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Postgastrectomy Syndromes
Nonmalignant Gastrointestinal Disease
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Postgastrectomy Syndromes E. R. Woodward, M.D.,* and Michael P. Hocking, M.D.t
Operative procedures designed for the control of peptic ulcer disease can result in new iatrogenic disorders. These most discouraging complications of surgery for benign disease are collectively referred to as "the postgastrectomy syndromes." Although a large number of disorders have been delineated, two distinct entities account for the vast majority; these are the dumping syndrome and alkaline reflux gastritis. A third problem, the Roux-en-Y syndrome, results largely from secondary treatment efforts in postgastrectomy patients. By far the most important factor in the pathogenesis of all postgastrectomy disorders is ablation or bypass of the pyloric sphincter.
THE DUMPING SYNDROMES There are two types of dumping: the early postprandial and the delayed or hypoglycemic. Although the two may coexist, the early type is far more common. The clinical syndrome was first reported in 1913, by Hertz, who correlated the symptoms with rapid drainage of the stomach on bismuth contrast radiography. 14 The term "dumping" was coined by Mix in 1922, referring to the x-ray findings. 26
EARLY POSTPRANDIAL DUMPING History Symptoms usually begin in the early postoperative period with resumption of oral intake. They occur during or soon after eating, often while the patient is still at the table. Vasomotor and cardiovascular symptoms usually predominate, sometimes to the complete exclusion of gastrointestinal symptoms. The patient notes the rather rapid onset
* Professor, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida
t Assistant Professor, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida
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of weakness, faintness, and dizziness and will have an immediate urgent desire to adopt a reclining position. The patient breaks out in a cold sweat and is conscious of the heart pounding. At the same time, he or she may note a feeling of fullness in the epigastrium and a sense of churning in the mid-abdomen. The patient rarely feels nauseated, and vomiting is unusual. In some patients these symptoms are followed by a series of wavelike intestinal cramps culminating in explosive diarrhea. Many patients note particular foods that precipitate an attack; high carbohydrate liquids are most often named. The thought of ingesting a milkshake often causes mental distress! Breakfast, with its high carbohydrate intake, is often associated with the most severe attacks. There is a close parallel between the severity of the dumping syndrome and the degree of weight loss and malnutrition. There is an unconscious restriction of food intake to avoid the dumping attacks. Patients literally feel better when they do not eat, which can lead to rapid and severe weight loss. Incidence The dumping syndrome occurs with exceedingly high frequency after gastric resection. We found that two thirds of 343 patients had dumping symptoms and that the disturbance persisted over 2 years in 20 per cent. 12 The incidence seems to vary directly with the amount of stomach resected and may occur less frequently after the Billroth I type of reconstruction. The syndrome seems to be less frequent after vagotomy and a drainage operation, particularly pyloroplasty. We observed clinically significant dumping in 14 per cent of 443 cases. 9 Seven years later the incidence had dropped to 4 per cent, indicating a spontaneous tendency toward recovery.27 It appears that preservation of storage function may playa role, albeit a secondary one. Pathogenesis Absence, disruption, or bypass of the pylorus permits rapid, continuous, and uncontrolled emptying of the stomach into the intestine. Rapid gastric emptying alone does not produce the dumping syndrome since radiologic determination reveals that emptying may be just as rapid in asymptomatic patients. The crux of the problem is the high carbohydrate content of the meal. This was well demonstrated in the classic study reported by Machella. 22 He passed a tube into the jejunum of normal volunteers and infused 50 per cent glucose directly into the intestine. Severe symptoms developed within 5 minutes. At the same time there was an increase in pulse rate and an elevation of blood pressure with widening of the pulse pressure. Roberts and coworkers studied 21 postgastrectomy patients using the same hypertonic glucose challenge. 3o The plasma volume measured by the Evans blue method was reduced by 400 to 800 ml. They postulated that intravascular fluid was rapidly attracted into the jejunal lumen because of the hyperosmolarity of intestinal content. In 1961 Johnson and J esseph produced evidence that there might
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be a humoral factor involved in the early postprandial dumping syndrome. 18 They pointed out that the subjective symptoms begin before changes can be measured in the plasma volume. They postulated that hyperosmolar materials caused release of a substance from the small intestinal mucosa passing through the circulation to produce symptoms. Because of the high concentration of enterochromaffin cells in the duodenum and proximal jejunum, these investigators proposed that the humoral agent might be serotonin. They pointed out the similarity between dumping and the carcinoid syndrome. Drapanas and associates measured serotonin in the portal and systemic blood of dogs after instillation of hypertonic glucose into the upper small intestine. 8 There was a 50 per cent increase in portal blood serotonin levels. Silver and colleagues, however, found that peripheral blood serotonin was not increased following a glucose challenge in patients with the dumping syndrome. 34 Zeitlin and Smith reported release into the circulation of a bradykininlike polypeptide in patients with dumping. 42 MacDonald and coworkers confirmed in the experimental animal the presence of bradykinin in the circulation. 21 It seems probable that a number of vasoactive polypeptides play a role in the dumping syndrome. Blackburn and associates found that plasma neurotensin increases sharply during a dumping attack. 2 Sagor and coworkers found that vasoactive intestinal peptide (VIP) also increased during dumping. 31 Sirinek and colleagues found that neurotensin increases in some dumping patients whereas VIP increases in others, suggesting that there may be two types of dumping. 35 Adrian and coworkers found also that plasma peptide YY increases in dumping attacks. 1 The possibility that inhibition of intestinal secretion might control dumping was suggested by Reasbeck and Van Rij. They found that somatostatin, with its profound inhibition of intestinal secretion, tended to control dumping, particularly the intestinal manifestations. 29 Prevention and Treatment The early postprandial dumping syndrome can be prevented or at least reduced in incidence and severity by proper selection of the operative procedure for the individual patient. Parietal cell vagotomy should be utilized whenever this is a reasonable approach for the patient with a duodenal ulcer diathesis. The vagally innervated pyloric sphincter mechanism is preserved. As a consequence, dumping is exceedingly rare. Vagotomy and pyloroplasty have a lower incidence of dumping than vagotomy and antrectomy and should be utilized when this procedure has a reasonable likelihood of being adequate. Moreover, in patients in whom the pyloric sphincter has been either divided, bypassed, or resected as a part of the operative procedure, the dumping symptoms can usually be prevented by proper postoperative dietary management. This is begun during the in-hospital postoperative period and continued following hospital discharge. It is our experience in this regard that a dietitian is of inestimable
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assistance to the surgeon because the dietitian can provide detailed menus. The treatment of the dumping syndrome is largely, in fact almost exclusively, dietary. The empiric observation that carbohydrates, particularly liquid sugars, precipitate an attack has been amply supported. The basis of dietary treatment is, therefore, a low carbohydrate diet. Liquid foods or solid foods flushed through the gastric remnant with liquids provide the basic components for the precipitation of dumping. Therefore, we utilize what we refer to in the vernacular as "the dry diet routine." This requires repeated detailed explanation to the patients. It is hard for them to grasp that breakfast can be eaten without two cups of coffee and without being prefaced by orange juice. The patient should take only the solid part of the meal at breakfast and 112 to 1 hour later take whatever (sugar-free) liquids are desired. Most patients respond favorably to such a program, not only with relief of their subjective symptoms, but also with obvious improvement in their nutritional status as measured by weight gain. In addition to diet, certain gel-forming carbohydrates can be used to modify glucose absorption. Jenkins and colleagues found that the addition of 14.5 gm pectin to a 50 gm oral glucose load prevented hypoglycemic symptoms in dumping patientsY This has been confirmed by Leeds and coworkers.20 Harju and Larmi reported that a similar substance, guar gum, also obviates the effect of a glucose challenge. l l We have found that the addition of a small dose of ephedrine sulfate (4 ml ephedrine elixir containing 11.5 mg) seems to potentiate the therapeutic value of pectin. 24 Surgical Treatment A small number of patients become permanent gastric cripples as a result of the early postprandial dumping syndrome refractory to medical therapy. These patients should be considered candidates for surgical revision. In patients with a Billroth II gastrectomy, conversion to a Billroth I reconstruction is frequently followed by improvement. We found that 5 of 11 patients became completely asymptomatic and 3 others clearly improved. 40 Jejunal pouches interposed between the gastric remnant and duodenum have been less satisfactory, with only three of nine cases showing persistent improvement. 41 Symptoms of prolonged retention often associated with bezoar formation have been frequent complications. On the basis of the work of Hammer and associates, reversed jejunal segments have been interposed between the gastric remnant and duodenum. lO Although this procedure was initially successful in controlling dumping symptoms, 13 later development of alkaline reflux gastritis has been a frequent occurrence. During the 1970s we used Roux-en-Y duodenal diversion for patients who had both alkaline reflux gastritis and the early postprandial dumping syndrome. We had not expected the dumping symptoms to improve and had advised the patients accordingly. Much to our surprise, all patients reported their dumping symptoms to be markedly
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improved. This unanticipated effect of the Roux-en- Y procedure will be discussed later. In any event, we treated 15 patients with medically intractable dumping using Roux-en- Y diversion with uniform success. 25 We continue to find this the treatment of choice in patients with medically intractable dumping. We have seen several patients who are converted from too rapid emptying of the stomach to too slow. Symptoms of dumping are replaced by symptoms of gastric retention. To date we have been unable to determine preoperatively when this might be a hazard, and we find that sluggish emptying often responds to bethanechol stimulation. Therefore, we consider the Roux-en- Y procedure to be the method of choice in patients with medically intractable early postprandial dumping syndrome.
