The Pancreas
The Management of
Acute Pancreatitis
Angela LaFace, MD, Donald Davis, MD,
and Vic Velanovich, MD
A cute pancreatitis is a pathologic condition with far-reaching con-
sequences and is the leading cause of gastrointestinal-related
hospitalizations in the United States. The annual incidence of acute
pancreatitis ranges from 13 to 45 per 100,000 persons and appears
to be on the rise. Common causes include gallstone disease, alcohol
use, and hypertriglyceridemia, all of which are conditions concordant
with the U.S. obesity epidemic. When a cause cannot be determined,
the disease is considered idiopathic, which is not uncommon in acute
pancreatitis. Acute pancreatitis affects men and women equally.
Increasing age confers higher risk and a twofold to threefold increased
risk is seen in African Americans as compared with Caucasians.
Symptomatology ranges from a mild, self-limited course to severe,
complicated disease that may lead to infected pancreatic necrosis,
organ failure, and death. Although a low mortality rate of 1% is seen
in acute pancreatitis overall, advanced age, comorbidities, and severe
disease are associated with increased risk of mortality. There is a
continuum of disease progression in which acute pancreatitis may
become recurrent in 20% to 30% and chronic in 10% of patients.
DIAGNOSIS AND EVALUATION
The diagnosis of pancreatitis requires two of the three following
criteria: clinical (upper abdominal pain), laboratory (serum amylase
>3 times normal), and imaging (computed tomography [CT], mag-
netic resonance imaging [MRI], ultrasonography). A detailed medical
history, including family history of pancreatic disease, should be
taken on presentation. Important considerations include previous
diagnoses of pancreatitis, gallstone disease, alcohol use, hypertriglyc-
eridemia, trauma, medications, and recent biliary or pancreatic
instrumentation including endoscopic retrograde cholangiopancrea-
tography (ERCP). Careful physical examination is performed along
with laboratory testing to detect hematologic, metabolic, or electro-
lyte disturbance. Measurement of transaminases and a right upper
quadrant ultrasound may aid in diagnosing a biliary cause.
Radiologic evaluation with CT scan is not required for diagnosis
of acute pancreatitis in most patients, although it may be necessary
in cases of diagnostic uncertainty. Consequently, routine early CT
scanning is not indicated and should be avoided. There is no evidence
to support improved outcomes, clinical management is rarely influ-
enced, and increased duration of hospitalization has been reported
with this practice. However, early CT evaluation is indicated in
patients who have acute pancreatitis as well as severe abdominal pain
where bowel ischemia or hollow viscus perforation is suspected. The
extent of pancreatic and peripancreatic necrosis typically becomes
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apparent 72 hours after symptom onset; therefore optimal initial CT
assessment is performed after 72 to 96 hours. Several earlier guide-
lines advocated routine serial CT scans obtained weekly throughout
the course of acute pancreatitis; however, current guidelines have
abolished this practice, as there is no evidence to support its benefit.
Follow-up imaging with CT or MRI is indicated in cases of treatment
failure or clinical deterioration or before any invasive intervention.
Both CT and MRI are excellent radiographic modalities to assess
pancreatic tissue viability; however, MRI may be preferred to dis-
criminate necrotic collections from pseudocysts and in patients
where ionizing radiation is contraindicated.
ASSESSMENT OF SEVERITY
Numerous scoring systems historically have been used to predict
disease severity and outcomes in acute pancreatitis. The oldest and
best known, Ranson’s criteria, published in 1974, uses several labora-
tory parameters gathered at presentation and at 48 hours to identify
patients who are likely to have severe disease. One point is given for
each criterion met and a score of 3 or greater supports a diagnosis
of severe acute pancreatitis. The Atlanta classification, revised in
2012, is a comprehensive tool that combines early clinical assessment
of severity with radiologic evaluation of late sequelae of acute pan-
creatitis. Four distinct pancreatic morphologies are described by this
image-based classification system: (1) interstitial edematous pancre-
atitis, (2) necrotizing pancreatitis, (3) acute peripancreatic fluid col-
lection, and (4) pancreatic pseudocyst. These data may be used to
guide treatment in later disease stages. It appears, however, that the
presence of systemic inflammatory response syndrome (SIRS) is the
most predictive of severe acute pancreatitis. Presence of two or more
