Gallstones, alcohol, idiopathic (80%) of cases o AP due to alcohol is rare in pts <30yrs Other o Infections o Post ERCP o Trauma o Drugs azathioprine, NSAIDs o Hyperlipidemia o inherited What are the presenting features of AP in hx and examination? Pain epigastric, LUQ, chest pain which is severe and constant with radiation to the back Associated sx: nausea, vomitting, abdo distension Hx of PC: gallstones, excess alcohol, recent ERCP, recent trauma, drugs and viral illness Family hx: possible On examination: -hydration, postural BP, JVP and capillary refill o Fever o Resp distress o Pleural effusions o Abdo exam: distension, guarding, tenderness, ascites, flank bruising, silent abdomen o Signs of underlying disorder: eg. CF, malignancy hypercalcaemia, jaundiced carcinoma What are the local and systemic complications of acute pancreatits in the early and late phase?
Local Systemic Early Ileus, pain Renal failure, hypokalaemia, hypocalcaemia, ARDS Late Necrosis, infected necrosis, pseudocyst, abscess Intestinal failure, muscle wasting
How is pancreatitis diagnosed clinically? Clinical hx, signs Confirm pancreatic enzymes 3x ULN Lipase o Imaging US for gallstones, CT
What other conditions can be associated with a high serum lipase? Acute pancreatitis Chronic pancreatitis Acute cholecystitis Duodenal ulcer Pancreatic calculus Diabetic ketoacidosis HIV Post-ERCP/trauma Coeliac disease Drugs Idiopathic What MDT members are involved in the mx of acute pancreatiits? Gastroenterologist Surgeons Intensive care Endoscopists Radiologists Pathologists What is the management for acute pancreatiis? Resuscitate: ABCD o Line bore IVC, IDC (if in ICU art line and CVC) o O2 aim for O2sats >95% Analgesia narcotic via PCA or epidural Rehydrate balanced electrolyte solutions Reassess regularly temp, HR, BP, UO, JVP IV fluids titrate to volume status o Once gorss vol status corrected, set infusion rate for basal fluid requirements (35ml/kg/day), plus ongoing third space loses o KCl should be added to IVF aim for 100mmol/day Proton pump inhibitors prevent stress ulcers Fasting and refeeding o Pancreas exocrine organ which secretes in response to oral diet Fasting until resolution established No clear protocols for when to restart oral intake use clinical judgement for resolution of sx, but prolonged fasting adverse outcomes due to gut disuse mucosal atrophy Stat clear fluids, graduate to solid foods as tolerated Start enteral refeeding (jejunal feeding tube) if oral refeeding not established after 5 days Monitor closely o Labs: FBC, CRP, UEC, glucose, arterial pH, lipids Magnesium and calcium monitoring and replacement if required If glucose >13.9 start insulin Blood transfusion if Hb <100, haematocrit <25% o Monitoring: O2 sats, aim >95% If resp insufficiency urgent CXR for APO or ARDS Vomitting if protracted AXR to assess for ileus, NGT for comfort and to prevent aspiration What is the ranson score? What does it determine? How is it calculated? Ranson score for predicting severity of acute pancreatitis It can determine both severity and predict mortality 11 points, scored at admission and 48 hours after admission Score >3 severe pancreatitis, score <3 severe pancreatitis unliekly Mortality o 0-2 = 2% mortality o 3-4 = 15% mortality o 5-6 = 40% mortality o 7 8 = 100% mortality Criteria: o On admission (GALAW) Glucose >11.1mM AST > 250 u/L LDH > 350 u/L Age > 55yrs WCC > 16,000/mm3 o At 48hrs (CHOBBS) Calcium <2 mM/L Haematocrit drop >10% PO2 <60mmHg Base excess >-4Meq/L BUN >1.8mM/l despite fluids Sequestration of fluid >6L What other factors are useful in determining severity? Mortality predictors multiple organ failure, elderly, shock on arrival, SIRS o SIRS: temp >38.5 or <35, HR>90, RR >20 or PO2 <32mmHg, WCC >12,000 or <4000, or >10% immature bands o Body weight: obesity, BMI >40kg/m2 o CRP tends to rise slowly and peaks day 3-4, if >300mg/L necrosis likely Do not send the pt home! o Imaging CT What is the utility of CT scanning in acute pancreatits? When should it be performed? What is the CT scan severity index? IV contrast-enhanced CT can distinguish from oedematous and necrotising pancreatic tissue more accurate than U/S CT scanning should be ordered at 72hrs unless critically ill, in need of emergency surgery, or to rule out other diagnoses takes time for necrosis to develop, may be equivocal in 24- 48hrs Follow-up CT scanning should be performed at 7-10 days if change in pts clinical status that suggests complications o Psuedocysts can take several weeks to develop, repeat/prorgess scan at time of hospital discharge CT severity index: o Stage A: normal pancreas score 0 o Stage B: intrinsic pancreatic changes Score 1 Focal or diffuse gland enlargement, mild heterogenity of the gland parenchyma, small intrapancreatic fluid collections o Stage C: Intrinsic and mild extrinsic changes Score 2 Inflammatory changes o Stage D: Extrinsic inflammation Score 3 But not more than one ill defined fluid collection o Stage E: Multiple extensive extra-pancreatic fluid collections of abscesses Score 4 o Plus necrosis percent score 0% necrosis 0 <33% necrosis 2 33-50% necrosis 4 >or=50% necrosis -6 Index Morbidity rates Mortality rates 0-3 8% 3% 4-6 35% 6% 7-10 92% 17%
