Transcript Cirrhosis - Portal Hypertension - AGA

Prevention and Management of
Esophageal Variceal and Portal
Hypertensive Hemorrhage
Thomas Hargrave, M.D.
March 24, 2012
Gastroesophageal Variceal
Hemorrhage
 Gastroesophageal variceal hemorrhage is one of
the major complications of portal hypertension
from cirrhosis
 Variceal hemorrhage occurs in 25-35% of
cirrhotics and accounts for 70-80% of UGIB in
these patients.
 Aprroximately 50% of cirrhotics will have varices
at the time of diagnosis
 7-8% develop de novo varices each year
PREVALENCE AND SIZE OF ESOPHAGEAL VARICES IN PATIENTS WITH NEWLY DIAGNOSED CIRRHOSIS
Prevalence and Size of Esophageal Varices in
Patients with Newly-Diagnosed Cirrhosis
100
80
Large
%
60
Patients
with varices 40
Medium
20
Small
0
Overall
Child A
Child B
Child C
n=494
n=346
n=114
n=34
Pagliaro et al., In: Portal Hypertension: Pathophysiology and Management, 1994: 72
Gastroesophageal Variceal
Hemorrhage
 The 1-year risk of a first variceal hemorrhage is
approximately 12% (5% for small varices and
15% for large varices).
 The 6-week mortality with each episode of
variceal hemorrhage is approximately 15 -20%,
 From 0% among patients with Child class A disease
to 30% among patients with Child class C disease.
 The 1-year rate of recurrent variceal
hemorrhage is approximately 60%.
Pathophysiology
Portal Venous Anatomy
Hepatic/Portal Blood Flow
 Blood accounts for 25-30% of the volume of the
liver
 Total Hepatic Blood Flow: Hepatic arterial and
portal venous blood flow
 Approximately 25% of the cardiac output
 Males: 1860 cc/min
 Females: 1550 cc/min
 Portal venous blood flow averages 1500 cc/min
 Normal portal venous pressure is 4-8 mmHg
Hepatic Lobular Anatomy
Pathophysiology
 Gastroesophageal varices are a direct
consequence of portal hypertension that, in
cirrhosis, results from
 Increased resistance to portal flow
 Structural (distortion of liver vascular
architecture by fibrosis and regenerative
nodules) and
 Dynamic (increased hepatic vascular tone due
to endothelial dysfunction and decreased nitric
oxide bioavailability).
 Increased portal venous blood inflow.
Intracellular Spaces (of Disse) in the Portal Sinusoids
Large Enough for Chylomicroms to Pass
Garcia-Tsao G, Bosch J. N Engl J Med 2010;362:823-832.
A THRESHOLD PORTAL PRESSURE OF ~12 mmHg IS NECESSARY FOR VARICES TO FORM
A Threshold Portal Pressure of ~12 mmHg is
Necessary for Esophageal Varices to Form
Varices Present
Varices Absent
(n=72)
(n=15)
35
30
Hepatic
Venous
Pressure
Gradient
(mmHg)
25
20
P<0.01
15
12
10
5
Garcia-Tsao et. al., Hepatology 1985; 5:419
Venous Layers of the Esophagus
VARICES INCREASE IN DIAMETER PROGRESSIVELY
Varices Increase in Diameter
Progressively
No varices
Small varices
7-8%/year
Large varices
7-8%/year
Merli et al. J Hepatol 2003;38:266
Grade II Varices
Grade III Varices
LARGE VARICES ARE MORE LIKELY TO RUPTURE
Large Varices Are More Likely To Rupture
No Varices
100
p<0.01 *
Small Varices
75
%
Patients
without
bleeding
Large Varices * *
50
2-year probability of first bleed:
 Small varices: 7%
 Large varices: 30%
25
0
0
12
24
12
36
24
Time (months)
*Merli et al., Hepatol 2003; 38:266, **Conn et al., Hepatology 1991; 13:902
36
Punctum
Variceal hemorrhage
Varix with red wale sign
Management of Variceal Bleeding
 Primary Prophylaxis
 Pharmacologic
 Endoscopic
 Acute Variceal Hemorrhage
 Pharmacologic
 Endoscopic
 TIPS
 Secondary Prophylaxis
 Pharmcologic
 Endoscopic
 TIPS
Primary Prophylaxis
 In view of the relatively high rate of bleeding
from esophageal varices and the high
associated mortality, an important goal of
management of patients with cirrhosis is the
primary prevention of variceal hemorrhage.
