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.
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 (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
by Bushra Ibnauf as part of SAMA's Visiting Faculty Program in Salam Rotana Hotel on June 24th 2011. This was in collaboration with the Sudanese Society for Gastroenterology.
Ventral hernia is protrusion of peritoneal sac through anterior abdominal wall defects except Groin hernias. In this presentation I have discussed Epigastric, Umbilical, Para umbilical, Incisional, Spigelian and Lumbar hernias.
Extended totally extraperitoneal repair (eTEP) is a novel technique that was first introduced by Jorge Daes in 2012 to address difficult inguinal hernias.
OPEN INGUINAL HERNIA REPAIR- OPERATIVE SURGERY
#surgicaleducator #operativesurgery #openinguinalherniarepair #usmle #babysurgeon #surgicaltutor
Dear viewers,
• Greetings from “Surgical Educator”
• Because of the popular demand by viewers of the YouTube channel “Surgical Educator”, I have decided to create and upload videos on common surgeries.
• I have already uploaded videos on open and Laparoscopic Appendicectomy, Thyroidectomy, Modified Radical Mastectomy and open and
Laparoscopic Cholecystectomy
• In this video today, I have discussed Open Inguinal Hernia Repair.
• However, these videos are not real surgeries but the theoretical aspect of operative surgery like going through an atlas of operative surgery.
• Along with these videos, I recommend you to watch real operative surgery videos as well and I will give a link for each surgery in the end of the video as end-cards, which I think will be very useful.
• This will give a very good opportunity for the surgical trainees to mentally rehearse various surgical steps in a sequential manner prior to actual surgery. You can watch the video in the following links:
• surgicaleducator.blogspot.com
• youtube.com/c/surgicaleducator
• Thank you for watching the videos.
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
by Bushra Ibnauf as part of SAMA's Visiting Faculty Program in Salam Rotana Hotel on June 24th 2011. This was in collaboration with the Sudanese Society for Gastroenterology.
Ventral hernia is protrusion of peritoneal sac through anterior abdominal wall defects except Groin hernias. In this presentation I have discussed Epigastric, Umbilical, Para umbilical, Incisional, Spigelian and Lumbar hernias.
Extended totally extraperitoneal repair (eTEP) is a novel technique that was first introduced by Jorge Daes in 2012 to address difficult inguinal hernias.
OPEN INGUINAL HERNIA REPAIR- OPERATIVE SURGERY
#surgicaleducator #operativesurgery #openinguinalherniarepair #usmle #babysurgeon #surgicaltutor
Dear viewers,
• Greetings from “Surgical Educator”
• Because of the popular demand by viewers of the YouTube channel “Surgical Educator”, I have decided to create and upload videos on common surgeries.
• I have already uploaded videos on open and Laparoscopic Appendicectomy, Thyroidectomy, Modified Radical Mastectomy and open and
Laparoscopic Cholecystectomy
• In this video today, I have discussed Open Inguinal Hernia Repair.
• However, these videos are not real surgeries but the theoretical aspect of operative surgery like going through an atlas of operative surgery.
• Along with these videos, I recommend you to watch real operative surgery videos as well and I will give a link for each surgery in the end of the video as end-cards, which I think will be very useful.
• This will give a very good opportunity for the surgical trainees to mentally rehearse various surgical steps in a sequential manner prior to actual surgery. You can watch the video in the following links:
• surgicaleducator.blogspot.com
• youtube.com/c/surgicaleducator
• Thank you for watching the videos.
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
Abnormal abdominal CT is best powerpoint presentation for radiologist, radiology resident and gastroenterologist, this include pancreatitis, all abdominal trauma grading with systemic manner. Thanks
Pancreatitis is a dreaded 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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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How to Give Better Lectures: Some Tips for Doctors
Revised Atlanta classification of Acute Pancreatitis
1. The Revised Atlanta
Classification of Acute
Pancreatitis: Its Importance
for the Radiologist and Its Effect
on Treatment
Volume 262: Number 3—March 2012
radiology.rsna.org
Dr M Venkatesh
2. Learning Objectives
Define acute pancreatitis in its early
phase and later phase, and the
persistent organ failure that can
accompany its occurance.
List the various fluid collections
encountered in acute pancreatitis as
defined by the revised Atlanta
classification.
