Anterior segment conditions in childhood – Part 1

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IntroductionWhen a child presents with an anterior segment eye condition, the optometrist must be able to identify potentially serious ocular conditions that will require urgent referral to an ophthalmologist and accurately diferentiate these from other less serious conditions that can be managed by the optometrist perhaps without referral at all. Conditions requiring urgent referral will be discussed in Part 1 below and less urgent conditions will be considered in Part 2.

Taking a good historyA full history is always important and should include the following questions:

• Onset of any ocular redness – was the development gradual or sudden?

• What are the associated symptoms? For example itchiness, lymphadenopathy, lid crusting, and lash matting.

• Is there any discharge? If so, what type and how much? The discharge may be important in distinguishing viral, bacterial and allergic conjunctivitis (see below).

• Does the child wear contact lenses? If so, the suspicion for Pseudomonas infection needs to be raised.

• Is there any swelling of the periorbital area?

• Does the child have photophobia?

• Is the child’s vision blurred?

• Is there any ocular pain? If so, what type of pain? Scratchy, gritty, well-deined pain is more likely to indicate a corneal problem. A deep, dull pain tends to indicate a more serious condition such as iritis.

• Is there a personal or family history of atopy? Is it spring or summer? Yes, to any of these questions suggests allergic conjunctivitis.

• What is the age of the child? Is he/she of school age?

• Is there any recent history of trauma?

• Does the child sufer with headaches? If so, for how long?

Ocular examination• Note the general well-being of the child. Does the child look

unwell?

• Visual acuity using Snellen or preferably LogMAR

• Check pupil reactions

• Slit lamp biomicroscope (wherever possible) to check the anterior segments

• Fundus examination

• Fluorescein to check for corneal staining e.g. corneal ulcers or abrasions.

• If any of the diagnoses discussed below are conirmed or suspected, then urgent referral to an ophthalmologist is necessary

Anterior segment conditions in childhood – Part 1by Chris Steele, BSc(Hons) FCOptom DCLP DipOC DipTp(IP) FBCLA

Outline:This article discusses anterior segment eye conditions which can present in childhood and require urgent referral. It will cover the importance of a comprehensive history and examination before looking at a number of these conditions in detail.

About the author:Chris Steele graduated from City University in 1988 and qualiied in July 1989 after his pre-registration year at The Royal East Sussex Hospital, Hastings. He is Consultant Optometrist, Head of Optometry at Sunderland Eye Inirmary (SEI) in Sunderland. Over the past 20 years he has developed a wide range of extended roles involving hospital optometrists undertaking cataract, anterior segment, diabetes, glaucoma, paediatrics

and medical retina case loads. He has authored over 60 publications re: glaucoma, diabetes, specialist medical contact lenses, refractive surgery and clinical risk management and has undertaken many presentations both nationally and internationally on these topics.

UK This article ofers 1 non-interactive CET point (C-52336)

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It is extremely important to rule out serious ocular presentations. Ocular pain and sudden change in vision are usually indications for referral to an ophthalmologist. The main causes of serious anterior segment conditions seen in children are considered below.

Preseptal and orbital (post-septal) cellulitisPreseptal cellulitis and orbital cellulitis are two distinct diseases that share a few clinical symptoms and signs. Preseptal cellulitis usually begins supericial to the orbital septum. Orbital cellulitis usually begins beneath the orbital septum. Both are more common among children, but preseptal cellulitis is far more common than orbital cellulitis.

Preseptal cellulitis usually presents as unilateral periorbital oedema (Figure 1). Preseptal cellulitis may have a variety of causes including eyelid trauma, extraocular infections and bacterial upper respiratory infections (caused by Haemophilus inluenzae and Streptococcus) which afect the para-nasal sinuses1. The proximity of the paranasal sinuses to the orbital walls and the interconnection between the venous system of the orbit and the face allow infection to spread from the sinuses to the orbit either directly or via the blood stream. It is less common in adults where it usually follows trauma or orbital surgery.

