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SOMATOSTATIN IN GASTROINTESTINAL FISTULAE
1381 SOMATOSTATIN IN GASTROINTESTINAL FISTULAE
SiR,-Somatostatin inhibits both the release of gastrointestinal hormones and gastric and pancreatic secretion. Some of these effects are probably related to its action in reducing splanchnic blood flow, and it has been used in the management of gastrointestinal haemorrhage.l However, its antisecretory properties seemed potentially useful in the management of persistent upper gastrointestinal fistulae which have not responded to other measures. We report three cases where somatostatin was used in this way. A 49-year-old man who had undergone a partial gastrectomy for carcinoma 3 years previously was readmitted with acute smallbowel obstruction. At laparotomy obliterative peritonitis was found. Several loops of small bowel were decompressed. Postoperatively several small-bowel fistulae developed and radiologically complete obstruction at the duodenojejunal flexure and at several other points in the small bowel was demonstrated. A gastrostomy stoma was created and he was fed intravenously. The fistulae continued to discharge large volumes (up to 1700 ml in a day). After a week in which the average daily output had been more than 1 litre somatostatin was given intravenously (6 mg per 24 h for 2 days and then 3 mg per 24 h for 5 days) with a reduction in average fistula output to 700 ml. After discontinuation of somatostatin output remained low for a week (240 ml), allowing the skin to heal and the smaller amounts of effluent to be trapped much more effectively. In the next 7 days output rose to 530 ml daily, but in the next 27 days the average was only 150 ml (range 0-360 ml). The patient died 4 months later with recurrent carcinoma. A 68-year-old woman had had endoscopic sphincterotomy for common bileduct stones which had resulted in septicaemic shock and renal failure. She bled from the sphincterotomy site and two operations were required to control the bleeding. A high duodenal fistula then developed which did not respond to 2 weeks of total parenteral nutrition and complete bowel rest. Somatostatin was given intravenously for 6 days and resulted in a reduction in fistula output from an average of 840 ml (range 300-1400 ml) for 13 days to 380 ml (range 250-700 ml) in the somatostatin period. When the somatostatin was stopped output remained low at 170 ml (range 80-220 ml) and 4 days later the fistula had dried up and healed. 3 weeks later she was discharged eating normally, and she remains well. A 45-year-old woman with Crohn’s disease had a chronic right iliac fossa fistula originating from the ileum, with evidence ofa more distal stricture. Several attempts to excise the affected segment had failed and she had lost a lot of weight. Despite parenteral feeding and restriction of oral intake she found her fistula difficult to manage because of large fluid losses and excoriation. 5 days of intravenous somatostatin reduced the fistula output from 1800 to 400 ml daily, and this improvement was maintained when she returned home. A further course of somatostatin 10 weeks later resulted in a small further reduction. She remains on home parenteral nutrition and can manage the reduced amount of fistula discharge with a stoma bag. Adequate nutritional support is essential in the management of enterocutaneous fistulae2 and complete bowel rest reduces the volume of experimental fistulae by up to 90%.3 However, not all fistulae close spontaneously, even with parenteral nutrition and bowel rest rigorously applied.4 Failure is usually associated with high fistula output, intercurrent sepsis, distal obstruction, or wound disruption,sand such patients may benefit from hormonal manipulation of gastrointestinal secretions. Somatostatin reduces gastrointestinal secretions but it is not clear in these cases why the reduction was maintained when the infusions stopped. Fistula tracks are often colonised with bacteria, so that reducing the flow of potential substrates lowers the bacterial count and reduces their irritant byproducts. This may allow healing or at least a manageable discharge from a fistula surrounded by healthy skin. Somatostatin may be a significant advance over conventional conservative therapy for persistent gastrointestinal fistulae, offering shorter hospital stays (against which must be set the cost of somatostatin, L980 for 5 days). We suggest that somatostatin be
reserved for patients with high-output fistulas5 or where parenteral nutrition and complete intake restriction for one month have not resulted in spontaneous closure.Somatostatin may allow an operative approach to be delayed until septic foci have been treated and nutritional status improved, and the patient may be able to convalesce at home. We thank Mr R. M. R. Taylor, Mr I. F. McNeill, and Mr B. V. McEvedy for permission to publish details of these cases.
