Postgastrectomy Syndromes

Dumping Syndrome

DS is a constellation of GI and vasomotor symptoms, which present postprandially due to rapid gastric emptying. It is caused by loss of pyloric regulation of gastric emptying and/or decreased gastric compliance. The human stomach possesses the remarkable capability of adapting to large volumes of orally administered liquids and solids through vagally mediated accommodation and receptive relaxation. These intragastric contents, usually hypertonic, are then acted on by secreted acid and pepsin along with muscular churning to prepare an isosmotic gastric chyme that is slowly discharged into the duodenum for further digestion and absorption. If there has been a vagotomy, or a portion of the stomach has been removed, or the normal pyloric sphincter has been disrupted or bypassed, the ingested meal may be incompletely processed by the stomach and/or prematurely discharged into the proximal small intestine. The flow of liquid out of the stomach is determined partly by intragastric pressure and partly by pyloric resistance. Procedures that alter the normal intragastric pressure/volume relationship (proximal gastric vagotomy, sleeve gastrectomy, fundoplication) or outflow resistance (pyloroplasty, gastrojejunostomy [GJ]) predispose to DS. Procedures that alter both have the highest incidence of dumping (gastrectomy, Roux-en-Y gastric bypass [RYGBP]). Dumping symptoms have been reported in up to 70% of Billroth II patients and up to 75% of patients after RYGBP for obesity. Similarly, after gastrectomy for cancer, 67% of patients present with early dumping symptoms and 38% with late dumping. Depending on the speed of liquid emptying and the osmolarity of the contents being discharged, a variety of symptoms may result that have been referred to as the dumping syndrome. Both an early and late form of this disorder have been identified. The role of surgically induced microbiome changes in the etiology of DS is unknown.

Early dumping is more common and includes systemic and abdominal symptoms. Systemic manifestations include palpitations, tachycardia, fatigue, a need to lie down following meals, flushing or pallor, diaphoresis, lightheadedness, hypotension, headache, and possibly syncope. Abdominal symptoms include early satiety, epigastric fullness or pain, diarrhea, nausea, cramps, bloating, and borborygmi. Early dumping begins within 30 minutes following a meal and is attributable to bowel distention, relative hypovolemia, GI hormone hypersecretion, and autonomic dysregulation. Late dumping is characterized by symptoms that occur 1 to 3 hours postprandially. Symptoms of late dumping consist of perspiration, faintness, decreased concentration, and altered levels of consciousness, among others. These symptoms are related to a reactive hypoglycemia that occurs 1 to 3 hours postprandially. Patients with late dumping often have early dumping as well.

Most patients with DS have mild to moderate symptoms, but some patients have disabling symptoms that may be severe enough to cause protein-energy malnutrition. The differential diagnosis of DS includes gastroparesis, partial small bowel obstruction, anastomotic stricture, postvagotomy diarrhea, inflammatory bowel disease, irritable bowel disease, and bacterial overgrowth. Dumping symptoms are triggered by rapid gastric emptying of hyperosmolar voluminous chyme that causes bowel distention, hypermotility, and splanchnic blood pooling. This leads to both the GI and vasomotor symptoms that characterize early DS. Hormones play an important role as mediators of this pathophysiologic response (e.g., vasoactive intestinal peptide [VIP], serotonin, bradykinin, norepinephrine). Late dumping involves a reactive hypoglycemia brought on by the rapid and high initial glucose load presented to and absorbed by the small intestine, leading to a GLP-1–mediated inappropriately high insulin response and hypoglycemia.

An oral glucose challenge will confirm the diagnosis of DS. Patients fast for 10 hours overnight and then ingest 50 g of glucose. It is reported to have a sensitivity and specificity of up to 100% and 94%, respectively. The diagnosis of early DS in a patient with clinical symptomatology may also be confirmed with a scintigraphic gastric emptying study, in which greater than 50% of an isotope-labeled solid meal has emptied within 1 hour.

