After a limited ileal resection (often under about 100 cm), bile acids spill into the colon where they stimulate secretion of water and electrolytes, causing watery diarrhoea. Synthesis can still keep the pool topped up, so a bile acid sequestrant works. After an extensive resection (often over about 100 cm), losses outstrip even maximal synthesis, the pool shrinks, fat is malabsorbed, and a sequestrant makes things worse by removing what little bile acid is left.
The two syndromes
| Limited resection (often <~100 cm) | Extensive resection (often >~100 cm) | |
|---|---|---|
| What breaks | Ileal uptake falls; hepatic synthesis compensates | Losses exceed maximal synthesis; the pool shrinks |
| Pool size | Maintained | Depleted |
| Mechanism of diarrhoea | Bile acids in the colon drive secretion | Unabsorbed fat — steatorrhoea |
| Stool | Watery, often urgent, worse after meals | Greasy, pale, offensive, hard to flush |
| Sequestrant | Helps | Makes it worse |
| Management | Colestyramine or another sequestrant | Low-fat diet, medium-chain triglycerides, fat-soluble vitamin replacement |
The 100 cm figure is a teaching guide, not a rule. What actually matters is how much ileum remains, whether the colon is in continuity, how much adaptation has occurred, and the underlying disease.
What else to look for after an ileal resection
- Vitamin B12 deficiency. The same last stretch of ileum absorbs B12 bound to intrinsic factor. After an ileal resection, think of both problems together.
- Gallstones. A depleted bile acid pool makes bile relatively cholesterol-rich and lithogenic.
- Oxalate kidney stones. Unabsorbed fat binds calcium in the gut, leaving oxalate free to be absorbed and excreted in the urine — enteric hyperoxaluria.
- Fat-soluble vitamin deficiency — A, D, E and K, because micelles cannot form without an adequate bile acid pool.
Bile acid diarrhoea with a normal ileum
Not every case follows surgery. Bile acid diarrhoea also occurs with an entirely normal terminal ileum, when the FGF19 feedback signal is deficient. The ileum fails to send the hormone that switches off CYP7A1, synthesis runs unchecked, and more bile acid reaches the colon than it can handle. The synthesis marker serum C4 is raised. This form is frequently mislabelled as diarrhoea-predominant irritable bowel syndrome, and it responds well to a sequestrant.
Other causes worth knowing
- Crohn's disease of the terminal ileum, even without resection
- Cholecystectomy — a minority get persistent loose stools because bile now trickles continuously rather than being released in a bolus
- Radiation enteritis
- Coeliac disease and small bowel bacterial overgrowth
How it is confirmed
The SeHCAT scan measures retention of a synthetic bile acid; retention below 15% at seven days supports the diagnosis. Where SeHCAT is unavailable, serum C4 or FGF19, or simply a carefully observed trial of a sequestrant, are used instead.
The question to ask yourself
Two patients, both with diarrhoea after ileal resection — one of about 60 cm, one of about 180 cm. Which gets a sequestrant? The shorter one. In the longer resection the pool is already depleted, and binding what remains turns a secretory diarrhoea into worse steatorrhoea.