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Pancreatitis (Acute)

Background Information

Aetiology

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 by eating
    • Pain improves with learning 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% 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

 

  • 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 commoner 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 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 upper limit of normal
  • CT / MRI findings consistent with acute pancreatitis

If a patient presents with typical clinical features of acute pancreatitis and has an elevated serum amylase or lipase levels (>3x upper limit of normal), this is sufficient to diagnose acute pancreatitis and initiate treatment, without waiting for imaging confirmation.

Diagnostic Tests

Blood Tests

Blood tests: [Ref1][Ref2]

  • Serum amylase and/or lipase (to diagnose acute pancreatitis)
  • LFT (cholestatic pattern suggests gallstone pancreatitis)
  • Serum triglyceride and calcium (to look for hypertriglyceridaemia and hypercalcaemia)
  • FBC, renal function, glucose
  • IgG4 levels (if autoimmune pancreatitis is suspected)

Serum lipase is preferred over serum amylase for the diagnosis of acute pancreatitis due to higher sensitivity, specificity, and a longer elevation period. [Ref]

In a patient with delayed presentation of acute pancreatitis, serum lipase should be measured, as it remains elevated for a longer period. [Ref]

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

Risk Assessment

The presence of the following features is associated with severe disease[Ref]

  • >55 y/o
  • Hypocalcaemia (**hypercalcaemia can cause acute pancreatitis, but severe pancreatitis causes hypocalcaemia!)
  • Hyperglycaemia (due to insulin deficiency)
  • ↑ WBC
  • ↑ LDH
  • ↑ AST
  • ↑ Urea (indicative of renal failure)
  • ↓ PaO2 (indicative of ARDS)

Disclaimer: multiple validated scoring systems exist to assess severity in acute pancreatitis. The criteria listed above represent common markers and variables frequently used for initial risk assessment, but may not include all scoring parameters.

Being aware of the trends noted above should be sufficient for the UKMLA.

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. Hartman’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]
  • Same-admission cholecystectomy is recommended to prevent recurrence
  • ERCP should NOT be performed routinely, only if there is concurrent cholangitis or persistent biliary obstruction
Alcohol-induced pancreatitis
Hypertriglyceridaemia-induced pancreatitis [Ref]
  • Acute: IV insulin OR plasmapheresis in selected cases to rapidly lower triglyceride levels
  • Long-term: dietary modification, lipid-lowering agents
Drug-induced pancreatitis
  • Withdrawal of the implicated medication is recommended if no alternative aetiology is identified

References

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