If an optometrist suspects this diagnosis, then an urgent referral is required the same day as preseptal and orbital cellulitis constitute medical emergencies. Mild preseptal cellulitis is usually treated initially with Co-amoxiclav 500/125mm p.o.t.d.s or Flucloxacillin 500mg p.o.t.d.s for 10 days. If the patient does not respond or is less than 5 years old, then the patient should be admitted for e.g. ceftriaxone 1-2g intravenously (IV) daily divided into doses until the patient responds to treatment.

Orbital (post-septal) cellulitis frequently presents as a unilateral swollen, red and tender lid but with proptosis, limitation of ocular movement and possibly decreased vision. Orbital cellulitis is most often caused by extension of infection from adjacent sinuses, especially the ethmoid sinus (75 to 90%). It is less commonly caused by direct infection accompanying local trauma (e.g. insect or animal bites, penetrating eyelid injuries) or contiguous spread of infection from the face or teeth. The child is often unable to open the lids and is usually unwell with a fever. The orbital septum is a sheet of connective tissue that is attached to the rim of the orbit and separates the lids from the orbit and its contents. If infection spreads beyond this septum then this can easily reach the brain via the cavernous sinus with ~4% of cases developing intracranial complications. Orbital cellulitis is, therefore, a true ocular emergency

being potentially life-threatening owing to the development of meningitis or encephalitis. Lid infections (preseptal cellulitis) are not life-threatening as the orbital septum stops the spread of infection.

All conirmed or suspected cases of orbital cellulitis require immediate referral to an A and E department for intensive intravenous antibiotic treatment. The patient should be admitted and treated with e.g. ceftriaxone 1-4g IV daily plus lucloxacillin 1-2g IV q.d.s. It may take 24-36 hours for any signiicant improvement to be seen. Where patients do not respond to treatment, an orbital CT scan is required to look for the presence of an abscess and spinal lumber puncture to conirm or exclude the presence of meningitis.

Dacryoadenitis Acute dacryoadenitis is a rare inlammatory condition of the lacrimal gland most often seen in children as a complication of viral infections such as mumps and herpes simplex. Acute dacryoadenitis presents as a painful swelling in the outer region of the upper lid with some degree of ptosis. Lifting the lid reveals the swollen palpebral portion of the gland bulging under the conjunctiva. There may also be pain in the area of swelling, excess tearing or discharge and swelling of lymph nodes in front of the ear (pre-auricular).

Chronic dacryoadenitis may occur in association with lymphoma, leukaemia or tuberculosis. Sometimes, it occurs bilaterally in sarcoidosis. Also bilateral dacryoadenitis has been reported in association with Epstein-Barr virus.

Treatment is with systemic antibiotics if there is bacterial infection. Surgical drainage is rarely necessary.

DacryocystitisDacryocystitis is usually caused by a blockage of the nasolacrimal duct, which allows luid to drain into the nasal passages. When the lacrimal sac does not drain, bacteria can grow in the trapped luid. This condition is quite common in infants. Acute dacryocystitis requires systemic antibiotics and therefore should be managed and treated in much the same way as preseptal cellulitis (see above). Probing should not be attempted in infants (<12 months) since this may cause permanent damage to the immature nasolacrimal duct which may even lead to orbital cellulitis.

Chronic dacryocystitis is more common and usually occurs in only one eye. Symptoms include:

• recurrent episodes of epiphora, plus swelling, tenderness and redness at medial canthus

• persistent redness at medial canthus

• persistent painless swelling at or below the medial canthus

• chronic epiphora

A warm compress applied to the area can help relieve pain and promote drainage.

In infants, gentle massage of the lacrimal sac four times daily for up to nine months can drain the sac and sometimes clear a blockage. As the infant grows, the duct may open by itself. If the duct does not open, it may need to be dilated with a minor surgical procedure.

