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home - Pancreas - Pancreatitis - Chronic Pancreatitis Written by Dr Sebastian Zeki

Knows the aetiology of acute pancreatitis Understands the means by
which the condition is diagnosed

Is aware of the risk stratification and prognostic scoring systems such
as Glasgow and Ranson; can apply this to the
management plan for individual patients

Knows the complications of severe attacks and the indications for

Knows how to initiate investigation of patients with recurrent
unexplained attacks of pancreatitis

Shows ability to make early risk stratification and involve multidisciplinary team and/or intensive care staff when appropriate

Collaborates closely with radiological and surgical colleagues where

Transfers patient to a specialist centre in accordance with guidelines



Understands the causes presentation investigation and
management of chronic pancreatitis

Knows the potential value of the various imaging modalities
Recognises the potential of blood and stool tests

Aware of the exocrine and endocrine consequences of the condition
Recognises complications

Knows the value of endoscopic non-invasive (ESWL) and surgical

Can diagnose the condition promptly
Knows possible avenues of treatment both to treat the consequences
of pancreatic insufficiency and to control pain where appropriate

Can recognise complications
Works within multi-disciplinary team and liaises with colleagues in
pain management

Shows empathy with patient and relatives


Chronic Pancreatitis

Chronic Calcific Chronic Obstructive (periductal fibrosis and duct dilatation)Causes:Congenital anomaliesTraumaIdiopathic fibrosing pancreatitisSclerosing pancreatocholangitisChronic Inflammatory Types DM -Pain (85%)- Epigastric Radiates to back Occasionally assoc with N+V Helped by sitting upright Worse 30 mins after eating Episodes may become continuous Disappearance of pain can signify onset of insufficiency -Malabsorption Fat (vit ADEK and B12) Protein Malabsorption (late) -Diabetes More common in calcifying disease Usually insulin requiring. Also affects glucagon producing alpha cells so get hypo’s. DKA rare -Hypocalcaemia (common) 1. Pain management -Stop drinking (doesnt always help) -Small meals, low fat -Try opiates with NSAID and amitryptylline -Other -Surgery 2. Exocrine Insufficiency -Pancreatic enzymes and PPI Reduces CCK stimulation of pancreas/ stops breakdown by gastric acid- For less advanced disease (ie, no large ducts/steatorrhea involved) Women, + those with idiopathic chronic pancreatitis may benefit the most -Treat with 30,000 IU lipase each meal- look at % normal pancreatic secretion -Give vitamin supps if lots of steatorrhoea -Give MCT’s if weight loss as dont need bile acids and more easily absorbed 3. Endocrine Insufficiency -Oral hypoglycaemics usually enough -Insulin sometimes but diabetes is brittle Imaging:-AXR 30% have calcifications)-USS 70% (duct dilatation most sensitive)-CT 80% (duct dilatation (- beaded, irregular or smooth) calcification, cysts)-EUS-Features include: visible side branches, cysts, lobularity, an irregular main pancreatic duct, hyperechoic foci and strands, dilation of the main pancreatic duct, and hyperechoic margins of the main pancreatic duct. Also: ductal and parenchymal findings-ERCP (Gold standard)Gradesa)Normal b)Equivocal c)Mild d)Moderate e) Severe-MRCP not as sensitive as ERCP but secretin MRCP may be better at helping with dx of early pancreatitis LabsAmylase/lipase high or normalFaecal fats (affected when exocrine function is <10% normal. Diagnos-tic when >7g fat on a 100g fat diet over 72 hoursFeacal elastase- < 200 ug/g are suggestive. Secretin test (inject CCK and collect pancreatic juices. 70-90% sensitive) PseudocystsOccur in 10% of CP.Due to ductal disruptions and communicate with the pancreatic ductsBile duct or duodenal obstructonDevelops in 10%Due to either inflammation and fibrosis in the head of the pancreas or to a pseudocyst.Pancreatic Ascites and Pleaural EffusionTreatment -If ductal disruption is present, endoscopically-placed stents are effective in the short-term.Many patients subsequently undergo surgery with anastomosis of a Roux-en-Y loop of jejunum to the pancreatic duct or to a leaking pseudocyst. a) Celiac nerve blocks b) Endoscopic stenting of the pancreatic duct or pancreatic sphincterotomy c) Extracorporeal shock wave lithotripsy Causes:EtOH- most commonHereditary pancreatitisCystic fibrosisMetabolic disorders.TropicalHistology:CystsChains of Lakes EtOH stops lithostatin which stops stones forming.Progression accelerated by smoking. Presentation Medical management Complications Chronic Pancreatitis Splenic vein thrombosisAs splenic vein runs along pancreas therefore get thrombosis due to inflammation. Subsequent portal hypertension and gastric varices Pseudoaneurysms A rare complication For surgical options consider: Areas of the pancreas involved + Pancreatic duct dilatationa)Decompression —For dilated main pancreatic duct; >2 yrs pain relief= 60%; Frey probably better than Whipple.;Surgery better than endoscopyb)Resection — Usually of tail or head, (uncommonly the entire pancreas)Usually for small duct disease. Usually for patients who have failed other forms of therapy.Procedures include:-Whipple-Pylorus-preserving pancreaticoduodenectomy-Duodenal-preserving resection of the pancreatic head = pancreatoduodenectomy for relief of pain.-Distal pancreatectomy--for disease confined to the body and tail of the pancreas (eg, occluded mid pancreatic duct, or a tail pseudocyst) -Total pancreatectomy (show figure 4) doesnt always achieve pain relief so only for those who fail all other therapies. -Lateral pancreaticojejunostomy-Patients who have undergone pancreatectomy may develop exocrine and endocrine dysfunction. c) Denervation procedures — 50% pain relief after 2 years. Surgical Treatment Investigations Written by Dr Sebastian Zeki

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