Pancreatitis Flashcards
What is acute pancreatitis?
An acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems.
What characterises mild and severe pancreatitis? Name of classification?
MILD: associated with minimal organ dysfunction and uneventful recovery; SEVERE: associated with organ failure and/or local complications such as necrosis, abscess or pseudocyst. 1992 ATLANTA CLASSIFICATION.
What is the aetiology of acute pancreatitis?
Insult results in activation of pancreatic proenzymes within the duct/acini resulting in tissue damage and inflammation.
What are the causes of acute pancreatitis?
GET SMASHED: Gallstones, ethanol, trauma, steroids, mumps/malignancy, autoimmune, scorpion sting, hyperlipidaemia/hyperparathyroidism, ERCP, drugs (azathioprine, thiazides, valproate).
What is the epidemiology of acute pancreatitis: Incidence? Age? Cause for each gender?
Common. Annual UK incidence – 1/1000. Peak age is 60. Males – most common cause is alcohol-induced; females – most common cause is gallstones.
What are the symptoms of acute pancreatitis? (x3)
o PAIN: severe, epigastric (upper or RUQ because affects head) or abdominal. Radiating to BACK (because pancreas partly retroperitoneal). Relieved by sitting forward. Aggravated by movement.
o Anorexia
o Nausea and vomiting, worse when eating
o Dehydration (from fluid shifts and oedema leading to hypovolaemia)
What are the signs of acute pancreatitis? (x5)
o Epigastric tenderness
o Fever
o Shock: tachycardia and tachypnoea.
o Reduced bowel sounds (due to ileus)
o If severe and haemorrhagic: Turner’s sign or Cullen’s sign.
What is the aetiology of Turner’s and Cullen’s sign?
Bruising due to blood vessel auto-digestion and retroperitoneal haemorrhage.
What are the investigations for acute pancreatitis? (x5)
o BLOODS: raised amylase (usually at least 3 times normal), raised lipase (especially alcoholic pancreatitis), FBC (increased WCC), U&Es, increased glucose, hypocalcaemia, LFTs may be deranged if gallstone pancreatitis or alcohol pancreatitis), ABG (for hypoxia and metabolic acidosis).
o USS: for gallstones or biliary dilatation
o ERECT CXR: there may be pleural effusion. Mainly for excluding other causes.
o AXR: to exclude other causes of acute abdomen. Psoas shadow may be lost (muscle; if no shadow, can be an indication of increased retroperitoneal fluid). ‘Sentinel loop’ of proximal jejunum from ileus (solitary air-filled dilatation).
o CT SCAN: if diagnostic uncertainty or if persisting organ failure, signs of sepsis or deterioration.
What is diagnostic of acute pancreatitis?
Bloods (high amylase) and symptoms alone are diagnostic. The point of other investigations is to EXCLUDE other differentials which you may suspect.
How may amylase levels be obscured in a patient without pancreatitis? (x2)
Renal failure results in reduced amylase clearance, so amylase is high though pancreatitis not present. AND amylase is non-specific; you may see elevated levels in cholecystitis, mesenteric infarction and GI perforation.
What is the cause of hypovolaemic shock in acute pancreatitis? Precipitated?
Oedema and fluid shifts e.g. ascites, extracellular fluid trapped in the gut, peritoneum and retroperitoneum. NB that hypovolaemia is worsened by vomiting – obviously.
Note about severity of acute pancreatitis and amylase?
Does not correlate with severity.
How can LFTs distinguish between alcoholic and gallstone pancreatitis?
ALCOHOLIC: increased ALT as this indicates hepatic injury. GALLSTONE: increased ALP and GGT
How can ALT and AST ratio determine pancreatitis cause?
Higher ALT than AST indicates chronic; higher AST than ALT indicates acute alcoholic or liver cirrhosis.
How is acute pancreatitis severity assessed? (x3)
o Modified Glasgow combined with CRP
o APACHE-II score
o Ranson’s criteria
Specificity of Modified Glasgow criteria vs APACHE-II score?
Glasgow is specific to pancreatitis; APACHE-II is non-specific and used in ITU settings.
What is the Modified Glasgow criteria for predicting pancreatitis severity?
