Pancreatitis Flashcards
What are the causes of acute pancreatitis
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Gallstones
Ethanol
Trauma
Steroids
Mumps
Automimmune
Scorpion bite
Hyperlipidaemia, Hypothermia, hypercalcaemia
ERCP, emboli
Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)
What is the pathophysiology behind acute pancreatitis
Each cause results in a premature and exaggerated activation of pancreatic enzymes –> pancreatic inflammatory response –> increase in vascular permeability –> fluid loss into third spaces (peritoneal cavity)
Enzymes are also released into systemic circulation causing fat necrosis and autodigestion of blood vessels leading to haemorrhage –> cullens and grey turners
Fat necrosis –> release of fatty acids –> reacts with serum calcium causing chalky deposits –> hypocalcaemia
What are the clinical features of acute pancreatitis
Sudden/gradual epigastric pain or central abdo pain Radiates to back Sitting forward may release pain Vomiting is prominent Cullens sign - periumbilical bruising Grey turners - Flank bruising (both due to retroperitoneal haemorrhage) Fever Jaundice Tachycardia hypovolaemic shock (severe) Rigid abdomen with guarding (severe) Normally soft abdomen with bowel sounds present
How is acute pancreatitis investigated
Bedside Obs
Bloods - FBC, U+Es, LFTs, Serum amylase (3fold upper limit of normal), Serum lipase, CRP
ABG - monitor acid base status
Erect CXR - exclude perforatio
ERCP if LFTs worsen
AXR - sentinel loop sign - dilated proximal bowel adjacent to pancreas secondary to localised infection
CT
How is acute pancreatitis managed
High flow oxygen
NBM
NG tube needed to decrease pancreatic stimulation
IV fluids (0.9% Saline) to counteract 3rd space sequestration
Catheterise
Fluid balance chart
Analgesia
- morphine = may ccause sphincter of oddi to contract
- Pethidine IM
Broad spectrum Abx in confirmed cases of pancreatic necrosis
What are the complications of acute pancreatitis
Local
- Pancreatic necrosis –> ongoing inflammation - ischaemic infarction of pancreatic tissue. Confirmed by CT an prone to infection
- Pancreatic pseudocyst - collection of fluid within the pancreatic tissue, formed weeks after initial acute episode
inflammatory reaction produces a necrotic space in the pancreas full of pancreatic fluid surrounded by fibrous tissue (prone to haemorrhage and rupture) may be found incidentally or be producing symptoms of mass effect e.g. biliary obstruction
Pancreatic abscess
peripancreatic fluid collections
SYSTEMIC
- DIC
- ARDS
- Hypocalcaemia
- Hyperglycaemia - secondary to disturbances to insulin metabolism
- Hypovolaemic shock and organ failure
Which score is used to assess severity of acute pancreatitis
Glasgow score used within the first 48hrs of admission PANCREAS PO2 <8kPA Aage >55 yrs Neutrophils >15x109 Calcium <2mmol Renal function urea >16mmol Enzymes ((LDH or AST) Albumin <32g/l Sugar >10mmol
How high does the serum amylase have to be to be diagnostic for actue pancreatitis
3x the upper limit of normal
What are the other causes for a raised serum amylase
Mesenteric ischaemia Perforated viscus Ruptured ectopic pregnancy Acute cholecystitis DKA
What is chronic pancreatitis
Chronic fibro-inflammatory disease of the pancreas with progressive and irreversible damage to the pancreas parenchyma
What causes chronic pancreatitis
Chronic alcohol abuse (60%) Idiopathic Metabolic - hyperlipidaemia -hypercalcaemia Infection - viral = HIV, mumps and Coxsackie - Bacterial = echinococcus Genetic - CF Autoimmune - Autoimmune pancreatitis - SLE Obstruction (of the pancreatic duct) - stricture formation - Neoplasm (carcinoma of the head of the pancreas)
Congenital
- Pancreas divisum
- Annular pancreas
What is the pathophysiology behind chronic pancreatitis
Large duct disease - dilatation and dysfunction, visible on imaging. Pancreatic fluid changes composition and facilitates the deposition of precursors to calcium carbonate stones –> diffuse pancreatic calcification. Males predominantly
Small duct disease - normal imaging and no pancreatic calcification. Difficult to diagnose. Females predominantly
What are the clinical features of chronic pancreatitis
Chronic pain - epigastrium, radiates to back
Pain tends to be worse 15-30 mins after eating
Nausea and vomiting
Symptoms secondary to endocrine dysfunction e.g. diabetes
Exocrine dysfunction - steatorrhoea and malabsorption
Epigastric tenderness on palpation
what are the differentials for chronic pancreatitis
Acute cholecystitis
Peptic ulcer disease
Acute hepatitis
Sphincter of oddi dysfunction
How would you investigate suspected chronic pancreatitis
Bedside Obs - temp (to rule out acute infection), HR, RR, BP
BM - raised glucose
Bloods
- FBC
- U+Es
- LFT - may show hepatic aetiology
- Bone profile - Calcium –> asses for hypercalcaemia
- Blood glucose
- Lipids
- Serum amylase and lipase are rarely high in established disease
- faecal elastase - abnormally low incases (sensitive for chronic pancreatitis)
Imaging
- Abdo USS - first line
- CT Abdo pelvis - for pancreatic calcification and pseudocysts
MRCP - will identify the presence of biliary obstruction and assess pancreatic duct
ERCP - more accurate in elicting the antomy of the pancreatic duct and can be combined with intervention
Administration of IV secretin may be used to cause the pancreas to produce a bicarb rich fluid - may reveal a stricture
