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Surgery_Schwartz_9602 | Surgery_Schwartz | episodes (or a prolonged course) of pancreatic injury ultimately leads to chronic disease is widely accepted as the pathophysiologic sequence119 (Fig. 33-18).Although direct alcohol exposure to the pancreatic ductal system, or elevated levels of alcohol in the bloodstream, has been shown to alter the integrity and function of pancreatic ducts and acini directly,120 most investigators believe that alco-hol metabolites such as acetaldehyde, combined with oxidant injury, result in local parenchymal injury that is preferentially targeted to the pancreas in predisposed individuals. Repeated or severe episodes of toxin-induced injury activate a cascade of cytokines, which, in turn, induces pancreatic stellate cells (PSCs) to produce collagen and cause fibrosis (Fig. 33-19).A high-protein, low-bicarbonate, low-volume secretory output is seen after chronic alcohol exposure, which may con-tribute to the precipitation of proteins in secondary ducts in the early stages of chronic | Surgery_Schwartz. episodes (or a prolonged course) of pancreatic injury ultimately leads to chronic disease is widely accepted as the pathophysiologic sequence119 (Fig. 33-18).Although direct alcohol exposure to the pancreatic ductal system, or elevated levels of alcohol in the bloodstream, has been shown to alter the integrity and function of pancreatic ducts and acini directly,120 most investigators believe that alco-hol metabolites such as acetaldehyde, combined with oxidant injury, result in local parenchymal injury that is preferentially targeted to the pancreas in predisposed individuals. Repeated or severe episodes of toxin-induced injury activate a cascade of cytokines, which, in turn, induces pancreatic stellate cells (PSCs) to produce collagen and cause fibrosis (Fig. 33-19).A high-protein, low-bicarbonate, low-volume secretory output is seen after chronic alcohol exposure, which may con-tribute to the precipitation of proteins in secondary ducts in the early stages of chronic |
Surgery_Schwartz_9603 | Surgery_Schwartz | low-bicarbonate, low-volume secretory output is seen after chronic alcohol exposure, which may con-tribute to the precipitation of proteins in secondary ducts in the early stages of chronic pancreatitis.121 Calcium is complexed to protein plugs in small ductules, secondary ducts, and, eventu-ally, in the main ductal system, which causes ductal cell injury and obstruction of the secretory system, which further promotes an inflammatory response.Cigarette smoking has been strongly associated with chronic pancreatitis,122 but until recently it was unclear whether this was a causative risk factor. Studies have now shown that smoking actually accelerates the development of alcoholic pancreatitis,123 and the risk of cancer in chronic pancreatitis is increased significantly by smoking. In hereditary pancreatitis, smoking has been found to lower the age of onset of carcinoma by about 20 years.124 Smoking therefore appears to be an inde-pendent risk factor for the late complications of | Surgery_Schwartz. low-bicarbonate, low-volume secretory output is seen after chronic alcohol exposure, which may con-tribute to the precipitation of proteins in secondary ducts in the early stages of chronic pancreatitis.121 Calcium is complexed to protein plugs in small ductules, secondary ducts, and, eventu-ally, in the main ductal system, which causes ductal cell injury and obstruction of the secretory system, which further promotes an inflammatory response.Cigarette smoking has been strongly associated with chronic pancreatitis,122 but until recently it was unclear whether this was a causative risk factor. Studies have now shown that smoking actually accelerates the development of alcoholic pancreatitis,123 and the risk of cancer in chronic pancreatitis is increased significantly by smoking. In hereditary pancreatitis, smoking has been found to lower the age of onset of carcinoma by about 20 years.124 Smoking therefore appears to be an inde-pendent risk factor for the late complications of |
Surgery_Schwartz_9604 | Surgery_Schwartz | hereditary pancreatitis, smoking has been found to lower the age of onset of carcinoma by about 20 years.124 Smoking therefore appears to be an inde-pendent risk factor for the late complications of alcoholic pan-creatitis, if not an early cofactor for the development of fibrosis.HyperparathyroidismHypercalcemia is a known cause of pancreatic hypersecretion,125 and chronic hypercalcemia caused by untreated hyperparathyroidism is associated with chronic calcific pancreatitis.126 Hypercalcemia is also a stimulant for pancreatic calcium secretion, which contributes to calculus formation and obstructive pancreatopathy. The treatment is correction of the hyperparathyroidism and assessment of any additional endocrinopathies.HyperlipidemiaIn addition to the risk of acute pancreatitis, hyperlipidemia and hypertriglyceridemia predispose women to chronic pancreatitis when they receive estrogen replacement therapy.127 Fasting tri-glyceride levels <300 mg/dL are below the threshold for this to | Surgery_Schwartz. hereditary pancreatitis, smoking has been found to lower the age of onset of carcinoma by about 20 years.124 Smoking therefore appears to be an inde-pendent risk factor for the late complications of alcoholic pan-creatitis, if not an early cofactor for the development of fibrosis.HyperparathyroidismHypercalcemia is a known cause of pancreatic hypersecretion,125 and chronic hypercalcemia caused by untreated hyperparathyroidism is associated with chronic calcific pancreatitis.126 Hypercalcemia is also a stimulant for pancreatic calcium secretion, which contributes to calculus formation and obstructive pancreatopathy. The treatment is correction of the hyperparathyroidism and assessment of any additional endocrinopathies.HyperlipidemiaIn addition to the risk of acute pancreatitis, hyperlipidemia and hypertriglyceridemia predispose women to chronic pancreatitis when they receive estrogen replacement therapy.127 Fasting tri-glyceride levels <300 mg/dL are below the threshold for this to |
Surgery_Schwartz_9605 | Surgery_Schwartz | and hypertriglyceridemia predispose women to chronic pancreatitis when they receive estrogen replacement therapy.127 Fasting tri-glyceride levels <300 mg/dL are below the threshold for this to occur, and the mechanism of estrogen potentiation of hyperlip-idemia-induced chronic pancreatitis is unknown. It is assumed that chronic changes occur after repeated subclinical episodes of acute inflammation. Aggressive therapy of hyperlipidemia is therefore important in perior postmenopausal patients who are candidates for estrogen therapy.ClassificationA major impediment to a better understanding of the etiology, frequency, and severity of chronic pancreatitis has been the dif-ficulty with which investigators and clinicians have struggled to identify a useful classification system. Multiple classification systems have been proposed. The TIGAR-O scheme catego-rizes chronic pancreatitis according to risk factors and etiolo-gies, such as (a) toxic-metabolic, (b) idiopathic, (c) genetic, (d) | Surgery_Schwartz. and hypertriglyceridemia predispose women to chronic pancreatitis when they receive estrogen replacement therapy.127 Fasting tri-glyceride levels <300 mg/dL are below the threshold for this to occur, and the mechanism of estrogen potentiation of hyperlip-idemia-induced chronic pancreatitis is unknown. It is assumed that chronic changes occur after repeated subclinical episodes of acute inflammation. Aggressive therapy of hyperlipidemia is therefore important in perior postmenopausal patients who are candidates for estrogen therapy.ClassificationA major impediment to a better understanding of the etiology, frequency, and severity of chronic pancreatitis has been the dif-ficulty with which investigators and clinicians have struggled to identify a useful classification system. Multiple classification systems have been proposed. The TIGAR-O scheme catego-rizes chronic pancreatitis according to risk factors and etiolo-gies, such as (a) toxic-metabolic, (b) idiopathic, (c) genetic, (d) |
Surgery_Schwartz_9606 | Surgery_Schwartz | systems have been proposed. The TIGAR-O scheme catego-rizes chronic pancreatitis according to risk factors and etiolo-gies, such as (a) toxic-metabolic, (b) idiopathic, (c) genetic, (d) autoimmune, (e) recurrent and severe acute pancreatitis, or (f) obstructive.128 A recent classification system based on his-topathology as well as etiology was delineated by Singer and Chari.129Chronic Calcific (Lithogenic) PancreatitisThis type is the largest subgroup in the classification scheme proposed by Singer and Chari and includes patients with calcific pancreatitis of most etiologies. Although the majority of patients with calcific pancreatitis have a history of alcohol abuse, stone formation and parenchymal calcification can develop in a variety of etiologic subgroups; hereditary pancreatitis and tropical pan-creatitis are particularly noteworthy for the formation of stone disease. The clinician should therefore avoid the assumption that calcific pancreatitis confirms the diagnosis of alcohol | Surgery_Schwartz. systems have been proposed. The TIGAR-O scheme catego-rizes chronic pancreatitis according to risk factors and etiolo-gies, such as (a) toxic-metabolic, (b) idiopathic, (c) genetic, (d) autoimmune, (e) recurrent and severe acute pancreatitis, or (f) obstructive.128 A recent classification system based on his-topathology as well as etiology was delineated by Singer and Chari.129Chronic Calcific (Lithogenic) PancreatitisThis type is the largest subgroup in the classification scheme proposed by Singer and Chari and includes patients with calcific pancreatitis of most etiologies. Although the majority of patients with calcific pancreatitis have a history of alcohol abuse, stone formation and parenchymal calcification can develop in a variety of etiologic subgroups; hereditary pancreatitis and tropical pan-creatitis are particularly noteworthy for the formation of stone disease. The clinician should therefore avoid the assumption that calcific pancreatitis confirms the diagnosis of alcohol |
Surgery_Schwartz_9607 | Surgery_Schwartz | tropical pan-creatitis are particularly noteworthy for the formation of stone disease. The clinician should therefore avoid the assumption that calcific pancreatitis confirms the diagnosis of alcohol abuse.Brunicardi_Ch33_p1429-p1516.indd 145201/03/19 6:44 PM 1453PANCREASCHAPTER 33Normal pancreasAlcoholMetabolic / oxidative stressSentinel eventAcinar cell injury(+ / – Necrosis)Inflammatory response:proinflammatory(Early)Anti-inflammatory (Later)Alcoholmetabolic/oxidative stressRecurrent acute pancreatitis(RAP)Anti-inflammatoryFibrosisHealedStressRAPNormal (Recovered):Normal:Stellate cells(Inactive)CytokinesChronicpancreatitis:FibrosisEarly acutepancreatitis: NeutrophilLymphocyteMacrophageStellate cell(Active)Collagen, etc.Late acutepancreatitis:M(Anti-inflam-matory)Necrosis = Stress, ETOHxxxxxxxxxxxxxFigure 33-19. The sentinel acute pancreatitis event (SAPE) hypothesis for the development of chronic pancreatitis. A critical episode of acute pancreatitis activates cytokine-induced | Surgery_Schwartz. tropical pan-creatitis are particularly noteworthy for the formation of stone disease. The clinician should therefore avoid the assumption that calcific pancreatitis confirms the diagnosis of alcohol abuse.Brunicardi_Ch33_p1429-p1516.indd 145201/03/19 6:44 PM 1453PANCREASCHAPTER 33Normal pancreasAlcoholMetabolic / oxidative stressSentinel eventAcinar cell injury(+ / – Necrosis)Inflammatory response:proinflammatory(Early)Anti-inflammatory (Later)Alcoholmetabolic/oxidative stressRecurrent acute pancreatitis(RAP)Anti-inflammatoryFibrosisHealedStressRAPNormal (Recovered):Normal:Stellate cells(Inactive)CytokinesChronicpancreatitis:FibrosisEarly acutepancreatitis: NeutrophilLymphocyteMacrophageStellate cell(Active)Collagen, etc.Late acutepancreatitis:M(Anti-inflam-matory)Necrosis = Stress, ETOHxxxxxxxxxxxxxFigure 33-19. The sentinel acute pancreatitis event (SAPE) hypothesis for the development of chronic pancreatitis. A critical episode of acute pancreatitis activates cytokine-induced |
Surgery_Schwartz_9608 | Surgery_Schwartz | ETOHxxxxxxxxxxxxxFigure 33-19. The sentinel acute pancreatitis event (SAPE) hypothesis for the development of chronic pancreatitis. A critical episode of acute pancreatitis activates cytokine-induced transformation of pancreatic stellate cells, which results in collagen production and fibrosis. ETOH = ethyl alcohol. (Adapted with permission from Schneider A, Whitcomb DC: Hereditary pancreatitis: a model for inflammatory diseases of the pancreas, Best Pract Res Clin Gastroenterol. 2002 Jun;16(3):347-363.)Chronic Obstructive PancreatitisThis refers to chronic inflammatory changes that are caused by the compression or occlusion of the proximal ductal system by tumor, gallstone, posttraumatic scar, or inadequate duct caliber (as in pancreas divisum). Obstruction of the main pancreatic duct by inflammatory (posttraumatic) or neoplastic processes can result in diffuse fibrosis, dilated main and secondary pan-creatic ducts, and acinar atrophy. The patient may have little in | Surgery_Schwartz. ETOHxxxxxxxxxxxxxFigure 33-19. The sentinel acute pancreatitis event (SAPE) hypothesis for the development of chronic pancreatitis. A critical episode of acute pancreatitis activates cytokine-induced transformation of pancreatic stellate cells, which results in collagen production and fibrosis. ETOH = ethyl alcohol. (Adapted with permission from Schneider A, Whitcomb DC: Hereditary pancreatitis: a model for inflammatory diseases of the pancreas, Best Pract Res Clin Gastroenterol. 2002 Jun;16(3):347-363.)Chronic Obstructive PancreatitisThis refers to chronic inflammatory changes that are caused by the compression or occlusion of the proximal ductal system by tumor, gallstone, posttraumatic scar, or inadequate duct caliber (as in pancreas divisum). Obstruction of the main pancreatic duct by inflammatory (posttraumatic) or neoplastic processes can result in diffuse fibrosis, dilated main and secondary pan-creatic ducts, and acinar atrophy. The patient may have little in |
Surgery_Schwartz_9609 | Surgery_Schwartz | duct by inflammatory (posttraumatic) or neoplastic processes can result in diffuse fibrosis, dilated main and secondary pan-creatic ducts, and acinar atrophy. The patient may have little in Brunicardi_Ch33_p1429-p1516.indd 145301/03/19 6:44 PM 1454SPECIFIC CONSIDERATIONSPART IINormal pancreasAbsence of duct of SantoriniNormal pancreaswith duct of SantoriniPancreas divisumSmall ductof WirsungPancreas divisumNo duct of WirsungABCDFigure 33-20. Pancreas divisum. Normal pancreatic duct anatomy and the variations of partial or complete pancreas divisum are shown. (Reproduced with permission from Beger HG: The pancreas: an integrated textbook of basic science, medicine, and surgery. London: Blackwell-Science; 1998.)the way of pain symptoms or may present with signs of exo-crine insufficiency. Intraductal stone formation is rare, and both functional and structural abnormalities may improve when the obstructive process is relieved or removed. Trauma to the pan-creas frequently results in | Surgery_Schwartz. duct by inflammatory (posttraumatic) or neoplastic processes can result in diffuse fibrosis, dilated main and secondary pan-creatic ducts, and acinar atrophy. The patient may have little in Brunicardi_Ch33_p1429-p1516.indd 145301/03/19 6:44 PM 1454SPECIFIC CONSIDERATIONSPART IINormal pancreasAbsence of duct of SantoriniNormal pancreaswith duct of SantoriniPancreas divisumSmall ductof WirsungPancreas divisumNo duct of WirsungABCDFigure 33-20. Pancreas divisum. Normal pancreatic duct anatomy and the variations of partial or complete pancreas divisum are shown. (Reproduced with permission from Beger HG: The pancreas: an integrated textbook of basic science, medicine, and surgery. London: Blackwell-Science; 1998.)the way of pain symptoms or may present with signs of exo-crine insufficiency. Intraductal stone formation is rare, and both functional and structural abnormalities may improve when the obstructive process is relieved or removed. Trauma to the pan-creas frequently results in |
Surgery_Schwartz_9610 | Surgery_Schwartz | Intraductal stone formation is rare, and both functional and structural abnormalities may improve when the obstructive process is relieved or removed. Trauma to the pan-creas frequently results in duct injury and leakage, which may result in pseudocyst formation as well as local scar formation. Inadequately treated pancreatic trauma may result in persistent inflammatory changes in the distal gland.130Pancreas divisum represents a special case of obstruc-tive pancreatitis. It is the most common congenital anomaly involving the pancreas and occurs in up to 10% of children. It is thought to predispose the pancreas to recurrent acute pan-creatitis and chronic pancreatitis, due to functional obstruction of a diminutive duct of Santorini that fails to communicate with Wirsung’s duct (Fig. 33-20). However, the classic pic-ture of obstructive pancreatopathy with a dilated dorsal duct is unusual in pancreas divisum, so a decompressive opera-tion or a lesser papilla sphincteroplasty is | Surgery_Schwartz. Intraductal stone formation is rare, and both functional and structural abnormalities may improve when the obstructive process is relieved or removed. Trauma to the pan-creas frequently results in duct injury and leakage, which may result in pseudocyst formation as well as local scar formation. Inadequately treated pancreatic trauma may result in persistent inflammatory changes in the distal gland.130Pancreas divisum represents a special case of obstruc-tive pancreatitis. It is the most common congenital anomaly involving the pancreas and occurs in up to 10% of children. It is thought to predispose the pancreas to recurrent acute pan-creatitis and chronic pancreatitis, due to functional obstruction of a diminutive duct of Santorini that fails to communicate with Wirsung’s duct (Fig. 33-20). However, the classic pic-ture of obstructive pancreatopathy with a dilated dorsal duct is unusual in pancreas divisum, so a decompressive opera-tion or a lesser papilla sphincteroplasty is |
Surgery_Schwartz_9611 | Surgery_Schwartz | 33-20). However, the classic pic-ture of obstructive pancreatopathy with a dilated dorsal duct is unusual in pancreas divisum, so a decompressive opera-tion or a lesser papilla sphincteroplasty is frequently not fea-sible or unsuccessful. Endoscopic stenting through the lesser papilla may result in temporary relief of symptoms, and this response would increase the possibility that a permanent sur-gical or endoscopic intervention will be successful. Although some authors emphasize the pathologic implications of pan-creas divisum,131 others express skepticism that it represents a true risk to pancreatic secretory capacity or contributes to the development of chronic pancreatitis.132,133A recent French study reveals that pancreas divisum is equally prevalent among patients with idiopathic chronic pancreatitis and normal con-trols (7%), and is minimally increased in patients with PRSS1 and SPINK1 mutations. It is accompanied by CFTR mutations in 47% of patients, however, suggesting that | Surgery_Schwartz. 33-20). However, the classic pic-ture of obstructive pancreatopathy with a dilated dorsal duct is unusual in pancreas divisum, so a decompressive opera-tion or a lesser papilla sphincteroplasty is frequently not fea-sible or unsuccessful. Endoscopic stenting through the lesser papilla may result in temporary relief of symptoms, and this response would increase the possibility that a permanent sur-gical or endoscopic intervention will be successful. Although some authors emphasize the pathologic implications of pan-creas divisum,131 others express skepticism that it represents a true risk to pancreatic secretory capacity or contributes to the development of chronic pancreatitis.132,133A recent French study reveals that pancreas divisum is equally prevalent among patients with idiopathic chronic pancreatitis and normal con-trols (7%), and is minimally increased in patients with PRSS1 and SPINK1 mutations. It is accompanied by CFTR mutations in 47% of patients, however, suggesting that |
Surgery_Schwartz_9612 | Surgery_Schwartz | pancreatitis and normal con-trols (7%), and is minimally increased in patients with PRSS1 and SPINK1 mutations. It is accompanied by CFTR mutations in 47% of patients, however, suggesting that the presence of pancreas divisum together with mutational events may increase the susceptibility to pancreatitis.134Chronic Inflammatory PancreatitisChronic inflammatory pancreatitis is characterized by diffuse fibrosis and a loss of acinar elements with a predominant mono-nuclear cell infiltration throughout the gland.A variant of chronic pancreatitis is a nonobstructive, diffusely infiltrative disease associated with fibrosis, a mono-nuclear cell (lymphocyte, plasma cell, or eosinophil) infiltrate, and an increased titer of one or more autoantibodies.135 This type, referred to as autoimmune pancreatitis (AIP), is associated with a variety of illnesses with suspected or proven autoimmune etiology, such as Sjögren’s syndrome, rheumatoid arthritis, and type 1 diabetes mellitus. AIP has been | Surgery_Schwartz. pancreatitis and normal con-trols (7%), and is minimally increased in patients with PRSS1 and SPINK1 mutations. It is accompanied by CFTR mutations in 47% of patients, however, suggesting that the presence of pancreas divisum together with mutational events may increase the susceptibility to pancreatitis.134Chronic Inflammatory PancreatitisChronic inflammatory pancreatitis is characterized by diffuse fibrosis and a loss of acinar elements with a predominant mono-nuclear cell infiltration throughout the gland.A variant of chronic pancreatitis is a nonobstructive, diffusely infiltrative disease associated with fibrosis, a mono-nuclear cell (lymphocyte, plasma cell, or eosinophil) infiltrate, and an increased titer of one or more autoantibodies.135 This type, referred to as autoimmune pancreatitis (AIP), is associated with a variety of illnesses with suspected or proven autoimmune etiology, such as Sjögren’s syndrome, rheumatoid arthritis, and type 1 diabetes mellitus. AIP has been |
Surgery_Schwartz_9613 | Surgery_Schwartz | (AIP), is associated with a variety of illnesses with suspected or proven autoimmune etiology, such as Sjögren’s syndrome, rheumatoid arthritis, and type 1 diabetes mellitus. AIP has been characterized as either type I, with accompanying systemic or multiorgan dysfunction, or type II, which is restricted to the pancreas.Compressive stenosis of the intrapancreatic portion of the common bile duct is frequently seen in both types of AIP, along with symptoms of obstructive jaundice. Increased levels of serum β-globulin or immunoglobulin G4 are also present. Steroid therapy is uniformly successful in ameliorating the dis-ease, including any associated bile duct compression.136 CFTR mutations that result in dislocation of the transmembrane pro-tein have been found in AIP, and steroid therapy results in a nor-malization of the CFTR localization and a resumption of normal chloride and bicarbonate secretion.137 The differential diagnosis includes lymphoma, plasmacytoma (“pseudotumor” of the | Surgery_Schwartz. (AIP), is associated with a variety of illnesses with suspected or proven autoimmune etiology, such as Sjögren’s syndrome, rheumatoid arthritis, and type 1 diabetes mellitus. AIP has been characterized as either type I, with accompanying systemic or multiorgan dysfunction, or type II, which is restricted to the pancreas.Compressive stenosis of the intrapancreatic portion of the common bile duct is frequently seen in both types of AIP, along with symptoms of obstructive jaundice. Increased levels of serum β-globulin or immunoglobulin G4 are also present. Steroid therapy is uniformly successful in ameliorating the dis-ease, including any associated bile duct compression.136 CFTR mutations that result in dislocation of the transmembrane pro-tein have been found in AIP, and steroid therapy results in a nor-malization of the CFTR localization and a resumption of normal chloride and bicarbonate secretion.137 The differential diagnosis includes lymphoma, plasmacytoma (“pseudotumor” of the |
