Postgastrectomy Syndromes

Postgastrectomy Syndromes are caused by changes in gastric emptying as a consequence of gastric operations. They may occur in up to 20% of patients who undergo gastric surgery, depending on the extent of resection, disruption of the vagus nerves, status of the pylorus, type of reconstruction, and presence of mechanical or functional obstruction. Clearly defining the syndrome that is present in a given patient is critical to developing a rational treatment plan (World J Surg 2003;27:725). Most are treated nonoperatively and resolve with time.

A. Nutritional disturbances

Nutritional disturbances occur in 30% of patients after gastric surgery, either as a result of functional changes or postgastrectomy syndromes. Prolonged iron, folate, vitamin B12, calcium, and vitamin D deficiencies can result in anemia, neuropathy, dementia, and osteomalacia. These can be prevented with supplementation.

B. Dumping syndrome

Dumping syndrome is thought to result from the rapid emptying of a high-osmolar carbohydrate load into the small intestine. Gastric resection leads to the loss of reservoir capacity and the loss of pylorus function. Dumping syndrome is most common after Billroth II reconstruction.
  • Early dumping occurs within 30 minutes of eating and is characterized by nausea, epigastric distress, explosive diarrhea, and vasomotor symptoms (dizziness, palpitations, flushing, diaphoresis). It is presumably caused by rapid fluid shifts


    in response to the hyperosmolar intestinal load and release of vasoactive peptides from the gut. Symptoms are relieved by recumbence or saline infusion.

  • Late dumping symptoms are primarily vasomotor and occur 1 to 4 hours after eating. The hormonal response to high simple carbohydrate loads results in hyperinsulinemia and reactive hypoglycemia. Symptoms are relieved by carbohydrate ingestion.
  • Treatment is primarily nonsurgical and results in improvement in nearly all patients over time. Meals should be smaller in volume but increased in frequency, liquids should be ingested 30 minutes after eating solids, and simple carbohydrates should be avoided. Use of the long-acting somatostatin analog octreotide results in significant improvement and persistent relief in 80% of patients when behavioral modifications fail (Clin Endocrinol 1999;51:619). If reoperation is necessary, conversion to Roux-en-Y gastrojejunostomy is usually successful.

C. Alkaline reflux gastritis

Alkaline reflux gastritis is most commonly associated with Billroth II gastrojejunostomy and requires operative treatment more often than other postgastrectomy syndromes. It is characterized by the triad of constant (not postprandial) epigastric pain, nausea, and bilious emesis. Vomiting does not relieve the pain and is not associated with meals. Endoscopy reveals inflamed, beefy-red, friable gastric mucosa and can rule out recurrent ulcer as a cause of symptoms. Bile reflux into the stomach is occasionally seen. Enterogastric reflux can be confirmed by hydroxy iminodiacetic acid (HIDA) scan. Mechanical obstruction is absent, distinguishing alkaline reflux gastritis from loop syndromes. Nonoperative therapy consists of frequent meals, antacids, and cholestyramine to bind bile salts but is usually ineffective. Surgery to divert bile flow from the gastric mucosa is the only proven treatment. The creation of a long-limb (45-cm) Roux-en-Y gastrojejunostomy effectively eliminates alkaline reflux and is the preferred option for most patients (Gastroenterol Clin North Am 1994;23:281).

D. Roux stasis syndrome

Roux stasis syndrome may occur in up to 30% of patients after Roux-en-Y gastroenterostomy (Am J Surg 2003;186:269). It is characterized by chronic abdominal pain, nausea, and vomiting that is aggravated with eating. It results from functional obstruction due to disruption of the normal propagation of pacesetter potentials in the Roux limb from the proximal duodenum, as well as altered motility in the gastric remnant. Near-total gastrectomy to remove the atonic stomach can improve gastric emptying and is occasionally useful in patients with refractory Roux stasis. Use of an “uncut” Roux-en-Y reconstruction (Am J Surg 2001;182:52) may preserve normal pacemaker propagation and prevent the development of the syndrome.

E. Loop syndromes

Loop syndromes result from mechanical obstruction of either the afferent or efferent limbs of the Billroth II gastrojejunostomy. The location and etiology of the obstruction are investigated by plain abdominal x-rays, CT scan, upper GI contrast studies, and endoscopy. Relief of the obstruction may require adhesiolysis, revision of the anastomosis, occasionally bowel resection, or conversion of Billroth II to Roux-en-Y gastrojejunostomy.
  • Afferent loop syndrome can be caused acutely by bowel kink, volvulus, or internal herniation, resulting in severe abdominal pain and nonbilious emesis within the first few weeks after surgery. Lack of bilious staining of nasogastric drainage in the immediate postoperative period suggests this complication. Examination may reveal a fluid-filled abdominal mass, and laboratory findings may include elevated bilirubin or amylase. Duodenal stump blowout results from progressive afferent limb dilation, leading to peritonitis, abscess, or fistula formation. In the urgent setting, jejunojejunostomy can effectively decompress the afferent limb. A more chronic form of afferent loop syndrome results from partial mechanical obstruction of the afferent limb. Patients present with postprandial right upper quadrant pain relieved by bilious emesis that is not mixed with recently ingested food. Stasis can lead to bacterial overgrowth and subsequent bile salt deconjugation in the obstructed loop, causing blind loop syndrome (steatorrhea and vitamin B12, folate, and iron deficiency) by interfering with fat and vitamin B12 absorption.

  • Efferent loop syndrome results from intermittent obstruction of the efferent limb of the gastrojejunostomy. Patients complain of abdominal pain and bilious emesis months to years after surgery, similar to the situation with regard to a proximal small bowel obstruction.

F. Postvagotomy diarrhea

Postvagotomy diarrhea has an incidence of 20% after truncal vagotomy and is thought to result from alterations in gastric emptying and vagal denervation of the small bowel and biliary tree. The diarrhea is typically watery and episodic. Treatment includes antidiarrheal medications (loperamide, diphenoxylate with atropine, cholestyramine) and decreasing excessive intake of fluids or foods that contain lactose. Symptoms usually improve with time, and surgery is rarely indicated.