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J. Kleeff et al.
Key Steps
The procedures for chronic pancreatitis described above are usually performed as
open surgery using a midline or transverse laparotomy. The evidence on minimally
invasive approaches is limited to small case series from specialized centers and case
reports [20–22]. These reports include very few patients who received an operation
other than the Frey procedure. In cases with a more extensive procedure, the rate of
conversion to open surgery was high [21]. Therefore, in light of the often- pronounced
inammatory adhesions and the relevant risk of hemorrhage in procedures involving pancreatic transection, minimally invasive surgery for combined resection, and
drainage procedures for chronic pancreatitis cannot be generally recommended, but
can be performed in experienced centers.
Open combined resection and drainage procedures for chronic pancreatitis
require a setup equivalent to that of oncologic pancreatic resections. Patients require
multiple large bore iv catheters, a central venous catheter when indicated and usually also an arterial line for continuous blood pressure management. A nasogastric
tube is to be placed for the operation and may remain in situ postoperatively if
needed. Placement of a Foley catheter allows for more accurate intra- and postoperative uid management, but it should be removed shortly after the operation to
facilitate early mobilization.
The most important surgical steps of the procedures can be summarized as
follows.
Common Steps
• Timely antibiotic prophylaxis (see above)
• Supine position with the right or both arms at the sides
• Prepping and draping of the entire abdomen
• Midline or transverse laparotomy, depending on the conguration of the patient’s
abdomen/coastal arches and previous laparotomies
• Entering the lesser sac by dividing the gastrocolic ligament (caution must be
exerted not to injure the gastroepiploic vascular arch)
• Mobilization of the caudal border of the pancreatic body and tail. The right gastroepiploic artery and vein usually need to be ligated and divided for exposure of
the ventral plane of the pancreatic head and neck (caution: possible portal venous
collaterals)
• Mobilization of the right colonic exure and Kocher’s maneuver, allowing for
ventral and dorsal palpation of the pancreatic head (transduodenal biopsy of a
suspicious mass for frozen section possible)
• Exposure of the portal and superior mesenteric vein at the caudal border of the
pancreas and division of venous and arterial tributaries next to the pancreatic
head and uncinate process
• Cholecystectomy (if not performed in a previous surgery)
9 Combined Procedures (Open Vs. MIS)
151
Frey Procedure/Hamburg Modication
• Localization of the pancreatic duct by palpation or puncture with a small gauge
needle and aspiration
• Incision of the ventral pancreas at the location of the duct, identication of duct
orientation using an angulated clamp
• Opening of the duct to within 1.5 cm of the pancreatic tail and 1 cm of the
ampulla, removal of all visible stones
• Verication of ampullary patency by placing a small probe through the ampulla
into the duodenum (caution: due to invagination of the pancreatic head into the
duodenum, the duct turns posterior-laterally from the ventral surface of the pancreas next to the duodenal margin until the ampulla is reached)
• Excision of the ventral portion of the pancreatic head up to the dorsal wall of the
pancreatic duct; some tissue should be left along the duodenal curve and right of
the superior mesenteric vein; frozen section of excised tissue is possible if malignancy cannot be ruled out
• Hamburg modication: V-shaped extension of excision into the uncinate process
• Identication and preservation of the intrapancreatic common bile duct, removal
of periductal inammations, thus relieving compression (in case of persisting
stricture or duct injury, choledochojejunostomy can or must be performed)
• Roux-en-Y reconstruction with two-layered retrocolic pancreaticojejunostomy
(outer layer: interrupted sutures, jejunal serosa and muscularis to pancreatic capsule; inner layer: continuous suture, full-thickness jejunum to the incised pancreatic surface) and end-to-side jejunojejunostomy 40 cm aborally from the
pancreaticojejunostomy
DPPHR/Berne Modication
• Ligation of the gastroduodenal artery at its origin from the common hepatic artery
• Exposure of the common bile duct in the hepatoduodenal ligament up to the
cranial pancreatic border
• Exposure of the conuence of the superior mesenteric vein and the splenic vein
and of the portal vein dorsally to the pancreatic head (caution: adhesions of the
pancreatic tissue to the veins, portal venous collaterals)
• Division of the pancreatic neck at the level of the mesenteric-portal axis
• Berne modication: no division of the pancreatic neck, avoiding complete dissection of the portal vein
• Subtotal excision of the pancreatic head by dividing small venous and arterial
tributaries and dissecting the pancreatic tissue from the common bile duct
towards the papilla and the uncinate process; frozen section of excised tissue is
possible if malignancy cannot be ruled out
152
• Removal of inammatory tissue around the common bile duct, thus relieving
compression (in case of persisting stricture or duct injury, choledochojejunostomy can or must be performed); some pancreatic tissue must be left along the
duodenal curve between the common bile duct and the duodenal wall
• Retrocolic Roux-en-Y pancreatojejunostomy: two-layered end-to-side anastomosis between the left pancreas and jejunum (outer layer: interrupted or continuous suture, jejunal serosa and muscularis to pancreatic capsule; inner layer:
interrupted or continuous suture, jejunal mucosa to pancreatic duct)
• Latero-lateral pancreatojejunostomy between the same jejunal limb and the pancreatic head remnant (outer layer: interrupted or continuous suture, jejunal serosa
and muscularis to pancreatic capsule; inner layer: interrupted or continuous
suture, full-thickness jejunum to the incised pancreatic surface)
