Treatment of Acute Pancreatitis 2013 PDF

14.01.
13 Treatment of acute pancreatitis
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Treatment of acute pancreatitis
Author Section Editor Deputy Editor

Santhi Swaroop Vege, MD David C Whitcomb, MD, PhD Shilpaнет
Grover, MD, MPH
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Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Dec 2012. | This topic last updated: Thu Oct 25 00:00:00 GMT 2012.
INTRODUCTION — Acute pancreatitis can be divided into two broad categories [1]:
Edematous, interstitial, or mild acute pancreatitis

Necrotizing or severe acute pancreatitis
Treatment of acute pancreatitis is based upon the severity of the condition, as determined by the clinical,
laboratory and a severity scoring system (algorithm 1). (See "Predicting the severity of acute pancreatitis".)
Treatment is aimed at correcting any underlying predisposing factors and at the pancreatic inflammation itself.
Most attacks of acute pancreatitis are mild with recovery occurring within five to seven days. Death is unusual in
such patients. In contrast, severe necrotizing pancreatitis is associated with a high rate of complications and
significant mortality.
A subgroup of patients with severe pancreatitis has early severe acute pancreatitis or fulminant acute
pancreatitis characterized by extended pancreatic necrosis with organ failure either at admission or within 72
hours. Early severe acute pancreatitis or fulminant acute pancreatitis has a high mortality of 25 to 30 percent [2-
4].
An intermediate group of patients with "moderately severe acute pancreatitis", comprised of patients with local
complications but no organ failure, has also been recognized [5]. Moderately severe acute pancreatitis has a
low mortality like mild acute pancreatitis but morbidity (requiring prolonged hospital stay and interventions)
similar to severe acute pancreatitis.
This topic reviews the treatment of acute pancreatitis. Our recommendations are largely consistent with the
American Gastroenterological Association (AGA) and the American College of Gastroenterology (ACG)
guidelines for the treatment of acute pancreatitis [6,7]. The etiology, clinical manifestations, diagnosis of acute
pancreatitis, methods to predict its severity, and the diagnosis and management of pancreatic pseudocysts are
discussed separately. (See "Etiology of acute pancreatitis" and "Clinical manifestations and diagnosis of acute
pancreatitis" and "Predicting the severity of acute pancreatitis" and "Diagnosis and management of
pseudocysts of the pancreas".)
PRETREATMENT ASSESSMENT OF DISEASE SEVERITY — The first step in managing patients with acute
pancreatitis is determining the severity. The severity of acute pancreatitis can be predicted based upon clinical,
laboratory, and radiologic risk factors, severity grading systems, and serum markers. Some of these can be
performed on admission to assist in triage of patients, while others can only be obtained after the first 48 to 72
hours or later. (See "Predicting the severity of acute pancreatitis".)
SUPPORTIVE CARE — Mild acute pancreatitis is treated with supportive care including pain control,
intravenous fluids, and correction of electrolyte and metabolic abnormalities. The majority of patients require no
further therapy, and recover and eat within three to seven days. (See "Predicting the severity of acute
Sci-Hub
pancreatitis" and 'Pain management' below and 'Nutrition' below.)
In severe acute pancreatitis, intensive care unit monitoring and support of pulmonary, renal, circulatory, and
hepatobiliary function may minimize systemic sequelae [8].
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14.01.13 Treatment of acute pancreatitis
Vital signs and urine output should be monitored every few hours in the first 24 to 48 hours. Patients with
severe pancreatitis will need ongoing monitoring for other complications that might arise. (See
"Abdominal compartment syndrome".)
Sustained hypoxemia, hypotension refractory to a bolus of IV fluids, and possibly renal insufficiency that
does not respond to a fluid bolus warrant prompt transfer to an intensive care unit for close monitoring.
The importance of fluid replacement in the initial stages has been accepted as standard of care [9]. Fluid
replacement is important because patients with necrotizing pancreatitis develop vascular leak syndrome
[10]. At least one report suggested that inadequate fluid replacement (as evidenced by persistent
hemoconcentration at 24 hours) was associated with development of necrotizing pancreatitis [11].
Inadequate hydration can lead to hypotension and acute tubular necrosis. In addition, fluid depletion
damages pancreatic microcirculation and results in further pancreatic necrosis. Faster initial hydration
was associated with decreased mortality [12].
The exact amount and composition of fluid resuscitation that is required has not been extensively studied
but several approaches have been published [13]. After initial resuscitation with 20 cc/kg of intravenous
fluid given over 60 to 90 minutes, approximately 250 to 300 cc of intravenous fluids per hour are typically
required for 48 hours if the cardiac status permits [14]. Adequate fluid replacement can be assessed by
improvement in vital signs and urine output and reduction in hematocrit and blood urea nitrogen (BUN)
over 24 hours, particularly if they were high at the onset. Monitoring the BUN may be particularly
important, as both the BUN at the time of admission and the change in BUN during the first 24 hours of
hospitalization predict mortality [15]. Increased fluid resuscitation should be considered in patients
whose BUN levels stay the same or increase.
Fluids should be titrated to maintain urine output greater than 0.5 cc/kg/hour [16]. However, a low urine
output may reflect the development of acute tubular necrosis rather than persistent volume depletion. In
