Parietal Cell Vagotomy and Dilatation for Peptic Duodenal Stricture
ALI $. MENTE$, M.D.
Gastric outlet obstruction due to peptic duodenal stricture (pyloric stenosis) was treated with parietal cell vagotomy and dilatation of the stricture in 32 patients. Follow-up is in the range of 5 years in 37.4% of the patients, while 6 to 10 years follow-up is available in 62.4% of the patients. At their last follow-up, 74.9% of the patients were in either Visick 1 or 2 clinical status. Recurrence rates have been 3.1% at 1 year, 9.3% at 5 years, and 21.8% after 6 to 10 years follow-up. There has been only one instance (3.1%) of restenosis. Two patients required reoperation because of recurrence and one of them died.
T n HE FREQUENCY OF peptic duodenal ulcer surgery declined after the introduction of H2 receptor blockers. However gastric outlet obstruction continues to be a principal indication for surgery.' An ideal operation for obstructing peptic duodenal stricture must relieve the obstruction, control the primary ulcer diathesis, and be free of late complications2; also it must have a negligible mortality rate and an acceptable rate of postoperative morbidity. Johnston et al.3 have advocated parietal cell vagotomy and dilatation for the surgical treatment of peptic duodenal stricture. We began performing this procedure in 1979 in unselected patients. Here we report our late results with parietal cell vagotomy and dilatation for peptic duodenal stricture.
Materials and Methods Parietal cell vagotomy and dilatation was performed in 32 patients with gastric outlet obstruction due to peptic duodenal stricture. Their ages were within the range of 17 to 70 years (mean, 41 years). Twenty eight patients (87.5%) were male and four (12.5%) were female. They had medical histories of duodenal ulcer between 4 and 40 years of age (mean, 12.8 years). All patients had a full Address reprint requests to Dr. Ali Mentes, Department of Surgery, Agean University Hospital, 35100, Bornova, Izmir, Turkey. Accepted for publication December 4, 1989. Accepted for publication December 4, 1989.
From the Department of Surgery, Agean University Faculty of
Medicine, Izmir, Turkey
diagnosis of 'pyloric stenosis' at the time of admission. Barium studies of the upper gastrointestinal tract revealed atonic and dilated stomachs in every patient. Similarly all patients had the typical symptomatology of gastric outlet obstruction. Peptic duodenal stricture was due to a duodenal ulcer in most patients (81.2%). Pyloric channel ulcers constituted 18.7% of the series. Preoperative nasogastric decompression was used for an average of 2 days. Fluid and electrolyte replacement was necessary as a rule. Basal acid output and maximal acid output were determined in all patients. All patients were operated on either personally or under direct supervision of the author. Parietal cell vagotomy was performed in all patients with the same method. Both anterior and posterior vagal trunks were identified and isolated on separate nontraumatic tapes as the initial step of the procedure. The esophagus was isolated on a penrose drain and retracted to the left. Lesser curve dissection was started immediately above the crow's foot. The posterior pancreatogastric attachments were cleared off and the angle of His was emptied from all neurovascular and connective tissue. The esophageal dissection was carried up to approximately 10 cm above the esophagogastric junction. A slight myotomy was performed at the lower esophagus to cut intramuscular vagal fibers, if present. The denervated lesser curvature was closed with interrupted 3/0 silk stitches in every case.
A small gastrotomy was performed at the denervated portion of the corpus, next to the gastric antrum, anteriorly, and toward the greater curvature. Hegar dilators were introduced through this opening, starting from the smallest-calibered dilator. The probe that could not pass the stricture without forceful manipulation was recorded
597
598
Ann. Surg. * November 1990 MENTE8 refers to excellent clinical status, Visick 2 to a good result, as the caliber of the outlet. The initial outlet was between Visick 3 to a fair result, and Visick 4 to a poor result, 6 to 12 Hegar (mean, 8.5 Hegar) in these 32 patients. Patients with less than a I 0-Hegar outlet were considered including recurrences and reoperations related to a reto have a severe obstruction (75%, 24 patients), while those currence. At last follow-up 59.3% of the patients were with an outlet between 10 to 12 Hegar had a moderate classified as Visick 1 and 15.6% were Visick 2. Those with obstruction (25%, 8 patients). Dilatation was continued a good or excellent clinical outcome 1 to 10 years after in a stepwise fashion, leaving the dilator within the stricoperation for 74.9% of the patients in this series (Tature for a few seconds in each step. Dilatation was carried ble 1). on until the stricture was felt to be relieved without doubt Seven patients (21.8%) have had recurrence. Two of or until the largest dilator was introduced or until there these patients (6.2%) were reoperated on in other hospitals. was a duodenal rupture at the site of the stricture. DuoOne patient was a 52-year-old woman with a moderate denal rupture complicated the dilatation process in five stricture dilated to 26 Hegar. She had been symptomatic patients (15.6%) and was closed transversely with interstarting from her third postoperative year and underwent rupted 3/0 silks sutures in every instance. A penrose drain a Billroth 2 gastrectomy 8 years after operation. The other was placed to the lesser curvature and maintained for 24 patient was a 43-year-old man with severe stricture, dilated hours in patients without duodenal rupture and for 3 days from 7 to 25 Hegar. At 1 year follow-up he was Visick 1. In his second postoperative year he had a recurrence and for those with a rupture. The nasogastric catheter was