510 Gallstone Pancreatitis
nn SUMMARY
Acute pancreatitis is a common but potentially life-­threatening
disease. Imaging is not always necessary to establish a diagnosis
and is more helpful in delineating the demarcation of necrosis
from healthy tissue later in the disease process. Patients should
be expeditiously fluid-­ resuscitated early in the course of dis-
ease while remaining conscious of the potential complications of
over-­resuscitation. Institution of an oral diet early in the course of
mild pancreatitis and enteral tube feeding in severe disease form
the foundation of nutritional support, parenteral nutrition being
reserved for patients who cannot tolerate enteral feeding. Antibi-
otics should not be administered prophylactically in the absence
of clinical suspicion or evidence for infection. Infected necrosis is
the primary indication for mechanical intervention in acute pan-
creatitis. Infection is usually diagnosed by a combination of radio-
graphic and clinical factors. Intervention, when indicated, should
be initiated with a step-­up approach; decisions about the best mode
and route for intervention should optimally be made by a multi-
disciplinary group of surgeons, interventional radiologists experi-
enced with percutaneous drainage, and interventional endoscopists
capable of endoscopic transluminal intervention. A variety of tech-
niques are now available for interventional management of necro-
tizing pancreatitis and its sequelae with the different strengths and
weaknesses of the alternatives as described previously. An individ-
ualized approach based on patient anatomy, physiology, and prefer-
ence should be used to choose the best technique in each case to
obtain optimal results.
Gallstone Pancreatitis
John C. Alverdy, MD, FACS, Richard A. Jacobson, MD, and
Fons van den Berg, MD
A cute pancreatitis (AP) remains a leading cause of emergency
department visits, hospital admissions, and healthcare costs
worldwide. In the United States, the incidence has risen concordantly
with an aging population and the increased prevalence of obesity. AP
resulting from gallstones is the most common etiology in the devel-
oped world, followed by alcohol ingestion, although locoregional
rates vary based on population characteristics.
In patients with mild disease, cholecystectomy should be per-
formed during the same admission to prevent complications of recur-
rent disease. Twenty percent of all patients admitted with a diagnosis
of AP develop severe disease for which intensive care therapy and
interventional procedures other than cholecystectomy may be appro-
priate. In this latter population, the surgical community has been
slow to fully adopt more minimally invasive techniques that are asso-
ciated with lower morbidity and improved survival.
nn EPIDEMIOLOGY
AP accounts for more than 330,000 emergency department visits and
contributes to roughly 5400 deaths per year in the United States. More
than US$2.5 billion are spent annually on the treatment of AP and its
complications. Gallstone pancreatitis (GSP) is the most common etiol-
ogy, accounting for up to 60% of all cases, followed by alcoholic AP. Risk
factors for GSP are patient related, stone related, or anatomic. Factors
such as age, female gender, gallstones smaller than 5 mm, biliary sludge,
20 or more gallstones, and a large cystic duct diameter have been dem-
onstrated to influence the incidence, course, and outcome of the disease.  onset, constant visceral-­
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Suggested Readings
Bakker OJ, van Santvoort HC, van Brunschot S, et al. Endoscopic transgastric
vs surgical necrosectomy for infected necrotizing pancreatitis: a random-
