Gastro 55 Pancreatitis

• Two of the following three features:
• (1) abdominal pain consistent with acute pancreatitis
• (acute onset of a persistent, severe, epigastric pain often radiating to the back);
• (2) serum lipase activity (or amylase activity) at
• least three times greater than the upper limit of normal; and
• (3) Radiological evidence of acute pancreatitis on CECT, USG or MRI

• Interstitial oedematous pancreatitis - Acute inflammation of the pancreatic parenchyma and peripancreatic
• tissues, but without recognisable tissue necrosis. 
• CECT criteria
• ▸ Pancreatic parenchyma enhancement by intravenous contrast agent
• ▸ No findings of peripancreatic necrosis 

• 2. Necrotising pancreatitis
• - Inflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis
• CECT criteria
• ▸ Lack of pancreatic parenchymal enhancement by intravenous contrast agent and/or
• ▸ Presence of findings of peripancreatic necrosis

• Extraluminal gas in the pancreatic and/or peripancreatic tissues on CECT
• Percutaneous, image-guided FNA is positive for bacteria and/or fungi on Gram stain and culture

• < 2weeks - MODS
• >2 weeks -Septic complications

• Obstructive theory - Excessive pressure in pancreatic duct
• Reflux theory - Stone impacted in ampulla, reflux of bile

• Alcohol triggers proinflammatory pathways such as nuclear factor κB (NF-κB), which increase the production of TNF-α and IL-1.
• It also increases the expression and activity of caspases. Caspases are proteases that mediate apoptosis.
• Alcohol decreases pancreatic perfusion.
• It induces sphincter of Oddi spasm.
• It obstructs pancreatic ducts through the precipitation of proteins inside the ducts

• Peptic Ulcer disease
• GI perforation
• Mesenteric Ischemia
• Retroperitoneal Hematoma
• Renal failure
• Salpingitis
• Salivary gland inflammation

• Give IV secretin - Increases pancreatic duct secretion, causes transient distension of pancreatic duct, useful for recurrent pancreatitis with no evidence of predisposing factors -
• - Pancreas Divisum
• - Intraductal Papillary Mucinous Neoplasm
• - Small tumor of pancreatic duct

• Ranson Scoring system
• APACHE (Acute Physiologic and Chronic Health Evaluation) - age, health status, 12 physiological measurements , APACHE >8 - Severe Pancreatitis
• BISAP
• Modified CTSI
• Modified Marshall scoring system 
• CRP Level - >150mg/ml - Severe

• 11 Parameters - 5 on admission, 6 after 48 hours
• Different for Gallstone and Alcoholic Pancreatitis

Mortality was 0 to 3 percent when the score was <3, 11 to 15 percent when the score was ≥3, and 40 percent when the score was ≥6

• On admission
• WBC count > 16000/mm3
• Age > 55 years
• LDH > 700 units/L
• Liver enzyme (AST) > 250 Sigma Frankel units per cent
• Blood Sugar > 10 mmol/L

• Within 48 hours
• Fluid sequestration > 6 liters
• Arterial Oxygen saturation (PaO2) < 8 kPa (60 mmHg)
• Serum Calcium < 2.0 mmol/L (8mg/dl)
• Hematocrit - fall by>10%• Blood Urea nitrogen rise > 5 mg%
• Base deficit > 4 mmol/L
• [@ WALLS FOr CHUB]

• Does not assess the severity at the time of admission, 6 parameters are assessed after 48 hours
• Low PPV, high NPV - used to rule out severe pancreatitis

• Bedside index for severity of Acute Pancreatitis (≥3 in first 24 hours - severe)
• BUN >25mg/dl
• Impairment of conciousness
• Evidence of SIRS
• Age > 60 years
• Pleural effusion

• 
• 

Mild acute pancreatitis - absence of organ failure and the absence of local or systemic complications

• Moderately severe acute pancreatitis - presence of transient organ failure or local or systemic complications in the absence of persistent organ failure.
• An example of a symptomatic local complication is a peripancreatic collection resulting in prolonged abdominal pain, leucocytosis and fever, or that prevents the ability to maintain nutrition orally.
• An example of a symptomatic systemic complication is exacerbation of coronary artery disease or chronic lung disease precipitated by the acute pancreatitis.

Severe acute pancreatitis is characterised by persistent organ failure.

