(1) Acute pancreatitis is an inflammatory condition of the pancreas most commonly caused by gallstones or alcohol abuse. (2) Damage to the pancreas leads to release of enzymes that autodigest pancreatic tissue. (3) Treatment involves fluid resuscitation, pain management, monitoring for complications like infection or pseudocyst formation, and identifying and addressing the underlying cause.

1. Group: WinnerzKlub
Year: 2020
ACUTE PANCREATITIS

2. ACUTE PANCREATITIS:
• An inflammatory condition of the pancreas.
• Most commonly caused by biliary tract disease or alcohol abuse.
• Damage to the pancreas leads to release of pancreatic enzymes (proteolytic) which
autodigests pancreatic tissue.
• Acute pancreatitis usually resolves within one-to-two weeks.
• Solid foods are generally avoided for a while in order to reduce the strain on the
pancreas.
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3. ETIOLOGY:
• Most common causes:
i. Biliary pancreatitis (e.g. gallstones, constriction of ampulla of Vater) ~40% cases.
ii. Alcohol-induced (~30% of cases).
iii. Idiopathic (~15% - 25% of cases).
• Other causes:
• Severe hypertriglyceridemia (> 1,000 mg/dl), hypercalcemia
• Post-ERCP (upto 10% patients develop pancreatitis post-ERCP).
• Certain drugs:
• Steroids, Sulfonamides, Loop & thiazide diuretics, Estrogen, Anticonvulsants.
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4. PATHOPHYSIOLOGY:
• Intrapancreatic activation of pancreatic enzymes: 2° to pancreatic ductal outflow
obstruction (e.g. gallstones, cystic fibrosis) or direct injury to pancreatic acinar cells (e.g.
alcohol, drugs).
• Increased proteolytic & lipolytic enzyme activity – destruction of pancreatic parenchyma.
• Attraction of pancreatic cells (neutrophils, macrophages) – release of inflammatory
cytokines – pancreatic inflammation (pancreatitis).
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5. CLINICAL FEATURES:
• Constant, severe epigastric pain
• Classically radiating towards the back
• Worse after meals & when supine
• Improves on leaning forwards
• Nausea, vomiting
• General physical examination:
• Signs of shock: tachycardia, hypotension, oliguria/anuria.
• Possibly jaundice in patients with biliary pancreatitis.
• Abdominal examination:
• Abdominal tenderness, distension (ascites), guarding
• Ileus with reduced bowel sounds & tympany on percussion.
• Pathognomonic sign:
• Cullen sign – bluish discoloration
preumbilical area).
• Grey-Turner sign – flank ecchymosis
with discoloration.
• Fox sign – ecchymosis over the
inguinal ligament.
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6. CLINICAL FEATURES:
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7. DIAGNOSIS:
• Pancreatitis can be diagnosed both clinically and chemically.
• Acute pancreatitis is diagnosed based on a typical clinical presentation, with abdominal
pain radiating to the back, and either detection of highly elevated pancreatic enzymes or
characteristic findings on imaging.
• Diagnosis tests which will be discussed here includes:
• Laboratory tests
• Imaging.
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8. DIAGNOSIS – LABORATORY TESTS:
i. Tests to confirm clinical diagnosis
• Increased serum pancreatic enzymes (Normal enzyme levels does not rule out
pancreatitis).
• Lipase: if upper reference range increases by 3 times or more.
• Amylase (nonspecific as increased level seen in may conditions).
ii. Tests to assess severity:
• Hematocrit (Hct)
• Should be conducted at presentation as well as 12hrs & 24hrs after admissions.
• Increased: (hemoconcentration) indicates 3rd space fluid loss & inadequate fluid
resuscitation.
• Decreased: indicates the rarer acute hemorrhagic pancreatitis.
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9. • WBC count (leukocytosis is an indication of severe pancreatitis).
• Blood urea nitrogen (Rising level >48hrs of resuscitation indicates persistent
third spacing of fluid & is a predictor of severe pancreatitis.
• Increased CRP and procalcitonin levels
• Increased ALT (Alanine aminotransferase) levels
iii. Tests to determine etiology:
• Alkaline phosphatase, bilirubin levels (evidence of gallstone pancreatitis).
• Serum calcium levels
• Serum triglyceride levels (fasting).
• NB: Hypercalcemia may cause pancreatitis, which may then, in turn, cause
hypocalcemia!
