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Portal Hypertensive Gastropathy
This complication results from venous congestion in the
gastric wall, resulting in engorged, friable mucosa, which
can lead to indolent bleeding from the stomach.
Splenomegaly
factor to the formation of ascites is the presence of
hypoalbuminemia as a result of hepatocellular damage.
A third important factor is retention of sodium and
water due to increased secretion of adrenocortical
hormones. Ascites does not occur in prehepatic portal
hypertension.
Portal hypertension causes splenomegaly through engorgement of the intrasplenic vascular spaces. Splenomegaly
results in sequestration and destruction of blood elements
by immune mechanisms. The process, known as hypersplenism, causes leukopenia (WBC <4000/mm
thrombocytopenia (platelet count <100,000mm
3
) and
3
Although the spleen is always enlarged in hypersplenism,
there is no correlation between spleen size and degree of
hypersplenism, indicating the importance of immune
destruction in the process.
Ascites
Postsinusoidal and hepatic venous obstruction lead to
increased hepatic lymph formation. The increased lymph
formed extravasates into the peritoneal cavity through the
liver capsule (Figure 6.5). An important contributing
Encephalopathy and Hepatic Coma
Portasystemic encephalopathy—which occurs in patients
with marked decrease in hepatic function—is due largely
to hyperammonemia, increased levels of g-aminobutyric
).
acid (GABA), and false neurotransmitters. Hence, it rarely
occurs in extrahepatic portal hypertension. Hyperammonemia is due to both impaired liver function and
hepatic bypass through portasystemic collaterals. Normally, all the ammonia produced in the gut is deactivated
in the liver by conversion into urea.
The neuropsychiatric manifestations of encephalopathy include altered consciousness, depressed motor activity, and decreased deep tendon reflexes. A characteristic
sign is the liver flap, that is, when the patient, with arm
outstretched, wrist extended, and fingers straight, exhibits
repeated involuntary flexions of the wrist and fingers.
FIGURE 6.5. In portal hypertension, ascites is caused by discharge of increased hepatic lymph into the
peritoneal cavity through the liver capsule. This supine x-ray shows large and small bowel gathered in
the center of the abdomen with ascites fluid appearing as a gray background occupying both flanks
(arrows). (Courtesy of Henry I. Goldberg, MD.)
P athophysiology ................................................................................................................................. 169
As the condition worsens, delirium gives way to stupor,
then coma. Electroencephalogram (EEG) is a sensitive
way to detect encephalopathy. In hepatic coma, blood
levels of ammonia are frequently elevated to 125mg/dL or
more.
MANAGEMENT: PORTAL HYPERTENSION
Portal hypertension is an important condition that
requires team management by gastroenterologists, radiologists, and surgeons. Variceal hemorrhage and intractable
ascites are the usual reasons for surgical treatment. Over
the years, surgeons have developed several ingenious ways
of decompressing portal hypertension. Recently, the availability of liver transplantation as an option for definitive
treatment has resulted in the use of radiological or surgical procedures that leave the portal vein intact to treat
acute variceal hemorrhage.
ACUTE VARICEAL HEMORRHAGE
Encephalopathy may be worsened and hepatic coma
precipitated by severe variceal hemorrhage, which leads to
decreased liver blood flow, and increased ammonia formation from blood in the GI tract due to action of gut
flora.
Esophageal varices may develop without causing bleeding,
but 25% to 35% of patients with esophageal varices will
eventually bleed (Figure 6.6).
responsible for approximately 25% to 30% of deaths in
patients with cirrhosis.
4
3
Variceal hemorrhage is
Most commonly, the varices that
rupture are within 2 to 3cm of the gastroesophageal junction. Bleeding may be minor or massive. Massive bleeding
has a 50% mortality rate when associated with severe liver
dysfunction. Approximately 50% to 60% of patients with
esophageal varices bleed from a cause other than the
varices.
3
Nevertheless, patients with esophageal varices will
often have the stigmata of chronic liver disease, including
jaundice, ascites, splenomegaly, spider nevi, gynecomastia,
and testicular atrophy. The management is discussed
below and depicted in Figure 6.7.
