S1794 Refractory Hypokalemia in the Setting of Ogilvie Syndrome

Abstract

Introduction: Ogilvie Syndrome often results from a disruption of the parasympathetic nervous system due to electrolyte abnormalities. This case study examines a unique presentation of Ogilvie Syndrome involving secretory diarrhea with increased fecal potassium losses resulting in refractory hypokalemia. This case explores the use of cholinesterase inhibitors, aldosterone antagonists and potassium sparing diuretics in the management of such cases of colonic pseudo-obstruction. Case Description/Methods: An 83 year-old male presented with encephalopathy and abdominal pain. Physical examination was notable for significant abdominal distention. Labs demonstrated severe hypokalemia. CT abdomen revealed massive colonic distention with cecal diameter at 10 cm. Neither CT nor contrast enema study showed signs of mechanical obstruction. Initial management was focused on replacing potassium prior to considering other pharmacologic therapy. Despite aggressive replacement, the hypokalemia persisted. Further workup of the hypokalemia was consistent with non-renal losses. Stool studies were consistent with fecal potassium losses. A potassium-sparing diuretic and aldosterone antagonist were used to increase potassium levels, but with ongoing diarrhea, hypokalemia continued to recur. The patient was subsequently treated with neostigmine with swift resolution of the pseudo-obstruction. Once the diarrhea resolved, the patient was able to maintain his response to hypokalemia therapy. Discussion: Ogilvie syndrome is a functional obstruction thought to be due to disturbance in the parasympathetic system that has been associated with electrolyte abnormalities and is usually treated with conservative management including electrolyte replacement and physical therapy. Colonic pseudo-obstruction is often associated with secretory diarrhea and hypokalemia. In some patients, most commonly, end stage renal patients, an overexpression of potassium cotransporters helps eliminate potassium when kidneys are unable. This has been thought to contribute to hypersecretion of potassium with diarrhea. Our patient had severe hypokalemia despite aggressive electrolyte replacement with high fecal potassium losses. As aldosterone increases urinary excretion of potassium in the urine, antagonists are used to treat hypokalemia. While it is not yet the standard of care, it is important to recognize that potassium-sparing aldosterone antagonists can improve and aid in the management of this type of Ogilvie Syndrome.