Hamrahian Amir H, Fleseriu Maria
Endocr Pract. 2017 Jun;23(6):716-725. doi: 10.4158/EP161720.RA. Epub 2017 Mar 23.
The definition of normal adrenal function in critically ill patients remains controversial, despite a large body of literature. We review the clinical presentation, diagnosis, and treatment of adrenal insufficiency in critically ill patients and discuss the authors' personal approach to patient management.
Extensive literature review, guidelines from professional societies, and personal experience.
A decrease in cortisol breakdown rather than an increase in cortisol production has been suggested as the main contributor to elevated cortisol levels in critically ill patients. The concept of relative adrenal insufficiency has multiple pathophysiologic flaws and is not supported by current evidence. Patients with septic shock who are pressor dependent or refractory to fluid resuscitation may receive a short course of hydrocortisone regardless of their serum cortisol levels or their response to a cosyntropin stimulation test (CST). Patients without septic shock who are suspected to have adrenal insufficiency should have their random cortisol levels measured. In patients with low and near-normal cortisol-binding proteins, a serum cortisol of <10 or 15 μg/dL, respectively, may trigger need for glucocorticoid treatment. Assays of free cortisol levels offer an advantage over total cortisol levels in patients with low binding proteins. Most critically ill patients have a normal random free cortisol level of >1.8 μg/dL, although further studies are needed to define a normal range in critically ill patients based on both severity and duration of illness. A CST may be used to further evaluate adrenal function in patients without septic shock who have borderline random serum or free cortisol levels.
Evaluation of adrenal function in critically ill patients is complex. Recent findings of decreased cortisol breakdown in critically ill patients as the main contributor to elevated cortisol levels calls for better-designed studies to explore the optimal evaluation and treatment of adrenal insufficiency in critically ill patients.
ACTH = adrenocorticotropic hormone; AI = adrenal insufficiency; CBG = corticosteroid-binding globulin; CORTICUS = Corticosteroid Therapy of Septic Shock; CRH = corticotropin-releasing hormone; CST = cosyntropin stimulation test; GC = glucocorticoid; GR = glucocorticoid receptor; HPA = hypothalamic-pituitary-adrenal; IL = interleukin; RAI = relative adrenal insufficiency.
尽管有大量文献，但危重症患者正常肾上腺功能的定义仍存在争议。我们回顾危重症患者肾上腺功能不全的临床表现、诊断和治疗，并讨论作者个人的患者管理方法。
广泛的文献综述、专业学会的指南以及个人经验。
有人提出，皮质醇分解减少而非皮质醇产生增加是危重症患者皮质醇水平升高的主要原因。相对肾上腺功能不全的概念存在多个病理生理缺陷，且未得到现有证据的支持。依赖血管加压药或对液体复苏无效的感染性休克患者，无论其血清皮质醇水平或对促肾上腺皮质激素刺激试验（CST）的反应如何，均可接受短期氢化可的松治疗。怀疑有肾上腺功能不全但无感染性休克的患者，应检测其随机皮质醇水平。对于皮质醇结合蛋白水平低及接近正常的患者，血清皮质醇分别<10或15μg/dL可能提示需要糖皮质激素治疗。在结合蛋白水平低的患者中，游离皮质醇水平检测比总皮质醇水平检测更具优势。大多数危重症患者随机游离皮质醇水平正常，>1.8μg/dL，不过还需要进一步研究以根据疾病的严重程度和持续时间确定危重症患者的正常范围。CST可用于进一步评估无感染性休克、随机血清或游离皮质醇水平处于临界值的患者的肾上腺功能。
危重症患者肾上腺功能的评估很复杂。最近关于危重症患者皮质醇分解减少是皮质醇水平升高主要原因的发现，要求开展设计更完善的研究，以探索危重症患者肾上腺功能不全的最佳评估和治疗方法。
ACTH = 促肾上腺皮质激素；AI = 肾上腺功能不全；CBG = 皮质类固醇结合球蛋白；CORTICUS = 感染性休克的皮质类固醇治疗；CRH = 促肾上腺皮质激素释放激素；CST = 促肾上腺皮质激素刺激试验；GC = 糖皮质激素；GR = 糖皮质激素受体；HPA = 下丘脑 - 垂体 - 肾上腺；IL = 白细胞介素；RAI = 相对肾上腺功能不全
