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PORTAL HYPERTENSION 427
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Endoscopic Therapy for
Esophageal Variceal
Hemorrhage
Julie A. Conyers, MD
PORTAL HYPERTENSION AND VARICES
Hemorrhage resulting from rupture of gastroesophageal varices is
one of the most lethal complications of portal hypertension. Portal
hypertension is a common clinical syndrome defined by the indirect
measurement of the hepatic venous pressure gradient (HVPG) > 10
mm Hg. The HVPG is determined by the difference between the
free hepatic venous pressure (FHVP) and the wedged hepatic venous
pressure (WHVP) or HVPG = WHVP – FHVP (Fig. 1). HVPG
Starzl TE, Todo S, Fung J, Demetris AJ, Venkataramanan R, Jain A. FK
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Duct-to-duct reconstruction in liver transplantation for primary sclerosing cholangitis is associated with fewer biliary complications in comparison with hepaticojejunostomy. Liver Transpl. 2014;20(4):457–463.
Tzakis AG, Kirkegaard P, Pinna AD, etal. Liver transplantation with cavopor-
tal hemitransposition in the presence of diffuse portal vein thrombosis.
Transplantation. 1998;65(5):619–624.
Weiss S, Schmidt SC, Ulrich F, et al. Biliary reconstruction using a side-to-
side choledochocholedochostomy with or without T-tube in deceased
donor liver transplantation: a prospective randomized trial. Ann Surg.
2009;250(5):766–771.
Zamboni F, Franchello A, Ricchiuti A, Fop F, Rizzetto M, Salizzoni M. Use of
arterial conduit as an alternative technique in arterial revascularization
during orthotopic liver transplantation. Dig Liver Dis. 2002;34(2):122–
126.
serves as a surrogate measurement of portal pressure in sinusoidal
causes of portal hypertension.
Endoscopic ultrasound (EUS)-guided measurements of the portal pressure gradient (PPG) as the difference between hepatic
venous pressure (HVP) and direct portal venous pressure (PVP), or
PPG = PVP – HVP, has been recently been described and theoretically may be accurate for presinusoidal, sinusoidal, and postsinusoidal etiologies of portal hypertension (Fig. 2).
The development of clinically significant esophageal and gastric
varices is the result of porto-systemic collaterals secondary to portal
hypertension. As the radius of the variceal vessel increases, wall tension exceeds tissue strength resulting in vessel rupture in accordance
with Laplace’s law and Pascal’s principle (Fig. 3). As portal pressure
increases, the likelihood of gastroesophageal variceal rupture and
hemorrhage also increases.
Although liver cirrhosis is the most common etiology of portal hypertension in Western cultures, schistosomiasis is the most
FIG. 1 Hepatic venous pressure gradient (HVPG). (A) Transjugular wedge balloon for measuring HVPG. (B) HVPG is calculated as the difference between
free hepatic vein pressure (FHVP) and wedged hepatic vein pressure (WHVP), which is a surrogate for portal vein pressure in sinusoidal causes of portal
hypertension. (From Jirapinyo P, Thompson CC, Ryou M. Effects of endoscopic gastric plication on portal pressure gradient in a patient with nonalcoholic steatohepatitis
cirrhosis. VideoGIE. 2021;6:491–494.)
428 ENDOSCOPIC THERAPY FOR ESOPHAGEAL VARICEAL HEMORRHAGE
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FIG. 2 Endoscopic ultrasound-guided portal pressure gradient (PPG) measurement. (A) Hepatic venous pressure (HVP) measurement. (B) Portal venous
pressure (PVP) measurement. (C) PPG represents the difference between the PVP and HVP. (From Jirapinyo P, Thompson CC, Ryou M. Effects of endoscopic gastric
plication on portal pressure gradient in a patient with nonalcoholic steatohepatitis cirrhosis. VideoGIE. 2021;6:491–494.)
FIG. 3 Laplace’s law and Pascal’s principle. (From HyperPhysics by Rod Nave,
Georgia State University.)
common cause of varices in countries in sub-Saharan Africa, with
chronic infection in an estimated 440 million people, resulting in
200,000 deaths annually. Although liver function is often well maintained in these patients, hemorrhage from varices is the main cause
of death. In absolute numbers, varices from schistosomiasis may be
more common than liver cirrhosis.
ENDOSCOPIC SCREENING FOR
ESOPHAGEAL VARICES
Prospective studies of the natural history of liver cirrhosis have
demonstrated that 50% to 90% develop esophageal varices, and 30%
will bleed. Bleeding from esophageal varices is associated with a
mortality rate of at least 20% at 6 weeks despite spontaneous resolution of bleeding in 40% to 50%. Mortality from bleeding episodes
depends on the severity of underlying liver disease ranging from less
than 10% in patients with Child-Pugh grade A compared with over
70% in patients with advanced Child-Pugh grade C. Patients with
very high portal pressure (HVPG >20 mm Hg) are at higher risk
of rebleeding within 1 week of hemorrhage, have up to 84% risk of
failure to control initial bleeding, and demonstrate a 1-year mortality
rate of 64%.
