This document summarizes an article from the New England Journal of Medicine about acute pancreatitis. It provides details on the pathogenesis, diagnosis, and management of acute pancreatitis. It discusses risk factors, causes, predictors of severe disease, and treatments including fluid resuscitation, determining the cause, imaging studies, ERCP, and predicting outcomes. Key points are that acute pancreatitis results from inappropriate activation of pancreatic enzymes, risk factors are gallstones and alcohol, and predictors of severe disease include scoring systems assessing inflammation and organ failure.
This document discusses pancreatitis, including its anatomy, physiology, etiology, clinical presentation, diagnosis, prognosis, management, and complications. Pancreatitis is defined as inflammation of the pancreas and can be acute or chronic. Acute pancreatitis is commonly caused by gallstones or alcohol and may range from mild to severe, with severe cases involving pancreatic necrosis and multi-organ failure. Diagnosis involves blood tests measuring amylase and lipase along with imaging like CT. Management depends on severity but generally involves hospitalization, IV fluids, pain control, and monitoring for complications.
Acute Pancreatitis - Diagnosis and ManagementRobert Robinson
This document discusses signs, symptoms, diagnostic tests, severity scoring, and treatment strategies for pancreatitis. It provides sensitivity and specificity data for diagnostic tests like amylase, lipase, ultrasound, MRI, and CT scans. It also outlines a CT severity index scoring system for grading pancreatitis severity. Finally, it lists the key treatment aspects of pancreatitis management as fluids, pain control, antibiotics, nutrition, DVT prophylaxis, and potential interventions.
A 22-year-old male presented with sudden onset of epigastric pain radiating to the back with no significant past medical history. On examination, he was in pain with normal vital signs and abdominal tenderness. This raises concern for acute pancreatitis. The document discusses definitions, diagnosis, assessment of severity, management of fluid replacement, antibiotics, nutrition, and other issues related to acute pancreatitis. Enteral nutrition is preferred over total parenteral nutrition for acute pancreatitis as it reduces mortality, organ failure, infections, and length of hospital stay.
Revised Atlanta classification of Acute PancreatitisDr M Venkatesh
The most important change in Atlanta classification is the categorization of the various pancreatic collections.
In acute IEP, collections that do not have an enhancing capsule are called APFCs; after development of a capsule, they are referred to as
pseudocysts
In necrotizing pancreatitis,a collection without an enhancing capsule is called an ANC (usually in the first 4 weeks) and thereafter a WON, which has an enhancing capsule.
The most important distinction between collections in necrotizing pancreatitis and those associated with acute IEP is the presence of nonliquefied material in collections due to necrotizing pancreatitis.
This document summarizes key points about the management of acute pancreatitis. It discusses the epidemiology, etiology, clinical presentation, diagnostic evaluation, determination of severity, treatment approaches, and complications of acute pancreatitis. Management depends on determining if the pancreatitis is mild, moderate, or severe based on the presence of organ failure or local complications on imaging. Nutritional support, antibiotics, and drainage of fluid collections are addressed.
Acute pancreatitis is a potentially lethal condition that requires careful treatment and management. It involves sudden inflammation of the pancreas that can lead to the release of digestive enzymes within the abdomen. These enzymes can damage normal tissues, especially fat, and cause inflammation. The document discusses definitions of acute pancreatitis and classifications based on severity. Mild cases involve only inflammation while more severe cases can lead to pancreatic necrosis and organ failure. Treatment depends on the classification and complications. The pathogenesis involves trypsinogen activation within pancreas cells leading to autodigestion and an inflammatory response.
severe acute pancreatitis has high mortality rate and there is always confusions in between physicians. This topic is about management of acute pancreatitis its complications and ongoing controvercies. hope this will help and clear the doubts among physicians, residents and medical students
This document summarizes the diagnosis, etiology, management, and treatment of acute pancreatitis based on guidelines from the American College of Gastroenterology. It presents a case study of a 47-year-old female diagnosed with gallstone pancreatitis based on abdominal pain, elevated lipase, and ultrasound findings of cholelithiasis. Her case is used to illustrate the guidelines, including IV fluid hydration, no antibiotics given due to mild symptoms resolving in 48 hours, and cholecystectomy before discharge due to gallstone etiology.
This document discusses pancreatitis, including its anatomy, physiology, etiology, clinical presentation, diagnosis, prognosis, management, and complications. Pancreatitis is defined as inflammation of the pancreas and can be acute or chronic. Acute pancreatitis is commonly caused by gallstones or alcohol and may range from mild to severe, with severe cases involving pancreatic necrosis and multi-organ failure. Diagnosis involves blood tests measuring amylase and lipase along with imaging like CT. Management depends on severity but generally involves hospitalization, IV fluids, pain control, and monitoring for complications.
Acute Pancreatitis - Diagnosis and ManagementRobert Robinson
This document discusses signs, symptoms, diagnostic tests, severity scoring, and treatment strategies for pancreatitis. It provides sensitivity and specificity data for diagnostic tests like amylase, lipase, ultrasound, MRI, and CT scans. It also outlines a CT severity index scoring system for grading pancreatitis severity. Finally, it lists the key treatment aspects of pancreatitis management as fluids, pain control, antibiotics, nutrition, DVT prophylaxis, and potential interventions.
A 22-year-old male presented with sudden onset of epigastric pain radiating to the back with no significant past medical history. On examination, he was in pain with normal vital signs and abdominal tenderness. This raises concern for acute pancreatitis. The document discusses definitions, diagnosis, assessment of severity, management of fluid replacement, antibiotics, nutrition, and other issues related to acute pancreatitis. Enteral nutrition is preferred over total parenteral nutrition for acute pancreatitis as it reduces mortality, organ failure, infections, and length of hospital stay.
Revised Atlanta classification of Acute PancreatitisDr M Venkatesh
The most important change in Atlanta classification is the categorization of the various pancreatic collections.
In acute IEP, collections that do not have an enhancing capsule are called APFCs; after development of a capsule, they are referred to as
pseudocysts
In necrotizing pancreatitis,a collection without an enhancing capsule is called an ANC (usually in the first 4 weeks) and thereafter a WON, which has an enhancing capsule.
The most important distinction between collections in necrotizing pancreatitis and those associated with acute IEP is the presence of nonliquefied material in collections due to necrotizing pancreatitis.
This document summarizes key points about the management of acute pancreatitis. It discusses the epidemiology, etiology, clinical presentation, diagnostic evaluation, determination of severity, treatment approaches, and complications of acute pancreatitis. Management depends on determining if the pancreatitis is mild, moderate, or severe based on the presence of organ failure or local complications on imaging. Nutritional support, antibiotics, and drainage of fluid collections are addressed.
Acute pancreatitis is a potentially lethal condition that requires careful treatment and management. It involves sudden inflammation of the pancreas that can lead to the release of digestive enzymes within the abdomen. These enzymes can damage normal tissues, especially fat, and cause inflammation. The document discusses definitions of acute pancreatitis and classifications based on severity. Mild cases involve only inflammation while more severe cases can lead to pancreatic necrosis and organ failure. Treatment depends on the classification and complications. The pathogenesis involves trypsinogen activation within pancreas cells leading to autodigestion and an inflammatory response.
severe acute pancreatitis has high mortality rate and there is always confusions in between physicians. This topic is about management of acute pancreatitis its complications and ongoing controvercies. hope this will help and clear the doubts among physicians, residents and medical students
This document summarizes the diagnosis, etiology, management, and treatment of acute pancreatitis based on guidelines from the American College of Gastroenterology. It presents a case study of a 47-year-old female diagnosed with gallstone pancreatitis based on abdominal pain, elevated lipase, and ultrasound findings of cholelithiasis. Her case is used to illustrate the guidelines, including IV fluid hydration, no antibiotics given due to mild symptoms resolving in 48 hours, and cholecystectomy before discharge due to gallstone etiology.
This document discusses the diagnosis and management of acute pancreatitis in a 22-year-old male patient presenting with epigastric pain. It examines the use of amylase and lipase tests to diagnose acute pancreatitis, describes clinical features and scoring systems to assess severity, and discusses management issues including fluid resuscitation, antibiotics, nutrition, ERCP, surgery, and monitoring organ function with Ranson's criteria and CT severity index.
