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Dumping syndrome in children
Dumping syndrome in children Dumping syndrome d e v e l o p e d in seven children after gastric surgery, (Nissen fundoplication in six, Whipple procedure in one). The patients ranged from a g e 10 months to !3 years, and four of the seven were neurologically impaired. The diagnosis was m a d e by demonstrating an abnormal response to an orally administered glucose challenge. The pediatric literature records only eight cases, but we believe that dumping syndrome is more c o m m o n in children than once believed. Dietary m a n a g e m e n t can often dramatically diminish the associated symptoms. (J PEDIATR1987;110:212-5) M a u r e e n E. Caulfield, M.D., Robert Wyllie, M.D., Hugh V. Firor, M.D., a n d William Michener, M.D. From the Departments of Pediatrics and Adolescent Medicine, Gastroenterology, a0d General Surgery, The Cleveland Clinic Foundation, Cleveland
Dumping syndrome is a complex of postprandial symptoms including abdominal discomfort, diaphoresis, pallor, lethargy, and diarrhea, and may occur after gastric surgery. It is well described in adults but rarely considered in the symptomatic postoperative pediatric patient, t We review our experience with a group of seven patients, aged 10 months to 13 years, four of whom were neurologically impaired, who developed dumping syndrome after Nissen fundoplication (six patients) or Whipple procedure (1). METHODS We saw seven patients with dumping syndrome at our institution from February 1984 through December 1985. We suspected dumping syndrome from their histories of postprandial irritability and diaphoresis, and diagnosed it by demonstrating an abnormal response to a glucose tolerance test. For this test, each child received orally a bolus of 1.75 g/kg glucose; blood samples were collected every 30 to 60 minutes for 3 hours. For each child, dietary modifications reduced the postprandial symptoms. Pertinent historical data are summarized in the Table.
RESULTS Typically, these patients began having postprandial symptoms of irritability and diaphoresis 1 to 2 weeks after gastric surgery, most often after Nissen fundoplication. Associated complaints included abdominal distention, diarrhea, and failure to gain weight. All of the children underwent additional testing (endoscopy and esophageal pH probe) before the diagnosis of dumping syndrome was made. Less than half of the patients had their operations a t our institution; the majority were referred after gastric operations done elsewhere. Each patient's fasting blood sugar concentration was normal. All children had hyperglycemia within 1 hour of receiving an orally administered glucose load, followed by significant hypoglycemia (Figure). The mean peak glucose concentration was 333 mg/dL, occurring 30 to 60 minutes after the oral challenge. The mean trough glucose value was 50 mg/dL, occurring 60 to 120 minutes after the peak. Dietary modifications were prescribed for all patients, ranging from small, frequent, low-carbohydrate meals to continuous gastric tube feeding of carbohydrate-free formula. All children had fewer symptoms after dietary changes and were able to gain weight. DISCUSSION
Submitted for publication July 14, 1986; accepted Sept. 24, 1986. Reprint requests: Robert Wyllie, M.D., The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44106.
