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Jaundice

By Brent Garcia,2014-05-09 20:38
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Jaundice

    Jaundice

    Hx:

    1) Age of patient (Crigler-Najjar affects newborns)

    2) Fever/chills (obstruction ; inflammation and infection)

    3) N/V (obstruction; vomiting blood? ; think cirrhosis)

    4) Location of pain and radiation (i.e. to R shoulder: Boas sign) 5) Itching (b/c of bile salts in dermis)

    6) Hemorrhoids (think cirrhosis)

    7) Appetite changes/weight loss (think obstruction, cancer) 8) Urine changes (i.e. dark, tea-colored)

    9) Bowel changes (i.e. pale stools)

    10) Recent surgeries (adhesions forming fistulas)

    11) Meds

    a. Acetaminophen overuse ; drug hepatitis

    12) Allergies (i.e. sulfa, nitrofurantoin, quinidine) 13) Recent stress (i.e. fasting, infection); think mono, herpes, Gilbert’s syndrome

    14) Social hx:

    a. Smoking hx: liver mets from lung cancer

    b. EtOH hx: alcoholic cirrhosis

    c. Drug use: needle-sharing ; hepatitis

    PE:

    1) Look under tongue (sometimes first place that jaundice appears) 2) Check eyes for kernicterus, Keyser-Fleischer rings 3) Murphy’s sign (pain upon attempted palpation of gallbladder)

    4) Courvoisier’s sign: palpable gall bladder in jaundiced patient ; think cancer of pancreatic

    head causing obstruction and dilatation of gallbladder; 5) Signs of liver cirrhosis ; esophageal varices, caput medusa, hemmorhoids

    Studies:

    1) U/S: see stones (better in gallbladder than in ducts), dilated ducts, thickened gallbladder

    2) AXR: look for stones, dilated biliary duct, or mass 3) Percutaneous Transhepatic Cholangiogram (PTC) or Intraoperative Cholangiogram (IOC):

    contrast injected into bile duct to visualize obstructions like gallstones 4) HIDA scan: radioactive substance injected IV, picked up by liver, and excreted wherever bile is

    sent; used to determine location of obstructions and leaks 5) CT/MRI

    6) ERCP: visualization and extraction of pancreatic or bile duct stones 7) CA 19-9: pancreatic tumor antigen for staging/prognosis/followup 8) CXR: check for lung metastases

    9) Bx of liver: determine if liver cancer

    Labs:

    1) Bilirubin levels: direct and indirect (non-conjugated)

    a. jaundice when bilirubin levels >2.5

    2) LFTs: AST, ALT, alkaline phosphatase, albumin

    3) PT/PTT coagulation studies

    4) UA: check urine bilirubin, urine urobilinogen, Cu levels 5) CBC, peripheral blood smear, lactate dehydrogenase: check for hemolysis 6) IgM anti HAV antibody, anti-HbsAg Ab: serologic test for hepatitis

    7) Serologic tests for CMV, mononucleosis, herpes

    8) Ceruoplasmin levels

    9) Fe studies: serum Fe, Ferritin, TIBC

    DDx:

    1) Non-bilirubin related yellowing of skin

    a. Hypercarotenemia

    i. Mechanism: drug related

    ii. Sx: yellow skin, normal bilirubin levels, sclera white

    2) Pre-hepatic (aka indirect hyperbilirubinemia)

    a. Definition: ; unconjugated bilirubin

    b. Causes:

    i. Hemolytic disorders (i.e. Sickle cell dz, thalassemia, hereditary spherocytosis)

    ii. Defect in glucoronyl transferase enzyme (needed to conjugate bilirubin)

    1. Gilbert’s syndrome

    a. Mild in enzyme

    b. Sx: usually asymptomatic

    2. Cragler-Najjar

    a. Enzyme absent

    b. Type I: autorec, severe

    c. Type II: autodom, less severe

    d. Sx:

    i. newborns, die within few years

    ii. jaundice, kernicterus if bilirubin >20mg/dl

    e. Tx: plasmapheresis, phototherapy; Type II: phenobarbital c. Labs:

    i. ; unconjugated bilirubin

    ii. UA:

