Acute Pancreatitis Symptoms

The most common symptom of acute pancreatitis is pain. Almost everybody with
acute pancreatitis experiences pain.

• The pain may come on suddenly or build up gradually. If the pain begins
suddenly, it is typically very severe. If the pain builds up gradually, it starts
out mild but may become severe.

• The pain is usually centered in the upper middle or upper left part of the belly
(abdomen). The pain is often described as if it radiates from the front of the
abdomen through to the back.

• The pain often begins or worsens after eating.

• The pain typically lasts a few days.

• The pain may feel worse when a person lies flat on his or her back.

People with acute pancreatitis usually feel very sick. Besides pain, people may have
other symptoms and signs.

• Nausea (Some people do vomit, but vomiting does not relieve the symptoms.)

• Fever, chills, or both

• Swollen abdomen which is tender to the touch

• Rapid heartbeat (A rapid heartbeat may be due to the pain and fever,
dehydration from vomiting and not eating, or it may be a compensation
mechanism if a person is bleeding internally.)

In very severe cases with infection or bleeding, a person may become dehydrated and
have low blood pressure, in addition to the following symptoms:

• Weakness or feeling tired (fatigue)

• Feeling lightheaded or faint

• Lethargy

• Irritability

• Confusion or difficulty concentrating

• Headache

If the blood pressure becomes extremely low, the organs of the body do not get
enough blood to carry out their normal functions. This very dangerous condition is
called circulatory shock and is referred to simply as shock.

Chronic Pancreatitis Symptoms

Pain is less common in chronic pancreatitis than in acute pancreatitis.

Some people have pain, but many people do not experience pain. For those people
who do have pain, the pain is usually constant and may be disabling; however, the
pain often goes away as the condition worsens. This lack of pain is a bad sign because
it probably means that the pancreas has stopped working.

Other symptoms of chronic pancreatitis are related to long-term complications, such

as the following:

• Inability to produce insulin (diabetes)

• Inability to digest food (weight loss and nutritional deficiencies)

• Bleeding (low blood count, or anemia)

• Liver problems (jaundice)

Acute pancreatitis
URL of this page: http://www.nlm.nih.gov/medlineplus/ency/article/000287.htm

Acute pancreatitis is sudden swelling and inflammation of the pancreas.

Causes
The pancreas is an organ located behind the stomach that produces chemicals called
enzymes, as well as the hormones insulin and glucagon. Most of the time, the
enzymes are only active after they reach the small intestine, where they are needed to
digest food.

When these enzymes somehow become active inside the pancreas, they eat (and
digest) the tissue of the pancreas. This causes swelling, bleeding (hemorrhage), and
damage to the pancreas and its blood vessels.

Acute pancreatitis affects men more often than women. Certain diseases, surgeries,
and habits make you more likely to develop this condition.
Acute Pancreatitis
Definitions

Acute pancreatitis (AP) is an acute inflammatory condition of the pancreas that may
extend to local and distant extrapancreatic tissues. AP is broadly classified as mild or
severe. Mild AP is often referred to as interstitial pancreatitis, based on its
radiographic appearance. Severe AP implies the presence of organ failure, local
complications, or pancreatic necrosis. Interstitial pancreatitis implies preservation of
pancreatic blood supply; necrosis suggests the disruption of pancreatic blood supply,
with resulting ischemia.

Figure 1: Click to Enlarge

Different types of fluid collections develop in the setting of AP, including acute fluid
collections, acute pseudocysts, and pancreatic abscesses. Acute fluid collections occur
early in AP in the peripancreatic areas and are not encapsulated by a fibrous wall.
Acute pseudocysts are well-developed collections of pancreatic juice encapsu-lated by
a nonepithelialized wall of granulation tissue (Fig. 1). Pseudocysts typically form 4 to
6 weeks after an episode of AP. A pseudocyst that has become infected is a pancreatic
abscess. Pancreatic abscesses may also form through encapsulation of areas of
infected pancreatic necrosis. The terms pancreatic phlegmon and hemorrhagic
pancreatitis are no longer used in the current American College of Gastroenterology
(ACG) guidelines.

When acute pancreatitis occurs on two or more occasions (evidenced by elevation of

serum pancreatic enzyme levels), it is classified as acute recurrent pancreatitis. In
some cases, acute recurrent pancreatitis progresses to chronic pancreatitis, implying
the presence of parenchymal fibrosis and loss of glandular function.

