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A manometry report reading esophagogastric junction outflow obstruction is not yet a diagnosis, and on its own it is often a false positive. The episode follows a fifty-nine-year-old man on daily opioids with obesity and dysphagia. It first defines the three tracing requirements, then explains why the diagnosis is clinically inconclusive without fitting symptoms and a confirmatory test. Next it works through the imitators: opioids, obesity, hernia, eosinophilic esophagitis, cancer, prior fundoplication, and evolving achalasia. It then confirms obstruction with a timed barium esophagram or FLIP, and ends by choosing treatment according to the cause the workup finds.
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Welcome to Board Pearls. This is episode two of four of the Esophageal Motility chapter, in the Esophageal Disorders module. This episode is the patient whose manometry shows a sphincter that doesn't relax fully but whose peristalsis is still there. That pattern is called esophagogastric junction outflow obstruction, and on manometry alone it's often a false positive. A fifty-nine-year-old man on daily opioids, with obesity and dysphagia, is followed from his first tracing. His case teaches why the tracing alone isn't a diagnosis, which conditions raise the relaxation pressure without any disease of the sphincter and how each is checked, which tests prove a real obstruction and how they're read, and how the cause, once found, decides the treatment.
Here's the patient. A fifty-nine-year-old man has had a year of solid food sticking low in his chest, a few times a week. Liquids go down fine. He has chronic back pain and takes hydrocodone every day. His body mass index is thirty-four. He has mild heartburn. His primary care doctor ordered high-resolution manometry, and the report says outflow obstruction at the junction. He's been told he might need a procedure on his sphincter.
His report says outflow obstruction, so the starting point is what his tracing actually shows. His integrated relaxation pressure, the IRP, is elevated both lying down and sitting up. But unlike achalasia, in which no swallow produces peristalsis, his body still has peristalsis: most swallows are intact or weak, not failed. And on more than a fifth of swallows, the bolus is pressurized above the sphincter. Esophagogastric junction outflow obstruction is impaired relaxation of the junction with partly preserved function of the esophageal body, and it's a heterogeneous diagnosis that covers every patient with that combination.
Those are the three manometric requirements in version four of the Chicago classification, and each is there for a reason. The median IRP has to be elevated in both positions, with an upright threshold of twelve millimeters of mercury on the most widely used system. The upright requirement was added because a high supine IRP alone has a high false-positive rate: in one study, an upright IRP over twelve had a sensitivity of ninety-eight percent for obstruction confirmed on barium, but its specificity was low, so many positives weren't real. Some peristalsis has to be preserved, because if every swallow fails, the diagnosis is achalasia instead. And at least twenty percent of swallows need increased intrabolus pressure, because a real obstruction squeezes the bolus against a sphincter that won't open, and that trapped, compartmentalized pressure is the physical sign of it. He meets all three, so on manometry he has outflow obstruction.
That pattern isn't yet a disease. The current classification says a manometric diagnosis of outflow obstruction is always clinically inconclusive on its own. Many patients with this tracing have nothing wrong with their sphincter. Calling it clinically relevant takes three things together: the manometric pattern, symptoms that fit, meaning dysphagia, chest pain, or both, and a second test that confirms an actual obstruction. That three-part rule is the most important practical change in the current version for this diagnosis, and it removes a large share of incidental findings from the disease pool.
The rule exists because the alternative is putting a balloon or a knife to a normal sphincter. A patient with this tracing found incidentally, with no dysphagia, doesn't have a disease and doesn't get a procedure. This patient has dysphagia, so he has two of the three. He still needs the confirmation. But before confirming it, the question is what else could be raising his IRP, because this pattern has a long list of imitators, and he already carries several of them, so those are checked first.
His opioid is the first to address, because it's the most common reversible cause. Opioids impair sphincter relaxation and raise the IRP. They also make contractions come too early and too hard, so a patient on daily opioids can produce almost any abnormal pattern, including this one. Opioid-induced outflow obstruction resolves when the opioid stops. So the first step for him isn't a test. It's a taper of his hydrocodone, together with whoever manages his back pain, and then a repeat study. If the tracing normalizes, the cause is found and he's spared a procedure. If the opioid truly can't stop, only his symptoms are treated, because cutting a sphincter that's being held shut by a drug doesn't make sense.
