Microscopic colitis and short bowel syndrome

• Microscopic colitis is one of the commonest causes of chronic, watery, non-bloody diarrhoea in older adults, especially women in older adulthood. The colon looks normal at endoscopy; the diagnosis comes from biopsies.
• Its two main forms are collagenous colitis, with a thickened collagen band under the surface, and lymphocytic colitis, with excess lymphocytes in the lining. A mixed or incomplete form also occurs.
• Essential treatment is oral budesonide 9 mg once daily for 8 weeks, which induces remission in most patients; mesalazine, systemic steroids and antibiotics are not recommended ^[1][2].
• Short bowel syndrome (SBS) follows extensive resection of the small intestine. It is the commonest cause of chronic intestinal failure: the remaining bowel cannot absorb enough nutrients and fluid, so patients need specialised diets, adaptations support and sometimes parenteral nutrition.
• With a remnant of under about 180 to 200 cm of small bowel, adults are defined as having SBS; preservation of the colon turns a desperate prognosis into an adaptable one ^[5][3].
• Nutritional care is gradual adaptation over 1 to 3 years: hyperphagia, small frequent meals, oral rehydration, micronutrient replacement, parenteral support when needed, and drugs such as teduglutide 0.05 mg/kg/day subcutaneously in selected patients ^[3][5].

By the end of this page you should be able to:

1. Define microscopic colitis, its three histological forms, and its diagnostic histology.
2. Recognise the typical presentation in an older adult and plan the investigation that confirms or excludes it.
3. Explain why oral budesonide is first-line and state its induction dose and duration, plus the alternatives that are not recommended.
4. Define short bowel syndrome and intestinal failure, classify the SBS anatomy types, and interpret a residual bowel length.
5. Outline intestinal adaptation and the dietary, pharmacological and surgical measures that support it.
6. Design a parenteral nutrition and micronutrient plan and list the common complications and how to monitor them.

Microscopic colitis is a chronic inflammatory condition of the colon that produces watery, non-bloody diarrhoea while the mucosa looks normal or almost normal at colonoscopy. The diagnosis is histological: a pathologist recognises characteristic changes in colonic biopsies ^[1].

Three forms are recognised:

• Collagenous colitis (CC): a thickened subepithelial collagenous band of 10 micrometres or more, combined with increased inflammatory cells in the lamina propria.
• Lymphocytic colitis (LC): twenty or more intraepithelial lymphocytes per 100 surface epithelial cells, with increased inflammation in the lamina propria and no significant collagen thickening (under 10 micrometres).
• Incomplete microscopic colitis (MCi): inflammatory, collagen or intraepithelial lymphocyte changes that do not reach the thresholds above, but still form a coherent clinical picture. UEG/EMCG 2021 defines this as a collagen band over 5 but under 10 micrometres and/or more than 10 but fewer than 20 intraepithelial lymphocytes per 100 cells ^[1]; the Münch 2021 trial used a broader inclusion range of an abnormally thickened collagen band (5 to 9 micrometres) and/or more than 5 but fewer than 20 intraepithelial lymphocytes per 100 cells ^[2].

MCi is not a rarity: about 6% of cases in a large US series, 14% in a European registry and 19% in a Danish series fall into the incomplete category, and patients respond to treatment much as they do for the classical forms ^[2]. The line between MC and functional diarrhoea is often thin, which is why random biopsies matter even when the mucosa looks normal.

MC is an increasingly recognised cause of chronic diarrhoea in the West. The pooled incidence is about 11.4 cases per 100,000 person-years, with CC ranging from 0.6 to 16.4 and LC from 0.6 to 16.0 per 100,000 person-years ^[1]. Prevalence is around 119 per 100,000 people. Among patients who actually have chronic watery diarrhoea, MC is found in about 12.8% of cases ^[1].

and women are affected more often than men. Smoking, both past and current, raises the risk of both CC and LC. Chronic or frequent use of proton pump inhibitors, NSAIDs and SSRIs is associated with MC, although this does not prove causation; if a drug clearly predates and overlaps with the diarrhoea, it should be reviewed and withdrawn where possible ^[1]. Patients with MC do not carry an increased risk of colorectal cancer or adenoma, so a special surveillance colonoscopy programme is not recommended ^[1].

