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Acute Pancreatitis
Joshua G. Barton · Michael G. Sarr · Moshe Schein
“Acute pancreatitis is the most terrible of all the calamities that occur in connec-
tion with the abdominal viscera.” (Berkeley Moynihan, 1865–1936)
God put the pancreas in the back because He did not want surgeons messing with it.
Editorial Introduction
In this edition, we decided to invite Drs. Sarr and Barton from the Mayo Clinic
to write this chapter on the surgical management of acute pancreatitis. As the treatment of this condition has become less aggressive, increasingly non- invasive, and
tailored to the individual patient, it requires a dedicated multispecialty team, which
includes surgeons, radiologists, endoscopists, and intensivists. If possible, patients
suffering from complications of severe pancreatitis should not be treated in community or rural hospitals but transferred to centers that can offer the best care—
based on the multiple modalities of treatment mentioned by Drs. Sarr and Barton.
But, in the real world where many of you readers practice, not all such
patients can be transferred to the Mayo Clinic or your local university hospital.
It is important, therefore, that general surgeons, wherever they practice, develop
understanding of this complex and multifaceted disease. The following text is
aimed to provide an introduction to emphasize basic concepts before turning to
Drs. Sarr and Barton’s contribution to the chapter.
19
The Basics
Moshe Schein
Natural History
Uncomplicated acute pancreatitis (AP) is “a 1-week disease.” Failure to re-
cover or the persistence of local and systemic signs of pancreatic inflammation
beyond the seventh day are signs that a complication may be brewing. You will
best understand this complicated disease, and develop a rational clinical approach
to its treatment, when you consider its evolution week by week (> Fig. 19.1).
Michael G. Sarr
Department of Surgery, Mayo Clinic, Rochester, MN 55902, USA
M. Schein et al. (eds.), Schein’s Common Sense Emergency Abdominal Surger y,
DOI: 10.1007/978-3-540-74821-2_19, © Springer-Verlag Berlin Heidelberg 2010
167
168 Joshua G. Barton · Michael G. Sarr · Moshe Schein
Week 1Week 2 Week 3 Week 4
Inflammation
phlegmon
Necrosis
Always nonoperative
management
Usually nonoperative
management
Operative
management
Infected necrosis
Reolution
Abscess
infected pseudocyst
Fig. 19.1. Natural history of complicated acute pancreatitis (AP) and its
management
First Week: Inflammation
Inflammation in the first week is the phase of acute inflammation resulting in
an inflammatory mass, which consists of the pancreas and adjacent structures—the
so-called pancreatic phlegmon. Proinflammatory mediators (e.g., cytokines) are
present in the beerlike (we refer here to real European dark beer, not the insipid pilsner consumed in the United States) hemorrhagic exudate of severe AP and are responsible for producing the characteristic local and systemic clinical inflammation
(SIRS, systemic inflammatory response syndrome). The systemic repercussions of
AP (e.g., respiratory or renal failure) depend on the intensity of the process and the
quantity of mediators entering the retroperitoneum, the peritoneal cavity, and the
circulation. In most patients, the inflammation is mild and will resolve in a few days.
Patients with a severe inflammatory process tend to progress into the second week.
Second Week: Necrosis
The phase of necrosis starts toward the end of the first week. The necrotizing process may involve the pancreas and its surroundings; retroperitoneal
spread is hastened by activated proteolytic pancreatic enzymes. The severity of
disease and therefore the prognosis depend on the quantity and extent of necrotic tissue (sometimes involving the entire retroperitoneum) and whether secondary infection supervenes. Pooling of the exudate in the lesser sac and beyond
forms the so-called acute peripancreatic fluid collections, which may resolve
spontaneously or gradually develop an inflammatory wall to become a pancreatic
pseudocyst. The necrotic process may resolve spontaneously over a period of
weeks. It may, however, become secondarily infected, a process that may occur
as early as the second week but usually later.
19 Acute Pancreatitis 169
Third Week: Infection
The third week is the phase of infection. The diagnostic modalities described in this chapter may point to infection of the necrotic tissue by the middle
of the second week, but its peak incidence is the third week. The causative organisms probably originate from the nearby colon by translocation, but superinfection with Candida species is not uncommon. The resulting infection of necrotic
tissue produces infected pancreatic or peripancreatic necrosis, whereas secondary infection of a pseudocyst results in an infected pseudocyst (a late, rarer, and
more benign process). The combined effects of necrosis and infection give rise to
the clinical manifestations of local and systemic inflammatory syndromes.
