The Sphincter of Oddi and Gallbladder Function: *

Click here to load reader

  • date post

  • Category


  • view

  • download


Embed Size (px)

Transcript of The Sphincter of Oddi and Gallbladder Function: *

  • The Sphincter of Oddi and Gallbladder Function: *

    I. Preservation of Function after Section and Resectionof the Sphincter


    From the Department of Surgery, Veterans Administration Hospital and IndianaUniversity Medical Center, Indianapolis, Indiana

    SECTION of the sphincter of Oddi in dogshas been followed almost routinely by thedevelopment of acute and chronic inflam-matory lesions of the biliary tract.3' 6, 13, 14Stasis in the gallbladder resulting from theoperation, with or without reflux of duo-denal contents into the bile ducts, hasbeen incriminated in the development ofthese complications. 4 6, 11, 13 For this reasoncholecystectomy has been recommendedand usually performed whenever thesphincter of Oddi is sectioned, resected orbypassed in man.4'8' 1' It was with con-siderable interest, therefore, that we ob-served not only the absence of clinicallyovert cholecystitis, but also the preserva-tion of function by oral cholecystographyin every patient known to us who had hadthe sphincter defunctionalized withoutprior or concomitant cholecystectomy.These patients, eight in number, are thesubject of this report.

    Case ReportsCase 1: 0. L. H., a 45-year-old white man,

    had increasingly more frequent attacks of re-current pancreatitis for 16 months before opera-tion on July 17, 1950. A "stenosed" ampulla ofVater through which a "small probe couldbarely be inserted" was incised a distance of5 mm. The gallbladder appeared to be normaland was not removed. The patient continued tohave occasional mild episodes of epigastric painand tenderness when last seen in February 1954.

    An oral cholecystogram six days preopera-tively showed normal concentrating ability and

    motor function (Fig. 1). On January 31, 1951,six months following sphincter section, a repeatexamination was interpreted as being withinnormal limits (Fig. 2) although the opaquemedium was less concentrated than in the pre-operative film.

    Case 2: R. L. T., a 54-year-old white man,had a perforated duodenal ulcer closed elsewherein September 1955. On May 22, 1957 a subtotalgastrectomy for complete pyloric obstruction wasundertaken. During dissection of the foreshortenedduodenum the common bile duct and duct ofWirsung were transected at their point of entryinto the muscularis. A T-tube was placed in thecommon duct with one long limb projectingthrough the severed end. One end of a poly-ethylene tube (O.D. 1.7 mm.) was threaded intothe pancreatic duct and the other end passed upthe common duct and through the abdominalwall beside the T-tube. The duodenum wassutured to the ulcer bed and pancreas around theostia of the ducts as shown in Figure 3. Theoperation was completed with a subtotal gastricresection and antecolic gastrojejunostomy. Thegallbladder was grossly normal and was not dis-turbed. Convalescence was uncomplicated. Therewas no clinical or laboratory evidence of biliaryobstruction.

    On June 26, a month following operation, anoral cholecystogram visualized a normal gall-bladder with satisfactory contraction following afat meal. The patient has remained well for twoyears with no complaints referable to the biliarytract. Serum alkaline phosphatase and bilirubinconcentrations have remained within normal limits.A cholecystogram on June 10, 1959 revealed airin the common and cystic ducts, but the gall-bladder was well visualized and considered nor-mal (Fig. 4).

    Case 3: W. W. J., a 58-year-old white man,had a four-week history of progressive, painless,


    * Submitted for publication December 7, 1959.

  • LEMPKE Annals of SurgeryNovember 1960

    FIG. 1. (left) Case 1. Normal oral cholecystogram six days before sphincterotomy. FIG. 2.(right) Case 1. Cholecystography performed six months after section of the sphincter ofOddi did not result in as dense opacification of the gallbladder as it did preoperatively,although it was considered to be within normal limits. No calculi were visualized. The gall-bladder contracted in response to a meal of fat.

