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Chapter 2 / Acute Pancreatitis 21
often necessary to supplement caloric needs. Feeding gastrojejunostomy
or jejunostomy tube placement is appropriate if more than 30 days of
nutritional support are expected. Reinitiation of oral feeding is appro-
priate when abdominal pain improves, and many patients in the “hold-
ing pattern” of the second phase of SAP will derive nutrition from some
combination of oral, enteral, and parenteral nutrition. It is important to
remember that all SAP patients will remain catabolic until the inamma-
tory focus has resolved.
Indications for ERCP
Recent meta-analysis of seven prospective, randomized trials found that
routine ERCP does not aect outcome in AP. erefore, ERCP should be
reserved for those patients with biliary obstruction or cholangitis. Early
consultation with endoscopists is appropriate for patients with SAP.
Venous Thromboembolism
Venous thromboembolism incidence is remarkably common (>50%) in AP
patients, commonly aecting splanchnic vessels (splenic vein, superior
mesenteric vein, and portal vein) in addition to extremity veins. Venous
thrombosis may be associated with vascular catheterization. In general, we
do not routinely anticoagulate patients with splanchnic thrombosis (these
will usually not resolve until the underlying inammatory focus and mass
eect from adjacent collections have resolved). Peripheral deep vein throm-
bosis, however, should be treated with anticoagulation. In addition, screen-
ing for peripheral DVT seems warranted in all patients with SAP/NP.
Bleeding
Bleeding severe AP/NP may be due to disruption of retroperitoneal veins
(which is almost always self-limiting) or from visceral arterial pseudoan-
eurysm (PSA). In NP patients, PSA may present with sudden increase of
abdominal pain, GI hemorrhage, or blood in a surgical or percutaneously
placed drain. CT angiography is an excellent rst-line test with which to
diagnose (or exclude the presence of) PSA. Treatment of PSA is by transar-
terial embolization, which is successful in virtually all patients.
Ischemic Viscera—Colon and Gallbladder
Ischemia of the colon or gallbladder should be considered in any patient
with SAP who suddenly decompensates. Colon ischemia may occur in up
to 8% of SAP patients; the mechanism of colonic ischemia is likely related
to venous occlusion with subsequent tissue congestion. Unfortunately, the
only method to securely diagnose (or rule out) colon ischemia is by lapa-
rotomy. Ischemic cholecystitis may be treated initially with tube cholecys-
tostomy; however, these patients should be followed very closely with a low
threshold for operative exploration in those who do not demonstrate rapid
improvement after cholecystostomy tube placement.
Fine Needle Aspiration
Fine needle aspiration (FNA) may diagnose infected (peri)pancreatic
necrosis; however, no indication currently exists for routine FNA. Clinicians
should be aware of the signicant (12% to 25%) false-negative rate associ-
ated with FNA.
Intervention in Necrotizing Pancreatitis
Infected pancreatic necrosis is nearly always mandates intervention to
achieve source control. e management of sterile necrosis is more contro-
versial. Clearly, some patients with symptomatic sterile necrosis wi ll benet
Section I / Pancreas22
from debridement. In addition, a number of patients with presumed sterile
necrosis will harbor occult infection. Experience has shown that denitive
intervention should not be undertaken earlier than 4 weeks from the dis-
ease onset. is time frame allows (peri)pancreatic collections to mature
and wall o, making debridement safer and easier to achieve at a single
setting. Earlier operation results in incomplete debridement of immature
necrosis. In addition, early operation is fraught with hazard and potentially
catastrophic bleeding complication.
e goals of treating NP include (1) safe debridement of all solid
necrotic material, (2) drainage of any pancreatic stula (externally or if pos-
sible internally), (3) gaining access to the alimentary tract, and (4) cholecys-
tectomy (if technically possible and safe) in patients with biliary etiology.
e classic approach to treating NP has been open operative debridement.
Recently, enthusiasm for minimally invasive approaches to NP patients has
grown. ese minimally invasive approaches include percutaneous drain-
age, endoscopic debridement, a combination of percutaneous/endoscopic
approach, retroperitoneal debridement (sinus tract necrosectomy or vid-
eoscopic assisted retroperitoneal debridement), laparoscopic transabdom-
inal debridement, and transgastric debridement (open or laparoscopic).