LATE OR HYPOGLYCEMIC DUMPING
The late postprandial or hypoglycemic dumping syndrome is much less common than the immediate variety. Symptoms appear from 1 to 3 hours after a meal. They are similar to those of the early type except for the absence of gastrointestinal symptoms. The syndrome depends on the absence of an effective pyloric sphincter for its pathogenesis. Rapid emptying of soluble carbohydrate into the intestine causes a more rapid rise in postprandial serum glucose, which also reaches higher levels than usual. Hyperosmolar material in the upper intestine causes excessive release of enteroglucagon. 32 This substance sensitizes the beta cells of the pancreatic islets to release excessive amounts of insulin. 33 Therefore, the postprandial hyperglycemia is overcorrected and is followed by hypoglycemia. Unlike the early postprandial type, symptoms are relieved by the ingestion of liquids containing sugar. Prevention and treatment of the late postprandial dumping syndrome is the same as that of the early or immediate variety. After a period of several months on a low carbohydrate diet, the small bowel mucosa ceases to release excessive enteroglucagon. Patients note that they can tolerate larger and larger amounts of carbohydrate in their diet without developing symptoms. Response to medical therapy is so successful that medical intractability is extremely rare and revisional surgery almost never necessary.
ALKALINE REFLUX GASTRITIS For many years it was generally considered that all patients with epigastric pain and chronic bilious vomiting after gastrectomy or gastroenterostomy had chronic afferent loop syndrome with intermittent afferent loop obstruction. However, reoperation in many of these patients revealed no evidence for a mechanical problem. It also became apparent that the syndrome appeared in patients without an afferent
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loop, that is, Billroth I gastrectomy or pyloroplasty. It was then realized that there is usually a striking difference in the patients' history as well. With the relatively uncommon afferent loop syndrome, pain is immediately postprandial, causes cramping, and is associated with projectile vomiting that completely relieves the pain, and the vomitus contains no food debris. It is now understood that afferent loop obstruction is a very uncommon syndrome. In the more common patient with alkaline reflux gastritis, the epigastric pain is more likely to be burning, is much less closely related to meal taking, and is often not relieved completely by vomiting, and the vomitus often contains some admixture of food debris. Pathogenesis As with the dumping syndrome, the fundamental defect is ablation, destruction, or bypass of the pyloric sphincter. In addition to regulation of gastric emptying, this structure also regulates reflux from the duodenum into the stomach. The uncontrolled reflux of duodenal fluid produces gastritis, with the associated pain and bilious vomiting. Which constituent of duodenal fluid causes gastric mucosal injury? This fascinating question remains unanswered to date. Are two or even several constituents necessary to produce the pathologic result? The use of the term "alkaline" is a confession of ignorance since the mild alkalinity of duodenal fluid resulting largely from pancreatic bicarbonate is certainly nontoxic to any gastrointestinal mucosa. There is a vast array of data from experimental laboratories that is often confusing and even contradictory. Some of these discrepancies may be due to species variations. Since bile acids are the most toxic material present in duodenal fluid, much attention has been directed to them. In the clinical setting, however, binding of bile acid with cholestyramine does not afford either symptomatic relief or objective endoscopic improvement. On the other hand, bile acids are known to break the barrier of the gastric mucosa, permitting back diffusion of hydrogen ions, which suggests that this could be the mechanism of injury. However, chronic diversion of bile directly into the stomach of both the dog and the pig have failed to reproduce the injury.39 Lawson was able to reproduce the lesion in the dog by diversion of both pancreatic juice and bile into the stomach. 19 It is possible that pancreatic enzymes associated with bile acids, particularly trypsin, result in gastritis. Diagnosis and Pathology In patients with epigastric pain and bilious vomiting, the diagnosis of alkaline reflux gastritis is confirmed by fiberoptic endoscopy and gastric mucosal biopsy. The body of the stomach is more or less diffusely involved. The mucosa appears erythematous and friable and bleeds readily on contact with the tip of the endoscope. Frequent suctioning is usually needed because of the continuous regurgitation of heavily bile-stained duodenal fluid. There are interspersed areas
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of atrophy with abnormal visibility of the submucosal blood vessels. In addition, superficial erosions are often seen, particularly along the lesser curvature. Histologic examination of the gastric mucosa shows three characteristic changes. First, there is complete absence of parietal cells. Second, there is an accumulation of chronic inflammatory cells in the submucosa. Third, the gastric glands are markedly distorted, dilated, and elongated, giving a corkscrew appearance. The mucosa is frequently superficially ulcerated and in other areas atrophic. The lesion may progress to intestinal metaplasia with the appearance of small intestinal villi and sometimes Paneth cells. Unfortunately, the severity of clinical symptoms and the severity of the pathologic lesion often correlate poorly in both directions. Moreover, mucosal abnormalities are often seen in asymptomatic postoperative patients who undergo endoscopy for some other reason. Treatment No medical treatment provides relief in patients with alkaline reflux gastritis. A patient with clinically significant symptoms who desires relief should be offered revisional surgery. We initially utilized an isoperistaltic segment of jejunum interposed between the gastric remnant and duodenum, the so-called Henle loop.5 It was thought that this would provide a peristaltic valve that inhibited duodenogastric reflux and at the same time restored normal gastrointestinal continuity. Unfortunately, of 10 patients undergoing this procedure, only 4 have had enduring satisfactory results. We have since used Roux-en-Y duodenal diversion for the treatment of the syndrome of alkaline reflux gastritis. In 1976 we reported 24 cases with favorable outcome. 4 We have continued to use this procedure as the treatment of choice for this disorder. Clinical recovery is usually dramatic. Frequently the patient notes the absence of the pre-existing chronic epigastric distress even during the period of maximum wound pain. The patient can ingest solid food within a few days, and notices no discomfort and a complete absence of vomiting. Fiberoptic endoscopy was performed in the first 24 patients 3 to 4 months postoperatively. All showed marked improvement in the gross endoscopic picture. Biopsies demonstrated improvement in 22 of the 24 patients, and 17 of the biopsies were reported to be histologically normal. Parietal cells return with recovery of the gastric mucosa and the gastric remnant recovers the capacity to secrete hydrochloric acid. Since the Roux-en-Y procedure is potentially ulcerogenic, it is important that complete vagotomy be present in all patients to prevent marginal ulceration.
