Pancreatitis

Mx of acute pancreatitis Supportive Analgesia

- Do not give NSAIDs as they can worsen pancreatitis & cause renal failure (since there is already decreased renal perfusion in acute pancreatitis) - Use opioid analgesics (tramadol, pethidine) other than morphine (causes increased tone of sphincter of Oddi)

Mx of acute pancreatitis Supportive Abx

- Either prophylactic or therapeutic - Not shown to have any benefit in mild pancreatitis - Prophylactic in severe acute pancreatitis to prevent infection of necrosis (infection will occur in 40-70% of patients with necrosis and increases the mortality rate from 12 to 33%) - Carbapenem (only imipenem has been shown to prevent sepsis) - Therapeutic in cholangitis (coexisting with gallstone disease or as a complication of pancreatitis) & infection of pancreatic necrosis/ pseudocyst - Duration: 14 day

Ix for chronic pancreatitis Assess Cx

1. Abdominal X-Ray - Identify diffuse calcification of the pancreas 2. CT / MRI - CT → Good for diagnosing pancreatic parenchyma or ductal disease - Useful to evaluate mass lesions and sequelae of chronic pancreatitis - MRCP → good for evaluating dilated duct and strictures

What are the endocrine cells in the pancreas?

Alpha (glucagon) Beta (insulin and amylin) Delta (somatostatin) PP/Gamma (pancreatic polypeptide) Epsilon (ghrelin)

Mx of chronic pancreatitis Indication for Whipple

Indicated in cases where pancreatitis mainly affects head of the pancreas

Mx of acute pancreatitis Monitoring of Cx

LOCAL Cx 1. Acute fluid collections - (30-50%) - Due to increased vascular permeability - 70-80% resolve spontaneously 2. Pseudocyst - (10-20%) - Persistent fluid collection (enzymes, blood, necrotic tissue) walled off by fibrosis and not an epithelium-lined surface (after 4 weeks) - Presents as persistent pain, mass on examination, persistently ↑amylase or lipase - 50% resolve spontaneously if not surgical intervention - Can be further complicated by GOO, infx, peritonitis, h'ge (erosion of splenic vessels) 3. Sterile Pancreatic necrosis - (20%) - Areas of no contrast uptake on CT with intravenous contrast - ? prophylactic antibiotics with imipenem - Supportive measures, KIV surgery if patient unstable - Consider surgery if patient doing poorly 4. Infection (5%) - usually 2' enteric G-ve Rods a. Pancreatic Abscess - Circumscribed collection of pus (w/o pancreatic tissue) - Treat with antibiotics + drainage (CT guided if possible) b. Infected pancreatic necrosis - Gas bubbles on CT scan - FNA in deteriorating patient with necrosis 5. Chronic pancreatitis, exocrine insufficiency & endocrine insufficiency SYSTEMIC Cx 1. Peritoneal sepsis 2. Pancreatic ascites (massive accumulation of pancreatic fluid in peritoneum) -- lead to abdominal compartment syndrome 3. Pleural Effusion 5. Intra-abdominal haemorrhage (erosion of splenic vessels) - shock 6. Multiple organ failure (ARDS, acute renal failure, hypovolemicshock, DIVC) 7. Hypocalcaemia, hyper/ hypoglycaemia

Indications for ERCP to Mx Cx of acute pancreatitis

No benefit in mild biliary pancreatitis Indications: - Severe pancreatitis - Evidence of ductal stones - Cholangitis - No response to treatment within 48 hours ERCP should be done within first 48-72 hours for maximum benefit

What is interstitial edematous pancreatitis (IEP)?

Non-necrotising = interstitial edematous pancreatitis (IEP) - Fluid around pancreatitis = Acute pancreatic or peripancreatic fluid collection (APFC) -- Can be sterile or infected - After 28 days, the name changes to pancreatic pseudocyst -- Can be sterile or infected

When does pancreatic necrosis happen?

Only starts at day 5 and ends at week 5 (Hence CT imaging before day 5 is useless, only do for DIAGNOSIS) - Fluid around pancreas = Acute necrotic collection, -- Can be sterile or infected After 4 weeks it is called walled off necrosis

Mx of chronic pancreatitis Why must both the pancreas and duodenum be removed?

