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.
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 discusses acute cholecystitis, which is inflammation of the gallbladder. It defines the condition and discusses its most common causes and risk factors. The main symptoms are abdominal pain in the right upper quadrant, nausea, vomiting, and fever. Diagnosis involves physical exam findings like Murphy's sign as well as imaging tests and bloodwork. Treatment involves intravenous fluids, antibiotics, and early cholecystectomy if symptoms worsen or complications arise. Both open and laparoscopic cholecystectomy are discussed as surgical treatment options.
This document discusses peritoneal tuberculosis and tuberculous mesenteric lymphadenitis. It provides details on the clinical presentation, pathology, types, investigations and treatment for each condition. Peritoneal tuberculosis typically presents with abdominal distension, obstruction, pain and weight loss. Chronic cases can lead to ascites or adhesions. Tuberculous lymphadenitis most commonly involves the right mesenteric lymph nodes and may cause obstruction, presenting like appendicitis. Investigations include imaging, fluid analysis and Mantoux testing. Both conditions are generally treated with anti-tubercular drugs, and sometimes surgery is needed for complications like obstruction.
This document provides an overview of pancreatic surgery and management of pancreatic conditions. It discusses the anatomy of the pancreas, classification and management of acute pancreatitis including necrotizing pancreatitis. It covers the indications, timing and approaches for intervention in infected pancreatic necrosis, including radiologic drainage, minimally invasive techniques like VARD and nephroscopic debridement, and open necrosectomy. It also summarizes the principles and techniques of surgical management of pancreatic cancer.
This document provides an overview of the management of obstructive jaundice. It begins with definitions and classifications of jaundice. Obstructive jaundice can be intrahepatic or extrahepatic in origin. Common causes of intrahepatic cholestasis include viral hepatitis, alcoholic hepatitis, and drug toxicity. Extrahepatic obstructions are often due to choledocholithiasis (gallstones in the common bile duct), tumors, or strictures. Diagnostic imaging includes ultrasound, MRCP, ERCP, and intraoperative cholangiography. Treatment depends on whether the obstruction is pre-operative or discovered during cholecystectomy, and may involve ERCP, laparoscopic or open CBD exploration, or
The document discusses acute cholangitis, including its pathogenesis, clinical manifestations, diagnostic criteria, severity assessment, imaging, and management. Regarding diagnostic criteria, it summarizes that Charcot's triad has low sensitivity for diagnosing acute cholangitis compared to the Tokyo Guidelines 2007 and 2013 criteria. It also notes that the Tokyo Guidelines 2007 criteria for severity assessment were insufficient and have been revised in subsequent guidelines to better distinguish mild from moderate cases in the initial diagnosis.
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 discusses acute cholecystitis, which is inflammation of the gallbladder. It defines the condition and discusses its most common causes and risk factors. The main symptoms are abdominal pain in the right upper quadrant, nausea, vomiting, and fever. Diagnosis involves physical exam findings like Murphy's sign as well as imaging tests and bloodwork. Treatment involves intravenous fluids, antibiotics, and early cholecystectomy if symptoms worsen or complications arise. Both open and laparoscopic cholecystectomy are discussed as surgical treatment options.
This document discusses peritoneal tuberculosis and tuberculous mesenteric lymphadenitis. It provides details on the clinical presentation, pathology, types, investigations and treatment for each condition. Peritoneal tuberculosis typically presents with abdominal distension, obstruction, pain and weight loss. Chronic cases can lead to ascites or adhesions. Tuberculous lymphadenitis most commonly involves the right mesenteric lymph nodes and may cause obstruction, presenting like appendicitis. Investigations include imaging, fluid analysis and Mantoux testing. Both conditions are generally treated with anti-tubercular drugs, and sometimes surgery is needed for complications like obstruction.
This document provides an overview of pancreatic surgery and management of pancreatic conditions. It discusses the anatomy of the pancreas, classification and management of acute pancreatitis including necrotizing pancreatitis. It covers the indications, timing and approaches for intervention in infected pancreatic necrosis, including radiologic drainage, minimally invasive techniques like VARD and nephroscopic debridement, and open necrosectomy. It also summarizes the principles and techniques of surgical management of pancreatic cancer.
This document provides an overview of the management of obstructive jaundice. It begins with definitions and classifications of jaundice. Obstructive jaundice can be intrahepatic or extrahepatic in origin. Common causes of intrahepatic cholestasis include viral hepatitis, alcoholic hepatitis, and drug toxicity. Extrahepatic obstructions are often due to choledocholithiasis (gallstones in the common bile duct), tumors, or strictures. Diagnostic imaging includes ultrasound, MRCP, ERCP, and intraoperative cholangiography. Treatment depends on whether the obstruction is pre-operative or discovered during cholecystectomy, and may involve ERCP, laparoscopic or open CBD exploration, or
The document discusses acute cholangitis, including its pathogenesis, clinical manifestations, diagnostic criteria, severity assessment, imaging, and management. Regarding diagnostic criteria, it summarizes that Charcot's triad has low sensitivity for diagnosing acute cholangitis compared to the Tokyo Guidelines 2007 and 2013 criteria. It also notes that the Tokyo Guidelines 2007 criteria for severity assessment were insufficient and have been revised in subsequent guidelines to better distinguish mild from moderate cases in the initial diagnosis.
Acute cholangitis is an infection of the bile ducts caused by obstruction and bacterial overgrowth. It presents with fever, jaundice, and right upper quadrant pain (Charcot's triad). Obstruction leads to increased pressure and bacterial growth in the bile ducts. Diagnosis involves blood tests, imaging like ultrasound or CT, and testing bile if drained. Treatment is antibiotics, hydration, and relieving obstruction endoscopically or surgically. Antibiotics are continued until obstruction is fully resolved to prevent recurrence.
Preparation of a patient of obstructive jaundice and periampullary carcinomaDr.Manojit Sarkar
This document discusses the preoperative preparation and management of a patient with obstructive jaundice. It notes that such patients are usually anemic so blood transfusions may be needed. It also discusses correcting dehydration, vitamin K deficiency, renal impairment, infection risk and malnutrition. The case involves a 60-year old male with jaundice, clay-colored stools and weight loss being evaluated for obstructive jaundice. On examination, a lump is palpated in the right upper abdomen. Further sections discuss periampullary anatomy and carcinomas, investigations including blood tests, imaging and biopsies, and treatment options like Whipple procedure or palliative surgeries.
This document discusses jaundice and diseases of the biliary tract. It covers the anatomy and physiology of the biliary system, pathophysiology of jaundice, etiologies including gallstones and cancer, clinical features such as itching and pale stools, diagnostic tests like liver enzymes and imaging, and treatment modalities for various biliary diseases. Key topics include cholecystitis, cholangitis, choledocholithiasis, biliary atresia, choledochal cysts, and hepatobiliary cancers.
Hepatic Encephalopathy -Pathophysiology,Evaluation And ManagementSantosh Narayankar
Hepatic encephalopathy is a brain dysfunction caused by liver disease or portosystemic shunting. It presents as a wide range of neurological or psychiatric abnormalities from mild alterations to coma. The prevalence is 30-40% in those with cirrhosis and risk of first episode is 5-25% within 5 years of cirrhosis diagnosis. Recurrence risk after an initial episode is 40% within 1 year. Ammonia, systemic inflammation, manganese, genetics, and oxidative stress may all contribute to pathogenesis. Diagnosis involves clinical exam and testing like serum ammonia levels or neuropsychological tests on phone apps. Management involves treating precipitating factors, lactulose, antibiotics like rifaximin, and
The document discusses acute epigastric pain, dividing it into causes such as acute gastritis, exacerbation of duodenal ulcer, biliary colic, acute cholecystitis, and acute pancreatitis. For each cause, it describes the typical history, examination findings, diagnostic tests, and treatment approach. For example, it notes that acute gastritis is often caused by H. pylori or NSAIDs, while acute cholecystitis presents with right upper quadrant tenderness and Murphy's sign on examination. Ultrasound is useful for gallstones, while lipase checks for pancreatitis. Treatment focuses on conservative measures, though cholecystectomy may be considered for cholecystitis.
1. Abdominal tuberculosis refers to tuberculosis infection of the gastrointestinal tract, mesenteric lymph nodes, peritoneum, and organs like the liver and spleen.
2. It is commonly caused by Mycobacterium tuberculosis or M. bovis bacteria and spreads via ingestion, hematogenous spread, or lymphatic spread.
3. Common presentations include abdominal pain, fever, weight loss, and the formation of masses, strictures, or ascites in the abdomen. Investigations include imaging tests, blood tests, and microbiological analysis of samples.
Chronic pancreatitis is a progressive inflammatory condition of the pancreas characterized by irreversible morphological changes and loss of function. It is most commonly caused by long term heavy alcohol use. Symptoms include recurrent abdominal pain, steatorrhea due to exocrine insufficiency, and diabetes mellitus due to endocrine insufficiency. Diagnosis involves functional tests like fecal elastase and imaging modalities like CT, MRI, ERCP and EUS which demonstrate findings of pancreatic duct abnormalities, parenchymal changes and calcifications.
Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe. Mild cases involve pancreatic edema while severe cases involve pancreatic necrosis and multi-organ failure. The main causes are gallstones and alcohol use. Diagnosis is based on abdominal pain and elevated pancreatic enzymes. Severity is assessed using criteria like Ranson score, CT severity index, and Atlanta criteria. Treatment of mild cases involves fluids and pain control while severe cases require intensive care monitoring, fluids, nutrition, and may involve ERCP or surgery for complications.
1. Abdominal pain is a common presenting symptom that can be caused by many intra-abdominal and extra-abdominal processes.
2. A thorough history and physical exam is important to help determine the cause, including assessing location, character, and timing of pain.
3. Differential diagnosis depends on factors like location of pain and patient characteristics, and may include conditions like appendicitis, cholecystitis, pancreatitis, or diverticulitis. Laboratory tests, imaging, and other evaluations can help make the diagnosis.
1. Acute appendicitis is caused by obstruction of the appendix lumen, leading to increased intraluminal pressure, edema, and bacterial invasion.
2. The classic presentation includes initially vague periumbilical pain that later localizes to the right lower quadrant, accompanied by anorexia, nausea, and low-grade fever.
3. On examination, tenderness is elicited over McBurney's point with guarding and rebound tenderness. Diagnosis is suggested by clinical scoring systems and confirmed by ultrasound or CT scan showing a thick-walled, inflamed appendix.
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.
This document discusses peritonitis and intra-abdominal abscesses. It begins with an anatomy section describing the peritoneum. Peritonitis is defined as inflammation of the peritoneum caused by microorganisms, chemicals, irradiation or foreign bodies. The pathophysiology involves an influx of fluid and immune cells into the peritoneal cavity in response to injury or infection. Management involves treating both the infection source and with antibiotics. Localized peritonitis can occur when anatomical or pathological factors limit the spread of infection.
1) Acute pancreatitis is defined as an acute inflammatory process of the pancreas with variable involvement of other tissues. It is diagnosed when a patient presents with abdominal pain consistent with the disease as well as serum amylase or lipase levels over three times the upper limit of normal.
2) Common causes of acute pancreatitis include gallstones, alcohol use, hypertriglyceridemia, endoscopic retrograde cholangiopancreatography (ERCP), trauma, postoperative complications, and certain drugs.
3) Management involves adequate hydration, analgesia, monitoring for organ failure, cautious administration of fluids and insulin, and consideration of endoscopic procedures or surgery in severe cases with complications like necrosis
1. A 60-year-old male presented with yellowish discoloration of the eye, itching all over the body, pale stools, loss of appetite, and weight loss.
2. Obstructive jaundice and periampullary carcinoma were suspected given his age, painless progressive jaundice, pruritis, pale stools, and weight loss.
3. Key clinical features of obstructive jaundice include jaundice, intense pruritis, pale stools, loss of appetite and weight in patients typically aged 50-70 years.
Acute calculous cholecystitis is caused by obstruction of the cystic duct by a gallstone. Symptoms include biliary colic, fever, and right upper quadrant pain. Ultrasound and hepatobiliary scintigraphy can diagnose thickened gallbladder walls and obstruction. Treatment involves early laparoscopic cholecystectomy for mild cases, or initial conservative treatment with antibiotics and potential percutaneous cholecystostomy for severe cases presenting with sepsis, with delayed cholecystectomy once the patient improves. Guidelines recommend early surgery for mild disease and initial medical management for severe acute cholecystitis.
Intestinal obstruction occurs when the normal passage of intestinal contents is blocked. It can involve the small intestine, large intestine, or both. Obstructions are classified as mechanical, which involve a physical blockage, or dynamic/adynamic, which involve ineffective motility without a blockage. Common causes include adhesions, hernias, tumors, and volvulus. Symptoms vary based on the location and severity of the obstruction but often include colicky abdominal pain, vomiting, distention, and constipation. Diagnosis involves physical exam findings like distention and hyperperistalsis as well as imaging tests showing gas/fluid levels and other signs of obstruction.
This document provides an overview of chronic pancreatitis, including its definition, epidemiology, pathology, classification, clinical features, diagnosis and treatment. Chronic pancreatitis is defined as permanent and irreversible damage to the pancreas resulting in inflammation, fibrosis and destruction of pancreatic tissue. It has an annual incidence of 3-9 cases per 100,000 people. Alcohol is a major risk factor. Diagnosis involves evaluating pancreatic function and structure through imaging, endoscopy and genetic/serological testing. Treatment focuses on pain management, pancreatic enzyme supplementation and surgery for severe cases.
Acute Pancreatitis (According to American College of Gastroenterology 2013 gu...Jibran Mohsin
This Presentation focuses on definition, new classification, different scoring systems for severity, rationale for radiological signs and new management recommendations as per 2013 American College of Gastroenterology guidelines
This document summarizes acute pancreatitis, including its definition, causes, symptoms, pathogenesis, complications, diagnostic tests, severity scoring systems, and management. Acute pancreatitis is characterized by inflammation of the pancreas and is most commonly caused by gallstones or alcoholism. It presents with severe epigastric pain and other gastrointestinal symptoms. The pathogenesis involves premature activation of digestive enzymes within the pancreas that can lead to autodigestion. Complications include pseudocysts, abscesses, necrosis, and systemic complications like shock. Diagnosis involves blood tests showing elevated pancreatic enzymes and imaging tests. Severity is assessed using scoring systems like Ranson criteria, APACHE II, and CT severity index. Treatment focuses on fluid
Acute cholangitis is an infection of the bile ducts caused by obstruction and bacterial overgrowth. It presents with fever, jaundice, and right upper quadrant pain (Charcot's triad). Obstruction leads to increased pressure and bacterial growth in the bile ducts. Diagnosis involves blood tests, imaging like ultrasound or CT, and testing bile if drained. Treatment is antibiotics, hydration, and relieving obstruction endoscopically or surgically. Antibiotics are continued until obstruction is fully resolved to prevent recurrence.