Investigations
Helpful investigations in acute variceal hemorrhage include laboratory studies, endoscopy, radiological studies,
and duplex ultrasonography.
Laboratory Studies
Liver function test results are nearly always abnormal and
include elevated bilirubin and depressed serum albumin
levels. These findings—combined with the presence or
absence of ascites and neurological and nutritional disorders—must be used to determine the patient’s hepatic
functional reserve according to Child’s criteria (see Table
6.1). The hemogram and coagulation profile should be
determined. If the presence of hepatoma is suspected,
serum alpha protein and a CT scan may be required.
FIGURE 6.6. This esophagram demonstrates thick wavy linear
structures in the body of the esophagus, representing varices.
(Courtesy of Henry I. Goldberg, MD.)
170 ................................................................................................................................................. Liver
Endoscopy
Esophagogastroduodenoscopy, the most important investigation to identify the cause of bleeding, should be
performed as soon as hemodynamic stability is restored.
Large, tortuous submucosal varices may be seen. The
bleeding varix may be visible. If no bleeding is seen
from the varices, the absence of a bleeding lesion in the
stomach and duodenum strongly suggest variceal hemorrhage. Patients with cherry red spots and red wale markings on large thin-walled varices are likely to bleed from
varices.
Radiology
Barium swallow is of little investigative use in variceal
hemorrhage, but it is often on barium swallow that the
presence of varices is detected.
Duplex Ultrasonography
Doppler duplex ultrasonography is useful in defining
portal venous anatomy, patency of the portal vein, and the
presence of splenomegaly. This study is more useful preoperatively than during acute hemorrhage.
Treatment
Treatment of acute variceal hemorrhage requires resuscitation, prevention of encephalopathy, and control of
bleeding.
Resuscitation and Prevention of Encephalopathy
Rapid hemodynamic resuscitation and oxygen administration are important to prevent further deterioration of
hepatocellular function. Central venous or pulmonary
FIGURE 6.7. Decision tree for management of acute variceal hemorrhage. Abbreviation: TIPS, trans-
jugular intrahepatic portasystemic shunt.
M anagement: P ortal H ypertension ..................................................................................................... 171
artery pressure as well as urine output monitoring may
be required. The patient may have or may develop
encephalopathy and obtundation. Should these conditions
become a problem, the airway should be controlled
quickly to prevent aspiration, and mechanical ventilation
should be instituted. Saline solutions should be avoided
and potassium chloride given as soon as adequate urine
output is established. Parenteral vitamin K should also be
given. Measures to prevent encephalopathy should be
instituted early, including protection of hepatic function
by prompt hemodynamic resuscitation, administration of
oxygen, evacuation of blood from the gastrointestinal tract
(using nasogastric lavage, magnesium sulfate, enemas),
and luminal acidification of the gut (using lactulose) and
reduction of gut flora using neomycin.
Control of Bleeding
Acute bleeding may be controlled by endoscopic sclerotherapy, balloon tamponade, radiological measures, or
emergency surgery:
Endoscopic sclerotherapy. Injection of a sclerosant (e.g.,
5% sodium morrhuate or 5% ethanol amine oleate) into
either the varices or the paravariceal mucosa may control
acute hemorrhage. Obliteration of varices usually requires
repeated endoscopic sclerotherapy at weekly intervals for
3 or more weeks. Endoscopic sclerotherapy has emerged
as the best initial technique to control hemorrhage.
However, it has significant complications, including recurrent bleeding from mucosal ulceration in 20% of patients,
esophageal stricture in up to 15%, pleural effusion, and,
rarely, esophageal perforation.
Endoscopic variceal ligation. Also known as variceal
banding, endoscopic variceal ligation (EVL) is safer than
sclerotherapy but more difficult to perform. The varices
are grasped serially and elastic O-rings applied to the base
of each, much as is done in hemorrhoid banding.