removed on the first post- a subsequent perforation. He presented to a rural hospital, operative day and patients generally were allowed to take was treated with primary closure, but later died. This death oral fluids by the second day. Regular diet was resumed apparently was related to recurrence. after the third postoperative day. Basal acid output and Recurrence rates showed a stepwise increase in relation maximal acid output was determined when the patient to the extent of the follow-up. The recurrence rate was was to be discharged from the hospital or 7 to 10 days 3.1% at 1 year, 9.3% at 5 years, and increased to 21.8% after operation if the patient had been discharged. Gastric after 6 to 10 years follow-up. The recurrence rate for those emptying was controlled with a barium meal when the patients initially diagnosed with a pyloric ulcer was 16.6% and for those patients with a duodenal ulcer the recurrence patient resumed a regular diet and at 1 year follow-up. The patients were followed through a questionnaire and/ rate was 23%. or interview. Postoperative endoscopy was performed in Apart from seven patients with a proved recurrence, all patients at the first year follow-up and then as indicated. there have been three other patients in whom a recurrence Even slight symptoms were considered indications for a has been suspected. In two of these patients the reason for suspicion of a recurrence was gastrointestinal bleeding. thorough search for recurrence. However in both patients bleeding was attributed to gastric erosions with endoscopic examination. Both patients were Results under considerable stress related to family problems just before their episodes. Apart from this both patients have There were no hospital deaths. Significant morbidity been classified as Visick 1 throughout their follow-up 7 was not encountered, except for one patient with proand 8 years after operation. The third patient is the only longed gastrointestinal malfunction. This patient was a one in whom a Visick 3 status has been assigned in this 59-year-old man with long-standing duodenal ulcer disseries. He had a severe stricture dilated from 8 to 24 Hegar, ease. The stricture in this patient was dilated from 7 to with a duodenal rupture and transverse closure. He had 19 Hegar, without rupture. He was discharged on the fifth symptoms that interfered with his everyday life, but a day after operation but was readmitted 3 days later with recurrent ulcer could not be detected despite careful abdominal distention, gastric retention, and faintness. search. He has been lost to follow-up 1 year after operation
There was no evidence of peritonitis. He was treated with nasogastric decompression, supportive measures, and intravenous fluids and he recovered in a few days. He has been Visick 1 since then.
and his current status is unknown. TABLE 1. Clinical Results After I to 10 Years Following
Parietal Cell Vagotomy and Dilatation
Clinical Status The patients have been followed for 1 to 10 years. A 5-year follow-up is available for 37.4% of the series, while 6- to 10-year follow-up is available for 62.4%. Late results were evaluated according to the Visick criteria. Visick 1
Visick Score
Percentage
1 2
59.3
1 +2
15.6 74.9
3
3.1 21.8
4
Vol. 212 -No. S
PCV AND DILATION FOR PEPTIC STRICTURE
Dilatation The maximal dilatation performed in 32 patients with peptic duodenal stricture was between 17 and 26 Hegar (mean, 21.5 Hegar). Barium studies for gastric emptying revealed a free outlet in every patient, both immediately after surgery and during the first year of follow-up. Early restenosis did not take place. There has been only one instance of late restenosis (3.1%). This patient was a 70year-old man with a severe stricture, dilated from 8 to 17 Hegar. He had been classified as Visick 1 for 5 years. After this time he experienced epigastric fullness and occasional vomiting; however repeated barium studies and endoscopy failed to reveal an ulcer. At his last follow-up, 9 years after operation, a recurrent ulcer and restenosis was detected. He responded very well to H2-receptor blocker therapy and is completely free of symptoms. Gastric Acidity Gastric acidity was analyzed before operation and 7 to 10 days after operation in every patient. However nine patients refused to undergo acid studies at first year followup. Five of these were convinced for reanalysis during the second year follow-up. Hence acid secretory figures for preoperative, 7 to 10 days, and 1 or 2 years postoperative determinations are available in 28 of the 32 patients (87.5%). The mean basal acid output (BAO) was 5.6 mEq/hour before parietal cell vagotomy (PCV) and dilatation. The mean early postoperative level of BAO, 7 to 10 days after surgery was 3.2 mEq/hour. Thus BAO was reduced by 42.86% immediately after PCV and dilatation. The mean BAO in the late postoperative period was 1.4 mEq/hour. Thus BAO was reduced by 75% 1 to 2 years after PCV and dilatation. Maximal acid output (MAO) was determined after an intravenous injection of histamine dichloride, 0.04 mg/ kg. The mean MAO was 30.1 mEq/hour before and 17.2 mEq/hour 7 to 10 days after PCV and dilatation. The immediate response of MAO to PCV thus was again 42.86%. There was a further reduction by 57.81% in the maximal acid output after 1 to 2 years after operation. The mean MAO, 1 to 2 years after PCV and dilatation was 12.7 mEq/hour. Gastric acidity showed a different pattern in patients with a proved recurrence. Although the preoperative mean BAO was lower in patients with a subsequent recurrence (4.7 mEq/hour versus 5.6 mEq/hour for the entire group), the immediate response to PCV was not as marked. The mean BAO 7 to 10 days after operation decreased by 35% to a level of 3.1 mEq/hour. However late postoperative mean BAO was at the level of 1.5 mEq/hour 1 to 2 years after PCV and exhibited a 69% reduction compared to the preoperative level.
