The Role of Endoscopy in the Diagnosis, Grading,

and Treatment of Portal Hypertensive Gastropathy

Eugene C. Lam, MD, Dennis M. Jensen, MD, and Ian M. Gralnek, MD, MSHS

Portal hypertensive gastropathy (PHG) is an extremely common endoscopic finding in

patients with portal hypertension. This article examines the various endoscopic grading
systems that have been developed for PHG with further discussion on the risk of bleeding
with PHG and if endoscopic grading can predict the risk of bleeding. Finally, both the
nonendoscopic and endoscopic treatment modalities for acute and chronic bleeding sec-
ondary to PHG are discussed.
Tech Gastrointest Endosc 7:37– 40 © 2005 Elsevier Inc. All rights reserved.

P ortal hypertensive gastropathy (PHG) is recognized as a

common endoscopic finding and as a potential source of
both acute and chronic blood loss in patients with cirrhosis.
Endoscopic Grading of Portal
Hypertensive Gastropathy
PHG refers to the characteristic mosaic or snakeskin gastric There is ongoing debate regarding the accuracy and reliabil-
mucosal appearance defined by endoscopy in patients with ity of available PHG grading systems. No scoring system has
portal hypertension (Fig. 1). The point prevalence of PHG is been validated among international experts or large numbers
estimated to range between 50 and 80% in patients with of endoscopists. The lack of a universally accepted grading
portal hypertension secondary to cirrhosis.1-6 Severe PHG system has brought criticism to the published data regarding
ranges from 10 to 25% of cases, but not all “severe” PHG is the significance of PHG lesions and their implications regard-
associated with significant GI blood loss.5,6 ing clinically relevant endpoints such as bleeding, transfu-
The etiology of these gastric mucosal lesions is unclear and sion requirements, and mortality.
may be multi-factorial. There have been a number of theories Currently, there are several PHG grading schema available
regarding possible mechanisms of PHG development includ- to the endoscopist. These PHG severity-grading schemes
ing congestive gastropathy,1 altered blood flow,7 increased range from the simple to complex.
susceptibility to gastric mucosal damage,8-10 or increased ni- Yoo and colleagues compared a 2-category (2-CCS) and a
tric oxide, gastrin, and TNF-alpha levels.11 In addition, oblit- 3-category classification system (3-CCS) (see Table 1). The
eration of esophageal varices by endoscopic treatments has mean percentage agreement among different endoscopists
been associated with an increased prevalence of PHG.3,6 In- was significantly lower for the 3-CCS compared with the
vestigators have suggested a significant increase in PHG as-
sociated with esophageal variceal sclerotherapy.12,13 How-
ever, Primignani and colleagues followed the natural history
of PHG in a study of 373 patients and concluded that the
incidence of PHG over time was similar in patients with no
prior history of endoscopic sclerotherapy versus those receiv-
ing ongoing sclerotherapy.
The incidence of acute PHG bleeding has been noted to be
3% at 3 years, while chronic GI bleeding secondary to PHG is
seen in 10 to 15% of patients at 3 years as found by Sarin and
colleagues.13

Department of Medicine, Division of Gastroenterology & Hepatology; David

Geffen School of Medicine at UCLA, Los Angeles, CA.
Address reprint requests to: Dr. I.M. Gralnek, Assistant Professor of Medicine,
David Geffen School of Medicine at UCLA, VA Greater Los Angeles Health-
care System, CURE Digestive Diseases Research Center, Center for the Study
of Digestive Healthcare Quality and Outcomes, 11301 Wilshire Blvd.,
Cure Bldg 115, Room 215D, Los Angeles, CA 90073. E-mail: Figure 1 Snake skin appearance of portal hypertensive gastropathy.
igralnek@mednet.ucla.edu (Color version of figure is available online.)

1096-2883/05/$-see front matter © 2005 Elsevier Inc. All rights reserved. 37

doi:10.1016/j.tgie.2004.10.009
38 E.C. Lam, D.M. Jensen, and I.M. Gralnek

Table 1 Comparison of 2-Category Classification System versus 3-Category Classification System

2-Category Classification System (2-CCS) 3-Category Classification System (3-CCS)
Mild PHG Fine pink speckling (scarlatina-type rash) Mild PHG Mild reddening
Superficial reddening Congestive mucosa
Mosaic pattern Diffuse pink areola
Severe PHG Discrete red spots Moderate PHG Flat red spot in center of a pink areola
Diffuse hemorrhagic lesion Severe redness and a fine reticular
pattern separating the areas of
raised edematous mucosa
Severe PHG Diffuse red areola
Pinpoint bleeding
Discrete or confluent red mark
lesion
PHG, portal hypertensive gastropathy.

