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... pathogenesis is multi- faceted, including duct, stone, and genetic related. 8 The passage of a gallstone or sludge causes local edema or transient spasm of the ampulla of Vater (Fig 1), causing transient obstruction of the pancreatic duct, resulting in increased pancreatic secretion, pancreatic edema, and/or necrosis. 9 The risk is increased with small gallstones 5 mm, cystic duct diameter 5 mm, multiple gallstones (20), excess cholesterol crystals, and good gallbladder emptying. ...
Context 2
... pancreas, a retroperitoneal gland that is often quoted as an organ of mystery, has both endocrine and exocrine functions ( Fig 1). Approximately 80% of the gross weight of the pancreas supports exocrine function, while the remaining 20% is involved with endocrine function. 1 Enzymes are produced within the pancreatic acinar cells, packaged into storage vesicles called zymogens, and then released via the pancreatic ductal cells into the pancreatic duct, from where they are secreted into the small intestine to begin the metabolic process needed to affect the major digestive activity of the gastrointestinal tract. The pancreas secretes 1500-3000 mL of iso-osmotic alkaline (pH Ͼ 8.0) fluid per day containing many enzymes and zymogens. We searched MEDLINE using the keywords acute pancreatitis (AP) AND etiology, diagnosis, laboratories, imaging, clinical features, treatment, management, complications, and differential diagnosis. The infor- mation is synthesized from the review articles, guidelines from gastroenterology societies, and original articles (1974-2011). Following ingestion of food, the vagal nerves, vasoactive intestinal peptide, gastrin releasing peptide, secretin, cholecystokinin (CCK), and encephalins stimulate enzymatic release into the pancreatic duct. The pancreas secretes amylolytic, lipolytic, and proteolytic enzymes. Amylase, the major amylolytic enzyme, hydrolyzes starch to oligosaccharides. The lipolytic enzymes include lipase, phospholipase A, and cholesterol esterase. Proteolytic enzymes which include trypsin, chymotrypsin, carboxypeptidases, aminopeptidases, and elastases act on peptide bonds of proteins and polypeptides. The proteolytic enzymes are secreted as inactive precursors (zymogens). These precursor enzymes reach the duodenum where trypsinogen, the proenzyme for trypsin, is activated by the brush border enzyme enterokinase. Trypsin then facilitates the conversion of the other pro-enzymes to their active form. Autodigestion of the pancreas is prevented by the packaging of proteases in precursor form and by the synthesis of protease inhibitors, such as pancreatic secretory trypsin inhibitor and serine protease inhibitor (SPINK1). 2 In addition, the acidic pH and a low calcium concentration in the zymogen granules guard against premature activation of the proenzymes. Whenever there is a loss of any of these protective mechanisms, zymogen activation and autodigestion occur, leading to AP. Pancreatic enzyme secretion is controlled by a negative feedback mechanism induced by the presence of active unbound proteases in the duodenum. Pancreatic inflammatory disease may be classified as AP and chronic pancreatitis. The pathologic spectrum of AP varies from a mild self- limited form of interstitial pancreatitis to a severe systemic form of necrotizing pancreatitis. 3 AP is defined by the presence of 2 of the 3 criteria : 1. Abdominal pain characteristic of AP; 2. Serum amylase and/or lipase Ն 3 times the upper limit of normal; and 3. Characteristic findings of AP on computed tomography (CT) scan. In 1992, the Atlanta International Symposium classified AP into mild AP (edematous/interstitial pancreatitis), which has a mortality of 1%, and severe AP (necrotizing pancreatitis), which constitutes about 20% to 30% of the AP with a mortality rate around 20% to 30%. 5 Determining the etiology of AP is crucial in the management of an acute episode and in the prevention of recurrent pancreatitis. Biliary and alcoholic pancreatitis constitute the majority of cases. In up to 30% of cases, etiology cannot be determined and they are labeled as “Idiopathic pancreatitis.” The potential causes are outlined in Table 1. Biliary pancreatitis is the most common cause of AP in the western world, accounting for 35% to 60% of patients with AP. The incidence of biliary pancreatitis has been increasing over the past decade. A higher incidence of gallstone pancreatitis is noted in Hispanics, whites, women, and persons over the age of 75 years. 