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• W2027816237 abstract "Ramsay Hunt Syndrome (RHS) is caused by reactivation of varicella-zoster virus (VZV) infection. As early as 1907, Hunt pointed out that both facial paralysis and auditory or vestibular complications could accompany trigeminal, occipital, or even cervical herpes zoster infection. 1 RHS refers to either of 2 conditions, herpes zoster oticus or any cephalic zoster complicated by facial paralysis and/or by vestibulocochlear dysfunction. Facial paralysis due to VZV reactivation has been well described. 2–4 However, little is reported about RHS following dental procedures 5,6 and there are no reports associated with dental infection. We report the first case of an unusual presentation of RHS associated with a dental infection. The literature is reviewed and we discuss the reactivation of VZV related to oral inflammation caused by dental procedures, surgery, and infection. Although this patient did not develop the pathognomic vesicles of herpes zoster oticus, he presented with clinical signs that were characteristic for RHS. Due to diagnostic uncertainty among the clinicians, VZV reactivation was not considered in the initial differential diagnosis, which resulted in delayed antiviral treatment. CASE REPORT A 95-year-old man with no significant past medical history presented to an otolaryngologist 3 days after treatment of a root canal infection of the right cuspid on the lower jaw (tooth #27). His chief complaint was progressive pain in his right ear that started 1 day after dental work, which consisted of opening the area of the root canal and placement of a cotton pledget to allow drainage. No direct root canal therapy occurred at that time. Fourteen days prior to that, the patient had received adjustments for a new lower partial denture. The ear, nose, and throat examination revealed swelling and erythema of the skin around the right ear canal. No specific lesions around the ear, pharynx, or elsewhere were noted. The patient was started on oral amoxicillin/clavulanate for treatment of otitis externa. Two days after starting oral antibiotics, the right ear pain had worsened, the patient developed vertigo, and his voice became hoarse. The right pinna and auricle were significantly more swollen and a yellow discharge from the ear canal was noted. The oral cavity showed no lesions. Laryngoscopy revealed a right vocal cord paralysis, vocal cord edema, and a possible ulcerative lesion on the false cord on the right. He was admitted to the hospital for intravenous antibiotics and further management. One day after being hospitalized (4 days after the initial presentation to the otolaryngologist), the patient developed a right peripheral facial paresis. At that time, the infection had advanced to a severe auricular perichondritis and treatment was changed to tobramycin, vancomycin, piperacillin/tazobactam, ciprofloxacin, and fluconazole. A biopsy of the right pinna the following day showed many inclusions characteristic of herpes virus infection. An immunoperoxidase stain for herpes simplex virus showed focal faint positivity, suggestive of VZV. Six days after the initial presentation, the patient was started on intravenous acyclovir. Twenty-four hours later, he developed respiratory failure with large amounts of necrotic debris obstructing the airway. He expired on hospital day 32 due to complications of aspiration pneumonia requiring prolonged intubation and mechanical ventilation. Postmortem immunostains for VZV protein were performed on the surgical biopsy with monoclonal antibody C90.2.8 (Novacastra, Vector Laboratories, Burlingame, CA). Prior pepsin digestion for 30 minutes (Research Genetics, Huntsville, AL) and primary overnight incubation at 4°C were required. The chromogen was 3-3′diaminobenzidine (Ventana, Tucson, AZ). Figure 1 shows cytoplasmic positivity for VZV protein in multinucleated cells and in most keratinocytes in the area of the ulcerated vesicle.FIGURE 1: Stains on surgical biopsy of the pinna show brown cytoplasmic positivity for VZV. Note the large positive multinucleated giant cell in the center of the picture.DISCUSSION RHS typically presents with the classic triad of ear pain, herpetic auricular rash, facial paralysis, and/or vestibulocochlear dysfunction. The patient we describe presented without the pathognomic vesicles. The rapid progression from auricular skin swelling to necrotizing cellulitis might have masked the presence of herpetic vesicles. Thus, this presentation cannot be called a zoster sine