Anterior Segment Conditions in Childhood

Home , Herpes simplex keratitis, Neonatal conjunctivitis, Periorbital cellulitis

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Anterior segment conditions in childhood – Part 1 by Chris Steele, BSc(Hons) FCOptom DCLP DipOC DipTp(IP) FBCLA Outline: About the author: This article discusses anterior Chris Steele graduated from City University in 1988 and qualiied in July 1989 after segment eye conditions which can his pre-registration year at The Royal East Sussex Hospital, Hastings. He is Consultant present in childhood and require Optometrist, Head of Optometry at Sunderland Eye Inirmary (SEI) in Sunderland. Over urgent referral. It will cover the the past 20 years he has developed a wide range of extended roles involving hospital importance of a comprehensive optometrists undertaking cataract, anterior segment, diabetes, glaucoma, paediatrics history and examination before and medical retina case loads. He has authored over 60 publications re: glaucoma, diabetes, specialist looking at a number of these medical contact lenses, refractive surgery and clinical risk management and has undertaken many conditions in detail. presentations both nationally and internationally on these topics.

• Is there any ocular pain? If so, what type of pain? Scratchy, Introduction gritty, well-deined pain is more likely to indicate a corneal When a child presents with an anterior segment eye condition, problem. A deep, dull pain tends to indicate a more serious the optometrist must be able to identify potentially serious ocular condition such as iritis. conditions that will require urgent referral to an ophthalmologist and • Is there a personal or family history of atopy? Is it spring or accurately diferentiate these from other less serious conditions that summer? Yes, to any of these questions suggests allergic can be managed by the optometrist perhaps without referral at all. conjunctivitis. Conditions requiring urgent referral will be discussed in Part 1 below and less urgent conditions will be considered in Part 2. • What is the age of the child? Is he/she of school age? • Is there any recent history of trauma? Taking a good history • Does the child sufer with headaches? If so, for how long? A full history is always important and should include the following questions: Ocular examination • Onset of any ocular redness – was the development gradual or sudden? • Note the general well-being of the child. Does the child look unwell? • What are the associated symptoms? For example itchiness, • Visual acuity using Snellen or preferably LogMAR lymphadenopathy, lid crusting, and lash matting. • Check pupil reactions • Is there any discharge? If so, what type and how much? The • Slit lamp biomicroscope (wherever possible) to check the discharge may be important in distinguishing viral, bacterial and anterior segments allergic conjunctivitis (see below). • Fundus examination • Does the child wear contact lenses? If so, the suspicion for • Fluorescein to check for corneal staining e.g. corneal ulcers or Pseudomonas infection needs to be raised. abrasions. • Is there any swelling of the periorbital area? • If any of the diagnoses discussed below are conirmed or suspected, then urgent referral to an ophthalmologist is • Does the child have photophobia? necessary • Is the child’s vision blurred?

It is extremely important to rule out serious ocular presentations. being potentially life-threatening owing to the development of Ocular pain and sudden change in vision are usually indications for meningitis or encephalitis. Lid infections (preseptal cellulitis) are not referral to an ophthalmologist. The main causes of serious anterior life-threatening as the orbital septum stops the spread of infection. segment conditions seen in children are considered below. 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 Preseptal and orbital (post-septal) 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 cellulitis seen. Where patients do not respond to treatment, an orbital CT scan Preseptal cellulitis and orbital cellulitis are two distinct diseases that is required to look for the presence of an abscess and spinal lumber share a few clinical symptoms and signs. Preseptal cellulitis usually puncture to conirm or exclude the presence of meningitis. 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. Dacryoadenitis Preseptal cellulitis usually presents as unilateral periorbital oedema Acute dacryoadenitis is a rare inlammatory condition of the lacrimal (Figure 1). Preseptal cellulitis may have a variety of causes including gland most often seen in children as a complication of viral infections eyelid trauma, extraocular infections and bacterial upper respiratory such as mumps and herpes simplex. Acute dacryoadenitis presents infections (caused by Haemophilus inluenzae and Streptococcus) as a painful swelling in the outer region of the upper lid with some 1 which afect the para-nasal sinuses . The proximity of the paranasal degree of ptosis. Lifting the lid reveals the swollen palpebral portion sinuses to the orbital walls and the interconnection between the of the gland bulging under the conjunctiva. There may also be pain venous system of the orbit and the face allow infection to spread from in the area of swelling, excess tearing or discharge and swelling of the sinuses to the orbit either directly or via the blood stream. It is less lymph nodes in front of the ear (pre-auricular). common in adults where it usually follows trauma or orbital surgery. 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.