2-CCS (P ⫽ 0.0001). The mean interobserver kappa statistic
values were 0.44 for the 3-CCS and 0.52 for the 2-CCS and
the intraobserver kappa statistic values were 0.43 for the
3-CCS and 0.63 for the 2-CCS (P ⫽ 0.002).14
The New Italian Endoscopic Club (NIEC) sought to
produce a more universally accepted classification system
and defined four elementary lesions (see Table 2). There
was fair to good interobserver agreement in assessing the
elementary lesions of PHG by 32 different endosco-
pists.6,15
Stewart and Sanyal used the Baveno II gastropathy scoring
system (see Table 3) and sought to evaluate its reproducibil-
ity and validity. In a prospective study of 100 consecutive
patients with cirrhosis and portal hypertensive gastropathy,
there was high interobserver agreement (kappa ⬎0.75) re-
garding the presence of gastric mucosal mosaic pattern and
red marks, yet only fair interobserver agreement (kappa sta-
tistic ⫽ 0.4) was seen with assessment of lesion extent.16,17
Portal Hypertensive Gastropathy
Progression
The lesions of PHG can be static or fluctuate between
improvement and deterioration in terms of severity grad-
ing and changes in the severity of portal hypertension.
Primignani and colleagues studied the natural history of
PHG in 315 Italian patients with proven cirrhosis. These
patients were followed with endoscopy every 6 months for
up to 3 years. PHG was noted in 80% of these patients at
initial endoscopy. Portal hypertensive gastropathy became
more severe in 23%, improved in 23%, fluctuated in 25%,
and remained stable in 29% using the NIEC classification
system.6 In another study, Sarin followed a group of pa-
tients who had received esophageal variceal sclerotherapy
and noted that patients with preexisting PHG lesions were
more likely to have worsened PHG and bleeding, while
those without PHG before sclerotherapy had more transi-
tory and less severe PHG.13
Using the NIEC definitions of portal hypertensive gas-
tropathy, the natural history of PHG was observed by Prim-
ignani and coworkers (see Tables 4 and 5). PHG was found in
80% (299/373 patients) of cirrhotic patients. Mild disease
was seen in 127/373 patients (34%) and severe disease was
seen in 172/373 patients (46%).6
Bleeding Risk from Portal
Hypertensive Gastropathy
Primignani and coworkers again using the NIEC estab-
lished definitions of lesions of PHG in which there was fair
to good interobserver agreement showed that 2.5% of pa-
tients had acute bleeding and 12% had chronic bleeding
from PHG.6 Acute bleeding was defined as those with en-
doscopic evidence of actively bleeding lesions while
chronic bleeders had a 2 g/dL drop in hgb in consecutive
visits 6 months apart. McCormack and coworkers in a
series of 127 patients found that (28/127) 22% of studied
patients with portal hypertensive gastropathy had clini-
cally significant bleeding.2
Using the Baveno II scoring system, Stewart and Sanyal
showed that there was a clear association with increasing
PHG scores and an increasing risk of bleeding.16 Mild
gastropathy was defined as a score ⱕ3 and severe as ⱖ4.
Scores ⱕ3 were predictive of a nonbleeding tendency,

