Ординатура / Офтальмология / Английские материалы / Pediatric Opthalmology_Mukherjee_2005

F = Face wash (personal hygiene)

E= Environmental changes (availability of running water, disposal of human waste, vector control)

Surgery is not required in children.

Allergic conjunctivitis in children32

Allergic conjunctivitis is almost pandemic ocular disorder. Its frequency in children may surpass infective conjunctivitis in developed countries. In under developed countries its presentation and outcome may be over shadowed by prevailing infective conjunctivitis and vitamin A deficiency. Presenting features of allergic conjunctivitis are variable, its symptoms may be so mild and insidious that it is accepted as natural phenomenon or may be so troublesome as to cause loss of manpower in adults and absenteeism from school in children.

All allergic conjunctivitis are—self limiting, duration vary from few minutes to few years. Allergic conjunctivitis are generally bilateral, may be asymmetrical. No race, sex or age is immune.

Clinical presentation33, 34

Allergic conjunctivitis is influenced by many factors which may work separately or in various combinations. These factors are—Geography, climate, race, age, sex, genetic predisposition and reaction to allergen.

1.Immediate hypersensitivity (humoral),

2.Delayed hypersensitivity (cellular) or

3.Auto immune.

Allergic conjunctivitis may be seen both in atopic and non atopic patients. The allergen responsible for immediate (humoral) hypersensitivity are exogenous. Those responsible for delayed (cellular) hypersensitivity are endogenous. The exogenous allergen are organic matters either of vegetable origin i.e. pollen, hay, husk, moulds or of animal origin i.e. fur, wool, dust, mites, dander, drugs, cosmetics, plastics. Polymers are also capable of producing allergic conjunctivitis. Food and additives are known to produce allergic conjunctivitis. Many a times it is impossible to find out the allergen.

Exact mechanism of allergic conjunctivitis is not well understood. Factors that make conjunctiva vulnerable to allergic reaction are :

(i) Conjunctiva is most exposed mucous membrane of the body. (ii) It is rich in blood supply.

(iii) It is very loose.

(iv) It is rich in lymphatic.

(v) It is constantly bombarded with exogenous allergen.

Most accepted theory regarding allergic conjunctivitis is that exogenous allergens disrupt the mast cell membrane and cause degeneration, releasing a host of chemicals that cause—vasodilatation, edema, inflammation and exudation. The chemicals released in this process are—histamine, various prostaglandins, leucotriens. The reaction is type one allergy

and IgE mediated. In milder cases there is preponderance of mast cells. In severe cases there is increase in T cell lymphocytes.

Classification of allergic conjunctivitis is difficult. However, following classification may fulfil many of the clinical criteria and possible mode of management.

1.Immediate (humoral) hypersensitivity33 (a) Acute allergic conjunctivitis.

(b) Seasonal allergic conjunctivitis. (c) Perennial allergic conjunctivitis. (d) Vernal kerato conjunctivitis.

(f) Atopic kerato conjunctivitis.

(g) Giant papillary conjunctivitis.

All are caused due to exogenous allergen. The first three are more common, less troublesome and easy to manage than latter three which are less frequent but difficult to manage.

2.Delayed hypersensitivity (cellular)

3.Auto immune disease

(a) Cicatricial pemphigoid (seen in elders)

(b) Erythema multi formis (Stevens Johnson syndrome) minor and major.

1. Acute allergic conjunctivitis. Acute allergic conjunctivitis is equivalent to urticaria of the skin. It is very common among children. It can manifest as early as first year of life. It is due to large inoculum of exogenous allergen. The patient complains of sudden onset of copious watering from the eye which may be unilateral or bilateral. Fast developing chemosis of congested conjunctiva. The conjunctiva may be so edematous as to protrude through the inter palpebral fissure. The cornea forms the floor of the crater (well) of the chemosed conjunctiva. The lids are swollen. There may be moderate papillary reaction, no follicles are seen. Cornea remains unaffected. There is no anterior chamber reaction, vision may be blurred due to over hanging chemosed conjunctiva. There is no lymphadenopathy. The symptoms pass off within half an hour to one hour without leaving any trace. Muco purulent discharge, corneal involvement and lymphadenopathy point towards anti microbial conjunctivitis.

