|Year : 2021 | Volume
| Issue : 4 | Page : 674
Commentary: Post-fever retinitis and inflammatory angiogenesis
Srinivasan Sanjay, Ankush Kawali, Padmamalini Mahendradas
Department of Uvea and Ocular Immunology, Narayana Nethralaya Super Speciality Hospital and Post-Graduate Institute of Ophthalmology, Bangalore, Karnataka, India
|Date of Web Publication||09-Oct-2021|
Department of Uvea and Ocular Immunology, Narayana Nethralaya Super Speciality Hospital and Post-Graduate Institute of Ophthalmology, Bangalore, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Sanjay S, Kawali A, Mahendradas P. Commentary: Post-fever retinitis and inflammatory angiogenesis. Indian J Ophthalmol Case Rep 2021;1:674
Ocular manifestations in typhoid or enteric fever are varied and profound and can lead to visual impairment.,
WIDAL test dilution and blood culture will add more value to this case report. Toxoplasma is a differential diagnosis to consider in lieu of full-thickness retinal involvement with epiretinal membrane formation.
The role of Salmonella More Details typhi bacilli or immune-mediated reaction causing ocular manifestations is a matter of debate. There is a possible role of molecular mimicry inducing autoimmunity is being considered.
Our experience with post typhoid immune-mediated ocular manifestations include vitritis, multifocal retinitis, retinal vasculitis, choroidal neovascular membrane, neuroretinitis, retinal detachment and optic atrophy.,
Retinal neovascularization (NVE) is a rare complication of post fever immune-mediated retinitis.,
In their case, the authors have described a combined NVE and a choroidal neovascular membrane (CNVM). Fundus fluorescein angiography of the retinal periphery is of paramount importance to determine capillary nonperfusion areas in these cases. If available, optical coherence tomography angiography is a useful tool to monitor the NVE and CNVM before and after treatment.
Multiple optical coherence tomography (OCT) scans across retinitis, and CNVM as a composite image will add value in differentiating the features.
NVE in uveitis is seen only in a small proportion, occurs in those with active posterior uveitis (especially retinal vasculitis), a younger age group, those with uveitis (1–5 years duration) and bilateral inflammation. Patel et al. also observed that even though the inflammation was controlled the presence of pro-angiogenic molecules could last in the eye for much longer time.
During inflammation cytokines like IL-1β and TNF-α which cause capillary loss could also promote endothelial proliferation and pathologic angiogenesis. Other cytokines like IL-6 and IL-8 and TNF-α are upregulated in ocular inflammation-causing NVE.
Presence of CNVM may be partly driven by an inflammatory process. Vitreous findings in this case may be useful, although CNVM with posterior uveitis may have no vitreous activity or haze. There is uncertainty as to the role of vitreous cells and haze relating to risk of CNVM as they are two distinct entities.
Dhingra et al. identified leukocytes and chronic chorioretinal inflammation as being critical for the development of CNVM. They postulate the role of activated macrophages and other inflammatory mediators damage retinal pigment epithelium (RPE) and destroy Bruch's membrane. The cytokines released by these inflammatory cells may promote the growth of CNVM through the break in Bruch's membrane and into the sub-RPE space, potentially leading to edema, exudation, hemorrhages, and fibrosis which result in CNVM.
Baxter et al. studied the risk of CNVM in uveitis patients. They found that posterior uveitis was more likely than panuveitis to cause CNVM. The diseases like multifocal choroiditis and panuveitis affecting RPE and choroid were more likely to present with CNVM. Eyes with active inflammation, unilateral involvement, contralateral eye with CNVM previously were more likely to develop CNVM.
An interesting observation in their series was that eyes diagnosed with pre-retinal neovascularization (simultaneous with or before the diagnosis of CNV) had an over three-fold higher risk of developing CNVM.
As in the case report, treatment with steroids consolidation of CNVM occurred, revealing their role in inhibition of pro-angiogenic factors with a decrease in vascular permeability. It would have been interesting to see the effect of Anti VEGF if the patient had not declined. There may be a role for scatter photocoagulation of ischemic retina.
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