Acute pancreatitis is acute inflammation of the pancreas that commonly causes abdominal pain and hospitalization. It has two phases - early and late. The early phase lasts 2 weeks and severity is defined by clinical parameters like organ failure. Most patients experience systemic inflammatory response syndrome. Organ failure in more than one organ system is considered multiorgan failure. In the late phase, imaging can identify complications like necrotizing pancreatitis which prolongs hospital stay. Acute pancreatitis is classified as interstitial edema or necrotizing based on imaging and as mild, moderate or severe based on presence and duration of organ failure.

1. Acute pancreatitis
Presenter: Dr.Mohamed Hufane (R1/IM)
Moderator: Dr.Nuredin, MD (internist at
Haramaya university)
8/APRIL/2023

2. Outline
• Definition
• Epidemiology
• Pathogenesis
• Etiology
• Clinical symptoms and diagnosis
• Management
• Complications

3. Definition
• Acute pancreatitis is acute inflammation of the
pancreas and a common cause of acute
abdominal pain causing hospitalization.
• In the majority of patients, the illness settles over
a few days but in 25% of cases it is more severe
and associated with organ failure or pancreatic
necrosis, requiring critical care and a prolonged
hospital stay.

4. Epidemiology
• Per 100,000 people in the general population,
the yearly global incidence of acute pancreatitis
is 34 cases(nature).
• 3% of all cases of abdominal pain admitted to
hospital.

5. Pathophysiology
• A consequence of premature intracellular
trypsinogen activation, releasing proteases
that digest the pancreas and surrounding
tissue  acute pancreatitis
• Triggers for this are many, including
– alcohol
– gallstones and
– pancreatic duct obstruction

6. Pathophysiology

7. Pathophysiology

8. Pathophysiology

9. Pathophysiology
• The normal pancreas has only a poorly developed capsule,
thus, adjacent structures are commonly involved in the
inflammatory process, including the
– common bile duct,
– duodenum,
– splenic vein and
– transverse colon,.
• The severity of acute pancreatitis is dependent on the
balance between the activity of
– Released proteolytic enzymes  antiproteolytic factors.
• The antiproteolytic factors  comprise an
– intracellular pancreatic trypsin inhibitor protein and
– circulating β2-macroglobulin, α1-antitrypsin and C1-esterase
inhibitors.

10. Etiology

12. CLINICAL FEATURES
History
• Abdominal pain
– Present at the onset of most attacks of acute pancreatitis.
– Biliary colic may herald or progress to acute pancreatitis.
– Pain in pancreatitis usually involves the entire upper
abdomen.
– However, it may be epigastric, in the right upper quadrant,
or, infrequently, confined to the left side.
– Pain in the lower abdomen may arise from the rapid
spread of pancreatic exudation to the left colon.
– Onset of pain is rapid but not as abrupt as that of a
perforated viscus.
• Usually it is at maximal intensity in 10 to 20 minutes.

13. • Abdominal pain
– Occasionally, pain gradually increases and takes several
hours to reach maximum intensity.
– Pain is steady and moderate to very severe.
– There is little pain relief with changing position.
– Frequently, pain is unbearable, steady, and boring.
– Band-like radiation of the pain to the back occurs in half of
patients.
– Pain that lasts only a few hours and then disappears
suggests a disease other than pancreatitis, such as biliary
colic or peptic ulcer.
– Pain is absent in 5% to 10% of attacks, and a painless
presentation may be a feature of serious fatal disease

14. • Abdominal pain
– 90% of affected patients have N/V.
– Vomiting may be severe, may last for hours,
may be accompanied by retching, and may
not alleviate pain.
– Vomiting may be related to severe pain or to
inflammation involving the posterior gastric
wall.

