PDF(Pubmed)
Abstract：
Delayed cerebral ischemia is a clinical entity commonly encountered in patients presenting with acute neurological injury and is often complicated by dysnatremias, such as the cerebral salt wasting syndrome. In this case report, we described an exceptional case of polyuria attributed to an initial cerebral salt wasting phenomenon and iatrogenic-induced medullary washout.
A 53-year-old woman was admitted to our hospital for the management of a Modified Fisher scale grade 4 subarachnoid hemorrhage due to a ruptured posterior communicating aneurysm. She was initially managed with coil embolization and external ventricular drain due to secondary hydrocephalus. Throughout the course of her hospitalization, she developed severe polyuria reaching up to 40L per day. To keep up with the excessive urinary losses and maintain appropriate cerebral perfusion, fluid replacement therapy was adjusted every hour, reaching up to 1.3 L of crystalloid per hour in addition to aminergic support. An initial diagnosis of partial diabetes insipidus, followed by a cerebral salt wasting syndrome was suspected. While the urine output continued to increase, her serum urea concentration progressively decreased to a point of almost being undetectable on day 9. At that time, the presence of an interstitial medulla washout was hypothesized. Various pharmacological and non-pharmacological interventions were progressively introduced to regain normal renal homeostasis, including non-steroidal anti-inflammatory drugs, fludrocortisone, oral urea and high-protein intake. Medications were progressively weaned, and the patient was successfully discharged from the ICU.
Cerebral salt wasting should be considered in the initial differential diagnosis of a patient presenting with polyuria in the context of acute neurological injury. Early recognition of this entity is critical to quickly implement proper management. However, as shown in this case report, the concomitance of delayed cerebral ischemia may complexify that management.
A 53-year-old woman was admitted to our hospital for the management of a Modified Fisher scale grade 4 subarachnoid hemorrhage due to a ruptured posterior communicating aneurysm. She was initially managed with coil embolization and external ventricular drain due to secondary hydrocephalus. Throughout the course of her hospitalization, she developed severe polyuria reaching up to 40L per day. To keep up with the excessive urinary losses and maintain appropriate cerebral perfusion, fluid replacement therapy was adjusted every hour, reaching up to 1.3 L of crystalloid per hour in addition to aminergic support. An initial diagnosis of partial diabetes insipidus, followed by a cerebral salt wasting syndrome was suspected. While the urine output continued to increase, her serum urea concentration progressively decreased to a point of almost being undetectable on day 9. At that time, the presence of an interstitial medulla washout was hypothesized. Various pharmacological and non-pharmacological interventions were progressively introduced to regain normal renal homeostasis, including non-steroidal anti-inflammatory drugs, fludrocortisone, oral urea and high-protein intake. Medications were progressively weaned, and the patient was successfully discharged from the ICU.
Cerebral salt wasting should be considered in the initial differential diagnosis of a patient presenting with polyuria in the context of acute neurological injury. Early recognition of this entity is critical to quickly implement proper management. However, as shown in this case report, the concomitance of delayed cerebral ischemia may complexify that management.
摘要：
背景：迟发性脑缺血是表现为急性神经损伤的患者中常见的一种临床实体，并且通常会并发呼吸困难，比如脑性盐耗综合征。在这个案例报告中,我们描述了一个特殊的多尿病例，该病例归因于最初的脑盐消耗现象和医源性引起的髓质冲洗。
方法：一名53岁的妇女因破裂后交通动脉瘤而入院治疗改良Fisher评分4级蛛网膜下腔出血。由于继发性脑积水，她最初接受了线圈栓塞和外部心室引流的治疗。在她住院的整个过程中，她出现了严重的多尿，每天高达40L。为了跟上过多的尿流失并保持适当的脑灌注，补液治疗每小时调整一次,除了胺能支持外，每小时最高可达到1.3L的晶体。部分尿崩症的初步诊断，随后怀疑是脑性盐耗综合征。虽然尿量持续增加，在第9天，她的血清尿素浓度逐渐降低到几乎无法检测到的程度。当时,假设存在间质髓质冲洗。逐步引入各种药物和非药物干预措施以恢复正常的肾脏稳态，包括非甾体抗炎药,氟氢可的松,口服尿素和高蛋白摄入。药物逐渐断奶，患者成功从ICU出院。
结论：在急性神经损伤中表现为多尿的患者的初步鉴别诊断中，应考虑脑性盐消耗。尽早认识到这一实体对于快速实施适当的管理至关重要。然而,如案例报告所示，迟发性脑缺血的伴随可能使治疗复杂化。
方法：一名53岁的妇女因破裂后交通动脉瘤而入院治疗改良Fisher评分4级蛛网膜下腔出血。由于继发性脑积水，她最初接受了线圈栓塞和外部心室引流的治疗。在她住院的整个过程中，她出现了严重的多尿，每天高达40L。为了跟上过多的尿流失并保持适当的脑灌注，补液治疗每小时调整一次,除了胺能支持外，每小时最高可达到1.3L的晶体。部分尿崩症的初步诊断，随后怀疑是脑性盐耗综合征。虽然尿量持续增加，在第9天，她的血清尿素浓度逐渐降低到几乎无法检测到的程度。当时,假设存在间质髓质冲洗。逐步引入各种药物和非药物干预措施以恢复正常的肾脏稳态，包括非甾体抗炎药,氟氢可的松,口服尿素和高蛋白摄入。药物逐渐断奶，患者成功从ICU出院。
结论：在急性神经损伤中表现为多尿的患者的初步鉴别诊断中，应考虑脑性盐消耗。尽早认识到这一实体对于快速实施适当的管理至关重要。然而,如案例报告所示，迟发性脑缺血的伴随可能使治疗复杂化。
