Fascia lata graft repair of esophageal hiatal hernia

Fascia Lata Graft Repair of Esophageal Hiatal Hernia Be not the first by whom the new are tried. Nor yet the last to lay the old aside.

R.H. F.BRAIN, MS., F.R.C.S. ANDJOHNMAYNARD,MS., F.R.c.s., London, England

From the Department London, England.

of

Surgery,

Guy’s

Hospital,

HIS QUOTATION is thought to be singularly T inappropriate when applied to surgeons in

general, and particularly to those concerned with the problem of herniation. Dissatisfaction with existing ideas and methods has in the past led naturally to a reappraisal and inevitably to a change, usually for the better. This paper sets out the details that motivated such a change, with its results over a ten year period during which 281 patients have been operated upon for esophageal hiatal hernias. One hundred of this series have been carefully followed up and the results assessed. HISTORICAL SURVEY The familiar surgical problem of sliding hiatus hernia and associated gastroesophageal reflux has been discussed in innumerable papers from all parts of the world after the publication of Allison’s classical treatise on the subject [I]. Two aspects of the syndrome, an anatomic esophageal hiatal hernia and esophagitis, were well recognised long before this even though the two were not connected. Mackenzie [Z] in 1884 discussed chronic esophagitis, the main symptom of which was dysphagia. His treatment was hot foot baths, bismuth pastilles, and counterirritation with croton oil. Tileston [3] described the rare occurrence of chronic peptic ulcers in the lower end of the esophagus which were liable to perforate. Jackson [P] discussed peptic ulceration of the lower end of the esophagus, showed the importance of esophagoscopy in diagnosis, and

noticed the interesting feature that 75 per cent of his patients had symptoms of regurgitation. He suggested that the diaphragmatic pinchcock was inefficient but could find no supporting evidence. He was misled into associating peptic ulceration with focal infection in the tonsils, mouths, and sinuses of his patients. Winkelstein [5] described a new clinical entity of peptic esophagitis in five of his patients. They complained of regurgitation and retrosternal pain, which latter symptom he thought to be due to the effect of acid on the esophagus. He demonstrated esophagitis by biopsy in all his patients. A year later Truesdale [6] discussed the problem of diaphragmatic hernia in some detail. He noticed that hiatal hernias were more common in pregnancy and advancing age, recognised the so-called “short esophagus,” and the association of anaemia, haemorrhage, esophageal erosion, ulcer, and occasionally neoplasm with esophageal hiatus hernia. However, he did not recognise reflux and retrosternal pain as symptoms, and he thought the crural hiatus milked food from the esophagus into the stomach. He repaired the hiatus by suturing in front or behind the esophagus or even laterally and frowned on the habit in those days of crushing the left phrenic nerve to prevent strain on the suture line. Harrington [7,8], with an extensive experience of diaphragmatic hernia of all kinds, recognised that herniation of the cardiac end of the stomach through the esophageal hiatus was by far the most common diaphragmatic hernia that he encountered. In the course of 1,000 abdominal operations he noted that on digital examination of the esophageal hiatus 2 per cent 488

American Journal of Surgery

Esophageal

Hiatal

would admit three fingerbreadths and 8 per cent two fingerbreadths. At that time he thought that paraesophageal hiatal hernias were the most common. In later years, by which time he had collected 343 cases of hiatus hernia, he had recognised that only 25 per cent of these were paraesophageal and the remainder of the sliding type [9,10]. His indications for operation, however, were based on the size of the gastric hernia and the danger of incarceration. He did not stress the importance of reflux esophagitis although he noted ulceration of the lower end of the esophagus which normally healed if the hernia was reduced. His method of repair was to close the hiatus around the esophagus after reduction of the hernia, using strips of fascia lata to approximate the edges of the hiatus lateral, posterior, or anterior to the esophagus. Allison [1] in 1951 classified hiatal hernias into three groups: (1) paraesophageal, with no esophagitis; (2) sliding, with reflux and varying degrees of esophagitis; (3) mixed or rolling hernias. Bowers [II] recognised that 90 per cent of his cases were sliding hiatus hernias with the gastroesophageal junction above the diaphragm whereas paraesophageal hernias with the junction below accounted for the remaining 10 per cent. He pointed out that there was by definition no such thing as a combined type. INDICATIONSFOROPERATION

It is now generally agreed that paraesophageal hiatus hernias should always be reduced and repaired because of the dangers of incarceration, bleeding, ulceration due to retention, and, rarely, strangulation. It is realised that sliding hiatal hernias are relatively common. Approximately 5 per cent [12] of all barium swallows show an incompetent cardia, the vast majority of which are due to hernias, often too small to be reported. Many authors in the past have stressed that few patients with sliding hernias need surgery [13--161 whereas Rex et al. [17] in a ten year follow-up of 301 patients with hiatus hernia treated medically noted that approximately 60 per cent were asymptomatic or improved. We are generally in agreement that it is the presence of reflux esophagitis and its complications demonstrable on esophagoscopic examination in a patient with symptoms, that makes surgery necessary. However, it must be stressed that many paVol. 115. April 1968

Hernia Repair

489

tients with relatively minor symptoms undergo an unnecessarily prolonged trial by “fire and waterbrash” whereas approximately 10 per cent of patients in whom esophageal stricture ultimately develops have had very few or no previous symptoms. PATHOLOGICANATOMY

