Herpes Zoster Ophthalmicus Clinical
Presentation and Risk Factors for Loss of Vision
RACHEL LOUISE NIEDERER, JAY J. MEYER, KEVIN LIU, AND HELEN V. DANESH-MEYER
• PURPOSE: To determine the rate of moderate and severe
vision loss following herpes zoster ophthalmicus (HZO)
and to identify associated factors.
• DESIGN: Retrospective cohort study.
• METHODS: All subjects with acute HZO seen at a sin-
gle center from 2006 to 2016 were included in the study.
The primary outcome measure was the proportion of indi-
viduals with moderate and/or severe loss of vision follow-
ing an acute episode of HZO. Secondary outcome mea-
sures included causes and factors associated with perma-
nent loss of vision owing to HZO.
• RESULTS: A total of 869 patients with acute HZO
were identified with a median follow-up time of 6.3 years
(interquartile range 3.7-8.9 years). Ocular involvement
of HZO was diagnosed at or within the first month
of presentation in 737 individuals (84.8%). The most
common sites of ocular involvement were conjunctivi-
tis (76.1%), followed by keratitis (51.2%) and uveitis
(47.6%). Moderate vision loss (≤20/50) secondary to
HZO occurred in 83 eyes (9.6%) while severe vision loss
(≤20/200) occurred in 31 eyes (3.6%). Causes of loss of
vision included corneal scarring (94.0%), corneal perfo-
ration (4.8%), and secondary glaucoma (1.2%). Severe
vision loss was associated with older age (hazard ratio
[HR] 1.059, P = .001), immunosuppression (HR 3.125,
P = .028), poor presenting visual acuity (HR 2.821,
P = .002), and uveitis (HR 4.777, P = .004) on multi-
variate analysis.
• CONCLUSIONS: Among individuals with HZO, approx-
imately 1 in 10 individuals may develop moderate or
severe vision loss, primarily owing to corneal scarring.
Older age, immunosuppression, and uveitis are associated
with severe permanent loss of vision secondary to HZO.
(Am J Ophthalmol 2021;226: 83–89. © 2021 Published
by Elsevier Inc.)
H
erpes zoster (HZ), also known as shingles, re-
sults from reactivation of the varicella-zoster virus
(VZV) and typically manifests as a dermatomal
Accepted for publication February 3, 2021.
Department of Ophthalmology, Auckland District Health Board, Auck-
land, New Zealand; and Department of Ophthalmology, University of
Auckland, Auckland, New Zealand
Inquiries to Rachael Niederer, Department of Ophthalmology, Auckland
District Health Board, New Zealand.; e-mail: rachaeln@adhb.govt.nz
0002-9394/$36.00 © 2021 PUBLISHED BY ELSEVIER INC..
https://doi.org/10.1016/j.ajo.2021.02.002
rash with associated pain. This condition may affect up to a
third of individuals throughout their lifetime, with an in-
creased risk occurring with age.1 Reactivation along the
ophthalmic branch of the trigeminal nerve, or herpes zoster
ophthalmicus (HZO), represents approximately 10%-20%
of HZ cases.2 , 3 Herpes zoster ophthalmicus results in ocular
involvement in over 50% of cases and may cause inflamma-
tion throughout the eye, including conjunctivitis, keratitis,
iritis/uveitis, episcleritis/scleritis, retinal perivasculitis and
necrosis, and optic neuritis.2-4 There is evidence that both
the incidence of HZ and the rate of associated ocular com-
plications have risen in recent decades.2
Herpes zoster ophthalmicus can result in permanent loss
of vision, persistent pain, and a decreased quality of life.2-7
The loss of vision owing to HZO can be immediate or de-
layed, with over 20% developing a chronic course that can
result in further complications and loss of vision over time.8
There are limited data describing the causes of vision loss as
well as the rates and degrees of visual impairment following
acute HZO. We investigated a large cohort of individuals
with acute HZO to determine the rate of subsequent mod-
erate and severe vision loss owing to HZO and analyzed po-
tential factors associated with loss of vision.
