Medical Care
The medical care of uremic encephalopathy (UE) includes correcting the metabolic disturbance, which usually requires dialysis (hemodialysis or peritoneal dialysis) or renal transplantation. Symptoms improve as renal function improves.
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Seizures may be treated with anticonvulsants.
These drugs should be administered at lower-than-usual doses to accommodate the low albumin levels observed in chronic renal failure (RF). These low albumin levels can lead to higher levels of unbound anticonvulsant.
The unbound drug is the therapeutically active fraction.
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Emergency treatment of subdural hematoma or intracranial hemorrhage is addressed in other articles.
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Cerebrovascular disease is a significant cause of morbidity and mortality in patients with chronic renal failure. The main causes of ischemic stroke are atherosclerosis and thromboembolic or intradialytic hypotension. Patients with chronic renal failure have a high prevalence of hyperhomocysteinemia, an independent risk factor for atherosclerosis. Most hemodialysis and renal transplant patients are partially refractory to treatment intended to reduce homocysteine levels. Dialysis itself appears to promote the development of arterial disease, perhaps due to oxidative stress. The progression of atherosclerosis is further speculated to be influenced by the use of immunosuppressive agents. Thromboembolic ischemic cerebrovascular accidents may result from cardiac disease (dilated cardiomyopathy, arrhythmia) or artery-to-artery embolism due to severe atherosclerosis.
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Ultrafiltration-related arterial hypotension is a common complication in hemodialysis, especially in older patients with anemia. Severe arterial hypotension can cause cerebral hypoperfusion leading to ischemic stroke in the boundary zones between vascular territories. Treatment consists of fluid repletion.
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Caution must be exercised in administering drugs whose metabolism is affected by impaired renal function because their levels can rise to toxic levels.
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Hypertension and diabetes mellitus can both exacerbate the encephalopathic symptoms. Hypertensive encephalopathy is thought to be caused by vasogenic edema due to impaired cerebrovascular autoregulation, endothelial injury, and elevated plasma concentrations of natriuretic peptides. Hypertensive encephalopathy is thought to occur in 5% of uremic patients. Recombinant human erythropoietin for correction of renal anemia can cause hypertension in up to 35% of patients. Patients with diabetes tend to do worse.
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Infections need to be treated appropriately.
Surgical Care
The role of surgery in managing UE is limited to cases involving renal transplantation, neurosurgical care for subdural hematoma or intracranial hemorrhage, and vascular access.
Consultations
Consultation with the following may prove helpful:
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Specialist in critical care medicine
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Nephrologist
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Vascular surgeon
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Neurosurgeon
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Infectious disease specialist: Bacterial meningitis remains a high cause of mortality in hemodialyzed patients, often because of delay in treatment. [13]
Diet
Patients must maintain a low-salt, low-protein (ie, renal) diet.
Activity
In general, patients with UE are ill, and in the acute phase, their activity is limited to bed rest.
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EEG in a 56-year-old man with uremic encephalopathy. He became increasingly lethargic, requiring intubation. EEG shows absence of a posterior dominant alpha rhythm and diffuse bilateral slowing with mixed theta- and delta-frequency signal. A single sharp wave is present in the left occipital region, phase reversing at O1. From top to bottom: Fp1-F7, F7-T3, T3-T5, T5-O1, O1-O2, O2-T6, T6-T4, T4-F8, F8-Fp2, Fp2-Fp1, F3-C3, C3-P3, P3-O1, F4-C4, C4-P4, P4-O2, Fz-Cz, and ECG.
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EEG in a 56-year-old man with uremic encephalopathy. From top to bottom: Fp1-F7, F7-T3, T3-T5, T5-O1, Fp2-F8, F8-T4, T4-T6, T6-O2, Fp1-F3, F3-C3, C3-P3, P3=O1, Fp2-F4, F4-C4, C4-P4, P4-O2, Fz-Cz, ECG.
