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Re: TIPS for gastric varices

Dear Editor

We recently read with interest the study by Tripathi and colleagues[1] investigating the outcome of TIPS in patients with gastric (GV) compared to oesophageal varices (OV). This study confirmed the previous finding of lower mean portosystemic pressure gradient (PPG) in patients with GV bleeding relative to those with a history of OV bleeding.[2] Indeed in this study 35% (14/40) of GV patients compared to only 8% (20/2320 of OV patients had a PPG < 12 mm Hg1.

The group of patients who bleed at PPG < 12 mm Hg (group 1) is particularly intriguing. As mentioned by the authors, low PPG in GV patients has been shown to correlate with the presence and size of a spontaneous gastrorenal shunt (GRS) which is present in up to 85% of GV patients but present in only about 20% of OV patients.[3] Previously, Sanyal et al. found that 50% (6/12) of patients who underwent TIPS for prevention of GV re-bleeding failed to de-compress the varices as documented by endoscopy. 4/6 of these patients had a large GRS and a PPG < 12 mm Hg. Thus based on probability, the group 1 patients in the current study (both GV and OV) are likely to have had a spontaneous GRS already de-compressing the portal system. It would be valuable to know if the authors have any data on the presence of GRS in their patient population, perhaps documented by portogram taken at the time of TIPS? Also, did they document decompression of varices post-TIPS as an indicator of the clinical efficacy of the procedure? For example, it would be interesting to know if patients in group 1 failed to decompress varices post-TIPS more often than patients in group 2. Anecdotally, we have experience of a number of patients with large GV who had a baseline PPG of < 12 mm Hg and a large GRS. Following TIPS in these patients, there was a minimal or no reduction in PPG and filling of the GV was not shown to be reduced on post-TIPS portogram.

Finally the authors noted in group 2 (baseline PPG > 12 mm Hg) that lower post-TIPS PPG was associated with a lower risk of bleeding, as would be hoped. However in group 1, there was no difference in post-TIPS PPG between patients who did and did not re-bleed, suggesting that PPG may not be a critical determinant of variceal bleeding in patients who have a low PPG to start with. The role of PPG in dictating the natural history of GV is not known. Conceptually, insertion of an artificial portosystemic shunt into a patient who already has a large spontaneous shunt effectively offloading the portal pressure would not seem to confer much benefit. Do these GV (and possibly OV) patients with low PPG pre-TIPS and with a possible GRS really benefit from TIPS?

MR angiography can accurately assess for presence of a spontaneous GRS.[4] There is a compelling argument that this should be an essential part of the assessment algorithm of patients with GV. If a large spontaneous shunt is present, and PPG (as measured by hepatic vein wedge pressure gradient (HVPG)) is < 12 mm Hg, then perhaps other therapeutic options such as B-RTO (balloon occluded-retrograde transvenous obliteration) should be considered.

Hopefully more prospective data, examining the role of PPG, TIPS and B-RTO in the management and outcome of GV will help clarify these issues.

References

(1) Tripathi D, Therapondos G, Jackson E, Redhead DN, Hayes PC. The role of the transjugular intrahepatic portosystemic stent shunt (TIPSS) in the management of bleeding gastric varices: clinical and haemodynamic correlations. Gut 2002;51(2):270-4.

(2) D'Amico G, Pagliaro L, Bosch J. The treatment of portal hypertension: a meta-analytic review. Hepatology 1995;22:332-54.

(3) Watanabe K, Kimura K, Matsutani S, Ohto M, Okuda K. Portal hemodynamics in patients with gastric varices. A study in 230 patients with esophageal and/or gastric varices using portal vein catheterization. Gastroenterology 1988;95(2):434-40.

(4) Ono N, Toyonaga A, Nishimura H, Hayabuchi N, Tanikawa K. Evaluation of magnetic resonance angiography on portosystemic collaterals in cirrhotic patients. Am J Gastroenterol 1997;92(9):1515-9.