CASE REPORT
Afferent Loop Obstruction Presenting as Obstructive Jaundice R A J K U M A R K. W A R R I E R , MD, and F R A N C I S U. S T E I N H E B E R , MD
The clinical s y m p t o m o t o l o g y resulting from obstruction of the afferent limb of a Bilroth II gastrojejunostomy has generally been divided into an acute and a chronic form (1, 2). The acute form usually occurs in the immediate postoperative period and is characterized by sudden upper-abdominal pain, vomiting, and rapid clinical deterioration. On rare occasions, marked elevations of serum amylase have lead to confusion with acute pancreatitis. The chronic form presents a stereotyped picture of early postprandial distress relieved after an hour or two by copious vomiting of bilious material. A third form which has received little attention is characterized by progressive, insidious obstruction without evidence of clear-cut symptoms. This latter form is illustrated by our patient who presented with typical signs of obstructive jaundice. This represents the first reported instance of this complication.
CASE REPORT G.B., a 76-year-old white female was admitted to the surgical service of Coney Island Hospital with a twoweek history of jaundice. She was well until about six weeks prior to admission, when she noted a decrease in appetite and began to lose weight. Two weeks prior to admission, she noted the onset of pruritus which became increasingly severe. She denied any history of abdominal pain, vomiting, fever, drug ingestion, or gallbladder disease. Twenty-five years prior to admission, she had undergone a partial gastrectomy and gastrojejunostomy for peptic ulcer. On physical examination she was a cheerful elderly lady in no distress. Skin was icteric with multiple excoFrom the Gastroenterology Division, Coney Island Hospital, Brooklyn, New York. Dr. Warrier's present address is Gastroenterology Division, Pointe Basse Plaza Mall, Ste. Genevieve, Missouri 63670. Address for reprint requests: Dr. Francis U. Steinheber, Chief of G a s t r o e n t e r o l o g y Division, Coney Island Hospital, 2601 Ocean Parkway, Brooklyn, New York 11235.
74
riations due to scratching. There was an upper-abdominal midline scar from previous surgery. On palpation, a firm liver was felt 5 cm below the costal margin. A smooth cystic globular mass, assumed to be gall bladder, was felt below liver edge which moved with the liver on respiration. The spleen was not palpable. There was no ascites. Extremities were normal. Stool was pale, and was negative on Hematest. Laboratory Data. Hemoglobin 12 g, hematocrit 36%, WBC 9500, total protein 5.6 g, albumin 3.6 g, bilirubin 10.5 mg/dl, alkaline phosphatase 1056 units (upper limit of normal 80 units), SGOT 124 units, LDG 203 units, cholesterol 248 mg, blood sugar 221 mg, BUN 13 mg, prothrombin time, 11 sec with control of 10 sec. An upper-gastrointestinal series showed previous partial gastrectomy with normal efferent loop but the afferent loop failed to fill. Because of the diagnosis of obstructive jaundice, an exploratory laparotomy was performed. At surgery, the gall bladder was large and distended with bile. A huge, tense mass in the upper abdomen was found to be the afferent limb of the previous gastrojejunostomy. This was explored back to the stomal anastomasis where infiltrating tumor of the gastric remnant was found to be completely obstructing the afferent loop stoma. The pancreas was entirely normal. After a cholecystectomy, the afferent loop was opened and copious amounts of dark-green foulsmelling bile were withdrawn. The common duct, which was dilated to 2 cm, was incised and a T-tube placed. On intraoperative T-tube cholangiography, dye flowed freely from the common duct into the duodenum (Figures 1 and 2). There were no stones in the common duct. Biopsy of the tumor at the a-loop stoma revealed poorly differentiated mucus producing adenocarcinoma. An anastomosis was performed between the afferent and efferent loop. Postoperatively, the patient's icterus abated and the bilirubin dropped to 1.6 mg and alkaline phosphatase to 221. Three months later, her bilirubin was 0.5 mg/100 ml and alkaline phosphatase 136 I.U./ml. DISCUSSION This case is notable in several regards. Feiss found only four reported cases of cancer of the gastric pouch causing afferent loop obstruction (3, 4). More important, our case represents the first reported instance of obstructive jaunDigestive Diseases and Sciences, Vol. 24, No. 1 (January 1979)
0163-2116/79/0100-0074503.00/1 9 1979DigestiveDisease Systems, inc.