Microscopic colitis often coexists with coeliac disease, so screening for coeliac disease is recommended ^[1].

The cause is multifactorial and not fully settled: luminal factors, immune dysregulation and genetic predisposition all play parts ^[1]. Patients present with chronic or recurrent watery, non-bloody diarrhoea lasting weeks to years. Characteristic accompaniments include faecal urgency, nocturnal stools, faecal incontinence, abdominal pain and weight loss ^[1]. The picture overlaps heavily with irritable bowel syndrome, which is why routine care can miss it ^[2].

Examination is usually unremarkable beyond weight loss in active disease. There is no specific physical sign. Health-related quality of life falls with disease activity and with comorbid disease, and improves when remission is achieved ^[1].

Because presentation is non-specific, a guiding question is "chronic watery stool in an older adult, especially a woman, with no blood and no fever?".

The main imitators in this age group are infective colitis, inflammatory bowel disease, coeliac disease, bile acid diarrhoea, pancreatic exocrine insufficiency, laxative use and medication-induced diarrhoea. A table of separating features is below.

Work-up begins with the standard panel for any chronic diarrhoea: a full blood count, electrolytes, albumin, urea, C-reactive protein, thyroid function and coeliac serology ^[6]. Stool tests for infection, parasites and fat are added when relevant, and calcium and vitamin D when indicated. Abdominal imaging is reserved for alarm features.

Faecal calprotectin is not useful for excluding or monitoring MC, because inflammation is microscopic ^[1]. Colonoscopy (or ileocolonoscopy) with biopsies is the investigation that changes the diagnosis. Random biopsies should be taken from at least the right and left colon; endoscopic appearance is often normal and can even show subtle, non-specific vascular changes ^[1][6]. This is supported by the Japanese chronic diarrhoea guideline recommendation to perform random biopsies throughout the colon in any chronic diarrhoea, in order not to miss microscopic colitis, eosinophilic gastroenteritis and amyloidosis ^[6]. Random biopsies detect abnormal findings in a substantial minority (17 to 28%) of patients meeting Rome criteria ^[6].

Further tests have defined roles only:

• Coeliac screen for every patient with MC ^[1].
• Bile acid diarrhoea testing is not routine in MC, but can be considered when a patient does not respond to budesonide ^[1].
• Histological monitoring after starting treatment is not recommended ^[1].

The histological criteria are the definition, and they are applied to haematoxylin and eosin stained slides:

• Collagenous colitis: collagen band 10 micrometres or more, plus increased inflammatory infiltrate.
• Lymphocytic colitis: 20 or more intraepithelial lymphocytes per 100 surface epithelial cells, plus increased lamina propria inflammation, collagen band under 10 micrometres.
• Incomplete forms: collagen band 5 to 9 micrometres, and/or more than 10 but fewer than 20 intraepithelial lymphocytes per 100 cells (UEG/EMCG 2021) ^[1]; a broader range of more than 5 to fewer than 20 lymphocytes per 100 cells was used in the Münch 2021 trial ^[2].

MC should be considered, and ruled out, in any patient who meets criteria for functional bowel disease but who has risk factors or fails to respond to standard treatment ^[1].

Disease activity is judged by the Hjortswang criteria, which are also the usual remission endpoint: clinical remission is a mean of fewer than 3 stools a day and a mean of fewer than 1 watery stool a day, recorded over one week ^[1][2].

The UEG/EMCG guideline recommends oral budesonide to induce remission in both collagenous and lymphocytic colitis ^[1]. The trial basis for dosing is budesonide 9 mg once daily (as gastro-resistant granules) for 8 weeks, taken in the morning ^[2]. In that randomised, placebo-controlled multicentre trial in incomplete microscopic colitis, the remission rate at 8 weeks was 71.4% with budesonide versus 43.5% with placebo (not statistically significant at the 0.05 level because the study was stopped early for poor recruitment), with a fall in soft or watery stools from 16.3 to 7.7 per week (p = 0.0186) and improved quality of life; side effects were minimal ^[2]. Budesonide is recommended as a first-line treatment for microscopic colitis in general ^[2].

For maintenance, oral budesonide is effective in collagenous colitis and can be considered in lymphocytic colitis; decisions about tapering and duration should be guided by activity and by local practice, with attention to bone mineral density when treatment is prolonged ^[1].

