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Complications of Vagotomy and Pyloroplasty
Symposium on Complications of Common Procedures
Complications of Vagotomy and Pyloroplasty
Mark E. Skellenger, M.D.,* and Paul H. Jordan, Jr., M.D., F.A.C.S. t
The combination of truncal vagotomy or selective vagotomy and pyloroplasty is a synthesis of two operations used primarily for treatment of duodenal ulcers and less frequently for treatment of gastric ulcers. In the absence of pyloric obstruction the only necessity for combining pyloroplasty with vagotomy is to compensate for gastric stasis, a frequent complication of total gastric vagotomy. Vagotomy and pyloroplasty were developed independently, and each has its own historical background and specific complications.
HISTORICAL BACKGROUND OF PYLOROPLASTY
A discussion of pyloroplasty must include gastroenterostomy since this was the first gastric drainage operation described. Gastroenterostomy was introduced by Wolfler73 in 1881 to bypass a carcinoma at the pylorus. By 1900 this procedure was applied to cases of nonmalignant inflammatory strictures of the pylorus. It was popularized for this use by Berkley Moynihan and W. J. Mayo and remained in vogue for nearly 4 decades. Pyloroplasty was originally performed by Reineke and described by his student, Fronmiiller, 18 in 1886. Reineke's first patient had severe gastric outlet obstruction due to a pyloric mass, which was a duodenal ulcer penetrating into the pancreas. His operation consisted of a longitudinal incision involving the distal stomach, pylorus, and proximal duodenum. This opening was closed transversely (Fig. 1). Mikulicz44 objected to gastroenterostomy because it did not permit access to the disease in the pylorus. Eleven months later he described an *Instructor in Surgery, Cora and Webb Mading Department of Surgery, Baylor College of Medicine and the Veterans Administration Medical Center, Houston, Texas tProfessor of Surgery, Cora and Webb Madii:tg Department of Surgery, Baylor College of Medicine and Veterans Administration Medical Center, Houston, Texas
Surgical Clinics of North America-Yo!. 63, No. 6, December, 1983
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Figure 1. The most common forms of gastric drainage procedures used in combination with vagotomy.
operation similar to that reported by Fronmiiller. He opened the pylorus of his first patient for hemorrhage and cauterized a posterior duodenal ulcer. The longitudinal opening was closed transversely using a double row of sutures. Because of the close temporal relationship between these two reports, the enlargement of the pylorus by this means carries the eponym, Reineke-Mikulicz pyloroplasty. Subsequently, various drainage procedures developed that, according to their originators, provided specific advantages over gastroenterostomy and Heineke-Mikulicz pyloroplasty. In 1899 Richardson 54 advocated resection of the anterior and lateral walls of the pyloroduodenal junction and primary reanastomosis when there was circumferential cicatrix in this area. In 1922 Judd, 37 disturbed by the number of jejunal ulcers that occurred after gastroenterostomy, excised the anterior wall of the pylorus, including the ulcer if possible, and performed a two-layer transverse closure. In 1933 Horsley25 excised the ulcer as part of a longitudinal incision of the pylorus. The incision was closed transversely. Other modifications of the HeinekeMikulicz pyloroplasty include those by Moschel, 46 Wangensteen, 67 Aust, 2 and Ballinger3 (Fig. 2). In 1956 Weinberg69 made a significant modification of the HeinekeMikulicz pyloroplasty. He used a one-layer closure of interrupted sutures. The major advantage of this procedure was that the amount of enfolded tissue that acts as a barrier to stasis was reduced to a minimum. Weinberg objected to gastroenterostomy because the abnormal continuity of the intestinal tract interfered with digestion. It resulted in regurgitation of
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'
I
I
~ Judd-1922
Moschel-1958
Horsley-1933
JeJun~~P.yljs
,
.
'
~ Wangensteen-1958
Ballinger-1966
Figure 2. Some of the modifications of pyloroplasty less frequently used in combination with vagotomy.
jejunal contents into the stomach leading to diffuse inflammation of the gastric mucosa, antral hyperfunction, and anastomotic ulcerations. Other methods of gastric drainage include gastroduodenostomy (see Fig. 1) performed by Jaboulay27 in 1892 for the treatment of an obstructing malignant lesion of the pylorus. So that the patient would not vomit bile, he performed duodenojejunostomy in addition to gastroduodenostomy. Later he simplified the operation and performed gastroduodenostomy alone. 28 In 1902 Finney15 described a method of pyloroplasty that in effect was also a gastroduodenostomy, but the opening was enlarged by connecting the gastric and duodenal incisions before making the side-to-side anastomosis (see Fig. l.) The Weinberg modification of the Heineke-Mikulicz pyloroplasty is probably the most common procedure for gastric drainage. Nevertheless, it shares an undesirable consequence of all drainage procedures-that is, the problem of bypassing or destroying the pyloric sphincter mechanism responsible for metering small amounts of gastric contents into the duodenum.
HISTORICAL BACKGROUND OF VAGOTOMY Abdominal vagotomy was performed by Exner14 in 1911 for abdominal pain and vomiting associated with tabes dorsalis. In 1922 Latarjet40 reported the use of vagotomy in 24 patients, 6 of whom had peptic ulcer. He performed a complementary gastrojejunostomy in each patient to prevent gastric stasis. This operation was not widely accepted, and gastroenterostomy or subtotal gastric resection became the standard operation for duodenal ulcer.
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Dissatisfied with the high rate of ulcer recurrence after gastroenterostomy and the mortality and morbidity associated with subtotal gastric resection, Dragstedt introduced transthoracic truncal vagotomy in 1943. 12 The frequency with which gastric stasis and gastric ulcers developed led Dragstedt to modify his operation and to perform transabdominal truncal vagotomy combined first with gastrojejunostomy and later with pyloroplasty to facilitate gastric drainage. In 1948 Jackson 29 and Franksson, 16 feeling that it was unnecessary to perform total intra-abdominal vagotomy to reduce acid secretion, described selective vagotomy that also required a drainage procedure. Despite its theoretical advantages, this operation did not gain wide acceptance because it was difficult to demonstrate its superiority and it was more difficult to perform than truncal vagotomy. Finally, the concept of denervating only the acid-secreting portion of the stomach developed and was described by Griffith and Harkins. 21 This type of vagotomy, parietal cell vagotomy or one of a number of other synonyms, was performed first on patients by Holle. 24 He combined the operation with pyloroplasty but later Johnston 32 and Amdrup, 1 independently, performed parietal cell vagotomy without a drainage procedure. Parietal cell vagotomy preserved antral function, which allowed for almost normal gastric emptying. Diarrhea, dumping, and bilious vomiting that complicated other types of vagotomy requiring a drainage operation were virtually eliminated.
OPERATIVE COMPLICATIONS OF VAGOTOMY The immediate postoperative morbidity after vagotomy involved complications common to all major intra-abdominal surgery. 35• 36 Major operative complications related to vagotomy occurred in 53 of 1096 patients in one series. 72 In this study, perforation of the esophagus was reported in 5 patients. 72 Death occurred in one patient in whom perforation was unrecognized. In a study of 4414 patients who underwent vagotomy, 53 3 of 24 patients with perforations died. The perforation was unrecognized at the original operation in 2 of the 3 patients. We have experienced esophageal perforation but have always recognized the complication and successfully repaired the esophagus. In our opinion, this complication is usually the consequence of blind finger dissection of the esophagus in obese individuals, in patients with portal hypertension, or in those with periesophageal inflammation secondary to esophagitis. Since we have begun to perform primarily selective vagotomy or parietal cell vagotomy, we have not encountered the complication and attribute this to the precise dissection that these operations demand. Splenic rupture (2. 7 per cent)72 was once considered an inconsequential complication of vagotomy except for the possibility of a subphrenic abscess. Incidental splenectomy is now a recognized complication in children and perhaps in adults as well. Therefore, every effort to avoid splenic injury should be taken.
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Figure 3. A, Severe dysphagia developed in this patient after vagotomy. The esophagogram gave the appearance of classic achalasia. The resistance of the lower esophageal sphincter was so great that initially it was impossible to pass safely a dilator of any size. B, In the early phase of recovery, the pressure of the lower esophageal sphincter was 60 mm Hg. The lower esophageal sphincter relaxed on swallowing, but the pressure did not fall to the intragastric pressure level. The patient recovered in nine days.
