van Onselen, B

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OPHTHALMOLOGYBrian van Onselen, ME CkB, FCS (Opth) (SA)Ophthalmologist in privau pracri€e~Sandum, GaurmgTreatment consists of oral valaciclovir (Zelitrex) for 10 daysas well as topical mupirocin (Bactroban) ointment for thescabs. It is vital not to let the lesions dry out, as this canlead to cicatrisation and lid disorders such as entropionwith resultant corneal scarring. Pain can be debilitating andis alleviated by topical EMLA cream, capsacain and oralcarbamazepine ITegretol).THf SOUTHfRN AFRICAN JOURNAL OF HIV MfOlCINfKAPOSI'S SARCOMAHerpetic ulcers of the cornea in HIV-infected patients tendto be peripheral rather than central, and to be largedendritic ulcers. Treatment is with acyclovir (Zovirax)ointment 5 times a day, and patients should be monitoredfor uveitis.Lesions are multiple and large, and accumulate on the lids.Cryotherapy is used to treat clinically significant lesions.Uveitis and an accompanying rise in intraocular pressureare seen in up to 40% of patients. Referral to anophthalmologist is prudent to avoid complications.SQUAMOUS CARCINOMA OF THE CONJUNCTNAMOllUSCUM CONTAGIOSUMThese blue-black vascular tumours can affect the eyelids orconjunctiva. Treatment is necessary for large, sight-threatening lesions and is normally accomplished bycryotherapy.Squamous carcinoma of the conjunctiva has rapidlybecome a new marker for HIV in young patients (Figs 2 and3). Typically they are younger than 40 years, whereas thenormal age for appearance of this tumour is 65 years.The spectrum of disease extends from pterygium throughdysplasia to carcinoma in situ. Typical lesions are raised,with large feeder blood vessels and uneven, rough surfaces.Pigmentation is common.Treatment involves careful excision using Moh'smicrographic technique. It is important not to breach thecorneal Bruch's membrane as this can lead to localrecurrence. Adjuvant therapies include mitomycinantimetabolite, radiotherapy and enucleation of eyes ifHERPES ZOSTERFig. 1. Herpes zoster.SURFACE PATHOLOGYAlmost 7(JJ/o of untreated AIDS patients will develop ocularmanifestations, more than half of which are associatedwith ocular infiammation or uveitis. It is the aim of thisarticle to highlight the common and important conditionsthat the practitioner might come across.OCULAR MANIFESTATIONS OF HIV/AIDSThe practice of the ophthalmologist who looks after peoplewith HN has changed.The widespread use of highly active antiretroviral therapy(HAARn has reduced the incidence of cytomegalovirus(CMY) retinitis as well as other opportunistic infections. Itmust be remembered that iatrogenic complications alsoarise, e.g. colour vision impairment by zidovudine anduveitis associated with cidofovir and rifabutin.For convenience, we can group the conditions into surfacedisorders, neuro-ophthalmological complications, vascularmanifestations and uveitis.Herpes zoster has become a prominent marker for HIVinfection (Fig. 1). Traditionally this condition affectspatients older than 60 years. With HIV, we are seeingpatients younger than 45 years. The disease tends to bevery aggressive, with prominent crusting and neuralgia. TheCD4+ count is usually 75 - 150 cells/~1.NOVfMHfR 2003THf SOUTHfRN AmlCAN JOURNAL O~ HIV MfOlCINf ----------- NOVfM9m 2003UVEITISAg. 4. Early CMValong vascular arcade.Ag. 5. Established CMV with retinal oedema.Necrotising retinitis is caused by CMV, varicella and herpeszoster. CMV is the most common, and usually occurs witha CD4+ count of less than 50 cells/~1.Other causes of uveitis include:• Toxoplasmosis [llJlltl of HIV patients). Can be single ormultiple white foci with overlying vitritis.• Lymphoma with infiltrates.• Endogenous endophthalmitis in intravenous drug users,leading to retinal abscess.