Surgery_Schwartz_9614 | Surgery_Schwartz | results in a nor-malization of the CFTR localization and a resumption of normal chloride and bicarbonate secretion.137 The differential diagnosis includes lymphoma, plasmacytoma (“pseudotumor” of the pan-creas) and diffuse infiltrative carcinoma. Although the diagnosis is confirmed on pancreatic biopsy, presumptive treatment with steroids is usually undertaken, especially when clinical and lab-oratory findings, such as an elevation in IgG4 levels, support the diagnosis. Failure to obtain a cytologic specimen may lead to an unnecessary resectional procedure, and an untreated inflam-matory component may cause sclerosis of the extrahepatic or intrahepatic bile ducts, with eventual liver failure.138Brunicardi_Ch33_p1429-p1516.indd 145401/03/19 6:44 PM 1455PANCREASCHAPTER 33Tropical (Nutritional) PancreatitisChronic pancreatitis is highly prevalent among adolescents and young adults in Indonesia, southern India, and tropical Africa. Abdominal pain develops in adolescence, followed by | Surgery_Schwartz. results in a nor-malization of the CFTR localization and a resumption of normal chloride and bicarbonate secretion.137 The differential diagnosis includes lymphoma, plasmacytoma (“pseudotumor” of the pan-creas) and diffuse infiltrative carcinoma. Although the diagnosis is confirmed on pancreatic biopsy, presumptive treatment with steroids is usually undertaken, especially when clinical and lab-oratory findings, such as an elevation in IgG4 levels, support the diagnosis. Failure to obtain a cytologic specimen may lead to an unnecessary resectional procedure, and an untreated inflam-matory component may cause sclerosis of the extrahepatic or intrahepatic bile ducts, with eventual liver failure.138Brunicardi_Ch33_p1429-p1516.indd 145401/03/19 6:44 PM 1455PANCREASCHAPTER 33Tropical (Nutritional) PancreatitisChronic pancreatitis is highly prevalent among adolescents and young adults in Indonesia, southern India, and tropical Africa. Abdominal pain develops in adolescence, followed by |
Surgery_Schwartz_9615 | Surgery_Schwartz | PancreatitisChronic pancreatitis is highly prevalent among adolescents and young adults in Indonesia, southern India, and tropical Africa. Abdominal pain develops in adolescence, followed by the development of a brittle form of pancreatogenic diabetes. Parenchymal and intraductal calcifications are seen, and the pancreatic duct stones may be quite large.139 Many of the patients appear malnourished, some present with extreme emaciation, and a characteristic cyanotic coloration of the lips may be seen.140 In addition to protein-caloric malnutrition, toxic products of some indigenous foodstuffs have also been thought to contribute to the disease. Because of the geographic concentration of this early-onset form of chronic pancreatitis, it has been termed tropical pancreatitis, although the exact etiology remains unclear.Clinically, tropical pancreatitis presents much like heredi-tary pancreatitis, and a familial pattern among cases is not unusual. SPINK1 mutations have been documented in | Surgery_Schwartz. PancreatitisChronic pancreatitis is highly prevalent among adolescents and young adults in Indonesia, southern India, and tropical Africa. Abdominal pain develops in adolescence, followed by the development of a brittle form of pancreatogenic diabetes. Parenchymal and intraductal calcifications are seen, and the pancreatic duct stones may be quite large.139 Many of the patients appear malnourished, some present with extreme emaciation, and a characteristic cyanotic coloration of the lips may be seen.140 In addition to protein-caloric malnutrition, toxic products of some indigenous foodstuffs have also been thought to contribute to the disease. Because of the geographic concentration of this early-onset form of chronic pancreatitis, it has been termed tropical pancreatitis, although the exact etiology remains unclear.Clinically, tropical pancreatitis presents much like heredi-tary pancreatitis, and a familial pattern among cases is not unusual. SPINK1 mutations have been documented in |
Surgery_Schwartz_9616 | Surgery_Schwartz | etiology remains unclear.Clinically, tropical pancreatitis presents much like heredi-tary pancreatitis, and a familial pattern among cases is not unusual. SPINK1 mutations have been documented in 20% to 55% of patients with tropical pancreatitis, and CFTR mutations have been reported as well.106,107 The accelerated deteriora-tion of endocrine and exocrine function, the chronic pain due to obstructive disease, and the recurrence of symptoms despite decompressive procedures characterize the course of disease. As immigrants from the tropical regions increasingly find their way to all parts of the world, an awareness of this severe form of chronic pancreatitis is helpful for those who treat patients with pancreatic disease.Asymptomatic Pancreatic FibrosisPancreatic fibrosis is seen in some asymptomatic elderly patients, in tropical populations, or in asymptomatic alcohol users. There is diffuse perilobar fibrosis and a loss of acinar cell mass, but there is not a main ductular component. | Surgery_Schwartz. etiology remains unclear.Clinically, tropical pancreatitis presents much like heredi-tary pancreatitis, and a familial pattern among cases is not unusual. SPINK1 mutations have been documented in 20% to 55% of patients with tropical pancreatitis, and CFTR mutations have been reported as well.106,107 The accelerated deteriora-tion of endocrine and exocrine function, the chronic pain due to obstructive disease, and the recurrence of symptoms despite decompressive procedures characterize the course of disease. As immigrants from the tropical regions increasingly find their way to all parts of the world, an awareness of this severe form of chronic pancreatitis is helpful for those who treat patients with pancreatic disease.Asymptomatic Pancreatic FibrosisPancreatic fibrosis is seen in some asymptomatic elderly patients, in tropical populations, or in asymptomatic alcohol users. There is diffuse perilobar fibrosis and a loss of acinar cell mass, but there is not a main ductular component. |
Surgery_Schwartz_9617 | Surgery_Schwartz | elderly patients, in tropical populations, or in asymptomatic alcohol users. There is diffuse perilobar fibrosis and a loss of acinar cell mass, but there is not a main ductular component. In addition, the presence of fibrosis and decreased exocrine function in patients with diabetes has raised the question of whether long-standing diabetes is a cause of chronic pancreatitis.141 Patients with this entity are usually asymptomatic in terms of typical pancreatic pain, and a recent histopathologic study of patients with typi-cal chronic pancreatitis and “diabetic exocrine pancreatopathy” reveals significant differences in morphology, including a virtual absence of duct distortion or obstruction (Fig. 33-21).142 It remains unknown whether this form of chronic inflammation precedes or contributes to the roughly twofold increase in the risk of pancreatic cancer in patients with long-standing diabetes.Idiopathic PancreatitisWhen a definable cause for chronic pancreatitis is lacking, the term | Surgery_Schwartz. elderly patients, in tropical populations, or in asymptomatic alcohol users. There is diffuse perilobar fibrosis and a loss of acinar cell mass, but there is not a main ductular component. In addition, the presence of fibrosis and decreased exocrine function in patients with diabetes has raised the question of whether long-standing diabetes is a cause of chronic pancreatitis.141 Patients with this entity are usually asymptomatic in terms of typical pancreatic pain, and a recent histopathologic study of patients with typi-cal chronic pancreatitis and “diabetic exocrine pancreatopathy” reveals significant differences in morphology, including a virtual absence of duct distortion or obstruction (Fig. 33-21).142 It remains unknown whether this form of chronic inflammation precedes or contributes to the roughly twofold increase in the risk of pancreatic cancer in patients with long-standing diabetes.Idiopathic PancreatitisWhen a definable cause for chronic pancreatitis is lacking, the term |
Surgery_Schwartz_9618 | Surgery_Schwartz | to the roughly twofold increase in the risk of pancreatic cancer in patients with long-standing diabetes.Idiopathic PancreatitisWhen a definable cause for chronic pancreatitis is lacking, the term idiopathic is used to categorize the illness. Classically, the idiopathic group includes young adults and adolescents who lack a family history of pancreatitis but who may represent indi-viduals with spontaneous gene mutations encoding regulatory proteins in the pancreas. A variable percentage of SPINK1 and CFTR mutations have been described in various studies. In addi-tion, the idiopathic group has included a large number of older patients for whom no obvious cause of recurrent or chronic pan-creatitis can be found.143 However, because the prevalence of biliary calculi increases steadily with age, it is not surprising that, as methods of biliary stone detection have improved, many elderly “idiopathic” pancreatitis patients are found to have bili-ary tract disease.144An increasing number of | Surgery_Schwartz. to the roughly twofold increase in the risk of pancreatic cancer in patients with long-standing diabetes.Idiopathic PancreatitisWhen a definable cause for chronic pancreatitis is lacking, the term idiopathic is used to categorize the illness. Classically, the idiopathic group includes young adults and adolescents who lack a family history of pancreatitis but who may represent indi-viduals with spontaneous gene mutations encoding regulatory proteins in the pancreas. A variable percentage of SPINK1 and CFTR mutations have been described in various studies. In addi-tion, the idiopathic group has included a large number of older patients for whom no obvious cause of recurrent or chronic pan-creatitis can be found.143 However, because the prevalence of biliary calculi increases steadily with age, it is not surprising that, as methods of biliary stone detection have improved, many elderly “idiopathic” pancreatitis patients are found to have bili-ary tract disease.144An increasing number of |
Surgery_Schwartz_9619 | Surgery_Schwartz | it is not surprising that, as methods of biliary stone detection have improved, many elderly “idiopathic” pancreatitis patients are found to have bili-ary tract disease.144An increasing number of mutations of the SPINK1 and CFTR genes have been identified in association with various forms of chronic pancreatitis. However, the role of genetic analysis in the management of these patients remains unclear, as guidelines have yet to be developed to allow physicians to use the data consistently. Although the clinical management of patients who harbor a minor CFTR mutation and chronic pan-creatitis, for example, is still dictated by the clinical manifesta-tions of the pancreatitis, recent data suggest that the etiology of chronic pancreatitis, rather than the morphology, may determine the response to surgical treatment.145A shortcoming of these clinical classification systems is the lack of histologic criteria of chronic inflammation due to the usual absence of a biopsy specimen. The | Surgery_Schwartz. it is not surprising that, as methods of biliary stone detection have improved, many elderly “idiopathic” pancreatitis patients are found to have bili-ary tract disease.144An increasing number of mutations of the SPINK1 and CFTR genes have been identified in association with various forms of chronic pancreatitis. However, the role of genetic analysis in the management of these patients remains unclear, as guidelines have yet to be developed to allow physicians to use the data consistently. Although the clinical management of patients who harbor a minor CFTR mutation and chronic pan-creatitis, for example, is still dictated by the clinical manifesta-tions of the pancreatitis, recent data suggest that the etiology of chronic pancreatitis, rather than the morphology, may determine the response to surgical treatment.145A shortcoming of these clinical classification systems is the lack of histologic criteria of chronic inflammation due to the usual absence of a biopsy specimen. The |
Surgery_Schwartz_9620 | Surgery_Schwartz | response to surgical treatment.145A shortcoming of these clinical classification systems is the lack of histologic criteria of chronic inflammation due to the usual absence of a biopsy specimen. The differentiation of recurrent acute pancreatitis from chronic pancreatitis with exac-erbations of pain can be difficult to establish and is not facili-tated by the current system. Similarly, cystic fibrosis is known to cause fibrosis and acinar dysfunction but is not included in the classification despite increasing evidence for its possible role in idiopathic chronic pancreatitis.146 Therefore, further refinements in the classification system for chronic pancreatitis Interacinarfibrosis0102030405060708090100AcinaratrophyInterlobularfibrosisStromalinflammationDuctaldistortionDuctalepithelialattenuationIslet amyloidCPDEPFigure 33-21. Comparative frequencies of key histolopathologic features of chronic pancreatitis (CP n = 7) and diabetic exocrine pancrea-topathy (DEP n = 9) (Reproduced with | Surgery_Schwartz. response to surgical treatment.145A shortcoming of these clinical classification systems is the lack of histologic criteria of chronic inflammation due to the usual absence of a biopsy specimen. The differentiation of recurrent acute pancreatitis from chronic pancreatitis with exac-erbations of pain can be difficult to establish and is not facili-tated by the current system. Similarly, cystic fibrosis is known to cause fibrosis and acinar dysfunction but is not included in the classification despite increasing evidence for its possible role in idiopathic chronic pancreatitis.146 Therefore, further refinements in the classification system for chronic pancreatitis Interacinarfibrosis0102030405060708090100AcinaratrophyInterlobularfibrosisStromalinflammationDuctaldistortionDuctalepithelialattenuationIslet amyloidCPDEPFigure 33-21. Comparative frequencies of key histolopathologic features of chronic pancreatitis (CP n = 7) and diabetic exocrine pancrea-topathy (DEP n = 9) (Reproduced with |
Surgery_Schwartz_9621 | Surgery_Schwartz | amyloidCPDEPFigure 33-21. Comparative frequencies of key histolopathologic features of chronic pancreatitis (CP n = 7) and diabetic exocrine pancrea-topathy (DEP n = 9) (Reproduced with permission from Majumder S, Zhang L, Philip N, et al. Exocrine Pancreatopathy (EP) Associated With Diabetes Mellitus (DM) Is Histologically Distinct From Chronic Pancreatitis (CP): An International Multi-Reader Blinded Study, Gastroenterol 2016 April;150(4) Suppl 1: S191 (abstr).)Brunicardi_Ch33_p1429-p1516.indd 145501/03/19 6:44 PM 1456SPECIFIC CONSIDERATIONSPART IIFigure 33-22. Histology of early chronic pancreatitis. High-power microscopic (40x) histology of chronic pancreatitis shows an infil-tration of mononuclear inflammatory cells throughout the inter-stitium of the pancreas, with little fibrosis. (Used with permission from Rhonda Yantiss, Weill Cornell Medical College.)Figure 33-23. Gross appearance of chronic pancreatitis. Areas of fibrosis and scarring are seen adjacent to other areas | Surgery_Schwartz. amyloidCPDEPFigure 33-21. Comparative frequencies of key histolopathologic features of chronic pancreatitis (CP n = 7) and diabetic exocrine pancrea-topathy (DEP n = 9) (Reproduced with permission from Majumder S, Zhang L, Philip N, et al. Exocrine Pancreatopathy (EP) Associated With Diabetes Mellitus (DM) Is Histologically Distinct From Chronic Pancreatitis (CP): An International Multi-Reader Blinded Study, Gastroenterol 2016 April;150(4) Suppl 1: S191 (abstr).)Brunicardi_Ch33_p1429-p1516.indd 145501/03/19 6:44 PM 1456SPECIFIC CONSIDERATIONSPART IIFigure 33-22. Histology of early chronic pancreatitis. High-power microscopic (40x) histology of chronic pancreatitis shows an infil-tration of mononuclear inflammatory cells throughout the inter-stitium of the pancreas, with little fibrosis. (Used with permission from Rhonda Yantiss, Weill Cornell Medical College.)Figure 33-23. Gross appearance of chronic pancreatitis. Areas of fibrosis and scarring are seen adjacent to other areas |
Surgery_Schwartz_9622 | Surgery_Schwartz | (Used with permission from Rhonda Yantiss, Weill Cornell Medical College.)Figure 33-23. Gross appearance of chronic pancreatitis. Areas of fibrosis and scarring are seen adjacent to other areas within the gland in which the lobar architecture is grossly preserved. A dilated pancreatic duct indicates the presence of downstream obstruction in this specimen removed from a patient with chronic pancreatitis. (Used with permis-sion from Rhonda Yantiss, Weill Cornell Medical College.)Figure 33-24. Histology of severe chronic pancreatitis. High-power microscopic (40x) histologic appearance of advanced chronic pancre-atitis shows extensive sheets of fibrosis and loss of acinar tissue, with preservation of islet tissue in scattered areas. (Used with permission from Rhonda Yantiss, Weill Cornell Medical College.)are needed to allow a better prediction of its clinical course and a more accurate diagnosis of a likely etiologic agent.PathologyHistology. In early chronic pancreatitis, the histologic | Surgery_Schwartz. (Used with permission from Rhonda Yantiss, Weill Cornell Medical College.)Figure 33-23. Gross appearance of chronic pancreatitis. Areas of fibrosis and scarring are seen adjacent to other areas within the gland in which the lobar architecture is grossly preserved. A dilated pancreatic duct indicates the presence of downstream obstruction in this specimen removed from a patient with chronic pancreatitis. (Used with permis-sion from Rhonda Yantiss, Weill Cornell Medical College.)Figure 33-24. Histology of severe chronic pancreatitis. High-power microscopic (40x) histologic appearance of advanced chronic pancre-atitis shows extensive sheets of fibrosis and loss of acinar tissue, with preservation of islet tissue in scattered areas. (Used with permission from Rhonda Yantiss, Weill Cornell Medical College.)are needed to allow a better prediction of its clinical course and a more accurate diagnosis of a likely etiologic agent.PathologyHistology. In early chronic pancreatitis, the histologic |
Surgery_Schwartz_9623 | Surgery_Schwartz | College.)are needed to allow a better prediction of its clinical course and a more accurate diagnosis of a likely etiologic agent.PathologyHistology. In early chronic pancreatitis, the histologic changes are unevenly distributed and are characterized by induration, nodular scarring, and lobular regions of fibrosis (Fig. 33-22). As the disease progresses, there is a loss of normal lobulation, with thicker sheets of fibrosis surrounding a reduced acinar cell mass and dilatation of ductular structures (Fig. 33-23). The ductular epithelium is usually atypical and may display features of dysplasia, as evidenced by cuboidal cells with hyperplastic features, accompanied by areas of mononuclear cell infiltrates or patchy areas of necrosis. Cystic changes may be seen, but areas of relatively intact acinar elements and normal-appearing islets persist. In severe chronic pancreatitis, there is considerable replacement of acinar tissue by broad, coalescing areas of fibrosis, and the islet size and | Surgery_Schwartz. College.)are needed to allow a better prediction of its clinical course and a more accurate diagnosis of a likely etiologic agent.PathologyHistology. In early chronic pancreatitis, the histologic changes are unevenly distributed and are characterized by induration, nodular scarring, and lobular regions of fibrosis (Fig. 33-22). As the disease progresses, there is a loss of normal lobulation, with thicker sheets of fibrosis surrounding a reduced acinar cell mass and dilatation of ductular structures (Fig. 33-23). The ductular epithelium is usually atypical and may display features of dysplasia, as evidenced by cuboidal cells with hyperplastic features, accompanied by areas of mononuclear cell infiltrates or patchy areas of necrosis. Cystic changes may be seen, but areas of relatively intact acinar elements and normal-appearing islets persist. In severe chronic pancreatitis, there is considerable replacement of acinar tissue by broad, coalescing areas of fibrosis, and the islet size and |
Surgery_Schwartz_9624 | Surgery_Schwartz | acinar elements and normal-appearing islets persist. In severe chronic pancreatitis, there is considerable replacement of acinar tissue by broad, coalescing areas of fibrosis, and the islet size and number are reduced (Fig. 33-24). Small arteries appear thickened, and neural trunks become prominent.147Tropical pancreatitis and hereditary pancreatitis are histo-logically indistinguishable from chronic alcoholic pancreatitis. In obstructive chronic pancreatitis, calculi are absent, although periacinar fibrosis and dilated ductular structures are prominent. In pancreatic lobular fibrosis seen in elderly subjects, small ducts are dilated, sometimes with small calculi trapped within. Hypertrophy of ductular epithelia is thought to cause this small-duct disease, which is accompanied by perilobular fibrosis.148Fibrosis. A common feature of all forms of chronic pancreatitis is the perilobular fibrosis that forms surrounding individual acini, then propagates to surround small lobules, and | Surgery_Schwartz. acinar elements and normal-appearing islets persist. In severe chronic pancreatitis, there is considerable replacement of acinar tissue by broad, coalescing areas of fibrosis, and the islet size and number are reduced (Fig. 33-24). Small arteries appear thickened, and neural trunks become prominent.147Tropical pancreatitis and hereditary pancreatitis are histo-logically indistinguishable from chronic alcoholic pancreatitis. In obstructive chronic pancreatitis, calculi are absent, although periacinar fibrosis and dilated ductular structures are prominent. In pancreatic lobular fibrosis seen in elderly subjects, small ducts are dilated, sometimes with small calculi trapped within. Hypertrophy of ductular epithelia is thought to cause this small-duct disease, which is accompanied by perilobular fibrosis.148Fibrosis. A common feature of all forms of chronic pancreatitis is the perilobular fibrosis that forms surrounding individual acini, then propagates to surround small lobules, and |
Surgery_Schwartz_9625 | Surgery_Schwartz | fibrosis.148Fibrosis. A common feature of all forms of chronic pancreatitis is the perilobular fibrosis that forms surrounding individual acini, then propagates to surround small lobules, and eventually coalesces to replace larger areas of acinar tissue. The pathogenesis of this process involves the activation of pancreatic stellate cells (PSCs) that are found adjacent to acini and small arteries.149 The extended cytoplasmic processes of PSCs encircle the acini but appear quiescent in the normal gland, where they contain lipid vacuoles and cytoskeletal proteins. In response to pancreatic injury, the PSCs become activated and proliferate (similarly to hepatic stellate cells), lose their lipid vesicles, and transform into myofibroblast-like cells. These cells respond to proliferative factors such as transforming growth factor ®, platelet-derived growth factor, and proinflammatory cytokines that synthesize and secrete type I and III collagen and fibronectin. Studies indicate that vitamin | Surgery_Schwartz. fibrosis.148Fibrosis. A common feature of all forms of chronic pancreatitis is the perilobular fibrosis that forms surrounding individual acini, then propagates to surround small lobules, and eventually coalesces to replace larger areas of acinar tissue. The pathogenesis of this process involves the activation of pancreatic stellate cells (PSCs) that are found adjacent to acini and small arteries.149 The extended cytoplasmic processes of PSCs encircle the acini but appear quiescent in the normal gland, where they contain lipid vacuoles and cytoskeletal proteins. In response to pancreatic injury, the PSCs become activated and proliferate (similarly to hepatic stellate cells), lose their lipid vesicles, and transform into myofibroblast-like cells. These cells respond to proliferative factors such as transforming growth factor ®, platelet-derived growth factor, and proinflammatory cytokines that synthesize and secrete type I and III collagen and fibronectin. Studies indicate that vitamin |
Surgery_Schwartz_9626 | Surgery_Schwartz | such as transforming growth factor ®, platelet-derived growth factor, and proinflammatory cytokines that synthesize and secrete type I and III collagen and fibronectin. Studies indicate that vitamin A metabolites, similar to those present in quiescent PSCs, can inhibit the collagen production of activated cultured PSCs.150 This raises the possibility that early intervention may be possible to interrupt or prevent the fibrosis resulting from ongoing activation of PSCs.The overall pathogenic sequence proposed by Schneider and Whitcomb151 whereby alcohol induces acute pancreati-tis and, with ongoing exposure, promotes the development of chronic fibrosis, is summarized in Fig. 33-19. PSCs surround-ing the acinus are activated in acute pancreatitis but may be inactivated by anti-inflammatory cytokines and, in the absence of further injury, may revert to a quiescent state. The role of proinflammatory macrophages, cytokines, and PSCs in models of acute and chronic pancreatitis represents an | Surgery_Schwartz. such as transforming growth factor ®, platelet-derived growth factor, and proinflammatory cytokines that synthesize and secrete type I and III collagen and fibronectin. Studies indicate that vitamin A metabolites, similar to those present in quiescent PSCs, can inhibit the collagen production of activated cultured PSCs.150 This raises the possibility that early intervention may be possible to interrupt or prevent the fibrosis resulting from ongoing activation of PSCs.The overall pathogenic sequence proposed by Schneider and Whitcomb151 whereby alcohol induces acute pancreati-tis and, with ongoing exposure, promotes the development of chronic fibrosis, is summarized in Fig. 33-19. PSCs surround-ing the acinus are activated in acute pancreatitis but may be inactivated by anti-inflammatory cytokines and, in the absence of further injury, may revert to a quiescent state. The role of proinflammatory macrophages, cytokines, and PSCs in models of acute and chronic pancreatitis represents an |
