treatment oesophagus associated hernia - thorax.bmj.com · phreno-oesophageal ligament in hiatal...

PHRENO-OESOPHAGEAL LIGAMENT IN HIATAL HERNIA REPAIR

part of the oesophagus in these cases is completelyfreed by dividing all the fibrous mediastinal attach-ments which have resulted from peri-oesophagitis,the normal part of the tube is nearly alwayssufficiently elastic to allow the hernia to be reducedwithout undue tension. I am sure that placing theanchoring stitches from the insertion of thephreno-oesophageal ligament to the under surfaceof the hiatal muscle as described and tighteningthem all together is an important factor in makingan oesophagus which is apparently short lengthensufficiently for good repair of the hernia. Bringingthe oesophagus through the anterior part of thehiatus is also important, i.e., always placing thehiatal stitches behind the oesophagus, never at thesides or in front, because the plane of the hiatus istilted forwards very little from the vertical so thatthe most anterior part is also the highest.There is another condition which has been called

" short oesophagus." Those who believe that onlythe part of the tube lined by squamous epitheliumcan rightly be called oesophagus consider that astate of short oesophagus exists when columnarepithelium extends further than usual up the tube,whether the tube itself is shortened or not. In theprevious paper I have explained why I do notrecognize reduction in the length of the part ofthe tube lined by squamous epithelium as a type ofshort oesophagus.

The insertion of the phreno-oesophagealligament into the oesophagus is at a level about2 cm. above the oesophago-gastric junction.The fixation of this insertion to the lower edge

of the hiatus is an essential step in the repair of ahiatal hernia. A method of doing this is described.

Neither the wall of the oesophagus nor of thestomach should be included in any stitches usedin the repair.

Repair by the method described makes anoesophagus too short to allow restoration of thestomach to the abdomen a rare finding.

REFERENCESAllison, P. R. (1951). Surg. Gynec. Obstet., 92, 419.Burke, J. B. (1959). Lancet, 2, 787.Clarebrough, J. K., and Connell, J. L. (1959). Aust. N.Z. J. Surg.,

29, 21.Groves, L. K., Martinez, W. V., and Effler, D. B. (1959). J. thorac.

Surg., 38, 537.Hagarty, G. (1959). Med. J. Aust., 2, 515.Harrington, S. W. (1955). Surg. Gynec. Obstet., 100, 277.Laimer, E. (1883). Beitrag Zur Anatomie Des Oesophagus, Med.

Jahrbucher (Wien), p. 333. (Quoted by Hagarty, S.)Lerche, W. (1950). The Esophagus and Pharynx in Action, p. 65.

Thomas, Springfield, Illinois.Marchand, P. (1959). J. thorac. Surg., 37, 81.Peters, P. M. (1955). Thorax, 10, 27.Sweet, R. H. (1948). New Engl. J. Med., 238, 649.Tanner, N. C. (1955). Lancet, 2, 1050.

THE TREATMENT OF FIBROUS STRICTURE OF THEOESOPHAGUS ASSOCIATED WITH HIATAL HERNIA

When a patient with a sliding hiatal herniadevelops dysphagia, this symptom may be dueto inflammatory hyperaemia and oedema in theoesophagus, to oesophageal muscular incoordina-tion or spasm, or to the laying down circumferen-tially of dense, contracted fibrous tissue in themucosa, the mucosa and submucosa, or

all layers of the oesophageal wall. Thesechanges can occur separately or together. Inthis paper a stricture is regarded as fibrous whenthere is convincing evidence at oesophagoscopyand at operation of the presence of circumferentialfibrosis in the oesophagus sufficient in itself tocause significant oesophageal obstruction whetherthe other factors are also present or not. Thesefibrous strictures complicating sliding hiatalhernias are difficult to treat satisfactorily, and an

extraordinarily wide range of procedures has been

suggested-a sure sign that the best solution to theproblem has yet to be found.Most authors favour some sort of resection

(Allison, 1951; Allison, Wooler, and Gunning,1957; Barrett, 1952, 1957; Belsey, 1953; Ellis,1956; Ellis, Andersen, and Clagett, 1956; Linds-kog and Kline, 1957; MacLean and Wangensteen,1956; Mustard, 1957; Sweet, Robbins, Gephart,and Wilkins, 1954; Tanner, 1955; Wooler, 1956),but few agree on what is to be removed or howbest to reconstitute the alimentary canal after-wards. Many variations of resection of oesophagus,or stomach, or both, with all sorts of anastomoseswhich may or may not involve the jejunum orcolon, have been advocated. Sometimes nostomach, sometimes the upper part of it, sometimesthe lower part, sometimes the upper and lowerparts leaving a portion of the greater curvature in

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the middle, is removed. No one as yet seems toremove all the stomach for this condition. Theresults are always said to be satisfactory. I donot believe it. If the results really satisfied thesurgeons and patients, ingenious new pieces ofalimentary mutilation would not continue to bedevised for this condition.Some reports favour more conservative

measures. Benedict and Nardi (1957) prefer nooperation at all. They advise dilatations withbougie olives guided along a swallowed thread.Presumably these dilatations are repeated for therest of the patients' lives. They resort to surgeryif this treatment fails or severe haemorrhageoccurs, and then occasionally do an oesophago-plasty; but usually advise resections. Severalauthors advise repair of the hernia, if possible,followed by post-operative endoscopic dilatationof the stricture (Holinger, Johnston, Potts, anddaCunha, 1954), or by dilatation during operationby bougies passed by the anaesthetist and guidedby the surgeon (Byrnes, 1958), or by retrogradedilatation via the stomach at the time of operation(Burke, 1959; Groves, Martinez, and Effler, 1959).Cross, Smith, and Kay (1959) stated that " repairof the associated hiatal hernia, rather than one ofthe more complicated procedures," was their treat-ment of choice, but they did not give any detailsabout what they did to the stricture. Berman andBerman (1959) also think that the hernia should berepaired, followed by post-operative endoscopicdilatations, but they added vagotomy, restorationof the cardio-oesophageal angle by oesophago-gastropexy, and pyloroplasty with excision of theanterior third of the pyloric sphincter to theoperation. They cannot have much faith in theirmethod of repair of the hernia.

