This slides highlight you about acute pancreatitis. it is wisely selected from Harrison 21st edition.

1. ACUTE PANCREATITIS
Most common inpatient principal GI diagnosis.
Incidence continues to rise.
Common causes
Gallstones
Alcohol
Hypertriglyceridemia
ERCP
Idiopathic.

2. Etiology and Pathogenesis
Has many causes.
Mechanism not known.
Gallstone and alcohol 80-90%.
Gallstone is leading cause 30-60%.
Alcohol second most common 15-30%.
After ERCP 5-10%.
Can be prevented by prophylactic stent and/or Rectal
Indomethacin.

3. Risk factor for Post ERCP Pancreatitis are:
Papillary sphincterotomy.
Suspected sphincter of Oddi dysfunction.
Prior history.
Age <60.
More than 2 contrast injection.
Endoscopist experience.
Hypertriglyceridemia 1-4%
Serum triglyceride >1000mg/dl.

4. Have undiagnosed or uncontrolled DM.
Underlying derangement in lipid metabolism.
Alcohol or medication like OCP can precipitate acute pancreatitis.
Drugs by either hypersensitivity or generation of toxic metabolite.

5. Pathology: ranges from interistial pancreatitis with pancreas blood
supply maintained to necrotizing pancreatitis with blood supply
interrupted.
Autodigestion when proteolytic enzymes are activated in acinar cells
rather than intestinal lumen.
 SIRS and ARDS as well as multi organ failure as result of cascade of
local and distant effects.

6. Approach to the patient:
Abdominal pain is the major symptom of acute pancreatitis.
From mild discomfort to sever constant and incapacitating distress.
Steady and boring in character, located in epigastrium, may radiate to
the back, chest, flanks and lower abdomen.
Nausea, vomiting and abdominal distention due to gastric and
intestinal hypomotility.

7. P/E:
Distressed and anxious patient.
Low grade fever, tachycardia and hypotension.
Shock is not unusual and due to
Exudation of blood and plasma proteins in to retroperitoneal space.
Increased formation and release of kinin peptides-causes
vasodilation and increased vascular permeability.
Systemic effects of proteolytic and lipolytic enzymes.

8. Jaundice infrequently-extirinisic compression due to peripancreatic
edema or pancreatic head mass.
Basilar rales, atelectasis and pleural effusion commonly left sided in
10-20%
Abdominal tenderness and muscle rigidity.

9. Diminished or absent bowel sound.
Palpable enlarged pancreases latter on.
Cullen's sign is faint blue discoloration of flanks as result of
hemoperitoneum.
Turners sign green- brown discoloration of flanks as result of tissue
breakdown from hemoglobin.

10. Laboratory Data
Serum amylase and lipase >3x strongly suggests when other causes
excludes like gut perforation. Ischemia and infarction.
No correlation between severity of pancreatitis and degree of serum
lipase and amylase elevations.
After 3-7 days amylase returns to normal despite ongoing pancreatitis
Lipase may remain 7-14 days.
Lipase is more specific than amylase.
Amylase may be low in hypertriglyceridemia.

11. Lipase level differentiate hyperamylasemia weather from pancreatic
or not.
Leukocytosis 15,000-20,000.
Hemoconcentration HCT>44%.
Hemoconcentration is harbinger of more sever disease.
BUN>22mg/dl pre renal azotemia.
Azotemia is significant risk for mortality.

12. Hyperglycemia common and due to multiple factors.
Decreased insulin release.
Increased glucagon.
Increased output of adrenal glucocorticoids and catecholamines.
Hypocalcemia 25%.
Hyperbilirubinemia 10%. Returns to normal in 4-7 days.
ALT> 3X strongly associated to gallstone.
5-10% have hypoxemia-heralds onset of ARDS.

13. ECG: ST and T wave abnormalities simulating MI.
Abdominal U/S initial diagnostic imaging.
CT Scan with Atlanta Criteria:
Interstitial pancreatitis.
Necrotizing pancreatitis.
Acute pancreatic fluid collection
Pancreatic fluid collection.
Acute necrotic collection.

