- This document describes the case of a 62-year-old male (Mr. JR) presenting for follow up of chronic liver disease and a recent episode of hematemesis. - His past medical history included esophageal variceal bleeding managed with band ligation four years prior. Current evaluation showed features of cirrhosis on ultrasound and severe diffuse gastric antral varices (GAVE) on endoscopy. - He was managed conservatively with blood transfusion, medications, and three sessions of endoscopic band ligation of the GAVE over three weeks. No further bleeding episodes occurred on eight months of follow up.

1. 12-02-2013
↓GE2 Services

2.  Mr. JR
 62/M
 R/O Jammu
 GUT clinic follow up

3.  Haematemesis – 1 day

4.  Haematemesis – 1 day
 3 bouts
 300ml of altered blood per bout
 Associated with melena
 No postural symptoms
 No H/o jaundice, abdominal distension, altered
sensorium

5.  Past History
 H/O Haematemesis – 4 yrs back
 Evaluated in PGI, found to have esophageal varices
 USG showed features of CLD with ascites
 Etiologic work up was negative
 EVL was done and varices were eradicated and he
was on GUT clinic follow up for 4 yrs
 Ascites improved with diuretics and he was off
diuretics for last 2 yrs
 Beta blocker prophylaxis for varices

6.  Type 2 DM – 10 yrs
 Sugars controlled with OHA
 Personal History
 No addictions
 Family History
 No H/o similar illness in the family

7.  Conscious , oriented
 Vitals
 Blood pressure – 130/80 mm Hg
 Pulse rate – 100/ min , regular
 Respiratory rate – 14/min
 Pallor present, no icterus, no cyanosis, no clubbing, no
pedal edema

8.  Abdomen
 Soft, non tender
 Spleen palpable 4 cm below left costal margin
 No free fluid
 Other systems – normal

9. Hb 4.6 gm % Bilirubin o.8 mg%
TC 6700 SGOT 23
Platelet count 95,000 SGPT 18
PTI 74% ALP 89
aPTT 28” Prot 5.0
Urea 40
Alb 2.6
Creatinine 0.8
USG Abdomen
Liver -12 cm, coarsened echotexture, irregular outline,
PV – 12 mm
No ascites

10.  HBS Ag / anti-HCV – neg
 Autoimmune markers – neg
 Hemochromatosis w/u – neg
 IgA Anti tTG – normal

11.  UGIE
 Esophagus: Eradicated varices
 Stomach
 Fundus , body – normal
 Antrum – severe diffuse GAVE present
 D1, D2 - normal

14. • This 45 years male with history of chronic Liver disease (NAFLD
related) for the last 4 yrs, with past H/O EVL for variceal
bleed, now presented with history of hemetemesis and melena
• Managed with blood transfusion , terlipressin, PPI
• UGIE showed no varices , however severe diffuse GAVE was
present
• 3 sessions of Endoscopic band ligation were done every 3 weekly
• No further episodes of UGI bleed
• No further requirement of transfusions on follow up for last 8
months

15.  Type 2 Diabetes Mellitus
 Chronic liver disease (? NAFLD related )
 Upper Gastrointestinal Bleed
 Diffuse GAVE related
 Managed with Endoscopic Band ligation

16.  Mrs. AK
 54/F
 R/o Chandigarh
 GUT clinic follow up

17.  Haematemesis – 1 day

18.  Haematemesis – 1 day
 5 bouts of ~ 200 ml each
 Associated with melena
 Associated with postural symptoms
 No H/o abdominal distension, altered
sensorium, jaundice

19.  Past History
 Diabetes mellitus – 5 yrs
 No history of any complications
 Personal History
 No addictions
 Family History
 No H/o similar illness in the family

20.  Conscious , oriented
 Vitals
 Blood pressure – 96/60 mm Hg
 Pulse rate – 120/ min , regular
 Respiratory rate – 18/min
 Pallor present, no icterus, no cyanosis, no clubbing, no
pedal edema

