9 
Esophageal Varicosities
Esophageal varices are diagnosed in almost one-third of compensated cases
and almost two-thirds of decompensated cases of cirrhosis. Bleeding may
occur in one-third of cases and is related to the size of the varix and the
severity of the liver disease. There is a 1 in 8 chance of bleeding annually
if varices are present. Each bleed has up to a 20% risk of resulting in death.
Varicosities occur secondary to portal hypertension and are defined
as dilatations of various alternative pathways when cirrhosis obstructs
the portal return of blood (Fig. 9.1). Varicosities occur most often in
the distal third but may occur throughout the esophagus. Acute variceal
hemorrhage is the most lethal complication of portal hypertension. The
median age of these patients is 52 years, and 73% are men.
The most common cause of portal hypertension, affecting 94% of
patients, is cirrhosis. The most common causes of cirrhosis are alcohol-
ism (57%), hepatitis C virus (30%), and hepatitis B virus (10%).
Mortality rates from the initial episode of variceal hemorrhage range
from 17% to 57%. Larger vessels bleed more frequently. Hospitalizations
for acute bleeding from esophageal varices have been declining in recent
years; this is believed to be a result of more active primary and secondary
prophylaxis. Bleeding occurs when the tension in the venous wall leads to
rupture, and shock may follow. Occasionally the bleeding may stop spon-
taneously, but more often it will recur. Thrombocytopenia and impaired
hepatic synthesis of coagulation factors both interfere with hemostasis.
CLINICAL PICTURE
Cardinal symptoms of esophageal varicosities are recurrent hematemesis
and melena. Patients with acute variceal bleeding have hemodynamic
instability (61%), tachycardia (22%), hypotension (29%), and orthostatic
hypotension (10%).
DIAGNOSIS
To prevent a first variceal hemorrhage, patients with cirrhosis should
undergo upper endoscopy to screen for esophageal varices and, if present,
characterize them. Endoscopy should be performed when the patient’s
condition is stable. The risk of initiating bleeding from the varices is
negligible. Endoscopy should also be performed for any patient who
has hemorrhage of unexplained cause. In 25% of patients with varices
that present with upper intestinal bleeding, the diagnosis hemorrhage
from a source other than the varices. Esophageal varices are believed
to be the cause of bleeding if no other source of the bleeding is found.
Other causes include gastric or duodenal ulcers, gastritis, a Mallory-
Weiss tear, and gastric varices.
At endoscopy, the varices are blue, round, and surrounded by con-
gested mucosa as they protrude into the lumen of the distal esophagus.
They are soft and compressible, and an esophagoscope can easily be
passed beyond them. Erosion of the superficial mucosa with an adher-
ent blood clot signifies the site of a recent hemorrhage. On establishing
the presence of esophageal varices, the clinician should also search for
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Neil R. Floch
gastric varicosities, because the surgical treatment may have to be modi-
fied if these have developed.
Imaging is not part of the screening process. Only 40% of varicosi-
ties can be seen on radiographs. A typical finding is a “honeycomb”
formation produced by a thin layer of barium surrounding the venous
protrusion that does not constrict the lumen. Endoscopic color Doppler
ultrasonography is a useful modality for obtaining color-flow images
of esophageal varices and their hemodynamics. Capsule endoscopy is
now being studied as a possible screening tool for esophageal varices;
it has a sensitivity and specificity of 84% and 88%, respectively. Recently,
64-row multidetector computed tomography (CT) portal venography
reliably displayed the location, morphology, origin, and collateral types
of esophageal varices, showing promise as a diagnostic tool. CT was
found to have 90% sensitivity and 50% specificity in finding esophageal
varices. It also has the benefit of detecting extraluminal pathology that
cannot be seen by endoscopy.
TREATMENT AND MANAGEMENT
Variceal management encompasses three phases: (1) prevention of initial
bleeding, (2) management of active bleeding, and (3) prevention of rebleed-
ing. Treatment includes pharmacology, endoscopy, radiologic shunting,
and surgery. Preprimary prophylaxis attempts to prevent varices from
developing in patient with portal hypertension. In these individuals, liver
disease should be treated, but nonselective beta blockers have not proven
to be beneficial. The goal of primary prophylaxis is to prevent hemorrhage
from occurring in patients with known esophageal varices. There are two
acceptable treatments that have been shown to be better than observation.
Endoscopic variceal ligation (EVL) has been demonstrated in studies to
prevent an initial bleed; however, it does not ensure a lower mortality risk,
and EVL carries potential complications. When beta-blockers are used
and tolerated, they may result in a low incidence of side effects and may
be beneficial in reducing the development of both ascites and spontaneous
bacterial peritonitis. Secondary prophylaxis aims to prevent individuals
with a history of bleeding varices from having another variceal bleed.
Prophylaxis can then be instituted according to categorization. Low-
risk patients with hepatitis C are found to have platelet counts
≥150,000/µL and liver stiffness below 20 kPa on transient elastography;
such individuals may avoid endoscopy as long as these parameters are
not exceeded. In other patients who, on screening, do not have varices
and compensated cirrhosis, endoscopy can be repeated every 2 to 3
years. If small varices are found, esophagogastroduodenoscopy (EGD)
should be performed every 1 to 2 years. Those with decompensated
cirrhosis should have yearly endoscopies.
Although many endoscopists categorize them simply as small or
large, the North Italian Endoscopic Club has categorized esophageal
varices as follows:
• F1: Small varices, straight in appearance
• F2: Large tortuous varices involving less than 33% of the esophagus
43
44 SECTION I Esophagus