599
The mean preoperative MAO was higher in patients with a subsequent recurrence (34.9 mEq/hour versus 30.1 mEq/hour in the entire series). The mean MAO was 10.5 mEq/hour 7 to 10 days after operation, thus decreased by 70% in the immediate postoperative period. However this time a further decrease could not be seen 1 to 2 years after operation and the mean MAO increased to the level of 14.9 mEq/hour (a 58% decrease compared to the preoperative value or a 12% increase compared to the immediate postoperative level).
Discussion More than 15 years have passed since the first report3 ofPCV and dilatation of the obstruction caused by chronic duodenal ulcer. The original intention was to reproduce the favorable early results of PCV in patients presenting with complications. Since then there have not been many published experiences with this procedure, and not surprisingly the results of PCV and dilatation have been conflicting.4-6 The largest reported experience is based on 70 patients7 and most ofthe reports are based on populations not exceeding 20 patients.F"8'10 Furthermore the followup periods are variable, ranging from 0.7 to 10 years (Table 2). These factors may render results reported by individual authors less significant. An analysis of the collective data from 249 patients provided by the published literature4'2 and this present series may lead to a more reliable decision on the results of PCV and dilatation. The argument on the effectiveness of PCV and dilatation for the surgical treatment of peptic duodenal stricture ('pyloric stenosis') is based on the recurrence and restenosis rates. The recurrence rates reported vary between 6.6% after a minimum follow-up of 18 months5 and 22.2% after 1 to 3 years follow-up.4 The recurrence rate in this present series is 21.8%. On the other hand, there are reports with less6'7"0 or no recurrence at all.8"'1
TABLE 2. Failure (Recurrence and Restenosis) Rates in 249 Patients (Including This Series) Collected from the Literature, Following PCV and Dilatation
Reference
n
McMahon, 1976" Delaney, 19788 Ferraz, 19814 Rossi, 19819 Dunn, 19815 Blackett, 19817 Gorey, 198412 Hooks, 19866 Hom, 1989'0 Menteq, 1989 Total
23 11 11 19 15 70 44 14 10 32 249
Visick 4
Restenosis
(%)
(%)
Follow-up (Years)
-
1-5 1-3 1-3 1.5 (minimum) 4-5
10 18 5
4 (mean) 5-7 0.7-5 4
22.2 16 6.6 9 16 11
10 21.8 12
3.1 6.8
1-10
Patients with duodenoplasty or drainage have been excluded.
600
Ann. Surg. * November 1990
MENTE$
The overall recurrence rate 1 to 10 years after PCV and dilatation in 249 patients is 12%. This is similar to the recurrence rates obtained after a mean follow-up of 10 years in 183 elective patients treated with PCV.'3 A recent review of the literature on PCV'4 also has presented data comparable with this rate. However almost all series on PCV and dilatation have follow-up periods shorter than 10 years and the late recurrence rate after PCV can be as high as 30% after 15 years.'5 The stepwise increase of recurrences from 3.1% after 1 year to 21.8% after 6 to 10 years in our series also suggests that the actual failure rate of PCV cannot be correctly determined before 10 years follow-up is completed. This trend justifies an expectation of a higher long-term recurrence rate than that after elective PCV in patients treated with PCV and dilatation. One of the reasons why PCV and dilatation has not been used extensively seems to be related to the fear of failure to achieve a persistently patent and competent gastric outlet. At least two groups have suggested that poor results following PCV and dilatation could be improved if a drainage procedure had been added to PCV.4'9 However there is both theoretical and clinical evidence that favors avoidance of a drainage procedure. Because motor nerves to the gastric antrum are preserved, it is assumed that PCV helps to maintain the propulsive activity of the stomach in an attempt to overcome the pre-existing obstruction and provides protection from restenosis.3 l Clinical evidence supports this point of view. Hooks et al.6 compiled a series of 229 patients from the literature, with a restenosis rate of 4%. However their collective data consists of patients treated with PCV plus dilatation or duodenoplasty. We calculated a 6.8% restenosis rate in our collective series of 249 patients treated with PCV and dilatation. Most of the restenoses have been reported in two series.7 2 Gorey et al.'2 have reported a restenosis rate of 18%, in which eight of the nine patients with recurrent stenosis had previously undergone patch closures for duodenal ulcer perforation. The ninth patient had an omental patch closure because of duodenal rupture during dilatation. Omental patches drawn to the duodenum are known to cause dense fibrosis'6 and these restenoses cannot be directly accepted as failures due to recurrent peptic strictures. Nevertheless restenosis does not seem to be a matter of major concern after PCV and dilatation and we share the view that a drainage procedure or duodenoplasty is unnecessary.S Two possible methods for dilatation exist: finger dilatation and bougie dilatation. We have preferred bougie dilatation because the greatest diameter that can be achieved with finger dilatation would be 14 or 15 Hegar. The stricture in our patients were dilated to a mean of 21.5 Hegar (maximum, 26 Hegar) and we believe this has an influence on the low restenosis rate that we achieved. Despite the high rate of ulcer recurrence, only one patient
