These slides includes information about histoical background, Anatomy, physiology and pathology of pancreas. pancreatitis it's types, etiology, pathology and it's management both conservative and surgical.

2. Contents:
 Historical background
 Surgical anatomy
 Physiology
 Pancreatitis
 Types of pancreatitis in detail
 Management of pancreatitis

3. Beginning of pancreatology:
 Herophilus – father of anatomy is believed to be the founder of pancreas, but no where
mentioned.
 Rufus of Ephesus – gave the term Pancreas, who believed that pancreas was just extension of
digestive system.
 Johann georje wirsung introduced main duct of pancreas.
 Accessary duct was discovered by Giovanni Domenico Santorini
 Claude Bernard introduced digestive functions of pancreatic juice
 Fredrick grant banting 1921 introduced effect of pancreatic juice on DM by experimenting on
dog.

4. Introduction:
Pancreas is a gland which is partly endocrine and partly
exocrine.
Rufus gave the term pancreas, which is a Greek word.
Pan + Kreas
(All + Flesh/meat)
Homers named it as Sweet Bread (Animal Flesh)
Moynihan gave name as Abdominal Tiger

5. Surgical Anatomy of Pancreas
Pancreas is situated across posterior wall of abdomen involving
epigastric and left hypochondriac region, deep in abdomen between
stomach and L2, L3 vertebrae.
Extends from duodenum to spleen.
It is long, flat, irregular prismatic in shape.
Weight – 100gms
Measurement – 15 cm in length, 3 cm in width, and 1.5 cm in thickness.
Parts of Pancreas:
Head, Neck, Body, and tail.

6. Head of Pancreas:
 Broadest part of pancreas
 Situated in the C curve of duodenum
 On right side of superior mesenteric vein
 Head extended posteriorly and inferiorly behind
superior mesenteric vein – uncinated process
Relationship:
Posteriorly: Right Kidney, Right renal vessel, IVC, Left
Renal Vein entering IVC, Right crus of diaphragm,
Pancreaticoduodenal arcade, Right Gonadal vein,
Distal CBD.

7. Neck:
 Constricted part of pancreas
 1.5 cm in length
 Lies between celiac trunk and superior mesenteric
vessels
 Its junction with head lie over imaginary line joining
sup. Mesentric vessel and portal vein
 Relations:
Ant – Gastroduodenal artery giving a branch, ant. Sup.
Gastroduodenal artery.
Post – Sup. Mesenteric vein joining splenic vein to form
portal vein, few small veins entering portal vein, rarely
inferior mesenteric vein may join portal vein.

8. Body:
 Horizontal segment, on the left side of sup. Mesentric
vessel.
 Relations:
Sup – celiac axis, CHA, splenic vessel
Inf – 4th part of duodenum, suspensory ligament of trietz,
first part of jejunum left side of transverse colon, sup.
Mesentric vein and artery.
Front – omental bursa, stomach, transverse colon with
mesocolon, inf mesenteric vein joining splenic vein.
Behind – devoid of peritoneum, aorta, sup. Mesentric
artery, left crus of diaphragm, left supra renal gland, laft
kidney and, its vessels, splenic vein.

9. Tail:
 Distal most part, tip related to spleen, enveloped in splenorenal ligamengt with splenic vessel.
 Blood supply:
pancreatic branch of splenic Artery
superior pancreaticoduodenal artery
inferior pancreaticoduodenal artey
Venous drainage: into portal vein.
Nerve supply:
parasympathetic – vagus
sympathetic – splenic

10. Ducts of pancreas:
 Main duct (Duct of Wirsung) :
 Begins at tail, runs posteriorly on body and head of pancreas receiving numerous
tributaries at its right angle. Then joins CBD at 2nd part of duodenum to form
pancreaticoduodenal vater (Ampula of vater) and opens on major summit of papilla 8
– 10 cm from pylorus.
 Accessory pancreatic duct (Duct of santorini):
 Ampula of vater
Muscular spincter complex:
 Sup. bile duct spincter
 Inf. Bile duct spincter
 Pancreatic spincter
 Ampular spincter

11. Physiology of pancreas (functional anatomy of pancreas)
Exocrine part: made up of alveoli/ acini with central lumen. Each alveolus has
duct which joins to interlobular duct which further connects main pancreatic
duct.
Exocrine part deals with pancreatic juice secretion.

