Dialysis disequilibrium syndrome (DDS) is a serious and rare complication of dialysis that involves a range of neurological symptoms that are primarily considered to be a consequence of cerebral edema and increased intracranial pressure. Though DDS can occur with continuous renal replacement therapy (CRRT), it is more common with traditional hemodialysis.
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Who is at risk for DDS?
Dialysis disequilibrium syndrome is most likely to affect someone newly starting dialysis or a patient that has missed consecutive dialysis appointments. Other factors that increase the risk for DDS are:
- age (very young or very old), more common in children than adults
- significantly elevated BUN
- any condition that causes increased permeability of the blood-brain barrier (such as sepsis, meningitis and encephalitis)
- a pre-existing neurological disorder (such as stroke or seizure disorder)
- any condition that is related to cerebral edema (such as hyponatremia and hypertensive crisis)
- individuals who retain CO2 may be at higher risk (such as those with COPD)
Disequilibrium syndrome pathophysiology
Though we know the symptoms of DDS are essentially due to cerebral edema, why cerebral edema occurs is not fully understood. Disequilibrium syndrome was first reported in 1962 when it was noticed that the mental status of many patients improved after dialysis completed, but in some patients there was no improvement and they continued to have headaches, be confused, and have muscle twitches.
Key theories suggest it is due to osmotic shifts of urea and pH changes in brain cells secondary to increases in CO2 retention. Let’s take a closer look at the theory that suggests it is due to a reverse osmotic shift.
As the patient undergoes hemodialysis there is a rapid decrease in blood urea, especially in patients who had a markedly elevated BUN prior to the session. This shift lowers the osmolality of the plasma, which creates an osmotic gradient between cells in the plasma and cells of the brain. Water follows this gradient and moves from the plasma into the brain cells, causing cerebral edema.
Another theory for the pathophysiology of DDS is the CO2 theory. Dialysis may involve the creation of a CO2 gradient between the plasma and the CSF, which lowers the pH of the brain tissue. This, in turn, may cause the brain cells to increase in osmolality due to a higher concentration of hydrogen ions and acid radicals. A higher osmolality pulls water into the cell, leading to cerebral edema.
If not prevented or treated, DDS may produce significant increases in intracranial pressure that can lead to brain herniation and death.
Taking care of patients with (and at risk for) DDS
Now that you have a better understanding of what DDS is, let’s go through how we care for these patients using the Straight A Nursing LATTE method.
L: How does the patient LOOK? What are the signs and symptoms of dialysis disequilibrium syndrome?
The signs and symptoms of DDS tend to occur together and soon after dialysis is initiated or completed, though they can occur up to 24 hours later. The key signs/symptoms are headache, blurred vision, dizziness, nausea/vomiting, asterixis and changes in LOC. The patient may be restless, confused, somnolent or even manic. Severe cases of DDS result in seizure, coma and death.
Though not a neurological symptom, it is also believed that DDS is the cause for muscle cramping that can occur toward the end of dialysis treatment.
A: How do you ASSESS a patient for DDS?
Your key assessments as you monitor for DDS will involve keeping a close eye on your patient’s neurological status. Take any complaints of headache, blurred vision, nausea and dizziness seriously. Notice if your patient is becoming more agitated, more somnolent or confused. All of these are signs that DDS could be occurring.
You’ll also want to get a set of VS prior to beginning dialysis, making note of the patient’s blood pressure. A patient experiencing hypertensive crisis is at higher risk for DDS.
T: What TESTS are conducted for DDS?
While there isn’t a specific diagnostic test for disequilibrium syndrome, lab tests that will be conducted for your patient at risk for the condition are:
- BUN – This is a blood test that assesses the amount of urea in the blood. Individuals with markedly high BUN levels (greater than 100 mg/dL) are at greater risk for experiencing DDS.
- Na – Measuring sodium level prior to HD is important since patients with hyponatremia are at higher risk for DDS. Additionally, one of the treatments for DDS will necessitate monitoring Na levels as they can become elevated.
- Serum osmolality – Treatments for DDS can increase serum osmolality, so this may need to be monitored as well.
- Blood glucose – This simple test is conducted to rule out hypoglycemia as the cause for the neurological signs and symptoms
- MRI – Utilized to evaluate the extent of cerebral edema and for the presence of herniation
- CT scan – Conducted to rule out other possible causes for neurological changes
- Lumbar puncture – This test is performed to rule out another cause for the change in neurological status such as meningoencephalitis
- Ammonia level – This blood test may be performed to rule out hepatic encephalopathy as the cause for neurological deterioration.
- EEG – Evaluates the brain for seizure activity
T: What TREATMENTS are provided for DDS?
The most important component of treating DDS is preventing it from occurring. The three key ways we do this is by slowing the dialysate blood flow (which decreases how quickly urea is removed from the bloodstream), shortening the duration of the hemodialysis session, and mitigating osmotic shifts through a process called sodium modeling.
Using the sodium modeling technique, the sodium content of the dialysate changes throughout the duration of the dialysis treatment in an effort to slow the removal of sodium from the bloodstream. This is either done through a machine with a special sodium modeling feature, or changing the dialysate sodium solution.
Another method utilized to prevent DDS is to use a dialysis solution that has a lower concentration of sodium bicarbonate in patients who retain carbon dioxide, such as those with COPD. This is because CO2 is a potent cerebral vasodilator and can lead to increases in intracranial pressure.
Should DDS occur, treatment also involves utilizing sodium modeling with the goal of keeping the patient on dialysis if possible. In many cases, improvements can be seen within 30 minutes and the patient will likely be switched to more frequent dialysis sessions that are shorter in duration and slower in flow rate. If improvement is not seen, additional measures may be necessary.
Additional measures that may be utilized for DDS:
- Administration of hypertonic saline or mannitol (an osmotic diuretic). Both of these fluids will cause fluid to leave the brain cells and reduce cerebral edema.
- Switch the patient to a slow, gentle continuous mode of renal replacement therapy.
- Hyperventilate the patient to remove excess CO2 and reduce intracranial pressure. Note this is only an option in mechanically ventilated patients.
- Manage symptoms such as nausea and restlessness with appropriate pharmacologic measures such as ondansetron and benzodiazepines.
E: How do you EDUCATE a patient about DDS?
- Teach the patient that advances in the way we administer hemodialysis means symptoms, if noted, are usually mild and transient.
- Teach the patient to attend all their dialysis appointments, as missing treatments increases their risk of experiencing DDS.
- Teach the patient to report any neurological symptoms during or after dialysis such as nausea, confusion, headache and muscle twitching.
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