Dumping syndrome is a common complication following gastric, esophageal, and bariatric surgery. It affects about 20% of patients after vagotomy with pyloroplasty, up to 30% after Roux-en-Y gastric bypass (RYGB), around 15% after sleeve gastrectomy, and as many as 50% after esophagectomy. These procedures alter the anatomy of the stomach and its innervation, causing undigested food to enter the small intestine too rapidly. Dumping syndrome includes symptoms that may appear together or separately, allowing for a classification into early and late dumping syndrome. These symptoms are often debilitating, emotionally distressing, and may lead to weight loss and reduced quality of life. 
 
Typically, symptoms of early dumping syndrome occur within the first hour after a meal and include gastrointestinal symptoms (such as abdominal pain, bloating, nausea, vomiting, and diarrhea) and vasomotor symptoms (such as pallor, palpitations, sweating, tachycardia, hypotension, fatigue, a desire to lie down, and rarely, syncope). The underlying mechanisms involve osmotic effects, autonomic neuronal responses, and the release of peptide hormones, including vasoactive substances (like neurotensin and vasoactive intestinal peptide), incretins (like glucagon-like peptide 1 [GLP1]), YY gastric inhibitory polypeptide, and glucose modulators (such as insulin and glucagon). 
 
The symptoms of late dumping syndrome usually appear between one and three hours after a meal and primarily result from hypoglycemia (nadir <2.8-3.0 mmol/L). This is largely due to an incretin-driven hyperinsulinemic response following carbohydrate intake. Symptoms of hypoglycemia include neuroglycopenic symptoms (such as fatigue, weakness, concentration difficulties, intense hunger, and clouded consciousness) and signs of vagal and sympathetic activation (such as sweating, palpitations, tremors, and irritability). 

There is no specific need for macro- or micronutrients in dumping syndrome. Carbohydrate restriction is discussed in detail in the section 'Practical tips for dietary modification. 

Aims of Nutritional Therapy

• Aims of Nutritional Therapy
• Relieve postprandial discomfort
• Increase energy and protein intake
• Maintain/improve nutritional status and body function
• Prevent malnutrition/nutrient deficiencies

To identify malnourished patients early, a nutritional risk screening should be conducted at least twice a year.

Energy and protein requirements should be met through oral nutrition whenever possible. If less than 75% of requirements are covered, even with fortification, snacks, or sip feeds, supplementary enteral nutrition should be provided within five days. Complementary parenteral nutrition is indicated if less than 75% of requirements are covered by oral and/or enteral nutrition.

 
Oral Nutrition

The first step should be conservative management of dumping syndrome. Adjusting the diet is crucial, and support from a dietician is highly recommended.

Practical Tips for Dietary Modification (Initial Measures)

• Eat at least six times throughout the day.
• Eat slowly and chew thoroughly.
• Limit very salty snacks (chips, salted nuts, French fries, etc.) and sugary foods (sorbet, sweetened drinks, honey, caramel, etc.).
• Avoid meals consisting solely of carbohydrates; always combine carbohydrates with other (ideally all) macronutrients (protein, fat, dietary fiber).
• Carbohydrates, quantity: Limit to ≤30 g CH per meal (adjust as needed based on glucose levels).
• Carbohydrates, quality: Choose high-fiber foods (nutrition label: total carbohydrate-to-fiber ratio ≤5:1). Increase resistant starch (cool starchy foods for 12 hours after heating), select foods with a low glycemic index, and minimize processed carbs (table sugar and white flour).
• If having dessert, consume it 90 minutes after the main meal, ideally as a protein- or fat-rich option. For sweeteners, use small amounts of fructose, erythritol, or non-caloric alternatives.
• Protein/amino acids: Try arginine- or glutamine-rich foods to stimulate glucagon (supplementation possible, e.g., 2.5 g arginine).
• For nocturnal hypoglycemia (substrate deficiency due to malnutrition): Consider taking Glycosade® or Maizena® (starting with 15–20g).
• Consider adding soluble dietary fiber supplements: guar (Digesan®, Optifibre®), pectin. These slow carbohydrate absorption and reduce the release of insulinotropic factors; e.g., take 5-15 g before/with meals.
• Drink about 20 minutes before or after meals, but avoid drinking during meals.
• Limit alcohol and caffeine intake significantly.
• If necessary, lie down for 15–30 minutes after eating or consider eating while lying down.

Enteral Nutrition

In cases with a high risk of dumping syndrome, enteral nutrition (via gastric or jejunal route) should be administered continuously using an enteral feeding pump. Bolus feeding or excessively high infusion rates can exacerbate dumping-like symptoms. As tolerance improves, continuous feeding can be gradually switched to intermittent, slow administration of larger volumes overnight at the highest tolerated infusion rate.

Parenteral Nutrition

With complementary or total parenteral nutrition, severe symptoms of dumping syndrome can be significantly reduced, and with total parenteral nutrition, they may be entirely eliminated.

Diagnostic

A suspicion of dumping syndrome arises from the simultaneous occurrence of multiple suggestive symptoms (see Introduction), particularly in patients who have undergone stomach or esophageal surgery.

It is essential to inquire about trigger foods, such as salty snacks and sugary items like sweetened yogurts, sweets, or sugary drinks.