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Prevalence

The yearly incidence of AP in the United States is approximately 17 new cases per
100,000. Acute pancreatitis results in 100,000 hospitalizations per year. Eighty
percent of cases of AP are interstitial and mild; the remaining 20% are necrotizing and
severe. Approximately 2000 patients per year die from complications related to AP.

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Causes

Gallstones and alcohol are the two most common causes of AP in western countries,
accounting for 80% of cases. Gallstone pancreatitis results from transient obstruction
of the ampulla of Vater by small stones or edema. Clinical features include preceding
biliary colic, the presence of cholelithiasis or biliary dilation on gallbladder
ultrasound, and liver function test abnormalities. Gallstone pancreatitis typically does
not recur after cholecystectomy or endoscopic therapy (biliary sphincterotomy and
stone extraction). Alcohol is the second leading cause of AP, which typically occurs
after episodes of binge drinking. After recurrent episodes, most alcoholics go on to
develop chronic pancreatitis.

Numerous less common causes have been described (Box 1). Hypertriglyceridemia
produces acute pancreatitis if triglyceride levels are above 1000 mg/dL. Markedly
elevated triglyceride levels may be encountered in the setting of diabetes, alcoholism,
and inherited disorders of lipoprotein metabolism (Fredrickson types I, II, and V).
Hypercalcemia produces AP through calcium-mediated activation of trypsinogen and
subsequent glandular autodigestion. Hypercalcemia-associated AP may occur in the
setting of primary and secondary hyperparathyroidism, malignancy, and metabolic
bone disease. In recent years, numerous genetic mutations have been associated with
the development of pancreatitis. These include mutations of cationic trypsinogen
(hereditary pancreatitis), serine protease inhibitor Kazal type 1 (SPINK1), and the
cystic fibrosis transmembrane regulator (CFTR) gene. Numerous case reports and
case series have implicated specific medications (e.g., sulfa drugs, 6-mercaptopurine,
didanosine, furosemide, valproate) as causes of acute pancreatitis; however, the
strength of these associations is variable.

Box 1: Causes of Acute Pancreatitis

Gallstones (45%)
Alcohol (35%)
Other (10%)

• Medications
• Hypercalcemia
• Hypertriglyceridemia
• Obstructive
• Post-ERCP
• Hereditary
• Trauma—viral, vascular-ischemic

• Postcardiac bypass
Idiopathic (10%)

ERCP, endoscopic retrograde cholangiopancreatography.

Obstruction of the pancreatic duct may produce acute or chronic pancreatitis. Causes
of obstructive AP include ductal adenocarcinoma, ampullary tumors and polyps,
neuroendocrine and cystic pancreatic tumors, and intraductal papillary mucinous
tumors. Pancreatic tumors should be kept in the differential diagnosis, particularly in
older patients. Occasionally, congenital abnormalities of the pancreas, such as
pancreas divisum and annular pancreas, produce obstructive AP in adult patients.

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Pathophysiology

The pathogenesis of AP has been studied extensively using animal models. Although
various causes produce distinct inciting events, the final common pathway is
premature activation of digestive enzymes within the acinar cells. Ordinarily,
pancreatic proenzymes become activated on release within the duodenum. Pancreatitis
results from early activation of pancreatic enzymes, producing autodigestion of the
pancreas and surrounding tissues. Exposure of trypsinogen to lysosomal enzymes
such as cathepsin B has recently been elucidated as a mechanism for early trypsin
activation. Digestive enzyme release is amplified as acinar cells lyse, leading to a
vicious cycle of inflammation and necrosis.

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Signs and symptoms

Acute pancreatitis manifests with the sudden onset of epigastric pain radiating to the
back. The pain may be severe and characterized as deep and boring. Eating food
worsens pain; bending forward ameliorates pain. In AP precipitated by alcohol, pain
occurs from hours to days after binge drinking. Abdominal pain lasts for days and is
associated with anorexia, nausea, and vomiting. Most patients present to the
emergency department; however, occasional patients manage their symptoms at home
by minimizing oral intake for a few days.

