1. Pancreatitis
Dr. Faiez Alhmoud
Albashir Hospital
Surg. Department
Dr. Faiez

2. Pancreas.. little anatomy & Physiology
• Retroperitoneal organ that extends obliquely from the
duodenal C loop to the hilum of the spleen.
• It is divided into 4 portions: head, neck body and tail.
• The head is 30% of size and intimately associated with the
second portion of the duodenum, and they are BOTH
supplied by the pancreaticoduodenal arteries.
• The aorta and the superior mesenteric vessels lie behind
the neck of the gland.
• It incorporates endocrine and exocrine function.

4. Pancreas…….little anatomy & physiology
• Behind the neck of the pancreas, near its
upper border, the superior mesenteric vein
joins the splenic vein to form the portal vein.
• The tip of the pancreatic tail extends up to
the splenic hilum.
• The main pancreatic duct branches into
interlobular and intralobular ducts, ductules
and, finally, acini.

5. Pancreas……. little anatomy & physiology
• In response to a meal, the pancreas secretes
digestive enzymes in an alkaline (pH 8.4)
bicarbonate-rich fluid.
• The pancreatic enzymes are secreated in an
inactive form, the maintenance of this is
important in preventing pancreatitis.

6. Pancreas……. little anatomy & physiology
• 1-2 L alkaline, clear, isoosmolar enzyme rich
fluid
• Na & K at plasma levels
• 20 enzymes are secreted
• Secretion is regulated by: Secretin, CCK,
Vagus n. and low Ph
• Proteolytic enzymes (Tryp, Chemotryp,
elastase …etc
• Lipolytic (lipase, colipase, phospholipase..etc)
• amyloytic
• Endocrine function: insulin, glucagon,
somatostatin..etc)
Dr. Faiez

7. Pancreatitis
Inflammation of the pancreatic
parenchyma
Acute or Chronic
 Acute pancreatitis represents a
transient inflammation that resolves
with or without Complications.
 Chronic pancreatitis defined as
continuous inflammation resulting
in progressive anatomic and
functional damage to the pancreas.
Dr. Faiez

8. ?Who gets pancreatitis
 Biliary tract stones  Idiopathic
 Ethanol Abuse  Infections
 Drugs  Ischemia
 ERCP  Parasites
 Hypercalcemia  Postoperative
 Hyperlipidemia
 Scorpion sting
 Trauma
 Pancreatic duct
obstruction
– Tumour
– Pancreas divisum

9. Pancreatitis..causes
Gallstone Disease (Alcohol abuse (35%
Fewer than 10% of •
((45% alcoholics develop
Gallstones impacted at • pancreatitis
S.o.O
In general, smaller stones • First attack after 6-10 •
more likely to cause years
pancreatitis than larger of beginning alcohol
abuse
ones
mm 5 >
Direct effects on •
Microlithiasis • pancreatic intracellular
Microlithiasis felt- metabolism
responsible for many
“idiopathic” cases Decreased pancreatic •
Dr. Faiez

10. Pancreatitis….causes
Alcohol
Pancreatitis is a consequence of chronic -
alcohol abuse; usually 6 to 10 years
-Daily consumption averages 100-150
g/day;
-10% of heavy drinkers develop
pancreatitis
-May cause spasm or inflammation of
sphincter of Oddi
-May decrease solubility of intraductal
proteins, promoting stone formation
-Decrease in pancreatic blood flow and
alterations of lipid metabolism may
contribute as well

11. Pancreatitis…causes
Drugs
 5-Aminosalicylate  Furosemide
 6-Mercaptopurine  Metronidazole
 Azathioprine  Pentamidine
 Cytosine arabinoside  Tetracycline
 Dideoxyinosine  Thiazide
 Diuretics  Trimethoprim-
 Estrogens
sulfamethoxide
 Valproic acid

12. Pancreatitis... causes
Iatrogenic Trauma
Accounts for about 1.5% •
of acute pancreatitis
Post-ERCP( 1) cases
Possibly the 3rd most • Abdominal blunt trauma •
common cause
May crush gland against •
Risk approximately 4- • spine
8%
May disrupt pancreatic •
duct
Post-surgical( 2 ) Penetrating trauma •
Direct injury • Dissection and disruption •
of pancreatic duct
Dissection of vessels •

