Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe. It is most often caused by gallstones or heavy alcohol use. A patient presents with acute upper abdominal pain that may radiate to the back. Laboratory tests show elevated pancreatic enzymes and imaging can identify gallstones or complications. Severity is assessed by the presence of organ failure or local complications like necrosis. Treatment involves fluid resuscitation and management of complications. The Ranson criteria uses factors at admission and within 48 hours to predict severe acute pancreatitis.
By Dr. Usama Ragab, Zagazig Faculty of Medicine
PSC incidence ranges from 0.5 to 1.25 cases/100 000.
The prevalence of the disease ranges between six and 20 cases/100 000.
Men are more likely to be affected (70%).
Prevalence of PSC may be increased in first degree relatives of PSC patients
By Dr. Usama Ragab, Zagazig Faculty of Medicine
PSC incidence ranges from 0.5 to 1.25 cases/100 000.
The prevalence of the disease ranges between six and 20 cases/100 000.
Men are more likely to be affected (70%).
Prevalence of PSC may be increased in first degree relatives of PSC patients
Acute Pancreatitis - Diagnosis and ManagementRobert Robinson
Overview of the diagnosis and management of acute pancreatitis with a target audience of first year internal medicine residents at SIU Medicine in Springfield IL, USA.
Acute Pancreatitis - Diagnosis and ManagementRobert Robinson
Overview of the diagnosis and management of acute pancreatitis with a target audience of first year internal medicine residents at SIU Medicine in Springfield IL, USA.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
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.
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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!
2. Outline
Introduction
The normal pancrease
Definition and pathogenesis of acute pancreatitis
Causes of acute pancreatitis
Clinical presentation
History
Physical examination
Laboratory examination findings
Assement of severity & hospital triage
Management
Complications
3. Introduction
The pancrease is an organ in the digestive system and
endocrine system.
◦ Endocrine hormones: Insulin, glucagon, and pancreatic
polypeptide
◦ Digestive secretions: Trypsinogen, Chymotrypsinogen,
Carboxypeptidase, elastases, Pancreatic lipase, Pancreatic
amylase
◦ Exocrine secretions: Secretin, Cholecystokinin (CCK), Gastric
inhibitory peptide (GIP), Somatostatin
4. Auto protection of the pancrease
Protection of the pancreatic tissue is facilitated by:
• The packaging of pancreatic proteases in precursor (proenzyme) form
• Intracellular calcium homeostasis
• Acid-base balance
• The synthesis of protective protease inhibitors
5. Acute pancreatitis
• Acute pancreatitis is the sudden onset of reversible inflammation of the pancrease,
•It is estimated to affect between 4.5 and 35 in every 100,000 individuals per year.
• Acute pancreatitis can vary from mild (mortality rate less than 1%; typically resolves in several days)
to severe (mortality rate up to 30%).
• Mortality rates are highest in patients with:
•hemorrhagic pancreatitis,
•multiorgan dysfunction or failure,
•necrotizing pancreatitis.
•The incidence of acute pancreatitis increases with age. Onset in the first decade suggests a hereditary
cause, infection, or trauma.
6. Pathogenesis
The pathogenesis of this disorder is not fully understood, but Acute pancreatitis occurs
when there is abnormal activation of digestive enzymes within the pancrease.
6
Inappropriate activation of inactive enzyme precursors called zymogens
(Trypsinogen)
Trypsin leads to further activation of other digestive enzymes
Inflammation, edema, vascular injury, and cellular death.
Endotoxins, exotoxins, viral infections, ischemia, oxidative
stress, lysosomal calcium, and direct trauma
10. Etiology (Gall stones)
•Gallstones account for 35 to 40 % of cases, but only 3 to 7% of patients with gallstones develop
pancreatitis.
•Mechanism by which the passage of gallstones induces pancreatitis is unknown, but suggested
mechanisms include:
Reflux of bile into the pancreatic duct due to transient obstruction of the ampulla during
passage of gallstones
Obstruction at the ampulla secondary to stone or edema resulting from the passage of a
stone
•An elevated serum ALT is the most clinically useful parameter in predicting a gallstone etiology in
patients with acute pancreatitis.
11. Etiology (Biliary sludge and microlithiasis)
•Most patients with biliary sludge are asymptomatic.
