What is the effect of the diaphragm on intraluminal pressure in the hiatal hernia patient?
P.J. Kahrilas (Chicago)
Gastroesophageal acid reflux occurs by two major mechanisms: during transient lower esophageal sphincter relaxations (TLESRs) that are preceded by periods of normal lower esophageal sphincter (LES) pressure, during abrupt increases in intraabdominal pressure that overcome a feeble or absent LES [1, 2]. Clinical experience suggests that exercise, tight fitting garments, and activities that involve bending at the waist exacerbate heartburn, especially after having consumed meals that reduce LES pressure. These observations, along with the observation that during periods of cigarette smoking acid reflux occurs predominantly by abrupt increases in intraabdominal pressure associated with coughing or deep inspiration [3], support the importance of abrupt increases in intraabdominal pressure inherent in normal daily activity overcoming a feeble LES as an important reflux mechanism in symptomatic individuals.
Recent physiologic investigations in humans and animals have advanced the "two sphincter hypothesis" of gastroesophageal junction competence, suggesting that both the smooth muscle LES and the crural diaphragm encircling the LES serve a sphincteric function [4-8]. In particular, the diaphragm augments the LES during transient periods of increased intraabdominal pressure such as occur during inspiration, coughing, or a Müller maneuver. The augmentation of LES pressure observed during sustained inspiration corresponds both temporally and quantitatively with the augmentation of crural electromyographic (EMG) activity and this augmented LES pressure is observed to obscure the intrinsic LES relaxation induced by esophageal distention [8]. Electrical and mechanical inhibition of the crural diaphragm has also been demonstrated during TLESRs in humans further supporting the notion that the crural diaphragm functions independently of the diaphragmatic dome [9]. Reflex inhibition of the diaphragmatic crus disappears with vagotomy [10]. An attractive feature of the two sphincter hypothesis of gastroesophageal junction competence is that it suggests a mechanism by which hiatus hernia might impair gastroesophageal junction competence and thereby exacerbate reflux disease. Specifically, if hiatus hernia compromises the diaphragmatic sphincter, and if the diaphragmatic sphincter is important in minimizing the number of reflux events, the presence of a hiatal hernia could increase an individual's susceptibility to reflux disease.
Observations of the antireflux mechanism during stress maneuvers such as leg raising and abdominal compression suggest a "pinchcock effect" of crural contraction that effectively augments the antireflux barrier [11]. Recent combined manometric and fluoroscopic studies suggest that patients with a substantial hiatal hernia, regardless of whether or not they had a hypotensive LES, incur an increased number of acid reflux episodes in response to stress maneuvers (leg lifts, cough, Valsalva maneuver, abdominal compression, and Müller maneuver) [12]. Modeling of the determinants of gastroesophageal junction competence suggests that the relative vulnerability inherent in a hypotensive LES was greatly compounded by hiatus hernia [12]. Although LES pressure is a significant determinant of competence, an individual with a hypotensive LES and a large hernia was several times more likely to incur gastroesophageal reflux during an abrupt increase in intraabdominal pressure than an individual with a hypotensive LES but without a hiatal hernia. These data suggest that the "diaphragmatic sphincter" (comprised of the crural diaphragm) is functionally impaired with hiatus hernias and that this impairment predisposes to gastroesophageal reflux during abrupt transients in intraabdominal pressure, events normally associated with contraction of the diaphragmatic crus.
A further twist in the interrelationship between a hiatal hernia and the LES is that a hernia in itself may diminish LES pressure. Surgical division of the phrenoesophageal ligament in dogs led to a decreased LES pressure that was then restored by reanastomosing the ligament [13]. In recent experiments in which a metal clip was attached to the squamocolumnar junction prior to combined fluoroscopy and manometry, the peak pressure within the LES high pressure zone correlated closely in position with the squamocolumnar junction [14]. However, individuals with hiatus hernia exhibited both a decreased overall length of the high pressure zone, principally because of loss of the segment distal to the squamocolumnar junction, and diminished LES pressure. This distal segment of the LES may be attributable to the sling fibers and clasp fibers of the gastric cardia, also referred to as the intraabdominal segment of the esophagus [15]. With progressive proximal displacement of the squamocolumnar junction above the hiatus, this segment of the high pressure zone eventually becomes disrupted and splays open, creating a radiographically evident saccular structure identifiable as a non-reducing hiatal hernia [16]. These observations also suggest that the observed shortening of the LES high pressure zone commented on by surgeons as indicative of a mechanically defective sphincter [17] is probably largely a manometric correlate of a non-reducing hiatal hernia.
