Review

Portal hypertensive
gastropathy with a focus
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on management
Expert Rev. Gastroenterol. Hepatol. 9(9), 1207–1216 (2015)

Patrick Snyder1, Portal hypertensive gastropathy (PHG) is a painless condition of gastric mucosal ectasia and
Rabia Ali1, impaired mucosal defense, commonly seen in patients with elevated portal pressures. While it
Michael Poles1 and is typically asymptomatic and incidentally discovered on upper endoscopy, acute and chronic
bleeding may occur. There are no definitive recommendations for treatment of asymptomatic
Seth A Gross*2
PHG. Non-selective b-blockers represent the mainstay of therapy for chronic bleeding, while
1
New York University Medical School, somatostatin and vasopressin and their derivatives may be used in conjunction with
550 1st Avenue, New York,
NY 10016, USA supportive measures for acute bleeding. Salvage therapy with transjugular intrahepatic
2
New York University Medical School, portosystemic shunt or rarely surgical shunt is appropriate when medical management fails.
240 E 38 St, 23 FL, New York, The role of endoscopic therapy for PHG is controversial. Liver transplantation should be
NY 10016, USA
considered as a final resort in cases of refractory bleeding due to PHG.
*Author for correspondence:
Seth.gross@nyumc.org
For personal use only.

KEYWORDS: anemia . cirrhosis . congestive gastropathy . hemorrhage . portal hypertension . portal hypertensive
gastropathy

Portal hypertension is defined as an elevated etiology of PHG is thought to involve hyper-

portal pressure gradient, the difference between
the pressure in the portal vein and the inferior
vena cava [1]. Cirrhosis is the leading cause of
portal hypertension in the world, accounting for
over 90% of cases in the West [1]. Non-cirrhotic
portal hypertension, particularly as related to
schistosomiasis, is prevalent in southeast Asia
and the Middle East [2,3]. Complications of por-
tal hypertension include abdominal ascites,
spontaneous bacterial peritonitis, hepatorenal
syndrome, hepatopulmonary syndrome, high
output heart failure cardiomyopathy and gastro-
intestinal (GI) bleeding. Perhaps most concern-
ing among potential complications, however,
both in terms of prevalence and morbidity and
mortality, is GI bleeding. Specifically, acute var-
iceal bleeding is the most life-threatening
manifestation of portal hypertension. Portal
hypertensive gastropathy (PHG) is a prevalent
cause of GI blood loss among cirrhotics. While
the prevalence of PHG in patients with cirrhosis
is between 20 and 80%, only 10–15% of those
with PHG experience significant GI hemor-
rhage [4,5]. PHG is diagnosed endoscopically
and has a mosaic ‘snake skin’ mucosal appear-
ance. These findings are most commonly visual-
ized in the gastric body and fundus [6–9]. The
emia and stasis, with impaired mucosal defense
mechanisms playing a role in its development,
but the exact pathogenesis is not completely
understood [10–15]. Eradication of varices, both
esophageal and gastric, promotes the pathogene-
sis of PHG, often in a transitory pattern [16–19],
which has been suggested to be due to increased
shunting of blood and elevation of mucosal
vasculature pressure.
The aim of treatment of PHG is to mitigate
bleeding complications and includes both
medical therapy and invasive salvage therapy
when medical management is unsuccessful.
Invasive therapy includes percutaneous, surgi-
cal and endoscopic modalities. The goal of
percutaneous and surgical approaches is to
reduce portal pressures, while that of endo-
scopic therapy is to use thermal coagulation or
desiccant powder to achieve hemostasis. Recent
advancements have been made in the realm of
endoscopic therapy, and ongoing research into
the pathophysiology of PHG is yielding novel
therapeutic targets.
Epidemiology/natural history
Given a 20–80% prevalence of PHG among
patients with elevated portal pressures, it

informahealthcare.com 10.1586/17474124.2015.1059275  2015 Informa UK Ltd ISSN 1747-4124 1207

