Abstract: FR-PO583
SIADH as the Initial Presentation in Guillain Barre Syndrome
Session Information
- Trainee Case Reports - III
October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Reports
- 902 Fluid and Electrolytes: Clinical
Authors
- Fuca, Nicholas, Staten Island University Hospital, Staten Island, New York, United States
- Asti, Divya, Northwell Health, Staten Island, New York, United States
- Mudduluru, Bindu, Northwell Health, Staten Island, New York, United States
- El-Charabaty, Elie, Staten Island University Hospital, Staten Island, New York, United States
Group or Team Name
- SIUH Internal Medicine / Nephrology
Introduction
Guillain-Barre Syndrome (GBS) is an autoimmune disease damaging the peripheral nervous system that commonly presents as rapidly progressive symmetrical motor weakness. Autonomic dysfunction occurs in about 70% of GBS patients. Although there is a known association of SIADH in GBS patients, it usually occurs late in the disease course when there is maximal motor deficit. SIADH as an initial finding in patients with GBS is rare which is reported in this case.
Case Description
72-year old female with history of dyslipidemia presented with subjective complaints of bilateral lower extremity weakness and difficulty ambulating. Her initial neurological exam was normal, with no deficits. She was found to have hyponatremia at 128 mEq/l that continued to drop to 115 mEq/l despite normal saline. Her serum Osmolality was 245 Osm/L, with elevated Urine Osmolality 702 Osm/L, suggestive of SIADH. Fluid restriction 1L daily was initiated, and her sodium continued to decline to 113 mEq/l. By day 6 she was found to have lower extremity weakness with strength 1/5. CSF analysis showed an albuminocytologic dissociation (total protein 288 & WBC 3) – suggestive of GBS. Therapeutic Plasmapheresis Exchange and oral Tolvaptan was initiated. Her sodium stabilized 134-137 mEq/l. With aggressive treatment and physical therapy, she regained her strength and walked without assistance at discharge.
Discussion
GBS commonly presents as progressive symmetrical muscle weakness with absent/decreased deep tendon reflexes. Incidence of SIADH in GBS is ~4.8%. Pathogenesis of SIADH in GBS is hypothesized to be: (1) Resetting of the osmoreceptor (2) Increased sensitivity of ADH at renal tubules. Hyponatremia in our case was present on admission prior to motor deficits from GBS. Urine and serum studies confirmed SIADH requiring tolvaptan. Her GBS was treated with plasmapheresis and her sodium stabilized only after treatment of the underlying GBS. Only 2 cases of GBS with SIADH at presentation have been reported. Observational and prospective studies have shown hyponatremia in GBS is associated with poor outcomes and increase mortality.
Our case report emphasizes that SIADH may precede the development of profound motor deficit in GBS. Physicians should be aware of this rare presentation to prevent delays in treatment. Further studies are necessary to understand the cause behind SIADH in GBS and its impact on prognosis.