14. Diagnosis
Two of the following 3 criteria required
Typical abdominal epigastric pain radiates to the back.
Three fold or greater elevation in serum lipase and/amylase.
Confirmatory finding of acute pancreatitis in cross sectional
abdominal imaging.

15. Markers of severity
Hemoconcentration HCT> 44%.
Admission azotemia BUN> 22g/dl
SIRS and signs of Organ failure.

17. DDx
Perforated viscus PUD.
Acute cholecystitis.
Acute intestinal obstruction.
Mesenteric vascular occlusion.
Renal colic.
Inferior MI.
Dissecting aortic aneurysm
CTD with vasculitis
Pneumonia
DKA

18. Acute cholecystitis and acute pancreatitis both have elevated serum
amylase.
Pain of biliary origin is more on right side or epigastric than
periumbilical or LUQ.
Ultrasound establish diagnosis of cholelithiasis and cholecystitis.
Intestinal obstruction due to mechanical factors has crescendo-
Decrescendo pain, finding in abdominal examination and CT of
abdomen.
Acute mesenteric ischemia in elderly debilitated with leukocytosis,
abdominal distention and bloody diarrhea.
Confirmed by CT/MR angiography.

19. Vasculitis due to SLE and PAN can be confused because pancreatitis
develops as complication of the disease.

20. Clinical course, Definition and Classification
Atlanta criteria
Phases of acute pancreatitis
Early< 2 weeks
Severity by clinical parameters not morphologic
Most exhibit SIRS-predispose to Organ failure.
Three organs, Respiratory, CVS and Renal.
Two or more from one of those organs.
Modified marshal score
CT not recommended during 1st 48 hours.

21. Late phase >2 weeks
Protracted course.
Many require imaging to determine for complication.
Sign of severity is persistent organ failure.
Many require supportive measure like renal dialysis, ventilation
support and supplemental nutrition.
Development of necrotizing pancreatitis on CT Scan.

22. Severity of acute pancreatitis
Mild
With out local complications or organ failure.
Self limited disease, 3-7 days.
Oral intake possible if patient is hungry, has normal bowel function,
no nausea and vomiting.
Clear and full liquid diet as initial meal.

23. Moderately sever acute pancreatitis
Transient organ failure <48 hours.
Local or systemic complications in the absence of persistent organ
failure.
May or may not have necrosis, develop local complication-fluid
collection.
Low mortality.

24. Sever acute pancreatitis
Persistent organ failure >48hours.
Involves one or more organ.
CT/MRI should be obtained to detect necrosis or complications.
• Local complication encountered-management guided by
Clinical symptoms
Evidence of infection
Maturity of fluid collection
Clinical stability of the patient.
Prophylactic antibiotics not recommended.

25. Imaging
CT imaging with contrast
When patient not responding tosupportive care.
To asses for local complications like necrosis.
After 3-5 days post admission.
Interstitial pancreatitis 90-95%.
Diffuse gland enlargement
Homogenous contrast enhancement.
Mild inflammatory changes.
Peripancreatic stranding.

26. Patient with infected or sterile necrosis is greatest risk for mortality.
Organ failure >50% in necrotizing pancreatitis.
Higher in infected than sterile necrosis.
Mortality 3-10% with single organ failure and 50% with multiorgan
failure.

27. Acute pancreatitis management
85-90% are self limited with in 3-7 days.
Early aggressive fluid resuscitation is critical.
IV analgesics.
Search for etiology that may impact acute care.
Hemodynamic monitoring and management of any organ failure.
Fluid resuscitation and monitoring to therapy.
Aggressive fluid resuscitation to prevent systemic complications from
secondary SIRS.

28. Keep NPO.
IV narcotics.
Supplemental oxygen as needed.
NS/RL bolus 15-20ml/kg followed by 2-3ml/kg/hr.
Urine output target >0.5ml/kg/hr.
Vital sign Q6/8hr
RL better because it decreases SIRS and CRP level.
Measurement of HCT and BUN Q8/12hr.

29. Less aggressive fluid management in mild form.
Rising BUN suggests lesser resuscitation and high mortality.
Decrease in HCT and BUN 1st 12-24 hours is strong evidence of
sufficient fluids are administered.
Rise in HCT and BUN during serial measurement, Repeat volume
challenge with bolus 2lt and increased by 1.5ml/kg/hr.
If BUN and HCT persists to rise transfer to ICU for continuous
hemodynamic monitoring.

