Dialysis disequilibrium syndrome: Difference between revisions

Revision as of 10:06, 27 April 2017

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
- 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

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

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

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]

The mainstay of treatment is ICP reduction^[3]
- Can give mannitol or hypertonic saline IV
- Can hyperventilate patient
Symptomatic management for mild symptoms (nausea, headache, restlessness)
Symptoms are self-limiting and typically resolve within several hours

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

↑ 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
↑ Zepeda-Orozco D and Quigley R. Dialysis disequilibrium syndrome. Pediatr Nephrol. 2012 Dec; 27(12): 2205–2211.
↑ ^3.0 ^3.1 ^3.2 ^3.3 Zepeda-orozco D. et al. Dialysis disequilibrium syndrome. Pediatr Nephrol. 2012;27(12):2205-11.Pubmed
↑ Mahoney CA. et al. Uremic encephalopathies: clinical, biochemical, and experimental features. Am J Kidney Dis. 1982;2(3):324-36. Pubmed
↑ 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
↑ 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
↑ 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

Authors:

@@ Line 32: / Line 32: @@
 *[[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>
-{{Dialysis complications DDX}}
-===Other===
-*[[Hypoglycemia]]
-*[[Hyponatremia]]
 *[[Hypocalcemia]]
-*[[Uremia]]
 *Intracranial Bleed
 *[[Hypertensive Emergency]]
 *[[Stroke]]
 *Supratheurapeutic Medication Effects
-*PRES
+*[[PRES]]
+{{Dialysis complications DDX}}
 ==Evaluation==