Duodenal Bezoar: A Rare Cause of Acute Pancreatitis
Article information
Abstract
Gastrointestinal bezoars often occur as a complication of previous gastric surgery or in patients with altered gastrointestinal motility. Complications associated with gastrointestinal bezoars include perforation, peritonitis, protein-losing enteropathy, and acute appendicitis. Acute pancreatitis secondary to a duodenal bezoar is rare, and few studies have reported this complication. We report a case of acute pancreatitis and subsequent duodenal obstruction caused by a large duodenal phytobezoar.
INTRODUCTION
Bezoars are retained concretions of indigestible foreign material that accumulate and conglomerate in the gastrointestinal tract [1]. There is a relatively rare disease entity as described in the literature [2,3]. The gastrointestinal bezoars often occur as a complication of previous gastric surgery or altered gastrointestinal motility in which there is a loss of normal peristaltic activity, compromised pyloric function, or reduced gastric acidity [1]. However, bezoars have been described in patients with normal gastrointestinal anatomy and physiology [2]. Endoscopic examinations play the most important role in the detection of gastrointestinal bezoars, as well as in the treatment [4]. The currently available treatment options for a gastrointestinal phytobezoar include dissolution of the bezoar, endoscopic removal, and surgical removal [3,4]. Once the diagnosis of bezoar is made, the bezoar needs to be generally dissolved or removed because it can cause gastric outlet obstruction, ileus, ulcerations due to pressure necrosis, and subsequent gastrointestinal bleeding [4]. Acute pancreatitis is a rare complication of duodenal bezoar and has been rarely reported [5,6]. We report a case of acute pancreatitis and subsequent duodenal obstruction caused by a large duodenal phytobezoar.
CASE REPORT
A 66-year-old woman visited the emergency room complaining of severe epigastric abdominal pain and vomiting lasting for 1 month. She underwent subtotal gastrectomy with Billorth I anastomosis for early gastric cancer 17 years ago, and no recurrence was reported during follow-up. Other comorbid illnesses were hypertension, diabetes mellitus, hyperlipidemia and an old cerebral infarction. Her medications included irbesartan, metformin, ezetimibe/atorvastatin, and cilostazole.
The vital signs were normal (blood pressure 145/78 mmHg, pulse rate 67 beats per minute, respiration rate 20 cycles per minute, and body temperature 36.6°C). She appeared to have an alert mental status and was without jaundice. Her abdomen was soft and flat with a mild tenderness at the epigastric area without rebound tenderness and a normal bowel sound. There were no signs of peritoneal inflammation or mass.
Laboratory studies elicited the following results: a normal cell blood count with a leukocyte count of 6770/μL, hemoglobin count at 12.9 g/dL, and platelet count of 240000/μL. The liver function test, renal function test, and electrolyte levels were normal. The C-reactive protein was elevated (4.75 mg/dL [reference, 0–0.30 mg/dL]). The serum amylase and lipase were elevated 3 times higher than the upper limit of normal, at 349 U/L (reference, 0–99 U/L) and 441 U/L (reference, 0–60 U/L), respectively.
The plain abdomen showed ill-defined food materials on the duodenum (Fig. 1A). On the abdomen computer tomography (CT), a bezoar was suggested with findings of a lowdensity mottled intraluminal mass containing air bubbles at the duodenum, and an ill-defined low attenuated area was found at the pancreatic head and a groove between the duodenal second portion with a focal compression at the abutting proximal superior mesenteric vein (Fig. 1B and C). In addition, there was a mild swelling of the pancreatic parenchyma with a scanty peripancreatic fluid, without pancreatic duct dilatation. On the magnetic resonance cholangiopancreatography, the lumen of the remnant stomach body was markedly distended, and there was acute pancreatitis accompanying a large bezoar on the proximal duodenum (Fig. 2).
Imaging studies at initial patient presentation. A: On the plain abdomen, suspected large food materials were observed at the duodenum (arrows). B and C: Abdomen computed tomography showed swelling and ill-defined low attenuated area at the pancreatic head (arrows), a large bezoar obstructing the duodenal lumen (asterisk) (B) and mild swelling of the pancreatic parenchyma (arrows) (C).
Magnetic resonance cholangiopancreatography showed a marked distended remnant stomach and proximal duodenum with a large bezoar obstructing the duodenal lumen (asterisk) and ampulla of Vater (arrow) (A), and related acute pancreatitis (arrows) (B).
Initially, conservative treatments with intravenous fluid replacement, nutritional support, and pain control were provided. Then, esophagogastroduodenoscopy was performed, and a large yellowish bezoar was observed blocking the duodenal lumen with nearly total obstruction of the ampulla of Vater (AoV) (Fig. 3A). Endoscopic treatment was performed on the same day. After 500 mL coke injection, the bezoar was pulverized with a rat tooth alligator-jaw grasping forceps and a snare. Then the endoscopic removal of the bezoar was performed by a net retrieval device (Fig. 3B-F). The size of the bezoar was at least 6 cm long. After 2 sessions of endoscopic treatment, the patient’s symptoms improved. Serum amylase and lipase levels became normal, and the patient was discharged on the hospital day 7. A follow-up endoscopy was performed one month later, and a bezoar was no longer observed.
Esophagogastroduodenoscopy showed a large yellowish phytobezoar just below the gastroduodenostomy anastomosis site (A). Endoscopic treatment was started after Coca-Cola injection (B). Mechanical fragmentation of the bezoar was performed using rat tooth alligatorgrasping forceps (C) and snare (D). Then, the fragmented bezoars were removed by the Roth net retrieval device (E), and finally, bezoars were completely removed by endoscopic treatment (F).
