Prevalence and natural history of subclinical hepatic encephalopathy in cirrhosis

Das, Ananya; Dhiman, Radha K.; Saraswat, Vivek A.; Verma, Meera; Naik, S. R.

doi:10.1046/j.1440-1746.2001.02487.x

Cited by 265 publications

(235 citation statements)

References 21 publications

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“…[7][8][9][10][11] Overt HE develops in >50% of MHE patients within three years. 10 These patients pose a significant burden to their care givers depending on the severity of cognitive dysfunction. 2,12 Considering all these facts together, early detection and treatment of MHE is warranted and recommended.…”

Section: H Epatic Encephalopathy (He) Is a Neurocognitivementioning

confidence: 99%

“…16 Prevalence of MHE increases with increasing severity of liver dysfunction 2,7,10,[16][17][18][19] and is not affected by etiology of cirrhosis once patients with recent alcohol intake were excluded.…”

Section: Epidemiologymentioning

confidence: 99%

“…14 The prevalence of MHE in patients with cirrhosis who do not have the evidence of overt HE is high and has been reported to vary between 30% and 84%. 2,10,15 Large variability in these studies were due to different diagnostic criteria used and population studied. Prevalence of MHE in our population varies between 48% and 67.7% as shown by our previous studies using psychometric tests.…”

mentioning

confidence: 99%

“…Prevalence of MHE in our population varies between 48% and 67.7% as shown by our previous studies using psychometric tests. 2,10,11 Patients who develop MHE are …”

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confidence: 99%

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Minimal Hepatic Encephalopathy Impairs Quality of Life

Agrawal

Umapathy

Dhiman

2015

Journal of Clinical and Experimental Hepatology

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Minimal hepatic encephalopathy (MHE) is the mildest form of the spectrum of neurocognitive impairment in cirrhosis. It is a frequent occurrence in patients of cirrhosis and is detectable only by specialized neurocognitive testing. MHE is a clinically significant disorder which impairs daily functioning, driving performance, work capability and learning ability. It also predisposes to the development of overt hepatic encephalopathy, increased falls and increased mortality. This results in impaired quality of life for the patient as well as significant social and economic burden for health providers and care givers. Early detection and treatment of MHE with ammonia lowering therapy can reverse MHE and improve quality of life. ( J CLIN EXP HEPATOL 2015;5:S42-S48) H epatic encephalopathy (HE) is a neurocognitive disorder in which brain function is impaired and is associated with both acute and chronic liver dysfunction. 1 It is a major complication that develops in some form and at some stage in a majority of patients with liver cirrhosis. Minimal HE (MHE) is the mildest form of spectrum of HE which is characterized by subtle cognitive and psychomotor deficits in the absence of recognizable clinical symptoms of HE. 2 It occurs in patients with liver dysfunction and/or portosystemic shunts. In MHE, neurocognitive abnormalities primarily affect attention, speed of information processing, executive control, motor ability and coordination in an individual. 3 In 1970, Zeegen et al 4 first described this condition when they discovered that 38% of patients who had undergone portal decompression surgery scored abnormal in Reitan trail making test (number connection test). Eight years later, the term subclinical HE 5 was introduced to describe these patients. Since then, this condition was described under various names like early HE, latent HE, subclinical HE and finally minimal HE. The latest classification combines MHE and grade 1 HE into covert HE while higher grades are classified as overt HE, thus simplifying the clinical schema so that HE can be uniformly diagnosed. 6 Covert HE means that the mental defect is not detectable by the clinician using conventional testing and is not noticeable to the patient. However, it is significant because these patients usually have neuropsychiatric and neurophysiological abnormalities on advanced testing which are not enough to cause disorientation or asterixis. MHE is regarded as a preclinical stage of HE and ammonia and systemic inflammation plays an important role in its pathogenesis similar to HE. Ammonia lowering therapies were used in the treatment of MHE and found to be effective.MHE is clinically significant as it impairs daily functioning, health related quality of life (HRQOL) and driving skills, predicts the development of overt HE and is associated with poor survival. 7-11 Overt HE develops in >50% of MHE patients within three years. 10 These patients pose a significant burden to their care givers depending on the severity of cognitive dysfunction. 2,12 Considering all ...

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Section: H Epatic Encephalopathy (He) Is a Neurocognitivementioning

confidence: 99%

Section: Epidemiologymentioning

confidence: 99%

mentioning

confidence: 99%

“…Prevalence of MHE in our population varies between 48% and 67.7% as shown by our previous studies using psychometric tests. 2,10,11 Patients who develop MHE are …”

mentioning

confidence: 99%

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Minimal Hepatic Encephalopathy Impairs Quality of Life

Agrawal

Umapathy

Dhiman

2015

Journal of Clinical and Experimental Hepatology

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“…8 The prevalence of MHE in patients with cirrhosis has been estimated to lie between 30% and 84%, with variations in the diagnostic criteria thought to be responsible for this wide range. 9 THE ROLE OF AMMONIA IN THE SYNDROME OF HEPATIC ENCEPHALOPATHY Ammonia was first implicated in the pathogenesis of HE 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. Hahn and colleagues demonstrated the induction of an encephalopathic state in dogs following the formation of a surgical shunt, known as Eck's fistula, which served to divert nitrogen-rich blood from the portal vein directly to the inferior vena cava, therein bypassing the liver.…”

mentioning

confidence: 99%

Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

Aldridge

Tranah

Shawcross

2015

Journal of Clinical and Experimental Hepatology

246

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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Minimal Hepatic Encephalopathy

Mattarozzi¹,

Stracciari²,

Vignatelli³

et al. 2004

Arch Neurol

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Background: The long-term effects of liver transplantation (LT) on minimal hepatic encephalopathy are poorly documented. Objective: To assess the cognitive performance of patients with cirrhosis and without overt encephalopathy, before and after LT. Design: Longitudinal study comparing cognitive performance of patients with cirrhosis before LT and 6 to 18 months after LT, with matched control patients. Setting: University medical center. Results: Six months after LT, patients had improved their performance in visuospatial and selective attention, vi-suospatial short-term and long-term memory, and language tasks. After 18 months, a further improvement was found for selective attention and verbal short-term memory, while no other cognitive functions varied over time. Conclusions: The present findings confirm preliminary studies showing that LT improves cognitive functions in patients with cirrhosis. The cognitive improvement is not generalized, but appears prominent in attention and memory and, once achieved, remains stable. Rates of recovery differ, being early for some functions and later for others.

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Prevalence and natural history of subclinical hepatic encephalopathy in cirrhosis

Abstract: We conclude that SHE is common in cirrhosis. The natural history of SHE is worse in patients with advanced cirrhosis and SHE probably predisposes the cirrhotic patient to overt hepatic encephalopathy.

Cited by 265 publications

References 21 publications

Minimal Hepatic Encephalopathy Impairs Quality of Life

Minimal Hepatic Encephalopathy Impairs Quality of Life

Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

Minimal Hepatic Encephalopathy

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