Acute Pancreatitis

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

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

Acute Pancreatitis

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

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

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

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

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

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

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

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

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

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

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%.

Clinical Presentation Acute Pancreatitis Clinical Presentation

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

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

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

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)

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

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%

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

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

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

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

Acute Pancreatitis Prognosis

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

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)

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

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

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.

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

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

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

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

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

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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