• Local complications are
• - Acute peripancreatic fluid collection
• - Pancreatic pseudocyst
• - Acute necrotic collection and
• - Walled-off necrosis

Walled-off pancreatic fluid collections include pseudocysts and walled-off pancreatic necrosis. The majority of walled-off pancreatic fluid collections are now classified as walled-off pancreatic necrosis rather than pseudocysts

• Though the revised classification has brought uniformity in terminology and has been validated in recent studies, as its application  has grown, a number of criticisms have arisen about it being complete.
• It has been pointed out that it does not give due credence to  infected pancreatic necrosis and the dynamics of organ failure are not accounted for in it.
• The category of moderately severe pancreatitis  is rather not well defined.
• Moreover the emerging data on extrapancreatic necrosis needs to be considered in severity stratification.
• The classification of acute pancreatitis seems to be a continuous process  which is like a “work in progress”.

• Refer to - The Revised Atlanta Classification of Acute Pancreatitis: A Work Still in Progress?
• http://pancreas.imedpub.com/the-revised-atlanta-classification-of-acute-pancreatitis-a-work-still-in-progress.pdf

• Peripancreatic fluid associated with interstitial oedematous pancreatitis with no associated peripancreatic necrosis. Fluid collections usually develop in the early phase of pancreatitis. Acute peripancreatic fluid collections (APFC) do not have a well defined wall, usually remain asymptomatic, and resolve spontaneously without the need for drainage
• CECT criteria
• ▸ Occurs in the setting of interstitial oedematous pancreatitis
• ▸ Homogeneous collection with fluid density
• ▸ Confined by normal peripancreatic fascial planes
• ▸ No definable wall encapsulating the collection
• ▸ Adjacent to pancreas (no intrapancreatic extension

A pancreatic pseudocyst is an encapsulated collection of fluid with a well defined inflammatory wall usually outside the pancreas with minimal or no necrosis. This entity usually occurs more than 4 weeks after onset of interstitial oedematous pancreatitis to mature.

• CECT criteria
• ▸ Well circumscribed, usually round or oval
• ▸ Homogeneous fluid density
• ▸ No non-liquid component
• ▸ Well defined wall; that is, completely encapsulated
• ▸ Maturation usually requires >4 weeks after onset of acute pancreatitis; occurs after interstitial oedematous pancreatitis.

Necrotizing pancreatitis most commonly manifests as necrosis involving both the pancreas and peripancreatic tissues. Necrosis may result in an acute necrotic collection (ANC) that contains a variable amount of fluid and necrosis but lacks a definable wall or walled-off necrosis (WON), which consists of a mature, encapsulated collection of pancreatic and/or peripancreatic necrosis that has developed a well defined inflammatory wall. Both ANC and WON are initially sterile but may become infected.

• CECT criteria for acute nectrotic collection 
• ▸ Occurs only in the setting of acute necrotising pancreatitis
• ▸ Heterogeneous and non-liquid density of varying degrees in different locations (some appear homogeneous early in their course)
• ▸ No definable wall encapsulating the collection
• ▸ Location—intrapancreatic and/or extrapancreatic

• CECT criteria for walled off necrosis 
• ▸ Heterogeneous with liquid and non-liquid density with varying degrees of loculations (some may appear homogeneous)
• ▸ Well defined wall, that is, completely encapsulated
• ▸ Location—intrapancreatic and/or extrapancreatic
• ▸ Maturation usually requires 4 weeks after onset of acute necrotising pancreatitis

• Mucosal Atrophy
• Decreased intestinal blood flow, increased risk of bacterial overgrowth and small bowel antegrade colonization with increased colonic bacteria translocation
• Metabolic complications – Hyperglycemia, electrolyte imbalance, central line infection

• Mild pancreatitis – Same setting
• Severe pancreatitis – After 6 weeks

• Normal Pancreatic Parenchyma – 100-150
• Necrotic Pancreatic Tissue <40-50 HU

• IV antibiotics – Carbapenem is DOC
• Step Up approach
• Surgical debridement with necrosectomy

• Postpone Intervention to facilitate safe necrosectomy and improved prognosis
• Percutaneous drainage
• Endoscopic transgastric necrosectomy
• Percutaneous retroperitoneal necrosectomy
• Video assisted retroperitoneal debridement
• Open necrosectomy

