Uremic Encephalopathy Workup: Laboratory Studies, Imaging Studies, Other Tests

Laboratory Studies

See the list below:

• Electrolytes, BUN, creatinine, and glucose
  • Markedly elevated BUN and creatinine levels are seen in uremic encephalopathy.
  • Obtain serum electrolyte and glucose measurements to rule out hyponatremia, hypernatremia, hyperglycemia, and hyperosmolar syndromes as the cause of encephalopathy.
• Obtain a complete blood cell count to detect leukocytosis, which may suggest an infectious cause and determine whether anemia is present. (Anemia may contribute to the severity of mental alterations.)
• Obtain serum calcium, phosphate, and PTH levels to determine the presence of hypercalcemia, hypophosphatemia, and severe hyperparathyroidism, which cause metabolic encephalopathy.
• Serum magnesium levels may be elevated in a patient with renal insufficiency, particularly if the patient is ingesting magnesium-containing antacids. Hypermagnesemia may manifest as encephalopathy.
• Order a toxicology screen in all patients.
• Medication levels
  • Determine drug levels because medications may accumulate in patients with kidney failure and contribute to encephalopathy (eg, digoxin, lithium).
  • Some medications cannot be detected and are excreted by the kidney. These may also accumulate in patients with kidney failure, resulting in encephalopathy (eg, penicillin, cimetidine, meperidine, baclofen).

Imaging Studies

See the list below:

• Severe symptoms
  • Obtain an MRI or head CT scan for a uremic patient who presents with severe neurologic symptoms to rule out structural abnormalities (eg, cerebrovascular accident, intracranial mass, subdural hematoma).
  • A CT scan does not demonstrate any characteristic findings for uremic encephalopathy.
  • Typical MRI findings include increased signal intensity either in the cerebral cortex or in the basal ganglia.
• With milder symptoms, initially treat the patient with dialysis and observe for neurologic improvement.

Other Tests

See the list below:

• Electroencephalogram
  • An EEG is commonly performed on patients with metabolic encephalopathy. Findings typically include the following: (1) slowing and loss of alpha frequency waves, (2) disorganization, and (3) intermittent bursts of theta and delta waves with slow background activity.
  • Reduction in frequency of EEG waves correlates with the decrease in renal function and the alterations in cerebral function. After the initial period of dialysis, clinical stabilization may occur while the EEG findings do not improve. Eventually, EEG results move toward normal.
  • Aside from the routine EEG, evoked potentials (EPs) (ie, EEG signals that occur at a reproducible time after the brain receives a sensory stimulus [eg, visual, auditory, somatosensory]) may be helpful in evaluating uremic encephalopathy.
  • Chronic renal failure prolongs latency of the cortical visual-evoked response. Auditory-evoked responses are generally not altered in uremia, but delays in the cortical potential of the somatosensory-evoked response do occur.
• Cognitive function tests: Several cognitive function tests are used to evaluate uremic encephalopathy.
  • Uremia may result in worse performance on the trail-making test, which measures psychomotor speed; the continuous memory test, which measures short-term recognition; and the choice reaction time test, which measures simple decision making.
  • Alterations in choice reaction time appear to correlate best with renal failure.

Procedures

See the list below:

• Lumbar puncture
  • Lumbar puncture is not routinely performed; however, it may be indicated to find other causes of encephalopathy if a patient's mental status does not improve after initiation of dialysis.
  • No specific CSF finding indicates uremic encephalopathy.

Treatment & Management

James W Lohr, MD Professor, Department of Internal Medicine, Division of Nephrology, Fellowship Program Director, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, Central Society for Clinical and Translational Research

Disclosure: Partner received salary from Alexion for employment.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Ajay K Singh, MB, MRCP, MBA Associate Professor of Medicine, Harvard Medical School; Director of Dialysis, Renal Division, Brigham and Women's Hospital; Director, Brigham/Falkner Dialysis Unit, Faulkner Hospital

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Acknowledgements

Donald A Feinfeld, MD, FACP, FASN Consulting Staff, Division of Nephrology and Hypertension, Beth Israel Medical Center

References

1. Bolton CF, Young GB. Encephalopathy of chronic renal failure. Neurological Complications of Renal Disease. 1990. 49-74.
2. Brouns R, De Deyn PP. Neurological complications in renal failure: a review. Clin Neurol Neurosurg. 2004 Dec. 107(1):1-16. [Medline].
3. Arieff AI. Nervous system manifestations of renal failure. Schrier RW, ed. Diseases of the Kidney. Lippincott; 2007. 2460-2482.
4. Seifter JL, Samuels MA. Uremic encephalopathy and other brain disorders associated with renal failure. Semin Neurol. 2011 Apr. 31(2):139-43. [Medline].
5. Biasioli S, D'Andrea G, Feriani M, Chiaramonte S, Fabris A, Ronco C, et al. Uremic encephalopathy: an updating. Clin Nephrol. 1986 Feb. 25(2):57-63. [Medline].
6. Biasioli S. Neurologic aspects of dialysis. Nissenson A, Fine R, eds. Clinical Dialysis. 2005. 855-876.
7. Moe SM, Sprague SM. Uremic encephalopathy. Clin Nephrol. 1994 Oct. 42(4):251-6. [Medline].
8. Deguchi T, Isozaki K, Yousuke K, Terasaki T, Otagiri M. Involvement of organic anion transporters in the efflux of uremic toxins across the blood-brain barrier. J Neurochem. 2006 Feb. 96(4):1051-9. [Medline].
9. De Deyn PP, Vanholder R, Eloot S, et al. Guanidino compounds as uremic (neuro)toxins. Semin Dial. 2009 Jul-Aug. 22(4):340-5. [Medline].
10. Liu M, Liang Y, Chigurupati S, Lathia JD, Pletnikov M, Sun Z, et al. Acute kidney injury leads to inflammation and functional changes in the brain. J Am Soc Nephrol. 2008 Jul. 19(7):1360-70. [Medline].
11. Nomoto K, Scurlock C, Bronster D. Dexmedetomidine controls twitch-convulsive syndrome in the course of uremic encephalopathy. J Clin Anesth. 2011 Dec. 23(8):646-8. [Medline].
12. Yamamoto T, Satomura K, Okada S, et al. Risk factors for neurological complications in complete hemolytic uremic syndrome caused by Escherichia coli O157. Pediatr Int. 2009 Apr. 51(2):216-9. [Medline].
13. Schmidt M, Sitter T, Lederer SR, Held E, Schiffl H. Reversible MRI changes in a patient with uremic encephalopathy. J Nephrol. 2001 Sep-Oct. 14(5):424-7. [Medline].