Pancreatitis

Ranson's criteria

-Admission: Age WBC elevated glucose LDH AST -Within 48 hrs: Drop Hct BUN increase Calcium decrease Hypoxemia Acidosis Fluid requirement

Etiologies of pancreatitis

-Biliarylithiasis -EtOH -Trauma -Viral -Posterior duodenal or gastric ulcer -Drugs, prednisone, Hctz, methotrexate * -Cystic fibrosis -Hypercalcemia, hyperlipidemia -Pancreas is a "shock organ"- responds adversely to injury from systemic cytokines, hypovolemic, cardiogenic + septic shock, heart-lung pump ...

Most accurate imaging & associated findings in pancreatitis

-CT and MR most accurate: CT scanning is essential to accurate dx and surveillance for complications -CT and MR with IV contrast can demonstrate viability/necrosis of pancreatic tissue, hematoma, gas

Chronic pancreatitis tx

-Chronic pain difficult to treat -Eliminate EtOH -Replacement of enzymes with oral supplements -Pain meds, risky due to addiction with opiates, renal/liver toxicity NSAIDS -Endoscopic surgical correction of pancreatic ductal obstruction -Internal drainage of pseudocysts -Surgery is treatment of last resort

Mechanisms of injury in acute pancreatitis

-Ductal obstruction secondary to CBD stone -Premature activation of pancreatic proenzymes within cell leads to autodigestion of acinar cell and destruction of adjacent tissues -Mechanism of EtOH? -Systemic effects of enzymes on remote organs due to cytokine release

Pathophys of chronic pancreatitis

-Gland becomes scarred, segmental stenosis of duct -Calcification of gland typical

Findings of acute pancreatitis

-Grey-Turner's or Cullen's Sign due to retroperitoneal hemorrhage* -Left pleural effusion -Ascites -Abdominal mass from pseudocyst, hematoma or phlegmon -ARDS 2o to breakdown of alveolar capillary membranes* -Acute renal failure

When might CT changes be minimal in pancreatitis?

-In the first 24 hours of the disease CT changes may be minimal and may NOT be helpful when the diagnosis is secure. -Only perform CT early if dx is in doubt, i.e. bowel obstruction, perforation and results will change management

Prognosis of Pancreatic Pseudocyst: <4 cm vs >4 cm

< 4cm usually resolve spontaneously > 4cm persist cause chronic ↑ amylase and pose risk of recurrent pancreatitis, jaundice, infection enlargement with rupture into retroperitoneum or peritoneal cavity + hemorrhage

When should you suspect pancreatitis?

Always suspect pancreatitis in an acutely ill pt with abdominal pain /findings without other simple explanation

Tx of chronic pancreatitis

Chronic pain difficult to treat

Pancreatic ascites complication

Leads to severe peritonitis

Presentation of chronic pancreatitis

Obstructive jaundice can occur 2o to CBD obst Exocrine insufficiency> fat malabsorption, wt loss Endocrine insufficiency> diabetes mellitus May mimic pancreatic CA

Pancreatic ascites cause

Occurs after severe edematous pancreatitis or rupture of pseudocyst

Probably causes of drug induced pancreatitis

phenformin rifampicin ethacrynic acid diphenoxylate metronidazole cimetidine indomethacin chlorthalidone

Causes of increased amylase & lipase other than pancreatitis

Checking a serum amylase/lipase is key to NOT missing the diagnosis in pancreatitis

Pancreatitis CT appearance

(Compare densities of normal and inflamed intraabdominal fat w/ normal CT)

Initial tx of pancreatitis

-Large bore or multi lumen central venous catheter -IV fluid challenge -O2 (if indicated) -Foley catheter if hypotensive, azotemic -NG tube benefit is controversial most beneficial when nutrition infused distal to atonic stomach -Antibiotics may benefit as prophylaxis with necrotizing pancreatitis -PPI? Somatostatin? Don't alter course of dz -Nutritional support extremely important

Damaged acinar cell structure

-Loss of acinar cell polarity and the process of cytoplasmic fusion of lysosomes and zymogen granules -Disordered basolateral discharge of activated proteases from the acinar cell follows.

Complications & prognosis of acute pancreatitis

-May resolve spontaneously without permanent damage is minimal -May recur if more stones pass, or continued EtOH ingestion -Edematous pancreas may liquefy to become pseudocyst (which may lead to pancreatic ascites); if < 4cm usually resolve, larger lesions may bleed, rupture or become infected -Necrotic pancreas or adjacent tissue may become infected>pancreatic abscess -Necrotic pancreas or adjacent tissue may bleed i.e. hemorrhagic pancreatitis -Repeated bouts may lead to chronic pancreatitis

Tx of acute pancreatitis

-No targeted treatment available to heal pancreas -ERCP with stone extraction if gallstone impacted in Common Bile Duct -NPO, any food intake stimulates pancreatic exocrine secretion via secretin -Somatostatin can decrease exocrine secretion -IV fluid replacement 3rd space losses -Nasogastric suction for gastric ileus/obstruction -IV nutritional support when dz persists> 3 days -Treat infection with antibiotics/drainage of fluid or pus collections, surgical debridement of nonviable tissue

Presentation of pancreatitis

-RUQ-epigastric-LUQ-back pain pt sitting upright with thoracic spine flexed -Nausea-emesis -Ileus -Fever, tachycardia, 3rd space losses -May present as mild discomfort (subtle) or abdominal catastrophe with peritoneal tenderness and shock state

Lab findings of acute pancreatitis

-Serum Amylase (also in salivary glands and commonly increased in renal failure) -Lipase remains elevated longer than amylase -LFT elevation suggestive/not diagnostic of biliary pancreatitis or any other pancreatitis -Albumin decreased 2o to malnutrition and inflammatory leakage from damaged capillaries -Obstructive pattern conjugated hyperbilirubinemia, due to CBD stone or edema around CBD

Tx of pancreatic pseudoycyst

-establishing drainage into stomach or small intestine -Must be drained externally if infected (abscess)

APACHE criteria

-physiology: temperature BP HR PaO2 pH [Na+] [K+] Creat Hct WBC Glascow coma score [HCO3-] -Age points -Chronic health points

Pancreatic ascites tx

Can be treated with peritoneal dialysis

Normal acinar cell ultrastructure

Cytoplasmic processing of the proenzymes is depicted, with apical discharge into the acinar ductule by means of zymogen granule exocytosis

Causes of Chronic pancreatitis

Majority secondary to EtOH Cystic fibrosis, developmental abnormalities, hypertriglyceridemia

Lab finding of pancreatic ascites

Peritoneal fluid c high amylase-lipase levels

Why is US not the best imaging modality for pancreatitis?

US often disrupted by overlying gas, suitable for detection of gallstones and for following large fluid collections

Why is risk stratification beneficial?

allows for more accurate planning of management, appropriate monitoring, imaging, duration of hospitalization

Use of APACHE criteria

assessing severity (Acute Physiology and Chronic Health Evaluation)

Use of Ranson's criteria

assessing severity and outcome

Prognostic criteria for acute pancreatitis

incorporate a variety of inputs to assist prediction of severity of disease, duration of illness and morbidity-mortality

Definite causes of drug induced pancreatitis

thiazides azathioprine tetracyclines sodium valproate furosemide estrogens corticosteroids sulphonamides