• Biliary sludge is found in 20-40% of patients with acute pancreatitis with no obvious cause.
•In the absence of any other etiology, biliary sludge should be suspected in patients with acute
pancreatitis with a transient elevation in liver tests.
•Sludge is found in patients with stasis, which may be secondary to:
•Prolonged fast
•Total parenteral nutrition
•Ceftriaxone use
12. Etiology (Alcohol)
•Responsible for approximately 30% of cases of acute pancreatitis in the US.
•Exact mechanism is unknown, but suggested ideas include:
increased synthesis of enzymes that are thought to be responsible for acute pancreatitis
over-sensitization of acini to cholecystokinin
abnormal sphincter of Oddi motility
small duct obstruction by protein plug formation
direct toxic and metabolic effects,
•The diagnosis should not be entertained unless a person has a history of over 5 years of heavy alcohol
consumption.
13. Etiology (Drugs)
•Pancreatitis due to medications is rare (0.3 to 1.4%)
•Suggested mechanisms include:
immunologic reactions (eg, 6-mercaptopurine, aminosalicylates, sulfonamides),
direct toxic effect (eg, diuretics, sulfonamides),
accumulation of a toxic metabolite (valproic acid, didanosine, pentamidine, tetracycline),
ischemia (diuretics, azathioprine)
intravascular thrombosis (estrogen),
increased viscosity of pancreatic juice (diuretics and steroids).
•The prognosis of drug-induced pancreatitis is generally excellent and mortality is low.
14. Determining the etiology of acute
pancreatitis
•The etiology of acute pancreatitis can be established in at least 75 % of patients.
•History- focus on previous symptoms or documentation of gallstones, alcohol use, history of
hypertriglyceridemia or hypercalcemia, family history of pancreatic disease, drug history, history
of trauma, and the presence of concomitant autoimmune diseases.
•Labs- on admission, all patients should have a serum amylase or lipase, triglyceride level,
calcium level, and liver biochemistries.
•Imaging- abdominal ultrasound should be obtained on admission in all patients with acute
pancreatitis to evaluate for cholelithiasis or choledocholithiasis. Repeat after recovery if clinical
suspicion for gallstones remains.
-
* Extensive or invasive evaluation is usually not recommended in those with a single episode of
pancreatitis who are younger than 40.
16. Symptoms
•The disease varies in severity and the diagnosis is often missed at the extreme ends of the spectrum.
•Almost all patients with acute pancreatitis have acute upper abdominal pain at the onset.
Location: mid-epigastrium, right upper quadrant, diffuse (infrequently confined to the left side)
Character: steady, gnawing
Radiation: may radiate to the back (50% of cases), or throughout the abdomen and into the chest
Severity : usually very sever (mild or absent in some cases)
Aggravating and alleviating factors: Initially, the pain worsens after eating or drinking, especially fatty foods,
and then typically becomes constant over time. Leaning forward may relieve the pain.
Associated symptoms: Nausea, vomiting, anorexia, frequent hiccups.
Onset: rapid, reaching maximum intensity in 10-20 min.
* The intensity and location of the pain do not correlate with severity.
17. Physical signs
•The physical examination findings may be normal or reveal fever, hypotension, tachycardia,
tachypnea, or diaphoresis.
•Abdominal examination typically reveals
Notable tenderness to palpation,
Guarding,
Signs of peritoneal irritation,
Distension, or rigidity,
Decreased bowel sounds,
Jaundice may be present.
• Basilar rales, and signs of atelectasis, & pleural effusion may be present in 10-20%.
•In severe disease, patients may present with altered mental status.
18. Physical signs (less common)
Grey-Turner's sign: hemorrhagic discoloration of the flanks
Cullen's sign: hemorrhagic discoloration of the umbilicus
Grunewald sign: appearance of ecchymosis, large bruise, around the umbilicus due to local toxic lesion of the
vessels
Körte's sign: pain or resistance in the zone where the head of pancreas is located (in epigastrium, 6–7 cm above
the umbilicus.
