Acute Pancreatitis Treatment & Management

Acute Pancreatitis Treatment & Management 4/9/15, 12:10 PM
Acute Pancreatitis Treatment & Management

Author: Timothy B Gardner, MD; Chief Editor: BS Anand, MD more...
Updated: Apr 1, 2015
Approach Considerations
Medical management of mild acute pancreatitis is relatively straightforward. The patient is kept NPO (nil per os
that is, nothing by mouth), and intravenous (IV) fluid hydration is provided. Analgesics are administered for pain
relief. Antibiotics are generally not indicated.
If ultrasonograms show evidence of gallstones and if the cause of pancreatitis is believed to be biliary, a
cholecystectomy should be performed during the same hospital admission. Feeding should be introduced enterally
as the patients anorexia and pain resolves. Patients can be initiated on a low-fat diet initially and need not
invariably start their dietary advancement using a clear liquid diet.
Serum amylase and lipase levels can be elevated in patients with brain injury (eg, cerebrovascular accident or
brain trauma). These patients are generally cared for in an intensive care unit (ICU) and require mechanical
ventilation. Pancreatic enzyme elevations may rise and fall considerably over many days to weeks. The elevation
is believed to result from hyperstimulation of the pancreas via a central mechanism, but no evidence of acute
pancreatitis is present on imaging studies.
Patients with severe acute pancreatitis require intensive care. Within hours to days, a number of complications (eg,
shock, pulmonary failure, renal failure, gastrointestinal [GI] bleeding, or multiorgan system failure) may develop.
The goals of medical management are to provide aggressive supportive care, to decrease inflammation, to limit
infection or superinfection, and to identify and treat complications as appropriate.
Autoimmune pancreatitis is a rare condition. Corticosteroids should not be used to treat this condition in the short
term in patients who are suspected of having autoimmune pancreatitis and who present with acute pancreatitis.
No evidence-based guidelines specify when a patient should be transferred to a more experienced or skilled
medical center. However, if severe acute pancreatitis is suggested either by the Atlanta criteria[3] or by a C-reactive
protein (CRP) level above 10 mg/dL, Ranson score of 4 or higher, or Acute Physiology and Chronic Health
Evaluation (APACHE) II score of 9 or higher, consider transfer to an institution where an intensivist staffs the
critical care unit and an interested subspecialist experienced in the diagnosis and treatment of pancreatitis is
available.
Further inpatient care depends on whether any of the complications of severe pancreatitis develop and how well
patients respond to treatment. This ranges from a few days to several months of intensive care.
Patients can be discharged when their pain is well controlled with oral analgesia, they are able to tolerate an oral
diet that maintains their caloric needs, and all complications have been addressed adequately.
Initial Supportive Care

Fluid resuscitation
Patients with acute pancreatitis lose a large amount of fluids to third spacing into the retroperitoneum and intra-
abdominal area. Accordingly, they require prompt IV hydration within the first 24 hours. Especially in the early
phase of the illness, aggressive fluid resuscitation is critically important. This cannot be overemphasized.
There is no universal consensus definitively favoring one type of fluid over another type; both crystalloids and
colloids are used. Resuscitation should be sufficient to maintain hemodynamic stability. This usually involves
administration of several liters of fluid as a bolus, followed by continuous infusion at a rate of 250-500 mL/h.
Central venous pressure, pulmonary artery wedge pressure, and urine output (>0.5 mL/kg/h) can be followed up
as markers of adequate hydration. Careful attention should be paid to signs of overhydration, such as pulmonary
edema causing hypoxia.