7 The significance of determining a biliary etiology is important as it needs invasive treatment, and failure to identify it can lead to recurrent pancreatitis. The pathogenesis is multi- faceted, including duct, stone, and genetic related. 8 The passage of a gallstone or sludge causes local edema or transient spasm of the ampulla of Vater (Fig 1), causing transient obstruction of the pancreatic duct, resulting in increased pancreatic secretion, pancreatic edema, and/or necrosis. 9 The risk is increased with small gallstones Ͻ 5 mm, cystic duct diameter Ͼ 5 mm, multiple gallstones ( Ͼ 20), excess cholesterol crystals, and good gallbladder emptying. 10 Common bile duct diameter Ͼ 13 mm and a wide angle between bile duct and pancreatic duct are known ductal risk factors for AP. 11 Duodenal exclusion of pancreatic juices has been postulated in the pathogenesis. 12 The lack of trypsin results in an increase in CCK- releasing peptide because it is inactivated by trypsin. As a result, there is an increased level of CCK, resulting in increased pancreatic secretion. 13 During ampullary obstruction, the pressure gradient between pancreatic duct and biliary duct disappears, resulting in a reflux of infected bile juice into the pancreatic duct, which triggers pancreatitis. Genetic defects have also been postulated in the etiology of AP, the most important being the SPINK1 mutation, which results in decreased production of trypsin inhibitor. 14 Other genetic causes for acute recurrent biliary pancreatitis include mutations in the ABCB4 and CFTR genes. Alcohol is considered the leading cause of AP in patients with a history of alcohol consumption. Heavy alcohol use is the second most common cause of AP in developed countries. Moderate drinkers are defined as having 4-14 drinks/week in men and 4-7 drinks/week in women. Heavy drinkers are defined as having more than 14 drinks/week in men and more than 7 drinks/week in women. Alcohol does not cause AP directly. There has to be a cofactor involved with alcohol in the causation of pancreatitis. The cofactors identified are smoking, African American race, and a high-fat, high-protein diet. 15 Likewise, only a small proportion of alcohol abusers develop pancreatitis. Alcohol decreases the threshold for trypsin activation, which leads to pancreatic injury and also alters the severity of pancreatic inflammation. There is no established threshold for the amount of alcohol that causes pancreatitis. Several studies have postulated that the consumption of more than 80-100 g/d of alcohol for 5 years is a threshold for causing pancreatitis. Papachristou et al. identified chronic alcohol consumption ( Ͼ 2 drinks/day) as a major risk factor for the development of pancreatic necrosis in AP. 16 The theory is that the alcohol exposure shifts the mechanism of cell death from apoptosis to necrosis. 17 Recent studies have demonstrated smoking as an important cause of both chronic and idiopathic pancreatitis. 18-20 It is an independent risk factor and the risk is dose dependent. 20 It also has an additive/synergistic effect, with alcohol in the progression of pancreatitis. 21 The role of oxidative stress in the induction of pancreatitis has been postulated in active smokers. 22 Genetic influence has also been shown to affect the complex alcohol–smoking interaction. 23 The gastroenterology commu- nity continues to raise awareness of smoking as a risk factor for pancreatitis. 19 The 1991 consensus definition for Post-ERCP Pancreatitis (PEP) is “new onset of pancreatic type abdominal pain associated with a rise in serum amylase Ն 3-fold above the upper limit of normal within 24 hours of ERCP and also requiring more than one additional night of hospital stay.” The severity of PEP is based on the length of stay after the procedure. A length of stay of 2-3 days is graded as mild, 4-10 days as moderate and Ͼ 10 days or requiring intensive care and/or intervention for complications as severe PEP. 24 The consensus definition of PEP is distinct from the clinical definition of AP per 2006 American College of Gastroenterology (ACG) practice guidelines. 4 The combined use of CT scan with lipase level increases the diagnostic yield for PEP. 25 There are various mechanisms proposed for the etiology of PEP. The most common theory is mechanical trauma to the papilla, causing obstruction to the outflow of pancreatic juice. This is supported by prophylactic placement of a pancreatic duct stent, which decreased the incidence of PEP. Another theory is increased pancreatic duct pressure from the injection of contrast or saline, causing acinarization of the pancreas. Pancreatic infection from instrumentation is another hypothesis supported by prophylactic antibiotic usage decreasing the rate of post- procedure pancreatitis. ...
