clinical support for the notion that portal diversion accelerated the decline of liver function in patients
with cirrhosis and they are no longer performed for this indication.
Endoscopic Sclerotherapy and Variceal Ligation. In the past, prophylactic sclerotherapy to prevent
variceal bleeding was an accepted practice but technical challenges and esophageal and pulmonary
complications have led to abandonment of endoscopic sclerotherapy (ES) for the primary prevention of
variceal bleeding. Initial investigations of the effectiveness of endoscopic variceal ligation (EVL) as a
method of primary prophylaxis to prevent initial bleeding in high-risk patients with esophageal varices
reported mixed results.218,219 In one study, no statistically significant differences in the incidence of
initial bleeding and mortality were found in a comparison of patients after variceal ligation with
controls,220 though subgroup analysis revealed a significant decrease in the incidence of initial bleeding
for Child–Pugh class B patients.219 Furthermore, there seems to be a significant prognostic divergence
related to variceal size. As data have accumulated, consensus recommendations regarding prophylaxis
have emerged as presented in recent practice guidelines from the AASLD. Briefly summarized, patients
with cirrhosis with small, low-risk varices should be managed with beta-blocker prophylaxis. In those
with medium or large varices with high-risk features (Child B or C, red wale markings), either EVL or
beta blockade is acceptable primary prophylaxis. In the absence of the above high-risk features, beta
blockade is preferred, with EVL reserved for those patients who have contraindications to, or are
intolerant of beta blockers.198
Treatment of Esophageal Variceal Bleeding
Initial Management. Initial management of the patient with acute variceal bleeding includes the
following: (a) establishment and maintenance of an airway; (b) hemodynamic monitoring; (c)
placement of large-bore intravenous lines; (d) full laboratory investigation, including measurement of
hemoglobin and hematocrit, coagulation profile, liver function tests, measurement of electrolytes, and
assessment of renal function; (e) administration of blood products as needed, including packed red cells,
platelets, and fresh frozen plasma; and (f) intensive care unit monitoring. Hemoglobin concentration
should be maintained around 8 g/dL.221,222 Transfusion to higher hemoglobin concentrations has been
associated with higher portal pressure and worse outcomes. Furthermore, as gastrointestinal bleeding is
associated with a high risk of subsequent spontaneous bacterial peritonitis in patients with cirrhosis, a 7-
day course of antibiotics (typically a quinolone such as norfloxacin or ciprofloxacin) is also
recommended as standard therapy for acute variceal bleeding.223
Pharmacologic Therapy. The administration of vasoactive medications can be commenced almost
immediately after patient presentation if the history and physical findings suggest variceal bleeding.
This practice decreases the rate of bleeding and enhances the endoscopic ability to visualize the site(s)
of bleeding.
Vasopressin (antidiuretic hormone) has potent splanchnic vasoconstrictive properties that decrease
portal venous and collateral flow and reduce portal pressure. In randomized prospective trials, as well
as in a meta-analysis, continuous intravenous administration of vasopressin has proved to reduce
variceal bleeding, an observation initially made in 1962.224–226 When vasopressin was compared with
placebo, bleeding stopped in an average of 52% of patients who received vasopressin and 18% of
patients who received placebo. Rates of rebleeding as high as 45% were noted, however. Because of
coronary vasoconstrictive effects, vasopressin is often used in combination with a vasodilator, such as
nitroglycerin. The combination provides protection from adverse cardiac events and increases the
effectiveness of vasopressin by decreasing intrahepatic and collateral resistance.227 A meta-analysis of
three randomized controlled trials confirmed the increased effectiveness of vasopressin and
nitroglycerin in comparison with vasopressin alone.228
Somatostatin and octreotide, its longer-acting eight-amino acid derivative, have been used extensively
for the treatment of variceal bleeding. These agents decrease splanchnic blood flow indirectly by
reducing the levels of other factors, such as glucagon, vasoactive intestinal peptide, and substance P,
rather than by direct vasoconstriction.229 The effects of somatostatin are limited to the splanchnic
circulation, so that side effects are minimized.230 A somatostatin and octreotide combination has proved
to be as effective as vasopressin, sclerotherapy, and balloon tamponade in multiple studies.231–233
Because of the lack of complications related to somatostatin therapy, octreotide is the initial drug of
choice for the treatment of acute variceal hemorrhage. Dosing typically consists of a bolus of 50 μg
followed by an infusion of 50 μg/hr, to be initiated as soon as variceal bleeding is suspected and
continued for 3 to 5 days after the diagnosis has been verified.198
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Endoscopic Interventions. Esophageal variceal ligation has become the principal approach to the
initial control and ongoing treatment of variceal bleeding; it is performed at the bedside in acute
bleeding and has replaced variceal sclerosis.
The technique of ligation (Fig. 59-6) includes placing an endoscope over a sheath (which allows
multiple insertions and removal of the endoscope), suctioning of a varix into the lumen of a plastic
channel, and then placing a rubber band around the tissue. The procedure is similar to the ligation of
hemorrhoids. The tissue then sloughs in 1 to 3 days, leaving a shallow ulcer. Up to six bands can be
placed at each session. Newer endoscopes allow for the placement of multiple bands without removal of
the endoscope.
