Ординатура / Офтальмология / Английские материалы / Pediatric Opthalmology_Mukherjee_2005

are seen in adults. Most characteristic sign of herpetic ulcer is diminish corneal sensation. The ulcer is unilateral, generally central and dendritic in shape without much redness and pain. Initially the ulcer stains poorly with fluorescein and better with rose bengal. In later stage with disquamation of epithelium fluorescein stain becomes prominent. Herpetic ulcer does not develop hypopyon unless secondarily infected by bacteria.

The other symptoms of viral keratitis are foreign body sensation, lacrimation, photophobia, diminished vision, sometimes diminished corneal sensation. Initially there is hardly any circumciliary congestion. The ulcers are small and numerous. They stain with fluorescein. Smaller ulcers may require cobalt blue filter to become visible many viral ulcers are bilateral.

Characteristics of sterile corneal ulcer. These ulcers are generally peripheral, mostly bilateral, relatively quiet, without circumcorneal congestion. Corneal infiltrates and epithelial defect are minimal or absent. There is no anterior chamber reaction, no hypopyon, corneal sensation is normal. Vision is diminished if the lesion is central. Other symptoms are mild redness and pain. Etiological factors are generally systemic.

Morphological distribution of corneal ulcer. Corneal ulcers can be central or peripheral, both can be superficial, deep, infective or non infective.

Central corneal ulcers42, 43. Central corneal ulcers are mostly infective, may be caused by bacteria, fungi and viruses. As they develop in front of pupil, diminished vision is early and marked that becomes worse with extension of ulcer. Even successful treatment leaves residual central opacity that causes diminished vision. Diminished vision is not only due to obstruction of light to pass through pupil but also due to accompanied irregular astigmatism. Diminished vision following central corneal ulcer puts child at an added disadvantage of intractable amblyopia and squint. Opacity developing in infancy may cause nystagmus.

Peripheral (marginal) corneal ulcers35, 44. Marginal corneal ulcers are as common as central ulcers. They are less dramatic than central ulcers and have a more benign course, hence draw less and late attention than central ulcers. However incidence of peripheral ulcer is less in children than adults. Marginal ulcers in children do not perforate unless secondary bacterial infection is superimposed. Causes of their being superficial and non perforating is better nutrition on the periphery of cornea and enhanced thickness of corneal periphery.

Causes of peripheral corneal ulcers are :

1.Extension of conjunctival disease in the cornea i.e. trachoma, phlycten, rosacea, staphylococcal blepharoconjunctivitis.

2.Allergic—phlycten

3.Toxin

4.Metabolic

Marginal ulcers according to their position can be (1) sectorial, (2) circumferential - may form a ring ulcer. Circumferential ulcers generally result due to coalescence of more than one peripheral ulcer. Circumferential ulcers have tendency to develop heavy superficial vascularisation.

Identification of specific causative organism is done by : (a) Corneal scrapping and examination of stained slide. (b) Culture of organism

(c) Sensitivity of organism to antibiotic.

Identification of other ocular diseases that may influence treatment of corneal ulcer i.e. lagophthalmos, lid deformity, loss of sensation, chronic dacryocystitis, raised intraocular tension.

Systemic diseases. Malnutrition, vitamin A deficiency, measles. Diabetes is generally not a problem in children but should be kept in mind if it is associated with symptoms of juvenile diabetes.

Specific treatment : 1. Anti microbial drugs.

Local antibiotics. Once it has been established that the ulcer is infective and its causative organism identified, specific anti microbial drops in suitable strength and frequency will eliminate the organism and enhance healing. However it is not always practical to get smear, culture and sensitivity done, result of sensitivity to antibiotic for bacterial infection takes minimum 24 hours to 48 hours. Fungal culture takes as much as a fortnight to be informative. Culture of virus is done only in few selected and advanced centres. Most practical method is to decide an antibiotic according to clinical feature. Generally a long acting antibiotic that is effective against both gram positive and negative organisms is used as aqueous drops. Frequency depends upon severity of the condition.

