Fiser Chapter 31. LIVER Flashcards
Right hepatic artery variant
Off SMA: courses behind pancreas, posterolateral to CBD
Left hepatic artery variant
Off L gastric artery: in gastrohepatic ligament medially
Falciform ligament
Separates medial and lateral left lobe, attaches liver to anterior abdominal wall, extends to umbilicus and carries remnant of umbilical vein
Ligamentem teres
Carries obliterated umbilical vein to undersurface of the liver, extends from falciform ligament
Cantlie’s line separating right and left liver
Middle of gallbladder fossa to IVC (aka portal fissure)
Couinaud’s segments
1-4 clockwise starting with caudate
5-8 clockwise (5 is inferior medial)
Glisson’s capsule
Peritoneum that vocers liver
Bare area
Posterior-superior surface not covered by Glisson’s capsule
Triangular ligaments
Lateral and medial extensions of the coronary ligament on the posterior surfact of the liver; made up of peritoneum
Where does portal triad enter
Segments IV and V
Where does the gallbladder lie
Under segments IV and V
Kupffer cells
Liver macrophages
Portal triad
CBD (lateral), PV (posterior), proper hepatic artery (medial)
Pringle maneuver
Clamp porta hepatic, will not stop HV bleeding
Entrance to lesser sac
Foramen of windslow (anterior is portal triad, posterior is IVC, inferior is duo, superior is liver)
What forms PV?
SMV joining splenic vein
IMV enters splenic vein
There are two portal veins in liver, and they may 2/3 of hepatic blood flow. Left goes to segments 2-4, right goes to 5-8.
Arterieal blood supply of liver
R, M, and L hepatic arteries (follow hepatic vein system)
Middle most commonly a branch off left hepatic
Most primary and secondary liver tumors are supplied by what blood flow?
Hepatic artery
Hepatic veins
R, M, L
R: 6-8
M: 5 and inferior 4
L: 2, 3, and superior 4
Middle HV comes into LHV before going into IVC in 80%, in remaining goes directly into IVC
Accessory R hepatic veins
Drain medial aspect of R lobe directly to IVC
Inferior phrenic veins
Drain directly into IVC
Caudate lobe blood flow
Receives separate R and L portal and arterial blood flow
Drains directly into IVC via separate hepatic veins
Where is alkaline phosphatase normal located?
Canalicular membrane
Where does nutrient uptake occur?
Sinusoidal membrane
Usual enrgy source for liver
Ketones
Glucose is converted to glycogen and stored
Excess glucose converted to fat
Where is urea synthesized
Liver
Where is vWF and factor 8 synthesized?
Endothelium
What does liver store?
Fat-soluble vitamins and B12
Most common problems with hepatic resection
Bleeding and Bile leak
Hepatocytes most sensitive to ischemia
Central lobular (acinar zone III)
How much of a normal liver can be resected?
75%
Bilirubin synthesis
Hgb -> heme -> biliverdin -> bilirubin
What does bilirubin do?
Conjugated to glucuronic acid with glucuronyl transferse in the liver, which improves bili’s water solubility
Conjugated bili is actively secreted into bile
Breakdown of conjugated bilirubin by bacteria in TI
Free bili reabsorbed andconverted to urobilinogen, and eventually released in urine as urobilin. Excess urobilinogen turns urine dark like cola
Bile contains what?
85% bile salts; proteins; phospholipids (lecithin); cholesterol; bilirubin
What determines the final bile composition?
Active (Na/K ATPase) reabsorption of water in gallbladder
What is used to make bile salts/acids?
Cholesterol
What happens to bile salts?
There are conjugated to taurine or glycine (improves water solubility)
Primary and secondary bile acids (salts)
Primary: cholic and chenodeoxycholic acid
Secondary: Deoxycholic and lithocholic (dehydroxylated primary bile acids by bacteria in gut)
Main biliary phospholipid
Lecithin
What does bile do?
Solubilizes cholesterol and emulsifies fats in the intestine, forming micelles, which enter enterocytes by fusing with membrane
At what level does jaundice occur?
Tbili > 2.5
First evident under tongue
Maximum bilirubin
30, unless patient had underlying renal disease, hemolysis, or bile duct-hepatic vein fistula
Elevated unconjugated versus conjugated bilirubin
Unconjugated: prehepatic causes (hemolysis); hepatic deficiencies or uptake or conjugation
Conjugated: Secretion defects into bile ducts; excretion defects into GI tract (stones, strictures, tumor)
Gilbert’s disease
Abnromal conjugation; mild defect in glucuronyl transferase
Crigler-Najjar disease
Inability to conjugate; sevre deficiency of glucuronyl transferase; high unconjugated bilirubin causing life threatening disease
Physiologic jaundice of newborn
Immature glucuronyl transferase; high unconjugated bilirubin
Roto’s syndrome
Deficiency in storage ability; high conjugated bilirubin
Dubin-Johnson syndrome
Deficiency in secretion ability; high conjugated bilirubin
What viral hepatitis can cause fulminant hepatic failure?
