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1. Dumping syndrome
By solomon(MD,R)

2. • Dumping Syndrome
• Dumping is a phenomenon caused by the destruction or bypass of the pyloric sphincter
• However, other factors undoubtedly play a role because dumping can occur after operations that
preserve the pylorus, such as parietal cell vagotomy
• The appropriate stimulus can provoke dumping symptoms, even in some patients who have not
undergone surgery
• Clinically significant dumping occurs in 5% to 10% of patients after pyloroplasty, pyloromyotomy, or
distal gastrectomy
• The symptoms are thought to be the result of the abrupt delivery of a hyperosmolar load into the small
bowel due to ablation of the pylorus or decreased gastric compliance

3. • Sabiston……. Dumping syndrome can be early (20 to 30 minutes after eating)
or late (2 or 3 hours after a meal)
• Early dumping is more common, with more GI and fewer cardiovascular effects
• GI symptoms------nausea and vomiting, a sense of epigastric fullness, cramping abdominal pain, and
often explosive diarrhea
• The cardiovascular symptoms ---- palpitations, tachycardia, diaphoresis, fainting, dizziness, flushing,
and occasionally blurred vision
• This symptom complex can develop after any operation on the stomach but is more common after partial
gastrectomy with the Billroth II reconstruction
• It is much less commonly observed after the Billroth I gastrectomy or after vagotomy and drainage
procedures

4. • Early dumping occurs because of the rapid passage of food of high osmolarity from the stomach into the small
intestine
• This occurs because gastrectomy, or any interruption of the pyloric sphincteric mechanism, prevents the
stomach from preparing its contents and delivering them to the proximal bowel in the form of small particles
in isotonic solution
• The resultant hypertonic food bolus passes into the small intestine, which induces a rapid shift of extracellular
fluid into the intestinal lumen to achieve isotonicity
• After this shift of extracellular fluid, luminal distention occurs and induces the autonomic responses listed
earlier
• The basic defect of late dumping is also rapid gastric emptying; however, it is related specifcally to
carbohydrates being delivered rapidly into the proximal intestine
• When carbohydrates are delivered to the small intestine, they are quickly absorbed, resulting in
hyperglycemia, which triggers the release of large amounts of insulin to control the increasing blood sugar
level
• An overcompensation results so that profound hypoglycemia occurs in response to the insulin
• This hypoglycemia activates the adrenal gland to release catecholamines, which results in diaphoresis,
tremulousness, light-headedness, tachycardia, and confusion
• The symptom complex is indistinguishable from insulin shock

5. • The symptoms associated with early dumping syndrome appear to be secondary to the release of several
humoral agents, such as serotonin, bradykinin-like substances, neurotensin, and enteroglucagon
• Dietary measures are usually sufficient to treat most patients
• These include
– avoiding foods containing large amounts of sugar,
– frequent feeding of small meals rich in protein and fat, and
– separating liquids from solids during a meal
• In some patients without a response to dietary measures, long acting octreotide agonists have
ameliorated symptoms
• These peptides not only inhibit gastric emptying but also affect small bowel motility so that intestinal
transit of the ingested meal is prolonged
• The side effects associated with administration of these synthetic peptides are relatively benign;
however, the peptides are expensive
• Many operative procedures have been advocated for the surgical treatment of these patients
• The paucity of patients treated for PUD with gastrectomy or vagotomy has made remedial procedures
for dumping exceedingly rare

6. .

7. • Early dumping
• Typically, 15 to 30 minutes after a meal,
• the patient becomes diaphoretic, weak, light-headed, and tachycardic
• These symptoms may be ameliorated by recumbence or saline infusion
• Crampy abdominal pain is not uncommon and diarrhea often follows
• A variety of hormonal aberrations have been observed in early dumping, including increased
VIP, CCK, neurotensin, peripheral hormone peptide YY, renin-angiotensin-aldosterone
• late dumping
• postprandial (reactive) hypoglycemia
• usually occurs later (2–3 hours following a meal), and is relieved by the administration of
sugar
• decreased atrial natriuretic peptide
• Late dumping is associated with hypoglycemia and hyperinsulinemia

8. • The medical therapy for the dumping syndrome consists of dietary management and somatostatin
analogue (octreotide)
• Often, symptoms improve if the patient avoids liquids during meals
• Hyperosmolar liquids (e.g., milk shakes) may be particularly troublesome
• There is some evidence that adding dietary fiber compounds at mealtime may improve the syndrome
• If dietary manipulation fails, the patient is started on octreotide, 100 μg subcutaneously twice daily
• This can be increased up to 500 μg twice daily if necessary
• The long-acting depot octreotide preparation is useful
• Octreotide not only ameliorates the abnormal hormonal pattern seen in patients with dumping
symptoms, but also promotes restoration of a fasting motility pattern in the small intestine (i.e.,
restoration of the MMC)

9. • The α-glucosidase inhibitor acarbose may be particularly helpful in ameliorating the symptoms of late
dumping
• Only a very small percentage of patients with dumping symptoms ultimately require surgery
• Most patients improve with time (months and even years), dietary management, and medication
• Therefore, the surgeon should not rush to reoperate on the patient with dumping symptoms
• Multidisciplinary nonsurgical management must be optimized first

10. • Before reoperation, a period of in hospital observation is useful to define the severity of the patient’s
symptoms, and patient compliance with prescribed dietary and medical therapy
• The results of remedial operation for dumping are variable and unpredictable
• There are a variety of surgical approaches, none of which work consistently well
• Patients with disabling refractory dumping after gastrojejunostomy can be considered for simple
takedown of this anastomosis provided that the pyloric channel is open endoscopically
• The reversed intestinal segment is rarely used today—and rightly so
• This operation interposes a 10-cm reversed segment of intestine between the
stomach and the proximal small bowel
• This slows gastric emptying, but often leads to obstruction, requiring reoperation

11. • Isoperistaltic interposition (Henley loop) has not been successful in ameliorating severe dumping over
the long term
• The Roux-en-Y gastrojejunostomy is associated with delayed gastric emptying,
probably on the basis of disordered motility in the Roux limb
• Taking advantage of this disordered physiology, surgeons have used this operation successfully in the
management of the dumping syndrome
• Although this is probably the procedure of choice in the small group of patients requiring operation for
severe dumping following gastric resection, gastric stasis may result, particularly if a large gastric
remnant is left
• In the presence of significant gastric acid secretion, marginal ulceration is common after both jejunal
interposition and Roux-en-Y procedures; thus concomitant vagotomy and hemigastrectomy should be
considered

12. • The theoretical possibility of treating postpyloroplasty dumping with a Roux-en-Y to the proximal
duodenum (the duodenal switch, a potentially reversible operation) has not yet been reported (Fig. 26-
68)
• Because pyloric ablation seems to be the dominant factor in the etiology of dumping, it is not surprising
that conversion of Billroth II to Billroth I anastomosis has not been successful in the treatment of
dumping

13. Reference
• 1.schwartz 10th ed
• 2.sabiston 20th ed
• 3.mannipal 4th ed

14. Thank you