the role of the hiatus hernia in gastro-oesophageal

Review article: the role of the hiatus hernia in gastro-oesophagealreflux disease

C. GORDON, J. Y. KANG, P. J . NEILD & J. D. MAXWELL

Department of Gastroenterology, St George’s Hospital, London, UK

Accepted for publication 26 June 2004

SUMMARY

A sliding hiatus hernia disrupts both the anatomy and

physiology of the normal antireflux mechanism. It

reduces lower oesophageal sphincter length and pres-

sure, and impairs the augmenting effects of the

diaphragmatic crus. It is associated with decreased

oesophageal peristalsis, increases the cross-sectional

area of the oesophago-gastric junction, and acts as a

reservoir allowing reflux from the hernia sac into the

oesophagus during swallowing. The overall effect is that

of increased oesophageal acid exposure. The presence of

a hiatus hernia is associated with symptoms of gastro-

oesophageal reflux, increased prevalence and severity of

reflux oesophagitis, as well as Barrett’s oesophagus and

oesophageal adenocarcinoma. The efficacy of treatment

with proton pump inhibitors is reduced. Our view on the

significance of the sliding hiatus hernia in gastro-

oesophageal reflux disease has changed enormously in

recent decades. It was initially thought that a hiatus

hernia had to be present for reflux oesophagitis to occur.

Subsequently, the hiatus hernia was considered an

incidental finding of little consequence. We now appre-

ciate that the hiatus hernia has major patho-physiolo-

gical effects favouring gastro-oesophageal reflux and

hence contributing to oesophageal mucosal injury,

particularly in patients with severe gastro-oesophageal

reflux disease.

INTRODUCTION

Winklestein first described gastro-oesophageal reflux

disease (GERD) in 1935,1 and Allison2 highlighted the

association between oesophagitis and hiatus hernia. For

many years it was thought that a hiatus hernia had to

be present for reflux to occur.3 In 1972, Cohen et al.

drew attention to the role of a persistently hypotensive

lower oesophageal sphincter (LOS) in patients with

GERD.4 However, many patients with GERD were then

found to have basal LOS pressure within the normal

range.5 In 1982, Dodds et al.6 emphasized transient

lower oesophageal sphincter relaxations (TLOSRs) not

associated with swallowing and their role in the

aetiology of GERD. Subsequent studies have shown that

TLOSRs are in fact physiological,7, 8 and they underlie

the majority of reflux events in healthy subjects.9 The

pathogenesis of GERD is now recognized to be multi-

factorial, involving the LOS, diaphragmatic crus, oeso-

phageal acid clearance, gastric acid secretion, gastric

emptying and intra-abdominal pressure. But what of

the hiatus hernia?

The association between hiatus hernia and GERD has

long been recognized.2, 10 Much work has been done

recently to elucidate the effect of the hiatus hernia in the

pathophysiology of GER, and we are now beginning to

understand this complex relationship.11 The pendulum

has swung back, and like flared trousers and other icons

of the 1960s, the hiatus hernia is coming back into

fashion. This review looks at how the hiatus hernia

influences antireflux mechanisms, GERD and its

complications in adults.

Correspondence to: Dr J. Y. Kang, Department of Gastroenterology, St

George’s Hospital, Blackshaw Road, London SW17 0QT, UK.

E-mail: [email protected]

Aliment Pharmacol Ther 2004; 20: 719–732. doi: 10.1111/j.1365-2036.2004.02149.x

� 2004 Blackwell Publishing Ltd 719

METHODS

A Medline search was performed, limited to English lan-

guage, using keywords: hiatus hernia/gastro-oesopha-

geal reflux disease/aetiology/prevalence/classification/

diagnosis/Barrett’s/proton pump inhibitors/oesophageal

neoplasia/genetics/therapy, from the 1966 to 2003

database and PreMedline. Other relevant publications

known to the authors were also reviewed. Studies on

paediatric subjects were not included.

OESOPHAGEAL ANATOMY AND PHYSIOLOGY IN

NORMAL SUBJECTS

The oesophagus is a hollow muscular tube extending

from the pharynx to the stomach. It is composed of both

striated and smooth muscle and functionally comprises

three portions: (i) posterior cricoid portion – contains

striated muscle under voluntary control, and initiates

swallowing; (ii) body of the oesophagus – smooth

muscle which propagates peristalsis under control of

both the extrinsic (vagus) and intrinsic (Auerbach’s)

plexus; and (iii) the LOS. The distal end of the

oesophagus is anchored to the diaphragm by the

phreno-oesophageal ligament/membrane, which is

formed by the fused endothoracic and endoabdominal

fascia.12

The longitudinal muscles of the oesophagus shorten

during swallowing,13, 14 and the gastric cardia tents

through the diaphragmatic hiatus,13 but reduces after-

wards. This is commonly seen on barium studies,

provided a careful examination is performed,15 and is

termed the phrenic ampulla. Traditionally, it was

regarded as part of the oesophagus and hence a

physiological finding. However, simultaneous fluoro-

scopic and manometric studies of the gastro-oesopha-

geal junction (GOJ) by Lin et al.16 suggested that the

phrenic ampulla is physiologically distinct from the

oesophagus, and is analogous to a small reducing hiatus

hernia.16

The LOS is a manometrically distinct entity, identified

by a rise in pressure over the gastric baseline pressure as

a pressure transducer is withdrawn from the stomach to

the oesophagus. It is a functional barrier with no

anatomical landmarks, and represents an intraluminal

zone with a basal pressure greater than that of the

stomach and oesophagus. In adults, this zone has a

pressure of approximately 20 mmHg (in one study with

a range of 10–35 mmHg17). It has been suggested that

a pressure of 6 mmHg or less is required for GER,18

although there is a great deal of overlap and many

patients with milder forms of GERD will have normal

LOS pressure.

