173 Section 7: Digestive system
PANCREAS
Chapter 173 Acute pancreatitis
DEFINITION
● Acute pancreatitis is an inflammatory process of the pancreas
with intrapancreatic activation of enzymes that may also in-
volve peripancreatic tissue and/or remote organ systems.
PHYSICAL FINDINGS AND CLINICAL PRESENTATION
● Epigastric tenderness and guarding; pain usually developing
suddenly, reaching peak intensity within 10 to 30 minutes,
severe and lasting several hours without relief
● Hypoactive bowel sounds (secondary to ileus)
● Tachycardia, shock (secondary to decreased intravascular
volume)
● Confusion (secondary to metabolic disturbances)
● Fever
● Tachycardia, decreased breath sounds (atelectasis, pleural
effusions, ARDS)
● Jaundice (secondary to obstruction or compression of bili-
ary tract)
● Ascites (secondary to tear in pancreatic duct, leaking pseu-
docyst)
● Palpable abdominal mass (pseudocyst, phlegmon, abscess,
carcinoma)
● Evidence of hypocalcemia (Chvostek’s sign [see Fig. 269–3A],
Trousseau’s sign [see Fig. 269–3B])
● Evidence of intra-abdominal bleeding (hemorrhagic pan-
creatitis):
1. Gray-bluish discoloration around the umbilicus (Cullen’s
sign) (Fig. 173–1)
2. Bluish discoloration involving the flanks (Grey Turner’s
sign) (Fig. 173–2)
● Tender subcutaneous nodules (caused by subcutaneous fat
necrosis) (Fig. 173–3)
CAUSE
● In ⬎90% of cases: biliary tract disease (calculi or sludge) or
alcohol
● Drugs (e.g., thiazides, furosemide, corticosteroids, tetracy-
cline, estrogens, valproic acid, metronidazole, azathioprine,
Fig 173–1
Periumbilical purpura (Cullen’s sign) associated with acute hemorrhagic
pancreatitis.
(From Callen JP, Jorizzo JL, Bolognia JL, et al: Dermatological Signs of In-
608 ternal Disease, 3rd ed. Philadelphia, WB Saunders, 2003.)
methyldopa, pentamidine, ethacrynic acid, procainamide,
sulindac, nitrofurantoin, ACE inhibitors, danazol, cimeti-
dine, piroxicam, gold, ranitidine, sulfasalazine, isoniazid,
acetaminophen, cisplatin, opiates, erythromycin)
● Abdominal trauma
● Surgery
● ERCP
● Infections (predominantly viral infections)
● Peptic ulcer (penetrating duodenal ulcer) (see Fig. 155–1)
● Pancreas divisum (congenital failure to fuse of dorsal or
ventral pancreas)
● Idiopathic
● Pregnancy
● Vascular (vasculitis, ischemic) (see Fig. 194–4)
● Hypolipoproteinemia (types I, IV, and V)
● Hypercalcemia
● Pancreatic carcinoma (primary or metastatic) (see Fig.
175–4)
● Renal failure
● Hereditary pancreatitis
● Occupational exposure to chemicals: methanol, cobalt, zinc,
mercuric chloride, creosol, lead, organophosphates, chlori-
nated naphthalenes
● Others: scorpion bite, obstruction at ampulla region (neo-
plasm, duodenal diverticula, Crohn’s disease), hypotensive
shock
DIFFERENTIAL DIAGNOSIS
● Peptic ulcer disease (PUD) (see Fig. 155–1)
● Acute cholangitis, biliary colic (see Fig. 186–1)
● High intestinal obstruction (See Fig. 157–2)
● Early acute appendicitis (See Fig. 161–1)
● Mesenteric vascular obstruction (see Fig. 194–4)
● Diabetic ketoacidosis
● Pneumonia (basilar)
Fig 173–2
Purpura of the left flank (Grey Turner’s sign) in a patient with acute
hemorrhagic pancreatitis.
(From Callen JP, Jorizzo JL, Bolognia JL, et al: Dermatological Signs of
Internal Disease, 3rd ed. Philadelphia, WB Saunders, 2003.)

