Short Bowel Syndrome(SBS)
Dr. Yuvraj (M.S.)
Associate Professor
General Surgery
Outline
• Anatomy
• Physiology
• Definition
• Pathophysiology
• Classification(including etiology)
• Clinical Presentation
• Workup
Anatomy
Length of small gut* Neonate 250 cm
Adult Average 600 cm (Range 260- 800 cm)
Short Gut Syndrome 200 cm viable (Adult)
>50 %-80% lost
Lifelong TPN Dependence
(Minimal gut length required for
life)
Adult With intact colon 60 cm
Without colon 100 cm
Infant With ileocecal valve 11 cm
Without ileoceal valve 12-25 cm
*As a consequence, the infant and the young child have a favorable long-term
prognosis compared to an adult in regards to potential intestinal growth after
intestinal resection
Physiology
Jejunum Ileum
Villi Long Shorter
Absorptive surface area Large Less
Tight Junction Relatively large
• epithelium more porous to
larger molecules
• free and rapid flux of water
and electrolytes
Tighter
• permitting less flux of
water and electrolytes
from the vascular space
into the intestinal lumen
Water absorption Less effective More efficient
Absorption Carbohydrates, proteins, fat,
vitamins (iron-duodenum)
Bile acids, vitamin B-12
GI hormones that affect
intestinal motility
enteroglucagon and
peptide YY
Etymology:
• Duodenum (Latin: duodēnum Twelve ) (duodenum is 12 fingerbreadth long)
• Jejunum (Latin: jejunus  fasting )(because it was usually found to be empty after death).
• Ileum (Greek: eilein  to twist up tightly)
Physiology
Proximal jejunal resection is better tolerated than distal ileum resection
Definition
Clinically defined by malabsorption, diarrhea,
steatorrhea, fluid and electrolyte disturbances,
and malnutrition due to ≥ 50 % (viable gut <200
cm) of structural or functional loss of small gut.
Pathophysiology
Underlying
Disease
extensive
bowel
resection
affects normal
intestinal
physiology
alteration of
intestinal
digestion and
absorption
nutritional,
metabolic,
and infectious
consequences
Pathophysiology
• Loss of ileocecal valve
– transit time is faster, and loss of fluid and
nutrients is greater
– Colonic bacteria colonize the small bowel,
worsening diarrhea and nutrient loss.
Pathophysiology
Preservation of the colon
MERITS DEMERITS
colonic water absorption could be increased
to as much as five times its normal capacity
following small bowel resection
increase incidence of urinary calcium
oxalate stone formation
(Oxalate is normally bound by calcium in the
small bowel and thus is insoluble when it
reaches the colon.
After massive enterectomy, much of this
calcium is bound by free intraluminal fats)
Colonic bacteria  metabolize undigested
carbohydrates(starch & fibres) into short-
chain fatty acids, such as butyrate,
propionate, and acetate.
(up to 500 kcal/day)
small intestinal bacterial overgrowth.
( in absence of ileocecal valve)
Natural History
( 3 Phases)
• Acute Phase
• Adaption Phase
• Maintenance Phase
Acute Phase
• Starts immediately after bowel resection and lasts 1-4
months
• Ostomy output of greater than 5 L/day (as high as 6-8
L/day)
• Life-threatening dehydration and electrolyte imbalances
• Extremely poor absorption of all nutrients
• Development of hypergastrinemia and hyperbilirubinemia
Adaption Phase
• Enterocyte hyperplasia + villous hyperplasia + increased crypt depth
increased surface area;
• intestinal dilatation and lengthening  increased capacity/Low transit
time(reduction in volume and frequency of bowel movements)
• Begins within 48 hours of resection and lasts up to 1-2 years
• ~ 90% of the bowel adaptation takes place during this phase
• Luminal nutrition is essential for adaptation and should be initiated as
early as possible; parenteral nutrition is also essential throughout this
period
Maintenance Phase
• Absorptive capacity of the intestine is at its
maximum
Classification
Congenital versus Acquired
CONGENITAL ACQUIRED
Congenital Short Small Bowel * NEONATAL PERIOD ADULT
Necrotizing enterocolitis Crohn disease
Intestinal atresias radiation enteritis
Intestinal volvulus mesenteric vascular
accidents
OLDER INFANTS and
CHILDREN
Trauma
Intussusception with
ischemic small-intestinal
injury
recurrent intestinal
obstruction
* Also associated with gastroschisis ,omphalocele and meconium peritonitis.