Surgery_Schwartz_9627 | Surgery_Schwartz | and, in the absence of further injury, may revert to a quiescent state. The role of proinflammatory macrophages, cytokines, and PSCs in models of acute and chronic pancreatitis represents an important area of current research.Stone Formation. Pancreatic stones are composed largely of calcium carbonate crystals trapped in a matrix of fibrillar and other material. The fibrillar center of most stones contains no Brunicardi_Ch33_p1429-p1516.indd 145601/03/19 6:44 PM 1457PANCREASCHAPTER 33calcium but rather a mixture of other metals. This suggests that stones form from an initial noncalcified protein precipitate, which serves as a focus for layered calcium carbonate precipita-tion. The same low molecular weight protein is present in stones and protein plugs and was initially named pancreatic stone pro-tein, or PSP.152 PSP was found to be a potent inhibitor of calcium carbonate crystal growth and has subsequently been renamed lithostathine.153 Independently, a 15-kDa fibrillar protein | Surgery_Schwartz. and, in the absence of further injury, may revert to a quiescent state. The role of proinflammatory macrophages, cytokines, and PSCs in models of acute and chronic pancreatitis represents an important area of current research.Stone Formation. Pancreatic stones are composed largely of calcium carbonate crystals trapped in a matrix of fibrillar and other material. The fibrillar center of most stones contains no Brunicardi_Ch33_p1429-p1516.indd 145601/03/19 6:44 PM 1457PANCREASCHAPTER 33calcium but rather a mixture of other metals. This suggests that stones form from an initial noncalcified protein precipitate, which serves as a focus for layered calcium carbonate precipita-tion. The same low molecular weight protein is present in stones and protein plugs and was initially named pancreatic stone pro-tein, or PSP.152 PSP was found to be a potent inhibitor of calcium carbonate crystal growth and has subsequently been renamed lithostathine.153 Independently, a 15-kDa fibrillar protein |
Surgery_Schwartz_9628 | Surgery_Schwartz | stone pro-tein, or PSP.152 PSP was found to be a potent inhibitor of calcium carbonate crystal growth and has subsequently been renamed lithostathine.153 Independently, a 15-kDa fibrillar protein iso-lated from the pancreas was named pancreatic thread protein, and it has been shown to be homologous with lithostathine. Finally, a protein product of the reg gene, so named because it is expressed in association with regenerating islets in models of pancreatic injury, was isolated and called reg protein and was subsequently found to be homologous with lithostathine.154 The PSP/pancreatic thread protein/reg/lithostathine gene encodes for a 166-amino acid product that undergoes posttranslational modification to produce isoforms present in pancreatic juice. The protein is expressed in all rodents and mammals, both in the pancreas as well as in brain tissue, where it is found in particu-larly high concentrations in pyramidal neurons in Alzheimer’s disease and Down syndrome. It is also found | Surgery_Schwartz. stone pro-tein, or PSP.152 PSP was found to be a potent inhibitor of calcium carbonate crystal growth and has subsequently been renamed lithostathine.153 Independently, a 15-kDa fibrillar protein iso-lated from the pancreas was named pancreatic thread protein, and it has been shown to be homologous with lithostathine. Finally, a protein product of the reg gene, so named because it is expressed in association with regenerating islets in models of pancreatic injury, was isolated and called reg protein and was subsequently found to be homologous with lithostathine.154 The PSP/pancreatic thread protein/reg/lithostathine gene encodes for a 166-amino acid product that undergoes posttranslational modification to produce isoforms present in pancreatic juice. The protein is expressed in all rodents and mammals, both in the pancreas as well as in brain tissue, where it is found in particu-larly high concentrations in pyramidal neurons in Alzheimer’s disease and Down syndrome. It is also found |
Surgery_Schwartz_9629 | Surgery_Schwartz | and mammals, both in the pancreas as well as in brain tissue, where it is found in particu-larly high concentrations in pyramidal neurons in Alzheimer’s disease and Down syndrome. It is also found in the renal tubules, which is consistent with its biologic action of prevent-ing calcium carbonate precipitation.Calcium and bicarbonate ions are normally present in pan-creatic juice in high concentrations, and the solubility product of calcium carbonate is greatly exceeded under normal condi-tions. Microcrystals of calcium carbonate can be seen in normal pancreatic juice but are usually clinically silent. Lithostathine is a potent inhibitor of calcium carbonate crystal formation, at a concentration of only 0.1 μmol/L. However, lithostathine con-centrations in normal pancreatic juice are in the range of 20 to 25 μmol/L, so a constant suppression of calcium carbonate crystal formation is present in the normal pancreas.In alcoholics and in patients with alcoholic chronic pan-creatitis, | Surgery_Schwartz. and mammals, both in the pancreas as well as in brain tissue, where it is found in particu-larly high concentrations in pyramidal neurons in Alzheimer’s disease and Down syndrome. It is also found in the renal tubules, which is consistent with its biologic action of prevent-ing calcium carbonate precipitation.Calcium and bicarbonate ions are normally present in pan-creatic juice in high concentrations, and the solubility product of calcium carbonate is greatly exceeded under normal condi-tions. Microcrystals of calcium carbonate can be seen in normal pancreatic juice but are usually clinically silent. Lithostathine is a potent inhibitor of calcium carbonate crystal formation, at a concentration of only 0.1 μmol/L. However, lithostathine con-centrations in normal pancreatic juice are in the range of 20 to 25 μmol/L, so a constant suppression of calcium carbonate crystal formation is present in the normal pancreas.In alcoholics and in patients with alcoholic chronic pan-creatitis, |
Surgery_Schwartz_9630 | Surgery_Schwartz | in the range of 20 to 25 μmol/L, so a constant suppression of calcium carbonate crystal formation is present in the normal pancreas.In alcoholics and in patients with alcoholic chronic pan-creatitis, lithostathine expression and secretion are dramati-cally inhibited155 (Fig. 33-25). In addition, elevated levels of precipitated lithostathine in the duct fluid in chronic pancreati-tis patients suggests that the availability of the protein may be further reduced by the action of increased proteases and other proteins present in the duct fluid of alcoholic patients. Increased pancreatic juice protein levels in alcoholic men are reversible by abstinence from alcohol,156 so the availability and effectiveness of lithostathine may be restored in patients with early-stage dis-ease by timely intervention. Nevertheless, calcific stone forma-tion represents an advanced stage of disease, which can further promote injury or symptoms due to mechanical damage to duct epithelium or obstruction of the | Surgery_Schwartz. in the range of 20 to 25 μmol/L, so a constant suppression of calcium carbonate crystal formation is present in the normal pancreas.In alcoholics and in patients with alcoholic chronic pan-creatitis, lithostathine expression and secretion are dramati-cally inhibited155 (Fig. 33-25). In addition, elevated levels of precipitated lithostathine in the duct fluid in chronic pancreati-tis patients suggests that the availability of the protein may be further reduced by the action of increased proteases and other proteins present in the duct fluid of alcoholic patients. Increased pancreatic juice protein levels in alcoholic men are reversible by abstinence from alcohol,156 so the availability and effectiveness of lithostathine may be restored in patients with early-stage dis-ease by timely intervention. Nevertheless, calcific stone forma-tion represents an advanced stage of disease, which can further promote injury or symptoms due to mechanical damage to duct epithelium or obstruction of the |
Surgery_Schwartz_9631 | Surgery_Schwartz | Nevertheless, calcific stone forma-tion represents an advanced stage of disease, which can further promote injury or symptoms due to mechanical damage to duct epithelium or obstruction of the ductular network.Duct Distortion. Although calcific stone disease is normally a marker for an advanced stage of disease, parenchymal and ductular calcifications do not always correlate with symptoms. Obstructing main duct stones are commonly observed and are thought to be an indication for endoscopic or surgical removal. The ball-valve effect of a stone in a secreting system produces inevitable episodes of duct obstruction, usually accompanied by pain. But some patients with complete duct obstruction have prolonged periods of painlessness. Ductular hypertension has been documented in patients with proximal stenosis of the main pancreatic duct, and prolonged ductular distention after secre-tin administration is taken as a sign of ductular obstruction.157 Although calculus disease and duct | Surgery_Schwartz. Nevertheless, calcific stone forma-tion represents an advanced stage of disease, which can further promote injury or symptoms due to mechanical damage to duct epithelium or obstruction of the ductular network.Duct Distortion. Although calcific stone disease is normally a marker for an advanced stage of disease, parenchymal and ductular calcifications do not always correlate with symptoms. Obstructing main duct stones are commonly observed and are thought to be an indication for endoscopic or surgical removal. The ball-valve effect of a stone in a secreting system produces inevitable episodes of duct obstruction, usually accompanied by pain. But some patients with complete duct obstruction have prolonged periods of painlessness. Ductular hypertension has been documented in patients with proximal stenosis of the main pancreatic duct, and prolonged ductular distention after secre-tin administration is taken as a sign of ductular obstruction.157 Although calculus disease and duct |
Surgery_Schwartz_9632 | Surgery_Schwartz | with proximal stenosis of the main pancreatic duct, and prolonged ductular distention after secre-tin administration is taken as a sign of ductular obstruction.157 Although calculus disease and duct enlargement appear together as late stages of chronic pancreatitis, controversy persists over whether they are associated, are independent events, or are caus-ally related.Radiology. Radiologic imaging of chronic pancreatitis assists in four areas: (a) diagnosis, (b) the evaluation of severity of disease, (c) detection of complications, and (d) assistance in determining treatment options.158 With the advent of cross-sectional imaging techniques such as CT and MRI, the contour, content, ductal pattern, calcifications, calculi, and cystic disease of the pancreas are all readily discernible. Transabdominal ultrasonography is frequently used as a screening method for patients with abdominal symptoms or trauma, and the extension of ultrasonic imaging to include endoscopic ultrasound (EUS) and | Surgery_Schwartz. with proximal stenosis of the main pancreatic duct, and prolonged ductular distention after secre-tin administration is taken as a sign of ductular obstruction.157 Although calculus disease and duct enlargement appear together as late stages of chronic pancreatitis, controversy persists over whether they are associated, are independent events, or are caus-ally related.Radiology. Radiologic imaging of chronic pancreatitis assists in four areas: (a) diagnosis, (b) the evaluation of severity of disease, (c) detection of complications, and (d) assistance in determining treatment options.158 With the advent of cross-sectional imaging techniques such as CT and MRI, the contour, content, ductal pattern, calcifications, calculi, and cystic disease of the pancreas are all readily discernible. Transabdominal ultrasonography is frequently used as a screening method for patients with abdominal symptoms or trauma, and the extension of ultrasonic imaging to include endoscopic ultrasound (EUS) and |
Surgery_Schwartz_9633 | Surgery_Schwartz | ultrasonography is frequently used as a screening method for patients with abdominal symptoms or trauma, and the extension of ultrasonic imaging to include endoscopic ultrasound (EUS) and laparoscopic US have resulted in the highest-resolution images that are capable of detecting very small (<1 cm) abnormalities in the pancreas. EUS is now frequently used as a preliminary step in the evaluation of patients with pancreatic disease, and magnetic resonance cholangiopancreatography (MRCP) is increasingly being used to select patients who are candidates for the most invasive imaging method, ERCP. The staging of disease is important in the care of patients, and a combination of imaging methods is usually used (Table 33-12).Ultrasonography is frequently used as an initial imaging method in patients with abdominal symptoms, and changes con-sistent with pancreatic duct dilatation, intraductal filling defects, cystic changes, and a heterogeneous texture are seen in chronic pancreatitis (Fig. | Surgery_Schwartz. ultrasonography is frequently used as a screening method for patients with abdominal symptoms or trauma, and the extension of ultrasonic imaging to include endoscopic ultrasound (EUS) and laparoscopic US have resulted in the highest-resolution images that are capable of detecting very small (<1 cm) abnormalities in the pancreas. EUS is now frequently used as a preliminary step in the evaluation of patients with pancreatic disease, and magnetic resonance cholangiopancreatography (MRCP) is increasingly being used to select patients who are candidates for the most invasive imaging method, ERCP. The staging of disease is important in the care of patients, and a combination of imaging methods is usually used (Table 33-12).Ultrasonography is frequently used as an initial imaging method in patients with abdominal symptoms, and changes con-sistent with pancreatic duct dilatation, intraductal filling defects, cystic changes, and a heterogeneous texture are seen in chronic pancreatitis (Fig. |
Surgery_Schwartz_9634 | Surgery_Schwartz | with abdominal symptoms, and changes con-sistent with pancreatic duct dilatation, intraductal filling defects, cystic changes, and a heterogeneous texture are seen in chronic pancreatitis (Fig. 33-26). The sensitivity of transabdominal ultrasonography ranges from 48% to 96%, and it is operator dependent.159 However, the contour, texture, and ductal pattern are usually quite discernible, and it is a reliable method for peri-odic reexamination to determine the efficacy of treatment.EUS has heavily impacted the evaluation and manage-ment of patients with chronic pancreatitis. Although it is more operator dependent than transabdominal ultrasonography, EUS provides not only imaging capability but also adds the capac-ity to obtain cytologic and chemical samples of tissue and fluid aspirated with linear array monitoring (Fig. 33-27). EUS images obtained through a high-frequency (7.5to 12.5-mHz) transducer are able to evaluate subtle changes in 2to 3-mm 50102030µg lithostathine/mg total | Surgery_Schwartz. with abdominal symptoms, and changes con-sistent with pancreatic duct dilatation, intraductal filling defects, cystic changes, and a heterogeneous texture are seen in chronic pancreatitis (Fig. 33-26). The sensitivity of transabdominal ultrasonography ranges from 48% to 96%, and it is operator dependent.159 However, the contour, texture, and ductal pattern are usually quite discernible, and it is a reliable method for peri-odic reexamination to determine the efficacy of treatment.EUS has heavily impacted the evaluation and manage-ment of patients with chronic pancreatitis. Although it is more operator dependent than transabdominal ultrasonography, EUS provides not only imaging capability but also adds the capac-ity to obtain cytologic and chemical samples of tissue and fluid aspirated with linear array monitoring (Fig. 33-27). EUS images obtained through a high-frequency (7.5to 12.5-mHz) transducer are able to evaluate subtle changes in 2to 3-mm 50102030µg lithostathine/mg total |
Surgery_Schwartz_9635 | Surgery_Schwartz | with linear array monitoring (Fig. 33-27). EUS images obtained through a high-frequency (7.5to 12.5-mHz) transducer are able to evaluate subtle changes in 2to 3-mm 50102030µg lithostathine/mg total proteinCCPAlc.OPDControlsFigure 33-25. Lithostathine levels in chronic calcific pancreatitis (CCP) patients, patients with alcohol abuse (Alc.), patients with other pancreatic disease (OPD), and controls. (Reproduced with permis-sion from Beger HG: The pancreas: an integrated textbook of basic science, medicine, and surgery. London: Blackwell-Science; 1998.)Brunicardi_Ch33_p1429-p1516.indd 145701/03/19 6:44 PM 1458SPECIFIC CONSIDERATIONSPART IITable 33-12Cambridge classification of pancreatic morphology in chronic pancreatitisCLASSIFICATIONERCP FINDINGSCT AND US FINDINGSNormalNo abnormal SBDsNormal gland size, shape; homogeneous parenchymaEquivocalMPD normalOne of the following: less than three abnormal SBDs; MPD 2–4 mm; gland enlarged more than two times normal size; heterogeneous | Surgery_Schwartz. with linear array monitoring (Fig. 33-27). EUS images obtained through a high-frequency (7.5to 12.5-mHz) transducer are able to evaluate subtle changes in 2to 3-mm 50102030µg lithostathine/mg total proteinCCPAlc.OPDControlsFigure 33-25. Lithostathine levels in chronic calcific pancreatitis (CCP) patients, patients with alcohol abuse (Alc.), patients with other pancreatic disease (OPD), and controls. (Reproduced with permis-sion from Beger HG: The pancreas: an integrated textbook of basic science, medicine, and surgery. London: Blackwell-Science; 1998.)Brunicardi_Ch33_p1429-p1516.indd 145701/03/19 6:44 PM 1458SPECIFIC CONSIDERATIONSPART IITable 33-12Cambridge classification of pancreatic morphology in chronic pancreatitisCLASSIFICATIONERCP FINDINGSCT AND US FINDINGSNormalNo abnormal SBDsNormal gland size, shape; homogeneous parenchymaEquivocalMPD normalOne of the following: less than three abnormal SBDs; MPD 2–4 mm; gland enlarged more than two times normal size; heterogeneous |
Surgery_Schwartz_9636 | Surgery_Schwartz | SBDsNormal gland size, shape; homogeneous parenchymaEquivocalMPD normalOne of the following: less than three abnormal SBDs; MPD 2–4 mm; gland enlarged more than two times normal size; heterogeneous parenchymaMildMPD normalTwo or more of the following: less than three abnormal SBDs; MPD 2–4 mm; slight gland enlargement; heterogeneous parenchymaModerate MPD changesSmall cysts <10 mm; MPD irregularitySBD changesFocal acute pancreatitis; increased echogenicity of MPD walls; gland-contour irregularitySevereAny of the above changes plus one or more of the following: cysts <10 mm; intraductal filling defects; calculi; MPD obstruction or stricture; severe MPD irregularity; contiguous organ invasion—Abbreviations: CT = computed tomography; ERCP = endoscopic retrograde cholangiopancreatography; MPD = main pancreatic duct; SBD = side-branch duct; US = ultrasound.Reproduced with permission from Beger HG: The Pancreas. London: Blackwell-Science; 1998.Figure 33-26. Sonography in chronic | Surgery_Schwartz. SBDsNormal gland size, shape; homogeneous parenchymaEquivocalMPD normalOne of the following: less than three abnormal SBDs; MPD 2–4 mm; gland enlarged more than two times normal size; heterogeneous parenchymaMildMPD normalTwo or more of the following: less than three abnormal SBDs; MPD 2–4 mm; slight gland enlargement; heterogeneous parenchymaModerate MPD changesSmall cysts <10 mm; MPD irregularitySBD changesFocal acute pancreatitis; increased echogenicity of MPD walls; gland-contour irregularitySevereAny of the above changes plus one or more of the following: cysts <10 mm; intraductal filling defects; calculi; MPD obstruction or stricture; severe MPD irregularity; contiguous organ invasion—Abbreviations: CT = computed tomography; ERCP = endoscopic retrograde cholangiopancreatography; MPD = main pancreatic duct; SBD = side-branch duct; US = ultrasound.Reproduced with permission from Beger HG: The Pancreas. London: Blackwell-Science; 1998.Figure 33-26. Sonography in chronic |
Surgery_Schwartz_9637 | Surgery_Schwartz | MPD = main pancreatic duct; SBD = side-branch duct; US = ultrasound.Reproduced with permission from Beger HG: The Pancreas. London: Blackwell-Science; 1998.Figure 33-26. Sonography in chronic pancreatitis. Transabdomi-nal sonogram of patient with chronic pancreatitis demonstrates het-erogeneity of the pancreatic parenchyma, dilated ductal systems, and cyst formation. (Reproduced with permission from Bolondi L, Li Bassi S, Gaiani S, et al: Sonography of chronic pancreatitis, Radiol Clin North Am. 1989 Jul;27(4):815-833.)Figure 33-27. Endoscopic ultrasound of chronic pancreatitis. The endoscopic ultrasound appearance of the parenchyma is heteroge-neous, and dilated ducts are seen, indicating early obstructive pan-creatopathy. (Used with permission from Mark Topazian, Division of Digestive Diseases, Department of Medicine, Mayo Clinic.)structures within the pancreas and can detect indolent neoplasms in the setting of chronic inflammation. Small intraductal lesions, intraductal mucus, | Surgery_Schwartz. MPD = main pancreatic duct; SBD = side-branch duct; US = ultrasound.Reproduced with permission from Beger HG: The Pancreas. London: Blackwell-Science; 1998.Figure 33-26. Sonography in chronic pancreatitis. Transabdomi-nal sonogram of patient with chronic pancreatitis demonstrates het-erogeneity of the pancreatic parenchyma, dilated ductal systems, and cyst formation. (Reproduced with permission from Bolondi L, Li Bassi S, Gaiani S, et al: Sonography of chronic pancreatitis, Radiol Clin North Am. 1989 Jul;27(4):815-833.)Figure 33-27. Endoscopic ultrasound of chronic pancreatitis. The endoscopic ultrasound appearance of the parenchyma is heteroge-neous, and dilated ducts are seen, indicating early obstructive pan-creatopathy. (Used with permission from Mark Topazian, Division of Digestive Diseases, Department of Medicine, Mayo Clinic.)structures within the pancreas and can detect indolent neoplasms in the setting of chronic inflammation. Small intraductal lesions, intraductal mucus, |
Surgery_Schwartz_9638 | Surgery_Schwartz | Diseases, Department of Medicine, Mayo Clinic.)structures within the pancreas and can detect indolent neoplasms in the setting of chronic inflammation. Small intraductal lesions, intraductal mucus, cystic lesions, and subtle ductular abnormali-ties are recognizable by EUS (Table 33-13). This allows ERCP to be reserved for these patients who require therapeutic maneu-vers, or for the evaluation of more complex problems. EUS is comparable to ERCP in the detection of advanced changes in chronic pancreatitis and may be more sensitive than ERCP in the detection of mild disease.160CT scanning has affected the diagnosis of pancreatic dis-ease more broadly than any other method. With the advent of faster helical CT scanning and CT angiography, visualization of the nature, extent, location, and relative relationships of pancre-atic structures and lesions is possible with great clarity. Duct dil-atation, calculous disease, cystic changes, inflammatory events, and anomalies are all detectable | Surgery_Schwartz. Diseases, Department of Medicine, Mayo Clinic.)structures within the pancreas and can detect indolent neoplasms in the setting of chronic inflammation. Small intraductal lesions, intraductal mucus, cystic lesions, and subtle ductular abnormali-ties are recognizable by EUS (Table 33-13). This allows ERCP to be reserved for these patients who require therapeutic maneu-vers, or for the evaluation of more complex problems. EUS is comparable to ERCP in the detection of advanced changes in chronic pancreatitis and may be more sensitive than ERCP in the detection of mild disease.160CT scanning has affected the diagnosis of pancreatic dis-ease more broadly than any other method. With the advent of faster helical CT scanning and CT angiography, visualization of the nature, extent, location, and relative relationships of pancre-atic structures and lesions is possible with great clarity. Duct dil-atation, calculous disease, cystic changes, inflammatory events, and anomalies are all detectable |