13. Pancreatitis…causes
Infections Metabolic
:Viral • Hypercalcemia (of any •
mumps, coxsackie, measles, ( cause
varicella, EBV, CMV
Hypertriglyceridemia •
: Bacterial• Causes pancreatitis at -
TB, mycoplasma, salmonella, levels above 1000
campylobacter mg/dL
: Helminthic•
ascariasis

14. Pancreatitis…..Pathology
Major Pathological Processes
Lipolysis
Proteolysis
Necrosis of blood vessels
Inflamation
Dr. Faiez

15. Pathogenesis
Tissue necrosis – activation of several pancreatic enzymes,
including trypsin and phospholipase A2.
 Hemorrhage -extensive activation of pancreatic elastase,
which dissolves elastic fibers of blood vessels
 Exudate containing toxins, activated pancreatic enzymes
permeates the retroperitoneum and at times the peritoneal
cavity, inducing a chemical burn and increasing the
permeability of blood vessels- third space
 Circulating activated enzymes - may damage tissue directly
causing remote systemic effects or generalized systemic
inflammatory response (shock, ARDS, multisystem organ
failure)

16. Acute Pancreatitis
Clinical Presentation
Mid epigastric abdominal pain•
Steady, boring pain•
Radiation to the back•
Anorexia, nausea ± vomiting ± diarrhea•
Low grade fever•
Presentations associated with complications•
Secondary infection-
Shock-
.Multi-system failure-

17. Acute Pancreatitis
Exam Findings
Abdominal tenderness•
(Fever (66%•
(Abdominal guarding (68%•
(Abdominal distension (65%•
(Tachycardia (75%•
Hypoactive bowel sounds•
(Dyspnea (10%•
(Hemodynamic changes (10%•
(Melena or hematemesis (5%•
Cullen’s sign•
Grey-Turner and Fox sign•
Left pleural effusion•
(Jaundice (28%•

18. Cullen’s sign Fox sign Grey-Turner sign
Periumbilical ecchymosis usually results from hemoperitoneum,
and the diffusion of blood along Periumbilical
tissues produces the discoloration around the navel.
Diffusion of blood via the falciform ligament may also
. produce Periumbilical blood staining

19. Differential diagnosis
Look for other causes
of abdominal pain

20. Differential diagnosis
 Biliary System Disease:
 Biliary Colic.
 Cholangitis.
 Cholecystitis.
 Cholelithiasis.
 Acute Gastritis.

21. Differential diagnosis
 Duodenal Ulcers.
 Hollow viscus Perforation.
 Myocardial Infarction.
 Omental Torsion.
 Mesenteric Artery Thrombosis.
 Intra-abdominal Sepsis.
 Extra-abdominal cuases.

22. Diagnosis
Serum amylase •
Not specific for pancreatitis: intestinal ischemia,-
,CRF
SBO, macroamylasemia, parotitis
Short half-life: rise early, returns to normal early (2- -
(3 d
Serum lipase •
More specific to pancreas-
Long half-life: rise later, stay elevated longer (7-14 -
(d
Liver enzymes • Dr. Faiez

23. Causes of hyperamylasaemia
 Perforated peptic ulcer
 Cholecystitis
 Generalised peritonitis
 Intestinal obstruction
 Mesenteric infarction
 Ruptured AAA
 Ruptured ectopic pregnancy

24. Acute pancreatitis
amylase - lipase
Both must be at least 2-3x normal -
. value
Magnitude of increase does not -
. correlate with disease severity
Together sensitivity increases to -
. 94%
Persistent hyperamylasemia beyond the initial week
may indicate the development of pancreatic
pseudocyst ,phlegmon, abscess or ongoing acute
.pancreatic inflammation

25. Diagnosis..
 Complete Blood Count
Hct > 44 risk factor for pancreatic necrosis-
Part of Ranson criteria -
 C-reactive protein
Not specific, but if > 10 mg/dL suggests severe-
inflammation
 serum glucose
elevated level indicate pancreatic endocrine dysfunction -
 serum calcium
maybe decreased -
 Ultrasound
Most useful initial test for gallstone etiology-
Dr. Faiez