• Bilateral multifocal choroiditis caused by Pneumocystiscarinii or cryptococcus. This tends to occur as anepiphenomenon of systemic/central nervous systemdisease.cryptococcosis. Optic neuritis is treated by antivirals andcorticosteroids according to severity. Causative organismsare often not isolated, leading to the hypothesis that HIVitself causes optic neuritis.CMV retinitis can have various appearances [Figs 4 and 5).The traditional description of 'cottage cheese and ketchup'with haemorrhages can follow an indolent or granularappearance. The leading edge of the lesion can assume a'brushfire' appearance around the necrotic, pale retina [Fig.6). Sheathing of the vessels can produce a spectacularVASCULOPATHYAg. 2. Squamaus carcinama af the canjunctiva.Ag. 3. Neglected squamous carcinoma.NEURO-OPHTHALMOLOGICAL PATHOLOGYthere is local invasion. Spread to adjacent tissues requiresexenteration of the orbital contents.Neuro-ophthalmological disease includes optic neuritis,papilloedema, cranial nerve palsies and visual field deficitsdue to intracranial disease such as toxoplasmosis andThese lesions usually resolve spontaneously and can beconfused with early CMV retinitis.Vasculopathy takes the form of a microangiopathy thatmanifests as cottonwool spots in the retina. It occurs in50 - 7lJlltl of AIDS patients and can look like early diabeticretinopathy. Small dot haemorrhages are common.Rg. 6. '8rushfire' edge ofCMVretinitis.Rg. 7. 'Frosted-branch' angiitis.Rg. 8. Healed CMV with retinal atrophy and pigmentation.'frosted-branch angiitis' (Fig. 7). In response to treatment,the active white border turns grey (Fig. 8). Haemorrhagescan persist for months. Fibrosis and pigmentation arecommon in healed lesions.On HAART, patients with previously quiescent disease canexperience the phenomenon of immune-ret:overy uveitis.This usually occurs after elevation of the CD4+ count above60 cells/~1. No concurrent relapse of CMV retinitis is noted.Vitreous haze, retinal and optic nerve oedema andformation of epiretinal membranes are noted. Treatment iswith periocular and systemic steroids.NOVfMllfR 2003Various agents have been used to treat CMV retinitis.Intravenous agents have the advantage of treating botheyes and systemic disease. These include:• Foscarnet - daily dose with side-effet:ts of nausea(40'1'0) and renal impairment• Cidofovir - induction and then weekly. Complicationsare uveitis and hypotony.• Ganciclovir - induction and then daily 5 times a weeilThis can cause bone-marrow suppression.Relapse of disease within months is common on IVtreatment.Ganciclovir implants have proven effective but carry therisk of haemorrhage and retinal detachment (12%) andneed to be replaced every 6 - 8 months.Intravitreal ganciclovir injmions (Fig. 9) have provedvery effective in the South African setting where HAART isstill not freely available. These are cheap (20 treatments pervial of ganciclovir) and after the initial twice-weeklyinduction are given weekly and then every 2 weeks. Theaddition of oral ganciclovir improves the outcome.Rg. 9. Introvitreal ganciclovir injection.Recent studies have shown that it may not be necessary tocontinue CMV therapy in patients on HAART. Normally,without immune restitution or maintenance therapy CMVretinitis relapses within 3 weeks. In patients on HAART,relapses occur up to 6 months. After this period, if theC04+ count is above 50 cellsM the patient can bemonitored without CMV therapy.After 18 months on HAART, if there has been no ret:urrenceof CMV it is highly unlikely to recur even if the C04+ countdoes not rise above 100 cells/~1. Any drop below 50 cells/~I,however, can lead to recurrence.REFERENa51. Ash S. Erlitorial BtJ Ophrholmo/ 1998; 82: 981-S82.2. bmbarakIi eraJ. HAART and Olo/ therapy. BrJOphrhalmo/2001: 85:837-841-3. Kanski Jl OinicaJ Ophrhafm%g'l_ 2003 Edition.THf SOUTHERN AmlCAN JOURNAL Of HIV MfOlCINf

Ocular manifestations of HIV/AIDS

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Ocular manifestations of HIV/AIDS

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