CLINICAL CHALLENGES AND IMAGES IN GI A Woman With Chronic Postprandial Abdominal Pain and Vomiting Raj Shah,1 Bradley Anderson,2 and Andrew Greenlund3 1
Department of Internal Medicine, University of Missouri-Kansas City, Kansas City, Missouri; 2Division of Gastroenterology and Hepatology, and 3Division of Primary Care Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota
Question: A 35-year-old woman presented with a 3-month history of postprandial abdominal discomfort and vomiting. The patient’s history included left jugular foramen schwannoma with involvement of the vagus and spinal accessory nerves (cranial nerves X and XI) treated with left level II/III neck dissection 4 months before presentation; intraoperatively, electromyography (EMG) monitoring confirmed transection of both nerves in the process of tumor resection. Physical examination yielded a soft, nondistended abdomen with bowel sounds present; no guarding, rebound, or bruits were found. The only laboratory abnormality included a mildly elevated leukocyte count of 11.7 109/L (normal range, 3.5-10.5 109/L). Abdominal computed tomographic imaging demonstrated pronounced gallbladder contraction (Figure A [transverse plane] and Figure B [coronal plane]; arrows) without additional intra-abdominal pathology. Subsequent abdominal ultrasound performed in the fasting state also demonstrated gallbladder contraction (Figure C). The patient proceeded to cholecystectomy for diagnostic and therapeutic intent. Postoperative surgical pathology revealed chronic inflammation and thickened muscularis mucosa of the gallbladder (Figure D; star indicates thickened muscularis mucosa). After cholecystectomy, the patient reported complete symptomatic resolution. What are the diagnosis and the likely etiology? Look on page 47 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. © 2016 by the AGA Institute 0016-5085/$36.00 http://dx.doi.org/10.1053/j.gastro.2015.11.001
Gastroenterology 2016;150:46–47
CLINICAL CHALLENGES AND IMAGES IN GI Answer to Image 4 (page 46): Chronic Cholecystitis Resulting From Surgical Vagotomy Altered biliary motility is a known but frequently unrecognized complication after vagal denervation. Gallbladder contraction is principally governed by the interaction between the parasympathetic motor function of the vagus nerve and cholecystokinin (CCK). Although the precise physiologic mechanism remains unclear, in postvagotomy states, including truncal vagotomy and pyloroplasty, an increase in the basal plasma CCK level occurs1 and is accompanied by the augmented sensitivity of gallbladder contractile response to CCK.2 The subsequent impairment in gallbladder motility as a result of sustained contraction potentiates hydrophobic bile salt cholestasis and cholecystitis. This mechanism is supported in this case by EMG-confirmed surgical transection of the left vagus nerve (the origin of the anterior vagal trunk transected during truncal vagotomy), followed by the onset of postprandial symptoms with radiographic confirmation of pronounced gallbladder contraction in the fasting state. Postoperative pathologic review confirmed the presence of chronic cholecystitis. In addition to alterations in gallbladder kinetics, vagal deinnervation has also been associated with symptoms of dumping, diarrhea, and bilious vomiting in patients with a history of gastroenterostomy and pyloroplasty.3 Despite these associations, vagotomy serves as a historic clue that can be overlooked in patients presenting with chronic abdominal discomfort. Chronic gastrointestinal complaints in patients with histories of surgery or trauma affecting the vagus nerves should prompt further exploration in this regard. This case illustrates the importance of such history gathering and contextualization of historical conditions with seemingly unrelated symptoms. Early recognition of this association may facilitate expedited symptomatic relief and minimize unnecessary diagnostic evaluation.
References 1. 2. 3.
Huang YS, Huang TJ, McKay D, et al. Effect of vagotomy on cholecystokinin release and gallbladder contraction in patients with complicated duodenal ulcer. Eur Surg Res 1994;26:362–371. Masclee AA, Jansen JB, Driessen WM, et al. Effect of truncal vagotomy on cholecystokinin release, gallbladder contraction, and gallbladder sensitivity to cholecystokinin in humans. Gastroenterology 1990;98:1338–1344. McMahon MJ, Johnston D, Hill DL, et al. Treatment of severe side effects after vagotomy and gastroenterostomy by closure of gastroenterostomy without pyloroplasty. Br Med J 1978;1:7–8.
