The intrapancreatic location of the distal common bile duct is critical to many pancreatic disease

processes. Gallstone pancreatitis, the second most common cause of pancreatitis in the United States, is

caused by gallstones passed into the common bile duct. These gallstones can obstruct the duct distally

and lead to transient obstruction of the pancreatic duct with resulting reflux of pancreatic juice and bile

into the pancreatic duct, causing pancreatitis.

In benign pancreatic diseases such as chronic pancreatitis, disease in the pancreatic head may cause

benign biliary strictures and jaundice, whereas disease in the body and tail more often presents with

abdominal pain. Pancreatic ductal anatomy and the presence or absence of ductal dilation dictate the

choices for operative management. In the setting of a dilated pancreatic duct, drainage procedures may

impact pancreatic pain and recurrent acute episodes. Conversely, in the setting of small duct disease,

ablative therapy with resection (duodenum-preserving pancreatic head resection,

pancreaticoduodenectomy, and distal pancreatectomy) is the treatment of choice when medical

management fails.

Figure 52-11. Large pancreatic pseudocyst in the lesser sac. The pseudocyst is compressing the stomach anteriorly.

In the setting of acute or chronic pancreatitis, ductal disruption can lead to the formation of a

pancreatic pseudocyst. In many cases, these pseudocysts occur anterior to the pancreas in the lesser sac

(Fig. 52-11). This often leads to early satiety and abdominal pain. When large pseudocysts abut the

stomach, drainage can be achieved with endoscopic or operative cystgastrostomy.

Trauma and Pancreatic Injury

The pancreatic body lies anterior to the second lumbar vertebra deep in the retroperitoneum. In cases of

blunt abdominal trauma, specifically deceleration injury, the pancreatic body is crushed against the

second vertebral body and can be transected at this point. In trauma patients with elevated amylase and

lipase levels, the trauma surgeon should be aware of this possibility and obtain cross-sectional

pancreatic imaging to rule out ductal disruption. In the case of complete ductal disruption distal

pancreatectomy or drainage of the pancreas into the intestine may be necessary.

Penetrating injury to the duodenum or pancreas often involves major vascular injury and in many

cases is not survivable. In the case of injury to the IVC, the pancreas and duodenum must be mobilized

out of the retroperitoneum (Kocher maneuver) in order to expose the vessels.

DIAGNOSTIC APPROACH TO PATIENTS WITH PANCREATIC DISEASE

Pancreatic Imaging (Studies of Pancreatic Structure)

If pancreatic disease is suspected, the pancreas can be imaged by several radiographic modalities

including plain abdominal x-rays, upper gastrointestinal series, abdominal ultrasonography, CT MRCP,

endoscopic retrograde cholangiopancreatography (ERCP), and EUS.

Abdominal Plain Films

Plain films of the abdomen may be useful in patients with acute and chronic pancreatitis. In patients

with acute pancreatitis, the most common finding on plain film include a generalized ileus with air fluid

levels, a localized ileus or “sentinel loop” of jejunum or duodenum in the area of the inflamed pancreas,

1360

or a cutoff of the colon due to distention of the transverse colon. In the setting of acute pancreatic fluid

collections or pseudocysts, one may see an actual mass on plain film with displacement of the stomach

or duodenum.24 These findings are not sensitive or specific for acute pancreatitis, but in the setting of

elevated amylase and lipase and associated abdominal symptoms can provide support for the diagnosis

and an indication for more sensitive pancreatic imaging studies.

In the setting of chronic pancreatitis the most common finding on plain film is the presence of

calcifications within the pancreas. These are most commonly seen at the level of the second lumbar

vertebrae, where the pancreas lies in the retroperitoneum.

Upper Gastrointestinal Series

In the setting of a mass or mass effect on plain film, an upper gastrointestinal series can demonstrate

displacement of the stomach or duodenum by a retroperitoneal mass. Displacement or narrowing of the

duodenal C-loop suggests the presence of a pancreatic mass. However, the character of the mass

(inflammatory, neoplastic, cystic, etc.) cannot be further defined on upper gastrointestinal series.24 For

this reason, upper gastrointestinal series has been largely replaced by ultrasound and other crosssectional imaging modalities such as CT or MRCP.

