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.
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.
This document provides an overview of acute pancreatitis, including:
- The definition, classification, and pathophysiology of the disease. It involves inflammation of the pancreas that can range from mild to severe.
- Common causes or etiologies like gallstones, alcohol use, hyperlipidemia.
- Typical clinical presentation including severe abdominal pain, nausea, vomiting. Findings on physical exam can include abdominal tenderness.
- Tests and severity scores used to evaluate patients and monitor for complications. Treatment involves pain control, fluid resuscitation, and treating any underlying causes or complications. Outcomes depend on the severity of the attack.
Seminar presentation by 5th-year medical students under the supervision of in house lecturer. He was previously working as a consultant surgeon in Syria. Reference as mentioned in the slides.
Hepatic encephalopathy is a brain dysfunction caused by liver disease or portosystemic shunting. It manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subtle alterations to coma. The main neurotoxin involved is ammonia, which is normally cleared by the liver. In liver disease, ammonia builds up in the blood and brain, where it interferes with neurotransmission. Symptoms include impaired cognition, personality changes, asterixis, and eventually coma. Hepatic encephalopathy is classified based on the underlying liver disease, time course, presence of precipitating factors, and severity of symptoms.
This document provides information on pancreatic neoplasms. It begins with the anatomy of the pancreas and its blood supply. It then discusses the different types of pancreatic neoplasms, including cystic neoplasms and ductal adenocarcinoma. Risk factors for ductal adenocarcinoma are outlined. The pathogenesis and molecular progression of pancreatic cancer from pancreatic intraepithelial neoplasia to invasive cancer is described. Clinical presentation, diagnostic imaging modalities, staging, treatment options including surgery and adjuvant therapy, palliative care, and recent advances are summarized. Finally, cystic neoplasms of the pancreas including mucinous cystic neoplasms are briefly covered.
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.
This document provides an overview of acute pancreatitis, including:
- The definition, classification, and pathophysiology of the disease. It involves inflammation of the pancreas that can range from mild to severe.
- Common causes or etiologies like gallstones, alcohol use, hyperlipidemia.
- Typical clinical presentation including severe abdominal pain, nausea, vomiting. Findings on physical exam can include abdominal tenderness.
- Tests and severity scores used to evaluate patients and monitor for complications. Treatment involves pain control, fluid resuscitation, and treating any underlying causes or complications. Outcomes depend on the severity of the attack.
Seminar presentation by 5th-year medical students under the supervision of in house lecturer. He was previously working as a consultant surgeon in Syria. Reference as mentioned in the slides.
Hepatic encephalopathy is a brain dysfunction caused by liver disease or portosystemic shunting. It manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subtle alterations to coma. The main neurotoxin involved is ammonia, which is normally cleared by the liver. In liver disease, ammonia builds up in the blood and brain, where it interferes with neurotransmission. Symptoms include impaired cognition, personality changes, asterixis, and eventually coma. Hepatic encephalopathy is classified based on the underlying liver disease, time course, presence of precipitating factors, and severity of symptoms.
This document provides information on pancreatic neoplasms. It begins with the anatomy of the pancreas and its blood supply. It then discusses the different types of pancreatic neoplasms, including cystic neoplasms and ductal adenocarcinoma. Risk factors for ductal adenocarcinoma are outlined. The pathogenesis and molecular progression of pancreatic cancer from pancreatic intraepithelial neoplasia to invasive cancer is described. Clinical presentation, diagnostic imaging modalities, staging, treatment options including surgery and adjuvant therapy, palliative care, and recent advances are summarized. Finally, cystic neoplasms of the pancreas including mucinous cystic neoplasms are briefly covered.
An intestinal stoma is an artificial opening in the abdominal wall that connects the intestinal tract to the outside of the body. There are different types of stomas including ileostomies, colostomies, and urostomies. Ileostomies divert small intestine contents and have a liquid effluent that is discharged continuously. Colostomies divert large intestine contents and have solid, intermittent effluent. Stomas can be temporary or permanent depending on the clinical situation and are constructed in different ways including as an end stoma or loop stoma. Proper stoma care and use of appliances is important for managing stomas.
Portal hypertension is defined as elevated portal pressure above 10-12 mm Hg. It is classified as pre-hepatic, intra-hepatic, or post-hepatic based on the location of blockage. Common causes include liver cirrhosis and blockages in the portal vein. Clinical features include upper GI bleeding, splenomegaly, ascites, and hepatic encephalopathy. Management involves treating acute bleeding episodes endoscopically and use of beta-blockers for prevention, along with diuretics and paracentesis for ascites. More advanced treatments include TIPSS, surgical shunting, and liver transplantation.
Abdominal tuberculosis is a common extrapulmonary manifestation of tuberculosis that most commonly involves the ileocaecal region of the small intestine. It can present with nonspecific constitutional symptoms like fever, weight loss, or abdominal pain. Diagnosis is challenging as findings can mimic other diseases like Crohn's disease, but imaging modalities like ultrasound, CT scan, and barium studies can reveal features suggestive of abdominal tuberculosis like enlarged lymph nodes, bowel wall thickening, strictures, and ascites. Blood tests are often nonspecific but may show elevated ESR or mild anemia. Sputum tests have low yield for diagnosis but help evaluate for concurrent pulmonary tuberculosis. Tissue sampling is often needed for confirmation.
Gallbladder disease is common, affecting around 5% of the population. Gallstones are the most common cause of gallbladder disease and occur more often in women, with increasing age. Symptoms include biliary colic, acute cholecystitis, and in rare cases gallbladder cancer. Treatment options include oral medication, lithotripsy for single stones, and cholecystectomy for symptomatic or complicated cases. Complications can include cholangitis, pancreatitis, and choledocholithiasis requiring ERCP.
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.
The document provides information on the anatomy, physiology, and common diseases of the stomach. It describes the stomach's layers, blood supply, innervation, and motor activity. It discusses acid secretion and the roles of parietal cells, gastrin, and histamine. Common benign diseases mentioned include peptic ulcer disease and gastric lymphoma. Gastric adenocarcinoma risk factors and staging are outlined. Post-gastrectomy syndromes such as dumping syndrome and afferent loop obstruction are also summarized.
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.
Chronic pancreatitis is a chronic inflammatory condition of the pancreas characterized by progressive fibrosis of the pancreatic parenchyma and loss of function. It has multiple etiologies but alcohol use is the most common cause. Patients experience abdominal pain, steatorrhea from maldigestion, and can develop diabetes. Treatment involves pain management, pancreatic enzyme replacement, and in severe cases, surgery such as drainage procedures or pancreatic resections.
