Br. J. Surg. Vol. 70 (1983) 406-407 Printed in Great Britain

Gastric ulceration after Nissen f undoplication

Thirteen patients developed gastric ulcers between 6 months and 8.5 years after Nissen fundoplication. Eight patients presented with epigastric pain alone, 3 with bleeding alone and 2 with both pain and bleeding. Nine ulcers (69 per cent) were high on the lesser curve, close to the fundoplication and 7 of these patients had recurrent hernias. Anatomical distortion produced by fundoplication is probably the most important aetiological factor, though gastric distension, bile reflux gastritis and ischaemia may be contributory.

R. CAMPBELL*, T. KENNEDY AND G. W. JOHNSTON

Belfast BT126BJ. Correspondence to: T . Kennedy.

Royal Victoria Hospital. Grosvenor Road,

The operation of fundoplication, introduced by Nissen in 1956 (l), is probably the procedure most commonly used in the United Kingdom for oesophageal reflux. Gastric ulceration in unoperated hiatus hernia has been recognized for many years (2, 3), but only recently has this complication been described after fundoplication (4-9). Bushkin (4) reported 5 gastric ulcers in 160 fundoplications, and Scobie (9) observed that in all 3 of his cases the ulcer was high on the lesser curve. High lesser curve gastric ulcer has also been reported after intrathoracic fundoplication (10, 11). This gastric ulceration has been variously attributed to alkaline reflux gastritis, gastric stasis and distension, hypergastrinaemia and vagal damage, but there is no entirely adequate explanation.

Patients and methods Thirteen patients who had Nissen fundoplication between 1968 and 1978 later developed gastric ulcers. Various units both in the Royal Victoria Hospital and elsewhere were the source of these patients, so that the total number of fundoplications performed in this period is unknown. Ulcers occurred in 4.7 per cent of our series of 170 fundoplications. Any patient with pre-existing gastric ulcer has been excluded from this study. Two patients in the series also had duodenal ulcer, and one had gallstones. Fundoplication was performed through the chest in 5 cases and via the abdomen in 8. In addition 3 of the patients had proximal gastric vagotomy, truncal vagotomy and gastro- jejunostomy and cholecystectomy respectively. The average age at operation was 55 yr (range 33-72 yr).

After mobilization of the oesophagus a 360 fundoplication was made about 4cm in length and usually loose. One or two short gastric vessels were sometimes divided. With large hiatal defects the crura were approximated with a few linen stitches, after reduction of the hernia. The completed fundoplication was always intra-abdominal.

Five patients had post-cibal gaseous distension and inability to belch after operation, fulfilling the criteria of the 'gas-bloat' syndrome (12).

Results Gastric ulcer was suspected from the patients' symptoms, and confirmed by barium meal, endoscopy or operation. The average interval between fundoplication and the appearance of ulcer symptoms was 4.5 yr (range 6 mth-8.5 yr).

Presenting complaint Epigastric pain was the major symptom in 10 patients; 2 of these later bled from their ulcer. Bleeding was the only symptom of ulceration in 3 cases. Three patients had taken aspirin or other anti-inflammatory drugs, but only 1 of these had bleeding.

Investigations Twelve patients had barium meals, but in only 4 was gastric ulcer correctly diagnosed. Seven cases had a fixed recurrent hiatus hernia. Endoscopy correctly diagnosed gastric ulcer in 11 cases; in 1 further patient the diagnosis was missed because the stomach was full of blood and clot. In 2 patients the diagnosis was only established at emergency operation for bleeding. In 3 patients serum gastrin levels were normal.

Site of ulcer Nine ulcers (69 per cent) were situated high on the lesser curve, close to the fundoplication (Fig. 1). Seven of these were associated with recurrence of hiatus hernia.

Fig. 1. Location of 13 post-Nissen fundoplication gastric ulcers

Medical treatment Eight patients were treated with either carbenoxolone or cimetidine. All the ulcers healed, but 4 later recurred and 3 responded to further medical treatment.