The LOS is approximately 4 cm long, 2 cm of which

lies intra-abdominally. The intrinsic muscles of the

distal oesophagus and the proximal stomach, with

the sling fibres of the cardia, form the intrinsic part of

the LOS. This is augmented externally by a number of

adjacent structures:

1 The crural diaphragm forms a sling around the GOJ

and has been shown to have a sphincteric action

distinct from that of the LOS.19, 20 It enhances the

LOS pressure,21 and augments the oesophago-gastric

junction (OGJ) when abrupt rises in intra-abdominal

pressure occur, such as coughing or abdominal

straining.22

2 The angle of His is the acute angle formed between

the greater curvature of the stomach and the

oesophagus, and this is thought to function as a

valve.23, 24 If the angle becomes less acute then

reflux is more likely to occur.25

3 The distal portion (approximately 2 cm) of the

oesophagus is thought to act as a valve. This portion

of the oesophagus is within the abdominal cavity,

and thus any increase in intra-abdominal pressure

will be transmitted equally to the stomach and the

intra-abdominal oesophagus.26, 27 Thus, as long as

the LOS maintains an intraluminal pressure incre-

ment greater than intragastric pressure, the reflux

barrier is maintained.

4 The phrenoesophageal ligament inserts circumferen-

tially into the oesophageal musculature close to the

squamo-columnar junction,16 and contributes to the

competence of the GOJ.28, 29 In patients with hiatus

hernia, the phrenoesophageal ligament is stretched

in an orad direction, forming a sac which contains

part of the proximal stomach and distal oesophagus.

DeMeester et al. proposed that this functions as an

extension of the abdomen into the mediastinum, and

allows for transmission of intra-abdominal pressure

to that portion of the LOS contained within the sac.30

The importance of the length of oesophagus within

the hernia sac is seen in the autopsy study of 55

patients by Bombeck et al.28 Eight patients had a

hiatus hernia, five of whom had no evidence of

oesophagitis (and hence a competent cardia). The

phrenoesophageal membrane in these five patients

720 C. GORDON et al.

� 2004 Blackwell Publishing Ltd, Aliment Pharmacol Ther 20, 719–732

inserted a mean of 3.6 cm above the GOJ. In the three

patients with oesophagitis (and hence an incompet-

ent cardia), the ligament inserted a mean of 0.5 cm

above the GOJ. This difference was significant and

emphasizes the importance of an adequate length of

intra-abdominal oesophagus in maintaining a com-

petent antireflux mechanism, even in patients with a

hiatus hernia.

Transient lower oesophageal sphincter relaxations

The TLOSRs are spontaneous relaxations to baseline of

LOS pressure, and are distinct from swallow-induced

LOS relaxations. In normal subjects, they allow belching

to occur.7, 8 They underlie the majority of reflux events

in healthy individuals and patients with mild GERD, i.e.

those with normal basal LOS pressure.5, 31, 32 In

patients with severe GERD other factors such as low

basal LOS pressure, defective LOS function, or a hiatus

hernia, are more important.32, 33 Over the whole

spectrum of GERD, the proportion of reflux episodes

that can be ascribed to TLOSRs varies inversely with the

severity of the disease.34

PATHOPHYSIOLOGICAL MECHANISMS

UNDERLYING GERD IN SUBJECTS WITHOUT

HIATUS HERNIA

Gastric acid is kept in the stomach by a combination of

oesophageal motility, LOS function and gastric empty-

ing. Coordinated peristaltic waves deliver the food

boluses to the distal oesophagus from the mouth. This

is achieved by voluntary (pharyngeal) and involuntary

(oesophageal) muscle, coordinated by the Auerbach’s

plexus. Oesophageal peristalsis can be primary (initiated

by a swallow), or secondary (initiated by distension of

the oesophagus because of retained food or refluxed

material). Tertiary contractions refer to non-peristaltic

oesophageal activity. The LOS relaxes completely during

swallowing to allow passage of the ingested material. As

mentioned earlier, a low LOS pressure is an important

determinant of GERD. LOS pressure is reduced by

cigarette smoking,35 alcohol36 and by some foods, e.g.

peppermint.

In adults about 1000–1500 mL of saliva is secreted

per day, with a pH of approximately 7.0.37 This large

volume of saliva contributes to the buffering of refluxed

acid, and induces primary peristalsis.38 Although

salivary flow in patients with GERD is similar to that

in age-matched controls,39 it can be doubled by

chewing gum, and this has been proposed as a non-

pharmacological treatment for GERD.40

Delayed emptying of the proximal stomach may make

reflux more likely due to a pressure backflow effect.

Many patients with GERD have an enhanced or

prolonged postprandial fundic relaxation, with delayed

emptying of the proximal stomach.41, 42 Gastric outlet

obstruction, as in peptic ulcer disease43, 44 and delayed

gastric emptying, as in diabetes,44 can be associated

with GERD.