Congenital dacryostenosis In newborn infants, the nasolacrimal duct may fail to form an opening. This condition is called dacryostenosis.

Congenital dacryostenosis can result from inadequate development

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Figure 1. Preseptal cellulitis. Courtesy P Tiin


of any part of the nasolacrimal ducts. Most often, the far end of the nasolacrimal duct is blocked. The result is an overlow of tears that run down the cheek (epiphora) or persistent crusting. One or both eyes can be afected. The problem is usually irst noticed in 3 to 12-week-old infants. Congenital dacryostenosis is frequently associated with neonatal conjunctivitis. This should be suspected in children with unilateral conjunctivitis and epiphora who have a relux of mucopurulent material from the lacrimal punctae after massaging the nasolacrimal sac. Dacyrocsystitis may develop secondary to dacryostenosis and progress to periorbital cellulitis.

This type of blockage (dacryostenosis) usually disappears without treatment by the age of 6 to 9 months, as the nasolacrimal system develops. Until the child is about 1 year old, doctors often suggest that parents gently massage the nasolacrimal sac four or ive times per day to help relieve the blockage.

If the blockage is not relieved by the time the child is about 1 year old, an ear, nose, and throat (ENT) specialist or ophthalmologist may have to open the nasolacrimal duct with a small probe, which is usually inserted through the nasolacrimal duct punctum. The child is usually given a general anaesthetic for this procedure.

Sight-threatening keratitisThe most common forms of keratitis in children are those associated with acute viral infections but these are almost invariably self-limiting except in sick children.

Microbial keratitis This is relatively rare in children, but for a small group, can be a cause of blindness. Underlying causes in children (most frequently afecting young children) may include systemic infections, immunodeiciency, orbital malignancies, corneal exposure, trauma or dry eyes (Figure 2). At particular risk are children wearing soft contact lenses2,3. Pseudomonas should always be suspected in any contact lens wearer with corneal infection. This is a virulent organism that is mobile and produces collagenase which gives rise to a rapidly spreading liquefactive ulcer in the form of a yellowish white corneal opacity, with hypopyon. This is a collection of white blood cells in the inferior anterior chamber. The symptoms and signs are very similar to acute anterior uveitis.

Other forms of keratitis can be diagnosed from their clinical presentation e.g. dendritic ulcers in herpetic keratitis (see below).

Fungal infections are rare in the UK but more common in other parts of the world. In children, they tend to occur in those predisposed to

severe systemic disease. The most common fungal corneal pathogens include Candida sp. (yeast like) and Fusarium sp. (ilamentous). Fungal keratitis produces similar signs to bacterial keratitis, although the infection may develop more slowly. Fusarium infection can progress rapidly and invasively.

Symptoms and signs of sight-threatening keratitis may include:

• Moderate to severe pain with acute onset and rapid progression

• Redness

• Photophobia (may be severe)

• Mucous discharge

• Blurred vision (worse if the lesion is on the visual axis as opposed to peripherally)

• Usually white or yellow corneal lesion caused by excavation of epithelium, Bowman’s layer and stroma as a result of tissue necrosis

• Stromal iniltration beneath the epithelial lesion often associated with stromal oedema and folds in Descemet’s membrane and even an endothelial ibrin plaque beneath

• Anterior chamber lare, cells and possible hypopyon

If a child is complaining of severe pain which appears to be disproportionate to relatively minor clinical indings on slit lamp examination, refer immediately as this may indicate an Acanthamoeba infection4. A good history is very important as discussed above. Children may be exposed to Acanthamoeba infection by swimming in rivers with brackish (slightly salty) and standing water or chlorinated swimming pools and hot tubs.

In severe corneal infections, particularly where there are axial lesions or lesions larger than 6mm in diameter, hospital admission is required. This would also be required if poor compliance with intensive treatment (round the clock) using topical antibiotics is considered likely. Identiication of the causative organism is undertaken by corneal scrape, culture and determination of antibiotic sensitivities. Polymerase chain reaction [PCR] is a technique that may be used to identify fungal organisms.