Kamenchik's sign: pain with pressure under the xiphoid process
Mayo-Robson's sign: pain while pressing at the top of the angle lateral to the Erector spinae muscles and below
the left 12th rib (left costovertebral angle (CVA)
Pandiaraja's sign: ecchymosis of right axilla
19. Laboratory examination
•Overall, history and physical examination have moderate accuracy, especially when findings are
abnormal.
•Laboratory testing can assist in diagnosis, classify the severity of disease, and predict outcomes.
• Serum amylase and lipase values threefold or more above normal virtually clinch the diagnosis if gut
perforation, ischemia, and infarction are excluded.
•Other tests that should be ordered at presentation include a
complete blood count;
comprehensive metabolic panel including renal and hepatic function
urinalysis;
lipase, calcium, LDH, and triglyceride levels
If alcohol abuse is a factor, magnesium and phosphorous levels should be assessed.
20. Laboratory examination(2)
•In acute pancreatitis, the serum amylase and lipase are usually elevated within 24 h of onset and
remain so for 3–7 days.
•Approximately 85% of patients with acute pancreatitis have a threefold or greater elevated
serum lipase and amylase levels.
•The values may be normal if:
(1) there is a delay (of 2–5 days) before blood samples are obtained,
(2) the underlying disorder is chronic pancreatitis rather than acute pancreatitis, or
(3) hypertriglyceridemia is present.
•Lipase is the single best enzyme to measure for the diagnosis of acute pancreatitis.
There is no correlation between the severity of pancreatitis and the degree of serum lipase and
amylase elevations.
22. Laboratory examination(3)
•Leukocytosis (15,000–20,000 leukocytes/μL) occurs frequently in acute pancreatitis.
•Hemoconcentration may be the harbinger of more severe disease (i.e., pancreatic necrosis), whereas azotemia is
a significant risk factor for mortality.
•Hyperglycemia is common and is due to multiple factors, including decreased insulin release, increased glucagon
release, and an increased adrenal glucocorticoids and catecholamines.
•Hypocalcemia occurs in ~25% of patients, and its pathogenesis is incompletely understood.
•Hyperbilirubinemia (serum bilirubin>4.0 mg/dL) occurs in ~10% of patients.
•Hypertriglyceridemia occurs in 5–10% of patients, and serum amylase levels in these individuals are often
spuriously normal.
•Hypoxemia (arterial PO2 ≤60 mmHg) in 5-10% , may herald the onset of ARDS.
•Electrocardiogram is occasionally abnormal in acute pancreatitis with ST-segment and T-wave abnormalities
simulating myocardial infarction.
23. Imaging findings
•Abdominal ultrasound is recommended in the emergency ward as the initial diagnostic imaging
modality and is most useful to evaluate for gallstone disease and the pancreatic head.
•Contrast-enhanced CT (CECT) and / or MRI of the pancreas should be reserved for patients in
whom the diagnosis is unclear or who fail to improve clinically within the first 48 – 72 h after
hospital admission or to evaluate complications.
24. Diagnosis
Any severe acute pain in the abdomen or back should suggest the possibility of acute
pancreatitis. The diagnosis is established by two of the following three criteria:
(1) Typical abdominal pain in the epigastrium that may radiate to the back,
(2) Threefold or greater elevation in serum lipase and/or amylase,
(3) Confirmatory findings of acute pancreatitis on cross-sectional abdominal imaging.
26. Clinical course
EARLY PHASE (< 2 WEEKS )
- severity is defined by clinical parameters
rather than morphologic findings.
- If SIRS, persists, patients are predisposed to
organ failure.
-Three organ systems should be assessed to
define organ failure: respiratory,
cardiovascular, and renal.
-Persistent organ failure (>48 h) is the most
important clinical finding in regard to severity
of the acute pancreatitis episode.
LATE PHASE (> 2 WEEKS )
- characterized by a protracted course of illness
and may require imaging to evaluate for local
complications.
-The important clinical parameter of severity, as
in the early phase, is persistent organ failure
-These patients may require supportive measures
such as renal dialysis, ventilator support, or need
for supplemental nutrition via the nasojejunal or
parenteral route.
-The radiographic feature of greatest importance
to recognize in this phase is the development of
necrotizing pancreatitis on CT imaging.
27. Primary Assessment
1. Hemodynamic status should be assessed immediately upon presentation and resuscitative
measures begun as needed.
