A 46‐year‐old man presented with a 1‐week history of bilateral lower facial nerve paralysis and 3 weeks of fever, headache, mild transaminitis, and hepatosplenomegaly. Illness began with acute onset of fever (103°F), headache, chills, and night sweats followed by generalized joint swelling and pain and a dry cough 24 hours (day 1) after a fishing trip. He was initially given doxycycline, then got jaundiced on day 3 and was started on atovaquone and azithromycin. Symptoms were getting worse, and he developed new bilateral lower motor facial nerve paralysis and 2 days of generalized, diffuse macular rash and was admitted on day 15. A extensive workup was positive for mild transaminitis, and hepatosplenomegaly. Other negative workups included cultures, hepatitis panel, serologies for Lyme (IgG and IgM) twice, Ehrlichia, Rickettsia, cytomegalovirus, West Nile, Leptospira, Babesia, smear and serology, rapid plasma reagin, HIV, ANA, and RF. Lumbar puncture showed 44 WBCs (55% lymphocytes, 37% neutrophils, 8% monocytes), protein of 100 mg/dL, and glucose of 70 mg/dL. By day 19 he had received short courses of doxycycline, atovaquone, azithromycin, and ceftriaxone without any improvement. Then he was started on acyclovir for possible herpers simplex virus encephalitis and was transferred to a tertiary‐care center. Tests were repeated and were negative as above. Considering his travel history and living environment, neuroborreliosis was suspected, although tests were negative. He was treated with 2 weeks of intravenous ceftriaxone and 7 days of steroids, and the symptoms improved almost to baseline.
Fever, arthralgia, bilateral or unilateral lower motor facial nerve paralysis, and transaminitis are encountered by the hospitalists and internist commonly. Differential diagnoses for acute presentation of these could be broad: infections like otitis media, neuroborreliosis, rickettsial disease, acute retroviral infection, and herpes zoster; autoimmune conditions like neurosarcoid and Guillain–Barré; and any primary or secondary tumors in the affected site. Early disseminated Lyme infection occurs within weeks to months after getting infected. Between 10% and 20% of Lyme patients can get neurological manifestations in the peripheral or central nervous system. Lyme disease is diagnosed with serologic tests that are not very sensitive during the first 2 weeks of infection; only 59% of patients with early‐stage Lyme disease have positive serology test results. IgM antibodies appear 2– 4 weeks and IgG antibodies appear 4–6 weeks after the onset of the rash. IgG antibody levels will remain low, even with successful treatment, whereas IgM usually drops off to very low levels 6 months after disease onset.
Hospitalists should be familiar with clinical features, stages, and diagnosis and management of Lyme disease and related complications. It is important to know that serological tests may be negative at the initial stage of the disease, and treatment should be started in a suspected patient to prevent progression and complications and to decrease cost.
P. Ranasinghe ‐ Johns Hopkins School of Medicine, employment; K. Praksa ‐Johns Hopkins School of Medicine, employment.
To cite this abstract:Ranasinghe P, Prakasa K. Acute Bilateral Facial Nerve Paralysis and Negative Workup. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 380. Journal of Hospital Medicine. 2011; 6 (suppl 2). https://www.shmabstracts.com/abstract/acute-bilateral-facial-nerve-paralysis-and-negative-workup/. Accessed May 24, 2019.