Bleeding after vagotomy, requiring operation, ranged from 0.3 per cent to 1 per cent and was a major cause of death associated with vagotomy. Bleeding occurred from the edge of the left lobe of the liver if mobilized, from the esophagus, from a transected vessel accompanying the vagus nerve, from varices, or from the splenic bed following splenectomy. Chylous ascites has occasionally been reported to occur following vagotomy. Dysphagia is a common problem after vagotomy. We concur with Cox7 that mild dysphagia occurs in about 20 per cent of patients following vagotomy. The onset begins after operation with the ingestion of solid foods. It is transient and usually disappears within two weeks. In most patients, dysphagia disappears spontaneously or after a simple bougienage. Routine roentgenograms almost never demonstrate any abnormalities. The cause of mild dysphagia may be due to operative trauma and edema of the lower esophagus. Dysphagia of consequence occurs in 1 to 2 per cent of patients treated by vagotomy. The onset may be early or months after operation. More troublesome dysphagia may be due to hematoma, fibrosis, periesophageal granuloma, injury and possible denervation of the lower esophagus. These patients usually can be satisfactorily managed by one or more esophageal dilatations. We have reoperated on only two patients after vagotomy because of dysphagia. Both patients had chronic periesophageal inflammatory reaction, one of which was thought to be a suture granuloma. These patients differ from those that appear as achalasia in that they also have odynophagia and their motility studies demonstrate sphincter relaxation with deglutition. Occasionally a patient becomes dysphagic; and esophageal roentgenograms suggest a classic picture of achalasia that did not exist preoperatively. (Fig. 3). High resistance at the esophagogastric junction can prevent endoscopy and necessitate several dilatations before the patient becomes asymptomatic. Such tightness of the sphincter is not characteristic of achalasia. This problem has been associated with transthoracic vagotomy more often than with transabdominal vagotomy.
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Dysphagia after vagotomy has also been attributed to reflux esophagitis, esophageal stricture, or both. The factors responsible for gastroesophageal reflux after vagotomy are not completely understood. Mobilization and loss of the normal tethering mechanism of the gastroesophageal junction that permit it to move into the mediastinum and escape the influence of positive intra-abdominal pressure have been suggested as causes. Loss of lower esophageal sphincter tone was proposed in one study performed two weeks after truncal vagotomy-pyloroplasty. 71 There are several studies, however, demonstrating that the lower esophageal sphincter pressure is unaltered by any type of vagotomy. 4• 8• 9•65 Evidence accumulating from our own service suggests that gastroesophageal reflux recognized after vagotomy may have been present but unrecognized preoperatively. This view is shared by others 10• 43 • 49 and indicates the need for careful evaluation prior to operation for duodenal ulcer.
OPERATIVE COMPLICATIONS OF PYLOROPLASTY
Pyloroplasty is performed to overcome gastric stasis caused by vagotomy. A major complication of pyloroplasty, therefore, is its failure to permit adequate gastric drainage. Several modifications of pyloroplasty were specifically made in an effort to avoid this complication. Of all the modifications of the Heineke-Mikulicz pyloroplasty, there seems to be little advantage of one over the other except for the single-layer closure advocated by Weinberg. Even so, in a prospective studl6 of truncal vagotomy and Heineke-Mikulicz pyloroplasty there was stomal dysfunction in 7 of 94 patients. Reoperation was required in 2 patients. If there is excessive inflammation at the pylorus, a Finney pyloroplasty, a Jaboulay gastroduodenostomy, or a gastroenterostomy may be preferable. If the antral portion of the stomach lies transversely, any of these alternatives are satisfactory. If the stomach lies primarily in a longitudinal axis, the efferent limb of a stoma created by the Jaboulay pyloroplasty may be acutely angulated causing gastric emptying to be impaired.
NUTRITIONAL CONSEQUENCES OF VAGOTOMY AND PYLOROPLASTY
Failure to maintain weight is a common problem after all gastric operations including truncal vagotomy-pyloroplasty. The cause for weight loss is probably multifactorial. Unlike high, subtotal gastrectomy where reduced food intake is related to reduction in size of the gastric reservoir, limitation of eating after any type of vagotomy results from early satiety due to the loss of receptive relaxation of the stomach. This reflex is usually regained, but early satiety and reduced caloric intake may remain a persistent problem after vagotomy. Dumping after truncal vagotomy-pyloroplasty can be sufficiently distressing to cause a patient to severely restrict his food intake to avoid producing these symptoms. Intestinal hurry and episodic diarrhea associated
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with vagotomy or the diarrhea associated with dumping may be severe enough to contribute to steatorrhea, creatorrhea, and ultimate weight loss. After vagotomy or gastric resection of any type some patients develop an intolerance for dairy products. This problem may be due to a relative lactose deficiency as a consequence of the increased rate in which liquids leave the stomach after operation. Studies show reduced production of pancreatic enzyme after truncal vagotomy-pyloroplasty. In conjunction with decreased transit time, this does not allow adequate mixing of enzyme and food to permit satisfactory absorption. 41 • 61 There is recent convincing evidence for the existence of an enteropancreatic reflex that mediates the early pancreatic enzyme response to intestinal stimulants. 60 Loss of this reflex after vagotomy of the small bowel also may contribute to improper mixing of food and pancreatic enzymes and malabsorption observed after truncal vagotomy-pyloroplasty. Following truncal vagotomy-pyloroplasty, defects in the absorption of iron, folate, vitamin B12 , and calcium, if they occur, are usually mild. 68 Occasionally they can be severe, and in the presence of steatorrhea, calcium loss can be large. Among 66 patients undergoing truncal vagotomy-pyloroplasty and followed for 10 to 16 years in our clinic, only one patient had anemia on the basis of malabsorption.