2. Risk assessment should be performed to stratify patients into higher- and lower-risk
categories to assist triage, such as admission to an intensive care setting.
3. Patients with organ failure should be admitted to an intensive care unit or intermediary care
setting whenever possible.
28. Severity of acute pancreatitis
•Mild acute pancreatitis is without local complications or organ failure.
- the disease is self-limited and subsides spontaneously, usually within 3–7 days after treatment
is instituted.
•Moderately severe acute pancreatitis is characterized by transient organ failure (resolves in <48
h) or local or systemic complications in the absence of persistent organ failure.
- These patients may or may not have necrosis, but may develop a local complication such as a
fluid collection that requires a prolonged hospitalization greater than 1 week.
•Severe acute pancreatitis is characterized by persistent organ failure (>48 h). Organ failure can
be single or multiple.
Organ failure is defined as a score of 2 or more for any one of three organ systems (respiratory,
cardiovascular, or renal) using the modified Marshall scoring system.
29. Severity of acute pancreatitis
INTERSTITIAL PANCREATITIS
•Acute inflammation of the pancreatic
parenchyma and peripancreatic tissues, but
without recognizable tissue necrosis
•occurs in 90–95% of admissions for acute
pancreatitis
•is characterized by diffuse gland enlargement,
homogenous contrast enhancement, and mild
inflammatory changes or peripancreatic
stranding.
•Symptoms generally resolve with a week of
hospitalization.
NECROTIZING PANCREATITIS
•Inflammation associated with pancreatic
parenchymal necrosis and/or peripancreatic
necrosis
•occurs in 5–10% of acute pancreatitis
admissions
•Does not evolve until several days of
hospitalization
•is characterized by lack of pancreatic
parenchymal enhancement by intravenous
contrast agent and/or presence of findings of
peripancreatic necrosis.
30. Predicting severe acute pancreatitis
•Clinicians have been largely unable to predict which patients with AP will develop severe
disease.
•The new scoring systems, such as the BISAP, have not shown to be more accurate than the other
scoring systems.
• Also no laboratory test is practically available or consistently accurate to predict severity in
patients with AP.
•CT and/or MRI imaging also cannot reliably determine severity early in the course of AP, as
necrosis usually is not present on admission and may develop after 24– 48 h.
•Thus, in the absence of any available test to determine severity, close examination to assess
early fluid losses, hypovolemic shock, and symptoms suggestive of organ dysfunction is crucial.
* Rather than depending on a scoring system to predict severity of AP, clinicians need to be aware of intrinsic
patient-related risk factors, including laboratory and imaging risk factors, for the development of severe disease.
31. During the first 48 to 72 hours, a rising hematocrit or blood urea nitrogen or creatinine level,
persistent SIRS after adequate fluid resuscitation, or the presence of pancreatic or peripancreatic
necrosis on cross-sectional imaging constitutes evidence of evolving severe pancreatitis.
32. Predicting severe acute pancreatitis
RANSON CRITERIA
◦ At admission:
◦ Age in years > 55 years
◦ WBC count > 16000 cells/mm3
◦ Blood glucose > 11 mmol/L (> 200 mg/dL)
◦ Serum AST > 250 IU/L
◦ Serum LDH > 350 IU/L
◦ Within 48 hours:
◦ Serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
◦ Hematocrit fall > 10%
◦ Oxygen (hypoxemia PaO2 < 60 mmHg)
◦ BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after
IV fluid hydration
◦ Base deficit (negative base excess) > 4 mEq/L
◦ Sequestration of fluids > 6 L
BISAP
– Parameters should be obtained within the
first 24 hours of hospitalization:
BUN > 25mg/dl.
Impaired mental status(GCS<15).
SIRS
Age > 60 years.
Pleural effusion on radiography.
33. Management (principles)
• 85-90% of cases of acute pancreatitis are self-limited & subside spontaneously, (usu. 3-7 days
after start of Rx) & do not exhibit organ failure or local complications.
•Administer aggressive fluid resuscitation,
IV fluids( NS or LR ) – initially bloused at 15cc – 20cc/kg, followed by 3ml/kg/hr, to
maintain urine output >0.5cc/kg/hr.