Regardless of the approach chosen, one physician must be willing to accept
responsibility for the duration of the NP patient’s care in what is commonly
a long-term (months to even years) recuperation.
Patient Selection for Intervention
NP is a very heterogeneous disease. It is critical for the practitioner to real-
ize that one approach does NOT t all patients. Individual patients must be
approached on a case-by-case basis, ideally in the context of an interested
multidisciplinary group that includes pancreatic surgeons, therapeutic
endoscopists, and interventional radiologists. e appropriate interven-
tion in SAP/NP depends principally upon the location of the peripancreatic
collections and the volume of solid necrosis present. An important consid-
eration is the presence of pancreatic parenchymal necrosis, particularly
when this is associated with a major pancreatic duct disruption (Fig. 2.4).
is common nding will lead to the so-called disconnected pancreatic
duct syndrome (DPDS), which will predictably result in persistent pancre-
atic stula when drained externally. Figure 2.5 depicts common patterns
of necrosis.
Antibiotic Treatment Alone
Several small and one moderately larger series have shown ecacy of anti-
biotic treatment alone in highly select patients with pancreatic necrosis.
is treatment strategy must be reserved for highly select patients, who
should be kept under very close follow-up. Mechanical intervention should
be applied for any sign of clinical deterioration.
FIGURE 2.4 CT of a patient with DPDS. Viable head (left panel, arrow) and tail (right
panel, arrow) are present; neck and body are necrotic, and subsequent drainage from the
tail is consolidated into a large lesser sac collection.
Chapter 2 / Acute Pancreatitis 23
Percutaneous Drainage
Recent reports suggest that as many as one-third of all NP patients may
be successfully treated with percutaneous drainage alone. Importantly, this
treatment strategy mandates frequent (72-hour) repeat cross-sectional
imaging with drain upsizing and/or additional drain placement. Patients
with DPDS, pancreatic head necrosis, or necrosis that extends down the
root of the small bowel mesentery are not good candidates for the per-
cutaneous approach. Patients who develop infected necrosis prior to the
4-week time point should have percutaneous drains placed. Percutaneous
drainage in the setting of early infection often successfully temporizes the
clinical situation until safe (i.e., 4 weeks) denitive debridement may be
undertaken. If a patient does not rapidly improve after percutaneous drain-
age, the surgeon should consider laparotomy to exclude ischemic viscera as
a source of deterioration.
Endoscopic Necrosectomy
Transgastric endoscopic debridement of NP was rst described in 1996.
is approach is attractive for its minimally invasive nature, as well as for
the concept of providing durable internal drainage for patients with DPDS.
Endoscopic debridement requires a dedicated endoscopist with advanced
procedural skills. Patients treated with this approach commonly require
multiple (4+) endoscopy sessions, each under general anesthetic.
Combined Endoscopic and Percutaneous Approach
e Virginia Mason group in Seattle has championed a combination pro-
cedure including endoscopic transgastric and percutaneous drainage. is
approach permits irrigation of the percutaneous drain, which may facilitate
mechanical egress of solid material into the alimentary tract. Dedicated cli-
nicians (both endoscopists and interventional radiologists) must follow the
patient treated with this combined approach, as they also require multiple
interventions.
FIGURE 2.5 Patterns of necrosis. Left image (collection conned to lesser sac) may be most
amenable to transgastric approach. Middle image (collection extending down left para-
colic gutter) may be most amenable to retroperitoneal debridement. Right image (necrosis
involving left paracolic gutter, pancreatic head, and/or root of the small bowel mesentery)
is a very challenging situation and may be best approached by open debridement.
Section I / Pancreas24
Retroperitoneal Approach
Select patients with appropriate anatomy may be debrided through the ret-
roperitoneum. e “step-up” approach of percutaneous drainage followed
at short interval by retroperitoneal debridement if necessary compared
favorably to direct open necrosectomy in the Dutch prospective, random-
ized PANTER trial. A multicenter North American study and another larger
series from Liverpool have also shown the ecacy of this approach in
select patients. Of particular interest is the nding that nearly one-third of
patients treated by the “step-up” approach resolved symptoms with percu-
taneous drainage alone. Further investigation is focusing on dening spe-
cic factors predicting success.
e etiology of AP must not be overlooked—minimally invasive
approaches such as percutaneous, endoscopic, and retroperitoneal do not
provide direct access for cholecystectomy.
