Annals of the Royal College of Surgeons of England (1976) vol 58

Gastro-oesophageal reflux and hiatal hernia

A re-evaluation of current data and dogma

A R Moossa FRCS

D B Skinner MD FACSDepartment of Surgery, University of Chicago, Pritzker Schlool of Medicine, Chicago,Illinois.

SummaryVarious methods of investigating and treatingpatients with gastro-oesophageal disorders aredescribed and the rationale of current con-cepts is outlined. Emphasis is placed through-out on gastro-oesophageal reflux and its seque-lae rather than on sliding hiatal hernias.Symptoms of gastro-oesophageal dysfunctioncan be misleading, and careful studies are es-sential in assessing its importance and the re-sults of various modes of therapy.

IntroductionControversy and confusion still rage over themechanisms and treatment of gastro-oesopha-geal reflux and hiatal hernia. A fairamount of misconception has gathered in theliterature over the past io years. This reviewattempts to correlate the various concepts cur-rently in vogue. It is based on our presentpolicy of evaluating and treating patients withlower oesophageal disorders at the Universityof Chicago Hospitals and on our experimentaldata with normal human volunteers andrhesus monkeys.

Hiatal hernia versus gastro-oesophagealrefluxIt has not been sufficiently emphasized thatthere are two separate conditions affecting thegastro-oesophageal junction-a hiatal herniais simply an anatomical abnormality, whilegastro-oesophageal reflux is the pathological re-sult of an incompetent cardia'. Although thesetwo conditions often coexist, each one mayoccur without the other. A causal relationshipbetween hiatal hernia and gastro-oesophageal

reflux is unproven-a coincidental correlationremains the more likely possibility.A small (Type i) hernia is of no clinical im-

portance unless it is associated with gastro-oesophageal reflux. We are at present exclud-ing all the paraoesophageal (Type 2) herniasfrom this discussion. Suffice it to say that theselarge hernias are not usually related to gastro-oesophageal reflux and they have to, be treatedon their own merit in the same way as anylarge internal or external hernia elsewhere inthe body. They are subject to such complica-tions as bleeding, ulceration, erosive gastritis,gastric volvulus, strangulation, perforation,and acute intrathoracic gastric dilatation.These events mav be sudden and often occurwithout any pnor warning symptom. Themortality and morbidity rise appreciably in thepresence of any such complication. Even whenthese large hernias are asymptomatic surgeryis usually advised to prevent these lethal com-plications provided the general condition ofthe patient is satisfactory2. This concept ofprophylactic operation for all asymptomaticType 2 hiatal hernias may be too drastic sinceno discrete information is available on thenatural history of the condition. The risk ofcomplications must be balanced against thehazards of sturgery in each individual patient.

Since a small hiatal hernia is inconsequen-tial, emphasis over recent years has moved onto the problem of gastro-oesophageal reflux.This can lead to such complications as oeso-phagitis, ulceration, bleeding. and strictureformation. The whole issue has been totallyconfused by various workers using differentclinical parameters and investigative methodsfor evaluating gastro-oesophageal reflux.

Gastro-oesophageal reflux anid hiatal hernia

Clinical assessment of gastro-oesopha-geal refluxA large number of patients with gastro-oeso-phageal reflux have typical symptoms-name-ly, a hIstory of retrosternal burning sensationor regurgitation of gastric contents made worseby stooping or lying flat and relieved by stand-ing up or by ingestion of alkalis. In some cases,however, the complaints are very non-specificand consist of indigestion, postprandial full-ness, belching, dysphagia, angina-like chestpain, aspiration pneumonitis, or upper gastro-intestinal bleeding. These symptoms are notdiagnostic of reflux on clinical grounds alone.Further, some of the patients have concomit-ant duodenal or gastric ulcer, gastritis, biliarytract or pancreatic disease, or cardiopulmonarydisease. An objective way of assessing the im-portance and severity of the gastro-oesopha-geal reflux and the results of its treatment istherefore essential.

