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6 SAGES Manual: Chronic Pancreatitis–Classication andMedical 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 deciencies
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 difcult symptoms to manage, especially in compli­cated disease processes like chronic pancreatitis, despite the availability of a wide range of pain management options [15]. Pain signicantly 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 inammation, 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.
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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 modication 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 specically 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 benet [24]. However, the studies that showed no benet 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]. Specically, combination therapy with β-carotene, vitamins C and E, selenium, and methionine leads to pain relief, whereas treatment with a single antioxidant has no signicant benet [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–Classication andMedical 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
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vitamin deciencies and malnutrition. Steatorrhea occurs due to lipase deciency, 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 benet 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 benet from enzyme replacement.
Nutritional Deciencies
Patients with chronic pancreatitis frequently suffer from nutritional deciencies [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 inammation.
Chronic pancreatitis can also lead to poor absorption of fat-soluble vitamins, including vitamins A, D, E, and K, resulting in vitamin deciencies. The quantica­tion of vitamin deciency incidence varies widely and has primarily focused on laboratory-identied deciencies rather than clinically signicant deciencies. Clinical manifestations of various vitamin deciencies in patients with chronic pan­creatitis have been published as case reports [3234], but the true incidence of sig­nicant vitamin deciencies in patients with chronic pancreatitis is unknown [30].
6 SAGES Manual: Chronic Pancreatitis–Classication andMedical Management
113

Conclusion

Overall, chronic pancreatitis remains a challenge to classify and manage. While several classication 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 classication 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 classication 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 classication 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

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2. Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, etal. Classication of acute pancreatitis—2012: revision of the Atlanta classication and denitions 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 classication of pancreatitis—Marseille 1984. Dig Dis Sci. 1985;30(6):573–4.
7. Sarner M, Cotton PB.Classication of pancreatitis. Gut. 1984;25(7):756–9.
8. Catalano MF, Sahai A, Levy M, Romagnuolo J, Wiersema M, Brugge W, etal. EUS-based criteria for the diagnosis of chronic pancreatitis: the Rosemont classication. Gastrointest Endosc. 2009;69(7):1251–61.
9. Etemad B, Whitcomb DC. Chronic pancreatitis: diagnosis, classication, and new genetic developments. Gastroenterology. 2001;120(3):682–707.
10. Schneider A, Löhr JM, Singer MV.The M-ANNHEIM classication of chronic pancreatitis: introduction of a unifying classication system based on a review of previous classications 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 classication 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 clas­sication of chronic pancreatitis. BMC Gastroenterol. 2009;9:93.
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14. Beyer G, Mahajan UM, Budde C, Bulla TJ, Kohlmann T, Kuhlmann L, etal. 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, etal. 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, etal. 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, etal. 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 insufciency. N Engl J Med. 1973;288(16):813–5.
32. Yokota T, Tsuchiya K, Furukawa T, Tsukagoshi H, Miyakawa H, Hasumura Y. Vitamin E deciency 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 de­ciency 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)
DhireshRohanJeyarajah andHoussamG.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 calcication 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 inammation, 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 inammatory 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
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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 insufciency (EPI) is a common and unrecognized issue with patients with CP.The usual manifestation of greasy stools can be easily identi­ed 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 deciencies. The authors routinely place these patients on bariatric multivitamin replacement and check bariatric labs on an ongoing basis.
Endocrine insufciency 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 inammation and diabetes mellitus (DM); one must use a fast-acting insulin in this case and evaluate glycemia 30min 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 signicant 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 forSurgery intheCP 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 specic indication for surgery. The authors are careful to be very specic in the expectations for resolution of pain. In addition to the type of surgery performed, the pathophysiology of pain in a specic 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 300mg 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 3days with a constant level of drug), an intermediate acting agent, such as oxycontin ER, which lasts for 12h, 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.
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Procedures andTechnical Details
Operative Approach forPancreatic 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 inammatory pseu­dotumor in the pancreatic head, that is often the dominant morphologic abnormality in CP. Pancreatic head inammatory 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 7mm 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 modi­cation [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 inamed 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