Endogenous Endophthalmitis and Other Ocular Manifestations of Injection Drug Use

Preston M. Luong; Edmund Tsui; Nikhil N. Batra; Michael E. Zegans


Curr Opin Ophthalmol. 2019;30(6):506-512. 

In This Article

HIV-associated Pathology

Although the advent of HAART has drastically reduced the burden of disease from opportunistic infections in patients with HIV, IDUs unaware of their HIV infection remain vulnerable.[34]

Herpes zoster ophthalmicus (HZO) occurs during reactivation of the varicella zoster virus along the V1 trigeminal nerve distribution affecting the eye and is substantially more common in those who are immunocompromised.[35] The typical age of patients presenting with HZO is in the 5th and 6th decade of life. Consequently, younger patients presenting with symptoms typical of HZO should be questioned about injection drug use and evaluated for an immunocompromised state, and HIV infection.[36] A nonspecific inflammatory prodrome may precede overt clinical signs. Classic signs include a unilateral periorbital vesicular and erythematous rash with symptoms of eye redness and diminished vision. If the nasolacrimal nerve of V1 is affected, Hutchinson's sign may manifest as lesions on the nose tip and folds. Associated findings may include keratitis, scleritis, iritis, uveitis, and retinitis.[37] HZO can be clinically diagnosed, although viral cultures and PCR may provide confirmatory support. Oral acyclovir, famciclovir, and valacyclovir have demonstrated efficacy in treating HZO.[38,39] Topical or systemic steroids may also play a role in reducing inflammatory damage.[40]

Cytomegalovirus (CMV) retinitis is an opportunistic infection that typically occurs when CD4 counts fall under 50 cells/μl, although it has been noted that those even with CD4 counts greater than 100 cells/μl may acquire CMV retinitis.[41,42] It is the most common manifestation of CMV infection in patients with HIV and affects almost half of patients who have developed AIDS.[43] Fundus exam typically reveals retinitis of either a fulminant hemorrhagic, granular, or perivascular pattern. Treatment involves intravitreal injection of antivirals for local control of the retinitis, as well as possible systemic initiation of HAART with additional valganciclovir, ganciclovir, foscarnet, or cidofovir as needed.[44]

Ocular syphilis manifestations are myriad. Anterior uveitis, vitritis, retinitis, and papillitis may be present. Large, placoid, yellow lesions with faded centers are characteristically observed within the retina.[44,45] Suspected ocular syphilis warrants investigation by serum treponemal testing such as fluorescent treponemal antibody absorption followed by nontreponemal testing such as rapid plasma reagent.[46–48] Treatment of ocular syphilis mirrors neurosyphilis, which involves a course of intravenous penicillin G.[49]

Ocular toxoplasmosis occurs twice as frequently in HIV-positive individuals compared with those with HIV-negative status.[50] Patients are typically young, with most presenting in their 20s or 30s. Quiescent chorioretinal scars from previous subclinical inflammation may already be present on exam when patients first present.[51] Substantial vitritis may obscure areas of active inflammation, which appear as fluffy yellow lesions with indistinct borders.[52,53] Anterior chamber inflammation is also present in the majority of patients.[54] Inflammation resolves usually over 6 weeks although reactivation is common. If ocular toxoplasmosis is suspected, serology for antitoxoplasma antibodies as well as PCR of intraocular fluids can lend supporting evidence.[55,56] Treatment with the classic 'triple therapy' consists of sulfadiazine, pyrimethamine, and prednisone, although clindamycin, trimethoprim–sulfamethoxazole, azithromycin, or atovaquone either alone or in combination have also been suggested.[57,58] Computed tomography or MRI scans may also be obtained to survey the possibility of central nervous system involvement.[59]

Even in the absence of an opportunistic infection, HIV infection itself causes a retinopathy characterized by cotton-wool spots and intraretinal hemorrhages, which are postulated to arise from immune complex deposition and increases in plasma viscosity.[37] Patients with CD4 counts of less than 100 cells/μl have retinal nerve fiber layer (RNFL) thinning, especially of the temporal, superior, and inferior retina.[60] HIV patients with CD4 count greater than 100 cells/μl appear to have no RNFL loss, highlighting the importance of prompt recognition of HIV infection and initiation of HAART.[60]