Esophageal care, reexamined: Dilation, dysmotility, and diagnostic debates

Dear colleagues,

Much of our clinical practice focuses on the diagnosis and management of upper gastrointestinal disorders, ranging from dysphagia due to mechanical obstruction to dyspepsia and abdominal pain related to dysmotility disorders. While presentations vary, patients consistently seek both an accurate diagnosis and durable relief.

In this issue, Dr. William Ravich shares practical insights on performing successful esophageal dilation of benign stenoses, addressing controversial topics such as the role of the barium esophagram — is it obsolete? — and the often quoted “rule of threes.”

Drs. Aylin Tansel and Yamini Natarajan examine upper GI dysmotility, reviewing the spectrum of medical therapies and outlining their approach to the nuanced care these patients require. We hope these contributions address common concerns and enhance your clinical practice in treating these disorders.

Gyanprakash A. Ketwaroo, MD, MSc, is associate professor of medicine, Yale University, New Haven, and chief of endoscopy at West Haven VA Medical Center, both in Connecticut. He is an associate editor for GI & Hepatology News. 

Is the esophagram obsolete?

By William J. Ravich, MD

A few years ago, I was asked to speak on the topic "Is the esophagram obsolete." The answer, to paraphrase Mark Twain, is that the report of the esophagram's demise is grossly exaggerated.

In my experience, the most frequent reason for the misdiagnosis or missed diagnosis in patients with dysphagia is the failure to perform a high-quality barium esophagram. Guidelines that reduce the esophagram to either secondary, or even optional, status are misguided. Endoscopy as the initial study is most appropriate for patients who have solid food dysphagia localized to the chest. These are patients with a high probability of a stricture beyond the cervical esophagus. Even in this situation, I have one proviso for skipping an esophagram; if no stenotic lesion is found on visual exam, the endoscopist must go ahead and dilate on an empiric basis. For most other dysphagia patients, a barium esophagram is a better choice for the initial evaluation. The esophagram should be tailored to the clinical question posed by the patient's clinical presentation.

Pharyngeal dysphagia should include a dynamic (video) evaluation of the pharynx in addition to the traditional esophagram. The gastroenterologist should make it a habit of reviewing the images with a focus on missed findings (it happens more than I would like to admit) and deficiencies in the examination (areas of inadequate distension in which a stenotic lesion might be hiding).

The "Rule of Three"

The "Rule of Three" states that you should "only dilate by three increments" (in dilator size) at a single session. Often attributed to H. Worth Boyce, MD, a legendary esophagologist, Boyce denied originating the rule, and believed he received the concept from his own mentor Eddy David Palmer, MD. Although superficially straight-forward, it contains a number of ambiguities.

What diameter dilator should you start with? I once had the opportunity of sharing my concerns about the rule with Dr. Boyce over lunch. He indicated that in practice he starts counting increments at the size at which he first appreciates "moderate resistance" — a rather subjective criterion.

What increments does the rule refer to? Depending on the manufacturer and type of dilator, dilators are sold in increments that vary from 2, 3, or 4 French units (1 French unit is equivalent to 1/3 mm in diameter). At the Johns Hopkins Hospital, where I cut my teeth as an endoscopist, non-guided serial dilators were available in 4 French increments. I only discovered later that they were available in 2 French increments. The brand of guidewire-directed dilators was sold in 3 French increments. So did the "Rule of Three" require limiting dilation to 2, 3, or 4 mm at a single session?

And how does the rule apply to balloon dilators? The reality is: it doesn’t! During the same discussion, Worth agreed that the rule couldn’t be applied to balloon dilators where the dilators don’t provide the type of tactile sense of resistance upon which the rule depends.

Does the "Rule of Three" matter? A retrospective study found that the risk of perforation does not appear to increase when the rule is not followed, so there appears to be at least some leeway in applying the rule in endoscopic practice. My approach is that as long as I sense no more than mild to moderate resistance, I will continue to dilate up to my ultimate goal for dilation. On the other hand, if I detect a significant jump in resistance at any point, and if I have already achieved a 4 mm dilation, I complete the passage of the dilator in my hand and then stop. When in doubt, I stop!

Schatzki’s Rule

Richard Schatzki, in his seminal work on the distal esophageal ring that bears his name, reported that rings that were 12 mm or less in diameter (as measured on an esophagram) always caused dysphagia, whereas those that were greater than 20 mm, rarely (he didn’t actually say never) cause dysphagia. Extrapolating this to strictures in general, the goal of dilation is to either resolve symptoms or to achieve a luminal diameter of 20 mm. In practice, a target of 18 mm with further dilation at a separate session up to 20 mm seems reasonable and consistent with Schatzki’s findings.

