# 31 - 358 Approach to the Patient with Pancreatic Disease

### 358 Approach to the Patient with Pancreatic Disease

Section 4	 Disorders of the Pancreas
Somashekar G. Krishna, 

Darwin L. Conwell, Phil A. Hart

Approach to the Patient 

with Pancreatic Disease
■
■GENERAL CONSIDERATIONS
Globally, pancreatic disorders, including acute and chronic pancreati­
tis, pancreatic cysts, and pancreatic cancer, are challenging to manage 
and associated with a high burden on health care resources. While the 
relationships between these diseases are multifaceted, there is ongoing 
scientific progress and a growing understanding in this field. Acute 
pancreatitis is one of the most common reasons for hospitalizations in 
gastroenterology, and there is increasing evidence of sequelae includ­
ing diabetes, exocrine pancreas insufficiency, and chronic pancreatitis. 
In elderly patients, acute pancreatitis may serve as an early symptom 
of pancreatic cancer. Chronic pancreatitis, an irreversible disease of the 
pancreas, associated with poor quality of life due to abdominal pain 
and associated exocrine insufficiency, is also an established risk factor 
for pancreatic cancer. Pancreatic cysts, mostly incidental, are increas­
ingly detected on cross-sectional abdominal imaging studies. Although 
only a small proportion of pancreatic cysts can progress to pancreatic 
cancer, the diagnostic uncertainty can introduce unwanted anxiety to 
patients and treating physicians. Meanwhile, with persistently high 
mortality rates, the incidence of pancreatic adenocarcinoma is increas­
ing and is the seventh leading cause of cancer-related death in the 
industrialized world and the third most common in the United States.
PART 10
Disorders of the Gastrointestinal System
As emphasized in Chap. 359, the etiologies and clinical manifesta­
tions of pancreatitis are quite varied. Although it is well-appreciated 
that acute pancreatitis is frequently secondary to biliary tract disease or 
alcohol abuse, it can also be caused by medications, genetic mutations, 
and trauma. In ~30% of patients with acute pancreatitis and 25–40% of 
patients with chronic pancreatitis, the etiology is initially unexplained.
The global pooled incidence of acute pancreatitis is ~33.7 cases 
(95% confidence interval [CI], 23.3–48.8) with 1.16 deaths (95% CI, 
0.85–1.6) per 100,000 person-years. The global pooled incidence of 
chronic pancreatitis is ~9.6 cases (95% CI, 7.9–11.8) with 0.09 attrib­
utable deaths (95% CI, 0.02–0.5) per 100,000 person-years. In the 
A
B
FIGURE 358-1  A. Side-branch intraductal papillary mucinous neoplasm (magnetic resonance imaging [MRI] with magnetic resonance cholangiopancreatography [MRCP]). 
T2-weighted MRCP image demonstrates a dominant, lobulated, hyperintense cystic structure (arrow) within the posterior body of the pancreas. The pancreatic duct 
upstream from the cyst is dilated and irregular. Endoscopic ultrasound and fine-needle aspiration of cyst fluid were consistent with a mucinous cyst. Surgical histopathology 
revealed an infiltrating moderately differentiated adenocarcinoma, 0.3 cm, arising in a background of an intraductal papillary mucinous neoplasm (IPMN). B. Mucinous 
cystic neoplasm (computed tomography [CT] scan). In the tail of the pancreas, there is a well-circumscribed hypodense cyst (arrow) without any nodular enhancing 
components. Endoscopic ultrasound and fine-needle aspiration of cyst fluid were suggestive of a mucinous cyst. Surgical histopathology revealed a mucinous cystic 
neoplasm (3.4 cm) with low-grade dysplasia. The stroma of the cyst demonstrated diffuse positivity for progesterone receptor and focal positivity for CD10 (ovarian stroma), 
confirming the diagnosis. C. Serous cystadenoma (MRI). A lobulated microcystic cyst (arrow) is observed in the tail of the pancreas. Neither a communication with the main 
pancreatic duct nor intracystic soft tissue enhancing nodular components were observed. However, the cyst continued to increase in size, and a distal pancreatectomy 
was performed. Histopathology revealed a serous microcystic adenoma. (Courtesy of Dr. Z.K. Shah, The Ohio State University Wexner Medical Center; with permission.)