    FIG. 3. Case 2. Method of re-establishingbiliary and pancreatic continuity with the duo-denum following accidental resection of theampulla of Vater.

    obstructive jaundice when admitted. The jaundicesubsided rapidly. On the fourth day of hospitaliza-tion an oral cholecystogram was attempted. Thegallbladder was not visualized. Periampullarycarcinoma was suspected and exploration per-formed on June 27, 1957. Gross evidence ofbiliary cirrhosis, a limited area of induration inthe head of the pancreas, and a normal gall-bladder without calculi were found. The commonduct was small and "fibrous," and would not ac-cept a 4 mm. Bakes dilator. A fine probe passedthrough the ampulla only with difficulty. Thesphincter of Oddi was sectioned 10 to 11 mm.transduodenally. A wedge removed for micro-scopic examination was "not diagnostic." Thegallbladder was not removed. Convalescence wasuncomplicated and liver function tests had re-turned to normal in three weeks. A final diag-nosis of nonspecific sclerosing choledochitis wasmade.

    Oral cholecystography two, eight and 21months postoperatively (Fig. 5) was interpretedon each occasion as showing normal concentrat-ing ability and contraction following a fat mealwithout evidence of calculi. The patient has re-mained asymptomatic and liver function tests havecontinued to be within normal limits.



    Case 4: J. L. C., a 38-year-old white man, hadhepatitis in 1942, following yellow fever vac-cination. Subsequently, he had recurrent episodesof anorexia and right upper quadrant pain radiat-ing to the right subscapular region. In June 1955,he was admitted for similar complaints associatedfor the first time with obstructive jaundice. Oralcholecystography did not visualize the gallbladder.Laparotomy on June 27 revealed a grossly normal,small gallbladder without calculi. The pancreasand liver were thought to be normal althoughthe latter showed evidence of biliary obstructionmicroscopically (Fig. 6a). The common duct wasthickened. A Randall stone forcep could not bepassed through the ampulla. Transduodenalsphincterotomy was performed and the commonduct drained with a 10 F catheter. The operativediagnosis was nonspecific sclerosing choledochitis.The patient's recovery was complicated by theaccidental removal of the biliary catheter on thenight of operation and bleeding from the sub-hepatic drain site and upper gastro-intestinal tracton the thirteenth postoperative day. An x-raystudy three days later did not disclose the bleed-ing site but did demonstrate reflux of barium intothe common and cystic ducts. Operation on July

    FIG. 4. Case 2. Oral cholecystogram two yearsafter operation. Air was demonstrated in theextrahepatic biliary tract. The concentrating andmotor functions of the gallbladder were preserved.No calculi.


    FIG. 5. Case 3. Normal cholecystogram 21 monthsafter sphincterotomy.

    FIC. 6a. Case 4. Liver biopsy at the time ofsphincterotomy. The architecture of the liver waswell preserved with no significant abnormality ofthe portal triads. Some retention of bile in thecentral area of the lobules with early lake forma-tion (solid black area immediately above centralvein) is compatible with the diagnosis of biliaryobstruction ( x 200).

  • 818 LEMPKE

    FIG. 6b. Case 4. Chronic cholecystitis seentwo years after a sphincterotomy that permittedreflux into the common duct (x 100).

    FIG. 6c. Case 4. Liver biopsy at the timeof cholecystectomy. The portal triads containsmall numbers of inflammatory cells includinglymphocytes and a few eosinophilic granulocytes.There is no evidence of biliary obstruction(x 200).

    Annals of SurgeryNovember 1960

    15 also failed to reveal the cause of the continuedbleeding. The sectioned sphincter of Oddi wasseen to be well healed and patent.The patient recovered but continued to have

    subelinical icterus until July 1957 when he de-veloped mild jaundice and constant pain in theright upper quadrant of the abdomen. Hepa-tomegaly was present. X-ray study of the duo-denum again revealed reflux of barium into thecommon duct (Fig. 7). The gallbladder was veryfaintly opacified on July 31 and somewhat moredensely six days later when a double dose ofcontrast media was given (Fig. 8). Motor func-tion in response to a fat meal was satisfactory.At operation the common duct was dilated andcontained amorphous sediment. A probe passedinto the duodenum readily and the sphincter wasdilated to 8 mm. with only moderate difficulty.The gallbladder, somewhat thickened and sur-rounded by adhesions, was removed. Pathologicdiagnosis was chronic cholecystitis (Fig. 6b).The ampulla was edematous and showed no evi-dence of the previous section. A 12 to 13-mm.incision was necessary to reopen it completely.Liver biopsy revealed only a mild pericholangiticinfiltration of inflammatory cells including lym-phocytes and a few eosinophilic leucocytes.There was no evidence of biliary obstruction(Fig. 6c). The patient convalesced uneventfullyand all liver function tests returned to normal.He was asymptomatic when last seen two monthsafter operation.

