85 CARBOHYDRATE MEALS INCREASE PORTAL VENOUS PRESSURE IN CIRRHOTICS WHO HAVE BLED FROM OESOPHAGEAL VARICES P.A. McCormick~ M. Graffeo, M. Morreale~ D. Wa~staff*, A. Madden*, R. Dick*~ N. Mclntyre, A.K. Burroughs Academic Department of Medicine and *Department of Radiology, Royal Free Hospital, London, U.K.

Protein but not carbohydrate or fat feeding is associated with a marked increase in hepatic blood flow in normal subjects (Am J Dig Dis 1965; I0: 239). We have shown that a high protein meal significantly increases hepatic venous pressure gradient (HVPG), in cirrhotics with varices (J Hepatol 1986; 3 (suppl i): $53). We examined the effects of a protein free meal containing 19 g carbohydrate, 5 g fat and 120 Kcal per i00 ml on wedged and free hepatic venous pressures in 16 cirrhotics (15 male: median age 49 range 20-56: alcoholic n=lO, cryptogenic n=5, autoimmune n=l) who had bled from oesophageal varices. 8 patients received a 600 Kcal (500 ml) and 8 a 300 Kcal (250 ml) meal. Pressures were measured before the meal and at subsequent intervals of 10 minutes for one hour. Free hepatic venous pressure did not change. HVPG increased in all patients after 600 Kcal rising 29% from 15.6+SD 5.1 mmHg to 20.2+SD 6.2 mmHg at 30 minutes (p<O.Ol) by 22% to 19.1+SD 6.0 mmHg at 60 minutes (p<O.Ol).- Following 300 Kcal HVPG increased in 7/8 patients? mean HVPG increased from 18.5+SD 7.7 mmHg by 15% to 21.2+7.1 mmHg at 3 minutes (ns) and by 6% to 19.6~8.2 mmHg at 60 minutes (ns). These results suggest that despite the findings in normal subjects non-protein meals significantly elevate portal venous pressure in cirrhotics with varices and that there is a dose effect. These physiological increases in portal pressure

may be of importance in .the management of the acute variceal bleedin~ episode and also in relation to long term administration of portal hypotensive drums which may not anta~onise the effects of feeding on portal pressure.

86 THE EFFECT OF CONTINUED ALCOHOL CONSUMPTION ON BLEEDING AND MORTALITY AFTER VARICEAL HAEMORRHAGE P.A. McCormick, T. Yin, D. Sprengers, N. Mclntyre, A.K. Burroughs Academic Dept of Medicine, Royal Free Hospital Medical School, London, NW3, UK.

It is a commonly held view that abstinence from alcohol reduces the incidence of variceal rebleeding. However this has not been properly documented. Moreover two large studies(l-3) suggests that abstinence after bleeding does not improve survival and one shows that rebleed- ing is not affected(3). We reviewed the alcohol history and clinical course of 176 consec- utive alcoholic cirrhotics subsequent to their initial admission to the Royal Free Hospital with documented variceal haemorrhage. Exclusions: died within 30 days of admission (n=66), abstinent prior to bleed (n=6), no follow up (n=4), concomitant alpha 1 anti-trypsin deficiency (n=4), hepatocellular carcinoma (n=2).

94 patients were followed up: median 20 months (range 2-97). Drinking was confirmed by history, corroboration from relatives and blood alcohol levels. 30 remained abstinent and 64 continued to drink. Pugh's grading at initial presentation and length of follow up were similar in both groups. Mortality was 12/30 (40%) in the abstinent and 24/64 (38%) in the drinkers. Upper gastrointestinal rebleeding (excluding peptic ulcers) occurred in 53% (16/ 30) of the abstinent versus 75% of the drinkers (48/64). There was no significant difference in the rebleeding or mortality rates between the 2 groups (logrank test) or in the number of rebleeds per patient. However there was a strong trend towards a reduction in the incidence of rebleeding after 8 months of abstinence. These results support those of previous studies. Although abstinence probably has a beneficial effect this does not occur early enough to alter the prognosis in alcoholics who have already bled from oesophageal varices.

i. Gastro 1978; 74: 64. 2. Lancet 1973; 2: 65. 3. Am J Med 1968; 44: 406.

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