United States, the number of patients admitted to the hospital with 
acute pancreatitis is increasing, with estimated rates of almost 300,000 
annually, whereas the number of patients hospitalized for chronic pan­
creatitis is decreasing, with recent estimates of ~13,000 admissions per 
year. Chronic pancreatitis has an annual prevalence of 42–73 cases per 
100,000 adults in the United States, although higher prevalence rates 
(0.04–5%) have been noted among adults at autopsy. Together, acute 
and chronic pancreatic disease costs an estimated $3 billion annually 
in health care expenditures. During the COVID-19 pandemic, it was 
noted that the infection was associated with elevated pancreas enzyme 
serum levels and presumed acute pancreatitis, though causal relation­
ships have not been definitively established.
The diagnosis of acute pancreatitis is generally defined based on a 
combination of laboratory, imaging, and clinical symptoms. The diag­
nosis of chronic pancreatitis, especially in mild disease, is hampered by 
the relative inaccessibility of the pancreas to direct examination and the 
nonspecificity of the associated abdominal pain. Many patients with 
chronic pancreatitis do not have elevated blood amylase or lipase levels. 
Some patients with chronic pancreatitis develop signs and symptoms 
of exocrine pancreatic insufficiency (EPI), and thus, objective evidence 
for pancreatic disease can be demonstrated. However, there is a large 
reservoir of pancreatic exocrine function. Maldigestion of fat and 
protein becomes evident only when more than 90% of the pancreas 
is functionally damaged or obstructed. Noninvasive, indirect tests of 
pancreatic exocrine function (e.g., fecal elastase) are much more likely 
to give abnormal results in patients with obvious advanced pancreatic 
disease (i.e., pancreatic calcification, steatorrhea, or diabetes mellitus) 
than in patients with occult disease. Invasive, direct tests of pancreatic 
secretory function (e.g., secretin stimulation test) are the most sensitive 
and specific tests to detect early chronic pancreatic disease when imag­
ing is equivocal or normal.
The increasing utilization of cross-sectional imaging modalities 
with their improved resolution has contributed to a high prevalence 
(2–5% with computed tomography [CT] scans, 20–30% with magnetic 
resonance imaging [MRI]) of incidentally detected pancreatic cysts. 
The most common cyst type encountered is an intraductal papillary 
mucinous neoplasm (IPMN), which is classified as a precancerous 
mucinous cyst. In the absence of high-risk features, radiographic 
surveillance is typically recommended (Fig. 358-1). Mucinous cystic 
neoplasms (MCNs) are relatively less common and occur almost exclu­
sively in women. Among the neoplastic cysts, serous cystadenomas 
have a negligible risk of progression to malignancy. Other infrequent 
neoplastic cysts include neuroendocrine tumors and solid pseudo­
papillary neoplasms. The most commonly encountered benign cyst 
is a pseudocyst, which can occur in patients with a history of acute 
C

or chronic pancreatitis. The challenges with accurately predicting the 
risk of malignant transformation of precancerous pancreatic cysts has 
contributed to the growing number of patients on imaging surveillance 
protocols placing a burden on health care systems in industrialized 
nations.
TABLE 358-1  Tests Useful in the Diagnosis of Acute and Chronic Pancreatitis and Pancreatic Neoplasms
TEST
PRINCIPLE
COMMENT
Pancreatic Enzymes in Body Fluids
Serum lipase
Pancreatic inflammation leads to increased serum 
enzyme levels
Amylase
 