A F F E R E N T LOOP OBSTRUCTION
Fig 1. Operative cholangiogram showing dilated common duct and dye filling dilated afferent loop
dice secondary to such obstruction. In view of the increasing awareness of carcinoma developing in a gastric remnant, with reported frequencies of 1-6%, it is somewhat surprising that afferent loop obstruction has been such an infrequent occurrence following stomal cancer (5-7). The most remarkable aspect of this case is the late presentation as obstructive jaundice. Little emphasis has been placed on the fact that complete obstruction of the afferent loop may be virtually asymptomatic. The case reported by Diba (8) represents an instance where massive distension of the afferent loop presented with a palpable mass which mimicked a pseudocyst. In our case, the rising pressure within the isolated loop led eventually to dilatation of the entire biliary tree and gall bladder. Dilatation of the common duct has been noted previously, but in the case of Bubrick and Hitchcock it is likely that this resulted from previous biliary surgery (9). One question that deserves comment is why pancreatitis failed to develop despite duodenal pressures substantial enough to dilate the biliary tree. In the Pffefer dog preparation for example, a closed-loop duodenal obstrucDigestive Diseases and Sciences, Vol. 24, No. 1 (January 1979)
tion with biliary exclusion regularly leads to severe pancreatitis. Unlike the usual clinical situation, however, factors other than simple obstruction may be involved in this model (10-12). In the one study using human volunteers, Greenfield was unable to demonstrate any biliary or pancreatic reflux after completely occluding both segments of the duodenum with balloons and raising intraduodenal pressure (13). Despite these conflicting experimental data there is ample clinical evidence that pancreatitis can result from obstruction of the duodenum (14). Had the obstruction in our case continued, pancreatitis might well have developed. We can only speculate on the reasons why the pancreas was spared for so long. It is possible that it was protected by the sphincter of Boyden. This submucosal muscular sheath is separate from the sphincter of Oddi and surrounds the intramural portion the individual pancreatic and bile ducts (15). The muscle fibers of this distinct sphincteric mechanism mix with the fibers of the intestinal and papillary muscles. Our case suggests that under some circumstances this more proximal mechanism can function as an independent pancreatic sphincter.
75
WARRIER AND STEINHEBER
Fig 2. Close-up of operative cholangiogram illustrating free flow of dye into duodenum from common duct
SUMMARY The first case of obstructive jaundice secondary to a chronic afferent loop obstruction has been reported. The cause of the obstructed afferent loop was found to be a carcinoma of the gastric pouch occurring 25 years after surgery for peptic ulcer disease. The failure to develop any evidence of pancreatitis despite marked dilatation of the biliary tree and gall bladder suggests the existence of an independent functioning pancreatic sphincter, perhaps the sphincter of Boyden.