Pancreas and duodenum share the same arterial blood supply (gastroduodenal artery) so both must be removed

Mx of chronic pancreatitis Aetio

Treat underlying cause → abstain from alcohol consumption

Mx of chronic pancreatitis Principles

Treatment aimed at underlying aetiology, symptoms and complication (1) lifestyle modifications (2) medical therapy (3) surgical

Mx of chronic pancreatitis How to do celiac plexus block?

Ganglionectomy or direct injection of sclerosing agents

CRP scoring

- As a single prognostic marker; <100 is unlikely severe - If CRP is >150mg/dL at 48 hours, the pancreatitis is more likely to be severe -- possibly an early indicator of progression of acute pancreatitis into a serious state - No relevance >3/7 of onset as other confounding factors come into the picture - Combination of Glasgow score and CRP improves overall prognostic value

Aetio of acute pancreatitis

(I GET SMASHED) 1. Idiopathic (15-25%) 2. Gallstones (38%) 3. Ethanol (36%) - Develops in pts whose alcohol ingestion is habitual over 5-15 years. - Alcoholics are usually admitted with an acute exacerbation of chronic pancreatitis. - Occasionally, however, pancreatitis can develop in a patient with a weekend binging habit. 4. Trauma 5. Steroids 6. Mumps and other infections (i.e. VZV, CMV, mycoplasma, parasitic infections) 7. Autoimmune - SLE, Sjogren's Syndrome 8. Scorpion toxin and other toxins (i.e. organophosphates poisoning) 9. Hypercalcaemia, hypertriglyceridemia (metabolic causes) 10. ERCP(2-5%)** - Post-ERCP pancreatitis in high risk patients might be prevented by a temporary pancreatic stent placement 11. Drugs(1-2%) - SAND: sulfamethoxazole-trimethoprim (co-trimoxazole), azathioprine (immunosuppressant), NSAIDs (valproic acid), Diuretics (Furosemide) 12. Rare causes: Neoplasm (i.e. pancreatic or ampullary tumour), Congenital (i.e. pancreas divisum), Genetics

Balthazar's CT Severity index

(consider a CT AP @ ~ 3-4/7 from onset) - Grades severity of disease according to CT findings - Rarely used

Atlanta classification

**Onset of acute pancreatitis is defined as the onset of abdominal pain (not the time of admission to the hospital) - time interval between onset of abdominal pain and first admission should be noted 1. Mild - Usually resolves in the first week - Mortality is rare 2. Moderate - Local complications or exacerbation of co-morbid disease 2. Severe - Local complications are: peripancreatic fluid collections, pancreatic and peripancreatic necrosis (sterile or infected), pseudocyst and walled-off necrosis (sterile or infected) - Mortality ranges from 36-50%

Hx taking for acute pancreatitis HOPC

- Acute and constant pain the epigastric area (or RUQ/LUQ) classically described as a boring sensation that radiates to the back - Patient is unable to get comfortable when lying supine with pain alleviated by sitting up and leaning forward - Pain might last for several days - Nausea, vomiting

Causes of chronic pancreatitis

- Alcohol abuse (70%) & Smoking - Autoimmune - Idiopathic - Metabolic (hypercalcaemia, hypertriglyceridemia, hyperparathyroidism) - Drugs -i.e. steroids, azathioprine - Trauma - Genetic (cystic fibrosis) - Congenital (sphincter of Oddi dysfunction, pancreas divisum) *Not all patients diagnosed with chronicpancreatitishave a history of recurrent acute pancreatitis

Mx of acute pancreatitis Supportive Monitoring

- In general ward if mild pancreatitis - HD/ICU monitoring if severe (≥3) - Fluid resuscitate with crystalloids to correct fluid losses in the 3rd space - Monitor vitals [SpO2, BP, HR, Temp.], urine output (aim: >0.5ml/kg/hr)& ± CVP - Frequent monitoring of electrolyte including calcium (every 6-8 hours initially) - Monitoring of ABG - assess oxygenation and acid-base status

Role for SX

- Infected necrotic pancreas (mortality 100% without operation) - Sterile necrotic pancreas (necrosectomy) - Diagnostic uncertainty - Complications e.g. intra-abdominal haemorrhage/ pseudocyst

PE for chronic pancreatitis

- LOW (secondary to anorexia and malabsorption) - Tenderness of upper abdomen - Enlarged pancreas is occasionally palpable, especially in thin patients (DDx: presence of pseudocyst) - ± jaundice (secondary to stricture of the common bile duct) - ± splenomegaly (secondary to thrombosis of the splenic vein) - ± ascites (secondary to a pancreatic peritoneal fistula)