 
1.	 Serum
Pancreatic inflammation leads to increased serum 
enzyme levels
2.	 Urine
Renal clearance of amylase is increased in acute 
pancreatitis
3.	 Ascitic fluid
Disruption of gland or main pancreatic duct leads to 
increased amylase concentration
4.	 Pleural fluid
Exudative pleural effusion with pancreatitis
False positives occur with carcinoma of the lung and esophageal perforation
Studies Pertaining to Pancreatic Structure
Radiologic and radionuclide tests
1.	 Plain film of the abdomen or 
Can demonstrate large calcifications in chronic 
pancreatitis
upper gastrointestinal x-rays
1.	 Ultrasonography (US)
Can provide limited information on edema, 
inflammation, calcification, pseudocysts, and mass 
lesions
2.	 Computed tomography (CT) 
Permits detailed visualization of pancreas and 
surrounding structures, pancreatic fluid collection, 
pseudocyst; assessment of necrosis or interstitial 
disease
scan
3.	 Magnetic resonance 
Permits noninvasive detailed evaluation of the 
pancreatic parenchyma, biliary and pancreatic 
ducts, adjacent soft tissues, and vascular 
structures.
imaging (MRI) and 
cholangiopancreatography 
(MRCP)
4.	 Endoscopic ultrasonography 
High-frequency transducer used with EUS produces 
very-high-resolution images permitting focused 
evaluation of pancreatic parenchyma and biliary 
and pancreatic ducts, and FNA/B provides targeted 
tissue acquisition
(EUS) and fine-needle 
aspiration/biopsy (FNA/B)
5.	 Endoscopic retrograde 
Cannulation of pancreatic and/or common bile duct 
permits visualization of pancreaticobiliary ductal 
system
cholangiopancreatography 
(ERCP)
Tests of Exocrine Pancreatic Function
Direct stimulation of the pancreas with analysis of duodenal contents
1.	 Secretin test
Secretin leads to increased output of pancreatic 
juice and HCO3
–; pancreatic secretory response is 
related to the functional mass of pancreatic tissue; 
involves duodenal intubation and fluoroscopic 
placement of gastroduodenal tube
2.	 Endoscopic pancreatic 
Secretin-stimulated collection of pancreatic juice 
performed during upper endoscopy; replaces need 
for tube placement in the duodenum
function test (ePFT)
3.	 EUS-ePFT
Combines endosonographic evaluation of the 
pancreas and endoscopic collection of pancreatic 
juice
4.	 Secretin-stimulated MRCP
Combines imaging evaluation of the pancreas and 
a semiquantitative estimation of pancreatic juice 
output in the duodenum
Measurement of intraluminal digestion products
1.	 Stool fat determination
Lack of lipolytic enzymes brings about impaired 
fat digestion; quantitative 72-h stool collection 
and estimation are more reliable than qualitative 
analysis of a random stool sample
Measurement of pancreatic enzymes in feces
1.	 Fecal elastase
Pancreatic secretion of proteolytic enzymes; not 
degraded in intestine

■
■TESTS USEFUL IN THE DIAGNOSIS OF 
PANCREATIC DISEASE
Several tests are of value in the evaluation of pancreatic disease. Examples 
of specific tests and their usefulness in the diagnosis of acute and chronic 
pancreatitis are summarized in Table 358-1 and Fig. 358-2. At some 