212
Dumping syndrome is divided clinically into early and late syndromes. 2,3 Early dumping symptoms, which occur 10 to 20 minutes after meals, include abdominal corn-
Volume 110 Number 2
Dumping syndrome
2 13
400 z~ Patient I v Patient 2 A Patient II Patient 4 13 Patient 5 o Patient 6 9 Patient 7
500
F 200 o
U E)
t00
0 i
1
I
t
I
0
30
45
(50
,,
I
1
I
1
90
t20
150
180
TIME {minutes)
Figure. Shaded area, normal range of blood glucose values after oral ingestion of t.75 g/kg glucose, with values for seven patients in our series superimposed. All fasting blood glucose values (at 0 minutes) were within normal range. After glucose challenge, all patients had marked hyperglycemia followed by hypoglycemia. plaints (bloating, nausea, eructation, colic, and explosive diarrhea) and systemic symptoms of weakness, diaphoresis, dizziness, pallor, and palpitations. Even in adults, the incidence of early dumping is unknown because the diagnosis is based on the patient'S description, although it is estimated to follow 8% to 15% of gastric operations because of peptic ulcer disease. Late dumping, better described as late postprandial hypoglycemia, occurs 1 to 4 hours after meals and is associated with complaints of diaphoresis, palpitations, weakness, and lethargy; gastrointestinal symptoms are usually mild or absent. The diagnosis of late dumping syndrome is made by demonstrating an abnormal response to an orally administered glucose challenge. Typically, blood glucose concentration rises rapidly to well above the normal range, then plunges to hypogtycemic levels. Late dumping is thought to occur less frequently than early dumping in adults, and although the two would be expected to occur in sequence, the relationship is clinically inconsistent and unpredictable. We could demonstrate late postprandial hypoglycemia in all of our patients, although in one patient initial results of glucose tolerance testing were normal. Five children seemed to have abdominal symptoms as well, which suggests that these patients may have had both early and
late dumping symptoms. In retrospective review, symptoms developed Within the first few postoperative months; the mean interval between operation and diagnosis of dumping syndrome was 12 months. The lag time was related to the nonspecific quality of the symptoms in a largely nonverbal population and to the absence of consideration of dumping syndrome in the differential diagnosis. The pathophysiology of the syndrome is complex and not fully understood. Early dumping is thought to occur most frequently when pyloric sphincter function is disrupted, resulting in abnormal gastric emptying of liquids.4-7 Rapid distention of the jejunum may account for most of the abdominal symptoms. In addition, hypertonicity of gastric fluid in the jejunum causes neuronal vasopeptidemediated changes that increase splanchnic blood flow and decrease circulating blood volume. These changes are clinically manifested by symptoms of autonomic instabilit y ) -1~ Late postprandial hypoglyemia is thought to be caused by hyperinsulinemia evoked by the rapid initial rise of blood glucose concentration. Nissen fundoplication, the most common gastric operation performed in children, eliminates the fundus as a storage area for gastric content and air. The vagus nerves are left intact, and most antireflux procedures do not
Z14
Caulfield et al.
The Journal of Pediatrics February 1987
Table. Clinical data
Patient
Age at operation
Age at diagnosis of dumping syndrome
(yr)
(yr)
Operative procedure Nissen fundoplication
2
~42
3~2
Nissen fundoplication
3
4
4~2
Whipple procedure
4
l~f2 2~2
2~2
Nissen fundoplication Revision of Nissen fundoplication and gastrostomy* Nissen fundoplication Gastrostomy*
5
13
13y2
6
~2
~,~2
Nissen fundoplication Gastrostomy
7
1
4
Nissen fundoplication Gastrostomy*
Medical therapy prior to surgery
Gastrointestinal diagnoses
Associated conditions
Tracheoesophageal fistula Gastroes0Phageal reflux Pyloric stenosis Gastroesophageal reflux Pyloric stenosis Pancreatic tumor: spindle cell Gastroesophageal reflux
Atrial septal defect Ventricular septal defect Scoliosis
Unknown
CHARGE syndrome Mental retardation None
Unknown
Williams syndrome Mental retardation
Metoclopramide Cimetidine
Gastroesophageal reflux
Severe mental retardation Severe growth failure None
Cimetidine
Gastroesophageal reflux Meconium ileus Gastroesophageal reflux
Cerebellar hypoplasia Mental retardation
None
Metoclopramide Bethanechol Antacids Bethanechol Cimetidine
