Following publication of the original article [1], we were notified that the collaborators’ names part of the “The TBI Collaborative” group has not been indexed in Pubmed. Below the collaborators names full list

Allen, G

Anstey, JR

Badenes, R

Baro, N

Bellomo, R

Citerio, G

Collaborative, TBI

Cooper, DJ

Duranteau, J

Ercole, A

Harrois, A

Helbok, R

Ichai, C

Kofler, M

Long, K

Lozano, A

Nelson, DW

Oddo, M

Prowle, JR

Quintard, H

Robba, C

Rodrigues, A

Saxby, E

Schneider, A

Sisson, A

Skrifvars, MB

Taccone, FS

Udy, AA

van Der Jagt, M

Vargiolu, A

Wolf, S

Annals of Intensive Care

Abstract
              
                Background
                In traumatic brain injury (TBI) patients desmopressin administration may induce rapid decreases in serum sodium and increase intracranial pressure (ICP).
              
              
                Aim
                In an international multi-centre study, we aimed to report changes in serum sodium and ICP after desmopressin administration in TBI patients.
              
              
                Methods
                We obtained data from 14 neurotrauma ICUs in Europe, Australia and UK for severe TBI patients (GCS ≤ 8) requiring ICP monitoring. We identified patients who received any desmopressin and recorded daily dose, 6-hourly serum sodium, and 6-hourly ICP.
              
              
                Results
                We studied 262 severe TBI patients. Of these, 39 patients (14.9%) received desmopressin. Median length of treatment with desmopressin was 1 [1–3] day and daily intravenous dose varied between centres from 0.125 to 10 mcg. The median hourly rate of decrease in serum sodium was low (− 0.1 [− 0.2 to 0.0] mmol/L/h) with a median period of decrease of 36 h. The proportion of 6-h periods in which the rate of natremia correction exceeded 0.5 mmol/L/h or 1 mmol/L/h was low, at 8% and 3%, respectively, and ICPs remained stable. After adjusting for IMPACT score and injury severity score, desmopressin administration was independently associated with increased 60-day mortality [HR of 1.83 (1.05–3.24) (p = 0.03)].
              
              
                Conclusions
                In severe TBI, desmopressin administration, potentially representing instances of diabetes insipidus is common and is independently associated with increased mortality. Desmopressin doses vary markedly among ICUs; however, the associated decrease in natremia rarely exceeds recommended rates and median ICP values remain unchanged. These findings support the notion that desmopressin therapy is safe

Harrois, A.

Anstey, J. R

Taccone, F. S

Udy, A. A

Citerio, G.

Duranteau, J.

Ichai, C.

Badenes, R.

Prowle, J. R

Ercole, A.

Oddo, M.

Schneider, A.

van der Jagt, M.

Wolf, S.

Helbok, R.

Nelson, D. W

Skrifvars, M. B.

Cooper, D. J

Bellomo, R.

Helsingin yliopiston digitaalinen arkisto

Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients : a multi-centre cohort study

Abstract: Background: In traumatic brain injury (TBI) patients desmopressin administration may induce rapid decreases in serum sodium and increase intracranial pressure (ICP). Aim: In an international multi-centre study, we aimed to report changes in serum sodium and ICP after desmopressin administration in TBI patients. Methods: We obtained data from 14 neurotrauma ICUs in Europe, Australia and UK for severe TBI patients (GCS ≤ 8) requiring ICP monitoring. We identified patients who received any desmopressin and recorded daily dose, 6-hourly serum sodium, and 6-hourly ICP. Results: We studied 262 severe TBI patients. Of these, 39 patients (14.9%) received desmopressin. Median length of treatment with desmopressin was 1 [1–3] day and daily intravenous dose varied between centres from 0.125 to 10 mcg. The median hourly rate of decrease in serum sodium was low (− 0.1 [− 0.2 to 0.0] mmol/L/h) with a median period of decrease of 36 h. The proportion of 6-h periods in which the rate of natremia correction exceeded 0.5 mmol/L/h or 1 mmol/L/h was low, at 8% and 3%, respectively, and ICPs remained stable. After adjusting for IMPACT score and injury severity score, desmopressin administration was independently associated with increased 60-day mortality [HR of 1.83 (1.05–3.24) (p = 0.03)]. Conclusions: In severe TBI, desmopressin administration, potentially representing instances of diabetes insipidus is common and is independently associated with increased mortality. Desmopressin doses vary markedly among ICUs; however, the associated decrease in natremia rarely exceeds recommended rates and median ICP values remain unchanged. These findings support the notion that desmopressin therapy is safe

