Varices: Esophageal, Gastric, and Rectal

Var ice s
Esophageal, Gastric, and Rectal
a, b,c
Thomas O.G. Kovacs, MD *, Dennis M. Jensen, MD
KEYWORDS
Esophageal varices Gastric varices Rectal varices Portal hypertension
UGI bleed Band ligation Sclerotherapy Hematochezia
KEY POINTS
Either esophageal band ligation and/or nonselective b-blockers (propranolol, nadolol, and
carvedilol) are recommended for the prevention of first hemorrhage.
For patients presenting with acute esophageal variceal bleed, volume resuscitation, vaso-
active medications (octreotide), and prophylactic antibiotics should be initiated followed
by urgent upper endoscopy and endoscopic hemostasis when variceal bleeding is
suspected.
Prevention of rebleeding from esophageal varices is best accomplished by an endoscop-
ist experienced in management of upper gastrointestinal bleeding and combination of
band ligation and/or sclerotherapy and nonselective b-blockers until varices are
obliterated.
For patients with gastric variceal hemorrhage, cyanoacrylate glue injection (if available),
sclerotherapy, or band ligation (if technically possible) is recommended management.
For patients with bleeding rectal varices, endoscopic treatment includes band ligation (if
technically feasible), sclerotherapy, or cyanoacrylate glue injection (if available).
INTRODUCTION
Gastrointestinal (GI) varices are abnormally dilated submucosal veins usually caused
by portal hypertension that can occur throughout the digestive tract, especially
the esophagus, stomach, and rectum. Sometimes they also occur at surgical anas-
tomotic sites. Among a large Center for Ulcer Research and Education (CURE) He-
mostasis Research Group cohort of approximately 1000 patients with severe
a
Division of Digestive Diseases, David Geffen School of Medicine at UCLA, Ronald Reagan –
UCLA Medical Center, Olive View-UCLA Medical Center, Sylmar, CA, USA; b Medicine-GI, VA
Greater Los Angeles Healthcare System, Ronald Reagan – UCLA Medical Center, David Geffen
School of Medicine at UCLA, CURE:DDRC, Room 318, Building 115, 11301 Wilshire Boulevard,
Los Angeles, CA 90073-1003, USA; c Human Studies Core and GI Hemostasis Research Unit, VA/
CURE Digestive Disease Research Center, Los Angeles, CA, USA
* Corresponding author.
E-mail address: [email protected]
Clin Liver Dis 23 (2019) 625–642

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626 Kovacs & Jensen
upper GI (UGI) bleeding, gastroesophageal varices (GOVs) comprised approximately

23% of cases1 (Fig. 1). Variceal hemorrhage is associated with significant morbidity
and mortality, which place a major burden on health care costs.2 The prevalence of
esophageal varices (EVs) increases with the severity of liver disease (Child-Pugh
class A, 43%; Child-Pugh class B, 71%; and Child-Pugh class C, 76%).3 Approxi-
mately 50% of patients with newly diagnosed cirrhosis have GOVs. Small EVs prog-
ress to large ones at a 10% annual rate. The annual variceal hemorrhage risk for
small varices is 5% and for large ones is 15%.4 The 6-week mortality rate after an
index EV bleed, however, is approximately 20%5 but ranges from 0% among pa-
tients with Child-Pugh class A to approximately 30% among patients with Child-
Pugh class C disease.6 Red wale marks on varices in addition to variceal size and
decompensated liver disease identify patients at higher risk of variceal
hemorrhage7,8.
RISK STRATIFICATION
Increased blood flow through the portosystemic collaterals due to portal hyperten-
sion leads to dilation of the submucosal venous plexus producing elevated intravar-
iceal pressure and increased wall tension in the varices (Fig. 2). The mechanism of
variceal rupture is best described by the Laplace law—wall tension is related to the
transmural pressure x variceal radius, divided by the variceal wall thickness.
Portal pressure increments produce increased flow through the varices and
increased intravariceal pressure. Randomized controlled trials (RCTs) have reported
that patients with hepatic venous pressure gradient (HPVG) less than 12 mm Hg
(where the normal is 3–5 mm HG) do not develop variceal hemorrhage.9 An HPVG
greater than 20 mm Hg, however, is associated with an increased risk of failure to con-
trol hemorrhage and early rebleeding and death.10 Reducing the HPVG greater than
Fig. 1. Prevalence of diagnoses for severe UGI bleeding: CURE Hemostasis Research Group.
CA, Cancer; Dx, Diagnoses; ESO, Esophageal; GD, Gastroduodenal; MWT, Mallory-Weiss tear;
PHTN, Portal hypertension; UCLA, University of California at Los Angeles; VA, Veteran’s
Administration Greater Los Angeles Health Care System.
Varices 627
Fig. 2. Veins of distal esophagus: normal venous anatomy and EVs with portal hypertension.
20% from baseline (by b-blockers or other drugs) decreases the risks of further
bleeding and death.11
Esophagogastroduodenoscopy (EGD) is the gold standard for the diagnosis of
esophagogastric varices and for estimating the size of the varices and finding high-
risk stigmata, such as red wale marks. Endoscopy can discern whether varices are ab-
sent, small (<5 mm), medium, large (>5 mm), or giant size (>10 mm). Large or giant
varices have a greater risk of bleeding due to higher wall tension. Red wale marks
are another indicator of higher bleeding risk. Expense of and limited diagnostic sensi-
tivity of current esophageal capsule endoscopy suggest it is not a useful alternative to
upper endoscopy for esophagogastric variceal screening12,13 or the detection of
gastric varices.
Noninvasive tests have been used to predict the presence of esophagogastric vari-
ces, without much success, and do not correlate well with HPVG changes. Recently,
in patients with compensated cirrhosis, a combination of liver stiffness (LS), measured
by transient elastography (with LS <20 kPa), and platelet count (>150,000/mm3) has
been recommended as a method of identifying patients with a very low probability
(<5%) of having high-risk varices.14 Potentially, with such low scores, endoscopy
could be avoided in these patients, representing approximately 20% to 25% of current
screening endoscopies. These guidelines were recently validated in a large cohort of
patients with hepatitis B virus–associated or hepatitis C virus–associated cirrhosis.
The study showed that none of the 80 patients with LS less than 20 kPa and platelet
counts greater than 150,000 had EVs requiring treatment.15 Approximately 25% of the
endoscopies could have been avoided, while missing only 1.3% of varices needing
therapy.15 Most cirrhotic patients with cirrhosis who do not meet those criteria, how-
ever, should have a screening upper endoscopy to diagnose and potentially treat
esophagogastric varices.
For compensated cirrhotic patients who undergo screening endoscopy, current
recommendations about esophagogastric varices include
1. If no varices are seen, screening endoscopy should be repeated every 2 years for
ongoing active liver injury or every 3 years if the liver disease is quiescent.
2. If small varices are noted, endoscopy should be repeated yearly in patients with
ongoing liver injury or every 2 years if the liver disease is quiescent.
3. Patients with compensated cirrhosis without varices who develop decompensation
should have a repeat EGD when this occurs.16
628 Kovacs & Jensen
There is no evidence to suggest that current medications, such as nonselective

