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Liver Flashcards

1
Q

What divides the right lobe of the liver?

A

The right hepatic vein divides the right lobe into anterior and posterior segments.

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2
Q

What divides the liver into right and left lobes?

A

The middle hepatic vein divides the liver into right and left lobes. This plane runs from the inferior vena cava to the gallbladder fossa.

-Cantlie’s Line (imaginary): separates R & L lobes of the liver; line between gallbladder fossa and IVC

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3
Q

How does the Falciform ligament divide the left lobe of the liver?

A

The Falciform ligament divides the left lobe into a medial segment (IV) and a lateral part (segments II and III).

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4
Q

What supplies primary and secondary tumors of the liver?

A

Primary and secondary tumors of the liver are supplied by the hepatic artery.

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5
Q

Where is the replaced right hepatic artery (RHA) most commonly located?

A

The replaced RHA from SMA is most commonly located behind the neck of the pancreas, posterior to the portal vein, and located posterior to the cystic duct.

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6
Q

Where is the replaced left hepatic artery (LHA) typically found?

A

The replaced LHA from left gastric is typically found in the gastro-hepatic ligament (lesser omentum) medially.

-During foregut surgery, take care not to ligate a replaced left traveling in the gastrohepatic ligament.

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7
Q

What segments do the hepatic veins correspond to?

A

Left: II, III and superior IV
Middle: V and inferior IV- represents an anatomical landmark and creates a resection plan for left and right hepatic resection
Right: VI, VII, VIII

3 hepatic veins -> drain into IVC
-Medial & left hepatic vein usually merge before draining into IVC

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8
Q

What does the ligamentum teres carry?

A

The ligamentum teres carries the umbilical vein remnant.

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9
Q

What is the rate limiting step for cholesterol synthesis?

A

HMGCoA reductase is the rate limiting step for cholesterol synthesis.

HMGCoA -> (HMGCoA reductase) -> cholesterol -> (7alpha-hydroxylase) -> bile salts

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10
Q

What does bile contain?

A

Bile contains 80% bile acids, phospholipids (mainly lecithin), cholesterol, bilirubin, and proteins.

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11
Q

How are primary bile acids conjugated?

A

Primary bile acids (cholic and chenodeoxycholic) are conjugated with taurine and glycine in hepatocytes -> improves water solubility -> secreted into bile -> goes into intestines

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12
Q

Where are the majority of conjugated bile salts absorbed?

A

The majority of conjugated bile salts (80%) are absorbed using active transport in the terminal ileum.

Conjugated bile salts only absorbed in terminal ileum); the remainder are deconjugated by bacteria in the colon

Only 5 percent of bile acids escape enterohepatic circulation and end up in the stool

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13
Q

What happens to deconjugated bile acids in the colon?

A

Deconjugated bile acids form secondary bile acids (deoxycholic and lithocholic) and are absorbed in the colon, returning to the liver.

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14
Q

What is the serum to ascites albumin gradient (SAAG)?

A

SAAG is calculated as serum albumin minus ascites albumin; > 1.1 indicates portal hypertension.

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15
Q

What is Budd-Chiari syndrome characterized by?

A

Budd-Chiari syndrome is characterized by a triad of ascites, RUQ pain, and hepatosplenomegaly. Also have Jaundice.

  • Post sinusoidal portal HTN
  • Classic CT in venous phase show hypertrophy of caudate lobe (that is brighter than the rest of segments) and inhomogeneous enhancement of whole liver
  • Dx: Duplex-> No flow in hepatic veins
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16
Q

What is the treatment for Budd-Chiari syndrome?

A

Acute treatment begins with heparin and percutaneous angioplasty +/- stent.

  • There are rare reports of successful thrombolysis, however if used, it is only used in the ACUTE setting
  • Subsequent treatment depends on the primary indication for intervention. If portal HTN then TIPS. If liver failure  then liver transplant
  • Patients will need lifelong anticoagulation
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17
Q

What is the most common cause of cirrhosis worldwide?

A

The most common cause of cirrhosis worldwide is hepatitis B.

MCC of cirrhosis in US  hepatitis C (likely) vs alcohol

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18
Q

What is the most common indication for liver transplantation?

A

The most common indication for liver transplantation is hepatitis C but shifting to NASH

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19
Q

What are the Milan criteria for liver transplantation for HCC?

A

Milan Criteria: Single lesion ≤ 5 cm or ≤ 3 lesions with largest < 3 cm with no metastasis.

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20
Q

What is the treatment for simple liver cysts?

A

Simple liver cyst
- Homogenous, anechoic.
- No septations!
- If any thickening of cyst wall or nodularity, septations, loculations, papillary projections think CA not simple liver cyst
- Will not enhance on CT

Treatment is unroofing fenestration; only perform if symptomatic. Don’t do aspiration, recurs

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21
Q

What is the most common symptom of hepatic cystadenoma?

A

The most common symptoms are anorexia and abdominal fullness.

Hepatic Cystadenoma
- They are CYSTS!!
- Have ovarian like stroma
- Pre-malignant  can progress to cystadenocarcinoma
- Can be serous or mucinous
- If bloody worry about CA
- Dx: Imaging  septations, papillary projections, thickened cyst wall = KEY.
- Tx: non-anatomic Surgical hepatectomy OR enucleation
o If it is cystadenocarcinoma  hepatectomy!

