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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_734_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Disclaimer
- •Contents
- •Contributors
- •Embryology
- •Lymphatics
- •Nerves
- •Clinically Relevant Anatomic Variations
- •Duodenum Inversum
- •Pancreas Divisum
- •Annular Pancreas
- •Ectopic Pancreas
- •Ansa Pancreatica
- •Pancreaticobiliary Maljunction
- •Duplication Anomalies
- •Physiology
- •Duodenal Physiology
- •Mechanical Function
- •Endocrine Function
- •Pancreatic Physiology
- •Exocrine Physiology
- •Normal Anatomy
- •Duodenal Anatomy
- •Pancreatic Anatomy
- •Ductal Anatomy
- •Vasculature
- •Endocrine Physiology
- •References
- •Etiology
- •Pathophysiology
- •Diagnosis
- •Clinical Presentation
- •Laboratory Tests
- •Imaging
- •Medical Management
- •Fluid Resuscitation
- •Analgesics
- •Prophylactic Antibiotics
- •Nutrition
- •Complications
- •Long-Term Sequelae of Acute Pancreatitis
- •References
- •Introduction
- •Initial Treatment
- •Reducing Severity of Acute Pancreatitis
- •Fluid Resuscitation
- •Pain Management
- •Nutrition
- •Preventing Infectious Complications
- •References
- •Introduction
- •Sterile Pancreatic Necrosis
- •Antibiotic Therapy
- •Catheter Drainage
- •Video-Assisted Retroperitoneal Drainage (VARD) Procedure
- •Sinus Tract Necrosectomy
- •Open Necrosectomy
- •Open Trans-Gastric Cystogastrostomy
- •Disconnected Distal Pancreatic Duct Syndrome
- •Introduction
- •References
- •Introduction
- •Venous Thrombosis
- •Intra-Abdominal Hypertension
- •Thoracic Complications
- •Gastrointestinal Complications
- •References
- •Pain
- •Endocrine Dysfunction
- •Exocrine Dysfunction
- •Conclusion
- •References
- •Background
- •Postoperative Care
- •References
- •Background
- •Head-Dominant Disease
- •Tail-Dominant Disease
- •Perioperative Management
- •Procedure Steps
- •Open Whipple
- •MIS Whipple
- •Open Distal Pancreatectomy
- •MIS Distal Pancreatectomy
- •Pearls
- •References
- •Introduction
- •Procedures
- •Indications
- •Contraindications
- •Preoperative Workup
- •Pediatrics
- •Patient Selection
- •Contraindications
- •Key Steps
- •Common Steps
- •Pitfalls/Tricks
- •Local Complications
- •Systemic Complications
- •References
- •History/Introduction
- •Indications
- •Adults
- •Procedural Aspects
- •Preoperative Care
- •Total Pancreatectomy
- •Islet Infusion
- •Minimally Invasive Surgery (MIS)
- •Postoperative Care
- •Outcomes
- •Perioperative Data
- •Perioperative Complications
- •Endocrine Function
- •References
- •Introduction
- •Duodenal Adenomas
- •Duodenal Adenocarcinomas
- •Duodenal Neuroendocrine Tumors (D-NETs)
- •Other Non-neoplastic Epithelial Lesions
- •Duodenal Gastrointestinal Stromal Tumors (DGISTs)
- •Leiomyoma
- •Lipoma
- •Choledochal Cysts
- •Duodenal Lymphoma
- •Conclusion
- •References
- •Introduction
- •Pre-procedural Considerations
- •Indications
- •Resection Techniques
- •Sporadic Non-ampullary Adenomas: Cold Snare Polypectomy
- •Sporadic Non-ampullary Adenomas: EMR
- •Sporadic Non-ampullary Adenomas: ESD
- •Sporadic Non-ampullary Adenomas: Full-Thickness Resection Device
- •Ampullary Adenomas: Endoscopic Papillectomy
- •Sporadic Non-ampullary Adenomas: Cold Snare Polypectomy
- •Sporadic Non-ampullary Adenomas: EMR
- •Endoscopic Papillectomy
- •Surveillance
- •References
- •Introduction
- •Benign Tumors
- •Genetic Syndromes
- •Pre-Malignant Tumors
- •Low-Grade Malignancies
- •Alternatives
- •Inclusion Criteria
- •Preoperative Planning
- •Open Transduodenal Ampullectomy
- •Minimally Invasive (Robotic-Assisted) Transduodenal Ampullectomy
- •Outcomes
- •Conclusions
- •References
- •Introduction
- •Anatomy
- •Laparoscopic Segmental Duodenectomy
- •Robotic Segmental Duodenectomy
- •Technique
- •Open Segmental Duodenectomy
- •Patient Positioning
- •Technique
- •Conclusion
- •References
- •Overview
- •Intraductal Papillary Mucinous Neoplasm (IPMN)
- •General Concepts
- •Novel Biomarkers
- •DNA-Based Biomarkers
- •MiRNA
- •Protein-Based Biomarkers
- •IPMNs
- •MCNs
- •SCNs
- •SPTs
- •Guidelines
- •Surveillance Discontinuation
- •Follow-Up Strategy
- •The Verona Policy
- •Conclusions
- •References
- •Introduction
- •Pathophysiology
- •Work-Up
- •Tissue Diagnosis
- •Serum Tumor Markers
- •Multidisciplinary Decision-Making
- •Adjuvant Trials
- •Systemic Chemotherapy