Pharmacologic control. Vasopressin and glypressin and
either somatostatin or the long-acting somatostatin analogue, octreotide, may stop bleeding by reducing portal
pressure. Vasopressin lowers portal pressure by causing
splanchnic arterial vasoconstriction, while octreotide acts
A B
FIGURE 6.8. The Sengstaken–Blakemore tube is indicated to control bleeding when endoscopic sclerotherapy is unavailable or fails. (A) The device creates a tamponade by putting traction on an
inflated gastric balloon (B); the esophageal balloon is inflated only if the gastric balloon fails to get
bleeding under control. (Adapted from Greenfield L, ed. Surgery: Scientific Principles and Practice.
2nd ed. Philadelphia: Lippincott-Raven; 1997.)
172 ................................................................................................................................................. Liver
Table 6.4. Proper Use of the Sengstaken–Blakemore Tube
Pre-insertion
䊏
Assess need for nasogastric intubation
䊏
Apply topical anesthesia to nasal passage
䊏
Evacuate stomach of blood
䊏
Label gastric and esophageal tubes
Insertion
䊏
Through nostril is preferred
䊏
Insert tube well into stomach
䊏
Inflate gastric balloon to 250 ml of air
䊏
Pull gastric balloon snugly to gastroesophageal junction
䊏
Plain abdominal x-ray to check placement
䊏
Insert #14 Salem into esophagus and apply suction
䊏
If bleeding is controlled, no need to inflate esophageal
balloon
䊏
If bleeding is not controlled, inflate esophageal balloon to
25–45 mm Hg
䊏
Chest and abdominal x-rays to check position of balloons
Follow-up
䊏
24–h/day nursing supervision
䊏
Tape scissors to head of bed to cut tubes in case of respiratory
difficulty
䊏
Serial hematocrit levels every 6 h
䊏
Deflate balloons in 24 h but leave tube in situ for additional
24 h
䊏
Remove tube if no bleeding occurs in 24 h
Source: Reprinted with permission from Rikker, Goldsmith, eds. Practice and
Surgery. Philadelphia: Harper & Row, 1981.
FIGURE 6.9. Transjugular intrahepatic portasystemic shunt (TIPS)
procedure. This subtraction angiogram shows a catheter entering the liver in the hepatic vein and passing through the metallic stent into the portal vein (arrow). (Courtesy of Henry I.
Goldberg, MD.)
on the venous side by inhibiting the release and action
of vasodilators. Vasopressin has an efficacy of only 50%;
it has the potential to reduce coronary blood flow and
cause myocardial infarction. Nitroglycerin has been
used concomitantly to block the coronary vasospastic
effects. Glypressin is an analogue with fewer side effects.
Somatostatin and octreotide are initially given as an
intravenous bolus of 250 mg/hr or 50 to 100 mg/hr, respec-
tively. In controlled trials, somatostatin therapy resulted
in control of bleeding in 63% compared to 46% with
vasopressin.
5
Balloon tamponade. Use of the Sengstaken–Blakemore
tube (Figure 6.8) to control bleeding is indicated when
endoscopic sclerotherapy fails or is not available. Balloon
tamponade provides effective and immediate control of
bleeding but must be used under strict protocol as outlined in Table 6.4. Bleeding is usually controlled by applying traction on the inflated gastric balloon. The esophageal
balloon is inflated only if the gastric balloon fails to
control the bleeding. The most common complication is
aspiration and aspiration pneumonia. The most dreaded
complications, both of which are rare, are migration of the
esophageal balloon to obstruct the airway and esophageal
perforation.
The balloon(s) is(are) deflated after 24h but kept in
place for another 24h in the event bleeding recurs. Balloon
tamponade controls bleeding in over 90% of patients, but
rebleeding after balloon deflation occurs in some 25%.
6
Radiologic control. Two techniques have been used to
control bleeding radiologically: percutaneous, transhep-
atic obliteration of varices by selective gel foam embolization into individual collaterals and transjugular intrahepatic portasystemic shunt (TIPS). Because of the success
of TIPS, percutaneous transhepatic obliteration is now
rarely used.
TIPS accomplishes intrahepatic portasystemic shunting using a flexible, expandable metal stent (Wall stent).