12. Functions of pancreatic juice:
 Neutralization
 Activation of enzymes.
 Digestion
 Digestion of proteins
 Trypsin: it activates only after entering small intestine. Its activation is controlled by inhibitors
secreted by ducts
 Functions: protein metabolism
 Curdling of milk
 Blood clotting
 Activation of other enzymes
 Autolytic action
Other ptotease enzymes has got similar actions

13. Digestion of lipids:
 Pancreatic lipase: it’s a strong lipolytic enyme, digests triglycerides into monoglycerides and fatty acids
 Fat digestion by pancreatic lipase requires:
 1. Bile salt: for emulsification
 2. Colipase: co-enzyme for digestion
 Rest of lipolytic enzymes has got similar action
 Digestion of carbohydrates: by pancreatic amylase into dextrin and maltose
 Hormones stimulating pancreatic secretions:
Secretin and CCK
 Hormones inhibiting pancreatic secretion:
Pancreatic polypeptide, somatostatin, peptide YY and, peptides like ghrelin & leptin

14. Endocrine part of pancreas:
 A cells – Glucagon
 B cells – Insulin
 D cells – somatostanin
 PP cells – pancreatic polypeptide

15. Pancreatitis
 Inflammation of pancreas
 It is most devastating condition of the abdomen
 Classification:
I. Marseilles’ classification
 A. Acute Pancreatitis
 B. Acute relapsing pancreatitis
 C. Chronic pancreatitis
 D. Chronic relapsing pancreatitis

16. Trapnell’s aetiologic classification
Major causes:
Biliary tract disease
Alcoholism
Other causes:
Trauma
Hyperparathyroidism; hypercalcemia; hyperlipidaemia.
Diabetes
Drugs
Viral infection
Vascular disease
Scorpion venom
Biliary ascariasis
Mycoplsma pneumonia

17. Acute pancreatitis
 Acute pancreatitis is an acute inflammation of the prior normal
gland parenchyma which is usually reversible (but acute attack
can occur in a pre-existing chronic pancreatitis) with raised
pancreatic enzyme levels in blood and urine.
 Acute relapsing pancreatitis: It may be first attack or relapsing
attacks with an apparently normal gland in between.
 Biliary tract disease is the commonest cause of acute
pancreatitis.
 Early phase lasts for 2 weeks with oedematous pancreatitis or
sterile necrosis which carry less mortality; death here occurs by
multiorgan failure.
 In late phase after 2–3 weeks pancreatic abscess or infective
necrosis can occur. Pancreatic abscess has got 40% mortality
which needs drainage.
 Infective necrosis usually develops after 3 weeks and carries 100%
mortality without surgical drainage (necrosectomy).

18. Pathogenesis
All the aetiological factors
↓
Either cause spasm of sphincter of Oddi and lead into the parenchyma (common channel theory), OR causes increased secretion
of pancreatic enzymes
↓
Trypsinogen gets activated forming trypsin which activates other enzymes.
↓ ↓
Proelastase to elastase. Prolipase to lipase.
↓ ↓
Causes capillary rupture. Metabolises triglycerides to glycerol + fatty acids and fatty acids
combine with calcium forming saponified fat.
↓ ↓
Sequestered fluid, saponified fat, blood, toxins all together forms a chicken broth fluid.

19. Lecithinase, amylase and factors like lysolecithinase, prostaglandins, bradykinins, kallikrein, myocardial depressant factor, free radicals,
cytokines, tumour necrosis factor, and platelet activation factor are also released to have local and systemic effects.
↓
Infection occurs causing bacteraemia, septicaemia.
↓
Large volume of fluid sequestration occurs causing hypovolemic shock.
Toxins released may lead to acute tubular necrosis and so acute renal failure.
Left sided diaphragm gets elevated and left sided pleural effusion occurs.
Lecithinase reduces the surfactant in the alveoli of lung, and infection leads to pulmonary insufficiency, ARDS and respiratory failure.
Because calcium is utilised for saponification, hypocalcaemia sets in.
Diffuse oozing in pancreatic bed occurs which utilizes platelets and causes disseminated intravascular coagulation (DIC).
In severe cases, extensive necrosis with haemorrhage occurs causing acute haemorrhagic necrotising pancreatitis (Fulminant
pancreatitis), which has got a high mortality.
Here enzymes seep across the retroperitoneum causing haemorrhagic spots and ecchymosis in the flanks (Grey-Turner’s sign),or
through falciform ligament causing discolouration around the umbilicus (Cullen’s sign), umbilical black eye or below the inguinal
ligament (Fox sign).
SIRS and later MODS set in.

