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Postvagotomy dysphagia
CASE REPORTS
PostvagotomyDysphagia Roy C. Orlando, MD, Chapel Hill, North Carolina Eugene M. Bozymski, MD, Chapel Hill, North Carolina
T h e incidence of d y s p h a g i a after v a g o t o m y has b e e n - r e p o r t e d as less t h a n 1 per cent to 36 per cent [I-4]. T h e highest rate occurs after transthoracic v a g o t o m y . Although a b n o r m a l i t i e s have been reported on x-ray, m a n o m e t r i c , and endocopic s t u d y in patients with p o s t v a g o t o m y dysphagia, no a g r e e m e n t exists as to the p r i m a r y cause. Our report is the first to detail a series of clinical, x-ray, a n d m a n o m e t r i c studies in a patient before, .during, a n d after the d e v e l o p m e n t of p o s t v a g o t o m y dysphagia.
vomiting, pain, and pyrosis were notably absent. Painless dysphagia persisted over the next few weeks. During this period, a cine esophagram demonstrated a smoothly tapered narrowing in the distal esophagus (Figure 2A) and delayed eml)tying of barium into the stomach. In contrast to the findings on preoperative manometric study, spontaneous synchronous contractions were observed in the body of the esophagus (Figure 2B and C), and the transit time was increased to 19.,5 seconds. Dysphagia completely cleared spontaneously six weeks after surgery. At that time, a cine esophagram (Figure 3A) showed the distal esophagus to be of normal caliber with no delay in the passage of
Case Report The patient (AF), a fifty-three year old man underwent transthoraeic vagotomy in January 1973 for recurrent peptic ulcer disease. Prior to that there was tm dysphagia or pyrosis, and contrast studies of the upper gastrointestinal tract demonstrated a normal esophagus. At endoscopy for evaluation of the ulcer, the esophagus appeared normal with no evidence of esophagitis or stricture. Using a triple lumen, constantly perfused system, preoperative esophageal manometry was performed prospectively to study the effect of transthoracic vagotomy. This motility study gave normal results. (Figure 1A and B.) The transit time, meas u r e d from onset of swallowing at the pharynx to the peak of a contraction 2 cm above the lower esophageal sphincter, was 15.5 seconds. Five days after transthoracic vagotomy, the patient experienced dysphagia during ingestion of his first solid meal. Postoperative From Division of Gastroenterology, Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina. This work was supported in part by USPHS grant AM-05503 and UNC Faculty Grant 1-0-160-4228 VB099. Reprint requests should be addressed to Dr Bozymski, Department of Medicine, Division of Gastroenterology. University of North Carolina School of Medicine. Chapel Hill, North Carolina 27514.
Volume 126, November 1973
mmH~
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Figure 1. A and B, pretransthoracic vagotomy. Note the normal resting pressure and the normal relaxation of the lower esophageal sphincter with swallows. Normal peristaltic activity is observed in the body of the esophagus.
683
Orlando and Bozymski
barium into the stomach. Spontaneous synchronous contractions were again noted on manometic study,and the lower esophageal sphincter was unchanged (Figure 3B and C); however, the transit time was 15.0 seconds, a return to the preoperative value. Ten weeks after vagotomy, a Hollander test, confirmed interruption of the vagal mechanism, with a basal acid output of 0.4 mEq/ hr and a maximal acid output of 0.7 mEq/hr after insulin. The lowest blood sugar level during this test was 26 rag/100 ml. Pertinent data from'these studies are presented in Table I. Comments In 1947 M o s e s [5] described the first case of p o s t v a g o t o m y dysphagia. Since t h a t time, vagal denervation of the distal esol~hagus has been cited as the most frequent cause (!f d y s p h a g i a after vagotomy [1]. O t h e r authors question this "neuroi
genie" m e c h a n i s m and support surgical injury of periesophageal tissue as the major etiologic factor [6, 7]. Postoperative esophagitis is a third cause of postvagotomy dysphagia which is reported to occur infrequently [l,4]. This factor was excluded in cur ease because of (I) the absence of pain with dysphagia, (2) the absence of pyrosis; (3) the disa p p e a r a n c e of s y m p t o m s without a n t a c i d therapy, and (4) the presence of a c o m p e t e n t lower esophageal sphincter, an effective barrier against esophageal reflux [8]. Abnormal results of motility studies a f t e r vagoto m y in animals provide the best evidence for a "neurogenic" cause of p o s t v a g o t o m y dysphagia [9, I0]. Also, esophageal motility disturbances have been reported in p a t i e n t s with po~tvagotomy dysphagia [11]; however, no serial studies have docu-
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Figure 2A. Two weeks alter transthoracic vagotomy, barium swallow demonstrates narrowing of the distal esophagus. The surgical clips de, note the area of recent vagotomy.