Commonly used antibiotic in infective corneal ulcer are Erythromycin 0.5%, Chloramphenicol 03.%-0.5%, Gentamycin 0.3%, Tobramycin 0.3%, Ciprofloxicin 0.3%, Framycetin 0.5%, Ofloxacin 0.3%, sparfloxacin 0.3%. Newer antibiotics are being added frequently replacing older antibiotics.

These drugs are instilled as drops, one drop each hour in the lower fornix. More than one drop at a time is not retained in the conjunctiva and flows out without additional therapeutic advantage.

Sometimes a combination of antibiotics that have synergistic effect is used. A common combination are Neomycin 0.35% + Polymyxine B. 10000 u and Bacitracin 500u. Another popular combination is combination of neomycin with chloramphenicol.

In adults and older children subconjunctival injection may be given. Whenever it is not possible to administer subconjunctival injection, fortified antibiotic solutions are instilled instead of ordinary drops.

Commonly used fortified solutions used for corneal ulcer are : Gentamycin 14 mg/ml,

Cephazoline 33 mg/ml, Tobracin 15 mg/ml

Ophthalmic ointment is used at bed time either with or without bandage.

Advantage of ophthalmic ointments are :

They act as lubricants, they have slow absorption, slow drainage from the conjunctival sac. They need not be applied frequently. They prevent sticking of the lids.

Subconjunctival injection. Commonly used subconjunctival injections are : Penicillin—1 million unit/ml

Gentamycin—20 mg-40 mg/ml Cephazoline—100 mg-125 mg /ml Tobramycin—20 mg-40 mg/ml

Subconjunctival injection of antibiotic gives a high but short lived peak of antibiotic concentration at the site of injection. Hence they are either given along with local instillation or at bed time with a pad and bandage.

Generally subconjunctival injections are given once a day for five to seven days. Systemic antibiotics do not have any added advantage over local antibiotics. (For anti fungal and anti-viral drugs used in corneal ulcer see under specific ulcers)

2.Removal of discharge. Bacterial and fungal corneal ulcers are generally associated with mucopurulent or purulent discharge. Efforts should be made to remove the discharge from the conjunctival sac and lid margin with sterile wet swab. Irrigation of the conjunctival sac has no added advantage. On the contrary it washes away tear lysozyme which has anti microbial property.

3.Cycloplegia. Cycloplegics should be used in all corneal ulcers with anterior chamber reaction. Cycloplegics have no action on cornea, they are not anti-inflammatory, analgesics or anti microbial. Main function of cycloplegic in corneal ulcer is to prevent and treat associated anterior uveitis that is main cause of pain and photophobia. Cycloplegics relive spasm of ciliary body, thus reduce pain indirectly. As all cycloplegics are strong mydriatic also, they dilate the pupil and break posterior synechea.

As such pure mydriatics have no role in management of corneal ulcer. Commonly used cycloplegics in corneal ulcer are :

(i) Atropine sulphate. Atropine is most potent cycloplegic and prompt mydriatic. Its action last for more than ten days following single instillation, however, in inflamed eye more than one instillation is required. Atropine should be used with caution in children. One drop of one percent atropine contain more than therapeutic dose. It is better to avoid atropine as drop in children. In no case should atropine be used more than twice in twenty four hours. If necessary short acting cycloplegic may be added to atropine to enhance effect of atropine. Prolonged use of atropine may cause allergic dermatitis. While prescribing atropine to children the parents should be appraised of the side effect of atropine i.e. flushed face, fever, and dryness of mouth which are not serious and can be managed by systemic antipyretic and plenty of fluids orally. Dilated pupil makes the child uncomfortable due to glare.

(ii) Home atropine hydrobromide 2%. It is less powerful cycloplegic than atropine. Its action does not last more than 48 hours. Its side effects are less than atropine so it can be used frequently. However in children who develop allergy to atropine are also allergic to home atropine. It is generally used in cases of superficial small ulcers.

