1 / 14

Pancreatitis chap. 87 tintinalli’s emergency medicine

Pancreatitis chap. 87 tintinalli’s emergency medicine. Robert Moosally, DO. acute pancreatitis. Most common causes: Alcohol* Biliary dz* Drugs* Infection Inflammation Trauma Metabolic disorders *make up most of the cases. pathophysiology.

keefer
Télécharger la présentation

Pancreatitis chap. 87 tintinalli’s emergency medicine

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Pancreatitischap. 87tintinalli’s emergency medicine Robert Moosally, DO

  2. acute pancreatitis • Most common causes: • Alcohol* • Biliary dz* • Drugs* • Infection • Inflammation • Trauma • Metabolic disorders *make up most of the cases

  3. pathophysiology • Activation of digestive zymogens in pancreatic acinar cells => autodigestion of pancreas • Edema • Interstitial hemorrhage • Vascular damage • Coagulation • Cellular necrosis

  4. clinical features • Midepigastric pain or LUQ pain • Constant, boring pain that radiates to the back, flanks, chest, or lower abdomen • Pain can be exacerbated by supine position; relieved by sitting with trunk & knees flexed • Nausea/vomiting • Abdominal bloating (gut hypomobility); dec. BS • Low grade fevers • Tachycardia • Hypotension (from 3rd spacing; shock; MODS) • Pleural effusion (left sided); rarely ARDS • Cullen sign – bluish discoloration around umbilicus • Grey Turner sign – bluish discoloration of the flanks

  5. diagnosis • Labs • Amylase – pancreas/salivary glands; low levels found in fallopian tubes, ovaries, testes, adipose tissue, small bowel, lung, thyroid, skeletal muscle & certain neoplasms; some excreted by kidneys so will also see elevations in renal failure; most sensitive at 36 hrs • Lipase – pancreas; also found in gastric and intestinal mucosa; liver; heparin administration can cause a release of lipase into the serum; also cleared by the kidneys so will be elevated in renal failure; longer half-life so will be elevated even when amylase at baseline **absolute levels do NOT correlate w/ severity of dz

  6. imaging • CXR • Used to r/o other causes; if you see calcifications of pancreas then indicates more chronic dz • May see sentinel loop indicating regional ileus • May see left sided pleural or pericardial effusions • US • Used to see dilatation of biliary tree or gallstones • Pancreatic edema or pseudocysts • CT • Better to visualize severity of dz and other anatomy

  7. prognostic markers • Usually pancreatitis is a self-limiting dz • 5-10% of cases suffer significant morbidity/mortality • Ranson criteria: • Age > 55 • BS > 200 mg/dL • WBC ct > 16,000/L • SGOT > 250 units/L • LDH > 700 IU/L

  8. treatment • “rest the pancreas” • NPO (no evidence to support the NGT, other than to remind the pt that they are NPO!) • FLUID RESUSCITATION!! • Parenteral narcotics • Antiemetics • If biliary pancreatitis, then requires emergent decompression • Antibiotics only in severe dz • Peritoneal lavage/laparotomy (ascites or hemor.)

  9. disposition • Mild dz that can be managed with outpt therapy can go home; pts tolerating PO and pain controlled • All others…….admit • Pancreatic abscesses need a surgeon

  10. chronic pancreatitis • Chronic inflammation of pancreas that causes irreversible damage to its structure and function • Most cases are alcohol related; second is idiopathic • Pathophysiology • Interstitial inflammation w/ duct obstruction & dilatation leading to parenchymal loss & fibrosis • Eventual impairment of both exocrine and endocrine pancreatic functions; the latter coming later in dz • Significant malabsorption syndrome does not occur until > 90% of glandular function is lost

  11. clinical features • Abdominal pain (midepigastric radiating to back) • Nausea/vomiting • Pain worse after alcohol or fatty meals • Pts will look chronically ill • Cachectic • Steatorrhea • Clubbing • Polyuria • Stigmata of liver dz (if alcoholic pancreatitis)

  12. diagnosis • Amylase/lipase may be normal • Glucose tolerance impaired (elev. fasting BS) • Elevated bilirubin & alk phos • CXR – will see calcifications in pancreas • CT or US will show complications of chronic pancreatitis (pseudocysts or abscesses)

  13. treatment • IV narcotics • Antiemetics • Correct fluid and electrolyte abnormalities • Relief of mechanical obstruction or complications • Correction of malabsorption • Alteration of dz course • 5 year mortality rate of chronic alcoholic pancreatitis in pts who continue to drink alcohol is 50%

  14. disposition • Most chronic pancreatitis pts can go home after any complications have been ruled out/addressed • Secure follow-up • Admit if pt has intractable pain

More Related