Acute Pancreatitis: When the Pancreas Goes Rogue

A fiery organ with a short fuse

If there’s one abdominal organ that holds a grudge, it’s the pancreas.
You can neglect it for years, overload it with alcohol, send gallstones tumbling past its duct, and most days, it’ll quietly get on with its enzyme-making duties.
But cross the line once, and it will explode in inflammation.

That, my friends, is acute pancreatitis, sudden, severe inflammation of the pancreas that can turn from mild discomfort to multi-organ failure in a matter of hours.

The basic plot

Under normal circumstances, pancreatic enzymes are produced in an inactive form, travel down the pancreatic duct, and get activated safely in the duodenum.

In acute pancreatitis, those same enzymes are activated prematurely within the pancreas, effectively digesting the gland from the inside out. Imagine pouring acid into your own kitchen sink.

Two main villains: stones and spirits

If you remember nothing else, remember GALLSTONES and ALCOHOL. Together, they account for roughly 80% of cases.

CauseMechanism
GallstonesObstruct the ampulla of Vater → reflux of bile → enzyme activation
AlcoholDirect toxic effect + ductal spasm + oxidative stress
Others (the A–G mnemonic)Autoimmune, Genetic (CFTR, PRSS1), Drugs (azathioprine, steroids, valproate), ERCP, Trauma, Infections (mumps, coxsackie), Hypertriglyceridemia, Hypercalcemia

But truly, in the exam, it’s stones and spirits.

The pain that makes people sweat

The classic story:

  • Severe, constant epigastric pain
  • Radiates to the back (“boring” pain, as if a drill is tunnelling through)
  • Worse after eating
  • Relieved by leaning forward

Patients look miserable. They often clutch their abdomen, sweating, sometimes vomiting continuously.

Diagnostic triad (trust me, this sticks)

You only need two of the following three to make the diagnosis:

  1. Typical abdominal pain
  2. Serum amylase or lipase > 3× upper limit of normal
  3. Imaging evidence (CT, MRI, or ultrasound showing swollen pancreas, peripancreatic fluid, fat stranding)

Lipase is preferred now, it stays elevated longer and is more specific.

The quiet danger, systemic inflammation

What kills in pancreatitis isn’t just local inflammation, it’s the cytokine storm that follows.
This can trigger SIRS (Systemic Inflammatory Response Syndrome) → shock → renal failure → ARDS → DIC.

In severe cases, necrosis of pancreatic tissue invites infection, cue abscesses, pseudocysts, and surgical headaches.

Assessing severity, because not all pancreatitis is equal

Use modified Glasgow criteria (PANCREAS):

| P | PaO₂ < 8 kPa |
| A | Age > 55 years |
| N | Neutrophils (WBC > 15 × 10⁹/L) |
| C | Calcium < 2.0 mmol/L |
| R | Renal function (urea > 16 mmol/L) |
| E | Enzymes (LDH > 600 IU/L, AST > 200 IU/L) |
| A | Albumin < 32 g/L |
| S | Sugar (glucose > 10 mmol/L) |

Score ≥3 → severe pancreatitis.
Those patients belong in HDU/ICU, not the ward.

Imaging pearls

  • Ultrasound: first-line, check for gallstones
  • CT scan (after 48–72 hours): to assess necrosis and complications
  • MRCP: non-invasive ductal visualization if stone suspected

Never rush a CT too early, the damage takes time to declare itself.

Management: less heroics, more support

There’s no “magic drug.” The pancreas heals itself if you support it properly:

Fluids, fluids, fluids
Aggressive IV resuscitation: third-space losses are enormous.

Pain control
Opiates, patient-controlled if needed.

Keep them NBM initially
Pancreas rests; early enteral feeding once tolerated is beneficial (don’t starve them for days unnecessarily).

Treat the cause

  • Gallstones → ERCP if biliary obstruction or cholangitis
  • Alcohol → strict abstinence + counselling
  • Triglycerides → insulin infusion or plasmapheresis if >1000 mg/dL

Monitor for complications
Necrosis, pseudocysts, abscess, ARDS, renal failure.

When things go wrong…

Complications are the stuff examiners live for:

LocalSystemic
Pancreatic necrosisShock, ARDS
PseudocystRenal failure
AbscessDIC
HaemorrhageHypocalcaemia

Late-stage chronic sequelae include diabetesmalabsorption, and recurrent attacks, the pancreas never quite forgets.

Clinical pearls

  • Pain radiating to the back? → think pancreas
  • Amylase normal but clinical suspicion high? → still pancreatitis (especially alcoholic)
  • Persistent fever? → suspect infected necrosis
  • Grey–Turner’s sign (flank bruising) or Cullen’s sign (periumbilical bruising) = retroperitoneal bleeding

A line to remember

“If you don’t respect the pancreas, it’ll remind you, violently.”

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