Following gastroesophageal reflux, the duration of time that the esophageal mucosa remains acidified is termed the esophageal acid clearance time. In either the controlled setting of the acid clearance time test or in the setting of spontaneous reflux, reflux patients have acid clearance times that are, on the average, two to three times longer than those of controls [18, 19]. A potential cause of prolonged esophageal acid clearance is impaired esophageal emptying. Recent investigations suggest that hiatal hernias impair the process of acid clearance by impairing emptying. Mittal et al. used concurrent pH recording and scintiscanning to examine the efficacy of acid and volume clearance in a group of patients with hiatus hernia (with or without esophagitis) and compared them to a group on esophagitis patients without hernias [20]. Irrespective of the presence of esophagitis, the hernia groups had delayed acid clearance because there was "rereflux" from the hernia sac during swallowing. Sloan and Kahrilas further analyzed the impact of hiatus hernia on esophageal emptying using simultaneous videofluoroscopy and manometry in 22 patients with axial hiatal hernias compared to normal subjects [21]. The overall efficacy of esophageal emptying was significantly impaired with hiatus hernia, being especially bad in the individuals with non-reducing hernias. The group with non-reducing hernias had complete emptying in only one third of the test swallows and exhibited early retrograde flow ("rereflux"), a phenomenon unique to this group, in almost half.
Possible explanations for the phenomenon of retrograde flow during esophageal emptying in non-reducing hernia patients were suggested by the observations in normal subjects. During normal swallow sequences, complete LES relaxation was evident within 3 seconds of the swallow. However, sphincter (ampullary) opening was not evident until it was distended by the barium bolus being propelled by esophageal peristalsis, an event that occurred 5-10 seconds after the swallow. Thus, LES relaxation and opening do not occur simultaneously. The reason LES opening does not occur at the time of relaxation is that the distal esophagus is intraabdominal; intragastric pressure acting from within to open the sphincter is negated by the external pressure of equal magnitude acting on the same esophageal segment. The effect of eliminating this intraabdominal segment is evident in non-reducing hernia patients; the LES opens from below immediately following swallow-induced LES relaxation. For this to occur, intragastric pressure being applied within the sphincter must have exceeded the extrasphincteric pressure, indicating that the extrasphincteric pressure was less than intraabdominal pressure in these individuals.
Another mechanism promoting gastroesophageal junction competence during esophageal emptying is the crural diaphragm. In normal individuals the esophageal ampulla fills from above as the bolus is propelled ahead of the peristaltic contraction. As the peristaltic contraction arrives at the distal esophagus, intra-ampullary pressure increases to about 10 mmHg at which time ampullary emptying began [22]. During emptying, the diaphragmatic crura functioned as a one-way valve. During expiration, at which time the esophageal-gastric pressure gradient favored antegrade flow, the crus is relaxed and visibly open. However, during inspiration when intraabdominal pressure was increased, the crura contract and close, thereby preventing gastroesophageal flow. The valvular effect of the crural diaphragm is grossly impaired with non-reducing hernias because a gastric pouch persists above the diaphragm thereby disabling this one-way valve function [23].
In summary, the emerging picture is that large hiatal hernias compromise the gastroesophageal junction during dynamic stresses such as swallowing or abrupt increases in intraabdominal pressure. During swallowing, large hernias impair the process of esophageal emptying thereby prolonging acid clearance time (especially while in the supine posture). During abrupt increases in intra-abdominal pressure the crural diaphragm normally serves as a "second sphincter" and this mechanism is probably substantially impaired in individuals with a gaping hiatus. The susceptibility to stress reflux inherent during periods of diminished LES pressure is dramatically increased by disabling the diaphragmatic sphincter. Thus, although hiatus hernia may or may not be involved at the inception of reflux disease, it clearly can be a significant contributor to the chronicity of the disease.
References