Classification
Structural versus functional
STRUCTURAL FUNCTIONAL
Any insult leading to  Length maintained BUT function
is lost
< 200 cm or loss of ≥ 50% of viable small bowel 
For example:
Increased risk of developing SBS ( NOT ALWAYS)
Radiation Enteritis
PREDISPOSING FACTORS
• premorbid length of small bowel Cloacal Extrophy
• segment of intestine that is lost,
• Age of the patient (infant tolerate better)
• Remaining length of small bowel and colon,
• Presence or absence of the ileocecal valve
Classification
SBS due to proximal jejunal resection
versus
SBS due to distal ileum resection
Clinical Presentation
• Diarrhea ± steatorrhea
– dehydration and electrolytes disturbances
• Significant weight loss, fatigue, malaise, and lethargy
• Malnutrition
– Mineral deficiencies (folate, iron, calcium, magnesium, zinc)
– Vitamins deficiencies (A,D, E, K , B complex esp B12)
– Macro-nutrient deficiencies (CHO,Protein,fat)
Clinical Presentation
• Recurrent bacterial enteritis
• Stones and related problems
– Gall stones due to altered bile metabolism
– Renal stones due to high oxalate
• Vomiting, bloating, GERD, gastric ulceration
• Failure to thrive
• Drug toxicities
• Bowel Obstruction (potential complication)
Clinical Presentation
• TPN related issues
– Line sepsis and fulminant liver failure
• Enteral Feeding related issues
– gastrostomy or nasogastric tube issues
Clinical Presentation
• During the physical examination, pay close attention to these clinical signs
– Vitals
– State of hydration
– State of nutrition, as measured by a patient's weight for height and
anthropometric measurements
– Signs of sepsis
– Form of nutritional therapy used in the patient (eg, central line access or
enteral access)
– Specific clinical signs of nutritional deficiency
– Signs of liver disease
Workup
• Hematological and Biochemical investigations
• Radiological investigations
• Microbiological investigations
• Histopathological investigations
• Miscellaneous
Workup
Hematological and Biochemical investigations
CBC • Anemia (MCH, MCHC, MCV)
• Thrombocytosis/thrombocytopenia
• Hyper segmented neutrophils
Albumin (half life 21 days) • good indicator of hepatic protein synthesis
• indicator of overall nutritional status
Prealbumin ( 3-5 days) • indicator of acute nutritional status
• monitor the efficacy of nutrition support regimens
AST/ALT • TPN induced liver failure
Electrolytes
(Na, K, Cl, Zn, Ca, Mg,Cr, Se, PO4
-3)
• TPN monitoring
BUN • Renal reserve
• Dehydration(>20:1)
• Overfed with protein
Vitamins Level
Coagulation Profile • Deranged Liver function
Workup
Hematological and Biochemical investigations Frequency*
Electrolytes, BUN, creatinine, calcium, magnesium, phosphorous Twice weekly
Comprehensive metabolic panel, CBC, triglycerides, cholesterol Weekly
Folate, vitamin B-12, vitamin E, copper, zinc, selenium Monthly
*both in initial phase and the late period or at the time of presentation for
instability
Workup
Radiological investigations
Plain Chest X-ray Post CV line insertion
Plain Abdominal X-ray Suspected bowel obstruction
Barium imaging of the bowel
Abdominal USG fungal balls in the kidney (sepsis)
Renal Stones and related problems
Gall stones and related problems
Liver failure (spleen, ascites, liver texture, Portal vein
flow-Duplex)
CT-Abdomen identify persistent sepsis
Potential Liver/Bowel transplant
Angiography
Workup
Histopathological investigations
• Liver biopsy(rare)
– TPN related liver problems
Workup
Miscellaneous
• Upper GI endoscopy
– to assess for peptic ulcer disease and possible signs of
liver disease e.g. esophageal varices, hypertensive
gastropathy
• Dual radiographic absorptiometry
– Bone density estimation in Metabolic Bone Disease
Available at surgicalpresentations

shortbowelsyndrome-150820110854-lva1-app6891 copy.pptx

  • 1.