The stent is introduced over a guidewire after an intrahepatic track is formed between the hepatic and portal
veins using a balloon catheter (Figure 6.9). Once the stent
is in place, portal pressure falls rapidly so that the portal
vein to inferior vena caval pressure gradient is less than
12 mm Hg, the threshold below which varices rarely bleed.
Complications occur in about 10%, but lifethreatening bleeding from puncture of the liver capsule
occurs in only approximately 1% to 2%.
7
Encephalopathy
develops frequently. Randomized clinical trials have
shown that the rebleeding rate after TIPS is consistently
lower than the rate following endoscopic sclerotherapy,
while mortality rates are comparable.
7
The best indication for using TIPS is failure of endoscopic sclerotherapy in patients who are candidates for
liver transplantation. In this case, TIPS serves as a bridge
to transplantation. It may also be the best option in Child
C patients who have failed sclerotherapy. The major
concern with TIPS is long-term stenosis or occlusion. In
the most experienced centers, TIPS patency has been
maintained in 90% of patients over a 2-year follow-up
period by performing TIPS revisions on an outpatient
basis when necessary.
8
M anagement: P ortal H ypertension ..................................................................................................... 173
174 ................................................................................................................................................. Liver
Emergency surgical treatment. Failure to control hemorrhage nonoperatively or recurrence of hemorrhage
within 48 h is an indication for expeditious operation.
Three surgical techniques are available: emergency
portasystemic shunt, esophageal transection, and variceal
ligation.
Several factors must be considered in selecting the procedure, including the patient’s Child’s class, the candidacy
of the patient for liver transplantation, and the surgeon’s
experience. Patients who are Child’s class A or B are not
candidates for liver transplantation, while Child’s C
patients may be. Whenever a patient is judged to be a candidate for liver transplantation, procedures that violate the
porta hepatis or portal vein should be avoided. In this case,
the remaining choices are then direct variceal ligation,
stapled esophageal transection, or mesocaval H-graft. Even
here, however, the procedure of choice, if available, is TIPS.
In Child’s A or B patients, the most expeditious operation
is emergency portacaval shunt. If bleeding can be controlled with balloon tamponade, however, a selective distal
splenorenal shunt may be possible.
1. Portasystemic shunt. Performed either as an end-toside portacaval or an H-mesocaval shunt, emergency portacaval shunt is 95% successful in controlling bleeding
(Figure 6.10). Mortalities rates are similar to endoscopic
sclerotherapy. In an NIH-funded prospective randomized
clinical trial comparing emergency portacaval shunt and
endoscopic sclerotherapy in unselected patients with
variceal hemorrhage, the 30-day survival was equal at
about 50%.
9
2. Esophageal transection. Esophageal transection is
accomplished using an end-to-end stapler to transect
and reanastomose the distal esophagus (Figure 6.11). In so
doing, the procedure disconnects the portal circulation
from the systemic circulation, and the doughnut of esophagus excised removes segments of the varices. Unfortunately, bleeding will recur as varices reform.
3. Variceal ligation. Performed by the thoracic or
abdominal approach, variceal ligation involves opening the distal esophagus and oversewing the varices
individually with suture. The procedure is now rarely
performed.
Prevention of Recurrent Hemorrhage
In acute variceal hemorrhage that has been successfully
controlled nonoperatively, the goal is to prevent further
hemorrhage. Available methods include pharmacotherapy,
obliteration of varices by endoscopic sclerotherapy, and
surgery.
P
HARMACOTHERAPY Nonselective b-blockade with
propranolol has been shown to reduce the likelihood of
recurrent bleeding by 30%.
10
Unfortunately, the drug
requires strict compliance, its effect on individual patients
is inconsistent, and it reduces cardiac output. Conse-
quently, this therapy has to date not proven to be a longterm option.
E
NDOSCOPIC OBLITERATION OF VARICES Long-term
results indicate that this procedure is effective in only 40%
to 60% of patients and that it decreases the mortality rate
of acute variceal hemorrhage by 25%.
11
The advent of this
form of therapy has reduced the incidence of shunt surgery.
Nevertheless, endoscopic sclerotherapy is associated with
a high rate of long-term mortality because of recurrent
hemorrhage.