PANCREAS: PaO2 low, Age over 55years, Neutrophilia high WCC, Calcium low, Renal function high urea, Enzymes high LDH and AST, Albumin low, Sugar high.
How is the Modified Glasgow criteria interpreted?
If you have at least three of the criterions, your pancreatitis is severe.
What is the APACHE-II score?
More physiological: PaO2, temp, MAP, pH, HR, RR, Na+, K+, creatinine, Hct, WCC, GCS.
What are the local complications of pancreatitis? (x10)
o Pancreatic necrosis from autodigestion by pancreatic enzymes
o Pseudocyst (peripancreatic fluid collection 4 weeks from onset; associated with fever, abdominal mass and persistent increased amylase/LFTs)
o Abscess: peripancreatic fluid from pancreatic necrosis, occurring more than 4 weeks after pancreatitis
o Ascites (fluid leakage from pancreas)
o Pseudoaneurysm (collection of blood between tunica media and adventitia – different from dissection which is between tunica intima and media)
o Venous thrombosis (of splenic vein)
o Bleeding from elastase eroding major vessels e.g. splenic artery.
o Pleural effusion
o Chronic pancreatitis
o Gastric varices
What makes a pancreatic pseudocyst ‘pseudo’?
It is a collection of fluid in the LESSER SAC i.e. not lined by epi or endothelium.
What is the difference in management of pancreatic pseudocyst and abscess?
Abscess NEEDS drainage; pseudocyst may need draining/may resolve.
How is recurrent oedematous pancreatitis managed?
Near-total pancreatectomy.
What are the systemic complications of pancreatitis? Aetiology of each? (x7)
o Multiorgan dysfunction from shock
o Sepsis
o Renal failure (from hypoxaemia, high amylase, decrease in renal perfusion pressure from shock and ascites)
o ARDS (acute respiratory distress syndrome; from pancreatic enzymes causing inflammation in the lungs)
o DIC (theorised that this is from early intravascular consumption of coagulation factors secondary to circulating pancreatic enzymes)
o Hypocalcaemia (unknown mechanism but the pancreas contains a lot of calcium)
o Diabetes
How do we reduce risk of renal failure in pancreatitis?
Give lots of fluid!
How is acute pancreatitis medically managed? (x7)
o Fluid and electrolyte resuscitation
o Urinary catheter
o NG tube if vomiting
o Nil by mouth, consider NJ feeding as it will result in decreased pancreatic stimulation. Enteral preferred to parenteral feeding is shown to reduce infective complications and mortality
o Analgesia
o Blood sugar control
o Prophylactic antibiotics for infective pancreatitis
How is acute pancreatitis managed non-conservatively for gallstone pancreatitis?
ERCP and sphincterotomy
How is acute pancreatitis managed when pancreatic necrosis or sepsis?
Undergo image-guided fine needle aspiration for culture
How is acute pancreatitis managed surgically?
Necrotising pancreatitis should be managed with minimal abscess or open necresectomy (drainage and debridement of necrotic tissue).
What is the prognosis of acute pancreatitis?
20% follow severe course with high mortality (infected pancreatic necrosis associated with 70% mortality). 80% run milder course, but mortality is still 5%.
What is chronic pancreatitis? What characterises it? (x3)
Chronic inflammatory disease of the pancreas characterised by irreversible atrophy, fibrosis leading to impaired endocrine and exocrine function, and recurrent abdominal pain.
What is the aetiology of chronic pancreatitis? Contribution of each cause? (x10)
o Alcohol (70%)
o Idiopathic (20%) – unknown, spontaneous
o Recurrent acute pancreatitis
o Ductal obstruction
o Pancreas divisum – congenital abnormality a single pancreatic duct is not formed, but rather remains as two distinct dorsal and ventral ducts
o Hereditary pancreatitis
o Tropical pancreatitis
o Autoimmune pancreatitis
o Hyperparathyroidism
o Hypertriglyceridemia
o NOT gallbladder as this would be acute
What is the epidemiology of chronic pancreatitis: Incidence? Prevalence? Age?
1/100 000 incidence; 3/100 000 prevalence. Mean age 40-50 years.
