Liver Review

Dr. Ahmed Kandil, MD,PhD.

Consultant Surgeon
Head of Surgery Department
Shifa Hosp. - Gaza

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 Anatomy
 Anatomical lobes: Liver seems to divide
into big Rt & Small Lt lobes by falciform
ligament.
 Surgical lobes: Liver divided into 2 ± lobes
by the portal fissure or Cantlies line. It is a
plane passing from the left side of the
gallbladder fossa to the left side of the
IVC.

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Anatomy

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 Anatomy
Segments:
 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.
 This after French surgeon Henry Bismuth.

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Segments

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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 liver’s 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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 Liver Trauma
Predisposing factors:
1- Hepatomegally
2- Diseased liver
Causes:
1- Closed trauma
2- Open (penetrating) injury
3- Iatrogenic injury
4- Spontaneous rupture

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 Liver Trauma
Types of injury:
 Subcapsular hematoma or intrahepatic
hematoma.
 Contusion
 Laceration
 Hepatic vascular disruption
 Bile duct injury
 Most of injuries have stopped bleeding at time of
exploration.
 Decreased transfusion req. with conservative

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Liver Trauma – Scaling system

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 Liver Trauma
Clinical Assessment:
 Unstable patients (systolic BP>90mmHg)
Should go immediately to OR.
 Stable patients but with obvious signs of
internal bleeding, preparation and sent
rapidly to OR.
 Stable patients with equivocal signs we
have time to investigate and observe.
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 Liver Trauma
Investigations:
 Routine investigations
 U S abdomen
 DPL
 C T abdomen
 Laparoscopy

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 Liver Trauma
Management:
 Immediate operation
 Rapid operation after some preperations
 non operative management
 Delayed operation

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 Liver Trauma
Different surgical procedures:
 Cautary , local haemostatic agents
 Suturing
 Omental packing
 perihepatic packing
 Wrapping of the lacerated liver
 Others

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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).
 TTT: Antibiotics 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 >90%, eosinophilia (10-30%).
 Surgical drainage, hypertonic saline, removal of
cyst wall, don’t 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). 10%
malig trans, rupture. Surgical.
 Focal nodular hyperplasia (FNH).Women 20-
50, stellate scar on CT. Kupffer cells on
scan.Non surgical.

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 Liver cysts
 Simple Cysts: If sympt, rupture, infection,
bleed, or suspicious. Surgical treatment;
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, Wilson’s, 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 <5%.
 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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 History
 Directed towards determining the cause,
the presence of complications of portal
hypertension.
 Jaundice, transfusions, pruritis, hereditary
liver disease,…
 Hematemesis, melena, mental status,
abdominal girth, pain, fever,
hematochezia?

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 Physical Examination
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
 Testicular atrophy, gynecomastia
 Muscle wasting, Dupuytren contracture
 Splenomegaly

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Dilated veins

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Ascites

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Palmer Erythema

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Gynecomastia

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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! It’s
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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Sengstaken Tube

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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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 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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 Child’s Classification
 A: 2% mortality
 B: 10% mortality
 C: 50% mortality

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 Tips= Transjugular Intrahepatic
Portasystemic Shunt
 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.

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Liver Review

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