Treatment often involves dual therapy with fortiied antibiotic agents e.g. cephalosporin and an aminoglycoside (e.g. Gentamycin 1.5%). Where monotherapy is deemed appropriate this involves the use of luoroquinolones (e.g. oloxacin, levoloxacin). Fourth-generation luoroquinolones (e.g. moxiloxacin and gatiloxacin) are now considered good alternatives to standard treatment of bacterial keratitis using combined fortiied topical antibiotics5.

Herpes simplex keratitisHerpes simplex virus (HSV) eye disease is an important cause of ocular morbidity and a very common cause of corneal opaciication and visual loss worldwide. During childhood years, it generally afects a small group of older children with chronic disease. Approximately 90% of the UK population is sero-positive for this double stranded DNA virus. HSV eye disease can have a highly variable and unpredictable course. HSV has a predilection for mucous membranes innervated by the trigeminal Vth cranial nerve and this disease may manifest as blepharitis, conjunctivitis, epithelial keratitis (dendritic or geographic), stromal keratitis (necrotizing or non-necrotizing), irido-cyclitis and endotheliitis. Corneal endotheliitis is a fascinating clinical entity manifested by corneal oedema, keratic precipitates, and mild anterior chamber reaction. There is increasing evidence that the cause involves various viral infections including herpes simplex virus, varicella zoster virus, and cytomegalovirus. Corneal endotheliitis can be classiied clinically into four forms: linear, sectorial, disciform, and difuse. Antiviral treatment in combination with topical corticosteroids is generally efective to suppress the inlammation;

Figure 2. Corneal central ulcer with hypoyon

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however, irreversible corneal endothelial dysfunction may develop in some cases6.

History of previous attacks of herpes simplex infection is a key diagnostic feature. Inlammation with attendant structural damage and scarring is responsible for most of the visual impairment encountered with HSV eye disease. Topical and systemic antiviral agents e.g. Aciclovir are the mainstay of treatment. Corticosteroids are powerful anti-inlammatory agents which must be used cautiously and appropriately with this condition, especially in children.

HSV is categorised into two main types: HSV-2 generally infects the genitalia i.e. ‘below the waist’ and is sexually acquired. The much more common HSV-1 generally infects ‘above the waist’ and has a predilection for the orofacial area (i.e. lips, face, eyes). Primary infection usually occurs in childhood, following which the virus lies dormant in the trigeminal ganglion. Although the initial attack is sub-clinical and is often unnoticed by the individual, recurrence can lead to destructive sequelae. Reactivation of the virus is often triggered in HSV seropositive individuals if their general health is poor, they are stressed or fatigued and particularly if there is immunodeiciency. Systemic or topical steroids, or other immunosuppressive drugs may also be possible aggravating factors7.

Once reactivated the virus travels along branches of the trigeminal nerve to cause local infection e.g. cold sores or herpes keratitis. Potential reactivating stimuli include: sunlight (UV), fever, extreme heat or cold, infection (systemic or ocular) and ocular trauma.

HSV not only afects the anterior segment, but can also afect (rarely) the posterior segment causing retinal necrosis. It is therefore recommended that consideration is given to performing an examination of the vitreous (checking for haze) and fundus, following pupil dilatation, on all patients exhibiting signs of HSV eye disease. HSV eye disease can be divided into four main categories:

• Epithelial (Figure 3)

• Stromal (Figure 4)

• Disciform keratitis

• Metaherpetic ulcer (trophic keratitis)

• Herpes simplex epithelial keratitis

Typically, patients with HSV keratitis present with blurry vision, extreme photophobia, pain, redness, and epiphora. If on clinical examination, only the epithelium is involved this is characterised by arborising luorescein staining dendritic ulcers. Terminal end bulbs allow the practitioner to distinguish this condition from other possible causes of dendritiform lesions e.g. varicellar zoster, healing corneal abrasions and Acanthamoeba infection. As with many corneal conditions, corneal sensitivity may also be reduced.

