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Portal-Systemic Encephalopathy Workup

  • Author: Gagan K Sood, MD; Chief Editor: BS Anand, MD  more...
Updated: Dec 18, 2014

Laboratory Studies

Studies include the following:

  • Serum calcium
  • Serum ammonia, preferably arterial
  • Elevated blood levels are not diagnostic of hepatic encephalopathy, and normal levels do not rule out hepatic encephalopathy. Very high levels may suggest an unsuspected urea cycle enzyme deficiency. They are helpful to suggest a diagnosis of hepatic encephalopathy when the cause is obscure.
  • Serum glucose
  • Serum albumin
  • Serum aspartate aminotransferase: A very high aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT) level (eg >1000) may suggest widespread hepatic necrosis as a consequence of acetaminophen toxicity and may help guide appropriate diagnostic evaluations and therapy accordingly (with acetaminophen levels and N -acetylcysteine). However, very high AST and ALT values may be observed in other settings (notably ischemic hepatitis and other causes of submassive or massive hepatic necrosis) and, therefore, are not specific.
  • Serum alanine aminotransferase: ALT is more specific for liver origin because AST also may be released from muscle.
  • Serum bilirubin
  • Complete blood cell (CBC) count
  • Blood and urine screen for drugs
  • Blood alcohol level
  • Serum electrolytes: levels may be disturbed for a variety of reasons in patients with advanced liver disease. Hyponatremia resulting from diuretic use, renal failure, water intoxication, or the syndrome of inappropriate secretion of antidiuretic hormone is particularly important to consider as a contributing cause of encephalopathy.
  • Serum transaminases: This measurement is useful as an index of hepatocellular inflammation, although a poor correlation exists with respect to hepatocellular function. Very high transaminase values (eg, >500 U/L) suggest the possibility of acute hepatitis of indeterminate etiology, and, in the context of encephalopathy, consider the possibility of FHF.
  • Prothrombin time, albumin, and bilirubin: Measurements are true liver function tests that provide an estimate of the severity of liver damage. They also allow the clinician to anticipate certain potential complications (eg, bleeding) and adjust therapy appropriately.

Imaging Studies

See the list below:

  • Computed tomography scan of the head
    • The rationale for CT scan is to exclude structural considerations in the differential diagnosis, including intracranial hemorrhage (epidural, subdural, subarachnoid, intraparenchymal), cerebral infarct, intracranial infections (brain abscess with mass effect, meningoencephalitis), and hydrocephalus.
    • CT scan of the head may not be necessary in patients with well-documented liver disease and a typical history, especially if no focal or localizing signs are evident. However, if the circumstances leave any doubt, then CT scan is critical in helping exclude structural causes for encephalopathy.
    • This test is more widely available than MRI and generally can be performed more rapidly. Therefore, it is the imaging modality of first choice in most instances.
    • Patients may develop portosystemic encephalopathy and subsequently sustain head trauma. This is particularly common among patients with alcoholism, and the event may not be volunteered upon taking the history or may not be evident upon physical examination. However, in uncomplicated portosystemic encephalopathy, no characteristic clues or findings are present.
  • Magnetic resonance imaging
    • The availability and speed with which CT scans can be performed make them preferable in most instances for helping exclude mass lesions and, especially, intracranial hemorrhage. However, MRI findings may be of particular value in cases in which a diagnosis is not clear-cut based on other clinical and laboratory data.
    • The presence of hyperintense-appearing regions on T1-weighted MRI studies of the brains of patients with cirrhosis is described as a characteristic feature. The increased MRI signal intensity may be the result of Mn deposition in these structures.
    • The globus pallidus, putamen, and caudate nucleus of the basal ganglia and the frontal and occipital cortex of patients with cirrhosis who died with hepatic encephalopathy are demonstrated to contain increased Mn concentrations when compared to matched control specimens. Pallidal hyperintensity on T1-weighted MRI does not appear to be present in well-compensated patients with cirrhosis who do not have hepatic encephalopathy. This finding appears to correlate with blood ammonia levels but not the severity of hepatic encephalopathy itself.
    • The amount of Mn deposition that can be identified at autopsy following hepatic coma appears to be independent of patient age, etiology of cirrhosis, or the presence of chronic hepatic encephalopathy. In an experimental model using both cirrhotic and portacaval-shunted rats, Mn levels in the basal ganglia were significantly elevated above control values. These levels also were significantly higher in portacaval-shunted rats when compared to those with experimental cirrhosis; therefore, while the precise etiology responsible for Mn deposition is unclear, it is enhanced by portal hypertension.
    • Therefore, signs of extrapyramidal toxicity in hepatic encephalopathy conceivably may result from Mn deposition. The neurologic and radiologic changes may resolve gradually with time following liver transplantation. Deposition of Mn also may potentiate the effects of BZPs, natural or otherwise, by increasing the number of available peripheral-type BZP binding sites (possibly by promoting receptor expression).
    • These intriguing issues unveiled by the advent of MRI are complemented by metabolic data derived from the application of MRS. This technique has demonstrated findings of altered glutamine metabolism. Its role in clinical evaluation and management of hepatic encephalopathy is unclear. In one series, MRS findings (ie, decreased myoinositol, increased glutamine) correlated poorly with neurological status. These markers were suggested to be more representative of the underlying chronic hepatic dysfunction.
  • Positron emission tomography scanning has demonstrated reduced metabolic activity for glucose utilization in the parietal cortex of patients with cirrhosis with mild hepatic encephalopathy. At present, this technique is best reserved for research applications because no clear clinical guidelines are available for its use and its availability is limited.

