Liver Review

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Liver Review

• Vic Vernenkar, D.O.
• St. Barnabas Hospital
• Bronx, NY

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Major Structures and Landmarks

• Glissons capsule the peritoneal lining that
  surrounds the liver.
• Bare area posterior surface of the liver not
  covered.
• Coronary ligaments reflections of peritoneum on
  the posterior surface.

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Major Structures and Landmarks

• Triangular ligaments lateral extensions of the
  coronary ligaments.
• Falciform from umbilicus to diaphragm, contains
  obliterated umbilical vein.
• Ligamentum teres, extends from falciform on
  undersurface of liver.

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Anatomy

• Eight segments, based on arterial and portal
  venous inflow.
• Segment 1 is the caudate lobe of the liver.
• Segments 2-4 are segments of the left lobe
  resected during left hepatic lobectomy.
• Segments 5-8 are segments of the right lobe
  resected during right hepatic lobectomy.

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Segments
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Anatomy

• Falciform ligament does not divide right and left
  lobes of liver, the portal fissure or Cantlies
  line is a plane passing from the left side of the
  gallbladder fossa to the left side of the IVC. It
  defines the physiologic division between left and
  right lobes of liver.
• It does separate medial and lateral segments of
  left lobe

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Anatomy

• A right trisegmentectomy includes a resection of
  the right lobe plus segment 4.
• A left lateral segmentectomy includes resection
  of segments 2 and 3 to the left of the falciform.
• Resection of 80 of parenchyma is compatible with
  life.

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Anatomy

• Portal vein is a valveless vein formed by SMV and
  splenic vein behind head of pancreas.
• Passes posteriorly to the bile duct and hepatic
  artery in the hepatoduodenal ligament.
• 75 of livers blood supply.

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Anatomy

• Portal vein drains blood from the small and large
  intestines, stomach, spleen, pancreas,and
  gallbladder.
• The portal trunk divides in to 2 lobar veins, the
  right drains the cystic vein, the left receives
  umbilical and paraumbilical veins that enlarge to
  form the caput medusae. The coronary vein drains
  the distal esophagus, which also enlarge in PHTN.

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Anatomy

• Common hepatic artery arises from the celiac
  artery and becomes the proper hepatic artery
  after the GD branches.
• Passes medial to the bile duct and anterior to
  portal vein.
• Bifurcates into right and left hepatics in liver
  parenchyma.
• Can come off SMA (right) or Left gastric (left).
• Pringle maneuver.

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Infections of Liver

• Pyogenic liver abscesses (80 of all liver
  abscesses).
• Routes of infection are portal, ascending biliary
  tree, bacteremia via hepatic artery, direct
  extension (appendicitis), primary infection post
  trauma.
• Intra-abdominal infection most common
  identifiable source (biliary, colonic).
• ABX plus drainage, look for source.

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Infections of Liver

• Amebic Liver abscess, entamoeba histolytica.
• Via portal venous system after intestinal
  infection after a trophozoite is ingested.
• Contains necrotic tissue and blood, anchovy
  paste.
• Right lobe (80), solitary (80).
• CT scan (? One?) Antibody test specific.
• Non surgical, Flagyl. Surgery if rupture or
  secondary infection.

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Infections of Liver

• Hydatid Liver Cysts are rare liver cysts, right
  lobe, echinococcal, dogs that eat sheep
  (carrier).
• Vague abdominal pain, jaundice.
• Ct characteristic (calcified wall), ELISA test
  for antibody gt90, eosinophilia (10-30).
• Surgical drainage, hypertonic saline, removal of
  cyst wall, dont spill it!? anaphylaxis.
• Mebendazole

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Benign Tumors

• Hemangiomas (most common). Symptomatic, Surgical.
  Rupture rare, most asympt.Women.
• Adenomas (exclusively in women 30-50, OCP risk
  factor). 10 malig trans, rupture. Surgical.
• Focal nodular hyperplasia (FNH).Women 20-50,
  stellate scar on CT. Kupffer cells on scan.Non
  surgical.
• Simple Cysts. Surgical if sympt, rupture,
  infection, bleed, or suspicious. Unroof, oversew.
• Polycystic liver disease associated with renal
  failure. Women 30-80, 50 PC kidneys as well.

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Malignant Tumors

• Hepatocellular carcinoma (HCC) most common, men,
  40-70. Risks cirrhosis, Hep B, Hep C,
  carcinogens, hemachromatosis, tyrosinemia,
  glycogen storage, Wilsons, adenoma,
  schistosomiasis, alpha-1 antitrypsin deficiency,
  blood group B.

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Malignant Tumors

• Dx AFP (elevated 40-70), US, CT, MRI
• TX 5-y survival 31 for resectable tumors. With
  no treatment, 1-4 months,11 operative mortality,
  cirrhosis is the limiting factor, recurrence 50,
  so transplant an option.
• Chemo is no benefit, transarterial embolization,
  ethanol injection may help.