• Mesalazine is not recommended for inducing remission ^[1].
• Systemic prednisolone and other corticosteroids apart from budesonide are not recommended ^[1].
• Antibiotics and probiotics are not recommended ^[1].
• There is insufficient evidence to recommend bismuth subsalicylate ^[1].
• Loperamide has no trial evidence in MC, but because it works in chronic diarrhoea it is favoured by expert opinion for mild disease ^[1].
• Bile acid binders are suggested when MC coexists with bile acid diarrhoea ^[1].

For patients who fail budesonide, thiopurines, anti-TNF drugs or vedolizumab can be used to induce and maintain remission; methotrexate is not recommended ^[1]. Surgery is an option of last resort in selected patients after all medical therapy has failed ^[1]. Testing for bile acid diarrhoea can be considered in non-responders ^[1]. Drugs with a suspected chronological relationship to the diarrhoea, such as proton pump inhibitors, NSAIDs and SSRIs, should be reviewed and withdrawn where possible ^[1].

Bone health deserves attention: the fracture risk does not appear to increase with budesonide in MC, but prolonged use may reduce bone mineral density ^[1]. No specific colon cancer surveillance is needed ^[1].

Short bowel syndrome (SBS) is a malabsorptive disorder that follows surgical resection of the small intestine. It is the commonest cause of chronic intestinal failure worldwide ^[3].

Intestinal failure itself is defined by two elements: reduced assimilation of macronutrients and/or water and electrolytes because of impaired gastrointestinal function, plus a requirement for intravenous supplementation ^[3]. An adult has SBS when the remaining functional small intestine measures fewer than about 180 to 200 cm (normal length 275 to 850 cm) ^[5].

Three anatomical types are recognised, and they determine both symptoms and prognosis ^[4]:

• Type 1, SBS-J: a short bowel ending in an end jejunostomy. Highest fluid and electrolyte losses.
• Type 2, SBS-JC: jejunal stump anastomosed to the colon, with no ileocaecal valve.
• Type 3, SBS-JIC: jejuno-ileal anastomosis with the ileocaecal valve and the whole colon preserved. Best prognosis.

A colon in continuity can be decisive: even with only 50 cm of small bowel, an intact ileocaecal valve and whole colon can maintain hydration and progress towards enteral autonomy ^[4]. Conversely, an end jejunostomy requires the gut to absorb all the fluid it secretes. ^[3]

For children, intestinal failure has been defined as a need for parenteral nutrition for more than 60 days (NASPGHAN) or for more than 60 days within the last 74 days (ASPEN), because of intestinal disease, dysfunction or resection; the paediatric forms carry a different set of problems and often grow into adult patients on long-term support ^[3].

The worldwide prevalence of SBS is estimated at 0.12 to 2.74 per 100,000 people, depending on region ^[4]. In a large ESPEN registry, SBS accounted for 67% of cases of intestinal failure across 65 centres in 22 countries ^[3]. Roughly 15% of adults who undergo intestinal resection develop SBS ^[4].

Adult causes differ from paediatric ones. The most common adult causes are mesenteric ischaemia, Crohn's disease and malignancy; volvulus and trauma matter too ^[4]. Paediatric cases come largely from congenital atresias, gastroschisis, midgut volvulus and necrotising enterocolitis. In the ESPEN data, Crohn's disease predominates in end-jejunostomy disease (SBS-J), while mesenteric ischaemia predominates in the colon-in-continuity types ^[3].

Knowing which segments remain is clinically essential. The jejunum absorbs most carbohydrate; the ileum absorbs bile acids, vitamin B12 and iron; the colon ferments carbohydrate to short-chain fatty acids and salvages fluid. A surgeon's note of resected length and remaining segments is often the most useful single document for long-term management ^[4].

The gastrointestinal tract normally secretes 7 to 9 litres of fluid a day and receives 2 to 3 litres of intake, and almost all of this is normally absorbed. After major resection, unabsorbed fluid and nutrients cause high-volume diarrhoea, dehydration and electrolyte loss ^[4].

