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Short bowel syndrome (short gut syndrome)

Short bowel syndrome (Definition): Condition resulting from Intestinal malabsorption related to massive surgical bowel resection -- ranges from mild intestinal dysfunction responsive dietary and pharmacological measures to severe intestinal failure requiring 100% parenteral support.
 
Most important metabolic consequences of short bowel syndrome:
  1. Sodium and fluid depletion
  2. Hypocalcemia
  3. Hypomagnesemia
  4. Normal anion gap metabolic acidosis (GI bicarbonate losses)
  5. Elevated anion gap metabolic acidosis (D-lactic acidosis -- see below)
  6. Hyperoxaluria (see below)
Banerjee A, Warwicker P. Acute renal failure and metabolic disturbances in the
short bowel syndrome. QJM. 2002 Jan;95(1):37-40. PubMed PMID: 11834771.
 

 

Intestinal failure (Definition): the reduction of gut function below the minimum necessary for the absorption of macronutrients and/or water and electrolytes, such that intravenous supplementation is required to maintain health and/or growth.  
 
Pironi L. Definitions of intestinal failure and the short bowel syndrome. Best Pract Res Clin Gastroenterol. 2016 Apr;30(2):173-85. doi: 10.1016/j.bpg.2016.02.011. Epub 2016 Feb 18. Review. PubMed PMID: 27086884.

 

Common diagnosis in pediatrics include:

  1. Necrotizing entercolitis
  2. Gastroschisis
  3. Small bowel atresia
  4. Malrotation with midgut volvulus
  5. Mesenteric ischemia 
 
Individualized nutritional management depends upon:
  • Physiology 
  • Anatomy - portion resected, colon in continuity
  • Stage of adaptation - under stimulus of enteral nutrition
Water and electrolyte losses need replacement
- Gastric hypersecretion in the first month post-operatively.  Although commonly used, there is little evidence that H2 blockers or PPI are effective.
- Sodium and chloride losses are high and require replacement.
 
Goal: Optimize linear growth and lean mass accrual as well as to achieve appropriate developmental milestones while parenteral nutrition weaned and enteral nutrition advanced.
 

 

short bowel

 

Bielawska B, Allard JP. Parenteral Nutrition and Intestinal Failure. Nutrients. 2017 May 6;9(5). pii: E466. doi: 10.3390/nu9050466. Review. PubMed PMID: 28481229; PubMed Central PMCID: PMC5452196.

Duggan CP, Jaksic T. Pediatric Intestinal Failure. N Engl J Med. 2017 Aug 17;377(7):666-675. doi: 10.1056/NEJMra1602650. Review. PubMed PMID: 28813225.

Gosselin KB, Duggan C. Enteral nutrition in the management of pediatric intestinal failure. J Pediatr. 2014 Dec;165(6):1085-90. doi: 10.1016/j.jpeds.2014.08.012. Epub 2014 Sep 18. Review. PubMed PMID: 25242686; PubMed Central PMCID: PMC4253063.

 

D-Lactic Acidosis

Symptoms:

  • Encephalopathy
  • Coma
  • Slurred speech
  • Ataxia
  • Gait disturbance
  • Weakness
  • Tachypnea
  • Feeling drunk

Diagnosis:

  • Clinical suspicion
  • Anion gap acidosis
  • D-lactate (send out test)
  • Rule-out alternate diagnosis (intoxications)

Treatment

  • Correct acidemia with IV fluids with bicarbonate (avoid lactated ringer's which contains both D-and L-lactate.
  • Intravenous fluids with dextrose to augment pyruvate dehydrogenase activity.
  • Consider thiamine supplementation to augment pyruvate dehydrogenase activity.
  • Poorly absorbable oral antibiotics to change intestinal flora (treat lactobacillus), such as clindamycin, vancomycin, neomycin, ciprofloxacin and flagyl.
  • Limit offending agent (fermented foods such as sour milk, yogurt, and pickles)
  • Long-term control measures.
  • In extreme acute situations, may use dialysis.
  • In recurrent episodes, consider surgery to address bowel dilation.

 

Pathophysiology

Unabsorbed carbohydrates act as a substrate for colonic bacteria.

Short Gut

 

Bianchetti DGAM, Amelio GS, Lava SAG, Bianchetti MG, Simonetti GD, Agostoni C, Fossali EF, Milani GP. D-lactic acidosis in humans: systematic literature review. Pediatr Nephrol. 2017 Dec 7. doi: 10.1007/s00467-017-3844-8. [Epub ahead of print] PubMed PMID: 29218437.
 
Kowlgi NG, Chhabra L. D-lactic acidosis: an underrecognized complication of short bowel syndrome. Gastroenterol Res Pract. 2015;2015:476215. doi: 10.1155/2015/476215. Epub 2015 Apr 22. Review. PubMed PMID: 25977687; PubMed Central PMCID: PMC4421027.
 

HYPEROXALURIA

  • Occurs w/ small intestinal resection in continuity w/ colon.
  • Calcium usually binds to oxalate in small intestine.  However, with significant fat malabsorption occurring -- the unabsorbed fatty acids bind to calcium in small intestine.
  • Free oxalates pass into colon, and absorbed in the colon.
  • Bile acid malabsorption leads to additional bile salts in the colon, which increase colon permiability to oxalate, too.
  • In the kidney, free oxalate binds to calcium leading to oxalate nepholithiasis.
  • Persistent oxalate nephrolithiasis over time leads to progressive obstructive nephropathy. 
Peña de la Vega L, Lieske JC, Milliner D, Gonyea J, Kelly DG. Urinary oxalate excretion increases in home parenteral nutrition patients on a higher intravenous ascorbic acid dose. JPEN J Parenter Enteral Nutr. 2004 Nov-Dec;28(6):435-8. PubMed PMID: 15568291.

  

Johnson E, Vu L, Matarese LE. Bacteria, Bones, and Stones: Managing Complications of Short Bowel Syndrome. Nutr Clin Pract. 2018 Aug;33(4):454-466. doi: 10.1002/ncp.10113. Epub 2018 Jun 21. Review. PubMed PMID: 29926935.

 

Infant with short bowel syndrome and PN associated cholestasis.

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Upper GI small bowel follow-through with contrast progressing through duodenocolonic anastamosis after 35 minutes.

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