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1. Acute Pancreatitis
Moderator: Dr. Semir ( MD, Internist )
Presentor : Dr. Hussen ( R1 )

2. Out lines
• Introduction
• Etiology and pathophysiology
• Clinical presentation
• Diagnosis
• Severity assessment
• Complications & treatment

3. Introduction

4. Introduction
• Acute pancreatitis : acute inflammatory process pancrease
• With involvement regional tissues or remote organ system
• Should be suspected in Pt with severe acute upper abdominal pain
• But requires biochemical/radiologic evidence to confirm the diagnosis.
• The incidence of acute pancreatitis in United States ranges from 4.9
to 35/100,000 population
• Mortality rate about 5%.

5. ETIOLOGY AND PATHOGENESIS
• Many causes of AP ,but how to cause inflammation not fully
understood
• Gallstones and alcohol account for 2/3 in the USA.
• Others include: idiopathic, metabolic, iatrogenic, medication, genetic
risk, trauma, autoimmune, neoplasia, structural, vascular, infection and
toxins.

6. Gallstones
 Most common cause- ~40-70%- of cases.
 Only 3% to 7% of patients with gallstones develop AP.
 risk of AP in patients with at least one gallstone <5 mm in diameter is >4x than
patients with larger stones!
 Two factors have been suggested as the possible initiating event in gallstones:
1. reflux of bile into the pancreatic duct due to transient obstruction of the ampulla during
passage of gallstones , or
2. obstruction at the ampulla secondary to stone or edema resulting from the passage of a
stone.

7. Alcohol
Alcohol : the second most common cause, responsible for 25–35% of cases in the
USA.
 Only 10% of chronic alcoholic pts develop chronic pancreatitis.
Proposed mechanism;
 direct toxicity vs toxic-metabolic theory.
 Alcohol modulates exocrine function to increase the lithogenicity of pancreatic
fluid.
 Cigarette smoking increases the risk of alcoholic and idiopathic pancreatitis, but
not gallstone pancreatitis.

8. Post-ERCP….
 Acute pancreatitis occurs in 5–25% of patients undergoing diagnostic or
therapeutic ERCP.
 Risk factors for post-ERCP pancreatitis include
• minor papilla sphincterotomy,
• sphincter of Oddi dysfunction,
• prior history of post-ERCP pancreatitis,
• age<60 years, >2 contrast injections into the pancreatic duct, and endoscopic
trainee involvement.

9. Hypertriglyceridemia
 Third most common identifiable couse
 in 1–14% of cases;
 serum TG levels are usually (>1000 mg/dL).
 are prone to recurrent episodes of pancreatitis.
 any factor (e.g., drugs or alcohol, obesity,DM, Px and hypothyroidism) that causes
an abrupt increase in serum TG can precipitate about of AP
 Pathogenesis: Unclear
 The hydrolysis of TGs by pancreatic lipase and release of free fatty acids that
induce free radical damage can directly injure cell membranes..

10. Drugs:
 Probably accounts for about less than 5% of cases.
 Cause pancreatitis either by
 a hypersensitivity reaction, direct toxic effect, accumulation of a toxic
metabolite, ischemia, intravascular thrombosis and increased viscosity of
pancreatic joice.
 Classified ( class I—IV ) based on the number of case reported, latency period
and reaction with rechallenge.
 Hypersensitivity reaction.
 occur a few weeks after starting the drug and not dose related.
 On rechallenge with the drug, pancreatitis recurs within hours to days.
 Eg.: Aminosalicylates, metronidazole, and tetracycline

11. Drugs…
 Accumulation of a toxic metabolite that may cause pancreatitis
 Typically after several months of use.
 Eg. Valproic acid and didanosine; drugs that induce hypertriglyceridemia
(e.g., thiazides, isotretinoin, tamoxifen) are also in this category

12. Pathophysiology
 Pancreatic autodigestion results when:
 Intraacinar activation of proteolytic enzymes (e.g.trypsinogen, chymotrypsinogen,
proelastase,
 and lipolytic enzymes such as phospholipase A)
 The initial step is conversion of trypsinogen to trypsin, in sufficient quantities to
overwhelm normal mechanisms to remove active trypsin.
 Trypsin, in turn, catalyzes conversion of proenzymes
 The activation, chemoattraction, and sequestration of leukocytes and macrophages
in the pancrease lead to release of cytokines and oxidative stress.
 The active enzymes and cytokines then digest cellular membranes and cause
proteolysis, edema, interstitial hemorrhage, vascular damage, coagulation necrosis,
fat necrosis, and parenchymal cell necrosis.

