CLINICAL CHALLENGES AND IMAGES IN GI Now You See It, Now You Don’t: An Unusual Cause of the “Double Duct Sign” Richard S. Kalman,1 Morgan A. Bresnick,2 and Christopher S. Huang1 1 Section of Gastroenterology, Boston Medical Center, Boston, Massachusetts; and 2Department of Surgery, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Question: An 80year-old Haitian man presented to our hospital with a 1-day history of crampy, diffuse abdominal pain associated with nausea and vomiting. He reported similar symptoms occurring intermittently over the past 5 years, and he lost 30 pounds over the last 12 months. Prior investigation included an esophagogastroduodenoscopy (EGD) in Haiti 2 years ago that reportedly showed a “mass” of uncertain nature, but subsequent EGD apparently showed no abnormality. On presentation to our hospital, physical examination revealed epigastric tenderness without rebound, guarding, or palpable mass. Laboratory testing revealed abnormal liver function tests (total/direct bilirubin level, 1.4/0.9 mg/dL; alkaline phosphatase, 237 U/L; alanine aminotransferase, 87 U/L; aspartate aminotransferase, 138 U/L) and elevated pancreatic enzymes (amylase, 1274 U/L; lipase, >1000 U/L). Computed tomography of the abdomen and pelvis revealed a 4.5-cm mass in the duodenum likely intussuscepting from the stomach, associated with common bile duct and pancreatic duct dilation to 1.3 cm and 8 mm, respectively (Figure A, B). EGD revealed a long, broad stalk of gastric mucosa prolapsing along the lesser curvature, through the pylorus. Retroflexion demonstrated that this stalk arose from the gastric fundus (Figure C). The endoscope was advanced with some difficulty alongside the stalk and ultimately into the duodenal bulb, where the views of the lumen were completely obliterated. Upon endoscope withdrawal, the prolapsing stalk reduced back into the stomach, and a large subepithelial mass with focal ulceration was visualized in the gastric fundus (Figure D). What is the most likely diagnosis to explain these laboratory and radiographic findings? Look on page 591 for the answer and see the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.
Conflicts of interest The authors disclose no conflicts. © 2014 by the AGA Institute 0016-5085/$36.00 http://dx.doi.org/10.1053/j.gastro.2013.10.001
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web and ZD remains unknown, but the index of suspicion at time of endoscopy should be high as the barium esophagram may not fully reveal this coexisting pathology. Given the comorbidities of our patient, the web was disrupted by passage of an 18-mm over-the-wire rigid dilator without performing a cricopharyngeal myotomy. This resulted in complete resolution of dysphagia and illustrates that identification and treatment of a coexistent cervical web may obviate the need for myotomy.
References 1. 2.
3.
Siddiq MA, Sood S, Strachan D. Pharyngeal pouch (Zenker’s diverticulum). Postgrad Med J 2001;77:506. Evrard S, Le Moine O, Hassid S, et al. Zenker’s diverticulum: a new endoscopic treatment with a soft diverticuloscope. Gastrointest Endosc 2003;58:116. Low DE, Hill DE. Cervical esophageal web associated with Zenker’s diverticulum. Am J Surg 1998;156:34–37.
For submission instructions, please see the Gastroenterology web site (www.gastrojournal.org).
Answer to the Clinical Challenges and Images in GI Question: Image 3 (page 347): Olmesartan-Induced Enteropathy On careful review of his medical records and after a detailed history, it was found that the patient was started on olmesartan 20 mg/d (previously on lisinopril) in 2008 for hypertension. The dose was subsequently increased to 40 mg/d in the subsequent months for better blood pressure control. His primary care physician was contacted and confirmed the reported history. The patient began experiencing symptoms in March 2009. A recent case series from the Mayo clinic describes 22 patients with symptoms of chronic diarrhea and weight loss who reported marked clinical improvement after stopping olmesartan.1 Small bowel biopsy slides from our patient, as seen in the Figures, showed partial villous blunting and increased intraepithelial lymphocytes. These findings were similar to the reported histologic findings in the Mayo case series. In our patient, olmesartan was held indefinitely and he was discharged home. Telephone follow-up 4 weeks after discharge confirmed our diagnosis of olmesartan-induced enteropathy with complete resolution of diarrhea, improvement in appetite, and a 15-lb weight gain. He is scheduled for a follow-up visit with his local gastroenterologist, at which time a repeat endoscopy with biopsies will be performed to establish histologic response. This case will hopefully shed light on a new entity of olmesartan-induced enteropathy and provide an impetus for further studies and research in this field.
Reference 1.
Rubio-Tapia A, Herman ML, Ludvigsson JF, et al. Severe spruelike enteropathy associated with olmesartan. Mayo Clin Proc 2012;87:732–738.
For submission instructions, please see the Gastroenterology web site (www.gastrojournal.org).