- •Chemoradiation
- •Neoadjuvant Trials
- •Chemotherapy
- •Chemoradiation
- •Pancreatectomy
- •Summary
- •References
- •Introduction
- •Diagnosis
- •Imaging
- •Functionality
- •Insulinoma
- •Gastrinoma
- •VIPoma
- •Glucagonoma
- •Staging/Surgical Decision-Making
- •Nonmetastatic Disease
- •Metastatic Disease
- •Multidisciplinary Decision-Making
- •Surgical Resection
- •Systemic Treatments
- •Open Trials
- •Surveillance
- •References
- •Renal Cell Carcinoma
- •Introduction/Epidemiology
- •Diagnosis/Radiology/Pathology
- •Treatment/Outcome
- •Colorectal Carcinoma
- •Introduction/Epidemiology
- •Diagnosis/Radiology/Pathology
- •Treatment/Prognosis
- •Melanoma
- •Introduction/Epidemiology
- •Diagnosis/Radiology/Pathology
- •Treatment/Prognosis
- •Sarcoma
- •Introduction/Epidemiology
- •Diagnosis/Radiology/Pathology
- •Treatment/Prognosis
- •Conclusion
- •References
- •Preoperative Considerations
- •Key Steps
- •Staging Laparoscopy
- •Specimen Removal
- •Vascular Resection
- •Reconstruction
- •Pancreaticojejunostomy
- •Hepaticojejunostomy
- •Gastro- or Duodeno-Jejunostomy
- •Final Steps
- •References
- •Randomized Controlled Trials
- •Surgical Technique
- •Resection Phase
- •Reconstruction Phase
- •Postoperative Course
- •Conclusions
- •References
- •Introduction
- •Preoperative Workup
- •Preoperative Planning
- •Surgical Management
- •Patient Preparation
- •Surgical Steps
- •Step 1: Kocher Maneuver
- •Step 4: Pancreatic Transection
- •Reconstruction
- •Hepaticojejunostomy
- •Pancreaticojejunostomy
- •Duodenojejunostomy
- •References
- •Introduction
- •Preoperative Planning
- •Diagnostic Laparoscopy
- •Radical Antegrade Modular Pancreatosplenectomy (RAMPS)
- •Splenic Vein Stump Length
- •Ligamentum Teres/Falciform Pedicle Flap
- •References
- •History
- •Early Exploration
- •Trends Over Time
- •Morbidity
- •Safety
- •Oncologic Safety
- •Preoperative Planning
- •Clinical Considerations
- •Anatomical Considerations
- •Surgical Technique
- •Conclusion
- •References
- •Introduction
- •Indications
- •Preoperative Testing
- •Operative Approach
- •Peritoneal Access
- •Specimen Extraction
- •Closure
- •Clinical Outcomes
- •Conclusions
- •References
- •Introduction
- •Preoperative Preparation
- •Key Shared Operative Steps
- •Trocar Placement
- •Splenic Flexure Mobilization
- •Pancreas Mobilization
- •Identify Pancreatic Pathology
- •Pancreatic Transection
- •Splenic Vein Dissection
- •Splenic Artery Dissection
- •Conclusion
- •References
- •Introduction
- •Historical Evolution
- •Perioperative Outcomes
- •Oncologic Outcomes
- •Neoadjuvant Therapy
- •Preoperative Adjuncts
- •Preoperative Coiling
- •Aortic Stenting
- •Robotic DP-CAR Surgical Technique
- •Positioning
- •Port Placement
- •Surgical Steps
- •Perioperative Care
- •Conclusion
- •References
- •Introduction
- •Preoperative Considerations
- •Laparoscopic Enucleation
- •Patient Positioning
- •Procedure
- •Robotic Enucleation
- •Patient Positioning
- •Procedure
- •Open Enucleation
- •Postoperative Management
- •Postoperative Outcomes
- •References
- •Introduction
- •Indications
- •Preoperative Assessment
- •Serologic Testing
- •Surgical Management
- •Patient Preparation
- •Diagnostic Laparoscopy
- •Surgical Steps
- •Step 1: Gastric Mobilization
- •Step 2: Pancreatic Resection
- •Step 3: Reconstruction
- •Jejunojejunostomy
- •Pancreaticojejunostomy
- •Discussion
- •References
- •Introduction
- •Biliary Obstruction
- •Endoscopic Interventions
- •Plastic Versus Metal Stents
- •Covered Versus Uncovered Metal Stents
- •Stent Obstruction
- •Surgical Options
- •Endoscopic Versus Surgical Intervention
- •Duodenal Obstruction
- •Duodenal Stents
- •Venting Percutaneous Gastrostomy Tubes (PEG)
- •Surgical Gastrojejunostomy (Duodenal Bypass)
- •Endoscopic Versus Surgical Intervention
- •Abdominal Pain
- •Celiac Plexus Neurolysis
- •Surgical Celiac Plexus Block
- •Summary
- •References

6 SAGES Manual: Chronic Pancreatitis–Classication andMedical Management
109
Psychiatric
interventions
Spinal cord
stimulation
Neurolytic therapy
Analgesia
(nonopioid, opioid,
antidepressants,
Fig. 6.1 Options for medical management of chronic pancreatitis, addressing pain, endocrine
dysfunction, exocrine dysfunction, and nutritional deciencies
Risk factor
modification
(smoking, alcohol)
Pancreatic enzyme
supplementation
Antioxidants
etc.)
