The Liver disease.
Surgical anatomy and physiology. The dual afferent blood supply,
consisting of the hepatic artery and portal vein, singles out the liver from
all other organs. That the portal vein has no valves is the understanding of
portal hypertension.
The blood in the sinusoids is derived from two sources:
1. The portal system conveys between 60 and 80 % of the afferent blood
to the liver.
2. The hepatic artery, which supplies 25% of the 1500-ml blood that
enters the liver each minute, provides oxygen for the liver.
The pressure relationship of the hepatic artery (100 – 150 mm Hg),
the portal vein (8 –12 mm Hg) and the hepatic veins (1-4 mm Hg) testify
further as to the unique nature of the circulation through the liver. During
exercise the blood flow through the liver, normally about 40% of the
cardiac output, falls sharply in favor of the heart, brain and muscles.
Surgical lobes of the liver. The right and left branches of the hepatic
artery do not supply the two main anatomical lobes as such. Their territory
has a boundary running along the gall – bladder bed. The biliary ducts and
branches of the portal vein follow the hepatic arterial branches.
In this way, the liver is divided in to two surgical lobes, right and
left, by a major avascular fissure.
The blood from the liver is drained by three major hepatic veins: right
and left, the middle one of which is located in the major fissure.
Knowledge of the anatomy of the surgical lobes and of the segments is
particularly important in planning hepatic resection for injury or tumors.
Segmental structure of the liver. Now that resection of primary and
secondary tumors of the liver is regularly performed, more detailed
segmental anatomy of the liver is needed. One or two segments may be
resected leaving the blood supply and bile drainage of the other segments
undisturbed. As much as whole lobe plus two other segments can be
removed, providing two healthy segments are spared. Intaoperative
ultrasound is used to detect the vessels and ducts inside the liver.
Functions of the liver.
1. The formation of the bile and the metabolism of bilirubin and of bile
salts.
2. The synthesis of albumin, fibrinogen, and prothrombin.
3. Storage and metabolism of carbohydrates, including the conversion
monosaccharides (e. d. dextrose) into glycogen, and vise versa.
4. Formation of phospholipids and cholesterol, synthesis of fatty acids
from carbohydrate, and other steps in fat metabolism.
5. Desamination of amino – acids with formation of urea. Removal of
ammonia from portal blood.
6. Heat production. Intermediate metabolism, both anabolic and catabolic,
in the liver requires a large amount of energy derived from the conversion
of adenosine triphosphate (ATF) to adenosine diphosphate (ADR) as well
as aerobic oxygenation via the Krebs cycle. A byproduct of these
activities is the production of an excessive amount of energy in the form
of heat.
7. Reticuloendothelial activities.
8. Storage of vitamin B12 (cyancobalamin) and vit. A.
9. Iron and copper storage.
10. Destruction of bacteria.
11. Detoxication of drugs and hormones.
Regeneration. Unlike other organs, the liver possesses a completely
by compensatory cellular hypertrophy and hyperplasia.
Special methods of liver investigation. Usually several tests are
undertaken in each patients, and in some instances the individual test must
be repeated. No less than 80 %of the liver can be out of action without
affecting individual tests, and in patients with cirrhosis they may be within
normal limits. Among a large number of tests available the following are
the most useful:
I. 1. Serum bilirubin estimation. 7 mmol/ l (0.4 mg) 100 ml,
2. Serum alkaline phosphatase. [N = 3 – 13 king - Armstrong (K- A), 5 –
30 iu/ l, ar 1.5 – 4 Bodansky units.]A high alkaline phosphatase (>40 KA units or > 100 in/l) with low transaminase levels favors obstructive
jaundice but the alkaline phosphatase can be high in cholestatic jaundice
and hepatitis.
3. Estimation of serum albumin is a good general test of hepatic function.
A level below 25 g/l (2.5 / 100 ml) indicates that liver function is greatly
impaired. Above 30 g/l (3.0 g/ 100 ml) is satisfactory and safe.
4. Serum transaminases (aminotransferase). In creased values (over 100
units) are found in hepatocellular disease.
5. Plasma prothrombin index, if low is an indication for preoperative
vitamin K therapy.
6. 5–nucleotidase and  - glutamynly transferase is raised particularly in
alcoholic liver disease.
