Evidence of Persistent Cognitive Impairment After Resolution of Overt Hepatic Encephalopathy

Riggio, Oliviero; Ridola, Lorenzo; Pasquale, Chiara; Nardelli, Silvia; Pentassuglio, I.; Moscucci, Federica; Merli, Manuela

doi:10.1016/j.cgh.2010.10.002

Cited by 95 publications

(80 citation statements)

References 10 publications

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“…However, recent studies have shown the persistence of cognitive impairment in cirrhotics even after complete resolution of HE despite ammonia lowering therapy suggesting role of other factors. [30][31][32] Small intestinal bacterial overgrowth correlates with MHE in patients with cirrhosis suggesting the role of gut derived bacterial toxins. 32 Recent studies have implicated infection and systemic inflammation in the pathogenesis of HE.…”

Section: Pathogenesis Of Minimal Hepatic Encephalopathymentioning

confidence: 99%

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: Pathogenesis Of Minimal Hepatic Encephalopathymentioning

confidence: 99%

Minimal Hepatic Encephalopathy Impairs Quality of Life

Agrawal

Umapathy

Dhiman

2015

Journal of Clinical and Experimental Hepatology

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“…Patients underwent testing using two validated modalities at baseline and retesting between 7 and 30 days apart without intervening change in liver disease severity based on prior studies [6][7][8]. We aimed to study (1) intra-visit learning: improvement in ICT lures at baseline and separately at the retesting visit and (2) inter-visit learning: improvement in individual PHES sub-tests, total score, and total ICT lures and targets at the retesting visit compared to the baseline visit.…”

Section: Methodsmentioning

confidence: 99%

“…While mental status changes in overt HE improve after treatment, there is some evidence that the metabolic insult associated with overt HE may lead to chronic neurological injury that is not readily reversible [3][4][5]. Cognitive issues, such as learning impairment, have been reported in patients with prior overt HE episodes from single-center studies, accompanied by pathological evidence of neuronal death [6][7][8][9]. However, multicenter confirmation using more than one testing methodology is lacking.…”

Section: Introductionmentioning

confidence: 94%

Hepatic Encephalopathy Is Associated with Persistent Learning Impairments Despite Adequate Medical Treatment: A Multicenter, International Study

et al. 2016

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“…[3][4][5][6][7][8][9][10] While it was once thought that cognitive impairment with CHE or OHE was reversible, data from studies evaluating medical treatment or liver transplantation suggest that the associated cognitive changes may not be totally reversible. [66][67][68] Moreover, it has been demonstrated that even after therapy and improvement to normal mental status, a single episode of OHE may continue to have residual negative effects on cognitive function. 66 Therefore, it would only seem logical to consider prophylactic treatment for HE in patients with cirrhosis.…”

Section: Management Guidelines For Covert Hepatic Encephalopathymentioning

confidence: 99%

Management of Covert Hepatic Encephalopathy

Waghray

Mullen

2015

Journal of Clinical and Experimental Hepatology

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Hepatic encephalopathy is a reversible progressive neuropsychiatric disorder that encompasses a wide clinical spectrum. Covert hepatic encephalopathy is defined as patients with minimal hepatic encephalopathy and Grade I encephalopathy by West-Haven Criteria. Terminology such as "sub-clinical", "latent", and "minimal" appear to trivialize the disease and have been replaced by the term covert. The lack of clinical signs means that covert hepatic encephalopathy is rarely recognized or treated outside of clinical trials with options for therapy based on patients with episodic hepatic encephalopathy. This review discusses the current available options for therapy in covert hepatic encephalopathy and focuses on non-absorbable disacharides (lactulose or lactitol), antibiotics (rifaximin), probiotics/synbiotics and L-ornithine-L-aspartate. ( J CLIN EXP HEPATOL 2015;5:S75-S81)

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Evidence of Persistent Cognitive Impairment After Resolution of Overt Hepatic Encephalopathy

Cited by 95 publications

References 10 publications

Minimal Hepatic Encephalopathy Impairs Quality of Life

Minimal Hepatic Encephalopathy Impairs Quality of Life

Hepatic Encephalopathy Is Associated with Persistent Learning Impairments Despite Adequate Medical Treatment: A Multicenter, International Study

Management of Covert Hepatic Encephalopathy

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