Acute Pancreatitis 2018, Current Medical diagnosis and treatment 2018 and Harrison edition 19

1. ACUTE PANCREATITIS
Dr. Ansari

2. Case presentation
• 30 years old patient with epigastric region pain
for 24 hours without any significant alleviation
with the use of antiacids and IV PPI, presented
in the OPD room. By Physical exam, NAD just
had a local tenderness in epigastric region by
palpation.
• After 1 day, jaundice was noted in sclera with
increased in the severity of pain.

4. General Consideration
• The pancreas secrets 1 500-3000 mL of
isosmotic alkaline (pH >8) fluid per day
containing about 20 enzymes.
• The pancreatic secretions provide the enzymes
and bicarbonate needed to affect the major
digestive activity of the gastrointestinal tract

5. Bicarbonate
• Bicarbonate : Bicarbonate is the ion of primary
physiologic importance within pancreatic secretion.
The ductal cells secrete bicarbonate predominantly
derived from plasma (93%) more than from
intracellular metabolism (7%).
• Function: Intraluminal bicarbonate secreted from
the ductal cells helps neutralize gastric acid and
creates the appropriate pH for the activity of
pancreatic enzymes and bile salts on ingested food.

6. Enzyme secretion
The pancreas secretes
• amylolytic，
• lipolytic， and
• proteolytic enzymes into the duct lumen.

7. Auto-digestion of the pancreas is
prevented by :
• the packaging of pancreatic proteases in
precursor (proenzyme) form，
• Intracellular calcium homeostasis (low
intracellular calcium in the cytosol of the acinar cell
promotes the destruction of spontaneously activated
trypsin)
• acid-base balance，
•
• and the synthesis of protective protease
inhibitors

8. ACUTE PANCREATITIS
• The incidence of acute pancreatitis also varies in
different countries and depends on cause (e.g.， alcohol
， gallstones, metabolic factors， drugs).
• The annual incidence ranges from 1 3-45/ 1 00,000
persons.
• The median length of hospital stay is 4 days，with a
median hospital cost of $6,096 and a mortality of 1 %.
• Hospitalization rates increase with age， are 88%
higher among blacks， and are higher among males
than females.

10. Etiology

12. Approach to Acute Pancreatitis
• Abdominal pain is the major symptom o f acute
pancreatitis. Pain may vary from a mild discomfort to
severe， constant.
• Characteristically， the pain， which is steady and
boring in character， is located in the epigastrium and
periumbilical region， and may radiate to the back
， chest， flanks， and lower abdomen.
• Nausea， vomiting， and abdominal distention
due to gastric and intestinal hypomotility and chemical
peritonitis are also frequent complaints.

13. Physical examination
• Physical examination frequently reveals a distressed
and anxious patient.
• Low-grade fever， tachycardia, and hypotension
are fairly common. Shock is not unusual.
• Jaundice occurs infrequently; when present， it
usually is due to edema of the head of the
pancreas with compression of the intra-pancreatic
portion of the common bile duct or passage of a
biliary stone or sludge.

14. Cont’d
• Chest: In 10-20% of patients， there are pulmonary
findings， including basilar rales， atelectasis， and
pleural effusion， the latter most frequently left sided.
• Abdomen: Abdominal tenderness and muscle
rigidity are present to a variable degree， but
compared with the intense pain， these signs may be
less impressive. Bowel sounds are usually diminished
or absent. An enlarged pancreas from acute fluid
collection， walled off necrosis，or a pseudocyst may be
palpable in the upper abdomen later in the course of the
disease (i.e.， 4-6 weeks)

15. Cont’d
• Cullen’s sign: A faint blue discoloration
around the umbilicus (Cullen's sign) may occur as
the result of hemoperitoneum，
• Grey Turner’s sign: and a blue-red-purple or
green-brown discoloration of the flanks
reflects tissue catabolism of hemoglobin from
severe necrotizing pancreatitis with hemorrhage.

17. Lab tests
• Serum amylase and lipase values threefold or more above
normal.
• Serum lipase is the preferred test. However， it should be noted
that there is no correlation between the severity of pancreatitis
and the degree of serum lipase and amylase elevations.
• After 3-7 days，even with continuing evidence of pancreatitis，
total serum amylase values tend to return toward normal.
• However， pancreatic lipase levels may remain elevated for 7- 1 4
days.
• Acidosis could increase serum amylase levels such as DKA.
• A serum lipase measurement can be instrumental in
differentiating a pancreatic or non-pancreatic cause for
hyperamylasemia.

18. Cont’d
• Leukocytosis ( 1 5 ，000-20，000 )occurs
frequently.
• Prerenal azotemia with a blood urea nitrogen
(BUN) level >22 mg/dL resulting from loss of
plasma into the retroperitoneal space and
peritoneal cavity.
• Hyperglycemia is common and is due to multiple
factors， including decreased insulin release，
increased glucagon release.
• Hyperbilirubinemia in 10% of cases, normalizes in
4-7 days.

