Chapter 31: Liver Flashcards
Right hepatic artery variants
Off SMA (#1 hepatic artery variant, 20%) courses behind pancreas, posterolateral to the common bile duct
1 hepatic artery variant
Right hepatic artery off SMA
Left hepatic artery variant
Off left gastric artery (about 20%) - found in gastrohepatic ligament medially
Separates medial and lateral segments of the left lobe; attaches liver to anterior abdominal wall; extends to umbilicus and carries remnant of umbilical vein
Falciform ligament
What does the falciform ligament contain?
Remnant of umbilical vein
Carries the obliterated umbilical vein to the undersurface of the liver; extends from the falciform ligament
Ligamentum teres
Line drawn from the middle of the gallbladder fossa to IVA ; separates right and left liver lobes
Portal fissure or Cantlie’s line
Liver segments
1: caudate
2: superior left lateral
3: inferior left lateral
4: left medial (quadrate lobe)
5: inferior right anteromedial
6: inferior right posterolateral
7: superior right posterolateral
8: superior right anteromedial
Liver segment: 1
Caudate
Liver segment: 2
Superior left lateral segment
Liver segment: 3
Inferior left lateral segment
Liver segment: 4
Left medial segment (quadrate lobe)
Liver segment: 5
Inferior right anteromedial segment
Liver segment: 6
Inferior right posterolateral segment
Liver segment: 7
Superior right posterolateral segment
Liver segment: 8
Superior right anteromedial segment
Peritoneum that covers the liver
Glisson’s capsule
Area on the posterior-superior surface of liver not covered by Glisson’s capsule
Bare area
Lateral and medial extensions of the coronary ligament on the posterior surface of the liver; made up of peritoneum
Triangular ligaments
Where does the portal triad enter?
Segments 4 and 5
Where does the gallbladder lie?
Segments 4 and 5
Liver macrophages
Kupffer cells
What composes the portal triad?
Common bile duct (lateral), portal vein (posterior), and proper hepatic artery (medial); come together in the hepatoduodenal ligament (porta hepatis)
Porta hepatis clamping; will not stop hepatic vein bleeding
Pringle maneuver
Entrance to lesser sac
Foramen of Winslow
Borders of Foramen of Winslow (entrance to lesser sac)
- Anterior: portal triad
- Posterior: IVC
- Inferior: duodenum
- Superior: liver
What forms the portal vein?
Forms from superior mesenteric vein joining splenic vein (no valves)
Where dose inferior mesenteric vein drain?
Enters splenic vein
2 in liver
- 2/3 of hepatic blood flow
Portal veins
Where are L / R portal vein located?
Left: goes to segment 2, 3, 4
Right: goes to segment 5, 6, 7, 8
Arterial blood supply of the liver
Right, left, and middle hepatic arteries (follows hepatic vein system below)
What is the middle hepatic artery a branch of?
MC a branch off the left hepatic artery
Arterial supply of most primary and secondary liver tumors
Hepatic artery
How many hepatic veins are there? Where do they drain?
3 hepatic veins
- Drain into IVC
Location left hepatic vein
2, 3 and superior 4 segments
Location of middle hepatic vein
5 and inferior 6 segments
Location of right hepatic vein
6, 7, and 8 segments
What does middle hepatic vein come off of?
Left hepatic vein in 80% before going to IVC; other 20% goes directly into IVC
Drain medial aspect of right lobe directly to IVC
Accessory right hepatic veins
Where do inferior phrenic veins drain?
Also drain directly into the IVC
Liver lobe: receives separate right and left portal and arterial blood flow; drains directly into IVC via separate hepatic veins
Caudate lobe
Where is alkaline phosphatase located?
Normally located in canalicular membrane
Where does nutrient uptake occur?
Sinusoidal membrane
Usual energy source for liver; glucose is converted to glycogen and stored.
- Excess glucose converted to fat
Ketones
Where is urea synthesized?
Liver
Coagulation factors not made in the liver
von Willebrand factor and factor 8 (endothelium)
Type of vitamins stored in the liver
Liver stores large amount of fat-soluble vitamins
The only water-soluble vitamin stored in the liver
b12
Most common problems with hepatic resection
Bleeding and bile leak
Hepatocytes most sensitive to ischemia
Central lobular (acinar zone 3)
How much of the liver can be safely resected?