b-blockers (NSBBs), prevent the formation of EVs in patients who do not have them
at baseline EGD.17
PREVENTION OF FIRST HEMORRHAGE IN ESOPHAGEAL VARICES
Primary prophylaxis of EV hemorrhage is indicated in patients at increased risk of

bleeding. Patients with medium, large, or giant EVs; patients with small varices with
red wale marks; and decompensated patients with small varices are candidates for
primary prophylaxis.7,15
In patients with medium or large varices, meta-analyses of RCTs have shown that
both NSBBs and band ligation are effective in preventing first variceal hemorrhage.18
By consensus, either NSBBs (propranolol, nadolol, and carvedilol) or band ligation are
recommended to prevent first variceal bleed in high-risk patients with EVs with me-
dium or large varices (Table 1).19
Table 1
Prevention of first hemorrhage in cirrhotic patients: management recommendations
Therapy Recommended Dose Therapy Goals Maintenance/Follow-up

EVL Every 4–6 wk until the Variceal eradication First EGD performed
eradication of varices (no further ligation 3–6 mo after
possible) eradication and every
6–12 mo thereafter
Propranolol 20–40 mg orally Resting heart rate At every outpatient
twice a day of 55–60 beats per visit check heart rate
Adjust every 2–3 d minute Continue indefinitely
until treatment goal Systolic blood pressure If used in combination
is achieved should not decrease with EVL, continue
Maximal daily dose: <90 mm Hg until EVs are
320 mg/d in patients Titrate dose to reduce eradicated
without ascites resting pulse to by
160 mg/d in patients 20%–25%
with ascites
Nadolol 20–40 mg orally Resting heart rate of At every outpatient
once a day 55–60 beats per visit check heart rate
Adjust every 2–3 d minute Continue indefinitely
until treatment goal Systolic blood pressure If used in combination
is achieved should not decrease with EVL, continue
Maximal daily dose: <90 mm Hg until EVs are
160 mg/d in patients Titrate dose to reduce eradicated
without ascites resting pulse to by
80 mg/d in patients 20%–25%
with ascites
Carvedilol Start with 6.25 mg Systolic arterial blood Continue indefinitely
once a day pressure should not If used in combination
After 3 d increase to decrease <90 mm Hg with EVL, continue
6.25 mg twice-daily until EVs are
Maximal dose: eradicated
12.5 mg/d (except in
patients with persistent
arterial hypertension)
Abbreviations: EV, Esophageal varices; EVL, Esophageal variceal ligation.
Varices 629
The potential advantages of NSBBs are low cost, no requirement for specific
expertise to administer, and no need for surveillance endoscopy. Disadvantages of
NSBBs include that approximately 15% to 20% of patients have absolute or relative
contraindications to their use and another 15% to 20% develop side effects, such
as shortness of breath, fatigue, and weakness, and need to discontinue or reduce
dosage. Another major disadvantage is that patients with advanced cirrhosis and por-
tal hypertension may respond poorly and that decreasing the pulse by 20% to 25%
does not predictably reduce HPVG and the risk of bleeding in substantial proportion
of patients.19
Advantages of band ligation are that it can be done during the initial screening
endoscopy and there few contraindications. It is also well tolerated in patients.19 Dis-
advantages are that sedation is required; procedural complications, such as post-
banding ulcer bleeding and postbanding ulcers, may occur or bleed; and
surveillance endoscopy is needed to monitor variceal obliteration and recurrence.
The combination of NSBBs and band ligation was not more effective than banding
alone in preventing bleeding or mortality in a RCT20 and thus combination therapy
is not usually recommended. The authors’ preference based on relative patient intol-
erance to NSBBS and on outcomes with band ligation is for endoscopic
intervention.19
In patients with small EVs at a high risk of bleeding, with red wale marks, and/or
in decompensated cirrhotics, NSBBs are the suggested therapy.16 For low-risk small
varices, management is controversial, but limited evidence suggests that NSBBs
may slow the growth of the small varices.21 Individualization of management for pri-
mary prophylaxis is highly recommended. The main focus should be on whether
high-risk varices are present and whether a patient prefers endoscopic, medical,
or no therapy.
TREATMENT OF ACUTE ESOPHAGEAL VARICEAL HEMORRHAGE
Acute variceal hemorrhage is a medical emergency requiring urgent and intensive

