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Chronic complications of short bowel syndrome in children

Chronic complications of short bowel syndrome in children
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Gastrointestinal complications
Diarrhea Acute or chronic; multiple mechanisms.
  • Early management involves acid suppression and gradual advancement of feeds
  • Chronic management varies with patient characteristics; involves trials of dietary changes and, sometimes, pharmacotherapy
Dysmotility Common in patients with intestinal dilatation or gastroschisis. Treatment may involve prokinetic drugs and/or surgical tapering procedures.
Anastomotic ulcers Develop at site of intestinal resection; may present with acute or chronic gastrointestinal bleeding, anemia, and elevated markers of gastrointestinal inflammation.
Allergic and eosinophilic disease Increased risk for food protein-induced proctocolitis and eosinophilic enteritis and esophagitis. Management is similar to patients without SBS and may include elimination diets.
Esophagitis/peptic ulcer disease Risk related to gastric acid hypersecretion and dysmotility. Acid suppression should be given routinely in the early phase after intestinal resection but only continued if there is clear evidence of active peptic disease.
Small intestine bacterial overgrowth Risk increases with dysmotility, dilated bowel, acid-suppressive drugs, and lack of enteral feeds. Symptoms include exacerbation of diarrhea and weight loss.
Hepatobiliary disease
Intestinal failure-associated liver disease Cholestatic liver disease associated with prolonged PN, especially in infants. Refer to UpToDate content on this disorder.
Gallstones Multiple causes; best prevention is maximizing enteral feeds and reducing PN.
Catheter-related complications
Infection Highest risk shortly after transition to home PN. Patients with fever and a CVC should be treated promptly with empiric intravenous antibiotics.
Mechanical failure Occlusion, thrombosis, or damage to CVCs.
Nutritional complications
Common deficiencies Highest risk during and shortly after transition off of PN. Common deficiencies are fat-soluble vitamins (A, E, D and K), iron, vitamin B12, and calcium*.
Metabolic bone disease and rickets Usually caused by vitamin D and calcium deficiencies; monitor with serial laboratory and bone densitometry screening*.
Skin complications
Ileostomy or colostomy – Infection, skin breakdown Monitor skin; use barrier cream or other measures.
Gastrostomy – Granulation tissue Ensure proper fit of gastrostomy device; chemical cautery if needed.
Kidney complications
Kidney stones (calcium oxalate) Fat malabsorption leads to hyperoxaluria and calcium oxalate stones.
Kidney dysfunction Increased risk in SBS compared with healthy population. Avoid acute or chronic dehydration.
Neurologic dysfunction
Neurocognitive development Risk for cognitive delay and learning disabilities, only partly explained by prematurity.
D-lactate encephalopathy A complication of D-lactic acidosis. Symptoms are acute or intermittent neurologic dysfunction including confusion, cerebellar ataxia, and slurred speech. Primarily occurs in patients with an intact colon and with underlying small intestine bacterial overgrowth.
Other issues
Feeding problems and oral aversion Common complication in infants who are not orally fed.
Dental disorders High prevalence of caries; occasional tooth discoloration.
Psychosocial burden Families have high financial and caregiving burden.

CVC: central venous catheter; PN: parenteral nutrition; SBS: short bowel syndrome.

* Refer to UpToDate topic and table for schedule of laboratory monitoring for nutritional deficiencies in SBS.
Courtesy of Christopher Duggan, MD, and Alexandra Carey, MD.
Graphic 107859 Version 4.0

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