Neurology of Uremia
CASE
A 64-year-old man with end-stage renal failure tells you that at night his legs “bother him.” Just after he lies down in bed, his legs feel “odd,” and he has to get up and walk. He can’t quite put the feeling into words, but it keeps him from having a restful sleep.
Diagnosis
Restless leg syndrome, associated with renal disease.
Patients with impaired renal function have a variety of neurologic problems. They are at a higher risk of mental status changes, peripheral neuropathy, neurologic infection, and other manifestations of their underlying disease state.
MENTAL STATUS CHANGES
One of the most common features of renal failure is an altered mental status. It may range from irritability and difficulty concentrating (e.g., performing “serial 7s”), to psychotic reactions or coma.
Mental status changes in uremia fluctuate; periods of confusion are interspersed with periods of lucidity. Acute changes in mental status generally are encountered after dialysis, when there have been rapid electrolyte shifts; although actual electrolyte values are improved (“dysequilibrium syndrome”). Metabolic shifts in brain pH or urea often lag behind the changes in the blood values. Slowly developing renal failure causes fewer cognitive changes than does rapidly developing failure. Acute uremia may be accompanied by tremor, fasciculations, myoclonus, chorea, or convulsions. Patients undergoing dialysis are at risk for complex partial status epilepticus, and patients with an unexplained encephalopathy should have an electroencephalogram (EEG).
EEG changes are usual with an altered mental status, and slowing usually parallels the degree of metabolic encephalopathy.
Most patients with a blood urea nitrogen level higher than 60 mg/100 mL have EEG abnormalities (generalized slowing). With complex partial status, continuous focal seizure activity or rhythmic slowing may be seen.
Most patients with a blood urea nitrogen level higher than 60 mg/100 mL have EEG abnormalities (generalized slowing). With complex partial status, continuous focal seizure activity or rhythmic slowing may be seen.
Although most mental status changes in uremia are not secondary to treatable nervous system disease, keep other possibilities in mind:
Infection. Listeria, fungal, or other central nervous system (CNS) pathogens are not uncommon in patients with uremia. When there is unexplained confusion or fever in the patient with uremia, after performing a CT scan or magnetic resonance imaging (MRI) to rule out subdural hematoma or other mass lesion, perform a lumbar puncture (LP). Remember to do an India ink preparation for Cryptococcus or test for cryptococcal antigen if there are cells in the cerebrospinal fluid (CSF) (see Chapter 30).
Subdural hematoma. Patients with uremia have an increased bleeding tendency, and subdural collections may develop with mild head trauma or during dialysis. If a subdural hematoma is suspected because of lateralizing signs or persistent lethargy with headache, obtain a CT or MRI scan.
Hypertensive encephalopathy. Hypertension frequently accompanies uremia, and hypertensive crisis may mimic the clinical features of uremic encephalopathy. Look for markedly elevated blood pressure, papilledema, and retinal hemorrhages. MRI changes that are bilateral, subcortical, and suggestive of edema may be dramatic, and are reversible with resolution of the hypertensive encephalopathy. Patients with cyclosporine toxicity may be especially sensitive to mild hypertension, which can cause a reversible posterior hemisphere leukoencephalopathy (otherwise known as PRESS, posterior reversible encephalopathy syndrome). Clinically, these patients present with confusion, lethargy, and visual symptoms. They respond to lowering blood pressure and withholding cyclosporine.Related posts:
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