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Ovid: Oxford Handbook of Genitourinary Medicine, HIV, and Aids

Editors: Pattman, Richard; Snow, Michael; Handy, Pauline; Sankar, K. Nathan; Elawad, Babiker Title: Oxford Handbook of Genitourinary Medicine, HIV, and Aids, 1st Edition Copyright ©2005 Oxford University Press > Table of Contents > HIV/AIDS > Chapter 44 – HIV: disorders of the eye Chapter 44 HIV: disorders of the eye P.434
Introduction Ocular manifestations have been reported in up to 60% of those infected with HIV, ↑ in frequency as the CD4 count ↓. Patients with CD4 count <200/µL should be closely examined for signs of ocular disease which may be asymptomatic in the early stages. Close cooperation with ophthalmology is essential to ensure timely therapeutic interventions to ↓ risk of visual impairment and blindness. Widespread use of HAART has dramatically altered the incidence and natural history of many opportunistic eye infections. HIV-related vasculopathy 70–80% of patients with advanced HIV disease have asymptomatic transient microvascular changes that may occur simultaneously in the conjunctiva and retina. Conjunctival changes are found near the limbus and only detected by slit-lamp examination. Features include vascular narrowing, dilatation, and microaneurysms. No treatment needed. Retinal changes are detected by fundal examination. Cotton-wool spots (infarcts of nerve fibre layer) most common feature of retinal vasculopathy. Differentiated from early CMV lesions by their small size, superficial retinal location, and transient nature with less frequent retinal haemorrhages and microaneurysms. Iridocyclitis Seen in association with toxoplasmic, syphilitic, bacterial, and fungal retinitis. Drugs such as rifabutin, (especially with concurrent azole and macrolide use) and cidofovir are frequent causes. Diagnosed by slit-lamp examination. Treatment Treat underlying infection(s) and/or ↓ or discontinue implicated drug(s). Topical steroids may be used but not if active infection. Neurological eye manifestations Occur in 10%. Most common features include papilloedema, cranial nerve palsies, ophthalmoplegia, and visual field defects. Caused by lymphoma and any CNS infection, most frequently cryptococcal meningitis, neurosyphilis, and toxoplasmosis. HIV encephalopathy and progressive multi-focal leukoencephalopathy may have similar complications. Investigate by magnetic resonance imaging, lumbar puncture (CSF—cell count, cytology, culture, and serology). Immune-recovery uveitis Mainly involves anterior uveal tract and vitreous, commonly associated with a marked disturbance of visual function due to macular oedema and epi-retinal membrane formation. Believed to be a consequence of the marked reconstitution of immune function induced by HAART. Marked cellular infiltration of the vitreous (in the absence of an active retinal or chorioretinal lesion) is a hallmark of this phenomenon. Responds well to systemic steroids. P.435
Opportunistic infections (OIs) Cytomegalovirus infection (CMV) CMV retinitis results from reactivation of infection acquired in childhood or early adult life. Prior to HAART it was the most common eye OI occurring in 30–40% of those with a CD4 count <50cells/µL. Bilateral in 30–50% of cases with optic nerve involvement in 5%. Serious visual complications can be avoided by the detection of its early features with regular dilated examination of the fundi for those at risk (CD4 <100cells/µL). Clinical features Symptoms depend on site and extent of retinal involvement. Peripheral retinal lesions are asymptomatic. Earliest and most common symptoms are multiple floaters, representing foci of inflammatory cells in the vitreous attempting to contain the infection. Other symptoms include bluring/loss of central vision, flashing lights, and scotomata. Initial focus of retinal inflammation expands peripherally inducing retinal necrosis. Early active lesions appear as multiple granular white dots with occasional haemorrhages. With further progress areas of retinitis enlarge by following the vascular arcades, resulting in an arcuate or triangular zone of infection. Areas of active infection may also be linear, following the retinal vessels or nerve fibre layer into the periphery. Early CMV lesions may be confused with cotton-wool spots (due to HIV vasculopathy) which may coexist. Serial drawings or retinal photographs are helpful in differentiation. Continuing activity of the necrotic process results in atrophic features with thinning of the retina resulting in visualization of the underlying choroid. Other features of CMV retinitis include vascular attenuation, vessel occlusion, vitritis, and anterior uveitis (Plate 21). May be complicated by retinal detachment and cataract. Occasionally it may be difficult to establish the cause of retinitis. Diagnosis Usually clinical. Confirmed by obtaining a vitreous sample for CMV using PCR testing. CMV viraemia may be a useful predictor of CMV disease. A rising CMV viral load detected by PCR is associated with ↑ eye and other organ disease. Treatment

