Dialysis disequilibrium syndrome

Revision as of 10:01, 27 April 2017 by Rossdonaldson1 (talk | contribs)

Background

  • Dialysis Disequilibrium Syndrome (DDS) is 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
  • 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


  • Characterized by neurological symptoms that is thought to be secondary to cerebral edema affecting dialysis patients
  • Tends to occur in patients who are initially started on dialysis, particularly with high initial BUN
  • 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

Clinical Features

  • Headache
  • Disorientation
  • Nausea and vomiting
  • Restlessness
  • Can progress to seizure, coma & death [3]


  • Signs and symptoms develop during or after dialysis or during renal replacement therapy, usually self limited but can occasionally progress
  • Headache
  • Nausea
  • Visual disturbances
  • Asterixis
  • Altered mental staus
  • Seizures
  • Coma
  • Muscle Cramps

Differential Diagnosis

Dialysis Complications


Other

Evaluation

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

Workup

  • Diagnosis suggested by development of neurologic symptoms associated with dialysis, however DDS is a diagnosis of exclusion (rule out SDH, CVA).


Management

Prevention

  • 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]

Treatment

  • The mainstay of treatment is ICP reduction[3]
  • Symptomatic management for mild symptoms (nausea, headache, restlessness)
  • Symptoms are self-limiting and typically resolve within several hours


Management

  • Supportive in most cases
  • Limit the rate of urea removal during first few session of dialysis to prevent dysequilibrium syndrome
  • For severe symptoms such as seizure, consider stopping dialysis

Disposition

  • Most cases can be discharged with followup

See Also

References

  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
Retrieved from "https://www.wikem.org/w/index.php?title=Dialysis_disequilibrium_syndrome&oldid=132718"