A variety of gastric procedures may give rise to early dumping. More than half of the patients who have had RYGBP for obesity or total gastrectomy experience early dumping symptoms, and approximately 30% of those with partial gastrectomy have early dumping. The risk of problematic dumping after sleeve gastrectomy is low (1.6%), although up to 30% to 40% of patients may have very mild symptoms. Up to 15% of patients with pyloroplasty or simple GJ experience early dumping, as do 2% of patients with proximal gastric vagotomy and fundoplication. The type of GI reconstruction after distal gastrectomy influences the risk of DS because Roux-en-Y GJ (11%) has a lower rate of dumping than either Billroth I (B1) or Billroth II (B2). DS after B1 (17%) is less than after B2, (70%), perhaps because B1 gastric effluent enters the duodenum and triggers a neuroendocrine response that slows gastric emptying (duodenal brake). The risk of dumping with pyloroplasty and loop GJ are similar, but the latter gastric drainage procedure is easily reversible. Dumping symptoms tend to improve with time in most patients.

Late dumping, less common than the early variant, is caused by hyperinsulinemic hypoglycemia and occurs 2 to 3 hours postprandially. In late dumping the rapid delivery of monosaccharides and disaccharides into the small intestine causes hyperglycemia. The pancreas is subsequently triggered to release insulin by glucagon-like peptide 1 (GLP-1) and in the process actually “overshoots” so that marked hypoglycemia is induced. This insulin shock condition stimulates the adrenal glands to release catecholamines, which cause a constellation of symptoms, including tachycardia, tachypnea, diaphoresis, and lightheadedness. Late DS is more frequent in patients who had early DS. Late DS has been reported in more than 50% of bariatric patients after gastric bypass. In some of these patients, late DS developed 1 to 8 years after the surgery and was significantly more common in patients with type 2 diabetes mellitus (44.9% vs. 5.6%). One must rule out an unrelated islet cell tumor as the cause of a severe refractory hypoglycemia by documenting the fasting plasma glucose, serum insulin, and C-peptide level. A prolonged oral glucose tolerance test will also confirm the diagnosis of late dumping. Early dumping tends to improve with time, whereas late dumping tends to persist or exacerbate.

In most patients with DS, symptoms are not severe and medical management is successful. Consultation with an experienced dietitian is helpful. Dietary modification is the first-line treatment for DS. Daily intake should be divided into at least 6 meals. Liquids and solids should be separated. Diets should be high in protein and fat, and simple sugars should be avoided. Vasomotor symptoms can often be ameliorated if the patient lies down for 30 minutes after meals. Elimination of milk and dairy products has been successful in many patients. Another simple therapy is adding dietary fiber. Guar gum and pectin are useful in increasing the viscosity of the food, but their poor taste limits patient compliance. Hard candy can be consumed to abort the hypoglycemia of late DS. Acarbose is an α-glycosidase hydrolase inhibitor that delays carbohydrate digestion and absorption and is efficient in the treatment of late dumping. Side effects include excess flatulence and hypoglycemia if carbohydrate absorption is excessively inhibited.

A number of pharmacologic options exist for the treatment of the DS. Tincture of opium is especially effective in relieving diarrhea associated with DS. Symptomatic treatment of DS may be addressed with over the counter medications. Treatment for diarrhea (e.g., Imodium), nausea (e.g., meclizine, promethazine, proton pump inhibitors [PPIs]), or antigas measures may be helpful. Inadequate digestion of nutrients can cause gas and bloating when they reach colonic bacteria; therefore probiotics may be a useful adjunct. Anticholinergic agents, such as dicyclomine, hyoscyamine, and propantheline, slow gastric emptying and are also antispasmodic, thus decreasing abdominal pain related to small bowel motility. Diazoxide is a potassium channel activator that inhibits the secretion of insulin. Thus diazoxide has showed success in recent studies in treating late dumping hypoglycemia and can be used when acarbose and lifestyle modifications are insufficient.

