WHAT IS DDS?

The dialysis disequilibrium syndrome is defined as a clinical syndrome of neurologic deterioration that is
seen in patients who undergo hemodialysis 

DDS is a neurological disorder that is associated with cerebral edema

RISK FACTORS

First dialysis treatment

Children

Elderly

High BUN

Hypernatremia

Hyperglycemia

Metabolic acidosis

Preexisting neurologic abnormalities

Preexisting cerebral edema

Conditions associated with an increased permeability of the blood brain barrier, eg, meningitis,
vasculitis, CNS tumors, hemolytic uremic syndrome or thrombotic thrombocytopenic purpura

Signs and symptoms

Disequilibrium syndrome of dialysis has essentially the same symptoms as cerebral edema: dizzy, faint,
lightheaded, ringing in the ears, racing pulse, feeling warm, sweating, nausea, vomiting, yawning, itching
and severe muscle cramps (anywhere on the body). It is due to a shift of water to the intracellular
spaces as a result of the loss of urea. Actually, I think hypotension is more of the problem because of the
loss of water and solutes.

CAUSES:

The cause of DDS is currently not well understood. There are two theories to explain it; the first theory
postulates that urea transport from the brain cells is slowed in chronic kidney disease, leading to a
large urea concentration gradient, which results in reverse osmosis. The second theory postulates that
organic compounds are increased in uremia to protect the brain and result in injury by, like in the first
theory, reverse osmosis. More recent studies on rats noted that brain concentrations of organic
osmolytes were not increased relative to baseline after rapid dialysis. Cerebral edema was thus
attributed to osmotic effects related to a high urea gradient between plasma and brain
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.

WHAT HAPPENS:

Need for hospitalization

Risk of neurological permanent damage (demyelination of the pontine and extrapontine areas, rare)

Death (in severe form, rare)

 Blood glucose (to exclude hypoglycemia)

 Serum calcium (to exclude hypocalcemia or hypercalcemia)
 Serum sodium (to exclude hyponatremia)
 Head CT scan or brain MRI (to exclude a cerebrovascular accident or subdural
hematoma; dialysis disequilibrium syndrome is characterized by diffuse cerebral
edema)

Management

When DDS is suspected, strong consideration should be given to discontinuing the dialysis treatment.

If symptoms are very mild, blood flow rate should be reduced to decrease urea clearance.

The patient should be closely monitored and the dialysis session discontinued immediately if
symptoms worsen or if severe. Evaluation for other causes of neurologic deterioration should be
undertaken

Conclusion

The population with renal failure at risk for developing DDS is large, yet the syndrome is rare because
measures to prevent it are already part of routine practice.

Recognition of patients at high risk, slowing down the efficiency and rate of urea clearance, limiting
the decrease in plasma osmolality and avoiding bicarbonate-based rapid correction of metabolic
acidosis are strategies for prevention of this syndrome.