Physical examination frequently reveals systemic signs such as fever, tachycardia, and
hypotension. Abdominal examination reveals epigastric tenderness, with localized
guarding and rebound. Sluggish or absent bowel sounds indicate coexisting ileus.
Less frequent findings signal complications, including Grey Turner's (flank
ecchymosis) or Cullen's (umbilical ecchymosis) signs suggestive of retroperitoneal
hemorrhage, a palpable mass suggestive of a pseudocyst, panniculitis suggestive of
subcutaneous fat necrosis, and dullness to percussion of lung fields suggestive of
pleural effusion. The differential diagnosis of upper gastrointestinal bleeding in acute
pancreatitis includes erosion of a pseudocyst into the splenic artery (“hemosuccus
pancreaticus”) or bleeding from gastric varices that arise secondary to splenic vein
thrombosis.

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Diagnosis

The diagnosis of AP is supported by an elevation of the serum amylase and lipase

levels in excess of three times the upper limit of normal. These enzyme levels are
elevated because of leakage from pancreatic acinar cells into the interstitial space and
subsequent absorption into the circulation. The amylase level becomes elevated within
hours of the development of pain and may remain elevated for 3 to 5 days. The
differential diagnosis for hyperamylasemia includes intestinal obstruction, visceral
perforation, tubo-ovarian abscess, renal failure, and salivary gland disease.
Macroamylasemia is a condition in which amylase is chronically elevated because of
its binding to an abnormal serum protein, leading to delayed clearance. Serum lipase
has higher specificity for pancreatic disease but its level may be elevated in other
conditions as well. The severity of pancreatitis does not correlate well with the
magnitude of elevation of the serum amylase and lipase levels. There is no value in
following daily trends of serum amylase and lipase levels, because they do not
correlate with recovery or prognosis.

Laboratory abnormalities encountered in AP include hyperglycemia, hypocalcemia,

leukocytosis, and mild elevations of liver function test results. Elevation of the serum
alanine aminotransferase level to higher than 80 U/mL is highly specific but poorly
sensitive for gallstone pancreatitis. Experimental biochemical markers that may hold
promise for assessing the severity of disease include trypsinogen activation peptide,
interleukin-6, interleukin-10, and C-reactive protein levels.

Simple plain films of the chest and abdomen are appropriate for the initial
radiographic assessment of AP. An abdominal radiograph is helpful for excluding
other causes of acute abdominal pain, such as obstruction and perforation. In AP, the
abdominal radiograph is frequently normal or may demonstrate ileus. A chest
radiograph can detect pulmonary complications of AP such as atelectasis, pleural
effusions (most commonly left-sided), or infiltrates suggestive of adult respiratory
distress syndrome.

Although transabdominal ultrasound is poorly reliable for imaging the pancreas itself,
it is the best initial radiographic test for the evaluation of mild AP because of the
following:

1. It detects gallstones as a potential cause,

2. It rules out acute cholecystitis as a differential cause of pain and
hyperamylasemia, and
3. It detects biliary dilation suggestive of the need for early endoscopic
retrograde cholangiopancreatography (ERCP).

Figure 2: Click to Enlarge

Contrast-enhanced computed tomography (CT) of the abdomen is the preferred test

for evaluating severe pancreatitis and detecting complications. CT features in
interstitial pancreatitis include homogenous contrast enhancement; diffuse or
segmental pancreatic enlargement; irregularity, heterogeneity, and lobularity of the
pancreas; and obliteration of the peripancreatic fat planes. CT detects areas of
pancreatic necrosis (Fig. 2), which significantly influences subsequent management.
The presence of necrosis confers a substantial increase in mortality compared with
interstitial pancreatitis. A CT should not be routinely ordered for all patients with AP;
however, the ACG practice guidelines state that “a dynamic contrast-enhanced CT is
recommended at some point beyond the first 3 days in severe acute pancreatitis (on
the basis of a high APACHE score or organ failure) to distinguish interstitial from
necrotizing pancreatitis.” A CT should also be considered for those in whom a
localized pancreatic complication is suspected (e.g., pseudocyst, splenic vein
thrombosis, splenic artery aneurysm). CT is also appropriate after resolution of AP to
exclude a tumor if the cause of the attack is unclear. It is highly controversial whether
intravenous contrast worsens or precipitates pancreatic necrosis, and abdominal CT
should generally not be withheld on this basis.

Endoscopic ultrasound (EUS) and magnetic resonance cholangiopancreatography

(MRCP) are emerging as potentially valuable tests in the evaluation of AP. Both are
helpful in detecting stones in the common bile duct and directly assessing the
pancreatic parenchyma. Magnetic resonance imaging is similar or superior to contrast
CT in its ability to stage AP and detect necrosis and complications, and it does not
require intravenous contrast. Operator dependence and expense limit the widespread
availability of EUS and MRCP.

