Effect of Furosemide on Urinary Oxygenation in Patients with Septic Shock.


Journal

Blood purification
ISSN: 1421-9735
Titre abrégé: Blood Purif
Pays: Switzerland
ID NLM: 8402040

Informations de publication

Date de publication:
2019
Historique:
received: 25 02 2019
accepted: 16 06 2019
pubmed: 25 7 2019
medline: 16 5 2020
entrez: 24 7 2019
Statut: ppublish

Résumé

Renal medullary hypoxia precedes the development of acute kidney injury in experimental sepsis and can now be assessed by continuous measurement of urinary oxygen tension (PuO2). We aimed to test if PuO2 measurements in patients with septic shock would be similar to those shown in experimental sepsis and would detect changes induced by the administration of furosemide. Pilot prospective observational cohort study in a tertiary intensive care unit (ICU). Seven adult patients with septic shock admitted to ICU had PuO2 measurements recorded minutely. There were 29 episodes of intravenous furosemide (20 mg n = 19; 40 mg n = 10). The median pre-furosemide PuO2 was low at 21.2 mm Hg (interquartile range [IQR] 17.73-24.86) and increased to 26 mm Hg (IQR 20.27-29.95) at 20 min (p < 0.01), to 27.5 mm Hg (IQR 24.06-33.18) at 40 min (p < 0.01) and to 28.5 mm Hg (IQR 22.65-31.03) at 60 min (p < 0.01). The increase in PuO2 was greater in episodes with a diuretic response >2 mL/kg/h than during episodes without such a response (p < 0.01). PuO2 measurements in patients are reflective of the low values reported in experimental models of sepsis. PuO2 values increased following furosemide administration with a response independently associated with greater diuresis.

Sections du résumé

BACKGROUND
Renal medullary hypoxia precedes the development of acute kidney injury in experimental sepsis and can now be assessed by continuous measurement of urinary oxygen tension (PuO2).
OBJECTIVES
We aimed to test if PuO2 measurements in patients with septic shock would be similar to those shown in experimental sepsis and would detect changes induced by the administration of furosemide.
METHOD
Pilot prospective observational cohort study in a tertiary intensive care unit (ICU). Seven adult patients with septic shock admitted to ICU had PuO2 measurements recorded minutely. There were 29 episodes of intravenous furosemide (20 mg n = 19; 40 mg n = 10).
RESULTS
The median pre-furosemide PuO2 was low at 21.2 mm Hg (interquartile range [IQR] 17.73-24.86) and increased to 26 mm Hg (IQR 20.27-29.95) at 20 min (p < 0.01), to 27.5 mm Hg (IQR 24.06-33.18) at 40 min (p < 0.01) and to 28.5 mm Hg (IQR 22.65-31.03) at 60 min (p < 0.01). The increase in PuO2 was greater in episodes with a diuretic response >2 mL/kg/h than during episodes without such a response (p < 0.01).
CONCLUSIONS
PuO2 measurements in patients are reflective of the low values reported in experimental models of sepsis. PuO2 values increased following furosemide administration with a response independently associated with greater diuresis.

Identifiants

pubmed: 31336370
pii: 000501512
doi: 10.1159/000501512
doi:

Substances chimiques

Diuretics 0
Furosemide 7LXU5N7ZO5
Oxygen S88TT14065

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

336-345

Informations de copyright

© 2019 S. Karger AG, Basel.

Auteurs

Eduardo Atsushi Osawa (EA)

Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia, eduardoosawa@yahoo.com.

Salvatore Lucio Cutuli (SL)

Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia.
Department of Anesthesiology and Intensive Care, Fondazione Policlinico Universitario A. Gemelli, Universita Cattolica del Sacro Cuore, Rome, Italy.

Laurent Bitker (L)

Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia.

Emmanuel Canet (E)

Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia.

Luca Cioccari (L)

Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia.
Department of Intensive Care Medicine, University Hospital, University of Bern, Bern, Switzerland.
Australian and New Zealand Intensive Care Research Centre, School of Public Health and Preventive Medicine, Monash University, Prahran, Victoria, Australia.

Naoya Iguchi (N)

Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia.
Pre-clinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria, Australia.
Department of Anesthesiology and Intensive Care Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.

Yugeesh R Lankadeva (YR)

Pre-clinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria, Australia.

Glenn M Eastwood (GM)

Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia.

Roger G Evans (RG)

Department of Physiology, Cardiovascular Disease Program, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.

Clive N May (CN)

Pre-clinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria, Australia.

Rinaldo Bellomo (R)

Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia.
Centre for Integrated Critical Care, Department of Medicine and Radiology, School of Medicine, The University of Melbourne, Parkville, Victoria, Australia.
Australian and New Zealand Intensive Care Research Centre, School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia.

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