This seminar outlines the latest diagnostic and management guidelines for Viral Keratitis.

1. Viral Keratitis
Presenter: Dr Sahil Thakur
Moderator: Professor Sudesh Arya

2. INTRODUCTION • Infective keratitis is suppurative infection of cornea
which may be associated with epithelial defects and or
signs of inflammation.
• Worldwide 45 million blind
• 1.5-2.0 million blind due to corneal diseases added
every year.
• Prevalence of corneal blindness (<6/60 in worse eye) in
Indian population is 0.66% i.e (one out of every 150
people in India)
• In India ,incidence of corneal ulcer is 113 per 100,000
per year i.e. 8,40,000 corneal ulcers develop annually in
India.
BJO 2003;87:133-141

3. VIRALKERATITIS:
EPIDEMIOLOGY
• Viral keratitis is the commonest cause of keratitis in
the developed world.
• The virus can infect individual layers of the cornea or
in more severe form it may involve all the layers of
cornea.
• The various viral infections that can affect the cornea
can be broadly grouped under the following
categories herpes simplex keratitis, varicella zoster
induced keratitis and the adenoviral keratitis.

4. HSVKERATITIS:
EPIDEMIOLOGY
• The global incidence of HSV keratitis is roughly 1.5
million, including 40,000 new cases of severe
monocular visual impairment or blindness each year.
Farooq, A. V., & Shukla, D. (2012). Herpes Simplex Epithelial and Stromal Keratitis: An Epidemiologic
Update. Survey of Ophthalmology, 57(5), 448–462.

5. HSVKERATITIS
• Herpes simplex virus is a large and complex enveloped
virus measuring 150-200 nm.
• It has a double stranded DNA core, which is surrounded by
a protein capsid that is made up of 162 subunits called
capsomer.
• The capsid is surrounded by the tegument, membrane of
the infected cell that has been altered by virus-induced
proteins.
• Humans are the only natural reservoirs of herpes.
• The sources of infection are by direct contact with infected
lesions, by salivary droplets or fomites from children and
adults with active disease and also of asymptomatic virus
shedding carriers.

6. HSVKERATITIS
• The most common type of herpes simplex virus is HSV-1
which causes cold sore or fever blister in the mouth, face
and upper body and may affect the eye.
• HSV-2 causes genital herpes, a sexually transmitted
disease. Ocular herpes is caused primarily by HSV-1 and
occasionally by HSV type-2 virus.

7. HSVKERATITIS:
PATHOPHYSIOLOGY
• The main route of HSV spread is via
direct contact.
• Ocular infection can occur as primary
or recurrent episodes.
• HSV epithelial keratitis begins as a
superficial punctate lesion, progressing
to a stellate erosion and, finally, a
dendritic ulcer.
• HSV stromal keratitis is thought to
occur more commonly in recurrences.
• The morbidity in stromal disease is
thought to result from CD4+ T-cell
destruction in the inflammatory
response to the virus, in addition to
direct viral effects.

8. HSVKERATITIS:INFECTION
•Congenital
•Neonatal
•Primary Ocular HSV
•Recurrent Ocular HSV

9. CONGENITALHSVKERATITIS
• HSV-1 and HSV-2 can be acquired in utero,
by transplacental or ascending infection,
by exposure to genital lesions during
delivery, or postnatally from relatives or
attendants.
• Of all the neonatal HSV, 4 percent is
acquired during intrauterine life, 86
percent infection occurs at the time of
birth and remaining 10 percent occurs in
the postnatal period.
• Congenital HSV infection is characterized
by the triad of skin vesicles, eye disease
and microencephaly.

10. NEONATALHSVKERATITIS • Neonatal HSV infection usually presents as a bilateral
disease at 2 days to 2 weeks of age.
• HSV keratitis in a neonate is invariably associated with
conjunctivitis.
• Keratitis may manifest as diffuse microdendritis,
serpiginous epithelial defects or a punctate keratitis.
• The diagnosis of ocular HSV must be considered in any
infant with nonpurulent conjunctivitis or keratitis.
• Treatment of neonatal ocular herpetic disease comprises of
topical antivirals (1% Trifluridine ophthalmic solution or 3%
acyclovir ophthalmic ointment) in addition to systemic
Acyclovir (2 g/day IV every 8 hourly for 14 days).

