VZV affects patients both young and old. Here’s how to manage the associated ocular complications.
Goal Statement:
Despite the relatively recent advent of multiple vaccines for both
chickenpox and shingles, the overall incidence of herpes zoster is on
the rise. This article will review the ocular complications associated
with varicella zoster virus (VZV) in both children and adults, as well
as discuss potential treatment options for shingles and postherpetic
neuralgia.
Faculty/Editorial Board:
William Marcolini, OD
Credit Statement:
This course is COPE approved for 2 hours of CE credit. COPE ID
36847-AS. Check with your local state licensing board to see if this
counts toward your CE requirements for relicensure.
Joint-Sponsorship Statement:
This continuing education course is joint-sponsored by the Pennsylvania College of Optometry.
Disclosure Statement:
Dr. Marcolini has no relationships to disclose.
As primary care optometrists, we often see pediatric
patients with chickenpox
or older individuals with
herpes zoster--commonly known
as shingles. Despite the relatively
recent advent of multiple vaccines
for both chickenpox and shingles,
the overall incidence of herpes zoster is on the rise.1
In an effort to provide the best
possible care, this article will
review the ocular complications
associated with varicella zoster
virus (VZV) in both children and
adults, as well as discuss potential
treatment options for shingles and
postherpetic neuralgia.
Chickenpox
Upon primary infection, VZV
causes the development of chickenpox in children and young teenagers. Most children become infected
with VZV between the ages of
five and 10 years.2 Typically, this
initial infection--coupled with
intermittent environmental exposure--provides the patient with a
lifetime of immunity against the
recurrence of chickenpox.2
VZV is one of eight strains of
herpes viruses known to infect
humans. Most often, the primary
infection persists for two weeks
and causes vesicular, macular and
papular eruptions on the face and
trunk that crust over within a few
weeks. Fever and general malaise
are the most common symptoms,
with the potential for long-term
cutaneous scarring.
Although the course of chickenpox is usually benign, there
are exceptions. In fact, associated
cases of pneumonia, encephalitis
and even death have been reported
in the literature.2
VZV is highly contagious. In
the past, parents have hosted "pox
parties" in an effort to expose
their kids to other infected children. This would ensure simultaneous infection throughout the
household and confer immunity
going forward.
Shingles
Shingles manifest following the
reactivation of latent VZV during
adulthood. The Centers for Disease
Control and Prevention (CDC)
estimates that 500,000 to one million cases of shingles are reported
each year. Shingles typically present with a characteristic rash that
respects the midline. Typically, this
rash is found in the lower thoracic
region, but also may be located on
the scalp, forehead and periorbital
structures.
Both chickenpox and shingles are caused by VZV. A child is first
infected when the virus enters the
respiratory mucosa or the conjunctiva. After the initial varicella
infection, the virus becomes dormant. Subsequent reactivation is
predicated on certain triggers. Such
triggers are heavily influenced by
the condition of the host, and are
believed to include the presence of
an immunocompromising condition, use of immunosuppressive
medications or long-standing emotional stress.2,3
During the latency period, the
virus remains in the dorsal root
ganglia. The dorsal root ganglia
are located throughout the body
and along the spinal cord, and
are part of the afferent sensory
system. This explains how the
virus can travel via axonal transport to the skin or mucous membranes. As optometrists, we are
most concerned with eruptions
along the trigeminal dermatome.
However, just 13% to 20% of all
cases involve one of the 12 cranial
nerves, including the trigeminal
(CN V).3
The primary clinical trial for the
herpes zoster vaccine Zostavax
(live zoster virus, Merck) included
more than 38,000 adults aged 60
to 80 years who had previous history of shingles.4 Subjects who
were treated with Zostavax were
51% less likely to develop shingles
and 66% less likely to experience
postherpetic neuralgia.4 Further,
patients who still developed shingles following treatment with Zostavax exhibited less severe signs
and symptoms.4 The researchers
also determined that the efficacy of
Zostavax declined proportionately
with advanced age.
