Interesting Case

Dendritic Keratitis

Yohanes Firmansyah
406162018

Supervisor:
dr. Soviana, Sp.M

Ophthalmology Department Sumber Waras Hospital

Faculty of Medicine Tarumanagara University
2018
 Patient’s General Information
• Title : Mr
• Full name :S
• Date of birth : March 6th, 1977
• Place of birth : Klaten
• Gender : Male
• Address : Jl. Bugem RT 01/ RW 03.
• Occupation : Cleaning Service
• Education : Junior High School
• Marital Status : Married
• Religion : Mosloem
• Race : Sundaenese
 Anamnesis
• Auto-anamnesis is done on May 12nd, 2018 in
Ophthalmology Department Sumber Waras
Hospital

• Chief complaint: Decreased vision on right eye

since one week ago
 History of Present Illness
• Patient came to Ophthalmology Department of
Sumber Waras Hospital complaining about his
decreased vision since one week ago. He complains
that he has blurred vision and unclear view. It
happened mostly every time especially in his right eye
and keep getting worse.

• He complains that he has redness, watering and mild

discomfort in his right eye. It was only happened when
day time or working time.
• He didn’t complain any pain, itchy, dizziness and
headache, nausea and vomit.
 Anamnesis
• He had been diagnosed with Ocular Chemical
Injury (Porstex) previously from general
practioner (workplace) and ophthalmologist at
RS Sumber Waras, Jakarta.
 Anamnesis
• Family history:
– no family member experience the same complaint

• Eye history:
– History of eye surgery or trauma
– No History of Contact Lens

• Medical history: Hypertension (-), NIDDM (-), CHF

(-), Varisela (+) when Junior High School

• Social history: smoking (+), alcohol (-)

 Physical Examination
• Visual Acuity:
– VOD : 6/20 ; PH 6/15
– VOS : 6/6
 OD OS
Benjolan (-) Benjolan (-)
Edema (-) Edema (-)
Hiperemis (-) Hiperemis (-)
Palpebra Ptosis (-) Ptosis (-)
Lagophthalmus (-) Lagophthalmus (-)
Ectropion (-) Ectropion (-)
Entropion (-) Entropion (-)

Physical Warna: transparan Warna: transparan

Vaskularisasi: Vaskularisasi:

Examination Bulbi
injeksi (+)
Nodul (-)
injeksi (-)
Nodul (-)
Edema (-), kemosis Edema (-), kemosis
Conjunctiva
(-). Pigmentasi (+) (-), Pigmentasi (+)
Hiperemis (-) Hiperemis (-)
Folikel (-) Folikel (-)
Tarsal
Papil (-) Papil (-)
Korpus alineum (-) Korpus alineum (-)
Sclera Warna: putih Warna: putih
Inflamasi (-) Inflamasi (-)
 Kejernihan: jernih Kejernihan: jernih
Stellate lesions and bed Infiltrat (-)
of dendritic ulcer stained Defek (-)
Cornea
with fluorescein Edema (-)
(geographic Ulcer)
Edema (-)
Kedalaman: cukup Kedalaman: cukup
Anterior Chamber Hifema (-) Hifema (-)

Physical Hipopion (-)

Warna: coklat
Hipopion (-)
Warna: coklat

Examination Iris
Sinekia (-)
Iridodenesis (-)
Sinekia (-)
Iridodenesis (-)
Neovaskularisasi (-) Neovaskularisasi (-)
Ukuran: 3 mm Ukuran: 3 mm
Bentuk: bulat, simetris Bentuk: bulat, simetris
Reflex cahaya langsung (+) Reflex cahaya langsung
Pupil
Reflex cahaya tidak (+)
langsung (+) Reflex cahaya tidak
langsung (+)
Kejernihan: jernih Kejernihan: jernih
Lens Luksasio (-) Luksasio (-)
IOL (-) IOL (-)
 Physical Examination
• Visual field: no visual field defects

• Extraocular muscles: no extraocular muscles

defects

• Intra-Ocular Pressure (IOP):

– OD : 13
– OS : 14
 Direct Ophthalmoscopy
• OD
– Cup-to-disc ratio 0.3
– A:V ratio 2/3
– Macula light reflex (+)
– No retinal tear, bleeding, exudate, neovascularization
• OS
– Cup-to-disc ratio 0.3
– A:V ratio 2/3
– Macula light reflex (+)
– No retinal tear, bleeding, exudate, neovascularization
Slit Lamp + Fluorescent
Slit Lamp + Fluorescent
 Diagnosis
• Working Diagnosis:
– Epithelial Keratitis (Dendritic Keratitis) ec susp. HSV 1

