(Radiology. 2000;216:142-145.)
© RSNA, 2000
Case 24: Afferent Loop Syndrome1
Scott W. Wise, MD
1 From the Department of Radiology, Penn State College of Medicine, Milton S Hershey Medical Center, Hershey, Pa. Received January 22, 1999; revision requested March 22; revision
received April 16; accepted August 4. Address correspondence to the author, 116 Racehorse Dr, Jonestown, PA 17038 (e-mail: swise@paonline.com).
Index terms: Diagnosis Please Gastrointestinal tract, CT, 74.12112 Gastrointestinal tract, diseases, 74.297 Gastrojejunostomy, 72.1267, 74.1267 Intestines, stenosis or obstruction, 74.297
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HISTORY
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A 52-year-old woman presented to our emergency department with diffuse severe abdominal pain, nausea, and vomiting of a duration of approximately 6 hours. Her medical history was positive only for a perforated gastric ulcer necessitating surgery approximately 6 years previously. At physical examination, the patient had mild diffuse abdominal tenderness. Otherwise, physical examination results were unremarkable. Clinically important laboratory findings included an alkaline phosphatase level of 170 U/L (normal, 39117 U/L), an amylase level of 772 U/L (normal, 25115 U/L), and a lipase level of more than 11,000 U/L (normal, 23300 U/L). The patient subsequently underwent abdominopelvic computed tomography (CT) (Fig 1).

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Figure 1a. (a, b) Transverse contrast material-enhanced CT images obtained through the liver and pancreas demonstrate intrahepatic and extrahepatic biliary dilatation (arrow in a and b), as well as peripancreatic inflammation (arrowheads in b) consistent with acute pancreatitis. (c-f) Transverse contrast-enhanced CT images obtained caudad to a and b reveal massively dilated small bowel (* in c-f) with an abnormal swirled transition (arrow in d-f) between the dilated small bowel and the body of the stomach. The anatomic configuration, along with an absent gastric antrum, is consistent with a dilated afferent limb after a Billroth II procedure. Small calcifications that may be dystrophic in nature or related to the prior surgery are seen in the wall of the afferent loop in c.
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Figure 1b. (a, b) Transverse contrast material-enhanced CT images obtained through the liver and pancreas demonstrate intrahepatic and extrahepatic biliary dilatation (arrow in a and b), as well as peripancreatic inflammation (arrowheads in b) consistent with acute pancreatitis. (c-f) Transverse contrast-enhanced CT images obtained caudad to a and b reveal massively dilated small bowel (* in c-f) with an abnormal swirled transition (arrow in d-f) between the dilated small bowel and the body of the stomach. The anatomic configuration, along with an absent gastric antrum, is consistent with a dilated afferent limb after a Billroth II procedure. Small calcifications that may be dystrophic in nature or related to the prior surgery are seen in the wall of the afferent loop in c.
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Figure 1c. (a, b) Transverse contrast material-enhanced CT images obtained through the liver and pancreas demonstrate intrahepatic and extrahepatic biliary dilatation (arrow in a and b), as well as peripancreatic inflammation (arrowheads in b) consistent with acute pancreatitis. (c-f) Transverse contrast-enhanced CT images obtained caudad to a and b reveal massively dilated small bowel (* in c-f) with an abnormal swirled transition (arrow in d-f) between the dilated small bowel and the body of the stomach. The anatomic configuration, along with an absent gastric antrum, is consistent with a dilated afferent limb after a Billroth II procedure. Small calcifications that may be dystrophic in nature or related to the prior surgery are seen in the wall of the afferent loop in c.
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Figure 1d. (a, b) Transverse contrast material-enhanced CT images obtained through the liver and pancreas demonstrate intrahepatic and extrahepatic biliary dilatation (arrow in a and b), as well as peripancreatic inflammation (arrowheads in b) consistent with acute pancreatitis. (c-f) Transverse contrast-enhanced CT images obtained caudad to a and b reveal massively dilated small bowel (* in c-f) with an abnormal swirled transition (arrow in d-f) between the dilated small bowel and the body of the stomach. The anatomic configuration, along with an absent gastric antrum, is consistent with a dilated afferent limb after a Billroth II procedure. Small calcifications that may be dystrophic in nature or related to the prior surgery are seen in the wall of the afferent loop in c.
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Figure 1e. (a, b) Transverse contrast material-enhanced CT images obtained through the liver and pancreas demonstrate intrahepatic and extrahepatic biliary dilatation (arrow in a and b), as well as peripancreatic inflammation (arrowheads in b) consistent with acute pancreatitis. (c-f) Transverse contrast-enhanced CT images obtained caudad to a and b reveal massively dilated small bowel (* in c-f) with an abnormal swirled transition (arrow in d-f) between the dilated small bowel and the body of the stomach. The anatomic configuration, along with an absent gastric antrum, is consistent with a dilated afferent limb after a Billroth II procedure. Small calcifications that may be dystrophic in nature or related to the prior surgery are seen in the wall of the afferent loop in c.