● Myocardial infarction (inferior wall)
● Renal colic
● Ruptured or dissecting aortic aneurysm
● Mesenteric ischemia (see Fig. 194–3)
LABORATORY TESTS
Pancreatic enzymes
● Amylase is increased, usually elevated in the initial 3 to 5
days of acute pancreatitis.
● Serum lipase levels are elevated in acute pancreatitis; the
elevation is less transient than serum amylase; concomitant
evaluation of serum amylase and lipase increases diagnostic
accuracy of acute pancreatitis. An elevated lipase/amylase
ratio is suggestive of alcoholic pancreatitis.
● Elevated serum trypsin levels are diagnostic of pancreatitis
(in absence of renal failure); measurement is made by radio-
immunoassay. Although not routinely available, the serum
trypsin level is the most accurate laboratory indicator for
pancreatitis.
● Rapid measurement of urinary trypsinogen-2 (if available)
is useful in the ER as a screening test for acute pancreatitis
in patients with abdominal pain; a negative dipstick test for
urinary trypsinogen-2 generally rules out acute pancreatitis
with a high degree of probability, whereas a positive test
indicates need for further evaluation.
Additional tests
● CBC: reveals leukocytosis; Hct may be initially increased
secondary to hemoconcentration; decreased Hct may indi-
cate hemorrhage or hemolysis.
● BUN is increased secondary to dehydration.
● Elevation of serum glucose in previously normal patient
correlates with the degree of pancreatic malfunction and
may be related to increased release of glycogen, catechol-
amines, and glucocorticoid release and decreased insulin
release.
● Serum chemistry: AST and LDH are increased secondary to
tissue necrosis; bilirubin and alkaline phosphatase may be
increased secondary to common bile duct obstruction. A
threefold or greater rise in serum ALT concentrations is an
excellent indicator (95% probability) of biliary pancreatitis.
Fig 173–3
Painful nodules and plaques as a result of subcutaneous fat necrosis.
(From Callen JP, Jorizzo JL, Bolognia JL, et al: Dermatological Signs of In-
ternal Disease, 3rd ed. Philadelphia, WB Saunders, 2003.)
Chapter 173: Acute pancreatitis 173
● Serum calcium is decreased secondary to saponification,
precipitation, and decreased PTH response.
● ABGs: Pao2 may be decreased secondary to ARDS, pleural
effusion(s); pH may be decreased secondary to lactic acido-
sis, respiratory acidosis, and renal insufficiency.
● Serum electrolytes: potassium may be increased secondary
to acidosis or renal insufficiency, sodium may be increased
secondary to dehydration.
IMAGING STUDIES
● Abdominal plain film is useful initially to distinguish other
conditions that may mimic pancreatitis (perforated viscus);
it may reveal localized ileus (sentinel loop), pancreatic cal-
cifications (chronic pancreatitis) (Fig. 173–4), blurring of
left psoas shadow, dilation of transverse colon, calcified
gallstones.
● Chest x-ray may reveal elevation of one or both diaphragms,
pleural effusions, basilar infiltrates, platelike atelectasis.
● Abdominal ultrasonography is useful in detecting gallstones
(sensitivity of 60% to 70% for detecting stones associated
with pancreatitis). It is also useful for detecting pancreatic
pseudocysts (see Fig. 173–8); its major limitation is the
presence of distended bowel loops overlying the pancreas.
● CT scan (Fig. 173–5) is superior to ultrasonography in iden-
tifying pancreatitis and defining its extent, and it also plays
a role in diagnosing pseudocysts (they appear as a well-
defined area surrounded by a high-density capsule); GI fis-
tulation or infection of a pseudocyst can also be identified
by the presence of gas within the pseudocyst.
● Magnetic resonance cholangiopancreatography (MRCP) is
also a useful diagnostic modality if a surgical procedure
is not anticipated.
● ERCP (Fig. 173–6) should not be performed during the
acute stage of disease unless it is necessary to remove an
impacted stone in the ampulla of Vater; patients with severe
or worsening pancreatitis but without obstructive jaundice
(biliary obstruction) do not benefit from early ERCP and
papillotomy.
TREATMENT
● Bowel rest with avoidance of PO liquids or solids during the
acute illness
● Avoidance of alcohol and any drugs associated with pancre-
atitis
General measures
● Maintain adequate intravascular volume with vigorous IV
hydration.
● Patient should remain NPO until clinically improved, sta-
ble, and hungry. Enteral feedings are preferred over total
parenteral nutrition (TPN). Parenteral nutrition may be
necessary in patients who do not tolerate enteral feeding or
in whom an adequate infusion rate cannot be reached
within 2 to 4 days.
● Nasogastric suction is useful only in severe pancreatitis to
decompress the abdomen in patients with ileus.
● Control pain: IV morphine or fentanyl
● Correct metabolic abnormalities (e.g., replace calcium and
magnesium as necessary).
Specific measures
● Pancreatic or peripancreatic infection develops in 40% to
70% of patients with pancreatic necrosis (Fig. 173–7). How-
ever, IV antibiotics should not be used prophylactically for
all cases of pancreatitis; their use is justified if the patient 609
173 Section 7: Digestive system

A B
Fig 173–4
Calcification in chronic pancreatitis. Rarely on a plain film of the abdomen (A), a horizontal band of calcification can be seen extending across the
upper midabdomen (arrows). Calcification within the pancreas is much easier to see on a transverse computed tomography scan of the upper ab-
domen (B). Calcification is seen as white speckled areas within the pancreas (arrows). The darker areas within the pancreas represent dilated
common and pancreatic ducts. L ⫽ liver; GB ⫽ gallbladder; St ⫽ stomach; K ⫽ kidney; Sp ⫽ spleen.
(From Mettler FA, Guibertau MJ, Voss CM, Urbina CE: Primary Care Radiology. Philadelphia, Elsevier, 2000.)