3. Identify the two phases of acute
Pancreatitis, the parameters that
determine care, and the treatment for
an infected walled-off necrosis.
4. The modifications (a) address the
clinical course and severity of disease
(b) divide acute pancreatitis into
interstitial edematous
pancreatitis and necrotizing
pancreatitis
5. (c) distinguish an early phase (1st
week) and a late phase (after the 1st
week), and
(d) emphasize systemic inflammatory
response syndrome and multisystem
organ failure
6. In the 1st week, only clinical
parameters are important for
treatment planning.
After the 1st week,morphologic
criteria defined on the basis of
computed tomographic findings are
combined with clinical parameters to
help determine care.
7. In 1992, the Atlanta classification
for acute pancreatitis was introduced
as a universally applicable
classification system for the various
manifestations of acute pancreatitis
It defined acute pancreatitis as an
acute inflammatory process of the
pancreas with variable involvement of
other local tissues and remote organ
systems.
9. It was found that the definitions of
severity and local complications of
acute pancreatitis were not used
consistently and that characterization
of severity based on presence of
organ failure had limitations
10. The definition of necrotizing
pancreatitis was determined to be
inadequate because it included sterile
and infected necrosis and did not
distinguish between pancreatic and
peripancreatic necrosis
11. The initial Atlanta classification
system also did not include exact
radiologic criteria for local
complications and controversy
developed over the natural course of
pancreatic and peripancreatic fluid
collections.
12. In 2008, a global consensus
statement was developed that
included broad and international
participation of many experts in the
field of pancreatitis and was led by
the Acute Pancreatitis
Classification Working Group
13. Precise description of pancreatic
collections is particularly important,
because treatment varies with
collection type.
This revised classification is directly
applicable only to adults (>18 years
of age).
14. Radiologic imaging has become
increasingly important in staging
and treating acute pancreatitis
The revision of the Atlanta
classification focuses heavily on
morphologic criteria for defining
the various manifestations of acute
pancreatitis
16. Clinical Definition, Course,
and Severity of Disease
Acute pancreatitis (regardless of
presence or absence of chronic
pancreatitis) is clinically defined by at
least the two of three features
(a) abdominal pain suggestive of
pancreatitis with the start of such
pain considered to be the onset of
acute pancreatitis
17. (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.
18. Course and severity
Introduces two distinct phases of
acute pancreatitis:
First or early phase that occurs
within the 1st week of onset of
disease
Second or late phase that takes place
after the 1st week of onset
19. In the early phase, severity is
entirely based on clinical parameters,
because the need for treatment is
determined primarily by presence
or absence of organ failure
20. It is standard clinical practice within
the first 3 days of admission of a
patient with acute pancreatitis to
record markers of severity
21. Hematocrit
APACHE II, Ranson Scores
Pulmonary complications on chest
radiograph, including pleural effusion;
and serum levels of CRP)
Other severity markers
CT severity index
Modified CT severity index
Other parameters of acute
pancreatic injury
24. The ideal time for assessing the
complications with CT is after 72
hours from onset of symptoms.
CT should be repeated when the
clinical picture drastically
changes, such as with sudden onset
of fever, decrease in hematocrit or
sepsis.
25. Furthermore, in patients with their
first episode of pancreatitis who are
over 40 years of age and have no
identifiable cause for pancreatitis,
contrast enhanced CT should be used
to exclude a possible neoplasm
26. ROLE OF RADIOLOGIST
Address whether pancreatic necrosis
is present, characterize pancreatic
parenchymal and extrapancreatic
fluid collections, and describe the
presence of ascites, extrapancreatic
findings such as gallstones, biliary
dilatation,venous thrombosis,
aneurysms
27. And contiguous inflammatory
involvement of the gastrointestinal
tract.
MR imaging is reserved for detection
of choledocholithiasis not
visualized on contrast-enhanced CT
images and to further characterize
collections for the presence of
nonliquefied material
28. Nonliquefied material refers to
solid and semisolid components
usually pancreatic and extra-
pancreatic debris and necrotic fatty
tissue and may appear on contrast-
enhanced CT images as a
homogeneous or heterogeneous
fluid collection.