Ultrasonography

Abdominal ultrasound can be useful in the setting of acute pancreatitis, chronic pancreatitis, pancreatic

cystic lesions, pancreatic pseudocysts, and pancreatic cancer. In acute pancreatitis, the abdominal

ultrasound may demonstrate gallstones, suggesting a potential etiology. In addition, the ultrasound can

identify an enlarged pancreas, pancreatic edema and peripancreatic fluid collections consistent with the

diagnosis of acute pancreatitis. Ultrasound can also identify pancreatic pseudocysts, cystic lesions, and

other pancreatic masses.24 Pancreatic pseudocysts usually appear as a smooth, round fluid collection

without acoustic shadowing. A pancreatic cancer is more likely to distort the underlying pancreatic

anatomy and appear as a localized, solid lesion on ultrasound, also without acoustic shadowing. Cystic

neoplasms of the pancreas can have both solid and cystic components. They can be uniloculated or

multiloculated and contain cysts of varying size. A large uniloculated neoplastic cyst is difficult to

differentiate from a pancreatic pseudocyst.

Ultrasound examination can be limited by obesity, overlying bowel gas, recently performed barium

contrast studies. Small masses or fluid collections can be easily missed. The presence of a mass on

ultrasound is an indication for more extensive workup via CT or MRCP imaging.

Computed Tomography

Contrast enhanced, multidetector helical 3D CT is the most commonly performed study for the detection

and characterization of pancreatic solid and cystic tumors. It is also useful in defining the pancreatic

anatomy in the presence of chronic pancreatitis and identifying and following the complications of acute

pancreatitis. CT is very sensitive for identifying pancreatic masses as small as 1 cm and can accurately

distinguish solid from cystic lesions. The density of the lesion on CT can provide clues as to the

diagnosis. Pancreatic adenocarcinomas are usually solid and hypodense, whereas pancreatic

neuroendocrine tumors are vascular and appear hyperdense. Both pseudocysts and cystic lesions have

components with fluid density.

CT is sensitive for the diagnosis of a malignant pancreatic adenocarcinoma. However, it is less

sensitive and accurate in the diagnosis of cystic lesions. As CT scans are more commonly performed for

a variety of indications, many cystic lesions are found incidentally. CT can be useful in identifying the

characteristics associated with malignancy including tumor size greater than 3 cm, a dilated main

pancreatic duct, and solid components within the cystic lesion.54 However, significant controversy

remains regarding observation versus resection of pancreatic cystic lesions.

Endoscopic Ultrasound

Compared to transabdominal ultrasound, EUS provides higher-resolution images of the pancreatic

parenchyma and pancreatic duct. This procedure uses a transducer fixed to an endoscope that can be

directed to the surface of the pancreas through the stomach or duodenum. EUS provides a useful adjunct

to CT in the diagnosis of mucinous cystic lesions and malignancies. Pancreatic masses and cystic lesions

can be well visualized on EUS, providing information about tumor size and invasion of major vascular

structures. While more invasive than CT, EUS can provide useful additional information. EUS allows for

fine-needle aspiration and/or biopsy, providing a tissue diagnosis, which is critical in the setting of

1361

planned neoadjuvant therapy for pancreatic adenocarcinoma. EUS can also provide information about

pancreatic ductal anatomy without the risk of invasive ERCP, which can cause severe pancreatitis.

A list of 11 EUS criteria has been defined for the diagnosis of chronic pancreatitis. The ductal criteria

include pancreatic duct stones, echogenic ductal walls, irregular ductal walls, pancreatic duct strictures,

visible side branches, and ductal dilatation. The parenchyma criteria include echogenic strands,

echogenic foci, calcifications, lobular contour, and pancreatic cysts. Recent studies have determined that

three or more EUS criteria provides the best balance of sensitivity and specificity for histologic

pancreatic fibrosis.55

Finally, in the setting of intractable pain in unresectable pancreatic cancer, chemical neurolysis of the

celiac ganglion can be performed under EUS guidance. As with any endoscopic procedure, the risks

include perforation of the stomach and/or duodenum.