of the most common etiologies for chronic pancreatitis and also leads to recurrent
episodes of acute pancreatitis [16]. Therefore, cessation of alcohol use is recommended in patients with chronic pancreatitis or those at risk for its development
caused by known genetic factors [15]. Similarly, smoking cessation is also recommended for these patients. While it was previously believed that the apparent link
between smoking and chronic pancreatitis was due to the confounding effect of
alcohol use, smoking has now been shown to be an independent risk factor for the
development of chronic pancreatitis as well as for episodes of acute pancreatitis
[17, 18].
Pain
Pain remains one of the most difcult symptoms to manage, especially in complicated disease processes like chronic pancreatitis, despite the availability of a wide
range of pain management options [15]. Pain signicantly impacts on patients’
quality of life, which can be improved by reducing the frequency and intensity of
attacks. Pain in patients with chronic pancreatitis can be caused by pancreatic
inammation, complications of the disease, or even neurogenic causes. Thus, medical management may need to be tailored to the individual patient and requires a
multimodal approach.

110
E. Hensler and S. Ayloo
The rst step in the treatment of pain due to chronic pancreatitis is pain assessment. Several pain severity assessment tools have been validated in patients with
chronic pancreatitis. The Brief Pain Inventory is one such tool and has been used in
patients with chronic pain from a wide range of causes, including chronic pancreatitis [19]. Although the Brief Pain Inventory does include an assessment of pain
severity, it also assesses how pain affects a patient’s mood, sleep, ability to work,
and relationships. This tool has been found to correlate well with the overall quality
of life in patients with chronic pancreatitis. The McGill Pain Questionnaire is
another tool that focuses on more than disease severity [20]. It uses descriptors of a
patient’s pain and asks the patient to choose from a list of words that apply to their
pain and then to further describe their pain as mild, moderate, or severe [21]. Most
of the pain descriptors are conventional words describing physical sensations, such
as sharp, stabbing, and cramping, but others address other aspects of pain, including
emotional responses, such as exhaustion, fear, cruelty, and sickening.
Quantitative sensory testing has also been used in patients with chronic pancreatitis to determine treatment effects [15]. Quantitative sensory testing involves the
presentation of standardized noxious stimuli to patients and the evaluation of their
responses. In patients with chronic pancreatitis, this method has allowed the comparison of treatment options and their effects on pain. For example, visceral pain is
better managed by oxycodone than by morphine [22], and pregabalin can reduce
patient hypersensitivity caused by central sensitization [23].
As described above, risk factor modication can be used as one facet of pain
management in patients with chronic pancreatitis [15]. Alcohol abstinence is associated with a reduction in frequency of acute pancreatitis episodes. Smoking also
correlates with an increase in acute episodes, but no studies have specically examined a link between smoking cessation and a reduction in pain in patients with
chronic pancreatitis.
Supplementation with pancreatic enzymes may also reduce pain. In healthy individuals, nutrient ingestion leads to secretion of cholecystokinin-releasing factor,
which stimulates the release of cholecystokinin, which triggers normal pancreatic
secretions. Some patients with chronic pancreatitis have an obstructed pancreatic
duct; thus, ongoing pancreatic secretion stimulated by nutrient ingestion is hypothesized to increase pressure in the duct, which causes pain. However, supplemental
pancreatic enzymes degrade cholecystokinin-releasing factor, preventing downstream pancreatic secretion. Several studies have shown a reduction in pain in
patients treated with tablets of supplemental pancreatic enzymes, whereas several
studies have shown no benet [24]. However, the studies that showed no benet
used capsules that may not have dissolved in the duodenum because of an acidprotective coating [15].