What are the symptoms of chronic pancreatitis? (x5)
o Recurrent severe epigastric pain, radiating to back, relieved by sitting forward or hot water bottles, can be exacerbated by eating or drinking alcohol
o Weight loss over many years
o Bloating
o Pale offensive stool (steatorrhea) – some lipases are secreted in the pancreas
o Erythema ab igne (mottled, scaly, hyperpigmented skin from chronic application of hot water bottles)
What are the signs of chronic pancreatitis? (x3)
Epigastric tenderness, weight loss, malnutrition.
What is the pathogenesis of chronic pancreatitis? (x3)
Disruption of normal pancreatic glandular architecture due to chronic inflammation and fibrosis, calcification, parenchymal atrophy, ductal dilatation, cyst and stone formation. Pancreatic stellate cells are thought to play a role, converting from quiescent fat storing cells to myofibroblast-like cells forming ECM, cytokines and growth factors in response to injury. Pain is associated with raised intraductal pressures and inflammation.
What are the investigations for chronic pancreatitis? (x6)
o BLOOD: glucose (increase may indicate endocrine dysfunction), glucose intolerance test, amylase and lipase (usually NORMAL), increased immunoglobulins especially IgG4 in autoimmune pancreatitis.
o USS: percutaneous or endoscopic showing hyperechoic foci (bright-coloured) with post-acoustic shadowing – sign of inflammation
o ERCP or MRCP: early changes include main duct dilatation and stumping of branches. Late manifestations are duct strictures with alternative dilatation (‘chain of lakes’ appearance – see photo)
o AXR: pancreatic calcification may be visible
o CT SCAN: pancreatic cysts, calcification. Calcifications are DIAGNOSTIC
o TESTS OF PANCREATIC EXOCRINE FUNCTION: faecal elastase
What are the local complications of chronic pancreatitis? (x8)
Pseudocysts, biliary duct stricture, duodenal obstruction, pancreatic ascites, pancreatic carcinoma, splenic vein thrombosis, local arterial aneurysm, gastric varices
What are gastric varices? Relationship with pancreatitis?
Dilated gastric submucosal veins associated with thrombosis of the splenic vein, into which the short gastric veins which drain the fundus of the stomach flow.
What are the systemic complications of chronic pancreatitis? (x4)
Diabetes, steatorrhea, chronic pain syndromes, dependence on strong analgesics.
What is the nature of diabetes in pancreatitis?
It is BRITTLE, meaning hard to control.
What is the prognosis of chronic pancreatitis: Surgery? Life expectancy reduction?
Difficult to predict. Surgery improves symptoms in 60-70% but results are often sustained. Life expectancy can be reduced by 10-20 years.
How is chronic pancreatitis managed conservatively? (x5)
TREATMENT IS MAINLY SYMPTOMATIC AND SUPPORTIVE e.g. dietary advice (especially low fats as lipase function of pancreas is compromised), abstinence (self-enforced restraint from indulging in bodily activities that are widely experienced as giving pleasure) from alcohol and smoking, treatment of diabetes, oral pancreatic enzyme replacements, analgesia for pain exacerbations.
What is oral pancreatic enzyme replacement?
Creon – lipase.
What specialist pain relief can be offered to patients with chronic pancreatitis? (x2)
The sensory nerves to the pancreas transverse the coeliac ganglia and splanchnic nerve: therefore, COELIAC PLEXUS BLOCK (CT or EUS-guided neurolysis) and TRANSTHORACIC SPLANCHIOCECTOMY (surgical excision of one or more segments of the splanchnic nerves) can offer variable degrees of pain relief.
How is chronic pancreatitis managed endoscopically? (x5)
Sphincterotomy, stone extraction, dilatation, or stenting of strictures. Extracorporeal shock-wave lithotripsy (shock waves used to physically destroy/fragment stones; done from outside the body) is sometimes used for fragmentation of larger pancreatic stones prior to endoscopic removal.
When is surgical management of chronic pancreatitis indicated?
When medical management has failed.
How is chronic pancreatitis surgically managed? (x2 (x1 and x3))
o DRAINAGE PROCEDURES: lateral pancreaticojejunal drainage (modified Puestow procedure)
o RESECTIONAL PROCEDURES: pancreaticoduodenectomy (or Whipple’s), limited resection of the pancreatic head (Beger procedure), combined opening of the pancreatic duct and excavation of the pancreatic head (Frey procedure).
