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Sudden Onset of Steatorrhea Due to Surgical Occlusion of the Main Pancreatic Duct
GASTROENTEROLOGY 67:717- 719, 1974 Copyright © 1974 by The Williams & Wilkins Co.
Vol. 67 , No.4
Printed in U.S .A.
SUDDEN ONSET OF STEATORRHEA DUE TO SURGICAL OCCLUSION OF THE MAIN PANCREATIC DUCT Report of a case JuAN-R. MALAGELADA, M.D ., AND DouGLAS
B. McGILL, M .D .
Division of Gastroenterology and Internal M edicine, Mayo Clinic and Mayo Foundation , Rochester, Minnesota
A patient is described who had complete occlusion of the distal end of the main pancreatic duct after a Billroth II gastrectomy for duodenal ulcer. This occlusion resulted in a very unusual course with prolonged, severe steatorrhea and painless pancreatic atrophy. Partial gastrectomy is often performed for the treatment of peptic ulcer. Subclinical pancreatic exocrine insufficiency is a relatively frequent sequela, 1 although its pathogenesis often is unclear. This report describes a patient who had severe painless pancreatic atrophy after a Billroth II gastrectomy for chronic duodenal ulcer. Subsequently, this patient was found to have a complete occlusion of the main pancreatic duct near the duodenum; the occlusion completely blocked secretion. Although similar accidental lesions may cause acute, often fatal, postoperative pancreatitis, 2 a prolonged course leading to pancreatic fibrosis and atrophy has not previously been reported.
Report of a Case A 39-year-old lumberyard worker had had symptoms of peptic ulcer since he was 10 years old. In January , 1971, at the age of 37 years, because of chronic intractable pain, he underwent operation at another hospital. The operative report described a penetrating posteroinferior ulcer in the duodenal bulb. The pancreas was normal on inspection and palpation . The
ulcer bed was freed by surgical dissection through extensive scarring that surrounded the crater; the duodenum was transected; and the duodenal stump was closed. A truncal vagotomy with antrectomy and a Billroth II anastomosis was performed. Within a few days of the operation, coincident with the beginning of oral feedings, the patient developed severe diarrhea, with 6 to 12 daily bowel movements . The stools were sometimes large and foul-smelling, and contained oil droplets . The patient lost weight progressively despite a ravenous appetite that forced him to eat large and frequent meals. A trial period on a gluten-free diet did not relieve his symptoms. In August, 1971, 7 months after his initial operation, the patient was seen for the first time at the Mayo Clinic. There was no personal or familial history of pancreatic, biliary, or endocrine disease, and the patient drank very little alcohol. He was a thin, ill-appearing man, 68.0 inches (172.72 em) tall, who weighed 116 lb (52.7 kg) ; his weight before gastrectomy was 156 lb (70 .8 kg) . Vital signs were normal. There was a midline surgical scar on his abdomen , but otherwise, results of the examination were unremarkable. Laboratory data included hemoglobin 13.6 g per dl, leukocyte count 10,000 per mm 3 , sedimentation rate 11 mm in 1 hr, fasting blood sugar 78 mg per dl , creatinine 0.9 mg per dl, potassium 4.0 mEq per liter, calcium 8.9 mg per dl , total bilirubin 0.3 mg per dl , serum glutamic oxaloacetic transaminase 27 Karmen units per liter, alkaline phosphatase 86 IU per liter, prothrombin time 20 sec , cholesterol 117 mg per dl, and total protein in serum 6.8 g per dl (albumin 3.4 g, -y-globulins 1.6 g). Amylase
Received January 18, 1974. Accepted April 22, 1974. Address requests for reprints to : Dr. Juan-R. Malagelada , Section of Publications, Mayo Clinic , 200 First Street, SW , Rochester, Minnesota 55901. This investigation was supported in part by Research Grant AM-5259 from the National Institutes of Health , United States Public Health Service . 11 7
718
CASE REPORTS
