1. Diseases of the pancreas
Dept. of General and Transplant Surgery
Diseases of the pancreas
Jakub Szmytkowski

2. Anatomy - location
Retroperitoneal (except part of the tail) in the epigastrium and left infracostal region
Approximate dimensions: L 15 cm, W 3-4 cm, T 1-2 cm; weight g

3. Anatomy - parts
head
Isthmus (notch)
uncinate process
body
tail

4. Pancreatic ducts
The pancreatic duct, or duct of Wirsung (also, the major pancreatic duct)  a duct joining the pancreas to the common bile duct to supply pancreatic juices which aid in digestion provided by the "exocrine pancreas". The pancreatic duct joins the common bile duct just prior to the ampulla of Vater, after which both ducts perforate the medial side of the second portion of the duodenum at the major duodenal papilla.

5. Pancreatic ducts
Accessory pancreatic duct (duct of Santorini) connects straight to the duodenum at the minor duodenal papilla
In some cases, the main pancreatic duct is smaller than the accessory pancreatic duct and the two may not be connected. In such people, the accessory duct carries most of the pancreatic juice.

6. Pancreatic duct

7. Anatomical relations anterior: transverse colon (head) pylorus (body)
posterior: VCI, CBD, aorta, superior mesenteric a., renal veins
left: splenic hilus, splenic flexure
right: duodenum
superior: celiac trunk, splenic a.

8. Surgical diseases of the pancreas
Acute pancreatitis
Chronic pancreatitis
Cysts
Tumors

9. Goals of pancreatic surgery
Completion of diagnosis
Treatment of pancreatitis
Treatment of infection and complications
Pain control
Malignant tumors
curative
palliative
Management of endocrine disorders

10. Acute pancreatitis
Acute pancreatitis is a complex disorder of the exocrine part of the pancreas. Its exact patomechanism has not been fully explained, but can be described as acute injury to the acinar cells with a local and generalized inflammatory response.
Overall mortality %
Necrotizing – hemorrhagic (5 – 15%) %
Morbidity (Poland) / / year
No specific therapy

11. Types interstitial edematous pancreatitis
sterile necrotizing pancreatitis
infected pancreatic necrosis/abscess
hemorrhagic pancreatitis

12. Frequent causes 80% gallstones alcohol idiopathic hyperlipidemia
hypercalcemia
drugs and toxins ( steroids, immunosuppressants: Azathioprine, Thiazide, Valproic acid, Tetracycline, and Trimethoprim-sulfamethoxazole )
endoscopic retrograde cholangiopancreatography
trauma
surgery
80%

13. Less frequent causes Malignancies of the ampulla of Vater
Pancreatic carcinoma
Diverticulum of the duodenum
Vasculitis

14. Even less frequent causes
infection: viral (Coxsackie, mumps , HIV), parasites
Autoimmune disorders: lupus, Sjögren’s syndrome
alpha1-antitripsin deficiency
Anorexia
Repeated marathon running
Scorpion venom
Pancreas divisum

15. Physiology
The pancreas secretes ml/ day of transparent, anodorous, isoosmotic juice with a high pH, containing bicarbonates and digestive enzymes
Stimulants: secretin, duodenal pH <4.0
Cholinergic stimulation – vagus nerve

16. Physiology
The proportions of different enzymes differ; various nutrients stimulate the secretion of various enzymes
Cholecystokinin (CCK) i s the primary regulator
Secondary mediators include Ca++ and diacylglycerol

17. Pancreatic enzymes Inhibitors: Amylase Active
Proteases ( trypsin) Inactive
Lipases Inactive
Inhibitors:
Alpha 1-antitrypsin
Beta 2-macroglobulin
Pancreatic secretory trypsin inhibitor (PSTI)

18. Pathology overpressure in Wirsung’s duct
abnormal inhibition of secretion of zymogens and inappropriate activation of pancreatic zymogens inside the pancreas, most notably trypsinogen
during an acute pancreatitis episode there is colocalization of lysosomal enzymes, specifically cathepsin, with trypsinogen. Cathepsin activates trypsinogen to trypsin leading to further activation of other molecules of trypsinogen and immediate pancreatic cell death according to either the necrosis or apoptosis mechanism (or a mix between the two)