of the following criteria defines SIRS: (1) temperature less than 36°C
or greater than 38°C, (2) heart rate greater than 90/min, (3) respira-
tory rate greater than 20/min, (4) white blood cell count less than
4000 cells/mm3 or greater than 12,000 cells/mm3 or greater than 10%
bands. Multisystem organ failure is associated with the persistence of
SIRS physiology past 48 hours and, in turn, persistent multisystem
organ failure (>48 hours) is the leading predictor of mortality in
acute pancreatitis. A 25% mortality is associated with persistent SIRS,
with a high sensitivity and specificity of 77% to 89% and 79% to
86%, respectively. Ultimately, a holistic approach that accounts for
host risk factors, clinical risk stratification, and response to therapy
is most appropriate and accurate for prognostication in acute
pancreatitis.
INITIAL MANAGEMENT
Resuscitation
The presentation of patients with acute pancreatitis varies from
mild abdominal pain to systemic shock. Many patients with acute
pancreatitis need significant resuscitation at presentation. Initial
aggressive fluid replacement is required as these patients are hypo-
volemic for multiple reasons, including vomiting, poor oral intake,
increased respiratory losses, diaphoresis, and edema. Patients with
489
490 The Management of Acute Pancreatitis
signs of shock need aggressive fluid boluses and often vasopressive
medications to restore end organ perfusion. Pancreatitis causes
pancreatic edema and microangiopathic effects that decrease blood
flow to pancreatic cells resulting in cellular death and unregulated
release of pancreatic enzymes. This in turn leads to increased
inflammation, vascular permeability, and edema with subsequent
worsened perfusion of the pancreas. Restoration of the intravascular
volume and perfusion is imperative to help prevent propagation
of this cycle.
Classically, resuscitation of patients with acute pancreatitis has
included continued isotonic solution infusion at up to 20 mL/kg/h
after initial stabilization. However, recent evidence suggests that more
judicious regimens for continued resuscitation significantly decrease
morbidity and possibly mortality. Avoiding fluid overload is espe-
cially important in patients who have concurrent heart and renal
disease. Avoiding overresuscitation reduces complications such as
pulmonary edema, acute respiratory distress syndrome (ARDS), and
abdominal compartment syndrome.
Initial resuscitation should aim at restoring normal hemodynam-
ics and end organ perfusion. Lactated Ringer’s solution is the fluid
of choice for fluid resuscitation, as well-designed prospective studies
have demonstrated its superiority over normal saline. Boluses should
be given as quickly as possible in 500- to 1000-mL increments.
Improvement or maintenance of normal values of surrogate markers,
such as hematocrit, blood urea nitrogen (BUN), and creatinine, can
be reassuring. Once initial resuscitation is completed and euvolemia
is restored, appropriate vasopressive support should be provided
if hemodynamic instability and shock persist. Determination of
euvolemia or adequate resuscitation will vary by institution and criti-
cal care group.
As mentioned earlier, previous guidelines recommended continu-
ous infusion with lactated Ringer’s solution at a rate of 10 to 20 mL/
kg/h for the first 24 to 48 hours. In recent years, many other groups,
including the Surviving Sepsis Campaign, have advocated goal-
directed guidelines for resuscitation. Both of these approaches may
be appropriate at many institutions, especially those without the
ability to provide continuous monitoring of patients by a multidis-
ciplinary critical care team. Parameters for goal-directed therapy may
include central venous pressure (CVP), pulmonary arterial wedge
pressure (PAWP), mixed venous saturation (SvO2), lactate level, and
hourly urine output. However, multiple large, multicenter, random-
ized control trials in numerous countries have now demonstrated
that early goal-directed therapy is not superior to careful resuscita-
tion performed by experience critical care teams.
Indeed, many of these patients also have multisystem dysfunction,
making their hourly urine output, lactate, and renal function inac-
curate markers for resuscitation. Our experience has found that using
these parameters in isolation or continuously infusing Lactated
Ringer’s solution at the recommended rates often results in fluid
overload with increasing complications. Our institution’s preference
is to rely heavily on the SvO2 measured by a pulmonary arterial
catheter when euvolemia is in question. Numerous studies have chal-
lenged the reliability of both CVP and PAWP in measuring volume
status. Similar to the Surviving Sepsis Campaign, we have found that
