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Gastric Antral Vascular Ectasia (“Watermelon Stomach”) as a Cause of Chronic Gastrointestinal Bleeding (Full title below)

  • Fri, 9/11/09 - 7:58am
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Citation: 

Pages 32 - 35

Author(s): 

Alexander Rabinovich, MD, Yaffa Lerman, MD, and Faina Rozenberg, MD

Gastric Antral Vascular Ectasia (“Watermelon Stomach”) as a Cause of Chronic Gastrointestinal Bleeding in an Elderly Bedridden Patient

Introduction

Gastric antral vascular ectasia (GAVE), or “watermelon stomach,” is a relatively uncommon cause of gastrointestinal (GI) blood loss. The entity is well described in the gastroenterological and endoscopic literature, but it is not as familiar to most readers of geriatric journals. The mean age of affected individuals is around 70 years, with female preponderance. It is widely believed that GAVE is underrecognized and that it is often misdiagnosed as antral gastritis. Tsai et al1 reported an average latency of five years before antral vascular ectasias are identified as the origin of GI blood loss. Therefore, it is important to keep in mind the possibility of GAVE in the differential diagnosis of chronic occult upper GI bleeding in a patient with iron deficiency anemia that is resistant to conventional treatment. We present a case of GAVE in an elderly woman and review the current literature in order to raise the level of awareness of this condition among geriatricians and others caring for older patients.

The Case

Mrs. C is a 73-year old female of Iraqi-Jewish origin. She was diagnosed by her family physician as having chronic iron deficiency anemia in 2004, and was suspected of having hyperplasia with polyposis on gastroscopy in 2006. She has type 2 diabetes mellitus and chronic progressive renal failure. All of her liver tests were normal, and her history was negative for Raynaud’s syndrome or any other autoimmune disorder. Mrs. C was treated with proton pump inhibitors (PPIs) and an iron supplement. Her hemoglobin values were stable between 10 g/dL and 11 g/dL. In 2007, she was hospitalized in the department of Neurology with a right hemispheric cerebral vascular accident and left flaccid hemiplegia. There were no signs of intracranial bleeding on the initial computed tomography (CT) scan, and treatment with aspirin and low-molecular-weight heparin (LMWH) was started. Mrs. C’s admission hemoglobin level was 9.1 g/dL, the iron level was low (25 mcg/dL), and the B12 and folate levels were normal.

On the following day, the hemoglobin decreased to 8.7 g/dL, and Mrs. C received a transfusion of packed red blood cells. She was transferred to the Rehabilitation department 6 days after admission, where she was hospitalized for a total of 110 days. The rehabilitation process was slow and generally unsuccessful. The left hemiplegia did not improve, and general frailty and weakness were prominent throughout hospitalization. Mrs. C remained totally dependent on permanent nursing care. Cognitive evaluation revealed moderate dementia (Mini-Mental State Examination score of 19/30).

The main medical problem throughout the period of hospitalization was persistent upper GI bleeding with recurrent anemia. The LMWH and then aspirin were stopped when rehabilitation was begun because of continuous blood loss. Melena was observed several times, but the blood loss was usually occult. A PPI (omeprazole) was prescribed at maximal dosage (40 mg bid), but the occult bleeding failed to respond to treatment. Mrs. C was transfusion-dependent during her stay at the Rehabilitation department, and she received a total of 18 units of packed red blood cells. Gastroduodenoscopy was performed three times; the main finding was antral erosive gastritis with no evidence of Helicobacter pylori infection.

Mrs. C’s not responding to standard therapy for gastric bleeding raised the suspicion that the origin of bleeding was the small intestine, so she underwent enteroscopy and a video capsule endoscopy; however, the results were noninformative. She then had a repeat gastroduodenoscopy, and this time (2.5 mo after admission to the Rehabilitation department), the gastroenterologist observed that the antral lesions were compatible with GAVE (Figure 1).

References: 

1. Tsai HH, Smith J, Danesh BJ. Successful control of bleeding from gastric antral vascular ectasia (watermelon stomach) by laser photocoagulation. Gut 1991;32:93-94.

2. Selinger CP, Ang YS. Gastric antral vascular ectasia (GAVE): An update on clinical presentation, pathophysiology and treatment. Digestion 2008;77:131-137. Published Online: April 4, 2008.

3. Chaves DM, Sakai P, Oliveira CV, et al. Watermelon stomach: Clinical aspects and treatment with argon plasma coagulation. Arq Gastroenterol 2006;43(3):191-195.

4. Rider JA, Klotz AP, Kirsner JB. Gastritis with veno capillary ectasia as a source of massive gastric haemorrhage. Gastroenterology 1953;24:118-123.

5. Jabbari M, Cherry R, Lough JO, et al. Gastric antral vascular ectasia: the watermelon stomach. Gastroenterology 1984;87:1165-1170.

6. Al-Haddad M, Ward EM, DeVault KR, et al. Vascular ectasia of the proximal stomach. Dig Dis Sci 2007;52:1367-1369. Published Online: March 20, 2007.

7. Suit P, Petras RE, Bauer TW, Petrini JL Jr. Gastric antral vascular ectasia. A histologic and morphometric study of ‘the watermelon stomach.’ Am J Surg Pathol 1987;11:750-757.

8. Gostout CJ, Viggiano TR, Ahlquist DA, et al. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol 1992;15(3):256-263.

9. Ward EM, Raimondo M, Rosser BG, et al. Prevalence and natural history of gastric antral vascular ectasia (GAVE) in patients undergoing orthoptic liver transplantation. J Clin Gastroenterol 2004;38:898-900.

10. Spahr L, Villeneuve JP, Dufresne MP, et al. Gastric antral vascular ectasia in cirrhotic patients: Absence of relation with portal hypertension. Gut 1999;44(5):739-742.

11. Sebastian S, O’Morain CA, Buckley MJM. Review article: Current therapeutic options for gastric antral vascular ectasia. Aliment Pharmacol Ther 2003;18:157-165.

12. Shibukawa G, Irisawa A, Sakamoto N, et al. Gastric antral vascular ectasia (GAVE) associated with systemic sclerosis: Relapse after endoscopic treatment by argon plasma coagulation. Intern Med 2007;46(6):279-283. Published Online: March 15, 2007.

13. Izquierdo S, Rey E, Gutiérrez Del Olmo A, et al. Polyp as a complication of argon plasma coagulation in watermelon stomach. Endoscopy 2005;37:921.

14. Probst A, Scheubel R, Wienbeck M. Treatment of watermelon stomach (GAVE syndrome) by means of endoscopic argon plasma coagulation (APC): Long-term outcome. Z Gastroenterol 2001;39:447-452.

15. Yusoff I, Brennan F, Ormonde D, Laurence B. Argon plasma coagulation for treatment of watermelon stomach. Endoscopy 2002;34(4):407-410.

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