DIAGNOSIS – LABORATORY TESTS:
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10. i. Ultrasound: (most useful initial test)
• Indicated in all patients with acute pancreatitis
• Main purpose – detection of gallstones and/or dilatation of the biliary tract (indicating
biliary origin).
• Signs of pancreatitis:
• Indistinct pancreatic margins
• Peripancreatic build-up of fluid (hypoechogenic): evidence of ascites in some cases.
• Evidence of necrosis, abscesses, pancreatic pseudocysts.
ii. CT scan: not routinely indicated.
• Useful to assess severity and complications of acute pancreatitis.
DIAGNOSIS – IMAGING:
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11. iii. MRCP and ERCP
• Indications: suspected biliary or pancreatic duct obstructions.
• MRCP is noninvasive but less sensitive than ERCP.
• ERCP can be combined with sphincterotomy & stone extraction; but may worsen pancreatitis.
iv. Conventional X-ray:
• Sentinel loop sign: dilatation of a loop of small intestine in the upper abdomen
(duodenum/jejunum)
• A specific radiological sign of acute pancreatitis.
• Caused due to a functional ileus of small intestine adjacent to the pancreas due to
pancreatic inflammation.
• Colon cut-off sign: gaseous distention of the ascending & transverse colon that abruptly
terminates at the splenic flexure.
• Evidence of possible complications: pleural effusions, pancreatic calcium stones, helps rule
out intestinal perforation with free air.
DIAGNOSIS – IMAGING:
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12. DIFFERENTIAL DIAGNOSES:
• Intestinal manifestations:
• Acute peritonitis
• Appendicitis
• Acute mesenteric ischemia
• Acute cholecystitis
• Acute cholangitis
• Peptic ulcer disease
• Biliary colic
• Abdominal aorta aneurism
• Extra-intestinal manifestations:
• Myocardial infarction
• Bacterial pneumonia
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13. TREATMENT:
i. General measures:
• Admission to hospital and assessment of disease severity (consider ICU admission).
• Fluid resuscitation: aggressive hydration with crystalloids (e.g., lactated Ringer’s
solution, normal saline).
• Analgesia: IV opioids (e.g. fentanyl)
• Nil-by-mouth & IV fluids are recommended until the pain subsides.
• Nasogastric tube insertion: not routinely recommended; indicated in patients with
vomiting and/or significant abdominal distention.
• Nutrition:
• Begin enteral feeding (oral/ nasogastric/ nasojejunal) as soon as pain subsides.
• Total parental nutrition: only in patients who cannot tolerate enteral feeds (e.g.
those with persistent ileus & abdominal pain).
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14. ii. Drug Therapy:
• Analgesics: e.g. fentanyl or hydromorphone
• Antibiotics:
• Prophylactic antibiotic therapy is not recommended.
• Antibiotics should only be used in patients with evidence of infected necrosis
• (Samples from CT-guided fine needle aspiration sent for culture and Gram
staining to identify the appropriate antibiotic).
• Fenofibrates: in hyperlipidemia-induced acute pancreatitis.
• *Fenofibrates – a fibric acid derivative that functions to lower triglycerides.
• *Hyperlipidemia – condition of elevated serum concentration of both
triglycerides (>200 mg/dL) and cholesterol (>190 mg/dL).
TREATMENT:
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15. • Surgery/Procedure:
• Gallstone pancreatitis
• Urgent ERCP & sphincterotomy (within 24 hours): in patients with evidence of
choledocholithiasis and/or cholangitis, followed by cholecystectomy.
• Cholecystectomy (preferably during same admission once patient is stabilized;
or within 6 weeks): in all patients with gallstone pancreatitis.
• NB: *there is a 30% risk of recurrent acute pancreatitis if cholecystectomy is not
performed!
• “PANCREAS” – Perfusion (fluid resuscitation), Analgesia, Nutrition, Clinical (observation),
Radiology (imaging), ERC (endoscopic stone extraction), Antibiotics, Surgery (surgical
intervention, if necessary).
TREATMENT:
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16. • Localized:
• Bacterial superinfection of necrotic
tissue
• Pancreatic pseudocysts
• Pancreatic abscess
• Systemic:
• SIRS, sepsis, DIC
• Pneumonia, respiratory failure, ARDS
• Shock
• Prerenal failure due to volume
depletion
• Hypocalcemia
• Pleural effusion, pancreatic ascites
• Paralytic ileus
COMPLICATION(S):
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17. THE END:
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