Acute pancreatitis has an incidence of 17 per 100,000 people and a mortality of 2-3%. The most common causes are gallstones (50% of cases) and alcohol abuse (20-25% of cases). Necrotizing pancreatitis can lead to pancreatic infections which are most often polymicrobial. Treatment involves fluid resuscitation, pain control, nutritional support via enteral feeding when possible, and antibiotics only for infected necrosis or cholangitis. Complications include pancreatic pseudocysts and abscesses which may require percutaneous or surgical drainage.
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 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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
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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
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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.
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.
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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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
2. EPIDEMIOLOGY
17 per 100,000
2-3% overall mortality from acute pancreatitis
Male: female ratio is 1:3- in those with gallstones
and 6:1 in those with alcoholism
The median age at onset depends on the etiology
AIDS-related - 31 years
Vasculitis-related - 36 years
Alcohol-related - 39 years
Drug-induced etiology - 42 years
ERCP-related - 58 years
Trauma-related - 66 years
Biliary tract–related - 69 years
4. Idiopathic Acute Pancreatitis
The etiology of acute pancreatitis should be
determined in at least 80% of cases and no more
than 20% should be classified as idiopathic
Gall stone disease represents approximately half
the cases of acute pancreatitis, and 20–25% are
related to alcohol abuse
The correct diagnosis of acute pancreatitis should
be made in all patients within 48 hours of
admission.
The diagnosis of idiopathic pancreatitis should not
be accepted in the absence of a vigorous search
for gall stones as a minimum, it is necessary to
obtain at least two good quality ultrasound
examinations.
5. Clinical Presentation
Pain (95%)
◦ Acute onset
◦ Mid-abdominal or mid-epigastric
◦ Radiates to the back (50%)
◦ Peak intensity in 30 minutes
◦ Lasts for several hours
Nausea and vomiting (80%)
Fever
Shock
Abdominal distension (75%)
Abdominal guarding and tenderness (50%)
Restlessness and agitation
Grey-Turner's sign (hemorrhagic discoloration of the flanks)
Cullen's sign (hemorrhagic discoloration of the umbilicus)
8. Laboratory Diagnosis
BASELINE INVESTIGATION
LFT’S
Increased amylase and/or lipase >3 times
◦ Amylase levels rise w/in 2-12h
Peak w/in first 48hr
Remain elevated 3-5days before return to baseline
◦ Lipase much more specific
Height of elevation does not correlate with severity
No utility in following daily levels after the diagnosis
Serum Ca+
LDH
VIRAL ANTIBODY TITERS
10. PREDICTION OF SEVERITY
Available prognostic features which
predict complications in acute
pancreatitis are
clinical impression of severity
Obesity
APACHE II >8 in the first 24 hours
C reactive protein levels >150 mg/l
Glasgow score 3 or more
Persisting organ failure after 48 hours in
hospital
13. Signs of Organ Failure
Cardiovascular
◦ Hypotension
◦ Septic physiology
HR, CO and
◦ DIC
◦ Thrombocytosis
SVR
Respiratory
Renal
◦ ATN
◦ Oliguria
Hepatic
◦ Encephalopathy
◦ T bili (3 mg/dl)
◦ AST/ALT 2X nl
◦ Hypoxemia
◦ Pleural effusions
Hematologic
GI
◦ Stress ulcer
◦ Acalculous cholecystitis
14. Determining severity
Clinical assessment,
fluid status
vitals
UOP
pulse oximetry
Clinical criteria
Radiographic criteria
◦ Ranson criteria
◦ Atlanta criteria
◦ POP score
◦ CT severity index
necrosis may not be evident until 48-72h
15. Ranson Score
At admission
age in years > 55 years
white blood cell count > 16000 cells/mm3
blood glucose > 11 mmol/L (> 200 mg/dL)
serum AST > 250 IU/L
serum LDH > 350 IU/L
At 48 hours
Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
Hematocrit fall > 10%
Oxygen (hypoxemia PO2 < 60 mmHg)
BUN increased by 1.8 or more mmol/L (5 or more
mg/dL) after IV fluid hydration
Base deficit (negative base excess) > 4 mEq/L
Sequestration of fluids > 6 L
18. When Do I Order A CT?
If the patient has…..
