Incidence	1 in 2000 population require hospital admission for acute pancreatitis every year - < 10% have necrotising haemorrhagic pancreatitis - incidence is increasing
Age	- peak incidence between 50 and 60 years
Sex	F > M
Geography	- aetiology varies with country; e.g. 2/3 of patients in UK have gallstone aetiology, 2/3 of patients in US have alcohol aetiology
Aetiology	- GET SMASHED: - Gallstones - ETOH - Trauma - Steroids - Mumps - Autoimmune - Scorpion - Hypertrygliceridaemia - ERCP - Drugs - Gallstones and alcoholism account for 80% of acute pancreatitis worldwide - stone obstruction of ampulla of Vater allows bile reflux into pancreatic duct - small stones may cause transient obstruction as they pass through - longstanding high alcohol intake is required - ? obstructive element to acute pancreatitis in alcoholics as well as gallstones - sudden onset of acute inflammation of the pancreas -> inappropriate activation of zymogens - trypsin activation may be key event -> interstitial oedematous pancreatitis - more severe pancreatitis leads to fat saponification; if this is extensive, there may be sequestration of calcium - in severe cases, there is extensive local damage and activation of the complement and kinin systems -> shock, ARDS, renal failure, DIC, pancreatic necrosis with peripancreatic fluid collections - 50% of patients with pancreatic necrosis develop diffuse pancreatic infection; usually Gram -ves Obstruction - gallstones - 30-70% of cases - ampullary or pancreatic tumours - 3% - congenital abnormalities - 5% - abnormally high pressure in sphincter of Oddi - 1-2% - Ascariasis - common cause in endemic areas Drugs and toxins - alcoholism - 30-70% - drugs - azathioprine, 6-mercaptopurine, metronidazole, tetracycline, H2 blockers - 1-2% Iatrogenic and traumatic causes - following ERCP or endoscopic sphincterotomy - following cardiopulmonary bypass - blunt pancreatic trauma (rare) Metabolic - hypertriglyceridaemia - 2% - hypercalcaemia (rare) Infection - AIDS - secondary CMV infection - incidence about 10% in AIDS patients - other viruses - Coxsackie, HAV, HBV, HCV Idiopathic pancreatitis - about 10% have no cause identified following investigation; 2/3 probably have microlithiasis
Presentation	- acute abdomen - sudden onset severe and continuous pain, poorly localised in upper abdomen, radiating to back - pain spreads throughout abdomen; may be referred to shoulder tips if diaphragmatic hernia is affected - eary vomiting - patient restless, changes posture constantly; "pancreatic position" - patient leans forwards - patient tends to lie still with the onset of peritonitis, as movement exacerbates the pain Mild acute pancreatitis - patient generally well, few systemic features and little abdo tenderness - pain is often severe Moderate acute pancreatitis - moderate systemic features; tachycardia - abdoment distended, diffusely tender with guarding - inflammatory ileus -> bowel sounds absent Severe acute pancreatitis - patient apathetic, shocked, grey - signs of generalised peritonitis; tenderness, guarding, rigidity - may develop ARDS
Investigations	Bloods - serum amylase - > 1200 iu/mL is dianostic, but levels tend to be lower in alcoholics; rapid rise at outset of attack; peak levels are not predictive of outcome - ? lipase estimation in difficult or late-presenting cases - ALT elevated to > 3x normal is indicative of gallstone pancreatitis X-ray - chest (erect) - - abdomen (supine) - "ground glass" appearance if peritoneal exudate present, may be sentinel loop of bowel USS - detection of gallstones in biliary tree - pancreatic swelling and necrosis, presence/absence of peripancreatic fluid collections - pancreas may be obscured by gas in severe pancreatitis Contrast-enhanced dynamic CT scanning - pancreatic swelling, necrosis, fluid collections - diffuse inflammatory changes in retroperitoneum - presence/absence of gallstones MRI - can distinguish between fluid and inflammatory masses ERCP - cause can be found in 50% of patients where it was not apparent on history or inital imaging Peritoneal tap - clear fluid in moderate pancreatitis - "prune juice" in severe necrotising pancreatitis; sterile - foul-smelling fluid containing bacteria suggests intestinal perforation - estimation of amylase in fluid Exploratory laparotomy - if diagnosis is in doubt, to exclude any other cause
Macro
Micro
Staging
Serum markers
Management	Medical Mild cases - nil-by-mouth - nasogastric suction (reduces vomiting and abdominal distension - resuscitate - water and electrolytes - opiate analgesia (not morphine) - lexipafant (platelet activating factor antagonist) improves mortality and complications - if there is direct evidence that gallstones are the cause, an ERCP will be necessary for stone removal
Prognosis	Poor prognostic indicators - Age > 55 years - WBC > 15x109/L - blood glucose > 10 mmol/L - serum urea > 16 mmol/L - serum albumin < 30 g/L - serum aminotransferase > 200 U/L - serum calcium < 2 mmol/L - serum LDH > 600 U/L - PaO2 < 8.0 kPa Mild cases - 1% mortality Severe cases - 50% mortality - with multiple complications and presence of all bad prognostic signs, mortality is nearer 100% - depending on aetiology, patient may have recurrent attacks
Complications	Pancreatic - acute fluid collection (30-50% of patients; spontaneous regression in 50%) - necrosis - infected pancreatic necrosis has a bad prognosis - pseudocyst - evolve from acute fluid collections > 4 weeks after start of acute attack; if suspected of infection, can be aspirated under USS guidance or surgically - abscess - intra-abdominal collection of pus arising some weeks after start of attack; can often be treated by percutaneous drainage - ascites - high amylase content; carries a poor prognosis Intestinal - paralytic ileus - GI haemorrhage Hepatobiliary - jaundice - obstruction of CBD - portal vein thrombosis Systemic - metabolic - malnutrition, hypoglycaemia, hypocalcaemia - haematological - DIC, portal vein thrombosis - renal - acute renal failure - cardiovascular - shock - respiratory - hypoxic acute respiratory failure

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