Lessons from look-back in acute liver failure? A single centre experience of 3300 patients

Bernal, William; Hyyrylainen, Anna; Gera, A; Audimoolam, Vinod K.; McPhail, Mark; Auzinger, G.; Rela, Mohammed; Heaton, Nigel; O’Grady, John; Wendon, Julia; Williams, Roger

doi:10.1016/j.jhep.2013.02.010

Cited by 344 publications

(346 citation statements)

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“…48 However, there have been steady advances in the management of patients with alcohol-related liver disease, endoscopic banding of varices, terlipressin treatment of hepatorenal syndrome, and in intensive care. [74][75][76] There have been steady year-on-year improvements in in-hospital mortality across acute trusts in the UK (figure 8). Baseline data for longer-term survival has been calculated using NHS data supplied by liver units in Southampton, Plymouth, Newcastle, and Sunderland (figure 9).…”

Section: Metric 5·7: Survival Of Alcohol Related Liver Disease Admissmentioning

confidence: 99%

New metrics for the Lancet Standing Commission on Liver Disease in the UK

et al. 2017

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Section: Metric 5·7: Survival Of Alcohol Related Liver Disease Admissmentioning

confidence: 99%

New metrics for the Lancet Standing Commission on Liver Disease in the UK

et al. 2017

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“…This mirrored a fall in the markers of disease severity on intensive care admission reflecting earlier recognition, improved care, and use of salvage emergency liver transplantation. 4 In patients with CLF, the symptoms of HE tend to be far less severe and occur insidiously in keeping with the chronic nature of this disease. Factors such as sepsis, upper gastrointestinal bleeding, constipation or electrolyte disturbances, can precipitate the clinical decompensation of pre-existing cirrhosis and may lead to the development of organ dysfunction; a state sometimes referred to as acute-on-chronic liver failure (AoCLF).…”

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Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

Aldridge

Tranah

Shawcross

2015

Journal of Clinical and Experimental Hepatology

224

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The syndrome we refer to as Hepatic Encephalopathy (HE) was first characterized by a team of Nobel Prize winning physiologists led by Pavlov and Nencki at the Imperial Institute of Experimental Medicine in Russia in the 1890's. This focused upon the key observation that performing a portocaval shunt, which bypassed nitrogen-rich blood away from the liver, induced elevated blood and brain ammonia concentrations in association with profound neurobehavioral changes. There exists however a spectrum of metabolic encephalopathies attributable to a variety (or even absence) of liver hepatocellular dysfunctions and it is this spectrum rather than a single disease entity that has come to be defined as HE. Differences in the underlying pathophysiology, treatment responses and outcomes can therefore be highly variable between acute and chronic HE. The term also fails to articulate quite how systemic the syndrome of HE can be and how it can be influenced by the gastrointestinal, renal, nervous, or immune systems without any change in background liver function. The pathogenesis of HE therefore encapsulates a complex network of interdependent organ systems which as yet remain poorly characterized. There is nonetheless a growing recognition that there is a complex but influential synergistic relationship between ammonia, inflammation (sterile and non-sterile) and oxidative stress in the pathogenesis HE which develops in an environment of functional immunoparesis in patients with liver dysfunction. Therapeutic strategies are thus moving further away from the traditional specialty of hepatology and more towards novel immune and inflammatory targets which will be discussed in this review. ( J CLIN EXP HEPATOL 2015;5:S7-S20) H epatic encephalopathy (HE) is the term used to encapsulate the broad spectrum of neuropsychiatric disturbances associated with both acute and chronic liver failure (ALF and CLF, respectively), as well as porto-systemic bypass in the absence of hepatocellular disease. The clinical manifestations of HE can be extremely heterogeneous in nature, with symptoms presenting anywhere on a continuum spanning from seemingly normal cognitive performance, right the way through to states of confusion, stupor and coma. In between these extremes, patients with HE may exhibit signs such as inattentiveness, blunted affect, impairment of memory or reversal of the sleep-wake cycle, as well as physical manifestations such as tremor, myoclonus, asterixis and deep tendon hyperreflexia.ALF is defined by the onset of coagulopathy alongside any degree of encephalopathy in patients with no evidence of pre-existing liver disease. 1 The presence of HE in those with ALF is prognostic, with up to a quarter of cases developing raised intracranial pressure. 2 Patients presenting with ALF are at risk of developing its cardinal, lifethreatening feature, cerebral edema. Left untreated, cerebral edema can rapidly progress to cause herniation of the uncus through the falx cerebri, leading to compression of the brainstem and, ultimately, death. H...

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“…This may be due to earlier recognition of the severity of the disease, leading to better medical care and use of salvage emergency transplant. 2,13,14 The brain lacks an effective urea cycle, thus leaving the removal of ammonia exclusively to the glutamate synthetase in the astrocytes. In ALF, the brain edema is primarily cytotoxic in nature, resulting from astrocyte swelling.…”

Section: Correct Answers: D and Ementioning

confidence: 99%