it covers all the major topics on pancreas from a surgeon's point of view. contains comprehensive texts with diagrams and radiological findings.

1. Pancreas
Dr Bijendra Mishra

2. Surgical Anatomy
• Also known as abdominal tiger.
• Pan = All, kreas = Flesh.
• Elongated retroperitoneal organ; 15-20 cm long; lies against
L1-L2 vertebra.
• It lies posterior to stomach, separated by lesser sac.
• Parts
 Head lies in the concavity of duodenum and Tail reaches the hilum of
spleen.
 Posterior surface of the neck is related to the terminal part of superior
mesenteric vein and beginning of portal vein.
• Ducts-
 Duct of Wirsung – main duct, begins at tail, joins the bile duct in the
wall of second part od duodenum to form ampulla of vater and opens
on the summit of major duodenal papilla (8-10cm from pylorus).
 Duct od Santorini – accessory duct, begins in the lower part of head
and opens at the minor duodenal papilla(6-8cm from pylorus).

4. Acute pancreatitis
• Acutenonbacterialinflammatoryconditioncausedby
activation,interstitialliberationandauto-digestionof
pancreaspresentingas acuteabdominalpain.
• Stings like a scorpion (severe pain)
• Drinks like a fish (dehydration)
• Eats like a wolf (pancreatic necrosis)
• Burrows like a rodent (produces fistula)
• Kills like a leopard (life-threatening)

5. Mechanism

6. 6
Pathophysiology
• Co-localization theory “Steer & Saluja” 1998
– Most acceptable
– Stones  pancreatic duct hypertension  ductal
rupture
– Ductal pH = 9 …… parenchymal pH = 7
– trypsinogen + cathepsin B  trypsin 
autodigestion cascade

7. Pathogenesis

8. 8
Diagnosis
“Acute pancreatitis is a diagnosis of exclusion” Schwartz’s
• History:
– Epigastric pain
– Radiating to back
– Nausea, vomiting
– Precipitating factor?
• Physical
– V/S  variable
– Epigastric tenderness
– Cullen’s / Grey Turner’s (1%)
– Findings of complication(s)

9. 9
Diagnosis

10. 10
Cullen’s sign
bluish discoloration around umbilicus

11. 11
Grey Turner’s sign
bluish discoloration in flanks

12. 12
Diagnosis
 Serum markers
 Amylase
• Easiest to measure and most widely used
• Rises immediately
• Peaks in few hours
• Remains for 3-5 days
• “Three fold rise is diagnostic”
• May be normal in severe attacks
• May be falsely negative in hyperlipedimic patients
• Inverse correlation between severity and serum amylase level
• No need to repeat
 Urine amylase
• Remains elevated for a few more days
• Increase excretion of amylase with attacks of AP
• Of great value when dealing with severe pancreatitis

13. 13

14. 14
Radiology
• Diagnostic role
– X-ray
– U/S
– CE-CT

15. 15
Radiology
• X-ray
– Air in the duodenal C loop
– Sentinel loop sign
– Colon cutoff sign
– All these signs are non
specific

16. 16
Radiology
• CE-CT
– Enlargement of the pancreas
• (focal/diffuse)
– Irregular enhancement
– Shaggy Pancreatic contour
– Thickening of fascial planes
– fluid collections.
• Intraperitoneal / retroperitoneal
– Retroperitoneal air

17. 17
Radiology
• U/S
– Diagnosis of gallstones
– F/U of pseudocysts.
– Dx pseudoaneurysms
– EAUS vs. EUS

18. 18
Course
– Mild = edematous pancreatitis
– Severe = necrotic pancreatitis
– Very severe = infected necrosis
– No such thing as moderate pancreatitis

19. 19
Prognosis
• Serum markers
• CT
• Systemic complications
• Prognostic scores
– Ranson
– Apache II
– Modified Glasgow
– Atlanta

20. 20
Prognostic scores
• Ranson’s
– Published in 1974
– Predictor of morbidity/mortality
• <2 0% mortality
• 3-5 10-20%
• >7 >50% mortality
• Drawbacks of Ranson’s
– 11 parameters
– 48 hours
– No predictor value beyond 48hrs
– Too pessimistic for today’s healthcare system

21. 21

22. 22
Prognostic scores
• APACHE II
– Immediate
– Acute and chronic parameters
– Complicated
– >7 = severe pancreatitis

23. 23
Prognostic biochemical markers
• Biochemical markers of prognosis
– Ideally
• High sensitivity
• High specificity
• Discriminate severe from mild
• Immediate
• Widely available
– Amylase & lipase
• Highly sens./spec.
• Lack prognostic value