HIATUS HERNIA

Hiatus hernia refers to the herniation of parts of

the abdominal contents through the oesophageal hiatus

of the diaphragm. There are three recognized types:45, 46

Type I

This is the commonest type, and is characterized by

widening of the muscular hiatal aperture of the

diaphragm, with laxity of the phrenoesophageal mem-

brane, allowing some of the gastric cardia to herniate

upwards.

Type II

A type II hernia results from a localized defect in the

phrenoesophageal membrane. The GOJ remains fixed

to the preaortic fascia and the arcuate ligament,

and the gastric fundus forms the leading part of the

herniation.

Type III

Type III hernias are mixed types I and II, with a sliding

element to the type II hernia. Type III hernias associated

with a large defect can allow other organs to herniate,

e.g. spleen, pancreas.

The remainder of this review will concentrate on the

type I hiatus hernia, as it accounts for about 90% of the

hiatal hernias seen in clinical practice.47

DIAGNOSIS

The GOJ moves during swallowing in relation to the

diaphragmatic crus. While large hiatal herniae are easily

identified in radiological, endoscopic and manometric

REVIEW: HIATUS HERNIA AND GERD 721


studies, the diagnosis of a small hiatus hernia is not

well-standardized.

Radiography

On barium studies, the lower oesophageal mucosal ring

demarcates the union of the oesophagus with the

stomach,48 and thus its presence above the diaphrag-

matic hiatus is used as a sign of a hiatus hernia. As

discussed previously, the distal oesophagus and gastric

cardia move cranially during swallowing and form the

phrenic ampulla. There is no precise consensus regard-

ing the differentiation of a phrenic ampulla, which is

physiological, from a hiatus hernia, which is patholo-

gical. Most authors agree that the lower oesophageal

ring must be at least 1–2 cm above the level of the

diaphragmatic hiatus to diagnose a hiatus hernia,45

although in practice the distinction can be quite

arbitrary. In particular, there is no standardized proto-

col in assessing and recording the reducibility of a

hiatus hernia in between swallows or when getting

upright from the supine position.

Upper gastrointestinal endoscopy

At upper GI endoscopy, the GOJ is recognized as the

Z-line, where the dark pink columnar stomach mucosa

changes to the lighter pink squamous oesophageal

mucosa above the visible stomach folds. In a normal

subject, the GOJ is usually seen just above the diaph-

ragmatic crus.49 Most authors consider a hiatus hernia

to be present if diaphragmatic indentation is seen 2 cm

or more distal to the Z-line and the top of the stomach

mucosal folds.46, 49

The current practice of diagnosing a hiatus hernia and

measuring its size using the centimetre markings on the

endoscope is inaccurate. There is no standardization

regarding the degree of air insufflation or which phase

of respiration the measurement is made at.49 It is also

difficult to be certain that the tip of the endoscope is

precisely at the Z-line or diaphragmatic crus while the

distance from these landmarks to the incisors can vary

circumferentially.

There are few published data on the correlation

between upper endoscopy and barium studies in the

diagnosis of hiatus hernia. Panzuto et al. studied

21 patients with large hiatus hernias, using both upper

GI endoscopy and barium studies.50 They noted that

upper GI endoscopy significantly underestimated the

size of hiatus hernias compared with barium studies.

Small hiatus hernias were not included in this study. In

contrast, of 34 patients in whom hiatus hernias were

diagnosed at upper GI endoscopy, only 20 met the

radiological criteria for hiatus hernia.51

At present, radiology is the only accurate method of

measuring hiatus hernia size. However, upper GI

endoscopy is now the standard tool for assessing upper

GI symptoms. If a simple, standardized, endoscopic

method of diagnosing a hiatus hernia and measuring its

size could be developed, our knowledge of the role of the

hiatus hernia in GERD could be much advanced.

