Concerning the surgical physiology of duodenal ulcer

CONCERNING

THE SURGICAL PHYSIOLOGY OF DUODENAL ULCER

VERNE

G.

BURDEN,

M.D.,

P.A.C.S.

Attending Surgeon, St. Joseph’s HospitaI PHILADELPHIA, PENNSYLVANIA

T

HE pyIorus forms the dista1 fixed extremity of the stomach. It Iies a IittIe to the right of the midIine of the body, opposite the first Iumbar vertebra, with the pancreas beIow and behind and the left Iobe of the Iiver above and in front. The cardia forms the proximal fixed extremity and between these two points the stomach is suspended from the gastrohepatic Iigament. The cardiac sphincter guards the entrance and the pyIoric sphincter the exit, the former being reIated to the motor activity of the esophagus and the Iatter to that of the stomach. The pyIoric sphincter is a definite anatomic structure, the best deveIoped of a11 the sphincters of the gastrointestina1 tract, being represented by a IocaI increment of circuIar muscle fibers about >/4 to >4 inch in width. During operations under genera1 anesthesia the sphincter is reIaxed, making definition difYicuIt, but its Iocation is readiIy marked by the transverse pyIoric veins. The arteries of the stomach do not reach the pyIorus; the Iatter is suppIied from above by the pyIoric artery, a branch of the hepatic from which are also derived the branches supplying the first portion of the duodenum. The anterior and posterior branches of the vagus nerve suppIy the respective aspects of the stomach but onIy as far as the pyIorus. The Iatter structure is innervated from above by fibers of the hepatic branch of the vagus which probabIy aIso carry sympathetic fiIaments. Since the nerve suppIy of the pyIoric sphincter has been the subject of much controversy it may be we11 to dea1 with it more fuIIy. EmbryoIogic and comparative anatomic studies cited by ‘GaskeII show that the sphincters of the gastrointestina1

tract have deveIoped from the derma1 muscuIature and at one time formed a continuous muscuIar investment of the gut. In the course of deveIopment most of the derma1 muscuIature disappeared from the gut and that which remained became IocaIized at certain points to form the sphincters. It is well estabIished that the sympathetic nerves which represent the thoracicoIumbar outff ow of the involuntary nervous system supply motor fibers to a11 bIood vesseIs and sweat gIands, to a11 unstriped muscIe under the skin and to tubuIar structures derived from the segmented duct. Structures with a common origin usuaIIy have a common nerve suppIy. It has been proved that the motor nerve for the iIeoceca1 sphincter is from the superior mesenteric ganglion. The pyIoric sphincter in a11 Iikelihood beIongs to this group and is supplied by motor nerves from the sympathetic. The vagus, a parasympathetic nerve, supplies inhibitory and diIator fibers to this sphincter and has its gangIion ceIIs Iocated in the waI1 of the gut. Experimenta attempts to IocaIize the nerve suppIy of the pyIoric sphincter have shown conff icting resuIts, probabIy because of faiIure to differentiate between sphincter and antra1 activity as reIated to the emptying of the stomach, and because of the diffIcuIty of separating vagus from sympathetic fibers. The vagus is not onIy the motor nerve for the stomach but it is aIso the inhibitor and diIator nerve for the pyIoric sphincter. Cutting it does not disturb the intrinsic mechanism of the stomach which is controIIed by IocaI gangIonic ceIIs. The motor activity of the sphincter is under sympathetic contro1 which is niceIy correIated with the motor function of the stomach and is aIso ex-

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tremeIy sensitive to extraneous stimuli not onIy from the abdomen but from the entire body. Horton showed by anatomic studies that the muscuIature of the pyIoric sphincter is made up principaIIy of circuIar fibers whose contraction cIoses the orifice. He demonstrated aIso that Iooped around the circuIar fibers are muscle bundIes proIonged from the IongitudinaI muscIe coat of the stomach. Contraction of these Iatter fibers which are under vagus contro1 serves to diIate the sphincteric orifice and to hoId it open. Thus it becomes apparent that the mechanism of the pyIoric sphincter resembIes that of the iris of the eye. The norma function and behavior of the pyIoric sphincter have to do with reguIating the passage of food from the stomach to the duodenum and probabIy with the regurgitation of duodena1 contents into the stomach. Recent investigations indicate that acidity on the gastric or duodena1 side of the pylorus does not normaIIy contro1 the activity of the sphincter. Each advancing peristaltic wave in conjunction with increased tonus of the stomach overcomes the tonus of the pyIorus and forces some of the thyme into the duodenum regardIess of whether the reaction of the thyme is neutra1, acid or aIkaIine. The pyIoric tone normaIIy onIy keeps the sphincter closed when the pressure on either side is insuffIcient to overcome it. Structures which are controIIed by the sympathetic nervous system exhibit reactions which are pecuIiarIy responsive to many stimuIi. Perspiration and paIIor of the skin, invoIuntary evacuation of the bIadder and rectum induced by fright and emotional shock; hyperpiesis resuIting from worry and nervous strain and from trauma to an extremity may be cited as resuIts of overstimuIation of the sympathetic nervous system. Indeed many of the symptoms of surgica1 shock may be expIained in a simiIar manner. Postoperative intestina iIeus is not caused by paraiysis of the intestine, but is due to a preponderance of sympathetic activity, causing inhibition of

