This document discusses the principles underlying short bowel syndrome (SBS). It begins with an introduction that defines SBS as a condition that occurs when a significant length of small intestine is resected, leaving insufficient bowel length to maintain nutritional and fluid balance. The document then covers the relevant anatomy and physiology, etiology, pathophysiology, clinical features, investigations, treatment options, and complications of SBS. It provides detailed information on how the condition disrupts normal digestive and absorptive processes.

1. PRINCIPLES UNDERLYING
SHORT BOWEL SYNDROME
PRESENTER: DR. OBIORA NWAFULUME
CENTRE: GENERAL SURGERY, UNTH

2. OUTLINE
 INTRODUCTION
 RELEVANT SURGICAL ANATOMY AND
PHYSIOLOGY
 AETIOLOGY
 PATHOPHYSIOLOGY
 CLINICAL FEATURES
 INVESTIGATIONS
 TREATMENT OPTIONS
 COMPLICATIONS
 FOLLOW UP
 PROGNOSIS / FUTURE TRENDS
 CONCLUSION / REFERENCES

3. INTRODUCTION
 The GIT has a wide range of normal
variation in length and anatomy.
 It has a large functional reserve and a
tremendous capacity to compensate
for loss of long segments.
 However, when a length beyond its
adaptive capacity is lost, life-
threatening nutritional and metabolic
complications ensue.

4. INTRODUCTION
 SBS encompasses a spectrum of
metabolic and physiologic
disturbances associated with the
inability to maintain protein-energy,
fluid-electrolytes, or micronutrient
balances while on a conventionally
accepted normal diet as a result of
anatomical or functional loss of a
significant length of the intestine.

5. INTRODUCTION
 Essentially a mal-absorptive condition
when there is severe loss of functional
absorptive surface area.
 There is inadequate functional bowel
to support nutrient and fluids
requirements for that individual,
regardless of the length of the GIT in
the setting of normal fluid and nutrient
intake.

6. INTRODUCTION
 Defined as the presence of less than
200 cm of residual small bowel in
adult patients when 70-75% of the
small intestine is resected.
OR
 less than 100-120cm of SI without a
colon,
OR
 less than 50- 70 cm of SI with a colon.

7. INTRODUCTION
 Resection of the colon alone typically
does not result in SBS.
 Diarrhoea and steatorrhoea , cardinal
symptoms of SBS, occur when the
fluid-substrate load exceeds the
absorptive capacityof the remaining
viable mucosa.

8. INTRODUCTION
 Massive small intestinal resection
compromises digestive and absorptive
processes and proper nutritional
status cannot be maintained without
supportive care.

9. Epidemiology
 Incidence and prevalence of SBS are
difficult to make.
 Estimates based on data on patients
requiring long-term home TPN for SBS
 UK: 2/1,000,000 (Lennard-Jones)
 US: 10,000-20,000 patients (Byrne et al)
 Spain: prevalence 1.8/1,000,000
(Moreno et al, 2002)
 Locally no records
 Costs about $100,000 per annum to
maintain a patient on TPN.

10. ANATOMY AND PHYSIOLOGY
 The intestine consists of small and
large intestine.
 The normal adult SI is about 600cm in
length and one inch in diameter (200-
250cm in neonate).
 Parts: duodenum, jejunum, and ileum.

11. ANATOMY AND PHYSIOLOGY
 The duodenum:
(25-30cm)
-no mesentery; most
fixed part
-merges into the
jejunum at the DJ
flexure.
 The upper 2/5th of
the small intestine is
termed the jejunum,
the remainder is the
ileum

12.  Jejunum: (160-
200cm, 8 feet)
 Wider, thicker &
more vascular than
the ileum.
 Circular folds of
mucous membrane
(valvulae
conniventes).
 Ileum: (about
350cm, 12 feet)
 The distal 3/5

13.  Large intestine: about 1.5m (5 feet)
long and 3 inches in diameter
 Parts: caecum, colon, rectum, anal
canal

14. Anatomy and physiology...
 Mucosal
comprises of
 Villi
 Crypts
 Laminal propia
 Muscularis mucosa
 Receptor sites on
the epithelial cells
 Mucus on the
surface
 Brushborder
enzymes

16. Anatomy and physiology...
 Roles of jejunum
 Site of absorption for most macronutrients
and minerals(Ca, Mg and Fe)
 Absorption of Vitamins B,C and folic acid
 Production of CCK and Secretin
 90% of digestion and absorption in the
proximal 150 cm as it has taller villi, deeper
crypts and greater enzyme activity than the
ileum.