B, D, E
Very rare with A and C
What viruses can cause chronic hepatitis and hepatoma?
B, C, D
MOst common virus leading to OLT and HCC
HCV
Cofactor for HBV
D (worsens prognosis)
Virus with fulminant hepatic failure in pregnancy
E, most often in 3rd timester
Most common cause of liver failure
Cirrhosis (palpable liver, jaundice, ascites)
Best indicator of synthetic function in cirrhosis
PT
Acute liver failure (fulminant hepatic failure) mortality
80%
Outcome determines by course of encephalopathy
Consider urgent liver txp if King’s College criteria met
King’s College Criteria of Poor Prognostic Indicators
Tylenol-ALF:
- If pH < 7.3, OR
- INR > 6.5, Cr > 3.4, Grade 3/4 HE
Non-Tylenol ALF:
- INR > 6.5, OR 3 of:
- Age < 10 or > 40, drug toxicity or undetermined etiology, jaundice > 7 days before encephalopathy, INR > 3.5, bilirubin > 17
HE
Liver failure -> inability to metabolize -> buildup of ammonia, mercanatanes, false neurotransmitters
Causes other than liver failure: GIB, SBP, electrolytes, drugs
HE treatment
May need to embolize shunts or other major collaterals
Lactulose: cathartic that gets rid of bacteria and acidifies colon (preventing NH3 uptake by converting it to ammonium), titrate to 2-3 stools/day
Limit protein intake (<70 g/day)
Branched-chain aa’s (metabolized by skeletal muscle, may be of some value)
No abx unless for specific infection
Neomycin (gets rid of ammonia producing bacteria from gut), rifaximin?
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
Paracentesis for ascites
Replace with albumin
Ascites
From hepatic/splanchnic lymph
Tx: water restriction (1-1.5 L/day), decrease NaCl (1-2g/day), diuretics (spironolactone counteracts hyperaldosteronism seen with liver failure), paracentesis, TIPS, prophylactic abx to prevent SBOP (norfloxacin; used if previous SBP or current UGIB)
Aldosterone in liver failure
Elevated due to impaired hepatic metabolism and GFR
HRS
Progressive renal failure, same lab findings as prerenal azotemia, usually a sign of ESLD
Tx: Stop diuretics, give volume, no good tx other than OLT
Neurologic changes in liver failure
Asterixis; sign that liver failure is progressing
Postpartum liver failure with ascites
From HVT; has an infectious component
Dx: SMA arteriogram with venous phase contrast
Tx: Heparin and antibiotic
Fever, abd pain, PMNs >250 in fluid, positive cultures
SBP
MCC organisms in SBP
E coli
Pneumococcus
Streptococcus
If polymicrobial, worry about bowel perf
SBP risk factors
Prior SBP
UGIB (variceal hemorrhage)
Low-protein ascites
SBP tx
3rd gen cephalosporins; usually respond within 48 hr
Esophageal varices
Bleed by rupture
Tx: Banding and sclerotherapy (95% effective); vasopressin (splanchnic artery constriction) and ocreotide (decrease portal pressure by decreasing blood flow) can be used to temporize; patients with history of CAD should receive NTG while on vasopression; Sengstaken-Blakemore esophageal tube (has a balloon used to control variceal bleeding; risk of esophageal rupture so hardly used anymore); propranolol may help prevent re-bleeding but no good role acutely; can get later strictures from sclerotherapy usually easily managed with dilatation; TIPS for refractory variceal bleeding
Portal HTN: pre-sinusoidal, sinusoidal, and post-sinusoidal
Pre-sinusoidal obstruction: schistosomiasis, congenital hepatic fibrosis, PVT (50% of portal HTN in children)
Sinusoidal: cirrhosis
Post-sinusoidal obstruction: Budd-Chiari syndrome (HVT), constrictive pericarditis, CHF
Normal portal vein pressure
<12mmHg
Coronary veins in portal HTN
Act as collaterals between PV and systemic venous system of lower esophagus (azygous vein)
Portal HTN consequences
Esophageal variceal hemorrhage
Ascites
Splenomegaly
HE
Portal HTN tx
Shunts to decompress portal system: TIPS, splenorenal
TIPS uses
protracted bleeding, progression of coagulopathy, visceral hypoperfusion, or refractory ascites
allows antegrade flow
complication: HE
Splenorenal shunt
Low rate of HE
Need to ligate L adrenal vein, L gonadal vein, IMV, coronary vein, and pancreatic branches of splenic vein
Splenoreal shunt uses
Used only for Child’s A cirrhotics who present just with bleeding (rarely used anymore)
Contraindicated in patients with refractory ascites, as splenorenal shunts can WORSEN ascites
Child’s B or C with need for shunt
TIPS
Child’s A that has just bleeding
Consider splenorenal shunt (more durable), otherwise TIPS
Mortality after open shunt placement
CTP correlates
Child-Pugh Scoring
BEIAA
Bilirubin Encephalopathy INR Albumin Ascites
Child’s A: 2% mortality with shunt
Child’s B: 10%
Child’s C: 50%
Portal HTN in children
Usually caused by extra-hepatic PVT
Most common cause of massive hematemesis in children
Budd-Chiari syndrome
Hepatic vein or IVC occlusion
Dx: Angiogram with venous phase, CT angiogram; liver biopsy shows sinusoidal dilatation, congestion, centrilobular congestion
Tx: Pora-caval shunt (needs to connect to the IVC above obstruction)
RUQ pain, hepatosplenomegaly, ascites, fulminant hepatic failure, muscle wasting, variceal bleeding
Budd-Chiari syndrome
Isolated gastric varices without elevated pressure in rest of portal system
Splenic vein thrombosis.
