1. THE PAINFUL RED EYE
PART 3
KERATITIS
Lorrimer Esselaar

2. EVALUATION OF KERATITIS
CLINICAL FEATURES
SYMPTOMS
Stimulation of corneal nerves causes superficial pain.
It also causes reflex spasm of the ciliary muscle and iris sphincter to produce deep seated pain and photophobia.
Movement of the upper lid worsens the pain and causes a scratchy sensation with resultant blepharospasm.
Vision is often affected and reflex tearing occurs.
Halos are seen around lights when corneal oedema is present.
Redness
Pain
Photophobia
Blepharospasm
Tearing
Reduced vision
Halos around lights
SIGNS
The cornea must be examined with a bright light. A magnifying glass helps to see less obvious lesions. Remember that your ophthalmoscope acts as a magnifying glass when set on a high plus.
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.

3. The pattern of redness is typically more intense towards the limbus and less intense towards the fornices. This pattern of redness is known as ciliary or circumcorneal injection. Compare the generalised conjunctival injection of conjunctivitis.
Local anaesthetic is often indispensable in making an examination possible.
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!

4. Central zone
Danger zone
Bacteria
Fungi
Viruses
Immune complex
Peripheral zone
Safer zone
LOCATION
The location of the lesion may be an important clue to the nature of the problem.
Central cornea: Usually caused by direct infection by bacteria, fungi and viruses.
Peripheral cornea: Usually caused by immune complex reactions in which the lesions themselves do not contain microorganisms. They may also be caused by direct infection by viruses.

5. PRINCIPLES OF MANAGEMENT
Use the following features to categorise the lesion: (a) History (b) Nature of the discharge (c) Location of the lesion (d) Appearance of the lesion (e) Corneal sensation
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.
Refer immediately: (a) Any corneal lesion reducing visual acuity. (b) Any discrete corneal lesion which stains with fluorescein.
Exception: A confidently diagnosed, noncentral, Herpes simplex dendritic ulcer.
(c) Any hypopyon, whatever the cause.
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.

6. BACTERIAL KERATITIS EPIDEMIOLOGY
Most causative organisms are opportunists which cause infection only when local resistance is low.
The 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.
The three commonest organisms that cause bacterial ulceration are:
Pneumococcus This is the primary corneal pathogen.
Pseudomonas Rapidly enlarging ulcer due to proteolytic enzymes which cause lysis of the corneal stroma. Perforation is a real danger.
Staphylococcus aureus and epidermidis

7. INVESTIGATIONS MANAGEMENT
Corneal opacification secondary to corneal ulceration is a common cause of permanent loss of vision which is to a large extent preventable if an aetiological diagnosis is made and the correct treatment instituted early.
Thus MC&S should be performed whenever available. Corneal scrapings from the edge of the ulcer yield the best results, and these should preferably be done by an ophthalmologist.
MANAGEMENT
Management is often difficult and prolonged. The response to treatment and the development of complications must be carefully monitored. If possible refer to an ophthalmologist immediately. Alternatively treatment should be commenced without delay but in telephonic consultation with an ophthalmologist.
Irrigate the eye with normal saline to remove any purulent discharge from the conjunctival sac and eyelid margins. This must be performed regularly throughout treatment to reduce the load of organisms and debris and so increase antibiotic efficacy.
Cycloplegic drops should always be administered to relieve ciliary spasm and the resultant pain (vide infra).
Local antibiotic drops (vide infra).
Do not pad the eye unless specifically advised to do so by the ophthalmologist. A closed eye with a static and debris filled tear film may act as a culture medium.

8. LOCAL ANTIBIOTIC DROPS
CYCLOPLEGIC DROPS
For cycloplegia use Cyclopentolate HCI (Cyclogyl ®) 1% tid.
Do not use tropicamide (Mydriacyl®). It is too weak and too short acting.
Do not use atropine. It is too potent and too long acting.
LOCAL ANTIBIOTIC DROPS
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.
Start with a loading dose: 1 drop every minute for 5 minutes. Then one drop every half hour for 24 hours. Then one drop every hour for 48 hours while keeping close surveillance. Then adjust the regime to the response. Remember to keep the eye closed for a minute after administering the drop.

9. COMPLICATIONS Permanent corneal thinning.
Permanent corneal opacification.
Corneal perforation.
Anterior uveitis with hypopyon.
Endophthalmitis: the infection affects the lens and posterior segment.
Permanent loss of vision can occur as a result of any of the above.
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.

