1. Acute Pancreatitis

2. Acute Pancreatitis - Objectives
Discuss basic physiology
Etiology
Clinical Presentation
Diagnosis
Prognosis
Management
Complications

3. Pancreatic Physiology
(1) Production of bicarbonate-rich fluid to neutralize gastric fluid in the duodenum – duct cells primarily (CFTR gene = chloride / bicarbonate channel)
(2) Synthesis of digestive enzymes – acinar cells
(3) Insulin production = islet cells

4. Acute Pancreatitis

5. Acute Pancreatitis – Epidemiology
180,000 - >200,000 Hospital Admissions / Year
20% have a severe course
10-30% mortality for this group, which has not significantly changed during the past few decades despite improvement in critical care and other interventions

6. Etiology Alcohol (30-40%) Mechanism not fully understood
Not all alcoholics get pancreatitis (only about 15%)
This suggests a subset of the population predisposed to pancreatitis, with alcohol acting more as a co-precipitant

7. Etiology Gallstones (35%-60%)
Gallstone pancreatitis risk is highest among patients with small GS < 5mm and with microlithiasis
GS pancreatitis risk is also increased in women > 60 yrs

8. Etiology – Drugs and Toxins (5%)
Azathioprine
Cimetidine
Estrogens
Enalapril
Erythromycin
Furosemide
Multiple HIV medications
Scorpion Bites
Sulfonamides
Thiazides
TMP/SMX

9. Etiology – Trauma Blunt Trauma Iatrogenic – ERCP (1-7%) Automobile
Bicycle handlebar injuries
Abuse
Iatrogenic – ERCP (1-7%)
Likely secondary to contrast but also very operator dependant
Risk is also increased with Sphincter of Oddi manometry

10. Etiology – Multi-System Disease
Diabetic Ketoacidosis (10-15%)
Hemochromatosis
HUS
Hypercalcemia
Hyperparathyroidism
Hypertriglyceridemia
IBD
Malnutrition
Severe PUD
Renal Failure
SIRS
SLE and other connective tissue dissorders
Status-Post solid organ and BM transplant
Vasculitis

11. Etiology – Multi-System Disease
Cystic Fibrosis
2-15% of patients
Ductal obstruction from thickened secetions

12. Etiology – Multi-System Disease
Malnutrition and Re-feeding
Anorexia Nervosa
Pancreatic acinar cells atrophy but true cause of pancreatitis unknown

13. Etiology – Infection Ascaris Campylobacter CMV Coxsackie B EBV
Enterovirus
HIV/AIDS
Influenza
MAC
Measles
Mumps Rubella
Mycoplasma
Rubeola
Viral Hepatitis
Varicella

14. Etiology – Anatomical Anomalies
Pancreas Divisum
Failure of dorsal and ventral fusion (5-15% of population)
Annular Pancreas
Any Ductal Anomalies
Sphincter of Oddi dysfunction
Always consider a primary malignancy as a possible cause of new onset pancreatitis in older patients without other obvious risk factors

15. Etiology – Idiopathic
Experts suggest that idiopathic pancreatitis should account for no more than 5-10% of the total cases, yet the broadly quoted percentage in the literature at this time in the US is currently 20-25%.

16. Clinical Presentation
Acute Pancreatitis
Clinical Presentation

17. Clinical Presentation
Continuous mid-epigastric / peri-umbilical abdominal pain  Radiating to back, lower abdomen or chest
Emesis
Fever
Aggravated by eating
Progressive
Restless and uncomfortable

18. Clinical Presentation
More severe cases
Jaundice
Ascites
Pleural effusions – generally left-sided
Cullen’s sign – bluish peri-umbilical discoloration
Grey Turner’s sign – bluish discoloration of the flanks

19. Diagnosis – Initial work-up
Med intake
Family History
Alcohol intake
Viral exposures
Lipase
LFTs
GB US

20. Diagnosis – Amylase
Elevates within HOURS and can remain elevated for 4-5 days
High specificity when using levels >3x normal
Many false positives (see next slide)
Most specific = pancreatic isoamylase (fractionated amylase)

21. Diagnosis – Amylase Elevation
Pancreatic Source
Biliary obstruction
Bowel obstruction
Perforated ulcer
Appendicitis
Mesenteric ischemia
Peritonitis
Salivary
Parotitis
DKA
Anorexia
Fallopian tube
Malignancies
Unknown Source
Renal failure
Head trauma
Burns
Postoperative

22. Diagnosis – Lipase The preferred test for diagnosis
Begins to increase 4-8H after onset of symptoms and peaks at 24H
Remains elevated for days
Sensitivity % and Specificity 60-99%
>3X normal S&S ~100%