(iii) Cyclopentolate hydrochloride. This is used as 1% drop, has action faster than home atropine but action lasts for twenty four hours to forty eight hours, can be used frequently.

Tropicamide 1% is very short acting unless used repeatedly has hardly any beneficial effect in corneal ulcer.

4.Pad and bandage. Pad and bandage prevent movement of lid over the ulcer this stabilises the epithelial growth during healing. It does not abolish movement of eye, it only reduces movement of lid that helps epithelisation of ulcer. However pad and bandage raise the temperature of the conjunctiva which encourages proliferation of micro organism, hence, application of pad is contra indicated in presence of copious discharge.

5.Bandage contact lenses are good substitute for usual pad and bandage.

6.Destruction of ulcer :

(i) Cauterisation of ulcer. If ulcer fails to respond to usual treatment within a week, debridement of the ulcer is done under local anaesthesia and edges are cauterised by pure carbolic with caution.

Other drugs used to cauterise the ulcer are 7% alcoholic solution of iodine, trichlor acetic acid.

(ii) Physical methods of destruction of ulcers are Heat cautery, cryo and laser. 7. In case of non healing corneal ulcer, penetrating keratoplasty is indicated.

Management of hypopyon corneal ulcer. Hypopyon corneal ulcer denotes presence of severe anterior uveitis due to corneal ulcer. All bacteria are capable of producing hypopyon. Some organisms characteristically produce severe hypopyon, others cause minimal hypopyon.

Hypopyon is acculumation of sterile pus in anterior chamber. It contains mostly polymorphonuclear leucocytes, occasional mononeuclear cells, macro-phages and fibrin. The pus is due to out pouring of exudates from iris and ciliary body. In bacterial corneal ulcer, the pus remains sterile so long as Descemet’s membrane is intact. The pus gets infected following perforation of ulcer. It is a prominent feature in central corneal ulcers and penetrating injury. The pus in bacterial corneal ulcer is worsened by absorption of toxin liberated by causative organism.

Hypopyon in fungal ulcer is generally infected because fungus can penetrate intact Descemet’s membrane. Bacteria produce hypopyon earlier than fungi.

Virus by themselves do not produce hypopyon. Presence of pus in viral keratitis denotes presence of secondary bacterial infection.

Development of pus is preceded by severe anterior chamber reaction. The aqueous becomes plasmoid and fibrinous that entangles leucocytes. Presence of pus cells in the anterior chamber gives it characteristic white colour, however the pus is tinged green in pseudomonas infection, and is yellowish in fungus, it may be occasionally tinted with blood. As pus is heavier than aqueous, hypopyon settles down at the most dependent part of anterior chamber, it assumes a horizontal level at the upper part. Though hypopyon is thicker than aqueous yet it freely moves unless it gets organised as is seen in fungal ulcer. Amount of hypopyon is directly proportionate to virulence of organism. Some organisms produce early

and severe hypopyon. Organisms that produce severe hypopyon are—pneumococci, pseudomonas, streptococci pyogenes, gonococcus. Extent of hypopyon is measured by its height from bottom of anterior chamber in millimeters or roughly as trace, mild, moderate, half of AC or full of AC. Best position of the eye to look for early hypopyon is to make the patient sit up for few minutes and allow hypopyon to settle down and ask the patient to look down, light is thrown from the above in front of the iris. In recumbent position the pus spreads all over the iris or may pass through the pupil, making it difficult to be visualised.

Hypopyon in fungal corneal ulcer takes more time to develop, it is associated with severe anterior chamber reaction. The pus is generally thick, does not move freely with change in position of the eye, is fluffy, yellowish in colour and infected with fungal element. The ulcer has multiple satellite lesion and an endothelial plaque under the original ulcer.