These gastric varices can bleed
Most often caused by pancreatitis
Tx: Splenectomy if symptomatic
Diagnosis and treatment of amebic abscess
Serology and imaging (culture may be sterile, protozoa exist only in peripheral rim)
Tx: flagyl; aspiration only if refractory; surgery only if free rupture
Starts with amebic colitis, reaches R liver by PV
Dx and Tx of hydatid cyst (echinococcus)
Positive serology and Casoni skin test
CT showing ectocyst (calcified) and endocyst (double walled); do NOT aspirate (anaphylaxis)
Tx: albendazole x2 weeks, then surgical removal (intraop inject cyst with EtOH to kill organisms then aspirate out) and remove entire wall without spilling contents; preop ERCP if jaundice, transaminitis, or cholangitis to check for communication with biliary system
Maculopapular rash and eosinophilia with liver abscess
Schistosomiasis
Primary infection in sigmoid
Fine granulation tissue, petechiae, ulcers; can cause variceal bleeding
Tx: Praziquantel and control of variceal bleeding
MCC liver abscess
Pyogenic (bacterial are 80%
Fever, chills, weight loss, RUQ pain, high LFTs, high WBC, sepsis, R liver lobe abscess
Pyogenic abscess
15% mortality with sepsis
MCC pyogenic abscess
E coli
Secondary to contiguous infection from biliary tract
Can occur following bacteremia from other infections (diverticulitis and appendicitis)
Dx and Tx of pyogenic abscess
Aspiration
Tx: CT-guided drainage and abx; surgical drainage for unstable condition and continued signs of sepsis
Women with OCPs or steroid use, has R liver mass
Hepatic adenoma
20% risk rupture and bleed
5% malignant potential
CT or MRI with hypervascular tumor
No uptake of sulfur colloid (cold): adenoma (no Kupffer cells)
Uptake of sulfure colloid: FNH
Tx of hepatic adenoma
Asymptomatic: stop OCPs, if still no regression then need resection
Symptomat: resect for bleeding and malignancy risk; embolization if multiple and unresectable
Central stellate scar in liver mass
Focal nodular hyperplasia
No malignancy risk, very rare rupture
Tx of FNH
Conservative, no resection
MCC benign hepatic tumor
Hemangioma: rupture is rare (but avoid biopsy due to risk of hemorrhage), more common in women, most asymptomatic
MRI or CT with peripheral to central enhancement of a hypervascular lesion
Hemangioma
Tx of hemangioma
Conservative
If symptomatic: surgery +/- preop embolization; steroids (possible XRT) for unresectable disease
Liver mass with CHF or a consumptive coagulopathy
Kasabach-Merritt syndrome (coagulopathy with hemangioma); usually seen in children
Solitary liver cysts
Congenital; women; right lobe; walls have blue hue; rare complications, leave alone
Malignant liver tumors
20x more likely to be mets
Primary are hypervascular, metastatic are hypovascular
Most common cancer worldwide
HCC
Risk factors for HCC
HepB, HepC, EtOH, hemochromatosis, alpha-1 antitrypsin def, PSC, aflatoxins, hepatic adenoma, steroids, pesticides
(PBC and Wilson’s are NOT risk factors)
HCC types with best prognosis
clear cell
lymphocyte infiltrative
fibrolamellar (young people)
Risk factors for hepatic sarcoma
PVC, thorotrast, arsenic -> rapidly fatal
Survival after CRC liver met resection
35% at 5 years
