Acute Pancreatitis

Anatomy• The pancreas is a retroperitoneal organ that lies

in an oblique position, sloping upward from the C-loop of the duodenum to the splenic hilum.

• Weighs about 75 to 100gm• Length is about 15 to 20cm• It can be divided into Head, Uncinate process,

neck, body and tail.• Neck lies over L1 and L2 vertebrae

Anatomical Relations• The neck of the pancreas lies directly over the

portal vein.• At the inferior border of the neck, the superior

mesenteric vein joins the splenic vein and then continues as the portal vein.

• The common bile duct runs in a deep groove on the posterior aspect of the head.

• The body and tail lie just anterior to the splenic artery and vein.

• The body overlies the aorta at the origin of the superior mesenteric artery.

Arterial Supply

Venous Drainage

Variations of Portal Vein

Lymphatic Drainage

Nervous Supply

Pancreatic Duct• Embryologically pancreas develops from a ventral

bud and a dorsal bud.• The duct of ventral bud is called as duct of

Wirsung, which is joined by common bile duct.• The duct of dorsal bud is called as duct of

Santorini and it drains directly into the duodenum.

• With the gut rotation, the two buds and their respective ducts fuse. The ventral bud becomes the inferior portion of head and uncinate process while the dorsal bud becomes the body and tail of pancreas.

• Most of the pancreas drains through the duct of Wirsung, the main pancreatic duct, and drains into duodenum through ampulla of Vater/ major papilla.

• In 60% of the people the duct of Santorini persists as the lesser pancreatic duct and drains into duodenum through lesser papilla.

• The lesser papilla is usually about 2 cms proximal to ampulla of Vater.

• In 30% the duct of Santorini ends as blind accessory duct and does not empty into duodenum.

• In 10% the duct of Wirsung and Santorini fail to fuse, this results in majority of pancreas draining through the duct of Santorini and lesser papilla. This is know as pancreas divisum

• In minority of patients with pancreas divisum the lesser papilla can be inadequate to handle the flow of pancreatic juice resulting in outflow obstruction leading to pancreatitis.

Ampulla Of Vater

Sphincter Of Oddi

Histology• Pancreas secretes approximately 500ml to 800ml

of pancreatic juice per day.• Exocrine pancreas accounts for 85% • Endocrine pancreas accounts only for 2% • only approximately 20% of the normal pancreas is

required to prevent insufficiency.• The acinar cells secrete amylase, proteases, and

lipases enzymes• The centroacinar and intercalated duct cells

secrete the water and electrolytes

Endocrine FunctionHormones Islet Cell Functions

Insulin Beta Cell Decreased gluconeogenesis, glycogenolysis, fatty acid breakdown, and ketogenesisIncreased glycogenesis, protein synthesis

Glucagon Alpha Cell Opposite effects of insulin; increased hepatic glycogenolysis and gluconeogenesis

Somatostatin Delta Cell Inhibits GI secretionInhibits secretion and action of all GI endocrine peptidesInhibits cell growth

Pancreatic polypeptide

PP Cell Inhibits pancreatic exocrine secretion and secretion of insulinFacilitates hepatic effect of insulin

Hormones Islet Cell Functions

Amylin Beta Cell Counterregulates insulin secretion and function

Pancreastatin Beta Cell Decreases insulin and somatostatin releaseIncreases glucagon releaseDecreases pancreatic exocrine secretion

Ghrelin Epsilon Cell

Decreases insulin release and insulin action

Pancreatitis

Acute Pancreatitis

Acute Relapsing

Pancreatitis

Chronic Pancreatitis

Acute Pancreatitis• Inflammatory disease of pancreas that is

associated with little or no fibrosis of the gland.

OR• An acute condition presenting with abdominal

pain and is usually associated with raised pancreatic enzymes levels in the blood or urine as a result of pancreatic inflammation.

Acute v/s Chronic• Acute pancreatitis is reversible pancreatic

parenchymal injury associated with inflammation.• Chronic pancreatitis is defined as inflammation of

the pancreas with irreversible destruction of exocrine parenchyma, fibrosis, and, in the late stages, the destruction of endocrine parenchyma.

Clinical Classification

Acute Pancreatitis

Mild Severe

• Mild acute pancreatitis: Interstitial oedema of the gland and minimal organ dysfunction.

• 80% of case fall under Mild category, which has about 1% mortality.

• Severe acute pancreatitis: pancreatic necrosis, severe systemic inflammatory response and often multi-organ failure.

• Mortality rate is as high as 20 to 50%

Aetiology• Alcohol• Biliary tract disease• Hyperlipidemia• Hereditary• Hypercalcemia• Trauma

o Externalo Surgicalo ERCP

•   Ischemiao Hypoperfusiono Atheroembolico  Vasculitis

• Pancreatic duct obstructiono  Neoplasmso Pancreas divisumo Ampullary and duodenal lesions

• Infections• Venom• Drugs• Idiopathic

Aetiology

Biliary Tract

Diseases70%

Alcohol25%

Others5%

Incidence

Biliary Tract disease• Choledocholithiasis is the most common form of

associated biliary abnormality• Various Theories:

o Common channel hypothesis o Sphincter Incompetence o Ductal Pressureo Colocalization theory

Alcohol• Pancreatitis can result with single or little alcohol

intake.• Usually > 2 years of intake, and often history of >

10 years.• In individuals taking 100 to 150gm/day of alcohol,

10 to 15% can develop pancreatitis. • It can become recurrent with continued alcohol

intake. • Theories: secretion with blockage mechanism • It is a metabolic toxin to pancreatic acinar cells. • Alcohol also transiently decreases blood flow to

pancreas

Tumors• Should be considered in a non alcoholic patient

with no demonstrable biliary tract disease. • 1 to 2% of patients with acute pancreatitis have

pancreatic carcinoma • It could be the first clinical manifestation of

periampullary tumor.

Iatrogenic • Pancreatic biopsy, biliary duct exploration, distal

gastrectomy and splenectomy are associated with acute pancreatitis.

• It is associated post op with billroth II gastrectomy and jejunostomy.

• ERCP results in pancreatitis in 2 to 10% of cases.

Drug Induced• Thiazides• furosemide• estrogens• azathioprines• l-asparaginase• 6-marcaptopurine• methyldopa• sulfonamides• tetracyclines• pentamide

• procainamide• nitrofurantoin• dideoxyinosine• valproic acid• acetylcholinesterase

inhibitors

Infections• Mumps, coxsackievirus, and m.pneumoniae are

believed to be capable of inducing pancreatitis by infecting acinar cells.

• Infection by ascaris lumbricoides, and clonorchis sinensis are also implicated.

Hereditary• Cationic trypsinogen/PRSS1: It is a missense

mutation, which results in premature, intrapancreatic activation of trypsinogen.

• It accounts for about two-thirds of cases of hereditary pancreatitis

• A failure to express a normal trypsinogen inhibitor, pancreatic secretory trypsin inhibitor (PSTI) or SPINK1, is a cause of familial pancreatitis.