an SvO2 above 65% correlates with adequate tissue perfusion in most
patients. It should be stressed that most patients can be resuscitated
without a pulmonary artery catheter but we have found that it is an
invaluable tool in patients with persistent hypotension and oliguria
despite initial aggressive fluid resuscitation.
The method of resuscitation varies between groups and institu-
tions. Resuscitation performed with goal-directed therapy or con-
tinuous infusion of resuscitative fluid may be appropriate, especially
if intensive, continuous monitoring by a critical care team is not
feasible. Hypervolemia may result but this is preferable to hypoperfu-
sion. Otherwise, patients with signs of shock should be resuscitated
in a thoughtful, diligent, and continuous manner by a critical care
team in an intensive care unit (ICU) until SIRS physiology has
resolved.
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Antibiotics
Antibiotics should be given to patients with acute pancreatitis and
an active infection. This may include cholangitis, urinary tract infec-
tion, pneumonia, catheter-related infections, bacteremia, and, indeed,
infected pancreatic necrosis.
Acute pancreatitis itself may cause fever, tachypnea, tachycardia,
hypotension, oliguria, and other symptoms that may be clinically
indistinguishable from sepsis and septic shock resulting from a
profound systemic inflammatory response. If an infection is sus-
pected, broad-spectrum antibiotics should be initiated with anti-
fungal coverage in select cases. Cultures should be obtained and
antibiotic therapy tailored based on organism sensitivities; immedi-
ate cessation is warranted if culture results do not support con-
comitant infection.
Patients with infected pancreatic necrosis have a significantly
higher mortality rate when compared with patients with sterile pan-
creatic necrosis. Historically, prophylactic antibiotics were given to
patients with pancreatic necrosis to prevent conversion of sterile
pancreatic necrosis to infected pancreatic necrosis, as previous
studies suggested that prophylactic antibiotics may be able to prevent
this transition. However, a meta-analysis of more recent, well-
designed, randomized controlled trials demonstrated no significant
benefit from prophylactic antibiotics in this setting. Currently, anti-
biotics do not appear to be beneficial in a prophylactic role in acute
pancreatitis.
Nutrition
Long-held dogma in acute pancreatitis is that patients should be kept
without enteral nutrition, allowing the pancreas to “rest” based on
the belief that enteral feeding exacerbates pancreatic inflammation.
To that end, many patients with acute pancreatitis have been main-
tained on total parenteral nutrition (TPN) to avoid additional enteral
simulation. In recent years, multiple studies based on both clinical
and laboratory observations demonstrate that such an approach is
harmful to patients with acute pancreatitis, and the evidence does
not support the claim that enteral feeding exacerbates pancreatic
inflammation.
In mild pancreatitis (patients without SIRS or need for ICU
admission), immediate enteral feeding should be initiated. Multiple
studies have demonstrated that patients can be started safely on a
low-fat solid diet and that restricting the diet to clear liquids is
without benefit. Initiating a solid diet early increases caloric intake
and shortens hospital stays.
The timing of initiation of enteral nutrition in severe pancreatitis
is controversial but should be attempted before TPN is considered.
Multiple randomized controlled trials and meta-analyses have shown
that infectious complications, organ failure, and mortality were
increased with the use of TPN in patients with severe pancreatitis.
Enteral feeding prevents atrophy and breakdown of the gastrointes-
tinal tract mucosal barrier and may prevent bacterial translocation.
Some studies also demonstrate a decreased incidence of infected
pancreatic necrosis.
In patients who are unable to maintain their nutritional require-
ment with oral intake alone, nutritional supplementation should be
provided in the form of tube feedings. Nasojejunal positioning of
the feeding tube was long considered optimal to avoid pancreatic
stimulation but numerous studies have now demonstrated that naso-
gastric tubes are safe and effective for most patients with acute
pancreatitis. Given the theoretical risk of aspiration with the use of
this feeding modality and potential associated complications, an
aspiration precaution protocol is advised. Placement of a nasojejunal
feeding tube is often more difficult than a nasogastric tube and
may require some form of radiographic assistance, but should
be attempted if nasogastric feeding is not tolerated and before
considering TPN.