This document discusses obstructive jaundice, providing definitions, pathophysiology, effects on various body systems, etiology, history and examination findings, laboratory investigations, imaging modalities, and causes of biliary obstruction. It defines obstructive jaundice as a failure of bile to reach the intestine due to mechanical obstruction. Pathophysiological changes include bile duct dilation, hepatic fibrosis, and portal hypertension. Causes include gallstones, strictures, tumors, and congenital anomalies. A thorough history, physical exam, and lab tests can localize the level and cause of obstruction, while imaging modalities like ultrasound and MRCP can identify and characterize obstructive lesions.
The document discusses Entamoeba histolytica, a parasite that can cause liver abscesses. The most common extraintestinal symptoms are fever, right upper quadrant pain, anorexia and point tenderness in the right upper quadrant area, with jaundice being rare. Diagnostic tests for liver abscesses caused by E. histolytica include ultrasonography, CT scan, MRI, and Elisa antibody tests. Treatment is generally metronidazole, with 90% seeing a good response within 72 hours.
This document provides an overview of acute and chronic pancreatitis. Regarding acute pancreatitis, it defines the condition, discusses etiology, pathophysiology, clinical features, investigations, management, complications like pseudocyst, and outcomes. It emphasizes that acute pancreatitis is a biochemical diagnosis based on elevated serum amylase and lipase levels. For chronic pancreatitis, it defines the condition as irreversible progressive destruction of pancreatic tissue causing loss of exocrine and endocrine function and pain. Key investigations and treatments are also summarized.
This document discusses the evaluation and management of cystic tumors of the pancreas. It notes that the most common types are serous cystadenomas, mucinous cystic neoplasms, and intraductal papillary mucinous neoplasms. Initial imaging includes MRI with MRCP and EUS with FNA to characterize the cyst. Cyst fluid analysis is important to distinguish malignant potential. Small asymptomatic cysts may only need follow up imaging. Surveillance is recommended for certain non-surgical cases, monitoring for changes or malignant progression over multiple years.
This document provides an overview of the management of acute pancreatitis. It defines acute pancreatitis as the inflammation of the pancreas often associated with pancreatic duct dilation. It discusses the epidemiology, etiology, pathogenesis, clinical forms, investigations, risk assessment, treatment and prognosis of acute pancreatitis. The management involves resuscitation, assessing severity, treating any underlying causes, and monitoring for complications which can include pancreatic necrosis, infection and multi-organ failure. Severity is assessed using scoring systems like Ranson's criteria or CT severity index to determine prognosis and guide management.
1. Chronic pancreatitis represents a continuous inflammatory process of the pancreas resulting in permanent endocrine and exocrine dysfunction.
2. Chronic pancreatitis most commonly presents with abdominal pain in 95% of cases, along with weight loss, steatorrhea, and diabetes mellitus in some cases.
3. Diagnosis involves tests of pancreatic function like secretin stimulation tests and fecal elastase, as well as imaging with CT, MRI, and ERCP to detect features like pancreatic enlargement, calcifications, and ductal abnormalities.
This document outlines a seminar plan on carcinoma of the pancreas presented by Dr. Jyotindra Singh. The seminar will cover topics such as the anatomy and surgical anatomy of the pancreas, pancreatic tumors, modes of presentation, pre-operative workup, various surgeries and surgical videos, recent updates, studies and trials, and a take home message. The seminar introduction discusses that carcinoma of the exocrine pancreas accounts for over 90% of pancreatic tumors and remains an oncologic challenge with a 5-year survival rate of 3%.
The document discusses gastric outlet obstruction (GOO), which refers to any mechanical impediment to gastric emptying. It can be caused by benign or malignant conditions. Common benign causes include peptic ulcer disease and gastric polyps, while pancreatic cancer is a frequent malignant cause. Symptoms include vomiting, weight loss, and dehydration. Diagnosis involves imaging like barium studies and endoscopy. Treatment of GOO focuses on rehydration, nutritional support, and correcting electrolyte imbalances. Surgical intervention may be needed for persistent or malignant obstructions.
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 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.
An intestinal stoma is an artificial opening in the abdominal wall that connects the intestinal tract to the outside of the body. There are different types of stomas including ileostomies, colostomies, and urostomies. Ileostomies divert small intestine contents and have a liquid effluent that is discharged continuously. Colostomies divert large intestine contents and have solid, intermittent effluent. Stomas can be temporary or permanent depending on the clinical situation and are constructed in different ways including as an end stoma or loop stoma. Proper stoma care and use of appliances is important for managing stomas.
Portal hypertension is defined as elevated portal pressure above 10-12 mm Hg. It is classified as pre-hepatic, intra-hepatic, or post-hepatic based on the location of blockage. Common causes include liver cirrhosis and blockages in the portal vein. Clinical features include upper GI bleeding, splenomegaly, ascites, and hepatic encephalopathy. Management involves treating acute bleeding episodes endoscopically and use of beta-blockers for prevention, along with diuretics and paracentesis for ascites. More advanced treatments include TIPSS, surgical shunting, and liver transplantation.
Abdominal tuberculosis is a common extrapulmonary manifestation of tuberculosis that most commonly involves the ileocaecal region of the small intestine. It can present with nonspecific constitutional symptoms like fever, weight loss, or abdominal pain. Diagnosis is challenging as findings can mimic other diseases like Crohn's disease, but imaging modalities like ultrasound, CT scan, and barium studies can reveal features suggestive of abdominal tuberculosis like enlarged lymph nodes, bowel wall thickening, strictures, and ascites. Blood tests are often nonspecific but may show elevated ESR or mild anemia. Sputum tests have low yield for diagnosis but help evaluate for concurrent pulmonary tuberculosis. Tissue sampling is often needed for confirmation.
Gallbladder disease is common, affecting around 5% of the population. Gallstones are the most common cause of gallbladder disease and occur more often in women, with increasing age. Symptoms include biliary colic, acute cholecystitis, and in rare cases gallbladder cancer. Treatment options include oral medication, lithotripsy for single stones, and cholecystectomy for symptomatic or complicated cases. Complications can include cholangitis, pancreatitis, and choledocholithiasis requiring ERCP.
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.
The document provides information on the anatomy, physiology, and common diseases of the stomach. It describes the stomach's layers, blood supply, innervation, and motor activity. It discusses acid secretion and the roles of parietal cells, gastrin, and histamine. Common benign diseases mentioned include peptic ulcer disease and gastric lymphoma. Gastric adenocarcinoma risk factors and staging are outlined. Post-gastrectomy syndromes such as dumping syndrome and afferent loop obstruction are also summarized.
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.
Chronic pancreatitis is a chronic inflammatory condition of the pancreas characterized by progressive fibrosis of the pancreatic parenchyma and loss of function. It has multiple etiologies but alcohol use is the most common cause. Patients experience abdominal pain, steatorrhea from maldigestion, and can develop diabetes. Treatment involves pain management, pancreatic enzyme replacement, and in severe cases, surgery such as drainage procedures or pancreatic resections.