Enzyme measurement of choice for the diagnosis of acute pancreatitis; 
increased specificity if the level is more than three times the upper limit of 
normal (3× ULN)
Simple; increased specificity if the level is >3× ULN; may be falsely normal in 
patients with hypertriglyceridemic pancreatitis
Infrequently used
Can help establish source of ascites; false positives occur with intestinal 
obstruction and perforated ulcer; can also measure lipase
Infrequently used
Simple, noninvasive; sequential studies quite feasible; useful in diagnosis 
of gallstones; pancreas visualization limited by interference from overlying 
bowel gas
CHAPTER 358
Useful in the diagnosis of pancreatic calcification, dilated pancreatic ducts, 
and pancreatic tumors; may not be able to distinguish between inflammatory 
and neoplastic mass lesions; multiphasic CT scans are the preferred 
imaging modality for staging pancreatic cancer; IV contrast is needed for 
characterization of most features
Approach to the Patient with Pancreatic Disease 
Has mostly replaced ERCP for diagnostic assessment of the pancreatic duct; 
more sensitive than CT scan for detection of mild pancreatitis, necrosis, 
choledocholithiasis, pancreatic ductal abnormalities, and cystic neoplasms; 
no exposure to ionizing radiation
Can be used to assess gallstones, choledocholithiasis, chronic pancreatitis, 
pancreatic masses, and cystic neoplasms; FNA/B facilitates diagnostic and 
therapeutic management of pancreatic diseases
Primarily a therapeutic procedure; invasive with risks for iatrogenic 
complications
Sensitive to detect occult disease; poorly defined normal enzyme response; 
large secretory reserve capacity of the pancreas; rarely performed
Sensitive to detect occult disease; high negative predictive value for chronic 
pancreatitis; requires sedation
Single endoscopic evaluation of pancreatic structure and function
Improved visualization of pancreatic ductal anatomy; functional evaluation is 
less accurate than ePFT; noninvasive
Reliable reference standard for defining severity of fat malabsorption; 
does not distinguish between pancreatic and nonpancreatic cause of 
malabsorption
Diagnostic accuracy is highest when the pretest probability is high and the 
value is <100 μg/g; false positives will occur in patients with nonformed stools

• Clinical signs and symptoms suggestive of chronic pancreatic disease: abdominal pain,
 nausea, weight loss, steatorrhea, malabsorption, history of alcohol abuse, recurrent
 pancreatitis, fatty-food intolerance
• Perform history, physical examination, review of laboratory studies; consider fecal elastase
 measurement
Step 1
• Contrast-enhanced CT scan
• CP diagnostic criteria: calcifications in combination with atrophy and/or dilated duct
• Diagnostic criteria met; no further imaging needed
• Inconclusive or nondiagnostic results; continue to step 2
Step 2
• MRI and MRCP, with or without secretin enhancement (sMRCP)
• CP diagnostic criteria: Cambridge class III,a dilated duct, atrophy of gland, filling
 defects in duct suggestive of stones
• Diagnostic criteria met; no further imaging needed
• Inconclusive or nondiagnostic results; continue to step 3
Step 3
• EUS with quantification of parenchymal and ductal criteria
• CP diagnostic criteria: ≥5 EUS CP criteria
• Diagnostic criteria met; no further imaging needed
• Inconclusive or nondiagnostic results; continue to step 4
Step 4
• Pancreas function test (with secretin)—endoscopic (ePFT) collection method
 preferred; consider combining ePFT with EUS
• CP diagnostic criteria: peak [bicarbonate] <80 mEq/L
• Diagnostic criteria met; no further imaging needed
• Inconclusive or nondiagnostic results require monitoring of signs and symptoms and repeat 
 testing in 6 months–1 year
FIGURE 358-2  A stepwise diagnostic approach to the patient with suspected chronic pancreatitis (CP). Endoscopic ultrasonography (EUS) and magnetic resonance 
imaging (MRI) with secretin-stimulated magnetic resonance cholangiopancreatography (sMRCP/MRCP) are appropriate diagnostic alternatives to endoscopic retrograde 
cholangiopancreatography (ERCP). CT, computed tomography; ePFT, endoscopic pancreas function test. aCambridge classification of pancreatic duct findings: class 0: normal—
visualization of complete normal ductal anatomy; class I: equivocal—normal main duct, 1–3 abnormal side branches; class II: mild—normal main duct, >3 abnormal 
side branches; class III—dilated and irregular main duct, >3 abnormal side branches, small (<10 mm) cysts; class IV—irregular main duct, intraductal calculi, strictures, 
obstruction with dilation, or large (>10 mm) cysts.
PART 10
Disorders of the Gastrointestinal System
institutions, pancreatic function tests are available and performed if the 
diagnosis of chronic pancreatitis remains a possibility after noninvasive 
tests (i.e., ultrasound, CT scan, MRI with magnetic resonance cholangio­
pancreatography [MRCP]) or invasive tests (i.e., endoscopic retrograde 
cholangiopancreatography [ERCP], endoscopic ultrasound [EUS]) have 
given normal or inconclusive results. In this regard, tests using direct 
stimulation of the pancreas with secretin are the most sensitive.
Pancreatic Enzymes in Body Fluids 
The serum amylase and 
lipase levels are widely used as screening tests for acute pancreatitis 
in the patient with acute abdominal pain or back pain. Lipase is more 
specific for the pancreas, and values greater than three times the upper 
limit of normal (3× ULN) in combination with epigastric pain strongly 
suggest the diagnosis of acute pancreatitis. In acute pancreatitis, the 
serum amylase and lipase are usually elevated within 24 h of onset 
and remain so for 3–7 days. Levels usually return to normal within 7 days 
unless there is pancreatic ductal disruption, ductal obstruction, or 
pseudocyst formation. Approximately 85% of patients with acute pan­
creatitis have threefold or greater elevated serum lipase and amylase 
levels. The values may be normal if (1) there is a delay (2–5 days) before 
blood samples are obtained, (2) the underlying disorder is chronic 
pancreatitis rather than acute pancreatitis, or (3) hypertriglyceridemia 
is present. Patients with hypertriglyceridemia and acute pancreatitis 
have been found to have spuriously low levels of amylase and perhaps 
lipase activity. In the absence of objective evidence of pancreatitis by 
abdominal ultrasound, contrast-enhanced CT scan, MRI with MRCP, 
or EUS, mild to moderate elevations of amylase and/or lipase are not 
helpful in making a diagnosis of chronic pancreatitis.
It should be noted that the serum amylase can be elevated in other 
conditions (Table 358-2), in part because the enzyme is found in many 
organs. In addition to the pancreas and salivary glands, small quantities 
of amylase are found in the tissues of the fallopian tubes, lung, thyroid, 
and tonsils and can be produced by various tumors (carcinomas of the 
lung, esophagus, breast, and ovary). Isoamylase determinations do not 
accurately distinguish elevated blood amylase levels from pancreatic 
or nonpancreatic sources. In patients with unexplained hyperamylas­
emia, the measurement of macroamylase can avoid numerous tests in 
patients with this rare disorder.

