Case Presentation: 66 year old man with a history of eosinophilic granulomastosis with polyangiitis presented with ascending numbness and unsteadiness that worsened over two days and finally manifested as paraesthesia and weakness in all extremities, gait imbalance, and diplopia. Three weeks prior to presentation, the patient had received the flu vaccine. Neurology was consulted upon admission and physical exam was notable for diplopia on horizontal gaze, absent deep tendon reflexes, dysmetria, and a wide based gait. Otherwise, his exam was benign. His labs revealed normal values including normal blood cell count, electrolytes, Erythrocyte Sedimentation Rate (ESR), C-reactive protein (CRP) and IgG level. Imaginings of the head and whole spine were all negative. A lumbar puncture was performed that showed elevated protein of 68.5 mg/dL and IgG of 6.6 mg/dL. Further fluid analysis was negative for infection. Given his clinical symptoms of ataxia, diplopia, and areflexia with albuminocytologic dissociation, patient was diagnosed with Miller Fisher variant of Guillain-Barre Syndrome (GBS). Patient was started on intravenous immunoglobin therapy (IVIG) with significant improvement in his neurological exam. But his course was complicated by acute development of hyponatremia with serum sodium of 124 mEq/L (initial 143) after four sessions of IVIG therapy. Nephrology was consulted. His measured osmolality was 261 mOsm/kg and calculated osmolality was 257 mOsm/kg. Urine osmolality and sodium were 250 mOsm/kg and 28, respectively. Patient was diagnosed with glycine induced hyponatremia secondary to IVIG therapy, a phenomenon usually seen post Transurethral Resection of the Prostrate (TURP). He was started on 3% hypertonic saline for a day and then 2 doses of Ure-Na. He ultimately autocorrected his sodium. IVIG therapy was continued for 1 more session without any complications. He was then discharged to rehabilitation center.

Discussion: GBS is a clinical diagnosis that is often supported by albuminocytologic dissociation. The main features of the disease are progressive, bilateral paraesthesia/weakness and areflexia. In the Miller Fisher variant of GBS, patients usually have areflexia, ataxia, and diplopia, which our patient had. Based on Brighton Criteria, our patient reached level 1 in all diagnostic criteria except for the nerve conduction study that was not performed. CSF analysis for antibodies against GQ1B was also sent out but the results were still pending during the case write-up. There also have been well-documented cases of GBS in the setting of recent vaccination, mostly due to H1N1 “swine flu” or influenza A vaccines. Our patient had a flu vaccine 3 weeks prior to presentation. Finally, his neurological symptoms and exam improved markedly after IVIG therapy.His acute development of hyponatremia was initially an enigma. After confirming with the pharmacist, we learned that IVIG therapy namely Gammagard, that our patient received, has glycine in it. Studies have shown that glycine can cause hypotonic hyponatremia acutely in post TURP patients. During the infusion, similar phenomenon occurs and fluid is drawn towards the extravascular space by the osmotically active glycine particles, causing hyponatremia.

Conclusions: In patients presenting with acute onset of bilateral ascending weakness and areflexia, GBS should always be considered. Moreover, patient showed be closely monitored when treated with IVIG therapy as it can cause acute onset of hyponatremia.