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120 R. E. Roses and D. L. Fraker
after pancreaticoduodenectomy, Yeo and associ­ates defined DGE as either (1) nasogastric tube requirement for 10 or more days plus one of the following: (a) emesis after nasogastric tube re­moval, (b) postoperative use of prokinetic agents after postoperative day 10, (c) reinsertion of a na­sogastric tube, or (d) failure to progress with diet; or (2) nasogastric tube requirement fewer than 10 days plus two of (a) through (d) above [7]. The 10-day cutoff for nasogastric tube require­ment has been adopted in some, but certainly not all subsequent studies.
In practice, DGE or postoperative gastropa­resis are often diagnoses of exclusion. Anasto­motic leak (particularly an evolving pancreatic fistula after pancreatoduodenectomy) may pres­ent with proximal ileus and be accompanied by leukocytosis, tachycardia, or turbid output from a postoperative drain. Mechanical obstruction can likewise be difficult to differentiate from gastro­paresis on clinical grounds alone. A CT scan with enteric contrast is often an appropriate first im­aging modality and can identify undrained fluid collections, extraluminal air, or transition points between enhanced and collapsed viscera. A dy­namic upper GI contrast study may be more sen­sitive in identifying partial mechanical obstruc­tion. The experienced gastrointestinal radiologist will often identify delayed transit time as contrast traverses the stomach and proximal bowel. The use of barium for these studies may further en­hance sensitivity but should be reserved for those cases in which the index of suspicion for an en­teric leak or high-grade mechanical obstruction is low, as barium extravasation into the perito­neal cavity or retained barium can be problem­atic in these settings, respectively. Furthermore, retained barium can limit interpretation of subse­quent CT scans.
Gastric emptying scintigraphy provides per­haps the most nuanced assessment of gastric emptying; however, the role of this study in eval­uating the postoperative patient remains poorly defined and standardized definitions of normal scintigraphic findings after gastric resection re­main elusive. In general, there is delay in the emptying of solids and accelerated emptying of liquids after partial gastrectomy [8]. After Roux-
en-y reconstruction, there is often retention of solids in both gastric remnant and the Roux limb [9]. Scintigraphy does allow assessment of re­gional emptying of the fundic and antral regions and can be helpful in explaining dyspeptic symp­toms, particularly when global gastric emptying values are normal [10]. For example, nausea, early satiety, and abdominal distention have been associated with proximal gastric retention; in contrast, vomiting is more often associated with delayed distal GE.
Management
In the early postoperative period, gastroparesis often necessitates prolonged NG tube decom­pression. Early dysmotility often improves with time, and a deliberate management approach is justified. Correction of hyperglycemia, electro­lyte abnormalities, and the reduction of narcotic use are recommended. While waiting for recov­ery, nutritional support is requisite, in the form of either enteral feeding (if the patient has a je­junostomy feeding tube) or parenteral nutrition. Depending on the severity of symptoms and the scope of the initial operation, placement of a je­junostomy feeding tube or a decompressive gas­trostomy tube may expedite recovery.
The use of promotility agents is sometimes helpful and fairly safe although convincing evi­dence of efficacy in the postoperative setting is lacking. Macrolide antibiotics (e.g., erythromy­cin) agonize the motilin receptor. In patients with diabetes mellitus and delayed gastric empty­ing, intravenous administration of erythromycin 200 mg before a test meal has been shown to nor­malize gastric emptying of liquids and solids [11]. The clinical efficacy of oral erythromycin, how­ever, has not been consistently demonstrated. In a randomized placebo controlled trial, intravenous erythromycin after pancreaticoduodenectomy did not significantly reduce delayed gastric emp­tying as defined by the authors; though, fewer pa­tients required reinsertion of a nasogastric tube or retained liquids by scintigraphy in the treatment group [7]. Even in those patients who do appear to respond favorably, a tolerance phenomenon is
12112 Bile Reflux and Gastroparesis
frequently observed and drug interactions with agents that are metabolized by CYP3A4 further limit utility.