Surgery_Schwartz_9639 | Surgery_Schwartz | relative relationships of pancre-atic structures and lesions is possible with great clarity. Duct dil-atation, calculous disease, cystic changes, inflammatory events, and anomalies are all detectable with a resolution of 3 to 4 mm (Fig. 33-28). CT scanning has a false-negative rate of <10% for chronic pancreatitis, but early or mild chronic disease may go undetected by CT imaging. The earliest changes are dilatation of secondary ducts and heterogeneous parenchymal changes, which are detectable by EUS and ERCP. Another drawback of CT scanning is its lower sensitivity for detecting small neo-plasms, which are seen with increased frequency in chronic pancreatitis and may be invisible to all modalities except EUS.An MRI, in both the cross-sectional mode and the coro-nally oriented heavily weighted T2 or high spin ratio imaging Brunicardi_Ch33_p1429-p1516.indd 145801/03/19 6:44 PM 1459PANCREASCHAPTER 33Table 33-13Endoscopic ultrasound features of chronic pancreatitisENDOSCOPIC | Surgery_Schwartz. relative relationships of pancre-atic structures and lesions is possible with great clarity. Duct dil-atation, calculous disease, cystic changes, inflammatory events, and anomalies are all detectable with a resolution of 3 to 4 mm (Fig. 33-28). CT scanning has a false-negative rate of <10% for chronic pancreatitis, but early or mild chronic disease may go undetected by CT imaging. The earliest changes are dilatation of secondary ducts and heterogeneous parenchymal changes, which are detectable by EUS and ERCP. Another drawback of CT scanning is its lower sensitivity for detecting small neo-plasms, which are seen with increased frequency in chronic pancreatitis and may be invisible to all modalities except EUS.An MRI, in both the cross-sectional mode and the coro-nally oriented heavily weighted T2 or high spin ratio imaging Brunicardi_Ch33_p1429-p1516.indd 145801/03/19 6:44 PM 1459PANCREASCHAPTER 33Table 33-13Endoscopic ultrasound features of chronic pancreatitisENDOSCOPIC |
Surgery_Schwartz_9640 | Surgery_Schwartz | weighted T2 or high spin ratio imaging Brunicardi_Ch33_p1429-p1516.indd 145801/03/19 6:44 PM 1459PANCREASCHAPTER 33Table 33-13Endoscopic ultrasound features of chronic pancreatitisENDOSCOPIC ULTRASOUND FEATUREIMPLICATIONDuctal changes Duct size >3 mmDuctal dilation Tortuous pancreatic ductDuctal irregularity Intraductal echogenic fociStones or calcification Echogenic duct wallDuctal fibrosis Side-branch ectasiaPeriductal fibrosisParenchymal changes Inhomogeneous echo patternEdema Reduced echogenic foci (1–3 mm)Edema Enhanced echogenic fociCalcifications Prominent interlobular septaeFibrosis Lobular outer gland marginFibrosis, glandular atrophy Large, echo-poor cavities (>5 mm)PseudocystReproduced with permission from Catalano MF, Lahoti S, Geenen JE, et al. Prospective evaluation of endoscopic ultrasonography, endoscopic retrograde pancreatography, and secretin test in the diagnosis of chronic pancreatitis, Gastrointest Endosc. 1998 Jul;48(1):11-17.(MRCP) that can disclose | Surgery_Schwartz. weighted T2 or high spin ratio imaging Brunicardi_Ch33_p1429-p1516.indd 145801/03/19 6:44 PM 1459PANCREASCHAPTER 33Table 33-13Endoscopic ultrasound features of chronic pancreatitisENDOSCOPIC ULTRASOUND FEATUREIMPLICATIONDuctal changes Duct size >3 mmDuctal dilation Tortuous pancreatic ductDuctal irregularity Intraductal echogenic fociStones or calcification Echogenic duct wallDuctal fibrosis Side-branch ectasiaPeriductal fibrosisParenchymal changes Inhomogeneous echo patternEdema Reduced echogenic foci (1–3 mm)Edema Enhanced echogenic fociCalcifications Prominent interlobular septaeFibrosis Lobular outer gland marginFibrosis, glandular atrophy Large, echo-poor cavities (>5 mm)PseudocystReproduced with permission from Catalano MF, Lahoti S, Geenen JE, et al. Prospective evaluation of endoscopic ultrasonography, endoscopic retrograde pancreatography, and secretin test in the diagnosis of chronic pancreatitis, Gastrointest Endosc. 1998 Jul;48(1):11-17.(MRCP) that can disclose |
Surgery_Schwartz_9641 | Surgery_Schwartz | of endoscopic ultrasonography, endoscopic retrograde pancreatography, and secretin test in the diagnosis of chronic pancreatitis, Gastrointest Endosc. 1998 Jul;48(1):11-17.(MRCP) that can disclose fluid-filled ducts and cystic lesions, has added greatly to the imaging options for chronic pancreatitis (Fig. 33-29). The resolution of cross-sectional MRI scanning is now approaching that of CT scanning, although the availability of MRI scanners and the complexity of the images produced have limited their large-scale use for routine imaging of the pancreas. MRCP has been shown to be an effective screening technique for disclosing ductal abnormalities that correlates closely with the contrast-filled ducts imaged by ERCP.161 The advantages of MRCP include its noninvasive methodology and Figure 33-28. Computed tomographic imaging of chronic pancre-atitis. A dilated pancreatic duct is seen, with evidence of intraductal stones and parenchymal calcification. (Reproduced with permission from | Surgery_Schwartz. of endoscopic ultrasonography, endoscopic retrograde pancreatography, and secretin test in the diagnosis of chronic pancreatitis, Gastrointest Endosc. 1998 Jul;48(1):11-17.(MRCP) that can disclose fluid-filled ducts and cystic lesions, has added greatly to the imaging options for chronic pancreatitis (Fig. 33-29). The resolution of cross-sectional MRI scanning is now approaching that of CT scanning, although the availability of MRI scanners and the complexity of the images produced have limited their large-scale use for routine imaging of the pancreas. MRCP has been shown to be an effective screening technique for disclosing ductal abnormalities that correlates closely with the contrast-filled ducts imaged by ERCP.161 The advantages of MRCP include its noninvasive methodology and Figure 33-28. Computed tomographic imaging of chronic pancre-atitis. A dilated pancreatic duct is seen, with evidence of intraductal stones and parenchymal calcification. (Reproduced with permission from |
Surgery_Schwartz_9642 | Surgery_Schwartz | 33-28. Computed tomographic imaging of chronic pancre-atitis. A dilated pancreatic duct is seen, with evidence of intraductal stones and parenchymal calcification. (Reproduced with permission from Forsmark CE: Management of chronic pancreatitis, Gastroen-terology. 2013 Jun;144(6):1282-1291.)Figure 33-29. Coronal T2-weighted magnetic resonance image showing evidence of chronic pancreatitis, including a pancreatic duct dilatation and side-branch clubbing. (Used with permission from Mellena Bridges, MD, Mayo Clinic Jacksonville, Department of Radiology.)its ability to image obstructed ducts that are not opacified by ERCP injection. It is therefore a useful screening study to detect duct abnormalities and to confirm the need for interventional procedures. Oral, IV, and intraductal contrast are unnecessary for MRCP, and its lack of ionizing radiation makes this the saf-est method to image the ductal system in high-risk patients.For the diagnosis and staging of chronic pancreatitis, ERCP is | Surgery_Schwartz. 33-28. Computed tomographic imaging of chronic pancre-atitis. A dilated pancreatic duct is seen, with evidence of intraductal stones and parenchymal calcification. (Reproduced with permission from Forsmark CE: Management of chronic pancreatitis, Gastroen-terology. 2013 Jun;144(6):1282-1291.)Figure 33-29. Coronal T2-weighted magnetic resonance image showing evidence of chronic pancreatitis, including a pancreatic duct dilatation and side-branch clubbing. (Used with permission from Mellena Bridges, MD, Mayo Clinic Jacksonville, Department of Radiology.)its ability to image obstructed ducts that are not opacified by ERCP injection. It is therefore a useful screening study to detect duct abnormalities and to confirm the need for interventional procedures. Oral, IV, and intraductal contrast are unnecessary for MRCP, and its lack of ionizing radiation makes this the saf-est method to image the ductal system in high-risk patients.For the diagnosis and staging of chronic pancreatitis, ERCP is |
Surgery_Schwartz_9643 | Surgery_Schwartz | unnecessary for MRCP, and its lack of ionizing radiation makes this the saf-est method to image the ductal system in high-risk patients.For the diagnosis and staging of chronic pancreatitis, ERCP is considered to be the gold standard. It also serves as a vehicle that enables other diagnostic and therapeutic maneu-vers, such as biopsy or brushing for cytology, or the use of stents to relieve obstruction or drain a pseudocyst (Fig. 33-30). Figure 33-30. Pancreatic duct stenting. At endoscopic retrograde cholangiopancreatography, a stent is placed in the proximal pan-creatic duct to relieve obstruction and reduce symptoms of pain. Pancreatic duct stents are left in place for only a limited time to avoid further inflammation.Brunicardi_Ch33_p1429-p1516.indd 145901/03/19 6:44 PM 1460SPECIFIC CONSIDERATIONSPART IIFigure 33-31. Pain location in chronic pancreatitis. (Reproduced with permission from Greenfield LJ, Mulholland MW, Oldham KT, et al: Surgery, Scientific Principles and | Surgery_Schwartz. unnecessary for MRCP, and its lack of ionizing radiation makes this the saf-est method to image the ductal system in high-risk patients.For the diagnosis and staging of chronic pancreatitis, ERCP is considered to be the gold standard. It also serves as a vehicle that enables other diagnostic and therapeutic maneu-vers, such as biopsy or brushing for cytology, or the use of stents to relieve obstruction or drain a pseudocyst (Fig. 33-30). Figure 33-30. Pancreatic duct stenting. At endoscopic retrograde cholangiopancreatography, a stent is placed in the proximal pan-creatic duct to relieve obstruction and reduce symptoms of pain. Pancreatic duct stents are left in place for only a limited time to avoid further inflammation.Brunicardi_Ch33_p1429-p1516.indd 145901/03/19 6:44 PM 1460SPECIFIC CONSIDERATIONSPART IIFigure 33-31. Pain location in chronic pancreatitis. (Reproduced with permission from Greenfield LJ, Mulholland MW, Oldham KT, et al: Surgery, Scientific Principles and |
Surgery_Schwartz_9644 | Surgery_Schwartz | CONSIDERATIONSPART IIFigure 33-31. Pain location in chronic pancreatitis. (Reproduced with permission from Greenfield LJ, Mulholland MW, Oldham KT, et al: Surgery, Scientific Principles and Practice, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.)Unfortunately, ERCP also carries a risk of procedure-induced pancreatitis that occurs in approximately 5% of patients.161 Patients at increased risk include those with sphincter of Oddi dysfunction and those with a previous history of post-ERCP pancreatitis. Post-ERCP pancreatitis occurs after uncompli-cated procedures, as well as after those that require prolonged manipulation. Severe pancreatitis and deaths have occurred after ERCP. It should be reserved for patients in whom the diagnosis is unclear despite the use of other imaging methods, or in whom a diagnostic or therapeutic maneuver is specifically indicated.Presentation, Natural History, and ComplicationsPresenting Signs and Symptoms. Pain is the most common symptom of | Surgery_Schwartz. CONSIDERATIONSPART IIFigure 33-31. Pain location in chronic pancreatitis. (Reproduced with permission from Greenfield LJ, Mulholland MW, Oldham KT, et al: Surgery, Scientific Principles and Practice, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.)Unfortunately, ERCP also carries a risk of procedure-induced pancreatitis that occurs in approximately 5% of patients.161 Patients at increased risk include those with sphincter of Oddi dysfunction and those with a previous history of post-ERCP pancreatitis. Post-ERCP pancreatitis occurs after uncompli-cated procedures, as well as after those that require prolonged manipulation. Severe pancreatitis and deaths have occurred after ERCP. It should be reserved for patients in whom the diagnosis is unclear despite the use of other imaging methods, or in whom a diagnostic or therapeutic maneuver is specifically indicated.Presentation, Natural History, and ComplicationsPresenting Signs and Symptoms. Pain is the most common symptom of |
Surgery_Schwartz_9645 | Surgery_Schwartz | methods, or in whom a diagnostic or therapeutic maneuver is specifically indicated.Presentation, Natural History, and ComplicationsPresenting Signs and Symptoms. Pain is the most common symptom of chronic pancreatitis. It is usually midepigastric in location but may localize or involve either the left or right upper quadrant of the abdomen. Occasionally, it is perceived in the lower midabdomen but is frequently described as penetrating through to the back (Fig. 33-31). The pain is typically steady and boring, but not colicky. It persists for hours or days and may be chronic with exacerbations caused by eating or drink-ing alcohol. Chronic alcoholics also describe a steady, constant pain that is temporarily relieved by alcohol, followed by a more severe recurrence hours later.Patients with chronic pancreatic pain typically flex their abdomen and either sit or lie with their hips flexed, or lie on their side in a fetal position. Unlike ureteral stone pain or biliary colic, the pain | Surgery_Schwartz. methods, or in whom a diagnostic or therapeutic maneuver is specifically indicated.Presentation, Natural History, and ComplicationsPresenting Signs and Symptoms. Pain is the most common symptom of chronic pancreatitis. It is usually midepigastric in location but may localize or involve either the left or right upper quadrant of the abdomen. Occasionally, it is perceived in the lower midabdomen but is frequently described as penetrating through to the back (Fig. 33-31). The pain is typically steady and boring, but not colicky. It persists for hours or days and may be chronic with exacerbations caused by eating or drink-ing alcohol. Chronic alcoholics also describe a steady, constant pain that is temporarily relieved by alcohol, followed by a more severe recurrence hours later.Patients with chronic pancreatic pain typically flex their abdomen and either sit or lie with their hips flexed, or lie on their side in a fetal position. Unlike ureteral stone pain or biliary colic, the pain |
Surgery_Schwartz_9646 | Surgery_Schwartz | with chronic pancreatic pain typically flex their abdomen and either sit or lie with their hips flexed, or lie on their side in a fetal position. Unlike ureteral stone pain or biliary colic, the pain causes the patient to be still. Nausea or vomit-ing may accompany the pain, but anorexia is the most common associated symptom.Pain from chronic pancreatitis has been ascribed to multiple etiologies. Ductal hypertension, due to strictures or stones, may predispose to pain that is initiated or exacerbated by eating. Chronic pain without exacerbation may be related to parenchymal disease or retroperitoneal inflammation with per-sistent neural involvement. Acute exacerbations of pain in the setting of chronic pain may be due to acute increases in duct pressure or recurrent episodes of acute inflammation in the set-ting of chronic parenchymal disease. Nealon and Matin have described these various pain syndromes as being predictive of the response to various surgical procedures.162 Pain that | Surgery_Schwartz. with chronic pancreatic pain typically flex their abdomen and either sit or lie with their hips flexed, or lie on their side in a fetal position. Unlike ureteral stone pain or biliary colic, the pain causes the patient to be still. Nausea or vomit-ing may accompany the pain, but anorexia is the most common associated symptom.Pain from chronic pancreatitis has been ascribed to multiple etiologies. Ductal hypertension, due to strictures or stones, may predispose to pain that is initiated or exacerbated by eating. Chronic pain without exacerbation may be related to parenchymal disease or retroperitoneal inflammation with per-sistent neural involvement. Acute exacerbations of pain in the setting of chronic pain may be due to acute increases in duct pressure or recurrent episodes of acute inflammation in the set-ting of chronic parenchymal disease. Nealon and Matin have described these various pain syndromes as being predictive of the response to various surgical procedures.162 Pain that |
Surgery_Schwartz_9647 | Surgery_Schwartz | in the set-ting of chronic parenchymal disease. Nealon and Matin have described these various pain syndromes as being predictive of the response to various surgical procedures.162 Pain that is found in association with ductal hypertension is most readily relieved by pancreatic duct decompression, through endoscopic stenting or surgical decompression.The surgical relief of pain due to obstructive pancreatopa-thy may be dependent on the degree of underlying fibrosis and the etiology of the disease rather than the presence of ductal obstruction, per se, according to a recent studies from Johns Hopkins. Cooper et al studied 35 patients with chronic pain associated with evidence of duct obstruction who were treated with local resection of the pancreatic head and longitudinal pan-creaticojejunostomy (LR-LPJ), or Frey procedure.163 The degree of pain resolution after surgery was compared to the degree of underlying parenchymal fibrosis. After a follow-up that averaged 22 months, patients | Surgery_Schwartz. in the set-ting of chronic parenchymal disease. Nealon and Matin have described these various pain syndromes as being predictive of the response to various surgical procedures.162 Pain that is found in association with ductal hypertension is most readily relieved by pancreatic duct decompression, through endoscopic stenting or surgical decompression.The surgical relief of pain due to obstructive pancreatopa-thy may be dependent on the degree of underlying fibrosis and the etiology of the disease rather than the presence of ductal obstruction, per se, according to a recent studies from Johns Hopkins. Cooper et al studied 35 patients with chronic pain associated with evidence of duct obstruction who were treated with local resection of the pancreatic head and longitudinal pan-creaticojejunostomy (LR-LPJ), or Frey procedure.163 The degree of pain resolution after surgery was compared to the degree of underlying parenchymal fibrosis. After a follow-up that averaged 22 months, patients |
Surgery_Schwartz_9648 | Surgery_Schwartz | (LR-LPJ), or Frey procedure.163 The degree of pain resolution after surgery was compared to the degree of underlying parenchymal fibrosis. After a follow-up that averaged 22 months, patients with more than 80% fibrosis had 100% pain relief, whereas only 60% patients with less than 10% fibrosis experienced substantial or complete pain relief. Subsequently, this group studied 60 patients who had undergone either the Frey procedure or the Whipple procedure for refractory pain due to chronic pancreatitis.145 In addition to histopathologic findings, they also analyzed the etiology of the disease. Of patients with “toxic” etiologies of acquired disease (i.e., a history of alcohol or tobacco abuse), 89% experienced prolonged pain relief, whereas only 39% of those with hereditary or idiopathic disease achieved this result. Further, these results were independent of the degree of pancreatic fibrosis. These findings suggest that the etiology of the disease may be the most important predictor of | Surgery_Schwartz. (LR-LPJ), or Frey procedure.163 The degree of pain resolution after surgery was compared to the degree of underlying parenchymal fibrosis. After a follow-up that averaged 22 months, patients with more than 80% fibrosis had 100% pain relief, whereas only 60% patients with less than 10% fibrosis experienced substantial or complete pain relief. Subsequently, this group studied 60 patients who had undergone either the Frey procedure or the Whipple procedure for refractory pain due to chronic pancreatitis.145 In addition to histopathologic findings, they also analyzed the etiology of the disease. Of patients with “toxic” etiologies of acquired disease (i.e., a history of alcohol or tobacco abuse), 89% experienced prolonged pain relief, whereas only 39% of those with hereditary or idiopathic disease achieved this result. Further, these results were independent of the degree of pancreatic fibrosis. These findings suggest that the etiology of the disease may be the most important predictor of |
Surgery_Schwartz_9649 | Surgery_Schwartz | achieved this result. Further, these results were independent of the degree of pancreatic fibrosis. These findings suggest that the etiology of the disease may be the most important predictor of the ben-efit of a resectional or hybrid procedure, and that patients with idiopathic or hereditary disease might be considered for an alter-native approach, such as total pancreatectomy with islet auto-transplantation (see following section).The pain of chronic pancreatitis may decrease or disappear completely over a period of years, as symptoms of exocrine and endocrine deficiency become apparent.164 This is referred to as burned out pancreatitis and correlates with the progression of disease from a mild or moderate stage to severe destruction of the pancreas. Although this evolution of painful to nonpainful disease is sometimes used as a justification to avoid intervention in painful chronic pancreatitis, noninterventional approaches to the treatment of chronic pancreatitis are inevitably | Surgery_Schwartz. achieved this result. Further, these results were independent of the degree of pancreatic fibrosis. These findings suggest that the etiology of the disease may be the most important predictor of the ben-efit of a resectional or hybrid procedure, and that patients with idiopathic or hereditary disease might be considered for an alter-native approach, such as total pancreatectomy with islet auto-transplantation (see following section).The pain of chronic pancreatitis may decrease or disappear completely over a period of years, as symptoms of exocrine and endocrine deficiency become apparent.164 This is referred to as burned out pancreatitis and correlates with the progression of disease from a mild or moderate stage to severe destruction of the pancreas. Although this evolution of painful to nonpainful disease is sometimes used as a justification to avoid intervention in painful chronic pancreatitis, noninterventional approaches to the treatment of chronic pancreatitis are inevitably |
Surgery_Schwartz_9650 | Surgery_Schwartz | to nonpainful disease is sometimes used as a justification to avoid intervention in painful chronic pancreatitis, noninterventional approaches to the treatment of chronic pancreatitis are inevitably accompanied by the development of narcotic addiction, inability to work, and the sequelae of chronic illness.Although increased ductal pressure, and therefore paren-chymal pressure, has been thought to be the cause of pain in chronic obstructive pancreatitis, the role of chronic inflamma-tion per se, and the development of actual nerve damage in the diseased gland, are also thought to contribute to pain.165 Chronic inflammation results in the infiltration of tissue by macrophages, which secrete prostaglandins and other nociceptive agents that cause chronic stimulation of afferent neural fibers. Inflamma-tory damage to the perineurial layers surrounding the unmyelin-ated pancreatic nerves and a focal infiltration of inflammatory cells around nerves suggest that neural fibers are a target | Surgery_Schwartz. to nonpainful disease is sometimes used as a justification to avoid intervention in painful chronic pancreatitis, noninterventional approaches to the treatment of chronic pancreatitis are inevitably accompanied by the development of narcotic addiction, inability to work, and the sequelae of chronic illness.Although increased ductal pressure, and therefore paren-chymal pressure, has been thought to be the cause of pain in chronic obstructive pancreatitis, the role of chronic inflamma-tion per se, and the development of actual nerve damage in the diseased gland, are also thought to contribute to pain.165 Chronic inflammation results in the infiltration of tissue by macrophages, which secrete prostaglandins and other nociceptive agents that cause chronic stimulation of afferent neural fibers. Inflamma-tory damage to the perineurial layers surrounding the unmyelin-ated pancreatic nerves and a focal infiltration of inflammatory cells around nerves suggest that neural fibers are a target |
Surgery_Schwartz_9651 | Surgery_Schwartz | Inflamma-tory damage to the perineurial layers surrounding the unmyelin-ated pancreatic nerves and a focal infiltration of inflammatory cells around nerves suggest that neural fibers are a target for the cellular response to inflammation in the pancreas.166Strategies to relieve pain are therefore based on three approaches: (a) reducing secretion and/or decompress the secre-tory compartment, (b) resecting the focus of chronic inflamma-tory change, or (c) interrupting the transmission of afferent neural impulses through neural ablative procedures. A trial of antisecre-tory therapy or endoscopic duct drainage may select those patients who will benefit preferentially from a decompressive procedure.Brunicardi_Ch33_p1429-p1516.indd 146001/03/19 6:45 PM 1461PANCREASCHAPTER 33Central Nervous System Abnormalities• Functional reorganization• Central sensitization (cortical)Central NervousSystem Abnormalities• Central sensitization (spinal)Obstructive Abnormalities• Pancreatic duct | Surgery_Schwartz. Inflamma-tory damage to the perineurial layers surrounding the unmyelin-ated pancreatic nerves and a focal infiltration of inflammatory cells around nerves suggest that neural fibers are a target for the cellular response to inflammation in the pancreas.166Strategies to relieve pain are therefore based on three approaches: (a) reducing secretion and/or decompress the secre-tory compartment, (b) resecting the focus of chronic inflamma-tory change, or (c) interrupting the transmission of afferent neural impulses through neural ablative procedures. A trial of antisecre-tory therapy or endoscopic duct drainage may select those patients who will benefit preferentially from a decompressive procedure.Brunicardi_Ch33_p1429-p1516.indd 146001/03/19 6:45 PM 1461PANCREASCHAPTER 33Central Nervous System Abnormalities• Functional reorganization• Central sensitization (cortical)Central NervousSystem Abnormalities• Central sensitization (spinal)Obstructive Abnormalities• Pancreatic duct |