Another study of 22,000
adults aged 50 through 59 years
showed that the risk of shingles
was reduced by 69.8% following
the administration of Zostavax.2 Although the FDA approved Zostavax for individuals age 50 years
and older in March 2011, CDC
officials recommended that the
vaccine only be used in patients
60 years and older.2 This recommendation likely is explained, in
part, by lingering concerns about
vaccine supply and a lower overall
risk of herpes zoster in the 50 to
59 years of age cohort.
Ocular Manifestations of Chickenpox
Eighty-five percent of chickenpox infections occur before age 15.2 Optometrists with significant
pediatric populations will see a
larger volume of ocular complications. Vesicular eruptions can
occur externally, along the periorbital skin around the eyelids. The
eyelids often become infected, and
scarring and/or pockmarks may
result. Further, the conjunctiva can
be infected by vesicles as well as a
non-specific papillary conjunctivitis.
Most significantly, the cornea
can be scarred by vesicular eruption.5 Similar to the dendritic
appearance caused by herpes simplex virus (HSV) keratitis, active
varicella can invade the cornea
and cause punctate or dendritic
keratitis (see "How to Differentiate Herpes Simplex from Varicella
Zoster," above).5
An immune-mediated disciform
keratitis, with or without uveitis,
may be documented.5 Cases of
cranial nerve palsies, retinopathy
and optic neuropathy also have
been reported. Carefully examine
each ocular structure--from the
cornea to the retina--in all pediatric patients who present with
chickenpox.
Ocular Manifestations of Shingles
In most instances, herpes zoster
patients who present to my office
have already been diagnosed with
active shingles. Occasionally, the
patient exhibits the characteristic
unilateral, dermatomal rash on the
forehead, periorbital region and
nose. If the rash is present on the
nose, the virus has spread sufficiently enough along the V1 nasociliary branch of the trigeminal
nerve. This presentation, known
as Hutchinson's sign, indicates a
high probability of ophthalmic
involvement.5 It must be noted that the absence of Hutchinson's sign
should in no way be reassuring, as
significant ocular involvement is
often seen without frank evidence
of this indicator.
Because the outbreak occurs
along the trigeminal dermatome,
the rash respects the midline and
manifests on only one side of the
patient's face or scalp.5
Whether you make the initial
diagnosis or participate in a consult, your clinical responsibilities
are the same. The eye must be
inspected from cornea to retina,
with a special emphasis on intraoc-ular pressure. The goal is to arrest
viral replication, control inflammation, prevent scarring and educate
the patient about the possibility of
postherpetic neuralgia.
* Symptoms. Shingles presents
with prodromal symptoms a few
days before the onset of a macular
rash, which rapidly progresses to
papular and vesicular eruptions
within 24 hours.5 The prodromal
symptoms include pain, redness,
hypesthesia, fever, malaise and
headache.5 While these symptoms
can be associated with a host of
diseases, it is the characteristic
rash and respect of the midline
that makes the diagnosis straightforward. Occasionally, an immunologic test from vesicular fluid or
a serologic workup that reveals a
high IgM titer against VZV is necessary to confirm a confusing case.
Inform the patient that the rash
usually continues to develop and
proliferate for three to four days.
The acute phase often lasts two
weeks or more, until the rash
crusts over.5 Acute pain tends to
lessen during the course of the disease; however, pain may persist in
the affected dermatome for months
to years--a condition known as
postherpetic neuralgia.6
* Pertinent anatomy. Typically,
shingles reactivation occurs in
the thoracic region. Less commonly, it may affect the trigeminal
nerve. Herpes zoster ophthalmicus
(HZO) is defined as a reactivation
of VZV that originates from the
trigeminal ganglion and includes
ocular involvement. The trigeminal
nerve provides both sensory and
motor functions. It is primarily
responsible for facial sensation.
