Operative management of chronic pancreatitis: A review

Tillou, John; Tatum, Jacob A.; Jolissaint, Joshua S.; Strand, Daniel S.; Wang, Andrew Y.; Zaydfudim, Victor M.; Adams, Reid B.; Brayman, Kenneth L.

doi:10.1016/j.amjsurg.2017.03.004

“…Endoscopic sphincterotomy and/or stenting of the pancreas can assist in alleviating anatomical obstruction of the pancreas. There are a number of well‐described drainage procedures (eg, Frey procedure, Berger procedure, Berne procedure) that can alleviate anatomical abnormalities not amenable to endoscopic decompresion . Pancreatic resection can be an option in cases of a pancreatic mass, common bile duct obstruction, and previously failed drainage .…”

Section: Pancreatic Surgery and Effect On Nutritionmentioning

confidence: 99%

“…There are a number of well‐described drainage procedures (eg, Frey procedure, Berger procedure, Berne procedure) that can alleviate anatomical abnormalities not amenable to endoscopic decompresion . Pancreatic resection can be an option in cases of a pancreatic mass, common bile duct obstruction, and previously failed drainage . Importantly, there may be a need for postoperative pancreatic enzyme replacement and there is a risk of diabetes mellitus, depending on the extent of pancreatic resection.…”

Section: Pancreatic Surgery and Effect On Nutritionmentioning

confidence: 99%

Chronic Pancreatitis and Nutrition Therapy

O’Brien

¹

,

Omer

²

2019

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Chronic pancreatitis is a complex and irreversible disease of the pancreas and is associated with significant morbidity and mortality. Nutrition deficiencies in chronic pancreatitis are common and can be atypical in nature. As such, the management of these deficiencies can be individualized for patients. The aim of this review is to discuss the components of nutrition deficiencies in chronic pancreatitis, their management, and the current areas of research that are being explored. The clinical guidelines of major national and international societies were analyzed for recommendations on the nutrition management of chronic pancreatitis. The etiology of nutrition deficiencies in chronic pancreatitis is multifactorial and includes aspects of exocrine and/or endocrine dysfunction, significant abdominal pain, often persistent alcohol consumption, and increased metabolic activity. A large number of patients with nutrition deficiencies are underrecognized and undertreated. Although the majority of these patients can be managed by oral and pancreatic enzyme supplementation, some patients may require enteral tube feeding and, in rare cases, parenteral feeding. Current areas of research include the accurate identification of patients at risk for nutrition deficiencies, optimization of feeding regimens, and research into islet cell autotransplantation. (Nutr Clin Pract. 2019;34(suppl 1):S13-S26)

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“…The modified Puestow is least morbid and preserves the most pancreatic parenchyma but has only around 50% long-term pain relief. Total pancreatectomy is associated with a high rate of post-operative morbidity (40–50%) and results in brittle insulin-dependent diabetes that is especially challenging to manage 67 . Total pancreatectomy is rarely indicated for the treatment of CP and is reserved only for patients who failed previous surgical interventions, who have severe pain with complete exocrine and endocrine pancreatic failure, who meet IPMN criteria for resection 67 , or who have hereditary pancreatitis or familial pancreatic cancer as a prophylactic procedure for pancreatic cancer 68 .…”

Section: Clinical Features Of Chronic Pancreatitis and Their Managemementioning

confidence: 99%

“…Total pancreatectomy is associated with a high rate of post-operative morbidity (40–50%) and results in brittle insulin-dependent diabetes that is especially challenging to manage 67 . Total pancreatectomy is rarely indicated for the treatment of CP and is reserved only for patients who failed previous surgical interventions, who have severe pain with complete exocrine and endocrine pancreatic failure, who meet IPMN criteria for resection 67 , or who have hereditary pancreatitis or familial pancreatic cancer as a prophylactic procedure for pancreatic cancer 68 . Despite the relatively high morbidity and mortality of operative management of CP, nearly half of all patients with CP will eventually require some form of surgical intervention to treat chronic pain that is unmanageable via less-invasive means 69 – 71 .…”

Section: Clinical Features Of Chronic Pancreatitis and Their Managemementioning

confidence: 99%

Chronic pancreatitis: review and update of etiology, risk factors, and management