17. Anatomy and physiology...
 Roles of Ileum
 Absorption of
Vitamin B12 and fat
soluble vitamins
 Absorption of bile
acids
 Immune function

18. Anatomy and physiology...
Functions of:
 Ileoceccal valve
 Prevent reflux of
colonic content
◦ limits the degree of
bacterial
colonization of the
SI.
 Increase nutrient
transit time
 regulates the
movement of chyme
into the large
 Colon
 Site for Na and fluid
absorption
 Synthesis of SCFA,
Vitamin K and folate
 Excretion of K and
HCO3

19. Anatomy and physiology.
 Most CHO and protein absorbed in the
duodenum and jejunum.
 Fats bound to bile salts, fat-soluble vitamins
and vitamin B12 bound to intrinsic factor
absorbed in the ileum.
 Ca, Mg, Fe and folic acid predominantly
absorbed in the duodenum.
 Vit. B1, B2, B6 and C are absorbed along the
entire SI.
 Most fluids and electrolytes absorbed in the
ileum and large intestine.
 Water is absorbed by passive diffusion.

20. Anatomy and physiology.
 The ileum and right colon produce
meal-stimulated glucagon-like peptide
2 important for intestinal mucosal
repair and absorption.
 Massive SI resection compromises
digestive and absorptive processes.
 SBS with colectomy or with residual
colon not in continuity with the SI is
difficult to manage.

21. AETIOLOGY: Children
 Intestinal atresias
 Malrotation syndromes causing midgut
volvulus
 Congenital short small bowel
 Gastroschisis
 Necrotizing enterocolitis
 Meconium peritonitis
 Hirschsprung disease

22. AETIOLOGY: Adults
 Crohn’s disease
 Radiation enteritis
 Mesenteric vascular accidents (thrombosis,
embolism)
 Trauma
 Small bowel volvulus
 Multiple or extensive intestinal resections eg
for Crohn’s disease, malignancies etc
 Gangrene from volvulus, intestinal
obstruction
 Iatrogenic- eg irepairable damage to
mesenteric vessels, Jejuno-Ileal by-pass for
morbid obesity

23. PATHOPHYSIOLOGY
 Decreased Transit time:
-Short length
-loss of ileo-caecal junction
-loss of “Ileal break” and “colonic break”.
Hence not enough contact time to allow
absorption
 Decreased absorptive capacity as a result
of loss of functional surface area for
absorption

24. PATHOPHYSIOLOGY:
Jejunal resection
 Jejunal fluid and electrolyte losses often
exceed absorption. At least 100cm necessary
to maintain positive fluid and electrolyte
balance.
 With loss of significant portion or all, the
absorption of proteins, CHOs, vitamins and
minerals can be unaffected due to ileal
adaptation.
 Iron is absorbed in the duodenum hence
deficiency uncommon
 Calcium deficiency could manifest despite
absorption in the duodenum due to vitamin D
malabsorption.

25. Pathophysiology...
 Loss jejunum
 Loss of enteric
hormones
 Decreased biliary and
pancreatic secretions
 Increase gastrin level,
gastric hypersecretion
and peptic ulceration
 Decrease enzymatic
activity
 Diarrhea
 Gall bladder stasis,
gallstones
 Loss of ileum
 Decreased water
and electrolyte
absorption,
diarrhoea
 Reduced Vitamin B12
 Loss of bile salts,
steatorrhoea

26. PATHOPHYSIOLOGY:
ILEAL RESECTION...
 Loss of bile salts  fat malabsorption,
steatorrhoea and fat-soluble vitamins
deficiencies
 Increased bile salt spillage into the colon
 diminished bile salt pool (and
cholesterol gall stones) & increased
colonic permeability/ secretion 
choleretic diarrhoea
 High colonic bile salt levels solubilize
unconjugated bilirubin and promote its
absorption  high concentration of
bilirubin in bile  pigment gall stones