Ulcer

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peristaIsis and spasm of the sphincters. SpinaI anesthesia or severence of the sympathetic nerves promptIy reIieves or prevents this condition. Mere sudden forcibIe contraction of the stomach wouId cause ejection of its contents into the duodenum; therefore, for vomiting to occur there must be coincident cIosure of the pyIorus by contraction of its sphincter and reversa1 of gastric peristalsis. AI1 stimuIi which affect the sympathetic nervous system do so by causing an increase in the output of the adrena gIands. The action of epinephrine is Iimited to structures having sympathetic innervation, there being no effect on nerves of the autonomic system. The sphincters are made to contract by sympathetic stimuIation and their tone is probabIy increased by atropine which paraIyzes the IocaI inhibitory ganglia. By appIication of this genera1 knowIedge of sphincters to the pyIoric sphincter it is presumabIy correct to say that norma tonus maintains cIosure of the pyIorus, that it reIaxes and opens in response to vagus stimuIation as it occurs in gastric periastaIsis, and that spasm of the pyIoric sphincter occurs from IocaI or reflex irritation. Surgical diagnosis must frequentIy differentiate between gastric symptoms caused by intrinsic disease of the stomach and gastric symptoms which are manifestations of extragastric Iesions. UIcer of the stomach or duodenum is a IocaI irritative Iesion whose symptoms are directIy reIated to the functiona activity of the stomach. The regularity and periodicity of symptoms, especiaJIy of duodena1 uIcer, are constant from day to day. The stomach often exhibits hypermotiIity and there is usuaIIy spasm or achaIasia of the pyIoric sphincter. The etioIogy of duodena1 uIcer is as vague as ever. Its experimenta reproduction has not simuIated the conditions found in the human. Infection seems to pIay a part but the predisposing factors, especiaIIy those which promote chronicity, ‘remain unknown. The fact that duodena1 uIcer occurs so often in certain

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individua1.s of a characteristic habitus described by Draper and Hurst, that it is often found in severa members of a famiIy of the same and succeeding generations, that it is often prone to recur after surgica1 treatment, that it seems to bear some reIationship to the use of tobacco (nicotine paralyzes the vagus terminaIs), and that the symptoms of uIcer are often accentuated by worry or nervous strain are highIy significant and suggestive of a nervous inff uence in etioIogy. RefIex spasm of the pyIorus may be caused by any abdomina1 Iesion which irritates the peritoneum. It is often a seque1 of abdomina1 operations, and may even arise from the Iigation of the sac of an inguina1 hernia done under IocaI anesthesia. Spasm from the above causes is usuaIIy temporary, sometimes recurrent at irreguIar intervaIs and rarely of much significance. Continua1 cIonic spasm produces hypertrophy of the sphincter as seen in earIy infancy. The etioIogy of this condition seems to be best expIained by overstimuIation of the sympathetic fibers to the sphincter. It has been suggested that hyperadrenaIism causes the overstimuIation. Mere cutting of the sphincter, however, sufhces for cure. Reffex spasm of the pyIorus in the absence of duodena1 uIcer and other abdomina1 Iesions may give rise to symptoms which often simuIate duodena1 uIcer and justify operation. BastianeIIi speaks of such cases, which he has treated successfuIIy by the Ramstedt operation. Gastroenterostomy in the absence of uIcer does not reIieve the symptoms of pyIorospasm, but may cause additiona symptoms which are 0nIy reIieved by undoing the anastomosis. The significant features of duodena1 uIcer which may be explained by the activity of the pyIoric sphincter are the chronicity and periodicity of symptoms; the unchanging cycIe of pain-food-ease-pain; the hypermotiIity and hyperacidity of the stomach; the selective Iocation of the uIcer in the anterior superior waI1 of the duodena1 cap about I inch from the pyIorus; the absence