21. Sequence of events:
Acute oedematous →→→→→Severe acute pancreatitis pancreatitis
→ Acute sterile necrosis
→ Acute infected necrosis
↓ ↓ ↓ ↓
Resolution/recovery/ Local or systemic complications with high mortality.
complications (rare) (pseudocyst /abscess /ARDS /MODS /haemorrhage, etc.)
Less mortality
Moynihan described acute pancreatitis as “The most terrible of all the calamities that occur in connection
with abdominal viscera”.

22. Organisms Involved
 Infection is commonly polymicrobial (60%). It may be from gallbladder, colon or small bowel via transmural
migration or by haematogenous spread.
 Infection rate in one week is 24% and in 3 weeks it is 70%.
 E. coli (35%).
 Klebsiella (25%).
 Enterococcus (25%).
Others—staphylococci, Pseudomonas, Proteus, Enterobacter, Anaerobes, Candida (10%).
Other types of pancreatitis :
Hereditary pancreatitis
Autoimmune pancreatitis
Idiopathic pancreatitis

23.  Clinical Features
 Clinical features may be mild, severe or fulminant.
 xSudden onset of upper abdominal pain which is referred to back. Pain is severe, agonizing and refractory. Pain may be relieved or
reduced by leaning forward.
 x Vomiting and high fever, tachypnoea with cyanosis.
 x Tenderness, rebound tenderness, guarding, rigidity and abdominal distension, severe illness.
 x Often mild jaundice (due to cholangitis). Jaundice may also be due to bile duct disease/obstruction or cholestasis.
 x Features of shock and dehydration.
 x Oliguria, hypoxia and acidosis.
 x Grey-Turner’s sign, Cullen’s sign, Fox sign.
 x Haematemesis / malaena due to duodenal necrosis, gastric erosions, decreased coagulability / DIC.
 x Hiccough when present is refractory.
 x Ascites may be present. Paralytic ileus is common.
 x Pleural effusion (20%), pulmonary oedema, consolidation, features of rapid onset ARDS is often observed.
 x Neurological derangements due to toxaemia, fat embolism, hypoxia, respiratory distress can occur. It may be mild Psychosis to
coma.
 x Occasionally haematemesis or melaena can occur.

24.  Fluid, Metabolic, Haematologic and Biochemical Changes
 x Hypovolemia.
 x Hypoalbuminaemia which is more revealed after fluid correction.
 x Hypocalcaemia is either due to decreased albumin level or specific loss of ionized calcium. Hypocalcaemia due
to reduced ionised calcium carries poor prognosis. Response of calcium reserve in bone to PTH is also reduced.
 x Total count is raised with neutrophilia. Thrombocytopaenia, raised FDP, decreased fibrinogen, prolonged
partial thromboplastin time and PT—are common. DIC can develop later.
 x Hypochloraemic metabolic alkalosis is common due to repeated vomiting.
 x Reduced insulin secretion, increased glucagon and catecholamine secretion causes hyperglycaemia, more so
in diabetic patients.
 x Hyperbilirubinaemia may be due to biliary stone/obstruction or cholangitis or non-obstructive cholectasis.
 Hypertriglyceridaemia is common especially in hyperlipidaemic patients.
 x Methemalbuminemia, when it occurs in acute pancreatitis indicates poor prognosis.

25.  Differential diagnosis
 Perforated duodenal ulcer
 Cholecystitis
 Mesenteric ischaemia
 Ruptured aortic aneurysm
 Ectopic pregnancy
 Salpingitis
 Intestinal obstruction
 Diabetic ketoacidosis

26.  Investigations
 Serum amylase is very high (>1000 Somogyi units) or shows rising titre.
 Amylase creatinine clearance ratio is increased. Normal value is 1–4%. More than 6% signifies acute pancreatitis.
 Serum lipase more specific than amylase. Pancreas is the only source unlike amylase, hence more specific.
 Serum lactescence (related to triglyceride metabolism)—Most specific in hereditary hyperlipidaemia or alcohol
pancreatitis.
 Serum trypsin is the most accurate indicator but it is not commonly used.
 Trypsinogen activation polypeptide (TAP) assay in serum and urine reveals the severity of the acute pancreatitis.
CRP (>150 mg/L) is also useful. Phospholipase A2, LDH levels are also often assessed.
 Liver function tests: Serum bilirubin, albumin, prothrombin time, alkaline phosphatase.
 x Blood urea, serum creatinine.
 x Blood glucose (hyperglycaemia is seen).
 x Serum calcium level (hypocalcaemia occurs).
 x Arterial PO2 and PCO2 level to assess pulmonary insufficiency(or ARDS).