*Operation performedat our institution. include pyloroplasty. Thus, in contrast to adult gastric operations, vagotomy and pyloroplasty cannot account for the initiation of dumping after fundopiication. A number of factors may predispose children to dumping. The first is the elimination of fundus storage capacity, which leads to increased transpyloric pressure by reducing adaptive relaxation and ultimately accelerating gastric emptying. Second is the common practice of placing gastrostomy tubes in patients with feeding problems secondary to gastrointestinal anomalies Or severe retardation. These children are given carbohydrate-rich and osmotically active liquid feedings, which may provoke intravascular fluid shifts and hyperinsulinism. The third factor includes disruption of pytoric function by vagotomy (deliberate or inadvertent), gastrectomy, or py|oroplasty; the indications for these procedures in children are rare. Nissen fundoplication effectively prevents the gastroesophageal reflux that persists after a trial of medical management. 1~ It is a relatively common operation in children with tracheoesophagea! fistulas and hiatal hernias, and is being done more often in severely retarded children, who have a high incidence of gastroesophageal reflux.12
We found only eight documented cases of dumping syndrome ~>18in the pediatric literature. All eight l~atients were younger than age 13 months and were not neurologically impaired. Because we have Seen nearly as many cases as have been recorded, we believe that dumping syndrom e as a comPlication of fundoplication occurs more frequently than previously reported. In addition, five of the seven children in our series were older than age 3 years when the syndrome was first diagnosed; four of these five patients were neurologically impaired. Our treatment of dumping syndrome was usually conservative. The diet was modified to decrease the amount of food and glucose delivered to the stomach at each meal and to increase the intake of solid food. i9'20 Specific nutritional changes included limiting the daily carbohydrate intake to approximately 2 g/kg. Several Children were given a carbohydrate-free formula supplemented with 2 g / k g / d a y fructose; medium-chain triglycerides provided additional calories when needed. Like adults with dumping syndrome, most of our patients appeared to have fewer symptoms after their diets were modified. There are no reports of refractory pediatric cases managed more aggressively with pectin, insulin, tolbutamide, or somatostatin, 1~ nor have
Volume 110 Number 2
surgical procedures been used to delay gastric emptying, as in reversed jejunal loop interposition between the stomach and duodenum, the Roux-en-u jejunal pouch operation of Lygidakis (which creates a recirculating loop), or pyloric reconstruction.22. 23 Our experience suggests that dumping syndrome occurs frequently but often is not recognized. The majority of cases occur in children at high risk for gastroesophageal reflux, such as infants with tracheoesophageal fistula or hiatal hernia, and the severely mentally retarded. To make a timely diagnosis, pediatricians should suspect dumping syndrome in these nonverbal patients. Oral glucose tolerance testing should be part of the evaluation of symptoms in postoperative pediatric patients, and the glucose challenge may need to be repeated if the initial test results are normal and the symptoms continue. Once the diagnosis has been es'tablished, the patient should be given frequent, small, low-carbohydrate feedings. REFERENCES
1. Rodgers BM, Talbert JL. Complications following gastric surgery in children. Major Probl Clin Surg 1976;20:147. 2. Woodward ER. The early postprandial dumping syndrome: clinical manifestations and pathogenesis. Major Probl Clin Surg 1976;20:1. 3. Woodward ER, Neustein CL. The late postprandial dumping syndrome. Major Probl Clin Surg 1976;20:28. 4. Lawaeltz O, Aritas Y, Blackburn AM, Ralphs DNL. Gastric emptying after peptic ulcer surgery: some pathophysiological mechanisms of the dumping syndrome. Scand J Gastroenterol 1982;17:1065. 5. Lawaetz O, Blackburn AM, Bloom SR, Aritas Y, Ralphs DNL. Gut hormone profile and gastric emptying in the dumping syndrome: a hypothesis concerning pathogenesis. Scand J Gastroenterol 1983;18:73. 6. Moir IH. The role of altered gastric emptying in the initiation of clinical dumping. Scand J Gastroenterol 1979;14:463. 7. Sagor GR, Bryant MG, Ghatei MA, Kirk RM, Bloom SR. Release of vasoactive intestinal peptide in the dumping syndrome. Br Med J 1981;282:507. 8. Ralphs DNR, Thomson JPS, Haynes S, Lawson-Smith C,
Dumping syndrome
9. 10. 11.
12. 13.
14.
15.
16.
17.
18.
19. 20. 21.
22.
23.