Nutritional support
General guidelines for nutritional support of patients with acute pancreatitis include the following:
In patients with mild uncomplicated pancreatitis, no benefit is observed from nutritional support, and the
energy (caloric) intake received with IV dextrose 5% in water (D5W) suffices; oral feedings should be
initiated once the patients pain and anorexia resolve
In patients with moderate-to-severe pancreatitis, begin nutritional support early in the course of
management, as soon as stabilization of fluid and hemodynamic parameters permits; optimally, nasojejunal
feedings with a low-fat formulation should be initiated at admission
Total parenteral nutrition (TPN) may be required when patients cannot meet their caloric needs with enteral
nutrition or when adequate jejunal access cannot be maintained; the TPN solution should include fat
emulsions in amounts sufficient to prevent essential fatty acid deficiency
If surgery is required for diagnosis or complications of the disease, place a feeding jejunostomy at the time
of the operation; use a low-fat formula
Begin oral feedings once abdominal pain has resolved and the patient regains appetite; the diet should be
low in fat and protein
Theoretical considerations regarding the ability of the enterocyte to maintain a barrier against bacterial
http://emedicine.medscape.com/article/181364-treatment Page 1 of 7
translocation favor nasojejunal feedingshence the recommendation to attempt initiating nasojejunal feedings at
admission in all patients admitted to the ICU. For patients with mild acute pancreatitis, nasojejunal feedings can be
avoided unless patients are unable to tolerate oral intake for over 1 week.
Research has not established whether nasojejunal tubes have an advantage over nasogastric tubes for enteral
feeding.
Although TPN, which has been shown to reduce mortality, may be necessary in certain situations, it should
generally be reserved for use as a second-line therapy, behind enteral feeding.
A prospective, randomized study showed that initiating oral feeding with a low-fat solid diet was as well tolerated
as initiating feeding with a clear liquid diet, but it did not result in a shorter length of stay.[21]
In a 2014 randomized, multicenter study of 208 patients with acute pancreatitis, early nasoenteric tube feeding
was not superior to an oral diet initiated 72 hours after presentation.[22] Tube feeding was provided if the oral diet
was not tolerated.
During 6 months of follow-up, major infection or death occurred in 30 of 101 patients (30%) in the early nasoenteric
tube feeding group and in 28 of 104 patients (27%) in the oral diet group (risk ratio, 1.07; 95% confidence interval,
0.79 to 1.44; P = 0.76).[22] Of the 104 patients in the oral diet group, 72 (69%) did not require tube feeding.
Antibiotic Therapy
Antibiotics, usually drugs of the imipenem class, should be used in any case of pancreatitis complicated by
infected pancreatic necrosis. However, they should not be given routinely for fever, especially early in the disease
course, because this symptom is almost universally secondary to the inflammatory response and typically does not
reflect an infectious process.
Several controlled trials have evaluated the role of empiric antibiotics in patients with severe acute necrotizing
pancreatitis for infectious prophylaxis.
One such trial evaluated the role of imipenem-cilastatin initiated at admission to prevent infected pancreatic
necrosis. This drug combination penetrates the pancreatic parenchyma and reduces the risk of intra-abdominal
infection. It appeared to offer some benefit in preventing infectious complications. Unfortunately, fungal
superinfection tends to develop later in the clinical course, although this risk is probably overemphasized.[23]
A randomized trial failed to show any benefit from giving ciprofloxacin and metronidazole to prevent infectious
complications. Accordingly, this drug combination is not routinely used for prophylaxis in the setting of acute
pancreatitis.[24]
The bottom line is that antibiotic prophylaxis in severe pancreatitis is controversial. At this time, the routine use of
antibiotics as prophylaxis against infection in severe acute pancreatitis is not recommended.
Emerging Pharmacologic Treatments

Although the role that cytokines play in the systemic inflammatory response syndrome (SIRS) appears to be
important, a large clinical trial of lexipafant, a platelet-activating factor antagonist, has shown no benefit in patients
with severe acute pancreatitis. Because multiple pathways are involved in the inflammatory response, further
research is needed in order to define which cytokine or combination of cytokines should be targeted to ameliorate
the complications of acute pancreatitis.[25]
Therapy directed against tumor necrosis factor-alpha (TNF-) has been targeted as a potential treatment of acute
pancreatitis; however, clinical trials have not yet determined its value in this setting.
Surgical Interventions
Surgical intervention, whether by minimally invasive or conventional open techniques, is indicated when an
anatomic complication amenable to a mechanical solution is present (eg, acute necrotizing pancreatitis in which
the necrotic phlegmon is excised to limit a potential site of sepsis, or hemorrhagic pancreatitis in which surgical
control of bleeding is warranted). Depending on the situation and local expertise, this may require the talents of an
interventional radiologist, an interventional endoscopist, or surgeon (individually or in combination).