Oesophageal manometry

When the manometry probe is in the stomach, a deep

inspiration is recorded as a positive deflection, as

abdominal pressure rises. When the probe is in the

thoracic cavity a deep inspiration causes a negative

deflection as thoracic pressure is lowered. When the

probe is at the level of the diaphragm, deep inspiration

causes a positive deflection followed by a negative

deflection, as the probe lying in the stomach moves into

the oesophagus as the diaphragm descends. This is called

the respiratory reversal point. The LOS is identified as a

pressure rise above gastric baseline as the probe is pulled

back from the stomach to the oesophagus – this falls back

to baseline during swallows and periodically after eating

(TLOSRs). In a normal subject, the distal border of the

LOS is below the respiratory reversal point, and hence

part of the LOS appears intra-abdominal. With a small

hiatus hernia, an accurate measurement can be difficult

because the diaphragm changes position with respir-

ation. It is only in large hernias that the LOS is proximal

to the respiratory reversal point. Therefore,manometry is

not a sensitive tool for the diagnosis of a hiatus hernia.46

AETIOLOGY

Simplistically, the hiatus hernia can be caused by one or

more of three mechanisms: (i) widening of the diaph-

ragmatic hiatus, (ii) pulling up of the stomach by

oesophageal shortening, and (iii) pushing up of the

stomach by increased intra-abdominal pressure.52

During a normal swallow, the oesophagus shortens by

up to 2 cm. The elasticity of supporting structures,

especially the phrenoesophageal ligament, returns the

anatomy to its normal position.46 Age-related ‘wear and

tear’ of the phrenoesophageal ligament could loosen the



attachment of the GOJ to the diaphragmatic crus,16 and

thus over time contribute to the formation of a hiatus

hernia. Intraoesophageal acid perfusion causes proximal

migration of the LOS.53 Mittal46 proposed a unifying

hypothesis relating GER and oesophagitis to the patho-

genesis of hiatus hernia. Frequent TLOSRs with resultant

acid reflux could be the initiating factor causing oesopha-

gitis, which leads secondarily to oesophageal shortening

through acid-induced contraction of the longitudinal

muscles. This may lead to subsequent fibrosis, exacerba-

ted by age-related loss of elasticity of the surrounding

structures. A hiatus hernia then results, which in turn

enlarges the oesophageal hiatus, impairing the sphincter

function of the crural diaphragm. The development of

hiatus hernia and crural diaphragmatic incompetence

introduces further mechanisms of GER leading to exacer-

bation of oesophagitis and setting up a vicious cycle.54

A high prevalence of hiatus hernia of up to 80%55

amongst power athletes suggests a role for raised intra-

abdominal pressure.55, 56 However, the extreme intra-

abdominal pressures seen in this setting (up to

365 mmHg amongst those who wear a lifting belt55)

is far beyond that normally encountered in the normal

subjects, and thus is unlikely to be a major factor in the

causation of hiatus hernia in the general population.

Familial clusters of hiatus hernia have been des-

cribed.57–59 In a recent study by Carre et al.,60 38

members of a family pedigree across five generations

were studied. Twenty-three had radiological evidence of

a hiatal hernia. No individual with a hiatus hernia

was born to unaffected parents. In one case direct male-

to-male transmission was shown. This raises the

possibility of genetic inheritance, which Carre proposed

occurs in an autosomal dominant fashion.60 However,

since the frequency of hiatus hernia in the general

population is still not clear, it is difficult to draw definite

conclusions from these data.

OBESITY AND HIATUS HERNIA

It is commonly thought that obesity is a risk factor for

reflux symptoms, and indeed weight loss forms part of

the lifestyle advice given to patients with GERD.

However, it is unclear whether obesity in itself increases

the risk for GERD,47 whether the association arises

through the types of food obese people eat, or by a

common relationship with hiatus hernia.

In a retrospective case–control study of 1205 patients

who underwent upper endoscopy, Wilson et al. analysed

the risk of reflux oesophagitis on the basis of their body

mass index61 and showed that obesity is a significant

risk factor for oesophagitis. Excessive body weight was

also significantly associated with the presence of hiatus

hernia, the probability of hiatus hernia increasing with

each level of obesity. Wilson et al.61 proposed that

although obesity was a significant risk factor for

oesophagitis, it was largely through an association with

hiatus hernia, a view shared by Barak et al.62 Logistic

regression analysis of 385 dyspeptic patients in the UK

and Singapore showed that body mass index was an

independent risk factor for both hiatus hernia and reflux

oesophagitis.63 Stein-Larson et al. also described an

association between obesity and the occurrence of both

hiatus hernia and reflux oesophagitis in a prospective

study of 1224 patients undergoing upper endoscopy.63

Wu et al. examined the relationship between hiatus

hernia, reflux symptoms and body size as part of a

population-based, case–control study of the risk of upper

GI cancers.64 A positive trend was found between

increasing body size and hiatus hernia presence,

although this did not reach statistical significance.

There is therefore an association between obesity and

hiatus hernia, but the nature of this association is

unclear. Is it a pure pressure effect? Or is it related to a

lax hiatal orifice? It would be interesting to study the

effect of weight loss on the size of a hiatus hernia.

PREVALENCE AND INCIDENCE OF HIATUS HERNIA

The frequency of hiatus hernia, like that of oesophagitis,

increases with age.65–67 There is, however, no definite

gender effect, different series showing male predomin-

ance,68 female predominance,69 or no difference.65–67

Prevalence data relating to the hiatus hernia are

difficult to interpret. They generally relate to patients

attending for upper endoscopy rather than community

subjects, and as selection criteria for this procedure vary,

such data are not strictly comparable across series.

Details such as age and body mass index are seldom

presented. Furthermore, diagnostic criteria for hiatus

hernia vary between studies, and in some reports are not

even described. While there is geographical variation in

the prevalence of hiatus hernia, it is uncertain if these

differences are genuine, because of genetic or lifestyle

variations, or whether they merely reflect variability in

patient selection and diagnostic criteria.

In a literature review by Pridie,70 the frequency of

hiatus hernias found incidentally during barium studies



varied widely depending on when the studies were

performed. Throughout the 1930s and 1940s, the

reported prevalence was between 0.8 and 2.9%.

However, in the 1950s and early 1960s, when

abdominal pressure was routinely applied during bar-

ium examinations, the prevalence rose to between 11.8

and 29.6%.70

The GERD is generally thought to be uncommon in the

Far East, and the prevalence of hiatus hernia seems to

follow this trend. Of patients undergoing upper endo-

scopy, the proportion with a hiatus hernia was 2.2% of

2044 subjects71 and 7% of 464 subjects72 in Taiwan,

2.9% of 11 943 subjects in Singapore,73 and 4.1% of

1010 patients in Korea.68 In a recent Japanese series of

6010 individuals undergoing upper endoscopy between

1996 and 1998, 17.5% had a hiatus hernia.65 This

prevalence is higher than that shown by other studies in

Far Eastern populations, and may reflect the fact that

the frequency of GERD is thought to be increasing in the

East in recent years.74 However, for this study, the

diagnostic criteria for hiatus hernia were not described.