ized trial. JAMA. 2012;307:1053–1061.
Carter CR, McKay CJ, Imrie CW. Percutaneous necrosectomy and sinus tract
endoscopy in the management of infected pancreatic necrosis: an initial
experience. Ann Surg. 2000;232:175–180.
Fagenholz PJ. Sinus tract endoscopic debridement of pancreatic necrosis;
2018. https://youtu.be/e05-­SVI-­7rA.
Fagenholz PJ. Video assisted retroperitoneal debridement of pancreatic necro-
sis; 2018. https://youtu.be/9ErPBAnrOAU.
Fagenholz PJ, Thabet A, Mueller PR, et al. Combined endoscopic transgastric
drainage and video assisted retroperitoneal pancreatic debridement: The
best of both worlds for extensive pancreatic necrosis with enteric fistulae.
Pancreatology. 2016;16(5):788–790.
Madenci AL, Michailidou M, Chiou G, et  al. A contemporary series of pa-
tients undergoing open debridement for necrotizing pancreatitis. Am J
Surg. 2014;208(3):324–331.
Räty S, Pulkkinen J, Nordback I, et al. Can laparoscopic cholecystectomy pre-
vent recurrent idiopathic acute pancreatitis?: a prospective randomized
multicenter trial. Ann Surg. 2015;262(5):736–741.
van Brunschot S, Hollemans RA, Bakker OJ, et al. Minimally invasive and en-
doscopic versus open necrosectomy for necrotising pancreatitis: a pooled
analysis of individual data for 1980 patients. Gut. 2018;67(4):697–706.
van Santvoort HC, Besselink MG, Bakker OJ, et al. A step-­up approach or open
necrosectomy for necrotizing pancreatitis. N Engl J Med. 2010;362:1491–1502.
Working Group IAP/APA Acute Pancreatitis Guidelines. IAP/APA evidence-­
based guidelines for the management of acute pancreatitis. Pancreatology.
2013;13(4 suppl 2):e1–e15.
Zyromski NJ, Nakeeb A, House MG, Jester AL. Transgastric pancreatic necro-
sectomy: how I do it. J Gastrointest Surg. 2016;20(2):445–449.
nn PATHOPHYSIOLOGY
The molecular pathophysiology of GSP is defined by inappropri-
ate and excessive activation of intrapancreatic proteases that lead to
autodigestion of the pancreatic tissue. The subsequent inflammatory
response results in local and systemic complications of AP as outlined
in the following section. Anatomically, it is recognized that obstruc-
tive biliary events incite this cascade of pancreatic inflammation and
autodigestion; however, the full process is incompletely understood.
Three leading theories include: (1) obstruction of the sphincter of
Oddi leading to back-­pressure and stasis in the pancreatic duct;
(2) bile reflux into the pancreatic duct; and (3) duodenal contents
refluxing into the pancreatic duct. Irrespective of these mechanical
events, the burst of protease activation that follows is what damages
the pancreatic acini, which in some cases leads to ductal disrup-
tion, local inflammation, secondary infection, and all subsequent
complications.
Infection of a peripancreatic fluid collection or necrotic pancre-
atic parenchyma is the leading cause of morbidity and mortality in
AP. Importantly, these are not primary necrotizing infections that
destroy pancreatic tissue, but rather secondary infections by translo-
cated bacteria presumed to originate from the gastrointestinal tract.
The morbidity and mortality associated with infected pancreatic
necrosis has resulted in several attempts to prevent the transloca-
tion of intestinal bacteria with prophylactic intravenous antibiotics,
selective digestive decontamination with oral antibiotics, or probiotic
regimens. The timing, dose, route, and utility of microbiome-­altering
regimens remains controversial in GSP. 
nn CLINICAL PRESENTATION
Patients presenting with AP appear constitutionally similar to those
in septic shock. They often appear unwell and complain of acute
type pain in the epigastrium generally

