Rapid gastric emptying is the constellation of symptoms including abdominal symptoms (diarrhea, nausea, bloating, early satiety, and epigastric pain) as well as systemic symptoms (tachycardia, palpitations, hypotension, headache, and flushing) usually presenting within 30 min following a meal. The cause of rapid gastric emptying, commonly referred to as dumping syndrome (DS), is typically multifactorial, or caused by several different factors. Gastric surgeries, such as vagotomy and pyloroplasty (V&P), bariatric surgeries, and pylorectomy/pyloroplasty have been well-known as causes of dumping syndrome since the early 1900s. More recently, diabetes mellitus, including type II, as well as viral illnesses, have been associated with DS. This syndrome usually develops in adults, but can affect children who have had surgeries for gastroesophageal reflux disease. Around 20–50% of individuals who have undergone gastric surgery have some clinical features of DS, but only 1–5% of individuals have severe symptoms [1]. The incidence related to diabetes and viral illnesses is unknown due to the similarity of symptoms to other gastrointestinal disorders such as gastroparesis; current research efforts are helping to differentiate these entities.

Dumping syndrome can be divided into early and late forms, depending on the timing and type of symptoms associated with a meal. A majority of individuals have early dumping, approximately 25% of people have late dumping, and few have features of both [2]. Clinical appearances of dumping syndrome include two broad categories, gastrointestinal (abdominal) and vasomotor (systemic) symptoms. Gastrointestinal symptoms include early satiety, nausea, cramps, bloating, diarrhea, and vomiting. Vasomotor symptoms include sweating, flushing, tachycardia, palpitations, hypotension, headache, and syncope. Early dumping syndrome is defined as symptoms that occur within 10–30 min of consuming a meal and is related to bowel distention, gastrointestinal hormone hypersecretion, and autonomic dysregulation [3]. Most people have both gastrointestinal and vasomotor symptoms with early dumping syndrome. On the other hand, late dumping syndrome is defined as symptoms that occur 1–3 h postprandial and is related to reactive hypoglycemia that occurs during this time period. The symptoms of late dumping syndrome are predominantly vasomotor in origin. If the symptoms are severe enough, individuals can develop protein-wasting malnutrition [4], and late dumping syndrome may be associated with food aversion.

The diagnosis of dumping syndrome is largely related to clinical presentation, as well as several other measurable parameters in an individual who has risk factors for the disease (e.g., previous gastric surgeries, diabetes mellitus, or recent viral illness). Sigstad developed a diagnostic scoring system in 1970 that is based on the symptoms of dumping syndrome [5]. The scoring system is easy to use, the more points that an individual has, the higher the likelihood of the disease. A score of greater than 7 on this scale is suggestive of dumping syndrome, while a score of less than 4 suggests another disease. This system is very helpful in evaluating the effectiveness of a treatment when a baseline value is obtained prior to the initiation of treatment and reassessed at specific intervals. The disadvantage of the Sigstad score is separating the similar symptoms seen postprandial from those of dumping syndrome. The Sigstad scoring system can be used in conjunction with other diagnostic criteria.

The oral glucose challenge is a useful test for the diagnosis of dumping syndrome and helps to evoke the symptoms associated with it. The test includes a 10 h fast prior to the administration of an oral 50 gram glucose bolus. Blood pressure and pulse rate are monitored before, during, and after ingestion. An increase in heart rate by ten beats per minute in the first hour after glucose ingestion is considered a positive result [6]. Hematocrit and blood glucose levels are monitored during the test to provide additional information. A hematocrit increase of 3% in the first 30 min suggests early dumping syndrome and hypoglycemia 2–3 h after ingestion suggests late dumping syndrome [7]. The oral glucose test is reported to have a sensitivity and specificity of 100 and 94%, respectively [6].

Radionuclide scintigraphy , also known as gastric scintigraphy , is a useful tool for diagnosing the functional ability of the stomach to empty a meal (whether delayed or rapid) and other symptoms related to dumping syndrome. The presence of rapid gastric emptying is the hallmark of dumping syndrome, and must be present in order to be diagnosed with this disorder. The ingestion of a Technetium (TC)-99m sulfur colloid radiolabeled meal consisting of scrambled egg substitute, two slices of whole wheat bread, and 120 mL of water is the standard of practice. Imaging (both anteriorly and posteriorly) of the stomach is taken at 0, 1, 2, 3, and 4 h after ingestion [8]. Rapid gastric emptying is defined as <30% isotope retention at 1 h, and recent studies have shown gastric emptying percentages of 25.2, 10.2, and 3.5% at 1, 2, and 4, respectively [9]. Delayed gastric emptying is defined as >90% retention at 1 h, >60% at 2 h, and >10% at 4 h. Gastric scintigraphy is most specific at the 4-h mark necessitating the need for studies to be continued for the whole duration rather than relying on the 2 h scan.

