Cornea

Question 1

ANATOMY: Layers

Answer 1

From the exterior inwards, the cornea consists of 5 layers:
1. Epithelium: 5-6 layers cells and bm and is continuous with the epithelium of the bulbar conjunctiva.–> sensory nn supply
2. Bowman’s layer: Dense layer of modified stroma.
3. Stroma: 90% of the corneal thickness, and consists of lamellar fibres that run parallel to the corneal surface.
The size and periodicity of these fibres play an important rôle in the optical clarity of the cornea.
4. Descemet’s membrane: clear, elastic, basement membrane of the endothelium.
5. Endothelium: single layer of cells covering the posterior surface of the cornea.

Question 2

PHYSIOLOGY: Function

Answer 2

1. Transparent–> uniform structure, avascularity and state of relative dehydration of the stroma: Allows light to enter the eye and fall on the retina.
2. Its anterior surface–> covered by the tear film, is a powerful convex lens.
3. Nutrition: Limbal blood vessels, aqueous humour and tears.
4. Receive oxygen from atmospheric oxygen dissolved in the tear film.
5. Active pump mechanism in the endothelium: transports water from the stroma –> anterior chamber
   - -> Dehydration

Question 3

CORNEAL INFILTRATION and ULCERATION

Presentation
Location
Treatment

Answer 3

CLINICAL FEATURES SYMPTOMS
1. Redness
2. Pain: Upper lid move over lesion
3. Photophobia: Stim corneal nn
4. Scratchy sensation cause Blepharospasm
5. Tearing
6. Reduced vision
7. Halos around lights: corneal oedema
SIGNS
1. Full thickness epithelial defects (ulcers) stain with fluorescein–> Minims (single dose bottles) or fluorescein impregnated strips should be used, and not multidose bottles as these are vulnerable to contamination.
2. Redness has a ciliary or circumcorneal distribution.
3. Testing of corneal sensation and comparison with the healthy eye is important, taking great care not to contaminate the healthy eye with material from the symptomatic eye, and remembering that this test is not useful after instilling local anaesthetic

LOCATION

1. Central cornea: cause by direct infection by bacteria, fungi and viruses.
2. Peripheral cornea: caused by immune complex reactions in which the lesions themselves do not contain microorganisms. They may also be caused by direct infection by viruses.

MANAGEMENT

1. categorise the lesion:
   (a) History
   (b) Nature of the discharge
   (c) Location of the lesion
   (d) Appearance of the lesion (e) Corneal sensation
2. Categorise the lesion into one of the following clinical diagnostic groups:
   (a) Acute bacterial or fungal (b) Viral
   (c) Immune complex (marginal)
   (d) Miscellaneous: neurotrophic, exposure, xerofthalmia.
3. Refer immediately:
   (a) Any corneal lesion reducing visual acuity.
   (b) Any discrete corneal lesion which stains with fluorescein except a noncentral. Herpes simplex dendritic ulcer where the diagnosis is certain.
   (c) Any hypopyon, whatever the cause.
4. Treat other lesions according to the category in which you’ve placed them.
   (a) Review daily.
   (b) Refer if there is any deterioration and refer early if there is no improvement.

Question 4

BACTERIAL KERATITIS

Pathophysiology
Causes
Investigations
Management
Complications

Answer 4

Pathophysiology:

• Opportunists infection due to poor local resistance.
• Corneal epithelium is resistant to invasion by most microorganisms, but epithelial damage exposes the avascular stroma, which forms an excellent culture medium.
• Neisseria gonorrhoea, Neisseria meningitidis and Corynebacterium diphtheriae can invade the cornea without prior corneal damage and always lead to a purulent keratoconjunctivitis.

Cause
• Strep pneumoniae (pneumococcus): Primary path
• Pseudomonas: Rapidly > ulcer due to proteolytic enzymes which cause lysis of the corneal stroma–> Perforation is a real danger.
• Staphylococcus aureus
• Staphylococcus epidermidis

INVESTIGA TIONS
1. MC&S: Corneal scrapings from the edge of the ulcer yield the best results

MANAGEMENT
1. If possible refer to an ophthalmologist immediately.
2. Irrigate the eye with normal saline to remove any purulent discharge from the conjunctival sac and eyelid margins.
3. Cycloplegic drops: Relieve ciliary spasm and the resultant pain.
4. Local antibiotic drops.
5. Do not pad the eye unless specifically advised to do so by the ophthalmologist–> closed eye with a
static and débris filled tear film may act as a culture medium.
5. Local AB drops:
a) Start treatment with a 4th generation fluoroquinolone if possible: gatifloxacin, moxifloxacin.
If these are not available use a 2nd or 3rd generation fluoroquinolone: ciprofloxacin, ofloxacin.
b) Start with a loading dose: 1 drop every minute for 5 minutes.
Then 1 drop/half hour for 24 hours.
Then 1 drop/hour for 48 hours
Then adjust the regime to the response.
Remember to keep the eye closed for a minute after administering the drop.
6. If the infection cannot be brought under control, or if severe complications set in, an emergency corneal transplant is sometimes necessary to save the eye.

