Acute Pancreatitis

dr. Tjatur Winarsanto SpPD

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
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 secretions

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%.

Acute Pancreatitis
Clinical Presentation

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

Clinical Presentation
More severe cases
Jaundice Ascites Pleural effusions generally left-sided Cullens sign bluish peri-umbilical discoloration Grey Turners 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

Unknown Source
Renal failure Head trauma Burns Postoperative

Biliary obstruction Bowel obstruction Perforated ulcer Appendicitis Mesenteric ischemia Peritonitis
Parotitis DKA Anorexia Fallopian tube Malignancies

Salivary

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 (610 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 Ransons (Severe > 3)

Ransons Score 5 on Admission
Age > 55 y Glucose >200 WBC > 16000 LDH > 350 ALT > 250 Hct > 10% decrease Calcium < 8 Base Deficit > 4 BUN > 5 Fluid Sequestration > 6L PaO2 < 60

6 after 48 hours from presentation

Ransons Criteria
3 is severe

Prognosis CT Severity Index

CT Grade
Normal Focal or diffuse enlargement Intrinsic change or fat stranding Single ill-defined fluid collection Multiple collections of fluid or gas 0 points 1 point 2 points 3 points 4 points

Necrosis Score
None 1/3 of pancreas 1/2 of pancreas > 1/2 of pancrease 0 points
2 points 4 points 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

TREATMENT
AGGRESSIVE FLUID RESUSCITATION
May require 250-500 cc/hr for first 48 hrs
6 L of fluid is sequestered in abdomen alone Third spacing can consume up to 1/3 of total plasma volume

1/3 of people die in the first phase 50% of these are associated to ARDS

PULMONARY EDEMA CHF

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

ANTIOBIOTICS
Imipenem Cipro + metronidazole

One study showed 24% of pts had fungus

Very poor prognosis

Complications Local
Necrosis
Sterile Infected - abscess

Pseudocyst Ascites Intraperitoneal hemorrhage Thrombosis Bowel infarction Obstructive jaundice

Complications Systemic
Pulmonary
Pleural effusions Atelectasis Mediastinal abscess ARDS

Gastrointestinal

PUD Erosive gastritis Blood vessel erosion Portal vein thrombosis

Oliguria Azotemia Renal artery/vein throbosis ATN

Cardiovascular
Hypotension Sudden death Pericardial effusion

Renal

Hematologic
DIC

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

fin