    Case 5: V. L. D. B., a 44-year-old Negro man,had recurrent episodes of epigastric distress at-tributed to duodenal ulcer for ten years andproven recurrent pancreatitis with calcificationfor two years. A 10-mm. transduodenal sphincter-otomy was performed on April 17, 1958. Explora-tion of the duct of Wirsung and an operativepancreatogram demonstrated the presence ofcalcification and dilatation of the duct, and apseudocyst. The gallbladder appeared to be nor-mal and was not removed. The patient made anuneventful recovery and has had no recurrenceof symptoms in one year. Evidence of pancreaticislet cell injury, manifested by abnormal glucosetolerance preoperatively, progressed to clinicaldiabetes in that time. Oral cholecystography per-formed two months preoperatively (Fig. 9), andtwo weeks, ten weeks and one year postopera-tively (Fig. 10) showed normal function.

    Case 6: W. C. B., a 41-year-old white man,had the diagnosis of Laennec's cirrhosis estab-lished clinically in 1955 at which time his gall-bladder did not visualize on oral cholecystography.


    FIG. 7. (left) Case 4. Gastroduodenal x-ray study two years after sphincterotomy demon-strating reflux of barium into the common duct and what appeared, on multiple views, tobe stenosis or constriction by the duodenal wall of the distal duct with proximal dilatation.The radiolucent area in the supraduodenal portion of the common duct corresponds to thebiliary sediment found at operation. FIG. 8. (right) Case 4. Faint opacification of the gall-bladder obtained with a "double dose" of contrast material two years after sphincterotomy.Contraction in response to the ingestion of fat occured. No calculi.

    FIG. 9. (left) Case 5. Normal preoperative cholecystogram. FIG. 10. (right) Case 5. Chole-cystogram one year after sphincter section showing normal opacification and no evidence ofcalculi. Pancreatic calcification was not increased over that present preoperatively.


  • 820 LEMPKE Annals of SurgeryNovember 1960

    FIG. 11. (left) Case 6. Oral cholecystogram 16 days after section of the sphincter ofOddi and internal drainage of a pancreatic pseudocyst. There was no impairment of motorfunction. FIG. 12. (right) Case 7. Normal preoperative cholecystogram.

    FIG. 13. Case 7. Oral cholecystogram five weeks after a sphincterotomy that probably rendered thethe choledochoduodenal junction incompetent. Opacification of the gallbladder is considerably less densethan preoperatively.


    FIG. 14. Case 8. Normal preoperative cholecystogram. FIG. 15. Case 8. Normal cholecystogram18 days after sphincterotomy.

    Two years later the onset of epigastric and backpain, hematemesis, weight loss and a mass in theupper abdomen led to operation on November 5,1957. A pseudocyst of the pancreas was found anddrained intemally by a Roux-en-Y cystojejunostomy.The sphincter of Oddi was sectioned a distanceof 10 mm. transduodenally. The patient con-valesced smoothly and remained asymptomaticwhen last seen three months later. An oralcholecystogram 16 days after operation was withinnormal limits (Fig. 11).

    Case 7: E. C. E., a 37-year-old white man, hadrepeated episodes of alcoholic gastritis for fouryears and acute pancreatitis recurrent three timesin as many months before operation on March 25,1959. A 15-mm. transduodenal sphincterotomywas performed. An operative pancreatogramdemonstrated a uniformly dilated duct of Wirsungand a pseudocyst of the head of the pancreas infree communication with the duct. The gall-bladder and common duct were normal grossly.Postoperatively there was an early mild exacerba-tion of pancreatitis. Slow but progressive reduc-tion in the tumefaction of the head of the pan-creas as evidenced by its impression on thecommon duct was demonstrated by serial cho-langiograms. An upper gastro-intestinal x-ray studyshowed reflux of barium at least into the intra-mural portion of the common duct. At the time ofdischarge from the hospital the patient had beenasymptomatic for a month.