(3.1%) experienced restenosis among our patients. The symptoms in this patient quickly resolved with H2-receptor blocker therapy 9 years after operation. Hence there is a high probability that even this was not a genuine restenosis. One other important aspect of PCV and dilatation is that there is limited postoperative morbidity and almost no Visick 3 results during follow-up. Gastric emptying after PCV and dilatation is not different than that found after PCV alone for uncomplicated duodenal ulcer.'7 Although excellent results have been reported after PCV and drainage for obstructing duodenal ulcer,2 this is not the case in every instance.10"8 An additional drainage procedure does not have a significant influence on the recurrence rates'9 but may lead to immediate mechanical problems, as well as to late side effects, which are out of the question if the stricture is dilated instead. Dilatation has led to duodenal rupture in five patients (15.6%) in this series. However there is no other report of rupture comparable to our rate. This high rate may be due to the vigorous dilatation we used. A comparison of PCV and dilatation and truncal vagotomy and drainage has provided Visick 3 results of 4% and 22%, respectively."I On the other hand, when combined with dilatation, results after truncal vagotomy are comparable with those after PCV.20 The only Visick 3 patient in this series probably should have ended with a recurrence if he could have been followed longer than 1 year. In this present series, PCV resulted with a 43% reduction in BAO during the early postoperative period and with a 75% reduction 1 or 2 years after surgery. A similar decrease in MAO by 43% was achieved in the early postoperative period, while a 58% decrease was detected 1 or 2 years after PCV. These findings do not correlate with the assumption that PCV leads to a greater reduction in acid output during the initial phase and that there is a relative increase in gastric acidity after 1 year.'" The acid secretion results in this series reveal that there is a stepwise reduction in both basal and maximal acid output during the first 2 years after PCV. This trend was impaired in relation to maximal acid output in response to a dose of histamine dichloride in patients with a subsequent recurrence. Data has been presented on the prediction of a recurrence,'4 however uniformly valid predictive acid secretory criteria are not present. Because almost all recurrences in this series occurred after the third postoperative year, our data suggest that an increase in MAO within 2 years after an initial decline may raise concern of a recurrence for the patient in question. References 1. Weiland D, Dunn DH, Humphrey EW, Schwartz ML. Gastric outlet obstruction in peptic ulcer disease: an indication for surgery. Am
J Surg 1982; 143:90-93.
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PCV AND DILATION FOR PEPTIC STRICTURE
2. Donahue PE, Yoshida J, Richter HM, et al. Proximal gastric vagotomy with drainage for obstructing duodenal ulcer. Surgery 1988; 104:757-763. 3. Johnston D, Lyndon PJ, Smith RB, Humphrey CS. Highly selective vagotomy without a drainage procedure in the treatment of haemorrhage, perforation and pyloric stenosis due to peptic ulcer. BrJ Surg 1973; 60:790-797. 4. Ferraz EM, Filho HAF, Bacelar TS, et al. Proximal gastric vagotomy in stenosed or perforated duodenal ulcer. Br J Surg 1981; 68: 452-454. 5. Dunn DC, Thomas WEG, Hunter JO. Highly selective vagotomy and pyloric dilatation for duodenal ulcer with stenosis. Br J Surg 1981; 68:194-196. 6. Hooks VH, Bowden TA, Mansberger AR, Sisley JF. Highly selective vagotomy with dilatation or duodenoplasty. Ann Surg 1986; 203: 545-548. 7. Blackett RL, Axon ATR, Barker MC, et al. Highly selective vagotomy with pyloric dilatation for pyloric stenosis due to peptic ulcer. Br J Surg 1982; 69:289(Abstr). 8. Delaney P. Peroperative grading of pyloric stenosis: a long term clinical and radiological follow-up of patients with severe pyloric stenosis treated by highly selective vagotomy and dilatation of the stricture. Br J Surg 1978; 65:157-160. 9. Rossi RL, Braasch JW, Cady B, Sedgwick CE. Parietal cell vagotomy for intractable and obstructing duodenal ulcer. Am J Surg 1981; 141:482-485. 10. Hom S, Sarr MG, Kelly KA, Hench V. Postoperative gastric atony after vagotomy for obstructing peptic ulcer. Am J Surg 1989; 157:282-286.
601
11. McMahon MJ, Greenall MJ, Johnston D, Goligher JC. Highly selective vagotomy plus dilatation of the stenosis compared with truncal vagotomy and drainage in the treatment of pyloric stenosis secondary to duodenal ulceration. Gut 1976; 17:471-476. 12. Gorey TF, Lennon F, Heffernan SJ. Highly selective vagotomy in duodenal ulceration and its complications. Ann Surg 1984; 200: 181-184. 13. Schache DJ, Masters A, Tovey FH, et al. Long term recurrence patterns following proximal gastric vagotomy. Aust NZJ Surg 1989; 59:387-390. 14. Schirmer BD. Current status of proximal gastric vagotomy. Ann Surg 1989; 209:131-148. 15. Hoffman J, Olesen A, Jensen HE. Prospective 14 to 18 year followup study after parietal cell vagotomy. Br J Surg 1987; 74:10561059. 16. Ballinger W, Solanke T. Serosal patch pyloroplasty. Surg Gynecol Obstet 1966; 122:1283. 17. White CM, Harding LK, Keighley MRB, et al. Gastric emptying after treatment for stenosis secondary to duodenal ulceration by proximal gastric vagotomy and duodenoplasty or pyloric dilatation. Gut 1978; 19:783-786. 18. Gleysteen JJ, Droege EA. Expedient surgical treatment of chronic ulcer stenosis: a case for proximal gastric vagotomy. J Clin Gastroenterol 1988; 10:619-622. 19. Nilsell K. Five to nine years results of selective proximal vagotomy with and without pyloroplasty for duodenal ulcer. Acta Chir Scand 1979; 145:251-255. 20. Thomson JD, Galloway JBW. Vagotomy and pyloric dilatation in chronic duodenal ulceration. Br Med J 1979; 1:1453-1455.
