– Liver

  Hepatic artery variants

•  Right hepatic artery off superior mesenteric artery (#1 hepatic artery variant; 20%) courses behind pancreas, posterolateral to the common bile duct

•  Left hepatic artery off left gastric artery (about 20%) – found in gastrohepatic ligament medially

  Falciform ligament – separates medial and lateral segments of the left lobe; attaches liver to anterior abdominal wall; extends to umbilicus and carries remnant of the umbilical vein

  Ligamentum teres – carries the obliterated umbilical vein to the undersurface of the liver; extends from the falciform ligament

  Line drawn from the middle of the gallbladder fossa to IVC (portal fissure or Cantlie’s line) separates the right and left liver lobes


•  I – caudate

•  II – superior left lateral segment

•  III – inferior left lateral segment

•  IV – left medial segment (quadrate lobe)

•  V – inferior right anteromedial segment

•  VI – inferior right posterolateral segment

•  VII – superior right posterolateral segment

•  VIII – superior right anteromedial segment

  Glisson’s capsule – peritoneum that covers the liver

  Bare area – area on the posterior-superior surface of liver not covered by Glisson’s capsule

  Triangular ligaments – lateral and medial extensions of the coronary ligament on the posterior surface of the liver; made up of peritoneum

  Portal triad enters segments IV and V

  Gallbladder lies under segments IV and V

  Kupffer cellsliver macrophages

  Portal triadcommon bile duct (lateral), portal vein (posterior), and proper hepatic artery (medial); come together in the hepatoduodenal ligament (porta hepatis)

  Pringle maneuver – porta hepatis clamping; will not stop hepatic vein bleeding

  Foramen of Winslow (entrance to lesser sac)

•  Anterior – portal triad

•  Posterior – IVC

•  Inferior – duodenum

•  Superior – liver

  Portal vein

•  Forms from superior mesenteric vein joining splenic vein (no valves)

•  Inferior mesenteric vein – enters splenic vein

•  Portal veins – 2 in liver; ⅔ of hepatic blood flow

  Left – goes to segments II, III, and IV

  Right – goes to segments V, VI, VII, and VIII

  Arterial blood supply

•  Right, left, and middle hepatic arteries (follows hepatic vein system below)

•  Middle hepatic artery MC a branch off the left hepatic artery

•  Most primary and secondary liver tumors are supplied by the hepatic artery

  Hepatic veins – 3 hepatic veins; drain into IVC

•  Left – II, III, and superior IV

•  Middle – V and inferior IV

•  Right – VI, VII, and VIII

•  Middle hepatic vein comes off left hepatic vein in 80% before going into IVC; other 20% goes directly into IVC

•  Accessory right hepatic veins – drain medial aspect of right lobe directly to IVC

•  Inferior phrenic veins – also drain directly into the IVC

  Caudate lobe – receives separate right and left portal and arterial blood flow; drains directly into IVC via separate hepatic veins

  Alkaline phosphatase – normally located in canalicular membrane

  Nutrient uptake – occurs in sinusoidal membrane

  Ketones – usual energy source for liver; glucose is converted to glycogen and stored

•  Excess glucose converted to fat

  Urea – synthesized in the liver

  Not made in the liver – von Willebrand factor and factor VIII (endothelium)

  Liver stores large amount of fat-soluble vitamins

  B12 – the only water-soluble vitamin stored in the liver

  Bleeding and bile leak – most common problems with hepatic resection

  Hepatocytes most sensitive to ischemia – central lobular (acinar zone III)

  75% of normal liver can be safely resected


  A breakdown product of hemoglobin (Hgb → heme → biliverdin → bilirubin)

  Conjugated to glucuronic acid (glucuronyl transferase) in the liver → improves water solubility

  Conjugated bilirubin is actively secreted into bile


•  Breakdown of conjugated bilirubin by bacteria in the terminal ileum occurs

•  Free bilirubin is reabsorbed, converted to urobilinogen, and eventually released in the urine as urobilin (yellow color)

•  Excess urobilinogen turns urine dark like cola


  Contains bile salts (85%), proteins, phospholipids (lecithin), cholesterol, and bilirubin

  Final bile composition determined by active (Na/K ATPase) reabsorption of water in gallbladder

  Cholesterol – used to make bile salts/acids

  Bile salts are conjugated to taurine or glycine (improves water solubility)

•  Primary bile acids (salts) – cholic and chenodeoxycholic

•  Secondary bile acids (salts) – deoxycholic and lithocholic (dehydroxylated primary bile acids by bacteria in gut)

  Lecithin – main biliary phospholipid

  Bile solubilizes cholesterol and emulsifies fats in the intestine, forming micelles, which enter enterocytes by fusing with membrane


  Occurs when total bilirubin > 2.5; 1st evident under the tongue

  Maximum bilirubin is 30 unless patient had underlying renal disease, hemolysis, or bile duct–hepatic vein fistula

  Elevated un-conjugated bilirubin – prehepatic causes (hemolysis); hepatic deficiencies of uptake or conjugation

  Elevated conjugated bilirubin – secretion defects into bile ducts; excretion defects into GI tract (stones, strictures, tumor)


•  Gilbert’s disease – abnormal conjugation; mild defect in glucuronyl transferase

•  Crigler–Najjar disease – inability to conjugate; severe deficiency of glucuronyl transferase; high unconjugated bilirubin → life-threatening disease

•  Physiologic jaundice of newborn – immature glucuronyl transferase; high unconjugated bilirubin

•  Rotor’s syndrome – deficiency in storage ability; high conjugated bilirubin

•  Dubin–Johnson syndrome – deficiency in secretion ability; high conjugated bilirubin


  All hepatitis viral agents can cause acute hepatitis

  Fulminant hepatic failure can occur with hepatitis B, D, and E (very rare with A and C)

  Hepatitis B, C, and D can cause chronic hepatitis and hepatoma

  Hepatitis A (RNA) – serious consequences uncommon

  Hepatitis B (DNA)

•  Anti-HBc-IgM (c = core) is elevated in the first 6 months; IgG then takes over

•  Vaccination – have ↑ anti-HBs (s = surface) antibodies only

•  ↑ anti-HBc and ↑ anti-HBs antibodies and no HBs antigens (HBsAg) → patient had infection with recovery and subsequent immunity

  Hepatitis C (RNA) – can have long incubation period; currently most common viral hepatitis leading to liver TXP

  Hepatitis D (RNA) – cofactor for hepatitis B (worsens prognosis)

  Hepatitis E (RNA) – fulminant hepatic failure in pregnancy, most often in 3rd trimester


  Most common cause of liver failurecirrhosis (palpable liver, jaundice, ascites)

  Best indicator of synthetic function in patient with cirrhosis – prothrombin time (PT)

  Acute liver failure (fulminant hepatic failure) – 80% mortality

•  Outcome determined by the course of encephalopathy

•  Consider urgent liver TXP listing if King’s College criteria are met

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Jun 24, 2017 | Posted by in GENERAL SURGERY | Comments Off on – Liver

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