This document discusses obstructive jaundice, providing definitions, pathophysiology, effects on various body systems, etiology, history and examination findings, laboratory investigations, imaging modalities, and causes of biliary obstruction. It defines obstructive jaundice as a failure of bile to reach the intestine due to mechanical obstruction. Pathophysiological changes include bile duct dilation, hepatic fibrosis, and portal hypertension. Causes include gallstones, strictures, tumors, and congenital anomalies. A thorough history, physical exam, and lab tests can localize the level and cause of obstruction, while imaging modalities like ultrasound and MRCP can identify and characterize obstructive lesions.
The document discusses Entamoeba histolytica, a parasite that can cause liver abscesses. The most common extraintestinal symptoms are fever, right upper quadrant pain, anorexia and point tenderness in the right upper quadrant area, with jaundice being rare. Diagnostic tests for liver abscesses caused by E. histolytica include ultrasonography, CT scan, MRI, and Elisa antibody tests. Treatment is generally metronidazole, with 90% seeing a good response within 72 hours.
This document provides an overview of acute and chronic pancreatitis. Regarding acute pancreatitis, it defines the condition, discusses etiology, pathophysiology, clinical features, investigations, management, complications like pseudocyst, and outcomes. It emphasizes that acute pancreatitis is a biochemical diagnosis based on elevated serum amylase and lipase levels. For chronic pancreatitis, it defines the condition as irreversible progressive destruction of pancreatic tissue causing loss of exocrine and endocrine function and pain. Key investigations and treatments are also summarized.
This document discusses the evaluation and management of cystic tumors of the pancreas. It notes that the most common types are serous cystadenomas, mucinous cystic neoplasms, and intraductal papillary mucinous neoplasms. Initial imaging includes MRI with MRCP and EUS with FNA to characterize the cyst. Cyst fluid analysis is important to distinguish malignant potential. Small asymptomatic cysts may only need follow up imaging. Surveillance is recommended for certain non-surgical cases, monitoring for changes or malignant progression over multiple years.
This document provides an overview of the management of acute pancreatitis. It defines acute pancreatitis as the inflammation of the pancreas often associated with pancreatic duct dilation. It discusses the epidemiology, etiology, pathogenesis, clinical forms, investigations, risk assessment, treatment and prognosis of acute pancreatitis. The management involves resuscitation, assessing severity, treating any underlying causes, and monitoring for complications which can include pancreatic necrosis, infection and multi-organ failure. Severity is assessed using scoring systems like Ranson's criteria or CT severity index to determine prognosis and guide management.
1. Chronic pancreatitis represents a continuous inflammatory process of the pancreas resulting in permanent endocrine and exocrine dysfunction.
2. Chronic pancreatitis most commonly presents with abdominal pain in 95% of cases, along with weight loss, steatorrhea, and diabetes mellitus in some cases.
3. Diagnosis involves tests of pancreatic function like secretin stimulation tests and fecal elastase, as well as imaging with CT, MRI, and ERCP to detect features like pancreatic enlargement, calcifications, and ductal abnormalities.
This document outlines a seminar plan on carcinoma of the pancreas presented by Dr. Jyotindra Singh. The seminar will cover topics such as the anatomy and surgical anatomy of the pancreas, pancreatic tumors, modes of presentation, pre-operative workup, various surgeries and surgical videos, recent updates, studies and trials, and a take home message. The seminar introduction discusses that carcinoma of the exocrine pancreas accounts for over 90% of pancreatic tumors and remains an oncologic challenge with a 5-year survival rate of 3%.
The document discusses gastric outlet obstruction (GOO), which refers to any mechanical impediment to gastric emptying. It can be caused by benign or malignant conditions. Common benign causes include peptic ulcer disease and gastric polyps, while pancreatic cancer is a frequent malignant cause. Symptoms include vomiting, weight loss, and dehydration. Diagnosis involves imaging like barium studies and endoscopy. Treatment of GOO focuses on rehydration, nutritional support, and correcting electrolyte imbalances. Surgical intervention may be needed for persistent or malignant obstructions.
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 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.
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
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.
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.
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
Acute pancreatitis is a condition where pancreatic enzymes leak into the pancreas and cause its auto-digestion. Common causes include gallstones, alcohol use, and idiopathic factors. Patients present with epigastric pain radiating to the back that is exacerbated by eating or lying down. Lab tests show elevated pancreatic enzymes and imaging shows changes to the pancreas. Treatment is supportive with NPO, IV fluids, pain control and monitoring for complications like necrosis, pseudocysts, shock and respiratory failure. Severe cases may require ERCP, surgery or drainage procedures.
1. The document discusses chronic pancreatitis, providing details on its history, anatomy, physiology, classification, types, risk factors, and symptoms.
2. Chronic pancreatitis is characterized by persistent inflammation and irreversible fibrosis of the pancreas that decreases quality of life and can cause pain and exocrine/endocrine insufficiency.
3. Heavy alcohol consumption is the most common cause, accounting for 70-80% of cases, while other risks include genetic mutations, duct obstructions, trauma, and tropical or autoimmune etiologies.
This document summarizes the updated 2013 classification of acute pancreatitis published in the journal Gut. It defines acute pancreatitis diagnosis requiring two of three criteria: abdominal pain, elevated lipase/amylase, characteristic CT findings. CT is indicated if clinical diagnosis is doubtful, severity is high, or complications are suspected and can identify two types: interstitial edematous pancreatitis and necrotizing pancreatitis. Collections are also defined including acute peripancreatic fluid collections in interstitial cases, acute necrotic collections in necrotizing cases, and pseudocysts or walled-off necrosis in later encapsulated collections. Reporting requirements for imaging findings are discussed.
Acute pancreatitis atlanta classification & managementSeneeth Peramuna
Acute Pancreatitis
Definition,
Etialogy and pathogenesis
Atlanta Revised classification
Initial risk assesment
Management of general condition, local and systemic complications
BISAP score
Modified Marshall score
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.
Evidence Based Treatment of Acute Pancreatitis 2013Waleed Mahrous
The document summarizes guidelines for the diagnosis and management of acute pancreatitis. It addresses criteria for diagnosis, risk stratification based on severity (mild, moderately severe, severe), initial assessment including fluid resuscitation goals, nutritional support, and recommendations for enteral versus parenteral nutrition based on severity. The guidelines emphasize early aggressive fluid resuscitation, monitoring for organ failure, and initiating enteral nutrition in severe cases to prevent infectious complications while avoiding parenteral nutrition.
severe acute pancreatitis has high mortality rate and there is always confusions in between physicians. This topic is about management of acute pancreatitis its complications and ongoing controvercies. hope this will help and clear the doubts among physicians, residents and medical students
The document discusses acute pancreatitis, including its increasing incidence, mortality rates, definition, etiology, pathophysiology, clinical features, diagnosis, and assessments like Ranson's criteria. It notes that acute pancreatitis is defined as acute inflammation of the pancreatic parenchyma leading to injury or destruction of acinar cells. Common causes include gallstones, alcohol abuse, metabolic factors like hypertriglyceridemia, drugs, trauma, and infections. Clinical features may include epigastric pain, nausea, vomiting, and jaundice. Diagnosis involves blood tests like serum amylase and lipase levels, as well as imaging like ultrasound and CT scan. Prognosis can be assessed using tools like Ranson
Este documento trata sobre la pancreatitis. Explica la anatomía, fisiología, etiología, patogenia y clasificación de la pancreatitis aguda y crónica. También discute los factores de riesgo como la litiasis biliar y el consumo excesivo de alcohol, así como los síntomas, complicaciones y tratamiento de esta enfermedad.