PE for acute pancreatitis General apperance

- Lying motionless = Diffuse Peritonitis - Sitting Up, Leaning Forward = Pancreatitis - Small red tender nodules on skin and legs = subcutaneous fat necrosis (rare)

Course of disease of acute pancreatitis

- Most episodes (75%) are mild and self-limiting, needing only brief hospitalization - 20-25% patients develop a severe disease with local and extra-pancreatic complications characterized by early development and persistence of hypovolemia and multiple organ dysfunction (mortality rates as high as 40%)

Mx of chronic pancreatitis What is Whipple procedure?

- Pancreaticoduodenectomy - En-bloc removal of distal segment of the stomach, duodenum, proximal 15cm of jejunum, head of pancreas, common bile duct, gallbladder - Pancreatic and biliary anastomosis placed 45-60cm proximal to gastrojejunostomy

How do the classifications compare?

- Predicts severity - There are many systems but none are ideal 1. Now, Marshall score preferred -- uses organ failure score - Or SOFA score (validated for ICU patients) - In TTSH -- SOFA used 2. Ranson and glasgow can only be done after 48h - But Marshall to differentiate moderately severe and severe is to see after 48h if organ failure persists

Pathophysio of chronic pancreatitis

- Progressive destruction of the pancreas by repeated flare-ups of mild and subclinical types of acute pancreatitis - Characterized by diffuse scarring and strictures in the pancreatic duct - The Islet of Langerhans (endocrine function) have a greater resistance to injury than do the exocrine tissues

Hx taking for acute pancreatitis DDx

- Rule out other differential diagnosis 1. Gastric causes (PUD) 2. Hepatobiliary causes (hepatitis, GB/CBD disease) 3. Medical causes (AMI, DKA, lower lobe pneumonia) 4. Important to rule out (perforated viscus)

Role for MRCP

- Substitute for CT scan in patients allergic to iodinated contrast or in acute renal failure - MRCP good for visualizing cholelithiasis, choledocholithiasis, anomalies of the pancreatic and common bile ducts

PE for acute pancreatitis Vitals

- Tachycardia and Hypotension (due to fluid shifts with IV volume becoming markedly depleted) - Low Grade Fever - Tachypnoea → herald development of ARDS (auscultate lungs - crepitations, reduced air-entry)

Mx of chronic pancreatitis Indications for SX

- Unremitting Pain - Inability to rule out neoplasm - Treatment of complications: pseudocyst, aneurysm and fistula, local obstruction secondary to fibrosis (CBD, duodenum)

Role for Contrast-Enhanced CT Abdomen (CECT)

- Useful in confirming diagnosis of pancreatitis if haematological results are inconclusive - Useful in severely ill patients with suspicion of necrotizing pancreatitis (only after aggressive volume resuscitation to diminish risk of contrast-associated nephrotoxicity) - Patients with persisting organ failure, signs of sepsis or deterioration in clinical status 6-10 days after admission - CT assess local complications such as fluid collections and necrosis

Disadv of Ransons

- Validated for alcoholic pancreatitis only → revised Ranson's score was created for gallstone pancreatitis (same parameters but different cut-off values) - Difficult to tell aetiology in acute setting & cumbersome to wait for 48 hours, and difficult to assess for negative fluid balance

Mx of acute pancreatitis Supportive Organ failure

- Ventilate with PEEP if hypoxemic (e.g. ARDS) - Dialysis& CVP monitoring if in ARF - Fluid resuscitation & inotropes if Hypotensive

Pathophysio of acute pancreatitis

1. Acute pancreatitis is caused by unregulated activation of trypsin within pancreatic acinar cells - Activating pro-enzymes leading to auto-digestion - Activates an inflammatory cascade that both amplifies the local inflammatory response and can result in a progression to SIRS 2. Gallstones are thought to cause acute pancreatitis due to obstruction of the pancreatic duct - Causing interstitial oedema which impairs blood flow to the pancreatic cells → ischaemic cellular injury → activation of pro-enzymes→ destruction of pancreatic acinar cells 3. Alcohol is postulated to cause acute pancreatitis via its direct toxic effects and/or its metabolites (acetaldehyde, fatty acid ethyl esters (FAEEs), generation of oxidant stress) on acinar cells which predisposes the gland to autodigestive injury. - i.e. FAEEs which are generated when O2 levels in the pancreas is low trigger anexcessive increase in calcium ion concentration in the cell water inside the pancreatic cell which in turn activates the digestive enzymes