GIT Journal club acute pancreatitis ACG Practice guidelines.Shaikhani.
The document contains questions regarding the diagnosis, etiology, management, and treatment of acute pancreatitis. Specifically, it asks 11 multiple choice questions testing knowledge about the required findings for diagnosis of acute pancreatitis, indications for endoscopic retrograde cholangiopancreatography and nutrition in acute pancreatitis, definitions of severe acute pancreatitis, and risk factors for hereditary and idiopathic acute pancreatitis.
1) Autoimmune pancreatitis is characterized by lymphoplasmacytic infiltration and fibrosis of the pancreas that often dramatically responds to steroid therapy.
2) Diagnosis involves a combination of clinical, imaging, histological, and serological findings including elevated serum IgG4 levels and involvement of other organs.
3) Two subtypes exist - type 1 is associated with elevated IgG4, other organ involvement and a good response to steroids, while type 2 involves granulocytic epithelial lesions and is less responsive to steroids.
This document provides an overview of acute pancreatitis, including its definitions, etiology, pathogenesis, and diagnostic assessment. It discusses the major causes of acute pancreatitis such as alcohol use, gallstones, medications, and genetic factors. The pathogenesis involves the abnormal activation of pancreatic enzymes leading to immune response and microcirculatory disturbances. Diagnosis is based on clinical features, elevated serum amylase and lipase levels, and imaging findings on ultrasound or CT scan. Several scoring systems are described to assess the severity of acute pancreatitis, including ATLANTA criteria, Ranson score, APACHE-II score, and Marshall score. Biochemical markers like CRP, PCT, and hematocrit can also help predict
Acute pancreatitis has an incidence of 17 per 100,000 people and a mortality of 2-3%. The most common causes are gallstones (50% of cases) and alcohol abuse (20-25% of cases). Necrotizing pancreatitis can lead to pancreatic infections which are most often polymicrobial. Treatment involves fluid resuscitation, pain control, nutritional support via enteral feeding when possible, and antibiotics only for infected necrosis or cholangitis. Complications include pancreatic pseudocysts and abscesses which may require percutaneous or surgical drainage.
The document discusses the anatomy, functions, diseases, and management of liver injuries. It describes the liver's dual blood supply and ability to regenerate after partial resection. Evaluation and treatment of liver trauma involves resuscitation, imaging to assess injuries, and management may include suturing lacerations, resection for vascular injuries, or packing for diffuse parenchymal injuries.
Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe. It is most often caused by gallstones or heavy alcohol use. A patient presents with acute upper abdominal pain that may radiate to the back. Laboratory tests show elevated pancreatic enzymes and imaging can identify gallstones or complications. Severity is assessed by the presence of organ failure or local complications like necrosis. Treatment involves fluid resuscitation and management of complications. The Ranson criteria uses factors at admission and within 48 hours to predict severe acute pancreatitis.
Evidence Based Treatment of Acute Pancreatitis 2013Waleed Mahrous
The document summarizes guidelines for the diagnosis and management of acute pancreatitis. It addresses criteria for diagnosis, risk stratification based on severity (mild, moderately severe, severe), initial assessment including fluid resuscitation goals, nutritional support, and recommendations for enteral versus parenteral nutrition based on severity. The guidelines emphasize early aggressive fluid resuscitation, monitoring for organ failure, and initiating enteral nutrition in severe cases to prevent infectious complications while avoiding parenteral nutrition.
1) Acute pancreatitis is an inflammation of the pancreas that can range from mild to severe. It involves autodigestion of the pancreas by its own enzymes.
2) There are two main types - edematous pancreatitis which is mild and necrotizing/hemorrhagic pancreatitis which is more severe and can lead to loss of pancreatic function.
3) Causes include gallstones, alcohol abuse, medications, trauma, hyperlipidemia and sometimes the cause is unknown. Clinical features include severe abdominal pain, nausea and tenderness on examination. Investigations include blood tests and imaging. Management involves IV fluids, nil by mouth, antibiotics if infected, and sometimes
Gastrocon 2016 - Dr S.K Sinha's observation on Acute PancreatitisApolloGleaneagls
The patient is a 40-year old male alcohol abuser presenting with abdominal pain, vomiting, and distension. Investigations show elevated lipase and CT scan shows bulky pancreas and gallbladder sludge. The patient meets criteria for acute pancreatitis and CT severity index of 8/10 suggests severe disease. While antibiotics are not routinely recommended, they may be considered for infected necrosis seen on imaging or clinical deterioration. Aggressive fluid resuscitation and pain management with tramadol are the primary treatments, with nutritional support and monitoring for organ dysfunction.
This document describes the case of a 33-year-old male patient presenting with severe acute pancreatitis following an alcohol binge. Initial tests showed signs of severe illness including a CT scan showing over 30% necrosis of the pancreas. The patient was found to have a high Ranson score of 8, predicting a 60% mortality rate. Though not initially started on antibiotics, the patient later developed multiple organ dysfunction and infection was detected in a peripancreatic fluid collection via fine needle aspiration, identifying Proteus mirabilis. The patient underwent surgery to drain the infection and was treated with meropenem, subsequently making a full recovery.
This document summarizes the updated 2013 classification of acute pancreatitis published in the journal Gut. It defines acute pancreatitis diagnosis requiring two of three criteria: abdominal pain, elevated lipase/amylase, characteristic CT findings. CT is indicated if clinical diagnosis is doubtful, severity is high, or complications are suspected and can identify two types: interstitial edematous pancreatitis and necrotizing pancreatitis. Collections are also defined including acute peripancreatic fluid collections in interstitial cases, acute necrotic collections in necrotizing cases, and pseudocysts or walled-off necrosis in later encapsulated collections. Reporting requirements for imaging findings are discussed.
This document discusses acute pancreatitis. It begins with a case presentation of a 30-year-old patient presenting with epigastric pain. It then provides general information on the pancreas and its secretions of bicarbonate and enzymes. It describes the signs, symptoms, lab tests, imaging studies, differential diagnosis, phases, severity, treatment, and recurrence risks of acute pancreatitis. Treatment involves NPO, IV fluids, analgesics, and treating any underlying causes like gallstones.
The document discusses the embryology, anatomy, clinical features, investigations and imaging findings of acute pancreatitis. Regarding embryology, it describes how the pancreas develops from dorsal and ventral buds that fuse. For anatomy, it outlines the relationships of different parts of the pancreas. It also summarizes the etiology, pathophysiology and scoring systems used to classify severity of acute pancreatitis. Imaging findings on ultrasound, CT and MRI are summarized to diagnose and characterize acute pancreatitis and its complications.
Acute pancreatitis atlanta classification & managementSeneeth Peramuna
Acute Pancreatitis
Definition,
Etialogy and pathogenesis
Atlanta Revised classification
Initial risk assesment
Management of general condition, local and systemic complications
BISAP score
Modified Marshall score
Acute pancreatitis is defined as an acute inflammatory process of the pancreas that can involve other tissues. It is caused by premature activation of digestive enzymes within pancreatic cells leading to autodigestion. Acute pancreatitis is clinically defined by abdominal pain and elevated pancreatic enzymes. Gallstones and alcohol are common causes. Severity is classified based on organ failure and local complications. Treatment involves supportive care, pain management, intravenous fluids, nutritional support, and treating complications. New research focuses on modulating the immune response to reduce organ damage.
The document discusses acute pancreatitis, which occurs when the pancreas becomes inflamed. It describes the pancreas's normal functions and the pathophysiology of acute pancreatitis, which involves premature activation of digestive enzymes that digest the pancreas itself. Symptoms include severe abdominal pain. Complications can include multi-organ failure if the inflammation spreads beyond the pancreas. Risk factors, signs, symptoms, classification, complications, and treatment approach are outlined.