 Review Snyder, Ali, Poles & Gross
should be considered on the differential diagnosis for GI hem-
orrhage among this patient population. In a 2004 study of
222 asymptomatic patients with liver cirrhosis and portal
hypertension, PHG was detected in a total of 48 patients [4].
The study population was followed with upper endoscopy every
12 months for 3 years, revealing an increased incidence over
the duration of the study (3 at 1 year, 10 at 2 years and 24%
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at 3 years). The severity of disease also typically worsened over
time; on follow-up of the initial 43 patients with mild PHG,
approximately 30% developed severe PHG and 60% main-
tained a stable level of disease, while only 10% experienced dis-
appearance of disease. The overall prevalence of endoscopic
PHG was 50% by the end of the study. The study also moni-
tored acute bleeding, defined as overt bleeding (hematemesis or
melena) with concurrent endoscopic evidence of PHG with
active bleeding. Chronic bleeding was defined as a decrease in
hemoglobin of >2 g/dl between consecutive 6-month visits in
the absence of acute bleeding or NSAID use. In this study, 8%
of PHG patients bled acutely and 6% bled chronically. Acute
bleeding was more common in patients with endoscopic evi-
dence of severe PHG. The authors also found that both the
initial prevalence of PHG and progression of PHG correlated
with the presence of advanced cirrhosis (Child–Pugh class B or
C) [4]. In contrast, Primignani et al. found an overall prevalence
For personal use only.
of PHG of 80% in patients with cirrhosis [5]. In this study,
which utilized similar definitions, 2.5% of the study population
bled acutely and 11% bled chronically. Acute bleeding was
again noted to be more common in patients with endoscopic
evidence of severe PHG. The presence of PHG correlated with
the duration of cirrhosis, and PHG was also more commonly
seen in patients with esophageal varices and positively corre-
lated to variceal size. Perhaps counterintuitively, this study
found that Child–Pugh class B patients had a greater preva-
lence of PHG than did Child–Pugh class C patients [5]. Based
on these studies, it appears that while PHG is common in cir-
rhotics, bleeding from PHG occurs more rarely and with a bias
toward those with severe PHG [4,5].
Some investigators have considered the possibility that
Helicobacter pylori infection may alter the gastric environment
in a manner that would increase the risk of development of
PHG in cirrhotic patients. On the contrary, the prevalence of
H. pylori infection, including those strains producing virulence
factors (cagA and cagE), was found to be either neutrally or
inversely correlated with the presence and severity of
PHG [20–22].
Eradication of gastric and esophageal varices by endoscopic
variceal sclerotherapy (EVS) and endoscopic variceal ligation
(EVL) has been shown to be a risk factor for the development
and progression of PHG [16–19]. Similarly, gastric variceal erad-
ication by balloon-occluded retrograde transvenous obliteration
(BRTO) has been linked with progression of PHG [23]. Vari-
ceal eradications by EVS or endoscopic variceal ligation (EVL)
causes are distribution of local mucosal gastric blood flow,
overwhelming other collaterals and leading to the development
of PHG [17,19]. Although the mechanism underlying PHG
1208
exacerbation following balloon-occluded retrograde transve-
nous obliteration (BRTO) has not been investigated, it is
likely that gastrorenal shunt obliteration overwhelms the
remaining gastric collateral circulation in an analogous fashion.
Exacerbation of PHG may occur dynamically at the time of
eradication or in a sub-acute time frame [17]. Primignani et al.
suggested the relationship between variceal eradication and
PHG may be overestimated, as patients who are candidates for
variceal eradication are at higher baseline risk of developing
PHG [5].
Pathophysiology
The pathogenesis of PHG has been extensively studied but is
still not well understood. Portal hypertension is thought to be
a prerequisite for PHG [4,12,24–28]. Several studies, however,
have failed to exhibit a direct relationship between portal
venous pressure and PHG [10,12,24]. It is also unclear to what
extent the severity of underlying liver disease correlates with
prevalence or progression of PHG, as noted above [4,5,11,12].
Hemodynamic studies of the hepatic venous system in
patients with PHG have revealed unique changes in mucosal
blood flow compared with patients with portal hypertension
without PHG [10,15]. In comparing these two groups,
Ohta et al. noted similar systemic indices of portal hyperten-
sion, including portal venous pressure, volumetric portal venous
blood flow and portal venous flow velocity [10]. Volumetric gas-
tric mucosal blood flow in the fundus was noted to be higher
in the PHG group, supporting the theory PHG is a result of
localized active congestion [10]. In contrast, Gupta et al. found
decreased volumetric blood flows in the gastric mucosa of
patients with PHG, suggesting a model of passive conges-
tion [15]. Piasecki et al. utilized an endoscopic probe to measure
mucosal tissue oxygenation and found that PHG patients had
gastric mucosa that was relatively oxygen deficient compared
with those without PHG. This finding supported the role of
mucosal hypoxia and passive congestion in the pathogenesis of
PHG [29]. Curvelo et al., in accordance with Ohta et al., found
no correlation between systemic hemodynamic indices and
PHG, supporting the theory of localized congestion [12]. On
the contrary, a multivariate analysis by Kumar et al. concluded
that PHG is a consequence of systemic, rather than local, vas-
cular derangements of cirrhosis and portal hypertension. In this
study, cirrhotics with and without PHG were compared; those
with PHG were found to have increased mean cardiac output
and mean cardiac index and decreased median systemic vascular
resistance [11]. Regardless, gastric mucosal hyperemia and con-
gestion play a critical role in PHG and PHG related bleeding.
Elevated gastric mucosal levels of inducible nitric oxide syn-
thase and correspondent increases in nitric oxide mediate vaso-
dilation and promote active hyperemia [30].
Mucosal hyperemia and congestion may contribute to PHG
related bleeding by lowering the threshold for mucosal
injury [13,14]. Alcohol, bile salts, NSAIDs and intestinal endo-
toxin are intraluminal stressors inpatients with PHG [14,31,32].
An animal model study demonstrated that treatment with
Expert Rev. Gastroenterol. Hepatol. 9(9), (2015)
 PHG with a focus on management Review

