by Varicella - Zoster virus which is morphologically similar to HSV, but differs immunologically and clinically. Primary infection occurs is childhood. After that the virus becomes dormant in the trigeminal ganglion ready for reactivity.
Old age and immuno-deficient patients.
Affection of the ophthalmic division of trigeminal occurs in 10% of HZV cases. It runs in three stages:
Stage I: The acute stage (3 weeks):-
1. Skin maculo-papular eruptions involve one or more of the branches of the ophthalmic division of trigeminal nerve. Affection of the nasociliary nerve case characteristic eruption a the tip of the nose (Huchinson’s sign) because the external nasal nerve is the terminal branch of nasociliary nerve.
2. Ocular affection:
- Conjunctivitis, scleritis and episcleritis.
- Keratitis which is usually punctate and superficial with positive rose bengal stain. Microdendrites, nummular infiltrates and disciform keratitis may be seen.
- Iridocyclitis with secondary glaucoma may occur.
This stage is treated by:-
- Zovirax tablets 400 mg 5 times daily.
- Steroid and antibiotic skin ointment.
- Steroid and antibiotic eye drops (it is not responding to local antiviral drugs).
Stage II: Chronic stage:-
- Skin scarring may occur leading to ptosis, ectropion, trichiasis or madarosis.
- Corneal scarring, vascularization and neurotrophic corneal ulcer may occur.
- Neuralgic pain due to scarring of the nerve. It is avoided by systemic zovirax in the acute stage. When it occurs it is difficult to treat.
Stage III: Stage of recurrence.
Fungal corneal ulcer
Fungi are opportunistic infection that rarely infect a healthy cornea.
1. Corneal trauma especially with plant materials as wood.
2. Abuse of topical steroids and antibiotics.
3. Bad hygiene of contact lenses.
* Usually there is a history of trauma with a plant material.
* The ulcer appears as a greyish white stromal abscess. Stromal satellites separated from the main lesion by clear stroma is diagnostic. Hypopyon is very common.
Corneal scraping of even biopsy is taken for culture and direct film.
Local and systemic antifungal drugs are necessary. Treatment takes several weeks.
Acanthameba corneal ulcer
Acanthameba is a protozoan found in soil, fresh water and swimming pools. It is present in a trophozoite form (vegetative form) during favourable conditions. During unfavourable conditions, it becomes encysted and resists several injurious agents as heat and chlorine.
Acanthameba can infect the cornea only when there is a corneal abrasion, for example by extended wear contact lenses. It produces several enzymes that help tissue penetration.
Since acanthameba corneal ulcer is rare, it is suspected resistant corneal ulcers. A corneal biopsy stained by special a stain is necessary for diagnosis.
Non infective corneal ulcers
1. Marginal (catarrhal) corneal ulcers
They are the commonest corneal ulcers. They are hypersensitivity reactions to various bacterial infections as staphylococcus blepharitis (50%), Koch-Week’s bacillus and proteus.
Catarrhal ulcers are unilateral tiny peripheral ulcers separated from the limbus by a clear space. They may be single or multiple. They may be rounded or rectangular.
2. Ulcer with lagophthalmos
It is a primary corneal ulcer in the lower 1/3 of cornea caused by corneal exposure.
All causes of lagophthalmos especially facial nerve palsy (See the chapter of "EYELID").
- Exposure of the cornea will lead to dryness of corneal epithelium leading to erosions and ulcerations of the cornea. It may be followed by secondary infection.
NB. As the cornea is rolled upwards during sleep (Bell's phenomenon), exposure affects its lower part only causing dryness and secondary bacterial infection. So that the ulcer occurs in the lower 1/3 with straight upper border (characteristic feature).
1. Symptoms of lagophthalmos: Burning sensation and sense of dryness.
2. Symptoms of corneal ulcer: Pain & redness, but no diminution of vision because it is peripheral.
* General signs of ulcer as ciliary injection, loss of lustre and transparency and positive fluorescein stain.
* The ulcer occurs in the lower 1/3 with straight upper border.
* Incomplete lid closure and its cause are seen.
1. Treatment of lagophthalmos (See EYELID).
2. Treatment of the ulcer by artificial tears and therapeutic contact lens. In some cases atropine and topical antibiotics are indicated.