Gut injury plays a key role in the pathogenesis and outcome of severe acute pancreatitis (SAP). Intestinal ischemia-reperfusion injury during SAP can damage the gut barrier and lead to bacterial translocation from the gut to the mesenteric lymph nodes and bloodstream, resulting in sepsis, systemic inflammatory response syndrome (SIRS), and multiple organ dysfunction syndrome (MODS). Evidence indicates gut injury is common in SAP, shown by intestinal atrophy, ischemia, increased permeability, bacterial translocation, and endotoxemia, all of which correlate with increased severity of disease and risk of complications.
Acute pancreatitis is an inflammatory process of the pancreas that can involve surrounding tissues or remote organ systems. The most common causes are gallstones and alcohol. The pathogenesis involves premature activation of digestive enzymes within the pancreas that cause autodigestion. Clinical presentation includes severe upper abdominal pain and elevated pancreatic enzymes. Diagnosis requires abdominal pain consistent with pancreatitis plus elevated pancreatic enzymes or radiologic findings. Complications can include pancreatic necrosis, pseudocyst formation, and systemic inflammatory response.
This document discusses the diagnosis and management of acute pancreatitis in a 22-year-old male patient presenting with epigastric pain. It examines the use of amylase and lipase tests to diagnose acute pancreatitis, describes clinical features and scoring systems to assess severity, and discusses management issues including fluid resuscitation, antibiotics, nutrition, ERCP, surgery, and monitoring organ function with Ranson's criteria and CT severity index.
GIT Journal club acute pancreatitis ACG Practice guidelines.Shaikhani.
The document contains questions regarding the diagnosis, etiology, management, and treatment of acute pancreatitis. Specifically, it asks 11 multiple choice questions testing knowledge about the required findings for diagnosis of acute pancreatitis, indications for endoscopic retrograde cholangiopancreatography and nutrition in acute pancreatitis, definitions of severe acute pancreatitis, and risk factors for hereditary and idiopathic acute pancreatitis.
1) Autoimmune pancreatitis is characterized by lymphoplasmacytic infiltration and fibrosis of the pancreas that often dramatically responds to steroid therapy.
2) Diagnosis involves a combination of clinical, imaging, histological, and serological findings including elevated serum IgG4 levels and involvement of other organs.
3) Two subtypes exist - type 1 is associated with elevated IgG4, other organ involvement and a good response to steroids, while type 2 involves granulocytic epithelial lesions and is less responsive to steroids.
This document provides an overview of acute pancreatitis, including its definitions, etiology, pathogenesis, and diagnostic assessment. It discusses the major causes of acute pancreatitis such as alcohol use, gallstones, medications, and genetic factors. The pathogenesis involves the abnormal activation of pancreatic enzymes leading to immune response and microcirculatory disturbances. Diagnosis is based on clinical features, elevated serum amylase and lipase levels, and imaging findings on ultrasound or CT scan. Several scoring systems are described to assess the severity of acute pancreatitis, including ATLANTA criteria, Ranson score, APACHE-II score, and Marshall score. Biochemical markers like CRP, PCT, and hematocrit can also help predict
Acute pancreatitis has an incidence of 17 per 100,000 people and a mortality of 2-3%. The most common causes are gallstones (50% of cases) and alcohol abuse (20-25% of cases). Necrotizing pancreatitis can lead to pancreatic infections which are most often polymicrobial. Treatment involves fluid resuscitation, pain control, nutritional support via enteral feeding when possible, and antibiotics only for infected necrosis or cholangitis. Complications include pancreatic pseudocysts and abscesses which may require percutaneous or surgical drainage.
The document discusses the anatomy, functions, diseases, and management of liver injuries. It describes the liver's dual blood supply and ability to regenerate after partial resection. Evaluation and treatment of liver trauma involves resuscitation, imaging to assess injuries, and management may include suturing lacerations, resection for vascular injuries, or packing for diffuse parenchymal injuries.
Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe. It is most often caused by gallstones or heavy alcohol use. A patient presents with acute upper abdominal pain that may radiate to the back. Laboratory tests show elevated pancreatic enzymes and imaging can identify gallstones or complications. Severity is assessed by the presence of organ failure or local complications like necrosis. Treatment involves fluid resuscitation and management of complications. The Ranson criteria uses factors at admission and within 48 hours to predict severe acute pancreatitis.
Evidence Based Treatment of Acute Pancreatitis 2013Waleed Mahrous
The document summarizes guidelines for the diagnosis and management of acute pancreatitis. It addresses criteria for diagnosis, risk stratification based on severity (mild, moderately severe, severe), initial assessment including fluid resuscitation goals, nutritional support, and recommendations for enteral versus parenteral nutrition based on severity. The guidelines emphasize early aggressive fluid resuscitation, monitoring for organ failure, and initiating enteral nutrition in severe cases to prevent infectious complications while avoiding parenteral nutrition.
1) Acute pancreatitis is an inflammation of the pancreas that can range from mild to severe. It involves autodigestion of the pancreas by its own enzymes.
2) There are two main types - edematous pancreatitis which is mild and necrotizing/hemorrhagic pancreatitis which is more severe and can lead to loss of pancreatic function.
3) Causes include gallstones, alcohol abuse, medications, trauma, hyperlipidemia and sometimes the cause is unknown. Clinical features include severe abdominal pain, nausea and tenderness on examination. Investigations include blood tests and imaging. Management involves IV fluids, nil by mouth, antibiotics if infected, and sometimes
Gastrocon 2016 - Dr S.K Sinha's observation on Acute PancreatitisApolloGleaneagls
The patient is a 40-year old male alcohol abuser presenting with abdominal pain, vomiting, and distension. Investigations show elevated lipase and CT scan shows bulky pancreas and gallbladder sludge. The patient meets criteria for acute pancreatitis and CT severity index of 8/10 suggests severe disease. While antibiotics are not routinely recommended, they may be considered for infected necrosis seen on imaging or clinical deterioration. Aggressive fluid resuscitation and pain management with tramadol are the primary treatments, with nutritional support and monitoring for organ dysfunction.
This document describes the case of a 33-year-old male patient presenting with severe acute pancreatitis following an alcohol binge. Initial tests showed signs of severe illness including a CT scan showing over 30% necrosis of the pancreas. The patient was found to have a high Ranson score of 8, predicting a 60% mortality rate. Though not initially started on antibiotics, the patient later developed multiple organ dysfunction and infection was detected in a peripancreatic fluid collection via fine needle aspiration, identifying Proteus mirabilis. The patient underwent surgery to drain the infection and was treated with meropenem, subsequently making a full recovery.
This document summarizes the updated 2013 classification of acute pancreatitis published in the journal Gut. It defines acute pancreatitis diagnosis requiring two of three criteria: abdominal pain, elevated lipase/amylase, characteristic CT findings. CT is indicated if clinical diagnosis is doubtful, severity is high, or complications are suspected and can identify two types: interstitial edematous pancreatitis and necrotizing pancreatitis. Collections are also defined including acute peripancreatic fluid collections in interstitial cases, acute necrotic collections in necrotizing cases, and pseudocysts or walled-off necrosis in later encapsulated collections. Reporting requirements for imaging findings are discussed.
This document discusses acute pancreatitis. It begins with a case presentation of a 30-year-old patient presenting with epigastric pain. It then provides general information on the pancreas and its secretions of bicarbonate and enzymes. It describes the signs, symptoms, lab tests, imaging studies, differential diagnosis, phases, severity, treatment, and recurrence risks of acute pancreatitis. Treatment involves NPO, IV fluids, analgesics, and treating any underlying causes like gallstones.
The document discusses the embryology, anatomy, clinical features, investigations and imaging findings of acute pancreatitis. Regarding embryology, it describes how the pancreas develops from dorsal and ventral buds that fuse. For anatomy, it outlines the relationships of different parts of the pancreas. It also summarizes the etiology, pathophysiology and scoring systems used to classify severity of acute pancreatitis. Imaging findings on ultrasound, CT and MRI are summarized to diagnose and characterize acute pancreatitis and its complications.