• End-to-side jejunojejunostomy 40 cm aborally from the
pancreaticojejunostomy
J. Kleeff et al.
Pitfalls/Tricks
• To facilitate dissection of the ventral side of the superior mesenteric and portal
vein, a suture can be placed through the pancreatic tissue at the level of the neck
in order to lift the pancreas ventrally.
• In case of pronounced hemorrhage during vessel dissection, compression of the
pancreas can compress the portal and splenic vein and reduce blood ow, allowing for portal vein exposure and repair of its wall.
• To avoid injuring the common bile duct, a thin probe can be inserted through the
orice of the cystic duct (if no prior cholecystectomy had been performed) or
through a small incision into the duct.
Specic Postoperative Outcomes
The postoperative complications specic to combined resection and drainage procedures for chronic pancreatitis mostly overlap with complications after pancreatic
surgery for other indications (see dedicated chapters in this manual).
Local Complications
• Postoperative pancreatic stula (POPF), classiable according to the ISGPS consensus [23]
• Delayed gastric emptying (DGE), classiable according to the ISGPS consensus [24]
9 Combined Procedures (Open Vs. MIS)
153
• Postpancreatectomy hemorrhage (PPH), classiable according to the ISGPS
consensus [25]
• Postpancreatectomy Acute Pancreatitis (PPAP), classiable according to the
ISGPS consensus [26]
• Bile leak, classiable according to the ISGPS consensus [27]
• Bile duct stricture with cholestasis
• Leak of the entero-enterostomy
• Chyle leak
• Surgical site infection
Systemic Complications
• Pneumonia
• Acute kidney failure
• Catheter infection/sepsis
• Endocrine pancreatic failure with newly onset or deteriorating diabetes mellitus
• Hypoglycemia in case of insulin overdosing and insufcient oral intake
• Exocrine pancreatic failure with bloating, abdominal pain, and malabsorption
Management of these complications is described in detail in other chapters of
this manual.
References
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4. Bockman DE, Buchler M, Malfertheiner P, Beger HG.Analysis of nerves in chronic pancreatitis. Gastroenterology. 1988;94(6):1459–69.
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head resection in chronic pancreatitis. Chirurg. 1980;51(5):303–7.
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18. Ratnayake CBB, Kamarajah SK, Loveday BPT, Nayar M, Oppong K, White S, etal. A network meta-analysis of surgery for chronic pancreatitis: impact on pain and quality of life. J
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19. Pezzilli R, Bini L, Fantini L, Baroni E, Campana D, Tomassetti P, et al. Quality of life in
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20. Kilburn DJ, Chiow AKH, Leung U, Siriwardhane M, Cavallucci DJ, Bryant R, etal. Early
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27. Koch M, Garden OJ, Padbury R, Rahbari NN, Adam R, Capussotti L, etal. Bile leakage after
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28. Traverso LW, Frey CF, Mayer K, Beger HG, Rau B, Schlosser W. Chronic pancreatitis. In:
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Chapter 10
Total Pancreatectomy withIslet Cell
Autotransplantation
JennyChang, RobertSimon, andR.MatthewWalsh
History/Introduction
The rst documented interest in total pancreatectomy dates from the late 1800s with
experiments on canines by Joseph von Mering and Oska Minkowski of Strasbourg
that demonstrated the lethality of the surgery due to severe hyperglycemia, as insulin was not available until 1922 [1]. Fifty years later, the rst successful human total
pancreatectomy was performed for hyperinsulinism by Dr. James Priestly at the
Mayo Clinic in 1944 [1, 2]. The revolutionary work of isolating and transplanting
islet cells in rodent and canine models turned into human trials of isolated islet
transplantation from cadaveric donors which paved the foundation for the rst
reported human total pancreatectomy with islet cell autotransplantation (TPIAT)
performed in 1977 by Dr. David Sutherland at the University of Minnesota [3, 4].