Metoclopramide is a dopamine-2 (D2) an­tagonist with apparent efficacy in a subset of patients with gastroparesis. Sedative effects can limit utility and extrapyramidal side effects, though not as frequent as with older antipsychot­ic drugs (e.g., haloperidol and chlorpromazine), can be irreversible. A majority of cases of tardive dyskinesia occur with longer-term use, and limit­ing metoclopramide use to less than 3 months is prudent.
Pyloroplasty when applicable has also been proposed, and botulinum toxin injections may transiently improve gastric emptying in a sub­set of patients. In the majority of postsurgical patients who have undergone either gastric or pancreatic resection, these approaches are not relevant. Historically, completion or subtotal gastrectomy was offered to patients with refrac­tory gastroparesis. A number of reports from single institutions support the efficacy of such an approach [12, 13]. Importantly, these should represent options of last resort considered only after exhausting all more conservative measures. In most cases, enteral access with a jejunostomy feeding tube with or without a decompressive gastrostomy and dietary modification affords prompter improvement in the quality of life than does near-total gastrectomy. Placement of a percutaneous endoscopic gastrostomy (PEG) tube with jejunostomy tube extension represents a useful alternative to traditional enteral access procedures in selected patients requiring gastric decompression and distal enteral access for nu­trition support.
More recent experiences with gastric electri­cal stimulation (GES) suggest an alternative ther­apeutic option. Initial studies in dogs demonstrat­ed increased peristaltic pressure waves and the gastric emptying rate with electrical stimulation [14]. A series of small trials using implantable electronic devices in patients with diabetic gas­troparesis followed. Recently, patients with re­fractory postsurgical gastroparesis were reported to achieve symptomatic improvement with GES [15, 16]. Interestingly, the stimulation impulses
used (5 mA, duration 330 ms) are too weak to excite gastric smooth muscles (hence the term “gastric pacemaker” is a misnomer). Moreover, objective measurements of gastric emptying have not consistently demonstrated effect [17].
Bile Reflux
Etiology
Pancreaticobiliary reflux into the stomach is obli­gate after resection or ablation of the pylorus (e.g., pyloroplasty or Billroth I) or loop reconstruction to a gastric remnant (e.g., gastrojejunostomy or Billroth II). Only a subset of patients, however, develop bile reflux gastritis or esophagitis as a result. Billroth II reconstruction to a small gas­tric pouch may anticipate particularly severe bile esophagitis and should be avoided (Fig. 12.1). Resection of greater than 60 % of the distal stom­ach should be reconstructed with a Roux-en-Y gastrojejunostomy to prevent this complication. The syndrome of bile reflux has also been rec­ognized after cholecystectomy. In this setting, it has been attributed to loss of gallbladder reser­voir function and continuous passage of biliary
Fig. 12.1 Enlarged hyperemic folds in gastric remnant, after Billroth II reconstruction. (Image courtesy of Greg­ory Ginsberg, MD)
122 R. E. Roses and D. L. Fraker
Fig. 12.2 Erosive alkaline reflux esophagitis. (Image courtesy of Gregory Ginsberg, MD)
secretions, more of which reflux into the stom­ach than would otherwise be the case (Fig. 12.2). Delayed gastric emptying or gastric stasis may be contributory in many cases as well, and the denervating procedures of the past era of peptic ulcer disease surgery (i.e., truncal vagotomy) yielded an experience that informs the current understanding of this clinical syndrome. In the presence of gastric stasis, exposure of gastric mucosa to duodenal fluids is increased. A higher gastric pH may allow bacterial overgrowth and subsequent conversion of bile salts to unconju­gated bile acids, which are particularly noxious to the gastric mucosa. Pathological changes in the gastric mucosa develop over time and include foveolar hyperplasia, glandular cystic degenera­tion, edema of the lamina propria, and vasocon­gestion of the mucosal capillaries [18].
Clinical Presentation and Evaluation
The occasional patient complains of profound re­flux pain in the early postoperative period. More often, symptoms evolve a year or more after the index operation. A symptom complex of nausea, pain, and bilious emesis is characteristic but, by no means, specific to bile reflux. As with gastro­paresis, other more common etiologies must be excluded. Cross-sectional imaging or dynamic upper gastrointestinal contrast studies are useful
for excluding mechanical obstruction. The for­mer can rule out fluid collections as well, more relevant in the early postoperative period. Upper endoscopy may identify marginal ulceration or mucosal irritation. Scintigraphy (bile reflux scan or HIDA scan) may be useful, particularly in de­termining a role for remedial surgery. An abnor­mal study is not that informative. A normal study, however, anticipates a poor response to surgical management.