Elevation of ascitic fluid amylase occurs in acute pancreatitis as well 
as in (1) ascites due to disruption of the main pancreatic duct or a leak­
ing pseudocyst and (2) other abdominal disorders that simulate pan­
creatitis (e.g., intestinal obstruction, intestinal infarction, or perforated 
peptic ulcer). Elevation of pleural fluid amylase can occur in acute 
pancreatitis, chronic pancreatitis, carcinoma of the lung, and esopha­
geal perforation. Serum lipase is the single best enzyme to measure 
for the diagnosis of acute pancreatitis. It is important to acknowledge 
that levels are often mildly elevated in the setting of renal disease, so 
determining whether a patient with renal failure and abdominal pain 
has pancreatitis remains a challenging clinical problem. One study 
found that serum amylase levels were elevated in patients with renal 
dysfunction only when creatinine clearance was <0.8 mL/s (<50 mL/min). 
In such patients, the serum amylase level was invariably <500 IU/L in 
the absence of objective evidence of acute pancreatitis. In that study, 
serum lipase and trypsin levels paralleled serum amylase values. With 
these limitations in mind, the recommended screening test for acute 
pancreatitis in renal disease is serum lipase, but a high index of clinical 
suspicion is needed based on symptoms. Elevations in serum lipase 
>3× ULN due to nonpancreatic etiology can be observed in hepato­
biliary or gastrointestinal malignancies, septicemia, liver cirrhosis, 
systemic lupus erythematosus, severe head injury, chronic alcoholism, 
diabetes mellitus, and post-ERCP without any associated evidence of 
pancreatitis.
COVID-19 infection has been associated with asymptomatic eleva­
tions of both amylase and lipase. In a systematic review of 21 studies 
involving 36,496 patients during the COVID-19 pandemic, the pooled 
prevalence of hyperlipasemia (>3 × ULN) and hyperamylas­
emia (>3 × ULN) was 5.6% (95% CI, 2.8–9.3%) and 4.0% (95% CI, 
0.9–8.7%), respectively. Importantly, the overall prevalence of acute 
pancreatitis in this cohort was 1.7%. Abnormal levels of amylase and 
lipase were more closely associated with the severity of COVID-19 
than a diagnosis of acute pancreatitis.
Studies Pertaining to Pancreatic Structure 
• 
RADIOLOGIC 
TESTS  Plain films of the abdomen rarely provide useful informa­
tion related to pancreatic disease and have been superseded by more 
detailed imaging studies (ultrasound, EUS, CT, and MRI with MRCP).