This document discusses the diagnosis and management of acute pancreatitis in a 22-year-old male patient presenting with epigastric pain. It examines the use of amylase and lipase tests to diagnose acute pancreatitis, describes clinical features and scoring systems to assess severity, and discusses management issues including fluid resuscitation, antibiotics, nutrition, ERCP, surgery, and monitoring organ function with Ranson's criteria and CT severity index.
Acute pancreatitis is a common medical problem. Initial phase of acute pancreatitis is characterized by inflammation. This is caused by release of cytokines and other pro inflammatory mediators. These further cause vasodilatation, intravascular volume depletion, and end organ hypoperfusion. The etiology can be varied but common causes are biliary (stone in CBD) and alcohol. Other causes are drugs, infections, trauma, idiopathic, post ERCP etc. Patients with severe pancreatitis have high risk of mortality (10%) which can go upto 30% if necrosis gets infected, which occurs in about 40% patients. Further, persistent organ failure increases the mortality up to 34–55% as compared to 0.3% with transient organ failure. Traditionally as per Atlanta classification, acute pancreatitis has been classified as mild or severe depending upon organ failure or local complications. Acute pancreatitis is a hyper-catabolic state. Moreover some of these patients may be malnourished to begin with (alcoholics). Thus their nutritional requirements are much more than ordinary person. There are good quality studies available to show that in absence of cholangitis, there is no benefit of doing early ERCP. Also, technically it is more difficult to do in such situations, and procedure related complication may be more. If in doubt, it may be worthwhile to do endoscopic ultrasound to document the presence of CBD stone before attempting to cannulate the CBD.
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.
This document discusses pancreatitis, including its anatomy, physiology, etiology, clinical presentation, diagnosis, prognosis, management, and complications. Pancreatitis is defined as inflammation of the pancreas and can be acute or chronic. Acute pancreatitis is commonly caused by gallstones or alcohol and may range from mild to severe, with severe cases involving pancreatic necrosis and multi-organ failure. Diagnosis involves blood tests measuring amylase and lipase along with imaging like CT. Management depends on severity but generally involves hospitalization, IV fluids, pain control, and monitoring for complications.
The document discusses acute pancreatitis, including causes, clinical features, diagnosis, severity grading, management, and prognosis. Gallstones and alcohol are the most common causes. Scoring systems like Ranson criteria and APACHE II can help indicate severity and prognosis. Management involves treatment of the underlying cause, supportive care, and monitoring for complications like pancreatic necrosis which may require intervention.
This document summarizes an article from the New England Journal of Medicine about acute pancreatitis. It provides details on the pathogenesis, diagnosis, and management of acute pancreatitis. It discusses risk factors, causes, predictors of severe disease, and treatments including fluid resuscitation, determining the cause, imaging studies, ERCP, and predicting outcomes. Key points are that acute pancreatitis results from inappropriate activation of pancreatic enzymes, risk factors are gallstones and alcohol, and predictors of severe disease include scoring systems assessing inflammation and organ failure.
The document provides guidelines for the management of acute pancreatitis (AP). It summarizes that AP is one of the most common gastrointestinal diseases, leading to significant burden. The incidence of AP has been increasing. Recent studies have identified two phases of AP - early (within 1 week) characterized by systemic inflammatory response and late (>1 week) characterized by local complications. Key recommendations include establishing the diagnosis of AP using clinical criteria including abdominal pain and elevated serum amylase/lipase. Imaging such as CT should be reserved for unclear or non-improving cases. Early management focuses on hemodynamic support and aggressive hydration to decrease morbidity and mortality. Guidelines are provided for evaluating etiology, risk stratification, nutritional support, antibiotic use
The document provides guidelines for the management of acute pancreatitis (AP). It summarizes that AP diagnosis is typically established by abdominal pain and elevated serum amylase and/or lipase levels. Contrast-enhanced CT or MRI is only recommended if diagnosis is unclear or patient fails to improve to evaluate for complications. It outlines recommendations for early medical management including aggressive hydration and nutrition, as well as management of complications like pancreatic necrosis with antibiotics, endoscopic or radiologic drainage, or surgery.
The document provides guidelines for the management of acute pancreatitis (AP). It summarizes that AP is one of the most common gastrointestinal diseases, leading to significant burden. The incidence of AP has been increasing. Recent studies have identified two phases of AP - early (within 1 week) characterized by systemic inflammatory response and late (>1 week) characterized by local complications. Key recommendations include establishing the diagnosis of AP using clinical criteria including abdominal pain and elevated serum amylase/lipase. Imaging such as CT should be reserved for unclear or non-improving cases. Early management focuses on hemodynamic support and aggressive hydration to decrease morbidity and mortality. Guidelines are provided for evaluating etiology, risk stratification, nutritional support, antibiotic use
This document discusses acute pancreatitis in children. It provides information on the definition, diagnosis, etiology, biomarkers, imaging, management, and outcomes of pediatric acute pancreatitis. The main points are:
- Acute pancreatitis is defined as abdominal pain with serum lipase or amylase levels over 3 times the normal limit and imaging findings consistent with pancreatitis.
- Common causes in children include gallstones, trauma, medications, infections, and genetic disorders.
- Lipase is the preferred biomarker as it remains elevated longer than amylase. Imaging like ultrasound and CT scan are used but usually not needed for diagnosis.
- Management involves fluid resuscitation, monitoring for complications, pain
This document discusses the approach to patients with pancreatic diseases, including acute and chronic pancreatitis. It begins with definitions of incidence and diagnostic tests used. It then describes the etiology, pathogenesis, clinical features, management, and complications of acute pancreatitis. Etiology of recurrent pancreatitis is discussed. Chronic pancreatitis is defined, and its pathophysiology, imaging, treatment, and complications are outlined. Throughout, key definitions from the Revised Atlanta Classification are provided to stage and characterize pancreatic conditions.
This guideline presents recommendations for the management of acute pancreatitis (AP). Key recommendations include: assessing hemodynamic status upon presentation and providing resuscitation as needed; admitting patients with organ failure to intensive care; providing aggressive intravenous hydration within the first 12-24 hours; using ERCP within 24 hours for patients with AP and cholangitis; not routinely using prophylactic antibiotics for severe AP or sterile necrosis; considering infected necrosis in patients not improving after 7-10 days and using antibiotics known to penetrate pancreatic necrosis; and providing enteral nutrition for severe AP to prevent infectious complications while avoiding parenteral nutrition.