Anstey, J. R.

Taccone, F. S.

Udy, A. A.

Prowle, J. R.

Nelson, D. W.

Cooper, D. J.

Apollo (Cambridge)

English

Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients: a multi-centre cohort study

Following publication of the original article [1], we were notified that the collaborators' names part of the "The TBI Collaborative" group has not been indexed in Pubmed. Below the collaborators names full list

van der Jagt, M

University of Melbourne Institutional Repository

Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients: a multi-centre cohort study (vol 9, 99, 2019)

van der Jagt, Mathieu

EUR Research Repository

Following publication of the original article [1], we were notified that the collaborators' names part of the "The TBI Collaborative" group has not been indexed in Pubmed. Below the collaborators names full list:
Te TBI collaborative group: Long K (Intensive Care
Unit, Royal Melbourne Hospital, Parkville, Victoria,
Australia), Rodrigues A (Department of Anesthesia
and Surgical Intensive Care, CHU de Bicetre, Le Kremlin Bicêtre, France), Lozano A (Department of Intensive
Care, Erasme Hospital, Université Libre de Bruxelles,
Brussels, Belgium), Saxby E (Intensive Care Unit, Te
Alfred Hospital, Melbourne, Victoria, Australia), Vargiolu A (School of Medicine and Surgery, University
Milano Bicocca-Neurointensive Care, San Gerardo Hospital, ASSTMonza, Monza, Italy), Quintard H (Université Côte d’Azur, Centre hospitalier Universitaire de Nice,
Service de Réanimation polyvalente, Hôpital Pasteur
2. Nice, France), Robba C (Department of Anesthesiology and Surgical-Trauma Intensive Care, Hospital Clinic
Universitari de Valencia, University of Valencia, Valencia, Spain), Sisson A (Adult Critical Care Unit, Te Royal
London Hospital, Barts Health NHS Trust, London, UK),
Allen G (Neurosciences and Trauma Critical Care Unit,
Cambridge University Hospitals NHS Foundation Trust,
Cambridge, UK), Baro N (Department of Neurosurgery,
Charité Universitätsmedizin Berlin), Kofer M (Neurological Intensive Care Unit, Department of Neurology,
Medical University of Innsbruck, Innsbruck, Austria)

TBI Collaborative

Queen Mary Research Online

Correction to: Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients: a multi-centre cohort study.

Following publication of the original article [1], we were notified that the collaborators’ names part of the “The TBI Collaborative” group has not been indexed in Pubmed. Below the collaborators names full list: The TBI collaborative group: Long K (Intensive Care Unit, Royal Melbourne Hospital, Parkville, Victoria, Australia), Rodrigues A (Department of Anesthesia and Surgical Intensive Care, CHU de Bicetre, Le Kremlin Bicêtre, France), Lozano A (Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium), Saxby E (Intensive Care Unit, The Alfred Hospital, Melbourne, Victoria, Australia), Vargiolu A (School of Medicine and Surgery, University Milano Bicocca-Neurointensive Care, San Gerardo Hospital, ASSTMonza, Monza, Italy), Quintard H (Université Côte d’Azur, Centre hospitalier Universitaire de Nice, Service de Réanimation polyvalente, Hôpital Pasteur 2. Nice, France), Robba C (Department of Anesthesiology and Surgical-Trauma Intensive Care, Hospital Clinic Universitari de Valencia, University of Valencia, Valencia, Spain), Sisson A (Adult Critical Care Unit, The Royal London Hospital, Barts Health NHS Trust, London, UK), Allen G (Neurosciences and Trauma Critical Care Unit, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK), Baro N (Department of Neurosurgery, Charité Universitätsmedizin Berlin), Kofler M (Neurological Intensive Care Unit, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria)

