Pancreatitis

Pancreatitis

Your friend and mine... actually scratch that, pancreatits is pretty sucky as diseases go, mainly because the pancreas is not encased in a protective lining like other organs are.

Consequently, when it gets damaged and starts releasing its digestive enzymes it has no where to go but on itself - leading to a sort of auto-digestion, and the surrounding organs - ew. This creates all sorts of inflammation. As I said, pretty sucky. Plus, ma-hoo-sive 3rd space losses means gallons of extracellular fluids get trapped in the gut, peritoneum and retroperitoneum (meaning 'behind the peritoneum', from the original Greek - peritoni-, meaning 'lining', and retro- 'meaning from the 70s' - due to the tiny disco ball found lying behind there*). The body decompensates rapidly in this condition, and so the patient, as a result, becomes very unpredictable - able to be chatting one minute, and in severe shock the next.

There are several kinds:
Acute
Chronic
Obstructive
(due to obstruction of the pancreatic duct, but basically shares features with the acute and chronic forms)

Acute Pancreatitis

10-20/100 000 West society

*mild/self-limiting

1/5 - severe = shock/organ failure/death

Symptoms

Central/epigastric pain radiating to the back. +/- nausea, vomiting. Possibly relieved on sitting forwards.
Tachycardia

Causes
Using the infamous GET SMASHED

Gallstones
Ethanol
Trauma

Steroids
Mumps
Autoimmune (PAN)
Scorpion Sting (Trinidadian)
Hyperlipidaemia/Hypercalcaemia/Hypothermia
ERCP
Drugs

plus Pregnancy and Idiopathic, Infections, Ischaemia

Gallstones & Chronic alcoholism = 70%
Idiopathic = 20%

Poor ol', IDIOtic Amy, she got SMASHED, & woke up PREGNANT. You'd think she's have more sense.

Pathogenesis

Enzymatic auto-digestion of pancreas

Acinar cell damage = release of pro-enzymes into interstitium, where activated

Mechanisms

 - Direct - Trauma/infection/alcohol

 - Oxidative stress

 - Acinar cell ischaemia (retained pancreatic secretion, inflammation, oedema, vascular constriction)

leading to...

Acute inflammation

Microvascular leakage

Oedema

Fat necrosis

Proteolysis

Vascular destruction

Haemorrhage

Ix
Increased WCC

Increased plasma pancreatic enzyme levels x3 (within 24 hours)
RANSON criteria indicates clinical outcome

Glasgow Criteria for assessing severity of pancreatitis
(NB only validated for gallstones & ethanol as the cause)

PANCREAS

PaO2 <8kPA

Age >55yrs

Neutrophils WBC >15x10

Calcium <2mmol/L

Renal function Urea >16mmol/L

Enzymes LDH >600iu/L & AST>200iu/L

Albumin >32g/L

Sugar BM>10mmol/L

3/3+ positives within 48hrs = severe pancreatitis. Transfer to ITU/HDU.

Pathology
Mild

Interstitial oedema

Focal fat necrosis

Pancreas swollen

Superficial white plaques of fat necrosis (fatty acids + Ca)

Severe

Necrotizing
Affects acini, ducts, islets

= w/spread necrosis and Hg

Macro

Yellow/white chalky fat necrosis, with areas of black haemorrhage

Peritoneum = brown, serous fluid - fat globules & chalky deposits
Micro

Interstitial oedema
Peri-pancreatic fat necrosis

Severe
Extending necrosis

Acini and blood vessels destruction
With septal acute inflammation cell reaction and haemorrhage

Tx

Mild episode & majority of cases
Resolve with supportive treatment
Min organ dysfunction

Course and Cx

Severe episode

Pancreatic necrosis (Dx at CT)

Local damage

Pancreatic abscesses

Pancreatic pseudocysts

Duodenal obstruction

Path = complete resolution/focal fibrosis

Multi-organ failure

DIC

ARDS
Death - 30% in severe acute pancreatitis
Early deaths = organ failure

Late deaths = infection

5% mortality = shock w/i 1 week of perforation

*Total BS