A tailored approach to dilation

Schatzki’s rings. Schatzki’s rings are isolated non-inflammatory webs composed of mucosa and submucosal without muscularis propria. The traditional approach to a Schatzki’s ring is to disrupt (“rupture”) it. Any dilator can achieve this end. For non-guided serial dilators, which I would only use with a patient under conscious sedition, I usually start by passing a fairly narrow dilator (e.g., 32 or 34 Fr) in order to determine whether there is a problem with its passage and to observe how the patient reacts. I then take a large diameter dilator (usually 56 or 60 Fr) to disrupt the ring. I use a similar approach when using a guidewire-direct serial dilator under conscious sedation but skip the preliminary dilator if the patient is under deep sedation or general anesthesia. With a balloon dilator, I attempt to pull through the ring but deflate the ballon and reposition it across the ring if I encounter more than mild to moderate resistance. Dilation is almost always effective at resolving symptoms, although recurrent dysphagia occurs in about 50% in the months or years to follow. Dilation can be repeated on an as-needed basis, if and when symptoms recur. Although there have been reports of using a four-quadrant biopsy technique (often using forceps with large cups) or electrocautery to disrupt the ring, I am not convinced that these approaches are superior or provide more durable responses. I reserve them for the rare Schatzki’s ring that is refractory to dilation.

Simple strictures. Through-the-scope balloon dilators are particularly suited for relatively short strictures (less than 4 cm in length). The balloon is passed through the scope, positioned to straddle the stricture, and inflated to a specified diameter. For a compliant stricture, one that seems to distend without much resistance, I will sequentially inflate the graded balloon in steps, waiting about 15 to 30 seconds between each step. For more fibrotic strictures, I will usually inflate to the first of the balloon’s three diameters for the same period, deflate briefly to assess effect and to decide whether to continue additional dilation, and then if appropriate inflate the balloon to the next diameter. I would use a similar approach with thin webs occasionally found in the tubular esophagus or PE segment.

Complex strictures. Complex strictures can be divided into three categories: those that are too long to straddle the stricture with a balloon dilator; those are two stenotic to pass even a slim (pediatric) endoscope through the stricture and those in which the remaining channel is highly irregular – often found to be malignant strictures. If possible, the full length of the stricture should be examined prior to dilation as bleeding from the dilation can make a careful examination of the stricture impossible. Information obtained from a previously performed barium esophagram can be invaluable with dealing with a stricture in which an endoscope can’t pass.

For long, and for most tight, strictures, I usually use guidewire-directed dilators, starting with a dilator diameter slightly above the diameter of the stricture. If the stricture is too tight to permit intubation before the dilation, a guidewire can be advanced carefully under fluoroscopic monitoring. I occasionally perform a pre-dilation with a balloon dilator (which requires a standard diameter endoscope) to sufficient diameter to permit passage of a slim endoscope, permitting placement of the guidewire directly into the stomach. It is helpful if you already know the length and contour of the stricture, either by a barium esophagram or information obtained from a previous endoscopy. With long or very tight stricture, I tend to adhere to the “Rule of Threes” closely. Long strictures can be dilated with balloon dilators by modifying the technique to dilate the stricture sequentially along its axial length, either starting at its distal or proximal end. However, this can prove cumbersome and is practical primarily for strictures in which the standard endoscope (required for the use of balloon dilators) can be passed through the stricture before dilation begins.

Fibrotic strictures. Occasionally, strictures are extremely fibrotic and resistant to dilation. This is particularly common in radiation-induced strictures. Balloon dilators are often too compliant to effectively dilate these strictures and guidewire-direct bougie dilators are preferred for this situation. Occasionally guidewire-direct bougie dilators may fail to dilate them effectively as well or require excessive pressure to do so safely. Marked resistance is a warning sign to suspend further attempts at dilation. Fortunately, patients with radiation-induced strictures often have developed compensatory eating behaviors that minimize obstructive symptoms, and dysphagia may be satisfied with a lumen of 15 mm or less. If the patient is happy, I’m happy!

Eosinophilic esophagitis (EoE) strictures. Strictures complicating eosinophilic esophagitis may appear as isolated webs, short strictures, multiple fibrotic-looking rings, or long strictures (referred to a small caliber esophagus). One of the characteristics of eosinophilic esophagitis is that the mucosa is fragile and any attempt at dilation causes a mucosal tear. I prefer balloon dilators for EoE strictures whenever practical, as it allows recognition of superficial mucosal disruptions that serve as signs to suspend further dilation at that session. For a small caliber esophagus, serial dilation with guidewire-directed bougie may be unavoidable. In this situation, I meticulously adhere to the “Rule of Three.” My concern is that a stricture that has already developed a deep tear during initial dilation, is unlikely to provide the reliable sense of resistance required to determine the extent of dilation. I once had a discussion with Dr. Ikuo Hirano about our respective techniques for dilating EoE strictures. I knew that he used guidewire-directed dilators and I expressed this concern. He explained that his practice was to examine the esophagus with the endoscope between each pass of a dilator. [Lymphocytic esophagitis, a much less common condition which can look and behave identically to eosinophilic esophagitis and should be handled in the same way.]