Radiological examination The bariummeal examination is most useful for visualizinglarge hiatal hernias. A small hiatal hernia canalso be diagnosed, depending on the diagnos-tic criteria employed and the aggressiveness ofthe radiologist concerned. However, radiologyis not an accurate way of diagnosing gastro-oesophageal reflux. The incidence of false neg-ative reports following standard barium swal-low examination in patients ultimately provedto have gastro-oesophageal reflux is as high as

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6o% according to some authorities3. In anattempt to improve the efficacy of radiologyin the diagnosis of reflux Donner and his col-leagues4 at the Johns Hopkins Hospital, Balti-more, evaluated acid barium studies. By thismethod oesophageal motility disorders can beprovoked and visualized by cineradiographyin a proportion of patients with symptomaticreflux. However, the technique depends solelyon the sensitivity of the individual's oesophagusto acid and therefore yields a large numberof false positive and false negative results. Themethod is also unreliable as a pain reproduc-tion test since the amount of acid barium istoo small and the transit time along the oeso-phagus too short to elicit any oesophagealpain.The water siphonage test, first advocated by

deCarvalho', has been strongly recommendedby several authorities'-8. It is simple, but istotally unphysiological since the patient has tolie in the supine position while drinking a largevolume of fluid rapidly. The technique is alsounreliable since the lower oesophagus relaxesduring swallowing and gastro-oesophageal re-flux will therefore occur in a large proportionof normal individuals subjected to this test.

Gastro-oesophageal motility studiesSince Fyke et al.9 popularized manometricmethods of studying gastro-oesophageal motorfunction in the I950S the technique has beenwidely applied in clinical investigative work.

FIG. I Gastro-oesophagealmanometry recorded duringa pull-through with contin-uous perfusion technique.

§ The tracing from only one27 26.5 catheter is shown in each

case. Note the high-pressureDW zone which relaxes on swal-

lowing in both rhesus monkeyand man. (s mm Hg=o.I33

.A. kPa.)

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128 Al R Moossa and D B Skinner

A continuously perfused triple-lumen poly-vinyl catheter is usually used. After it has beenpassed through the nose into the stomach thecatheter is gradually withdrawn at half-centi-metre intervals while the pressure is con-tinuously recorded with external pressure trans-ducers and direct-writing recorders. Basically,pressure in the stomach is higher than that inthe oesophagus, and a high-pressure zone ex-ists at the cardia (Fig. i). This intraluminalhigh-pressure zone has been termed 'lower oeso-phageal sphincter pressure' and is generallyregarded as a barrier to reflux. It relaxes onswallowing (Fig. i) and its amplitude providesa statistical separation between the populationof normal individuals and those with an in-competent cardia (Fig. 2). Rightly or wrongly,the intraluminal high-pressure zone at the low-er end of the oesophagus has been regardedas the manometric manifestation of an intrinsicsphincter. No anatomical sphincter has beendemonstrated in man or primates. In recentyears hormones such as gastrin, secretin, gluca-gon, and prostaglandins have been shown toalter the amplitude of this high-pressure zoneto a varying degree'0"1. No correlation hasbeen demonstrated between the reportedchanges in 'sphincter' pressures and the re-flux status of the subjects12. The effect of suchhormones may well be a non-specific one onthe smooth muscle of the upper gastrointesti-nal tract. Further, studies on our patients withZollinger-Ellison syndrome or Addisonianpernicious anaemia who have abnormallyhigh circulating levels of gastrin have failed toshow unusually high lower oesophageal 'sphinc-ter' pressures. These patients certainly do notpossess any immunity to gastro-oesophagealreflux and its sequelae. We cannot thereforeoveremphasize the importance of the followingfacts-a high lower oesophageal pressure doesnot invariably equate with gastro-oesophagealcompetence, either symptomatically or byusing the more sensitive method of pHmeasurement. Conversely a low high-press-ure zone value does not always indicate gastro-oesophageal reflux.The technique of performing oesophageal

motility studies has not yet been standardized.The consistency and the diameter of the tubes,the type of orifice (terminal or side holes), andthe rate of saline infusion are important vani-

ables which are currently being evaluated atthe University of Chicago Hospitals. Prelimin-ary data indicate that these factors have animportant bearing on the reproducibility ofresults under similar conditions in fasting sub-jects.

