Short bowel syndrome (SBS) refers to a condition characterized by malnutrition, diarrhea, electrolyte imbalance, and metabolic disturbances caused by a significant reduction in effective intestinal absorption area. This occurs following extensive resection or bypass of the small intestine, leaving the remaining functional intestine unable to sustain adequate nutrient absorption for the body.
This syndrome commonly occurs in individuals who undergo extensive small bowel resections due to conditions such as mesenteric vascular embolism or thrombosis, intestinal volvulus, strangulated hernias, trauma, or Crohn’s disease. It can also occur in patients with extensive functional impairment of the intestine, such as those with radiation enteritis, or as a complication of inappropriate surgical procedures like jejunocolic or gastroduodenal anastomosis.
Pathophysiology
The development of short bowel syndrome is primarily related to the following factors:
Reduction in Effective Absorptive Area
The normal absorptive area of the small intestinal mucosa exceeds the requirements of nutritional absorption. Resection of 50–70% of the small intestine can result in malabsorption, while severe symptoms leading to short bowel syndrome can develop if less than 75 cm of intestine remains (with an intact colon) or if the ileocecal valve is lost and the remaining intestine is less than 100 cm.
Reabsorption Impairment
The ileum is the primary absorption site for bile salts and vitamin B12. Loss of this segment can lead to symptoms such as diarrhea and anemia.
Gastrointestinal Hormone Dysregulation
Extensive small bowel resection can elevate levels of hormones such as gastrin, leading to increased gastric acid secretion and accelerated gastrointestinal transit. These changes can result in peptic ulcers and exacerbate diarrhea.
Effect of Ileocecal Valve Removal
Removal of the ileocecal valve eliminates its “check valve” function, accelerating intestinal transit. Additionally, pathologic overgrowth of colonic bacteria into the small intestine exacerbates malabsorption and diarrhea.
After extensive small bowel resection, the remaining intestinal segments can undergo compensatory changes to enhance digestion and absorption, such as elongation of intestinal villi, thickening of mucosal folds, deepening of crypts, and widening and lengthening of the intestinal tract.
Clinical Manifestations
The severity and prognosis of short bowel syndrome depend on factors such as the underlying disease, the length and location of the remaining intestine, the presence of the ileocecal valve and colon, and the success of intestinal adaptation.
In the early stage, the primary clinical manifestations include diarrhea, water and electrolyte imbalance, acid-base disturbances, and malnutrition. Over time, diarrhea tends to decrease, and the patient’s nutritional status may stabilize depending on the residual bowel length and compensatory capacity. In cases of progressive malnutrition, symptoms such as weight loss, muscle atrophy, anemia, liver dysfunction, hypoproteinemia, metabolic bone disease, and deficiencies in various vitamins and electrolytes may emerge.
Treatment
The prevention of short bowel syndrome remains the primary goal, with unnecessary extensive resections during the management of small bowel diseases needing to be avoided. The main treatment objectives are the correction of fluid and electrolyte imbalances, maintenance of nutrition, and prevention of complications associated with nutritional support. Treatment is typically divided into three phases based on the progression of the disease:
Phase 1 – Acute Phase
This phase occurs within the first 2 months after surgery, during which intestinal adaptation has not yet occurred. Daily intestinal fluid loss can reach 5–10 liters, leading to significant risks of water and electrolyte imbalance. Treatment during this phase primarily focuses on maintaining stability in the internal milieu of the patient. After achieving stable vital signs, early initiation of parenteral nutrition, along with the use of medications to suppress intestinal motility and reduce gastrointestinal secretions (such as proton pump inhibitors, histamine H2 receptor antagonists, and octreotide), can help reduce diarrhea frequency. When diarrhea volume falls below 2 L/day, small amounts of isotonic enteral nutrition formulations may be introduced to promote intestinal compensation.
Phase 2 – Adaptation Phase
This phase spans from 2 months to 2 years postoperatively. During this time, intestinal adaptation and compensatory mechanisms emerge, significantly reducing diarrhea. Individualized nutritional support plans can be developed, with active efforts to promote bowel rehabilitation and adaptation. Initial diets include small amounts of isotonic foods with gradual increases in volume, caloric content, and osmolarity. Insufficient nutrition and fluids at this stage are supplemented parenterally. The use of agents such as glutamine, growth hormone, and glucagon-like peptide-2 (GLP-2) analogs can further promote the compensatory function of the small intestine.
Phase 3 – Maintenance Phase
This phase begins 2 years postoperatively, by which point intestinal adaptation is largely complete. Diarrhea is substantially controlled, and metabolic and nutritional states tend toward stabilization. If patients are unable to maintain normal metabolic demands, long-term or even lifelong parenteral nutrition or specialized enteral nutrition may be required, with attention to the prevention of complications associated with prolonged parenteral nutrition.
Surgical Management
Surgical treatments for short bowel syndrome primarily fall into two categories:
Slowing Intestinal Transit
Techniques include creating intestinal valves or sphincters, reversing bowel segments, or performing colonic interposition.
Increasing Intestinal Surface Area
Procedures such as intestinal lengthening and tapering surgeries or small bowel transplantation may be performed.