Arterial ammonia concentration determined by point of care testing in acute liver failure; clinical associations and utility in prediction of complications and outcome

Vishal C. Patel, Beatriz Mateos Munoz, Elizabeth Sizer, Charalambos G. Antoniades, Christopher Willars, Georg Auzinger, Julia Wendon, William Bernal

    Research output: Contribution to journalPoster abstractpeer-review


    Background: Though ammonia is implicated as central to the pathogenesis of hepatic encephalopathy (HE) and cerebral edema (CE) in acute liver failure (ALF), there is limited data on the clinical relevance of measurement of its arterial concentration (AAC), and changes with therapeutic interventions. In a very large cohort of patients with ALF we examined the clinical associations of AAC and its utility in the prediction of complications.

    Patients and Methods: Patients with ALF admitted to a single intensive therapy unit (ITU) over a 10 year period were studied. AAC was measured on and after ITU admission using the Point of care (POC) PocketChem BA Blood Ammonia Analyser. Its relation to development of HE, CE and survival was assessed. Changes in AAC following introduction of hemofiltration for renal replacement and after liver transplantation (LT) were examined, as was their relation to progression of HE and development of CE.

    Results: 729 patients of median age 37 years (IQR 28-49) were studied; 59% were female. 413 (57%) had acetaminophen (APAP) and 316 (43%) non-APAP aetiologies. 496 (68%) had or developed HE grade ≥3 (high-grade), in 81 (16%) with evidence of CE. 400 survived with medical management alone, 176 underwent LT and 155 died without LT. Median AAC was 102 (66-156) in those awith high-grade HE and 73 (45-103) in those without (p<0.001). In those admitted without HE, AAC on admission was higher in those who progressed to high-grade (n=97) than those who did not (n=221) 88 (60-146) vs. 65 (43-89) (p<0.001). In patients with high grade HE who developed CE (n=81) AAC was higher than those who did not (n=396) on admission (132 (99-203) vs. 84 (64-144)) and on ITU day 2 (122 (71-156) vs. 82 (61-124)) (both p<0.001). AAC was the best laboratory measure for prediction of HE progression (AUROC 0.730) or the development of CE (AUROC 0.660). In those with HE, AAC did not differ between survivors and non-survivors (87 (56-134) vs.93 (64-145) p=0.16) but did at day 3 (68 (49-101) vs. 98 (66-139) (p<0.001)) In those with high-grade HE, hemofiltration on admission was associated with a median 16% fall in AAC on day 2 as compared to 5% when not treated in this way (p<0.03). LT was associated with a fall in AAC by 70% from 116 (77-170) to 38 (19-55) (p<0.0001). 

    Conclusions: Elevations of AAC, particularly if sustained, relate closely to the development and severity of cerebral complications of ALF. POC testing may assist in the prediction of HE progression and the development of CE. Elevated AAC is rapidly reversed by transplantation and to a lesser degree by standard hemofiltration.
    Original languageEnglish
    Article number729
    Pages (from-to)554A-554A
    Number of pages1
    Publication statusPublished - 2014
    Event65th Annual Meeting of the American-Association-for-the-Study-of-Liver-Diseases - Boston, MA, United Kingdom
    Duration: 7 Nov 201411 Nov 2014


    • Ammonia
    • Acute liver failure


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