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Figure 1f. (a, b) Transverse contrast material-enhanced CT images obtained through the liver and pancreas demonstrate intrahepatic and extrahepatic biliary dilatation (arrow in a and b), as well as peripancreatic inflammation (arrowheads in b) consistent with acute pancreatitis. (c-f) Transverse contrast-enhanced CT images obtained caudad to a and b reveal massively dilated small bowel (* in c-f) with an abnormal swirled transition (arrow in d-f) between the dilated small bowel and the body of the stomach. The anatomic configuration, along with an absent gastric antrum, is consistent with a dilated afferent limb after a Billroth II procedure. Small calcifications that may be dystrophic in nature or related to the prior surgery are seen in the wall of the afferent loop in c.
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IMAGING FINDINGS
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Transverse CT images of the upper abdomen (Fig 1a, 1b) demonstrated intra- and extrahepatic biliary dilatation, along with peripancreatic inflammatory stranding representative of an acute pancreatitis. More caudal images (Fig 1c1f) revealed dilated small bowel adjacent to the pancreas, which corresponded to the second and third parts of the duodenum. The most inferior CT image (Fig 1f) revealed a transition just below the body of the stomach into dilated small bowel in the left side of the abdomen. An abnormal twisted configuration was noted between the body of the stomach cephalad and the dilated small bowel in the left side of the abdomen caudad.
The differential diagnosis would include pancreatic pseudocyst and a right upper quadrant abscess if only the CT images of the pancreatic region were presented for evaluation. The lack of clearly identifiable small-bowel folds, possibly owing to effacement from the dilatation, could suggest this alternative explanation of and confusion with a peripancreatic fluid collection. However, the pattern of small-bowel dilatation in this case, along with the absence of an identifiable gastric antrum, is most consistent with a dilated afferent loop in a patient with known prior gastric surgery.
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DISCUSSION
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Review of this patient's medical records at hospital admission confirmed that the patient underwent a Billroth II surgical procedure 4 years previously. Endoscopy performed the day after admission was clinically important only for the inability of the endoscopist to enter the afferent loop. Conversely, the efferent small bowel could be entered during the endoscopy. Thereafter, the patient underwent a laparotomy in which gastrojejunal adhesions were lysed to relieve obstruction of the afferent limb. No obstruction of the efferent limb was identified during the surgery. The common bile duct also was explored during the surgery and revealed no evidence of a biliary obstruction. It was presumed that back pressure from the dilated afferent loop was the underlying cause for both the biliary dilatation and the acute pancreatitis.
Afferent loop syndrome is an uncommon complication following a Billroth II procedure and occurs in approximately 0.3% of cases (1). Most cases are due to mechanical obstruction of the afferent loop from adhesions, kinking at the anastomosis, internal hernia, stomal stenosis, malignancy, or inflammation surrounding the anastomosis (2). Obstruction of the afferent bowel with ongoing accumulation of biliary, pancreatic, and intestinal secretions results in afferent loop dilatation. The back pressure from the dilated afferent loop can cause biliary dilatation, gallbladder dilatation, and acute pancreatitis (3,4). The frequency of acute pancreatitis in afferent loop syndrome, however, has not been established in a large series, to our knowledge.
Uncommonly, afferent loop syndrome can be secondary to preferential gastric emptying into the afferent loop rather than to mechanical obstruction. In this form of afferent loop syndrome, there is excessive accumulation of gastric contents, usually secondary to a left-to-right surgical anastomosis rather than a right-to-left connection (5). Another form of afferent loop syndrome that may have an upper gastrointestinal appearance similar to a left-to-right surgical anastomosis is obstruction of the efferent loop with preferential filling of the afferent loop. In the early postoperative period, anastomotic edema, hemorrhage at the origin of the efferent limb, or both can prevent gastric emptying and, similarly, result in fluid accumulation in the afferent loop.
The clinical features of afferent loop syndrome are variable and depend on whether the afferent loop obstruction is acute or chronic. Most of the findings are relatively nonspecific and include abdominal pain, nausea and vomiting, postprandial fullness, and, rarely, postobstructive jaundice. The classic presentation of chronic afferent loop syndrome has been described as bilious vomiting with relief of the abdominal pain (6). This classic presentation presumably is due to intermittent release of pressure from the afferent loop into the stomach. In the case presented, the clinical presentation had a relatively lengthy list of differential considerations, including peptic ulcer disease, gastritis, gastric outlet obstruction, small-bowel obstruction, mesenteric ischemia, acute cholecystitis, and pancreatitis. The elevated amylase and lipase levels in this case supported the presence of acute pancreatitis.