Signs of biliary obstruction?
Yes
Suspicion of cholangitis?
Yes No
Signs of
Emergent
obstruction
ERCP with
resolved within
sphincterotomy
24–48 hours?
Yes No
Follow Follow
ERCP with
non-obstructed non-obstructed
sphincterotomy
algorithm algorithm
Follow non
obstructed algorithm
FIGURE 1 Management algorithm for acute pancreatitis resulting from gallstones with and without common bile duct obstruction. ERCP, Endoscopic
retrograde cholangiopancreatography.
Endoscopic Retrograde
Cholangiopancreatography and Cholecystectomy
The preferred treatment of biliary pancreatitis has changed and many
previous questions about the role of ERCP and cholecystectomy have
been clarified. Large randomized controlled trials and meta-analyses
have failed to demonstrate benefit of routine ERCP and it should be
avoided unless there is evidence of biliary obstruction. If cholangitis
is suspected, urgent ERCP should be performed as soon as feasible,
ideally within 24 hours of admission. Delay up to 48 hours is reason-
able in patients who have biliary obstruction in the absence of chol-
angitis, as spontaneous stone passage may result in resolution of the
obstruction without intervention (Figure 1).
Cholecystectomy is recommended for patients with biliary pan-
creatitis but optimal timing depends on disease severity. In mild cases
of acute pancreatitis, surgery should be performed during the index
admission. A 6-week interval before cholecystectomy should be
granted for patients with severe disease and peripancreatic fluid col-
lections. Allowing such fluid collections to resolve or mature decreases
the incidence of infectious complications (Figure 2).
ERCP with sphincterotomy effectively prevents recurrent biliary
pancreatitis and can be used alone in patients with life-threatening
comorbidities and prohibitive surgical risk. Cholecystectomy should
be performed after sphincterotomy in those who are deemed accept-
able surgical candidates, as these patients remain at risk for gallstone-
related disease complications.
SURGICAL MANAGEMENT
Historically, the treatment for necrotizing pancreatitis was pancreatic
necrosectomy. This approach was abandoned because of the high
morbidity and mortality of the procedure and the observation that
many of these patients recovered without operation. Surgery was
then reserved for infected pancreatic necrosis or other complica-
tions such as gastric outlet obstruction or bile duct obstruction.
However, recent evidence suggests that necrosectomy often may
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T HE PANCREAS 491
No
Severe pancreatitis with
peripancreatic fluid?
Yes No
Cholecystectomy
Wait 6 weeks during index
admission
High risk
for operation?
Yes No
ERCP with
Cholecystectomy
sphincterotomy
be unnecessary, even in infected cases. If infected pancreatitis is
suspected or proven, either by imaging or culture obtained by
image-guided fine-needle aspiration (FNA), empiric antibiotics with
adequate pancreatic tissue penetration (i.e., carbapenems) should
be initiated. If FNA is performed and is negative for infection,
empiric antibiotic therapy should cease. FNA should not be per-
formed routinely and should be avoided if clinical suspicion for
infection is low or the patient is clinically improving.
In cases of antibiotic therapy failure in infected pancreatic necro-
sis, all attempts at stabilization should be made for at least 4 weeks
before performing invasive procedures. Allowing time for sequestra-
tion of necrotic pancreatic tissue has been shown to decrease the
morbidity of these procedures. The first invasive intervention that
should be attempted is percutaneous drainage or endoscopic trans-
luminal drainage. If a percutaneous approach is taken, this tract
subsequently can be dilated for further débridement. Laparoscopic
or open necrosectomy is indicated in cases of treatment failure with
these modalities. This “step-up” approach should be utilized when
feasible and has been shown to reduce major complication and mul-
tisystem organ failure.
An intra-abdominal catastrophe or persistent clinical instability
necessitates the appropriate immediate intervention that may reach
across multiple specialties. Indicated interventions may include
angioembolization, endoscopic intervention, laparotomy with perfo-
ration repair, diverting ileostomy or colostomy, or even open necro-
sectomy with blunt removal of all pancreatic tissue and two large-bore
drains for postoperative lavage. These interventions should be dic-
tated by the individual patient’s immediate, life-threatening needs.
SUMMARY
The management of acute pancreatitis continues to evolve. Every-
thing from the diagnosis to the treatment of this disease has changed
significantly over the last 20 years. Radiographic imaging, specifically
CT scans, is no longer considered required for diagnosis and subse-
quent CT scans are no longer used to monitor the progression of the
492 The Management of Acute Pancreatitis