glutamine, an antioxidant, might improve PHG by tempering Table 1. Classification schemes for portal
these stressors [13]. Additional studies have suggested that PHG hypertensive gastropathy.
is a state of increased mucosal apoptosis [33]. Lan et al. studied
Classification NIEC Tanoue et al.
rat models with PHG injected with endotoxin to evaluate its
scheme
effect on gastric mucosa. The PHG rats demonstrated histo-
logic evidence of greater mucosal cell damage and higher Mild/Grade 1 Isolated MLP Mild reddening
without MLP
mucosal concentrations of TNF-a, which plays a significant
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role in inflammation and apoptosis, in response to endotoxin Moderate/Grade 2 Not defined Severe redness and MLP
injection when compared with controls [14,34]. Tan et al. investi- Severe/Grade 3 Presence of Presence of point bleeding
gated the role p53-upregulated modulator of apoptosis among red marks
in vivo mouse models of PHG and in vitro human gastric cell MLP: Mosaic like pattern; NIEC: New Italian Endoscopic Club.
lines from subjects with PHG. The study suggested PHG
drives stress to the endoplasmic reticulum, which upregulates
pink areola and a central red spot and severe with a red are-
expression of p53-upregulated modulator of apoptosis, resulting
ola [7]. Tanoue et al. proposed a three-tier classification system
in increased levels of gastric mucosal cell apoptosis [33].
for PHG in which grade 1 disease was characterized by mild
reddening without a MLP, grade 2 disease by severe redness
Presentation
and a MLP and grade 3 by the presence of point
PHG is typically asymptomatic and incidentally diagnosed but
bleeding TABLE 1 & FIGURE 1 [9]. The necessity of such classification
may present with slow, chronic or acute GI bleeding. Approxi-
schemes is questionable, given that it does not impact therapeu-
mately 10 – 15% of cirrhotic patients with PHG experience GI
tic decisions.
hemorrhage [4,5]. The remaining 85–90% of cases are diagnosed
incidentally during an endoscopy performed for alternative indi-
PHG and GAVE
cations (i.e., variceal screening). In patients with chronic bleed-
PHG is often considered alongside gastric antral vascular ectasia
ing from PHG, the bleeding may be low volume and
For personal use only.

(GAVE), otherwise known as watermelon stomach. While these

intermittent and occur in the absence of clinical melena, result-
syndromes are distinct entities, in some instances they overlap.
ing only in iron deficiency anemia. Well-established guidelines
for endoscopic variceal screening facilitate monitoring of
PHG [35].
The clinical sequelae of acute GI bleeding from PHG are A B
similar to those of any other cause of acute upper GI bleeding.
Hematemesis or coffee ground emesis may accompany melena
with higher volume bleeding. Hematochezia is an uncommon
finding with PHG-related hemorrhage as the volume typically
is not great enough to cause a brisk upper GI bleed.