OTHER PHYSIOLOGIC COMPLICATIONS OF VAGOTOMY AND PYLOROPLASTY Epigastric fullness, vomiting of food, dyspepsia, or heartburn occurred in approximately 10 per cent of patients after vagotomy and pyloroplasty in most series. 11 • 23 · 38· 55 Epigastric fullness that occurs immediately after operation owing to loss of receptive relaxation is usually self-limiting. Prolonged epigastric fullness and vomiting of food are more likely the consequences of gastric stasis due to an unsatisfactory pyloroplasty. Construction of a new drainage procedure may eventually be necessary. Dyspepsia or heartburn may herald recurrent ulcer or they may represent symptoms of reflux that existed preoperatively. The method of treatment depends on the severity of reflux. Bilious vomiting occurs in 1.852 to 7.5 per centl 9 of patients after truncal vagotomy and pyloroplasty. This is less than after subtotal gastrectomy (10.1 per cent), vagotomy-antrectomy (12. 9 per cent), or vagotomygastroenterostomy (18.5 per cent). 19 Some patients with bilious vomiting have painful alkaline reflux gastritis, reflux esophagitis, or both. The presence of gastroesophageal reflux requires that an antireflux procedure be performed. It is more difficult to determine whether a Roux-en-Y diversion procedure is also required. Before performing a diversionary procedure it is recommended that the patient have weight loss, constant epigastric pain, endoscopic gastritis, and objective evidence of duodenogastric reflux. It is recommended that the antrum be removed before performing the Roux-en-Y drainage operation. Dumping occurs in approximately 20 per cent of patients after truncal vagotomy-pyloroplasty. In most patients these symptoms are easily con-
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trolled by reclining after eating and minor diet alterations. An occasional patient may have disabling dumping requiring remedial operation. Diarrhea occurs in one half of the patients with dumping symptoms 57 and is related to the pyloroplasty and rapid gastric emptying. Diarrhea related to vagotomy can be of three types: 33 transitory diarrhea that clears within a few weeks of operation, episodic diarrhea that is explosive and unpredictable with periods of normal bowel movements in between, and continuous diarrhea with multiple, loose watery stools. Episodic diarrhea occurs more often than the continuous form. 6 Diarrhea occurs with about the same frequency after truncal vagotomy-pyloroplasty as it does after any operation in which the pylorus is nonfunctioning and truncal vagotomy has been performed. 19 The frequency and severity of postvagotomy diarrhea is less after selective vagotomy than after truncal vagotomy, 11 • 38· 57 and the severe incapacitating varieties of postvagotomy diarrhea are virtually eliminated by parietal cell vagotomy. The severity of dumping symptoms and diarrhea frequently improve with time. 33 The long-term results of truncal vagotomy-pyloroplasty from the Mayo Clinic indicated that gastrointestinal disturbance, including diarrhea, dumping, bilious vomiting, bloating, dysphagia, or postprandial pain, occurred in 40 per cent of all patients and were significant in 5.8 per cent. 5°
THERAPY FOR PHYSIOLOGIC COMPLICATIONS
Complications occur less frequently after truncal vagotomy-pyloroplasty than after resectional surgery and Billroth II anastomosis or truncal vagotomy-gastroenterostomy because of the absence of afferent and efferent limbs of a gastrojejunostomy that may become partially or totally obstructed and require reoperation. Even the symptoms of dumping, diarrhea, and bilious vomiting are less severe after truncal vagotomy-pyloroplasty than after other forms of therapy. These symptoms can usually be managed medically and in our experience remedial surgery after truncal vagotomypyloroplasty is rarely required. Before a patient is considered a candidate for reconstructive operation for dumping, he is challenged with a cocktail of 150 ml of 50 per cent glucose and 100 ml of half milk and half cream. This is administered through a tube without the patient's knowledge at the conclusion of a gastric analysis. If the symptoms of dumping are not reproduced, it is unlikely the patient is a candidate for operation. One advantage of gastroenterostomy over pyloroplasty is that if dumping does occur after gastroenterostomy it can be successfully treated by dismantling the anastomosis. No further drainage procedure need be done in the absence of pyloric stenosis; the stomach will have regained its intrinsic motility and will empty satisfactorily. Although pyloroplasty was likened to an incurable disease, 70 we have successfully treated dumping by restoration of the pylorus after a HeinekeMikulicz pyloroplasty. The pylorus is opened transversely and closed longitudinally so that the pyloric musculature is reapproximated. 17• 42 Reoperation after a Finney pyloroplasty or Jaboulay gastroduodenostomy is more
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difficult. 30 • 42 If reconstitution of the pylorus is unsuccessful, antral resection and Roux-en-Y gastrojejunostomy can be performed. For patients with postvagotomy diarrhea following truncal vagotomy-pyloroplasty without dumping, a reversed jejunal segment in the upper jejunum has been recommended. 34 Antrectomy with a Roux-en-Y limb is a useful operation for patients who meet the criterion for alkaline reflux gastritis mentioned previously. 22 For patients with dumping as well as alkaline reflux gastritis or postvagotomy diarrhea, the Roux-en-Y gastrojejunostomy plus a reversed segment of a jejunum between the stomach and Roux-en-Y limb may be beneficial, 22 although this is not universally successful. 45 Patients with alkaline or acid reflux esophagitis require a fundoplication operation with or without one of the preceding operative procedures. These complicated remedial operations are not without risk, as Martin noted, 42 and may best be reserved until the simpler procedure of reconstruction of the pylorus has been tried.
GALLSTONES Johnson 31 reported dilatation of the gallbladder following truncal vagotomy and suggested a relationship between gallbladder pathology and its size. There are conflicting reports concerning the relationship of gallstone formation and the effects of truncal vagotomy. Total vagotomy has been reported to increase the incidence of gallstones by 16 to 24 per cent. 26 It has been suggested that increased gallstone formation after vagotomy is due to an increase in the lithogenic index of bile. There is now significant evidence that the lithogenicity of bile does not increase after vagotomy. 47 · 58 · 61 Ihasz 26 reported an increased frequency of gallstones after truncal vagotomy in patients who developed dilatation and noncontractility of the gallbladder, whereas selective vagotomy was not associated with this sequence of events. Increased resistance to flow through the sphincter of Oddi, as was reported after truncal vagotomy-pyloroplasty in the prairie dog, 51 may cause dilatation and loss of compliance of the gallbladder with eventual gallstone formation. Gallbladder dilatation and bile stasis may be related to precipitation of solid pigment material in bile, but this is probably not the only factor related to gallstone formation after truncal vagotomy.
RECURRENT ULCER In a review of the literature, the long-term recurrence rate after truncal vagotomy-pyloroplasty and selective vagotomy-pyloroplasty ranged from 5 to 15 per cent. In one study the recurrence rate was 27.3 per cent. 62 In some of the same studies the recurrence rate after truncal vagotomy was unaffected by the type of pyloroplasty performed. 50• 66 The recurrence rate after selective vagotomy has been reported lower after Finney pyloroplasty than after Heineke-Mikulicz pyloroplasty.·56 • 59 The location of recurrent ulceration following truncal vagotomy-pyloroplasty can be in the stomach, the duodenum, or at the pyloroplasty.
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Burge5 and Tanner64 reported that ulcers recurred most often in the stomach. In each of Burge's patients, there was an associated pyloroduodenal stenosis. In their opinion antral stasis and antral hyperfunction due to incomplete drainage of the stomach contributed to the recurrence of gastric ulcer when pyloroplasty complemented vagotomy. Sawyers56 reported that the recurrence rate 6 months to 4 years after selective vagotomy and a Finney pyloroplasty was similar to that of truncal vagotomy and antrectomy. He attributed the low recurrence rate to improved gastric emptying after the larger and more dependent Finney pyloroplasty and to a more complete gastric vagotomy owing to the greater operative precision required to perform selective vagotomy. Reoperation for recurrent ulcer after truncal vagotomy-pyloroplasty is performed for intractability or hemorrhage in 90 per cent of patients and obstruction or perforation in 10 per cent. 20 Before reoperation for recurrent ulcer after truncal vagotomy-pyloroplasty, it is essential to exclude the diagnosis of a gastrinoma. Revagotomy alone is perhaps the most unsatisfactory operative choice for treatment of recurrent ulcer after vagotomy and pyloroplasty. On the other hand, in patients with elevated basal acid secretion, maximal acid secretion, or a clear-cut vagal response to insulin, revagotomy alone is indicated. In carefully selected cases, one is likely to find the major posterior vagus trunk intact. In a prospective, random study, not only was the recurrence rate higher after truncal vagotomy-pyloroplasty than after truncal vagotomyantrectomy, but we found that the number of positive insulin responses after truncal vagotomy-pyloroplasty was significantly greater than after truncal vagotomy-antrectomy. 35 These data suggest to us that antrectomy compensated for continued vagal function by reducing the synergism between the neural and hormonal phases of gastric secretion. In our opinion, antrectomy provided protection from an incomplete vagotomy and is the operation of choice for recurrent ulcer after truncal vagotomy-pyloroplasty. Revagotomy alone is acceptable only when a major nerve trunk is found that was clearly not sectioned previously. This view is supported by Kennedy's 39 report of 142 patients with recurrent ulcers. His re-recurrent ulcer rate was 16 per cent after revagotomy alone, 6 per cent after gastric resection alone, and 1.4 per cent after revagotomy and antrectomy.
MORTALITY OF VAGOTOMY AND PYLOROPLASTY IN ELECTIVE SURGERY
The ultimate complication of operation is death. In the study referred to above, 36 the mortality rate was 2.1 per cent. One patient developed a leak at the pyloroplasty site and a second patient died from a pulmonary embolus. The mortality rate associated with truncal vagotomy-pyloroplasty performed under elective conditions should be in the vicinity of 1. 0 per cent. 13 One objective that stimulated the development of truncal vagotomypyloroplasty was to reduce the mortality rate of gastric surgery for duodenal ulcers. The mortality rate for subtotal gastrectomy by experienced surgeons
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was 3.5 per cent63 when truncal vagotomy-pyloroplasty was introduced; however, the mortality rate for elective gastric resection has been reduced, equivalent to that achieved by truncal vagotomy-pyloroplasty, 48 and the newest surgical treatment, parietal cell vagotomy, has an associated mortality rate of less than 0. 5 per cent.