Management
A variety of pharmacologic agents have been utilized in the treatment of bile reflux; none are consistently effective. Sucralfate may buffer the stomach or gastric remnant and provide symp­tomatic relief and is often a good first choice. Cholestyramine has been advocated but is prob­ably of little utility [19]. Promotility agents (e.g., metaclopromide) may have a role, particularly if a contribution of gastroparesis is suspected. Per­sistent symptoms over months despite pharmaco­logic intervention in the face of an abnormal bile reflux scan point to a role for remedial surgery.
In the patient with severe symptoms, objective signs of bile reflux (e.g., endoscopic evidence of gastritis, scintigraphy confirming duodenal re­flux into the stomach) surgery can be considered. A variety of operative approaches can be utilized for the remediation of bile reflex. The most com­monly chosen and most familiar is Roux-en Y gastrojejunostomy; however, Braun entero-enter­ostomy and the Henley procedure (antiperistal­tic jejunal interposition) are reasonable alterna­tives (Fig. 12.3). If Roux-en Y reconstruction is selected, a limb in excess of 40 cm (some have advocated > 60 cm) should be constructed to maximize isolation of the stomach from duode­nal secretions. Longer limbs (> 80 cm) should be avoided to decrease the risk of malabsorption and Roux stasis. Assuming careful patient selection, a high rate of success can be expected.
The major disadvantage of Roux-en Y re­construction is an incidence of “Roux stasis syndrome,” generally attributed to small bowel denervation and diminished prograde peristalsis
12312 Bile Reflux and Gastroparesis
Fig. 12.3 Isoperistaltic jejunal loop interposition. (Henley procedure)
in the Roux limb. Bacterial overgrowth, diarrhea, jejunal ulceration, and impaired protein digestion may result. Abdominal pain and vomiting are typical symptoms and there is often overlap with gastroparesis, as this syndrome is observed with greater frequency in patients with larger gastric remnants. These concerns may necessitate com­pletion antrectomy or even subtotal gastrectomy, and truncal vagotomy at the time of remediation in the appropriate clinical setting.
While bilious emesis is mitigated by Roux-en Y reconstruction, a number of larger published experiences suggested recurrent symptoms in ap­proximately 30 % of patients long term [20]. This substantial rate of long-term morbidity justifies consideration of other remedial approaches. Per­haps the simplest of these is creation of a Braun enteroenterostomy. This is most applicable in the setting of prior Billroth II construction and is achieved by side-to-side anastomosis of the af-
124 R. E. Roses and D. L. Fraker
Fig. 12.4 “Uncut Roux” reconstruction
ferent limb to the jejunum at least 40 cm distal to the gastrojejunostomy. Diminution of duo­denal fluid into the stomach or gastric remnant can be achieved with the application of a staple line across the afferent limb just proximal to the gastrojejunostomy. Use of a thoracoabdominal (TA) stapler facilitates the creation of a partition without transection, and may, therefore, preserve prograde peristalsis through the small bowel. Importantly, this partition is temporary in most cases (recanalization is a likelihood over time). For this reason, this so-called uncut Roux may not be the best option in a younger patient for whom effective long-term remediation is neces­sary (Fig. 12.4).
Interposition of an isoperistaltic segment of small bowel between the gastric remnant and du­odenum was advocated by Henley in the 1950s for the management of dumping syndrome. The Henley procedure has been used with reported success for the treatment of Bile reflux. In the
setting of prior Billroth II reconstruction, the af­ferent limb just proximal to the gastrojejunosto­my is divided. The jejunum is divided 20–45 cm distal to the anastomosis at a point that allows for convenient anastomosis to the proximal duode­num. Jejuno-duodenstomy and downstream jeju­nojejunostomy are performed to restore continu­ity. This configuration has been associated with effective amelioration of biliopancreatic reflux on scintigraphic examination [21] and may result in less of the long-term morbidity associated with Roux reconstruction.