ALI $. MENTE$, M.D.
Gastric outlet obstruction due to peptic duodenal stricture (pyloric stenosis) was treated with parietal cell vagotomy and dilatation of the stricture in 32 patients. Follow-up is in the range of 5 years in 37.4% of the patients, while 6 to 10 years follow-up is available in 62.4% of the patients. At their last follow-up, 74.9% of the patients were in either Visick 1 or 2 clinical status. Recurrence rates have been 3.1% at 1 year, 9.3% at 5 years, and 21.8% after 6 to 10 years follow-up. There has been only one instance (3.1%) of restenosis. Two patients required reoperation because of recurrence and one of them died.
T n HE FREQUENCY OF peptic duodenal ulcer surgery declined after the introduction of H2 receptor blockers. However gastric outlet obstruction continues to be a principal indication for surgery.' An ideal operation for obstructing peptic duodenal stricture must relieve the obstruction, control the primary ulcer diathesis, and be free of late complications2; also it must have a negligible mortality rate and an acceptable rate of postoperative morbidity. Johnston et al.3 have advocated parietal cell vagotomy and dilatation for the surgical treatment of peptic duodenal stricture. We began performing this procedure in 1979 in unselected patients. Here we report our late results with parietal cell vagotomy and dilatation for peptic duodenal stricture.
Materials and Methods Parietal cell vagotomy and dilatation was performed in 32 patients with gastric outlet obstruction due to peptic duodenal stricture. Their ages were within the range of 17 to 70 years (mean, 41 years). Twenty eight patients (87.5%) were male and four (12.5%) were female. They had medical histories of duodenal ulcer between 4 and 40 years of age (mean, 12.8 years). All patients had a full Address reprint requests to Dr. Ali Mentes, Department of Surgery, Agean University Hospital, 35100, Bornova, Izmir, Turkey. Accepted for publication December 4, 1989. Accepted for publication December 4, 1989.
From the Department of Surgery, Agean University Faculty of
Medicine, Izmir, Turkey
diagnosis of 'pyloric stenosis' at the time of admission. Barium studies of the upper gastrointestinal tract revealed atonic and dilated stomachs in every patient. Similarly all patients had the typical symptomatology of gastric outlet obstruction. Peptic duodenal stricture was due to a duodenal ulcer in most patients (81.2%). Pyloric channel ulcers constituted 18.7% of the series. Preoperative nasogastric decompression was used for an average of 2 days. Fluid and electrolyte replacement was necessary as a rule. Basal acid output and maximal acid output were determined in all patients. All patients were operated on either personally or under direct supervision of the author. Parietal cell vagotomy was performed in all patients with the same method. Both anterior and posterior vagal trunks were identified and isolated on separate nontraumatic tapes as the initial step of the procedure. The esophagus was isolated on a penrose drain and retracted to the left. Lesser curve dissection was started immediately above the crow's foot. The posterior pancreatogastric attachments were cleared off and the angle of His was emptied from all neurovascular and connective tissue. The esophageal dissection was carried up to approximately 10 cm above the esophagogastric junction. A slight myotomy was performed at the lower esophagus to cut intramuscular vagal fibers, if present. The denervated lesser curvature was closed with interrupted 3/0 silk stitches in every case.
A small gastrotomy was performed at the denervated portion of the corpus, next to the gastric antrum, anteriorly, and toward the greater curvature. Hegar dilators were introduced through this opening, starting from the smallest-calibered dilator. The probe that could not pass the stricture without forceful manipulation was recorded
597
598
Ann. Surg. * November 1990 MENTE8 refers to excellent clinical status, Visick 2 to a good result, as the caliber of the outlet. The initial outlet was between Visick 3 to a fair result, and Visick 4 to a poor result, 6 to 12 Hegar (mean, 8.5 Hegar) in these 32 patients. Patients with less than a I 0-Hegar outlet were considered including recurrences and reoperations related to a reto have a severe obstruction (75%, 24 patients), while those currence. At last follow-up 59.3% of the patients were with an outlet between 10 to 12 Hegar had a moderate classified as Visick 1 and 15.6% were Visick 2. Those with obstruction (25%, 8 patients). Dilatation was continued a good or excellent clinical outcome 1 to 10 years after in a stepwise fashion, leaving the dilator within the stricoperation for 74.9% of the patients in this series (Tature for a few seconds in each step. Dilatation was carried ble 1). on until the stricture was felt to be relieved without doubt Seven patients (21.8%) have had recurrence. Two of or until the largest dilator was introduced or until there these patients (6.2%) were reoperated on in other hospitals. was a duodenal rupture at the site of the stricture. DuoOne patient was a 52-year-old woman with a moderate denal rupture complicated the dilatation process in five stricture dilated to 26 Hegar. She had been symptomatic patients (15.6%) and was closed transversely with interstarting from her third postoperative year and underwent rupted 3/0 silks sutures in every instance. A penrose drain a Billroth 2 gastrectomy 8 years after operation. The other was placed to the lesser curvature and maintained for 24 patient was a 43-year-old man with severe stricture, dilated hours in patients without duodenal rupture and for 3 days from 7 to 25 Hegar. At 1 year follow-up he was Visick 1. In his second postoperative year he had a recurrence and for those with a rupture. The nasogastric catheter was removed on the first post- a subsequent