Acute pancreatitis atlanta classification & managementSeneeth Peramuna
Acute Pancreatitis
Definition,
Etialogy and pathogenesis
Atlanta Revised classification
Initial risk assesment
Management of general condition, local and systemic complications
BISAP score
Modified Marshall score
Acute pancreatitis is defined as an acute inflammatory process of the pancreas that can involve other tissues. It is caused by premature activation of digestive enzymes within pancreatic cells leading to autodigestion. Acute pancreatitis is clinically defined by abdominal pain and elevated pancreatic enzymes. Gallstones and alcohol are common causes. Severity is classified based on organ failure and local complications. Treatment involves supportive care, pain management, intravenous fluids, nutritional support, and treating complications. New research focuses on modulating the immune response to reduce organ damage.
The document discusses acute pancreatitis, which occurs when the pancreas becomes inflamed. It describes the pancreas's normal functions and the pathophysiology of acute pancreatitis, which involves premature activation of digestive enzymes that digest the pancreas itself. Symptoms include severe abdominal pain. Complications can include multi-organ failure if the inflammation spreads beyond the pancreas. Risk factors, signs, symptoms, classification, complications, and treatment approach are outlined.
Gut injury plays a key role in the pathogenesis and outcome of severe acute pancreatitis (SAP). Intestinal ischemia-reperfusion injury during SAP can damage the gut barrier and lead to bacterial translocation from the gut to the mesenteric lymph nodes and bloodstream, resulting in sepsis, systemic inflammatory response syndrome (SIRS), and multiple organ dysfunction syndrome (MODS). Evidence indicates gut injury is common in SAP, shown by intestinal atrophy, ischemia, increased permeability, bacterial translocation, and endotoxemia, all of which correlate with increased severity of disease and risk of complications.
Acute pancreatitis is an inflammatory process of the pancreas that can involve surrounding tissues or remote organ systems. The most common causes are gallstones and alcohol. The pathogenesis involves premature activation of digestive enzymes within the pancreas that cause autodigestion. Clinical presentation includes severe upper abdominal pain and elevated pancreatic enzymes. Diagnosis requires abdominal pain consistent with pancreatitis plus elevated pancreatic enzymes or radiologic findings. Complications can include pancreatic necrosis, pseudocyst formation, and systemic inflammatory response.
This document discusses acute pancreatitis, including:
- Definitions of mild and severe acute pancreatitis.
- Common causes like gallstones and alcohol.
- Presenting signs of abdominal pain, nausea, and elevated amylase/lipase levels.
- Imaging like CT scans can assess severity and complications.
- Treatment focuses on supportive care like fluid resuscitation, pain control, and enteral nutrition.
This document summarizes acute pancreatitis (AP), including its causes, presentation, diagnosis, severity assessment, treatment, and complications. AP ranges from mild to severe and is commonly caused by gallstones or alcohol abuse. Clinically it presents with abdominal pain and elevated pancreatic enzymes. Imaging like CT can help determine severity and guide management, which involves supportive care, pain control, and treating any underlying conditions or complications like pancreatic necrosis. More severe cases may require antibiotics, minimally invasive drainage procedures, or surgery.
The document discusses acute pancreatitis, including causes, clinical features, diagnosis, severity grading, management, and prognosis. Gallstones and alcohol are the most common causes. Scoring systems like Ranson criteria and APACHE II can help indicate severity and prognosis. Management involves treatment of the underlying cause, supportive care, and monitoring for complications like pancreatic necrosis which may require intervention.
SEVERE ACUTE PANCREATITIS PRESENTATION 2020karanchhabra75
This document discusses the diagnosis and management of severe acute pancreatitis. It provides details on the case of a 40-year-old male diagnosed with severe acute pancreatitis induced by alcohol. Imaging showed multiple fluid collections surrounding the pancreas. The document then reviews diagnostic criteria, severity assessments, nutritional support, antibiotic use, and approaches to managing complications like necrosis and collections.
Acute pancreatitis is a common medical problem. Initial phase of acute pancreatitis is characterized by inflammation. This is caused by release of cytokines and other pro inflammatory mediators. These further cause vasodilatation, intravascular volume depletion, and end organ hypoperfusion. The etiology can be varied but common causes are biliary (stone in CBD) and alcohol. Other causes are drugs, infections, trauma, idiopathic, post ERCP etc. Patients with severe pancreatitis have high risk of mortality (10%) which can go upto 30% if necrosis gets infected, which occurs in about 40% patients. Further, persistent organ failure increases the mortality up to 34–55% as compared to 0.3% with transient organ failure. Traditionally as per Atlanta classification, acute pancreatitis has been classified as mild or severe depending upon organ failure or local complications. Acute pancreatitis is a hyper-catabolic state. Moreover some of these patients may be malnourished to begin with (alcoholics). Thus their nutritional requirements are much more than ordinary person. There are good quality studies available to show that in absence of cholangitis, there is no benefit of doing early ERCP. Also, technically it is more difficult to do in such situations, and procedure related complication may be more. If in doubt, it may be worthwhile to do endoscopic ultrasound to document the presence of CBD stone before attempting to cannulate the CBD.
Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe. It commonly results from gallstones or alcohol use. Symptoms include abdominal pain and elevated pancreatic enzymes. Severe cases can lead to organ failure and death in up to 30% of patients. Treatment focuses on fluid resuscitation, treating the underlying cause, and managing complications which may include pancreatic necrosis, pseudocysts, or systemic inflammatory response. Prognosis depends on severity with most patients recovering if the attack is mild but severe cases carrying significant morbidity and mortality.
This document provides information about acute pancreatitis including its anatomy, pathogenesis, clinical presentation, diagnosis, severity assessment, complications and management. Some key points:
- Acute pancreatitis can range from mild to severe and is commonly caused by gallstones or alcohol use.
- Diagnosis involves elevated pancreatic enzymes and imaging such as CT scan which can also assess severity. Several scoring systems exist to evaluate prognosis.
- Management of mild cases is usually conservative while severe cases require ICU monitoring, IV fluids, nutritional support and antibiotics if infected necrosis is present.
- Complications include fluid collections, pancreatic necrosis, pseudocysts and vascular issues which may require drainage or surgical debridement.
The document provides guidelines for the management of acute pancreatitis (AP). It summarizes that AP is one of the most common gastrointestinal diseases, leading to significant burden. The incidence of AP has been increasing. Recent studies have identified two phases of AP - early (within 1 week) characterized by systemic inflammatory response and late (>1 week) characterized by local complications. Key recommendations include establishing the diagnosis of AP using clinical criteria including abdominal pain and elevated serum amylase/lipase. Imaging such as CT should be reserved for unclear or non-improving cases. Early management focuses on hemodynamic support and aggressive hydration to decrease morbidity and mortality. Guidelines are provided for evaluating etiology, risk stratification, nutritional support, antibiotic use
The document provides guidelines for the management of acute pancreatitis (AP). It summarizes that AP diagnosis is typically established by abdominal pain and elevated serum amylase and/or lipase levels. Contrast-enhanced CT or MRI is only recommended if diagnosis is unclear or patient fails to improve to evaluate for complications. It outlines recommendations for early medical management including aggressive hydration and nutrition, as well as management of complications like pancreatic necrosis with antibiotics, endoscopic or radiologic drainage, or surgery.
The document provides guidelines for the management of acute pancreatitis (AP). It summarizes that AP is one of the most common gastrointestinal diseases, leading to significant burden. The incidence of AP has been increasing. Recent studies have identified two phases of AP - early (within 1 week) characterized by systemic inflammatory response and late (>1 week) characterized by local complications. Key recommendations include establishing the diagnosis of AP using clinical criteria including abdominal pain and elevated serum amylase/lipase. Imaging such as CT should be reserved for unclear or non-improving cases. Early management focuses on hemodynamic support and aggressive hydration to decrease morbidity and mortality. Guidelines are provided for evaluating etiology, risk stratification, nutritional support, antibiotic use
The document discusses acute calculous cholecystitis, a complication of gallstones where the gallbladder becomes inflamed. It provides details on the pathogenesis, symptoms, diagnosis and treatment strategies. Regarding treatment strategies, it indicates that early laparoscopic cholecystectomy within 1 week of symptoms starting is considered the best treatment for most patients based on randomized trials showing shorter hospital stays compared to delayed surgery 2-3 months later. However, it notes the risk of bile duct injuries may be higher for early surgery on an inflamed gallbladder based on large registry studies, though randomized trials were too small to definitively assess this risk. It concludes that while early laparoscopy is usually best, open surgery or postponing surgery may
A Case of Chronic Pancreatitis Due to Hyper ParathyroidismApollo Hospitals
Chronic pancreatitis is the progressive and permanent destruction of the pancreas resulting in exocrine and endocrine insufficiency and, often, chronic disabling pain. The etiology is multifactorial. 60 to 70% of patients with chronic pancreatitis have a long history of heavy consumption of alcohol before the onset of clinically apparent disease. Primary hyperparathyroidism is a rare cause of chronic pancreatitis and there is paucity of data on this interesting association. The relationship of cause and effect between the two diseases has been debated.
