etiology,clinical features of chr.pancreatitis,medical management,reason for pain,indications of LPJ

1. Chronic pancreatitis &
Indications for LPJ
Discussion - G.P.Chakravarthy
(Gen.Surgery PG)
Moderators - Dr.A.Satish Babu sir
(Prof. in Gen.Surgery)
Dr.Viswanath sir
(Asst.Prof in GenSurgery)

2. Anatomy
• Weight: 75 - 125 g
• Size: 10 to 20 cm
• It lies in the retro peritoneum just anterior to the
first lumbar vertebrae
• Anatomically divided into four portions, the
head, neck, body and tail.

3. Pancreatic ducts
Main duct of pancreas (Duct of Wirsung): It begins in
the tail of pancreas and runs along its posterior surface ,
receives numerous tributaries at right angle along its length
(‘Herring bone pattern’). It joins the bile duct to form
hepatopancreatic ampulla (of Vater)
• Accessory pancreatic duct (Duct of Santorini): It begins
in the lower part of the head
opens into the duodenum at
minor duodenal papilla
(6-8 cm from the pylorus).

4. Arterial supply

5. Nerve supply

6. Chronic Pancreatitis
Definition :
it is a benign inflammatory process and
fibrosing disorder characterized by
• irreversible morphologic changes,
• Progressive and
• permanent loss of exocrine and endocrine
function

7. Chronic Pancreatitis
• Clinically, the disease is characterized by recurrent
episodes of severe and uncontrollable upper
abdominal pain and by a loss of exocrine function
(diarrhea, steatorrhea) and endocrine function
(diabetes mellitus)

8. Chronic Pancreatitis
• Incidence – 3-10 / 1lakh population
• More common in men
• Middle aged > 40 yrs
• 2/3 rds are alcoholics

9. Etiology – (TIGAR –O classification)
• Toxic – Metabolic
• Idiopathic
• Genetic / hereditary
• Autoimmune / immunologic
• Recurrent acute pancreatitis
• Obstructive / mechanical

10. Toxic / metabolic
• alcohol consumption 60 – 90 %
• Tobacco (changes in composition , oxidative stress)
• Hypercalcemia (trypsinogen & trypsin stabilisation ,
calculi formation , direct acinar cell injury)
• CRF – uremia

11. Idiopathic
• Up to 20% of patients with CP have no known risk
factors
• Based on the bimodal age of onset of the clinical
symptoms – 2 distinct entities
• Early onset idiopathic CP -
1. first 2 decades of life,
2. abdominal pain - predominant clinical feature,
3. pancreatic calcifications and exocrine and
endocrine pancreatic insufficiency are very rare
at the time of diagnosis

12. Idiopathic
• Late onset idiopathic CP :
1. Fifth decade of life,
2. Usually painless course
3. associated with significant exocrine and endocrine
pancreatic insufficiency and
4. Pancreatic calcifications

13. Tropical pancreatitis
• Tropical pancreatitis is one of the most common forms
of chronic pancreatitis in certain areas of southwest
India.
• Tropical pancreatitis is generally a disease of youth and
early adulthood, with a mean age at onset of 24 years.
• The disease classically manifests as abdominal pain,
severe malnutrition, and exocrine or endocrine
insufficiency.

14. Genetic factors / hereditary :
1. CFTR : Cystic fibrosis is assosiated with ductal
dilatation, precipitate formation, pancreatic
atrophy
2. PRSS1 : chromosome 7 and regulates
trypsinogen production; mutations - intra-
acinar trypsinogen activation - resistant to
inactivation - activate other proenzymes -
episodes of acute pancreatitis – chronic
pancreatitis

15. Genetic factors / hereditary :
3 . SPINK 1 - serine protease inhibitor Kazal type 1
• regulates the premature activation of trypsinogen
• SPINK1 mutations are not enough to trigger
pancreatic inflammation.
• they lower the threshold for its development and
influence the severity of the disease.

16. Auto immune / immunological
• rare but distinct form of CP characterized by specific
histopathologic and immunologic features
• Autoimmune diseases , viral infections (coxsackie)
• hallmarks are
1. periductal infiltration by lymphocytes and
plasma cells
2. granulocytic epithelial lesions & destruction of the
duct epithelium
3. venulitis

17. Auto immune / immunological
• minimal abdominal pain
• diffuse enlargement of the pancreas without
calcifications or pseudocysts
• most commonly involves the head of the
pancreas and the distal bile duct.

