Patients with cirrhosis experience worse health-related quality of life (HRQoL), and attempts are warranted further exploration of modifiable factors to improve HRQoL. Data on the impact of malnutrition risk on HRQoL among cirrhosis are limited; thus, we aimed to strengthen understanding by clarifying the relationship between nutritional status and low HRQoL in patients with decompensated cirrhosis. Consecutive inpatients with cirrhosis attending our department within a tertiary hospital were studied. Generic health profiles and malnutrition risk were evaluated by the EuroQol-5D (EQ-5D) and Royal Free Hospital-Nutritional Prioritizing Tool (RFH-NPT) score, respectively. Multiple linear regression analysis was used to determine association of malnutrition risk with low HRQoL. In this cohort of 364 patients with median age of 64 years and 49·5 % male, 55·5 % of the study population reported impairment pertinent to HRQoL in at least one dimension in terms of the EQ-5D. Moreover, malnutrition risk (RFH-NPT score: β coefficient = −0·114, P = 0·038) was proved to be independently associated with poor HRQoL in multiple analysis, after adjustment for significant variables like age, BMI and markers of decompensation. Notably, we found that health dimensions representing physical function (i.e. mobility, self-care and usual activities) are substantially affected, while malnourished patients reported less frequencies of complaints in other domain such as anxiety/depression. In conclusion, the risk of malnutrition assessed by the RFH-NPT score is independently associated with low HRQoL. It is operational to improve HRQoL by identifying patients at high malnutrition risk and providing timely nutrition treatment.

In this review the most important hypotheses for the occurrence of the clinical picture of hepatic encephalopathy are discussed. As possible pathogenetic mechanisms are raised: dysfunction of the serotonergic system due to an increased tryptophan uptake in the brain, an elevated intracerebral ammoniac concentration and glutamine synthesis, and a heightened intracerebral GABA-activity.

The dysregulation of the serotonergic system as a consequence of the increased intracerebral tryptophan uptake is described as one of the most important pathogenetic mechanisms. The elevated intracerebral ammoniac concentration and the elevated intracerebral glutamine synthesis play in this a facilitating role. The similarity in symptomatology of the clinical picture of HE and the serotonergic syndrome support this hypothesis. Due to contradictory research findings the role of the GABA-ergic system and the occurrence of HE remains unclear.

Cirrhotic patients are prone to having infections, which may aggravate hepatic encephalopathy (HE). However, the effect of infections on mortality in HE cirrhotic patients is not well described. The National Health Insurance Database, derived from the Taiwan National Health Insurance Programme, was used to identify 4150 adult HE cirrhotic patients hospitalized between 1 January 2004 and 31 December 2004. Nine hundred and eighty-five patients (23·7%) had one or more co-existing infections during their hospitalization. After Cox proportional hazard regression modelling adjusted by the patients' gender, age, and medical comorbidity disorders, the hazard ratios (HRs) in HE patients with infections for 30-day, 30- to 90-day, and 90-day to 1-year mortalities were 1·66 [95% confidence interval (CI) 1·42–1·94], 1·51 (95% CI 1·23–1·85) and 1·34 (95% CI 1·13–1·58), respectively. Compared to the non-infection group, the HRs of pneumonia, spontaneous bacterial peritonitis, urinary tract infection, sepsis without specific focus (SWSF), cellulitis, and biliary tract infection were 2·11, 1·48, 1·06, 2·21, 1·06, and 0·78, respectively, for 30-day mortality; 1·82, 1·22, 0·93, 2·24, 0·31, and 2·82, respectively, for 30- to 90-day mortality; and 2·03, 0·82, 1·24, 1·64, 1·14, and 0·60, respectively, for 90-day to 1-year mortality for HE cirrhotic patients. We conclude that infections increase the mortality of HE cirrhotic patients, especially pneumonia and SWSF.

This purpose of this article is to promote comprehensive assessment, differential evaluation and provision of care which optimizes benefit while minimizing burden. Delirium is a debilitating neuropsychiatric complication that is highly prevalent in palliative care. It is multifactorial and may be related to infection, disease progression, metabolic state or medication toxicity. There are three proposed sub-types of delirium with the hypoactive/ hypoalert variant being most often underdiagnosed and undertreated. The inadequate management of all types of delirium is associated with increased personal and family distress, lengthier hospital stays, and escalating healthcare costs. This article reviews the assessment, diagnosis and treatment for delirium in general and hepatic encephalopathy in particular. A number of valid and reliable tools are discussed, as they assist in screening, symptom appraisal, diagnosis, and treatment planning. It is recognized that nurses are particularly well positioned to make bedside observations, to document changes over time, and to educate and support patients and their families. Searching for the etiology of delirium, developing individualized plans of care consistent with patient goals, and endorsing the benefit of consultation/referral are discussed as key roles for palliative care providers from all disciplines. New and novel therapies in the management of hepatic encephalopathy are discussed, as they expand treatment options for patients at all points along the trajectory of liver disease.

Although the exact pathophysiology of hepatic encephalopathy (HE) is not fully understood, for more than a century ammonia has been thought to play a critical role. However, the interpretation and utility of ammonia levels in patients with chronic liver disease (CLD) presenting with HE has been a long-standing source of confusion. It is a common belief in the emergency department and on the wards that a single elevated ammonia level in a patient with CLD can confirm the diagnosis of HE, and a normal level essentially rules it out. This confusion stems from the fact that early studies showed a correlation between degree of encephalopathy and the ammonia level, but numerous subsequent studies have shown that severely encephalopathic patients often have normal ammonia levels. This paper reviews the published literature on ammonia levels in patients with CLD in an attempt to clarify its value as a clinical decision-making tool in patients with suspected HE.

This report describes an association between hepatic encephalopathy and central anticholinergic syndrome(CAS). A 60-year-old anaemic woman was admitted unconscious and with a delayed reaction to pain but with no focal neurological deficits. She had signs of portal hypertension and a history of non-alcoholic liver cirrhosis grade Child B. Suspecting upper gastrointestinal bleeding, she was intubated for gastroduodenoscopy and a fibrin-covered ulcer was revealed. Raised intra-abdominal pressure resultingfrom ascites caused cardiopulmonary failure, which required mechanical ventilation for 24 h, but extubation was possible after drainage of the ascites and blood volume replacement therapy. However, her neurological state remained unchanged despite normal blood ammonia concentration and no sedation. CAS was considered and physostigmine injected with immediate effect. The patient opened her eyes immediately and was fully orientated to personal and medical history. We suggest that hepatic encephalopathy may trigger CAS, although the significance of physostigmine in the treatment of hepatic encephalopathy remains to be addressed by controlled investigations.

Hepatic encephalopathy is a neuropsychiatric disorder usually associated with severe hepatic insufficiency. It may however be divided into clinical and subclinical groupings. Psychometric testing, serial EEG's, EEG spectral analysis and event related potentials are all presently being used to quantify and differentiate between the various stages of hepatic encephalopathy. We review the use of psychometrics in hepatic encephalopathy and discuss evidence that these findings are comparable with the more objective data of electrophysiological studies. An adequate, simple and inexpensive assessment may be carried out using a battery of psychometric tests which include number connection tests and five pointed star construction.