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Figure 2B. Two weeks postoperatively, the resting pressure and the response of the lower esophageal sphincter to swallowing remain normal. Spontaneous synchronous contractions a r e now evident.
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Figure 2C. Two weeks postoperatively the peristaltic activity in the bG~ ; of the esophagus remains normal on swallowing, Spontaneous synchronous contractions are noted.
The American Journal of Surgery
Postvagotomy Dysphagia
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Figure 3A. Eight weeks after transthoracic vagotomy~, the barium swallow demonstrates a normal distal esophagus, Figure 3B. Eight weeks after transthoracic vagotomy, the lower esophageal sphincter pressure and relaxation with swaflows remain normal
Figure 3C. Spontaneous synchronous contractions are still noted eight weeks after transthoracic vagotomy. Peristaltic activity with swallows remains normal
,
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mented a causal relationship between the observed motor abnormalities and clinical symptoms. This latter point is important pathophysiologically because it is well known that esophageal motor abnormalities may be present without accompanying symptoms [12,13]. In our patient, the esophagus was shown t o b e normal preoperatively by endoscopic, x-ray, and manometric st/adies. Since surgery consisted of only transthoracic vagotomy, all postoperative changes could be attributed to the operative procedure itself or to vagal denervation of th e distal esophagus. In the postoperative period two motit-
V o l u m e 126, N o v e m b e r 1973
•
•
~
/'.
~
~ "~x,,)Vu W
~
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ity changes were noted: (1) spontaneous synchronous contractions in the body of the esophagus and (2) an increased transit time compared with that noted in the preoperative study. Both motor disturbances coincided with x-ray evidence of narrowing in the distal esophagus and the patient's complaint of dysphagia. Concomitant with the disappearance o f dysphagia and the returz~ of x-ray findings to normal, esophageal transit time decreased t o the preoperative value. In contrast, spontaneous synchronous contractions persisted unabated. T h e s e observations suggest that the two motor disturbances do not have a common Or-
685
Orlando and Bozymski
TABLE I
Serial Studies in a Patient with Pcstvagotomy Dysphagia Postoperative Preoperative
Symptoms Barium swallow of esophagus
Lower esophageal sphincter (mean resting pressure) Lower esophageal sphincter (relaxation) Peristalsis with swallows Transit time Abnormal motility pattern Fasting serum gastrin level
Two Weeks
None Normal
Dysphagia for solids Smooth tapered narrowing, delayed emptying by cine 17 tore Hg 18 mm Hg
None Normal esophagus, normal emptying by cine 18 mm Hg
Normal
Normal
Normal
Normal 15.5 sec None
Normal 19.5 sec Spontaneous synchronous contrac. tions <100 pg/rol
Normal 15,0 sec Spontaneous synchronous contractions <100 pg/ml
igin and that the synchronous contractions are not causally related to the symptom of dysphagia. Increased transit time has previously been reported in patients with postvagotomy dysphagia [6], but the mechanism for its production remains speculative. Motility studies in animals have demonstrated 1hat the transit time is unchanged or decreased hy cervical vagotomy [9,10]. Therefore, it appears that vagal denervation is not responsible for the increased transit time in our case. An alternative explanation is that periesophageal e d e m a or hemorrhage resulting from surgery is the major factor producing the increase in transit time. Conceivably, edema and hemorrhage around the distal esophagus could increase resistance to muscular contraction and thereby delay the peristaltic wave [6]. In addition, injury of pertesophageal tissue appears to adequately explain the narrowing of the distal esophagus noted on x-ray study and the presence of dysphagia. As healing occurs, spontaneous improvement in x-ray appearance, symptoms, and transit time would be