27.  Urinary lipase estimation.
 Total count, haematocrit, platelet count, coagulation profile.
 Peritoneal tap fluid shows high amylase and protein level (very useful method). Lipase level in ascitic fluid is also
useful.
 Plain X-ray shows ‘Sentinel loop’ of dilated proximal small bowel. Distension of transverse colon with collapse of
descending colon (colon cut off sign). Air-fluid level in the duodenum. Renal halo sign. Obliteration of psoas
shadow. Localized ground glass appearance.
 US abdomen.
 Spiral CT (CECT–contrast enhanced CT) is better—gold standard.
 CT-guided aspiration (fluid should be sent for Gram’s stain and bacterial culture);
 CECT gives diagnosis of AP;
 MRI, MRCP — should be done at a later date.
 ERCP is usually not done in acute phase.
 x Chest X-ray for effusion and ARDS.
 x EUS—to see necrosis, calcifications and to assess CBD.

29.  Treatment
 Conservative Treatment
 Rehydration is essential (250–400 ml/hour) as there is lot of fluid sequestration and 3rd space fluid loss. It is
done by using ringer lactate, normal saline, dextrose saline, plasma and fresh blood transfusion/packed cells.
 Pain relief by pethidine and other analgesics. Morphine is not used as it causes spasm of sphincter of Oddi.
 In severe haemorrhagic episodes, fresh frozen plasma and platelet concentrate may be required in anticipation
of DIC and haemorrhage.
 Nasogastric aspiration, urinary catheterisation to maintain and monitor urine output 50 ml hourly. Nasojejunal
tube placement for feeding is very useful.
 Antibiotics like third generation cephalosporins, imipenem, meropenem, cefuroxime are used even though its
role is not clear but it is commonly used to reduce the anticipated sepsis.
 Calcium gluconate 10 ml 10% IV 8th hourly is given as patient will be hypocalcaemic.
 CVP line is essential to monitor, for rapid fluid therapy and for Total Parenteral Nutrition (TPN) using
carbohydrate, amino acids, vitamins, essential elements.
 IV ranitidine 50 mg 6th hourly or IV omeprazole 40 mg BD or IV pantoprazole 80 mg BD to prevent stress ulcers
and erosive bleeding.

31.  Proper electrolyte management with monitoring is needed.
 It is always better to manage the patient in an intensive care set up so that when needed
endotracheal intubation, ventilator support, tracheostomy can be done as an emergency basis.
 In case of renal failure haemodialysis is required.
 Somatostatin/octreotide is often used to reduce pancreatic secretion.
 Anticholinergics, protease inhibitors and calcitonin are other agents used. Their efficacy is not sure.
 Steroid injection in initial phase of shock is beneficial. It is also useful in respiratory distress and ARDS.
Nebulisation, bronchodilators are also tried.
 Nasojejunal tube placement and feeding should be started as early as possible once ileus subsides so that it
reduces the infection rate by transmucosal migration of bacteria and it also improves nutritional status. During
recovery period nasogastric feeding or jejunostomy feeding can be undertaken.
 Repeated calcium estimation, US examination to see the response is useful.
 Dopamine or low molecular weight dextran (to improve renal perfusion) is also often used.
 Management of complications like acute lung injury, atelectasis, renal failure, GI bleeding, metabolic
encephalopathy, electrolyte deficiency as and when needed by repeated observation and evaluation.

32.  Surgery
 Indications for Surgical Intervention (10% cases)
1. If condition of patient deteriorates in spite of good conservative treatment.
2. If there is pancreatic infected necrosis.
3. In severe necrotizing pancreatitis as a trial to save the life of the patient which has got very high mortality.
 Surgical management of acute pancreatitis
 Surgery removes intra- and extra-pancreatic necrotic materials, pancreatic fluid, and toxins. It permits
preservation of viable pancreatic tissue. Open surgery is the gold standard for infected pancreatic necrosis.

33.  Laparotomy–necrosectomy–wide debridement–wash–wide packing. Wound is left open. Repeated wash and
packings are done until healthy granulation develops – open method.
 Laparotomy–necrosectomy and closure with drain and re-laparotomy later — semi-open method.
 Zip technique can be used to give repeated wash to remove toxins and necrotic tissues until healthy granulation
tissue develops in the pancreatic bed—Bradley’s repeated laparotomies and wash.
 Continuous closed peritoneal lavage of the pancreatic bed and lesser sac is done with 10–12 liters of normal
saline or hyperosmolar, potassium free dialysate fluid 2 liters / hour using multiple tubes to remove toxic
material in the peritoneal cavity/retroperitoneal area until return fluid becomes clear—Beger’s lavage.
Procedure is done after initial surgical debridement.
 Extra peritoneal lavage through bilateral flank incisions is also used. But being a blind procedure it is technically
difficult and one may not be sure about the adequacy of the procedure.