DISCUSSION
Acute pancreatitis is a sudden inflammatory condition of the pancreas induced by various agents, and the most common causes of the disease are alcohol consumption and gallstones. Dyslipidaemia, drugs, trauma, and infection are additional contributing factors to the pathogenesis of acute pancreatitis [7]. Duodenal bezoars are an infrequent cause of acute pancreatitis, and cases have been reported rarely in the literature [5,6,8]. In a previous case report, acute pancreatitis was caused by irritation and secondary duodenal obstruction due to the progression of jejunal bezoars [5]. Other case reports showed that pancreatitis develops when a bezoar obstructs the AoV as shown in pancreatitis due to common bile duct stones [6,8]. Some cases required surgical treatment for the removal of bezoars due to the combined bezoars at other sites of small bowel or failure of endoscopic removal [5,8]. Our case accounts for one of the few reports of a patient with acute pancreatitis caused by a duodenal bezoar, and the bezoars were removed by the endoscopic procedure without the need of surgical treatment. She had no history of excessive alcohol consumption and the abdomen CT did not show any common bile duct stones or gallstones. The obstruction of the AoV by the large bezoar was the apparent cause of the pancreatitis.
Of various types of bezoars, phytobezoars are the most common type [1]. Previous gastric surgery and diabetes mellitus are the most common predisposing factors for developing phytobezoars [1,4,9,10]. The interval between gastric operation and phytobezoar detection could range from 9 months to 30 years [10]. Clinical manifestations vary from no symptoms to acute abdominal syndrome depending on the location of the bezoar [4]. Recognizing the clinical symptoms and predisposing risk factors may enhance clinical suspicion leading to prompt diagnosis, treatment, and avoidance of potential complications related to bezoars [1]. The complications include perforation, peritonitis, protein-losing enteropathy, acute appendicitis, very seldom as in our case, acute pancreatitis [2,4,5,9]. Physical examination has limited utility in diagnosing bezoars. Occasionally, a palpable mass may be appreciated on the abdominal exam or halitosis recognized from the putrefying material within the stomach [1]. However, these findings are nonspecific and often difficult to discern. Similar to a previous case report [6], the present case had the most common predisposing risk factors for phytobezoars including previous gastric surgery and diabetes mellitus. In addition, initial laboratory findings and clinical symptoms were highly suggestive of acute pancreatitis. However, liver function tests including alkaline phosphatase and γ-glutamyl transpeptidase were normal at the emergency room. We speculated that the timing of AoV obstruction might be early, and only the pancreatic duct was affected.
Endoscopic examinations play the most important role in the detection of upper gastrointestinal bezoars as well as in the treatment [1,4,11]. The most common location for bezoars are the stomach, ileum, and jejunum, whereas the duodenum is a rare location [3,9,10]. Conservative or endoscopic treatments are provided to dissolve or remove the gastrointestinal bezoars. Several studies have reported that Coca-Cola chemical dissolution alone or endoscopic fragmentation and extraction with the coadministration of Coca-Cola by drinking, gastric lavage, or via endoscopic spraying or endoscopic injection was effective for the gastrointestinal phytobezoars [3,9,10,12,13]. Endoscopic treatment is acceptable as a primary treatment option and has fewer complications than surgery, whereas surgical interventions are needed for intestinal obstructions or perforations, and in cases where endoscopic treatment fails to resolve the bezoar [11,13]. In some cases, bezoars could migrate to the distal part of the gastrointestinal tract after partial dissolution with Coca-Cola administration and result in complications including acute pancreatitis and small bowel obstruction [14]. Thus, it is safer to provide combined mechanical fragmentation and extraction of bezoars by endoscopic treatment than oral Coca-Cola ingestion only. In the present case, the endoscopy access was relatively easy because of the gastrectomy state, although the bezoar was located in the duodenal 2nd portion. Thus, we successfully removed large bezoars (more than 6 cm) by endoscopic treatment with Coca-Cola injection and mechanical fragmentations, and the patient improved symptoms and findings of acute pancreatitis without any complications.
Acute pancreatitis by duodenal bezoar is a rare disease which necessitates an early diagnosis and rapid treatment to avoid surgical intervention and complications, especially in elderly patients. Upper gastrointestinal endoscopy after chemical dissolution is a safe and effective procedure for diagnostic and therapeutic purposes of duodenal phytobezoars.
Notes
Availability of Data and Material
Data sharing not applicable to this article as no datasets were generated or analyzed during the study.
Conflicts of Interest
Young-Il Kim, a contributing editor of the Korean Journal of Helicobacter and Upper Gastrointestinal Research, was not involved in the editorial evaluation or decision to publish this article. All remaining authors have declared no conflicts of interest.
Funding Statement
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Authors’ Contribution
Conceptualization: Young-Il Kim. Data curation: Henriette Ya Kissi Anzouan Kacou, Young-Il Kim. Writing—original draft: Henriette Ya Kissi Anzouan Kacou, Young-Il Kim. Writing—review & editing: Henriette Ya Kissi Anzouan Kacou, Young-Il Kim. Approval of final manuscript: all authors.
Ethics Statement
The informed consent was waived by the Institutional Review Board of the National Cancer Center due to the minimal risk of the case report.
Acknowledgements
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