Dialysis disequilibrium syndrome: Difference between revisions
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==Background== | ==Background== | ||
* | *Abbreviation: DDS | ||
**Occurs most commonly during initial | *A rare clinical syndrome occurring at end of dialysis or the beginning of continuous renal replacement therapy | ||
**Large solute | **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== | ||
* | ''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 | ===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== | ||
* | ===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]] | ||
==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
- Headache
- Disorientation
- Nausea and vomiting
- Restlessness
- Visual disturbances
- Asterixis
- Muscle Cramps
- Can progress to seizure, coma, and death[3]
Differential Diagnosis
- Subdural hematoma
- Uremia
- Nonketotic hyperosmolar coma
- Acute cerebrovascular event
- Dialysis dementia
- Excessive ultrafiltration and seizure
- Metabolic disturbances
- Meningitis
- Malignant hypertension[3][4]
- Hypocalcemia
- Intracranial Bleed
- Hypertensive Emergency
- Stroke
- Supratheurapeutic Medication Effects
- PRES
Dialysis Complications
- Dialysis-associated hypotension
- Dialysis disequilibrium syndrome
- Air embolism
- Missed dialysis (pulmonary edema)
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
Management
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[3]
- Can give mannitol or hypertonic saline IV
- Can hyperventilate patient
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
- Consider hemofiltration rather than hemodialysis[7]
See Also
References
- ↑ 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