radiating to the back. Associated symptoms include nausea and vom-
iting. The pain is exacerbated by oral intake and may be relieved when
the patient leans forward. Other diagnoses to be considered are acute
cholecystitis, choledocholithiasis, and peptic ulcer disease.
On examination, patients can present with tachycardia driven,
in part, by the pain associated with AP in mild cases or by severe
hypovolemia in more moderate to severe cases. Low-­grade fevers are
common and not necessarily indicative of an acute infectious pro-
cess. Abdominal tenderness can be a prominent finding on physical
examination. The presence of bruising in the flank areas, umbili-
cus, or inguinal regions indicates hemorrhagic pancreatitis that has
resulted in dissection of blood along the retroperitoneal planes. The
presence of fever, jaundice, or acholic stools may indicate obstructive
choledocholithiasis or cholangitis. 
nn DIAGNOSIS
The diagnosis of GSP is generally made in the emergency setting and
is based on clinical, radiographic, and biochemical factors. Blood
chemistries suggestive of AP in the setting of gallstones documented
by ultrasound usually confirm the diagnosis. The pancreatic enzymes
amylase and lipase are usually elevated in patients with AP. Sensitiv-
ity and specificity of these assays depends on the specific enzyme
measured and the threshold used to define a positive test. Amylase
is considered nonspecific, whereas lipase is considered specific for
AP, but neither delineates GSP from other etiologies. Most centers
use a threshold of positivity defined as three to four times the normal
value; however, the duration of symptoms should be considered when
interpreting levels of these enzymes. Other circulating factors such
as C-­reactive protein and interleukin 6 have been validated as useful
markers of the severity of AP, but they do not discriminate AP from
other inflammatory or infectious processes. Elevated alanine amino-
transferase or lymphocyte/neutrophil ratio may distinguish GSP from
other etiologies of AP; however, this distinction is generally based on
the absence of a history of alcohol abuse and evidence of obstructing
biliary stones or sludge on imaging. Other markers of the acute phase
response induced by AP such as interleukin 8 have been validated to
rise in the setting of AP but are uncommonly used in clinical practice.
Ultrasound is the initial imaging test of choice as it is a noninvasive
and highly sensitive test to detect the presence of gallstones. Because
patients with GSP may present with a significant ileus, the sensitivity of
ultrasound may be decreased by overshadowing of bowel gas. A limita-
tion of ultrasound in this setting, however, is that it cannot assess the
severity of pancreatic inflammation and therefore contrast-­enhanced
computed tomography (CT) is the test of choice to determine the
extent of the AP. Ideally, a pancreas protocol CT with arterial and por-
tal phases is most useful to delineate the degree of inflammation and
disruption of the pancreatic parenchyma and main duct. Most authors
recommend a CT scan at least 72 hours after the onset of symptoms
because radiographic signs of local complications may not be evident
before this and therefore are not actionable. On CT, peripancreatic
edema (in the anterior pararenal space, transverse mesocolon, or small
bowel mesentery), fat stranding, or nonenhancement of the pancreatic
parenchyma (indicating necrosis) are indicative of AP.
Severity
The severity of GSP is a function of the degree of acute cholecystitis
and the degree of pancreatic necrosis and inflammation that is pres-
ent. Most often, the gallbladder is not inflamed because the disease is
more of a consequence of the migration of gallstones into the com-
mon bile duction than acute gallbladder inflammation. However, it is
important to recognize the severity of both as an important aspect of
the treatment strategy. Stratification by severity is of prognostic value
and predicts which patients will require intensive care and invasive
drainage procedures. The severity of systemic inflammation gener-
ally dictates the need for intensive care monitoring and can usually
be assessed on admission. Although most patients present with mild
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PA N C R E A S 511
TABLE 1  Severity of AP According to 2012
Revision of the Atlanta Criteria
Severity Characteristics
Mild No organ failure
No local or systemic complications
Moderately severe Transient organ failure (<48 hours)
Local or systemic complications without
persistent organ failure
Severe Persistent organ failure
TABLE 2  Organ Failure as Defined by the
Marshall Criteria
Organ system Criteria for failure
Pulmonary PaO2/FiO2 ratio <300
Renal Serum creatinine >1.9 (if normal at baseline)
Cardiovascular SBP <90 mm Hg, not responsive to fluids
From Marshall JC. A scoring system for multiple organ dysfunction syn-
drome. Sepsis. 1994;38-49.
SBP, systolic blood pressure.
or moderate disease, up to 20% of patients can present with severe
AP as defined by the 2012 revision of the Atlanta criteria (Table 1).
This revision classifies organ dysfunction as transient (<48 hours) or
persistent. When organ failure develops, the systems most commonly
affected are the respiratory, renal, and cardiovascular systems (in this
