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410 T.S. Wahl and J.D. Christein
Pancreaticojejunostomy
• Orient the Roux jejunal limb according to patient’s anatomy with anas-
tomoses starting from the tail with incremental openings to avoid an
overly long jejunotomy
Postoperative Management
A monitored setting may be required for 24–48 h postoperatively in patients with
high blood loss, given risk of further bleeding postoperatively. High fluid
requirements may be needed if active inflammation is present or extensive adhesiolysis performed. Monitor urine output closely with a urinary catheter initially
until patient is adequately resuscitated.
Early enteral nutrition initiation (feeding jejunostomy among malnourished
patients) with enteral liquids by postoperative day (POD) 1. Check a drain amylase
on POD 2 or 3 once diet is advanced with drain removal according to the International Study Group on Pancreatic Fistula (ISGPF) criteria. Projected goal for
discharge on POD 4 or 5, once the patient tolerates diet with return of bowel
function and ambulating with adequate pain control.
Patients shoul d be encouraged to continue lifestyle modification, since alcohol
and smok ing cessation is associated with decreased risk of disease progression and
morbidity. Patients need regular follow-up for exocrine and endocrine insufficiency,
as they may require pancreatic enzyme supplementation or insulin.
Alternative Management
• Malnourished patients need nasojejunal feeding for enteral nutrition for 2–
4 weeks preoperatively to promote an anabolic state. A feeding jejunostomy tube should be placed intraoperatively.
• Bile duct strictures should receive a preoperative biliary stent to assist duct
identification prior to intra-pancreatic biliary sphincteroplasty following
partial pancreatic head resection, to allow biliary drainage into the
pancreaticojejunostomy,
31 Chronic Pancreatitis: Frey Procedure 411
Global Pearls
• Utilize lifestyle modification, when feasible, pre- and postoperatively
• Assess exocrine and endocrine function along with nutritional status for
optimization
• Ensure adequate exposure of the pancreatic duct for complete debris removal
• Early initiation of enteral nutrition is a key postoperatively
References
1. Etemad B, Whitcomb DC. Chronic pancreatitis: diagnosis, classification, and new genetic
developments. Gastroenterology. 2001;120(3):682–707.
2. Homma T, Harada H, Koizumi M. Diagnostic criteria for chronic pancreatitis by the Japan
Pancreas Society. Pancreas. 1997;15(1):14–5.
3. Kloppel G, Maillet B. Pseudocysts in chronic pancreatitis: a morphological analysis of 57
resection specimens and 9 autopsy pancreata. Pancreas. 1991;6(3):266–74.
4. Kloppel G, Maillet B. Pathology of acute and chronic pancreatitis. Pancreas. 1993;8(6):659–
70.
5. Whitcomb DC, Frulloni L, Garg P, Greer JB, Schneider A, Yadav D, et al. Chronic
pancreatitis: an international draft consensus proposal for a new mechanistic definition.
Pancreatology. 2016;16(2):218–24.
6. Lin Y, Tamakoshi A, Hayakawa T, Ogawa M, Ohno Y. Cigarette smoking as a risk factor for
chronic pancreatitis: a case-control study in Japan. Research Committee on Intractable
Pancreatic Diseases. Pancreas. 2000;21(2):109–14.
7. Talamini G, Bassi C, Falconi M, Frulloni L, Di Francesco V, Vaona B, et al. Cigarette
smoking: an independent risk factor in alcoholic pancreatitis. Pancreas. 1996;12(2):131–7.
8. Yadav D, Hawes RH, Brand RE, Anderson MA, Money ME, Banks PA, et al. Alcohol
consumption, cigarette smoking, and the risk of recurrent acute and chronic pancreatitis. Arch
Intern Med. 2009;169(11):1035–45.
9. Yadav D, Whitcomb DC. The role of alcohol and smoking in pancreatitis. Nat Rev
Gastroenterol Hepatol. 2010;7(3):131–45.
10. Ramstedt M. Alcohol and pancreatitis mortality at the population level: experiences from 14
western countries. Addiction. 2004;99(10):1255–61.