    An oral cholecystogram preoperatively demon-strated normal function (Fig. 12). Five weeks afteroperation the ability of the gallbladder to con-centrate the contrast material was considerablyreduced (Fig. 13).

    Case 8: W. C. C., a 37-year-old Negro man,an alcoholic, had chronic pancreatitis of unknownduration associated with the recent developmentof glucosuria and an epigastric mass. At operationon May 15, 1959 the gallbladder and commonduct were normal in appearance. Pancreatic andretroperitoneal inflammation was responsible forthe mass. A transduodenal sphincterotomy wasperformed and the patient recovered unevent-fully.

    Oral cholecystography two weeks beforeoperation (Fig. 14) and 18 days postoperatively(Fig. 15) demonstrated good concentration ofthe contrast material and no evidence of calculi.


    Filling of the gallbladder is consideredto occur passively as a result of the lateralpressure in the common duct developedby the resistance to bile flow offered by thesphincteric mechanism at the choledocho-duodenal junction.8' 11, 15 This mechanismhas two components: the sphincter of Oddi

    Volume 152Number 5

  • Annals of SurgeryNovember 1960

    and the duodenal musculature. The formeris thought to be the one of physiologicsignificance in this regard.4' However, theevidence for a functional relationship be-tween the sphincter and the gallbladder inman is largely theoretical and indirect.

    Phylogenetically the sphincter of Oddiand the gallbladder are associated. Speciessuch as the horse and rat that do not havegallbladders also lack sphincters. In manthe sphincter is more significant anatom-ically in relation to the duodenal com-ponent than in other animals.'

    Reduction of the resistance to the flowof bile into the duodenum in the resting,fasting state by approximately one-third,and the abolition of sphincter spasm inresponse to intraduodenally administeredhydrochloric acid by sphincterotomy wasdemonstrated in dogs by Colp, Doubiletand Gerber.3 The significance of thesefindings is decreased by the additional ob-servations that at the time of the post-operative measurement both dogs hadacute and chronic cholecystitis and that inanother series of animals cholecystectomyachieved an equal reduction in sphincterresistance that was not altered by sub-sequent sphincterotomy. Shoemaker, Ulinand Gambescia 17 have demonstrated a re-duction in the peak common duct pressurefollowing Decholing stimulation of bilesecretion in dogs with experimental chole-cystitis and following cholecystectomy.Data on the effect of sphincterotomy

    upon sphincteric resistance in man are lessextensive than in the dog. For obviousreasons the opportunity to measure com-mon duct pressures in subjects with normalbiliary tracts while in a resting state occursinfrequently. In one patient with a trau-matic intrahepatic-cutaneous fistula Ryan,Doubilet and Mulholland 16 recorded aresistance of 150 mm. of water. Otherpatients have been shown to have valuesof 100 to 120 mm. after combined sphincter-otomy and cholecystectomy. While these

    results are in agreement with those foundin dogs, the definitive experiment of serialmeasurements in the same individual be-fore and after sphincter section alone hasnot been reported. In the human studies ofEiseman and his colleagues 5 the pre-section determinations were made at opera-tion in subjects with abnormal ducts andfollowing cholecystectomy. Therefore, thequestion of the effect of sphincterotomy onthe resistance to bile flow and hence thecommon duct pressure available for fillingof the gallbladder in man appears to beunresolved.The almost universal incidence of chole-

    cystitis, choledochitis and, to a lesser ex-tent, hepatitis in dogs after section of thesphincter without concurrent cholecystec-tomy also has been advanced as evidencefor the integral relationship of that struc-ture to gallbladder function.3 6, 13, 14 If, in-deed, destroying the sphincter converts thegallbladder to a flaccid diverticulum of theextrahepatic biliary tract, the resultingstasis in that organ would make infection alikely consequence. In studying this prob-lem, however, ampullary incisions of 10mm. or more, that admittedly render thecholedochoduodenal junction incompetent,have been used most commonly.5 6, 13 Theresulting reflux of duodenal content intothe biliary tree, not seen after a properlyperformed operation in man,4 provides analternative explanation for the ensuingcomplication. An 8-mm. sphincterotomywas used in three dogs by Colp et al.3and manometric studies in two of themsuggested that the duodenal musculaturewas preserved and capable of preventingregurgitation. This was not proven, how-ever. Although all the animals developedcholecystitis, the fact that the sphinctersections were performed endocholedochallyby way of a cholecystostomy adds anotherpossibly significant variable.Two patients on whom a sphincterotomy