Whatever the true incidence may be of patients with esophagitis who will progress despite medical treatment to esophageal stricture and dysphagia, the mechanical problem facing the surgeon who deals with these hernias is the prevention of reflux. Naturally this has led to conjecture concerning the normal mechanism at play in maintaining gastroesophageal competence. Allison [1] considered that the muscle fibres of the right crus of the diaphragm played an important part in maintaining the oblique angle of entry of the esophagus into the stomach. They counteracted suction of the stomach into the chest during inspiration by contraction of the sling fibres of the right crus. He drew an analogy between this mechanism and the puborectalis muscle sling around the anorectal junction. He was aware, however, of an intrinsic mechanism which helped prevent reflux and was related to the oblique junction between the stomach and esophagus. Since this classical paper, controversy has raged around the intrinsic and extrinsic factors involved in gastroesophageal competence. Although no morphologic sphincter is demonstrable at the lower end of the esophagus, there is considerable evidence in favour of a physiologic sphincter. Fyke, Code, and Schlegel [18] demonstrated a definite band at the lower end of the normal esophagus which underwent prolonged contraction at a pressure some 10 cm. of water above intragastric pressure. Atkinson et al. [19] demonstrated a band of higher pressure of 1 to 3 cm. at the junction of the esophagus and stomach in thirteen of eighteen patients with hiatus hernia. They demonstrated a similar pressure band in a patient with a fixed hiatus hernia at the gastroesophageal junction at a level higher than the hiatus muscle sling. Botha, Astley, and Carre [20] produced evidence of a lower esophageal sphincter by a combination of cineradiographic and manometric investigations. Creamer, Harrison, and Pierce [21] demonstrated a “sphincteric zone” at the lower end of the esophagus which together with the abrupt changes of pressure at the hiatus pro-

Brain and Maynard

490

duced a “pressure barrier” at this level. Gahagan [.22] believed that part of the inner muscle layer of the stomach which loops around the insertion of the esophagus is the most important part of the sphincteric mechanism preventing reflux. Barrett [23,24] had already stressed the importance of this sling of fibres which narrowed the angle of His. The general consensus seems to accept the presence of a weak physiologic sphincter, in itself perhaps not enough to maintain competence. In combination with the pressure differences present between the thoracic and abdominal esophagus [21], obliquity of entry of the esophagus and mucosal flap valve [I1 1, or mucosal rosette [25], it is enough to prevent reflux. The pinchcock effect of the diaphragmatic “scissors” effect of the oblique and transverse muscle fibres [26] was considered doubtful by Lyons, Ellis, and Olsen [27]. Braasch and Ellis [28] produced no experimental evidence in favour of the diaphragmatic sling as a factor involved in the prevention of reflux. Whatever is thought of the merits of the various factors now listed as being involved in the control of the cardia, incompetence follows the disruptive influence of a bulky stomach within the confines of the hiatus, which can be cured by its replacement within the abdomen. This simple view forms the basis for the majority of operations recommended. Different features of the anatomy are considered by various authors best to achieve this end and are consequently exaggerated in each method of repair. As different surgical methods have evolved, the argument of thoracic versus abdominal approach has developed. ASSOCIATED

PATHOLOGY

Such controversy is largely based on the frequent association of other upper abdominal disease with hiatus hernia; some of these problems are more easily dealt with surgically through an abdominal incision. Palmer [29] reported, in association with hiatus hernia in 214 patients, diverticulosis of the colon in thirty-one patients, gallstones in thirty-two, duodenal ulcer in thirty-four, and gastric ulcer in twentyfour. Rex et al. [17] collected 365 cases of hiatal hernias, seventy of which were associated with gallbladder disease, and in a series of 801 cases of hiatal hernia he found fourteen patients with duodenal ulceration. Lord and Imparato [30] stressed the frequent association of hiatal

hernia, duodenal and gastric ulceration, and gallbladder disease. Eyring and Amendola [31] in a series of 365 hiatal hernias noted an incidence of gallstones in 20 per cent and duodenal ulceration in 15 per cent. Herrington, Edwards, and Sawyers [32] raised these figures to 35 and 25 per cent, respectively, and finally Casten [33] found duodenal ulceration in no less than thirty-four cases in a series of sixty-five patients with symptomatic hiatus hernia. This apparently frequent association of duodenal ulceration and hiatus hernia with esophagitis suggested that the degree of esophagitis associated with reflux might be related to the amount of acid secreted in the stomach. Hill, Chapman, and Morgan [34] had measured the pH of the lower part of the esophagus and used a reading below pH 5 to confirm the presence of reflux not demonstrable on radiography. Morgan [35] considered a pH of less than 4 in the lower esophagus as direct evidence of reflux. Casten et al. [36] measured the total night gastric secretion and found more than 20 mEq. of hydrochloric acid in 82 per cent of his patients with symptomatic hiatus hernia and this amount of acid in only 12 per cent of patients with asymptomatic hiatus hernia. Surgical thinking along these lines led to an alternative attack on esophagitis, that of decreasing gastric secretion. Pyloroplasty alone had seemed a logical procedure to encourage gastric drainage but was obviously by itself dangerous if gastric secretion was high. In fact, pyloroplasty does not increase the rate of gastric emptying except in patients with pyloric stenosis. Miller and Veloso [37] found it unsatisfactory and advocated vagotomy and antrectomy. Woodward, Schapiro, and Eisenberg [38] obtained good results in eleven patients from herniorrhaphy alone, but on followup examination eight still had evidence of reflux. In five patients in whom pyloroplasty alone was added to repair, the results were good in four but reflux was still present in two. Eleven further patients had pyloroplasty and vagotomy in addition to herniorrhaphy; nine good results and only two cases of reflux were obtained. Bowers [II ] tailored his operations to the degree of gastric secretion. He performed herniorrhaphy alone but added vagotomy and pyloroplasty if there was a high level of acid secretion. When there was an associated duodenal ulcer, he performed gastrectomy. Dorsey and Helbing [13] performed vagot-

Esophageal

Hiatal

omy and pyloroplasty in addition to repairing the hernia and pointed out that in difficult cases in which the esophagus was shortened as a result of esophagitis and fibrosis, division of the vagal nerves appreciably increased the length of the esophagus. Casten et al. [36] practised vagotomy and pyloroplasty in addition to repairing the hiatus hernia in forty-seven patients and found duodenal ulceration in twenty-three. Their patients had no postoperative diarrhoea. On the other hand Clarke, Gordon, and Winner [39] practised vagotomy in addition to repair and produced dumping and diarrhoea in nine of thirty patients. Bemhang, Nach, and Casten [4Oo]performed vagotomy and drainage in their patients who secreted a high amount of acid whereas Berman and Berman in two papers [14,41] advocated for all cases a “balanced operation” for hiatus hernia which again included vagotomy and pyloroplasty

.