19. Pathology
an extensive inflammatory response due to pancreatic cells synthesizing and secreting inflammatory mediators: primarily TNF-alpha and IL-1
inflammatory response leads to the secondary manifestations of pancreatitis: hypovolemia from capillary permeability, acute respiratory distress syndrome, disseminated intravascular coagulations, renal failure, cardiovascular failure, and gastrointestinal hemorrhage

20. Physiology

21. Pathology

22. Signs and symptoms
SEVERE abdominal pain – usually (95-100%) first symptom, often radiates to the back
Nausea,vomiting without relief ( 80%)
Fever (onset crucial for correct management: 1st week – SIRS; 2 weeks and later – necrosis infection)
Epigastric tenderness
Peristaltic sounds weak or absent (paralytic ileus)

23. Signs and symptoms
Tender epigastric mass – parapancreatic infiltration
Shock
Pancreatic encephalopathy
Tachycardia (often)
Hypotonia (due to hypovolemia)
Jaundice – (20-30%)

24. Rare sypmtoms
Kamenchik's sign (pain with pressure under the xiphoid process)
Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the Erector spinae muscles and below the left 12th rib (left costovertebral angle (CVA))
Loeffler’s sign – facial erythema
Clairmont’s sign – left pleural effusion
Körte's sign (pain or resistance in the zone where the head of pancreas is located (in epigastrium, 6–7 cm above the umbilicus))

25. Grey Turner's sign
bruising of the flanks, appearing as a blue discoloration
a sign of retroperitoneal hemorrhage
Also seen in:
Blunt abdominal trauma
Ruptured abdominal aortic aneurysm
Ruptured / hemorrhagic ectopic pregnancy

26. Cullen's sign
superficial edema and bruising in the subcutaneous fatty tissue around the umbilicus

27. Fox’s sign
bruising along inguinal ligament

28. Symptoms - summary All of them non -specific Abdominal pain 85-100%
Nausea and vomiting %
Anorexia %
Tachycardia %
Fever %
Bowel obstruction %
Tender abdominal mass %
All of them non -specific
Baron TH, Morgan DE. Acute Necrotizing Pancreatitis, NEJM, 1999

29. Lab results indicative of AP
Elevated serum amylase and lipase levels  no role in assessing disease severity.
Serum lipase rises 4 to 8 hours from the onset of symptoms and normalizes within 7 to 14 days after treatment
Serum amylase may be normal (in 10% of cases) for cases of acute or chronic pancreatitis (depleted acinar cell mass) and hypertriglyceridemia.
Reasons for false positive elevated serum amylase include salivary gland disease (elevated salivary amylase), bowel obstruction, infarction, cholecystitis, and a perforated ulcer.
If the lipase level is about 2.5 to 3 times that of amylase, it is an indication of pancreatitis due to alcohol
Decreased serum calcium
Glycosuria
Increased CRP

30. Acute pancreatitis: US imaging
Abdominal US usually performed  pancreas often invisible (intestinal gasses, obesity)
US in acute pancreatitis: pancreas enlarged, boundaries not clearly defined (inflammatory infiltration), heterogenous echogenicity
US important for ID of causative factor (gallstones)
Monitoring of complications (abcess, cyst, necrosis)

31. US

32. Computed tomography
„Gold standard” in AP imaging; enables assessment of severity and necrotic changes (Balthasar score A-E)
Helps assess severity (CTSI index)
Recommended after 72 h from onset of symptoms,
In critical patients – immediate CT
Further scans after 7-10 days or upon significant changes of patient’s condition

33. Balthasar score Balthazar Grade Appearance on CT CT Grade Points
Normal CT
0 points
Grade B
Focal or diffuse enlargement of the pancreas
1 point
Grade C
Pancreatic gland abnormalities and peripancreatic inflammation
2 points
Grade D
Fluid collection in a single location
3 points
Grade E
Two or more fluid collections and / or gas bubbles in or adjacent to pancreas
4 points

