(1435) Syndrome of Inappropriate Antidiuretic Hormone via the Oculo-Hypothalamic Reflex

Introduction: This case outlines the diagnosis and stepwise approach to treatment of a patient with refractory SIADH and recognizes the connection between the eye and the posterior pituitary gland.

Description: An 82-year-old woman presented to the hospital with left eye pain and redness after cataract surgery. Upon ophthalmologic examination, she was diagnosed with bacterial endophthalmitis and started on antibiotics. Lab work was consistent with euvolemic hyponatremia. Her TSH, cortisol, and blood glucose were within normal limits. She was started on balanced crystalloid infusion and repeat testing revealed continued euvolemic hypotonic hyponatremia. Given concern for syndrome of inappropriate anti-diuretic hormone (SIADH), she was fluid restricted and given hypertonic saline infusion. Due to persistent severe hyponatremia, urea powder and sodium chloride tablets were initiated. Given the persistent hyponatremia, she underwent enucleation of her left eye and hyponatremia improved afterwards.

Discussion: This case reflects persistent and refractory SIADH due to endophthalmitis that ultimately corrected upon enucleation. Diagnosis of SIADH involves excluding other causes of the patient’s hyponatremia and understanding the timeline of serum sodium changes. Our patient had no known history of malignancy, pulmonary disease, CNS disorders, or medications typical of causing SIADH. Given the clinical scenario, the etiology of SIADH was secondary to endophthalmitis. This can be explained by ophthalmologic innervation of the vagus nerve. Through vagal efferents to the solitary nucleus, chemoreceptors have projection into the posterior pituitary gland. As demonstrated in our case, persistent activation of this reflex can lead to profound SIADH and hyponatremia.

The approach toward the treatment of SIADH should involve treatment of the cause, free water restriction, and sodium chloride administration. If this is ineffective for improvement in serum sodium levels, then additional therapy with urea or vasopressin receptor antagonists are required. In our case, activation of the ocular-hypothalamic reflex from endophthalmitis led to persistent SIADH that required a treatment approach concentrated around antibiotics and eventual surgical correction.