Key Facts

SIBO occurs when bacteria that normally colonise the colon proliferate in the small intestine. This leads to malabsorption through bile salt deconjugation, mucosal inflammation, and competitive nutrient consumption.

Epidemiology

True prevalence is uncertain due to diagnostic challenges. More common in the elderly, post-surgical patients, and those with motility disorders. Estimated to affect 30-50% of patients with Crohn's disease, 50-60% of patients with systemic sclerosis, and up to 50% of chronic PPI users in some studies.

Aetiology

• Structural: blind loops (Billroth II, Roux-en-Y), strictures (Crohn's), small bowel diverticulae, fistulae, post-surgical adhesions
• Motility disorders: diabetic autonomic neuropathy, scleroderma, chronic intestinal pseudo-obstruction, opioid use
• Reduced gastric acid: PPI use (controversial), autoimmune gastritis, vagotomy
• Immunodeficiency: IgA deficiency, hypogammaglobulinaemia, HIV
• Miscellaneous: elderly, chronic renal failure, cirrhosis

Pathophysiology

Bacteria in the small bowel: (1) deconjugate bile salts → reduced micelle formation → fat malabsorption and steatorrhoea, (2) consume vitamin B12 → B12 deficiency, (3) produce folate → serum folate often normal or raised, (4) produce gas (hydrogen, methane) → bloating and flatulence, (5) damage enterocyte brush border → disaccharidase deficiency → carbohydrate malabsorption. D-lactate-producing bacteria may cause D-lactic acidosis (encephalopathy, ataxia) in short bowel syndrome.

Symptoms

• Bloating and abdominal distension (most common)
• Flatulence (excessive)
• Watery diarrhoea or steatorrhoea
• Abdominal discomfort/cramping
• Weight loss
• Nausea

Signs of Malabsorption

• B12 deficiency: macrocytic anaemia, peripheral neuropathy, glossitis
• Fat-soluble vitamin deficiency: osteomalacia, night blindness
• Iron deficiency (mucosal damage)
• Protein malabsorption: oedema

Red Flags

• Significant weight loss (exclude structural cause/malignancy)
• Recurrent/refractory SIBO (consider underlying motility disorder or immunodeficiency)
• D-lactic acidosis: confusion, ataxia, slurred speech after carbohydrate meals (short bowel syndrome)

Bloods

• FBC: macrocytic anaemia (B12 deficiency)
• B12: low (consumed by bacteria)
• Folate: normal or raised (produced by bacteria) — this pattern (low B12, raised folate) is characteristic
• Iron studies: may be low (mucosal damage)
• Albumin: low if severe protein malabsorption
• CRP: usually normal (unless underlying Crohn's)
• Vitamin D, calcium: may be low

Special Tests

• Glucose hydrogen breath test: patient drinks glucose solution; serial breath hydrogen/methane measured; rise of >12 ppm hydrogen within 90 minutes = positive for SIBO
  • Sensitivity ~60-70%; specificity ~80%
• Jejunal aspirate culture: gold standard (>10⁵ CFU/mL) but invasive, rarely performed
• Lactulose hydrogen breath test: alternative but less specific (lactulose also fermented by colonic bacteria)

Imaging

• CT/MR enterography: assess for structural causes (strictures, blind loops, diverticulae)
• Small bowel follow-through: structural assessment
• Gastric emptying studies: if motility disorder suspected

Non-pharmacological

• Address underlying cause: correct structural abnormality if possible, optimise diabetic control, stop unnecessary PPIs, reduce opioids
• Dietary: low-FODMAP diet may help symptoms; dietitian involvement
• Probiotics: limited evidence; some benefit in selected patients

Pharmacological

• First-line: rifaximin 400 mg TDS × 14 days (non-absorbed, well-tolerated; response rate ~50-70%)
• Alternatives: metronidazole 400 mg TDS × 14 days, co-amoxiclav 625 mg TDS × 14 days, ciprofloxacin 500 mg BD × 14 days, doxycycline 100 mg BD × 14 days
• Relapsing SIBO: cyclical antibiotics — 1-2 weeks every month; rotate between agents to reduce resistance
• Nutritional supplementation: B12 (hydroxocobalamin IM if deficient), fat-soluble vitamins, iron as needed
• Prokinetics: consider if motility disorder contributing (erythromycin 250 mg TDS, prucalopride 1-2 mg OD)

Surgical/Interventional

• Revision of blind loop or surgical cause if amenable
• Stricturoplasty for Crohn's-related strictures

Referral Criteria

• Gastroenterology: for investigation and management of refractory/relapsing SIBO
• Dietitian: nutritional assessment
• Surgery: if correctable structural cause identified

Prognosis depends on the underlying cause. If a correctable cause is identified and treated, SIBO can be cured. Many patients have relapsing disease requiring cyclical antibiotics. Response to antibiotics is typically seen within days. Rifaximin has the best evidence and tolerability. Long-term outcomes are generally good with appropriate management, but persistent malabsorption can occur if the underlying condition is not addressed.

SIBO Diagnostic Approach

B12 vs Folate Pattern in SIBO