Antioxidant therapy has also been shown to reduce pain in patients with chronic
pancreatitis [25]. Specically, combination therapy with β-carotene, vitamins C and
E, selenium, and methionine leads to pain relief, whereas treatment with a single
antioxidant has no signicant benet [15]. Combination antioxidant therapy with
pregabalin has also been shown to reduce pain in patients who suffer from recurrent
pain despite endoscopic or surgical intervention [26].

6 SAGES Manual: Chronic Pancreatitis–Classication andMedical Management
More traditional pain management options also exist. The World Health
Organization provides a framework for escalation of pain management that was
initially developed for the management of chronic pain in cancer patients [27]. The
rst level uses nonopioid medications, including acetaminophen, ibuprofen, and
pregabalin. Antidepressants, which have been successfully used in patients with
pain from neuropathic causes, are also included in this level. The second level uses
weak opiates, such as tramadol or codeine, with or without the non-opiate medications from the rst level. The third level includes stronger opiate medications, such
as morphine, oxycodone, and methadone. Other medications such as octreotide,
ketamine, benzodiazepines, clonidine, cannabinoids, and antipsychotics are also
used as adjuvants at any level to assist in pain management.
Neurolytic therapy, such as a celiac plexus block, can also be used to control a
patient’s pain if other treatment options fail, but this is only a short-acting option
with a risk of side effects [15]. Spinal cord stimulators have also been studied in
patients with chronic pancreatitis, and most patients experiencing relief from pain
using this method [28]. However, this option is invasive and carries the risk of complications from placement in the spinal cord region [15]. Transcranial magnetic
stimulation has been studied as a treatment for depression in patients with chronic
pancreatitis and may also have some effect on pain levels [29]. Psychiatric interventions, such as cognitive behavioral therapy and hypnosis, have also been successfully used in the management of chronic pain, but there is minimal data for their use
in patients with chronic pancreatitis [15].
111
Endocrine Dysfunction
Endocrine dysfunction from chronic pancreatitis results in type 3c diabetes, also
known as pancreatogenic diabetes [30]. Patients with type 3c diabetes also have
impaired glucagon and pancreatic polypeptide secretion. This leads to low insulin
sensitivity in the liver, which then increases glucose production. Patients with type
3c diabetes from chronic pancreatitis tend to have more brittle diabetes than patients
with type 2 diabetes. The incidence of diabetes increases with the duration of
chronic pancreatitis, and diabetes is also more common in patients who have undergone pancreatectomy. Management of endocrine dysfunction in patients with
chronic pancreatitis requires close attention to nutrition and blood glucose levels.
Patients must be especially careful to avoid hypo- and hyperglycemic episodes.
Exocrine Dysfunction
Exocrine dysfunction from chronic pancreatitis is a result of the loss of the acinar
cells that normally produce pancreatic enzymes [30]. Steatorrhea is the hallmark of
pancreatic exocrine dysfunction and puts these patients at a high risk of fat-soluble

112
E. Hensler and S. Ayloo
vitamin deciencies and malnutrition. Steatorrhea occurs due to lipase deciency,
which leads to poor fat breakdown and malabsorption, therefore increasing fat
excretion in stool. Symptoms include fatty diarrhea, cramping, bloating, and atulence. It is important to note that subclinical exocrine dysfunction can also occur.
Exocrine dysfunction can be diagnosed in several ways. Lipase secretion following
hormone administration can be assessed by intubation of the duodenum, but this is
an invasive option. More commonly, levels of fecal fat or fecal elastase-1 are
measured.
The mainstay of treatment of exocrine dysfunction in patients with chronic pancreatitis is the replacement of pancreatic enzymes. Administration of these enzymes
to patients results in improved fat breakdown and reduced malabsorption, leading to
improved nutrition. As previously discussed, enzyme replacement may have the
added benet of pain reduction in this population. As the pancreas produces less
bicarbonate under conditions of chronic pancreatitis, patients may also require acidsuppression treatment in order to reduce denaturation of pancreatic enzymes. In
addition, enzyme replacement should be uptitrated as needed, as many patients may
be inadvertently undertreated.
It was previously believed that patients must have a loss of at least 90% of their
pancreatic function to exhibit signs of exocrine dysfunction [31], but the study that
this is based on compared only patients with severe symptoms of exocrine dysfunction with healthy controls. Therefore, this study may have missed important information from patients with milder symptoms or even subclinical dysfunction [30].