this setting, aggressive fluid replacement can lead to peripheral and pulmonary edema without improving
the urine output. (See "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute
kidney injury (acute renal failure)".)
There is some evidence that fluid resuscitation with lactated Ringer’s solution may be superior to normal
saline [17]. In one small randomized trial of 40 patients, patients who received lactated Ringer’s had
significantly lower mean C-reactive protein levels compared with patients who received normal saline (52
versus 104 mg/dL) and a significant reduction in systemic inflammatory response syndrome (SIRS) after
24 hours (84 versus 0 percent). However, in rare patients with acute pancreatitis due to hypercalcemia,
lactated Ringer’s is contraindicated because it contains 3 mEq/L calcium. In these patients normal
saline is the preferred fluid for volume resuscitation.
Oxygen saturation needs to be assessed routinely and supplemental oxygen administered to maintain
arterial oxygen saturation of greater than 95 percent. Blood gas analysis should be done if oxygen
saturation is less than 95 percent or if clinical situation demands. Hypoxia may be due to splinting,
atelectasis, pleural effusions, opening of intrapulmonary shunts, or acute respiratory distress syndrome
(ARDS). Persistent or progressive hypoxia may require mechanical ventilation. (See "Acute respiratory
distress syndrome: Clinical features and diagnosis" and "Supportive care and oxygenation in acute
respiratory distress syndrome".)
Electrolytes should be monitored in patients with acute pancreatitis based on disease severity.
Hypocalcemia should be corrected if ionized calcium is low or if there are signs of neuromuscular
instability (Chvostek’s or Trousseau’s sign). Low magnesium levels may cause hypocalcemia and should
be corrected.
Serum glucose levels should be carefully monitored hourly in patients with severe pancreatitis and sliding
scale insulin should be used to keep blood sugar levels under good control. Hyperglycemia may result
from parenteral nutritional therapy, decreased insulin release, increased gluconeogenesis, and decreased
glucose utilization, and may increase the risk of secondary pancreatic infections.
Deep vein thrombosis prophylaxis should be considered in bedridden patients. (See "Prevention of
venous thromboembolic disease in surgical patients".)
PAIN MANAGEMENT — Abdominal pain is often the dominant symptom. Patients with hypovolemia from
vascular leak and hemoconcentration may have ischemic pain. Markers of ischemia include metabolic acidosis
and elevated serum lactate. Uncontrolled pain can contribute to the hemodynamic instability.
Attention to adequate fluid resuscitation should be the first priority in addressing severe abdominal pain
(see 'Supportive care' above).
Adequate pain control requires the use of intravenous opiates, usually in the form of a patient controlled
analgesia pump. (See "Pain control in the critically ill adult patient".) Hydromorphone or
fentanyl (intravenous) may be used for pain relief in acute pancreatitis. Fentanyl is being increasingly
used due to its better safety profile, especially in renal impairment. As with other opiates, fentanyl can
depress respiratory function. It can be given both as boluses as well as constant infusion. The typical
dose for bolus regimen ranges from 20 to 50 micrograms with a 10-minute lock-out period (time from the
end of one dose infusion to the time the machine starts responding to another demand). Patients on
patient-controlled analgesia should be carefully monitored for side effects. (See "Pain control in the
critically ill adult patient", section on 'Opioid side effects'.)
Meperidine has been favored over morphine for analgesia in pancreatitis because studies showed that
morphine caused an increase in sphincter of Oddi pressure. However, there are no clinical studies to
suggest that morphine can aggravate or cause pancreatitis or cholecystitis [18]. It is important to note
that meperidine has a short half-life and repeated doses can lead to accumulation of the metabolite
normeperidine that causes neuromuscular irritation and, rarely, seizures.
NUTRITION — Patients with mild pancreatitis can often be managed with intravenous hydration alone since
recovery often occurs rapidly, allowing patients to resume an oral diet within a week. Nutritional support is often
required in patients with severe pancreatitis.
Nutritional support should be provided to those who are unlikely to resume oral intake for more than five to seven
days. Nasojejunal tube feeding (using an elemental or semi-elemental formula) is preferred to total parenteral
nutrition. Early enteral nutrition (24 to 48 hours) should be initiated upon transfer to an intensive care unit,
development of organ dysfunction, or systemic inflammatory response syndrome (SIRS) persisting for 48 hours
if severe acute pancreatitis is confirmed [19-22].
Enteral — Enteral feeding is recommended in patients with severe acute pancreatitis [6,7].
A benefit of enteral nutrition is its ability to maintain the intestinal barrier and prevent bacterial translocation from
the gut, which may be a major cause of infection. (See "Pathogenesis of acute pancreatitis".) Another
advantage is the avoidance of the complications associated with parenteral nutrition including catheter sepsis
(which occurs in 2 percent even if the catheter is managed appropriately) and less frequent complications such
as arterial laceration, pneumothorax, vein thrombosis, thrombophlebitis, and catheter embolism. In patients with
a partial gastric outlet obstruction due to inflammation or a fluid collection, a few weeks of enteral feeding allows
for the inflammation to subside or the fluid collection to mature and be drained, leading to resolution of the
obstruction and resumption of oral feeding. Consistent with previous meta-analyses, a 2010 meta-analysis of
