Case Presentation: A 52-year-old man with HIV on HAART (CD4 count of 644) and recently treated early latent syphilis, was admitted for abdominal pain and hematochezia of 2 days duration. On exam, he had normal vital signs and diffuse tenderness to palpation but no rigidity or guarding. Labs were notable for hemoglobin drop to 11 from baseline of 14. CMP and lipase were normal. CT scan revealed new prominent perirectal lymph nodes. EGD showed non-bleeding gastric ulcers and colonoscopy revealed proctitis with shallow ulcerations, which were felt to be the source of bleeding. He received empiric treatment for syphilis, gonorrhea, and chlamydia in addition to pantoprazole. Hospital course was complicated by severe left sided facial pain on hospital day 2. This was initially attributed to an impacted left third molar found on CT maxillofacial; however, dental evaluation was unremarkable. On day 6, he developed erythema and swelling of the left ear associated with drainage, tender periauricular lymphadenopathy, as well as pink papular lesions on the left posterior neck. Oral acyclovir was empirically started for concern of varicella zoster (VZV) infection. PCR swab of the area was positive for VZV. Despite empiric oral treatment, he rapidly developed neurological symptoms including vertigo, left-sided hearing loss, facial droop, and blurred vision. No ocular or retinal involvement was noted on fundoscopic exam. Patient was diagnosed with Herpes Zoster Oticus, or Ramsay Hunt Syndrome (RHS). MRI head was significant for abnormal enhancement in the left internal auditory canal, left facial nerve, and left geniculate ganglion, indicating cerebellitis due to VZV. He was promptly switched to IV acyclovir for a total of 14 days and a prolonged steroid taper. Despite modifications to his regimen, the patient continues to have persistent neurological symptoms as of 5 months later including vertigo, left-sided hearing loss, facial pain and weakness, as well as left-sided upper and lower extremity paresis.
Discussion: Despite presenting initially for gastrointestinal bleeding, the patient unexpectedly developed Herpes Zoster reactivation. It has been found that HIV patients are at higher risk than the general population of having complicated Herpes Zoster infection even if the patient is on HAART with an adequate CD4 count. While immunocompromised patients benefit from antiviral therapy beyond 72 hours after initial presentation, reports suggest better outcomes when treatment is initiated within the first 72 hours. Although treatment was started within 24 hours of rash development, it had already been about 96 hours since onset of neuralgia. It can be argued that treatment could have been initiated earlier had there been less anchoring on imaging as it skewed clinical reasoning.
Conclusions: Unilateral facial pain without evidence of an overt rash could be the first sign of RHS. While imaging can be useful in most situations, it can also prove to be a red herring or false reassurance. Therefore, high clinical suspicion and careful monitoring of signs and symptoms are critical to early identification and treatment of RHS. This is especially important in immunocompromised patients, such HIV patients, who appear to be at a higher risk of developing this complication of Herpes Zoster infection even when they are on HAART and have an adequate CD4 count. Despite prompt treatment with intravenous antiviral and steroids after obvious signs of RHS emerge, patients may still unfortunately suffer from long-term neurological sequelae.