Short Bowel Syndrome (SBS) 

Short bowel syndrome is a malabsorptive state resulting from extensive resection or functional loss of small intestine, leading to fluid, electrolyte, and nutrient deficiency.

1. Definition

Short Bowel Syndrome (SBS) is defined as:

Malabsorption resulting from <200 cm of functional small intestine remaining (normal length ≈ 300–800 cm).

Severe intestinal failure:

• <100 cm jejunum without colon
• <50–60 cm small bowel with colon

2. Anatomy 

Outcome depends on:

• Remaining bowel length
• Presence of ileum
• Presence of colon
• Presence of ileocaecal valve

 Jejunum

• Major site of:
• Carbohydrate absorption
• Protein absorption
• Water-soluble vitamins
• Highly adaptable
• Loss is better tolerated

 Ileum

• Absorbs:
• Vitamin B12
• Bile salts
• Less adaptable than jejunum
• Resection → severe consequences

 Colon

• Absorbs:
• Water
• Sodium
• Short-chain fatty acids (SCFAs)
• Presence markedly improves prognosis

3. Types of SBS 

4. Causes of SBS

Adults

• Crohn’s disease (most common in adults)
• Mesenteric ischemia
• Trauma
• Radiation enteritis
• Volvulus

Children

• Necrotizing enterocolitis
• Congenital atresia
• Midgut volvulus

5. Phases of SBS 

 1. Acute Phase (First 3–4 weeks)

• Massive diarrhea
• Fluid & electrolyte loss
• Gastric hypersecretion
• High stoma output (>2L/day)

Management:

• IV fluids
• Electrolyte correction
• PPI/H2 blocker
• TPN

 2. Adaptation Phase (Up to 1–2 years)

Structural adaptation:

• Villous hypertrophy
• Increased crypt depth
• Increased diameter

Hormonal mediators:

• GLP-2
• Growth hormone
• EGF

 3. Maintenance Phase

• Stabilised absorption
• Chronic nutritional management

6. Pathophysiology 

A. Fluid Loss

• Jejunum absorbs poorly without ileum
• Loss of colon → severe dehydration

B. Bile Salt Malabsorption

• Ileal resection <100 cm → bile salt diarrhea
• 100 cm → fat malabsorption → steatorrhea

C. Vitamin B12 Deficiency

• Terminal ileum resection → megaloblastic anemia

D. Hypergastrinemia

• Loss of inhibitory hormones → ↑ acid
• Inactivates pancreatic enzymes

E. D-lactic Acidosis 

Seen in:

• Colon present
• High carbohydrate intake

Mechanism:

• Colonic bacterial fermentation → D-lactate

Features:

• Confusion
• Ataxia
• Slurred speech

7. Clinical Features

Early

• High-output diarrhea
• Dehydration
• Hypomagnesemia
• Hypokalemia

Chronic

• Weight loss
• Steatorrhea
• Vitamin deficiencies:
• A → night blindness
• D → osteomalacia
• K → bleeding
• B12 → neuropathy

8. Complications 

 —TPN-Related

• Catheter sepsis
• Liver disease (cholestasis)
• Steatosis
• Cirrhosis

 —Renal Stones

• Oxalate stones
  Mechanism:
• Fat binds calcium
• Free oxalate absorbed

— Gallstones

• Due to bile salt depletion

— Metabolic Bone Disease

9. Investigations

• FBC → anemia
• U&E → electrolyte imbalance
• Magnesium (often low)
• Vitamin levels
• 72-hour fecal fat
• B12 level
• D-lactate if suspected

10. Management 

1. Fluid Management

Avoid:

• Hypotonic fluids
• Sugary drinks

Use:

• Oral rehydration solution (WHO-type)
• High sodium (90 mmol/L)

2. Diet

• High complex carbs
• High protein
• Moderate fat (if colon present)
• Low oxalate
• Small frequent meals

 3. Drugs

Teduglutide4

Mechanism:

• GLP-2 analogue
• Enhances mucosal growth
• Reduces TPN dependence

4. Parenteral Nutrition

Indications:

• <100 cm bowel
• High-output stoma
• Severe malnutrition

Complication to remember:
TPN-induced liver disease

5. Surgery

• Intestinal lengthening (Bianchi procedure)
• STEP procedure
• Intestinal transplant (last resort)

11. Prognostic Factors

Good prognosis:

• Colon present
• 100 cm bowel
  
• Ileocaecal valve present

Poor prognosis:

• End jejunostomy
• <50 cm bowel
• No colon

12. Clinical cases