The trigeminal nerve has three
main branches: the V1 ophthalmic
branch (sensory), the V2 maxillary
branch (sensory) and the V3 mandibular branch (motor for chewing). The V1 ophthalmic relays
sensory information from the
scalp, forehead, eyelids, periorbital
skin, nose and, most importantly,
the cornea and conjunctiva.
The V1 branch is further divided
into the frontal, nasociliary and
lacrimal nerves. The frontal nerve
is most commonly affected by
VZV reactivation, which is why
shingles often appears on the
forehead. The nasociliary branch
innervates the skin of both eyelids
as well as the tip of the nose, conjunctiva, sclera, cornea, iris and
choroid.5
Considering the extensive nerve
involvement, it becomes increasingly evident that the virus easily
can spread to any nearby ophthalmic component. That's why I
examine herpes zoster patients in a
similar fashion as victims of blunt
force trauma--from the adnexa to
optic nerve.
When the forehead and scalp
are affected (indicative of frontal
nerve involvement), the upper eyelid may exhibit vesicles and edema.
These symptoms often resolve
without sequelae; however, if
scarring results, lid retraction and
exposure may develop.6 Associated
conjunctivitis can be follicular or
necrotizing, and may occasionally yield conjunctival vesicles and
potential scarring.6 Also, the sclera
can be involved with a scleritis or
an episclerits.
* Herpes zoster ophthalmicus.
Approximately two-thirds of HZO
cases have corneal involvement.7 All layers of the cornea potentially
can be infected--from the epithelium to the endothelium. Further,
corneal involvement can occur
during the acute event or years
after the infection has subsided.7
The epithelial dendrite present in HZO often is termed a
"pseudodendrite." The pseudodendrite may begin as clusters of
swollen epithelial cells that are
infected with live zoster virus.
At this stage, the inflamed lesion
commonly is referred to as punctate epithelial keratopathy. Over
time, the lesion resolves, develops
anterior stromal infiltrates, or
coalesces to form into a dendritiform pattern.6 In most instances,
though, these lesions tend to
resolve spontaneously over weeks
without topical treatment.
A neurotrophic keratitis can
be seen in patients who have corneal nerve damage. Because of
decreased innervation and sensation, the cornea can develop a
non-healing neurotrophic ulcer
that is neither infectious nor
inflammatory, and therefore must
be managed differently. In general,
patients with HZO are more likely
to experience severely reduced
corneal sensitivity than those with
HSV keratitis.6 During evaluation, test corneal sensitivity with a
simple cotton wisp to detect areas
of denervation.
Stromal disease represents an
immune reaction to retained viral
antigen in the corneal epithelium,
and is not a sign of active HZO.
Nonetheless, resultant inflammation can yield devastating visual
consequences. This immune reaction can occur within three to four
months following the reactivation of varicella, or it may present
several years later.6,7 So, you may
think of HZO as a reactivation of
VZV, and stromal disease as a subsequent immune response to the
reactivation.
HZO can cause anterior uveitis,
iris atrophy, choroiditis, retinitis,
optic neuritis and even acute retinal necrosis.6,7 A dilated fundus
examination is of paramount
importance in any suspected case
of HZO. Be certain to investigate
for inflammatory lesions or necrosis in the retina as well as optic
nerve edema.
Additionally, it is essential to
inspect the anterior chamber for
the presence of cells and flare,
because significant iridocyclitis can
develop. Iridocyclitis usually presents within the first week of herpes
zoster infection, but can be seen
months after.6
HZO is notorious for causing
chronic complications associated
with recurrent inflammation,
including increased intraocular
pressure and/or trabeculitis.8 Such persistent inflammation is
believed to be caused by the presence of inactivated viral antigens
in the eye or ongoing low-grade
viral replication.8-10
Treatment for Shingles
Primary treatment for active
herpes zoster should be aimed at
curtailing viral replication, minimizing inflammation, preventing
secondary infection and limiting
the potential for future postherpetic neuralgia. Ultimately, the
location and the extent of ocular
involvement will drive your treatment regimen.