Preparation of a patient of obstructive jaundice and periampullary carcinomaDr.Manojit Sarkar
This document discusses the preoperative preparation and management of a patient with obstructive jaundice. It notes that such patients are usually anemic so blood transfusions may be needed. It also discusses correcting dehydration, vitamin K deficiency, renal impairment, infection risk and malnutrition. The case involves a 60-year old male with jaundice, clay-colored stools and weight loss being evaluated for obstructive jaundice. On examination, a lump is palpated in the right upper abdomen. Further sections discuss periampullary anatomy and carcinomas, investigations including blood tests, imaging and biopsies, and treatment options like Whipple procedure or palliative surgeries.
This document discusses jaundice and diseases of the biliary tract. It covers the anatomy and physiology of the biliary system, pathophysiology of jaundice, etiologies including gallstones and cancer, clinical features such as itching and pale stools, diagnostic tests like liver enzymes and imaging, and treatment modalities for various biliary diseases. Key topics include cholecystitis, cholangitis, choledocholithiasis, biliary atresia, choledochal cysts, and hepatobiliary cancers.
Hepatic Encephalopathy -Pathophysiology,Evaluation And ManagementSantosh Narayankar
Hepatic encephalopathy is a brain dysfunction caused by liver disease or portosystemic shunting. It presents as a wide range of neurological or psychiatric abnormalities from mild alterations to coma. The prevalence is 30-40% in those with cirrhosis and risk of first episode is 5-25% within 5 years of cirrhosis diagnosis. Recurrence risk after an initial episode is 40% within 1 year. Ammonia, systemic inflammation, manganese, genetics, and oxidative stress may all contribute to pathogenesis. Diagnosis involves clinical exam and testing like serum ammonia levels or neuropsychological tests on phone apps. Management involves treating precipitating factors, lactulose, antibiotics like rifaximin, and
The document discusses acute epigastric pain, dividing it into causes such as acute gastritis, exacerbation of duodenal ulcer, biliary colic, acute cholecystitis, and acute pancreatitis. For each cause, it describes the typical history, examination findings, diagnostic tests, and treatment approach. For example, it notes that acute gastritis is often caused by H. pylori or NSAIDs, while acute cholecystitis presents with right upper quadrant tenderness and Murphy's sign on examination. Ultrasound is useful for gallstones, while lipase checks for pancreatitis. Treatment focuses on conservative measures, though cholecystectomy may be considered for cholecystitis.
1. Abdominal tuberculosis refers to tuberculosis infection of the gastrointestinal tract, mesenteric lymph nodes, peritoneum, and organs like the liver and spleen.
2. It is commonly caused by Mycobacterium tuberculosis or M. bovis bacteria and spreads via ingestion, hematogenous spread, or lymphatic spread.
3. Common presentations include abdominal pain, fever, weight loss, and the formation of masses, strictures, or ascites in the abdomen. Investigations include imaging tests, blood tests, and microbiological analysis of samples.
Chronic pancreatitis is a progressive inflammatory condition of the pancreas characterized by irreversible morphological changes and loss of function. It is most commonly caused by long term heavy alcohol use. Symptoms include recurrent abdominal pain, steatorrhea due to exocrine insufficiency, and diabetes mellitus due to endocrine insufficiency. Diagnosis involves functional tests like fecal elastase and imaging modalities like CT, MRI, ERCP and EUS which demonstrate findings of pancreatic duct abnormalities, parenchymal changes and calcifications.
Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe. Mild cases involve pancreatic edema while severe cases involve pancreatic necrosis and multi-organ failure. The main causes are gallstones and alcohol use. Diagnosis is based on abdominal pain and elevated pancreatic enzymes. Severity is assessed using criteria like Ranson score, CT severity index, and Atlanta criteria. Treatment of mild cases involves fluids and pain control while severe cases require intensive care monitoring, fluids, nutrition, and may involve ERCP or surgery for complications.
1. Abdominal pain is a common presenting symptom that can be caused by many intra-abdominal and extra-abdominal processes.
2. A thorough history and physical exam is important to help determine the cause, including assessing location, character, and timing of pain.
3. Differential diagnosis depends on factors like location of pain and patient characteristics, and may include conditions like appendicitis, cholecystitis, pancreatitis, or diverticulitis. Laboratory tests, imaging, and other evaluations can help make the diagnosis.
1. Acute appendicitis is caused by obstruction of the appendix lumen, leading to increased intraluminal pressure, edema, and bacterial invasion.
2. The classic presentation includes initially vague periumbilical pain that later localizes to the right lower quadrant, accompanied by anorexia, nausea, and low-grade fever.
3. On examination, tenderness is elicited over McBurney's point with guarding and rebound tenderness. Diagnosis is suggested by clinical scoring systems and confirmed by ultrasound or CT scan showing a thick-walled, inflamed appendix.
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.
This document discusses peritonitis and intra-abdominal abscesses. It begins with an anatomy section describing the peritoneum. Peritonitis is defined as inflammation of the peritoneum caused by microorganisms, chemicals, irradiation or foreign bodies. The pathophysiology involves an influx of fluid and immune cells into the peritoneal cavity in response to injury or infection. Management involves treating both the infection source and with antibiotics. Localized peritonitis can occur when anatomical or pathological factors limit the spread of infection.
1) Acute pancreatitis is defined as an acute inflammatory process of the pancreas with variable involvement of other tissues. It is diagnosed when a patient presents with abdominal pain consistent with the disease as well as serum amylase or lipase levels over three times the upper limit of normal.
2) Common causes of acute pancreatitis include gallstones, alcohol use, hypertriglyceridemia, endoscopic retrograde cholangiopancreatography (ERCP), trauma, postoperative complications, and certain drugs.
3) Management involves adequate hydration, analgesia, monitoring for organ failure, cautious administration of fluids and insulin, and consideration of endoscopic procedures or surgery in severe cases with complications like necrosis
1. A 60-year-old male presented with yellowish discoloration of the eye, itching all over the body, pale stools, loss of appetite, and weight loss.
2. Obstructive jaundice and periampullary carcinoma were suspected given his age, painless progressive jaundice, pruritis, pale stools, and weight loss.
3. Key clinical features of obstructive jaundice include jaundice, intense pruritis, pale stools, loss of appetite and weight in patients typically aged 50-70 years.
Acute calculous cholecystitis is caused by obstruction of the cystic duct by a gallstone. Symptoms include biliary colic, fever, and right upper quadrant pain. Ultrasound and hepatobiliary scintigraphy can diagnose thickened gallbladder walls and obstruction. Treatment involves early laparoscopic cholecystectomy for mild cases, or initial conservative treatment with antibiotics and potential percutaneous cholecystostomy for severe cases presenting with sepsis, with delayed cholecystectomy once the patient improves. Guidelines recommend early surgery for mild disease and initial medical management for severe acute cholecystitis.
Intestinal obstruction occurs when the normal passage of intestinal contents is blocked. It can involve the small intestine, large intestine, or both. Obstructions are classified as mechanical, which involve a physical blockage, or dynamic/adynamic, which involve ineffective motility without a blockage. Common causes include adhesions, hernias, tumors, and volvulus. Symptoms vary based on the location and severity of the obstruction but often include colicky abdominal pain, vomiting, distention, and constipation. Diagnosis involves physical exam findings like distention and hyperperistalsis as well as imaging tests showing gas/fluid levels and other signs of obstruction.
This document provides an overview of chronic pancreatitis, including its definition, epidemiology, pathology, classification, clinical features, diagnosis and treatment. Chronic pancreatitis is defined as permanent and irreversible damage to the pancreas resulting in inflammation, fibrosis and destruction of pancreatic tissue. It has an annual incidence of 3-9 cases per 100,000 people. Alcohol is a major risk factor. Diagnosis involves evaluating pancreatic function and structure through imaging, endoscopy and genetic/serological testing. Treatment focuses on pain management, pancreatic enzyme supplementation and surgery for severe cases.
Acute Pancreatitis (According to American College of Gastroenterology 2013 gu...Jibran Mohsin
This Presentation focuses on definition, new classification, different scoring systems for severity, rationale for radiological signs and new management recommendations as per 2013 American College of Gastroenterology guidelines
This document summarizes acute pancreatitis, including its definition, causes, symptoms, pathogenesis, complications, diagnostic tests, severity scoring systems, and management. Acute pancreatitis is characterized by inflammation of the pancreas and is most commonly caused by gallstones or alcoholism. It presents with severe epigastric pain and other gastrointestinal symptoms. The pathogenesis involves premature activation of digestive enzymes within the pancreas that can lead to autodigestion. Complications include pseudocysts, abscesses, necrosis, and systemic complications like shock. Diagnosis involves blood tests showing elevated pancreatic enzymes and imaging tests. Severity is assessed using scoring systems like Ranson criteria, APACHE II, and CT severity index. Treatment focuses on fluid
This document summarizes acute and chronic pancreatitis. It covers the anatomy and physiology of the pancreas, pathophysiology, causes, symptoms, signs, diagnostic testing including labs and imaging, medical and surgical treatment options, and prognosis. The main causes of acute pancreatitis are biliary disease and alcohol use, while chronic pancreatitis is primarily caused by alcohol use long-term. Complications can include pseudocysts, abscesses, pancreatic necrosis, and pancreatic duct disruption. Treatment depends on the severity and includes pain control, antibiotics, nutritional support, enzyme replacement, and possible surgery.
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.
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 pancreatitis, including its anatomy, physiology, classification, signs and symptoms, diagnosis, and management. It addresses both acute and chronic pancreatitis. Acute pancreatitis is commonly caused by gallstones or alcohol and can be mild, moderately severe, or severe based on organ dysfunction. It presents with abdominal pain and elevated pancreatic enzymes. Chronic pancreatitis is usually due to alcohol abuse and causes pain, digestive issues, and diabetes over time. Management involves treating the underlying cause, supportive care, and surgery for complications.
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.
Acute pancreatitis is inflammation of the pancreas that results from premature activation of pancreatic enzymes. It commonly presents with severe upper abdominal pain requiring hospital admission. The pathophysiology involves release of enzymes that damage pancreatic and surrounding tissues through increased capillary permeability, cell membrane destruction, and fat necrosis. Treatment focuses on fluid management, nutritional support, pain control, and supporting other organ systems to prevent complications like respiratory failure and multi-organ dysfunction.
1. Acute pancreatitis is inflammation of the pancreas that can range from mild to severe. It is most often caused by gallstones or excessive alcohol use.
2. Diagnosis is supported by laboratory tests showing elevated pancreatic enzymes in blood and urine, along with abdominal imaging showing swelling or inflammation of the pancreas.
3. The clinical course and severity can be predicted using scoring systems like Ranson's criteria that evaluate markers of organ failure over the first 48 hours. Early identification of severe cases allows for more aggressive management to reduce mortality risk.
1. The pancreas is an elongated organ located in the abdominal cavity behind the stomach. It has three parts - head, body, and tail.
2. The pancreas has both exocrine and endocrine functions. Exocrine functions include producing pancreatic juice containing enzymes that digest carbohydrates, proteins, and fats. Endocrine functions include production of insulin, glucagon, and somatostatin by islets of Langerhans cells.
3. Pancreatitis is inflammation of the pancreas that can be acute or chronic. Acute pancreatitis symptoms include severe abdominal pain and its causes include gallstones and alcohol use. Chronic pancreatitis involves long-term inflammation that destroys the pancreas over
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.
This document discusses acute pancreatitis, including its anatomy, etiology, diagnosis, assessment of severity, treatment, complications, and management guidelines. It covers the key roles of the pancreas in enzyme and electrolyte secretion. Common causes of pancreatitis like gallstones and alcohol are described. Diagnosis involves serum markers, imaging, and severity scores. Treatment focuses on hydration, nutrition, and managing complications. Local complications like pseudocysts and necrosis are defined and approaches to their management are provided. Surgical debridement indications and timing are outlined.
The pancreas is a 15-20cm long organ located in the retroperitoneum. It has a head, body, and tail. The pancreas contains exocrine tissue that produces enzymes to aid digestion and endocrine tissue clustered in islets of Langerhans that produce hormones like insulin and glucagon. The pancreas develops from dorsal and ventral buds that fuse during embryogenesis. It receives blood supply from various arteries and drains into veins like the portal vein. The pancreas secretes enzymes and bicarbonate to digest nutrients in the small intestine. Removal of the pancreas results in diabetes and digestive issues due to lack of enzymes.
Pancreatitis is an inflammation of the pancreas that can be acute or chronic. Acute pancreatitis is often caused by gallstones blocking the pancreatic duct or heavy alcohol use, while chronic pancreatitis results from repeated acute attacks or long-term alcohol abuse. Symptoms include abdominal pain radiating to the back, tender swollen abdomen, fever, nausea, and increased heart rate. Blood tests measuring amylase and lipase levels indicate pancreatitis. Treatment focuses on pain management, intravenous fluids, dietary changes like a low-fat diet, and potentially surgery to drain fluid or remove diseased tissue. Maintaining a healthy diet and lifestyle through modifications can help manage and prevent pancreatitis.
This document outlines various local, regional, and systemic complications that can arise from acute pancreatitis. Local complications include fluid collections, pancreatic pseudocysts, necrosis, abscesses, and hemorrhage. Regional complications involve neighboring organs through thrombosis, ileus, obstruction, or ischemia. Systemic complications consist of inflammatory response syndrome, multiple organ dysfunction, respiratory or renal failure, and disseminated coagulopathy. Management depends on the specific complication but may involve drainage, debridement, resection, or supportive care.
This document provides information on ischemia, necrosis, and their causes and types. It defines ischemia as insufficient blood supply causing oxygen and nutrient shortage. Causes include embolism, thrombosis, and aneurysm. Signs include tissue damage within minutes in highly aerobic tissues. Types are discussed like cardiac and limb ischemia. Necrosis is defined as cell death from loss of membrane integrity. Causes include anoxia, ischemia, chemicals and infections. Changes include cytoplasmic and nuclear changes. Necrotic cells may persist or be digested. Types discussed are coagulative, liquefactive, and caseous necrosis.
This document discusses various gastrointestinal conditions including dysphagia, hiccups, esophageal rupture, pneumomediastinum, esophageal foreign bodies, food impaction, caustic ingestions, peptic ulcer disease, bilirubin, and hepatitis. It provides details on symptoms, diagnostic findings, treatment options, and complications for each condition. Key diagnostic tests mentioned include esophagram, endoscopy, and motility studies for dysphagia and chest x-ray for esophageal rupture or foreign bodies. Treatment depends on the specific condition but may include antibiotics, acid suppressants, anti-ulcer medications, endoscopy, or surgery.
This document discusses nutritional support in acute pancreatitis. It begins by assessing the severity of acute pancreatitis using the Ranson criteria and CT severity index. It then discusses the impact of adequate nutritional support on clinical outcomes and the benefits and risks of enteral versus parenteral nutrition. It recommends enteral nutrition over parenteral nutrition when possible, starting with a jejunal tube and peptide-based formula. For severe acute pancreatitis requiring mechanical ventilation, it suggests decreasing or stopping enteral nutrition and starting parenteral nutrition instead.
Capurso G. Le Pancreatiti Acute: quelle vere e quelle false. ASMaD 2014Gianfranco Tammaro
1. The document discusses the management of acute pancreatitis, noting that contrast-enhanced CT or MRI should be reserved for unclear diagnoses or patients who do not improve clinically within 48-72 hours of admission.