18. Obstructive
• scars of the pancreatic duct,
• tumors of the ampulla of Vater & head of the
pancreas,
• Trauma
• Main pancreatic duct obstruction may lead to
stagnation and stone formation by pancreatic
juice
• Leads to recurrent pancreatitis – periductal
fibrosis - chronic pancreatitis

19. Pathogenesis
Protein Plug hypothesis :
Alcohol
Protein conc in pancreatic secretion &
Glycoprotein2 secretions in acinar cells
formation of protein precipitates & protein plug
calcification of ppt.
ductal stone formation
duct obstruction
Ulceration of epithelium , fibrosis

20. Pathogenesis
Toxic metabolite hypothesis :
fatty acid ethyl esters and reactive O2 species
Increase fragility in intraacinar oraganelles
such as zymogen granules and lysosomes,
Damage acinar cells
scarring of the pancreatic parenchyma
Impair microcirculation
• Acetaldehyde causes direct acinar injury.

21. Pathogenesis
• Pancreatic stellate cells (PSCs) :
PSCs – quiescent fibroblasts
(base of acinar cells.)
PDGF, TNF, IL-1, IL-6 Alcohol & its metabolites
activated myofibroblasts
Synthesize proteins
(collagen I and III, fibronectin, laminin,MMP)
FIBROSIS

22. pathogenesis
Primary duct hypothesis :
immune reactions cause – periductal inflammation
– scarring of the ducts – outflow obstruction -
destruction and fibrosis

23. Clinical features
• Abdominal Pain
• Exocrine insufficiency occurs in 80% to 90%
• steatorrhea,
• diarrhea,
• fat-soluble vitamin deficiency, such as bleeding,
osteopenia, and osteoporosis,
• Endocrine insufficiency - diabetes mellitus
• Jaundice or cholangitis
• Rarely upper GI bleed

24. Abdominal Pain
• most common and most debiliating
• Initially pain manifests after consumption of food ,
later on it becomes continuous and affects quality
of life
• Loses apetite , wt loss , addiction to narcotic
analgesics

25. Abdominal Pain
• epigastrium, often with radiation to the back.
• boring, deep, and Penetrating
• relieved by leaning forward, by assuming the
knee-chest position on 1 side
• Loses apetite , wt loss , addiction to narcotic
analgesics
,

26. Abdominal Pain
• Proposed 2 mechanisms for pain
1. increased pressure and ischemia
2. injury and alterations in peripheral and central
nociceptive nerves

27. Pain
• increased pressure and ischemia :
• Obstruction in ducts leads to Increased pressure
• Similar to compartment syndrome where
increased pressure leads to ischemia which
causes pain
• Proven in animal studies and decreased
Pancreatic blood flow, measured at ERCP and
basis for surgical intervention

28. Pain
Alterations in Peripheral and Central
Nociceptive Nerves :
• Demonstrated increase in the diameter and
number of intrapancreatic nerves, foci of
inflammatory cells associated with nerves and
ganglia, and damage to the perineural sheath
• The disruption of the perineural sheath may allow
inflammatory mediators to gain access to the neural
elements.

29. Pain
• The accumulation of inflammatory mediators and
nerve injury can sensitize the nerve, making it
hyper-responsive
• Chronic pain due to chronic peripheral nerve
injury or inflammation leads to changes in
nociceptive processing that involve both the
spinal cord and CNS.
• Chronic pain can produce a centrally
sensitized pain state in which elimination of the
original source of pain does not relieve pain

30. Exocrine insufficiency :
• Steatorrhea and azotorrhea (protein maldigestion) do
not usually occur until pancreatic enzyme secretion is
reduced to less than 10% of the maximum output
• Advanced chronic pancreatitis, maldigestion of fat,
protein, and carbohydrates occur - present with
diarrhea and weight loss
• median time to development of exocrine insufficiency
was 13.1 years in patients with alcoholic chronic
pancreatitis

31. Exocrine insufficiency :
• Deficiencies of fat-soluble vitamins
• Significant vitamin D deficiency and osteopenia or
even osteoporosis occur
• Bleeding manifestations

32. Endocrine insufficiency :
• Chronic pancreatitis also affects islet cell
populations - 40% to 80% of patients will have
clinical manifestations of diabetes mellitus
• Islet cells appear to be relatively resistant to
destruction in chronic pancreatitis - Diabetes
mellitus typically manifests late

33. Extrapancreatic complications
• Jaundice may be seen in the presence of coexistent
alcoholic liver disease or bile duct compression within
the head of the pancreas. & duodenal obstruction
• A palpable spleen may also rarely be found in patients
with thrombosis of the splenic vein as a consequence
of chronic pancreatitis or in patients with portal
hypertension due to coexistent chronic liver disease.