For submission instructions, please see the Gastroenterology web site (www.gastrojournal.org).
47
Department of Internal Medicine, University of Missouri-Kansas City, Kansas City, Missouri; 2Division of Gastroenterology and Hepatology, and 3Division of Primary Care Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota
Question: A 35-year-old woman presented with a 3-month history of postprandial abdominal discomfort and vomiting. The patient’s history included left jugular foramen schwannoma with involvement of the vagus and spinal accessory nerves (cranial nerves X and XI) treated with left level II/III neck dissection 4 months before presentation; intraoperatively, electromyography (EMG) monitoring confirmed transection of both nerves in the process of tumor resection. Physical examination yielded a soft, nondistended abdomen with bowel sounds present; no guarding, rebound, or bruits were found. The only laboratory abnormality included a mildly elevated leukocyte count of 11.7 109/L (normal range, 3.5-10.5 109/L). Abdominal computed tomographic imaging demonstrated pronounced gallbladder contraction (Figure A [transverse plane] and Figure B [coronal plane]; arrows) without additional intra-abdominal pathology. Subsequent abdominal ultrasound performed in the fasting state also demonstrated gallbladder contraction (Figure C). The patient proceeded to cholecystectomy for diagnostic and therapeutic intent. Postoperative surgical pathology revealed chronic inflammation and thickened muscularis mucosa of the gallbladder (Figure D; star indicates thickened muscularis mucosa). After cholecystectomy, the patient reported complete symptomatic resolution. What are the diagnosis and the likely etiology? Look on page 47 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. © 2016 by the AGA Institute 0016-5085/$36.00 http://dx.doi.org/10.1053/j.gastro.2015.11.001
Gastroenterology 2016;150:46–47
CLINICAL CHALLENGES AND IMAGES IN GI Answer to Image 4 (page 46): Chronic Cholecystitis Resulting From Surgical Vagotomy Altered biliary motility is a known but frequently unrecognized complication after vagal denervation. Gallbladder contraction is principally governed by the interaction between the parasympathetic motor function of the vagus nerve and cholecystokinin (CCK). Although the precise physiologic mechanism remains unclear, in postvagotomy states, including truncal vagotomy and pyloroplasty, an increase in the basal plasma CCK level occurs1 and is accompanied by the augmented sensitivity of gallbladder contractile response to CCK.2 The subsequent impairment in gallbladder motility as a result of sustained contraction potentiates hydrophobic bile salt cholestasis and cholecystitis. This mechanism is supported in this case by EMG-confirmed surgical transection of the left vagus nerve (the origin of the anterior vagal trunk transected during truncal vagotomy), followed by the onset of postprandial symptoms with radiographic confirmation of pronounced gallbladder contraction in the fasting state. Postoperative pathologic review confirmed the presence of chronic cholecystitis. In addition to alterations in gallbladder kinetics, vagal deinnervation has also been associated with symptoms of dumping, diarrhea, and bilious vomiting in patients with a history of gastroenterostomy and pyloroplasty.3 Despite these associations, vagotomy serves as a historic clue that can be overlooked in patients presenting with chronic abdominal discomfort. Chronic gastrointestinal complaints in patients with histories of surgery or trauma affecting the vagus nerves should prompt further exploration in this regard. This case illustrates the importance of such history gathering and contextualization of historical conditions with seemingly unrelated symptoms. Early recognition of this association may facilitate expedited symptomatic relief and minimize unnecessary diagnostic evaluation.
References 1. 2. 3.
Huang YS, Huang TJ, McKay D, et al. Effect of vagotomy on cholecystokinin release and gallbladder contraction in patients with complicated duodenal ulcer. Eur Surg Res 1994;26:362–371. Masclee AA, Jansen JB, Driessen WM, et al. Effect of truncal vagotomy on cholecystokinin release, gallbladder contraction, and gallbladder sensitivity to cholecystokinin in humans. Gastroenterology 1990;98:1338–1344. McMahon MJ, Johnston D, Hill DL, et al. Treatment of severe side effects after vagotomy and gastroenterostomy by closure of gastroenterostomy without pyloroplasty. Br Med J 1978;1:7–8.
For submission instructions, please see the Gastroenterology web site (www.gastrojournal.org).
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