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22
Q

What is the treatment for cystic intrapapillary mucinous neoplasm of the bile duct?

A

Cystic intrapapillary mucinous neoplasm of the bile duct (Intrahepatic) - similar to ipmn of pancreas
- No ovarian like stroma
- High risk of CA
- Dx: Imaging same as above but have bile duct nodules
- Tx: Surgical hepatectomy. all need IOC.

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23
Q

What is the classic CT finding for Entamoeba histolytica liver abscess?

A

Entamoeba hystolytica - Contaminated food
Mexico! Southeast Asia, Africa, India
Fecal oral route
Associated with alcoholics
amebic colitis 1st (diarrhea). Reaches liver via portal vein.
Anchovy paste appearance
More likely to only have a SINGLE abscess
Classic CT finding: fluid collection in right lobe with a THICK rim (enhancing) and peripheral edema
Cultures of the collection or stool usually DO NOT grow anything
Dx: CT, but BEST is ELISA combined with indirect hemagglutination
Tx: Flagyl. Aspiration if that fails. Surgery only for free rupture

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24
Q

How does a pyogenic liver abscess differ from an amebic liver abscess?

A

Pyogenic liver abscess is more likely to have multiple abscesses, while amebic is more likely to have a single abscess.
- Rim enhancing on CT
- Will enhance on CT
- MCC is E. Coli and Klebsiella pneumoniae

Pyogenic abscess (most common, > 80%)
-2/2 biliary tract infection (E. coli MC), GI source (diverticulitis, appendicitis)
-Tx: percutaneous drain and antibiotics

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25
Q

What is the most common cause of pyogenic liver abscess?

A

E. Coli and Klebsiella pneumoniae.

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26
Q

What is the definitive host for Echinococcus (Hydatid disease)?

A

The dog is the definitive (primary) host, while sheep are the intermediate host.

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27
Q

What are the main causes of cystic disease in humans infected with Echinococcus?

A

Humans infected: fecal-oral
E. Granulosus and Vogeli.

Alveolar disease Multilocularis does not cause cyst See pseudotumor on CT all need formal hepatic resection

Dx: ELISA + CT. Casoni’s skin test is old gold standard
- Will see mural calcifications or daughter cysts
Pre-op ERCP if jaundiced  can cause cholangitis

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28
Q

What is the diagnosis method for Echinococcus?

A

ELISA and CT. Casoni’s skin test is an old gold standard.

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29
Q

What is the treatment for Echinococcus?

A

Preoperative albendazole, followed by aspiration, injection of a sclerosing agent, and surgical removal.

Now for large simple cyst: PAIR treatment with transhepatic drain, aspiration, then injection of hypertonic saline/alcohol recommended before surgery

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30
Q

What is the diagnosis for Schistosoma infection?

A

ELISA and eosinophilia.

Schistosoma – Presinusoidal normal liver, and LFT
Travel to africa
Can cause portal HTN and esophageal varices bleed without cirrhosis
See a maculopapular rash

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31
Q

What is the treatment for Schistosoma infection?

A

Praziquantel.

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32
Q

What imaging is best for benign liver lesions?

A

MRI is the best for all benign liver lesions.

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33
Q

What are the characteristics of a hepatic adenoma?

A

Hypervascular, homogeneous, no Kupfer cells, and no uptake on sulfur colloid.

Risk of rupture/bleeding and malignancy

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34
Q

What is the first step in managing a hepatic adenoma in women?

A

Stop OCP and weight loss, then get an MRI after 6 months.

  • If persistently > 5 cm or if increase in size  resection
  • If < 5 cm and stable, or decrease in size to < 5 cm  yearly MRI
  • If found in a male  ALL NEED to be resected regardless of size or symptoms. They have a high rate of malignant transformation
    If not on OCP or steroids: resect
    NEED FORMAL RESECTION with NEGATIVE MARGINS

-Rare; OCP & androgen steroid us; 10% malignant
-Rupture risk inc with size; > 5 cm= 30% risk spontaneous bleeding
-Pain, abdominal fullness, abnormal LFTs, bleeding from rupture
-Imaging:
-CT: arterial enhancement w washout on portal phase; smooth surface w tumor capsule; no central scar
-MRI: mildly hyperintense on T1 & T2
-Tx
-Small lesions= d/c OCPs, may regress
-Larger lesions (> 4 cm) or no regression after d/c OCPs= resect
-Ruptured -> IR embolization, recover, then resect in elective setting
-Negative sulfur colloid uptake = absent Kupffer cells, from hepatocytes -> adenoma

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35
Q

What is the treatment for a bleeding hepatic adenoma?

A

Angioembolization.

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36
Q

What is the treatment for a ruptured hepatic adenoma?

A

Definitive management is exploratory laparotomy with resection.

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37
Q

What are the imaging characteristics of a hepatic hemangioma?

A

CT arterial phase shows peripheral enhancement, centripetal filling in portal venous phase, with retention of contrast in delayed phase.