Anstey, J.R. (J. R.)

Taccone, F.S. (Fabio)

Udy, A.A. (A. A.)

Citerio, G. (Giuseppe)

Duranteau, J. (Jacques)

Ichai, C. (Carole)

Badenes, R. (R.)

Prowle, J.R. (J. R.)

Ercole, A. (Ari)

Oddo, M. (Mauro)

Schneider, A. (A.)

Jagt, M. (Mathieu) van der

Wolf, S. (Stefan)

Helbok, R. (Raimund)

Nelson, D. (David)

Skrifvars, M.B. (M. B.)

Cooper, D.J. (D. J.)

Bellomo, R. (R.)

Long, K. (K.)

Rodrigues, A. (A.)

Lozano, A. (A.)

Saxby, E. (E.)

Vargiolu, A. (Alessia)

Quintard, H. (H.)

Robba, C. (C.)

Sisson, A. (A.)

Allen, G. (G.)

Baro, N. (N.)

Kofler, M. (M.)

Erasmus University Digital Repository

Correction to: Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients: a multi-centre cohort study (Annals of Intensive Care, (2019), 9, 1, (99), 10.1186/s13613-019-0574-z)

Anstey, J R

Taccone, F S

Udy, A A

Prowle, J R

Nelson, D W

Skrifvars, M B

Cooper, D J

Harrois et al. Ann. Intensive Care           (2019) 9:136  https://doi.org/10.1186/s13613-019-0610-zCORRECTIONCorrection to: Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients: a multi-centre cohort studyA. Harrois1,2* , J. R. Anstey1, F. S. Taccone3, A. A. Udy4,16, G. Citerio5, J. Duranteau2, C. Ichai6, R. Badenes7, J. R. Prowle8, A. Ercole9, M. Oddo10, A. Schneider10, M. van der Jagt11, S. Wolf12, R. Helbok13, D. W. Nelson14, M. B. Skrifvars15, D. J. Cooper3,16 and R. Bellomo1,16,17,18 on behalf of The TBI Collaborative© The Author(s) 2019. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.Correction to:  Ann Intensive Care (2019) 9:99  https ://doi.org/10.1186/s1361 3-019-0574-zFollowing publication of the original article [1], we were notified that the collaborators’ names part of the “The TBI Collaborative” group has not been indexed in Pub-med. Below the collaborators names full list:The TBI collaborative group: Long K (Intensive Care Unit, Royal Melbourne Hospital, Parkville, Victoria, Australia), Rodrigues A (Department of Anesthesia and Surgical Intensive Care, CHU de Bicetre, Le Krem-lin Bicêtre, France), Lozano A (Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium), Saxby E (Intensive Care Unit, The Alfred Hospital, Melbourne, Victoria, Australia), Var-giolu A (School of Medicine and Surgery, University Milano Bicocca-Neurointensive Care, San Gerardo Hos-pital, ASSTMonza, Monza, Italy), Quintard H (Univer-sité Côte d’Azur, Centre hospitalier Universitaire de Nice, Service de Réanimation polyvalente, Hôpital Pasteur 2. Nice, France), Robba C (Department of Anesthesiol-ogy and Surgical-Trauma Intensive Care, Hospital Clinic Universitari de Valencia, University of Valencia, Valen-cia, Spain), Sisson A (Adult Critical Care Unit, The Royal London Hospital, Barts Health NHS Trust, London, UK), Allen G (Neurosciences and Trauma Critical Care Unit, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK), Baro N (Department of Neurosurgery, Charité Universitätsmedizin Berlin), Kofler M (Neuro-logical Intensive Care Unit, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria).Author details1 Intensive Care Unit, Royal Melbourne Hospital, Parkville, VIC, Australia. 