SHORT BOWEL SYNDROME

Michael D. Sitrin, MD
SUNY at Buffalo
 CASE HISTORY

CC: 52 yo man referred for Crohns disease, short bowel

syndrome, and hypomagnesemia

HPI: Hx of Crohns for 34 years. Total colectomy in 1972

and 5 small bowel resections for obstruction; last surgery
in 2000 for stomal dysfunction. Weight stable. Empties
ostomy bag 6-8 x/d. Recently ostomy output somewhat
looser. Hospitalized with marked fatigue and weakness,
eyes twitching, palpitations. Noted to be severely
hypomagnesemic and hypocalcemic.
 CASE HISTORY 2

PMH: GERD, cholecystectomy, hypertension, multiple

kidney stones
Medications: Norvasc, Asacol, Cortisone 25 mg bid,
Nexium, Calcitriol 0.5 mcg qd, Nasal cobalamin, Ambien,
Xanax, Mg oxide 2000 mg/d; Citracal+D 4/d, Centrum
PE: Abd: multiple scars; ostomy; Neuro: neg Trousseaus,
Chvosteks
Lab: SB xray 6 mo. ago reported no recurrence; Mg 0.2
mg/dl; Ca 5.2 mg/dl; 24 hr urinary calcium 7 mg/d
 CASE HISTORY 3

Recommendations:
1. Mg sulfate 50% 2cc IM weekly
2. 24 hr ostomy collection for fat, weight
3. Check 25 OH D and 1,25 (OH)2 D levels
4. Lomotil regularly
5. Small bowel xray and ileoscopy to look for recurrent
Crohns
6. Change Asacol to Azathioprine
 CASE HISTORY 4

Follow up:
1. Weight gain 4 lbs
2. Some improvement in fatigue, strength
2. Thicker ostomy output
24 hr weight 2454 gm; fecal fat 122 gm/d
3. Serum Mg 1.2 mg/dl; calcium nl
4. 25 D 17 ng/ml; 1,25 D 50 pg/ml
5. SB x-ray, ileoscopy: recurrent Crohns
 SHORT BOWEL SYNDROME

Clinical consequences of small intestinal

resection, with or without some additional
loss of colon
 COMMON CAUSES OF SHORT
BOWEL SYNDROME
Adults Children
Vascular Prenatal
Thrombosis or embolus Vascular accidents
Volvulus Atresia
Strangulated hernia Volvulus
Post-surgical Abdominal wall defect
J-I bypass Postnatal
Trauma Necrotizing enterocolitis
Miscellaneous Trauma
Crohns Crohns
Radiation enteritis Volvulus
Neoplasms Thrombosis or embolus
 FACTORS INFLUENCING THE
METABOLIC CONSEQUENCES OF
INTESTINAL RESECTION
Extent of resected bowel
Site of resected bowel
Presence of ileo-cecal region
Condition of remaining bowel and digestive
organs
Degree of adaptation in the residual small
and large intestine
 EXTENT OF RESECTED
BOWEL
Resection of 50% of small bowel little
problem in sustaining normal nutritional
status
Less than 1 foot of small bowel remaining
__ will almost require permanent TPN