-Contrast MRI in T1 is hypointense, while T2 is strong hyperintense
-Can use tagged RBC scan to dx

-NOT associated with OCP, don’t need to stop OCP if asymptomatic

-Imaging follow up is not required because its benign

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38
Q

What is the treatment for symptomatic hepatic hemangioma?

A

Resection or enucleation.
Leave alone if asymptomatic

-If bleeding or ruptured: 1st line is angioembolization
- If kassabach merit syndrome: angioembolization or steroids and vincristine

Hemangioendothelioma (infants, liver hemangomia) can lead to Kasabach-Merritt syndrome
- Arteriovenous shunting causing CHF and consumptive thrombocytopenia. Can cause DIC
- Treatment  Embolization and steroids
- Congenital papillary malformation (port of wine stain)  pulsed dye laser

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39
Q

What is focal nodular hyperplasia characterized by?

A
  • Hyperintense in arterial phase, hypodense central scar
    -CT shows well demarcated lesion with rapid arterial enhancement and central scar.
  • Venous phase, central scar is hyperintense
  • T1 shows no attenuation of central scar, T2 shows hyperintense central scar
  • Usually in periphery of liver
  • Has Kupfer cells. Hot on sulfur colloid scan
  • Caused by embryologic disturbance in liver blood flow
  • Associated with OCP use
    -The second most common liver tumor, benign, usually asymptomatic.

-2nd MC liver tumor, women 30-50 years old * Completely benign, usually asymptomatic
-Imaging
-CT: well demarcated; rapid arterial enhancement with central stellate scar
-MRI: hypointense with central scar on T1; isointense with hyperintense scar on T2
-Tx: none; no malignant potential, no bleeding risk
-Sulfur colloid uptake = functioning Kupffer cells -> FNH

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40
Q

What is the treatment for symptomatic focal nodular hyperplasia?

A

Resect only if symptomatic; no need for follow-up imaging. No need to stop OCP.

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41
Q

What is required for resection of colon cancer metastasis to the liver?

A

Needs a 1 cm margin with resection. Non-anatomical resection

  • No evidence to suggest simultaneous liver and colon resection, colon resection 1st, or liver resection 1st superiority
  • Simultaneous resection is best for young, favorable operative risk, who do not need major hepatic resection (lobectomy)
  • If doing colon resection first, do liver resection after 8 weeks with repeat imaging 1st
  • Prognostic indicator for survival after resection of hepatic-colorectal mets:
  • Disease free survival > 12 months, negative margin, tumor number < 3, CEA < 200, size < 5 cm, negative nodes

Primary liver tumor – hypervascular. Metastatic  hypovascular
Incidental colorectal CA mets to liver during colectomy for CA  if amenable and curable with just wedge resection  do it
- If needs formal resection  just Bx it

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42
Q

What is the most common primary liver tumor?

A

Hepatocellular carcinoma (HCC)

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43
Q

What correlates with tumor size in hepatocellular carcinoma?

A

AFP (Alpha-fetoprotein) correlates with tumor size; higher levels indicate worse prognosis.

MC 2/2 to Chronic liver disease from hepatitis C, alcoholic liver disease and NASH
RFs: alcoholism, smoking, aflatoxin (from aspergillus, grains), nitrites, hydrocarbons, vinyl chloride, thorotrast, hemochromatosis
All patients with cirrhosis need surveillance US +/- AFP every 6 months to screen for HCC
- If there is a lesion >1 cm or AFP > 20 then this is a positive screen  MRI or CT
MRI IS BEST, better than CT- rapid enhancement of homogenous poorly circumscribed mass with rapid wash out in portal venous phase and a psuedocapsule. Has necrotic areas
Diagnosis of HCC CAN be made with only CT/MRI in a patient WITH cirrhosis if the lesion is > 1 cm and consistent with HCC (don’t need biopsy). If doesn’t have cirrhosis, imaging CANNOT diagnose it  need biopsy here
Need CT chest to rule out lung mets MC location of mets

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44
Q

What is the first-line treatment for Child A cirrhotic patients with HCC?

A

Hepatic resection.

-Anatomic resection is treatment of choice with 1 cm margin
-Resection only attempted if negative margin possible, no mets and no vascular invasion

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45
Q

What are the Milan criteria for liver transplantation in HCC?

A

Single lesion ≤ 5 cm or ≤ 3 lesions with the largest < 3 cm, with no nodes or metastasis.

-If NOT a TXP candidate, child A/B or no cirrhosis then: 1-2 tumors, all < 5 cm, no vascular invasion: Ablation
-If > 3 tumors or any > 5 cm, no vascular invasion: TACE, embolization. Embolization can also be used as bridge to transplant
-If NOT a TXP candidate, Child C: Supportive care
-Metastasis, extrahepatic spread or vascular invasion with preserved liver: sorafenib + transarterial chemo-embolization (TACE); improves survival in patients with non-curable HCC

External beam radiation therapy indicated: unresectable disease not amenable to ablation or TACE due to tumor location.

5-year surival is 65-90% after transplantation

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46
Q

What is the treatment for Child B or C cirrhosis or portal HTN with HCC?

A

First-line treatment is liver transplantation if the patient is a candidate. No alcohol, other cancers, etc and Milan criteria

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47
Q

What is the treatment for ruptured HCC?