2 Department of Anesthesia and Surgical Intensive Care, CHU de Bicetre, APHP, Université Paris Sud, 78 Rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France. 3 Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium. 4 Intensive Care Unit, The Alfred Hospital, Melbourne, VIC, Australia. 5 School of Medicine and Surgery, University Milano Bicocca-Neurointensive Care, San Gerardo Hospital, ASST-Monza, Monza, Italy. 6 Université Côte d’Azur, Centre hospitalier Universitaire de Nice, Service de Réanimation Polyvalente, Hôpital Pasteur 2, Nice, France. 7 Depart-ment of Anesthesiology and Surgical-Trauma Intensive Care, Hospital Clinic Universitari de Valencia, University of Valencia, Valencia, Spain. 8 Adult Critical Care Unit, The Royal London Hospital, Barts Health NHS Trust, London, UK. 9 Neurosciences and Trauma Critical Care Unit, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK. 10 Department of Medical-Surgical Intensive Care Medicine, Faculty of Biology and Medicine, Centre Hospitalier Universitaire, Vaudois (CHUV), University of Lausanne, Lausanne, Switzerland. 11 Department of Intensive Care, Erasmus MC-University Medical Center, Rotterdam, The Netherlands. 12 Department of Neurosurgery, Charité Uni-versitätsmedizin Berlin, Berlin, Germany. 13 Neurological Intensive Care Unit, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. 14 Section for Perioperative Medicine and Intensive Care, Department of Physi-ology and Pharmacology, Karolinska Institute, Stockholm, Sweden. 15 Division of Intensive Care, Department of Emergency Care and Services, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. 16 Australian and New Zealand Intensive Care Research Centre, School of Public Health and Preventative Medicine, Monash University, Melbourne, VIC, Australia. 17 Department of Intensive Care, Austin Health, Melbourne, VIC, Australia. 18 School of Medicine, University of Melbourne, Melbourne, Australia. Open AccessThe original article can be found online at https ://doi.org/10.1186/s1361 3-019-0574-z.*Correspondence:  harroisanatole@yahoo.fr2 Department of Anesthesia and Surgical Intensive Care, CHU de Bicetre, APHP, Université Paris Sud, 78 Rue du Général Leclerc, 94270 Le Kremlin Bicêtre, FranceFull list of author information is available at the end of the articlePage 2 of 2Harrois et al. Ann. Intensive Care           (2019) 9:136 Reference 1. Harrois A, Anstey JR, Taccone FS, Udy AA, Citerio G, Duranteau J, Ichai C, Badenes R, Prowle JR, Ercole A, Oddo M, Schneider A, van der Jagt M, Wolf S, Helbok R, Nelson DW, Skrifvars MB, Cooper DJ, Bellomo R. Ann Intensive Care. 2019;9:99. https ://doi.org/10.1186/s1361 3-019-0574-z.Publisher’s NoteSpringer Nature remains neutral with regard to jurisdictional claims in pub-lished maps and institutional affiliations.