    Short Bowel Syndrome(SBS) Dr.Yuvraj (M.S.) Associate Professor General Surgery
  • 2.
    Outline • Anatomy • Physiology •Definition • Pathophysiology • Classification(including etiology) • Clinical Presentation • Workup
  • 3.
    Anatomy Length of smallgut* Neonate 250 cm Adult Average 600 cm (Range 260- 800 cm) Short Gut Syndrome 200 cm viable (Adult) >50 %-80% lost Lifelong TPN Dependence (Minimal gut length required for life) Adult With intact colon 60 cm Without colon 100 cm Infant With ileocecal valve 11 cm Without ileoceal valve 12-25 cm *As a consequence, the infant and the young child have a favorable long-term prognosis compared to an adult in regards to potential intestinal growth after intestinal resection
  • 4.
    Physiology Jejunum Ileum Villi LongShorter Absorptive surface area Large Less Tight Junction Relatively large • epithelium more porous to larger molecules • free and rapid flux of water and electrolytes Tighter • permitting less flux of water and electrolytes from the vascular space into the intestinal lumen Water absorption Less effective More efficient Absorption Carbohydrates, proteins, fat, vitamins (iron-duodenum) Bile acids, vitamin B-12 GI hormones that affect intestinal motility enteroglucagon and peptide YY Etymology: • Duodenum (Latin: duodēnum Twelve ) (duodenum is 12 fingerbreadth long) • Jejunum (Latin: jejunus  fasting )(because it was usually found to be empty after death). • Ileum (Greek: eilein  to twist up tightly)
  • 5.
    Physiology Proximal jejunal resectionis better tolerated than distal ileum resection
  • 6.
    Definition Clinically defined bymalabsorption, diarrhea, steatorrhea, fluid and electrolyte disturbances, and malnutrition due to ≥ 50 % (viable gut <200 cm) of structural or functional loss of small gut.
  • 7.
  • 8.
    Pathophysiology • Loss ofileocecal valve – transit time is faster, and loss of fluid and nutrients is greater – Colonic bacteria colonize the small bowel, worsening diarrhea and nutrient loss.
  • 9.
    Pathophysiology Preservation of thecolon MERITS DEMERITS colonic water absorption could be increased to as much as five times its normal capacity following small bowel resection increase incidence of urinary calcium oxalate stone formation (Oxalate is normally bound by calcium in the small bowel and thus is insoluble when it reaches the colon. After massive enterectomy, much of this calcium is bound by free intraluminal fats) Colonic bacteria  metabolize undigested carbohydrates(starch & fibres) into short- chain fatty acids, such as butyrate, propionate, and acetate. (up to 500 kcal/day) small intestinal bacterial overgrowth. ( in absence of ileocecal valve)
  • 10.
    Natural History ( 3Phases) • Acute Phase • Adaption Phase • Maintenance Phase
  • 11.
    Acute Phase • Startsimmediately after bowel resection and lasts 1-4 months • Ostomy output of greater than 5 L/day (as high as 6-8 L/day) • Life-threatening dehydration and electrolyte imbalances • Extremely poor absorption of all nutrients • Development of hypergastrinemia and hyperbilirubinemia
  • 12.
    Adaption Phase • Enterocytehyperplasia + villous hyperplasia + increased crypt depth increased surface area; • intestinal dilatation and lengthening  increased capacity/Low transit time(reduction in volume and frequency of bowel movements) • Begins within 48 hours of resection and lasts up to 1-2 years • ~ 90% of the bowel adaptation takes place during this phase • Luminal nutrition is essential for adaptation and should be initiated as early as possible; parenteral nutrition is also essential throughout this period
  • 13.
    Maintenance Phase • Absorptivecapacity of the intestine is at its maximum
  • 14.
    Classification Congenital versus Acquired CONGENITALACQUIRED Congenital Short Small Bowel * NEONATAL PERIOD ADULT Necrotizing enterocolitis Crohn disease Intestinal atresias radiation enteritis Intestinal volvulus mesenteric vascular accidents OLDER INFANTS and CHILDREN Trauma Intussusception with ischemic small-intestinal injury recurrent intestinal obstruction * Also associated with gastroschisis ,omphalocele and meconium peritonitis.