Specialized centers that perform TPIAT have evolved further with surgical innovation and improved outcomes.
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978- 3- 031- 78409- 5_10.
J. Chang · R. Simon · R. M. Walsh (*)
Department of General Surgery, Digestive Disease Institute, Cleveland Clinic,
Cleveland, OH, USA
e-mail: Changj7@ccf.org; walshm@ccf.org
Switzerland AG 2025
E. P. Ceppa et al. (eds.), The SAGES Manual of Evolving Techniques in
Pancreatic Surgery, https://doi.org/10.1007/978-3-031-78409-5_10
157© The Author(s), under exclusive license to Springer Nature
158
J. Chang et al.
Indications
Adults
The primary indications for TPIAT are intractable abdominal pain of visceral origin
due to chronic pancreatitis or recurrent acute pancreatitis leading to impaired quality of life. The decision for TPIAT vs. other surgical procedures is an individualized
one, based on the patient’s etiology, disease morphology, comorbidities including
diabetes, symptom burden, rate of disease progression, and thorough evaluation by
a multidisciplinary team [5]. Patients with a known hereditary cause of chronic or
recurrent acute pancreatitis such as alteration in the CFTR, SPINK1, and PRSS1
genes should be given special consideration as their disease is unlikely to remit and
affects the entire gland making other surgical options untenable, while subjecting
these patients to a lifetime risk of pancreatic cancer. Historically, TPIAT was considered after all other medical, endoscopic, and surgical therapies have failed.
Currently, an argument can be made for earlier intervention to prevent lower islet
cell yield from the brosis of ongoing pancreatitis or prior partial pancreatectomies.
Additionally, an improved pain response may occur with earlier intervention for
chronic pancreatitis, which is particularly inferred from experience in pediatric
patients. Central sensitization from recurrent inammation may permanently damage nociceptive neurons. Additionally, in those patients treated with chronic opioid
therapy, earlier intervention can help eliminate the possibility of opioid-induced
hyperalgesia, a lower threshold for pain that may be a consequence of a prolonged
duration of chronic pain, and can be extremely problematic in this era of opioid
crisis [5, 6].
Pediatrics
The indications for TPIAT in chronic pancreatitis are the same in children as in
adults. Children have distinct considerations, ranging from a high rate of idiopathic
and hereditary etiologies, small body size, higher caloric needs for growth, and
crucial psychosocial developmental periods. The largest series of pediatric TPIAT is
from the University of Minnesota, with an average age of 13.8year old [7].
In pediatric populations, the most common causes of chronic pancreatitis cannot
be altered because they include idiopathic and hereditary etiologies. Additional etiologies of chronic pancreatitis in children include trauma, congenital anatomic
variations including pancreatic divisum and annular pancreas. Of children with
hereditary etiologies, the lifetime estimated cumulative risk of pancreatic cancer is
up to 40–70% [8]. Therapeutic intervention, endoscopic or surgical, as described in
previous chapters should be considered when an accurate diagnosis has been established and signicant alterations in quality of life are noted, which often include
10 Total Pancreatectomy withIslet Cell Autotransplantation
159
disruptions in schooling. Early treatment to prevent opioid dependency is advisable
to avert impairment of growth and development.
Patient Selection
Pancreatitis Etiology andPreoperative Workup
A multidisciplinary team assessment of prospective candidates is ideal, and at our
center, this includes involvement of the primary treating physician, gastroenterologist, endocrinologist, surgeon, chronic pain anesthesiologist, and clinical psychologist specializing in chronic pain.
A careful history and understanding of the underlying etiology of CP is required.