11. PRIMARYOCULARHSV • Atypical presentation
• Unilateral blepharoconjuctivitis
-Follicular conjuctivitis
-Skin or eyelid vesicles
• Epithelial keratitis
• Stromal keratitis is rare.
• Primary ocular herpes (1st encounter with virus) should
not be confused with First ocular occurrence (1st eye
involvement with HSV in a patient who has subclinical
infection and is immune)

12. RECURRENTOCULARHSV
• Reactivation of virus in latently infected sensory ganglion.
• Patients have both cellular and humoral immunity against virus.
• It can present in any one of the combinations:
Blepharoconjuctivitis Episcleritis, Scleritis
Corneal keratitis:
• Epithelial keratitis
• Infectious ulcerative
• Trophic (Metaherpatic)
ulceration
Stromal keratitis:
• Necrotizing keratitis
• Non necrotizing keratitis
• Disciform
• Diffuse
• Linear
Endotheliitis
Iridocyclitis and
Trabeculitis

13. •Clinical disease develops in less than 1 % of
population infected with virus
•Corneal scarring occurs in 18% - 28%.
•Corneal disease is broadly divided into:
oEpithelial
oStromal
oEndothelial
CLINICALMANIFESTATIONS

14. • Involved in two- third of cases.
• Earliest lesion- fine or coarse granular spots with epithelial
bedewing forming a punctuate epithelial keratopathy.
• Within 12-24 hours cell nuclei become laden with
replicating virus and infected cell swells up prior to releasing
the virus into adjacent areas.
EPITHELIALKERATITIS

15. •Clinically manifests first as a
raised dendritiform lesion
that displaces fluorescein to
produce ‘negative staining’
but stains with Rose
Bengal.
•This progress to destruction
of Bowman’s Membrane
and forms dendritic ulcer.
(base stains with
fluorescein)
EPITHELIALKERATITIS

16. • Characteristic branching
linear shape with large
terminal bulbs and swollen
epithelial borders.
• Epithelial borders are areas
of epitheliolysis that stain
negative with fluorescein
but can be demarcated with
Rose Bengal or Lissamine
Green.
• Enlargement of ulcer leading
to Geographic (amoeboid)
ulcer in upto 22% of all
cases.
Amoeboid ulcer
EPITHELIALKERATITIS

17. • Patients with Marginal or
Limbal herpetic ulcers are
more symptomatic and less
responsive to treatment.
Resembles staphylococcal
catarrhal ulcer.
• Epithelial disease usually
resolves, sequelae may
ensue such as a persistent
punctate epithelial
keratopathy, recurrent
corneal erosions or
epithelial granularity.
EPITHELIALKERATITIS
Persistent Punctate Epithelial Keratopathy
Recurrent Corneal Erosion
Persistent Epithelial Defect

18. • Secondary bacterial infection of
ulcer may occur- many features
may no longer be recognized
• Impairment of corneal sensation
neurotrophic keratopathy with
loss of corneal lustre and
irregularity of corneal surface
• Punctate epithelial erosions may
develop and progress to
persistent epithelial or
metaherpatic ulcer with shallow
smooth borders of grey, elevated,
thickened and rolled epithelium.
It shows ‘reverse staining’.
• It is not associated with live virus.
EPITHELIALKERATITIS

19. • Accounts for 2% of initial
presentation and 20-48% of
recurrent herpetic disease.
• Viral invasion of stroma, either
from reactivation of latent virus
from direct invasion from
epithelium in the supplying sensory
nerves.
• Or from reactivation of latent virus
within stroma together with
marked immune response produce
stromal keratitis.
STROMALKERATITIS

20. •Necrosis, ulceration and dense infiltration of stroma
usually with an overlying epithelial defect
•HSV-1 antigens and HSV DNA are present.
•Grayish white homogenous abscesses with edema,
KPs, severe iridocyclitis and raised IOP.
•Super added infection may lead to thinning and
perforation.
NECROTIZINGKERATITIS