eight trials demonstrated that enteral nutrition significantly reduced mortality, multiple organ failure, systemic
infections, and the need for surgery compared with those who received parenteral nutrition [23-26].
Radiologic or endoscopic placement of a jejunal feeding tube beyond the ligament of Treitz and enteral feeding
should be attempted. If this is not possible, nasogastric feeding has been proposed as an easier alternative. A
controlled trial comparing nasogastric with nasojejunal feedings found no significant differences in APACHE II
score, CRP measurement, pain levels, or analgesic requirement [27]. However, another small study comparing
nasogastric feeding with TPN noted increased pulmonary and total complications in the nasogastric group [28].
Further studies are needed before the nasogastric approach can be recommended.
We use high protein, low fat, semi-elemental feeding formulas (eg, Peptamen AF®) because of a reduction in
pancreatic digestive enzymes. We start at 25 cc per hour and advance as tolerated to at least 30 percent of the
calculated daily requirement (25 kcal/kg ideal body weight), even in the presence of ileus. Signs that the formula
is not tolerated include gastric residual volumes >400 cc (with nasogastric feeding), vomiting (with nasogastric
feeding), bloating, or diarrhea (>5 watery stools or >500 mL per 24 hours with exclusion of C. difficile toxin and
medication-induced diarrhea) that resolves if the feeding is held.
The presence of fluid collections or elevated pancreatic enzymes is not necessarily a contraindication to oral or
enteral feeding. However, in a subgroup of patients there is clear correlation of pain, recurrence of pancreatitis,
or worsening of fluid collections, with feeding, either oral or enteral. These patients often have disrupted
pancreatic ducts with fluid collections. Drainage of fluid collections may allow resumption of oral intake. If the
fluid collections are not considered suitable for drainage or if the target rate of enteral feeding is not achieved
within 48 to 72 hours, supplemental parenteral nutrition should be provided. (See 'Parenteral' below.)
Parenteral — Parenteral nutrition should be initiated in patients who do not tolerate enteral feeding. The use of
parenteral nutrition as an adjunct to enteral nutrition to improve provision of calories and protein to critically ill
patients may be harmful according to two studies. The first study was a multicenter trial that randomly assigned
4640 critically ill adults who were already receiving enteral nutrition to have supplemental parenteral nutrition
initiated early (within 48 hours of ICU admission) or late (after the eighth day of ICU admission) [29]. Those who
received early parenteral nutrition were more likely to develop a new infection and had a longer duration of
mechanical ventilation, ICU stay, and hospitalization. The second study was an observational study that
compared three groups: enteral nutrition alone, enteral nutrition plus early parenteral nutrition, and enteral
nutrition plus late parenteral nutrition in mechanically ventilated critically ill adults [30]. Enteral nutrition plus
either early or late parenteral nutrition was associated with increased mortality compared with enteral nutrition
alone. (See "Nutrition support in critically ill patients: An overview", section on 'Parenteral nutrition'.)
Initiation of oral feeding — When to begin oral feedings depends on the severity of the pancreatitis.
In mild pancreatitis, in the absence of ileus, nausea or vomiting, oral feeds can be initiated as soon as
the pain starts improving and narcotic requirements are decreasing. This usually occurs 24 to 48 hours
after the onset of pancreatitis. Traditionally, patients have been advanced from a clear liquid diet to solid
food as tolerated. More recent data suggest that starting first with a solid, low fat diet is safe, although it
does not necessarily decrease length of stay [31-34].
In moderate to severe pancreatitis, oral feeding is frequently not tolerated due to postprandial pain,
nausea, or vomiting, probably related to gastroduodenal inflammation and/or extrinsic compression from
fluid collections leading to gastric outlet obstruction. Patients are generally placed on enteral or
parenteral feeding as discussed above. When the local complications start improving, oral feeds are
initiated and advanced as tolerated.
INFECTION — The occurrence of pancreatic infection is a leading cause of morbidity and mortality in acute
necrotizing pancreatitis. Approximately one-third of patients with pancreatic necrosis develop infected necrosis
[6]. Patients who develop infection tend to have more extensive necrosis. Although infection can occur early in
the course of necrotizing pancreatitis, it is more often seen late in the clinical course (after 10 days) [35,36].
The important organisms causing infection in necrotizing pancreatitis are predominantly gut-derived, including
Escherichia coli, Pseudomonas, Klebsiella, and Enterococcus. The majority of infections (about 75 percent) are
monomicrobial. Fungal infection and infection with gram-positive organisms are uncommon but occur more
frequently in the setting of prophylactic antibiotic use for severe acute pancreatitis, especially when used for
more than 10 to 14 days. Fungal infections occur in approximately 9 percent of necrotizing pancreatitis and it is
not clear if they are associated with higher mortality [6].
Approaches taken to decrease bacterial infections in acute necrotizing pancreatitis include enteral feeding,
systemic antibiotics, percutaneous computerized tomography (CT) guided aspiration, and necrosectomy. Our
approach based upon these data is summarized in the following algorithm (algorithm 1). (See 'Percutaneous CT-
guided aspiration' below and 'Necrosectomy' below.)