    1. ;; urine bilirubin (b/c bilirubin never conjugated, so insoluble, never

    makes it to urine)

    2. ; urine urobilinogen (formed directly from heme metabolism) d. Studies:

    i. Blood smears: look for hemolysis

    3) Hepatic

    a. Causes:

    i. Viral hepatitis (A, B, C, CMV, mononucleosis, herpes)

    ii. Cirrhosis (chronic alcoholism)

    iii. Wilson’s dz

    1. Mechanism: accumulation of copper in liver, brain, cornea b/c failure of

    transport into serum

    2. Sx: liver cirrhosis, asterixis, parkisonian Sx, Kayser-Fleischer rings,

    dementia

    3. Labs: ceruloplasmin, ; Cu in liver, ; Cu in urine

    4. Tx: Cu chelators (i.e. O-penacilliamine), liver transplant

    iv. Hemochromatosis

    1. Mechanism: deposition of hemosiderin (Fe)

    2. Sx: liver cirrhosis, pancreatic fibrosis, skin pigmentation (bronze diabetes)

    3. Complications: CHF, DM, liver cirrhosis/cancer

    4. Labs: Fe studies: ; ferritin, ; serum Fe, TIBC

    5. Tx: repeated phlebotomy, Fe chelator

v. Liver cancer

    1. Sx: RUQ pain, referred pain to R shoulder, weight loss, hepatomegaly vi. Toxic drug hepatitis: i.e. acetaminophen overdose

    b. Labs:

    i. LFTs:

    1. ;;; AST, ALT

    2. ; Alkaline phophatase

    3. Albumin

    ii. PT/PTT: ; b/c coagulation factors

    iii. ; conjugated bilirubin only or ; in both conjugated/unconjugated

    iv. UA:

    1. ; urine bilirubin (b/c conjugated bilirubin is soluble and can go to urine)

    2. normal urine urobilinogen (breakdown of heme)

    4) Post-hepatic

    a. Causes:

    i. Defective excretion of conjugated bilirubin

    1. Dubin-Johnson syndrome

    a. Sx: grossly black liver, usually asymptomatic

    2. Rotor’s syndrome

    a. Sx: milder for of Dubin-Johnson syndrome, no black liver ii. Obstruction of biliary tree

    1. Choledocholithiasis ; cholangitis

    a. Mechanism

    i. Cholesterol supersaturation of bile ; precipitation ; stone

    formation ; obstruction ; inflammation of bile ducts

    ii. Mixed > cholesterol > pigment stones

    b. Risk factors: 4 F’s (fat, female, forty, fertile), hyperlipidemia

    c. Sx:

    i. Fever, pain after fatty meals, (+) Murphy’s sign, writhing

    (can’t keep still), pruritis, dark urine, pale stools, loss of

    appetite, N/V, pain RUQ and in R shoulder (Boas sign)

    ii. Charcot’s triad: jaundice, RUQ pain, fever w/chills

    iii. Reynold’s pentad: Charcot + hypotension, mental confusion

    d. Labs:

    i. LFTs: ;; alkaline phosphatase, ; AST, ALT

    ii. Amylase: ;

    iii. CBC: ; WBC

    e. Studies

    i. U/S: visualize stones, percholecystic fluid, thickened GB

    ii. AXR: visualize stones

    iii. HIDA scan

    f. Tx:

    i. Abx, NPO with IVFs

    ii. ERCP: sphincterectomy (to remove stone) + stent (to allow

    easier drainage of bile) OR stent + simple decompression

    iii. PTC: decompress

    iv. Surgery: cholecystectomy + T-tube (placed in bile duct to

    decompress, allow healing of bile duct, and act as access

    point to remove later stones if present) OR transduodenal

    sphincteroplasty (if stone in ampulla of Vater)