To confirm the diagnosis, a provocation test based on oral intake of 50 grams of glucose can be conducted. Various bodily responses are measured, with a diagnosis of dumping syndrome confirmed if any of the following criteria are met:

• Heart rate increases by more than ten beats per minute after glucose intake 
• Hematocrit value decreases by more than three percent 
• Hydrogen excretion in the breath increases (indicating early dumping syndrome; sensitivity 100%) 
• After an initial hyperglycemic response, blood glucose drops significantly (hypoglycemia), or typical hypoglycemia symptoms occur (indicating late dumping syndrome). 

Screening

• 10-day continuous glucose monitoring (CGM) with blinded data, alongside a detailed diary of food intake, symptoms, and activities 
• To improve sensor accuracy, calibrate the sensor with capillary measurements, fasting in the morning, at least every 2–3 days during stable euglycemia 
• CGM Evaluation:
• Minimum of 7 days of data, with typical eating patterns and behaviors recorded during monitoring 
  % of sensor glucose in 3–3.9 mmol/L range, % of sensor glucose >10.0 mmol/L, number of hypoglycemic events (<3.0 mmol/L for ≥15 min), nadir glucose, peak glucose, glucose variability (CV), distribution, correlation of hypoglycemia with food intake, symptoms, and activity 
  Differentiation between endogenous and exogenous correction of hypoglycemia 

Confirmation

• Mixed Meal Test for post-bariatric hypoglycemia 
• Assessment:
• Postprandial hypoglycemia (plasma glucose <3.0 mmol/L), symptomatic (autonomic, neuroglycopenic, or other symptoms) vs. asymptomatic 
• Inadequate insulin suppression (insulin >5.0 mU/L when plasma glucose <3.0 mmol/L) 
• Inadequate counter-regulation (glucagon <10.0 pmol/L when plasma glucose <3.0 mmol/L) 
• Rebound effect after hypoglycemia correction 
• Early dumping component (heart rate increase >10 bpm 30 minutes after baseline) 

Monitoring

Correction of postprandial hypoglycemia (gain experience with CGM), caution: standard recommendations for correction in diabetes patients (15-rule) may lead to rebound hypoglycemia: 

• 5 g glucose (about 2 glucose tablets, depending on the product) 
• Optionally, add a protein bar (10 g protein, max. 5 g carbs) or nuts 

Medikamente

Therapy

• First Measure: Dietary modification (see Section 1.3) 
• Second Measure: Pharmacotherapy (off-label use) 
• First Choice: Acarbose 50–100 mg before each meal containing carbohydrates (1–1–1 dosing; also situationally for high-carbohydrate meals)
• May also impact early dumping symptoms 
• Frequent gastrointestinal side effects like flatulence 
• Coverage Approval ("Kostengutsprache") required and supply from Germany 
• Second Choice: Octreotide 25–50 µg subcutaneously before meals. If well tolerated and effective for glycemic response, consider Octreotide LAR (10–20 mg once/month intramuscularly) or low-dose Pasireotide (150 µg).
• Suitable for early dumping as well 
• Common gastrointestinal side effects: steatorrhea, cholelithiasis 
• Caution: Non-specific action; also suppresses glucagon 
• Emerging Options (Not Yet Widely Available):
• Dasiglucagon (stable glucagon analogue): 80 mcg subcutaneously (fixed-dose pen) immediately after peak hypoglycemia; more of a rescue medication than daily therapy 
• Exendin-9-39 (GLP-1 antagonist): 0.025 mg/kg subcutaneously before meal
• Limited Evidence Options:
• Diazoxide 100–150 mg (1–1–1): Directly inhibits insulin; common side effects include edema, nausea, hypotension, and headache (beneficial for cases with high insulin excess, demonstrated by MMTT) 
• Verapamil 120 mg: Inhibits GLUT1-mediated insulin release
• Possibly an indirect effect via reduced intake of “trigger” foods: GLP-1 analogues (liraglutide, semaglutide), but with a lower glucose nadir in the meal test (glucagonostatic effect); no effect on gastric emptying in bariatric surgery patients! 
• GLP-1 Analogues (liraglutide, semaglutide): Potentially reduces intake of “trigger” foods but lowers glucose nadir in meal tests without affecting gastric emptying in bariatric surgery patients 
• SGLT-2 Inhibitors (particularly canagliflozin 300 mg/day, also affects SGLT1 in intestines) 
• Third Measure: If conservative measures do not lead to an improvement in symptoms, surgical corrective procedures can be evaluated (surgical restraint with RYGB)
• Emergency Measure for Severe Hypoglycemia: gastrostomy (↓incretins, ↓insulin) 
• So far no evidence (objectified reduction of hypoglycemia): restoration of possibly missing restriction, most likely indirect effect due to reduced meal intake (transient) 
• Laparoscopic pouch revision (reduces proximal gastric pouch size) 
• Endoscopic constriction of gastrojejunal anastomosis (e.g., Apollo Endosurgery) 
• RYGB (Roux-en-Y Gastric Bypass) reversal 
• Distal pancreatectomy (limited evidence, as Nesidioblastosis, the underlying cause, is rare in post-bariatric hypoglycemia and more often a separate disease entity)

Special Considerations

Continuous Glucose Monitoring (CGM) Therapy

• Enhance understanding of the effects of food choices and physical activity on blood glucose (BG) and symptoms 
• Optimizes hypoglycemia correction, especially for asymptomatic cases 
• Recommended for higher-risk situations (e.g., driving, pregnancy) 
  For improved sensor accuracy, conduct capillary calibration on an empty stomach every 2–3 days during stable euglycemia 
• Use capillary checks to verify sensor accuracy at BG levels <3.9 mmol/L, as sensors may be less accurate at lower BG levels 
• Note: Coverage Approval required