Although oesophageal manometry does notdirectly measure gastro-oesophageal reflux,its real importance must be carefully under-lined. It provides a method of exactly locatingthe intraluminal high-pressure zone and thishelps in the correct placement of the pH probefor measuring gastro-oesophageal reflux. Italso gives a semiquantitative measure of theintraluminal high-pressure zone before andafter treatment. Most important, it can identi-fy motility disorders of the body of the oeso-phagus, such as tertiary or spastic contractions,which may be due to reflux and be the source

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FIG. 2 High-pressure zone values in 197human subjects with normal and abnormalpH reflux tests. The difference between themean values is statistically significant (p <0.0005), but the overlap indicates that mano-metry alone does not diagnose gastro-oeso-phageal reflux. (I mm Hg = 0.133 kPa.)

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Gastro-ocsophageal re/lux and hiatal hernia

of (lysphagia and chest pain. It is essential inthe diagnosis of early achalasia when the intra-luminal high-pressure zone is found to be ex-

ceedingly high. Lack of oesophageal motilityor aperistalsis in the distal two-thirds of theoesophagus is also diagnostic of sclerodermna,which is commonly associated with gastro-oesophageal reflux.

Oesophageal pH The pH probe for detect-ing gastro-oesophageal reflux was first intro-duiced by Tuttle and Grossmann in I958".The probe is gradually withdrawn from thestomach into the oesophagus and, in mostnormal subjects, a sharp rise in pH occurs over

a distance of approximnately I cm at thecardia. With an incompetent gastro-oesopha-geal junction a more gradual rise in pH occurs

over a more prolonged distance. False positiveand negative results abound with this method.We adopted the method advocated by Skinnerand Booth'4 in 1970 and place the pH probea set distance (5 cm in man and 3 cm in therhesus monkey) above the cardia and takethe measurements tinder standardized condi-tions. The pH is measured under resting con-

ditions and after the patient has performed a

series of respiratorv and postural manoeuvres

in sequence-namely, deep breathing, cough-ing, Muller manoeuvre, and Valsava man-

oeuvre. Next I50 ml of o.I N hydrochloricacid is placed in the patient's stomach and theoesophageal pH taken at rest and after thefour manoeuvres already mentioned. Thepatient is turned into the right lateral, leftlateral, and 200 head-down positions and I5more pH readings are obtained. The result ispositive when more than two repeated falls inoesophageal pH to less than 4 occur. We haveestimated that about 40%/O of normal asympto-matic subjects will have one or two occasionalfalls in pH during these extreme manoeuvres.

Until recently we felt that this was the mostaccurate method of diagnosing reflux. In more

than Ioo normal subjects studied at the JohnsHopkins and University of Cl-iicago Hospitalsthe incidence of false positive results was about20/%. Over 300 patients ultimately proved tohave gastro-oesophageal reflux were analysedand the incidence of false negative results was

less than I%. The role of acid and pepsin inacute experimental oesophagitis has been deter-

mined by Goldberg and his colleagues"5. Theyshowed that mucosal exposure to a pH ofI-1.3 for one hour can produce oesophagitis.However, pepsin activity for the substrate ofoesophageal mucosa is maximal at pH 1.3-2.3.It is becoming apparent that the pH of 4 asthe upper limit previously used to indicatepositive reflux is too high and is beyond therange neces-sary for peptic or acid digestion ofthe oesophageal mucosa. Further, the numberof reflux episodes and their duration as well asthe clearing response to refluxed fluid by theoesophagus are being recognized as importantfactors in the pathogenesis of oesophagitis.We are now changing to continuous pH

monitoring techniques for the diagnosis of re-flux. Dr DeMeester in our department is col-lecting data on 24-h pH monitoring in thelower oesophagus. Two patterns of abnormalreflux are emerging-'nocturnal supine' and'diurnal upright'. Patients with the former-type would benefit from an antireflux proced-ure if an indication for surgerv exists. Thelatter type is probably associated with inade-quate gastric emptying due to pyloric dysfunc-tion; in addition there may or may not beprimary gastro-oesophageal incompetence.However, in patients with diurnal upright re-flux an antireflux procedure will probablylead to the gas-bloat syndrome. Whether thevare best treated by vagotomv and adrainage procedure supplemented bv anantireflux wrap is unknown. We are currentlyinvestigating the patterns of gastric emptyingin normal individuals and in refluxers.

