Acute Pancreatitis Complicating Diagnostic Endosonography

Richard A. Erickson, M.D., F.A.C.P., F.A.C.G.

 

Keywords

Endosonography, pancreatitis

Introduction

Endoscopic ultrasound (EUS) has proved to be very sensitive for assessing pancreatic and biliary pathology (1, 2). EUS's accuracy in pancreaticobiliary disease is complimented by its low morbidity. As long as the echoendoscope is not being forced through a stricture, EUS is reported to have only the rare major complications generally associated with upper endoscopic, i.e. perforation and cardiopulmonary problems (3). Because of the combination of low morbidity and high pancreaticobiliary accuracy, EUS is often used in preference to diagnostic ERCP specifically to avoid the potential for ERCP-induced pancreatitis. We report the second case of acute pancreatitis associated with diagnostic EUS and believe this very rare complication may need to be added to the rare risks associated with diagnostic EUS.

Methods for EUS Capture

Images were scanned from original thermal prints.

Case Summary

The patient is a 33 year old white male with at least twelve bouts of relatively mild recurrent pancreatitis over the past five or six years. His last attack resulted in being briefly hospitalized two weeks earlier at which time his maximum amylase was only 240 and an abdominal CT showed minimal generalized pancreatic enlargement. The patient drank only 3 to 4 beers per month and his lipids and calcium have been normal. Previous abdominal ultrasounds had not shown any gallbladder pathology and he had never had an ERCP. Interestingly, the patient's father, a heavy alcohol user, also had recurrent pancreatitis starting in his early thirties and died from pancreatic cancer in his fifties.

Figure 1

As part of his initial evaluation at our institution, the patient underwent a diagnostic EUS. He was totally asymptomatic at the time. EUS was performed as previous described (4) with a pre-EUS endoscopy (5) with the Pentax EG 2901 videoendoscope (Pentax Precision Instrument Corp., Orangeburg, NY). This showed only some mild changes of reflux esophagitis. Diagnostic EUS was then performed using the Olympus GF-UM20 echoendoscope (Olympus America, Inc., Lake Success, NY) at both 7.5 and 12 MHz. The echoendoscope was initially handled by a senior gastroenterology fellow (AC) and subsequently by a staff gastroenterologist (RAE). The total duration of the procedure was 60 minutes with 45 minutes being spent in the duodenum assessing the pancreatic and biliary ductal anatomy to rule out pancreas divisum and examining the gallbladder. The patient required 15 mg of midazolam and 150 mg of meperidine to maintain sedation throughout the procedure. Approximately 200 ml of sterile water was insufflated into the duodenum throughout the duodenal exam to optimize endosonographic visualization using the Olympus endoscopic water insufflator Model UWS-1.

Figure 2

EUS showed the pancreatic duct was only 2 mm in maximal diameter but there were some changes, primarily in the pancreatic head, consistent with chronic pancreatitis (2). These changes included echogenic foci and stranding, nodularity and echogenicity of the pancreatic duct wall (fig. 1). The patient had a prominent duct of Santorini with a "crossed-duct sign" suggestive of a pancreas divisum (6). However, after further evaluation, he appeared to have a normal "stack sign" with the common bile duct and main pancreatic duct simultaneously seen arising out of the main ampulla which would make a classic pancreas divisum unlikely (7). His common bile duct measured only 3 mm but the gallbladder neck contained a 5-6 mm sessile somewhat echogenic polypoid lesion which shadowed slightly (fig. 2). This lesion was most consistent with a cholesterol polyp (8). The patient had a prolonged, four hour stay in our endoscopy recovery room after the procedure complaining of nausea which was eventually relieved by 25 mg of intramuscular promethazine. However, approximately ten hours after the procedure the patient came back to our Emergency Room complaining of progressively increasing, severe abdominal pain and nausea.