27. PATHOPHYSIOLOGY:
ILEAL RESECTION……
 Loss of entero-hepatic circulation of bile
salts---further impairment of absorption
of fat and fat soluble vitamins----
steatorrhea
 Small Bowel Bacterial overgrowth -----
Inflammation of bowel mucosa,
increased permeability of mucosa,
deconjugation of bile salts--------
worsening of steatorhoea and Vit B12
deficiency. Also produces D-lactic Acid---
--Lactic acidosis

28. PATHOPHYSIOLOGY:
ILEOCAECAL VALVE
RESECTION Faster transit time
and fluid, electrolyte
loss
 Colonization of small
bowel by colonic
bacteria, diarrhoea,
D-lactic acidosis
 Risk of calcium
oxalate stone
increases

29. PATHOPHYSIOLOGY:
Preservation of colon:
 Oxalate is normally bound to calcium
in the SI, and therefore insoluble in the
colon
 Free fatty acids will bind to calcium----
 increased level of unbound oxalate
reaching the colon------ increased
oxalate absorption--hyperoxaluria---
---oxalate stones in urinary tract
 SI bacterial overgrowth

30. PATHOPHYSIOLOGY:
Preservation of colon…..
 In extensive bowel resection,
secretion of motility-regulating factors-
GLP-1, GLP-2, peptide YY – is lost ,
leading to rapid gastric emptying 
worsening diarrhoea and
malabsorption.
 GLP-2: impt for SI hypertrophy during
adaptation.

31. Factors that determine the
development of SBS
 The pre-morbid length of the SI
 The segment of the gut is lost
 The age of the patient at the time of
bowel loss
 The remaining length of the small bowel
and colon
 Preservation or loss of the Ileo-caecal
valve
 Presence of colon
 Persisting disease in remnant bowel

32. PATHOPHYSIOLOGY:
Intestinal adaptation
 Inherent ability to increase the absorptive surface
area of remnant bowel
 Starts 24—48 hours after resections, and
continues for about 2 yrs
 Changes occur in morphology, and functional
capacity
 Ileum adapts better than jejunum
 Adaptation better with preservation of the
terminal ileum and ileo caecal valve
 Luminal content & GIT secretions helpful in
adaptation
 Vitamins and minerals supplements required. eg
Mg, Zn, Vit. A , B12

33. Pathophysiology... changes
 Acute phase:
 Immediate, last 3-4
months
 Ostomy output of
>5L/day
 Life threatening
dehydration and
electrolyte imbalances
 Hypergastrinemia and
hyperbilirubinemia,
Abnormal LFT
 Extremely poor
absorption of all
nutrients
 Associated
malnutrition with life-
threatening fluid and
electrolyte loss, up to
6-8L/day.
 Initiate enteral
feeding slowly.
 TPN necessary in
those with SI
<100cm.

34. Pathophysiology... changes
 Adaptation phase:
 Begins 2-3 days may
last up 1-2years
 Early continuous feeding
with elemental diet may
reduce TPN
 Mediated by
 Enteroglucagon, gastrin,
cholesytokinin, EGF, GH,
GLP 2, neurotensin
 EN essential for
adaptation and
initiated early.
 Up to 90% adaptation
occur- enterocyte &
villous hyperplasia,
increased crypt depth,
bowel dilatation &
lenghtening… 
surface area
 TPN usually required
in combination with
high viscosity
elemental diet until
sufficient bowel
remodelling of bowel.

35. Pathophysiology... changes
 Maintenance
phase:
 Absorptive capacity at
its maximum
 Absorptive capacity
of the GIT at its
maximum
 Nutritional and
metabolic
homeostasis
achievable by oral
feeding
 May still require
supplemental PN.
 Chronic phase:
 Intrinsically unstable
 Long term
maintenance of
calories and
nitrogen balance
 Gall stones
 Urinary stones
 Mineral, Amino acid,
Fatty acid, Vitamins
and Trace element
deficiency

36. COMPLICATIONS
 DEHYDRATION
 ELECTROLYTE DERANGEMENT
 MALNUTRITION-----MACRO AND MICRO
NUTRIENT DEFICIENCY
 GASTRIC HYPERSECRETION
 CHOLESTEROL STONES
 OXALATE STONES
 PEPTIC ULCERATIONS
 BACTERIAL OVERGROWTH IN GIT
 OSTEOPOROSIS
 METABOLIC ACIDOSIS-----D-LACTIC
ACIDOSIS

