HERPES ZOSTER OPHTHALMICUS

Herpes zoster ophthalmicus is an acute infection of
Gasserian ganglion of the fifth cranial nerve by the
varicella-zoster virus (VZV). It constitutes
approximately 10 percent of all cases of herpes zoster.
Etiology
Varicella -zoster virus. It is a DNA virus and produces
acidophilic intranuclear inclusion bodies. It is
neurotropic in nature.

Mode of infection. The infection is contracted in
childhood, which manifests as chickenpox and the
child develops immunity. The virus then remains
dormant in the sensory ganglion of trigeminal nerve.
It is thought that, usually in elderly people (can occur
at any age) with depressed cellular immunity, the virus
reactivates, replicates and travels down along one or
more of the branches of the ophthalmic division of
the fifth nerve.
Clinical features
In herpes zoster ophthalmicus, frontal nerve is
more frequently affected than the lacrimal and
nasociliary nerves.
About 50 percent cases of herpes zoster
ophthalmicus get ocular complications.
The Hutchinson's rule, which implies that ocular
involvement is frequent if the side or tip of nose
presents vesicles (cutaneous involvement of
nasociliary nerve), is useful but not infallible.
Lesions of herpes zoster are strictly limited to
one side of the midline of head.
Clinical phases of H. zoster ophthalmicus are :
i. Acute, which may totally resolve.
ii. Chronic, which may persist for years.
iii. Relapsing, where the acute or chronic lesions
reappear sometimes years later.
Clinical features of herpes zoster ophthalmicus
include general features, cutaneous lesions and
ocular lesions. In addition, there may be associated
other neurological complications as described below:
A. General features. The onset of illness is sudden
with fever, malaise and severe neuralgic pain along
the course of the affected nerve. The distribution of
pain is so characteristic of zoster that it usually
arouses suspicion of the nature of the disease before
appearance of vesicles.
B. Cutaneous lesions. Cutaneous lesions (Fig. 5.10)
in the area of distribution of the involved nerve appear
usually after 3-4 days of onset of the disease. To
begin with, the skin of lids and other affected areas
become red and oedematous (mimicking erysipelas),
followed by vesicle formation. In due course of time
vesicles are converted into pustules, which
subsequently burst to become crusting ulcers. When
crusts are shed, permanent pitted scars are left. The
active eruptive phase lasts for about 3 weeks. Main
symptom is severe neuralgic pain which usually
diminishes with the subsidence of eruptive phase;
but sometimes it may persist for years with little
diminution of intensity. There occurs some anaesthesia
of the affected skin which when associated with
continued post-herpetic neuralgia is called
anaesthesia dolorosa.
C. Ocular lesions. Ocular complications usually
appear at the subsidence of skin eruptions and may
present as a combination of two or more of the
following lesions:
1. Conjunctivitis is one of the most common
complication of herpes zoster. It may occur as
mucopurulent conjunctivitis with petechial
haemorrhages or acute follicular conjunctivitis with
regional lymphadenopathy. Sometimes, severe
necrotizing membranous inflammation may be seen.
2. Zoster keratitis occurs in 40 percent of all patients
and sometimes may precede the neuralgia or skin
lesions. It may occur in several forms, which in order
of chronological clinical occurrence are (Fig. 5.11) :
Fine or coarse punctate epithelial keratitis.
Microdendritic epithelial ulcers. These unlike
dendritic ulcers of herpes simplex are usually
peripheral and stellate rather than exactly dendritic
in shape. It contrast to Herpes simplex dendrites,
they have tapered ends which lack bulbs.
Nummular keratitis is seen in about one-third
number of total cases. It typically occurs as
multiple tiny granular deposits surrounded by a
halo of stromal haze.
Disciform keratitis occurs in about 50 percent of
cases and is always preceded by nummular keratitis.