Context 3
... pancreas, a retroperitoneal gland that is often quoted as an organ of mystery, has both endocrine and exocrine functions ( Fig 1). Approximately 80% of the gross weight of the pancreas supports exocrine function, while the remaining 20% is involved with endocrine function. 1 Enzymes are produced within the pancreatic acinar cells, packaged into storage vesicles called zymogens, and then released via the pancreatic ductal cells into the pancreatic duct, from where they are secreted into the small intestine to begin the metabolic process needed to affect the major digestive activity of the gastrointestinal tract. The pancreas secretes 1500-3000 mL of iso-osmotic alkaline (pH Ͼ 8.0) fluid per day containing many enzymes and zymogens. We searched MEDLINE using the keywords acute pancreatitis (AP) AND etiology, diagnosis, laboratories, imaging, clinical features, treatment, management, complications, and differential diagnosis. The infor- mation is synthesized from the review articles, guidelines from gastroenterology societies, and original articles (1974-2011). Following ingestion of food, the vagal nerves, vasoactive intestinal peptide, gastrin releasing peptide, secretin, cholecystokinin (CCK), and encephalins stimulate enzymatic release into the pancreatic duct. The pancreas secretes amylolytic, lipolytic, and proteolytic enzymes. Amylase, the major amylolytic enzyme, hydrolyzes starch to oligosaccharides. The lipolytic enzymes include lipase, phospholipase A, and cholesterol esterase. Proteolytic enzymes which include trypsin, chymotrypsin, carboxypeptidases, aminopeptidases, and elastases act on peptide bonds of proteins and polypeptides. The proteolytic enzymes are secreted as inactive precursors (zymogens). These precursor enzymes reach the duodenum where trypsinogen, the proenzyme for trypsin, is activated by the brush border enzyme enterokinase. Trypsin then facilitates the conversion of the other pro-enzymes to their active form. Autodigestion of the pancreas is prevented by the packaging of proteases in precursor form and by the synthesis of protease inhibitors, such as pancreatic secretory trypsin inhibitor and serine protease inhibitor (SPINK1). 2 In addition, the acidic pH and a low calcium concentration in the zymogen granules guard against premature activation of the proenzymes. Whenever there is a loss of any of these protective mechanisms, zymogen activation and autodigestion occur, leading to AP. Pancreatic enzyme secretion is controlled by a negative feedback mechanism induced by the presence of active unbound proteases in the duodenum. Pancreatic inflammatory disease may be classified as AP and chronic pancreatitis. The pathologic spectrum of AP varies from a mild self- limited form of interstitial pancreatitis to a severe systemic form of necrotizing pancreatitis. 3 AP is defined by the presence of 2 of the 3 criteria : 1. Abdominal pain characteristic of AP; 2. Serum amylase and/or lipase Ն 3 times the upper limit of normal; and 3. Characteristic findings of AP on computed tomography (CT) scan. In 1992, the Atlanta International Symposium classified AP into mild AP (edematous/interstitial pancreatitis), which has a mortality of 1%, and severe AP (necrotizing pancreatitis), which constitutes about 20% to 30% of the AP with a mortality rate around 20% to 30%. 5 Determining the etiology of AP is crucial in the management of an acute episode and in the prevention of recurrent pancreatitis. Biliary and alcoholic pancreatitis constitute the majority of cases. In up to 30% of cases, etiology cannot be determined and they are labeled as “Idiopathic pancreatitis.” The potential causes are outlined in Table 1. Biliary pancreatitis is the most common cause of AP in the western world, accounting for 35% to 60% of patients with AP. The incidence of biliary pancreatitis has been increasing over the past decade. A higher incidence of gallstone pancreatitis is noted in Hispanics, whites, women, and persons over the age of 75 years. 7 The significance of determining a biliary etiology is important as it needs invasive treatment, and failure to identify it can lead to recurrent pancreatitis. The pathogenesis is multi- faceted, including duct, stone, and genetic related. 8 The passage of a gallstone or sludge causes local edema or transient spasm of the ampulla of Vater (Fig 1), causing transient obstruction of the pancreatic duct, resulting in increased pancreatic secretion, pancreatic edema, and/or necrosis. 9 The risk is increased with small gallstones Ͻ 5 mm, cystic duct diameter Ͼ 5 mm, multiple gallstones ( Ͼ 20), excess cholesterol crystals, and good gallbladder emptying. 10 Common bile duct diameter Ͼ 13 mm and a wide angle between bile duct and pancreatic duct are known ductal risk factors for AP. 11 Duodenal exclusion of pancreatic juices has been postulated in the pathogenesis. 12 The lack of trypsin results in an increase in CCK- releasing peptide because it is inactivated by trypsin. As a result, there is an increased level of CCK, resulting in increased pancreatic secretion. 