This summary indicates that a surgeon, facedwith the problem of a patient with hiatal hernia andoesophageal stricture and seeking guidance, willturn to the literature in vain. It will only confusehim. I have found it best to ignore the literatureand work out the management of my patients inmy own way. This paper is based on 14 consecu-tive patients, all with tough fibrous strictures andpersistent dysphagia. Patients with mild or inter-mittent dysphagia due to superficial oesophagitisare excluded.The experience of these patients has led to the

,conclusion that resections are seldom, if ever,needed and that good results can be obtained byrepair of the hernia, dilatation of the stricture tothe point of internal splitting at the time ofoperation, and post-operative dilatation by self-bouginage with Hurst's mercury bougies for alimited period when necessary. The evidence

presented here is purely clinical. Since no resec-tion was done pathological specimens were notavailable for study.

PRE-OPERATIVE ASSESSMENTThe history of peptic oesophagitis, often for a

long period, followed by dysphagia, sometimesrapidly developing and sometimes present formany years or from infancy, and perhaps asso-ciated with haemorrhage and anaemia, is verycharacteristic in all its variations and should leadto the correct provisional diagnosis. Bariumstudies must be adequate, with full outlining of thestomach and duodenum. If no barium orinsufficient barium passes the stricture at the firstexamination, it must be repeated after dilatationof the stricture through the oesophagoscope. Theradiological examination is not complete until thehiatal hernia is properly shown and until it is provedwith reasonable certainty that there is no chroniculcer in the stomach or duodenum and nocarcinoma in the stomach. If these conditionsare found, gastric resection is necessary, as it wouldbe if there were no associated hernia and oeso-phageal stricture. They are the only indicationsfor resection. The stricture in the oesophagus isnot an indication for resection of oesophagus orstomach.At oesophagoscopy the possibility of oeso-

phageal carcinoma is excluded by inspection andbiopsy. Solid pieces of food which have failed topass the stricture may be present and need to beremoved. The stricture is dilated with bougies asfar as is possible with safety, and, if the stricturesplits at this stage, there will be less dilatation todo at operation. In these cases one commonlyfeels a second, lesser resistance to the passage ofthe bougies, usually 2 or 3 cm. below the stricture.This is due to muscular spasm at the oesophago-gastric junction.

This spasm also makes it very difficult forradiologists to fill the oesophagus below thestricture. Often they fail to do so. Then in thefilms the stricture looks as if it extends down tothe oesophago-gastric junction, and even when itis only a narrow ring at the top of the length ofapparent narrowing, it seems to be 2 or 3 cm. long.The stricture never extends down as far as theoesophago-gastric junction (Hayward, 1961a). Itmay, however, extend upwards (ascending oeso-phagitis) making a long length of narrowing, or beshort but situated as high as the aortic arch witha long length of unstrictured oesophagus belowinstead of the usual 2 or 3 cm. Long stricturesare usually relatively easily dilatable with bougiesas far as their lower ends. The bougie may not

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pass the extreme lower end, because the densestfibrous tissue is usually limited to the lower endof the stricture. The rest is largely due to hyper-trophy and spasm of the muscular wall of theoesophagus. Thus, in my experience, howeverlong they may look, tough fibrous strictures inthese cases are usually relatively short and some-times annular.Having established the nature and position of

the stricture and excluded associated gastric orduodenal disease, the patient is prepared foroperation. Blood transfusion to correct anaemiamay be required and a period on high-protein,high-vitamin fluids and vitaminized food may benecessary. The oesophagoscopic dilatation alreadydone usually relieves the dysphagia for at least 10to 14 days and enables the patient to ingest enoughfluid and soft food to be brought into reasonablecondition for surgery. If dilatation has failed anddysphagia is complete, intravenous fluids arenecessary. The patient should have the operationas soon as he is fit. He may feel so much betterafter the endoscopic dilatation that he wishes todefer it. He should be advised against this andwarned that his dysphagia will surely recur asseverely as ever, probably in a very short time.

THE OPERATIONAs many fibrous strictures are associated with

peri-oesophagitis which has produced densemediastinal adhesions, the approach must givedirect access to the stricture to enable this partof the oesophagus to be dissected free. The chestmust, therefore, be opened; a purely abdominalapproach in this type of case is inadequate. Ifthere is chronic peptic ulceration in the stomachor duodenum requiring gastrectomy, a thoraco-abdominal incision is best. Otherwise an ordinarypostero-lateral thoracotomy is used, usually on theleft side, but occasionally on the right side for aa very high stricture which would require difficultdissection under the aortic arch if approachedfrom the left. The hernia can be satisfactorilyrepaired through a right thoracotomy.

