Abstract
BackgroundHepatic encephalopathy (HE) is a frequent and severe complication of cirrhosis. A single determination of ammonia in venous blood correlates poorly with neurological symptoms. Thus, a better biological marker is needed.AimTo make a diagnosis of HE, we explored the value of ammonia in capillary blood, an equivalent to arterial blood, measured at bedside following an oral glutamine challenge.MethodsWe included 57 patients (age 56 yrs; M/F: 37/20) with cirrhosis (alcoholic = 42; MELD score 13.8 [7-29], esophageal varices = 38) and previous episodes of HE (n = 19), but without neurological deficits at time of examination, and 13 healthy controls (age 54 yrs). After psychometric tests and capillary (ear lobe) blood ammonia measurements, 20 gr of glutamine was administered orally. Tests were repeated at 60 minutes (+ blood ammonia at 30'). Minimal HE was diagnosed if values were > 1.5 SD in at least 2 psychometric tests. Follow-up lasted 12 months.ResultsThe test was well tolerated (nausea = 1; dizziness = 1). Patients showed higher values of capillary blood ammonia over time as compared to controls (0'-30'-60 minutes: 75, 117, 169 versus 52, 59, 78 umol/L, p < 0.05). At baseline, 25 patients (44%) had minimal HE, while 38 patients (67%) met the criteria for HE at 60 minutes (chi2: p < 0.01). For the diagnosis of minimal HE, using the ROC curve analysis, baseline capillary blood ammonia showed an AUC of 0.541 (CI: 0.38-0.7, p = 0.6), while at 60 minutes the AUC was 0.727 (CI: 0.58-0.87, p < 0.006). During follow-up, 18 patients (31%) developed clinical episodes of HE. At multivariate analysis, the MELD score (1.12 [1.018-1.236]), previous episodes of HE (3.2[1.069-9.58]), but not capillary blood ammonia, were independent predictors of event.ConclusionsIn patients with cirrhosis and normal neurological examination, bedside determination of ammonia in capillary blood following oral glutamine load is well tolerated and achieves a better diagnostic performance for minimal HE than basal capillary ammonia levels. However, capillary blood ammonia is a poor predictor of development of clinically overt HE.
Highlights
Hepatic encephalopathy (HE) is a frequent and severe complication of cirrhosis
Capillary blood ammonia is a poor predictor of development of clinically overt HE
Oral glutamine load and blood ammonia The oral glutamine challenge was completed in all patients and the healthy subjects
Summary
Hepatic encephalopathy (HE) is a frequent and severe complication of cirrhosis. Hepatic encephalopathy (HE) is a common complication of cirrhosis that affects quality of life, increases the risk of accidents, and is an independent predictor of poor outcome [1,2]. Neurological alterations observed in HE are postulated to result from the exposure of the brain to abnormally elevated concentrations of ammonia present in the general circulation in response to liver insufficiency and portosystemic collaterals [6]. High ammonia levels have been associated with large portosystemic collaterals such as esophageal varices in patients with cirrhosis [7]. Ammonia determination is not currently accepted as a reliable marker to identify patients with HE [8]. The pathogenesis of HE is still incompletely elucidated, the ammonia hypothesis remain central [10] and a large number of experimental data support the role of hyperammonemia in the direct and indirect alterations of brain function that characterize HE [11]
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