Magnetic Resonance Cholangiopancreatography

MRCP is now being used more commonly as a noninvasive way to image both the biliary and pancreatic

ducts. MRCP can provide excellent images and detect abnormalities of the common bile duct and main

pancreatic duct, but it is more limited in its ability to detect abnormalities in the secondary ducts. This

noninvasive imaging technique is very useful in high-risk patients and pregnant patients. It is also useful

in diagnosis of persistent choledocholithiasis in the setting of gallstone pancreatitis. MRCP is most

useful in settings where intervention such as biopsy or biliary drainage are unnecessary, thereby

avoiding the risk of ERCP. MRCP can be a good modality for defining pancreatic ductal anatomy in

patients with chronic pancreatitis and pancreatic pseudocysts to help plan operative management.

Endoscopic Retrograde Cholangiopancreatography

ERCP is the gold standard for providing information about pancreatic ductal anatomy. However, it is

associated with significant complications and can often be avoided by using the previously described

noninvasive tests. Five percent to 20% of patients develop clinical pancreatitis after ERCP and 25% to

75% have elevated amylase and lipase levels.24 There is no way to prevent post-ERCP pancreatitis;

however, high-pressure injection of the pancreatic duct is thought to contribute. Perforation of the

gastrointestinal tract is a potential complication of ERCP.

ERCP is performed less commonly since much of the information can now be obtained with CT,

MRCP, and/or EUS. However, it remains the procedure of choice when there is a high likelihood for the

need of therapeutic intervention. For example, in patients with persistently elevated liver function tests

in the setting of common duct stones ERCP is both diagnostic and therapeutic.

Pancreatic cancer is characterized by obstruction or stenosis of the pancreatic duct and or common

bile duct (double-duct sign). ERCP remains the primary modality for palliation of obstructive jaundice

with endostent placement. In chronic pancreatitis, the pancreatic duct may have irregularities including

stenosis, dilation, sacculation, and ectasia. Pancreatic duct stones may be present within the pancreatic

duct. Similar ductal changes can be observed immediately following acute attacks of pancreatitis.

However, these abnormalities can be detected on MRCP or CT.

References

1. Klein SD, Affronti JP. Pancreas divisum, an evidence-based review: part II, patient selection and

treatment. Gastrointest Endosc 2004;60(4):585–589.

2. Levy MJ, Geenen JE. Idiopathic acute recurrent pancreatitis. Am J Gastroenterol 2001;96(9):2540–

2555.

3. Testoni PA. Aetiologies of recurrent acute pancreatitis: acute or chronic relapsing disease? JOP

2001;2(6):357–367.

4. Delhaye M, Engelholm L, Cremer M. Pancreas divisum: controversial clinical significance. Dig Dis

1988;6(1):30–39.

5. Delhaye M, Engelholm L, Cremer M. Pancreas divisum: congenital anatomic variant or anomaly?

Contribution of endoscopic retrograde dorsal pancreatography. Gastroenterology 1985;89(5):951–

958.

6. Cotton PB. Congenital anomaly of pancreas divisum as cause of obstructive pain and pancreatitis.

Gut 1980;21(2):105–114.

7. Khalid A, Slivka A. Approach to idiopathic recurrent pancreatitis. Gastrointest Endosc Clin N Am

1362

2003;13(4):695–716, x.

8. Manfredi R, Costamagna G, Brizi MG, et al. Pancreas divisum and “santorinicele”: diagnosis with

dynamic MR cholangiopancreatography with secretin stimulation. Radiology 2000;217(2):403–408.

9. Ravitch MM, Woods AC, Jr. Annular pancreas. Ann Surg 1950;132(6):1116–1127.

10. Theodorides T. [Annular Pancreas]. J Chir (Paris) 1964;87:445–462.

11. Chevillotte G, Sahel J, Raillat A, et al. Annular pancreas. Report of one case associated with acute

pancreatitis and diagnosed by endoscopic retrograde pancreatography. Dig Dis Sci 1984;29(1):75–

77.

12. Glazer GM, Margulis AR. Annular pancreas: etiology and diagnosis using endoscopic retrograde

cholangiopancreatography. Radiology 1979;133(2):303–306.

