MON-007 - Acute Colonic Pseudo-obstruction in Patient with Adipsic AVP Deficiency: A Case Report

Background: Adipsic Arginine Vasopressin Deficiency (AVP-D) is a rare disorder characterized by the loss of osmotic thirst triggers, leading to high-risk water homeostasis. While metabolic derangements are known to incite Acute Colonic Pseudo-obstruction (ACPO), or Ogilvie’s Syndrome, its occurrence during the correction of profound hyponatremia in a patient with panhypopituitarism presents unique diagnostic and therapeutic challenges.

Case Presentation: A 46-year-old male with craniopharyngioma status post radiation therapy and transsphenoidal surgeries complicated by blindness, panhypopituitarism and adipsic AVP-D presented with one week of progressive confusion, emesis, and diarrhea. As per collateral history from his spouse, the patient was following his prescribed desmopressin (DDAVP) regimen but he was drinking more than his prescribed volume of free water. Initial labs showed profound hyponatremia (106 mmol/L) with serum osmolality of 226 mOsm/kg and urine osmolality of 480 mOsm/kg. CT head/neck ruled out any acute intracranial pathology. Initial CT abdomen and pelvis did not reveal an obstruction or colitis. Cortisol level and free thyroxine level were within normal range. While correcting the serum sodium at a rate of no more than 8–10 mmol/L/24h using fluid restriction and intermittent desmopressin dosing, the patient developed massive abdominal distension. Abdominal X-ray confirmed diffuse colonic dilation consistent with ACPO without mechanical blockage. He was maintained on nil per os (NPO) status. Neostigmine was considered but withheld due to sinus bradycardia down to heart rate of 49 beats per minute. A Malecot rectal tube was placed and was followed by endoscopic decompression. He was started on polyethylene glycol (PEG) three times a day and docusate twice a day. Daily abdominal X-Rays were obtained to monitor for improvement of colonic distension. While being managed for his ACPO, there were instances of unpredictable brisk hypotonic urine output resulting in hypernatremia despite the scheduled oral DDAVP use. As some doses of DDAVP were co-administered with PEG, it was surmised that PEG could have led to poor absorption of DDAVP and thus DDAVP doses were separated from PEG by at least 4 hours. This change led to the return of the expected pharmacokinetics of DDAVP. The pseudo-obstruction resolved in 10 days.

Conclusion: This case demonstrates that severe hyponatremia and its subsequent correction can potentiate ACPO. Clinicians must maintain suspicion for pseudo-obstruction in patients with profound hyponatremia, particularly as serum sodium values reach target levels. Given the vital nature of DDAVP in a patient with adipsic AVP-D, it is also important to ensure there are no agents that are interfering with its absorption which can lead to significant hypernatremia in a patient that is unable to compensate due to an impaired thirst mechanism.

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