kathmandu medical college, department of surgery

1. Chronic pancreatitis

2. Definition
• Inflammatory and fibrosing disease of
pancrease of the exocrine pancrease
characterized by irreversible morphological
changes and permanent loss of function

3. Classification
• Marseille-Rome classification
– Chronic obstructive
• Exocrine pancreatic atrophy
• Duct stenosis by tumors, psedocyst, scarring
– Chronic calcifying
• Intraductal calcifications and protein plugs, associated with
atrphy, stenotic ducts, areas of acute inflammation or
pesudocyst
– Chronic inflammatory
• Dense infiltration of mononuclear inflammatory cells

4. Epidemiology
• 3-10/1 lakh persons

5. Etiology
• Metabolic/ toxic
– alcohol, tobacco,hypercalcemia (hypoparathyroidism,
dietary, nutrional therapy
– Hyperlipidemia
– Chronic renal failure
• Anatomic/ physiological
– FunctionalSphincter oddi dysfunction
– Congenital- pancreatic divism, annular pancreas
– Acquired- primary pancreatic stones, malignant obst
– choledochocele

6. • Genetic
– PRSS1,PRSS2
– SPINK1
– CFTR
– Chymotrypsin C
• Immunologic
– Autoimmune
• Other- recurrent and sever acute pancreatitis

7. Etiopathogenesis
Alcohol
Increases total protein concentration in pancreatic juice
Promotes the synthesis and secretion of lithostathine by
acinar cells and increase glycoprotein 2 in pacreatic juice
• Protein precipitation plug formation calculi
acinar cells cannot secete autodigestion
• Product of alcohol ROS acinar injury abdnormal
acitvation of zymogen

8. Etiopathogenesis
• Chronic alcohol consumptionenhance NF-
Kbeta activity decresed perfusion in the
microcirculation of the pancreas and
increased intracellular calcium levels

9. Etiopathogenesis
• Pancreatic stellate cells
– Specilized queisent cell in base of acini
– Once stimulated activated myofibroblasts
synthesize proteins which form proteins 
collagen I and III an fibronectin, laminin, matrix
metalloproteinases fibrosis

10. Etiopathogenesis
• Smoking

11. Etiopathogenesis
• Genetics
Mutation in proteins that regulate activation
– Protein serine 1 ( PRSS 1)- Ch 7 regulate
trypsinogen production
Mutations intracinar activation of trypsinogen
– SPINK 1- peptide secreted by acinar cells that
regulate premature activation of trypsinogen
Lower the threshold to develop the disease

12. Etiopathogenesis
• CFTR gene mutation
– Rsecreation of bicarbonate and chloride in
repiratory and pancreatic secreations
– It s mutation affects normal secretion of HCO3,
decrease pancrease juice volume and augments
the concentration of pancreatic enzymes inside
the ducts
– Homozygous CFTR gene mutation- cystic fibrosis
– Heterozygous mutation- pancreatic exocrine
insufficiency and chronic pancreatitis

13. • Autoimmune
• Common In men, >50 years ( 80%)
– Type 1
• Most common
• Dense, periductal lymphoplasmacytic infiltrates
• Storiform fibrosis
• Obliterative veuliti
• IgG4 positive
– Type 2
• Infiltrated by neutrophils, lymphocytes, and plasma cells that
obliterate the epithelium in the pancreatic duct

14. Etiopathogenesis
• Tropical pancreatitis
– Tropical areas in 30 degree of equator ( india)
– Unknown pathophysiology
– Associated with cassava ingestio and SPINK 1
mutations

15. Etiopathogenesis
• Idiopathic
10-20%

16. presentation
• Pain in left upper quadrant or epigastrium radiating to back
– Precipitated by food
– Qualy affected
– Nausea vomit as disease progresses
– Stetorrhoea, diarrhoes, other symptom of malabsorption90% gland
destroy
– Severe cases- deficiency of Vit ADEK,bleeding, osteopenia,
osteoporosis
– Exocrine insuffiecieny- 80-90%of patients with long standing disease
– Diabetes- 40-80%
– Jaudince, cholangitis- 5-10%distal CBD fibrosis
– Duodenal scarrring- GOO
– UGI bleeding- portal, splenic vein thrombosis

17. Diagnosis
• History
• Physical examination
• Investigation

18. Diagnosis
• Investigation
• Laboratory investigations limited value
– Amylase/lipase sometime raised in acute
exacerbation
– LFT deraged
– PT/INR

19. Diagnosis-Imaging
• Ultrasound
– The pancreas might appear atrophic, calcified or fibrotic.
– hyperechogenicity (often diffuse) often indicates fibrotic changes
– pseudocysts
– pseudoaneurysms
– presence of ascites
• Ultrasound may also be assist to differentiate between the
autoimmune type vs acquired:
– the pancreas is enlarged (either focally or diffusely) in the
autoimmune type
– calcifications are visible in acquired types

21. Diagnosis-Imaging
• CT scan
– Dilated duct (68%)
– Parenchymal atrophy 54%
– Pancreatic calcification 50%
– Peripancreatic fluid
– Focal pancreatic enlargement
– Irregular pancreatic parenchyma
– Sensitivity 56-95%
– Specificity-85-100%

22. Diagnosis-Imaging
• CT
– Assess complications like pancreatic duct
disruptions, psedocyst, portal and splenic vein
thrombosis
– Splenic and pancreaticoduodenal artery
pseudoaneurysm

23. Diagnosis-Imaging
• MRI
• May be undertaken both as morphological and functional imaging
• Morphological
Features of chronic pancreatitis can be divided into early and late findings:
• early findings
– low-signal-intensity pancreas on T1-weighted fat-suppressed images
– decreased and delayed enhancement after IV contrast administration
– dilated side branches
• late findings
– parenchymal atrophy or enlargement
– pseudocyst formation
– dilatation and beading of the pancreatic duct often with intraductal calcifications, could give a
'chain of lakes' appearance.