Pancreatitis is inflammation of the pancreas that can be acute or chronic. Acute pancreatitis presents as an emergency with abdominal pain and elevated pancreatic enzymes. It can lead to complications affecting other organ systems. Chronic pancreatitis is a lifelong condition resulting in irreversible damage and pain or loss of pancreatic function. Management depends on severity, with mild cases treated conservatively and severe cases requiring intensive care monitoring. Local complications include fluid collections, necrosis, abscesses, and pseudocysts.
Acute pancreatitis is an inflammatory process of the pancreas that can involve surrounding tissues or remote organ systems. The most common causes are gallstones and alcohol. The pathogenesis involves premature activation of digestive enzymes within the pancreas that cause autodigestion. Clinical presentation includes severe upper abdominal pain and elevated pancreatic enzymes. Diagnosis requires abdominal pain consistent with pancreatitis plus elevated pancreatic enzymes or radiologic findings. Complications can include pancreatic necrosis, pseudocyst formation, and systemic inflammatory response.
This document 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.
An inflammatory condition of the pancreas
Acute pancreatitis is a reversible process,
whereas Chronic pancreatitis (CP) is irreversible
Acinar Cell Injury
This document discusses delirium, which is an acute disturbance of consciousness and cognition. It defines delirium and describes its subtypes. Delirium is associated with increased mortality, longer hospital stays, and permanent cognitive impairment in some patients. Risk factors include infection, withdrawal, metabolic abnormalities, trauma, and various medical conditions. Delirium results from neurotransmitter imbalances and inflammation in the brain. It should be monitored using scales like the Richmond Agitation Sedation Scale and Confusion Assessment Method. Treatment involves managing the underlying causes, minimizing sedation, promoting mobility, and in some cases using antipsychotics or dexmedetomidine. Delirium usually develops within the first 48 hours and can last up to two weeks.
Colistin is a polymyxin antibiotic produced by Bacillus polymyxa that is effective against most gram-negative bacteria. It fell out of favor due to nephrotoxicity but remains a treatment of last resort for multidrug-resistant infections. There are two forms, colistin sulfate and colistimethate sodium, which are dosed differently and have different mechanisms of action, pharmacokinetics, and toxicity profiles. Resistance can develop with use but remains relatively rare currently.
This document discusses various methods for monitoring the central nervous system (CNS) during and after surgery. It describes cerebral perfusion monitoring techniques like cerebral blood flow measurements, transcranial Doppler ultrasonography, near-infrared spectroscopy, and jugular bulb oximetry. Regional perfusion is also monitored using brain tissue partial oxygen tension. Cerebral metabolism is assessed using cerebral microdialysis. Cerebral function is evaluated with the bispectral index, approximate entropy, and auditory evoked potentials. The document provides details on how each technique is performed and what clinical information it provides about CNS oxygenation, blood flow, and function.
This document discusses ventricular tachycardia (VT) clusters and incessant VT. It defines a VT cluster as 3 or more sustained VTs within 24 hours. Treatment options discussed include antiarrhythmic drugs, ablation, anesthesia, and LVAD. Amiodarone, lidocaine, and procainamide dosages are provided. Left stellate ganglion blockade is suggested as superior to antiarrhythmic drugs for electrical storms. The document also discusses therapies for VT including ablation and digitalis toxicity management.
This document discusses various calculations used to diagnose and distinguish between different types of acid-base disorders, including anion gap, delta gap, urine anion gap, and osmolar gap. It provides detailed explanations of how to calculate each value and what they indicate. The anion gap is useful for determining the cause of metabolic acidosis. The delta gap can identify mixed acid-base disorders. A negative urine anion gap suggests GI bicarbonate loss while a positive value suggests renal tubular acidosis. An increased osmolar gap may indicate ethylene glycol or methanol poisoning in the setting of an unexplained metabolic acidosis.
Chest x. ray interpretation and teachingsamirelansary
1. The document discusses various radiological signs seen on chest x-rays related to different disease processes and conditions. It provides descriptions of abnormalities indicative of conditions like pneumonia, lung cancer, tuberculosis, pulmonary edema and others.
2. Examples and descriptions are given for interpreting findings related to mediastinal masses, pleural effusions, atelectasis, pneumothorax and other lung abnormalities. Signs related to vascular structures like aneurysms are also outlined.
3. The document serves as a teaching guide for radiological interpretation and diagnosis, summarizing key signs and patterns seen for different diseases on chest x-rays.
Colistin is a polymyxin antibiotic produced by Bacillus polymyxa that is effective against most gram-negative bacteria. It fell out of favor due to nephrotoxicity but remains a treatment of last resort for multidrug-resistant infections. There are two forms, colistin sulfate and colistimethate sodium, which are not interchangeable. Dosing is complicated due to lack of standardization. Colistin works by disrupting bacterial membranes. While resistance is still rare, its increased use has led to some resistant strains emerging.
Chest x. ray interpretation and teachingsamirelansary
1. The document discusses various radiological signs seen on chest x-rays related to different disease processes and conditions. It provides descriptions of findings related to lung lesions, pleural diseases, pulmonary vascular abnormalities and other pathologies.
2. Examples of signs described include the appearance of mediastinal lesions, pleural effusions, lung opacities, findings associated with lobar collapse, and distributions of opacities related to specific conditions.
3. The document aims to aid in the interpretation of chest x-rays and teaching of radiological findings for different diseases. It covers topics such as cavitary lung lesions, mediastinal abnormalities, signs of pneumonia, and characteristics of vascular anomalies amongst other pathologies.
This document discusses various methods for monitoring the central nervous system (CNS) during and after surgery. It describes cerebral perfusion monitoring techniques like cerebral blood flow measurements, transcranial Doppler ultrasonography, near-infrared spectroscopy, and jugular bulb oximetry. Regional perfusion is also monitored using brain tissue partial oxygen tension. Cerebral metabolism is assessed using cerebral microdialysis. Cerebral function is evaluated with the bispectral index, approximate entropy, and auditory evoked potentials. The document provides details on how each technique is performed and what insights it provides about CNS oxygenation, blood flow, and electrical activity.
1) An arterial line allows continuous monitoring of a patient's blood pressure by connecting an arterial catheter to a pressure transducer. The transducer converts pressure oscillations into an electrical waveform displayed on a monitor.
2) The arterial waveform provides information about cardiovascular physiology and hemodynamics. An accurate waveform depends on proper catheter placement, monitoring equipment setup, and avoiding issues like dampening or resonance.
3) Key portions of the arterial waveform include the anacrotic limb, anacrotic notch, dicrotic limb, and dicrotic notch, which reflect events in the cardiac cycle and can be affected by conditions like vascular resistance.