TABLE 358-2  Causes of Hyperamylasemia 
Pancreatic Disease
I.	 Pancreatitis
A.	 Acute
B.	 Chronic: ductal obstruction
C.	 Complications of pancreatitis
1.	 Pancreatic pseudocyst
2.	 Ascites caused by pancreatic duct disruption
3.	 Pancreatic necrosis
II.	 Pancreatic trauma
III.	 Pancreatic adenocarcinoma
Nonpancreatic Disorders
I.	 Renal insufficiency
II.	 Salivary gland lesions
A.	 Mumps
B.	 Calculus
C.	 Irradiation sialadenitis
D.	 Maxillofacial surgery
III.	 “Tumor” hyperamylasemia
A.	 Carcinoma of the lung, esophagus, breast, or ovary
IV.	 Macroamylasemia
V.	 Burns
VI.	 Diabetes mellitus, particularly when ketoacidosis is present
VII.	 Pregnancy
VIII.	 Renal transplantation
IX.	 COVID-19 infection
X.	 Cerebral trauma
XI.	 Drugs: opiates
Other Abdominal Disorders
I.	 Biliary tract disease: cholecystitis, choledocholithiasis
II.	 Intraabdominal disease
A.	 Perforated or penetrating peptic ulcer
B.	 Intestinal obstruction or inflammation
C.	 Ruptured ectopic pregnancy
D.	 Peritonitis
E.	 Aortic aneurysm
F.	 Postoperative hyperamylasemia
Ultrasonography (US) can provide important information in the 
initial emergency ward evaluation of patients with acute pancreatitis, 
chronic pancreatitis, pseudocysts, and pancreatic adenocarcinoma. 
Sonographic changes can indicate the presence of edema, inflamma­
tion, and calcification (not obvious on plain films of the abdomen), 
as well as gallstones, biliary dilation, pseudocysts, and mass lesions. In 
acute pancreatitis, the pancreas is characteristically enlarged. In pan­
creatic pseudocyst, the usual appearance is primarily that of a smooth, 
round fluid collection. Pancreatic adenocarcinoma distorts the usual 
landmarks, and mass lesions >3.0 cm are usually detected as localized, 
solid lesions. US is often the initial investigation for patients with sus­
pected pancreatic disease. However, obesity and excess intestinal bowel 
gas can interfere with pancreatic imaging, limiting its sensitivity.
CT with intravenous contrast is the best imaging study for the 
assessment of complications of acute and chronic pancreatitis. It is 
especially useful in the detection of pancreatic and peripancreatic 
acute fluid collections, fluid-containing lesions such as pseudocysts, 
walled-off necrosis (see Chap. 359, Figs. 359-1, 359-2, and 359-4), 
and pancreatic neoplasms. Acute pancreatitis is characterized by (1) 
enlargement of the pancreas, (2) distortion of the pancreatic contour 
with peripancreatic stranding of adjacent fat tissue, and/or (3) the 
presence of pancreatic fluid that has a different attenuation coeffi­
cient than normal pancreas. When possible, CT scans should ideally 
be performed with oral and intravenous contrast to detect areas of 
pancreatic necrosis. The major benefit of CT scan in acute pancreatitis 