Mx for acute pancreatitis Treating aetio

1. Avoid alcohol, stop all offending medication & control hyperlipidaemia 2. ERCP + endoscopic sphincterotomy - Done in acute setting (within 72hours) for patients with severe biliary pancreatitis 3. Cholecystectomy for biliary pancreatitis - Patients with biliary pancreatitis who do not undergo cholecystectomy have a 40% 6 week recurrence risk - Cholecystectomy can be done in the same admission for patients with mild biliary pancreatitis - In patients with severe pancreatitis, there is reluctance to do the surgery early, as the patient may develop complications that require surgical intervention - better to do all surgery in the same operation instead of opening the patient twice

Mx of pseudocyst

1. Don't need to operate unless symptomatic - LOA or early satiety due to compression on stomach 2 Operate if > 6cm and persisting for > 6 weeks + pain as the chance of spontaneous resolution is low and risk of complications (infection, haemorrhage, rupture) is high 3. Tx by surgery, can be open, laparoscopic, endoscopic - Endoscopic - internal drainage via a cystogastrostomy, cystoduodenostomy or cystojejunostomy - Stomach if head of pancreas vs jejunum if tail of pancreas vs duodenum (depends on location of cyst) 4. Percutanoues draingage is relative contraindication if pancreatic pseudocyst - Leads to pancreaticocutanous fistula with secodnary skin complications because the amylase that comes out will digest skin - And body will be deprived amylase

Mx of chronic pancreatitis SX options

1. Drainage (Preferable for patients with dilated ducts) - Puestow procedure - Partington-Rochelle 2. Resection (pancreatectomy) - Whipple procedure - Subtotal/total pancreatectomy 3. Combined duct drainage and resection - Beger procedure - Frey procedure 4. Nerve block - Celiac plexus block

Ix for chronic pancreatitis (categories)

1. Dx 2. Assess Cx

Ix for acute pancreatitis (categories)

1. Dx 2. Risk stratification 3. Aetio

Mortality distribution in acute pancreatitis

1. Early: Within 1/52 - Due to severe organ failure, SIRS - Very little can be done in terms of treatment 2. Late - Most common cause is infection with resultant sepsis - Multi-organ failure can be the cause of death

Findings on Erect CXR & Supine AXR

1. Erect CXR may show: - Air under the diaphragm (perforated viscus) - Pleural effusion - Elevated hemidiaphragm - Pulmonary infiltrates - Complete whiteout (ARDS) 2. Supine AXR may show: - Sentinel loop sign: dilated proximal jejunal loop near the pancreas or - Colon cut-off sign: distended colon from ascending to mid-transverse with no air distally) due to localized ileus 2 to inflammationaround the pancreas 3. Presence of calcifications within the pancreas may indicate chronic pancreatitis

Hx taking for acute pancreatitis Aetiology

1. Gall stone disease: biliary colic, cholecystitis, CBD stone, cholangitis 2. Recent alcohol abuse or chronic alcohol abuse 3. Recent blunt trauma or ERCP done 4. PMHx: metabolic disease, autoimmune disease 5. Recent symptoms of mumps (viral fever + bilateral jaw pain/swelling) 6. Recent drug history: steroids, NSAIDs, diuretics

PE for acute pancreatitis (categories)

1. General appearance 2. Vitals 3. Abdo exam 4. Complete exam by

Hx taking for acute pancreatitis (categories)

1. HOPC 2. TRO DDx 3. Aetio

PE for acute pancreatitis Abdo exam

1. Inspection (from the foot of the bed) - Abdominal Distension 2. Palpation (patient in supine position, eyes fixed on patient's eye) a. Focal Epigastric Tenderness b. Palpable Mass (i.e. pseudocysts, pancreatic phlegmon) c. Signs of Peritonism: rebound tenderness, guarding, board-like rigidity d. Signs of Haemorrhagic Pancreatitis - Grey-Turner Sign (flank ecchymosis) - Cullen's Sign (periumbilical ecchymosis) -- exudates from pancreatic necrotic areas tracking along the falciform ligament and into the retroperitoneal and seen in the periumbilical region - Fox's Sign (inguinal ecchymosis) 3. Auscultation Diminished / Absent bowel sounds paralytic ileus from diffuse peritonitis