There may be a delay in the management of exocrine dysfunction in patients with
mild or subclinical exocrine dysfunction who may benet from enzyme replacement.
Nutritional Deciencies
Patients with chronic pancreatitis frequently suffer from nutritional deciencies
[30]. This can result from recurrent pain, ongoing alcoholism, and other gastrointestinal symptoms resulting from complications of the disease itself or medications
used to manage it. Patients may have reduced muscle mass [30] and can be underweight, with the authors of the COPPS system noting an inverse relationship
between BMI and severity of chronic pancreatitis [14]. Patients with chronic pancreatitis also suffer from osteopenia and osteoporosis as a result of low dietary vitamin D and calcium and chronic inammation.
Chronic pancreatitis can also lead to poor absorption of fat-soluble vitamins,
including vitamins A, D, E, and K, resulting in vitamin deciencies. The quantication of vitamin deciency incidence varies widely and has primarily focused on
laboratory-identied deciencies rather than clinically signicant deciencies.
Clinical manifestations of various vitamin deciencies in patients with chronic pancreatitis have been published as case reports [32–34], but the true incidence of signicant vitamin deciencies in patients with chronic pancreatitis is unknown [30].

6 SAGES Manual: Chronic Pancreatitis–Classication andMedical Management
113
Conclusion
Overall, chronic pancreatitis remains a challenge to classify and manage. While
several classication systems have been proposed, they focus on a wide range of
factors with varying degrees of clinical relevance, including imaging ndings, clinical symptoms, laboratory tests, etiology, etc. These classication systems are also
limited in that the majority have not been prospectively validated or tested in a
multi-institutional setting. In addition, many of these classication systems only
group patients with common ndings, without providing guidance on treatment or
prognosis. These limitations have likely contributed to the lack of a widely accepted
and utilized classication system for this disease process. Medical management of
chronic pancreatitis often requires a multi-pronged approach, targeting pain, endocrine dysfunction, exocrine dysfunction, and nutrition. Patients may present with
varying degrees of these symptoms, necessitating individualized treatment plans.
References
1. Rahman A, O’Connor DB, Gather F, Koscic S, Gilgan J, Mockler D, etal. Clinical classication and severity scoring systems in chronic pancreatitis: a systematic review. Dig Surg.
2020;37(3):181–91.
2. Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, etal. Classication of
acute pancreatitis—2012: revision of the Atlanta classication and denitions by international
consensus. Gut. 2013;62(1):102–11.
3. Blamey SL, Imrie CW, O’Neill J, Gilmour WH, Carter DC.Prognostic factors in acute pancreatitis. Gut. 1984;25(12):1340–6.
4. Ranson JH, Pasternack BS.Statistical methods for quantifying the severity of clinical acute
pancreatitis. J Surg Res. 1977;22(2):79–91.
5. Larvin M, McMahon MJ.APACHE-II score for assessment and monitoring of acute pancreatitis. Lancet. 1989;2(8656):201–5.
6. Sarles H.Revised classication of pancreatitis—Marseille 1984. Dig Dis Sci. 1985;30(6):573–4.
7. Sarner M, Cotton PB.Classication of pancreatitis. Gut. 1984;25(7):756–9.
8. Catalano MF, Sahai A, Levy M, Romagnuolo J, Wiersema M, Brugge W, etal. EUS-based
criteria for the diagnosis of chronic pancreatitis: the Rosemont classication. Gastrointest
Endosc. 2009;69(7):1251–61.
9. Etemad B, Whitcomb DC. Chronic pancreatitis: diagnosis, classication, and new genetic
developments. Gastroenterology. 2001;120(3):682–707.
10. Schneider A, Löhr JM, Singer MV.The M-ANNHEIM classication of chronic pancreatitis:
introduction of a unifying classication system based on a review of previous classications of
the disease. J Gastroenterol. 2007;42(2):101–19.
11. Bank S, Singh P, Pooran N.Proposal for a new grading system for chronic pancreatitis: the
ABC system. J Clin Gastroenterol. 2002;35(1):3–4.
12. Bagul A, Siriwardena AK.Evaluation of the Manchester classication system for chronic pancreatitis. Jop. 2006;7(4):390–6.
13. Büchler MW, Martignoni ME, Friess H, Malfertheiner P.A proposal for a new clinical classication of chronic pancreatitis. BMC Gastroenterol. 2009;9:93.

114
14. Beyer G, Mahajan UM, Budde C, Bulla TJ, Kohlmann T, Kuhlmann L, etal. Development and
validation of a chronic pancreatitis prognosis score in 2 independent cohorts. Gastroenterology.
2017;153(6):1544–54.e2.
