Iskandar Idris Dumping syndrome is a frequent complication of bariatric surgery. The prevalence of dumping syndrome depends on the type and extent of surgery, but current data suggests a prevalence of up to 40% of patients after Roux‐en‐Y gastric bypass or sleeve gastrectomy. In addition to the two procedures, dumping syndrome may also occur after vertical banded gastroplasty and the laparoscopic adjustable gastric band, all of which reduce the volume capacity of the proximal stomach. Although the majority of patients have mild symptoms, for some patients, symptoms of dumping syndrome can be debilitating and emotionally distressing, and are associated with a significant reduction in quality of life. It has been proposed that food intolerance that often accompany dumping syndrome plays an important role of weight loss following bariatric surgery; multiple studies have not shown that patients who have dumping syndrome symptoms lose more weight than those who do not have dumping syndrome (Table 24.1). Table 24.1 Treatment of dumping syndrome. Dumping syndrome consists of a constellation of symptoms that can be categorised as early or late dumping symptoms. Early dumping syndrome typically occurs within the first hour after a meal and include gastrointestinal symptoms (abdominal pain, bloating, borborygmi, nausea and diarrhoea) and vasomotor symptoms (flushing, palpitations, perspiration, tachycardia, hypotension, fatigue, desire to lie down and, rarely, syncope). The pathophysiology involves the introduction of hyperosmolar nutrients in the small bowel. This causes a shift of fluid from the intravascular compartment to the intestinal lumen, resulting in a reduction in plasma volume, tachycardia and, rarely, syncope. Movement of fluid into the small bowel may also cause distention and contribute to cramp‐like contractions, bloating and diarrhoea. In addition, increased release of multiple GI hormones including vasoactive agents (e.g. neurotensin and vasoactive intestinal peptide [VIP]), incretins (e.g. gastric inhibitory polypeptide [GIP] and GLP‐1) and glucose modulators (e.g. insulin and glucagon) may contribute to the vasomotor symptoms. Late dumping syndrome meanwhile usually occurs between 1 and 3 hours after a meal and mainly includes symptoms of hypoglycaemia due to incretin‐driven hyperinsulinaemic response after carbohydrate ingestion. Hypoglycaemia‐related symptoms are attributable to neuroglycopenia (which is indicated by fatigue, weakness, confusion, hunger and syncope) as well as sympathetic activation (indicated by perspiration, palpitations, tremor and irritability). In contrast, the pathophysiology of early dumping, late dumping is largely attributable to the development of hyperinsulinemic or reactive hypoglycaemia. Rapid delivery of undigested carbohydrates to the small intestine results in high glucose concentrations that induce a hyperinsulinemic response, resulting in subsequent hypoglycaemia and related late dumping symptoms. An exaggerated endogenous GLP‐1 response plays an important role in mediating the hyperinsulinemic and hypoglycaemic effect that is characteristic of late dumping syndrome (Figure 24.1). Since early and late dumping is a spectrum of disease presentation, many patients can be affected by both early and late dumping syndrome. A thorough medical history and symptom assessment in the context of a person who recently had a bariatric surgery are important for the diagnosis of dumping syndrome. Symptom‐based questionnaires, such as the Sigstad’s score and the Arts’ dumping questionnaire, can be used to help identify patients with dumping symptoms. For the Sigstad score, the total points are summarised into a calculated diagnostic index; score of >7 is suggestive of dumping syndrome and if the score is <4 then other diagnoses need to be considered. Scores of 5 and 6 represent diagnostic uncertainties (Figure 24.2). Arts’ dumping questionnaire meanwhile was designed to differentiate between early and late dumping symptoms, where symptoms of early and late dumping (eight and six symptoms, respectively) were scored on a four‐point Likert scale (Figure 24.3). Unfortunately, the diagnostic accuracy of both these questionnaires and its accuracy for response to treatment have not been established. Both these scores can therefore be utilised as a diagnostic aid. However, in its original description, Sigstad’s scoring system was shown to identify early dumping syndrome by diagnosing signs and symptoms such as a high pulse rate or increased haematocrit level that are indicative of hypovolaemia during an oral glucose tolerance test. In the modified glucose tolerance test, patients with suspected dumping syndrome