    without concomitant cholecystectomy wasperformed and who subsequently devel-

    822 LEMPKE


    oped cholecystitis have been reportedby Large."1 One became symptomatic"soon" and the other "almost two years"later. What incidence this representsand whether or not regurgitation of duo-denal contents into the common duct waspresent can not be determined. Jones andSmith 7 described four patients with nor-mal gallbladders who remained well fromthree months to one year after sphincter-oplasty, an operation designed to producesphincteric incompetence and proven tohave done so in one case. Among the eightpatients presented here, one (Case 4) isknown to have had chronic cholecystitistwo years following sphincterotomy. Al-though the possibility exists that this rep-resented either an extension of his originaldisease or a complication of subsequentpartial common duct obstruction, its re-lationship to the operation can not beignored. Reflux of barium into the commonduct was observed shortly after thesphincterotomy and again two years later,prior to the cholecystectomy. X-ray studyof another patient (Case 7) suggests thatincompetence may have been produced.In the brief period of five weeks that hehas been observed there is no evidence ofbiliary tract infection.

    Reflux of air and presumably duodenalcontents was demonstrated in one otherpatient (Case 2). This man, who had acholedochoduodenostomy performed in thecourse of a Hofmeister subtotal gastrec-tomy, has not developed clinically apparentcholecystitis in two years. This is in ac-cord with the observation of Mallet-Guyand his coworkers 12, 13 who found that apyloric exclusion operation in one dogprotected that animal from the biliary tractinfection otherwise produced by section ofthe sphincter and resultant refiux. Thisauthor13 and others 9, 18 have also usedsubtotal gastrectomy with duodenal exclu-sion in the treatment of cholangitis, sec-ondary to choledochoduodenal fistula or

    choledochoduodenostomy. These observa-tions suggest that it is not the loss ofOddian sphincter action that leads to chole-cystitis and choledochitis but rather theestablishment of reflux of intestinal con-tents, and particularly chyme, into thecommon duct and gallbladder.

    Oral cholecystography is a simple di-rect method of evaluating the effect ofsphincter destruction on gallbladder func-tion. If that organ does not fill, the con-trast material obviously can not be visual-ized by x-ray. This procedure has beenused little in the study of this problem.Cadili and Sommariva 2 incised the am-pulla transduodenally and cannulated itwith a glass tube in four dogs. The gall-bladder of each was visualized by oralcholecystography 20, 60 and 90 days post-operatively and considered to functionnormally although not quite as well aspreoperatively. Incompetence of the sphinc-ter mechanism presumably was producedbut not actually demonstrated. Three ofthe four patients reported by Jones andSmith 7 were examined by this method fol-dowing sphincteroplasty and showed nofunction. Reflux of duodenal contents wasproven in one and was probably present inthe remaining patients. Of the eight patientsin the present report, six retained essen-tially normal and two reduced gallbladderfunction as determined by oral cholecys-tography. Reflux of barium into the com-mon duct during upper gastro-intestinalx-ray study was suspected in one of thelatter patients (Case 7) and was definitein the other (Case 4). This was the onlysubject in the group of eight to developcholecystitis.

    Preservation of function on oral chole-cystography does not preclude the exist-ence of cholecystitis 11 even in the absenceof definite symptomatology. Neither doesan apparent decrease in the density of thegallbladder image necessarily indicate dis-ease of that organ since absorption of the

    Volume 152Number 5 823

  • Annals of SurgeryNovember 1960

    contrast material may be impaired byintestinal factors such as increased motilitysecondary to pancreatic insufficiency. It issignificant for the purposes of this study,however, that the gallbladder did fill wellenough to exhibit some function in everycase and that the reduced function in twopatients as well as the absence of visualiza-tion in previously reported cases was as-sociated with choledochoduodenal incom-petence.