VARIOUS

METHODS

OF REPAIR

To leave the problem of associated pathologic conditions for the moment, it will be seen that the approach to the hernia depends to a certain extent on the type of repair considered advisable. Allison [1] stressed the importance of the phrenoesophageal ligament which had become stretched by the shift of the gastroesophageal junction into the chest. He approached the problem via the chest and a small radial incision in the diaphragm, excised the excess phrenoesophageal ligament, and sutured the esophageal end of the ligament to the under surface of the diaphragm. In this way he believed he returned the gastroesophageal junction below the hiatus and restored normal anatomy. Finally he approximated the vertical fibres of the right crus with thread sutures posterior to the esophagus to narrow the hiatus. This latter manoeuvre has been the main feature of most abdominal repairs. Allison [42] stressed the importance of the function of the crural fibres and thought it important that suturing of the hiatus should not distort the anatomy and function of the hiatus. He was against anterior and lateral suture as advocated by Farrar and Sanders [43] and Harrington [8,10,44]. As theories concerning the functions of the crural fibres declined in popularity, other methVol. 115, April

1968

Hernia

Repair

491

ods of maintaining the obliquity of the gastroesophageal junction were sporadically reported. Boerema [45] suggested that there was a combination of three upward forces tending to displace the stomach into the chest: suction due to negative intrathoracic pressure, positive intra-abdominal pressure, and contraction of the longitudinal muscle of the esophagus. He therefore sutured the lesser curve to the anterior abdominal wall to pull the cardia downwards. He reported a 7 per cent recurrence rate in seventy patients. Nissen [46] combined this operation, gastropexy, with fundoplication of the gastroesophageal junction and reported seven relapses on follow-up radiography in ninety-six cases. Bettex and Stillhart [47] advised fundoplication alone for hiatus hernia in children. Farrar and Sanders [43] in 1952 increased the acuteness of the angle between the stomach and esophagus by suturing the fundus to the diaphragm. Twelve years later they had modified their procedure [48] by suturing the reflected phrenoesophageal ligament to the under surface of the diaphragm. Watkins [49] in 1959 and Amendola [50] in 1963 combined suture of the fundus to the diaphragm with fundoplication. Hayward [51] however was against suturing the fundus as he thought it unnecessary and that it interfered with normal gastric motility. More exotic attempts to replace the physiologic sphincter at the lower end of the esophagus have been made in dogs. McGannon, Williams, and Friesen [52] interposed the pylorus between the esophagus and stomach with successful results. Ingram [53] produced a muscle flap from the diaphragm which, when wrapped around the gastroesophageal junction, prevented reflux in dogs in which the lower end of the esophagus had been resected. These methods have not yet been applied in patients with reflux. The ileocaecal valve has been used successfully by one of us (R.H.F.B.) in a number of patients with special reflux problems such as those associated with achalasia. All these different operations are designed ultimately to prevent reflux of gastric contents into the esophagus. Barrett [54] echoed general surgical opinion when he stated, “the barrier against reflux is restored when the gastroesophageal junction is put below the diaphragm.”

Brain and Maynard

492

Since 1957 this objective has been achieved by the following operation. FASCIA LATA GRAFTING

This operation was developed ten years ago because of the poor results in our experience with the Allison type repair. A reappraisal of the problem was prompted by a 25 per cent recurrence rate and the finding on reoperation in several patients of incisional hernias through the central tendon, two such incisional hernias constituting emergency cases. Fresh emphasis was given to the importance of the fascial lining of the abdominal cavity in controlling herniation from the abdominal cavity. Moschowitz [55] in 1915 first drew attention to the importance of this, the transversalis fascia of the anterior abdominal wall, which is continuous over the diaphragm to the hiatus. It here leaves the crura to cross to the esophagus and ascend into the chest. At first loosely attached, it becomes firmly fixed and inseparable from the esophagus 2 cm. above the apparent esophagogastric junction [51] at or a little above the level at which the squamous epithelium of the esophagus changes to columnar epithelium of the cardia [56]. Dorsey and Helbing [13] and Casten et al. [36] in 1963 accepted the phrenoesophageal ligament as suitable material for fixation and sutured the cut esophageal ends to the under surface of the diaphragm. Harrington [57] was however well aware of the phrenoesophageal ligament and had examined it histologically. He noted that it atrophied in old age and was attenuated and atrophied in large sliding hernias. He dismissed it as unimportant. Paulson, Shaw, and Kee [58] had observed that the elastic fibres were stretched in hiatus hernias, but anchored the esophageal ends of the ligament to the under surface of the diaphragm. Sherman and Lyon [59] devised a more satisfactory method of suturing the ligament to the diaphragm. Barrett [23] thought the ligament played little or no part in keeping the gastroesophageal junction below the diaphragm and suggested that the left gastric artery was the significant structure which tethered the stomach in place, He was moved to describe the phrenoesophageal ligament two years later as “these strands of tissue which can be dissected out with the eye of faith” [24]. Hayward [51] who examined the whole re-