THE ROUX-EN-Y SYNDROME In 1975 Davidson and Hersh suggested that delayed gastric emptying might playa role in the pathogenesis of alkaline reflux gastritis. 6
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They later reported that patients with evidence of delayed gastric emptying preoperatively did not fare well after Roux-en-Y doudenal diversion. 7 Boren and Way reported a high incidence of delayed gastric emptying following Raux diversion for alkaline reflux gastritis. 3 In a more recent study, Pellegrini and coworkers found no single pattern of gastric emptying in patients with alkaline reflux gastritis. 28 They reported that Roux-en-Y diversion resulted in delayed gastric emptying in 45 per cent of their patients, half of whom developed gastric bezoars after surgery. In 1980 a retrospective study was conducted on 97 patients who had undergone Roux-en-Y duodenal diversion for alkaline reflux gastritis at the University of Florida. 37 Follow-up was obtained by telephone interview or clinic visit with additional examinations as indicated. Pre-existing signs or symptoms of gastric stasis were present in 35 per cent of these patients. Gastric emptying was not routinely studied preoperatively, however. Postoperatively, all patients experienced dramatic relief from their epigastric pain. However, 50 (52 per cent) of these patients had moderate to severe symptoms of delayed gastric emptying. The symptoms consisted of postprandial fullness, "gas bloating," and even painful abdominal distention relieved by vomiting. Many of these patients avoided solid foods and exist on a nearly all-liquid diet. Despite these new symptoms, however, half of these 50 patients still consider themselves improved, mainly because of the relief of their previous epigastric pain. Barium upper gastrointestinal x-ray studies of these patients were frequently normal because this test does not reliably evaluate gastric emptying of solids. Endoscopy revealed no evidence of mechanical obstruction. In the latter part of the series we found radionuclide evaluation of gastric emptying of solids to be quite useful, utilizing a poached egg white method incorporating technetium-99m sulfur colloid. 23 Research Data On the basis of our clinical evaluation, an animal model was developed to study this problem further. 15 Vagotomy with antrectomy was performed with reconstruction as either a Roux-en-Y or a standard Billroth II gastrojejunostomy. Gastric emptying was studied by washing out the residue of a meal through a large bore gastric cannula. Gastric emptying of liquids and solids was delayed in the Roux-enY animals compared with the Billroth II group. In a more recent study, we assessed gastric emptying with the radionuclide poached egg white technique, which allowed continuous monitoring of gastric emptying with the gamma camera. 38 Gastric emptying was assessed in control animals with vagal innervation intact. Roux-en-Y diversion without vagotomy resulted in more rapid gastric emptying of the test meal. The addition of truncal vagotomy led to delayed gastric emptying in 25 per cent of Roux-en-Y animals. It appears clear, therefore, that the Roux-en-Y syndrome is dependent on vagal denervation of the gastric remnant. This observation was confirmed in the dog by
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pharmacologic replacement of the vagus nerve. Both parenteral and oral administration of bethanechol markedly improved gastric retention in vagotomized Roux-en-Y animals. 16 Interestingly, metoclopramide had no effect on delayed gastric emptying in this model. These findings have been utilized in the clinic for patients with symptoms of delayed gastric emptying after the Roux-en-Y procedure. Approximately half of such patients have responded clinically to bethanechol administration, and a similar improvement in gastric emptying is observed using the technetium-99m-Iabeled test meal. Clinical Experience In the experimental model, delayed gastric emptying after the Roux-en-Y procedure can be markedly lessened by subtotal gastrectomy.15 This finding in the animal has also been applied to the patient with medically intractable symptoms of delayed gastric emptying after the Roux-en-Y procedure. Although a substantial number of the patients have improved after this further operative procedure, in several unimproved patients it has been necessary to proceed with total gastrectomy to provide relief. For the past 5 years we have studied gastric emptying in all patients with alkaline reflux gastritis who are candidates for Roux-en-Y duodenal diversion. 36 In patients in whom there is a pre-existing delay in gastric emptying, subtotal gastrectomy has been performed at the time of the Roux-en-Y procedure. This has been successful in limiting postoperative symptoms of gastric retention. However, in patients with normal gastric emptying, and even in patients with the dumping syndrome as well as alkaline gastritis, Rouxen-Y duodenal diversion without extensive gastrectomy has been associated with a high incidence of postoperative gastric retention. At this time we cannot find any clinically useful method to determine which patient will have postoperative difficulties with gastric emptying. It is our current policy, therefore, to perform subtotal gastrectomy as a routine procedure in conjunction with Roux-en-Y duodenal diversion for alkaline reflux gastritis. SUMMARY Operations on the stomach for benign peptic ulcer frequently result in a variety of symptoms collectively referred to as "the postgastrectomy syndromes." These iatrogenic disorders are numerous and varied, but the vast majority fall into two categories: the postprandial dumping syndrome and alkaline reflux gastritis. Both disorders result from ablation or bypass of the pyloric sphincter. The early postprandial dumping syndrome results from hyperosmolar food rapidly reaching the mucosa of the small intestine. This causes, release of a variety of vasoactive materials. Severe peripheral vasodilatation is accompanied by stimulation of intestinal motility. The patient usually has a mixture of vasomotor symptoms along with abdominal cramping and diarrhea.
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Dumping can be prevented by preserving the innervated pylorus when possible and by proper postoperative dietary instructions. Treatment is largely dietary, consisting of a low carbohydrate, sugar-free diet with the liquid part of the meal separated from solids. Medicinal treatment with pectin and ephedrine is sometimes helpful. Intractable patients can be treated best by revisional surgery, with Roux-en-Y duodenal diversion providing the best results. The delayed or hypoglycemic form of the dumping syndrome is less common and is due to excessive release of insulin in response to postprandial hyperglycemia and release of enteroglucagon from the upper small intestine. Dietary treatment with a low carbohydrate intake is usually successful. Destruction of the pylorus permits unrestrained reflux of duodenal content into the stomach. This produces gastritis in some patients, with epigastric pain and intractable bilious vomiting. Multiple substances present in bile and pancreatic juice are probably necessary for creation of the lesion. The disorder is prevented only by preservation of the pylorus. Treatment is exclusively surgical. The procedure of choice is Rouxen-Y duodenal diversion, which provides immediate relief of symptoms. However, a substantial number of these patients will later have symptomatic gastric retention. The Roux-en-Y syndrome often follows use of this procedure in the treatment of alkaline reflux gastritis. This problem is present only in the absence of vagal innervation. The mechanisms involved are unclear at this time. Studies in the dog have indicated that subtotal gastrectomy usually minimizes the defect, and this principle has proved moderately satisfactory in the patient. Animal studies also indicated that bethanechol is useful for the medical treatment of gastric retention after the Roux-en-Y procedure. This has also been successfully applied to patients. The disorder is particularly frequent and severe in patients who have delayed gastric emptying along with alkaline reflux gastritis. However, preoperative testing of gastric emptying has not been helpful in patient selection, and we propose that subtotal gastrectomy should usually be performed as a part of Rouxen-Y duodenal diversion for alkaline reflux gastritis.