Management of hypopyon corneal ulcer is basically the same as any infective ulcer with severe uveitis. Hypopyon corneal ulcer should be treated as an emergency. It is better to hospitalise the patient and start vigorous antibiotic drop instillation. Subconjunctival injection in children is difficult to administer. Hence frequent local instillation of suitable fortified antibiotic is most important part of treatment. In bacterial ulcers hypopyon may disappear with in twenty four hours only to appear after frequency of instillation is reduced unless infection has been eradicated.

Bandage lenses and occuserts are good alternative when available and possible.

In children sub-conjunctival injection and cauterisation should be done under short acting general anaesthesia or good sedation.

All cases of hypopyon should receive atropine sulphate 1% as an ointment. Atropinisation should be done under supervision of trained person. Atropine drops are better avoided because an illiterate attendant may instil atropine frequently in place of antibiotic without anticipating serious complication.

Outline of treatment of hypopyon—Corneal ulcer should be as follows :

1.Hospitalise the child.

2.Affective and safe atropinisation.

3.Frequent instillation of single or combination of two broad spectrum synergestic antibiotic drops that will eradicate both gram positive and gram negative cocci and bacilli.

4.Corneal scrapping :

(i) Examine part of scrapped material after staining with Gram’s stain, Giemsa stain, 10% KOH to identify bacteria and fungus and find out if the characteristics present are in favour of bacteria or fungi.

(ii) Inoculate part of the material to grow bacteria or fungi. (iii) Identify organism and test for sensitivity to antibiotic.

5.Once best possible antibiotic has been identified, replace initial antibiotic with sensitive antibiotic as fortified drops. If possible give sub-conjunctival injection of the same antibiotic.

(ii) Introduction of exogenous infection by way of contaminated drops i.e. fluorescein drops, local anaesthetic agent.

(iii) Over enthusiastic chemical cauterisation.

Management of non healing corneal ulcer is basically treatment of simple corneal ulcer with suitable antibiotic, cycloplegic and correction of above mentioned factors. In case of penicillinase producing organism i.e. staphylococci, methicillin should be used. Pseudomonas corneal ulcers generally require two antibiotic drops one aminoglycocide and other cefazolin. Common ancillary management consists of cauterisation of ulcer edge, sub-conjunctival antibiotic injection, bandage lens, local beta blockers or systemic acetazolamide, cauterisation of superficial vascularisation. Under no condition should a subconjunctival injection or cauterisation be tried in a struggling child. The child should be properly sedated for such procedures. Predisposing factors should be eliminated i.e. epilate the misdirected lash, perform a tarsorrhaphy in lagophthalmos and neurotropic keratitis.

All malnourished children should get full dose of vitamin A as per WHO recommendation.

Corneal ulcer threatening to perforate :

There are two groups of ulcers that perforate :

1.Very fast developing ulcer like pneumococcal, and pseudomonas ulcers and keratomalacia.

2.Slow developing ulcers - Fungal ulcer, stromal involvement in HSV, Herpes simplex keratitis.

Perforation of an ulcer is a catastrophe that must be avoided. Once an ulcer perforates, the prognosis changes to worst. It may lead to endophthalmitis or even panophthalmitis. If perforation seals, it leads to adherent leucoma or corneal staphyloma.

Management of impending perforation are :

1.Anticipation of perforation. A fast developing ulcer, especially in depth with large hypopyon, severe anterior chamber reaction and pain is most likely to perforate. Intensive instillation of two synergistic antibiotic with subconjunctival injection may stop the progress.

2.Prevent

(i) A sudden rise of intraocular pressure by preventing cough, sneezing, vomiting, and constipation. Protect the eye from direct trauma by metal or plastic shield placed properly. Otherwise the edge of shield itself can traumatise cornea.

(ii) Fast build up of intraocular tension is managed by local beta blocker two times a day or acetazolamide 15 mg/kg body weight in divided doses for short period.

Pilocarpine is contra indicated.

(iii) Paracentesis. Paracentesis is a guarded and planned perforation on the corneal periphery. It should be done under general anaesthesia in children. It lowers intraocular tension instantaneously. Advantage of paracentesis are :

1.Pus drains out through the wound.

