Abstract
Background:
Guillain-Barré Syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy. Hyponatremia, often caused by Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH), is a recognized but underappreciated complication of GBS. SIADH typically arises after neurological symptoms; however, rare cases may present with hyponatremia preceding neuromuscular features, complicating early diagnosis and management.
Case Presentation:
A previously well man in his 50s presented with acute confusion and drowsiness. Initial investigations revealed profound hyponatremia (serum sodium 110 mmol/L), low serum osmolality (260 mOsm/kg), and inappropriately elevated urine osmolality (550 mOsm/kg) with high urine sodium, consistent with SIADH. Thyroid and adrenal functions were normal; brain imaging was unremarkable. Over several days, he developed bilateral lower limb weakness, areflexia, and unsteadiness. Nerve conduction studies demonstrated demyelinating features confirming acute inflammatory demyelinating polyneuropathy (AIDP). Lumbar puncture revealed albuminocytologic dissociation.
Outcome:
Management included cautious sodium correction with fluid restriction and hypertonic saline, alongside IVIG (0.4 g/kg/day for 5 days). The patient showed gradual neurological recovery. At 3-month follow-up, he regained functional independence with minimal residual weakness and no recurrence of hyponatremia.
Discussion:
SIADH may rarely precede the classical neuromuscular symptoms of GBS. Early recognition of this atypical sequence is vital, as profound hyponatremia may delay the diagnosis of GBS, leading to potentially worse outcomes. Clinicians should maintain a high index of suspicion for GBS in patients presenting with unexplained hyponatremia and evolving neurological symptoms.