Conclusion
Gastroparesis and bile reflux after foregut sur­gery remain distinct clinical challenges. Both diagnoses require exclusion of other correctable surgical complications, particularly mechanical obstruction or undrained infection. Scintigraphic studies can be used to confirm either diagnosis. Even when the diagnosis has been secured, a trial of conservative management is almost always in order during which time attention to nutritional status, correction of metabolic disturbances, and reduction of narcotic exposure are critical. Phar­macologic therapies are associated with only modest benefit, but may be helpful in selected cases and are relatively safe. In the setting of persistent severe refractory symptoms, remedi­al surgery should be considered. In the case of gastroparesis, distal enteral feeding access with gastric decompression may be an appropriate intermediate step before subtotal gastrectomy. A role for gastric electrical stimulation is evolving. A variety of remedial operations for bile reflux have been used with moderate success including conversion to Roux-en Y reconstruction, Braun enteroenterostomy, and Henley jejunal interposi­tion.
Key Points (Prevention)
1. Although definitive data are lacking, antecolic reconstruction after pylorus-preserving pan­creaticoduodenectomy may be associated
12512 Bile Reflux and Gastroparesis
with a lower rate of delayed gastric emptying compared to retrocolic reconstruction.
2. Gastric and intestinal denervation may con­tribute to the incidence of gastroparesis after gastric resection favoring Billroth II over Roux-en Y in appropriate circumstances.
3. Correction of hyperglycemia and electrolyte abnormalities and the reduction of narcotic use are self-recommending after abdominal surgery and may decrease the incidence of postoperative gastrointestinal dysmotility.
4.
Loop reconstruction to a small gastric pouch
may anticipate particularly
severe bile esoph-
agitis and should be avoided.
Key Points (Management)
1. Initial priorities in the management of postop­erative gastroparesis include decompression and treatment of postsurgical infection.
2. Bile reflux is most often a late complication and must be distinguished from mechanical obstruction.
3. Nutritional repletion is critical in the initial management of gastroparesis or bile reflux. When appropriate, surgical or percutaneous enteral access should be obtained early.
4. Remedial surgery for gastroparesis or bile re­flux should be reserved for refractory cases after exclusion of reversible etiologies, nutri­tional repletion, and confirmatory scintigraph­ic studies.
References
1. Tani M, et al. Improvement of delayed gastric empty-
ing in pylorus-preserving pancreaticoduodenectomy: results of a prospective, randomized, controlled trial. Ann Surg. 2006;243(3):316–20.
2.
Qu H, et al. Clinical
emptying in patients after pancreaticoduodenectomy: a systematic review and meta-analysis. Eur J Surg Oncol. 2013;39(3):213–23.
3. Tran KT, et al. Pylorus preserving pancreaticoduo-
denectomy versus standard Whipple procedure: a prospective, randomized, multicenter analysis of 170 patients with pancreatic and periampullary tumors. Ann Surg. 2004;240(5):738–45.
risk factors of delayed gastric
4. Fraser AG, Brunt PW of highly selective vagotomy with truncal vagotomy and pyloroplasty–one surgeon’s results after 5 Br J Surg. 1983;70(8):485–8.
5. Stoddard CJ, V tive vagotomy or truncal vagotomy and pyloroplasty for chronic duodenal ulceration: a randomized, pro­spective clinical study. Br J Surg. 1978;65(11):793–6.
6. Traverso LW ing: the state of the highest level of evidence. J Hepa­tobiliary Pancreat Surg. 2008;15(3):262–9.
7. Yeo CJ, et al. Erythromycin accelerates tying after pancreaticoduodenectomy. A prospective, randomized, placebo-controlled trial. Ann Surg. 1993;218(3):229–37. Discussion 237–8.
8. Fich A, et al. Stasis syndromes following gastric sur­gery: clinical patients. J Clin Gastroenterol. 1990;12(5):505–12.
9. Miedema BW, et al. Human gastric sit and motility after Roux gastrojejunostomy. Gas­troenterology. 1992;103(4):1133–43.
10.