Octreotide, a somatostatin analogue, should be considered for patients with severe postgastrectomy DS refractory to diet therapy. Octreotide can markedly improve the quality of life in DS patients, but the data are limited for long-term efficacy. Octreotide alleviates both early and late dumping symptoms through inhibition of hormone mediators. It also delays gastric emptying time and inhibits splanchnic vasodilation. Short-acting and long-acting octreotide are equally effective in blunting dumping symptoms, but the long-acting preparation scored significantly better on quality-of-life measures. Long-term octreotide therapy loses its efficacy because side effects such as diarrhea and steatorrhea as well as cost lead to lack of compliance.

Only a small percentage of patients with dumping symptoms ultimately require surgery. Most patients improve with time (months and even years), dietary management, and medication. Therefore the surgeon should not rush to reoperate on the patient with DS. Multidisciplinary nonsurgical management must be optimized first. Before reoperation, a period of in-hospital observation is useful to define the severity of the patient's symptoms, and patient compliance with prescribed dietary and medical therapy. The results of remedial operation for dumping are variable and unpredictable. There are a variety of surgical approaches, none of which work consistently well. In addition, there is not a great deal of experience reported in the literature with any of these methods. Long-term follow-up is rare.

Patients with disabling refractory dumping after GJ can be considered for simple takedown of this anastomosis provided that the pyloric channel is patent endoscopically. For dumping following pyloroplasty, pyloric reconstruction is described, but modern day experience with this is rare and today's surgeon should view pyloroplasty as irreversible. Distal gastrectomy with Roux reconstruction ( Fig. 62.4A ), or a “duodenal switch” with division of the postbulbar duodenum and anastomosis to a Roux jejunal limb, is currently the best option for the uncommon patient with refractory postpyloroplasty dumping. For severe dumping after Billroth I or II gastrectomy, conversion to Roux-en-Y GJ should be considered because the motility of the Roux limb tends to slow gastric emptying. However, gastric stasis and/or marginal ulceration may result particularly in the presence of a large gastric remnant. Lifelong acid suppression should be considered. The reversed intestinal interposition is rarely used currently for DS—and rightly so. This operation interposes a 10-cm reversed segment of intestine between the stomach and the proximal small bowel (see Fig. 62.4B ). This slows gastric emptying but often leads to obstruction, requiring reoperation. Isoperistaltic interposition (Henley loop) between the gastric remnant and the duodenum has not been successful in sustained improvement of DS. Because pyloric ablation is a dominant factor in the etiology of postgastrectomy dumping, it is not surprising that conversion of Billroth II to Billroth I anastomosis cannot ensure resolution of dumping symptoms. Newer surgical techniques, such as pylorus-preserving segmental gastrectomy for early cancer of the midbody of the stomach, have been reported and may significantly decrease the incidence of postoperative dumping.

Postvagotomy Diarrhea

Truncal vagotomy is associated with clinically significant diarrhea in 5% to 10% of patients. It occurs soon after surgery and usually is not associated with other GI or systemic symptoms, a fact that helps to distinguish it from dumping. The diarrhea may be a daily occurrence, or there may be significant periods of relatively normal bowel function. The symptoms tend to improve over the months and years after the index operation, and long-term significant postvagotomy diarrhea occurs in only 1% to 2% of vagotomy patients. The cause of postvagotomy diarrhea is unclear. Although rare, it can even occur after proximal gastric vagotomy or fundoplication, suggesting that intestinal vagal denervation may not be the sole cause. Factors contributing to postvagotomy diarrhea include intestinal dysmotility and accelerated transit, bile acid malabsorption, rapid gastric emptying, altered microbiome, and bacterial overgrowth. The latter problem is facilitated by decreased gastric acid secretion and (even small) blind loops. Although bacterial overgrowth can be confirmed with the hydrogen breath test, a simpler test is an empirical trial of oral antibiotics and/or probiotics. Some patients with postvagotomy diarrhea respond to cholestyramine, whereas in others codeine or loperamide may be useful. It has been shown experimentally that the total bile acid content in the stools of patients with postvagotomy diarrhea, although not significantly greater than in those without this problem, has more than twice the amount of chenodeoxycholic acid. Such findings lend support to the hypothesis that bile acid malabsorption may contribute to postvagotomy diarrhea in some patients.

