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 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 13  |  Issue : 3  |  Page : 215-220

Herpes zoster oticus among pediatric patients: Our experiences at a tertiary care teaching hospital


1 Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University, Bhubaneswar, Odisha, India
2 Department of Pediatrics, IMS and SUM Hospital, Siksha “O” Anusandhan University, Bhubaneswar, Odisha, India

Date of Submission25-Mar-2020
Date of Acceptance13-Jul-2020
Date of Web Publication05-Oct-2020

Correspondence Address:
Prof. Santosh Kumar Swain
Department of Otorhinolaryngology, IMS and SUM Hospital, Kalinga Nagar, Bhubaneswar - 751 003, Odisha
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/kleuhsj.kleuhsj_100_20

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  Abstract 

Introduction: Herpes zoster oticus (HZO) occurs due to the reactivation of the varicella zoster virus (VZV) in the geniculate ganglion of the facial nerve. It is characterized by erythematous vesicular eruptions on the pinna and external auditory canal with severe otalgia. When it is associated with ipsilateral facial nerve paralysis, a diagnosis of Ramsay Hunt syndrome (RHS) can be made. It is rare in the pediatric age group but with low immunity, so prone for increased risk of disseminated infections, neurological complications, and recurrence of infections.
Objective: The aim of this study was to evaluate the clinical profile and management of the HZO among pediatric patients at a tertiary care teaching hospital.
Materials and Methods: In this prospective study, 24 pediatric patients of HZO were reviewed those presented during the period of December 2015–January 2020. All pediatric patients underwent thorough clinical examinations before getting the diagnosis. All the participants also underwent thorough neuro-otological and otolaryngological examinations.
Results: Out of 24 pediatric patients, 15 were boys and 9 were girls. All were in the pediatric age group with age ranging from 5 years to 16 years. After the diagnosis of HZO/RHS, all were treated with acyclovir for 10 days along with tapering dose of deflazacort, labyrinthine sedatives, and eye care in case of facial palsy. All the pediatric patients were recovered by our treatment protocol except 3 cases those are still in follow-up with facial weakness.
Conclusions: Adequate awareness for the HZO in pediatric patients is required, and the management of RHS patients is paramount among pediatrician or pediatric otorhinolaryngologists.

Keywords: Facial nerve palsy, herpes zoster oticus, pediatric patients, Ramsay hunt syndrome


How to cite this article:
Swain SK, Choudhury J, Acharya S. Herpes zoster oticus among pediatric patients: Our experiences at a tertiary care teaching hospital. Indian J Health Sci Biomed Res 2020;13:215-20

How to cite this URL:
Swain SK, Choudhury J, Acharya S. Herpes zoster oticus among pediatric patients: Our experiences at a tertiary care teaching hospital. Indian J Health Sci Biomed Res [serial online] 2020 [cited 2020 Oct 23];13:215-20. Available from: https://www.ijournalhs.org/text.asp?2020/13/3/215/297181


  Introduction Top


Herpes zoster oticus (HZO) is characterized by erythematous vesicular rashes on the pinna and external auditory canal with severe otalgia. When it is associated with ipsilateral facial nerve paralysis, a diagnosis of Ramsay Hunt syndrome (RHS) can be done. HZO is a viral infection characterized by severe otalgia and erythematous vesicular rashes on the pinna and in the external auditory canal. In RHS, the facial nerve paralysis occurs due to inflammation of the facial nerve by reactivation of the varicella zoster virus (VZV). The primary infection of the VZV causes chicken pox. The presence of the VZV in the vesicles on either pinna or tongue often enter the sensory fibers of the facial nerve and travel to the geniculate ganglion, where the virus remains latent. On reactivation, VZV moves back through the sensory branches of the facial nerve toward the auricular and external auditory canal and makes rash. During the same time, the adjacent motor branches of the facial nerve are inflamed, causing facial palsy.[1] The reactivation of the latent VZV is triggered by low cell-mediated immunity of the host.[2] There is perivascular, perineural, or intraneural aggregations of the inflammatory cells such as round cells in the facial nerve have been seen in the patients of RHS.[3] There are certain neurological complications include alterations in cerebrospinal fluids (CSFs), peripheral motor neuropathy, aseptic meningitis, and cranial neuropathy.[4] Out of these, vestibulocochlear symptoms such as vertigo, tinnitus, and hearing loss are common among patients with RHS. RHS shows poor prognosis for recovery of the facial nerve palsy in comparison to idiopathic facial nerve palsy (Bell's palsy).[5] The vestibulocochlear symptoms such as hearing loss, vertigo, and tinnitus are often found in patients with HZO or RHS. RHS was first described in 1907 which included vesicular rash, otalgia, inner ear dysfunction, and facial palsy.[6] Although HZO is rarely found in clinical entity, it is more often seen in immunocompromised patients. It is very important for clinicians to suspect, diagnose, and manage the HZO among pediatric patients. However, there have been, to our best of knowledge, not many studies that emphasized on pediatric HZO in this region of the world. The purpose of this study is assessing the clinical manifestations and management of the pediatric HZO, although these are rarely found in day-to-day clinical practice.


