Dialysis disequilibrium syndrome

Background
  • Abbreviation: DDS
  • A rare clinical syndrome occurring at end of dialysis or the beginning of continuous renal replacement therapy
    • Does not occur with peritoneal dialysis[1]
    • 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 [2]
    • Pre-dialysis urea in CSF lower than in blood[3]
    • 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

Evaluation

Workup
  • Bedside Glucose
  • CBC
  • Chem-10
  • LFTs
  • CT Brain

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

Management

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

Severe

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

Prevention
  • Response to treatment is typically poor, so preventive measures are important[4]
  • Add an osmotic agent to mitigate the osmotic gradient
    • Elevate the sodium concentration in the diasylate[6]
    • Elevate the glucose concentration in the diasylate (717 mg/dl) or add IV mannitol (1g/kg)[7]
  • Consider hemofiltration rather than hemodialysis[8]

See Also

References
  1. Wolfson AB. Renal failure. In: Walls RM, Hockberger RS, Gausche-Hill M, et al., eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th ed. Elsevier; 2018:(Ch) 87.
  2. 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
  3. Zepeda-Orozco D and Quigley R. Dialysis disequilibrium syndrome. Pediatr Nephrol. 2012 Dec; 27(12): 2205–2211.
  4. Zepeda-orozco D. et al. Dialysis disequilibrium syndrome. Pediatr Nephrol. 2012;27(12):2205-11.Pubmed
  5. Mahoney CA. et al. Uremic encephalopathies: clinical, biochemical, and experimental features. Am J Kidney Dis. 1982;2(3):324-36. Pubmed
  6. 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
  7. 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
  8. 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
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