METHODS
• PARTICIPANTS: This study was approved by the Auck-
land Health Regional Ethics Committee (#000027). Partic-
ipants were identified by a search for the key words “shin-
gles,” “zoster,” “VZV,” “HZV,” “HZO,” or “herpes zoster
ophthalmicus” on discharge paperwork for subjects re-
viewed at the Department of Ophthalmology, Auckland
District Health Board, Auckland, New Zealand, between
January 1, 2006, and December 31, 2016, with follow-up
concluded June 1, 2019, or on subject death or moving care
to another center. Participants were considered eligible for
inclusion in the study if they were diagnosed with their first
episode of HZO with a classic shingles rash in the V1 dis-
tribution. Ocular involvement of HZO was defined as any
involvement of structures of the eye/globe. Involvement of
only the eyelid or only a cranial nerve palsy was not con-
sidered ocular involvement. Subjects were excluded if they
had HZO sine herpete (absence of classic shingles rash) or
if the presentation was atypical and the diagnosis was not
clear. Notes were reviewed for 1,010 patients, of whom 141
83
were excluded owing to final diagnosis being herpes sim-
plex (26 subjects); first episode outside of study period or TABLE 1. Patient Demographics
reviewed at a different medical facility (76 subjects); chick-
enpox not HZO (9 subjects); herpes zoster sine herpete (9 Demographic Result (N = 869 Patients)

subjects); non-V1 dermatome (7 subjects); diagnosis uncer- Age, y Median 65.5 (IQR 52.9-75.4)
tain (9 subjects); and alternative diagnosis (5 subjects). Male 456 (52.5%)
Ethnicity
• OUTCOME MEASURES: Visual acuity was recorded as White 621 (71.5%)
Snellen acuity and converted to logMAR for the purpose of Pacific Peoples 47 (5.4%)
analyses. Moderate visual loss was defined as best-corrected Maori 42 (4.8%)
visual acuity (BCVA) ≤20/50 and severe vision loss was vi- Chinese 61 (7.0%)
sion ≤20/200.9 Visual loss was classified as permanent vi- Indian 44 (5.1%)
Other Asian 27 (3.1%)
sual loss owing to HZO if visual acuity did not improve by
Other 13 (1.5%)
the final visit after resolution of inflammation, or as visual
Unknown 14 (1.6%)
loss owing to non-HZO causes or nonpermanent visual loss
Immunosuppressed 83 (9.6%)
(such as cataract). Oral corticosteroid 35 (4.0%)
Recurrence of disease was considered an increase in an- DMARD 36 (4.1%)
terior chamber cells of ≥1 grade or uveitis or corneal dis- Anti–tumor necrosis factor 4 (0.5%)
ease requiring an escalation of treatment. Neurotrophic ker- Rituximab 3 (0.4%)
atopathy was defined as a chronic keratopathy or epithelial Chemotherapy 18 (2.1%)
defect attributed to a neurotrophic cornea by the treating Leukemia or lymphoma 21 (2.4%)
clinician, as corneal sensation was not routinely checked HIV 5 (0.6%)
for all patients. Diabetes 102 (11.7%)

DMARD = disease-modifying antirheumatic drugs;

• STATISTICAL ANALYSIS: Results were entered into an
Excel database and analyzed in STATA version 15 (Stat-
aCorp, College Station, Texas, USA). Categorical data are
reported as n (%) and continuous data as median (in-
terquartile range [IQR]). For time to vision loss, subjects
were censored at June 1, 2019, or at time of death or trans-
fer of care to another district health board or private clinic.
Cox regression was used to examine risk factors for vision
loss. Goodness-of-fit tests were employed and the most par-
simonious model presented. A P value of <.05 was consid-
ered statistically significant.
HIV = human immunodeficiency virus.
subjects (4.0%). Human immunodeficiency virus (HIV) in-
fection was rare, present in 5 subjects (0.6%). Diabetes
was present in 102 subjects (11.7%) and was more com-
mon in Pacific Peoples (36.2%) and Māori (26.2%) subjects
presenting with HZO, compared with white (10.5%) and
Asian (9.1%) individuals (P < .001). No subjects reported
or had a record of having previously received vaccination
for the prevention of shingles.

• CLINICAL PRESENTATION: The clinical features of the

RESULTS
• DEMOGRAPHICS: A total of 869 patients were included
for analysis with a median follow-up time of 6.3 years
(IQR 3.7-8.9 years), with a total of 5,504.4 patient-years
of follow-up. Patient demographics are reported in Table 1.
