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30 Chronic Pancreatitis: Puestow and Frey Procedures 399
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Chronic Pancreatitis: Frey Procedure
31
Tyler S. Wahl and John D. Christein
Case Presentation
A 57-year-old white male with chronic obstructive pulmonary disease (COPD) and
chronic pancreatitis from alcohol abuse of 40 years presents to your clinic with
chronic abdominal pain. Patient notes having significant post-prandial abdominal
bloating and boring epigastric pain radiating to his back in a band-like fashion,
intermittently associated with diarrhea. His pain, nausea, and steatorrhea have
progressed over several years, resulting in a 15-lb weight loss this past year,
requiring initiation of pancreatic enzyme replacement with some improvement.
First episode of pancreatitis occurred in 2008, followed by episodes in August 2014
and March 2015, requiring hospitalizations with a serum lipase of 1,544 units/L and
normal liver function tests during his latest admission. Notable past medical history
is significant for COPD, osteoarthritis, and pancreatitis, without evidence of
choledocholithiasis, jaundice, abnorm al liver function tests, or cirrhosis during prior
hospitalizations. Your patient has no surgical history and has abstained from
alcohol for 14 months; however, he continues to smoke half a pack of tobacco per
day. Physical exam reveals stable vital signs and a non-tender epigastrum without
guarding or rebound tenderness.
The patient received an abdominal computed tomography (CT) scan with
intravenous and oral contrast (Fig. 31.1a–d) showing extensive dystrophic calcifications throughout the pancreatic head, with diffuse dilation of the proximal
T.S. Wahl J.D. Christein (&)
Department of Surgery, University of Alabama at Birmingham (UAB),
1922 7th Avenue South, Kracke Building 428, Birmingham, AL 35249, USA
e-mail: jchristein@uabmc.edu
T.S. Wahl
e-mail: twahl@uabmc.edu
© Springer International Publishing AG 2017
T.M. Pawlik et al. (eds.), Case-Based Lessons in the Management of Complex
Hepato-Pancreato-Biliary Surgery, DOI 10.1007/978-3-319-50868-9_31
401
402 T.S. Wahl and J.D. Christein
main-pancreatic duct from an intra-pancreatic duct calculus. The pancreatic duct
was dilated to the level of the pancreatic tail. The patient also underwent an
endoscopic retrograde cholangiopancreatography (ERCP) with scout imaging
showing numerous calcifications in the pancreatic gland and large mass of calcium
in the pancreatic head. Cholangiogram was deferred given normal preoperative
liver function tests. The pancreatogram revealed a pancreatic duct stricture in the
head with some filling into a large mass of calcification.
Fig. 31.1 CT abdomen with IV/PO contrast showing a extensive dystrophic calcifications
throughout the pancreatic head with diffuse dilation of b the proximal main-pancreatic duct
(9 mm), with an intra-pancreatic duct calculus associated with mild edema and peri-pancreatic
stranding suggestive of acute on chronic pancreatitis. c coronal image of the pancreatic head with
calculi and dilated duct. d pancreatic duct dilation extends to the body and tail
31 Chronic Pancreatitis: Frey Procedure 403
Diagnosis and Assessment
Chronic pancreatitis is a fibro-inflammatory syndrome of the pancreas provoked by
inflammatory or stress conditions incited through genetic and/or environmental risk
factors, leading to morphologic (parenchymal injury, irregular fibrosis) and physiologic (exocrine and endocrine) changes with acinar and islet cell loss [1–5]. The
pathophysiology of chronic pancreatit is is multifactorial and complex. The
TIGAR-O (toxic/metabolic, idiopathic, genetic, autoimmune, recurrent pancreatitis,
obstructive) classification system identifies risk-factor categories associated with
chronic pancreatitis [1].
Our patient demonstrates a common presentation of chronic pancreatitis with
chronic alcohol and tobacco abuse, recurrent acute pancreatitis, post-prandial
abdominal pain, malabsorption (exocrine insufficiency), and weight loss. His
exposure to long-term use of alcohol and tobacco places him at an elevated risk for
pancreatic disease development and progression [6 – 9 ]. The correlation between
alcohol use and pancreatic disease is common worldwide, including the United
States [10]. Recurrent acute pancreatitis attacks destroy parenchymal tissue over
time through chronic inflammatory changes, including fibrosis and calcification,
leading to impaired exocrine and endocrine functions [11]. Chronic pancreatitis in
the advanced phases is associated with an increased risk for pancreatic cancer [12–
14]. Exocrine insufficiency largely takes place when more than 90% of acinar cell
function is lost leading to malabsorption [15]. Steatorrhea (fat malabsorption)
precedes azotorrhea (protein malabsorption), leading to weight loss over months to
years, as seen in our patient. Patients commonly present with boring epigastric pain
radiating to the back in a band-like fashion. Pancreatic pseudocyst formation (not
found in our patient) may also cause pain, early satiety, weight loss, and inability to
eat, resulting in weight loss in the more acute setting.