gion anatomically and histologically in some detail pointed out that the ligament was easily missed through an abdominal approach and on the whole was ignored by those surgeons who practised such an approach to hiatus hernia. Muscle suture of the right crus was compared with suture of the conjoint tendon in the Bassini repair of inguinal hernia and the resulting muscle atrophy that occurred in the latter procedure. Despite reports of primary muscle atrophy associated with hiatal hernia [60], our experience has contradicted this view. The operation to be described was based on two premises: first, that the phrenoesophageal ligament when normal does help to tether the stomach in the abdomen and by closing the hiatus prevents herniation of the stomach in much the same way as the transversalis fascia prevents direct inguinal hernias; second, that in cases of hiatus hernia, the ligament becomes stretched and attenuated. (A parallel can again be drawn with direct inguinal hernias.) Instead of using the inefficient and atrophic ligament for repair of the hernia [32], it was decided to replace the fascia with fascia lata. In order to avoid crural muscle atrophy from tuturing and yet to reduce the size of the stretched hiatus, a patch of fascia lata was sewed around the esophagus in such a way as to close the natural hiatus behind the esophagus and to increase the esophagogastric “angle” at the same time. In view of the importance of a complete reduction of the hernia, meticulous dissection of the under surface of the diaphragm under direct vision is essential, and this together with the need for assessment of possibly associated upper abdominal disease suggested a new approach to the problem. The abdominal route was rejected as being far too restrictive whereas the abdominothoracic route, now used successfully by Collis [61], was also rejected because of a reluctance to divide the costal margin, A transthoracic incision through the bed of the eighth rib on the left side, with division of the anterolateral attachment of the diaphragm, has successfully survived a ten year trial. This approach gives an excellent exposure and avoids all the dangers associated with incisions of the central tendon, such as damage to the phrenic nerve or subsequent hemiation . The patient is placed in the lateral position with the left side uppermost. A trapezium of American Journal of Surgery

Esophageal Hiatal Hernia Repair

FIG. 1. Left thoracotomy FIG. 2. The diaphragmatic

and the anterior end of the circumferential incision completed

revealing the spleen, stomach, and left lobe of the liver.

fascia lata measuring approximately 2.5 by 2 by 1 inch is excised from the left thigh. The chest is opened and the diaphragm is incised circumferentially 1 cm. from its costal attachment anteriorly backwards for approximately 6 to 7 inches. (Fig. 1.) Division of the left coronary ligament is continued to its junction with the lesser omentum and the falciform ligament, enabling the left lobe of the liver to be mobilised and later the hiatus to be more easily visualised and its limits defined. (Fig. 2.) After starting the dissection below the diaphragm laterally, the peritoneum is divided along the splenorenal ligament transversely across the front of the esophagus and into the lesser omentum. Dissection is continued to the hiatus in the subperitoneal extrafascial layer with full mobilisation of the spleen to avoid its damage. (Fig. 3.) The phrenoesophageal ligament is carefully dissected as it crosses the front of the hiatus to be reflected on to the esophagus. Its esophageal attachment is now eased upwards with a small dissecting swab until its firm attachment to the esophagus is clearly demonstrated. (Fig. 4.) This point roughly demarcates the upper end of the cardia as defined by Hayward [56] and is Vol. 115, A#ril 1968

incision into the diaphragm.

the junction zone between the columnar and squamous epithelium. The fascia is then divided transversely leaving a cuff approximately 1.5 cm. in length attached to the esophagus. (Fig. 5 and 6.) Care is taken not to damage the vagi perforating the ligament at this point. It is essential that this level be replaced and retained below the hiatus for a successful repair. Although division of the fascial reflection at this stage facilitates reduction of the hernia, it may be necessary to mobilise further the thoracic esophagus at its lower end where the full brunt of reflux has been received and where esophagitis and periesophagitis are at their worst. In those patients with organic strictures and without enough esophageal shortening to prevent replacement of the gastroesophageal junction below the diaphragm, an esophageal bougie can at this stage be passed by the anaesthetist and assisted through the stricture manually by the surgeon. The fascia lata graft is now split in its long axis for three quarters of its length and its edges sutured to the fascia over the under surface of the diaphragm well wide of the hiatus. It is so placed as to cover the hiatal gap behind the

494

Brain and Maynard

FIG. 4. Exposure of the edge of the phrenoesophageal

FIG. 5. Incision into the phrenoesophageal

ligament and commencement

of its upward dissection.

ligament.

FIG. 6. The esophageal hiatus dissected clean and demonstration

of the attached cuff of phrenoesophageal American

Journal

ligament.

of Surgery

Esophageal Hiatal Hernia Repair

7

8

FIG.7. The right border of the fascia lata graft sutured to the right half of the right CNSjust revealing the inferior vena cava. FIG.8. The graft suturedin place and the free border of the cuff of the phrenoesophageal ligamentsuturedto the

graft.

in a taut fashion, enfolding the latter anteriorly in such a way as to pull the esophagus backwards and thereby exaggerating the esophagogastric angle. (Fig. 7.) The muscular margins of the hiatus are allowed to approximate naturally above the graft in the hope that they will regain their normal anatomic site, size, tonus, and function. The size of the new hiatus behind the esophagus is critical; it must allow the passage of a normal bolus, yet not encourage further herniation. Room for the loosely fitting index finger alongside the esophagus at the level of the distal interphalangeal joint is a satisfactory measure. The operation in its latest form is completed by resuturing the esophageal cuff of the divided phrenoesophageal ligament about 2 cm. anterolaterally to the new hiatus, helping further to exaggerate the “angle” and to retain a suitable length of the abdominal esophagus. (Fig. 8.) An indwelling esophagogastric tube passed preoperatively to decompress the stomach greatly facilitates the operation and is retained postoperatively for twenty-four hours to prevent swallowed air from producing abdominal esophagus