anticipated. This, in fact, was observed in our study. However, further studies documenting this relationship between transit time and postvagotomy dysphagia will be necessary to ascertain its true significance. In contrast to the increased transit" time, there is good experimental evidence that synchronous contractions after vagotomy in animals are a direct result of vagal denervation [9,10]. Therefore, the persistence of synchronous" contractions despite symptomatic and x-ray evidence of improvement in the patient casts doubt on vagal denervation as a cause of postvagotomy dysphagia. In addition, reports of "achalasia" after vagotomy are based on the concept that vagal denervation alters the lower esophageal sphincter and esophageal peristalsis to produce dysphagia [14,15]. In this
686
Eight Weeks
patient as well as in three cases of postvagotomy dysphagia reported by Edwards [6}, no adverse effect on the lower esophageal sphincter or peristalsis could be detected. Therefore, the results of this detailed study cast further doubt on vagal denervation as an etiologic factor and support the concept that the primary cause of dysphagia after vagotomy is surgical injury of periesophageal tissue. Finally, serum gastrin levels have not been reported previously in patients with postvagotomy dysphagia althm~gh alteratior~s in gastrh~ levels have been proposed as a contributing factor in some cases [I6]. In our patient, fasting serum gastrin levels were determined postoperatively during dysphagia and after the disappearance of symp. toms. Both were less than 100 pg/ml. These low levels of gastrin were consistent with the patient's history of antrectomy [17], and their persistence at this low level militates against any causal role for gastrin in producing dysphagia in this case. Summary
A detailed series of x-ray and manometric studies is reported in a patient with postvagotomy dysphagia. The results of this study cast doubt on vagal denervation as an etiologic factor and support t h e concept that the primary cause of dysphagia after vagotomy is injury of periesophagea] tissue at surgery. References
1. Guillory JR, Clagett OT: Post-vagotoroy dysphagia. Surg C/in North Am 47; 833, 1967. 2. Dagradi A, Stempien SJ, Siefer H, et al: Terminal esOphageal (vestibular) spasm after vagotoPny. Arch Surg 85: 955, 1962/ 3. Grimson KS, Baylen GJ, Taylor HM; et al: Transthoracic vagotomy. The effects in 57 patients with peptic ulcer
The AmericanJournalof Surgery
Postvagotomy bysphagia
and the clinical limitations. JAMA 134: 925, 1947. 4. Posllethwait RW, Kim SK, Dillon ML', Esophageal complications of vagotomy~ Surg Gynecol Obstet 128: 461, 1969. 5. Moses WR: Critique on vagotomy, N Eng/ J Med 2;37: 603, 1947. 6. Edwards IDAW: Post-vagotomy dysphagia. Lancet 2: 90, 1970. 7. Bruce J, Small WP: Dysphagia following vagotomy, J R Co//Sur9 Edinb 4:170, 1959. 8. Benz LJ, Hootkin LA, Margulies S, et ah A comparison of clinical measurements of gastroesophageal reflux. Gastroenterology62: 1, 1972. 9. Binder HJ, Bloom DL, Stern H, et al: Effect of vagectomy on esophageal function in the monkey. Surgery 64: 1075, 1968. 10. Carveth SW, Schlegel 3F, Code CF, el al: Esophageal motility after vagotomy, phrenicotomy, myotomy, and myomectomy in dogs. Surg Gynecol Obstet 114: 31,
Volume 126, November lg73
1962, 11, Andersen HA, Schlegel JF, Olsen AM: Post-vagectomy dysphagia, Gastrointest Endosc 12: 13, 1966, 12, Bennett JR, Hendrix TR: Diffuse esophageal spasm: a disorder with more than one cause. Gastroentero/ogy 59: 273, 1970, 13. Soergel KH, Zboratske FF, Amberg JR: Presbyesophagus: esophageal motility in nonagenarians. J C/in Invest 43: 1472, 1964. 14. Harris J, Miller CM: Cardiospasm following vagotomy. Surgery 47: 568, 1960. 15. Pierandezzi JS, Ritler JH: Transient achalasia: a complication of vagotomy. Am J Surg 111: 356, 1966. 16. Blackman AH, Rakatansky H, Nasruelah M, et ah Transabdominal vagectomy and lower esophageal function. Arch $urg 102: 6, 1971. 17. McOuigan JE, Trudeau Wh Serum gastrin levels before and after vagotomy and pyloroplasly or vagotomy and antreetomy. N Engl J Med 286: 184, 1972.