75%
Breakdown product of hemoglobin (Hgb -> heme -> biliverdin -> bilirubin)
Bilirubin
What improves water solubility of bilirubin?
Conjugated to glucuronic acid (glucuronyl transferase) in the liver
Where is conjugated bilirubin secreted?
Bile
- Breakdown of conjugated bilirubin by bacteria in the terminal ileum occurs
- Free bilirubin is reabsorbed and converted to this
- Excess turns urine dark like cola
Urobilinogen
What is urobilinogen released in the urine as?
Urobilin (yellow color)
free bilirubin -> urobilinogen -> urobilin
What does bile contain?
Bile salts (85%), proteins, phosopholipids (lecithin), cholesterol, and bilirubin
What determines the final bile composition?
Active (Na/K ATPase) reabsorption of water in gallbladder
Used to make bile salts / acids
Cholesterol
What improves water solubility of bile salts?
Bile salts are conjugated to taurine or glycine
What are primary bile acids (salts)?
Cholic and chenodeoxycholic
What are secondary bile acids (salts)?
Deoxycholic and lithocholic (dehydroxylated primary bile acids by bacteria in gut)
Main biliary phospholipid
Lecithin
Solubilizes cholesterol and emulsifies fats in the intestine, forming micelles, which enter enterocytes by fusing with membrane
Bile
When does jaundice occur?
When total bilirubin > 2.5
Where is jaundice first evident?
Under the tongue
What is the maximum bilirubin?
30: unless patient had underlying renal disease, hemolysis, or bile duct-hepatic vein fistula
Causes of elevated un-conjugated bilirubin
Prehepatic causes (hemolysis); hepatic deficiencies of uptake or conjugation
Causes of elevated conjugated bilirubin
Secretion defects into bile ducts; excretion defects into GI tract (stones, strictures, tumor)
Abnormal conjugation; mild defect in glucuronyl transferase
Gilbert’s disease
Inability to conjugate; sever deficiency of glucuronyl transferase; high unconjugated bilirubin -> life-threatening disease
Crigler-Najjar disease
Immature glucuronyl transferase; high unconjugated bilirubin
Physiologic jaundice of newborn
Deficiency in storage ability; high conjugated bilirubin
Rotor’s syndrome
Deficiency in secretion ability, high conjugated bilirbuin
Dubin-Johnson syndrome
All hepatitis viral agents can cause…
Acute hepatitis
What can cause fulminant hepatic failure in viral hepatitis?
Can occur with hepatitis B, D, and E (very rare with A and C)
Viral hepatitis: can cause chronic hepatitis and hepatoma
Hepatitis B, C, and D
Consequences of hepatitis A (RNA)
Serious consequences uncommon
Hepatitis B: elevated in the first 6 months; IgG then takes
Anti-HBc-IgM (c = core)
Hepatitis B vaccination serum
Have increased anti-HBs (s=surface) antibodies only
Hepatitis B: patient had infection with recovery and subsequent immunity
Increased anti-HBc and increased anti-HBs antibodies and no HBs antigens (HBsAg)
Can have long incubation period; currently most common viral hepatitis leading to liver TXP
Hepatitis C (RNA)
Cofactor for hepatitis B (worsens prognosis)
Hepatitis D (RNA)
Viral hepatitis: fulminant hepatic failure in pregnancy, most often in 3rd trimester
Hepatitis E (RNA)
MCC liver failure
Cirrhosis (palpable liver, jaundice, ascites)
Best indicator of synthetic function in patient with cirrhosis
Prothrombin time (PT)
- 80% mortality
- Outcome determined by the course of encephalopathy
- Consider urgent liver TXP listing if King’s College criteria are emt
Acute liver failure (fulminant hepatic failure)
King’s college criteria of poor prognostic indicators:
- Acetaminophen-induced ALF
- Arterial pH 6.5, creatinine > 3.4 mg/dL (300 umol/L), grade 3/4 encephalopathy
King’s college criteria of poor prognostic indicators:
- Non-Acetaminophen-induced ALF
-INR > 6.5
(or any three of the following)
- Age 40, drug toxicity or undetermined etiology, jaundice > 7 d before encephalopathy, INR > 3.5, bilirubin > 17 mg/dL (300umol/L)
What causes hepatic encephalopathy?