COMPLICATIONS

1. Permanent corneal thinning.
2. Permanent corneal opacification.
3. Corneal perforation.
4. Anterior uveitis with hypopyon.
5. Endophthalmitis: the infection affects the lens and posterior segment.
6. Permanent loss of vision can occur as a result of any of the above.

Question 5

FUNGAL KERATITIS

Causes
Presentation
Trearment

Answer 5

Cause:
Injury involving plant or animal matter.

Presentation:

1. The eye is usually extremely red and inflamed.
2. Satellite lesions are often present, and this sign is highly suggestive of fungal keratitis.
3. A hypopion containing fungi is often present.
4. Fungal ulcers progress relatively slowly.

TREATMENT
Conservatice Rx in superficial infection
1. Natamycin or Amphoteracin B topically for up to 3 months.
2. Systemic Fluconazole for up to 3 months.

Infection invaded the deeper cornea
1. Emergency corneal transplant is the only definitive treatment.

Question 6

VIRAL KERATITIS: HERPES SIMPLEX

Presentation
Complications
Treatment

Answer 6

PRIMARY HERPES SIMPLEX KERATOCONJUNCTIVITIS

Presentation:

1. children and young adults.
2. mild malaise
3. vesicular skin rash may occur on the eyelids.
4. follicular conjunctivitis
5. punctate epithelial keratitis.
6. After about a week, dendritic keratitis may occur.

RECURRENT HERPES SIMPLEX KERATITIS
SYMPTOMS
1. Irritation
2. tearing
3. moderate photophobia.
SIGNS
1. Dendritic ulcer with the typical linear branching pattern (Greek: dendron = tree).
2. dendritic ulcer may enlarge to become a geographic ulcer.
3. Corneal sensation over the ulcer is reduced or absent.

TREATMENT
1. Acyclovir (Zovirax) ointment 5 times daily.
2. Cycloplegia: Cyclopentolate (Cyclogyl) to relieve the pain of reflex ciliary spasm, expecially
if a secondary uveitis is present.

COMPLICATIONS (caused by steroid RX)

1. Disciform keratitis: A round, dull, central area of corneal oedema develops due to an immune response–> VA ««
2. Stromal keratitis: cornea becomes oedematous+ anterior uveitis

Question 7

VIRAL KERATITIS: HERPES ZOSTER OPHTHALMICUS

Presentation
Treatment

Answer 7

Pathophysiology:
When Herpes zoster affects the ophthalmic branch of trigeminal, ocular involvement may occur.

Presentation

1. typical skin rash is present, the condition is easy to diagnose.
2. Hutchinson’s sign: the appearance of typical lesions at the tip, side, or root of the nose –> areas are innervated by a branch of the nasociliary nerve, which also innervates the cornea, such lesions may herald ocular involvement.
3. blepharitis
4. keratitis
5. uveitis
6. optic neuritis.
7. Herpes zoster in a young patient should raise suspicion of HIV related immune suppression.

TREATMENT

1. Early referral
2. Systemic acyclovir in high doses
3. Local acyclovir
4. Careful use of steroids
5. Pain control for the neuralgia

Question 8

PERIPHERAL CORNEAL ULCERATION and THINNING: MARGINAL INFILTRATES and ULCERATION

Cause
Presentation
Treatment

Answer 8

Cause
1. antigen-antibody reaction
2. Secondary to chronic bacterial conjunctivitis, especially Staphylococcal blepharoconjunctivitis.
Bacterial antigens diffuse into the cornea –> contact with antibodies diffusing from the limbal blood vessels.
3. systemic collagen vascular disease such as rheumatoid arthritis.

CLINICAL FEATURES

1. Marginal infiltrates usually begin as whitish oval or linear opacities adjacent to the limbus.
2. They may later lead to extremely painful ulceration and vascularisation.

TREATMENT
1. The local lesions respond to topical steroids.
2. Cycloplegia for pain.
3. ID and treat the underlying cause.
•Treat conjunctivitis and blepharoconjunctivitis with local antibiotics.
•Manage systemic collagen vascular diseases appropriately, with systemic steroids if necessary.

Question 9

PERIPHERAL CORNEAL ULCERATION & THINNING: PHLYCTENULOSIS

Cause
Presentation
Treatment

Answer 9

EPIDEMIOLOGY
Delayed hypersensitivity response to bacterial antigens: TB, staphylococcal antigens.