Diagnosis
The diagnosis of PHG is made visually during endoscopic
examination. Mucosal biopsy is rarely required and may result
in post-biopsy bleeding in patients with underlying liver disease C D
and a high risk for coagulopathy. McCormack et al. initially
described PHG as a distinct mucosal lesion located in the gas-
tric fundus and body. Histologic samples were characterized by
hyperemia and minimal inflammation [6]. Since that time,
several classification schemes have emerged. In 1992, the New
Italian Endoscopic Club (NIEC) reached a consensus describ-
ing three general patterns of PHG [7]. The first was a mosaic-
like pattern (MLP), or ‘snake skin’ pattern, of polygonal areas
with white depressed borders. The second pattern was
described as red marks and the third pattern was brown black Figure 1. Portal hypertensive gastropathy and gastric
spots with irregular borders attributed to intramucosal hemor- antral vascular ectasia on endoscopy. (A) Mild PHG in the
fundus of the stomach, characterized by a MLP with pink areola.
rhage [7]. This schema only designated two levels of severity of (B) Moderate severity MLP: diffuse polygonal markings with pink
PHG: mild in the instance of an isolated MLP and severe in areolae with central red spots. (C) Severe PHG with red marks,
the instance of red marks regardless of the presence or absence indicating a higher predisposition to bleeding. (D) GAVE: longitu-
of a MLP [7,8]. Further, the MLP was subcategorized into three dinal columns of ectatic vessels coursing through the antrum of
levels of severity: mild with a pink areola, moderate with a the stomach.

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 Review Snyder, Ali, Poles & Gross

Unlike PHG, portal hypertension is not a prerequisite for Treatment

GAVE and is present in approximately 30% of cases [26].
Endoscopically, GAVE is characterized by discrete columns of
ectatic vessels running longitudinally through the antrum of the
stomach, resulting in a ‘striped watermelon’ appearance. In
some instances, GAVE may present with punctate lesions and
extend into the body of the stomach, making differentiation
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Management of PHG depends on the clinical context, as strate-
gies differ between treatment of asymptomatic PHG and treat-
ment of chronic and acute bleeding related to PHG. In
general, medical therapy is first line, and surgical salvage ther-
apy is recommended only if medical therapy is unsuccessful.
Liver transplantation may be considered in instances of refrac-

from PHG more difficult [26].
Although diagnosis of PHG is based on visualization of the
mucosa and identification of the distinct pattern, biopsy may
be necessary to differentiate PHG and GAVE in ambiguous
cases. In the instance that biopsy is performed, PHG is charac-
terized by vascular ectasia of the capillaries and veins without
inflammation or thrombi at the level of the mucosa and sub-
mucosa [6]. While GAVE also is characterized histologically by
dilated mucosal capillaries, the presence of fibrin thrombi,
lamina propria hyperplasia and spindle cell proliferation differ-
entiates it from PHG [26].
Capsule endoscopy (CE) has been investigated as a less inva-
sive means of identifying bleeding sources in patients with por-
tal hypertension and chronic anemia. Canlas et al. studied
19 cirrhotic patients evaluated with CE, detecting PHG in
68% of the study population [36]. A recent randomized con-
trolled trial compared the efficacy of CE in identifying PHG
For personal use only.
tory bleeding due to PHG or other complications of advanced
cirrhosis in which all other management modalities have failed.
Although most of the established management strategies for
PHG are based on studies performed on cirrhotics, the recom-
mendations below can be cautiously extended to subjects with
non-cirrhotic portal hypertension.
Medical therapy
Asymptomatic PHG
No guidelines exist for prophylaxis against bleeding in asymp-
tomatic PHG [27,28]. Notwithstanding, given the frequent coex-
istence of PHG and esophageal varices, primary or secondary
prophylaxis against variceal bleeding with b-blockade may offer
a theoretical benefit in the prevention of bleeding in asymp-
tomatic PHG (FIGURE 2) [27,35].
Chronic bleeding and prophylaxis against recurrent bleeding

with upper endoscopy, the gold standard. The sensitivity of CE
was 69%. It appeared the location of the lesion was the pri-
mary limiting factor, as the sensitivity of CE in picking up
PHG in the gastric body was 100 verses 48% for PHG located
in the fundus [37].
Non-selective b-blockers were established as effective primary
and secondary prophylaxis for esophageal variceal bleeding in
patients with portal hypertension before their role in the man-
agement of PHG was understood. b-blockers reduce portal
hypertension by blocking b-receptors in mesenteric arterioles