REFERENCES 1. Adrian TE, Long RG, Fuessl HS: Plasma peptide YY (PYY) in dumping syndrome. Dig Dis Sci 30:1145-1148, 1985 2. Blackburn AM, Christofides ND, Ghatei MA, et al: Elevation of plasma neurotensin in the dumping syndrome. Clin Sci 59:237-243, 1980 3. Boren CH, Way LW: Alkaline reflux gastritis: A reevaluation. Am J Surg 140:4046, 1980 4. Bushkin FL, Wickbom G, Woodward ER: Use of Roux-en-Y diversion of duodenal secretions in the treatment ofreflux gastritis. South Med J 69:132-137, 1976 5. Bushkin FL, Woodward ER: Postgastrectomy Syndromes, xx. Philadelphia, WB Saunders, 1976, p 56 6. Davidson ED, Hersh T: Bile reflux gastritis. Am J Surg 130:514-518, 1975
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7. Davidson ED, Hersh T: The surgical treatment of bile reflux gastritis. Ann Surg 192:175-178,1980 8. Drapanas T, McDonald JC, Stewart JD: Serotonin release following instillation of hypertonic glucose into the proximal intestine. Ann Surg 156:528-536, 1962 9. Eisenberg MM, Woodward ER, Carson TJ: Vagotomy and drainage procedure for duodenal ulcer: The results often years' experience. Ann Surg 170:785-792,1969 10. Hammer JM, Seay PH, Johnston RL, et al: The effect of antiperistaltic bowel segments on intestinal emptying time. Arch Surg 79:537-541, 1959 11. Harju E, Lanni TKI: Efficacy of guar gum in preventing the dumping syndrome. JPEN 7:470-472, 1983 12. Hastings N, Halsted JA, Woodward ER, et al: Subtotal gastric resection for benign peptic ulcer. Arch Surg 76:74-80, 1958 13. Herrington JL Jr: Remedial operations for post-gastrectomy syndromes. In Current Problems in Surgery. Chicago, Year Book Medical Publishers, 1970 14. Hertz AF: The cause and treatment of certain unfavorable aftereffects of gastroenterostomy. Ann Surg 58:466-472, 1913 15. Hocking MP, Vogel SB, Falasca CA, et al: Delayed gastric emptying of liquids and solids following Roux-en-Y biliary diversion. Ann Surg 194:494-501, 1981 16. Hocking MP, Vogel SB, Webb S, et al: Medical therapy of delayed gastric emptying after Roux-en-Y gastrojejunostomy. Surg Forum 33:124-126, 1982 17. Jenkins DJA, Gassull MA, Leeds AR, et al: Effect of dietary fiber on complications of gastric surgery: Prevention of postprandial hypoglycemia by pectin. Gastroenterology 72:215-217, 1977 18. Johnson LP, J esseph JE: Evidence for a humoral etiology of the dumping syndrome. Surg Forum 12:316-317, 1961 19. Lawson HH: Effect of duodenal contents on the gastric mucosa under experimental conditions. Lancet 1:469-472, 1964 20. Leeds AR, Ebied F, Ralphs DNL, et al: Pectin in the dumping syndrome: Reduction of symptoms and plasma volume changes. Lancet 16:1075-1078,1981 21. MacDonald JM, Webster MM Jr, Tennyson CH, et al: Serotonin and bradykinin in the dumping syndrome. Am J Surg 117:204-213,1969 22. Machella TE: The mechanism of postgastrectomy dumping syndrome. Ann Surg 130:145-159, 1949 23. Martin JL, Beck WJ, McDonald AP, et al: 99m Tc-labeled solid-phase meal: A quantitative clinical measurement of human gastric emptying. J Clin Gastroenterol 5:315-319, 1983 24. Mathias JR, Woodward ER: Unpublished data 25. Miranda R, Steffes BC, O'Leary JP, et al: Surgical treatment of the postgastrectomy dumping syndrome. Am J Surg 139:40-43, 1980 26. Mix CL: Dumping following gastrojejunostomy. Surg Clin North Am 2:617-622, 1922 27. O'Leary JP, Woodward ER, Hollenbeck JI, et al: Vagotomy and drainage procedure for duodenal ulcer: The results of seventeen years' experience. Ann Surg 183:613-618, 1976 28. Pellegrini CA, Patti MG, Lewin M, et al: Alkaline reflux gastritis and the effect of biliary diversion on gastric emptying of solid food. Am J Surg 150:166-171, 1985 29. Reasbeck PG, Van Rij AM: The effect of somatostatin on dumping after gastric surgery: A preliminary report. Surgery 99:462-468, 1986 30. Roberts KE, Randall HT, Farr HW, et al: Cardiovascular blood volume alterations resulting from intrajejunal administration of hypertonic solutions to gastrectomized patients: The relationship of these changes to the dumping syndrome. Ann Surg 140:631-640, 1954 31. Sagor GR, Bryant MG, Ghatei MA, et al: Release of vasoactive intestinal peptide in the dumping syndrome. Br Med J 282:507-510, 1981 32. Samols E, Tyler J, Marri G, et al: Stimulation of glucagon secretion by oral glucose. Lancet 2: 1257-1259, 1965 33. Shultz KT, Neelon FA, Nilson LB, et al: Mechanism of postgastrectomy hypoglycemia. Arch Intern Med 128:240-246, 1971 34. Silver D, McGregor FH Jr, Porter JM, et al: The mechanism of the dumping syndrome. Surg Clin North Am 46:425-439, 1966
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35. Sirinek KR, O'Dorisio TM, Howe B, et al: Neurotensin, vasoactive intestinal peptide, and Roux-en-Y gastrojejunostomy: Their role in the dumping syndrome. Arch Surg 120:605-609, 1985 36. Vogel SB, Hocking MP, Woodward ER: Radionuclide evaluation of gastric emptying in patients undergoing Roux-Y biliary diversion for alkaline reflux gastritis and po~tgastrectomy dumping. Surg Forum 34:173-175,1983 37. Vogel SB, Hocking MP, Woodward ER: Unpublished data 38. Vogel SB, Vair DB, Woodward ER: Alterations in gastrointestinal emptying of99mtechnetium-labeled solids following sequential antrectomy, truncal vagotomy and Roux-Y gastroenterostomy. Ann Surg 198:506-515, 1983 39. Wickbom G, Bushkin FL, Linares C: On the corrosive properties of bile and pancreatic juice on various living tissues in dogs. Arch Surg 108:680-684, 1974 40. Woodward ER, Desser PL, Gasster M: Surgical treatment of the postgastrectomy dumping syndrome. West J Surg Obstet Gynecol 63:567-573, 1955 41. Woodward ER, Hastings N: Surgical treatment of the postgastrectomy dumping syndrome. Surg Gynecol Obstet 3:429-437, 1960 42. Zeitlin IJ, Smith AN: 5-Hydroxinoles and kjpins in the carcinoid and dumping syndrome. Lancet 2:986-991, 1966 Box J-286, JHMHC University of Florida College of Medicine Gainesville, Florida 32610
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Postgastrectomy Syndromes E. R. Woodward, M.D.,* and Michael P. Hocking, M.D.t
Operative procedures designed for the control of peptic ulcer disease can result in new iatrogenic disorders. These most discouraging complications of surgery for benign disease are collectively referred to as "the postgastrectomy syndromes." Although a large number of disorders have been delineated, two distinct entities account for the vast majority; these are the dumping syndrome and alkaline reflux gastritis. A third problem, the Roux-en-Y syndrome, results largely from secondary treatment efforts in postgastrectomy patients. By far the most important factor in the pathogenesis of all postgastrectomy disorders is ablation or bypass of the pyloric sphincter.