14. Con’t

15. Con’t
 AP evolves in three phases.
 Initial phase: intrapancreatic digestive enzyme activation and acinar cell
injury.
 Second phase: Activation, chemoattraction, and sequestration of leukocytes
and macrophages in the pancreas, resulting in an enhanced intrapancreatic
inflammatory reaction.
 Third phase: Effects of activated proteolytic enzymes and cytokines,
released by the inflamed pancreas, on distant organs,SIRS,ARDS

16. Clinical Evaluation
History:
 abdominal pain is the most common symptom.
 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.
 Pain may vary from a mild discomfort to severe, constant, and
incapacitating distress. Hx of etiology [alcolhol…]
 characteristically, the pain, which is steady and boring.
 is located in the epigastrium and periumbilical region, and may radiate to
the back, chest, flanks, and lower abdomen.

17. Cont…
 There is little pain relief with changing position(leanigforeword).
 Pain is absent in 5% to 10% of attack.
 90% of affected patients have nausea and vomiting.
 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.
 Fever and yellowish discoloration of eye may associated with pain

18. Physical Examination
 Physical findings vary with the severity of an attack.
 Low-grade fever, tachycardia, hypoxemia and hypotension are common.
 Shock can found in severe case
 severe pancreatitis, patients look severely ill and often have abdominal distention,
especially epigastric, which is due to gastric, small bowel, or colonic ileus
 bowel sounds are reduced and may be absent.
 Jaundice occurs infrequently(chledocholithiasis)
 Dyspnea may accompany pleural effusions, atelectasis, ARDS.

19. Cont…
 In 3%, ecchymotic discoloration along the flank or in the periumbilical
region
 Grey Turner’s sign &Cullen’s sign,
 Retroperitoneal bleeding
 Some physical findings point to a specific cause of acute pancreatitis.
 Hepatomegaly, spider angiomas, and thickening
of palmar sheaths favor alcoholic pancreatitis.
• Parotid pain and swelling are features of mumps.
• Xanthomas in hyperlipidemic pancreatitis
• Palpable epigastric mass-pseudocyst or a large inflammatory mass

21. Laboratory diagnosis
Pancreatic Enzymes;
In general, the diagnosis of acute pancreatitis relies on at least a 3-fold elevation of serum
amylase or lipase in the blood.
Serum Amylase Level;
 It is usually increased on the first day of symptoms, and it remains elevated for 3 to5 days
in uncomplicated attacks.
 Sensitivity is ( 67 to 83%%)
 Limitations
 may be not upper normal of limit in alcoholic pacre
 may be falsely negative in hyperlipedimic patients.
 false positive.
 doesn’t tell severity, prognosis.

22. Serum Lipase Level and Others Lab
 the sensitivity ~85% to 100%.
 have greater specificity for pancreatitis than amylase.
 Serum lipase always is elevated on the first day of illness and remains elevated
longer than does the serum amylase, providing a higher sensitivity
 Levels usually return to normal within 8 to 14 days unless there is pancreatic
ductal disruption, ductal obstruction, or pseudocyst formation.
 Other Lab ( CRP, serum TG, procalcitonin )
 CBC leukocytosis and hemaconcetration
 OFT BUN
 Eletrolyte hypocalcemia

23. Imaging
Abdominal Plain Film;
 range from normal-to-localized ileus of a segment of small intestine;
 (“sentinel loop”) or the colon cut-off sign in more severe disease.
 helps exclude other causes of abdominal pain, such as bowel obstruction
,calcified gallstone and pancre abscess ( gas in retroperiton)
 CXR; including elevation of a hemidiaphragm,
 pleural effusion(s), basal or
 plate-like atelectasis secondary to limited respiratory excursion, and pulmonary infiltrates.

24. Imaging

25. Abdominal ultrasound and CT Scan
 used during the first 24 hours of hospitalization to search for;
 gallstones, ascites
 dilation of the bile duct due to choledocholithiasis.
 it is usually diffusely enlarged and hypoechoic.
 US can be used to evaluate progression of a pseudocyst.
 The 3 main indications for a CT in acute pancreatitis are to:
 (1) exclude other serious intra-abdominal conditions (e.g., mesenteric infarction or a perforated
ulcer),
 (2) stage the severity of acute pancreatitis, and
 (3) determine whether complications of pancreatitis are present.
 the presence of gas in the pancreas suggests pancreatic infection with a gas-forming organism

26. Cont…
 Helical CT is the most common technique.
 If possible, scanning should occur after the patient receives oral contrast,
followed by IV contrast to identify any areas of pancreatic necrosis
 Pancreatic necrosis manifested as perfusion defects after IV contrast may not
appear until 48 to 72 hours after onset of acute pancreatitis!!
 Acute pancreatitis is characterized by
 (1) enlargement of the pancreatic outline,
 (2) distortion of the pancreatic contour, and/or
 (3) a pancreatic fluid that has a different attenuation coefficient than
normal pancreas.

