• Dialysis

    July 25, 2022 admin

    Can Hemodialysis Cause Seizures

    Seizures among hemodialysis patients:

    Seizures are common among hemodialysis patients. Seizures in hemodialysis patients can have a variety of causes. Seizures usually occur during or shortly after hemodialysis because of the hemodynamic and biochemical changes that occur during the procedure.
    This topic discusses the causes and treatment of seizures in hemodialysis patients. The treatment of seizures in patients who do not have kidney failure is discussed elsewhere.



    The evaluation of a new-onset seizure is similar to that of non-dialysis patients. End-stage kidney disease (ESKD) or hemodialysis treatment can result in the following complications: uremic encephalopathy, dialysis dysequilibrium syndrome (DDS), intradialytic hemodynamic instability, aluminum-associated dialysis dementia, air embolism, hypoglycemia, hypocalcemia, and hyponatremia.

    Other causes of seizures in hemodialysis patients are similar to those in the general population, but may be more common. Cerebrovascular disease (infarction, cerebral emboli [distinct from infarction because dialysis vascular access can lead to infections and septic emboli], haemorrhage, and subdural hematoma) is a major concern in the hemodialysis population. Because of their significantly reduced clearance, patients on hemodialysis are more vulnerable to drug-induced seizures with certain drugs such as carbapenem and ertapenem when compared to patients who are not on dialysis. The following sections go over the most common causes of seizures in the dialysis population. Some are unrelated to dialysis, while others are a direct result of the procedure.

    Uremic encephalopathy:

    Central nervous system (CNS) dysfunction is seen in patients with severe, untreated uremia but not in patients receiving maintenance hemodialysis unless multiple treatments are missed. Irritability and restlessness are common symptoms, as are seizures, coma, and death. Seizures are most commonly generalised and occur prior to dialysis, frequently prompting the start of emergent dialysis. CNS dysfunction resolves within days to weeks of starting adequate kidney replacement therapy.

    Dialysis disequilibrium syndrome (DDS):

    Dialysis disequilibrium syndrome (DDS) can occur in severely uremic patients who are starting hemodialysis for the first time, but it rarely occurs in patients on maintenance hemodialysis. DDS is distinguished by a range of neurologic symptoms. Symptoms usually appear during or immediately after hemodialysis. Headache, nausea, disorientation, restlessness, blurred vision, and asterixis are common early symptoms. Patients who are more severely affected develop confusion, seizures, coma, and even death. However, DDS includes many milder dialysis-related signs and symptoms, such as muscle cramps and dizziness that develop near the end of a dialysis treatment.

    Toxins or drugs:

    Toxins or drugs Many medications in the general population can cause seizures (table 1). Patients on hemodialysis are especially vulnerable to certain drugs due to decreased clearance:
    1. Antibiotics such as penicillin, cephalosporins, carbapenem, and ertapenem, especially when given in high doses
    2. Meperidine (due to toxic metabolite accumulation, normeperidine)
    3. Metoclopramide
    4. Theophylline
    5. L-dopa
    6. Lithium
    7. Acyclovir
    8. Iodinated contrast material administered intravenously (IV) (in high doses)
    In dialysis patients, star fruit consumption can result in severe neurologic dysfunction, including seizures and death.

    Dialysis dementia:

    Dialysis dementia is a progressive neurologic disorder that occurs exclusively in dialysis patients and can manifest as seizures. Aluminum exposure is the root cause. Because of improved hemodialysis water treatment and the use of non-aluminum-containing phosphate binders for chronic hyperphosphatemia management, the incidence of dialysis dementia has significantly decreased.

    Immediate management of seizures:

    The emergency treatment of seizures in dialysis patients includes the following:
    • Stop dialysis and begin IV fluid and oxygen infusion if necessary.
    • Keep the vascular access safe during the seizure.
    • Ascertain that the patient is in a safe environment and is not in danger of injury (eg, fall risk). Place the patient on their side if possible, during the seizure. During an active seizure, do not put anything in their mouth.
    • Although most seizures last less than five minutes and spontaneously resolve, (if hemodialysis is performed in an outpatient clinic) or a rapid response (if hemodialysis is performed in a hospital setting) should be called in most cases.
    • If a patient continues to seize, paramedics or the rapid response team must protect the patient’s airway and stabilise the patient. The first-line treatment is IV benzodiazepines to stop the ongoing seizure activity. A clinician should then evaluate the patient to determine the best course of treatment (eg, with IV antiseizure medications)

    Serum levels of glucose, calcium, sodium, magnesium, and other electrolytes should be measured in blood, as significant abnormalities may indicate the underlying cause of the seizure. If hypoglycemia is suspected, IV glucose and IV thiamine should be administered, especially in at-risk individuals (eg, history of heavy alcohol use).


