A Closer Look at Glucagon for Esophageal Foreign Body

Reaching for that vial (or two) of glucagon to manage the patient who presents to your emergency department with an esophageal foreign body obstruction (EFBO)? Think again.

The first reports of its use for managing patients with EFBOs came about in the 1970s, when it was first discovered that glucagon had direct relaxation properties on the lower esophageal sphincter (LES), which is comprised of smooth muscle. This, in turn, will help decrease the resting pressure of the LES. There were a number of promising small studies and case reports that followed this discovery that showed the benefits of glucagon in disimpacting esophageal foreign bodies, with high rates of success.

What dose of glucagon will effectively work in relaxing the lower esophageal sphincter? The results of one study demonstrated that doses of 0.25 mg and 0.5 mg significantly reduced the resting pressure of the LES. Interestingly enough, not only did a dose of 1 mg not have any significant benefit in reducing the resting pressure, but it was also found to delay transit time within the esophagus, which can potentially worsen the event (and defeats the purpose of using glucagon in the first place).

The investigators of the above-mentioned study found that more patients were likely to experience symptoms of nausea and/or vomiting with the higher dose of 1 mg. This adverse effect can be expected, as the incidence of nausea and vomiting associated with glucagon is known to be dose-related (as well as related to the frequency of administration). This is particularly worrisome, as not only is the vial conveniently available for administration as a 1-mg dose, but in the setting of EFBO, the incidence of nausea and/or vomiting can increase the risk of aspiration. If the ingested foreign body is made up of sharp or jagged edges, one also runs into the risk of esophageal perforation.

Sodeman and colleagues conducted a retrospective case series of 222 patients who presented to the emergency department with EFBO. Of these patients, nearly half (106 patients) received intravenous glucagon, of which only 10 experienced complete symptom resolution following administration. In contrast, of the 116 patients who did not receive glucagon, 20 (17%) had spontaneous resolution. In addition, the investigators evaluated those patients who were not likely to respond to glucagon for the removal of EFBOs. They found that patients with a history of esophageal strictures and rings and those who present with meat impaction were less likely to respond to treatment with intravenous glucagon.

Other studies that have been conducted have not demonstrated any significant benefit of using glucagon in the setting of EFBO, a review of which can be found here. With the inconsistencies in dosing and outcomes as well as the potential harms associated with its use, one should reconsider glucagon as the “go-to” intervention for EFBO.

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