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
Segments
• 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 cells – liver macrophages
Portal triad – common 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
BILIRUBIN
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
Urobilinogen
• 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
BILE
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
JAUNDICE
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)
Syndromes
• 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
VIRAL HEPATITIS
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
LIVER FAILURE
Most common cause of liver failure – cirrhosis (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