intervention. The essential treatment aims are the control of active bleeding, preven-
tion of rebleeding, and reduction of early mortality (the main therapeutic outcome
metric). All patients with variceal hemorrhage should be aggressively resuscitated to
achieve hemodynamic stability and to protect the airway from aspiration, which is
life threatening. Elective intubation is highly recommended in any patient with ongoing
hematemesis, neurologic impairment, altered mental or respiratory disorders, or diffi-
culty sedating with intravenous (IV) conscious sedation.
A recent RCT in patients with GI hemorrhage reported that restrictive packed red
blood cell (pRBC) transfusion strategy (starting pRBC transfusion at a hemoglobin
level of 7 g/dL and maintaining it at 7–9 g/dL) significantly reduced mortality
compared with a liberal transfusion strategy (starting pRBC transfusion at a hemo-
globin level of 9 g/dL and maintaining it at 9–11 g/dL).22 The greatest benefit was
observed in the subgroup of cirrhotic patients randomized to the restrictive transfu-
sion protocol, who had significantly decreased early rebleeding and mortality rates.
The benefits were for the Child-Pugh class A and Child-Pugh class B groups but not
Child-Pugh class C.22 This trial excluded patients with severe GI bleeding or comor-
bidities: active hemorrhage, severe hemodynamic compromise, and cardiac comor-
bidities. Therefore, the appropriate transfusion strategy needs to be carefully
individualized for elderly patients with active bleeding, hypotension, and hypoperfu-
sion and associated cardiovascular disorders, such as myocardial ischemia. In
contrast, in a study of unselected patients at CURE (of no patients excluded)
630 Kovacs & Jensen
reported that adequate hemodynamic resuscitation and limiting red blood cell trans-
fusions in cirrhotic patients did not increase mortality.23 Clearly cirrhotic patient man-
agement before and after endoscopy needs to be individualized based on acute,
severity of liver disease, and comorbidities.
Because cirrhotic patients with GI bleeding are at increased risk of developing bac-
terial infections, antibiotic prophylaxis has been demonstrated in RCTs to reduce in-
fections, rebleeding, and mortality. Therefore, short-term (no longer than 7 days)
antibiotic prophylaxis should be started in any cirrhotic patient and GI bleed. For
example, IV ceftriaxone, 1 g/24 h, is the antibiotic of choice.14
Vasoactive medications (such as octreotide, somatostatin, vasopressin, and terli-
pressin) cause splanchnic vasoconstriction and can decrease portal pressure
HVPG. One of these agents should be administered as an IV infusion as soon as var-
iceal hemorrhage is suspected. A meta-analysis of 30 RCTs reported that vasoactive
drug in acute EV bleeding decreased 7-day all-cause mortality and reduced transfu-
sion requirements.24 A selected vasoactive agent should be initiated prior to endos-
copy. Octreotide is the only vasoactive medication available in the United States
and a meta-analysis showed that it significantly reduced acute bleeding.24 There
were no significant differences in outcomes among patients treated with different
agents—octreotide, somatostatin, or a vasopressin analog, terlipressin.25 Vasoactive
agents should be continued for 2 days to 5 days.
Currently, routine use of plasma products and platelet transfusions is not recom-
mended. Similarly, platelet transfusions are not suggested for patients on antiplate-
let medications with a normal platelet count. Although empirical, it seems
reasonable to aim for an International Normalized Ratio score less than 2.0 and
platelet count greater than 50,000/mm3 in hemodynamically unstable patients
with active variceal hemorrhage. Evidence-based data are lacking to document
this recommendation.
Erythromycin (250 mg IV) or metoclopramide (10 mg IV) given 30 minutes to 60 mi-
nutes before endoscopy increases gastric motility and may improve visualization dur-
ing endoscopy. Clinical outcome improvements, however, have not been reported
with use of these medications.
Upper endoscopy is recommended within 12 hours after presentation in cirrhotic
patients with severe UGI hemorrhage once hemodynamic resuscitation has been
achieved.16 Initially, a therapeutic endoscope with a large suction channel and target
irrigation is recommended. This facilitates suctioning of blood clots, target irrigation,
and better visualization compared with a smaller diagnostic scope. A diagnosis of
EVs as the source of a patient’s UGI hemorrhage is based on the finding of a stigmata
of recent hemorrhage, such as active bleeding (Fig. 3), a platelet plug (white nipple
sign) (Fig. 4), or overlying clot or a combination of these, which indicates the bleeding
site. Red markings on varices, veins-on-veins, or blood in the stomach and presence
of varices without other potential sources of bleeding are less definitive but indicate
that in the absence of other UGI findings that the EVs are the presumptive source of
severe UGI hemorrhage. Red color signs or red wale marks on varices (Fig. 5) are pre-
dictors of higher risk for future bleeding and are not a definitive sign of recent
hemorrhage.
Esophageal band ligation, first described by Van Stiegmann and Goff,26 is the cur-
rent treatment of choice for bleeding and nonbleeding EVS.
Band ligation results are excellent for most cases and provide high rates of initial he-
mostasis, low rates of rebleeding, few side effects, and improved survival compared
with sclerotherapy. Variceal ligation with a diagnostic-sized endoscope can be used to
control active variceal bleeding with bands placed over the actively bleeding varix or
Varices 631
Fig. 3. Active variceal bleeding from an EV.
on the platelet plug (Fig. 6). The authors recommend that bands are placed distally,
within 2 cm of the gastroesophageal junction (GEJ) (Fig. 7) and 4 cm to 6 cm proxi-
mally above the GEJ. Each bleeding and nonbleeding column of EVs should be treated
similarly, with 2 bands per variceal column, placed in a spiral manner starting at the
GEJ and moving proximally.
Brisk variceal hemorrhage may preclude the ability to do band ligation, either due to
limited visibility or in adequate suctioning of the varix into the band housing. Endo-
scopic sclerotherapy is a useful alternative in such cases to control active bleeding
prior to banding all varices (2 bands per column—1 distally and another proximally).
The authors recommend injecting a sclerosant solution into (intravariceal) or adjacent
(paraesophageal) the bleeding EV to control active bleeding. Several sclerosant solu-
tions are available, with ethanolamine oleate (5%), polidocanol (1%–2%), and cyano-
acrylate used most commonly. The authors’ sclerotherapy technique through a
therapeutic endoscope is to inject 1-mL to 1.5-mL aliquots per injection of
Fig. 4. Platelet plug on an EV.
632 Kovacs & Jensen
Fig. 5. Large EV with red wale marks.
ethanolamine oleate (5%) through a 25-gauge sclerotherapy needle, distal and prox-
imal to the bleeding varix. Subsequently, all nonbleeding varices are treated with 2
bands/columns, as described previously with band ligation.
Other endoscopic modalities, such as clipping, thermal contact devices (such as
multipolar coagulation or heater probe), or argon plasma coagulation, are not recom-
mended for esophageal or gastric variceal hemostasis. These should be used for non-
variceal hemostasis.
The initial surveillance endoscopy is usually scheduled 1 week to 2 weeks after the
index treatment of patients hospitalized for EV hemorrhage. Then, repeat EGDs are
recommended at 4-week to 6-week intervals until all the EVs are completely obliter-
ated. The use of a Doppler endoscopic probe (DEP) to monitor blood flow as guide
to endoscopic therapy27 improves clinical outcomes for cirrhotic patients with severe
variceal bleeding. The DEP produces an audible signal related to the underlying
venous blood flow of varices, allowing a distinction between arterial (higher-pitched
pulsatile signal) and venous (low-pitched continuous signal) blood flow. A recent
RCT of DEP monitoring in patients with severe variceal hemorrhage showed that
Fig. 6. Band ligation over a platelet plug.
Varices 633
Fig. 7. Band ligation of a distal EV. (A) Acutely. (B) Follow-up band ligation.
DEP-guided endoscopic hemostasis reduced 30-day rates of rebleeding, transfusion

requirement, and hospital stay.28 Residual variceal blood flow after visually guided
endoscopic therapy was strongly associated with variceal rebleeding. These
improved outcomes suggest that DEP is extremely valuable in risk assessment and
as a guide to completion of endoscopic treatment of patients with bleeding varices.
TREATMENT FAILURE
If variceal hemorrhage is not controlled by a combination of a vasoactive agent and

