食管压力测定的临床应用英文-AGA.doc

POLICY AND POSITION STATEMENTAn American Gastroenterological Association Medical Position Statement on the Clinical Use of Esophageal ManometryThe following guidelines were developed to assist physicians in the appropriate use of esophageal manometry in patient care. They emanate from a comprehensive review of the medical literature pertaining to manometric technique and application.1 Manometry is widely available, but the limited specificity of manometric data and the low prevalence rates of clinically significant motility disorders in symptomatic patients speak for the necessity of practice guidelines. This position statement is intended to help the clinician apply manometric studies most beneficially within the context of other available tests of esophageal structure and function. Guidelines1.Manometry may be requested by any physician in compliance with the remainder of these guidelines. 2.Manometry is indicated to establish the diagnosis of suspected cases of achalasia or diffuse esophageal spasm. Because of the low prevalence of these diagnoses in patients with esophageal symptoms, more common esophageal disorders should be excluded with barium radiographs or endoscopy before manometric evaluation. 3.Manometry is indicated for detecting esophageal motor abnormalities associated with systemic diseases (e.g., connective tissue diseases) if their detection would contribute to establishing a multisystem diagnosis or to other aspects of management. 4.Manometric techniques are indicated for placement of intraluminal devices (e.g., pH probes) when positioning is dependent on the relationship to functional landmarks, such as the lower sphincter. 5.Manometry is possibly indicated for the preoperative assessment of peristaltic function in patients being considered for antireflux surgery and is indicated in this setting if uncertainty remains regarding the correct diagnosis. 6.Manometry is not indicated for making or confirming a suspected diagnosis of gastroesophageal reflux disease. 7.Manometry should not be routinely used as the initial test for chest pain or other esophageal symptoms because of the low specificity of the findings and the low likelihood of detecting a clinically significant motility disorder. (Approved by the American Gastroenterological Association Patient Care Committee on May 15, 1994. Approved by the American Gastroenterological Association Governing Board on July 15, 1994.) References1. Kahrilas PJ, Clouse RE, Hogan WJ. American Gastroenterological Association technical review on the clinical use of esophageal manometry. Gastroenterology 1994;107:1865-1884. American Gastroenterological Association Technical Review on the Clinical Use of Esophageal Manometry Manometric recordings from within the gastrointestinal tract were first obtained more than a century ago. However, these first balloon kymograph studies of Kronecker and Meltzer in 1894 were clearly limited to the experimental domain.1 The era of clinical esophageal manometry dates from the first atlas of esophageal manometry published by Code et al. in 1958.2 Since that time, methodological improvements have steadily occurred, and esophageal manometry has evolved to the point that it is now widely used in the clinical evaluation of esophageal contractile activity. Nonetheless, the dichotomy persists between the use of manometry as an investigational technique or as a useful clinical test, leading to pervasive uncertainty regarding the clinical indications for an esophageal manometric evaluation. Thus, the object of this review is threefold. First, our current understanding of esophageal physiology will be summarized, emphasizing aspects evaluated by manometric techniques. Secondly, the technical aspects and limitations of performing an esophageal manometric evaluation will be discussed. Finally, the use of manometric evaluation in terms of patient outcomes will be reviewed. However, note that this review pertains to adult patients, and some conclusions and recommendations might differ for pediatric patients. What Physiological Data Can be Obtained From Esophageal Manometry?There are three functional regions of the esophagus: the upper esophageal sphincter (UES), the esophageal body, and the lower esophageal sphincter (LES). Each region has physiological attributes that can be assessed by manometry. In the case of the sphincters, resting tone, timing of relaxation, completeness of relaxation, and response to exogenous stimuli can be measured. In the case of the esophageal body, the presence, propagation, and vigor of peristalsis or the presence of nonperistaltic contractions can be determined. The following sections detail the physiological activity of each esophageal region, emphasizing aspects detectable by manometric recordings. The UESThe muscles of the UES are striated, consisting of the cricopharyngeus and adjacent portions of the esophagus and inferior constrictor. The cricopharyngeus muscle inserts bilaterally at the inferior-lateral margins of the cricoid lamina, and the zone of maximal intraluminal pressure is ≈1 cm in length at precisely this location.3 The closed sphincter has a slitlike configuration with the lamina of the cricoid cartilage anterior and the cricopharyngeus attached in a C configuration, making up the lateral and posterior walls. Because the only insertion of the cricopharyngeus is to cartilage of the larynx, the sphincter and larynx are obliged to move in unison. This axial mobility is facilitated by a posterior tissue fissure lined with adipose tissue.4 Resting UES pressure is markedly asymmetric with greater values anteriorly and posteriorly than laterally.5,6 This asymmetry is understandable in view of the slitlike configuration of the sphincter; indeed, the radial asymmetry disappears