2. Early fluid resuscitation, with 2 ml/kg/hour and an initial bolus of 20 ml/kg within 30-45 minutes is recommended, preferably with crystalloids like lactated Ringer's solution.
3. For mild pancreatitis, early oral feeding is recommended once pain resolves, while for severe cases enteral nutrition within 48 hours is recommended to prevent infectious complications.
Este documento describe la pancreatitis aguda. Define la pancreatitis aguda como una enfermedad inflamatoria del páncreas causada por la activación y autodigestión del páncreas por sus propias enzimas. Explica los principales factores etiológicos, la patofisiología, la clasificación de la severidad, los síntomas clínicos, los índices de severidad, el diagnóstico y el tratamiento inicial para la pancreatitis aguda.
Acute pancreatitis anatomy pathogenesis and management Suhas G
The document provides information on acute pancreatitis including its anatomy, definition, etiology, pathogenesis, clinical presentation, diagnosis, classification of severity, management, and intervention. Some key points:
- The pancreas has a head, body, and tail and receives its blood supply primarily from the splenic artery and splenic vein.
- Acute pancreatitis is defined as abdominal pain with elevated pancreatic enzymes and may be associated with acute swelling and inflammation of the pancreas.
- Etiologies include systemic infections, trauma, anomalies of pancreaticobiliary ducts, drugs, metabolic abnormalities, and idiopathic causes.
- Management involves fluid resuscitation, pain relief, prevention of infection typically
Pancreatitis is an inflammation of the pancreas that can be acute or chronic. Acute pancreatitis involves reversible injury to the pancreas and can range from mild to severe, with severe cases involving organ failure. Chronic pancreatitis is characterized by irreversible damage to the pancreas that typically causes pain and loss of pancreatic function over time. Treatment for acute pancreatitis depends on severity and may involve hospitalization, IV fluids, monitoring for organ failure, and antibiotics for severe cases. Treatment for chronic pancreatitis focuses on pain management, treating complications, and sometimes surgical interventions.
1. The pancreas is a retroperitoneal organ that produces enzymes to aid digestion and hormones like insulin and glucagon.
2. Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe, with the most common causes being gallstones and alcohol abuse.
3. Management of acute pancreatitis involves fluid resuscitation, pain control, predicting severity based on criteria like Ranson's or CT severity index, treating any organ failure, and considering ERCP if cholangitis or gallstones are present.
The document provides an overview of pancreatitis, including:
- The pancreas is a retroperitoneal glandular organ involved in digestion and hormone production. Pancreatitis is inflammation of the pancreas.
- Acute pancreatitis is defined as abdominal pain associated with elevated pancreatic enzymes due to pancreatic inflammation, and may recur.
- The annual incidence of acute pancreatitis ranges from 5 to 50 per 100,000 people worldwide, with higher rates in young men and older women.
- Causes include biliary tract diseases, alcohol, certain viral infections, drugs, scorpion bites, hyperlipidemia, and hyperparathyroidism. Trauma and idiopathic cases also occur
Acute pancreatitis is defined clinically by abdominal pain consistent with pancreatitis along with elevated serum amylase or lipase levels and imaging findings. It has an incidence of 4.9 to 73.4 per 100,000 patients in the US. The natural history involves an initial inflammatory phase lasting about a week followed by potential complications like pancreatic necrosis in 20% of patients. The pathogenesis involves inappropriate activation of digestive enzymes within the pancreas. Common causes include gallstones, alcohol use, hypertriglyceridemia, and post-ERCP. Diagnosis relies on abdominal pain and at least a 3-fold elevation of serum amylase or lipase.
Abnormal abdominal CT is best powerpoint presentation for radiologist, radiology resident and gastroenterologist, this include pancreatitis, all abdominal trauma grading with systemic manner. Thanks
The document describes the pancreas, pancreatitis, and pancreatic tumors. It discusses the anatomy and function of the pancreas, including that it produces digestive enzymes and hormones. Pancreatitis can be acute or chronic and is defined as inflammation of the pancreas. Acute pancreatitis causes severe abdominal pain and its severity ranges from mild to severe based on organ dysfunction. Chronic pancreatitis is progressive destruction of the pancreas due to recurrent inflammation, causing severe pain and pancreatic insufficiency over time. The document also outlines evaluation and management of pancreatic disorders.
This document summarizes a presentation on acute pancreatitis. It begins with an overview of the anatomy of the pancreas and then discusses the etiology, pathophysiology, clinical approach, differential diagnosis, investigations, assessment of severity, management, and complications of acute pancreatitis. The two most common causes are gallstones and alcohol abuse. Clinically, it presents with abdominal pain and elevated pancreatic enzymes. Investigations include blood tests and imaging like ultrasound, CT, and MRI. Management involves treating the underlying cause, pain control, and monitoring for local complications like pseudocysts or systemic complications like respiratory failure.
Pancreatitis is an inflammatory condition of the pancreas. Two major forms : acute pancreatitis (is reversible) and chronic pancreatitis(is irreversible).
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 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.
This document discusses acute pancreatitis, including:
- It is a common disease causing significant morbidity and mortality, with over 250,000 US hospital admissions per year and 3,000 deaths.
- The most common causes are gallstone obstruction and alcohol abuse.
- Symptoms include severe abdominal pain, nausea, vomiting, and tenderness. Diagnosis involves blood tests showing elevated lipase, amylase, and imaging studies like CT or MRI.
- Risk stratification systems like Ranson's criteria and the Atlanta classification are used to determine severity and risk of complications like organ failure. Early goal-directed fluid resuscitation is important for severe cases while avoiding excessive fluids.
chronic panreatitis surgery presentationsrujankatta
This document provides an overview of chronic pancreatitis, including:
- It defines chronic pancreatitis as an ongoing inflammatory and fibrosing disorder of the pancreas characterized by irreversible damage and loss of function.
- Risk factors include alcohol use, genetics, anatomical abnormalities. It classifies risk factors using the TIGAR-O system.
- Signs and symptoms involve pain, diabetes, maldigestion from exocrine insufficiency.
- Diagnosis involves blood tests, imaging like CT, MRI, ERCP. Management focuses on pain control, enzyme replacement, endoscopic or surgical interventions for complications.
- Surgical options include drainage procedures or resections for refractory pain or disease complications.
- Acute pancreatitis has varying levels of severity from mild to severe cases with high mortality. Nonoperative management is the mainstay involving fluid resuscitation, nutritional support, symptomatic treatment, and monitoring for complications.
- In severe cases, aggressive fluid resuscitation is important to prevent shock while enteral nutrition via nasogastric or nasojejunal tubes is preferred over total parenteral nutrition or prolonged nil per os.
- ERCP is indicated for cholangitis or significant biliary obstruction but not for mild biliary pancreatitis without obstruction. Infected necrosis is best drained after 4 weeks to allow development of fibrous walls.
This document provides an overview of acute pancreatitis including its anatomy, etiology, pathophysiology, diagnosis, severity assessment, treatment, and complications. Some key points:
- The pancreas is located in the retroperitoneum and has a head, neck, body and tail supplied by various arteries and veins.
- Acute pancreatitis is defined as inflammation of the pancreas with abdominal pain and elevated pancreatic enzymes. Common causes include gallstones, alcohol use, and hyperlipidemia.
- Inflammation occurs when pancreatic enzymes prematurely activate within the pancreas, causing injury. Systemic complications can develop depending on severity.
- Diagnosis involves history, exam, and lab tests
This topic is very important for an MBBS Students as it is one of the common cases a Medical Officer will come across during their Surgical Postings. Moreover it is always a Debate in treating the patient either an Physician or a Surgeon...Always it is one of the Devastating conditions of abdomen...
Acute pancreatitis is acute inflammation of the pancreas that commonly causes abdominal pain and hospitalization. It has two phases - early and late. The early phase lasts 2 weeks and severity is defined by clinical parameters like organ failure. Most patients experience systemic inflammatory response syndrome. Organ failure in more than one organ system is considered multiorgan failure. In the late phase, imaging can identify complications like necrotizing pancreatitis which prolongs hospital stay. Acute pancreatitis is classified as interstitial edema or necrotizing based on imaging and as mild, moderate or severe based on presence and duration of organ failure.
This document provides an overview of acute pancreatitis, including:
- The epidemiology, with highest rates in the US and among males related to alcohol use.
- The pathophysiology, involving premature activation of digestive enzymes within the pancreas.
- Diagnosis is based on abdominal pain plus elevated pancreatic enzymes or imaging findings. Severity is assessed using scores like Ranson's criteria or CT severity index.
- Treatment involves fluid resuscitation, nutritional support, pain management, and antibiotics only for proven or suspected infected pancreatic necrosis. The goals are to prevent complications and infections.
1. The document discusses acute pancreatitis, including its causes, pathogenesis, clinical presentation, imaging findings, and lab investigations. It describes the three phases of pathogenesis involving trypsin activation, leukocyte infiltration, and effects on distant organs.
2. Common causes include gallstones, alcohol, hypertriglyceridemia, while complications can be local like pseudocysts or systemic like metabolic and pulmonary issues.
3. Imaging like CT and MRI are used to identify necrosis and collections, while lab tests show elevated lipase and amylase with other markers of organ dysfunction indicating severity.
This document discusses ways to improve patient satisfaction by putting the patient first. It emphasizes that patients are customers and the purpose of healthcare work is to serve them. It outlines factors related to doctors, patients, and the organization that can influence satisfaction. Doctors are advised to communicate effectively, respect patients, and address complaints. Hospitals should aim to minimize wait times, obtain feedback, and maintain a service-oriented culture. The document concludes that delivering patient-centered care and continually improving quality are important for satisfaction.
The presence of haematuria may be the sole symptom of an underlying disease, either benign or malignant. It is one of the most common presentations of patients with urinary tract diseases and of patients referred for urinary imaging. Painless visible haematuria (VH) is the commonest presentation of bladder cancer.
CBDSs are one of the medical conditions leading to surgical intervention. They may occur in 3%–14.7% of all patients for whom cholecystectomies are preformed. When patients present with CBD, the one important question that should be answered: what is the best modality of treatment under the giving conditions? There are competing technologies and approaches for diagnosing CBDS with regard to diagnostic performance characteristics, technical success, safety, and cost effectiveness. Management of CBDS usually requires two separate teams: the gastroenterologist and the surgical team. One of the main factors in the management is initially the detection of CBDS, before, during, or after cholecystectomy. The main options for treatment are pre- or postoperative ERCP with endoscopic biliary sphincterotomy (EST), laparoscopic or open surgical bile duct clearance. There are other options for the treat- ment of CBDS such as electrohydraulic lithotripsy (EHL), extracorporeal shockwave lithotripsy (ESWL), dissolving solutions, and laser lithotripsy. It is unlikely that one option
will be appropriate for all clinical circumstances in all centers. Variables such as disease status, patient demographics, availability of endoscopic, radiological and surgical expertise, and healthcare economics will all have significant influence on practice
The incidence of biliary injury after laparoscopic cholecystectomy (LC) has shown a declining trend though it may still be twice that as with open cholecystectomy. Major biliary or vasculobiliary injury is associated with significant morbidity. As prevention is the best strategy, the concept of a culture of safe cholecystectomy has been recently introduced to educate surgeons and apprise them of basic tenets of safe performance of LC. Various aspects of safe cholecystectomy include: (1) thorough knowledge of relevant anatomy, various anatomical landmarks, and anatomical variations; (2) an understanding of the mechanisms involved in biliary/vascular injury, the most important being the misidentification injury; (3) identification of various preoperative and intraoperative predictors of difficult cholecystectomy; (4) proper gallbladder retraction; (5) safe use of various energy devices; (6) understanding the critical view of safety, including its doublet view and documentation; (7) awareness of various error traps (e.g., fundus first technique); (8) use of various bailout strategies (e.g., subtotal cholecystectomy) in difficult gallbladder cases; (9) use of intraoperative imaging techniques (e.g., intraoperative cholangiogram) to ascertain correct anatomy; and (10) understanding the concept of time-out. Surgeons should be facile with these aspects of this culture of safety in cholecystectomy in an attempt to reduce the incidence of biliary/vascular injury during LC.
Ageing, also spelled aging, is the process of becoming older. The term refers especially to human beings, many animals, and fungi, whereas for example bacteria, perennial plants and some simple animals are potentially immortal. In the broader sense, ageing can refer to single cells within an organism which have ceased dividing (cellular senescence) or to the population of a species (population ageing).
In humans, ageing represents the accumulation of changes in a human being over time,[1] encompassing physical, psychological, and social change. Reaction time, for example, may slow with age, while knowledge of world events and wisdom may expand. Ageing is among the greatest known risk factors for most human diseases:[2] of the roughly 150,000 people who die each day across the globe, about two thirds die from age-related causes.
The causes of ageing are uncertain; current theories are assigned to the damage concept, whereby the accumulation of damage (such as DNA oxidation) may cause biological systems to fail, or to the programmed ageing concept, whereby internal processes (such as DNA methylation) may cause ageing. Programmed ageing should not be confused with programmed cell death (apoptosis).
As we enter in the Modern day, we are witnessing dawn of the new trend in which closed body operating procedures are more often being performed through minimal access. This development is the consequence of vision and work of many dedicated individuals. They include early pioneers of endoscopy who planted the seed and lastly the current pioneers who pushed and expanded these frontiers to give rise the birth of modern laparoscopy. Therapeutic laparoscopic surgery was introduced into the surgical practice recently and within a short span of time, it has become established as defacto standard for the treatment of chronic cholelithiasis and many advanced laparoscopic procedures can be performed safely. Laparoscopic surgery, what we should witness today, may be the culmination of over a hundred years of painstaking efforts from the number of pioneers within the fields of optics, instrumentation and video laparoscopic camera. Few advances in medicine occur in isolation. The innate human curiosity to peer within the body cavities can be traced back to ancient times. However, due to primitive technology and crude instruments, several ambitions were not realized. It is probably safe to say that first laparoscopy would not have been performed had it not been for the efforts of many physicians in 1800s to develop endoscope. The device developed by Theodore Stein in mid 1880 contains all the aspects of the current endoscopic documentation system. There was a crude endoscope and a high intensity light source. Illumination was made by continuously feeding a magnesium wire into an ignition chamber utilizing a clockwise mechanism. Light from this combustion was reflected to the tube utilizing a mirror. Finally the look was focused on to some photographic plate through coupling optics.
Constipation refers to bowel movements that are infrequent or hard to pass. Constipation is a common cause of painful defecation. Severe constipation includes obstipation (failure to pass stools or gas) and fecal impaction, which can progress to bowel obstruction and become life-threatening.
Constipation is a symptom with many causes. These causes are of two types: obstructed defecation and colonic slow transit (or hypo mobility). About 50 percent of people evaluated for constipation at tertiary referral hospitals have obstructed defecation. This type of constipation has mechanical and functional causes. Causes of colonic slow transit constipation include diet, hormonal disorders such as hypothyroidism, side effects of medications, and rarely heavy metal toxicity. Because constipation is a symptom, not a disease, effective treatment of constipation may require first determining the cause. Treatments include changes in dietary habits, laxatives, enemas, biofeedback, and in particular situations surgery may be required.