REFERENCES 1. Woodward ER: The pathophysiology of afferent loop syndrome. Surg Clin North Am 46:411-423, 1966 2. Dahlgren S: The afferent loop syndrome. Acta Chir Scand, (Suppl) 327, 1964 3. Feiss JS, Plevy DJ, Luckman GS, Lenit OS Jr: A case of postgastrectomy afferent loop obstruction secondary to cancer of the stomach simulating pseudocyst of the pancreas. Am J Dig Dis 20:995-998, 1975 4. Feiss JS, Raskin MM, Wolfe J, Plevy DJ, Luckman GS: A case of afferent loop obstruction secondary to recurrent carcinoma of the stomach with ultrasound and C.T. scan findings. Am J Gastroenterol 68:77-80, 1977 5. Morgenstern L, Yamakawa T, Seltzer D: Carcinoma of the
76
gastric stump. Am J Surg 125:29-38, 1973 6. Terjesen T, Erichsen HG: Carcinoma of the gastric stump after operation for benign gastroduodenal ulcer. Acta Chir Scand 142:256-260, 1976 7. Domeloff L, Eriksson S, Janunger KG: Carcinoma and possible precancerous changes of the gastric stump after Billroth 11 resection. Gastroenterology 73:462-468, 1977 8. Diba A, Grossman ET, Dolan EP: Afferent loop syndrome: A different picture. Am J Gastroenterol 166:72-75, 1976 9. Bubrick MP, Hitchcock CR: Renal cyst causing afferent loop obstruction and acute pancreatitis. Am Surg 41:440-443, 1975 10. Rosato EF, Cowan RP, Rosato FE: Duodenal pressure as a cause of pancreatitis. Surgery 68:837-841, 1970 11. Strack R, Dreizin DH, Ketyer S, Lazaro EJ: Duodenal reflux in the genesis of acute pancreatitis. Can J Surg 10:68-74, 1967 12. Johnson RH, Doppman J: Duodenal reflux and the etiology of pancreatitis. Surgery 62:462-467, 1967 13. Greenfield H, Siegel LH, DeFrancis N: Attempted visualization of the pancreatic ducts by ampullary reflux. Gastroenterology 29:280-284, 1955 14. Dreiling DA, Kirschner PA, Nemser H: Chronic duodenal obstructions: A mechanovascular etiology of pancreatitis. Am J Dig Dis 5:991-1005, 1960 15. Boyden EA: The anatomy of the choledochoduodenal junction in man. Surg Gynecol Obstetr 104:641, 1975 Digestive Diseases and Sciences, Vol. 24, No. l (January 1979)
Afferent Loop Obstruction Presenting as Obstructive Jaundice R A J K U M A R K. W A R R I E R , MD, and F R A N C I S U. S T E I N H E B E R , MD
The clinical s y m p t o m o t o l o g y resulting from obstruction of the afferent limb of a Bilroth II gastrojejunostomy has generally been divided into an acute and a chronic form (1, 2). The acute form usually occurs in the immediate postoperative period and is characterized by sudden upper-abdominal pain, vomiting, and rapid clinical deterioration. On rare occasions, marked elevations of serum amylase have lead to confusion with acute pancreatitis. The chronic form presents a stereotyped picture of early postprandial distress relieved after an hour or two by copious vomiting of bilious material. A third form which has received little attention is characterized by progressive, insidious obstruction without evidence of clear-cut symptoms. This latter form is illustrated by our patient who presented with typical signs of obstructive jaundice. This represents the first reported instance of this complication.
CASE REPORT G.B., a 76-year-old white female was admitted to the surgical service of Coney Island Hospital with a twoweek history of jaundice. She was well until about six weeks prior to admission, when she noted a decrease in appetite and began to lose weight. Two weeks prior to admission, she noted the onset of pruritus which became increasingly severe. She denied any history of abdominal pain, vomiting, fever, drug ingestion, or gallbladder disease. Twenty-five years prior to admission, she had undergone a partial gastrectomy and gastrojejunostomy for peptic ulcer. On physical examination she was a cheerful elderly lady in no distress. Skin was icteric with multiple excoFrom the Gastroenterology Division, Coney Island Hospital, Brooklyn, New York. Dr. Warrier's present address is Gastroenterology Division, Pointe Basse Plaza Mall, Ste. Genevieve, Missouri 63670. Address for reprint requests: Dr. Francis U. Steinheber, Chief of G a s t r o e n t e r o l o g y Division, Coney Island Hospital, 2601 Ocean Parkway, Brooklyn, New York 11235.