Vol. 115. April 1968

distention. Normal swallowing is begun on the day after operation. CLINICALPRESENTATION There were twenty-nine male and seventyone female patients in the series. Three were children, fourteen were between nineteen and forty-five years of age, fifty-nine between fortysix and sixty-five years, twenty-one between sixty-six and seventy-five years, and three between seventy-six and eighty-five years of age. As can be seen, there is the usual preponderance in women and in the fifth, sixth, and seventh decades in this series. The different types of hiatus hernia have been classified as follows : sliding hiatus hernia (eighty-three cases), paraesophageal hernia (ten), sliding and rolling hernia (two), congenital short esophagus (four), and reflux after Heller’s operation (one). Paraesophageal hiatus hernias account for 10 per cent of the cases seen, which is similar to other series. Four cases of the entity usually termed a congenital short esophagus, in contradistinction to acquired short esophagus, have been included. Barium

Brain and Maynard

496

TABLE I SYMPTOMATOLOGY

symptoms Epigastric pain Retrosternal pain Flatulence Regurgitation Vomiting Relation to food Relation to position Dysphagia Haematemesis and malaena Onset during pregnancy Radiation of pain to neck and ears

meal in these four cases showed the usual hiatal hernia whereas esophagoscopy and biopsy revealed esophagitis with a squamocolunmar epithelial junction high in the esophagus. One case of reflux esophagitis after a Heller cardiomyotomy is included. The symptoms of the patients with uncomplicated hernias are analysed in Table I. The most common symptoms were pain and regurgitation. Surprisingly, half the patients with paraesophageal hernias complained of regurgitation. Ten per cent had frank bleeding in the form of small haematemeses or obvious melaena. Forty-six per cent complained of dysphagia and sixteen of these were found on investigation to have organic strictures. In view of the many reports of associated disease in other series it is interesting to report that in this particular group, despite a careful appraisal of the stomach, duodenum, and gallbladder at operation, no cases were associated with duodenal or gastric ulceration. One patient had gallstones, and cholecystectomy was performed through the same incision, The majority of these patients were referred because of failure of medical treatment. Patients in whom symptoms of peptic ulceration predominated despite their hiatal hernias may have been referred elsewhere. Two patients not included in this series have recently been found by one of us (J.M.) to have gastric ulcers in addition to a sliding hiatus hernia and have been treated by gastrectomy as well as fascia lata graft repair. Two patients had had previous operations at

Sliding Hiatus Hernia (EightyThree Cases)

Paraesophageal Hiatus Hernia (Ten Cases) 8 5 5 5 2 3 6 3

37 64 13 51 30 33 61 43 (16 organic strictures) 10 6

1

... 5

...

other hospitals. One had an unsuccessful repair of a paraesophageal hiatus hernia and the other had partial gastrectomy for a tight esophageal stricture due to reflux. RESULTS

OF OPERATION

Since Allison [I] reported thirty-three cases of sliding hiatus hernia with one death, one recurrent hernia, and one patient with radiographic evidence of reflux, innumerable reports of the results of different kinds of repair of hiatus hernia have followed. These results seem to vary widely, from Berman and Berman [la] reporting on nineteen patients who underwent repair, vagotomy, pyloroplasty, and esophagogastropexy with no recurrences, to Miller and Veloso [37] who reported a 45 per cent recurrence and from Weisel, Raine, and Watson [62] with one recurrence in thirty cases and Nissen [46] with seven recurrences after ninety-six operations, to Morgan [35] with four patients with evidence of reflux in a series of twenty-two repairs and Woodward, Schapiro, and Eisenberg [38] with eight patients with reflux in a small series of eleven patients. Brintnall, Blame, and Tidrick [63] emphasised that long-term follow-up study was necessary before publishing the results of any operation for hiatus hernia and reported fourteen recurrences in a series of twenty-nine abdominal repairs. Boerema [45] who sutured the lesser curve to the anterior abdominal wall stressed the importance of clinical and radiographic follow-up examination and reported a 7 per cent recurrence in seventy patients. American Journal of Surgery

Esophageal

Hiatal Hernia Repair

TABLE II DETAILED RESULTS OF FOLLOW-UP STUDY IN THREE Results

497

GROUPS

No. of Patients

OF PATIENTS

Comments ---

A. Group I: Normal Roentgenograms and Minor Symptoms (Seventeen Patients) Retrosternal

pain

3

Regurgitation LTomiting Dysphagia

1 1 9

Pain in scar

3

Mild in 1 Questionable angina in 1 (coronary thrombosis in 1) Slight Every few weeks Mild in 8; 1 occasional bad attacks

.

B. Group II: Abnormal Roentgenograms and No Symptoms Recurrent hernia Reflux Slight delay in emptying Diaphramatic pinchcock not sustained Left diaphragm paralyzed Left diaphragm poor excursion C. Group III:

2 5 6

(Fifteen Patients)

Two mechanical

and due to tight repair

2 1 1

.

Abnormal Roentgenograms and Symptoms (Thirty Patients)

Recurrent Reflux

hernia

Failed repair Pinchcock not sustained Mechanical delay in emptying Functional delay in emptying

One hundred patients who underwent this operative repair of hiatal hernias during the years 1957 to 1963 have been carefully followed up and the results assessed. Patients who had excision of esophageal strictures and replacement by jejunal transplant have been excluded. The majority of the patients were operated on by one of us (R.H.F.B.). Each patient on follow-up study, with a few exceptions, was examined and screened radiographically by the other author with the assistance of Dr. Roebuck of the X-ray Department of Guy’s Hospital. The movements of the left diaphragm were examined critically while barium was swallowed. Delay in emptying of the esophagus was assessed and gastroesophageal reflux was not excluded until the patient had been tipped head Vol. 115. Afwil 1968

