What are the potential causes of dyskinesia in a patient with end-stage renal disease (ESRD) undergoing dialysis?

Dyskinesia in Dialysis Patients: Causes and Evaluation

Dyskinesia in dialysis patients is primarily caused by electrolyte fluctuations (particularly magnesium, calcium, and potassium), uremic toxin accumulation, dialysis disequilibrium syndrome, or medication effects—not true dyskinesia as seen in movement disorders. The term "dyskinesia" in this context typically refers to abnormal involuntary movements that are metabolic or toxic in origin rather than basal ganglia pathology 1.

Primary Metabolic Causes

Electrolyte-Induced Neuromuscular Irritability

The dominant mechanism is electrolyte fluctuations during and after dialysis, creating neuromuscular irritability that manifests as muscle jerking, twitching, or choreiform movements 1.

• Hypomagnesemia occurs in 60-65% of critically ill patients on continuous kidney replacement therapy and is the most commonly overlooked cause of refractory muscle twitching 1

• Target serum magnesium should be ≥0.70 mmol/L (approximately 1.7 mg/dL) 1

• Hypomagnesemia causes refractory hypokalemia and hypocalcemia that cannot be corrected without magnesium replacement first 1

• Hypocalcemia and hypokalemia often coexist with hypomagnesemia and will not respond to replacement unless magnesium is corrected first 1

• The intermittent nature of hemodialysis creates wide swings in potassium, ionized calcium, magnesium, and other divalent ions between treatments 1

• These fluctuations are exacerbated by dialysate composition and variable dietary adherence affecting calcium-phosphate product control 1

Uremic Encephalopathy

• Inadequate dialysis leads to uremia with symptoms including nausea, vomiting, appetite suppression, and neurological manifestations 2
• Decreased ultrafiltration and decreased clearance from inappropriate dialysate dextrose concentration can lead to uremia 2

Dialysis Disequilibrium Syndrome

Dialysis disequilibrium syndrome (DDS) is a rare but serious central nervous system complication caused by rapid removal of urea during hemodialysis, presenting with neurological symptoms including abnormal movements, seizures, and altered mental status 3, 4.

• Common risk factors include extreme age, high blood urea nitrogen, sudden change in dialysis regimen, preexisting neurological diseases, and increased permeability of the blood-brain barrier 4
• DDS can be potentially fatal with poor prognosis when manifesting with serious neurological symptoms like seizures and obtundation 3
• Successful management includes administration of mannitol and 3% hypertonic saline 3

Aluminum Neurotoxicity (Less Common but Critical)

If muscle twitching is accompanied by speech disturbances, personality changes, or occurs shortly after dialysis, consider aluminum neurotoxicity 1.

• Dialysis encephalopathy presents with twitching, myoclonic jerks, and motor apraxia 1
• Plasma aluminum levels are typically 150-350 µg/L in dialysis encephalopathy 1
• Acute aluminum neurotoxicity causes agitation, confusion, myoclonic jerks, and major motor seizures with plasma aluminum 400-1,000 µg/L 1

Medication-Related Dyskinesia

• Drug-induced dyskinesias from dopamine receptor blocking agents (antipsychotics) can occur in dialysis patients, particularly those with psychiatric comorbidities 5
• Almost 9% of all dialysis patients are hospitalized with a mental disorder, with depression, dementia, and drug-related disorders being especially common 6
• Levodopa-induced dyskinesia in Parkinson's disease patients on dialysis can lead to rhabdomyolysis, a life-threatening complication 7

Ischemia-Related Movement Abnormalities

• Intradialytic hypotension occurs in approximately 25% of hemodialysis sessions and can cause cerebral ischemic events manifesting as abnormal movements 8
• Defined as a decrease in systolic blood pressure by ≥20 mm Hg or mean arterial pressure by ≥10 mm Hg, accompanied by symptoms 8

Diagnostic Algorithm

Check electrolytes immediately: magnesium, calcium (ionized if possible), potassium, and phosphate 1.

1. Correct magnesium FIRST if low—use dialysis solutions containing magnesium rather than IV supplementation 1
2. Assess dialysate composition: determine current magnesium, calcium, and potassium concentrations 1
3. Evaluate for uremic symptoms: check adequacy of dialysis clearance (Kt/V) 2
4. Consider aluminum levels if symptoms worsen after dialysis or include speech/cognitive changes 1
5. Review medication list for dopamine blockers, levodopa, or other movement disorder medications 5
6. Assess for DDS risk factors if patient is new to dialysis or had recent regimen changes 4

Critical Management Pitfalls to Avoid

• Do not treat hypokalemia or hypocalcemia without checking and correcting magnesium first—these will be refractory to replacement 1
• Do not give IV magnesium supplementation to patients on dialysis—adjust dialysate composition instead 1
• Do not assume post-dialysis electrolytes are stable—fluctuations continue for 4-5 hours after treatment 1
• Do not overlook aluminum toxicity if symptoms worsen after dialysis or include speech/cognitive changes 1
• Avoid exogenous IV supplementation during dialysis—it carries severe clinical risks 1