Troncon LE, et al. Abnormal intragastric distribution
of food during gastric emptying in functional dys­pepsia patients. Gut. 1994;35(3):327–32.
11. Janssens J, et al. Improvement of gastric emptying in diabetic gastroparesis by erythromycin. Preliminary studies. N Engl J Med. 1990;322(15):1028–31.
12.
Speicher JE, et al. Results of completion
mies in 44 patients with postsurgical gastric atony. J Gastrointest Surg. 2009;13(5):874–80.
13. Forstner-Barthell AW, et al. Near-total completion gastrectomy for severe postvagotomy gastric stasis: analysis of early and long-term results in 62 patients. J Gastrointest Surg. 1999;3(1):15–21. Discussion 21–3.
14. Familoni BO, et al. Efficacy of electrical stimulation at frequencies higher than basal rate in canine stom­ach. Dig Dis Sci. 1997;42(5):892–7.
15.
McCallum R, et al. Clinical response to gastric
electrical cal gastroparesis. Clin Gastroenterol Hepatol. 2005;3(1):49–54.
16. Oubre B, et al. Pilot study on gastric electrical stimu­lation on surgery-associated gastroparesis: long-term outcome. South Med J. 2005;98(7):693–7.
17. Abrahamsson H. Treatment options for patients with severe gastroparesis. Gut. 2007;56(6):877–83.
18. Dixon MF, et al. Reflux gastritis: distinct histopatho­logical entity? J Clin Pathol. 1986;39(5):524–30.
19. Meshkinpour H, et al. Effect of cholestyramine on the symptoms of reflux gastritis. A randomized, double blind, crossover study. Gastroenterology. 1977;73(3):441–3.
20. Zobolas B, et al. Alkaline reflux gastritis: early and late results of surgery. World J Surg. 2006;30(6):1043–9.
21. Sousa JE, et al. Comparison between Henley jejunal interposition and Roux-en-Y anastomosis as con­cerns enterogastric biliary reflux levels. Ann Surg. 1988;208(5):597–600.
, Hashimoto Y. Delayed gastric empty-
stimulation in patients with postsurgi-
, Matheson NA. A comparison
years.
assilakis JS, Duthie HL. Highly selec-
gastric emp-
and motility features of 60 symptomatic
and jejunal tran-
gastrecto-
Dealing with Dumping Syndrome
Kyung Ho Pak and Sung Hoon Noh
13
Introduction
Although gastric surgery for ulcer disease has decreased, gastric cancer surgery and bariatric surgery are still frequently performed world­wide. Accordingly, the number of patients suf­fering from dumping syndrome has increased. In particular, in Korea and Japan, early gastric cancer (EGC) comprises up to 60–70 % of gastric cancer; therefore, the life expectancy of patients with gastric cancer is quite high. Surgeons, there­fore, must better understand dumping syndrome and be familiar with its management. Previously, there was a greater focus on finding a radical cure rather than on improving quality of life to increase the survival rate for gastric cancer; in contrast, concerns regarding the development of postgastrectomy syndromes such as dumping syndrome or reflux disease are now increasing.
Dumping syndrome is one of the most com­mon complications after gastric surgery. Ap­proximately 25–50 % of patients develop some manifestation of dumping syndrome. Among
S. H. Noh () Department of Surgery, Yonsei University Health System, Yonsei University College of Medicine, Seoul, Republic of Korea e-mail: sunghoonn@yuhs.ac
K. H. Pak Department of Surgery, Dongtan Sacred Heart Hospital, Hallym University College of Medicine, Hwasung, Kyunggi-do, Republic of Korea e-mail: sweetpkh@hallym.or.kr
them, 5–10 % have clinically significant symp­toms, and 1–2 % are debilitated by them. [1] Mallory et al.[2] reported that the incidence of dumping syndrome after gastric bypass was as high as 75 % in the early postoperative period, and most symptoms disappeared 15–18 months after surgery. However, many patients exhibit symptoms throughout life. Dumping syndrome has also been reported after Nissen fundoplica­tion in children and adults [35], and in pedi­atric and adult patients receiving gastrostomy feeding with a persistent vegetative state [6, 7]. In recent years, bariatric surgery has become the principal cause of postoperative dumping syn­drome [8].