Liver failure leads to inability to metabolize -> get buildup of ammonia, mercantanes, and false neurotransmitters
Causes other than liver failure for encephalopathy
GIB, infection (SBP), electrolyte imbalances, drugs
May need to do what in hepatic encephalopathy
May need to embolize previous therapeutic shunts or other major collaterals
Treatment: hepatic encephalopathy
- Lactulose
- Limit protein intake (
Cathartic that gets rid of bacteria in the gut and acidifies colon (preventing NH3 uptake by converting it to ammonium), titrate to 2-3 stools/d
Lactulose
Protein intake suggested for hepatic encephalopathy
Hepatic encephalopathy: metabolized by skeletal muscle, may be of some value
Branched-chain amino acids
Gets rid of ammonia-producing bacteria from gut
Neomycin
Cirrhosis mechanism
Hepatocyte destruction -> fibrosis and scarring of liver -> increased hepatic pressure -> portal venous congestion -> lymphatic overload -> leakage of splanchnic and hepatic lymph into peritoneum -> ascites
Management of albumin with paracentesis for ascites
Replace with albumin (1g for every 100 cc removed)
Treatment: ascites (from hepatic/splanchnic lymph)
Water restriction (1-1.5 L/d), decreased NaCl (1-2 g/d), diuretics (spironolactone counteracts hyperaldosteronism seen with liver failure), paracentesis, TIPS, prophylactic antibiotics to prevent SBP (norfloxacin; used if previous SBP or current UGIB)
Why is aldosterone elevated with liver failure?
Secondary to impaired hepatic metabolism and impaired GFR
Progressive renal failure; same lab findings as preener azotemia; usually a sign of end-stage liver disease
Hepatorenal syndrome
Treatment: hepatorenal syndrome
Stop diuretics, give volume; no good therapy other than liver TXP
What are neurological changes seen with progressive liver failure?
Asterixis; sign that liver failure is progressing
What causes postpartum liver failure with ascites?
From hepatic vein thrombosis; has an infectious component
Dx / Tx: postpartum liver failure with ascites
Dx: SMA arteriogram with venous phase contrast
Tx: heparin and antibiotic
- Fever, abdominal pain, PMNs > 250 in fluid, positive cultures
- Risk factors: prior SBP, UGIB, low-protein ascites
Spontaneous bacterial peritonitis
MCC spontaneous bacterial peritonitis
E. coli (#1), pneumococci, streptococci
- Most commonly mono-organism; if not, need to worry about bowel perforation
Tx: spontaneous bacterial peritonitis
3rd-generation cephalosporins; patients usually respond within 48 hours
How do esophageal varices bleed?
Bleed by rupture
Treatment: esophageal varices
- Banding and sclerotherapy (95% effective)
- Vasopressin, octreotide
- NGT (h/o CAD)
- Propranolol (no good role acutely)
Why is vasopressin good for esophageal varices?
Splanchnic artery constriction
Why is octreotide good for esophageal varices?
Decreases portal pressure by decreasing blood flow
Has a balloon used to control variceal bleeding; risk of rupture of the esophagus (hardly used anymore)
Sengstaken-Blakemore esophageal tube
Esophageal varices: may help prevent re-bleeding; no good role acutely
Propranolol
Esophageal varices: complication of sclerotherapy
Can get stricture from sclerotherapy; usually easily managed with dilatation
Needed for refractory variceal bleeding
TIPS
Portal hypertension: pre-sinusoidal obstruction
Schistosomiasis, congenital hepatic fibrosis, portal vein thrombosis (50% of portal HTN in children)
What causes 50% of portal HTN in children?