37. CLINICAL FEATURES
History:
 Weight loss
 Diarrhea
 Dehydration
 Malaise
 Lethargy
 Weight loss
 Steatorrhea
 Poor growth
performance
 Abdominal pain
 Vomiting
 Diet history:
 Appetite, oral intake,
tube feeds, parenteral
nutrition
 Past Medical
History- radiation
enteritis
 Past Surgical
History-
 Intestinal surgeries
(for Crohns disease,
bowel volvulus)

38. symptoms
 Vitamin and mineral deficiencies can
lead to specific symptoms
 Vit. A - night blindness and
xerophthalmia
 Vit. B 12, folic acid, iron - dyspnea
on exertion and lethargy (anaemia)
 Vit. D - paresthesia , tetany
 Vit. E - paresthesia ,ataxic gait ,
visual disturbance ( retinopathy )
 Vit. K - easy bruisability, prolonged
bleeding

39. symptoms
 Calcium , magnesium - paresthesia ,
tetany
 Zinc - anorexia , diarrhea
 Fever
 Yellowish discoloration of the sclera
 Abdominal pain ( RUQ ) - gallstones
 Loin to groin pain , haematuria -
urinary stones

40. SIGNS
 On examination
 WASTED
 sunken eye ball, temporal wasting,
loss of digital muscle mass,
peripheral edema
 skin - dry and flaky
 nails - prominient ridges
 lingual papillae - blunted and
atrophic
 vital signs - pyrexia, tachycardia,

41. Investigation
 A. Methods of nutritional assessment
 1. clinical history
 weighing , subjective assessment
 2. biochemical measurement ( mst )
 serum proteins - used as indices
of malnutrition
 .. albumin - < 30g/dl - an
indication for nutritional support
 .. transferrin - < 200mg/dl
 .. Prealbumin

42. signs
 Children - poor growth performance
 Essential fatty acid deficiency - growth
retardation, alopecia
 Vit. A - corneal ulcerations, growth delay
 Vit. B complex - stomatitis, cheilosis,
glossitis
 Vit. B1 - edema, tachycardia,
ophthalmoplegia, depressed DTRs
 Vit. B6 - peripheral neuropathy, seizure
 Vit. B12 - ,, ,,
 Vit. D - growth delay, bowed extremities
 Vit. E - ataxia, edema, depressed DTRs

43. signs
 Vit. K - petechiae, ecchymosis,
purpura, bleeding diathesis
 Iron - pallor, spooned nails, glossitis
 Zinc - angular stomatitis, poor wound
healing, alopecia, scaly erythematous
rash around mouth, eyes, nose,
perineum
 Abdomen
 tenderness - RUQ
 - EPIGASTRIUM
 - LOINS

44. Investigations
 Geared towards nutritional
assessment
 Monitoring during TPN

45. INVESTIGATIONS
FBC
Urea Electrolytes &
Creatinine
Serum proteins, albumin
• Indicates overall nutritional
status
• Half life 21days
• Level <2.5g/dl is associated
with increased morbidity and
mortality
Prealbumin
• Indicator of acute nutritional status
• Half life 3-5days
Serum Ca, PO4, LFT
BUN
Vitamins and trace elements
Stool fat
Coagulation profile

46. Investigation
 NUTRITIONAL ASSESSMENT: Aim-
 facilitate institution of TPN
 determine efficacy of nutritional
intervention

47. investigation
 3. Anthropometric mst
 a. ideal body weight ( IBW ) -
used to calculate caloric needs
 b. arm muscle circumference and
triceps skin fold thickness - reflect
muscle and fat stores

48. investigation
 4. measurement nitrogen balance ( N.bal.)
 5. measurement of immunologic status
 6.body composition analysis
a. Bioelectric impedance - estimates
TBW and LBM ( lean body mass)
b. Total exchange of labeled ions
c. Cross sectional imaging
d. MRI - may accurately assess LBM
 e. CT - radiographic tissue density
 7. Indirect Calorimetry:
 02 consumption , respiratory quotient

