Early and Late Dumping Syndromes

Dumping syndrome comprises symptoms of nausea, abdominal pain, palpitations, and light-headedness after eating. Dumping syndrome may have an early or late manifestation. Unlike late dumping, which is mostly incretin-driven, early dumping is related to the physical attributes of a meal but may also stimulate the secretion of vasoactive gastrointestinal hormones. Early dumping occurs within 1 h of a meal, when hyperosmolar nutrients such as carbohydrates and fats arrive directly into the jejunum. This causes fluid shifts into the intestinal lumen to dilute the food load, shifts that can cause hypotension, palpitations, light-headedness, and a feeling of impending collapse. Dilation of the intestinal lumen causes nausea, abdominal pain, distension, and diarrhea. Unlike early dumping, late dumping or neuroglycopenia (hyperinsulinemic hypoglycemia) may be seen years after surgery and is generally seen later after a meal. Gastrointestinal manifestations are much less prominent than adrenergic symptoms such as agitation, anxiety, sweating, tremors, tachycardia, and palpitations. Those symptoms specifically thought of as “neuroglycopenic” include confusion, fatigue, memory loss, speech problems, weakness, light-headedness, dizziness, blurry vision, ataxia, personality changes, confusion, seizures, and loss of consciousness. If untreated, neuroglycopenia can progress to coma and death. Both early and late dumping respond to dietary modification, with higher-protein meals. Pharmacologic agents may also be helpful. The last resorts are a variety of surgical approaches including enteral feeding through the bypassed stomach, stomal reduction to slow the passage of food, and finally bypass reversal. The latter carries a higher risk of complications, weight regain, and recurrent comorbidities.