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CASE REPORT
Year : 2020  |  Volume : 47  |  Issue : 1  |  Page : 45-47

Herpes zoster laryngitis


Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University (Deemed to be), Bhubaneswar, Odisha, India

Date of Submission06-Feb-2020
Date of Acceptance20-Mar-2020
Date of Web Publication23-Jun-2020

Correspondence Address:
Prof. Santosh Kumar Swain
Department of Otorhinolaryngology, IMS&SUM Hospital, Siksha “O” Anusandhan University (Deemed to be), Bhubaneswar, Odisha
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jss.JSS_10_20

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  Abstract 


Herpes zoster infection is due to reactivation of the latent varicella zoster virus. It is often seen in persons with impaired immunity or stress and characterized by one-side herpetic vesicular eruptions and neuralgia. A 45-year-old male presented with sore throat, hiccups, voice changes, and dry cough. Laryngeal examinations showed edema and eruptions over the left side of the larynx. He had herpetic vesicles over the left concha and external auditory canal. Elevated complement fixation titer confirmed the diagnosis of the herpes zoster. The patient was treated with acyclovir and steroid. Patients improved symptomatically after 10 days of treatment. This clinical condition should be kept in mind when the patient will present with unilateral sore throat, voice changes, and hiccups.

Keywords: Acyclovir, herpes zoster laryngitis, varicella zoster virus


How to cite this article:
Swain SK, Acharya S, Shajahan N, Agrawala R. Herpes zoster laryngitis. J Sci Soc 2020;47:45-7

How to cite this URL:
Swain SK, Acharya S, Shajahan N, Agrawala R. Herpes zoster laryngitis. J Sci Soc [serial online] 2020 [cited 2020 Jul 15];47:45-7. Available from: http://www.jscisociety.com/text.asp?2020/47/1/45/287475




  Introduction Top


Herpes zoster infection is caused by the reactivation of the latent varicella zoster virus (VZV).[1] The primary infections are by VZV, a DNA virus of the Herpesviridae family causes a typical picture of the chickenpox. The most common sites of latency of the VZV include not only trigeminal nerve and the dorsal ganglia but also other cranial nerves and autonomic ganglion. Reactivation of the VZV during adult period can produce zoster (shingles), which leads to painful vesicles at the skin segmental distribution.[2] Two common cranial nerves are widely known to be affected by VZV are ophthalmic division of the trigeminal nerve (herpes zoster ophthalmicus) and the facial nerve (herpes zoster oticus).[2] Other cranial nerves are rarely affected by this viral infection. Here, we are presenting a case of herpes zoster laryngitis. In this case, the patient is presenting with involvement of the vagus nerve by VZV.


  Case Report Top


A 45-year-old male attended the outpatient department of the otorhinolaryngology with the complaints of sore throat, odynophagia, voice change, and hiccup for 5 days. He had associated complaint of right otalgia. He was not known case of diabetes mellitus, hypertension, and tuberculosis. Examination showed the presence of herpetic eruptions at the right postaural area [Figure 1]. Direct laryngoscopy revealed edematous, erythematous, and erosive lesions at the left side of the larynx [Figure 2]. The patient was unable to eat and speak comfortably. White blood cell count was 7100 mm3 with raised segmented cells (74%) and decreased lymphocytes (13%). The diagnosis of herpes zoster laryngitis was done provisionally. Immunoglobulin M (IgM) for VZV and herpes simplex virus were negative at the time of clinical diagnosis, whereas complement fixation (CF) test for VZV revealed an elevated titter. Elevated CF titer confirmed the diagnosis of the herpes zoster infection. He was treated with valaciclovir for 10 days. Intravenous steroid (100 mg hydrocortisone sodium succinate) for 2 days treatment was given for managing the laryngeal mucosal edema. His hiccup gradually disappeared along with lesions of the larynx. His hiccup was treated by metoclopramide but with little effect. The hiccup was subsided slowly after disappearance of the erosive lesions of the larynx. The hiccups relapsed transiently along with vomiting and then resolved completely. The mucosal edema and erosions gradually subsided and resolved on the 8th day. Although severe hiccups present, magnetic resonance imaging of the brain and cervical computed tomography scan were within normal limits. He was discharged from the hospital on the 10th day of admission. Informed consent of the patient was obtained for publication along with approval from the institutional ethical committee of our hospital.
Figure 1: Vesicular eruptions in the postaural region (arrow mark)