Herpetic epithelial keratitis may occur unilaterally or bilaterally (most often in patients with atopic disease) and be accompanied by a blepharoconjunctivitis, involving lesions of the lid and a follicular response of the conjunctiva. In addition, a palpable pre-auricular lymph node may be present.

Medical management is relatively straight forward with HSV epithelial disease. Topical Occ. Aciclovir 3% or ganciclovir 0.15% (often preferred by patients) instilled ive times daily for two weeks is usually suicient to resolve the dendritic ulcer(s) in most cases8. Topical corticosteroids are contraindicated in the treatment of active HSV epithelial keratitis.

• Herpes simplex stromal keratitis

Since treatment of stromal keratitis may become prolonged with use of steroids and associated with signiicant ocular morbidity, all patients seen in community practice with stromal HSVK should be referred urgently to an ophthalmologist within 48 hours.

After resolution of dendritic epithelial keratitis, non-suppurative subepithelial iniltration and scarring can occur just beneath the area of previous epithelial ulceration, resulting in a “ghost” image of the previous dendrite within the anterior stroma. The lesion usually resolves without additional therapy, but may leave a permanent imprint of prior epithelial keratitis. Children with herpetic keratitis may have bilateral ocular involvement and are at risk for recurrent keratitis and amblyopia9.

Acute anterior uveitis (AAU) (iritis)10

Uveitis is inlammation of the uveal tract i.e. iris, ciliary body and choroid. Acute anterior uveitis (incidence 12 per 100,000) is the most common type of uveitis and can present as an isolated event or secondary to another eye condition (herpes zoster, herpes simplex) or systemic disease. Although 50% are idiopathic, around 60% are associated with human leukocyte antigen (HLA) B27. A second acute presentation of anterior uveitis (in less than 6-12 weeks) is referred to as recurrent acute uveitis. A third presentation reclassiies the condition as recurrent uveitis, which requires complete medical evaluation11.

The important symptoms of AAU are:

• Photophobia

• Rapid onset of pain in irst episodes (gradual at subsequent episodes)

• Reduced vision

• Pain (dull ache)

• Lacrimation

It is rare for it to be accompanied by symptoms of discharge, stickiness, irritation, itching, nausea or vomiting.

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Figure 3. Herpes simplex dendritic ulcers

Figure 4. Stromal herpes simplex


Important signs include:

• Hyperaemia - circum-corneal (ciliary injection)

• Keratic precipitates (Figure 5)

• Aqueous cells

• Aqueous lare

• Raised intraocular pressure in some cases (this may be reduced particularly if the ciliary body is afected)

• Posterior synechiae possibly causing pupil block and iris bombé

• Iris nodules: Koeppe (small, near pupil), Bussaca (large, far from pupil)

• Anterior vitreous cells indicate intermediate ± posterior uveitis

• Posterior segment examination is essential: check for cystoid macular oedema and posterior uveitis

• Other signs include sluggish pupil reactions, cataract, chronic corneal oedema

Speciic underlying causes of anterior uveitis in children:

• Trauma – traumatic iridocyclitis is common in childhood, wherever there is a history of blunt injury to the eye.

• Infectious disease – Iritis can be associated with childhood measles, mumps and chickenpox.

• Ankylosing spondylitis – characterised by presence of axial skeletal arthritis.

• Reiter’s syndrome – characterised by recurrent iridocyclitis, mucosal mouth lesions, polyarthritis conjunctivitis and urethritis.

• Behcet’s disease – this is very rarely a cause of iritis in children.