CLINICAL FEATURES

1. Acute phlyctenulosis is very painful usually with severe lacrimation, photophobia and blepharospasm.
2. A conjunctival phlycten begins as a raised pink nodule with surrounding hyperaemia close to the limbus. This nodule then ulcerates and heals spontaneously.
3. A corneal phlycten begins at the limbus and may spread onto the cornea, ulcerate or heal spontaneously.

TREATMENT

1. short course of topical steroids.
2. Treat cause

Question 10

XEROPHTHALMIA (VITAMIN A DEFICIENCY)

Pathophysiology
Presentation

Answer 10

Pathophysiology

1. The ocular manifestations of vitamin A deficiency are known as xerophthalmia.
2. Loss of mucus secreting goblet cells results in a severely dry eye.
3. The conjunctival epithelium keratinises and the cornea becomes dull.
4. The cornea may later soften, undergo necrosis and perforate.

Presentation
Night blindness occurs in xerophthalmia.

Question 11

ARCUS CORNEALIS

Pathophysiology
Presentation
Treatment

Answer 11

Pathophysiology

1. Arcus cornealis is a very common peripheral corneal degeneration that affects mainly older people.
2. It consists of a grey-white ring of stromal lipid deposition in the corneal periphery with a clear interval between the ring and the limbus. It usually begins as discontinuous superior and inferior arcs which gradually join to form a complete ring.
3. Younger people–> Sign of hyperlipidaemia

Presentation
grey-white ring of stromal lipid deposition in the corneal periphery with a clear interval between the ring and the limbus. It usually begins as discontinuous superior and inferior arcs which gradually join to form a complete ring.

treatment
Not indicated.
Test cholesterol

Question 12

HAEMA TOCORNEA

Pathophysiology

Answer 12

Pathophysiology:

1. When a hyphaema is present–> cornea may be stained with haemoglobin, especially when the hyphaema is longstanding or the intraocular pressure is raised.
2. It may take many years to clear, and may be permanent.

Question 13

KERATOCONUS

Pathophysiology
Presentation
Treatment

Answer 13

Pathophysiology
Ectatic corneal dystrophy.
Weakening of the corneal stroma –> thinning and bulging of the central and inferior paracentral cornea.

Presentation:

1. myopia
2. astigmatism.
3. Munson’s sign: when the patient looks down, the conic shape can be seen to thrust the centre of the lower lid margin forwards.
4. Initially, good vision may be obtained with hard contact lenses.
5. Progression may be an indication for chemical stabilisation of the cone by collagen cross linking.

Treatment:
1. Initially: Hard contact lenses
2. Conrneal Implants
3 Corneal transplant

Question 14

Conditions of the Cornea

Answer 14

Infiltration and Ulceration:

1. Kerrititis
   - Bacterial
   - Viral
   - Fungal
2. Peripheral corneal ulceration and thining
   - Marginal infiltrates and ulceration
   - Phlyctenulosis
   - Xerophthalmia
   - Neurotrophic corneal ulceration
   - Exposure Keratopathy
   - Carneal Flash burn (Arc eye)
3. Miscellaneous:
   - Arcus Cornealis
   - Haematocornea
   - Keratoconus

Question 15

PHYSIOLOGY: Corneal pathology

Answer 15

malfunction of the endothelium –> corneal oedema–> swelling and loss of transparency of the stroma–> > intraocular pressure rises–> difficult for the endothelial pump to pump water out of the stroma and into the anterior chamber against the increased pressure gradient–> > IOP –> corneal oedema–> acute angle closure glaucoma.

Question 16

NEUROTROPHIC CORNEAL ULCERATION

Pathophysiology
Causes
Treatement

Answer 16

Pathophysiology:
Loss of corneal sensation due to damage to the ophthalmic division of the trigeminal results in neurotrophic corneal damage.

Causes:

1. Ulceration
2. secondary infection

Treatment:

1. Early temporary or permanent tarsorrhaphy,
2. tear supplements
3. infection control

Question 17

EXPOSURE KERATOPATHY

Pathophysiology
Cause
Treatment

Answer 17

Pathophysiology:
Any condition resulting in the eyelids not closing completely (lagophthalmos) or interfering with the blink mechanism will result in drying out of the corneal epithelium with the risk of secondary ulceration and infection.

Causes:

1. Patients under anaesthesia
2. Unconscious patients
3. Exophthalmos
4. Bell’ s palsy with lagophthalmos
5. Severe ectropion

Treatment
Tear supplements to prevent corneal drying.

Question 18

CORNEAL FLASH BURN (ARC EYE)

Pathophysiology
Cause

Answer 18

Pathophysiology
UV light irradiation burn of the cornea.

Cause
welding without a visor and sunlamp tanning without eye shields.