What is the utility of ERCP in the diagnosis of acute pancreatitis? When should ERCP be used? ERCP has no role in diagnosis of acute pancreatits Alcohol and gallstone diease 80% of cases Indications: o Cholangitis or impacted stones o Early ERCP and sphincterotomy within first 72hrs of onset of pain
What are the 4 commandments of ERCP in acute pancreatitis? Acute pancreatitis with gallstones and elevated bilirubin early ERCP <72hrs All pts undergoing early ERCP for severe gallstone pancreatitis require endoscopic sphincterotomy regardless of whether stones are found in bile duct Cholangitis should be treated with sphincterotomy and duct drainage by stenting to decompress biliary obstruction All pts with biliary pancreatitis need definitive management of gallstones after their recovery for acute pancreatitis
What is the signifiance of infected pancreatic necrosis as a local late complication? Is CT scan good at differentiating infected necrosis from non-infected, how can the diagnosis be confirmed? What bacterial strains are found in pancreatic tissue or blood cultures? Infected pancreatic necrosis mortality increase (70-80%) o 25-70% of pancreatic necroses become infected, gram negative gut organisms via bacterial translocation Frequently develops 2-4 weeks from onset CT scan cannot determine if infected or not need to watch for signs of sepsis o Diagnosis: guided FNA under CT /US Gram stain or culture +ve surgical or percutaneous drainage Bacterial strains: o Escherichia coli o Enterococcus o Klebsiella o Staphylococcus o Pseudomonas o What is the role of prophylactic antibiotic use in acute pancreatitis? When ABs be initiated? What ABs? Prophylactic antibiotic treatment in mild AP no beneficial effect, leads to selection of AB resistant bacteria But, early AB treatment inidicated in pts with pancreatic necrosis significant beneficial effect on outcome and mortality Initiation of ABs: o If there is CT evidence of necrosis and fever Start carbepenem o If CRP> 300 and fever Start carpenem o Culture positive collection drain Anbibiotics: o Carbepenems (imipenem, meropenem), metronidazole, fluoroquinolones, cephalosporins o Aminoglycosides (gent) does not reach pancreatitic tissue at high enough concentration
Pathology of pancreatitis What is the pathogenesis underlying acute pancreatitis?
What are the histological features macroscopically and microscopically of acute pancreatitis? Macro: swollen, oedematous, fat necrosis and haemorrhage Microscopic: neutrophils, focal fat necrosis (within, surrounding and occasionally distant from pancreas), blood vessel damage and bleeding
What is a pancreatitic pseudocyst? What is the pathogenesis of the pseudocyst? Localised collection of necrotic haemorrhage material rich in pancreatic enzymes Pathogenesis: walling off of area of pancreatic haemorrhagic fat necrosis by fibrous tissue What are the macro and microscopic features of pancreatic pseudocysts? What are the complications of pancreatic pseudocysts? Macro: range in size from 2-30cm in diameter Micro: cyst wall has no epithelial lining, lining is a fibrous wall of granulation tissue Complications: compression of surrounding structures (eg. Bile ducts), infection, abscess, rupture (severe chemical peritonitis) and haemorrhage What are the main causes of chronic pancreatitis? What are the other causes? Common: alcohol, idiopathic and others Causes: TIGARO o Toxins (etoh, metabolic hyercalcaemia, hypertriglyceridaemia), idiopathic, genetic (hereditary pancreatitis, CF), autoimmune, recurrent acute pancreatitis, obstruction tumours, pseudocysts What are the macroscopic and microscopic features of chronic pancreatitis? Macro: dilated pancreatic ducts, calcification, firm Micro: o Early: fibrosis, exocrine gland atrophy, islet often preserved, blocked pancreatic duct o Late: extensive fibrosis, exocrine gland atrophy, islets preserved
Micro: early Late:
What are the complications of chronic pancreatitis?
Pancreatic tumours
What are the tumours of the pancreas?
Most are epithelial o Exocrine origin Ductal adenocarcinoma (90%) Serous cystic tumours Acinar cell carcinoma (unusual) Mucinous neoplasms (unusual)
What are the risk factors of pancreatic carcinoma? M>F Smoking x2 non-smokers Chronic pancreatitis Diabetes Hereditary pancreatitis
What are the macroscopic and microscopic features of pancreatic carcinoma? Macro: o Location: head 70%, body 20% o Hard, grey-white mass o Evidence of local infiltration and systemic mets liver, LNs Microscopic o Granular structures infiltrating stroma and lobules o Desmoplastic reaction o DD is chronic pancreatitis
What should be on the path report for pancreatic neoplasm? Type of specimen Location of tumour head/body/tail o Unifocal/multifocal Type of tumour Tumour grade Tumour size =<2cm Tumour borders circumscribed/infiltrative Surgical margins o Clear/involved where there is extension Lymphatic/vascular invasion LNs Other pathology chronic pancreatitis
Pancreatic anatomy
What is the blood supply to the pancreas?
What are the components of the pancreas? Head, neck, tail and body