A

Ligation of the hepatic artery and embolization; do not perform hepatectomy.

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48
Q

What is fibrolamellar carcinoma characterized by?

A

Occurs in younger patients (median age 25), usually without cirrhosis/hepatitis B/elevated AFP.

Associated with neurotensin levels
-Tumor has central scar area: hard to distinguish from FNH. But central scar does not enhance like FNH does in venous phase
-Prognosis better than HCC

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49
Q

What is the main cause of death in fulminant hepatic failure?

A

Cerebral edema and high intracranial pressure (ICP).

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50
Q

Correction of cirrhotic hyponatremia

A

Use tolvaptan (ADH antagonist) (improves mental health scores) OR spironolactone

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51
Q

Coronary veins in portal HTN

A

Coronary veins – act as collaterals between portal vein and systemic venous system (Azygmous/hemiazygous) of lower esophagus in portal HTN

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52
Q

Cirrhotics and branched chain amino acid

A

Give Cirrhotics branched chain amino acid: metabolized by skeletal muscle-> Decreases hepatic encephalopathy

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53
Q

Hepatorenal syndrome

A

Hepatorenal syndrome – vasodilation of splanchnic vessels, release Nitric oxide CO increases, SVR and MAP decreases renal vaso-constriction and activation of RAS  decreases sodium secretion
Treatment
- Critically ill (ICU)  levophed (or vasopressin) and albumin
- Not critically ill  Terlipressin (vasopressin analog decreases splanchnic vasodilation) and albumin
o If terlipressin not available  midodrine, octreotide, albumin
- If medical management fails the next step is: TIPS!!!!!!!! Not liver TXP
Hepatorenal syndrome type I – 2 fold increase in Cr > 2.5 in < 2 weeks with oliguria – very severe, leads to death

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54
Q

Umbilical hernia in cirrhotic

A

Umbilical hernia in cirrhotic with ascites should be repaired – Do not wait, these should be repaired electively
- Do not use mesh if patient has ascites

For elective cases with no overlying skin issues:
- Child Pugh A  proceed with elective surgery
- Child B  medically optimize first then surgery
- Child C  contraindicated
If overlying skin is perforated, infected, or necrotic  emergent repair regardless of Child Pugh score primary repair without mesh if patient has ascites
Surgery for both emergent and non-emergent:
- First thing to do preop is remove ascites  Give albumin 1 gram for every 100 cc removed, use 25% (low salt) only
- If medical management of ascites fails pre-operatively the patient needs TIPS FIRST before surgery
- Alternative, if the patient is a liver transplant candidate, can repair at time of liver transplant
- Then fix coagulopathy
- Primary closure if infected or perforated

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55
Q

Vasopressin for esophageal varices, in a patient with angina

A

Also give nitroglycerin

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56
Q

Complication from esophageal varices banding/sclerotherapy

A

-Stricture
-Tx: dilation

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57
Q

Hepatic venous pressure gradient (HVPG)

A

Hepatic venous pressure gradient (HVPG) = difference in pressure in portal (wedge pressure) and systemic.
- > 5 = portal HTN. > 10 = clinically significant, > 12 = variceal bleeding may occur
- Normal HVPG – 3-4 mmHg

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58
Q

Predictors of variceal bleeding from portal HTN

A
  • Liver stiffness measured by US  < 20 kPa = low risk of variceal bleed
  • Platelets > 150k = low risk of variceal bleed
  • DO not need endoscopic screening for EV if you have above values

Every cirrhotic needs a baseline EGD to evaluate for EV

59
Q

Post partum liver failure with ascites

A

Post partum liver failure with ascites from hepatic vein thrombosis from ovarian vein thrombophlebitis (pelvic thrombophlebitis)
- Has infectious and hypercoagulability component.
- RUQ pain, jaundice, ascites
- Ovarian vein thrombosis -> IVC thrombus formation
- Dx: CT angio with venous phase
- Tx: heparin AND abx

60
Q

PV thrombosis

A

PV thrombosis can cause portal HTN and esophageal varices or ascites WITHOUT liver failure
- Presinusoidal portal HTN  LFT are normal here
- Can occur after umbilical vein catheterization in children
- Can be caused by: pancreatitis, post splenectomy, trauma, cirrhosis
- MCC of massive Hematemesis in children
- Dx: duplex
- Tx: heparin (avoid if UGIB)
- Consider shunt after 1st bleed (spleno-renal, meso-caval or REX (SMV to left portal)
- DON’T DO TIPS, does not work here

61
Q

Pyelophlebitis

A

Pyelophlebitis = infectious inflammation of portal system
- MC occurs after diverticulitis or appendicitis. In children occurs with omphalitis (umbilical cord)
- Sx: Fever and abdominal pain, can have liver abscesses
- Dx: CT shows air AND thrombus portal system.
- Tx: treat infection (appendectomy), abx, and heparin

62
Q

Portal triad:

A

Portal triad:
-Common bile duct
-Proper hepatic artery (medial)
-Portal vein (posterior)
-Runs in hepatoduodenal ligament

63
Q

-Anatomic liver segments
-Segments in liver resection:

A

-Anatomic liver segments:
-I = caudate lobe
-II-III = left lateral segments
-IV = left inferior anteromedial
-V = right inferior anteromedial
-VI-VII = right posterior lateral
-VIII = right superior anteromedial

-Segments in liver resection:
-Right= 5-8
-Left= 2-4 +/- caudate (1)
-Left lateral segmentectomy: 2-3
-Extended right: 5-8 + 4
-Extended left: 2-4 + 5 and 8

64
Q

Liver Tumor Flow Chart

A
65
Q

Systemic, portal, and collateral circulation

A
66
Q

Comparison of image findings of benign liver lesions

A
67
Q

What is the best method to prevent first bleed in large or medium size varices?