15. Drewes AM, Bouwense SAW, Campbell CM, Ceyhan GO, Delhaye M, Demir IE,
et al. Guidelines for the understanding and management of pain in chronic pancreatitis.
Pancreatology. 2017;17(5):720–31.
16. Samokhvalov AV, Rehm J, Roerecke M. Alcohol consumption as a risk factor for acute
and chronic pancreatitis: a systematic review and a series of meta-analyses. EBioMedicine.
2015;2(12):1996–2002.
17. Maisonneuve P, Lowenfels AB, Müllhaupt B, Cavallini G, Lankisch PG, Andersen JR,
et al. Cigarette smoking accelerates progression of alcoholic chronic pancreatitis. Gut.
2005;54(4):510–4.
18. Yuhara H, Ogawa M, Kawaguchi Y, Igarashi M, Mine T.Smoking and risk for acute pancreatitis: a systematic review and meta-analysis. Pancreas. 2014;43(8):1201–7.
19. Olesen SS, Juel J, Nielsen AK, Frøkjær JB, Wilder-Smith OH, Drewes AM. Pain severity
reduces life quality in chronic pancreatitis: Implications for design of future outcome trials.
Pancreatology. 2014;14(6):497–502.
20. Seicean A, Grigorescu M, Tanţău M, Dumitraşcu DL, Pop D, Mocan T.Pain in chronic pancreatitis: assessment and relief through treatment. Rom J Gastroenterol. 2004;13(1):9–15.
21. Melzack R. The McGill Pain Questionnaire: major properties and scoring methods. Pain.
1975;1(3):277–99.
22. Staahl C, Dimcevski G, Andersen SD, Thorsgaard N, Christrup LL, Arendt-Nielsen L, etal.
Differential effect of opioids in patients with chronic pancreatitis: an experimental pain study.
Scand J Gastroenterol. 2007;42(3):383–90.
23. Bouwense SA, Olesen SS, Drewes AM, Poley JW, van Goor H, Wilder-Smith OH.Effects of
pregabalin on central sensitization in patients with chronic pancreatitis in a randomized, controlled trial. PLoS One. 2012;7(8):e42096.
24. Warshaw AL, Banks PA, Fernández-Del CC. AGA technical review: treatment of pain in
chronic pancreatitis. Gastroenterology. 1998;115(3):765–76.
25. Ahmed Ali U, Jens S, Busch OR, Keus F, van Goor H, Gooszen HG, etal. Antioxidants for
pain in chronic pancreatitis. Cochrane Database Syst Rev. 2014;(8):Cd008945.
26. Talukdar R, Lakhtakia S, Nageshwar Reddy D, Rao GV, Pradeep R, Banerjee R, et al.
Ameliorating effect of antioxidants and pregabalin combination in pain recurrence after ductal
clearance in chronic pancreatitis: results of a randomized, double blind, placebo-controlled
trial. J Gastroenterol Hepatol. 2016;31(9):1654–62.
27. Jadad AR, Browman GP.The WHO analgesic ladder for cancer pain management. Stepping up
the quality of its evaluation. JAMA. 1995;274(23):1870–3.
28. Kapural L, Cywinski JB, Sparks DA.Spinal cord stimulation for visceral pain from chronic
pancreatitis. Neuromodulation. 2011;14(5):423–6; discussion 6–7
29. Fregni F, Potvin K, Dasilva D, Wang X, Lenkinski RE, Freedman SD, etal. Clinical effects
and brain metabolic correlates in non-invasive cortical neuromodulation for visceral pain. Eur
J Pain. 2011;15(1):53–60.
30. Duggan SN.Negotiating the complexities of exocrine and endocrine dysfunction in chronic
pancreatitis. Proc Nutr Soc. 2017;76(4):484–94.
31. DiMagno EP, Go VL, Summerskill WH.Relations between pancreatic enzyme outputs and
malabsorption in severe pancreatic insufciency. N Engl J Med. 1973;288(16):813–5.
32. Yokota T, Tsuchiya K, Furukawa T, Tsukagoshi H, Miyakawa H, Hasumura Y. Vitamin E
deciency in acquired fat malabsorption. J Neurol. 1990;237(2):103–6.
33. Reynaert H, Debeuckelaere S, De Waele B, Meysman M, Goossens A, Devis G.The brown
bowel syndrome and gastrointestinal adenocarcinoma. Two complications of vitamin E deciency in celiac sprue and chronic pancreatitis? J Clin Gastroenterol. 1993;16(1):48–51.
34. Kurtulmus N, Yarman S, Tanakol R, Alagol F.Severe osteomalacia in a patient with idiopathic
chronic pancreatitis. Scott Med J. 2005;50(4):172–3.