29. MR imaging has an important role in
patients in whom contrast-enhanced
CT is contraindicated
ERCP has no role in this morphologic
imaging–based classification of acute
pancreatitis
30. Morphologic Stages of Acute
Pancreatitis
In the 1992 Atlanta classification, a
distinction was made between
interstitial pancreatitis and sterile or
infected necrosis.
In the revised Atlanta classification,
these two types are defined similarly
as IEP and acute necrotizing
pancreatitis
31. Necrotizing pancreatitis is further
subdivided into
-Parenchymal necrosis alone
-Peripancreatic necrosis alone
-Combined type (peripancreatic and
parenchymal necrosis) with or
without infection
32. It is important for the radiologist to
adopt this new nomenclature so that
imaging descriptions are standardized
and communication with clinical and
surgical colleagues is precise.
33. Interstitial Edematous
Pancreatitis(IEP)
Contrast-enhanced CT demonstrates
acute pancreatitis as localized or
diffuse enlargement of the
pancreas with normal
homogeneous enhancement or
slightly heterogeneous enhancement
of the pancreatic parenchyma related
to edema
34. Coronal CT image of Interstitial edematous pancreatitis
(IEP) in a 34-year-old man. Pancreas (arrows) is
heterogeneously enhanced, with indistinct margins due
to inflammation of peripancreatic fat. Some stranding
and minimal fluid are also present
35. In early/mild disease-
peripancreatic and retroperitoneal
tissue may appear normal or may
show mild inflammatory changes in
the peripancreatic soft tissue that
appear as “mistiness” or mild fat
stranding with varying amounts of
Peripancreatic fluid
36. First several days of acute onset of
pancreatitis, the pancreas
occasionally demonstrates increased
heterogeneous enhancement of the
parenchyma that cannot be
characterized definitively as either
IEP or illdefined necrosis.
37. Axial multidetector CT image of IEP in a 39-year-old man
obtained 48 hours after onset of pain. Note focal
heterogeneous low-attenuation area in pancreas body
and neck (arrows). At this stage, the appearance could
not be definitively characterized as IEP or patchy
necrosis and was classified as indeterminate.Follow-up
multidetector CT study did not show any necrosis.
38. With these findings, the presence or
absence of pancreatic necrosis needs
to be described initially as
indeterminate.
CECT performed 5–7 days later
permits definitive characterization.
39. Necrotizing Pancreatitis
Three forms of acute necrotizing
pancreatitis, depending on location.
All three types can be sterile or
infected
Pancreatic parenchymal necrosis
Peripancreatic necrosis alone
Pancreatic parenchymal necrosis
with peripancreatic necrosis
40. Pancreatic parenchymal
necrosis alone
Appears on contrast-enhanced CT
images as lack of parenchymal
enhancement
1st week-CT demonstrates necrosis
as a more homogeneous non-
enhancing area of variable
attenuation
41. Later in the course of the disease, as
a more heterogeneous area.
Often the extent of parenchymal
necrosis is divided into
less than 30%
30%–50%
greater than 50% of the gland
involved
42. Axial CT image in a 38-year-old man obtained
5 days after onset of symptoms. Tail and body
of the pancreas are nonenhancing(arrows) and
slightly heterogeneous in appearance.
43. On coronal reformation CT image obtained 4
weeks after onset, capsule (arrows) is evident
and some heterogeneity (arrowheads) is seen
within this collection, reflecting presence of
nonliquefied material.
44. At times, areas of no or poor
enhancement that are estimated to
be less than 30% in the early phase
may actually be findings of edema
rather than necrosis.
A definitive diagnosis in these
patients requires a follow-up
study.
45. Peripancreatic necrosis alone
Difficult to confirm,its presence is
diagnosed when heterogeneous areas
of nonenhancement are visualized
that contain nonliquefied
components.
Peripancreatic necrosis is commonly
located in the retroperitoneum and
lesser sac.
46. Coronal CT reconstruction shows extent of the
peripancreatic WONs (white arrows) with
percutaneous drain (black arrow) and debris
(arrowheads).
