Welcome back to the tasty morsels of critical care podcast.
SBS is not a common thing to find in the ICU and the most likely context here is going to be receiving someone from the operating theatre who has had rather more bowel removed than one would like. There are some poor souls who as a result of SBS are dependant on long term TPN who may also appear in ICU from time to time and a working knowledge would be useful. Neither LITFL not Deranged Physiology have an entry for this (which is more reflective of its non importance rather than a reflection on the comprehensiveness of the two resources.)
Surgical causes of this are typically going to be surgery for things like Crohn’s disease or ischaemic bowel. The decision to resect enough bowel to put someone at risk of long term TPN is a huge intraop decision and not taken lightly. However it is frequently not one that can be made until the abdomen is entered (especially in the emergency mesenteric ischaemia situation).
A useful definition of the syndrome would be insufficient gut to maintain homeostasis and nutrition. Lengths are not particularly useful in predicting outcomes but having <180cm puts you at risk and <100 cm means you’re almost undoubtedly in trouble. Having some colon left is protective.
The part of the small bowel removed will have a different impact depending on which bit. As revision
Jejunum function (proximal 2/5 of small bowel)
- lots of nutrient absorption
- lots of fluid resorption (the gut secretes about 9L/day of fluids so it’s important to take most of it back)
Ileal function (distal 3/5 small bowel)
- vit B12 absorption
- bile acid absorption (loss of bile acids impairs fat soluble vitamin absorption)
In some bizarre hostage like situation where someone asked you which bit of your small bowel you had to remove it would be best to say jejenum as the ileum seems to be more adaptable overall and gives you a better chance of sufficient intestinal function.
in the post op period we’ll be faced with the “acute phase” of SBS where there is generally significant fluid losses and metabolic derangements from whatever kind of “ostomy” is left behind.
Management options at this stage include:
- Acid suppression (eg PPI or H2RA) – gastric secretions are a major contributor to fluid losses here and typically there are more secretions than normal that cause fluid loss and also impair pancreatic enzyme function.
- Fluids to replace losses – and the answer is probably hartmans as always
- PN with trial of EN (the EN is the best stimulant of intestinal adaptation needed to establish a functioning intestinal tract)
- loperamide can be used (though often not in the ICU period)
- Octreotide (typically when >3L IV fluid a day are required)
- ICU favourite clonidine can also reduce stool output apparently.
Pironi L, Corcos O, Forbes A, Holst M, Joly F, Jonkers C, Klek S, Lal S, Blaser AR, Rollins KE, Sasdelli AS, Shaffer J, Van Gossum A, Wanten G, Zanfi C, Lobo DN; ESPEN Acute and Chronic Intestinal Failure Special Interest Groups. Intestinal failure in adults: Recommendations from the ESPEN expert groups. Clin Nutr. 2018 Dec;37(6 Pt A):1798-1809. doi: 10.1016/j.clnu.2018.07.036. Epub 2018 Aug 18. PMID: 30172658.