SUMMARY The development of truncal vagotomy-pyloroplasty provided an opportunity to study gastric physiology altered by gastric operations. These investigations were particularly valuable in demonstrating the importance of the vagi in the control of acid secretion in patients with duodenal ulcer. Truncal vagotomy-pyloroplasty is a safe procedure and under elective conditions the mortality rate should be 1 per cent or less. Vagotomy and pyloroplasty are associated with technical complications, the most important being rupture of the esophagus, splenic injury, leak at the pyloroplasty, and intra-abdominal bleeding. This operation can also be associated with other complications including epigastric fullness, dysphagia, vomiting of food, bilious vomiting, dumping, and diarrhea. These complications may lead to malabsorption and significant weight loss. Some complications, particularly dumping, bilious vomiting, and diarrhea result from loss of the pylorus, the major function of which is to meter small aliquots of gastric contents into the duodenum. The long-term recurrence rate of ulcer after truncal vagotomy-pyloroplasty is 5 to 15 per cent and is high in comparison with other possible surgical options for the treatment of peptic ulcer disease. The recurrent ulcer rate after selective vagotomy and Finney pyloroplasty may be less than after truncal vagotomy-pyloroplasty. Parietal cell vagotomy without drainage also has a recurrence rate of 5 to 10 per cent at 10 years when performed properly. The operation is preferred by many, however, because it has few technical complications, it is associated with the lowest mortality rate of any operation for peptic ulcer, and most important, physiologic complications of truncal vagotomy-pyloroplasty resulting from loss of the pylorus are virtually eliminated. Truncal vagotomy-pyloroplasty is no longer the dominant operation in the field of gastric surgery but, in spite of its shortcomings, will continue to be a widely used operation.
REFERENCES l. Amdrup, E., and Jensen, H. E.: Selective vagotomy of the parietal cell mass preserving innervation of the undrained antrum. Gastroenterology, 59:522-527, 1970. 2. Aust, J. B.: A new technique for pyloroplasty. Surgery, 53:309-310, 1963. 3. Ballinger, W. F., II, and Solanke, T. F.: Serosal patch pyloroplasty. Surg. Gynecol. Obstet., 122:1283-1288, 1966. 4. Braash, J. W., Sala, L. E., Ellis, F. H., eta!.: Parietal cell vagotomy: Its effect on lower esophageal sphincter function. Arch. Surg., 115:699-701, 1980.
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5. Burge, H. W.: Vagal nerve section in chronic duodenal ulcer. Ann. R. Coli. Surg. Engl.. 26:231-244, 1960. 6. Cox, A. G.: Vagotomy on Trial. London, William Heinemann Medical Books, Ltd., 1973, page 70. 7. Cox, A. G., Spencer, J., and Tinker, J.: Clinical results reviewed. In After Vagotomy. New York, Appleton-Century-Crofts, 1969, pages 119-130. 8. Csendes, A., 0ster, M., Brandsborg, 0., et a!.: The effect of vagotomy on human gastroesophageal sphincter pressure in the resting state and following increases in intraabdominal pressure. Surgery, 85:419-424, 1979. 9. Csendes, A., 0ster, M., Mpller, J., eta!.: The effect of extrinsic denervation of the lower part of the esophagus on resting and cholinergic stimulated gastroesophageal sphincter in man. Surg. Gynecol. Obstet., 148:375-399, 1978. 10. Csendes, A., 0ster, M., Mpller, J. T., eta!.: Gastroesophageal reflux in duodenal ulcer patients before and after vagotomy. Ann. Surg., 188:804-808, 1978. 11. De Miguel, J.: Late results of bilateral selective vagotomy and pyloroplasty for duodenal ulcer: 5-9 year follow-up. Br. J. Surg., 61:264-270, 1974. 12. Dragstedt, L. R., and Owens, F. M., Jr.: Supradiaphragmatic section of the vagus nerves in treatment of duodenal ulcer. Proc. Soc. Exp. Bioi. Med., 53:152-154, 1943. 13. Eisenberg, M. M., Woodward, E. R., Carson, T. J., et a!.: Vagotomy and drainage procedure for duodenal ulcer: The results of ten years' experience. Ann. Surg., 170:317328, 1969. 14. Exner, A.: Ein neues Operationsverfahren bei tabischen Crises gastriques. Dtsch. Z. Chir., 111:576, 1911. 15. Finney, J. M. T.: A new method of pyloroplasty. Johns Hopkins Bull., 13:155-161, 1902. 16. Franksson, C.: Selective abdominal vagotomy. Acta Chir. Scan d., 96:409-412, 1948. 17. Frederiksen, H. J. B., Staehr Johansen, T., and Christiansen, P. M.: Post vagotomy diarrhea and dumping treated with reconstruction of the pylorus. Scand. J. Gastroenterol., 15:245-248, 1980. 18. Fronmiiller, F.: Operation der Pylorusstenose (Erlangen dissertation). Furth, Schroder, 1886, pages 1-19. 19. Goligher, J. C., Feather, D. B., Hal, R., eta!.: Several standard elective operations for duodenal ulcer: Ten to 16 year clinical results. Ann. Surg., 189:18-24, 1979. 20. Griffin, W. 0.: Recurrent ulcer. In After Vagotomy. New York, Appleton-Century-Crofts, 1969, page 192. 21. Griffith, C. A., and Harkins, H. N.: Partial gastric vagotomy: An experimental study. Gastroenterology, 32:96-102, 1957. 22. Herrington, J. L., and Sawyers, J. L.: Remedial operations. In Nyhus, L. M., and Wastell, C. (ed.): Surgery of the Stomach and Duodenum. Edition 3. Boston, Little, Brown & Company, 1977, page 545. 23. Hojlund, B., and Madsen, P.: The clinical results of selective vagotomy and pyloroplasty 6-9 years later. Dan. Med. Bull., 27:164-167, 1980. 24. Holle,. F., and Bauer, H.: Selective proximal vagotomy with pyloroplasty in surgery of gastroduodenal ulcer. In Nyhus, L. M., and Wastell, C. (ed.): Surgery of the Stomach and Duodenum. Edition 3. Boston, Little, Brown & Company, 1977, pages 329-338. 25. Horsley, J. S.: Surgery of the Stomach and Duodenum. St. Louis, C. V. Mosby Co., 1933. 26. Ihasz, M., and Griffith, C. A.: Gallstones and vagotomy. Am. J. Surg., 141:48-50, 1981. 27. Jaboulay, M.: LaGastro-enterostomie. La Jejuno-duodenostomie. La Resection du pylore. Arch. Prov. Chir., 1:11-12, 1892. 28. Jaboulay, M.: Inconvenients de Ia gastro-enterostomie simple, et moyons d'y remedier. Prov. Med., 6:63, 1894. 29. Jackson, R. G.: Anatomic study of the vagus nerves with a technique of transabdominal selective gastric vagus resection. Arch. Surg., 57:333-352, 1948. 30. Jensen, H. E., Damgaard Nielsen, S. A., and Balslev, I.: Operative technique for recurrent ulcer of vagotomy and Jaboulay gastroduodenostomy. Acta Chir. Scan d., 144:499-501, 1978. 31. Johnson, F. E., and Boyden, E. A.: The effect of double vagotomy on the motor activity of the human gallbladder. Surgery, 32:591-601, 1952. 32. Johnston, D., and Wilkinson, A. R.: Highly selective vagotomy without a drainage procedure in the treatment of duodenal ulcer. Br. J. Surg., 57:289-295, 1970.
