From the Guidelines
Hepatic encephalopathy is typically associated with elevated blood ammonia levels, with normal serum ammonia ranges from 15-45 μg/dL, and other laboratory values such as elevated bilirubin, AST, ALT, decreased albumin, prolonged prothrombin time (PT) and international normalized ratio (INR), electrolyte abnormalities, and thrombocytopenia. The diagnosis of hepatic encephalopathy involves a combination of clinical findings and laboratory values, including blood ammonia levels, which correlate with the severity of the condition, as stated in the easl clinical practice guidelines on the management of hepatic encephalopathy 1. Key lab values to monitor include:
- Ammonia levels: often elevated due to the liver's inability to convert ammonia to urea
- Liver function tests: such as elevated bilirubin, AST, ALT, and decreased albumin, which indicate liver dysfunction
- Coagulation studies: often show prolonged prothrombin time (PT) and international normalized ratio (INR) due to decreased production of clotting factors
- Electrolyte abnormalities: particularly hyponatremia (sodium <135 mEq/L), can worsen encephalopathy
- Blood glucose: should be monitored as hypoglycemia can occur
- Arterial blood gases: may show respiratory alkalosis due to hyperventilation
- Complete blood count: may reveal thrombocytopenia and anemia According to the kasl clinical practice guidelines for liver cirrhosis, diagnostic tests such as complete blood count, C-reactive protein, chest X-ray, urinalysis and urine culture, blood culture, and diagnostic paracentesis can help identify precipitating factors of hepatic encephalopathy 1. Management includes lactulose and rifaximin to reduce ammonia production, with lactulose administered orally or via nasogastric tube, and an enema solution for severe cases 1. These lab values help diagnose hepatic encephalopathy, assess its severity, guide treatment decisions, and monitor response to therapy.
From the FDA Drug Label
The primary endpoint was the time to first breakthrough overt HE episode. A breakthrough overt HE episode was defined as a marked deterioration in neurological function and an increase of Conn score to Grade ≥2. In patients with a baseline Conn score of 0, a breakthrough overt HE episode was defined as an increase in Conn score of 1 and asterixis grade of 1 Patients had MELD scores of either ≤10 (27%) or 11 to 18 (64%) at baseline. No patients were enrolled with a MELD score of >25. Nine percent of the patients were Child-Pugh Class C
The typical laboratory values associated with Hepatic (Liver) Encephalopathy are not directly stated in the provided text. However, the text mentions the following relevant information:
- MELD scores: ≤10 (27%) or 11 to 18 (64%) at baseline
- Child-Pugh Class: 9% of patients were Class C
- Conn score: used to define breakthrough overt HE episodes, with a score of ≥2 indicating a marked deterioration in neurological function These values are related to the severity of liver disease and hepatic encephalopathy, but they do not provide a direct answer to the question about typical laboratory values associated with Hepatic (Liver) Encephalopathy 2.
From the Research
Laboratory Values for Hepatic Encephalopathy
The typical laboratory values associated with Hepatic (Liver) Encephalopathy include:
- Serum ammonia levels, which remain the diagnostic gold standard 3
- Other laboratory tests, such as electroencephalogram to identify metabolic encephalopathy, or specific abnormalities on cerebral magnetic resonance imagery, may also support the diagnosis 4
Diagnostic Criteria
The diagnosis of Hepatic Encephalopathy is essentially clinical, characterized by various neuropsychiatric symptoms, possibly associated with hyperammonemia 4
- Clinical scales, such as the West-Haven scale, can be used to diagnose overt hepatic encephalopathy 5
- Psychometric tests, such as the PSE-syndrome test, and neurophysiological tests, such as EEG and Critical flicker frequency (CFF), can be used to diagnose minimal hepatic encephalopathy 5
Treatment and Management
The management of Hepatic Encephalopathy is essentially based on treatment of triggering factors, such as ionic disorders or sepsis, and symptomatic therapy with non-absorbable disaccharides (notably lactulose) or polyethylene glycol, possibly combined with rifaximin 4