Asthma and COPD are important causes of morbidity and mortality worldwide. Asthma is characterized by fluctuating symptoms of wheeze, shortness of breath, chest tightness and/or cough and by variable expiratory airflow limitation secondary to airway hyperreactivity and bronchospasm . COPD presents with persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities . Also, asthma/COPD both have in common airflow limitation. During acute exacerbations such flow limitation results in hyperinflation, which seems to be related with sustained post-inspiratory activity of the inspiratory muscles . We hypothesized that hyperinflation and accessory muscle recruitment result in pleural vertical displacement and could explain the findings described. As airflow limitation is reversed, hyperinflation ameliorates and accessory muscles are no longer recruited, thus the pleural vertical displacement will decrease.
We could not find any previous description of such pleural movement in our bibliography research.
Dr. Lichtenstein described two signals detected in M-mode LUS in cases of severe acute dyspnea: the Ifrac and the Nogue-Armendariz phenomena. The Ifrac phenomenon is secondary to accessory respiratory muscle activation, creating a pattern of “muscular sliding” in addition to usual lung sliding. This muscular sliding shows a “seashore pattern” on M-Mode, identifiable above the pleural line, unlike lung sliding that produces a “seashore pattern” under the same line. The Nogue-Armendariz phenomenon represents the rare occurrence of perfect synchrony between such muscular and lung sliding, resulting in a permanent “sand pattern” on M-mode arising at the muscular line and paralleled with the “sand pattern” caused by the movement of the pleural layers . In our case, these phenomena are visible in inspiration during the first evaluation (line A of Fig. 1). Although such findings seem to be present in cases of severe acute dyspnea, they were not correlated with airflow limitation itself and might be difficult to detect in the short time evaluations of the emergency setting.
Some case reports also mentioned absence of B-mode pleural sliding, with loss of its M-mode correspondent “seashore sign” and appearance of “bar-code sign”, in cases of severe airflow impairment [10, 11]. This is also assumed to be a consequence of hyperinflation with pleural over-tension. However, such findings are not specific of those diseases, being more commonly associated with pneumothorax (which can itself present as a complication of severe asthma/COPD exacerbations), but also described in other conditions such as atelectasis, pleural adhesions, severe emphysema or severe fibrosis. Furthermore, a reduction/absence of pleural movement cannot be quantified and therefore would not be suitable to assess the degree of bronchospasm and its response to treatment.
Bronchospasm monitorization is difficult even with standard tests. Although COPD and asthma guidelines underline spirometry and/or peak expiratory respiratory flow (PERF) as pivotal tools for diseases diagnosis and monitorization, they also recognize that those tests show low sensitivity and variation according to age. Also, both techniques need patient collaboration and training to a correct measurement, and PERF monitoring did not prove to ameliorate asthma control in addition to symptom score [12, 16, 17], neither could it predict the need of hospital admissions .Those features imply that such complementary tests lack practical applicability in the acute setting; and the American College of Emergency Physicians has already released a statement emphasizing that evidence does not support PERF monitoring for all adult asthma patients .
Therefore, currently there is an absence of practical and easily performable tests to diagnose and monitor the airflow limitation, particularly in the emergency setting. The pleural displacement index could be a quick, simple method to indirectly monitor airflow impairment at bedside, independent of patient collaboration.