Rodriguez Lopez Armando F, Ameduite Messanh K, Maddipati Veeranna, Coore Hunter
Nephrology, East Carolina University Health Medical Center, Greenville, USA.
Pulmonary and Critical Care, East Carolina University Health Medical Center/East Carolina University Brody School of Medicine, Greenville, USA.
Cureus. 2025 Aug 4;17(8):e89369. doi: 10.7759/cureus.89369. eCollection 2025 Aug.
Dialysis disequilibrium syndrome (DDS) is a rare but potentially fatal complication of renal replacement therapy, typically characterized by cerebral edema and often precipitated by the rapid correction of severe azotemia. Clinical symptoms are often non-specific, and, in some cases, the condition can be fatal. While the role of azotemia in DDS is well established, alternative mechanisms, such as the brain acidosis paradox, have also been proposed. We present the case of a 57-year-old African American woman with chronic kidney disease who was admitted with urosepsis and respiratory distress. Initial laboratory evaluation revealed a serum bicarbonate level <5 mEq/L and blood urea nitrogen of 116 mg/dL (baseline = 40-50 mg/dL). Due to the severity of her metabolic acidosis and signs of impending hypoxic respiratory failure, she underwent urgent hemodialysis. After 80 minutes of treatment, the patient became hypotensive and was transferred to the intensive care unit. Subsequent imaging revealed worsening cerebral edema with associated herniation, which was refractory to osmotherapy. The patient was transitioned to palliative care, and organ procurement was arranged. Most reported cases of fatal DDS are associated with chronic azotemia >150 mg/dL, a threshold not reached in this case. While preventive strategies for DDS emphasize limiting the urea reduction ratio (URR), there are currently no established guidelines for the safe rate of bicarbonate correction. In this case, the URR was 57% using a standard blood flow rate, and the bicarbonate level increased by more than 10 mEq/L. We hypothesize that rapid correction of metabolic acidosis may contribute to fatal DDS by worsening cerebral edema through mechanisms such as the brain acidosis paradox.
透析失衡综合征(DDS)是肾脏替代治疗中一种罕见但可能致命的并发症,通常表现为脑水肿,常由严重氮质血症的快速纠正引发。临床症状往往不具特异性,在某些情况下,病情可能致命。虽然氮质血症在DDS中的作用已得到充分证实,但也有人提出了其他机制,如脑酸中毒悖论。我们报告一例57岁患有慢性肾脏病的非裔美国女性,因尿脓毒症和呼吸窘迫入院。初始实验室检查显示血清碳酸氢盐水平<5 mEq/L,血尿素氮为116 mg/dL(基线值=40 - 50 mg/dL)。由于其代谢性酸中毒严重且有即将发生的低氧性呼吸衰竭迹象,她接受了紧急血液透析。治疗80分钟后,患者出现低血压并被转入重症监护病房。随后的影像学检查显示脑水肿加重并伴有脑疝形成,对渗透性疗法无效。患者转为姑息治疗,并安排了器官获取事宜。大多数报告的致命性DDS病例与慢性氮质血症>150 mg/dL相关,本病例未达到该阈值。虽然DDS的预防策略强调限制尿素清除率(URR),但目前尚无关于碳酸氢盐安全纠正率的既定指南。在本病例中,使用标准血流量时URR为57%,碳酸氢盐水平升高超过10 mEq/L。我们推测,代谢性酸中毒的快速纠正可能通过脑酸中毒悖论等机制加重脑水肿,从而导致致命性DDS。