Laparoscopic Transabdominal Debridement
Several small reports have documented the feasibility of laparoscopic (and
hand-assisted laparoscopic) debridement of peripancreatic and pancre-
atic necrosis, again in very select patients. Basic principles of pancreatic
debridement—that is, proper timing, thorough debridement, wide pan-
creatic drainage, and addressing underlying etiology (gallbladder) must
be followed in this approach. e totally laparoscopic approach is chal-
lenging due to lack of haptic feedback. General advantages of minimally
invasive surgery (i.e., shorter hospital stay, earlier return to work, etc.) may
be dicult to realize in this challenging group of patients.
Transgastric Debridement
Transgastric debridement can be accomplished endoscopically or surgi-
cally and is ideal for collections that are conned to the lesser sac and
for those patients with DPDS. Surgical transgastric debridement may be
approached laparoscopically or through a short upper midline incision.
Intraoperative ultrasound localizes the retrogastric collection; ultra-
sound is particularly helpful in patients with predominantly solid necro-
sis. Anterior gastrotomy is created, posterior gastrotomy is placed with
ultrasound guidance, and blunt necrosectomy performed through the
back wall of the stomach. Many NP patients have splenic vein thrombo-
sis with left-sided (sinistral) portal hypertension; gastric varices potenti-
ate signicant hemorrhage in this situation. Long posterior gastrotomy is
incorporated into what essentially amounts to cyst-gastrostomy. Feeding
tube placement and cholecystectomy may be performed at the same set-
ting, if indicated.
Several reports of surgical transgastric debridement have been pub-
lished recently. is approach appears to be an excellent choice for select
patients with necrosis conned to the lesser sac but may not be as useful
for those with necrosis extending down the paracolic gutters or the small
bowel mesentery root. Long-term follow-up is accruing; patients should be
counseled regarding the potential for reaccumulation of retroperitoneal
collections or the potential for recurrent AP.
Open Debridement
Open pancreatic debridement represents the time-tested standard as a
safe, eective method to achieve thorough debridement of necrotic tis-
sue, wide drainage of the pancreas and debridement bed, access to the
alimentary tract, and cholecystectomy (if indicated by biliary etiology).
Contemporary outcomes of open debridement at experienced centers doc-
ument improved morbidity and mortality rates compared to earlier eras,
Chapter 2 / Acute Pancreatitis 25
despite the fact that open surgical debridement is being reserved for those
patients with the most severe pathology.
Generous exposure should be obtained; the inammatory response
is generally quite dense and mild venous oozing seen during mobiliza-
tion of tissue is usually self-limited. Intraoperative ultrasound comple-
ments preoperative imaging as a surgical “road map” to ensure thorough
debridement. Collections in the paracolic gutters provide a safe route by
which to access contiguous lesser sac collections. Special care should be
taken debriding necrosis around the pancreatic head; catastrophic hem-
orrhage may accompany inadvertent injury to the superior mesenteric or
portal veins. e vascular walls are commonly weakened by the surround-
ing inammatory mass, and proximal/distal vascular control is extremely
challenging in this densely inamed operative eld. Gentle debridement
should only take tissue that is easily dislodged from the retroperitoneum.
Wide drainage of the necrosis bed is important to control pancreatic stula
externally. In patients with biliary AP, the decision to perform simultane-
ous cholecystectomy should be based on the patient’s clinical condition; if
cholecystectomy is deferred, it should be performed in the near future (as
the patient recuperates) to avoid recurrent biliary problems or recurrent
pancreatitis. Enteral access is routine in patients requiring open pancreatic
debridement; our preference is to place a gastrojejunostomy feeding tube.
OUTCOMES
Most patients with mild AP will recuperate without major clinical conse-
quence. Up to 20% of patients with a rst episode of AP will have recur-
rent AP, some of whom will progress to chronic pancreatitis. Patients with
NP, particularly those requiring debridement, often take several months
to return to baseline quality of life. Few data exist to document the true
incidence of long-term NP complications, which in addition to recurrent
AP may include exocrine and endocrine insuciency, biliary stricture, duo-
denal stricture (particularly in patients with head necrosis), disconnected
pancreatic duct with pancreatic stula, pseudocyst, or recurrent retro-
peritoneal collections/abscess. A pragmatic approach to long-term care
includes educating the patient as well as their primary care providers to the
possibility of long-term complication.