 As a result, all patients with cirrhosis should
undergo diagnostic endoscopy to document
the presence of varices and to determine their
risk for variceal hemorrhage.
MANAGEMENT OF PATIENTS WITHOUT VARICES
Treatment of Varices / Variceal Hemorrhage
No varices
Varices
No hemorrhage
Variceal
hemorrhage
Recurrent
hemorrhage
Can we prevent formation of
varices ?
NON-SELECTIVE BETA BLOCKERS DO NOT PREVENT DEVELOPMENT OF VARICES
Prevention of Esophageal
Varices w/ Beta-Blockers?
 Multicenter, randomized, placebo-controlled trial
of timolol (non-selective beta-blocker) vs.
placebo in patients
 Beta-blockers did not prevent the development of
varices and were associated with a higher rate of
serious adverse events
 In patients without varices, treatment with
nonselective beta-blockers is not recommended
Groszmann, et al., Hepatology 2003;38 (suppl 1):206A
MANAGEMENT OF PATIENTS WITHOUT VARICES
Treatment of Varices / Variceal Hemorrhage
No varices
No specific therapy
Repeat endoscopy in 2-3 yrs*
Varices
No hemorrhage
Variceal
hemorrhage
Recurrent
hemorrhage
* Sooner with cirrhosis decompensation
PREVENTION OF FIRST VARICEAL HEMORRHAGE
Treatment of Varices / Variceal Hemorrhage
No varices
Varices
No hemorrhage
Variceal
hemorrhage
Recurrent
hemorrhage
Prevention of first
variceal hemorrhage
Primary Prophylaxis for Variceal
Hemorrhage
 Pharmacologic Therapy
 Beta Blockers
 Nitrates
 Endoscopic Therapies
 Band Ligation
 Sclerotherapy (historican interest only)
DECREASE IN HEPATIC VENOUS PRESSURE GRADIENT (HVPG) REDUCES THE RISK OF VARICEAL BLEEDING
Decrease In Hepatic Venous Pressure Gradient
(HVPG) Reduces Risk of Variceal Bleeding
100
80
46-65%
%
60
Rebleeding 40
7-13%
20
0%
0
HVPG
decrease to
< 12 mmHg
HVPG decrease
> 20% from
baseline
No change in
HVPG
Bosch and García-Pagán, Lancet 2003; 361:952
Primary Prophylaxis for Variceal
Hemorrhage: Beta Blockers
 Non-selective beta-blockers preferred
 Beta-1 antagonism: reduced cardiac output
 Beta-2 antagonism: splanchnic vasoconstriction
 Goal of therapy to reduce portal pressure by 20%
or below 12 mm Hg
 Dose titrated to a resting HR of 55, or a 25%
reduction in baseline
 Initial dose propranolol 40 mg bid, Average dose
160 mg/day
 Up to 1/3 intolerant to side effects resulting in
discontinuation
NON-SELECTIVE BETA-BLOCKERS PREVENT FIRST VARICEAL HEMORRHAGE
Non-Selective Beta-Blockers Prevent
First Variceal Hemorrhage: 11 Trials
Bleeding rate
Control
Beta-blocker
Absolute rate
difference
25%
15%
-10%
(n=600)
(n=590)
(-16 to -5)
30%
14%
-16%
(n=411)
(n=400)
(-24 to -8)
7%
2%
-5%
(n=100)
(n=91)
(-11 to 2)
(~2 year)
All varices
(11 trials)
Large varices
(8 trials)
Small varices
(3 trials)
D’Amico et al., Sem Liv Dis 1999; 19:475
Primary Prophylaxis against Variceal
Hemorrhage.
Garcia-Tsao G, Bosch J. N Engl J Med 2010;362:823-832.
THE RISK OF FIRST VARICEAL HEMORRHAGE IS NOT REDUCED BY ADDING ISOSORBIDE MONONITRATE (ISMN) TO BETA-BLOCKERS
The Risk of First Bleeding is Not Reduced
by Adding Isosorbide Mononitrate (ISMN) to
b-blockers
Free of a first variceal bleeding
Survival
100
100
75
%
ns
ns
75
50
50
25
Propranolol + ISMN
Propranolol + placebo
25
0
1
Years
Propranolol + ISMN
Propranolol + placebo
0
2
1
Years
García-Pagán et al., Hepatology 2003; 37:1260
2
ENDOSCOPIC VARICEAL BAND LIGATION
Endoscopic Variceal Band Ligation
Primary Prophylaxis for Variceal
Hemorrhage
 3 randomized controlled trials published
comparing band ligation to no treatment,
showing lower bleeding rates and mortality.