Additional tests, such as colonoscopy, endoscopy, stool studies, and other lab tests (complete blood count, comprehensive metabolic panel, tissue transglutaminase IgA, and breath tests), are also performed on a routine basis to help diagnose other diseases that may present with similar symptoms. These include gastroparesis, irritable bowel disease (IBS), idiopathic diarrhea, pancreatic insufficiency, lactose intolerance, and celiac disease, to name a few.

The mechanisms involved in dumping syndrome are beginning to be understood, but are likely multifactorial in nature, from ideas related to chyme characteristics, fluid shifts, and hormone mediated factors. The hallmark of dumping syndrome is the rapid introduction of chyme (partially digested food) into the small intestine. This decreased transit time of food from the stomach to the small intestine causes a cascade of events leading to the symptoms of dumping syndrome. Chyme is both hyperosmolar and voluminous [10], and the consumption of liquids is more likely to cause the symptoms of dumping syndrome than solids alone. The enteric nervous system, or network of nerves that control aspects of the gastrointestinal tract, such as gastric motility and distensibility, are tightly linked to the symptomatology of dumping syndrome. The adaptation of the enteric nervous system also plays a key role in dumping syndrome, allowing some individuals to have resolution of symptoms, and others to have persistence of symptoms. When the chyme enters the small intestine at a faster rate than normal, this causes distention. The small bowel reflexively contracts via the muscular layer (muscularis muscosa) and relaying this to the enteric nervous system causes the postprandial abdominal pain observed in dumping syndrome. The rapid infusion of glucose into the small bowel has demonstrated these symptoms, even in healthy individuals [11, 12].

Early dumping syndrome is defined as symptoms that occur within 10–30 min postprandially. Hormone secretion, such as VIP, serotonin, and GLP-1, and parasympathetic responses cause a fluid shift from the intravascular space to the intestinal lumen and intestinal blood supply [13]. This physiological response is also known as splanchnic blood pooling [14]. In an unaffected individual, the sympathetic activity, which consists of an increase in heart rate, vasoconstriction, and plasma norepinephrine levels, helps to keep the blood pressure from fluctuating during this time [15–17]. The fluid shift seen in dumping syndrome overwhelms the sympathetic activity and results in symptoms such as fatigue, weakness, dizziness, and hypotension. Reflex sympathetic activation then causes diaphoresis and palpitations.

Several hormone abnormalities have been implicated in dumping syndrome [18], during the period in which nutrient-rich chyme reaches the small intestine and causes bowel distention. The influence of vasoactive intestinal peptide (VIP) and serotonin have been studied widely in dumping syndrome. Vasoactive intestinal peptide is a potent vasodilator, regulating smooth muscle activity, epithelial cell secretion, and blood flow in the gastrointestinal tract [19]. Serotonin also may play a role in dilating intestinal blood supply. These physiological factors lead to the rapid fluid shift seen in dumping syndrome and the subsequent systemic sequelae. Higher plasma levels of adrenaline and noradrenaline were also found in early dumping syndrome, which correlates to the increased sympathetic drive [20].

Late dumping syndrome is defined as symptoms that occur 1–3 h postprandially. Glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide (GLP-1) are released as a result of the hyperosmolar chyme that enters the small intestine. These two hormones stimulate insulin secretion from the pancreas due to the high glucose load in the intestine. This rise in insulin causes a reactive hypoglycemia [21] and symptoms of low blood sugar such as diaphoresis and fainting episodes. GLP-1 levels as well as GIP are found to peak around 1 h following ingestion of a meal [22] and correlate with these episodes. In addition to the increased insulin release, GLP-1 also inhibits glucagon, the hormone responsible for increasing the serum glucose levels by mobilizing the stored glucose, compounding the hypoglycemia seen in dumping syndrome.

Dumping syndrome has both surgical and non-surgical causes. Diabetes mellitus has been linked to dumping syndrome, but many other idiopathic cases have been reported. As opposed to gastroparesis, which is characteristically associated with chronic diabetes mellitus, dumping syndrome is often seen in individuals with new onset diabetes mellitus, specifically type II diabetes mellitus, but is not exclusive [23]. Multiple mechanisms for the role of diabetes mellitus have been proposed, including Wallerian degeneration (early vagal nerve damage) and increased contractility or motor activity in the gastric fundus [24]. The resulting motor abnormality of the stomach is one of the leading hypotheses related to diabetes induced dumping syndrome.