Prior to CT and ultrasonography (US), radiographic barium examinations of the upper gastrointestinal tract were the primary means of assessing for afferent loop syndrome (7,8). Two classic findings were described at radiographic upper gastrointestinal examinations. First, nonfilling of the afferent limb suggests afferent loop syndrome. However, this finding can be problematic in that some patients without afferent loop syndrome may have nonfilling of their afferent limbs (9). Second, preferential filling and retention of barium in a dilated afferent limb for at least 60 minutes is consistent with afferent loop syndrome (Fig 2).

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Figure 2. Anteroposterior radiograph from an upper gastrointestinal examination in a different patient shows Billroth II anatomy and preferential filling of the afferent loop (arrow). This distribution of barium and retention of barium in the afferent limb on subsequent radiographs is one appearance of afferent loop syndrome at upper gastrointestinal examination.
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CT and US are useful in establishing the diagnosis of afferent loop syndrome (10,11). The fluid-filled dilated, afferent portion of small bowel can be identified readily by means of both imaging modalities. One finding that has been described as diagnostic of afferent loop syndrome is a large transversely oriented portion of small bowel anterior to the spine in the middle of the abdomen (Fig 3) (11). The case presented in this article is particularly illustrative of this finding. The tubular nature of the dilated bowel combined with the appropriate anatomic distribution for the afferent limb is useful in distinguishing afferent loop syndrome from pancreatic pseudocysts. Complications of afferent loop syndrome such as a dilated gallbladder, biliary dilatation, and pancreatitis also are identified readily at CT and US.
In summary, afferent loop syndrome is an important diagnosis to establish, as surgery is usually necessary to relieve the mechanical obstruction and possibly revise the anastomosis of the gastrojejunostomy. CT and US play a major role in the diagnosis of this entity, as the clinical signs and symptoms are generally nonspecific.
Our congratulations to the 104 individuals who submitted the most likely diagnosis (afferent loop syndrome) for Diagnosis Please, Case 24. The names and locations of the individuals, as submitted, are as follows:
- Hisashi Abe, Osaka, Japan
- Patrik Aerts, MD, Roeselare, Belgium
- Gholamali Afshang, MD, Tinley Park, Ill
- Jonathan R. Arnow, MD, Lexington, Mass
- Peter Bach, MD, Hemer, Germany
- Cung H. Bae, MD, Kenmore, NY
- Angus Baird, Alabama
- Edward L. Baker, MD, San Francisco, Calif
- Ken Baliga, Rockford, Ill
- Antonio Medina Benítez, Granada, Spain
- Grazia Bitti, Cagliari, Italy
- Frank S. Bonelli, MD, PhD, Rockford, Ill
- John W. Breckenridge, MD, Abington, Pa
- Eric Bressler, Minnetonka, Minn
- Doug Brown, MD, Durham, NC
- Michael P. Buetow, MD, Okemos, Mich
- Josè Burgos-Flor, La Rioja, Argentina
- Charles H. Bush, MD, Gainesville, Fla
- Robert A. Camele, MD, Uniontown, Pa
- Yvette Cheong, MD, Vancouver, British Columbia, Canada
- Martin I. Cohen, MD, Westlake Village, Calif
- Christopher J. Conners, MD, Rosemont, Pa
- Manoel de Souza Rocha, MD, Sao Paulo, Brazil
- Jonathan H. DeMeo, MD, Yorktown, Va
- Dr. Gloria Diaz, Buenos Aires, Argentina
- Olivier Dourthe, MD, Sophia Antipolis, France
- Seyed A. Emamian, MD, PhD, Washington, DC
- Steven M. Epstein, MD, Cherry Hill, NJ
- Milton R. Fuentealba, MD, General Roca, Rio Negro, Argentina
- Akira Fujikawa, Tokyo, Japan
- Gerrit Fund, Germany
- M. Elon Gale, MD, Boston, Mass
- Cristine Norwig Galvão, MD, Barretos, Brazil
- Douglas Gardner, MD, Windsor, Ontario, Canada
- Jorge M. Garin Ferreira, Malaga, Spain
- Guillermo Geisse, MD, St Louis, Mo
- Brad S. Gluck, MD, Southampton, NY
- Burton M. Gold, MD, Mineola, NY
- Herbert F. Gramm, Boston, Mass
- Mark A. Guenin, MD, Harrisburg, Pa
- Flavius F. Guglielmo, MD, Basking Ridge, NJ
- Yong H. Hahn, MD, Flushing, NY