34. Diagnosis
• Functional tests
• Imaging

35. Functional tests
• fecal elastase 1 level is the preferred
noninvasive study to diagnose pancreatic
exocrine insufficiency
• Normal - > 200 μg/g feces
• mild to moderate 100 - 200 μg/g
• severe pancreatic exocrine insufficiency< 100 μg/g
• Lipase and amylase are of minimal diagnostic value

36. Imaging
• Test of choice previously - ERCP
• Test of choice now - CECT
• CT has specificity of 85% to 100% for the diagnosis of
chronic pancreatitis
• dilated pancreatic duct (68%), parenchymal
atrophy (54%), and pancreatic calcifications (50%).
• Other findings include
peripancreatic fluid, focal pancreatic enlargement,
biliary duct dilation, and irregular pancreatic
parenchyma contour

37. CECT

38. CECT

39. Imaging
• MRI is a reliable alternative
• MRCP with secretin injection - particularly useful
- intraductal
strictures and
pancreatic duct
disruption.

40. MRCP

41. Imaging role of ERCP
• ERCP was historically considered the “gold
standard” for the diagnosis of chronic pancreatitis
• Indications include patients for whom CT and
MRCP, are contraindicated/failed to corroborate
the diagnosis
• Therapeutic modality - pancreatic duct
complications amenable to endoscopic therapy,
such as stricture, stone, pseudocysts, and biliary
stenosis

42. Imaging - EUS
• EUS has emerged during the past 25 years as the
most accurate technique to diagnose - in the
early stages.
• Rosemont criteria – to diagnose chronic
pancreatitis
• Features - Hyperechoic foci with postacoustic
shadowing , Honeycombing lobularity
• Main pancreatic duct calculi , Main pancreatic
duct dilation , Dilated side branches

43. Imaging - EUS

44. Management
• Abdominal pain
• Pancreatic insufficiency - steatorrhea

45. Pain management
• most debilitating symptom of chronic
pancreatitis, as well as the one most often
requiring medical care
• Identify associated conditions for which specific
therapy exists – pseudocysts, duodenal
obstruction, carcinoma

46. Pain – Medical management
• Some pts’ pain may be managed with
acetaminophen;
• NSAIDs should be avoided.
• Pain management clinics should start with non
narcotic analgesics
• Mostly they fail, it is useful to begin with lower
potency opioid agents like tramadol.
• gradually increase the dosage , while focusing the
patient on the goal of control of pain to an
acceptable level rather than complete relief of
pain

47. Pain – Medical management
• The risk of opiate addiction is estimated to be 10% to
30% - BUT
• Pain relief is the first priority
• Adjuncts - Tricyclic antidepressants , SSRI ,SNRI -
modulating central pain perception , potentiate
narcotics
• Gabapentoids - gabapentin & pregabalin

48. Pain management
• Cessation of alcohol and smoking :
• Most studies, have documented an apparent
decrease in pain or painful relapses in patients
who stop drinking alcohol

49. Pain management
• Anti oxidants :
• As such there is no clear evidence to support the use
of these in pain management….
• But in a large study conducted in india – tropical
pancreatitis – there is improvement in pain and other
symptoms
• Not found useful in elderly pts with chr.pancreatitis

50. Pain management
• Pancreatic Enzyme Therapy :
• Proteases supplementation to duodenum /
proximal jejunum
• Reduce CCK release by destroying an intestinal
CCK-releasing factor
• Octreotide – reduces circulating CCK levels

51. Endoscopic management
• goal of endoscopic therapy is to improve drainage
of the pancreatic duct by relieving ductal
obstruction.
• limited to a subgroup of patients with amenable
pancreatic ductal anatomy (single dominant
stricture or an obstructing stone in the head of the
pancreas)

52. Pain management
• Stent placement and sphincterotomy :
• stenosis of the sphincter has produced obstructive
chronic pancreatitis
• complications are clogging of stents (producing
recurrent pain, attacks of acute pancreatitis, or
pancreatic sepsis), stent migration (which may
require surgical extraction) and ductal perforation

53. Pain management
• ESWL :
• removal of large or impacted stones requires
lithotripsy
• A survey from Japan in 555 patients reported
complete stone clearance in 73% of patients.308 Pain
improvement or relief is seen in about 75% to 90% of
patients who undergo this type of therapy.
• there is some other effect on pancreatic pain separate
from the ability to fragment pancreatic stones.

