- Clinical science
Acute pancreatitis is an inflammatory condition of the pancreas most commonly caused by biliary tract disease or alcohol abuse. Damage to the pancreas causes local release of digestive proteolytic enzymes that autodigest pancreatic tissue. Acute pancreatitis usually presents with epigastric pain radiating to the back, nausea and vomiting, and epigastric tenderness on palpation. The diagnosis is made based on the clinical presentation, elevated serum pancreatic enzymes, and findings on imaging (CT, MRI, ultrasound) that suggest acute pancreatitis. Treatment is mostly supportive and includes bowel rest, fluid resuscitation, and pain medication. Enteral feeding is usually quickly resumed once the pain and inflammatory markers begin to subside. Interventional procedures may be indicated for the treatment of underlying conditions, such as ERCP or cholecystectomy in gallstone pancreatitis. Localized complications of pancreatitis include necrosis, pancreatic pseudocysts, and abscesses. Systemic complications involve sepsis, ARDS, organ failure, and shock and are associated with a considerable rise in mortality.
- Most common causes
- Severe hypertriglyceridemia (> 1,000 mg/dl),
- Certain drugs
- Scorpion stings
- Viral infections (e.g., coxsackievirus B, mumps)
- Trauma (especially in children)
- Autoimmune and rheumatological disorders (e.g., Sjögren syndrome)
- Pancreas divisum
- Hereditary (e.g., mutation of the trypsinogen gene, cystic fibrosis)
To remember the most common causes of acute pancreatitis, think: "I GET SMASHED" (Idiopathic, Gall stones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion poison, Hypercalcemia, Hypertriglyceridemia, ERCP, Drugs).
Mechanisms of development
Sequence of events leading to pancreatitis
- Intrapancreatic activation of pancreatic enzymes: secondary to pancreatic ductal outflow obstruction (e.g., gallstones, cystic fibrosis) or direct injury to pancreatic acinar cells (e.g., alcohol, drugs)
- Increased proteolytic and lipolytic enzyme activity → destruction of pancreatic parenchyma
- Attraction of inflammatory cells (neutrophils, macrophages) → release of inflammatory cytokines → pancreatic inflammation (pancreatitis)
Sequelae of pancreatitis (depending on the severity of pancreatitis)
- Capillary leakage: release of inflammatory cytokines and vascular injury by pancreatic enzymes → vasodilation and increased vascular permeability → shift of fluid from the intravascular space into the interstitial space (third space loss) → hypotension, tachycardia →
- Pancreatic necrosis: uncorrected hypotension and third space loss → decreased organ perfusion → multiorgan dysfunction (mainly renal) and pancreatic necrosis
- Hypocalcemia: lipase breaks down peripancreatic and mesenteric fat; → release of free fatty acids that bind calcium → hypocalcemia (fatty saponification) 
Constant, severe epigastric pain
- Classically radiating towards the back
- Worse after meals and when supine
- Improves on leaning forwards
- Nausea, vomiting
- General physical examination
- Abdominal tenderness, distention, guarding
- Ileus with reduced bowel sounds and tympany on percussion
- Skin changes (rare)
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. Serum hematocrit is an easy test that should be conducted to help quickly predict disease severity.
- Tests to confirm clinical diagnosis
- Tests to assess severity
- Tests to determine etiology
- Ultrasound (most useful initial test): indicated in all patients with acute pancreatitis
CT scan: not routinely indicated
- At admission: only when the diagnosis is in doubt (e.g., not very highly elevated pancreatic enzymes, non-specific symptoms)
- > 72 hours of symptom onset: if complications such as necrotizing pancreatitis or pancreatic abscess (e.g., persistent fever and leukocytosis, no clinical improvement or evidence of organ failure > 72 hours of therapy) are suspected
- Sentinel loop sign: dilatation of a loop of small intestine in the upper abdomen (duodenum/jejunum)
- Colon cut off sign: gaseous distention of the ascending and 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
- 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)
- Bowel rest (NPO)and IV fluids are recommended until the pain subsides
- Nasogastric tube insertion: not routinely recommended; indicated in patients with vomiting and/or significant abdominal distention
- Analgesics: fentanyl or hydromorphone; consider pump administration (patient controlled analgesia = PCA)
- Fenofibrates: in hyperlipidemia-induced acute pancreatitis
- Biliary pancreatitis
"PANCREAS" - Perfusion (fluid replacement), Analgesia, Nutrition, Clinical (observation), Radiology (imaging), ERC (endoscopic stone extraction), Antibiotics, Surgery (surgical intervention, if necessary).
- IV access with two large-bore peripheral IV lines
- Identify and treat sepsis, if present.
- Aggressive IV fluid resuscitation 
- Electrolyte repletion
- Early enteral nutrition (if able to tolerate PO) 
- Acute pain management: parenteral analgesics with NSAIDs (e.g., ketorolac ) and/or opioids (e.g., morphine ) 
- IV antiemetics (e.g., ondansetron )
- Assess severity (e.g., )
- Consider an early general surgery consult if pancreatitis is severe or pancreatic necrosis is present.
- Vitals and urine output every 1–2 hours
- Serial abdominal examination
- Serial BMP, electrolytes, and CBC every 6–12 hours
- Consider continuous telemetry if electrolyte abnormalities are present or the patient is critically ill.
- Transfer to ICU if there is evidence of multiorgan dysfunction.
- Identify and treat the underlying cause.
- Gallstone pancreatitis 
- Lipid profile for hypertriglyceridemia: If present, initiate fibrate therapy at discharge.
- Alcohol use: alcohol cessation counseling
- Bacterial superinfection of necrotic tissue → fever
- Walled-off infected necrotic tissue; or pancreatic pseudocyst; typically develops > 4 weeks after an attack of acute pancreatitis
- Abdominal CT: visible contrast-enhanced abscess capsule with evidence of fluid (pus)
- Ultrasound: complex cystic, fluid collection with irregular walls and septations
- Treatment: cannulation and drainage; necrosectomy if other measures are not effective
- Pleural effusion
- Blood vessel erosion with bleeding
- SIRS, sepsis,
- Pneumonia, respiratory failure,
- Prerenal failure due to volume depletion
- Pleural effusion, pancreatic ascites
- Paralytic ileus
We list the most important complications. The selection is not exhaustive.
Important predictors of severity
- Age > 55
- Gastrointestinal bleeding
- Abnormal hematocrit within 48 hours
- Hypocalcemia and/or hyperglycemia
- Inflammatory markers: ↑↑ CRP, ↑ IL-6, ↑ IL-8
- Evidence of shock and/or organ failure
- CT findings: pancreatic edema, peripancreatic fluid collection, and/or necrosis of > 33% of the pancreas
- Numerous scoring systems exist (e.g, pancreatitis ) for assessing the severity and predicting the prognosis of acute