E. Hensler and S. Ayloo

Chapter 7
Chronic Pancreatitis: Drainage Procedures
(Open Vs. MIS)
DhireshRohanJeyarajah andHoussamG.Osman
Background
In the West, chronic pancreatitis (CP) is mostly seen in patients with alcohol abuse
as well as smoking. However, CP can develop in patients for other reasons including
genetic predisposition (hereditary pancreatitis), tropical pancreatitis, and pancreas
divisum. It is important to note that biliary pancreatitis does not lead to CP in the
absence of disconnected pancreatic duct which can result in recurrent pancreatitis
attacks. The common end pathway is calcication of the gland itself, or stone formation within the pancreatic ducts, that do not allow for adequate drainage of the
exocrine function of the gland. This results in inammation, initially, and then a
cycle of scarring and brosis that can result in large duct or small duct obstruction.
There is associated irritation of the nerves in the retroperitoneum that results in a
dull, boring, and unrelenting pain that typically radiates to the back. This is truly
miserable for the patient and abstinence from alcohol or tobacco may improve some
of the inammatory changes but will not completely reverse it. This nerve pain can
be managed in many ways, mostly using a combination of NSAID, narcotic, and
nerve stabilizing agents such as gabapentin. Intervention with celiac ganglia blockade can be achieved with endoscopic ultrasound guidance or percutaneously.
Psychiatric medications may be needed to manage the anxiety and depression that
comes with chronic pain. Psychological tools, such as cognitive behavioral therapy
(CBP) or biofeedback, can be very helpful in providing coping strategies for the
patient with CP. It is imperative that the pancreatic surgeon have a working
D. R. Jeyarajah (*)
Department of Surgery, Methodist Health System, Dallas, TX, USA
Department of Surgery, TCU Burnett School of Medicine, Fort Worth, USA
e-mail: drj@tscsurgical.com
H. G. Osman
Department of Surgery, Methodist Health System, Dallas, TX, USA
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_7
115© The Author(s), under exclusive license to Springer Nature

116
D. R. Jeyarajah and H. G. Osman
knowledge of non-surgical management of chronic pain. One of the most common
issues with these CP patients is the lack of insight into management of their pain
syndrome. Unexperienced physicians will often withhold analgesics for patients
that have been on high doses of narcotics at home; weaning a patient from their pain
medications is not appropriate in the immediate postoperative period or during an
admission for an acute episode of pancreatitis.
Exocrine pancreatic insufciency (EPI) is a common and unrecognized issue
with patients with CP.The usual manifestation of greasy stools can be easily identied by the caring physician. However, many caregivers miss that increased gas,
bloating, and looser stools that oat may indeed be a manifestation of EPI. Aggressive
treatment of the EPI symptoms is essential in the CP patient. The authors will commonly nd that the bathroom that the EPI patient uses cannot be used by any family
member for days after the patient has used it! Such is the manifestation of fat malabsorption that makes stool smell so odious. The authors ask the patient to increase
their pancreatic enzymes until they reach constipation, and then back off slightly.
Constipation will occur when there is minimal fat content in the stool and is an easy
sign that the patient has reached a state of fat absorption. Conversely, eating a high
fat meal will require an increase in pancreatic enzyme supplementation. Many of
these patients need to gain weight and avoiding all fat will make this tough. Of
course, in the patient who has high triglycerides driving the CP process, the patient
must be on a triglyceride lowering agent and obey a low-fat diet. Many of these
patients will be diabetic also, and triglycerides will rise with blood sugar, making
blood sugar control a critical element to their CP management.
Associated with EPI is vitamin malabsorption and, much like the post bariatric
surgery patient, the CP patient must be watched carefully for vitamin deciencies.
The authors routinely place these patients on bariatric multivitamin replacement
and check bariatric labs on an ongoing basis.
Endocrine insufciency must also be watched carefully. The pancreatic surgeon
must have a working knowledge of the current state of diabetic management, especially a grasp of the several types of insulin on the market. The CP patient may have
delayed gastric emptying (DGE) based on pancreatic inammation and diabetes
mellitus (DM); one must use a fast-acting insulin in this case and evaluate glycemia
30min after the meal to ensure that the patient does not become hypoglycemic.
Questioning the patient regarding their “lows” will indicate how much glucagon
“window” is available from the native pancreas. This will give the surgeon an idea
of whether a total pancreatectomy will cause any disturbance to the existing glycemic control. The presence of signicant swings in blood sugar with low readings
frequently will tell the surgeon that the pancreas is effectively burnt out with lack of
both insulin and glucagon production. In this case, the authors are more likely to
consider total pancreatectomy. Understanding the severity of the patient’s DM will
help guide the pancreatic surgeon in selecting from the surgical options for therapy.
