Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients: a multi-centre cohort study.
Desmopressin
Diabetes insipidus
Natremia
Sodium
Traumatic brain injury
Journal
Annals of intensive care
ISSN: 2110-5820
Titre abrégé: Ann Intensive Care
Pays: Germany
ID NLM: 101562873
Informations de publication
Date de publication:
05 Sep 2019
05 Sep 2019
Historique:
received:
27
01
2019
accepted:
26
08
2019
entrez:
6
9
2019
pubmed:
6
9
2019
medline:
6
9
2019
Statut:
epublish
Résumé
In traumatic brain injury (TBI) patients desmopressin administration may induce rapid decreases in serum sodium and increase intracranial pressure (ICP). In an international multi-centre study, we aimed to report changes in serum sodium and ICP after desmopressin administration in TBI patients. 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. 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)]. 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.
Sections du résumé
BACKGROUND
BACKGROUND
In traumatic brain injury (TBI) patients desmopressin administration may induce rapid decreases in serum sodium and increase intracranial pressure (ICP).
AIM
OBJECTIVE
In an international multi-centre study, we aimed to report changes in serum sodium and ICP after desmopressin administration in TBI patients.
METHODS
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
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
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.
Identifiants
pubmed: 31486921
doi: 10.1186/s13613-019-0574-z
pii: 10.1186/s13613-019-0574-z
pmc: PMC6728106
doi:
Types de publication
Journal Article
Langues
eng
Pagination
99Commentaires et corrections
Type : ErratumIn
Références
Clin Endocrinol (Oxf). 2004 May;60(5):584-91
pubmed: 15104561
Am Surg. 2004 Jun;70(6):500-3
pubmed: 15212402
J Clin Endocrinol Metab. 2004 Dec;89(12):5987-92
pubmed: 15579748
J Cereb Blood Flow Metab. 2005 Aug;25(8):1012-9
pubmed: 15744246
Eur J Endocrinol. 2005 Mar;152(3):371-7
pubmed: 15757853
PLoS Med. 2008 Aug 5;5(8):e165; discussion e165
pubmed: 18684008
J Am Coll Surg. 2008 Oct;207(4):477-84
pubmed: 18926448
J Neurotrauma. 2008 Dec;25(12):1459-65
pubmed: 19118456
Crit Care Med. 2009 Apr;37(4):1433-41
pubmed: 19242317
Crit Care. 2009;13(4):R110
pubmed: 19583864
Acta Neurochir Suppl. 2010;106:221-4
pubmed: 19812953
J Neurosurg. 2010 Sep;113(3):581-4
pubmed: 19929195
Neurol Res. 2010 Dec;32(10):1021-6
pubmed: 20810023
Pediatr Neurosurg. 2010;46(4):318-23
pubmed: 21196800
Endocrine. 2011 Aug;40(1):67-74
pubmed: 21626284
Crit Care. 2011;15(5):R260
pubmed: 22035596
Pediatr Crit Care Med. 2013 Feb;14(2):203-9
pubmed: 23314181
J Trauma Acute Care Surg. 2013 Feb;74(2):639-46
pubmed: 23354263
J Trauma Acute Care Surg. 2013 Aug;75(2):195-201
pubmed: 23823614
BMJ. 1989 Jan 7;298(6665):2-3
pubmed: 2492841
J Clin Med. 2015 Jul 13;4(7):1448-62
pubmed: 26239685
J Neurotrauma. 2016 Apr 1;33(7):615-24
pubmed: 26472056
BMJ Open. 2017 Aug 18;7(8):e016248
pubmed: 28821524
Lancet Neurol. 2017 Dec;16(12):987-1048
pubmed: 29122524
Crit Care. 2017 Dec 28;21(1):328
pubmed: 29282104
N Engl J Med. 2018 Aug 02;379(5):428-439
pubmed: 30067922
Neurosurgery. 1982 Sep;11(3):402-7
pubmed: 7133357