21. • Occurs in 20%.
• There may be no history of previous
symptomatic epithelial keratitis and
epithelium is usually intact.
• Focal, multifocal or diffuse.
• May have associated anterior uveitis.
• Chronic, recurrent or leading to stromal
scarring, thinning, neovascularisation and
lipid deposition.
• Occasionally an immune ring is present.
• Marginal keratitis or limbitis is usually
accompanied by inflammatory or
immune response.
• Stromal neovascularisation may be
sectoral or diffuse.
NONNECROTIZINGKERATITIS/
IMMUNEKERATITIS

22. • Disc-shaped area of
stromal edema in the
central or par central
cornea.
• Usually involving the
entire stromal thickness
giving a ground glass
appearance.
• KPs are present
underlying the areas of
stromal edema.
• Mild to moderate iritis is
usually present.
DISCIFORMKERATITIS

23. • Diffuse stromal edema with
underlying KPs.
• Mild-to-moderate iritis.
• Dense retro corneal plaque of
inflammatory cells may follow.
DIFFUSEKERATITISLINEARKERATITIS
• Appears as a serpiginous line of
KPs, that progresses centrally
from the limbus.
• Accompanied by peripheral
stromal and epithelial oedema.
Schwab et al, Interstitial Linear Keratitis, AJO, 1999.

24. •Progressive Endotheliitis
with or without uveitis
may be associated with
dendritic ulceration,
disciform edema or
marked elevation of IOP
•Pure HSV Endotheliitis is
characterized by line of
KPs demarcating
edematous and non-
edematous corneal
zones.
ENDOTHELITIIS

25. • Recurrent non granulomatous HSV iridocyclitis may
occur without known prior keratitis or without
concomitant keratitis.
• Due to inflammation caused either by reaction to viral
antigen in the iris or by irritative effects of keratitis.
• Circumlimbal ciliary flush, KPs, cells and flare in
aqueous.
• Multiple recurrence: diffuse iris atrophy, posterior
synechiae.
• High intraocular pressure is a common complication
of HSV iritis and can serve as a diagnostic hallmark.
• High IOP is due to trabeculitis, as well as inflammatory
cells clogging the trabecular meshwork.
• Although antiglaucoma therapy may be required in
the acute setting, once the inflammation is controlled,
typically the intraocular pressure will normalize and
the patient will not require ongoing antiglaucoma
treatment.
IRIDOCYCLITISAND
TRABECULITIS
Candy Cane Hypopyon

26. •Clinically active disease.
•Cutaneous lid or corneal lesions are
typical.
•Laboratory tests are aimed at :
oCell cytology
oViral antigen detection(Immunoassays)
oViral DNA detection(PCR)
oVirus isolation(Tissue Culture)
DIAGNOSIS

27. Progress in Retinal and Eye Research 25 (2006) 355–380
DIAGNOSIS

28. •Fever
•UV light
•Systemic illness, surgery
•Menstruation
•Minor local trauma
•Immunosuppression
•Contact Lens Use
REACTIVATIONFACTORS
Arch Ophthal 2000:118:1617-1625

29. • Prior to HEDS the standard therapy for all forms of
HSV keratitis was topical antivirals.
• The HEDS was undertaken to assess the effect of
adding steroids and acyclovir to conventional
therapy with trifluridine.
• It was a prospective, randomized, double masked,
placebo controlled, multicentric study derived into
six trials: three therapeutic, two preventive , and 1
cohort.
HEDS

30. HEDSIHEDSII

31. MEDICALMANAGEMENT
EPITHELIALKERATITIS

32. MEDICALMANAGEMENT
STROMALKERATITIS

33. MEDICALMANAGEMENT
ENDOTHELIALKERATITIS

34. MEDICALMANAGEMENT
PROPHYLAXIS

35. TROPHICULCERNOTRESPONDING
TOMEDICATION

36. •Topical steroids: 1% Prednisolone
•Mannitol/Glycerol/Acetazolamide for acute
IOP control
•Non prostamide analog antiglaucoma:
Brimonidine or a Beta blocker
•Cycloplegics
•Acyclovir 400mg BD
•Topical antibiotic ointment at bedtime
•Artificial tears
SECONDARYGLAUCOMADUETO
TRABECULITIS

37. •HSV Non Necrotizing stromal keratitis can be
treated with topical cyclosporine and acyclovir
ointment.
•Treatment of HSV stromal keratitis unresponsive
to topical prednisolone 1% with topical
cyclosporine 0.05% has also been demonstrated
in case series.
ROLEOFCYCLOSPORINE
Graefe's Arch Clin Exp Ophthalmol, May, 1999.
AJO 2006,141,771-772.