II. Liver biopsy is a common procedure of: considerable diagnostic value.
III. Imaging techniques.
A. Noninvasive methods: a. A plain x- ray of the abdomen is only of
limited diagnostic value (calcification).
b. Ultrasound. This is a safe, simple and noninvasive method that is
of particular value in demonstrating dilatation of bile ducts and stones in
the gallbladder as well as primary and secondary liver tumors and cysts.
c. Computed axial tomography. This is of considerable value in
showing the nature and relations of tumors and cysts in the liver.
(Expansive).
d. Radioactive scanning. A gamma emitting isotope such as 198
colloidal gold and Techetium 99 is taken by the reticuloendothelial system
and can be useful in local lesions in the liver.
Rose – Bengal labeled with 131 I is taken up by the liver parenchyma.
The normal liver presents as even distribution of activity, and lesion that
do not take up isotopes, e. d. abscesses, cysts and tumors, appear as
defects in the scan.
Generalized decrease in up take suggests a diffuse hepatocellular disorder
such as cirrhosis.
B. Invasive methods: a. Angiography by means of coeliac axis or
superior mesenteric arteriogram can show vascular obstruction or an
avascular lesion, or a vascular tumor.
In case of portal hypertension films in the venous phase of superior
mesenteric angiography are useful. Splenic punctures are more hazardous
but if a fine needle is used it is an acceptable alternative.
b. Percutaneous transhepatic cholangiography (RTC).
c. Endoscopic retrograde cholangeopancreatography (E R C R).
Hydatid Disease of the Liver.
Although the larval stage of the parasite Echinococcus granulosus can
thrive in many parts of the body, in 80% of cases it does so in the liver;
after ingestion it enters this organ through a radical of the portal vein,
and usually the right lobe is affected.
Source of infection. Dogs are the chief mediators of hydatid disease
to human beings by direct contact. Humans may also eat salads on
which the ova hake been deposited. Animals, particularly sheep, are
infected by eating contaminated grass. Once in the stomach, the ova
burrow through the stomach wall to enter the portal system and the liver.
Dogs become infected by feeding on offal of infested sheep.
The disease is relatively common in the sheep - rearing districts of
Australia and South America, Greece, Turkey, Iran and Iraq.
In other parts of the world the life – cycle can be completed in other
animals: the wolf → moose → wolf ( in the frozen north ) often
maintains the cycle.
Pathology
A hydatid cyst consist of thee layers. 1) The adventitia (pseudocyst),
consisting of fibrous tissue, the result of reaction of the liver to parasite,
is grey in color and blended intimately with the liver, from which it is
inseparable.
2) The laminated membrane (ectocyst) formed of parasite itself is whitish
and elastic and contains the hydatid fluid. The membrane peels readily
from the adventitia. Hydatid fluid is crystal – clear, contains no albumin.
The cyst grows very slowly.
3) The only living part of the hydatid cyst is a single layer of cells
(germinal epithelium) lining the cyst (endocyst). This secreted: a)
internally: the hydrated fluid; b) externally: the laminated membrane.
Brood capsules within thy cyst develop from the germinal epithelium and
are attached by pedicles to its innermost wall. Within the brood capsules,
scolices (heads of the future worms) develop.
Should the laminated membrane become damaged, it disintegrates, and
the brood capsules, becoming free, grow into daughter cysts. In this event
the mother cyst ceases to exist as such, the hydatid fluid and its content
being confined by the adventitia only.
Clinical features.
For a long time, perhaps for some years after the original infestation
(which often occurs in childhood), a hydatid cyst remains symptomless.
In the course of time a visible and palpable swelling in the upper abdomen
is discovered. An unruptured cyst present as a rounded calcified shadow
in the liver. Ultrasound and CT scanning can localize the cyst and ERCP
can show the cyst communicates with bile duct.
The intradermal test (Casoni’s test) is positive in 75 % of cases, but gives
up to 40% of false positives.
Recent
serologic
tests
are
of
greater
accuracy
be
indirect
haemagglutination reaction.
A blood count often shows an eosinophilia (6% or more).
Course of the disease.
1. Occasionally the parasite dies. The fluids absorbed, and all that remains
is encapsulated, laminated, bile – stained membrane the walls of the cyst
may calcify.
2. Usually the cyst enlarges gradually and becomes manifest by its size.
Sometimes sessile cyst float in the peritoneal cavity, or they may be
confused with mesenteric, pancreatic or renal cysts.