Acid perfusion test'6 This te-t was designedto measure the sensitivity of the lower oeso-phaztus to acid. It is a pain reprodtuction testand in n)atients with atypical symptocms orwith multiple pathology it helns to docuimentthat their pain is due to rezurgitation of oTastricacid into the lower oesophagus. Hvdrochloricacid (O.T N) and isotonic saline qre llternatelyperfused into the mid-oesophagus without in-forming the patient which solution is beingused. A positive result is recorded if theTatient's pain is provoked by acid alone. Apositive-unrelated result is scored when symp-toms other than the natient's original com-Dlaints are precipitated bv acid alone. A nega-tive result is one in wvhich no symptom is re-

12 9

130 A R Moos.sa and D B Skinner

produced by either acid or saline. An indeter-minate result is obtained when both acid andsaline provoke the symptom.The acid or saline perfusion may have to be

continued for a minimum of 20 min beforeany conclusion can be drawn. It should alsobe emphasized that the acid perfusion test mayhave to be repeated on more than one oc-casion and the patient observed withoutprompting or interpretation by the in-vestigator. A positive result does not necessari-ly indicate the presence of oesophagitis. Con-versly, not all patients with oesophagitis aresymptomatic or have pain on perfusion ofacid.

Acid clearing test17 This is the last of thefour investigations that we perform on indivi-dual patients with documented gastro-oeso-phageal refluix. The pH probe is placed at5 cm above the cardia and a bolus of i 9 mlof o. i N hydrochloric acid is introduced intothe oesophagus i o cm proximal to the elec-trode. The patient is asked to perform 'dryswallows' at about 30-S intervals and the pHis continuously monitored. Normal subjectsclear this acid from the oesophaguis within i oswallows. If the acid clearance is delayed oeso-phageal peristaltic activity is considered to beinadequate. Any regurgitated gastric acidwould thus remain in prolonged contact withthe lower oesophagus. Under these circum-stances oesouhagitis is a likely result. A pro-longed acid clearing test in a patient withdemonstrable reflux can therefore be regardedas an absolute indication for oesophagoscopy.

Oesophagoscopy Oesophagoscopy withor without biopsy remains the mostaccurate method of diagnosing oesopha-gitis. It is our practice to perform oeso-pha,goscopv on every patient with demon-strable reflux who has a history of uppergastrointestinal bleeding or dysphagia, whoshows radiological features of spasm or irregu-lar mucosa, or who has a delayed acid clear-ing test. The battery of four oesophageal func-tion tests-namely, oesophageal manometry,the pH reflux test, the acid perfusion test, andthe acid clearing test-form a sound basisfor evaluation of all our patients who aresuspected of refluix. They can be adequately

handled by an experienced technician nurseunder close supervision. We used to perform allfour tests at one sitting over a period of aboutone hour. The wisdom of this is now beingquestioned. Oesophageal manometry, standardacid reflux test, and acid clearing test areusually well tolerated at the same sitting. Theacid perfusion test may need to be performedat one or more subsequent sessions.

Potential difference measurement Thepioneering work of Helm et al." showedthat the difference in electric potential betweenthe gastric and oesophageal mucosa in rela-tion to the skin is relatively easy to measure.The gastric mucosa has a negative potentialvoltage and the oesophageal mucosa a slightlypositive one compared with the reference elec-trode. Meckeler and Inglefinger'9 showed thatthe mucosal potential difference change cor-related with a change in the mucosa fromparietal-cell to columnar junctional or squam-ous epithelium. Beck and Hernandez20 addeda fourth polyvinyl tube to, the assembly ofthree manometric catheters and demonstratedthat the potential difference starts to rise ap-proximately 2 cm distal to the beginning ofthe high-pressure zone and becomes positive3-4 cm above that level. In patients with a longpotential difference transitional zone mucosalabnormalities such as oesopha,gitis, ulcer, car-cinoma, and ectopic gastric mucosa are usuallyfound. The technique has not received wideaccceptance and further improvement in itsnerformance and interpretation is necessarybefore it can be advocated as a screening testto detect oesophaveal mucosal abnormalitiesprior to oesophagoscopy.

The place of surgeryNot all patients wvith documented gastro-oeso-phageal reflux need to have an operation. Sur-gery is reserved for those with intrprtable refluxsymptoms which cannot be controlled by medi-cal means and those with comnlications such asulcerative oesophazitis, haemorrhage, strictureformation, and chronic aspiration pneumon-itis.