24. 24
Prognostic biochemical markers
• Alternatives
• CRP
• 2 macroglobulin
• PMN elastase
• 1 antitrypsin
• Phospholipase A2
– “CRP seems to be the marker of choice in these
settings”
– CRP >150 is diagnostic of severe pancreatitis

25. Management - ABCDEF
• Aspiration with ryle’s tube
• Blood transfusion
• Charts- increasing pulse, temp indicates pancreatic abscess
• Drugs- IV cefuroxime or imipenem or ciprofloxacin with
metronidazole. Low molecular Dextran given to increase
renal perfusion
• Exploratory laparotomy only when diagnosis in doubt,
patient is not improving, or when complications such as
pancreatic abscess, fistula, necrosis is present.
• Fluids given early. Rapid infusion of 2-3L of RL used to treat
hypovolemic shock. Plasma or albumin may also be given.

26. Principles of management

27. Key notes

28. Complications

29. Chronic Pancreatitis
• Diffuseinflammatoryprocessof pancreasinvolvinghead,body
andtailresultingin permanent structuralandfunctional
damage.

30. Causes
• Alcohol
• Idiopathic- due to malnutrition, a.k.a tropical
pancreatitis
• Hereditary- transmitted as a mendelian-
dominant trait
• Cystic fibrosis
• Hyperparathyroidism
• Autoimmune pancreatitis

31. Pathology

32. Clinical features
• Malabsorption
• Obstructive jaundice
• Pain abdomen- due to multiple strictures in
the pancreatic duct increasing the intraductal
pressure. Relieved on stooping forward.
• Exploratory laparotomy- diagnosed at
laparotomy done for obstructive jaundice.
• Diabetes

33. Investigations
• Plain X-ray
• USG
• ERCP (chain of lakes)
• CT Scan

34. Complications
• Obstructive jaundice due to a mass lesion in
the head region
• Carcinoma pancreas
• Pseudocyst
• Steroids in autoimmune pancreatitis

35. Treatment
• Analgesics., epidural analgesia, slow release
opioid skin patches.
• Supplement pancreatic enzymes, diet should be
low in fat and vitamin D supplements given.
• Surgery-
 Distal Pancreatectomy (tail involvement)
 Puestow’s operation (longitudinal pancreaticojejunostomy)
 Pancreaticoduodenectomy (head involvement)
 choledochojejunostomy (bile duct obstruction)
 Hans beger’s procedure- duodenum preserving pancreatic head
resection.

36. Pseudocyst
• Collectionof amylaserichfluidin thelessersac,dueto
pancreaticpathology.
• Fluid collection in the first 4 weeks is acute
fluid collection, after 4 weeks it becomes
acute Pseudocyst.
• It is called Pseudocyst because it has no
epithelial lining.
• Fluid is enclosed by a wall of fibrous
granulation tissue and is called Pseudocyst.

37. sagittal-sectional view of lesser sac

38. cross-sectional view of lesser sac

39. Aetiology
• Following an attack of Acute pancreatitis
• Blunt injury causing ductal disruption
• Chronic pancreatitis
Location-
b/w stomach and transverse colon
b/w stomach and liver
Behind or below transverse colon

40. D’EGIDIO Classification
• Type 1- after an episode of acute pancreatitis and
is associated with normal duct anatomy and
rarely communicate with pancreatic duct.
• Type 2- after an episode of acute on chronic
pancreatitis and have a diseased but not
strictured ducts, and there is after
communication between duct and Pseudocyst
• Type 3- retention cyst, occurs in chronic
pancreatitis, uniformly associated with duct
stricture and a communication between duct and
Pseudocyst.

41. Clinical features
• Tensely cystic mass feels firm on palpation.
• Classically upper border of the mass is not felt.
• It is retroperitoneal so does not move with respiration.
• May have transverse mobility
• It does not fall forward
• Resonant note on percussion because of stomach or
intestine anterior to it
• Transmitted pulsation from aorta can be felt
• Baid sign- if ryle’s tube is passed, it is felt above the
swelling.
• Depending upon the tension within the cyst, it can be
tender or non tender

42. Investigations
• USG/CT- confirm that there is no neoplasm
before doing cystogastrostomy.
• ERCP- shows communication between duct
and cyst

43. Treatment
• Majority of the cysts following acute pancreatitis resolve
spontaneously within 4 weeks, hence regular USG is required.
• Increased size, pain, unresolved needs surgery.
• Cystogastrostomy is done for cyst arising from head and body of
pancreas. Done after 6 weeks because that’s the time required for
the wall to become fibrous. Size of the cyst should be at least 6cm,
and stoma size should be about 6cm. For reasons not known, the
food does not enter the cyst. This procedure can also be done by
endoscopic method.
• Distal pancreatectomy done for cyst arising from tail of pancreas
• Cystojejunostomy done for large cysts.