 Meta-analysis of 8 trial show banding superior
to beta blockers but no difference in survival
 One trial of band ligation and beta blockers: no
benefit
 Prophylactic sclerotherapy definitely of no
proven benefit, probably harmful.
VARICEAL BAND LIGATION (VBL) VS. BETA-BLOCKERS (BB) IN THE PREVENTION OF FIRST VARICEAL HEMORRHAGE
Variceal Band Ligation (VBL) vs. Beta-Blockers
(BB) in the Prevention of First Variceal Bleed
First hemorrhage
Survival
Chen 1998
Sarin 1999
De 1999
Jutabha 2000
De la Mora 2000
Lui 2002
Lo 2004
Schepke 2004
Total
0
1
Favors VBL
10
Favors BB
0
1
Favors VBL
10 40
Relative
risk
Favors BB
Khuroo, et al., Aliment Pharmacol Ther 2005; 21:347
MANAGEMENT ALGORITHM FOR THE PROPHYLAXIS OF VARICEAL HEMORRHAGE - SUMMARY
Prophylaxis of Variceal Hemorrhage
Diagnosis of Cirrhosis
Endoscopy
No Varices
Small Varices
Follow-up EGD in 2-3 years*
Follow-up EGD in 1-2 years*
*EGD every year in decompensated cirrhosis
•Stepwise increase until maximally tolerated dose
•Continue beta-blocker (life-long)
•No role for repeated endoscopy!!
Medium/Large Varices
Child’s C or Stigmata
Beta-blocker therapy
No Contraindications
Contraindications
or
Beta-blocker intolerance
Endoscopic Variceal Band Ligation
No role for sclerotherapy or nitrates
Primary Prophylaxis for Variceal Hemorrhage:
Conclusions
 Propranolol is the most cost-effective treatment for
the prevention of initial variceal bleeding
 The documented benefits of prophylactic beta
blockers may be lost if discontinued due to a rebound
in bleeding/ mortality.
 Life-long beta blocker treatment is therefore
indicated
 Non-compliant patients may be better served by band
ligation therapy, although at substantially higher
costs ($1425 vs $4284)
Hepatology 2001; 34(6):1096-02
Management of Variceal Bleeding
 Primary Prophylaxis
 Pharmacologic
 Endoscopic
 Acute Variceal Hemorrhage
 Pharmacologic
 Endoscopic
 TIPS
 Secondary Prophylaxis
 Pharmcologic
 Endoscopic
 TIPS
TREATMENT OF ACUTE VARICEAL HEMORRHAGE
Treatment of Acute Variceal Hemorrhage
General Management:
 IV access and fluid resuscitation
 Antibiotic prophylaxis
 Correct coagulopathy
 Do not overtransfuse (hemoglobin ~ 7-8 g/dL)
 Empiric lactulose?