26. Diagnosis..
 CXR and PA non-specific findings
– Sentinel loop
– Ileus
– Cutoff sign
– Pleural effusion (Left)
– Calcifications

27. Cutoff sign Sentinel loop
Dr. Faiez

28. Diagnosis
 Dynamic Contrast CT Scan
( May help identify etiology (e.g. pancreatic tumor -
Useful to assess grade or complications, especially -
after
initial 72 hours as fluid collections or pancreatic
necrosis
 MRCP
Non invasive

29. Pancreatitis Severity
Acute
 Mild – interstitial edema and response of
inflammatory cells with little necrosis
 Severe – necrosis, thrombosis, vascular
disruption, hemorrhage.
Chronic – fibrosis, loss of
exocrine/endocrine
elements, perineural inflammation, neural
enlargement; may have superimposed acute
changes

30. Severity - Scoring
Ranson Criteria - > 3 indicates severe AP
At Admission:
Age > 55; WBC > 16K; Glucose > 200; •
;AST > 250 LDH >350
During first 48 hours:
Hct decrease by > 10% with hydration •
BUN increase > 5 mg/dL •
Calcium < 8 mg/dL •
pO2 < 60 mm Hg •
Evidence of fluid sequestration •
( 6L replacement )<

31. Markers of Severity within 24 Hours
SIRS [temperature >38° or < 36°C, Pulse > 90,
[ Tachypnea > 24, WBC > 12,000
( Hemoconcentration (Hct >44%
(BISAP (Bedside Index of Severity in Acute Pancreatitis
% B) Blood urea nitrogen (BUN) >22 mg)
I) Impaired mental status)
S) SIRS: 2/4 or more present)
A) Age >60 years)
P) Pleural effusion)
Organ Failure
Cardiovascular: systolic BP <90 mmHg, heart rate >130
Pulmonary: Pao2 <60 mmHg
%Renal: serum creatinine >2.0 mg
Gastrointestinal: bleeding >500 ml/24 hours

32. Pancreatitis….Severity
Risk Factors
Age > 60 years
Obesity & overweight, BMI > 30
Comorbid disease
Markers during Hospitalization
Persistent organ failure
Pancreatic necrosis
Hospital-acquired infection

33. Contrast-enhanced CT scoring system
A Normal
B • Focal or diffuse glandular enlargement .
• Small intra-pancreatic fluid collection
C • Any of the above
• Peripancreatic inflammatory changes
• Less than 25% gland necrosis
D • Any of the above
• Single extrapancreatic fluid collection
• 25-50% gland necrosis
E •Any of the above
•Extensive extrapancreatic fluid collection
•Pancreatic abscess
•More than 50% gland necrosis

34. Ranson Criteria Prognosis
Mortality correlates with number of criteria
1% 0-2 •
15% 3-4 •
40% 5-6 •
100% 7-8 •

35. Severe Acute Pancreatitis Definition
Organ failure. 1
,Shock, pulmonary insufficiency •
renal failure, GI bleeding
Local complications. 2
Pseudocyst, abscess, pancreatic •
necrosis
Ranson criteria 3< . 3

36. Edematous acute pancreatitis

37. Necrotizing acute pancreatitis

38. How do you treat acute pancreatitis
 Pain control
 Fluid and electrolyte management
 Lots of fluid
 Foley’s catheter
 Supplemental oxygen
 NGT???
 Mechanical ventilation, inotropes
 Eliminate cause (i.e. gallstones,
hypoperfusion ,scorpions,
etc.) Dr. Faiez

39. What is the Target for
.treatment
Pain control
Correction of fluid and
electrolyte
derangement
 Reduction of
pancreatic secretory
stimuli

40. Mild Acute Pancreatitis
Management
Mild AP (Ranson score 2) = 85% patients•
Most cases will resolve in several days•
NPO, IV fluids, Analgesia•
Advance diet as tolerated•
Gallstone pancreatitis = cholecystectomy•
Failure to improve, status worsens•
.CT abdomen -

41. Severe ACUTE PANCREATITS
Management
Severe AP (Ranson score 3) 15% patients•
ICU with close monitoring, strict VS charting•
NPO, NGT?, aggressive IV fluid replacement, •
analgesia
Early ERCP + sphincterotomy if due to gallstone •
disease
Pancreatic necrosis on CT = start IV antibiotics•
Maintain nutrition•
Enteral nutritional support•
NJ tube within 3-4 days•