A

Endoscopic ligation is superior to beta-blockers for prevention. Best when combined.

68
Q

What are the indications for TIPS?

A

Refractory bleeding, ascites, visceral hypoperfusion, hepato-renal syndrome, hepato-pulmonary syndrome, selective cases of Budd Chiari.

  • Really good to use as a bridge for candidates of liver TXP who have refractory varices bleeding awaiting TXP
  • Non-selective shunt
  • Not meant for long term portal decompression
69
Q

When is TIPS contraindicated?

A

Encephalopathy, PCOS, Caroli’s disease, right heart failure, severe pulmonary hypertension, polycystic liver disease.

70
Q

What is the risk of TIPS in patients with MELD >19 and Child C?

A

Significant risk of hepatic failure due to shunting blood away from the liver; these patients need liver transplantation.

71
Q

In which Child classes is TIPS indicated?

A

TIPS is indicated for Child A or B.

72
Q

What does prehepatic portal hypertension not relieved by TIPS indicate?

A

Portal vein thrombosis.

73
Q

When are surgical shunts indicated?

A

For chronic and current bleeding when medical management and TIPS have failed or TIPS has thrombosed.

74
Q

In which Child classes should surgical shunts be performed?

A

Only in Child A or B; never for Child C.

75
Q

What is a selective shunt?

A

Decompresses the portal-azygous system while preserving portal inflow to the liver.

Decompress only part of the portal venous system; good for variceal bleeding but does not help ascites.

76
Q

What is a distal splenorenal shunt and its contraindication?

A

Do not perform in patients with ascites as it worsens ascites.

o Has lower hepatic encephalopathy
o Used only for Child’s A cirrhotic with JUST BLEEDING
o Technically demanding, long operation, that is not well suited for emergent indications
o Best indicated for patients who need long term decompression, in a semi-elective manner, who are NOT candidates for TXP who have recurrent variceal bleeding (once bleeding has been medically controlled!!!!)

77
Q

What is the Rex Recessus (Rex shunt) used for?

A

For children with portal vein thrombosis and refractory upper gastrointestinal bleeding.

SMV to left portal vein – reduces portal HTN and improves blood flow to liver

78
Q

What are non-selective shunts?

A

Divert all portal flow away from the liver.

Most common type of nonselective portosystemic shunt: Side to side portocaval shunt.

-Divert flow from liver to caval system
- end-to-side portacaval shunts – rarely performed and only done in emergent settings
o Has unacceptably high hepatic encephalopathy, never done anymore
o Discouraged if patient is liver transplant candidate
- side to side portacaval shunts - rarely performed and only done in emergent settings
o Increases risk of liver failure and hepatic encephalopathy
o Discouraged if patient is liver transplant candidate
- Mesocaval shunt – SMV to IVC- rarely performed and only done in emergent settings
o Avoids dissection in porta hepatis  can still do liver transplant after this
o Use H type shunt if wanting to bridge to liver TXP
All portosys¬temic shunts decrease gastroesophageal varices and reduce the risk of hemorrhage

79
Q

What is the risk associated with end-to-side portacaval shunts?

A

Has unacceptably high hepatic encephalopathy; rarely performed.

80
Q

What is the indication for mesocaval shunt?

A

To avoid dissection in porta hepatis; can still do liver transplant after this.

81
Q

What is the purpose of LeVeen or Denver shunt?

A

Used for ascites.

LeVeen or Denver shunt = peritoneovenous shunt  used for ascites
- Complications - DIC

82
Q

What are the contraindications for LeVeen or Denver shunt?

A

Severe liver failure, previous spontaneous bacterial peritonitis, previous variceal bleed, coagulopathy.

83
Q

What condition is splenic vein thrombosis associated with?

A

Sinistral portal hypertension.

84
Q

What is the MELD score threshold for elective surgery?

A

Most elective surgery is OK for Child A and B only.

85
Q

What is the MELD score threshold for liver resection?

A

MELD > 9 indicates no liver resection due to 20% mortality risk.

Liver resection only for child A only

86
Q

What is the MELD score threshold for elective general surgery?

A

MELD > 15 indicates no elective general surgery.

87
Q

What is the MELD score threshold for TIPS?

A

MELD > 19 indicates no TIPS.

Portal vein embolization only for Child A
TIPS for Child A or B only
Surgical shunt ok for Child A and B

88
Q

What is the significance of indocyanine green retention in plasma at 15 minutes?

A

Major resection of HCC should not be performed if it exceeds 15% in cirrhotic patients.

89
Q

What are hepatic stellate cells (Ito cells) responsible for?