13 During ampullary obstruction, the pressure gradient between pancreatic duct and biliary duct disappears, resulting in a reflux of infected bile juice into the pancreatic duct, which triggers pancreatitis. Genetic defects have also been postulated in the etiology of AP, the most important being the SPINK1 mutation, which results in decreased production of trypsin inhibitor. 14 Other genetic causes for acute recurrent biliary pancreatitis include mutations in the ABCB4 and CFTR genes. Alcohol is considered the leading cause of AP in patients with a history of alcohol consumption. Heavy alcohol use is the second most common cause of AP in developed countries. Moderate drinkers are defined as having 4-14 drinks/week in men and 4-7 drinks/week in women. Heavy drinkers are defined as having more than 14 drinks/week in men and more than 7 drinks/week in women. Alcohol does not cause AP directly. There has to be a cofactor involved with alcohol in the causation of pancreatitis. The cofactors identified are smoking, African American race, and a high-fat, high-protein diet. 15 Likewise, only a small proportion of alcohol abusers develop pancreatitis. Alcohol decreases the threshold for trypsin activation, which leads to pancreatic injury and also alters the severity of pancreatic inflammation. There is no established threshold for the amount of alcohol that causes pancreatitis. Several studies have postulated that the consumption of more than 80-100 g/d of alcohol for 5 years is a threshold for causing pancreatitis. Papachristou et al. identified chronic alcohol consumption ( Ͼ 2 drinks/day) as a major risk factor for the development of pancreatic necrosis in AP. 16 The theory is that the alcohol exposure shifts the mechanism of cell death from apoptosis to necrosis. 17 Recent studies have demonstrated smoking as an important cause of both chronic and idiopathic pancreatitis. 18-20 It is an independent risk factor and the risk is dose dependent. 20 It also has an additive/synergistic effect, with alcohol in the progression of pancreatitis. 21 The role of oxidative stress in the induction of pancreatitis has been postulated in active smokers. 22 Genetic influence has also been shown to affect the complex alcohol–smoking interaction. 23 The gastroenterology commu- nity continues to raise awareness of smoking as a risk factor for pancreatitis. 19 The 1991 consensus definition for Post-ERCP Pancreatitis (PEP) is “new onset of pancreatic type abdominal pain associated with a rise in serum amylase Ն 3-fold above the upper limit of normal within 24 hours of ERCP and also requiring more than one additional night of hospital stay.” The severity of PEP is based on the length of stay after the procedure. A length of stay of 2-3 days is graded as mild, 4-10 days as moderate and Ͼ 10 days or requiring intensive care and/or intervention for complications as severe PEP. 24 The consensus definition of PEP is distinct from the clinical definition of AP per 2006 American College of Gastroenterology (ACG) practice guidelines. 4 The combined use of CT scan with lipase level increases the diagnostic yield for PEP. 25 There are various mechanisms proposed for the etiology of PEP. The most common theory is mechanical trauma to the papilla, causing obstruction to the outflow of pancreatic juice. This is supported by prophylactic placement of a pancreatic duct stent, which decreased the incidence of PEP. Another theory is increased pancreatic duct pressure from the injection of contrast or saline, causing acinarization of the pancreas. Pancreatic infection from instrumentation is another hypothesis supported by prophylactic antibiotic usage decreasing the rate of post- procedure pancreatitis. ...
Context 4
... pathogenesis is multi- faceted, including duct, stone, and genetic related. 8 The passage of a gallstone or sludge causes local edema or transient spasm of the ampulla of Vater (Fig 1), causing transient obstruction of the pancreatic duct, resulting in increased pancreatic secretion, pancreatic edema, and/or necrosis. 9 The risk is increased with small gallstones 5 mm, cystic duct diameter 5 mm, multiple gallstones (20), excess cholesterol crystals, and good gallbladder emptying. ...
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Background:
Patients with acute pancreatitis usually exhibit dyslipidemia and oxidative stress. However, the significance of high-density lipoprotein cholesterol (HDL-C) level, low-density lipoprotein cholesterol (LDL-C) level and the HDL-C/LDL-C ratio (H/L ratio) as markers for disease progression remain unknown.
Aim:
The aim of this study was...
Introducción:
Las complicaciones torácicas secundarias a pancreatitis aguda son excepcionales y más aún la presencia de un pseudoquiste mediastinal.
Caso Clínico:
Hombre de 36 años. Consumidor de marihuana y alcohol. Historia de 6 meses de dolor abdominal y adelgazamiento de 20 kilos. Instalando en la evolución sintomatología respiratoria.
Discus...