Surgical treatment Billroth I gastrectomy was performed in 4 cases, without taking down the fundoplication, but in 1 case ulceration recurred high on the new lesser curve, 4 years later, and a more extensive gastrectomy is now contemplated. In 1 patient emergency vagotomy and pyloroplasty was used for bleeding-the ulcer was biopsied and undersewn. Emergency operation for bleeding was necessary in 1 further patient who relapsed after medical treatment. The ulcer lay very high on the lesser curve, and was biopsied and undersewn. She was too frail for a definitive procedure and died soon after operation.

Pathology All ulcers were examined histologically, either from endoscopic biopsies or the resected specimens and all were benign. Histological gastritis was present in 8 patients.

Discussion In this series of post-fundoplication gastric ulcers nearly 70 per cent were high on the lesser curve, close to the wrap. In previous reports most ulcers were at or distal to the angulus (4-8). These low ulcers could be unrelated, but high ulcers do seem to be a specific complication of fundoplication.

In the Nissen fundoplication a complete 360 ' wrap of fundus around the oesophagus is performed (1). The Belsey Mark IV operation is a partial or 240-270 O wrap (13), and in the Hill gastropexy there is effectively a 180 O wrap (14). We have little experience of these last two procedures, and gastric ulcer after

* Present address: R. Campbell. Kantonsspital Basel. Basel 4031, Switzerland.

Gastric ulceration

them has not been reported in the literature. This suggests that a complete wrap is an important feature.

Gastritis, probably induced by bile reflux, is important in the development of gastric ulcer. Bremner (6,s) reported that alkaline reflux was present in all 6 of his cases, and felt that gastric ulcer resulted from bile reflux. Whether the reflux was present before fundoplication, or followed operation was unknown.

Bushkin (4) suggested that gastric distension, as evidenced by the ‘gas-bloat’ syndrome, could stimulate gastrin release from the antrum. This hypergastrinaemia has not been found in our patients or by others (5 , s ) . ‘Gas-bloat’ was present in 4 of Bushkin’s 5 cases of post-Nissen gastric ulcer, but in only 20 per cent of his total series of fundoplications. ‘Gas-bloat’ syndrome was present in 5 of our cases, and may be a manifestation of a wrap which has been constructed too tightly. Recent experimental work has shown that only a ‘floppy’ fundoplication allows the normal reflux activity of eructation and vomiting (15).

Fundoplication undoubtedly produces anatomical distortion in the upper stomach and Scobie (9) suggested that there was an important mechanical factor related to angulation a t the upper lesser curve. The ‘riding’ gastric ulcer seen in unoperated hiatus hernia has been attributed to trauma from the right crus of the diaphragm (2) . Seven of our 9 cases of high gastric ulcer had a recurrent hiatus hernia. Four high ulcers recurred after treatment-all had a recurrent hernia, suggesting a continuing process. Occasionally, when the fundoplication must be left in the chest, perforation and gastric ulceration can occur (10, 11).

Oi (16) described oblique muscular bands in anterior and posterior positions on the lesser curve, and others a t right angles to these at the angulus. He further showed that gastric ulcers develop distal to epithelial junctions (1 7). These epithelial junctions must lie in relation to the muscular bands for ulceration to occur.

Not all the arteries supplying the mucosa of the lesser curve anastomose freely. Piasecki (1 8, 19) has described mucosal-end arteries of extramural origin which pierce the gastric musculature and each supplies a limited area of mucosa. Relatively few of these vessels are found in the upper lesser curve. but their division or compression could be expected to produce a degree of mucosal ischaemia and ulceration. Ligation of one or two short gastric vessels is sometimes needed during mobilization of the fundus, which could be another factor causing ischaemia.

We have seen three cases of acute lesser curve necrosis after proximal gastric vagotomy and all occurred in patients having concomitant fundoplication; they were probably due to a combination of ischaemia and gastric distension (20).

Perhaps a combination of factors is responsible for the development of gastric ulcer after fundoplication, but anatomical distortion is probably the most important single cause.

407

Acknowledgements We wish to thank our many colleagues for permission to study their cases.

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57: 250-93.

118: 295-335.

Paper accepted 7 January 1983