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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1649_Библиотеки_им_академика_М_И_Перельмана.pdf
Acute Pancreatitis in Childhood
31
Education: MBBS, Dip Paed, FRACP, PhD
Address: Sydney Children’s Hospital Randwick, High Street, Randwick
NSW 2031, Australia
Research and Professional Experience: Dr Ooi is a Clinical Academic at
the School of Women’s and Children’s Health, Medicine at University of New
South Wales, Australia and a Paediatric Gastroenterologist at Sydney
Children’s Hospitals Network. Dr Ooi’s area of interest and expertise is in
pancreatic diseases in childhood, and in the spectrum of diseases related to
defects in the CFTR gene, in particular genotype and phenotype correlations in
CFTR-related pancreatitis..
Publications and Awards: https://research.unsw.edu.au/people/dr-keith-
ooi
Name: Gilles Duvoisin
Affiliation: Department of Gastroenterology, Sydney Children’s Hospital
Randwick, Sydney, Australia
Department of Paediatrics (Département Médico-Chirurgical de Pédiatrie),
Lausanne University Hospital (CHUV), Lausanne, Switzerland
Date of Birth: October 10
th
Education: MBBS (equivalent), Dip Paed (equivalent), MD, Master of
advance studies in Health Organisation.
Address: Sydney Children’s Hospital, High Street, Randwick NSW 2031
Australia
Research and Professional Experience: Dr Duvoisin is the Fellow of
Gastroenterology at the Sydney Children’s Hospital, Sydney, Australia. Dr
Duvoisin areas of interest are general gastroenterology and paediatric
pancreatitis. Dr Duvoisin is conducting several international multicentric
studies in the field of Paediatric Gastroenterology. Dr Duvoisin obtained his
MD in studying the field of risks of early-onset neonatal sepsis and the use of
IV antibiotics.
In: Acute Pancreatitis ISBN: 978-1-63485-229-6
Editor: Shane Copeland © 2016 Nova Science Publishers, Inc.
Chapter 2
WALLED-OFF PANCREATIC NECROSIS
V. Arteaga Peralta
1
, MD, PhD,
A. A. Medina Velasco
1
, MD,
R. de la Plaza Llamas
1
, MD,
J. M. Ramia Angel
1,*
, MD, PhD, FACS, FRCS
and J. D. Gonzales Aguilar
1
, MD
1
Hepato-Pancreato-Biliary Surgical Unit, Department of Surgery,
Hospital Universitario de Guadalajara, Guadalajara, Spain
ABSTRACT
The term “walled-off pancreatic necrosis” (WOPN) refers to the
presence of a variable amount of necrotic tissue encapsulated within a
wall of reactive tissue four weeks after acute pancreatitis. The diagnosis
is based on radiological evidence of a well-defined wall around an intra-
or extra-pancreatic collection in a patient with a history of pancreatitis or
pancreatic trauma, always including some necrotic tissue inside. Initial
management is medical observation. Therapeutic action in patients
WOPN is only recommended in the case of infection or in sterile WOPN
causing clinical symptoms. The best treatment of WOPN is not clearly
defined.
WOPN patients should be treated by a multidisciplinary team.
Several therapeutic options are available, including percutaneous
**
E-mail: jose_ramia@hotmail.com, Tlf: 0034-616292056.
V. Arteaga Peralta, A. A. Medina Velasco, R. de la Plaza Llamas et al.
34
drainage, endoscopic drainage, transluminal endoscopic necrosectomy or
retroperitoneal video-assisted surgery when necessary. Open surgery is
reserved for patients who do not meet the criteria for endoscopic or
percutaneous treatment, for complications of endoscopic or laparoscopic
treatment, or when such treatments have failed. In this chapter we review
the literature and present an update on the current state of WOPN.
WALLED-OFF PANCREATIC NECROSIS
The term “walled-off pancreatic necrosis” (WOPN) was first used in 2005
to define a mixed solid-liquid collection with an appearance similar to a
pancreatic pseudocyst, occurring four weeks after a severe acute pancreatitis
[1-3]. We conducted an exhaustive review of the literature on the
epidemiological, clinical, diagnostic and therapeutic aspects of WOPN. An
unlimited PubMed search (updated on December 15, 2015) was performed
using the following search strategy: (Walled off necrosis) OR (Walled off
pancreatic necrosis) OR (WOPN). One hundred and sixty-four results were
obtained, of which 26 were studied.