    2. Cancer

    a. Gallbladder polyp

    i. <1cm ; probably inflammation; F/U with U/S in one month

    ii. >1cm ; take out with open, not laproscopic, procedure

    (concern that polyp may be maligant)

    iii. Porcelain gallbladder may be premaligant

    1. calcified so if suspect, order AXR

    b. Bile ducts (Klatskin’s tumor adenocarcinoma that can invade R

    hepatic artery, so need reconstruction of that artery)

    c. Pancreas, duodenum

    d. Metastatic colorectal cancer (enlarged LN that can obstruct bilary

    tree)

    3. Stricture (iatrogenic, usually caused by previous surgery in that area)

    4. Primary sclerosing cirrhosis

    a. Mechanism: inflammation and fibrosis of biliary ducts; associated

    with UC

    b. Studies: ERCP shows “beading” pattern

    5. Annular pancreas

    a. Mechanism: ring of pancreatic tissue partially/fully obstructs

    duodenum

    b. Sx: N/V

    c. Studies: UGI, CT, endoscopy

    d. Tx: duodenojejunostomy

    6. Duodenal diverticulitis

    b. Labs:

    i. ; conjugated bilirubin

    ii. LFTs: ; alkaline phosphatase

    iii. UA: ; urine bilirubin, urine urobilinogen (b/c can’t make it into bile where it is

    converted to urobilinogen)

Whipple procedure (aka radical pancreaticduodenectomy)

    1) resection of distal stomach, distal bile duct, part of duodenum, and pancreatic head

    2) blood supply of head of pancreas and duodenum connected

Bilirubin General

    1) Function: component of bile salts, which help emulsifies digested fats; other constituents of bile

    salts are cholesterol, lecithin, and bile acids. Bile salts are reabsorbed in distal ileum and

    recycled in liver

    2) Origin: breakdown product of hemoglobin (unconjugated); extracted from blood by liver and

    conjugated by UDP-glucoronyl transferase

    3) CCK (from duodenum) and vagal stimulation ; gallbladder emptying

Other factoids:

    -watch out for R hepatic artery during cholecystectomy

    -triangle of Calot: cystic duct, cystic artery, common hepatic duct -liver has dual blood supply (hepatic artery and portal vein); lung also has dual blood supply -clamp hepatic artery, no much would happen; clamp portal vein, blood flow in hepatic artery (“arterialized” as in liver cirrhosis)

    -Zones 1, 2, 3 of liver (artery ; central vein)

    -Ascites (?pressure in portal vein ; extravasation of fluid into Space of Disse)

    1) pre-sinusoid ascites: portal vein thrombosis

    2) hepatic ascites: portal vein hypertension

3) post-sinusoid ascites: i.e Budd-Chiari syndrome: obstruction of hepatic vein, polycythemia

    -9 segments of liver divided by right, middle, and left hepatic veins -Middle hepatic vein divides liver into R and L parts

    1) R and L lobectomy

    2) R trisegmentectomy (R of falciform ligament)

    3) L lateral segmentation (L of falciform ligament)

    -don’t operate on hepatitis induced jaundice!

    -distal 1/3 of bile duct lies in pancreas

Benign Liver dz

    1) cystic dz

    2) cystadenoma

    3) infection

    a. abscess ; percutaneous drain

    b. hyatid ; abscess parasitic infection where humans eat fecal matter from dogs infected;

    anaphylaxis if spilled in peritoneum

    4) hemangioma: arteriovenous malformation of vessels

    5) adenoma

    6) focal nodular hyperplasia: hamartoma of liver (normal disorganized tissue)

Malignant Liver dz

    1) hepatic cell carcinoma

    a. ?b/c hepatitis C rates

    b. resect SEGMENT of liver

    2) colorectal cancer with mets to liver

    3) melanoma mets to liver

    4) resect any non-GI mets to liver (i.e. melanoma) and colorectal mets

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