endoscopic treatment, other techniques can be used as bridge to more definitive
treatment. Sengstaken-Blakemore tubes have been utilized to tamponade varices.
The rate of hemostasis ranges from 50% to 80%, with a rebleeding rate of approxi-
mately 50% after deflation of the balloons (usually within 24 hours).16 Furthermore, re-
ported serious side effects, including aspiration, esophageal ulcer formation, and
esophageal perforation, occur frequently. Currently most physicians and surgeons
have limited experience with tamponade tubes and their utilization should be limited.
Endoscopically placed self-expanding covered metal stents also can provide hemo-
stasis of bleeding EVs. The stents expand inside the esophagus and tamponade the
varices to produce hemostasis. The stents can be left in for up to 2 weeks (although
stent retrieval is recommended after 7 days). Side effects, such as stent migration,
ulcers, and rebleeding, after stent removal are less severe than for the Sengstaken-
Blakemore tubes. Compared with balloon tamponade tubes, stents have been re-
ported to have lower transfusion requirements and fewer serious adverse events
but no survival advantage.29 For patients with uncontrolled EV hemorrhage, stents
may be a safer than balloon tamponade tubes and more effective bridge to definitive
therapy.
Patients with persistent bleeding despite medical and endoscopic therapy should be
considered for early transjugular intrahepatic portosystemic shunting (TIPS) with poly-
tetrafluoroethylene stents.30,31 TIPS involves the formation of a low-resistance channel
between the hepatic vein and the intrahepatic portion of the portal vein using angio-
graphic techniques. The shunt is kept open by using an expandable metal stent across
it to allow blood to return to the systemic circulation. RCTs report that early TIPS
(placed within 72 hours of admission) significantly decreased rates of treatment failure
and mortality in Child-Pugh class B patients with active bleeding or Child-Pugh class C
patients compared with standard management. Studies showing these benefits had
multiple exclusion criteria, however, and therefore included only approximately 20%
of the total patient group with variceal hemorrhage. The authors recommend that
any patient with persistent bleeding or severe rebleeding, despite combination phar-
macologic and endoscopic intervention, be considered for a TIPS. The availability of
634 Kovacs & Jensen
radiologists and of TIPS placement within the recommended time frame, however,
may be problematic in many smaller centers. In patients with TIPS placed, vasoactive
medications may be stopped. Portosystemic encephalopathy is a relative contraindi-
cation to TIPS placement, because TIPS may worsen encephalopathy.
When all other therapeutic interventions fail, shunt surgery may be a last option. Por-
tosystemic shunts can control portal hypertension and reduce variceal rebleeding.
The tradeoff, however, is the high encephalopathy rates and other perioperative sur-
gical complications after the procedure. One RCT did report that emergency porto-
caval shunt surgery compared with TIPS provided improved rates of hemostasis
and survival and a decreased rate of encephalopathy.32 Distal shunts (such as sple-
norenal types) are reported to cause less encephalopathy than central shunts, such
as portacaval or mesocaval shunts. Further studies are needed before the use of por-
tocaval shunts after failure of combined medical and endoscopic treatment is recom-
mended. Another problem currently is that experienced surgeons to perform
emergency shunts for variceal bleeding are not available in most hospitals, including
referral centers.
PREVENTION OF REBLEEDING
There is a high risk of rebleeding (60%–70% within 2 years) after a first episode of
active variceal hemorrhage in high-risk patients, such as those with Child-Pugh class
C cirrhosis, with accompanying mortality up to 33% on medical therapy alone. There-
fore, it is critical to prevent rebleeding and appropriate treatment should be initiated
while the patient is still in the hospital. This risk can be decreased to 45% by NSBB
use,33 to approximately 30% by band ligation,34 and to approximately 25% by
combining both treatments. Therefore, optimal secondary prophylactic therapy in-
cludes a combination of NSBBs (propranolol or nadolol) plus endoscopic band ligation
(Table 2).14 Band ligation should occur initially and within 1 week to 2 weeks of the in-
dex bleed with follow-up endoscopic surveillance and banding scheduled at 4-week
to 6-week intervals until EVs are obliterated. Each EV should be banded near the
GEJ and 4 cm to 6 cm above for 2 bands per variceal column. If EVs are too small
to band, are scarred down, and/or have blood flow by DEP, the intravariceal sclero-
therapy is recommended.28 The authors recommend that junctional varices in a hiatal
hernia be treated endoscopically similar to distal EVs.
A meta-analysis comparing band ligation or NSBBs to a combination of the 2
showed that the combined treatments were significantly more effective than either
intervention alone.35 Adding a long-acting nitrate (isosorbide mononitrate) to NSBBs
decreased portal pressures further and was shown in a meta-analysis of the combina-
tion of NSBBs and nitrates compared with NSBBs to improve rebleeding and mortality
while causing more side effects.36 Reports suggest that patients with higher portal
pressures respond better to NSBBs than patients with a lower HVPG.37 Controversy
exists about the safety and efficacy of NSBBs in patients with advanced liver disease,
dating to a 2010 study implying that NSBBs increase mortality in patients with refrac-
tory ascites.38 Subsequent studies, however, have not shown a harmful effect of
NSBBs39 if they are carefully titrated, and doses of propranolol over 160 mg/d or of
nadolol over 80 mg/d are avoided.40 NSBBs may not be appropriate in patients with
hemodynamic instability or renal dysfunction. Current guidelines recommend a com-
bination of band ligation and NSBBs for the prevention of recurrent variceal bleeding
even in patients who bled while receiving primary prophylaxis with band ligation or
NSBBs alone. If a patient is unable to tolerate NSBBs, band ligation alone is sug-
gested, although TIPS may be a useful alternative, especially if the patient has
Varices 635
Table 2
Prevention of recurrent esophageal variceal hemorrhage: management recommendations
Therapy Recommended Dose Therapy Goals Maintenance/Follow-up

EVL Every 4–6 wk until the Variceal eradication First EGD performed
eradication of varices (no further ligation 3–6 mo after
possible) eradication and every
6–12 mo thereafter
Propranolol 20–40 mg orally twice Resting heart rate At every outpatient
a day of 55–60 beats per visit check heart rate
Adjust every 2–3 d minute Continue indefinitely,
until treatment goal Systolic blood or if used in
is achieved pressure should not combination with
Maximal daily dose: decrease <90 mm Hg EVL, until EVs are
320 mg/d in patients Reduction of resting eradicated
without ascites pulse by 20%–25%
160 mg/d in patients
with ascites
Nadolol 20–40 mg orally once Reduction of resting At every outpatient
a day pulse by 20%–25% visit check heart rate
Adjust every 2–3 d Resting heart rate of Continue indefinitely
until treatment goal 55–60 beats per or, if used in
is achieved minute combination with
Maximal daily dose: Systolic blood pressure EVL, until EVs are
160 mg/d in patients should not decrease eradicated
without ascites <90 mm Hg
80 mg/d in patients
with ascites
A combination of EV ligation and either propranolol or nadolol is recommended.