  Materials and Methods Top


We evaluated 24 pediatric patients of HZO those attended the outpatient department of otorhinolaryngology during the period between December 2015 and January 2020. This prospective study was approved by the Institutional Ethical Committee (IEC) with reference number IEC/IMS/SOAU/72/2014. Out of 24 pediatric patients, 15 were male and 9 were female. All the patients of HZO were diagnosed accompanying at least one of the symptoms of 7th and 8th cranial nerve dysfunction (CN VII and CN VIII). All were pediatric patients with age range from 5 years to 16 years. All the patients underwent thorough clinical examinations by pediatricians and otorhinolaryngologists before coming to the diagnosis. All the participants also underwent thorough neuro-otological and otolaryngological examinations. Those with prior history of neuro-otological diseases or otologic surgery in either ear were excluded from this study. Immune status of the children and their parents was evaluated. Parents were asked regarding the chicken pox of the children earlier. One patient was diagnosed with acute myeloid leukemia and just completed immunosuppressive chemotherapy. Birth histories of all the children were uneventful. There was no history of the herpes infections among the parents of the children with HZO. Patients with chronic ear discharge, headache, weakness of the limbs, and seizures were excluded from this study. All the children were examined for hearing loss, tinnitus, facial weakness, and vertigo. Tzanck smears were taken from the lesions over the pinna and external auditory canal which showed giant cells. All the study patients underwent pure-tone audiometry (PTA) for the assessment of hearing. A bithermal caloric test was performed by irrigating with a constant flow of water at alternating temperatures of 30°C and 44°C for a period of 30 s in each ear. Using an infrared video-based system (CHARTR VNG, ICS Medical, Schaumburg), the maximum slow-phase velocity of nystagmus was calculated. Jongkees' formula was utilized for determining the canal paresis (CP), and a CP ≥25% was considered as abnormal.


  Results Top


Out of the 24 pediatric patients of HZO in this study, 15 were boys and 9 were girls. The male-to-female ratio was 1.7:1 with male preponderance. Their age ranged from 5 years to 16 years. In this study, the youngest patient was 5 years and eldest was 16 years. The mean age group was 11.20 years. All patients presented with vesicles over the pinna and external auditory canal [Figure 1] except one child who had extensive vesicles spreading to neck area [Figure 2].
Figure 1: A child with vesicular eruption over pinna and external auditory canal

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Figure 2: A child with extensive vesicular eruption in pinna, external auditory canal with spread to neck and cheek area

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Out of 24 patients, 4 children presented with facial palsy. Out of the 4 children with facial palsy, one was diagnosed with acute myeloid leukemia and just completed full course of the chemotherapy. Except one who was under immunosuppressive agents, the rest of the children and all the parents were evaluated as immunocompetent. The most common symptom was severe otalgia after vesicular eruption on the pinna and external auditory canal. Our 24 patients, 12 patients presented with vertigo and nine patients presented with tinnitus [Table 1].
Table 1: Clinical profile of the pediatric patients of herpes zoster oticus

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There were 17 patients presented with sensorineural hearing loss (SNHL). Out of 17 patients with SNHL, 12 showed high-frequency hearing loss. All were with mild-to-moderate degree of SNHL. Out of 24 pediatric patients, only 9 had a history of chicken pox in the past. In this study, 22 children presented with otalgia (91.66%), 17 children presented with hearing loss (70.83%); out of the three clinical presentations such as hearing loss, facial palsy, vertigo, and tinnitus. Among patients without hearing loss (n = 7), vertigo was seen in 2 patients. Out of 24 patients, 4 were associated with ipsilateral facial nerve paralysis [Figure 3] were further diagnosed as RHS. Out of 4 patients, 2 were with Grade-II House-Brackmann grading and 1 was with III grading and one with Grade-IV.
Figure 3: A child of Herpes zoster oticus with ipsilateral facial nerve palsy (Ramsay Hunt syndrome)

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Caloric test showed CP in 12 patients. Tzanck smears from the pinna lesions revealed giant cells [Figure 4].
Figure 4: Tzanck smear preparation showing multinuclear giant cells (Giemsa stain, ×200)

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After the diagnosis of HZO/RHS, all were treated with acyclovir for 10 days along with tapering dose of deflazacort, labyrinthine sedatives, and eye care in case of facial palsy. All were reviewed after 2 weeks. The vesicles over the pinna were resolved with the improvement of facial nerve functions. In case of facial palsy, facial nerve rehabilitations such as facial massage, facial nerve exercises such as grimacing, smiling, and whistling and biofeedback training with a mirror was done. All of our cases were recovered with the help of above treatment except three cases those are still on follow-up with facial exercises.