Median age at presentation was 65.5 years (mean 62.5 ±
18.3 years), ranging from 1.3 years to 100.2 years (Figure).
Three hundred and eighteen subjects (36.6%) were aged
<60 years at presentation and 116 subjects (13.4%) were
aged <40 years at presentation. Age at presentation differed
between ethnicities, with median age at presentation 67.9
(IQR 55.9-77.5) years in white, 62.0 (IQR 49.1-68.9) years
in Māori, 60.9 (IQR 44.5-73.6) years in Pacific Peoples, and
56.5 (IQR 37.2-69.4) years in Asian subjects (P < .001).
Eighty-three subjects (9.6%) were immunosuppressed at
presentation, with disease-modifying antirheumatic drugs
used in 36 subjects (4.1%) and oral corticosteroid in 35
study cohort at presentation are described in Table 2. The
median time from development of rash to presentation to
ophthalmology was 5 days (IQR 3-7 days). Median BCVA
was 20/30 (IQR 20/25-20/40). Two hundred and ten sub-
jects (26.6%) had BCVA ≤20/50 at presentation and 48
(5.6%) had BCVA ≤20/200 at presentation.
Ocular involvement was diagnosed at or within the
first month of presentation in 737 individuals (84.8%).
The most common presentation was with conjunctivitis
(76.1%). Isolated conjunctivitis occurred in 177 subjects
(20.4%). Corneal involvement was present in 445 individ-
uals (51.2%), with pseudodendrites in 255 (29.3%), disci-
form keratitis in 102 (11.7%), punctate epithelial erosions
in 132 (15.2%), and epithelial defect in 11 (1.3%). Four
hundred and thirteen individuals (47.6%) had uveitis ei-
ther at presentation or within a month of presentation. The
median time from the onset of rash to diagnosis with uveitis
was 10 days (IQR 6-14 days).

84 AMERICAN JOURNAL OF OPHTHALMOLOGY JUNE 2021

 80
Frequency 60
40
20
0
0 20 40
Age at onset
FIGURE. Age at presentation with herpes zoster ophthalmicus.
Age at onset was associated with an increased risk of pre-
senting with corneal involvement (OR 1.017, P < .001),
translating to an 18.3% increased risk for every decade.
There was no association between corneal involvement and
sex, ethnicity, immunosuppression, or diabetes.
Age at onset was also associated with an increased risk of
presenting with uveitis (OR 1.010, P = .006), translating to
a 10.8% increased risk for every decade. There was no as-
sociation between corneal involvement and sex, ethnicity,
immunosuppression, or diabetes.
Cranial nerve palsy occurred in 30 subjects (3.5%), most
frequently CN III (14 subjects, 1.6%) and CN VI (12 sub-
jects, 1.4%). Twenty-seven subjects had an isolated cranial
nerve palsy and 3 had multiple cranial nerves involved. Op-
tic neuropathy was present in 15 subjects (1.8%) and prop-
tosis in 3 subjects (0.3%).
• MANAGEMENT: Oral or intravenous antiviral therapy
(acyclovir or valacyclovir) was started in 765 subjects
(88.0%; 741 oral, 24 intravenous followed by oral), not used
in 95 (10.9%), and not documented in 9 subjects (1.0%).
Median time from onset of rash to commencing oral an-
tiviral therapy was 3 days (IQR 1-5 days). Intravenous an-
tiviral was given to 24 subjects (2.8%). Four hundred and
sixty-eight subjects (54.9%) received antiviral therapy ≤72
hours after the onset of rash (termed “prompt antiviral” for
study purposes). Median duration of antiviral therapy was 7
days (IQR 7-7 days). No difference was observed in the like-
lihood of prompt antiviral by ethnicity. Oral corticosteroid
was started in 24 subjects (2.8%).
Topical corticosteroid was initiated in 437 subjects
(50.4%), most commonly prednisolone acetate 1.0% (407
VOL. 226 HERPES ZOSTER OPHTHALMICUS
60 80 100
subjects). Median daily drop frequency at initiation was 4
(IQR 4-6). Median duration of topical steroid therapy was
54 days (IQR 34-108 days). One hundred and twenty-nine
subjects (14.9%) required topical antihypertensive treat-
ment at presentation and 11 subjects (1.8%) required oral
acetazolamide for intraocular pressure management.
