Achinger Steven G, Ayus Juan Carlos
1Department of Nephrology, Watson Clinic LLP, Lakeland, FL. 2Renal Consultants of Houston, Department of Research, Houston, TX. 3Department of Nephrology, Hospital Italiano, Buenos Aires, Argentina. 4Department of Nephrology, Hospital Austral, Austral University, Buenos Aires, Argentina. 5Department of Nephrology, University of California, Irvine, CA.
Crit Care Med. 2017 Oct;45(10):1762-1771. doi: 10.1097/CCM.0000000000002595.
Hyponatremic encephalopathy, symptomatic cerebral edema due to a low osmolar state, is a medical emergency and often encountered in the ICU setting. This article provides a critical appraisal and review of the literature on identification of high-risk patients and the treatment of this life-threatening disorder.
DATA SOURCES, STUDY SELECTION, AND DATA EXTRACTION: Online search of the PubMed database and manual review of articles involving risk factors for hyponatremic encephalopathy and treatment of hyponatremic encephalopathy in critical illness.
Hyponatremic encephalopathy is a frequently encountered problem in the ICU. Prompt recognition of hyponatremic encephalopathy and early treatment with hypertonic saline are critical for successful outcomes. Manifestations are varied, depending on the extent of CNS's adaptation to the hypoosmolar state. The absolute change in serum sodium alone is a poor predictor of clinical symptoms. However, certain patient specific risks factors are predictive of a poor outcome and are important to identify. Gender (premenopausal and postmenopausal females), age (prepubertal children), and the presence of hypoxia are the three main clinical risk factors and are more predictive of poor outcomes than the rate of development of hyponatremia or the absolute decrease in the serum sodium.
In patients with hyponatremic encephalopathy exhibiting neurologic manifestations, a bolus of 100 mL of 3% saline, given over 10 minutes, should be promptly administered. The goal of this initial bolus is to quickly treat cerebral edema. If signs persist, the bolus should be repeated in order to achieve clinical remission. However, the total change in serum sodium should not exceed 5 mEq/L in the initial 1-2 hours and 15-20 mEq/L in the first 48 hours of treatment. It has recently been demonstrated in a prospective fashion that 500 mL of 3% saline at an infusion rate of 100 mL per hour can be given safely. It is critical to recognize the early signs of cerebral edema (nausea, vomiting, and headache) and intervene with IV 3% sodium chloride as this is the time to intervene rather than waiting until more severe symptoms develop. Cerebral demyelination is a rare complication of overly rapid correction of hyponatremia. The principal risk factors for cerebral demyelination are correction of the serum sodium more than 25 mEq/L in the first 48 hours of therapy, correction past the point of 140 mEq/L, chronic liver disease, and hypoxic/anoxic episode.
低钠血症性脑病是一种因低渗状态导致的症状性脑水肿，属于医疗急症，在重症监护病房（ICU）环境中经常遇到。本文对关于识别高危患者以及治疗这种危及生命疾病的文献进行了批判性评价和综述。
数据来源、研究选择和数据提取：对PubMed数据库进行在线搜索，并人工查阅涉及低钠血症性脑病危险因素及危重病中低钠血症性脑病治疗的文章。
低钠血症性脑病是ICU中经常遇到的问题。迅速识别低钠血症性脑病并尽早用高渗盐水治疗对于取得成功的治疗结果至关重要。其表现因中枢神经系统对低渗状态的适应程度而异。仅血清钠的绝对变化并不能很好地预测临床症状。然而，某些患者特定的危险因素可预测不良预后，识别这些因素很重要。性别（绝经前和绝经后女性）、年龄（青春期前儿童）以及缺氧的存在是三个主要的临床危险因素，比低钠血症的发展速度或血清钠的绝对降低更能预测不良预后。
对于出现神经学表现的低钠血症性脑病患者，应迅速给予100毫升3%盐水，在10分钟内静脉推注。这一初始推注的目的是快速治疗脑水肿。如果症状持续，应重复推注以实现临床缓解。然而，血清钠的总变化在最初1 - 2小时内不应超过5 mEq/L，在治疗的头48小时内不应超过15 - 20 mEq/L。最近有前瞻性研究表明，以每小时100毫升的输注速度给予500毫升3%盐水是安全的。识别脑水肿的早期迹象（恶心、呕吐和头痛）并使用静脉注射3%氯化钠进行干预至关重要，因为此时是进行干预的时机，而不是等到出现更严重的症状。脑脱髓鞘是低钠血症过快纠正的一种罕见并发症。脑脱髓鞘的主要危险因素包括在治疗的头48小时内血清钠纠正超过25 mEq/L、纠正至超过140 mEq/L、慢性肝病以及缺氧/无氧发作。
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