•NPO; IV narcotic analgesics; supplemental Oxygen (2L via nasal cannula).
•Assess for etiology and severity.
•Serial bedside evaluations: every 6-8 hrs.
Assess: Vital signs, Oxygen saturation , Change in Physical examination.
•Targeted resuscitation strategy – 8-12hrs.
Measure BUN & Hematocrit.
33
34. Management
INITIAL MANAGEMENT
1. Aggressive hydration, (250 – 500 ml per hour of
isotonic crystalloid solution) should be provided to all
patients, unless cardiovascular, renal, or other related
comorbid factors exist. Early aggressive intravenous
hydration is most benefi cial during the first 12 – 24 h,
and may have little benefi t beyond this time period
2. In a patient with severe volume depletion, manifest
as hypotension and tachycardia, more rapid repletion
(bolus) may be needed
3. Lactated Ringer’s solution may be the preferred
isotonic crystalloid replacement fluid
4. Fluid requirements should be reassessed at frequent
intervals within 6 h of admission and for the next 24 –
48 h. Th e goal of aggressive hydration should be to
decrease the BUN
ANTIBIOTICS IN AP
1. Antibiotics should be given for an extrapancreatic
infection, such as cholangitis, catheter-acquired infections,
bacteremia, urinary tract infections, pneumonia
2. Routine use of prophylactic antibiotics in patients with
severe AP is not recommended
. 3. Th e use of antibiotics in patients with sterile necrosis
to prevent the development of infected necrosis is not
recommended
4. Infected necrosis should be considered in patients with
pancreatic or extrapancreatic necrosis who deteriorate or
fail to improve aft er 7 – 10 days of hospitalization. In
these patients, either (i) initial CT-guided fi ne-needle
aspiration (FNA) for Gram stain and culture to guide use of
appropriate antibiotics or (ii) empiric use of antibiotics aft
er obtaining necessary cultures for infectious agents,
without CT FNA, should be given
35. Management (2)
NUTRITION IN AP
1. In mild AP, oral feedings can be started
immediately if there is no nausea and vomiting,
and the abdominal pain has resolved
2. In mild AP, initiation of feeding with a low-fat
solid diet appears as safe as a clear liquid diet
3. In severe AP, enteral nutrition is recommended
to prevent infectious complications. Parenteral
nutrition should be avoided, unless the enteral
route is not available, not tolerated, or not
meeting caloric requirements
4. Nasogastric delivery and nasojejunal delivery
of enteral feeding appear comparable in efficacy
and safety.
SURGERY IN AP
1. In patients with mild AP, found to have gallstones in the
gallbladder, a cholecystectomy should be performed before
discharge to prevent a recurrence of AP
2. In a patient with necrotizing biliary AP, in order to prevent
infection, cholecystectomy is to be deferred until active infl
ammation subsides and fluid collections resolve or stabilize
3. Asymptomatic pseudocysts and pancreatic and/or
extrapancreatic necrosis do not warrant intervention
regardless of size, location, and/or extension
4. In stable patients with infected necrosis, surgical, radiologic,
and /or endoscopic drainage should be delayed preferably for
more than 4 weeks to allow liquefi cation of the contents and
the development of a fibrous wall around the necrosis (walled-
off necrosis)
5. In symptomatic patients with infected necrosis, minimally
invasive methods of necrosectomy are preferred to open
necrosectomy
39. Follow-up care
Evaluate for the development of:
Diabetes
Exocrine insufficiency
Recurrent cholangitis
Development of infected fluid collections.
40. References
•Harrison’s principles of internal medicine 19th edition.
•Up-to-date version 21.6
•Acute pancreatitis; JEFFREY D. QUINLAN, MD, Uniformed Services University of the Health
Sciences, Bethesda, Maryland; Am Fam Physician. 2014;90(9):632-639
•American College of Gastroenterology Guideline: Management of Acute Pancreatitis (2013)
• Acute pancreatitis; Chris E. Forsmark, M.D. et.al N Engl J Med 2016;375:1972-81.
41. Recommended readings
•American College of Gastroenterology Guideline: Management of Acute Pancreatitis (2013 or
later versions)
•Acute pancreatitis; Chris E. Forsmark, M.D. et.al N Engl J Med 2016;375:1972-81.