Acquired Immunodeficiency Syndrome (AIDS) is now a global pandemic with more than 40 million people in the world being affected, causing enormous human, social and economic toll in the world. According to WHO, soon India will have the highest number of HIV-infected Ocular (eye) lesions, occuring in 40 to 70 per cent of AIDS patients, reveals Dr. Binita Thakore and Dr. Alay S Banker. Currently, about eight million people (about 0.8 per cent of the entire population) are infected with HIV in India. Also, the epidemic is growing outside high-risk groups to the general population, and is moving from urban to rural districts. Ocular lesions in AIDS Ocular (eye) lesions occur in 40 to 70 percent of AIDS patients. They can be as follows:
Anterior segment lesions in AIDS patients
- Dry eye
- Infective keratitis (infection of the cornea)
- Anterior uveitis
Posterior segment lesions in AIDS patients
- HIV retinopathy
- Cytomegalovirus retinitis
- Toxoplasmic retinochoroiditis
- Cytomegalovirus optic neuritis
- Pneumocystis carinii choroidopathy
- Acute retinal necrosis
- Herpes zoster retinopathy
- Progressive outer retinal necrosis
- Endogenous endophthalmitis
Ocular adnexal lesions in AIDS patients
- Conjunctival microvasculopathy
- Herpes zoster ophthalmicus
- Kaposi’s sarcoma of eyelid, conjunctiva
- Molluscum contagiosum of the eyelid
Orbital lesions in AIDS patients
- Burkitt’s lymphoma
- H Orbital cellulitis (aspergillus)
Neuro-ophthalmic lesions in AIDS patients
- Cranial nerve palsies
- Optic atrophy
Posterior segment lesions: Posterior segment lesions are the most common ocular manifestations in AIDS patients occurring in up to 50 per cent of cases. The patients can be asymptomatic or have complaints of floaters, flashes of light, visual field defect and dimness of vision.
CMV retinitis: CMV retinitis is the most common infection in patients with HIV disease, seen in 15 to 40 percent of patients with HIV disease, more so when CD4 cell count is less than 100 cells per cubit mm. The classic description of CMV retinitis (cottage cheese with catsup or pizza pie retinopathy) is one of scattered yellow-white areas of necrotising retinitis with variable degree of haemorrhage. There is not much vitreous involvement, a hallmark of CMV retinitis. It usually starts in the periphery and so patients either have no subjective complaints, or may complain of floaters. If the retinitis begins in the centre (the posterior pole), the patient may notice a visual field deficit. Retinal detachment has been reported in 13.5 to 29 per cent of patients with CMV retinitis and may occur during the active or healed phase of the disease. Other findings associated with CMV retinitis include: perivasculitis, vascular attenuation, vessel closure, and venous occlusions, as well as vitritis, anterior uveitis, and papillitis.
Mycobacterial infection: Extra pulmonary and disseminated tuberculosis is seen more commonly in HIV positive patients. However, choroidal tuberculosis has not been so commonly reported. It is possible that many cases of choroidal tuberculosis remain asymptomatic and probably regress with the anti-tubercular treatment for extra ocular tuberculosis. It usually presents as multifocal choroiditis with discrete yellow choroidal lesions mainly at posterior pole. It may be associated with an exudative retinal detachment with variable vitreous inflammation.
Ocular manifestations of HIV in the era of HAART: The advent of potent antiretroviral has made a profound effect in the ophthalmologic manifestations of AIDS patients. As these drugs lead to improved immune function, patients have fewer opportunistic infections. It has been estimated that the frequency of new CMV retinitis cases was decreased by 80 per cent or more. Other HIV related ophthalmic disorders like Kaposi’s sarcoma are seen infrequently. Patients who develop CMV retinitis can be divided into several distinct subpopulations, based on the history of whether or not they have used antiretroviral drugs and their potential for improved immune function. The approach to disease management for patients who have never received potent antiretroviral therapy is, that they should be placed on a combination of agents in an attempt to improve immune function.
For those with evidence of immune reconstitution (elevated CD4+ T-lymphocyte counts, lower HIV blood levels), control of CMV retinitis becomes easier, and in many cases it is possible to discontinue specific anti-CMV therapy altogether. However, immune reconstitution can take eight weeks or longer. Thus, aggressive\ anti-CMV therapy may be needed during the period immediately after diagnosis. An emerging problem among patients with CMV retinitis is ‘immune recovery uveitis.’ As immune function improves following the initiation of potent antiretroviral therapy, some patients will develop heightened intraocular inflammatory responses, presumably to CMV antigens. Although the vitreous humour reaction may be transient, patients can be left with complications of inflammation, such as persistent macular oedema, epiretinal membranes, and decreased vision. Inflammation and macular oedema with respond to corticosteroid therapy, and possibly to nonsteroidal anti-inflammatory agents, but improvement tends to be limited in duration and recovery of normal vision is rarely achieved in patients with macular oedema.