38. •Topical interferon alpha-2a appears to be an
effective treatment adjunct for refractory herpes
simplex keratitis.
•Actipol (0.007% paraaminobenzoic acid) is a new
interferon inductor. The reparogenic effect on the
corneal stroma and antithrombotic, fibrinolytic, and
antioxidant activity attributed to PABA.
•Effective drug for the treatment of stromal herpetic
keratitis
•No side effects.
ROLEOFINTERFERON
Cornea, May, 2000.
Vestn Oftalmol. 2000 Jan-Feb;116(2):16-8.

39. • The first antivirals, idoxuridine and vidarabine, seem better than no treatment in healing
HSV dendritic keratitis within two weeks.
• Topically applied trifluridine, acyclovir, or brivudine are better and safer than idoxuridine,
cure about 90% of treated eyes within two weeks, and have no significant differences in
effectiveness. The evidence is conflicting whether ganciclovir is as good as or better than
acyclovir.
• Interferon, a natural part of the immune system that can be given as an eye drop, is active
against HSV infection of the cornea.
• The integrated use of interferon and an antiviral drug might be slightly better than an
antiviral drug by itself.
• Another treatment is to debride, but debridement followed by an antiviral drug is not
consistently better than just an antiviral medication.

40. •Lateral tarsorrhaphy adjunctively with a
therapeutic lens
•Lamellar keratoplasty
•Conjunctival flap
•Penetrating keratoplasty
SURGICALMANAGEMENT

41. Surv Ophthalmol. 2012 Sep; 57(5): 448–462.
•HSV is one of the most important indication for repeat
PKP’s after primary graft failure.

42. •Procedure of choice for visual restoration of
significantly scarred or chronically inflamed
herpetic eyes
•Higher post op complications:
more corneal vascularisation, more epithelial defects,
lower corneal sensitivity, more graft rejection
episodes, and require larger grafts
Br J Ophthalmol. 2002 Jun;86(6):646-52
•Return of corneal sensitivity negligible
•Incidence of recurrence of keratitis
PENETRATINGKERATOPLASTY

43. •Use of fine, interrupted sutures.
•Use of intensive postoperative topical
steroids.
•Oral acyclovir prophylaxis for 12-18 months.
•Administration of full antiviral prophylaxis
during intensive topical steroid therapy for
graft rejection.
KEYTOGOODVISUALOUTCOME

44. • Once a visually disabling corneal scar
occurs options for improving vision are
limited to surgery either in the form of
penetrating or lamellar keratoplasty or
rarely photo keratectomy.
• Recurrence after PK -12% to 27%
• Incidence of newly acquired HSV
keratitis after PK is 14 fold higher than
in the general population.
• Antiviral prophylaxis translates to
treatment postoperatively.
• Both topical and systemic antivirals
have led to a significant reduction in
post-transplant recurrence of HSK.
RECURRENCEAFTERKERATOPLASTY

45. • It reviews three trials, current up to 2016, involving 126 participants, comparing the
use of oral acyclovir to no treatment or placebo.
• People in the studies either took antiviral medication for six months after the
corneal graft surgery or they took a placebo (or no treatment).
• The antiviral medication was oral acyclovir in all three studies but the dose varied
from 200 to 800 mg/day.
• The review concludes that oral acyclovir may lower the chance of herpetic keratitis
(low-certainty evidence). It may also reduce the risk of graft failure (low-certainty
evidence).
• Based on data from the included trials, this corresponds to approximately 23 fewer
cases of HSK recurrence per 100 corneal graft operations if oral acyclovir is used.
This also corresponds to approximately 13 fewer cases of graft failure per 100
corneal graft operations if oral acyclovir is used.