19. Cont’d lab test
• Serum alkaline phosphatase and aspartate
aminotransferase levels are also transiently elevated
， and they parallel serum bilirubin values and may
point to gallbladder-related disease or inf1ammation in
the pancreatic head.
• Hypertriglyceridemia occurs in 5 - 1 0% of patients.
• Approximately 5- 1 0% of patients have hypoxemia
(arterialPO， <60 mmHg) ， which may herald the
onset of ARDS.
• Hypocalcemia occurs in -25% of patients， and its
pathogenesis is incompletely understood. Intra-
pretoneal saponification.

20. ECG and Imaging studies
• Electrocardiogram is occasionally abnormal in
acute pancreatitis with ST-segment and T-
wave abnormalities simulating myocardial
ischemia.
• An 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.

21. Abdominal CT scan
• The revised Atlanta criteria have clearly outlined the
morphologic features of acute pancreatitis on computed
tomography (CT) scan as follows:
• ( 1 ) interstitial pancreatitis，
• (2) Necrotizing pancreatitis，
• (3) acute pancreatic f1uid collection，
• (4) pancreatic pseudocyst，
• (5) acute necrotic collection (ANC) ，
• and (6) walled-off pancreatic necrosis (WON)
• CT imaging is best evaluated 3-5 days into hospitalization
when patients are not responding to supportive care to 100k
for l0cal complications such as necrosis.

23. D/DX
• The differential diagnosis should include the
following disorders:
• ( 1 ) perforated viscus， especially peptic ulcer;
• (2) acute cholecystitis and biliarγ colic;
• (3) acute intestinal obstruction;
• 4) mesenteric vascular occlusion;
• (5) renal colic;
• (6) inferior myocardial infarction;
• (7) dissecting aortic aneurysm;
• (8) connective tissue disorders with vasculitis;
• (9) pneumonia;
• and ( 1 0) diabetic ketoacidosis

24. Phases of acute pancreatitis
• Two phases of acute pancreatitis have been defined， early
(<2 weeks) and late (>2 weeks).
• Early: which lasts 1-2 weeks， severity is defined by clinical
parameters rather than morpho1ogic findings.
• Most patients exhibit SIRS， and if this persists， patients
are predisposed to organ failure.
• Three organ systems shou1d be assessed to define organ
failure: respiratory，cardiovascu1ar， and renal.
• Late: The late phase is characterized by a protracted course of
illness and may require imaging to evaluate for 10ca1
complications. The important clinica1 parameter of severity
， as in the early phase， is persistent organ failure.

25. Severity of Acute Pancreatitis
• Mild acute pancreatitis
• is without 10cal complications or organ failure.
• Most patients with interstitia1 acute pancreatitis have mild
pancreatitis.
• In mild aιute pancreatitis， the disease is se1f-limited and
subsides spontaneous1y，usually within 3-7 days after
treatment is instituted.
• Ora1 intake can be resumed if the patient is hungry， has
norma1 bowe1 function， and is without nausea and
vomiting.
• Typiιally， a clear or full liquid diet has been recommended
for the initia1 meal; however， a 10w-fat solid diet is a
reasonab1e choice following recovery from mild acute
pancreatitis.

26. • Moderate severe acute pancreatitis is
characterized by transient organ failure (reso1ves in
<48 h) or l0cal or systemic complications in the
absence of persistent organ failure.
• These patients may or may not have necrosis， but
may deve10p a 10ca1 complication such as a fluid
co11ection that requires a pro1onged hospitalization
greater than 1 week.
• Severe acute pancreatitis is characterized by
perrsistent organ failure (>48 h). Organ failure can
be sing1e or multip1e. A CT scan or magnetic
• resonance imaging (MRI) shou1d be obtained to
assess for necrosis and/or complications

28. Treatment
• The most important treatment intervention for acute pancreatitis is safe， aggressive
intravenous fluid resuscitation.
1. NPO to rest the pancreas
2. and is given intravenous narcotic analgesics( Morphine or Mepridine 100-
150mg IM every 3-4 hours to control abdominal pain and
3. supplemental oxygen (2 L) via nasal cannula.
4. Intravenous fluids of lactated Ringer's or normal saline are initially bolused at 1 5-20
cc/kg ( 1 050- 1 400 mL， followed by(200-250 mL/hour， to maintain urine output >0.5
cc/kg per hour.
• A decrease in hematocrit and BUN during the first 12-24 h is strong evidence that sufficient
fluids are being administered. Serial measurements and bedside assessment for fluid
overload are continued，and fluid rates are maintained at the current rate.
5. Serial bedside evaluations are required every 6-8 h to assess vital signs， oxygen
saturation， and change in physical examination. Lactated Ringer's solution has been shown
to decrease systemic inflammation and may be a better crystalloid than normal saline.

29. GALLSTONE PANCREATITIS
• Patients with evidence of ascending cholangitis
(rising white blood cell count， increasing liver
enzymes) should undergo ERCP within 24-48
h of admission.
• Patients with gallstone pancreatitis are at
increased risk of recurrence， and consideration
should be given to performing a
cholecystectomy during the same
admission or within 4-6 weeks of
discharge.

30. • Serum triglycerides > 1 000 mg/ dL are
associated with acute pancreatitis. Initial
therapy may include insulin， heparin， or
plasmapheresis. Outpatient therapies include
control of diabetes.
• Approximately 25% of patients who have had an
attack of acute pancreatitishave a recurrence.
The two most common etiologic factors
• are alcohol and cholelithiasis.