* Oral antiviral therapy is a
mainstay treatment for HZO, and
should be initiated within the first
72 hours following diagnosis of
herpes zoster.6 This accelerates
resolution of the skin rash and
lesions, shortens the period of
lesion formation and viral shedding, and reduces the incidence
of episcleritis, keratitis and iritis.6 Oral antiviral agents also appear
to limit, but not prevent, the symptoms of postherpetic neuralgia. For
patients who have scalp involvement or ocular complications that
are limited to the eyelids, prescribe
one of the following systemic treatment regimens:
- 800mg acyclovir five times a day for seven to 10 days.
- 1,000mg valacyclovir TID for seven days.
- 500mg famciclovir QD for seven days.
* Systemic corticosteroids, such
as oral prednisone, are a useful adjunct to antiviral agents in
patients who have moderate to
severe pain. Patients on combination systemic steroids/antiviral therapy have been shown to experience
shorter healing times and decreased
pain during the acute infection
period.6 But remember, immunocompromised patients are at risk
for disseminated disease and should
not be placed on systemic steroids.
Additionally, posterior uveitis
and/or acute retinal necrosis must
be managed aggressively with a
combination of intravenous/oral
antivirals and systemic steroids.
These patients require immediate
referral to a retina specialist for
proper management.
* Topical agents in conjunction with oral antiviral therapy
may be necessary if a herpes zoster patient exhibits conjunctival
or corneal involvement, or develops a keratouveitis. However,
because patient circumstances
vary and viral response is not
always predictable, there is no
consensus on the clinical utility
of topical treatment.
In the presence of conjunctival
lesions, conjunctivitis or a corneal
pseudodendrite, antibiotic ointments, such as erythromycin or
bacitracin, may be used TID. In the
past, antiviral ointments, such as
Vira-A (vidarabine, Monarch Pharmaceuticals) QID, sometimes were
used. (Vira-A ointment is no longer available in the US and has no
generic equivalent.) Viroptic (trifluridine, Monarch Pharmaceuticals) also has been used in the past, but
was not proven effective.
Generic ganciclovir ointment
or Zirgan (0.15% ganciclovir
ophthalmic gel, Bausch + Lomb)
may be beneficial for individuals
with active lesions; however, ganciclovir's role and clinical efficacy
has not been formally established.
Nonetheless, off-label applications
of ganciclovir have demonstrated
good activity against HSV, VZV,
cytomegalovirus, Epstein-Barr
virus and multiple strains of
adenovirus.11
Once the corneal stroma is
involved, permanent scarring and
damage can occur. Thus, disciform
keratitis must be treated promptly
with topical corticosteroids. Prednisolone acetate 1% QID to Q4H
is recommended, with a slow taper
over a few months. Cycloplegic agents, such as scopolamine 0.25%, should be used two to four
times daily.
Take note that topical antivirals
have little to no effect on inflammation associated with elevated
intraocular pressure and/or iridocyclitis. Instead, prescribe topical
hypotensive agents for pressure
control, as needed.
Postherpetic Neuralgia
After the patient has recovered
from the acute rash that characterizes HZO, he or she may
experience pain in the affected
dermatome that persists for weeks,
months or even years. The pain
from postherpetic neuralgia is
often unbearable.
Approximately half of patients
with shingles or postherpetic neuralgia describe their pain as "horrible" or "excruciating," ranging
in duration from a few minutes
to constant, on a daily or almost
daily basis.1 In fact, there have
been reports of suicide in elderly
patients because of the unbearable
pain.12
The mechanism that causes
postherpetic neuralgia is not well
understood. Injury to peripheral
nerves and altered central nervous
system signal processing may contribute to its onset. According to
the CDC, "Pathologic observations
thought to distinguish postherpetic
neuralgia from uncomplicated
zoster include axonal and cell
body degeneration, atrophy of the
spinal cord dorsal horn, scarring
of the dorsal root ganglion and
loss of epidermal innervation of
the affected area."13 This neuronal
damage might be caused by ongoing viral replication.13 Regardless
of the exact mechanism, you may
see herpes zoster patients who
present with postherpetic neuralgia. In many instances, these individuals require timely referral to a
pain management specialist.
