Lyme Neuroborreliosis Presenting as the Syndrome of Inappropriate Antidiuretic Hormone Secretion

CPT Michael P. Perkins, MD; CPT Nathan Shumway, DO; MAJ William L. Jackson, Jr, MD, FACP, FCCP

In This Article

Abstract and Case Presentation

We describe a case of a patient presenting with the syndrome of inappropriate hormone secretion (SIADH) caused by Lyme neuroborreliosis.

A 73-year-old female presented to our emergency department with hyponatremia and a 1-month history of progressively worsening unsteady gait, falls, decreased mental acuity, and excessive daytime somnolence. Additional history revealed a rash that developed 2 months prior to presentation after a weekend of gardening. The rash was characterized by large erythematous ellipsoid lesions on her lower abdomen which eventually spread to her entire abdomen. These lesions were nonpruritic and spared her hands and feet. Onset of the rash was followed by symptoms of generalized fatigue, malaise, and myalgia that abated after approximately 1 week. She felt well until the onset of her presenting symptoms.

Her vital signs included a blood pressure of 140/72 mm Hg without significant orthostatic changes, heart rate of 67 beats per minute, respiratory rate of 19 breaths per minute, and a temperature of 98.7˚ F (37˚ C). Her physical exam was significant for a Mini-Mental State Examination of 26/30 with deficits in recall and concentration, an ataxic gait, 3/5 strength in her left deltoid, 4/5 strength in her left biceps, and 4+/5 strength in her left triceps. Additionally, her mucous membranes were moist, she had normal skin turgor, and no peripheral edema.

Her outpatient medications included pravastatin, cyclobenzaprine, and acetaminophen. Initial laboratory data were remarkable for a serum sodium of 118 mmol/L (137-145). Additional standard laboratory evaluation was unremarkable, including a normal complete blood count, liver associated enzymes, and the remainder of a serum chemistry panel. Of note, she had normal renal function with a blood urea nitrogen of 8 mg/dL (7-17) and serum creatinine of 0.5 mg/dL (0.7-1.2). Chart review revealed a serum sodium level of 138 mmol/L 1 month prior to admission.

Further laboratory evaluation of her hyponatremia demonstrated serum osmolality of 250 mOsm/kg (285-300), urine osmolality of 475 mOsm/kg (50-1400), urine sodium of 64 mmol/L (23-283), and a uric acid of 1.2 mg/dL (2.5-7.5). A lumbar puncture was performed and yielded 316 white blood cells per cubic mm (205 lymphocytes, 19 polymorphonuclear cells, 73 monocytes), glucose 60 mg/dL (40-70), protein 278 mg/dL (12-60), and a Lyme indirect fluorescent antibody titer of 1:1024. Concomitant serum Lyme antibody was 6.19 (0-1.09) by enzyme-linked immunoassay (ELISA) with positive confirmatory Western immunoblot. MRI studies of the brain showed scattered foci of T2 and FLAIR signal hyperintensity in the periventricular and diffuse subcortical white matter and pons.

Our patient was placed on fluid restriction for initial management of SIADH and then started a course of ceftriaxone for early Lyme neuroborreliosis (LNB). After 5 days of antibiotics and fluid restriction, her serum sodium returned to 130 mmol/L with improvement in her neurologic symptoms. After completion of 21 days of antibiotics, her serum sodium was within normal limits and her neurologic symptoms had almost completely resolved. Her MMSE was 30/30 and she had a normal gait. Her only residual deficit was a mild weakness in her left deltoid.

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