after laryngectomy.5 Another complicating attribute of intraluminal UES pressure is that the technique of measurement in and of itself stimulates sphincter contraction. The less movement applied to the recording catheter during measurement, the lower the recorded pressures.6,7 Furthermore, intraluminal UES pressure is comprised of both an active component related to cricopharyngeal contraction and a passive component, on the order of 10 mm Hg, attributable to elasticity.7-9 With UES pressure measurement so dependent on methodology, it is not surprising that there is little consensus on normal values. Representative studies are summarized in Table 1,5,6,10-13 most of which allude to the great variability observed in UES pressure values among subjects and among trials for a given subject. Thus, at present, it is impossible to define a meaningful normal range for UES pressure. TABLE 1Normal Values of UES PressureManometric technique UES pressure (mm Hg) (mean SEM) Sleeve sensor658 5 (anterior), 55 5 (posterior)Sleeve sensor1049 5 (anterior)Sleeve sensor1183 32 (posterior)Rapid pull-through6193 29 (anterior), 218 41 (posterior), 60 16 (right), 75 15 (left)Rapid pull-through5130 10 (anterior), 130 15 (posterior), 50 5 (right), 50 5 (left)Station pull-through658 5 (anterior), 55 5 (posterior)Station pull-through (circumferential)1284 38Station pull-through1140 15Station pull-through (circumferential)5121 ?Station pull-through (circumferential)1379 14Resting UES pressure is augmented by balloon distention of the tubular esophagus,6 emotional stress,10 and inspiration14 but not by esophageal acidification.14,15 On the other hand, sleep,14 anesthesia,16 or esophageal distention as occur during belching or esophageal air insufflation17 cause complete UES relaxation. The most predictable modifier of UES pressure is swallowing. Exacting videofluoroscopic studies performed concurrently with intraluminal manometry have shown that UES relaxation occurs during swallow-associated laryngeal elevation and precedes opening of the sphincter by about 0.1 second.3,18,19 Sphincter opening results from traction on the anterior sphincter wall caused by contraction of the suprahyoid and infrahyoid musculature. Both the diameter and duration of deglutitive sphincter opening increase with increased swallow bolus volumes. Representative timing values of deglutitive UES relaxation and opening are summarized in Table 2.3,19,20 TABLE 2Modulation of Deglutitive UES Relaxation and Opening With Swallow VolumeSwallow volumeMethod Dry 5 mL 10 mL 20 mL Opening (fluoroscopic)30.48 0.040.51 0.050.59 0.08Opening (fluoroscopic)190.30 0.020.48 0.050.55 0.050.62 0.07Sleeve sensor30.38 0.020.52 0.050.55 0.050.65 0.08Proximally placed side hole30.30 0.020.43 0.040.48 0.040.52 0.09Proximally placed side hole190.50 0.140.56 0.120.65 0.12Proximally placed circumferential transducer200.43 0.030.56 0.030.60 0.02NOTE. Time is expressed in minutes as mean SEM. The Tubular EsophagusThe body of the esophagus is a 20-22-cm tube composed of skeletal and smooth muscle. The proximal 5% of the esophagus is striated muscle, the middle 35%-40% is mixed (showing an increasing proportion of smooth muscle distally), and the distal 50%-60% is entirely smooth muscle.21,22 The bundles of the outer longitudinal muscle arise from the cricoid cartilage and pass dorsolaterally to fuse posteriorly about 3 cm below the cricoid cartilage. The esophagus contains a nerve network, the myenteric plexus, situated between the longitudinal and circular muscle layers. These enteric neurons are the relay neurons between the vagus and the smooth muscle. Although the relationship between morphology and function of the nerve plexuses has yet to be determined, it is apparent that there are two main types of effector neurons within the esophageal myenteric plexus. Excitatory neurons mediate contraction of both longitudinal and circular muscle layers via cholinergic receptors.23 Inhibitory neurons predominantly affect the circular muscle layer via a nonadrenergic, noncholinergic neurotransmitter.24 Both types of neurons innervate the distal tubular esophagus and the LES. A multitude of recent investigations suggests that the long elusive nonadrenergic, noncholinergic neurotransmitter is nitric oxide.25-27 Significantly, inhibitors of NO activity have been shown to prevent LES relaxation.28,29 Before the explosion of research exploring the role of NO as the inhibitory neurotransmitter of the intestine, vasoactive intestinal polypeptide was a leading candidate for this role.30 Vasoactive intestinal polypeptide does colocalize with NO synthase,31 and it is still possible that vasoactive intestinal polypeptide and NO collaborate as mediators of LES relaxation. The extrinsic innervation of the esophagus is via the vagus nerve. Fibers innervating the striated muscle are axons of lower motor neurons with cell bodies situated in the nucleus ambiguus, whereas the innervation of the smooth muscle is provided by the dorsal motor nucleus of the vagus.32,33 The vagus nerves also provide sensory innervation; in the cervical esophagus, this is via the superior laryngeal nerve with cell bodies in the Nodose ganglion, whereas the remainder of the esophagus sensory fibers travel via the recurrent laryngeal nerve or, in the most distal esophagus, via the esophageal branches of the vagus. These vagal afferents are strongly stimulated by esophageal distention. Primary esophageal peristalsis is initiated by swallowing and is evident shortly after the pharyngeal contraction traverses the UES, progressing at a velocity of 2-4 cm/s. Secondary peristalsis can be elicited at any level of the esophagus in response to luminal distension by air, fluid, or a balloon. A key property of the peristaltic mechanism is deglutitive inhibition. A