54. Pain management – surgery
• surgical treatment of CP is based on two main
concepts:
1. Resection of tissue : nondilated pancreatic
ducts, pancreatic head enlargement, or if a
pancreatic carcinoma is suspected
2. Drainage & preservation of tissue : to
prevent further loss of pancreatic function

55. Indications
• Intractable pain
• Symptomatic local complications
• Unsuccessful endoscopic management
• Suspicion of malignancy

56. Drainage / Decompression procedures
• Duval described using distal pancreatectomy and
splenectomy with an end-to-end
pancreaticojejunostomy
between the cut end of the
body or tall of the pancreas
and a Roux-en-Y limb of
jejunum to decompress
the pancreatic duct.

57. Drainage -
• Puestow and Gillesby. 'Ihey modified Duval's
procedure
longitudinal opening along
the main pancreatic duct
through the tail and body
of the pancreas and then
invaginating the distal
gland into a Roux-en-Y limb
of jejunum

58. Longitudinal pancreaticojejunostomy
• Partington and Rochelle described the side-to-
side longitudinal pancreaticojejunostomy that is
currently referred to as the modified Puestow
procedure.
• Remains as a standard approach to pancreatic
ductal decompression
• best applied to patients with parenchymal disease
and pancreatic ductal dilatation diffusely
involving the pancreatic head. neck. body,
and tail of the gland

59. Longitudinal pancreaticojejunostomy
• Minimal diameter of pancreatic duct should be >7
mm
• Should not be any mass in the pancreatic tissue
• Omitted splenectomy , distal pancreatectomy

60. Longitudinal pancreaticojejunostomy

61. Longitudinal pancreaticojejunostomy

62. LPJ – RESULTS
• 75–80% of patients with diffusely dilated main
pancreatic ducts (>7 mm) and no dominant
inflammatory mass, have achieved durable pain
relief over 5–10 years of followup
• morbidity is low
• because no pancreatic parenchyma is removed,
endocrine and exocrine functions are
generally preserved

63. Resection procedures
• patients with focal disease largely confined to the
head of the pancreas without duct dilation -
pancreaticoduodenectomy [PD]
• resection of the
head of the pancreas with
• the distal CBD,
• distal stomach,
• duodenum,
• proximal jejunum

64. Resection procedures
• Beger introduced duodenum-preserving pancreatic
head resection (DPPHR)
• division of the neck of pancreas and removal of the
head of the pancreas, leaving a small rim of
pancreatic tissue along the duodenum.

65. Hybrid procedures - FREY procedure
• Frey introduced a procedure that combines
duodenum-sparing resection of the pancreatic
head, without formal division of the neck of the
pancreas, combined with longitudinal
pancreaticojejunostomy of the dorsal duct .

66. Hybrid procedures - FREY procedure

67. TOTAL PANCREATECTOMY WITH
ISLET AUTOTRANSPLANTATION
• small duct disease
• diffuse parenchymal inflammation,
• hereditary syndromes,
• failures of prior pancreatic operations
• Complete or near complete pain relief in about
75% of patients, with 60% to 70% achieving
narcotic independence

68. Nerve blocks and Neurolysis
• The celiac plexus transmits visceral afferent
impulses from the pancreas
• The greater, lesser, and least splanchnic nerves
travel from the celiac plexus and then pass through
the diaphragm to reach the spinal cord.

69. Nerve blocks and Neurolysis
• Celiac plexus block (usually using a
combination of a glucocorticoid and a long-
acting local anesthetic like bupivacaine)
• celiac plexus neurolysis (using an injection
of absolute alcohol) can be administered by CT-
or EUS-guided techniques
• These are used in pancreatic carcinoma

70. splanchnicectomy
• block central perception of
nociceptive inputs.
• involves sectioning the greater
splanchnic nerve on 1 or both sides using thoracoscopy
• 50 – 75 % will get pain releif
• The multiple spinal levels that receive input from
the splanchnic nerves and the variation in the
number of splanchnic roots, makes complete
neurotomy difficult

71. Summary
 Benign inflammatory process and
fibrosing disorder characterized by irreversible
morphologic changes, Progressive and permanent
loss of exocrine and endocrine function
Alcohol consumption is the most common cause
Pain is the most common symptom
 CECT is 1st investigation of choice and best being
EUS

72. Summary
Treatment
• Local inflammation - Pharmacotherapy (pancreatic
enzymes,analgesics,narcotics)
• Ductal hypertension - Decompression (Puestow,
endoscopic stenting)
• Organ hypertension - Resection(Whipple,Frey)
• Retroperitoneal - Neuroablation (celiac block,
damage splanchnicectomy)

73. Thank you