S
URGERY: SHUNT PROCEDURES Total shunts or selec-
tive shunts can be used to prevent recurrent hemorrhage.
All shunt procedures reduce the rebleeding rate to less
than 10%, but this success comes at the price of a high
mortality rate (5%–20%) and an increased incidence of
encephalopathy.
12
In general, the incidence of encephalopathy in selective distal splenorenal shunt is 50% of that seen
in nonselective shunts.
In selecting the procedure, the distal splenorenal shunt
is the first choice. When it cannot be performed, either
mesocaval or end-to-side portacaval shunt is selected.
Central splenorenal shunt is now rarely performed, as is
side-to-side portacaval shunt.
Total shunts. Total procedures include end-to-side or
side-to-side portacaval shunt and mesocaval shunts. Endto-side portacaval shunt provides effective and longlasting protection from rebleeding. The side-to-side shunt
is usually reserved for treating Budd–Chiari syndrome and
ascites. The incidence of encephalopathy after portacaval
shunt is 20% to 40% with nonselective shunts and 10% to
20% with selective shunts.
13
Mesocaval shunt is accomplished by interposing a
segment of vein or prosthetic graft between the superior
mesenteric vein and the inferior vena cava. Mesocaval
shunts that use grafts of 12 to 20 mm result in total diversion of portal flow. If the shunt is limited to 8mm, portal
liver flow is preserved and the incidence of encephalopathy is significantly reduced.
Selective shunts. The distal splenorenal (Warren) shunt
is accomplished by anastomosing the distal end of the
transected splenic vein to the side of the left renal vein,
then transecting the coronary vein, the right gastroepiploic vein, and the veins in the splenocolic ligament. The
operation is complex, requires special expertise, and is
contraindicated in several situations, including too great a
distance between the splenic and renal veins to permit
anastomosis, previous splenectomy, and ascites. Distal
splenorenal shunt is not an effective treatment for ascites.
With time, this selective shunt becomes less selective as
new collaterals form.
Liver Transplantation
Liver transplantation not only resolves the problem of varices, but it restores normal liver function. Unfortunately, the
A
FIGURE 6.10. Emergency portacaval shunt is effective in controlling bleeding by decompressing the portal system flow into the
B
inferior vena cava and other lower-pressure systems. A number
of procedures can by used, including (A) end-to-side portacaval
shunt and (B) H-mesocaval shunt.
Continued on next page
M anagement: P ortal H ypertension ..................................................................................................... 175
C
FIGURE 6.10. Continued
The H-mesocaval shunt may be either proximal
(C) or distal, also known as the Warren shunt (D).
(Adapted from Greenfield L, ed. Surgery: Scientific Principles and Practice. 2nd ed. Philadelphia:
Lippincott-Raven; 1997.)
Ligated coronary
vein
D
gastric artery
masentaric vein
176 ................................................................................................................................................. Liver
A
B
FIGURE 6.11. Esophageal transection. (A and B) An end-to-end stapler is used to transect and reanastomose the distal esophagus to remove segments of the varices and disconnect the portal circulation
from the systemic circulation. (Adapted from Greenfield L, ed. Surgery: Scientific Principles and Practice. 2nd ed. Philadelphia: Lippincott-Raven; 1997.)
scarcity of donor organs makes liver transplantation a less
viable option. Acute alcoholic patients and drug users are
not candidates. It is also difficult to justify liver transplantation to treat varices when end-stage liver disease is not
develops, relative deficit of circulating volume occurs.
Patients with abdominal wall hernias—particularly umbilical hernias—have the additional risk of spontaneous perforation.
present. In such cases, either selective shunts or the TIPS
procedure may be used.
Medical Therapy
Medical therapy has a large measure of success in treating
ASCITES
ascites, but some patients must be treated surgically.