Neuroparalytic ulceration may occur as a
sequelae of acute infection and Gasserian ganglion
destruction.
Exposure keratitis may supervene in some cases
due to associated facial palsy.
Mucous plaque keratitis develops in 5% of cases
between 3rd and 5th months characterised by
sudden development of elevated mucous plaque
with stain brilliantly with rose bengal.

3. Episcleritis and scleritis occur in about one-half
of the cases. These usually appear at the onset of the
rash but are frequently concealed by the overlying
conjunctivitis.
4. Iridocyclitis is of a frequent occurrence and may
or may not be associated with keratitis. There may be
associated hypopyon and hyphaema (acute
haemorrhagic uveitis).
5. Acute retinal necrosis may occurs in some cases.
6. Anterior segment necrosis and phthisis bulbi. It
may also result from zoster vasculitis and ischemia.
7. Secondary glaucoma. It may occur due to
trabeculitis in early stages and synechial angle
closure in late stages.

D. Associated neurological complications. Herpes
zoster ophthalmicus may also be associated with
other neurological complications such as :
1. Motor nerve palsies especially third, fourth, sixth
and seventh.
2. Optic neuritis occurs in about 1 percent of cases.
3. Encephalitis occurs rarely with severe infection.
Treatment
Therapeutic approach to herpes zoster ophthalmicus
should be vigorous and aimed at preventing severe
devastating ocular complications and promoting rapid
healing of the skin lesions without the formation of
massive crusts which result in scarring of the nerves
and postherpetic neuralgia. The following regime may
be followed:
I. Systemic therapy for herpes zoster
1. Oral antiviral drugs. These significantly decrease
pain, curtail vesiculation, stop viral progression
and reduce the incidence as well as severity of
keratitis and iritis. In order to be effective, the
treatment should be started immediately after the
onset of rash. It has no effect on post herpetic
neuralgia.
Acyclovir in a dose of 800 mg 5 times a day
for 10 days, or
Valaciclovir in a dose of 500mg TDS
2. Analgesics. Pain during the first 2 weeks of an
attack is very severe and should be treated by
analgesics such as combination of mephenamic
acid and paracetamol or pentazocin or even
pethidine (when very severe).
3. Systemic steroids. They appear to inhibit
development of post-herpetic neuralgia when
given in high doses. However, the risk of high
doses of steroids in elderly should always be
taken into consideration. Steroids are commonly
recommended in cases developing neurological
complications such as third nerve palsy and
optic neuritis.
4. Cimetidine in a dose of 300 mg QID for 2-3 weeks
starting within 48-72 hours of onset has also
been shown to reduce pain and pruritis in acute
zoster - presumably by histamine blockade.
5. Amitriptyline should be used to relieve the
accompanying depression in acute phase.

II. Local therapy for skin lesions
1. Antibiotic-corticosteroid skin ointment or lotions.
These should be used three times a day till skin
lesions heal.
2. No calamine lotion. Cool zinc calamine
application, as advocated earlier, is better avoided,
as it promotes crust formation.
III. Local therapy for ocular lesions
1. For zoster keratitis, iridocyctitis and scleritis
i. Topical steroid eye drops 4 times a day.
ii. Cycloplegics such as cyclopentolate eyedrops
BD or atropine eye ointment OD.
iii. Topical acyclovir 3 percent eye ointment
should be instilled 5 times a day for about 2
weeks.
2. To prevent secondary infections topical antibiotics
are used.
3. For secondary glaucoma
i. 0.5 percent timolol or 0.5% betaxolol drops BD.
ii. Acetazolamide 250 mg QID.
4. For neuroparalytic corneal ulcer caused by
herpes zoster, lateral tarsorrhaphy should be
performed.
5. For persistent epithelial defects use :
i. Lubricating artificial tear drops, and
ii. Bandage soft contact lens.
6. Keratoplasty. It may be required for visual
rehabilitation of zoster-patients with dense
scarring. However, these are poor risk patients.