Although the primary indication for TPIAT is pain relief, it is imperative to recognize that the degree of symptoms does not always correlate with morphologic
changes. Minimal change disease is a form of chronic pancreatitis where minimal
objective morphologic changes are notable, yet patients may report debilitating pain
affecting their quality of life.
Patients with chronic pancreatitis often undergo multiple radiographic studies
prior to presentation, variably including CT, MRI/MRCP, ERCP, and/or upper
EUS.These imaging modalities are crucial for evidence of neoplasm, demonstration of brosis (diffuse or localized), and anatomical considerations such as pancreatic ductal obstruction.
A key factor in selecting patients for TPIAT is assessing the extent of islet cell
dysfunction to predict future islet yields. There are varying prevalence estimates of
patients with diabetes from chronic pancreatitis, ranging from 25% to 80% [9].
Diabetic patients are still candidates for the operation, provided their beta cell mass
is sufcient to produce c-peptide. Evaluation of beta cell mass includes measurement of endogenous insulin production with the following labs: hemoglobin A1c
), fasting serum glucose, fasting plasma c-peptide levels, C-peptide with
(HbA
1c
arginine, fasting insulin levels, and glucose with mixed meal tolerance tests.
Pancreatic exocrine function is evaluated with fecal elastase for enzymatic
replacement to mitigate perioperative malnutrition. As portal hypertension and
hepatic disease are a relative contraindication for TPIAT, LFTs are required. In our
institution, prior liver transplant is not a contraindication for TPIAT.
Patients who have failed prior surgical intervention(s) are still candidates for
TPIAT, and studies have demonstrated that 10–20% of TPIAT patients have undergone prior pancreatic resection [10]. A prior Whipple procedure has not demonstrated a consequential decreased yield in islets, as most pancreatic islets are
concentrated in the body and tail [11]. However, because the method of islet isolation involves disruption of the main pancreatic duct, a prior lateral pancreaticojejunostomy or distal pancreatectomy will decrease up to 50% of the islet cell yield
[5, 11].
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J. Chang et al.
As one of the main indications for this procedure is pain, conrmation that the
pancreas represents the largest factor in the etiology of pain cannot be understated.
A retrograde epidural differential neuroaxial blockade is a diagnostic test that allows
differentiation of the visceral or non-visceral (centralized or somatosensory) origin
of chronic abdominal pain based on the patient’s response to injection of normal
saline then local anesthetic via an epidural [12, 13]. A celiac plexus block is not a
requirement prior to TPIAT, but can also be a useful therapeutic and diagnostic
adjunct to target the visceral afferent pain bers to the pancreas. At our institution,
each patient undergoes a thorough standardized evaluation of the patient’s pain,
mood, and function with a psychologist specializing in chronic pain. Psychosocial
factors such as pain catastrophizing, depression and anxiety, post-traumatic stress
disorder and unaddressed prior trauma, as well as ongoing litigation are predictors
of a chronic pain syndrome which is unlikely to remit after surgery, and therefore
must be addressed prior to continuing workup for TPIAT.
Contraindications
Contraindications to TPIAT include active alcohol abuse, which can be determined
by measurement of phosphatidylethanol (PEth), a direct alcohol biomarker with
nearly 100% sensitivity and detectability for up to 3weeks after consumption of
alcohol [14]. Other contraindications include illicit substance use excluding moderate uses of marijuana, poorly controlled psychiatric illness, litigation related to pain,
or the lack of support system that could impair the patient’s ability to adhere to the
complicated medical management including diabetes, pancreatic enzyme therapy,
and opioid pain medication taper. Additionally, current smoking is a contraindication, as it is associated with lower rates of insulin independence after TPIAT [15],
presumably due to brosis exacerbated by active habitual smoking in chronic pancreatitis and increased perioperative complications.
Because some acinar and ductal tissue is transplanted with islets, pancreatic cancer or precancerous lesions including IPMN is an absolute contraindication.
C-peptide negative diabetes and type 1 diabetes are contraindications to TPIAT
as these patients do not have adequate islet yield. However, these patients may be
candidates for a total pancreatectomy without islet cell autotransplantation.
Portal vein thrombosis, portal hypertension, or signicant liver diseases are contraindications due to the injection of islets into the portal system although research
into other islet repository sites, such as the peritoneal cavity, is ongoing.