The gut does adapt, but slowly. Structural and functional changes (taller villi, deeper crypts, slower transit, increased surface area) continue for about 2 to 3 years after resection ^[4][5]. Most adaptation is thought to occur within 12 to 24 months ^[5]. Trophic signals come from enteral nutrients in contact with the mucosa, pancreatic and biliary secretions, blood flow, and hormones such as glucagon-like peptide-1 and peptide YY. The colon's microbiota contribute by fermenting unabsorbed carbohydrate into short-chain fatty acids that can act as a fuel. For optimal adaptation in adults, more than 100 cm of healthy small intestine generally needs to be preserved ^[3].

A plateau can be reached where weaning from parenteral support stalls; at that point pharmacological enhancement of adaptation is considered ^[4].

Presentation depends on anatomy and on how long after surgery the patient is seen. Acute features are high stoma output or watery diarrhoea, thirst, dehydration and rapid weight loss, with electrolyte disturbance, especially of sodium, potassium and magnesium. In the large US inpatient series, fluid and electrolyte imbalance accounted for 52.5% of hospital admissions and sepsis or bacteraemia for 41.1%; in-hospital mortality averaged 3.8% ^[3]. Chronic features are steatorrhoea, fat-soluble vitamin deficiency (A, D, E, K), vitamin B12 deficiency, oxalate nephropathy and kidney stones, metabolic bone disease and small-bowel bacterial overgrowth with bloating and acidosis. ^[5]

Useful assessment:

• Residual anatomy: the operative note and any postoperative imaging or contrast study; plain film estimates of bowel length are unreliable, but CT or MR enterography estimates length better.
• Citrulline: a plasma marker that can be used tentatively as a measure of absorptive mass and of the likelihood of achieving enteral autonomy ^[4].
• Output and absorption: stool weight, the wet weight (the difference between weight of ingested food and excrement), and comparison of absorbed energy with predicted needs. Avoidance of home parenteral nutrition was associated with wet weights over about 1.4 kg per day and absorption of about 84% of predicted energy needs in one series ^[4].
• Nutritional and micronutrient profile: including the panel of vitamins and trace elements listed below.
• Small-bowel bacterial overgrowth: diagnosed by culture counts over 10^5 colony-forming units per millilitre in a duodenal or jejunal aspirate; treatment can improve enteral tolerance ^[3].
• Bone density: in patients on long-term parenteral support, because osteoporosis develops in up to 46% ^[3].

A practical threshold for starting oral or enteral intake is a faeculent output under 800 mL on nil per os; above that, the gut is not yet ready ^[4].

The first aim is to preserve bowel length. A second look at 24 to 48 hours after an emergency operation allows the surgeon to reassess marginally viable bowel. Trophic enteral feeding and oral intake should start as soon as the gut functions, to stimulate adaptation. Parenteral nutrition is usually needed in the early weeks for maintenance and for fluids and electrolytes ^[3].

Nutrition is the cornerstone of long-term management, and because every patient's anatomy differs, diets must be personalised ^[4].

• Hyperphagia: patients with SBS eat at least 1.5 times their predicted resting energy expenditure in some cases; at least 83% show hyperphagia. Intake must rise to at least 50% above predicted needs to compensate for malabsorption ^[4][3].
• Meal pattern: multiple small meals (5 to 6 a day), separating liquids from solids ^[4][3].
• Fluid: avoid large volumes of plain water with meals; use oral rehydration solution; add salt. The gut must handle 7 to 9 litres of secretions plus 2 to 3 litres of intake daily ^[4].
• Macronutrients: all three macronutrients daily, using whole foods; high-quality protein spread through the day; complex carbohydrate with meals; limit concentrated sweets and juice. Type matters:
  • End jejunostomy (Type 1): monitor steatorrhoea; moderate fat; medium-chain triglyceride oil 1 to 3 tablespoons a day, spread out, if tolerated. ^[4]
  • Colon in continuity (Types 2 and 3): a higher carbohydrate, lower fat pattern (around 60% carbohydrate, 20% fat) with monitoring of steatorrhoea and bile acid diarrhoea; restrict oxalate if kidney function is impaired or stones occur ^[4][3].
• Introduce oral nutrition gradually as stoma output falls, moving from nil per os when output is under 800 mL.
• Enteral nutrition can be valuable when dependence on parenteral support is low, using polymeric formulas, often infused continuously overnight to free the day ^[3].
• Parenteral nutrition: cycle it over 12 to 16 hours whenever possible to improve quality of life and oral intake; use appropriate vascular access; monitor line care and use antibiotic or ethanol locks to reduce sepsis; educate the patient; keep PN volume as low as oral intake allows ^[3].
• Home parenteral nutrition is for patients who cannot maintain adequate nutrition enterally, with education, suitable access and regular monitoring; the aim is always to wean ^[3].