TABLE 1 EGD Surveillance for Cirrhosis
Patient EGD Findings Repeat EGD
Compensated Cirrhosis No Varices Every 2–3 years
Compensated Cirrhosis Small Varices Every 1–2 years
Decompensated Cirrhosis Ye ar ly
In patients diagnosed with liver cirrhosis, the gold standard for
screening for gastroesophageal varices is by esophagogastroduodenoscopy (EGD). Varices <5 mm are considered small. Findings
at risk for bleeding include varices >5 mm and red whale markings. Figure 4 demonstrates the spectrum of esophageal varices.
Table 1 summarizes EGD surveillance consensus recommendations
in patients with cirrhosis.
PRIMARY PREVENTION
The strategy for preventing variceal hemorrhage is either by decreasing portal hypertension with nonselective β-blockers (NSBBs),
carvedilol, or by endoscopic variceal ligation (EVL). NSBBs may
help reduce the progression from small to large varices and the risk
of mortality from hemorrhage, but they often are not well tolerated.
Also, one must use caution with NSBBs in patients with refractory ascites. Carvedilol is a NSBB with mild anti-α
decreasing hepatic vascular resistance. However, carvedilol tends to
drop mean arterial pressure (MAP), but may be more effective than
EVL in preventing a first bleed if tolerated. The use of isosorbide
mononitrate (ISMN) in randomized controlled trials demonstrated
higher mortality rates in patients who received ISMN. Consensus
among experts is that NSBB and EVL have similar efficacy in preventing a first esophageal bleed, and there is no benefit to combining
the two treatments. Table 2 summarizes primary prevention thera-
pies for esophageal hemorrhage.
If β-blockers are not tolerated, elective EVL is an option to prevent
esophageal variceal hemorrhage. Banding is recommended only in
the distal 5 cm of the esophagus, where the varices are more superficial. Banding more proximal may result in delayed hemorrhage from
effect, thereby
1
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A B
FIG. 4 (A and B) Endoscopic appearances of esophageal varices. (A) EGD demonstrating dilated and straight veins (small esophageal varices) in the
distal esophagus (arrow). (B) EGD demonstrating large esophageal varices, greater than 5 mm in diameter, with a fibrin plug (arrow) indicating the site of a
recent bleed. (C–E) Large esophageal varices. Endoscopic view of the lower third of the esophagus demonstrating varices greater than 5 mm in diameter.
(C)Large varix (arrow) with a red wale sign. (D) Red wale sign—longitudinal whip mark on varix (arrow). (E) Large varix with hematocystic spot (arrow).
(A and B from Friedman LS, Brandt LJ, Feldman M. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. 11th ed.
Elsevier; 2021; C–E from Sanyal AJ, etal: Zakim and Boyer’s Hepatology: A Textbook of Liver Disease. 6th ed. Elsevier; 2012.)
the varix as the band sloughs, leaving the posterior vessel wall still
intact. Also, because bleeding is a potential complication of EVL, this
procedure may better serve patients if performed in a high-resource
environment. An EVL session every 1 to 8 weeks until eradication is
effective. Proton pump inhibitors are used as adjunctive treatment
for the 0.3% to 3% of ligation-related esophageal ulcers. Surveillance
EGD should be performed in 1 to 3 months after eradication, then
every 6 to 12 months to assess for recurrence.
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TABLE 2 Primary Prevention of Variceal Hemorrhage in Patients With Small Varices With Red Spots
or Varices >5 mm
Therapy Therapy Dose Therapy Goals Maintenance
Propranolol 20–40 mg BID HR 55–60 per minute Check HR
Max: 320 mg/day SBP >90 mm Hg Indefinitely
160 mg/day with ascites No F/U EGD
Nadolol 20–40 mg daily HR 55–60 per minute Check HR
Max: 160 mg/day SBP >90 mm Hg Indefinitely
80 mg/day with ascites No F/U EGD
Carvedilol 6.25 mg daily SBP >90 mm Hg Indefinitely
After 3 days 6.25 mg BID No F/U EGD
Max: 12.5 mg/day
EVL Every 2–8 weeks until eradication Variceal eradication EGD 3–6 months after eradication
then every 3–6 months
BID, Twice a day; EGD, esophagogastroduodenoscopy; EVL, endoscopic variceal ligation; FU, follow-up; HR, heart rate; S BP, systolic blood pressure.