27. Diagnosis
• AP should be suspected in a patient with acute onset of a persistent,
severe, epigastric pain with tenderness on palpation.
 Diagnosis of acute pancreatitis require presences of 2 of the following 3 criteria:
1. symptoms (e.g., epigastric pain) consistent with pancreatitis,
2. a serum amylase or lipase level greater than 3 times the laboratory’s upper
limit of normal, and
3. radiologic imaging consistent with pancreatitis, using CT or MRI.

28. Complications
• About 20% of PT have moderately severe or severe AP with local or
systemic complications or organ failure
• Local complication include: acute peripancreatic fluid collection,
pancreatic pseudocyst, acute necrodsis collection and walled off
necrosis
• Systemic complication include: acute respiratory failure, Shock, and
renal failure may resolve in within 48hr or persistent for > 48hr

29. Predicting The Severity Of AP
• The ability to predict severity can help identify PT at increased risk for morbidity
and mortality, thereby assisting in appropriate early triage to intensive care units
and selection of PT for specific intervention.
• Many of predictive models have been developed to predict the severity of AP
based on clinical, laboratory, and radiologic risk factors, and various severity
grading systems. no “gold standard” prognostic score for predicting severe pancreatitis
• Severity is now defined by the presence of organ failure or complications
• Among these are:
• Ranson’s Criteria, Revised Atlanta classification, BISAP score, The APACHE II
score.

30. According to the revised Atlanta classification there are 3 grades of
severity of AP . Phase of AP,[early ,late] and imaging classif [interstial,
necrotizing]

31. acute pancreatitis varies from:
• Interstitial pancreatitis (pancreas blood supply maintained), which is
generally self-limited.
• Necrotizing pancreatitis (pancreas blood supply interrupted), in which
the extent of necrosis may correlate with the severity of the attack and
its systemic complications.

32. • Interstitial pancreatitis have a normally perfused gland, manifesting on contrast-enhanced
CT as a normal bright appearance.
• Necrotizing pancreatitis have greater than 30% of the gland that is not perfused, with low
attenuation.
• Pancreatic necrosis consists of focal or diffuse nonviable
pancreatic parenchyma and is usually accompanied by peripancreatic fat necrosis.
• Peripancreatic necrosis describes necrotic fatty and tissue debris around the pancreas.

35. • Pancreatic necrosis can be sterile or infected.
• An acute fluid collection occurs in 30% to 50% of cases of acute
pancreatitis, and most resolve spontaneously.
• A pseudocyst is a fluid collection that persists for 4 to 6 weeks and
becomes encapsulated by a wall of fibrous or granulation tissue.
• Pseudocysts are located adjacent to or off the body of the pancreas.

36. • The term for a walled-off fluid appearing pseudocyst-like structure
involving the pancreas is walled-off necrosis (WON).
• A pancreatic abscess is a circumscribed intra-abdominal collection of
pus occurring after an episode of acute pancreatitis or pancreatic
trauma.
• It usually develops close to the pancreas and contains little pancreatic
necrosis.

40. Ranson’s Criteria

42. Factors Assocaited With Severity
• Age >60 years
• Obesity, BMI >30
• Comorbid disease (Charlson Comorbidity Index)
Markers of Severity at Admission or Within 24 h
• • SIRS—defined by presence of 2 or more criteria:
• • Core temperature <36° or >38°C
• • Heart rate >90 beats/min
• • Respirations >20/min or Pco2 <32 mmHg
• • White blood cell count >12,000/μL, <4000/μL, or 10% bands
• • APACHE II
• • Hemoconcentration (hematocrit >44%)
• • Admission BUN (>22 mg/dL)
• BISAP Score

43. Management
• 1 General management
• 2 Management of complications
• 3 Management of underlying Predisposing conditions
The first step in managing patients with acute pancreatitis is
determining whether the pancreatitis is mild or severe
 Mild -is self-limited and subsides spontaneously, usually within 3-7
days after treatment is instituted
ICU care – severe AP

44. General managment
• Supportive care includes:
 Oxygen saturation maintenance
 NPO
 Intravenous fluids
 Pain control
 Correction of electrolyte and metabolic abnormality
 Nutritional therapy