Dacryocystitis Dacryocystitis 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 Figure 1. Preseptal cellulitis. Courtesy P Tiin may cause permanent damage to the immature nasolacrimal duct which may even lead to orbital cellulitis.

If an optometrist suspects this diagnosis, then an urgent referral is Chronic dacryocystitis is more common and usually occurs in only required the same day as preseptal and orbital cellulitis constitute one eye. Symptoms include: medical emergencies. Mild preseptal cellulitis is usually treated • recurrent episodes of epiphora, plus swelling, tenderness and initially with Co-amoxiclav 500/125mm p.o.t.d.s or Flucloxacillin redness at medial canthus 500mg p.o.t.d.s for 10 days. If the patient does not respond or is • persistent redness at medial canthus 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 • persistent painless swelling at or below the medial canthus patient responds to treatment. • chronic epiphora Orbital (post-septal) cellulitis frequently presents as a unilateral A warm compress applied to the area can help relieve pain and swollen, red and tender lid but with proptosis, limitation of ocular promote drainage. movement and possibly decreased vision. Orbital cellulitis is most In infants, gentle massage of the lacrimal sac four times daily for up often caused by extension of infection from adjacent sinuses, to nine months can drain the sac and sometimes clear a blockage. especially the ethmoid sinus (75 to 90%). It is less commonly As the infant grows, the duct may open by itself. If the duct does not caused by direct infection accompanying local trauma (e.g. insect open, it may need to be dilated with a minor surgical procedure. 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 Congenital dacryostenosis and separates the lids from the orbit and its contents. If infection spreads beyond this septum then this can easily reach the brain In newborn infants, the nasolacrimal duct may fail to form an via the cavernous sinus with ~4% of cases developing intracranial opening. This condition is called dacryostenosis. complications. Orbital cellulitis is, therefore, a true ocular emergency Congenital dacryostenosis can result from inadequate development