MANAGEMENT OF ACUTE
GASTROESOPHAGEAL VARICEAL
HEMORRHAGE
Resuscitation
Patients who present with upper gastrointestinal bleeding (UGIB)
(hematemesis, melena, currant jelly stools) with findings suggestive
of portal hypertension or cirrhosis (ascites, thrombocytopenia, elevated prothrombin time, history of cirrhosis) should be suspected
of gastroesophageal variceal hemorrhage. Patients often present in
hemorrhagic shock with altered mental status. Initial resuscitation
should focus on the orderly evaluation of airway, breathing, and circulation. Hematemesis can result in aspiration, especially in patients
with developing encephalopathy caused by hyperammonemia, so
one should consider early intubation. Intravenous access with at least
two large-bore IVs is essential. Restrictive balanced blood volume
resuscitation should be initiated based on the physiologic response
rather than hemoglobin levels while avoiding fluid overload from
crystalloid, which may increase portal pressures. Quantification of
blood loss is more challenging in gastrointestinal bleeds, but initiation of a massive transfusion protocol may help facilitate blood
products and resources in patients at risk of exsanguination. Many
cirrhotic patients have an existing coagulopathy that may require
earlier initiation of platelet and fresh-frozen plasma transfusions.
Resuscitation of a hemodynamically unstable patient precludes
waiting for laboratory values. However, restrictive resuscitation
studies are mostly based on laboratory values and may be considered in hemodynamically stable patients. Restrictive resuscitation in
previous prospective studies, defined by a hemoglobin transfusion
threshold of <7 g/dL, was associated with higher survival, decreased
rebleeding, and no significant increases in HVPG or portal pressures compared with a liberal hemoglobin transfusion threshold of
<9 g/dL. Interestingly, in one prospective study, patients received
significant volumes of crystalloid recorded averaging 5.5 L within
the first 72 hours in both restrictive and liberal arms. More studies
may be indicated to determine whether survival is influenced by
also practicing restrictive crystalloid resuscitation in the setting of
gastroesophageal variceal hemorrhage. A recent randomized clinical
trial (HALT-IT) of over 12,000 patients with gastrointestinal bleeding
demonstrated no benefit of tranexamic acid.
Intravenous Antibiotics
The risk of infection is about 60% in cirrhotic patients with gastrointestinal hemorrhage, with the exception of patients with Child-Pugh
grade A cirrhosis, whose infection risk is only 5%. Antibiotics will
significantly reduce the rate of infections, mortality, rebleeding, and
transfusion requirements as demonstrated in clinical trials. Ceftriaxone 1 g/day for 7 days seems to be favored in patients with encephalopathy, ascites, malnutrition, and known quinolone resistance.
Vasoactive Agents
Vasoactive agents, such as octreotide, somatostatin, terlipressin,
and vasopressin, have been shown to reduce all-cause mortality and
decrease transfusion requirements. Octreotide and vasopressin are
available in the United States. An octreotide IV bolus of 50 µg followed by an infusion of 50 µg/hour should be given over 2 to 5 days
and should be initiated before endoscopy.
Prokinetics
The use of metoclopramide or erythromycin may help with visualization at endoscopy and is associated with a lower incidence of need
for repeat EGD in UGIBs, but it has not affected survival. NGTs and
lavage are not effective in evacuating clotted blood from the stomach
or diagnosing UGIBs.
Balloon Tamponade
In patients for whom definitive treatment is not available, balloon
tamponade with an esophagogastric tube is very effective until the
patient can reach definitive treatment. Figure 5 illustrates three
different variations of balloon tamponade tubes. Patients should be
intubated before placing these tubes because of the risk of aspiration
and poor tolerance. The Minnesota tube has four separate ports
including a suction port and a balloon port for the esophagus. The
tube must be placed well into the stomach (at least 50 cm) before
inflating the gastric balloon to avoid esophageal perforation. Traction is placed on the tube until mild resistance is met. The placement
must be verified by x-ray demonstrating the air-filled balloon in the
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FIG. 5 Esophageal tamponade tubes. (A) Sengstaken-Blakemore tube. (B) Linton-Nachlas tube. (C) Minnesota tube.
(From Urden LD, etal. Priorities in Critical Care Nursing. 5th ed. Mosby, 2008.)
stomach. Because most gastroesophageal varices are at the gastroesophageal junction, tamponade can usually be accomplished by
only filling the gastric balloon. Mild traction is placed on the balloon
of 0.5 kg to 1.0 kg using saline IV bags. If bleeding is seen from the
esophageal suction port, the esophageal balloon can be carefully
inflated. For clinicians practicing in low-resource areas, familiarity
with the operation and location of a balloon tamponade tube can
be life saving. The tube should not remain for more than 24 hours.
Although these tubes can control bleeding in 80% of patients, they
are associated with complications secondary to aspiration, migration,
esophageal perforation, or esophageal necrosis.