Initial workup should include well-validated radiologic imaging, typically with
CT, ERCP, endoscopic ultrasound (EUS) with biopsy, or magnetic resonance
cholangiopancreatography (MRCP). CT imaging with a pancreas protocol (with
and without IV contrast, IV contrast in arterial and portal venous phases, and water
as oral contrast) is the first-line noninvasive imaging modalit y of choice, and our
initial gold standard. Studies using this protocol are able to diagnose chronic
pancreatitis and its complications with 90% confidence [1]. Endoscopic methods of
imaging with ERCP and EUS can provide imaging and tissue for diagnosis with
therapeutic intervention using ERCP technique. The risks of bleeding, bowel or
duct perforation, and acute pancreatitis must be taken into account with perceived
benefits on a case-by-case basis. It is essential to assess the pancreatic and biliary
duct anatomy for evidence of obstruction preoperatively to optimize intraoperative
intervention.
In terms of pancreatic exocrine dysfunction, functional testing is invasive and
not necessarily diagnostic, and should have a limited role in chronic pancreatitis
workup. Instead, history and clinical evidence of steatorrhea/azotorrhea with or
without weight loss may be a signa l of malabsorption and a malnourished, catabolic
state. It is critical to evaluate the patient’s nutritional status preoperatively throu gh a
404 T.S. Wahl and J.D. Christein
metabolic and nutritional panel not limited to fat-soluble vitamins, liver function
tests, pre-albumin, and albumin. Malnourished patients need nasojejunal enteral
feedings for 2–4 weeks to reestablish an anabolic state to prepare for surgery.
Patients with chronic pancreatitis often present with glucose intolerance from
endocrine insufficiency, as up to 60% of patients will require insulin replacement
[16]. Further, chronic pancreatitis patients are at an increased risk for spontaneous
or treatment-related hypoglycemia, likely attributed to glucagon insufficiency,
malnutrition, and alcohol consumption [ 16]. Our patient did not have endocrine
insufficiency.
Management
Whenever feasible, lifestyle modifications should be implemented for chronic
pancreatitis patients prior to surgical intervention. In addition to multimodal pain
therapies, alcohol and smoking cessation can further decrease pain and complications in chronic pancreatitis, with further risk mitigation of pancreatic calcification
through smoking cessation [17–19]. Reductions in dietary fats for patients with
severe refractory steatorrh ea offer some benefit, yet medium-chain triglyceride
supplementation are not indicated and require additional enzyme supplementation
for proper digestion and absorption [11, 20]. Parenteral vitamin supplementation of
fat-soluble vitami ns and enteral pancreatic enzyme replacement is beneficial for
patients with exocrine insufficiency and malabsorption [11]. Pancreatic enzyme
supplementation normalizes fat-soluble vitamin, pre-albumin, and ferritin levels in
chronic pancreatitis patients without steatorrhea [21]. Enzyme supplementation can
be given in the absence of fecal-fat testing in patients with clinical malabsorption
(loose, foul-smelling stool; weight loss; muscle wasting; osteopenia) [22]. A 72-h
fecal-fat study is the gold standard to detect steatorrhea; however, this test may not
be convenient or feasible given the sensitivity and specificity (100 and 95%,
respectively) and positive predictive value (90%) of the acid steatocrit random-spot
test [23].
Surgical intervention is warranted in our patient presenting with progressive
frequency of pancreatitis episodes, severe and recurrent pain, signs of malabsorption, and evidence of pancreatic duct obstruction and dilation. Our patient warrants
a duodenal-preserving partial resection of the pancreatic head, longitudinal ductotomy, and lateral pancreaticojejunostomy (Frey Procedure).
Indications for Frey Procedure
• Disabling or severe pain with ductal dilation 7 mm or dilated with
multiple strictures
• Asymptomatic with ductal dilation 7 mm or dilated with multiple
stricture
31 Chronic Pancreatitis: Frey Procedure 405
• Symptomatic inflammatory mass/calcification in pancreatic head causing
ductal dilation
• Consideration: dilated with multiple strictures has a “chain of lakes”
appearance
Intraoperative Technique
Positioning and Preparation
The patient is placed on the operating room table in the supine position. Intravenous
access with two large-bore intravenous cannulas or one central venous line is
established, along with arterial wave monitoring via a radial arterial line. Appropriate prophylactic antibiotics, urinary catheter, and compression hose-stockings
with a sequential compression device are administered or placed prior to incision.
Exposure of the Pancreas
We begin with a bilateral subcostal incision with thorough exploration of the
abdomen prior to exposing the pancreas (Fig. 31.2). The greater omentum is elevated off the transverse mesocolon to its origin on the stomach, and the gastrocolic
ligament is divided to provide access into the lesser sac exposing the anterior
pancreas body and tail (Fig. 31.3a, b). Exposure of the pancreas is challenging in
the setting of chronic inflammation, as the posterior wall of the stomach is frequently densely adherent to the pancreas.