11. Frulloni L, Falconi M, Gabbrielli A, Gaia E, Graziani R, Pezzilli R, et al. Italian consensus
guidelines for chronic pancreatitis. Digest Liver Dis. 2010;42(Suppl 6):S381–406.
12. Guidelines for the diagnosis and treatment of chronic pancreatitis (Nanjing, 2005). Chin J
Digest Dis. 2005;6(4):198–201.
13. Tandon RK, Sato N, Garg PK. Chronic pancreatitis: Asia-Pacific consensus report.
J Gastroenterol Hepatol. 2002;17(4):508–18.
14. Warshaw AL, Banks PA, Fernandez-Del Castillo C. AGA technical review: treatment of pain
in chronic pancreatitis. Gastroenterology. 1998;115(3):765–76.
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malabsorption in severe pancreatic insufficiency. N Engl J Med. 1973;288(16):813–5.
16. Mergener K, Baillie J. Chronic pancreatitis. Lancet. 1997;350(9088):1379–85.
17. Imoto M, DiMagno EP. Cigarette smoking increases the risk of pancreatic calcification in
late-onset but not early-onset idiopathic chronic pancreatitis. Pancreas. 2000;21(2):115–9.
18. Maisonneuve P, Lowenfels AB, Mullhaupt B, Cavallini G, Lankisch PG, Andersen JR, et al.
Cigarette smoking accelerates progression of alcoholic chronic pancreatitis. Gut. 2005;54
(4):510–4.
412 T.S. Wahl and J.D. Christein
19. Talamini G, Bassi C, Falconi M, Sartori N, Vaona B, Bovo P, et al. Smoking cessation at the
clinical onset of chronic pancreatitis and risk of pancreatic calcifications. Pancreas. 2007;35
(4):320–6.
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pancreatitis. Am J Gastroenterol. 2004;99(7):1350–4.
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Total Pancreatectomy with Islet Autotransplantation
William P. Lancaster and Katherine A. Morgan
Case Scenarios
Case 1: Diffuse Small Duct Disease
A 42-year-old-woman presents for evaluation of chronic pancreatitis. She reports a
4-year history of disease, marked by progressiv e epigastric and left-sided abdominal pain with periodic episodes of signi ficant exacerbation, requiring hospitalization for intravenous opiates. Between episodes, she requires daily narcotic pain
medication. She has nausea and pain with eating and has had significant weight loss
of 20 lb over the past year. She has oily stools with fatty meals. Her quality of life is
poor and has deteriorated to the point that she has had to quit working. She has a
history of endoscopic retrograde cholangiopancreatography (ERCP) with endoscopic stent placement, which provided no relief. She also has history of celiac
plexus block, which provided temporary relief of her symptoms, but proved nondurable. She has no other significant medical problems and does not take medications. Her surgical history is significant for a laparoscopic cholecystectomy. She
denies alcohol use, but admits to smoking one-half pack per day. She denies family
history of pancreatitis or pancreatic cancer. On physical exam she appears older
than her stated age and is thin. Her laboratory work is significant for an albumin of
3.2 g/dL and a vitamin D level of 8 ng/mL (normal 20–50 ng/ml).
32
W.P. Lancaster
Department of Surgery, Indiana University, 545 Barnhill Drive, EH 545,
Indianapolis, IN 46202, USA
e-mail: wplancas@iupui.edu
K.A. Morgan (&)
Medical University of South Carolina, 114 Doughty Street, Suite 249, Charleston,
SC 29425, USA
e-mail: morganka@musc.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_32
413
414 W.P. Lancaster and K.A. Morgan
Imaging findings are notable for a magnetic resonance cholangiopancreatography (MRCP) demonstrating diminished parenchymal enhancement on T1 weighted
imaging and, on T2 weighted images an irregular main pancreatic duct 3 mm in
diameter along with multiple dilated side branche s consistent, with chronic pancreatitis. Endoscopic retrograde cholangiopancreatography (ERCP) shows a similarly abnormal topography of the pancreatic duct, consistent with Cambridge
classification type III, and endoscopic ultrasound (EUS) is high probability of
chronic pancreatitis, revealing six criteria of chronic pancreatitis.