45. Fluid Resuscitation
• 5 to 10 mL /kg /hr or 250 to 500 mL /hr of isotonic solution probably RL,
preferably during the first 24 hours after admission ( previous guideline)
• We use moderate resuscitation ( 1.5 ml/kg /hr in the firs 24 – 48hr,
preceded by a bolus of 10--20ml/kg in 1 -2hr only in Pt with hypovolemia,
moderately severe, severe, AKI, and other por predictive indication )
• The rate of fluid resuscitation is adjusted based on clinical assessment
• Fluid requirements reassessed at frequent intervals in the first 24 hrs and
for next 24 to 48 hrs.
• Adequate fluid replacement can be assessed by an improvement in V/S
(goal HR <120 , MAP 65 to 85 mmHg), UOP (>0.5 to 1 cc/kg/Hr) and
reduction in HCT (goal 35 to 44 percent) and BUN over 24 hours,
particularly if they were high at the onset

48. Pain management
• pain can be treated with opiate analgesics
• Opiate dosing is monitored and adjusted on a daily basis according to
ongoing needs
• Fentanyl, hydromorphone, or meperidine may be used for pain relief
• Severe pain can be treated with Pethidine (morphine causes the
sphincter of Oddi to contract and should be avoided).
• Pt should be monitored by V/S, UOP, laboratory for complic and
treatment response.
• The use of antibiotics in patients with suspected or confirmed
infected pancreatic necrosis

49. Nutritional Therapy
• 1 Oral Feeding ; In mild pancreatitis, a low-fat soft diet can be started after the
abdominal pain has resolved [ usualy after 24 hr] . In severe panc after local complic
resolving
• 2 Enteral Nutrition : 2–3 days after admission in more severe pancreatitis instead of
TPN. -Nasojejunal tube or NGT
 Enteral feeding maintains
• gut barrier integrity,
• limits bacterial translocation,
• is less expensive, and has fewer complications than TPN.
• 3 Parenteral — Parenteral nutrition should be initiated in patients
 who do not tolerate enteral feeding
 nutritional goals cannot reached within two days

50. MANAGEMENT OF COMPLICATIONS

51. Pseudocyst
• patients who are symptomatic, have rapidly enlarging pseudocysts or have
systemic illness as a result of an infected pseudocyst should be drained
with surgery or endoscopy or by percutaneous route.
Infected necrosis : CT-guided perc. Aspr. [FNAC] with Gram’s stain and
culture is recommended
• If it reviled G-ve - carbipenem,
• fluoroquinolone plus metronidazole, or a
• third generation cephalosporin plus metronidazole
• If G+ve -vancomycin
• In patients who fail to improve, we perform debridement necrosis
(necrosectomy)

52. Sterile necrosis
• Continue conservative treatment for four to six weeks
• If abdominal pain persists for more than 8 weeks and prevents oral
intake, debridement should be considered
Splanchnic venous thrombosis
 Effective treatment of underlying pancreatitis may result spontaneous resolution
 Anticoagulation should be initiated if there is extension of the clot into the portal or
superior mesenteric vein resulting in hepatic decompensation or compromise of bowel
perfusion
Pseudoaneurysm: Life-threatening bleeding from a ruptured can be
diagnosed and treated with mesenteric angiography and embolization.

53. MANAGEMENT OF UNDERLYING
PREDISPOSING CONDITIONS
• Gallstone pancreatitis:
• Urgent ERCP (within 24 hours of admission) with endosocopic biliary
sphincterotomy and stone removal
-concomitant cholangitis
- common bile duct obstruction (visible stone on imaging)
• Cholecystectomy
• after recovery in all patients with gallstone pancreatitis prior to
hospital discharge
• including those patients who have undergone an endoscopic
sphincterotomy

54. Biliary sludge
• perform EUS to look for microlithiasis in the gallbladder or bile duct.
• Cholecystectomy should be performed in patients who have had an episode of
pancreatitis and have biliary sludge
• Alcoholic pancreatitis
AGA recommends brief alcohol counseling intervention during admission
• Hypertriglycerdemia
Serum triglycerides >1000 mg/dL are associated with AP.
Initial therapy as other AP and Insulin, plasmapheresis in selected pt
Outpatient therapies include
 control of diabetes if present,
administration of lipid-lowering agents,
weight loss, and avoidance of drugs that elevate lipid level

57. References
• Harrison,21st edition
• Up-to-date 2023
• ACG Guideline 2013
• Schwartz’s principles of surgery,11th edition

58. .