DEFINITION OF WOPN
The Atlanta Classification for Acute Pancreatitis (AP) [4] was created in
1992, in an attempt to standardize and classify AP according to its severity and
complications.
This classification did not include WOPN. With time, some authors found
that a subgroup of patients diagnosed with pancreatic pseudocyst had poor
clinical outcomes for reasons that were unclear, and began to postulate the
existence of a distinct entity. Today, we know that certain patients who were
diagnosed with pseudocysts in fact had WOPN and therefore received
inadequate treatment [5].
A review of the Atlanta Classification (6) was begun in 2007. It was
completed after an international consensus meeting and published in the
journal Gut in January 2013 [2, 7].
According to the revised classification, inflammatory accumulations of
pancreatic fluid include acute peripancreatic fluid collections, pseudocysts,
acute necrotic collections and WOPN [2, 7-9]. In this classification the WOPN
is defined as an encapsulated collection of pancreatic necrosis that may
Walled-Off Pancreatic Necrosis
35
contain liquids and solids (with or without loculation) and develops after four
weeks of the start of the AP, and can be located at either intra- or extra-
pancreatic levels [2].
PATHOLOGY
The evolution of AP and the reasons for the subsequent formation of
WOPN or pseudocyst remain unclear. The evolution and natural history of
WOPN have not been definitively established [10, 11]. Several hypotheses
have been put forward, proposing that the pathophysiology of WOPN depends
on its location and on the pathological background. All authors agree that it is
the result of a severe, intense inflammatory process [5, 9, 10, 12, 13].
According to location:
Extra-pancreatic onset: AP with necrosis of peripancreatic tissue may
progress to the liquefaction and subsequent organization and
evolution of a walled-off accumulation of fluid that may communicate
with the pancreatic duct [12].
Intra-pancreatic onset: A collection of walled-off fluid may result
from parenchymal necrosis, which can lead to complete ductal
disruption and leakage of pancreatic fluid [12].
According to pathological background:
In chronic pancreatitis: A walled-off pancreatic fluid accumulation
may be induced by an acute exacerbation of pancreatitis or by
progressive ductal obstruction. The resulting increase in intraductal
pressure can then induce ductal leakage, with the accumulation of a
collection of peripancreatic liquid [5, 12].
In trauma: blunt or penetrating pancreatic trauma (including
iatrogenic injury, such as pancreatic surgery) can directly alter the
pancreatic duct and lead to the formation of a walled-off fluid
collection [5-10].
V. Arteaga Peralta, A. A. Medina Velasco, R. de la Plaza Llamas et al.
36
EPIDEMIOLOGY
In the literature, no significant differences in the frequency of WOPN
formation have been reported between men and women [1, 14]. WOPN occurs
in 1-9% of cases of necrotizing AP [1, 15-17]. Acute biliary pancreatitis is the
most common cause of WOPN, representing 50-70% of cases. Other less
common causes are alcohol abuse and idiopathic AP [1, 15, 18-19]. It is
estimated that chronic pancreatitis may be the cause of WOPN in between 4%
and 16% of cases [1, 20, 21]. The most common sites are the body and tail of
the pancreas (80-92% of cases), and the spread to paracolic gutters is frequent
[1, 18, 19]. The mean size is between 11 and 17 cm [1, 18, 19].
CLINICAL FEATURES
After the first episode of AP around half of WOPN patients are
asymptomatic, while the other half report symptoms such as abdominal pain,
malaise, relapsing or recurrent pancreatitis, feeding intolerance or weight loss
[1, 20]. These symptoms are mainly due to the mass effect created by the
WOPN which produces abdominal pain, duodenal or biliary obstruction,
fistula formation in adjacent viscera, pancreatic ascites and pleural effusion
due to the disruption of the pancreatic duct, with fistula in the abdomen or
chest, vascular occlusion or erosion/digestion of a vessel inside or adjacent to
the WOPN which may cause pancreaticus hemosuccus [12]. The WOPN may
also develop a spontaneous infection.
DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS OF WOPN
WOPN consists of a variable amount of necrotic tissue encapsulated in a
reactive tissue wall four weeks after AP. Radiological images show a well-
defined wall around the intra- or extra-pancreatic collection in a patient with a
history of pancreatitis or pancreatic trauma [11, 12].
