Effect of beta-blocker therapy on early mortality after emergency colonic cancer surgery.


Journal

The British journal of surgery
ISSN: 1365-2168
Titre abrégé: Br J Surg
Pays: England
ID NLM: 0372553

Informations de publication

Date de publication:
03 2019
Historique:
received: 09 05 2018
revised: 18 06 2018
accepted: 28 07 2018
pubmed: 28 9 2018
medline: 7 9 2019
entrez: 28 9 2018
Statut: ppublish

Résumé

Emergency colorectal cancer surgery is associated with significant mortality. Induced adrenergic hyperactivity is thought to be an important contributor. Downregulating the effects of circulating catecholamines may reduce the risk of adverse outcomes. This study assessed whether regular preoperative beta-blockade reduced mortality after emergency colonic cancer surgery. This cohort study used the prospectively collected Swedish Colorectal Cancer Registry to recruit all adult patients requiring emergency colonic cancer surgery between 2011 and 2016. Patients were subdivided into those receiving regular beta-blocker therapy before surgery and those who were not (control). Demographics and clinical outcomes were compared. Risk factors for 30-day mortality were evaluated using Poisson regression analysis. A total of 3187 patients were included, of whom 685 (21·5 per cent) used regular beta-blocker therapy before surgery. The overall 30-day mortality rate was significantly reduced in the beta-blocker group compared with controls: 3·1 (95 per cent c.i. 1·9 to 4·7) versus 8·6 (7·6 to 9·8) per cent respectively (P < 0·001). Beta-blocker therapy was the only modifiable protective factor identified in multivariable analysis of 30-day all-cause mortality (incidence rate ratio 0·31, 95 per cent c.i. 0·20 to 0·47; P < 0·001) and was associated with a significant reduction in death of cardiovascular, respiratory, sepsis and multiple organ failure origin. Preoperative beta-blocker therapy may be associated with a reduction in 30-day mortality following emergency colonic cancer surgery.

Sections du résumé

BACKGROUND
Emergency colorectal cancer surgery is associated with significant mortality. Induced adrenergic hyperactivity is thought to be an important contributor. Downregulating the effects of circulating catecholamines may reduce the risk of adverse outcomes. This study assessed whether regular preoperative beta-blockade reduced mortality after emergency colonic cancer surgery.
METHODS
This cohort study used the prospectively collected Swedish Colorectal Cancer Registry to recruit all adult patients requiring emergency colonic cancer surgery between 2011 and 2016. Patients were subdivided into those receiving regular beta-blocker therapy before surgery and those who were not (control). Demographics and clinical outcomes were compared. Risk factors for 30-day mortality were evaluated using Poisson regression analysis.
RESULTS
A total of 3187 patients were included, of whom 685 (21·5 per cent) used regular beta-blocker therapy before surgery. The overall 30-day mortality rate was significantly reduced in the beta-blocker group compared with controls: 3·1 (95 per cent c.i. 1·9 to 4·7) versus 8·6 (7·6 to 9·8) per cent respectively (P < 0·001). Beta-blocker therapy was the only modifiable protective factor identified in multivariable analysis of 30-day all-cause mortality (incidence rate ratio 0·31, 95 per cent c.i. 0·20 to 0·47; P < 0·001) and was associated with a significant reduction in death of cardiovascular, respiratory, sepsis and multiple organ failure origin.
CONCLUSION
Preoperative beta-blocker therapy may be associated with a reduction in 30-day mortality following emergency colonic cancer surgery.

Identifiants

pubmed: 30259967
doi: 10.1002/bjs.10988
doi:

Substances chimiques

Adrenergic beta-Antagonists 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

477-483

Informations de copyright

© 2018 BJS Society Ltd Published by John Wiley & Sons Ltd.

Auteurs

R Ahl (R)

Department of Surgery, Karolinska University Hospital, Stockholm, Sweden.
School of Medical Sciences, Orebro University, Orebro, Sweden.

P Matthiessen (P)

School of Medical Sciences, Orebro University, Orebro, Sweden.
Department of Surgery, Orebro University Hospital, Orebro, Sweden.

X Fang (X)

Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Y Cao (Y)

Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Clinical Epidemiology and Biostatistics, School of Medical Sciences, Orebro University, Orebro, Sweden.

G Sjolin (G)

School of Medical Sciences, Orebro University, Orebro, Sweden.
Department of Surgery, Orebro University Hospital, Orebro, Sweden.

R Lindgren (R)

Department of Surgery, Orebro University Hospital, Orebro, Sweden.

O Ljungqvist (O)

Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
School of Medical Sciences, Orebro University, Orebro, Sweden.

S Mohseni (S)

School of Medical Sciences, Orebro University, Orebro, Sweden.
Department of Surgery, Orebro University Hospital, Orebro, Sweden.

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