The symptoms of early and late dumping syn­drome are believed to have distinct underlying pathophysiologies (Fig. 13.1). Early dumping, typically starting 20–30 min after a meal, usu­ally causes both vasomotor and gastrointestinal complaints such as sweating, palpitation, weak­ness and faintness, abdominal bloating, cramp­ing, and profound diarrhea. These symptoms, in severe cases, can occur during meals, but usually happen after meals. Although these symptoms can occur after any type of gastrointestinal sur­gery, Billroth-II reconstruction after gastrecto­my is the leading cause of dumping syndrome. The probability of occurrence increases when a greater amount of stomach is resected. Early dumping appears to be caused by the excessive secretion of gastrointestinal hormones after the rapid flow of a hypertonic diet into the small in­testine, which shifts intravascular fluid into the
T. M. Pawlik et al. (eds.), Gastrointestinal Surgery, DOI 10.1007/978-1-4939-2223-9_13, © Springer Science+Business Media New York 2015
127
128 K. H. Pak and S. H. Noh
Fig. 13.1 Pathophysiology of dumping syndrome
small intestine [9]. It causes the abrupt expansion of the small bowel, which causes increased fre­quency and amplitude of bowel contractility. Up to 25 % of the blood circulation can be utilized in this process.
Late dumping, often occurring 2–3 h postpran­dially, involves mainly vasomotor complaints characterized by perspiration, palpitation, mental confusion, and sometimes syncope. Rapid deliv­ery of a meal to the small intestine leads to an ini­tial higher concentration of carbohydrates in the proximal small bowel, followed by rapid absorp­tion of glucose into the blood. This is countered by the excessive release of insulin, the so-called “hyperinsulinemic response,” responsible for the subsequent reactive hypoglycemia [10]. The majority of patients exhibit early dumping, ap­proximately 25 % of them exhibit late dumping, and only a minority of patients have symptoms of both [11].
Diagnosis
Dumping syndrome is diagnosed based on a group of symptoms in patients who have under­gone gastric surgery, or by the dumping provoca­tion test. In 1970, Sigstad [12] proposed a scor­ing system based on the occurrence of different symptoms of dumping syndrome, to calculate a diagnostic index (Table 13.1). A diagnostic index > 7 is suggestive of dumping syndrome. This system is simple to use, but its disadvantage is that it is difficult to distinguish other postpran­dial symptoms from dumping. The score index is helpful in clinical practice to assess response to therapy.
A provocative test for assessing dumping syndrome can be used to confirm clinical sus­picions. This test is a modification of the oral glucose tolerance test (OGTT) and involves the ingestion of 50 or 75 g glucose in solution after an overnight fast. Immediately before and up to
Table 13.1  Sigstad score. Weighting factors allocated to the symptoms and signs of dumping syndrome
Sigstad score Preshock, shock 5 Almost fainting, syncope, loss of consciousness 4 Desire to lie or sit down 3 Breathlessness, dyspnea 3
Weakness,
Sleepiness, drowsiness, yawning, apathy Palpitation 3 Restlessness 2 Dizziness 2 Headache 1 Feeling of warmth, sweating, pallor, clammy skin 1 Nausea 1 Fullness in the abdomen, meteorism 1 Borborygmus 1 Eructation V
omiting
exhaustion 3
, falling asleep 3
1 4
12913 Dealing with Dumping Syndrome
180 min after ingestion of this solution, the blood glucose concentration, hematocrit, pulse rate, and blood pressure are measured at 30 min inter­vals. The provocative test is considered positive if late (120–180 min) hypoglycemia occurs, or if an early (30 min) increase in hematocrit of more than 3 % occurs. The best predictor of dumping syndrome seems to be a rise in pulse rate of more than 10 bpm (beat per min) after 30 min [13]. Assessments of the speed of gastric emptying might show that this process occurs rapidly in patients with dumping syndrome—especially for liquid nutrients—but this test does not seem to have good diagnostic sensitivity or specificity, probably because rapid emptying occurs early after meal ingestion, a phase that is not analyzed closely or separately in most protocols that test gastric emptying [10, 13, 14].