Fat malabsorption should also be considered in the differential diagnosis of postvagotomy diarrhea. This can be caused by acid inactivation of pancreatic enzymes, poorly coordinated mixing of food and digestive juices, or bacterial overgrowth. This can be confirmed with a qualitative test for fecal fat. It is best treated with acid suppression and pancreatic enzyme supplements, and if appropriate oral antibiotics. Postvagotomy diarrhea usually does not respond to these modalities.

In the rare patient who is debilitated by postvagotomy diarrhea unresponsive to maximal medical management for at least 1 year, operation might be considered but outcomes can be problematic. The operation of choice is probably a 10-cm reversed jejunal interposition placed in continuity 100 cm distal to the ligament of Treitz ( Fig. 62.5 ). Another option is the onlay antiperistaltic distal ileal graft. Both operations can cause obstructive symptoms and/or bacterial overgrowth.

Gastric Stasis

In the rare patient with acute gastric stasis after gastric surgery, persistent nausea and vomiting prevent removal of the nasogastric tube. If the nasogastric tube cannot be removed within a period of 7 to 10 days after surgery, a gastrostomy may be placed either laparoscopically or endoscopically. Alimentation can then be given via a J tube extension placed during one of these procedures. If the gastric remnant is not of sufficient size to accommodate these approaches, a decompressing gastric tube can often be passed retrograde through the efferent limb and exited through the skin via a Witzel technique. Distal to this placement, another tube may be placed antegrade as a Witzel feeding jejunostomy. In patients in whom these enteral approaches to alimentation are not possible, total parenteral nutrition is an alternative. In any event, reoperative surgery should generally be delayed for at least 3 months as the majority of patients will regain satisfactory GI function without surgery. Only after this period should reexploration be considered.

Chronic gastric stasis following gastric surgery may be due to a problem with gastric motor function or be caused by an obstruction. The gastric motility abnormality may have been preexisting and unrecognized by the operating surgeon. More commonly it is secondary to some aspect of the operation, such as deliberate or unintentional vagotomy or resection of the dominant gastric pacemaker. Truncal vagotomy is more likely to cause chronic gastric stasis than proximal gastric (parietal cell) vagotomy because it denervates the antropyloric pump mechanism. Obstruction may be mechanical (e.g., anastomotic stricture, efferent limb kink from adhesions or constricting mesocolon, or a proximal small-bowel obstruction) or functional (e.g., retrograde peristalsis in a Roux limb).

Chronic gastric stasis presents with vomiting (often of undigested food), bloating, epigastric pain, and weight loss. Symptoms are usually improved by a liquid diet and always improved by prolonged fasting. Differential diagnosis includes primary gastroparesis, chronic small bowel obstruction, anastomotic stricture, afferent loop syndrome, internal hernia, GERD, and achalasia. The evaluation includes esophagogastroduodenoscopy (EGD), upper GI series, gastric emptying scan (scintigraphy), and gastric motor testing. Endoscopy shows gastritis and retained food or bezoar in the stomach. The gastroenteric anastomosis and efferent limb should be evaluated for stricture or narrowing. A dilated efferent limb suggests chronic stasis, either from a motor abnormality (e.g., Roux syndrome) or mechanical small bowel obstruction (e.g., chronic adhesion). If the problem is thought to be primarily a disorder of intrinsic motor function, newer techniques, such as electrogastrography and GI manometry, should be considered. However, it should be recognized that chronic distal mechanical obstruction may result in disordered motility in the proximal organ.