perforation. He presented to a rural hospital, operative day and patients generally were allowed to take was treated with primary closure, but later died. This death oral fluids by the second day. Regular diet was resumed apparently was related to recurrence. after the third postoperative day. Basal acid output and Recurrence rates showed a stepwise increase in relation maximal acid output was determined when the patient to the extent of the follow-up. The recurrence rate was was to be discharged from the hospital or 7 to 10 days 3.1% at 1 year, 9.3% at 5 years, and increased to 21.8% after operation if the patient had been discharged. Gastric after 6 to 10 years follow-up. The recurrence rate for those emptying was controlled with a barium meal when the patients initially diagnosed with a pyloric ulcer was 16.6% and for those patients with a duodenal ulcer the recurrence patient resumed a regular diet and at 1 year follow-up. The patients were followed through a questionnaire and/ rate was 23%. or interview. Postoperative endoscopy was performed in Apart from seven patients with a proved recurrence, all patients at the first year follow-up and then as indicated. there have been three other patients in whom a recurrence Even slight symptoms were considered indications for a has been suspected. In two of these patients the reason for suspicion of a recurrence was gastrointestinal bleeding. thorough search for recurrence. However in both patients bleeding was attributed to gastric erosions with endoscopic examination. Both patients were Results under considerable stress related to family problems just before their episodes. Apart from this both patients have There were no hospital deaths. Significant morbidity been classified as Visick 1 throughout their follow-up 7 was not encountered, except for one patient with proand 8 years after operation. The third patient is the only longed gastrointestinal malfunction. This patient was a one in whom a Visick 3 status has been assigned in this 59-year-old man with long-standing duodenal ulcer disseries. He had a severe stricture dilated from 8 to 24 Hegar, ease. The stricture in this patient was dilated from 7 to with a duodenal rupture and transverse closure. He had 19 Hegar, without rupture. He was discharged on the fifth symptoms that interfered with his everyday life, but a day after operation but was readmitted 3 days later with recurrent ulcer could not be detected despite careful abdominal distention, gastric retention, and faintness. search. He has been lost to follow-up 1 year after operation
There was no evidence of peritonitis. He was treated with nasogastric decompression, supportive measures, and intravenous fluids and he recovered in a few days. He has been Visick 1 since then.
and his current status is unknown. TABLE 1. Clinical Results After I to 10 Years Following
Parietal Cell Vagotomy and Dilatation
Clinical Status The patients have been followed for 1 to 10 years. A 5-year follow-up is available for 37.4% of the series, while 6- to 10-year follow-up is available for 62.4%. Late results were evaluated according to the Visick criteria. Visick 1
Visick Score
Percentage
1 2
59.3
1 +2
15.6 74.9
3
3.1 21.8
4
Vol. 212 -No. S
PCV AND DILATION FOR PEPTIC STRICTURE
Dilatation The maximal dilatation performed in 32 patients with peptic duodenal stricture was between 17 and 26 Hegar (mean, 21.5 Hegar). Barium studies for gastric emptying revealed a free outlet in every patient, both immediately after surgery and during the first year of follow-up. Early restenosis did not take place. There has been only one instance of late restenosis (3.1%). This patient was a 70year-old man with a severe stricture, dilated from 8 to 17 Hegar. He had been classified as Visick 1 for 5 years. After this time he experienced epigastric fullness and occasional vomiting; however repeated barium studies and endoscopy failed to reveal an ulcer. At his last follow-up, 9 years after operation, a recurrent ulcer and restenosis was detected. He responded very well to H2-receptor blocker therapy and is completely free of symptoms. Gastric Acidity Gastric acidity was analyzed before operation and 7 to 10 days after operation in every patient. However nine patients refused to undergo acid studies at first year followup. Five of these were convinced for reanalysis during the second year follow-up. Hence acid secretory figures for preoperative, 7 to 10 days, and 1 or 2 years postoperative determinations are available in 28 of the 32 patients (87.5%). The mean basal acid output (BAO) was 5.6 mEq/hour before parietal cell vagotomy (PCV) and dilatation. The mean early postoperative level of BAO, 7 to 10 days after surgery was 3.2 mEq/hour. Thus BAO was reduced by 42.86% immediately after PCV and dilatation. The mean BAO in the late postoperative period was 1.4 mEq/hour. Thus BAO was reduced by 75% 1 to 2 years after PCV and dilatation. Maximal acid output (MAO) was determined after an intravenous injection of histamine dichloride, 0.04 mg/ kg. The mean MAO was 30.1 mEq/hour before and 17.2 mEq/hour 7 to 10 days after PCV and dilatation. The immediate response of MAO to PCV thus was again 42.86%. There was a further reduction by 57.81% in the maximal acid output after 1 to 2 years after operation. The mean MAO, 1 to 2 years after PCV and dilatation was 12.7 mEq/hour. Gastric acidity showed a different pattern in patients with a proved recurrence. Although the preoperative mean BAO was lower in patients with a subsequent recurrence (4.7 mEq/hour versus 5.6 mEq/hour for the entire group), the immediate response to PCV was not as marked. The mean BAO 7 to 10 days after operation decreased by 35% to a level of 3.1 mEq/hour. However late postoperative mean BAO was at the level of 1.5 mEq/hour 1 to 2 years after PCV and exhibited a 69% reduction compared to the preoperative level.