1) The document presents several radiographic signs seen on chest x-rays and CT scans related to various pulmonary and mediastinal abnormalities.
2) Examples include the deep sulcus sign indicating pleural free air, the air crescent sign seen in invasive aspergillosis, the silhouette sign depicting a pericardial cyst, and the CT halo sign associated with various conditions including invasive aspergillosis.
3) Accompanying each sign is an illustration and example chest x-ray or CT image, with a brief explanation of the clinical significance of each radiographic finding.
The document provides updates on infectious diseases from Clostridium difficile infection to new vaccines and antimicrobial agents. It discusses the increasing severity and prevalence of C. difficile, new diagnostic tests and treatment options including fidaxomicin and stool transplants. New antimicrobial agents for gram-positive infections like daptomycin, linezolid and ceftaroline are mentioned. Vaccine recommendations are updated for herpes zoster, pertussis and pneumococcus.
1. Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space between the brain's outermost layers caused by a ruptured aneurysm in 70% of cases.
2. Presentation includes sudden severe headache, reduced consciousness, vomiting, neck stiffness, and seizures. Investigations include CT scan and lumbar puncture to detect blood.
3. Treatment aims to prevent rebleeding through securing the aneurysm via coiling or clipping, and managing complications like hydrocephalus, vasospasm, seizures, and hyponatremia which can occur in the weeks following SAH.
SYSTEMIC LUPUS ERYTHEMATOSUS Sle pathophysiology and managementsamirelansary
This document provides an overview and update on systemic lupus erythematosus (SLE). It discusses the definition and classification criteria for SLE, including revisions to the criteria. Genetic factors contributing to SLE susceptibility are described. Increased levels of interferon alpha are implicated in the disease pathogenesis. Clinical manifestations and leading causes of mortality in SLE patients are summarized. Current therapeutic approaches for SLE, including hydroxychloroquine, belimumab, and targeted therapies in development are outlined.
This case describes a 45-year-old male presenting with agitation, fever, hypertension, tachycardia, and other signs consistent with serotonin syndrome after ingesting Paxil, Gravol, ibuprofen, and smoking crack cocaine. The document discusses the diagnostic criteria and causes of serotonin syndrome and recommends supportive care and medications like cyproheptadine, benzodiazepines, beta-blockers, chlorpromazine, and dantrolene for treatment. Cyproheptadine appears to be an effective and safe treatment option for mild to moderate cases based on case reports and series.
This document defines key terms and concepts related to mechanical ventilation and interprets blood gas results to guide ventilator adjustments. It describes various ventilator modes, appropriate initial settings, priorities for weaning, and criteria for extubation. Volume control delivers a set tidal volume while pressure control uses a fixed pressure. Pressure-regulated volume control aims for a target minute ventilation. Complications include barotrauma, pneumonia, and cardiac/GI issues. Physical exams and pressure patterns can localize causes of acute deterioration. Neurologic, cardiovascular, and pulmonary status must be optimized before extubation.
This document discusses new insights into treatment strategies for critically ill patients, including optimal antibiotic dosing and the potential benefits of extended infusion of antibiotics. It also reviews evidence on the use of aerosolized colistin, inhalation antibiotics, statins, probiotics, and prophylactic antibiotics in preventing infections like ventilator-associated pneumonia in ICU patients. While some studies found decreased infection rates, ICU stay, or ventilation time with these approaches, larger trials are still needed to determine clear effects on mortality or define best practices. The document emphasizes individualizing care based on pharmacokinetic factors and calls for more research on optimization of antibiotic use in critical illness.
Mixed connective tissue disease (MCTD) is a rare autoimmune disorder with features of lupus, scleroderma, rheumatoid arthritis, and polymyositis. It is characterized by high levels of antibodies against ribonucleic proteins. Diagnostic criteria require 3 of 5 clinical features plus positive serology. Over time, many patients evolve symptoms meeting criteria for other connective tissue diseases. Pulmonary, renal, and cardiac involvement are common complications. Prognosis depends on degree of organ involvement, with 5-year mortality of 8-19% reported.
This document discusses normal and increased intracranial pressure (ICP). It begins by defining normal ICP ranges in adults and babies. ICP is influenced by several factors and shows pressure fluctuations with cardiac systole and respiration. Increased ICP can be caused by factors that increase brain volume such as tumors or hematomas. Treatment aims to reduce ICP through general measures, induced cerebral vasoconstriction using techniques like hyperventilation, and osmotherapy using agents like mannitol. Careful monitoring of ICP is important for guiding therapy to prevent secondary brain injury.
This document contains summaries of several research points related to critical care. It discusses findings that propofol may limit recovery after brain injury in adults, that cardiac dysfunction is associated with mortality after traumatic brain injury, that vitamin D deficiency predicts sepsis in critically ill patients, and that neuromuscular blocking agents are associated with lower mortality in mechanically ventilated sepsis patients. It also summarizes research showing that a bundle of measures was effective at reducing ventriculitis associated with external cerebral ventricular drainage. Finally, it finds that critical illness is characterized by reduced intestinal absorption of glucose and lower expression of glucose transporters and taste receptors.
- 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
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share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
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• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
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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.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
3. Acute pancreatitis
AP is an inflammatory condition of the pancreas
that has a broad spectrum of severity ranging
from mild and self-limited to severe and
associated with multiorgan failure.
Clinically it is associated with the acute onset of
abdominal pain and elevation of serum
biochemical markers.
The underlying pathophysiology is early and
inappropriate activation of digestive enzymes
within acinar cells.
4. •Different degrees of AP, and how are they
defined?
Mild AP
Pancreatic inflammation (of any cause) without
persistent organ failure or local complications.
Severe acute pancreatitis (SAP)
Associated with systemic complications,
including multiple-organ failure, and local
complications, such as necrosis, abscess,
and/or pseudocyst.
This degree of pancreatitis requires aggressive therapy in an
intensive care setting to prevent significant morbidity or mortality.
5. Causes of AP?
Gallstone-related disease and excessive
alcohol intake comprising 70% of all cases.
hypertriglyceridemia (serum triglyceride level
above 1500 mg/dL), trauma, and
hypercalcemia.
Smoking is a risk factor for AP in a time- and
dose-dependent manner.
6. Causes of AP?
A large number of medications have been
implicated in causing AP, including angiotensin-
converting enzyme inhibitors, furosemide,
tetracycline, aminosalicylic acid, corticosteroids,
procainamide, thiazides, metronidazole, and
ranitidine.
Because of the varied duration between exposure and
development of symptoms, and the usual lack of a clear
mechanism, it is often difficult to identify a drug as the
sole cause of AP.
7. Causes of AP?
True idiopathic cases of AP are diminishing as
more genetic causes of the disease are
discovered.
Endoscopic retrograde
cholangiopancreatography (ERCP) causes
pancreatitis in approximately 5% of individuals
who undergo this procedure.
8. The presenting signs and symptoms of
AP?