Surgery_Schwartz_9652 | Surgery_Schwartz | System Abnormalities• Functional reorganization• Central sensitization (cortical)Central NervousSystem Abnormalities• Central sensitization (spinal)Obstructive Abnormalities• Pancreatic duct hypertension• Pancreatic parenchymal hypertension• Pancreas morphologyPancreatic and extrapancreatic complications• Pseudocysts• Duodenal or/and bile duct obstruction• Peptic ulcer• Splenic vein thrombosisAdditional causes• CCK elevation• Increased norepinephrine levels• Mesenteric ischemia (Type 3c diabetes)• Diabetic neuropathy (Type 3c diabetes)Peripheral NervousSystem Abnormalities• Pancreatic nociception• Pancreatic neuropathy and neuroplasticityAdverse effects to treatment• Opioid induced bowel dysfunction• Complications to surgery and endoscopic therapy• Bacterial overgrowth due to changed bowel motilityCentral Nervous System Abnormalities• Impaired inhibitory pain modulationFigure 33-32. Pain mechanisms in chronic pancreatitis. (Reproduced with permission from Demir IE, | Surgery_Schwartz. System Abnormalities• Functional reorganization• Central sensitization (cortical)Central NervousSystem Abnormalities• Central sensitization (spinal)Obstructive Abnormalities• Pancreatic duct hypertension• Pancreatic parenchymal hypertension• Pancreas morphologyPancreatic and extrapancreatic complications• Pseudocysts• Duodenal or/and bile duct obstruction• Peptic ulcer• Splenic vein thrombosisAdditional causes• CCK elevation• Increased norepinephrine levels• Mesenteric ischemia (Type 3c diabetes)• Diabetic neuropathy (Type 3c diabetes)Peripheral NervousSystem Abnormalities• Pancreatic nociception• Pancreatic neuropathy and neuroplasticityAdverse effects to treatment• Opioid induced bowel dysfunction• Complications to surgery and endoscopic therapy• Bacterial overgrowth due to changed bowel motilityCentral Nervous System Abnormalities• Impaired inhibitory pain modulationFigure 33-32. Pain mechanisms in chronic pancreatitis. (Reproduced with permission from Demir IE, |
Surgery_Schwartz_9653 | Surgery_Schwartz | to changed bowel motilityCentral Nervous System Abnormalities• Impaired inhibitory pain modulationFigure 33-32. Pain mechanisms in chronic pancreatitis. (Reproduced with permission from Demir IE, Tieftrunk E, Maak M, et al: Pain mechanisms in chronic pancreatitis: of a master and his fire, Langenbecks Arch Surg. 2011 Feb;396(2):151-160.)Patients with chronic pain due to chronic pancreatitis are often treated for years with escalating doses of narcotics, which imposes the additional problem of opioid dependency on this population. Further, it is now apparent that the pain pattern of many patients may be described as being either “visceral pain,” caused by inflammation in and around the pancreas, or “central sensitization of pain,” which is a syndrome of increased pain perception and sensitivity caused by the prolonged presence of pain167 (Fig. 33-32). Recent studies have suggested a method to differentiate these pain processes and further suggest that drugs that decrease or | Surgery_Schwartz. to changed bowel motilityCentral Nervous System Abnormalities• Impaired inhibitory pain modulationFigure 33-32. Pain mechanisms in chronic pancreatitis. (Reproduced with permission from Demir IE, Tieftrunk E, Maak M, et al: Pain mechanisms in chronic pancreatitis: of a master and his fire, Langenbecks Arch Surg. 2011 Feb;396(2):151-160.)Patients with chronic pain due to chronic pancreatitis are often treated for years with escalating doses of narcotics, which imposes the additional problem of opioid dependency on this population. Further, it is now apparent that the pain pattern of many patients may be described as being either “visceral pain,” caused by inflammation in and around the pancreas, or “central sensitization of pain,” which is a syndrome of increased pain perception and sensitivity caused by the prolonged presence of pain167 (Fig. 33-32). Recent studies have suggested a method to differentiate these pain processes and further suggest that drugs that decrease or |
Surgery_Schwartz_9654 | Surgery_Schwartz | and sensitivity caused by the prolonged presence of pain167 (Fig. 33-32). Recent studies have suggested a method to differentiate these pain processes and further suggest that drugs that decrease or ameliorate the central sensitization of pain, such as pregabalin and tramadol, may be especially useful in chronic pancreatitis patients.168 These methods of differential diagnosis of pain syndromes now appear to offer the means by which it is possible to further identify and predict which patients will ben-efit from a surgical approach to chronic pancreatitis.169Malabsorption and Weight Loss. When pancreatic exocrine capacity falls below 10% of normal, diarrhea and steatorrhea develop170 (Fig. 33-33). Patients describe a bulky, foul-smelling, loose (but not watery) stool that may be pale in color and float on the surface of toilet water. Frequently, patients will describe a greasy or oily appearance to the stool, or may describe an “oil slick” on the water’s surface. In severe | Surgery_Schwartz. and sensitivity caused by the prolonged presence of pain167 (Fig. 33-32). Recent studies have suggested a method to differentiate these pain processes and further suggest that drugs that decrease or ameliorate the central sensitization of pain, such as pregabalin and tramadol, may be especially useful in chronic pancreatitis patients.168 These methods of differential diagnosis of pain syndromes now appear to offer the means by which it is possible to further identify and predict which patients will ben-efit from a surgical approach to chronic pancreatitis.169Malabsorption and Weight Loss. When pancreatic exocrine capacity falls below 10% of normal, diarrhea and steatorrhea develop170 (Fig. 33-33). Patients describe a bulky, foul-smelling, loose (but not watery) stool that may be pale in color and float on the surface of toilet water. Frequently, patients will describe a greasy or oily appearance to the stool, or may describe an “oil slick” on the water’s surface. In severe |
Surgery_Schwartz_9655 | Surgery_Schwartz | pale in color and float on the surface of toilet water. Frequently, patients will describe a greasy or oily appearance to the stool, or may describe an “oil slick” on the water’s surface. In severe steatorrhea, an orange, 6040207010255075Fecal fat excretion (g/day)Normal lipase output (%)Figure 33-33. Relationship of lipase output to fat malabsorption. Excess fecal fat appears when the pancreatic lipase output falls below 10% of normal secretory values. (Data from DiMagno EP, Go VL, Summerskill WH. Relations between pancreatic enzyme out-puts and malabsorption in severe pancreatic insufficiency, N Engl J Med. 1973 Apr 19;288(16):813-815.)Brunicardi_Ch33_p1429-p1516.indd 146101/03/19 6:45 PM 1462SPECIFIC CONSIDERATIONSPART IIoily stool is often reported. As exocrine deficiency increases, symptoms of steatorrhea are often accompanied by weight loss. Patients may describe a good appetite despite weight loss or diminished food intake due to abdominal pain.In severe symptomatic chronic | Surgery_Schwartz. pale in color and float on the surface of toilet water. Frequently, patients will describe a greasy or oily appearance to the stool, or may describe an “oil slick” on the water’s surface. In severe steatorrhea, an orange, 6040207010255075Fecal fat excretion (g/day)Normal lipase output (%)Figure 33-33. Relationship of lipase output to fat malabsorption. Excess fecal fat appears when the pancreatic lipase output falls below 10% of normal secretory values. (Data from DiMagno EP, Go VL, Summerskill WH. Relations between pancreatic enzyme out-puts and malabsorption in severe pancreatic insufficiency, N Engl J Med. 1973 Apr 19;288(16):813-815.)Brunicardi_Ch33_p1429-p1516.indd 146101/03/19 6:45 PM 1462SPECIFIC CONSIDERATIONSPART IIoily stool is often reported. As exocrine deficiency increases, symptoms of steatorrhea are often accompanied by weight loss. Patients may describe a good appetite despite weight loss or diminished food intake due to abdominal pain.In severe symptomatic chronic |
Surgery_Schwartz_9656 | Surgery_Schwartz | symptoms of steatorrhea are often accompanied by weight loss. Patients may describe a good appetite despite weight loss or diminished food intake due to abdominal pain.In severe symptomatic chronic pancreatitis, anorexia or nausea may occur with or separate from abdominal pain. The combination of decreased food intake and malabsorption of nutrients usually results in chronic weight loss. As a result, many patients with severe chronic pancreatitis are below ideal body weight.Lipase deficiency tends to manifest itself before trypsin deficiency, so the presence of steatorrhea may be the first func-tional sign of pancreatic insufficiency.171 As pancreatic exocrine function deteriorates further, the secretion of bicarbonate into the duodenum is reduced, which causes duodenal acidification and further impairs nutrient absorption.172 Pancreatic exocrine insufficiency is frequently asymptomatic, however, and pancre-atic exocrine function is difficult to measure, so a diagnosis of chronic | Surgery_Schwartz. symptoms of steatorrhea are often accompanied by weight loss. Patients may describe a good appetite despite weight loss or diminished food intake due to abdominal pain.In severe symptomatic chronic pancreatitis, anorexia or nausea may occur with or separate from abdominal pain. The combination of decreased food intake and malabsorption of nutrients usually results in chronic weight loss. As a result, many patients with severe chronic pancreatitis are below ideal body weight.Lipase deficiency tends to manifest itself before trypsin deficiency, so the presence of steatorrhea may be the first func-tional sign of pancreatic insufficiency.171 As pancreatic exocrine function deteriorates further, the secretion of bicarbonate into the duodenum is reduced, which causes duodenal acidification and further impairs nutrient absorption.172 Pancreatic exocrine insufficiency is frequently asymptomatic, however, and pancre-atic exocrine function is difficult to measure, so a diagnosis of chronic |
Surgery_Schwartz_9657 | Surgery_Schwartz | and further impairs nutrient absorption.172 Pancreatic exocrine insufficiency is frequently asymptomatic, however, and pancre-atic exocrine function is difficult to measure, so a diagnosis of chronic pancreatitis is sufficient to justify a trial of pancreatic enzyme supplements. Each meal should be followed by 90,000 United States Pharmacopeia units of lipase, and the metabolic and symptomatic status of the patients should be followed.173Pancreatogenic Diabetes. The islets comprise only 2% of the mass of the pancreas, but they are preferentially conserved when pancreatic inflammation occurs. In chronic pancreatitis, acinar tissue loss and replacement by fibrosis is greater than the degree of loss of islet tissue. Islets are typically smaller than normal and may be isolated from their surrounding vascular network by the fibrosis. With progressive destruction of the gland, endocrine insufficiency commonly occurs. Frank diabetes is seen initially in about 20% of patients with chronic | Surgery_Schwartz. and further impairs nutrient absorption.172 Pancreatic exocrine insufficiency is frequently asymptomatic, however, and pancre-atic exocrine function is difficult to measure, so a diagnosis of chronic pancreatitis is sufficient to justify a trial of pancreatic enzyme supplements. Each meal should be followed by 90,000 United States Pharmacopeia units of lipase, and the metabolic and symptomatic status of the patients should be followed.173Pancreatogenic Diabetes. The islets comprise only 2% of the mass of the pancreas, but they are preferentially conserved when pancreatic inflammation occurs. In chronic pancreatitis, acinar tissue loss and replacement by fibrosis is greater than the degree of loss of islet tissue. Islets are typically smaller than normal and may be isolated from their surrounding vascular network by the fibrosis. With progressive destruction of the gland, endocrine insufficiency commonly occurs. Frank diabetes is seen initially in about 20% of patients with chronic |
Surgery_Schwartz_9658 | Surgery_Schwartz | vascular network by the fibrosis. With progressive destruction of the gland, endocrine insufficiency commonly occurs. Frank diabetes is seen initially in about 20% of patients with chronic pancreatitis, and impaired glucose metabolism can be detected in up to 70% of patients. In a study of 500 patients with predominantly alcoholic chronic pancreatitis, diabetes developed in 83% within 25 years of the clinical onset of chronic pancreatitis, and more than half of the diabetic patients required insulin treatment.174 Ketoacidosis and diabetic nephropathy are relatively uncommon in pancreato-genic diabetes (see Table 33-3), but retinopathy and neuropathy are seen to occur with a similar frequency as in type 1 and type 2 diabetes.175Pancreatogenic diabetes is most common in cases of chronic pancreatitis, and it is often seen after surgical resec-tion for benign or malignant disease176,177 (Fig. 33-34). Distal Hemochromatosis8%Cystic ÿbrosis4%Pancreatic resection3%Chronic | Surgery_Schwartz. vascular network by the fibrosis. With progressive destruction of the gland, endocrine insufficiency commonly occurs. Frank diabetes is seen initially in about 20% of patients with chronic pancreatitis, and impaired glucose metabolism can be detected in up to 70% of patients. In a study of 500 patients with predominantly alcoholic chronic pancreatitis, diabetes developed in 83% within 25 years of the clinical onset of chronic pancreatitis, and more than half of the diabetic patients required insulin treatment.174 Ketoacidosis and diabetic nephropathy are relatively uncommon in pancreato-genic diabetes (see Table 33-3), but retinopathy and neuropathy are seen to occur with a similar frequency as in type 1 and type 2 diabetes.175Pancreatogenic diabetes is most common in cases of chronic pancreatitis, and it is often seen after surgical resec-tion for benign or malignant disease176,177 (Fig. 33-34). Distal Hemochromatosis8%Cystic ÿbrosis4%Pancreatic resection3%Chronic |
Surgery_Schwartz_9659 | Surgery_Schwartz | of chronic pancreatitis, and it is often seen after surgical resec-tion for benign or malignant disease176,177 (Fig. 33-34). Distal Hemochromatosis8%Cystic ÿbrosis4%Pancreatic resection3%Chronic pancreatitis76%Pancreaticneoplasia9%A Distribution of T1DM, T2DM and T3cDMB Distribution of causes of T3cDMT3cDM8%T1DM12%T2DM80%Figure 33-34. Distribution of types of diabetes (A) and causes of type 3c (pancreatogenic) diabetes (B) based on studies of 1922 diabetic patients referred to an academic medical center as reported by Hardt et al. (Data from Hardt PD, Brendel MD, Kloer HU et al: Is pancreatic diabetes (type 3c diabetes) underdiagnosed and misdiagnosed? Diabetes Care. 2008 Feb;31 Suppl 2:S165-S169.)pancreatectomy and Whipple procedures have a higher inci-dence of diabetes than do drainage procedures, and the severity of diabetes is usually worse after subtotal or total pancreatec-tomy. Pancreatogenic, or type 3c diabetes (T3cDM), is seen in cystic fibrosis, in association with | Surgery_Schwartz. of chronic pancreatitis, and it is often seen after surgical resec-tion for benign or malignant disease176,177 (Fig. 33-34). Distal Hemochromatosis8%Cystic ÿbrosis4%Pancreatic resection3%Chronic pancreatitis76%Pancreaticneoplasia9%A Distribution of T1DM, T2DM and T3cDMB Distribution of causes of T3cDMT3cDM8%T1DM12%T2DM80%Figure 33-34. Distribution of types of diabetes (A) and causes of type 3c (pancreatogenic) diabetes (B) based on studies of 1922 diabetic patients referred to an academic medical center as reported by Hardt et al. (Data from Hardt PD, Brendel MD, Kloer HU et al: Is pancreatic diabetes (type 3c diabetes) underdiagnosed and misdiagnosed? Diabetes Care. 2008 Feb;31 Suppl 2:S165-S169.)pancreatectomy and Whipple procedures have a higher inci-dence of diabetes than do drainage procedures, and the severity of diabetes is usually worse after subtotal or total pancreatec-tomy. Pancreatogenic, or type 3c diabetes (T3cDM), is seen in cystic fibrosis, in association with |
Surgery_Schwartz_9660 | Surgery_Schwartz | procedures, and the severity of diabetes is usually worse after subtotal or total pancreatec-tomy. Pancreatogenic, or type 3c diabetes (T3cDM), is seen in cystic fibrosis, in association with pancreatic cancer, and in cases of severe hemochromatosis.178The etiology and pathophysiology of pancreatogenic diabetes is distinct from that of either autoimmune (type 1) or obesity-related (type 2) diabetes. In type 3c diabetes, the loss of functioning pancreatic tissue by disease or surgical removal results in a global deficiency of all three glucoregulatory islet cell hormones: insulin, glucagon, and PP. In addition, there is a paradoxical combination of enhanced peripheral sensitivity to insulin and decreased hepatic sensitivity to insulin.178,179 As a result, insulin therapy is frequently difficult; patients are hyper-glycemic when insulin replacement is insufficient (due to unsup-pressed hepatic glucose production) or hypoglycemic when insulin replacement is barely excessive (due to | Surgery_Schwartz. procedures, and the severity of diabetes is usually worse after subtotal or total pancreatec-tomy. Pancreatogenic, or type 3c diabetes (T3cDM), is seen in cystic fibrosis, in association with pancreatic cancer, and in cases of severe hemochromatosis.178The etiology and pathophysiology of pancreatogenic diabetes is distinct from that of either autoimmune (type 1) or obesity-related (type 2) diabetes. In type 3c diabetes, the loss of functioning pancreatic tissue by disease or surgical removal results in a global deficiency of all three glucoregulatory islet cell hormones: insulin, glucagon, and PP. In addition, there is a paradoxical combination of enhanced peripheral sensitivity to insulin and decreased hepatic sensitivity to insulin.178,179 As a result, insulin therapy is frequently difficult; patients are hyper-glycemic when insulin replacement is insufficient (due to unsup-pressed hepatic glucose production) or hypoglycemic when insulin replacement is barely excessive (due to |
Surgery_Schwartz_9661 | Surgery_Schwartz | difficult; patients are hyper-glycemic when insulin replacement is insufficient (due to unsup-pressed hepatic glucose production) or hypoglycemic when insulin replacement is barely excessive (due to enhanced periph-eral insulin sensitivity and a deficiency of pancreatic glucagon secretion to counteract the hypoglycemia). This form of diabetes is referred to as brittle diabetes and requires special attention.PP deficiency correlates with the severity of chronic pan-creatitis, and impairments in the hepatic action of insulin are reversed in PP-deficient chronic pancreatitis patients by admin-istration of PP.180 In addition, a study of type 1 and type 3c diabetic patients treated with insulin pump therapy revealed that the addition of a continuous subcutaneous infusion of PP reduced the insulin requirements needed for glycemic control.181 Studies are currently underway to identify a clinically suitable PP analog or PP receptor agonist.Laboratory Studies. The diagnosis of chronic | Surgery_Schwartz. difficult; patients are hyper-glycemic when insulin replacement is insufficient (due to unsup-pressed hepatic glucose production) or hypoglycemic when insulin replacement is barely excessive (due to enhanced periph-eral insulin sensitivity and a deficiency of pancreatic glucagon secretion to counteract the hypoglycemia). This form of diabetes is referred to as brittle diabetes and requires special attention.PP deficiency correlates with the severity of chronic pan-creatitis, and impairments in the hepatic action of insulin are reversed in PP-deficient chronic pancreatitis patients by admin-istration of PP.180 In addition, a study of type 1 and type 3c diabetic patients treated with insulin pump therapy revealed that the addition of a continuous subcutaneous infusion of PP reduced the insulin requirements needed for glycemic control.181 Studies are currently underway to identify a clinically suitable PP analog or PP receptor agonist.Laboratory Studies. The diagnosis of chronic |
Surgery_Schwartz_9662 | Surgery_Schwartz | the insulin requirements needed for glycemic control.181 Studies are currently underway to identify a clinically suitable PP analog or PP receptor agonist.Laboratory Studies. The diagnosis of chronic pancreatitis depends on the clinical presentation, a limited number of indirect measurements that correlate with pancreatic function, and selected imaging studies (Table 33-14). The direct measurement of pancreatic enzymes (e.g., lipase and amylase) by blood test is highly sensitive and fairly specific in acute pancreatitis but is seldom helpful in the diagnosis of chronic pancreatitis. The pancreatic endocrine product that correlates most strongly with chronic pancreatitis is the PP response to a test meal (Fig. 33-35). Severe chronic pancreatitis is associated with a blunted or absent PP response to feeding but, as with many other tests, a normal PP response does not rule out the presence of early disease.14Brunicardi_Ch33_p1429-p1516.indd 146201/03/19 6:45 PM 1463PANCREASCHAPTER | Surgery_Schwartz. the insulin requirements needed for glycemic control.181 Studies are currently underway to identify a clinically suitable PP analog or PP receptor agonist.Laboratory Studies. The diagnosis of chronic pancreatitis depends on the clinical presentation, a limited number of indirect measurements that correlate with pancreatic function, and selected imaging studies (Table 33-14). The direct measurement of pancreatic enzymes (e.g., lipase and amylase) by blood test is highly sensitive and fairly specific in acute pancreatitis but is seldom helpful in the diagnosis of chronic pancreatitis. The pancreatic endocrine product that correlates most strongly with chronic pancreatitis is the PP response to a test meal (Fig. 33-35). Severe chronic pancreatitis is associated with a blunted or absent PP response to feeding but, as with many other tests, a normal PP response does not rule out the presence of early disease.14Brunicardi_Ch33_p1429-p1516.indd 146201/03/19 6:45 PM 1463PANCREASCHAPTER |
Surgery_Schwartz_9663 | Surgery_Schwartz | response to feeding but, as with many other tests, a normal PP response does not rule out the presence of early disease.14Brunicardi_Ch33_p1429-p1516.indd 146201/03/19 6:45 PM 1463PANCREASCHAPTER 33The measurement of pancreatic exocrine secretion requires aspiration of pancreatic juice from the duodenum after nutrient (Lundh test meal) or hormonal (CCK or secretin) stimulation.182,183 Direct aspiration of pancreatic juice by endoscopic cannulation of the duct is performed in some centers, but it is not risk free, comfortable for the patient, or more sensitive than luminal intubation methods.184Indirect tests of pancreatic exocrine function are based on the measurement of metabolites of compounds that are altered (“digested”) by pancreatic exocrine products and can be quantified by serum or urine measurements. A commonly used indirect test is the bentiromide test, in which N-benzoyl-Ltyrosyl-p-aminobenzoic acid is ingested by the subject, and the urinary excretion of the | Surgery_Schwartz. response to feeding but, as with many other tests, a normal PP response does not rule out the presence of early disease.14Brunicardi_Ch33_p1429-p1516.indd 146201/03/19 6:45 PM 1463PANCREASCHAPTER 33The measurement of pancreatic exocrine secretion requires aspiration of pancreatic juice from the duodenum after nutrient (Lundh test meal) or hormonal (CCK or secretin) stimulation.182,183 Direct aspiration of pancreatic juice by endoscopic cannulation of the duct is performed in some centers, but it is not risk free, comfortable for the patient, or more sensitive than luminal intubation methods.184Indirect tests of pancreatic exocrine function are based on the measurement of metabolites of compounds that are altered (“digested”) by pancreatic exocrine products and can be quantified by serum or urine measurements. A commonly used indirect test is the bentiromide test, in which N-benzoyl-Ltyrosyl-p-aminobenzoic acid is ingested by the subject, and the urinary excretion of the |
Surgery_Schwartz_9664 | Surgery_Schwartz | by serum or urine measurements. A commonly used indirect test is the bentiromide test, in which N-benzoyl-Ltyrosyl-p-aminobenzoic acid is ingested by the subject, and the urinary excretion of the proteolytic metabolite p-aminobenzoic Table 33-14Tests for chronic pancreatitis I. Measurement of pancreatic products in blood A. Enzymes B. Pancreatic polypeptide II. Measurement of pancreatic exocrine secretion A. Direct measurements 1. Enzymes 2. Bicarbonate B. Indirect measurement 1. Bentiromide test 2. Schilling test 3. Fecal fat, chymotrypsin, or elastase concentration 4. [14C]-olein absorption III. Imaging techniques A. Plain film radiography of abdomen B. Ultrasonography C. Computed tomography D. Endoscopic retrograde cholangiopancreatography E. Magnetic resonance cholangiopancreatography F. Endoscopic ultrasonography04080120160Time (min)206010014018004080120160200–40IR-pancreatic polypeptide (pmol/L)NLCPFigure 33-35. Pancreatic polypeptide (PP) response to a test | Surgery_Schwartz. by serum or urine measurements. A commonly used indirect test is the bentiromide test, in which N-benzoyl-Ltyrosyl-p-aminobenzoic acid is ingested by the subject, and the urinary excretion of the proteolytic metabolite p-aminobenzoic Table 33-14Tests for chronic pancreatitis I. Measurement of pancreatic products in blood A. Enzymes B. Pancreatic polypeptide II. Measurement of pancreatic exocrine secretion A. Direct measurements 1. Enzymes 2. Bicarbonate B. Indirect measurement 1. Bentiromide test 2. Schilling test 3. Fecal fat, chymotrypsin, or elastase concentration 4. [14C]-olein absorption III. Imaging techniques A. Plain film radiography of abdomen B. Ultrasonography C. Computed tomography D. Endoscopic retrograde cholangiopancreatography E. Magnetic resonance cholangiopancreatography F. Endoscopic ultrasonography04080120160Time (min)206010014018004080120160200–40IR-pancreatic polypeptide (pmol/L)NLCPFigure 33-35. Pancreatic polypeptide (PP) response to a test |