Constipation is common; in the general population rates of constipation varies from 2–30 percent. In elderly people living in care homes the rate of constipation is 50–75 percent.[4] In the United States expenditures on medications for constipation are greater than US$250 million per year.
The definition of constipation includes the following:
infrequent bowel movements (typically three times or fewer per week)
difficulty during defecation (straining during more than 25% of bowel movements or a subjective sensation of hard stools; straining in this context is a strong effort to push out stool often by holding one's breath and by pushing the respective muscles in the abdominal area hard), or
the sensation of incomplete bowel evacuation.
The Rome III criteria are widely used to diagnose chronic constipation, and are helpful in separating cases of chronic functional constipation from less-serious instances.
Another definition states that less than three bowel movements per week and straining on more than 75% of occasions represents constipation in clinical surveys.
This document discusses laparoscopic common bile duct exploration (LCBDE) for the treatment of CBD stones. It outlines the advantages of the laparoscopic approach, including reduced costs, hospitalization and recovery time compared to open surgery. It describes the two main laparoscopic techniques for CBD stone removal - trans-cystic duct approach and laparoscopic choledochotomy. Key factors that determine technique selection include stone size and location, cystic/CBD duct anatomy and size, and surgeon skill. Standard port placements and step-by-step descriptions of each technique are provided. Complications are discussed. The document concludes with a brief overview of bilioenteric bypass indications and options.
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Orthopedic surgery to help stabilize joints
Repair ligaments
Ligate vessels or tis
Robotic Surgery means computer/ Robotic assisted surgery.
It was developed to overcome the limitations of MAS and to enhance the capabilities of surgeons performing open Surgery History of Robotic surgery
The first robot to assist in surgery was the Arthrobot, which was developed and used for the first time in Vancouver in 1983.[43] Intimately involved were biomedical engineer, Dr. James McEwen, Geof Auchinleck, a UBC engineering physics grad, and Dr. Brian Day as well as a team of engineering students. The robot was used in an orthopaedic surgical procedure on 12 March 1984, at the UBC Hospital in Vancouver.
Over 60 arthroscopic surgical procedures were performed in the first 12 months, and a 1985 National Geographic video on industrial robots, The Robotics Revolution, featured the device. Other related robotic devices developed at the same time included a surgical scrub nurse robot, which handed operative instruments on voice command, and a medical laboratory robotic arm. A YouTube video entitled Arthrobot illustrates some of these in operation .
Every upcoming surgeon practising minimal access surgery should know the basics of urology , so that he or she can put his or her,s capabilities as a surgeon
Common symptoms of depression:
Lost of interest in the things that were previously pleasurable
Depressed and Sadness
Hopelessness
Other may Include:
Anxiety
Increased feeling of guilt
Irritability
Impatience
Sleep disturbances
Tearfulness
Difficulty concentrating
Appetite changes (loss/gain)
Increased Isolation
Somatic Pain
Substance abuse
Wound dehiscence is a complication of surgery where the surgical incision ruptures or reopens. It can lead to evisceration of internal organs. Risk factors include obesity, diabetes, wound infection, and surgical factors like tension on the incision. Symptoms include pain, swelling, and drainage at the wound site. Treatment depends on the severity but may involve antibiotics, packing the wound, or re-suturing the incision. Negative pressure wound therapy can also be used to help close wounds at high risk of dehiscence. Preventing wound dehiscence requires proper surgical technique like layered closure with adequate suture length and tissue bites.
Laparoscopic Urologic surgery, is a part of the curriculum of Minimal Access Surgery, and requires lot of skills and patience. All new surgeons carrying out Basic Laparoscopic surgery should aim at also doing Lap. Urological surgeries, which has a steep learning curve, but with with excellent outcomes.
This document discusses bariatric surgery as a treatment for obesity, diabetes, and hypertension - known as the "dangerous triad". It outlines the obesity epidemic globally and in India. Bariatric surgery is presented as the most effective long-term treatment, as other options like diet, exercise, and medication often only achieve temporary weight loss. The document describes various bariatric surgical procedures and their mechanisms for weight loss and resolving comorbidities. Case studies are presented demonstrating successful weight loss and comorbidity resolution through bariatric surgery. Risks are low but include leaks, strictures, and potential for weight regain. A multidisciplinary team approach is emphasized for best outcomes.
This document discusses the pathophysiology of bariatric surgery. It notes that obesity is a global epidemic impacting over 1.7 billion people. Obesity is associated with numerous serious health conditions and comorbidities. Diet and pharmaceutical interventions have proven ineffective for treating severe or morbid obesity. The document outlines the various medical comorbidities of obesity including metabolic, mechanical, degenerative, neoplastic, and psychological conditions. It discusses the criteria for indicating bariatric surgery including BMI over 40 or over 35 with comorbidities. The goals and various procedures of bariatric surgery including restrictive, malabsorptive, and hybrid techniques are summarized.
This document discusses the pathophysiology of bariatric surgery. It notes that obesity is a global epidemic impacting over 1.7 billion people. Bariatric surgery is effective for weight loss and treating obesity-related comorbidities. The main procedures discussed are sleeve gastrectomy, Roux-en-Y gastric bypass, and biliopancreatic diversion with duodenal switch. These work through restriction, malabsorption, or both. Gut hormones like ghrelin and GLP-1 play an important role in appetite and glucose regulation after surgery. The author also shares their experience performing various bariatric procedures in India.
What is MIS?
A minimally invasive medical procedure is defined as one that is carried out by entering the body through the skin or through a body cavity or anatomical opening, but with the smallest damage possible to these struct uresIncludes laparoscopic, endoscopic, and other approaches.
Why MIS?
Decreased patient pain
Decreased patient recovery period
Possible decrease in inflammatory response in the patient which may prove to have a better outcome in oncologic operations.
Distant future
In the distant future, there will be a para- digm shift with the development of non-inva- sive surgical techniques in combination with nanotechnologies and a new era in the devel- opment of surgery, and subsequently in surgi- cal techniques, will be opened.
Nanotechnology is an umbrella term for materials and devices that operate at the nanoskill (1 billionth of a meter). In terms of scale, a nanometer is approximately one 1/8000 of a human hair or 10 times the diam- eter of a hydrogen atom. The size of the device can vary but starts from a ten thou- sand-logic element system that will occupy a cube of no more than one hundred nanome- ters. This is a volume slightly larger than 0.001 cubic microns. This would be sufficient to hold a small computer. For example, if red blood cells are approximately eight microns in diameter, the 100 nanomicroprocessor will be 80 times smaller than a red blood cell. Devices this size could easily fit into the circulatory system and could even conceivably enter indi- vidual cells.
This document provides an overview of bariatric surgery in Odisha, India. It begins with definitions of bariatric surgery and classifications of BMI. It then discusses the comorbidities of obesity and guidelines for determining who is a suitable candidate for bariatric surgery. The document outlines various bariatric procedures including restrictive, malabsorptive, and combination procedures. It also discusses pre-op assessment, investigations, tools used in bariatric surgery, pathophysiology including the role of GI hormones, and videos demonstrating sleeve gastrectomy and Roux-en-Y gastric bypass procedures.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
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The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
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Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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Acute pancreatitis SP
1. Acute Pancreatitis
lethal condition care & cure
what should be the approach
Acute Pancreatitis
lethal condition care & cure
what should be the approach
DR SREEJOY PATNAIKDR SREEJOY PATNAIK
2. DEFINITIONDEFINITION
• Pancreatitis is a condition associated with development of acute and
sudden inflammation of the pancreas.
• Pancreatic enzymes are released in the abdomen and cause
inflammation by the damage from digestion of normal body
structures, especially fat in the abdomen.
• Mortality ranges from 3 percent in patients with interstitial
edematous pancreatitis to 17 percent in patients who develop
pancreatic necrosis.
• Pancreatitis is a condition associated with development of acute and
sudden inflammation of the pancreas.
• Pancreatic enzymes are released in the abdomen and cause
inflammation by the damage from digestion of normal body
structures, especially fat in the abdomen.
• Mortality ranges from 3 percent in patients with interstitial
edematous pancreatitis to 17 percent in patients who develop
pancreatic necrosis.
Acute Pancreatitis
3. Revised definitions and classification
of acute pancreatitis
Revised definitions and classification
of acute pancreatitis
• Definition of diagnosis of acute pancreatitis
• The diagnosis of acute pancreatitis requires two of the
following three features:
• (1) abdominal pain consistent with acute pancreatitis (acute
onset of a persistent, severe, epigastric pain often radiating to
the back)
• (2) serum lipase activity (or amylase activity) at least three
times greater than the upper limit of normal.
• (3) characteristic findings of acute pancreatitis on CECT and
less commonly MRI) or USG abdomen.
• Definition of diagnosis of acute pancreatitis
• The diagnosis of acute pancreatitis requires two of the
following three features:
• (1) abdominal pain consistent with acute pancreatitis (acute
onset of a persistent, severe, epigastric pain often radiating to
the back)
• (2) serum lipase activity (or amylase activity) at least three
times greater than the upper limit of normal.
• (3) characteristic findings of acute pancreatitis on CECT and
less commonly MRI) or USG abdomen.
Acute Pancreatitis
4. Definition of onset of acute pancreatitisDefinition of onset of acute pancreatitis
• The onset of AP is defined as the time of onset of abdominal pain (not the
time of admission to the hospital).
• The time interval between onset of abdominal pain and first admission to
the hospital should be noted.
• When patients with severe disease are transferred to a tertiary hospital,
the intervals between onset of symptoms, first admission and transfer
should be noted.
• Data recorded from a tertiary care hospital should be stratified to allow
separate consideration of the outcomes of patients who were admitted
directly and those admitted by transfer from another hospital.
• The onset of AP is defined as the time of onset of abdominal pain (not the
time of admission to the hospital).
• The time interval between onset of abdominal pain and first admission to
the hospital should be noted.
• When patients with severe disease are transferred to a tertiary hospital,
the intervals between onset of symptoms, first admission and transfer
should be noted.
• Data recorded from a tertiary care hospital should be stratified to allow
separate consideration of the outcomes of patients who were admitted
directly and those admitted by transfer from another hospital.
Acute Pancreatitis
5. Why we are worriedWhy we are worried
• Acute pancreatitis (AP) is one of the most common disease of the gastrointestinal tract, leading to
tremendous emotional, physical, and financial human burden.
• Recent studies show the incidence of AP varies between 4.9 and 73.4 cases per 100,000 worldwide
• Mortality
– 2-3% overall mortality from acute pancreatitis
• Tertiary centers report rates of 15- 30%
– Interstitial pancreatitis (1%)
– Necrotizing pancreatitis/organ failure (30%)
• Physician office visits
– 911,000 per year
Hospitalizations
– 230,000 in 2002
• Deaths
– 2500 per year
• Acute pancreatitis (AP) is one of the most common disease of the gastrointestinal tract, leading to
tremendous emotional, physical, and financial human burden.
• Recent studies show the incidence of AP varies between 4.9 and 73.4 cases per 100,000 worldwide
• Mortality
– 2-3% overall mortality from acute pancreatitis
• Tertiary centers report rates of 15- 30%
– Interstitial pancreatitis (1%)
– Necrotizing pancreatitis/organ failure (30%)
• Physician office visits
– 911,000 per year
Hospitalizations
– 230,000 in 2002
• Deaths
– 2500 per year
Acute Pancreatitis
6. Definition of types of acute pancreatitisDefinition of types of acute pancreatitis
Acute Pancreatitis
According to the Atlanta
classification, Acute Pancreatitis can
be divided into two broad categories
According to the Atlanta
classification, Acute Pancreatitis can
be divided into two broad categories
1. Interstitial edematous pancreatitis.
2. Necrotizing pancreatitis
1. Interstitial edematous pancreatitis.
2. Necrotizing pancreatitis
7. Interstitial edematous pancreatitisInterstitial edematous pancreatitis
Acute Pancreatitis
The majority of patients with AP have diffuse (or occasionally localised)
enlargement of the pancreas due to inflammatory oedema. (75-80% )
On CECT, the pancreatic parenchyma shows
relatively homogeneous enhancement, and the peripancreatic fat usually
shows some inflammatory changes of haziness or mild stranding.
There may also be some peripancreatic fluid .
The clinical symptoms of interstitial oedematous pancreatitis usually
resolve within the first week.
The majority of patients with AP have diffuse (or occasionally localised)
enlargement of the pancreas due to inflammatory oedema. (75-80% )
On CECT, the pancreatic parenchyma shows
relatively homogeneous enhancement, and the peripancreatic fat usually
shows some inflammatory changes of haziness or mild stranding.
There may also be some peripancreatic fluid .
The clinical symptoms of interstitial oedematous pancreatitis usually
resolve within the first week.
9. Acute Pancreatitis
Necrotising pancreatitisNecrotising pancreatitis
About 5–10% of patients develop necrosis of the pancreatic
parenchyma, the peripancreatic tissue or both.
Necrotising pancreatitis most commonly manifests as necrosis
involving both the pancreas and peripancreatic tissues and less
commonly as necrosis of only the peripancreatic tissue, and
rarely of the pancreatic parenchyma alone.
About 5–10% of patients develop necrosis of the pancreatic
parenchyma, the peripancreatic tissue or both.
Necrotising pancreatitis most commonly manifests as necrosis
involving both the pancreas and peripancreatic tissues and less
commonly as necrosis of only the peripancreatic tissue, and
rarely of the pancreatic parenchyma alone.
11. Infected pancreatic necrosisInfected pancreatic necrosis
• Necrosis is variable, may remain solid or liquefy, remain sterile or
become infected, persist, or disappear over time.
• occurs > the first week.
• Infected pancreatic necrosis is important because of the need for
antibiotic treatment and likely active intervention.
• The presence of infection - extraluminal gas in the pancreatic and/or
peripancreatic tissues on CECT or PFNA is positive for bacteria and/or
fungi on Gram stain and culture.
• There may be suppuration (pus) associated with the infected
pancreatic necrosis, leading to liquefaction – abscess
• Necrosis is variable, may remain solid or liquefy, remain sterile or
become infected, persist, or disappear over time.
• occurs > the first week.
• Infected pancreatic necrosis is important because of the need for
antibiotic treatment and likely active intervention.
• The presence of infection - extraluminal gas in the pancreatic and/or
peripancreatic tissues on CECT or PFNA is positive for bacteria and/or
fungi on Gram stain and culture.
• There may be suppuration (pus) associated with the infected
pancreatic necrosis, leading to liquefaction – abscess
Acute Pancreatitis
13. FLUID COLLECTIONS IN AP REVISED ATLANTA
CLASSIFICATION & ITS INTERVENTION
FLUID COLLECTIONS IN AP REVISED ATLANTA
CLASSIFICATION & ITS INTERVENTION
Acute Pancreatitis
15. Phases of acute pancreatitisPhases of acute pancreatitis
Systemic disturbances result from the host response to local pancreatic injury.
Is usually over by the end of the 1st wk or extend to 2nd wk.
Cytokine cascades are activated by the pancreatic inflammation which manifest
clinically as the SIRS. An increased risk of developing OF.