Prophylactic antibiotics — Although this is still an area of debate, in the author's practice, we initiate
antimicrobial therapy with imipenem/meropenem and continue it for 7 to 10 days if there is necrotizing
pancreatitis (involving more than approximately 30 percent of the pancreas). Because of the risk of fungal
superinfection, antibiotics should be stopped after 7 to 10 days unless infection is documented. Given that the
data are equivocal regarding a benefit to prophylactic antibiotics, it is also reasonable to withhold antibiotics
until there is clinical evidence of infection (eg, fever, leukocytosis) or infection has been demonstrated after
sampling the necrotic tissue [6]. We do not routinely recommend prophylactic antifungal therapy with
fluconazole.
Studies evaluating the benefits [37-40] and harms [41-46] of prophylactic antibiotics have produced disparate
results. Contradictory results on the use of prophylactic antibiotics may be due to differences in methodological
quality, inconsistent presence of organ failure in these studies, differences in antibiotic regimens and feeding
used, and lack of data on adverse effects, making direct comparisons difficult [47-50].
One systematic review concluded prophylactic antibiotics decreased mortality in severe pancreatitis, but
not the rate of infected pancreatic necrosis [51].
In contrast, a subsequent meta-analysis of seven trials detected no mortality benefit or reduction in the
incidence of infected necrosis [41].
Further casting doubt on the benefit of prophylactic antibiotics is recognition that it can be associated
with the selection of resistant organisms and the development of fungal infection [44-46].
Guidelines issued by multiple societies also differ in their recommendations:
The American College of Gastroenterology guidelines [6] do not recommend prophylactic antibiotics.
Guidelines from the American Gastroenterological Association [52] do not make a firm recommendation
with regard to prophylactic antibiotics, but note that: "Antibiotic prophylaxis, if used, should be restricted
to patients with substantial pancreatic necrosis (>30 percent of the gland necrotic by CT criteria) and
should continue for no more than 14 days."
Guidelines from the Italian Association for the Study of the Pancreas [53] recommend antibiotics for
patients with CT-proven necrosis.
Whether there is a benefit to a specific class of antibiotics is also unclear. However, the authors suggest
imipenem or meropenem for 14 days for patients with proven necrosis based on the following data:
In a randomized controlled trial, 60 patients with severe acute pancreatitis with necrosis affecting at least
50 percent of the pancreas were randomly assigned to receive two weeks of pefloxacin, 400 mg twice
daily, or imipenem, 500 mg three times daily, within 120 hours of symptom onset. Rates of infected
necrosis were significantly lower in patients treated with imipenem as compared with pefloxacin (10 and
34 percent, respectively), although mortality was not significantly different in the two groups. [50].
A meta-analysis of five trials showed reduced sepsis and mortality but not a reduction in prevention of
necrosis with antibiotics (imipenem or meropenem) [54]. However, a subgroup of patients receiving
prophylactic imipenem had reduction in infected necrosis.
Percutaneous CT-guided aspiration — CT-guided percutaneous aspiration with Gram's stain and culture is
recommended when infected pancreatic necrosis is suspected (clinical instability or sepsis physiology,
increasing white blood cell count, fevers) [55,56]. Sterile necrosis does not usually require antibiotics and acute
fluid collections do not require therapy in the absence of infection or obstruction of a surrounding hollow viscus
[7].
Continued conservative management in a stable patient allows organization of necrotic fluid collections
permitting a minimally invasive debridement either by endoscopic or percutaneous route to clear necrotic debris
[57-60]. However, if there has been no improvement after one week of empiric antibiotics in a patient with >30
percent pancreatic necrosis and there are clinical signs of infection without another obvious site of infection, we
perform a percutaneous CT-guided aspiration [61-63]. We repeat percutaneous CT-guided aspiration if the
conditions of probable infection remain and no other source is found.
If there is evidence of a bacterial infection, we consider performing a necrosectomy (see 'Necrosectomy' below)
change the antibiotics according to the culture and sensitivity results (picture 1) [35,64]. If the aspirated material
is sterile, we continue conservative treatment for four to six weeks. A repeat aspiration in five to seven days may
be indicated in patients with signs of systemic toxicity since a negative fine needle aspiration does not
confidently exclude infection [65].
Necrosectomy — Indications for necrosectomy include infected pancreatic necrosis and sterile symptomatic
pancreatic necrosis with abdominal pain preventing oral intake. Surgical debridement of pancreatic necrosis
(necrosectomy) can be accomplished by open surgery or a minimally invasive approach (endoscopic or
percutaneous radiologic). In a randomized controlled trial, compared to open necrosectomy, a minimally invasive
step-up approach consisting of percutaneous drainage followed, if necessary, by open necrosectomy, reduced
the rate of the composite end point of major complications or death among patients with necrotizing pancreatitis
and infected necrotic tissue [66,67]. (See "Pancreatic debridement".)
Protease inhibitors — The role of protease inhibitors in the treatment of acute pancreatitis remains unclear as
evidence from clinical trials and a meta-analysis show only marginal benefit in patients with severe pancreatitis
[64,65,68-70].
TREATMENT OF ASSOCIATED CONDITIONS — In addition to the above treatment for pancreatic