• COMPLICATIONS: Complications are reported in
Table 3. Five hundred and fifty-one recurrences were
observed during the study period, with at least 1 recurrence
in 200 subjects (23.0%). The median final visual acuity was
20/25 (IQR 20/20-20/40). Moderate vision loss occurred
in 170 eyes (19.8%), of which 83 (9.6%) were permanent
loss owing to HZO. Severe vision loss occurred in 64 eyes
(7.6%), of which 31 (3.6%) were permanent loss owing to
HZO. In 4 subjects, vision loss was owing to perforation (2
enucleated, 1 eviscerated, 1 developed phthisis following
perforation). One subject lost vision secondary to glaucoma
(owing to HZO). In the remaining 78 subjects (94.0%)
with visual loss, loss of vision was secondary to corneal
scarring. Complete vision loss (no perception of light)
developed in 6 eyes (0.7%).
Causes of vision loss in this cohort that were either
not secondary to HZO or not permanent included cataract
(n = 27), age-related macular degeneration (n = 26), pre-
existing glaucoma (n = 4), optic neuropathy unrelated to
HZO (n = 4), retinal vein or artery occlusion (n = 4), am-
85
 TABLE 4. Factors Associated With Moderate Visual Loss
TABLE 2. Clinical Presentation of Individuals With Acute (≤20/50)
Herpes Zoster Ophthalmicus
Univariate Multivariate
Feature Result (N = 869 Patients)
HR P Value HR P Value
Time from rash to Median 5 days (IQR 3-7
presentation days) Age 1.057 <.001∗ 1.038 <.001∗
Right eye 439 (50.5%) Female 1.106 .690
BCVA Median 20/30 (IQR White 3.064 .005∗ 2.344 .036∗
20/25-20/40) Immunosuppressed 1.553 .246
Intraocular pressure Median 15 mm Hg (IQR Diabetes 1.090 .830
12-19 mm Hg) Presenting BCVA 3.354 <.001∗ 1.978 .010∗
≥24 mm Hg 112 (13.6%) Presenting IOP 1.043 <.001∗
≥30 mm Hg 56 (6.8%) Conjunctivitis 2.768 .011∗
Lid swelling 483 (55.6%) Corneal involvement 3.262 <.001∗
Conjunctivitis 661 (76.1%) Uveitis 4.881 <.001∗ 3.882 <.001∗
Corneal involvement 445 (51.2%) Prompt acyclovir 0.741 .239
Pseudodendrites 255 (29.3%) BCVA = best-corrected visual acuity; HR = hazard ratio;
Disciform keratitis 102 (11.7%) IOP = intraocular pressure.
Punctate epitheliopathy 132 (15.2%) Cox proportional hazards regression model.
Epithelial defect 11 (1.3%) Asterisk indicates statistically significant P values.
Stromal keratitis 6 (0.7%)
Uveitis 413 (47.6%)
Phakic 762 (87.7%)
Cataract at presentation 202 (23.2%)
blyopia (n = 4), other macular pathology (n = 3), unable to
Optic neuropathy 15 (1.7%)
be ascertained owing to dementia (n = 2), ocular ischemia
Cranial nerve palsy 30 (3.5%) (n = 1), previous retinal detachment (n = 1), previous
CN III 14 (1.6%) complicated cataract surgery (n = 2), and large pterygium
CN IV 6 (0.7%) (n = 1). In 10 subjects, there was pre-existing poor vision
CN VI 12 (1.4%) of unspecified etiology.