`
The determinant of the severity in this phase is primarily the presence and
duration of OF.
Transient OF -if the organ failure resolves within 48 h
Persistent OF - if organ failure persists for >48 h.
Multiple organ failure (MOF) – If OF affects > 1organ system.
Systemic disturbances result from the host response to local pancreatic injury.
Is usually over by the end of the 1st wk or extend to 2nd wk.
Cytokine cascades are activated by the pancreatic inflammation which manifest
clinically as the SIRS. An increased risk of developing OF.
`
The determinant of the severity in this phase is primarily the presence and
duration of OF.
Transient OF -if the organ failure resolves within 48 h
Persistent OF - if organ failure persists for >48 h.
Multiple organ failure (MOF) – If OF affects > 1organ system.
Acute Pancreatitis
EARLY PHASEEARLY PHASE
16. Signs of systemic inflammatory response syndrome
(SIRS)
Signs of systemic inflammatory response syndrome
(SIRS)
• SIRS—defined by presence of two or more criteria:
• HR >90 beats/min
• Core temperature <36°C or >38°C
• WBC count <4000 or >12000/mm3
• Respiration >20/min or PCO2 <32 mm Hg
• SIRS—defined by presence of two or more criteria:
• HR >90 beats/min
• Core temperature <36°C or >38°C
• WBC count <4000 or >12000/mm3
• Respiration >20/min or PCO2 <32 mm Hg
Acute Pancreatitis
17. Late phaseLate phase
• The late phase is characterised by
-Persistence of systemic signs of inflammation or by the presence of local complications, - -
occurs only in patients with moderately severe or severe acute pancreatitis.
• - Local complications evolve during the late phase.
• -It is important to distinguish the different morphologic characteristics of the local complications
by radiologic imaging.
• - Persistent OF, however, remains the main determinant of severity, so characterisation of AP in
the late phase requires both clinical and morphologic criteria.
• The SIRS of the early phase may be followed by a Compensatory anti-inflammatory response
syndrome (CARS) that may contribute to an increased risk of infection.
• The late phase is characterised by
-Persistence of systemic signs of inflammation or by the presence of local complications, - -
occurs only in patients with moderately severe or severe acute pancreatitis.
• - Local complications evolve during the late phase.
• -It is important to distinguish the different morphologic characteristics of the local complications
by radiologic imaging.
• - Persistent OF, however, remains the main determinant of severity, so characterisation of AP in
the late phase requires both clinical and morphologic criteria.
• The SIRS of the early phase may be followed by a Compensatory anti-inflammatory response
syndrome (CARS) that may contribute to an increased risk of infection.
Acute Pancreatitis
18. CLASSIFICATION ACCORDING TO SEVERITYCLASSIFICATION ACCORDING TO SEVERITY
Acute Pancreatitis
1. Mild acute pancreatitis, which is characterized by the absence
of organ failure and local or systemic complications
2. Moderately severe acute pancreatitis, which is characterized
by no organ failure or transient organ failure (<48 hours) with
systemic or local complications
3. Severe acute pancreatitis, which is characterized by
persistent organ failure (>48 hours) that may involve single or
multiple organs
1. Mild acute pancreatitis, which is characterized by the absence
of organ failure and local or systemic complications
2. Moderately severe acute pancreatitis, which is characterized
by no organ failure or transient organ failure (<48 hours) with
systemic or local complications
3. Severe acute pancreatitis, which is characterized by
persistent organ failure (>48 hours) that may involve single or
multiple organs
19. Revised Atlanta classificationRevised Atlanta classification
• According to the revised Atlanta classification of AP is clinically defined by at
least the first two of three features:
• (a) abdominal pain (epigastric often radiating to the back),
• (b) serum amylase and lipase levels three or more times normal (imaging is
to be used if the elevated values are ,3 times normal)
• (c) characteristic findings on CT, magnetic resonance (MR) imaging, or
transabdominal ultrasonographic (US) studies.
• If AP is diagnosed on the basis of the first two criteria with no systemic sign of
severe SIRS or persistent OF , CECT may not be necessary for determining
patient care.
• According to the revised Atlanta classification of AP is clinically defined by at
least the first two of three features:
• (a) abdominal pain (epigastric often radiating to the back),
• (b) serum amylase and lipase levels three or more times normal (imaging is
to be used if the elevated values are ,3 times normal)
• (c) characteristic findings on CT, magnetic resonance (MR) imaging, or
transabdominal ultrasonographic (US) studies.
• If AP is diagnosed on the basis of the first two criteria with no systemic sign of
severe SIRS or persistent OF , CECT may not be necessary for determining
patient care.
Acute Pancreatitis
22. Pancreatic InjuryPancreatic Injury
Abnormal Pancreatic enzyme
Activation inside acinar cells
Abnormal Pancreatic enzyme
Activation inside acinar cells
Colonization of zymogen granules
&lysosomes inside acinar cells
Colonization of zymogen granules
&lysosomes inside acinar cells
Pancreatic edemaPancreatic edema
Auto-digestion of normal
pancreatic parenchyma
Release of Pro-inflammatory
Cytokines from acinar cells
Release of Pro-inflammatory
Cytokines from acinar cells
TNF-αTNF-α IL-1,2,& 6IL-1,2,& 6 IL-10 & IL-1IL-10 & IL-1
(Anti inflammatory mediators)
PathophysiologyPathophysiology
23. These mediators propagate the response locally &
systemically >
These mediators propagate the response locally &
systemically >
TNF ,IL, neutrophils & macrophages are released into
the pancreatic parenchyma > release of more
TNF ,IL, neutrophils & macrophages are released into
the pancreatic parenchyma > release of more
TNF ,IL, reactive o2 metabolites, PG, platelet activating
factors & Leucotrienes.
TNF ,IL, reactive o2 metabolites, PG, platelet activating
factors & Leucotrienes.
Aggravation of AP occurs by local inflammatory
response>
Aggravation of AP occurs by local inflammatory
response>
Increased permeability & damage of the pan.micro-
circulation
Increased permeability & damage of the pan.micro-
circulation
Severe cases- inflamm. Response > localised
haemorrhage & pancreatic necrosis.
Severe cases- inflamm. Response > localised
haemorrhage & pancreatic necrosis.
Inflammatory cascade is self limiting – 80- 90% casesInflammatory cascade is self limiting – 80- 90% cases
10 % cases- vicious cycle of rec. panc. Injury &
localised SIR
10 % cases- vicious cycle of rec. panc. Injury &
localised SIR
Rest 10%- massive release of inflam. Mediators into
systemic circulation > SIRS and OF.
Rest 10%- massive release of inflam. Mediators into
systemic circulation > SIRS and OF.
24. Clinical manifestations:Clinical manifestations:
• ABDOMINAL PAIN- ( cardinal symptom) characteristically dull,boring &
steady; sudden in onset ,gradually becomes severe > constant ache.
• Location- epigastric & or peri-umbilical that radiates to the back & is
constant
• NAUSEA & VOMITING – 90%- does not relieve pain. sometimes anorexia
/diarrhea
• Fever (76%),Tachycardia (65%), Hypotension ( 73%)
• Abdominal tenderness, muscle guarding (68%),distension (65%),diminished or
absent bowel sounds.
• Jaundice (28%),Dyspnea (10%),tachypnea, basal rales left lung.
• Severe cases- haemodynamic instability (10%),haematemesis or malena (5%);
pale, diaphoretic, & listless appearance.
• Occasionally, muscular spasm of extremities secondary to hypocalcemia.
• ABDOMINAL PAIN- ( cardinal symptom) characteristically dull,boring &
steady; sudden in onset ,gradually becomes severe > constant ache.
• Location- epigastric & or peri-umbilical that radiates to the back & is
constant
• NAUSEA & VOMITING – 90%- does not relieve pain. sometimes anorexia
/diarrhea
• Fever (76%),Tachycardia (65%), Hypotension ( 73%)
• Abdominal tenderness, muscle guarding (68%),distension (65%),diminished or
absent bowel sounds.
• Jaundice (28%),Dyspnea (10%),tachypnea, basal rales left lung.
• Severe cases- haemodynamic instability (10%),haematemesis or malena (5%);
pale, diaphoretic, & listless appearance.
• Occasionally, muscular spasm of extremities secondary to hypocalcemia.
Acute Pancreatitis
25. Clinical manifestations:Clinical manifestations:
• Uncommon findings associated with severe necrotizing pancreatitis:
• 1.Cullens sign- bluish discolouration around the umbilicus resulting from
haemoperitoneum.
• 2.Grey-Turner sign- reddish brown discoloration along the flanks resulting from
retroperitoneal blood dissecting along tissue planes, more commonly patients have a
ruddy erythema in the flanks secondary to extravasated pancreatic exudate.
• Erythematous skin nodules, usually < 1 cm,typically located on extensor skin
surfaces; polyarthritis.
• Pleural effusions (fluid in the bases of the pleural cavity)
• Grünwald sign (appearance of ecchymosis, large bruise, around the umbilicus due to
local toxic lesion of the vessels)
• Körte's sign (pain or resistance in the zone where the head of pancreas is located (in
epigastrium, 6–7 cm above the umbilicus))
Kamenchik's sign (pain with pressure under the xiphoid process)
Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the Erector
spinae muscles and below the left 12th rib (left costovertebral angle (CVA))
• Uncommon findings associated with severe necrotizing pancreatitis:
• 1.Cullens sign- bluish discolouration around the umbilicus resulting from
haemoperitoneum.
• 2.Grey-Turner sign- reddish brown discoloration along the flanks resulting from
retroperitoneal blood dissecting along tissue planes, more commonly patients have a
ruddy erythema in the flanks secondary to extravasated pancreatic exudate.
• Erythematous skin nodules, usually < 1 cm,typically located on extensor skin
surfaces; polyarthritis.
• Pleural effusions (fluid in the bases of the pleural cavity)
• Grünwald sign (appearance of ecchymosis, large bruise, around the umbilicus due to
local toxic lesion of the vessels)
• Körte's sign (pain or resistance in the zone where the head of pancreas is located (in
epigastrium, 6–7 cm above the umbilicus))
Kamenchik's sign (pain with pressure under the xiphoid process)
Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the Erector
spinae muscles and below the left 12th rib (left costovertebral angle (CVA))
26. P/E
• MILD TO MODERATE EPIGASTRIC TENDERNESS
• ABDOMINAL DISTENSION
• GENERAL REBOUND & ABDOMINAL RIGIDITY
• CHEST RT. SIDE – DULLNESS ON PERCUSSION > RT. PLEURAL
EFFUSION.
• DECREASED BREATH SOUNDS ON RT SIDE
• MILD TO MODERATE EPIGASTRIC TENDERNESS
• ABDOMINAL DISTENSION
• GENERAL REBOUND & ABDOMINAL RIGIDITY
• CHEST RT. SIDE – DULLNESS ON PERCUSSION > RT. PLEURAL
EFFUSION.
• DECREASED BREATH SOUNDS ON RT SIDE
Acute Pancreatitis
29. CLINICAL PREDICTORSCLINICAL PREDICTORS
• Clinical judgment
• Older age
• Alcoholic pancreatitis
• Short time interval to symptom onset
• Obesity
• Organ failure
• LABORATORY AND RADIOLOGIC
PREDICTORS
• Hemoconcentration
• C-reactive protein
• Blood urea nitrogen
• Serum creatinine
• Other serum markers
• Chest radiographs
• CT scan
• MRI and MRCP
• Clinical judgment
• Older age
• Alcoholic pancreatitis
• Short time interval to symptom onset
• Obesity
• Organ failure
• LABORATORY AND RADIOLOGIC
PREDICTORS
• Hemoconcentration
• C-reactive protein
• Blood urea nitrogen
• Serum creatinine
• Other serum markers
• Chest radiographs
• CT scan
• MRI and MRCP
Acute Pancreatitis
SCORING SYSTEMS
Ranson's criteria
The APACHE II score
SIRS score
BISAP score
Harmless acute pancreatitis score
Organ failure-based scores
CT severity index Balthazar score
SCORING SYSTEMS
Ranson's criteria
The APACHE II score
SIRS score
BISAP score
Harmless acute pancreatitis score
Organ failure-based scores
CT severity index Balthazar score
30. INVESTIGATIONS - BIOCHEMICALINVESTIGATIONS - BIOCHEMICAL
• CBC and hematocrit
• Amylase and lipase
• LFT , GGT
• Serum electrolytes, BUN, creatinine, glucose, Lipid Profile.
• C-reactive protein
• Other tests
• -ABG
• -Lactic dehydrogenase (LDH), and HCO3 levels
• - IgG4 levels
• -Trypsin and its precursor trypsinogen-2 in both the urine and the peritoneal
fluid
• CBC and hematocrit
• Amylase and lipase
• LFT , GGT
• Serum electrolytes, BUN, creatinine, glucose, Lipid Profile.
• C-reactive protein
• Other tests
• -ABG
• -Lactic dehydrogenase (LDH), and HCO3 levels
• - IgG4 levels
• -Trypsin and its precursor trypsinogen-2 in both the urine and the peritoneal
fluid
Acute Pancreatitis
31. • Amylase or lipase levels at least > 3 times above -diagnostic of AP.
• Serum amylase determinations are not specific for AP
• Amylase P level is more specific to pancreatic pathology
• False + in- SAIO, mesenteric ischemia, tubo-ovarian disease, renal insufficiency, or
macroamylasemia.
• The serum half-life of amylase is short, and elevations generally return to reference
ranges within a few days.
• Lipase has a slightly longer half-life .
• Elevated lipase levels are more specific. Lipase levels remain high for 12 days
• ALP, SB, AST, and ALT levels to search for evidence of gallstone pancreatitis.
• An ALT level higher than 150 U/L suggests gallstone pancreatitis and a more
fulminant disease course.
• Amylase or lipase levels at least > 3 times above -diagnostic of AP.
• Serum amylase determinations are not specific for AP
• Amylase P level is more specific to pancreatic pathology
• False + in- SAIO, mesenteric ischemia, tubo-ovarian disease, renal insufficiency, or
macroamylasemia.
• The serum half-life of amylase is short, and elevations generally return to reference
ranges within a few days.
• Lipase has a slightly longer half-life .
• Elevated lipase levels are more specific. Lipase levels remain high for 12 days
• ALP, SB, AST, and ALT levels to search for evidence of gallstone pancreatitis.
• An ALT level higher than 150 U/L suggests gallstone pancreatitis and a more
fulminant disease course.
Acute Pancreatitis
32. • CBC (leukocytosis) > 12,000/µL with > segmented polymorphonuclear (PMN) cells.
• On admission hematocrit value greater than 47% - has been proposed as a sensitive
measure of more severe disease
• C-reactive protein (CRP) value can be obtained 24-48 hours after presentation to provide
some indication of prognosis.
• Higher levels have been shown to correlate with a propensity toward OF .
• A CRP value in double figures (ie, ≥ 10 mg/dL) strongly indicates severe pancreatitis.
• CRP is an acute-phase reactant that is not specific for pancreatitis.
• CBC (leukocytosis) > 12,000/µL with > segmented polymorphonuclear (PMN) cells.
