1. HERPES ZOSTER OTICUS
• Herpes zoster oticus (HZ oticus) is a viral
infection of the inner, middle, and external
ear.
• HZ oticus manifests as severe otalgia and
associated cutaneous vesicular eruption,
usually of the external canal and pinna.
• When associated with facial paralysis, the
infection is called Ramsay Hunt syndrome.
2. • Ramsay Hunt syndrome accounts for up to
12% of all facial paralyses and generally causes
more severe symptoms and has a worse
prognosis than Bell palsy.
• An additional complication of herpes zoster
viral infection is postherpetic neuralgia.
• The incidence rates of HZ oticus in males and
females are equal, and incidence increases
significantly in patients older than 60 years.
3. PATHOPHYSIOLOGY
• Reactivation of the varicella-zoster virus (VZV)
along the distribution of the sensory nerves
innervating the ear, which usually includes the
geniculate ganglion, is responsible for herpes
zoster (HZ) oticus.
• Associated symptoms, such as hearing loss and
vertigo, are thought to occur as a result of
transmission of the virus via direct proximity of
cranial nerve (CN) VIII to CN VII at the
cerebellopontine angle or via vasa vasorum that
travel from CN VII to other nearby cranial nerves.
5. Patient history
• Painful, burning blisters in and around the ear,
on the face, in the mouth, and/or on the
tongue
• Vertigo, nausea, vomiting
• Hearing loss, hyperacusis, tinnitus
• Eye pain, lacrimation
6. • Onset of pain may precede the rash by several
hours or days. Also, in patients with Ramsay Hunt
syndrome, vesicles may appear before, during, or
after facial palsy (zoster sine herpete).
• When asked, patients may recall a distant history,
perhaps in childhood, of chickenpox (varicella).
• A minority of patients (< 10%) give a history of
previous herpes zoster viral infection.
7. Physical examination
• Physical examination shows a vesicular exanthem,
usually of the external auditory canal, concha, and
pinna. The rash also may appear on postauricular skin,
lateral nasal wall, soft palate, and anterolateral tongue.
• Vertigo and sensorineural hearing loss may be noted,
and paralysis of the facial nerve, mimicking Bell palsy,
may be present. Complete loss of the ability to wrinkle
the ipsilateral brow distinguishes a peripheral lesion of
cranial nerve VII from a central lesion of the same
nerve, which spares the forehead.
8. Associated findings include the following:
• Dysgeusia (alteration in taste)
• Inability to fully close the ipsilateral eye, which
may lead to the occasional presentation of
drying and irritation of the cornea.
11. • Herpes zoster (HZ) oticus is caused by the
reactivation of latent varicella-zoster virus (VZV)
that has remained dormant within sensory
ganglia (commonly the geniculate ganglion) of
the facial nerve. Individuals with decreased cell-
mediated immunity resulting from carcinoma,
radiation therapy, chemotherapy, or HIV infection
are at greater risk for reactivation of latent VZV.
• Physical stress and emotional stress often are
cited as precipitating factors.
14. TESTS
• Herpes zoster oticus (HZ oticus) is primarily a
clinical diagnosis in the ED.
• Prior to initiating treatment with acyclovir,
consider a baseline set of the following
laboratory studies:
1. Blood urea nitrogen (BUN)
2. Creatinine
3. Blood cell counts
4. Electrolytes
15. TREATMENT
Until recently, therapy for herpes zoster (HZ)
oticus has been generally supportive,
including warm compresses, narcotic
analgesics, and antibiotics for a secondary
bacterial infection.
16. 1. Antiviral agents
• Antiviral agents clearly play a role in limiting the severity and
duration of symptoms if given early in the course of the illness.
Early administration (< 72 h) of acyclovir showed an increased rate
of facial nerve function recovery and prevented further nerve
degeneration. Furthermore, use of antivirals has been shown to
decrease the incidence and severity of postherpetic neuralgia.[7, 8, 9,
4]
• Evidence is accumulating that varicella-zoster virus (VZV) may be
responsible for many cases of Bell palsy that go unrecognized
because of a lack of cutaneous findings (zoster sine herpete).
Accordingly, the clinician should entertain more liberal use of
antivirals such as acyclovir, valacyclovir, and famciclovir.[2, 3] Studies
have shown no difference between oral and IV acyclovir in
immunocompetent patients with facial nerve paralysis.[10]
17. 2. Corticosteroids
• Systemic corticosteroids are used to relieve acute pain,
decrease vertigo, and limit the occurrence of postherpetic
neuralgia. The prevailing wisdom states that treatment with
acyclovir plus prednisone has more effective return to facial
nerve function and prevention of nerve degeneration than
treatment with prednisone alone; however, a recent review
uncovered very little data to support or negate this
theory.[7] Patients treated with acyclovir plus prednisone
had better outcomes (time to healing of rash, time to
cessation of acute neuritis, time to return to usual activity
and sleep, and time to cessation of analgesics) than those
treated with either prednisone or acyclovir alone.
18. Treatment in HIV patients
• For treatment of herpes zoster in patients with HIV,
inpatient parenteral regimens should be reserved for those
with severe immunosuppression, trigeminal nerve
involvement, ocular lesions, or multidermatomal
involvement. Treatment of VZV is the same for both HIV-
seronegative and seropositive patients. For acyclovir-
resistant VZV, IV foscarnet is an appropriate alternative
therapy (famciclovir and valacyclovir are not effective
against acyclovir-resistant VZV). For outpatient regimens,
famciclovir or valacyclovir for 7-10 days is recommended
(both have the advantage of easier dosing regimens).
Routine use of steroids is discouraged secondary to its
immunosuppressive effects.
19. Treatment in other situations
• Treatment of pregnant women with VZV is the
same as that of nonpregnant women.
• When secondary impetigo is present, a suitable
antistaphylococcal antibiotic should be
prescribed.
• Cyclic antidepressants, anticonvulsants, opioids,
and topical analgesics are sometimes used in the
treatment of postherpetic neuralgia.[4] These
agents are more appropriately started by a pain
management specialist in an outpatient setting.
20. • Prevention of herpes zoster by vaccination is
recommended for all persons older than 60
years, even if they have had chickenpox or
zoster in the past. This age group suffers
significant morbidity from zoster and may,
therefore, benefit from the vaccine.
Contraindications to vaccine administration
include age younger than 60 years, current
use of antivirals, pregnancy, and certain
immunosuppressive conditions.
21. Emergency department care
• Adequate analgesia is important for
individuals with significant pain from herpes
zoster. Nausea and vomiting may require ED
treatment. Complications, such as corneal
irritation or secondary bacterial infection of
the vesicles, should be managed with routine
therapies. Involvement of more than one
dermatome is atypical and should prompt the
search for possible immunoincompetence.
22. Consider admission for any of the following
situations:
• Severe symptoms
• Involvement of multiple (>2) dermatomes
• Immunocompromised