The images below provide examples of the treatment of severe acute pancreatitis by means of minimally invasive
techniques.
Endoscopic retrograde cholangiopancreatography excluded suppurative cholangitis and established presence of anular pancreas
divisum. Dorsal pancreatogram showed extravasation into retroperitoneum, and sphincterotomy was performed on minor papilla. Pigtail
nasopancreatic tube was then inserted into dorsal duct and out into retroperitoneal fluid collection. The other end of the tube was
attached to bulb suction and monitored every shift.
While percutaneous drains remove loculated fluid collections elsewhere in the abdomen, nasopancreatic tube is containing
retroperitoneal fluid collection. By 1 week later, retroperitoneal fluid collection is much smaller (image is reversed in horizontal direction).
By this time, patient is off pressors and is ready to be extubated.
Gallstone pancreatitis
It is optimal for patients admitted with gallstone pancreatitis to undergo cholecystectomy before discharge, rather
than (for example) being scheduled for a later date as an outpatient. Patients discharged with gallstone
pancreatitis without a cholecystectomy are at high risk for recurrent bouts of pancreatitis.
Aboulian et al found that in patients with mild gallstone pancreatitis, performing laparoscopic cholecystectomy
within 48 hours of admissionregardless of whether abdominal pain or laboratory abnormalities had resolved
resulted in a shorter hospital stay and had no apparent impact on the technical difficulty of the procedure or the
perioperative complication rate.[26]
If the imaging and laboratory study findings are consistent with severe acute gallstone pancreatitis that is not
responding to supportive therapy or with ascending cholangitis with worsening signs and symptoms of obstruction,
early endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy and stone extraction is
indicated.
Pancreatic duct disruption
Damage to the pancreatic ductal system may allow the pancreatic juice to leak from the gland. The sudden
development of hypocalcemia or a rapid increase in retroperitoneal fluid on computed tomography (CT) is
suggestive of this condition.
When imaging studies provide corroborating evidence, the condition is initially managed by percutaneous
placement of a drainage tube into the fluid collection under the guidance of ultrasonography or CT scanning.[5]
Fluid amylase or lipase levels in the 10,000s strongly suggest the presence of a ductal disruption.
In the appropriate clinical setting, ERCP confirms the diagnosis and provides a treatment option. Transpapillary
stent placement or, preferably, placement of a 6 French nasopancreatic tube attached to an external bulb suction
device can successfully treat leaks by removing the sphincter tone and changing the dynamics of fluid flow in favor
of ductal healing. Occasionally, leaks are associated with downstream stenoses that are also amenable to
endoscopic treatment.
Refractory cases may warrant surgery. If a persistent leak is present in the tail of the gland, a distal
pancreatectomy is preferred. If the leak is in the head of the gland, a Whipple procedure is the operation of choice.
Pseudocysts
Peripancreatic fluid collections persisting for more than 4 weeks are referred to as acute pseudocysts.
Pseudocysts lack an epithelial layer and thus are not considered true cysts. They also differ from true cysts in that
they are usually filled with necrotic debris rather than fluid. Accordingly, pseudocysts may be better described by
the term organized necrosis.
Most pseudocysts can be followed clinically. However, when they are symptomatic (ie, associated with pain,
bleeding, or infection) or are larger than 7 cm and are rapidly expanding in an acutely ill patient, intervention is
indicated. Several different therapeutic approaches may be implemented, depending on the anatomic relations and
on the duration of the natural history of the complication.
In selected patients with very large fluid collections, percutaneous aspiration of pancreatic pseudocysts is a
reasonable approach. Even though treatment failures are common when the pseudocyst communicates with the
pancreatic ductal system, percutaneous drainage serves as a temporizing measure that may later lead to
successful endoscopic or surgical intervention. Often, an infected pseudocyst (which by definition is regarded as a
pancreatic abscess) can be successfully managed by means of percutaneous drainage.
Pseudocysts may also be managed endoscopically with transpapillary or transmural techniques. Transpapillary
drainage requires the main pancreatic duct to communicate with the pseudocyst cavity, ideally in the head or body
of the gland. The proximal end of the stent (which should be smaller than the diameter of the pancreatic duct) is
placed into the cavity. The technical success rate is 83%, the complication rate 12%. Generally, however,
pancreatic stents are difficult to monitor, are prone to obstruction, and carry an increased risk of infection and
ductal injury.