Department of Surgery, Royal Victoria Infirmary, Newcastle upon Tyne NE1 1 4LP
A.
J.
J. RICH R. C. SAINSBURY
KW, Henry DA, Davies JG, Hine KR, Hawkey CJ, Langman MJS. Somatostatin in treatment of haematemesis and melaena. Lancet 1985; i: 130-32. 2. Chapman R, Foran R, Dunphy JE. Management of intestinal fistulas. Am J Surg 1964; 1. Somerville
108: 157-64. 3. Wolfe
BM, Keltner RM, Willman VL. Intestinal fistula output in regular, elemental and intravenous alimentation. Am J Surg 1972; 149: 333-36. 4. Reber HA, Roberts C, Way LV, et al. Management of external gastrointestinal fistulas. Ann Surg 1978; 188: 460-67. 5. Sitges-Serra A, Jaurrieta E, Sitges-Creus A. Management of postoperative enterocutaneous fistulas: the roles of parenteral nutrition and surgery. Br J Surg 1982; 69: 147-50.
GENESIS OF GASTRIC STUMP CARCINOMA
SIR,—Dr Caygill and colleagues (April 26, p 929) demonthat gastric surgery for benign disease, whether gastrec-
strate
tomy or vagotomy and drainage, significantly increases the risk of carcinoma developing in the remaining stomach. They implicate "bile reflux" in the aetiology of the disease. Evidence from animal studies suggests that surgically induced duodenogastric reflux will produce neoplastic change within a year.’ Which fraction of the reflux is responsible, bile or pancreaticoduodenal secretions, is not known. Our study2was done to find out, by surgery designed to produce reflux of bile or pancreaticoduodenal secretions or both, which fraction of duodenogastric reflux is responsible. The controls were animals with a gastrotomy but no reflux. After 9 months the animals were killed and the stomachs removed and examined for the presence of adenocarcinoma. Adenocarcinoma was detected in 17/26 animals with pancreaticoduodenal reflux alone (10/14) or with bile reflux (7/12) but in none of the 8 controls and in none of the 6 rats with bile reflux only. The differences in frequency between controls and animals with pancreaticoduodenal secretions (p<001) and reflux of both secretions (p < 0-05) were significant (X2 test) as was the difference between pancreaticoduodenal secretions and bile reflux only (p < 0-02). These findings suggest that duodenogastric reflux plays an important part in the aetiology of gastric stump carcinoma in the rat and that pancreaticoduodenal secretions and not bile are implicated. This may help to explain the findings of Caygill and colleagues, and emphasises the need to use the term duodenogastric reflux rather than bile reflux since this term ignores the pancreatic and duodenal components of the reflex.
Department of Surgery and Histopathology Guy’s Hospital, London SE1 9RT
R. C. MASON P. R. TAYLOR P. H. ROWE N. O. ASTON M. I. FILIPE W. J. OWEN
Langhans P, Heger RA, Hohenstein J, Schlake W, Bunter H. Operation-sequel carcinoma of the stomach: Experimented studies of surgical techniques with or without resection. World J Surg 1981; 5: 595-605. 2. Mason RC. Duodenogastric reflux in rat gastric carcinoma. Br J Surg (in press). 3. Mason RC, Brame KG, Filipe MI, Owen WJ. The long term effects of duodenogastric reflux on rat gastric mucosa. Gut 1986; 27: A634. 1.