Duodenal duplication cyst is not a common congenital anomaly and the pathophysiology may become very complicated if the cyst is situated at the ampulla of Vater. Here we report a very rare female case of duodenal duplication cyst at the ampulla of Vater, which caused acute pancreatitis due to massive protein plaques in the pancreatic duct. She had...
Citations
... These are typical pancreatic pain, an increase in the level of serum amylase or lipase to over three times the upper limit of normal and/or radiological evidence of AP. There is some agreement that smaller increases in serum pancreatic enzymes could be accepted for the diagnosis of ACP [50][51][52][53][54][55] which is consistent with a decreased acinar cell mass, secondary to the fibroinflammatory process and pancreatic atrophy associated with CP [56]. In a study of ACP patients, serum amylase and lipase levels were increased to at least three times the upper limit of normal in only 20% and 60% of episodes and were within normal range in 36% and 24%, respectively [5]. ...
Abstract
Background
Acute on chronic pancreatitis (ACP) is a relatively common condition, but there are significant gaps in our knowledge on the definition, incidence, diagnosis, treatment and prognosis.
Methods
A systematic review that followed PICO (Population; Intervention; Comparator; Outcome) recommendation for quantitative questions and PICo (Population, Phenomenon of Interest, Context) for qualitative research was done to answer 10 of the most relevant questions about ACP. Quality of evidence was judged by the GRADE criteria (Grades of Recommendation, Assessment, Development and Evaluation). The manuscript was sent for review to 12 international experts from various disciplines and continents using a Delphi process.
Results
The quality of evidence, for most statements, was low to very low, which means that the recommendations in general are only conditional. Despite that, it was possible to reach strong levels of agreement by the expert panel for all 10 questions. A new consensus definition of ACP was reached. Although common, the real incidence of ACP is not known, with alcohol as a major risk factor. Although pain dominates, other non-specific symptoms and signs can be present. Serum levels of pancreatic enzymes may be less than 3 times the upper limit of normal and cross-sectional imaging is considered more accurate for the diagnosis in many cases. It appears that it is less severe and with a lower mortality risk than acute pancreatitis.
Conclusions
Although the evidence base is poor, this position statement provides a foundation from which to advance management of ACP.
... Typically, the PPCs form as a result of pancreatic duct disruption with subsequent fluid leakage or by the maturation of peripancreatic necrosis. Ninety percent of them occur in the context of pancreatitis, while only 10% are caused by trauma (surgery, gunshots, and blunt abdominal trauma) [6]. Regarding the acute pancreatitis, PPCs formation (approximately 15%) is infrequent Figure 1. ...
Pancreatic pseudocysts frequently occur in the context of acute or chronic pancreatitis and seldom appear as a post-surgical outcome or trauma. Complicated pancreatic pseudocysts represent extremely rare entities but still life-threatening situations, including infection, hemorrhage, rupture, pseudoaneurysms, pancreatic fistulas, obstructions, and splenic complications. Premature diagnosis, based on transabdominal ultrasonography or computed tomography, is crucial for the early therapeutic approach. Conservative treatment, surgical and endoscopic intervention consist the therapeutic options. Thus, management of the complicated pseudocysts demands a multidisciplinary team eligible to cope with complications that might even occur due to the intervention. Pancreatic pseudocysts represent a challenge for clinical doctors.
... In these cases, prolongation of hospital stay and admission to intensive care units are common. Mortality rates of severe forms of pancreatitis vary by around 20 -30% [2], corresponding to the 14 th largest cause of death of gastrointestinal origin [3]. Early detection of prognosis of severity, are of fundamental importance in the management of these patients. ...
it talk about prognosis in acute pancreatitis
... The mortality rates vary from 1% in the mild form to 20-30% in the severe form, corresponding to the 14th main cause of death of gastrointestinal origin. 1,2 Clinically Acute pancreatitis was defined as two or more of the following: ...
Background: Acute pancreatitis presents as acute abdomen, is an inflammatory process of the pancreas associated with local and systemic complications requiring, in such cases, an intensive care. At present, there are lots of scores (such as Ranson’s, APACHE II, bedside index for severity in acute pancreatitis) that help us in predicting severity at the time of admission, but these are time consuming or require complex calculation and are costly. Our aim here is to analyse the simplified stratification system of the PANC 3 score, and its assessment in Predicting Severity of Acute Pancreatitis as decided by modified Marshals score.Methods: It is a prospective analytical observational study in which 74 patients were evaluated with PANC 3 scoring, who were diagnosed with acute pancreatitis and admitted to Dept. Of General Surgery, MKCG.Results: The results showed that PANC3 score had a 95.91% specificity, 68% sensitivity, 89.47% positive predictive value, and 85.45% negative predictive value, 86.48% diagnostic accuracy.Conclusions: PANC3 scoring system is one of the better systems because the three criteria used (haematocrit, body mass index, and pleural effusion) are simple, easy to assess, readily available, and economic Hence, the PANC3 score is a cost-effective, promising score that helps in predicting the severity of acute pancreatitis and triaging the patient, leading to prompt management.