Ix for acute pancreatitis Assess severity

1. Lactate Dehydrogenase (serum LDH) 2. Liver Function Test - Enzymes (serum AST) - aspartate - Albumin 3. Glucose 4. Full Blood Count - Elevated white cell count (WCC) → associated with worse prognosis - Haematocrit levels higher than 44% a/w worse prognosis (patients with inadequate fluid resuscitation as evidence by persistence of hemoconcentration at 24 hours are at increased risk of developing necrotizing pancreatitis) 5. Renal Panel + Ca2+ - Urea, any electrolyte imbalance, dehydration, degree of renal impairment - Hypocalcaemia 6. ABG - Calculate base deficit (negative base excess) 7. C-Reactive Protein (CRP) - Marker of severity 8. ECG / Cardiac Enzymes →AMI 9. Erect CXR & Supine AXR 10. Contrast-Enhanced CT Abdomen (CECT) 11. MRI / MR cholangiopancreatography (MRCP)

Ix for acute pancreatitis Aetio

1. Liver Function Test (LFTs) - Elevation of ALT > 150mg/dl → gallstone pancreatitis - Elevation of Br > 5mg/dl that does not fall after 6-12 hours → impacted stone in ampulla of Vater - Elevation of AST for Ranson and Glasgow scoring system 2.Ultrasound Abdomen - Pancreas is not visualized in up to 40% of patients due to overlying bowel gas and body habitus - Good for visualising biliary tree and picking up gallstones (can intervene!) -- Dilated CBD → ERCP to remove gallstones/Bx tumour -- Not dilated → MRCP (suspparenchymal disease) 3. Ca/Mg/PO4 with albumin → hypercalcaemia 4. Fasting Lipids → hyperlipidaemia

Cx of chronic pancreatitis

1. Local Complications - Persistent Pseudocyst - Splenic vein thrombosis (splenomegaly) - Fistula (pancreatico-enteric, pancreaticopleural fistula) 2. Common Bile Duct Obstruction - Result from transient obstruction from pancreatic inflammation and oedema or from strictures on the intrapancreatic common bile duct 3. Duodenal Obstruction - Occur due to acute pancreatic inflammation, chronic fibrotic reaction, pancreatic pseudocyst or neoplasm 4. Pancreatic Cancer - Chronic pancreatitis suggested to increase risk by 2-3 x 5. Pancreatic Insufficiency - Type 1 DM - Steatorrhoea, Vitamin deficiency, Malnutrition

Mx of chronic pancreatitis Sx

1. Malabsorption / steatorrhoea → pancreatic enzyme supplements 2. Diabetes → lifestyle choices, OHGA, Insulin 3. Pain Relief → narcotics / TCAs, abstinence from alcohol

Mx of acute pancreatitis based on aetio and severuity

1. Mild gall stone pancreatitis = lap chole 2. Mild alcoholic pancreatitis = watchful waiting - But still look for gall stones 3. Severe gall stone pancreatitis = either watchful waiting or ERCP - In High D or ICU

Pancreas morphology on CT (categories)

1. Non-necrotising 2. Necrotising

Mx of pancreatic necrosis

1. Only infected necrosis must do necrosectomy - How to know if it is infected? Culture the necrosis, using EUS / ?CT guided - Can give Abx: Carbapenem and Floroquinolones 2. Too much to early and too little too late are detrimental for outcomes - The right time is 4-5 weeks later because the necrosis progresses after 5 days, then by 5 weeks whatever is necrosising will have necrosed, and the remaining is good - Delay surgery till as late as possible for demarcation/organization of necrotic areas (repeated surgeries required) 3. Step-up approach - 1st: Retroperiotneal percutaneous drainage - 2nd: Minimally access surgery - 3rd: Necrosectomy/debridement 4. Lavage and drainage procedure is done after necrosectomy to decrease infective load Summary: Masterful inaction

Presentation of chronic pancreatitis

1. Pain (upper mid epigastric pain radiating to the back, getting progressive worse) - Can last from hours to days - Mostly episodic, some have persistent relentless pain - Cardinal symptom and is present in 85-90% of patients 2. Change in bowel habits (diarrhoea) followed later by steatorrhoea 3. Newly diagnosed DM (30%) - late 4. LOW (secondary to anorexia and malabsorption)