Case 2: Hereditary Pancreatitis
A 12-year-old-male presents with a history of pancreatitis since the age of 6. He
reports episodes of pancreatitis marked by epigastric abdominal pain and intolerance of oral intake, which have become progressively more frequent and more
severe over the past two years. He is well between episodes, but has had four
episodes this past year, and has missed a significant amount of school. He has
undergone multiple ERCPs with stent placement, which have resulted in transient
symptom improvement. A celiac plexus block was not helpful. Most recent axial
imaging shows diffuse calcifications throughout the gland, with associated atrophy.
The pancreatic duct is 7 mm in maximal diameter on MRCP. He takes oral pancreatic enzyme supplementation with meals. He is not diabetic. Genetic testing is
significant for a mutation at the PRSS1 gene. His father had chronic pancreatitis and
died at age 42 from pancreatic cancer. His sister has pancreatitis as well.
Case 3: Salvage Pancreatectomy
A 48-year-old-female presents with a 6-year history of idiopathic chronic pancreatitis. She underwent a Frey procedure (local pancreatic head resection with a lateral
pancreaticojejunostomy) 3 years ago for debilitating pain. She did well, with resolution of pain for approximately 2 years after surgery, but has had recurrence of
her abdominal pain over the past year. She has developed diabetes requiring insulin
over the past 3 months. Her past medical history and surgical history are otherwise
unremarkable. She takes daily narcotic medication and oral pancreatic enzyme
supplementation. She went back to school after her Frey and completed her degree,
but is now unable to work. Her exam is benign and her labwork unremarkable. She
underwent MRCP, which shows significant calcific disease and fibrosis in the
remnant pancreas.
Case 4: Recurrent Acute Pancreatitis
A 37-year-old-female presents with recurrent episodes of acute pancreatitis. She
reports her first episode was 3 years ago, and has since had progressively more
32 Total Pancreatectomy with Islet Autotransplantation 415
frequent and severe bouts of acute pancreatitis. Her episodes are marked by severe
epigastric abdominal pain with nausea, emesis, and intolerance of oral diet. These
bouts are associated with elevated serum lipase and require hospitalization for
intravenous hydration, antiemetics, and narcotics. The episodes last days to weeks,
and she had four such episodes last year. She is well, without pain, between bouts .
Her past medical history is unremarkable. Her surgical history is significant for a
cholecystectomy. A CT scan during an episode reveals peripancreatic fat stranding
and fluid. An MRI with MRCP done between episodes shows no evidence of
chronic pancreatitis. EUS is low probability for chronic pancreatitis.
Preoperative Evaluation
The goals of the preoperative evalua tion for total pancreatectomy with islet autotransplantation (TPIAT) are to establish the diagnosis of chronic pancreatitis or
recurrent acute pancreatitis, to assess whether disease severity warrants intervention, to consider whether lesser interventions may be successful, to evaluate the
physiologic fitness of the patient for surgery, and to consider the psychological
preparedness of the patient [1].
Patients with diffuse small duct pancreatitis, those with genetic pancreatitis [2],
patients who have failed lesser surgeries [3], and patients with recurrent acute
pancreatitis may benefit from TPIAT.
History
The clinical hallmark of chronic pancreatitis is progressive, severe, debilitating
abdominal pain. High healthcare utilization is common, and chronic narcotic use is
frequently present. Patients report a severely diminished quality of life. Patients
often have attendant nutritional failure due to PO intolerance, as well as to exocrine
pancreatic insufficiency. Diabetes due to islet cell loss during parenchymal
replacement with fibrosis occurs in late stages.
During the initial evaluation, risk factors for chronic pancreatitis should be
sought. Alcohol use has traditionally been implicated in many cases with chronic
pancreatitis, although direct causation is not evident, and suscep tibility to
alcohol-induced pancreatitis has been linked to genetic variation on the X chromosome. Alcohol is less commonly implicated in the morphologic patterns of
pancreatitis that present as appropriate for TPIAT (diffuse small duct disease), and
patients with alcoholic pancreatitis have been shown to have inferior outcomes after
TPIAT [4]. Tobacco use has been found to be a significant factor for promoting
fibrosis and for enhancing susceptibility to pancreatitis development, and has been
found to correlate with lower islet yields and function after islet autotransplantation.