42. ACUTE
PANCREATITS
COMPLICATION
S

43. Local Complications
 Pseudocyst
 Pancreatic necrosis
Sterile – treat with antibiotics
Infected – urgent surgical debridement
If infection suspected
CT-guided needle aspiration to decide
 Peri-pancreatic fluid collections
of patients 57% •
Initially ill-defined •
Usually managed conservatively •
Dr. Faiez

44. Pseudocyst
 The most common complication of acute
pancreatitis (occurring in approximately 25% of
patients).
 Pseudocyst is a collection of pancreatic juice
enclosed in a wall of fibrous or granulation tissue.
 Formation of Pseudocyst require 4 weeks or more
from the onset of acute pancreatitis.
Dr. Faiez

45. Pseudocyst
Classification
of Investigation of
Pseudocyst Pseudocyst
• Type 1 - normal duct • Ultrasound will allow
anatomy. No fistula assessment of changes
between duct and in the size of the cyst
cyst • Endoscopic ultrasound
• Type 2 - abnormal increasingly used
duct anatomy - No • CT to define
fistula relationship to adjacent
• Type 3 - abnormal organs
duct anatomy and
fistula

46. :Pancreatic necrosis
Pancreatic necrosis is a significant complication
of acute pancreatitis, and may result in mortality
rates as high as 15%. Whatever the mechanism of
acute pancreatitis, in necrotizing pancreatitis,
there is obstruction of the pancreatic
microcirculation
Dr. Faiez

47. Pancreatic Infections
 Ideal culture media
 Pathways of contamination :
-Hematogenous spread
-Duodenal reflux via pancreatic duct
-Biliary contamination
-Colonic translocation
Dr. Faiez

48. Systemic Complications
 CV collapse, pulmonary and renal
compromise
( Due to significant third spacing and
hypovolemia )
 DIC and GI bleeding
( Proinflammatory mediators activate
coagulation cascade )
 Retinopathy and Encephalopathy
( Pathogenesis unknown )
 Hypocalcaemia
( Due to extravasation of albumin into

49. ?What bugs are we talking about
Pancreatic infections are nearly always bacterial,
are commonly polymicrobial, and are most often
due to gut flora
Aerobic gram negative bacilli
 Enterococcus
 Staphylococcus
 Increasing fungus
 Similar in pancreatic necrosis and
abscesses

50. The Role of Antibiotic Prophylaxis“
in Severe Acute Pancreatitis
Antibiotic prophylaxis appeared to be associated with-
significantly decreased mortality but not infected pancreatic
necrosis
Antibiotics are sometime prescribed to prevent infection of-
dead tissue (pancreatic necrosis) in acute pancreatitis (a
serious acute abdominal disease) because this complication
. carries a high risk of death. Their role is unproven
Non-protocol antibiotic-

51. ?What should we use
…Don’t use …Use
Aminopenicillins  3rd generation
1st generation cephalosporins
cephalosporins  Piperacillin
Aminoglycosides  Mezlocillin
 Quinolones
 Imipenem
 Metronidazole

52. …Conclusions
 Give prophylactic antibiotics to:
Severe acute pancreatitis with necrosis -
Disruption of the pancreatic ductal system -
 Antibiotic must pass blood-pancreas barrier and
achieve minimum inhibitory
concentration
 Give antibiotics early; duration yet to be
determined

53. …When Rushing to
surgery

54. Indicated in 4 specific circumstances
 Uncertainty of Clinical Diagnosis
(rare)
 Treatment of Pancreatic Sepsis
Abscess up to 5%
 Correction of Associated
Biliary Tract Disease
 Deterioration of Clinical Status
(controversial)

55. Treat complications
Early Late
• Bleeding • Endo or exocrine
• Fluid collection insufficiency
• Sepsis • Pseudocyst
• Colon ischemia • Recurrent pancreatitis
• Pancreatic fistula • Sinistral hypertension
• Intestinal fistula
• Renal dysfunction
Dr. Faiez

56. ?What is role of endoscopy in acute pancreatitis

58. Prevention of pancreatitis

59. Thank you
 finished !!

60. Dr. Faiez