... The development in radiology has not only improved the diagnostic capabilities but also paved the way for interventions (Muniraj et al., 2012). ...
... The complications of acute pancreatitis are listed in table 8 (Muniraj et al., 2012). (Muniraj et al., 2012). ...
... The complications of acute pancreatitis are listed in table 8 (Muniraj et al., 2012). (Muniraj et al., 2012). ...
Complications are an integral component of the outcome of an intervention such as ERCP. Pancreatitis remains the most common and most feared complication after ERCP. The recognition of the risk factors for PEP and high risk patients is highly desirable so as to avoid the procedure at all in case of diagnostic ERCP, also to avoid high risk techniques during ERCP and for close follow up for these patients after the procedure and for early therapeutic approach during or after the procedure.
The primary aim of this study was to evaluate the commonest postulated risk factors for post-ERCP pancreatitis in patients with obstructive jaundice. Identification and evaluation of overall ERCP related complications was prospectively evaluated as a secondary goal of this study.
This prospective study was performed on 581 consecutive adult patients with obstructive jaundice referred to gastro-intestinal endoscopy unit of Assuit University hospital (540 patients) and gastro-intestinal endoscopy unit of surgery department of Sohag University hospital (141 patients) between June 2010 and June 2012. They were 225 male (38.7%) and 356 female (61.3%), their ages ranged between 18 and 73 years with a mean of 44.8 ± 13.9.
All patients were subjected pre-endoscopically to initial evaluation in the form of history taking, clinical examination and laboratory and imaging investigations. During ERCP, time of the whole procedure, time of manipulation of papilla, number of attempts of cannulation, number of pancreatic duct cannulation and injection, degree of difficulty of stone extraction, sphincterotomy, precut, balloon sphincteroplasty and trainee participation were recorded. After ERCP patients were monitored for at least six hours to detect symptoms and signs of pancreatitis, together with measurement of serum amylase four hours after the procedure.
The Cannulation of the papilla of vater was successful in 96.7% (562 patients) and failed in 3.3% (19 patients). Causes of failure were as follows: small and stenosed papilla was found in 10 patients (1.7%), duodenal diverticulum in 5 patients (0.9%), and ampullary tumor in 4 patients (0.7%).
The overall morbidity rate was 12.7% (74 cases), and the mortality rate was 0.51% (3 cases). The first died from sever pancreatitis, the second from pulmonary embolism, and the third from sever bradyarrthymia.
Estimation of serum amylase level after ERCP showed that 25% of cases had no hyperamylasemia, 66.1% of cases had asymptomatic hyperamylasemia and 8.9% of cases had acute pancreatitis.
Pancreatitis was the most common complication, and it was mild in 63.5%, moderate in 28.8% and sever in 7.7% of cases. Pancreatitis-related median hospital stay was 2.9, 6.5 and 17.5 days for mild, moderate and severe disease. The PEP related mortality rate was 1.9% (1 case) due to sever acute pancreatitis, No deaths were reported for mild or moderate pancreatitis.
Bleeding occurred in 11 patients (1.89%), Cholangitis developed in 4 cases (0.69 %), perforation occurred in 2 cases (0.34%), bradyarrthymia occurred in 2 cases (0.34%), cholecystitis in 1 case (0.17%), pulmonary embolism in 1 case (0.17%) and basket trapping occurred in 1 case (0.17%).
Technique-related risk factors are probably more numerous and potent than patient-related ones in the risk of post-ERCP pancreatitis. 7 risk factors were identified to be independently associated with pancreatitis, 2 were patient-related risk factors (i.e., history of previous pancreatitis and history of previous PEP), and 5 were procedure-related risk factors (i.e., precut sphincterotomy, difficult cannulation, pancreatic duct cannulation, ≥ 2 pancreatic duct injection, and difficult stone extraction).
History of previous PEP and history of previous pancreatitis were associated with 8-fold risk for recurrent attack of PEP.
