hiatus hernia and heartburn · gations have been along two lines: (1) the upward reflux of a...

Gut, 1969, 10, 609-613

Hiatus hernia and heartburnE. W. GILLISON,l W. M. CAPPER, G. R. AIRTH,

M. J. GIBSON, AND I. BRADFORD

From the Department of Gastroenterology, Southmead Hospital, Bristol

SUMMARY The symptoms in a group of 80 patients with a pure sliding hiatus hernia were investigatedusing the pyloric regulation test (Capper, Airth, and Kilby, 1966). It was found that there was a

high correlation between the symptoms of heartburn and the reflux of duodenal barium intothe stomach.

Heartburn is one of the most distressing ofpresentingsymptoms in patients with hiatus hernia. The de-finition followed here resembles that of Tuttle,Rufin, and Bettarello (1961); it is described as 'awarm discomfort situated in the epigastrium orretrosternal region, usually radiating up to the throator more rarely across the chest, and is usuallyassociated with intake of food or change in posture'.The evidence for the pain of heartburn originating

from the lower oesophagus is strong and investi-gations have been along two lines: (1) the upwardreflux of a noxious fluid from the stomach; and(2) response of the lower oesophagus in the form ofinflammatory changes, motility changes, or both.We decided to investigate the former aspect, ie, thepossible nature of the fluid. So far, the evidence hasbeen in favour of gastric rather than duodenal juicebeing responsible for heartburn.

Evidence for gastric juice has been gathered inseveral ways. Aylwin (1953) and Flood, Wells, andBaker (1955) have used aspiration techniques, andfound a fluid of low pH containing pepsin in symp-tomatic patients. Tuttle, Bettarello, and Grossman(1960) and Tuttle et al (1961) measured thepH at thelower end of the oseophagus and found the level tofall to pH 4 coinciding with the onset of heartburn,and a rise to a more neutral value coinciding withrelief. Bernstein and Baker (1958) perfused the lowerend of the oesophagus with N/10 hydrochloric acidin order to differentiate chest pain due to oesophagitisfrom chest pain of cardiac origin. They found that ahigh proportion of patients in the former group gavea positive response.

Interest in the evidence for duodenal juice isincreasing today and has been prompted by the factthat heartburn is known to occur after total gastrec-tomy, after acid-reducing operations (Brain, 1966),and in the presence of achlorhydria (Palmer, 1960).'Present address: Department of Surgery, Royal Hospital, Sheffield

Excellent experimental work by Levrat, Lambert,and Kirshbaum (1962), using a delicate surgical tech-nique in rats, showed that diverting the pancreaticjuice and also bile onto the mucosa of the oeso-phagus caused a much more severe oesophagitisthan would pure gastric juice. Though the oeso-phagus of the rat is histologically different from thatof man, this work adds interest to comparativepathology.Davenport (1967) by means of experimental work

in dogs showed that duodenal juice caused structuraland functional damage to the gastric mucosa as aresult of the lytic action of duodenal juice on the pro-tective mucous layer of the stomach. It thereforeseems reasonable to us that when the cardia isincompetent this same juice can equally affect theoesophageal mucosa. The observation volunteeredby several of our patients that they spat 'green bileinto their handkerchiefs' prompted us to investigatethis problem more fully.

MATERIAL

The assessment was made by separate clinical and radio-logical teams, the latter team not aware of the clinicalfindings, its sole duty being to report on the behaviourof the pyloric sphincter.

Eighty patients attending general surgical, generalmedical, or thoracic surgical departments, either asinpatients but mostly as outpatients, were selected. Allhad a full barium meal examination and were found tohave no other radiological lesion than a hiatus hernia.

All but two of these 80 patients were interviewed by oneof us (E.W.G.) and their histories were based on the fol-lowing questionnaire:

1 Heartburn The patient's description had to be in hisor her own words, but to correspond more or less to ourdefinition. He or she had to have experienced heartburnon the day of the test or the day before.2 Vomiting More than twice in the previous six

months.609

on January 17, 2021 by guest. Protected by copyright.

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E. W. Gillison, W. M. Capper, G. R. Airth, M. J. Gibson, and L Bradford

FIG. 2.

FIG. 1.

FIG. 1. Group A: the normal competent pylorus.

FIG. 2. Group B: incompetent pylorus, erect position.

FIG. 3. Group B: incompetent pylorus, supine position.

FIG. 3.