X-ray
Azygos vein

Esophagoscopic
view (at cardia)

Splenogram

Cirrhotic liver

Diaphragm

Coronary vein

Short gastric vein

Fig. 9.1  Esophageal Varicosities.

• F3: Large coiled varices involving more than 33% of the esophageal
lumen
The Child-Pugh classification is a predictor of surgical risk in patients
with cirrhosis. It has been modified from the Child-Turcotte classifica-
tion, which was based on the variables of serum albumin, bilirubin,
ascites, encephalopathy, and nutritional status. Nutritional status was
replaced with the prothrombin time in the new classification. A score
of 5 or 6 is Child-Pugh class A cirrhosis with a 10% mortality risk, 7
to 9 is class B cirrhosis with a 30% mortality risk, and 10 to 15 is class
C cirrhosis with an 82% mortality risk after undergoing nonshunting
abdominal surgery.
Prophylaxis is started with nonselective beta blockers, of which
nadolol 40 mg/day is the treatment of choice. It reduces portal pressure
and variceal blood flow and decreases the risk of bleeding by 50%. The
medication can be adjusted according to the patient’s response. Carvedilol
may be used as an alternative. The goal of beta blockade is to reduce
the HVPG (hepatic venous portal gradient). “Red signs” are the appear-
ance of varices on endoscopy that appear as red wale marks or long
red marks, red, flat spots known as cherry-red spots, red, raised spots
or hematocystic spots or the presence of diffuse erythema. Prophylaxis
is given to patients who have small varices with red signs or Child B
or C cirrhosis and those with medium or large varices. Other patients