UIcer

JUNE,1939

of symptoms for weeks or months when an unheaIed uIcer is known to be present and the occasiona occurrence of uIcer symptoms in the absence of uIcer. CertainIy the supposition is justified that the behavior of the pyloric sphincter has much to do with the symptoms of uIcer. Is it possibIe that misbehavior of the sphincter from direct or reflex nervous influence is a factor in the production of duodena1 uIcer? Mere excision of duodena1 uIcer has not been foIIowed by satisfactory resuIts, and various types of pIastic operations on the pyIorus have yieIded a Iarge percentage of faiIures. The reason for faiIure in the Iatter may be that the sphincter is rendered onIy temporariIy inactive because subsequent operations have often shown Iittie change in the appearance and caIiber of the pyIorus. The procedure which Judd has used with eminentIy satisfactory resuIts in a Iarge number of cases is excision of the uIcer combined with remova of the anterior haIf of the pyIoric sphincter. By this operation sphincteric activity is more or Iess permanentIy aboIished. There can be no doubt that the remova of a Iarge part of the pyrIoric sphincter is the major factor in the good resuIts which foIIow this operation. Excision of the anterior haIf of the sphincter probabIy removes many of the IocaI ganglionic ceIIs and the attachments of many sympathetic fibers. It is possible that after a time the sphincter may hea and resume activity. In this event, if certain predisposing factors persist, there may be recurrence of duodena1 ulceration. The soIution of the permanent contro1 of duodena uIcer remains invoIved with its etioIogy in which dysfunction of the pyIoric sphincter resuIting from reffex nervous inffuence shouId seriousIy be considered. Hyperacidity is the most constant Iaboratory finding in cases of duodena1 ulcer. Just what is hyperacidity? Does it mean a Iarger amount of acid, or acid that is stronger than norma or both? Certain basic facts of the chemistry of the stomach must be kept in mind. The acidity is due entireIy to hydrochloric acid. PavIov showed that the gastric juice as it flows

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from the gIands possesses a constant acidity-0.3 per cent-never more, never Iess. The optimum acidity for digestive purposes is 0.2 per cent. The reduction is accompIished by reguIation of the amount of acid secreted, by diIution with food and fIuid entering the stomach, by neutraIization from any aIkaIi in food, fluid, and stomach mucus, and at specia1 times by regurgitation of duodena1 contents into the stomach. The acid-secreting mechanism maintains the optimum IeveI of acidity when there is digestive work to be done, and as PavIov says, the exactitude of the work of the gIands is astonishing; that which is demanded of them they furnish each time to a hair’s breadth, no more and no Iess. SurgicaI duodena1 drainage, evuIsion of pancreatic ducts, and formation of a pancreatic fistuIa are among the most successful experimenta methods for the reproduction of peptic uIcer. In these experiments it is a significant fact that one starts with a norma gastric function. Later, in spite of the fact that an uIcer has been produced just beyond the outIet of the stomach, and that a11 Iikelihood of duod&aI regurgitation has been eIiminated, nevertheless gastric function, especiaIIy the behavior of the acidity remains unchanged. In view of these findings can we maintain that uIcer causes hyperacidity? Can there be any doubt that the norma stomach reguIates its own acidity? I am aware of no experimenta method which has been successfu1 in producing a maintained hyperacidity. From the practica1 standpoint, hyperacidity means not stronger acid, but the secreting of norma acid beyond the quantity required for digestion and probabIy when there is no digestive work to be done. Hyperacidity then is reaIIy hypersecretion. Where does the fauIt Iie? Not in the stomach itseIf. It seems very probabIe that this dysfunction of gastric secretion originates in the centra1 nervous system, and for reasons not necessary to expIain here, it is part of a fixed constitutiona pattern. The

