|Year : 2017 | Volume
| Issue : 2 | Page : 159-161
Herpes zoster infection of the face: A case report with review of literature
Seetharamiah Sunder Raj, Pradhuman Verma, Princy Mahajan, Ankush Puri
Department of Oral Medicine and Radiology, Surendera Dental College and Research Institute, Sriganganagar, Rajasthan, India
|Date of Submission||04-Aug-2016|
|Date of Acceptance||19-Oct-2017|
|Date of Web Publication||9-Nov-2017|
Department of Oral Medicine and Radiology, Surendra Dental College and Research Institute, Sriganganagar - 335 001, Rajasthan
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Varicella zoster virus (VZV) is a DNA virus and a member of the alpha herpes viridae family, causing both primary and recurrent infection. Herpes zoster (HZ), commonly called shingles, is a distinctive syndrome caused by reactivation of VZV. This reactivation occurs when immunity to VZV declines because of aging or immune-suppression. HZ can occur at any age but most commonly affects the elderly population. HZ may affect any sensory ganglia and its cutaneous nerve. Most of the infections affect dermatomes of T3 to L2, but approximately 13% of the patients present with infections involving any of the three branches of the trigeminal nerve. Prodromal symptoms include neuropathic pain, headache, malaise, and disrupted sleep. HZ causes pruritic, localized, vesicular rash which usually appears unilaterally in the distribution of one or more adjacent sensory nerves accompanied by neuropathic pain in the affected dermatome. This is a case report of HZ infection in a 55-year-old male patient who was managed with comprehensive medical treatment.
Keywords: Herpes, shingles, trigeminal, varicella, zoster
|How to cite this article:|
Raj SS, Verma P, Mahajan P, Puri A. Herpes zoster infection of the face: A case report with review of literature. J Indian Acad Oral Med Radiol 2017;29:159-61
|How to cite this URL:|
Raj SS, Verma P, Mahajan P, Puri A. Herpes zoster infection of the face: A case report with review of literature. J Indian Acad Oral Med Radiol [serial online] 2017 [cited 2020 Nov 24];29:159-61. Available from: https://www.jiaomr.in/text.asp?2017/29/2/159/217921
| Introduction|| |
Varicella zoster virus (VZV) is a ubiquitous DNA virus belonging to the alpha herpes viridae family causing both primary and recurrent infection. Chicken pox (varicella) is a generalized primary infection. After the primary infection, it remains latent in the cranial nerve, dorsal root, and autonomic nervous system ganglia along the entire neuraxis. The reactivation causes herpes zoster (HZ) also known as shingles. HZ cases present with the characteristic unilateral, localized, vesicular eruptions accompanied by neuropathic pain in the affected dermatome. This neuropathic pain is known as post-herpetic neuralgia (PHN), and usually occurs 30 or 120 days after the onset of acute rash. This is a case report of HZ infection in a 55-year-old male patient who was managed with comprehensive medical treatment.
| Case Report|| |
A 55-year-old old male patient reported to the department of oral medicine and radiology with the chief complaint of painful blisters on the right side of the face since 1 week. History dates back to 10 days, when the patient felt some weakness and fatigue along with a history of itching and redness on the right side of the face. The lesions appeared 1 week later as multiple papules on the right side of the face, which was sudden in onset, increased in extent that developed into fluid-filled vesicles which ruptured to form ulcers with fluid discharge, and there was a history of intraoral painful fluid-filled vesicles with the same onset as that of the vesicles on the face. He gave a history of pain which was gradual in onset, sharp, continuous and tingling, itching, pricking, which aggravated on facing wind and slashing water on face, and did not get relieved on taking medication. Patient visited the local chemist and was taking medication (analgesics) for the symptoms, which relieved him off the pain to some extent.