34.  Under laparoscopic visualisation, necrosectomy, wash and drainage can be done. But often it is difficult to
create pneumoperitoneum in acutely ill patient. But it is increasingly becoming popular.
 A jejunostomy is often done along with these procedures to have early enteral nutrition.
 Endoscopic necrosectomy is often done in some centres. Early endoscopic intervention (within 48 hours) with
ERCP, biliary stone removal and stenting in biliary pancreatitis is done and favored in many centres.
 Further management is important to prevent recurrence. Gallstones should be dealt by laparoscopic
cholecystectomy in 2 weeks after acute attack during same admission period. Endoscopic sphincterotomy
(ERCP) and often stenting may be needed if there are CBD stones.

35.  COMPLICATIONS OF ACUTE PANCREATITIS
 Shock—Hypovolemic and septic
 Respiratory failure and ARDS—Common in 7 days
 Septicaemia—Common after 7 days
 Hypocalcaemia
 Disseminated intravascular coagulation (DIC)
 Acute renal failure
 Pancreatic pleural effusion (left sided 20%)
 Pancreatic pseudoaneurysm
 Pancreatic ascites
 Colonic stricture
 Pseudocyst of pancreas
 Chronic pancreatitis
 Splenic vein thrombosis

36.  Abdominal compartment syndrome (ACS)
 Pancreatic endocrine (15%) and exocrine (20%) insufficiency as
 late sequelae can occur.
 Acute fluid collection
 Acute pseudocyst
 Pancreatic pseudocyst
 Pancrteatic necrosis (walled of necrosis)
 Infection of necrotic area

37.  CHRONIC PANCREATITIS
It is persistent progressive irreversible damage of the pancreas due to chronic inflammation.
Chronic pancreatitis is more common in males, common in Kerala (induced by diet, rich in Tapioca).
Chronic
pancreatitis
Persistant
chronic
pancreatitis
calcific
In the duct In the
parenchyma
Non calcific
Relapsing
chronic
pancreatitis

38.  Alcohol reduces pancreatic blood flow, alters cell viability,
releases the free radicals, creates pancreatic ischaemia, and
activates the pancreatic stellate cells which produce abundant
extracellular matrix and collagen.
 Genetic predisposition may be the cause of idiopathic
pancreatitis. Mutation in pancreatic secretory trypsin inhibitor
causes activation of trypsin causing pancreatitis.
 Hereditary pancreatitis is an autosomal disorder with mutation
in trypsinogen gene in chromosome 7. It causes recurrent
painful episodes of acute pancreatitis in childhood, leading to
chronic pancreatitis and pancreatic cancer in adulthood.

39.  Theories and Concepts in Pathogenesis of Chronic Pancreatitis
 Oxidative stress hypothesis — Reactive by-products of hepatic mixed function oxidase activity damage the
pancreas through chronic reflux of bile into the pancreatic duct.
 The toxic-metabolic theory — Alcohol is directly toxic to the acinar cell where it brings changes in intracellular
metabolism causing pancreatic lipid accumulation, fatty degeneration, cellular necrosis, and eventual
widespread fibrosis.
 Stone and duct obstruction theory — Alcohol increases the lithogenicity of pancreatic juice, leading to stone
formation. Chronic contact of stones with duct epithelial cells produces ulceration, scarring, atrophy, fibrosis
and chronic obstruction of the acini.
 The necrosis-fibrosis theory — Acute and chronic pancreatitis represents a spectrum of disease. Inflammation
from acute pancreatitis leads to scarring, extrinsic compression of the pancreatic ductules, obstruction, stasis,
atrophy and stone formation.