75% or greater small bowel resection

severe malabsorption
 SITE OF SMALL BOWEL
RESECTION
Jejunal resection generally better tolerated
Ileum
Bile salt, B12, transcellular magnesium absorption
Ileo-cecal nutrients regulate gastric empting and small
bowel transit (ileal brake)
Ileal hormones important in adaptation
Less than 100 cm of ileal resection leads to watery
diarrhea. Hepatic bile salt synthesis increased to
compensate for losses. Bile salts cause colonic
secretion of fluid and electrolytes
More than 100 cm of ileal resection leads to
steatorrhea. Hepatic synthesis cannot compensate for
losses, and bile salt depletion occurs
 ILEO-CECAL REGION
Ileal brake slows gastric emptying and
decreases intestinal transit (GLP-1, GLP-2,
Peptide YY)
Loss of this segment may result in increased
bacterial colonization of the small intestine,
i.e. bacterial overgrowth
 CONDITION OF THE REMAINING
BOWEL AND DIGESTIVE ORGANS
Colon
Absorption of water and electrolytes; those
with short bowel and preserved colon have less
diarrhea, electrolyte and acid-base disturbances
Energy salvage, e.g. short chain fatty acids
Increased absorption of other nutrients, e.g.
possibly calcium, folate
Crohns disease even mild recurrence may
severely affect the patient with short bowel
 INTESTINAL ADAPTATION
Gradual improvement
in absorption of
energy, protein, and
other nutrients after
resection
Hyperplasia of
remaining intestine
Absorption generally
proportional to
mucosal weight, # of
cells per unit length;
calcium absorption
may be increased in
individual cells
 FACTORS STIMULATING
INTESTINAL ADAPTATION
Exposure of remaining intestine to nutrients
TPN results in intestinal hypoplasia
Bulk or non-nutritive agents generally do not stimulate
adaptation
Pancreatic and biliary secretions
Trophic effects of hormones (GLP-2) and other
factors
Stimulation by polyamines
Neural factors
Increased blood flow to the remaining bowel
GLUCAGON-LIKE PEPTIDE 2 (GLP-
2)
Secreted by L-cells in
ileum and colon
Secretion stimulated by
CHO>fat>protein
Induces proliferation in
small bowel and colon by
stimulation of crypt cell
proliferation and
inhibition of apoptosis
GLP-2 analogue improves
absorption in short bowel
syndrome
 CLINICAL FEATURES OF THE
SHORT BOWEL SYNDROME
Diarrhea
Rapid transit
Osmotic (carbohydrate)
Increased water and electrolyte secretion
Bile acids
Steatorrhea
Gastric hypersecretion and peptic ulceration
Related to length or resection, not clearly site
Loss of inhibitory factors from small bowel
May contribute to malabsorption (similar to Z-E
syndrome)
 RENAL CALCULI AND ENTERIC
HYPEROXALURIA
Calcium oxalate stones
Increased absorption of
dietary oxalate, mainly in
colon; patients with short
bowel and ileostomy do
not have hyperoxaluria
Increased oxalate
solubility and increased
colonic permeability; fatty
acids and bile acids
increase permeability
Other factors such as
decreased urine volume,
citrate
 CLINICAL FEATURES OF THE
SHORT BOWEL SYNDROME
Gall stones
Ileal resection causes a 2-3 fold increase in incidence
Loss of bile salt enterohepatic circulation, leading to
increased hepatic cholesterol synthesis
Effect of cholesterol saturation variable
Up to 40% of gallstones after ileal resection are radio-
opaque pigment stones
 MALABSORPTION AND
NUTRITIONAL DEFICITS
Can have any nutritional deficiency
Most common micronutrient deficiencies are fat
soluble vitamins, B12, divalent cations,
particularly with ileal resection
Folate deficiency -- IBD on sulfasalazine
Iron deficiency -- present in 20-25%, particularly
in those with ongoing blood loss, e.g. Crohns
Zinc deficiency -- losses proportional to fecal
output
 MEDICAL MANAGEMENT OF THE
SHORT BOWEL SYNDROME 1
Anti-diarrheal agents
Increase intestinal contact and improve absorption
Encourage food intake by diminishing post-prandial
symptoms
Narcotic derivatives are most useful
Liquid medications often helpful
Cholestyramine only useful with small ileal resections
and little steatorrhea
Octreotide (somatostatin analogue) may decrease stool
volume; however, may worsen malabsorption,
increased risk of gall stones; effect on diarrhea may be
transient
 MEDICAL MANAGEMENT OF THE
SHORT BOWEL SYNDROME 2
Antisecretory agents (H2 blockers, PPI)
Prevent post-operative peptic ulcers
Decreases stool output (about 20%) in stable, ambulatory
short bowel patients
Antibiotics for bacterial overgrowth
Pancreatic enzymes
Rarely indicated
Proximal resections decreased CCK and secretin release
Severe protein-calorie malnutrition
Teduglutide
GLP-2 analogue increases salt and water absorption and
decreases TPN requirement
 NUTRITIONAL THERAPY -- TPN

Premature feeding causes massive diarrhea,

dehydration, electrolyte and acid-base
disturbances
Limited oral intake to stimulate adaptation
>30-50 cm of small bowel + colon off TPN in 1
year; need >60 cm of small bowel without colon
to avoid permanent TPN (Gouttebel)
Once stabilized, home TPN while oral feeding is
resumed and intestinal adaptation is occurring
Long-term home TPN for gut failure
 DIETARY MANAGEMENT OF THE
SHORT BOWEL SYNDROME

Traditional recommendation
Low fat
Low lactose
Low fiber
 SHORT BOWEL SYNDROME
DIETARY FAT
Jejunostomy or ileostomy
No difference in ostomy output with high fat vs high
carbohydrate diet
Not at risk for enteric hyperoxaluria
Fat soluble vitamin and divalent cation losses
No benefit from severe fat restriction
Short bowel + residual colon
Fatty acids stimulate colonic water and electrolyte
secretion
At risk for enteric hyperoxaluria
May benefit from fat restriction (50-60 gm/d); need to
be certain that energy intake is sufficient
 SHORT BOWEL SYNDROME
CARBOHYDRATES
Lactose intolerance common
Rapid transit
Immature enterocytes
Avoid concentrated sweets (dumping)
May be helpful to separate liquids and
solids
 SHORT BOWEL SYNDROME
DIETARY FIBER
Effects on motility depend on type
Bran accelerates transit; pectin decreases gastric
emptying and decreases intestinal transit
Some fibers bind bile salts and/or have water
retaining capacity
Some fiber metabolized by gut bacteria to short
chain fatty acids, which are a colonic fuel and
stimulate proliferation in small bowel and colon
Individualize fiber intake to control symptoms
 SHORT BOWEL SYNDROME
VITAMIN/MINERAL SUPPLEMENTS
Therapeutic multiple vitamin
Ileal resection
Fat soluble vitamins; may need high doses; monitor
serum levels
Divalent cations
Oral Mg supplementation difficult as it induces more diarrhea;
IM or IV supplements often needed
Zinc losses proportional to severity of diarrhea
B12; can be supplemented im, po, or by nasal spray
Osteoporosis or osteomalacia
Calcium and vitamin D
Monitor bone density
 SHORT BOWEL SYNDROME
HYPOMAGENSEMIA
Hypomagnesemia may
cause muscle cramps,
tetany, cardiac
arrhythmias, etc.
A greater number of
short bowel patients
have cellular
depletion, causing
weakness, fatigue, etc.
 SHORT BOWEL SYNDROME
HYPOCALCEMIA
Hypocalcemia is not due to dietary calcium
lack or calcium malabsorption; mobilization
from bone will defend the serum calcium
Hypocalcemia reflects impairment of the
PTH-vitamin D endocrine system
Hypomagnesemia interferes with PTH
secretion and action and the synthesis of
1,25(OH)2 vitamin D
TRUSSEAUS SIGN