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Treatment

Supportive Care

Figure 3: Click to Enlarge

The primary goals of therapy in AP are meticulous supportive care and prevention of
pancreatic necrosis, infection, and organ failure. The primary treatment is pancreatic
rest and analgesia. Patients should be kept NPO, and intravenous fluids should be
given with careful attention to volume status. The ACG guidelines state, “all patients
should receive close supportive care including pain control, fluid resuscitation, and
nutritional support.” A therapeutic algorithm closely based on the ACG guidelines is
shown in (Fig. 3).

The importance of vigorous hydration to optimize outcomes has been increasingly

recognized. The ACG guidelines stress, “Patients with evidence of significant third-
space losses require aggressive fluid resuscitation.” Many patients sequester
substantial amounts of fluid into the retroperitoneal space, producing very high fluid
requirements. Intravascular volume depletion may lead to tachycardia, hypotension,
renal failure, hemoconcentration, and generalized circulatory collapse. More than 6 L
of fluid sequestration within the first 48 hours is considered a marker of increased
severity, according to the Ranson criteria ( Table 1 ). Patients with evidence of
hemoconcentration resulting from intravascular water loss appear to be at increased
risk for the development of pancreatic necrosis and organ failure. In addition to
maintenance fluid requirements, the amount sequestered should be monitored and
replaced with isotonic fluids such as normal saline, with a goal of euvolemia and
hemodilution. Some patients may require as much as 250 to 350 mL/hr, particularly in
the early phases of AP. Of course, the aggressiveness of fluid replacement must be
tempered in the presence of underlying cardiac or renal disease.

Table 1: Ranson Criteria for Severity of Acute Pancreatitis

At Admission At 48 hr
Age > 55 yr Hematocrit decrease > 10%
WBC > 16,000/mL BUN increase > 5 mg/dL
LDH > 50 IU/L Calcium < 8 mg/dL
AST > 250 IU/L PaO2 < 60 mm Hg
Glucose > 200 mg/dL Base deficit > 4 mg/dL Fluid sequestration > 6 L

AST, aspartate aminotransferase; BUN, blood urea nitrogen; LDH, lactate

dehydrogenase; PaO2, partial pressure of arterial carbon dioxide; WBC, white blood
cell.

Oral intake should be severely limited initially and then carefully advanced as pain
subsides and hunger returns. Carbohydrate-containing foods are best for early
refeeding because they do not stimulate the pancreas as much as fat- and protein-
containing foods. A nasogastric tube is necessary only in the presence of vomiting or
ileus. Intravenous narcotics by injection or patient-controlled analgesia should be used
liberally during the attack and tapered as the diet is advanced to enable prompt bowel
recovery.

Nutritional support may be withheld in mild pancreatitis for several days. The ACG
guidelines advise nutritional support if NPO status is maintained for longer than 5 to 7
days. All patients with severe AP should receive nutritional support because of the
inherently high level of stress and hypercatabolism. Nasojejunal feeding past the
ligament of Treitz does not stimulate the pancreas and is preferred over parenteral
feeding because of decreased infection complication rates. Studies have shown
improved humoral and cellular immunity, decreased systemic inflammatory response,
and decreased bacterial translocation for enteral feeding compared with parenteral
nutrition. The presence of a severe intestinal ileus or delay in tube placement may
limit the use of enteral feeding. Many patients with AP develop gastric and colonic
ileus but maintain adequate small bowel motility, permitting enteral feeding.

Assessment of Severity

An important initial step in management is the assessment of severity by clinical and

radiographic criteria. Although AP is usually mild, a subset of patients develops a
severe course. Severe AP implies organ failure or pancreatic necrosis and carries a
mortality rate of 10% to 30%. Patients with severe AP should be administered close
supportive care in an intensive care unit (ICU) setting. According to the ACG
guidelines, severe pancreatitis is recognized on the basis of early clinical prognostic
signs, evidence of organ failure, or local complications (pancreatic necrosis or
abscess). Early recognition of severe pancreatitis improves outcomes by prompting
aggressive fluid resuscitation and transfer of the patient to an intensive care unit.