Treatment. Best is to avoid the allergen if it is known, otherwise local vasoconstrictors, astringent and short acting systemic antihistamine tablets are sufficient. Cold compress applied within few minutes may give relief. Local steroids are not necessary. Mast cell inhibitors have no role, recurrence are common.

2. Seasonal allergic conjunctivitis. Seasonal allergic conjunctivitis is equivalent to hay fever, hence may be associated with rhinitis, sore throat. They have seasonal predilection. Conjunctival reaction consists of mild to moderate papillae or follicle formation.

Cornea is bright. There is no AC reaction. There is no lymphadenopathy. Condition is invariably bilateral with mild itching and slight ropy discharge. Conjunctival scrapping show eosinophils. Symptoms coincide with release of allergen in the atmosphere (pollen, hay etc.) Main symptoms are itching, redness, watering. The condition is to be differentiated from trachoma, dry eye syndrome which are not seasonal nor produce itching.

Management of seasonal allergic conjunctivitis consists of :

(i) Oral non sedative antihistamine. Possible side effects of anti histamines should be weighed against its therapeutic benefits while prescribing to children specially when administration has to last longer than few days.

(ii) Instillation of combination of astringent, vasoconstrictor, antihistamine several times a day.

(iii) Local mast cell inhibitor – 2% NedoCromil two times a day is better than 4% sodium cromoglycate BD 2% cromoglycate has less therapeutic value. It is best used as prophylactic in between the attacks three to four times a day. Mast cell inhibitors are almost devoid of any side effect.

(iv) NSAID like ketorolac tromethamine 0.5% drops three times or Flurbiprophen 0.03% drops three times a day.

(v) Steroids are best avoided.

Perennial allergic conjunctivitis

As the name suggests the condition lingers throughout the year without remission or exacerbation. In the past perennial and seasonal allergic conjunctivitis were grouped under single category of chronic allergic conjunctivitis. Seasonal allergic conjunctivitis have definite seasonal predilection which lacks in perennial conjunctivitis. The allergen in perennial allergic conjunctivitis is present in the environment throughout the year which could be vegetable, animal or chemical in nature like house dust mite, animal dander, food allergen and locally used drugs.

The symptoms are : (i) Itching, redness and watering. (ii) Signs comprise of conjunctival congestion, follicle formation and papillary reaction. Cornea is never involved. The condition may be confused with trachoma, dry eye syndrome or angular conjunctivitis.

Management consists of removal of offending allergen which is not always possible. Local NSAID, mast cell inhibitor specially long acting Nedocromil 2% two times a day are effective. Low dose of non sedative antihistamine tablets give additional relief. In milder cases local anti histamine drops in combination with long acting vaso constrictor are sufficient. Steroids are best avoided.

Vernal (spring) kerato conjunctivitis34, 35, 36

It is most troublesome allergic conjunctivitis in children. In spite of its name it need not manifest in spring always. It is more common in summer in tropical and sub-tropical countries. It is a bilateral condition, may be a symmetrical specially when it develops first time. It has remission and exacerbations. It has been reported as early as first year of life. More common age is between six years to sixteen years, after which it may automatically heal. It is a self limiting disease lasting for six to ten years. It is more common in boys who outnumber girls in ratio of six to one. In girls the condition is milder, duration is shorter. It is more common in coloured races and in warmer climate. The disorder is seen in two age groups i.e. pre puberty which forms the bulk of patients, and post puberty. The post puberty cases are less in number, generally not seen in females, are less severe and last for shorter i.e. two to three years. Some authors consider this as variation of atopic kerato conjunctivitis. There

may be a positive history of vernal catarrh in the parents. Sometimes more than one sibling may be affected. Atopic dermatitis is a frequent dermatological disorder in children with spring catarrh.

