The Fundal Pile: Bleeding Gastric Varices
By A.J.W. Millar, R.A. Brown, I.D. Hill, H. Rode, and S. Cywes
Cape Town, South Africa
0 Bleeding from esophageal varices is a common cause of
major upper gastrointestinal tract blood loss in children with
portal hypertension but usually ceases spontaneously or is
satisfactorily managed by nonoperative measures. Massive
hemorrhage from gastric fundal varices may be difficult to
control with compression and sclerotherapy; in these cases,
a direct surgical approach may be indicated. Since 1964.27
children have undergone aggressive injection sclerotherapy
for bleeding esophageal/gastric varices. Nine (6 with portal
vein thrombosis) bled from gastric fundal varices. In 5 of
these, medical management and sclerotherapy failed to
control the acute bleed. In all 5 there was “rupture” of a large
gastric fundal varix or “pile” and bleeding was controlled at
emergency laparotomy by underrunning the varices through
a high anterior gastrotomy. Four have subsequently been
successfully managed by continued sclerotherapy and one
patient with cirrhosis has died of liver failure. In 3 of the
survivors both esophageal and gastric fundal varices have
been completely obliterated. No further life-threatening hem-
orrhage has occurred in any case during a follow-up period of
1 to 6 years. Bleeding from gastric varices is more common
than previously recorded and more difficult to control by
nonoperative management, including injection sclerother-
apy. In uncontrolled hemorrhage from gastric varices, surgi-
cal underrunning offers a means of providing initial control.
Thereafter, the inevitable variceal recurrence may be success-
fully treated with sclerotherapy.
Copyright o 7997 by W.B. Saunders Company
INDEX WORDS: Portal hypertension; gastric varices.
E SOPHAGEAL VARICES are a common cause
of serious upper gastrointestinal tract hemor-
rhage in children.‘” Morbidity and mortality are
worse in those with varices secondary to an intrahe-
patic cause rather than extrahepatic portal vein
obstruction.4 In most cases the bleeding site in the
esophagus can be identified at endoscopy and con-
trolled with sclerosant injection.*x’jThereafter, preven-
tion of further bleeding from esophageal varices is
possible with repeated endoscopic injection sclerother-
apy.j,’
A small proportion of patients presenting with an
acute variceal bleed fail to respond to conservative
measures, including intravenous vasopressin infusion,
balloon tamponade, and injection sclerotherapy. One
reason for failure is bleeding from gastric varices.8,9
Not only are they difficult to identify while there is
active bleeding, but they may be inadequately com-
pressed by a Sengstaken tube; are difficult to inject,
particularly when they protrude into the lumen of the
gastric fundus at the esophagogastric junction; and
they may be associated with major complications.‘O,ll
In these patients emergency surgery must be consid-
JournalofPediafricSufgery, Vol26,No6(June),1991: ~~707-709
ered. This report describes the management and
outcome of 5 patients who underwent emergency
operation to control continued bleeding from gastric
fundal varices.
MATERIALS AND METHODS
Over the period from 1984 through 1988, 27 patients were
treated at Red Cross War Memorial Children’s Hospital, Cape
Town for upper gastrointestinal tract bleeding from varices second-
ary to portal hypertension (Table 1). Their ages at first presenta-
tion ranged from 2 to 11 years. There were 12 boys and 15 girls.
Initial management included resuscitation with restoration of
blood volume and clotting factors, followed within 24 hours by
endoscopic identification of the bleeding site. A total of 5 to 10 mL
of ethanolamine oleate was injected at the site of the bleed as well
as proximally in an upward spiral fashion for a distance of 10 cm.
Initially the sclerosant was injected into the varices using a rigid
esophagoscope. Since 1985 paravariceal injections using a flexible
fiberoptic endoscope have been used. Gastric varices were identi-
fied as the source of bleeding in 2 patients at initial endoscopy and
in 7 patients subsequently4 after 1 injection and 3 after 2
injections. In 5 of these 9 cases sclerotherapy and other conserva-
tive measures were unable to control active bleeding (Tables 1 and
2).
Surgical exploration was performed through an upper midline
abdominal incision and a high anterior gastrotomy. Blood clot was
evacuated, and the gastric varices were identified. In 4 cases a
continuous jet of blood was seen arising from one of approximately
4 large varices that coursed from the gastric fundus toward the
esophagogastric junction. In the fifth patient a fresh blood clot
identified the site of the bleed. Commencing with the actively
bleeding varix, each of the varices was underrun throughout its
extent from the esophagogastric junction distally using a 2/O
absorbable suture. In all 5 patients there was complete control of
the bleeding.
Table 2 shows the long-term follow-up of the 5 patients. One
patient with cirrhosis of the liver died of liver failure 6 months after
surgery. A further patient developed an esophageal stricture that
responded well to dilatation. The surviving patients are well 26 to
59 months later, with completely obliterated varices in 3. These 4
patients have continued to undergo follow-up endoscopy at increas-
ing intervals.
DISCUSSION
Most acute variceal bleeds in children respond to
nonoperative management and bleeding ceases spon-
From the Departments of Paediam’c Surgery and Paediam’cs,
Institute of Child Health and Red Cross War Memorial Children’s
Hospital, Cape Town, South Africa.
Date accepted: May 9, 1990.
Address reprint requests to A.J. W. Millar, MD, Department of
Paediatric Surgery, Institute of Child Health, Red Cross War Memorial
Children’s Hospital, Rondebosch 7700, Cape Town, South Africa.
Copyright o 1991 by W.B. Saunders Company
0022-3468/91/2606-0015$03.00/0
707
708 MILLAR ET AL