Endoscopic Variceal Ligation
Once the patient is hemodynamically stable, an urgent EGD should
be performed within 12 hours of admission with the patient intubated
to avoid the risk of aspiration. EVL is the favored treatment over
endoscopic sclerotherapy (EST) for controlling esophageal variceal
hemorrhage as well as for secondary prevention. Several prospective,
randomized trials comparing EVL to EST demonstrated that EVL
was superior to EST for rapidly eradicating varices, less recurrent
bleeding, increased survival, and fewer complications. These findings were validated in a meta-analysis. One study demonstrated
432 ENDOSCOPIC THERAPY FOR ESOPHAGEAL VARICEAL HEMORRHAGE
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decreased rebleeding with EVL combined with a β-blocker. Several
commercial multiband preloaded devices are available with transparent caps. Once the varix is identified, the cap or tip is placed
up to the varix with application of continuous suction to bring the
varix within the cap for deployment of the band. Visualization of the
bleeding varix may be a challenge in a bloody field requiring active
flushing and suction. Consensus guidelines recommend EVL every
1 to 2 weeks until eradication to avoid rebleeding in the absence of
prospective trials typically requiring 2 to 4 sessions. During secondary prophylaxis sessions, bands are placed at the gastroesophageal
junction working proximally in a helical fashion within the palisade
and perforating zones (Fig. 6). Because esophageal varices can recur,
surveillance EGD should be performed every 3 to 6 months after
EVL. The presentation of EVL band-induced bleeding ulcer may
occur in up to 14% of patients. PPIs may provide adjunctive therapy
in preventing bleeding after EVL, but prospective trials are lacking.
Endoscopic Sclerotherapy
EST has been used to treat variceal hemorrhage for over 50 years and
was adopted more widely in the 1970s. The advent of flexible endoscopy in the 1980s resulted in rapid progress of endoscopic treatment
of variceal hemorrhage. Commonly used agents include ethanolamine oleate, polidocanol, sodium morrhuate, sodium tetradecyl
sulfate, and ethanol at varying concentrations, volumes, and intervals. Trials have not defined a single most effective agent. EST is 90%
effective in controlling esophageal variceal bleeding and may be performed in patients in whom EVL may be technically difficult. EST is
also a less expensive option in lower-resource locations. Techniques
include paravariceal injection adjacent to the varix or direct intravariceal injection of the sclerosant. Gastric varices in continuity with
esophageal varices (GOV1) below the gastroesophageal junction may
be treated with EST. Reported local and systemic complications of
EST vary greatly in trials and may be related to operator experience
and follow-up of patients. Complications may include retrosternal
chest pain, dysphagia, esophageal ulcers with subsequent bleeding,
esophageal strictures, esophageal perforation secondary to extensive
necrosis, mediastinitis, bronchoesophageal fistula, bacteremia, acute
respiratory distress syndrome, and death in 2%.
Other Endoscopic Techniques
Argon plasma coagulation has been combined with EVL to eradicate
esophageal varices with a low recurrence rate and no recorded complications. However, this technique is expensive, and this equipment
is not available in many endoscopic centers.
The technique of endoscopic clipping has also been described in
treating acute variceal bleeding and for prevention, with favorable
outcomes in small controlled trials, but it is not widely implemented
or studied.
The use of detachable nylon mini-loops with similar efficacy as
EVL has been largely abandoned after the development of preloaded
multiband devices for EVL.
Injection of adhesives (e.g., cyanoacrylate-based tissue adhesives)
compared with EVL for the treatment of esophageal varices demonstrated more minor complications and higher variceal recurrence
rates. Complications include embolic events and equipment damage.
MANAGEMENT OF ENDOSCOPIC
TREATMENT FAILURES
Transjugular Intrahepatic Portosystemic Shunt
Placement
Placement of a transjugular intrahepatic portosystemic shunt (TIPS)
by interventional radiology in the setting of acute variceal hemorrhage may be a salvage procedure for refractory or recurrent bleeding. This shunt is created by placing a covered metal stent between
the hepatic vein and portal vein with the goal of decreasing portal
pressure and decompressing esophageal varices as well as GOV1 and
GOV2 gastric varices.
FIG. 6 Schema of the lower esophagus anatomy drawn by deCarvalho in
1966. Zone 3 is the junction of the area drained by the portal vein system
and the systemic circulation. This segment begins caudally from the transition between the esophageal and gastric mucosa and ends cranially at the
level of diaphragmatic penetration, spanning the entire abdominal portion
of the esophagus. These longitudinal vessels, called palisade vessels, present
in the mucosal layer of the lower esophagus, are detected by endoscopy. EGJ, Esophagogastric junction. (From Ishimura N, Amano Y, Kinoshita
Y. Endoscopic definition of esophagogastric junction for diagnosis of Barrett’s
esophagus: importance of systematic education and training. Dig Endosc.
2009;21:213–218; adapted from De Carvalho C. Sur I’angio-architecture veineuse de la zone de transition oesophagogastrique et son interpretation fonctionelle.
Cells Tissues Organs. 1966;64:125–162.)
Esophageal Stent for Refractory Bleeding
In small studies, the use of self-expandable esophageal covered metal
stents as a bridge therapy for refractory bleeding shows promise.