  Discussion Top


HZO is characterized by severe otalgia and erythematous rashes over the pinna and external auditory canal caused by reactivation of the latent VZV. If it is associated with ipsilateral facial nerve paralysis, called as RHS. HZO accounts for 2%–10% of all the cases with facial nerve palsy.[7] CN poly-neuropathy is associated with VZV infection in 1.8%–3.2% and involved CN s are VII, VIII, IX, and X.[7] The peripheral facial nerve weakness occurs due to inflammation of the facial nerve by reactivation of the VZV. The histopathological study shows perivascular, perineural and intra-neural aggregation of the round cells in the facial nerve of the patients with RHS.[3] The occurrence of the varicella in the first year of life is considered as a risk factor for HZO in childhood.[8] Patients of HZO usually present with otalgia, cutaneous, and mucosal lesions due to involvement of the sensory branch to the external auditory meatus, concha or hard palate, and facial nerve palsy or weakness due to reactivation of VZV DNA at the ganglion of CN VII.[9] VZV infection often spread from dehiscent facial nerve to the labyrinth through the round window or oval window has been thought as possible routes for inner ear involvement.[10] Both cochlear and retro-cochlear types of audiological dysfunctions have been reported in HZO.[11] Inflammation of the superior vestibular nerve may be an important factor for causing vertigo in HZO as facial nerve is directly connected to the superior vestibular nerve inside the internal auditory canal.[12] The prodromal symptoms include pain, a burning and tingling sensation, which are followed by the eruption of the vesicles. It is characterized by the unilateral presence of vesicles and neuralgia. HZO occurs when VZV reactivates and involves the facial nerve, trigeminal nerve, vestibulocochlear nerve, glossopharyngeal nerve, vagus nerves, and or cervical nerves.[13] Patients of HZO usually complain symptoms associated with 7th and 8th CN dysfunctions.

HZO often have cochleovestibular symptoms, so proper evaluation for hearing and vertigo are important part in the clinical assessment. Patients with facial weakness along with vertigo and worse electroneuronography (ENoG) values indicate poor prognosis. Hearing loss is frequently found where mild-to-moderate degree in majority of cases that due to cochlear and/or retro-cochlear involvement.[14] However, 54% patients of HZO presents with no cochlear symptoms may show hearing loss of isolated high frequency in PTA and only 19% has hearing loss at speech frequency.[14] The vertigo in HZO is often similar to vestibular neuritis patients.

In this study, data showed that the degree of hearing loss is significantly more severe in high-frequency range than in the low-frequency range. Superior vestibular nerve is directly connected with the facial nerve in the internal auditory canal.[12] The vestibular dysfunction in patients of RHS has been attributed to the direct spread of VZV through neural anastomosis.[15] In contrast, direct connection between cochlear nerve and facial nerve has not been documented, even though the anastomosis between cochlear nerve and saccular nerve has been reported.[16] Hence, cochlear dysfunction may be due to the spread of viral infection from the facial nerve into the CSF or perilymph inside the internal auditory canal rather than direct contact. If the viral infection spreads from the internal auditory canal to the cochlea through CSF and perilymphatic fluid, tissues at the basal turn will be damaged earlier and more extensively in comparison to the apical part of the cochlear. If viral infection spreads from the CSF occurs along the perineural tissue of the cochlear nerve, then outer circumference of this nerve will be damaged first and more extensively than inner part of the nerve of low frequency range. Neural fibers in cochlear nerve are found to be arranged orderly according to their frequency.[17]

The diagnosis of HZO is based on the patient history and clinical findings.[18],[19] The diagnosis is done without any difficulty when the clinical presentations are present. The presenting symptom is often deep ear pain which is paroxysmal in nature at first but after a day to 2 days, the pain may radiates to outward into the pinna and then become constant in nature. The patients also present rash or blisters in the distribution of the nervus intermedius which may also include anterior two third of the tongue, soft palate, external auditory canal, and pinna. Lower motor neuron ipsilateral facial nerve palsy is obvious in patients of RHS. There may be hyperacusis on the side of facial paralysis due to paralysis of stapedius and tensor tympani. The other features include vertigo, ipsilateral hearing loss, and tinnitus. The diagnosis is often missed if there is no rash. For the diagnosis, virological studies are available, but often the diagnosis in pediatric patients is based on clinical presentations and a good medical history of the patient.

