HIV-Positive Veteran with Progressive Visual Changes
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VA BOSTON MEDICAL FORUM HIV-Positive Veteran With Progressive Visual Changes Lakshmana Swamy, MD; Nicholas J. Butler, MD; Richard Serrao, MD; and Anthony C. Breu, MD Case Presentation. This case involves a 49-year-old U.S. Army veteran (service included time in Somalia and Panama) with a history of HIV, diabetes mellitus, and hypertension who presented with progressive visual changes. Three years prior to the current presentation, he was diagnosed with HIV and started highly active antiretroviral therapy (HAART) therapy. About 1 year prior to presentation, he was off therapy for a month. When laboratory results indi- cated a detectable viral load, HAART was restarted (abacavir, lamivudine, and efavirenz). Four months prior to presentation, he noted a flicker in his left eye, followed 2 months later by a shadow over his left upper visual field along with occasionalROUND floaters- and blurry vision in his left eye. In the days leading to the presentation, the shadowTABLE worsened, prompting evaluation. Lakshmana Swamy, MD, chief medical sis. Likewise, ongoing fevers in an advanced resident, VA Boston Healthcare System AIDS patient with concomitant colitis, hepa- (VABHS) and Boston Medical Center. Dr. titis, and pneumonitis is strongly suspicious Serrao, when you hear about vision changes for cytomegalovirus (CMV) retinitis with in a patient with HIV, what differential diag- wide dissemination. nosis is generated? What epidemiologic or Geographic epidemiologic factors can historical factors can help distinguish these suggest pathogens more prevalent to certain entities? regions of the world, such as histoplasma chorioretinitis in a resident of the central Richard Serrao, MD, Infectious Dis- and eastern U.S. or tuberculosis in a return- ease Service, VABHS and assistant pro- ing traveler. Likewise, a cat owner or one fessor of medicine, Boston University who consumes steak tartare increases the School of Medicine. The differential diag- likelihood for toxoplasma retinochoroidi- noses for vision changes in a patient with tis, or syphilis in men who have sex with HIV is based on the overall immunosup- men (MSM) in the U.S. given that the ma- pression of the patient: the lower the pa- jority of new cases occur in this patient pop- tient’s CD4 count, the higher the number of ulation. Other clues one should consider etiologies.1 The portions of the visual path- include the presence of splinter hemor- way as well as the pattern of vision loss are rhages in the extremities in an intravenous useful in narrowing the differential. For ex- drug user, raising the possibility of embolic ample, monocular visual disturbances with endophthalmitis from bacterial or fungal en- dermatomal vesicles within the ophthalmic docarditis. A variety of other diagnoses can division of the trigeminal nerve strongly im- certainly occur as a result of drug treatment plicates varicella zoster retinitis or keratitis; (uveitis from rifampin, for example), im- abducens nerve palsy could suggest granulo- mune reconstitution from HAART, infec- matous basilar meningitis from cryptococco- tions with other HIV-associated pathogens, such as Pneumocystis jiroveci, and many Dr. Breu is a hospitalist and the director of resident education at VA Boston Healthcare System and an assistant professor non-HIV-related ocular diseases. of medicine at Harvard University in Massachusetts. He is the corresponding author and supervises the VA Boston Medical Dr. Swamy. Dr. Butler, what concerns Forum chief resident case conferences. All patients or their do you have when you hear about an HIV- surogate decision makers understand and have signed ap- propriate patient release forms. This article has received an infected patient with vision loss from the abbreviated peer review. ophthalmology perspective? 18 • FEDERAL PRACTITIONER • NOVEMBER 2017 www.fedprac.com Nicholas Butler, MD, Ophthalmology Table 1. Blood Test Analysis Service, Uveitis and Ocular Immunology, Tests Reference Result VABHS and assistant professor of oph- thalmology, Harvard Medical School. Of White blood cell count (x 109/L) 4.5-11.0 5.8 course, patients with HIV suffer from com- Differential count (%) mon causes of vision loss—cataract, glau- Neutrophils 40-75 62.6 coma, diabetes, macular degeneration, for instance—just like those without HIV infec- Bands 0-10 0.3 tion. If there is no significant immunodefi- Lymphocytes 10-55 24.5 ciency, then the patient’s HIV status would Monocytes 2-12 9.8 be less relevant, and these more common causes of vision loss should be pursued. My Eosinophils 0-7 2.1 first task would be to determine the patient’s Basophils 0-2 0.7 most recent CD4 T-cell count. Hemoglobin (g/dL) 10.3 13.1 Assuming an HIV-positive individual is ex- periencing visual symptoms related to his/her Hematocrit (%) 40-52 38 underlying HIV infection (especially in the Mean corpuscular volume (fL) 80-98 91.8 