    Several explanations for this continuedfunction are possible. These include in-adequacy and healing of the sphincter-otomy. The former seems likely in patient0. L. H. (Case 1) whose ampulla was in-cised only 5 mm. instead of the customary10 to 12 mm. Failure of the operation toabolish his symptoms completely supportsthis assumption. However, the remainingpatients with chronic or recurrent pan-creatitis (Cases 5-8) have been free of thecomplaints for which the operation wasdone, suggesting that the sections wereadequate and permanent. Although theperiod of observation in three instances hasbeen brief, one patient (Case 5) has beenfollowed a year without recurrent difficulty.Two other patients (Cases 2, 3) have beenasymptomatic with functioning gallbladdersfor two years after sphincter destructionfor other reasons. If the ampullary incisionshave healed, it would appear that this hasoccurred in such a way as to avoid thereestablishment of the original anatomicor abnormal functional state of the sphinc-ter. However, the fact that function oncholecystography was observed in five pa-tients before the four to six-week intervalreportedly required for healing of a sphinc-terotomy,5 indicates that reconstruction ofthe sphincter is not a necessary conditionfor filling of the gallbladder.A more likely explanation would appear

    to be that the resistance to bile flow neces-sary for gallbladder filling is low enoughthat, in some men at least, the component

    contributed by an intact sphincter of Oddiis not essential.15 Following the usualsphincterotomy the resistance offered bythe intact circular muscle coat of the duo-denum probably performs this function.Other sources of resistance are possible inthe more unusual cases in which thismechanism is destroyed also. For example,in the two patients who exhibited reflux ofbarium into the common duct, partial ob-struction by biliary sediment (Case 4) orby extrinsic pressure from an enlarged,indurated head of the pancreas (Case 7)may have produced the resistance neces-sary to fill the gallbladder. In the case ofthe patient whose ampulla was resected(Case 2), either stenosis of the newcholedochoduodenal junction or the tonusof the intrinsic musculature of the dis-tal common duct 10, 19 conceivably couldachieve the same result. An investigationof the hydrodynamics of the extrahepaticbiliary tract designed to elucidate the roleof the sphincter of Oddi in gallbladderfunction in man is currently in progress.

    Summary and Conclusions

    Eight consecutive patients in whom thesphincter of Oddi was sectioned or re-sected without prior or concomitant chole-cystectomy are reported. Contrary to whatmight be expected on the basis of experi-mental work using dogs, all were shownto have a functioning gallbladder as de-termined by oral cholecystography andonly one was proven to have developedcholecystitis during periods of observationvarying from two weeks to two years afteroperation. While some other explanationfor continued gallbladder filling followingdestruction of the sphincter of Oddi ispossible, and in certain of the cases evenlikely, it is considered probable that theresistance to bile flow necessary to producedistension of that organ is maintained bythe duodenal musculature. The major por-tion of the resistance in the intact indi-

    824 LEMPKE

  • Volume 152 THE SPHINCTER OF ODDI AND GALLBLADDER FUNCTION 825Number 5vidual apparently is contributed by thiscomponent of the sphincteric mechanismand is of such magnitude that it can reason-ably be assumed to be capable of perform-ing this function alone. Healing so as tore-establish sphincter action has not beenexcluded, but demonstration of gallbladderfilling two weeks postoperatively, wellwithin the four to six-week period re-portedly required for such healing to oc-cur, and the relief of symptoms for whichthe operations were performed for periodsextending to two years, suggest that it hasnot occurred.The intact duodenal musculature also

    prevents reflux of duodenal contents intothe common duct and apparently preventsthe development of inflammatory biliarytract complications in man. Incompetenceof the choledochoduodenal junction at-tributable to an overly extensive sphinc-terotomy was demonstrated in two patients.The ability of the gallbladder to concen-trate orally administered contrast materialwas reduced in each. One patient whooriginally had a diffuse, sclerosing inflam-mation of the biliary tract was found tohave chronic cholecystitis when operatedupon two years later for partial obstructionof the common duct by biliary sediment.The other patient has demonstrated noevidence of this complication in a muchshorter period of observation. Normal gall-bladder function and absence of symptomsin another patient two years after acholedochoduodenostomy and Hofmeistergastrectomy, who exhibits radiographicevidence of duodenal reflux, confirms theexperience of others that diversion ofchyme from the anastomosis protects thebiliary tree from inflammatory sequelae.The evidence from observations on these

    eight patients certainly is not sufficient towarrant a conclusion that the gallbladdershould not be removed when the sphincterof Oddi is sectioned or resected. The seriesis small and the period of observation in

    many patients is brief. Furthermore, chole-cystectomy ordinarily adds little to thetechnical difficulty or morbidity of theseoperations. However, these observationsare of interest in that they cast some doubton the significance of the sphincter ofOddi in gallbladder function in man andfurther illustrate the discrepancies thatfrequently are observed between the ef-fects of a given procedure in man and otherspecies.