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Figure 2: Endoscopic examination of the larynx showed edema, inflammation, and vesicles over the left side vocal fold

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  Discussion Top


Herpes zoster occurs due to the reactivation of the latent VZV infection which has been acquired with chickenpox. Herpes zoster is a common clinical entity caused due to the reactivation of the dormant VZV at the dorsal root ganglia, which may affect the sensory and/or motor nerves. The prodromal clinical presentations are burning sensation, pain, and tingling sensation, followed by vesicular eruption. Herpes zoster occurs when there are unilateral eruptions of the vesicles and neuralgia. Herpes zoster laryngitis is a rare clinical entity.[3] Patients of herpes zoster laryngitis may present with burning sensation in one side of the throat, odynophagia, hoarseness of voice, and occipital headache.[4] Although rare, sometimes patients may present with vocal cord paralysis.[5] The present patient was not accompanied with vocal fold paralysis. It, sometimes, presents with unilateral vocal fold palsy, laryngeal edema and mimics to laryngeal tumor, fungal infections, laryngeal tuberculosis, syphilis, abscess, or nonspecific laryngeal inflammation, so requires a differential diagnosis.[6] Hiccups are uncommon symptom found in herpes zoster infections. It represents an involuntary spasmodic contraction of the diaphragm where the inspiratory muscles following sudden closure of the glottis. There is a reflex pathway that mediates hiccups. The vagus nerve, phrenic nerve, pharyngeal plexus (C2–C4), and sympathetic chain (T6–T12) form afferent for the reflex mediating hiccups, whereas the phrenic motor nerve (C3–C5) acts as the efferent pathway. The role of the central nervous system is still obscure. Irritation at any part of this reflex may lead to hiccups.[7] The sensation of the supraglottic part of the larynx, base of the tongue, vallecula, and pyriform fossa is provided by the superior laryngeal nerve, which is a branch of the vagus nerve.[8] In addition to these, the auricular branch of the vagus supplies to the posterior wall of the external auditory canal. The vagus nerve is involved with nausea, vomiting, and anorexia.[9] However, the trigeminal nerve is involved with herpetic eruptions and neuralgia of the concha and external auditory canal.[9] Sore throat and ear pain are induced by the involvement of the glossopharyngeal nerve, which mediates the sensation of the tonsils, tongue base, and nasopharynx.[9] The sensation of the pinna is mediated by cervical nerves (C2 and C3).[9] In this case, the vagus nerve is affected by herpes zoster.

Laryngeal endoscopic examination or fiberoptic nasopharyngolaryngoscopic examination is a useful tool for the direct assessment of the larynx and hypopharynx. The exact site of lesions and extent of the pathology in the larynx can be assessed by laryngeal endoscopic examination. Certain serological tests available for these viral infections include IgM or immunoglobulin G (IgG) tests, CF test, and polymerase chain reaction (PCR), which are often used for the diagnosis of the herpes zoster. Although the IgM was not increased in this case, the complement test confirmed the diagnosis for varicella zoster infection. In case of varicella zoster infection, the IgM antibodies are seen at 8 to 10 days after the onset of the mucosal or dermatological lesions, whereas the increased level of IgG takes more than 2 weeks.[3] The DNA of the VZV is often positive in pinna skin exudates by PCR.[10] Hence, PCR analysis of VZV DNA may be a rapid investigation for the diagnosis of the herpes zoster laryngitis.

The treatment of herpes zoster infection is greatly improved by the advent of the new virostatic drugs, particularly acyclovir. Antiviral agents prevent further proliferation or spread of the VZV in the facial nerve. These antiviral treatments cause shortening of the duration of the viral infections and reduce the morbidity. Antiviral treatment such as acyclovir, valaciclovir, and famciclovir are recommended in herpes zoster infection, and sometimes, steroids are required in case of inflammatory edema. For the antiviral drug such as acyclovir to act against the virus must be phosphorylated within the herpes virus. The acyclovir is degraded or metabolized to monophosphate form in infected cells containing the virus-specific thymidine kinase. Then, the monophosphate is converted into acyclovir triphosphate by host cell enzymes which finally terminate the DNA of the virus. The treatment of the herpes zoster laryngitis includes antiviral therapy such as intravenous acyclovir or oral valaciclovir. Steroid is often recommended along with antiviral therapy for minimizing the laryngeal edema in acute respiratory distress.[6] Steroids help to reduce the inflammation of the cranial nerves and alleviate the neurological symptoms and pain. In this case, valaciclovir and corticosteroids were effective for reducing laryngeal edema. At present, a live attenuated vaccine is available for herpes zoster.[11] In case of hiccup, drugs such as metoclopramide, baclofen, chlorpromazine, and haloperidol are common medication.[12] Recently, a live attenuated vaccine is proven to be effective for herpes zoster infections such as herpes zoster which may be used in the future.