Higher frequencies of hiatus hernia have been reported

in Western populations. For example, 16.6% of 670

subjects (Norway),75 22% of 293 subjects (USA),10 and

14.5% of 1000 subjects (Sweden)76 undergoing upper

endoscopy were found to have a hiatus hernia. A

comparative study by a single endoscopist between

English and Singaporean patients with dyspepsia found

that the proportion of patients with hiatus hernia was

49% and 4% respectively (P < 0.005).66

Loffeld and Van der Putten67 calculated the incidence

of hiatus hernia for a cohort of patients with a normal

index upper endoscopy, who had a second procedure

(for newly developed or recurrent symptoms) over a

study period of up to 8 years. Ninety of 353 patients

developed a hiatus hernia, defined as a distance of more

than 2 cm between the OGJ and the diaphragmatic

indentation. The incidence of hiatus hernia in this

highly selected group of patients was 19.9%. Patients

who developed hiatus hernia were older, more likely to

be female and had a higher incidence of reflux

oesophagitis or Barrett’s metaplasia compared with

those who did not develop a hiatus hernia. However, an

annual incidence of 19.9% seems high. The reproduc-

ibility of the endoscopist’s diagnosis of hiatus hernia

was not assessed, and it was not stated if any of the

patients with a hiatus hernia at the index upper

endoscopy were found not to have a hiatus hernia at

a subsequent upper endoscopy.

The frequency of hiatus hernia in asymptomatic

individuals would be of great interest, but reliable data

are unavailable. Most studies relate to symptomatic

subjects undergoing investigation, rather than commu-

nity subjects or asymptomatic individuals. One radiolo-

gical study reported a 33% prevalence of hiatus hernia

in asymptomatic individuals,15 but the protocol inclu-

ded the application of abdominal pressure, a practice

which is now obsolete, and thus the results are difficult

to interpret. In the Far East, upper GI endoscopy is

frequently performed as part of a routine medical check

up. Hiatus hernia has been reported in about 11% of

such individuals in one Korean series, most of whom

were asymptomatic.77 However, these subjects repre-

sent a self-selected group who may not be comparable

with community subjects.

PHYSIOLOGICAL EFFECTS OF HIATUS HERNIA

LOS function

In a patient with a hiatus hernia, the portion of the LOS

exposed to intra-abdominal pressure is shorter.30, 78, 79

LOS pressure is reduced,80 and this is proportional to

the size of the hiatus hernia.79 These changes in LOS

pressure and function seem to be due to the spatial

separation of the pressure components derived from the

intrinsic LOS and compression of the oesophagus within

the hiatal canal.80

Impairment of the diaphragmatic sphincter

A hiatus hernia compromises the diaphragmatic sphinc-

ter independently of its effects on the LOS. A patient

with a hypotensive LOS and a large hiatus hernia is

more likely to develop GER during straining man-

oeuvres compared to a patient with a hypotensive

sphincter alone.51 Similarly, the presence of a hiatus

hernia is an independent risk factor, in addition to a

defective LOS, for abnormal oesophageal acid expo-

sure.78 It has been proposed that in the presence of a

structurally normal LOS, a hiatus hernia alters the

anatomy of the cardia and facilitates the ability of the

gastric wall tension to pull open the LOS.78

Oesophageal peristalsis

The presence of a large hiatus hernia is associated

with decreased peristaltic amplitude in the distal



oesophagus.78, 79 This may impair the clearance

of refluxed acid.81 It is uncertain whether this defect-

ive peristalsis is caused by the hiatus hernia, or if it

is secondary to oesophageal damage because of GER.

Transient lower oesophageal sphincter relaxations

What about the effect of a hiatus hernia on TLOSRs?

Van Herwaarden et al.5 studied GERD patients with and

without hiatus hernia. While those with a hiatus hernia

had greater oesophageal acid exposure and more reflux

episodes, the frequency of TLOSRs and proportion

associated with acid reflux was similar in the two

groups. However, patients with hiatus hernia did have

more reflux associated with low LOS pressure, swallow-

associated LOS relaxations and straining during periods

with low LOS pressure.

Kahrilas et al.82 studied the effects of gastric distension

(by gaseous infusion) on TLOSRs in GERD patients.While

the amount of reflux and frequency of TLOSRs at baseline

were unaffected by the presence of a hiatus hernia, gastric

distension elicited a greater increase in the frequency of

TLOSRs in patients with a hiatus hernia compared to

those without. The resultant TLOSR frequency was

proportional to the size of the hiatus hernia.

The conflicting conclusions reached by these two

studies could be due to differences in study design.

Van Herwaarden’s subjects were semiambulant, had

small standardized meals and were studied over 24 h.

Kahrilas et al.82 performed their study in recumbent

patients over 212 h, with the stomach distended with

200 mL saline and 1800 mL air. More work needs to be

done to determine if TLOSRs are a significant cause of

GER in the presence of a hiatus hernia.

Cross-sectional area of the gastro-oesophageal junction

Using a barostat filled with radioactive contrast, Pan-

dalfino et al.83 were able to study the opening of the GOJ

and to measure its cross-sectional area and compliance

during low pressure distension. Compliance was

increased in GERD patients compared with controls.