More than 90% of patients can be treated satisfactorily
Ascites can be a major problem in patients with portal
hypertension, especially in those with Budd–Chiari syndrome and postsinusoidal portal hypertension. As ascites
M anagement: P ortal H ypertension ..................................................................................................... 177
with medical therapy, including sodium restriction
(to a maximum of 2–3 g/day) and spironolactone therapy
(100–400 mg/day). Other diuretics (e.g., furosemide,
178 ................................................................................................................................................. Liver
hydrochlorothiazide) may also be used, but they can cause
hypokalemia, which can precipitate or aggregate encephalopathy. Hence, spironolactone is the diuretic of first
choice. Intermittent large-volume paracentesis and colloid
administration are also effective.
Surgical and Radiologic Therapy
Approximately 5% to 10% of patients will develop
diuretic-resistant ascites. Therapeutic options include
peritoneovenous shunt, TIPS, side-to-side portacaval
shunt, or liver transplantation.
Peritoneovenous Shunt
A shunt with a one-way valve is placed under local anesthesia between the peritoneal cavity and the superior vena
cava or right atrium. The transfer of fluid from the peritoneum into the bloodstream reverses most of the pathophysiological factors that produce ascites or are caused by
it. Circulating volume and cardiac output are restored.
Plasma levels of renin, aldosterone, and antidiuretic
hormone become normal, and renal function improves.
Despite the simplicity of the procedure, the peritoneovenous shunt is associated with complications in 40% to
50% of patients. The most common complications are
sepsis, disseminated intravascular coagulopathy, and shunt
occlusion. Mortality rates of approximately 25% have
also been reported, but these rates represent the seriousness of the underlying liver disease.
14
Controlled trials have
shown that peritoneovenous shunt does not improve
survival.
14
TIPS
TIPS, increasingly replacing peritoneovenous shunt in the
treatment of resistant ascites, is rapidly effective, but longterm results are not encouraging because of the higher rate
of encephalopathy and liver failure. Of course, in patients
with end-stage liver disease, TIPS serves as an excellent
bridge to liver transplantation.
Side-to-side Portocaval Shunt
When ascites is associated with variceal bleeding, side-toside portocaral shunt is indicated. Even then, the advent of
TIPS has made surgical shunts less common except in
treating the Budd–Chiari syndrome.
Liver Transplantation
Liver transplantation is indicated as a definitive procedure
in selected patients when ascites is associated with endstage liver disease.
MANAGEMENT: LIVER ABSCESS
Abscess of the liver may be caused by bacteria, fungi, or
ameba. In surgical practice, the most important of these
are bacterial and amebic abscesses (Table 6.5 and Figure
6.12).
BACTERIAL ABSCESS
Bacterial liver abscess may develop as a result of hematogenous spread from biliary tract infection or extension
from adjacent septic focus. Hematogenous spread from
acute appendicitis and diverticulitis was common prior to
the advent of antibiotics. The abscess may or may not be
preceded by infection of the portal vein (pylephlebitis).
Both aerobes and anaerobes are usually involved as a
polymicrobial infection. The most common aerobes are
Escherichia coli, Klebsiella pneumoniae, Pseudomonas,
Proteus, Enterococcus, and Streptococcus pyogenes. The
most common anaerobic organisms are bacteroides and
streptococci. Bacterial abscesses tend to be multiple and
are often found in both lobes. They present in a subacute
fashion with fever, with chills developing later. Mild jaundice may be present, and about a third of patients will
complain of right upper quadrant pain.
AMEBIC ABSCESS
Amebiasis is endemic in several parts of Africa, Southeast
Asia, Mexico, and South America. In North America, the
infection may be acquired either from travels to these
regions or from individuals who acquired amebiasis in
these parts of the world. Outside the body, Entameba his-
tolytica exists in trophozoite or cyst forms. In infection,
amebic cysts enter the gastrointestinal tract and, in the
colon, become trophozoites, which invade the mucosa and
result in typical flask-shaped ulcers. From there,the organism is transported via the portal circulation to the liver,
where the amebic abscess forms.
Amebic abscesses present more acutely than bacterial
abscesses. An antecedent history of bloody diarrhea is
obtained in only 10% of cases. Fever can be high and
is often intermittent. Moderate jaundice may also be
present.
Investigations
Laboratory and radiological studies can help determine
the causative factors.
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