• ●Indication - patients with pancreatic necrosis and progressive clinical sepsis as a complication of severe acute pancreatitis. Infected pancreatic necrosis and symptomatic sterile necrosis are both accepted indications for debridement.
• ● Goal - to excise all dead and devitalized pancreatic and peripancreatic tissue, while preserving viable functioning pancreas, controlling resultant pancreatic fistulas, and limiting extraneous organ damage.
• ●Timing - 3-4 weeks following the onset of acute pancreatitis. Delayed debridement allows clinical stabilization of the patient, resolution of early organ failure, and a decrease in the intense inflammatory reaction in the retroperitoneum.
• ●Minimally invasive techniques can be employed in selected patients. Percutaneous catheter drainage is primarily a bridging technique for patients who are too unstable to undergo surgical debridement,
• ●Open surgical debridement is the gold standard for management of pancreatic necrosis. Laparoscopic debridement is primarily limited to patients with walled-off pancreatic necrosis.
• ● Complications after pancreatic debridement include intra-abdominal fluid collections, bleeding, pancreatic fistulas, incisional hernias, and pancreatic insufficiency.

• Within 14 days – 75%
• 15-29 days – 45%
• >29 days – 8%

The longer the patient be medically optimized and managed with enteral nutrition and antibiotics (as indicated), the more mature the fluid collection, and operation will be better tolerated

• Pseudocyst <4cm indiameter
• Located in tail
• No evidence of pancreatic duct obstruction or communication with main pancreatic duct

• Infection - abscess, systemic sepsis
• Rupture
• - Into gut - GI bleeding, internal fistual
• - Into peritoneum - Peritonitis
• Enlargement
• - Pressure effects - Obstructive jaundice form biliary compression , Bowel obstruction
• - Pain
• Erosion in vessels - Hemorrhage into the cyst, hemoperitoneum

• Symptomatic patients
• Difference between cystic neoplasm and pseudocyst not possible

• Transgastric/ transduodenal endoscopic drainage
• Endoscopic dilatation and stent placemet 
• Surgical – Those who fail Endoscopic techniques
• - Cystogastrostomy
• - Cystoduodenostomy
• - Roux-en-Y Cystojejunostomy
• Percutaneous drainage – Only in septic patients

• Endoscopic drainage should only be considered if
• - there is confidence in the diagnosis (d/d -cystic neoplasm)
• - surgical backup is available in the event of a serious complication

Choice of endoscopic procedure will depend on the clinical setting

● Relatively small pseudocysts in communication with the main pancreatic duct are candidates for transpapillary stent placement. This technique reduces the incidence of bleeding compared with transmural drainage but may carry an increased risk of infection, especially if the pseudocyst contains debris. Transpapillary stent placement is often reserved for pseudocysts that are not amenable to transmural drainage. Transmural drainage is preferred because it permits placement of multiple larger-bore stents.

● Endoscopic dilatation and stent placemet – If pancreatic duct stricture is associated with pancreatic pseudocyst

●Transmural puncture through the gastric or duodenal wall into the cyst can be performed in patients who have a large, symptomatic walled-off pancreatic fluid collection that is compressing the stomach or duodenum when there is close apposition (<1cm) of the fluid collection to the bowel lumen. In addition, for patients with pseudocysts who have complete obstruction of the pancreatic duct, transmural puncture is the only feasible technique. In the absence of an endoscopically visible bulge, endoscopic ultrasound (EUS) is used to localize and direct drainage of the fluid collection.

• „ Grossly infected cyst
• „ Cysts associated with hemorrhage
• „ Free rupture of the cyst requiring immediate laparotomy
• „ Cysts with a soft wall which will not hold sutures.

• After laparotomy the cyst wall is broken down, all debris removed and closed suction drain is placed in the cavity.
• If there is bleeding the cavity may be packed.

• „ Pancreatic fistula
• „ Recurrence
• „ Increased mortality and morbidity

• Persistent Inflammation
• Irreversible fibrosis
• Atrophy of pancreatic parenchyma
• Chronic Pain
• Endocrine / Exocrine insuffiency

• - That significantly decreases the quality of life
• - 90% pancreas should be malfunctional before symptoms develop

Obstruction of the main pancreatic duct leads to increased ductal pressure (that may in turn be transmitted to secondary ducts and the surrounding parenchyma), leading to pain through stretch-activated neural pathways.

