COMMENTARY

Limb Muscle Dysfunction After Acute Exacerbation of COPD

Aaron B. Holley, MD

Disclosures

March 26, 2018

Acute exacerbation of COPD (AECOPD) is associated with considerable morbidity and mortality. Much work has gone into preventing AECOPD and minimizing the consequences of its occurrence, but we tend to focus more on associated lung function decline than on the effects from decreased mobility.[1]

Consider that the median duration of hospitalization for AECOPD is 7 days,[2] during which time these patients spend little time out of bed.[3] Even outpatient exacerbations are associated with decreased activity.[4] Given what we know about the profound physiologic effects of bed rest on healthy persons,[5,6] what happens to patients with COPD during extended periods of immobility?

In what the journal calls a "concise clinical review," the causes of lower-limb dysfunction in the setting of AECOPD are summarized.[3] Although this review is not concise, nor is it particularly clinical, it is well done. The causes of limb dysfunction include disuse, hypoxia, hypercapnia, drugs (glucocorticoids being one of the major culprits), and tobacco use. Add all other factors to the consequences expected from disuse, which is practically synonymous with bed rest, and patients are left profoundly weak, with poor functional status.

This will translate to worsened dyspnea regardless of whether there is an associated lung function decline. Afferent feedback from skeletal muscle triggers a heightened ventilatory response (respiratory drive), and this feedback is augmented in the presence of limb muscle dysfunction.[7] This leads to inefficient ventilation, air trapping, and earlier respiratory mechanical constraints.[7,8] It is easy to see how this extends and even exacerbates the functional decline after AECOPD, and how chasing said decline with medications (particularly corticosteroids) could worsen the problem.

Per this concise clinical review,[3] attempts at a pharmacologic solution are being made. Various agents with anabolic properties have been studied; however, all have adverse effects that are likely to limit their use.

The reality is that the best thing for muscle wasting and deconditioning is a slow, targeted pulmonary rehabilitation program. The challenges inherent to getting patients to participate in physical activity programs have been well chronicled,[9] but there are no short cuts. As physicians, we have an obligation to educate and facilitate targeted exercise. The alternative is adding more medications that are unlikely to fix the problem and may even exacerbate it.

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