Acetazolamide for metabolic alkalosis complicating respiratory failure with chronic obstructive pulmonary disease or obesity hypoventilation syndrome: a systematic review.


Journal

Thorax
ISSN: 1468-3296
Titre abrégé: Thorax
Pays: England
ID NLM: 0417353

Informations de publication

Date de publication:
10 2023
Historique:
received: 03 01 2023
accepted: 03 03 2023
medline: 18 9 2023
pubmed: 23 5 2023
entrez: 22 5 2023
Statut: ppublish

Résumé

Metabolic alkalosis may lead to respiratory inhibition and increased need for ventilatory support or prolongation of weaning from ventilation for patients with chronic respiratory disease. Acetazolamide can reduce alkalaemia and may reduce respiratory depression. We searched Medline, EMBASE and CENTRAL from inception to March 2022 for randomised controlled trials comparing acetazolamide to placebo in patients with chronic obstructive pulmonary disease, obesity hypoventilation syndrome or obstructive sleep apnoea, hospitalised with acute respiratory deterioration complicated by metabolic alkalosis. The primary outcome was mortality and we pooled data using random-effects meta-analysis. Risk of bias was assessed using the Cochrane RoB 2 (Risk of Bias 2) tool, heterogeneity was assessed using the I Four studies with 504 patients were included. 99% of included patients had chronic obstructive pulmonary disease. No trials recruited patients with obstructive sleep apnoea. 50% of trials recruited patients requiring mechanical ventilation. Risk of bias was overall low to some risk. There was no statistically significant difference with acetazolamide in mortality (relative risk 0.98 (95% CI 0.28 to 3.46); p=0.95; 490 participants; three studies; GRADE low certainty) or duration of ventilatory support (mean difference -0.8 days (95% CI -7.2 to 5.6); p=0.36; 427 participants; two studies; GRADE: low certainty). Acetazolamide may have little impact on respiratory failure with metabolic alkalosis in patients with chronic respiratory diseases. However, clinically significant benefits or harms are unable to be excluded, and larger trials are required. CRD42021278757.

Sections du résumé

BACKGROUND
Metabolic alkalosis may lead to respiratory inhibition and increased need for ventilatory support or prolongation of weaning from ventilation for patients with chronic respiratory disease. Acetazolamide can reduce alkalaemia and may reduce respiratory depression.
METHODS
We searched Medline, EMBASE and CENTRAL from inception to March 2022 for randomised controlled trials comparing acetazolamide to placebo in patients with chronic obstructive pulmonary disease, obesity hypoventilation syndrome or obstructive sleep apnoea, hospitalised with acute respiratory deterioration complicated by metabolic alkalosis. The primary outcome was mortality and we pooled data using random-effects meta-analysis. Risk of bias was assessed using the Cochrane RoB 2 (Risk of Bias 2) tool, heterogeneity was assessed using the I
RESULTS
Four studies with 504 patients were included. 99% of included patients had chronic obstructive pulmonary disease. No trials recruited patients with obstructive sleep apnoea. 50% of trials recruited patients requiring mechanical ventilation. Risk of bias was overall low to some risk. There was no statistically significant difference with acetazolamide in mortality (relative risk 0.98 (95% CI 0.28 to 3.46); p=0.95; 490 participants; three studies; GRADE low certainty) or duration of ventilatory support (mean difference -0.8 days (95% CI -7.2 to 5.6); p=0.36; 427 participants; two studies; GRADE: low certainty).
CONCLUSION
Acetazolamide may have little impact on respiratory failure with metabolic alkalosis in patients with chronic respiratory diseases. However, clinically significant benefits or harms are unable to be excluded, and larger trials are required.
PROSPERO REGISTRATION NUMBER
CRD42021278757.

Identifiants

pubmed: 37217290
pii: thorax-2023-219988
doi: 10.1136/thorax-2023-219988
doi:

Substances chimiques

Acetazolamide O3FX965V0I

Types de publication

Systematic Review Meta-Analysis Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1004-1010

Informations de copyright

© Author(s) (or their employer(s)) 2023. No commercial re-use. See rights and permissions. Published by BMJ.

Déclaration de conflit d'intérêts

Competing interests: None declared.

Auteurs

Timothy John Bemand (TJ)

Wagga Wagga Base Hospital, Wagga Wagga, New South Wales, Australia timothy.bemand@health.nsw.gov.au.
Rural Clinical School Wagga Wagga Campus, University of New South Wales, Wagga Wagga, New South Wales, Australia.
Sydney School of Public Health, The University of Sydney, Sydney, New South Wales, Australia.

Richard Chatoor (R)

Wagga Wagga Base Hospital, Wagga Wagga, New South Wales, Australia.
Rural Clinical School Wagga Wagga Campus, University of New South Wales, Wagga Wagga, New South Wales, Australia.
Malcolm Fisher Department of Intensive Care Medicine, Royal North Shore Hospital, St Leonards, New South Wales, Australia.

Patrizia Natale (P)

Sydney School of Public Health, The University of Sydney, Sydney, New South Wales, Australia.
Department of Precision and Regenerative Medicine and Ionian Area (DIMEPRE-J), University of Bari Aldo Moro, Bari, Italy.
Nephrology, Dialysis and Transplantation Unit, Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy.

Giovanni Strippoli (G)

Sydney School of Public Health, The University of Sydney, Sydney, New South Wales, Australia.
Department of Precision and Regenerative Medicine and Ionian Area (DIMEPRE-J), University of Bari Aldo Moro, Bari, Italy.

Anthony Delaney (A)

Malcolm Fisher Department of Intensive Care Medicine, Royal North Shore Hospital, St Leonards, New South Wales, Australia.
Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia.
Division of Critical Care, The George Institute for Global Health, Newtown, New South Wales, Australia.
Department of Epidemiology and Preventative Medicine, Monash University, ANZIC-RC, Melbourne, Victoria, Australia.

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