Surgery_Schwartz_9665 | Surgery_Schwartz | ultrasonography04080120160Time (min)206010014018004080120160200–40IR-pancreatic polypeptide (pmol/L)NLCPFigure 33-35. Pancreatic polypeptide (PP) response to a test meal. Immunoreactive PP (IR-PP) responses in control subjects (NL, n = 6) and patients with severe chronic pancreatitis (CP) accom-panied by PP deficiency (CP, n = 5) are shown. A test meal was administered at 0 minutes. Means ± standard error of the mean are shown. (Reproduced with permission from Brunicardi FC, Chaiken RL, Ryan AS, et al. Pancreatic polypeptide administration improves abnormal glucose metabolism in patients with chronic pancreatitis, J Clin Endocrinol Metab. 1996 Oct;81(10):3566-3572.)acid (PABA) is measured.185 Although the sensitivity of the test is as high as 100% in patients with severe chronic pancreati-tis, it identifies only 40% to 50% of patients with mild disease, and reduced PABA excretion is found in patients with a variety of other GI, hepatic, and renal diseases. The quantification of stool | Surgery_Schwartz. ultrasonography04080120160Time (min)206010014018004080120160200–40IR-pancreatic polypeptide (pmol/L)NLCPFigure 33-35. Pancreatic polypeptide (PP) response to a test meal. Immunoreactive PP (IR-PP) responses in control subjects (NL, n = 6) and patients with severe chronic pancreatitis (CP) accom-panied by PP deficiency (CP, n = 5) are shown. A test meal was administered at 0 minutes. Means ± standard error of the mean are shown. (Reproduced with permission from Brunicardi FC, Chaiken RL, Ryan AS, et al. Pancreatic polypeptide administration improves abnormal glucose metabolism in patients with chronic pancreatitis, J Clin Endocrinol Metab. 1996 Oct;81(10):3566-3572.)acid (PABA) is measured.185 Although the sensitivity of the test is as high as 100% in patients with severe chronic pancreati-tis, it identifies only 40% to 50% of patients with mild disease, and reduced PABA excretion is found in patients with a variety of other GI, hepatic, and renal diseases. The quantification of stool |
Surgery_Schwartz_9666 | Surgery_Schwartz | it identifies only 40% to 50% of patients with mild disease, and reduced PABA excretion is found in patients with a variety of other GI, hepatic, and renal diseases. The quantification of stool fat has also been used as a measure of pancreatic lipase secretion, either through the direct measurement of total fecal fat levels while the subject consumes a diet of known fat con-tent, or by the measurement of exhaled 14CO2 after ingestion of [14C]-triolein or [14C]-olein. This so-called triolein breath test is less cumbersome than intubation methods and avoids the necessity of stool collections and analysis, but it also has a high false-negative rate.186Fecal levels of chymotrypsin187 and elastase188 have been proposed as simpler, less expensive tests of exocrine function and correlate well with loss of pancreatic function. As with other test methods, however, these tests lose their sensitivity in patients with mild to moderate chronic pancreatitis and may be more sensitive for other | Surgery_Schwartz. it identifies only 40% to 50% of patients with mild disease, and reduced PABA excretion is found in patients with a variety of other GI, hepatic, and renal diseases. The quantification of stool fat has also been used as a measure of pancreatic lipase secretion, either through the direct measurement of total fecal fat levels while the subject consumes a diet of known fat con-tent, or by the measurement of exhaled 14CO2 after ingestion of [14C]-triolein or [14C]-olein. This so-called triolein breath test is less cumbersome than intubation methods and avoids the necessity of stool collections and analysis, but it also has a high false-negative rate.186Fecal levels of chymotrypsin187 and elastase188 have been proposed as simpler, less expensive tests of exocrine function and correlate well with loss of pancreatic function. As with other test methods, however, these tests lose their sensitivity in patients with mild to moderate chronic pancreatitis and may be more sensitive for other |
Surgery_Schwartz_9667 | Surgery_Schwartz | with loss of pancreatic function. As with other test methods, however, these tests lose their sensitivity in patients with mild to moderate chronic pancreatitis and may be more sensitive for other causes of pancreatic dysfunction, including cystic fibrosis. Fecal elastase C1 measurements have become widespread in their use, and levels above 200 μg/g are considered normal, whereas levels below 100 μg/g are indica-tive of pancreatic exocrine insufficiency.189 The sensitivity and specificity of fecal elastase C1 measurements fall short of those needed for definitive diagnosis of pancreatic exocrine insuffi-ciency, however.190Radiologic imaging has become the principal method of diagnosis of chronic pancreatitis, with the codification of clas-sification systems that correlate with proven disease. ERCP has been considered the most sensitive radiologic test for the diagnosis of chronic pancreatitis, with specific ERCP findings that are highly correlative with the degree or stage of chronic | Surgery_Schwartz. with loss of pancreatic function. As with other test methods, however, these tests lose their sensitivity in patients with mild to moderate chronic pancreatitis and may be more sensitive for other causes of pancreatic dysfunction, including cystic fibrosis. Fecal elastase C1 measurements have become widespread in their use, and levels above 200 μg/g are considered normal, whereas levels below 100 μg/g are indica-tive of pancreatic exocrine insufficiency.189 The sensitivity and specificity of fecal elastase C1 measurements fall short of those needed for definitive diagnosis of pancreatic exocrine insuffi-ciency, however.190Radiologic imaging has become the principal method of diagnosis of chronic pancreatitis, with the codification of clas-sification systems that correlate with proven disease. ERCP has been considered the most sensitive radiologic test for the diagnosis of chronic pancreatitis, with specific ERCP findings that are highly correlative with the degree or stage of chronic |
Surgery_Schwartz_9668 | Surgery_Schwartz | ERCP has been considered the most sensitive radiologic test for the diagnosis of chronic pancreatitis, with specific ERCP findings that are highly correlative with the degree or stage of chronic disease191 (Table 33-15). CT scanning is sensitive for the diag-nosis of chronic pancreatitis when calcification, duct dilata-tion, or cystic disease is present, but it is not accurate in the absence of these findings. CT is helpful as a screening study to guide interventional therapy or other diagnostic modalities,158 although EUS has become the preferred method for the diagno-sis of pancreatic disease and offers the advantage of very-high-resolution images of the pancreatic parenchyma, the main and secondary ductal systems, cystic lesions, and calcific changes. Table 33-15Cambridge classification of chronic pancreatitis by endoscopic retrograde cholangiopancreatographyGRADEMAIN PANCREATIC DUCTSIDE BRANCHESNormalNormalNormalSuggestiveNormal<3 AbnormalMildNormal≥3 AbnormalModerateAbnormal>3 | Surgery_Schwartz. ERCP has been considered the most sensitive radiologic test for the diagnosis of chronic pancreatitis, with specific ERCP findings that are highly correlative with the degree or stage of chronic disease191 (Table 33-15). CT scanning is sensitive for the diag-nosis of chronic pancreatitis when calcification, duct dilata-tion, or cystic disease is present, but it is not accurate in the absence of these findings. CT is helpful as a screening study to guide interventional therapy or other diagnostic modalities,158 although EUS has become the preferred method for the diagno-sis of pancreatic disease and offers the advantage of very-high-resolution images of the pancreatic parenchyma, the main and secondary ductal systems, cystic lesions, and calcific changes. Table 33-15Cambridge classification of chronic pancreatitis by endoscopic retrograde cholangiopancreatographyGRADEMAIN PANCREATIC DUCTSIDE BRANCHESNormalNormalNormalSuggestiveNormal<3 AbnormalMildNormal≥3 AbnormalModerateAbnormal>3 |
Surgery_Schwartz_9669 | Surgery_Schwartz | of chronic pancreatitis by endoscopic retrograde cholangiopancreatographyGRADEMAIN PANCREATIC DUCTSIDE BRANCHESNormalNormalNormalSuggestiveNormal<3 AbnormalMildNormal≥3 AbnormalModerateAbnormal>3 AbnormalSevereAbnormal plus at least one of the following: large cavity, duct obstruction, dilation or duct irregularity, intraductal filing defects Reproduced with permission from Axon AT, Classen M, Cotton PB, et al: Pancreatography in chronic pancreatitis: international definitions, Gut. 1984 Oct;25(10):1107-1112.Brunicardi_Ch33_p1429-p1516.indd 146301/03/19 6:45 PM 1464SPECIFIC CONSIDERATIONSPART II246810060NonalcoholicsPancreatico-duodenectomyalcoholicsAlcoholics; 40–80%distal pancreatectomyAlcoholics; 80–95%distal pancreatectomyYears after surgical procedurePercent surviving1214708090100Figure 33-36. Effect of alcohol use on survival after surgical procedures. The cumulative survival of patients with chronic pancreatitis fol-lowing pancreaticoduodenectomy or distal pancreatectomy | Surgery_Schwartz. of chronic pancreatitis by endoscopic retrograde cholangiopancreatographyGRADEMAIN PANCREATIC DUCTSIDE BRANCHESNormalNormalNormalSuggestiveNormal<3 AbnormalMildNormal≥3 AbnormalModerateAbnormal>3 AbnormalSevereAbnormal plus at least one of the following: large cavity, duct obstruction, dilation or duct irregularity, intraductal filing defects Reproduced with permission from Axon AT, Classen M, Cotton PB, et al: Pancreatography in chronic pancreatitis: international definitions, Gut. 1984 Oct;25(10):1107-1112.Brunicardi_Ch33_p1429-p1516.indd 146301/03/19 6:45 PM 1464SPECIFIC CONSIDERATIONSPART II246810060NonalcoholicsPancreatico-duodenectomyalcoholicsAlcoholics; 40–80%distal pancreatectomyAlcoholics; 80–95%distal pancreatectomyYears after surgical procedurePercent surviving1214708090100Figure 33-36. Effect of alcohol use on survival after surgical procedures. The cumulative survival of patients with chronic pancreatitis fol-lowing pancreaticoduodenectomy or distal pancreatectomy |
Surgery_Schwartz_9670 | Surgery_Schwartz | 33-36. Effect of alcohol use on survival after surgical procedures. The cumulative survival of patients with chronic pancreatitis fol-lowing pancreaticoduodenectomy or distal pancreatectomy is shown for nonalcoholic and alcoholic patients. (Reproduced with permission from Frey CF, Child CG, Fry W. Pancreatectomy for chronic pancreatitis, Ann Surg. 1976 Oct;184(4):403-413.)EUS findings may be inconclusive in mild or “minimal change” pancreatitis, however, and improved criteria for an EUS-based diagnosis are still a work in progress.192 Most importantly, EUS is highly reliable in ruling out pancreatic carcinoma when CT findings are normal or equivocal.Prognosis and Natural History. The prognosis for patients with chronic pancreatitis is dependent on the etiology of the disease, the development of complications, and on the age and socioeconomic status of the patient. The influence of treat-ment is less evident in long-term studies, although the general absence of randomized, prospective | Surgery_Schwartz. 33-36. Effect of alcohol use on survival after surgical procedures. The cumulative survival of patients with chronic pancreatitis fol-lowing pancreaticoduodenectomy or distal pancreatectomy is shown for nonalcoholic and alcoholic patients. (Reproduced with permission from Frey CF, Child CG, Fry W. Pancreatectomy for chronic pancreatitis, Ann Surg. 1976 Oct;184(4):403-413.)EUS findings may be inconclusive in mild or “minimal change” pancreatitis, however, and improved criteria for an EUS-based diagnosis are still a work in progress.192 Most importantly, EUS is highly reliable in ruling out pancreatic carcinoma when CT findings are normal or equivocal.Prognosis and Natural History. The prognosis for patients with chronic pancreatitis is dependent on the etiology of the disease, the development of complications, and on the age and socioeconomic status of the patient. The influence of treat-ment is less evident in long-term studies, although the general absence of randomized, prospective |
Surgery_Schwartz_9671 | Surgery_Schwartz | of complications, and on the age and socioeconomic status of the patient. The influence of treat-ment is less evident in long-term studies, although the general absence of randomized, prospective trials clouds the issue of whether specific forms of therapy alter the long-term outlook for patients with the disease.Several studies have demonstrated that, although symp-toms of pain decrease over time in about half of the patients, this decline is also accompanied by a progression of exocrine and endocrine insufficiency.193 In general, the likelihood of eventual pain relief is dependent upon the stage of disease at diagnosis, and the persistence of alcohol use in patients with alcoholic chronic pancreatitis. Miyake and colleagues found that pain relief was achieved in 60% of alcoholic patients who suc-cessfully discontinued drinking, but in only 26% who did not.194The long-term survival of patients with chronic pancreatitis is less than for patients without pancreatitis. In an | Surgery_Schwartz. of complications, and on the age and socioeconomic status of the patient. The influence of treat-ment is less evident in long-term studies, although the general absence of randomized, prospective trials clouds the issue of whether specific forms of therapy alter the long-term outlook for patients with the disease.Several studies have demonstrated that, although symp-toms of pain decrease over time in about half of the patients, this decline is also accompanied by a progression of exocrine and endocrine insufficiency.193 In general, the likelihood of eventual pain relief is dependent upon the stage of disease at diagnosis, and the persistence of alcohol use in patients with alcoholic chronic pancreatitis. Miyake and colleagues found that pain relief was achieved in 60% of alcoholic patients who suc-cessfully discontinued drinking, but in only 26% who did not.194The long-term survival of patients with chronic pancreatitis is less than for patients without pancreatitis. In an |
Surgery_Schwartz_9672 | Surgery_Schwartz | patients who suc-cessfully discontinued drinking, but in only 26% who did not.194The long-term survival of patients with chronic pancreatitis is less than for patients without pancreatitis. In an international multicenter study of >2000 patients, Lowenfels and colleagues found that the 10and 20-year survival rates for patients with chronic pancreatitis were 70% and 45%, respectively, compared to 93% and 65% for patients without pancreatitis.195 The mortality risk was found to be 1.6-fold higher in patients who continued to abuse alcohol, compared to those who did not. Continued alcohol abuse has a similar effect on the response to surgical treatment (Fig. 33-36), and results in a twofold increase in mortality over a 10to 14-year follow-up period.195In addition to progressive endocrine and exocrine dysfunc-tion, and the risk of the specific complications outlined here and in Table 33-16, the other significant long-term risk for the patient with chronic pancreatitis is the development | Surgery_Schwartz. patients who suc-cessfully discontinued drinking, but in only 26% who did not.194The long-term survival of patients with chronic pancreatitis is less than for patients without pancreatitis. In an international multicenter study of >2000 patients, Lowenfels and colleagues found that the 10and 20-year survival rates for patients with chronic pancreatitis were 70% and 45%, respectively, compared to 93% and 65% for patients without pancreatitis.195 The mortality risk was found to be 1.6-fold higher in patients who continued to abuse alcohol, compared to those who did not. Continued alcohol abuse has a similar effect on the response to surgical treatment (Fig. 33-36), and results in a twofold increase in mortality over a 10to 14-year follow-up period.195In addition to progressive endocrine and exocrine dysfunc-tion, and the risk of the specific complications outlined here and in Table 33-16, the other significant long-term risk for the patient with chronic pancreatitis is the development |
Surgery_Schwartz_9673 | Surgery_Schwartz | exocrine dysfunc-tion, and the risk of the specific complications outlined here and in Table 33-16, the other significant long-term risk for the patient with chronic pancreatitis is the development of pancre-atic carcinoma.196 There is a progressive, cumulative increased risk of carcinoma development in patients with chronic pancre-atitis, which continues throughout the subsequent lifetime of the patient (Fig. 33-37). The incidence of carcinoma in patients with chronic pancreatitis ranges from 1.5% to 6%,196 which is at least 10-fold greater than that of patients of similar age seen in a hospital setting. In patients with chronic pancreatitis accom-panied by diabetes, the risk of carcinoma has been found to be increased 12to 33-fold compared to healthy, comparably aged controls.197,198 In patients with advanced chronic pancreatitis referred for surgical therapy, indolent, undiagnosed carcinoma can be seen in as many as 10% of patients.199The development of carcinoma in the setting of | Surgery_Schwartz. exocrine dysfunc-tion, and the risk of the specific complications outlined here and in Table 33-16, the other significant long-term risk for the patient with chronic pancreatitis is the development of pancre-atic carcinoma.196 There is a progressive, cumulative increased risk of carcinoma development in patients with chronic pancre-atitis, which continues throughout the subsequent lifetime of the patient (Fig. 33-37). The incidence of carcinoma in patients with chronic pancreatitis ranges from 1.5% to 6%,196 which is at least 10-fold greater than that of patients of similar age seen in a hospital setting. In patients with chronic pancreatitis accom-panied by diabetes, the risk of carcinoma has been found to be increased 12to 33-fold compared to healthy, comparably aged controls.197,198 In patients with advanced chronic pancreatitis referred for surgical therapy, indolent, undiagnosed carcinoma can be seen in as many as 10% of patients.199The development of carcinoma in the setting of |
Surgery_Schwartz_9674 | Surgery_Schwartz | patients with advanced chronic pancreatitis referred for surgical therapy, indolent, undiagnosed carcinoma can be seen in as many as 10% of patients.199The development of carcinoma in the setting of chronic pancreatitis is no doubt related to the dysregulation of cellu-lar proliferation and tissue repair processes in the setting of chronic inflammation, as is seen throughout the alimentary tract and elsewhere. In the setting of chronic pancreatitis, car-cinoma development can be especially cryptic, and the diagno-sis of early-stage tumors is particularly difficult. Awareness of this risk justifies close surveillance for cancer in patients with chronic pancreatitis. Periodic measurement of tumor markers such as CA19-9, and periodic imaging of the pancreas with CT scan and EUS seem logical in order to detect the development Table 33-16Complications of chronic pancreatitisIntrapancreatic complications Pseudocysts Duodenal or gastric obstruction Thrombosis of splenic | Surgery_Schwartz. patients with advanced chronic pancreatitis referred for surgical therapy, indolent, undiagnosed carcinoma can be seen in as many as 10% of patients.199The development of carcinoma in the setting of chronic pancreatitis is no doubt related to the dysregulation of cellu-lar proliferation and tissue repair processes in the setting of chronic inflammation, as is seen throughout the alimentary tract and elsewhere. In the setting of chronic pancreatitis, car-cinoma development can be especially cryptic, and the diagno-sis of early-stage tumors is particularly difficult. Awareness of this risk justifies close surveillance for cancer in patients with chronic pancreatitis. Periodic measurement of tumor markers such as CA19-9, and periodic imaging of the pancreas with CT scan and EUS seem logical in order to detect the development Table 33-16Complications of chronic pancreatitisIntrapancreatic complications Pseudocysts Duodenal or gastric obstruction Thrombosis of splenic |
Surgery_Schwartz_9675 | Surgery_Schwartz | EUS seem logical in order to detect the development Table 33-16Complications of chronic pancreatitisIntrapancreatic complications Pseudocysts Duodenal or gastric obstruction Thrombosis of splenic vein Abscess Perforation Erosion into visceral artery Inflammatory mass in head of pancreas Bile duct stenosis Portal vein thrombosis Duodenal obstruction Duct strictures and/or stones Ductal hypertension and dilatation Pancreatic carcinomaExtrapancreatic complications Pancreatic duct leak with ascites or fistula Pseudocyst extension beyond lesser sac into mediastinum, retroperitoneum, lateral pericolic spaces, pelvis, or adjacent visceraBrunicardi_Ch33_p1429-p1516.indd 146401/03/19 6:45 PM 1465PANCREASCHAPTER 33Table 33-17Definitions of pancreatic fluid collectionsTERMDEFINITIONPeripancreatic fluid collectionA collection of enzyme-rich pancreatic juice that occurs early in the course of acute pancreatitis, or that forms after a pancreatic duct leak; located in or near the | Surgery_Schwartz. EUS seem logical in order to detect the development Table 33-16Complications of chronic pancreatitisIntrapancreatic complications Pseudocysts Duodenal or gastric obstruction Thrombosis of splenic vein Abscess Perforation Erosion into visceral artery Inflammatory mass in head of pancreas Bile duct stenosis Portal vein thrombosis Duodenal obstruction Duct strictures and/or stones Ductal hypertension and dilatation Pancreatic carcinomaExtrapancreatic complications Pancreatic duct leak with ascites or fistula Pseudocyst extension beyond lesser sac into mediastinum, retroperitoneum, lateral pericolic spaces, pelvis, or adjacent visceraBrunicardi_Ch33_p1429-p1516.indd 146401/03/19 6:45 PM 1465PANCREASCHAPTER 33Table 33-17Definitions of pancreatic fluid collectionsTERMDEFINITIONPeripancreatic fluid collectionA collection of enzyme-rich pancreatic juice that occurs early in the course of acute pancreatitis, or that forms after a pancreatic duct leak; located in or near the |
Surgery_Schwartz_9676 | Surgery_Schwartz | fluid collectionA collection of enzyme-rich pancreatic juice that occurs early in the course of acute pancreatitis, or that forms after a pancreatic duct leak; located in or near the pancreas; it lacks a well-organized wall of granulation or fibrous tissueEarly pancreatic (sterile) necrosisA focal or diffuse area of nonviable pancreatic parenchyma, typically occupying >30% of the gland and containing liquefied debris and fluidLate pancreatic (sterile) necrosisAn organized collection of sterile necrotic debris and fluid with a well-defined margin or wall within the normal domain of the pancreasAcute pseudocystA collection of pancreatic juice enclosed within a perimeter of early granulation tissue, usually as a consequence of acute pancreatitis that has occurred within the preceding 3–4 wkChronic pseudocystA collection of pancreatic fluid surrounded by a wall of normal granulation and fibrous tissue, usually persisting for >6 wkPancreatic abscessAny of the above in which gross | Surgery_Schwartz. fluid collectionA collection of enzyme-rich pancreatic juice that occurs early in the course of acute pancreatitis, or that forms after a pancreatic duct leak; located in or near the pancreas; it lacks a well-organized wall of granulation or fibrous tissueEarly pancreatic (sterile) necrosisA focal or diffuse area of nonviable pancreatic parenchyma, typically occupying >30% of the gland and containing liquefied debris and fluidLate pancreatic (sterile) necrosisAn organized collection of sterile necrotic debris and fluid with a well-defined margin or wall within the normal domain of the pancreasAcute pseudocystA collection of pancreatic juice enclosed within a perimeter of early granulation tissue, usually as a consequence of acute pancreatitis that has occurred within the preceding 3–4 wkChronic pseudocystA collection of pancreatic fluid surrounded by a wall of normal granulation and fibrous tissue, usually persisting for >6 wkPancreatic abscessAny of the above in which gross |