CONCLUSION
AP is a common, serious medical condition causing signicant morbidity
and mortality. Surgeons caring for AP patients should be prepared to lead a
multidisciplinary team and be prepared to care for these patients over the
long term of their illness. e challenges of caring for this complex disease
process are rewarded by seeing the patients return to good life quality after
this debilitating, potentially fatal illness. Research eorts are focused on
understanding the disease biology in order to identify specic treatment.
Suggested Readings
Balthazar EJ, Robinson DL, Megibow AJ, et al. Acute pancreatitis: value of CT in estab-
lishing prognosis. Radiology 1990;174:331–336.
Banks PA, Bollen TL, Dervenis C, et al.,; Acute Pancreatitis Classication Working
Group. Classication of acute pancreatitis—2012: revision of the Atlanta classi-
cation and denitions by international consensus. Gut 2013;62(1):102–111.
Banks PA, Gerzof SG, Langevin RE, et al. CT-guided aspiration of suspected pancreatic
infection: bacteriology and clinical outcome. Int J Pancreatol 1995;18:265–270.
Büchler MW, Glo or B, Müller CA, et al. Acute necrotizing pancreatitis: treatment strat-
egy according to the status of infection. Ann Surg 2000;232:619–626.
Section I / Pancreas26
Dellinger EP, Forsmark CE, Layer P, et al. Determinant-based classication of acute
pancreatitis severity. An international multidisciplinary consultation. Ann Surg
2012;256:875–880.
Petrov MS, Shanbhag S, Chakraborty M, et al. Organ failure and infection of pancre-
atic necrosis as determinants of mortality in patients with acute pancreatitis.
Gastroenterology 2010;139:813–820.
van Santvoort HC, Besselink MG, Bakker OJ, et al. A step-up approach or open
necrosectomy for necrotizing pancreatitis (PANTER trial). N Engl J Med
2010;362:1491–1502.
27
Adventures are all very well in their place, but there’s a lot to be said for regular
meals and freedom from pain
Neil Gaiman
INTRODUCTION
Chronic pancreatitis (CP) is a vexing disorder, marked clinically by
intractable debilitating abdominal pain and attendant nutritional failure.
CP is complex in its pathogenesis, clinical management, and psychoso-
cial implications. us, management challenges arise on all levels in the
endeavor to understand and treat this dicult disease.
EPIDEMIOLOGY
CP is a signicant public health care concern. e incidence and preva-
lence of CP in the United States have been estimated to be 4/100,000 and
41/100,000, respectively. Mortality from CP is increased up to 3.5 times the
average population, with a 10-year survival approximating 50%. US health
care costs for pancreatitis were estimated at $3.7 billion in 2009.
PATHOGENESIS
e etiology and pathophysiology underlying CP are poorly understood.
Pancreatitis is likely a heterogenous grouping of dierent diseases, mani-
festing as a similar end histologic result of pancreatic inammation and
brosis. Risk factors, most evidently excessive alcohol consumption, have
been implicated in disease pathogenesis. More likely, however, an intricate
interplay of environmental factors, genetic susceptibility, and host immu-
nologic response results in disease development.
Several theories on the etiology of CP have been put forth. e necro-
sis–brosis hypothesis holds that repeated bouts of acute pancreatitis
result in organ injury, resulting in brosis and CP. A similar model is the
sentinel acute pancreatitis event hypothesis, where an environmental
stress in a susceptible host leads to an inammatory response (acute pan-
creatitis), which then incites a host-specic immune response resulting in
brosis (CP).
Alcohol causes oxidative stress and mitochondrial damage, and it
lowers the threshold for trypsinogen activation. It also shifts cell death
from apoptosis to necrosis and stimulates immune-related inammatory
brosis. While excessive alcohol consumption is liable in alcoholic pancre-
atitis, it is not a lone causative agent, as evidenced by the fact that most
alcoholics do not develop pancreatitis. Clearly, there is an underlying host
susceptibility factor involved. Similarly, tobacco is implicated as a risk
f
actor for CP, with increasingly recognized importance.
