creation date: 2025-11-20 15:52
tags: Pathologies
Acute Pancreatitis
Background
Definitions
Acute pancreatitis refers to an inflammatory condition of the pancreas characterized by abdominal pain and elevated pancreatic enzymes.
Etiology
The causes of pancreatitis can be summarized by the mnemonic I GET PP SMASHED:
- Idiopathic
- Gallstones
- Ethanol
- Trauma
- Posterior duodenal ulcer rupture
- Pancreas divisum (congenital)
- Steroids
- Mumps
- Autoimmune
- Scorpion venom
- Hypercalemia/Hypertriglyceridemia
- ERCP
- Drugs
Gallstones
Accounts for 40-70% of cases of acute pancreatitis. Stones <5 mm were more likely to pass through the cystic duct and thus cause obstruction at the ampulla.
Two factors are hypothesized to cause pancreatitis:
- Reflux of bile into pancreatic duct due to obstruction from gallstone
- Reflux of bile due to edema/secondary to stone passage
Alcohol
Accounts for 25-35% of cases and typically attributed to chronic alcohol use disorder. There are debates regarding whether alcohol-induced pancreatitis is a strictly acute process or if chronic pancreatitis is present in many cases but only present acutely during a alcohol-induced episode.
The mechanism is through to be related to alcohol-induced increased synthesis of pancreatic enzymes. The digestive and lysosomal enzymes are thought to be responsible for pancreatic injury.
Hypertriglyceridemia
In 1-14% of cases, serum triglyceride concentrations above 11 mmol/L can result in acute pancreatitis. Concentration above 7 mmol/L puts patient at risk.
Iatrogenic
Acute pancreatitis is a possible complication of ERCP (3-5% of patients).
Medications that may induce pancreatitis may result from:
- Immunologic reactions (eg. aminosalicylates, sulfonamides)
- Direct toxicity (eg. diuretics, sulfonamides)
- Accumulation of toxic metabolic (eg. valproic acid)
- Overstimulation of acinar cells (eg. GLP-1 agonists)
- Ischemia (eg. diuretics, azathioprine)
- Intravascular thrombosis (eg. estrogen)
- Increased pancreatic juice viscosity (eg. diuretics, steroids)
Idiopathic / Genetic Risk
In rare circumstances, patients may be genetically predisposed to recurrent acute pancreatitis. This may be notable in younger patients.
Pathophysiology
Following an inciting event due to the various etiology, digestive enzymes (particularly trypsin) are activated prematurely in the pancreatic acinar cells rather than the intestinal lumen. This could be due to elevated intraductal pressure (eg. with obstruction), or change in signalling.
The activation of trypsin results in an activation cascade of proteolytic enzymes. This mediates pancreatic autodigestion and trigger the release of proinflammatory mediators.
Inflammatory cascade causes endothelial injury, increased vascular permeability, and microvascular thrombosis which manifest as systemic inflammatory response. The systemic effects can range from self-limiting edema to necrosis, organ failure, and death which can be classified as interstitial edematous pancreatitis and necrotizing pancreatitis, respectively.
Clinical Presentation
Signs & Symptoms
Most patients present with acute onset of persistent, severe epigastric and LUQ abdominal pain. Additional RUQ pain may be present and rarely present as confined LUQ pain. Other symptoms include:
- Nausea and vomiting which can persist
- Radiation of pain to back
- Pain may be relieved by sitting up or bending forward (Inglefinger’s sign)
- Abdominal distention due to secondary ileus
- Scleral icterus due to obstructive jaundice (choledocholithiasis or pancreatic head edema)
In patients with gallstone pancreatitis:
- Well localized and rapid onset of pain
- Maximum intensity in 10-20 minutes
In patients with hereditary, metabolic, or alcohol-induced pancreatitis:
- Less abrupt onset
- Poorly localized
Presentation can vary based on the severity of the pancreatitis:
Mild
- Absence of organ failure and local/systemic complications
Moderately severe - Transient organ failure (resolves <48 hrs) and/or local/systemic complications without persistent organ failure
Severe - Persistent organ failure that may involve one or multiple organs
- Dyspnea due to diaphragmatic inflammation, pleural effusions, ARDS
- Fever, tachypnea, hypoxemia, hypotension
If hemorrhage is induced, findings include:
- Grey Turner’s sign (bruising along the flanks downwards)
- Cullen’s sign (bruise just under umbilicus)
History & Physical Exam
History should assess for features of illness which may be suggestive of etiology. Relevant components include:
- History of gallstones
- Alcohol consumption
Similarly, physical exam may have findings suggestive of underlying etiology:
- Hepatomegaly - alcoholic pancreatitis
- Xanthomas - hyperlipidemic pancreatitis
- Parotid swelling - mumps
Risk factors
Diagnosis
Criteria
Diagnosis is made with the presence of two of the following criteria:
- Acute onset of persistent, severe, epigastric pain which may radiate to the back
- Elevation in serum lipase or amylase to ≥3x the ULN
- Characteristic findings of acute pancreatitis on imaging
Work-up
Laboratory studies
Pancreatic enzymes and products:
- Serum amylase - rise within 6-12 hrs; ≥3x ULN has Sn 67-83%, Sp 85-98%
- Serum lipase - rise within 4-8 hr, peak at 24hrs; Sn 82-100%, Sp high
- Trypsinogen activation peptide (TAP) may be useful for early detection due to rapid rise
- CRP - >150 mg/L at 48 hours associated with severe pancreatitis
Imaging
Typically starts with ultrasound but a CT is often used subsequently. Abnormal findings depend on modality:
Abdominal and chest radiographs
- Generally unremarkable in mild disease
- Severe may see localized ileus or colon cutoff sign (paucity of air in colon distal to splenic flexure due to functional spasm)
Abdominal ultrasound
- Diffusely enlarged and hypoechoic pancreas
- Gallstones may be visualized
- Peripancreatic fluid (anechoic)
CT abdomen with contrast
- Interstitial edematous pancreatitis: focal or diffuse enlargement of pancreas with heterogeneous enhancement
- Necrotic pancreatitis: areas of necrosis seen as lack of enhancement from IV contrast
- Pancreatic mass if underlying cancer
MRI
- Highest sensitivity for early acute pancreatitis but is rarely used due to availability and longer scanning time (not ideal for acutely ill patients)
Assessment of disease severity
Following diagnosis, evaluation for organ failure and complications should be performed.
Every 24 hours, the following should be obtained:
- CBC
- Complete metabolic panel
- CRP
- Lactate
Differential
Other causes of epigastric abdominal pain include:
- Peptic ulcer disease
- Choledocholithiasis or cholangitis
- Cholecystitis
- Perforated viscus
- Intestinal obstruction
- Mesenteric ischemia
- Hepatitis
Red Flags / Complications
Local complications include:
- Acute peripancreatic fluid collection
- Pancreatic pseudocyst
- Acute necrotic collection (infection risk)
- Walled-off necrosis (infection risk)
Systemic complications include exacerbation of underlying comorbidity, ARDS SIRS, DIC, and organ failure.
Management
Initial Management
Fluid replacement
IV hydration with lactated Ringer’s solution is recommended:
- Initial 10 mL/kg bolus if hypovolemic and 1.5 mL/kg/hr following
- Goal-directed therapy for fluid management
Pain control
Abdominal pain should be treated for patient comfort and to avoid hemodynamic instability. Options include:
- Oral opioids
- NSAIDs
In severe cases, hydromorphone or fentanyl can be used.
Monitoring
Close monitoring is indicated for 24-48 hours. This includes:
- Vitals and O2 sat
- Electrolytes and kidney function
- Glucose
- Urinary bladder pressures (if ICU)
Nutrition
Patients are kept on NPO status for acute pancreatitis.
In patients with mild pancreatitis without nausea, vomiting, or paralytic ileus, an oral diet can be resumed as soon as tolerated. In moderate-to-severe cases, enteral nutrition may be needed.
Antibiotic Use
Antibiotics are not routinely recommended for acute pancreatitis without infection. However, if extrapancreatic infection is suspected, empiric antibiotics with broad-spectrum coverage (eg. vancomycin, cefepime) should be initiated until cultures are shown to be negative.
Treatment of Complications
Peripancreatic fluid collection
Typically develops within 4 weeks of onset and asymptomatic. In most cases, they resolve without drainage.
Acute necrotic collection
Need for intervention depends on whether the necrotic collection is infected or if it is sterile but may cause other complications. Management may include antibiotics and/or percutaneous drainage.
Pancreatic pseudocyst and Walled-off necrosis
Typically develops >4 weeks after onset and has a well-defined inflammatory wall. Management ranges from monitoring for gradual self-resolution to drainage if symptomatic.
Abdominal compartment syndrome
Severe pancreatitis is a risk factor for abdominal compartment syndrome, characterized by a systained intra-abdominal pressure >20 mmHg with new onset organ failure.
Long-term complications
Acute pancreatitis can exacerbate underlying comorbidities such as CAD, lung disease. Additionally, patients should be treated for alcohol withdrawal and hyperglycemia is applicable.
Management of Underlying Etiology
Gallstone pancreatitis
In patients with gallstone pancreatitis, most stones pass to the duodenum without intervention. However, in patients with persistent obstruction, ERCP for stone removal and cholecystectomy should be performed.
Alcohol-associated pancreatitis
Patients should receive brief alcohol intervention as inpatients for unhealthy alcohol use. Alcohol use disorder and its treatment are discussed separately.
Others
Other rarer etiologies include hypertriglyceridemia, hypercalcemia, and medications.