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of any part of the nasolacrimal ducts. Most often, the far end of severe systemic disease. The most common fungal corneal pathogens the nasolacrimal duct is blocked. The result is an overlow of tears include Candida sp. (yeast like) and Fusarium sp. (ilamentous). that run down the cheek (epiphora) or persistent crusting. One or Fungal keratitis produces similar signs to bacterial keratitis, although both eyes can be afected. The problem is usually irst noticed in the infection may develop more slowly. Fusarium infection can 3 to 12-week-old infants. Congenital dacryostenosis is frequently progress rapidly and invasively. associated with neonatal conjunctivitis. This should be suspected in Symptoms and signs of sight-threatening keratitis may include: children with unilateral conjunctivitis and epiphora who have a relux of mucopurulent material from the lacrimal punctae after massaging • Moderate to severe pain with acute onset and rapid progression the nasolacrimal sac. Dacyrocsystitis may develop secondary to • Redness dacryostenosis and progress to periorbital cellulitis. • Photophobia (may be severe) This type of blockage (dacryostenosis) usually disappears without • Mucous discharge treatment by the age of 6 to 9 months, as the nasolacrimal system • Blurred vision (worse if the lesion is on the visual axis as develops. Until the child is about 1 year old, doctors often suggest opposed to peripherally) that parents gently massage the nasolacrimal sac four or ive times per day to help relieve the blockage. • Usually white or yellow corneal lesion caused by excavation of epithelium, Bowman’s layer and stroma as a result of tissue If the blockage is not relieved by the time the child is about 1 year necrosis old, an ear, nose, and throat (ENT) specialist or ophthalmologist • Stromal iniltration beneath the epithelial lesion often may have to open the nasolacrimal duct with a small probe, which is associated with stromal oedema and folds in Descemet’s usually inserted through the nasolacrimal duct punctum. The child is membrane and even an endothelial ibrin plaque beneath usually given a general anaesthetic for this procedure. • 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 Sight-threatening keratitis lamp examination, refer immediately as this may indicate an The most common forms of keratitis in children are those associated Acanthamoeba infection4. A good history is very important as with acute viral infections but these are almost invariably self-limiting discussed above. Children may be exposed to Acanthamoeba except in sick children. 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 Microbial keratitis lesions or lesions larger than 6mm in diameter, hospital admission is required. This would also be required if poor compliance with This is relatively rare in children, but for a small group, can be a intensive treatment (round the clock) using topical antibiotics cause of blindness. Underlying causes in children (most frequently is considered likely. Identiication of the causative organism is afecting young children) may include systemic infections, undertaken by corneal scrape, culture and determination of antibiotic immunodeiciency, orbital malignancies, corneal exposure, trauma sensitivities. Polymerase chain reaction [PCR] is a technique that may or dry eyes (Figure 2). At particular risk are children wearing soft be used to identify fungal organisms. contact lenses2,3. Pseudomonas should always be suspected in any contact lens wearer with corneal infection. This is a virulent organism Treatment often involves dual therapy with fortiied antibiotic that is mobile and produces collagenase which gives rise to a rapidly agents e.g. cephalosporin and an aminoglycoside (e.g. Gentamycin spreading liquefactive ulcer in the form of a yellowish white corneal 1.5%). Where monotherapy is deemed appropriate this involves opacity, with hypopyon. This is a collection of white blood cells in the the use of luoroquinolones (e.g. oloxacin, levoloxacin). Fourth- inferior anterior chamber. The symptoms and signs are very similar generation luoroquinolones (e.g. moxiloxacin and gatiloxacin) are to acute anterior uveitis. now considered good alternatives to standard treatment of bacterial keratitis using combined fortiied topical antibiotics5.

Herpes simplex keratitis Herpes 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), iridocyclitis and endotheliitis. Corneal endotheliitis is a fascinating clinical Figure 2. Corneal central ulcer with hypoyon 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, Other forms of keratitis can be diagnosed from their clinical varicella zoster virus, and cytomegalovirus. Corneal endotheliitis can presentation e.g. dendritic ulcers in herpetic keratitis (see below). be classiied clinically into four forms: linear, sectorial, disciform, Fungal infections are rare in the UK but more common in other parts and difuse. Antiviral treatment in combination with topical of the world. In children, they tend to occur in those predisposed to corticosteroids is generally efective to suppress the inlammation;

