Diaphragm dysfunction, lung aeration loss and weaning-induced pulmonary oedema in difficult-to-wean patients.

Diaphragm Difficult weaning Lung ultrasound Pulmonary oedema

Journal

Annals of intensive care
ISSN: 2110-5820
Titre abrégé: Ann Intensive Care
Pays: Germany
ID NLM: 101562873

Informations de publication

Date de publication:
28 Jun 2021
Historique:
received: 06 03 2021
accepted: 09 06 2021
entrez: 28 6 2021
pubmed: 29 6 2021
medline: 29 6 2021
Statut: epublish

Résumé

Diaphragm dysfunction and weaning-induced pulmonary oedema are commonly involved during weaning failure, but their physiological interactions have been poorly reported. Our hypothesis was that diaphragm dysfunction is not particularly associated with weaning-induced pulmonary oedema. It was a single-centre and physiological study conducted in patients who had failed a first spontaneous breathing trial and who underwent a second trial. The diaphragm function was evaluated by measuring the tracheal pressure generated in response to a bilateral magnetic phrenic nerves stimulations. Weaning-induced pulmonary oedema was diagnosed in case of failure of the spontaneous breathing trial if patients exhibited signs of plasma concentration or echocardiographic diagnosis of pulmonary artery occlusion pressure elevation. Fifty-three patients were included and 31/53 (58%) failed the spontaneous breathing trial, including 24/31 (77%) patients with weaning-induced pulmonary oedema. Diaphragm dysfunction was present in 33/53 (62%) patients. Diaphragm dysfunction or weaning-induced pulmonary oedema were present in 26/31 (84%) of the patients who failed the spontaneous breathing trial. Weaning-induced pulmonary oedema occurred in 20/33 (61%) patients with a diaphragm dysfunction and in 4/20 (20%) patients without (p = 0.005). Weaning-induced pulmonary oedema was three times more frequent in case of diaphragm dysfunction. Even in case of diaphragm dysfunction, physicians might be encouraged to investigate the presence of weaning-induced pulmonary oedema during weaning failure.

Sections du résumé

BACKGROUND BACKGROUND
Diaphragm dysfunction and weaning-induced pulmonary oedema are commonly involved during weaning failure, but their physiological interactions have been poorly reported. Our hypothesis was that diaphragm dysfunction is not particularly associated with weaning-induced pulmonary oedema.
METHODS METHODS
It was a single-centre and physiological study conducted in patients who had failed a first spontaneous breathing trial and who underwent a second trial. The diaphragm function was evaluated by measuring the tracheal pressure generated in response to a bilateral magnetic phrenic nerves stimulations. Weaning-induced pulmonary oedema was diagnosed in case of failure of the spontaneous breathing trial if patients exhibited signs of plasma concentration or echocardiographic diagnosis of pulmonary artery occlusion pressure elevation.
RESULTS RESULTS
Fifty-three patients were included and 31/53 (58%) failed the spontaneous breathing trial, including 24/31 (77%) patients with weaning-induced pulmonary oedema. Diaphragm dysfunction was present in 33/53 (62%) patients. Diaphragm dysfunction or weaning-induced pulmonary oedema were present in 26/31 (84%) of the patients who failed the spontaneous breathing trial. Weaning-induced pulmonary oedema occurred in 20/33 (61%) patients with a diaphragm dysfunction and in 4/20 (20%) patients without (p = 0.005).
CONCLUSION CONCLUSIONS
Weaning-induced pulmonary oedema was three times more frequent in case of diaphragm dysfunction. Even in case of diaphragm dysfunction, physicians might be encouraged to investigate the presence of weaning-induced pulmonary oedema during weaning failure.

Identifiants

pubmed: 34181105
doi: 10.1186/s13613-021-00886-6
pii: 10.1186/s13613-021-00886-6
pmc: PMC8237539
doi:

Types de publication

Journal Article

Langues

eng

Pagination

99

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Auteurs

Martin Dres (M)

Service de Pneumologie, Médecine intensive - Réanimation (Département "R3S"), AP-HP. Sorbonne Université, Hôpital Pitié-Salpêtrière, 75013, Paris, France. martin.dres@aphp.fr.
Sorbonne Université, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France. martin.dres@aphp.fr.

Emmanuel Rozenberg (E)

Service de Pneumologie, Médecine intensive - Réanimation (Département "R3S"), AP-HP. Sorbonne Université, Hôpital Pitié-Salpêtrière, 75013, Paris, France.

Elise Morawiec (E)

Service de Pneumologie, Médecine intensive - Réanimation (Département "R3S"), AP-HP. Sorbonne Université, Hôpital Pitié-Salpêtrière, 75013, Paris, France.

Julien Mayaux (J)

Service de Pneumologie, Médecine intensive - Réanimation (Département "R3S"), AP-HP. Sorbonne Université, Hôpital Pitié-Salpêtrière, 75013, Paris, France.

Julie Delemazure (J)

Service de Pneumologie, Médecine intensive - Réanimation (Département "R3S"), AP-HP. Sorbonne Université, Hôpital Pitié-Salpêtrière, 75013, Paris, France.

Thomas Similowski (T)

Service de Pneumologie, Médecine intensive - Réanimation (Département "R3S"), AP-HP. Sorbonne Université, Hôpital Pitié-Salpêtrière, 75013, Paris, France.
Sorbonne Université, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France.

Alexandre Demoule (A)

Service de Pneumologie, Médecine intensive - Réanimation (Département "R3S"), AP-HP. Sorbonne Université, Hôpital Pitié-Salpêtrière, 75013, Paris, France.
Sorbonne Université, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France.

Classifications MeSH