HYPOREFLEXIA, HYPOTONIA, AND HYPONATREMIA: A CASE OF GUILLAIN-BARRÉ SYNDROME AND SIADH

Abstract

SESSION TITLE: Wednesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Guillain-Barré Syndrome (GBS) is an acute inflammatory radiculoneuropathy that is characterized by acute or subacute areflexic paralysis with albumin-cytologic dissociation evident on cerebrospinal fluid (CSF) analysis. In patients with critical neurologic disease, hyponatremia is one of the most severe metabolic complications. Even with mild hyponatremia the consequences can be grave ranging from severe neurologic deficits to death. The association between hyponatremia and GBS has been reported in the past, however, the underlying pathophysiology is not completely understood. CASE PRESENTATION: A 57-year-old female presented to the emergency department due to bilateral distal extremity weakness, worse in the lower extremities, and unsteady gait. The patient stated that her symptoms progressed over the last week with significant numbness, tingling, and weakness bilaterally and difficulty walking. Other than a recent upper respiratory tract infection, she had not experienced any other changes in lifestyle or medications. Upon arrival, CT and MRI of the head and spine were negative for acute changes. Initial labs were within normal limits. Lumbar puncture was performed and the patient was noted to have a CSF protein of 116 mg/dL, WBC 2 per μL, RBC 6 per μL, and glucose 65 mg/dL. Based on these results, the patient was diagnosed with GBS. Over the next 24 hours, the patient’s sodium level dropped from 136 to 119 mEq/L. Urine sodium was greater than 40 mEq and serum osmolality was 248 mOsm/kg. Intravenous immunoglobulin (IVIG) and hypertonic saline were initiated. Over the next 4 days the patient’s hyponatremia resolved with the initiation of fluid restriction and hypertonic saline. Her neurologic symptoms substantially improved prior to discharge. DISCUSSION: The incidence of hyponatremia in GBS patients is reported to be as high as 48% and is typically present in more severe cases. The mechanism of hyponatremia is usually attributed to syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and has been documented as an initial symptom prior to flaccid paralysis. The association between SIADH and GBS is attributed to hypothalamic inflammation. Risk factors for hyponatremia in the setting of GBS include: age > 50 years and preexisting co-morbidities including anemia, alcohol abuse, hypertension, and coagulopathy. Administration of IVIG is associated with a 33% increased likelihood of hyponatremia in patients with GBS. It has been demonstrated that hyponatremia is an indicator of more severe pathology regardless of the underlying disease. CONCLUSIONS: Hyponatremia can occur in the setting of GBS, typically in association with severe clinical states. Although SIADH is the most common cause of hyponatremia in GBS, the exact underlying pathophysiology is unknown. Treatment should be directed at the underlying cause. Reference #1: Sejvar JJ. Population incidence of GBS: a systematic review and meta-analysis. Neuroepidemiology. 2011;36:123-33 Reference #2: Hiew F, Winer J, Rajabally Y. Hyponatremia in Guillain-Barre syndrome revisited. Acta Neurol Scand. 2015;133:295-301. Reference #3: Rabinstein AA. Hyponatremia in critically ill neurological patients. Neurologist. 2003;290-300. DISCLOSURES: No relevant relationships by Hussein Asad, source=Web Response No relevant relationships by Daniel Griffin, source=Web Response