Endocrine Abstracts

Introduction: Acute Colonic Pseudo-Obstruction (Ogilvie’s syndrome) is characterized by colonic distention in the absence of mechanical obstruction. Those without ischaemia/perforation is treated conservatively by withdrawing offending drugs, correcting electrolytes/underlying risk factors, neostigmine and colonic decompression.

Case Presentation: 90-year-old frail lady from care home with HTN, CVA, and dementia, admitted with recurrent falls and unwell. After 2 days, developed abdominal distention and vomiting. She was mostly constipated. Seen by surgical team. X-ray/CT abdomen showed colonic pseudo-obstruction. Electrolytes were normal on admission. Hypokalaemia - 2 days after vomiting. Not on any drugs to cause hypokalemia. Magnesium was normal. Correction of hypokalemia was virtually impossible. She was started on spironolactone and referred to endocrine. Aldosterone, renin, and urine potassium can’t be done as on spironolactone. ODST ruled out Cushing. Sando-K and spironolactone (400mg/day) failed to maintain potassium. Distention continued despite this and flatus tube for 4 months. Age and comorbidities limited colonoscopic/surgical options. Decided for palliative discharge.

Discussion: Ogilvie’s syndrome develops in hospitalised patients with serious underlying medical/surgical conditions, with risk factors being critical illness, surgery, metabolic imbalance and nonoperative trauma. Precise mechanism - unknown. Alterations in autonomic nervous system and colonic atony is proposed. Main clinical feature is abdominal distension. 80% have abdominal pain. Nausea and vomiting in 60%. Constipation and, paradoxically, diarrhoea in 50-60% and 40%, respectively. Two variants: classical variant (common) is associated with constipation. Secretory Diarrhoea variant (less common) is associated with secretory diarrhoea, profound hypokalemia, resistance to neostigmine and decompression, and increased mortality. The latter variant may have only minimal episodes of diarrhoea. However, they will have pooling of potassium rich secretions within the distended colon, causing volume repletion, secondary hyperaldosteronism, upregulation of BK channel in colonic mucosa and raised colonic potassium secretion. Spironolactone suppress BK channel and reduce colonic (and renal) potassium secretion.