Topographically there are three types of vernal kerato conjunctivitis :

1.Palpebral (tarsal). This is most common.

2.Bulbar (limbal). This causes early and more corneal involvement is more. Common in black races.

3.Mixed. Least common but most difficult to treat.

Symptoms. Commonest symptom is intense itching that may last throughout the day. Besides discomfort itching becomes social embarrassment to the child. Itching is associated with redness that becomes more intense following itching, there is a ropy discharge. There may be watering from the eyes. The child finds it difficult to open the eye in the morning but the lids do not get stuck as seen in acute bacterial conjunctivitis. Itching and watering leads to excoriation of the outer canthus. After sometime a pseudo ptosis develops which gives sleepy look to the child. The skin over the lid may be darker than the surrounding area.

Most frequent physical finding is presence of moderate size papillae in upper tarsal conjunctiva, these papillae are flat topped in the area that come in contact with the globe firmly and pointed on the lateral side of the tarsus. The flat topped papillae are polygonal in shape. In between adjacent papillae there are deep furrows that zigzag in between the papillae. There may be pseudo membrane over the papillae (Maxwell Lyons sign)35 in untreated cases. With treatment the papillae shrink in size both in height and width. The surface loose its roughness and becomes velvety. There is a tenacious ropy discharge which is alkaline in nature. The discharge can be pulled out in form of fine threads. The discharge which fills the gap between the papillae, the appearance is called milk spilled over cobble stone as the large papillae have appearance of cobble stone. The papillae are not seen in the lower lid or fornices.

In the bulbar form there are mucoid confluent nodular papillae at the limbus. Most commonly at the upper part, these nodules are generally seen in segments but may encircle whole of the cornea. In untreated cases there may be formation of Horner-Tranta’s spot35 which are discrete white spots at the limbus.

The corneal changes in spring catarrh are the cause of lacrimation, photophobia and diminished vision.

The corneal changes in spring catarrh comprise of following, they may be present as isolated lesion or in various combination :

1.Epithelial micro erosion generally seen in the upper part of cornea 1mm inside the limbus.

2.Epithelial macro erosion—There is large area of epithelial loss leading to sterile ulcer formation due to their shape. They are called shield or amaeboid ulcers seen in the upper part of the cornea.

3.Plaque over the macro erosion.

4.Superficial vascularisation.

5.Sub epithelial scarring.

6.Pseudo arcus. This is segmental in nature.

7.Keratoconus has been observed more frequently with vernal kerato conjunctivitis. The exact cause of keratoconus is not understood, may be a genetic feature. Frequent rubbing of the eye has also been blamed for development of keratoconus.

Differential diagnosis. Generally there is no problem in diagnosis of vernal kerato conjunctivitis due to its typical clinical feature of chronic, bilateral, papillary reaction in a male child intense periodic itching with remission and exacerbation that responds dramatically to local steroid drops. Common conditions that mimic as vernal conjunctivitis are—Other type of allergic conjunctivitis, chronic follicular conjunctivitis, dry eye status, acnerosacea, blepharo conjunctivitis, trachoma, drug induced conjunctivitis. In under developed countries, clinical features may be overshadowed by infective conjunctivitis and xerophthalmia.

Management35, 38, 39

Management of vernal kerato conjunctivitis has special significance as it is seen mostly in children, is chronic and requires prolonged treatment. Children with vernal conjunctivitis try to skip school as perpetual redness of eyes and constant itching is not socially acceptable to the children. Parents should be informed that the condition is recurrent, runs a prolonged course, is self limiting and by itself does not produce blindness but blindness can set in by indiscriminate use of steroids that gives prompt relief.

1.Parents should be persuaded to use nonspecific astringents vasoconstrictor and antihistamine drops in various combinations as local drops rather prompt relief giving steroids.

2.Frequent cold compress.

3.Dark glasses.