13. Zyromski NJ, Sandoval JA, Pitt HA, et al. Annular pancreas: dramatic differences between children

and adults. J Am Coll Surg 2008;206(5):1019–1025; discussion 1025–1017.

14. Ikeda Y, Irving IM. Annular pancreas in a fetus and its three-dimensional reconstruction. J Pediatr

Surg 1984;19(2):160–164.

15. Guillou L, Nordback P, Gerber C, et al. Ductal adenocarcinoma arising in a heterotopic pancreas

situated in a hiatal hernia. Arch Pathol Lab Med 1994; 118(5):568–571.

16. Makhlouf HR, Almeida JL, Sobin LH. Carcinoma in jejunal pancreatic heterotopia. Arch Pathol Lab

Med 1999;123(8):707–711.

17. Kleinman R, Gingerich R, Wong H, et al. Use of the Fab fragment for immunoneutralization of

somatostatin in the isolated perfused human pancreas. Am J Surg 1994;167(1):114–119.

18. Greenberger N, Toskes P. Chapter 307. Acute and chronic pancreatitis (chapter). In: Fauci AS,

Braunwald E, Kasper DL, et al., eds. Harrison’s Principles of Internal Medicine. 17th ed: McGraw Hill:

http://www.accessmedicine.com/content.aspx?aid=2875598. Accessed January 4, 2009.

19. Valenzuela JE, Weiner K, Saad C. Cholinergic stimulation of human pancreatic secretion. Dig Dis Sci

1986;31(6):615–619.

20. Konturek SJ, Becker HD, Thompson JC. Effect of vagotomy on hormones stimulating pancreatic

secretion. Arch Surg 1974;108(5):704–708.

21. Oh HC, Kim MH, Choi KS, et al. Analysis of PRSS1 and SPINK1 mutations in Korean patients with

idiopathic and familial pancreatitis. Pancreas 2008; 38(2), 180–183.

22. Masamune A, Kume K, Shimosegawa T. Differential roles of the SPINK1 gene mutations in alcoholic

and nonalcoholic chronic pancreatitis. J Gastroenterol 2007;42 suppl 17:135–140.

23. Dreiling D, Wolfson P. New Insights into Pancreatic Disease Revealed by the Secretin Test (chapter). Vol

2. Philadelphia, PA: Lea and Febiger; 1979.

24. Toskes P, Greenberger N. Chapter 306. Approach to the patient with pancreatic disease (chapter).

In: Fauci AS, Braunwald E, Kasper DL, et al., eds. Harrison’s Principles of Internal Medicine. 17th ed:

McGraw Hill: http:///www.accessmedicine.com/content.aspx?aID=2875521. Accessed January 4,

2009.

25. Noda A, Hayakawa T, Kondo T, et al. Clinical evaluation of pancreatic excretion test with

dimethadione and oral BT-PABA test in chronic pancreatitis. Dig Dis Sci 1983;28(3):230–235.

26. Goff JS. Two-stage triolein breath test differentiates pancreatic insufficiency from other causes of

malabsorption. Gastroenterology 1982;83(1 Pt 1):44–46.

27. Smith RC, Southwell-Keely J, Chesher D. Should serum pancreatic lipase replace serum amylase as

a biomarker of acute pancreatitis? ANZ J Surg 2005; 75(6):399–404.

28. Kemppainen E, Hedstrom J, Puolakkainen P, et al. Increased serum trypsinogen 2 and trypsin 2-

alpha 1 antitrypsin complex values identify endoscopic retrograde cholangiopancreatography

induced pancreatitis with high accuracy. Gut 1997;41(5):690–695.

29. Kemppainen EA, Hedstrom JI, Puolakkainen PA, et al. Rapid measurement of urinary trypsinogen-2

as a screening test for acute pancreatitis. N Engl J Med 1997;336(25):1788–1793.

30. Nanjo K, Sanke T, Miyano M, et al. Diabetes due to secretion of a structurally abnormal insulin

(insulin Wakayama). Clinical and functional characteristics of [LeuA3] insulin. J Clin Invest

1986;77(2):514–519.

31. Opara EC, Atwater I, Go VL. Characterization and control of pulsatile secretion of insulin and

glucagon. Pancreas 1988;3(4):484–487.

1363