34. Necrosis score CTSI score = Balthasar + necrosis score
Necrosis Percentage
Points
No necrosis
0 points
0 to 30% necrosis
2 points
30 to 50% necrosis
4 points
Over 50% necrosis
6 points
CTSI score = Balthasar + necrosis score

35. CT scan of AP patient

36. Other imaging modalities
Chest X-ray
Interstital atelectasis, pleural effusion, ARDS
Abdominal X-ray
Fluid levels, bowel distension (signs of paralytic ileus) MR
 indication for imaging of patients with an allergy to CT's contrast material

37. Course of the disease
Edematous AP (60-70%) of the patients – treatment of symptoms, no complications, mortality < 1%
Severe AP (30-40% )– mortality between 10% (sterile necrosis) and 25% (infected necrosis); if organ – specific complications arise, the mortality rates increase to 20% and 50-80% , respectively.
in severe AP there are two periods of increased mortality:
early (~60% deaths) – first 7-14 days: early MOF, severe ARDS due to SIRS
late (~40% deaths) – 3-4 weeks from onset  infection of necrotic tissues, abscess formation  sepsis  septic shock  MOF

38. AP severity scores Ranson criteria for non – gallstone AP
At admission:
Age in years > 55 years
White blood cell count > cells/mm3
Blood glucose > 10 mmol/L (> 200 mg/dL)
Serum AST > 250 IU/L
Serum LDH > 350 IU/L

39. After 48 hrs Serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
Hematocrit fall > 10%
Oxygen (hypoxemia PO2 < 60 mmHg)
BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration
Base deficit (negative base excess) > 4 mEq/L
Sequestration of fluids > 6 L

40. Ranson for gallstone AP
At admission:
Age in years > 70 years
White blood cell count > cells/mm3
Blood glucose > 12.2 mmol/L (> 220 mg/dL)
Serum AST > 250 IU/L
Serum LDH > 400 IU/L

41. After 48 hrs Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
Hematocrit fall > 10%
Oxygen (hypoxemia PO2 < 60 mmHg)
BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration
Base deficit (negative base excess) > 5 mEq/L
Sequestration of fluids > 4 L

42. Ranson - interpretation
If the score ≥ 3, severe pancreatitis likely.
If the score < 3, severe pancreatitis is unlikely
Or:
Score 0 to 2 : 2% mortality
Score 3 to 4 : 15% mortality
Score 5 to 6 : 40% mortality
Score 7 to 8 : 100% mortality

43. Conservative treatment
Anti –shock treatment
Pain control
Nil-by-mouth regime
Nasogastric tube placement
Total parenteral nutrition
Stress ulcer prevention
Wide - spectrum antimicrobial
Fluid replacement therapy

44. Endoscopic retrograde cholangiopancreatography (ERCP)
 combines the use of endoscopy and fluoroscopy to diagnose and treat certain problems of the biliary or pancreatic ductal systems
plastic catheter inserted through the ampulla, and radiocontrast is injected into the bile ducts and/or pancreatic duct. Fluoroscopy is used to look for blockages, or other lesions such as stones

45. ERCP
opening of the ampulla can be enlarged (sphincterotomy) with an electrified wire (sphincterotome) and access into the bile duct obtained 
trawling of the common bile duct with a basket or balloon to remove gallstones and the insertion of a plastic stent to assist the drainage of bile
direct electrohydraulic lithotripsy

46. ERCP

47. Indications for surgery
Diagnosis uncertain( peritoneal signs)
Symptoms of necrosis infection or abscess
Complications: bowel necrosis, perforation, hemorrhage

48. Timing of surgery
Almost never before 10th day after onset – unless fulminating necrosis occurs
surgery 0 – 7th day - mortality 38%
surgery 8 – 14th day - mortality 28%
surgery >21 day - mortality. 15%
Complete necrosis facilitates removal

49. The role of surgery in severe AP
Necrectomy, lavage / drainage of the bursa omentalis
laparostomy
abscess drainage
debridement of the retroperitoneal space

51. Video – Assisted Retroperitoneal Debridement (VARD)

52. Chronic pancreatitis
Long-standing inflammation of the pancreas that alters the organ's normal structure and functions.
It can present as episodes of acute inflammation in a previously injured pancreas, or as chronic damage with persistent pain or malabsorption.
Damage is non – reversible.