The correct categorization of WOPN is the vital first step in the
management of the condition. Differentiation from pseudocyst (on the grounds
of the solid content in collections) is clinically relevant because each condition
has its own prognosis and requires specific treatment strategies. Pseudocysts
Walled-Off Pancreatic Necrosis
37
usually have a better prognosis than WOPN and, if necessary, are easier to
drain via endoscopy [5, 7].
Currently, computed tomography (CT) is considered the gold standard in
the evaluation of AP images, not just because of its effectiveness but because
of its speed and wide availability [7]. Intravenous iodinated contrast should be
used to define the criteria and the therapeutic approach to WOPN, bearing in
mind that the morphological changes provide guidance for treatment [7, 12].
On CT, the WOPN appears as a heterogeneous collection (mixture of fat,
liquid and solid) generally without gas [1, 22, 23], with varying degrees of
loculation and a well-defined capsule (Figure 1) [11, 12]. The presence of gas
within a WOPN collection does not always indicate infection: it may be due to
a stomach or duodenum fistula, in which case the collection may be sterile.
When WOPN fistulizes to the colon there is always WOPN infection [1]. The
accuracy of CT for the differential diagnosis between WOPN and pseudocyst
is around 80% [1, 22].
Figure 1. CT: WOPN: mixed solid- liquid collection.
In some cases the use of magnetic resonance imaging (MRI) or ultrasound
(US) may be required to confirm the diagnosis, since the presence of necrotic
tissue may produce a variable attenuation on CT [24]. MRI is superior to CT
for characterizing collections of pancreatic/peripancreatic liquid, and is an
alternative to CT in situations in which the use of iodinated contrast is
contraindicated. It also offers the advantage of avoiding ionizing radiation [5,
7, 25]. However, MRI has drawbacks of its own in the clinical setting: it takes
V. Arteaga Peralta, A. A. Medina Velasco, R. de la Plaza Llamas et al.
38
more time, requires patient cooperation (e.g., immobility during prolonged
periods or apnea), and is more expensive [7].
Some authors suggest that MRI can determine the need for necrosectomy
or other interventions, because it allows the identification of solid waste inside
a necrotic collection [5].
This is particularly relevant because the CT with contrast cannot reliably
detect necrotic debris after an endoscopic or surgical procedure [5]. In
addition, MRI cholangiopancreatography is highly sensitive for detecting
cholelithiasis and for assisting in the selection of patients who may require
endoscopic cholangiopancreatography [7].
Assessment of ductal pancreatic disease in all patients with WOPN is
vital. If the transmural resolution of the collection is not accompanied by a
correct diagnosis and treatment of the underlying ductal pathology, the risk of
recurrence is high [11, 26]. Ductal disruption or stenosis must be ruled out.
Currently, the least invasive technique for assessing the integrity of the
pancreatic duct is secretin-enhanced pancreatic MRI [11].
Alternative diagnoses should be considered if the clinical history is not
compatible with WOPN (i.e., acute and chronic pancreatitis, trauma, surgery),
especially if radiological images presented intracystic septa and no signs of
inflammation [12]. Among the conditions that may resemble WOPN are
certain cystic neoplasms of the pancreas, cystic degeneration of a solid
pancreatic tumor and rare non-neoplastic pancreatic cysts (e.g., retention cysts)
[12]. When diagnosis is doubtful, it may be necessary to take a sample of fluid
from the cyst [27], by ultrasound CT or endoscopy punction, and measure
tumor markers (carcinoembryonal antigen –CEA- and carbohydrate antigen
19-9) and amylase. If there is communication with the pancreatic ductal
system, the amylase level in the cyst fluid will be raised. WOPN has high
amylase and low CEA, whereas intraductal papillary mucinous neoplasm and
mucinous cystadenoma present high CEA and low amylase [5, 11-25, 27, 28].
If infection is suspected, Gram stain and culture [12] are recommended.
MANAGEMENT OF WOPN
The latest Atlanta classification (mentioned above in the Definition of
WOPN section) provides a detailed definition of the condition, but indications
and guidelines for its management remain unclear. At present the literature is
scarce and of little value, probably because WOPN is a recently defined entity.