Specific therapy:
 Pharmacological therapy: octreotide, vasopressin +
nitroglycerin
 Early endoscopic therapy: band ligation
 Shunt therapy: TIPS, surgical shunt
Cautious Transfusion Improves Outcome
in Cirrhotics with Variceal Hemorrhage
 214 cirrhotics with UGIB randomized to restricted (Hgb
7-8 gm) or liberal transfusion (Hgb 9-10 gm)
 69% esophageal variceal 7% gastric variceal
 15% peptic ulcer
3% gastropathy
 Therapeutic failure occurred in 16% of restricted and
28% of liberal group (p<0.04)
 In subgroup with esophageal variceal bleed, the 6 week
survival without therapeutic failure was better in
restrictive group (84% vs 69%: p<0.02)
 38% in restrictive group required no transfusion vs 9%
in liberal group
Colomo A. et al , Abstract 232A (AASLD 2008)
Cautious Transfusion Improves Outcome
in Cirrhotics with Variceal Hemorrhage
P= 0.02
P= 0.04
6-week survival
in variceal
bleeders who did
not have
therapeutic
failure
Colomo A. et al , Abstract 232A (AASLD 2008)
Prophylactic Antibiotics Improve Outcomes in
Cirrhotic Patients with GI Hemorrhage
PROPHYLACTIC ANTIBIOTICS IMPROVE OUTCOMES IN CIRRHOTIC PATIENTS WITH GI HEMORRHAGE
 The use of prophylactic antibiotics in cirrhotics
with GI hemorrhage has been shown by metaanalysis to reduce infection, increase survival, and
reduce recurrent hemorrhage (13 prospective
trials)
 Recommended antibiotics include oral
norfloxacin, ciprofloxin, ofloacin, and amoxicillin
clavulanate, ceftriaxone IV
Scand J. Gastro 2003;38:193-200
PROPHYLACTIC ANTIBIOTICS IMPROVE OUTCOMES IN CIRRHOTIC PATIENTS WITH GI HEMORRHAGE
Prophylactic Antibiotics Improve Outcomes in
Cirrhotic Patients with GI Hemorrhage
Control
Antibiotic
(n=270)
(n=264)
Absolute rate
difference
(95% CI)
Infection
45%
14%
-32%
(-42 to –23)
SBP / Bacteremia
27%
8%
-18%
(-26 to –11)
Death
24%
15%
-9%
(-15 to –3)
Meta-analysis of 5 randomized trials
Bernard et al., Hepatology 1999; 29:1655
PROPHYLACTIC ANTIBIOTICS PREVENT EARLY VARICEAL REBLEEDING
Prophylactic Antibiotics Reduce Probability of
Recurrent Variceal Hemorrhage
1.0
Prophylactic antibiotics (n=59)
0.8
No antibiotics (n=61)
0.6
%
free of
0.4
variceal
hemorrhage
Greatest benefit
in first 7 days
0.2
0
0
1
3
2
12
18
24
30
Follow-up (months)
Ofloxacin 200 mg iv q12 hr for 2 days,
then oral 200 bid for 5 days
Hou M-C et al., Hepatology 2004; 39:746
Phamacologic Treatment for Acute
Variceal Hemorrhage
 Octreotide:
 50 microgram bolus and 25-50 mcg/hr for up to 5
days (range 2-5 days)
 Vasopressin:
 Too dangerous for empiric initial therapy
 Contiunuous infusion 0.2-0.4 U/min up to 1.0 U/min
 Recommended only in combination with i.v. TNG: 1050 mcg/min
 Titrate TNG infusion to maintain systolic BP >90
mmHg
 Continuous vasopressin> 24 hr not recommended
Prophylaxis of HSE in Acute Variceal Bleed
Lactulose 30 mL TID_QID until pts
had non-melenic stools and then the
dose was reduced so that patients
had two to three semiformed stools
per day
PROPHYLACTIC ANTIBIOTICS IMPROVE OUTCOMES IN CIRRHOTIC PATIENTS WITH GI HEMORRHAGE
Endoscopic Therapy Now Standard in
the Management of Variceal
Hemorrhage
Non-Pharmacologic Treatment of
Acute Variceal Hemorrhage
 Endoscopic Band Ligation
 Transjugular Intrahepatic Portalsystemic Shunting (TIPS)
 Mostly Historical Interest




Sengstaken-Blakemore Tube
Embolization of varices
Portacaval shunt surgery
Injection Sclerotherapy
ENDOSCOPIC VARICEAL BAND LIGATION
Endoscopic Variceal Band Ligation
 Bleeding controlled in 90%
 Rebleeding rate 30%
 Compared with sclerotherapy:
 Less rebleeding
 Lower mortality
 Fewer complications
 Fewer treatment sessions
Erythromycin improves visibility during
endoscopy for variceal bleeding
 Study involved 90 patients with cirrhosis who
had been vomiting blood due to variceal
bleeding during the previous 12 hours.
 The 47 patients randomized to the intervention
group received an intravenous bolus infusion of
125 mg erythromycin lactobionate in 50 mL
normal saline. The other 43 patients received
only the saline. (All patients also received
octreotide, esmoprazole, and ceftriaxone.)
Gastrointest Endosc 2010.
Erythromycin improves visibility during
endoscopy for variceal bleeding
 On multivariate analysis, erythromycin was the
only predictor of an empty stomach.
 As a result, the average time needed for
endoscopy was also shorter after erythromycin
(19 vs 26 min, p < 0.005).