order); dysfunction is defined by the Marshall criteria (Table 2).
As many as 20% of patients with severe AP (SAP) will progress to
develop necrotizing disease of the pancreas or peripancreatic tissues.
Up to 20% of these patients can develop infected necrosis, which will
significantly complicate their course and worsen their prognosis.
This so-­called rule of 20s (20% of all AP is severe, 20% of SAP is
necrotizing, 20% of necrotizing disease develops infection) is a useful
clinical pearl. 
nn MANAGEMENT: INITIAL TREATMENT
Patients diagnosed with GSP are admitted to the hospital and, if
determined to have severe disease, will require monitoring in an
intensive care unit. Aggressive fluid resuscitation, preferably with
lactated Ringer’s solution, remains the cornerstone of initial manage-
ment and is recommended for all patients. Pain should be managed
adequately with standard-­of-­care protocols. Patients presenting with
mild AP should resume oral intake as early as is feasible once the pain
is receding. Initiation of enteral feeding, be it with oral intake or naso-
enteric feeding of a chemically defined diet, has been shown to have
no adverse effect on the natural history of pancreatitis even when the
feeding is poorly tolerated, at which point it can be discontinued. The
Pancreatitis, Very Early Compared with Selective Delayed Start of
Enteral Feeding trial compared very early with on-­demand enteral
feeding in patients with predicted severe pancreatitis and found no
difference in infectious complications or death. Tube feeding, either
nasogastric or nasojejunal, should be reserved for patients that do not
respond to a trial of oral nutritional intake.
An absolute indication for an emergency endoscopic retrograde
cholangiopancreatography (ERCP) with endoscopic sphincterotomy
(ES) is acute cholangitis. Evidence indicates that mild GSP does
not warrant ERCP. The risks of the procedure itself coupled with
the likelihood of spontaneous passage of gallstones and/or sludge
diminishes enthusiasm for an aggressive approach using ERCP in
GSP. Whether ERCP with ES should be applied in cases of severe
512 Gallstone Pancreatitis
GSP remains controversial and will require further research before
it is recommended.  ence in mortality and major complications; however, the endoscopic
nn SYSTEMIC COMPLICATIONS OF GSP
In severe GSP, persistent multiple organ failure is a dreaded complica-
tion that warrants admission to an intensive care unit and treatment
by both critical care specialists and pancreatic surgeons. Persistent
organ failure in the first 2 weeks of admission is a function of a dys-
regulated systematic inflammatory response, an altered microbiome,
and thus immune dysregulation. Late-­onset sepsis associated with
highly resistant and virulent pathogens generally occurs after 2 weeks
when nonresolving organ dysfunction mandates dialysis, ventilator
support, vasopressors, total parenteral nutrition, and multiple anti-
biotics. The initial hyperinflammatory response can develop into
an immunosuppressive state, allowing highly resistant healthcare-­
associated pathogens opportunity to cause life-­threatening infected
pancreatic necrosis, pneumonia urinary tract infections, catheter-­
associated bloodstream infections, and spontaneous bacteremias.
Continuous vigilance is imperative for these infections and applica-
tion of multiple infection control measures such as daily chlorhexi-
dine baths, oral hygiene, and enteral nutrition are useful.
Necrotizing Gallstone Pancreatitis
Patients who develop necrotizing GSP should be managed in specialty
centers where an experienced interdisciplinary team of surgeons,
gastroenterologists, and interventional radiologists are available.
Secondary bacterial infections that invade the necrotic pancreas
can arise from multiple sources and can lead to infected pancreatic
necrosis (IPN), a dreaded and often fatal complication with mortal-
ity rates as high as 30% and reaching nearly 100% when endoscopic,
radiologic, or surgical services are not immediately available. The
diagnosis of IPN is made by the presence of gas in the peripancreatic
collections seen on CT scan, ultrasound, or endoscopic ultrasound
with or without fine-­needle aspiration confirming the presence of
bacteria. Clinical suspicion of IPN is based on new onset of organ
failure after 2 weeks of hospital admission combined with fever and
rising inflammatory markers in the absence of other infectious foci.
Confirmed infection by fine-­needle aspiration is not mandatory for
treatment but is useful to guide antibiotic treatment. Most antibiotic
treatment targets presumptive organisms because cultures often do
not represent all pathogens present in a given sample. It is preferable
to use antibiotics with a known penetration profile into the pancreatic
parenchyma and necrotic pancreatic collections.
Because the gallbladder per se is noninflamed in most cases of
GSP, treatment strategies are largely similar to those of nonobstruc-
tive SAP. The past several decades of experience have taught surgeons
that the longer surgery can be safely delayed, the more favorable the
outcome. Aggressive, early surgical intervention for SAP is no longer
recommended because of the attendant high mortality rates associ-
ated with this approach. The step-­up approach (first described in the