Abbreviations: EV, Esophageal varices; EVL, Esophageal variceal ligation.
difficult-to-treat ascites.16 Carvedilol has been compared with both band ligation
alone and combined NSBBS and nitrates but not to the combination of banding and
NSBBS. Therefore, carvedilol cannot be recommended for secondary prophylaxis
at this time.
TIPS is the recommended rescue treatment in patients with recurrent bleeding
despite combination therapy with band ligation and NSBBs. An RCT reported that
TIPS (with covered stents) significantly reduced rebleeding compared with endo-
scopic hemostasis and NSBBs (0% vs 29%). TIPs, however, did not improve survival
and increased early encephalopathy.41 If TIPS is placed successfully, band ligation
and NSBBs can be discontinued. HPVG responders (defined as an HPVG reduction
<12 mm Hg or >20% decrease from baseline) have the lowest rebleeding rates. There-
fore, HPVG measurement and monitoring during therapy are an ideal strategy in
centers where available. Currently in the United States, HPVG is not available in
most medical centers and is not the standard of care for secondary (or primary)
management.19
GASTRIC VARICES
Gastric varices are less prevalent than EVs and occur in approximately 20% of cirrhotic
patients. Sarin and colleagues’42 classification of gastric varices includes GOV type 1,
EVs extending below the GEJ along the lesser curve (most common—75% of all gastric
varices); GOV type 2 , EVs extending into the stomach along the greater curve into the
fundus (Fig. 8); isolated gastric varix type 1 (IGV1), isolated in the fundus; and isolated
636 Kovacs & Jensen
Fig. 8. Gastric varix in the fundus.
gastric varix type 2, located elsewhere in the stomach (body, antrum, or pylorus).
Bleeding risk is associated with localization (IGV1> GOV2> GOV1), large size, presence
of red color signs, and severity of hepatic disease. Gastric varices bleed less often than
EVs but have a higher mortality due to the severity of the hemorrhage and response
to medical and endoscopic therapies. Because fundic varices occur more frequently
with portal or splenic vein thrombosis, especially in the context of malignancy or
pancreatitis, radiologic imaging should be done to exclude venous thrombosis. Gastric
varices are best diagnosed at endoscopy in resuscitated patients because they may
not be seen on EGD in hypovolemic patients.
The guidelines for the management of gastric varices are much less evidence based
than for EVs.
PREVENTION OF FIRST HEMORRHAGE FROM GASTRIC VARICES
To date, there has been only 1 RCT published on the primary prevention of gastric vari-
ces. It compared NSSBs, endoscopic cyanoacrylate glue injection, and observation of
patients with large GOV2 and IGV1 varices. The glue group had decreased bleeding
(10%) compared with the NSSBs group (38%) and observation group (53%). There
was significantly better survival of the glue group (93%) compared with the observa-
tion group (74%) but not significantly better than the NSBBs group (83%).43 Preven-
tion of first hemorrhage from GOV1 varices has not been reported yet. GOV1
varices usually are managed based on the EV guidelines.16
Current recommendations for primary prophylaxis of gastric variceal bleeding are
based on limited data but include for GOV2 and IGV1 varices—NSBBs may be
used, and for GOV1 varices—follow the EVs guidelines. Neither TIPS nor balloon-
occluded retrograde transvenous obliteration (BRTO) is recommended for preventing
the first bleed in patients with fundic varices.
TREATMENT OF ACUTE HEMORRHAGE FROM GASTRIC VARICES
The initial management of patients with gastric variceal hemorrhage is similar to

that of esophageal bleeding. Rudiments are airway protection, hemodynamic and
volume resuscitation, blood transfusion (the authors recommended based on
CURE studies of hemoglobin to 8 g)23 and treatment of severe coagulopathies,
Varices 637
admission to a monitored care area, vasoactive medications, and antibiotics prior