46. •Amniotic membrane
transplantation can be used
in severe neurotrophic
corneal ulcers.
•AMT promotes rapid
epithelialization and reduces
stromal inflammation and
ulceration in HSV-1 keratitis.
Br J Ophthalmol. 2000 Aug;84(8):826-33
ROLEOFAMNIOTICMEMBRANE

47. • Study to evaluate Quality of Life (QoL) in 33
patients with a unilateral and relapsing
herpes simplex keratitis (HSK group) that
was quiescent during evaluation (no acute
episode in the past 3 months) and compared
with 66 patients with no history of HSK.
• Even during a quiescent phase of the
disease, unilateral and relapsing HSK
significantly impairs the QoL of patients to a
similar level as most sight-threatening
diseases.
• The decrease of VA has the greatest overall
effect, but other factors also significantly
affect QoL, such as the frequency of
relapses.
Ophthalmology 2017;124:160-169

48. • The wide use of acyclovir for the treatment of genital, orofacial, and other herpetic diseases,
and the over-the-counter availability of the drug in certain countries, has raised concern over
the development of resistance, particularly in immunosuppressed patients.
• The mechanism of resistance in the majority of cases appears to be a mutation or deletion of
the thymidine kinase gene, which may be difficult to interpret due to gene polymorphisms.
• It appears that antiviral resistance remains low in immunocompetent individuals, likely
because the immune system drives the virus into a latent state, whereas resistance is much
higher in the immunocompromised.
• However there is no clear indication at this time that long-term prophylactic antivirals in the
form of nucleoside analogues should be avoided in the management of ocular herpes.
ACYCLOVIRRESISTANCE
Surv Ophthalmol. 2012 Sep; 57(5): 448–462.

49. • The estimated average overall incidence of HZ is about 3.4–4.82
per 1000 person years which increases to more than 11 per 1000
person years in those aged at least 80 years.
• Between 20% and 70% of patients with HZO develop
complications that can include blepharitis, keratoconjunctivitis,
iritis, scleritis and acute retinal necrosis.
• Neurological complications are less frequent than ocular
complications and may include ophthalmoplegia, optic neuritis
and ptosis.
HERPESZOSTER:
EPIDEMIOLOGY
Johnson, Robert W. et al. “Herpes Zoster Epidemiology, Management, and Disease
and Economic Burden in Europe: A Multidisciplinary Perspective.” Therapeutic
Advances in Vaccines 3.4 (2015): 109–120.

50. • Varicella zoster virus (VZV) belongs to the herpes virus family and
cause varicella that is the chickenpox and the herpes zoster that is
the shingles.
• The varicella zoster keratitis occurs in two forms:
• Primary (varicella)
• Recurrent (herpes zoster)
• The ocular manifestations are uncommon in varicella but common in
ophthalmic zoster.
• The various ocular manifestations in ophthalmic VZV include:
Eye lesions which are manifested as pocks on lids and lid margins.
Keratitis occurs rarely in cases of VZV.
Epithelial keratitis with or without pseudodendrites occurs more
rarely.
Disciform keratitis with uveitis of varying duration can occur.
VARICELLAZOSTER

51. • The rash of chickenpox begins as macules and progresses
to papules, vesicles, and then pustules that dry, crust over,
and may leave individual scars.
• Ocular involvement may include follicular conjunctivitis,
occasionally associated with a vesicular lesion on the
bulbar conjunctiva or eyelid margins.
• Punctate or dendritic epithelial keratitis is uncommon.
Although subepithelial infiltrates, microdendritic keratitis,
stromal keratitis, disciform keratitis, uveitis, and elevated
IOP are rare, recurrent varicella keratouveitis may cause
significant morbidity in some patients.
CLINICALPRESENTATION

52. • Laboratory confirmation of acute or recurrent VZV
infection is possible by immunodiagnostic methods, viral
culture, and PCR.
• Serologic testing is used primarily to identify varicella-
naive adults who might benefit from prophylactic
vaccination.
• As with HSV, scrapings from a vesicle base can be tested by
cytology, PCR, or culture, or for the presence of VZV
antigen.
• Conjunctival scrapings or corneal impression cytology
specimens can be similarly analyzed by culture, antigen
detection, or PCR.
DIAGNOSIS