23. Diagnosis
Elevated ALT > 3x normal (in a non-alcoholic) has a positive predictive value of 95% for GS pancreatitis

24. Diagnosis – Imaging CT Excellent pancreas imaging
Recommended in all patients with persisting organ failure, sepsis or deterioration in clinical status (6-10 days after admission)
Search for necrosis – will be present at least 4 days after onset of symptoms; if ordered too early it will underestimate severity
Follow-up months after presentation as clinically warranted for CT severity index of >3

25. Diagnosis - Imaging ERCP / EUS Diagnostic and Therapeutic
Can see and treat:
Ductal dilatation
Strictures
Filling defects / GS
Masses / Biopsy

26. Diagnosis – Imaging
ERCP indications (should be done in the first 72hr)
GS etiology with severe pancreatitis – needs sphincterotomy
Cholangitis
Jaundice
Dilated CBD
If no GS found sphincterotomy is indicated anyway
Poor surgical candidate for laparoscopic cholecystectomy
Clinical course not improving sufficiently to allow timely laparoscopic cholecystectomy and intraoperative cholangiogram
Pregnant patient
Uncertainty regarding biliary etiology of pancreatitis

27. Acute Pancreatitis
Prognosis

28. Prognosis – Ranson’s (Severe > 3)
Ranson’s Score
5 on Admission
Age > 55 y
Glucose >200
WBC > 16000
LDH > 350
ALT > 250
6 after 48 hours from presentation
Hct > 10% decrease
Calcium < 8
Base Deficit > 4
BUN > 5
Fluid Sequestration > 6L
PaO2 < 60

29. Prognosis – CT Severity Index
CT Grade
Normal points
Focal or diffuse enlargement 1 point
Intrinsic change or fat stranding 2 points
Single ill-defined fluid collection 3 points
Multiple collections of fluid or gas 4 points
Necrosis Score
None points
1/3 of pancreas 2 points
1/2 of pancreas 4 points
> 1/2 of pancrease 6 points
Severe = Score > 6 (CT Grade + Necrosis)

30. Management
All patients with biliary pancreatitis should undergo definitive treatment of gallstones during the same hospital admission, unless a clear plan has been made for definitive treatment within the next two weeks
Delay exposes the patient to the risk of potentially fatal recurrent acute pancreatitis
Surgery should be delayed in severe pancreatitis and ERCP is preferred

31. Management Mainly supportive
Hydration, pain relief, and pancreatic rest
NPO – to decrease pancreatic secretion
Remember stress ulcer prophylaxis always
Look for complications

32. Management - Feedings Enteral nutrition is preferred
There is a push for nasojejunal feeds however nasogastric feeds have been shown to be effective in 80% of cases¶
NGTs should be used with caution in patients with AMS however
More risk with TPN / IL but if cannot feed enterally >5 days may be needed
¶ Eatock FC. Nasogastric feeding in severe acute pancreatitis. Radiology 1994: 193,

33. Management – Necrosis
All severe pancreatitis should be managed in the ICU
Necrosis associated Infection generally requires debridement (surgical or IR) best outcomes are reports associated with >30 after admission

34. Management – Pain Med Myths and Truths
Morphine not ideal but can still be used – it can theoretically worsen symptoms by increasing spasm of the Sphincter of Oddi
Demerol
Hydromorphone
All narcs cause Sphincter of Oddi spasm
PCA is generally preferred in the beginning
Always use the gut if you can to transition off IV pain meds

35. Complications – Local Necrosis Pseudocyst Ascites
Sterile
Infected - abscess
Pseudocyst
Ascites
Intraperitoneal hemorrhage
Thrombosis
Bowel infarction
Obstructive jaundice

36. Complications – Systemic
Pulmonary
Pleural effusions
Atelectasis
Mediastinal abscess
ARDS
Cardiovascular
Hypotension
Sudden death
Pericardial effusion
Hematologic
DIC
Gastrointestinal
PUD
Erosive gastritis
Blood vessel erosion
Portal vein thrombosis
Renal
Oliguria
Azotemia
Renal artery/vein throbosis
ATN

37. Complications – Long Term
Chronic Pancreatitis
Abdominal Pain
Steatorrhea
Exocrine insufficiency (pancreas has a 90% reserve for the secretion of digestive enzymes)
DM, i.e.Endocrine Insufficiency
Pseudocyst

38. Conclusions Do not assume alcohol is the primary cause of pancreatitis
Always consider further work-up for “idiopathic” pancreatitis
Severe acute pancreatitis should be managed in ICU/SD
Infected necrosis carries a high mortality
Antibiotics for suspected infected necrosis
Tube feedings preferred, post ligament of Triez
Always look for the myriad of complications

39. fin