Blood lactate as an early predictor of outcome in paracetamol-induced acute liver failure: a cohort study

Bernal, William; Donaldson, Nora; Wyncoll, Duncan; Wendon, Julia

doi:10.1016/s0140-6736(02)07743-7

Cited by 450 publications

(307 citation statements)

References 22 publications

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“…12,17,25,26 In this study, a difference in MELD score was already detectable 24 to 48 hours after ingestion of the acetaminophen overdose between patients who eventually developed FHF and those who did not. Because all 3 MELD components contributed to the difference between groups, the MELD score was significantly better than each single component at predicting FHF.…”

Section: Discussionmentioning

confidence: 61%

“…11 It has therefore been of interest to discover prognostic indicators with the capability of identifying transplant candidates at an earlier stage of liver failure, perhaps even prior to the onset of hepatic encephalopathy (HE). 10,12 The Model for End-Stage Liver Disease (MELD) scoring system was originally designed for the assessment of short-term prognosis in patients with liver cirrhosis undergoing a transjugular intrahepatic portosystemic shunt (TIPS) to alleviate portal hypertension. 13 Subsequently, its use has been expanded to predict survival in end-stage chronic liver disease in general, and the MELD score has been applied as a disease severity index in organ allocation decisions for liver transplantation in patients with chronic liver disease.…”

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confidence: 99%

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MELD score as a predictor of liver failure and death in patients with acetaminophen-induced liver injury

2007

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The Model for End-Stage Liver Disease (MELD) scoring system has been established as a reliable measure of short-term mortality risk in patients with end-stage chronic liver disease. The aim of this study was to evaluate the prognostic value of the MELD scoring as a predictor of fulminant hepatic failure (FHF) and death in patients with acetaminophen poisoning. Prospectively, serial measurements of the 3 MELD components-INR, bilirubin, and creatinine-were performed in 460 patients with acetaminophen-induced liver injury. Starting on the first day after the day of overdose, MELD score was significantly higher in patients who eventually developed hepatic encephalopathy (HE) than in those who did not. HE developed in 63 of 142 patients with a MELD score above 18 at 48-72 hours after the overdose (positive predictive value 44%) compared with 2 of 182 patients with a MELD score of 18 or below (negative predictive value 99%). Among 124 patients with FHF, a threshold MELD score of 33 on the day after the onset of HE had sensitivity of 60%, specificity of 69%, positive predictive value of 65%, and negative predictive value of 63%. However, the discriminative power of

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Section: Discussionmentioning

confidence: 61%

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confidence: 99%

MELD score as a predictor of liver failure and death in patients with acetaminophen-induced liver injury

2007

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“…53 The implications of energy failure in ALF have largely been disregarded despite the presence of higher lactate levels in patients with ALF, which is a consequence of energy failure. 54 In an experimental rodent model of ALF, 55 in the early (pre-coma) stages of HE there was a significant 2-4.5-fold increase in total brain glutamine and lactate but in the severe (coma) stages of HE and brain edema, there was a further significant increase in brain lactate but no such increase in glutamine implying that impaired glucose oxidative pathways rather than intracellular glutamine accumulation per se may play a more dominant role. 56,57 …”

Section: Ammonia and The Brain: The Sick Astrocytementioning

confidence: 99%

Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

Aldridge

Tranah

Shawcross

2015

Journal of Clinical and Experimental Hepatology

235

190

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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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“…Currently, serum lactate is considered an established early prognostic marker of survival in patients with FHF. 7,8 Although the mechanisms of hyperlactemia in severe liver dysfunction are not elucidated precisely, lactate may reflect multiple-organ (for example, hepatic and renal) dysfunction. Thus, not surprisingly, lactate has been found to be an independent factor of mortality in patients with acute complications of cirrhosis.…”

mentioning

confidence: 99%

Prognostic impact of lactate in acute liver failure

Betrossian¹,

Senzolo²,

Shaw

et al. 2007

Liver Transpl

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Blood lactate as an early predictor of outcome in paracetamol-induced acute liver failure: a cohort study

Cited by 450 publications

References 22 publications

MELD score as a predictor of liver failure and death in patients with acetaminophen-induced liver injury

MELD score as a predictor of liver failure and death in patients with acetaminophen-induced liver injury

Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

Prognostic impact of lactate in acute liver failure

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