44. Cystogastrostomy

45. Insulinoma
• Isletcelltumour,involvingtailandbody.
• Majority are benign, 1/3rd are malignant and
1/3rd are multiple.
• Hypoglycaemia is seen-> hunger pain, mimicking
duodenal ulcer
• Dizziness, syncopal attack, blurring of vision,
epilepsy and coma are later symptoms.
• Whipple’s triad of insulinoma- attack of
hypoglycaemia in morning hours, relieved on
taking glucose and blood sugar in fasting state
below 45mg%

46. Investigation
• Serum insulin
• Persistent hypoglycaemia (<50%)
• USG- if mass >2cm
• Selective angiography- tumour blush

47. Treatment
• Enucleation is treatment of choice
• Resection of the tumour and distal
pancreatectomy
• Diazoxide given to supress insulin release
• Streptozocin is best chemotherapeutic agent
for inoperable insulinoma

48. Treatment
• Duodenoduodenostomy is the treatment of
choice.
• Duodenojejunostomy can be done otherwise.

49. Annular pancreas
• Rare anomaly which occurs due
to persistence of the ventral
pancreatic anlage which fails to
rotate.
• As a result of this, second part
of the duodenum is surrounded
by a thin rim of pancreatic
tissue.
• Associated anomalies- intrinsic
duodenal atresia or stenosis

50. Embryology
• The pancreas develops from one dorsal and two ventral buds. Due
to selective expansion of the duodenum, by approximately the
seventh week, the ventral bud rotates with the gut, passing behind
the duodenum from the right to left and eventually fusing with the
dorsal bud.
• The ventral bud forms the inferior part of the head of the pancreas
and the uncinate process, whereas the dorsal bud becomes the tail
and the body.
• Fusion of the ductular network of the two buds gives rise to the
main pancreatic duct. The accessory pancreatic duct, which often
persists, is derived from the dorsal pancreatic duct proximal to the
site of fusion
• Annular pancreas results from failure of the ventral bud to rotate
with the duodenum, causing envelopment of duodenum.

51. Clinical features
• Neonatal type- early in life. Produces symptoms
of acute intestinal obstruction with vomiting and
inability to take food.
• Adult type- after age 20. vomiting is bile stained.
Due to stasis in the antrum, features of duodenal
ulcer may present.
• Investigation
 Xray- double bubble sign, due to dilated stomach and
dilated proximal duodenum
 Barium meal- obstruction to 2nd part of duodenum seen.

52. Double bubble sign

53. Carcinoma pancreas
• 70 % occur in head including periampullary
region
• 70% are Adenocarcinoma of duct cell origin.
• Rate of death in male due to cancer:-
Lung>Colon>Prostate>Pancreas
 Periampullary refers to carcinoma arising from ampulla of
vater, the duodenal mucosa or the lower end of common bile
duct

54. Aetiology
• Chronic tropical pancreatitis
• Hemochromatosis
• Diabetes
• Alcohol and smoking
• Westernization of diet- fatty food, animal
proteins
• Industrial carcinogens- benzidine, gasoline

55. Types- Microscopically
• Mucus
• Non mucus
• Anaplastic
• Cyst adenocarcinomas

56. Clinical features
• Obstructive jaundice – involving head of pancreas
or periampullary
• Backache (L1-L2) - retroperitoneal, so neural
spread is fast
• Weight loss
• Severe pain
• Vomiting- duodenal obstruction
• Trousseau’s sign (Thrombophlebitis migrans)- due to
sluggish blood flow resulting in thrombus formation,
affects long saphenous vein commonly.

57. Investigation
• USG-
Rules out calculus obstruction
Detects mass as small as 2cm
• CECT
• ERCP
• Carbohydrate antigen CA19-9

58. Treatment
• Whipple’s operation for periampullary ca.
• Total pancreatectomy with involved lymph nodes
if the tumour is very small and diagnosed early.
• Many cases are diagnosed late. They are
inoperable either due to fixity to portal vein or
due to mets. Only palliative treatment is given.
Palliative radiotherapy- 4000-6000 cGy units given