599
The mean preoperative MAO was higher in patients with a subsequent recurrence (34.9 mEq/hour versus 30.1 mEq/hour in the entire series). The mean MAO was 10.5 mEq/hour 7 to 10 days after operation, thus decreased by 70% in the immediate postoperative period. However this time a further decrease could not be seen 1 to 2 years after operation and the mean MAO increased to the level of 14.9 mEq/hour (a 58% decrease compared to the preoperative value or a 12% increase compared to the immediate postoperative level).
Discussion More than 15 years have passed since the first report3 ofPCV and dilatation of the obstruction caused by chronic duodenal ulcer. The original intention was to reproduce the favorable early results of PCV in patients presenting with complications. Since then there have not been many published experiences with this procedure, and not surprisingly the results of PCV and dilatation have been conflicting.4-6 The largest reported experience is based on 70 patients7 and most ofthe reports are based on populations not exceeding 20 patients.F"8'10 Furthermore the followup periods are variable, ranging from 0.7 to 10 years (Table 2). These factors may render results reported by individual authors less significant. An analysis of the collective data from 249 patients provided by the published literature4'2 and this present series may lead to a more reliable decision on the results of PCV and dilatation. The argument on the effectiveness of PCV and dilatation for the surgical treatment of peptic duodenal stricture ('pyloric stenosis') is based on the recurrence and restenosis rates. The recurrence rates reported vary between 6.6% after a minimum follow-up of 18 months5 and 22.2% after 1 to 3 years follow-up.4 The recurrence rate in this present series is 21.8%. On the other hand, there are reports with less6'7"0 or no recurrence at all.8"'1
TABLE 2. Failure (Recurrence and Restenosis) Rates in 249 Patients (Including This Series) Collected from the Literature, Following PCV and Dilatation
Reference
n
McMahon, 1976" Delaney, 19788 Ferraz, 19814 Rossi, 19819 Dunn, 19815 Blackett, 19817 Gorey, 198412 Hooks, 19866 Hom, 1989'0 Menteq, 1989 Total
23 11 11 19 15 70 44 14 10 32 249
Visick 4
Restenosis
(%)
(%)
Follow-up (Years)
-
1-5 1-3 1-3 1.5 (minimum) 4-5
10 18 5
4 (mean) 5-7 0.7-5 4
22.2 16 6.6 9 16 11
10 21.8 12
3.1 6.8
1-10
Patients with duodenoplasty or drainage have been excluded.
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Ann. Surg. * November 1990
MENTE$
The overall recurrence rate 1 to 10 years after PCV and dilatation in 249 patients is 12%. This is similar to the recurrence rates obtained after a mean follow-up of 10 years in 183 elective patients treated with PCV.'3 A recent review of the literature on PCV'4 also has presented data comparable with this rate. However almost all series on PCV and dilatation have follow-up periods shorter than 10 years and the late recurrence rate after PCV can be as high as 30% after 15 years.'5 The stepwise increase of recurrences from 3.1% after 1 year to 21.8% after 6 to 10 years in our series also suggests that the actual failure rate of PCV cannot be correctly determined before 10 years follow-up is completed. This trend justifies an expectation of a higher long-term recurrence rate than that after elective PCV in patients treated with PCV and dilatation. One of the reasons why PCV and dilatation has not been used extensively seems to be related to the fear of failure to achieve a persistently patent and competent gastric outlet. At least two groups have suggested that poor results following PCV and dilatation could be improved if a drainage procedure had been added to PCV.4'9 However there is both theoretical and clinical evidence that favors avoidance of a drainage procedure. Because motor nerves to the gastric antrum are preserved, it is assumed that PCV helps to maintain the propulsive activity of the stomach in an attempt to overcome the pre-existing obstruction and provides protection from restenosis.3 l Clinical evidence supports this point of view. Hooks et al.6 compiled a series of 229 patients from the literature, with a restenosis rate of 4%. However their collective data consists of patients treated with PCV plus dilatation or duodenoplasty. We calculated a 6.8% restenosis rate in our collective series of 249 patients treated with PCV and dilatation. Most of the restenoses have been reported in two series.7 2 Gorey et al.'2 have reported a restenosis rate of 18%, in which eight of the nine patients with recurrent stenosis had previously undergone patch closures for duodenal ulcer perforation. The ninth patient had an omental patch closure because of duodenal rupture during dilatation. Omental patches drawn to the duodenum are known to cause dense fibrosis'6 and these restenoses cannot be directly accepted as failures due to recurrent peptic strictures. Nevertheless restenosis does not seem to be a matter of major concern after PCV and dilatation and we share the view that a drainage procedure or duodenoplasty is unnecessary.S Two possible methods for dilatation exist: finger dilatation and bougie dilatation. We have preferred bougie dilatation because the greatest diameter that can be achieved with finger dilatation would be 14 or 15 Hegar. The stricture in our patients were dilated to a mean of 21.5 Hegar (maximum, 26 Hegar) and we believe this has an influence on the low restenosis rate that we achieved. Despite the high rate of ulcer recurrence, only one patient
