Loading presentation...

Present Remotely

Send the link below via email or IM


Present to your audience

Start remote presentation

  • Invited audience members will follow you as you navigate and present
  • People invited to a presentation do not need a Prezi account
  • This link expires 10 minutes after you close the presentation
  • A maximum of 30 users can follow your presentation
  • Learn more about this feature in our knowledge base article

Do you really want to delete this prezi?

Neither you, nor the coeditors you shared it with will be able to recover it again.



No description

Macy Martinson

on 2 August 2010

Comments (0)

Please log in to add your comment.

Report abuse

Transcript of Jaundice

stones in the gallbladder
stones in the CBD
obstruction of cystic duct induces
inflammation of gallbladder wall
infection of biliary tract 2/2 obstruction Jaundice overproduction or underclearance of bilirubin Conjugated (direct) bilirubin
water soluble
excreted in urine (dark)
normal levels 0-0.2
decreased intrahepatic excretion
hepatocellular disease (EtOH)
Dubin-Johnson, Rotor's
Drugs (OCPs)
extrahepatic biliary obstruction
stones, CA, atresia
Bilirubin metabolism most of our bilirubin comes from RBC breakdown
Hg--->bilirubin in spleen; this unconjugated bilirubin is albumin bound, not H2O soluble
dissociates from albumin in liver, conjugated and excreted in intestine
intestinal bacteria take bilirubin to urobilinogen and urobilin Unconjugated (indirect) bilirubin urine negative for bilirubin
normal level 0-0.8
excess production of bilirubin
hemolytic anemias
reduced hepatic uptake of bilirubin or impaired conjugation
Crigler-Najjer syndrome
Physiologic jaudice of newborn
Drugs (PCN, rifampin, contrast, sulfonamides) Initial approach clinical signs of jaundice when bili > 2.5
if indirect: CBC, retic count, haptoglobin, LDH, peripheral smear
if direct: US or CT to assess for obstruction intially Medical Emergencies hyperbilirubinemia is generally not urgent, excluding these select situations massive hemolysis (clostridium perfringens sepsis, falciparum malaria)
ascending cholangitis
neonatal kernicterus
fulminant hepatic failure Summary
not all jaundice is benign
many clues to etiology can be obtained from H&P (travel, HIV, EtOH, drugs, operations, etc.)
start with LFTs, CBC, coags; RUQ US
involve surgery/GI early
monitor patients closely for sx of cholecystitis and cholangitis as these can quickly lead to sepsis Ultrasound
55-91% sensitive for detection of dilated bile ducts
sensitivity increases with elevation of serum bilirubin
can demonstrate cholelithiasis; less so if stone is in common duct
advantage: cheap, non-invasive, easy to obtain ERCP
endoscopic retrograde cholangiopancreatography
directly visualize biliary tree and pancreatic duct
procedure of choice for choledocolithiasis
major advantage: therapeutic
disadvantage: pancreatitis, cholangitis, bleeding MRCP
magnetic resonance cholangiopancreatography
90-100% sensitive and specific for dx of choledocolithiasis and bile duct stones
advantage: non-invasive; diagnostic
disadvantage: not therapeutic, expensive, requires contrast EUS
endoscopic ultrasound
US transducer placed in duodenum, visualize CBD
similar accuracy to ERCP for detecting CBD stones
advantages: also detects pancreatic tumors, even small ones, no risk of pancreatitis
disadvantages: semi-invasive, not therapeutic PTC
percutaneous transhepatic cholangiography
needle passed through skin into hepatic parenchyma and advanced in bile duct, contrast injected
advantages: 100% sensitive and specific for dx, esp good in proximal obstruction or anatomical anomalies, can drain bile
disadvantages: technically limited, temporary solution Helical CT
better than a conventional CT for dx of obstruction
advantage: more comprehensive analysis of liver, abd, pelvis than US
disadvantage: cost, availability, contrast terms and diagnostic techniques Cholelithiasis "gallstones"
4 F's (female, fat, forty, fertile)
Native Americans
drugs: OCP, estrogens, clofibrate, octreotide, ceftriaxone
ileal resection; Crohn's Pathogenesis & stone types
combination of increased cholesterol saturation in bile and GB hypomotility
80% mixed stones; 10% cholesterol; 10% pigmented
black- unconj bili (chronic hemolysis) and
brown- anaerobic infxn of bile-->increased
unconj bili and calcium

Symptoms and diagnosis
episodic RUQ pain precipitated by fatty foods
afebrile, +/- RUQ pain, epigastric pain
Diagnose with RUQ US, ideally after fasting Treatment: cholecystectomy
ursodeoxycholic acid for non-surgical candidates
cholecystoenteric fistula- erosion through GB into bowel
GB cancer
Mirizzi's syndrome- cystic duct stone compresses common hepatic duct--> jaundice and biliary obstruction Choledocholithiasis Gallstone lodged in CBD
Occurs in 15% pts with gallstones
Sx: biliary pain, jaundice, nausea, pruritis
Dx: elevated direct bili, LFTs; transient spike in ALT/amylase suggests stone passage
RUQ US: dilated CBD >6mm, stone 50% time
ERCP; EUS/MRCP when suspicion low
Tx: ERCP and papillotomy with stone extraction
Complications: cholangitis, pancreatitis, cholecystitis, stricture
Cholecystitis due to stone impacting cystic duct or may be acalculous (GB stasis and ischemia 2/2 nflammatory response: TPN, sepsis, burns, opiates, immune suppression, infxn) Clinical manifestations
RUQ pain, radiates to R shoulder or back, N/V, fever
Murphy's sign: increased RUQ pain and inspiratory arrest with deep breath during palpation
leukocytosis with only mild elevation in bilirubin; if high direct bili and LFT's think choledocholithiasis Diagnosis:
RUQ US- pericholecystic fluid, GB wall thickening, sonographic Murphy's sign
HIDA scan- most sensitive test; in acute cholecysitis, radiolabeled HIDA enters CBD, not the GB
NPO, IVF, abx (zosyn, quinolone + flagyl)
E. coli, Klebsiella, enterococcus, Enterobacter
cholecystectomy within 72 hrs
ERCP to r/o choledocholithiasis in pts with jaundice or dilated CBD Complications:
cholecystoenteric fistula-->gallstone ileus
emphysematous cholecystitis- secondary infxn with gas-forming organism (clostridium)
crepitus and unconj hyperbilirubinemia Cholangitis CBD obstruction results in ascending infection proximal to the obstruction Etiology:
stone, stricture, neoplasm, fluke (clonorchis)
same bacteriology and abx as cholecystitis
Clinical sx:
Charcot's triad: RUQ pain, jaundice, fever
Reynold's pentad: triad + shock and AMS
leukocytosis, LFTs, blood clx
US, then ERCP or PTC
Broad spectrum abx (ceftriaxon or fluoroquinolone+flagyl; zosyn)
decompression via ERCP (stent, stone extraction); surgery
Full transcript