An emerging correlation between dumping syndrome and cyclic vomiting syndrome (CVS) has also begun to be established. In one study, nearly three-quarters of individuals with CVS met the criteria for dumping syndrome [25]. A link to autonomic dysfunction can be seen as a result of dumping syndrome occurring during the vomiting-free period of CVS [26].

Dumping syndrome has also been seen as a complication of fundoplication for gastroesophageal reflux disease (GERD) , resulting in accidental vagal nerve injury. Both delayed and rapid gastric emptying have been reported following this procedure [27]. Reduced pyloric relaxation, resulting in decreased gastric accommodation as well as impaired feedback inhibition to slow gastric emptying, can be seen after vagotomy. Functional dyspepsia, or chronic pain of the upper abdomen, has also been correlated with dumping syndrome. Nearly one-third of individuals with the diagnosis also exhibited rapid gastric emptying on gastric scintigraphy [28]. In addition, a small subset of patients who initially presented with symptomatology of abdominal pain and cramping and were diagnosed with irritable bowel syndrome, have a component of dumping syndrome [29].

The surgical treatment of peptic ulcer disease was the primary cause of this syndrome prior to the treatment of H. pylori. The anatomic alterations related to resection or bypass of the pylorus and vagotomy (whether intentional or accidental) altered the innervations of the stomach, resulting in the symptoms of dumping syndrome. It is reported that 15–20% of patients after partial gastrectomy [2] and 6–14% of patients after truncal vagotomy [30] experienced some form of dumping syndrome, but only 10% of these individuals had symptoms severe enough to be diagnosed with dumping syndrome [31]. The most common surgical cause of dumping syndrome in adults today is gastric bypass, with an incidence as high as 75% of patients [32]. In children, Nissen fundoplication for GERD is the leading surgical cause of dumping syndrome [33]. The surgical modifications change the anatomy of the gastrointestinal tract, resulting in rapid transit of chyme from the stomach to the small intestine. The pylorus and antrum function to inhibit gastric emptying. After gastric surgeries such as antrectomies and pyloroplasties, both the gastric remnant and pylorus are disrupted, resulting in the rapid transit of chyme seen in dumping syndrome. In regard to bariatric surgery, Roux-en-Y is the most common cause of surgically induced dumping syndrome [34], but with the newer technique of sleeve gastrectomy, the incidence of dumping syndrome has decreased with regard to this modality [35].

The first-line recommendations for the treatment of DS are related to dietary modifications. Food intake should be divided into smaller and more frequent meals (around six per day), with particular attention in reducing the amount of carbohydrates. Complex carbohydrates (e.g., oatmeal, brown rice, potatoes, pasta, and beans) are preferred and better tolerated over simple sugars (e.g., soda, candies, cookies, and other sweets). Fluid intake during meals should be limited and ideally occur 1 h after ingestions of solids, since liquids tend to accelerate gastric transit. Milk and other dairy products usually exacerbate symptoms and generally should be avoided by individuals with DS. Increasing the overall consumption of proteins, as well as fats, has been shown to decrease symptoms and help make the meal nutritionally complete, despite the limit in carbohydrates. Increasing dietary fiber has also helped treat the reactive hypoglycemia by slowing gastric emptying [36]. Pectins and guar gum have been shown to be an effective dietary additive, especially in children, delaying glucose absorption and prolonging chyme transit time by forming a gel with the carbohydrates [37]. For individuals who have low blood pressure and feel light headed after eating, lying down for 30 min may help, delaying gastric emptying and increasing venous return. If cases of severe DS, malnutrition may occur and dietary intake must be closely monitored and supplemented where needed. Some may need the expertise of a registered dietician to find a dietary plan that suits their specific symptoms. Many individuals improve with these dietary modifications, but other therapies exist in cases of persistent symptoms.

Despite dietary modifications, roughly 3–5% of individuals will continue to have symptoms of severe dumping. This can be frustrating for both the patient and clinician, but several other pharmacological interventions have been found to be of benefit in controlling symptoms, as noted below. As a perceived failure with dietary changes, patients can develop a fear of eating with progressive weight loss. It is important to control these symptoms so as to not persist in a state of malnutrition. Several over-the-counter medications can help with symptoms such as diarrhea (e.g., loperamide), nausea (e.g., promethazine, meclizine), or anti-gas (e.g., simethicone). Tincture of opium has been shown to be helpful in treating diarrhea associated with dumping syndrome [38]. Simple ingestion of a hard candy can relieve the hypoglycemia of late dumping syndrome. The gas and bloating associated with the rapid emptying of chyme into the intestines may be controlled with probiotics. These medications target only the symptoms of dumping syndrome and not the underlying causes.