One of the major sequelae in cirrhosis of the liver is esophageal variceal bleeding due to portal hypertension. The effective therapeutic modalities, those used with endoscopy for treating and eradicating acutely bleeding esophageal varices, are endoscopic injection sclerotherapy (EIS) and endoscopic variceal ligation (EVL)¹⁾. But, EIS is not a benign process and has many complications^2–7), and one of those is the change in esophageal motor function^8–11).

A recently developed method that uses small rubber bands for treating variceal bleeding, EVL, is similar to the technique of EIS, and the technique is easy and simple, has a lower complication rate, and the results with EVL are as effective as EIS for controlling esophageal variceal bleeding, so it is recommended as a new desirable therapeutic modality^12–17). But there are few reports about lower esophageal complications.

The method of EVL sucks the protruded superficial esophageal varix, then the varices are mechanically ligated and Strangulated, and the histological changes are limited to esophageal mucosa and submucosa. So, there are no disturbances in esophageal motility^18,19). Since there are few prospective studies done on it²⁰⁾, we designed this study to investigate the effect of EVL on lower esophageal motor function.

The overview of 27 patients who underwent EVL is summarized in Table 1. As scheduled, all 27 patients underwent 1–3 sessions of EVL and second esophageal motility evaluation done postoperatively at 21 days. There had been 21 patients at first, 2 of them died with hepatic failure, 4 of them refused EVL and 1 of them died with infection.

With only 14 patients, a third evaluation was done at 6 months after the last EVL. When follow-up endoscopy was done at one week after the last EVL session, the grade of varix was considered as 2; completely eradicated, 23: grade 1, 2: grade II. At 6 months after the last EVL session, the grade of varix were considered as 6: grade 0 to I, 7;grade II, 1; grade III. The procedures were tolerated well, and no serious side effects occurred. In the first EVL session, 21 patients complained of mild chest discomfort and dysphagia during or after the procedure. The complications such as epigastralgia (2), nausea (1) and bradycardia (1) developed, but they spontaneously subsided within 3 days. At the end of 3 weeks and 6 months, there were no complaints of dysphagia and no stricture developed.

EVL is an effective alternative method for controlling variceal bleeding with minimal complications, compared to EIS. Also there are few studies on EVL effects on esophageal motility^2,18). This study was designed to compare the effects of EVL on the lower esophageal motility in patients who had undergone variceal ligation.

Our manometric results after EVL in cirrhotic patients with esophageal varices show that, when compared with pre-EVL in the same patients, the effects of EVL in lowere sophageal motility can be divided into intermediate effects and late effects. The former effects are characterized by 1) the amplitude of the peristaltic wave that is significantly increased in the lower esophagus and 2) longer contraction duration of peristaltic wave in lower esophageal body. The latter effects are characterized by 1) longer LES relaxation duration and 2) speedier peristaltic wave progression. Discordant results have been published regarding esophageal motility of EVL effect¹⁹⁾. Although we could not exclude these differences, they are due to differences in observation period and methods (3 weeks, 6 months vs mean 8, 9 weeks), subjects (same patients vs different subjects), any possible site of EVL (chiefly LES portion vs no mention) and number of ligators which was used. The intermediate effects of post-EVL in lower esophageal peristaltic amplitude of our results could be supported by other authors^19,22) and possible explanations of these finding were proposed by Passaretti et al. They hypothesized that the presence of a ‘cushion’ of blood within the varices might have a damping effect on pressure wave, leading to a decrease in the amplitude and to an apparent increase in duration of contraction. This hypothesis can be supported by our results that lower esophageal peristaltic amplitude increased at intermediate post-EVL as the size of varix diminishes, and then the pressure decreased after late post-EVL as the size of varix diminishes, and then the pressure decreased after late post-EVL when the size of it enlarged²²⁾. But there is a discrepancy that does not support the hypothesis about the peristaltic duration in the lower esophageal body. Both peristaltic pressure and duration were similar to the level of those of pre-EVL and late post-EVL.

Also it is known that there is a continuing inflammatory response in the submucosa with maturing scar tissue at 3 weeks, and complete healing process in 50–60 days after EVL¹⁸⁾. The prolongation of the duration of peristalsis of intermediate post-EVL might be related to some inflammatory reaction in the submucosa as an acute effect of EIS⁹⁾.

In the long-term effect of post-EVL, even though there were no demonstrable changes in the percentage of LES relaxation after deglutitiion, there is no relationship between prolongation of LES relaxation time in our results in those when the site of variceal ligation was done chiefly within 3 cm from the gastroesophageal junction, healing process of submucosal fibrosis which appear in 50–60 days after EVL and the esophageal stricture after EVL in lower esophagus. There was some technical faults, even though there were no reliable clinical complications over 6 months. At present, it remains unclear why the duration of it was so prolonged.

Also, the late effects of post-EVL could not explain the increase of peristaltic velocity in the lower esophagus, which still remains unclear now. But a possible suggestion is that the speed of peristalsis is faster in cirrhotic patients with esophageal varix than without any varix and after EIS^9,22,23).

Following EIS, there have been reports of variable ranges of esophageal motor abnormalities^{8–11,23–26)}. These variabilities may explain the various factors for the study. Nevertheless, there is general agreement that one of the variabilities is in different schedules of motility study after EIS^9,11). Like this there is some difference in EVL effects with others, and our results might be related to different schedules, methods and subjects of study.

Even the intermediate EVL-induced motility changes continue over 3 weeks, at least, after the last EVL session. It appeats to be reversible and tends to return to basal motility. We speculate that this dysmotility is caused by submucosal inflammatory changes, injured nerve plexuses and possible muscular fibers due to EVL of those chiefly done in LES region. But the late EVL-induced dysmotility might start before 6 months after the last EVL session, and be permanent. We speculate that this dysmotility is caused by submucosal fibrosis, disturbed nerve plexus and possible fibrosis of muscle due to EVL.