Surgical access having been obtained, theoperation proceeds in a series of clearly definedsteps.FREEING THE OESOPHAGUS. This may be easy,

but is more often tedious and difficult. It shouldbe done in the plane outside the vagi and the para-oesophageal lymph glands which in these cases areenlarged, so that these structures remain intact onthe oesophageal wall. The inflammation round theoesophagus may have obliterated the tissue planes.Then it is best to define the correct plane round

the normal oesophagus above or below the stric-ture and work down or up from this. Much ofthe dissection will need to be sharp. As theinflammatory tissue is very vascular, many smalland often very short arteries entering it from thedescending aorta will be divided and requirecareful ligation. The opposite pleura will prob-ably be opened: with controlled respirationanaesthesia this does not matter. I have notdrained the opposite pleural cavity when it hasbeen opened and have not needed to aspirate itpost-operatively. When the strictured area is quitefree, the dissection continues easily downwards inthe same plane over the lower oesophagus andthoracic stomach with its associated peritoneal sacto the muscular margins of the hiatus in the sameway as is done for repair of a hiatal hernia withouta stricture.The whole lower oesophagus and hernia are

now lying quite free in the mediastinum, and thestrictured part of the oesophagus looks and feelsvery thick, but its longitudinal muscle coat isclearly visible on the outside and appears intactin spite of the violence of the inflammatory processaround it. The abnormal thickness of the oeso-phageal wall may continue up from the stricturefor a few centimetres. The thickened part abovethe stricture does not feel quite so firm and seemsto be due largely to hypertrophy of the muscularcoat. Presumably this is a normal response to thepresence of the obstruction in the lumen, as wouldbe expected in any tube with a muscular coat.

SPLITTING THE STRICTURE FROM WITHIN.-At thisstage the anaesthetist is asked to pass Hurstmercury bougies, beginning with No. 22 (English).The surgeon palpates the tip of the bougiethrough the oesophageal wall as it approaches thestricture and with one hand directs it into thestricture while the other hand encircles the oeso-phagus lightly to judge the progress of the bougieand help guide it through. With this guidance ofthe tip, the anaesthetist may safely use all the forcethe bougie will take short of kinking or curling upin the throat. After being held up for a fewseconds the bougie may suddenly go throughbecause it has split the constricting fibrous tissuein the mucosa and submucosa, probably togetherwith any epithelium that may be over it. It issurprising how often this will occur with thismethod even when a much smaller bougie couldnot be passed safely at the pre-operative oeso-phagoscopy. Once the first bougie has passed onecan usually proceed easily through the series up toNo. 30 (English). The dilatation is not adequateuntil No. 30 will pass freely without being gripped,

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i.e., until all the constricting fibrous tissue in themucosa and submucosa has been split. Thestricture, which was easily palpable from theoutside before, is now impalpable, though thepalpable muscular hypertrophy, of course, remains.

If the bougies fail to pass the stricture, retrogradedilatation is necessary. For low strictures this isdone through a small gastrotomy in the thoracicpart of the stomach after exposing it by dividingthe phreno-oesophageal ligament and sac justabove the hiatus. For high strictures at the levelof the aortic arch it is done through a smalllongitudinal oesophagotomy in the normally patentoesophagus just below the stricture.The stricture is first palpated with the finger up

the oesophagus. Sometimes the finger succeeds insplitting it. If not, instruments must be used.After trying various implements, I have come tothe conclusion that the best are Hegar's dilatorsup to the size of Brock's expanding aortic valvedilator followed by this instrument openedcautiously but with considerable force untilsplitting suddenly occurs. This has happenedbefore it was fully open. I have not needed toopen it fully and have hesitated to do so for fearof splitting the muscle. As with the bougies, theseretrograde instruments are guided very carefullythrough the stricture with the hand encircling it onthe outside. After the stricture has split the proofthat dilatation is adequate is given by retrogradepalpation by the finger and the passage of theNo. 30 Hurst bougie from above. Neither shouldbe gripped. A little bleeding into the oesophageallumen results from the splitting, but, from myexperience, it can be ignored.

After dilatation of the stricture the anaesthetistpasses a Ryle's tube into the stomach and bringsit out through the nose, where it is fixed withstrapping at the correct length. This is for post-operative gastric aspirations until intestinal peri-stalsis is resumed. If retrograde dilatation hasbeen necessary the gastrotomy or oesophagotomyis closed.

REPAIRING THE HERNIA.-The details are as forrepair of any sliding hiatal hernia. If the strictureis to disappear post-operatively, the repair mustcompletely stop all oesophageal reflux. Thismethod of dealing with these cases will assuredlyfail if the repair of the hernia is imperfect.I believe that the repair is imperfect if theattachment of the phreno-oesophageal ligament tothe oesophagus is not properly fixed below thehiatus (Hayward, 1961b). If the oesophagus isfully freed, as described above, there will rarely beany difficulty in achieving this. It is uncommon

for the oesophagus to be too short. Though Ihave never found it so, my colleague, Mr. IanMcConchie, did on one occasion when he wasperforming this operation on a boy of 15 with acongenital hernia and ascending oesophagitis andfibrous stricture. He managed the reduction bytransposing the oesophagus to an opening in thehigher, membranous portion of the left diaphragm,and, in the ensuing months, the boy's stricture hasdisappeared. A newly created hiatus can, there-fore, be adequate.