• On admission hematocrit value greater than 47% - has been proposed as a sensitive
measure of more severe disease
• C-reactive protein (CRP) value can be obtained 24-48 hours after presentation to provide
some indication of prognosis.
• Higher levels have been shown to correlate with a propensity toward OF .
• A CRP value in double figures (ie, ≥ 10 mg/dL) strongly indicates severe pancreatitis.
• CRP is an acute-phase reactant that is not specific for pancreatitis.
Acute Pancreatitis
33. • Evaluate ABG if a patient is dyspneic.
• Whether tachypnea is due to acute respiratory distress syndrome (ARDS) or
diaphragmatic irritation must be determined.
• LDH, BUN, and HCO3 levels should be measured both at admission and at 48 hours
in order to help determine the Ranson criteria for survival.
• Immunoglobulin G4 (IgG4) levels can be checked to evaluate for autoimmune
pancreatitis
• Trypsin and its precursor trypsinogen-2 - in both the urine and the peritoneal fluid
have been evaluated as possible markers for acute pancreatitis (especially post-
ERCP pancreatitis.
• Evaluate ABG if a patient is dyspneic.
• Whether tachypnea is due to acute respiratory distress syndrome (ARDS) or
diaphragmatic irritation must be determined.
• LDH, BUN, and HCO3 levels should be measured both at admission and at 48 hours
in order to help determine the Ranson criteria for survival.
• Immunoglobulin G4 (IgG4) levels can be checked to evaluate for autoimmune
pancreatitis
• Trypsin and its precursor trypsinogen-2 - in both the urine and the peritoneal fluid
have been evaluated as possible markers for acute pancreatitis (especially post-
ERCP pancreatitis.
Acute Pancreatitis
34. Abdominal RadiographyAbdominal Radiography
• Abdominal radiographs have a limited
role in acute pancreatitis.
• KUB radiography in upright position is
primarily performed to detect free air in
the abdomen, indicating a perforated
viscus, as would be the case in a
penetrating, perforated duodenal ulcer.
• In some cases, the inflammatory process
may damage peripancreatic structures,
resulting in a colon cut-off sign, a sentinel
loop, or an ileus.
• The presence of calcifications within or
around the pancreas may indicate chronic
pancreatitis.
• Abdominal radiographs have a limited
role in acute pancreatitis.
• KUB radiography in upright position is
primarily performed to detect free air in
the abdomen, indicating a perforated
viscus, as would be the case in a
penetrating, perforated duodenal ulcer.
• In some cases, the inflammatory process
may damage peripancreatic structures,
resulting in a colon cut-off sign, a sentinel
loop, or an ileus.
• The presence of calcifications within or
around the pancreas may indicate chronic
pancreatitis.
Acute Pancreatitis
35. UltrasonographyUltrasonography
• USG ( screening )of the abdomen is
the most useful initial test in
determining the etiology of
pancreatitis and is the technique of
choice for detecting gallstones.
• Sensitivity is reduced to 70-80%.
( Pancreatitis )
• In addition, the ability to identify
choledocholithiasis is limited.
• Not specific if overlying gas
shadows secondary to bowel
distention are present.
• Cannot measure the severity of
disease.
• USG ( screening )of the abdomen is
the most useful initial test in
determining the etiology of
pancreatitis and is the technique of
choice for detecting gallstones.
• Sensitivity is reduced to 70-80%.
( Pancreatitis )
• In addition, the ability to identify
choledocholithiasis is limited.
• Not specific if overlying gas
shadows secondary to bowel
distention are present.
• Cannot measure the severity of
disease.
36. Endoscopic ultrasonography- EUSEndoscopic ultrasonography- EUS
•
• -Is an endoscopic procedure that allows a
high-frequency ultrasound transducer to be
inserted into the gastrointestinal (GI) tract to
visualize the pancreas and the biliary tract.
• Its principal role is in detection of
microlithiasis and periampullary lesions.
• A secretin-stimulated EUS study –
• -may reveal resistance to ductal outflow at
the level of the papilla, for evaluation of
recurrent idiopathic pancreatitis.
•
• -Is an endoscopic procedure that allows a
high-frequency ultrasound transducer to be
inserted into the gastrointestinal (GI) tract to
visualize the pancreas and the biliary tract.
• Its principal role is in detection of
microlithiasis and periampullary lesions.
• A secretin-stimulated EUS study –
• -may reveal resistance to ductal outflow at
the level of the papilla, for evaluation of
recurrent idiopathic pancreatitis.
Acute Pancreatitis
37. Computed TomographyComputed Tomography
• Abdominal CT is not indicated for patients with mild pancreatitis.
• Always indicated in severe AP and is the imaging study of choice for assessing
complications.
• Scans done after > 72 hours after symptom onset unless the diagnosis is
uncertain, because inflammatory changes are often not radiographically present
until this time.
• Abdominal CT scans also provide prognostic information based on the
following grading scale developed by Balthazar & colleagues.
• Grade A - Normal pancreas
• Grade B - Focal or diffuse gland enlargement
• Grade C - Intrinsic gland abnormality recognized by haziness on the scan
• Grade D - Single ill-defined collection or phlegmon
• Grade E - Two or more ill-defined collections or the presence of gas in
or nearby the pancreas
• Abdominal CT is not indicated for patients with mild pancreatitis.
• Always indicated in severe AP and is the imaging study of choice for assessing
complications.
• Scans done after > 72 hours after symptom onset unless the diagnosis is
uncertain, because inflammatory changes are often not radiographically present
until this time.
• Abdominal CT scans also provide prognostic information based on the
following grading scale developed by Balthazar & colleagues.
• Grade A - Normal pancreas
• Grade B - Focal or diffuse gland enlargement
• Grade C - Intrinsic gland abnormality recognized by haziness on the scan
• Grade D - Single ill-defined collection or phlegmon
• Grade E - Two or more ill-defined collections or the presence of gas in
or nearby the pancreas
Acute Pancreatitis
43. • The chances of infection and death are virtually nil in grades A and B
but steadily increase in grades C through E.
• Patients with grade E pancreatitis have a 50% chance of developing an
infection and a 15% chance of dying.
• The chances of infection and death are virtually nil in grades A and B
but steadily increase in grades C through E.
• Patients with grade E pancreatitis have a 50% chance of developing an
infection and a 15% chance of dying.
Acute Pancreatitis
44. Magnetic Resonance Cholangiopancreatography
MRCP
Magnetic Resonance Cholangiopancreatography
MRCP
• ed. MRCP has an emerging role in the diagnosis of suspected biliary and pancreatic
duct obstruction in the setting of pancreatitis.
• MRCP is not as sensitive as ERCP , it is safer, noninvasive, and fast, and it
provides images useful in guiding clinical care decisions.
• MRCP should be used if choledocholithiasis is suspected but there is concern that
pancreatitis might worsen is
• If ERCP is performed.
• ed. MRCP has an emerging role in the diagnosis of suspected biliary and pancreatic
duct obstruction in the setting of pancreatitis.
• MRCP is not as sensitive as ERCP , it is safer, noninvasive, and fast, and it
provides images useful in guiding clinical care decisions.
• MRCP should be used if choledocholithiasis is suspected but there is concern that
pancreatitis might worsen is
• If ERCP is performed.
Acute Pancreatitis
45. ERCPERCP
• ERCP is an endoscopic procedure used to
evaluate the biliary and pancreatic ductal
system and is indicated in a subset of patients
with acute pancreatitis.
• Extreme caution in patients with acute
pancreatitis and should never be used as a first-
line diagnostic tool in this disease.
• It should be performed only in the following
situations:
• INDICATIONS :
• The patient has biliary pancreatitis and is
experiencing worsening jaundice and clinical
deterioration despite maximal supportive
therapy.
• When combined with sphincterotomy and
stone extraction, ERCP may reduce the length
of hospital stay, the complication rate, and,
possibly, mortality.
• ERCP is an endoscopic procedure used to
evaluate the biliary and pancreatic ductal
system and is indicated in a subset of patients
with acute pancreatitis.
• Extreme caution in patients with acute
pancreatitis and should never be used as a first-
line diagnostic tool in this disease.
• It should be performed only in the following
situations:
• INDICATIONS :
• The patient has biliary pancreatitis and is
experiencing worsening jaundice and clinical
deterioration despite maximal supportive
therapy.
• When combined with sphincterotomy and
stone extraction, ERCP may reduce the length
of hospital stay, the complication rate, and,
possibly, mortality.
Acute Pancreatitis
46. CT Image-Guided Aspiration and DrainageCT Image-Guided Aspiration and Drainage
• CT-guided needle aspiration is used to differentiate infected necrosis from sterile
necrosis in patients with severe necrotizing pancreatitis.
• The needle is placed into an area of low attenuation in or around the pancreas of a
patient with fever and tachycardia or other signs of a SIRS , generally following the
first week of severe pancreatitis.
• The procedure may be repeated weekly if clinically indicated.
• The specimen should be delivered to the laboratory within an hour and interpreted
promptly.
•
• The specimen should always be evaluated for Gram stain, and C/S study.
• If the Gram stain shows bacteria or fungi, surgical debridement of the infected
necrosis is generally indicated.
• An exception would be if the patient could not tolerate surgery; in this case, CT-
guided catheter drainage may be more effective.
• CT-guided needle aspiration is used to differentiate infected necrosis from sterile
necrosis in patients with severe necrotizing pancreatitis.
• The needle is placed into an area of low attenuation in or around the pancreas of a
patient with fever and tachycardia or other signs of a SIRS , generally following the
first week of severe pancreatitis.
• The procedure may be repeated weekly if clinically indicated.
• The specimen should be delivered to the laboratory within an hour and interpreted
promptly.
•
• The specimen should always be evaluated for Gram stain, and C/S study.
• If the Gram stain shows bacteria or fungi, surgical debridement of the infected
necrosis is generally indicated.
• An exception would be if the patient could not tolerate surgery; in this case, CT-
guided catheter drainage may be more effective.
Acute Pancreatitis
47. Histological FindingsHistological Findings
• The infinite spectrum of pancreatitis severity is usually subdivided into mild
and severe categories as follows:
• Mild pancreatitis - The gland exhibits interstitial edema and an inflammatory
infiltrate without hemorrhage or necrosis, usually with minimal or no organ
dysfunction
• Severe pancreatitis - Extensive inflammation and necrosis of the pancreatic
parenchyma are present, often associated with severe gland dysfunction and
multi organ failure.
• The infinite spectrum of pancreatitis severity is usually subdivided into mild
and severe categories as follows:
• Mild pancreatitis - The gland exhibits interstitial edema and an inflammatory
infiltrate without hemorrhage or necrosis, usually with minimal or no organ
dysfunction
• Severe pancreatitis - Extensive inflammation and necrosis of the pancreatic
parenchyma are present, often associated with severe gland dysfunction and
multi organ failure.
Acute Pancreatitis
49. ASSESSMENT OF SEVERITY –STAGING OF A.PASSESSMENT OF SEVERITY –STAGING OF A.P
• Ranson Scoring
• Acute Physiology and Chronic Health Evaluation (APACHE) II,
• Glasgow
• BISAP Scoring
• Balthazar CTSI scoring systems.
• Each has advantages and disadvantages, and none is currently recognized as a
criterion standard.
Evidence of ORGAN FAILURE:
Systolic B.P below 90 mm Hg,
Arterial partial pressure of oxygen [Pa O2] 60 mm Hg or lower,
Serum Creatinine level -2 mg/dL or lower,
GI bleeding amounting to 500 mL or more in 24 hrs
• Local complications (eg, necrosis, abscess, pseudocyst)
• Ranson score of 3 or higher or
• APACHE score of 8 or higher
•
• .
• Ranson Scoring
• Acute Physiology and Chronic Health Evaluation (APACHE) II,
• Glasgow
• BISAP Scoring
• Balthazar CTSI scoring systems.
• Each has advantages and disadvantages, and none is currently recognized as a
criterion standard.
Evidence of ORGAN FAILURE:
Systolic B.P below 90 mm Hg,
Arterial partial pressure of oxygen [Pa O2] 60 mm Hg or lower,
Serum Creatinine level -2 mg/dL or lower,
GI bleeding amounting to 500 mL or more in 24 hrs
• Local complications (eg, necrosis, abscess, pseudocyst)
• Ranson score of 3 or higher or
• APACHE score of 8 or higher
•
• .
Acute Pancreatitis
50. Ranson ScoreRanson Score
• Ranson criteria is a clinical prediction rule for predicting the severity of
acute pancreatitis. It was introduced in 1974.
• At admission
• age in years > 55 years
• TLC > 16000 cells/mm3
• BG > 10 mmol/L (> 200 mg/dL)
• Serum AST > 250 IU/L
• Serum LDH > 350 IU/L
• At 48 hours
• Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
• Hematocrit fall >10 mmol/l
• Oxygen (hypoxemia PO2 < 60 mmHg)
• BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid
hydration
• Base deficit (negative base excess) > 4 mEq/L
• Sequestration of fluids > 6 L
• Ranson criteria is a clinical prediction rule for predicting the severity of
acute pancreatitis. It was introduced in 1974.
• At admission
• age in years > 55 years
• TLC > 16000 cells/mm3
• BG > 10 mmol/L (> 200 mg/dL)
• Serum AST > 250 IU/L
• Serum LDH > 350 IU/L
• At 48 hours
• Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
• Hematocrit fall >10 mmol/l
• Oxygen (hypoxemia PO2 < 60 mmHg)
• BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid
hydration
• Base deficit (negative base excess) > 4 mEq/L
• Sequestration of fluids > 6 L
Acute Pancreatitis
51. Ranson ScoreRanson Score
• Ranson's score of ≥ 8 –OF / Substantial pancreatic necrosis (at least
30% glandular necrosis according to CECT)
• Interpretation
• If the score ≥ 3, severe pancreatitis is likely. If the score < 3, severe
pancreatitis is unlikely
• Or
• Score 0 to 2 : 2% mortality/ Score 3 to 4 : 15% mortality /Score 5 to
6 : 40% mortality/ Score 7 to 8 : 100% mortality
• Ranson's score of ≥ 8 –OF / Substantial pancreatic necrosis (at least
30% glandular necrosis according to CECT)
• Interpretation
• If the score ≥ 3, severe pancreatitis is likely. If the score < 3, severe
pancreatitis is unlikely
• Or
• Score 0 to 2 : 2% mortality/ Score 3 to 4 : 15% mortality /Score 5 to
6 : 40% mortality/ Score 7 to 8 : 100% mortality
Acute Pancreatitis
52. APACHE II
"Acute Physiology And Chronic Health Evaluation"
APACHE II
"Acute Physiology And Chronic Health Evaluation"
APACHE-II score based patient’s age, previous health status, and 12routine physiologic
measurements, general measure of the severity of disease 8 or higher defines severe
pancreatitis. Used on admission and repeated at any time. Positive predictive value of 43%
and a negative predictive value of 89%. It is an online calculator.
