Dialysis Disequilibrium Syndrome Revisited

Abstract

An aggressive dialysis in a grossly azotemic patient, especially one with severe metabolic acidosis, can lead to dialysis disequilibrium syndrome (DDS). Mild forms present as nausea, vomiting, restlessness, and headache. Severe manifestations include seizures, obtundation, coma, and even death. This clinical picture is caused by cerebral edema induced by one or more of the following mechanisms: "Reverse urea effect" - Dialysis removes urea faster from the blood than from the brain; consequently, water enters the brain. "Cerebrospinal fluid acidosis" - Correction of systemic acidosis engenders the condition due to a lowering of brain pH. "Idiogenic osmoles" - As a response to blood hyperosmolar state, osmoles are produced in the brain. As blood osmolality decreases under relatively quick dialysis, idiogenic osmoles tend to induce brain edema. Because the symptoms of DDS can be life-threatening, preventive measures in patients with severe uremia are important. The first strategy relies on raising blood osmolality by introducing solutes (osmoles) into the blood. The second approach, which is the most common, decreases the efficiency of the dialysis treatment by shortening the duration of a dialysis run to 25% - 30% of normal, by lowering dialyzer blood flow or dialysate flow rate, by using a less efficient dialyzer, or by a combination of these maneuvers. Dialysis frequency is increased instead. Anticonvulsant drugs are needed in cases where the preventive measures have not been used or have been unsuccessful.

Fellows’ Forum Fellows’ Forum in Dialysis Edited by Mark A. Perazella: Dialysis Disequilibrium Syndrome: A Narrative Review

“…As convective/ultrafiltrative urea removal does not contribute to the blood CSF osmotic gradient, this element of overall Kt/V can theoretically be ignored. If the patient can tolerate this dialysis treatment, then the efficacy of dialysis can gradually be increased in subsequent dialysis treatments until conventional treatments are performed (37)(38)(39)(40)(41)(42)(43).…”

“…One reported approach is to start urea and osmotic gradients with a dialysate urea concentration approximately 10% lower than serum urea concentration. Over a series of dialysis treatments, the patient's blood urea concentration is gradually reduced, thereby avoiding DDS (37,38,42,43).…”

Composition and clinical use of hemodialysates

“…13 However, at the same time, the intradialytic fall in plasma urea and osmolality levels tends to direct water to move in the opposite direction. 14 In terms of increasing dialysate sodium concentration, an array of different approaches have been suggested, including ones with a continuously high sodium concentration and ones that start out with a high sodium value (e.g., 145-150 mmol/L), which subsequently falls in a linear, step, or logarithmic manner to a lower level (e.g., 135-140 mmol/L) as dialysis progresses (sodium profiling). 15 Noteworthy that a patient' s postdialysis plasma sodium value is a function of a treatment' s time-averaged dialysate sodium value, not the terminal dialysate sodium concentration.…”

Successful management of severe hyponatremia in CKD‐VD: In a cost limited setting

“…DDS results from the urea removal (HD) from the extracellular space, which is quicker than urea leaving the brain cells, resulting in osmotic dysequilibrium due to water movement into the brain cells. 4 The pathophysiology of DDS is opposite to ODS, and thus brain cell urea disequilibration during HD may help prevent cellular dehydration caused by raising the extracellular serum Na too rapidly during a HD treatment. 5 ODS rarely occurs following correction of hyponatremia in uremic patients receiving HD.…”