The discussions focus on the need to define the timing, duration and type of
Walled-Off Pancreatic Necrosis
39
treatment [1, 16, 21]. Several factors influence the choice of the initial
approach for the treatment of pancreatic collections, such as the duration of the
collection, anatomical factors, previous surgeries, and the state and the
integrity of the pancreatic duct [11]. Thus, the ideal approach in the treatment
of WOPN is unclear at present and in many cases a combination of different
techniques is recommended if the decision is taken to intervene [11].
In around 70% of patients with necrotizing pancreatitis, the necrosis
remains sterile. The vast majority of sterile pancreatic necrotic collections can
be treated conservatively, and most of the collections resolve spontaneously
[3, 29, 30]. However, there is no absolute time frame and intervention is based
upon the severity of clinical symptoms and degree of organization. Several
treatment options are available: percutaneous drainage, endoscopic drainage,
laparoscopic drainage, surgical necrosectomy and combinations of techniques
[1, 20, 21, 23]. WOPN was initially believed to be less amenable to
endoscopic or percutaneous treatment because of non-viable solid
components. More recently, there has been a paradigm shift in the
management of WOPN toward less invasive approaches [18]. The goal of
these techniques is to provide minimal access necrosectomy with success rates
equivalent to those of open necrosectomy [18].
Intervention in patients with sterile WOPN is only indicated if they
present clinical deterioration despite appropriate treatment, in the form of
obstructive symptoms (constant abdominal pain, persistent vomiting, intestinal
or biliary obstruction) due to the mass effect of the WOPN. In case of
persistent symptoms such as pain and failure to thrive, intervention is more
controversial and current guidelines suggest that it should be considered some
eight weeks after onset [3, 23, 29, 30]. In severe cases, WOPN may fistulize
into adjacent anatomical areas, compress or erode blood vessels, or cause
portal vein thrombosis [1, 11, 23] and in these situations intervention is
indicated. Splenic vein thrombosis is seen in 40% of cases [16].
Infected WOPN is almost always an indication for intervention [31].
Infection is suspected on the grounds of clinical criteria (sepsis), analytical
criteria (increased acute phase reactants and positive blood cultures) and
radiology results [1, 8, 29]. Fine needle aspiration to demonstrate infection is
rarely necessary; in addition, it delays the intervention and may give rise to
false negatives and secondary infection [29, 32, 33]. WOPN infection is
suspected if gas is detected on CT [8, 29], although fistulization must be ruled
out and so confirmation with positive cultures is necessary [1]. A third of
patients have infected WOPN, sometimes due to percutaneous drainage or
endoscopy treatment. There is no clear correlation between the symptoms and
V. Arteaga Peralta, A. A. Medina Velasco, R. de la Plaza Llamas et al.
40
WOPN infection. The most commonly isolated bacteria in WOPN are E. coli,
K. pneumoniae, E. faecalis and S. aureus [1, 14, 16].
Despite the enthusiasm surrounding new developments and minimally
invasive techniques, we must not forget that conservative treatment with
antibiotics can also produce satisfactory results in selected, clinically stable
patients [27]. Therefore, since there is little evidence of results and treatments
for WOPN, all the decisions regarding whether and when to operate should be
discussed by a multidisciplinary team. Local experience and the location of the
collection are probably the most important factors in determining the choice of
approach.
THERAPEUTIC OPTIONS IN WOPN
“Wait and See”
“Wait and see” is an option in WOPN patients with minimal or no
symptoms and without evidence of complications [12]. Peripancreatic fluid
collections occur frequently in acute and chronic pancreatitis; fortunately, over
50% will resolve spontaneously and so watchful waiting is a good initial
decision [3, 27, 29, 30].
Drainage
Drainage is currently one of most widely used treatments. There are
several options: percutaneous drainage, endoscopic drainage alone, endoscopic
ultrasound-guided (ED-US) drainage, laparoscopic drainage and combinations.
It is unclear which of these techniques should be offered to patients as initial
therapy; no randomized controlled trials have been performed to date [12].
All these treatments present disadvantages. Surgical drainage is the most
invasive approach, percutaneous drainage requires the maintenance of a
prolonged external drainage with possible formation of an external pancreatic
fistula, and endoscopic drainage often requires multiple procedures in order to
function adequately [34]. At present, there is no single fully effective
treatment.