What are the posterior segment ocular manifestations in HIV infection?

Updated: Jun 12, 2019
  • Author: Robert A Copeland, Jr, MD; Chief Editor: Andrew A Dahl, MD, FACS  more...
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Answer

Complications of CMV retinitis include papillitis, seen in about 5% of these patients, and it can lead to significant visual loss. If left untreated or if inadequately treated, CMV retinitis progresses (usually less rapidly than HSV or HZV retinitis) to involve a larger area of the retina including the macular and/or foveal. Cystoid macular edema, retinal vein or artery occlusion, rhegmatogenous retinal detachment (RRD), or blindness may result from inadequately treated CMV retinitis in these patients. [20]

The incidence of RRDs tends to increase with time in patients with CMV retinitis, with a cumulative probability of 26-61% in different studies.

Immune recovery uveitis (IRU) is a HAART-dependent inflammatory response that may occur in up to 63% of patients with regressed CMV retinitis and elevated CD4+ counts. IRU is caused by a response to CMV antigens, which is made possible by immune recovery. IRU generally is recognized in its most severe form by an increase in intraocular inflammatory reactions within weeks after starting HAART, or it may manifest later by the presence of inflammation and may be associated with vision loss from epiretinal membrane, cataract, neovascularization of the retina or optic disc, and cystoid macular edema.

Patients with large areas of CMV retinitis and a history of cidofovir use have an increased risk for IRU. To reduce the risk of IRU, delay HAART use until induction of CMV therapy.

Acute retinal necrosis (ARN) frequently is complicated by anterior uveitis, retinal and choroidal vasculitis, vitritis, and papillitis. Episcleritis, scleritis, or optic neuropathy also may be present. During the initial phase of the infection, the severity of the retinitis can lead to exudative retinal detachment. Following the resolution of the retinitis, however, traction between the vitreous and the resulting gliotic scar of the necrotic retina may occur and can cause retinal breaks at the interface between the normal and necrotic retina. Subsequently, this may result in RRD. In as many as 75% of cases, ARN may be complicated by RRD 2-3 months after onset. [21]

Complications of herpes zoster ophthalmicus (progressive outer retinal necrosis, or PORN) may include macular retinitis, optic nerve disease, acute vitreous hemorrhage, and/or retinal detachment. Up to 66% of patients diagnosed with PORN become blind within 6 weeks of diagnosis despite aggressive treatment.

Syphilitic anterior uveitis may be complicated by cataract and glaucoma formation. Posterior segment complications may include posterior placoid chorioretinitis, neuroretinitis, vitritis, pigmentary chorioretinopathy, choroiditis, papillitis, choroidal neovascular membranes, and retinal vasculitis.

Complications of tuberculosis include the following:

  • Conjunctivitis

  • Oculoglandular syndrome

  • Interstitial keratitis

  • Phlyctenular keratitis

  • Anterior uveitis (most common)

  • Endophthalmitis

  • Scleritis

  • Chorioretinitis

  • Disseminated choroiditis

  • Choroidal neovascularization

  • Optic atrophy

These ocular manifestations tend to occur in patients with other extrapulmonary disease.

With Pneumocystis jiroveci choroidopathy, usually minimal vitreous inflammation occurs. The major cause of morbidity and/or mortality in patients with P jiroveci infection results from the debilitating pneumonia.

Ocular complications of Toxoplasma gondii infection depend on the mode of infection. Infection with T gondii may be congenital or acquired. In general, ocular complications include infantile retinochoroiditis, leukocoria, and anterior and posterior uveitis.

Disseminated histoplasmosis has a high mortality rate in AIDS patients. This disease tends to have a fulminant course, usually complicated by disseminated intravascular coagulation. Ocular complications of disseminated histoplasmosis include retinitis, choroiditis, optic neuritis, or uveitis. Secondary choroidal neovascularization also may develop.

The most frequent intraocular sequela of cryptococcal infection is chorioretinitis. In the absence of treatment, or because of poor management, endophthalmitis may result. Other reported ocular complications of cryptococcal infection include papilledema, optic atrophy, and ophthalmoplegia.

For neuro-ophthalmologic manifestations, the most common complications include papilledema due to increased intracranial pressure, cranial nerve palsies, ocular motility disorders, and visual field defects.


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