15. CLINICAL FEATURES
Physical exam
• Physical findings vary with the severity of an attack.
• Mild pancreatitis- may not appear acutely ill.
– Abdominal tenderness may be mild, and abdominal
guarding absent.
• Severe pancreatitis- Patients look severely ill and
often have abdominal distention, especially epigastric,
which is due to gastric, small bowel, or colonic ileus.
– Almost all patients are tender in the upper abdomen, which
may be elicited by gently shaking the abdomen or by
gentle percussion.
– Guarding is more marked in the upper abdomen.
– Tenderness and guarding can be less than expected,
considering the intensity of discomfort.

16. • Abdominal rigidity, as occurs in diffuse
peritonitis, is unusual but can be present, and
differentiation from a perforated viscus may be
impossible in these instances.
• Bowel sounds are reduced and may be absent.

17. • Ecchymosis in 1 or both flanks (Grey Turner’s
sign) or about the periumbilical area (Cullen’s
sign), owing to extravasation of hemorrhagic
pancreatic exudate to these areas.
– These signs occur in less than 1% of cases
and are associated with a poor prognosis.
• Rarely there is a brawny erythema of the flanks
caused by extravasation of pancreatic exudate
to the abdominal wall.
• A palpable epigastric mass may appear during
the disease from a pseudocyst or a large
inflammatory mass.

19. Vital Signs
– Pulse: commonly 100 to 150 beats/minute
– BP: Initially higher (due to pain) then low than
normal (3rd space losses and hypovolemia)
– Temperature: Normal initially; Increases
within 1 to 3 days (to 101°F to 103°F)
• Due to the severe retroperitoneal inflammatory
process and the release of inflammatory mediators
from the pancreas
– Respiration: Tachypnea with shallow
respirations (if the subdiaphragmatic
inflammatory exudate causes painful
breathing)

20. • Dyspnea may accompany pleural effusions,
atelectasis, ARDS, or congestive heart failure.
• Chest examination
– Limited diaphragmatic excursion if abdominal pain
causes splinting of the diaphragm, or
– Dullness to percussion and decreased breath sounds at
the lung bases if there is a pleural effusion.
• There may be disorientation, hallucinations,
agitation, or coma, which may be due to
– Alcohol withdrawal,
– Hypotension,
– Electrolyte imbalance such as hyponatremia,
hypoxemia,
– Fever, or
– Toxic effects of pancreatic enzymes on the central
nervous system.

21. • Conjunctival icterus, if present, may be due to
– Choledocholithiasis (gallstone pancreatitis) or
– Bile duct obstruction from edema of the head of the
pancreas, or
– From coexistent liver disease

22. • Uncommon findings in acute pancreatitis include
– Panniculitis with subcutaneous nodular fat necrosis
May be accompanied by polyarthritis (PPP
syndrome) and thrombophlebitis in the legs, and
polyarthritis.
Subcutaneous fat necroses are 0.5- to 2-cm
tender red nodules that usually appear over the
distal extremities but may occur over the scalp,
trunk, or buttocks.
They occasionally precede abdominal pain or
occur without abdominal pain, but usually they
appear during a clinical episode and disappear
with clinical improvement

23. • Some physical findings point to a specific cause
of acute pancreatitis.
– Hepatomegaly, spider angiomas, and thickening of
palmar sheaths favor alcoholic pancreatitis.
– Eruptive xanthomas and lipemia retinalis suggest
hyperlipidemic pancreatitis.
– Parotid pain and swelling are features of mumps.
– Band keratopathy (an infiltration on the lateral margin
of the cornea) occurs with hypercalcemia

24. Diagnosis
• The diagnosis is established by two of the
following three criteria:-
– Acute, severe, persistent epigastric pain +/- radiation
to back
– Elevated serum lipase 3x upper limit of normal
– Characteristic CT, U/S or MRI findings

25. Why amylase isn’t that preffered
anymore

26. • Other associated clinical and lab features may
include:-
Nausea/emesis(90%), fever, tachycardia, and
abnormal findings on abdominal examination.
Laboratory studies may reveal leukocytosis,
hypocalcaemia, and hyperglycemia.

