Esophageal motility testing: The spastic truthdownloads.hindawi.com/journals/cjgh/2007/893258.pdf · disorder. There are case reports of patients with a scleroderma-type esophagus,

Can J Gastroenterol Vol 21 No 3 March 2007 147

Dr William Paterson is a Professor of Medicine at Queen’sUniversity (Kingston, Ontario) and the current President

of the Canadian Association of Gastroenterology. He began hiscareer in esophageal motility research atHarvard University (USA) with Dr Raj Goyaland has an ongoing Canadian Institutes ofHealth Research-funded program that focuseson basic esophageal physiology and pathophysi-ology. He also directs the gastrointestinalfunction laboratory at Hotel Dieu Hospital(Kingston, Ontario).PA: You are called in to see a patient in thecardiology ward who has just had an angiogramand an angioplasty, but continues to haveangina-like chest pain. The patient has beenreceiving proton pump inhibitor (PPI) therapy.The cardiologist told him/her that he/she hasminimal heart problems (although he/she justhad an angioplasty) and most likely a spasticesophagus. What is your approach to thiscommon type of referral? If manometry is notreadily available at your centre, can you com-ment on the use of endoscopy and barium stud-ies within this setting?WP: Actually, at least at our centre, referrals from cardiologistsfor patients with so-called noncardiac chest pain are no longerthat common. We have noted a dramatic reduction in the num-ber of patients who are referred to our centre with this problem,both in the inpatient and outpatient setting. I am not sureexactly why this is the case. It may be that family doctors andcardiologists realize that we are no longer very enthusiasticabout pursuing various diagnostic tests in the workup of thesepatients. Since the Canadian Association of Gastroenterologyand the American Gastroenterological Association guidelines(1,2) on noncardiac chest pain and esophageal manometrywere published approximately 10 years ago, we have seen a sig-nificant change in the referral pattern for esophageal motilitystudies. Whereas in the past, probably two-thirds of the patientsundergoing manometry were referred because of noncardiacchest pain, that number has now decreased to less than 20%.The majority are referred for evaluation of nonstructural dys-phagia. This change in practice is due to our increasing realiza-tion that although esophageal manometry and provocativetesting may provide us with some insight into the pathogenesisof the patient’s chest pain, it lacks sensitivity and specificity andrarely guides us toward a specific therapy. More commonly, theapproach being taken in these patients, once cardiac disease isexcluded, is to treat empirically with either a PPI or a tricyclic

antidepressant. Barium studies are of no value unless the patienthas associated dysphagia. The yield on endoscopy is also verylow. It is nice if you find reflux esophagitis in these patients

because you then have a firm rationale for PPItherapy. However, in practice you will likelygive a treatment trial for reflux irrespective ofwhether there is macroscopic esophagitis.PA: Often these patients may have symptomsthat have been more traditionally associatedwith angina such as radiation of pain down thearm, diaphoresis or pain during exercise. Couldsome of these patients have microvascularangina?WP: Yes, microvascular angina or so-calledcardiac syndrome X may be present in some ofthese patients. It is more common in woman.Usually, this syndrome is characterized byclassic, exertionally related chest pain. Patientsusually do not present with sporadic chest painunrelated to exercise. I am, therefore, veryreluctant to consider esophageal origin of thepain in patients that have typical exertionalpain irrespective of the angiographic findings.In these patients, I usually ask the cardiologist