• Differential Diagnosis
– Herpes Zoster Keratitis
– Healing Corneal Abrasion (pseudo-dendrite)
– Acanthamoeba keratitis
– Toxic keratopathy secondary to topical medications
 Treatment
• Medical
– Acyclovir 3% ointment
– Artificial Tears
 Prognosis
• Ad vitam : Bonam
• Ad sanationam : dubia ad malam
• Ad functionam : dubia ad malam
CASE ANALYSIS
HERPES SIMPLEX KERATITIS
 Epithelial Keratitis (Dendritic)
• Definition
– Herpes simplex virus (HSV) keratitis is an infectious
disease of the cornea.
– Herpetic eye disease is the most common infectious
cause of corneal blindness in developed countries.
 Epithelial Keratitis (Dendritic)
• Epidemiology
– As many as 60% of corneal ulcers in developing
countries may be the result of herpes simplex virus
and 10 million people worldwide may have herpetic
eye disease.
 Herpes Simplex Virus (HSV)
• HSV is enveloped with a cuboidal capsule and has
a linear doublestranded DNA genome.
• The two subtypes are HSV-1 and HSV-2, and
these reside in almost all neuronal ganglia.
• HSV-1 causes infection above the waist
(principally the face, lips and eyes), whereas HSV-
2 causes venereally acquired infection (genital
herpes).
• Rarely HSV-2 may be transmitted to the eye
through infected secretions, either venereally or
at birth (neonatal conjunctivitis).
 Primary Infection
• HSV transmission is facilitated in conditions of
crowding and poor hygiene.
• Primary infection, without previous viral exposure,
usually occurs in childhood and is spread by droplet
transmission, or less frequently by direct inoculation.

• Due to protection by maternal antibodies, it is

uncommon during the first 6 months of life, though
occasionally severe neonatal systemic disease may
occur in which early diagnosis and intravenous antiviral
treatment are critical to reduce mortality and
disability; the presence of maternal antibodies means
that dendritic corneal ulcers may be seen.
 Primary Infection – Sign and
Symptons
• Most primary infections with HSV are subclinical
or cause only mild fever, malaise and upper
respiratory tract symptoms.
• Blepharitis and follicular conjunctivitis may
develop but are usually mild and selflimited.
• Treatment, if necessary, involves topical aciclovir
ointment for the eye and/or cream for skin
lesions, and occasionally oral antivirals.
• There is unfortunately no evidence that antiviral
treatment at this stage reduces the likelihood of
recurrent disease.
 Reccurent Infection
(reactivation in the presence of cellular andhumoral
immunity)
1. After primary infection the virus is carried to
the sensory ganglion for that dermatome
(e.g. trigeminal ganglion) where latent
infection is established. Latent virus is
incorporated in host DNA and cannot be
eradicated with presently available
treatment.
2. Subclinical reactivation can periodically
occur, during which HSV is shed and patients
are contagious.
 Clinical reactivation
A variety of stressors such as
• Fever, hormonal change,
• Ultraviolet radiation, trauma,
• Trigeminal injury

May cause clinical reactivation, when the virus

replicates and is transported in the sensory
axons to the periphery.
 The pattern of disease
Depends on the site of reactivation, which may
be remote from the site of primary disease.
Hundreds of reactivations can occur during a
lifetime.
 The rate of ocular recurrence
• After one episode is about 10% at 1 year and
50% at 10 years.
• The higher the number of previous attacks the
greater the risk of recurrence.
 Risk factors for severe disease
• Recurrent, include atopic eye disease,
childhood,
• Immunodeficiency or suppression,
malnutrition,
• Measles and malaria.
• Inappropriate use of topical steroids may
enhance the development of geographic
ulceration
 Morphology of Herpes Simplex
Keratitis (1)
• Epithelial Keratitis
 Morphology of Herpes Simplex
Keratitis (2)
• Disciform Keratitis
 Morphology of Herpes Simplex
Keratitis (3)
• Necrotizing Stromal Keratitis
EPITHELIAL KERATITIS
 Epithelial Keratitis
• Epithelial (dendritic or geographic) keratitis is
associated with active virus replication.
• Presentation:
– May be at any age
– Mild–moderate discomfort,
– redness,
– photophobia,
– watering
– blurred vision.
 Sign of Epithelial Keratitis (1)