687
PostvagotomyDysphagia Roy C. Orlando, MD, Chapel Hill, North Carolina Eugene M. Bozymski, MD, Chapel Hill, North Carolina
T h e incidence of d y s p h a g i a after v a g o t o m y has b e e n - r e p o r t e d as less t h a n 1 per cent to 36 per cent [I-4]. T h e highest rate occurs after transthoracic v a g o t o m y . Although a b n o r m a l i t i e s have been reported on x-ray, m a n o m e t r i c , and endocopic s t u d y in patients with p o s t v a g o t o m y dysphagia, no a g r e e m e n t exists as to the p r i m a r y cause. Our report is the first to detail a series of clinical, x-ray, a n d m a n o m e t r i c studies in a patient before, .during, a n d after the d e v e l o p m e n t of p o s t v a g o t o m y dysphagia.
vomiting, pain, and pyrosis were notably absent. Painless dysphagia persisted over the next few weeks. During this period, a cine esophagram demonstrated a smoothly tapered narrowing in the distal esophagus (Figure 2A) and delayed eml)tying of barium into the stomach. In contrast to the findings on preoperative manometric study, spontaneous synchronous contractions were observed in the body of the esophagus (Figure 2B and C), and the transit time was increased to 19.,5 seconds. Dysphagia completely cleared spontaneously six weeks after surgery. At that time, a cine esophagram (Figure 3A) showed the distal esophagus to be of normal caliber with no delay in the passage of
Case Report The patient (AF), a fifty-three year old man underwent transthoraeic vagotomy in January 1973 for recurrent peptic ulcer disease. Prior to that there was tm dysphagia or pyrosis, and contrast studies of the upper gastrointestinal tract demonstrated a normal esophagus. At endoscopy for evaluation of the ulcer, the esophagus appeared normal with no evidence of esophagitis or stricture. Using a triple lumen, constantly perfused system, preoperative esophageal manometry was performed prospectively to study the effect of transthoracic vagotomy. This motility study gave normal results. (Figure 1A and B.) The transit time, meas u r e d from onset of swallowing at the pharynx to the peak of a contraction 2 cm above the lower esophageal sphincter, was 15.5 seconds. Five days after transthoracic vagotomy, the patient experienced dysphagia during ingestion of his first solid meal. Postoperative From Division of Gastroenterology, Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina. This work was supported in part by USPHS grant AM-05503 and UNC Faculty Grant 1-0-160-4228 VB099. Reprint requests should be addressed to Dr Bozymski, Department of Medicine, Division of Gastroenterology. University of North Carolina School of Medicine. Chapel Hill, North Carolina 27514.
Volume 126, November 1973
mmH~
mmHQ
'°C
Scm 40 1 PROXIMAL20 to LES
i
0
,o. "°I /
LES
PROXIMAL20
AO 2 ¢m
GASTRIC 20 P~ESSU~
IOsec
PROXIMAL20 to L£S
O
A S*A~LOW ,
t
,
B
SWALLOW 1
t
Figure 1. A and B, pretransthoracic vagotomy. Note the normal resting pressure and the normal relaxation of the lower esophageal sphincter with swallows. Normal peristaltic activity is observed in the body of the esophagus.
683
Orlando and Bozymski
barium into the stomach. Spontaneous synchronous contractions were again noted on manometic study,and the lower esophageal sphincter was unchanged (Figure 3B and C); however, the transit time was 15.0 seconds, a return to the preoperative value. Ten weeks after vagotomy, a Hollander test, confirmed interruption of the vagal mechanism, with a basal acid output of 0.4 mEq/ hr and a maximal acid output of 0.7 mEq/hr after insulin. The lowest blood sugar level during this test was 26 rag/100 ml. Pertinent data from'these studies are presented in Table I. Comments In 1947 M o s e s [5] described the first case of p o s t v a g o t o m y dysphagia. Since t h a t time, vagal denervation of the distal esol~hagus has been cited as the most frequent cause (!f d y s p h a g i a after vagotomy [1]. O t h e r authors question this "neuroi
genie" m e c h a n i s m and support surgical injury of periesophageal tissue as the major etiologic factor [6, 7]. Postoperative esophagitis is a third cause of postvagotomy dysphagia which is reported to occur infrequently [l,4]. This factor was excluded in cur ease because of (I) the absence of pain with dysphagia, (2) the absence of pyrosis; (3) the disa p p e a r a n c e of s y m p t o m s without a n t a c i d therapy, and (4) the presence of a c o m p e t e n t lower esophageal sphincter, an effective barrier against esophageal reflux [8]. Abnormal results of motility studies a f t e r vagoto m y in animals provide the best evidence for a "neurogenic" cause of p o s t v a g o t o m y dysphagia [9, I0]. Also, esophageal motility disturbances have been reported in p a t i e n t s with po~tvagotomy dysphagia [11]; however, no serial studies have docu-
mmH9
~OX|M~L ~0 to LES
i
o
I
LE$
20
1 , GASTRtC
PRESSURE
A
I0 seC. -.
| 20
SWALLOW t
f
t
Figure 2A. Two weeks alter transthoracic vagotomy, barium swallow demonstrates narrowing of the distal esophagus. The surgical clips de, note the area of recent vagotomy.