to upper endoscopy. The definitive diagnosis of acute gastric variceal hemorrhage
is based on the endoscopic findings of active bleeding, a platelet plug, or a clot
overlying a gastric varix. A meta-analysis of endoscopic therapy showed that
both band ligation and cyanoacrylate injection provided similar initial hemostasis
rates, with significantly less rebleeding in the cyanoacrylate group.44 The investiga-
tors of this Cochrane review, however, cautioned about their findings for all-cause
and bleeding-related mortality, failure of intervention, adverse events, and control
of bleeding because of the very low quality of the available studies and their results.
Band ligation has a limited application in the treatment of gastric varices, because
only small varices (1 cm) can be effectively banded and adjacent varices need to
be banded to prevent early rebleeding. Cyanoacrylate used in most clinical trials
has been N-butyl-2-cyanoacrylate. Another glue, 2-octyl cyanoacrylate, which
has a longer polymerization time, has also been reported to produce beneficial out-
comes in acute gastric variceal hemorrhage.45 Neither of these glues is Food and
Drug Administration approved for treating gastric varices in the United States.
Although glue injection is widely recommended as the treatment of choice for
gastric variceal bleeding, endoscopic therapeutic skill and experience are required.
Several major complications are reported, including stroke, pulmonary embolism,
paraplegia, gastric ulcers and ulcer hemorrhage, and portal and splenic vein throm-
bosis. Combined glue injection and band ligation for gastric variceal hemorrhage
has been advocated46 but cannot be recommended at present because data
from evidence-based studies, such as RCTs, are not available.
As described previously for EVs, DEP monitoring in gastric variceal bleeding can
also significantly reduce rates of rebleeding, transfusion requirements, and duration
of hospitalization.28 Furthermore, residual blood flow after endoscopic therapy core-
lates closely with rebleeding.28 Other endoscopic approaches, such as endoscopic ul-
trasound (EUS)–guided insertion of coils and/or cyanoacrylate, show promise. Studies
in gastric variceal hemorrhage patients have reported that EUS-guided coil and glue
injection reduced bleeding rates, transfusions, and mortality compared with glue in-
jection.47 No confirmatory larger studies or RCTs have been reported to confirm or
expand these results.
For patients with uncontrolled gastric variceal bleeding despite endoscopic therapy,
balloon tamponade with a Linton-Nachlas or Sengstaken-Blakemore tube may be a
temporary bridge to more definitive intervention. If available, the Linton tube with its
larger gastric balloon (500 mL), is recommended.
TIPS may be effective in some patients with continued bleeding from gastric vari-
ces. TIPS has not been compared in an RCT to either glue injection or band ligation
for acute gastric variceal hemorrhage. TIPS should be considered early for bleeding
fundic varices, which often are associated with early rebleeding after endoscopic or
medical therapy.
The authors recommend that if bleeding occurs from GOV1 varices, either band
ligation, if feasible, or glue injection be used for endoscopic hemostasis. If that fails
or is unavailable, TIPS should be used for fundic varices (GOV2 or IGV1).16
PREVENTION OF REBLEEDING FROM GASTRIC VARICES
For patients who had index bleeding from GOV1 varices, a combination of endoscopic
treatment (band ligation or cyanoacrylate injection) and NSBBs is the recommended
therapy, as for EVs.16 For patients with fundic gastric varices, repeated cyanoacrylate
injection can reduce rebleeding and mortality compared with NSBBs48 Combination
638 Kovacs & Jensen
therapy with glue injection and NSBBs did not improve outcomes in comparison to in-
jection alone in fundic variceal patients.49
An RCT of patients with GOV1 and GOV2 varices showed that TIPS was associated
with lower early rebleeding (11% vs 38%) and transfusion needs, compared with glue
injection. There was no benefit, however, in initial hemostasis or survival and there was
a higher rate of encephalopathy after TIPS.50
Patients with gastric fundic varices and gastro-splenorenal collaterals also can be
managed with BRTO. This intervention is performed using angiographic techniques
and includes retrograde cannulation of the left renal vein by the jugular or femoral
vein, followed by balloon occlusion and slow infusion of sclerosant and/or coils to
obliterate the gastro-splenorenal collateral and fundic varices.51 Compared with
TIPS, BRTO does not divert portal blood flow away from the liver but may increase
portal pressure, potentially promoting EV bleeding and exacerbating ascites.8 When
BRTO was compared with TIPS in patients with acutely bleeding gastric varices, the
BRTO group had significantly less rebleeding (9% vs 20%) at 1 year, but there was
no survival advantage.52 A recent retrospective study of patients with gastric variceal
bleeding reported that BRTO improved rates of early hemostasis, rebleeding, and sur-
vival compared with TIPS.53
In summary, combination therapy with NSBBs and endoscopic hemostasis (band
ligation or glue injection) is recommended for prevention of rebleeding in patients
with GOV1 varices. TIPS or BRTO is recommended for patients with prior GOV2 or
IGV1 variceal hemorrhage to reduce rebleeding.16
Rectal Varices
Rectal varices are defined as dilated rectal veins that originate at least 4 cm above the
anal verge and are distinct from internal hemorrhoids and do not extend to the dentate
line.54 They originate from portosystemic anastomosis between the superior hemor-
rhoidal veins and the middle or inferior hemorrhoidal veins. The prevalence of rectal
varices varies between 40% and 56% in cirrhotic patients and increases to 63% to
94% in patients with extrahepatic portal vein obstruction.55 Clinically severe bleeding
is uncommon, occurring in 0.5% to 5% of cirrhotic patients.56 There are no estab-
lished management guidelines to treat rectal variceal hemorrhage. Colonoscopy
and flexible sigmoidoscopy are the main methods for diagnosing the presence of
rectal varices, and these are best visualized in both retroflexed and end-on views in
hemodynamically resuscitated patients (Fig. 9). Endoscopic band ligation is the
Fig. 9. Rectal varices.
Varices 639
recommended treatment modality. Sclerotherapy or glue injection can be utilized also,

but rebleeding rates are high. Sclerotherapy is associated with frequent postinjection
ulcer formation and glue is associated with an embolization rate of up to 4.3%.55 EUS-
guided coil and glue injection also may be useful in large bleeding rectal varices, which
cannot be treated with band ligation. Subsequently, TIPS and BRTO are possible
options, but the optimal management of rectal varices is currently uncertain.
SUMMARY
Despite current guidelines for the optimal management of variceal hemorrhage,

morbidity and mortality related to bleeding are still substantial, especially in poor-
risk cirrhotic patients. Although advances in medical, endoscopic, and radiologic in-
terventions have improved patient outcomes by preventing the first bleed, treating
acute hemorrhage, and preventing rebleeding, further innovations are needed to
lessen the dire consequences of variceal hemorrhage in patients with decompensated
liver disease.
ACKNOWLEDGMENTS
The research studies included in this article from the CURE: Digestive Diseases
Research Center-Human Studies Core of Dennis M. Jensen, MD, were funded by
grants from the VA Research Service (VA Clinical Merit Review CLIN-013–07F) and
the NIH-NIDDK grant (P30 DK041301) to CURE: Digestive Diseases Research
Center–Human Studies Core.
REFERENCES
1. Kovacs TO, Jensen DM. Gastrointestinal hemorrhage. In: Goldman L, Schafer A,

editors. Goldman-cecil medicine. 25th edition. Elsevier Saunders; 2016.
p. 879–84.
2. Gralnek IAM, Jensen DM, Kovacs TOG, et al. The economic impact of esopha-
geal variceal hemorrhage: cost-effectiveness implications of endoscopic therapy.
Hepatology 1999;29:44–50.
3. Kovalak M, Lake J, Mattek N, et al. Endoscopic screening for varices in cirrhotic
patients: data from a national endoscopic database. Gastrointest Endosc 2007;
65:82–8.
4. North Italian Endoscopic Club for the Study and Treatment of Esophageal Vari-
ces. Prediction of the first variceal hemorrhage in patients with cirrhosis of the
liver and esophageal varices. A prospective multicenter study. N Engl J Med
1988;319:983–9.
5. Amitrano L, Guardascione MA, Manguso F, et al. The effectiveness of current
acute variceal bleed treatments in unselected cirrhotic patients: refining short-
term prognosis and risk factors. Am J Gastroenterol 2012;107:1872–8.
6. Bosch J, Thabut D, Albillos A, et al. Recombinant factor VIIa for variceal bleeding
in patients with advanced cirrhosis: a randomized controlled trial. Hepatology
2008;47:1604–14.
7. Jensen DM. Endoscopic screening for varices in cirrhosis: findings, implications,
and outcomes. Gastroenterology 2002;122:1620–30.
8. Park JK, Saab S, Kee ST, et al. Balloon-occluded retrograde transvenous obliter-
ation (BRTO) for treatment of gastric varices: review and Meta-analysis. Dig Dis
Sci 2015;60:1543–53.
640 Kovacs & Jensen
9. Groszmann RJ, Bosch J, Grace ND, et al. Hemodynamic events in a prospective