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psychic phase of gastric secretion produces the most potent juice; it anticipates food in the stomach. “Appetite speIIs gastric juice.” I believe that in the patient with duodena1 uIcer the psychic phase of gastric secretion is not onIy overactive but active at unnatura1 times. The resuIt in the uIcer patient is a constant effort, conscious or unconscious, to satisfy and neutraIize the Hence the increased excessive acidity. appetite, the comfort from food in the stomach and the soIace from aIkaIine powders. Why do not a11persons with hyperacidity have uIcer? Is the uIcer the cause of sofor caIIed hyperacidity ? Is it responsibIe achaIasia and spasm of the pyIoric sphincter? The symptomatoIogy of duodena1 uIcer is expIained by hyperacidity and achaIasia or spasm of the pyIoric sphincter and not by uIcer. UIcer is the resuIt of the above and not the cause. RemovaI of the uIcer does not affect hyperacidity nor does it reIieve the symptoms, but the Iatter are cured in many instances by gastroenterostomy even though the uIcer remains for a varying period of time untii healing occurs. In the remission periods the patient with duodena1 uIcer stiI1 has his uIcer although it is probabIy in a heaIing stage. It is not uncommon to see a patient who has the typica symptoms of duodena1 uIcer but no uIcer. Reflex spasm of the pyIoric sphincter has been known to surgeons for many years. Moynihan painted its word picture in cases of chronic appendicitis. BastianeIIi cut the sphincter and relieved patients who had the symptoms of uIcer without actua1 uIcer. If these patients had been aIIowed to go on without treatment, wouId they have degives rise to veIoped uIcer ? PyIorospasm IocaI pain and discomfort, but not to hyperacidity. Spasm of the sphincter is a reffex sympathetic nervous mechanism. Its cause may be any peritonea1 irritation, any mechanica derangement, such as partia1 obstruction, an adherent appendix, an omenta1 attachment to an incisiona scar. Food aIIergy may be a factor-there

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is aIways spasm of the sphincter during an attack of migraine. Out of a11 the experimenta work in the search for the cause of chronic duodena1 uIcer one fact stands unshaken, that is, that the hydrochIoric acid of the stomach has a great inffuence and is probabIy the singIe direct cause of uIcer in the human being. The mechanism and factors by which this is brought about amount essentiaIIy to this : hypersecretion of hydrochIoric acid, due to a constitutiona fauIt, is combined with faiIure or inadequacy of the norma safety controIs (stomach mucus, aJkaIine pyIoric secretion, and duodena1 regurgitation, which carries the strongest aIkaIine secretion in the body). There is ample evidence of duodena1 regurgitation in the norma person, i.e., the frequent finding of biIe in the stomach; reverse duodena1 peristaIsis, demonstrated by the x-ray; and the intractabIe nature of a postoperative duodena1 f%tuIa. Interference with duodena1 regurgitation depends primariIy upon the pyIoric sphincter, either its faiIure to reIax, known as achaIasia, or actua1 spasm. The Iatter has been frequentIy demonstrated in patients with duodena1 uIcer. The surgeon does not have to seek outside his clinica experience for a demonstration of the experimenta production of peptic uIcer. Every gastrojejuna1 uIcer is an exampIe of experimenta peptic uIcer in the human being. There have been many types of operations used in the treatment of duodena1 uIcer. Their success depends essentiaIIy on the contro1 of the hypersecretion of hydrochIoric acid. In the evaIuation of postoperative resuIts it is important to remember that the patient continues to have hypersecretion aIthough his symptoms may be reIieved and his uIcer heaIed. SimpIe excision of the duodena1 uIcer has been abandoned because of the high rate of recurrence and mere cIosure of a perforated uIcer is foIIowed by unsatisfactory permanent resuIts in about 35 per cent of cases. Evidently the uIcer aIone does not warrant therapeutic attack.

UIcer

PIastic procedures designed to enIarge the pyIoric-duodena1 avenue, when we11 done, have been foIIowed by remarkabIy few recurrences of uIcer. Their faiIures have been due to mechanica interference with the emptying of the stomach caused by extensive IocaI adhesions which so often foIIow these procedures. Gastroenterostomy aImost invariabIy brings about heaIing of the origina uIcer in the duodenum, but in a varying percentage of cases a new uIcer forms in the jejunum near the anastomotic stoma. We have Iearned to know that a person with a gastroenterostomy is never free of the potentia1 danger of a margina uIcer. I have notes of a patient who was under my care for this condition twenty-eight years after a gastroenterostomy had been done for duodena1 uIcer. The answer to the faiIures after gastroenterostomy may be found in the expIanation of its successes. I have no doubt that the successfu1 surgica1 treatment of duodena1 uIcer by any type of operation depends upon efficient contro1 of hyperacidity. The test of this does not Iie in the resuIts of gastric anaIysis but in the continued weII-being of the patient. No operation yet devised can aIter the cerebra1 stimuIus upon which hyperacidity depends. It is a human faiIing to carry on to extremes, even in therapeutics. An exampIe of this is the practice of partia1 gastrectomy for duodena1 uIcer. The stated reasons have to do with remova of the uIcer-bearing area of the stomach and duodenum and its associated gastritis, and with a supposed contro1 of hyperacidity by remova of part of the secretory area of the stomach. Gastritis has nothing to do with the cause of uIcer aIthough the two may have a common origin. RemovaI of part of the secretory area does not sIow up the activity of the part that remains, which actuaIIy may undergo functiona hypertrophy. MarginaI uIcer may occur after partia1 gastrectomy for duodena1 uIcer and its incidence is aImost the same as when gastroenterostomy has been done in we11 seIected cases. If anything can be said in justification for gastrectomy for uIcer in