Other Tests

See the list below:

  • Psychometric testing
    • Psychometric evaluations are of value for establishing the diagnosis and perhaps for monitoring response to therapy in subclinical portosystemic encephalopathy. The number-connection test and the Trail-Making Test are pragmatic approaches and are used widely at the bedside.
    • More formal testing may not be feasible with many patients, in part due to the length of time taken to administer the tests, and also because of uncooperativeness. However, the results of psychometric testing in subclinical portosystemic encephalopathy may be of prognostic value independent of the Child-Pugh score of disease severity.
    • Patients with alcohol-induced liver disease exhibit poorer test scores than those with liver disease from other causes, presumably due to cerebral toxicity intrinsic to chronic alcohol use and independent of the hepatic insufficiency.
    • A grading scheme that incorporates the level of consciousness, personality and intellect, neurologic signs, and electroencephalogram (EEG) abnormalities is proposed for hepatic encephalopathy. The clinical portion of this grading approach has the advantage of being easily administered at the bedside, and it is helpful as a guide to progress.
  • Electroencephalography
    • EEG studies of patients in portosystemic encephalopathy grades 1-3 may demonstrate high voltage and low-frequency triphasic waves of 1-3 Hz. These also may be seen in uremia but are characteristic of hepatic encephalopathy. With progression to coma, the EEG typically shows delta-wave activity, representing a generalized slowing of the cortex, a nonspecific pattern seen in toxic and metabolic encephalopathies.
    • The EEG is most helpful in excluding the presence of other causes for encephalopathies, such as status epilepticus and akinetic seizures, or the demonstration of postictal slowing with or without focal spike and wave activity that suggests prior seizures.
    • EEG monitoring frequently is useful in assisting with the diagnosis of hepatic encephalopathy, especially subclinical hepatic encephalopathy. Computer-assisted or spectral EEG analysis may demonstrate characteristic abnormalities, but the incremental benefit over conventional EEG is unclear.
  • Evoked potentials
    • Further electrophysiologic assessment may be performed with evoked-potential studies, but whether this approach is of value remains unclear, except when significant doubt exists with respect to the underlying diagnosis of portosystemic encephalopathy as the cause for neuropsychiatric dysfunction. This is rarely the case in practice. These studies include visual-evoked potentials, somatosensory-evoked potentials, or brainstem auditory–evoked potentials, and they represent the externally recorded voltage from synchronous firing of neurons in a network response to specific stimuli.
    • The chief value of this approach may be to document abnormal cortical function in subclinical portosystemic encephalopathy and establish the diagnosis. Brainstem auditory–evoked responses appear particularly sensitive as a marker of perturbed cortical function. Evoked-potential studies in acute hepatic encephalopathy conceivably may be useful for monitoring clinical response to treatment; however, the use of these electrophysiologic diagnostic modalities currently is not widespread.

Histologic Findings

In neuropathological studies of hepatic encephalopathy, Alzheimer type II astrocytosis is typical and likely represents the end result of these mechanisms. Astrocytes demonstrate swollen nuclei, margination of the chromatin, and a prominent nucleolus.

Contributor Information and Disclosures

Gagan K Sood, MD Associate Professor, Department of Medicine and Surgery, Baylor College of Medicine

Gagan K Sood, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association

Disclosure: Nothing to disclose.

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.

Noel Williams, MD, FRCPC FACP, MACG, Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada

Noel Williams, MD, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

Ann Ouyang, MBBS Professor, Department of Internal Medicine, Pennsylvania State University College of Medicine; Attending Physician, Division of Gastroenterology and Hepatology, Milton S Hershey Medical Center

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthor, Blake A Jones, MD, to the development and writing of this article.

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