10. VIRAL KERATITIS HERPES SIMPLEX
PRIMARY HERPES SIMPLEX KERATOCONJUNCTIVITIS
This condition represents the primary infection with the virus and usually occurs in children and young adults.
There is usually mild malaise and the typical vesicular skin rash may occur on the eyelids. This is followed by a follicular conjunctivitis and punctate epithelial keratitis. After about a week, dendritic keratitis may occur.
Treatment is the same as for the recurrent form (see below).
RECURRENT HERPES SIMPLEX KERATITIS
SYMPTOMS
Irritation, tearing and moderate photophobia. Some loss of vision is usually present.
SIGNS
Dendritic ulcer with the typical linear branching pattern (Greek: dendron = tree).
A dendritic ulcer may enlarge to become a geographic ulcer.
Dendritic ulcer
Geographic ulcer

11. in any case of Herpes simplex keratitis.
Corneal sensation over the ulcer is reduced or absent. This is an extremely important finding. Reduced corneal sensation is highly suggestive of Herpes simplex keratitis.
TREATMENT
Acyclovir (Zovirax) ointment 5 times daily.
Cycloplegia: Cyclopentolate (Cyclogyl) to relieve the pain of reflex ciliary spasm, expecially if a secondary uveitis is present.
COMPLICATIONS
Disciform keratitis
This is the commonest complication.
A round, central area of corneal oedema develops
due to an immune response.
The patient’s vision is usually dramatically decreased.
Stromal keratitis
The involved area of cornea becomes oedematous.
There is usually a severe associated anterior uveitis.
The condition tends to be chronic and extremely painful and has a poor prognosis.
It occurs when Herpes simplex keratitis is erroneously treated with steroids.
Treatment of both of the above complications involves steroids and should under no circumstances be undertaken by the general practitioner.
Disciform keratitis
As far as the general practitioner is concerned, steroids are absolutely contraindicated
in any case of Herpes simplex keratitis.

12. HERPES ZOSTER OPHTHALMICUS
Typical skin rash
CLINICAL PICTURE
When Herpes zoster affects the ophthalmic branch of trigeminal, ocular involvement may occur.
When the typical skin rash is present, the condition is easy to diagnose. However, at the time of onset, patients may have only ocular involvement without the skin rash.
A strong prognostic indicator of ocular involvement is Hutchinson’s sign: the appearance of typical lesions at the tip, side, or root of the nose. Because these areas are innervated by a branch of the nasociliary nerve, which also innervates the cornea, such lesions may herald ocular involvement.
Herpes zoster can involve the visual system in many ways, including blepharitis, keratitis, uveitis and optic neuritis.
Herpes zoster in a young patient should raise suspicion of HIV related immune suppression.
Hutchinson’s
sign

13. TREATMENT Early referral Systemic acyclovir in high doses
Local acyclovir
Careful use of steroids
Pain control (neuralgia)

14. PERIPHERAL KERATITIS INFILTRATES & ULCERATION EPIDEMIOLOGY
Most marginal infiltrates and ulcerations are caused by an antigen-antibody reaction, and do not contain any organisms.
They are often secondary to chronic bacterial conjunctivitis, especially Staphylococcal blepharoconjunctivitis. Bacterial antigens diffuse into the cornea and come into contact with antibodies diffusing from the limbal blood vessels.
CLINICAL FEATURES
Staphylococcal blepharoconjunctivitis
Marginal infiltrates usually begin as whitish oval or linear opacities adjacent to the limbus.
They may later lead to extremely painful ulceration and vascularisation.
TREATMENT
The local lesions respond to topical steroids.
Cycloplegia for pain.
Identify and treat the underlying cause.
Treat conjunctivitis and blepharoconjunctivitis with local antibiotics.
Manage systemic collagen vascular diseases appropriately, with systemic steroids if necessary.

15. PHLYCTENULOSIS EPIDEMIOLOGY CLINICAL FEATURES TREATMENT
Phlyctens form due to a delayed hypersensitivity response to bacterial antigens. In high risk areas, tuberculosis is the most important cause, but elsewhere the cause is usually a reaction to staphylococcal antigens.
CLINICAL FEATURES
Acute phlyctenulosis is very painful usually with severe lacrimation, photophobia and blepharo- spasm.
A conjunctival phlycten begins as a raised pink nodule with surrounding hyperaemia close to the limbus. This nodule then ulcerates and heals spontaneously.
A corneal phlycten begins at the limbus and may spread onto the cornea, ulcerate or heal spontaneously.
TREATMENT
Treat the cause appropriately.
Phlyctens respond well to a short course of topical steroids.

16. Topic completed