- Howard T. Heller, MD, Garden City, NY
- Gary M. Israel, MD, New York, NY
- Hirotsugu Kado, Fukui, Japan
- Douglas S. Katz, MD, Mineola, NY
- Reiley Kidd, MD, Seattle, Wash
- Eung-Yeop Kim, MD, Seoul, Korea
- Minyeong Kim, Seoul, Korea
- Mitchell A. Klein, MD, Milwaukee, Wis
- Eito Kozawa, Bryn Mawr, Pa
- Richard Krauthamer, MD, Rolling Hills, Calif
- Mahesh Kumar, Bolton, United Kingdom
- Stefanos Lachanis, MD, Athens, Greece
- Stephen Lastig, MD, Woodbury, NY
- Wen-jeng Lee, MD, Taipei, Taiwan
- Wolf G. Liu, Taipei, Taiwan
- Dr. Laura Marini, General Roca, Rio Negro, Argentina
- Dr. Luis Méndez-Uriburu, Tucumán, Argentina
- Edward Menges, MD, Aptos, Calif
- Harlan D. Meyer, MD, Bexley, Ohio
- Manabu Minami, MD, Tokyo, Japan
- Robert E. Mindelzun, MD, Palo Alto, Calif
- Hidetoshi Miyake, MD, Oita, Japan
- Sergio J. Moguillansky, MD, Cipolletti, Rio Negro, Argentina
- Eduardo Mondello, Buenos Aires, Argentina
- Toshio Moritani, Rochester, NY
- Carlos J. Nassar, MD, Humacao, Puerto Rico
- Dr. Carlos Ocampo, Buenos Aires, Argentina
- Sanford M. Ornstein, MD, Phoenix, Ariz
- David M. Panicek, MD, New York, NY
- Harish Panicker, MD, Pontiac, Mich
- Benedito Pinheiro de Abreu Neto, São Paulo, Brazil
- John M. Plotke, Naperville, Ill
- Daniel Portalez, MD, Toulouse, France
- Shawn P. Quillin, MD, Charlotte, NC
- Enrique Remartinez Escobar, MD, Melilla, Spain
- Randall Rhodes, MD, Rockford, Ill
- Luiz Antonio Rossi, São Paulo, SP, Brazil
- Pierre-Jean Sauvage, MD, Mâcon, France
- Dennis Scholl, MD, Gig Harbor, Wash
- Steven M. Schultz, MD, Fort Worth, Tex
- Raymond Selouan, MD, Beirut, Lebanon
- Carlos Antonio Serrano, Olavarria, Argentina
- Matt Shapiro, MD, Lowell, Mass
- Taro Shimono, MD, Kyoto, Japan
- Nigel Sommerfeld, MBBS (Qld), South Brisbane, Australia
- Stacy Stevens, MD, San Antonio, Tex
- Peter M. Stroz, MD, Toronto, Ontario, Canada
- Denis Tack, MD, Charleroi, Belgium
- J. Takasugi, Mercer Island, Wash
- Douglas L. Teich, MD, Brookline, Mass
- Shendee Teng, MD, Woodbridge, NJ
- D. Dean Thornton, MD, Kirkwood, Mo
- Real Thuot, MD, Iberville, Quebec, Canada
- Dr. Edgardo Fabián Torres, General Roca, Río Negro, Argentina
- Carlos E. Triana Rodriguez, Santafe de Bogota, Colombia
- Philippe Vanlede, MD, Izegem, Belgium
- Angelo Vanzulli, MD, Milan, Italy
- Philip Wadyko, MD, Belle Vernon, Pa
- David Warshauer, MD, Chapel Hill, NC
- Jeff West, MD, Jacksonville, Fla
- Joe Yut, Olathe, Kan
- Marc Zins, MD, Paris, France
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FOOTNOTES
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There was one individual who submitted the highest number of most likely diagnoses for cases 1324. The name of this person will be announced in an upcoming issue of the Journal.
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Dahlgren S, Stenram U. Acute pancreatitis and hepatic necrosis in the acute afferent loop syndrome: a histopathological study in the rat. Ups J Med Sci 1976; 81:61-64.[Medline]
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Bubrick MP, Hitchcock CR. Renal cyst causing afferent loop obstruction and acute pancreatitis. Am Surg 1975; 41:440-443.[Medline]
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Burhenne HJ. The iatrogenic afferent-loop syndrome. Radiology 1968; 91:942-947.
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Beranbaum SL, Lewis L, Schwartz S. Roentgen exploration of the afferent loop. Radiology 1968; 91:932-941.[Medline]
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Op den Orth JO. Tubeless hypotonic examination of the afferent loop of the Billroth II stomach. Gastrointest Radiol 1977; 2:1-5.[Medline]
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Gale ME, Gerzof SG, Kiser LC, et al. CT appearance of afferent loop obstruction. AJR Am J Roentgenol 1982; 138:1085-1088.[Abstract/Free Full Text]
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Lee DH, Lim JH, Ko YT. Afferent loop syndrome: sonographic findings in seven cases. AJR Am J Roentgenol 1991; 157:41-43.[Abstract/Free Full Text]
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