Answer to the Clinical Challenges and Images in GI Question: Image 4 (page 348): Pancreaticobiliary Obstruction From Gastric GIST Intussuscepting Into the Duodenum Endoscopic ultrasonography revealed a large, round, slightly hypoechoic mass located in the submucosal layer, containing a few cystic foci. Examination of the ampullary region by endoscopy and endoscopic ultrasonography was normal. The patient’s symptoms immediately improved after endoscopy, and liver function tests and pancreatic enzymes subsequently normalized. A follow-up transabdominal ultrasound 1 day after the EGD showed resolution of the biliary and pancreatic ductal dilation. The patient underwent laparoscopic wedge resection of the gastric mass (Figure E). Histologic examination of the specimen revealed a 4.5-cm, encapsulated, spindle cell tumor with low mitotic rate (
Question: An 80year-old Haitian man presented to our hospital with a 1-day history of crampy, diffuse abdominal pain associated with nausea and vomiting. He reported similar symptoms occurring intermittently over the past 5 years, and he lost 30 pounds over the last 12 months. Prior investigation included an esophagogastroduodenoscopy (EGD) in Haiti 2 years ago that reportedly showed a “mass” of uncertain nature, but subsequent EGD apparently showed no abnormality. On presentation to our hospital, physical examination revealed epigastric tenderness without rebound, guarding, or palpable mass. Laboratory testing revealed abnormal liver function tests (total/direct bilirubin level, 1.4/0.9 mg/dL; alkaline phosphatase, 237 U/L; alanine aminotransferase, 87 U/L; aspartate aminotransferase, 138 U/L) and elevated pancreatic enzymes (amylase, 1274 U/L; lipase, >1000 U/L). Computed tomography of the abdomen and pelvis revealed a 4.5-cm mass in the duodenum likely intussuscepting from the stomach, associated with common bile duct and pancreatic duct dilation to 1.3 cm and 8 mm, respectively (Figure A, B). EGD revealed a long, broad stalk of gastric mucosa prolapsing along the lesser curvature, through the pylorus. Retroflexion demonstrated that this stalk arose from the gastric fundus (Figure C). The endoscope was advanced with some difficulty alongside the stalk and ultimately into the duodenal bulb, where the views of the lumen were completely obliterated. Upon endoscope withdrawal, the prolapsing stalk reduced back into the stomach, and a large subepithelial mass with focal ulceration was visualized in the gastric fundus (Figure D). What is the most likely diagnosis to explain these laboratory and radiographic findings? Look on page 591 for the answer and see the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.
Conflicts of interest The authors disclose no conflicts. © 2014 by the AGA Institute 0016-5085/$36.00 http://dx.doi.org/10.1053/j.gastro.2013.10.001
348
February 2014
Clinical Challenges and Images in GI 591
web and ZD remains unknown, but the index of suspicion at time of endoscopy should be high as the barium esophagram may not fully reveal this coexisting pathology. Given the comorbidities of our patient, the web was disrupted by passage of an 18-mm over-the-wire rigid dilator without performing a cricopharyngeal myotomy. This resulted in complete resolution of dysphagia and illustrates that identification and treatment of a coexistent cervical web may obviate the need for myotomy.
References 1. 2.
3.
Siddiq MA, Sood S, Strachan D. Pharyngeal pouch (Zenker’s diverticulum). Postgrad Med J 2001;77:506. Evrard S, Le Moine O, Hassid S, et al. Zenker’s diverticulum: a new endoscopic treatment with a soft diverticuloscope. Gastrointest Endosc 2003;58:116. Low DE, Hill DE. Cervical esophageal web associated with Zenker’s diverticulum. Am J Surg 1998;156:34–37.
For submission instructions, please see the Gastroenterology web site (www.gastrojournal.org).
Answer to the Clinical Challenges and Images in GI Question: Image 3 (page 347): Olmesartan-Induced Enteropathy On careful review of his medical records and after a detailed history, it was found that the patient was started on olmesartan 20 mg/d (previously on lisinopril) in 2008 for hypertension. The dose was subsequently increased to 40 mg/d in the subsequent months for better blood pressure control. His primary care physician was contacted and confirmed the reported history. The patient began experiencing symptoms in March 2009. A recent case series from the Mayo clinic describes 22 patients with symptoms of chronic diarrhea and weight loss who reported marked clinical improvement after stopping olmesartan.1 Small bowel biopsy slides from our patient, as seen in the Figures, showed partial villous blunting and increased intraepithelial lymphocytes. These findings were similar to the reported histologic findings in the Mayo case series. In our patient, olmesartan was held indefinitely and he was discharged home. Telephone follow-up 4 weeks after discharge confirmed our diagnosis of olmesartan-induced enteropathy with complete resolution of diarrhea, improvement in appetite, and a 15-lb weight gain. He is scheduled for a follow-up visit with his local gastroenterologist, at which time a repeat endoscopy with biopsies will be performed to establish histologic response. This case will hopefully shed light on a new entity of olmesartan-induced enteropathy and provide an impetus for further studies and research in this field.
Reference 1.
Rubio-Tapia A, Herman ML, Ludvigsson JF, et al. Severe spruelike enteropathy associated with olmesartan. Mayo Clin Proc 2012;87:732–738.
For submission instructions, please see the Gastroenterology web site (www.gastrojournal.org).
Answer to the Clinical Challenges and Images in GI Question: Image 4 (page 348): Pancreaticobiliary Obstruction From Gastric GIST Intussuscepting Into the Duodenum Endoscopic ultrasonography revealed a large, round, slightly hypoechoic mass located in the submucosal layer, containing a few cystic foci. Examination of the ampullary region by endoscopy and endoscopic ultrasonography was normal. The patient’s symptoms immediately improved after endoscopy, and liver function tests and pancreatic enzymes subsequently normalized. A follow-up transabdominal ultrasound 1 day after the EGD showed resolution of the biliary and pancreatic ductal dilation. The patient underwent laparoscopic wedge resection of the gastric mass (Figure E). Histologic examination of the specimen revealed a 4.5-cm, encapsulated, spindle cell tumor with low mitotic rate (