Success rates for variceal ligation range from 80% to 100%, in comparison with 77% to 94% for
sclerotherapy, in controlled trials.234 In patients with profuse bleeding, however, the type of endoscope
used for variceal ligation may make visualization of the bleeding varices difficult leading some
investigators to choose sclerotherapy in these patients, and use variceal ligation once bleeding is
somewhat controlled.
Balloon Tamponade. The vast majority of patients (75% to 90%) with bleeding esophageal varices
respond to endoscopic or pharmacologic therapy. For patients who fail these interventions, balloon
tamponade (Fig. 59-7) is an alternative therapy with a high success rate in controlling bleeding. It
entails the placement of a specialized nasogastric tube with two balloons that can be inflated separately
and to different pressures to apply direct compression to the gastroesophageal junction and the
esophagus. Once the mainstay in the initial management of variceal bleeding, use of these tubes is
becoming a lost art, most suitable for initial stabilization of patients in a facility with limited
availability of endoscopic or radiologic support. Because these tubes are difficult to use, and may cause
fatal complications with esophageal injury, it remains important for surgeons and gastroenterologists
with responsibility for managing gastrointestinal bleeding to understand principles for safe use. The
most commonly used tubes are the Sengstaken–Blakemore tube and the Minnesota tube. The former
consists of a gastric balloon and an esophageal balloon with a sump port for gastric suctioning. The
latter tube has an additional port above the esophageal balloon for the aspiration of saliva and other
material from the esophagus and pharynx.
Figure 59-6. Endoscopic ligation of esophageal varices. The device used for ligation is based on the standard Barron-type ligator
for the treatment of anal hemorrhoids. The esophageal varix is drawn up into the ligating device with suction (A), and the base of
the varix is ligated with an O-ring (B). Up to six varices can be treated at a single session.
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Figure 59-7. The Sengstaken–Blakemore tube is used to tamponade acutely bleeding gastroesophageal varices. The tube has three
lumina—one to aspirate the stomach, another to inflate the gastric balloon, and a third to inflate the esophageal balloon. Patients
treated with balloon tamponade should be in an intensive care unit, and endotracheal tubes should be placed in almost all to
prevent aspiration.
Placement of these tubes begins with the establishment of a safe airway by endotracheal intubation.
The tube is then passed through the nose and into the stomach. Radiographic confirmation that the tip
of the tube is in the stomach is required before balloon inflation to prevent inadvertent intraesophageal
inflation of the gastric balloon and resultant perforation. The gastric balloon is inflated with 200 mL of
air and firmly pulled backward against the gastroesophageal junction to tamponade any proximal
gastric bleeding. The esophageal balloon is then inflated to a pressure of 30 to 40 mm Hg, and the tube
is secured to the patient by means of a facemask or helmet to ensure adequate stability of the tube and
prevent inadvertent removal.
Because of the possible complications of balloon tamponade (e.g., aspiration, esophageal and gastric
perforations, necrosis), which occur in 10% to 20% of patients, its use is restricted to approximately 24
hours. Success rates for cessation of bleeding are 70% to 80%, but more than half of all patients rebleed
when the balloons are deflated. Although this method is highly effective in the initial control of
bleeding, with an efficacy similar to that of pharmacologic agents, because of its transient effects it can
be used only as a temporizing measure in anticipation of a more definitive procedure (e.g., TIPS,
placement of a surgical shunt, or transplantation) and is used only after endoscopic and pharmacologic
therapies have failed.
Transjugular Intrahepatic Portosystemic Shunt. In the 10% to 20% of patients who continue to
bleed or who have early rebleeding, a shunt procedure (to bypass the high-pressure hepatic vascular
bed) may be indicated (Algorithm 59-1). The mortality rate associated with failure to control bleeding
can be as high as 90%, and surgically created shunts in this setting are associated with a high morbidity
and mortality rate.
10 The TIPS (Fig. 59-8) has become first-line treatment for bleeding esophageal varices when the
aforementioned attempts fail.235 Absolute contraindications to TIPS include congestive heart failure,
uncontrolled sepsis, multiple hepatic cysts, severe pulmonary hypertension, and uncontrolled biliary
obstruction. Relative contraindications include HCC, hepatic vein obstruction, severe coagulopathy or
thrombocytopenia, and moderate pulmonary hypertension.236 After ultrasonographic confirmation of
patency of the portal vein, the procedure is performed in the interventional radiology suite, where a
wire-guided stent (8 to 12 mm in diameter) is placed percutaneously into the jugular vein. The wire is
then guided through the superior vena cava, right atrium, and inferior vena cava into a hepatic vein,
after which the catheter traverses the hepatic parenchyma and joins the hepatic vein to a portal vein.
This connection effectively creates a side-to-side portacaval shunt. Success rates in the cessation of
variceal bleeding are as high as 90% to 100%, with an incidence of recurrent bleeding of approximately
10%.237,238
As discussed earlier, the ideal portosystemic shunt lowers the pressure in the portal system without
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