THE DUMPING SYNDROMES There are two types of dumping: the early postprandial and the delayed or hypoglycemic. Although the two may coexist, the early type is far more common. The clinical syndrome was first reported in 1913, by Hertz, who correlated the symptoms with rapid drainage of the stomach on bismuth contrast radiography. 14 The term "dumping" was coined by Mix in 1922, referring to the x-ray findings. 26
EARLY POSTPRANDIAL DUMPING History Symptoms usually begin in the early postoperative period with resumption of oral intake. They occur during or soon after eating, often while the patient is still at the table. Vasomotor and cardiovascular symptoms usually predominate, sometimes to the complete exclusion of gastrointestinal symptoms. The patient notes the rather rapid onset
* Professor, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida
t Assistant Professor, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida
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of weakness, faintness, and dizziness and will have an immediate urgent desire to adopt a reclining position. The patient breaks out in a cold sweat and is conscious of the heart pounding. At the same time, he or she may note a feeling of fullness in the epigastrium and a sense of churning in the mid-abdomen. The patient rarely feels nauseated, and vomiting is unusual. In some patients these symptoms are followed by a series of wavelike intestinal cramps culminating in explosive diarrhea. Many patients note particular foods that precipitate an attack; high carbohydrate liquids are most often named. The thought of ingesting a milkshake often causes mental distress! Breakfast, with its high carbohydrate intake, is often associated with the most severe attacks. There is a close parallel between the severity of the dumping syndrome and the degree of weight loss and malnutrition. There is an unconscious restriction of food intake to avoid the dumping attacks. Patients literally feel better when they do not eat, which can lead to rapid and severe weight loss. Incidence The dumping syndrome occurs with exceedingly high frequency after gastric resection. We found that two thirds of 343 patients had dumping symptoms and that the disturbance persisted over 2 years in 20 per cent. 12 The incidence seems to vary directly with the amount of stomach resected and may occur less frequently after the Billroth I type of reconstruction. The syndrome seems to be less frequent after vagotomy and a drainage operation, particularly pyloroplasty. We observed clinically significant dumping in 14 per cent of 443 cases. 9 Seven years later the incidence had dropped to 4 per cent, indicating a spontaneous tendency toward recovery.27 It appears that preservation of storage function may playa role, albeit a secondary one. Pathogenesis Absence, disruption, or bypass of the pylorus permits rapid, continuous, and uncontrolled emptying of the stomach into the intestine. Rapid gastric emptying alone does not produce the dumping syndrome since radiologic determination reveals that emptying may be just as rapid in asymptomatic patients. The crux of the problem is the high carbohydrate content of the meal. This was well demonstrated in the classic study reported by Machella. 22 He passed a tube into the jejunum of normal volunteers and infused 50 per cent glucose directly into the intestine. Severe symptoms developed within 5 minutes. At the same time there was an increase in pulse rate and an elevation of blood pressure with widening of the pulse pressure. Roberts and coworkers studied 21 postgastrectomy patients using the same hypertonic glucose challenge. 3o The plasma volume measured by the Evans blue method was reduced by 400 to 800 ml. They postulated that intravascular fluid was rapidly attracted into the jejunal lumen because of the hyperosmolarity of intestinal content. In 1961 Johnson and J esseph produced evidence that there might
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be a humoral factor involved in the early postprandial dumping syndrome. 18 They pointed out that the subjective symptoms begin before changes can be measured in the plasma volume. They postulated that hyperosmolar materials caused release of a substance from the small intestinal mucosa passing through the circulation to produce symptoms. Because of the high concentration of enterochromaffin cells in the duodenum and proximal jejunum, these investigators proposed that the humoral agent might be serotonin. They pointed out the similarity between dumping and the carcinoid syndrome. Drapanas and associates measured serotonin in the portal and systemic blood of dogs after instillation of hypertonic glucose into the upper small intestine. 8 There was a 50 per cent increase in portal blood serotonin levels. Silver and colleagues, however, found that peripheral blood serotonin was not increased following a glucose challenge in patients with the dumping syndrome. 34 Zeitlin and Smith reported release into the circulation of a bradykininlike polypeptide in patients with dumping. 42 MacDonald and coworkers confirmed in the experimental animal the presence of bradykinin in the circulation. 21 It seems probable that a number of vasoactive polypeptides play a role in the dumping syndrome. Blackburn and associates found that plasma neurotensin increases sharply during a dumping attack. 2 Sagor and coworkers found that vasoactive intestinal peptide (VIP) also increased during dumping. 31 Sirinek and colleagues found that neurotensin increases in some dumping patients whereas VIP increases in others, suggesting that there may be two types of dumping. 35 Adrian and coworkers found also that plasma peptide YY increases in dumping attacks. 1 The possibility that inhibition of intestinal secretion might control dumping was suggested by Reasbeck and Van Rij. They found that somatostatin, with its profound inhibition of intestinal secretion, tended to control dumping, particularly the intestinal manifestations. 29 Prevention and Treatment The early postprandial dumping syndrome can be prevented or at least reduced in incidence and severity by proper selection of the operative procedure for the individual patient. Parietal cell vagotomy should be utilized whenever this is a reasonable approach for the patient with a duodenal ulcer diathesis. The vagally innervated pyloric sphincter mechanism is preserved. As a consequence, dumping is exceedingly rare. Vagotomy and pyloroplasty have a lower incidence of dumping than vagotomy and antrectomy and should be utilized when this procedure has a reasonable likelihood of being adequate. Moreover, in patients in whom the pyloric sphincter has been either divided, bypassed, or resected as a part of the operative procedure, the dumping symptoms can usually be prevented by proper postoperative dietary management. This is begun during the in-hospital postoperative period and continued following hospital discharge. It is our experience in this regard that a dietitian is of inestimable
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assistance to the surgeon because the dietitian can provide detailed menus. The treatment of the dumping syndrome is largely, in fact almost exclusively, dietary. The empiric observation that carbohydrates, particularly liquid sugars, precipitate an attack has been amply supported. The basis of dietary treatment is, therefore, a low carbohydrate diet. Liquid foods or solid foods flushed through the gastric remnant with liquids provide the basic components for the precipitation of dumping. Therefore, we utilize what we refer to in the vernacular as "the dry diet routine." This requires repeated detailed explanation to the patients. It is hard for them to grasp that breakfast can be eaten without two cups of coffee and without being prefaced by orange juice. The patient should take only the solid part of the meal at breakfast and 112 to 1 hour later take whatever (sugar-free) liquids are desired. Most patients respond favorably to such a program, not only with relief of their subjective symptoms, but also with obvious improvement in their nutritional status as measured by weight gain. In addition to diet, certain gel-forming carbohydrates can be used to modify glucose absorption. Jenkins and colleagues found that the addition of 14.5 gm pectin to a 50 gm oral glucose load prevented hypoglycemic symptoms in dumping patientsY This has been confirmed by Leeds and coworkers.20 Harju and Larmi reported that a similar substance, guar gum, also obviates the effect of a glucose challenge. l l We have found that the addition of a small dose of ephedrine sulfate (4 ml ephedrine elixir containing 11.5 mg) seems to potentiate the therapeutic value of pectin. 24 Surgical Treatment A small number of patients become permanent gastric cripples as a result of the early postprandial dumping syndrome refractory to medical therapy. These patients should be considered candidates for surgical revision. In patients with a Billroth II gastrectomy, conversion to a Billroth I reconstruction is frequently followed by improvement. We found that 5 of 11 patients became completely asymptomatic and 3 others clearly improved. 40 Jejunal pouches interposed between the gastric remnant and duodenum have been less satisfactory, with only three of nine cases showing persistent improvement. 41 Symptoms of prolonged retention often associated with bezoar formation have been frequent complications. On the basis of the work of Hammer and associates, reversed jejunal segments have been interposed between the gastric remnant and duodenum. lO Although this procedure was initially successful in controlling dumping symptoms, 13 later development of alkaline reflux gastritis has been a frequent occurrence. During the 1970s we used Roux-en-Y duodenal diversion for patients who had both alkaline reflux gastritis and the early postprandial dumping syndrome. We had not expected the dumping symptoms to improve and had advised the patients accordingly. Much to our surprise, all patients reported their dumping symptoms to be markedly
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improved. This unanticipated effect of the Roux-en- Y procedure will be discussed later. In any event, we treated 15 patients with medically intractable dumping using Roux-en- Y diversion with uniform success. 25 We continue to find this the treatment of choice in patients with medically intractable dumping. We have seen several patients who are converted from too rapid emptying of the stomach to too slow. Symptoms of dumping are replaced by symptoms of gastric retention. To date we have been unable to determine preoperatively when this might be a hazard, and we find that sluggish emptying often responds to bethanechol stimulation. Therefore, we consider the Roux-en- Y procedure to be the method of choice in patients with medically intractable early postprandial dumping syndrome.