    References1. Boyden, E. A.: The Anatomy of the Choled-

    ochoduodenal junction in Man. Surg.Gynec. & Obst., 104:641, 1957.

    2. Cadili, G. and V. Sommariva: Studio Colecist-ografico per Os Dopo Abolizione Anatomicae Funzionale dello Sfintere di Oddi. Minervachir., 13:215, 1958.

    3. Colp, R., H. Doubilet and I. E. Gerber:Endocholedochal Section of the Sphincterof Oddi. Arch. Surg., 33:696, 1936.

    4. Doubilet, H. and J. H. Mulholland: TheSurgical Treatment of Recurrent AcutePancreatitis by Endocholedochal Sphincter-otomy. Surg. Gynec. & Obst., 86:295, 1948.

    5. Eiseman, B., W. H. Brown, S. Virabutr andS. Gottesfeld: Sphincterotomy-An Evalua-tion of Its Physiologic Rationale. A. M. A.Arch. Surg., 79:294, 1959.

    6. Gray, S. H., J. G. Probstein and L. A. Schar:Chronic Cholecystitis Produced by Divisionof the Sphincter of Oddi. Arch. Surg., 59:1007, 1949.

    7. Jones, S. A. and L. L. Smith: TransduodenalSphincteroplasty for Recurrent Pancreatitis.A Preliminary Report. Ann. Surg., 136:937,1952.

    8. Jones, S. A., L. L. Smith and G. Gregory:Sphincteroplasty for Recurrent Pancreatitis:A Second Report. Ann. Surg., 147:180, 1958.

    9. Jordan, P. H. Jr. and L. Stirrett: Treatmentof Spontaneous Internal Biliary FistulaCaused by Duodenal Ulcer. Am. J. Surg.,91:307, 1956.

    10. Kelsey, J. R. and E. F. Beard: CommonBile Duct Pressures. Results of an Experi-mental Study in Human Subjects with Useof a Strain Gauge Manometer. Gastro-enterology, 32:1122, 1957.

    11. Large, A. M.: Regurgitation Cholecystitisand Cholelithiasis. Ann. Surg., 146:607,1957.

  • 826 LEMPKE Annals of SurgeryNovember 196012. Mallet-Guy, P. and L. Auger: Sur l'Etude

    Experimentale des Anastomoses de la VoieBiliaire Principale: l'Angiocholite apresSection du Sphincter d'Oddi. Lyon chir.,29:629, 1932.

    13. Mallet-Guy, P. and L. Auger: R6le Protecteurdu Sphincter d'Oddi contre les InfectionsAscendantes des Voies Biliaires. Compt.rend. Soc. de biol., 111:813, 1932.

    14. Mallet-Guy, P., L. Auger and M. Billa: EtatBacteriologique des Voies Biliaires apresSection Experimentale du Sphincter d'Oddi.Compt. rend. Soc. de biol., 112:899, 1933.

    15. Mulholland, J. H.: Discussion of Large."

    16. Ryan, J. D., H. Doubilet and J. H. Mulhol-land: Observations on Biliary-PancreaticDynamics in a Normal Human. Gastro-enterology, 13:1, 1949.

    17. Shoemaker, W. C., A. W. Ulin and J. M.Gambescia: Studies of the Reservoir Func-tion of Normal and Inflamed Gallbladdersin Dogs. Gastroenterology, 29:1024, 1955.

    18. Walker, G. L. and A. M. Large: Choledo-choduodenal Fistula: Its Surgical Manage-ment. Ann. Surg., 139:510, 1954.

    19. Waters, Waltman: Spasm of the CommonDuct Producing Pain after Sphincterotomy.A. M. A. Arch. Surg., 73:547, 1956.