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33. Johnston, I. D. A.: The management of side effects of surgery for peptic ulceration. Br. J. Surg., 57:787-790, 1970. 34. Jordan, G. L., Jr.: Surgical management of postgastrectomy problems. Arch. Surg., 102:251-259, 1971. 35. Jordan, P. H., Jr.: A followup report of a prospective evaluation of vagotomy-pyloroplasty and vagotomy-antrectomy for treatment of duodenal ulcer. Ann. Surg., 180:259-264, 1974. 36. Jordan, P. H., Jr., and Condon, R. E.: A prospective evaluation of vagotomy-pyloroplasty and vagotomy-antrectomy for treatment of duodenal ulcer. Ann. Surg., 172:547-560, 1970. 37. Judd, E. S.: Excision of ulcer of duodenum. Journal-Lancet, 42:381, 1922. 38. Kennedy, T., Connell, A. M., Love, A. G. H., eta!.: Selective or truncal vagotomy? Five year results of a double blind, randomized controlled trial. Br. J. Surg., 60:944948, 1973. 39. Kennedy, T., and Roger Green, W. E.: Stomal and recurrent ulceration: Medical or surgical management. Am. J. Surg., 139:18-21, 1980. 40. Latarjet, A.: Resection des nerfs de l'estomac. Technique operatoire. Resultats cliniques. Bull. Acad. Med., 87:681, 1922. 41. Malagelada, J. R., Go, V. L. W., and Summerskill, W. H. J.: Altered pancreatic and biliary function after vagotomy and pyloroplasty. Gastroenterology, 66:22-27, 1974. 42. Martin, C. J., and Kennedy, T.: Reconstruction of the pylorus. World J. Surg., 6:221225, 1982. 43. Mazur, J. M., Skinner, D. B. Jones, E. L., eta!.: Effect of transabdominal vagotomy on the human gastroesophageal high pressure zone. Surgery, 73:818-822, 1973. 44. Mikulicz, J.: Zur operativen behandlung des stenosirenden Magengeschwiires. Arch. Klin. Chir., 37:79-90, 1888. 45. Miranda, R., Steffes, B., O'Leary, J.P., eta!.: Surgical treatment of the post-gastrectomy dumping syndrome. Am. J. Surg., 139:40-43, 1980. 46. Moschel, D. M., Walske, B. R., and Neumeyer, F.: A new technique of pyloroplasty. Surgery, 44:813-814, 1958. 47. Matson, R. W.: Bile acid pool size and biliary lipid composition before and after truncal vagotomy in man .. Gastroenterology, 78:1226, 1980. 48. Ochsner, A., Zehnder, P. P., and Trammell, S. W.: The surgical treatment of peptic ulcer: A critical analysis of results from subtotal gastrectomy and from vagotomy plus partial resection. Surgery, 67:1017-1028, 1970. 49. O'Sullivan, G. C., De Meester, T. R., Smith, R. B., eta!.: Twenty-four hour pH monitoring of esophageal function: Its use in evaluation in symptomatic patients after truncal vagotomy and gastric resection or drainage. Arch. Surg., 116:581-590, 1981. 50. Pemberton, J. H., and Van Heerden, J. A.: Vagotomy and pyloroplasty in the treatment of duodenal ulcer: Long term results. Mayo Clin. Proc., 55:10-18, 1980. 51. Pitt, H.: Comments. Am. J. Surg., 141:46, 1981. 52. Postlethwait, R. W.: Five year follow-up results of operations for duodenal ulcer. Surg. Gynecol. Obstet., 137:387-392, 1973. 53. Postlethwait, R. W., Kim, S. K., and Dillon, M. L.: Esophageal complications of vagot01:~y. Surg. Gynecol. Obstet., 128:481-488, 1969. 54. Richardson, M. H.: Three cases of pyloroplasty for stricture of the pylorus. Boston Med. Surg. J., 141:537-542, 1899. 55. Robb, J. V., Banks, S., Marks, I. N., eta!.: A comparison between selective vagotomy and truncal vagotomy with drainage in duodenal ulceration. S. Afr. Med. J., 47:13911396, 1973. 56. Sawyers, J. H., and Scott, H. W., Jr.: Antrectomy or pyloroplasty? A prospective study with selective gastric vagotomy. South. Med. J., 66:98-101, 1973. 57. Sawyers, J. L., Scott, H. W., Jr., Edwards, W. H., eta!.: Comparative studies of the clinical effects of truncal and selective gastric vagotomy. Am. J. Surg., 115:165-172, 1968. 58. Schaffer, E. A.: The effect of vagotomy on gallbladder function and bile composition in man. Ann. Surg., 195:413-418, 1982. 59. Siim, C., Lubkin, H. K. F., and Jensen, H. E.: Selective vagotomy and drainage for duodenal ulcers: A 10-13 year follow-up. Ann. Surg., 194:687-691, 1981.
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60. Singer, M. V., Solomon, T. E., Wood, J., eta!.: Latency of pancreatic enzyme response to intraduodenal stimulants. Am. J. Physiol., 238:G23-G29, 1980. 61. Smith, R. B., Edward, J. P., and Johnston, D.: Effect of vagotomy on exocrine pancreatic and biliary secretions in man. Am. J. Surg., 141:40--47, 1981. 62. Stempien, S. J., Dagradi, A. E., Lee, E. R., eta!.: Status of duodenal ulcer patients ten years or more after vagotomy-pyloroplasty (V-P). Am. J. Gastroenterol., 56:99-108, 1971. 63. Strauss, A. A., Strauss, S. F., Schwartz, A. H., eta!.: Results of subtotal gastrectomy for gastric and duodenal ulcer since 1917. J.A.M.A., 149:1095-1101, 1952. 64. Tanner, N. G.: Drainage operations for vagotomy. Proc. R. Soc. Med., 60:221-223, 1967. 65. Temple, J. G., Goodall, R. J. R., Hay, D. J., eta!.: Effect of highly selective vagotomy upon the lower esophageal sphincter. Gut, 22:368-370, 1981. 66. Thompson, B. W., and Read, R. C.: Long term randomized, prospective comparison of Finney and Heineke-Mikulicz pyloroplasty in patients having vagotomy for peptic ulceration. Am. J. Surg., 129:78-81, 1975. 67. Wangensteen, 0. H.: A critique of operations for peptic ulcer. Postgrad. Med., 23:466483, 1958. 68. Wastell, C.: Long term clinical and metabolic effects of vagotomy with either gastrojejunostomy or pyloroplasty. Ann. R. Coli. Surg. Engl., 45:193-211, 1969. 69. Weinberg, J. A., Stempien, S. J., Movius, H. J., eta!.: Vagotomy and pyloroplasty in the treatment of duodenal ulcer. Am. J. Surg., 92:202-207, 1956. 70. Williams, J. A.: Surgery of the Stomach and Duodenum. Edition 3. Boston, Little, Brown & Company, 1977, page 274. 71. Williams, J. A., and Woodward, D. A. K.: The effect of subdiaphragmatic vagotomy on function of the gastro-esophageal sphincter. SURG. CLIN. NORTH AM., 47:1341-1344, 1967. 72. Wirthlin, L. S., and Malt, R. A.: Accidents of vagotomy. Surg. Gynecol. Obstet., 135:913916, 1972. 73. Wiilfler, A.: Gastro-enterostomie. Zentralbl. Chir., 45:705-708, 1881. (Dr. Jordan) 1200 Moursund Avenue Houston, Texas 77030
Complications of Vagotomy and Pyloroplasty
Mark E. Skellenger, M.D.,* and Paul H. Jordan, Jr., M.D., F.A.C.S. t
The combination of truncal vagotomy or selective vagotomy and pyloroplasty is a synthesis of two operations used primarily for treatment of duodenal ulcers and less frequently for treatment of gastric ulcers. In the absence of pyloric obstruction the only necessity for combining pyloroplasty with vagotomy is to compensate for gastric stasis, a frequent complication of total gastric vagotomy. Vagotomy and pyloroplasty were developed independently, and each has its own historical background and specific complications.
