Evidence map›Paper›PMID 30776686›Full record

ArticleThrombosis research2019

Fluid resuscitation with 0.9% saline alters haemostasis in an ovine model of endotoxemic shock.

Margaret R Passmore, Nchafatso G Obonyo, Liam Byrne, Ai-Ching Boon, Sara D Diab, Kimble R Dunster, Yoke L Fung, Michelle M Spanevello, Mohd H Fauzi, Sanne E Pedersen and 6 more

Open access · greenAbstract read
In one paragraph

Article in Thrombosis research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 9 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 9 institutions in 5 countries.

Margaret R PassmoreCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia; University of Queensland, Brisbane, Australia. Electronic address: M.Passmore@uq.edu.au.
Nchafatso G ObonyoCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia; KEMRI-Wellcome Trust Research Programme, Kenya. Electronic address: gnchafatso@gmail.com.
Liam ByrneCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia; Intensive Care Unit, The Canberra Hospital, Canberra, Australia. Electronic address: liambyrne.syd@gmail.com.
Ai-Ching BoonCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia; University of Queensland, Brisbane, Australia. Electronic address: c.boon0207@gmail.com.
Sara D DiabCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia. Electronic address: sara_diab5@hotmail.com.
Kimble R DunsterCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia; Queensland University of Technology, Brisbane, Australia. Electronic address: Kimble.Dunster@health.qld.gov.au.
Yoke L FungCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia; School of Health and Sport Sciences, University of the Sunshine Coast, Sippy Downs, Australia. Electronic address: ylfung@usc.edu.au.
Michelle M SpanevelloUniversity of Queensland, Brisbane, Australia; Cancer Care Services, Royal Brisbane and Women's Hospital, Brisbane, Australia. Electronic address: mmspanevello@gmail.com.
Mohd H FauziSchool of Medical Sciences, Universiti Sains Malaysia Health Campus, Kelantan, Malaysia. Electronic address: hashairi@usm.my.
Sanne E PedersenCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia. Electronic address: sanne.pedersen.work@gmail.com.
Gabriela SimonovaCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia; University of Queensland, Brisbane, Australia; Research and Development, Australian Red Cross Blood Service, Brisbane, Australia. Electronic address: GSimonova@redcrossblood.org.au.
Chris M AnsteyCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia; Sunshine Coast University Hospital Intensive Care, Birtinya, Australia. Electronic address: Chris.Anstey@health.qld.gov.au.
Kiran ShekarCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia. Electronic address: kiran.shekar@health.qld.gov.au.
John-Paul TungCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia; Research and Development, Australian Red Cross Blood Service, Brisbane, Australia. Electronic address: JTung@redcrossblood.org.au.
Kathryn MaitlandKEMRI-Wellcome Trust Research Programme, Kenya; Wellcome Trust Centre for Clinical Tropical Medicine and Department of Paediatrics, Faculty of Medicine, Imperial College, London, UK. Electronic address: kathryn.maitland@gmail.com.
John F FraserCritical Care Research Group, Prince Charles Hospital, Brisbane, Australia; University of Queensland, Brisbane, Australia. Electronic address: j.fraser@uq.edu.au.
The University of Queensland · AUPrince Charles Hospital · AUKenya Medical Research Institute · KEAustralian Red Cross Lifeblood · AUCanberra Hospital · AUQueensland University of Technology · AUSunshine Coast University Hospital · AUUniversiti Sains Malaysia · MYUniversity of the Sunshine Coast · AU

Funding

Medical Research Council G0601027Wellcome Trust 203077
6 · The paper itself

Abstract

introductionFluid resuscitation is a cornerstone of severe sepsis management, however there are many uncertainties surrounding the type and volume of fluid that is administered. The entire spectrum of coagulopathies can be seen in sepsis, from asymptomatic aberrations to fulminant disseminated intravascular coagulation (DIC). The aim of this study was to determine if fluid resuscitation with saline contributes to the haemostatic derangements in an ovine model of endotoxemic shock. MATERIALS AND

methodsTwenty-one adult female sheep were randomly divided into no endotoxemia (n = 5) or endotoxemia groups (n = 16) with an escalating dose of lipopolysaccharide (LPS) up to 4 μg/kg/h administered to achieve a mean arterial pressure below 60 mmHg. Endotoxemia sheep received either no bolus fluid resuscitation (n = 8) or a 0.9% saline bolus (40 mL/kg over 60 min) (n = 8). No endotoxemia, saline only animals (n = 5) underwent fluid resuscitation with a 0.9% bolus of saline as detailed above. Hemodynamic support with vasopressors was initiated if needed, to maintain a mean arterial pressure (MAP) of 60-65 mm Hg in all the groups.

resultsRotational thromboelastometry (ROTEM®) and conventional coagulation biomarker tests demonstrated sepsis induced derangements to secondary haemostasis. This effect was exacerbated by saline fluid resuscitation, with low pH (p = 0.036), delayed clot initiation and formation together with deficiencies in naturally occurring anti-coagulants antithrombin (p = 0.027) and Protein C (p = 0.001).

conclusionsEndotoxemia impairs secondary haemostasis and induces changes in the intrinsic, extrinsic and anti-coagulant pathways. These changes to haemostasis are exacerbated following resuscitation with 0.9% saline, a commonly used crystalloid in clinical settings.

Indexed as

HemostasisAnimalsBlood PressureDisease Models, AnimalEndotoxemiaFemaleFluid TherapyResuscitationSaline SolutionSheepSaline SolutionCoagulationCoagulation factorsFibrinogenSepsisThromboelastometry

Identifiers

PMID30776686
PMCPMC7613520
OpenAlexW2911482087

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.