Fellows’ Forum Fellows’ Forum in Dialysis Edited by Mark A. Perazella Dialysis Disequilibrium Syndrome: A Narrative Review Nilang Patel,* Pranav Dalal,† and Mandip Panesar* *Division of Nephrology, Department of Internal Medicine, Erie County Medical Center, State University of New York, Buffalo, New York, and †Department of Internal Medicine, Chicago Medical School, Mount Sinai Hospital, Chicago, Illinois ABSTRACT Dialysis Disequilibrium Syndrome (DDS) is characterized by neurological symptoms caused by rapid removal of urea during hemodialysis. It develops primarily from an osmotic gradient that develops between the brain and the plasma as a result of rapid hemodialysis. This results in brain edema that manifests as neurological symptoms such as headache, nausea, vomiting, muscle cramps, tremors, dis- turbed consciousness, and convulsions. In severe cases, patients can die from advanced cerebral edema. Recent advancements in cell biology implicate the role of urea dis- equilibrium (with a smaller contribution from organic osm- olytes) as the pathophysiological mechanism responsible for this syndrome. In this review, we discuss the pathogenesis, clinical features and prevention of DDS. Case A 54-year-old male with a past medial history of lupus nephritis, hypertension, and hypercholesterolemia pre- sented to the emergency department with anorexia and generalized malaise. On physical examination, the patient had bilateral lower extremity edema and blood chemistries showed elevated concentrations of potas- sium (6.3 mEq/l), blood urea nitrogen (BUN) (131 mg/ dl), and creatinine (13.3 mg/dl). A diagnosis of acute on chronic renal failure due to progressive lupus nephri- tis was made. Hyperkalemia failed to correct with medi- cal management and emergent hemodialysis was initiated via a right internal jugular dialysis catheter. The treatment was carried out for 4 hours with the fol- lowing dialysate composition: potassium 2 mEq/l, cal- cium 2.5 mEq/l, bicarbonate 35 mEq/l, and sodium 140 mEq/l. The dialysate flow rate was 500 ml/min and the blood flow rate was 250–300 ml/minute. Postdialy- sis laboratory results showed lower levels of serum potassium (3.2 mEq/l), BUN (71 mg/dl), and creatinine (8.9 mg/dl). About an hour after the completion of the dialysis treatment, the patient developed a generalized tonic–clonic seizure and was treated with intravenous lorazepam. Repeat laboratory evaluation demonstrated no electrolyte or divalent ion abnormalities. Computed tomography (CT) scan and magnetic resonance imag- ing (MRI) of the brain were both unremarkable. Elec- troencephalogram showed changes suggestive of diffuse metabolic encephalopathy. Dialysis disequilibrium syn- drome (DDS) was considered as a possible cause of the seizure. Subsequently, the patient was dialyzed with low blood flow rates and shorter time periods with a gradual increase in dialysis clearance. No further sei- zures developed. Introduction Dialysis Disequilibrium Syndrome, defined initially in 1962 (1), is an acute neurological complication of hemodialysis characterized by signs and symptoms that can include fatigue, mild headache, nausea, vomiting, blurred vision, muscle cramps, tremors, disturbed con- sciousness, convulsions, and coma. It can lead to death due to cerebral edema (2,3). The neurological symptoms are more common toward the end of a dialysis treatment that is characterized by rapid urea clearance in which accentuates the plasma cerebrospinal fluid (CSF) urea concentration gradient. The term disequilibrium is employed because the syndrome typically occurs when the blood biochemistry parameters are improving (3,4). Address correspondence to: Mandip Panesar, MD, Divi- sion of Nephrology, Department of Internal Medicine, Erie County Medical Center, State University of New York, 462 Grider Street, 10th Floor, Buffalo, NY 14215, or e-mail: mpanesar@buffalo.edu. Seminars in Dialysis—Vol 20, No 3 (September–October) 2008 pp. 493–498 DOI: 10.1111/j.1525-139X.2008.00474.x ª 2008 Copyright the Authors. Journal compilation ª 2008 Wiley Periodicals, Inc. 493