inflammation, treatment of acute pancreatitis is aimed at correcting any underlying predisposing factors, such
as gallstones and hypertriglyceridemia, and treating complications such as splenic vein thrombosis and
abdominal compartment syndrome.
Gallstone pancreatitis — Gallstone pancreatitis requires specific therapeutic considerations, in addition to the
above recommendations. In this disorder, obstructive stones in the biliary tract or ampulla of Vater are
responsible for the pancreatitis. (See "Etiology of acute pancreatitis".)
The diagnosis of gallstone pancreatitis is discussed separately. (See "Clinical manifestations and diagnosis of
acute pancreatitis", section on 'Alcoholic versus gallstone pancreatitis'.)
Endoscopic retrograde cholangiopancreatography — Early endoscopic retrograde cholangiogram

(ERCP) with papillotomy or surgical intervention to remove bile duct stones may lessen the severity of gallstone
pancreatitis [71]. Multiple studies suggest that early endoscopic papillotomy is of benefit in patients with acute
biliary pancreatitis [72-74]. Endoscopic papillotomy is typically accompanied by placement of a plastic biliary
stent to decrease the risk of post-ERCP pancreatitis, which can occur in a patient who already has gallstone
pancreatitis. (See "Endoscopic management of bile duct stones: Standard techniques and mechanical
lithotripsy" and "Prophylactic pancreatic stents to prevent ERCP-induced pancreatitis: When do you use
them?", section on 'Pancreatic sphincterotomy'.)
In general, ERCP should be performed within 72 hours in those with a high suspicion of persistent bile duct
stones (ie, visible common bile duct stone on noninvasive imaging, persistently dilated common bile duct,
jaundice or rising liver chemistries) [7].
In the absence of cholangitis or a high suspicion of a persistent common bile duct stone, early ERCP (within 24
to 48 hours) is controversial. Three meta-analyses and one multicenter study reached different conclusions [73-
76]. Two meta-analyses found that early ERCP in patients without cholangitis did not lead to a significant
reduction in the risk of overall complications and mortality regardless of the predicted severity [74,76]. In another
meta-analysis of five prospective randomized trials that included 702 patients, early ERCP reduced
complications but not mortality in predicted severe pancreatitis; no benefit was observed in predicted mild
pancreatitis [75].
We suggest early ERCP should be performed within 24 to 48 hours if there is concomitant cholangitis,
persistently abnormal liver tests, or increasing liver tests (indicating the presence of a stone in the common bile
duct).
In the absence of persistent bile duct stones, cholangitis, persistently abnormal liver tests, or increasing liver
tests, patients with biliary pancreatitis, can undergo ERCP before the cholecystectomy.
Endoscopic ultrasound (EUS) or magnetic resonance cholangiopancreatogram (MRCP) to determine the need
for ERCP should be considered in patients in whom the clinical course is not improving sufficiently to allow
timely laparoscopic cholecystectomy and intraoperative cholangiogram, pregnant patients, patients with high
risk of difficult ERCP (altered surgical anatomy or coagulopathy), or if there is intermediate concern regarding
the possibility of a retained common bile duct stone, and the patient is not felt to be a good candidate for
cholecystectomy with cholangiogram within the near future.
Cholecystectomy — Cholecystectomy should be performed after recovery in all patients with gallstone
pancreatitis. Failure to perform a cholecystectomy is associated with a 25 to 30 percent risk of recurrent acute
pancreatitis, cholecystitis, or cholangitis within 6 to 18 weeks [77]. The risk of recurrent pancreatitis is highest
in patients who have not undergone a sphincterotomy.
In patients who have had mild pancreatitis, cholecystectomy can usually be performed safely within seven days
after recovery [78]. In a randomized prospective study of 50 patients with mild gallstone pancreatitis,
laparoscopic cholecystectomy performed within 48 hours of admission resulted in a shorter hospitalized stay
than one performed after resolution of pain and laboratory abnormalities [79].
On the other hand, in patients who have had severe necrotizing pancreatitis, delaying cholecystectomy for at
least three weeks may be reasonable because of an increased risk of infection [78]. Cholecystectomy after
sphincterotomy in elderly and sick patients is controversial [80]. (See "Endoscopic management of bile duct
stones: Standard techniques and mechanical lithotripsy", section on 'Safety of outpatient sphincterotomy'.)
If the clinical suspicion of common bile duct stones is high (eg, in those with persistent or worsening liver test
abnormalities or cholangitis), a preoperative ERCP is the best test as there is a high likelihood that therapeutic
intervention (sphincterotomy, stone extraction) will be required (see 'Endoscopic retrograde
cholangiopancreatography' above). On the other hand, if the suspicion of persistent common bile duct stones is
low (eg, if liver tests normalize), an intraoperative cholangiogram during cholecystectomy may be preferable to
avoid the morbidity associated with ERCP. MRCP and EUS are other imaging options that can exclude
common bile duct stones [81]. A preoperative ERCP can then be performed only in those with stones or sludge
in the common bile duct. (See "Magnetic resonance cholangiopancreatography" and "Endoscopic ultrasound in
patients with suspected choledocholithiasis".)
Biliary sludge — Most patients with biliary sludge are asymptomatic. However, biliary sludge is commonly
found in 20 to 40 percent of patients with acute pancreatitis with no other obvious cause. On ultrasound, sludge
appears as a mobile, low-amplitude echo that layers in the most dependent part of the gallbladder and is not
associated with shadowing. We recommend cholecystectomy in patients who have had an episode of
pancreatitis and have biliary sludge because of the high risk of recurrence [31,34]. (See "Etiology of acute
pancreatitis", section on 'Biliary sludge and microlithiasis'.)
Although there are no randomized trials documenting that intervention in patients with pancreatitis and biliary
sludge or microcrystals prevents further attacks of pancreatitis, two studies suggest that biliary sludge can lead
to pancreatitis, and that these patients may benefit from intervention [82,83].
In one prospective study of 86 patients with acute pancreatitis of which 31 were idiopathic, 23 (74
percent) had either biliary sludge on ultrasonography (11 patients) and/or cholesterol monohydrate or
calcium bilirubinate crystals on biliary microscopy [83]. Of the 21 patients in whom biliary sludge was the
only finding (two patients also had dilated bile ducts when restudied), the 10 patients treated by
cholecystectomy or papillotomy had fewer recurrences of acute pancreatitis during follow-up (up to seven
years) than the 11 untreated patients.
Another report evaluated the efficacy of biliary drainage in 51 patients recovering from an attack of acute
"idiopathic" pancreatitis [82]. Clusters of cholesterol monohydrate crystals, calcium bilirubinate granules,
and/or calcium carbonate microspheroliths were found in 67 percent. Examination of the gallbladder bile
at cholecystectomy or serial ultrasonography of the gallbladder for up to 12 months showed that 73
percent of the patients with unexplained pancreatitis had biliary sludge or microlithiasis. Dissolution of
gallstones by ursodeoxycholic acid (UDCA) or cholecystectomy prevented further attacks, while those
with a delay in surgery or failed UDCA therapy continued to have episodes of pancreatitis.
Hypertriglyceridemic pancreatitis — The treatment of hypertriglyceridemic pancreatitis is discussed