Causes of chronic uveitis in children include:

• Juvenile rheumatoid arthritis (Still’s disease) – usually presenting in afected children 15 years or younger

• Sarcoidosis

• Fuch’s heterochromic cyclitis

• Tuberculosis

• Syphilis

The aims of treatment in AAU are to suppress inlammation, alleviate symptoms, prevent complications and treat complications. This usually consists of the following treatment:

• Cycloplegia (guttae(g). cyclopentolate 1%) three times daily

• Topical steroid (e.g. g. Dexamethasone 0.1% or g. Prednisolone acetate 1%) initially 2 hourly with steroid ointment at night until

there is an improvement, then reduced over 5-7 days if settling 8x/6x/4x/3x/2x/once daily).

• Treat secondary glaucoma with carbonic anhydrase inhibitors e.g. Brinzolamide (Azopt) or alpha-antagonists e.g. Brimonidine.

• Possible systemic immunosuppression

Intensive steroids reduce inlammation and mydriatics/cycloplegics make the eye more comfortable by relaxing the ciliary body and preventing posterior synechiae formation. In certain cases, further investigations will be conducted to check for underlying systemic conditions, but this is not always necessary and usually only undertaken after a third episode.

Chemical and thermal burnsChemical and thermal burns to the eye are a common occurrence, even in children12. If a chemical injury has just occurred it is one of the few occasions where immediate commencement of treatment with irrigation of the eye with sterile saline for at least 15-30mins (or until pH 7-8) with a high low of luid over the anterior segment is indicated13,14. If sterile saline is not immediately available, use tap water, and ensure all debris is removed from the eye. Alkali injuries cause considerably more damage than acid or thermal burns.

Always check what chemical agent is the cause. Alkalis e.g. ammonia compounds, sodium hydroxide, lime (i.e. calcium hydroxide) cause the most severe ocular trauma by a process of liquefactive necrosis with rapid penetration of ocular tissue. In contrast, acids e.g. sulphuric, hydroluoric and hydrochloric cause coagulative necrosis which slows the penetration into ocular tissues. Other common causes of burns involve detergents (sodium hypochlorite - bleach), solvents and ixatives. Contact lens solutions, including hydrogen peroxide may also cause minor ocular burns if used inappropriately.

Chemical burns can cause signiicant discomfort but usually heal quite quickly if relatively minor. In severe cases patients are often admitted and treated with topical antibiotics, steroids, ascorbic acid, sodium citrate and cycloplegics (Figures 6a and 6b). Acetazolamide may be required in cases with raised IOP. Surgical options may involve amniotic membrane grafts or even limbal stem cell transplantation in severe cases15.

Penetrating injuriesChildren and adolescents account for a disproportionate share of ocular trauma. Boys between 11 and 15 years old are the most vulnerable compared with girls, as they are injured in a ratio of approximately 4 to 1 respectively. Penetrating eye injuries in children cause long-term morbidity, and are of considerable socioeconomic importance. The list of clinical circumstances and the various possible sharp objects that can be implicated in causing ocular trauma are endless (Figure 7). Most injuries in children are related to rough sports and projectiles, including toys, guns, darts, sticks, stones and

Figure 5. Keratic precipitates in uveitis

Figure 6a. Chemical burn. Right:

corneal epithelial defect

Figure 6b. Epithelial defect after

luorescein instilled

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airguns.

It is important to take a full history to ascertain whether it is likely that a foreign body (FB) has actually penetrated the globe. If so try and ascertain its size and approximate speed on impact depending on the circumstances of the injury. Always attempt to check VA although this may be diicult if there is signiicant lid swelling or pain. Instillation of topical anaesthetics is often useful in making the eye more comfortable and therefore easier to examine with a slit lamp biomicroscope. Under no circumstances should pressure be applied to the globe, either for opening the lids or applanation, where full thickness lacerations or other penetrating injuries are suspected16. Do not to try and remove any deeply embedded foreign body or attempt to push back any protruding iris. Use an eye shield taped over the eye for protection during transit to A&E. Signs of a penetrating injury include:

• lacerations

• irregular pupils,

• lens dislocation or subluxation

• commotio retinae

• vitreous haemorrhage17.