Pancreatitis, Necrosectomy versus Step up Approach [PANTER] trial
in 2010) is recommended and follows international guidelines that
have become the standard of care. Briefly, management of IPN con-
sists of percutaneous catheter drainage, followed by video-­assisted
retroperitoneal debridement (VARD) and failing that, necrosectomy.
The PANTER trial showed that the step-­up approach significantly
decreased mortality and major complications, including new-­onset
multiple organ failure, perforation of a visceral organ, bleeding, and
or the development of an enterocutaneous fistula. Aggregate compli-
cations were decreased from 69% for open necrosectomy to 40% for
patients in the step-­up group. A management algorithm based on step-
­up therapy is illustrated in Fig. 1. The more recent Transluminal Endo-
scopic Step-­up Approach Versus Minimally Invasive Surgical Step-­up
Approach in Patients With Infected Pancreatic Necrosis superiority
trial compared an endoscopic with a surgical step-­up approach, with
the former consisting of endoscopic ultrasound-­guided transluminal
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drainage followed by endoscopic necrosectomy. There was no differ-
step-­up was associated with a reduced incidence of pancreatic fistulas
and a reduction in length of hospital stay. Centers with immediate
access to interventional endoscopists experienced in this procedure
are encouraged to use this approach. The optimal timing of interven-
tion is still unclear; the ongoing Postponed or Immediate Drainage of
Infected Necrotizing Pancreatitis trial is comparing early with post-
poned drainage until the infected collections are completely walled
off, which is the current standard of care.
The first step in surgical step-­up management is CT-­guided per-
cutaneous catheter drainage, preferably through the left retroperi-
toneum to later facilitate abscess access for the VARD procedure, if
indicated. Furthermore, because the catheter remains in the retroper-
itoneal space, it avoids contamination of the abdominal cavity. If sep-
sis persists and drainage is deemed to be inadequate, drains should be
upsized to the largest size available. Repeat imaging and the clinical
course should dictate whether further drainage is indicated. In this
circumstance, a VARD procedure can be performed to facilitate more
complete source control. A 5-­cm incision is made in the left flank at
the drain site and the retroperitoneal space is accessed for debride-
ment of necrotic tissue under direct vision. Laparoscopic instruments
are introduced in the cavity for debridement, irrigation, and suction.
The catheter drain is removed, replaced by two surgical drains, and
lavaged as needed. This hybrid minimal invasive procedure reduced
major complications and mortality to 35% and 13%, respectively,
compared with 34% to 95% and 11% to 39% in open necrosectomy.
Although open and intraperitoneal laparoscopic necrosectomy
were once considered standard of care, today these approaches have
become outdated in favor of VARDS. However, if indicated during
an intra­abdominal emergency, an open or an intra-­abdominal lapa-
roscopic approach can be used. Several endoscopic techniques have
been described, and the major interventions for IPN are increasing
in popularity owing to their minimally invasive nature. The first
step is the endoscopic ultrasound-­guided placement of transgastric
or transduodenal stents to provide temporary decompression and
drainage. If further intervention is needed, the stents can be used as
guides to facilitate endoscopic necrosectomy. Recent innovations in
stents, such as the lumen-­apposing metal stent, make it possible to
safely drain collections even when the distance between the gastric
or duodenal wall and necrotic collection exceeds 1 cm. The estab-
lished tract can be used for endoscopic debridement of the necrotic
cavity. 
Prophylactic Interventions for Infectious
Complications
The mechanism by which pancreatic collections and parenchymal
necrosis become infected remains speculative, but it is hypothesized
to occur from intestinally derived bacterial and fungal pathogens.
Clinically, bacteremia does not occur in most cases and therefore
the route by which pathogens travel from the gut to the necroma
remains unknown. The “Trojan horse” hypothesis suggests that
pathogens enter neutrophils or macrophages, which then silently
home to pancreatic tissues. Tissue conditions of the pancreas with
pancreatitis or necrosis are receptive to these bacteria-­carrying
immune cells, which can lodge and release their infectious pay-
load into pancreatic tissue, causing infection. Such processes may
explain why many patients develop infected necrosis late after the
acute inflammatory process has abated and when blood cultures
are negative. Further work will be needed to establish causality of
such a mechanism. The gut is considered the origin of pathogens
that cause IPN. However, attempts to preemptively eliminate poten-
tially translocating pathogens have been tested with controversial
results. In general, neither selective digestive decontamination nor
aggressive intravenous antibiotics are recommended to achieve this
because of the inability to completely defaunate the gut and for fear
of emergence of antibiotic resistance. Thus, the role of prophylactic
 PA N C R E A S 513

