Short bowel syndrome is characterized by the loss of a significant length of the small intestine, rendering the small intestine unable to absorb the body's nutritional demands without either oral or intravenous (IV) supplementation. The loss of small bowel length can either be due to congenital disease (eg, microvillous inclusion disease, congenital short bowel), or it can be acquired with a need for resection of a large amount of small bowel (eg, Crohn disease, small bowel infarction). Short bowel syndrome is defined as having less than 25% of expected bowel length or requiring parenteral nutrition 60 days after bowel resection.

In pediatrics, the most common cause of short bowel syndrome is necrotizing enterocolitis with small bowel resection. Intestinal atresia, gastroschisis, malrotation with volvulus, and Hirschsprung disease with proximal resection are other common causes of short bowel syndrome in children.

In adults, Crohn disease with small bowel resection, malignancy, volvulus, and vascular compromise with bowel infarction are the most common etiologies.

Symptoms depend on the phase of illness and can vary based on the length and location of resected bowel. Acute-phase symptoms include large volume gastrointestinal fluid losses and metabolic disarray; they begin immediately following surgical resection and can last for approximately 1 month. Over time, the bowel adapts to increase nutrient absorption. This may last for 1-2 years.  

Most symptoms are attributed to malabsorption (weight loss, diarrhea, abdominal discomfort, steatorrhea, dehydration, cholelithiasis) and malnutrition due to mineral and vitamin deficiencies (eg, zinc, magnesium, calcium, iron, folic acid, fat-soluble vitamins). These symptoms can include fatigue, scaling rash, muscle spasms, and impaired clotting.