With pain and regurgitation Dysphagia, regurgitation, and pain in 1 Slight regurgitation in 2 Slight retrosternal pain in 4 Slight dysphagia only in 2 True short esophagus, slight dysphagia but no reflux Mild dysphagia All with mild dysphagia Mild dysphagia in 3 Moderate to severe dysphagia in 5

down in all positions and pressure had been applied to the abdomen. The exceptions in this series who were not fully followed up include one patient who died postoperatively and four patients who died some years after operation from other causes. Six further patients examined at another hospital were not satisfactorily examined radiologically. Twenty-two patients were followed up two years after operation whereas the remainder had been operated on from three to six years previously. The assessment of the value of any operation purporting to cure hiatus hernia must include not only an evaluation of the major postoperative symptoms and presence of recurrent hernia

Brain and Maynard

498

One of the more important postoperative symptoms has been dysphagia, which is further analysed in Table III. Seventeen patients had dysphagia before operation which was due in seven cases to a preoperative stricture. Radiologic follow-up study failed to demonstrate a reason for the symptoms of dysphagia in seven cases whereas in the remainder the reason was obvious. In three cases there was definite radiologic evidence of a mechanical hold up due presumably to too tight a repair. In one case there was a functional delay in relaxation of the lower esophagus resulting in delayed emptying. In the remaining eighteen patients who did not have preoperative dysphagia, six had normal follow-up roentgenographic screening, two had a mechanical hold up, and five had a functional temporary failure of relaxation. Five patients had too tight a repair of the hiatus with consequent mild dysphagia which in three cases was severe enough to warrant further operation. Six patients had a narrow segment in the lower esophagus which ultimately completely relaxed and allowed the delayed passage of barium into the stomach. All six patients had mild dysphagia which appeared to be intermittent. This curious phenomenon needs further investigation. Six further operations were necessary after the original repair. These included widening of the hiatus in the fascia lata graft and narrowing of the hiatus in a recurrent hernia in one; in two, reduction of the hernia failed due to eso-

or reflux on roentgenogram but also the minor symptoms and minor radiographic abnormalities. The crude results of follow-up study were as follows : recurrent hiatus hernia developed in five patients The crude results of follow-up study were as follows: recurrent hiatus hernia in five patients and immediate failed repair in four caused by stricture in one requiring jejunal transplant, a short esophagus in two but with no reflux after operation, and inability to reduce the hernia in one. The latter patient still has regurgitation and evidence of reflux. The findings of follow-up study were analysed in more detail and divided into three groups. Group I (Table IIA) consisted of those patients who were radiographically normal but who had minor symptoms still. Group II patients (Table IIB) had abnormal results on roentgenograms but were symptom free. Group III (Table IIC) had both radiographic abnormalities and symptoms. The follow-up study in this series has been detailed and searching. Although there have been only five recurrent hernias, four failed repairs due to esophageal shortening, and fourteen patients with radiographic evidence on detailed screening of reflux, only twenty-nine of eightynine patients completely evaluated are quite normal. These findings may explain the widely conflicting reports of other writers and again stress the importance of long-term follow-up study and full clinical and radiographic assessment.

TABLE III POSTOPERATIVEDYSPHAGIA (THIIzTY-IWE PATIENTS) No. of Patients

Symptom Preoperative dysphagia Preoperative strictures

No preoperative

No preoperative

stricture

dysphagia

Follow-Up

Results

17 7

10

18

Normal barium swallows (2) Strictures, improving (2) Short esophagus (1) Recurrent hernia (1) Functional delay in emptying (1) Normal roentgenograms (5) Stricture (1) Reflux (1) Mechanical hold up (3) Normal barium swallows (6) Recurrent hernias (2) Reflux (3) Mechanical hold up (2) Functional delay in emptying (5)

American Journal

ofSuvgcry

Esophageal

Hiatal

phageal shortening and a jejunal transplant was later required. COMMENTS

Although the over-all gross recurrence rate (5 per cent) in this series is low, it seems at first disturbing to find that only 32 per cent (twentynine of eight-nine patients) are free of all symptoms and signs. However, we believe that the strict criteria utilised in this assessment give a much fairer picture than does the more usual assay based on a clinical appraisal of the good, improved, and not improved variety, in which bias on the part of both patients and assessor cannot be excluded. We believe that both the transthoracic subphrenic approach, using the circumferential diaphragmatic incision, and the replacement of the attenuated part of the subphrenic fascia, called the phrenoesophageal ligament, by a free fascia lata graft are based on sound reasoning. Perusal of the detailed results shows postoperative dysphagia in varying degrees of severity to be primarily responsible for the poor overall picture. The following analysis has been both interesting and helpful: 1. Too narrow a hiatus which is too small for passage of a normal food bolus. 2. Mechanical fixation of the cardia preventing “snakelike” action of the esophageal musculature during peristalsis. 3. Oversecure cardiac mechanism which, although it allows the passage of a normal mixed bolus, will not allow the free regurgitation of air during a meal. As a result the gas pressure in the stomach builds up to a degree barring further swallowing. These patients complain of an “air lock” relieved only by belching or the passage of the air much later per rectum. Colic may be a feature of its transit. 4. Alterations in esophageal tonus are now recognised to be common in patients with hiatal hernia. If unrecognised preoperatively, the postoperative course may be marred by dysphagia. The hypertonic type simulates the socalled corkscrew of diffuse spasm esophagus and the hypotonic type may masquerade as achalasia. Recognition of these various causes had led to a great improvement in recent results. Overtight suturing of the graft around the esophagus is avoided. Three patients have had to have further thoracotomies for this complication. The esophageal wall is no longer sutured to Vol. 115, Afwil 1968

Hernia

Repair

the new fascial edges of the hiatus, a procedure which was part of our original technic. The resuture of the edges of the phrenoesophageal cuff 1.5 cm. anterior and lateral to the new hiatus allows mobility of the cardia which is able to slide smoothly with peristaltic activity. Recognition of the aforementioned and the consequent modification in our technic have led us to believe that our present results will be superior to those in our past cases tabulated herein. SUMMARY