Repletion must be guided by anatomy and by measurement. A practical panel is vitamin A, B1, B12, C, D and E, folate, iron, zinc, copper and selenium, plus magnesium ^[4]. B12 deficiency follows terminal ileal resection; magnesium is often lost with high stomal output; fat-soluble vitamins and D follow any disturbance of fat absorption. Metabolic bone disease and osteoporosis are common on long-term parenteral support, so bone health is monitored proactively ^[3].

• Antidiarrhoeal and antisecretory drugs reduce fluid loss and slow transit, and are timed before meals for best effect ^[4].
• Glucagon-like peptide-2 (GLP-2) analogues: teduglutide is given as 0.05 mg/kg/day subcutaneously in adults with SBS who remain dependent on parenteral support. Randomised trials show a fall in parenteral support volume of about 252 mL per day on average, with roughly a doubling of the responder rate (at least 20% volume reduction) and few additional adverse events. Newer analogues such as glepaglutide weekly and apraglutide are under investigation ^[5][3]. Teduglutide was licensed for adults in 2012 ^[3].
• Small-bowel bacterial overgrowth is treated with targeted antibiotics when present; treating it improves tolerance and weight gain ^[3].

The principle is to preserve and recruit bowel: a second look after emergency resection, restoring continuity to use all available bowel, and, when weaning has stalled despite full medical therapy, autologous intestinal lengthening (for example STEP or LILT) or reversal procedures. Intestinal transplantation remains the option of last resort. These steps belong in specialised intestinal rehabilitation centres ^[3][4].

• Microscopic colitis: dehydration and electrolyte upset from chronic watery stool, weight loss, impaired quality of life. Prolonged budesonide may reduce bone mineral density ^[1]. No increased risk of colorectal cancer ^[1].
• Short bowel syndrome: catheter-related infection and sepsis, thrombosis, IFALD, renal impairment and oxalate stones, metabolic bone disease (osteoporosis in up to 46% on long-term home parenteral nutrition) ^[3], micronutrient deficiency and bacterial overgrowth. Long-term outcomes are improved by early referral to an intestinal rehabilitation programme.

Adaptation in SBS continues for 2 to 3 years, so realistic counselling and regular reassessment are needed; patients who are younger and who retain colon in continuity do best ^[4][3].

• Microscopic colitis: routine screening colonoscopy for cancer is not needed ^[1]; screening for coeliac disease is recommended ^[1]. Older women are the commonest group affected, so a low threshold for biopsies in this population is appropriate. No modifiable risk factor is established apart from smoking and review of relevant medications.
• Short bowel syndrome: children who survive on parenteral nutrition grow into a new adult population with SBS; they need planned transition of care, and attention to growth, puberty, neurodevelopment and quality of life ^[3]. Prevention of SBS means careful surgical practice to preserve bowel length at the first operation.

• Microscopic colitis needs only histology for its diagnosis, so where endoscopy is unavailable the diagnosis cannot be confirmed; empirical treatment for chronic diarrhoea and referral are the fallback. Where endoscopy exists, learn to take random biopsies even when the mucosa looks normal ^[6].
• Short bowel syndrome can often be managed with oral rehydration, high-energy small frequent meals and micronutrient replacement where parenteral nutrition and specialised centres are unavailable; referral before chronic complications develop is essential, because the treatment that preserves life and independence is best delivered in a rehabilitation centre ^[3].

Microscopic colitis neighbours: chronic diarrhoea and its differential (coeliac disease, inflammatory bowel disease, bile acid diarrhoea), histopathology of inflammatory bowel disease, nutrition in inflammatory bowel disease.

Short bowel syndrome neighbours: intestinal adaptation, home parenteral nutrition, intestinal failure associated liver disease, Crohn's disease, mesenteric ischaemia, paediatric short bowel and transition to adult care, small-bowel bacterial overgrowth.