Mild AP SAP

Supportive care Aggressive resuscitation

Early enteral feeds Intensive monitoringb
Same admission CCYa

Interstitial
Necrotizing
edematous

APFC ANC

Supportive Supportive
WON Symptomatic
carec care

Percutaneous or
No further Symptomatic Clinically Clinically
endoscopic
complications pseudocyst deteriorating improving
drainage

Concern for ACS, Concern for CCY after clinical

necrotic bowel local infection stabilization, 4-6
weeks after
onset
Internal or external drainage: Antibiotics,
CCY
Percutaneous drainage, Exploratory Percutaneous
4-6 weeks
endoscopic or surgical laparotomy drainage via Open
after onset
cystogastrostomy retroperitoneumd necrosectomy

Improving Deteriorating Deteriorating

Upsize drain

Deteriorating

VARD via drain tract

Endoscopic necrosectomy

FIG. 1  Management algorithm for acute pancreatitis based on the step-­up approach. Video-­assisted retroperitoneal debridement drawbacks are that these
approaches can lead to intraperitoneal dissemination of the infection, bleeding, fistulas, and a more aggressive postoperative inflammatory response. If concern
for hemorrhagic pancreatitis with ongoing bleeding, endovascular embolization is the preferred first-­line intervention, followed by surgical hemostasis. aEarly
cholecystectomy (within 48 hours of onset for mild AP) is currently under investigation. bEarly ERCP in predicted severe AP is currently under investigation.
cEarly drainage of sterile peripancreatic collections is currently under investigation. dFecal microbiota transplantation to prevent secondary infection in severe

AP is currently under investigation. ACS, abdominal compartment syndrome; ANC, acute necrotic collection; AP, acute pancreatitis; APFC, acute peripancreatic
fluid collection; CCY, cholecystectomy; SAP, severe acute pancreatitis; VARD, video-­assisted retroperitoneal debridement; WON, walled-­off necrosis.

antibiotics in SAP or GSP in the absence of cholangitis remains
debated. Once infected SAP is confirmed or suspected, antibiotics
are indicated.
Probiotics have been tested in severe AP as a strategy to contain
potential pathogens that drive systemic inflammation, translocate,
and cause IPN. The use of probiotics has been shown to have a benefi-
cial effect on the outcome of pancreatitis in animal models and small
human studies. However, a randomized controlled trial designed to
evaluate the efficacy of Prophylactic Probiotics in Patients With Pre-
dicted Severe Acute Pancreatitis demonstrated an increase in mortal-
ity in the treatment group presumed to be due to bowel ischemia.
Prophylactic treatment with probiotics is therefore contraindicated
in the treatment of pancreatitis. Possible explanations for these par-
adoxical results may involve the choice of bacteria in the probiotic
mixture, the route of administration (oral feeding) or an inappropri-
ate metabolic microenvironment. Fecal microbiota transplantation is
an emerging research field and could potentially be applied to prevent
infections in SAP. 
nn FOLLOW-­UP
Among the most contentious aspects of the treatment of GSP
beyond halting the progression of the pancreatitis is the timing
of the cholecystectomy. If the presentation of GSP is mild and the

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514 Gallstone Pancreatitis

TABLE 3  Current Trials

Population Intervention Outcomes Country
Mild AP Rectal indomethacin Systemic inflammatory markers, organ failure, US
disease progression
Mild AP Cholecystectomy within 72 hours of onset Hospital stay, perioperative complications Chile
AII AP Contrast-­enhanced CT with additional Microvascular permeability markers as France
­image processing ­predictors of severe disease
SAP Early percutaneous drainage of sterile acute Mortality, secondary infection, hemorrhage, China
peripancreatic collections fistula formation
SAP Goal-­directed fluid resuscitation based on Organ failure, change in APACHE II score Germany
PICCO parameters JCU days
SAP Fecal microbiota transplant via retention Mortality, infectious complications, China (3 separate
enema ­inflammatory markers trials)
SAP Oral ketorolac Inflammatory markers, organ failure, local Iran
­complications
AP with SIRS Experimental compound CM4620 Drug safety, radiographic disease severity USA
Necrotizing AP Pancreatic duct stenting 1–2 weeks after the Incidence of walled-­off necrosis, rates of USA
onset of symptoms ­intervention, procedural complications
Necrotizing AP Early drainage of necrotic collections Mortality, major complications, length of stay The Netherlands
before walling off
Predicted SAP Early ERCP Mortality, major complications, length of stay The Netherlands
­without
­cholangitis
Idiopathic Diagnostic endoscopic ultrasound Incidence of previously undetected gallstone The Netherlands
­pancreatitis disease