Sterile and infected pancreatic necrosis (IPN) are clinically indistinguishable.
IPN may occasionally produce a relatively mild systemic illness, while widespread
sterile necrosis may cause the patient’s demise, the outcome probably depending
on the intensity of the inflammatory response in the individual patient.
Fourth Week and Beyond
Patients with noninfected pancreatic or peripancreatic necrosis whose
hitherto relatively benign clinical course did not mandate an operation (and only
very rarely should an operation be performed at such an early phase) enter this
“late” phase. We do not know what quantity of necrotic pancreatic parenchyma
is capable of spontaneous resolution. We know, however, that large necrotic
zones may be reabsorbed and thus resolve or, alternatively, undergo secondary
infection, to present weeks later as a pancreatic abscess. This is an infective local-
ized process developing after the resolution of the acute pancreatic inflammatory process. Therefore, its presentation, management, and prognosis differ
drastically from those of IPN. Pseudocysts may also develop at this stage.
Estimation of the Severity of Illness
Severe AP will eventually declare itself either by failing to resolve or by its
dramatic systemic effects. It is important for you to recognize early that the attack is severe to optimize patient care, prevent infective complications, and estimate the prognosis.
Early attempts to estimate severity of disease revolved around measurement of levels of specific pancreatic enzymes or acute phase reactants, but it became obvious that one or two biochemical tests would not suffice. Beerlike,
murky peritoneal fluid is diagnostic of necrotizing-hemorrhagic pancreatitis
(i.e., severe AP), but this observation requires peritoneal aspiration, which is an
invasive procedure and is unacceptable as a routine in the early phase of AP.
170 Joshua G. Barton · Michael G. Sarr · Moshe Schein
A number of scoring systems have been developed to estimate the severity
of AP. Most are based on the estimation of clinical and laboratory variables that
reflect the intensity of the inflammatory process. Imrie’s (Clement Imrie, contemporary, Glasgow) method is popular in the United Kingdom, whereas elsewhere most medical students and enthusiastic medical residents can recite the
lengthy list of early and late Ranson’s criteria (John C. Ranson, 1938–1995). The
APACHE II (Acute Physiological and Chronic Health Evaluation II) scoring system is useful in measuring the severity of any acute disease and has been shown
to prognosticate the outcome of AP better than any other system. We advise you
to use this uniform and user-friendly scoring system (> Chap. 6). A patient with
an APACHE II score of more than 8 has severe AP.
Contrast-enhanced dynamic computed tomography (CT) has been reported to be useful in diagnosing AP and grading its severity. The clinical diagnosis of AP is, however, straightforward, and scoring can assess the severity of
disease better. Not uncommonly, we see patients with CT images of “horrendous
pancreatitis” who feel well and go home after a few days without any complications. Moreover, contrast-enhanced CT examination has been implicated in the
aggravation of microvascular damage in the pancreatic parenchyma. In addition, CT findings during the first week of AP will very rarely influence management decisions. We suggest that you avoid (as much as possible) CT scanning the
AP patient in the early phase of the disease and reserve this examination for
patients in whom the diagnosis of AP is uncertain. Please do not treat severe AP
with daily CT scans. Ultrasound should, however, be performed early to confirm
or exclude cholelithiasis as a possible cause of AP.
Diagnostic and Therapeutic Approach
Inflammation: The First Week
Generally, the approach to early severe AP is conservative and the treatment
supportive. Historically, many different approaches have been tried in attempts to
limit the effects of this disease. For example, since proinflammatory mediators
cause the clinical manifestations, there were attempts to prevent or diminish such
responses with early pancreatectomy o r peritoneal lavage, respectively. Pancreatic
resection in early severe AP is associated with a horrendous mortality rate and
anyway does not prevent the development of intra-abdominal infection. Although
continuous peritoneal lavage, if started within a day or two, may improve systemic manifestations, it is clear that it does not prevent the late major complications (and mortality) we are talking about. “Hemofiltration” of the blood of the
noxious mediators liberated by AP has been tried but remains experimental.
It appears, therefore, that you should offer these patients nothing more
(and nothing less) than supportive care, preferably in the surgical intensive care
19 Acute Pancreatitis 17 1
unit. You should remember that severe AP represents a major abdominal “chem-
ical burn,” with many liters of fluid sequestrated in the retroperitoneum and
peritoneal cavity. Optimal fluid balance and replacement are mandatory to protect the kidneys and provide an adequate venous return to the heart, which may
be adversely affected by the pancreatitis-related myocardial-depressing factor.
Overhydration, on the other hand, should be prevented especially in the presence
of an associated ARDS (acute respiratory distress syndrome).