HISTORICAL BACKGROUND OF PYLOROPLASTY
A discussion of pyloroplasty must include gastroenterostomy since this was the first gastric drainage operation described. Gastroenterostomy was introduced by Wolfler73 in 1881 to bypass a carcinoma at the pylorus. By 1900 this procedure was applied to cases of nonmalignant inflammatory strictures of the pylorus. It was popularized for this use by Berkley Moynihan and W. J. Mayo and remained in vogue for nearly 4 decades. Pyloroplasty was originally performed by Reineke and described by his student, Fronmiiller, 18 in 1886. Reineke's first patient had severe gastric outlet obstruction due to a pyloric mass, which was a duodenal ulcer penetrating into the pancreas. His operation consisted of a longitudinal incision involving the distal stomach, pylorus, and proximal duodenum. This opening was closed transversely (Fig. 1). Mikulicz44 objected to gastroenterostomy because it did not permit access to the disease in the pylorus. Eleven months later he described an *Instructor in Surgery, Cora and Webb Mading Department of Surgery, Baylor College of Medicine and the Veterans Administration Medical Center, Houston, Texas tProfessor of Surgery, Cora and Webb Madii:tg Department of Surgery, Baylor College of Medicine and Veterans Administration Medical Center, Houston, Texas
Surgical Clinics of North America-Yo!. 63, No. 6, December, 1983
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JABOULAY
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Figure 1. The most common forms of gastric drainage procedures used in combination with vagotomy.
operation similar to that reported by Fronmiiller. He opened the pylorus of his first patient for hemorrhage and cauterized a posterior duodenal ulcer. The longitudinal opening was closed transversely using a double row of sutures. Because of the close temporal relationship between these two reports, the enlargement of the pylorus by this means carries the eponym, Reineke-Mikulicz pyloroplasty. Subsequently, various drainage procedures developed that, according to their originators, provided specific advantages over gastroenterostomy and Heineke-Mikulicz pyloroplasty. In 1899 Richardson 54 advocated resection of the anterior and lateral walls of the pyloroduodenal junction and primary reanastomosis when there was circumferential cicatrix in this area. In 1922 Judd, 37 disturbed by the number of jejunal ulcers that occurred after gastroenterostomy, excised the anterior wall of the pylorus, including the ulcer if possible, and performed a two-layer transverse closure. In 1933 Horsley25 excised the ulcer as part of a longitudinal incision of the pylorus. The incision was closed transversely. Other modifications of the HeinekeMikulicz pyloroplasty include those by Moschel, 46 Wangensteen, 67 Aust, 2 and Ballinger3 (Fig. 2). In 1956 Weinberg69 made a significant modification of the HeinekeMikulicz pyloroplasty. He used a one-layer closure of interrupted sutures. The major advantage of this procedure was that the amount of enfolded tissue that acts as a barrier to stasis was reduced to a minimum. Weinberg objected to gastroenterostomy because the abnormal continuity of the intestinal tract interfered with digestion. It resulted in regurgitation of
1169
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'
I
I
~ Judd-1922
Moschel-1958
Horsley-1933
JeJun~~P.yljs
,
.
'
~ Wangensteen-1958
Ballinger-1966
Figure 2. Some of the modifications of pyloroplasty less frequently used in combination with vagotomy.
jejunal contents into the stomach leading to diffuse inflammation of the gastric mucosa, antral hyperfunction, and anastomotic ulcerations. Other methods of gastric drainage include gastroduodenostomy (see Fig. 1) performed by Jaboulay27 in 1892 for the treatment of an obstructing malignant lesion of the pylorus. So that the patient would not vomit bile, he performed duodenojejunostomy in addition to gastroduodenostomy. Later he simplified the operation and performed gastroduodenostomy alone. 28 In 1902 Finney15 described a method of pyloroplasty that in effect was also a gastroduodenostomy, but the opening was enlarged by connecting the gastric and duodenal incisions before making the side-to-side anastomosis (see Fig. l.) The Weinberg modification of the Heineke-Mikulicz pyloroplasty is probably the most common procedure for gastric drainage. Nevertheless, it shares an undesirable consequence of all drainage procedures-that is, the problem of bypassing or destroying the pyloric sphincter mechanism responsible for metering small amounts of gastric contents into the duodenum.
HISTORICAL BACKGROUND OF VAGOTOMY Abdominal vagotomy was performed by Exner14 in 1911 for abdominal pain and vomiting associated with tabes dorsalis. In 1922 Latarjet40 reported the use of vagotomy in 24 patients, 6 of whom had peptic ulcer. He performed a complementary gastrojejunostomy in each patient to prevent gastric stasis. This operation was not widely accepted, and gastroenterostomy or subtotal gastric resection became the standard operation for duodenal ulcer.
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Dissatisfied with the high rate of ulcer recurrence after gastroenterostomy and the mortality and morbidity associated with subtotal gastric resection, Dragstedt introduced transthoracic truncal vagotomy in 1943. 12 The frequency with which gastric stasis and gastric ulcers developed led Dragstedt to modify his operation and to perform transabdominal truncal vagotomy combined first with gastrojejunostomy and later with pyloroplasty to facilitate gastric drainage. In 1948 Jackson 29 and Franksson, 16 feeling that it was unnecessary to perform total intra-abdominal vagotomy to reduce acid secretion, described selective vagotomy that also required a drainage procedure. Despite its theoretical advantages, this operation did not gain wide acceptance because it was difficult to demonstrate its superiority and it was more difficult to perform than truncal vagotomy. Finally, the concept of denervating only the acid-secreting portion of the stomach developed and was described by Griffith and Harkins. 21 This type of vagotomy, parietal cell vagotomy or one of a number of other synonyms, was performed first on patients by Holle. 24 He combined the operation with pyloroplasty but later Johnston 32 and Amdrup, 1 independently, performed parietal cell vagotomy without a drainage procedure. Parietal cell vagotomy preserved antral function, which allowed for almost normal gastric emptying. Diarrhea, dumping, and bilious vomiting that complicated other types of vagotomy requiring a drainage operation were virtually eliminated.
OPERATIVE COMPLICATIONS OF VAGOTOMY The immediate postoperative morbidity after vagotomy involved complications common to all major intra-abdominal surgery. 35• 36 Major operative complications related to vagotomy occurred in 53 of 1096 patients in one series. 72 In this study, perforation of the esophagus was reported in 5 patients. 72 Death occurred in one patient in whom perforation was unrecognized. In a study of 4414 patients who underwent vagotomy, 53 3 of 24 patients with perforations died. The perforation was unrecognized at the original operation in 2 of the 3 patients. We have experienced esophageal perforation but have always recognized the complication and successfully repaired the esophagus. In our opinion, this complication is usually the consequence of blind finger dissection of the esophagus in obese individuals, in patients with portal hypertension, or in those with periesophageal inflammation secondary to esophagitis. Since we have begun to perform primarily selective vagotomy or parietal cell vagotomy, we have not encountered the complication and attribute this to the precise dissection that these operations demand. Splenic rupture (2. 7 per cent)72 was once considered an inconsequential complication of vagotomy except for the possibility of a subphrenic abscess. Incidental splenectomy is now a recognized complication in children and perhaps in adults as well. Therefore, every effort to avoid splenic injury should be taken.
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Figure 3. A, Severe dysphagia developed in this patient after vagotomy. The esophagogram gave the appearance of classic achalasia. The resistance of the lower esophageal sphincter was so great that initially it was impossible to pass safely a dilator of any size. B, In the early phase of recovery, the pressure of the lower esophageal sphincter was 60 mm Hg. The lower esophageal sphincter relaxed on swallowing, but the pressure did not fall to the intragastric pressure level. The patient recovered in nine days.
Bleeding after vagotomy, requiring operation, ranged from 0.3 per cent to 1 per cent and was a major cause of death associated with vagotomy. Bleeding occurred from the edge of the left lobe of the liver if mobilized, from the esophagus, from a transected vessel accompanying the vagus nerve, from varices, or from the splenic bed following splenectomy. Chylous ascites has occasionally been reported to occur following vagotomy. Dysphagia is a common problem after vagotomy. We concur with Cox7 that mild dysphagia occurs in about 20 per cent of patients following vagotomy. The onset begins after operation with the ingestion of solid foods. It is transient and usually disappears within two weeks. In most patients, dysphagia disappears spontaneously or after a simple bougienage. Routine roentgenograms almost never demonstrate any abnormalities. The cause of mild dysphagia may be due to operative trauma and edema of the lower esophagus. Dysphagia of consequence occurs in 1 to 2 per cent of patients treated by vagotomy. The onset may be early or months after operation. More troublesome dysphagia may be due to hematoma, fibrosis, periesophageal granuloma, injury and possible denervation of the lower esophagus. These patients usually can be satisfactorily managed by one or more esophageal dilatations. We have reoperated on only two patients after vagotomy because of dysphagia. Both patients had chronic periesophageal inflammatory reaction, one of which was thought to be a suture granuloma. These patients differ from those that appear as achalasia in that they also have odynophagia and their motility studies demonstrate sphincter relaxation with deglutition. Occasionally a patient becomes dysphagic; and esophageal roentgenograms suggest a classic picture of achalasia that did not exist preoperatively. (Fig. 3). High resistance at the esophagogastric junction can prevent endoscopy and necessitate several dilatations before the patient becomes asymptomatic. Such tightness of the sphincter is not characteristic of achalasia. This problem has been associated with transthoracic vagotomy more often than with transabdominal vagotomy.