POST-OPERATIVE CAREAfter this operation the oesophageal lining is

left split by the dilatation as well as eroded by anyulceration that was present pre-operatively. Asthe reflux has been stopped this will heal, but, untilthe epithelialization of denuded areas is complete,more fibrous tissue will form and may contract.After epithelialization is complete any fibroustissue present underneath will gradually thin outand cease to constrict.

In addition to routine post-operative treatmentthese patients need watching for the least sign ofa return of dysphagia. The cessation of refluxmakes all medical measures such as dietary restric-tions, alkalis, antispasmodics, and sleeping proppedup unnecessary. I put them on ordinary solidfood as soon as the alimentary canal will take it,usually early in the second week. Good boluses ofsolid food are useful dilators and, by being held upin their passage down the oesophagus, immediatelyindicate any return of the narrowing. Thishappens in more than half the cases, and, when itdoes, the patient must start self-bouginage at once,aiming at size No. 26 Hurst. If this size will gothrough there will be no trouble with a full normaldiet.

Self-bouginage may be required daily at first,but, as soon as possible, the intervals arelengthened. The patient goes home with hisNo. 26 (English) bougie, and when he can omitpassing it for a week without return of dysphagiaand without it being gripped when he swallows itafter this interval, he can discard it. This nor-mally happens within a few weeks or, at most,a few months. The aim is to keep the strictureopen until all ulceration has healed. Then it willstay open by itself. Patients will, as a rule, faceup to self-bouginage when it is explained that itis only to go on for a short time, not the rest oftheir lives. On occasion I have had difficulty inpersuading them to relinquish the bougie. Theyare so afraid of a return of the awful misery ofdysphagia that it may be hard to convince themthat it really will not recur.

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If self-bouginage has been started too late andNo. 26 will not pass the stricture, oesophagoscopicdilatation to size No. 28, which goes through theNegus full lumen oesophagoscope, is necessary.Then the patient will be able to swallow the No. 26,starting the next day. Lubricating it with xylo-caine jelly helps while the throat is still sore afteroesophagoscopy.

CLINICAL MATERIAL AND COMMENTSThe 14 cases on which this report is based were

consecutive in the author's practice during the pastfour years, but must not be taken to represent thetrue incidence of the condition or the relativefrequency of its variations. As the practiceincludes very little paediatric work, no infants orchildren are included. Also, being a purelythoracic surgical practice, cases with associatedchronic gastric or duodenal ulceration tend onlyto be referred from the general surgeon if heencounters thoracic trouble with which he needshelp. The incidence of this ulceration in this series(three out of 14) may therefore be too low.

The patient's ages varied from 17 to 84 andaveraged 53 years.~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~-FIG. IRadiograph of a low, short stricture in a msn aged 63 Two

views at the samne barium examination. In the film on the left theradiologist has ssucceeded in filling the oesophagus below thestricture. The second narrowing is due to muscular spasm at theoesophago-gastric junction.

FIG. 2.-Radiograph of a high, short stricture in a man aged 28.Two views at the same barium examination. Often, radiologistsonly produce films like the one on the left, which leave thepathology in doubt. The one on the right shows the full pictureof hiatal hernia and stricture.

There were eight men and six women. In twothe history of dysphagia began at the time ofweaning, strongly suggesting that the stricture wassecondary to a congenital hiatal hernia. In theremaining 12 the digestive troubles and dysphagiadid not begin till well into adult life and there waslittle doubt that they were all due to acquiredhiatal hernias.The strictures fell into three fairly well defined

groups: 10 low, short strictures (Figs. 1, 4, and 5),three high, short strictures (Fig. 2), and one longstricture (Fig. 3). In all of them the maximumnarrowing was localized to a portion of theoesophagus not more than 2 cm. long and usuallyless, and the narrowing seemed to be due to fibrosisinternal to the muscle coat, i.e., in the mucosa, orsubmucosa, or both.

In 12 it was impossible to be more specific thanthis because they were not seen from inside exceptthrough the oesophagoscope. In the remainingtwo the stricture was opened longitudinally for anoesophagoplasty, and in one of these the verynarrow part at the lower end was definitely dueto mucosal and submucosal fibrosis and was barely1 cm. long. The other 6 cm. of lesser narrowing

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muscle for a few centimetres above the strictureseemed hypertrophied, but, as it was only inspectedand palpated from the outside in these cases, it wasimpossible to be sure of this. The oesophagealwall of the second case in which oesophagoplastywas done seemed very fibrous in all layers at thesite of the stricture, which was a high short one. Thiswas also the only case in which the longitudinalmuscle coat did not appear normal from theoutside, but seemed fibrosed. Whether this stricturewould have been relieved by internal splitting ifI had been able to do this satisfactorily is notknown.

FIG. 3.-Radiograph of a long stricture in a tad aged 17, secondaryto a congenital hiatal hernia shown on the left. At this examina-tion the radiologist took no picture showing the hernia andstricture on the one film.

FIG. 4.-Radiograph of a low stricture in a man aged 64. Thisstricture was associated with muscular hypertrophy of the loweroesophagus, sufficient to be visible in the films as a line outsidethe column cf barium. No barium passed the stricture, so thehernia is not shown, but a small one was found at operation.

above, found at oesophagoscopy, was apparentlydue to hypertrophy of the muscle coat. In thelower centimetre which was incised for the oeso-

phagoplasty the muscle was seen to be 1 cm. thick(Fig. 4). In several other cases the oesophageal

FIG. 5.-Radiograph of a low, short stricture in a woman aged 32.A penetrating ulcer has leaked into the mediastinum (left-handfilm). The " waist " below the stricture at the oesophago-gastricjunction is well seen. At this stage the stricture had been dilatedsufficiently to allow the passage of a Ryle's tube for a continuousintragastric drip to supplement oral feedings. The ' leakingulcer" could have been due to a bougie, but all the bougiesseemed to pass normally and there was no pain after the oeso-phagoscopy, only delight at the improvement in the dysphagia.The film on the right was taken before oesophagoscopy. Insuffi-cient barium passed the stricture to distend the lower oesophagusand stomach at this examination.