AP, acute pancreatitis; AII, Acute Physiology, Age, Chronic Health Evaluation II (APACHE II); CT, computed tomography; ERCP, endoscopic retrograde
cholangiopancreatography; ICU, intensive care unit; PICCO, pulse contour cardiac output; SAP, severe acute pancreatitis; SIRS, systemic inflammatory response
syndrome.

pancreatitis resolves over a few days, cholecystectomy with intra-
operative cholangiogram is recommended. If choledocholithiasis
is found during cholecystectomy, postoperative ERCP with ES is
a safe and effective treatment. Although intraoperative common
bile duct exploration, lithotripsy, and stone removal are possible, in
most institutions, postoperative ERCP is performed. In many cases
of moderate to severe pancreatitis, cholecystectomy is deferred.
Imaging with magnetic resonance cholangiopancreatography as
an outpatient to rule out the need for ERCP once the pancreatitis
and its sequelae have resolved can be useful. If the pancreatitis has
been severe, however, cholecystectomy too soon after the acute epi-
sode is risky and complicated because of ongoing inflammation and
scarring. Clinical judgment as to the timing of the cholecystectomy
must be judiciously applied. Given the clear advantages of laparo-
scopic cholecystectomy over open cholecystectomy, the risk of an
open procedure if surgery is planned too soon following recovery
should be noted.
The Pancreatitis of Biliary Origin, Optimal Timing of Chole-
cystectomy trial compared same-­admission versus interval chole-
cystectomy (after 25–30 days) in mild AP and showed a significant
reduction in recurrence in favor of same-­admission cholecystec-
tomy. For reasons mentioned previously, it is advisable to post-
pone cholecystectomy in cases of necrotizing pancreatitis until
the time at which all collections are either successfully drained or
sufficiently walled off and the patient is fully stable and eating. In
cases in which gallstones are suspected but not observed, perform-
ing an ERCP or magnetic resonance cholangiopancreatography as
a method to identify microlithiasis and/or biliary sludge may be
useful. If positive, cholecystectomy should be performed to prevent
recurrence. Patients with recurrent idiopathic pancreatitis should
be referred for genetic counseling and evaluation for autoimmune
pancreatitis. Finally, pancreatic insufficiency of either endocrine or
exocrine function can occur after a bout of GSP. Timely recogni-
tion and treatment of these complications are needed to prevent
complications from diabetes and malnutrition in those patients that
develop chronic disease. 
nn CURRENT TRIALS
At least 12 trials are actively enrolling patients in interventional or
prognostic studies of GSP (Table 3).
Suggested Readings
Besselink Marc GH, et al. Minimally invasive “step-­up approach” versus maxi-
mal necrosectomy in patients with acute necrotising pancreatitis (PANT-
ER trial): design and rationale of a randomised controlled multicenter trial
[ISRCTN13975868]. BMC Surg. 2006;6(1):6.
Dellinger E Patchen, et al. Early antibiotic treatment for severe acute necrotiz-
ing pancreatitis: a randomized, double-­blind, placebo-­controlled study.
Ann Surg. 2007;245(5):674.
Da Costa, David W, et al. Same-­admission versus interval cholecystectomy for
mild gallstone pancreatitis (PONCHO): a multicentre randomised con-
trolled trial. The Lancet. 2015;386:1261–1268.
Tenner S, Baillie J, DeWitt J, Vege SS. American College of Gastroenterol-
ogy guideline: management of acute pancreatitis. Am J Gastroenterol.
2013;108(9):1400.

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