A 75–year–old male presented for inpatient treatment of major depression. A medicine consult was requested for evaluation of a pruritic facial rash that had been present for 2 weeks. Review of the systems was otherwise negative. Past history was significant for chronic systolic CHF, permanent pacemaker, hypothyroidism, BPH, and abdominal aortic aneurysm repair. Vital signs on presentation were normal, and physical examination revealed tender, sharply demarcated, erythematous, edematous patches with completely crusted vesicles in the right V1 and V2 distribution. Neurologic examination revealed unsteady gait, catatonic face, depressed affect, and orientation only to self. Ophthalmologic examination did not reveal corneal or retinal herpetic involvement. Initial laboratory values were significant for a serum sodium level of 122 mEq/L (reported to be 137 mEq/L 2 weeks before presentation), serum osmolality of 248 mOsm/kg, and urine osmolality of 515 mOsm/kg. The patient was diagnosed with facial cutaneous herpes zoster with secondary bacterial preseptal cellulitis, as well as SIADH. Given the duration of the lesions, the presence of crusting, and lack of ophthalmic involvement, antiviral therapy was not initiated. However, the SIADH improved only minimally with fluid restriction, the patient’s delirium worsened, and low–grade fevers began. With worsening delirium in the setting of facial cutaneous herpes zoster infection and no alternative infectious source identified, lumbar puncture was performed, revealing 67 lymphocytes including “atypical lymphocytes,” elevated protein, and normal glucose level. IV acyclovir was started empirically. Gram stain and cultures returned negative, and VZV PCR was positive. Acyclovir was continued with marked improvement in the skin lesions, mental status, sodium levels, and vision.
Zoster meningoencephalitis occurs in 1–2 per 10,000 varicella cases and has a variable time course, ranging from days to months. The concurrence of zoster meningoencephalitis, zoster ophthalmicus and SIADH in this immunocompetent patient is particularly noteworthy. The etiology of SIADH and altered mental status were both initially unclear, and a stepwise approach to both problems ultimately led to a lumbar puncture that revealed the unifying diagnosis. Given the aging population, it is likely we will see an increasing incidence of herpes zoster infections in elderly but otherwise immunocompetent patients. Lumbar puncture, looking for pleocytosis with atypical lymphocytes and positive VZV PCR testing, is an important step in detecting CNS involvement.
CNS complications of VZV are rare and have been traditionally thought to occur in immunocompromised patients. It is imperative that a strong clinical suspicion is maintained for CNS complications of herpes zoster infections in immunocompetent patients as well, however, especially considering the mortality rate of 5–10% of varicella encephalitis.