27. Differential diagnosis

28. Acute pancreatitis Vs Acute cholecystitis
Acute pancreatitis
• Elevated serum amylase
• Pain may be more
epigastric, periumbilical
or LUQ.
Acute cholecystitis
• Elevated serum amylase
• Pain may be more right
sided or epigastric.
• U/S is diagnostic for
acute cholecystitis.

29. Clinical course and classifications
• The Revised Atlanta Criteria:-
defines phases of acute pancreatitis
outlines severity of acute pancreatitis
clarifies imaging definitions

30. Phases of acute pancreatitis
• Two phases of acute pancreatitis have been
defined:-
– early (<2 weeks)
– late (>2 weeks)
• In the early phase of acute pancreatitis, which
lasts 1–2 weeks, severity is defined by clinical
parameters rather than morphologic findings.

31. • Most patients exhibit SIRS, and if this persists,
patients are predisposed to organ failure.
• Three organ systems should be assessed to
define organ failure: respiratory, cardiovascular,
and renal.
• Organ failure is defined as a score of 2 or more
for one of these three organ systems using the
modified Marshall scoring system.
• Persistent organ failure (>48 h) is the most
important clinical finding in regard to severity of
the acute pancreatitis episode.

33. • Organ failure that affects more than one organ is
considered multisystem organ failure.
• CT imaging is usually not needed or
recommended during the first 48 h of admission
in acute pancreatitis.

34. • The late phase is 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.

35. • The radiographic feature of greatest importance
to recognize in this phase is the development of
necrotizing pancreatitis on CT imaging.
• Necrosis generally prolongs hospitalization and,
if infected, may require operative, endoscopic, or
percutaneous intervention.

36. Classification
• According to the Atlanta classification, acute
pancreatitis can be divided into two broad
categories:-
 Interstitial edematous acute pancreatitis, which is
characterized by acute inflammation of the pancreatic
parenchyma and peripancreatic tissues, but without
recognizable tissue necrosis.
 Necrotizing acute pancreatitis, which is characterized
by inflammation associated with pancreatic
parenchymal necrosis and/or peripancreatic necrosis.

37. • According to the severity, acute pancreatitis is
divided into the following:-
 Mild acute pancreatitis, which is characterized by the
absence of organ failure and local or systemic
complications
 Moderately severe acute pancreatitis, which is
characterized by no organ failure or transient organ
failure (<48 hours) and/or local complications
 Severe acute pancreatitis, which is characterized by
persistent organ failure (>48 hours) that may involve
one or multiple organs

39. Severity

40. Mild acute pancreatitis
• Is without local complications or organ failure.
• Most patients with interstitial acute pancreatitis
have mild pancreatitis.
• The disease is self-limited and subsides
spontaneously, usually within 3–7 days after Rx
is instituted.
• Oral intake can be resumed if the patient is:-
 Hungry,
 Has normal bowel function,
 And is without nausea and vomiting.

41. • Typically, a clear or full liquid diet has been
recommended for the initial meal; however, a
low-fat solid diet is a reasonable choice following
recovery from mild acute pancreatitis.

42. 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 >1 week.

43. Severe acute pancreatitis
• Is characterized by persistent organ failure(>48
h). Organ failure can be single or multiple.
• A CT scan or magnetic resonance imaging
(MRI) should be obtained to assess for necrosis
and/or complications.
• If a local complication is encountered,
management is dictated by clinical symptoms,
evidence of infection, maturity of fluid collection,
and clinical stability of the patient.
• Prophylactic antibiotics are not recommended

44. Indications for monitoring or ICU admission
• Pulse <40 or >150 beats/minute
• Systolic arterial pressure <80 mmHg or mean arterial
pressure <60 mmHg or diastolic arterial pressure >120
mmHg
• Respiratory rate >35 breaths/minute
• Serum sodium <110 mmol/L or >170 mmol/L, serum
potassium <2.0 mmol/L or >7.0 mmol/L, serum glucose
>800 mg/dL, serum calcium >15 mg/dL
• PaO2 <50 mmHg
• pH <7.1 or >7.7
• Anuria
• Coma

45. Imaging in acute pancreatitis
• Two types of pancreatitis are recognized on
imaging based on pancreatic perfusion:-
 Interstitial
 Necrotizing
• CT imaging is best evaluated 3–5 days into
hospitalization when patients are not responding
to supportive care to look for local complications
such as necrosis.