(APACHE II) score > 8 points predicts 11% to 18% mortality
Hemorrhagic peritoneal fluid
•Obesity
Indicators of organ failure
•Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min
PO2 <60 mmHg
•Oliguria (<50 mL/h) or increasing BUN and creatinine
Serum calcium < 1.90 mmol/L (<8.0 mg/dL) or serum albumin <33 g/L (<3.2.g/dL)>
APACHE-II score based patient’s age, previous health status, and 12routine physiologic
measurements, general measure of the severity of disease 8 or higher defines severe
pancreatitis. Used on admission and repeated at any time. Positive predictive value of 43%
and a negative predictive value of 89%. It is an online calculator.
(APACHE II) score > 8 points predicts 11% to 18% mortality
Hemorrhagic peritoneal fluid
•Obesity
Indicators of organ failure
•Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min
PO2 <60 mmHg
•Oliguria (<50 mL/h) or increasing BUN and creatinine
Serum calcium < 1.90 mmol/L (<8.0 mg/dL) or serum albumin <33 g/L (<3.2.g/dL)>
Acute Pancreatitis
53. Glasgow criteriaGlasgow criteria
• The Glasgow criteria is valid for both gallstone and alcohol induced pancreatitis,
whereas the Ranson score is only for alcohol induced pancreatitis. If a patient
scores 3 or more it indicates severe pancreatitis and the patient should be
transferred to ITU.
• It is scored through the mnemonic, PANCREAS:
• P - PaO2 <8kPa
• A - Age >55 years old
• N - Neutrophilia - WCC >15x10(9)/L
• C - Calcium <2 mmol/L
• R - Renal function, Urea >16 mmol/L
• E - Enzymes: LDH >600iu/L; AST >200iu/L
• A - Albumin <3.2g/L (serum)
• S - Sugar: blood glucose >10 mmol/L
• The Glasgow criteria is valid for both gallstone and alcohol induced pancreatitis,
whereas the Ranson score is only for alcohol induced pancreatitis. If a patient
scores 3 or more it indicates severe pancreatitis and the patient should be
transferred to ITU.
• It is scored through the mnemonic, PANCREAS:
• P - PaO2 <8kPa
• A - Age >55 years old
• N - Neutrophilia - WCC >15x10(9)/L
• C - Calcium <2 mmol/L
• R - Renal function, Urea >16 mmol/L
• E - Enzymes: LDH >600iu/L; AST >200iu/L
• A - Albumin <3.2g/L (serum)
• S - Sugar: blood glucose >10 mmol/L
Acute Pancreatitis
54. BISAP score
Bedside index of severity in AP
BISAP score
Bedside index of severity in AP
• 1.BUN > 25MG/dL
• 2. Impaired mental status ( GCS score < 15)
• 3.SIRS score _>2
• 4.Age > 60 yrs.
• 5.Pleural effusion
• 1.BUN > 25MG/dL
• 2. Impaired mental status ( GCS score < 15)
• 3.SIRS score _>2
• 4.Age > 60 yrs.
• 5.Pleural effusion
Acute Pancreatitis
55. Balthazar criteriaBalthazar criteria
• Developed in the early 1990s by Emil J. Balthazar et al. the Computed
Tomography Severity Index (CTSI) is a grading system used to determine the
severity of acute pancreatitis. The numerical CTSI has a maximum of ten
points, and is the sum of the Balthazar grade points and pancreatic necrosis
grade points:
• Balthazar Grade Appearance on CT CT Grade Points
• Grade A Normal CT 0 points
• Grade B Focal or diffuse enlargement of the pancreas 1 point
• Grade C Pancreatic gland abnormalities and
• peripancreatic inflammation 2 points
• Grade D Fluid collection in a single location 3 points
• Grade E Two or more fluid collections and / or gas 4 points
bubbles in or adjacent to pancreas
• Developed in the early 1990s by Emil J. Balthazar et al. the Computed
Tomography Severity Index (CTSI) is a grading system used to determine the
severity of acute pancreatitis. The numerical CTSI has a maximum of ten
points, and is the sum of the Balthazar grade points and pancreatic necrosis
grade points:
• Balthazar Grade Appearance on CT CT Grade Points
• Grade A Normal CT 0 points
• Grade B Focal or diffuse enlargement of the pancreas 1 point
• Grade C Pancreatic gland abnormalities and
• peripancreatic inflammation 2 points
• Grade D Fluid collection in a single location 3 points
• Grade E Two or more fluid collections and / or gas 4 points
bubbles in or adjacent to pancreas
Acute Pancreatitis
56. Balthazar criteriaBalthazar criteria
• Necrosis Score
• Necrosis Percentage Points
• No necrosis 0 points
• 0 to 30% necrosis 2 points
• 30 to 50% necrosis 4 points
• Over 50% necrosis 6 points
• CTSI's staging of acute pancreatitis severity has been shown by a number of studies
to provide more accurate assessment than APACHE II, Ranson, and C-reactive
protein (CRP) level. However, a few studies indicate that CTSI is not significantly
associated with the prognosis of hospitalization in patients with pancreatic necrosis,
nor is it an accurate predictor of AP severity.
CTSI – 0-3 =mortality 3%, morbidity -8%
• CTSI- 4-6 = mortality 6%, morbidity -35%
• CTSI -7-10 = mortality 17%, morbidity- 92 %
• Necrosis Score
• Necrosis Percentage Points
• No necrosis 0 points
• 0 to 30% necrosis 2 points
• 30 to 50% necrosis 4 points
• Over 50% necrosis 6 points
• CTSI's staging of acute pancreatitis severity has been shown by a number of studies
to provide more accurate assessment than APACHE II, Ranson, and C-reactive
protein (CRP) level. However, a few studies indicate that CTSI is not significantly
associated with the prognosis of hospitalization in patients with pancreatic necrosis,
nor is it an accurate predictor of AP severity.
CTSI – 0-3 =mortality 3%, morbidity -8%
• CTSI- 4-6 = mortality 6%, morbidity -35%
• CTSI -7-10 = mortality 17%, morbidity- 92 %
Acute Pancreatitis
69. Imaging
An early CT may be misleading concerning the
severity of the pancreatitis, since it can underestimate
the presence and amount of necrosis.
Early CT is only recommended when the diagnosis is
uncertain, or in case of suspected early complications
such as perforation or ischemia.
An early CT may be misleading concerning the
severity of the pancreatitis, since it can underestimate
the presence and amount of necrosis.
Early CT is only recommended when the diagnosis is
uncertain, or in case of suspected early complications
such as perforation or ischemia.
golden rule
76. Management questionsManagement questions
• When should patients admitted with AP be monitored in an
ICU or step-down unit?
• When do I order a CT scan?
• Should patients with SAP receive prophylactic abx?
• What is the optimal mode and timing of nutritional support
for the patient with SAP?
• Under what circumstances should patients with gallstone
pancreatitis undergo interventions to clear the bile duct?
• What are the indications for surgery in AP; optimal timing
for intervention, and roles for less invasive approaches
including percutaneous drainage and laparoscopy?
• When should patients admitted with AP be monitored in an
ICU or step-down unit?
• When do I order a CT scan?
• Should patients with SAP receive prophylactic abx?
• What is the optimal mode and timing of nutritional support
for the patient with SAP?
• Under what circumstances should patients with gallstone
pancreatitis undergo interventions to clear the bile duct?
• What are the indications for surgery in AP; optimal timing
for intervention, and roles for less invasive approaches
including percutaneous drainage and laparoscopy?
Acute Pancreatitis
77. When Do I Transfer to the Unit ?When Do I Transfer to the Unit ?
• Severe pancreatitis
• Multi-organ failure
– Pulmonary
– Renal
• Consider it if you are placing the patient on
antibiotics and/or ordering a CT to evaluate
non-improvement
• Severe pancreatitis
• Multi-organ failure
– Pulmonary
– Renal
• Consider it if you are placing the patient on
antibiotics and/or ordering a CT to evaluate
non-improvement
Acute Pancreatitis
78. Severe Pancreatitis
Atlanta criteria
Severe Pancreatitis
Atlanta criteria
• Organ Failure
– i.e. systolic blood pressure <90 mm Hg, PaO2
<60 mm Hg, serum creatinine >2
mg/dL, >500 mL/24 h GI bleeding OR
• Local Complications
– Necrosis
– Abscess
– Pseudocyst OR
• Unfavorable Early Prognostic Signs
– ≥ 3 Ranson's signs OR
– ≥ 8 APACHE-II points
• Organ Failure
– i.e. systolic blood pressure <90 mm Hg, PaO2
<60 mm Hg, serum creatinine >2
mg/dL, >500 mL/24 h GI bleeding OR
• Local Complications
– Necrosis
– Abscess
– Pseudocyst OR
• Unfavorable Early Prognostic Signs
– ≥ 3 Ranson's signs OR
– ≥ 8 APACHE-II points
Acute Pancreatitis
80. When Do I Order A CT?When Do I Order A CT?
• If the patient has…..
– Signs of severe acute pancreatitis
– No signs of clinical improvement after several days
– Diagnostic dilemma
– Infection suspected
• T > 101o
F
• Positive blood cultures
• What kind of CT?
– Dynamic with rapid bolus IV contrast
• What are you looking for?
– Necrosis: Lack of enhancement with contrast
– Fluid Collections
– Alternate diagnosis
• If the patient has…..
– Signs of severe acute pancreatitis
– No signs of clinical improvement after several days
– Diagnostic dilemma
– Infection suspected
• T > 101o
F
• Positive blood cultures
• What kind of CT?
– Dynamic with rapid bolus IV contrast
• What are you looking for?
– Necrosis: Lack of enhancement with contrast
– Fluid Collections
– Alternate diagnosis
Acute Pancreatitis
81. CT FindingsCT Findings
• Pancreas
– Pancreatic enlargement
– Decreased density due to edema
– Intrapancreatic fluid collections
– Blurring of gland margins due to inflammation
• Peripancreatic
– Fluid collections and stranding densities
– Thickening of retroperitoneal fat
• Pancreas
– Pancreatic enlargement
– Decreased density due to edema
– Intrapancreatic fluid collections
– Blurring of gland margins due to inflammation
• Peripancreatic
– Fluid collections and stranding densities
– Thickening of retroperitoneal fat
Acute Pancreatitis
* It may take up to 72h for inflammatory changes to become apparent on CT ** It may take up to 72h for inflammatory changes to become apparent on CT ** It may take up to 72h for inflammatory changes to become apparent on CT ** It may take up to 72h for inflammatory changes to become apparent on CT *
82. Acute Pancreatitis
POINTSPOINTS
GradeGrade of Acute Pancreatitis
A = Normal pancreas 0
B = Pancreatic enlargement 1
C = Pancreatic/peripancreatic
inflammation 2
D = Single peripancreatic fluid collection 3
E = Multiple fluid collections 4
Grade E = 50% chance of developing an infection and 15% chance of deathGrade E = 50% chance of developing an infection and 15% chance of death
DegreeDegree of Necrosis
No necrosis 0
Necrosis of one third of pancreas 2
Necrosis of one half of pancreas 4
Necrosis of more than one half 6
CT Severity Index = Grade + Degree of necrosis
POINTSPOINTS
GradeGrade of Acute Pancreatitis
A = Normal pancreas 0
B = Pancreatic enlargement 1
C = Pancreatic/peripancreatic
inflammation 2
D = Single peripancreatic fluid collection 3
E = Multiple fluid collections 4
Grade E = 50% chance of developing an infection and 15% chance of deathGrade E = 50% chance of developing an infection and 15% chance of death
DegreeDegree of Necrosis
No necrosis 0
Necrosis of one third of pancreas 2
Necrosis of one half of pancreas 4
Necrosis of more than one half 6
CT Severity Index = Grade + Degree of necrosis
84. Management
Mild-Moderate
Management
Mild-Moderate
• NPO with IVF (crystalloids)
– Colloid (blood if Hct <25, albumin if serum alb <2)
– Patients with acute pancreatitis lose a large amount of fluids to third space
into the retroperitoneum and intra-abdominal area. Prompt IV hydration
within the first 24 hours. Especially in the early phase of the illness, aggressive
fluid resuscitation is critically important
• Central venous pressure, pulmonary artery wedge pressure, and urine
output (>0.5 mL/kg/h) can be followed up as markers of adequate
hydration.
• Generous narcotics
• NGT decompression
– if frequent emesis or evidence of ileus on plain films
• Start clear liquids when pain/anorexia resolve
• NPO with IVF (crystalloids)
– Colloid (blood if Hct <25, albumin if serum alb <2)
– Patients with acute pancreatitis lose a large amount of fluids to third space
into the retroperitoneum and intra-abdominal area. Prompt IV hydration
within the first 24 hours. Especially in the early phase of the illness, aggressive
fluid resuscitation is critically important
• Central venous pressure, pulmonary artery wedge pressure, and urine
output (>0.5 mL/kg/h) can be followed up as markers of adequate
hydration.
• Generous narcotics
• NGT decompression
– if frequent emesis or evidence of ileus on plain films
• Start clear liquids when pain/anorexia resolve
Acute Pancreatitis
85. • Nutritional support
• Mild uncomplicated pancreatitis, no benefit is observed from nutritional support,
only IV dextrose 5% in water (D5W) suffices; oral feedings should be initiated
early.
• Moderate-to-severe pancreatitis, begin nutritional support early in the course of
management, as soon as stabilization of fluid and hemodynamic parameters
permits; optimally, nasojejunal feedings with a low-fat formulation should be
initiated.
• Total parenteral nutrition (TPN) may be required when patients cannot meet their
caloric needs with enteral nutrition or when adequate jejunal access cannot be
maintained; the TPN solution should include fat emulsions in amounts sufficient
to prevent essential fatty acid deficiency
• If surgery is required a feeding jejunostomy at the time of the operation; use a
low-fat formula
• Begin oral feedings once abdominal pain has resolved and the patient regains
appetite; the diet should be low in fat and protein
• Nutritional support
• Mild uncomplicated pancreatitis, no benefit is observed from nutritional support,
only IV dextrose 5% in water (D5W) suffices; oral feedings should be initiated
early.
• Moderate-to-severe pancreatitis, begin nutritional support early in the course of
management, as soon as stabilization of fluid and hemodynamic parameters
permits; optimally, nasojejunal feedings with a low-fat formulation should be
initiated.
• Total parenteral nutrition (TPN) may be required when patients cannot meet their
caloric needs with enteral nutrition or when adequate jejunal access cannot be
maintained; the TPN solution should include fat emulsions in amounts sufficient
to prevent essential fatty acid deficiency
• If surgery is required a feeding jejunostomy at the time of the operation; use a
low-fat formula
• Begin oral feedings once abdominal pain has resolved and the patient regains
appetite; the diet should be low in fat and protein
Acute Pancreatitis
87. When Do I Start Antibiotics?When Do I Start Antibiotics?
• Acute pancreatitis is c/b infection ~ 10%
• 30-50% of those with necrosis get infection
• Prophylactic antibiotics
– Controversial
• No benefit in mild ALC. pancreatitis
• Imipenem or meropenem in necrotizing pancreatitis
• Selective gut decontamination may be beneficial
• Abx do not appear to promote fungal infection
• General recommendations for use:
– Biliary pancreatitis with signs of cholangitis
– > 30% necrosis on CT scan
• Acute pancreatitis is c/b infection ~ 10%
• 30-50% of those with necrosis get infection
• Prophylactic antibiotics
– Controversial
• No benefit in mild ALC. pancreatitis
• Imipenem or meropenem in necrotizing pancreatitis
• Selective gut decontamination may be beneficial
• Abx do not appear to promote fungal infection
• General recommendations for use:
– Biliary pancreatitis with signs of cholangitis
– > 30% necrosis on CT scan
Acute Pancreatitis
88. Antibiotics - EBMAntibiotics - EBM
Antibiotic therapy for prophylaxis against
infection of pancreatic necrosis in acute
pancreatitis.