2 15
Nobsley M, Le Quesne LP. The relationship between the rate of gastric emptying and the dumping syndrome. Br J Surg 1978;65:637. Stahlgren LH. The dumping syndrome: a study of its hemodynamics. Hosp Pract 1970;5:59. Long RG, Adrian TE, Bloom SR. Somatostatin and the dumping syndrome. Br Meal J 1985;290:886. Fonkalsrud EW, Ament ME, Byrne W J, Rachelefsky GS. Gastroesophageal fundoplication for the management of reflux in infants and children. J Thorac Cardiovasc Surg 1978;76:655. Sondheimer JM, Morris BA. Gastroesophageal reflux among severely retarded children. J PEDIATR 1979;94:710. Pellerin D, Fekete CN, Herbinet E. Traitement de la hernie hiatale et de l'oesophagite peptique de l'enfant par l'intervention combin~e: reposition-Nissen-pyloroplastine. Experience de 90 cas de 1960 a 1971. Ann Chir 1973;27:845. Kuffer F, Bettex M. Hiatus hernia in infants: early and late complications following fundoplication. Z Kinderchir 1974; 14:153. Safaie S, Zike W, Anuras S. Nissen fundoplication without crural repair: a cure for reflux esophagitis. Arch Surg 1974; 108:424. Villet R, Boureau M, Hayat P, Weisgerber G. Une complication grave de l'op~ration de Nissen: le dumping-syndrome. Chir Pediatr 1978;19:269. Meyer S, Deckelbaum R J, Lax E, Schiller M. Infant dumping syndrome after gastroesophageal reflux surgery. J PEDIATR 1981;99:235. Hersig J, Hartmud B, Tuchshmid P. Dumping syndrome following Nissen's fundoplication: a cause for refusal to feed. J Pediatr Surg 1984;19:155. Unser HL. Principles of diet therapy for postgastrectomy dumping syndrome. Major Probl Clin Surg 1976;20:159. Chaimoff C, Dintsman M. The long-term fate of patients with dumping syndrome. Arch Surg 1972;105:554. Leeds AR, Ralphs DN, Ebied F, Metz G, Dilawari JB. Pectin in the dumping syndrome: reduction of symptoms and plasma volume changes. Lancet 1981;1:1075. Miranda R, Steffes B, O'Leary JP, Woodward ER. Surgical treatment of the postgastrectomy dumping syndrome. Am J Surg 1980;139:40. Sawyers JL, Herrington JL. Treatment of postgastreetomy syndromes. Am Surg 1980;46:201.
Dumping syndrome is a complex of postprandial symptoms including abdominal discomfort, diaphoresis, pallor, lethargy, and diarrhea, and may occur after gastric surgery. It is well described in adults but rarely considered in the symptomatic postoperative pediatric patient, t We review our experience with a group of seven patients, aged 10 months to 13 years, four of whom were neurologically impaired, who developed dumping syndrome after Nissen fundoplication (six patients) or Whipple procedure (1). METHODS We saw seven patients with dumping syndrome at our institution from February 1984 through December 1985. We suspected dumping syndrome from their histories of postprandial irritability and diaphoresis, and diagnosed it by demonstrating an abnormal response to a glucose tolerance test. For this test, each child received orally a bolus of 1.75 g/kg glucose; blood samples were collected every 30 to 60 minutes for 3 hours. For each child, dietary modifications reduced the postprandial symptoms. Pertinent historical data are summarized in the Table.
RESULTS Typically, these patients began having postprandial symptoms of irritability and diaphoresis 1 to 2 weeks after gastric surgery, most often after Nissen fundoplication. Associated complaints included abdominal distention, diarrhea, and failure to gain weight. All of the children underwent additional testing (endoscopy and esophageal pH probe) before the diagnosis of dumping syndrome was made. Less than half of the patients had their operations a t our institution; the majority were referred after gastric operations done elsewhere. Each patient's fasting blood sugar concentration was normal. All children had hyperglycemia within 1 hour of receiving an orally administered glucose load, followed by significant hypoglycemia (Figure). The mean peak glucose concentration was 333 mg/dL, occurring 30 to 60 minutes after the oral challenge. The mean trough glucose value was 50 mg/dL, occurring 60 to 120 minutes after the peak. Dietary modifications were prescribed for all patients, ranging from small, frequent, low-carbohydrate meals to continuous gastric tube feeding of carbohydrate-free formula. All children had fewer symptoms after dietary changes and were able to gain weight. DISCUSSION
Submitted for publication July 14, 1986; accepted Sept. 24, 1986. Reprint requests: Robert Wyllie, M.D., The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44106.
