Dialysis disequilibrium syndrome: Difference between revisions

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==Background==
==Background==
*Clinical syndrome occurring at end of dialysis
*Abbreviation: DDS
**Occurs most commonly during initial dialysis or during hypercatabolic states
*A rare clinical syndrome occurring at end of dialysis or the beginning of continuous renal replacement therapy
**Large solute clearances -> cerebral edema
**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 <ref>Silver SM. et al. Dialysis disequilibrium syndrome (DDS) in the rat: role of the "reverse urea effect". Kidney Int. 1992;42(1):161-6. [http://www.ncbi.nlm.nih.gov/pubmed?term=1635345 Pubmed]</ref>
**Pre-dialysis urea in CSF lower than in blood<ref>Zepeda-Orozco D and Quigley R. Dialysis disequilibrium syndrome. Pediatr Nephrol. 2012 Dec; 27(12): 2205–2211.</ref>
**Post-dialysis urea in CSF higher, setting up osmotic gradient for water into CNS
**More uremic patients pre-dialysis at higher risk


==Clinical Features==
==Clinical Features==
*nausea and vomiting, hypertension; can progress to seizure, coma, death
''Signs and symptoms develop during or after dialysis or during renal replacement therapy, usually self limited but can occasionally progress''
*[[Headache]]
*Disorientation
*[[Nausea and vomiting]]
*Restlessness
*[[Visual disturbances]]
*Asterixis
*Muscle Cramps
*Can progress to [[seizure]], [[coma]], and [[death]]<ref name="DDS">Zepeda-orozco D. et al. Dialysis disequilibrium syndrome. Pediatr Nephrol. 2012;27(12):2205-11.[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491204/ Pubmed]</ref>


==Differential Diagnosis==
==Differential Diagnosis==
*[[Subdural hematoma]]
*[[Uremia]]
*Nonketotic hyperosmolar [[coma]]
*[[Acute cerebrovascular event]]
*Dialysis dementia
*Excessive ultrafiltration and seizure
*Metabolic disturbances
**[[Hypoglycemia]]
**[[Hyponatremia]]
*[[Meningitis]]
*[[Malignant hypertension]]<ref name="DDS"></ref><ref>Mahoney CA. et al. Uremic encephalopathies: clinical, biochemical, and experimental features. Am J Kidney Dis. 1982;2(3):324-36. [http://www.ncbi.nlm.nih.gov/pubmed/6756130 Pubmed]</ref>
*[[Hypocalcemia]]
*Intracranial Bleed
*[[Hypertensive Emergency]]
*[[Stroke]]
*Supratheurapeutic Medication Effects
*[[PRES]]
{{Dialysis complications DDX}}
{{Dialysis complications DDX}}


==Workup==
==Evaluation==
*Diagnosis of exclusion (rule out SDH, CVA)
===Workup===
*Bedside Glucose
*CBC
*Chem-10
*Liver Panel
*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==
==Management==
*Treat with mannitol
===Mild===
*Symptomatic management for mild symptoms (nausea, headache, restlessness)
**Symptoms are self-limiting and typically resolve within several hours
 
===Severe===
*For severe symptoms, the mainstay of treatment is ICP reduction<ref name="DDS"></ref>
**Can give [[mannitol]] or [[hypertonic saline]] IV
**Can hyperventilate patient


==Disposition==
==Disposition==
*Depends on severity
**Many cases can be discharged with followup
==Prevention==
*Response to treatment is typically poor, so preventive measures are important<ref name="DDS"></ref>
*Add an osmotic agent to mitigate the osmotic gradient
**Elevate the sodium concentration in the diasylate<ref> 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.[http://www.ncbi.nlm.nih.gov/pubmed/4792047/ Pubmed]</ref>
**Elevate the glucose concentration in the diasylate (717 mg/dl) or add IV mannitol (1g/kg)<ref>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. [http://www.ncbi.nlm.nih.gov/pubmed/851303/ Pubmed]</ref>
*Consider hemofiltration rather than hemodialysis<ref>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. [http://www.ncbi.nlm.nih.gov/pubmed/7396769/ Pubmed]</ref>


==See Also==
==See Also==
*[[Dialysis complications]]
*[[Dialysis complications]]
==External Links==


==References==
==References==
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[[Category:Renal]]
[[Category:Renal]]
[[Category:Neurology]]

Revision as of 16:18, 21 February 2018

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

Evaluation

Workup

  • Bedside Glucose
  • CBC
  • Chem-10
  • Liver Panel
  • 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[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

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