randomized trial ofpropranolol versus placebo in the prevention of a first variceal
hemorrhage. Gastroenterology 1990;99:1401–7.
10. Abraldes JG, Villanueva C, Banares R, et al, Spanish Cooperative Group for Por-
tal Hypertension and Variceal Bleeding. Hepatic venous pressure gradient and
prognosis in patients with acute variceal bleeding treated with pharmacologic
and endoscopic therapy. J Hepatol 2008;48:229–36.
11. D’Amico G, Garcia-Pagan JC, Luca A, et al. Hepatic vein pressure gradient
reduction and prevention of variceal bleeding in cirrhosis: a systematic review.
Gastroenterology 2006;131:1611–24.
12. McCarty TR, Afinogenova Y, Njei B. Use of wireless capsule endoscopy for the
diagnosis and grading of esophageal varices in patients with portal hypertension:
a systematic review and meta-analysis. J Clin Gastroenterol 2017;51:174–82.
13. Chavalitdhamrong D, Jensen DM, Singh B, et al. Capsule endoscopy is not as
accurate as esophagogastroduodenoscopy in screening cirrhotic patients for
varices. Clin Gastroenterol Hepatol 2012;10:254–8.
14. De Franchis R, Baveno VI Faculty. Expanding consensus in portal hypertension.
Report of the Baveno VI Consensus workshop: stratifying risk and individualizing
care for portal hypertension. J Hepatol 2015;63:743–52.
15. Thabut D, Bureau C, Layese R, et al. Validation of Baveno VI criteria for screening
and surveillance of esophageal varices in patients with compensated cirrhosis
and a sustained response to antiviral therapy. Gastroenterology 2019;156:
997–1009.
16. Garcia-Tsao G, Abraldes J, Berzigotti A, et al. Portal hypertensive bleeding in
cirrhosis: risk stratification, diagnosis, and management: 2016 practice guidance
by the American Association for the Study of Liver diseases. Hepatology 2017;65:
310–35.
17. Groszmann RJ, Garcia-Tsao G, Bosch J, et al. Beta-blockers to prevent gastro-
esophageal varices in patients with cirrhosis. N Engl J Med 2005;353:2254–61.
18. Gluud LL, Krag A. Band ligation versus beta-blockers for primary prevention in
oesophageal varices in adults. Cochrane Database Syst Rev 2012;(8):CD004544.
19. Jutabha R, Jensen DM, Martin P, et al. Randomized study comparing banding
and propranolol to prevent initial variceal hemorrhage in cirrhotics with high-
risk esophageal varices. Gastroenterology 2005;128:870–81.
20. Sarin SK, Wadhawan M, Agarwal SR, et al. Endoscopic variceal ligation plus pro-
pranolol versus endoscopic band ligation alone in primary prophylaxis of variceal
bleeding. Am J Gastroenterol 2005;100:797–804.
21. Bhardwaj A, Kedarisetty CK, Vashishtha C, et al. Carvedilol delays the progres-
sion of small oesophageal varices in patients with cirrhosis: a randomized
placebo-controlled trial. Gut 2017;66:1838–43.
22. Villanueva C, Colomo A, Bosch A, et al. Transfusion strategies for acute upper
gastrointestinal bleeding. N Engl J Med 2013;368:11–21.
23. Jensen DM, Markovic D, Jensen ME, et al. Red cell transfusions do not increase
30 day mortality rates for unselected patients with severe UGI hemorrhage.
Gastroenterology 2015;148:154.
24. Wells M, Chande N, Adams P, et al. Met-analysis: vasoactive medications for the
management of acute variceal bleeds. Aliment Pharmacol Ther 2012;35:
11267–78.
25. Seo YS, Park SY, Kim MY, et al. Lack of difference among terlipressin, somato-
statin and octreotide in the control of acute gastroesophageal variceal hemor-
rhage. Hepatology 2014;60:954–63.
Varices 641
26. Van Stiegman G, Goff JS. Endoscopic esophageal varix ligation: preliminary clin-
ical experience. Gastrointest Endosc 1988;34:113–7.
27. Jensen DM, Kovacs TOG, Ohning CV, et al. Doppler endoscopic probe moni-
toring for blood flow improves risk stratification and outcomes of patients with se-
vere non-variceal UGI hemorrhage. Gastroenterology 2017;152:1310–8.
28. Jensen DM, Jensen ME, Markovic D, et al. Doppler endoscopic probe improves
outcomes of severe UGI hemorrhage from varices and other portal hypertension
lesions. Gastroenterology 2018;154(Supplement 1):5529–30.
29. Escorsell A, Pavel O, Cardenas A, et al. Esophageal balloon tamponade versus
esophageal stent in controlling acute refractory variceal bleeding: a multicenter
randomized, controlled trial. Hepatology 2016;63:1957–67.
30. Garcia-Pagan JC, Caca K, Bureau C, et al. Early use of TIPS in patients with
cirrhosis and variceal bleeding. N Engl J Med 2010;362:2370–9.
31. Thabut D, Pauwels A, Carbonell N, et al. Cirrhotic patients with portal
hypertension-related bleeding and an indication for early-TIPS: a large multi-
centre audit with real-life results. J Hepatol 2018;68:73–81.
32. Oroff MJ, Hye R, Wheeler HO, et al. Randomized trials of endoscopic therapy and
transjugular intrahepatic portosystemic shunt versus portocaval shunt for emer-
gency and elective treatment of bleeding gastric varices in cirrhosis. Surgery
2015;157:1028–45.
33. Bernard B, Lebrec D, Mathurin P, et al. Beta-adrenergic antagonists in the pre-
vention of gastrointestinal rebleeding in patients with cirrhosis: a meta-analysis.
Hepatology 1997;25:63–70.
34. Thiele M, Krag A, Rohde U, et al. Meta-analysis: banding ligation and medical in-
terventions for the prevention of rebleeding from oesophageal varices. Aliment
Pharmacol Ther 2012;35:1155–65.
35. Puente A, Hernadez-Gea V, Graupera I, et al. Drugs plus ligation to prevent re-
bleeding in cirrhosis: an updated systematic review. Liver Int 2014;34:823–33.
36. Gluud LL, Langholz E, Krag A. Met-analysis: isosorbide -mononitrate alone or
with either beta-blockers or endoscopic therapy of oesophageal varices. Aliment
Pharmacol Ther 2010;32:859–71.
37. Villanueva C, Albillos A, Genesca J, et al. Development of hyperdynamic circula-
tion and response to B-blockers in compensated cirrhosis with portal hyperten-
sion. Hepatology 2016;63:197–206.
38. Serste T, Melot C, Francoz C, et al. Deleterious effects of beta-blockers on sur-
vival in patients with cirrhosis and refractory ascites. Hepatology 2010;52:
1017–22.
39. Facciorusso A, Roy S, Livadas S, et al. Nonselective beta-blockers do not affect
survival in cirrhotic patients with ascites. Dig Dis Sci 2018;63:1737–46.
40. Moctezuma-Velazquez C, Kalainy S, Abraldes JG. Beta-blockers in patients with
advanced liver disease: has the dust settled? Liver Transpl 2017;23:1058–69.
41. Holster IL, Tjwa ET, Moelker A, et al. Covered transjugular intrahepatic portosys-
temic shunt versus endoscopic therapy 1 beta-blocker for prevention of variceal
rebleeding. Hepatology 2016;63:581–9.
42. Sarin SK, Lahoti D, Saxena SP, et al. Prevalence, classification and natural history
of gastric varices: a long-term follow-up study in 568 portal hypertension patients.
Hepatology 1992;16:1343–9.
43. Mishra SR, Sharma BC, Kumar A, et al. Primary prophylaxis of gastric variceal
bleeding comparing cyanoacrylate injection and beta-blockers: a randomized
controlled trial. J Hepatol 2011;54:1161–7.
642 Kovacs & Jensen
44. Rios CE, Seron P, Gisbert JP, et al. Endoscopic injection of cyanoacrylate glue
versus other endoscopic procedures for acute bleeding gastric varices in people
with portal hypertension. Cochrane Database Syst Rev 2015;(5):CD010180.
45. Kahloon A, Chalasani N, DeWitt J, et al. Endoscopic therapy with 2- octyl-
cyanoacrylate for the treatment of gastric varices. Dig Dis Sci 2014;59:2178–83.
46. Mansour L, Ei-Kalla F, El-Bassat H, et al. Randomized controlled trial of scleroli-
gation versus band ligation alone for eradication of gastroesophageal varices.
Gastrointest Endosc 2017;86:307–15.
47. Bhat YM, Weilert F, Fredrick RT, et al. EUS-guided treatment of gastric fundal vari-
ces with combined injection of coils and cyanoacrylate glue: a large U.S. expe-
rience over 6 years (with video). Gastrointest Endosc 2016;83:1164–72.
48. Mishra SR, Chander SB, Kumar A, et al. Endoscopic cyanoacrylate injection
versus beta-blocker for secondary prophylaxis of gastric variceal bleed: a rand-
omised controlled trial. Gut 2010;59:729–35.
49. Hung HH, Chang CJ, Hou MC, et al. Efficacy of non-selective beta-blockers as
adjunct to endoscopic prophylaxis for gastric variceal bleeding: a randomized
controlled trial. J Hepatol 2012;56:1025–32.
50. Lo GH, Liang HL, Chen WC, et al. A prospective randomized controlled trial of
transjugular intrahepatic portosystemic shunt versus cyanoacrylate injection in
the prevention of gastric variceal rebleeding. Endoscopy 2007;39:679–85.
51. Saad WE. Endovascular management of gastric varices. Clin Liver Dis 2014;18:
829–51.
52. Lee SJ, Kim SU, Kim MD, et al. Comparison of treatment outcomes between balloon-
occluded retrograde transvenous obliteration and transjugular intrahepatic porto-
systemic shunt for gastric variceal bleeding hemostasis. J Gastroenterol Hepatol
2017;32:1487–94.
53. Gimm G, Chang Y, Kim H-C, et al. Balloon-occluded retrograde transvenous
obliteration versus transjugular intrahepatic portosystemic shunt for the manage-
ment of gastric variceal bleeding. Gut Liver 2018;12:704–13.
54. Ganguly S, Sarin SK, Bhatia V, et al. The prevalence and spectrum of colonic le-
sions in patients with cirrhotic and non-cirrhotic portal hypertension. Hepatology
1995;21:1226–31.
55. Al Khalloufi K, Laiyemo AO. Management of rectal varices in portal hypertension.
World J Hepatol 2015;7:2992–8.
56. Shudo R, Yazaki Y, Sakurai S, et al. Clinical study comparing bleeding and non-
bleeding rectal varices. Endoscopy 2002;34:189–94.