  Conclusion Top


Herpes zoster infection occurs due to VZV reactivation. If it is not diagnosed immediately and not timely treated, it leads to complications with severe morbidity. Herpes zoster laryngitis is an extremely rare clinical entity and should be considered as a possible cause for unilateral sore throat along with hiccups. This uncommon laryngeal pathology should be treated with acyclovir or valaciclovir along with steroids. Education to clinicians is vital for detecting these lesions at very early stage as it can be a rare cause for severe laryngeal airway compromise and thereby preventing the associated morbidity. Hence, adequate awareness is required among other clinicians for early detection and management of herpes zoster laryngitis 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.



 
  References Top

1.
Swain SK, Sahu MC, Behera IC. Management of Ramsay Hunt syndrome among HIV patients: Our experience in a tertiary care hospital of eastern India. Pol Ann Med 2016;23:92-6.  Back to cited text no. 1
    
2.
Steiner I, Kennedy PG, Pachner AR. The neurotropic herpes viruses: Herpes simplex and varicella-zoster. Lancet Neurol 2007;6:1015-28.  Back to cited text no. 2
    
3.
Watelet JB, Evrard AS, Lawson G, Bonte K, Remacle M, Van Cauwenberge P, et al. Herpes zoster laryngitis: Case report and serological profile. Eur Arch Otorhinolaryngol 2007;264:505-7.  Back to cited text no. 3
    
4.
Wu CL, Linne OC, Chiang CW. Herpes zoster laryngis with prelaryngeal skin erythema. Ann Otol Rhinol Laryngol 2004;113:113-4.  Back to cited text no. 4
    
5.
Yaguchi H, Hisatomi M, Sekine T, Matsui K, Nagatomo M, Inoue K. Case of zoster sine herpete presenting with dysphagia diagnosed by PCR analysis of VZV DNA in auricular skin exudated (in Japanese). Rinsho Shinkeigaku 2006;46:668-70.  Back to cited text no. 5
    
6.
Pinto JA, Pinto HC, Ramalho Jda R. Laryngeal herpes: A case report. J Voice 2002;16:560-3.  Back to cited text no. 6
    
7.
Reddy BV, Sethi G, Aggarwal A. Persistent hiccups: A rare prodromal manifestation of herpes zoster. Indian J Dermatol Venereol Leprol 2007;73:352-3.  Back to cited text no. 7
[PUBMED]  [Full text]  
8.
Watelet JB, Evrard AS, Lawson G, Bonte K, Remacle M, Van Cauwenberge P, et al. Herpes zoster laryngitis: Case report and serological profile. Eur Arch Otorhinolaryngol 2007;264:505-7.  Back to cited text no. 8
    
9.
Hirose H, Ichimura K, Iinuma T, Kaga K, Nibu K, Mizuno M, et al. Herpes zoster oticus (in Japanese). In: Nomura Y, editor. Modern Otorhino-Laryngology. 10th ed., Vol. 117. Tokyo: Nanzando Company, Limited; 2004. p. 165.  Back to cited text no. 9
    
10.
Murakami S, Honda N, Mizobuchi M, Nakashiro Y, Hato N, Gyo K. Rapid diagnosis of varicella zoster virus infection in acute facial palsy. Neurology 1998;51:1202-5.  Back to cited text no. 10
    
11.
Cunningham AL, Breuer J, Dwyer DE, Gronow DW, Helme RD, Litt JC, et al. The prevention and management of herpes zoster. Med J Aust 2008;188:171-6.  Back to cited text no. 11
    
12.
Launois S, Bizec JL, Whitelaw WA, Cabane J, Derenne JP. Hiccup in adults: An overview. Eur Respir J 1993;6:563-75.  Back to cited text no. 12
    


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