Acta Ophthalmologica 2016
However, their patient was also on
Letter to the Editor
Acute retinal necrosis and
ocular neovascularization
caused by cytomegalovirus
following intravitreal
dexamethasone implant
(Ozurdexâ) in an
immunocompetent patient
Alexander S. Thrane,1 Morten Hove,1
ard Kjersem1 and Jørgen Krohn1,2
B
1 vision. On examination, he was found
Department of Ophthalmology,
Haukeland University Hospital, Bergen,
Norway; 2Department of Clinical
Medicine, University of Bergen, Bergen,
Norway
doi: 10.1111/aos.13131
Editor,
O cular cytomegalovirus (CMV)
infection usually manifests as a
haemorrhagic retinitis in severely
immunocompromised patients. Previ-
ous reports have highlighted that other-
wise immunocompetent patients can
develop CMV or other types of viral
retinitis in the context of subtenonial or
intravitreal triamcinolone (Shah et al.
2010; Takakura et al. 2014). Recently,
Vannozzi et al. (2016) reported a case of
CMV retinitis following the use of a
dexamethasone implant (Ozurdex;
Allergan Inc., Irvine, CA, USA).
(A)
Fig. 1. (A) Fundus photograph of the right eye 1 month after onset of the cytomegalovirus infection, showing peripheral granular hyperpigmen-
tation. Dense vitritis and a small unresponsive pupil prevented photodocumentation of the peripheral lesions in the acute phase. (B) Ultra-widefield
angle fluorescein angiography (mid-venous phase) taken 1 month after onset of the infection, showing extensive peripheral non-perfusion and
blocking from peripheral granular pigmentation. (C) Gonioscopic photograph taken 3 months after presentation, showing florid iris and angle
neovascularisation.
fluorescein angiography (Spectralis;
systemic immunosuppression with
mycophenolate mofetil. The autho-
rs speculated whether the systemic
immunosuppression and/or central reti-
nal vein occlusion in this patient might
have contributed to the development of
CMV retinitis.
Here, we report a case of ocular
CMV infection in a 67-year-old
immunocompetent patient receiving
Ozurdex implants every 3–4 months
for 4 years for a chronic, bilateral
idiopathic panuveitis. Approximately
two weeks after administration of the
14th dexamethasone implant in his right
eye, the patient complained of redness,
photophobia, floaters and diminished
to have granulomatous keratic precipi-
tates, 3 + cells and flare in the anterior
chamber, iris haemorrhages, 2 + cells
in the vitreous, occlusive retinal vasculi-
tis and peripheral yellow-white areas of
retinal necrosis in 360o. Vitreous sam-
ples were taken, and intravenous acy-
clovir therapy was initiated for a
suspected herpes simplex or varicella-
zoster-related acute retinal necrosis
(ARN). However, quantitative poly-
merase chain reaction revealed
139 000 CMV units per ml, as well as
a small amount of Epstein–Barr virus
(EBV) DNA. Serology was CMV and
EBV IgG positive and IgM negative.
Therapy was changed to intravenous
ganciclovir, followed by oral valganci-
clovir, and the patient’s condition grad-
ually improved over the next weeks.
Eventually, granular hyperpigmenta-
tion occurred in the affected retina
(Fig. 1A). Ultra-widefield angle
(B)
Heidelberg Engineering, Heidelberg,
Germany) revealed extensive peripheral
retinal non-perfusion (Fig. 1B), likely
as a result of his occlusive CMV-related
retinal vasculitis. Panretinal photoco-
agulation was subsequently performed.
Three months after the onset of the
CMV infection, the patient was found
to have florid iris and angle neovascu-
larisation (rubeosis) (Fig. 1C), and a
localized superotemporal peripheral
retinal detachment. The latter was
treated conservatively, with laser reti-
nopexi. The visual prognosis for this
patient remains uncertain. Prior to the
CMV infection, he had a Snellen best-
corrected visual acuity of 0.8 in his right
eye, upon diagnosis it had dropped to
0.2, and after 4 months follow-up, the
visual acuity remained at 0.2. He also
had a concentric scotoma and persistent
ocular hypotony, likely as a result of
viral damage to the ciliary body.
Our case raises three important
issues. Firstly, ocular CMV infections
can have an atypical course in
immunocompetent patients and cause
a greater degree of anterior segment
inflammation with haemorrhagic iritis
and ciliary body damage, occlusive
retinal vasculitis and peripheral retinal
necrosis similar to ARN (Babiuch
et al. 2010; Pathanapitoon et al. 2013;
Schneider et al. 2013; Tyagi et al.
2015). Secondly, viral retinitis may
represent an underreported and/or
unrecognised risk of Ozurdex adminis-
tration. To our knowledge, there are
only four reports, including our
own, of viral retinitis following Ozur-
dex treatment (Ozturk et al. 2014;
(C)
1
Acta Ophthalmologica 2016
Kucukevcilioglu et al. 2015; Vannozzi
et al. 2016). Conversely, intravitreal
triamcinolone has been associated with
a 0.41% incidence of viral retinitis in
large systematic case series (Shah et al.
2010). Thirdly, the protracted course of
CMV retinitis in the context of local
corticosteroid treatment may cause
more widespread vascular damage and
increase the risk of ischaemia-induced
ocular neovascularisation, as was seen
in both our case and that reported by
Vanozzi et al. (2016) These patients
might therefore benefit from early pho-
tocoagulation if widefield angle angiog-
raphy reveals large ischaemic areas.
References
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Correspondence:
Alexander S. Thrane
Department of Ophthalmology
Haukeland University Hospital
Bergen N-5021, Norway
Tel: +47 55974130
Fax: +47 55974113
Email: alexander.thrane@gmail.com