The impact of organ dysfunction in cirrhosis: Survival at a cost?

Shawcross, Debbie L.; Austin, M; Abeles, R.D.; McPhail, Mark; Yeoman, Andrew D.; Taylor, Nicholas; Portal, A; Jamil, Khaleel; Auzinger, G.; Sizer, Elizabeth; Bernal, William; Wendon, Julia

doi:10.1016/j.jhep.2011.12.014

Cited by 59 publications

(45 citation statements)

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“…However, the acceptance of cirrhotic patients in ICU has been hampered by their high mortality, high costs per admission, and scarcity of ICU beds (5-7). As improved management of these patients led to improved outcomes in the intensive care setting, the refusal of admission of ACLF patients to an ICU may no longer be justifiable (6,8). Evidence on whom and when to transfer to an ICU is sparse, but recently it has been argued that ACLF should be managed in these units (9).…”

Section: Introductionmentioning

confidence: 99%

CLIF-C ACLF score is a better mortality predictor than MELD, MELD-Na and CTP in patients with Acute on Chronic Liver Failure admitted to the ward

et al. 2017

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Background and aims: Acute-on-chronic liver failure (ACLF) is a frequent syndrome associated with high mortality. The aims of the present study are: a) comparing the Chronic Liver Failure Consortium (CLIF-C) ACLF Model for End-Stage Liver Disease (MELD), MELD Sodium (MELD-Na) and Child-TurcottePugh (CTP) scores for prediction of short/medium term mortality; b) identifying ACLF prevalence in patients admitted to the ward; and c) comparing mortality between non-ACLF/ACLF.Methods: Retrospective cohort study of 177 patients admitted to the Gastroenterology ward for acute decompensation of cirrhosis.Results: We included 132 males. Alcohol was the cirrhosis cause/co-factor in 79.7% of cases. Infection was present in 40.7%. At admission, 19.8% of patients presented ACLF and 7.9% developed it during hospitalization (overall prevalence was 27.7%). ACLF grade 1 was diagnosed in 55.1% of the ACLF patients; grade 2, in 42.8%, and grade 3, in 2.0%. Infection (p < 0.001) and hepatic encephalopathy (p = 0.004) were more prevalent and C-reactive protein and leukocyte counts were higher in ACLF patients. ACLF 28 and 90-day mortality was 45.8% and 60.4%, respectively. The CLIF-C ACLF score was significantly superior to CTP, MELD, MELD-Na in predicting 28-day (AUROC 0.799 ± 0.078, 95% CI 0.637-0.891) and 90-day mortality (AUROC 0.828 ± 0.063, 95% CI 0.705-0.952).Conclusion: ACLF is highly prevalent in the ward. The new CLIF scores identify high mortality cirrhotic patients admitted to the ward and are better than their predecessors to predict ACLF patients' short/medium term mortality.

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Section: Introductionmentioning

confidence: 99%

CLIF-C ACLF score is a better mortality predictor than MELD, MELD-Na and CTP in patients with Acute on Chronic Liver Failure admitted to the ward

et al. 2017

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“…5 Great emphasis is put on actively seeking out and treating any precipitating factors in patients with cirrhosis presenting with overt HE, so as to minimize their risk of developing potentially fatal complications. 6 Minimal hepatic encephalopathy (MHE) cannot, by definition, be detected by the clinician alone, and its diagnosis therefore hinges on detailed assessment of the patient's history and comprehensive examination of the neurologic system, as well as formal psychometric testing. 7 It has therefore recently been redefined as covert HE.…”

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confidence: 99%

Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

Aldridge

Tranah

Shawcross

2015

Journal of Clinical and Experimental Hepatology

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248

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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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“…There has been growing interest in critically ill patients with cirrhosis due to the increased use of novel therapies. [5][6][7]9 Some patients in the final stages of cirrhosis, or those who have multiple-organ failure, can survive only for a short period of time, even when these patients receive supportive care in the ICU. 10 Furthermore, a number of studies have reported that the widespread use of health care has been associated with a high mortality in the ICU.…”

Section: Introductionmentioning

confidence: 99%

A modified prognostic score for critically ill patients with cirrhosis: An observational study

Bao

Wang

et al. 2016

J of Gastro and Hepatol

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The impact of organ dysfunction in cirrhosis: Survival at a cost?

Cited by 59 publications

References 36 publications

CLIF-C ACLF score is a better mortality predictor than MELD, MELD-Na and CTP in patients with Acute on Chronic Liver Failure admitted to the ward

CLIF-C ACLF score is a better mortality predictor than MELD, MELD-Na and CTP in patients with Acute on Chronic Liver Failure admitted to the ward

Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

A modified prognostic score for critically ill patients with cirrhosis: An observational study

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