4.If these failsmast cell inhibitors are added to above treatment. Sodium cromoglycate 2%-4% three to four times a day gives comfort to the child. Chromoglycate sodium in two percent strength can be used as prophylaxis in between exacerbation. Nedocromil sodium 2% BD has better effect that 4% sodium cromoglycate. Cromoglycates are mast cell inhibitors have almost no side effect.

5.Non steroidal anti inflammatory drugs have been used with good result. They have reduced use and dependence on steroid. They lack side effects of steroid are well tolerated.

Drugs used are :

1.Flurbiprophen 0.03% two to three times a day.

2.Ketorolac tromethamine 0.5% two to three times a day. Diclofenac sodium 0.1% may be used above twelve years of age.

3.Systemic aspirin, Ibuprofen, indomethacin, nemesulide have been used without uniform result.

4.In spite of all drawbacks local steroids have remained most effective treatment of choice. Local steroids are used as clear solution. Drawback of suspension is that the

suspended particles get lodged in between the papillae and act as irritant. The principle of local steroid therapy is to use weakest solution used least frequently should give maximum relief without side effect. Commonly used steroids used are -

Dexamethasone/Betamethasone 0.1% Prednisolone—0.125% to 0.5% Fluorometholone 0.1%

In severe cases any of the above drugs is instilled in conjunctival sac every two hourly for first twenty four hours, then frequency is gradually reduced over weeks. After a month the child may be comfortable in once a day instillation. All children under topical steroid should be under constant supervision of ophthalmologist who should monitor - vision, error of refraction, intra ocular pressure and any change in the disc. The lens should be examined for iatrogenic cataract.

Addition of mast cell inhibitors reduces requirement of steroid without jeopardising result.

8. Other drugs used in vernal kerato conjunctivitis are :

(i) Acetyl cysteine two to ten percent solution in methyl cellulose four times a day dissolves mucus.

(ii) Weak solution of acetic acid to change pH of tear from alkaline to acidic.

(iii) Tear film substitutes are given to manage ocular surface disorder that is too common.

(iv) Cyclosporine 2% in castor oil may be used in those cases that do not respond to steroids. These cases are generally associated with atopia.

(v) Shaving of papillae, cryo application to the papillae have not found to be very effective.

(vi) Plano T contact lenses may be helpful in persistent superficial keratitis.

(vii) Rarely low dose systemic steroid for a short period, may have to be used in severe corneal involvement under strict supervision.

Atopic kerato conjunctivitis

Fortunately this condition is rare, mostly seen in atopic adults but children in second decade may be affected. It has more systemic symptoms of atopic disease than ocular symptoms. Ocular manifestation consist of blepharitis, papillae formation, corneal epithelial defect, corneal plaque and atopic cataract, keratoconus. Systemic signs consist of eczema in the neck, antecubital fold, asthma, rhinitis.

Management consists of local low dose of steroid, sodium cromoglycate, sodium nedocromil, NSAID. Some cases may require topical cyclosporin in oil two times a day.

Giant papillary conjunctivitis41, 42, 43

The malady was first reported in 1974. By 1977 a syndrome consisting of contact lens intolerance, itching, mucus discharge, hyperemia, blurred vision has emerged. On

examination large papillae that are larger than 3mm across are seen in upper tarsal conjunctiva. The symptoms diminished on discontinuation of contact lens. Severity depends produce more encounter in on size of contact lens. Larger the lens more are the symptoms. However it was realised that contact lens was not the offending agent. It was the preservative and protein deposits on the lens that were the causative factors. Extendedwear lenses produced clinical features. It is not associated with atopia. It can affect any age both sexes are equally effected . On long run tops of papillae ulcerate and stain with fluorescein. Besides contact lens giant papillary conjunctivitis is also encountered in protruding mono filament sutures, corneal scleral shell, artificial eye, kerato prosthesis, ocular prosthesis, scleral buckle, cyno acrylate glue, multiple embedded foreign bodies.

Management comprises of discontinuation of CL, change of CL polymer and design, proper contact lens hygiene. Use of preservative free contact lens solution, steroids are best avoided. Local NSAID and cromoglycates give sufficient relief.