LATE OR HYPOGLYCEMIC DUMPING
The late postprandial or hypoglycemic dumping syndrome is much less common than the immediate variety. Symptoms appear from 1 to 3 hours after a meal. They are similar to those of the early type except for the absence of gastrointestinal symptoms. The syndrome depends on the absence of an effective pyloric sphincter for its pathogenesis. Rapid emptying of soluble carbohydrate into the intestine causes a more rapid rise in postprandial serum glucose, which also reaches higher levels than usual. Hyperosmolar material in the upper intestine causes excessive release of enteroglucagon. 32 This substance sensitizes the beta cells of the pancreatic islets to release excessive amounts of insulin. 33 Therefore, the postprandial hyperglycemia is overcorrected and is followed by hypoglycemia. Unlike the early postprandial type, symptoms are relieved by the ingestion of liquids containing sugar. Prevention and treatment of the late postprandial dumping syndrome is the same as that of the early or immediate variety. After a period of several months on a low carbohydrate diet, the small bowel mucosa ceases to release excessive enteroglucagon. Patients note that they can tolerate larger and larger amounts of carbohydrate in their diet without developing symptoms. Response to medical therapy is so successful that medical intractability is extremely rare and revisional surgery almost never necessary.
ALKALINE REFLUX GASTRITIS For many years it was generally considered that all patients with epigastric pain and chronic bilious vomiting after gastrectomy or gastroenterostomy had chronic afferent loop syndrome with intermittent afferent loop obstruction. However, reoperation in many of these patients revealed no evidence for a mechanical problem. It also became apparent that the syndrome appeared in patients without an afferent
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loop, that is, Billroth I gastrectomy or pyloroplasty. It was then realized that there is usually a striking difference in the patients' history as well. With the relatively uncommon afferent loop syndrome, pain is immediately postprandial, causes cramping, and is associated with projectile vomiting that completely relieves the pain, and the vomitus contains no food debris. It is now understood that afferent loop obstruction is a very uncommon syndrome. In the more common patient with alkaline reflux gastritis, the epigastric pain is more likely to be burning, is much less closely related to meal taking, and is often not relieved completely by vomiting, and the vomitus often contains some admixture of food debris. Pathogenesis As with the dumping syndrome, the fundamental defect is ablation, destruction, or bypass of the pyloric sphincter. In addition to regulation of gastric emptying, this structure also regulates reflux from the duodenum into the stomach. The uncontrolled reflux of duodenal fluid produces gastritis, with the associated pain and bilious vomiting. Which constituent of duodenal fluid causes gastric mucosal injury? This fascinating question remains unanswered to date. Are two or even several constituents necessary to produce the pathologic result? The use of the term "alkaline" is a confession of ignorance since the mild alkalinity of duodenal fluid resulting largely from pancreatic bicarbonate is certainly nontoxic to any gastrointestinal mucosa. There is a vast array of data from experimental laboratories that is often confusing and even contradictory. Some of these discrepancies may be due to species variations. Since bile acids are the most toxic material present in duodenal fluid, much attention has been directed to them. In the clinical setting, however, binding of bile acid with cholestyramine does not afford either symptomatic relief or objective endoscopic improvement. On the other hand, bile acids are known to break the barrier of the gastric mucosa, permitting back diffusion of hydrogen ions, which suggests that this could be the mechanism of injury. However, chronic diversion of bile directly into the stomach of both the dog and the pig have failed to reproduce the injury.39 Lawson was able to reproduce the lesion in the dog by diversion of both pancreatic juice and bile into the stomach. 19 It is possible that pancreatic enzymes associated with bile acids, particularly trypsin, result in gastritis. Diagnosis and Pathology In patients with epigastric pain and bilious vomiting, the diagnosis of alkaline reflux gastritis is confirmed by fiberoptic endoscopy and gastric mucosal biopsy. The body of the stomach is more or less diffusely involved. The mucosa appears erythematous and friable and bleeds readily on contact with the tip of the endoscope. Frequent suctioning is usually needed because of the continuous regurgitation of heavily bile-stained duodenal fluid. There are interspersed areas
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of atrophy with abnormal visibility of the submucosal blood vessels. In addition, superficial erosions are often seen, particularly along the lesser curvature. Histologic examination of the gastric mucosa shows three characteristic changes. First, there is complete absence of parietal cells. Second, there is an accumulation of chronic inflammatory cells in the submucosa. Third, the gastric glands are markedly distorted, dilated, and elongated, giving a corkscrew appearance. The mucosa is frequently superficially ulcerated and in other areas atrophic. The lesion may progress to intestinal metaplasia with the appearance of small intestinal villi and sometimes Paneth cells. Unfortunately, the severity of clinical symptoms and the severity of the pathologic lesion often correlate poorly in both directions. Moreover, mucosal abnormalities are often seen in asymptomatic postoperative patients who undergo endoscopy for some other reason. Treatment No medical treatment provides relief in patients with alkaline reflux gastritis. A patient with clinically significant symptoms who desires relief should be offered revisional surgery. We initially utilized an isoperistaltic segment of jejunum interposed between the gastric remnant and duodenum, the so-called Henle loop.5 It was thought that this would provide a peristaltic valve that inhibited duodenogastric reflux and at the same time restored normal gastrointestinal continuity. Unfortunately, of 10 patients undergoing this procedure, only 4 have had enduring satisfactory results. We have since used Roux-en-Y duodenal diversion for the treatment of the syndrome of alkaline reflux gastritis. In 1976 we reported 24 cases with favorable outcome. 4 We have continued to use this procedure as the treatment of choice for this disorder. Clinical recovery is usually dramatic. Frequently the patient notes the absence of the pre-existing chronic epigastric distress even during the period of maximum wound pain. The patient can ingest solid food within a few days, and notices no discomfort and a complete absence of vomiting. Fiberoptic endoscopy was performed in the first 24 patients 3 to 4 months postoperatively. All showed marked improvement in the gross endoscopic picture. Biopsies demonstrated improvement in 22 of the 24 patients, and 17 of the biopsies were reported to be histologically normal. Parietal cells return with recovery of the gastric mucosa and the gastric remnant recovers the capacity to secrete hydrochloric acid. Since the Roux-en-Y procedure is potentially ulcerogenic, it is important that complete vagotomy be present in all patients to prevent marginal ulceration.