30. Assessment of severity
Bedside Index of Sverity in Acute pancreatitis-BISAP Score.
Five clinical and laboratory parameters.
BUN >25g/dl.
GCS <15
Age >60
SIRS
Pleural effusion on CXR.
Presence of 3 or more are associated with high in hospital moertality.
Elevated HCT >44% and BUN >22g/dl more sever pancreatitis.

31. Special consideration based on etiology
Review medication
Selected laboratory studies like LFT, serum Triglycerides, serum
calcium.
Abdominal U/S- gallbladder, CBD and pancreatic head.
Gallstone pancreatitis-patients with cholangitis, increased WBC and
liver enzymes –do ERCP.
Gallstone-Cholecystectomy at the same admission for mild disease.
Endoscopic biliary sphincterotomy for no surgical candidates.

32. Hypertriglyceridemia- serum triglycerides >1000mg/dl.
Initial therapy-treatment of hyperglycemia with IV insulin.
Outpatient control DM, Administration of lipid lowering agents,
weight loss and avoidance drug that elevate lipids.
Hypercalcemia and ERCP pancreatitis
Treatment of hypoparathyroidism and malignancy reduces
calcium.
Pancreatic duct stenting and rectal indomethacin for Post ERCP
pancreatitis prevention.
Drugs that cause pancreatitis should be discontinued.

33. Nutritional therapy:
Low fat solid diet- mild acute pancreatitis once they able to take.
After 2-3 days of admission for patients with sever pancreatitis.

34. Management of local complications:
Patients who deteriorates with despite aggressive fluid resuscitation
and hemodynamic monitoring should be assessed for complications.
Complications may include
Necrosis
Pseudocyst formation.
Pancreatic duct disruption.
Peripancreatic vascular complications
Extra pancreatic infections.

35. Necrosis- multidisciplinary.
Empiric antibiotics in those with clinical decompensation.
Repeat CT/MRI when change in clinical course to monitor for
complications Eg, thrombosis, hemorrhage, abdominal compartment
syndrome.
Sterile necrosis managed conservatively.
Infected necrosis targeted antibiotics.
Pancreatic drainage and/or debridement-necrosectomy is definitive for
those not responding for antibiotics.

36. Step-up approach
Percutaneous/endoscopic
Trans gastric/trans duodenal drainage followed by surgical
necrosectomy.
If conservative therapy do it for 4-6 weeks. Either resolves or evolve
to develop more organized boundary- wall off.

37. Pseudocyst
Low incidence
Most resolves spontaneously.
<10% persists after 4 weeks.
Only symptomatic collections require intervention with endoscopic or
surgical drainage.

38. Pancreatic duct disruption
Presents with symptoms of increasing abdominal pain or SOB.
Enlarging fluid collection
Pancreatic ascites- ascitic fluid high in amylase level.
Confirmed by MRCP/ERCP.
Treatment: placing bridging pancreatic stent for at least 6 weeks.
Effective >90%.

39. Perivascular complications:
Splenic vein thrombosis with gastric varices and pseudoaneurysm.
Portal and superior mesenteric vein thrombosis.
Extra pancreatic infections
HAI- up to 20%.
Monitor for pneumonia, UTI and line infections.

40. Follow-up care
Asses for development of DM
Exocrine pancreatic insufficiency.
Recurrent cholangitis.
Necrotizing gallstone pancreatitis-timing for cholecystectomy should
be individualized.

41. Recurrent acute pancreatitis
25% have recurrence.
Alcohol and cholelithiasis two most common etiology.
If no obvious cause identified suspect
Microlithiasis
Hypertriglyceridemia.
Pancreatic Ca 2-4%.
Hereditary pancreatitis.

42. Pancreatitis in AIDS
Theoretically increased in AIDS.
High incidence of infections involving pancrease such as CMV,
cryptosporidium and MAC.
Frequent use of medications like pentamidine, CPT and PI.
Reduced after disuse of ddi.