Proper counseling should be undertaken with consideration of smoking cessation as
a requirement for surgery [5].
416 W.P. Lancaster and K.A. Morgan
Genetic Testing
Several genetic mutations have been identified that predispose to the development
of chronic pancreatitis, including PRSS1, SPINK1, and CFTR. Genetic testing is an
important component of preoperative evaluation, particularly in the setting of
early-onset disease, as the natural history of hereditary pancreatitis may differ from
pancreatitis of other etiologies. Patients with hereditary pancreatitis typically have
progressive disease with subsequent development of endocrine and exocrine dysfunction, and often have disease refractory to conventional medical and surgical
therapies. In addition, the lifetime risk of pancreatic cancer may be increased
compared to the general population. Thus, these patients are often well suited to
TPIAT [2]. Of the genetic mutations associated with pancreatitis, the best understood is PRSS1. The PRSS1 gene is located on the long arm of chromosome 7 and
encodes cationic trypsinogen. It is inherited in an autosomal dominant fashion with
an estimated penetrance of 80%. Disease onset is early, usually manifesting as
pancreatic pain. Patients progress to endocrine and exocrine insufficiency by the
third decade. The cumulative risk of pancreatic adenocarcinoma is approximately
50% at 75 years of age [6].
Recurrent Acute Pancreatitis
A subset of patients will have recurrent acute pancreatitis that is significantly
debilitating, without evidence of chronic pancreatitis. These patients may benefit
from TPIAT if disease progresses despite removal of aggravating environmental
factors and despite endoscopic interventions. Pancreatitis should be definitivel y
demonstrated to be causative of pain episodes by associated elevation in serum
lipase during events to three times normal, and/or evidence of peripancreatic
inflammation on axial imaging.
Imaging
Radiographic imaging is essential to the evaluation of patients for TPIAT. First,
confirming diagnosis of chronic pancreatitis in patients with longstanding abdominal
pain is fundamental, as abdominal pain can be multifactorial. Second, understanding
the anatomy of the pancreatic duct and parench ymal disease distribution can help
guide appropriateness of total pancreatectomy versus lesser intervention, such as a
drainage procedure for dilated duct pancreatitis, or partial resection for focal pancreatitis. The pancreas is well evaluated with several different modalities. Computed
tomography (CT) scan can demonstrate pancreatic inflammation as well as glandular
atrophy and pancreatic calcifications commonly seen with chronic pancreatitis,
though the overall sensitivity is low, particularly in early-stage disease and in the
absence of calcifications or overt ductal changes (Fig. 32.1) Magnetic resonance
cholangiopancreatography (MRCP), particularly with secretin administration, allows
32 Total Pancreatectomy with Islet Autotransplantation 417
Fig. 32.1 Diffuse small duct pancreatitis is demonstrated in this CT scan of a patient with
idiopathic chronic pancreatitis who underwent total pancreatectomy with islet autotransplantation.
Noted are a prominent, mildly dilated main pancreatic duct, parenchymal fibrosis, and punctate
calcifications
for reasonable ability to evaluate the pancreatic parenchyma as well as the pancreatic
ductal anatomy. ERCP is rarely used purely for diagnosis in the modern era of MRCP,
and is reserved for therapeutic use. The Cambridge classification system of pancreatic
abnormalities seen on ERCP is used to define features of chronic pancreatitis, and has
also been applied to MRCP. A sensitive assessment of the pancreas, although subject
to interobserver variability, is with EUS. EUS assesses for abnormal parenchymal
features as well as ductal abnormalities, and at least five features of pancreatitis
should be present in order for the test to be considered high probability for chronic
pancreatitis. Imaging features must be considered within the clinical context of these
often complex patients with chronic abdominal pain.