concentrations in serum and in urine were normal. Stool fat and nitrogen losses amounted to 70 g per 24 hr and 14.5 g per 24 hr, respectively, on a 100-g fat diet. Roentgenographic examination of the gastrointestinal tract confirmed a partial gastrectomy with gastrojejunostomy. The small bowel was normal. Esophagogastroscopy revealed no abnormalities . Various diagnostic possibilities, suggested by the sequence of events , led to exploratory laparotomy on August 18, 1971. The pancreas, surrounded by vestiges of fat necrosis , was small, hard , and irregular on palpation. · The body of the organ was then incised to the main pancreatic duct, and a gush of clear juice flowed through the opening. A pancreatogram showed complete occlusion of the main duct, very close to its duodenal opening, with no evidence of an accessory duct (fig. 1) . The pancreatic excretory system was slightly dilated and irregularly constricted. A biopsy specimen taken from the head of the pancreas showed pronounced atrophy of the exocrine gland, with advanced fibrosis. Islet cells were prominent (fig. 2). The remainder of the abdominal exploration revealed no other abnormalities , and an operative cholangiogram confirmed a normal biliary tree. The jejunum was then divided at approximately 30 em from the gastrojejunostomy site, and the distal cut end was anastomosed in a Raux-Y fashion to the pancreas at the site of the incision into the pancreatic duct to provide an intestinal route of drainage for the pancreatic
pancreatogram . Contrast material was injected into the duct of Wirsung through incision in the body of the gland. The duct is occluded near the duodenum, preventing entry of contrast material into the bowel lumen. Furthermore, the duct is dilated and irregularly constricted. No accessory duct is identified.
Vol. 67, No.4
FIG. 2. Surgical biopsy specimen from the head of the pancreas. Pronounced atrophy of the exocrine component of the gland, with advanced fibrosis. Most remaining cells are islet cells (hematoxylin and eosin, X
48).
secretion. The patient made an uneventful postoperative recovery and was dismissed from the hospital on September 2, 1971, on a therapeutic program of oral Viokase (pancreatin), 5 g six times daily. The patient was seen again at follow-up examination in April , 1972, when his weight had increased to 131 lb (59.5 kg) , his bowel habits were normal, without clinical evidence of steatorrhea, and his condition was considered satisfactory.
Comment We presume that the severe, painless pancreatic insufficiency that develcped immediately after gastric surgery in our patient, who had no preoperative evidence of pancreatic disease, resulted from complete occlusion of the main and only pancretic duct. Several considerations support such a direct relationship between the operation and subsequent pancreatic dysfunction: (1) lack of previous pancreatic disease clinically, absence of predisposing factors (that is , alcoholism or biliary disease), and a normal gland at the first operation; (2) the immediate and severe steatorrhea when oral feedings were begun in the postoperative period; and (3) the anatomic findings on reexploration, showing an isolated and well localized lesion in the duct of Wirsung near the duodenum, producing complete blockage of the secretion of the gland.
October 1974
719
CASE REPORTS
Chronic pancreatitis may produce strictures of the main pancreatic duct. However, chronic pancreatitis rarely presents with complete occlusion of the duct of Wirsung. 3 Furthermore, other pancreatographic or cholangiographic (or both) features commonly found in chronic pancreatitis• were not present. Thus, we think that the blockage of the distal portion of the main pancreatic duct in our patient was acquired, and that it resulted from injury at the initial surgical procedure. Surgical injuries to the ductal system, parenchyma, or vascular supply of the pancreas may be produced by transfixion, ligation, manipulation, or mobilization of different parts of the gland during partial gastrectomy. 