Note that the swollen pancreas, together with the edematous SIRS-affected
viscera, may easily produce intra-abdominal hypertension. You will not know
about it unless you measure the intra-abdominal pressure. When abdominal com-
partment syndrome complicates severe AP, the abdomen should be decompressed
(> Chap. 40). To us, this is the only indication for early laparotomy in AP.
We have always been told that “resting the pancreas,” by gastric decompression and an NPO (nil per os, nothing by mouth) regimen is beneficial. This
remains unproven. Gastric decompression with a nasogastric tube should be
employed only in the presence of gastric ileus or outlet obstruction due to the
swollen pancreas. Classically, the parenteral route was used for nutritional support, but recent evidence suggests that enteral nutrition via a transduodenal tube
is well tolerated and results in fewer local and systemic complications and better
outcome (> Chap. 46). Early enteral feeding may indeed be beneficial.
What about antibiotics? Some evidence suggests that intravenous antibiotics are to be started in any AP patient assessed as “severe.” This serves to prevent
superinfection of the necrotic tissue, thus reducing the incidence of IPN.
Imipenem, a wide-spectrum agent that achieves high levels within the pancreatic
parenchyma appears to be the drug of choice. Some authorities recommend the
addition of an antifungal agent (e.g., fluconazole) to prevent fungal superinfection of the necrotic pancreas. Others would administer antibiotics in all cases of
biliary pancreatitis; this, of course, would be the logical thing to do when there
are associated features of ascending cholangitis.
As mentioned, there is no indication at this stage to obtain a CT scan unless
you are insecure about your diagnosis. Laparotomy is almost contraindicated during early AP and should be allowed only when a life-threatening surgical catastrophe cannot be otherwise excluded or to decompress an abdominal compartment
syndrome. Indeed, exploratory laparotomy in AP is not innocuous; it adversely af-
fects the natural history of the disease by increasing the incidence of infective
complications. For this reason, no laparotomy for unexplained peritonitis should
be undertaken unless the diagnosis of AP has been excluded.
Endoscopic sphincterotomy is the only invasive therapeutic modality that
should be considered early, during the first week, in the course of severe biliary
172 Joshua G. Barton · Michael G. Sarr · Moshe Schein
AP, especially if features of ascending cholangitis are present and the presence
of common bile duct (CBD) stones is suspected (see > Chap. 20.3).
Your dedicated supportive care will result in the survival of most of these
patients until their disease process enters the second week.
Second Week and Beyond
The second week and beyond is the time of necrosis, infection, and other
complications. We are grateful to Drs. Sarr and Barton for the following section
that details the modern expert approach to the complex problems of AP.
Surgical Management of Acute Pancreatitis: State of the Art
Joshua G. Barton and Michael G. Sarr
It is fascinating to conjecture how an inflammatory process in a retroperitoneal
gland can produce abnormalities in so many organs. (Reginald Fritz, 1843–1913)
Although surgeons are often involved in the care of patients with AP, surgery is only rarely required unless the etiology is related to gallstones. When
operative intervention is required, the patients are usually extremely ill, and surgical intervention carries a substantial mortality (10–20%). Therefore, it is essential that practicing surgeons have a clear understanding of AP and the
decision-making processes used in determining appropriate treatment.
Classification
The Atlanta classification of AP was developed in 1992 to clarify and unify
the nomenclature used in describing AP. Unfortunately, it has not been adopted
consistently or universally. The Working Group Classification, devised in 2006, describes AP in terms that are more in keeping with the pathophysiology of the
disease (> Table 19.1).
Clinical Course
Mild Acute Pancreatitis
Acute pancreatitis has a mild clinical course in the vast majority of patients.
In patients with mild pancreatitis, the disease process is self-limiting and usually
19 Acute Pancreatitis 17 3
Table 19.1. Working Group Classification, 2006
Acute pancreatitis
Interstitial edematous pancreatitis
Necrotizing pancreatitis (pancreatic necrosis and/or peripancreatic necrosis)
Sterile necrosis··
Infected necrosis··
Fluid collections during acute pancreatitis
<4 weeks after onset of pancreatitis
Acute peripancreatic fluid collection
Sterile··
Infected··
Postnecrotic pancreatic/peripancreatic fluid collection (PNPFC)
Sterile··
Infected··
>4 weeks after onset of pancreatitis
Pancreatic pseudocyst (usually has increased amylase/lipase activity)
Sterile··
Infected··
Walled-off pancreatic necrosis (WOPN) (PNPFC with defined wall)
Sterile··
Infected··
subsides in 3–5 days with a mortality of less than 1%. Surgery or critical care
management is rarely required in these patients. A surgeon’s participation in the
care of patients with mild AP is usually limited to performing a cholecystectomy
during the same admission for cholelithiasis if present; a laparoscopic approach
is usually possible (see > Chap. 20.3).
