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Piers R. Boshier, Jeremy R. Huddy, Giovanni Zaninotto, George B. Hanna, Dumping syndrome after esophagectomy: a systematic review of the literature, Diseases of the Esophagus, Volume 30, Issue 1, January 2017, Pages 1–9, https://doi.org/10.1111/dote.12488
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INTRODUCTION
In recent years, a steady improvement in survival after radical surgery for esophageal carcinoma has been observed. Earlier detection, refinements in surgical technique, perioperative management, and adjunctive chemo/radiotherapy regimens1,2 have led to a substantial increase in both overall- and disease-free survival, with 40% of patients alive up to 5 years after radical surgery.3 As survival improves, symptoms unrelated to the original disease become relevant for the patient and impact on his/her quality of life. These symptoms include reflux, early satiety, malabsorption, diarrhea, and postprandial dumping.4,5
While commonly associated with gastrectomy and gastric bypass procedures, dumping syndrome is an intermittently reported and poorly understood complication of esophagectomy. Dumping syndrome may be classified into early and late dumping based on the relationship between the time elapsed following oral intake and the onset of symptoms. Early dumping, which typically occurs within 30 min of ingestion of a meal is characterized by palpitations, abdominal cramps, diarrhea, and nausea. These symptoms are believed to reflect the excessive secretion of gastrointestinal hormones and fluid shifts that accompany the rapid influx of hypertonic gastric chyme into the proximal small bowel. In contrast, late dumping typically occurs within 2–3 h of oral intake and is characterized by symptoms of hypoglycaemia (dizziness, faintness, cold sweats, and hunger). The pathophysiology of postesophagectomy dumping is incompletely understood. Factors believed to contribute to its development are principally related to disruption of gastric anatomy and function, including tubularization and transposition of the stomach into the thorax, reduced gastric capacity, vagotomy and gastric denervation, and disruption of mechanisms that regulate normal gastrointestinal function.6