After mechanical obstruction has been ruled out, medical treatment is successful in most cases of gastric motor dysfunction following gastric surgery. Management consists of dietary modification and promotility agents. One of several gastrokinetic agents, such as metoclopramide, domperidone, and erythromycin, will generally prove efficacious in a given patient. Metoclopramide is a dopamine antagonist that works on the stomach by facilitating acetylcholine release from enteric cholinergic neurons. It may cause irreversible movement disorder if used more than 3 months and/or at high doses. Domperidone works on both the stomach and the intestine by facilitating acetylcholine release from the mesenteric plexus of the gut. Erythromycin is a motilin agonist that works on both the stomach and intestine by binding to motilin receptors on GI smooth muscle. One of these agents is usually sufficient to enhance gastric tone so that improved gastric emptying results. Intermittent oral antibiotic therapy may be helpful in treating bacterial overgrowth, with its attendant symptoms of bloating, flatulence, and diarrhea. Probiotics should be tried because alterations in gut microbiome are likely.

Surgery should be considered when chronic postoperative gastric stasis is severe and resistant to medical management. At operation small bowel obstruction and efferent limb obstruction should always be ruled out. Gastroparesis following vagotomy and drainage procedures may be treated with subtotal (75%) gastrectomy. Billroth II anastomosis with Braun enteroenterostomy ( Fig. 62.6A ) may be preferable to Roux-en-Y reconstruction after subtotal gastrectomy in this setting because Roux reconstruction may result in persistent gastric emptying problems (Roux syndrome) ultimately necessitating near-total or total gastrectomy, a nutritionally unattractive option. Delayed gastric emptying following vagotomy and drainage or vagotomy and antrectomy may represent an anastomotic stricture due to recurrent (marginal) ulcer, or proximal small bowel obstruction. Recurrent ulcer may respond to medical therapy with PPI and abstinence from nonsteroidal antiinflammatory drugs (NSAIDs), aspirin, and smoking. Endoscopic dilation is occasionally helpful. Gastroparesis following subtotal gastric resection is best treated with near-total (95%) or total gastric resection and Roux-en-Y reconstruction. High-frequency gastric electrical stimulation (GES) may be an effective treatment for patients with postsurgical gastroparesis who failed standard medical therapy, but long-term follow-up and randomized controlled trials (RCTs) are lacking.

Afferent Loop Obstruction

Afferent loop obstruction, also called afferent loop syndrome, is a mechanical complication that infrequently occurs following construction of a GJ. The creation of a GJ leaves a segment of proximal small bowel (duodenum and proximal jejunum) upstream from the anastomosis. With Billroth II or loop GJ the afferent limb conducts bile, pancreatic juices, and other proximal intestinal secretions toward the GJ ; with Roux-en-Y the afferent limb conducts the succus toward the jejunojejunostomy and is also called the biliopancreatic limb. The operations most commonly associated with afferent loop obstruction are Billroth II and Roux-en-Y GJ (distal gastrectomy or gastric bypass), and Roux-en-Y esophagojejunostomy (total gastrectomy). The incidence of significant afferent loop obstruction after these procedures is low (0.3% to 1.0%) and is similar after open and laparoscopic surgery.

The etiologies of afferent loop obstruction include: (1) entrapment, compression, and kinking of the afferent loop by postoperative adhesions; (2) internal herniation, volvulus, and intussusception of the afferent loop; (3) scarring due to marginal ulceration of the GJ; (4) locoregional recurrence of cancer (lymph nodes, peritoneum, gastric remnant, anastomotic sites); (5) radiation enteritis of the afferent loop; and (6) enteroliths, bezoars, and foreign bodies impacted in the afferent loop ( Fig. 62.7 ). In patients with Billroth II anastomoses, afferent loop syndrome is seen more commonly in patients with redundant (longer than 30 to 40 cm) and antecolic afferent loops, which are more prone to kinking, volvulus, and entrapment by adhesions. Improperly closed mesocolic defects may predispose to internal herniation of the retrocolic afferent limb. In contrast, it is more common to find an obstruction or internal herniation of the Roux limb in the retrocolic retrogastric position than in the antecolic antegastric positioning after RYGBP. The role of closing the mesenteric defect remains unclear.

