This seems to be more than a little interesting and you think to yourself, “What the heck? Let me check this out.”
You then begin to recall that the patient looks a little familiar to you. In fact, SH has been to the ER more than a dozen times within the past three months. Her previous visits have all been related to asthma exacerbation secondary to ethanol abuse, and unfortunately, she has been non-compliant with her asthma medications. She has been intubated several times in the past and has required admission to the ICU.
She currently presents with tachypnea and acute shortness of breath. Physical exam reveals HR of 115 bpm, RR of 42 bpm with signs of accessory muscle use, and 88% oxygen saturation upon room air. SH also has decreased breath sound bilaterally with inspiratory and expiratory wheezing. In addition, readings from the peak flow meter are consistently in the red zone between 150 and 160 L/min.
Run of the mill treatment is started with oxygen therapy and nebulized solution of albuterol 2.5 mg and ipratropium 0.5 mg every 20 minutes times 3 doses. In addition, IV access is obtained, and a one-time dose of methylprednisolone 125 mg IV is ordered. SH does not show any improvement, and the decision is made to initiate a continuous solution of nebulized albuterol at a rate of 10 mg/hr.
Despite all these therapies, SH still shows no signs of improvement, and so “kitchen sink” therapy is started with a one-time dose of terbutaline 0.25 mg SQ and magnesium sulfate 2 g IV infusion. Even a loading dose of aminophylline 400 mg is ordered; after all, what harm can it do? With all these therapies being initiated, SH still is profoundly wheezing, and her oxygen saturation drops to 85% on room air. The ED attending physician looks to you and asks, “Can we try glucagon in this patient?”
You are stunned by this request. Theoretically, this makes sense. We know that glucagon is a 29-amino acid polypeptide hormone produced by the α-cells of the islets of Langerhans in the pancreas. It acts by stimulating adenyl cyclase to activate the synthesis of cyclic adenosine monophosphate (cAMP). So the next question you ask yourself is: are there any studies to support the use of glucagon in the management of asthma exacerbation?
A quick literature search on PubMed only reveals about a handful of studies related to this. One study demonstrated that approximately 60% of patients experienced a mean increase in peak expiratory flow rate by at least 60 L/min ten minutes after the administration of 1 mg of IV glucagon for patients with asthma exacerbation. However, in a randomized, double-blind, placebo-controlled trial simulated to evaluate the same study outcome, the administration of weight-based IV glucagon (0.03 mg/kg) showed no real benefit in improving bronchodilation in asthmatic patients who presented to the ED with bronchospasm. Interestingly enough, a study was conducted that evaluated the effect of nebulized glucagon in the management of bronchospasm in patients with a history of chronic stable asthma, which showed greater improvement in FEV1 compared to nebulized normal saline. Administration of glucagon through this route may be a reasonable option, especially in patients where IV access may be difficult to obtain.
Anecdotally, we have administered IV glucagon at a dose of 2 mg to select patients (including SH) at our institution for the management of bronchospasm associated with asthma exacerbation. Glucagon may be considered as a last-line option if patients with bronchospasm secondary to asthma do not show improvement with standard therapies.
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