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Hiatus hernia and heartburn6

3 Regurgitation This meant the awareness of un-pleasant fluid in amounts which could be swallowed or spatout.4 Abdominal pain Recorded when it occurred separ-

ately from heartburn.5 Dysphagia A sensation of food sticking in a

retrosternal position on swallowing. This had to be morethan twice in the previous six months.

6 Bleeding This had to be frank haematemesis. Astory of melaena alone was not accepted.

METHOD

The 80 patients were submitted to the pyloric regurgi-tation test as described by Capper et al (1966) and wereexamined by either of the two radiologists (G.R.A. orM.J.G.). The purpose of this radiological examinationwas to group patients according to their pyloric compe-tence: group A, competent (Fig. 1) and group B, incom-petent (Figs 2 and 3).The duodenal intubations were always done by the

same person (I.B.) in the ward or department, accordingto whether they were in-patients or out-patients. Aboutthree or four hours later they were taken to the X-rayDepartment for screening. When possible, patients ingroup B were tipped into a mild Trendelenburg position(about 200) to see if a hernial sac at the hiatus could bedemonstrated (Fig. 4).

RESULTS

According to the test, 24 patients fell into group Aand 56 into group B. The ratio of males to femaleswas 13:11 and 25:31, respectively. In the lattergroup it was not always possible to outline the hernialsac itself, but in the patient of Fig. 4 a few secondsafter demonstrating the sac an oesophageal stricturewas also seen (Fig. 5). Every drop of barium out-lining that stricture had originally been instilled intothe second part of the duodenum, and the tube hadbeen removed before the patient was tilted into theTrendelenburg position.The distribution of symptoms attributable to the

hiatus hernia was tabulated according to the twogroups (Table I). For ease of comparison, a histo-gram was constructed to show the percentages ofeach symptom (Fig. 6).The striking difference that can be seen in the two

groups is that heartburn in group B is so muchcommoner. While dysphagia and bleeding have not

TABLE ITHE ASSOCIATION OF HEARTBURN AND AN INCOMPETENT

PYLORIS

With Heartburn (159 cases) Without Heartburn (21 cases)

Competent Incompetent Competent Incompetent

7 52 17 4

Yates correction: P = <0-001

FIG. 4. Outlining ofhernial sac.

FIG. 5. Oesophageal stricture, seen in the patient illus-trated in Figure 4.

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E. W. Gillison, W. M. Capper, G. R. Airth, M. J. Gibson, and L. Bradford

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FIG. 6. Histogram showingpercentages of symptomsin 80 cases of hiatal hernia:a, in 56 cases of incompetentpylorus; b, in 24 cases ofcompetent pylorus.

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yet been shown to be significantly more common,the association of heartburn and an incompetentpylorus was highly significant (p = 0001, Table II).

TABLE IIDISTRIBUTION OF SYMPTOMS ATTRIBUTABLE TO HIATUS

HERNIA IN GROUPS A AND B

Symptom Pylorus

Competent (Group A) Incompetent (Group B)

HeartburnVomitingRegurgitationBelchingAbdominal painDysphagiaBleeding

7 (29%)13 (56%)17 (71 %)17 (71 %)17 (71 %)6 (25 %)4 (17%)

53 (93%)30 (54%)35 (65%)35 (65%)41 (71%)29 (52%)20 (36%)

DISCUSSION

The actual mechanism which leads to heartburnis still not clearly understood. Abnormal motilityfindings have been clearly shown in conjunctionwith heartburn by Jones (1938) and Texter (1967).Also, oesophagitis and heartburn definitely coexist.Siegel and Hendrix (1963) in a series of 25 patientswith heartburn found oesophagitis in 17. However,eight asymptomatic patients had biopsy evidence ofchronic oesophagitis. Palmer (1960) found that somepatients with heartburn had normal looking mucosabut biopsy revealed signs of submucosal inflam-mation.

In our own experience of 24 endoscopies, 19patients suffered from heartburn, and 15 of thosehad definite oesophagitis to the naked eye. On the

other hand, two out of the five without heartburnshowed mild inflammation.