3. Neurotrphic (neuroparalytic) corneal ulcer
It is a primary central corneal ulcer occurring due to corneal anaesthesia.
Etiology (causes corneal anaesthesia):-
The cornea is supplied by the ophthalmic division of trigeminal nerve. Damage of trigeminal nerve occurs in cases of:
- Intracranial lesions as:
* Herpes Zoster Ophthalmicus is the most important cause.
* Radical treatment of trigeminal neuralgia by alcohol injection into the trigeminal ganglion was the classical cause in the past.
* Intracranial tumours as acoustic neuroma.
- Damage of orbital nerves as in cases of:
* Superior orbital fissure (SOF) syndrome: Damage of III, IV. VI and branches of ophthalmic nerve.
* Orbital apex syndrome: As above + optic atrophy.
* Retrobulbar injection of alcohol.
Ulceration occurs because of loss of the nerve growth factor supplied by the sensory innervation. The centre is affected because it has been the most sensitive area and because it is the most exposed to trauma.
- Pain is absent.
- Marked drop of vision because the ulcer is central.
* Corneal anaesthesia (no blink response to corneal touch).
* Large central ulcer with ciliary injection, loss of corneal lustre and transparency in the area of ulcer and positive fluorescein stain.
* The ulcer is deep and liable to perforate.
Atropine and local antibiotics are used as usual. Covering of the cornea for a long time should be done by either:
- Long term bandage or therapeutic contact lens.
- Induction of ptosis by botulinum toxin injection into LPS.
- Median tarsorrhaphy (done without anaesthesia.. why).
NB. Keratoplasty is contraindicated because the lack of nerve growth factor will prevent healing.
4. Keratomalacia corneal ulcer
It is bilateral central corneal ulceration and melting due to acute severe vitamin A and protein deficiency. It is a primary central non infective ulcer.
- It occurs most commonly in marasmic infants in the first year of life.
- It occurs rarely in adults in cases of severe malabsorption syndrome or liver diseases.
The ulcer is bilateral and central. Ciliary injections usually mild.
1. Perforation is common due to melting of the corneal stroma leading to endophthalmitis.
2. Bilateral dens leukoma early in the life leading to nystagmus.
As the general treatment of ulcer + large doses of local and systemic vitamin A.
5. Mooren's corneal ulcer
It is a rare peripheral corneal ulcer. In this case ischemic necrosis of superficial corneal layers occur due to limbal vasculitis. Also there is release of proteolytic enzymes from the conjunctiva in the area adjacent to the ulcer. There are two types:
a. Bilateral progressive form usually in adults.
b. Unilateral limited form usually in old age.
- Severe neuralgic pain with lacrimation, photophobia and blepharospasm.
- Drop of vision.
* General signs of ulcer as ciliary injection, loss of lustre and transparency and positive fluorescein stain.
* The ulcer is characterized by:
- This ulcer is a superficial serpeginous ulcer. It starts at the limbus then progression occurs both circumferentially and centrally. As other serpeginous corneal ulcers it has two edges:
- an advancing undermined crescentic edge towards the centre.
- a peripheral healed vascular edge.
- Corneal opacification, thinning and vascularization occur at the site of ulcer.
1. treatment of the ulcer by atropine, steroids and bandage.
2. In resistant cases we do:
- Excision of conjunctiva in the area adjacent to the ulcer
- Systemic steroids and immunosuppressive drugs.
NB. Keratoplasty is of bad prognosis due to vascularization of the cornea and corneal thinning that will not match the normal thickness of the graft.
II. Degenerative corneal conditions
It is bilateral peripheral lipoid infiltration of the corneal stroma. It is a very common condition in old age. Uncommonly it occurs in young age due to hyperlipidemia or juvenile diabetes (arcus juvenilis).
No symptoms, it never affect vision because it does not reach the central area.
- It starts as an ark like opacity near the upper part of limbus. This opacity has a diffuse central border and a sharp peripheral border separated from the periphery by a clear zone (the lucid interval of Vogt).
- Then a similar arc develops lower down. Then both arks extend circumferentially till they fuse with each other forming a complete ring.
Differential diagnosis: from pannus siccus.