2.Pus and aqueous so drained can be examined for microbes.

3.If necessary, intra cameral antibiotics can be injected.

4.Following paracentesis, there is out pouring of fresh aqueous that has healing property.

4.Strengthening the thinned cornea by cynoacrylate substance when the ulcer is small.

5.Keratoplasty. In selected cases with rim of healthy cornea all round, penetrating keratoplasty may be tried. One of the advantages of penetrating keratoplasty is that it removes the infected part of the cornea, which harbours micro-organism, hypopyon is drained through the wound, AC can be washed with balanced salt solution antibiotics can be instilled directly in AC. Chances of dens central corneal opacity are reduced.

Complications of corneal ulcer. Aim of treatment of corneal ulcer is to eliminate infection and give a clear cornea. Corneal opacity is almost unavoidable even with best treatment unless it involves the epithelium only. The size and depth of opacity varies with extent of ulcer and promptness of treatment. Ulcers anterior to the Bowman’s membrane give faintest opacity unless they are vascularised. Full thickness extension with or without iris incarceration give most dense opacities. Corneal opacities in children not only diminish vision but lead to intractable amblyopia and squint. Opacity developing in infancy lead to nystagmus. Another complication of corneal ulcer that is often overlooked is gradually developing glaucoma specially following perforation. Presence of raised intraocular tension produces early disc changes in children that later on hampers with visual gain even after successful keratoplasty.

Commonest sequel of corneal ulcer is loss of transparency. Loss of transparency is commonly known as corneal opacity. The opacity is generally white in colour. According to colour of opacity which in turn depends upon its depth and incarceration of uvea opacities have been divided into following grades :

1.Nebula

2.Macula

3.Leucoma and

4.Leucoma adherent

Other sequel and complications are :

1.Ectasia

2.Perforation

Corneal opacity is produced due to replacement of keratocytes by fibrocytes, infiltration and edema. Infiltration and edema generally pass off with healing, may take weeks to months to disappear. Corneal opacities following destruction of Bowman’s membrane are always permanent.

Nebular opacities in corneal ulcer develop due to infiltrating edema and cicatrisation of epithelial defect. They are generally situated in front of the Bowman’s membrane. Small nebular opacities may be missed on oblique illumination but are best visualised on slit lamp biomicroscopy. On retinoscopy they cause irregular reflex. Though they do not cause much visual loss diminished vision due to nebulae are sufficient to cause amblyopia.

Macular opacities are denser than nebulae and visualised by ordinary flashlight. They are due to destruction of Bowman’s membrane and superficial stroma. They are permanent in nature.

Leucomass are densest opacities that are visible in diffuse light and when large, the parents may notice their presence. They are generally due to lesions extending from epithelium to Descemet’s membrane. They may cover whole of the cornea, may have facets in them, are often vascularised. They cause maximum loss of vision, amblyopia, and squint in children.

As corneal ulcer perforates following events take place :

1.Aqueous drains out causing softening of the eyeball, flattening of cornea, collapse of AC and miosis.

2.The iris is drawn towards the perforation and gets attached to it.

3.The iris plugs the wound over which fibrosis occurs and

4.A leucomatous opacity develops. This is called leucoma adherence.

Eye with leucoma adherence has following features :

1.A corneal opacity in which either the iris is adherent or there is an evidence that iris was once incarcerated, which is betrayed by presence of iris pigment in the centre of the opacity. Thus any corneal opacity with evidence of iris incarcerated is adherent leucoma.

2.Key hole pattern of pupil with narrow end towards the opacity.

3.Absence of AC at the site of iris incarceration.

4.Tent like appearance of the iris with apex at the opacity.