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Malignant Tumors

• Liver metastases are most common tumors of liver!
  Much more frequent than primary tumors.
• Colon, lung, breast, melanoma, carcinoid, renal
  cell.
• DX CEA a reliable indicator for recurrence of
  colon cancer previously treated. CT scan, IOUS.

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Malignant Tumors

• TX Liver resection other than for colon cancer
  show no reliable benefit.
• 5-y survival post resection 30-35(colorectal).
  Untreated lt5.
• 5 operative mortality.
• Size, number, location, extent of primary tumor,
  resectable lesions are a small minority of
  patients. If mets to other areas of body,
  contraindicated.

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Malignant Tumors

• Hepatoblastomas are primary malignant tumors of
  liver seen in boys younger than 2 years old.
• Cholangiocarcinomas are primary malignant tumors
  of biliary ductal epithelium, can present as
  intrahepatic or extrahepatic lesions.

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Portal Hypertension
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Background

• Portal pressure gradient 12 mmHg or more
• Often associated with varices and ascites.
• Many conditions are associated with it, the most
  common being cirrhosis of the liver.

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Causes of Portal HTN
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Four Major Consequences

• Ascites
• Portosystemic venous shunts and varices.
• Congestive splenomegaly
• Hepatic encephalopathy

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Mortality/Morbidity

• Variceal hemorrhage most common complication
• 90 with cirrhosis develop varices.
• 30 of these bleed.
• The first episode is estimated to carry a
  mortality of 30-50.

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Pathophysiology

• PFR, where P is pressure gradient thru the
  portal system, F is the volume of blood flowing
  thru the system, R is the resistance to flow.
• Changes in either F or R affect the pressure.
• In most types of portal hypertension, both flow
  and resistance are altered.

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History

• Directed towards determining the cause, the
  presence of complications of portal hypertension.
• Jaundice, transfusions, IVDA, pruritis,
  hereditary liver disease, ETOH?
• Hematemesis, melena, mental status, abdominal
  girth, pain, fever, hematochezia?

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Physical

• Signs of portosystemic collateral formation.
• Dilated veins in abdominal wall
• Caput medusa
• Rectal hemorrhoids
• Ascites
• Umbilical hernia

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Signs of Liver Disease

• Ascites
• Jaundice
• Palmar erythema
• Asterixis
• Testicular atrophy, gynecomastia
• Muscle wasting, Dupuytren contracture
• Splenomegaly

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Caput Medusa
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Lab Studies

• LFTs
• PT/PTT
• Albumin
• Hepatitis serology
• Platelets
• ANA, Antimitochondrial antibodies
• Alpha 1-antitrypsin deficiency

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Imaging Studies

• Duplex is safe, noninvasive. Demonstrates portal
  flow, portal vein thrombosis, splenic vein
  thrombosis
• Nodular liver surface, splenomegaly, presence of
  collateral circulation.
• Limitations include meals, meds, sympathetic
  nervous system affect flow.

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Imaging Studies

• CT scan when US inconclusive
• Look for collaterals from portal system
• Dilatation of the vena cava suggests portal
  hypertension.
• Limitations include not being able to use IV
  contrast in allergic patients or with renal
  failure.

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Incidental Finding on Barium Swallow
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Procedures

• Hemodynamic measurement of pressure, usually not
  performed due to invasive nature. Measures
  hepatic venous pressure gradient (HVPG). Similar
  to Swan Ganz, where balloon is inflated measuring
  wedged hepatic venous pressure, minus the
  unoccluded pressure is the HVPG.

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Procedures

• Endoscopy is performed to screen for varices.
• Gastroesophageal varices confirms diagnosis of
  portal hypertension, absence does not rule it
  out.
• Many times an incidental finding when scoped for
  something else.

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Varices on EGD
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Varix Banding
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Medical Care

• Treatment is directed at cause.
• Emergent treatment
• Primary prophylaxis
• Elective treatment

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Emergent Treatment

• Bleeding from varices ceases spontaneously in
  40. Rebleed in 40 within 6 weeks.
• Following resuscitation, treatment includes
  control of bleeding, prevention of recurrence,
  blood replacement, avoid over expansion of volume
  status.
• Diagnose source of bleed, specific treatment of
  bleeding lesion.

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Emergent Treatment

• All patients with cirrhosis and upper GI bleed
  are at risk for severe bacterial infections,
  which are associated with early rebleed.
• Use of antibiotics shown to increase survival,
  decrease rate of infection.
• Thus prophylactic use of antibiotics in acute
  bleeding is recommended.

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Pharmacologic Therapy

• Somatostatin-decreases portal flow, splanchnic
  vasoconstriction.
• Octreotide- 50mcg/h shown to reduce complications
  of bleeding after sclerotherapy.
• Vasopressin- reduces blood flow to all splanchnic
  organs, decreases portal pressure, venous blood
  flow. Use nitroglycerin with it! Its the most
  potent splanchnic vasoconstrictor.