It is tempting, but too soon, to draw clinicalapplications from this work and that of others.There has been a movement to perform a pyloro-plasty instead of repairing the hernia. Experimentalwork by Herron, Thomas, and Merendino (1957)showed a decrease from 72 to 9% in the incidenceof oesophagitis after Heller myotomy in dogs.Girvin and Merendino (1958) found that pyloroplastylessened the incidence of oesophagitis after oesopha-gogastrostomy. The suggestion was that drainageof the retained gastric juice was the importantfactor. We are not convinced yet that this alone isadequate in man. Franklin at Hammersmith Hos-pital, London, has been doing a Nissen fundoplica-tion combined with pyloroplasty for the last twoyears, and is satisfied with the results so far. Wells(1967) described how heartburn was cured by highgastrectomy and Roux-en-Y jejuno-jejunostomy, buthe abandoned this procedure because of the highincidence of postprandial dumping. Holt and Large(1961) have applied the same principle in achalasia,both after myotomy and oesophagogastrectomy.We need more knowledge of the physiology of theantroduodenal region and the cardia before decidingon the full comprehensive treatment of hiatus hernia.Our work has been done on the intact upper gastro-

intestinal tract using the pyloric regurgitation testwhich infers that if barium, which is introduced intothe duodenum, pours back into the stomach, thenduodenal juice should do the same. The evidence thatregurgitation does not occur in the normal person issupported by Kilby (1967) who found that in 27 non-dyspeptic controls, 26 had a competent pylorus, as

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Hiatus hernia and heartburn 613

in our group A. In time, we hope that this test willlead us to the ultimate goal of being able to pre-dict those patients at risk of developing the compli-cations of hiatus hernia and therefore requiring moreaggressive treatment at their initial presentation.We have found in this study that the concurrence

of heartburn with an incompetent pyloric sphincterwas highly significant, favouring the concept that thepresence of duodenal juice in the stomach of suchpatients is the decisive factor in heartburn.

We would like to thank Mr D. Mearns Milne, of theDepartment of Thoracic Surgery, Frenchay Hospital, inparticular, and the general surgeons in Bristol foradditional clinical material. Also we should like to thankDr J. M. Naish and Mr L. R. Celestin, both of theGastroenterological Unit of Frenchay Hospital, for theirhelpful criticism and advice during this study.

REFERENCES

Aylwin, J. A. (1953). The physiological basis of reflux oesophagitis insliding hiatal diaphragmatic hernia. Thorax, 8, 38-45.

Brain, R. (1966). Peptic strictures of the oesophagus associated withduodenal ulcer and operations for its relief. Proc. roy. Soc.Med., 59, 929-931.

Bernstein, L. M.. and Baker, L. A. (1958). A clinical test for esophagi-tis. Gastroeraterology, 34, 760-781.

Capper, W. M., Airth, G. R., and Kilby, J. 0. (1966). A test for pyloricregurgitation. Lancet, 2, 621-623.

Davenport, H. W. (1967). Personal communication.Flood, C. A., Wells, J., and Baker, D. (1955). Esophageal reflux in

simple heartburn. Gastroenterology, 28, 28-33.Girvin. G. W., and Merendino. K. A. (1956). The value of Finney

pyloroplasty in minimizing esophagitis after esophagogastrec -tomy with vagotomy and esophagogastrostomy. Surg. Forum.Philadelphia, 6, 328-333.

Herron, P. W., Thomas, G. I., and Merendino, K. A. (1957). Anexperimental approach to cardiospasm: appraisal of the Finneypyloroplasty in the prevention of oesophagitis following theHeller myotomy. J. thorac. Surg., 34, 609-614.

Holt, C. J., and Large, A. M. (1961). The surgical management ofreflux esophagitis. Ann. Surg., 153, 555-562.

Jones. C. M. (1938). Digestive Tract Pain. The Macmillan Co, NewYork.

Kilby, J. 0. (1967). Personal communication.Levrat, M., Lambert, R., and Kirshbaum, G. (1962). Esophagitis

produced by reflux of duodenal contents in rats. Amer. J.dig. Dis., 7, 564-573.

Lambert, R. (1962). Relative importance of biliary and pancreatic sec-retions in the genesis of esophagitis in rats. Ibid., 7, 1026-1033.

Palmer, E. D. (1960). Subacute erosive 'peptic' esophagitis associatedwith achlorhydria. New Engi. J. Med., 262, 927-929.

Siegel, C. I., and Hendrix, T. R. (1963). Esophageal motor abnormali-ties induced by acid perfusion in patients with heartburn.J. clin. Invest., 42, 686-695.

Texter, E. C. (1967). In The Stomach: the 13th Hahnemann Symposiumedited by C. Thompson, D. Berkewitz, and E. Polish, pp. 54-71.Grane and Stratton, New York.

Tuttle, S. G., Bettarello, A., and Crossman, !M. (1960). Esophagealacid perfusion test and a gastro-oesophageal reflux in patientswith esophagitis. Gastroenterology, 38, 861-872.Rufin, F., and Bettarello, A. (1961). The physiology of heartburn.Ann. intern. Med., 55, 292-300.

Wells, C. (1967). Personal communication.


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