Multiple clinical and radiographic severity scores have been proposed. Initially
studied in patients with alcoholic acute pancreatitis, the Ranson score comprises five
clinical criteria measured at admission and six clinical criteria measured at 48 hours
(see Table 1 ). The criteria measured at admission reflect the local inflammatory
effects of pancreatic enzymes; those measured at 48 hours represent the later systemic
effects. Three or more Ranson criteria predict a severe course and increased mortality
and should prompt ICU transfer and CT scanning to rule out pancreatic necrosis. The
APACHE II and III scores (acute physiology, age, chronic health evaluation) are
generated from multiple parameters and are considered highly accurate. Furthermore,
APACHE scores allow prediction of severity from the day of admission and may be
recalculated on a daily basis. Unfortunately, because of the time-consuming and
cumbersome nature of the APACHE evaluation, it is rarely used in clinical practice.

In addition to formal scoring systems, patients should be followed closely for other
markers of increased severity, including signs of hemodynamic instability or organ
failure. Respiratory failure may occur through the development of large pleural
effusions or adult respiratory distress syndrome. Rarely, hemorrhage into
retroperitoneal tissues results in further hemodynamic compromise. Hypervigilance
for these complications will result in more timely and aggressive management and
improved patient outcomes.

Preventive Measures
Prevention of Infection

Because superinfection of pancreatic necrosis dramatically increases the mortality rate

of AP compared with sterile necrosis, a major goal in management is the prevention
of infection. Some randomized trials have suggested a benefit for early initiation of
broad-spectrum antibiotics in preventing pancreatic infection. Antibiotics with good
pancreatic tissue penetration, such as imipenem (500 mg IV every 8 hours),
cefuroxime (1.5 g IV every 8 hours), or ciprofloxacin (400 mg IV every 12 hours) are
favored in this setting. Potential drawbacks of prophylactic antibiotics include the
development of resistant organisms and fungal infections. Although antibiotics have
been shown to decrease infection rates, they have not consistently demonstrated a
mortality benefit. The ACG guidelines recommend that “in patients with necrotizing
pancreatitis associated with organ failure, it is reasonable to initiate treatment with
antibiotics with good spectrum of activity against aerobic and anaerobic bacteria.”

Endoscopic Retrograde Cholangiopancreatography

Although the ACG guidelines state that “patients with severe pancreatitis caused by
gallstones should undergo urgent ERCP,” there has been much recent debate over the
benefit of early endoscopic removal of common bile duct stones in suspected
gallstone pancreatitis. There is strong evidence to suggest a benefit for ERCP with
papillotomy and stone extraction in the setting of stone impaction and cholangitis.
However, randomized trials of early ERCP in the management of all patients with
suspected gallstone pancreatitis have shown conflicting results. ERCP may further
exacerbate acute pancreatitis. Guidelines from the British Society of Gastroenterology
advise that “severe gallstone pancreatitis in the presence of increasingly deranged
liver function tests and signs of cholangitis (fever, rigors, and positive blood cultures)
require an immediate and therapeutic ERCP.” If there is only moderate suspicion of
retained stones, an MRCP is a “no-risk” alternative to ERCP, with excellent
sensitivity for the detection of common bile-duct stones.

Surgical Management

Surgical management of AP is indicated in two clinical settings—infected pancreatic

necrosis and gallstone pancreatitis.

Pancreatic Necrosis

Confirmation of the diagnosis of infected pancreatic necrosis is critical because

surgical management is indicated. Unfortunately, clinical and radiographic criteria are
not sufficiently reliable for detecting pancreatic infection. Infection is confirmed
through ultrasound- or CT-guided aspiration of areas of pancreatic necrosis or
suspected pancreatic abscesses. This procedure is safe and reliable, and has been
recommended for all patients with CT criteria for pancreatic necrosis and evidence of
sepsis or organ failure.

The ACG guidelines differentiate necrotizing pancreatitis with and without clinical
improvement. Patients with evidence of slow clinical improvement may be managed
expectantly, without needle aspiration; however, “in the absence of clinical
improvement, guided percutaneous aspiration should be performed.” This ap-proach
is reasonable if the patient is hemodynamically stable and has not developed
significant organ failure or septic syndrome. It is important to obtain a surgical
consultation before consider-ation of this procedure, given the possible need for
surgical débridement.