separately. (See "Hypertriglyceridemia-induced acute pancreatitis".)
Hypercalcemia — Hypercalcemia is a rare cause of acute pancreatitis. If present, treatment should be

directed at normalizing serum calcium levels and determining the underlying etiology. It is important to note that
Lactated Ringer’s solution is contraindicated in patients with hypercalcemia because it contains 3 mEq/L of
calcium and normal saline is the preferred fluid for volume resuscitation. (See "Etiology of hypercalcemia" and
"Diagnostic approach to hypercalcemia" and "Treatment of hypercalcemia".)
Splenic vein thrombosis — Splenic vein thrombosis is seen on imaging in up to 19 percent of patients with
acute pancreatitis [84].
Treatment should focus on the underlying pancreatitis since the effective treatment may be associated with
spontaneous resolution of the thrombosis. Anticoagulation may be needed if there is extension of the clot into
the portal or superior mesenteric vein resulting in hepatic decompensation or compromise of bowel perfusion.
However, this needs to be considered along with the theoretical possibility of hemorrhage into pancreatic
necrosis or fluid collections.
Complications such as variceal bleeding are uncommon (in contrast to chronic pancreatitis) and thus
prophylactic splenectomy is not recommended [85].
Abdominal compartment syndrome — Patients with severe pancreatitis are at increased risk for
intraabdominal hypertension and abdominal compartment syndrome. Factors that can contribute to abdominal
compartment syndrome in patients with acute pancreatitis include tissue edema from aggressive fluid
resuscitation, peripancreatic inflammation, ascites, and ileus [86]. Abdominal compartment syndrome is a life
threatening complication that results in visceral organ ischemia and tissue necrosis. Abdominal compartment
syndrome occurs when intra-abdominal pressure rises above 21 mmHg. Patients in the ICU should be
monitored for potential abdominal compartment syndrome with serial measures of urinary bladder pressures
[87].
Most patients who develop abdominal compartment syndrome are critically ill and unable to communicate. The
rare patient who is able to convey symptoms may complain of malaise, weakness, lightheadedness, dyspnea,
abdominal bloating, or abdominal pain. Nearly all patients with abdominal compartment syndrome have a
tensely distended abdomen. Progressive oliguria and increased ventilatory requirements are also common in
patients with abdominal compartment syndrome. Other findings may include hypotension, tachycardia, an
elevated jugular venous pressure, jugular venous distension, peripheral edema, abdominal tenderness, or acute
pulmonary decompensation. There may also be evidence of hypoperfusion, including cool skin, obtundation,
restlessness, or lactic acidosis.
If abdominal compartment syndrome is confirmed, either percutaneous catheter-based or surgical