Treatment: No treatment.
III. ECTATIC CORNEAL CONDITIONS
It is conical bulge in the central or paracentral or paracentral part of the cornea due to structural weakness in corneal tissue.
Type of patient:
It is more common in:
- Positive family history (10% of cases are autosmal dominant).
- Patients with atopic diseases as spring catarrhal.
* Gradual painless drop of vision due to:
- Myopia both axial and curvature.
- Irregular astigmatism because of the irregular bulge of cornea.
- Opacities at the apex of the cone.
* It is bilateral in 85% of cases, starting in one eye.
* It starts around puberty.
1. Early signs:
a. Retinoscopy shows spinning or scissoring of red reflex.
b. By ophthalmoscopic examination a tear droplet red reflex is seen.
c. Distorted image of Placido disc and keratoscope.
d. Corneal topography for earliest diagnosis.
2. Opacities at the apex of the cone due to folds of Descemet's membrane (the vertical stria of Vogt). Also there are opacities in Bowman’s membrane.
3. Fleischer's ring at the base of the cone. It occurs due to hemosiderin deposition in the epithelium.
4. The central part of cornea becomes thinner and bulges as a small cone. This can be seen by:
* Profile view in advanced cases.
* Notching of the lower lid on down looking (Munson's sign).
* Slit lamp: Thin apex of the cone and deep anterior chamber.
Acute hydrops of keratoconus:
- Acute rupture of Descemet’s membrane occurs in the centre of the cone leading to acute corneal edema.
- The patient will complain of marked acute drop of vision and pain.
- These cracks heal within 4 months, but scarring of the central cornea occurs.
- This condition is treated by hypertonic saline and bandage contact lens.
- After absorption of edema, keratoplasty is done the central part of cornea will be scarred.
The causes of corneal ectasia are:
A. Inflammatory conditions: - Anterior staphyloma.
B. Non inflammatory: - Keratoconus.
- Keratoglobus (stationary total spherical
bulge of the cornea since birth).
1. Rigid gas permeable contact lens to replace the power of the irregular corneal surface by the power or the regular surface or the contact lens.
2. Penetrating keratoplasty if the patient is intolerant to contact lenses, or if there are central opacities.
N.B. Glasses are tried, but they usually fail to correct irregular astigmatism. They can be used in the early cases.
NB. Intracorneal rings are used to stretch the conical cornea. They are very recent and still under investigations.
IV. Miscellaneous subjects
1. Causes of corneal opacities
1. Scars either nebula, leukoma non adherent or leukoma adherent.
2. Edema due to either:-
- Disruption of endothelial barrier in cases of buphthalmos, acute hydrops of keratoconus and blunt trauma.
- Endothelial pump failure due to iridocyclitis or acute glaucoma.
- Inflammatory edema min cases of keratitis and corneal ulcers
3. Corneal vascularization (mention the causes).
4. Degenerations as arcus senilis.
In this operation we remove an abnormal part of the cornea of a patient and replace it by a similar part of healthy donor's cornea. The donor may be:
- The cornea of the other eye if it is blind (autograft). There is no incidence of rejection in this case.
- The cornea of dead person taken maximally 6 - 10 hours post-mortem (homograft).
Types of keratoplasty:
1. Penetrating, i.e; transplantation of the whole corneal layers.
2. Lamellar: We dissect and transplant the superficial layers only. It is more difficult, but carries a less incidence of rejection.
Indications of keratoplasty:-
1. Optical: in cases of central corneal opacification and keratoconus.
2. Therapeutic in cases of resistant corneal ulcers and corneal fistula.
3. Structural and cases of perforated corneal ulcers and after multiple pterygium excision.
4. Cosmetic in cases of leukoma.
Contraindications of keratoplasty:-
1. Dryness and exposure because they lead to graft ulceration.
2. Corneal anaesthesia because loss of the nerve growth factor prevents healing of the graft.
3. Diseases as glaucoma and iridocyclitis should be treated at first.
NB. Corneal graft rejection is less common than other organs because the cornea is avascular and has a low cellular content. On the other hand, corneal vascularization will increase the risk of graft rejection.
3. Corneal vascularization
It means invasion of cornea by abnormal vessels. It may be superficial or deep