 Physicians found that with erythromycin, they
could control bleeding by band ligation more
often (70% vs 49%, p < 0.04) and that hospital
stays were shorter (3.4 vs 5.1 days, p < 0.002).
Gastrointest Endosc 2010.
COMBINATION DRUG/ENDOSCOPIC THERAPY IS MORE EFFECTIVE THAN ENDOSCOPIC THERAPY ALONE
Combination Drug / Endoscopic Therapy is More
Effective Than Endoscopic Therapy Alone in Achieving
Five-Day Hemostasis
Sclero + Octreotide
Ligation + Octreotide
Sclero + Octreotide / ST
Sclero + Octreotide
Sclero + Octreotide
Sclero + ST
Sclero + Octreotide
Sclero / ligation + Vapreotide
Besson, 1995
Sung, 1995
Signorelli, 1996
Ceriani, 1997
Signorelli, 1997
Avgerinos, 1997
Zuberi, 2000
Cales, 2001
TOTAL
Relative
Risk
0.8
1
Favors endoscopic
therapy alone
No Mortality Difference
1.2
1.4
1.6
1.8
2
Favors endoscopic
plus drug therapy
Bañares R et al., Hepatology 2002; 35:609
THE TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT
Transjugular Intrahepatic Portosystemic Shunt
Hepatic
vein
TIPS
Portal vein
Splenic
vein
Superior mesenteric
vein
TIPS IN THE TREATMENT OF VARICEAL HEMORRHAGE
TIPS in the Treatment of Variceal Hemorrhage
 TIPS is rescue therapy for recurrent variceal
hemorrhage
(at second rebleed for esophageal varices, at first
rebleed for gastric varices)
 TIPS is indicated in patients who rebleed on
combination endoscopic plus pharmacologic
therapy (10-20%)
 In patients with Child A/B cirrhosis, the distal
spleno-renal shunt is as effective as TIPS
(dependent on local expertise)
Early TIPS In Patients With Acute Variceal
Hemorrhage and HVPG > 20 mmHg (High Risk) May
Improve Survival
 116 cirrhotics with acute variceal bleed
 Urgent assessment of wedged hepatic vein
pressure
 64 HVPG < 20 mmHg: routine therapy
 52 HVPG > 20 mmHg randomized to TIPS vs
routine therapy
 Early TIPS in patients with HVPG>20
associated with reduced transfusion, rebleed,
in-hospital and 1 year mortality
Monescillo et al., Hepatology 2004; 40:793
EARLY TIPS IN PATIENTS WITH ACUTE VARICEAL HEMORRHAGE AND HVPG > 20 mmHg MAY IMPROVE SURVIVAL
Early TIPS In Patients With Acute Variceal Hemorrhage
and HVPG > 20 mmHg (High Risk) May Improve Survival
1
HVPG <20
0.8
HVPG >20 - TIPS
0.6
Probability
of survival
0.4
HVPG >20 – No TIPS
0.2
0
0
3
6
9
12
Months
Monescillo et al., Hepatology 2004; 40:793
Early Use of TIPS in Patients with
Cirrhosis and Variceal Bleeding
 63 patients with cirrhosis and acute variceal bleeding
who had been treated with vasoactive drugs plus
endoscopic therapy
 Randomized to treatment with a polytetrafluoroethylenecovered stent within 72 hours after randomization
(early-TIPS group, 32 patients)
 Vs continuation of vasoactive-drug therapy, followed
after 3 to 5 days by treatment with propranolol or
nadolol and long-term endoscopic band ligation (EBL),
with insertion of a TIPS if needed as rescue therapy
(pharmacotherapy–EBL group, 31 patients).
García-Pagán JC et al. N Engl J Med 2010;362:2370-2379.
Early Use of TIPS in Patients with
Cirrhosis and Variceal Bleeding
García-Pagán JC et al. N Engl J Med 2010;362:2370-2379.
Early Use of TIPS in Patients with
Cirrhosis and Variceal Bleeding
 During a median follow-up of 16 months, rebleeding or failure
to control bleeding occurred in 14 patients in the
pharmacotherapy–EBL group as compared with 1 patient in
the early-TIPS group (P=0.001).
 The 1-year actuarial probability of remaining free of this
composite end point was 50% in the pharmacotherapy–EBL
group versus 97% in the early-TIPS group (P<0.001).