In a small series of 14 cases it is unlikely thatall the possible variants would be encountered.There may be some with so much muscle fibrosisthat internal splitting is not feasible, but I thinkit can be accepted that, in most cases of stricturedue to peptic oesophagitis, the muscle coat isremarkably healthy and internal splitting of thestricture is effective and safe.Hypertrophy of the muscle coat of the

oesophagus in association with these strictures hasbeen noted by Barrett (1957). Groves et al. (1959)also observed it, even in some cases of peptic

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oesophagitis without stricture; they stated thatthey often did a myotomy for it. To damagemuscle which is reacting normally to the presenceof obstruction seems unnecessary and is useless,as they admitted, for tough fibrous strictures wherethe contracting fibrous tissue is in the mucosa andsubmucosa.

In the group of 10 low, short strictures therewere two in which the stricture consisted of atough, fibrous, annular diaphragm with a small,central hole, situated about 2 cm. above theoesophago-gastric junction. Similar strictures havepreviously been described as lower oesophagealring, lower oesophageal web and congenital oeso-phageal ring. MacMahon, Schatzki, and Gary(1958) noticed that these rings were always abovethe diaphragm and always associated with a hiatalhernia. They said that they always seemed to beat the junction of oesophagus and stomach, bywhich they meant at the junction of squamous andcolumnar epithelium, but this is above the oeso-phago-gastric junction as defined by me (Hayward,196 1a).

Allison et al. (1957) and Smith and Bradshaw(1959) advised submucous resection of them.Bugden (1957) described triradiate incisions in theweb, but thought circumferential removal might bebetter. Splitting them blindly, as described here,seems to be sufficient. However, the actual splitmust be felt as a sudden giving way, the stricturemust become impalpable from without, and neitherthe finger from below nor the No. 30 (English)bougie from above should be gripped afterwards.Mere stretching is not enough. They may bestretched enough, without splitting, to allow thepassage of the bougie and the finger, but in thatcase the bougie and finger will be gripped firmlyas they pass.

I believe that these annular strictures are merelyone variant of fibrous stricture due to pepticoesophagitis and that they are, therefore, notcongenital. One of the two cases reported hereoccurred in a woman aged 47 who had haddysphagia for one year, and the other occurred in awoman of 84 who had had dysphagia for 15 years.Thus the first had no dysphagia till the age of 46and the second till the age of 69. The symptomsof reflux oesophagitis due to the associated hiatalhernia preceded the dysphagia by a few months inthe first and by about 20 years in the second. Ontheir histories, it would be absurd to regard eitheras congenital. I do not know why peptic oeso-phagitis sometimes results in strictures of thisannular type with the fibrosis confined mainly tothe mucosa.

In two other cases with a low stricture the hiatalhernia and stricture were first noticed after lowersubtotal gastrectomy for chronic duodenal ulcera-tion. In both a careful history showed that refluxoesophagitis and dysphagia had begun before thegastrectomy.

The first was a woman, aged 59, who had a gall-bladder full of stones removed three years beforewithout relieving her indigestion. At this operation,scarring of the first part of the duodenum was noticed.During the following two and a half years she had sixsevere haematemeses, two requiring blood transfu-sions, all assumed to come from a duodenal ulcer.For three months the pain, previously confined tothe epigastrium, spread up behind the sternum andwas associated with regurgitation of food, which wasregarded as vomiting, and loss of weight. OnNovember 3, 1959, without any previous bariumexamination, a Polya gastrectomy was done. Nocomment on the hiatus was nade. A Ryle's tube wasleft for a few days down the oesophagus into thestomach remnant for post-operative aspirations inthe usual way. As soon as it was removed and shebegan to take fluid and soft food by mouth the retro-sternal pain and vomiting returned exactly as it hadbeen for the preceding three months, but it rapidlybecame worse. It was then noticed for the first timethat the " vomiting " was really regurgitation fromthe oesophagus, and a thoracic surgeon was consulted.Her first barium examination was ordered and showedcomplete obstruction in the lower oesophagus. Repe-tition of this examination after oesophagoscopicdilatation of the very tough stricture showed a largehiatal hernia. The operation described here was doneon January 6, 1960, and she is now well with no painand no dysphagia.The second was a man aged 64 who began to have

pain characteristic of duodenal ulcer at the beginningof 1959 and perforated his ulcer on May 24, 1959.It was oversewn. From then on he had typicalsymptoms of reflux oesophagitis, and early in Septem-ber, 1959, food began to be regurgitated and he rapidlylost weight. On September 30 a massive haematemesisrequired a transfusion of 5 pints of blood followedby an emergency laparotomy at which a Polyagastrectomy was done and the duodenal ulcer, whichwas not bleeding, was left in situ. The hiatus wasnot mentioned. Dysphagia and regurgitation of foodcontinued, but no notice was taken until his weightwas reduced to 5 st. (normal 10 st.) and he requiredintravenous fluids. He was then referred to thethoracic surgeon, and a barium examination (his first)showed complete lower oesophageal obstruction(Fig. 4). At oesophagoscopy easily dilatable narrow-ing was found from 31 to 36 cm., but at 36 cm. therewas a very tight, fibrous stricture which was dilatedwith difficulty using more force than usual in the hopeof enabling him to swallow for a period during whichhis general condition could be improved preparatoryto further surgery. This hope was not realized. A