Mx of chronic pancreatitis Cx

1. Pancreatic Pleural Effusions → tube thoracostomy 2. Pancreatic Ascites → paracentesis 3. Ductal Cx → Endoscopic Therapy (sphincterotomy, stenting, stone retrieval, lithotripsy) 4. Pseudocyst, aneurysm, fistula, local obstruction → surgical management

Ix for acute pancreatitis Risk stratification (criteria)

1. Ranson 2. Glasgow 3. Atlanta 4. CRP 5. Acute Physiology and Chronic Health Evaluation II Score (APACHE II) 6. Balthazar's CT severity index 7. Marshall score

Mx of acute pancreatitis Supportive (names)

1. Resus if needed 2. Monitoring 3. Nutrition NBM (gastric rest) with nutritional support 4. Analgesia 5. Treatment of fluid and electrolyte abnormalities - Hypocalcaemia, hypoglycaemia 6. Abx 7. Support for organ failure

Ix for acute pancreatitis Dx

1. Serum amylase(normal = 30-100U/L) - Levels ≥3 times the normal upper limit - Sensitivity 50% and spec. 99% - Levels rise within a 6-24 hours and normalizes in 3-7days - Elevation for > 10 days indicate complications (i.e. pseudocysts formation) - Magnitude of elevation not a/w disease severity or prognosis of disease 2. Serum lipase (normal =10-140 U/L) - Levels ≥ 3 times the normal upper limit - Sensitivity 64% & spec. 97% - Levels rise within 4-8hours and stays elevated for 8-14days - Useful for patients with delayed presentation of acute pancreatitis 3. Urinary diastase - Similar function to serum lipase, used when serum amylase is equivocally raised or normal

Mx of acute pancreatitis Categories

1. Supportive 2. Monitor and Mx for Cx 3. Tx aetio - Prevent further recurrance

APACHE II Score

APACHE II takes into account 12 continuous variables, age of the patient, pre-morbid conditions and the GCS. The major advantage is that it can be used to monitor a patient's response to therapy while the Ranson and the Glasgow scales are meant for assessment at presentation.

Mx of chronic pancreatitis What are Beger and Frey procedures?

Berger: Duodenum-preserving resection of a portion of the pancreatic head, pancreas transected at pancreatic neck Frey Procedure: Modification of Beger - Pancreatic neck not transected, parenchyma is extensively cored out from head to extent of diseased segment distally, lateral pancreaticojejunostomy

How to DDX cholangitis and acute pancreatitis?

Blood culture - Pancreatitis is sterile phenomenon until 1 week - Hence if positive then it is cholangitis - Only 1/3 of time is positive, because not taken during temperature spike - If negative then not helpful because cholangitis can have negative - But would not wait 48h for blood culture to come back - Hence do an urgent ERCP for possible cholangitis (for severe acute pancreatitis)

What are the danger signs of acute pancreatitis?

Danger signs in the first few hours: 1. Encephalopathy 2. Hypoxemia, Tachypnoea 3. Tachycardia >130/min, Hypotension <90mmHg, Haematocrit >44% 4. Presence of GreyTurner's/Cullen's sign 5. Oliguria <50mls/hr, Azotaemia

Other causes of elevated serum amylase

GI - PUD, Intestinal Obstruction, Perforated bowel, Ischaemic bowel (amylase > 1000), Cholecystitis, Cholangitis, Appendicitis - Complication of pancreatitis (pseudocyst, abscess, ascites), pancreatic cancer Non-GI - Renal Failure - ARDS - Ruptured ectopic pregnancy / Ovarian Cysts / PID - Salivary gland injury or inflammation - Macroamylasemia - Diabetic Ketoacidosis (DKA) or any acidosis (ketotic and non-ketotic) - Neoplasms (prostate, lung, oesophagus, breast, multiple myeloma, pheochromocytoma)

What is chronic pancreatitis?

Long-standing inflammation of the pancreas with diffuse scarring and structuring in the pancreatic duct leading to irreversible destruction of the exocrine and in the late stage the endocrine parenchyma

What is pancreatic divisum?

Most common congenital anomaly of the pancreas (3-10%) - Absence of fusion between the dorsal and ventral duct system during 6th week of development - Normally, distal dorsal duct joins to proximal ventral duct to form the main pancreatic duct (duct of Wirsung) which terminates at the papilla of Vater - In pancreas divisum, lack of fusion leads to a short duct of Wirsung and majority of pancreatic secretion having to drain through the minor pancreatic duct (duct of Santorini) → terminate at minor duodenal papilla - This lead to a stenosed or inadequately patent minor papilla preventing normal drainage of pancreatic secretions → lead to increased intra-ductal pressure.