3. Complications arise. Complications:
a/Jaundice: → due to pressure of cyst on the biliary ducts.
→ due to cyst within the bile ducts.
b/ Rupture → in to peritoneal cavity.
→in to alimentary canal.
→in to the biliary channels the most
common
complication.
→in to a plural cavity.
Rupture into the peritoneum is accompanied by profound shock,
and all the signs of diffuse peritonitis. As with any of rupture of a hydatid
cyst, anaphylactic phenomena, notably urticaria, are prone to occur.
The treatment of intraperitoneal rupture must be immediate, and directed
to combating shock and cleansing the peritoneal cavity. Even in those who
survive, the ultimate prognosis is poor, for if, as is usual, the cyst contains
brood capsules, however meticulous the cleansing the disease tends to
become disseminated within the peritoneum.
c/Suppuration.
Treatment of hydatid cyst of the liver
Small cysts do not require treatment.
For larger cysts surgical treatment is required because there is no safe
effective medical treatment. Recently the mebendasole, in doses of 400
to 600 mg three times a day for 21 to 30 days, has been found to be
effective in some patients.
Operation. The cyst is exposed by an incision that gives the best access.
Abdominal packs, wrung out in solutions of either hypertonic sodium
chloride (23 – 30 %) or sodium hydrochloride (0,5 %) are tucked around
the exposed liver.
The cyst is aspirated; a scolicidal solution (e. d. hypertonic saline solution
or sodium hypochloride solution) is injected so as to render the cyst about
three – quarters full.
An incision is made through the liver overlying the cyst, and the adventitia
is opened. The laminated membrane is separated from the adventitia with
a finger. The aim should be to deliver the cyst intact. When the intact cyst
can be enucleated, the resulting cavity in the liver can be closed
completely. In less favorable circum stances, it is advisable to drain the
cavity, particularly when infections present when the contents of the cyst
are bile stained, or when there is uncertainty of its complete removal.
Every precaution must be taken to prevent spilling the contents of the cyst
into the peritoneal cavity or the layers of abdominal wall, otherwise
dissemination is lively.
Where there are larger or multiple cysts, partial hepatectomy may be
necessary.
Mebendazole is recommended postoperatively to present recurrence.
Cirrhosis Of Liver
Hepatic cirrhosis is a necrosis of the liver followed by fibrosis and
regeneration of liver cells and involving the whole organ.
Portal Hypertension
Aetiology: increase of the portal vein blood pressure is due to an
obstruction which can be: (1)prehepatic, (2)intrahepatic,
(3)posthepatic.
1. Prehepatic. About 20% of patients belong to this group the
patients with prehepatic portal obstruction is nearly always young and
often a child. The most usual cause of for advice is being sought is either
a sudden hemorrhage or listlessness due to anemia. On examination :
liver is not palpable ,spleen is obviously enlarged.
The anemia usually due to oozing from esophageal varices but
sometimes hypersplenism is a factor .As the liver is normal ,or nearly so,
liver function test remains normal as disease advanced. Ascites does not
occur unless there is active phlebitis in the portal vein .The obstruction
arises in the one of two ways :
(a)
There is congenital abcenss or abnormality of the portal
vein.
(b)
Thrombosis of the portal vein due to extension of the
normal obliterative process of the umbilical vein and ductus
venosus sometimes associated with omphalitis in newborn.
(c)
Obstruction of portal vein in adult may be due to
chronic pancreatitis and carcinoma of the pancreas or thrombosis
of the vein may followed by acute pancreatitis ,but these may just
thrombosis the splenic vein may follow acute pancreatitis. The
vein becomes replaced by a mass of collateral channels.
2. Intrahepatic accounts for nearly 80% of all cases. The causes
are cirrhosis (fricvently alcogolic in origin) and schistosomiasis in
which blood flow through the liver is obstructed. Enlarged
portosystemic venous communications are present long before serious
oesophageal hemorrhage occurs. Oesophageal varices can be
demonstrated radiologically or seen through oesophagoscope.
Enlargement of veins of abdominal wall radiating from umbilicus may
be present. As long as hypertrophy of liver tissue is sufficient to
compensate for the cellular destruction by cirrhosis, the liver function
tests remain within normal limits.
