Acute Pancreatitis

Definition: Acute pancreatitis consists of inflammation of the pancreas and peripancreatic tissue from activation of potent pancreatic enzymes within the pancreas, particularly trypsin.

Acute Pancreatitis Causes:

    • EtOH abuse

    • Gallstones

ETOH and gallstones account for 70% - 80% of all cases.

    • Idiopathic

    • Blunt trauma to abdomen

    • ERCP, postop. biliary tract surgery

    • Hypertriglyceridemia, apolipoprotien CII deficiency

    • Hypercalcemia

    • Acute fatty liver of pregnancy

    • Viral hepatitis, mumps, echovirus, coxsackie virus,EBV, CMV, measles, ascariasis, Mycoplasma pneumoniae, Salmonella, Campylobacter, MAC, and Mycobacterium tuberculosis.

    • Penetrating PUD

    • Pancreas divisum, pancreatic CA, sphincter of Oddi dysfunction,

    • Scorpion venom

    • Drugs: azathioprine, 6MCP, thiazides, furosemide, sulfonamides, tetracyclines, estrogen, valproic acid, pentamidine, ddI, AZT, methyldopa, 5-ASA, sulindac, octreotide and corticosteroids.

  • Drugs probably associated with acute pancreatitis include chlorothiazide and hydrochlorothiazide, methandienone, metronidazole, nitrofurantoin, phenformin, piroxicam, procainamide, colaspase, chlorthalidone, combination cancer chemotherapy drugs (especially asparaginase), cimetidine, cisplatin, cytosine arabinoside, diphenoxylate, and ethacrynic acid.

Clinical Features: acute onset of epigastric abdominal pain, n/v, exacerbated by food intake. Systemic manifestations can include fever, SOB, altered mental status, anemia, and electrolyte imbalances.

Ranson's criteria: for Alcoholic Pancreatitis.

    • At presentation GA LAW

    • Age > 55, glucose > 200, WBC > 16,000, AST > 250, and LDH > 350

    • During the initial 48 hours: C HOBBS

    • Calcium < 8 mg/dL

    • Hct drop > 10%

    • PO2 < 60 mm Hg

    • Base deficit > 4

    • BUN increase > 5

    • Sequestration (third space fluid) > 6 L

Mortality: 0 - 2: <5%, 3 - 4: approx 15%, 5 - 6: approx 40%, 7 - 8: approx 100%.

Labs/Dxtic: CBC, CMP, LFTs, Sr. amylase, Sr. lipase (elevations of x 2 - 3 times the upper limit of normal), aPTT, PT/INR, Lipids, Hepatitis serology, T&C, AXR, CXR, ECG, troponin-I, U/S abdomen.

Pt's with renal impairment have elevated enzymes at baseline from impaired clearance.

Imaging: Dual-phase (pancreatic protocol) CT scanning. It is useful in the initial evaluation of severe acute pancreatitis and is considered the gold standard for diagnosis. It is usually reserved for Pts with prolonged and severe sx, or when the dx is not clear.

MRI with gadolinium can also be used but with less efficacy.

MRCP useful to detect biliary source for pancreatitis before ERCP is performed.

DDX:

    • Gastritis

    • PUD

    • Acute cholecystitis

    • Inferior MI

    • SBO

    • Mesenteric ischemia/infarction

    • Biliary colic

    • Pneumonia

Complications: Pseudocyst, abscess, inf, pancreatic necrosis, splenic/mesenteric/portal vessel rupture or thrombosis. Pancreatic ascites, pancreatic pleural effusion, DM, ARDS, sepsis, MOF, DIC, encephalopathy, severe hypocalcemia.

Tx:

    • NPO

    • IV access. Aggressive IVF, cyrstalloid and colloid. Monitor electrolytes, glucose.

    • Analgesia. Dilaudid is often use. Other are meperidine. PCA pump is frequently necessary for adequate relief of pain.

    • Hemodynamic unstable Pts go to ICU.

    • UO, hemodynamic parameters

    • TPN if resolution is slow (around 7 days) or if an ileus is present. Enteral nutriton - jejunal feeds, beyond ligament of Treitz is usually safer and more cost-effective than TPN.

    • Acid suppression: Protonix.

    • Prophylactic ABx is not necessary in the abscence of any signs or symptoms of systemic infection.

    • ERCP and biliary sphincterotomy done within 72 hours of presentation can improve outcome of severe gallstone pancreatitis in the presence of elevated LFT and/or dilated common bile duct. This is from reducing biliary sepsis rather than improving pancreatic inflammation.

Tx Complications:

    • Surgical debridement. Carbapenems or a combination of a fluoroquinolone and metronidazole have good penetration into necrotic tissue. CT-guided percutaneous aspiration for gram stain and culture can confirm the Dx of infected necrosis.

    • Pseudocysts presence is indicated by persistent pain and high amylase levels. Asymptomatic pseudocysts are follow up with serial imaging studies, and generally resolve within a few weeks. Decompression of infected or symptomatic pseudocyst can be done by percutaneous, endoscopic, or surgical techniques (marsupialization).

    • Infection. Potential sources of fever include infected pseudocyst, abscess, pancreatic necrosis, cholangitis, and aspiration pneumonia. Obtain cultures, continue with broad spectrum antimicrobials. In the absence of fever or other clinical evidence of infection, prophylactic antimicrobial therapy has no clear role in acute pancreatitis.

    • Pulmonary complicatons. Atelectasis, pleural effusion, pneumonia, and ARDS can develop in severely ill patients.

    • Renal failure. Severe intravascular volume depletion or acute tubular necrosis can cause renal failure.

    • Metabolic complications include hypoglycemia, hypomagnesemia, and hyperglycemia. GI bleeding from acute stress gastritis.