Hypopyon corneal ulcer Etiopathogenesis Causative organisms. Many pyogenic organisms (staphylococci, streptococci, gonococci, Moraxella) may produce hypopyon, but by far the most dangerous are pseudomonas pyocyanea and pneumococcus. Thus, any corneal ulcer may be associated with hypopyon, however, it is customary to reserve the term 'hypopyon corneal ulcer' for the characteristic ulcer caused by pneumococcus and the term 'corneal ulcer with hypopyon' for the ulcers associated with hypopyon due to other causes. The characteristic hypopyon corneal ulcer caused by pneumococcus is called ulcus serpens. Source of infection for pneumococcal infection is usually the chronic dacryocystitis. Factors predisposing to development of hypopyon. Two main factors which predispose to development of hypopyon in a paitent with corneal ulcer are, the virulence of the infecting organism and the resistance of the tissues. Hence, hypopyon ulcers are much more common in old debilitated or alcoholic subjects. Mechanism of development of hypopyon. Corneal ulcer is often associated with some iritis owing to diffusion of bacterial toxins. When the iritis is severe the outpouring of leucocytes from the vessels is so great that these cells gravitate to the bottom of the anterior chamber to form a hypopyon. Thus, it is important to note that the hypopyon is sterile since the outpouring of polymorphonuclear cells is due to the toxins and not due to actual invasion by bacteria. Once the ulcerative process is controlled, the hypopyon is absorbed. Clinical features Symptoms are the same as described above for bacterial corneal ulcer. However, it is important to note that during initial stage of ulcus serpens there is remarkably little pain. As a result the treatment is often undully delayed. Signs. In general the signs are same as described above for the bacterial ulcer. Typical features of ulcus serpens are : Ulcus serpens is a greyish white or yellowish disc shaped ulcer occuring near the centre of cornea (Fig. 5.6). The ulcer has a tendency to creep over the cornea in a serpiginous fashion. One edge of the ulcer, along which the ulcer spreads, shows more infiltration. The other side of the ulcer may be undergoing simultaneous cicatrization and the edges may be covered with fresh epithelium. Violent iridocyclitis is commonly associated with a definite hypopyon. Hypopyon increases in size very rapidly and often results in secondary glaucoma. Ulcer spreads rapidly and has a great tendency for early perforation. DISEASES OF THE CORNEA 97 Management Management of hypopyon corneal ulcer is same as for other bacterial corneal ulcer. Special points which need to be considered are : Secondary glaucoma should be anticipated and treated with 0.5% timolol maleate, B.I.D. eye drops and oral acetazolamide. Source of infection, i.e., chronic dacryocystitis if detected, should be treated by dacryocystectomy. Complications of corneal ulcer 1. Toxic iridocyclitis. It is usually associated with cases of purulent corneal ulcer due to absorption of toxins in the anterior chamber. 2. Secondary glaucoma. It occurs due to fibrinous exudates blocking the angle of anterior chamber (inflammatory glaucoma). 3. Descemetocele. Some ulcers caused by virulent organisms extend rapidly up to Descemet's membrane, which gives a great resistance, but due to the effect of intraocular pressure it herniates as a transparent vesicle called the descemetocele or keratocele (Fig.5.3). This is a sign of impending perforation and is usually associated with severe pain. 4. Perforation of corneal ulcer. Sudden strain due to cough, sneeze or spasm of orbicularis muscle may convert impending perforation into actual perforation (Fig. 5.4). Following perforation, immediately pain is decreased and the patient feels some hot fluid (aqueous) coming out of eyes. Sequelae of corneal perforation include : i. Prolapse of iris. It occurs immediately following perforation in a bid to plug it. ii. Subluxation or anterior dislocation of lens may occur due to sudden stretching and rupture of zonules. iii. Anterior capsular cataract. It is formed when the lens comes in contact with the ulcer following a perforation in the pupillary area. iv. Corneal fistula. It is formed when the perforation in the pupillary area is not plugged by iris and is lined by epithelium which gives way repeatedly. There occurs continuous leak of aqueous through the fistula. v. Purulent uveitis, endophthalmitis or even panophthalmitis may develop due to spread of intraocular infection. vi. Intraocular haemorrhage in the form of either vitreous haemorrhage or expulsive choroidal haemorrhage may occur in some patients due to sudden lowering of intraocular pressure. 5. Corneal scarring. It is the usual end result of healed corneal ulcer. Corneal scarring leads to permanent visual impairment ranging from slight blurring to total blindness. Depending upon the clinical course of ulcer, corneal scar noted may be nebula, macula, leucoma, ectatic cicatrix or kerectasia, adherent leucoma or anterior staphyloma (for details see pages 122). Management of a case of corneal ulcer [A] Clinical evaluation Each case with corneal ulcer should be subjected to: 1. Thorough history taking to elicit mode of onset, duration of disease and severity of symptoms. A B Fig. 5.6. Hypopyon corneal ulcer : A, Diagrammatic depiction; B, Clinical photograph. 98 Comprehensive OPHTHALMOLOGY 2. General physical examination, especially for built, nourishment, anaemia and any immunocompromising disease. 