Prevention
Prevention, rather than treatment, is recommend­ed for dumping syndrome. The introduction of proton pump inhibitors and Helicobacter pylori eradication decrease the need for elective sur­gery in peptic ulcer disease. In addition, highly selective gastric vagotomy, which causes mini­mal disturbance of the gastric emptying mecha­nism, results in a lower incidence of dumping
syndrome [15]. If more extensive surgery is nec­essary, a Roux-en-Y gastrojejunostomy (RYGJ) is preferable because of its decreased rate of dumping, when compared with pyloroplasty or loop gastrojejunostomy [1618].
The choice of reconstructional method after distal gastrectomy is still controversial. The use of the Billroth I procedure after distal gastrec­tomy is preferred in Japan, whereas Billroth II is more common in Korea because it facilitates wider dissection and less anastomotic tension. There are some advantages in Billroth I com­pared to Billroth II, as follows: a more natu­ral route for food passage, potentially less op­erative time due to one anastomosis, no risk of duodenal stump leakage, and less incidence of postoperative weight loss, anemia, and dump­ing syndrome. The disadvantage of Billroth I, however, is that the dissection area can be lim­ited in order to facilitate a tension-free anas­tomosis. Therefore, the Billroth I procedure is commonly used for benign disease or distally located EGC in Korea. However, Kim et al. [19] compared results from 122 gastric carci­noma patients undergoing Billroth I and Bill­roth II gastrectomy. They evaluated postgas­trectomy syndrome with a survey of abdominal symptoms, and dumping syndrome was mea­sured using the Sigstad dumping score. Accord­ing to their results, the occurrence of abdominal
130 K. H. Pak and S. H. Noh
symptoms and dumping syndrome was lower in the Billroth I group than in the Billroth II group. Furthermore, pylorus-preserving gastrectomy (PPG) is a kind of reduced-gastric operation that preserves the distal portion (1.5 cm) of the gastric antrum and reduces postoperative com­plications such as dumping syndrome and re­flux esophagitis [20]. However, a limitation of this operation is that complete lymph node (LN) dissection of the suprapyloric LN is undesirable for the preservation of the pyloric branch of the vagus nerve. Nowadays, some reports state that this procedure may be applicable in EGC con­fined to the mucosa and located at the gastric mid-body [21].
According to a recent Japanese large-scale in­vestigation into dumping syndrome after gastrec­tomy for gastric cancer, [22] many more patients suffer from early dumping syndrome (67.6 %) than from late dumping syndrome (38.4 %) after gastrectomy. This study revealed that patients suffering from at least one symptom of early dumping syndrome were significantly more like­ly to also experience symptoms of late dumping syndrome. The study also demonstrated that two clinical factors, the surgical procedures used and the amount of weight loss, were significantly as­sociated with the occurrence of both early and late dumping syndromes. Consistent with pre­vious reports, [23, 24] patients who underwent PPG showed the lowest incidence of dumping syndrome. In addition, patients who underwent PG (proximal gastrectomy with jejunal interpo­sition) showed the second highest incidence of early dumping syndrome. Patients who under­went RYGJ showed a lower incidence of dump­ing syndrome symptoms relative to Billroth I pa­tients. Taken together, RYGJ or Billroth I is less associated with dumping syndrome after distal gastrectomy than Billroth II.
Management of Dumping Syndrome
The first step in treating dumping syndrome is the introduction of dietary modification. If this ap­proach is insufficient, medical therapy and, in some cases, surgery might be considered (Fig. 13.2).
Fig.13 .2 Proposed treatment algorithm for dumping syn- drome
Diet
The resolution of dumping symptoms is achieved in most cases by dietary modification, in particu­lar by the reduction of carbohydrate intake, and lifestyle adjustment.
Dietary measures include advising patients to consume smaller amounts at one time by di­viding the recommended daily energy intake be­tween six meals. Dietary prohibitions are very important. Fluid intake during meals should be restricted. Drinking liquids should be avoided for at least one half-hour after a meal. Complex car­bohydrates (e.g., unsweetened cereals, pasta, po­tatoes, fresh fruit, and vegetables) are preferred. All rapidly absorbable carbohydrates (e.g., all