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few hours later he had severe abdominal pain andrigidity, and a radiograph showed gas under thediaphragm. He was returned to the theatre, openedthrough a left thoraco-abdominal incision and theperforation by a bougie found through the oesophagusjust below the phreno-oesophageal ligament into theperitoneal sac of a small hiatal hernia. Oesophago-plasty and repair of the hernia were done. When thephreno-oesophageal ligament was sewn to the undersurface of the hiatus the oesophagoplasty was entirelybelow the diaphragm. He died suddenly on the fifthday, probably of a coronary occlusion. The oeso-phagoplasty was intact. (This is the patient who hadthe enormous hypertrophy of the oesophageal muscle.)

These two cases correspond to those describedby Bingham (1958) and McCredie and McDowell(1958) in which oesophageal strictures becameevident after subtotal gastrectomy for duodenalulcer. McCredie and McDowell's attention was

focused on the possible part played by the stomachtube in causing the stricture, and they suggestedthat perhaps rubber stomach tubes should beavoided. Bingham realized that the main cause isthe missed hiatal hernia which was subsequentlyfound in all the cases, but he did not suggest thatthe way to avoid the calamity is to investigate thepatient properly before the gastric operation.Then the presence of the hiatal hernia would beknown and it would be repaired at the same time.Cases such as this show that lower subtotal gastrec-tomy for hiatal hernia with stricture is not alwaysas successful as MacLean and Wangensteen's (1956)experience suggested. It may make the oeso-

phagitis and stricture worse, possibly due to refluxof bile as stated by Wells and Johnston (1955).The operation, as described (freeing the

oesophagus, splitting the stricture internally, andrepairing the hernia), was done on eight patientsthrough a left thoracotomy. Of these, six hadlow short strictures (two of them annular), one hada high short stricture, and one a long stricture. Infive, bouginage from above sufficed to split thestricture. Retrograde dilatation through a gastro-tomy was necessary in the other three.One patient had a penetrating ulcer near the

stricture which had leaked into the mediastinum,making a narrow, fibrous track lined by granula-tion tissue (Fig. 5). This track was dissected to itsorigin from the oesophagus, cut off level with thesubmucosa and the small opening closed with a

catgut stitch and covered by closing the oeso-phageal muscle over it with two linen stitches.Otherwise the operation proceeded as described,with retrograde internal splitting through a gastro-tomy. Another patient shared with my colleague,Mr. E. E. Dunlop, had a high, short stricture whichwas split by bouginage through the oesophagoscope

followed by repair of the hiatal hernia through theabdominal route under the same anaesthetic.Four years before, dilatation of the stricture byanother surgeon, without repair of the hernia, hadproduced only temporary relief of dysphagia.The above 10 patients are now all well with no

dysphagia and need no dilatations, but six ofthem required a period of post-operative self-bouginage, and one, an irascible old man whoflatly refused to swallow the bougie, needed onepost-operative oesophagoscopic dilatation.One patient with a chronic duodenal ulcer and

hiatal hernia was referred to me for endoscopyonly. I found a tight low stricture which I wasonly able to dilate to size No. 22 (English). Hewas the patient of a general surgical colleaguewhom I advised to do a Polya gastrectomy, retro-grade splitting of the stricture, and repair of thehernia through a left abdomino-thoracic approach.He did the gastrectomy and repaired the hernia, asadvised, but omitted to split the stricture. Hesimply passed the size 22 bougie again. Thepatient's indigestion and pain were relieved, buthe was still unable to swallow solids when he wasreferred back to me five months later. Oesophago-scopic dilatation was then successful up to sizeNo. 28. Presumably the five months' freedomfrom reflux made it easier. A subsequent periodof a few months of self-bouginage with a sizeNo. 26 Hurst bougie prevented return of thedysphagia.Two patients had an oesophagoplasty. One,

whose oesophagus was perforated with a bougieduring endoscopic dilatation, has already beendescribed. His death was the only one in theseries. The other was the one with the highstricture already mentioned in which the fibrosisseemed to involve the whole oesophageal wall.The chest was opened through a right thoracotomy,but the stricture was so firmly attached to themembranous part of the lower trachea with noplane of cleavage that I was afraid of opening thetrachea and foolishly abandoned the dissection half-way. I made a small vertical oesophagotomybelow the stricture where the whole wall, includingthe mucosa, appeared macroscopically normal.Through this, I began retrograde dilatation withHegar's dilators. The stricture was about 2 cm.long and the lumen hard to find. Finally a smalldilator found it, but, when pushed, it emergedthrough the oesophageal wall half-way up thestricture. This would probably not have occurredif the stricture had been completely freed so thatthe dilator could be guided by encircling fingers.The abandoned dissection then had to be com-pleted (the trachea was not opened) and an

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oesophagoplasty done. He required one post-operative oesophagoscopic dilatation followed byself-bouginage.The last of the 14 cases did not have the

operation described because he was a cardio-respiratory cripple with hypertension and grossemphysema who could barely walk 20 yards. Hehad oesophagoscopic dilatation at intervals ofabout six months until the stricture becameimpassable. The dilatations were never satisfactorybecause he used to become more and morecyanosed under anaesthesia and I had to stop whenordered to by the anaesthetist. Then, since it wasthe only operation he was thought able to survive,he had a gastrotomy under local anaesthesia onMarch 29, 1957. He still lives, now aged 70, inbed and in his wheeled chair. Periods occur whenfluids will pass the stricture and then he takes lessby the gastrotomy tube. He is included in thisseries because he was treated during the sameperiod and because his story shows that dilatationswithout repair of the hernia are not of lastingbenefit.

