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Difficulty Swallowing, Pharyngeal Disorders, and Motility Disorders

Dysphagia is part of esophageal disease that you can do a great deal of your diagnosis based on history. If you talk to a patient and they say the have difficulty initiating swallow, the food is coming out their nose, it’s dribbling down their face, you know it’s probably not an esophageal problem. A lot of the patients I see say food sticks about here. When food sticks here, pretty much all bets are off. So a lot of the patients really don’t localize it well, but lower dysphagia, lower symptoms, almost always indicate a problem in the esophagus. We also were taught to segregate dysphagia into solids and liquids, and this works but not 100%. Intermittent solid food dysphagia, I strongly believe, is a lower esophageal ring until proven otherwise. In fact I’ll even disbelieve a lot of my testing up until I know where there are rings there and whether I’ve dilated it. Progressive solid food dysphagia worries me more. I’m thinking of a cancer. Perhaps a tight stricture. Intermittent liquid dysphagia may make me think of some of these esophageal disorders.

The test that we use in evaluating dysphagia is either radiographic, endoscopic and manometry. These are the three series of tests. I think what you get with a barium swallow depends a lot on two things, what you ask for and whether your radiologist is interested in esophageal radiology. Unfortunately, a lot of times barium swallows are done poorly.

A full column routine barium swallow with or without air contrast is okay for something like achalasia and it will show tight strictures and it will show stenoses or things like medication-related strictures. So it’s an okay study.

What about oropharyngeal dysphagia? I think, again, history is key. The way to understand it is to understand what normally happens. Normally oropharyngeal swallowing involves four phases. First is initiation. This involves chewing the material, you have to have intact teeth. Teeth are a big problem. If you have a patient with poorly fitting or no dentures, it’s no wonder they have dysphagia. I send a lot of patients off for dental-type consults whenever I can’t find another problem. The second thing that happens is the nasopharynx is sealed. This rarely goes astray but it has to be done to get the bolus to go the right way. The airway by the epiglottis flipping over is protected, which channels the food down in the correct direction, the bolus.

Finally, things can be left behind in the oropharynx. And it’s not that abnormal. Older patients tend to have a residual on barium swallow. If they don’t aspirate, that’s probably not pathology and you shouldn’t change the way you feed them just based on a small amount of residual on barium study.

What are the disorders that affect oropharyngeal dysphagia? They are multiple. I think this is a good way to divide them; anatomic, neurologic and muscular diseases. Anatomic: such things as webs, cervical osteophytes. You have to be careful with this. They are common. We heard from Rick dysphagia is common.

The upper esophageal sphincter itself is not a true sphincter. All the rest … I’ve finally come to believe that the remainder of sphincters in the GI tract, the smooth muscle ones at least, are all true sphincters including the ileocecal valve. The upper sphincter is more of a slit-like opening, has multiple muscles. The cricopharyngeus is only one.

We can measure that manometrically. If this is a catheter left within the upper esophageal sphincter, this is in the pharynx, we give a swallow. This UES relaxes, a little bit of post-relaxation contraction and the bolus passes through. Now this is very fast. This relaxation lasts no longer than about 500 milliseconds, or half a second.

This is what a tracing looks like when you are doing a clinical evaluation of UES relaxation using a solid-state, rapidly responding system. This is about equivalent to the tongue base, this is in the pharynx and this is at the upper esophageal sphincter. You look for ordered peristalsis. It’s not really peristalsis, it’s sequential contractions beginning in the tongue base and extending down into the pharynx. All this should happen while you get a lifting of the sphincter onto the catheter and relaxation. So this is actually the relaxation. This is actually an abnormal study. This is an achalasia patient.

When we are treating people for oropharyngeal dysphasia our goals of therapy are a little different. We want to protect the airway, maintain nutrition, and relieve dysphagia. Actually relieving dysphagia falls down a bit. I think the best person to work with is a speech swallowing therapist. They can do retraining, the can change bolus size, simply give patients thickeners for their food. They can recommend specific swallowing maneuvers, the Muller maneuver, the Valsalva.

Achalasia, this rare disorder that I see all the time but is pretty rare in the community. Achalasia is defined as incomplete relaxation of the lower sphincter with aperistalsis. These can either be absent waves or what’s called "isobaric simultaneous waves. Now ileus hypertension is shown on this slide but in reality that’s fairly rare.

How does achalasia happen? We know a lot about this disease. We don’t know why it happens but we know how it happens. The lower sphincter is under two controls. One is a tonic control provided to the cholinergic system, perhaps in substance P.

Treatment of achalasia. There’s four categories of treatment. Drug treatment has generally been poor. Nifedipine will drop the sphincter pressure but in no randomized study has it been shown to provide long term therapy. Botulinum toxin will actually provide relief of symptoms in a number of patients, perhaps half or more, by blocking acetylcholine reaction at the smooth muscle. But almost none of these patients gets long term relief, and everybody that I’ve ever treated has had to be re-treated. Now I have patients that I’ve kept in remission for 3-5 years by giving them repeated treatments.

Quickly going through the other neuropathic disorders; diffuse esophageal spasm is extraordinarily rare. Two percent of patients with dysphagia, or less. Some simultaneous contractions along with peristalsis. If you get any peristalsis within a manometry study it’s diffuse spasm and not achalasia. Nutcracker esophagus we will dismiss. This is high pressure contractions within the esophagus, probably a manometric curiosity but you’ll still see it in papers.

Now those are the neuropathies. I want to spend the last couple of minutes on the myopathic diseases of the esophagus, which perhaps are the more common cause of dysphagia. These are times whenever there are actually contractions but they are weak. We know that if a contraction doesn’t reach 35 mm of pressure it can’t propel the bolus. The most common cause of these weaknesses in the esophagus is reflux, although the classic finding is systemic sclerosis or sclerodermal esophagus. This is manifested by no LES pressure and aperistalsis. In contrast to achalasia where you have LES intact and aperistalsis. Sometimes it’s difficult to determine. Radiographically the classic picture is a stovepipe esophagus where you see no sphincter.

Finally, a problem with all of this is that we don’t have great therapy. I was misquoted a few years ago when I said, "The best therapy for reflux is a pro-motility agent." There was a big sign at a company that sells pro-motility agents that said that. It kind of shocked me because the actual sentence in the article said, " but there are no ideal pro-motility agents." They of course decided to leave that off. There is no ideal therapy for contraction failure. I certainly will try a pro-motility agent.