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the duodenum, it is that its mechanics insure more adequate neutraIization of gastric acidity. But the sacrifice of threefourths of the stomach is a big price to pay for the remova of a smaI1 uIcer in the duodenum. Assuming that the background of duodenal ulcer with its associated perversion of gastric physioIogy is of the nature depicted eIsewhere in this paper, what is a IogicaI soIution to the probIem? If hyperacidity and dysfunction of the pyIoric sphincter are at fauIt, is there any method to correct them? So far there is no mechanica1 means to attack the basic fauIt of hyperacidity. In duodena1 regurgitation nature has its own method of contro1, but in the uIcer patient its action is prevented by the pyIoric sphincter. This is not a new thought-surgeons Iong ago tried to render the sphincter inactive by cutting its fibers. The resuIts were immediateIy good, but were onIy temporary, because after heaIing the sphincter resumed its former activity. The method of Judd by which the anterior haIf of the sphincter is removed comes very near the idea1 procedure. Its success in cases in which it can be done far surpasses any other operation for uIcer. Its smaI1 percentage of faiIures is due not to recurrence of uIcer but to mechanica factors incident to IocaI adhesions. Judd’s operation opens the stomach and duodenum and is compIeted as a gastroduodenostomy. It is Iiable to the same faults due to adhesions which have foIIowed other pIastic procedures on the pylorus. The idea1 method to obtain our objective is remova of the anterior half of the pyloric sphincter without opening the stomach or duodenum. This we have done by a method described elsewhere, with exceIIent resuIts. The sphincter has been rendered permanentIy inactive or at Ieast no Ionger interferes with duodena1 regurgitation. The operation is suitabIe onIy for those duodena uIcers in which extensive scar tissue and fibrosis are absent, Otherwise identity and removal of the anterior haIf of the sphincter are not practica1.

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SUMMARY

The pyIoric sphincter is composed of constrictor and diIator muscIe fibers, the former under the contro1 of the sympathetic nerves and the Iatter under the parasympathetic or vagus nerves. The sphincter pIays a part in the emptying of the stomach and aIso in the regurgitation of duodena1 contents into the stomach. Its mechanism may be disturbed by IocaI or refIex irritation. Many of the cIinica1 features of duodena1 uIcer can be expIained by the activity of the pyloric sphincter. It may cause the typica symptoms of uIcer when no ulcer is present, since the uIcer itself does not cause the symptoms which identify its presence. Dysfunction of the pyloric sphincter is one of the two main factors in the etiology of duodenal uIcer. The other factor is hyperacidity. The norma stomach reguIates its own acidity. In certain individuaIs hypersecretion is a fixed constitutiona fauIt and its contro1 rests on the mechanism of duodena1 regurgitation. FaiIure of this contro1 means the deveIopment and maintenance of a duodena1 uIcer. The pyIoric sphincter because of spasm or faiIure to reIax becomes a potent hindrance to the regurgitation of aIkaIine duodena1 contents into the stomach. SuccessfuI treatment of duodena1 uIcer depends on the contro1 of hypersecretion. The administration of antacids and the use of sedative measures to sIow up the cerebra1 stimuIus constitute the accepted medica treatment, but faiIure is common. SurgicaI measures have been designed to utiIize the patient’s own control mechanism. FaiIure means the deveIopment of a new uIcer. Of the two factors concerned in the etioIogy and maintenance of duodenal uIcer, dysfunction of the pyIoric sphincter aIone is amenabIe to direct attack. Its function can be aboIished permanentIy by a simpIe operation which removes the anterior haIf of the sphincter without opening into the duodenum or stomach. This procedure has been carried out with enduring success in cases of duodena1 uIcer.