3.Posthepatic is rare. It may be caused by:
(a)
constrictive pericarditis and tricuspid valve
incompetence and it is also a component of the Budd-Chiari
syndrome. This syndrome is result from obstruction of the hepatic
veins.
(b)
Spontaneous thrombosis of the hepatic veins or
neoplastic encroachment from other organs account for the majority
of cases .The syndrome is also associated with clotting disease
especially polycythaemia and the use of hormones for contraception
and infertility. Some cases, presumably congenital are caused by an
obstruction of the suprahepatic portion of the inferior vena cava
with a membranous web. The importance lies in its potential
curability by operation.
Collateral circulation .When there is obstruction of blood flow to
or from the liver, the body responds by opening up normally
insignificant anastomotic channels.
When the obstruction is prehepatic, collaterals between the portal
vein above and below the obstruction enlarged. Depending upon the site
of the obstruction, some of the collaterals between the portal and
systemic venous systems, notably the oesophageal plexus, also becomes
dilated.
When the obstruction is intrahepatic, anastamotic channels outside
the liver between the portal and systemic systems become engorged,
dilated and so an increasing proportion of the obstructed portal venous
blood bypasses the liver.
The only dilated veins which are dangerous to life are those in the
submucosa of the oesophagus and upper end of the stomach. In patients
with portal hypertension hemorrhoids, if present are usually of the
idiopathic type but rectal varices are common and can lead to severe
haemorrhage.
Anastamoses between The portal and Systemic venous system.
Sites of
anastomos.
Portal
vessels
Systemic
vessels
Signs
and
Symptoms
1
.
Plexus
around
Oesop
hg.
lower End branches
Lower
systemic
Haema
temesis or
melena
of
of left
oesophageal
oesophagus
gastric
veins
vein &
short
Gastric
veins
2
.
Around
umbilicus
Parau
Superfici
mbilical
al veins of
veins
anterior
(accompan
abdominal
y the
wall
caput
medusae
round
Ligament
of the
liver)
3
.
Plexus
Superi
Middle
around
or
and inferior
lower Third
haemorrho
haemorrhoida
of rectum
idal veins
l veins
and
Rectal
varices
(heavy
bright red
bleeding)
Anal canal
4
.
Extrape
ritoneal
Tribut
aries of
superior
and
Subdiaph
ragmatic and
silent
Surface
s of
abdominal
inferior
retroperitonea
mesenteric
l veins
vein
Organs
Oesophageal varices are dilatations of the normal submucosal
oesophageal veins and are the most important collaterals of the portal
circulations. They may extend from below the gastro-oesophageal
junctions for 10-15cm up to oesophagus.
Bleeding, which is nearly always from the lower 5cm of the
oesophagus may be slow ooze or sudden and severe. The presence of
oesophageal varices can be demonstrated by several methods but it
cannot be assumed that they are the site of bleeding without
investigation.
1. Fibrooptic or rigid oesophagoscopy will demonstrate them
in all cases ,and should be carried out along with gastroscopy to
confirm the presence of varices and determine if they are the source
of bleeding .If the lower oesophagus is full of fresh blood it may be
impossible to see varical bleeding.
•
Duodenal and gastric lesion.
•
Reendoscoping an hour or two after.
2. Radiology after a barium swallow will show filling
defects but endoscopy is far more accurate.
The presence of varices and the cause of the portal hypertension
,e.g.: portal thrombosis or cirrhosis can be demonstrated by
angiography .The venous phase of a celiac angiogram is now preffered
to direct puncture of the spleen.
Treatment of massive hemorrhage from oesophageal varices.
By the time patients reach hospital about 1/3 will have stopped
bleeding heavily.
There are 4 stages in management :
1. Resuscitation of the patients. -Ensure a clear airway and
rapid replacement of blood volume is the priorities.
Fluids containing sodium should be avoided because patients with
liver diseases retain sodium excessively and great care must be taken
with sedation as opiates and the tranquilizers are normally metabolized
in the liver.
2. Arrest of haemorrhage.
(a) Tamponade is the most direct
and reliable method of arresting hemorrhage if carried out carefully
by an experienced team.
A Sengstaken-Blackmore type of tube with gastric and oesophageal
balloons is the most commonly used .
Which ever is used there must be some method of aspirating saliva
from the oesophagus to prevent inhalation pneumonia.