    Once the patients have been treated for seizure and dialysis has been discontinued, the seizure evaluation for patients on dialysis is the same as for other patients. Uremia, subdural hematoma, metabolic disturbances (hyponatremia, hypoglycemia), and drug-induced encephalopathy are all potential causes that should be ruled out. Furthermore, seizure causes that are not specific to dialysis patients must be ruled out.


    Seizure prevention is directed at specific causes.

    Causes specific:

    Uremic encephalopathy – Progressive uremic encephalopathy is a clear indication that dialysis should begin. Seizures are avoided by starting dialysis before the onset of mental status changes.

    Dialysis disequilibrium syndrome – Dialysis disequilibrium syndrome (DDS) is avoided by limiting the reduction in blood urea nitrogen (BUN) per treatment so that it is gradual and spread out over several days. This treatment prevents seizures but may not prevent mild symptoms like headaches and malaise.

    Erythropoietin therapy – Avoiding rapid increases in haemoglobin is the most important measure to prevent erythropoiesis-stimulating agent (ESA)-induced seizures. The optimal haemoglobin target, dosing, and route of administration are all discussed elsewhere.

    Dialysis-induced hypotension – A variety of manoeuvres are used to prevent dialysis hypotension. This is covered separately.


    Antiseizure medications are used for the same reasons in hemodialysis patients as they are in the general population. Long-term antiseizure medication therapy may not be necessary if the patient’s seizure is caused by a reversible cause.

    Medication selection:

    Among hemodialysis patients who are chosen for antiseizure medication, the choice of a specific medication is influenced by a number of factors, and no single antiseizure medication is clearly the most effective or well tolerated.

    We usually use levetiracetam for most hemodialysis patients. Levetiracetam is generally well tolerated, inexpensive due to the availability of generic forms, and has few drug-drug interactions. If levetiracetam is used, the recommended daily dose is 500 to 1000 mg, with an additional dose of 250 to 500 mg administered at the end of dialysis.

    A variety of other agents are effective. Lacosamide is an alternative that could be used. Lacosamide also has few interactions with other drugs, including immunosuppressive medications.

    We generally do not use phenytoin or valproic acid in hemodialysis patients unless the patient is already stable on one of these medications prior to starting hemodialysis. Phenytoin and valproic acid have numerous drug-drug interactions and have a higher rate of side effects.


    Dialysis removes many of the newer and more commonly used antiseizure medications. To prevent recurrent seizures in patients receiving a dialyzable antiseizure medication, the dosing regimen must be adjusted to avoid a subtherapeutic plasma level during or after dialysis, which could result in a seizure. Many antiseizure medications require dose adjustments based on the severity of kidney impairment, as detailed in the table for the most commonly prescribed antiseizure medications. The following drugs are removed in varying degrees by dialysis and must be supplemented to maintain therapeutic levels:
    • Levetiracetam
    • Lacosamide
    • Topiramate
    • Zonisamide
    • Lamotrigine
    • Primidone and phenobarbital
    • Gabapentin
    • Oxcarbazepine, carbamazepine

    We time the doses for patients on any of these agents so that the medication is administered at the end of each dialysis treatment. Another option is to administer an extra dose at the end of each dialysis session.

    Dialysis of carbamazepine and oxcarbazepine is minimal. However, even a small amount dialyzed out can cause a decrease in concentration. The strain of hemodialysis, combined with a slight drop in concentration, can lower the seizure threshold.

    We do not use long-acting formulations. An extended-release formulation will take longer to achieve a therapeutic concentration if given as a supplemental dose after dialysis.

    Some medications, such as phenytoin and valproic acid, are not dialyzed and therefore do not require postdialysis supplementation. As a result, phenytoin and valproic acid are commonly used among hemodialysis patients. However, as previously stated, these agents are less commonly used today in comparison to newer agents.

    Serum levels in patients taking phenytoin or valproic acid must be carefully interpreted. Phenytoin and valproic acid are highly protein bound, and the relationship between free and total drug concentrations is unpredictable. There is displacement of the drug from serum proteins with an increase in the volume of distribution in patients with hypoalbuminemia (which is very common in those with end-stage kidney disease [ESKD]).

    As a result, the patient has the same concentration of free drug (which has the pharmacologic effect) in serum while having a lower total blood concentration than a subject with normal kidney function and no hypoalbuminemia. If available, free levels should be monitored rather than total levels.

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