Pancreatitis

By Morris K Zhou
Learning Objectives
1. Describe basic physiology of the pancreas.
2. Recognize clinical features of acute and chronic pancreatitis.
3. Identify risk factors and etiologies of acute and chronic pancreatitis.
4. Interpret test results in the work-up of acute and chronic
pancreatitis.
Pancreas: is an elongated retroperitoneal organ
:It's about 15-20cm in length , lies against L1- L2
vertebra
:It lies posterior to stomach, separated by lesser sac
Pancreas means all flesh (Pan means all, kreas means flesh)
-It is divided into head, neck, body, and tail
:The head lies in the concavity of the duodenum and tail reaches
the hilum of the spleen.
 Pancreatitis
Inflammation of the pancreatic parenchyma.
Types
-Acute: means acute inflammatory changes which are
reversible(but acute attack can occur in pre-existing chronic
pancreatitis .
_Chronic: prolonged and frequently lifelong disorder resulting from
the development of fibrosis within the pancreas. Results in chronic
continuous inflammatory changes which are morphologically
irreversible.
 Endocrine

Exocrine OpenStax, Anatomy & Physiology. OpenStax CNX.

 Roles of the pancreas
Endocrine role- it is performed by the Islets of Langerhans
-Islets consist of 4 distinct cell types .
.Alpha- cells = glucagon
.Beta-cells= insulin
.Delta-cells= somatostatin
.C-cells = have no known function
Exocrine role - it is performed by the pancreatic acinar
cells .
-Acinar cells they produce digestive enzymes
(amylase ,lipase ,and protease) to break
down carbs, lipids and proteins.
Digestive Enzymes

Proenzyme Active Form

Lipase

Amylase

Trypsinogen Trypsin

Proelastase Elastase

Pandol SJ. The Exocrine Pancreas. San Rafael (CA): Morgan & Claypool Life Sciences; 2010. Digestive Enzymes.
Acute Pancreatitis
- sudden inflammation of the
pancreatic parenchyma due
to destruction by its own
digestive enzymes.
(autodigestion)
- It is a generally reversible
inflammatory change.

https://radiologyassistant.nl/abdomen/pancreas/acute-pancreatitis
 Measures to protect against autodigestion.
1.It produces proenzymes (zymogens)- are inactive forms of the enzyme
2. These zymogens are sequestered in vesicles called zymogen granules
3.In these granules, they are packaged with with protease inhibitors
which prevent them from doing damage if they become prematurely
active.
 Etiology
(I GET SMASHED)

I-Idiopathic
G-gall stones
E-Ethanol(alcohol)
T-Trauma
S-Steroids
M-Mumps
A-Autoimmune diseases
S-Scopion sting
H-Hypertriglycerides OR Hypercalcemia
E-ERCP
D-Drugs (eg: HCTZ, Didanosine,Bactrim, Azathioprine etc)
Causes: Duct obstruction Acinar cell injury Defective intracellular
transport

Alcohol
Cholelithiasis Drugs
Ampullary obstruction Trauma Metabolic injury (experimental)
Chronic alcoholism lschemia Alcohol
Ductal concretions Viruses Duct obstruction

Mechanisms:
!
Interstitial edema
l
Release of intracellular
l
Delivery of proenzymes to
i
Impaired blood now
proenzymes and lysosomal
hydrolases
lysosomal compartment

�
lschemia
l
Activation of enzymes Intracellular activation

1
(intra-or extracellular) of enzymes

Acinar cell injury

�
Activated enzymes

Interstitial
PToteolysis Fat necrosis Hemorrhage
Lesions: inflammation + + +
(proteases) {lipase, phospholipase) (e,lastase)
and edema

Acute pancreatitis
 Acute Pancreatitis Epidemiology

-Worldwide, the incidence of acute pacreatitis ranges

between 5-80 per 100,000 population.
-> 200,000 hospital admissions/year
-Hospitalization rates increases with age.
-About 20% have a severe course( 10-30% mortality for
this group, which has not significantly changed during the
past few decades despite improvement in critical care and
other interventions.
 Clinical presentation
.Epigastric Pain (constant, radiating to the back, worse when lying
supine, better when leaning forward)
.Anorexia predominates as any ingestion of anything( including
water ) exacerbates the pain.
.Abdominal distention , nausea and vomiting
.Ileus- local inflammation can decrease GI motility (reduced bowel
sounds)
.Hypotension & edema :inflammatory cytokines (IL-1, IL-6 & TNF-
alpha ) induce diffuse vasodilation and increase vascular permeability.
Clinical Presentation
- Grey Turner sign
- Cullen sign

https://www.registerednursern.com/four-abdominal-quadrants-regions/
http://www.60secondem.com/visual-diagnosis-16-answers/
Diagnosis
The diagnosis requires two of the following three criteria:

Epigastric abdominal pain.