Phlyctenular kerato conjunctivitis44,45,48

This is very common allergic conjunctivitis seen world-wide, more commonly in under developed countries where tuberculosis is endemic, malnutrition is frequent and lack of public health facility common. It is a cell mediated type four allergic reaction where sensitised corneal and conjunctival epithelium when exposed to causative endogenous allergen develops interstitial kerato conjunctivitis in the form of a nodule. Tubercular protein is commonest causative factor. The allergic response is attributed to lipid fraction of tubercular antigen. Other causative organisms that can produce phlycten are46 staphylococcus, strepto coccus, gonococcus, candida, coccidomycosis, lympho granuloma, ascariasis. Rarely it can be idiopathic as well. Common age to develop phlycten is between three to ten years. After ten years frequency becomes less. After fifteen it becomes very rare. Girls are effected more than boys. It is a bilateral disease, both eyes may be involved simultaneously, or separately. Number of nodules vary from single to multiple when more than one nodule is present they may be away from each other or may coalesce to involve a sector of limbus or in severe cases they may encircle the whole of the cornea. Phlyctens are self limiting in nature. They resolve in ten to fifteen days, never to recur on the same spot. However there may be crops of lesions one after another.

Perilimbal conjunctiva is the commonest site to develop phlyctenular conjunctivitis. It has been observed on the bulbar conjunctiva as well as tarsal conjunctiva and inter marginal strip. Other frequent part to be involved is cornea either primarily or due to spread from conjunctiva.

Typical conjunctival phlycten develops one to two millimetres away from limbus as a pale vescicle that form a nodule later44. The initial size may be that of a pin head, soon it enlarges to 1 mm to 2 mm. The conjunctiva round the nodule is congested, conjunctival vessels do not pass over the nodule. Two types of presentation are encountered i.e. only phlycten without muco purulent conjunctivitis or phlycten developing in infective conjunctivitis. Role of infective conjunctivitis in production of phlycten is not clear. Most of the time it is coincidental. Other possibility is that due to infection conjunctival epithelium gets sensitised and a phlycten ensues. Acute infective conjunctivitis may facilitate transfer of large amount of tubercular

protein to the limbus that results in formation of phlycten. Within four to five days the phlycten reaches its maximum size and the surface epithelium gives way to form an ulcer which takes another three to four days to heal without any scar on the conjunctiva. Though tuberculosis has been blamed as major cause of phlycten. Tubercle bacilli have never been isolated from the conjunctiva in phlyctenular keratoconjunctivitis. The histological changes do not show tubercle formation it resembles more or less of a micro abscess.

Other form of involvement in phlycten is when it develops at the limbus. It may either spread from conjunctiva and spill over the cornea or may develop directly on the limbus resulting in phlyctenular kerato conjunctivitis which is more congested than simple phlyctenular conjunctivitis.

Corneal involvement in phlycten can be of following types :

Cornea may be involved as (1) Primary lesion (2) The lesion may spread from conjunctiva. There are two main types of corneal involvement i.e. (1) Ulcerative (non vasularised) and (2) infiltrative (vascularisation)47. The ulcerative form may be (1) Marginal, (2) Fascicular.

Marginal corneal phlycten is generally due to a phlycten developing at the limbus. The phlycten sits astride the limbus i.e. half on cornea, half on conjunctiva. Like any phlycten in due course it ulcerates and heals with out any scar. However if the ulcer is deep it destroys the Bowman’s membrane and a permanent opacity is formed.

An opacity due to marginal phlycten has a typical dome shaped configuration with base at the limbus and convexity towards the pupil. There may be single or multiple marginal phlyctens. More than one may coalesce to form a sectorial ulcer.