The cricopharyngeus. Cricopharyngeal dysfunction is an under-appreciated cause of dysphagia. The diagnosis may be suggested on esophagram by the presence of hypopharyngeal bar. Remarkably, the pharyngoesophageal (PE) segment will almost invariably be intubated with a standard endoscope without any sense of resistance. Difficulty passing the endoscope suggests the presence of a fixed stricture rather than sphincteric dysfunction and should be treated as such. If cricopharyngeal dysfunction is suspected, my approach is to place a balloon dilator with a maximal diameter of 20 mm into the esophageal body, inflate it to its maximum diameter, maintaining traction on the inflated ballon against the tip of the scope, and withdraw the scope and balloon as a unit. In patients without cricopharyngeal dysfunction, the balloon can be pulled through the PE segment with minimal or no resistance. If I sense marked traction on the balloon, I deflate the balloon, position it across the PE segment and distend the balloon rapidly to 20 mm. A mucosal tear is a common finding after effective dilation and is a good prognosis for a clinical response. Although patients who are effectively dilated may have a sore throat, it almost always resolved within a few days.

Solid food dysphagia: "A stricture until proven otherwise"

A common wisdom in gastroenterology is that solid food dysphagia (dysphagia that only occurs with ingestion of solid food only), is "a stricture until proven otherwise." The problem is, what is required to prove otherwise — that a stricture has actually been excluded. An esophagram can miss a stenotic lesion and passage of a barium tablet (typically only 13 mm in diameter), does not exclude the presence of a significant stenosis (see the discussion of Schatzki’s Rule, above). Similarly, a clinically significant stenosis can be missed at endoscopy, especially when it occurs in the area of the PE segment or EG junction, regions where non-distensibility may be unappreciated or accepted as reflecting sphincter function. Another common wisdom — that "if the scope passes through there is not a significant stenosis," — is clearly incorrect, as the standard endoscopy is only 9-10 mm in diameter. Empiric dilation of the EG junction for symptoms that are clearly esophageal in nature, and of both the EG junction and PE segment when a cricopharyngeal dysfunction is also a possibility, represents the definitive proof that a stricture is — or is not— present. One advantage of a balloon dilator is that withdrawal of a fully inflated 20 mm balloon from the stomach to, or when symptoms warrant, through the PE segment, may unmasked a stenosis segment or resistant PE segment that was not appreciated during visual examination. If no resistance is encountered, a clinically significant esophageal stricture has effectively been excluded.

Dr. Ravich is a professor of medicine in the Department of Internal Medicine/Section of Digestive Diseases at Yale School of Medicine, New Haven, CT.

References

Hagel AF, Naegel A, Dauth W, et al. Perforation during esophageal dilatation: a 10-year experience. J Gastrointestin Liver Dis. 2013 Dec;22(4):385-9.

Pezzullo JC, Lewicki AM. Schatzki ring, statistically reexamined. Radiology. 2003 Sep;228(3):609-13.

Ravich WJ. The Art of Endoscopic Dilation: Lessons Learned Over 4 Decades of Practice. Gastroenterol Clin North Am. 2021 Dec;50(4):737-50.

Richter JE. Rule of three for esophageal dilation: like the tortoise versus the rabbit, low and slow is our friend and our patients' win. Gastrointest Endosc. 2017 Feb;85(2):338-9.

Management of esophageal dysmotility: A pragmatic, phenotype-based approach

By Aylin Tansel, MD, and Yamini Natarajan, MD

Introduction

Esophageal dysmotility can be a challenging disorder to manage. Despite advances in esophageal testing to categorize esophageal motility disorders, therapeutic management remains notably limited for esophageal disorders outside of achalasia. We have found the best approach is to evaluate the presence of five domains: hypomotility, hypercontractility or spasticity, hypersensitivity, reflux, and finally, other factors (such as medications, structural issues, dysmotility). By focusing on the processes of influencing dysmotility, care becomes more intentional and impactful. 

Hypomotility

Disorders of weak motility, including ineffective esophageal motility and absent peristalsis, are commonly encountered in patients with chronic reflux or connective tissue disorders. Because of the decreased contractility, bolus transit relies heavily on esophageal diameter and gravity. Pharmacologic options are limited and off label, but can be effective for some patients, ideally before meals for optimal effect. Prokinetic agents include bethanechol, pyridostigmine, and buspirone. In addition to pharmacologic therapy, lifestyle modifications such as smaller bites, staying upright, and walking after meals can provide substantial benefits.  Empiric esophageal dilation should be considered in patients with predominantly solid food dysphagia because of the reliance on gravity to aid in food bolus clearance. These patients are at risk for significant reflux-particularly supine reflux; antireflux teaching is essential.