Elevated lipase or amylase, > 3x the upper limit of normal .
Evidence of pancreatic inflammation on :Abdominal u/s (cost

effective) or Abdominal CT
Laboratory Testing
- Other tests are used to monitor overall patient
condition ,guide management and to assess
prognosis.
.WBC (Hb , HCT)
- .LDH levels
.Procalcitonin, CRP ,ESR
.LFT(Bilirubin, AST, ALT)
.Calcium levels
.Lipid profile
Lipase
- Secreted mainly by the pancreas
- The best test for acute pancreatitis; sensitivity and specificity 80-100%
- Increases in 4-8 hours and peaks at 24 hours with concentrations remaining
elevated for 7-14 days
- Increase in lipase is not proportional to severity
 https://www.istockphoto.com/illustrations/ultrasound?mediatype=illustration&phrase=ultrasound&sort=mostpopular

Imaging
- Ultrasound- best initial test
- Computed tomography (CT)
- Endoscopic retrograde cholangiopancreatography
(ERCP)- only reservesed for therapeutic intervention .

https://twitter.com/amergastroassn/status/1138140036753502211
https://www.radiologyinfo.org/en/info.cfm?pg=mrcp
 Severity of Acute Pancreatitis
The types of AP are interstitial edematous pancreatitis (IEP) and acute necrotizing pancreatitis

(ANP). The severity of the disease is classified as mild, moderately severe, and severe AP. Early

phase of AP is less than a week from the onset of symptoms. Late phase involves cases with more

than a week from the onset of symptoms and occurs only in patients with moderately severe or

severe AP. In mild AP, there is no organ dysfunction or failure nor local or systemic

complications. Spontaneous recovery usually takes place during the first week. New category in

RAC is moderately severe pancreatitis. It involves organ dysfunction (transient organ failure)

resolving in 48 h and/or local or systemic complications (e.g. peripancreatic fluid collections)

without organ failure. In severe or necrotizing form of AP, there is a persistent organ failure
(lasting for longer than 48h).
Revised Antlanta Criteria
Prognosis
 Management
- Most cases can be managed medically.
.Bowel rest, NPO
.IV hydaration- Lactated ringers(bolus at presentation, then
maintenance and electrolyte repletion as needed)
.Pain control( PCA pumps are superior to intermittent dosing)
.Antiemetics for nausea and vomiting
Nutritional management- initiation of oral feeding depends on the
severity . When the patient is hungry and in the absence of ileus,
nausea or vomiting you can reintroduce food slowly: water at first ,
clear liquids next, then bland foods.If there is pain with eating , go
back to NPO
If the patient does not appear to have a good velocity after some
time , introduce parenteral feeding(TPN)
NB:Early enteral feeding feeding decreases risk of infectious
complications by decreasing GI dysmotility and gut permeability.
Treating Infected Necrotizing Pancreatitis Fluid Collection
Infected necrotizing pancreatitis is an infection of an Fluid Collection Complication in
the setting of necrotizing pancreatitis (i.e., infected Acute Necrotic Collections or
infected Walled Off Necroses).
Superinfection of the FCC will present as refractory sepsis, deterioration of the
patient’s trajectory, or development of a nonpancreatic complication, but most often
as a new fever in a patient well into pancreatitis treatment.

Even if CT has already been performed, if infected necrotizing pancreatitis is suspected,

get a CT with IV contrast. In addition to routine cultures for fever (blood, urine),
perform fine-needle aspiration of the FCC. If there is evidence of infection on imaging (gas
in the fluid on CT), or the Gram stain shows organisms, start meropenem. When
cultures and sensitivities return, de-escalate to the lowest effective agent on the antibiotic
ladder. If the FCC cultures come back negative, discontinue treatment for infected
necrotizing pancreatitis.
complications of acute pancreatitis.
.LOCAL- phlegmon (ill-defined fluid collection) usually sterile
- pseudocysts( with defined non-epithelial wall)
-pancreatic abscess
- hemorrhage from pseudoaneurysm of splenic
artery(hemosuccus pancreaticus)

SYSTEMIC- ARDS (number 1 cause of mortality in pancreatitis,

pulmonary edema, pleural effusions.
-prerenal AKI
-Shock and dehydration
-multiorgan failure
-DIC
Outline
- Anatomy and physiology
- Acute Pancreatitis
- Chronic Pancreatitis
- Pathophysiology
- Clinical Features
- Diagnosis and Laboratory Testing
- Prognosis and Management
- Case Report
- Summary
Chronic Pancreatitis

- Progressive inflammation of the pancreas leading to irreversible damage

- Can result in exocrine and endocrine insufficiency
- Increased risk of pancreatic cancer over time

Aghani, Elham.(2015). Introduction to Pancreatic Disease: Chronic Pancreatitis. Pancreapedia: Exocrine Pancreas Knowledge Base.
Pathophysiology
- Not agreed upon or well understood
- Necrosis-Fibrosis theory: chronic fibrotic changes occur after recurrent acute
insults to the pancreas
- Probably more complex than this and multifactorial
- Degree of fibrosis doesn’t seem to correlate with degree of dysfunction