47. Interstitial pancreatitis
• occurs in 90–95% of admissions for acute
pancreatitis and is characterized by diffuse
gland enlargement, homogenous contrast
enhancement, and mild inflammatory changes
or peripancreatic stranding.
• Symptoms generally resolve with a week of
hospitalization.

49. Necrotizing pancreatitis
• Occurs in 5–10% of acute pancreatitis
admissions and does not evolve until several
days of hospitalization.
• It is characterized by lack of pancreatic
parenchymal enhancement by intravenous
contrast agent and/or presence of findings of
peripancreatic necrosis.
• CT identification of local complications, particularly
necrosis, is critical in patients who are not responding to
therapy because patients with infected and sterile
necrosis are at greatest risk of mortality.

51. • The median prevalence of organ failure is 54%
in necrotizing pancreatitis.
• The prevalence of organ failure is perhaps
slightly higher in infected versus sterile necrosis.
• With single-organ system failure, the mortality is
3–10% but increases to 47% with multisystem
organ failure

52. Acute management principles
1. Replace fluids
– Monitor volume status
• RL contraindicated in hypercalcemia induced
pancreatitis
2. Pain control
3. Nutrition
4. Monitor for complications
• All patients with Gallstone Pancreatitis should
also have ERCP on the same admission.

53. Fluid management
• NPO
• Intravenous fluids of RL or NS are initially
bolused at 15–20 mL/kg (1050–1400 mL),
followed by 2–3 mL/kg per hour (200–250 mL/h),
to maintain urine output >0.5 mL/kg per hour.
• Serial bedside evaluations are required every 6–
8 h to assess vital signs, oxygen saturation, and
change in physical examination to optimize fluid
resuscitation.

54. Aggressive Vs moderate fluid resuscitation

58. RL vs NS
• Lactated Ringer’s solution has been shown to
decrease systemic inflammation (lower CRP
levels from admission) and may be a better
crystalloid than normal saline.

59. • Targeted resuscitation strategy With
measurement of hematocrit and BUN every 8–
12 h is recommended to ensure adequacy of
fluid resuscitation and monitor response to
therapy.
• A rising BUN during hospitalization is not only
associated with inadequate hydration but also
higher in-hospital mortality.
• A decrease in hematocrit and BUN during the
first 12–24 h is strong evidence that sufficient
fluids are being administered
• Adjustments in fluid resuscitation may be
required in patients with cardiac, pulmonary, or
renal disease.

60. • A rise in hematocrit or BUN during serial
measurement should be treated with a repeat
volume challenge with a 2-L crystalloid bolus
followed by increasing the fluid rate by 1.5 mg/kg
per hour.
• If the BUN or hematocrit fails to respond (i.e.,
remains elevated or does not decrease) to this
bolus challenge and increase in fluid rate,
consideration of transfer to an intensive care unit
is strongly recommended for hemodynamic
monitoring

61. Pain control
• Hydromorphone or fentanyl (intravenous) may
be used for pain relief in acute pancreatitis.
Fentanyl is being increasingly used due to its
better safety profile, especially in renal
impairment.
• Meperidine has been favored over morphine for
analgesia in pancreatitis because studies
showed that morphine caused an increase in
sphincter of Oddi pressure.