We present here a case of a 42-year-old non-alcoholic man, diagnosed to be suffering from chronic calcific pancreatitis, the cause of which was found to be hypercalcemia due to a solitary parathyroid adenoma.
Cholecystitis is inflammation of the gallbladder, usually caused by a gallstone blocking the cystic duct. This study evaluated levels of liver enzymes and bilirubin in 60 patients with clinically diagnosed cholecystitis compared to 40 healthy controls. Levels of 5'NT, ALP, AST, ALT, and bilirubin were all significantly higher in patients, indicating cellular injury and cholestasis. 5'NT and bilirubin levels best distinguished between acute and chronic cholecystitis. Elevated enzyme levels helped diagnose cholecystitis and showed the extent of hepatic damage, with 5'NT specifically indicating bile duct obstruction or cholestasis.
This document discusses the approach to patients with pancreatic diseases, including acute and chronic pancreatitis. It begins with definitions of incidence and diagnostic tests used. It then describes the etiology, pathogenesis, clinical features, management, and complications of acute pancreatitis. Etiology of recurrent pancreatitis is discussed. Chronic pancreatitis is defined, and its pathophysiology, imaging, treatment, and complications are outlined. Throughout, key definitions from the Revised Atlanta Classification are provided to stage and characterize pancreatic conditions.
This document discusses acute pancreatitis, including its anatomy, risk factors, pathogenesis, symptoms, diagnosis, complications, and treatment approaches. It notes that acute pancreatitis is an inflammatory process of the pancreas caused by autolysis from abnormal activation of pancreatic enzymes. Treatment involves conservative management with pain control, fluid resuscitation, and prevention of infection. Operative intervention may be needed if conservative treatment fails or complications like necrosis or infection arise.
2. clinical practice
tive enzymes causes pancreatic injury and results
in an inflammatory response that is out of propor-tion
to the response of other organs to a similar
insult. The acute inflammatory response itself
causes substantial tissue damage and may pro-gress
beyond the pancreas to a systemic inflam-matory
response syndrome, multiorgan failure,
n engl j med 354;20 www.nejm.org may 18, 2006 2143
or death.
Strategies and Evidence
Diagnosis
The clinical diagnosis of acute pancreatitis is based
on characteristic abdominal pain and nausea, com-bined
with elevated serum levels of pancreatic en-zymes.
In gallstone pancreatitis, the pain is typi-cally
sudden, epigastric, and knife-like and may
radiate to the back. In hereditary or metabolic cas-es
or in those associated with alcohol abuse, the
onset may be less abrupt and the pain poorly local-ized.
Serum amylase levels that are more than
three times the upper limit of normal, in the set-ting
of typical abdominal pain, are almost always
caused by acute pancreatitis. Lipase levels are also
elevated and parallel the elevations in amylase lev-els.
The levels of both enzymes remain elevated
with ongoing pancreatic inflammation, with amy-lase
levels typically returning to normal shortly
before lipase levels in the resolution phase.
Tests that are more specific for acute pancreati-tis
but less widely available evaluate levels of tryp-sinogen
activation peptide10 and trypsinogen-2.11
Abdominal imaging by computed tomography
(CT), magnetic resonance imaging (MRI), or trans-abdominal
ultrasonography is useful in confirm-ing
the diagnosis of pancreatitis or ruling out
other intraabdominal conditions as the cause of
pain or laboratory abnormalities. Such imaging
may also identify the cause of pancreatitis or its
associated complications.
Management
Determination of the cause is important for guid-ing
immediate management and preventing recur-rence.
An elevated alanine aminotransferase level
in a patient without alcoholism who has pancre-atitis
is the single best laboratory predictor of bili-ary
pancreatitis; a level of more than three times
the upper limit of normal has a positive predictive
value of 95 percent for gallstone pancreatitis.12
However, the presence of normal alanine amino-transferase
levels does not reliably rule out the di-agnosis.
4 Laboratory testing may reveal hypertri-glyceridemia
or hypercalcemia as possible causes
of pancreatitis, although pancreatitis may also
cause mildly elevated triglyceride levels.
Imaging Studies
CT or MRI can identify gallstones or a tumor (an
infrequent cause of pancreatitis), as well as local
complications. MRI may also identify early duct
disruption that is not seen on CT.13 Transabdomi-nal
ultrasonography is more sensitive than either
CT or MRI for identifying gallstones and sludge
and for detecting bile-duct dilatation, but it is in-sensitive
for detecting stones in the distal bile
duct.4,5 Endoscopic ultrasonography may be the
most accurate test for diagnosing or ruling out
biliary causes of acute pancreatitis (Fig. 1) and may
guide the emergency use of endoscopic retrograde
cholangiopancreatography (ERCP).14
A
B
Figure 1. Endoscopic Ultrasonography of the Gall-bladder
and Common Bile Duct from the Duodenum.
Microlithiasis (sludge) is shown within the gallbladder
(Panel A, arrow) and within the common bile duct
(Panel B, arrow). Also visible in Panel B are the head of
the pancreas (curved arrow) and the pancreatic duct
(arrowhead). (Images courtesy of Neeraj Kaushik, M.D.)
3. The new england journal o f medicine
Table 1. Scoring Methods for the Prediction of Severe Acute Pancreatitis.
Criterion and Marker Threshold Value Severe Pancreatitis
Atlanta criteria* Indicated by any positive factor listed
Ranson’s score† ≥3
APACHE II score‡ ≥8
Organ failure
Shock Blood pressure of <90 mm Hg
Pulmonary insufficiency Partial pressure of arterial oxygen of ≤60 mm Hg5
Renal failure Creatinine level of >177 μmol/liter (2 mg/dl)
after hydration
Systemic complications
Disseminated intravascular coagulation Platelet count of ≤100,000/mm3
Fibrinogen level of <1 g/liter
Fibrin-split products level of >80 μg/ml
Metabolic disturbance Calcium level of ≤7.5 mg/dl
Local complications
Pancreatic necrosis Present
Pancreatic abscess Present
Pancreatic pseudocyst Present
Ranson’s score† Indicated by a total score ≥3, with
Age >55 yr
Blood glucose level >200 mg/dl (10 mmol/liter)
White-cell count >16,000/mm3
Lactate dehydrogenase level >350 IU/liter
Alanine aminotransferase level >250 IU/liter
Within 48 hr after presentation
Hematocrit >10% decrease
Serum calcium <8 mg/dl (2 mmol/liter)
Base deficit >4 mEq/liter
Blood urea nitrogen >5 mg/dl (1.8 mmol/liter) increase
Fluid sequestration >6 liters
Partial pressure of arterial oxygen§ <60 mm Hg
ERCP
Persistent biliary obstruction worsens the outcome
and increases the severity of acute pancreatitis and
predisposes the patient to bacterial cholangitis.