to reconsider the possibility of microvascular angina.PA: We have seen reports that patients can have manometricabnormalities with no symptoms and symptoms with no mano-metric abnormalities? How do you interpret these observations?WP: That is one of the basic problems with using manometryin patients with chest pain. There is rarely any direct correla-tion between the manometry abnormalities and the painepisodes. We do see a rare patient who has very prolonged dura-tion contractions that seem to coincide with pain episodes. Theusual high amplitude contractions seen in Nutcracker esopha-gus do not correlate with the pain. Many of us believe that thisis because the hypertensive peristaltic contractions seen inNutcracker esophagus may simply be a sign of hyperreactivity ofthe esophagus. Many of these patients have evidence of visceralsensory abnormality affecting the esophagus. The other reasonfor poor correlation with intraluminal manometry is that the‘muscle spasms’ that we have always presumed were the cause ofnoncardiac chest pain, are actually occurring in the longitudi-nal smooth muscle. These contractions lead to shortening ofthe esophagus but do not produce a detectable change in theintraluminal pressure. A study by Balaban et al (3), using intra-luminal ultrasound, has suggested that there are sustained con-tractions of the longitudinal muscle that correlate with certainpain episodes. We have also shown, in animal models, that acid

Esophageal motility testing: The spastic truth

William Paterson MD FRCPC1, Paul C Adams MD2, Editor-in-Chief

MEET THE EDITOR

1Department of Gastroenterology, Hotel Dieu Hospital, Kingston; 2London Health Sciences Centre, London, OntarioCorrespondence: Dr William Paterson, Department of Gastroenterology, Hotel Dieu Hospital, 166 Brock Street, Kingston, Ontario K7L 5G2.

Telephone 613-544-3400 ext 3376, fax 613-544-3114, e-mail [email protected]

Dr William Paterson is a Professor ofMedicine at Queen’s University(Kingston, Ontario) and the currentPresident of the Canadian Associationof Gastroenterology

©2007 Pulsus Group Inc. All rights reserved

paterson_9871.qxd 23/02/2007 10:04 AM Page 147

in the lumen can produce a sustained reflex contraction of thelongitudinal muscle.PA: One of the most well accepted indications for manometryis before fundoplication. Is this still a strong recommendation?WP: Although virtually all antireflux surgeons will requestesophageal manometry before proceeding with fundoplication,I am not sure if I would describe this as a well accepted indica-tion. In the updated American Gastroenterological Associationmedical position statement on the clinical use of esophagealmanometry published last year, it is stated that “manometry ispossibly indicated for the pre-operative assessment of peristalticfunction in patients being considered for anti-reflux surgery”(4). The main rationale for performing manometry beforesurgery is to rule out an unrecognized, severe, primary motordisorder. There are case reports of patients with a scleroderma-type esophagus, diffuse esophageal spasm or even achalasia whounderwent antireflux surgery and then developed severeunremitting dysphagia subsequently. This can lead to quite dis-astrous results, sometimes leading to esophagectomy. However,there is now abundant evidence in the literature that mostpatients with significant peristaltic dysfunction do not have asignificantly worse outcome after antireflux surgery, providingthe patient does indeed have underlying reflux disease. My ownview is that in patients with typical clinical and endoscopicevidence of reflux disease and no history of Raynaud’s phenom-enon, a well performed barium swallow is probably adequate.Manometry is probably important in patients being consideredfor surgery with atypical presentations or evidence of Raynaud’sdisease.PA: Can you describe any esophageal problems that are notwell demonstrated on barium studies or endoscopy but are wellsuited to a diagnosis by esophageal manometry?WP: The most important disorder that can be diagnosed mano-metrically, which may be overlooked by barium studies andendoscopy, is achalasia. We have recently reported that a sig-nificant minority of patients with manometrically confirmedachalasia will not have the classic barium x-ray findings. Thus,patients with persisting troublesome dysphagia, withoutevidence of mechanical obstruction (and this would includenegative biopsies for eosinophilic esophagitis), should haveesophageal manometry. On the other hand, it is worth pointingout that esophageal manometry does lack sensitivity. There aremany patients with normal stationary manometry testing whohave evidence of nonspecific contraction abnormalities duringvideofluoroscopy.PA: It seems that there is less interest in esophageal manome-try among community gastroenterologists. Is this because it hasnot been considered to be useful? Is it related to remunerationor inadequate training? Are manometry specialists at risk ofbecoming an extinct species?WP: I think the enthusiasm that was present 10 years agosurrounding motility disorders and motility testing in generalhas been waning. This is perhaps largely due to the fact thattreatment for esophageal motor disorders has not kept pacewith our ability to diagnose them. A diagnosis of achalasia onmanometry leads to very specific and useful therapies.Unfortunately, we do not have validated treatments for variousother motor disorders. Another factor I think is that traineesand training programs seem to be overwhelmed with proceduresand consultations at the expense of other aspects of ourspecialty, including manometry. Remuneration may also be afactor. It probably takes about the same time to perform a

