Diaphragm impairment in patients admitted for severe COVID-19

Abstract

Among patients affected by the virus COVID-19, physicians have observed ventilation disorders. It is relevant to assess neurological involvement, including the role of diaphragmatic function. Its possible impairment could be related to the systemic inflammatory response and disease progression that both typify COVID-19 infection. We distinguished two groups (severe group (SG) and mild group (MG)) according to the severity of respiratory symptomatology. We performed neurophysiological and sonography studies to evaluate the diaphragmatic function. Regarding the sonography variables, we identified statistically significant differences in the right mean diaphragmatic thickness along with the expiration, showing 1.56 mm (SEM: 0.11) in the SG vs 1.92 mm (SEM: 0.19) in the MG (p = 0.042). The contractibility of both hemidiaphragms was 15% lower in the severe group, though this difference is not statistically significant. In our examination of the neurophysiological variables, in the amplitude responses, we observed a greater difference between responses from both phrenic nerves as follows: the raw differences in amplitude were 0.40 μV (SEM: 0.14) in the SG vs 0.35 μV (SEM: 0.19) in the MG and the percentage difference was 25.92% (SEM: 7.22) in the SG vs 16.28% (SEM: 4.38%) in the MG. Although diaphragmatic dysfunction is difficult to detect, our combined functional and morphological approach with phrenic electroneurograms and chest ultrasounds could improve diagnostic sensitivity. We suggest that diaphragmatic dysfunction could play a relevant role in respiratory disturbance in hospitalised patients with severe COVID-19.

Prognostic Value of Diaphragm Diameter, Muscle Volume, and Bone Mineral Density in Critically Ill COVID-19 Patients

“…39 Parlak et al 21 found the cut-off value of diaphragm thickness as 3.67 mm for ICU admission and 3.47 mm for mortality. Many studies conducted with US also indicated that DD was lower in the severe patient group, 40 while the diaphragm was thinner in patients that developed complications, 9 and mechanical ventilation and mortality could be predicted by a diaphragm examination performed within 12 h of hospitalization. 41 Our results are in agreement with the literature data.…”

A Bilateral Diaphragmatic Paralysis Post-COVID-19 Infection: A Case Report and a Review of the Literature

“…According to observations, body tissues infected with SARS-CoV-2 have increased angiotensin-converting enzyme 2 (ACE-2) expression; hence, the ACE-2 receptors may play an essential role in promoting viral particle invasion into neurons and other body structures, such as the diaphragm muscle, causing breathing impairment [ 10 , 11 ]. Notably, researchers reported that epimysial and perimysial fibrosis was more than twofold more significant in the diaphragm muscles of COVID-19-infected ICU patients compared to control ICU patients in a study on the diaphragm musculature in COVID-19-infected ICU patients [ 12 ].…”

Cardiopulmonary Exercise Testing in Children and Young Adolescents after a Multisystem Inflammatory Syndrome: Physical Deconditioning or Residual Pathology?

“…This could be corroborated by the observed reduced VO 2 p values in many of them, and by the fact that this parameter can get better with physical training [ 39 , 40 , 41 ]. A possible alternative might lie in an altered central control of ventilation [ 42 , 43 , 44 , 45 ] or in an underlying vascular dysfunction, described in post-MIS-C children [ 23 ].…”