Fascicular ulcer is a typical corneal presentation of phlycten. It is generally preceded by marginal or keratoconjunctival phlycten. The ulcer starts on the corneal periphery, has a tendency to move towards centre followed by a leash of superficial vessels. The vessels are typically straight and do not branch. The fascicular ulcer while shifting from periphery towards pupil digs deep in the substance of cornea creating a shallow furrow. The vessels develop in this furrow. There may be more than one fascicular ulcer in the same cornea. The fascicular ulcer does not perforate, nor does it produce anterior chamber reaction. The final location of the ulcer where it may become stationary is uncertain. Once it stops shifting it starts healing, leaving a superficial opacity followed by fainter band shaped opacity extending upto limbus. This band represents the place of leash of vessels that followed the ulcer.

Third rare possibility is small pin point superficial ulcers all over the cornea. Infiltrative type of corneal phlycten may produce two types of vascularisation : First more common superficial vascularisation and a less frequent deep vascularisation. The superficial vascularisation may develop anywhere on the cornea even all around the cornea and called phlyctenular pannus. It differs from trachomatous pannus in the sense that latter has predilection for upper cornea. The vascularisation ultimately dies down leaving no scar. In a more severe case of longer duration there may be deep vascularisation which leaves permanent mark. Corneal involvement is more when tubercular protein is causative factor.

Symptoms. Symptoms of phlyctenular kerato conjunctivitis depend upon number of phlycten; associated bacterial conjunctivitis, and involvement of cornea. Simple conjunctival phlyctens do not produce much symptom except localised redness in the eye, slight irritation

and watering. Associated infective conjunctivitis invariably overshadows simple phlycten that may be missed altogether or it may become obvious when conjunctivitis has subsided. Though phlycten is an allergic manifestation it does not produce itching. Presence of itching with nodule at limbus points towards limbal spring catarrh.

Symptoms become more severe as cornea gets involved. A phlyctenular kerato conjunctivitis produces severe photophobia in children. Fascicular ulcer is associated with severe blepharospasm, photophobia, lacrimation and diminished vision. Vision is greatly reduced if the ulcer is positioned against the pupil.

Management

1.Simple phlycten without infective conjunctivitis—Local weak solution of steroid i.e. dexamethasone 0.1% 4 hourly for first day. This reduces symptoms promptly or FML 0.1% every one to two hourly till symptom subsides then the frequency is reduced.

2.Phlycten with infective conjunctivitis is treated as any catarrhal conjunctivitis along with local steroids under supervision.

3.If cornea is involved atropine is added to steroid to reduce ciliary spasm, this gives prompt relief. Keratitis due to tubercular antigen though produce severe symptoms responds better than in cases of staphylococcal antigen induced keratitis.

4.In under developed countries all children with phlycten should be investigated for both pulmonary as well as extra pulmonary tuberculosis. BCG does not prevent a child from developing phlycten. If the child is found to be tubercular a full course of anti-tubercular treatment should be ensured.

5.In case of staphylococcal allergy lid hygiene along with systemic anti staphylococcal antibiotic may be required. Children older than eight years should be put on doxycycline 100 mg once a day for 10 days while smaller children are put on erythromycin in dose of 25/mg/kg for seven to ten days along with local steroid.

6.Children suffering from intestinal helminths should get a course of anti helminth. Albendazole is an effective drug. This is given in form of chewable tablet in single dose. Children above 2 years should get 400 mg single dose to be repeated as required.

Differential diagnosis of phlycten comprise of nodules at limbus, trachoma, spring catarrh, interstitial keratitis.

Complication. Conjunctival phlycten is devoid of any complication. Corneal complications consist of peripheral dome shaped opacity, Salzmann’s nodular dystrophy46, corneal vascularisation and various grades of corneal opacities that may diminish distant vision leading to squint and amblyopia.

Erythema multiforme49, 50

Though this disorder is classified along with allergic conjunctivitis. It is not a true allergic conjunctivitis. The exact mechanism is not known. Most acceptable theory is an auto immune disease.51 It differs from both endogenous and exogenous allergic conjunctivitis by not producing - papillae, follicles or nodule. There is no itching either. It has profound systemic manifest, mostly cutaneous and mucous membrane involvement. It is a disease of children