◦
◦
◦
◦
◦
Persisting organ failure
Signs of sepsis
Deterioration in clinical status after 6-10days
Diagnostic dilemma
Infection suspected
T > 101o F
Positive blood cultures
What kind of CT?
What are you looking for?
Follow up scan are recommended only if the
patient’s clinical status deteriorates or fails to
show continued improvement.
◦ CT scan with pancreatic protocol
◦ Necrosis: Lack of enhancement with contrast
◦ Fluid Collections
◦ Alternate diagnosis
19. CT scan with pancreatic protocol
500 ml of oral contrast by mouth or
nasogastric tube. An initial scan
without iv contrast show extent of
peripancreatic change. A post contrast
series is obtained aftr iv inj of 100 ml
of nonionic contrast delivered at 3 ml/s
Images through the pancreatic bed
should be obtained with in 40 sec and
before 80 sec.
20. CT Findings
Pancreas
◦
◦
◦
◦
Pancreatic enlargement
Decreased density due to edema
Intrapancreatic fluid collections
Blurring of gland margins due to inflammation
Peripancreatic
◦ Fluid collections and stranding densities
◦ Thickening of retroperitoneal fat
* It may take up to 72h for inflammatory
changes to become apparent on CT *
23. Balthazar Scoring
CT grading of severity
POINTS
Grade of Acute Pancreatitis
A =Normal pancreas
B =Pancreatic enlargement
C =Pancreatic/peripancreatic
inflammation
D =Single peripancreatic fluid collection
E =Multiple fluid collections
0
1
2
3
4
Grade E = 50% chance of developing an infection and 15% chance of
death
Degree of Necrosis
No necrosis
Necrosis of one third of pancreas
Necrosis of one half of pancreas
Necrosis of more than one half
0
2
4
6
CT Severity Index = Grade + Degree of necrosis
24. When can he eat ?
TPN vs. enteral feeding
In patients with severe disease, oral intake is
inhibited by nausea; the acute inflammatory
response is associated with impaired gut
mucosal barrier function.
It has been suggested that nutritional support
may help to
limit the stimulus to the inflammatory response.
Reduce microbial translocation
Enhance gut mucosal blood flow
Promote gut mucosal surface immunity
In these circumstances enteral feeding seems to
be safer than parenteral feeding, with fewer septic
complications.It is also cheaper
25. Contd…
Tube
feed if anticipate NPO > 1 week.
Nasogastric feeding may be feasible in up to
80% of cases. Caution should be used when
administering nasogastric feed to patients
with impaired consciousness because of the
risk of aspiration of refluxed feed.
In that case nasojeujunal tube can be used.
The use of enteral feeding may be limited by
ileus. If this persists for more than five days,
and if can’t maintain adequate jejunal access
parenteral nutrition will be required.
26. Possible pathways for pancreatic infection
There are few mechanisms by which
bacteria may enter pancreatic and
peripancreatic necrosis
The haematogenous route via the
circulation.
Transmural migration through the colonic
bowel wall either to the pancreas
(translocation),or via ascites to the
pancreas, or via the lymphatics to the
circulation
The biliary duct system from the duodenum
via the main pancreatic duct.
Intra abdominal fungal infection can also
28. Management
All patients with acute pancreatitis should receive adequate
oxygen
Start IV fluids with crystalloid
Colloid (blood if Hct <25, albumin if serum alb <2)
Rate of fluid replacement should be monitored by frequent measurement of
central venous pressure
Closely follow input output charting
0.5ml/kg /hr in absence of renal failure
Analgseics
Opioids
Antiemetics
NGT decompression
if frequent emesis or evidence of ileus on plain films
Monitor & correct electrolytes.