The cross-sectional area was greater in patients with a

hiatus hernia and GERD than in patients with GERD but

no hiatus hernia, and this in turn was greater than that

in normal subjects. The larger cross-sectional area could

allow reflux of fluid rather than gas, and possibly a

higher volume of refluxate.

Oesophageal acid clearance

In a study combining barium examinations with

oesophageal pH studies, Ott et al. showed that patients

with larger (>2 cm) hiatus hernias were more likely to

have abnormal results on 24 h pH monitoring, com-

pared with normal subjects and those with hiatus

hernias <2 cm.84

The increase in oesophageal acid exposure with

hiatus hernia is not just due to increased frequency

and volume of refluxate. Mittal et al. instilled acid into

the oesophagus of patients with and without hiatus

hernia.85 In the absence of a hiatus hernia, a single

swallow resulted in restoration of a normal oesopha-

geal pH. However, patients with a hiatus hernia

showed a biphasic response – an initial episode of acid

reflux, seen as a fall in pH, followed by restoration of

pH towards normal. Simultaneous radionuclide studies

showed that the initial drop in pH coincided with

reflux from the hiatus hernia proximally. Mittal et al.85

proposed that gastric contents could be trapped in the

hiatus hernia limited by the LOS proximally and the

crural diaphragm distally. These contents could then

reflux into the oesophagus when the LOS relaxed

during swallowing.

Using concurrent videofluoroscopy and manometry,

Sloan and Kahrilas studied asymptomatic volunteers

and patients with symptomatic GERD who had hiatus

hernias noted during upper endoscopy. Ten of the 22

patients had endoscopic oesophagitis. In 10 of the

patients, the hiatus hernia was reducing while in the

other 12 it was non-reducing.86 Complete oesophageal

emptying without retrograde flow was seen in 86% of

test swallows in controls, 66% of swallows in the

reducing hiatus hernia group, and in 32% of swallows

in the non-reducing group.

Both these studies suggest that a hiatus hernia acts as

a reservoir, from which acid can reflux during a

swallow, thus contributing to the increased acid

exposure time seen in these patients.

In a detailed pathophysiological study of nine

controls and 38 patients with GERD, increasing

hiatus hernia size was associated with greater

oesophageal acid exposure, more prolonged episodes

of reflux and longer acid clearance times.87 However,

Massey argued that the presence of a hiatus hernia

is more important than its size in its effects on

GERD.88



Reducibility of hiatus hernia

Mattioli et al.89–91 recently drew attention to hiatus

hernia which reduce when the patient is in the upright

position. For this group of patients both the LOS

pressure, and the percentage time during which the

lower oesophageal pH is <4, are between those for

healthy volunteers and patients with irreducible hernias.

They suggested that hiatus hernias that reduce in the

upright position represent a stage in the development of

fixed hiatus hernias. They did not, however, report on

the effect of swallowing on the reducibility of hiatus

hernias. In contrast, Sloan and Kahrilas defined

reducing hiatus hernias as those occurring only during

mid-swallows, but reducing between swallows.86 The

frequency of incomplete oesophageal emptying during

swallows in these subjects was intermediate between

healthy controls and those with irreducible hiatus

hernias. In a later study,51 the same authors considered

these same subjects not to have hiatus hernias. Sloan

and Kahrilas86 studied patients only in the supine

position so the reducibility of hiatus hernias in the

upright position was not assessed.

In practice, there is no uniformity in the assessment or

reporting of the reducibility of hiatus hernias between

swallows and in the upright position during barium

studies. Furthermore endoscopy, which is always carried

out in the supine position and in which the effects of

swallowing are not assessed, is now the standard

modality of investigating upper GI anatomy. Thus,

although the reducibility or otherwise of hiatus hernias

is potentially important in terms of pathophysiological

considerations, its clinical effects cannot be studied easily.

In summary, a hiatus hernia reduces LOS length and

pressure, impairs the augmenting effect of the diaph-

ragmatic sphincter, is associated with decreased

oesophageal peristalsis, affects the opening characteris-

tics of the OGJ and acts as a reservoir allowing GER

during swallowing. The overall effect is that of increas-

ing oesophageal acid exposure and decreasing oesopha-

geal acid clearance.

CLINICAL EFFECTS OF HIATUS HERNIA

Reflux symptoms and hiatus hernia

In a study of 57 healthy subjects by Stal et al.,92 62%

with GER symptoms at computer interview had a hiatus

hernia at upper endoscopy, compared with only 14% of

asymptomatic subjects (P < 0.01). Subjects with GERD

had predominantly non-erosive disease: only one

quarter had oesophageal erythema or erosions.

Peterson et al.93 investigated 930 successive patients

who underwent endoscopy because of dyspepsia, and

looked at both GERD and non-erosive reflux (NERD)

patients. Even with exclusion of 131 patients with

reflux oesophagitis, patients with a hiatus hernia were

significantly more likely to have heartburn and regur-

gitation compared to those without.

Thus, it can be seen that reflux symptoms are more

common in subjects with a hiatus hernia than in those

without, even when reflux oesophagitis is not present at

upper endoscopy, i.e. non-erosive disease.