53. • Because infected individuals shed the virus in respiratory
secretions before the onset of the characteristic rash,
avoiding infected persons is not always possible.
• Vaccination against varicella is recommended for anyone
older than 12 months without a history of chickenpox or
with a negative serology.
• The severity of signs and symptoms may be reduced in
clinically ill patients by the administration of oral acyclovir.
• Significant keratitis or uveitis can be treated with topical
corticosteroids.
MANAGEMENT

54. • Following primary infection, VZV establishes latency in
sensory neural ganglia. Zoster (shingles) represents
endogenous reactivation of latent virus in people with a
waning level of immunity to infection.
• Most patients are in their sixth to ninth decades of life,
and the majority are healthy, with no specific predisposing
factors.
• However, zoster is more common in patients on
immunosuppressive therapy; in those with a systemic
malignancy, a debilitating disease, or HIV infection; and
after major surgery, trauma, or radiation.
• However, herpes zoster in otherwise healthy children has
been described in the literature.
HERPESZOSTEROPHTHALMICUS

55. • Zoster manifests as a painful vesicular
dermatitis typically localized to a single
dermatome on the thorax or face.
• Patients may complain initially of fever
and malaise, and warmth, redness, and
increased sensation in the affected
dermatome.
• The most commonly affected
dermatomes are on the thorax (T3
through L3) and those supplied by CN V.
• The ophthalmic division of the trigeminal
nerve is affected more often than the
maxillary and mandibular branches, and
its involvement is referred to as herpes
zoster ophthalmicus (HZO)
HERPESZOSTEROPHTHALMICUS

56. OCULARINVOLVEMENT
• Ocular involvement occurs in more than 70% of
patients with zoster.
• Eyelid vesicular eruption can lead to secondary
bacterial infection, eyelid scarring, marginal notching,
loss of cilia, trichiasis, and cicatricial entropion or
ectropion.
• Both punctate and dendritic epithelial keratitis
caused by viral replication in corneal epithelium are
common manifestations.
• Diminished corneal sensation develops in up to 50%
of patients.
• Nummular corneal infiltrates are said to be
characteristic of zoster stromal keratitis but the
interstitial keratitis, disciform keratitis, and anterior
uveitis with increased IOP in HZO are clinically
indistinguishable from those caused by HSV infection.
Liesegang TJ. Herpes zoster ophthalmicus: natural history, risk factors, clinical
presentation, and morbidity. Ophthalmology.2008;115(2 Suppl):S3–S12.

57. HERPESSIMPLEXVSZOSTER

58. COMPLICATIONSOFHZO • Focal choroiditis, occlusive retinal vasculitis, and retinal
detachment have been reported.
• Ipsilateral acute retinal necrosis (ARN) temporally
associated with HZO is uncommon.
• Orbital or central nervous system (CNS) involvement as a
result of an occlusive arteritis may lead to eyelid ptosis,
orbital edema, and proptosis.
• Papillitis or retrobulbar optic neuritis may also develop.
Cranial nerve palsies, when meticulously investigated, have
been reported to occur in up to one-third of cases of HZO,
with CN III (oculomotor) most commonly affected.
• Systemic dissemination is unusual in immunocompetent
patients but can occur in up to 25% of those who are
immunocompromised.

59. MANAGEMENT
• Oral antiviral therapy for HZO reduce viral shedding from
vesicular skin lesions, reduce the chance of systemic
dissemination of the virus, and decrease the incidence and
severity of the most common ocular complications.
• Oral antiviral therapy may reduce the duration if not the
incidence of postherpetic neuralgia if begun within 72
hours of the onset of symptoms.
• A varicella-zoster vaccine was approved by the US FDA,
after testing in 38,000 patients showed a 50% reduction in
incidence of zoster and a 66% reduction in postherpetic
neuralgia.
• The vaccine is recommended for immunocompetent
individuals older than 60 years but was recently made
available to those aged 50 years and older.
Schmader KE, Levin MJ, Gnann JW Jr, et al. Efficacy, safety, and tolerability of herpes zoster vaccine
in persons aged 50–59 years. Clin Infect Dis. 2012;54(7):922–928.