 Sixteen patients died (12 in the pharmacotherapy–EBL group
and 4 in the early-TIPS group, P=0.01).
 The 1-year actuarial survival was 61% in the
pharmacotherapy–EBL group versus 86% in the early-TIPS
group (P<0.001)
García-Pagán JC et al. N Engl J Med 2010;362:2370-2379.
Actuarial Probability of the Primary Composite End
Point and of Survival, According to Treatment Group.
No significant differences were observed between the two
treatment groups with respect to serious adverse events.
García-Pagán JC et al. N Engl J Med 2010;362:2370-2379.
Early Use of TIPS in Patients with
Cirrhosis and Variceal Bleeding
MANAGEMENT ALGORITHM IN ACUTE ESOPHAGEAL VARICEAL HEMORRHAGE
Management of Acute Variceal Hemorrhage
Variceal Hemorrhage Suspected
Initial Management
Acute Hemorrhage Controlled?
NO
YES
Balloon Tamponade
Early rebleeding?
YES
Rescue TIPS/Shunt surgery
NO
2nd Endoscopy
Further bleeding
Prophylaxis against recurrent hemorrhage
Management of Variceal Bleeding
 Primary Prophylaxis
 Pharmacologic
 Endoscopic
 Acute Variceal Hemorrhage
 Pharmacologic
 Endoscopic
 TIPS
 Secondary Prophylaxis
 Pharmcologic
 Endoscopic
 TIPS
LOWEST REBLEEDING RATES ARE OBTAINED IN HVPG RESPONDERS AND IN PATIENTS TREATED WITH VARICEAL BAND LIGATION + BETA-BLOCKERS
Lowest Rebleeding Rates are Obtained in HVPG
Responders and With Ligation + b-Blockers
80
60
%
Rebleeding
40
20
0
Untreated b-blockers
Sclerotherapy
(19 trials) (26 trials) (54 trials)
Bosch and García-Pagán, Lancet 2003; 361:952
b -blockers
+ ISMN
(6 trials)
Ligation
HVPGLigation
Responders*
+
b-blockers
(18 trials)
(6 trials)
(2 trials)
*  HVPG <12 mmHg or
>20% from baseline
MANAGEMENT ALGORITHM FOR THE PREVENTION OF RECURRENT VARICEAL HEMORRHAGE
Prophylaxis of Recurrent Variceal Hemorrhage
Control of Acute Variceal Hemorrhage
Prophylactic Pharmacotherapy
and/or
Endoscopic Variceal Band Ligation
Recurrent Hemorrhage
NO
Surveillance Endoscopy
and/or
Life-long Pharmacotherapy
YES
Is patient on EVL + Pharmacotherapy?
NO
YES
Initiate combination Rx
TIPS/Shunt Surgery
Further bleeding
SUMMARY OF MANAGEMENT OF VARICES AND VARICEAL HEMORRHAGE
Evolution of
Varices
Level of
Intervention
Cirrhosis with no
varices
Small varices
No hemorrhage
Medium / large varices
No hemorrhage
Pre-primary
prophylaxis
 Repeat endoscopy in 2-3 years
 No specific therapy
Small varices
 Repeat endoscopy in 1-2 years
 No specific therapy
 ? beta-blocker to prevent enlargement
Primary
prophylaxis
Medium/Large varices
 Non-selective beta-blockers
 EVL in those intolerant to drugs
 Endoscopic/pharmacologic therapy
 Antibiotics in all patients
 TIPS or shunt surgery as rescue therapy
Variceal hemorrhage
Secondary
prophylaxis
Recurrent variceal
hemorrhage
Management Recommendations
 Beta-blockers + nitrates or EVL
 Beta-blockers + EVL ?
 TIPS or shunt surgery as rescue therapy
GASTRIC VARICES
Gastric Varices
 10-15% of variceal bleeding episodes
 Limited data from controlled trials
 Optimal therapy not known
 Vasoactive drugs used, but not studied
 Endoscopic cyanoacrylate injection:
90% control of bleeding
 Balloon tamponade with Linton-Nachlas tube
 TIPS: 90% control of bleeding
CLASSIFICATION OF GASTRIC VARICES
Classification of Gastric Varices
GOV 2
GOV 1
IGV 1
IGV 2
Sarin et al, Am J Gastro 1989; 84:1244
MANAGEMENT ALGORITHM FOR PATIENTS BLEEDING FROM GASTRIC VARICES
Management of Acute Gastric (Fundal)
Variceal Bleeding
Variceal Hemorrhage Suspected
• Transfuse to hemoglobin ~8 g/dL
• Early pharmacotherapy
• Antibiotic prophylaxis
Initial Management
Variceal obturation possible?