colonoscopy than it does to perform a supervised manometry.The fee for colonoscopy is almost three times greater. However,I do not think that motility specialists are at risk of becomingextinct yet. I suspect motility testing will make a comebackonce better treatments are available. I am optimistic that a timewill come when we will use drugs to treat functional esophagealdisorders that are tailored to the specific motor or sensoryabnormality that is detected.PA: Can you describe some of the new technologies in theassessment of esophageal diseases?WP: There are a number of new techniques to study esophagealfunction. High-resolution manometry uses a 36-channel solidstate catheter and sophisticated computer software. By vastlyincreasing the number of recording sites and decreasing thespacing between them, one is able to markedly increase thesensitivity of esophageal manometry. The data are displayed inbeautiful isobaric contour plots that give high temporal andspatial resolution. While this will pick up subtle abnormalitiesthat can be missed with routine perfusion manometry, it is yetunclear whether this will improve outcome for our patients.Some laboratories also have the so-called Bilitech 2000(Medtronic of Canada Ltd) which is capable of detecting whenbilirubin makes contact with its sensor. This has been used toassess the degree of bile refluxing into the esophagus.Unfortunately, this device is somewhat inaccurate and has yetto show any clinical benefit.

There has also been a lot of interest in recent years insensory testing using either a barostat device or an impedanceplanimetry balloon. These devices are very useful to studypathophysiology and can ascertain whether the patient’s symp-toms are related to a sensory disorder. This in turn may guidetherapy toward drugs that interfere with visceral sensation, suchas tricyclic antidepressants. However, because sensory problemsare so prevalent, empirical treatment is certainly a reasonableoption to this sort of testing.

Finally, esophageal impedance monitoring is now being usedin many centres as an adjunct to standard manometry andambulatory pH testing. The impedance catheter detectschanges in electrical resistance between a series of paired elec-trodes, thereby detecting movement of air, solids and liquids ineither direction within the esophagus. It therefore provides auseful measure of bolus transport during peristalsis, as well asboth air and liquid reflux coming from the stomach. Whencombined with pH monitoring, it is able to detect ‘nonacid’reflux episodes. There is now a growing body of literaturesuggesting that a small subgroup of patients, with persistingsymptoms following PPI therapy, have symptoms caused bynonacid reflux events.

Can J Gastroenterol Vol 21 No 3 March 2007148

Meet the Editor

REFERENCES

1. Paterson WG. Canadian Association of Gastroenterology practiceguidelines: Management of noncardiac chest pain. Can J Gastroenterol 1998;12:401-7.

2. Kahrilas PJ, Clouse RE, Hogan WJ. American GastroenterologicalAssociation technical review on the clinical use of esophagealmanometry. Gastroenterology 1994;107:1865-84.

3. Balaban DH, Yamamoto Y, Liu J, et al. Sustained esophagealcontraction: A marker of esophageal chest pain identified byintraluminal ultrasonography. Gastroenterology 1999;116:29-37.

4. Pandolfino JE, Kahrilas PJ; American GastroenterologicalAssociation. AGA technical review on the clinical use of esophagealmanometry. Gastroenterology 2005;128:209-24.

5. El-Takli I, O’Brien P, Paterson WG. Clinical diagnosis of achalasia:How reliable is the barium x-ray? Can J Gastroenterol 2006;20:335-7.

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Esophageal motility testing: The spastic truthdownloads.hindawi.com/journals/cjgh/2007/893258.pdf · disorder. There are case reports of patients with a scleroderma-type esophagus,