decompression is indicated [88]. (See "Abdominal compartment syndrome", section on 'Surgical
decompression'.)
In patients with severe pancreatitis who require surgical decompression, this typically requires midline
laparotomy. Following decompressive laparotomy, temporary abdominal closure is used until the need for an
open abdomen has resolved. The abdomen is then closed primarily, functionally, or using skin grafts. (See
"Management of the open abdomen in adults", section on 'Temporary abdominal closure' and "Abdominal
compartment syndrome".)
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reading level, and they answer the four or five key questions a patient might have about a given condition. These
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comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
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Basics topics (see "Patient information: Pancreatitis (The Basics)")
Beyond the Basics topics (see "Patient information: Acute pancreatitis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
Acute pancreatitis can be divided into two broad categories: edematous, interstitial or mild acute
pancreatitis and necrotizing or severe acute pancreatitis. (See 'Introduction' above.) Treatment varies
depending on the severity of the condition. (See "Predicting the severity of acute pancreatitis".)
Mild pancreatitis is treated for several days with supportive care including pain control, intravenous fluids,
correction of electrolyte and metabolic abnormalities, and nothing by mouth. The majority of patients
require no further therapy, and recover and eat within three to seven days. (See 'Supportive care' above.)
In severe pancreatitis, intensive care unit monitoring and support of pulmonary, renal, circulatory, and
hepatobiliary function may minimize systemic sequelae. (See 'Supportive care' above.)
Abdominal pain is often the dominant symptom. Adequate pain control requires the use of intravenous
opiates, such as meperidine and fentanyl, usually in the form of a patient controlled analgesia pump.
(See 'Pain management' above.)
In patients with mild pancreatitis, recovery generally occurs quickly, making it generally unnecessary to
initiate supplemental nutrition. Soft diet can be started after resolution of pain. (See 'Initiation of oral
feeding' above.)
In patients with severe pancreatitis, we recommend attempting to provide early enteral nutrition in the first
72 hours through a nasojejunal tube placed endoscopically or radiologically (Grade 1B). If the target rate
is not achieved within 48-72 hours and if severe acute pancreatitis is not resolved, supplemental
parenteral nutrition should be provided. (See 'Enteral' above.)
The occurrence of pancreatic infection is a leading cause of morbidity and mortality in acute necrotizing
pancreatitis. We suggest prophylactic imipenem or meropenem in patients with necrosis that involves
more than 30 percent of the pancreas (Grade 2C). However, not all guidelines recommend the routine
use of antibiotics and it is reasonable to withhold antibiotics unless there is clinical or microbiologic
evidence of infection. (See 'Infection' above.)
We suggest the following algorithm (algorithm 1), based upon clinical and CT findings, to direct
percutaneous aspiration, antibiotic therapy, and minimally invasive or open surgical debridement as
needed (Grade 2B). (See 'Infection' above.)
In patients with gallstone pancreatitis, we recommend early ERCP and sphincterotomy for those who
have a high suspicion of cholestasis and those with cholangitis (Grade 1B). Cholecystectomy should be
performed after recovery in all patients with gallstone pancreatitis. (See 'Gallstone pancreatitis' above.)
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Topic 5633 Version 17.0
GRAPHICS
Management algorithm for severe acute pancreatitis
Image
CT: computed tomography; MRI: magnetic resonance imaging; TPN: total parenteral
nutrition.
* Controversial - see topic "Treatment of acute pancreatitis" for details.
• Choice depends upon the available expertise in tertiary centers.
Pancreatic abscess
Image
CT scan in a patient with abdominal pain, fever, and jaundice

