Current Management of the Short Bowel Syndrome

Thompson, Jon S.; Weseman, Rebecca A.; Rochling, Fedja A.; Mercer, David F.

doi:10.1016/j.suc.2011.02.006

Cited by 55 publications

(39 citation statements)

References 64 publications

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“…A detailed discussion of these conditions is beyond the scope of this article, but the topics are addressed in some detail by companion articles in this supplement. For further information, the reader is encouraged to refer to a recent review article by Thompson et al 91 …”

Section: Pathophysiology In the Gi Tract And Beyondmentioning

confidence: 99%

Pathophysiology of Short Bowel Syndrome

Tappenden

2014

J Parenter Enteral Nutr

160

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The human small intestine is organized with a proximal‐to‐distal gradient of mucosal structure and nutrient processing capacity. However, certain nutrients undergo site‐specific digestion and absorption, such as iron and folate in the duodenum/jejunum vs vitamin B12 and bile salts in the ileum. Intestinal resection can result in short bowel syndrome (SBS) due to reduction of total and/or site‐specific nutrient processing areas. Depending on the segment(s) of intestine resected, malabsorption can be nutrient specific (eg, vitamin B12 or fat) or sweeping, with deficiencies in energy, protein, and various micronutrients. Jejunal resections are generally better tolerated than ileal resections because of greater postresection adaptive capacity than that of the jejunum. Following intestinal resection, energy scavenging and fluid absorption become particularly important in the colon owing to loss of digestive and absorptive surface area in the resection portion. Resection‐induced alterations in enteroendocrine cell abundance can further disrupt intestinal function. For example, patients with end jejunostomy have depressed circulating peptide YY and glucagon‐like peptide 2 concentrations, which likely contribute to the rapid intestinal transit and blunted intestinal adaptation observed in this population. SBS‐associated pathophysiology often extends beyond the gastrointestinal tract, with hepatobiliary disease, metabolic bone disease, D‐lactic acidosis, and kidney stone formation being chronic complications. Clinical management of SBS must be individualized to account for the specific nutrient processing deficit within the remnant bowel and to mitigate potential complications, both inside and outside the gastrointestinal tract.

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Section: Pathophysiology In the Gi Tract And Beyondmentioning

confidence: 99%

Pathophysiology of Short Bowel Syndrome

Tappenden

2014

J Parenter Enteral Nutr

160

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“…4,5 Intestinal failure from SBS generally occurs with loss of approximately 50%-75% of the small intestine. [6][7][8] The insufficient quantity of surface absorption results in a broad diversity of metabolic and physiologic disturbances, including fluid, nutrient, and weight loss. 9 SBS may lead to liver failure, as prolonged intravenous alimentation is associated with cholestasis and progression to cirrhosis.…”

mentioning

confidence: 99%

A Multicellular Approach Forms a Significant Amount of Tissue-Engineered Small Intestine in the Mouse

Sala

Matthews

Speer

et al. 2011

Tissue Engineering Part A

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Tissue-engineered small intestine (TESI) has successfully been used to rescue Lewis rats after massive small bowel resection. In this study, we transitioned the technique to a mouse model, allowing investigation of the processes involved during TESI formation through the transgenic tools available in this species. This is a necessary step toward applying the technique to human therapy. Multicellular organoid units were derived from small intestines of transgenic mice and transplanted within the abdomen on biodegradable polymers. Immunofluorescence staining was used to characterize the cellular processes during TESI formation. We demonstrate the preservation of Lgr5-and DcamKl1-positive cells, two putative intestinal stem cell populations, in proximity to their niche mesenchymal cells, the intestinal subepithelial myofibroblasts (ISEMFs), at the time of implantation. Maintenance of the relationship between ISEMF and crypt epithelium is observed during the growth of TESI. The engineered small intestine has an epithelium containing a differentiated epithelium next to an innervated muscularis. Lineage tracing demonstrates that all the essential components, including epithelium, muscularis, nerves, and some of the blood vessels, are of donor origin. This multicellular approach provides the necessary cell population to regenerate large amounts of intestinal tissue that could be used to treat short bowel syndrome.

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“…Adult small intestine is approximately 480 cm and adults with residual small intestine of less than 180 cm are at risk for developing SBS and its complications and those who have less than 60 cm of small intestine (but with a colon) are more likely to be dependent on parental nutrition [2]. In our patient about 240 cm of the small bowel had been resected as a complication of appendicitis after which he was largely lost to follow up until he developed complications of SBS.…”

Section: Discussionmentioning

confidence: 80%

Delayed Presentation of Short Bowel Syndrome Complicated with Severe Degree of Nutritional Deficiencies, Nephrocalcinosis and Distal Renal Tubular Acidosis

Herath¹,

Kulatunga²

2017

J Gastrointest Dig Syst

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Background: Short bowel syndrome (SBS) is a malabsorptive state due to functional or anatomic loss of extensive segments of small intestine which can lead to nutritional deficiencies and metabolic disarrangements. Here we describe a young patient with short bowel presenting with severe nutritional deficiencies, nephrocalcinosis and distal renal tubular acidosis. Nephrocalcinosis and distal renal tubular acidosis are closely associated and each can lead to the other. There are only rare case reports of short bowel syndrome complicated with nephrocalcinosis and distal RTA and severe degree of metabolic derangement with nutritional deficiencies. And this case highlights the importance of early management of short bowel syndrome in order to prevent long-term complications.

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Current Management of the Short Bowel Syndrome

Cited by 55 publications

References 64 publications

Pathophysiology of Short Bowel Syndrome

Pathophysiology of Short Bowel Syndrome

A Multicellular Approach Forms a Significant Amount of Tissue-Engineered Small Intestine in the Mouse

Delayed Presentation of Short Bowel Syndrome Complicated with Severe Degree of Nutritional Deficiencies, Nephrocalcinosis and Distal Renal Tubular Acidosis

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