49. investigation
 C. Monitoring during TPN
 1. daily clinical assessment
overhydration / dehydration
daily I / O chart
daily weight chart
daily urine urea , electrolytes ,
osmolarity
 2. seucr - every 48 hours
 3. blood pH , clotting studies - every
48 hrs

50. Investigation
 Monitoring during TPN
 4. blood glucose- once daily, then
twice weekly
 5. urine - glycosuria , twice daily
 6. LFT , Serum Ca2+ , FBC - weekly

51. MANAGEMENT
A multidisciplinary team is
most effective at guiding
the rehab process
• Gastroenterologists
• Surgeons
• Dieticians
• Nurse coordinators

52. TREATMENT
 Challenging, painstaking, still evolving
 Involves both medical & surgical
modalities
 All pts initially require TPN
 50-70% of pts who initially require
TPN can subsequently be weaned off
it
 Most literature still document 30-50%
mortality

53. TREATMENT
• To sustain patient
• Minimize the inconvenience of malabsorption
& diarrhoea
• To wean patient from TPN
• To promote adaptation
AIM
• Adequate fluid and electrolyte replacement
• Important in the acute phase
Resuscitation

54. Treatment...medical
 Modalities of medical therapy include:
 Nutrition support and dietary modification
 Medications to reduce secretion,
diarrhoea and enhance digestion
 Trophic agents aimed at augmenting
bowel adaptation

55. Treatment...medical
Nutrition support and dietary modification:
 Intravenous fluids
 TPN
 Enteral; oral and tube feeding

56. MEDICAL TREATMENT
 NUTRITION
-TPN should be initiated within 72hrs of
surgery using a central vein
-calorie requirement to be calculated or
estimated
-Ideally lipid based regimen should be
used, volume(2-5L), calorie
content(1500-3200kcal)
-Strict monitoring for complications
-Pt education for possible home TPN

57. Treatment...
Parenteral
 Important in acute phase, post
operatively
 When Nutrition must be maintained in
the face of paralytic ileus
 Indispensable in chronic phase
 Central venous access to deliver
concentrated TPN solutions

58. Treatment...parenteral
 Require for long term survival
 Tailored to patient need
 Initiated on the 2-3DPO when CVS
and pulmonary system are stabilized.
 Energy 25-35kcal/day
 20-30% fat
 Amino acid 1-1.5g/kg/day
 CHO
 Large dose fat soluble vitamins

59. Treatment...parenteral
 Once oral caloric intake exceeds
1000kcal/day patient can be weaned
off parenteral nutrition
 Weaning is difficult in patient with
 Less 60cm of small intestine
 Loss of ileum and ileocecal valve
 Loss of colon

60.  Intact duodenum with 60cm of jejunum
or ileum may not need permanent TPN
 Patients with jejunostomy with total small
bowel remnant less than 100cm need
TPN
 Patients with less than 50cm jejunum
need TPN permanently ( even if most
colon is functional)
 Less than 30cm of small bowel with
competent ICV, and less than 60cm
without ICV require indefinite home TPN

61. .
 ENTERAL NUTRITION
-Should be commenced as soon as
feasible
 Start slowly
 Stimulate intestinal adaptation
-Pts with colonic continuity to be provided
with high complex CHO diet
-Enteral diets that maximize intestinal
adaptive response are prefered
-SCFAs have higher trophic effects

62. Medications to reduce secretion, diarrhoea
and
enhance digestion:
 Anti-secretory and bile salt binder agents:
 Cholestyramine
 H2 blockers / somatostatin / PPI
 Octreotide

63. Treatment...medical
 Anti-motility agents
 Codeine
 Loperamide, diphenoxylate
Trophic agents aimed at augmenting
bowel
Adaptation:
 Growth Hormone, Glutamine
 Glucagon-Like Peptide 2 (GLP 2) analog
(Teduglitide)

64. SURGICAL THERAPY
 Aim: is to increase intestinal
absorptive capacity Or slowing
intestinal transit.
 Mainly for those who fail to improve on
conservative care
 Various modalities/techniques
available
 Could be non transplant or transplant
surgery
 Outcome variable

65. Treatment...surgical
 Slowing intestinal transit time
 Interposition of a segment of colon between
segments of small bowel
 Creation of intestinal valves
 Reversed bowel segments
 Intestinal tapering
 Intestinal lengthening
 Bianchi procedure
 STEP