Diabetes
Patients with c hronic pancreatitis may develop pancreatic endocrine failure due to
islet cell loss (type 3c diabetes). Patients with diabetes may still benefit from islet
autotransplantation, as endogenous c-peptide production can ameliorate the severity
418 W.P. Lancaster and K.A. Morgan
of resultant surgical diabetes after pancreatectomy [7]. Patients with diabetes on
evaluation for TPIAT should be evaluated for their level of islet function, however,
to help weigh whether the potential benefits of islet autotransplantation war rant the
risks inherent. Stimulated c-peptide response should be assessed, often with a
mixed-meal tolerance test.
Nutritional Assessment
Patients with chronic pancreatitis are at risk for nutritional failure due to poor PO
intake and from pancreatic exocrine insufficiency. A full nutritional evaluation and
efforts to optimize nutritional status preoperatively are important for best outcomes.
Pancreatic enzyme replacement therapy is best instituted preoperatively. Evaluation
for malnutrition with assessment of serum albumin and pre-albumin levels are
requisite. Preopera tive oral supplementation or enteral feeds may be required in the
severely affected. Deficiencies in the fat-soluble vitamins should be addressed.
Physiologic Assessment
As with other major elective abdominal operations, attendant comorbidities,
including cardiac, pulmonary, and renal disease should be evaluated when considering patient candidacy for surgery. In particular, a history of hepatic disease is
important, as the islet infusion is an embolic event, which may be a significant
stressor to a previously compromised liver, increasing morbidity.
Behavioral Medicine Evaluation
Patients evaluated for TPIAT should undergo comprehensive psychological
assessment to evaluate relative preparedness for surgery [8]. Evaluation assesses
multiple psychological domains, including global cognitive functioning, quality of
life, and coping. The patient’s knowledge and expectations of the procedure are
assessed, as well as the support system available. A complete psychiatric evaluation
is performed to diagnose previously untreated psychiatric disorders, e.g. depression,
anxiety. The patient’s health behaviors and compliance are also assessed to screen
for narcotic dependence/abuse and ability to manage complex medication regimens,
e.g., pancreatic enzyme therapy, insulin.
Preoperative Counseling
In consideration of this radical, elective procedure, patient education is paramount.
Patients should demonstrate understanding of proper expectations. The goals of the
procedure are pain relief and improvements in quality of life. These expected
32 Total Pancreatectomy with Islet Autotransplantation 419
outcomes come at the cost of lifelong (ameliorated) surgical diabetes and exocrine
insufficiency.
Patient Selection Criteria for Total Pancreatectomy with Islet Auto-
transplantation for Chronic Pancreatitis
1. Chronic pancreatitis
Evidenced by: CT, MRCP, EUS (5 criteria, high probability), or prior
surgical pathology
OR
Recurrent acute pancreatitis
Evidenced by: at least two documented episodes with lipase >3 time
normal
2. Debilitating pain
Defined by daily narcotic use and/or inability to work, attend school, or
engage in normal societal roles
3. Not amenable to lesser interventions
Includes medical, endoscopic, and lesser surgical options
4. Physiologically fit
No prohibitive cardiopulmonary conditions, no significant hepatic disease
5. Psychologically fit
Requires behavioral medicine evaluation
Surgical Technique
The patient is positioned supine under general anesthesia. A triple lumen central
venous catheter is placed for durable intravenous access, primarily in anticipation of
the continuous infusions required during the initial postoperative period. Additional
large-bore peripheral intravenous access is also established because there is the
potential for rapid fluid shifts. An arterial line is placed and continuous hemodynamic monitoring is used to allow for goal-directed fluid management.
An upper midline laparotomy incision extending from the xiphisternum to above
the umbilicus is typically used. A wound protector is utilized. The gastrocolic
ligament is divided and the lesser sac is entered. The greater omentum and short
gastric vessels are taken down along the greater curvature of the stomach. The
hepatic flexure is mobilized and retracted inferomedially. A full Kocher maneuver
is performed, mobilizing the duodenum to the level of the aorta medially. The right
gastroepiploic vein and middle colic vein are identified and followed toward the
superior mesenteric vein. The right gastroepiploic vein is divided, taking care to
preserve the middle colic vein. The inferior margin of pancreatic neck is identified
over the superior mesenteric vein, and the plane between the portal vein and the