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In: Acute Pancreatitis ISBN: 978-1-63485-229-6
Editor: Shane Copeland © 2016 Nova Science Publishers, Inc.
Chapter 8
ANTIBIOTICS IN ACUTE PANCREATITIS
José Ramón Oliver Guillén, MD,
Ana Palomares Cano, MD, María Beltrán Martos, MD,
Mario Serradilla Martín MD,
and Alejandro Serrablo
*
, MD, PhD
Division of Hepato-Pancreatic-Biliary Surgery, Department of Surgery,
Miguel Servet University Hospital, Zaragoza, Spain
ABSTRACT
Acute pancreatitis is a local inflammatory response with systemic
effects and an adverse evolution in 20% of cases. Its mortality rate is 5–
10% in sterile and 15–40% in infected pancreatic necrosis. Infection is
widely accepted as the main reason of death in acute pancreatitis. The
evidence to enable a recommendation about antibiotic prophylaxis against
infection of pancreatic necrosis is conflicting and difficult to interpret. Up
to date, there is no evidence that supports the routine use of antibiotic
prophylaxis in patients with severe AP. Treatment on demand seems to be
the better option, avoiding excessive treatment and selection of bacterial.
In infected acute pancreatitis, antibiotics of choice are imipenem,
*
Corresponding author: Alejandro Serrablo, MD, PhD; Head of Division of Hepato-Pancreatic-
Biliary Surgery; Department of Surgery; Miguel Servet University Hospital; Paseo Isabel
La Católica 1-3, 50009 Zaragoza, Spain. E-mail: almaley@telefonica.net. Phone: +34
629675491.
José R. O. Guillén, Ana P. Cano, María B.Martos et al.
176
meronem or tigecycline in patients allergic to beta-lactams. Also
fluconazole must be given in determinate clinical situations.
Keywords: acute pancreatitis, antibitic treatment, antibiotic prophylaxis
1. DEFINITION OF ACUTE PANCREATITIS
Acute pancreatitis (AP) is a local inflammatory response with systemic
effects and an adverse evolution in 20% of cases [1].
The diagnosis requires two of the following three features:
a. abdominal pain consistent with AP (acute onset of a persistent, severe,
epigastric pain often radiating to the back);
b. serum lipase activity (or amylase activity) at least three times greater
than the upper limit of normal;
c. characteristic findings of AP on contrast-enhanced computed
tomography (CT) and less commonly magnetic resonance imaging
(MRI) or abdominal ultrasonography (US) [2].
2. TYPES, PHASES AND SEVERITY OF
ACUTE PANCREATITIS
Types, phases and severity of AP were revised by International Consensus
in 2012 [2].
Types of AP
There are two types of AP. Interstitial edematous pancreatitis (85%) is the
most common and is usually resolved within the first week. Pancreas develops
a diffuse enlargement due to inflammatory edema. CT may show
homogeneous enhancement of pancreatic parenchyma with inflammatory
changes of peripancreatic fat.
The other one, necrotizing pancreatitis (NP) (5-10%) is characterised by
the presence of necrosis of pancreatic parenchyma, peripancreatic tissue or
both, and usually evolve over several days. Early CT may underestimate the
Antibiotics in Acute Pancreatitis
177
extent of necrosis [2], although NP is strongly suspected if a poorly contrasted
area is observed by dynamic CT more than 2 weeks after onset [3].
Gadolinium-diethylenetriamine penta-acetic acid (GI-DTPA) dynamic MRI
can depict the foci of NP as a poorly contrasted area [4, 5].
NP may complicate with collections of necrosis. Two new terms are
defined:
a. Acute necrotic collection (ANC): an heterogeneous collection
containing variable amounts of both fluid and necrosis, involving
parenchyma and/or the peripancreatic tissues. Occurs only in the
setting of acute NP. There’s no definable wall encapsulating the
collection [2]. ANC can be differentiated from acute peripancreatic
fluid collection (APFC) using contrast-enhanced CT, eventhough in
many cases of early-onset pancreatitis (less than 1 week) it can be
difficult [3, 6]. APFC is an homogeneous collection with fluid density
without a definable encapsulating wall that is located adjacent to
pancreas (not intrapancreatic). APFC are only seen within the first 4
weeks after onset of interstitial oedematous pancreatitis [2, 6].
b. Walled-off necrosis (WON): mature, encapsulated and heterogeneous
collection of pancreatic and/or peripancreatic necrosis that has
developed a well defined inflammatory wall. It usually occurs > 4
weeks after onset of NP [2, 6]. WON can be differentiated from
pancreatic pseudocyst (PPC) using CT contrast level and MRI. PPC
are homogeneous, well circumscribed and liquid collections seen > 4
weeks after onset of interstitial oedematous pancreatitis [3, 5, 6].
The content of collections might be difficult to be differentiated using CT;
MRI may enable the diagnosis. Fatty necrosis presents higher signals in T1-
enhanced imaging and mildly lower signals in T2-enhanced imaging compared
with fluid [4, 5].
4 weeks after onset of pancreatitis
Necrosis (-)
APFC (sterile)
PPC (sterile)
APFC (infected)
PPC (infected)
Necrosis (+)
ANC (sterile)
WON (sterile)
ANC (infected)
WON (infected)
APFC: acute peripancreatic fluid collection.
ANC: acute necrotic collection.
PPC: pancreatic pseudocyst.
WON: walled-off necrosis.
José R. O. Guillén, Ana P. Cano, María B.Martos et al.
