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Gastric

This document discusses gastric varices, which occur in around 50% of cirrhosis patients and account for 10-30% of variceal hemorrhages. It describes three classification systems for gastric varices and focuses on the commonly used Sarin classification. The document then discusses various endoscopic, radiological, and combined treatment options for gastric variceal bleeding, their effectiveness and risks. It provides details on therapies including sclerotherapy, band ligation, thrombin injection, TIPS, and BRTO.

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201 views6 pages

Gastric

This document discusses gastric varices, which occur in around 50% of cirrhosis patients and account for 10-30% of variceal hemorrhages. It describes three classification systems for gastric varices and focuses on the commonly used Sarin classification. The document then discusses various endoscopic, radiological, and combined treatment options for gastric variceal bleeding, their effectiveness and risks. It provides details on therapies including sclerotherapy, band ligation, thrombin injection, TIPS, and BRTO.

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Anonymous ER8Y8sZGP
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© © All Rights Reserved
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Gastroesophageal varices have been seen in approximately 50% of patients with

cirrhosis of the liver. Their presence correlates with the severity of liver disease
Gastric varices (GV) bleed less frequently than esophageal varices and are responsible
for 10-30% of all variceal hemorrhages.[7] However, gastric variceal bleeding tends
to be more severe with higher mortality. In addition, a high proportion of patients,
around 35-90%, rebleed after spontaneous hemostasis

CLASSIFICATION OF GASTRIC VARICES


There are three types of classification commonly used for GV.
1. Sarin's classification
2. Hashizome classification
3. Arakawa's classification.
Most commonly used classification is Sarin's classification of GV.

SARIN'S CLASSIFICATION

Gastric varices are categorized into four types based on the relationship with
esophageal varices, as well as by their location in the stomach.

a Gastroesophageal varix (GOV) type 1: Extension of esophageal varices along lesser


b Gastroesophageal varix type 2: Extension of esophageal varices along great curve
c Isolated gastric varix (IGV) type 1 and
Isolated gastric varix type 2: Varices in stomach or duodenum as shown in figure.

HASHIZOME CLASSIFICATION

It is based on clinically significant endoscopic findings, and particularly from the


viewpoint of findings associated with the lightly risk of rupture, as in the
classification of esophageal varices. Thus, endoscopic findings of GV were classified
according to their form, location, and color.[9] The form was classified into three
types:

a. Tortuous (F1).
b. Nodular (F2).
c. Tumorous (F3).
The location was classified into five types and depends on hemodynamic factors;
a. Anterior (La).
b. Posterior (Lp).
c. Lesser curvature (Ll).
d. Greater curvature (Lg) of the cardia and.
e. Fundic area (Lf).
The colors can be classified in (a) white (Cw) or (b) red (Cr). The glossy, thin-walled
focal redness on the varix was defined as red color spot (RC spot). The Hashizume
group reported that the RC spot and larger forms were related to a significantly higher
risk of gastric variceal bleeding.
Arakawa's classification
Type I: Branches within the stomach wall are very few, and the supplying vessel,
varix and draining vessel form a single continuous vein of a nearly unchanged caliber.
 Ia: A single supplying vessel forms a fundic varix.
 Ib: Plural supplying vessels join and form a varix that drains into a single
draining vessel.
Type II: Beside the main supplying and the draining vessels, there are many branching
vessels that exist within the stomach wall, namely varix has communications with
vessels within the stomach wall.

Vascular anatomy
To achieve best results of treatment and at the same time minimizing the
complications it is very important to understand relevant vascular anatomy. This holds
true for all interventional modalities of treatment likely endoscopic, endoscopic
ultrasound (EUS) and radiological management of GV. GV drain into the systemic
vein via the esophageal-paraesophageal varices (gastroesophageal venous system), the
inferior phrenic vein (IPV) (gastrophrenic venous system), or both. These drainage
types generally correspond to the classification system of Sarin et al. GOV1 drains via
esophageal and paraesophageal varices, IGV1 drains via the left IPV, and GOV2
drains via both esophageal varices and the IPV. GV form at the hepatopetal collateral
pathway that develops secondary to localized portal hypertension and drain via the
gastric veins, thereby corresponding with IGV2

Modern imaging by computed tomography scan


The following venous systems are important to understand the venous anatomy of GV
on multi-detector computed tomography (CT) scan
Management
a. Endoscopic treatment modalities for gastric variceal bleeding.
1. Gastric variceal sclerotherapy (GVS).
2. Gastric variceal obturation (GVO) with glue.
3. Gastric variceal band ligation (GVL) with or without detachable
snares.
4. Thrombin injection (bovine or human).
5. Combined endoscopic therapy.
b. Endoscopic ultrasound-guided therapy.
c. Radiologic intervention - transjugular intrahepatic portosystemic shunt (TIPS)
and BRTO.

