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Acute Pancreatitis

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

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Acute Pancreatitis

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  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 • 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. Acute Pancreatitis Clinical Presentation

  17. Clinical Presentation • Clinical • 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 86-100% 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 0 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 0 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, 297-306.

  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 • 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

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