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 Figure 3. Herpes simplex dendritic ulcers 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. Figure 4. Stromal herpes simplex HSV eye disease can be divided into four main categories: • Epithelial (Figure 3) After resolution of dendritic epithelial keratitis, non-suppurative • Stromal (Figure 4) subepithelial iniltration and scarring can occur just beneath the • Disciform keratitis area of previous epithelial ulceration, resulting in a “ghost” image of the previous dendrite within the anterior stroma. The lesion usually • Metaherpetic ulcer (trophic keratitis) resolves without additional therapy, but may leave a permanent imprint of prior epithelial keratitis. Children with herpetic keratitis • Herpes simplex epithelial keratitis may have bilateral ocular involvement and are at risk for recurrent 9 Typically, patients with HSV keratitis present with blurry vision, keratitis and amblyopia . 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 Acute anterior uveitis (AAU) (iritis)10 bulbs allow the practitioner to distinguish this condition from other possible causes of dendritiform lesions e.g. varicellar zoster, healing Uveitis is inlammation of the uveal tract i.e. iris, ciliary body and corneal abrasions and Acanthamoeba infection. As with many corneal choroid. Acute anterior uveitis (incidence 12 per 100,000) is the conditions, corneal sensitivity may also be reduced. most common type of uveitis and can present as an isolated event or secondary to another eye condition (herpes zoster, herpes simplex) Herpetic epithelial keratitis may occur unilaterally or bilaterally or systemic disease. Although 50% are idiopathic, around 60% are (most often in patients with atopic disease) and be accompanied by associated with human leukocyte antigen (HLA) B27. A second acute a blepharoconjunctivitis, involving lesions of the lid and a follicular presentation of anterior uveitis (in less than 6-12 weeks) is referred response of the conjunctiva. In addition, a palpable pre-auricular to as recurrent acute uveitis. A third presentation reclassiies the lymph node may be present. condition as recurrent uveitis, which requires complete medical Medical management is relatively straight forward with HSV evaluation11. epithelial disease. Topical Occ. Aciclovir 3% or ganciclovir 0.15% The important symptoms of AAU are: (often preferred by patients) instilled ive times daily for two weeks is usually suicient to resolve the dendritic ulcer(s) in most cases8. • Photophobia Topical corticosteroids are contraindicated in the treatment of active • Rapid onset of pain in irst episodes (gradual at subsequent HSV epithelial keratitis. episodes) • Reduced vision • Herpes simplex stromal keratitis • Pain (dull ache) Since treatment of stromal keratitis may become prolonged with • Lacrimation use of steroids and associated with signiicant ocular morbidity, all It is rare for it to be accompanied by symptoms of discharge, patients seen in community practice with stromal HSVK should be stickiness, irritation, itching, nausea or vomiting. referred urgently to an ophthalmologist within 48 hours.

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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 burns Chemical 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 Figure 5. Keratic precipitates in uveitis 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 Important signs include: is indicated13,14. If sterile saline is not immediately available, use tap • Hyperaemia - circum-corneal (ciliary injection) water, and ensure all debris is removed from the eye. Alkali injuries • Keratic precipitates (Figure 5) cause considerably more damage than acid or thermal burns. • Aqueous cells Always check what chemical agent is the cause. Alkalis e.g. ammonia • Aqueous lare compounds, sodium hydroxide, lime (i.e. calcium hydroxide) cause the most severe ocular trauma by a process of liquefactive necrosis with • Raised intraocular pressure in some cases (this may be reduced rapid penetration of ocular tissue. In contrast, acids e.g. sulphuric, particularly if the ciliary body is afected) hydroluoric and hydrochloric cause coagulative necrosis which slows • Posterior synechiae possibly causing pupil block and iris bombé the penetration into ocular tissues. Other common causes of burns • Iris nodules: Koeppe (small, near pupil), Bussaca (large, far from involve detergents (sodium hypochlorite - bleach), solvents and pupil) ixatives. Contact lens solutions, including hydrogen peroxide may also cause minor ocular burns if used inappropriately. • Anterior vitreous cells indicate intermediate ± posterior uveitis • Posterior segment examination is essential: check for cystoid Chemical burns can cause signiicant discomfort but usually heal macular oedema and posterior uveitis quite quickly if relatively minor. In severe cases patients are often admitted and treated with topical antibiotics, steroids, ascorbic acid, • Other signs include sluggish pupil reactions, cataract, chronic sodium citrate and cycloplegics (Figures 6a and 6b). Acetazolamide corneal oedema may be required in cases with raised IOP. Surgical options may Speciic underlying causes of anterior uveitis in children: involve amniotic membrane grafts or even limbal stem cell • Trauma – traumatic iridocyclitis is common in childhood, transplantation in severe cases15. 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: Figure 6a. Chemical burn. Right: Figure 6b. Epithelial defect after • Juvenile rheumatoid arthritis (Still’s disease) – usually presenting corneal epithelial defect luorescein instilled in afected children 15 years or younger • Sarcoidosis • Fuch’s heterochromic cyclitis Penetrating injuries • Tuberculosis Children and adolescents account for a disproportionate share • Syphilis 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 The aims of treatment in AAU are to suppress inlammation, alleviate approximately 4 to 1 respectively. Penetrating eye injuries in children symptoms, prevent complications and treat complications. This cause long-term morbidity, and are of considerable socioeconomic usually consists of the following treatment: importance. The list of clinical circumstances and the various possible • Cycloplegia (guttae(g). cyclopentolate 1%) three times daily sharp objects that can be implicated in causing ocular trauma are • Topical steroid (e.g. g. Dexamethasone 0.1% or g. Prednisolone endless (Figure 7). Most injuries in children are related to rough acetate 1%) initially 2 hourly with steroid ointment at night until sports and projectiles, including toys, guns, darts, sticks, stones and

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.

