Findings were confirmed by spectral domain optical coherence tomography (OCT; Carl Zeiss Meditec, Dublin, CA), which showed retinal pigment elevation with thinning and disruption of the ellipsoid layer in the right eye (Figure 2), and normal foveal architecture in the left eye. Fundus photography, red-free, autofluorescence, and intravenous fluorescein angiography (IVFA; Kowa, Aichi, Japan) was performed, showing a leading edge of increased autofluorescence with initial blockage followed by late staining (Figures 3 and 4). She was started on 50 mg oral prednisone. A thorough laboratory workup, including Lyme, rapid plasma reagin (RPR), fluorescent treponemal antibody absorption (FTA-ABS), antinuclear antibody (ANA), angiotensin-converting enzyme (ACE), lysozyme, and antineutrophil cytoplasmic antibodies c-Antineutrophil Cytoplasmic Antibodies (ANCA) and p-ANCA, was negative. Her complete blood count was normal with a white cell count of 10.9, a hemoglobin level of 13.7, and hematocrit of 40.6. Her comprehensive metabolic panel including liver function tests was normal. Her creatinine was 0.6. A thorough laboratory workup was ordered and was negative except for five bands of immunoglobulin G (IgG) for Lyme and two bands of immunoglobulin M (IgM) for Lyme [4, 5]. The patient admitted to recently traveling to Maine, known for its high rate of Lyme disease according to the Centers for Disease Control and Prevention (CDC), and hiking extensively, but without a known tick bite. The infectious disease service was consulted and confirmed the diagnosis of suspected active Lyme disease. The patient was admitted to the hospital and received intravenous ceftriaxone 2 g twice daily for 4 weeks. At admission, her blood pressure was 106/69 mmHg, pulse 70 beats/minute, and temperature 97.4 F. At the end of February 2019, her visual acuity improved to 20/40 and prednisone was decreased to 40 mg. In March 2019, her prednisone was decreased to 30 mg and she completed 4 weeks of ceftriaxone. Her prednisone was further tapered, to 20 mg for 2 weeks, then 10 mg for 1 week, then 10 mg every other day for 1 week, then stopped. In June 2019, her vision returned to 20/20. At that visit, a new lesion was noted in the left eye (Figure 5). Optical coherence tomography angiography (OCTA) (Figure 6) and IVFA (Figure 7) revealed a hypoperfused outer retinal lesion in that area. She was restarted on 50 mg oral prednisone for 3 days with a taper by 10 mg every 3 days. Repeat Lyme testing was conducted, showing three positive IgG bands and two positive IgM bands. After repeat consultation with the infectious disease service, the patient was started on 100 mg oral doxycycline twice daily. In August 2019, after finishing her doxycycline and tapering off her prednisone, she was noted to have progression of the subretinal lesion in the left eye and decline in vision. She was restarted on 50 mg oral prednisone and sent to rheumatology for consideration of steroid-sparing immunosuppression. Figure 8 shows the progression of the OCTA, at the level of the choriocapillaris, over this period. The patient then received a dexamethasone intravitreal implant 0.7 mg (Ozurdex, Allergan, NJ) toward the end of August 2019 and was kept on high-dose prednisone (increased to 60 mg). Azithromycin 500 mg oral daily was also added, and doxycycline 100 mg oral twice daily was restarted. Rheumatology started the patient on adalimumab (Humira, Abbvie, IL) in September 2019, and then steroids were slowly tapered (by 5 mg every week). Repeat Lyme titers revealed four positive IgG bands and two positive IgM bands. She finished her azithromycin course in November 2019. In December 2019, she finished her prednisone taper, and in January 2020, she was taken off doxycycline and kept on adalimumab only. There has been no further recurrence of her findings or of her symptoms, and her vision remained between 20/20 and 20/25 for over a year. Figure 9 shows a timeline of her visual acuity since presentation (no known prior visual acuities but reportedly normal).
posterior eye disease and glaucoma a-z pdf free
Lyme disease is a tick-borne disease most commonly caused by the spirochete Borrelia burgdorferi. Eye involvement is rare, affecting less than 1% of Lyme cases and representing about 1% of all cases of uveitis [1]. The seroprevalence of B. burgdorferi among a large case series of uveitis patients from France was 7.9%, similar to the general population, the majority of whom had other etiologies to explain their uveitis, with only 1.6% found to be true Lyme uveitis cases (with history of tick bites and resistance to steroid-only treatment). Another large case series reported a rate of 4.4% [6]. For these reasons, it is not advised to screen all uveitis patients for Lyme disease as the seropositivity can be incidental. Of important note, IgM and IgG may persist for years without reactivation of borreliosis [7]. Lyme-associated uveitis has a very varied presentation: from anterior, to intermediate, to posterior uveitis [8]. It can be unilateral or bilateral, granulomatous or not, and with or without vasculitis. The main common feature is a history or risk of possible exposure to Lyme and extraophthalmic manifestations. The principal symptom is decreased vision in Lyme uveitis patients.
The main difference between the vitreous humor and the aqueous humor is that there is a set amount of the vitreous humor in your eye, and it does not move freely about between the two chambers. It remains in the posterior chamber.
A: The JVN system can identify most clinically evident eye diseases visible within the imaging fields used for evaluating diabetic retinopathy. This covers a wide range of diseases including macular degeneration, glaucoma, hypertensive retinopathy, and many other diseases with clinical finding in the posterior ocular fundus. 2ff7e9595c
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