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Dysphagia after vagotomy has also been attributed to reflux esophagitis, esophageal stricture, or both. The factors responsible for gastroesophageal reflux after vagotomy are not completely understood. Mobilization and loss of the normal tethering mechanism of the gastroesophageal junction that permit it to move into the mediastinum and escape the influence of positive intra-abdominal pressure have been suggested as causes. Loss of lower esophageal sphincter tone was proposed in one study performed two weeks after truncal vagotomy-pyloroplasty. 71 There are several studies, however, demonstrating that the lower esophageal sphincter pressure is unaltered by any type of vagotomy. 4• 8• 9•65 Evidence accumulating from our own service suggests that gastroesophageal reflux recognized after vagotomy may have been present but unrecognized preoperatively. This view is shared by others 10• 43 • 49 and indicates the need for careful evaluation prior to operation for duodenal ulcer.
OPERATIVE COMPLICATIONS OF PYLOROPLASTY
Pyloroplasty is performed to overcome gastric stasis caused by vagotomy. A major complication of pyloroplasty, therefore, is its failure to permit adequate gastric drainage. Several modifications of pyloroplasty were specifically made in an effort to avoid this complication. Of all the modifications of the Heineke-Mikulicz pyloroplasty, there seems to be little advantage of one over the other except for the single-layer closure advocated by Weinberg. Even so, in a prospective studl6 of truncal vagotomy and Heineke-Mikulicz pyloroplasty there was stomal dysfunction in 7 of 94 patients. Reoperation was required in 2 patients. If there is excessive inflammation at the pylorus, a Finney pyloroplasty, a Jaboulay gastroduodenostomy, or a gastroenterostomy may be preferable. If the antral portion of the stomach lies transversely, any of these alternatives are satisfactory. If the stomach lies primarily in a longitudinal axis, the efferent limb of a stoma created by the Jaboulay pyloroplasty may be acutely angulated causing gastric emptying to be impaired.
NUTRITIONAL CONSEQUENCES OF VAGOTOMY AND PYLOROPLASTY
Failure to maintain weight is a common problem after all gastric operations including truncal vagotomy-pyloroplasty. The cause for weight loss is probably multifactorial. Unlike high, subtotal gastrectomy where reduced food intake is related to reduction in size of the gastric reservoir, limitation of eating after any type of vagotomy results from early satiety due to the loss of receptive relaxation of the stomach. This reflex is usually regained, but early satiety and reduced caloric intake may remain a persistent problem after vagotomy. Dumping after truncal vagotomy-pyloroplasty can be sufficiently distressing to cause a patient to severely restrict his food intake to avoid producing these symptoms. Intestinal hurry and episodic diarrhea associated
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with vagotomy or the diarrhea associated with dumping may be severe enough to contribute to steatorrhea, creatorrhea, and ultimate weight loss. After vagotomy or gastric resection of any type some patients develop an intolerance for dairy products. This problem may be due to a relative lactose deficiency as a consequence of the increased rate in which liquids leave the stomach after operation. Studies show reduced production of pancreatic enzyme after truncal vagotomy-pyloroplasty. In conjunction with decreased transit time, this does not allow adequate mixing of enzyme and food to permit satisfactory absorption. 41 • 61 There is recent convincing evidence for the existence of an enteropancreatic reflex that mediates the early pancreatic enzyme response to intestinal stimulants. 60 Loss of this reflex after vagotomy of the small bowel also may contribute to improper mixing of food and pancreatic enzymes and malabsorption observed after truncal vagotomy-pyloroplasty. Following truncal vagotomy-pyloroplasty, defects in the absorption of iron, folate, vitamin B12 , and calcium, if they occur, are usually mild. 68 Occasionally they can be severe, and in the presence of steatorrhea, calcium loss can be large. Among 66 patients undergoing truncal vagotomy-pyloroplasty and followed for 10 to 16 years in our clinic, only one patient had anemia on the basis of malabsorption.
OTHER PHYSIOLOGIC COMPLICATIONS OF VAGOTOMY AND PYLOROPLASTY Epigastric fullness, vomiting of food, dyspepsia, or heartburn occurred in approximately 10 per cent of patients after vagotomy and pyloroplasty in most series. 11 • 23 · 38· 55 Epigastric fullness that occurs immediately after operation owing to loss of receptive relaxation is usually self-limiting. Prolonged epigastric fullness and vomiting of food are more likely the consequences of gastric stasis due to an unsatisfactory pyloroplasty. Construction of a new drainage procedure may eventually be necessary. Dyspepsia or heartburn may herald recurrent ulcer or they may represent symptoms of reflux that existed preoperatively. The method of treatment depends on the severity of reflux. Bilious vomiting occurs in 1.852 to 7.5 per centl 9 of patients after truncal vagotomy and pyloroplasty. This is less than after subtotal gastrectomy (10.1 per cent), vagotomy-antrectomy (12. 9 per cent), or vagotomygastroenterostomy (18.5 per cent). 19 Some patients with bilious vomiting have painful alkaline reflux gastritis, reflux esophagitis, or both. The presence of gastroesophageal reflux requires that an antireflux procedure be performed. It is more difficult to determine whether a Roux-en-Y diversion procedure is also required. Before performing a diversionary procedure it is recommended that the patient have weight loss, constant epigastric pain, endoscopic gastritis, and objective evidence of duodenogastric reflux. It is recommended that the antrum be removed before performing the Roux-en-Y drainage operation. Dumping occurs in approximately 20 per cent of patients after truncal vagotomy-pyloroplasty. In most patients these symptoms are easily con-
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trolled by reclining after eating and minor diet alterations. An occasional patient may have disabling dumping requiring remedial operation. Diarrhea occurs in one half of the patients with dumping symptoms 57 and is related to the pyloroplasty and rapid gastric emptying. Diarrhea related to vagotomy can be of three types: 33 transitory diarrhea that clears within a few weeks of operation, episodic diarrhea that is explosive and unpredictable with periods of normal bowel movements in between, and continuous diarrhea with multiple, loose watery stools. Episodic diarrhea occurs more often than the continuous form. 6 Diarrhea occurs with about the same frequency after truncal vagotomy-pyloroplasty as it does after any operation in which the pylorus is nonfunctioning and truncal vagotomy has been performed. 19 The frequency and severity of postvagotomy diarrhea is less after selective vagotomy than after truncal vagotomy, 11 • 38· 57 and the severe incapacitating varieties of postvagotomy diarrhea are virtually eliminated by parietal cell vagotomy. The severity of dumping symptoms and diarrhea frequently improve with time. 33 The long-term results of truncal vagotomy-pyloroplasty from the Mayo Clinic indicated that gastrointestinal disturbance, including diarrhea, dumping, bilious vomiting, bloating, dysphagia, or postprandial pain, occurred in 40 per cent of all patients and were significant in 5.8 per cent. 5°
THERAPY FOR PHYSIOLOGIC COMPLICATIONS
Complications occur less frequently after truncal vagotomy-pyloroplasty than after resectional surgery and Billroth II anastomosis or truncal vagotomy-gastroenterostomy because of the absence of afferent and efferent limbs of a gastrojejunostomy that may become partially or totally obstructed and require reoperation. Even the symptoms of dumping, diarrhea, and bilious vomiting are less severe after truncal vagotomy-pyloroplasty than after other forms of therapy. These symptoms can usually be managed medically and in our experience remedial surgery after truncal vagotomypyloroplasty is rarely required. Before a patient is considered a candidate for reconstructive operation for dumping, he is challenged with a cocktail of 150 ml of 50 per cent glucose and 100 ml of half milk and half cream. This is administered through a tube without the patient's knowledge at the conclusion of a gastric analysis. If the symptoms of dumping are not reproduced, it is unlikely the patient is a candidate for operation. One advantage of gastroenterostomy over pyloroplasty is that if dumping does occur after gastroenterostomy it can be successfully treated by dismantling the anastomosis. No further drainage procedure need be done in the absence of pyloric stenosis; the stomach will have regained its intrinsic motility and will empty satisfactorily. Although pyloroplasty was likened to an incurable disease, 70 we have successfully treated dumping by restoration of the pylorus after a HeinekeMikulicz pyloroplasty. The pylorus is opened transversely and closed longitudinally so that the pyloric musculature is reapproximated. 17• 42 Reoperation after a Finney pyloroplasty or Jaboulay gastroduodenostomy is more
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difficult. 30 • 42 If reconstitution of the pylorus is unsuccessful, antral resection and Roux-en-Y gastrojejunostomy can be performed. For patients with postvagotomy diarrhea following truncal vagotomy-pyloroplasty without dumping, a reversed jejunal segment in the upper jejunum has been recommended. 34 Antrectomy with a Roux-en-Y limb is a useful operation for patients who meet the criterion for alkaline reflux gastritis mentioned previously. 22 For patients with dumping as well as alkaline reflux gastritis or postvagotomy diarrhea, the Roux-en-Y gastrojejunostomy plus a reversed segment of a jejunum between the stomach and Roux-en-Y limb may be beneficial, 22 although this is not universally successful. 45 Patients with alkaline or acid reflux esophagitis require a fundoplication operation with or without one of the preceding operative procedures. These complicated remedial operations are not without risk, as Martin noted, 42 and may best be reserved until the simpler procedure of reconstruction of the pylorus has been tried.