THE ROUX-EN-Y SYNDROME In 1975 Davidson and Hersh suggested that delayed gastric emptying might playa role in the pathogenesis of alkaline reflux gastritis. 6
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They later reported that patients with evidence of delayed gastric emptying preoperatively did not fare well after Roux-en-Y doudenal diversion. 7 Boren and Way reported a high incidence of delayed gastric emptying following Raux diversion for alkaline reflux gastritis. 3 In a more recent study, Pellegrini and coworkers found no single pattern of gastric emptying in patients with alkaline reflux gastritis. 28 They reported that Roux-en-Y diversion resulted in delayed gastric emptying in 45 per cent of their patients, half of whom developed gastric bezoars after surgery. In 1980 a retrospective study was conducted on 97 patients who had undergone Roux-en-Y duodenal diversion for alkaline reflux gastritis at the University of Florida. 37 Follow-up was obtained by telephone interview or clinic visit with additional examinations as indicated. Pre-existing signs or symptoms of gastric stasis were present in 35 per cent of these patients. Gastric emptying was not routinely studied preoperatively, however. Postoperatively, all patients experienced dramatic relief from their epigastric pain. However, 50 (52 per cent) of these patients had moderate to severe symptoms of delayed gastric emptying. The symptoms consisted of postprandial fullness, "gas bloating," and even painful abdominal distention relieved by vomiting. Many of these patients avoided solid foods and exist on a nearly all-liquid diet. Despite these new symptoms, however, half of these 50 patients still consider themselves improved, mainly because of the relief of their previous epigastric pain. Barium upper gastrointestinal x-ray studies of these patients were frequently normal because this test does not reliably evaluate gastric emptying of solids. Endoscopy revealed no evidence of mechanical obstruction. In the latter part of the series we found radionuclide evaluation of gastric emptying of solids to be quite useful, utilizing a poached egg white method incorporating technetium-99m sulfur colloid. 23 Research Data On the basis of our clinical evaluation, an animal model was developed to study this problem further. 15 Vagotomy with antrectomy was performed with reconstruction as either a Roux-en-Y or a standard Billroth II gastrojejunostomy. Gastric emptying was studied by washing out the residue of a meal through a large bore gastric cannula. Gastric emptying of liquids and solids was delayed in the Roux-enY animals compared with the Billroth II group. In a more recent study, we assessed gastric emptying with the radionuclide poached egg white technique, which allowed continuous monitoring of gastric emptying with the gamma camera. 38 Gastric emptying was assessed in control animals with vagal innervation intact. Roux-en-Y diversion without vagotomy resulted in more rapid gastric emptying of the test meal. The addition of truncal vagotomy led to delayed gastric emptying in 25 per cent of Roux-en-Y animals. It appears clear, therefore, that the Roux-en-Y syndrome is dependent on vagal denervation of the gastric remnant. This observation was confirmed in the dog by
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pharmacologic replacement of the vagus nerve. Both parenteral and oral administration of bethanechol markedly improved gastric retention in vagotomized Roux-en-Y animals. 16 Interestingly, metoclopramide had no effect on delayed gastric emptying in this model. These findings have been utilized in the clinic for patients with symptoms of delayed gastric emptying after the Roux-en-Y procedure. Approximately half of such patients have responded clinically to bethanechol administration, and a similar improvement in gastric emptying is observed using the technetium-99m-Iabeled test meal. Clinical Experience In the experimental model, delayed gastric emptying after the Roux-en-Y procedure can be markedly lessened by subtotal gastrectomy.15 This finding in the animal has also been applied to the patient with medically intractable symptoms of delayed gastric emptying after the Roux-en-Y procedure. Although a substantial number of the patients have improved after this further operative procedure, in several unimproved patients it has been necessary to proceed with total gastrectomy to provide relief. For the past 5 years we have studied gastric emptying in all patients with alkaline reflux gastritis who are candidates for Roux-en-Y duodenal diversion. 36 In patients in whom there is a pre-existing delay in gastric emptying, subtotal gastrectomy has been performed at the time of the Roux-en-Y procedure. This has been successful in limiting postoperative symptoms of gastric retention. However, in patients with normal gastric emptying, and even in patients with the dumping syndrome as well as alkaline gastritis, Rouxen-Y duodenal diversion without extensive gastrectomy has been associated with a high incidence of postoperative gastric retention. At this time we cannot find any clinically useful method to determine which patient will have postoperative difficulties with gastric emptying. It is our current policy, therefore, to perform subtotal gastrectomy as a routine procedure in conjunction with Roux-en-Y duodenal diversion for alkaline reflux gastritis. SUMMARY Operations on the stomach for benign peptic ulcer frequently result in a variety of symptoms collectively referred to as "the postgastrectomy syndromes." These iatrogenic disorders are numerous and varied, but the vast majority fall into two categories: the postprandial dumping syndrome and alkaline reflux gastritis. Both disorders result from ablation or bypass of the pyloric sphincter. The early postprandial dumping syndrome results from hyperosmolar food rapidly reaching the mucosa of the small intestine. This causes, release of a variety of vasoactive materials. Severe peripheral vasodilatation is accompanied by stimulation of intestinal motility. The patient usually has a mixture of vasomotor symptoms along with abdominal cramping and diarrhea.
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Dumping can be prevented by preserving the innervated pylorus when possible and by proper postoperative dietary instructions. Treatment is largely dietary, consisting of a low carbohydrate, sugar-free diet with the liquid part of the meal separated from solids. Medicinal treatment with pectin and ephedrine is sometimes helpful. Intractable patients can be treated best by revisional surgery, with Roux-en-Y duodenal diversion providing the best results. The delayed or hypoglycemic form of the dumping syndrome is less common and is due to excessive release of insulin in response to postprandial hyperglycemia and release of enteroglucagon from the upper small intestine. Dietary treatment with a low carbohydrate intake is usually successful. Destruction of the pylorus permits unrestrained reflux of duodenal content into the stomach. This produces gastritis in some patients, with epigastric pain and intractable bilious vomiting. Multiple substances present in bile and pancreatic juice are probably necessary for creation of the lesion. The disorder is prevented only by preservation of the pylorus. Treatment is exclusively surgical. The procedure of choice is Rouxen-Y duodenal diversion, which provides immediate relief of symptoms. However, a substantial number of these patients will later have symptomatic gastric retention. The Roux-en-Y syndrome often follows use of this procedure in the treatment of alkaline reflux gastritis. This problem is present only in the absence of vagal innervation. The mechanisms involved are unclear at this time. Studies in the dog have indicated that subtotal gastrectomy usually minimizes the defect, and this principle has proved moderately satisfactory in the patient. Animal studies also indicated that bethanechol is useful for the medical treatment of gastric retention after the Roux-en-Y procedure. This has also been successfully applied to patients. The disorder is particularly frequent and severe in patients who have delayed gastric emptying along with alkaline reflux gastritis. However, preoperative testing of gastric emptying has not been helpful in patient selection, and we propose that subtotal gastrectomy should usually be performed as a part of Rouxen-Y duodenal diversion for alkaline reflux gastritis.