47. The clinical importance of
peripancreatic necrosis alone lies
in the fact that patients with this
condition have a better prognosis
than do patients with pancreatic
parenchymal necrosis
48. Pancreatic parenchymal
necrosis with peripancreatic
necrosis
It is the most common type and can
be seen in 75%–80% of patients with
acute necrotizing pancreatitis
Peripancreatic necrosis associated
with full width necrosis of the
pancreatic parenchyma may be
connected to the main pancreatic
duct
49. Pancreatic and Peripancreatic
Collections
In the revised Atlanta classification,
an important distinction is made
between fluid and nonliquefied
collections
The acute collections are referred to
as either APFCs or as ANCs,
depending on the absence or
presence of necrosis respectively.
50. IEP can be associated with APFC and
over time with pancreatic
pseudocysts.
Necrotizing pancreatitis in its three
forms can be associated with ANC
and over time with WON.
All of these collections can be
sterile or infected
51. APFCs-Acute peripancreatic
fluid collections
Peripancreatic fluid collections
without nonliquefied components
arising in patients with IEP during the
first 4 weeks are referred to as
APFCs
52. APFCs conform to the anatomic
boundaries of the retroperitoneum
(especially the anterior pararenal
fascia),
Are usually seen immediately next to
the pancreas and have no
discernable wall.
53. IEP in a 25-year-old woman with alcohol abuse and
epigastric pain for 72 hours. Axial CT image shows the
pancreas (arrowhead) to be slightly edematous and
heterogeneously enhancing.APFCs (arrows) are seen
surrounding the pancreas.
54. Fluid collections in the pancreatic
parenchyma should be diagnosed
as necrosis and not as APFCs
Most APFCs are reabsorbed
spontaneously within the first few
weeks and do not become infected.
Intervention at this stage is to be
avoided
55. In the 1st week of acute pancreatitis,
distinction between APFC and ANC
may be difficult or impossible,
because both collections may appear
as areas of nonenhancement
If nonenhancing areas of variable
attenuation are seen in these
collections, the diagnosis of peri -
pancreatic necrosis with nonliquefied
components is suggested.
56. Pseudocyst
Within 4 weeks from onset of acute
IEP, an APFC may gradually
transition into a pseudocyst
On CECT images, pseudocysts can be
diagnosed as well-circumscribed,
round or oval peripancreatic fluid
collections of homogeneously low
attenuation surrounded by a well-
defined enhancing wall (capsule
consisting of fibrous or granulation
tissue).
57. According to the revised Atlanta
classification, pseudocysts contain no
nonliquefied components within
the fluid collection
In the rare event in which an APFC
develops an enhancing capsule earlier
than 4 weeks after onset of acute
IEP, it should be characterized as a
pseudocyst.
58. Demonstrating the presence or
absence of communication of
pseudocyst with the pancreatic duct
may be important since it may help
determine management
59. Persistent communication with the
pancreatic duct can be shown on
contrast-enhanced CT images and
curved planar reconstructions, but
MRCP is usually more accurate.
60. Pancreatitis with pseudocyst in a 27-year-old woman.
Coronal CT reconstruction obtained 5 weeks after acute
episode shows pseudocyst(arrows) with well-defined rim
representingthe capsule near the tail of the pancreas.
Gastric folds are slightly thickened (arrowheads).
61. An infected pseudocyst is diagnosed
on CT images by the presence of
gas within the pseudocyst or in
absence of gas by means of fine-
needle aspiration (FNA) with Gram
staining and culture for bacteria or
fungal organisms
62. Pseudocyst in a 61-year-old man. (a) Coronal CT
reconstruction shows pseudocyst (arrows) next to body
of the pancreas with a well-defined capsule. The patient
complained of pain in the midabdomen to left upper
quadrant and early satiety. (b) Follow-up coronal CT
reconstruction was obtained after stent (arrow) had been
placed endoscopically through the stomach into the
sterile collection. There is no residual collection next to
the pancreas.
63. ANCs-Acute necrotic collections
In first 4 weeks after development of
necrotizing pancreatitis a persistent
collection is to be diagnosed as ANC
Contains both fluid and necrotic
material of various amounts(some of
which are loculated) and is to be
distinguished from APFC.
64. In these ANCs, liquefaction of the
necrotic tissue occurs gradually
(usually within 2–6 weeks)
Within the 1st week, both APFCs and
ANCs can manifest as homogeneous
nonenhancing areas. Usually, the
distinction on contrast-enhanced CT
images should become possible after
the 1st week.