Oesophagitis and hiatus hernia

The relationship between oesophagitis and hiatus

hernias has been recognized as far back as 1951.2

Both the presence and size of the hiatus hernia are

important.75, 88

Table 1 summarizes the results of various studies in

which this relationship was analysed by univariate

Table 1. Prevalence of hiatus hernia in

patients with and without oesophagitis

Location of

study

Number of

patients

Frequency of hiatus hernia

Patients with

oesophagitis (%)

Patients without

oesophagitis* (%)

Kang and Ho66 UK/Singapore 383 64 6

Yeom et al.68 Korea 1010 32 3

Kang et al.73 Singapore 11 943 13 2

Stein-Larson et al.63 Norway 1224 68 11

Berstad et al.75 Norway 670 63 8

Wright and Hurwitz10 USA 293 84 13

Cronstedt et al.76 Sweden 1000 72 9

* Statistically significant.



analysis. These studies included patients who had

an upper GI endoscopy done for a variety of indica-

tions,10, 63, 68, 73, 75, 76 or for dyspepsia only.66 The

association between hiatus hernia and reflux oesopha-

gitis is significant across different countries, irrespective

of the background prevalence of this condition.

Using multivariate analysis, Sontag et al. demonstrated

that the presence of a hiatus hernia was a more

important predictor of reflux oesophagitis than LOS

pressure.94 Jones et al. showed that increases in hiatal

hernia size were significantly correlated with total

oesophageal acid-exposure, acid clearance time and

oesophagitis severity,87 although the effect of presence

or absence of a hiatus hernia was not analysed. In a

third study by Cadiot et al.,95 the relationship between

hiatus hernia and reflux oesophagitis was not statisti-

cally significant on multivariate analysis, although an

association was demonstrable on univariate analysis.

Barrett’s oesophagus and hiatus hernia

Barrett’s oesophagus is associated with male sex, older

age, excess alcohol, cigarette smoking and frequent

reflux episodes. In a study of 229 patients with Barrett’s

oesophagus and 229 patients with non-erosive GERD,

the presence of Barrett’s oesophagus was strongly

associated with a hiatus hernia, more reflux episodes,

and excess smoking and alcohol.96

Cameron looked at the prevalence and size of hiatus

hernia in Barrett’s oesophagus.97 A hiatus hernia was

found in 96% of patients with classical Barrett’s

oesophagus, 72% of patients with short segment

(<2 cm) Barrett’s oesophagus, 71% of patients with

oesophagitis, and 29% of controls with no oesophagitis.

Among patients with hiatus hernias, those with

Barrett’s oesophagus had wider hiatal orifices, and

longer hiatal hernias compared to patients without

Barrett’s oesophagus.

Weston et al. prospectively followed up 99 patients

over a period of 24–106 months, and identified seven in

whom complete regression of the Barrett’s occurred.

Stepwise logistic regression analysis showed that only

the absence of a hiatus hernia and length of Barrett’s

<6 cm were significantly and independently predictive

of complete regression of the Barrett’s segment.98

Oesophageal adenocarcinoma and hiatus hernia

There is an established association between GERD and

oesophageal adenocarcinoma,99 but few studies specif-

ically examined the relationship between hiatus hernia

and oesophageal carcinoma. Chow et al. performed a

medical record based case–control study of 196 patients

with oesophageal adenocarcinoma and 196 controls,

and showed that the presence of a hiatus hernia doubled

the risk of oesophageal carcinoma. There was also a

cumulative increase in risk with a history of reflux,

dysphagia and previously documented oesophagitis.100

In a population-based, case–control study of patients

with oesophageal adenocarcinoma (n ¼ 222), both

hiatus hernia and reflux symptoms emerged as signifi-

cant risk factors. The risk was increased threefold in

those with reflux symptoms but no hiatus hernia,

sixfold in those with a hiatus hernia but no reflux

symptoms, and eightfold in those with both reflux

symptoms and a hiatus hernia.64

Avidan et al. reviewed 131 patients with high-grade

dysplasia or oesophageal adenocarcinoma, 2170

patients with no GERD, and 1189 patients with

Barrett’s oesophagus but no dysplasia. Logistic regres-

sion analysis showed the risk of high-grade dysplasia or

esophageal adenocarcinoma to be proportional to the

size of hiatus hernia and length of Barrett’s oesophagus.

Patients with high-grade dysplasia or oesophageal

adenocarcinoma shared many characteristics with

Table 2. Factors contributing to the antireflux mechanism in

normal subjects

Lower oesophageal sphincter (LOS)

Crural diaphragm

Angle of His

Intra-abdominal portion of the LOS

Phrenoesophageal ligament

Oesophageal peristalsis

Saliva

Table 3. Pathophysiological effects of a hiatus hernia

Decrease in intra-abdominal length of the lower oesophageal

sphincter (LOS)

Decreased LOS pressure

Impairment of the diaphragmatic sphincter

Impairment of oesophageal peristalsis

Increased cross-sectional area of the gastro-oesophageal

junction (GOJ)

Decreased oesophageal acid clearance

Increased oesophageal acid exposure



other forms of severe GERD, such as older age, male

gender and white ethnicity.101

Weston et al. prospectively followed up 108 patients

with Barrett’s oesophagus.102 Stepwise logistic regres-

sion analysis showed that progression to high-grade

dysplasia and oesophageal adenocarcinoma were signi-

ficantly and independently associated with hiatal hernia

size, dysplasia at diagnosis and the length of the

Barrett’s segment.

The association between hiatus hernia, and Barrett’s

oesophagus and oesophageal adenocarcinoma is con-

sistent with a promoting effect of the hiatus hernia on

GERD, and not necessarily by the presence of the hiatus

hernia per se.