Asymptomatic Chronic Acute

PHG bleeding bleeding

– ABC’s
– Non-selective
– Transfusion
beta blocker – Prophylactic
Associated with – Iron
Associated small varices with antibiotics
supplementation
with medium red signs or All other – Somatostatin or
– Transfusion
or large bleeding history or circumstances vasopressin drip
varices in patients with – PPI
Child-Pugh Class
B or C cirrhosis
Refractory
bleeding Refractory
Non-selective No formal bleeding
beta blocker recommendation
Non-selective
beta blocker

Portal venous Portal venous

decompression decompression
(TIPS vs (TIPS vs
surgical shunt) surgical shunt)

Figure 2. Treatment algorithm for portal hypertensive gastropathy.

1210 Expert Rev. Gastroenterol. Hepatol. 9(9), (2015)

 PHG with a focus on management Review

that mediate vasodilation, allowing for Table 2. Reviewing the evidence: important studies informing
unopposed a-receptor-mediated vasocon- management strategies for portal hypertensive gastropathy.
striction [38]. Blood flow is thereby prefer-
b-Blockers Somatostatin/ TIPS/surgical Endoscopic
entially shunted away from portal
vasopressin shunt therapy
circulation [38]. Hosking et al. published
the first trial investigating the use of pro- Hosking et al. [39] Kouroumalis Urata et al. [59] Herrera et al. [67]
Perez-Ayuso et al. [40] et al. [54] Mezawa et al. [60] Smith et al. [68]
pranolol specifically for the purpose of
Zhou et al. [55] Kamath et al. [61]
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treating PHG [39]. Twenty-four patients Orloff et al. [62]

with an established diagnosis of PHG Soin et al. [63]
were randomized to 160 mg propranolol
daily or placebo. After 6 weeks of inter-
vention, all participants were crossed over to the alternate arm. demonstrated that a more aggressive transfusion goal was actu-
The study demonstrated a significant improvement in endo- ally harmful in terms of 6-week mortality and incidence of
scopic grading of the PHG in the propranolol arm. Although adverse events, particularly in patients with cirrhosis. Transfu-
less bleeding was also demonstrated in the propranolol arm, sion above a hemoglobin of 7.0 g/dl may promote further
the study was underpowered to achieve statistical significance bleeding by increasing portal pressure, impairing clotting and
for this end point (TABLE 2) [39]. Perez-Ayuso et al. randomized inducing coagulopathy [46–48]. Furthermore, it has been pro-
54 cirrhotic patients with a history of acute or chronic bleeding posed that the immunosuppressive effect of allogeneic blood
from PHG to daily propranolol (with dose titrated to 25% products leads to higher rates of infection [49]. In the absence
reduction in resting heart rate) verses control. Absence of acute of studies specifically investigating transfusion strategies in
or chronic rebleeding at 12 months occurred in 65% of treated PHG patients, it is recommended that these guidelines be gen-
patients verses 38% in the control arm, and at 18 months in eralized to transfusion decisions in PHG. Therefore, in patients
52% of treated patients verses 7% in controls. Subgroup analy- bleeding acutely due to PHG, hemoglobin may be transfused
sis showed a statistically significant reduction in acute rebleed- to a goal of 7.0 g/dl, unless the patient has a need for greater
For personal use only.