SEROTYPING CAMPYLOBACTER
SIR,-Dr Fricker (March 8, p 554), referring to campyloserotyping schemes, proposes acceptance of the passive haemagglutination method based on heat-stable antigens as the bacter
SiR,-Somatostatin inhibits both the release of gastrointestinal hormones and gastric and pancreatic secretion. Some of these effects are probably related to its action in reducing splanchnic blood flow, and it has been used in the management of gastrointestinal haemorrhage.l However, its antisecretory properties seemed potentially useful in the management of persistent upper gastrointestinal fistulae which have not responded to other measures. We report three cases where somatostatin was used in this way. A 49-year-old man who had undergone a partial gastrectomy for carcinoma 3 years previously was readmitted with acute smallbowel obstruction. At laparotomy obliterative peritonitis was found. Several loops of small bowel were decompressed. Postoperatively several small-bowel fistulae developed and radiologically complete obstruction at the duodenojejunal flexure and at several other points in the small bowel was demonstrated. A gastrostomy stoma was created and he was fed intravenously. The fistulae continued to discharge large volumes (up to 1700 ml in a day). After a week in which the average daily output had been more than 1 litre somatostatin was given intravenously (6 mg per 24 h for 2 days and then 3 mg per 24 h for 5 days) with a reduction in average fistula output to 700 ml. After discontinuation of somatostatin output remained low for a week (240 ml), allowing the skin to heal and the smaller amounts of effluent to be trapped much more effectively. In the next 7 days output rose to 530 ml daily, but in the next 27 days the average was only 150 ml (range 0-360 ml). The patient died 4 months later with recurrent carcinoma. A 68-year-old woman had had endoscopic sphincterotomy for common bileduct stones which had resulted in septicaemic shock and renal failure. She bled from the sphincterotomy site and two operations were required to control the bleeding. A high duodenal fistula then developed which did not respond to 2 weeks of total parenteral nutrition and complete bowel rest. Somatostatin was given intravenously for 6 days and resulted in a reduction in fistula output from an average of 840 ml (range 300-1400 ml) for 13 days to 380 ml (range 250-700 ml) in the somatostatin period. When the somatostatin was stopped output remained low at 170 ml (range 80-220 ml) and 4 days later the fistula had dried up and healed. 3 weeks later she was discharged eating normally, and she remains well. A 45-year-old woman with Crohn’s disease had a chronic right iliac fossa fistula originating from the ileum, with evidence ofa more distal stricture. Several attempts to excise the affected segment had failed and she had lost a lot of weight. Despite parenteral feeding and restriction of oral intake she found her fistula difficult to manage because of large fluid losses and excoriation. 5 days of intravenous somatostatin reduced the fistula output from 1800 to 400 ml daily, and this improvement was maintained when she returned home. A further course of somatostatin 10 weeks later resulted in a small further reduction. She remains on home parenteral nutrition and can manage the reduced amount of fistula discharge with a stoma bag. Adequate nutritional support is essential in the management of enterocutaneous fistulae2 and complete bowel rest reduces the volume of experimental fistulae by up to 90%.3 However, not all fistulae close spontaneously, even with parenteral nutrition and bowel rest rigorously applied.4 Failure is usually associated with high fistula output, intercurrent sepsis, distal obstruction, or wound disruption,sand such patients may benefit from hormonal manipulation of gastrointestinal secretions. Somatostatin reduces gastrointestinal secretions but it is not clear in these cases why the reduction was maintained when the infusions stopped. Fistula tracks are often colonised with bacteria, so that reducing the flow of potential substrates lowers the bacterial count and reduces their irritant byproducts. This may allow healing or at least a manageable discharge from a fistula surrounded by healthy skin. Somatostatin may be a significant advance over conventional conservative therapy for persistent gastrointestinal fistulae, offering shorter hospital stays (against which must be set the cost of somatostatin, L980 for 5 days). We suggest that somatostatin be
reserved for patients with high-output fistulas5 or where parenteral nutrition and complete intake restriction for one month have not resulted in spontaneous closure.Somatostatin may allow an operative approach to be delayed until septic foci have been treated and nutritional status improved, and the patient may be able to convalesce at home. We thank Mr R. M. R. Taylor, Mr I. F. McNeill, and Mr B. V. McEvedy for permission to publish details of these cases.