29. When Do I Start Antibiotics?
Acute pancreatitis is c/b infection ~ 10%
30-50% of those with necrosis get infection
Prophylactic antibiotics
◦ Controversial
No benefit in mild EtOH pancreatitis
Selective gut decontamination may be beneficial
General recommendations for use:
◦ Biliary pancreatitis with signs of cholangitis
◦ > 30% necrosis on CT scan
31. A final word on antibiotics
Do not use empirically early in mild
pancreatitis
Fever early in the disease process is
almost universally secondary to the
inflammatory response and NOT an
infectious process
32. When Do I Consult GI ?
Evidence of biliary pancreatitis
◦ Elevated LFTs + pancreatitis
No matter what the US shows
Severe pancreatitis
Recurrent unexplained pancreatitis
Rule out infected necrosis
EUS FNA sampling of fluid collections
Endoscopic treatment of necrosis/abscess
33. GALL STONE PANCREATITIS AND
TREATMENT
OF GALL STONES
Q: When should I suspect it ?
◦ A: Always
Q: How do I evaluate for it ?
◦ A: (E)US and LFTs
Q: When is ERCP indicated ?
34. Contd….
Urgent therapeutic ERCP should be performed in
patients with acute pancreatitis of gall stone etiology
who satisfy the criteria for severe pancreatitis, or when
there is cholangitis, jaundice, or a dilated common bile
duct.
The procedure is best carried out within the first 72 hrs
after the onset of pain.
All patients undergoing early ERCP for severe gall
stone pancreatitis require endoscopic sphincterotomy
whether or not stones are found in the bile duct.
Patients with signs of cholangitis require endoscopic
sphincterotomy or duct drainage by stenting to ensure
relief of biliary obstruction
35. Timing of cholecystectomy
All
patients with biliary pancreatitis should
undergo definitive management of gall
stones during the same hospital admission.
For
unfit patients, endoscopic
sphincterotomy alone is adequate treatment
36. Complications of AP
Immediate
Shock
DIC
ARDS
Late
Pancreatic pseudocyst
Pancreatic abscess
Pancreatic necrosis
Progressive jaundice
Persistent duodenal ileus
GI bleeding
Pancreatic ascites
37. Management of Pancreatic
Complications
Acute fluid collections
◦ Occur early, seen but not felt
◦ No defined wall usually resolve spontaneously
◦ No routine percutaneous or operative drainage
require
Infected pancreatic necrosis
Pancreatic abscess
Pseudocysts
38. Infected necrosis
All patients with persistent symptoms
and greater than 30% pancreatic
necrosis, and those with smaller areas of
necrosis and clinical suspicion of sepsis,
should undergo image guided FNA to
obtain material for culture 7–14 days
after the onset of the pancreatitis.
Patients with infected necrosis will
require intervention to completely
debride all cavities containing necrotic
material.
39. Contd…
Radiological
percutaneous wide bore drainage
Surgical
Debridement of necrotic tissue following this abdomen can
be closed in three ways
Closed ovr drain
Packed and left open
Closed over drain and irrigated
A new approach for surgical debridement of infected
necrosis offers the potential to debride necrotic tissue
with minimal systemic disturbance, by approaching the
cavity along the track of a percutaneously placed
drain.The cavity is then debrided piecemeal with an
operating nephroscope. Several sessions may be
required in order to achieve complete debridement.
Postoperatively the cavity is continuously irrigated
40.
41. Pseudocysts
Collection of pancreatic fluid enclosed
by non-epithelialized wall of granulation
tissue
Complicates 5-10% cases of AP
~ 4 weeks after insult
25-50% resolve spontaneously
43. Pseudocyst Management
Old thought
◦ Pseudocysts > 5 cm that have been
present > 6 weeks must be drained
Current practice
◦ Asymptomatic pseudocysts, regardless of
size, do not require treatment
51. Pancreatic abscess
◦ CT or EUS guided drainage
Walled collection of pus
Similar to management of pseudocyst
52. Closing Points
Patients with severe acute pancreatitis
have an increased risk of death.
Patients who die usually have
evidence of organ failure.
All patients with severe acute
pancreatitis should be managed in a
high dependency unit or intensive
therapy unit with full monitoring and
systems support
The pancreas is mean