Some noncommunicating pseudocysts may be amenable to transmural enterocystostomy. Technical success

requires a mature cyst that bulges into the foregut, and the distance from the lumen to the cyst cavity should be
less than 1 cm. The success rate is 85%, the complication rate 17%. The transduodenal approach is associated
with fewer complications and recurrences than the transgastric approach.
On the basis of prospective studies in the 1970s, surgery was recommended for persistent large (> 7 cm)
pancreatic pseudocysts because complications developed in 41% of patients, 13% of whom died. Internal
pseudocyst-enteric anastomosis became the standard of care, with an operative mortality of 3-5%. This dogma
was subsequently challenged by 2 retrospective studies in which patients with smaller (ie, < 5 cm) asymptomatic
pseudocysts rarely (< 10%) developed complications.
Infected pancreatic necrosis
The clinician cannot rely on clinical findings alone to differentiate infected and sterile pancreatic necrosis. When
clinical signs of infection or SIRS are present in the setting of necrotizing pancreatitis, CT-guided needle aspiration
is indicated.
Surgery is recommended when large areas of the pancreas are necrotic and percutaneous CT-guided aspiration
demonstrates infection on the basis of a positive Gram stain. Antibiotic therapy alone is not sufficient to achieve a
cure. Aggressive surgical debridement and drainage are necessary to remove dead tissue and to clear the
infection.
A study of patients with necrotizing pancreatitis and infected necrotic tissue determined that a step-up approach to
treatment (consisting of percutaneous drainage followed, if necessary, by minimally invasive retroperitoneal
necrosectomy) yielded better results than standard care with open necrosectomy.[27] Patients who received step-
up treatment had a lower rate of major complications (new-onset multiorgan failure, multiple systemic
complications, perforation of a visceral organ, enterocutaneous fistula, or bleeding) and death.
Pancreatic abscess
Pancreatic abscesses generally occur late in the course of pancreatitis. Many of these respond to percutaneous
catheter drainage and antibiotics. Those that do not respond require surgical debridement and drainage.
Prevention
When the cause of pancreatitis can be determined, prevention depends on stopping the etiologic agent from
causing subsequent episodes.
In patients with documented gallstone pancreatitisand probably in those with idiopathic recurrent pancreatitis as
wellcholecystectomy is required. In patients who abuse alcohol, a dedicated person (eg, physician, psychologist,
addiction counselor) who can help the patient overcome the addiction to alcohol is required. When an uncommon
cause of pancreatitis is identified, the path of prevention is specific to the etiology.
Consultations
The most effective and soundly based treatment plan for any disorder is one aimed at the mechanism responsible
for the development of the disorder. With that axiom in mind, consultations must be obtained with an eye to
addressing the underlying cause of pancreatitis.
Treatment of patients with alcohol-induced pancreatitis should go beyond the physical manifestations of this
disease and address the underlying psychological addiction to alcohol. Simply telling patients they must stop
drinking alcohol is not satisfactory. Successful treatment often requires the involvement and expertise of a
chemical dependency counselor. The author favors in-hospital consultation for all patients admitted with alcoholic
pancreatitis.
Patients with hypertriglyceridemia- or hypercalcemia-induced pancreatitis require consultation with an

endocrinologist. Rarely, such patients require surgical intervention for treatment of hyperparathyroidism or control
of hyperlipidemia refractory to medical therapy.
Patients with gallstones or microlithiasis revealed on imaging studies should have a surgical consultation for
gallbladder removal. Because microlithiasis is the most common cause of idiopathic pancreatitis, a patient with
recurrent idiopathic pancreatitis should undergo cholecystectomy before procedures associated with a higher risk
of complications (eg, ERCP) are performed.
Patients with medication-induced acute pancreatitis may benefit from clinical pharmacology consultation during
their hospitalization to optimize their therapeutic regimen.
Long-Term Monitoring
Once the patient is stable enough to be discharged from the hospital, routine clinical follow-up care (typically
including physical examination and amylase and lipase assays) is needed to monitor for potential complications of
pancreatitis, especially pseudocysts.