Pancreatic
cell damage
Necrosis

Insult Fibrosis
Pancreatic Insufficiency
- Can’t be demonstrated until at least 50% of acinar cells are destroyed, clinical
signs at 90%
- Islet cells remain viable for longer than acinar cells
- Exocrine insufficiency leads to malnutrition due to protein and fat
malabsorption
- About two-thirds of patients have fat soluble vitamin deficiencies
- 65% of patients get osteopenia or osteoporosis
- Endocrine insufficiency can lead to type 3c diabetes
- 5-10% of patients develop this
Clinical Presentation
- Recurrent episodes of epigastric pain that spreads to the back
- Constant abdominal pain
- Steatorrhea
- Diabetes
- Weight loss
Differential Diagnosis
- Focal chronic pancreatitis
- Autoimmune pancreatitis
- Pancreatic adenocarcinoma
Risk Factors

Aghani, Elham.(2015). Introduction to Pancreatic Disease: Chronic Pancreatitis. Pancreapedia: Exocrine Pancreas Knowledge Base.
Diagnosis
- Establishing a diagnosis can be challenging, especially early
- Histology is the “gold standard”, but biopsies are not routinely done
- Requires combination of clinical history, imaging, and lab testing
 Normal Histology Chronic Pancreatits Histology

Lamps, LW. Pancreas. Image: Lobular pancreas. ExpertPath. Yerian, L. Chronic Pancreatitis. Image: Fibrosis and chronic inflammation. ExpertPath.
Laboratory Testing
- Lab tests have limited sensitivity early in disease
- Tests need to be used in combination with imaging, and clinical features to
make a diagnosis
- Some tests also help with risk assessment and guiding management
- Direct (invasive) and indirect (non-invasive) tests are available
Secretin-Cholecystokinin (CCK) Test
- Patient fasts overnight
- Tube is placed in the duodenum
- Secretin is given and duodenal fluid is
collected at 15 min intervals for an hour
- Stimulates secretion of pancreatic juices and
bicarbonate
- CCK is then given which stimulates the
secretion of pancreatic enzymes and fluid
is collected

https://courses.lumenlearning.com/atd-herkimer-nutrition/chapter/3-41-digestive-hormones-accessory-organs-secretions/
Pancreatic Elastase
- Quantitative determination of pancreatic elastase in stool is the primary test
for chronic pancreatitis
- Elastase is excreted by the pancreas and goes through the rest of the GI tract
without being degraded or inactivated
- Stool can’t be watery or the enzyme could be diluted out making the result
falsely low
- Treatment with pancreatic enzyme supplements does not interfere with
assays that are human-specific
Imaging
- Computed tomography (CT)- best initial test
- Endoscopic Ultrasound (EUS)
- Magnetic resonance imaging (MRI)
- Magnetic resonance cholangiopancreatography (MRCP)
- Endoscopic retrograde cholangiopancreatography (ERCP)

https://gastro.org/practice-guidance/gi-patient-center/topic/endoscopic-ultrasound-
https://en.wikipedia.org/wiki/CT_scan eus/?hilite=%27endoscopic%27%2C%27ultrasound%27
Management
- Pancreatic enzyme replacement therapy (PERT)
- Supplements and/or feeding tube if necessary
- Encourage abstinence from alcohol and smoking
- Pain management
- Imaging to surveil for pancreatic cancer (especially hereditary pancreatitis
patients)
- Surgery if there is an obstructive process, intractable pain, enlargement of
pancreatic head, suspicion for malignancy
References
OpenStax, Anatomy & Physiology. OpenStax CNX.

Pandol SJ. The Exocrine Pancreas. San Rafael (CA): Morgan & Claypool Life Sciences; 2010. Digestive Enzymes.

Lamps, LW. Pancreas. Images:Lobular pancreas, acinar parenchyma. ExpertPath. Accessed Nov 2020.

Waller A, Long B, Koyfman A, Gottlieb M. Acute pancreatitis: updates for emergency clinicians. J Emerg Med. 2018;55(6):769-779.

Choosing Wisely. An initiative of the ABIM Foundation. Accessed: Oct 2020

Banks PA, Freeman ML; Practice Parameters Committee of the American College of Gastroenterology. Practice guidelines in acute pancreatitis. Am J Gastroenterol. 2006
Oct;101(10):2379-400.

Yerian, L. Chronic Pancreatitis. Image: Fibrosis and chronic inflammation. ExpertPath. Accessed Nov 2020.

Panteghini, M and Bais, R. Serum Enzymes. In Rifai N, Horvath AR and Wittwer CT, eds. Tietz Textbook of Clinical Chemistry and Molecular Diagnostics, 6th ed. St. Louis, MO:
Elsevier, 2018.

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Diagnostics, 6th ed. St. Louis, MO: Elsevier, 2018.

DiaSorin LIAISON Elastase-1 Package Insert

Jalal M, Campbell JA, Hopper AD. Practical guide to the management of chronic pancreatitis. Frontline Gastroenterology 2019;10:253-260.

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