The holistic approach to the patient with CP is critical. The authors attempt to identify a single idea that captures what success looks like for each patient. This cannot
be a surgical measure of success, but rather a quality-of-life measure. For example,
the patient enjoys playing with their grandchildren and wishes that to be their main
aspect to return to after surgery. Returning to this activity would be the true endpoint
of success, not a surgical outcome per se.

7 Chronic Pancreatitis: Drainage Procedures (Open Vs. MIS)
117
Indications forSurgery intheCP Patient
As has been the case for decades, the indication for surgery in the CP patient remains
to treat pain or complications (e.g., bile duct obstruction, gastric outlet obstruction).
Drainage procedures will allow preservation of pancreatic parenchyma with its exocrine and endocrine function compared to surgical resection, but there is no good
data to support the suggestion that drainage procedures will allow for reversal of
EPI or endocrine already lost. As such, it is important that the pancreatic surgeon
counsel the patient and caregivers carefully with regard to the specic indication for
surgery. The authors are careful to be very specic in the expectations for resolution
of pain. In addition to the type of surgery performed, the pathophysiology of pain in
a specic patient and abstinence from alcohol and tobacco play a major role in pain
score improvement following surgery and duration of that improvement. The pain
relief will take months and the patient must be prepared for this slow weaning off
pain medications. This is a process that will be frustrating for all involved and clear
expectations must be laid out at the start of the surgery planning. The authors will
increase the dosing of gabapentin to 300mg TID to maximize non-narcotic effects
and nerve stabilizing effects. They will also add an SSRI, where appropriate, and try
to encourage the patient and family to seek counseling for non-pharmacologic measures that can be very helpful. Working with a pain management physician is very
helpful. However, this has become a real challenge as many anesthesia-pain management doctors have closed their practices in the private world. The surgeon who
deals with these patients must have a working knowledge of pain management.
Typically, the author will maximize non-narcotic medications. They will then add a
shorter acting narcotic and eventually ramp up to a long-acting agent (usually fentanyl patch that lasts for 3days with a constant level of drug), an intermediate acting
agent, such as oxycontin ER, which lasts for 12h, and a shorter acting agent that
will be used for breakthrough pain, such as hydrocodone. The plan for weaning will
be to gradually decrease the longest acting agent rst and gradually work down to
the short-acting agent. The aim is to gradually close the patients “pain gates” that
have been wide open for a while with their chronic pain. The patients are counseled
about the importance of quitting alcohol prior to surgical intervention. Smoking
cessation is paramount to successful outcome and is considered a requirement by
the authors prior to surgical intervention in CP patients.
A rare indication for surgery, but one that deserves some discussion, is the prevention of cancer. This can be an area of discussion for the hereditary pancreatitis
and the tropical pancreatitis patient. The authors are reticent to take a non-diabetic
patient and perform a total pancreatectomy. However, it is usual that the patients in
these group have brittle DM by the time that they ask for this discussion. The authors
have limited personal experience with total pancreatectomy in each of these groups.
When this has been performed, the patients follow the recovery of any total pancreatectomy patient.

118
D. R. Jeyarajah and H. G. Osman
Procedures andTechnical Details
Operative Approach forPancreatic Ductal Drainage
The patient that is well suited for a drainage procedure is one that has chronic pain
and a large, dilated main pancreatic duct (PD), but absence of inammatory pseudotumor in the pancreatic head, that is often the dominant morphologic abnormality
in CP. Pancreatic head inammatory masses may be accompanied by biliary or
duodenal obstruction, which also represent contraindications to a decompressive
surgical approach. In fact, drainage procedures are less invasive compared to resection and aim at simply decompressing a dilated PD but fail to tackle situations
where biliary or duodenal obstruction represents the “pacemaker,” propagating pain
development in the disease. The general thought in the choice of a drainage procedure is the presence of a PD greater than 7mm in size. However, the duct can always
be found even if smaller using several techniques that will be outlined below. A
patient with such a favorable duct is shown in Fig.7.1.
The most commonly performed decompressive procedures described in the literature include the Puestow procedure [1] and the Partington and Rochelle modication [2]. Both procedures include the transverse opening of the PD from tail to
body followed by a lateral pancreaticojejunostomy. The original Puestow procedure
also included pancreatic tail resection and splenectomy.
The Frey procedure (named for Charles Frey and rst described by Frey and
Smith) [3] is often referred to as a combined resection and drainage surgery but is
substantially a variant of the Puestow procedure and can be considered a drainage
procedure carried out more proximally to further decompress the PD.The primary
purpose of the local resection in the Frey procedure is not to remove the inamed
tissue from the pancreatic head, but rather to “core out” the pancreatic parenchyma,
which can improve the exposure of the proximal duct and facilitate the lateral
Fig. 7.1 Chronic
pancreatitis patient with
dilated pancreatic duct
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