ing and a reduction in chronic rebleeding and death which was oxygen-carrying capacity. Platelets may be transfused to a goal
not statistically significant [40]. The use of b-blockers became of 50  109/l in the same setting [50]. Coagulation factors may
well-accepted practice in the ensuing years, and the recommen- also require repletion in the form of fresh frozen plasma or
dation for their use in preventing rebleeding from PHG is prothombin complex concentrate.
reflected in the latest consensus guidelines [41]. Prophylactic antibiotics are recommended in any patient
A single study by Wagatsuma et al. investigated the use of with cirrhosis and GI hemorrhage. Oral norfloxacin 400 mg
angiotensin II receptor antagonist losartan in treating PHG [42]. twice daily or intravenous ceftriaxone 1 g daily up to 7 days
Sixteen patients with endoscopic evidence of PHG were treated are both acceptable regimens, although recent studies have
with daily losartan at a dose of 25 or 50 mg, and endoscopy shown an increased incidence of quinolone-resistant bacteria in
was repeated after 4 weeks of treatment. Improvement in endo- the fecal flora [41,51,52].
scopic mucosal findings was demonstrated in a dose-dependent The original study by Hosking et al. on the use of proprano-
fashion. However, the implications of the study are limited by lol in PHG investigated its efficacy in treating acute bleeds as
its small size and the uncertain utility of losartan in preventing well as in prophylaxis. Fourteen patients with acutely bleeding
PHG-related bleeding [42]. Given the alteration in metabolism PHG were started on 24–480 mg of propranolol daily. Thir-
of many angiotensin II receptor antagonists in cirrhosis, safety teen patients stopped bleeding by 3 days without further inter-
of administration must also be considered [43]. vention. Nine of 14 patients showed endoscopic improvement
Iron supplementation, either in the oral or intravenous form, in PHG with downgrading on the severity scale after cessation
is recommended in chronically bleeding PHG patients with of bleeding with propranolol therapy [39].
resultant iron deficiency anemia. Transfusion should also be per- Octreotide (a somatostatin analog) and terlipressin (a vaso-
formed if necessary with a restricted hemoglobin goal of 7.0 [44]. pressin analog) have become staples in the management of
acute bleeding due to PHG. Like propranolol, octreotide
Acute bleeding reduces portal hypertension via presplanchnic vasoconstriction
In the acutely bleeding patient, early management will focus on without causing hypotension or bradycardia [53]. Kouroumalis
stabilization, including protection of the airway, restoration of et al. investigated the use of somatostatin and octreotide in
intravascular volume with intravenous crystalloid or colloid 26 patients with acutely bleeding PHG. Eleven received
solutions and transfusion. Hemoglobin transfusion goals in the somatostatin (250 mg bolus followed by 250 mg/h) and
setting of acute GI bleeding have trended from a more liberal 15 received octreotide (100 mg bolus followed by 50 mg/h). All
goal of 10.0 g/dl to a more restricted goal of 7.0 g/dl [45,46]. 26 patients stopped bleeding within 48 h. Twenty-three had
Villanueva et al. compared a restrictive and liberal hemoglobin no relapse in bleeding after discontinuation of the drip. Of the
transfusion strategy in acute upper GI bleeding in nearly three patients who rebled, two responded to restarting somato-
900 patients, about 30% of whom had cirrhosis. It was statin intravenous therapy [54].