2 • 5 If a pancreatic duct is accidentally occluded at operation, the consequences may depend partly on the anatomic configuration of the pancreatic excretory system. Approximately half of the population (as was true of our patient) is without a functioning accessory duct, 5 and complete occlusion of the duct of Wirsung means total blockage of pancreatic secretion. There may be a similar result from obstruction of the duct of Santorini in the 10% of patients in whom this duct is the only duct conveying pancreatic secretions into the duodenum. 5 In man, accidental occlusion of the main duct of a normal pancreas at operation frequently results in acute postoperative pancreatitis, which carries a high mortality, 2 • 6 although a single instance of relapsing pancreatitis also has been described. 7 In contrast, no instances of acute pancreatitis were observed in 6 patients with chronic advanced pancreatitis who underwent ligation of the main and accessory pancreatic ducts for the purpose of reliev-
ing pain. 8 This procedure was followed, as in the canine model with experimental chronic pancreatitis, 9 by more (since there was, by definition, preexisting fibrosis and atrophy) atrophy and fibrosis of the gland. Our patient had a similar course. However, in this instance we think that the gland was normal prior to the injury which occluded the main duct leading to pancreatic atrophy. REFERENCES 1. Wormsley KG : Pancreatic exocrine function in patients with gastric ulceration before and after gastrectomy. Lancet 2:682-684, 1972 2. Hollender LF, Gillet M, Sava G, Staub D: Les pancreatites aigues post-operatoires: etude clinique et plaidoyer en faveur d'une reintervention plus systematique, avec pancreatectomie precoce. J Chir (Paris) 97 :177-198, 1969 3. Howard JM, Short WF: An evaluation of pancreatography in suspected pancreatic disease. Surg Gynecol Obstet 129:319-324, 1969 4. Ogoshi K, Niwa M, Hara Y, et al: Endoscopic pancreatocholangiography in the eva! uation of pancreatic and biliary disease. Gastroenterology 64:210- 216, 1973 5. Millboum E: On acute pancreatic affections following gastric resection for ulcer or cancer and the possibilities of avoiding them. Acta Chir Scand 98 :1-21, 1949 6. Peterson LM, Collins JJ Jr, Wilson RE: Acute pancreatitis occurring after operation. Surg Gynecol Obstet 127:23-28, 1968 7. Foley FE, Kilpatrick JT, Crabtree SF: Chronic recurrent pancreatitis due to injury to the duct of Santorini: a complication of subtotal gastrectomy. Ann Surg 144:87-92, 1956. 8. Cannon JA: Experience with ligation of the pancreatic ducts in the treatment of chronic relapsing pancreatitis. Am J Surg 90:266-279, 1955 9. Engel S, ReMine WH, Dockerty MB, et al: Effect of ligation of pancreatic ducts on chronic pancreatitis: experimental study. Arch Surg 85:1031-1035, 1962
Vol. 67 , No.4
Printed in U.S .A.
SUDDEN ONSET OF STEATORRHEA DUE TO SURGICAL OCCLUSION OF THE MAIN PANCREATIC DUCT Report of a case JuAN-R. MALAGELADA, M.D ., AND DouGLAS
B. McGILL, M .D .
Division of Gastroenterology and Internal M edicine, Mayo Clinic and Mayo Foundation , Rochester, Minnesota
A patient is described who had complete occlusion of the distal end of the main pancreatic duct after a Billroth II gastrectomy for duodenal ulcer. This occlusion resulted in a very unusual course with prolonged, severe steatorrhea and painless pancreatic atrophy. Partial gastrectomy is often performed for the treatment of peptic ulcer. Subclinical pancreatic exocrine insufficiency is a relatively frequent sequela, 1 although its pathogenesis often is unclear. This report describes a patient who had severe painless pancreatic atrophy after a Billroth II gastrectomy for chronic duodenal ulcer. Subsequently, this patient was found to have a complete occlusion of the main pancreatic duct near the duodenum; the occlusion completely blocked secretion. Although similar accidental lesions may cause acute, often fatal, postoperative pancreatitis, 2 a prolonged course leading to pancreatic fibrosis and atrophy has not previously been reported.
