Abstract
The dialysis disequilibrium syndrome is a rare but serious complication of hemodialysis. Despite the fact that maintenance hemodialysis has been a routine procedure for over 50 years, this syndrome remains poorly understood. The signs and symptoms vary widely from restlessness and headache to coma and death. While cerebral edema and increased intracranial pressure are the primary contributing factors to this syndrome and are the target of therapy, the precise mechanisms for their development remain elusive. Treatment of this syndrome once it has developed is rarely successful. Thus, measures to avoid its development are crucial. In this review, we will examine the pathophysiology of this syndrome and discuss the factors to consider in avoiding its development.
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1. E. Disequilibrium has been reported in a patient with a urea reduction ratio of 17 %. This patient had an initial urea concentration of 299 mg/dl. Thus, the initial BUN is critical. In addition, animal models have shown that the rate of reduction of urea is a crucial element in development of dialysis disequilibrium syndrome [15, 26, 36].
2. B. The microvascular endothelial cells of the BBB have low ion permeability, high reflection coefficient and high electrical resistance compared to other vascular beds. They regulate the movement of small organic solutes and ions [8, 9].
3. B. There is increased expression of AQP9 and AQP4 and decreased expression of UTB-1 [13].
4. C. This is a reduction of 40 % from the initial BUN over a time period of 2 h. While there are no studies to prove this is safe, there is consensus that this is a reasonable plan.
5. A. Infusing mannitol has been shown to reduce the symptoms of disequilibrium. Using a high dialysate sodium concentration (not low) would also help in preventing it.
Questions (answers are provided following the reference list)
Questions (answers are provided following the reference list)
1. What is/are the crucial element(s) involved in the development of dialysis disequilibrium syndrome
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a)
Pre-dialysis concentration of urea
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b)
Rate of urea removal
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c)
Pre-dialysis blood pressure
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d)
Patient’s volume status
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e)
a and b
2. What component of the neural microenviroment is responsible for regulating movement of small organic solutes and ions between the blood and the CNS extracellular space?
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a)
Choroid plexus
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b)
Microvacular unfenestrated endothelial cells with tight junctions
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c)
Astrocytes
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d)
Neurons
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e)
Glia
3. In uremic rats AQP4, AQP9 and UTB-1 are:
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a)
AQP4↑, AQP9↓, UTB-1↑
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b)
AQP4↑, AQP9↑, UTB-1↓
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c)
AQP4↓, AQP9↑, UTB-1↓
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d)
AQP4↑, AQP9↑, UTB-1↑
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c)
AQP4↓, AQP9↓, UTB-1↓
4. A patient presents with signs and symptoms of uremia and is found to have a BUN of 200 mg/dl. A reasonable plan to avoid disequilibrium for the first dialysis treatment would be to lower his BUN to:
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a)
40 mg/dl over 2 hours
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b)
80 mg/dl over 4 hours
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c)
120 mg/dl over 2 hours
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d)
120 mg/dl over 1 hour
5. In the above patient, an additional maneuver to avoid disequilibrium would be to:
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a)
infuse mannitol (1 gm/kg) over the first hour of treatment
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b)
use a dialysate sodium concentration of 130 mEq/liter
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c)
raise the dialysate bicarbonate concentration to 40 mEq/liter
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d)
avoid any ultrafiltration of fluid
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Zepeda-Orozco, D., Quigley, R. Dialysis disequilibrium syndrome. Pediatr Nephrol 27, 2205–2211 (2012). https://doi.org/10.1007/s00467-012-2199-4
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DOI: https://doi.org/10.1007/s00467-012-2199-4