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with Child A and small varices do not receive prophylactic treatment
and are followed by endoscopy. Patients with small varices with red
signs or Child B or C cirrhosis are treated with a nonselective beta
blocker. Those who cannot tolerate this are treated with EVL. In indi-
viduals with medium or large varices, either a nonselective beta blocker
or EVL is used, but EVL may be more effective with larger varices.
Measurements of hepatic venous pressure are used to monitor the
success of pharmacologic therapy, which has been shown to be superior
to sclerotherapy and possibly superior to band ligation. A recent meta-
analysis showed that a combination of endoscopic and pharmacologic
therapy reduces overall and variceal rebleeding in cirrhosis more than
either therapy alone.
If beta blockers are not tolerated or contraindicated or if patients are
at high risk for bleeding, endoscopic band ligation is preferred. The surveil-
lance of varices, with potential rebanding, should be repeated every 6 months.
Acute bleeding requires simultaneous control, resuscitation, and
prevention/treatment of complications. Medical treatment of bleeding
with vasopressin, terlipressin, somatostatin, or octreotide is started.
These medications stop the bleeding in 65% to 75% of patients, but
50% will bleed again within a week. Vasopressin is a posterior pituitary
hormone that constricts splanchnic arterioles and reduces portal flow
and pressure. Prophylactic intravenous antibiotics should also be started.
Endoscopy is performed to diagnose and treat hemorrhage.
Definitive therapy is first performed with sclerotherapy or band
ligation, which is successful in 90% of patients. Varices are injected
with sclerosing solutions to stop acute bleeding. Repeated injections
will cause variceal obliteration and may prevent recurrent bleeding.
However, recurrence is common before complete obliteration, and
esophageal strictures typically develop.
Endoscopic band ligation results in fewer strictures and ulcers than
sclerotherapy and faster eradication. Rebleeding is less frequent with
ligation than with sclerotherapy (26% vs. 44%), but the number of blood
transfusions, duration of hospital stay, and mortality risk are comparable.
When bleeding is under control, endoscopic ligation and sclerotherapy
are repeated every 1 to 2 weeks until the varices are eradicated. This
technique has the fewest complications and the lowest incidence of
recurrence. Surveillance is performed at 3- to 6-month intervals to
detect and treat any recurrence. Patients who have two or more rebleed-
ing episodes should be considered for surgery or transplantation.
Balloon tamponade is used as a bridge to definitive therapy in 6%
of patients when hemostasis is not achieved. Connected balloons in the
stomach and the esophagus compress the varices. Bleeding stops in 80% to
90% of patients but, unfortunately, 60% have recurrences. Complications
such as aspiration and esophageal rupture may also occur. A new method
involves the use of a self-expanding stent to stop acute variceal bleeding,
and initial studies reveal no method-related mortality or complications.
If medical and endoscopic therapies fail, transjugular intrahepatic
portosystemic shunt (TIPS) is the procedure of choice in case of emer-
gency. TIPS should be reserved for patients who have poor liver function.
It can be performed in 90% of patients but is used in only 7%. The
mortality rate with TIPS is low. Bleeding may recur in 15% to 20% of
patients over 2 years. Patients must be followed closely because the
shunt may occlude in up to 50% of cases within 18 months.
Shunt procedures are not the modality of choice because they result
in a high rate of complications compared with medical therapy. Shunts
are now used in less than 1% of patients. Emergency bleeding may be
controlled with a central portocaval shunt or with combined esophageal
transection, gastric devascularization, and splenectomy in patients hoping
for liver transplantation. Emergency shunt surgery carries a 50% mor-
tality risk and is rarely undertaken.
Surgical shunts should be used to prevent rebleeding in patients who
do not tolerate or who are noncompliant with medical therapy and who
have relatively preserved liver function. Portal decompression procedures
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CHAPTER 9  Esophageal Varicosities 45
create a connection between the high-pressure portal and low-pressure
systemic venous systems. Nonselective shunts include portacaval anas-
tomoses and TIPS, which decompress the entire portal system. Selective
shunts, such as the distal splenorenal shunt, decompress only esophageal
varices. Shunt surgery does not improve survival and may result in
hepatic encephalopathy. Elective shunt procedures are avoided in can-
didates for liver transplantation but may be performed in those with
Child A and B cirrhosis. Liver transplantation is the best therapy for
patients with Child C cirrhosis and is performed in only 1% of patients.
COURSE AND PROGNOSIS
Acute variceal hemorrhage occurs more often in patients with Child B and
C cirrhosis. Endoscopic banding is the most common single endoscopic
intervention. Early rebleeding occurs in 13% of patients within a week.
Although medical therapy, banding, and sclerotherapy are still used fre-
quently for rebleeding, balloon tamponade is necessary in 17%, TIPS in
15%, and surgical shunting in 3% of patients. Early complications after
acute variceal bleeding include esophageal ulceration (2%–3% of patients),
aspiration (2%–3%), medication adverse effects (0%–1%), dysphagia and
odynophagia (0%–2%), encephalopathy (13%–17%), and hepatorenal
syndrome (2%). The prognosis for patients with bleeding esophageal
varices depends directly on liver function. Overall short-term mortality
rates after acute bleeding are 10% to 15%. However, in patients with cir-
rhosis who have variceal bleeding, mortality risk is as high as 60% at 1 year.
Maintenance screening depends on the presence of varices and
whether the patient’s disease is chronic. Those with chronic disease
should have endoscopy every 1 to 2 years. Patients with compensated
cirrhosis but no varices should have endoscopy every 2 years, and those
with compensated cirrhosis and small varices should have yearly sur-
veillance. In patients where the liver injury has subsided, such as former
alcoholics and those cured of hepatitis C, an EGD every 2 to 3 years is
appropriate. Prophylactic treatment is started if varices increase in size
or red signs develop. Decompensation at any time warrants an endos-
copy. Patients with larger varices who are on beta blocker treatment
need endoscopy only if there is bleeding.
Patients who receive variceal banding should have a repeat EGD
every 1 to 2 weeks or until all the varices have been treated. Thereafter,
an endoscopy is repeated at 1 to 3 months and every 6 to 12 months
thereafter to rule out recurrences.
ADDITIONAL RESOURCES
Comar KM, Sanyal AJ: Portal hypertensive bleeding, Gastroenterol Clin North
Am 32:1079–1105, 2003.
De Franchis R, Eisen GM, Laine L, et al: Esophageal capsule endoscopy for
screening and surveillance of esophageal varices in patients with portal
hypertension, Hepatology 47(5):1595–1603, 2008.
Jamal MM, Samarasena JB, Hashemzadeh M, et al: Declining hospitalization
rate of esophageal variceal bleeding in the United States, Clin
Gastroenterol Hepatol 6(6):689–695, quiz 605, 2008.
Laine L, el-Newihi HM, Migikovsky B, et al: Endoscopic ligation compared
with sclerotherapy for the treatment of bleeding esophageal varices, Ann
Intern Med 119:1–7, 1993.
Perri RE, Chiorean MV, Fidler JL, et al: A prospective evaluation of
computerized tomographic (CT) scanning as a screening modality for
esophageal varices, Hepatology 47(5):1587–1594, 2008.
Sorbi D, Gostout CJ, Peura D, et al: An assessment of the management of
acute bleeding varices: a multicenter prospective member-based study, Am
J Gastroenterol 98:2424–2434, 2003.
Zaman A: Current management of esophageal varices, Curr Treat Options
Gastroenterol 6:499–507, 2003.
Zehetner J, Shamiyeh A, Wayand W, et al: Results of a new method to stop
acute bleeding from esophageal varices: implantation of a self-expanding
stent, Surg Endosc 22(10):2149–2152, 2008.