Treatment for Postherpetic Neuralgia
While there is no specific treatment course for postherpetic neuralgia, several oral and topical pain
management strategies could help
alleviate patient discomfort. Use
of Neurontin (gabapentin, Pfizer),
Lyrica (pregabalin, Pfizer), NSAID
analgesics, narcotics and/or tricyclic antidepressants (e.g., amitriptyline) may prove effective.
Further, topical options include:
Zostrix (capsaicin cream 0.025%,
Hi-Tech Pharmaceutical Co. Inc),
Qutenza patch (capsaicin 8%, NeurogesX) and Lidoderm patches
(lidocane 5.0%, Endo Pharmaceuticals) may be used as well.
Explanations for Increased Incidence
So, why has the number of herpes zoster cases increased during
the last two decades, despite the
availability of vaccines for both
chickenpox and shingles? The
higher disease incidence seems to
be independent of the population's
advancing age.
Interestingly, several studies
indicated that the overall incidence of shingles started increasing before the chickenpox vaccine
Varivax (live varicella virus,
Merck) was introduced in the
United States.1,14-16 Still, the underlying reasons for this increased
prevalence are not well understood. Most importantly, however,
no consistent evidence suggests
that the increased incidence of
shingles in the US has been accelerated by the widespread use of
the varicella vaccine.1
It is worth mentioning that there
have been cases of patients who
actually have experienced a reactivation of herpes zoster following
vaccination. Recently, researchers
reported the case of a patient with
a 3.5-year history of inactive herpes zoster who experienced a bout
of keratouveitis two weeks after
receiving Zostavax.17 The authors
proposed that an increase in cell-mediated immunity was augmented by vaccine administration.17
Vexed by Vaccination?
Whether widespread vaccination for chickenpox and shingles
ultimately is "good or bad" for
patient care is beyond the scope
of this article. Nonetheless, this
point must--at the very least--be
touched upon.
Critics have contended that
the recent increase in shingles
incidence has been caused by not
allowing children to be exposed to
VZV naturally at a young age--
effectively denying them a lifetime
of immunity. According to this
argument, widespread vaccinations
may prevent both children and
adults from having their natural
immunity boosted because they no
longer come into regular contact
with infected individuals.
Additionally, some advocates
believe that mass vaccination
for what often is regarded as a
benign childhood illness is neither
necessary nor cost effective.18 In
a recent article in the journal Vaccine, the authors argued that the
varicella vaccination is less effective than the natural immunity
experienced in pre-vaccine communities. Further, the researchers
noted that mass vaccination isn't
a cost-effective measure, because
more money now must be spent
treating the increased number of
herpes zoster patients.18
Evidence-based medicine shows
that mass vaccination does indeed
lower the overall incidence of
chickenpox and shingles in treated
individuals. However, experts
across many fields of the medical
community still are determining
the long-term, widespread impact
of VZV vaccination upon the population as a whole.
As a primary eye care provider,
you will encounter patients who
inquire about the benefits of vaccination. You can inform them
confidently that Zostavax is recommended for patients who are
over the age of 60 or for those
who have a history of shingles.
Treating herpes zoster can be
both rewarding and frustrating--for you and the patient. It is
important to recognize the signs
and symptoms, and begin treat
ment promptly. You must then
monitor these patients closely and
taper their medications accordingly. Finally, always remain vigilant
about the possibility of postherpetic neuralgia.
Dr. Marcolini is in a group practice at Omni Eye Services in Iselin,
N.J., and in private practice in
Clinton, N.J.
References
- The United States Centers for Disease Control and Prevention. Shingles (Herpes Zoster). Available at: www.cdc.gov/shingles/hcp/ clinical-overview.html. Accessed January 16, 2013.