60. MANAGEMENT
• The current recommendation for HZO is oral famciclovir 500
mg 3 times per day, valacyclovir 1g 3 times per day, or
acyclovir 800 mg 5 times per day for 7–10 days, best if
started within 72 hours of the onset of skin lesions.
• Intravenous acyclovir therapy(10 mg/kg every 8 hours) is
indicated in patients at risk for disseminated zoster due to
immunosuppression.
• Cutaneous lesions may be treated with moist warm
compresses and topical antibiotic ointment.
• Topical corticosteroids and cycloplegics are indicated for
keratouveitis.
• Oral corticosteroids are recommended by some for treating
patients with HZO over age 60 to reduce early zoster pain
and facilitate a rapid return to a normal quality of life.

61. POSTHERPETICNEURALGIA • Postherpetic neuralgia (PHN) may respond to capsaicin
cream applied to the involved skin, but low doses of
amitriptyline, desipramine, clomipramine, or
carbamazepine may be necessary to control severe
symptoms.
• Gabapentin (Neurontin) and pregabalin (Lyrica) have
recently been shown to be efficacious in managing PHN.
• Aggressive lubrication with nonpreserved tears, gels,
and ointments, combined with punctal occlusion and
tarsorrhaphy as necessary, may be indicated for
neurotrophic keratopathy.
• In a patient with significant pain, early referral to a pain
management specialist should be considered.

62. • It is causative agent for epidemic
keratoconjunctivitis which is predominantly
caused by the serotypes 8, 19, and 37.
• The infection is highly contagious.
• In Stage I corneal vesicles are present which are
25 to 30 microns and barely perceptible on slit
lamp.
• In Stage II, the lesions coalesce with each other ,
become clearly visible on slit lamp. These are the
classical deep epithelial punctuate keratitis
lesions which may resolve or progress further.
• In Stage III faint subepithelial infiltrates are
present beside the deep punctate keratitis.
• Stage IV is characterized by nummular opacities
which may be present months to weeks after the
initial episode
ADENOVIRALKERATITIS

63. •Supportive management of epidemic
keratoconjunctivitis includes the following:
Artificial tears
Cold compresses
Cycloplegic agents for severe photophobia
Topical corticosteroids
Topical agents that have antiviral activity
•Depending on the severity of the signs and
symptoms, patients should be followed up in
several days to weeks.
MANAGEMENT

64. • Cytomegalovirus (CMV) is a ubiquitous
herpesvirus that infects over 90% of humans
by age 80.
• Spread of CMV occurs through the sharing of
saliva, ingestion of breast milk, or sexual
contact.
• Recently, CMV has been increasingly
identified as a significant cause of anterior
uveitis and corneal endotheliitis.
• The anterior uveitis is characterized by an
acute or chronic iritis, with moderate to
severe rises in IOP that are variably
responsive to topical corticosteroids.
• The addition of keratic precipitates,
endothelial cell loss, and diffuse or local
corneal edema suggests CMV endotheliitis.
CMVKERATITIS

65. • Laboratory confirmation of disease is usually
accomplished through PCR testing of aqueous humor for
CMV.
• Aqueous humor is obtained by an anterior chamber tap,
which must be performed during an episode of active
disease.
DIAGNOSISMANAGEMENT
• CMV-associated anterior segment disease is treated with
ganciclovir and is not responsive to famciclovir, acyclovir, or its
derivatives.
• Resistance of a presumed HSV infection to these agents should
raise the suspicion of CMV.
• Recurrence can occur after keratoplasty. The role of corticosteroids
is unclear, as there is some suggestion that steroid use may
prolong or worsen CMV-associated anterior segment disease.

66. CONCLUSION
•Viral Keratitis is an important cause of considerable
ocular morbidity and loss of Quality of Life.
•Viral Keratitis can be managed effectively with good
observation, attention to details and good
therapeutic regime according to prescribed
guidelines.
•Steroids and Antivirals form the mainstay of
management for Viral Keratitis if used effectively
with newer modalities like interferons, cyclosporine
and interferon modulators.