74
riations due to scratching. There was an upper-abdominal midline scar from previous surgery. On palpation, a firm liver was felt 5 cm below the costal margin. A smooth cystic globular mass, assumed to be gall bladder, was felt below liver edge which moved with the liver on respiration. The spleen was not palpable. There was no ascites. Extremities were normal. Stool was pale, and was negative on Hematest. Laboratory Data. Hemoglobin 12 g, hematocrit 36%, WBC 9500, total protein 5.6 g, albumin 3.6 g, bilirubin 10.5 mg/dl, alkaline phosphatase 1056 units (upper limit of normal 80 units), SGOT 124 units, LDG 203 units, cholesterol 248 mg, blood sugar 221 mg, BUN 13 mg, prothrombin time, 11 sec with control of 10 sec. An upper-gastrointestinal series showed previous partial gastrectomy with normal efferent loop but the afferent loop failed to fill. Because of the diagnosis of obstructive jaundice, an exploratory laparotomy was performed. At surgery, the gall bladder was large and distended with bile. A huge, tense mass in the upper abdomen was found to be the afferent limb of the previous gastrojejunostomy. This was explored back to the stomal anastomasis where infiltrating tumor of the gastric remnant was found to be completely obstructing the afferent loop stoma. The pancreas was entirely normal. After a cholecystectomy, the afferent loop was opened and copious amounts of dark-green foulsmelling bile were withdrawn. The common duct, which was dilated to 2 cm, was incised and a T-tube placed. On intraoperative T-tube cholangiography, dye flowed freely from the common duct into the duodenum (Figures 1 and 2). There were no stones in the common duct. Biopsy of the tumor at the a-loop stoma revealed poorly differentiated mucus producing adenocarcinoma. An anastomosis was performed between the afferent and efferent loop. Postoperatively, the patient's icterus abated and the bilirubin dropped to 1.6 mg and alkaline phosphatase to 221. Three months later, her bilirubin was 0.5 mg/100 ml and alkaline phosphatase 136 I.U./ml. DISCUSSION This case is notable in several regards. Feiss found only four reported cases of cancer of the gastric pouch causing afferent loop obstruction (3, 4). More important, our case represents the first reported instance of obstructive jaunDigestive Diseases and Sciences, Vol. 24, No. 1 (January 1979)
0163-2116/79/0100-0074503.00/1 9 1979DigestiveDisease Systems, inc.
A F F E R E N T LOOP OBSTRUCTION
Fig 1. Operative cholangiogram showing dilated common duct and dye filling dilated afferent loop
dice secondary to such obstruction. In view of the increasing awareness of carcinoma developing in a gastric remnant, with reported frequencies of 1-6%, it is somewhat surprising that afferent loop obstruction has been such an infrequent occurrence following stomal cancer (5-7). The most remarkable aspect of this case is the late presentation as obstructive jaundice. Little emphasis has been placed on the fact that complete obstruction of the afferent loop may be virtually asymptomatic. The case reported by Diba (8) represents an instance where massive distension of the afferent loop presented with a palpable mass which mimicked a pseudocyst. In our case, the rising pressure within the isolated loop led eventually to dilatation of the entire biliary tree and gall bladder. Dilatation of the common duct has been noted previously, but in the case of Bubrick and Hitchcock it is likely that this resulted from previous biliary surgery (9). One question that deserves comment is why pancreatitis failed to develop despite duodenal pressures substantial enough to dilate the biliary tree. In the Pffefer dog preparation for example, a closed-loop duodenal obstrucDigestive Diseases and Sciences, Vol. 24, No. 1 (January 1979)
tion with biliary exclusion regularly leads to severe pancreatitis. Unlike the usual clinical situation, however, factors other than simple obstruction may be involved in this model (10-12). In the one study using human volunteers, Greenfield was unable to demonstrate any biliary or pancreatic reflux after completely occluding both segments of the duodenum with balloons and raising intraduodenal pressure (13). Despite these conflicting experimental data there is ample clinical evidence that pancreatitis can result from obstruction of the duodenum (14). Had the obstruction in our case continued, pancreatitis might well have developed. We can only speculate on the reasons why the pancreas was spared for so long. It is possible that it was protected by the sphincter of Boyden. This submucosal muscular sheath is separate from the sphincter of Oddi and surrounds the intramural portion the individual pancreatic and bile ducts (15). The muscle fibers of this distinct sphincteric mechanism mix with the fibers of the intestinal and papillary muscles. Our case suggests that under some circumstances this more proximal mechanism can function as an independent pancreatic sphincter.