Mx of chronic pancreatitis What are Puestow procedure and Partington-Rochelle?

Puestow: Distal pancreatectomy with a distal pancreaticojejunostomy anastomosis Partington-Rochelle: Modification of Puestow -eliminate distal pancreatectomy

Ix for chronic pancreatitis Dx

Radiological 1. ERCP - Gold standard imaging test for diagnosis of chronic pancreatitis) - Characteristic → "chain of lake" appearance of ductal anatomy - Can also evaluate pancreatic mass lesions, cytology, delineation of ductal anatomy and can be therapeutic - 3-7% risk of causing acute pancreatitis 2. Endoscopic Ultrasound (EUS) - Diagnosis for chronic pancreatitis based on Rosemont Criteria Laboratory -- Assessing pancreatic function 1. Pancreatic Secretin Stimulation Test - Gold standard but invasive - Patient is given IV secretin and the pancreatic secretions (released into the duodenum) are aspirated (removed with suction) and analysed over a period of about 2 hours 2. Pancreatic Endocrine Function - i.e. fasting blood glucose, 2hr post-prandial blood glucose or glucose tolerance test - Abnormal test results in 14-65% with early chronic pancreatitis - Abnormal results in 90% of patients when calcifications are present 3. 72hr faecal collection for estimation of daily faecal fat - Simple and cheap test for assessing pancreatic function → determine if patient has significant steatorrhoea - Limited role in definitive diagnosis of chronic pancreatitis (require high degree of pancreatic insufficiency to have a positive test) Note: serum amylase and lipase levels are elevated in acute pancreatitis but rarely useful in chronic pancreatitis and are commonly normal due to 'burn out' of the pancreas

Ranson's criteria

Ranson's criteria prognosticates mortality according to score - Any patient with a score of 3 and above is considered to have severe pancreatitis - Mortality -- 0-2 0-2% -- 3-415% -- 5-6 50% -- ≥7 70-90%

PE for acute pancreatitis Complete exam by

Request for input/output charts Respiratory Examination TRO pleura effusion, ARDS

Definition of acute pancreatitis

Reversible pancreatic parenchymal damage of varying severity owing to an acute inflammatory disease of the pancreas

What is hemorrhagic pancreatitis and how to Mx

Severe pancreatitis a/w 40% mortality rate, is usually seen in 1-3% of patients and usually develops within 48hours after onset of symptoms - Do angiography and embolisation of artery - And then if still cannot control bleeding: open up to control, on table death 30%

How to differentiate pseudocyst from cyst?

Test for amylase 1. High amylase is pseduocyst 2. If low then true cyst

Glasgow's criteria (Imrie's criteria)

The Glasgow system uses age and 7 laboratory values collected during the first 48 hours following admission for pancreatitis to predict for severe pancreatitis. It is used for both alcoholic and gallstone pancreatitis. (PaO2 < 60mmHg) - ≥ 3 criteria = severe - Preferred over Ranson's scoring in certain centres

Dx of acute pancreatitis

The diagnosis of acute pancreatitis requires 2 of the following 3 features 1. Abdominal pain consistent with epigastric pain (acute onset of a persistent, severe, epigastric pain often radiating to the back) 2. Serum lipase / amylase activity of at least 3x greater than the upper limit of normal 3. Characteristic findings of acute pancreatitis on CECT or MRI or trans-abdominal ultrasound

Mx of acute pancreatitis Supportive Nutrition

Tutorial: - Now not NBM, can eat and drink - But if N&V then can hold off - Enteral is better than parenteral Medbear: - May include gastric decompression with NGT if there is persistent vomiting, significant gastroparesis, or intestinal obstruction (ileus) - Acid suppression does not change course of disease, but protects against stress ulcer formation; octetride has no benefit (thought to reduce pancreatic secretions) - Fast patients for at least 2/7 until more stable - May start oral feeding early with fluids in mild pancreatitis if tolerated - Prolonged NBM results in poorer recovery due to nutritional debilitation - Think about NJ feeding, or open jejunostomy creation early in patients with severe pancreatitis; if not tolerable, then consider TPN