A

They are the principal mediators of fibrosis leading to cirrhosis.

90
Q

What defines acute liver failure?

A

Encephalopathy, jaundice, coagulopathy (INR > 1.5), elevated liver function tests.

Note does not have portal hypertensive bleeding

91
Q

What defines fulminant liver failure?

A

Encephalopathy (cerebral edema) and liver injury with an inciting event < 8 weeks.

Note does not have portal hypertensive bleeding

Chronic liver failure = no cerebral edema

92
Q

What are the indications for liver transplantation?

A

Acute failure, end-stage liver disease, hepatocellular carcinoma, cholangiocarcinoma, metastatic neuroendocrine tumor.

Indications in chronic liver disease:
- Hepatic encephalopathy
- High bili with intractable pruritus
- Portal HTN (bleeding, ascites, varices, hypersplenism)
- Coagulopathy
- Poor quality of life, failure to thrive

93
Q

What are the criteria for liver transplantation in acute liver failure?

A

King’s College criteria.

94
Q

What are the contraindications to liver transplantation?

A

Active substance abuse, sepsis, extra-hepatic cancer.

95
Q

What is polycystic liver disease associated with?

A

Autosomal dominant inheritance; seen with polycystic kidney disease 95% of the time.

  • Most asymptomatic.
  • Tx: leave alone unless symptomatic then laparoscopic fenestration is BEST
  • Definitive tx is liver transplant. Combined liver/kidney required in 40%
  • Avoid OCP (estrogen) will cause it to grow - Stop OCP if using it
96
Q

What should be avoided in polycystic liver disease?

A

Oral contraceptive pills (estrogen) as they can cause it to grow.

97
Q

What are the contraindications to liver resection in HCC?

A

Child B/C, portal hypertension, esophageal varices, ascites, metastasis, insufficient liver remnant.

98
Q

What is the purpose of pre-operative portal vein embolization prior to hepatic resection?

A

Used to increase the size of the remnant liver after resection.

  • Portal vein embolization OK in Child A, contraindicated in B/C
  • MC used for right hepatectomy and extended right (trisegmentectomy). So embolize right.
  • Left and extended left does not require this because it leaves enough behind
    75% of normal liver (Right trisegmentectomy) can be safely resected without liver failure.
    Diagnostic laparoscopy 1st
99
Q

What is the peak hypertrophy time after portal vein embolization?

A

Hypertrophy peaks at 2 weeks but is reassessed in 4 weeks.

100
Q

What is the minimum liver remnant required in healthy liver and cirrhosis?

A

At least 20% in healthy liver; at least 40% in cirrhosis.

101
Q

What is the risk factor for mortality after liver resection?

A

MELD > 9 is the number one risk factor.
Also: portal HTN

102
Q

What defines portal hypertension?

A

Portosystemic venous collaterals, ascites, hepatic encephalopathy, splenomegaly.

103
Q

What is portal hypertension indicated by?

A

Hepatic vein pressure gradient (HVPG) > 6 mmHg.

104
Q

What HVPG is required for variceal rupture?

A

HVPG of 12 mmHg.

105
Q

What is the Child-Turcotte-Pugh score based on?

A

Bilirubin, albumin, prothrombin time, encephalopathy, ascites.

106
Q

What is the MELD score based on?

A

Bilirubin, INR, creatinine.

107
Q

What is the MELD score at which patients have a survival benefit for transplantation?

A

MELD score of 15.

108
Q

What are the sites of increased portal resistance in portal hypertension?

A

Presinusoidal (schistosomiasis), sinusoidal (alcoholic cirrhosis, viral hepatitis), postsinusoidal (Budd-Chiari syndrome).

-Both presinusoidal and sinusoidal elements: primary biliary cirrhosis

109
Q

What are the sites of collateral circulation in portal hypertension?

A

-Sites of collateral circulation: where splanchnic venous system meets systemic drainage
-Distal esophagus/proximal stomach: esophageal submucosal veins to proximal gastric veins
-Rectum: IMV to pudendal vein
-Umbilicus: vestigial umbilical vein to left portal vein
-Retroperitoneum: mesenteric and ovarian veins

110
Q

What is the management for acute portal hypertension?

A

-Splanchnic vasoconstrictors in acute setting = vasopressin, octreotide
-Non-selective beta-blockers for prophylaxis = nadolol, propranolol
-Endoscopic variceal banding
-Transjugular intrahepatic portosystemic shunt (TIPS): acute or recurrent variceal bleeding, refractory ascites, Budd-Chiari syndrome, hepatic hydrothorax

111
Q

What is the management of acute esophageal variceal bleeding?

A

Resuscitate, transfuse, antibiotics, intubation for airway protection, octreotide, endoscopic treatment, TIPS if uncontrolled uncontrolled (balloon tamponade temporizing measure)
-If rebleed after initial endoscopic control: 2nd endoscopy -> consider TIPS

112
Q

What are the surgical options for portal hypertension?