Portal vein thrombosis
Portal hypertension: sinusoidal obstruction
Cirrhosis
Portal hypertension: post-sinusoidal obstruction
Budd-Chiari syndrome (hepatic vein occlusive disease), constrictive pericarditis, CHF
Normal portal vein pressure
Act as collaterals between the portal vein and the systemic venous system the lower esophagus (azygous vein)
Coronary veins
Leads to esophageal variceal hemorrhage, ascites, splenomegaly, and hepatic encephalopathy
Portal HTN
Can decompress portal system
Shunts
Used for protracted bleeding, progression of coagulopathy, visceral hypo perfusion or refractory ascites
- Allows integrate flow
TIPS (transjugular intrahepatic portosystemic shunt)
Low rate of encephalopathy; need to ligate left adrenal vein, left gonadal vein, inferior mesenteric vein, coronary vein, and pancreatic branches of splenic vein
Splenorenal shunt
When do you use splenorenal shunt for hepatic encephalopathy?
Used only for Child’s A cirrhotics who present just with bleeding (rarely used anymore)
When is splenorenal shunt contraindicated for hepatic encephalopathy?
Refractory ascites, as splenorenal can worsen ascites
Child’s B or C with indication for shunt
TIPS
Child’s A that just has bleeding as symptom
Consider splenorenal shunt (more durable); otherwise TIPS
Correlates with mortality after open shunt placement
Child-Pugh Score
What are the components of the Child-Pugh Score?
Albumin, bilirubin, encephalopathy, ascites, INR
Mortality with shunt: Child’s A (5-6 pts)
2% mortality with shunt
Mortality with shunt: Child’s B (7-9 pts)
10% mortality with shunt
Mortality with shunt: Child’s C (10 pts or greater)
50% mortality with shunt
Usually caused by extra-hepatic portal vein thrombosis
Portal HTN in children
MCC massive hematemesis in children
Portal HTN in children
- Occlusion of hepatic veins or IVC
- RUQ pain, hepatomegaly, ascites, fulminant hepatic failure, muscle wasting, variceal bleeding
Budd-Chiari Syndrome
Dx: budd-chiari syndrome
Angiogram with venous phase, CT angiogram; liver biopsy shows sinusoidal dilation, congestion, centrilobular congestion
Tx: budd-chiari syndrome
Porta-caval shunt (needs to connect to the IVC above the obstruction)
Can lead to isolated gastric varices without elevation of pressure in the rest of the portal system. These gastric varies can bleed.
Splenic vein thrombosis
What causes splenic vein thrombosis?
Most often caused by pancreatitis
Tx: Splenic vein thrombosis
Splenectomy if symptomatic
- Increased LFTs, increase in right lobe of liver, usually single
- Symptoms: fever, chills, RUQ pain, increased WBCs, jaundice, hepatomegaly.
- Can usually diagnose based on CT characteristics
Amebic liver abscess
Where does primary infection occur in amebic liver abscess?
Colon - amebic colitis
Risk factors: amebic liver abscess
Travel to Mexico, ETOH; fecal-oral transmission
What is serology positive for in amebic liver abscess?
Entamoeba histolytica - 90% have infection
How does ameba reach the liver to cause liver abscess?
Reaches liver via portal vein
What does culture usually reveal in amebic liver abscess?
Cultures of abscess often sterile -> protozoa exist only in peripheral rim
Tx: amebic liver abscess
Flagyl; aspiration only if refractory; surgery only if free rupture
- Forms cyst (hydatid cyst)
- Positive Casoni skin test, positive serology
- Sheep (carriers); dogs (human exposure); increase in right lobe of the liver
Echinococcus
Why do you not aspirate a hydatid cyst (echinococcus)?
Do not aspirate -> can leak out and cause anaphylactic shock
What does abdominal CT show in echinococcus (hydatid cyst)?
Ectocyst (calcified) and endocyst (double-walled cyst)
When do you do pre op ERCP in echinococcus (hydatid cyst)?
Jaundice, increased LFTs or cholangitis to check for communication with the biliary system
Treatment: echinococcus liver abscess
Pre-op albendazole (2 weeks) and surgical removal (intra-op can inject cyst with alcohol to kill organisms, then aspirate out); need to get all of cyst wall
What happens if you spill cyst contents in echinococcus?