Department of Surgery, Royal Victoria Infirmary, Newcastle upon Tyne NE1 1 4LP
A.
J.
J. RICH R. C. SAINSBURY
KW, Henry DA, Davies JG, Hine KR, Hawkey CJ, Langman MJS. Somatostatin in treatment of haematemesis and melaena. Lancet 1985; i: 130-32. 2. Chapman R, Foran R, Dunphy JE. Management of intestinal fistulas. Am J Surg 1964; 1. Somerville
108: 157-64. 3. Wolfe
BM, Keltner RM, Willman VL. Intestinal fistula output in regular, elemental and intravenous alimentation. Am J Surg 1972; 149: 333-36. 4. Reber HA, Roberts C, Way LV, et al. Management of external gastrointestinal fistulas. Ann Surg 1978; 188: 460-67. 5. Sitges-Serra A, Jaurrieta E, Sitges-Creus A. Management of postoperative enterocutaneous fistulas: the roles of parenteral nutrition and surgery. Br J Surg 1982; 69: 147-50.
GENESIS OF GASTRIC STUMP CARCINOMA
SIR,—Dr Caygill and colleagues (April 26, p 929) demonthat gastric surgery for benign disease, whether gastrec-
strate
tomy or vagotomy and drainage, significantly increases the risk of carcinoma developing in the remaining stomach. They implicate "bile reflux" in the aetiology of the disease. Evidence from animal studies suggests that surgically induced duodenogastric reflux will produce neoplastic change within a year.’ Which fraction of the reflux is responsible, bile or pancreaticoduodenal secretions, is not known. Our study2was done to find out, by surgery designed to produce reflux of bile or pancreaticoduodenal secretions or both, which fraction of duodenogastric reflux is responsible. The controls were animals with a gastrotomy but no reflux. After 9 months the animals were killed and the stomachs removed and examined for the presence of adenocarcinoma. Adenocarcinoma was detected in 17/26 animals with pancreaticoduodenal reflux alone (10/14) or with bile reflux (7/12) but in none of the 8 controls and in none of the 6 rats with bile reflux only. The differences in frequency between controls and animals with pancreaticoduodenal secretions (p<001) and reflux of both secretions (p < 0-05) were significant (X2 test) as was the difference between pancreaticoduodenal secretions and bile reflux only (p < 0-02). These findings suggest that duodenogastric reflux plays an important part in the aetiology of gastric stump carcinoma in the rat and that pancreaticoduodenal secretions and not bile are implicated. This may help to explain the findings of Caygill and colleagues, and emphasises the need to use the term duodenogastric reflux rather than bile reflux since this term ignores the pancreatic and duodenal components of the reflex.
Department of Surgery and Histopathology Guy’s Hospital, London SE1 9RT
R. C. MASON P. R. TAYLOR P. H. ROWE N. O. ASTON M. I. FILIPE W. J. OWEN
Langhans P, Heger RA, Hohenstein J, Schlake W, Bunter H. Operation-sequel carcinoma of the stomach: Experimented studies of surgical techniques with or without resection. World J Surg 1981; 5: 595-605. 2. Mason RC. Duodenogastric reflux in rat gastric carcinoma. Br J Surg (in press). 3. Mason RC, Brame KG, Filipe MI, Owen WJ. The long term effects of duodenogastric reflux on rat gastric mucosa. Gut 1986; 27: A634. 1.
SEROTYPING CAMPYLOBACTER
SIR,-Dr Fricker (March 8, p 554), referring to campyloserotyping schemes, proposes acceptance of the passive haemagglutination method based on heat-stable antigens as the bacter