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Endoscopic Therapy(EST, EVL)

• Hemostasis in 80, declines to 70 at day 5 due
  to very early rebleeding.
• No more than 2 sessions before deciding on TIPS
  or surgery.
• Complications include fever, stricture,
  perforation, mediastinitis, ulceration, pleural
  effusion.
• EVL and EST comparable in control of bleeding
• EST associated with more complications.

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Minnesota Tube

• Balloon tamponade only in massive bleeding as a
  temporizing measure.
• Complications
• Has 4 lumens, 1 for gastric aspiration, 2 to
  inflate the balloons, 1 above the esophageal
  balloon to prevent aspiration.
• Usually only need to inflate gastric balloon.

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Sengstaken Tube
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Prophylaxis

• Beta-blockers (propanolol, nadolol) are non
  cardioselective, reduce portal and collateral
  blood flow. Also reduces cardiac output,
  splanchnic vasoconstriction.
• First bleeding rates significantly reduced,
  mortality rates lower as well

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Prophylaxis

• No role for sclerotherapy in primary prophylaxis.
• EVL is more effective than no treatment to
  prevent first bleed. Similar efficacy to
  beta-blockers, with more adverse effects.
• Not recommended for primary prophylaxis except
  perhaps in patients with very large varices.

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Elective Treatment

• This is for prevention of rebleeding (2 year
  recurrence rate of 80).
• Propanolol and nadolol, reduce rebleed, increase
  survival.
• Beta blockers vs sclerotherapy have comparable
  rates of prevention
• EVL is considered treatment of choice in
  prevention of rebleeding, may combine with drugs.

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Surgical Treatment (Shunts)

• Total Portosystemic shunts include any shunt
  larger than 10mm between portal vein and IVC.
  Includes Eck (end to side) and side to side
  portocaval shunts.
• Eck fistula controls bleeding, but ascites
  unrelieved.
• Side to side controls bleeding and ascites, but
  encephalopathy a problem (40-50).

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Surgical Shunts

• Partial portal systemic shunts reduce the size to
  8mm in diameter.
• Use an interposition graft between portal vein
  and IVC.
• 90 control of bleeding, decreased incidence of
  encephalopathy and liver failure.

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Surgical Shunts

• Selective shunts aim to decompress varices whilst
  maintaining portal hypertension to maintain
  portal flow to liver.
• Warren distal splenorenal shunt, the most
  commonly used for patients with refractory
  bleeding and good liver function. Decompresses GE
  varices thru short gastrics, spleen, splenic vein
  to left renal vein. Lower incidence of
  encephalopathy (15), preserves some liver
  function. It does produce ascites.

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Splenorenal Shunt
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Devascularization Procedures

• Include splenectomy, gastroesophageal
  devascularization, esophageal transection.
• Incidence of encephalopathy is low, because of
  maintenance of portal flow.
• Used in patients who are not candidates for
  decompression in whom 1st line therapy has
  failed. This includes pts with splenic or portal
  vein thrombosis in addition to cirrhosis

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Denver and Leveen Shunts

• Subcutaneous shunts that drain ascitic fluid from
  the abdomen into the central venous system.
• Come with pressure valves.
• DIC is a known complication of peritoneovenous
  shunting of ascitic fluid.

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Devascularizaton

• Splenectomy- the spleen is a major inflow path to
  GE varices. Splenectomy gives better access to
  fundus and distal esophagus to complete the
  devascularization.
• Complicated by portal vein thrombosis, and
  ascites.

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Devascularization

• Sugiura procedure- devascularizes whole greater
  curve from pylorus to esophagus, upper two thirds
  of lesser curve. The esophagus is devascularized
  a minimum of 7 cm.

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Liver Transplant

• The ultimate shunt, as it relieves portal
  hypertension, prevents bleeding, manages ascites
  and encephalopathy by restoring liver function.
• Child class A shunt surgery
• Child class B shunt or TIPS
• Child class C TIPS or liver transplant

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Childs Classification

• A 2 mortality
• B 10 mortality
• C 50 mortality

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Tips

• For continued bleeding despite medical and
  endoscopic treatment in patients with Child C
  disease and selected Child B disease.
• It is only useful in portal hypertension of
  hepatic origin.
• Internal jugular to hepatic vein thru hepatic
  parenchyma to portal vein. Tract dilated and
  stented.

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TIPS
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Accepted Indications

• Active bleeding despite endoscopic or
  pharmacologic treatment
• Recurrent variceal bleeding despite adequate
  endoscopic treatment.
• Potential indications include bleeding gastric
  fundic varices, refractory ascites.
• A bridge to transplantation.

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Complications of TIPS

• Hematoma, cardiac arrythmias, bacteremia
• Perihepatic hematoma, rupture of liver capsule
• Extrahepatic punture of portal vein
• Arterioportal fistula, portobiliary fistula
• Encephalopathy (30)
• Liver failure

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Overview of Treatments
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Splenic Vein Thrombosis

• Can lead to isolated gastric varices without
  elevation of pressure in portal system
• These gastric varices can bleed
• Most often caused by pancreatitis
• Treatment is splenectomy.