CN VII 2 (0.2%) When classified according to age group, permanent visual
Proptosis 3 (0.3%) loss owing to HZO occurred in 2 subjects aged ≤40 years
BCVA = best-corrected visual acuity. (1.7%), 10 aged 41-59 years (5.0%), and 71 aged ≥60 years
Results are n (%) unless indicated. (14.9%). Looking specifically at those aged 50-65 years, per-
manent visual loss owing to HZO occurred in 16 of 232
subjects (6.9%). Permanent visual loss owing to HZO oc-
curred in 13 of 83 subjects who were immunosuppressed
TABLE 3. Complications of Herpes Zoster Ophthalmicus (15.7%), compared to 70 of 782 subjects who were not im-
munosuppressed (9.0%). Permanent visual loss occurred in
Result, n (%) 79 subjects (10.8%) with ocular involvement at or within
Complication (N = 869 Patients) 1 month of presentation, compared to 4 of 132 subjects
(3.0%) with no ocular involvement in the first month. All
Corneal scar 151 (17.4%)
Neurotrophic keratopathy 58 (6.7%)
severe vision loss occurred in subjects with ocular involve-
Band keratopathy 13 (1.5%) ment at presentation (31/733, 4.2%). The proportions of
Corneal melt 22 (2.5%) eyes that developed permanent moderate vision loss ow-
Corneal perforation 5 (0.6%) ing to HZO, according to corneal involvement at or within
Iris transillumination 19 (2.2%) a month of presentation, were as follows: disciform kerati-
Acute retinal necrosis 5 (0.6%) tis 27.5% (28/102), stromal keratitis 0% (0/6), pseudoden-
Intraocular pressure ≥24 mm Hg 169 (19.5%) drites 14.1% (36/255), and punctate epitheliopathy 8.3%
Intraocular pressure ≥30 mm Hg 106 (12.2%) (11/132).
Glaucoma 33 (3.8%) A Cox regression model was used to examine the risk
Moderate vision loss (≤20/50) 170 (19.7%)
of moderate and severe visual loss (Tables 4 and 5) ow-
Moderate vision loss owing to HZO 83 (9.6%)
ing to HZO. On multivariate analysis, older age (hazard
Severe vision loss (≤20/200) 64 (7.4%)
Severe vision loss owing to HZO 31 (3.6%)
ratio [HR] 1.038, P < .001), white ethnicity (HR 2.344,
P = .036), presenting visual acuity (HR 1.978, P = .010),
HZO = herpes zoster ophthalmicus. and uveitis (HR 3.882, P < .001) were associated with in-
creased risk of moderate vision loss owing to HZO. For

86 AMERICAN JOURNAL OF OPHTHALMOLOGY JUNE 2021

 thy,12 keratouveitis,13 and uveitis.13 Of significance is the
TABLE 5. Factors Associated With Severe Visual Loss rate of vision loss (6.9%) in the group of individuals aged
(≤20/200) 50-64 years, as funding of the zoster vaccine varies for this
cohort. Lowering the age of funding for vaccination could
Univariate Multivariate
potentially reduce the disease burden in this age group.
HR P Value HR P Value Uveitis was the strongest risk factor for loss of vision in
this study, similar to the findings of a smaller study of 64 pa-
Age 1.074 <.001∗ 1.059 .001∗
tients followed for 6 months.5 This association is not unex-
Female 1.366 .421
Caucasian 2.193 .149
pected, as uveitis is a recognized cause of many other vision-
Immunosuppressed 2.362 .083 3.125 .028∗ threatening complications, including glaucoma, cataract,
Diabetes 0.683 .604 band keratopathy, macular edema, and corneal decompen-
Presenting VA 4.355 <.001∗ 2.821 .002∗ sation.14 In addition, uveitis on initial presentation of HZO
Presenting IOP 1.052 .002∗ increases the risk of recurrent and chronic eye disease.10
Corneal involvement 5.717 .001∗ Immunosuppression, particularly cell-mediated immun-
Uveitis 7.108 <.001∗ 4.777 .004∗ odeficiency, is a well-established risk factor for HZ in any
Prompt acyclovir 0.625 .237 dermatome as well as HZ recurrence.15 , 16 In this study, im-
HR = hazard ratio; IOP = intraocular pressure; VA = visual munosuppression was also identified as a risk factor for vi-
acuity. sion loss on multivariate analysis. Immunosuppression may
Cox proportional hazards regression model. be caused by systemic disorders, such as malignancy or HIV,
Asterisk indicates statistically significant P values. or owing to immunosuppressive therapies. In this study,
the majority of patients were immunosuppressed owing to
therapies with systemic corticosteroid medications, disease-
severe vision loss owing to HZO, significant risk factors modifying antirheumatic drugs, or chemotherapy. Antivi-
were older age (HR 1.059, P = .001), immunosuppression ral treatment may be an important factor in the prevention
(HR 3.125, P = .028), presenting visual acuity (HR 2.821, of vision loss in immunosuppressed individuals. In 1 study,
P = .002), and uveitis (HR 4.777, P = .004). vision loss was identified in 56% of immunosuppressed pa-
tients who did not receive antiviral therapy.17 In contrast, a
prospective study promptly administered both systemic and
topical antivirals to 64 patients, including 37.5% with HIV,
DISCUSSION and only 4.7% developed vision loss over 6 months.5
No previous studies have examined the severity of vision
The present study is the largest to report the outcomes of loss according to ethnicity, likely because previous stud-
vision following HZO. In this study, among all presenting ies have largely described homogenous populations or be-
individuals with acute HZO, approximately 1 in 10 indi- cause study numbers were too few to stratify by ethnicity.