#
mmHQ L
l,
|
PROXIMAL 20
Figure 2B. Two weeks postoperatively, the resting pressure and the response of the lower esophageal sphincter to swallowing remain normal. Spontaneous synchronous contractions a r e now evident.
PROXIMAL 2 to LE$
¢__J
"°r;,
PROXIMAL 2 0
0 C
684
5WALLOW
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I0 sec.
i t ~: ~
"~
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Figure 2C. Two weeks postoperatively the peristaltic activity in the bG~ ; of the esophagus remains normal on swallowing, Spontaneous synchronous contractions are noted.
The American Journal of Surgery
Postvagotomy Dysphagia
mmHo
40 5,,%m FROXIMAL 2 0 to LES
40
LES
20
4O
lOsec.
GASTRIC 2 0 ~RESSURE •
A
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¢
¢
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12¢m
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Figure 3A. Eight weeks after transthoracic vagotomy~, the barium swallow demonstrates a normal distal esophagus, Figure 3B. Eight weeks after transthoracic vagotomy, the lower esophageal sphincter pressure and relaxation with swaflows remain normal
Figure 3C. Spontaneous synchronous contractions are still noted eight weeks after transthoracic vagotomy. Peristaltic activity with swallows remains normal
,
,RO×IMAL O
PROXIMAL 20
o C
SWALLOW
, _
~!
VWu,,V~
!
~
:i
, ,
.
.
.
.
.
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.
:!'
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-:~:m..~,o.,,.o.-k,v,//~ ~ E~ap~
mented a causal relationship between the observed motor abnormalities and clinical symptoms. This latter point is important pathophysiologically because it is well known that esophageal motor abnormalities may be present without accompanying symptoms [12,13]. In our patient, the esophagus was shown t o b e normal preoperatively by endoscopic, x-ray, and manometric st/adies. Since surgery consisted of only transthoracic vagotomy, all postoperative changes could be attributed to the operative procedure itself or to vagal denervation of th e distal esophagus. In the postoperative period two motit-
V o l u m e 126, N o v e m b e r 1973
•
•
~
/'.
~
~ "~x,,)Vu W
~
$
-~v,
~ t
ity changes were noted: (1) spontaneous synchronous contractions in the body of the esophagus and (2) an increased transit time compared with that noted in the preoperative study. Both motor disturbances coincided with x-ray evidence of narrowing in the distal esophagus and the patient's complaint of dysphagia. Concomitant with the disappearance o f dysphagia and the returz~ of x-ray findings to normal, esophageal transit time decreased t o the preoperative value. In contrast, spontaneous synchronous contractions persisted unabated. T h e s e observations suggest that the two motor disturbances do not have a common Or-
685
Orlando and Bozymski
TABLE I
Serial Studies in a Patient with Pcstvagotomy Dysphagia Postoperative Preoperative
Symptoms Barium swallow of esophagus
Lower esophageal sphincter (mean resting pressure) Lower esophageal sphincter (relaxation) Peristalsis with swallows Transit time Abnormal motility pattern Fasting serum gastrin level
Two Weeks
None Normal
Dysphagia for solids Smooth tapered narrowing, delayed emptying by cine 17 tore Hg 18 mm Hg
None Normal esophagus, normal emptying by cine 18 mm Hg
Normal
Normal
Normal
Normal 15.5 sec None
Normal 19.5 sec Spontaneous synchronous contrac. tions <100 pg/rol
Normal 15,0 sec Spontaneous synchronous contractions <100 pg/ml
igin and that the synchronous contractions are not causally related to the symptom of dysphagia. Increased transit time has previously been reported in patients with postvagotomy dysphagia [6], but the mechanism for its production remains speculative. Motility studies in animals have demonstrated 1hat the transit time is unchanged or decreased hy cervical vagotomy [9,10]. Therefore, it appears that vagal denervation is not responsible for the increased transit time in our case. An alternative explanation is that periesophageal e d e m a or hemorrhage resulting from surgery is the major factor producing the increase in transit time. Conceivably, edema and hemorrhage around the distal esophagus could increase resistance to muscular contraction and thereby delay the peristaltic wave [6]. In addition, injury of pertesophageal tissue appears to adequately