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).