Report of a Case A 39-year-old lumberyard worker had had symptoms of peptic ulcer since he was 10 years old. In January , 1971, at the age of 37 years, because of chronic intractable pain, he underwent operation at another hospital. The operative report described a penetrating posteroinferior ulcer in the duodenal bulb. The pancreas was normal on inspection and palpation . The
ulcer bed was freed by surgical dissection through extensive scarring that surrounded the crater; the duodenum was transected; and the duodenal stump was closed. A truncal vagotomy with antrectomy and a Billroth II anastomosis was performed. Within a few days of the operation, coincident with the beginning of oral feedings, the patient developed severe diarrhea, with 6 to 12 daily bowel movements . The stools were sometimes large and foul-smelling, and contained oil droplets . The patient lost weight progressively despite a ravenous appetite that forced him to eat large and frequent meals. A trial period on a gluten-free diet did not relieve his symptoms. In August, 1971, 7 months after his initial operation, the patient was seen for the first time at the Mayo Clinic. There was no personal or familial history of pancreatic, biliary, or endocrine disease, and the patient drank very little alcohol. He was a thin, ill-appearing man, 68.0 inches (172.72 em) tall, who weighed 116 lb (52.7 kg) ; his weight before gastrectomy was 156 lb (70 .8 kg) . Vital signs were normal. There was a midline surgical scar on his abdomen , but otherwise, results of the examination were unremarkable. Laboratory data included hemoglobin 13.6 g per dl, leukocyte count 10,000 per mm 3 , sedimentation rate 11 mm in 1 hr, fasting blood sugar 78 mg per dl , creatinine 0.9 mg per dl, potassium 4.0 mEq per liter, calcium 8.9 mg per dl , total bilirubin 0.3 mg per dl , serum glutamic oxaloacetic transaminase 27 Karmen units per liter, alkaline phosphatase 86 IU per liter, prothrombin time 20 sec , cholesterol 117 mg per dl, and total protein in serum 6.8 g per dl (albumin 3.4 g, -y-globulins 1.6 g). Amylase
Received January 18, 1974. Accepted April 22, 1974. Address requests for reprints to : Dr. Juan-R. Malagelada , Section of Publications, Mayo Clinic , 200 First Street, SW , Rochester, Minnesota 55901. This investigation was supported in part by Research Grant AM-5259 from the National Institutes of Health , United States Public Health Service . 11 7
718
CASE REPORTS
concentrations in serum and in urine were normal. Stool fat and nitrogen losses amounted to 70 g per 24 hr and 14.5 g per 24 hr, respectively, on a 100-g fat diet. Roentgenographic examination of the gastrointestinal tract confirmed a partial gastrectomy with gastrojejunostomy. The small bowel was normal. Esophagogastroscopy revealed no abnormalities . Various diagnostic possibilities, suggested by the sequence of events , led to exploratory laparotomy on August 18, 1971. The pancreas, surrounded by vestiges of fat necrosis , was small, hard , and irregular on palpation. · The body of the organ was then incised to the main pancreatic duct, and a gush of clear juice flowed through the opening. A pancreatogram showed complete occlusion of the main duct, very close to its duodenal opening, with no evidence of an accessory duct (fig. 1) . The pancreatic excretory system was slightly dilated and irregularly constricted. A biopsy specimen taken from the head of the pancreas showed pronounced atrophy of the exocrine gland, with advanced fibrosis. Islet cells were prominent (fig. 2). The remainder of the abdominal exploration revealed no other abnormalities , and an operative cholangiogram confirmed a normal biliary tree. The jejunum was then divided at approximately 30 em from the gastrojejunostomy site, and the distal cut end was anastomosed in a Raux-Y fashion to the pancreas at the site of the incision into the pancreatic duct to provide an intestinal route of drainage for the pancreatic
pancreatogram . Contrast material was injected into the duct of Wirsung through incision in the body of the gland. The duct is occluded near the duodenum, preventing entry of contrast material into the bowel lumen. Furthermore, the duct is dilated and irregularly constricted. No accessory duct is identified.
Vol. 67, No.4
FIG. 2. Surgical biopsy specimen from the head of the pancreas. Pronounced atrophy of the exocrine component of the gland, with advanced fibrosis. Most remaining cells are islet cells (hematoxylin and eosin, X
48).
secretion. The patient made an uneventful postoperative recovery and was dismissed from the hospital on September 2, 1971, on a therapeutic program of oral Viokase (pancreatin), 5 g six times daily. The patient was seen again at follow-up examination in April , 1972, when his weight had increased to 131 lb (59.5 kg) , his bowel habits were normal, without clinical evidence of steatorrhea, and his condition was considered satisfactory.