His weight is the second imitator he carries. Abdominal fat raises the pressure around the junction and pushes the baseline IRP up. It's a known confounder, not a disease of the sphincter, and it's one more reason a borderline number in a heavier patient needs confirmation before anyone acts on it.
The structural imitators need imaging, because manometry can't tell a stiff sphincter from a squeezed one. A paraesophageal hiatal hernia can narrow the junction mechanically, it's an underappreciated cause, and endoscopy and cross-sectional imaging show it. Eosinophilic esophagitis can cause enough fibrosis to stiffen the junction, impair its distensibility, and raise the IRP, which is why biopsies for eosinophils are required in any unexplained outflow obstruction, even when the mucosa looks normal. A cancer infiltrating the junction can produce anything from outflow obstruction to full pseudoachalasia, depending on how much of the wall it involves, so an older patient with rapid weight loss gets endoscopic ultrasound and cross-sectional imaging. A prior fundoplication reliably raises the IRP, because tightening the junction is what a wrap is built to do. And rarely, the aorta or a vascular ring compresses the esophagus from outside.
One more imitator is really the same disease in an earlier form: achalasia in evolution, particularly type three, where peristalsis is fragmenting but hasn't yet disappeared. That patient may look like outflow obstruction today and like achalasia in a year.
The manometry study itself can add support. A rapid drink challenge, two hundred milliliters of water through a straw, is abnormal when the IRP rises over twelve with pressurization along the whole esophagus in the first thirty seconds, and that supports outflow obstruction when the standard swallows are equivocal. Multiple rapid swallows during the same study can add support too.
So his workup has a sequence, and each step answers one item on that list. Endoscopy looks for mechanical narrowing, a mass at the junction, the anatomy of any hernia, and retained food that would suggest an achalasia variant, and it takes the eosinophil biopsies. Computed tomography, CT, of the chest and abdomen looks for compression from outside, a paraesophageal hernia, and a mass in the wall. Endoscopic ultrasound is added when a cancer is strongly suspected. And the opioid comes off.
His endoscopy is normal, with no stricture, no mass, no retained food, and biopsies without eosinophils. CT shows no hernia and no mass. He tapers off hydrocodone over a month with his pain doctor, moving to non-opioid treatment. Then the repeat manometry: the IRP is still elevated in both positions, peristalsis is still intact, and the bolus is still pressurized. So the opioid wasn't the cause, nothing structural is there, and his symptoms persist. Now he needs the third piece, a test that measures what manometry can't: whether the bolus is actually held up.
A timed barium esophagram with a barium tablet is the simpler confirmatory test. He drinks barium, and films at one, two, and five minutes show how quickly his esophagus empties. Then he swallows a barium tablet. A barium column more than five centimeters tall at five minutes, or a tablet that hangs up at the junction, supports a real obstruction. It's widely available, and it shows the thing the patient feels: food not getting through.
The functional lumen imaging probe, or FLIP, measures the junction directly. The catheter is passed through the mouth with the endoscope during a sedated procedure and positioned across the junction. It carries a sixteen-centimeter balloon with sixteen paired impedance electrodes and a pressure sensor inside. The balloon is filled with conductive saline in steps, typically thirty, forty, fifty, sixty, and seventy milliliters, and at each volume the impedance between electrode pairs is converted to a cross-sectional area at sixteen points along the segment, displayed as a real-time three-dimensional image. The narrowest cross-sectional area divided by the pressure in the balloon gives the distensibility index, in square millimeters per millimeter of mercury. It answers the real question: how stiff is this junction when something tries to get through?
FLIP is read by the Dallas consensus criteria. At a sixty-milliliter fill, a distensibility index of at least two and a maximum junction diameter of at least sixteen millimeters is normal opening. An index under two with a maximum diameter under twelve millimeters is reduced opening, which supports outflow obstruction or achalasia. Values in between are inconclusive.
FLIP also shows how the esophageal body responds to stretch, called FLIP panometry, because the body's response helps decide the treatment. The normal response is repetitive antegrade contractions, each at least six centimeters long, at six per minute, plus or minus three. Abnormal responses are absent, with no contraction in the body; spastic, with sustained occluding contractions in the body or at the sphincter; disordered, which is none of those with an intraballoon pressure over forty millimeters of mercury; and diminished, the same with a pressure under forty. Normal opening with a normal contractile response makes a major motility disorder very unlikely, so a normal FLIP is often the test that takes a patient off the procedure list. Reduced opening with a spastic or non-spastic obstructive response is common in achalasia.