Surgery_Schwartz_9677 | Surgery_Schwartz | 3–4 wkChronic pseudocystA collection of pancreatic fluid surrounded by a wall of normal granulation and fibrous tissue, usually persisting for >6 wkPancreatic abscessAny of the above in which gross purulence (pus) is present, with bacterial or fungal organisms documented to be presentModified with permission from Baron TH, Harewood GC, Morgan DE, et al. Outcome differences after endoscopic drainage of pancreatic necrosis, acute pancreatic pseudocysts, and chronic pancreatic pseudocysts, Gastrointest Endosc. 2002 Jul;56(1):7-17.Years after diagnosis of pancreatitisCumulative incidence of pancreatic cancer (%)12345605101520(1160)(599)(244)(64)Figure 33-37. Cumulative risk of pancreatic cancer in patients with chronic pancreatitis. The number of patients evaluated at different time intervals is shown in parentheses. (Reproduced with permis-sion from Lowenfels AB, Maisonneuve P, Cavallini G, et al. Pancre-atitis and the risk of pancreatic cancer. International Pancreatitis Study Group, N | Surgery_Schwartz. 3–4 wkChronic pseudocystA collection of pancreatic fluid surrounded by a wall of normal granulation and fibrous tissue, usually persisting for >6 wkPancreatic abscessAny of the above in which gross purulence (pus) is present, with bacterial or fungal organisms documented to be presentModified with permission from Baron TH, Harewood GC, Morgan DE, et al. Outcome differences after endoscopic drainage of pancreatic necrosis, acute pancreatic pseudocysts, and chronic pancreatic pseudocysts, Gastrointest Endosc. 2002 Jul;56(1):7-17.Years after diagnosis of pancreatitisCumulative incidence of pancreatic cancer (%)12345605101520(1160)(599)(244)(64)Figure 33-37. Cumulative risk of pancreatic cancer in patients with chronic pancreatitis. The number of patients evaluated at different time intervals is shown in parentheses. (Reproduced with permis-sion from Lowenfels AB, Maisonneuve P, Cavallini G, et al. Pancre-atitis and the risk of pancreatic cancer. International Pancreatitis Study Group, N |
Surgery_Schwartz_9678 | Surgery_Schwartz | is shown in parentheses. (Reproduced with permis-sion from Lowenfels AB, Maisonneuve P, Cavallini G, et al. Pancre-atitis and the risk of pancreatic cancer. International Pancreatitis Study Group, N Engl J Med. 1993 May 20;328(20):1433-1437.)of carcinoma in the patient with chronic pancreatitis, although no evidence exists to indicate that this alters the outcome of patients who develop pancreatic cancer. Surgical procedures, particularly drainage procedures performed for presumed chronic pancreatitis, should always include biopsy of the tissue to exclude the diagnosis of malignancy.ComplicationsPseudocyst. A chronic collection of pancreatic fluid surrounded by a nonepithelialized wall of granulation tissue and fibrosis is referred to as a pseudocyst. Pseudocysts occur in up to 10% of patients with acute pancreatitis, and in 20% to 38% of patients with chronic pancreatitis, and thus, they comprise the most com-mon complication of chronic pancreatitis.200-202 The identification and | Surgery_Schwartz. is shown in parentheses. (Reproduced with permis-sion from Lowenfels AB, Maisonneuve P, Cavallini G, et al. Pancre-atitis and the risk of pancreatic cancer. International Pancreatitis Study Group, N Engl J Med. 1993 May 20;328(20):1433-1437.)of carcinoma in the patient with chronic pancreatitis, although no evidence exists to indicate that this alters the outcome of patients who develop pancreatic cancer. Surgical procedures, particularly drainage procedures performed for presumed chronic pancreatitis, should always include biopsy of the tissue to exclude the diagnosis of malignancy.ComplicationsPseudocyst. A chronic collection of pancreatic fluid surrounded by a nonepithelialized wall of granulation tissue and fibrosis is referred to as a pseudocyst. Pseudocysts occur in up to 10% of patients with acute pancreatitis, and in 20% to 38% of patients with chronic pancreatitis, and thus, they comprise the most com-mon complication of chronic pancreatitis.200-202 The identification and |
Surgery_Schwartz_9679 | Surgery_Schwartz | patients with acute pancreatitis, and in 20% to 38% of patients with chronic pancreatitis, and thus, they comprise the most com-mon complication of chronic pancreatitis.200-202 The identification and treatment of pseudocysts requires definition of the various forms of pancreatic fluid collections that occur (Table 33-17). In chronic pancreatitis, a pancreatic duct leak with extravasa-tion of pancreatic juice results in a peripancreatic fluid collection (PPFC). Over a period of 3 to 4 weeks, the PPFC is sealed by an inflammatory reaction that leads to development of a wall of acute granulation tissue without much fibrosis. This is referred to as an acute pseudocyst. Acute pseudocysts may resolve spontane-ously in up to 50% of cases, over a course of 6 weeks or longer.203 Pseudocysts >6 cm resolve less frequently than smaller ones but may regress over a period of weeks to months. Pseudocysts are multiple in 17% of patients,202 or they may be multilobulated. They may occur | Surgery_Schwartz. patients with acute pancreatitis, and in 20% to 38% of patients with chronic pancreatitis, and thus, they comprise the most com-mon complication of chronic pancreatitis.200-202 The identification and treatment of pseudocysts requires definition of the various forms of pancreatic fluid collections that occur (Table 33-17). In chronic pancreatitis, a pancreatic duct leak with extravasa-tion of pancreatic juice results in a peripancreatic fluid collection (PPFC). Over a period of 3 to 4 weeks, the PPFC is sealed by an inflammatory reaction that leads to development of a wall of acute granulation tissue without much fibrosis. This is referred to as an acute pseudocyst. Acute pseudocysts may resolve spontane-ously in up to 50% of cases, over a course of 6 weeks or longer.203 Pseudocysts >6 cm resolve less frequently than smaller ones but may regress over a period of weeks to months. Pseudocysts are multiple in 17% of patients,202 or they may be multilobulated. They may occur |
Surgery_Schwartz_9680 | Surgery_Schwartz | >6 cm resolve less frequently than smaller ones but may regress over a period of weeks to months. Pseudocysts are multiple in 17% of patients,202 or they may be multilobulated. They may occur intrapancreatically or extend beyond the region of the pancreas into other cavities or compartments (Fig. 33-38).Pseudocysts may become secondarily infected, in which case they become abscesses. They can compress or obstruct adjacent organs or structures, leading to superior mesenteric-portal vein thrombosis or splenic vein thrombosis.204 They can erode into visceral arteries and cause intracystic hemorrhage or pseudoaneurysms (Fig. 33-39). They also can perforate and cause peritonitis or intraperitoneal bleeding.205Figure 33-38. Extensive pseudocyst disease. A computed tomo-graphic scan in a patient with alcoholic chronic pancreatitis dem-onstrates multiloculated pseudocyst disease.Pseudocysts usually cause symptoms of pain, fullness, or early satiety. Asymptomatic pseudocysts can be managed | Surgery_Schwartz. >6 cm resolve less frequently than smaller ones but may regress over a period of weeks to months. Pseudocysts are multiple in 17% of patients,202 or they may be multilobulated. They may occur intrapancreatically or extend beyond the region of the pancreas into other cavities or compartments (Fig. 33-38).Pseudocysts may become secondarily infected, in which case they become abscesses. They can compress or obstruct adjacent organs or structures, leading to superior mesenteric-portal vein thrombosis or splenic vein thrombosis.204 They can erode into visceral arteries and cause intracystic hemorrhage or pseudoaneurysms (Fig. 33-39). They also can perforate and cause peritonitis or intraperitoneal bleeding.205Figure 33-38. Extensive pseudocyst disease. A computed tomo-graphic scan in a patient with alcoholic chronic pancreatitis dem-onstrates multiloculated pseudocyst disease.Pseudocysts usually cause symptoms of pain, fullness, or early satiety. Asymptomatic pseudocysts can be managed |
Surgery_Schwartz_9681 | Surgery_Schwartz | with alcoholic chronic pancreatitis dem-onstrates multiloculated pseudocyst disease.Pseudocysts usually cause symptoms of pain, fullness, or early satiety. Asymptomatic pseudocysts can be managed expectantly and may resolve spontaneously or persist without complication.201,203 Symptomatic or enlarging pseudocysts require treatment, and any presumed pseudocyst without a documented antecedent episode of acute pancreatitis requires investigation to determine the etiology Brunicardi_Ch33_p1429-p1516.indd 146501/03/19 6:45 PM 1466SPECIFIC CONSIDERATIONSPART IIFigure 33-39. Pseudoaneurysm of the gastroduodenal artery. A pseudocyst can erode into an adjacent artery, which results in contained hemorrhage otherwise known as a pseudoaneurysm. A contrast-injected computed tomographic scan reveals active bleed-ing (area marked B) into a pseudocyst (arrows) as a result of this process. (Reproduced with permission from Balthazar EJ: CT diagnosis and staging of acute pancreatitis, Radiol Clin | Surgery_Schwartz. with alcoholic chronic pancreatitis dem-onstrates multiloculated pseudocyst disease.Pseudocysts usually cause symptoms of pain, fullness, or early satiety. Asymptomatic pseudocysts can be managed expectantly and may resolve spontaneously or persist without complication.201,203 Symptomatic or enlarging pseudocysts require treatment, and any presumed pseudocyst without a documented antecedent episode of acute pancreatitis requires investigation to determine the etiology Brunicardi_Ch33_p1429-p1516.indd 146501/03/19 6:45 PM 1466SPECIFIC CONSIDERATIONSPART IIFigure 33-39. Pseudoaneurysm of the gastroduodenal artery. A pseudocyst can erode into an adjacent artery, which results in contained hemorrhage otherwise known as a pseudoaneurysm. A contrast-injected computed tomographic scan reveals active bleed-ing (area marked B) into a pseudocyst (arrows) as a result of this process. (Reproduced with permission from Balthazar EJ: CT diagnosis and staging of acute pancreatitis, Radiol Clin |
Surgery_Schwartz_9682 | Surgery_Schwartz | active bleed-ing (area marked B) into a pseudocyst (arrows) as a result of this process. (Reproduced with permission from Balthazar EJ: CT diagnosis and staging of acute pancreatitis, Radiol Clin North Am. 1989 Jan;27(1):19-37.)of the lesion, including a cystic neoplasm.205 Although pseudocysts comprise roughly two-thirds of all pancreatic cystic lesions, they resemble cystadenomas and cystadenocarcinoma radiographically. An incidentally discovered cystic lesion should be examined by EUS and aspirated to determine whether it is a true pancreatic cystic neoplasm or a pseudocyst.The timing and method of treatment requires careful con-sideration. Pitfalls in the management of pseudocysts result from the incorrect (presumptive) diagnosis of a cystic neoplasm masquerading as a pseudocyst, a failure to appreciate the solid or debris-filled contents of a pseudocyst that appears to be fluid filled on CT scan, and a failure to document true adherence with an adjacent portion of the stomach | Surgery_Schwartz. active bleed-ing (area marked B) into a pseudocyst (arrows) as a result of this process. (Reproduced with permission from Balthazar EJ: CT diagnosis and staging of acute pancreatitis, Radiol Clin North Am. 1989 Jan;27(1):19-37.)of the lesion, including a cystic neoplasm.205 Although pseudocysts comprise roughly two-thirds of all pancreatic cystic lesions, they resemble cystadenomas and cystadenocarcinoma radiographically. An incidentally discovered cystic lesion should be examined by EUS and aspirated to determine whether it is a true pancreatic cystic neoplasm or a pseudocyst.The timing and method of treatment requires careful con-sideration. Pitfalls in the management of pseudocysts result from the incorrect (presumptive) diagnosis of a cystic neoplasm masquerading as a pseudocyst, a failure to appreciate the solid or debris-filled contents of a pseudocyst that appears to be fluid filled on CT scan, and a failure to document true adherence with an adjacent portion of the stomach |
Surgery_Schwartz_9683 | Surgery_Schwartz | failure to appreciate the solid or debris-filled contents of a pseudocyst that appears to be fluid filled on CT scan, and a failure to document true adherence with an adjacent portion of the stomach before attempting transgas-tric internal drainage.If the pseudocyst has failed to resolve with conserva-tive therapy and symptoms persist, internal drainage is usu-ally preferred to external drainage to avoid the complication of a pancreaticocutaneous fistula. Pseudocysts communicate with the pancreatic ductal system in up to 80% of cases,206 so external drainage creates a pathway for pancreatic duct leak-age to and through the catheter exit site. Internal drainage may be performed with either endoscopic methods (transgastric or transduodenal puncture and multiple stent placements, with or without a nasocystic irrigation catheter), or surgical methods (a true cystoenterostomy, biopsy of cyst wall, and evacuation of all debris and contents). Surgical options include a cystogastros-tomy | Surgery_Schwartz. failure to appreciate the solid or debris-filled contents of a pseudocyst that appears to be fluid filled on CT scan, and a failure to document true adherence with an adjacent portion of the stomach before attempting transgas-tric internal drainage.If the pseudocyst has failed to resolve with conserva-tive therapy and symptoms persist, internal drainage is usu-ally preferred to external drainage to avoid the complication of a pancreaticocutaneous fistula. Pseudocysts communicate with the pancreatic ductal system in up to 80% of cases,206 so external drainage creates a pathway for pancreatic duct leak-age to and through the catheter exit site. Internal drainage may be performed with either endoscopic methods (transgastric or transduodenal puncture and multiple stent placements, with or without a nasocystic irrigation catheter), or surgical methods (a true cystoenterostomy, biopsy of cyst wall, and evacuation of all debris and contents). Surgical options include a cystogastros-tomy |
Surgery_Schwartz_9684 | Surgery_Schwartz | without a nasocystic irrigation catheter), or surgical methods (a true cystoenterostomy, biopsy of cyst wall, and evacuation of all debris and contents). Surgical options include a cystogastros-tomy (Fig. 33-40), a Roux-en-Y cystojejunostomy, or a cysto-duodenostomy. Cystojejunostomy is the most versatile method, and it can be applied to pseudocysts that penetrate into the trans-verse mesocolon, the paracolic gutters, or the lesser sac. Cys-togastrostomy can be performed endoscopically207 (Fig. 33-41), laparoscopically,208 or by a combined laparoscopic-endoscopic method.209Because pseudocysts often communicate with the pan-creatic ductal system, two newer approaches to pseudocyst management are based on main duct drainage, rather than pseu-docyst drainage per se. Transpapillary stents inserted at the time Figure 33-40. Cystogastrostomy drainage of a retrogastric pancre-atic pseudocyst. A larger opening is made through the common wall of a retrogastric pseudocyst, and a portion of the | Surgery_Schwartz. without a nasocystic irrigation catheter), or surgical methods (a true cystoenterostomy, biopsy of cyst wall, and evacuation of all debris and contents). Surgical options include a cystogastros-tomy (Fig. 33-40), a Roux-en-Y cystojejunostomy, or a cysto-duodenostomy. Cystojejunostomy is the most versatile method, and it can be applied to pseudocysts that penetrate into the trans-verse mesocolon, the paracolic gutters, or the lesser sac. Cys-togastrostomy can be performed endoscopically207 (Fig. 33-41), laparoscopically,208 or by a combined laparoscopic-endoscopic method.209Because pseudocysts often communicate with the pan-creatic ductal system, two newer approaches to pseudocyst management are based on main duct drainage, rather than pseu-docyst drainage per se. Transpapillary stents inserted at the time Figure 33-40. Cystogastrostomy drainage of a retrogastric pancre-atic pseudocyst. A larger opening is made through the common wall of a retrogastric pseudocyst, and a portion of the |
Surgery_Schwartz_9685 | Surgery_Schwartz | at the time Figure 33-40. Cystogastrostomy drainage of a retrogastric pancre-atic pseudocyst. A larger opening is made through the common wall of a retrogastric pseudocyst, and a portion of the pseudocyst wall is submitted for histologic confirmation of the diagnosis. Suture reinforcement of the communication is performed to avoid the com-plication of bleeding. (Reproduced with permission from Bell RH, Rikkers LF, Mulholland M: Digestive Tract Surgery: A Text and Atlas. Philadelphia, PA: Lippincott Williams & Wilkins; 1996.)StomachFNAneedlePseudocystDuodenumPancreasLiverPseudocystDoublepigtailedstentsPancreasStomachEUSscopeABFigure 33-41. Technique of endoluminal cystogastrostomy. A. Endoscopic ultrasound (EUS)-guided transgastric puncture of pancreatic pseudocyst. B. Transgastric stents placed across fused posterior wall of stomach and anterior wall of pseudocyst. (Repro-duced with permission from Chauhan SS, Forsmark CE. Evidence-based treatment of pancreatic pseudocysts, | Surgery_Schwartz. at the time Figure 33-40. Cystogastrostomy drainage of a retrogastric pancre-atic pseudocyst. A larger opening is made through the common wall of a retrogastric pseudocyst, and a portion of the pseudocyst wall is submitted for histologic confirmation of the diagnosis. Suture reinforcement of the communication is performed to avoid the com-plication of bleeding. (Reproduced with permission from Bell RH, Rikkers LF, Mulholland M: Digestive Tract Surgery: A Text and Atlas. Philadelphia, PA: Lippincott Williams & Wilkins; 1996.)StomachFNAneedlePseudocystDuodenumPancreasLiverPseudocystDoublepigtailedstentsPancreasStomachEUSscopeABFigure 33-41. Technique of endoluminal cystogastrostomy. A. Endoscopic ultrasound (EUS)-guided transgastric puncture of pancreatic pseudocyst. B. Transgastric stents placed across fused posterior wall of stomach and anterior wall of pseudocyst. (Repro-duced with permission from Chauhan SS, Forsmark CE. Evidence-based treatment of pancreatic pseudocysts, |
Surgery_Schwartz_9686 | Surgery_Schwartz | stents placed across fused posterior wall of stomach and anterior wall of pseudocyst. (Repro-duced with permission from Chauhan SS, Forsmark CE. Evidence-based treatment of pancreatic pseudocysts, Gastroenterology. 2013 Sep;145(3):511-5113.)Brunicardi_Ch33_p1429-p1516.indd 146601/03/19 6:45 PM 1467PANCREASCHAPTER 33ABFigure 33-42. Transpapillary drainage of a pancreatic pseudocyst. A. Endoscopic passage of a flexible wire through the major papilla, through the pancreatic duct, and into a communicating pseudocyst. B. Placement of a stent over the wire into the pseudocyst with transpapillary drainage. (Reproduced with permission from Kozarek RA, Brayko CM, Harlan J, et al. Endoscopic drainage of pancreatic pseudocysts, Gastrointest Endosc. 1985 Oct;31(5):322-327.)of ERCP may be directed into a pseudocyst through the ductal communication itself (Fig. 33-42), or they can be left across the area of suspected duct leakage to facilitate decompression and cyst drainage, analogous to the | Surgery_Schwartz. stents placed across fused posterior wall of stomach and anterior wall of pseudocyst. (Repro-duced with permission from Chauhan SS, Forsmark CE. Evidence-based treatment of pancreatic pseudocysts, Gastroenterology. 2013 Sep;145(3):511-5113.)Brunicardi_Ch33_p1429-p1516.indd 146601/03/19 6:45 PM 1467PANCREASCHAPTER 33ABFigure 33-42. Transpapillary drainage of a pancreatic pseudocyst. A. Endoscopic passage of a flexible wire through the major papilla, through the pancreatic duct, and into a communicating pseudocyst. B. Placement of a stent over the wire into the pseudocyst with transpapillary drainage. (Reproduced with permission from Kozarek RA, Brayko CM, Harlan J, et al. Endoscopic drainage of pancreatic pseudocysts, Gastrointest Endosc. 1985 Oct;31(5):322-327.)of ERCP may be directed into a pseudocyst through the ductal communication itself (Fig. 33-42), or they can be left across the area of suspected duct leakage to facilitate decompression and cyst drainage, analogous to the |
Surgery_Schwartz_9687 | Surgery_Schwartz | into a pseudocyst through the ductal communication itself (Fig. 33-42), or they can be left across the area of suspected duct leakage to facilitate decompression and cyst drainage, analogous to the use of common bile duct stents in the setting of a cystic duct leak.206 In a surgical series of patients with chronic pancreatitis, ductal dilatation, and a coex-isting pseudocyst, Nealon and Walser showed that duct drainage alone, without a separate cystoenteric anastomosis, was as suc-cessful as a combined drainage procedure.92 Furthermore, the “duct drainage only” group enjoyed a shorter hospital stay and fewer complications than the group who underwent a separate cystoenterostomy. These observations suggest that transductal drainage may be a safe and effective approach to the manage-ment of pseudocystic disease.The complications of endoscopic drainage of pseudocysts often require surgical intervention. Bleeding from the cystoenterostomy and inoculation of a pseudocyst with failure of | Surgery_Schwartz. into a pseudocyst through the ductal communication itself (Fig. 33-42), or they can be left across the area of suspected duct leakage to facilitate decompression and cyst drainage, analogous to the use of common bile duct stents in the setting of a cystic duct leak.206 In a surgical series of patients with chronic pancreatitis, ductal dilatation, and a coex-isting pseudocyst, Nealon and Walser showed that duct drainage alone, without a separate cystoenteric anastomosis, was as suc-cessful as a combined drainage procedure.92 Furthermore, the “duct drainage only” group enjoyed a shorter hospital stay and fewer complications than the group who underwent a separate cystoenterostomy. These observations suggest that transductal drainage may be a safe and effective approach to the manage-ment of pseudocystic disease.The complications of endoscopic drainage of pseudocysts often require surgical intervention. Bleeding from the cystoenterostomy and inoculation of a pseudocyst with failure of |
Surgery_Schwartz_9688 | Surgery_Schwartz | of pseudocystic disease.The complications of endoscopic drainage of pseudocysts often require surgical intervention. Bleeding from the cystoenterostomy and inoculation of a pseudocyst with failure of resolution and persistence of infection may require surgical treatment. Bleeding risks may be lessened by the routine use of EUS in the selection of the site for transluminal stent placement.210 Endoscopic treatment of pseudocysts requires large-bore catheters or multiple stents and an aggressive approach to management for success to be achieved. Failure of nonsurgical therapy, with subsequent salvage procedures to remove infected debris and establish complete drainage, is associated with increased risks for complications and death.211,212 The most experienced therapeutic endoscopists report a complication rate of 17% to 19% for the treatment of sterile pseudocysts, and deaths as a result of endoscopic therapy have occurred.212 Therefore, the use of endoscopic methods to treat sterile or | Surgery_Schwartz. of pseudocystic disease.The complications of endoscopic drainage of pseudocysts often require surgical intervention. Bleeding from the cystoenterostomy and inoculation of a pseudocyst with failure of resolution and persistence of infection may require surgical treatment. Bleeding risks may be lessened by the routine use of EUS in the selection of the site for transluminal stent placement.210 Endoscopic treatment of pseudocysts requires large-bore catheters or multiple stents and an aggressive approach to management for success to be achieved. Failure of nonsurgical therapy, with subsequent salvage procedures to remove infected debris and establish complete drainage, is associated with increased risks for complications and death.211,212 The most experienced therapeutic endoscopists report a complication rate of 17% to 19% for the treatment of sterile pseudocysts, and deaths as a result of endoscopic therapy have occurred.212 Therefore, the use of endoscopic methods to treat sterile or |
Surgery_Schwartz_9689 | Surgery_Schwartz | a complication rate of 17% to 19% for the treatment of sterile pseudocysts, and deaths as a result of endoscopic therapy have occurred.212 Therefore, the use of endoscopic methods to treat sterile or infected pancreatic necrosis has a higher complication rate and is limited to specialized centers.Resection of a pseudocyst is sometimes indicated for cysts located in the pancreatic tail or when a midpancreatic duct disruption has resulted in a distally located pseudocyst. Distal pancreatectomy for removal of a pseudocyst, with or without splenectomy, can be a challenging procedure in the setting of prior pancreatitis. An internal drainage procedure of the com-municating duct or of the pseudocyst itself should be considered when distal resection is being contemplated.Pancreatic Ascites. When a disrupted pancreatic duct leads to pancreatic fluid extravasation that does not become sequestered as a pseudocyst, but drains freely into the peritoneal cavity, pan-creatic ascites occurs. | Surgery_Schwartz. a complication rate of 17% to 19% for the treatment of sterile pseudocysts, and deaths as a result of endoscopic therapy have occurred.212 Therefore, the use of endoscopic methods to treat sterile or infected pancreatic necrosis has a higher complication rate and is limited to specialized centers.Resection of a pseudocyst is sometimes indicated for cysts located in the pancreatic tail or when a midpancreatic duct disruption has resulted in a distally located pseudocyst. Distal pancreatectomy for removal of a pseudocyst, with or without splenectomy, can be a challenging procedure in the setting of prior pancreatitis. An internal drainage procedure of the com-municating duct or of the pseudocyst itself should be considered when distal resection is being contemplated.Pancreatic Ascites. When a disrupted pancreatic duct leads to pancreatic fluid extravasation that does not become sequestered as a pseudocyst, but drains freely into the peritoneal cavity, pan-creatic ascites occurs. |