AP is characterized by the sudden onset of
abdominal pain, classically located in the
epigastrium and usually associated with nausea
and/or vomiting.
Radiation of pain from the epigastrium
through to the back that is alleviated with the
patient leaning forward is a typical but not a
necessary feature.
Tachycardia related to pain or volume depletion
and low-grade fever may be present.
9. The presenting signs and symptoms of
AP?
Two additional findings associated with severe
pancreatitis may be present
the Grey Turner and Cullen signs.
•The Grey Turner sign is an ecchymosis of the
flank due to retroperitoneal hemorrhage.
When present, it usually occurs 3 to 7 days after the onset of pain
and is indicative of severe pancreatitis.
•The Cullen sign is periumbilical ecchymosis
associated with both severe necrotizing
pancreatitis and retroperitoneal hemorrhage of
various causes.
10. •Are amylase and/or lipase measurements
helpful in the diagnosis?
The most commonly used diagnostic markers are
serum amylase and lipase.
Although serum amylase levels have a high
sensitivity in the first 24 hours the specificity is
very low.
In addition to pancreatitis, elevated amylase
levels are seen with many other conditions
including bowel infarction, renal failure,
perforated peptic ulcer, trauma to the salivary
glands, and macroamylasemia.
11. •Are amylase and/or lipase measurements
helpful in the diagnosis?
In contrast, serum lipase levels are both more
specific and more sensitive than amylase
measurements.
Of note, no correlation exists between
the absolute levels of amylase and
lipase and the severity of pancreatitis.
12. Role of imaging in the diagnosis
of AP
Abdominal plain radiographs may be
nonspecific or reveal an ileus if the pancreatitis
is severe.
Ultrasound evaluation of the pancreas itself is
often limited by overlying bowel gas and/or
patient discomfort. This test may, however,
detect signs of biliary abnormalities in cases
where this cause is suspected.
13. Role of imaging in the diagnosis
of AP
Computed tomography (CT) with oral and
intravenous (IV) contrast
Can offer information regarding severity of
disease and development of complications.
Features that may be identified on CT include
evidence of inflammation (pancreatic
parenchymal edema or peripancreatic fat
stranding), peripancreatic or intrapancreatic
fluid collections, pancreas perfusion, and
presence and extent of pancreatic necrosis.
14. •Should all patients have imaging studies
done at the time of presentation?
The timing of performing CT in the evaluation of
AP has been frequently debated and studied.
Obtaining CT early in the course of illness has
not been shown to establish alternative
diagnoses or change clinical management.
The need for cross-sectional imaging should be
evaluated on a case-by-case basis and reserved
for those who do not improve clinically after
several days of supportive therapy and/or in
whom worrisome symptoms such as fever or
leukocytosis develop.
15. •Should all patients have imaging studies
done at the time of presentation?
Advanced imaging should be considered early in
a patient's course of illness if the diagnosis itself
is uncertain or if suspicion exists of a
complication from AP that, if identified, would
significantly alter management, or if alternative
diagnoses requiring surgical management are
considered.
16. •What if the patient cannot receive
contrast for imaging?
Magnetic resonance imaging (MRI) has a
growing role in the diagnosis and management
of AP and is a reasonable option in patients
who cannot receive iodinated contrast for CT.
Enhanced MRl requires the administration of
gadolinium, which has been implicated in
severe toxic side effects (nephrogenic
systemic fibrosis) in patients with
compromised renal function.
17. •What if the patient cannot receive
contrast for imaging?
Good correlation has been noted, however,
when comparing magnetic resonance
cholangiopancreatography (MRCP), with or
without gadolinium contrast, with CT in the
evaluation AP.
MRCP also has the added benefit of being able to
better define the pancreatic and biliary ductal system
in cases where this cause is suspected but the pretest
probability is too low to proceed directly to ERCP.
18. Determination of the severity and
prognosis of AP
Recognizing and differentiating mild AP from
Severe AP is important so that patients can be
triaged to the appropriate setting and
treatment plan.
Over decades, several clinical predictors have
emerged.
Although all are imperfect, they are
considered superior to clinical judgment alone.
19. Ranson criteria
Were one of the earliest and widely used
scoring systems.
Their major disadvantage was that they
required 48 hours to complete.
The Acute Physiology and Chronic Health
Evaluation (APACHE) II system, developed
to evaluate critically ill patients, has also been
used to differentiate mild AP from SAP {
Severe AP }.
The major disadvantage of this system is that many find it
cumbersome as it requires 12 physiologic measures to calculate.
20. A CT severity index
(Balthazar score )
Has been developed and often used to predict
severity of pancreatitis on the basis of
radiographic features.
The bedside index of severity in AP
(BISAP) score integrates the systemic
inflammatory response syndrome (SIRS)
criteria and can be calculated relatively
quickly on admission.
21. RANSON PROGNOSTIC SIGNS
ETIOLOGY OF PANCREATITIS
{ GALL STONES AND NON GALL STONES }
At initial presentation :
•70
•White blood cell count (k/mm3)
•Lactate dehydrogenase (U/L)
During first 48 hours
•Decrease in hematocrit
•Elevation in blood urea nitrogen (mg/dl )
•Base deficit (mmol/L)
•Fluid sequestration (L)
22. The treatment for AP
The mainstay of treatment in AP is aggressive
supportive and symptomatic therapy that
includes volume repletion, pain control,
nutritional support, correction of electrolyte
abnormalities, treatment of infection (if
present), and treatment of associated or
causative conditions.
23. Adequate volume repletion and restoration
of perfusion to pancreatic microcirculation is
imperative to stave off progression of disease
and development of local complications.
Inadequate volume repletion is associated
with higher rates of pancreatic necrosis.
No randomized trials exist to guide rate or
volume of fluid administration. Most experts
recommend isotonic crystalloid infusion rates
of 250 to 300 Ml/hr or greater for the first 48
hours or enough to maintain urine output at 0.5
ml/kg/hr.
24. Narcotics are usually necessary to establish
pain control.
IV morphine or hydromorphone at 2- to 4-hour
intervals should be considered.
Occasionally, continuous infusion with
additional patient-administered boluses is
necessary.
Antisecretory agents have been considered
for use in pancreatitis.
The inhibitory effect of octreotide, a
pharmaceutical analog of somatostatin, on
pancreatic enzyme secretion has led to its
study in the treatment of AP.
25. The largest randomized trial comparing
placebo with octreotide in the treatment of
moderate or severe pancreatitis
found no significant difference
With regard to mortality, rate of new
complications, rate of surgical intervention,
duration of pain, or length of hospital stay.
26. BALTHAZAR CT GRADING OF AP
AND CT SEVERITY INDEX
•A Normal pancreas
•B Enlarged pancreas
•C Inflammation of pancreas or
•D One peripancreatic fluid collection
•E More than one peripancreatic fluid
collection and /or air in retroperitoneum
NECROSIS FACTOR :
Percentage of necrosis .
