Dimopoulou Ioanna, Tsagarakis Stylianos, Anthi Anastasia, Milou Ema, Ilias Ioannis, Stavrakaki Krystallia, Charalambidis Charalambos, Tzanela Marinella, Orfanos Stylianos, Mandragos Konstantinos, Thalassinos Nikolaos, Roussos Charis
Departments of Critical Care Medicine, Evangelismos Hospital, Athens, Greece.
Crit Care Med. 2003 Apr;31(4):1113-7. doi: 10.1097/01.CCM.0000059644.54819.67.
To investigate the adrenocortical function in brain-dead patients, potential organ donors.
Prospective study.
Intensive care units in two teaching hospitals.
A total of 37 patients (28 men, nine women) with severe brain injury, having a mean age of 42 +/- 18 yrs, were included in the study. Group A consisted of 20 brain-injured patients who did not deteriorate to brain death. Group B included 17 brain-injured patients who were brain dead; of these, ten patients developed brain death during ICU stay and seven patients were admitted to the ICU after clinical brain death.
In all patients (group A and group B), a morning blood sample was obtained at admission to the ICU to determine baseline plasma cortisol. Subsequently, 1 microg of corticotropin (adrenocorticotropic hormone, Synacthen) was administered intravenously, and a blood sample was taken 30 mins after the injection. In group B patients who became brain dead while being treated in the ICU (n = 10), the same procedure was repeated the morning after the confirmation of brain death. Patients having a cortisol level of at least 18 microg/dL after the administration of adrenocorticotropic hormone were defined as responders.
After the occurrence of brain death, group B patients had significantly lower values for baseline (8.5 +/- 6.2 vs. 17.0 +/- 6.6 microg/dL, p <.001) and stimulated (16.9 +/- 6.3 vs. 23.9 +/- 5.7 microg/dL, p =.001) plasma cortisol compared with group A patients. Thirteen group B patients (76%) and two group A patients (10%) were nonresponders to adrenocorticotropic hormone (p <.001). In group B patients, baseline and stimulated cortisol concentrations were significantly related (r =.71, p =.001), whereas there was no correlation between baseline cortisol and the increment in cortisol (r = -.37, p =.15). Mean hormonal data of the ten brain-dead patients studied at admission in the ICU and after the occurrence of brain death were the following: baseline plasma cortisol (23.5 +/- 11.4 vs. 6.8 +/- 4.2 microg/dL, p =.003) and stimulated serum cortisol (28.8 +/- 9.9 vs. 16.3 +/- 4.3 microg/dL, p =.008).
Adrenal cortisol secretion after dynamic stimulation is deficient in a substantial proportion of brain-dead potential organ donors.
研究脑死亡患者（潜在器官捐献者）的肾上腺皮质功能。
前瞻性研究。
两家教学医院的重症监护病房。
共37例严重脑损伤患者（28例男性，9例女性）纳入研究，平均年龄42±18岁。A组由20例未恶化至脑死亡的脑损伤患者组成。B组包括17例脑死亡的脑损伤患者；其中，10例患者在重症监护病房住院期间发生脑死亡，7例患者在临床脑死亡后入住重症监护病房。
在所有患者（A组和B组）中，入住重症监护病房时采集晨起血样以测定基础血浆皮质醇。随后，静脉注射1微克促肾上腺皮质激素（促肾上腺皮质激素，辛纳科），注射后30分钟采集血样。对于在重症监护病房治疗期间发生脑死亡的B组患者（n = 10），在脑死亡确认后的早晨重复相同步骤。促肾上腺皮质激素给药后皮质醇水平至少为18微克/分升的患者被定义为反应者。
脑死亡发生后，B组患者的基础血浆皮质醇（8.5±6.2 vs. 17.0±6.6微克/分升，p <.001）和刺激后血浆皮质醇（16.9±6.3 vs. 23.9±5.7微克/分升，p =.001）值显著低于A组患者。13例B组患者（76%）和2例A组患者（10%）对促肾上腺皮质激素无反应（p <.001）。在B组患者中，基础皮质醇和刺激后皮质醇浓度显著相关（r =.71，p =.001），而基础皮质醇与皮质醇增加值之间无相关性（r = -.37，p =.15）。在重症监护病房入院时及脑死亡发生后研究的10例脑死亡患者的平均激素数据如下：基础血浆皮质醇（23.5±11.4 vs. 6.8±4.2微克/分升，p =.003）和刺激后血清皮质醇（28.8±9.9 vs. 16.3±4.3微克/分升，p =.008）。
相当一部分脑死亡潜在器官捐献者在动态刺激后肾上腺皮质醇分泌不足。
Zotero 插件