informahealthcare.com 1211
 Review Snyder, Ali, Poles & Gross
Zhou et al. compared octreotide, vasopressin and omepra-
zole in the treatment of acutely bleeding PHG in 68 patients
randomized to 48-h infusions of each drug. Twenty-four of
24 (100%) experienced remission in the octreotide arm,
14 of 22 (64%) in the vasopressin arm and 13 of 22 (59%)
in the omeprazole arm. All of the patients who did not
respond to omeprazole after 48 h were then treated with a
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combination of omeprazole and vasopressin resulting in
control of bleeding in all patients [55]. Terlipressin, an analog
of vasopressin that is not available in the USA or Canada,
was demonstrated by Bruha et al. to be as effective as
vasopressin [56].
Isolated case reports have described successful use of cortico-
steroids and thalidomide in controlling refractory bleeding due
to PHG [57,58]. However, larger studies will be needed before
the role of these agents in treating acute bleeding from PHG
can be determined.
Salvage therapy
In instances of chronic bleeding refractory to maximal beta
blockade or acute bleeding refractory to somatostatin or vaso-
pressin, invasive methods of hemostasis are recommended.
Portal venous decompression
For personal use only.
Transjugular intrahepatic portosystemic shunt (TIPS) is an inva-
sive means of portal venous decompression that may suppress
acute bleeding or reduce the incidence of chronic bleeding.
Urata et al. examined a population of 12 patients with portal
hypertension and its complications: esophageal or gastric varices,
refractory ascites or hemorrhage from severe PHG. Ten of
12 patients had endoscopic evidence of PHG. Nine of these
10 patients showed endoscopic improvement of PHG after
TIPS and one patient with uncontrollable bleeding from severe
PHG achieved hemostasis [59]. Mezawa et al. had a similar expe-
rience in a study investigating the effect of TIPS on 16 patients
with cirrhosis and PHG. Endoscopic improvement in PHG
after TIPS was noted in all four patients with severe PHG and
5 out of 12 patients with mild PHG [60]. Both of these studies
were limited in their short-term follow-up of 2–4 weeks. How-
ever, another study on a similar population showed that TIPS
induced endoscopic resolution of PHG in 75% of patients with
severe PHG and 89% of patients with mild PHG 6 months
after treatment [61].
Surgical decompression, either by formation of a portacaval
or splenorenal shunt, is another option. A prospective study of
12 cirrhotic patients with either active bleeding from PHG or
a history of previous hospitalizations for bleeding from PHG
demonstrated complete resolution of bleeding in all 12 patients
after surgical portacaval shunt with follow-up to nearly 7 years.
Several of these patients had failed previous trials of proprano-
lol therapy [62]. Another prospective study looked at 25 patients
with non-cirrhotic portal hypertension. Eight of these patients
were found to have endoscopic evidence of PHG initially; after
splenorenal shunting, six of the seven patients followed-up
demonstrated resolution of PHG [63].
1212
With multiple methods of portal venous decompression
available, guidance is needed in selecting the appropriate
modality. Helton et al. studied 40 patients with Child–Pugh
class A or B cirrhosis and a history of at least one bleeding epi-
sode from gastroesophageal varices or PHG. Patients either had
surgical shunting or TIPS. The TIPS arm had a higher 30-day
mortality and more rebleeding episodes, rehospitalizations and
need for shunt revisions, but long-term mortality was compara-
ble [64]. A subsequent prospective randomized trial comparing
distal splenorenal shunting and TIPS in patients with Child–
Pugh class A or B cirrhosis and refractory variceal bleeding
showed no significant difference in time to first encephalo-
pathic event, time to first rebleeding episode or mortality,
although shunt complications and need for reintervention were
higher in the TIPS arm [65]. Whether these findings generalize
to the population of those bleeding due to PHG is uncertain.
High operative and perioperative risks in advanced (Child–
Pugh class C) cirrhosis patients preclude surgical shunting as a
treatment option [66]. In other patients, it is recommended that
selection of decompression method be based on the specific
center’s capabilities and expertise.
Endoscopic techniques
Little investigation has been performed evaluating the applica-
tion of endoscopic techniques for controlling PHG-related
bleeding. One small prospective study examined the use of
argon plasma coagulation (APC) in 11 patients with bleeding
due to PHG among a broader field of patients with bleeding
due to various forms of gastric vascular ectasia [67]. None of the
11 patients had recurrence of acute GI bleeding over a follow-
up ranging from 18 to 37 months. The need for transfusion
was eliminated in 9 of 11 patients. The two remaining patients
were transfusion-dependent prior to the study and continued
to require transfusion after APC treatment, albeit at a reduced
level [67]. The study was limited by its size and in that all of
the patients were hemodynamically stable at the time of initial
presentation. One of the challenges posed by PHG is its often-
diffuse pattern, rendering it less amenable to APC treatment.
This challenge is perhaps being met by a new tool, Hemospray,
a hemostatic powder applied to bleeding sites that works by
rapidly absorbing water and forming a mechanical barrier over
a bleeding point [68]. It already has been successfully employed
to control bleeding due to peptic ulcers, varices and gastroduo-
denal malignancies [68,69]. Initial case reports for its use in PHG
are promising, but large prospective studies must be
performed [68]. The role of endosopic therapy in the treatment
of PHG is ill-defined, but its use is suggested either as a bridge
to more definitive therapy such as portal venous decompres-
sion, or as a surrogate to such measures when they are
contraindicated.
Liver transplantation
Liver transplantation is an option for the treatment of refrac-
tory bleeding due to PHG when all other management options
have been exhausted [70]. Evaluation for liver transplantation is
Expert Rev. Gastroenterol. Hepatol. 9(9), (2015)

