Herpes zoster ophthalmicus
BMJ 2009; 339 doi: https://doi.org/10.1136/bmj.b2624 (Published 13 August 2009) Cite this as: BMJ 2009;339:b2624All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
Lam et al[1] provide an excellent overview of ophthalmic varicella
virus (VZV) reactivation presentation and management. Although VZV rarely
manifests as progressive outer retinal necrosis (PORN), usually in immune
suppressed patients, PORN can occur in apparently immune competent
patients,[2, 3] with the outcome in most a visual acuity of no light
perception.
In contrast to the relatively older patients Lam et al[1] describe
(>50 year olds), PORN tends to occur in younger patients, often
associated with a rash. Rapidly progressive unilateral or bilateral visual
loss (to no light perception within days to weeks) may be associated with
or progress to optic neuritis,[4] retinal detachment, vitreous haemorrhage
and meningoencephalitis. It is most often seen in HIV positive patients
but also in those with haematological malignancies, organ or bone marrow
transplant, steroid therapy,[3, 4] anti-TNF therapy,[3] rituximab therapy,
lupus, rheumatoid arthritis[3]and nephrotic syndrome.
Management approaches include combinations of oral, intravenous and
intravitreal therapy.[2-5] Agents include highly active antiretroviral
therapy, valganciclovir, bromovinyldeoxyuridine, aciclovir, ganciclovir,
foscarnet and gammaglobulin (IVIg). Multiple surgical procedures are often
required, mainly for treating complications, including vitrectomy with
silicone oil tamponade, retinopexy, optic nerve fenestration, laser
photocoagulation and ganciclovir implant. However, profound visual
disability usually persists.
References
[1] Lam FC, Law A, Wykes W. Herpes zoster ophthalmicus. BMJ.
2009;339:b2624.
[2] Carrillo-Pacheco S, Vazquez-Marouschek MC, Lopez-Checa F, Sanchez
-Roman J. Progressive outer retinal necrosis in an immunocompetent
patient. Acta Ophthalmol Scand. 1996;74:506-8.
[3] Benz MS, Glaser JS, Davis JL. Progressive outer retinal necrosis
in immunocompetent patients treated initially for optic neuropathy with
systemic corticosteroids. Am J Ophthalmol. 2003;135:551-3.
[4] Nakamoto BK, Dorotheo EU, Biousse V, Tang RA, Schiffman JS,
Newman NJ. Progressive outer retinal necrosis presenting with isolated
optic neuropathy. Neurology. 2004;63:2423-5.
[5] Pérez-Blázquez E, Traspas R, Méndez Marín I, Montero M.
Intravitreal ganciclovir treatment in progressive outer retinal necrosis.
Am J Ophthalmol. 1997;124:418-21.
Competing interests:
None declared
Competing interests: No competing interests
Herpes zoster opthalmicus: Don’t forget HIV!
I read with great interest Lam and colleague’s 10-minute consultation
on Herpes zoster opthalmicus.1 However they failed to include a very
important point concerning possible HIV infection under the sub heading of
“what to do next”.
Herpes zoster is well recognised in persons aged over 60 years and is
commonly associated with malignancies, especially Hodgkin’s lymphoma.
However, Herpes zoster may also occur at any stage of HIV infection and
may be the first clinical presentation of undiagnosed HIV. Buchbinder and
colleagues reported that Herpes zoster was significantly higher among HIV
positive men (29.4 case/1000 person-year) than among HIV-seronegative men
(2.0 cases/1000 persons-year) 2. The risk of developing Herpes zoster was
not associated with duration of HIV infection or with rapid progression to
AIDS.
HIV infection should be always considered in patients with Herpes zoster
aged less than 65 years and since late presentation of HIV is a major
problem, awareness that Herpes zoster infection may be associated with
HIV will help to reduce the incidence of late presenters . 3
References:
1. Lam FC, Law A, Wykes W. Herpes zoster ophthalmicus. BMJ 2009;
339:457-8
2. Buchbinder SP, Katz MH, Hessol NA, Liu JY, O’Malley PM, Underwood
R, Holmberg SD. Herpes zoster and Human immunodeficiency virus infection.
JID 1992:166:1153-6
3. Sethupathi M, Miles S, Yoganathan K, Danino S. Late presenters
with HIV infection at a District General Hospital. D-39, 154. BASHH –
ASTDA conference, May 7 – 10, 2008, New York, USA.
Competing interests:
None declared
Competing interests: No competing interests
Herpes zoster ophthalmicus
Pictures of current Herpes Zoster Ophthalmicus should no longer
appear.
In my practice, since 1954, the very effective treatment of Herpes Zoster
Ophthalmicus and all cases of Herpes Zoster, has been with daily (2,500
micrograms) intramuscular injections of Vitamin B.12. (Cyanocobalamin).
This practice is shared by some Eye Specialists.
Yet it is not generally known.
This treatment was long before the expensive anti-virals, the
Cyclovirs, came on the market.
To warrant these injections it is sufficient to notice just one and a half
vesicles, with some pain, in the distribution of the Ophthalmic Division
of the Fifth Cranial Nerve.
Failure to notice and to treat early will lead to the pictures illustrated
and may indeed cause blindness.
This should not be.
No dilly-dallying.
Injection first and then referral same day to the Eye Specialist.
As a young doctor just entering General Practice in Yorkshire I visited a patient who was recovering from just this
lesion. Too late unfortunately to save his sight. He was 100% blind in
the eye opposite to the lesion, on which side he was 90% blind. Here is
the only site in the body where "Shingles" crosses to the other side.
We learned about Vitamin B.12 after this case.
There then should be no further cases of Post Herpetic Neuralgia. No
need again to hear that some doctor has casually remarked "It is
Shingles! There is no treatment. Take Panadol. Good Morning!" Which has
very often been the case, leaving the patient with permanent pain for the
remainder of their lives. Apart from B.12 injections there are many
helpful and comforting suggestions to ease the discomfort.
Vitamin B.12 you see restores the lost Myelin fatty insulation on the
damaged nerve fibres and so the lesions quickly disappear, even without
the modern Cyclovirs.
Treatment at the onset is imperative. No good three months later.
B.12 indeed might help at the onset of the many other Demyelination
Syndromes.
See a letter in the British Medical Journal of 15th June 1946 by Drs.
W. H. Marshall and Hugh Dickie. Hugh Dickie noted the effect of Liver
Extract injection while serving as a Medical Officer in Prisoner of War
camp in Germany, in 1944. Many other doctors all round the world, from
South Africa, India, Finland and Poland and USA, wrote and agreed that
Liver Extract or Vitamin B.12 worked equally well on their cases.
Competing interests:
None declared
Competing interests: No competing interests