Although both acute and chronic forms of afferent loop syndrome have been described, chronic partial obstruction is the more common clinical manifestation. The classic presentation of chronic afferent loop syndrome is postprandial abdominal pain relieved by bilious vomiting, but the latter may be lacking with Roux-en-Y GJ.

A meal elicits pancreatic, biliary, and duodenal secretion into the obstructed afferent limb. As the volume of these secretions increases, the obstructed duodenum and proximal jejunum become more distended. Eventually the pressure in the partially obstructed afferent limb overcomes the obstruction (usually 30 to 60 minutes postprandially), delivering a large volume of bilious secretions into the stomach or Roux limb. This leads to bilious vomiting and prompt relief of the pain, which was caused by the afferent limb distention. Weight loss and anemia are common. Bacterial overgrowth secondary to afferent limb stasis may contribute to these problems due to malabsorption of fat and other nutrients, such as vitamin B ₁₂ or iron.

If the obstruction is high grade or complete, the distended afferent loop may not sufficiently decompress. In this scenario, vomiting, if present, will be nonbilious, and a clinical picture of “closed loop obstruction” manifested as an acute abdomen will result. If this condition is not recognized early, the afferent loop may actually perforate and result in peritonitis. Urgent surgery is necessary to correct this problem.

Depending on the acuity and severity of the afferent loop obstruction, physical examination can reveal one or more of the following findings: weight loss, upper abdominal distention, upper abdominal mass, and abdominal tenderness. Peritoneal findings or pain out of proportion to physical findings are ominous. Rarely jaundice, cholangitis, or pancreatitis can confuse the clinical picture.

Abdominal multiple detector computed tomography (CT) is the diagnostic study of choice. CT appearance of the obstructed afferent loop consists of a C -shaped, fluid-filled tubular mass located in the midline between the abdominal aorta and the superior mesenteric artery (c-loop sign) with valvulae conniventes projecting into the lumen (keyboard sign). Adhesions are suspected when a point of transition from a dilated to a normal-caliber loop is observed without other apparent cause. An internal hernia is suspected when crowding, stretching, and crossover of mesenteric vessels and the whirl sign are observed. Local recurrence and radiation enteritis are suspected when focal and diffuse bowel wall thickening are observed. Carcinomatosis is suspected when ascites and peritoneal enhancement are present and bowel wall thickening around the level of obstruction is absent. Barium upper GI, contraindicated in patients with an acute abdomen, can be helpful in patients with chronic intermittent symptoms. Suggestive findings of afferent limb obstruction on this study include nonfilling of the afferent loop and/or retention of barium in the dilated afferent loop. However, these findings cannot be deemed conclusive because 20% of normal afferent loops are not filled after a barium meal. Although balloon dilation and/or stenting may be useful in special cases, the cornerstone of treatment for afferent loop obstruction in patients with curable cancer or benign disease is surgery. At operation the primary cause of afferent loop obstruction should be confirmed and treated. This may include resection for tumor or marginal ulcer, lysis of adhesions, or repair of internal hernia. Procedures to consider include addition of a Braun anastomosis in a former Billroth II reconstruction, excision of the redundant loop and conversion of Billroth II to Roux-en-Y GJ or Billroth I, and excision of the redundant loop and reconstruction of the former Roux-en-Y jejunojejunostomy ( Fig. 62.8 ). Endoscopic interventions and percutaneous approaches (percutaneous endoscopic gastrostomy [PEG], balloon dilation, double-pigtail stents traversing the afferent loop strictured area) have an important role in the management of patients with stage IV cancer. These techniques may also be useful as temporizing measures in high-risk patients.

In contrast to the relatively stereotypical manifestation of afferent loop obstruction, efferent loop obstruction generally mimics proximal small bowel obstruction. It is most commonly caused by adhesions, but internal hernia must also be considered.