Dialysis disequilibrium syndrome (DDS) is a neurological complication that has been known to occur after hemodialysis (HD). In recent years, the prevalence of DDS has been low as the symptoms are widely recognized; hence, preventive therapies, such as the slow and gentle procedure for HD, are often administered before starting dialysis. However, once DDS occurs, it may cause seizures, coma, and even death in severe cases. Since there has been no established treatment, recognizing risk factors and preventing the syndrome is important.
A 76-year-old man was admitted to our hospital due to exacerbation of chronic heart failure. He also had a history of chronic kidney disease and had consulted with his home doctor about the preparation for HD a month before admission. After treatment with diuretics, the symptoms ameliorated, but he experienced presyncope and malaise. Laboratory tests revealed acute anemia and a decrease in renal function. Upper gastrointestinal endoscopy revealed active bleeding from a gastric ulcer, which was successfully stopped. However, his consciousness deteriorated because of uremia; hence, HD was initiated. We used a cellulose triacetate membrane with a surface area of 1.3 m
2
and maintained a dialysate flow rate of 500 ml/min with a blood flow rate of 120 ml/min. Four hours after starting HD, he suddenly developed generalized tonic convulsions. The dialysis was immediately stopped, and the patient was transferred to an intensive care unit. A computed tomography scan of the head showed mild edematous change of the brain, and laboratory tests also revealed a rapid decrease of urea nitrogen. We rationalized that he might have developed DDS. After injection of levetiracetam for the treatment of seizures, we initiated continuous hemodiafiltration as renal replacement therapy. Fortunately, his consciousness gradually improved, and he was completely alert on day 18 after admission.
With reference to our current report, DDS can occur even following acute kidney injury, as the progression rate of the injury and accumulation of blood urea may not correlate with the risk of the syndrome.