Following publication of the original article [1], we were notified that the collaborators’ names part of the “The TBI Collaborative” group has not been indexed in Pubmed. Below the collaborators names full list: The TBI collaborative group: Long K (Intensive Care Unit, Royal Melbourne Hospital, Parkville, Victoria, Australia), Rodrigues A (Department of Anesthesia and Surgical Intensive Care, CHU de Bicetre, Le Kremlin Bicêtre, France), Lozano A (Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium), Saxby E (Intensive Care Unit, The Alfred Hospital, Melbourne, Victoria, Australia), Vargiolu A (School of Medicine and Surgery, University Milano Bicocca-Neurointensive Care, San Gerardo Hospital, ASSTMonza, Monza, Italy), Quintard H (Université Côte d’Azur, Centre hospitalier Universitaire de Nice, Service de Réanimation polyvalente, Hôpital Pasteur 2. Nice, France), Robba C (Department of Anesthesiology and Surgical-Trauma Intensive Care, Hospital Clinic Universitari de Valencia, University of Valencia, Valencia, Spain), Sisson A (Adult Critical Care Unit, The Royal London Hospital, Barts Health NHS Trust, London, UK), Allen G (Neurosciences and Trauma Critical Care Unit, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK), Baro N (Department of Neurosurgery, Charité Universitätsmedizin Berlin), Kofler M (Neurological Intensive Care Unit, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria).SCOPUS: er.jinfo:eu-repo/semantics/publishe

Harrois, Anatole

Anstey, James Richards

Taccone, Fabio

Udy, Andrew A

Citerio, Giuseppe

Duranteau, Jacques

Ichai, Carole

Badenes, Rafael

Prowle, John J.R.

Ercole, Ari

Oddo, Mauro

Schneider, Antoine

Wolf, Stefan

Helbok, Raimund

Nelson, David

Skrifvars, Markus M.B.

Cooper, James A.

Bellomo, Rinaldo

Long, K.

Rodrigues, Aurore

Lozano, Angels

Saxby, Edward Robert E.

Vargiolu, Alessia

Quintard, Hervé

Robba, Chiara

Sisson, A.

Allen, G.

Baro, N.

Kofler, Mario

DI-fusion

BACKGROUND: In traumatic brain injury (TBI) patients desmopressin administration may induce rapid decreases in serum sodium and increase intracranial pressure (ICP). AIM: In an international multi-centre study, we aimed to report changes in serum sodium and ICP after desmopressin administration in TBI patients. METHODS: We obtained data from 14 neurotrauma ICUs in Europe, Australia and UK for severe TBI patients (GCS ≤ 8) requiring ICP monitoring. We identified patients who received any desmopressin and recorded daily dose, 6-hourly serum sodium, and 6-hourly ICP. RESULTS: We studied 262 severe TBI patients. Of these, 39 patients (14.9%) received desmopressin. Median length of treatment with desmopressin was 1 [1-3] day and daily intravenous dose varied between centres from 0.125 to 10 mcg. The median hourly rate of decrease in serum sodium was low (- 0.1 [- 0.2 to 0.0] mmol/L/h) with a median period of decrease of 36 h. The proportion of 6-h periods in which the rate of natremia correction exceeded 0.5 mmol/L/h or 1 mmol/L/h was low, at 8% and 3%, respectively, and ICPs remained stable. After adjusting for IMPACT score and injury severity score, desmopressin administration was independently associated with increased 60-day mortality [HR of 1.83 (1.05-3.24) (p = 0.03)]. CONCLUSIONS: In severe TBI, desmopressin administration, potentially representing instances of diabetes insipidus is common and is independently associated with increased mortality. Desmopressin doses vary markedly among ICUs; however, the associated decrease in natremia rarely exceeds recommended rates and median ICP values remain unchanged. These findings support the notion that desmopressin therapy is safe

https://www.repository.cam.ac.uk/bitstream/handle/1810/314432/13613_2019_Article_610.pdf?sequence=3&isAllowed=y

Correction to: Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients : a multi-centre cohort study

Correction to: Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients : a multi-centre cohort study

Abstract

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Helsingin yliopiston digitaalinen arkisto

Apollo (Cambridge)

University of Melbourne Institutional Repository

EUR Research Repository

Queen Mary Research Online

Erasmus University Digital Repository

Apollo (Cambridge)

DI-fusion

Queen Mary Research Online

University of Melbourne Institutional Repository