GALLSTONES Johnson 31 reported dilatation of the gallbladder following truncal vagotomy and suggested a relationship between gallbladder pathology and its size. There are conflicting reports concerning the relationship of gallstone formation and the effects of truncal vagotomy. Total vagotomy has been reported to increase the incidence of gallstones by 16 to 24 per cent. 26 It has been suggested that increased gallstone formation after vagotomy is due to an increase in the lithogenic index of bile. There is now significant evidence that the lithogenicity of bile does not increase after vagotomy. 47 · 58 · 61 Ihasz 26 reported an increased frequency of gallstones after truncal vagotomy in patients who developed dilatation and noncontractility of the gallbladder, whereas selective vagotomy was not associated with this sequence of events. Increased resistance to flow through the sphincter of Oddi, as was reported after truncal vagotomy-pyloroplasty in the prairie dog, 51 may cause dilatation and loss of compliance of the gallbladder with eventual gallstone formation. Gallbladder dilatation and bile stasis may be related to precipitation of solid pigment material in bile, but this is probably not the only factor related to gallstone formation after truncal vagotomy.
RECURRENT ULCER In a review of the literature, the long-term recurrence rate after truncal vagotomy-pyloroplasty and selective vagotomy-pyloroplasty ranged from 5 to 15 per cent. In one study the recurrence rate was 27.3 per cent. 62 In some of the same studies the recurrence rate after truncal vagotomy was unaffected by the type of pyloroplasty performed. 50• 66 The recurrence rate after selective vagotomy has been reported lower after Finney pyloroplasty than after Heineke-Mikulicz pyloroplasty.·56 • 59 The location of recurrent ulceration following truncal vagotomy-pyloroplasty can be in the stomach, the duodenum, or at the pyloroplasty.
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Burge5 and Tanner64 reported that ulcers recurred most often in the stomach. In each of Burge's patients, there was an associated pyloroduodenal stenosis. In their opinion antral stasis and antral hyperfunction due to incomplete drainage of the stomach contributed to the recurrence of gastric ulcer when pyloroplasty complemented vagotomy. Sawyers56 reported that the recurrence rate 6 months to 4 years after selective vagotomy and a Finney pyloroplasty was similar to that of truncal vagotomy and antrectomy. He attributed the low recurrence rate to improved gastric emptying after the larger and more dependent Finney pyloroplasty and to a more complete gastric vagotomy owing to the greater operative precision required to perform selective vagotomy. Reoperation for recurrent ulcer after truncal vagotomy-pyloroplasty is performed for intractability or hemorrhage in 90 per cent of patients and obstruction or perforation in 10 per cent. 20 Before reoperation for recurrent ulcer after truncal vagotomy-pyloroplasty, it is essential to exclude the diagnosis of a gastrinoma. Revagotomy alone is perhaps the most unsatisfactory operative choice for treatment of recurrent ulcer after vagotomy and pyloroplasty. On the other hand, in patients with elevated basal acid secretion, maximal acid secretion, or a clear-cut vagal response to insulin, revagotomy alone is indicated. In carefully selected cases, one is likely to find the major posterior vagus trunk intact. In a prospective, random study, not only was the recurrence rate higher after truncal vagotomy-pyloroplasty than after truncal vagotomyantrectomy, but we found that the number of positive insulin responses after truncal vagotomy-pyloroplasty was significantly greater than after truncal vagotomy-antrectomy. 35 These data suggest to us that antrectomy compensated for continued vagal function by reducing the synergism between the neural and hormonal phases of gastric secretion. In our opinion, antrectomy provided protection from an incomplete vagotomy and is the operation of choice for recurrent ulcer after truncal vagotomy-pyloroplasty. Revagotomy alone is acceptable only when a major nerve trunk is found that was clearly not sectioned previously. This view is supported by Kennedy's 39 report of 142 patients with recurrent ulcers. His re-recurrent ulcer rate was 16 per cent after revagotomy alone, 6 per cent after gastric resection alone, and 1.4 per cent after revagotomy and antrectomy.
MORTALITY OF VAGOTOMY AND PYLOROPLASTY IN ELECTIVE SURGERY
The ultimate complication of operation is death. In the study referred to above, 36 the mortality rate was 2.1 per cent. One patient developed a leak at the pyloroplasty site and a second patient died from a pulmonary embolus. The mortality rate associated with truncal vagotomy-pyloroplasty performed under elective conditions should be in the vicinity of 1. 0 per cent. 13 One objective that stimulated the development of truncal vagotomypyloroplasty was to reduce the mortality rate of gastric surgery for duodenal ulcers. The mortality rate for subtotal gastrectomy by experienced surgeons
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was 3.5 per cent63 when truncal vagotomy-pyloroplasty was introduced; however, the mortality rate for elective gastric resection has been reduced, equivalent to that achieved by truncal vagotomy-pyloroplasty, 48 and the newest surgical treatment, parietal cell vagotomy, has an associated mortality rate of less than 0. 5 per cent.
SUMMARY The development of truncal vagotomy-pyloroplasty provided an opportunity to study gastric physiology altered by gastric operations. These investigations were particularly valuable in demonstrating the importance of the vagi in the control of acid secretion in patients with duodenal ulcer. Truncal vagotomy-pyloroplasty is a safe procedure and under elective conditions the mortality rate should be 1 per cent or less. Vagotomy and pyloroplasty are associated with technical complications, the most important being rupture of the esophagus, splenic injury, leak at the pyloroplasty, and intra-abdominal bleeding. This operation can also be associated with other complications including epigastric fullness, dysphagia, vomiting of food, bilious vomiting, dumping, and diarrhea. These complications may lead to malabsorption and significant weight loss. Some complications, particularly dumping, bilious vomiting, and diarrhea result from loss of the pylorus, the major function of which is to meter small aliquots of gastric contents into the duodenum. The long-term recurrence rate of ulcer after truncal vagotomy-pyloroplasty is 5 to 15 per cent and is high in comparison with other possible surgical options for the treatment of peptic ulcer disease. The recurrent ulcer rate after selective vagotomy and Finney pyloroplasty may be less than after truncal vagotomy-pyloroplasty. Parietal cell vagotomy without drainage also has a recurrence rate of 5 to 10 per cent at 10 years when performed properly. The operation is preferred by many, however, because it has few technical complications, it is associated with the lowest mortality rate of any operation for peptic ulcer, and most important, physiologic complications of truncal vagotomy-pyloroplasty resulting from loss of the pylorus are virtually eliminated. Truncal vagotomy-pyloroplasty is no longer the dominant operation in the field of gastric surgery but, in spite of its shortcomings, will continue to be a widely used operation.
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