(3.1%) experienced restenosis among our patients. The symptoms in this patient quickly resolved with H2-receptor blocker therapy 9 years after operation. Hence there is a high probability that even this was not a genuine restenosis. One other important aspect of PCV and dilatation is that there is limited postoperative morbidity and almost no Visick 3 results during follow-up. Gastric emptying after PCV and dilatation is not different than that found after PCV alone for uncomplicated duodenal ulcer.'7 Although excellent results have been reported after PCV and drainage for obstructing duodenal ulcer,2 this is not the case in every instance.10"8 An additional drainage procedure does not have a significant influence on the recurrence rates'9 but may lead to immediate mechanical problems, as well as to late side effects, which are out of the question if the stricture is dilated instead. Dilatation has led to duodenal rupture in five patients (15.6%) in this series. However there is no other report of rupture comparable to our rate. This high rate may be due to the vigorous dilatation we used. A comparison of PCV and dilatation and truncal vagotomy and drainage has provided Visick 3 results of 4% and 22%, respectively."I On the other hand, when combined with dilatation, results after truncal vagotomy are comparable with those after PCV.20 The only Visick 3 patient in this series probably should have ended with a recurrence if he could have been followed longer than 1 year. In this present series, PCV resulted with a 43% reduction in BAO during the early postoperative period and with a 75% reduction 1 or 2 years after surgery. A similar decrease in MAO by 43% was achieved in the early postoperative period, while a 58% decrease was detected 1 or 2 years after PCV. These findings do not correlate with the assumption that PCV leads to a greater reduction in acid output during the initial phase and that there is a relative increase in gastric acidity after 1 year.'" The acid secretion results in this series reveal that there is a stepwise reduction in both basal and maximal acid output during the first 2 years after PCV. This trend was impaired in relation to maximal acid output in response to a dose of histamine dichloride in patients with a subsequent recurrence. Data has been presented on the prediction of a recurrence,'4 however uniformly valid predictive acid secretory criteria are not present. Because almost all recurrences in this series occurred after the third postoperative year, our data suggest that an increase in MAO within 2 years after an initial decline may raise concern of a recurrence for the patient in question. References 1. Weiland D, Dunn DH, Humphrey EW, Schwartz ML. Gastric outlet obstruction in peptic ulcer disease: an indication for surgery. Am
J Surg 1982; 143:90-93.
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2. Donahue PE, Yoshida J, Richter HM, et al. Proximal gastric vagotomy with drainage for obstructing duodenal ulcer. Surgery 1988; 104:757-763. 3. Johnston D, Lyndon PJ, Smith RB, Humphrey CS. Highly selective vagotomy without a drainage procedure in the treatment of haemorrhage, perforation and pyloric stenosis due to peptic ulcer. BrJ Surg 1973; 60:790-797. 4. Ferraz EM, Filho HAF, Bacelar TS, et al. Proximal gastric vagotomy in stenosed or perforated duodenal ulcer. Br J Surg 1981; 68: 452-454. 5. Dunn DC, Thomas WEG, Hunter JO. Highly selective vagotomy and pyloric dilatation for duodenal ulcer with stenosis. Br J Surg 1981; 68:194-196. 6. Hooks VH, Bowden TA, Mansberger AR, Sisley JF. Highly selective vagotomy with dilatation or duodenoplasty. Ann Surg 1986; 203: 545-548. 7. Blackett RL, Axon ATR, Barker MC, et al. Highly selective vagotomy with pyloric dilatation for pyloric stenosis due to peptic ulcer. Br J Surg 1982; 69:289(Abstr). 8. Delaney P. Peroperative grading of pyloric stenosis: a long term clinical and radiological follow-up of patients with severe pyloric stenosis treated by highly selective vagotomy and dilatation of the stricture. Br J Surg 1978; 65:157-160. 9. Rossi RL, Braasch JW, Cady B, Sedgwick CE. Parietal cell vagotomy for intractable and obstructing duodenal ulcer. Am J Surg 1981; 141:482-485. 10. Hom S, Sarr MG, Kelly KA, Hench V. Postoperative gastric atony after vagotomy for obstructing peptic ulcer. Am J Surg 1989; 157:282-286.
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11. McMahon MJ, Greenall MJ, Johnston D, Goligher JC. Highly selective vagotomy plus dilatation of the stenosis compared with truncal vagotomy and drainage in the treatment of pyloric stenosis secondary to duodenal ulceration. Gut 1976; 17:471-476. 12. Gorey TF, Lennon F, Heffernan SJ. Highly selective vagotomy in duodenal ulceration and its complications. Ann Surg 1984; 200: 181-184. 13. Schache DJ, Masters A, Tovey FH, et al. Long term recurrence patterns following proximal gastric vagotomy. Aust NZJ Surg 1989; 59:387-390. 14. Schirmer BD. Current status of proximal gastric vagotomy. Ann Surg 1989; 209:131-148. 15. Hoffman J, Olesen A, Jensen HE. Prospective 14 to 18 year followup study after parietal cell vagotomy. Br J Surg 1987; 74:10561059. 16. Ballinger W, Solanke T. Serosal patch pyloroplasty. Surg Gynecol Obstet 1966; 122:1283. 17. White CM, Harding LK, Keighley MRB, et al. Gastric emptying after treatment for stenosis secondary to duodenal ulceration by proximal gastric vagotomy and duodenoplasty or pyloric dilatation. Gut 1978; 19:783-786. 18. Gleysteen JJ, Droege EA. Expedient surgical treatment of chronic ulcer stenosis: a case for proximal gastric vagotomy. J Clin Gastroenterol 1988; 10:619-622. 19. Nilsell K. Five to nine years results of selective proximal vagotomy with and without pyloroplasty for duodenal ulcer. Acta Chir Scand 1979; 145:251-255. 20. Thomson JD, Galloway JBW. Vagotomy and pyloric dilatation in chronic duodenal ulceration. Br Med J 1979; 1:1453-1455.