Age was not a significant independent risk factor for PEP although PEP had inverse relationship with age (the younger the patient the higher the percentage of pancreatitis – 10% vs. 5%). Also, sex of patients was not a significant independent risk factor for PEP although females were found to have higher rates of PEP compared to males (11.5 % vs. 4.9%).
Previous cholecystectomy, previous sphincterotomy, preoperative total serum bilirubin, cause of obstructive jaundice and CBD diameter were not a significant risk factors for PEP.
Increasing number of attempts at cannulating Vater’s papilla was the most risky independent factor for post-ERCP pancreatitis. More than 15 attempts raised the risk 10-fold while 6 to 15 attempts raised the risk threefold, independently of the other patient- and procedure-related risk factors.
Pancreatic duct cannulation (≥ 1 time) and pancreatic duct injection (≥ 2 times) were significant independent factors for PEP with a tripled risk.
The degree of difficulty of stone extraction was found to be a significant independent risk (two-fold) for PEP in patients with gall stone disease. PEP had inverse relationship with the degree of difficulty of stone extraction (the difficulty the stone extraction the higher the percentage of pancreatitis).
Precut was considered a barely risk factor for PEP. Moreover, this study found that early pre-cut was safer than either delayed pre-cut or multiple attempts at cannulating the papilla (13.6% versus 25.6% and 28.6%), supporting the concept that in expert hands pre-cut might be preferable to repeated cannulation attempts, especially in patients at high risk for post-procedure pancreatitis.
The total time of the procedure was not a significant independent risk factor for PEP (the mean time was 27.7 minutes vs. 32.4 minutes). Also, the mean time of cannulation of the papilla did not differ significantly between the pancreatitis and non pancreatitis group (6.6 minutes vs. 8.4 minutes).
Standard biliary sphincterotomy, balloon sphincteroplasty and Trainee participation were not associated with any increase in the incidence of PEP.
... 8,9 Early postoperative edema of the anastomosis, source of bleeding in the afferent loop or both may prevent gastric emptying, which favors the accumula- tion of fluids in the afferent loop. 1,10,11 Reported mortality reaches 57% and is closely associated with diagnostic delay, which causes intestinal ischemia, perforation and peritonitis. Prolonged stasis of the secretions favors bacterial overgrowth, which produces deconjugation of bile acids that, in turn, cause steatorrhea, malnutrition and vitamin B12 deficiency with subsequent megaloblastic anemia. ...
Background:
The afferent syndrome loop is a mechanic obstruction of the afferent limb before a Billroth II or Roux-Y reconstruction, secondary in most of case to distal or subtotal gastrectomy. Clinical case: Male 76 years old, with antecedent of cholecystectomy, gastric adenocarcinoma six years ago, with subtotal gastrectomy and Roux-Y reconstruction. Beginning a several abdominal pain, nausea and vomiting, abdominal distension, without peritoneal irritation sings. Amylase 1246 U/L, lipase 3381 U/L. Computed Tomography with thickness wall and dilatation of afferent loop, pancreas with diffuse enlargement diagnostic of acute pancreatitis secondary an afferent loop syndrome.
Conclusion:
The afferent loop syndrome is presented in 0.3%-1% in all cases with Billroth II reconstruction, with a mortality of up to 57%, the obstruction lead accumulation of bile, pancreatic and intestinal secretions, increasing the pressure and resulting in afferent limb, bile conduct and Wirsung conduct dilatation, triggering an inflammatory response that culminates in pancreatic inflammation. The severity of the presentation is related to the degree and duration of the blockage.
... 1,7 The pathogenesis of drug induced pancreatitis does not appear to differ from other causes of AP as discussed in several studies in the literature. [8][9][10] Exactly how medications induce AP is unknown, but postulated mechanisms include immune-mediated inflammatory response, direct cellular toxicity, pancreatic ductal constriction, arteriolar thrombosis, and metabolic effects. 1,7 Most of the 'evidence' supporting associations between drugs and AP are based on anecdotal case reports. ...
A wide variety of drugs have been reported to cause pancreatitis. Although the incidence of drug induced acute pancreatitis is low, the disease is associated with substantial morbidity and mortality, which makes timely identification of the causative agent important.
Herein, we report two patients with clinical, biochemical, and radiological evidence of acute pancreatitis. There were no etiologic factors except their prescribed drugs.
The majority of patients with acute pancreatitis recover uneventfully, but there remains an uncontrollable risk of mortality. It is prudent to withdraw a medication with a known association with acute pancreatitis. Necessity of multi-drug regimens especially in oncological patients however, presents a challenge.