Pham

¹

,

Forsmark

²

2018

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Chronic pancreatitis is a syndrome involving inflammation, fibrosis, and loss of acinar and islet cells which can manifest in unrelenting abdominal pain, malnutrition, and exocrine and endocrine insufficiency. The Toxic-Metabolic, Idiopathic, Genetic, Autoimmune, Recurrent and Severe Acute Pancreatitis, Obstructive (TIGAR-O) classification system categorizes known causes and factors that contribute to chronic pancreatitis. Although determining disease etiology provides a framework for focused and specific treatments, chronic pancreatitis remains a challenging condition to treat owing to the often refractory, centrally mediated pain and the lack of consensus regarding when endoscopic therapy and surgery are indicated. Further complications incurred include both exocrine and endocrine pancreatic insufficiency, pseudocyst formation, bile duct obstruction, and pancreatic cancer. Medical treatment of chronic pancreatitis involves controlling pain, addressing malnutrition via the treatment of vitamin and mineral deficiencies and recognizing the risk of osteoporosis, and administering appropriate pancreatic enzyme supplementation and diabetic agents. Cornerstones in treatment include the recognition of pancreatic exocrine insufficiency and administration of pancreatic enzyme replacement therapy, support to cease smoking and alcohol consumption, consultation with a dietitian, and a systematic follow-up to assure optimal treatment effect.

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“…[ 2 ] The main pathological manifestation of CP is fibrosis of the pancreas, which is due to the deposition of a large number of extracellular matrix. [ 3 ] In the past few years, the pathogenesis of pancreatic fibrosis has received increasing attention, along with the identification and characterization of pancreatic stellate cells (PSCs). [ 4 , 5 ] PSCs are the main source of extracellular matrix, and excessive activation of PSCs contributes to the development of pancreatic fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Thromboxane A2 receptor contributes to the activation of rat pancreatic stellate cells induced by 8-epi-prostaglandin F2α

Zhang

¹

,

Li

²

,

Cui

³

et al. 2020

Chinese Medical Journal

0

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Background Pancreatic stellate cells (PSCs) activation plays a critical role in the development of chronic pancreatitis. Previous studies confirmed that thromboxane A2 receptor (TxA 2 r) was overexpressed in activated PSCs in rats. The purpose of this study was to investigate the role of TxA 2 r in the activation of PSCs induced by 8-epi-prostaglandin F 2α (8-epi-PGF 2α ). Methods TxA 2 r expression in both quiescent and activated PSCs was detected by immunocytochemistry and immunoblot assay. Isolated PSCs were treated with 8-epi-PGF 2α (10 −6 , 10 −7 , 10 −8 mol/L) for 48 h, and SQ29548 (10 −4 , 10 −6 , and 10 −7 mol/L), a TxA 2 r-specific antagonist for 48 h, respectively, to identify the drug concentration with the best biological effect and the least cytotoxicity. Then isolated PSCs were treated with SQ29548 (10 −4 mol/L) for 2 h, followed by 10 −7 mol/L 8-epi-PGF 2α for 48 h. Real-time polymerase chain reaction was performed to detect the messenger RNA (mRNA) levels of α-smooth muscle actin (α-SMA) and collagen I. Comparisons between the groups were performed using Student's t test. Results TxA 2 r was up-regulated in activated PSCs in vitro compared with quiescent PSCs (all P < 0.001). Compared with the control group, different concentrations of 8-epi-PGF 2α significantly increased mRNA levels of α-SMA (10 −6 mol/L: 2.23 ± 0.18 vs. 1.00 ± 0.07, t = 10.70, P < 0.001; 10 −7 mol/L: 2.91 ± 0.29 vs. 1.01 ± 0.08, t = 10.83, P < 0.001; 10 −8 mol/L, 1.67 ± 0.07 vs. 1.00 ± 0.08, t = 11.40, P < 0.001) and collagen I (10 −6 mol/L: 2.68 ± 0.09 vs. 1.00 ± 0.07, t = 24.94, P < 0.001; 10 −7 mol/L: 2.12 ± 0.29 vs. 1.01 ± 0.12 , t = 6.08, P < 0.001; 10 −8 mol/L: 1.46 ± 0.15 vs. 1.00 ± 0.05, t = 4.93, P = 0.008). However, different concen...

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Operative management of chronic pancreatitis: A review

Cited by 30 publications

References 149 publications

Chronic Pancreatitis and Nutrition Therapy

Chronic Pancreatitis and Nutrition Therapy

Chronic pancreatitis: review and update of etiology, risk factors, and management

Thromboxane A2 receptor contributes to the activation of rat pancreatic stellate cells induced by 8-epi-prostaglandin F2α

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