Suspected or confirmed pancreatic necrosis?

Yes No

Stabilization and supportive

care (enteral feeds, physical
Stabilization and therapy, etc.)
antibiotics x 6 weeks
ERCP with sphincterotomy
if needed

Failure to thrive or gastric

Clinical decline? outlet obstruction after
6–8 weeks of supportive care?

Yes No

Lifesaving intervention
Persistent signs of
(laparotomy,
infection?
angioembolization, etc.)

Yes No Yes No

Disposition
CT-guided or Continue supportive CT-guided or
(home, skilled
transluminal drainage care transluminal drainage
nursing care, rehab, etc.)

Clinical decline? Clinical decline?

Yes No Yes No

Persistent signs of
Life-saving intervention Life-saving intervention Persistent failure to
infection, failure to
(laparotomy, (laparotomy, thrive or gastric outlet
thrive, or gastric outlet
angioembolization, etc.) angioembolization, etc.) obstruction?
obstruction?

Yes No Yes No

Consider laparoscopic Disposition

Laparoscopic or open Continue supportive
or open (home, skilled
necrosectomy care
necrosectomy nursing care, rehab, etc.)

FIGURE 2 Management algorithm for acute pancreatitis associated with pancreatic necrosis. CT, Computed tomography; ERCP, Endoscopic retrograde
cholangiopancreatography.

disease process. In fact, radiographic imaging is now considered
useful only if the diagnosis of pancreatitis or infected pancreatic
necrosis is in doubt.
Routine ERCP appears to be unnecessary but should be done as
soon as feasible if cholangitis is present, if signs of biliary obstruction
do not resolve, or if the patient with biliary pancreatitis is not a
suitable candidate for cholecystectomy. Cholecystectomy should be
done at the index admission if the pancreatitis is not severe and is of
biliary origin.
Resuscitation is still of primary importance in patients with severe
pancreatitis but there is increasing recognition that this must be done
with substantial thought, care, and diligence to avoid fluid overload
and once common complications such as ARDS and abdominal com-
partment syndrome.
Nutrition should be provided as soon as possible and in enteral
form. If the patient is not able to eat adequate calories by mouth,
nasogastric or nasojejunal feedings should be initiated. There is no
need to “cool down” the pancreas and TPN should be used only if
enteral nutrition is not feasible.
The role of antibiotics has been clarified. Antibiotics should not
be used for prophylaxis against infected pancreatic necrosis but have
become the first-line treatment for this disease process. Only once
antibiotics have failed should more invasive forms of treatment be
pursued. Image-guided or transluminal drainage should be attempted
before surgical intervention.
Surgical intervention was once the mainstay treatment for severe
acute pancreatitis. This is no longer the case. Aggressive, surgical
management has largely been replaced by more conservative, non­
operative, supportive care. This has significantly reduced wasted
resources while decreasing morbidity and mortality. Surgery is still
an important part of the treatment of severe acute pancreatitis but
only when all other measures have failed.

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Poropat G, Giljaca V, Hauser G, Stimac D. Enteral nutrition formulations for
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