explain the narrowing of the distal esophagus noted on x-ray study and the presence of dysphagia. As healing occurs, spontaneous improvement in x-ray appearance, symptoms, and transit time would be anticipated. This, in fact, was observed in our study. However, further studies documenting this relationship between transit time and postvagotomy dysphagia will be necessary to ascertain its true significance. In contrast to the increased transit" time, there is good experimental evidence that synchronous contractions after vagotomy in animals are a direct result of vagal denervation [9,10]. Therefore, the persistence of synchronous" contractions despite symptomatic and x-ray evidence of improvement in the patient casts doubt on vagal denervation as a cause of postvagotomy dysphagia. In addition, reports of "achalasia" after vagotomy are based on the concept that vagal denervation alters the lower esophageal sphincter and esophageal peristalsis to produce dysphagia [14,15]. In this
686
Eight Weeks
patient as well as in three cases of postvagotomy dysphagia reported by Edwards [6}, no adverse effect on the lower esophageal sphincter or peristalsis could be detected. Therefore, the results of this detailed study cast further doubt on vagal denervation as an etiologic factor and support the concept that the primary cause of dysphagia after vagotomy is surgical injury of periesophageal tissue. Finally, serum gastrin levels have not been reported previously in patients with postvagotomy dysphagia althm~gh alteratior~s in gastrh~ levels have been proposed as a contributing factor in some cases [I6]. In our patient, fasting serum gastrin levels were determined postoperatively during dysphagia and after the disappearance of symp. toms. Both were less than 100 pg/ml. These low levels of gastrin were consistent with the patient's history of antrectomy [17], and their persistence at this low level militates against any causal role for gastrin in producing dysphagia in this case. Summary
A detailed series of x-ray and manometric studies is reported in a patient with postvagotomy dysphagia. The results of this study cast doubt on vagal denervation as an etiologic factor and support t h e concept that the primary cause of dysphagia after vagotomy is injury of periesophagea] tissue at surgery. References
1. Guillory JR, Clagett OT: Post-vagotoroy dysphagia. Surg C/in North Am 47; 833, 1967. 2. Dagradi A, Stempien SJ, Siefer H, et al: Terminal esOphageal (vestibular) spasm after vagotoPny. Arch Surg 85: 955, 1962/ 3. Grimson KS, Baylen GJ, Taylor HM; et al: Transthoracic vagotomy. The effects in 57 patients with peptic ulcer
The AmericanJournalof Surgery
Postvagotomy bysphagia
and the clinical limitations. JAMA 134: 925, 1947. 4. Posllethwait RW, Kim SK, Dillon ML', Esophageal complications of vagotomy~ Surg Gynecol Obstet 128: 461, 1969. 5. Moses WR: Critique on vagotomy, N Eng/ J Med 2;37: 603, 1947. 6. Edwards IDAW: Post-vagotomy dysphagia. Lancet 2: 90, 1970. 7. Bruce J, Small WP: Dysphagia following vagotomy, J R Co//Sur9 Edinb 4:170, 1959. 8. Benz LJ, Hootkin LA, Margulies S, et ah A comparison of clinical measurements of gastroesophageal reflux. Gastroenterology62: 1, 1972. 9. Binder HJ, Bloom DL, Stern H, et al: Effect of vagectomy on esophageal function in the monkey. Surgery 64: 1075, 1968. 10. Carveth SW, Schlegel 3F, Code CF, el al: Esophageal motility after vagotomy, phrenicotomy, myotomy, and myomectomy in dogs. Surg Gynecol Obstet 114: 31,
Volume 126, November lg73
1962, 11, Andersen HA, Schlegel JF, Olsen AM: Post-vagectomy dysphagia, Gastrointest Endosc 12: 13, 1966, 12, Bennett JR, Hendrix TR: Diffuse esophageal spasm: a disorder with more than one cause. Gastroentero/ogy 59: 273, 1970, 13. Soergel KH, Zboratske FF, Amberg JR: Presbyesophagus: esophageal motility in nonagenarians. J C/in Invest 43: 1472, 1964. 14. Harris J, Miller CM: Cardiospasm following vagotomy. Surgery 47: 568, 1960. 15. Pierandezzi JS, Ritler JH: Transient achalasia: a complication of vagotomy. Am J Surg 111: 356, 1966. 16. Blackman AH, Rakatansky H, Nasruelah M, et ah Transabdominal vagectomy and lower esophageal function. Arch $urg 102: 6, 1971. 17. McOuigan JE, Trudeau Wh Serum gastrin levels before and after vagotomy and pyloroplasly or vagotomy and antreetomy. N Engl J Med 286: 184, 1972.
687