21.  Abdomen
 Soft, non tender
 No palpable organomegaly
 No free fluid
 Other systems – normal

22.  Hb- 4.5
 USG abdomen −Liver-12.5 cm,coarsened
echotexture,no ascites
 UGIE −Esophagus-no varices
Stomach- full of blood,could not be evaluated
completely
Referred to PGI

23. Hb 5.3gm % Bilirubin o.8 mg%
TC 8000
Platelet count 1,00,000 SGOT 65
SGPT 83
PTI 77% ALP 89
aPTT 28” Chol 152
Urea 39 TGL 122
Creatinine 0.8 LDL 66
HDL 52

24.  HBS Ag / anti-HCV – neg
 Autoimmune markers – neg
 Hemochromatosis w/u – neg
 IgA Anti tTG – normal

25.  USG Abdomen
 Liver -11.5 cm, mildly coarsened echotexture, mildly
irregular margins
 PV – 12mm, Hepatic veins - normal
 GB/ pancreas – normal
 No ascites
 UGIE
 Esophagus: no varices
 Stomach
 Fundus – no varices
 Body – normal
 Antrum – severe diffuse GAVE with ooze
 D1, D2 - normal

28. • This 54 yr female patient presented with haematemesis with significant
postural symptoms
• On evaluation, her USG showed features of CLD and UGIE showed
severe diffuse GAVE
• Her etiologic work up for CLD was negative and the possibility of NAFLD
related cirrhosis was kept
• She was managed with UGIE and 4 sessions of Argon plasma
coagulation for GAVE
• Vit E supplements, Beta Blocker, OHA were given at discharge
• Follow up : Weight reduction, good glycemic control, LFT has normalized
• No further episodes of UGI bleed

29.  Type 2 Diabetes Mellitus
 Chronic Liver Disease ( ? NAFLD related)
 UGI bleed
 Diffuse GAVE related
 Managed with APC

30.  Introduction
 Associations
 Diagnosis
 Treatment
 Newer Endoscopic treatment modalities

31.  Rider et al, described the first case of GAVE in
1953, noting – “an erosive type of atrophic gastritis with
marked veno-capillary ectasia” in a gastrectomy
specimen of an elderly woman with occult GI bleed
 In 1984, Jabbari et al,described the characteristic
endoscopic findings of GAVE and coined the term -
Watermelon Stomach Rider JA et al, Gastroenterology,1953
Jabbari et al, Gastroenterology,1984

32.  Approximately 30% of patients with GAVE syndrome
will have cirrhosis
 1 in 40 patients with endstage liver disease have
GAVE
 In Noncirrhotic patients, autoimmune disorders are
most common (particularly scleroderma or CREST )
with an incidence upto 62%
Ward EM et al, Clin Gastroenterol, 2004

33. Novitsky et al, J GI surgery,2003

34.  Quintero et al.first conceptualized a theory of
mechanical stress, peristaltic waves of loosely attached
antral mucosa draw the mucosa in longitudinal folds
and induce fibromuscular proliferation and secondary
formation of ectatic vessels
Quintero E et al.Gastroenterology 1987

35.  mechanical stress
 humoral factors
 autoimmune factors
 hemodynamic alterations
 portal hypertension does not play a role in the GAVE
development

36.  The histological pattern, although not pathognomonic is
characterized by four alterations:
 vascular ectasia of mucosal capillaries
 focal thrombosis
 spindle cell proliferation (= smooth muscle cell and
myofibroblast hyperplasia)
 fibrohyalinosis
Suit PF et al Am J Surg Pathol 1987
Gilliam JH et al. Dig Dis Sci 1989

37.  Iron deficiency anemia – requiring blood transfusions
(88%)
 Heme positive stool (42%)
 Haematemesis , melena
 Haematochezia
Gretz et al, Am J Gastroenterology,1998

38. 1. Classic raised convoluted ridges covered
by ectatic vascular tissue radiating out
from the pylorus
2. Lesions arranged in radiating flat stripes
3. Diffuse scattered multiple mucosal
lesions
4. A mixture of the above patterns
5. Coalesced angiodysplastic giant red
lesions, labeled as “honeycomb
Gostout et al, JCG, 1992
stomach” Chawla SK, Presti et al, GIE 1990

