Background Information
Causes and Risk Factors
3 most common causes (in descending order of prevalence) are: [Ref]
- Gallstone (→ obstruction of pancreatic duct → backup of pancreatic secretions) – most common overall
- Alcohol use (alcohol metabolism generates toxic metabolites that cause premature activation of digestive enzymes within the pancreas)
- Hypertriglyceridaemia
I GET SMASHED is a commonly used acronym to remember the causes of acute pancreatitis: [Ref]
- I: idiopathic
- G: gallstones
- E: ethanol (alcohol)
- T: trauma
- S: steroids
- M: mumps
- A: autoimmune (e.g. IgG4-related disease)
- S: scorpion venom (rare..)
- H: hypertriglyceridaemia, hypercalcaemia, hypothermia
- E: ERCP (risk of acute pancreatitis after undergoing ERCP is ~10% in average patients, up to 30-50% in high-risk groups)
- D: drugs (key drugs: azathioprine, mesalazine, sodium valproate, thiazide diuretics, GLP-1 agonists)
Clinical Features
Symptoms
Typical presentation: [Ref]
- Sudden-onset severe epigastric pain
- Pain classically radiates to the back
- Pain worsens when lying down and with eating
- Pain improves when leaning forward
- Fever
- Nausea and vomiting
Signs
Typical signs: [Ref]
- Signs of shock (e.g. tachycardia, hypotension etc.)
- Abdominal tenderness
- Abdominal distension
- Decreased bowel sounds
The following signs are rare: [Ref]
- Grey Turner’s sign: bruising of the flanks
- Cullen’s sign: periumbilical bruising
Grey Turner’s and Cullen’s signs are classic textbook signs of acute pancreatitis. However, they are rarely seen in practice (<1% of cases).
Both are signs of retroperitoneal haemorrhage, typically from pancreatic inflammation or necrosis damaging blood vessels. Their presence indicates severe disease and poor prognosis.
Complications
Local Complications
Pancreatic Necrosis (sterile)
- Diagnosis
- Suspect if there are persistent or worsening symptoms [Ref]
-
- Confirmation: cross-sectional imaging (CT/MRI with contrast) 3-4 days after pancreatitis onset
- Findings: non-enhancing areas of pancreatic or peripancreatic tissue
- Confirmation: cross-sectional imaging (CT/MRI with contrast) 3-4 days after pancreatitis onset
- Management
- Most cases: conservative (interventions risk introducing infections)
Infected Pancreatic Necrosis
- Suspect if any of the following are present:
- New or persistent fever
- Bacteraemia
- Worsening leukocytosis
- Clinical deterioration or persistent unwellness
- Cross-sectional imaging (CT or MRI) demonstrates gas within a pancreatic or peripancreatic collection (highly specific for infected necrosis)
- Management [Ref]
- All patients: IV antibiotics
- Additional: Debridement
- Preferred: minimally invasive (endoscopic transluminal / percutaneous catheter techniques)
- Refractory cases: surgical debridement
Infected pancreatic necrosis (not sterile ones) is the key local complication requiring active treatment with antibiotics and drainage / debridement.
Other complications are typically managed supportively / conservatively. A large pancreatic pseudocyst causing symptoms may require endoscopic drainage.
Pancreatic Pseudocyst
- Definition: encapsulated collection of pancreatic fluid
- Can occur in both acute/chronic pancreatitis, typically after ≥4 weeks of an acute attack [Ref]
- Clinical features:
- Often asymptomatic
- Palpable abdominal mass
- Pressure effects
- Gastric outlet obstruction
- Duodenal obstruction
- Diagnosis
- Cross-sectional imaging (CT or MRI) demonstrating well-circumscribed, fluid-filled lesion with a defined wall
- Management
- Asymptomatic → typically conservative (as they often spontaneously resolve)
- Complicated or symptomatic cysts → drainage
- Preferred technique: endoscopic drainage (esp. if near stomach/duodenum)
Other Complications
- Biliary / duodenal obstruction (due to inflammation compressing adjacent structures)
- Pancreatic endocrine and exocrine insufficiency (although more common in chronic pancreatitis)
- Endocrine insufficiency → diabetes mellitus
- Exocrine insufficiency → abdominal bloating, steatorrhoea, fat-soluble vitamin deficiency
Systemic Complications
Acute pancreatitis triggers a severe systemic inflammatory response that causes widespread organ injury
- ARDS
- AKI
- DIC
- Sepsis (often secondary to infected pancreatic necrosis)
Diagnosis
Diagnostic Tests
Blood Tests
Initial workup for suspected acute pancreatitis: [Ref1][Ref2]
| Blood test | Rationale |
|---|---|
| Serum amylase and/or lipase | ↑ Levels suggest acute pancreatitis (>3x the ULN – also see diagnostic criteria)
Serum lipase is preferred over serum amylase for the diagnosis of acute pancreatitis due to higher sensitivity, specificity, and a longer duration of elevation. [Ref] In a patient with delayed presentation of acute pancreatitis, serum lipase should be measured, as it remains elevated for a longer period. [Ref] |