A

-Gastroesophageal devascularization: patients with extensive portal venous thrombosis and no portosystemic shunt options

-Esophageal transection with division and anastomosis: rarely used since TIPS

-Devascularization procedures: total devascularization of the greater curvature and upper 2/3rd of the lesser curvature and circumferential devascularization of the lower 7.5 cm of the esophagus

-Portosystemic shunts
-Selective shunts (e.g. distal splenorenal or “Warren” shunt)
-Decompress only part of portal venous system
-Good for variceal bleeding but does not help ascites
-Partial portosystemic shunts
-Type of side to side shunt where flow is calibrated by the size of the synthetic interposition graft placed between the portal vein and vena cava
-Nonselective portosystemic shunts= ascites
-Decompress the entire portal venous system
-Side to side portocaval shunt is most common
-High rate of encephalopathy and complicate later liver transplant

113
Q

What is the difference between selective and non-selective portosystemic shunts?

A

Selective shunts decompress part of the portal venous system; non-selective decompress the entire system.

114
Q

What is the management for umbilical hernias in a cirrhotic with ascites?

A

Ideally elective repair after medically controlling ascites; urgent repair for complicated cases.

-Ideally elective (use mesh); medically control ascites first -> reduce recurrence wound infection, evisceration, ascites drainage, peritonitis
-If refrac to meds: intermittent paracentesis, temporary peritoneal dialysis catheter or transjugular intrahepatic portosystemic shunt
-If transplant eligible-> repair hernia at time of transplant
-Complicated= incarcerated, strangulated, ruptured= repair urgently- no mesh, close in layers (close peritoneum), sterile dressing, aggressive ascites control postop
-Avoid intraperitoneal drain on the exam – can get hypotensive. Intermittent paracentesis standard

115
Q

What is the treatment for echinococcal cysts?

A

-Hydatid cyst; characteristic double walled cyst on CT
* Check serology
* Tx= albendazole followed by surgical excision; do not aspirate or spill -> anaphylaxis

116
Q

What are choledochal cysts associated with?

A

Anomalous biliary-pancreatic duct junction with reflux of pancreatic enzymes (long common BP duct)
-Most identified/ treated early childhood; pain, biliary obstruction, cirrhosis; malignant potential

117
Q

What is the imaging characteristic of hepatic hemangioma?

A

-MC liver tumor, M > W, = distribution in liver
-Congenital vascular malformations, generally asx
-Pain, compressive sxs; rarely hemorrhage, inflammation, or coagulopathy
-Kasabach-Merritt Syndrome = hemangioma + consumptive coagulopathy
-Imaging
-CT: hypodense pre-contrast; peripheral -> central enhancement in the arterial phase; persistent contrast on delayed series
-MRI: hypointense on T1; hyperintense on T2
-Tx
-Asx: observation (regardless of size, no risk of rupture)
-Sx: resection

118
Q

What are the imaging characteristics of hepatocellular carcinoma?

A

CT shows hypervascular lesions; hyperintense during arterial phase, hypodense during delayed phase.

-Risk factors (causes of liver inflammation): HBV, HCV, cirrhosis of any cause, inherited errors of metabolism (hemochromatosis, alpha 1 antitrypsin deficiency), aflatoxin
-CT scan: hypervascular lesions; hyperintense during arterial phase; hypodense during delayed phase
-Characteristic lesion on imaging + elevated AFP = no biopsy needed
-No PET/CT
-Lung= most common site of metastasis
-Management=
-Resection indicated for cure if solitary mass without major vascular invasion and adequate liver function (low grade with normal function or Childs A without portal hypertension)
-FLR (future liver remnant) needed?
-No cirrhosis= 25%
-Childs= 30-40%
-Portal vein embolization= strategy to hypertrophy the anticipated FLR in advance of major hepatectomy.
-No cirrhosis or Childs A and early stage= resection
-Moderate to severe cirrhosis and early stage= transplant
-Must meet Milan criteria:
-One lesion < 5 cm
-3 or fewer lesions all less than 3 cm and no gross vascular or extrahepatic spread

-Neoadjuvant chemotherapy prior to transplant
-Locoregional therapies if not candidates for surgical curative treatments
-Ablation (radiofrequency, cryoablation, microwave)= best for small lesions < 5 cm
-Arterially directed therapies – transarterial chemoembolization (TACE)
-Consider for unresectable tumors > 5 cm
-External beam radiation therapy
-Unresectable disease; not amenable to ablation or TACE due to tumor location

119
Q

What is the management for solitary hepatocellular carcinoma without major vascular invasion?

A

Resection is indicated if there is adequate liver function.

120
Q

What are the common risk factors (RF) for cholangiocarcinoma?

A

Primary sclerosing cholangitis, ulcerative colitis, bile duct stones, choledochal cysts, liver fluke infections, HBV, HCV.

121
Q

What types of cholangiocarcinoma exist?

A

-Intrahepatic or extrahepatic disease

Sclerosing or periductal infiltrating (most common), nodular, papillary, diffusely infiltrating.

122
Q

What is the prognosis for papillary cholangiocarcinoma?

A

Better prognosis with improved outcomes.