24. Diagnosis-Imaging
• Functional
• Exocrine function may be assessed by secretin enhanced magnetic
resonance cholangiopancreatography, SMRCP (a.k.a. MRCP-S).
• This relatively new technique has shown promising results and may
replace endoscopic measuring techniques in the near future
• Imaging protocols to assess exocrine function may contain:
– measurement of secretory volume after intravenous secretin-
stimulation by assessing T2-high signal changes in the duodenum
– post-enhanced dynamic assessment of of pancreatic parenchyma,
revealing delayed and reduced peak values

25. Diagnosis-Imaging
• EUS
– Rosemont criteria
– More sensitive than ERCP or MRCP in detecting
early stage, minimal change disease when other
modalities fail

26. Diagnosis-Imaging

27. Diagnosis- functional
• Fecal elastase-1 level
– >200 microgram/gm feces is normal
– 100-200 mild to mod pancre insuffi
– <100- dx of pancre insuffi
– Fecal fat and weight
– 100 gm fat/day for 3 day
– Stool fat content >7gm/day –dx of stetorrhoea

28. Treatment
• Aim:
• Preventive- quit alcohol/ smoking, avoid high fat foods,
parenteral supplementations, pancreatic enzymes
• Curative
• Palliative- analgesics, decompressive surgery
• Rehabilitation- alchol rehab, nutrional rehan

29. • Psychosocial
– Counseling
• Medical management
– pain control
– NSAIDS, narcotics
– TCAs, antidepressants
– Gabapentin
– Invasive pain control – celiac plexus block( usg
guided, ct guided,100 % alcohol use
– Splanchnicectomy via thoracosopic approach

30. • Minima invasive procedures
– ERCP with stent placement
– Only after ruling out malignancy with other
modalities like CT/MRCP/EUS ERCP should be
done
– ERCP and ESWl 44%-77% success rate

31. Surgical management
• For patients with symptoms that are
otherwise intractable to pharmacotherapy
and other therapeutic approaches
• Other causes
– Relieve biliary or GIT obstruction
– Internally drain symptomatic pseudocyst
– Vascular complications- gastric variceal
hemorrhage secondary to splenic vein thrombosis

32. Choice of operation
• Depends on anatomic morphology

33. Large duct disease
• MPD >7- 8mm
• Puestow
– Longitudinal unroofing of dilated MPD in body and tail with pancreatic
tail resection
– With longitudinal PJ for enteric drainage
• Partington and Rochelle ( 1960)
– Abolished pancreatic tail resection
• Modified Puestow or Partington and Rochelle
– Lateral PJdiffusely dilated MPD with no signnificant biliary tract
obstruction and no mass in pancreatic head

35. Lateral PJ
• Outcomes
– 75-80% of patients with diffusely dilated MPD (>7mm)
and no dominant inflammatory mass  durable pain
relief over 5-10 years
– Low perioperative morbidity
• As no pancretic parenchyma removed
• Failure of LP
– Inappropriate patient selection ( under appreciated
extent of disease with presence of significant fibrosis
in pancreatic head) or on-going fibrosis with
progressive development of neuropathic pain

36. Chronic pancreatitis with a dominant
pancreatic head mass
• Inflammatory mass
• Extesive calcifications or duct stones in
pancreatic head
– Pure resectional procedure or with hyrid resention
and drainage procedures

37. Chronic pancreatitis with a dominant
pancreatic head mass
• 4 procedures
– Whipples procedure with or without pyloric
preservation
– 3 forms of duodenum preserving pancreatic head
resection ( DPPHR)
• Berger procedure
• Berne procedure
• Frey procedure

38. • Patient with dominant head mass withMPD
dilatation but no biliary dilatation– Frey
procedure ( limited duodenum preserving
resection of pancreatic head with extended
lateral PJ

39. Frey procedure
• DPHHR- does not address disease that may
coexist in pancreatic body and tail
• Poor drainage of pancreatic body and tail
• Frey- DPPHR with hybrid resection or drainage
procedure at pancreatic body and tail ( i.e
local resection of pancreatic head with
longitudinal PJ LR-LPJ)

40. Berger procedure
• PD unnecessary for benign pathology and that
more limited resection preserving the
duodenum avoid complications like delayed
gastric emptying and insulin dependent
dibetes
– Divide pancreatic neck, save CBD, coring
pancrease with electrocautery to leave bile duct
intact within the rim of pancrease nead
duodenum

41. • Berger result
– Good pain control (91.3% free of pain 5.7 year
median follow )
– Pancreatic fistula- 3.3%
– Delayed gastric emptying 15%
– Perioperative mortality -0.7%

42. • Dominant head mass without MPD dilatation
an no biliary obstruction Berne modification
of Berger procedure ( limited duodenum
preserving resection of pancreatic head
without extension of lateral PJ toward tail)

43. Berne procedure
• Modification Berger DPPHR

44. • Biliary obstruction or imaging characteristics
more suspicious for the presence of
malignancy Whipples than DHHPR