Chronic Pancreatitis
Katherine A. Morgan
3
Section I / Pancreas28
e past two decades have brought revolutionary understand-
ing to the paradigm of pancreatitis pathophysiology with the discovery
of the cationic trypsinogen gene (PRSS1) and the delineation of heredi-
tary
p
ancreatitis in 1996. is important revelation clearly demonstrates
the phenotypic result of alterations in the trypsinogen pathway, with an
autosomal dominant disorder resulting in potentially severe disease with
increased susceptibility for cancer development. It has become a milestone
model in the genetic basis of pancreatic disease. Since then, several other
genes have been implicated in the pathogenesis of pancreatitis, all involv-
ing the trypsinogen pathway, including SPINK 1 (serum protease inhibitor,
Kazal type 1), CFTR (cystic brosis transmembrane regulator), CTRC (chy-
motrypsin C), and CaSR (calcium-sensing receptor) (Table 3.1).
Important immunologic discoveries including correlations with vari-
ations in human leukocyte antigen antigens have come about in the past
decade. On a cellular level, pancreatic stellate cells are identied in their
important role of extracellular matrix formation and brosis development.
e understanding of the contribution of substance P, nerve growth factor,
brain-derived growth factor, and other cell signaling molecules to disease
pathogenesis is evolving. Elucidation of the mechanism of disease develop-
ment on the genetic and cellular level explicates the concept of individual
susceptibility in the face of environmental stressors.
CLINICAL PRESENTATION
Patients may present with complications of pancreatitis such as obstruction
(biliary, duodenal, mesenteric vascular thrombosis), perforation (pseudocyst,
pancreatic stula, pancreatic ascites), or bleeding (visceral arterial pseudoa-
neurysm). e clinical hallmark of CP, however, is intractable, debilitating
abdominal pain. Pain is reported by 80% to 94% of patients with CP. It is typi-
cally described as sharp and burning, located in the epigastrium and radiating
around to the back. Nausea, emesis, and food intolerance often accompany the
pain. Patients may not have objective ndings associated with pain exacerba-
tion episodes, such as serum amylase elevation, thus leading to challenges for
health care workers and patients alike. Commonly, patients with severe disease
are challenged in their relationships with family and health care workers and
may develop maladaptive behaviors and associated social marginalization.
Endocrine and exocrine organ failure develops with progressive disease.
Approximately 60% of CP patients will develop insulin-dependent diabetes.
Greater than 90% loss of exocrine function must occur to result in malab-
sorption, with absorption of fat more signicantly aected than protein.
Gene Mechanism
Cationic trypsinogen gene (PRSS1) Inappropriate activation of trypsin
Serum protease inhibitor, Kazal type
1 (SPINK 1)
Failed inhibition of activated trypsin
Cystic brosis transmembrane
regulator (CFTR)
Decreased pH and ow of pancreatic
juice
Chymotrypsin C (CTRC) Failed inhibition of prematurely
activated trypsin
Calcium sensing receptor (CaSR) Failed intraductal calcium
homeostasis
Genes Implicated in Chronic Pancreatitis
TABLE
3.1
Chapter 3 / Chronic Pancreatitis 29
DIAGNOSIS
e diagnosis of CP entails a consistent clinical history, notable for
p
ancreatic-type abdominal pain, along with radiographic evidence of dis-
ease. e most relevant imaging modalities include contrast-enhanced
computed tomography (CT), secretin-stimulated magnetic resonance pan-
creatography (MRP), endoscopic retrograde pancreatography (ERP), and
endoscopic ultrasound (EUS).
Abdominal CT may show calcications, parenchymal thickening or
atrophy, or pancreatic ductal dilation evidencing disease. Alterations in
parenchymal enhancement, decreased response to secretin stimulation,
and pancreatic ductal pathology such as strictures or dilation may be better
delineated by MRP. ERP can show ductal changes and historically has been
the gold standard of objective disease diagnosis, although MRP is quickly
replacing ERP for diagnostic purposes at many centers. e ERP-derived
Cambridge classication system is the standard disease grading system
derived from an international consensus (Table 3.2). EUS is touted as the
most sensitive of the imaging modalities, although its utility is limited by
interobserver variability. It, too, has a disease grading system based on the
identication of objective features of CP (Table 3.3).