53. Causes Alcohol Smoking Malnutrition Hereditary
Trypsinogen and inhibitory protein defects
Cystic fibrosis
Idiopathic (unknown)
Trauma
Hypercalcemia

54. Forms Calcifying chronic pancreatitis – alcohol
Proteins present within the pancreatic juice precipitate  secondary calcification

56. Chronic pancreatitis
Chronic obstruction of pancreatic juice flow may lead to chronic pancreatitis (tumors, gallstones, pancreas divisum, scarrring)

57. Signs & symptoms
pain – severe postprandial pain in the epigastrium, radiating to the left epigastrium or back; due to increase in intraductal pressure and / or inadequate blood supply
Weight loss & cachexia (loss of exocrine function, fear of pain after eating)
fatty diarrhea (steatorrhea)
dyspepsia
jaundice

58. Complications diabetes abscess cyst duodenal obstruction
biliary tree obstruction

60. US pancreas enlarged hypoechogenous distended Wirsung’s duct
calcifications within parenchyma, stones within Wirsung’s duct
pseudocysts

61. Conservative treatment
Dietary fat limited to 100 gram / d
Replacement pancreatic enzymes
Pain control
Parenteral nutrition in severe cachexia
Insulin

62. Indications for surgery
Debilitating pain nonresponsive to medical treatment
Duodenal obstruction
Ascites or pleural effusion
Suspected malignancy
Cysts, fistulae

63. Surgical treatment
Puestow procedure

64. Surgical treatment
anastomoses
gastrointestinal
biliary

65. Endoscopic treatment

66. Palliative treatment
neurolysis

67. Pancreatic cysts Pseudocysts (no epithelium) > 75%
Secondary to inflammation, trauma
True cysts – rare, usually in polycystic syndromes

68. Clinical presentation
Usually asymptomatic, present as abdominal mass
Serum amylase usually normal

69. Imaging

70. Complications
infection
hemorrhage
Fistula
external
internal

71. Treatment
Internal drainage
Jurasz procedure

72. Treatment
Percutaneous drainage

73. Tumors 90% - ductal adenocarcinoma
Neuroendocrine tumors (insulinoma, glukagonoma, vip-oma, gastrinoma etc.)
1% - benign cystic tumors (serous, mucous cysts)

74. Pancreatic cancer Morbidity 10/ 100.000 / year ♂ 30% more likely
3rd most frequent malignancy of the alimentary tract
More frequent after 60 years of age
3% of all malignancies
80% preceded by diabetes

75. Risk factors smoking alcohol abuse
chronic pancreatitis (linked but not causal)
diet: fat + red meat, soft drinks
genes (BRCA-2)
increased BMI

76. Location
Head 60-70%
Body 15-20%
Tail 5%
More than one part 20%

77. Signs and symptoms Late, non - specific Weight loss -90% Pain -75%
Anorexia -60%
Malnutrition -75%
Hepatomegaly -65%
Skin itch -40%
Courvoisier’s sign -30%
Diabetes -15%
Abdominal tenderness -20%
Palpable abdominal mass-10%
Ascites -5%
Jaundice -6%

78. Diagnosis CT ECPW EUS Diagnostic laparoscopy  laparoscopic US
Marker : CA 19-9

79. Prognosis 5 – year survival  approx. 5%
Tumor limited to pancreas, resectable – expected survival 17 months
Locally advanced tumor, non-resectable – mean expected survival 8-9 months
Metastases – mean expected survival 4-6 months
5 – year survival  approx. 5%

80. Treatment radical: resection + radiotherapy + chemotherapy
palliative: fecal diversion, stenting, brachytherapy

81. Surgical treatment
Whipple procedure – en bloc removal of the distal segment (antrum) of the stomach; the first and second portions of the duodenum; the head of the pancreas; the common bile duct; and the gallbladder

82. Longmire – Traverso ( resection of the head of the pancreas, preserving the pylorus)

83. Pancreatic tail resection (usually with splenectomy)