herpete. The initial diagnosis in our patient was otitis externa. Basilar skull osteomyelitis was included in the differential diagnosis at the time the infection advanced to a necrotizing cellulitis of the auricle. The organisms considered were Staphylococcus aureus, Pseudomonas aeruginosa, and fungal species. A biopsy of the pinna was performed after the clinical course worsened on broad-spectrum antibiotics, cultures of the otic discharge remained negative, and the patient developed a peripheral facial paresis. One week after the initial presentation, the patient was started on appropriate antiviral treatment. Various dentistry-related causes of facial palsy have been reported in the literature. Most are a direct effect of dental anesthetic injection, 7,8 or due to direct or indirect surgical trauma to the facial nerve. 9 We found only 5 cases documenting the association between dental procedures and facial paralysis due to reactivation of VZV. 5,6 These dental procedures were incision of the gingiva and fitting of a crown, treatment of carious teeth, extraction of a tooth, root canal therapy, and adjustment of dentures. The types of dental treatment took place in the mandibular or maxillar region and varied widely. Direct stimulation of the trigeminal nerve by incision, drilling, extraction, or root canal therapy might have triggered virus reactivation in most of these cases. In our patient, as well as in 1 reported case of RHS after adjustment of dentures, treatment did not directly stimulate the nerve. Although incidental occurrence of RHS in these cases could be considered, it is more likely that chronic irritation of the gingiva triggered virus reactivation. The time between dental treatment and onset of facial paralysis varied between 5 and 14 days in the reported cases. However, no information was given concerning the time between the procedure and the occurrence of herpetic lesions. As pathognomic vesicles of herpes zoster can occur before or after facial paralysis, it is difficult to comment on the time interval between dental procedures and the first symptoms of VZV reactivation. In our patient, ear pain started already 1 day after treatment of a root canal infection. This infectious process, probably subclinical for several days prior treatment, and/or the irritation of the gingiva by the denture adjustment may have triggered the VZV reactivation. The other uncommon manifestation of RHS was the presentation of a rapidly progressing cranial polyneuropathy. Initially cranial nerves V, VIII, and X were involved followed by 7th nerve palsy. The presence of a right vocal cord paralysis with debris obstructing the airway and the delay in antiviral treatment might have contributed to our patient’s poor outcome. There have been reports of RHS presenting with multiple cranial nerve involvement in the past. Aviel and Marshak 10 reviewed the literature and found that the following nerves are involved in order of decreasing frequency: VII, VIII, IX, V, X, and VI with involvement of cranial nerves I, II, III, IV, XI, and XII being rare. De and Pfleiderer 11 described an extreme and unusual variant of RHS with involvement of cranial nerves VII, VIII, X, IX, and XII, as well as C2-C4 sensory dermatomes. Therefore, it must be kept in mind that RHS should be considered a cranial polyneuropathy. The significance of early diagnosis and treatment of RHS is well established. Administration of acyclovir-prednisone within 72 hours of the onset of facial paralysis has been shown to reduce nerve degeneration. 12 In cases of diagnostic uncertainty, the presence of VZV can be confirmed by documenting viral antigen through PCR or viral serology. 2,13 In conclusion, reactivation of VZV following inflammation of oral tissue may be more common than previously documented, particularly in immunocompromised hosts. Independent of the clinical presentation, RHS should be included in the differential diagnosis of patients presenting with ear pain after dental procedures or dental infection, and when appropriate, should lead to early administration of antiviral treatment. ACKNOWLEDGMENTS The authors thank Melanie Maslow, MD, and Morel Fidler, DDS, for instructive help and assistance with this case report. This work was supported in part by the Research Enhancement Award Program from the Department of Veterans Affairs." @default.
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• W2027816237 title "Ramsay Hunt Syndrome: An Unusual Variant After Dental Infection" @default.
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