Knowingly or not, we in emergency medicine tend to lean into the Dutch hypothesis, a 1960s postulate that asthma and COPD are part of a spectrum of common disease (chronic obstructive lung disease), and should be considered a single disease with common genetic origins.

It’s an approach that allows us to cognitively coordinate the management of obstructive pulmonary disease to some degree.

Both patient populations universally receive the inhaled beta agonists and anticholinergics we reflexively call for as well as a hefty dose of corticosteroids and a call to the respiratory therapist to initiate bi-level positive airway ventilation. Nebs. Steroids. BiPAP.

But growing clinical experience understands these conditions as separate entities, which for all of their similarities uniting bronchoconstriction, bronchorrhea, and hypoventilation, have marked differences in the pattern of inflammation that occurs in the respiratory tract, with different inflammatory cells recruited, different mediators produced, distinct consequences of inflammation, and, importantly, differing responses to further therapy.

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