Figure 3

His vital signs were normal but his bowel sounds were hypoactive and he had diffuse abdominal tenderness without rebound. On admission his laboratories showed WBCs of 18,500, hemoglobin 15.8 g/dL, amylase 1,060 IU/L (28-100), lipase 6,110 IU/L (166-292), calcium 8.7 mg/dL, triglycerides 137 mg/dL, normal electrolytes and normal liver tests. An acute abdominal series showed only a non-specific bowel gas pattern with no free air. An abdominal CT the next day revealed mild heterogeneity of the pancreas with peripancreatic stranding (fig. 3), a few fluid-filled loops of bowel consistent with a local ileus, some free fluid around the tail of the pancreas and spleen, bibasilar atelectasis and small bilateral pleural effusions. The patient was treated with bowel rest, fluid resuscitation, analgesics and made a slow recovery over the next eight days and was discharged.

Discussion

Discussion: We believe this patient represents the second case of acute pancreatitis reported after diagnostic endoscopic ultrasound. Kulling et al. reported a remarkably similar case of acute pancreatitis after a diagnostic EUS (9). Like our case, their patient was young (a 22 year old woman) and had idiopathic recurrent pancreatitis for a number of years prior to the EUS. In addition, their patient had an anomaly of the pancreas on subsequent ERCP, ansa pancreatica (10). The etiology of recurrent pancreatitis in our patient is still uncertain. The cholesterol polyp may suggest microlithiasis; however, the history of pancreatitis in his father raises the possibility of familial pancreatitis. The prominent duct of Santorini may suggest our patient, like the previously reported case, may have some anomaly of the pancreatic ductal system. However, this has yet to be confirmed in our patient as he is understandably reluctant to consider having an ERCP at this time.

Although acute pancreatitis has been reported after diagnostic endoscopy (11), it is an extraordinarily rare complication. The mechanism by which endoscopy or diagnostic EUS could cause pancreatitis is unknown. Since mechanical trauma to the ampulla by either biopsy (12) or unsuccessful attempts at cannulation during failed ERCP (13) can cause acute pancreatitis, EUS- induced pancreatitis may likewise be secondary to excessive mechanical trauma to the ampulla in a patient predisposed to developing pancreatitis. This may lead to ampullary spasm or edema resulting in excessive pancreatic duct pressure and ensuing pancreatitis.

EUS may be more prone to inducing pancreatitis than standard endoscopy for at least three reasons. High risk patients with recurrent pancreatitis are often undergoing diagnostic EUS as part of their evaluation. This type of patient is clearly at higher risk for pancreatitis after ERCP or sphincter of Oddi manometry (13). Additionally, much more time is typically spent in the duodenum during EUS than with standard endoscopy since it is there that the pancreatic head, ampullary region and extrahepatic biliary tree is examined (14). Finally, the water-filled balloon used for acoustic coupling may also result in additional mechanical trauma to the ampullary region through compression or rubbing. It is doubtful that water insufflation into the duodenum could cause any clinically significant increase in luminal pressure as the water can flow freely proximally and distally through the duodenum. The acoustic energy produced by the transducer of an echoendoscope is quite small (15) and it would seem unlikely that it could induce pancreatitis itself.

Since this case and the one previously reported are nearly identical in their clinical circumstances, we believe that acute pancreatitis should be added to the list of rare complications associated with diagnostic EUS in patients with a history of recurrent pancreatitis. Since tens of thousands of EUS exams have been performed over the last decade with now only two reported cases of pancreatitis, the incidence of this complication must be very low. As demonstrated by these two cases, this risk may be limited to those younger patients with a significant previous history of recurrent acute pancreatitis. It is unknown whether any change in EUS technique could reduce the risk of pancreatitis in such high risk patients. However, in patients with a history of recurrent pancreatitis, it would make pathophysiologic sense to try and minimize mechanical trauma to the ampulla during diagnostic EUS by spending as short a time as possible in the duodenum, avoiding excessive balloon insufflation and minimizing physical contact between the echoendoscope and the ampulla.

References

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Editorial Board:
Manoop S. Bhutani, M.D.
Galveston, TX
William R. Brugge, M.D.
Boston, MA
Peter R. McNally, D.O.
Denver, CO
Iqbal S. Sandhu, M.D.
Salt Lake City, UT
Thomas J. Savides, M.D.
San Diego, CA

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