65. WON-Walled off necrosis
Over time (usually at or after 4
weeks), the ANC matures and
develops thickened nonepithelialized
wall between the necrosis and the
adjacent tissue. This maturing
collection is called a WON.
66. WON may involve
pancreatic parenchymal tissue and the
peripancreatic tissue,
peripancreatic tissue alone or
pancreas alone.
67. Any apparent fluid collection that
occupies or replaces portions of the
pancreatic parenchyma should be
called a WON after 4 weeks from
onset of necrotizing pancreatitis.
In contradistinction to a pseudocyst,
WON contains necrotic pancreatic
parenchyma or necrotic fat.
68. (a) Axial CT image obtained 6 weeks after acute onset
shows some areas of lower attenuation (arrowheads) in
a heterogeneous collection with a well-defined rim
(arrows), representing WON with fat necrosis involving
pancreas and peripancreatic tissues. (b) Axial CT image
obtained several centimeters caudal to a shows WONs
extending into right anterior pararenal and left anterior
and posterior pararenal space (arrows).
69. Sterile WON in a 45-year-old man with previous episodes
of pancreatitis. MR imaging was performed because the
patient had an allergy to iodinated contrast material. (a)
T2-weighted MR image obtained 5 weeks after the acute
episode shows encapsulated collection (arrows) near the
splenic hilus and next to tail of the pancreas.The
collection appears heterogeneous and contains
nonliquefied material (arrowheads) and fluid and can be
distinguished from a pseudocyst with fluid only
70. Most nonliquefied components
need to be removed by means
of a percutaneous image-guided
approach, a laparoscopic or
endoscopic procedure, or surgery.
A pseudocyst can be treated
effectively by draining the fluid in
most cases.
71. Therefore the distinction between a
collection containing fluid only and a
collection containing fluid and
nonliquefied material is very
important.
72. Complications of Acute
Pancreatitis
Collections that contain
nonliquefied material are more
likely to becomeinfected.
Distinction between a sterile and an
infected collection is important
because treatment and prognosis are
different
73. Infection can be suggested on CECT
images if gas bubbles are present in
the collection owing to the presence
of gas-forming organisms
Gas can also be present in collection
after marsupialization or other
drainage procedures
74. Axial CT image obtained 5 weeks after acute onset
shows pancreas replaced by low-attenuation collection
with well-defined rim (arrows) and multiple pockets of
gas (arrowheads)
75. Axial CT image obtained 3 days after placement of
percutaneous drainage catheters (arrows) shows large
residual WON with air bubbles, indicative of incomplete
drainage of an infected WON.
76. Treatment of IEP
IEP is usually self-limited, and
supportive measures alone suffice.
Most APFCs resolve spontaneously or
mature into pseudocysts.
The majority of these pseudocysts
disappear spontaneously over time
and do not require any treatment.
About 25% become symptomatic or
infected and necessitate drainage
77. Treatment of Necrotizing
Pancreatitis
No universally accepted treatment
algorithm currently exists.
The approach often is dictated by the
expertise of the surgeon and the
interventional radiologist
Image-guided drainage procedures
proved to be effective alternatives to
surgery
78. Treatment of Sterile Pancreatic
Necrosis
If the pancreatic fluid sample is
sterile, the patient is diagnosed as
having sterile necrosis.
Percutaneous drainage and surgey
depending on the clinical severity.
79. Treatment of Infected
Pancreatic Necrosis
Generally treated with surgical
débridement and antibiotics
If a patient is too unstable for
surgery, percutaneous catheter
drainage may help stabilize the
patient
80. Interventional radiology also is called
on for ancillary procedures.
Pseudoaneurysms or active
bleeding related to acute pancreatitis
are usually diagnosed on the basis of
contrast-enhanced CT findings
81. Most commonly, coil embolization
is used
Cases where coil embolization is too
risky or not feasible, a covered stent
can be placed.
Embolization may also be performed
in selected instances of a bleeding
vessel caused by pancreatitis.
82.
83. Conclusions
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
84. 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.
85. 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.
86. In the early phase of pancreatitis,
distinction between APFC and ANC by
CT may be impossible and if clinically
needed for treatment planning, MR
imaging or US may be used to
determine presence of nonliquefied
material
87. The revised Atlanta classification
system with CT helps guide
management and monitor the
success of treatment.