NO
YES
Bleeding controlled?
NO
TIPS*
YES
Variceal obliteration +beta-blockers
Not possible or rebleed
*Surgical shunt may be considered for Child’s Class A
MANAGEMENT OF GASTRIC VARICES
Management of Gastric Varices
 Gastric varices that are continuous with
esophageal varices and extend along the
lesser curve (GOV1) should be treated in the
same way as esophageal varices
 In patients with isolated fundal varices (IGV1),
splenic vein thrombosis should be
investigated. If present, treatment consists of
splenectomy
 Cirrhotic patients bleeding from gastric fundal
varices require specific treatment
ENDOSCOPIC IMAGES OF GASTRIC VARICES
Gastric Varices
Pretreatment cyanoacrylate
Post-treatment cyanoacrylate
PORTAL HYPERTENSIVE GASTROPATHY
Portal Hypertensive Gastropathy
 Endoscopic changes seen in most patients with
portal hypertension
 Characterized by a cobblestone appearance of
the mucosa and red signs on endoscopy
 Often confused with:
 Gastric Antral Vascular Estasia (GAVE)
 Watermelon Stomach
 May be associated with chronic occult bleeding,
anemia, and occasionally cause of acute UGI
hemorrhage
SEVERE PORTAL HYPERTENSIVE GASTROPATHY MAY BE DIFFICULT TO DISTINGUISH FROM DIFFUSE GAVE
Severe Portal Hypertensive Gastropathy May
be Difficult to Distinguish from Diffuse GAVE
Severe PHG
Diffuse GAVE
ENDOSCOPIC IMAGES OF THE TWO TYPES OF GASTRIC ANTRAL VASCULAR ECTASIA
Types of Gastric Antral Vascular Ectasia
Typical GAVE
“watermelon stomach”
Diffuse GAVE
GASTRIC ANTRAL VASCULAR ECTASIA
Gastric Antral Vascular Ectasia (GAVE)
 Endoscopic findings:
 Red spots without
background mosaic pattern
 Linear aggregates in
antrum: “watermelon
stomach”
 Diffuse lesions in proximal
and distal stomach
 May be difficult to differentiate
from portal hypertensive
gastropathy (PHG)
 Ideal therapy not known
Argon Plasma Coagulation for GAVE
Band Ligation for GAVE
VARICEAL WALL TENSION IS A MAJOR DETERMINANT OF VARICEAL RUPTURE
Variceal Wall Tension (T) is a Major
Determinant of Variceal Rupture
Esophagus
Wall thickness
(w)
Radius
(r)
Transmural
pressure (tp)
Varix
Tension (T)
r
T = tp x
w
Groszmann, Gastroenterology 1984; 80:1611
MANAGEMENT OF PATIENTS WITHOUT VARICES
Treatment of Varices / Variceal Hemorrhage
No varices
Prevent Formation of Varices ?
Varices
No hemorrhage
Prevent First Variceal
Hemorrhage
Variceal
hemorrhage
Control Bleeding: Reduce
Mortality
Recurrent
hemorrhage
Prevent Recurrent
Hemorrhage
Endoscopic Findings
Which is the best option?
1) Start atenolol
2) Start propranolol
3) Variceal band ligation
4) Propranol and isosorbide mononitrate
5) Band ligation and beta blockers
 Bleeding controlled with band ligation,
antibiotics an octreotide
 No bleeding for 5 days
 Child score 10. MELD 15 MAP 90 mmHg
Which is the best discharge regiment?
1) Beta blockers and nitrates
2) Serial ligation alone
3) Ligation and beta blockers
4) TIPS
5) Portacaval shunt
Prevention of Recurrent Bleeding TIPS
vs. Drug Therapy
 91 Childs-Pugh class B/C cirrhotic patients
who survived first variceal hemorrhage
 Randomized to TIPS(47) vs propranolol
plus isosorbide-5-mononitrate(44)
 Followed for 2 years
 Assess hepatic encephalopathy, recurrent
variceal hemorrhage, costs, number of
medical interventions, and survival
Hepatology 2002;35:385-92