This lecture was conducted during the Nephrology Unit Grand Ground by a Sub- intern under Nephrology Division, Department of Medicine in King Saud University. Nephrology Division is NOT responsible for the content of the presentation for it is intended for learning and /or education purpose only.

ACUTE PANCREATITIS Done by : Saad Alsaawy

pancreas  It’s account for 0.1% of total body weight but has 13 times the protein-producing capacity of the liver and the reticuloendothelial system combined.  Endocrine 20%.  Exocrine 80%.  Pancreatic acinar cells zymogens pancreatic ductal cells duodenum.

physiology Meal ingestion -ve Feeback the vagal nerves. vasoactive intestinal polypeptide (VIP) gastrin-releasing peptide (GRP). secretin. cholecystokinin (CCK). Digestive proenzymesTrypsinogen to trypsin Proenzymes to Active form

The Protection mecanism.  1. protein translation into proenzymes. 2. posttranlation modification and segregation. 3. packaging with protease inhibitors. 4. acidic PH and low calcium.  Intracellular enzyme activation and pancreatic autodigestion leading to acute pancreatitis.

Etiology  Most common causes due to : 1. Gallstones. 2. Alcohol abuse.  Other causes are : 3. Post ERCP. 4. viral infection. 5. Drugs. 6. hypercalcemia and hypertriglyceridemia. 7. Abdominal trauma.

pathogenesis  By activation of the proenzymes leads to autodigestion of the pancreas through : 1. Obstruction of the main pancreatic duct or the CBD a. Gallstones. b. alcohol. 2. Chemical injury to acinar cells. 3. Infection injry to acinar cells.

4. Mechanical injury. 5. Metabolic activation of proenzymes.  Trypsin also activate the proenzyme and lead to : 1. protease damage acinar cells. 2. lipase & phospholipase produce enzymtic fat necrosis. 3. Elastase damage vessels wall and produce hemorrhage.

Clinical findings  Fever  Nausea  Vomiting  Abdominal pain  Hypovolemic shock  Hypoxemia & (ARDS)  Tetany

Clinical findings  Grey- Turner sign.  Cullen’s sign.

Complication  Pancreatic necrosis : - systemic signs occur earlier. - peripancreatic infection.  Pancreatic pseudocyst: ( 20 %) - Abdominal mass with persistence of serum amylase up to 10 days. - treatment.

Complication  Pancreatic abscess : - Abdominal pain. - high fever duo to sepsis. - neutrophilic leuckocytosis. - persistent hyperamylsemia. - diagnosis. - tratment.

Complication  Pancreatic ascites : - duo to leaking of pseudosyct. - high amylase in peritoneal fluid. - resolve spontanously.  Hemorrhagic pancreatitis.  ARDS

Laboratory Findings  Serum Amylase. - sensitivity 85%, specificity 70 %. - increase in 2-12hrs. Peak over hrs. return to normal in 2-4 days. - present in urine 1-14 days. - persistent increase > 7day.  Serum lipase. - more specific for pancreatitis. - increase in 3-6 hrs. peak over hrs. return to normal in 7-10 days. - not excreted in urine.

 Serum immunoreactive trypsin.  Neutrophilic leuckocytosis.  Hypocalcemia, and hyperglycemia.

Imaging Studies  CT scan is gold standard for pancreatic imaging.  Most accurate test for diagnosis and identifiying complication.

 Abdominal radiograph.  Abdominal Ultrasound.  ERCP.

Tratment  Bowel rest (NPO).  IV fluids.  Pain control.  Nasogastric tube.  Oxygen.

prognosis  Ranson’s criteria. (GA LAW) (C HOBBS) Initial 48 hrs. criteriaAdmission criteria Ca < 8 mg/dlGlucose > 200 mg/dl Decrease in Hematocrit < 10%Age > 55 years Pao2 < 60 mm HgLDH > 350 IU/L BUN > 8 mg/dlAST > 250 U/L Base deficiet > 4 mg/dlWBC > 16,000 cells/mm3 Fluid Sequestration > 6L

 Mortality rate.  Patient with > 3-4 criteria should be monitord in an ICU setting. %points 1 %< 3 criteria 15%3-4 40% %>7

THANK YOU