HERPES ZOSTER OTICUS

RANDHEER KUMAR ANNARAPU

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 tympanic membrane, meatalskin,concha and posterior auricular groove.

• When associated with facial paralysis, the infection is called Ramsay Hunt syndrome.

ETIOLOGY

• 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.

• Causative agent: reactivated Varicella Zoster Virus

• Family: Herpeviridae (alphaherpevirinae)

• Structure: enveloped,icosahedrallinear ds DNA

RAMSAY HUNT SYNDROMES

• Ramsay Hunt Cerebellar Syndrome –cerebellar degeneration involving myoclonic epilepsy, progressive ataxia, tremors and a dementing process.

• Ramsay Hunt Syndrome II- reactivation of the herpes zoster in the geniculate ganglion.

• Ramsay Hunt Syndrome III-occupationally induced neuropathy of deep palmar branch of ulnar nerve.

• 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.

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) VII to CN VIII at the cerebellopontine angle or via vasa vasorum that travel from CN VII to other nearby cranial nerves.

CLINICAL MANIFESTATIONS

Patient history

• Painful, burning blisters on the tympanic membrane,meatal skin,concha,posteriorauricular sulcus, on the face, in the mouth, and/or on the tongue

• Vertigo, nausea, vomiting

• Hearing loss, hyperacusis, tinnitus

• Eye pain, lacrimation

• 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.

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.

• One sided weakness of face, facial drooping or eyelid drooping, difficulty in chewing food on the ipsilateralside.

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.

Complications

• Postherpetic neuralgia

• Residual paralysis

• Rarely, herpes zoster encephalitis

TESTS

• Herpes zoster oticus (HZ oticus) is primarily a clinical diagnosis in the emergency department.

• 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

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.

1. Antiviral agents

• 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.

• 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.Studies have shown no difference between oral and IV acyclovir in immunocompetent patients with facial nerve paralysis.

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(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) to facial nerve function and prevention of nerve degeneration than treatment with prednisone alone.

• However, only a very little data has been uncovered to support or negate this theory.

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 multidermatomalinvolvement. 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.

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.

• 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.

Emergency department care

• Adequate analgesia is important for individuals with significant pain from herpes zoster. Nausea and vomiting may require emergency department 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.

Consider admission for any of the following situations:

• Severe symptoms

• Involvement of multiple (>2) dermatomes

• Immunocompromised

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