These stents can stay in for days, allowing for optimization of the
patients. One small randomized controlled study comparing esophageal stenting versus balloon tamponade in 28 patients demonstrated
better control of bleeding, decreased transfusion requirements, and
lower serious adverse events in the stenting group. Figure 7 shows an
example of a self-expandable covered metal stent.
Gastric Varices
Gastric varices bleed less frequently than esophageal varices and
account for 10% to 30% of all variceal hemorrhages; however, gastric
variceal hemorrhages tend to be more severe, with higher mortality
and rebleeding rates. The endoscopic and interventional radiology
procedures are often predicated on the classification and pathophysiology of the gastric varices. As with esophageal varices, the risk of
rupture increases with the size of the varix. If possible, patients with
gastric varices may be better served at experienced, high-resource
multidisciplinary centers because of their complexity and acuity.
Classification
Sarin’s classification of gastric varices is the most commonly used,
and gastric varices are classified into four types based on location
(Fig. 8). Sarin’s classification of gastric varices, prevalence, and inci-
dence of bleeding are listed in Table 3.
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Endoscopic Treatment of Gastric Varices
Endoscopic treatment of bleeding gastric varices includes the
following:
■ Band ligation with or without detachable snares
■ Sclerotherapy
■ Obturation with tissue adhesives or glue
■ Thrombin injection
■ Combined therapy
■ Endoscopic ultrasound-guided therapy
Only limited data are available regarding the treatment of bleeding gastric varices. Results from limited prospective studies are often
variable and uncontrolled; therefore, it is difficult to draw conclusions about the efficacy of one treatment over another.
In contrast with esophageal varices, band ligation does not
appear to be the preferred treatment of gastric varices because of
FIG. 7 Self-expandable covered metal stent.
FIG. 8 Sarin’s classification is the most commonly used for risk stratifica-
tion and management of gastric varices. GOV type 1 (GOV1): EV extend
below the cardia into the lesser curvature. GOV2: EV extend into the
fundus. Isolated GV1 (IGV1) are located in the fundus. IGV2 are located elsewhere in the stomach. EV, Esophageal varices; GV, gastric varices;
GO V, gastroesophageal varices; IGV, isolated gastric varice. (From Elmunzer
BJ, Chandrasekhara V, Khashab MA, Muthsamy VR. Clinical Gastrointestinal
Endoscopy. 3rd ed. Elsevier; 2019.)
TABLE 3 Sarin’s Classification of Gastric Varices,
Prevalence, and Bleeding Risk
Bleeding
Classification Location Prevalence
Gastroesophageal
Lesser curvature 70%–74% 25%
varix type 1
(GOV1)
Gastroesophageal
varix type 2
Greater
curvature
21%–24% 60%
(GOV2)
Isolated gastric varix
type 1 (IGV1)
Isolated gastric varix
type 2 (IGV2)
Greater
curvature
Stomach/
duodenum
2%–7% 90%
1%–2% 15%
Risk
high rebleeding rates likely resulting from the failure to obliterate
the entire feeding vessel. Also, sclerotherapy has been less effective
in gastric varices as opposed to esophageal varices. Gastric varices
often require larger volumes of sclerosant, especially with GOV2 and
IGV1, resulting in more complications including large ulcerations,
perforations, and mediastinitis. In acute gastric variceal bleeding,
sclerotherapy may control bleeding in 60% to 100% of cases, with
unacceptable rebleeding rates up to 90%. Sclerotherapy may be
effective in treating GOV1 hemorrhage, but it should be avoided in
GOV2 and IGV1 bleeding varices because of low success of primary
hemostasis and the high rate of rebleeding.
Gastric variceal obturation (GVO) with tissue adhesives (e.g.,
N-butyl-2-cyanoacralate or fibrin glue) when compared with ligation
or sclerotherapy appears to be the most effective endoscopic intervention for the treatment of acute gastric variceal hemorrhage. The
endoscopic technique consists of injecting small aliquots (1–1.5 mL)
of cyanoacrylate into the varix followed by a normal saline flush of
volume equal to the needle catheter dead space as the needle is withdrawn from the varix. The tissue adhesives with fast polymerization
using small aliquots appear to be associated with lower incidents of
embolic complications that occur in 1% to 5%. Bacteremia is another
complication of GVO, so antibiotics should be administered. Equipment damage from tissue adhesives is another complication. Several
studies have reported initial hemostasis in 90%, with recurrent
rebleeding rates of 15% to 30%. One to three sessions may be required
for eradication, with success in GOV1, GOV2, and IGV1. Injection
therapy of cyanoacrylate-based compounds for the treatment of gastric varices is not approved by the US Food and Drug Administration.