ingest 75 g of glucose in solution after an overnight fast; blood concentrations of glucose, haematocrit level, pulse rate and blood pressure are measured before and at 30‐minute intervals up to 180 minutes after ingestion. The test is considered positive for early dumping syndrome based on the presence of an early (30 minutes) increase in haematocrit level >3% or an increase in pulse rate >10 bpm 30 minutes after ingestion. The modified OGTT is considered positive for late dumping syndrome based on the development of late (60–180 minutes after ingestion) hypoglycaemia <2.8 mmol l−1 (50 mg dl−1). Some studies have utilised a higher glycaemia threshold of 3.3 mmol l−1 (60 mg dl−1), usually occurring between 90 and 180 minutes after ingestion, as diagnostic of late dumping syndrome. Although hypoglycaemia is a marker of late dumping syndrome its absence does not exclude a diagnosis of dumping syndrome as early dumping syndrome might be present in the absence of late dumping syndrome. In complex cases, continuous glucose monitoring (CGM) has been used with some success although the diagnostic accuracy of CGM has not been validated against standard tests. Gastric emptying study is often used to support a diagnosis of dumping syndrome in combination with other tests. This involves eating a meal that contains a small amount of radioactive material and measuring the rate of gastric emptying at hourly intervals until four hours after the meal. This test however cannot be used following a total gastrectomy. Its sensitivity and specificity are low. Figure 24.1 Pathophysiology and symptoms of early and late dumping syndrome. Source: Taken from van Beek et al. (2017). Treatment approaches for dumping syndrome include dietary modifications, pharmacologic interventions and, possibly, surgical re‐intervention or continuous tube feeding. Dietary modification: For most patients, strict adherence to dietary intervention will result in a significant improvement or even complete resolution of symptoms. Dietary modification should therefore be the first‐line treatment approach. This involve advice to reduce the amount of food consumed at each meal, delay fluid intake until at least 30 minutes after meals, elimination of rapidly absorbable carbohydrates from the diet to prevent late dumping symptoms, such as hypoglycaemia, and to consume diet consisting of high‐fibre and protein‐rich foods. Fruit and vegetables should be encouraged, but alcoholic beverages should be avoided. Education about the glycaemic index of different foods may also be helpful. In protracted cases, patients can be advised to lie down for 30 minutes after meals to delay gastric emptying and reduce the symptoms of hypovolemia. Dietary supplement: Patients should also follow generic post bariatric eating behaviour advice, such as eating slowly and chew well. Dietary supplements, such as pectin (15 g), guar gum (5 g) and Glucomannan (1.3 g) with each meal, are good second‐line treatment for patients with dumping syndrome to increase the viscosity of food. However, many of these substances are not very palatable, which may adversely affect compliance. Figure 24.2 Dumping syndrome according to Sigstad scoring system. Figure 24.3 Dumping syndrome according to Art’s questionnaire. Each symptom is scored for severity on a 0–3 Likert scale (absent to severe). Early and late dumping syndrome scores are calculated as, respectively, the sum of the eight symptoms of early dumping syndrome and the six symptoms of late dumping syndrome. The total severity score for dumping syndrome is the sum of severities of all symptoms. Pharmacological
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Metabolic Complications of Bariatric Surgery
Dumping Syndrome
Dietary
Reduce food consumption
Delay fluid intake until at least 30 min after meals
Avoid simple carbohydrates
Consume diet consisting of high‐fibre, protein‐rich foods, low glycaemic index food
Lie down for 30 min after meals
Dietary supplements
Pectin (15 g), guar gum (5 g) and Glucomannan (1.3 g)
Pharmacological
Acarbose 50–100 mg three times a day
Octreotide 50–100 mcg three times a day (subcutaneous injection)
Octerotide LAR 20–40 mg 2–4 weekly (intramuscular injection)
Pasireotide LAR 10–40 mg every 4 wk (intramuscular injection)
Diazoxide 100–150 mg three times a day
Nifedipine 10 mg a day
Surgical
Gastric tube placement
Gastric bypass reversal with or without concomitant sleeve resection
Gastric pouch restriction
Pancreatic resection
Constant enteral feeding nutrition via a feeding jejunostomy
Diagnosis
Symptom‐Based Questionnaires
Modified Glucose Tolerance Test
Gastric Emptying Study
Treatment
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