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Transcript of 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
� 2004 Blackwell Publishing Ltd, Aliment Pharmacol Ther 20, 719–732
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
722 C. GORDON et al.
� 2004 Blackwell Publishing Ltd, Aliment Pharmacol Ther 20, 719–732
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
REVIEW: HIATUS HERNIA AND GERD 723
� 2004 Blackwell Publishing Ltd, Aliment Pharmacol Ther 20, 719–732
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
724 C. GORDON et al.
� 2004 Blackwell Publishing Ltd, Aliment Pharmacol Ther 20, 719–732
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
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� 2004 Blackwell Publishing Ltd, Aliment Pharmacol Ther 20, 719–732
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.
726 C. GORDON et al.
� 2004 Blackwell Publishing Ltd, Aliment Pharmacol Ther 20, 719–732
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
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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.
728 C. GORDON et al.
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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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