second swallow, initiated while an earlier peristaltic contraction is still progressing, causes complete inhibition of the contraction induced by the first swallow.34,35 With repeated swallows at short intervals, the esophagus remains inhibited with the LES relaxed. Primary peristalsis occurs after the last swallow in the series. Deglutitive inhibition is intricately involved in sequencing the peristaltic contraction. An elegant experiment using an intraesophageal balloon to quantify the period of deglutitive inhibition at different levels of the esophagus showed that inhibition commences nearly simultaneously but persists progressively longer at more distal esophageal locations.36 Excitation then follows the period of inhibition at each level, resulting in a sequenced peristaltic contraction. The mechanical effect of peristalsis is a stripping wave that milks the esophagus clean from its proximal to distal end. Progression of the stripping wave corresponds closely with that of the manometric contraction such that the point of the inverted V found fluoroscopically at each esophageal locus coincides with the upstroke of the pressure wave.37 However, it is important to note that any intraluminal pressure waveform is potentially either intrabolus pressure or squeeze pressure from within a closed lumen; manometry alone cannot reliably distinguish between these conditions.38 The longitudinal esophageal muscle also contracts at the onset of peristalsis with the net effect of transiently shortening the esophagus by 2-2.5 cm.39,40 The efficacy of esophageal emptying is inversely related to peristaltic amplitude such that emptying becomes progressively impaired with peristaltic amplitudes 40 mm Hg.37 Failed or feeble peristalsis (40 mm Hg in the distal esophagus) is not an unusual observation in a normal population. Richter et al. found 4.1% 8.3% of swallows in normal volunteers of varied age to result in nonperistaltic contractions.41 Kahrilas et al. found 10% incidence of peristaltic dysfunction in a young normal population and determined that the 95% confidence interval for peristaltic dysfunction was 50% in that population.42 More than any other peristaltic variable, the amplitude of peristaltic contractions has been the subject of substantial scrutiny during the past decade. Table 341-44 shows representative normal data on peristaltic amplitude obtained using modern methodology. The 40-60-year-old patients in the study by Richter et al. had slightly increased peristaltic amplitudes relative to the younger patients. Typical duration of peristaltic contractions in both studies was 4 1 seconds, and typical propagation velocity was 3.0 1 cm/s in the distal esophagus. Occasional double-peaked contractions were noted to occur in 44% of the normal subjects studied by Richter et al.,41 but these waveforms usually occur with no more than 10%-15% of swallows.44 An interesting perspective on double-peaked contractions was provided by a recent topographic analysis of esophageal peristalsis.45 That analysis confirmed a consistent pressure trough in the proximal esophagus corresponding to the junction between the striated and smooth muscle. Furthermore, the distal esophagus was separated into two contractile segments divided by another relative pressure trough. Slight malalignment of these distal contractile segments resulted in the most distal segment commencing its contraction late, when the proximal segment was past the peak of its contraction. A double-peaked contraction is then recorded where the slightly staggered contractile segments overlap. TABLE 3Normal Values of Primary Peristaltic Contraction Amplitude During Water SwallowsPosition of recording site above the LES (cm)3 6 9 12 15 18 n 98 60123 55100 4089 3568 2944 20314291 42124 67100 6487 5167 4950 244842a58 963 2465 3059 1870 4538 241043109 4590 41 (8 cm)70 32 (13 cm)109 45954132 or 137 (95% confidence interval for the distal esophagus)4144NOTE. Values are expressed as mm Hg (mean SEM). aPatient controls. The LESLiebermann-Meffert provided a detailed description of the muscular anatomy of the human LES, identifying a ring of thickened circular muscle angling obliquely upward from the lesser to the greater curvature of the stomach.46 Away from this ring, muscle thickness decreases both toward the esophagus and toward the stomach. Distally, the ring is split into two segments; one forming short transverse muscle clasps around the esophagus and the other forming long oblique loops to the stomach. The LES is normally situated within the diaphragmatic hiatus, typically formed by the right diaphragmatic crus. Recent studies discussed further suggest that a component of LES pressure results from extrinsic compression by the crural diaphragm. Physiologically, the LES is a 3-4-cm long segment of tonically contracted smooth muscle at the distal end of the esophagus. Resting LES pressure varies among individuals from 10 to 45 mm Hg relative to intragastric pressure. LES pressure is greatest at night and least in the postprandial period.47 LES tonic contraction results from both an intrinsic property of the muscle itself and modification of that tone by the nerves affecting the sphincter.48 Intra-abdominal pressure, gastric distention, peptides, hormones, various foods, and many drugs modify the LES pressure (Table 4).49 The LES is inhibited with swallowing concurrent with and presumably by the same mechanism as deglutitive inhibition in the smooth muscle esophagus. In fact, the sphincter should be viewed as identical to the adjacent circular muscle except that it maintains a tonic contraction by a myogenic mechanism. TABLE 4Substances Influencing LES PressureIncrease LES pressure Decrease LES pressure HormonesGastrinMotilinSubstance PSecretinCholecystokininGlucagonSomatostatinG