Direct injection of thrombin into a bleeding gastric varix published in several small series appears to show promise with high
efficacy and low complications and may have a treatment role. Combination endoscopic therapy using ligation and sclerotherapy, GVO
and ligation, and GVO with sclerotherapy have been described in
small series with mixed results. EUS-guided injection of tissue adhesives and/or EUS-guided coil embolization into perforating veins has
recently emerged as a possible tool for treatment of gastric varices in
several small series.
Radiologic Intervention for Gastric Varices
When endoscopic treatment fails, TIPS may provide salvage therapy
with initial hemostasis of 87% to 100% and a rebleeding rate of 10%
to 30%. Frequent complications of TIPS include encephalopathy and
shunt stenosis or occlusion.
Of note, gastric varices classified as IGV1 can be seen in patients
with cirrhosis and portal hypertension and in patients with splenic
vein or portal vein thrombosis. These patients may present with
massive hemorrhage. Because 80% to 85% of IGV1 drain via a gastrorenal shunt into the left renal vein, this provides a pathway to varix
outflow for interventional radiologists to perform balloon-occluded
retrograde transvenous obliteration (BRTO). During this procedure,
the varix is occluded with a balloon followed by the delivery of coils
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and sclerosants with the goal to obliterate the varix. Although BRTO
has been shown to be as effective as TIPS in the treatment of gastric
variceal bleeding, it does not produce encephalopathy, but BRTO
does increase portal pressure, which may worsen esophageal varices.
Major complications include shock and atrial fibrillation.
SUMMARY
Although mortality from gastroesophageal variceal hemorrhage has
decreased over the decades with the advent of advanced endoscopic
and image-guided treatments, variceal bleeds still result in significant morbidity and mortality. Hence, primary prevention of gastroesophageal bleeding plays an essential role in reducing morbidity
and mortality. The optimal management of acute gastroesophageal
variceal hemorrhage with early intubation, balanced, restrictive
resuscitation of blood products, IV antibiotics, vasoactive agents,
and endoscopic intervention remain the cornerstone of managing these patients. For bleeding esophageal varices, band ligation
remains the gold standard treatment. Tamponade by gastroesophageal balloon tubes or self-expandable fully covered esophageal stents
provide bridging treatments. Gastric variceal hemorrhage treatment
is often based on the classification, location, and drainage pattern of
the varix with gastric variceal obturation by tissue adhesives as the
most effective therapy. Image-guided interventions include TIPS,
EUS-guided embolization, and BRTO. High-resource centers are
able to provide these patients with the multidisciplinary treatment
options.
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Transjugular
Intrahepatic
Portosystemic Shunt
Andrew R. Kolarich, MD, Yvonne Tsitsiou, MBBS, and
Christos Georgiades, MD, PhD
INTRODUCTION
The creation of a transjugular, intrahepatic, portosystemic shunt
(TIPS) was put forth as a possible treatment for the symptoms of
portal hypertension in the early 1970s, with the first TIPS placement
performed in 1989. TIPS is an artificial connection between the
portal and hepatic vein, bypassing the liver, and a durable solution
for portal hypertension with a long-term efficacy of 90%. Meticulous
technique and stringent patient selection are critical to keep the
morbidity and mortality in patients with portal hypertension at a
minimum. Refinement of the technique and additional techniques
deployed by interventional radiologists, including direct intrahepatic
portosystemic shunt (DIPS) and adjunct techniques for treatment
of variceal bleeding (such as balloon- or plug-assisted transvenous
obliteration), have expanded treatment options for patients with
complications of portal hypertension.
INDICATIONS
Causes of portal hypertension are summarized in Table 1. Whatever
the causative pathophysiology, TIPS can directly reduce or normalize
the elevated portal pressure and reduce or ameliorate symptoms.
Current indications for TIPS, which are expanding, along with contraindications are summarized in Table 2. TIPS can be performed
on an emergent basis or as an elective procedure. Multidisciplinary
communication between hepatologists, interventional radiologists,
and transplant surgeons is necessary to identify and select appropriate patients for TIPS.