Figure 7. Previous penetrating injury due to a pencil poked in the eye. Note Iris partially missing 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: Figure 8. Blunt trauma • lacerations • irregular pupils, • lens dislocation or subluxation Non-accidental injuries • commotio retinae Ophthalmic signs of non-accidental injury (NAI) can be varied and include periorbital and conjunctival injuries, damage to the anterior • vitreous haemorrhage17. segments, lens and vitreoretinal injuries. If suspected, all cases must Ophthalmological management may include orbital X ray (to check be referred and child protection procedures followed accordingly. for intraocular foreign bodies), B scan ultrasound (if there is no All Specsavers’ stores should have child protection protocols that clear fundus view owing to media opacities), surgical wound repair must be followed. 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 Conjunctivitis or visual loss usually 1-12 months after the inciting event. Treatment Acute conjunctivitis in childhood can result from infection with of posterior uveitis is beyond the scope of this article but usually a vast array of organisms with the most common cause being involves corticosteroids as well as immunosuppressants e.g. the adenovirus virus (see part 2). Most cases of conjunctivitis, Mycophenolate, Ciclosporin, methotrexate and azathioprine. 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 Blunt ocular injuries newborn < 4weeks old. The infection may be acquired during delivery (if the mother has a vaginal infection) or if born in A detailed, relevant history will give a clear indication as to what unhygienic conditions. The main types are: level of damage the eye may have sustained. Examination of the eye should be systematically undertaken to check for: o Gonococcal conjunctivitis which is a rare disease, but • Blood in the anterior chamber - hyphaema still common in certain parts of the world. This is characterised by an acute purulent conjunctivitis with lid • Black (uveal tissue) protruding from the eye which would oedema, marked conjunctival hyperaemia, chemosis with indicate rupture of the globe or without membrane formation and prominent pre- • Sub-conjunctival haemorrhage indicating possible perforation auricular adenopathy. Treatment involves systemic and beneath

topical antibiotics. Gonococcal conjunctivitis is caused by the bacterium Neisseria gonorrhoeae. A newborn can be infected with these bacteria during childbirth. If conirmed, GOC’s Enhanced CET Scheme the child would need to be admitted and treated with CET and CPD regulators require practitioners to relect on their systemic antibiotics. learning. Additional activities are required to gain CET for distance learning. o Inclusion (chlamydial) conjunctivitis caused by the bacterium, Chlamydia. Signs include injected conjunctiva, Log into your CET dashboard via iLearn. On the menu you reach you lid swelling and a mucopurulent discharge that appear 5 will ind non-interactive CET for this unit of learning. to 12 days after birth. Chlamydia trachomatis is one of the For ‘non-interactive’ CET you have to pass (>60%) a six-question most common causes of neonatal conjunctivitis. This would multiple-choice quiz. usually be treated with systemic antibiotics. The learning objectives for this article are: 1.1.1 Therapeutic optometrists will have enhanced understanding Conclusions of signs, symptoms and management of childhood anterior segment diseases A range of serious anterior segment conditions presenting in childhood have been discussed in terms of clinical presentation 6.1.5 Optometrists will have enhanced understanding of signs, and management options. For most of these conditions, accurate symptoms and management of childhood anterior segment diagnosis by the community optometrist is required so that an diseases urgent referral can be made containing all relevant information. 8.1.2 Dispensing opticians will have enhanced understanding of In the second part of this series, less urgent anterior segment eye symptoms associated with childhood anterior segment diseases 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.

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