On extraoral examination, unilateral multiple crops of coalescing vesicles, along with few shallow ulcers and tissue tags were present on the whole of the right side of the face extending anteriorly from the midline to about 1.5 cm in front of tragus and superiorly involving the right eye to the angle of mouth of the same side. The lesions followed a dermatomal pattern with irregular borders having erythematous erosive areas and fluid discharge with swollen right upper eyelid, right side of nose, and swollen right side of upper lip with lip crusting [Figure 1]. On palpation, it was tender with a rough surface texture. One submandibular lymph node was palpable which was 1 cm in maximum diameter, soft, tender and not fixed to underlying structures.
On intraoral examination, unilateral multiple crops of coalescing vesicles and ulcers were present on the right side of the alveolar mucosa and palate extending anteriorly from the labial aspect of alveolar mucosa in relation to 11 and 12 region to involving the labial and palatal mucosa of 17 region. Erythematous regions extending up to soft palate were also present [Figure 2]. It was tender, soft in consistency, and had a rough surface texture. Based upon the history and clinical findings, provisional diagnosis of acute vesiculobullous lesion involving the right side of face was made, and a differential diagnosis of HZ infection, Ramsay Hunt syndrome, and erythema multiforme were considered.
Exfoliative cytology was done which was sent for cytopathological examination (10×, H and E stain), which revealed multinucleated giant cells. All the hematological investigations were normal except erythrocyte sedimentation rate which was raised up to 38 mm/1st h. Panoramic radiograph revealed multiple root stumps, missing teeth, and generalized bone loss. Based upon history, clinical examination and investigations, a final diagnosis of HZ virus infection of the right side of face involving the maxillary branch of the trigeminal nerve was made.
Patient was advised to have a bland diet, adequate hydration; Tab. acyclovir (800 mg) five times daily for 5 days, tab. prednisolone (5 mg) three times daily for 5 days, tab. paracetamol (650 mg) three times daily for 5 days, and topical application of calamine lotion on facial lesions 4–5 times daily were advised. Patient was recalled after 5 days. On first follow-up, extraoral and intraoral lesions had healed by 50%, healing was appreciated with the formation of dry scabs on extraoral lesions [Figure 3], pain subsided by 30%; acyclovir was continued for 5 more days. On second follow-up, extraoral and intraoral lesions almost resolved, and acyclovir was discontinued in a tapering manner. The patient was advised regular follow-up.
| Discussion|| |
HZ of the trigeminal nerve is a disease that falls within the diagnostic purview of all dentists and dental specialists. In 1892, Von Bokay  first suggested the relationship between the etiologies of varicella and HZ. The first suggestion was made by Garland and Hope-Simpson  that HZ is caused by reactivation of latent virus acquired during varicella. Initially, the lesions in the affected dermatome are clustered at a few sites. As the disease progresses, the vesicles often coalesce into larger, fluid-filled lesions. Prodromal symptoms include neuropathic pain, headache, malaise, and disrupted sleep. HZ may affect any sensory ganglia and its cutaneous nerve. Most of the infections affect dermatomes of T3 to L2, however, approximately 13% of the patients present with infections involving any of the three branches of the trigeminal nerve. Zoster-associated complications include neurologic components such as Guillian–Barre syndrome, encephalitis, myelitis, Ramsey–Hunt Syndrome, and Horner's syndrome. In general, ocular complications involve ulcerations, hemorrhage, conjunctivitis, and optic neuritis. The ophthalmic division of trigeminal nerve is most commonly affected, i.e., HZ opthalmicus. Involvement of the trigeminal nerve leads to lesions on the upper eyelid, forehead, and scalp with V1; midface and upper lip with V2; and lower face and lower lips with V3. In our case, maxillary division of trigeminal nerve was involved. The cranial and peripheral nerve palsies may occur as a complication such as Ramsay–Hunt Syndrome, in which patient develops Bell's palsy, vesicles of external ear, and loss of taste sensations in anterior 2/3rd of the tongue; these three signs were not present in our case. Complications can occur in 10–46% of the patients with HZ infection. The skin lesions involved in erythema multiforme may mimic these lesions, however, the unilateral lesions typically involving the dermatomes and absence of target lesions may help to exclude lesions with erythema multiforme.