FLIP takes about ten minutes, is done at the same session as an endoscopy, and carries about the same risk as an endoscopy alone. That's why it often makes sense to plan it with the diagnostic scope rather than as a separate visit.
His barium column is seven centimeters at five minutes, and the tablet stops at the junction. His FLIP shows a distensibility index of one point four and a maximum diameter of ten millimeters, with a normal contractile response in the body. Now he has all three: the manometric pattern, dysphagia, and a confirmed obstruction. His outflow obstruction is clinically relevant.
His treatment follows the mechanism the workup found, not the label. When barium and FLIP confirm obstruction in a patient with dysphagia, the physiology behaves like an early form of achalasia, so treatment mirrors achalasia: pneumatic dilation, Heller myotomy with a partial fundoplication, or peroral endoscopic myotomy, POEM, with the choice guided by the pattern of peristalsis in the body and whether there are spastic features.
The other mechanisms each change that plan. If his body showed spastic or hypercontractile features, the pattern would be managed as a type three achalasia variant, with POEM, because only a long myotomy reaches the spastic segment above the sphincter. If his peristalsis were normal or only weak and his symptoms were mild, he could be observed on a proton pump inhibitor, PPI, with diet changes, with botulinum toxin or pneumatic dilation kept for symptoms that become disabling; a mild symptom doesn't justify a permanent change to the sphincter. A mechanical cause gets the fix for that cause: hernia repair, treatment of eosinophilic esophagitis, or cancer care. And opioid-induced obstruction resolves with stopping the opioid; when that isn't possible, treatment is for symptoms only.
For him, with a confirmed obstruction, intact peristalsis without spasm, and dysphagia that now limits what he eats, a definitive achalasia-style treatment is reasonable, and he has a pneumatic dilation. His dysphagia improves.
FLIP solves three other diagnostic problems. A patient with classic achalasia symptoms but a borderline IRP, under fifteen lying down, can be confirmed as having achalasia by reduced opening on FLIP. A manometry study that fails, because of artifact or because the patient can't tolerate the swallows, can be replaced by FLIP at the time of endoscopy, without a separate visit. And during POEM or Heller myotomy, FLIP tells the operator when the myotomy is long enough: the endpoint is a normalized distensibility index and a wider junction, which correlate with better results afterward.
Here are the traps the boards set in this patient.
In reading the tracing, treating the manometric pattern without fitting symptoms and a confirmatory test treats a finding that's often a false positive. And accepting a supine IRP alone ignores the upright requirement that cuts those false positives.
In the workup, calling it a disease before stopping the opioid misses the most common reversible cause. Skipping eosinophil biopsies because the mucosa looks normal misses a fibrotic cause. Missing a paraesophageal hernia, a prior fundoplication, or an infiltrating cancer treats the wrong problem. And forgetting that obesity raises the IRP overreads a borderline number.
In treatment, choosing dilation when the body is spastic misses that POEM is the treatment for that pattern. And treating a confirmed, disabling obstruction with a PPI alone leaves the obstruction in place.
So, start to finish.
An elevated IRP lying and sitting, with some preserved peristalsis and bolus pressurization on a fifth of swallows, is outflow obstruction on manometry, and on its own it's inconclusive.
Before calling it a disease, stop opioids, think of obesity and a prior wrap, and look for a hernia, eosinophilic esophagitis, and cancer with endoscopy, biopsies, and CT.
It becomes clinically relevant only with fitting symptoms plus a confirmatory test: a barium column over five centimeters at five minutes or a tablet that hangs up, or a FLIP distensibility index under two with a maximum diameter under twelve millimeters.
Then treat the mechanism: achalasia-style treatment for confirmed obstruction, POEM when the body is spastic, observation for mild symptoms with weak or normal peristalsis, and the specific fix for a mechanical cause.
Episode three moves to the body of the esophagus: the patient whose sphincter relaxes normally but whose esophagus squeezes too early or too hard, causing chest pain and dysphagia.