Severe Acute Pancreatitis
In contrast, AP should be classified as severe when the disease process is
associated with organ failure for three consecutive days. A clinically relevant
174 Joshua G. Barton · Michael G. Sarr · Moshe Schein
SIRS and multiple organ dysfunction (MOD) often complicate severe AP. Local
complications are frequent and may include sterile or infected pancreatic or peripancreatic necrosis, fluid collections, and pancreatic, enteric, or colonic fistulae.
Operative intervention, when required, is directed at one of these complications.
Severe Acute Pancreatitis Manifests Two Different Temporal Phases
The first phase is characterized by the presence of distant organ dysfunction primarily and not by morphologic changes within the pancreas per se.
Hence, this phase is described best by clinical parameters, the hallmark of which
is organ dysfunction:
Occurs within the first week of disease onset·
Serum amylase or lipase activity more than three times the upper limit of ·
normal
Characteristic findings of AP on CT, ultrasonography, or magnetic reso-·
nance imaging
Organ dysfunction for three consecutive days·
The second phase, which occurs 1–2 weeks after the onset of symptoms, is
described more appropriately by morphologic changes within the pancreas itself.
Typically, CT will reveal changes within the pancreatic parenchyma consistent
with necrosis, marked interstitial edema of the pancreas, or fluid collections
(fluid or solid content) outside the pancreas (> Fig. 19.2).
Pathology that may require operation:
Gallstone pancreatitis (see ·
Pancreatic necrosis (sterile and infected)·
Pancreatic pseudocyst·
Pancreatic fistula·
>
Chap. 20.3)
Fig. 19.2. Computed tomography of the abdomen revealing changes of nonenhancement consistent with necrosis and marked interstitial edema of the pancreas
19 Acute Pancreatitis 17 5
Fig. 19.3. Computed tomography of the abdomen showing areas of extraluminal
gas (arrows) in the setting of AP
Pancreatic Necrosis
The issue of primary importance to determine when pancreatic necrosis
develops is if the necrotic tissue is sterile or infected. On contrast-enhanced CT,
extraluminal gas should be considered pathognomonic of infection (> Fig. 19.3).
In the absence of extraluminal gas, a CT-guided fine-needle aspiration can be
used to search for infection of the area of necrosis or fluid collection when clinical suspicion exists. The aspirated material should then be analyzed by both
Gram stain and culture.
The culture results in particular should guide the use of antibiotic suppression therapy in an attempt to delay operative intervention for at least 4 weeks
after the onset of pancreatitis. By so delaying the need for early operative intervention, mortality and morbidity can be decreased.
Sterile Necrosis
Over the last two decades, there has been a shift in viewpoints on the need
for operative treatment of sterile pancreatic necrosis:
Operating early in the course of sterile pancreatic necrosis with the goal of ·
removing the devitalized tissue to improve the SIRS and thereby prevent
MODS is no longer recommended.
176 Joshua G. Barton · Michael G. Sarr · Moshe Schein
Fig. 19.4. Computed tomography of the abdomen revealing walled-off pancreatic
necrosis (arrow)
The aggressive use of prophylactic, broad-spectrum antibiotics appears to ·
decrease the rate of infected necrosis but does not alter overall mortality.
Advances in critical care have allowed conservative management of sterile ·
pancreatic necrosis even when organ dysfunction is present.
These developments represent an important advance in the treatment of
severe AP because surgery in the first 3 weeks is associated with a risk of substantial blood loss and poor outcomes.
Therefore, every attempt should be made to delay laparotomy until 4 weeks
from the onset of AP and even then only in patients with persistent symptoms
(or the persistently “unwell” patient). These symptoms may include anorexia, early
satiety, vomiting, or fever. Waiting more than 4 weeks allows sterile necrosis, and
any accompanying acute peripancreatic fluid collection (APFC) or postnecrotic pancreatic fluid collection (PNPFC), to either resolve or mature into walled-off pancreatic necrosis (WOPN) (> Fig. 19.4) or a pseudocyst (detailed in a separate section).
Debridement for Sterile Necrosis
Removal or debridement of sterile necrosis (better termed “necrosectomy”)
has been approached traditionally by an open laparotomy through a midline or
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