REFERENCES 1. Adrian TE, Long RG, Fuessl HS: Plasma peptide YY (PYY) in dumping syndrome. Dig Dis Sci 30:1145-1148, 1985 2. Blackburn AM, Christofides ND, Ghatei MA, et al: Elevation of plasma neurotensin in the dumping syndrome. Clin Sci 59:237-243, 1980 3. Boren CH, Way LW: Alkaline reflux gastritis: A reevaluation. Am J Surg 140:4046, 1980 4. Bushkin FL, Wickbom G, Woodward ER: Use of Roux-en-Y diversion of duodenal secretions in the treatment ofreflux gastritis. South Med J 69:132-137, 1976 5. Bushkin FL, Woodward ER: Postgastrectomy Syndromes, xx. Philadelphia, WB Saunders, 1976, p 56 6. Davidson ED, Hersh T: Bile reflux gastritis. Am J Surg 130:514-518, 1975
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7. Davidson ED, Hersh T: The surgical treatment of bile reflux gastritis. Ann Surg 192:175-178,1980 8. Drapanas T, McDonald JC, Stewart JD: Serotonin release following instillation of hypertonic glucose into the proximal intestine. Ann Surg 156:528-536, 1962 9. Eisenberg MM, Woodward ER, Carson TJ: Vagotomy and drainage procedure for duodenal ulcer: The results often years' experience. Ann Surg 170:785-792,1969 10. Hammer JM, Seay PH, Johnston RL, et al: The effect of antiperistaltic bowel segments on intestinal emptying time. Arch Surg 79:537-541, 1959 11. Harju E, Lanni TKI: Efficacy of guar gum in preventing the dumping syndrome. JPEN 7:470-472, 1983 12. Hastings N, Halsted JA, Woodward ER, et al: Subtotal gastric resection for benign peptic ulcer. Arch Surg 76:74-80, 1958 13. Herrington JL Jr: Remedial operations for post-gastrectomy syndromes. In Current Problems in Surgery. Chicago, Year Book Medical Publishers, 1970 14. Hertz AF: The cause and treatment of certain unfavorable aftereffects of gastroenterostomy. Ann Surg 58:466-472, 1913 15. Hocking MP, Vogel SB, Falasca CA, et al: Delayed gastric emptying of liquids and solids following Roux-en-Y biliary diversion. Ann Surg 194:494-501, 1981 16. Hocking MP, Vogel SB, Webb S, et al: Medical therapy of delayed gastric emptying after Roux-en-Y gastrojejunostomy. Surg Forum 33:124-126, 1982 17. Jenkins DJA, Gassull MA, Leeds AR, et al: Effect of dietary fiber on complications of gastric surgery: Prevention of postprandial hypoglycemia by pectin. Gastroenterology 72:215-217, 1977 18. Johnson LP, J esseph JE: Evidence for a humoral etiology of the dumping syndrome. Surg Forum 12:316-317, 1961 19. Lawson HH: Effect of duodenal contents on the gastric mucosa under experimental conditions. Lancet 1:469-472, 1964 20. Leeds AR, Ebied F, Ralphs DNL, et al: Pectin in the dumping syndrome: Reduction of symptoms and plasma volume changes. Lancet 16:1075-1078,1981 21. MacDonald JM, Webster MM Jr, Tennyson CH, et al: Serotonin and bradykinin in the dumping syndrome. Am J Surg 117:204-213,1969 22. Machella TE: The mechanism of postgastrectomy dumping syndrome. Ann Surg 130:145-159, 1949 23. Martin JL, Beck WJ, McDonald AP, et al: 99m Tc-labeled solid-phase meal: A quantitative clinical measurement of human gastric emptying. J Clin Gastroenterol 5:315-319, 1983 24. Mathias JR, Woodward ER: Unpublished data 25. Miranda R, Steffes BC, O'Leary JP, et al: Surgical treatment of the postgastrectomy dumping syndrome. Am J Surg 139:40-43, 1980 26. Mix CL: Dumping following gastrojejunostomy. Surg Clin North Am 2:617-622, 1922 27. O'Leary JP, Woodward ER, Hollenbeck JI, et al: Vagotomy and drainage procedure for duodenal ulcer: The results of seventeen years' experience. Ann Surg 183:613-618, 1976 28. Pellegrini CA, Patti MG, Lewin M, et al: Alkaline reflux gastritis and the effect of biliary diversion on gastric emptying of solid food. Am J Surg 150:166-171, 1985 29. Reasbeck PG, Van Rij AM: The effect of somatostatin on dumping after gastric surgery: A preliminary report. Surgery 99:462-468, 1986 30. Roberts KE, Randall HT, Farr HW, et al: Cardiovascular blood volume alterations resulting from intrajejunal administration of hypertonic solutions to gastrectomized patients: The relationship of these changes to the dumping syndrome. Ann Surg 140:631-640, 1954 31. Sagor GR, Bryant MG, Ghatei MA, et al: Release of vasoactive intestinal peptide in the dumping syndrome. Br Med J 282:507-510, 1981 32. Samols E, Tyler J, Marri G, et al: Stimulation of glucagon secretion by oral glucose. Lancet 2: 1257-1259, 1965 33. Shultz KT, Neelon FA, Nilson LB, et al: Mechanism of postgastrectomy hypoglycemia. Arch Intern Med 128:240-246, 1971 34. Silver D, McGregor FH Jr, Porter JM, et al: The mechanism of the dumping syndrome. Surg Clin North Am 46:425-439, 1966
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35. Sirinek KR, O'Dorisio TM, Howe B, et al: Neurotensin, vasoactive intestinal peptide, and Roux-en-Y gastrojejunostomy: Their role in the dumping syndrome. Arch Surg 120:605-609, 1985 36. Vogel SB, Hocking MP, Woodward ER: Radionuclide evaluation of gastric emptying in patients undergoing Roux-Y biliary diversion for alkaline reflux gastritis and po~tgastrectomy dumping. Surg Forum 34:173-175,1983 37. Vogel SB, Hocking MP, Woodward ER: Unpublished data 38. Vogel SB, Vair DB, Woodward ER: Alterations in gastrointestinal emptying of99mtechnetium-labeled solids following sequential antrectomy, truncal vagotomy and Roux-Y gastroenterostomy. Ann Surg 198:506-515, 1983 39. Wickbom G, Bushkin FL, Linares C: On the corrosive properties of bile and pancreatic juice on various living tissues in dogs. Arch Surg 108:680-684, 1974 40. Woodward ER, Desser PL, Gasster M: Surgical treatment of the postgastrectomy dumping syndrome. West J Surg Obstet Gynecol 63:567-573, 1955 41. Woodward ER, Hastings N: Surgical treatment of the postgastrectomy dumping syndrome. Surg Gynecol Obstet 3:429-437, 1960 42. Zeitlin IJ, Smith AN: 5-Hydroxinoles and kjpins in the carcinoid and dumping syndrome. Lancet 2:986-991, 1966 Box J-286, JHMHC University of Florida College of Medicine Gainesville, Florida 32610