Swollen opaque
epithelial cells arranged
in a coarse punctate or
stellate pattern.
 Sign of Epithelial Keratitis (2)
Central desquamation
results in a linear-
branching (dendritic)
ulcer, most frequent
located centrally; the
branches of the ulcer
have characteristic
terminal buds and its bed
stains well with
fluorescein.
 Sign of Epithelial Keratitis (3)
• The virus-laden cells at
the margin of the ulcer
stain with rose Bengal,
and this may help
distinction from
alternative diagnoses,
particularly an atypical
recurrent corneal
abrasion.
 Sign of Epithelial Keratitis (4)
• Inadvertent topical
steroid treatment may
promote progressive
enlargement of the
ulcer to a geographical
or ‘amoeboid’
configuration
 Sign of Epithelial Keratitis (5)
• Corneal sensation is reduced.
• Mild associated subepithelial haze is typical.
• Anterior chamber activity may be present, but is
usually mild.
• Follicular conjunctivitis may be associated; topical
• antivirals can also cause this.
• Vesicular eyelid lesions may coincide with epithelial
ulceration.
• Elevated IOP is not uncommon (tonometry should be
performed on the unaffected eye first; a disposable
prism should be used, or a re-usable tonometer prism
carefully disinfected after use).
 Sign of Epithelial Keratitis (6)
• Following healing, there
may be persistent punctate
epithelial erosions and
irregular epithelium which
settle spontaneously and
should not be mistaken for
persistent active infection.
• A whorled epithelial
appearance commonly
results from assiduous,
especially prolonged,
topical antiviral instillation.
 Sign of Epithelial Keratitis (7)
• Mild subepithelial haze
may persist for weeks
after the epithelium
heals;
• in some cases mild
scarring may develop,
which tends to become
more evident after each
recurrence and may
eventually substantially
threaten vision.
 Investigations
• Generally unnecessary as the diagnosis is
principally clinical, but pre-treatment scrapings
can be sent in viral transport medium for culture.
• PCR and immunocytochemistry are also available.
Giemsa staining shows multinucleated giant cells.
• HSV serological titres rise only on primary
infection, but can be used to confirm previous
viral exposure, usually in cases of stromal disease
when the diagnosis is in doubt.
 Differential diagnosis
• Herpes zoster keratitis,
• Healing corneal abrasion (pseudodendrite),
• Acanthamoeba keratitis,
• Epithelial rejection in a corneal graft,
• Tyrosinaemia type 2,
• The epithelial effects of soft contact lenses,
• Toxic keratopathy secondary to topical
medication.
 Treatment
• Treatment of HSV disease is predominantly
with nucleoside (purine or pyrimidine)
analogues that disrupt viral DNA.
• The majority of dendritic ulcers will eventually
heal spontaneously without treatment,
though scarring and vascularization may be
more significant.
 Topical Medicine
• The most frequently used drugs are aciclovir 3%
ointment and ganciclovir 0.15% gel, each administered
five times daily.
• Trifluridine is an alternative but requires instillation up
to nine times a day.
• The drugs are relatively non-toxic, even when given for
up to 60 days.
• They have approximately equivalent effect, acting
preferentially on virus-laden epithelial cells, and
penetrating effectively into the stroma; 99% of ulcers
heal within two weeks.
• Idoxuridine and vidarabine are older drugs that are
probably less effective and more toxic.
 Debridement
• May be used for resistant cases.
• The corneal surface is wiped with a sterile cellulose
sponge or cottontipped applicator (cotton bud).
• Epithelium should be removed 2 mm beyond the edge
of the ulcer, since involvement extends beyond the
visible dendrite.
• The removal of the virus-containing cells protects
adjacent healthy epithelium from infection and
eliminates the antigenic stimulus to stromal
inflammation.
• A topical antiviral agent should be used in conjunction.
 Signs of treatment toxicity
• superficial punctate erosions,
• waves of whorled epithelium,
• follicular conjunctivitis and, rarely, punctal
occlusion.
• Absence of epithelial whorling with a
persistent epithelial lesion raises the
possibility of poor or non-compliance.
 Interferon monotherapy
• Interferon monotherapy does not seem to be
more effective than antivirals, but the
combination of a nucleoside antiviral with
either interferon or debridement seems to
speed healing.
 Others (1)
• Skin lesions may be treated with aciclovir cream five times
daily, as for cold sores, and if extensive an oral antiviral may
be given.
• Cycloplegia, e.g. homatropine 1% once or twice daily can
be given to improve comfort if necessary.
• Topical antibiotic prophylaxis is recommended by some
practitioners.
• IOP control. If glaucoma treatment is necessary,
prostaglandin derivatives should probably be avoided as
they may promote herpes virus activity and inflammation
generally.
• Topical steroids are not used unless significant disciform
keratitis is also present
 Others (2)
• Slow healing or frequent recurrence may indicate
the presence of a resistant viral strain, and an
alternative topical agent or debridement may be
tried.
• In especially refractory cases, a combination of
two topical agents with oral valaciclovir or
famciclovir may be effective.
• A significant minority of resistant cases are due to
varicella-zoster virus.
 References
• White LW, Chodosh J; Herpes Simplex Virus Keratitis : A
Treatment Guideline. Charles Street. 2014; 20: 4 - 30
• Kanski JJ. Clinical Opthalmology – A Systemaatic Approach 8
th ed. Butterworth-Heinemann; Sydney : Elsevier ; 2015
THANK YOU