Two hundred eighty-nine patients have been operated upon for hiatus hernia in the last ten years. A repair procedure has been developed in which a fascia lata graft is sutured to the under surface of the diaphragm. The approach is through a left thoracotomy incision and a circumferential incision in the diaphragm. The reason for adopting this technic are set out. One hundred patients have been followed up between three and six years after operation, and eight-nine have undergone a full and detailed evaluation. The results are described with emphasis on detailed facts rather than clinical qualitative impressions. Although the over-all recurrence rate is low (5 per cent), dissatisfaction is felt at the high incidence of postoperative dysphagia which, although mild in all but three patients, is undoubtedly due in the majority to failure to leave an adequate hiatus for the passage of a normal bolus. REFERENCES

1. ALLISON, P.

R. Reflux oesophagitis, sliding hiatal hernia and the anatomy of repair. Surg. Gynec.6 Obst.,92: 419, 1951. 2. MACKENZIE, M. Diseases of the Throat and Nose, vol. 2. London, 1884. J. & A. ChurchillLtd. 3. TILESTON, W. Peptic ulcer of the oesophagus. Am. J. M. Sci., 132: 240, 1906. 4. JACKSON, C. Peptic ulcer of the oesophagus. J.A.M.A.,92:369, 1929. 5. WINKELSTEIN,A. Peptic esophagitis: a new clinical entity. J.A.M.A., 104: 906, 1935. 6. TRUESDALE, P. E. Diaphragmatic hernia: its 7. 3.

varieties and surgical treatment of hiatus type. Am. J. Surg., 32: 204, 1936. HARRINCTON,S. W. Diaphragmatic hernia. Arch. Surg., 16: 386, 1928. HARRINGTON,S. W. The surgical treatment of 105 cases of diaphragmatic hernia. IVest. J. Surg., 44: 255. 1936.

500

Brain and Maynard

9. HARRINGTON, S. W. The surgical treatment of the more common types of diaphragmatic hernia, oesophageal hiatus, traumatic, pleuroperitoneal absence and foramen of hiatus, congenital Morgagni. Report of 404 cases. Ann. Surg., 122: 546, 1945. 10. HARRINGTON, S. W. Various types of diaphragmatic hernia treated surgically. Report of 430 cases. Surg. Gynec. & Obst., 86: 735, 1948. 11. BOWERS, W. F. Current status of surgery for oesophageal hiatal hernia, peptic oesophagitis and inflammatorv stricture. New York J. Med., 63: 2220, 1963. 12. HODSON, C. J. Discussion on hiatus hernia. Proc. Roy. Sot. Med., 47: 531, 1954. 13. DORSEY, J. M. and HELBING, E. J. Oesophageal hiatus diaphragmatic hernia. The selection of patients for surgical therapy. Arch. Surg., 86: 1000, 1963. 14. BERMAN, J. K. and BERMAN, E. J. Balanced operations for oesophagitis associated with oesophageal hiatal hernia. Arch. Surg., 78: 889, 1959. 15. HARDY, J. D. Diaphragmatic hernias. A general survey with emphasis upon oesophageal hiatal type. Am J. Surg., 103: 342, 1962. 16. MENSH, M. Management of symptomatic hiatal hernia, oesophagitis and gastritis. A doubleblind controlled study. Am. J. M. Sci., 247: 669, 1964. 17. REX, J. D., ANDERSON,H.A., BARTHOLOMEW,L. G., and CAIN, J. C. Esophageal hiatus hernia. A 10 year study of medically treated cases. J. A. M. A., 178: 271, 1961. 18. FYKE, F. E., CODE, C. F., and SCHLEGEL, J. F. The gastro-oesophageal sphincter in healthy human beings. Gastroenterologia, 86: 135, 1956. 19. ATKINSON, M., EDWARDS, D. A. W., HONOUR, A. V., and ROWLANDS E. N. Oesophago-gastric sphincter in hiatus hernia. Lancet, 2: 1138, 1957. 20. BOTHA, G. S. M., ASTLEY, R., and CARRE, I. J. A combined cineradiographic and manometric study of the gastro-oesophageal junction. Lance& 1: 659, 1957. 21. CREAMER, S., HARRISON, G. R., and PIERCE, J. W. Further observations on the gastro-oesophageal junction. Thorax, 14: 132, 1959. 22. GAHAGAN, T. The function of the musculature of the oesophagus and stomach in the oesophagogastric sphincter mechanism. Surg. Gynec. & Obst., 114: 293, 1962. 23. BARRETT, N. R. Discussion on hiatus hernia. Proc. Roy. Sot. Med., 45: 279, 1952. 24. BARRETT, N. R. Hiatus hernia: a review of some controversial points. &it. J. Surg., 42: 231, 1954. 25. DORNHORST, A. C., HARRISON, K., and PIERCE, J. W. The normal oesophagus and cardia. Lancet, 1: 695, 1954. 26. COLLIS, J. L., KELLY, T. D., and WILEY, A. M. Anatomy of the crura of the diaphragm and the surgery of hiatus hernia. Thorax, 9: 175, 1954. 27. LYONS, W. S., ELLIS, F. H., and OLSEN, A. M. The gastro-oesophageal “sphincter mechanism”: a review. Proc. Staff Meet. Mayo Cl&.. 31: 605.