Acute Variceal Bleeding and Secondary Prophylaxis
Portal hypertension can cause varices along the entire gastrointestinal
tract from the esophagus to the rectum to divert the elevated portal
flow to the heart. Gastroesophageal varices, formed between the
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TABLE 1 Causes of Portal Hypertension
Presinusoidal Perisinusoidal Postsinusoidal
Portal, splenic, or superior mesenteric vein
thrombosis
Idiopathic portal hypertension Congenital hepatic fibrosis Veno-occlusive disease (Sinusoidal obstruction
Mass effect (i.e., tumor) Sarcoidosis Chronic passive congestion (Nutmeg liver)
Schistosomiasis Mass effect (i.e., tumor)
Primary biliary cirrhosis
Alcoholic central sclerosis
Endothelitis (liver rejection, radiation injury)
Arterio-portovenous fistula (traumatic or
Osler-Weber-Rendu)
Hyperdynamic splenomegaly (infectious or
myelodysplastic)
Nodular regenerative hyperplasia
Cirrhosis Budd-Chiari syndrome
syndrome)
TABLE 2 Indications and Contraindications for TIPS
Indications Contraindications
Indication Condition Absolute Relative
Portal variceal hemorrhage Refractory to medical/
endoscopic management
Recurrent ascites Refractory to medical
management
Recurrent, hepatic hydrothorax Refractory to medical
management
Hepatorenal syndrome May help in Type 2 Severely elevated right heart
Hepatopulmonary syndrome Scant evidence Severe encephalopathy
Budd-Chiari syndrome Bridge to transplant Active infection
Portal gastropathy Refractory to β-blockers
coronary vein (also known as the left gastric vein) and the lower esophageal veins, are the most likely to rupture and bleed because of the
high transluminal pressure gradient caused by the negative esophageal
luminal pressure during inspiration. Primary treatment of bleeding
gastroesophageal varices is medical management (i.e., somatostatin or
octreotide) followed by endoscopic management (i.e., sclerotherapy/
epinephrine injection, band ligation, clip placement). Even though
endoscopic management is often temporarily successful, recurrent
bleeding is expected in more than half of the patients. Unlike medical
or endoscopic management, TIPS addresses the underlying portal
hypertension and, outside of liver transplant, is the only definitive
treatment. In patients at high risk of treatment failure (i.e., Child-Pugh
class B with active bleeding at index endoscopy or Child-Pugh class C
score lower than 14 points), TIPS placement is indicated at an early
time point, which is within 72 hours (ideally <24 hours).
Ascites
Ascites is the most common complication of cirrhosis. In addition
to severe limitations in lifestyle, ascites poses risks for bacterial
Uncorrectable bleeding diathesis Hepatic vein thrombosis
Portal vein thrombosis
Poor liver function reserve
pressure
peritonitis, renal failure, and increased mortality. Initial management
of ascites is medical and includes diuretics, aldosterone antagonists,
and sodium restriction. Intermittent paracentesis generally follows,
which is often done on an outpatient basis. In advanced stages,
ascites becomes refractory to medical management and repeat paracentesis becomes burdensome. TIPS is very effective in eliminating
ascites, but as the root causes of ascites are hemodynamic/hormone
related, the response is not immediate. It may take 2 to 4 weeks after
TIPS for ascites to resolve, during which time paracentesis may be
necessary. Often, drainage of ascites before TIPS placement is performed to decrease movement of the liver.
Hepatic Hydrothorax
Hepatic hydrothorax is defined as the accumulation of at least 500
mL of pleural fluid in a patient with cirrhosis, without cardiopulmonary disease. Even though this definition is not highly specific
to hepatic hydrothorax, additional signs such as isolated right-sided
hydrothorax and concurrent ascites help confirm the diagnosis. It
occurs in less than 10% of patients with cirrhosis as peritoneal fluid
436 TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT
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permeates via diaphragmatic communications. Initial management
is sodium restriction and diuretics; in nonresponsive patients, TIPS
will eliminate hydrothorax in most and decrease the frequency of
thoracentesis in the rest.
Hepatorenal Syndrome
Hepatorenal syndrome (HRS) portends a poor prognosis for the cirrhotic patient, as it occurs during the late stages of the hemodynamic
changes related to cirrhosis. Alterations in vasoactive hormones
responding to these hemodynamic changes result in splanchnic
vasodilation, renal artery vasoconstriction, and the opening of
small intrarenal arteriovenous communications. The result is renal
hypoperfusion and ensuing renal failure.
Two distinct forms of HRS have been identified: type 1 HRS,
which progresses rapidly, and type 2 HRS, which evolves slowly. Type
1 HRS is precipitated by either an event that incites acute-on-chronic
liver failure, an exaggerated systemic inflammatory response, or kidney dysfunction as part of a broader multiorgan failure. Targeting the
precipitating event is the hallmark of treatment for type 1 HRS. Type
2 HRS results from the reduction of effective arterial blood volume
created by a shift of fluid from the intravascular compartment to
the extravascular compartment (i.e., ascites). Noncontrolled studies
suggest using TIPS to reduce the production of ascites in type 2 HRS.
Hepatopulmonary Syndrome
Hepatopulmonary syndrome is the presence of intrapulmonary
vasodilation and multiple small right-to-left shunts that result
in impaired gas exchange. Because of the lack of data, TIPS cannot be recommended as standard treatment for hepatopulmonary
syndrome. However, in selected cases, especially in severely compromised patients on the liver transplant list, TIPS may prove a
lifesaving bridge to transplant.
Budd-Chiari Syndrome
Budd-Chiari syndrome is an uncommon condition caused by
obstruction of the hepatic venous outflow tract, resulting in cirrhosis
and portal hypertension. The etiology of Budd-Chiari syndrome
encompasses several conditions; it is deemed primary when the
hepatic venous outflow obstruction is primarily a venous problem
(patients with hypercoagulable states resulting in thrombus, venous
webs) and secondary when it relates to extrinsic compression (compression from tumors, cysts, or abscesses). Clinical presentation may
be asymptomatic, fulminant, acute, subacute, or chronic.