No evidence-based guidelines have been established for outpatient follow-up care. Generally, a reasonable time to
see the patient is within 7-10 days from the date of hospital discharge to evaluate how he or she is doing and to
check for signs or symptoms of complications. If the pancreatitis was moderate to severe and was associated with
peripancreatic fluid collections, subsequent imaging studies are indicated to determine if a pseudocyst has
developed.
Recurrent acute pancreatitis
Recurrent acute pancreatitis (see the image below) can be a challenging clinical problem. First, seek to determine
the etiology using modalities that subject the patient to the least risk while simultaneously assessing for treatable
causes.
Normal-appearing ventral pancreas in a patient with recurrent acute pancreatitis. Dorsal pancreas (not pictured) showed evidence of
chronic pancreatitis.
Abdominal CT is a reasonable first approach. If neoplasia or chronic pancreatitis is found, it must be addressed
and treated accordingly.
If the CT scan is not diagnostic, order magnetic resonance cholangiopancreatography (MRCP). If MRCP shows
developmental abnormalities, strictures, or evidence of chronic pancreatitis, remember that endoscopic or surgical
treatment may be of benefit in a subset of patients.
If the MRCP findings are normal, further evaluation with endoscopic ultrasonography (EUS) is indicated. EUS has
better sensitivity for detecting biliary sludge and microlithiasis, which are probably the most common causes of
recurrent idiopathic pancreatitis. It may also help detect periampullary lesions missed by abdominal CT scanning
or MRCP.
If previous studies showed evidence of microlithiasis or biliary sludge, cholecystectomy is indicated. If the patient
has already undergone cholecystectomy or if pancreatitis recurs, further evaluation by ERCP is indicated. This
may reveal papillary stenosis, in which case a pancreatic and, possibly, biliary sphincterotomy is indicated.
The role of genetic testing is emerging, and whether testing for cationic trypsinogen mutations, SPINK1 mutations,
or CFTR mutations should be performed remains unclear, because no effective treatment currently exists for these
diseases.
If recurrent pancreatitis continues, ERCP with sphincter of Oddi manometry is indicated. This procedure is placed
last in the evaluation because patients with suspected sphincter of Oddi dysfunction (especially that resulting from
dyskinesia of the sphincter) have a very high rate of post-ERCP pancreatitis, and the possibility that ERCP may
create iatrogenic complications rather than cure the recurrent pancreatitis is a concern.
Contributor Information and Disclosures

Author
Timothy B Gardner, MD Assistant Professor, Department of Medicine, Dartmouth Medical School; Director of
Pancreatic Disorders, Section of Gastroenterology, Dartmouth-Hitchcock Medical Center
Timothy B Gardner, MD is a member of the following medical societies: American College of Gastroenterology,
American College of Physicians-American Society of Internal Medicine, American Gastroenterological
Association, American Medical Association, American Pancreatic Association, and American Society for
Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Coauthor(s)
Brian S Berk, MD Assistant Professor, Department of Medicine, Dartmouth Medical School; Director of End
Stage Liver Disease, Section of Gastroenterology, Dartmouth Hitchcock Medical Center
Brian S Berk, MD is a member of the following medical societies: American Association for the Study of Liver
Diseases, American College of Gastroenterology, and American Gastroenterological Association
Chief Editor
BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of
Medicine
BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver
Diseases, American College of Gastroenterology, American Gastroenterological Association, and American
Society for Gastrointestinal Endoscopy
Additional Contributors
Tushar Patel, MB, ChB Professor of Medicine, Ohio State University Medical Center
Tushar Patel, MB, ChB is a member of the following medical societies: American Association for the Study of
Liver Diseases and American Gastroenterological Association
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Noel Williams, MD Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia,
Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta,
Edmonton, Alberta, Canada
Noel Williams, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of
Canada
Paul Yakshe, MD Assistant Professor of Medicine, University of Minnesota, Medical Director of Pancreas and
Biliary Clinic, Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, Fairview
University Medical Center
Paul Yakshe, MD is a member of the following medical societies: American College of Gastroenterology,
American Pancreatic Association, and American Society for Gastrointestinal Endoscopy
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