75
WARRIER AND STEINHEBER
Fig 2. Close-up of operative cholangiogram illustrating free flow of dye into duodenum from common duct
SUMMARY The first case of obstructive jaundice secondary to a chronic afferent loop obstruction has been reported. The cause of the obstructed afferent loop was found to be a carcinoma of the gastric pouch occurring 25 years after surgery for peptic ulcer disease. The failure to develop any evidence of pancreatitis despite marked dilatation of the biliary tree and gall bladder suggests the existence of an independent functioning pancreatic sphincter, perhaps the sphincter of Boyden.
REFERENCES 1. Woodward ER: The pathophysiology of afferent loop syndrome. Surg Clin North Am 46:411-423, 1966 2. Dahlgren S: The afferent loop syndrome. Acta Chir Scand, (Suppl) 327, 1964 3. Feiss JS, Plevy DJ, Luckman GS, Lenit OS Jr: A case of postgastrectomy afferent loop obstruction secondary to cancer of the stomach simulating pseudocyst of the pancreas. Am J Dig Dis 20:995-998, 1975 4. Feiss JS, Raskin MM, Wolfe J, Plevy DJ, Luckman GS: A case of afferent loop obstruction secondary to recurrent carcinoma of the stomach with ultrasound and C.T. scan findings. Am J Gastroenterol 68:77-80, 1977 5. Morgenstern L, Yamakawa T, Seltzer D: Carcinoma of the
76
gastric stump. Am J Surg 125:29-38, 1973 6. Terjesen T, Erichsen HG: Carcinoma of the gastric stump after operation for benign gastroduodenal ulcer. Acta Chir Scand 142:256-260, 1976 7. Domeloff L, Eriksson S, Janunger KG: Carcinoma and possible precancerous changes of the gastric stump after Billroth 11 resection. Gastroenterology 73:462-468, 1977 8. Diba A, Grossman ET, Dolan EP: Afferent loop syndrome: A different picture. Am J Gastroenterol 166:72-75, 1976 9. Bubrick MP, Hitchcock CR: Renal cyst causing afferent loop obstruction and acute pancreatitis. Am Surg 41:440-443, 1975 10. Rosato EF, Cowan RP, Rosato FE: Duodenal pressure as a cause of pancreatitis. Surgery 68:837-841, 1970 11. Strack R, Dreizin DH, Ketyer S, Lazaro EJ: Duodenal reflux in the genesis of acute pancreatitis. Can J Surg 10:68-74, 1967 12. Johnson RH, Doppman J: Duodenal reflux and the etiology of pancreatitis. Surgery 62:462-467, 1967 13. Greenfield H, Siegel LH, DeFrancis N: Attempted visualization of the pancreatic ducts by ampullary reflux. Gastroenterology 29:280-284, 1955 14. Dreiling DA, Kirschner PA, Nemser H: Chronic duodenal obstructions: A mechanovascular etiology of pancreatitis. Am J Dig Dis 5:991-1005, 1960 15. Boyden EA: The anatomy of the choledochoduodenal junction in man. Surg Gynecol Obstetr 104:641, 1975 Digestive Diseases and Sciences, Vol. 24, No. l (January 1979)