shows air (thin arrow) in the central pancreas, which is necrotic
and largely replaced by an acute fluid collection (thick arrows),
leaving only a small residual pancreatic head (P).
Courtesy of Jonathan Kruskal, MD, PhD.
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14.01.

13 Treatment of acute pancreatitis

Official reprint from UpToDate®

Treatment of acute pancreatitis

Author Section Editor Deputy Editor

Edematous, interstitial, or mild acute pancreatitis

Guidelines issued by multiple societies also differ in their recommendations:

TREATMENT OF ASSOCIATED CONDITIONS — In addition to the above treatment for pancreatic

Endoscopic retrograde cholangiopancreatography — Early endoscopic retrograde cholangiogram

Hypertriglyceridemic pancreatitis — The treatment of hypertriglyceridemic pancreatitis is discussed

Hypercalcemia — Hypercalcemia is a rare cause of acute pancreatitis. If present, treatment should be

If abdominal compartment syndrome is confirmed, either percutaneous catheter-based or surgical

comfortable with some medical jargon.

Basics topics (see "Patient information: Pancreatitis (The Basics)")

SUMMARY AND RECOMMENDATIONS

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Topic 5633 Version 17.0

Management algorithm for severe acute pancreatitis

CT scan in a patient with abdominal pain, fever, and jaundice

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