Neuropathic sensitization of peripheral and central sensory pathways – more accepted theory. Microscopic evaluation of pancreatic nerves has shown evidence of neural injury in setting of chronic pancreatitis.

Trypsin and capsaicin can cause activation of sensory pancreatic neuron.

Cholecystokinin, which is significantly raised in chronic pancreatitis, act directly on CNS via receptors in area postrema of medulla, that connect to central pain centre leading to pain sensation.

TIGAR-O

• Toxic metabolites - alcohol, tobacoo, smoking, hypercalcemia, CRF
• Idiopathic - tropical
• Genetic - Protease serine I (PRSSS1), SPINK 1, CFTR
• Autoimmune disorders
• Recurrent acute and severe - recurrent acute pancreatitis, post-radiation,
• Obstructive - Pancreatic divisum, sphinchter of oddi disfunction

• Valproate 
• Erythromycin 
• Retrovirals 
• Furesemide 
• Azathioprine 
• Thiazides /Tetracyclines 
• Statins/Steroids/Sulfonamides 
• Hydrochlorothiazide 
• Estrogen 
• Ethanol 
• Metronidazole 
• Acetaminophen (Paracetamol)

[@ VERy FAT SHEEMA suffered from pancreatitis.]

• EUS – Rosemont concesus – Based on Parenchyma and ductal features
• ERCP - Historically considered gold standard, however, with advent of secretin MRCP and EUS, has significantly decreased its role as diagnostic test

• - Measurement of fecal Elastase level
• - Fecal fat level – fecal fat after intake of 100gm of fat/day, if exceeds 7gm/day – steatorrhea is confirmed

• Medical
• Interventional therapy – Endoscopic treatment (Placement of Stent/ESWL )
• Surgical treatment
• 

• A) Decompression - When the main pancreatic duct is dilated more than 7 mm and there is no inflammatory pseudotumor at the pancreatic head.
• 1. Duval - pancreatic tail resection and end-to-end or end-to-side pancreaticojejunostomy of the residual pancreatic end and jejunum to achieve retrograde drainage of the pancreatic duct
• 
• 2. Puestow-Gillesby procedure (Side-side Roux-en-Y Pancreaticojejunostomy or lateral Pancreatico-jejunostomy) - to solve the problem of recurrent multiple strictures of the pancreatic duct in the DuVal procedure, Puestow and Gillesby first proposed the Puestow- Gillesby procedure. In this procedure, the spleen and pancreatic tail are resected, and the pancreatic duct is longitudinally opened. The longitudinally opened pancreatic duct is then connected with the jejunum via side-to-side pancreaticojejunostomy to drain the pancreatic juice and reduce the incidence of late-stage strictures.
• 
• 3. Partington-Rochelle procedure - splenectomy and pancreatic resection is not done
• 

• B. Resection –
• 1. Whipples
• 2. Pylorus preserving pancreatoduodenectomy
• 3. Distal pancreatectomy
• 4. Middle segment pancreatectomy
• 5. Total pancreatectomy

• C. Decompression combined with resection -
• 1. Beger - also called as Duodenum-preserving pancreatic head resection (DPPHR). Division of neck of pancreas, leaving small rim of pancreatic tissue along the duodenum – End-End and End-side Roux-en-Y PJ (Double anastomosis)
• 

• 2. Frey procedure - modified type of DPPHR, local resection of the pancreatic head combined with a longitudinal pancreaticojejunostomy.
• 3. Berne modification - Resection of pancreatic tissues at the portal vein level is usually difficult because of inflammation or portal hypertension. In the Berne procedure, this resection is not performed. The Berne procedure has a pancreatic head resection range similar to the Beger procedure. The pancreatic neck is preserved, and Roux-en-Y anastomosis is performed between the pancreatic head and the jejunum
• 
• 4. Hamburg modification - This procedure is applicable to patients with CP who have thin pancreatic ducts smaller than 3 mm in diameter. This procedure has a large range of pancreatic head resection, and the central part of the uncinate process is also resected. The pancreatic tissues are resected in a V  shape
• 5. Izbicki procedure

.

• o Frey’s Procedure 2072
• o Idiopathic acute pancreatitis 2070