In the setting of infected pancreatic necrosis, resection of all devitalized pancreatic

and surrounding tissue is performed. Multiple re-explorations, continuous irrigation,
or laparotomy formation may be required for adequate débridement. Recent studies
have suggested that a delayed approach to surgical débridement improves outcomes
by allowing time for adequate separation of necrotic and vital areas. Surgical
necrectomy is clearly indicated in the setting of infected necrosis; however, its benefit
in sterile necrosis is controversial. Cholecystectomy is indicated to prevent recurrence
of gallstone pancreatitis. In mild disease, an early cholecystectomy performed during
the same hospitalization is favored. In severe gallstone pancreatitis, cholecystectomy
may be delayed until clinical improvement or performed at the time of necrectomy.

Idiopathic Acute Pancreatitis

Ten percent of cases of acute pancreatitis are idiopathic acute pancreatitis (IAP).
Potential underlying causes of idiopathic pancreatitis include biliary microlithiasis,
sphincter of Oddi dysfunction, and undiagnosed genetic defects. Biliary microlithiasis
has been implicated as a common cause of IAP. Recurrent acute episodes of
pancreatitis may develop in the absence of gallstones on ultrasound, with or without
elevated liver enzyme levels. Repeat ultrasound examinations may eventually reveal
biliary sludge or small stones. The finding of cholesterol monohydrate or calcium
bilirubinate crystals on microscopic biliary analysis after cholecystokinin stimulation
strongly supports the diagnosis of microlithiasis; however, it is not completely
sensitive. Laparoscopic cholecystectomy prevents recurrence in patients with IAP and
should be considered in all patients with acute recurrent pancreatitis of unclear cause.
Endoscopic sphincterotomy or stone dissolution therapy with ursodiol (8 to 10
mg/kg/day, in two divided doses) are valid options in patients with high surgical risk.
Stone dissolution therapy is effective only for noncalcified, cholesterol monohydrate
stones smaller than 1 cm in diameter.

Figure 4: Click to Enlarge

ERCP may be helpful in elucidating the cause of IAP. ERCP allows the detection of
ampullary tumors, mucinous ductal ectasia, common bile duct stones, pancreas
divisum, and pancreatic ductal adenocarcinoma. Biliary manometry allows the
diagnosis of sphincter of Oddi dysfunction. ERCP is most strongly indicated for
patients who are older than 40 years to rule out neoplasia. MRCP is a safer alternative
to ERCP for detection of diseases of the pancreatic duct; however, it is less sensitive
for small duct processes, and does not allow inspection of the ampulla or functional
assessment of the sphincter of Oddi. Genetic screening for cationic trypsinogen,
SPINK1, or CFTR gene mutations may be considered in some patients with IAP,
although positive results are unlikely to change management.

There are no published guidelines for the approach to recurrent IAP. Laparoscopic
cholecystectomy, ERCP-MRCP, and genetic screening each have their advocates as
the initial step in the diagnostic workup. Most clinicians do not favor extensive
evaluation for the first episode of IAP, because it does not recur in most patients after
the first episode; however, CT after resolution is probably reasonable for excluding
pancreatic cancer. It is best to tailor the diagnostic approach individually based on
patient characteristics. We favor a laparoscopic cholecystectomy in any patient who
develops a second episode of IAP. One suggested approach to the patient with
idiopathic recurrent acute pancreatitis is demonstrated in Figure 4.

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Outcomes

Mortality rates for hospitalized patients vary from 5% to 10% in most series. In
patients with interstitial pancreatitis, mortality is close to zero. Mortality is
substantially increased in necrotizing pancreatitis (less than 1% for interstitial
pancreatitis, 10% for sterile necrosis, 30% for infected necrosis).

Summary

• Gallstones and alcohol are the most common causes of acute pancreatitis.
• The management of acute pancreatitis includes meticulous supportive care,
with careful attention to volume status.
• Assessment of severity is an important initial step in the care of all patients
with acute pancreatitis.
• A contrast-enhanced pancreatic CT scan should be considered for patients
with severe acute pancreatitis.
• Endoscopic retrograde cholangiopancreatography should be performed in
patients with gallstone pancreatitis and signs of ongoing biliary obstruction or
cholangitis.
• Nutritional support should be administered to all patients with prolonged NPO
status or severe acute pancreatitis.
• Surgical consultation and percutaneous aspiration of pancreatic necrosis
should be considered for patients with clinical deterioration or multiorgan
system failure.

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