ERCP is used with endoscopic sphincterotomy to
extract impacted gallstones and to drain infected
bile in severe acute pancreatitis.15-18 Although ERCP
has risks, including bleeding after sphincteroto-my
and causing acute pancreatitis, complications
are uncommon when the procedure is performed
by experienced endoscopists. Three randomized
trials involving a total of 511 patients with gall-stone
pancreatitis compared conservative manage-ment
1 point for each positive factor
with ERCP and endoscopic sphincterotomy
within 24 to 72 hours after admission. The stud-ies
showed a significantly lower risk of pancreati-tis-
associated complications in the ERCP group
(odds ratio, 0.27; 95 percent confidence interval,
0.14 to 0.53).16
Hospitalization
Patients who present with persistent or severe pain,
vomiting, dehydration, or signs of impending se-vere
acute pancreatitis (to be discussed later) should
be hospitalized. Clinical trials have failed to show
the efficacy of medications proposed to alter the
At presentation
2144 n engl j med 354;20 www.nejm.org may 18, 2006
4. clinical practice
Table 1. (Continued.)
Criterion and Marker Threshold Value Severe Pancreatitis
CT severity index¶ Indicated by a total score of >6
course of acute pancreatitis, including an inhibi-tor
of platelet-activating factor (lexipafant19), so-matostatin
and its analogues, and protease inhib-itors20;
treatment is primarily supportive. Patients
should receive nothing by mouth and receive in-travenous
pain medication and aggressive hydra-tion
to treat or prevent hemoconcentration (e.g.,
a bolus of fluids to achieve hemodynamic stabil-ity,
followed by 250 to 500 ml of crystalloid solu-tions
per hour in an average-sized patient without
substantial kidney or heart disease). Fluid balance
should be maintained and pulse oximetry should
be considered, especially when narcotic analgesics
are used.
Predicting Severe Acute Pancreatitis
The severity of acute pancreatitis is defined by the
presence or absence of organ failure, local com-plications,
or both21-25 (Table 1). It is critical to
identify patients who are at high risk for severe
(CT grade plus necrosis score)
disease, since they require close monitoring and
possible intervention. Recognized markers of the
risk of severe acute pancreatitis include specific
laboratory values that measure the systemic in-flammatory
response (such as C-reactive protein),
scoring systems that assess inflammation or or-gan
failure (such as Ranson’s score), and findings
on imaging studies13,23 (Table 2). The Acute Phys-iology
and Chronic Health Evaluation score (based
on initial values of 12 routine physiological mea-surements,
age, and previous health status) is
among the best predictors of severity on admission,
whereas elevated C-reactive protein levels are equal-ly
useful when measured 24 to 48 hours after the
onset of symptoms.27 Severity scores are useful in
predicting both complications and death (Table 3).
Other markers that are not included in standard
scoring systems should also be considered. Obe-sity
(a body-mass index of more than 30) is associ-ated
with an increase in the risk of a severe clinical
n engl j med 354;20 www.nejm.org may 18, 2006 2145
CT grade
Normal pancreas (grade A) 0 points
Focal or diffuse enlargement (grade B) 1 point
Intrinsic change; fat stranding (grade C) 2 points
Single, ill-defined collection of fluid (grade D) 3 points
Multiple collections of fluid or gas in or adja-cent
to pancreas (grade E)
4 points
Necrosis score
No pancreatic necrosis 0 points
Necrosis of one third of pancreas 2 points
Necrosis of one half of pancreas 4 points
Necrosis of >one half of pancreas 6 points
APACHE II score‡ Indicated by a score of ≥8
Initial values of 12 routine physiological measure-ments,
age, and previous health status
* Data are from Bradley.21 The Atlanta criteria were adopted in 1992 by the International Symposium on Acute Pancreatitis. The presence of
any condition in the five main categories indicates severe acute pancreatitis.
† Data are from Ranson et al.22 The original Ranson’s score is based on 11 clinical signs (5 measured on admission and 6 in the 48 hours af-ter
admission), with a higher score indicating greater correlation with the incidence of systemic complications and the presence of pancreat-ic
necrosis. The relationship between Ranson’s score and the CT severity index23 is given in Table 3.
‡ Data are from Knaus et al.24 and Larvin and McMahon.25 The Acute Physiology and Chronic Health Evaluation (APACHE II) score is based
on initial values of 12 routine physiological measurements, age, and previous health status, with a score of 8 or more commonly used as
the threshold for classification as severe pancreatitis.
§ The test was performed without the use of supplemental oxygen.
¶ The CT severity index23 is a combination of the sum of the necrosis score and points assigned to five grades of findings on CT. The index
ranges from 0 to 10, with higher scores indicating a greater severity of illness.
5. The new england journal o f medicine
Table 2. Value of Various Scoring Systems and Inflammatory Markers in the Prediction of Severe Acute Pancreatitis.*
Scoring System Sensitivity Specificity
course by a factor of 2 to 3.29 A hematocrit above
44 percent is a clear risk factor for pancreatic ne-crosis,
30 although it is a poor predictor of the sever-ity
of disease. Preliminary evidence suggests that
genetic factors, such as polymorphisms in the che-mokine
monocyte chemotactic protein 1 (MCP-1)
gene,31 may also predict severity, although such
genetic testing is not currently used in practice.
Several clinical findings — including thirst,
poor urine output, progressive tachycardia, tachyp-nea,
hypoxemia, agitation, confusion, a rising he-matocrit
level, and a lack of improvement in symp-toms
within the first 48 hours — are warning
signs of impending severe disease. If such symp-toms
develop, admission to an intensive care unit
should be considered. Intensive care may also be
warranted in patients at risk for rapid deteriora-tion
in their condition, including those over the
age of 55 years,22 those who need ongoing volume
resuscitation or invasive monitoring of fluid sta-tus
(e.g., central venous pressure monitoring), or
Positive
Predictive
Value
those with renal failure or respiratory compro-mise.
15
Pancreatic-Fluid Collections, Pseudocysts,
and Necrosis
Up to 57 percent of patients who are hospitalized
with acute pancreatitis will have fluid collections,
with 39 percent having two areas involved and 33
percent having three or more.32 Fluid collections
are initially ill defined,21 evolve over time, and are
usually managed conservatively. If the fluid col-lections
continue to enlarge, cause pain, become
infected (as suggested by the presence of unex-plained
fever, leukocytosis, or gas in the fluid col-lection),
or compress adjacent organs, then med-ical,
endoscopic, or surgical intervention may be
needed.33,34 Fluid collections with very high lev-els
of pancreatic enzymes are usually associated
with pancreatic-duct disruptions and may even-tually
form pseudocysts (usually over a period of
several weeks), ascites, or pleural effusions.34
2146 n engl j med 354;20 www.nejm.org may 18, 2006
Negative
Predictive
Value Accuracy
percent
On admission
APACHE II score†
≥6 83–99 33–54 28–40 80–97 45–65
≥8 68–71 48–67 30–40 84–87 53–68
≥10 52–63 66–81 32–64 81–89 63–77
Interleukin-6 level >400 pg/ml 89 87 80 93 88
At 24 hours
APACHE II score ≥8 63 73 38 88 71
C-reactive protein level >150 mg/dl 65 73 37 90 72
PMN elastase >300 μg/liter 93 99 97 98 98
Urinary TAP >35 nmol/liter 68 74 44 89 73
At 48 hours
APACHE II score ≥8 56–78 52–64 30–33 85–88 58–63
Ranson’s score ≥3 75–89 54–71 37–49 91–96 62–75
Modified Glasgow score ≥3‡ 45–75 63–89 28–66 79–93 59–84
C-reactive protein level >150 mg/dl 65 73 37 90 72
* PMN denotes polymorphonuclear leukocyte, and TAP trypsinogen activation peptide.
† Data are from Knaus et al.24 and Larvin and McMahon.25 The Acute Physiology and Chronic Health Evaluation
(APACHE II) score is based on initial values of 12 routine physiological measurements, age, and previous health status,
with a score of 8 or more commonly used as the threshold for the classification of severe pancreatitis.
‡ The Modified Glasgow score is similar to Ranson’s score but can be completed on admission. The score ranges from
0 to 8, with scores of 3 or more indicating a greater severity of illness.26 Data are from Papachristou and Whitcomb.27
6. clinical practice
Asymptomatic pseudocysts can be managed con-servatively,
whereas symptomatic pseudocysts can
often be drained endoscopically.35 ERCP may help
to define the anatomy of the pancreatic duct and
identify any duct disruptions to guide further in-tervention.