Surgery_Schwartz_9690 | Surgery_Schwartz | a disrupted pancreatic duct leads to pancreatic fluid extravasation that does not become sequestered as a pseudocyst, but drains freely into the peritoneal cavity, pan-creatic ascites occurs. Occasionally, the pancreatic fluid tracks superiorly into the thorax, and a pancreatic pleural effusion occurs. Referred to as internal pancreatic fistulae, both compli-cations are seen more often in patients with chronic pancreatitis rather than after acute pancreatitis. Pancreatic ascites and pleu-ral effusion occur together in 14% of patients, and 18% have a pancreatic pleural effusion alone.213Patients demonstrate the general demographics of chronic pancreatitis and usually present with a subacute or recent his-tory of progressive abdominal swelling despite weight loss. Pain and nausea are rarely present. The abdominal CT scan discloses ascites and the presence of chronic pancreatitis or a partially collapsed pseudocyst (Fig. 33-43). Paracentesis or thoracente-sis reveals noninfected fluid | Surgery_Schwartz. a disrupted pancreatic duct leads to pancreatic fluid extravasation that does not become sequestered as a pseudocyst, but drains freely into the peritoneal cavity, pan-creatic ascites occurs. Occasionally, the pancreatic fluid tracks superiorly into the thorax, and a pancreatic pleural effusion occurs. Referred to as internal pancreatic fistulae, both compli-cations are seen more often in patients with chronic pancreatitis rather than after acute pancreatitis. Pancreatic ascites and pleu-ral effusion occur together in 14% of patients, and 18% have a pancreatic pleural effusion alone.213Patients demonstrate the general demographics of chronic pancreatitis and usually present with a subacute or recent his-tory of progressive abdominal swelling despite weight loss. Pain and nausea are rarely present. The abdominal CT scan discloses ascites and the presence of chronic pancreatitis or a partially collapsed pseudocyst (Fig. 33-43). Paracentesis or thoracente-sis reveals noninfected fluid |
Surgery_Schwartz_9691 | Surgery_Schwartz | present. The abdominal CT scan discloses ascites and the presence of chronic pancreatitis or a partially collapsed pseudocyst (Fig. 33-43). Paracentesis or thoracente-sis reveals noninfected fluid with a protein level >25 g/L and a markedly elevated amylase level. Serum amylase may also be elevated, presumably from reabsorption across the parietal membrane. Serum albumin may be low, and patients may have Figure 33-43. Pancreatic ascites. Computed tomographic scan of a patient with a ruptured pancreatic pseudocyst resulting in intra-peritoneal pancreatic fluid. (Reproduced with permission from Cameron JL, Cameron AM: Current Surgical Therapy, 11th ed. Philadelphia, PA: Elsevier; 2014.)Brunicardi_Ch33_p1429-p1516.indd 146701/03/19 6:45 PM 1468SPECIFIC CONSIDERATIONSPART IIFigure 33-44. Internal drainage for leaking pancreatic duct. A Roux-en-Y pancreaticojejunostomy is performed at the site of duct rupture to accomplish internal drainage of the pancreatic duct leak. (Reproduced with | Surgery_Schwartz. present. The abdominal CT scan discloses ascites and the presence of chronic pancreatitis or a partially collapsed pseudocyst (Fig. 33-43). Paracentesis or thoracente-sis reveals noninfected fluid with a protein level >25 g/L and a markedly elevated amylase level. Serum amylase may also be elevated, presumably from reabsorption across the parietal membrane. Serum albumin may be low, and patients may have Figure 33-43. Pancreatic ascites. Computed tomographic scan of a patient with a ruptured pancreatic pseudocyst resulting in intra-peritoneal pancreatic fluid. (Reproduced with permission from Cameron JL, Cameron AM: Current Surgical Therapy, 11th ed. Philadelphia, PA: Elsevier; 2014.)Brunicardi_Ch33_p1429-p1516.indd 146701/03/19 6:45 PM 1468SPECIFIC CONSIDERATIONSPART IIFigure 33-44. Internal drainage for leaking pancreatic duct. A Roux-en-Y pancreaticojejunostomy is performed at the site of duct rupture to accomplish internal drainage of the pancreatic duct leak. (Reproduced with |
Surgery_Schwartz_9692 | Surgery_Schwartz | drainage for leaking pancreatic duct. A Roux-en-Y pancreaticojejunostomy is performed at the site of duct rupture to accomplish internal drainage of the pancreatic duct leak. (Reproduced with permission from Beger HG: The Pancreas. London: Blackwell-Science; 1998.)coexisting liver disease. Paracentesis is therefore critical to dif-ferentiate pancreatic from hepatic ascites.ERCP is most helpful to delineate the location of the pan-creatic duct leak and to elucidate the underlying pancreatic duc-tal anatomy. Pancreatic duct stenting may be considered at the time of ERCP, but if nonsurgical therapy is undertaken and then abandoned, repeat imaging of the pancreatic duct is appropriate to guide surgical treatment.Antisecretory therapy with the somatostatin analogue octreotide acetate, together with bowel rest and parenteral nutrition, is successful in more than half of patients.214,215 Reap-position of serosal surfaces to facilitate closure of the leak is considered a part of therapy, and | Surgery_Schwartz. drainage for leaking pancreatic duct. A Roux-en-Y pancreaticojejunostomy is performed at the site of duct rupture to accomplish internal drainage of the pancreatic duct leak. (Reproduced with permission from Beger HG: The Pancreas. London: Blackwell-Science; 1998.)coexisting liver disease. Paracentesis is therefore critical to dif-ferentiate pancreatic from hepatic ascites.ERCP is most helpful to delineate the location of the pan-creatic duct leak and to elucidate the underlying pancreatic duc-tal anatomy. Pancreatic duct stenting may be considered at the time of ERCP, but if nonsurgical therapy is undertaken and then abandoned, repeat imaging of the pancreatic duct is appropriate to guide surgical treatment.Antisecretory therapy with the somatostatin analogue octreotide acetate, together with bowel rest and parenteral nutrition, is successful in more than half of patients.214,215 Reap-position of serosal surfaces to facilitate closure of the leak is considered a part of therapy, and |
Surgery_Schwartz_9693 | Surgery_Schwartz | with bowel rest and parenteral nutrition, is successful in more than half of patients.214,215 Reap-position of serosal surfaces to facilitate closure of the leak is considered a part of therapy, and this is accomplished by com-plete paracentesis. For pleural effusions, a period of chest tube drainage may facilitate closure of the internal fistula.214 Surgi-cal therapy is reserved for those who fail to respond to medical treatment. If the leak originates from the central region of the pancreas, a Roux-en-Y pancreaticojejunostomy is performed to the site of duct leakage215 (Fig. 33-44). If the leak is in the tail, a distal pancreatectomy may be considered, or an internal drainage procedure can be performed. The results of surgical treatment are usually favorable if the ductal anatomy has been carefully delineated preoperatively.Pancreatic-Enteric Fistula. The erosion of a pancreatic pseu-docyst into an adjacent hollow viscus can result in a pancreatic-enteric fistula. The most common | Surgery_Schwartz. with bowel rest and parenteral nutrition, is successful in more than half of patients.214,215 Reap-position of serosal surfaces to facilitate closure of the leak is considered a part of therapy, and this is accomplished by com-plete paracentesis. For pleural effusions, a period of chest tube drainage may facilitate closure of the internal fistula.214 Surgi-cal therapy is reserved for those who fail to respond to medical treatment. If the leak originates from the central region of the pancreas, a Roux-en-Y pancreaticojejunostomy is performed to the site of duct leakage215 (Fig. 33-44). If the leak is in the tail, a distal pancreatectomy may be considered, or an internal drainage procedure can be performed. The results of surgical treatment are usually favorable if the ductal anatomy has been carefully delineated preoperatively.Pancreatic-Enteric Fistula. The erosion of a pancreatic pseu-docyst into an adjacent hollow viscus can result in a pancreatic-enteric fistula. The most common |
Surgery_Schwartz_9694 | Surgery_Schwartz | been carefully delineated preoperatively.Pancreatic-Enteric Fistula. The erosion of a pancreatic pseu-docyst into an adjacent hollow viscus can result in a pancreatic-enteric fistula. The most common site of communication is the transverse colon or splenic flexure. The fistula usually presents with evidence of GI or colonic bleeding and sepsis. If the fis-tula communicates with the stomach or duodenum, it may close spontaneously or persist as a pancreatic-enteric fistula. When the fistula involves the colon, operative correction is usually required.215Head-of-Pancreas Mass. In up to 30% of patients with advanced chronic pancreatitis, an inflammatory mass develops in the head of the pancreas.216 The clinical presentation includes severe pain and frequently includes stenosis of the distal common bile duct, duodenal stenosis, compression of the portal vein, and stenosis of the proximal main pancreatic duct (Table 33-18). Mutations and polymorphisms of p53 have been found in these | Surgery_Schwartz. been carefully delineated preoperatively.Pancreatic-Enteric Fistula. The erosion of a pancreatic pseu-docyst into an adjacent hollow viscus can result in a pancreatic-enteric fistula. The most common site of communication is the transverse colon or splenic flexure. The fistula usually presents with evidence of GI or colonic bleeding and sepsis. If the fis-tula communicates with the stomach or duodenum, it may close spontaneously or persist as a pancreatic-enteric fistula. When the fistula involves the colon, operative correction is usually required.215Head-of-Pancreas Mass. In up to 30% of patients with advanced chronic pancreatitis, an inflammatory mass develops in the head of the pancreas.216 The clinical presentation includes severe pain and frequently includes stenosis of the distal common bile duct, duodenal stenosis, compression of the portal vein, and stenosis of the proximal main pancreatic duct (Table 33-18). Mutations and polymorphisms of p53 have been found in these |
Surgery_Schwartz_9695 | Surgery_Schwartz | common bile duct, duodenal stenosis, compression of the portal vein, and stenosis of the proximal main pancreatic duct (Table 33-18). Mutations and polymorphisms of p53 have been found in these patients, and a focus of ductular carcinoma was found in 3.7% of patients with pancreatic head enlargement in one series.217 It was concluded that an accelerated transformation from hyperplasia to dysplasia exists in patients with pancreatic head enlargement, although the etiology for this process remains unclear.Splenic and Portal Vein Thrombosis. Vascular complications of chronic pancreatitis are fortunately infrequent because they are difficult to treat successfully. Portal vein compression and occlusion can occur as a consequence of an inflammatory mass in the head of the pancreas, and splenic vein thrombosis occurs in association with chronic pancreatitis in 4% to 8% of cases.218 Variceal formation can occur as a consequence of either portal or splenic venous occlusion, and splenic vein | Surgery_Schwartz. common bile duct, duodenal stenosis, compression of the portal vein, and stenosis of the proximal main pancreatic duct (Table 33-18). Mutations and polymorphisms of p53 have been found in these patients, and a focus of ductular carcinoma was found in 3.7% of patients with pancreatic head enlargement in one series.217 It was concluded that an accelerated transformation from hyperplasia to dysplasia exists in patients with pancreatic head enlargement, although the etiology for this process remains unclear.Splenic and Portal Vein Thrombosis. Vascular complications of chronic pancreatitis are fortunately infrequent because they are difficult to treat successfully. Portal vein compression and occlusion can occur as a consequence of an inflammatory mass in the head of the pancreas, and splenic vein thrombosis occurs in association with chronic pancreatitis in 4% to 8% of cases.218 Variceal formation can occur as a consequence of either portal or splenic venous occlusion, and splenic vein |
Surgery_Schwartz_9696 | Surgery_Schwartz | vein thrombosis occurs in association with chronic pancreatitis in 4% to 8% of cases.218 Variceal formation can occur as a consequence of either portal or splenic venous occlusion, and splenic vein thrombosis with gas-tric variceal formation is referred to as left-sided or sinistral por-tal hypertension. Although bleeding complications are infrequent, the mortality risk of bleeding is >20%. When gastroesophageal varices are caused by splenic vein thrombosis, the addition of splenectomy to prevent variceal hemorrhage is prudent when sur-gery is otherwise indicated to correct other problems.TreatmentMedical Therapy. The medical treatment of chronic or recurrent pain in chronic pancreatitis requires the use of analgesics, a cessation of alcohol use, oral enzyme therapy, and the selective use of antisecretory therapy. Interventional procedures to block visceral afferent nerve conduction or to treat obstructions of the main pancreatic duct are also an adjunct to medical | Surgery_Schwartz. vein thrombosis occurs in association with chronic pancreatitis in 4% to 8% of cases.218 Variceal formation can occur as a consequence of either portal or splenic venous occlusion, and splenic vein thrombosis with gas-tric variceal formation is referred to as left-sided or sinistral por-tal hypertension. Although bleeding complications are infrequent, the mortality risk of bleeding is >20%. When gastroesophageal varices are caused by splenic vein thrombosis, the addition of splenectomy to prevent variceal hemorrhage is prudent when sur-gery is otherwise indicated to correct other problems.TreatmentMedical Therapy. The medical treatment of chronic or recurrent pain in chronic pancreatitis requires the use of analgesics, a cessation of alcohol use, oral enzyme therapy, and the selective use of antisecretory therapy. Interventional procedures to block visceral afferent nerve conduction or to treat obstructions of the main pancreatic duct are also an adjunct to medical |
Surgery_Schwartz_9697 | Surgery_Schwartz | the selective use of antisecretory therapy. Interventional procedures to block visceral afferent nerve conduction or to treat obstructions of the main pancreatic duct are also an adjunct to medical treatment.Analgesia. Oral analgesics are prescribed as needed, alone or with analgesia-enhancing agents such as gabapentin.168 Ade-quate pain control usually requires the use of narcotics, but these should be titrated to achieve pain relief with the lowest effective dose. Opioid addiction is common, and the use of long-acting analgesics by transdermal patch together with oral agents for pain exacerbations slightly reduces the sedative effects of high-dose oral narcotics.Table 33-18Signs and symptoms of chronic pancreatitis with and without a pancreatic head massSIGNS AND SYMPTOMSWITH HEAD ENLARGEMENT (n = 138) (%)WITHOUT HEAD ENLARGEMENT (n = 141) (%)Daily severe pain6740Cholestasis4611Duodenal obstruction307Diabetes mellitus1830Vascular involvement158Reproduced with permission from | Surgery_Schwartz. the selective use of antisecretory therapy. Interventional procedures to block visceral afferent nerve conduction or to treat obstructions of the main pancreatic duct are also an adjunct to medical treatment.Analgesia. Oral analgesics are prescribed as needed, alone or with analgesia-enhancing agents such as gabapentin.168 Ade-quate pain control usually requires the use of narcotics, but these should be titrated to achieve pain relief with the lowest effective dose. Opioid addiction is common, and the use of long-acting analgesics by transdermal patch together with oral agents for pain exacerbations slightly reduces the sedative effects of high-dose oral narcotics.Table 33-18Signs and symptoms of chronic pancreatitis with and without a pancreatic head massSIGNS AND SYMPTOMSWITH HEAD ENLARGEMENT (n = 138) (%)WITHOUT HEAD ENLARGEMENT (n = 141) (%)Daily severe pain6740Cholestasis4611Duodenal obstruction307Diabetes mellitus1830Vascular involvement158Reproduced with permission from |
Surgery_Schwartz_9698 | Surgery_Schwartz | ENLARGEMENT (n = 138) (%)WITHOUT HEAD ENLARGEMENT (n = 141) (%)Daily severe pain6740Cholestasis4611Duodenal obstruction307Diabetes mellitus1830Vascular involvement158Reproduced with permission from Beger HG: The pancreas: an integrated textbook of basic science, medicine, and surgery. London: Blackwell-Science; 1998.Brunicardi_Ch33_p1429-p1516.indd 146801/03/19 6:45 PM 1469PANCREASCHAPTER 33It is essential for patients to abstain from alcohol. In addition to removing the causative agent, alcohol abstention results in pain reduction or relief in 60% to 75% of patients with chronic pancreatitis.219 Despite this benefit, roughly half of alcoholic chronic pancreatitis patients continue to abuse alcohol.Enzyme Therapy. Pancreatic enzyme administration serves to reverse the effects of pancreatic exocrine insufficiency. Adequate pancreatic enzyme replacement reverses the exo-crine insufficiency seen in most patients, and it prevents sec-ondary complications such as metabolic bone | Surgery_Schwartz. ENLARGEMENT (n = 138) (%)WITHOUT HEAD ENLARGEMENT (n = 141) (%)Daily severe pain6740Cholestasis4611Duodenal obstruction307Diabetes mellitus1830Vascular involvement158Reproduced with permission from Beger HG: The pancreas: an integrated textbook of basic science, medicine, and surgery. London: Blackwell-Science; 1998.Brunicardi_Ch33_p1429-p1516.indd 146801/03/19 6:45 PM 1469PANCREASCHAPTER 33It is essential for patients to abstain from alcohol. In addition to removing the causative agent, alcohol abstention results in pain reduction or relief in 60% to 75% of patients with chronic pancreatitis.219 Despite this benefit, roughly half of alcoholic chronic pancreatitis patients continue to abuse alcohol.Enzyme Therapy. Pancreatic enzyme administration serves to reverse the effects of pancreatic exocrine insufficiency. Adequate pancreatic enzyme replacement reverses the exo-crine insufficiency seen in most patients, and it prevents sec-ondary complications such as metabolic bone |
Surgery_Schwartz_9699 | Surgery_Schwartz | pancreatic exocrine insufficiency. Adequate pancreatic enzyme replacement reverses the exo-crine insufficiency seen in most patients, and it prevents sec-ondary complications such as metabolic bone disease due to inadequate absorption of the fat-soluble vitamins A, D, E, and K. In addition, pancreatic enzyme replacement may reduce or alleviate the pain experienced by patients. The choice of enzyme supplement and the dose should be selected based on whether malabsorption or pain (or both) are the indica-tions for therapy220 (Table 33-19). Conventional (nonen-teric-coated) enzyme preparations are partially degraded by gastric acid but are available within the duodenal and jejunal regions to bind to CCK-releasing peptide and downregulate the release of CCK. This theoretically reduces the enteric sig-nal for pancreatic exocrine secretion, which reduces the pres-sure within a partially or completely obstructed pancreatic duct.221 Enteric-coated preparations result in little to no pain | Surgery_Schwartz. pancreatic exocrine insufficiency. Adequate pancreatic enzyme replacement reverses the exo-crine insufficiency seen in most patients, and it prevents sec-ondary complications such as metabolic bone disease due to inadequate absorption of the fat-soluble vitamins A, D, E, and K. In addition, pancreatic enzyme replacement may reduce or alleviate the pain experienced by patients. The choice of enzyme supplement and the dose should be selected based on whether malabsorption or pain (or both) are the indica-tions for therapy220 (Table 33-19). Conventional (nonen-teric-coated) enzyme preparations are partially degraded by gastric acid but are available within the duodenal and jejunal regions to bind to CCK-releasing peptide and downregulate the release of CCK. This theoretically reduces the enteric sig-nal for pancreatic exocrine secretion, which reduces the pres-sure within a partially or completely obstructed pancreatic duct.221 Enteric-coated preparations result in little to no pain |
Surgery_Schwartz_9700 | Surgery_Schwartz | enteric sig-nal for pancreatic exocrine secretion, which reduces the pres-sure within a partially or completely obstructed pancreatic duct.221 Enteric-coated preparations result in little to no pain relief, presumably due to their reduced bioavailability in the proximal gut. Due to the loss of pancreatic enzymes by acid hydrolysis and proteolysis, relatively large doses are required to achieve effective levels of enzyme within the proximal small bowel. Enteric-coated preparations are protected from acid degradation but are presumably not released in the criti-cal proximal gut in sufficient quantity to inhibit the stimulus for endogenous pancreatic enzyme secretion. Nonalcoholic patients may experience more effective pain relief than alco-holic patients, but it is recommended that all patients with chronic pancreatitis pain begin a trial of nonenteric-coated enzyme supplements together with an acid-suppressive medi-cation for 1 month. If pain relief is achieved, therapy is con-tinued. | Surgery_Schwartz. enteric sig-nal for pancreatic exocrine secretion, which reduces the pres-sure within a partially or completely obstructed pancreatic duct.221 Enteric-coated preparations result in little to no pain relief, presumably due to their reduced bioavailability in the proximal gut. Due to the loss of pancreatic enzymes by acid hydrolysis and proteolysis, relatively large doses are required to achieve effective levels of enzyme within the proximal small bowel. Enteric-coated preparations are protected from acid degradation but are presumably not released in the criti-cal proximal gut in sufficient quantity to inhibit the stimulus for endogenous pancreatic enzyme secretion. Nonalcoholic patients may experience more effective pain relief than alco-holic patients, but it is recommended that all patients with chronic pancreatitis pain begin a trial of nonenteric-coated enzyme supplements together with an acid-suppressive medi-cation for 1 month. If pain relief is achieved, therapy is con-tinued. |
Surgery_Schwartz_9701 | Surgery_Schwartz | with chronic pancreatitis pain begin a trial of nonenteric-coated enzyme supplements together with an acid-suppressive medi-cation for 1 month. If pain relief is achieved, therapy is con-tinued. If enzyme therapy fails, further investigation of the pancreatic ductal system by ERCP guides the therapy based on specific anatomical findings (Fig. 33-45).Antisecretory Therapy. Somatostatin administration has been shown to inhibit pancreatic exocrine secretion and CCK Table 33-19Pancreatic enzyme preparationsPRODUCTFORMULATIONMANUFACTURERLIPASE CONTENT (USP)/PILL OR CAPSULEZenpepEnteric-coated porcineAptalis3000, 5000, 10,000, 15,000, 20,000CreonEnteric-coated porcineAbbott3000, 6000, 12,000, 24,000PancreazeEnteric-coated porcineOrtho-McNeil-Janssen4200, 10,500, 16,800, 21,000PertzyeEnteric-coated porcine mixed with bicarbonate granulesDigestive Care8000, 16,000UltresaEnteric-coated porcineAptalis13,800, 20,700, 23,000ViokaceTablet non-enteric-coated porcineAptalis10,440, 20,880Note: USP = | Surgery_Schwartz. with chronic pancreatitis pain begin a trial of nonenteric-coated enzyme supplements together with an acid-suppressive medi-cation for 1 month. If pain relief is achieved, therapy is con-tinued. If enzyme therapy fails, further investigation of the pancreatic ductal system by ERCP guides the therapy based on specific anatomical findings (Fig. 33-45).Antisecretory Therapy. Somatostatin administration has been shown to inhibit pancreatic exocrine secretion and CCK Table 33-19Pancreatic enzyme preparationsPRODUCTFORMULATIONMANUFACTURERLIPASE CONTENT (USP)/PILL OR CAPSULEZenpepEnteric-coated porcineAptalis3000, 5000, 10,000, 15,000, 20,000CreonEnteric-coated porcineAbbott3000, 6000, 12,000, 24,000PancreazeEnteric-coated porcineOrtho-McNeil-Janssen4200, 10,500, 16,800, 21,000PertzyeEnteric-coated porcine mixed with bicarbonate granulesDigestive Care8000, 16,000UltresaEnteric-coated porcineAptalis13,800, 20,700, 23,000ViokaceTablet non-enteric-coated porcineAptalis10,440, 20,880Note: USP = |
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