40.  The genetic defect of hereditary pancreatitis produces recurrent acute pancreatitis in early childhood, leading
to chronic pancreatitis in early adulthood.
 Cellular mechanisms of pancreatic fibrogenesis is due to pancreatic stellate cells which are stimulated and
activated by alcohol, oxidative stress, cytokines of acute pancreatitis; activated stellate cells migrate to the
periacinar areas to deposit collagen and fibronectin. Transforming growth factor beta 1 is an important
mediator of pancreatic fibrosis.
 The sentinel acute pancreatitis event (SAPE) hypothesis — An episode of acute pancreatitis, the sentinel
event, sets the stage for the attraction of collagen-secreting stellate cells. Heavy, prolonged alcohol use is the
most common cause of chronic pancreatitis. Alcohol-related chronic pancreatitis is associated with more
severe pain, more extensive calcification and ductal changes, and more rapid progression to endocrine and
exocrine insufficiency. Often recurrent episodes of acute pancreatitis for several years are seen in these
patients. Some cofactors amplify the effect of alcohol in these patients. Prevalence of some genetic mutations
linked with pancreatitis like cystic fibrosis transmembrane regulator (CFTR), serine protease inhibitor Kazal
type-1 (SPINK1) has been noted in alcoholic pancreatitis. A high-fat diet and smoking affect pancreatic
bicarbonate and water secretion adversely, inducing oxidative stress and increases the rate of pancreatic
calcification.
 Tropical pancreatitis is endemic in some regions of India (Kerala), Africa, and South America. Episodic
abdominal pain begins in childhood and is followed by rapid progression to endocrine and exocrine
insufficiency with pancreatic calculi in non-alcoholic individuals.

41. Dietary toxins (cyanogens in the cassava plant, tapioca) and micronutrients like zinc, copper, and selenium, vitamin
A deficiencies, genetic factors, ductal abnormalities are the probable causes of tropical pancreatitis. Linnamarin
and its methyl derivative, in acid pH of stomach releases hydrocyanic acid which is cytotoxic in presence of
rhodanase releases thiocyanates causing depletion of methionine, damaging pancreas → pancreatitis. Gross look is
small, firm fibrotic/adipose type.
 Early-onset idiopathic chronic pancreatitis manifests with severe abdominal pain in childhood, with relatively
few structural and functional changes. Late-onset idiopathic chronic pancreatitis manifests in middle and late
adulthood, often with minimal pain and pronounced exocrine insufficiency.

42.  Pathology
 It shows atrophy of acini, hyperplasia of duct epithelium, interlobular fibrosis, calcifications, ductal dilatation,
with strictures in the duct, focal necrosis.
 There is loss of exocrine function initially and endocrine functions eventually.
 Ductular metaplasia and acinar atrophy along with fibrosis and cyst formation develops.
Spectrum of chronic pancreatitis
 Early—pancreatic oedema—chronic inflammation—normal secretory function.
 Moderate—early fibrosis; only few acinar cells—exocrine dysfunction.
 Late—fibrosis—loss of secretory function—diabetes mellitus.
 Complications develop secondary to healing and fibrosis; deposition of inspissated proteinaceous material in
the duct; over expression of CTGF and TGF-B1 that stimulate extracellular matrix.

43.  Clinical Features
 Pain in epigastric region (80%)
 It is persistent and severe, which radiates to back.
 This pain is due to irritation of retropancreatic nerves, or due to ductal dilatation and stasis, or due to chronic inflammation itself.
 Two patterns of pain have been described (Ammann and Muellhaupt). Type A pain is short relapsing episodes lasting days to weeks,
with pain-free intervals. Type B pain is prolonged, severe, unrelenting pain.
 Pain exacerbations need not be always associated with rise in amylase and lipase levels.
 There is often a gradual diminish in pain over years due to “pancreatic burnout” by extensive calcifications, exocrine and endocrine
insufficiency.
 Exocrine dysfunction: Diarrhoea, asthenia, loss of weight and appetite, steatorrhoea (signifies severe pancreatic insufficiency) (90%),
malabsorption.
 Endocrine dysfunction: Diabetes mellitus. Pancreatic diabetes may often be typically brittle because of concomitant glucagon
deficiency and requires insulin.
 Mild jaundice is due to narrowing of retropancreatic bile duct and cholangitis.
 Mass per abdomen, just above the umbilicus, tender, nodular, hard, felt on deep palpation, not moving with respiration, not mobile,
resonant on percussion.

44.  Investigations presently used are:
 CT scan abdomen: It is 95% reliable; to see pseudocyst, calcification, ductal stones, duct stricture and dilatation,
vasculature, fibrosis, surrounding structures, CBD status. It shows 90% sensitivity; 95% specificity.
 ERCP is useful in chronic pancreatitis to see dilatations, strictures and altered ductal anatomy. It is mainly to
assess structural pathology of the pancreas.
 MRCP is non-invasive method to see ductal anatomy.
 Endosonography (EUS) to see possible malignant site and to take FNAC. Site, duct status, stricture, stones,
parenchyma, pseudocyst, CBD status, nodes are identified in EUS. Positive five parameters suggest chronic
pancreatitis. It also helps in assessing operability.