- The United States Centers for Disease Control and Prevention. Varicella. Available at: www.cdc.gov/vaccines/pubs/pinkbook/ downloads/varicella.pdf. Accessed January 16, 2013.
- Ragozzino MW, Melton LJ 3rd, Kurland LT, et al. Population-based study of herpes zoster and its sequelae. Medicine (Balti-more). 1982 Sep;61(5):310-6.
- Oxman MN, Levin MJ, Johnson GR, et al. A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults. N Engl J Med. 2005 Jun 2;352(22):2271-84.
- Lee WB, Liesegang TJ. Herpes Zoster Keratitis. In: Krachmer JH, Mannis MJ, Holland EJ, eds. Cornea, 2nd ed. Philadelphia: Elsevier Mosby; 2005:1075-89.
- Yanoff M, Duker JS. Infectious Keratitis. In: Ophthalmology, 2nd ed. Philadelphia: Mosby; 2004:469-81.
- Leisegang TJ. Corneal complications from herpes zoster ophthal-micus. Ophthalmology. 1985 Mar;92(3):316-24.
- Foster CS, Vitale AT. Herpes Viruses. In: Diagnosis and Treatment of Uveitis. Philadelphia: WB Saunders; 2002:317-23.
- Wenkel H, Rummelt V, Fleckenstein B, Naumann GO. Detection of varicella zoster virus DNA and viral antigen in human eyes after herpes zoster ophthalmicus. Ophthalmology. 1998 Jul;105(7):1323-30.
- Zaal MJ, Maudgal PC, Rietveld E, Suir EP. Chronic ocular zoster. Curr Eye Res. 1991;10 Suppl:125-30.
- Foster CS. Ganciclovir gel--a new topical treatment for herpetic keratitis. Availale at: www.touchbriefings.com/pdf/3200/foster.pdf. Accessed January 28, 2013.
- El-Ansary M. International Association for the Study of Pain. Chapter 24: Management of postherpetic neuralgia. Available at: www.iasp-pain.org/AM/Template.cfm?Section=Home&Template=/ CM/ContentDisplay.cfm&ContentID=12187. Accessed January 28, 2013.
- Harpaz R, Ortega-Sanchez IR, Seward JF. The United States Centers for Disease Control and Prevention. Prevention of Herpes Zoster: Recommendations of the Advisory Committee on Immunization Practices. Available at: www.cdc.gov/mmwr/preview/ mmwrhtml/rr5705a1.htm. Accessed January 16, 2013.
- Yawn BP, Saddier P, Wollan PC, et al. A population-based study of the incidence and complication rates of herpes zoster before zoster vaccine introduction. Mayo Clin Proc 2007 Nov;82(11):1341-9.
- Donahue JG, Choo PW, Manson JE, Platt R. The incidence of herpes zoster. Arch Int Med 1995 Aug 7-21;155(15):1605-9.
- Hales CM, Harpaz R, Joesoef MR, Bialek SR. Herpes zoster in the Medicare population, 1991-2009: Assessment of trends, risk factors and the impact of the varicella vaccination program. Poster presented at: IDWeek 2012; San Diego: October 17-21 2012.
- Hwang CW Jr, Steigleman WA, Saucedo-Sanchez E, Tuli SS. Reactivation of herpes zoster keratitis in an adult after varicella zoster vaccination. Cornea. 2012 Nov 26. [Epub ahead of print]
- Goldman GS, King PG. Review of the United States universal varicella vaccination program: Herpes zoster incidence rates, cost-effectiveness, and vaccine efficacy based primarily on the Antelope Valley Varicella Active Surveillance Project data. Vaccine. 2012 Jun 1. [Epub ahead of print]
- Prince A. Infectious diseases. In: Behrman RE, Lkiegman RM (eds.). Essentials of pediatrics, 2nd ed. Philadelphia: WB Saun-ders;1994:297-394. .
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