Ophthalmological management may include orbital X ray (to check for intraocular foreign bodies), B scan ultrasound (if there is no clear fundus view owing to media opacities), surgical wound repair and infection prevention with antibiotics. Patients are at risk of sympathetic ophthalmia so need appropriate follow up18. This is a bilateral panuveitis following ocular injury or surgery. This presents with bilateral sub acute discomfort with redness and photophobia or visual loss usually 1-12 months after the inciting event. Treatment of posterior uveitis is beyond the scope of this article but usually involves corticosteroids as well as immunosuppressants e.g. Mycophenolate, Ciclosporin, methotrexate and azathioprine.

Blunt ocular injuries A detailed, relevant history will give a clear indication as to what level of damage the eye may have sustained. Examination of the eye should be systematically undertaken to check for:

• Blood in the anterior chamber - hyphaema

• Black (uveal tissue) protruding from the eye which would indicate rupture of the globe

• Sub-conjunctival haemorrhage indicating possible perforation beneath

Immediate referral should be considered if any of the above is present or suspected and presenting with a recent history of trauma. Less serious (benign) causes of sub-conjunctival haemorrhage should irst be ruled out.

A “black eye” is commonly caused by direct trauma to the eye or face. The bruise is caused by bleeding under the skin (Figure 8). The tissue around the eye turns black and blue, gradually becoming purple, green, and yellow over several days. The abnormal color disappears within 2 weeks. Usually, swelling of the eyelid and tissue around the eye also occurs. Certain types of skull fractures can cause bruising around the eyes, even without direct injury to the eye. If there is any injury to the skull, it can be deined as a head injury and this would need a medical assessment if it is signiicant.

Non-accidental injuriesOphthalmic signs of non-accidental injury (NAI) can be varied and include periorbital and conjunctival injuries, damage to the anterior segments, lens and vitreoretinal injuries. If suspected, all cases must be referred and child protection procedures followed accordingly. All Specsavers’ stores should have child protection protocols that must be followed.

ConjunctivitisAcute conjunctivitis in childhood can result from infection with a vast array of organisms with the most common cause being the adenovirus virus (see part 2). Most cases of conjunctivitis, from whatever cause are usually self-limiting, but there are a few exceptions where urgent referral may be required. These include:

• Ophthalmia neonatorum - deined as conjunctivitis of the newborn < 4weeks old. The infection may be acquired during delivery (if the mother has a vaginal infection) or if born in unhygienic conditions. The main types are:

o Gonococcal conjunctivitis which is a rare disease, but still common in certain parts of the world. This is characterised by an acute purulent conjunctivitis with lid oedema, marked conjunctival hyperaemia, chemosis with or without membrane formation and prominent pre-auricular adenopathy. Treatment involves systemic and

Figure 7. Previous penetrating injury due to a pencil poked in the eye.

Note Iris partially missing

Figure 8. Blunt trauma

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topical antibiotics. Gonococcal conjunctivitis is caused by the bacterium Neisseria gonorrhoeae. A newborn can be infected with these bacteria during childbirth. If conirmed, the child would need to be admitted and treated with systemic antibiotics.

o Inclusion (chlamydial) conjunctivitis caused by the bacterium, Chlamydia. Signs include injected conjunctiva, lid swelling and a mucopurulent discharge that appear 5 to 12 days after birth. Chlamydia trachomatis is one of the most common causes of neonatal conjunctivitis. This would usually be treated with systemic antibiotics.

ConclusionsA range of serious anterior segment conditions presenting in childhood have been discussed in terms of clinical presentation and management options. For most of these conditions, accurate diagnosis by the community optometrist is required so that an urgent referral can be made containing all relevant information. In the second part of this series, less urgent anterior segment eye conditions that may be encountered in children will be discussed. For many of these conditions, referral may not be necessary at all and patients may be appropriately managed by the community based optometrist.