Table 2 Elementary Gastric Mucosal Lesions of PHG As Defined by the New Italian Endoscopic Club (NIEC)
Mild PHG Mosaic Like Pattern (MLP)
Severe PHG Red Point Lesions (RPLs)
Cherry Red Spots (CRSs)
Black Brown Spots (BBSs)
Presence of small, polygonal areas surrounded by a whitish-yellow
depressed border
-Mild (areola is uniformly pink)
-Moderate (if center is red)
-Severe (if the areola is uniformly red)
Small, flat, red point-like lesions <1 mm in diameter
Red colored, round lesions >2mm in diameter and slightly protrude
into the lumen of the stomach
Irregularly shaped flat spots, black or brown, persistently present after
washing and caused by intramucosal hemorrhage
Role of endoscopy in hypertensive gastropathy
Table 3 Portal Hypertensive Gastropathy Scoring System As
Proposed at Baveno II Consensus Conference
Parameter Score
Mucosal MP Mild 1 Body & Fundus
Severe 2 Body & Antrum
Red Markings Isolated 1 Fundus
Confluent 2 Body
GAVE Absent 0 Antrum
Present 2
Mild gastropathy ⴝ score < 3. Severe gastropathy ⴝ score > 4.
GAVE, Gastric Antral Vascular Ectasia. MP, Mosaic Pattern.
while scores ⱖ4 showed an association with bleeding (see
Table 3).
Treatment Options
Non-Endoscopic Treatments
As per the UCLA Hemostasis Group recommendations, sup-
portive care is the initial step in the treatment of bleeding
from PHG. In most cases of chronic bleeding, patients will
respond to iron replacement with or without epogen. In pa-
tients with acute GI bleeding from severe PHG, volume re-
suscitation, including possible packed red blood cell transfu-
sions, is needed before endoscopic evaluation. Correction of
any existing coagulopathies and cessation of antiplatelet
agents are keys to preventing early re-bleeding. Correction of
the INR to ⱕ1.5 and maintaining platelets ⱖ50K are impor-
tant goals. DDAVP may also be administered if there is sus-
pected platelet dysfunction from underlying renal disease.
For acute large volume or chronic, persistent bleeding as-
sociated with diffuse PHG, use of pharmacologic agents in-
cluding beta blockers or somatostatin/octreotide, Transjugu-
lar Intrahepatic Portosystemic Shunts (TIPS), shunt surgery
that lowers portal pressures, or liver transplantation, are the
treatment options.1
For acute bleeding thought to be secondary to PHG Garcia
and Sanyal suggest the following treatment regimen.17 (1)
Octreotide 100 ␮g bolus IV followed by 50 ␮g/hr infusion;
(2) Administration of propranolol to hemodynamically stable
patients if bleeding is not stopped or slowed appreciably in
24 to 48 hours (start dose of 40 mg/d PO in 2 divided doses
and titrated up); and (3) TIPS or (4) Shunt surgery if #1 and
2 are not successful.
Endoscopic Treatments
Most often, the portal hypertensive gastropathy associated
with significant UGI bleeding is severe, diffuse, and may not
be amenable to therapeutic endoscopy. However, endo-
scopic hemostasis should be considered in lesions that are
Table 4 NIEC Prevalence of Elementary PHG Lesions in n ⴝ
373 Italian Cirrhotic Patients
MLP 59%
RPLs 37%
CRSs 5.9%
BBSs 8.3%
MLP, mosaic like pattern. RPL, red point lesions. CRS, cherry red
spots. BBS, black brown spots.
39
Table 5 NIEC Location of PHG Lesions in n ⴝ 373 Italian
Cirrhotic Patients
Entire Stomach 50%
24%
8%
10%
3%
6%
focal or localized to the antrum and/or fundus of the stom-
ach. Dulai and colleagues reported on a subgroup of 8 pa-
tients with Watermelon Stomach (WMS) and concomitant
portal hypertension.18 The WMS patients with portal hyper-
tension had more diffuse, punctate gastric antral lesions that
were often actively bleeding as compared with WMS patients
without portal hypertension. WMS patients with PHG did
not have the classic mosaic or snakeskin gastric mucosal ap-
pearance. These patients were treated with endoscopic he-
mostasis and had significant decreases in transfusion require-
ments, fewer bleeding-related hospitalizations, and increased
hematocrits during extended follow-up, compared with
baseline or medical treatment.
In any acute upper GI bleeding case, we recommend the
use of a large single channel or double channel therapeutic
gastroscope for endoscopic evaluation and possible hemosta-
sis (Fig. 2). If using endoscopic hemostasis, we recommend
the use of a large-size (eg, 10F) thermal probe such as a
multipolar electrocautery probe or heater probe. When using
a multipolar electrocautery probe, we recommend a genera-
tor setting of 12 to 15W with a pulse duration of 1 to 10
seconds. Heater probes should be set at 10 to 15J, with sim-
ilar 1-second pulse duration. Argon plasma coagulator (APC)
can also be utilized with a gas flow rate of 1.0 to 1.4 liters per
minute and a generator setting of 50 to 60W. Frequent suc-
tioning is recommend to minimize gastric distension. Pa-
tients should be placed on acid suppression (eg, proton
pump inhibitor) after endoscopic hemostasis. Some endos-
copists recommend sucralfate, since acid secretion is often
reduced in older patients with WMS with or without PHG.19
Conclusion and
Recommendations
PHG can cause acute and/or chronic GI bleeding. The under-
lying pathophysiologic mechanisms of PHG and the endo-
scopic grading systems for PHG are controversial. In some
studies, simple PHG grading systems (eg, 2-category classifi-
cation system) appear to have better interobserver agreement
and may be more reliable than more complex endoscopic
grading systems. The gastric mucosal lesions seen in PHG are
dynamic and can worsen or improve in severity over time.
Overall, mild PHG appears to not cause acute or chronic GI
bleeding, while severe PHG lesions are more frequently asso-
ciated with blood loss. While endoscopy plays a role in the
diagnosis and grading of PHG, there is only a limited role for
therapeutic endoscopy with hemostasis in the treatment of
PHG. Supportive care and medical therapy appear to be the
mainstays of treatment at this time.
40 E.C. Lam, D.M. Jensen, and I.M. Gralnek

Figure 2 (A) Severe antral portal hypertensive gastropathy with hem-

orrhage. (B) Subepithelial hemorrhages in portal hypertensive gas-
tropathy (PHG). (C) Diffuse bleeding PHG treated with argon
plasma coagulation.

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