Anaphylactic shock
- Maculopapular rash, increased eosinophils
- Sigmoid colon: primary infection, fine granulation tissue, petechiae, ulcers
- Can cause variceal bleeding
Schistosomiasis
Tx: schistosomiasis
Praziquantel and control of variceal bleeding
- account for 80% of liver abscess
- Symptoms: fever, chills, weight loss, RUQ pain, increased LFTs/WBCs, sepsis
- increase in right lobe; 15% mortality with sepsis
Pyogenic abscess
1 organism in pyogenic liver abscess
E. coli (GNRs)
What causes pyogenic abscess?
Most commonly secondary to contiguous infection form biliary tract
- Can occur following bacteremia from other types of infections (diverticulitis, appendicitis)
Dx / Tx: pyogenic liver abscess
- Dx: aspiration
- Tx: CT-guided drainage and antibiotics; surgical drainage for unstable condition and continued signs of sepsis
What causes hepatic adenomas?
Women, steroid use, OCPs
- 80% are symptomatic, 20% risk of significant bleeding (rupture)
- Can become malignant
- More common in right lobe
- Symptoms: pain, increased LFTs, hypotension (from rupture), palpable mass
Hepatic adenomas
Dx: hepatic adenoma
No Kupffer cells in adenomas, thus no uptake on sulfur colloid scan (cold)
- MRI demonstrates a hypervascular tumor
Tx: asymptomatic hepatic adenoma
Stop OCPs; if regression, no further therapy is needed; if no regression, patient needs resection of the tumor
Tx: symptomatic hepatic adenoma
Tumor resection for bleeding and malignant risk; embolization if multiple and unresectable.
- Has central stellate scar that may look like cancer
- No malignant risk; very unlikely to rupture
- MRI / CT scan demonstrates a hypervascular tumor
Focal nodular hyperplasia
Dx: focal nodular hyperplasia
Abdominal CT; has Kipper cells; so will take up sulfur colloid on liver scan
Tx: focal nodular hyperplasia
Conservative therapy (No resection)
Most common benign hepatic tumor
Hemangiomas
- Rupture rare; most asymptomatic; more common in women
- Avoid biopsy -> risk of hemorrhage
Hemangiomas
Dx: hemangiomas
MRI and CT scan show peripheral to central enhancement
- Appears as hyper vascular lesion
Tx: hemangiomas
Conservative unless symptomatic, then surgery +/ pre-op embolization; steroids (possible XRT) for unresectable disease
Rare complications of hemangioma
Consumptive coagulopathy (Kasabach-Merritt syndrome) and CHF; these complications are usually seen in children
- Congenital; women, right lobe
- Walls have a characteristic blue hue
- Complications from these cysts are rare; most can be left alone
Solitary liver cysts
Malignant liver tumors:
- metastases:primary ratio
20:1
Most common cancer worldwide
Hepatocellular carcinoma (hepatoma)
Risk factors for hepatocellular carcinoma
HepB (#1 cause worldwide), HepC, ETOH, hemochromatosis, alpha1-antitrypsin deficiency, primary sclerosing cholangitis, aflatoxins, hepatic adenoma, steroids, pesticides
Not risk factors for hepatocellular carcinoma
Primary biliary cirrhosis, Wilson’s disease
What have the best prognosis for malignant liver tumors?
Clear cell, lymphocyte infiltrative, and fibrolamellar types (adolescents and young adults)
Correlates with tumor size in malignant liver tumors
AFP level
5 year survival rate with resection in hepatocellular carcinoma
30%
Why are few hepatic tumors resectable?
Secondary to cirrhosis, portohepatic involvement, or metastases
Margins for resection in hepatocellular carcinoma
1 cm margins
Where is tumor recurrence most likely after resection of hepatocellular carcinoma?
Tumor recurrence most likely in the liver after resection
Risk factors: PVC, thorotrast, arsenic -> rapidly fatal
Hepatic sarcoma
Management: Isolated colon carcinoma metastases to liver
Can resect if you leave enough liver for the patient to survive; 35% 5-year survival rate after resection for cure
Primary liver tumors
Hypervascular
Metastatic liver tumors
Hypovascualr