45.  Secretin cholecystokinin test is the gold standard for assessing pancreatic function. After over night fasting,
double lumen tube is placed into the duodenum at the level of ligament of Treitz under C ARM guidance.
Gastric and duodenal juices are aspirated. Continuous IV secretin 1 u/kg/hour and CCK are infused in 90
minutes. Sampling of duodenal juice is done in every 10 minutes for one hour for analysis of volume, HCO3,
amylase, lipase and proteases. It is to assess functional deficiency. In chronic pancreatitis volume is normal—
>2 ml/kg but less bicarbonate contents <80 mEq/L. In malignancy volume is reduced due to obstruction— < 2
ml/kg; bicarbonate level is normal—> 80 mEq/L; enzyme levels are normal.
 Pancreolauryl test: After overnight fasting, blood sample is taken. IV secretin is injected 1 u/kg in 3 minutes.
Test meal containing bread, butter, tea and fluorescein dilaurate is given to eat. IV metoclopramide 10 mg is
injected. Blood samples are taken at 2, 21⁄2, 3 and 4 hours to assess serum fluorescein concentration. It is also
quantified in urine after 2 days.
 LFT, prothrombin time is needed to manage the patient.
 Serum trypsinogen <20 ng/ml and fecal elastase < 200 mcg/g stool—severe exocrine insufficiency.
 Plain X-ray abdomen may show ductal calculi or parenchymal calcifications.

46.  Conservative
 Avoid alcohol.
 Low fat, high protein, high carbohydrate diet; small and more frequent meals.
 Pancreatic enzyme supplements, vitamins and minerals, medium chain fatty acids.
 For pain — analgesics, splanchnic nerve or coeliac plexus block. Pancreatic enzyme replacement therapy (PERT) is used to
relieve pain based on—negative feedback mechanism of pain; protease content responsible for pain relief (dose: >50,000
units). It may be beneficial only in females with idiopathic pancreatitis, small duct disease and pancreas divisum. Other drugs
used are—antioxidants, amitriptyline, fluoxitine, octreotide. Novel pain therapies like NGF, antinociceptive agents, mast cell
directed therapies are also used.
 Control of diabetes by oral hypoglycaemics or insulin.
 Somatostatin and its analogues. Its role is not clear.
 Repeated ascetic taps for pancreatic ascites.
 Steatorrhoea can be controlled by proton pump inhibitors with
 1,50,000 units of oral lipase with low fat diet. PPI inhibits acid in stomach to prevent lipase getting inactivated in stomach.

47.  Endoscopic Therapy in Chronic Pancreatitis
 It is used as it has got low morbidity.
 Main indications are—pain relief, ductal stones, main duct stricture, pseudocyst drainage, pancreatic ascites, effusion and
fistula.
 It is quite useful for main pancreatic duct obstruction and pseudocyst. It is less useful for biliary stricture.
 Procedures are—pancreatic duct sphincterotomy, main ductal stone extraction using Dormia basket, main ductal stenting in
strictures, stricture dilatation, ESWL of main duct stones, minor papillary sphincterotomy.
 Pseudocyst can be treated by transmural stenting across gastric wall if there is visible bulge, distance of cyst wall is less than
1 cm, no major vessel at puncture site. Transpapillary stenting is done if pseudocyst is communicating, if cyst is less than 6
cm, if there is no visible bulge in the stomach.
 Complications are—pancreatitis, stent displacement/occlusion, perforation, bleeding, sepsis, restenosis.
 Advantages of endotherapy are—less invasive, can be repeated, less severe complications, can be used as bridge therapy
prior to surgery.
 Disadvantages are—long-term benefits are less (50%). Definitive treatment is delayed. It is not useful in small duct disease;
main duct dilatation decides the success rate.

48.  Surgery
 Objectives of Surgery
 x Pain relief when endotherapy has failed.
 x Management of complications.
 x Procedure selected is one which shows less morbidity and mortality.
 x Quality of life (QOL) should be preserved. Problems and Limitations of Surgery
 x Disease is irreversible parenchymal and ductal damage and so surgery cannot cure or reverse completely.
 x Disease progression cannot be prevented or arrested by surgery.
 x Risk of development of cancer continues.
 x Complications of surgery are a drawback.
 Benefits of Surgery in Relation to Pain Relief and Obstruction
 x Relieves intraductal, interstitial, intracellular hypertension through drainage procedures.
 x Entrapped nerves are released and reduction in pancreatic enzyme reduces nerve irritation—resectional methods.
 x Pacemaker—head of pancreas is removed in head coring procedure (Frey’s) to relieve pain. It is less morbid and
acceptable method.
 x Resection is better than drainage procedure.