3. Ocular examination should include: i. Diffuse light examination for gross lesions of the lids, conjunctiva and cornea including testing for sensations. ii. Regurgitation test and syringing to rule out lacrimal sac infection. iii. Biomicroscopic examination after staining of corneal ulcer with 2 per cent freshlyprepared aqueous solution of fluorescein dye or sterilised fluorescein impregnated filter paper strip to note site, size, shape, depth, margin, floor and vascularization of corneal ulcer. On biomicroscopy also note presence of keratic precipitates at the back of cornea, depth and contents of anterior chamber, colour and pattern of iris and condition of crystalline lens. [B] Laboratory investigations (a) Routine laboratory investigations such as haemoglobin, TLC, DLC, ESR, blood sugar, complete urine and stool examination should be carried out in each case. (b) Microbiological investigations. These studies are essential to identify causative organism, confirm the diagnosis and guide the treatment to be instituted. Material for such investigations is obtained by scraping the base and margins of the corneal ulcer (under local anaesthesia, using 2 percent xylocaine) with the help of a modified Kimura spatula or by simply using the bent tip of a 20 gauge hypodermic needle. The material obtained is used for the following investigations: i. Gram and Giemsa stained smears for possible identification of infecting organisms. ii. 10 per cent KOH wet preparation for identification of fungal hyphae. iii. Calcofluor white (CFW) stain preparation is viewed under fluorescence microscope for fungal filaments, the walls of which appear bright apple green. iv. Culture on blood agar medium for aerobic organisms. v. Culture on Sabouraud's dextrose agar medium for fungi. [C] Treatment I. Treatment of uncomplicated corneal ulcer Bacterial corneal ulcer is a vision threatening condition and demands urgent treatment by identification and eradication of causative bacteria. Treatment of corneal ulcer can be discussed under three headings: 1. Specific treatment for the cause. 2. Non-specific supportive therapy. 3. Physical and general measures. 1. The specific treatment (a) Topical antibiotics. Initial therapy (before results of culture and sensitivity are available) should be with combination therapy to cover both gram-negative and gram-positive organisms. It is preferable to start fortified gentamycin (14 mg/ml) or fortified tobramycin (14mg/ml) eyedrops along with fortified cephazoline (50mg/ ml), every ½ to one hour for first few days and then reduced to 2 hourly. Once the favourable response is obtained, the fortified drops can be substituted by more diluted commercially available eye-drops, e.g. : Ciprofloxacin (0.3%) eye drops, or Ofloxacin (0.3%) eye drops, or Gatifloxacin (0.3%) eye drops. (b) Systemic antibiotics are usually not required. However, a cephalosporine and an aminoglycoside or oral ciprofloxacin (750 mg twice daily) may be given in fulminating cases with perforation and when sclera is also involved. 2. Non-specific treatment (a) Cycloplegic drugs. Preferably 1 percent atropine eye ointment or drops should be used to reduce pain from ciliary spasm and to prevent the formation of posterior synechiae from secondary iridocyclitis. Atropine also increases the blood supply to anterior uvea by relieving pressure on the anterior ciliary arteries and so brings more antibodies in the aqueous humour. It also reduces exudation by decreasing hyperaemia and vascular permeability. Other cycloplegic which can be used is 2 per cent homatropine eye drops. DISEASES OF THE CORNEA 99 (b) Systemic analgesics and anti-inflammatory drugs such as paracetamol and ibuprofen relieve the pain and decrease oedema. (c) Vitamins (A, B-complex and C) help in early healing of ulcer. 3. Physical and general measures (a) Hot fomentation. Local application of heat (preferably dry) gives comfort, reduces pain and causes vasodilatation. (b) Dark goggles may be used to prevent photophobia. (c) Rest, good diet and fresh air may have a soothing effect. II. Treatment of non-healing corneal ulcer If the ulcer progresses despite the above therapy the following additional measures should be taken: 1. Removal of any known cause of non-healing ulcer. A thorough search for any already missed cause not allowing healing should be made and when found, such factors should be eliminated. Common causes of non-healing ulcers are as under: i. Local causes. Associated raised intraocular pressure, concretions, misdirected cilia, impacted foreign body, dacryocystitis, inadequate therapy, wrong diagnosis, lagophthalmos and excessive vascularization of ulcer. ii. Systemic causes: Diabetes mellitus, severe anaemia, malnutrition, chronic debilitating diseases and patients on systemic steroids. 2. Mechanical debridement of ulcer to remove necrosed material by scraping floor of the ulcer with a spatula under local anaesthesia may hasten the healing. 3. Cauterisation of the ulcer may also be considered in non-responding cases. Cauterisation may be performed with pure carbolic acid or 10-20 per cent trichloracetic acid. 4. Bandage soft contact lens may also help in healing. 5. Peritomy, i.e., severing of perilimbal conjunctival vessels may be performed when excessive corneal vascularization is hindering healing. III. Treatment of impending perforation When ulcer progresses and perforation seems imminent, the following additional measures may help to prevent perforation and its complications: 1. No strain. The patient should be advised to avoid sneezing, coughing and straining during stool etc. He should be advised strict bed rest. 2. Pressure bandage should be applied to give some external support. 3. Lowering of intraocular pressure by simultaneous use of acetazolamide 250 mg QID orally, intravenous mannitol (20%) drip stat, oral glycerol twice a day, 0.5% timolol eyedrops twice a day, and even paracentesis with slow evacuation of aqueous from the anterior chamber may be performed if required. 4. Tissue adhesive glue such as cynoacrylate is helpful in preventing perforation. 5. Conjunctival flap. The cornea may be covered completely or partly by a conjunctival flap to give support to the weak tissue. 6. Bandage soft contact lens may also be used. 7. Penetrating therapeutic keratoplasty (tectonic graft) may be undertaken in suitable cases, when available. IV. Treatment of perforated corneal ulcer Best is to prevent perforation. However, if perforation has occurred, immediate measures should be taken to restore the integrity of perforated cornea. Depending upon the size of perforation and availability, measures like use of tissue adhesive glues, covering with conjunctival flap, use of bandage soft contact lens or therapeutic keratoplasty should be undertaken. Best is an urgent therapeutic keratoplasty.