setting of CD4 counts < 200 cells/mm3), oc- ular opportunistic infections (OOI) come to Red cell distribution width (%) 11.5-14.5 12.8 mind first. Despite a reduction in incidence of Platelets (per mm3) 130-450 327 75% to 80% in the HAART-era, CMV retini- Sodium (mmol/L) 135-145 140 tis remains the most common OOI in patients with AIDS and carries the greatest risk of oc- Potassium (mmol/L) 3.5-5.0 4.3 ular morbidity.2 In fact, based on enrollment Chloride (mmol/L) 100-110 101 data for the Longitudinal Study of the Ocu- Carbon dioxide (mmol/L) 20-30 29 lar Complications of AIDS (LSOCA), the prev- alence of CMV retinitis among patients with Urea nitrogen (mg/dL) 7-25 20 AIDS is more than 20-fold higher than all other Creatinine (mg/dL) 0.5-1.5 1.25 ocular complications of AIDS (OOIs and ocu- Glucose (mmol/L) 65-100 213 lar neoplastic disease), including Kaposi sar- coma, lymphoma, herpes zoster ophthalmicus, Albumin (g/dL) 3.2-5.0 3.6 ocular syphilis, ocular toxoplasma, necrotiz- Total protein (mg/dL) 6.0-8.5 7.1 ing herpetic retinitis, cryptococcal choroiditis, Alkaline phosphatase (U/L) 40-150 98 and pneumocystis choroiditis.3 Beyond ocu- lar opportunistic infections, the most common Aspartate aminotransferase (U/L) 5-34 24 retinal finding in HIV-positive people is HIV Alanine aminotransferase (U/L) 7-52 35 retinopathy, nonspecific microvascular findings Bilirubin, total (mg/dL) 0.2-1.2 0.2 in the retina affecting nearly 70% of those with advanced HIV disease. Fortunately, HIV reti- CD4 (cells/mm3) 410-1,590 730 4 nopathy is generally asymptomatic. HIV (copies/mL) Not detected < 20 Cytomegalovirus immunoglobulin G (IU/mL) Negative Positive Dr. Swamy. Thank you for those expla- nations. Based on Dr. Serrao’s differential, it Cytomegalovirus immunoglobulin M (AU/mL) Negative Negative is worth noting that this patient is MSM. He Antineutrophil cytoplasmic antibodies Negative Negative was evaluated in urgent care with the initial Angiotensin converting enzyme (U/L) 6-67 30 examination showing a temperature of 98.0° F, pulse 83 beats per minute, and blood pres- Rapid plasma reagin Nonreactive 1:32, Reactive sure 110/70 mm Hg. The eye exam showed Toxoplasma immunoglobulin G (IU/mL) Negative Negative no injection with normal extraocular move- ments. Initial laboratory data were notable Toxoplasma immunoglobulin M (AU/mL) Negative Negative for a CD4 count of 730 cells/mm3 with fewer Lyme antibody Not detected Positive than 20 HIV viral copies/mL. Cytomegalovi- Lyme immunoglobulin G Western blot Negative Negative rus immunoglobulin G (IgG) was positive, and immunoglobulin M (IgM) was negative. Lyme immunoglobulin M Negative Negative www.fedprac.com NOVEMBER 2017 • FEDERAL PRACTITIONER • 19 MEDICAL FORUM Table 2. Cerebrospinal Fluid Analysis evaluation. Dr. Butler, when should a generalist consider urgent ophthalmology referral? Tests Reference Result Turbidity Clear Clear Dr. Butler. In general, all patients with acute (and significant) vision loss should be Color Colorless Colorless referred immediately to an ophthalmologist. Nucleated cells (cells/cumm) 0-5 10 The challenge for the general practitioner is determining the true extent of the reported vi- Red blood cells (cells/cumm) 0-10 < 1,000 sion loss. If possible, some assessment of vi- Lymphocytes (%) 94 sual acuity should be obtained, testing each eye independently and with the correct glasses Mononucleocytes (%) 6 correction (ie, the patient’s distance glasses Protein (mg/dL) 15-45 30.9 if the test object is 12 feet or more from the patient or their reading glasses if the test ob- Glucose (mg/dL) 40-75 138 ject is held inside arm’s length). If the general Lactate dehydrogenase (U/L) < 25 33 practitioner does not have access to an eye chart or near card, any assessment of vision Lyme polymerase chain reaction Negative Negative with an appropriate description will be use- Venereal disease Nonreactive Nonreactive ful (eg, theROUND patient- can quickly count fingers at 15 feet TABLEin the unaffected eye, but the eye Cerebrospinal fluid fluorescent Nonreactive Reactive with reported vision loss cannot reliably treponemal antibody count fingers outside of 2 feet). Additional ocular symptoms associated with the vision A Lyme antibody was positive with nega- loss, such as pain, redness, photophobia, new tive IgM and IgG by Western blot. Additional flashes or floaters, increase the urgency of the tests can be seen in Tables 1 and 2. The pa- referral. The threshold for referral for any oc- tient has good immunologic and virologic ular complaint is lower compared with that of control. How does this change your thinking the general population for those with evidence about the case? of immunodeficiency, such as for this patient with HIV. Any CD4 count < 200 cells/mm3 Dr. Serrao. His CD4 count is well above should raise the practitioner’s concern for an 350, increasing the likelihood of a relatively ocular opportunistic infection, with the great- uncomplicated course and treatment.