62. Nutrition
• A low-fat solid diet can be administered to
subjects with mild acute pancreatitis after the
abdominal pain has resolved.
• Enteral nutrition should be considered 2–3 days
after admission in subjects with more severe
pancreatitis instead of total parenteral nutrition
(TPN).
• Enteral feeding maintains gut barrier integrity,
limits bacterial translocation, is less expensive,
and has fewer complications than TPN.
• The choice of gastric versus nasojejunal enteral
feeding is currently under investigation.

63. Monitoring & management of local
complications
• A multidisciplinary team approach is
recommended including gastroenterology,
surgery, interventional radiology, and intensive
care specialists.
• Local complications include:-
– Necrosis
– Psuedocyst
– Pancreatic duct disruption
– Perivascular complication
– Extrapancreatic infection

64. Necrosis
• Necrotizing pancreatitis (20%)
– Acute necrotic collection < 4weeks
– Walled off necrosis > 4 weeks
• The management of necrosis requires a
multidisciplinary team approach.
• The benefits of percutaneous aspiration of
necrosis with Gram stain and culture should be
considered or discussed if there are ongoing
signs of possible pancreatic infection such as
sustained leukocytosis, fever, or organ failure.

65. • There is currently no role for prophylactic
antibiotics in necrotizing pancreatitis.
• Start BS ABX while awaiting gram and stain and
culture in a pt who apear septic.
• If cultures are negative, the antibiotics should be
discontinued to minimize the risk of developing
opportunistic or fungal superinfection

66. • Repeated fine-needle aspiration and Gram stain
with culture of pancreatic necrosis may be done
every 5–7 days in the presence of persistent
fever.
• Repeated CT or MRI imaging should also be
considered with any change in clinical course to
monitor for complications (e.g., thromboses,
hemorrhage, abdominal compartment
syndrome)

67. • Necrosis
 Sterile
 Infected
• sterile necrosis is most often managed
conservatively unless complications arise.
• Once a diagnosis of infected necrosis is
established and an organism identified, targeted
antibiotics should be instituted.
• Pancreatic debridement (necrosectomy) should
be considered for definitive management of
infected necrosis, but clinical decisions are
generally influenced by response to antibiotic
treatment and overall clinical condition.

68. PSEUDOCYST
• The incidence of pseudocyst is low, and most
acute collections resolve over time.
• Less than 10% of patients have persistent fluid
collections after 6 weeks that would meet the
definition of a pseudocyst.
• Only symptomatic collections should be drained
with surgery or endoscopy or by percutaneous
route.

69. PANCREATIC DUCT DISRUPTION
• Pancreatic duct disruption may present with
symptoms of increasing abdominal pain or
shortness of breath in the setting of an enlarging
fluid collection.
• Diagnosis can be confirmed on MRCP or
ERCP.
• Placement of a bridging pancreatic stent for at
least 6 weeks is >90% effective at resolving the
leak.
• Nonbridging stents are less effective (25–50%).

70. PERIVASCULAR COMPLICATIONS
• Perivascular complications may include splenic
vein thrombosis with gastric varices and
pseudoaneurysms.
• Gastric varices bleed <5% of the time.
• Life-threatening bleeding from a ruptured
pseudoaneurysm can be diagnosed and treated
with mesenteric angiography and embolization.

71. EXTRAPANCREATIC INFECTIONS
• Hospital-acquired infections occur in up to 20%
of patients with acute pancreatitis.
• Patients should be continually monitored for the
development pneumonia, urinary tract infection,
and line infection.
• Continued culturing of urine, monitoring of chest
x-rays, and routine changing of intravenous lines
are important during hospitalization.

72. ACG guidelines on ABX

73. ACG guidelines on ERCP

74. References
• Harrisons internal medicine 21th edition
• Uptodate
• https://www.nejm.org/doi/pdf/10.1056/NEJ
Moa2202884?articleTools
• Fundamentals of pathology
• ACG guidelines on acute pancreatitis 2022
• Infographics from the internet

75. Thanks, any questions