| FBC, U&Es | To assess pancreatitis severity – ↑ WCC and ↑ urea are associated with severe pancreatitis |
| Calcium | To assess for underlying cause – hypercalcaemia can cause acute pancreatitis
To assess pancreatitis severity – hypocalcaemia is associated with severe pancreatitis |
| LFTs | To assess for underlying cause – cholestatic LFTs may suggest gallstone pancreatitis
To assess pancreatitis severity – ↑ AST and ↓ albumin are associated with severe pancreatitis |
| Lipid panel | To assess for underlying cause – hypertriglyceridaemia can cause acute pancreatitis |
| Glucose | To assess pancreatitis severity – hypoglycaemia is associated with severe pancreatitis |
| LDH | To assess pancreatitis severity – ↑ LDH is associated with severe pancreatitis |
| Blood gas | To assess pancreatitis – ↓ PaO2 is associated with severe pancreatitis |
| IgG4 levels | To be considered if autoimmune pancreatitis is suspected |
Imaging
Choice of imaging: [Ref1][Ref2]
- 1st line: trans-abdominal ultrasound
- Mainly to detect gallstones or biliary obstruction (NOT to diagnose acute pancreatitis)
- The pancreas may appear normal in early disease
- Findings suggestive of acute pancreatitis:
- Enlarged, hypoechoic pancreas /peripancreatic fluid collections
- Biliary pancreatitis: suggested by cholelithiasis, biliary sludge, stones within the CBD, or CBD dilation
- 2nd line: CT / MRI with contrast (reserved for diagnostic uncertainty, atypical presentation, assess complications)
- Findings suggestive of acute pancreatitis (similar to US, but with higher sensitivity):
- Diffuse/focal pancreatic enlargement
- Heterogeneous or homogeneous enhancement
- Peripancreatic fat stranding / fluid collections
- Findings suggestive of acute pancreatitis (similar to US, but with higher sensitivity):
Diagnostic Criteria
At least 2 out of 3 of the following are diagnostic of acute pancreatitis (revised Atlanta classification):
- Abdominal pain suggestive of pancreatitis
- ↑ Serum amylase and/or lipase >3x the ULN
- CT / MRI findings consistent with acute pancreatitis
If a patient presents with typical clinical features of acute pancreatitis + elevated serum amylase or lipase level (>3x ULN), this is sufficient to diagnose acute pancreatitis and initiate treatment, without imaging confirmation.
Risk Assessment
The presence of the following features is associated with severe disease (PANCREAS): [Ref]
- P: ↓ PaO2 (indicative of ARDS)
- A: age >55 y/o
- N: ↑ neutrophils / white cell count
- C: ↓ calcium (**hypercalcaemia can cause acute pancreatitis, but severe pancreatitis causes hypocalcaemia)
- R: renal function (↑ urea)
- E: enzyme (↑ AST or ↑ LDH)
- A: ↓ albumin
- S: ↑ sugar (hyperglycaemia) (severe acute pancreatitis can cause exocrine pancreatic insufficiency → insulin deficiency)
The factors above are based on the Glasgow-Imrie score, most commonly used in clinical practice. Several other validated scoring systems can be used to assess the severity of acute pancreatitis (e.g. APACHE II in critically unwell patients)
For exams, focus on recognising the general trends associated with severe pancreatitis rather than memorising every component of each score. In clinical practice, scores would be calculated using a checklist or electronic calculator
Severity assessment helps guide the appropriate level of care (e.g. ward-based care vs HDU vs ICU)
Management
Initial Management
Fluid resuscitation, supportive care & nutritional support are the 3 main cornerstones in the initial management of acute pancreatitis (regardless of the cause)
Do not routinely offer prophylactic antibiotics in acute pancreatitis; they are reserved for confirmed or strongly suspected infected pancreatic necrosis or extra-pancreatic infection.
Fluid Resuscitation
Aggressive IV fluid resuscitation should be started immediately once the diagnosis is made:
- Fluid type: Isotonic fluids (e.g. Hartmann’s solution, 0.9% saline)
- Goal-directed fluid resuscitation is recommended as part of ongoing fluid therapy to avoid fluid overload
Hypovolaemia is common in acute pancreatitis due to fluid 3rd spacing and vomiting
Supportive care
Involving:
- Analgaesia
- Anti-emetics
- Electrolyte replacement
Nutritional Support
Key points regarding nutritional support:
- Do not routinely make patients NBM
- Early oral feeding is advised as soon as tolerated
- If unable to tolerate oral feeding → enteral feeding
- Only offer parenteral feeding if enteral feeding is not appropriate
Early nutrition (oral preferred) has been shown to reduce infectious and metabolic complications in acute pancreatitis.
Management of Underlying Cause
| Underlying cause | Management |
|---|---|
| Gallstone (biliary) pancreatitis [Ref] |
|
| Alcohol-induced pancreatitis |
|
| Hypertriglyceridaemia-induced pancreatitis [Ref] |
|
| Drug-induced pancreatitis |
|