Sur,gical treatment fell into disrepute be-cause the aim of early pioneers was to correctan anatomical abnormality, the hiatal hernia.This did not always correct gastro-oesophageal

Gastro-ocsophageal reflux and hiatal hernia

reflux and therefore the operations advocatedby Allison2" and Sweet22 eventually fell intodisfavour. Since a hiatal hernia is of no signi-ficance surgeons in recent years have focusedon altering the mechanisms which control re-flux after reduction and repair of the hiatalhernia. Four operations satisfy the basic require-ment for any antireflux procedure. They arethe Collis gastroplasty2", the Hill posteriorgastropexy24, the Nissen fundoplication25, andthe Belsey Mark IV procedure2';.

Collis in 1954 devised his gastroplasty forpatients with early strictures and shortening ofthe lower oesophagus. Since the intra-abdomin-al oesophagus cannot be restored to its normalposition in these cases a tube of lesser curvatureof the stomach is used to construct a new loweroesophagus. The suiccess of the operation wasthought to be dependent on the restorationof the angle of His. Experiments on rhesusmonkeys in our laboratory have failed to sup-port this concept12. The success of the proce-dure is mainly if not entirely dependent onthe fact that there is an intra-abdominal mus-cular tube or neo-oesophagus continuous withthe intrathoracic oesophagus. We have de-monstrated that the intraluminal high-pressurezone is situated in that segment of stomachtube in the postoperative period. Gastrin andsecretin have similar effects on this neo-oeso-phagus as on the normal lower oesophagus.The other three operations mentioned basic-

allv restore a good intra-abdominal segment ofoesophagus. Creating an oesophagogastric flapvalve in an exaggerated fashion also helps toprevent further reflux. However, if the wrapof the stomach around the lower oesophagus isperformed too tightly a large number ofpatients will have the gas-bloat svndrome withdifficulty in vomiting or belching. This is easilyprevented by paying attention to two importantpoints. First, the outlet of the stomach is ad-equately verified to exclude incipient pyloricstenosis due to duodenal or prepyloric ulcera-tion. Second, a large Moloney bougie, at leastNo 50, is passed into the stomach before crea-ting any wrap arotind the lower oesophagus.The diaphragmatic hiatus is tusually narrowedbehind the oesophagus, but this is not necessaryunless the hiatal opening is very large. Preser-vation of the lower oesophageal musculatureand vagal nerve fibres must also be emphasized.

In an earlier group of I patients treatedby vagotomy and drainage without any anti-reflux procedure we found that the results werenot encouraging. There was no demonstrablechange in the intraluminal high-pressure zoneand reflux persisted in all cases. We thereforefeel that vagotomy and a drainage procedureought to be reserved for patients who haveconcomitant duodenal ulceration or its compli-cations. This can be done in conjunction withan antireflux operation if indicated.

All our Collis and Belsey Mark IV proced-ures were performed through the left chest andall the Nissen and Hill repairs were ap-proached through the abdomen. Basically, thethoracic approach is preferred in patients withsevere oesophagitis, perioesophagitis, oeso-phageal shortening, strictures, or very largeimpacted paraoesophageal hernias. Accessthrough a laparotomy is advocated in patientswith severely restricted pulmonary function orwith other intra-abdominal conditions suchas gallstones or duodenal ulcer which need tobe tackled at the same operation.The results of surgery are evaluated during

the second postoperative week by repeating thebarium swallow, oesophageal manometry, andpH reflux studies. The operative mortality foreach procedure is about i % and a successrate of over go'V, is currently being reported invarious series with a follow-up period of up to8 years2.

ConclusionsSymptoms of gastro-oesoDhageal refluxare often non-specific and overlap withthose of other conditions. Severe complicationsof oesophagitis and pulmonary aspiration mayoccur with minimal reflux symptoms. Clinicalevaluation alone can be misinterpreted andlead to inappropriate therapy. Our thesis isthat gastro-oesophageal reflux can be properlyevaluated only by means of a battery of oeso-phageal function tests-namely, radiology,oesophageal manometry, pH reflux test, oeso-phageal perfusion test, acid clearing test, andoesophagoscopy. The indications and results ofsurgical or medical treatment can thus be ob-jectively assessed, and in this way the relativemerits of the currently popular antirefluxoperations will become evident.

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I32 A IR Moossa and D B Skinner

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