Table 3. Relationship between Severity Scores and Outcomes in Acute Pan-creatitis.*
Index Score
Ranson’s score 0–2 3–4 5–6 7–8
percent of patients
Intensive care for >7 days and
survival
1 24 53 NA
Death 3 16 40 100
Either intensive care for >7 days
or death
4 40 93 100
CT severity index 0–3 4–6 7–10 NA
Complications 8 35 92 NA
Death 3 6 17 NA
* Data are from Balthazar et al.23 and Ranson.28 NA denotes not applicable.
n engl j med 354;20 www.nejm.org may 18, 2006 2147
33,34
Pancreatic necrosis, occurring as diffuse or fo-cal
areas of nonviable pancreatic parenchyma,21
is an important complication that can develop dur-ing
the first few days of pancreatitis; the condition
is associated with late complications and death if
the necrotic tissue becomes infected. The devel-opment
of necrosis is associated with pancreatic
inflammation, hypovolemia, and hypotension from
the shunting of blood from other organs, vascu-lar
spasm, and hemoconcentration.30 Pancreatic
necrosis can be demonstrated by a loss of tissue
perfusion on contrast-enhanced CT.23
Infection of necrotic tissue is suspected when
there is fever, leukocytosis, and a failure to improve
or unexpected deterioration — usually after the
first week of illness. Visualization of gas bubbles
within the necrotic tissue on CT is evidence of in-fection.
The diagnosis of infected necrosis is usu-ally
made by fine-needle aspiration of the necrotic
area guided by either CT or ultrasonography, with
Gram’s staining and culture of the aspirate.36
Lack of Improvement
If the condition of a patient whose pancreatitis is
predicted to be mild fails to improve within two or
three days, then contrast-enhanced CT (“pancreas
protocol”) should be considered to identify fluid
collections, pancreatic necrosis, or other compli-cations
that may require intervention. Antibiotic
therapy and nutritional support also warrant con-sideration
in patients whose condition fails to im-prove
promptly or in whom complications develop.
Use of Antibiotics
The proper role of antibiotics in acute pancreati-tis
remains controversial. No antibiotics are indi-cated
in mild cases. However, infectious compli-cations
are an important concern in severe cases,
especially cases of pancreatic necrosis. A potential
role for prophylactic antibiotics in severe pancre-atitis
was initially given support by a randomized
trial demonstrating that the administration of
imipenem reduced infectious complications, in-cluding
central-line sepsis, pulmonary infection,
urinary tract infection, and infected pancreatic ne-crosis.
37 Subsequent trials yielded mixed, but gen-erally
confirmatory, results.38 However, a recent
randomized trial failed to demonstrate differenc-es
in outcome among patients treated with ci p-rofloxacin
plus metronidazole, as compared with
placebo, leading some experts to recommend
against the routine use of prophylactic antibiot-ics.
39 Some centers use antifungal therapy as well
as antibacterial therapy, but this practice has not
been validated by randomized trials.
Nutritional Support
Ensuring adequate nutrition is important in pa-tients
with severe or complicated pancreatitis, but
the optimal means of doing so remains contro-versial.
40 Two small trials involving a total of 70
patients showed a nonsignificant reduction in ad-verse
outcomes with enteral feeding through na-soenteric
feeding tubes, as compared with total
parenteral nutrition.41 More recent meta-analy-ses
of six randomized trials involving a total of
263 patients demonstrated improved outcomes
with enteral nutrition,42,43 including decreased
rates of infection42,44 and surgical intervention,42
a reduced length of hospital stay,42 and reduced
costs (20 percent of the costs associated with to-tal
parenteral nutrition).43 Enteral feeding is usu-ally
well tolerated in patients with ileus.40 How-ever,
total parenteral nutrition may be necessary
for patients who cannot obtain sufficient calories
through enteral nutrition or in whom enteral ac-cess
cannot be maintained.45
Surgery
Surgical intervention is indicated in patients with
infected pancreatic necrosis. In most cases, the di-
7. The new england journal o f medicine
agnosis is confirmed by fine-needle aspiration be-fore
surgical intervention, but because false neg-ative
results can occur (reported sensitivity, 88
percent),46 surgery also warrants consideration
when there is a high index of suspicion of infected
necrosis even if infection is not documented.
Surgery within the first few days after the onset
of severe acute pancreatitis is associated with rates
of death up to 65 percent.47 Furthermore, there is
no clear demarcation between viable and nonviable
tissue early in the course of acute pancreatitis.47
Observational data support delaying surgical dé-bridement
of necrotic tissue for at least two weeks
if possible while the patient’s medical condition is
optimized and viable pancreatic tissue becomes
evident.47 This approach appears to improve sur-vival
and maximize organ preservation.47
Discharge Planning
Whenever possible, the cause of pancreatitis should
be determined and plans to prevent recurrence
should be devised before the patient is discharged
from the hospital. In patients with acute pancre-atitis
caused by gallstones, cholecystectomy should
be considered before discharge in those with mild
cases or within a few months in those with more
severe or complicated cases to allow inflamma-tory
processes or fluid collections to organize or
resolve.47 ERCP with sphincterotomy is an alter-native
in patients who are not surgical candidates
or in whom surgery must be delayed.47 If the cause
is hypertriglyceridemia, then dietary measures,
cessation of alcohol intake, weight reduction, and
possibly, treatment with the administration of gem-fibrozil
or fenofibrate should be initiated.48 The
identification of hypercalcemia requires attention
to the underlying cause, such as hyperparathyroid-ism
or cancer. Medications associated with acute
pancreatitis should be discontinued.49 Recurrent
pancreatitis — in the absence of biliary disease,
alcoholism, and toxic or metabolic causes — sug-gests
other causes, such as strictures, pancreas di-visum,
duct-obstructing masses, autoimmune pan-creatitis,
and genetic susceptibility.50 Systematic
approaches to idiopathic and recurrent acute pan-creatitis
have been reviewed elsewhere.50-52
Patients can be discharged when their pain is
controlled with oral analgesics and they are able
to eat and drink. Oral feeding can be started when
abdominal tenderness diminishes and the patient
becomes hungry. Clinical experience provides sup-port
for a recommendation that patients eat small,
low-fat meals of carbohydrates and proteins, with
a gradual increase in quantity over a period of
three to six days as tolerated.40 Patients who are
unable to eat because of persistent pain or gastric
compression from a pseudocyst have been suc-cessfully
treated as outpatients with nasoenteric
feeding tubes, surgical jejunal tubes, or total par-enteral
nutrition.
Areas of Uncertainty
Data from randomized trials are needed to identify
ways to improve the management of acute pan-creatitis,
including the optimization of nutrition-al
support and the prevention and treatment of in-fections
and other complications.
Guidelines
The prophylactic use of antibiotics in patients with
pancreatic necrosis is supported by the guidelines
of the International Association of Pancreatology
for the surgical management of acute pancreati-tis47
and the Japanese Society of Abdominal Emer-gency
Medicine53 but is discouraged by an expert
panel of the American Thoracic Society and other
organizations.15 No consensus was reached by the
United Kingdom Working Party on Acute Pancre-atitis.
17 The last three organizations15,17,53 favor
the use of enteral nutrition over total parenteral
nutrition in patients with severe acute pancreati-tis
whenever possible. Early intervention for gall-stone
pancreatitis with bile-duct obstruction with
the use of ERCP with endoscopic sphincterotomy
is consistently recommended.
