Acute/Chronic Pancreatitis

Question 1

How common is it?

Answer 1

150-420 cases per million (and rising)

Question 2

What causes it?

Answer 2

Acute - ‘I GET SMASHED’

• Iatrogenic
• Gallstones (38%) - blocking the bile duct, causing back pressure in the main pancreatic duct.
• Ethanol (35%)
• Trauma
• Steroids
• Mumps
• Autoimmune (PAN)
• Scorpion venom
• Hyperlipidaemia, hypothermia, hypercalcaemia
• ERCP (5%) and emboli
• Drugs

Chronic
- Alcohol (by far biggest cause), familial, CF, haemochromatosis, pancreatic duct obstruction, ↑PTH, congenital (pancreas divisum).

Question 3

How does it present?

Answer 3

Symptoms

• Acute - Gradual or sudden severe epigastric or central abdominal pain (radiates to back, sitting forward may relieve); vomiting prominent.
• Chronic – Epigastric pain ‘bores’ through to back, relieved by sitting forward or hot water bottle on epigastrium/back. Bloating, steatorrhoea, weight loss, brittle diabetes. Symptoms relapse and worsen.

Signs

• May be mild in serious disease.
• Tachycardia, fever, jaundice, shock, ileus, rigid abdomen +/- local/general tenderness.
• Periumbilical bruising (Cullen’s sign) or flanks (Grey Turner’s sign) from blood vessel autodigestion and retroperitoneal haemorrhage.

Complications

• Acute – (Early) Shock, ARDS, renal failure, DIC, sepsis, ↓Ca2+, ↑glucose. (Late) Pancreatic necrosis and pseudocyst, abscesses, bleeding, thrombosis, fistulae, recurrent oedematous pancreatitis.
• Chronic – Pseudocyst, diabetes, biliary obstruction, local arterial aneurysm , splenic vein thrombosis, gastric varices, pancreatic carcinoma.

Question 4

What other conditions may present similarly?

Answer 4

Any acute abdomen, myocardial infarct.

Question 5

Investigations?

Answer 5

Acute

• Raised serum amylase – degree of elevation not related to disease severity. Serum lipase more sensitive and specific for pancreatitis.
• ABG to monitor oxygenation and acid base status.
• AXR – No psoas shadow (retroperitoneal fluid↑), ‘sentinel loop’ of proximal jejunum from ileus.
• Erect CXR – helps exclude other causes.
• CT – assess severity and look for complications. MRI may be better.
• US (if gallstones and AST↑).
• ERCP if LFTs worsen.
• CRP >150mg/L at 36h post-admission is a predictor of severe pancreatitis.

Chronic

• US +/- CT (pancreatic calcifications confirm the diagnosis).
• MRCP + ERCP (risks acute attack).
• AXR – speckled calcification; ↑glucose…

Question 6

Treatments?

Answer 6

Acute
Severity assessment essential. Modified Glasgow criteria for predicting severity of pancreatitis (PANCREAS) – 3 or more positive factors within 48h of onset suggests severe pancreatitis. 
-	PaO2 55 yrs
-	Neutrophilia WBC >15 x 109/L
-	Calcium 16mmol/L
-	Enzymes LDH >600iu/L; AST >200iu/L
-	Albumin 10mmol/L

Management

• Nil by mouth – NG tube, IV fluids. Insert urinary catheter and consider CVP monitoring.
• Analgesia – pethidine or morphine.
• Hourly pulse, BP and urine output; daily FBC, U&E, Ca2+, glucose, amylase, ABG.
• If worsening – ITU, O2 if ↓PaO2.
• ERCP + gallstone removal may be needed if there is no progressive jaundice.
• Repeat imaging (CT) to monitor progress.

Chronic

• Drugs: analgesia, lipase, fat soluble vitamins. Insulin needs may be high or variable (beware hypoglycaemia).
• Diet: no alcohol; low fat may help.
• Surgery: For unremitting pain; narcotic abuse (beware of this; weight↓: eg. Pancreatectomy or pancreaticojejunostomy (duct drainage procedure).