Post-herpetic neuralgia is a neuropathia resulting from peripheral and central nervous system injury and altered central nervous system processing. Recommended therapy should include (1) patient isolation, (2) local management of skin lesions, (3) control and elimination of pain, (4) limitation of the extent, duration, and severity of the disease with antiviral agents, and (5) treatment of post-herpetic neuralgia.
Acyclovir has been the drug of choice; given in a dosage of 800 mg four times a day for 10 days. Recently, newer forms of antiviral drugs have been developed, specifically to address the acute stage of HZ (Famciclovir) and for use in immune-competent patients (Valacyclovir). In the former, the dosage is 500 mg every 8 h for 7 days; for the latter it is 1 g three times daily for 7 days.
Recent treatment modalities include lysine/arginine usually given at 300–1200 mg dosage per day. Topical zinc treatment is applied as topical solution of zinc sulphate (4%) in water four times daily for 4 days. Vitamin C is given as 200 mg ascorbic acid and 200 mg as water-soluble flavonoids (apparently from citrus) three times daily for 3 days. Oral zinc treatment includes oral administration of 23 mg zinc sulphate and 250 mg vitamin C, each twice daily for 6 weeks. Vitamin E was given in uncontrolled trials; topical application of vitamin E relieved pain and aided in the healing of oral herpetic lesions (gingivostomatitis or herpetic cold sores). The affected area was dried and cotton saturated with vitamin E oil (20000–28000 IU per ounce) was placed over it for 15 min. Adenosine monophosphate is also given; each injection contained 1.5–2.0 mg per Kg body weight and was administered every other day for a total of 9–12 treatments. Extracts of the leaves of lemon balm (Melissa officinalis) have been investigated as a topical treatment for Herpes simplex. The lithium preparation or a placebo was applied topically four times daily for seven days, beginning within 48 hours of the onset of lesions.
| Conclusion|| |
It is known that the patients with Herpes are infectious until the lesions have healed. Hence, the early diagnosis and treatment of the disease in the prodromal phase by the use of antiviral agents should be the main goal of its management. Therefore, dentists should have a thorough knowledge about the presentation of the condition, its treatment, and probable complications. Differential diagnosis is very important to ensure that correct treatment is performed.
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.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Arvin AM. Varicella zoster virus. Clin Microbiol Rev 1996;9:361-81.
Gilden D, Williams L, Cohers. Clinical features of varicella zoster virus infection of the nervous system. ANCR 2002;2:7-10.
Insingha RP, Itzler RF, Pellissier JM, Saddier P, Nikas AA. The incidence of herpes zoster in a United States Administrative Database. J Gen Intern Med 2005;20:748-53.
Munnangi A, Afteb A, Khurana N, Shah K. Post herpetic neuralgia. J Evol Med Dent Sci 2015;4:2278-4802.
Von Bokay J. Uber den atiologischen Zusammenhang der Varizellen mit gewissen. Fallen von Herpes Zoster Wien Zlin Wochenschr 1909;22:1323-6.
Hope-Simpson RE. The nature of herpes zoster: A long-term study and a new hypothesis. Proc R Soc Med 1965;58:9-20.
Chidiac C, Bruxelle J, Daures JP. Characteristics of patients with herpes zoster on presentation to practitioners in France. Clin Infect Dis 2001;33:62-9.
Burket LW, Greenberg MS, Glick M. Burket's Oral Medicine - Diagnosis and Treatment. 9th
ed. 1984. p. 64.
Wadhawan R, Luthra K, Reddy Y, Singh M, Jha J, Solanki G. Herpes zoster of right maxillary division of trigeminal nerve along with oral manifestations in a 46 year old male. Int J Adv Biol Res 2015;5:281-4.
[Figure 1], [Figure 2], [Figure 3]