Summary and Recommendations
In a patient presenting with acute pancreatitis,
such as the woman in the vignette, immediate con-siderations
include assessment of the severity and
cause of the condition. The patient in the vignette
has a Ranson’s score that indicates a high risk of
severe disease on the basis of her age, white-cell
count, and levels of lactate dehydrogenase and ala-nine
aminotransferase. She should be admitted to
the hospital, receive aggressive hydration, and be
closely monitored. Given her sex, age, absence of
alcohol intake, and alanine aminotransferase lev-els,
gallstones are the likely cause, and transab-dominal
or endoscopic ultrasonography should be
performed to look for stones or sludge in the gall-
2148 n engl j med 354;20 www.nejm.org may 18, 2006
8. clinical practice
bladder. If the findings on imaging or the clinical
presentation provide support for a biliary cause,
consultation or transfer to a facility with an expe-rienced
therapeutic endoscopist is warranted, since
emergency treatment with ERCP is useful in such
patients. Nasoenteric feedings are recommended
for most patients with severe pancreatitis; among
patients whose condition is stable, such feedings
should be started within two to three days after
presentation. Data and clinical guidelines con-flict
with respect to whether antibiotics are indi-cated
in severe acute pancreatitis. Pending more
data to inform this decision, the use of antibiotics
should be reserved for patients with necrosis of
more than 30 percent of the pancreas, since small
areas of necrosis seldom become infected; the
use of imipenem was associated with the preven-tion
of infectious complications in two random-ized
trials.37,54
Dr. Whitcomb reports having received consulting and lecture
fees from Solvay Pharmaceuticals. He reports being listed on a
patent for genetic testing for hereditary pancreatitis, which is
licensed to Ambry Genetics. No other potential conflict of inter-est
relevant to this article was reported.
I am indebted to Drs. Veronique Morinville, Kevin McGrath,
Georgios Papachristou, Scott Cooper, and Adam Slivka for their
critical review of the manuscript.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
n engl j med 354;20 www.nejm.org may 18, 2006 2149
References
DeFrances CJ, Hall MJ, Podgornik MN.
2003 National Hospital Discharge Survey.
Advance data from vital and health statis-tics.
No. 359. Hyattsville, Md.: National
Center for Health Statistics, 2005.
Lankisch PG, Lowenfels AB, Maison-neuve
P. What is the risk of alcoholic pan-creatitis
in heavy drinkers? Pancreas 2002;
25:411-2.
Venneman NG, Buskens E, Besselink
MG, et al. Small gallstones are associated
with increased risk of acute pancreatitis:
potential benefits of prophylactic chole-cystectomy?
Am J Gastroenterol 2005;100:
2540-50.
Chwistek M, Roberts I, Amoateng-
Adjepong Y. Gallstone pancreatitis: a com-munity
teaching hospital experience. J Clin
Gastroenterol 2001;33:41-4.
Levy P, Boruchowicz A, Hastier P, et
al. Diagnostic criteria in predicting a bili-ary
origin of acute pancreatitis in the era
of endoscopic ultrasound: multicentre pro-spective
evaluation of 213 patients. Pan-creatology
2005;5:450-6.
Drinking in the United States: main
findings from the 1992 National Longi-tudinal
Alcohol Epidemiologic Survey
(NLAES). Vol. 6. Bethesda, Md.: National
Institutes of Health, 1998. (NIH publica-tion
no. 99-3519.)
Whitcomb DC, Lowe ME. Pancreatitis:
acute and chronic. In: Walker WA, Goulet
O, Kleinman RE, Sherman PM, Shneider
BL, Sanderson IR, eds. Pediatric gastroin-testinal
disease: pathophysiology, diag-nosis,
management. 4th ed. Hamilton,
Ont., Canada: B.C. Decker, 2004:1584-97.
Whitcomb DC. Value of genetic test-ing
in management of pancreatitis. Gut
2004;53:1710-7.
McKay CJ, Imrie CW. The continuing
challenge of early mortality in acute pan-creatitis.
Br J Surg 2004;91:1243-4.
Neoptolemos JP, Kemppainen EA,
Mayer JM, et al. Early prediction of sever-ity
in acute pancreatitis by urinary tryp-sinogen
activation peptide: a multicentre
study. Lancet 2000;355:1955-60.
Kemppainen E, Hedstrom J, Puolak-
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
kainen P, et al. Increased serum trypsino-gen
2 and trypsin 2-alpha 1 antitrypsin
complex values identify endoscopic retro-grade
cholangiopancreatography induced
pancreatitis with high accuracy. Gut 1997;
41:690-5.
Tenner S, Dubner H, Steinberg W. Pre-dicting
gallstone pancreatitis with labora-tory
parameters: a meta-analysis. Am J
Gastroenterol 1994;89:1863-6.
Arvanitakis M, Delhaye M, De Maer-telaere
V, et al. Computed tomography and
magnetic resonance imaging in the as-sessment
of acute pancreatitis. Gastroen-terology
2004;126:715-23.
Romagnuolo J, Currie G. Noninvasive
vs. selective invasive biliary imaging for
acute biliary pancreatitis: an economic
evaluation by using decision tree analysis.
Gastrointest Endosc 2005;61:86-97.
Nathens AB, Curtis JR, Beale RJ, et al.
Management of the critically ill patient with
severe acute pancreatitis. Crit Care Med
2004;32:2524-36.
Ayub K, Imada R, Slavin J. Endoscop-ic
retrograde cholangiopancreatography
in gallstone-associated acute pancreati-tis.
Cochrane Database Syst Rev 2004;4:
CD003630.
Working Party of the British Society
of Gastroenterology, Association of Sur-geons
of Great Britain and Ireland, Pan-creatic
Society of Great Britain and Ire-land,
Association of Upper GI Surgeons of
Great Britain and Ireland. UK guidelines
for the management of acute pancreatitis.
Gut 2005;54:Suppl 3:iii1-iii9.
NIH state-of-the-science statement on
endoscopic retrograde cholangiopancrea-tography
(ERCP) for diagnosis and therapy.
NIH Consens State Sci Statements 2002;
19(1):1-26.
Johnson CD, Kingsnorth AN, Imrie
CW, et al. Double blind, randomised, pla-cebo
controlled study of a platelet activat-ing
factor antagonist, lexipafant, in the
treatment and prevention of organ failure
in predicted severe acute pancreatitis. Gut
2001;48:62-9.
Steinberg W, Schlesselman S. Treat-
12.
13.
14.
15.
16.
17.
18.
19.
20.
ment of acute pancreatitis: comparison of
animal and human studies. Gastroenter-ology
1987;93:1420-7.
Bradley EL III. A clinically based clas-sification
system for acute pancreatitis:
summary of the International Symposium
on Acute Pancreatitis, Atlanta, Ga., Sep-tember
11 through 13, 1992. Arch Surg
1993;128:586-90.
Ranson JH, Rifkind KM, Turner JW.
Prognostic signs and nonoperative perito-neal
lavage in acute pancreatitis. Surg
Gynecol Obstet 1976;143:209-19.
Balthazar EJ, Robinson DL, Megibow
AJ, Ranson JH. Acute pancreatitis: value
of CT in establishing prognosis. Radiolo-gy
1990;174:331-6.
Knaus WA, Draper EA, Wagner DP,
Zimmerman JE. APACHE II: a severity of
disease classification system. Crit Care
Med 1985;13:818-29.
Larvin M, McMahon MJ. APACHE-II
score for assessment and monitoring of
acute pancreatitis. Lancet 1989;2:201-5.
Blamey SL, Imrie CW, O’Neill J, Gil-more
WH, Carter DC. Prognostic factors in
acute pancreatitis. Gut 1984;25:1340-6.
Papachristou GI, Whitcomb DC. Pre-dictors
of severity and necrosis in acute
pancreatitis. Gastroenterol Clin North
Am 2004;33:871-90.
Ranson JH. Etiological and prognos-tic
factors in human acute pancreatitis:
a review. Am J Gastroenterol 1982;77:633-
8.
Martinez J, Sanchez-Paya J, Palazon
JM, Suazo-Barahona J, Robles-Diaz G,
Perez-Mateo M. Is obesity a risk factor in
acute pancreatitis? A meta-analysis. Pan-creatology
2004;4:42-8.
Baillargeon JD, Orav J, Ramagopal V,
Tenner SM, Banks PA. Hemoconcentra-tion
as an early risk factor for necrotizing
pancreatitis. Am J Gastroenterol 1998;93:
2130-4.
Papachristou GI, Sass DA, Avula H, et
al. Is the monocyte chemotactic protein-1
–2518 G allele a risk factor for severe
acute pancreatitis? Clin Gastroenterol
Hepatol 2005;3:475-81.