*CT grade points + necrosis points.
27. •How should patients with
pancreatitis be fed?
Enteral feeding
Is the preferred method of nutritional support
for all patients who are seen with pancreatitis.
It is thought to help maintain the intestinal
mucosal barrier, thereby preventing
translocation, which is thought to be a major
source of infection.
28. Enteral feeding
No strong evidence exists that nasojejunal
feeding is advantageous over nasogastric
feeding.
Still, many experts recommend fluoroscopic or
endoscopic placement of a jejunal, or
postpyloric, feeding tube if possible.
29. Parenteral nutrition
should be initiated in patients unable to
tolerate oral feeding because of pain,
ileus, and/or nausea.
Opinion with regard to the timing of
initiation of parenteral nutrition
ranges from 2 to 5 days after
presentation.
30. •Should all patients with AP
receive antibiotics?
No. The use of prophylactic antibiotics to
prevent infection of pancreatic necrosis has
been controversial but is not currently
recommended.
No significant benefit has been found with
regard to mortality, rates of infected
necrosis,need for operative treatment, or overall
infections when administering prophylactic
antibiotics.
31. Broad-spectrum antibiotics should be
administered if objective evidence exists of
infected necrosis on the basis of clinical status
(i.e., fever) or cultured aspirate.
Some experts believe antibiotics are warranted
when evidence is seen on CT of necrosis in >
30% of the pancreas.
In such cases, the use of antibiotics should be
limited to 7 to 14 days because of the risk of
fungal superinfection.
32. If the patient's condition continues to
deteriorate, he or she should be
evaluated for minimally invasive
and/or surgical debridement or
necrosectomy .
33. The bedside index of severity in AP
BlSAP SCORE :
1 point for each of the following if present. 0 ooints if absenl
•BUN >25 mg/dL (8.9 mmol/L)
•Impaired mental state status
•SIRS (two or more of the following) :
•Pulse > 90 beats/min
•Respiratory rate >20/min or
•PaC02 < 32 mm Hg
•Temperature >38" C or <36" C
•WBC >12,000 or <4000 cells/mm3
or > 10% immarure neutrophils
•Age > 60 yr
•Pleural effusion
34. The most common bacteria responsible
for infected pancreatic necrosis?
Culprit infective agents are usually gut derived,
including
Escherichia coli, Bacteroides, and
Enterococcus.
Staphylococcus and Pseudomonas
are also potential pathogens and should be
considered.
35. Fungal infection
of necrosis
Is rare but more common when prophylactic
antibiotics are given.
It is unclear whether fungal superinfection has
any impact on mortality.
36. Role of surgery for AP
Surgery may be necessary for delayed
complications of AP (i.e., pancreatic
pseudocysts, persistent sterile necrosis) or for
cholecystectomy to prevent future episodes of
biliary pancreatitis.
Surgical necrosectomy is the gold standard
treatment for infected pancreatic necrosis
resulting from severe AP.
37. Retrospective reviews addressing timing of
intervention found that postponing surgery
until 4 or 6 weeks after admission correlated
with decreased mortality compared with
earlier intervention.
Expert panels recommend delaying
necrosectomy at least 3 to 4 weeks after
hospitalization if possible, while
administering antibiotics and allowing the
necrosis to organize.
38. Principles of surgical management of
infected pancreatic necrosis include
debridement of all infected necrotic
material and drainage of the remaining
pancreatic bed.
Debridement is done bluntly and
gently, with hydrosonic irrigation
frequently used, to avoid vascular
injury.
39. Adequate debridement may require
multiple trips to the operating room.
The current favored drainage option
includes closure of the abdomen over
multiple large closed sump drains
with or without irrigation.
These patients are usually critically ill
and require vigorous supportive care.
40. •When should minimally invasive or image-
guided therapy be considered?
Although surgical necrosectomy remains the
gold standard for definitive management of
pancreatic necrosis, percutaneous and
endoscopic therapies have a growing role in
at least adjunctive management.
Percutaneous drainage (followed by surgery
if necessary) has been associated with fewer
major complications than open necrosectomy
alone but did not offer any mortality benefit.
41. •One third to one half of patients who undergo
percutaneous drainage have no need for surgical
necrosectomy. CT-guided percutaneous drainage of
necrotizing pancreatic collections may be considered
as a bridge to necrosectomy in patients with sepsis
who are too ill
to proceed directly to surgery.
Drainage of a walled-off necrotic cavity by
endoscopic ultrasonography (EUS) via transgastric
or transduodenal approach has been shown to be
effective; however, this modality should be considered
only in a carefully selected patient population and is
dependent on local expertise.
42. Additional treatment options for acute
biliary pancreatitis
Early ERCP has previously been the standard of
care for patients with AP suspected to be due to
gallstones.
All patients who have signs or symptoms of
cholangitis should have early ERCP to relieve
biliary obstruction.
43. Other patients with AP in which cholangitis
is not present should be evaluated on a
case-by-case basis with the understanding
that investigations have shown that early
ERCP in patients with predicted mild or
severe pancreatitis does not significantly
reduce the risk for overall complications or
mortality.
44. Pancreatic pseudocysts
Pancreatic pseudocysts are localized fluid
collections rich in amylase and other
pancreatic enzymes surrounded by a wall of
fibrous tissue that are not lined by epithelium.
Pseudocysts can form as a result of
pancreatic necrosis during an episode of
pancreatitis or because of disruption in the
normal duct anatomy due to stenosis,
calculus, or trauma.
45. Pancreatic pseudocysts may be
asymptomatic, present with pain alone, or
present with a variety of other clinical
complications including
bleeding, infection, or rupture.
Rare complications include gastric outlet
and/or biliary obstruction and thrombosis of
splenic or portal veins with development
of gastric varices.
Diagnosis is usually made on the basis of
clinical and radiographic evidence.
46. The best approach to the
management of pseudocysts
Pancreatic pseudocysts require treatment if
they become symptomatic or develop a
complication .
Surgical, percutaneous, and endoscopic
approaches have all been used to manage
these collections.
No randomized trials have been performed to
compare these modalities.
47. Endoscopic drainage has advantages of
being less invasive, more cost-effective, and
associated with lower lengths of stay than
surgery, but its use may be limited on the
basis of anatomy.
Modality of treatment for pancreatic
pseudocysts should be based on a
combination of factors including patient
comorbidities and clinical status, site and
characteristics of the lesion, and available
local expertise.
48. COMMON CAUSES OF ACUTE
PANCREATITIS :
•Biliary-Gallstones, parasites, or
malignancy
•Alcohol
•Drugs
•Trauma, toxins
•Idiopathic, ischemic, infectious, inherited
•Metabolic-hyperlipidemia, hypercalcemia
•ERCP
•Smoking
49. GOOD LUCK
SAMIRELANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
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Wellcome in our new group ..... Dr.SAMIR EL ANSARY