References1. Bedwell J, Bauman NM. Management of pediatric orbital cellulitis and abscess.Curr Opin Otolaryngol Head Neck Surg. 2011; 19(6):467-73.2. Stapleton F, Carnt N. Contact lens-related microbial keratitis: how have epidemiology and genetics helped us with pathogenesis and prophylaxis. Eye (Lond). 2012; 26(2): 185-93.3. Otri AM, Fares U, Al-Qababa et al. Proile of sight-threatening infectious keratitis: a prospective study. Acta Ophthalmol. 2012 Aug 3.4. Tetsuya M, Isao I, Yukihiro M, et el. A retrospective study of nine cases of Acanthamoeba keratitis. Clin Ophthalmol. 2010; 4: 1189–1192.5. Wong RL, Gangwani RA, Yu LW et al. New treatments for bacterial keratitis. J Ophthalmol. 2012; 2012: 831502. Published online 2012 September 66. Suzuki T, Ohashi Y. Corneal endotheliitis. Semin Ophthalmol. 2008, 23(4): 235-407. Heath G. (2010) Medical Management of common corneal conditions. Optometry in Practice, 11(4): 151-160.8. Wilhelmus KR, Coster DJ, Jones BR. (1981) Acyclovir and debridement in the treatment of ulcerative herpetic keratitis. Am J Ophthalmol 1981, 91: 323-7.9. Chong EM1, Wilhelmus KR, Matoba AY Herpes simplex virus keratitis in children. Am J Ophthalmol. 2004, 138(3): 474-5.10. http://www.college-optometrists.org/en/utilities/document-summary.cfm/docid/7489147E-0543-40C9-86286ABCFCE8AD98. Anterior uveitis11. Curl A, Mattos K, Pavésio C: Uveitis (acute anterior). Clin Evid 2005; 14: 179-43.12. Kuckelkorn R, Schrage N, Keller G, Redbrake C. Emergency treatment of chemical and thermal eye burns. Acta Ophthalmol Scand. 2002; 80(1): 4-10.13. Ikeda N, Hayasaka S, Hayasaka Y, Watanabe K. Alkali burns of the eye: efect of immediate copious irrigation with tap water on their severity. Ophthalmologica. 2006; 220(4): 225-8.14. Morgan SJ. Chemical burns of the eye: causes and management. Br J Ophthalmol. 1987; 71(11): 854–857.15. Meller D, Pires RTF, Mack RJS, Figueiredo F, et al. Amniotic membrane transplantation for acute chemical or thermal burns. Ophthalmology 2000; 107:980-990.16. Jonas JB, Knorr HLJ, Budde WM (2000). Prognostic Factors in Ocular Injuries Caused by Intraocular or Retrobulbar Foreign Bodies. Ophthalmology 107(5): 823-8.17. Ehlers JP, Shah CP, Fenton GL, and Hoskins EN. The Wills Eye Manual: Oice and Emergency Room Diagnosis and Treatment of Eye Disease (5th edition). Lippincott Williams & Wilkins, 2008.18. Wong T, Klein B, Klein R. The Prevalence and 5-year incidence of Ocular Trauma-The Beaver Dam Eye Study. Ophthalmology. 2000; 107: 2196-2202.

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GOC’s Enhanced CET Scheme CET and CPD regulators require practitioners to relect on their learning. Additional activities are required to gain CET for distance learning.

Log into your CET dashboard via iLearn. On the menu you reach you will ind non-interactive CET for this unit of learning.

For ‘non-interactive’ CET you have to pass (>60%) a six-question multiple-choice quiz.

The learning objectives for this article are:

1.1.1 Therapeutic optometrists will have enhanced understanding of signs, symptoms and management of childhood anterior segment diseases

6.1.5 Optometrists will have enhanced understanding of signs, symptoms and management of childhood anterior segment diseases

8.1.2 Dispensing opticians will have enhanced understanding of symptoms associated with childhood anterior segment diseases

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Anterior segment conditions in childhood – Part 1