178
Pancreatic and peripancreatic necrosis, ANC and WON can remain sterile
or become infected. Infected necrosis is rare during the first week [2].
Phases of AP
Two different phases have been identified according to two peaks of
mortality:
a. Early (within 1 week), characterized by the systemic inflammatory
response syndrome (SIRS) and/ or organ failure.
b. Late (> 1 week), characterized by persistence of systemic signs of
inflammation or by local complications. The SIRS appeared in the
early phase may be followed by a compensatory anti-inflammatory
response syndrome (CARS) that may contribute to an increased risk
of infection.
The presence and duration of organ failure is the main determinant of
severity in both phases.
Severity of AP
Several scoring systems have been proposed and are used at clinical sites
for severity assessments of AP: Ranson (1974) [7], APACHE-II (1989) [8],
Panc 3 score (2007) [9], POP (Pancreatitis Outcome Prediction, 2007) [10],
BiSAP (Bed-side for Severity in Acute Pancreatitis, 2008) [11], JSS (Japanese
Severity Score, 2008) [12], HAPS (Harmless Acute Pancreatitis Score, 2009)
[13] and revised Atlanta classification and definitions (2012) [2], among
others.
It is recommended to make a severity assessment immediately after
diagnosis and repeated over time; re-evaluations should be made 24 hours, 48
hours and 7 days after admission to the hospital [2, 3].
Following the latest revised Atlanta definitions [2], three new severity
grades were shaped: mild, moderately severe and severe AP.
a. In mild AP there’s neither organ failure or local or systemic
complications. Pancreatic imaging is not usually required, and
Antibiotics in Acute Pancreatitis
179
mortality is very rare. Antibiotic prophylaxis is not recommended, as
seen later.
b. In moderately severe AP there is transient organ failure (resolves
within 48 hours) or local or systemic complications in the absence of
persistent organ failure. Prolonged specialist care may be required.
Mortality is far less than that of severe AP.
c. Finally, severe AP is characterised by persistent organ failure. It may
be single or multiple. One or more local complications are usually
presented. Severe AP in the first few days associates a high risk of
death (36-50%) [14]; infection of necrosis associates an extremely
high mortality.
3. INCIDENCE
A large increase in the incidence of AP and a smaller increase in the
incidence of chronic pancreatitis have been reported in population studies.
Nowadays, the annual incidence of AP ranges from 13 to 45/100,000
population [15], with an overall prevalence rate of 49.4 per 100,000 population
[16].
It’s one of the most frequent causes of acute gastrointestinal, liver, and
pancreatic diseases requiring hospitalization, rising the third leading position
in US in 2012 (275,170 admissions).
It was also the 12
th
most common cause of the emergency department visit
(330,561 visits) and the 15
th
cause of death (2,844 patients as underlying cause
of death) from gastrointestinal, liver, and pancreatic diseases. In other words,
that means a crude mortality rate of 0.9%, [17], even though it can raise up to
50% in infected pancreatic necrosis as said before [14].
4. ETIOLOGY
The identification of the etiology is important for the management during
the early phase of the disease. Although there is no specific therapy for acute
pancreatitis, the causing factor must be investigated and eliminated if
identified [18].
José R. O. Guillén, Ana P. Cano, María B.Martos et al.
180
Acquired Conditions
a. Gallstone disease. Gallstone-induced pancreatitis is caused by duct
obstruction. This is produced as a consequence of an impacted stone
that obstructs the main pancreatic duct at the level of papilla of Vater,
or because of transient papillary edema or papillary orifice relaxation
following the passage of stones, that can obstruct the pancreatic juice
flow or favor duodenopancreatic reflux. Transient ampullary
obstruction may allow bile to reflux into the pancreas, even if the
pressure in the main pancreatic duct in normal conditions is generally
higher than in the common bile duct. Bile reflux into the pancreatic
ductal system is facilitated if there is a common channel at bilio-
pancreatic junction. The common channel theory has been confirmed
in 1993 by Hernández and Lerch [19]. These studies documented the
presence of amylase in the bile collected by a T-tube inserted into the
common bile duct, suggesting there might be a functional channel
between the two ductal systems. The gallstone disease may also be
manifested only by: 1) microlithiasis (stones less that 2 mm of
diameter), that can be seen or suspected mainly at endoscopic
ultrasound or endoscopic retrograde cholangio-pancreatography
(ERCP); 2) gallbladder sludge, which can only be visualized by
endoscopic ultrasound; and 3) calcium carbonate, cholesterol
monohydrate and calcium bilirubinate crystals [20].
b. Alcohol-induced AP. Alcohol abuse is the second most frequent cause
of AP [21]. Typically occurs in people who have consumed large
amounts of alcohol for at least 5-10 years. In most countries, the
proportions of alcohol-attributable mortality from pancreatitis fall
within the range between 40 and 80% [22]. Alcohol intake causes a
transient stimulation of exocrine pancreatic secretion by increasing
the synthesis and secretion of digestive and lysosomal enzymes in
pancreatic acinar cells. Ethanol has been proven not to cause AP itself
but sensitizes the pancreas to disease. It appears that the pancreas has
developed protective mechanisms that can partially compensate for
ethanol-induced cellular damage. Further defining the mechanisms of
ethanol-induced pancreatic injury may help define these protective
mechanisms. It is hoped that this strategy will lead to the development
of therapeutic targets that will prevent or reduce the severity of
alcoholic pancreatitis [23].