The diagnosis is confirmed by Tzanck smear which demonstrates the presence of the virus.[20] The severity of the facial nerve paralysis is evaluated with House-Brackmann grading system. It measures the movements of the eyebrow and corner of the mouth in the affected side of the face and compare to the unaffected side.[21] Magnetic resonance imaging (MRI) with contrast is helpful to identify the damaged part of the facial nerve. The normal facial nerve often shows minimal enhancement of the facial nerve at the geniculate ganglion whereas in contrast MRI, it shows enhancement of the facial nerve from the meatal segment of the facial nerve to the mastoid segment of the facial nerve. In addition to the facial nerve, enhancement of the VIIIth CN can also be visible.[22] The inflammatory infiltrates around the geniculate ganglion can be demonstrated in the histopathological evaluation of the temporal bone.[19] The histopathological examination reveals the perivascular, perineural, and intra-neural aggregation of the inflammatory cells in the facial nerve in patients of RHS. The DNA of the VZV can studied from the tear fluid and saliva from the salivary glands such as submandibular gland and parotid glands of the patients with HZO.[23] DNA of the VZV was found in 72% of the submandibular gland saliva and in 27% of the tear fluid of patient of this disease.[2]

Facial ENoG is an important electrophysiological method for assessing the facial nerve degeneration and disease progression. ENoG is useful for predicting the progression of the facial nerve recovery and determine the requirement of surgical decompression. It was documented that, patients with acute facial palsy, reduction in ENoG amplitude with <10% of the healthy side may be highly predictive for incomplete recovery.[24] Patients presenting with <90% degeneration on ENoG within 2 weeks were found to recover to H-B grade I or II in 7 months after the development of the facial nerve weakness and those with 95% degeneration within 2 weeks were documented to show 50% chance of poor recovery.[25]

The standard treatment of HZO is antiviral therapy and high dose of corticosteroids in tapering dose. Corticosteroids reduce otalgia, vertigo, posttherapeutic neuralgia, and speeds up the healing of dermatological herpetic lesions. It also reduces the inflammation and edema of the facial nerve.[26] Antiviral agents prevent further proliferation or spread of the varicella zoster virus in the facial nerve. These antiviral treatments cause shortening of the duration of the viral infections and reduce the dermatological manifestations of HZO.[27]

Antiviral treatment such as acyclovir, valaciclovir, or famciclovir is recommended in HZO, and sometimes, steroids are required in case of facial palsy which occurs due to inflammatory edema of the perifacial nerve.[28] Recently, a live attenuated vaccine is proven to effective for herpes zoster infections such as HZO which may be used in future.[29] The treatment is usually done by oral acyclovir which is a DNA nucleoside analog that interferes with the herpes virus DNA polymerase and inhibits DNA replication and halting the cell cycle. Hence, acyclovir is an effective antiviral drug against the virus replication. It is a nontoxic drug and can be safely administered to the pediatric patients. Acyclovir is effective intravenously for the prevention and treatment of the herpes infection in immunosuppressed patients and herpes encephalitis. The effectiveness of acyclovir along with adjunct high dose of steroids is useful in HZO.

All the pediatric patients were treated with intravenous acyclovir with dose of 13.3 mg/kg/day for 7 days and along with intravenous methylprednisolone for 10 days with gradual decreased dose from 80 to 40 mg. The rashes and vesicles on the pinna and external auditory canal are often disappeared after around 72 h treatment. Improvement of the facial nerve function will appear after 1 week treatment and often return to normal after 1 month. The prognosis of HZO in pediatric age is better than in the adult age group.[30] Audiovestibular symptoms, facial nerve paralysis, and late treatment result in bad prognosis.[31] Hearing loss often recovers well. The prognosis of the facial nerve paralysis in HZO or RHS is worse than in Bell's palsy where around 10% of the complete facial nerve paralysis in HZO or RHS recovers completely.[32],[33]


  Conclusions Top


HZO occurs due to VZV reactivation which may result in RHS. If not diagnosed immediately and not timely treated, HZO is in pediatric age progress to RHS. Education to clinicians is vital for detecting HZO at very early stage as it can be a rare cause for facial nerve paralysis in pediatric patients and thereby prevent the associated morbidity. Hence, adequate awareness is required among pediatricians and other clinicians for the early detection and management of HZO for preventing morbidity.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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