viduals (9.6%) developed moderate visual loss and 3.6% There is some epidemiologic evidence that nonwhite indi-
had severe visual loss attributable to HZO. As might be ex- viduals may be at lower risk for HZ in general.16 Potential
pected, poor presenting visual acuity was associated with explanations for this discrepancy include differences in age
both moderate and severe vision loss. Other factors associ- at varicella acquisition, genetic differences affecting reacti-
ated with vision loss in multivariate analyses included older vation, or differences in mortality rates affecting survival
age, uveitis, white ethnicity, and immunosuppression. to older age.16 While a lower incidence of HZO among
In the present study, older age was associated with Pacific Islanders has previously been reported, no analyses
corneal involvement and uveitis, both of which have been of severity of HZO or complications were reported.11 Fur-
associated with vision loss following HZO.4 , 5 However, ther studies are required to confirm the association of white
older age was also identified as an independent risk factor ethnicity with loss of vision and to investigate potential
for loss of vision in our multivariate model that included mechanisms.
uveitis and corneal involvement in the analysis. Indeed, the The wide range of ocular complications that can de-
rate of severe vision loss in those under age 40 was only velop following HZO are a result of the direct effects of the
1.7%, or 1 of 59. Herpes zoster results from the reactiva- virus, the host inflammatory/immune response, or both.3
tion of the VZV related to waning cell-mediated immunity Vision loss following HZO can occur acutely owing to con-
against VZV. This selective decline in cell-mediated immu- ditions such as keratitis, optic neuritis, or retinitis. How-
nity may occur with advancing age in the absence of im- ever, more commonly, as demonstrated in this study, severe
mune boosting from repeat exposure to the virus through complications resulting in permanent loss of vision may oc-
contact with wild-type virus or through vaccination.3 In ad- cur months or years after the initial presentation owing to
dition to increasing the risk of HZO,10 older age has been the sequelae of acute and chronic inflammation and neu-
associated with a higher rate of several complications,2 in- ropathy. These delayed complications include neurotrophic
cluding postherpetic neuralgia,11 , 12 neurotrophic keratopa- keratopathy, corneal scarring, corneal melting/perforation,

VOL. 226 HERPES ZOSTER OPHTHALMICUS 87

 TABLE 6. Summary of Studies Reporting Visual Outcomes Following Herpes Zoster Ophthalmicus
Study Number With HZO Ocular involvement
Current study 869 737 (84.8%)
Szeto et al4 259 170 (65.6%)
Babu et al21 249 Not specified
Yawn et al2 Not specified 184
Liesegang et al3 86 61 (70.9%)
Zaal et al18 73 46 (63.0%)
Nithyanandam et al5 64 Not specified
Kahloun et al13 51 45 (88.2%)
BCVA = best-corrected visual acuity; HZO = herpes zoster ophthalmicus; IQR = interquartile range.
a
Only decreased vision owing to HZO listed here for this study.
cataract, and secondary glaucoma. In our series, 6 eyes
ended up with total loss of vision (no perception of light).