DISCUSSIONSurgical treatment should always have a sound

pathological basis. The above treatment of thistype of case is based on the following beliefs aboutthe underlying pathology, which, I realize, aredifferent from any hitherto put forward and areas yet unproved, but which I nevertheless considerto be close to the truth, because the treatmentbased on them is usually effective and they seemto be in accord with the pathological findings andwith general pathological principles.Most cases of reflux oesophagitis show

hyperaemic mucosa with shallow superficialulceration and sloughs which may come and gofor years, with some spasm and dysphagia at times,but no fibrous stricture. Even at this superficialstage there may be oedema and enlarged lymphnodes in the surrounding mediastinum. In periodsof quiescence some healing occurs. The squamousepithelium may grow again in ulcerated areas andmay develop leucoplakia. In other cases, or atother times in the same case, the denuded areasmay be replaced by metaplastic junctional epithe-lium (Hayward, 1961b). This gives some protectionfrom acid-peptic digestion, and future inflammationwill be more marked in the area immediatelyabove still lined by squamous epithelium. Withcontinuation or repetition of the process ofsuperficial ulceration and healing in casescharacterized by replacement by metaplasticjunetional epithelium, this columnar epithelium

creeps higher and higher. It may reach the levelof the arch of the aorta.

In a few cases, probably as a rule quite suddenly,and for reasons still unknown, the previously verysuperficial inflammation undergoes violent trans-mural spread. This seems always to occur in theregion where the squamo-columnar junctionhappens to be at the time and may therefore beanywhere from about 2 cm. up the oesophagus tothe level of the arch of the aorta. The transmuralspread is circumferential and symmetrical. Withinweeks there is a circle of contracting fibrous tissuein the mucosa and submucosa and usually severeperi-oesophagitis outside with rigid fibrousadherence of the gullet to all surrounding structuresat this level. The muscle coat in between isastonishingly little affected. It is scarcely everdestroyed like the tissues of the mucosa andsubmucosa. On the contrary it is often hyper-trophied. There may be some oedema and a littleincrease in fibrous tissue between the muscle fibres.This evenly circumferential transmural inflamma-

tion is quite different from the transmural spreadin one place of a penetrating ulcer with destructionof all coats, though rarely a penetrating ulcer mayalso be present in the vicinity (Fig. 5). Usuallythe associated ulceration is still quite superficial.It may also be circumferential but is more oftenconfined to one part of the circumference. As theseverity of digestion by regurgitated gastric con-tents abates the superficial ulceration may healmore or less completely, but the fibrous tissue inthe mucosa and submucosa remains tough andcontracted so long as any reflux is occurring. Thesite of the stricture is therefore in the mucosaland submucosal layers, not the muscular layer.It is the intact muscle layer which makes internalsplitting, as described, feasible. When inflamma-tion spreads up above the stricture-so-calledascending oesophagitis-it usually remains super-ficial, and the narrowing which extends slowlyupwards is due mainly to muscular hypertrophyand spasm. The fibrous stricture which requiresinternal splitting is usually still quite short and atthe bottom of the narrowed area.There is a widespread delusion that abnormal

tough fibrous tissue is of necessity permanent.Once the adjectives "fibrous," "organic," or" chronic " are applied to a stricture, most surgeonsautomatically consider that it probably ought tobe cut out. This idea is false, and the operationdescribed here is based on the opposite view thatabnormal fibrous tissue anywhere in the body, nomatter how inert the fibrocytes and bundles ofcollagen may appear under the microscope, is

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JOHN HAYWARD

really a labile tissue which only persists if there isa cause continually acting to keep it there. Forinstance, pleural adhesions often disappear, a verythickened pleura may return to normal if the causeof the inflammation has been completely eradi-cated, and the thickest keloid may in time bereduced to paper thinness.

It so happens that in the type of fibrousoesophageal stricture under discussion the cause,namely oesophageal reflux, can be completelystopped (by efficient repair of the associated hiatalhernia). With the cause removed the ulcers canre-epithelialize and the fibrous tissue under themthin out like a keloid. This can occur even with-out the complete internal splitting advised here, aswas shown by MacLean and Wangensteen (1956).Restoration of the normal mucosal and sub-mucosal architecture where it has been destroyedis, of course, not to be expected, but the gulletcan function again as an efficient conductor offood to the stomach.The operation is also based on the belief that

these strictures are all acquired and all due tooesophageal reflux, which is in turn almost always,if not always, due to an associated hiatal hernia.This is at variance with other opinions. Forinstance, Berman and Berman (1959) state that" the diaphragmatic defect may well be ofancillary importance." MacLean and Wangensteen(1956) reported 18 cases of fibrous stricture inwhich, according to them, only eight had a hiatalhernia, and they only considered it worth while torepair the hernia in three of these eight. Sweetet al. (1954) reported 50 cases of which 48 hadhernias. Though all were treated surgically invarious ways they do not mention repairing thehernia in any of them. All my cases have had ahernia, though in three it was quite small. Thediscrepancies in the reported incidence of hiatalhernia with these strictures seem only to beexplicable by assuming that the hernia has oftenbeen missed. The fact that oesophageal dilatationalone gives only temporary relief of dysphagia,whereas repair of the hernia as well and no othertreatment, medical or surgical, has in my casesalways been followed by prolonged relief, isevidence which suggests that the hernias reallywere present and caused the strictures and wereresponsible for their persistence.As well as these pathological considerations,