39.  Endoscopic ultrasound(EUS ), the gastric antrum
appears hypertrophic with a spongy appearance of the
mucosa and submucosa and a well-preserved
muscularis propria
Shudo R et al. Gastrointest Endosc 2001

40. GAVE PHG
Predominant location Antrum Body and Fundus
Classic Endoscopic Linear red stripes Mosaic like pattern or red marks
appearance separated by normal
mucosa
Histology Marked dilatation of Mild to moderate dilatation of
capillaries and venules veins and capillaries
with areas of intimal no change in vessel wall
thickening and thrombi
Portal hypertension May or may not be Always present
present
Associations Cirrhosis ,connective Only with portal hypertension
tissue disorders,CKD
Endoscopic therapy Yes No
CD61(platelet marker) Yes No

41.  Medical and Supportive therapy
 Endoscopic therapy
 Surgical therapy

42. Medical therapy
o Hormonal therapy - estrogen-progesterone
o Tranexemic acid
o Octreotide
o methylprednisolone
o Cyclophosfamide
Supportive theapy – Hematinics and blood
transfusion

43. Contact devices
 Sclerotherapy
 Bipolar electrocautery
 Heater probe
 Cryotherapy
Non contact devices
 Laser photocoagulation
 Argon plasma coagulation
Band ligation

44.  The basic principle of all endoscopic treatments is safe
and effective hemostasis of mucosal and submucosal
ectasia
 The goal is to reduce or possibly eliminate the need for
blood transfusions
 Often several treatment sessions are required
Jensen D et al.Endoscopy, 2004

45. Endoscopic Laser Therapy
 Reduces/abolishes the need of blood transfusions in
about 50% to 80% of cases with a mean of 3
treatment sessions
 Complications
 gastric ulceration -gastric perforation
 Pyloric stenosis -hyperplastic polyps
 Multifocal Gastric cancer
Lasers Med Sci 2004; 18:213-218
Gastrointest Endosc 1994; 40: 584-587
Gastrointest Endosc 1996; 43: 54-56

46.  Argon plasma coagulation (APC) is a noncontact
technique with a controllable depth of coagulation (0.5-
3 mm)
 APC has been the most widely studied endoscopic
treatment and is the most frequently used for GAVE-
related bleeding.
 In comparison to Nd: YAG laser therapy, APC is easier
to use, more manageable, cheaper and, most
importantly, safer

47.  Different case series of APC treatment reported an
efficacy ranging from 90% to 100% with no further
need for blood transfusions and an increase of
hemoglobin level from 2.3 g/dL to 5.5 g/Dl
Wahab PJ et al, Endoscopy 1997
Roman S et al.Endoscopy, 2003
Yusoff I et al.Endoscopy ,2002

48.  Newer modality in the treatment of GAVE
 Standard band ligator as used in variceal banding
 Ligation bands are applied to the abnormal mucosa
working proximally, starting from the distal antrum

49. GIE,2006
 53/ M, presented with anemia and 1 episode of
haematemesis
 UGIE showed GAVE
 BMFT & Colonoscopy were normal
 Estrogen- progesterone had to be withdrawn due to
adverse reaction
 2 sessions of endoscopic band ligation

53.  Antrectomy – most common surgery
 Others – Partial / total gastrectomy
Novitsky et al, Journal of GI surgery,2003

54.  Over the last 6 years, 7 patients with GAVE related UGI
bleed have been treated
( 2 – CKD, 4 – CLD, 1 – SLE )
 3 patients were managed with APC (no. of sessions : 2
– 5)
 4 patients were managed with EBL (no. of sessions : 2
– 4)
 No recurrence of bleed in the follow up

55.  GAVE should be considered as a cause of UGIB in
chronic liver disease, auto immune disorders and CKD
 Endoscopic modalities are the mainstay of treatment

56. THANK YOU