is the diagnosis of pancreatic necrosis in patients not responding to 
conservative management within 72 h. It may take 48–72 h to develop 
perfusion defects indicative of pancreatic necrosis. Therefore, if acute 
pancreatitis is confirmed with serology and physical examination find­
ings, CT scan in the first 3 days is not recommended to minimize risk 
of contrast-induced nephropathy and unnecessary health care costs. 
Improved imaging technology and increased resolution are facilitated 
by multiphasic CT scans using multidetector technology (MDCT) 
in which a pancreas protocol consisting of dual-phase scanning with 
intravenous contrast is utilized for the detection and staging of pan­
creatic cancers. While the sensitivity of MDCT for detecting smaller 
(≤2 cm) lesions is lower, the reported overall sensitivity for pancreatic 
cancers is 76–97%. The contraindications to using intravenous contrast 
include renal failure (serum creatinine >2 mg/dL) and a history of 
severe allergic reaction to iodinated contrast agents. In situations where 
EUS is not available, CT-guided percutaneous aspiration or biopsy of a 
pancreatic mass can be performed. Prior to the major advance of EUSguided fine-needle aspiration (FNA), CT-guided biopsy was utilized in 
the preceding decades and is regarded as a safe procedure.

MRI and MRCP provide excellent imaging of the bile duct, pan­
creatic duct, and pancreas parenchyma in both acute pancreatitis and 
chronic pancreatitis. MRI is more sensitive than transabdominal US 
and CT scans and comparable to EUS for the detection of choledo­
cholithiasis. Similar to CT, MRI can evaluate for the severity of acute 
pancreatitis. Moreover, T2-weighted MRI of fluid collections can dif­
ferentiate necrotic debris from fluid in suspected walled-off necrosis, 
and T1 imaging can diagnose hemorrhage in suspected pseudoaneu­
rysm rupture. In chronic pancreatitis, secretin-enhanced MRCP is a 
method to enhance the evaluation of major and minor ductal changes. 
While imaging is comparable to CT for evaluating pancreatic mass 
lesions, MRI with MRCP is the preferred imaging modality for evalu­
ating pancreatic cystic lesions. Nephrogenic systemic fibrosis has been 
described in patients with chronic renal failure following exposure to 
the gadolinium contrast, but incidence rates are extraordinarily low 
with contemporary contrast agents.
CHAPTER 358
Approach to the Patient with Pancreatic Disease 
EUS produces high-resolution images of the bile duct, pancreatic 
parenchyma, and pancreatic duct with a transducer fixed to an endo­
scope that can be directed onto the surface of the pancreas through the 
stomach or duodenum. EUS is not beneficial for the evaluation of pan­
creas during acute pancreatitis. It is preferable to perform EUS after the 
resolution of acute pancreatitis (~4 weeks) to detect any predisposing 
factors, including malignancy, choledocholithiasis, pancreatic divisum, 
or ampullary lesions. EUS can be combined with ERCP in a single ses­
sion and is increasingly preferred for the diagnosis and management 
of choledocholithiasis in acute pancreatitis and pancreatic neoplasm 
with biliary obstruction. EUS has been studied as a diagnostic modal­
ity for chronic pancreatitis. Criteria for abnormalities on EUS in severe 
chronic pancreatic disease have been developed. There is general 
agreement that the presence of five or more of the nine criteria listed 
in Table 358-3 is highly predictive of chronic pancreatitis in the correct 
clinical context. The sensitivity of EUS (81%; 95% CI, 70–89%) to diag­
nose chronic pancreatitis is comparable to that of MRI/MRCP (78%; 
95% CI, 69–85%) and better than CT (75%; 95% CI, 66–83%); however, 
nonspecific changes are commonly seen in the pancreas that may be 
attributable to cigarette smoking, diabetes, or normal aging. EUS also 
facilitates the delivery of nerve-blocking agents via fine-needle injec­
tion in patients suffering from pancreatic pain from chronic pancre­
atitis (celiac plexus block) or cancer (celiac plexus neurolysis). When 
TABLE 358-3  Endoscopic Ultrasonographic Criteria for Chronic 
Pancreatitis (Total Criteria = 9)
DUCTAL
PARENCHYMAL
Stones
Echogenic strands
Hyperechoic main duct margins
Echogenic foci
Main duct irregularity
Lobular contour
Main duct dilatation
Cysts
Visible side branches