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
Intensive Care Unit, Royal Melbourne Hospital, Parkville, VIC, Australia.
Department of Anesthesia and Surgical Intensive Care, CHU de Bicetre, APHP, Université Paris Sud, 78 Rue du Général Leclerc, 94270, Le Kremlin Bicêtre, France.
Ann Intensive Care. 2019 Sep 5;9(1):99. doi: 10.1186/s13613-019-0574-z.
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.
在创伤性脑损伤(TBI)患者中,给予去氨加压素可能会导致血清钠迅速下降并升高颅内压(ICP)。
在一项国际多中心研究中,我们旨在报告TBI患者给予去氨加压素后血清钠和ICP的变化。
我们从欧洲、澳大利亚和英国的14个神经创伤重症监护病房获取了严重TBI患者(格拉斯哥昏迷量表评分≤8分)的数据,这些患者需要进行ICP监测。我们确定了接受任何去氨加压素治疗的患者,并记录每日剂量、每6小时的血清钠水平和每6小时的ICP。
我们研究了262例严重TBI患者。其中,39例患者(14.9%)接受了去氨加压素治疗。去氨加压素的中位治疗时长为1[1 - 3]天,各中心每日静脉给药剂量在0.125至10微克之间。血清钠每小时下降的中位速率较低(-0.1[-0.2至0.0]毫摩尔/升/小时),下降的中位时长为36小时。血钠纠正速率超过0.5毫摩尔/升/小时或1毫摩尔/升/小时的6小时时间段的比例较低,分别为8%和3%,且ICP保持稳定。在对IMPACT评分和损伤严重程度评分进行调整后,给予去氨加压素与60天死亡率增加独立相关[风险比为1.83(1.05 - 3.24)(p = 0.03)]。
在严重TBI中,给予去氨加压素(可能代表尿崩症情况)很常见,且与死亡率增加独立相关。各重症监护病房的去氨加压素剂量差异显著;然而,相关的血钠降低很少超过推荐速率,且ICP中位值保持不变。这些发现支持去氨加压素治疗是安全的这一观点。