The treatment for patients presenting with fulminant BuddChiari syndrome, which develops within a few days with severe liver
failure, abrupt onset of ascites, and hepatomegaly, is liver transplantation. If caused by a hepatic venous web, angioplasty and placement
of a TIPS or DIPS has proven to be a valuable tool in bridging these
patients with fulminant Budd-Chiari syndrome to transplant.
In the nonfulminant forms of Budd-Chiari syndrome, anticoagulation is the first-line therapy. When anticoagulation fails, TIPS is a
reasonable and accepted next step, as is DIPS if the hepatic veins are
occluded. The use of TIPS in this patient population was examined
in a large retrospective study that showed 1-year and 10-year transplant-free survival were much greater than expected. The American
Association for the Study of Liver Diseases (AASLD) now recommends creation of a TIPS in patients with Budd-Chiari syndrome
who fail to improve with anticoagulation.
Portal Hypertensive Gastropathy
Portal hypertensive gastropathy (which is distinguished from vascular ectasia) is the diffuse dilation of gastric veins that, along with the
inflamed and fragile mucosa of the stomach, predispose the patient
to bleeding. Gastric varices occur less frequently than esophageal
varices but are associated with massive bleeding events and higher
mortality rates. Various treatment modalities, including pharmacotherapy and endoscopic treatment, can be used as prophylactic
agents and acute treatment of bleeding portal gastropathy. However,
without portal decompression, rebleeding is imminent. TIPS can
help decrease portal pressures, which can help decompress and
control variceal bleeding, and is indicated in portal hypertensive
gastropathy. However, patients with poor hepatic reserve, as defined
by the Model for End-Stage Liver Disease (MELD) score >17–19,
are shown to have a significantly higher 3-month mortality rate
than those with lower MELD scores. In patients with isolated portal
hypertensive gastropathy, balloon-occluded retrograde transvenous
obliteration (BRTO) and TIPS have been well described in the literature as effective procedures in managing gastric varices with low
rebleeding rates.
TECHNIQUE
Patient Preparation
Many complications of TIPS can be avoided or reduced by proper
patient workup. Review of pertinent cross-sectional imaging confirms a patent (nonthrombosed) portal vein. This minimizes the
number of attempts to engage the portal vein and minimizes associated risk for bleeding. Good hydration minimizes risk of acute renal
failure. Initiation of metronidazole or lactulose mitigates the risk of
encephalopathy. Patients should be blood-typed and cross-matched
in the event of a bleeding complication. Finally, relevant risks, especially the 30-day mortality, which ranges from 1% to 3% for elective
procedures in well-compensated patients to 30% for emergent TIPS
in patients with advanced liver disease, should be understood by the
treating physicians, the patient, and their family. Detailed steps with
rationale for the TIPS placement procedure are shown in Figure 1.
Diagnostic Assessment
Optimizing the TIPS outcomes requires not only anatomic assessment, but also functional assessment of the patient’s hemodynamic
status. One strong contraindication to TIPS is elevated right heart
pressure; ensuring that the right atrial pressure is not severely elevated is mandatory. If this is not done, shunting of portal venous
blood to an overburdened right heart can result in pulmonary congestion, frequently necessitating intubation. Right atrial pressures
below 15 mm Hg are generally safe, whereas pressures above 20
mm Hg predispose patients to acute right heart failure. There are no
specific guidelines; thus, sound clinical judgment is important; for
example, an unstable patient with ongoing variceal bleeding and a
right atrial pressure of 16 mm Hg should not be automatically precluded from a potentially lifesaving TIPS.
After selecting the right hepatic vein, free and wedged hepatic
venous pressures are measured and usually confirm portal hypertension. Normal corrected pressures are not accurate in general and
should not necessarily terminate the procedure. In fact, they are
wholly inaccurate in cases of presinusoidal (e.g., Budd-Chiari syndrome) portal hypertension.
If the direct portal pressure is within normal limits, TIPS creation is abandoned irrespective of the clinical picture. If a TIPS is
not possible or contraindicated, the gastroesophageal varices can
be embolized via a catheter to stop the hemorrhage without placing
a TIPS. Balloon-assisted transvenous obliteration (BRTO) and its
derivative procedures are very effective but temporary; the ongoing
portal hypertension will likely cause new varices to form (Fig. 2).
If the direct portal pressure is elevated, the stent is advanced
through the larger sheath, keeping it constrained and in position.
The sheath is pulled back into the right atrium, uncovering the
stent. The distal 2 cm of the stent are uncovered and flare out on
withdrawal of the sheath. The rest of the stent is then fully expanded
under fluoroscopy.
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