Ectatic Changes in Cornea Following Perforation

1. Staphyloma. Perforation is very common catastrophic complication of corneal ulcer. They are most common in large central, untreated or poorly managed ulcers that extend deeper than Descemet’s membrane. Small corneal perforation is plugged by a knuckle of iris to form an adherent leucoma. A large perforation is not immediately sealed. As has been discussed earlier, a perforation leads to draining of aqueous, flattening of cornea, softening of eyeball, miosis and shift of iris lens diaphragm forwards. This forwarded shifted iris blocks the perforation and the constricted pupil is closed by exudate that acts as a scaffolding over which fibrocytes from stroma and epithelium develop to form a white scar or pseudocornea of uneven thickness which is very thin and plastered with iris on posterior surface at places the whole of the scar gets ectetic and bulges forward. This ectatic cicatrix with iris incarcerated is called corneal or anterior staphyloma. It can engulf whole of cornea and called total anterior staphyloma or may be partial. The anterior staphyloma may be vascularised, may have facets. There is always associated secondary glaucoma, which produces loss of vision which is very common. A large staphyloma may bulge through inter palpebral fissure. Generally the staphylomatous eyes are divergent and have nystagmus. Commonly they are not painful, uncontrolled glaucoma or break down of scar make them painful. In unfortunate children anterior staphyloma can be bilateral. Small pox used to be commonest

cause of large bilateral anterior staphyloma before small pox was eradicated. In under developed countries, keratomalacia still causes bilateral anterior staphyloma. Blast injury especially due to cracker burst is another cause of bilateral, total or partial staphyloma in children.

2. Descemetocele. Bulging of thin cornea is a common feature of poorly managed corneal ulcer. If there is incarceration of iris in ectatic cornea, it results in corneal staphyloma that has been discussed earlier. If there is no perforation, iris does not get incarcerated in the wound and the Descemet’s membrane bulges through the floor of the ulcer. It is called Descemetocele or keratocele. In the infiltrative stage of corneal ulcer, the ulcer can spread either towards the periphery or may infiltrate deep. In unfortunate conditions both may happen simultaneously. Deeper infiltration is rapid through Bowman’s membrane and stroma. The Descemet’s membrane offers real resistance and can withstand the infiltrative processes for sometime. As the ulcer reaches the Descemet’s membrane, the membrane bulges forward as a translucent blister through the floor of ulcer under normal intraocular pressure. If intraocular pressure is high, not only will the surrounding Descemet’s membrane bulge but also surrounding thin cornea.

Corneal ectasia may follow thinning of cornea without Descemet’s membrane bulging. In simple ectatic cicatrix of cornea, there is no incarceration of iris. The cicatrised ectasia is a weak spot in cornea hence is liable to perforate either following trauma or gradual rise of tension. Perforation of ectatic cornea is not sealed so perfectly as a simple small perforation seals. It may seal and anterior chamber may reform only to be lost following opening up of the wound resulting into a corneal fistula.

Corneal fistula45. Corneal fistula is a small track that allows anterior chamber to open externally permanently. In corneal ulcer it is generally seen in the centre of the cornea, is not wider than one to two millimetre. It is lined by corneal epithelium that grows down the wall of the fistula. The epithelium may spread over the corneal endothelium and iris. Traumatic corneal fistula may develop anywhere over the cornea.

Formation of corneal fistula may occur in following conditions

1.Perforation of a ectatic cicatrix that is not plugged by iris.

2.Perforation of centre of cornea -

(a) When pupil is widely dilated due to prolonged atropinisation and kept dilated following perforation. This prevents the iris from blocking the hole.

(b) A pre-existing wide iridectomy that prevents iris from reaching the perforation. (c) Coloboma of iris. In very rare instances aniridia.

The fistula gives all the features of a corneal perforation i.e. flat cornea, absent AC and soft eye. The only difference is that the pupil is not constricted, vision is very poor. Occasionally the fistula may be blocked by debris resulting in reformation of the AC. This allows intraocular pressure to build up, which does not last long as rise of intraocular pressure even within normal range forces the fistula to open and the AC is again lost.

The corneal fistula has a typical appearances of a translucent pit surrounded by a zone of infiltration. On careful examination, it will be noted that aqueous leaks through the pit or may be forced to leak on pressing the globe.