Acute Pancreatitis
Acute Pancreatitis (AP)
Causes:
Idiopathic, viral (mumps), medication (azathioprine and 6-MP, α methyldopa, DDI, DDC, estrogen, pentamidine, sulfas, salicylates) obstructive (divisum, SOD), metabolic (hypercalcemia, hypertriglyceridemia), alcohol, gallstones, toxins, trauma (surgery), tumor (IPMN, PanCA)
Diagnosis:
Pancreas enzyme elevation x3 above normal. Consider mesenteric ischemia, bowel perforation if amylase alone is elevated. GGT usually x2 normal in biliary pancreatitis.
Hyperlipidemia may cause a falsely low amylase level. Calcium levels may appear normal or low due to hypoalbuminemia.
Abdominal US to r/o GS. CT abdomen only if severe pancreatitis or necrosis is suspected or if pt does not improve (to r/o infection/abscess do FNA), otherwise not helpful.
Severe Acute Pancreatitis (SAP) 30% of acute pancreatitis
Ranson, APACHE II >8, multi organ failure (PaO2 ≤60, vent support, SBP <90, HR >120, Cr>2, GI bleed >500cc/24 hrs, >30% gland necrosis on contrast CT)
APACHE II score:
http://www.sfar.org/scores2/apache22.html (just punch in values)
Ranson Criteria
| Admission |
48 hrs |
Expected Mortality |
Age > 55 |
Hct drop 10% |
0-2-----------2% |
| WBC > 16,000 |
BUN incr >8 |
3/4-----------15% |
| Glucose > 200 |
Ca <8 |
5-6-----------40% |
| LDH > 350 |
Pa02 <60 |
|
| AST > 250 |
Base deficit > 4 |
|
| Fluid sequestration >6L |
|
|
Recurrent acute pancreatitis 10-30% of patients with AP
Microlithiasis #1 cause when GB is in-situ, SOD, pancreas divisum (present 8% population), periampullary diverticuli, duplication cysts, choledochocele, anomalous pancreatobiliary junction and annular pancreas, genetic mutations, chronic pancreatitis, pancreatobiliary neoplasia.
| Biliary SOD |
Pancreatic SOD |
Type I: Biliary-type pain, Elevated liver enzymes (2 x normal), Common bile duct (CBD) dilatation (> 6mm)
|
Pancreatic-type pain, Elevated pancreas enzymes (3 x normal), Dilated MPD |
Type II: Biliary-type pain, Either elevated liver enzymes or dilated CBD |
Pancreatic-type pain, Either elevated pancreas enzymes or dilated MPD |
| Type III: Biliary type pain alone |
Pancreatic-type pain alone |
| Genetic Mutations |
Cationic trypsinogen gene: autosomal dominant R122H or N29I mutation on chromosome 7q35. Risk PanCA 40%.
Cystic fibrosis transmembrane regulator: autosomal recessive, ΔF508 mutation most common.
Pancreatic secretory trypsin inhibitor: serum protease inhibitor Kazal type 1 (SPINK-1) a disease modifier, more of a role in tropical pancreatitis.
Consult medical genetics before testing.
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Management:
Patients with SAP need to be admitted to the ICU
Keep NPO until pain has subsided.
Initiate nutrition as soon as possible as patients are catabolic. Enteral nutrition to the jejunum is preferred once ileus has been ruled out.
NGT to LIS only if pt. has ileus or vomiting.
Start all patients with pancreas necrosis on Imipenem or a fluoroquinolone (less efficacy) if allergic, otherwise no need for antibiotics.
Vigurous IV hydration, keep hematocrit <43
ERCP only if pt has evidence of biliary obstruction or cholangitis.
Infected pancreas necrosis or abscess should be drained surgically, radiologically or endoscopically.
*Prognosis:
Mortality 10%, 30% SAP, >80% with infected necrosis. Half deaths are early (≤ 2 weeks, due to systemic inflammatory response and MOF), the other half late (≥ 2 weeks, due to infection).
Nagar AB, et al. Acute pancreatitis. Curr Opin Gastroenterol 2004;20:439-43
Banks PA, Practice guidelines in acute pancreatitis. Am J Gastroenterol 1997;92:377-86
Baron, TH, et al. Acute necrotizing pancreatitis. N Engl J Med 1999;340:1412-7
Bradley EL. A clinically based classification system for acute pancreatitis. Arch Surg 1993;232:619-26
Lara LF, et al. Idiopathic recurrent acute pancreatitis. MedGenMed. 2004 Nov 15;6(4):10 http://www.medscape.com/viewarticle/487185
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