66. Treatment...surgical
COLON
INTERPOSITION
INTESTINAL VALVE

67. Treatment...surgical
REVERSED INTESTINAL
SEGMENT INTESTINAL
TAPERING

68. Treatment...surgical
Longitudinal intestinal lengthening and
tailoring (LILT)
 Effective isoperistaltic propulsion
reduces:
 Intraluminal stasis and bacterial
translocation
 Longer mucosal contact over a greater
bowel length to enhances absorption and
 Stimulates the intestinal adaptation
process

69. INCREASING ABSORPTIVE SURFACE
AREA
• Bianchi Procedure
-intestinal lenghtning
procedure
-longitudinal stapler
division of loop of gut
based on the dual
vasculature + end to
end anastomosis

70. Serial Transverse Enteroplasty
Procedure(STEP)
-Involves serial transverse
application of a linear
stapler from alternate
directions
-Technically simpler than
Bianchi procedure

71. Treatment...surgical
 Serial transverse
enteroplasty
(STEP)

72. DILATED
BOWEL
NO
YE
S
Moderate
bowel length:
growth of bowel
expected
Very short
bowel; not
much growth
expected
Intestinal
lengthening
Tapering
enteroplasty
Intact colon
YE
S
NO
Isoperistaltic colon
interposition
Intestinal
valve
Reverse
d
intestinal
segment
MANAGEMENT ALGORITHM

73. Treatment...surgical
 Transplant surgery
 Intestinal transplant 45%
 Combined liver-intestinal transplantation
40%
 Indications
 For patients dependent on parenteral
nutrition
 Presence of life-threatening
complications:
 Thrombosis of major central vein
 Liver failure

74. Treatment...surgical
Postoperative care
 Ensure fluid and electrolyte balance
 Start enteral as soon as possible
 Commence immunosuppressive drugs
in patients with transplantation

75. COMPLICATIONS
From Disease
• Diarrhea
• Dyselectrolytaemia
• Malnutrition
• Stress ulcers
• Gall stones
• Renal stones
From Therapy
• Catheter sepsis
• Volume over load
• Metabolic acidosis
• Hyperglycemia
• Anaemia
• Liver cirrhosis
• Metabolic bone
disease
• Nephropathy
• Memory deficit

76. FOLLOW UP
 Lifetime follow-up
 Regular weighing
 Biochemical assays to identify any
metabolic derangement
 Treat bacteria overgrowth with cyclic
antibiotics

77. PROGNOSIS
 Age
 Site and amount of bowel resection
 Loss of ICV portends worse prognosis
 Loss of jejunum and ileum create a
poorer clinical condition than loss of
colon
 The longer it takes to tolerate full enteral
feeds the worse the prognosis
 Development of severe TPN liver
disease -poor prognosis

78. Prognosis...
 No cure yet
 Patients on parenteral nutrition-
4years survival -70%
 Non-transplant surgery- 80%
improvement
 Organ transplant- fraught with
problems
 Early postop mortality rate as high as 30%
 Information on survival among
patients with short-bowel syndrome is

79. FUTURE TRENDS
 Finding ways to maximize intestinal
adaptation
 Pharmacologic and biologic therapies
designed to expand intestinal mucosal
surface area or to enhance the efficiency of
intestinal absorption
 Refining technique of transplantation and
immune modulation
 Finding of donor specific immunologic
tolerance

80. CONCLUSION
 Short bowel syndrome is a disorder
with severe metabolic derangements
 Successful treatment will require a
multi-disciplinary approach and is
capital intensive
 Surgical mode of treatment poses
great challenge due to lack of
surgeons with these skills
 A lasting solution is still being awaited

81. Conclusion...
 For now, the short-bowel syndrome
remains a formidable challenge for
clinical surgeons and surgical
scientists

82. THANK YOU
FOR
LISTENING

83. REFERENCES
 Buchman AL, Scolapio J, Fryer J. AGA
technical review on short bowel syndrome
and intestinal transplantation.
Gastroenterology. 2003;124(4):1111–1134.
 Goulet O, Ruemmele J. Causes and
management of intestinal failure in children.
Gastroenterology 2006;130:S16–S28.
 SRB’S Manual of Surgery 3rd edition By
Sriram Bhat, pg 814