The gastric balloon should be inflated with 300-400 ml of air to
ensure that the tube does not fall out and to compress the varices round
the upper part of the stomach. The oesophageal balloon is inflated to a
volume which was found before insertion to procedure an even
distention.
The pressure should be 20-30mm Hg above that recorded before
insertion .The tube is secured to the forehead to prevent if advancing
into the stomach but strong traction is unnecessary .The tube is kept in
position until the bleeding point is treated. This should not be more
than 24 hours, preferably 12 hours.
(b)
Drugs. Vasopressin (20 IU in 200 ml i.v. over 20 min.
and then 0.4 U/minute for up to 24 hours) may be used to lower
portal venous pressure and so reduce bleeding (side effect :
abdominal gripping ; coronary artery vasoconstriction). The
hormone somatostatin is effective in lowering intravariceal blood
pressure and flow.
Morphine is contraindicated.
(c) Endoscopic ligation of esophageal varices: - The varix is
drawn into the ligator by suction. An “O” ring is applied.
(d)
Endoscopic sclerotherapy is now the simplest and
relatively safe way of treating hemorrhage from esophageal varices
and stops bleeding in over 90% of cases.
Technique. A fibroptic flexible oesophagoscope .
Sedation with pharyngeal analgesia. Blood will be sucked away
while the injection needle is in place.
1) In the intravariceal method: 5-6 ml of ethanolamine oleate or
other sclerosant is injected in each varix at or just above the
gastroesophageal junction to produce thrombosis.
2) In the paravariceal technique : very small quantities (0.5 ml) of
sclerosant is injected in many different sites along side each varix to
produce perivascular fibrosis Ballon compression maybe used for a short
time afterwards.Sclerotherapy may be repeated the following day.
3/ combined method.
(d)
Operations. Emergency operations are avoided if
possible because of the high mortality; but if bleeding persists after
sclerotherapy there is no alternative.
There are 2 alternatives: devascularization and transection or
portosystemic shunting.
Devascularization and transection operation. The Miles-Walker
and Borema-Crile procedures were transthoracic operations and involve
direct ligation of veins in the oesophagus and Tanner’s porto-azygos
disconnection used as abdominal approach with transaction of the upper
stomach.
Combined devascularization transection operation where upper
half of the stomach and lower part of the oesophagus are devascularised
and then the gastro-oesophageal junction transected and reanastamosed,
thereby interruption in intramural and submucosal veins.
The devascularisation must be continued well up the oesophagus
even an abdominal incision is used.
Oesophageal stapling(Johnston). The stapling gun makes the
transaction and reanastamosis relatively easy. To pass a stapling
instrument into the lower oesophagus through a small hole in the
anterior wall of stomach. When operated ,the instrument simultaneously
divides the oesophagus and joins it together again with staples which
occludes the vessels .The results of this operation are reasonably
effective and it has the merit of simplicity.
Portal vein shunt. The operation is not easy. It is best avoided in
the presence of active bleeding except by very experienced surgeons.
Portasystemic shunt operations. Premilinary investigation should
have determine the cause of the venous block and its site.
Portalcaval anastamosis:
a) end- to- side portacaval shunt
b) side-to-side portacaval anastomosis.
With careful selection of cases the mortality of an elective
portacaval operation is about 6% and recurrent bleeding from varices
after this operation is most unusual.
Up to 30% of patients may have post shunt encephalopathy because
of venous deprivation the liver and slow deterioration of the liver
function.
(c)
Splenorenal anastomosis. This may be performed if
there is thrombosis of the portal vein, but it is contraindicated if the
splenic vein is less than 1cm in diameter.
This operation is less effective than a portacaval anastomosis in
preventing further hemorrhages, but carries a lower risk of
encephalopathy.
The spleen is removed .The splenic vein is anatomized by end-toside anastomosis with the renal vein.
Distal splenorenal shunt (DSRS). The distal splenic vein is joined
to the renal vein without splenectomy.
(d)
Superior mesentericocaval anastomosis. When the
portal vein is thrombosed this alternative may be possible. The
inferior vena cava is divided .The proximal end is joined to the side
of the superior mesenteric vein in the root of mesentery.
(e)
Splenectomy. This has no place in treatment of portal
hypertension except in the rare cases of thrombosis confined to the
systemic vein or in combination with some other operation.