  • HAART ↑ response to treatment, prognosis, and ↓ relapse rates.
  • Oral valganciclovir 900mg twice daily for 3 weeks followed by 900mg once daily produces blood levels comparable to intravenous ganciclovir. Main side-effects are bone marrow suppression and gastrointestinal upset.
  • Intravitreous ganciclovir implant is very effective but needs to be replaced after 6–9 months and does not give protection to the other eye or protect against systemic disease.
  • Intravenous ganciclovir given as an induction course for 2–3 weeks (5mg/kg body weight 12 hourly) followed by maintenance therapy (5mg/kg body weight 7 days a week or 6mg/kg body weight 5 days a week). Side-effects include rigors and neutropenia that may require discontinuation of treatment or the use of granulocyte colony P.437
    stimulating factor. Oral ganciclovir (1g 3 times a day) may be given in place of intravenous formulation once retinitis has remained stable for at least 3 weeks.
  • Intravenous foscarnet given as an induction course for 2–3 weeks (60mg/kg body weight 8 hourly) followed by maintenance therapy (90–120mg/kg body weight once a day). Given when ganciclovir not tolerated due to its toxicity. Side-effects include nephrotoxicity, convulsions, meatal ulceration, and electrolyte disturbance. Has ↑ infusion time and requires an infusion pump.
  • Intravenous cidofovir (3–5mg/kg body weight once a week) given together with probenecid (2g orally 3 hours before the cidofovir infusion followed by 1g for 2 hours and 8 hours following its completion) and fluids. Effective in ganciclovir-resistant CMV but highly nephrotoxic and myelosuppressive.

Prognosis Response to therapy achieved in 80–90%. Without immune reconstitution, the median time to relapse is 50–120 days using standard anti-CMV treatment. Maintenance therapy can be stopped once immune reconstitution is achieved. P.438
Varicella zoster virus infection (VZV) Ophthalmic herpes zoster results from involvement of the ophthalmic division of the trigeminal nerve and is recognized by characteristic vesicular eruptions. May be associated with blepharitis, conjunctivitis, keratitis, and uveitis. Complications and post-herpetic neuralgia ↑ in the immunosuppressed. VZV is the 2nd most common cause of necrotizing retinitis which may occur at same time or follow recent herpes zoster. Early retinal lesions similar to CMV, but rapidly progressive, deep, and multifocal with ↑ risk of bilateral disease and retinal detachment which may lead to blindness in days without prompt treatment. Diagnosis Characteristic rash and its distribution are usually sufficient to establish the diagnosis. Serological tests and PCR rarely needed. Treatment Intravenous ganciclovir is the treatment of choice in addition to topical steroids. In the absence of anterior uveitis mydriatics (e.g. 1% atropine) also required. Herpes simplex keratitis HSV eye infection causes keratitis or rarely acute retinal necrosis. Keratitis leads to corneal ulcers, diminished corneal sensation, and ↑ intraocular pressure. Corneal ulcers are usually painful and have a dendritic appearance. Difficult to treat and relapses frequently. Treatment Oral aciclovir (400mg 5 times daily) or famciclovir (250–500mg 3 times daily). Acute retinal necrosis Commonly caused by VZV and HSV but CMV and other viruses may be implicated. Usually present with scotomata progressing rapidly to visual loss. Detailed fundal examination reveals peripheral white lesions that progress to widespread necrosis over a few days. May be complicated by proliferative retinopathy and retinal detachment. Treatment Responds poorly to antivirals but IV ganciclovir should be started immediately. Toxoplasma retinochoroiditis Rare, accounting for 1–2% of retinitis with 30–50% of patients having central nervous system involvement. Characteristically causes bilateral multifocal retinochoroidal lesions that invade the vitreous in the later stages. Majority of patients do not have pre-existing eye lesions. Diagnosis Fundal examination reveals characteristic extensive fluffy areas of retinal whitening with accompanying vitritis, but unlike CMV infection retinal P.439
haemorrhaging is less likely. Toxoplasma serological tests unreliable but absence of toxoplasma IgG antibodies makes its diagnosis less likely. Treatment Pyrimethamine in combination with sulfadiazine or clindamycin. Equally good response may be obtained with atovaquone. Long-term maintenance treatment with clindamycin and pyrimethamine usually required. Candidal eye infection Infection of the anterior segment of the eye results in superficial keratitis. Posterior segment infection seen in advanced HIV disease and presents as multiple often bilateral, white fluffy retinal lesions that may extend into the overlying vitreous. Majority of patients have systemic candidal infection. Culture and sensitivity of the causative yeast provides the best outcome on which to base therapy. Superficial keratitis responds well to topical antifungals. Systemic antifungals are needed for posterior segment infection e.g. voriconazole and liposomal amphotericin. Kaposi’s sarcoma (KS) Up to 20% of patients with skin KS have eyelid and conjunctival lesions recognized by their characteristic appearance, although conjunctival lesions may resemble traumatic haemorrhages. Treatment Options include surgical removal, cryotherapy, and intralesional vinblastine. Systemic chemotherapy is given if there are associated skin lesions. Radiation is effective but may be complicated by loss of eyelashes and conjunctivitis.

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