a complex process. In general, transplantation should be con-
sidered in subjects with acute liver failure or advanced cirrhosis
with complications and in whom the limits of medical therapy
have been reached [70]. Candidacy for liver transplantation is
largely assessed based on the Model for End-stage Liver Disease
score, a tool for estimating prognosis in the setting of liver dis-
ease [70]. Initial evaluation for liver transplantation in cirrhotics
Expert Review of Gastroenterology & Hepatology Downloaded from informahealthcare.com by Nanyang Technological University on 08/29/15
is indicated after the occurrence of an index complication or
deterioration of hepatic function resulting in a Model for End-
stage Liver Disease score ‡15 [70]. Index complications include
ascites, hepatic encephalopathy and hemorrhage due to esoph-
ageal varices or PHG [70]. Although refractory bleeding from
PHG is an indication for liver transplantation consideration,
most liver transplant candidates with PHG qualify for trans-
plant from other complications of cirrhosis. Patients with PHG
undergoing liver transplantation are highly likely to experience
resolution of PHG [71].
Expert commentary
PHG is most commonly seen in patients with elevated portal
pressures from cirrhosis. It is often asymptomatic and found
when patients undergo screening for esophageal varices, which
if present can cause acute active bleeding. The prevalence of
PHG has been reported to be as high as 80% in patients with
For personal use only.
cirrhosis. PHG has also been linked to causing bleeding but
usually chronic bleeding identified by a drop in hemoglobin.
This is in contrast to a variceal bleed, which is commonly
active bleeding associated with melena, hematemesis or hemato-
chezia. However, severe PHG can have active bleeding, which
is often related to patients having a long duration of cirrhosis
accompanied by esophageal varices. Patients may need follow-
up endoscopy for variceal surveillance, which secondarily allows
for the monitoring of PHG. There are classification schemas to
grade PHG, but they do not impact management. Manage-
ment of PHG is usually with medical therapy rather than inva-
sive intervention. PHG can be treated secondarily with non-
selective b-blockers, which is the main therapy for esophageal
varices. Additionally, iron supplementation can also be helpful
to manage iron deficiency anemia. Acute bleeding from PHG
is managed with somatostatin or terlipressin, which lower por-
tal pressures via splanchnic vasoconstriction. Portal venous
decompression, whether by TIPS or surgical decompression,
Key issues
. Portal hypertensive gastropathy (PHG) is a condition of gastric mucosal ectasia and congestion secondary to portal hypertension.
. PHG is diagnosed endoscopically and patients are often asymptomatic.
. Non-selective b-blockers are the mainstay of prophylaxis against acute and chronic bleeding from PHG.
. Somatostatin and vasopressin derivatives are first-line therapy in the setting of acute bleeding due to PHG.
. Salvage therapy with portal venous decompression via TIPS or surgical shunt is recommended in the management of acute or chronic
bleeding due to PHG when medical therapy alone is ineffective.
. Liver transplantation should be considered in patients with refractory bleeding due to PHG not responding to medical or invasive
treatment.
informahealthcare.com
PHG with a focus on management Review
has been shown to decrease portal pressure, which will decrease
risk of both acute and chronic bleeding in patients with PHG.
Endoscopic therapy can be performed on gastric mucosa by
using thermal cautery, such as APC, to control bleeding. Lastly,
if the above options fail patients can be considered for liver
transplantation.
Five-year view
PHG remains a common consequence of elevated portal pres-
sures. Fortunately, most patients with PHG are asymptomatic
and do not require intervention. The most common group of
patients are those with cirrhosis who are carefully monitored
for development of other consequences related to PHG, such
as esophageal varices. There are guidelines in place for esoph-
ageal variceal screening, which also allow for the screening and
surveillance of PHG. Medical therapy is the centerpiece of
treatment, with the use of non-selective b-blockers as first-line
therapy for varices also conferring protection against bleeding
complications related to PHG.
It is important to recognize PHG as a source of chronic
bleeding in patients with elevated portal pressures. Further-
more, the longer a patient has cirrhosis, the greater the chance
their PHG will worsen, which could result in both chronic and
acute bleeding. Hopefully, their PHG will remain under con-
trol with the use of medical therapy, such as non-selective
b-blockers.
Nonetheless, clinicians must be aware of both medical and
invasive treatments for PHG. Portal pressure shunts, either
TIPS or surgical, are well established options to help better
control PHG. Endoscopic thermal therapy is also a valuable,
established option, and there continue to be advances in endo-
scopic therapy with treatments such as hemospray powder,
which can achieve immediate hemostasis.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with
any organization or entity with a financial interest in or financial conflict
with the subject matter or materials discussed in the manuscript. This
includes employment, consultancies, honoraria, stock ownership or options,
expert testimony, grants or patents received or pending or royalties.
No writing assistance was utilized in the production of this
manuscript.
1213
 Review Snyder, Ali, Poles & Gross
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