3. Excision or drainage of necrotic or infected foci.

● Identification and treatment of complications:
Fig 173–5
Spread of acute pancreatitis. Enhanced CT demonstrates the inflam-
matory changes of acute pancreatitis spreading along the transverse
mesocolon (arrows) toward the transverse colon. Phlegmonous
extension through the small bowel mesentery is also present.
(From Grainger RG, Allison DJ, Adam A, Dixon AK [eds]: Grainger and
Allison’s Diagnostic Radiology, 4th ed. Philadelphia, Churchill Livingstone,
2001)
has evidence of septicemia, pancreatic abscess, or pancreati-
tis secondary to biliary calculi. Their use should generally be
limited to 5 to 7 days to prevent development of fungal su-
perinfection. Appropriate empirical antibiotic therapy
should cover: B. fragilis and other anaerobes, Enterococcus
● Surgical therapy has a limited role in acute pancreatitis; it is
indicated in the following:
1. Gallstone-induced pancreatitis: cholecystectomy when
acute pancreatitis subsides
610 2. Perforated peptic ulcer
1. Pseudocyst: round or spheroid collection of fluid, tissue,
pancreatic enzymes, and blood.
a. Diagnosed by CT scan (Fig. 173–8) or sonography
b. Treatment: CT scan or ultrasound-guided percutaneous
drainage (with a pigtail catheter left in place for continuous
drainage) can be used, but the recurrence rate is high; the
conservative approach is to re-evaluate the pseudocyst (with
CT scan or sonography) after 6 to 7 weeks and surgically
drain it if the pseudocyst has not decreased in size. Gener-
ally, pseudocysts ⬎5 cm in diameter are reabsorbed without
intervention, whereas those ⬎5 cm require surgical inter-
vention after the wall has matured.
2. Phlegmon: represents pancreatic edema. It can be diag-
nosed by CT scan or sonography. Treatment is supportive
measures because it usually resolves spontaneously.
3. Pancreatic abscess: diagnosed by CT scan (presence of
bubbles in the retroperitoneum) (Fig. 173–9); Gram stain-
ing and cultures of fluid obtained from guided percutane-
ous aspiration (GPA) usually identify bacterial organism.
Therapy is surgical (or catheter) drainage and IV antibiotics
4. Pancreatic ascites: usually caused by leaking of pseudo-
cyst or tear in pancreatic duct. Paracentesis reveals very high
amylase and lipase levels in the pancreatic fluid; ERCP may
demonstrate the lesion. Treatment is surgical correction if
exudative ascites from severe pancreatitis does not resolve
spontaneously.
5. GI bleeding: caused by concomitant alcoholic gastritis,
bleeding varices, stress ulceration, or DIC.
6. Renal failure: caused by hypovolemia resulting in oliguria
or anuria, cortical or tubular necrosis (shock, DIC), or
thrombosis of renal artery or vein.
7. Hypoxia: caused by ARDS, pleural effusion, or atelectasis.
 Chapter 173: Acute pancreatitis 173

B
Fig 173–6 Fig 173–8
Normal pancreatic duct. (A) Normal ERCP shows the accessory pan- Pancreatic pseudocyst. A well-defined fluid collection with a thick wall
creatic duct (APD) draining separately into the minor papillary (MiP), (arrows) lies superior to the pancreas.
and the major pancreatic duct (MPD) draining into the major papilla (From Grainger RG, Allison DJ, Adam A, Dixon AK [eds]: Grainger and
(MjP). (B) ERCP shows filling of the main pancreatic duct (MPD), com- Allison’s Diagnostic Radiology, 4th ed. Philadelphia, Churchill Livingstone,
mon bile duct (B) and gallbladder (G). The MPD and CBD drain into 2001.)
the major papillary (large arrow). The small accessory pancreatic duct
(small arrows) drains separately into the minor papilla (arrowhead).
(From Grainger RG, Allison DJ, Adam A, Dixon AK [eds]: Grainger and
Allison’s Diagnostic Radiology, 4th ed. Philadelphia, Churchill Livingstone,
2001.)

Fig 173–7 Fig 173–9

Acute necrotizing pancreatitis. Dynamic CT shows enlargement of the
pancreas, a thin rim of contrast-enhancement (arrows), and lack of en-
hancement of the pancreatic parenchyma indicating almost complete
gland necrosis (cursors 1 and 2 measure soft tissue density: 25 to 30
Hounsfield units). Small islands of normally enhancing parenchyma are
seen (P). Patient died despite surgery.
(From Grainger RG, Allison DJ, Adam A, Dixon AK [eds]: Grainger and
Allison’s Diagnostic Radiology, 4th ed. Philadelphia, Churchill Livingstone,
2001.)
Pancreatic abscess. Dynamic CT shows a fluid collection with a
contrast-enhancing capsure (arrowheads). Percutaneous aspiration
showed the fluid to be pus. The abscess was drained successfully
through percutaneous catheters.
(From Grainger RG, Allison DJ, Adam A, Dixon AK [eds]: Grainger and
Allison’s Diagnostic Radiology, 4th ed. Philadelphia, Churchill Livingstone,
2001.)
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