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Abstract: PO1122

Colonic Pseudo-Obstruction and Hypokalemia

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Hamid, Akbar H., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
  • Puri, Isha, SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
  • Mallappallil, Mary C., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
  • Oh, Man S., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
  • Salifu, Moro O., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
Introduction

Ogilvie's syndrome, or colonic pseudo-obstruction, is the pathologic dilation of the colon without underlying mechanical obstruction. It is caused by increased sympathetic activity or reduced parasympathetic activity. The common manifestation is constipation, but sometimes it may be associated with diarrhea when potassium secretion is greatly increased by stretch-activated maxi-K channel, also known as BK channel, resulting from dilatation of the colon. While exact mechanism is unclear, diagnosis is based on clinical and radiologic grounds.

Case Description

A 69 year old African American female with history of diabetes mellitus, hypertension, hyperlipidemia, and HIV infection presented with worsening lower back pain. Initial labs showed leukocytosis, anemia, mild renal impairment, and paraprotein gap. MRI of the spine showed extensive compression deformities and epidural extension, with lytic lesions on skeletal survey. Bone biopsy showed >80% blast cells with marked increase in circulating plasma cells, confirming plasma cell leukemia. Abdominal CT showed dilated ascending colon suggestive of obstruction, but she was having normal bowel movements. She successfully underwent induction therapy and was discharged. When she was readmitted for second cycle of chemotherapy, serum potassium of 1.8 mmol/L with U wave on ECG noted. She also complained of abdominal distension, diarrhea, and bilateral lower extremity edema. Despite aggressive potassium supplementation, her potassium level persistently remained below 3.5 mmol/L. Initial urine potassium was 23 mmol/L, which peaked at 45.8 mmol/L before becoming anuric. First stool potassium was >100 mmol/L with stool volume of 900 mL. Repeat stool study after a week showed stool potassium 95.9 mmol/L with stool sodium 42 mmol/L. Abdominal x-ray on admission showed colon distension measuring up to 11.4 cm at the cecum. Serial imaging of the bowel showed worsening diffused colonic dilation. Remarkably, our patient required large doses of potassium supplement while she remained anuric.

Discussion

Colonic pseudo-obstruction may result, in some patients, in dramatic upregulation of the maxi-K channel. When potassium secretion is greatly increased, diarrhea rather than constipation becomes predominant manifestation. Diarrhea is the result of high potassium content of the stool, unlike most other secretory diarrhea which contains sodium as the main cation.