212
Dumping syndrome is divided clinically into early and late syndromes. 2,3 Early dumping symptoms, which occur 10 to 20 minutes after meals, include abdominal corn-
Volume 110 Number 2
Dumping syndrome
2 13
400 z~ Patient I v Patient 2 A Patient II Patient 4 13 Patient 5 o Patient 6 9 Patient 7
500
F 200 o
U E)
t00
0 i
1
I
t
I
0
30
45
(50
,,
I
1
I
1
90
t20
150
180
TIME {minutes)
Figure. Shaded area, normal range of blood glucose values after oral ingestion of t.75 g/kg glucose, with values for seven patients in our series superimposed. All fasting blood glucose values (at 0 minutes) were within normal range. After glucose challenge, all patients had marked hyperglycemia followed by hypoglycemia. plaints (bloating, nausea, eructation, colic, and explosive diarrhea) and systemic symptoms of weakness, diaphoresis, dizziness, pallor, and palpitations. Even in adults, the incidence of early dumping is unknown because the diagnosis is based on the patient'S description, although it is estimated to follow 8% to 15% of gastric operations because of peptic ulcer disease. Late dumping, better described as late postprandial hypoglycemia, occurs 1 to 4 hours after meals and is associated with complaints of diaphoresis, palpitations, weakness, and lethargy; gastrointestinal symptoms are usually mild or absent. The diagnosis of late dumping syndrome is made by demonstrating an abnormal response to an orally administered glucose challenge. Typically, blood glucose concentration rises rapidly to well above the normal range, then plunges to hypogtycemic levels. Late dumping is thought to occur less frequently than early dumping in adults, and although the two would be expected to occur in sequence, the relationship is clinically inconsistent and unpredictable. We could demonstrate late postprandial hypoglycemia in all of our patients, although in one patient initial results of glucose tolerance testing were normal. Five children seemed to have abdominal symptoms as well, which suggests that these patients may have had both early and
late dumping symptoms. In retrospective review, symptoms developed Within the first few postoperative months; the mean interval between operation and diagnosis of dumping syndrome was 12 months. The lag time was related to the nonspecific quality of the symptoms in a largely nonverbal population and to the absence of consideration of dumping syndrome in the differential diagnosis. The pathophysiology of the syndrome is complex and not fully understood. Early dumping is thought to occur most frequently when pyloric sphincter function is disrupted, resulting in abnormal gastric emptying of liquids.4-7 Rapid distention of the jejunum may account for most of the abdominal symptoms. In addition, hypertonicity of gastric fluid in the jejunum causes neuronal vasopeptidemediated changes that increase splanchnic blood flow and decrease circulating blood volume. These changes are clinically manifested by symptoms of autonomic instabilit y ) -1~ Late postprandial hypoglyemia is thought to be caused by hyperinsulinemia evoked by the rapid initial rise of blood glucose concentration. Nissen fundoplication, the most common gastric operation performed in children, eliminates the fundus as a storage area for gastric content and air. The vagus nerves are left intact, and most antireflux procedures do not
Z14
Caulfield et al.
