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The patient with acute gastrointestinal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Rebecca Maindonald, Adrian Jugdoyal
Acute hepatic dysfunction can be classified according to the time interval between the onset of jaundice and encephalopathy, with hyperacute being less than 7 days, acute being 8–28 days and subacute being 29 days–12 weeks. Additionally, patients may have stable chronic liver disease that decompensates acutely. The most common causes of acute liver failure are drug-induced (e.g., Paracetamol) and acute viral hepatitis. Other causes are included in Table 10.1.
Gastroenterology
Published in Kristen Davies, Shadaba Ahmed, Core Conditions for Medical and Surgical Finals, 2020
Causes of acute liver failure include: Infection (viral hepatitis, Weil's disease)Toxins (paracetamol overdose, drug reactions)Budd–Chiari syndrome (liver venous outflow obstruction)Infiltrative diseases (Wilson's disease)If a patient already has established chronic liver disease, then infection, alcohol bingeing, GI bleeding and electrolyte disturbances can cause an acute-on-chronic liver failure
The liver
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
Liver transplantation is appropriate for some patients with acute liver failure, although the short-term results are poor in comparison with liver transplantation for chronic liver disease and suitable donor livers are frequently unavailable during the brief window of opportunity before death from liver failure.
Simple and feasible detection of hepatitis a virus using reverse transcription multienzyme isothermal rapid amplification and lateral flow dipsticks without standard PCR laboratory
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
Mao-ling Sun, Yang Zhong, Xiao-na Li, Jun Yao, Yu-qing Pan
Hepatitis A virus (HAV), classified as hepatovirus, is a small, unenveloped symmetrical RNA virus. It belongs to the micro ribonucleic acid viruses and is the cause of infectious or epidemic hepatitis [1]. HAV spreads through the fecal-oral route and is commonly contracted by ingesting food or water contaminated with the faeces of infected patients and vegetables fertilised with faeces and uncooked shellfish [2–4]. In developing regions, the source pollution of primary and processed agricultural products is still a serious problem. Although, the infection of HAV is more common in developing countries, an increased number of HAV cases has been reported in developed countries [5]. In developed cities, food may also be contaminated by unkilled HAV virus [6]. A 2019 HAV-mediated outbreak in the United States was linked to imported fresh blackberries [7]. HAV infections cause nausea, vomiting, abdominal pain, jaundice, fever, and diarrhoea [8]. Approximately 10 to 15% of infected patients will have recurring symptoms within six months of the initial infection. In severe cases, acute liver failure may be life-threatening [9]. Moreover, HAV infections during community-based, person-to-person outbreaks cannot be ignored [10].
Spotlight on liver macrophages for halting liver disease progression and injury
Published in Expert Opinion on Therapeutic Targets, 2022
Amit Khurana, Umashanker Navik, Prince Allawadhi, Poonam Yadav, Ralf Weiskirchen
Hepatic transaminases are the important biomarkers for the diagnosis of liver diseases and their levels have been reported to increase two- to three-fold in ALI with the involvement of jaundice and coagulation defects of hepatic origin in patients lacking a history of chronic liver disease. ALI can be caused by several factors including lipopolysaccharide, endotoxin, thioacetamide, D-galactosamine, acetaminophen, and several other physicochemical factors which generally show hallmark alterations such as inflammation and necrosis in hepatic tissue [36]. ALI can further lead to the development of the life-threatening condition acute liver failure (ALF), which may lead to an altered mental status known as hepatic encephalopathy. The time between the onset of jaundice and the emergence of hepatic encephalopathy has been used in several sub-categorizations of ALF to distinguish between patients with rapidly progressing ‘hyperacute’ disease and those with a more indolent (‘subacute’) clinical course, in whom the prognosis is typically worse [37]. The most common cause of ALF in the UK and the USA is an overdose of acetaminophen, which is marked by deteriorating symptoms over a few days [38]. Moreover, acute viral hepatitis, idiosyncratic drug reactions, autoimmune hepatitis, hepatotoxic drugs (phenprocoumon and antibiotics), and herbal or dietary supplements may also lead to the development of ALF. Unfortunately, liver transplantation is the only option for one-third to half of all patients with acute liver failure [38].
Identifying areas of improvement in nursing knowledge regarding hepatic encephalopathy management
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Aalam Sohal, Victoria Green, Sunny Sandhu, Marina Roytman
Development of HE is attributed to the accumulation of neurotoxic substances including ammonia in the bloodstream as well as the brain [4]. Hepatic encephalopathy can be divided into covert HE and overt HE. Covert HE is the preclinical stage of overt HE and refers to cognitive dysfunction (such as difficulty in decision-making and psychomotor slowing) without disorientation [5] while overt HE (OHE) is the presence of symptoms such as confusion, dysarthria, stupor, and coma. The development of OHE is a poor prognostic sign in the setting of chronic liver disease with the probability of survival of 44% at 1 year [6]. In the setting of acute liver failure, the development of HE is a harbinger of progressive hepatic failure. In both acute and chronic settings, development of OHE is an indication for transplant evaluation.