There are limited data describing loss of vision following
acute HZO, particularly with adequate follow-up to capture
those individuals with a chronic course and progressive, or
delayed, loss of vision. Comparison of our results with pre-
vious studies is limited owing to variable reported defini-
tions of vision loss, type of vision loss (temporary or per-
manent), underlying causes of vision loss (owing to HZO
or other causes), treatments employed, and immune status
of the studied populations.2 , 4 , 5 , 10 , 13 , 18-22 Some studies re-
ported vision loss as a percentage of all HZO cases, while
others only report cases of HZO with ocular involvement.
In addition, some studies only included patients who pre-
sented with acute HZO while others also included those re-
ferred with complications. A summary of studies reporting
visual outcomes is listed in Table 6.
Szeto and associates retrospectively studied 259 individ-
uals with acute HZO followed for 9.3 ±10.2 months.4 Of
these, 170 (66%) had ocular involvement and 59% had vi-
sion of 20/40 or worse after resolution of HZO. Visual loss
(reduction in BCVA ≥1 line after resolution of HZO com-
pared to BCVA at presentation) developed in 12% of pa-
tients, primarily owing to corneal involvement. Keratitis
(both epithelial and stromal) and number of ocular man-
ifestations were found to be risk factors associated with vi-
sion loss. Similar to the present study, the commonest man-
ifestations were conjunctivitis, followed by uveitis and ker-
atitis.
Yawn and associates retrospectively studied 184 individ-
uals with HZO and ocular involvement.2 Of these, 6.6%
had a “permanent vision decrement,” including 3.3% with
severe vision loss of 20/200 or worse.2 Recurrent keratitis
and uveitis each developed in approximately 7% of eyes.
88 AMERICAN JOURNAL OF OPHTHALMOLOGY
Follow-up Visual Outcome or Loss
Median 6.3 years 83/869 (9.6%) BCVA ≤20/50a
(IQR 3.7-8.9 years) 31/869 (3.6%) BCVA ≤20/200a
9.3 ±10.2 months 12% loss of ≥1 line of BCVA
Not specified 80/249 (32.1%) BCVA ≤20/60
23/249 (9.2%) BCVA <20/200
209 ±349 days 6/184 (3.3%) ≤20/200
Not specified 24/86 (16.3%) BCVA ≤20/50
10/86 (11.6%) BCVA <20/200
6 months 2/73 (2.7%) BCVA ≤20/50
0/73 (0%) BCVA ≤20/200
6 months 3/64 (4.7%) BCVA ≤20/200
Mean 12 months (range 11/51 (21.6%) BCVA ≤20/50
9-51 months) 4/51 (7.8%) BCVA <20/200
Zaal and associates prospectively studied 73 immuno-
competent patients, all treated with oral acyclovir.18 At
6 months, approximately 10% (7 eyes) had mild-to-
moderate vision loss (20/40 to 20/125), while no eyes
developed severe vision loss. Causes of vision loss in-
cluded optic neuropathy, corneal exposure, and corneal
opacities.
Limitations of the present study include the retrospec-
tive nature and possibility of referral bias, as it is possible
that some individuals with HZO were not referred for an
ophthalmic examination. However, the vast majority of pa-
tients in our community who are referred for an evaluation
are referred to our clinic, as it is the only department with a
designated acute eye service. In addition, the study period
was prior to the availability of a publicly funded vaccine to
reduce shingles in New Zealand and may not reflect disease
severity in populations with high proportions of vaccinated
individuals. The main strengths of this study are the large
number of individuals studied, the diversity of the studied
population, and the long duration of follow-up, which in-
creases the likelihood that individuals with chronic, or de-
layed, vision loss were identified. In addition, all outcomes
were determined by direct chart review rather than relying
on diagnosis codes, which can be inaccurate when deter-
mining HZ complications.23
In conclusion, HZO can result in moderate-to-severe loss
of vision in a significant proportion of patients with ocu-
lar involvement, even with timely and appropriate man-
agement. Vision loss can be delayed and occur months
or years after the initial acute HZO presentation. Further
research is needed to determine whether long-term pro-
phylactic antiviral treatment may be beneficial in treat-
ing or preventing chronic disease and subsequent vision
loss.
JUNE 2021
Funding/Support: The authors have none to declare. Financial Disclosures: The authors have none to declare. All authors attest that they meet the current
ICMJE criteria for authorship.
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