Comment We presume that the severe, painless pancreatic insufficiency that develcped immediately after gastric surgery in our patient, who had no preoperative evidence of pancreatic disease, resulted from complete occlusion of the main and only pancretic duct. Several considerations support such a direct relationship between the operation and subsequent pancreatic dysfunction: (1) lack of previous pancreatic disease clinically, absence of predisposing factors (that is , alcoholism or biliary disease), and a normal gland at the first operation; (2) the immediate and severe steatorrhea when oral feedings were begun in the postoperative period; and (3) the anatomic findings on reexploration, showing an isolated and well localized lesion in the duct of Wirsung near the duodenum, producing complete blockage of the secretion of the gland.
October 1974
719
CASE REPORTS
Chronic pancreatitis may produce strictures of the main pancreatic duct. However, chronic pancreatitis rarely presents with complete occlusion of the duct of Wirsung. 3 Furthermore, other pancreatographic or cholangiographic (or both) features commonly found in chronic pancreatitis• were not present. Thus, we think that the blockage of the distal portion of the main pancreatic duct in our patient was acquired, and that it resulted from injury at the initial surgical procedure. Surgical injuries to the ductal system, parenchyma, or vascular supply of the pancreas may be produced by transfixion, ligation, manipulation, or mobilization of different parts of the gland during partial gastrectomy. 2 • 5 If a pancreatic duct is accidentally occluded at operation, the consequences may depend partly on the anatomic configuration of the pancreatic excretory system. Approximately half of the population (as was true of our patient) is without a functioning accessory duct, 5 and complete occlusion of the duct of Wirsung means total blockage of pancreatic secretion. There may be a similar result from obstruction of the duct of Santorini in the 10% of patients in whom this duct is the only duct conveying pancreatic secretions into the duodenum. 5 In man, accidental occlusion of the main duct of a normal pancreas at operation frequently results in acute postoperative pancreatitis, which carries a high mortality, 2 • 6 although a single instance of relapsing pancreatitis also has been described. 7 In contrast, no instances of acute pancreatitis were observed in 6 patients with chronic advanced pancreatitis who underwent ligation of the main and accessory pancreatic ducts for the purpose of reliev-
ing pain. 8 This procedure was followed, as in the canine model with experimental chronic pancreatitis, 9 by more (since there was, by definition, preexisting fibrosis and atrophy) atrophy and fibrosis of the gland. Our patient had a similar course. However, in this instance we think that the gland was normal prior to the injury which occluded the main duct leading to pancreatic atrophy. REFERENCES 1. Wormsley KG : Pancreatic exocrine function in patients with gastric ulceration before and after gastrectomy. Lancet 2:682-684, 1972 2. Hollender LF, Gillet M, Sava G, Staub D: Les pancreatites aigues post-operatoires: etude clinique et plaidoyer en faveur d'une reintervention plus systematique, avec pancreatectomie precoce. J Chir (Paris) 97 :177-198, 1969 3. Howard JM, Short WF: An evaluation of pancreatography in suspected pancreatic disease. Surg Gynecol Obstet 129:319-324, 1969 4. Ogoshi K, Niwa M, Hara Y, et al: Endoscopic pancreatocholangiography in the eva! uation of pancreatic and biliary disease. Gastroenterology 64:210- 216, 1973 5. Millboum E: On acute pancreatic affections following gastric resection for ulcer or cancer and the possibilities of avoiding them. Acta Chir Scand 98 :1-21, 1949 6. Peterson LM, Collins JJ Jr, Wilson RE: Acute pancreatitis occurring after operation. Surg Gynecol Obstet 127:23-28, 1968 7. Foley FE, Kilpatrick JT, Crabtree SF: Chronic recurrent pancreatitis due to injury to the duct of Santorini: a complication of subtotal gastrectomy. Ann Surg 144:87-92, 1956. 8. Cannon JA: Experience with ligation of the pancreatic ducts in the treatment of chronic relapsing pancreatitis. Am J Surg 90:266-279, 1955 9. Engel S, ReMine WH, Dockerty MB, et al: Effect of ligation of pancreatic ducts on chronic pancreatitis: experimental study. Arch Surg 85:1031-1035, 1962