-Sclerosing & nodular: lower resectability and cure rates

-Intrahepatic
-Preop bx not necessary if radiographically and clinically suggested malignancy
-Diagnostic laparoscopy to rule out disseminated disease
-Lymph node metastasis past porta hepatis and distant metastases contraindicate resection
-Multifocal liver disease generally not amenable to resection
-Extrahepatic:
-Complete resection with negative margins and regional lymphadenectomy
-Location hilar: in order to be resectable, contralateral hemi-liver must have intact arterial/portal flow and biliary drainage uninvolved with tumor; reconstruction generally with Roux-en-Y hepaticojejunostomy
-Location distal: pancreaticoduodenectomy (Whipple)

123
Q

What is the next step for a patient with colorectal cancer and isolated liver metastasis after neoadjuvant FOLFOX therapy shows complete radiologic response?

A

Still perform hepatic resection as complete pathologic response is rare.

124
Q

What is the highest negative predictive value test for choledocholithiasis?

A

GGT (beta-glutamyl transpeptidase) -> normal GGT has 97% NPV.

125
Q

How do you manage choledocholithiasis in a patient with prior Roux-en-Y gastric bypass?

A

Transgastric ERCP or advanced double-balloon endoscopy.

126
Q

What is the significance of HCC found in a young patient without cirrhosis?

A

Fibrolamellar variant with better prognosis; recurrence is common. Marker = Neurotensin.

127
Q

Do you need to excise port sites after surgery?

A

No benefit

128
Q

What is the significance of isolated gastric varices?

A

Most commonly caused by splenic vein thrombosis secondary to pancreatitis. Treatment = splenectomy.

129
Q

What is the treatment for hemobilia from hepatic artery-biliary duct fistula?

A

Angioembolization.

130
Q

What is the management for injury to the extrahepatic biliary system?

A

For any injury to the CBD with ductal tissue loss, if unstable, perform percutaneous drainage or ligation of CBD.

131
Q

What is the treatment for distal CBD injury?

A

Roux-en-Y choledochojejunostomy.

-For any injury to the CBD with ductal tissue loss or when > 50% of the duct is involved
-If unstable patient: percutaneous drainage or ligation of CBD
-Roux-en-Y choledochojejunostomy (distal CBD injury)
-Roux-on-Y hepaticojejunostomy (proximal CBD injury): small bowel is divided & distal small bowel (Roux limb) is brought up and sutured to bile duct (end-to-side hepaticjejunostomy). End-to-side bowel-bowel anastomosis. Enterotomy is only made through the seromuscular layers.

132
Q

What is the treatment for proximal CBD injury?

A

Roux-en-Y hepaticojejunostomy.

133
Q

What is the most common cause of peritoneal dialysis catheter infection?

A

MCC by Staph aureus.

134
Q

What is the contraindication for placement of a PD catheter?

A

Active infection.

  • VP shunt and G tube are not contraindications to placement of PD catheter
  • Hernia is not a contraindication to placement, but they must be repaired during PD placement
135
Q

What is the treatment for exit site and tunneled infection of PD catheter?

A

Cephalexin and cipro (oral); get US to look for abscess. If + abscess, drain it.

136
Q

What is the treatment for peritonitis in PD catheter infection?

A

Need MRSA and pseudomonas coverage; intraperitoneal route is better than IV.

  • If fungal infxn: immediately remove catheter
137
Q

What is needed for SBP prophylaxis?

A

Previous SBP, ascitic protein < 1.0, bili > 2.5, GI bleed.

138
Q

What is the albumin treatment for a patient diagnosed with SBP?

A

1.5 g/kg at the time of diagnosis and another dose of 1 g/kg on day 3 of antibiotic treatment.

139
Q

Todani classification system and treatment by type?

A

Type III: intraduodenal or intrapancreatic dilations of the common bile duct; associated with cholangitis and pancreatitis; small- ERCP and sphincterotomy or excision; larger- transduodenal excision with reimplantation of pancreatic duct if involved

140
Q

Primary Sclerosing Cholangitis

A

-Hx of ulcerative colitis, pruritis, fatigue, abnormal liver enzymes
-Autoimmune disease that causes fibrosis and strictures in the biliary tree -> progressive cholestatic liver disease -> biliary sepsis, cirrhosis
-Cholangiography: “chain-of-lakes” or beaded appearance of bile ducts
-Bx dominant stricture because risk of cholangiocarcinoma

Tx: start with ursodeoxycholic acid= improves liver enzymes; ERCP with balloon dilation of dominant strictures= symptomatic treatment
-Definitive treatment= liver transplant; can occur in transplanted liver but less aggressive

141
Q

Lesion characteristics of CT scan

A

-Focal nodular hyperplasia: homogenous/ isodense enhancement of a hypodense lesion with an associated central scar

-Hepatic adenoma: heterogenous mass with rapid enhancement during arterial phase

-Hemangioma: low density and peripheral nodular enhancement

142
Q

Most accurate way to identify all pulmonary metastatic lesions

A

Intraoperative indocyanine green fluoroscopy
-Seen in lung at 24 hours; HB tissues retain ICG for up to two weeks

143
Q

Best test of liver function

A

Prothrombin time

Albumin indication of synthetic function

144
Q

Pneumobilia vs portal venous gas

A

Portal vein gas: patient’s usually ill- pneumatosis intestinalis, ischemic bowel; P for peripheral; flow of portal veins away from hilum

Pneumobilia: biliary tract infections, liver abscess, recent biliary instrumentation; C for CBD and Central gas patern

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