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Var ice s

Esophageal, Gastric, and Rectal

Clin Liver Dis 23 (2019) 625–642

upper GI (UGI) bleeding, gastroesophageal varices (GOVs) comprised approximately

There is no evidence to suggest that current medications, such as nonselective

PREVENTION OF FIRST HEMORRHAGE IN ESOPHAGEAL VARICES

Primary prophylaxis of EV hemorrhage is indicated in patients at increased risk of

Therapy Recommended Dose Therapy Goals Maintenance/Follow-up

Abbreviations: EV, Esophageal varices; EVL, Esophageal variceal ligation.

TREATMENT OF ACUTE ESOPHAGEAL VARICEAL HEMORRHAGE

Acute variceal hemorrhage is a medical emergency requiring urgent and intensive

Fig. 3. Active variceal bleeding from an EV.

Fig. 4. Platelet plug on an EV.

Fig. 5. Large EV with red wale marks.

Fig. 6. Band ligation over a platelet plug.

DEP-guided endoscopic hemostasis reduced 30-day rates of rebleeding, transfusion

If variceal hemorrhage is not controlled by a combination of a vasoactive agent and

Therapy Recommended Dose Therapy Goals Maintenance/Follow-up

A combination of EV ligation and either propranolol or nadolol is recommended.

Fig. 8. Gastric varix in the fundus.

PREVENTION OF FIRST HEMORRHAGE FROM GASTRIC VARICES

TREATMENT OF ACUTE HEMORRHAGE FROM GASTRIC VARICES

The initial management of patients with gastric variceal hemorrhage is similar to

admission to a monitored care area, vasoactive medications, and antibiotics prior

PREVENTION OF REBLEEDING FROM GASTRIC VARICES

Fig. 9. Rectal varices.

recommended treatment modality. Sclerotherapy or glue injection can be utilized also,

Despite current guidelines for the optimal management of variceal hemorrhage,

1. Kovacs TO, Jensen DM. Gastrointestinal hemorrhage. In: Goldman L, Schafer A,

9. Groszmann RJ, Bosch J, Grace ND, et al. Hemodynamic events in a prospective

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