Corticosteroid pulse therapy was easily detectable as the causative agent in our first case, but combined anti-neoplastic drug therapy and additional multi-drug regimen presented great difficulties in identifying single causative agent in our second patient.
Background:
The effect of chemotherapy induction on the pancreatic in patients with acute lymphoblastic leukemia is not described in Ethiopia. The study determined the chemotherapy drug-induced pancreatitis in patients with acute lymphoblastic leukemia.
Method:
A preexperimental study (pretest and posttests) was conducted in forty patients with acute lymphoblastic leukemia. For some skewed data, a log transformation was computed. The back transformation was then calculated. Descriptive statistics and a mixed-model ANOVA were used to analyze the data. A post hoc Bonferroni test was used. A p value < 0.05 was declared statistically significant.
Results:
In this study, no clinically significant acute pancreatitis occurred. Elevated amylase and lipase levels, indicating grade 2 acute pancreatitis, were observed in 25% and 17.5% of patients, respectively. Amylase enzyme levels in children differed significantly from preinduction to the second week of induction (p = 0.001) and fourth week of induction (p = 0.001), as well as between the second and fourth weeks of induction (p = 0.033), but adults' amylase enzyme levels did not differ significantly (p = 0.2). Lipase levels in adults are nearly identical in all three measures, implying that there is no statistically significant difference (p = 0.775). However, the level of lipase enzyme in children was significantly higher from baseline to two and four weeks of induction (p = 0.007) but not between two and four weeks of induction (p = 0.129).
Conclusion:
Clinically significant acute pancreatitis did not occur, but patients experienced mild (grade 2) acute pancreatitis. Amylase and lipase enzymes responded significantly to chemotherapy induction in children. Chemotherapy drugs should be given without altering pancreatic enzymes, specifically in children.
Acute pancreatitis can result from a variety of infections. The causative pathogens have been well established to be certain viruses and parasites. However, certain infections fail to find mention in standard literature and have been overlooked due to the trivial number of cases of pancreatitis that result from them. Among these are influenza, leptospirosis, acute viral hepatitis, and certain tropical infections such as dengue, chikungunya, scrub typhus, malaria, and typhoid. In this narrative review, we have conducted a literature search on PubMed and EMBASE databases for cases of pancreatitis occurring in these diseases and compiled the data. Most of these infections are prevalent in the developing world, and consequently, more cases are reported from these regions. The pathogenesis, predictors of outcome, and the response to antimicrobial therapy have not been studied extensively. The actual incidence is probably higher than what is reported, and this subject deserves more attention.
Background:
Acute pancreatitis (AP) is an inflammatory disease in which the regulatory pathway is complex and not well understood. Soluble suppression of tumorigenicity 2 (sST2) protein receptor functions as a decoy receptor for interleukin (IL)-33 to prevent IL-33/suppression of tumorigenicity 2L (ST2L)-pathway-mediated T helper (Th)2 immune responses.
Aim:
To investigate the role of sST2 in AP.
Methods:
We assessed the association between sST2 and severity of AP in 123 patients enrolled in this study. The serum levels of sST2, C-reactive protein (CRP) and Th1- and Th2-related cytokines, including interferon (IFN)-γ, tumor necrosis factor (TNF)-α, IL-2, IL-4, IL-5 and IL-13, were measured by highly sensitive ELISA, and the severity of AP in patients was evaluated by the 2012 Atlanta Classification Criteria.
Results:
Serum sST2 levels were significantly increased in AP patients, and further, these levels were significantly elevated in severe AP (SAP) patients compared to moderately severe AP (MSAP) and mild AP (MAP) patients. Logistic regression showed sST2 was a predictor of SAP [odds ratio (OR): 1.003 (1.001-1.006), P = 0.000]. sST2 cutoff point was 1190 pg/mL, and sST2 above this cutoff was associated with SAP. sST2 was also a predictor of any organ failure and mortality during AP [OR: 1.006 (1.003-1.009), P = 0.000, OR: 1.002 (1.001-1.004), P = 0.012, respectively]. Additionally, the Th1-related cytokines IFN-γ and TNF-α in the SAP group were higher and the Th2-related cytokine IL-4 in the SAP group was significantly lower than those in MSAP and MAP groups.
Conclusion:
sST2 may be used as a novel inflammatory marker in predicting AP severity and may regulate the function and differentiation of IL-33/ST2-mediated Th1 and Th2 Lymphocytes in AP homeostasis.