Gastric variceal sclerotherapy


The endoscopic sclerotherapy has been less effective in the treatment of gastric
variceal bleeding and eradication of GV as against esophageal varices where
endoscopic sclerotherapy is one of the effective modes of treatment. Because of the
high volume of blood flow through GV compared with EV, resulting in rapid flushing
away of the sclerosant in the bloodstream. GVS typically requires larger volumes of
sclerosant than for EV and fundal varices (GOV2 and IGV1) require significantly
more sclerosant than GOV1. This results in more side effects after GVS, such as
fever, retrosternal and abdominal pain, and large ulcerations. Perforations and
mediastinitis are complications that are more serious, and the latter results in mortality
in excess of 50%.
In acute GV bleeding, GVS has been reported to control bleeding in 60-100% of cases
but with unacceptably high rebleeding rates of up to 90%. Mucosal ulcers are also
commonly seen, and cause rebleeding. Approximately, 50% of rebleeding is caused
by sclerotherapy induced ulcers and is difficult to control, with a success rate between
9% and 44%.GVS appears to be least successful in controlling acute fundal variceal
bleeding.
Gastric variceal sclerotherapy is an effective and appropriate treatment for treatment
of acute GOV1 hemorrhage and for attempting secondary prophylactic GOV1
obliteration. It is not appropriate for patients with fundal varices (GOV2 or IGV1)
because of the low rate of primary hemostasis, the low success rate for secondary
variceal eradication, and the high rate of rebleeding and complications.

Combined endoscopic therapy (endoscopic variceal ligation-injection


sclerotherapy)
Endoscopic variceal ligation-injection sclerotherapy (EVLIS) is safe and effective in
achieving hemostasis and obliteration in all patients as shown by Chun and Hyun. The
combination of variceal ligation and cyanoacrylate injection in GV effectively
controlled acute bleed in 89% of patients; however 33% rebleed on follow-up.
Combination with sclerotherapy is unlikely to be accepted for the management of
acute bleeding in view of the increased risk of iatrogenic complications, and the need
for greater technical skill and procedure time. For secondary prophylaxis, combined
therapy should be compared with standard established treatments.
Other methods used for gastric varices treatment

Radiologic intervention
Transjugular intrahepatic portosystemic shunt
When patients with GV bleeding are unresponsive to initial endoscopic treatment, a
second endoscopic therapy should be attempted if possible. If a second attempt fails
or the severity of bleeding precludes further endoscopic therapy, salvage therapy
using surgical shunts or TIPSs should be considered for refractory GV bleeding. Most
current studies of TIPS focus on treatment for refractory GV bleeding and prevention
of GV rebleeding. A recent study showed that the primary hemostasis rate of TIPS for
acute GV bleeding is 92.3%. Other studies showed initial hemostasis of TIPS for
acute refractory GV bleeding is between 87% and 100%, 58-62 with an approximate
rebleeding rate of 10-30%.
Frequent complications of TIPS are encephalopathy and shunt stenosis/occlusion,
with post-TIPS encephalopathy occurring in 4-16% of patients. The shunt dysfunction
could be reduced by using polytetrafluoroethylene (PTFE)-covered stent. Considering
the currently available evidence, TIPS with PTFE-covered stent is the treatment of
choice for patients who failed first-line medical and endoscopic therapy.

Balloon-occluded retrograde transvenous obliteration


Kanagawa et al. first introduced the BRTO procedure in 1996. GVs are associated
with a gastro-renal shunt (GRS) in 60-85%. The GRS drains blood flow into systemic
circulation and provides a pathway for radiologists to treat GV. The outflow of GRS
was blocked by inflating the balloon, and 5% ethanolamine oleateiopamidol was
injected in a retrograde manner

The BRTO was used as either primary or secondary prophylaxis of GV in most series.
Initial hemostasis of BRTO for acute GV bleeding ranges between 76.9% and 100%.
It was noted that the re-bleeding rate was from 0% to 15.4%.BRTO had a similar
initial hemostasis and lower rebleeding rate, compared with GVO or band ligation for
acute GV bleeding. The BRTO had been shown to be as effective as TIPS for acute
GV bleeding, without increasing hepatic encephalopathy. Portal pressure also
increased significantly after BRTO, which caused worsening of esophageal variceal
pressure. Other common complications of BRTO are hemoglobinuria, abdominal
pain, pyrexia, and pleural effusion. Major complications are shock and atrial
fibrillation.

Dapus

Sugimoto N, Watanabe K, Watanabe K, Ogata S, Shimoda R, Sakata H, et al.


Endoscopic hemostasis for bleeding gastric varices treated by combination of variceal
ligation and sclerotherapy with N-butyl-2-cyanoacrylate. J
Gastroenterol. 2007;42:528–32.

Sarin SK, Lahoti D, Saxena SP, Murthy NS, Makwana UK. Prevalence, classification
and natural history of gastric varices: A long-term follow-up study in 568 portal
hypertension patients. Hepatology. 1992;16:1343–9

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