The Journal of Pediatrics February 1987
Table. Clinical data
Patient
Age at operation
Age at diagnosis of dumping syndrome
(yr)
(yr)
Operative procedure Nissen fundoplication
2
~42
3~2
Nissen fundoplication
3
4
4~2
Whipple procedure
4
l~f2 2~2
2~2
Nissen fundoplication Revision of Nissen fundoplication and gastrostomy* Nissen fundoplication Gastrostomy*
5
13
13y2
6
~2
~,~2
Nissen fundoplication Gastrostomy
7
1
4
Nissen fundoplication Gastrostomy*
Medical therapy prior to surgery
Gastrointestinal diagnoses
Associated conditions
Tracheoesophageal fistula Gastroes0Phageal reflux Pyloric stenosis Gastroesophageal reflux Pyloric stenosis Pancreatic tumor: spindle cell Gastroesophageal reflux
Atrial septal defect Ventricular septal defect Scoliosis
Unknown
CHARGE syndrome Mental retardation None
Unknown
Williams syndrome Mental retardation
Metoclopramide Cimetidine
Gastroesophageal reflux
Severe mental retardation Severe growth failure None
Cimetidine
Gastroesophageal reflux Meconium ileus Gastroesophageal reflux
Cerebellar hypoplasia Mental retardation
None
Metoclopramide Bethanechol Antacids Bethanechol Cimetidine
*Operation performedat our institution. include pyloroplasty. Thus, in contrast to adult gastric operations, vagotomy and pyloroplasty cannot account for the initiation of dumping after fundopiication. A number of factors may predispose children to dumping. The first is the elimination of fundus storage capacity, which leads to increased transpyloric pressure by reducing adaptive relaxation and ultimately accelerating gastric emptying. Second is the common practice of placing gastrostomy tubes in patients with feeding problems secondary to gastrointestinal anomalies Or severe retardation. These children are given carbohydrate-rich and osmotically active liquid feedings, which may provoke intravascular fluid shifts and hyperinsulinism. The third factor includes disruption of pytoric function by vagotomy (deliberate or inadvertent), gastrectomy, or py|oroplasty; the indications for these procedures in children are rare. Nissen fundoplication effectively prevents the gastroesophageal reflux that persists after a trial of medical management. 1~ It is a relatively common operation in children with tracheoesophagea! fistulas and hiatal hernias, and is being done more often in severely retarded children, who have a high incidence of gastroesophageal reflux.12
We found only eight documented cases of dumping syndrome ~>18in the pediatric literature. All eight l~atients were younger than age 13 months and were not neurologically impaired. Because we have Seen nearly as many cases as have been recorded, we believe that dumping syndrom e as a comPlication of fundoplication occurs more frequently than previously reported. In addition, five of the seven children in our series were older than age 3 years when the syndrome was first diagnosed; four of these five patients were neurologically impaired. Our treatment of dumping syndrome was usually conservative. The diet was modified to decrease the amount of food and glucose delivered to the stomach at each meal and to increase the intake of solid food. i9'20 Specific nutritional changes included limiting the daily carbohydrate intake to approximately 2 g/kg. Several Children were given a carbohydrate-free formula supplemented with 2 g / k g / d a y fructose; medium-chain triglycerides provided additional calories when needed. Like adults with dumping syndrome, most of our patients appeared to have fewer symptoms after their diets were modified. There are no reports of refractory pediatric cases managed more aggressively with pectin, insulin, tolbutamide, or somatostatin, 1~ nor have
Volume 110 Number 2