Table 1. Injection Schlerotherapy Management of Bleeding Esophageal and Gastric Varices, Red Cross War Memorial Children’s Hospital
(January lg84-June 1989)

Follow-Up

Total Gastric Mean No. of Outcome

No. of Patients Varices Surgery Injections Until Duration
Etiology (n = 27) (n = 9) (n = 5) Obliteration (mo) Cured Died

Portal vein thrombosis 20 7 4 4.3 20.2 18* 0

(5-59)
Cirrhosis 5 2 1 4.5 33.8 3 2
(45-46)
Hepatic fibrosis 2 0 0 5 41.5 2 0
(3746)

“Two still have a single residual varix after 6 and 7 injections, respectively.

taneously.1’3 Management of those patients who con-
tinue bleeding may include immediate injection scle-
rotherapy or emergency surgical procedures, such as
esophagogastric devascularization or portasystemic
shunting.4.‘2 Unfortunately, some postsurgery rebleed-
ing and development of long-term encephalopathy
can be anticipated in shunted patients.4Z13”4Because
of the high morbidity and occasional mortality with
emergency surgery, endoscopic sclerotherapy to con-
trol bleeding from varices has become popular.1X6Z7
Howard et al report variceal obliteration by injec-
tion sclerotherapy in 92% of children with an extrahe-
patic cause of portal hypertension and 75% with an
intrahepatic cause.’ Of the 108 patients in their
series, none had gastric varices identified as the
source of the initial bleed but one child died as a
result of uncontrolled hemorrhage from esophagogas-
tric varices. Twelve patients subsequently rebled and
4 were found to be bleeding from gastric varices.5 In
contrast, a third (9/27) of children with upper gas-
trointestinal bleeding secondary to portal hyperten-
sion in this series were found to be bleeding from
gastric varices. The diagnosis of bleeding from gastric
rather than esophageal varices may be difficult in the
acute phase because the field is obliterated by active
bleeding and the gastroesophageal cardia is relatively
inaccessible even with the flexible endoscope. Once
identified as the source of bleeding, it may still be
technically difficult to inject sclerosant into or around
a varix high up on the gastric fundus. As demon-
strated in 3 of the present patients, attempted gastric
variceal compression by tamponade with a Blakemore-
Sengstaken tube may be unsuccessful. In 2 patients it
did not control the initial hemorrhage; in the third,
bleeding recommenced immediately on deflation of
the balloon.
Recently, Hosking and Johnson proposed a classifi-
cation of gastric varices based on their dominant
location within the stomach.8 Their classification
divides gastric varices into 3 types. Type II, in which
there are gastric varices converging on the cardia, and
which may be accompanied by smaller esophageal
varices above the esophagogastric junction, repre-
sents the bleeding gastric varices encountered in the
children in this series. The incidence of gastric varices
causing variceal hemorrhage in Hosking’s series of
more than 200 patients was 6%. A further 9%
developed gastric varices during long-term follow-up,
many after repeated esophageal variceal sclerother-
apy. Controversy exists as to whether the gastric
varices occur ab initio or secondary to obliterative
sclerotherapy. The increased incidence of gastric
varices postsclerotherapy may be due to the develop-
ment of submucosal collaterals around the fundus. In
two of the present patients bleeding from gastric
varices occurred before any injection sclerotherapy,
suggesting that they were primary in nature.
The name “fundal pile” was thought appropriate
because of the resemblance of the dependant bleed-
ing fundal varix to a prolapsed bleeding hemorrhoid.

Table 2. Follow-Up After Surgical Control of Gastric Variceal Hemorrhage in 5 patients

Age at Duration of No. of Re- Further

Varices Operation Follow-Up bleeds From Variceal current
W Diagnosis &no) Varices Injections Status

4.5 PVT 59 0 3 No varices, stricture dilated

4.5 PVT 35 0 3 Grade II varix, injected at 24 mo
12 PVT 29 0 2 No varices
4 PW 26 0 2 No varices
10.9 Hepatitis, cirrhosis 5 5 3 Died; liver failure; varices still present

Abbreviation: PVT. portal vein thrombosis.

BLEEDING GASTRIC VARICES
In both conditions there is a submucosal varix protrud-
ing into the lumen of the gastrointestinal tract. They
both complicate with fresh bleeding and are related
to alimentary canal sphincters-the lower esophageal
sphincter and the internal anal sphincter. It is possi-
ble the pinch-cock action of these sphincters plays a
role in development of the varix and precipitation of
bleeding by impeding venous return and increasing
intravariceal pressure. The metaphor is further sus-
tained by a recent publication, in which it is suggested
that bleeding esophageal varices may be treated by
“banding” as advocated for hemorrhoids.‘5
The authors’ management of children with bleed-
ing varices entails resuscitation, followed by pitressin
and immediate injection sclerotherapy, with balloon
tamponade if necessary to temporarily control blood
loss. Subsequent injections are continued at weekly
intervals until there is complete variceal obliteration.
This has been most successful with bleeding from
esophageal varices and this experience is similar to
that reported previously.5,6.‘6However, this approach
is less successful when bleeding is from gastric varices
and in 50% of the patients in this series blood loss
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