MANAGEMENT
In CP patients with debilitating pain who have failed medical management
to include alcohol and tobacco abstinence, pain control, nutritional opti-
mization, and behavioral therapies, intervention is indicated for pain relief.
ENDOSCOPIC MANAGEMENT
erapeutic ERP interventions for CP are undertaken with the goal of
relieving an obstructive process. Maneuvers include sphincterotomy,
stone extraction, stricture dilation, and stenting. In practice, the endo-
scopic approach is exhausted prior to surgery, given the perceived
advantages of a less invasive procedure, despite two randomized con-
trolled trials demonstrating improved outcomes with surgery in patients
with obstructive pancreatopathy. In the rst trial by Dite and colleagues
from the Czech Republic, 72 patients were randomized to endoscopic or
Grade Severity of Pancreatitis ERCP Findings
1 Normal No abnormal features
2 Equivocal Less than 3 abnormal branches
3 Mild More than 3 abnormal branches
4 Moderate Abnormal main duct and branches
5 Marked As above with one or more of:
Large cavities (> 10mm)
Gross gland enlargement (> 2 × normal)
Intraductal lling defects or calculi
Duct obstruction, structure or gross
irregularity
Contiguous organ invasion
ERCP, endoscopic retrograde cholangiopancreatography
From Sarner M, Cotton PB. Classication of pancreatitis. Gut 1984;25:756–759.
Cambridge Classication System for Severity of Chronic
Pancreatitis by ERCP Imaging
TABLE
3.2
Section I / Pancreas30
surgical intervention for pancreatic duct obstruction and associated pain.
Endoscopic therapy consisted of 52% sphincterotomy and stenting and 23%
stone removal. Operative management included 20% drainage procedures
and 80% resections. At 5-year follow-up, the surgical group had a greater
proportion of patients who were pain free (34% vs. 15%), while the rate of
partial pain relief was equivalent between the groups (52% surgery, 46%
endoscopy). In another trial by Cahen and colleagues from the Netherlands,
39 patients were randomized to endoscopic or surgical intervention for
dilated duct pancreatitis and pain. Endoscopic therapy included sphincter-
otomy and stent, while operative therapy was with a longitudinal pancre-
aticojejunostomy (LR-LPJ). At 5-year follow-up, pain relief was achieved in
80% of the surgical group versus 38% of the endoscopic group (p=0.001).
e surgical group also had larger improvements in quality of life and
underwent fewer procedures. Equivalent morbidity, length of stay, and pan-
creatic function were seen in the two groups.
SURGICAL MANAGEMENT
e primary indication for surgical intervention in CP is intractable pain,
unresponsive to medical therapies. Forty percent to sixty-seven percent
of patients with CP will meet these criteria for surgery. e goals of sur-
gery are to eectively and durably relieve pain while minimizing morbidity
including preserving pancreatic parenchyma when possible. e etiology of
pancreatic pain is poorly understood and likely multifactorial. us, opera-
tive decision making can be challenging. e pancreatic ductal anatomy is
the primary determinant in surgical planning. Generally speaking, patients
with a large main pancreatic duct (> 6–7mm in diameter) are presumed to
have an obstructive component to their disease and are thus well served by
a drainage procedure. In patients with small duct disease, resection of dam-
aged and poorly drained parenchyma is typically eective. In patients with
head-predominant or tail-centered disease, a directed resection is optimal.
In patients with a small pancreatic duct and diuse organ involvement,
a total pancreatectomy (TP) with islet autotransplantation (IAT) may be
indicated.
e heterogenous nature of CP anatomical changes mandates the sur-
geon’s familiarity with several operative approaches—no one operation is
suitable for every patient.
Parenchymal Criteria Duct Criteria
Hyperechoic foci Irregular duct contour
Hyperechoic strands Visible side branches
Hyperechoic lobules, foci, or areas Hyperechoic duct margin
Cyst Dilated main duct
Normal (low probability) 0–2 criteria present
Indeterminate (intermediate
probability)
3–4 criteria present
High probability 5–9 criteria present
EUS, endoscopic ultrasound
From Wallace MB, Hawes RH, Durkalski V, et al. The reliability of EUS for the diagnosis for chronic
pancreatitis: interobserver agreement among experienced endosonographers. Gastrointest Endosc
2001;53:294–299.
Conventional EUS Criteria for Chronic Pancreatitis
TABLE
3.3