surgical procedures been used to delay gastric emptying, as in reversed jejunal loop interposition between the stomach and duodenum, the Roux-en-u jejunal pouch operation of Lygidakis (which creates a recirculating loop), or pyloric reconstruction.22. 23 Our experience suggests that dumping syndrome occurs frequently but often is not recognized. The majority of cases occur in children at high risk for gastroesophageal reflux, such as infants with tracheoesophageal fistula or hiatal hernia, and the severely mentally retarded. To make a timely diagnosis, pediatricians should suspect dumping syndrome in these nonverbal patients. Oral glucose tolerance testing should be part of the evaluation of symptoms in postoperative pediatric patients, and the glucose challenge may need to be repeated if the initial test results are normal and the symptoms continue. Once the diagnosis has been es'tablished, the patient should be given frequent, small, low-carbohydrate feedings. REFERENCES
1. Rodgers BM, Talbert JL. Complications following gastric surgery in children. Major Probl Clin Surg 1976;20:147. 2. Woodward ER. The early postprandial dumping syndrome: clinical manifestations and pathogenesis. Major Probl Clin Surg 1976;20:1. 3. Woodward ER, Neustein CL. The late postprandial dumping syndrome. Major Probl Clin Surg 1976;20:28. 4. Lawaeltz O, Aritas Y, Blackburn AM, Ralphs DNL. Gastric emptying after peptic ulcer surgery: some pathophysiological mechanisms of the dumping syndrome. Scand J Gastroenterol 1982;17:1065. 5. Lawaetz O, Blackburn AM, Bloom SR, Aritas Y, Ralphs DNL. Gut hormone profile and gastric emptying in the dumping syndrome: a hypothesis concerning pathogenesis. Scand J Gastroenterol 1983;18:73. 6. Moir IH. The role of altered gastric emptying in the initiation of clinical dumping. Scand J Gastroenterol 1979;14:463. 7. Sagor GR, Bryant MG, Ghatei MA, Kirk RM, Bloom SR. Release of vasoactive intestinal peptide in the dumping syndrome. Br Med J 1981;282:507. 8. Ralphs DNR, Thomson JPS, Haynes S, Lawson-Smith C,
Dumping syndrome
9. 10. 11.
12. 13.
14.
15.
16.
17.
18.
19. 20. 21.
22.
23.
2 15
Nobsley M, Le Quesne LP. The relationship between the rate of gastric emptying and the dumping syndrome. Br J Surg 1978;65:637. Stahlgren LH. The dumping syndrome: a study of its hemodynamics. Hosp Pract 1970;5:59. Long RG, Adrian TE, Bloom SR. Somatostatin and the dumping syndrome. Br Meal J 1985;290:886. Fonkalsrud EW, Ament ME, Byrne W J, Rachelefsky GS. Gastroesophageal fundoplication for the management of reflux in infants and children. J Thorac Cardiovasc Surg 1978;76:655. Sondheimer JM, Morris BA. Gastroesophageal reflux among severely retarded children. J PEDIATR 1979;94:710. Pellerin D, Fekete CN, Herbinet E. Traitement de la hernie hiatale et de l'oesophagite peptique de l'enfant par l'intervention combin~e: reposition-Nissen-pyloroplastine. Experience de 90 cas de 1960 a 1971. Ann Chir 1973;27:845. Kuffer F, Bettex M. Hiatus hernia in infants: early and late complications following fundoplication. Z Kinderchir 1974; 14:153. Safaie S, Zike W, Anuras S. Nissen fundoplication without crural repair: a cure for reflux esophagitis. Arch Surg 1974; 108:424. Villet R, Boureau M, Hayat P, Weisgerber G. Une complication grave de l'op~ration de Nissen: le dumping-syndrome. Chir Pediatr 1978;19:269. Meyer S, Deckelbaum R J, Lax E, Schiller M. Infant dumping syndrome after gastroesophageal reflux surgery. J PEDIATR 1981;99:235. Hersig J, Hartmud B, Tuchshmid P. Dumping syndrome following Nissen's fundoplication: a cause for refusal to feed. J Pediatr Surg 1984;19:155. Unser HL. Principles of diet therapy for postgastrectomy dumping syndrome. Major Probl Clin Surg 1976;20:159. Chaimoff C, Dintsman M. The long-term fate of patients with dumping syndrome. Arch Surg 1972;105:554. Leeds AR, Ralphs DN, Ebied F, Metz G, Dilawari JB. Pectin in the dumping syndrome: reduction of symptoms and plasma volume changes. Lancet 1981;1:1075. Miranda R, Steffes B, O'Leary JP, Woodward ER. Surgical treatment of the postgastrectomy dumping syndrome. Am J Surg 1980;139:40. Sawyers JL, Herrington JL. Treatment of postgastreetomy syndromes. Am Surg 1980;46:201.