Acid suppression treatment and hiatus hernia

Frazzoni et al. studied lower oesophageal pH in 50

patients with complications or atypical manifestations

of GERD, who had been referred for upper GI endoscopy.

A 30 mg dose of lansoprazole normalized oesophageal

acid exposure in 70% of subjects, whereas a 60 mg

daily dose was necessary in the remainder. The two

groups differed only in the presence of hiatal hernia

(28% vs. 100% respectively). However, hiatal hernia

size was not studied.103 Said et al. examined predictors

of early recurrence of peptic oesophageal strictures after

initial dilatation in 67 patients over a 1-year period.

Continued acid suppression was used in 94% of

patients. Both the presence and size of a hiatus hernia

were significantly associated with early recurrence on

multivariate analysis.104 Both these studies suggest that

a hiatus hernia affects the ability of acid suppressing

medication to normalize intraoesophageal pH. This

could be due to the promoting effect of hiatus hernia

on GER. It has been shown that on standard doses

of PPIs, nocturnal acid breakthrough commonly

occurs,105 and it may be that this residual acid refluxes

more easily in the presence of a hiatus hernia.

Surgical and endoscopic therapy for GERD in the presence of

hiatus hernia

In the infancy of antireflux surgery, it was thought that

a hiatus hernia was the only causative factor leading to

GERD. Thus, early surgery was designed only to treat

the hernia itself and was often ineffective for reflux

oesophagitis.106 We now know that the aetiology of

GERD is multifactorial, and an ideal operation, whether

open or laparoscopic, should address all the various

aspects,106 including (i) restoration of the intra-abdom-

inal oesophagus, (ii) reconstruction of the diaphragmat-

ic hiatus (with reduction of a hiatus hernia if present)

and (iii) reinforcement of the LOS by fundoplication.107

The operation most commonly used today is a

modification of the operation described by Nissen in

1956.106 During surgery the oesophagus is mobilized in

the thorax so that it can be brought down sufficiently to

restore the intra-abdominal portion. This reduces ten-

sion on the repair, and reduces the risk of late failure.108

However, in the context of a large or irreducible hiatus

hernia, there may be a short oesophagus despite

adequate mobilization.108–111 Oesophageal lengthening

(Collis gastroplasty) combined with fundoplication can

be performed during laparoscopic112 surgery, but may

require an open operation.107

A large hiatus may be seen in patients with a large

hiatus hernia,97 and reconstruction of the diaphragmatic

hiatus is an integral part of antireflux surgery.107, 113

Both the reconstruction of the oesophageal hiatus and

oesophageal lengthening can be achieved laparoscopi-

cally,107, 112 but the presence of a large hiatus hernia

might influence the surgeon to consider an open

operation.107

Antireflux surgery is indicated in patients affected by

severe GERD who are (i) not compliant with long-term

medical therapy, (ii) who require high doses of drugs and

(iii) who wish to avoid lifetime medical treatment.114

While the presence of a large hiatus hernia is associated

with severe GERD symptoms, erosive oesophagitis and

poorer response to treatment, a sliding hiatus hernia

per se is not an indication for surgery. In contrast,

surgery is recommended for para-oesophageal hernias

because, if left untreated, approximately 33% will suffer

complications such as intrathoracic incarceration of the

stomach, bleeding, strangulation or perforation115

A number of novel endoscopic techniques have

recently been described for the treatment of GERD.116

These include (i) endoscopic plicators which place

sutures around the LOS, (ii) bulking techniques in

which inert substances are injected into the lower

oesophagus, and (iii) the STRETTA procedure in which

radiofrequency energy is delivered to the LOS and

gastric cardia. To date subjects with hiatus hernia have

not been included in the case series that have been

published. However, none of these techniques correct

the anatomical abnormality, and thus are unlikely to be

effective in patients who have significant hiatus hernias.



CONCLUSIONS

Our view of the role of the hiatus hernia in GERD has

changed in recent decades. Initially thought to be

synonymous with GERD, then in the 1970s and 1980s

regarded as an incidental finding, the hiatus hernia is

now recognized to be an important aetiological factor at

the more severe end of the GERD spectrum. A hiatus

hernia impairs LOS competence, reduces LOS pressure

and length and alters the opening characteristics of the

GOJ, resulting in delayed oesophageal acid clearance

and increased oesophageal acid exposure. Numerous

studies have shown that hiatus hernia is associated

with GERD symptoms, endoscopic oesophagitis, Barr-

ett’s oesophagus and oesophageal adenocarcinoma.

Among patients with GERD, patients with hiatus hernia

have more severe disease and poorer response to

treatment.

Studies on hiatus hernia are hampered by a lack of

standardized diagnostic criteria, and hiatal hernia size is

frequently not taken into account. This may hamper

our understanding of the contribution of the hiatus

hernia to GERD, and thus prevent us from effectively

managing the condition. Development of a simple

method of diagnosing, measuring and reporting a

hiatus hernia endoscopically would help to advance

our understanding of this important subject.

The hiatus hernia is again emerging as an important

factor in the pathogenesis of GERD. Although our

understanding of its contribution to this condition has

advanced, we are still not seeing the full picture. Further

work is needed to understand how the hiatus hernia

influences the pathogenesis of GER, progression of GERD

and its complications, and the effects of therapy. At the

present time, the hiatus hernia is a marker of severe

GERD, but its presence per se does not alter management

strategies.

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