Dialysis disequilibrium syndrome

Revision as of 16:18, 21 February 2018 by DrKarb (talk | contribs) (Background)


  • Abbreviation: DDS
  • A rare clinical syndrome occurring at end of dialysis or the beginning of continuous renal replacement therapy
    • Occurs most commonly during initial hemodialysis or during hypercatabolic states
    • Tends to occur in patients who are initially started on dialysis, particularly with high initial BUN
    • Other risk factors: older or younger age, hyponatremia, pre-existing neurologic disease
    • Symptoms are thought to be secondary to the development of cerebral edema possibly due to urea removal during dialysis and from a decreased in pH in the cerebral intracelluar environment
  • Large and rapid solute clearance creates an osmotic gradient which can precipitate cerebral edema [1]
    • Pre-dialysis urea in CSF lower than in blood[2]
    • Post-dialysis urea in CSF higher, setting up osmotic gradient for water into CNS
    • More uremic patients pre-dialysis at higher risk

Clinical Features

Signs and symptoms develop during or after dialysis or during renal replacement therapy, usually self limited but can occasionally progress

Differential Diagnosis

Dialysis Complications



  • Bedside Glucose
  • CBC
  • Chem-10
  • Liver Panel
  • CT Brain


  • Is a clinical diagnosis, suggested by development of neurologic symptoms associated with dialysis
    • However, must first exclude more serious diagnoses (rule out SDH, CVA).



  • Symptomatic management for mild symptoms (nausea, headache, restlessness)
    • Symptoms are self-limiting and typically resolve within several hours



  • Depends on severity
    • Many cases can be discharged with followup


  • Response to treatment is typically poor, so preventive measures are important[3]
  • Add an osmotic agent to mitigate the osmotic gradient
    • Elevate the sodium concentration in the diasylate[5]
    • Elevate the glucose concentration in the diasylate (717 mg/dl) or add IV mannitol (1g/kg)[6]
  • Consider hemofiltration rather than hemodialysis[7]

See Also


  1. Silver SM. et al. Dialysis disequilibrium syndrome (DDS) in the rat: role of the "reverse urea effect". Kidney Int. 1992;42(1):161-6. Pubmed
  2. Zepeda-Orozco D and Quigley R. Dialysis disequilibrium syndrome. Pediatr Nephrol. 2012 Dec; 27(12): 2205–2211.
  3. 3.0 3.1 3.2 3.3 Zepeda-orozco D. et al. Dialysis disequilibrium syndrome. Pediatr Nephrol. 2012;27(12):2205-11.Pubmed
  4. Mahoney CA. et al. Uremic encephalopathies: clinical, biochemical, and experimental features. Am J Kidney Dis. 1982;2(3):324-36. Pubmed
  5. Port FK. et al. Prevention of dialysis disequilibrium syndrome by use of high sodium concentration in the dialysate. Kidney Int. 1973;3(5):327-33.Pubmed
  6. Rodrigo F. et al. Osmolality changes during hemodialysis. Natural history, clinical correlations, and influence of dialysate glucose and intravenous mannitol. Ann Intern Med. 1977;86(5):554-61. Pubmed
  7. Kishimoto T. et al. Superiority of hemofiltration to hemodialysis for treatment of chronic renal failure: comparative studies between hemofiltration and hemodialysis on dialysis disequilibrium syndrome. Artif Organs. 1980;4(2):86-93. Pubmed