  • 15.
    Classification Structural versus functional STRUCTURALFUNCTIONAL Any insult leading to  Length maintained BUT function is lost < 200 cm or loss of ≥ 50% of viable small bowel  For example: Increased risk of developing SBS ( NOT ALWAYS) Radiation Enteritis PREDISPOSING FACTORS • premorbid length of small bowel Cloacal Extrophy • segment of intestine that is lost, • Age of the patient (infant tolerate better) • Remaining length of small bowel and colon, • Presence or absence of the ileocecal valve
  • 16.
    Classification SBS due toproximal jejunal resection versus SBS due to distal ileum resection
  • 17.
    Clinical Presentation • Diarrhea± steatorrhea – dehydration and electrolytes disturbances • Significant weight loss, fatigue, malaise, and lethargy • Malnutrition – Mineral deficiencies (folate, iron, calcium, magnesium, zinc) – Vitamins deficiencies (A,D, E, K , B complex esp B12) – Macro-nutrient deficiencies (CHO,Protein,fat)
  • 18.
    Clinical Presentation • Recurrentbacterial enteritis • Stones and related problems – Gall stones due to altered bile metabolism – Renal stones due to high oxalate • Vomiting, bloating, GERD, gastric ulceration • Failure to thrive • Drug toxicities • Bowel Obstruction (potential complication)
  • 19.
    Clinical Presentation • TPNrelated issues – Line sepsis and fulminant liver failure • Enteral Feeding related issues – gastrostomy or nasogastric tube issues
  • 20.
    Clinical Presentation • Duringthe physical examination, pay close attention to these clinical signs – Vitals – State of hydration – State of nutrition, as measured by a patient's weight for height and anthropometric measurements – Signs of sepsis – Form of nutritional therapy used in the patient (eg, central line access or enteral access) – Specific clinical signs of nutritional deficiency – Signs of liver disease
  • 21.
    Workup • Hematological andBiochemical investigations • Radiological investigations • Microbiological investigations • Histopathological investigations • Miscellaneous
  • 22.
    Workup Hematological and Biochemicalinvestigations CBC • Anemia (MCH, MCHC, MCV) • Thrombocytosis/thrombocytopenia • Hyper segmented neutrophils Albumin (half life 21 days) • good indicator of hepatic protein synthesis • indicator of overall nutritional status Prealbumin ( 3-5 days) • indicator of acute nutritional status • monitor the efficacy of nutrition support regimens AST/ALT • TPN induced liver failure Electrolytes (Na, K, Cl, Zn, Ca, Mg,Cr, Se, PO4 -3) • TPN monitoring BUN • Renal reserve • Dehydration(>20:1) • Overfed with protein Vitamins Level Coagulation Profile • Deranged Liver function
  • 23.
    Workup Hematological and Biochemicalinvestigations Frequency* Electrolytes, BUN, creatinine, calcium, magnesium, phosphorous Twice weekly Comprehensive metabolic panel, CBC, triglycerides, cholesterol Weekly Folate, vitamin B-12, vitamin E, copper, zinc, selenium Monthly *both in initial phase and the late period or at the time of presentation for instability
  • 24.
    Workup Radiological investigations Plain ChestX-ray Post CV line insertion Plain Abdominal X-ray Suspected bowel obstruction Barium imaging of the bowel Abdominal USG fungal balls in the kidney (sepsis) Renal Stones and related problems Gall stones and related problems Liver failure (spleen, ascites, liver texture, Portal vein flow-Duplex) CT-Abdomen identify persistent sepsis Potential Liver/Bowel transplant Angiography
  • 25.
    Workup Histopathological investigations • Liverbiopsy(rare) – TPN related liver problems
  • 26.
    Workup Miscellaneous • Upper GIendoscopy – to assess for peptic ulcer disease and possible signs of liver disease e.g. esophageal varices, hypertensive gastropathy • Dual radiographic absorptiometry – Bone density estimation in Metabolic Bone Disease
  • 27.