General management of patients.
Stopping the bleeding is the first priority but the general state of the
patient must not be forgotten and the earlier support measures are
started, the better the outlook.
(a)
Encephalopathy. Absorption of protein metabolism
from the alimentary tracts leads to encephalopathy .The bowel
should be cleared of blood by enemas or purgatives (e.g.
magnesium sulphate). In addition neomycin are given by mouth
or tube to alter and reduce the proteolytic bacteria in the gut.
(b)
Corrections of clotting problems. Vitamin K is given to
correct the abnormal prothrombin time.
Table: Child’s table indicating suitability of a patient with
portal hypertension for shunt surgery
Observations Very suitable ,
Marginal , B
Unsuitable ,C
A
Serum bilirubin
mmol(mg %)
Below 34
34-50
(2.0)
Serum albumin
(2.0-3.0)
Over 35
30-35
g/l (mg %)
(3.5)
Ascitis
None
Neurological
Over 50
(3.0)
Below 30
(3.0-3.5)
(3.0)
Easily
Poorly
controlled
controlled
Minimal
Coma
Good
Poor
None
disorders
Nutritional
status
Excellent
Preventing of rebleeding
Long term treatment:
(a)
Repeated sclerotherapy with regular check
endoscopies at 2 weeks,
1 month, 3 months and then 6 month,
to diagnose and sclerose non thrombosed varices or new varices that
develop with time.
(b)
Devascularization and oesophageal transaction.
(c)
Portasystemic shunts.
Transjugular intrahepatic portasystemic shunt ( TIPS).
TIPS is placed via the right internal jugular vein. The right hepatic
vein is catheterized and a needle is punctured through the hepatic
parenchyma to enter the main right portal vein. A balloon is placed over
a guide wire to dilate this parenchymal tract and finally, a metallic stent
is placed in the dilated tract. Stents must bridge all the parenchyma
between the portal and hepatic veins but not protrude significantly into
either of the veins.
Portography before and after stent placement should document
both flow patterns to the liver and varices, as well as measuring
pressure. The portal to hepatic pressure gradients should be reduced to <
12mm Hg.
Currently, the wall stent, a self expanding stent is the most widely
used.
The risk for this procedure are similar to the risks for any portal
systemic shunt with bleeding, infection and precipitation of liver failure
as the main risks.
As with other minimally invasive surgical procedures, hospitals stay
can be shortened.
Immediate fluid management, antibiotic coverage, liver functions
monitoring guidelines should be followed strictly.
The major problem with TIPS at this time is stenosis or occlusion of
the shunts in the first 6 months.
Liver transplant.
The final surgical approach to portal hypertension and variceal
bleeding is liver transplantation.
However, the indication for transplantation is end stage liver
disease, not variceal bleeding. The decision to proceed to transplantation
should be based on full evaluation following stabilization of initial
bleeding.
Quantitative liver function testing can help make this definition. The
Child-Pugh class C patient with variceal bleeding may require liver
transplantation.
The benefits of liver transplantation in the patient with variceal
bleeding and end stage disease is that it not only decompresses the
varices and controls bleeding but also restores functional hepatic mass.
The disadvantage is that liver transplantation requires long term
immunosupression with its associated morbidity. However, survival rate
achieve in this patient subset are significantly better than the outcome
historically achieved with other forms of therapy.
Management Algorithm of varicceal bleeding.
Acute variceal bleed sclerotherapy
EVALUATION
Good liver function
Poor liver
function
Non-alcoholic disease
Alcoholic cirrhosis
Transplant candidate
SCLEROTHERAPY + B- BLOCK
No
Yes
DSRS
Transplant
TIPS
Transplant candidate
DSRS – Distal splenorenal shunt
TIPS - Transjugular intrahepatic portocaval stent
shunt
Transjugular intrahepatic portosystemic
shunt
Portal hypertension
TIPS-transjugular intrahepatic portosystemic shunt.
TIPS is placed via the right internal jugular vein.The
right hepatic vein is catheterized and a needle is
punctured through the hepatic parenchyma to enter
the main right portal vein.A ballon is placed over a
guide wire to dilate this parenchymal tract and
finally ,a metallic stend is placed in the dilated
tract.Stends must bridge all the parenchyma between
the portal and hepatic veins but not protrude