Hypercontractility and spasm

For the management of hypercontractile and spastic disorders (jackhammer esophagus or distal esophageal spasm), the goal is to promote smooth muscle relaxation and thereby relieve symptoms of dysphagia and/or chest pain. Eating habits should be assessed, with emphasis on slow, thorough chewing, as rapid eating can exacerbate hypercontractility and spasticity. For acute relief of chest pain and/or dysphagia, sublingual formulations are preferred. Peppermint oil can be a safe initial trial. For most with dysphagia/pain, consider prescribing an antispasmodic (hyoscyamine).  Severe spasms may require escalation to nitrates, such as nitroglycerin. For patients with frequent symptoms (with most meals), calcium channel blockers (diltiazem, nifedipine) can be taken prior to meals to reduce contraction amplitudes and thereby improve symptoms. For patients nonresponsive to medical management, consider esophageal Botox and possible dilation.  Some patients may benefit from specialized tailored therapy (such as POEM, Heller myotomy, etc). A low threshold to refer to tertiary centers is recommended.

Hypersensitivity

Symptoms of chest pain or discomfort can be particularly vexing for both provider and patient. If symptoms occur while eating, a hypercontractile or spastic esophagus may be the culprit, and management as outlined above can be considered. If worse after meals, suspect reflux. If constant and refractory to above, then the treatment can become more complicated involving the gut-brain axis. Short acting agents such as sucralfate or antacid-lidocaine mixtures can be used on demand for immediate symptom control but have limited long-term utility. For patients with predominant symptoms of chest pain, neuromodulators can be an effective tool. Tricyclic antidepressants have the best evidence for functional esophageal disorders. Other options include SSRIs, SNRIs, gabapentinoids, or trazodone. For isolated globus symptoms, consider a one-time gentle proximal esophageal dilation to see if this improves symptoms, and if fails, then consider trial with a gabapentinoid. Collaboration with a therapist and psychiatrist with expertise in functional gastrointestinal disorders can also be beneficial.

Reflux

Reflux can be both a cause and consequence of esophageal dysmotility. When reflux symptoms are present, they should be categorized by severity, frequency, and timing — whether postprandial, supine, or both. For postprandial symptoms, diaphragmatic breathing after meals and during acute episodes can be emphasized. For supine symptoms, left-sided or upright sleeping positions and avoidance of late meals are recommended.

The type of symptoms reported is also important. Regurgitation typically does not improve with acid suppression, whereas chest pain or burning may respond. If chest pain or burning persist despite optimized acid suppression, consideration can be given to possible bile reflux. For atypical symptoms such as cough or voice hoarseness, efforts should focus on reducing nighttime reflux, including elevating the head of the bed and considering a short trial of twice-daily PPI therapy. These patients may benefit from a multidisciplinary approach involving ENT and pulmonary specialists.

External and Systemic Influences

Finally, it is always important to step back and evaluate if any other factors could be further contributing to esophageal dysmotility. For instance, carefully review medications that can affect esophageal motility, such as opioids. If patients are on opioids, coniser peripherally acting mu-opioid receptor antagonists to help decrease the impact of opioids on esophageal dysmotility. The size and structure of pills are also important to consider. Large tablets can trigger symptoms, become impacted, and result in pill esophagitis. Consider alternate formulations such as liquids, crushed tablets, or open capsules whenever feasible. Consideration should be given to structural issues of the esophagus (e.g., epiphrenic diverticulum, peptic stricture, Schatzki ring), surrounding structures (such as a large left atrium or cervical hardware), and additional anatomical factors that may influence reflux or impair emptying (including hiatal hernia or prior surgeries). Treatment of these structural factors can often yield significant symptom improvement. Finally, evaluation of additional dysmotility issues, such as gastroparesis or constipation, can yield an additional target to optimize symptoms, particularly for patients with significant reflux.

Conclusion

Ultimately, the management of esophageal dysmotility is far more effective when we stop treating it as a single diagnosis and instead approach it as a set of underlying physiologic problems. It is helpful to focus on the processes influencing dysmotility — hypomotility, hypercontractility or spasticity, sensitivity, reflux, and other external or systemic factors. The goal is to improve how patients eat, feel, and function. This framework simplifies decision-making and helps align treatment more closely with patient symptoms.

Dr. Tansel practices at the University of Pittsburgh, Department of Medicine, Division of Gastroenterology. Dr. Natarajan practices at the Kelsey-Seybold Clinic in Houston, TX.

References

O’Rourke A, Tansel A. “Esophageal Disorders.” Bailey’s Head & Neck Surgery-Otolaryngology 6th edition. Lippincott Williams & Wilkins (LWW). 2022. ISBN: 978-1-97-516266-5.