Longitudinal Pancreatic Ductotomy
First, identify the gastroduodenal artery (GDA) near the head. If the GDA can be
palpated, ligate at the superior and inferior border of the pancreas for proximal and
distal control, respectively, with interrupted figure-of-eight 4-0 Prolene sutures. If
the GDA is not palpable due to extensive fibrosis, carefully dissect until the GDA is
encountered, and control with manual compression until ligated. Once dissection
approaches the neck, formal control of the GDA is performed superiorly and
inferiorly to the pancreas as described. The pancreatic duct is identified within the
pancreatic head with a needle and opened using cautery with a high setting (75–85)
on fulgurate mode. We insert an appropriately sized probe into the duct upstream
406 T.S. Wahl and J.D. Christein
Fig. 31.2 Sub-costal incision or an upper midline incision may be utilized
toward the tail and cut down along the probe with high cautery. The ductotomy is
then directed downstream toward the head to expose the entire main-pancreatic duct
up to 1 cm from the papilla of Vater. All pancreatic stones and debris are removed.
Pancreatic Head Resection
The portal vein above the pancreas and superior mesenteric vein (SMV) below are
visualized to ensure safe dissection of the anterior pancreatic head and uncinate
process. With the GDA ligated, use high cautery to partially resect the pancreatic
head, leaving only a thin rim of pancreatic tissue along the medial duodenal wall
31 Chronic Pancreatitis: Frey Procedure 407
(a)
Stomach
Pancreas under
gastrocolic
ligament
(b)
Esophagus
Spleen
Short gastric
arteries
Gastroepiploic
vessels
Gastrocolic
ligament
Transverse
colon
Stomach
Pancreas
Duodenum
Superior
mesenteric
vein
Fig. 31.3 a Divide the gastrocolic ligament to gain access into the lesser sac. b Reflect the
stomach cephalad to expose the anterior pancreas
408 T.S. Wahl and J.D. Christein
Fig. 31.4 The longitudinal
ductotomy should expose the
entire main duct from the tail
to approximately 1 cm from
the papilla of Vater. The
partial pancreatic head
resection is shown (note the
dissection does not extend
past the posterior border of
the main duct). Remove all
stones and debris from main
and side-branch ducts
(Fig. 31.4). Once lateral to the neck, dissection can continue down to the uncinate
process in a circular fashion with piece-meal resection of tissue, if necess ary.
Resection should not extend beyond the posterior border of the main duct, as deeper
resections increase the risk of pancreatic division, compromising vascular structures, and promoting a pancreatic leak into the retroperitoneal space. We do not
perform a Kocher maneuver as to avoid posterior capsule penetration. Meticulous
care is taken to remove stones and debris from the main duct and side branches.
Utilize suture ligation of brisk bleeding (5-0 Prolene sutures), as cautery temporarily seals arterial vessels. If the bile duct is encountered and opened unintentionally, the bile will ultimately drain into the pancreaticojejunostomy.
Roux-en-Y Pancreaticojejunostomy
A segment of jejunum is identified and divided 15 to 30 cm distal to the ligament of
Treitz. The common enterotomy is closed with 3-0 Prolene as the mesentery is
divided with ligation of bridging vessels toward the mesenteric origin to the right of
the middle colic vasculature. The distal jejunum segment is pulled through the
transverse mesocolon to deliver the Roux limb to the pancreas in a retrocolic
position, or according to the patient’s anatomy. Excess mesenteric defects are
closed with interrupted 3-0 silk suture. The transected end of the Roux limb is
oriented with the pancreatic tail to start a one-layer side-to-side pancreaticojejunostomy using multiple running 3-0 Prolene sutures, and secured to the transverse
mesocolon with interrupted 3-0 silk suture once complete. The pancreaticojejunostomy continues toward the pancreatic head to allow complete drainage of the
main duct, with progressive opening of the jejunum to avoid an excessively long
jejunotomy (Fig. 31.5).
31 Chronic Pancreatitis: Frey Procedure 409
Fig. 31.5 Lateral
pancreaticojejunostomy,
anterior view. Remember to
perform incremental opening
of the Roux jejunal limb
while performing the
anastomosis from the tail
toward the head, to avoid an
overly long jejunotomy
Following completion of the pancreaticojejunostomy, an end-to-side jejunojejunostomy is created to complete the Roux-en-Y, approximately 40–50 cm distal to
the pancreaticojejunostomy to reestablish intestinal continuity. One small, round
drain is placed in the lesser sac, and fascia is closed in two layers with 1-0 Prolene
sutures prior to skin irrigation and approximation with staples.
Technical Pearls
Exposure
• Enter the lesser scar through the gastrocolic ligament to expose the
anterior pancreas
Ductotomy
• Ligate the gastroduodenal artery
• Ensure ductotomy extends the entire length of the gland using high-setting
cautery (75–85) on fulgurate mode
Partial pancreatic head resection
• Pancreatic head tissue resection should leave only a thin rim of tissue
around the duodenum and not extend past the posterior border of the
main-pancreatic duct