some fundamental surgical principles are involved.Surely it is a surgical principle that a damagedorgan which can be restored to normal functionshould not be removed. These strictures fall intothis category and this should be reason enoughfor not resecting them. When, moreover, their

resection makes it necessary to cut out a piece ofjejunum or colon to bridge the gap the situationis comparable with a woman cutting up newclothes to patch old ones. This sort of thing isjustifiable when the stricture is malignant buthardly when it is benign and reversible.

Still worse is the practice of attacking perfectlynormal stomach, cutting it this way and that andremoving more or less of it here and there, orwrecking its nerve supply and its pyloric sphincter,to deal with a condition which involves theoesophageal hiatus and the oesophagus. This, ofcourse, followed the discovery that oesophago-gastrostomy with normal stomach merely increasedthe reflux and caused the stricture to recur at theanastomosis; so surgeons proceeded to make thestomach as abnormal as possible before theanastomosis. It is a good surgical principle, when-ever possible, to remove the cause of the troubleand not to try to minimize its effects by partialor complete destruction of the function of othernormal organs. The cause in this condition isacid-peptic reflux and the proper treatment is tostop the reflux, which is quite simply done byrepairing the hernia, not to stop the normalfunction of gastric secretion which is necessary togood health.Nothing can replace the satisfaction of

savouring food in the mouth and feeling it passfreely down the gullet into a normal stomach,normally situated in the abdomen and with itsvagal nerve supply intact. The treatmentdescribed here usually achieves this result.

SUMMARYThere is no agreement on the management of

patients with fibrous oesophageal strictures due topeptic oesophagitis. Many widely differentapproaches to the problem, often involving moreor less extensive resections, have been advised.

This paper is based on the experience of treating14 personal cases.This experience has led to the conclusion that

the best method of treatment for most of thesepatients consists of an operation in which thesteps are freeing the strictured part of the oeso-phagus, splitting the stricture internally andrepairing the hernia, followed by post-operativeself-bouginage for a limited period when necessary.The hernial repair must include proper fixationof the oesophageal attachment of the phreno-oesophageal ligament under the hiatus.

This treatment is based on the opinion that thesestrictures are acquired, are due to oesophagealreflux and can be relaxed permanently after the

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reflux is stopped. It is thought that the reflux isalmost always due to a sliding hiatal hernia whichmay be small and has probably often been missed.

Resections for this condition are condemned.

REFERENCESAllison, P. R. (1951). Surg. Gynec. Obstet., 92, 419.

Wooler, G. H., and Gunning, A. J. (1957). J. thorac. Surg., 33,738.

Barrett, N. R. (1952). Proc. roy. Soc. Med., 45, 279.- (1957). Surgery, 41, 881.Belsey, R. H. R. (1953). Trans. med. Soc. Lond., 68, 18.Benedict, E. B., and Nardi, G. L. (1957). Amer. J. Surg., 93, 238.Berman, J. K., and Berman, E. J. (1959). A.M.A. Arch. Surg., 78, 889.Bingham, J. A. W. (1958). Brit. med. J., 2, 817.Bugden, W. F. (1957). Amer. J. Surg., 93, 248.Burke, J. B. (1959). Brit. med. J., 2, 787.Byrnes, C. K. (1958). Irish J. med. Sci., p. 65.Cross, F. S., Smith, G. V., and Kay, E. B. (1959). J. thorac. Surg.,

38, 798.Ellis, F. H. (1956). Proc. Mayo Clin., 31, 615.

Ellis, F. H., Jr., Andersen, H. A., and Clagett, 0. T. (1956). A.M.A.Arch. Surg., 73, 578.

Groves, L. K., Martinez, W. V., and Effler, D. B. (1959). J. thorac.Surg., 38, 537.

Hayward, J. (1961a). Thorax, 16, 36.-(1961b). Ibid., 16, 41.Holinger, P. H., Johnston, K. C., Potts, W. J., and daCunha, F.

(1954). J. thorac. Surg., 28, 345.Lindskog, G. E., and Kline, J. L. (1957). New Engl. J. Med.,

257, 110.McCredie, J. A., and McDowell, R. F. C. (1958). Brit. J. Surg., 46,

260.MacLean, L. D., and Wangensteen, 0. H. (1956). Surg. Gynec.

Obstet., 103, 5.MacMahon, H. E., Schatzki, R., and Gary, J. E. (1958). New Engl.

J. Med., 259, 1.Mustard, R. A. (1957). Canad. med. Ass. J., 76, 811.Smith, L. C., and Bradshaw, H. H. (1959). Surg. Gynec. Obstet.,

109, 230.Sweet, R. H., Robbins, L. L., Gephart, T., and Wilkins, E. W.

(1954). Ann. Surg., 139, 258.Tanner, N. C. (1955). Lancet, 2, 1050.Wells, C., and Johnston, J. H. (1955). Ibid., 1, 937.Wooler, G. (1956). Thorax, 11, 275.

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