49.  Principles of Surgery
Pancreatic duct decompression (drainage) reduces the pain and retains the existing exocrine and endocrine
functions. But chances of malignant transformation are still high. In significant number of patients recurrence of
symptoms (50% recurrence of pain in 5 years) and progression of the disease pathology occurs and it does not give
a complete cure. Normal diameter of pancreatic duct 4 mm in head; 3 mm in body; 2 mm in tail of the pancreas.
Pancreatic duct diameter more than 7 mm is an indication for surgery (pancreaticojejunostomy).
Pancreatic resection (total pancreatectomy) is the actually ideal technique which relieves pain, removes entire
diseased tissue. But technical difficulty; high surgical mortality (21%); and severe exocrine and endocrine deficiency
(brittle diabetes) are the drawbacks. Head of pancreas is considered as pacemaker of the pancreatitis disease and
so pancreaticoduodenectomy (Whipple’s) is the other option to give adequate relief. It is preferred in patients who
are having relatively normal body and tail of the pancreas. Occasionally when disease is limited to tail and body
then distal pancreatectomy with or without splenectomy often with distal pancreatico-jejunostomy may be done.
But it is not beneficial if disease is extensive and diffuse. Resection is the main method of treatment if ductal
dilatation is not adequate.
A combined resection and drainage procedures are also done.
Head is decored at various levels and decompressed
duct is anastomosed to jejunum.

50. Surgeries:
Partington-Rochelle operation: Here longitudinal
pancreaticojejunostomy is done using almost
entire laid open pancreatic duct. Spleen is
retained in this procedure. This is now commonly
done procedure.
Puestow’s operation [Puestow-Gilesby (1958)]:
As the duct is dilated more than 8 mm, duct can
easily be opened longitudinally. After removing
all stones from the duct, it is anastomosed to the
jejunum as Roux-en-Y anastomosis. In Puestow’s
operation spleen is removed.

51. Frey procedure: Longitudinal
pancreaticojejunostomy after excision of
peripancreatic duct tissue. here superficial part of
the head of pancreas is removed to achieve
improved drainage. It is done when ductal
dilatation is not adequate; head is more than 4 cm
thick. Head coring is done with retaining 5 mm
thick tissue in front of veins, close to duodenum. It
shows 75% pain relief in 3 years
Duodenal preserving resection of head of
pancreas in front of portal vein with jejunal
loop anastomosis to transected neck of
pancreas - Beger procedure. Here extensive
resection of head (than Frey’s) is done.

52. x Total pancreatectomy is indicated when entire gland is
diseased. It relieves the pain and also prevents the diseased
pancreas from turning into malignancy. Patient has to take
insulin and oral pancreatic enzymes permanently (brittle
diabetes).
x The cause is treated like cholecystectomy for gallstones.
x Therapeutic ERCP is useful in removal of stones in dilated
duct.
x If disease mainly involves head of the pancreas, then
pancreaticoduodenectomy can be done — Whipple’s
procedure.

53.  95% subtotal pancreatectomy.
 x Distal pancreatectomy—Spleen, body and tail of the pancreas are
removed—Child’s operation Resection of tail of pancreas with retrograde
pancreatico-jejunostomy—Duval procedure.
 When duodenal, biliary and pancreatic obstruction is present—
choledochojejunal, pancreaticojejunal and gastrojejunal anastomosis
may be needed — triple anastomosis. Only biliary stricture which cannot
be managed by ERCP needs choledochojejunostomy.

54.  Complications of surgery:
 x Pancreatic leak/fistula (10%); infection; bleeding; recurrence; brittle diabetes.
 x Pain relief in chronic pancreatitis is achieved by drugs; decompression/drainage surgeries, resection surgeries,
epidural analgesia, coeliac ganglion block, operative chemical splanchnicectomy, extra/intra-peritoneal right and
left splanchnicectomy, transhiatal bilateral splanchnicectomy, thoracoscopic splanchnicectomy
 Post-operative care
 Nutrition—TPN/ jejunostomy feed
 Fluid and electrolyte management
 Prevention/control of sepsis
 Proper monitoring
 Octreotide on table and postoperatively—regular intervals or slow infusion—5 days