Cochrane Database of Systematic Reviews. 3, 2005
Antibiotic therapy for prophylaxis against
infection of pancreatic necrosis in acute
pancreatitis.
Cochrane Database of Systematic Reviews. 3, 2005
Acute Pancreatitis
Despite variations in drug agent, case mix, duration of treatment and
methodological quality (especially the lack of double blinded studies),
there was strong evidence that intravenous antibiotic prophylactic
therapy for 10 to 14 days decreased the risk of super-infection of
necrotic tissue and mortality in patients with severe acute pancreatitis
with proven pancreatic necrosis at CT
Despite variations in drug agent, case mix, duration of treatment and
methodological quality (especially the lack of double blinded studies),
there was strong evidence that intravenous antibiotic prophylactic
therapy for 10 to 14 days decreased the risk of super-infection of
necrotic tissue and mortality in patients with severe acute pancreatitis
with proven pancreatic necrosis at CT
89. A final word on antibioticsA final word on antibiotics
• Do not use empirically early in mild
pancreatitis
• Fever early in the disease process is almost
universally secondary to the inflammatory
response and NOT an infectious process
• Do not use empirically early in mild
pancreatitis
• Fever early in the disease process is almost
universally secondary to the inflammatory
response and NOT an infectious process
Acute Pancreatitis
90. When can he eat ?
Nutritional issues in AP
• TPN vs. enteral feeding
– Not TPN per meta-analysis but …*
– NJ not NG
• Early initiation of enteral nutrition in severe AP
• tube feed if anticipate NPO > 1 week
• may be unnecessary for mild AP
– Reduce microbial translocation
– Enhance gut mucosal blood flow
– Promote gut mucosal surface immunity
Acute Pancreatitis
Reduce incidence ofReduce incidence of
infected necrosisinfected necrosis
Reduce incidence ofReduce incidence of
infected necrosisinfected necrosis
** 6 older studies, relationship b/w glycemic control and infectious risk may confound vs. TPN6 older studies, relationship b/w glycemic control and infectious risk may confound vs. TPN
91. NutritionNutrition
• Mild pancreatitis
– Calories from IVF (D5W)
are sufficient
– No benefit from
additional nutritional
support
– Oral intake advancing to
low fat diet once
pain/anorexia resolve
• Mild pancreatitis
– Calories from IVF (D5W)
are sufficient
– No benefit from
additional nutritional
support
– Oral intake advancing to
low fat diet once
pain/anorexia resolve
• Moderate/Severe
– Begin nutritional support
as early as possible
• NJ tube preferred
– TPN only if :
• Can’t maintain adequate
jejunal access
• Unable to meet caloric
demands enterally
• Moderate/Severe
– Begin nutritional support
as early as possible
• NJ tube preferred
– TPN only if :
• Can’t maintain adequate
jejunal access
• Unable to meet caloric
demands enterally
Acute Pancreatitis
93. When Do I Consult GI Person ?When Do I Consult GI Person ?
• Evidence of biliary pancreatitis
– Elevated LFTs + pancreatitis
• No matter what the US shows
• Severe pancreatitis
• Recurrent unexplained pancreatitis
• Rule out infected necrosis
• EUS FNA sampling of fluid collections
• Endoscopic treatment of necrosis/abscess
• Evidence of biliary pancreatitis
– Elevated LFTs + pancreatitis
• No matter what the US shows
• Severe pancreatitis
• Recurrent unexplained pancreatitis
• Rule out infected necrosis
• EUS FNA sampling of fluid collections
• Endoscopic treatment of necrosis/abscess
Acute Pancreatitis
94. Biliary pancreatitisBiliary pancreatitis
• Q: When should I suspect it ?
– A: Always
• Q: How do I evaluate for it ?
– A: EUS and LFTs
• Q: When is ERCP indicated ?
– A: 3 studies looked at emergency (within 24-72h)
ERCP with EUS vs standard therapy in biliary AP
• Q: When should I suspect it ?
– A: Always
• Q: How do I evaluate for it ?
– A: EUS and LFTs
• Q: When is ERCP indicated ?
– A: 3 studies looked at emergency (within 24-72h)
ERCP with EUS vs standard therapy in biliary AP
Acute Pancreatitis
95. Management of Pancreatic
Complications- objectives
• Acute fluid collections
– Occur early, seen not felt
– No defined wall ∴ usually resolve spontaneously
– NO routine percutaneous or operative drainage
• may infect otherwise sterile tissue
• Infected pancreatic necrosis
• Pancreatic abscess
• Pseudocysts
• Gallstones with CBD stones
• Pancreatic duct disruption with ascites
• Acute fluid collections
– Occur early, seen not felt
– No defined wall ∴ usually resolve spontaneously
– NO routine percutaneous or operative drainage
• may infect otherwise sterile tissue
• Infected pancreatic necrosis
• Pancreatic abscess
• Pseudocysts
• Gallstones with CBD stones
• Pancreatic duct disruption with ascites
Acute Pancreatitis
96. Management of Pancreatic
Complications
• Infected Pancreatic
necrosis
– Organisms on gram stain
after aspirate
– Surgical drainage
– Trans-gastric drainage
– Try to delay necrosectomy 2-
3wk for demarcation of
necrosis
• Pancreatic abscess
– CT or EUS guided
drainage
• Walled collection of pus
• Similar to management
of pseudocyst
• Pancreatic abscess
– CT or EUS guided
drainage
• Walled collection of pus
• Similar to management
of pseudocyst
Acute Pancreatitis
100. Complications of PseudocystComplications of Pseudocyst
• Infection - 14%
• Rupture - 6.8%
• Hemorrhage - 6.5%
• Common bile duct obstruction - 6.3%
• GI obstruction - 2.6%
• Infection - 14%
• Rupture - 6.8%
• Hemorrhage - 6.5%
• Common bile duct obstruction - 6.3%
• GI obstruction - 2.6%
Acute Pancreatitis
101. Pseudocyst Management
• Old thought
– Pseudocysts > 5 cm that have been present > 6
weeks must be drained
• Current practice
– Asymptomatic pseudocysts, regardless of size, do
not require treatment
• Old thought
– Pseudocysts > 5 cm that have been present > 6
weeks must be drained
• Current practice
– Asymptomatic pseudocysts, regardless of size, do
not require treatment
Acute Pancreatitis
107. Pancreatic Ascites and Pancreaticopleural FistulasPancreatic Ascites and Pancreaticopleural Fistulas
Acute Pancreatitis
Abdominal drainage endoscopic placement pancreatic stent
across the disruption.
Surgical distal resection and closure of the proximal stump
Abdominal drainage endoscopic placement pancreatic stent
across the disruption.
Surgical distal resection and closure of the proximal stump
108. NecresectomyNecresectomy
Acute Pancreatitis
Surgical intervention - minimally invasive or conventional open
techniques, is indicated when an anatomic complication
amenable to a mechanical solution is present (eg, acute
necrotizing pancreatitis)
The necrotic phlegmon is excised to limit the source of sepsis or
hemorrhagic pancreatitis to control of bleeding
Depending on the situation and local expertise, this may require
the talents of an interventional radiologist, an interventional
endoscopist, or surgeon (individually or in combination).
Surgical intervention - minimally invasive or conventional open
techniques, is indicated when an anatomic complication
amenable to a mechanical solution is present (eg, acute
necrotizing pancreatitis)
The necrotic phlegmon is excised to limit the source of sepsis or
hemorrhagic pancreatitis to control of bleeding
Depending on the situation and local expertise, this may require
the talents of an interventional radiologist, an interventional
endoscopist, or surgeon (individually or in combination).
111. Vascular ComplicationsVascular Complications
Acute Pancreatitis
Splenic artery, superior mesenteric, cystic and gastroduodenal arteries
Pancreatic elastase damages the vessels with pseudoaneurysm
formation.
Spontaneous rupture massive bleeding sudden onset of abdominal pain,
tachycardia and hypotension,
T/T -
Arterial embolization. Refractory cases require ligation of the vessel
affected mortality 28% to 56%.
Vascular thrombosis splenic vein portal venous system.
Recurrent episodes of UGI l bleeding /venous hypertension >
splenectomy
Splenic artery, superior mesenteric, cystic and gastroduodenal arteries
Pancreatic elastase damages the vessels with pseudoaneurysm
formation.
Spontaneous rupture massive bleeding sudden onset of abdominal pain,
tachycardia and hypotension,
T/T -
Arterial embolization. Refractory cases require ligation of the vessel
affected mortality 28% to 56%.
Vascular thrombosis splenic vein portal venous system.
Recurrent episodes of UGI l bleeding /venous hypertension >
splenectomy
112. Gallstone pancreatitisGallstone pancreatitis
Acute Pancreatitis
Gallstone pancreatitis that is not responding to supportive
therapy or with ascending cholangitis with worsening signs
and symptoms of obstruction, early endoscopic retrograde
cholangiopancreatography (ERCP) with sphincterotomy and
stone extraction is indicated.
Gallstone pancreatitis that is not responding to supportive
therapy or with ascending cholangitis with worsening signs
and symptoms of obstruction, early endoscopic retrograde
cholangiopancreatography (ERCP) with sphincterotomy and
stone extraction is indicated.
Laparoscopic or open cholecystectomy to be done after 4
to 6 weeks
Laparoscopic or open cholecystectomy to be done after 4
to 6 weeks
113. Pancreatic duct disruptionPancreatic duct disruption
Acute Pancreatitis
Damage to the pancreatic ductal system may allow pancreatic
juice to leak from the gland. The sudden development of
hypocalcemia or a rapid increase in retroperitoneal fluid on
computed tomography (CT)
Damage to the pancreatic ductal system may allow pancreatic
juice to leak from the gland. The sudden development of
hypocalcemia or a rapid increase in retroperitoneal fluid on
computed tomography (CT)
Percutaneous placement of a drainage tube into the fluid collection
Transpapillary stent placement or, preferably, placement of a 6 French
nasopancreatic tube attached to an external bulb suction device
Refractory cases may warrant surgery. If the persistent leak is present in
the tail of the gland, a distal pancreatectomy is preferred. If the leak is in
the head of the gland, a Whipple procedure is the operation of choice.
Percutaneous placement of a drainage tube into the fluid collection
Transpapillary stent placement or, preferably, placement of a 6 French
nasopancreatic tube attached to an external bulb suction device
Refractory cases may warrant surgery. If the persistent leak is present in
the tail of the gland, a distal pancreatectomy is preferred. If the leak is in
the head of the gland, a Whipple procedure is the operation of choice.
114. Pancreatic abscessPancreatic abscess
Acute Pancreatitis
Pancreatic abscesses generally occur late in the course of pancreatitis. Many of
these respond to percutaneous catheter drainage and antibiotics. Those that
do not respond require surgical debridement and drainage.
Pancreatic abscesses generally occur late in the course of pancreatitis. Many of
these respond to percutaneous catheter drainage and antibiotics. Those that
do not respond require surgical debridement and drainage.
118. Famous people who have had
pancreatitis
Famous people who have had
pancreatitis
• Alexander the Great
• Ludwig von Beethoven
• Dizzie Gillespie
• Maximilian Schell
• Matthew Perry
• John Ashcroft
• Alexander the Great
• Ludwig von Beethoven
• Dizzie Gillespie
• Maximilian Schell
• Matthew Perry
• John Ashcroft
Acute Pancreatitis
119. Closing PointsClosing Points
• 4 out of 5 patients have mild uneventful pancreatitis
• If the patient is not getting considerably better in 36-
48 hrs, start thinking about that “5th patient”
• A CT is that 5th patient’s friend
• If you are thinking about antibiotics, you should be
thinking about a CT and a few consultations.
• The pancreas is a mean organ….respect it
• 4 out of 5 patients have mild uneventful pancreatitis
• If the patient is not getting considerably better in 36-
48 hrs, start thinking about that “5th patient”
• A CT is that 5th patient’s friend
• If you are thinking about antibiotics, you should be
thinking about a CT and a few consultations.
• The pancreas is a mean organ….respect it
Acute Pancreatitis
120. Take home messageTake home message
Severity of acute pancreatitis and pancreatic necrosis can only be reliably
assessed by imaging after 72 hours.
• Absence of pancreatic parenchymal necrosis does not preclude a serious
course of the illness.
• CT cannot reliably differentiate between collections that consist of fluid and
those that contain solid debris.
• In these cases MRI can be of additional value.
• Name collections always according to 2012 Atlanta definitions.
• Central gland necrosis is a subtype of necrotizing pancreatitis with important
implications.
• ERCP is the procedure of choice in mild to mod. Cases, with CBD stone
induced pancreatitis, Gallstone t/t after 4-6 weeks.
Severity of acute pancreatitis and pancreatic necrosis can only be reliably
assessed by imaging after 72 hours.
• Absence of pancreatic parenchymal necrosis does not preclude a serious
course of the illness.
• CT cannot reliably differentiate between collections that consist of fluid and
those that contain solid debris.
• In these cases MRI can be of additional value.
• Name collections always according to 2012 Atlanta definitions.
• Central gland necrosis is a subtype of necrotizing pancreatitis with important
implications.
• ERCP is the procedure of choice in mild to mod. Cases, with CBD stone
induced pancreatitis, Gallstone t/t after 4-6 weeks.
A 63-year-old man with acute interstitial oedematous pancreatitis. There is peripancreatic fat stranding (arrows) without an acute peripancreatic fluid collection; the pancreas enhances completely but has a heterogeneous appearance due to oedema.
(A) Acute necrotic collections (ANC) in a 44-year-old man with acute necrotising pancreatitis involving only the peripancreatic tissues. Note enhancement of the entire pancreatic parenchyma (white stars) and the heterogeneous, non-liquid peripancreatic components in the retroperitoneum (white arrows pointing at the borders of the ANC). (B) The ANC in the same patient as (A) but imaged a few weeks later demonstrate a heterogeneous collection with areas of fat (black arrowheads) surrounded by fluid density, and areas which have a slightly greater attenuation (black arrows) than seen in collections without necrosis such as shown in figure 7. This finding is typical for peripancreatic necrosis. White arrows denote border of ANC; white stars denote enhancement of pancreatic parenchyma. The ANC are not yet fully encapsulated.
A 47-year-old man with acute necrotising pancreatitis complicated by infected pancreatic necrosis. There is a heterogeneous, acute necrotic collection (ANC) in the pancreatic and peripancreatic area (white arrows pointing at the borders of the ANC) with presence of gas bubbles (white arrowheads), usually a pathognomonic sign of infection of the necrosis (infected necrosis).