28. BRAASCH, J. W. and ELLIS, F. H. The gastrooesophageal sphincter mechanism: an expcrimental studv. SurPerv. 39: 901. 1956. 29. PALMER, E. 6. Hi&‘hernia in adults: clinical manifestation. Am. J. Digest. Dis., 3: 45, 1958. 30. LORD, J. W. and IMPARATO, A. M. Case for transabdominal repair of oesophageal hiatal hernia. J.A.M.A., 179:30, 1962. 31. EYRING, E. J. and AMENDOLA, F. H. Oesophageal hiatus hernia. Surgery, 53: 222, 1963. 32. HERRINGTON,J. L., EDWARDS,W. H., and SAWYERS J. L. A physiologic and anatomic approach to the surgical treatment of sliding oesophageal hiatus hernia. J. Tennessee M. A., 56: 465, 1963. 33. CASTEN, D. F. Oesophageal hiatal hernia and gastric acid secretion. Arch. Surg., 88: 255, 1964. 34. HILL, L. D., CHAPMAN, K. W., and MORGAN, E. H. Objective evaluation of surgery for hiatus hernia and oesophagitis. J. Thoracic 6 Cardiovasc. Surg., 41: 60, 1961. 35. MORGAN, E. H. Objective assessment of gastrooesophageal reflux secondary to hiatal hernia. Dis. Chest., 43: 367, 1963. 36. CASTEN, D. F., BERNHANG, A., NACH, R. J., and SPINZIA, J. A physiological basis for the surgical treatment of sliding oesophageal hiatal hernia. Surg. Gynec. b Obst., 117: 87, 1963. 37. MILLER, F. A. and VELOSO, M. Esophageal hiatus hernia and esophagitis: an evaluation of treatment by inhibiting reflux of acid peptic gastric contents. S. Forum, 12: 292, 1961. 38. WOODWARD, E. R., SCHAPIRO, M. S., and EISENBERG, M. M. Hiatal hernia and peptic esophagitis. Am. Surgeon, 29: 779, 1963. 39. CLARKE, J. S., GORDON, H. E., and WINNER, R. B. Treatment of hiatus hernia by hiatus herniorvagotomy and drainage procedure. rhaphy, Am. J. Surg., 107: 253, 1964. 40. BERNHANG, A., NACH, R. J., and CASTEN, D. F. A study of nocturnal gastric acid secretion in patients with sliding oesophageal hiatus hernia. S. Forum, 13: 250, 1962. 41. BERMAN, E. J. and BERMAN, J. K. Hiatal hernia complex. Arch. Surg., 89: 179, 1964. 42. ALLISON, P. R. Observations on a conservative approach to non-malignant lesions at the cardia. J. Thoracic Surf.. 32: 150. 1956. 43. FARRAR, T. and SANDERS,’ R. L. Hiatus hernia. Am. Surgeon, 18: 919, 1952. 44. HARRINGTON, S. W. Oesophageal hiatal diaphragmatic hernia. Surg. Gynec. b Obst., 100: 277, 1955. 45. BOEREMA, I. Gastropexia anterior geniculate for sliding hiatus hernia and for cardiostasis. J. Innternat. Coll. Surneons. 29: 533. 1958. 46. NISSEN, R. Gastropexy ‘and “f&doplication” in surgical treatment of hiatal hernia. Am. J. Digest. Dis., 10: 954, 1961. 47. BETTEX, M. and STILLHART, H. Operation for hiatus hernia and cardio-oesophageal achalasia by fundoplication after Nissen. Surgery, 55: 451, 1964. 48. FARRAR, T., TOSH, J., and SANDERS, R. L. Oesophageal hiatus hernia. Arch. Surg., 88: 846, 1964. 49. WATKINS, D. H. Gastric cardia competence in American Journal

of Surgery

Esophageal Hiatal Hernia Repair

50 51. 52.

53.

54. 55.

56.

repair of esophageal hiatal hernia. Rocky Moue tain M. J., 56: 40, 1959. AMENDOLA, F. H. Transabdominal repair of hiatal hernia. Szlrg. Gynec. 6r Obst., 116: 373, 1963. HAYWARD, J. The phreno-oesophageal ligament in hiatal hernia repair. Thorax, 16: 41,196l. MCGANNON. P. T.. WILLIAMS. C.. and FRIESEN. S. R. The prevention of ’ oekphagitis afte; oesophago-gastrostomy in dogs by an interposed pedicled pylorus. S. Forum, 7: 348, 1956. INGRAM, P. R. An experimental study of a new operation to restore oesophago-gastric competence and repair hiatus hernia. Surg. Gynec. & Obst., 116: 203,1963. BARRETT, N. R. Hiatus hernia. Brit. M. J., 2: 247, 1960. JOHNSON,A. B. Operative therapeusis. In: Hernia. Edited by Moschowitz, A. V. New York, 1915. Appleton-Century-Crofts. HAYWARD, J. The lower end of the oesophagus. Thorax, 16: 36, 1961.

Vol. 115, A@

1968

501

57. HARRINGTON, S. W. Diagnosis and treatment of various types of diaphragmatic hernia. Am. J. Surg., 50: 381, 1940. 58. PAULSON, D. L., SHAW, R. R., and KEE, J. L. Esophageal hiatal diaphragmatic hernia and its complications. Ann. surg., 155: 957, 1962. 59. SHERMAN, C. D. and LYON, J. L. Simplified method for esophageal hiatal herniorrhaphy. Surgery, 43: 857, 1958. 60. MARCHAND, P. The gastro-oesophageal “sphincter” and the mechanism of regurgitation. Brit. J. Surg., 42: 504, 1954. 61. COLLIS, J. L. A review of surgical results in hiatus hernia. Thorax, 16: 114, 1961. 62. WEISEL, W., RAINE, F., and WATSON, R. R. The efficiency of esophageal hiatal hernia repair. Surg. Gynec. & Obst., 104: 471, 1957. 63. BRINTNALL, E. S., BLOME, R. A., and TIDRICK, R. T. Late results of hiatus hernia repair. Am. J. Surg., 101: 159, 1961.