The Neuropsychological Consequences of Alcohol and Drug Abuse
John Brick in Handbook of the Medical Consequences of Alcohol and Drug Abuse, 2012
Several studies have noted the indirect toxic effects of alcohol on brain memory systems due to severe nutritional depletion. Marchiafava-Bignami syndrome, a rare condition associated with severe malnourishment in chronic alcoholism involves demyelination or necrosis of the corpus callosum with accompanying damage to pericallosal white matter. Symptoms include dementia, dysarthria, spasticity, and inability to ambulate (Hartman, 1995). One of the many consequences of chronic alcohol abuse is cirrhosis (see Chapter 2). Liver disease represents an additional indirect toxic effect of alcohol that can give rise to hepatic encephalopathy and can account for a significant portion of neuropsychological performance deficits (Hartman, 1995). Hepatic encephalopathy is associated with brain damage in widespread areas including the basal ganglia, thalamus, red nucleus, pons, and cerebellum (Charness, 1994; cited in Hartman, 1995; also see Chapter 4 for additional review). Hepatic encephalopathy can produce impairment in multiple domains of behavior. Symptoms of hepatic encephalopathy include but are not limited to: forgetfulness, confusion, disorientation, delirium, loss of memory, intellectual changes, reasoning changes, and mood changes.
Patty
Walter J. Hendelman, Peter Humphreys, Christopher R. Skinner in The Integrated Nervous System, 2017
The diagnosis of hepatic encephalopathy is made on clinical grounds, with the support of simple laboratory tests. Our patient’s story is characteristic: a long history of chronic alcoholism and documented liver disease; a period of increasing confusion and intermittent agitation followed by coma, evidence of portal-systemic shunting (periumbilical venous tortuosity, splenomegaly, GI bleeding, spider nevi, palmar erythema) and evidence of hepatocellular dysfunction (jaundice, peripheral edema). As will be seen in the next section, she also demonstrated a typical collection of biochemical abnormalities including hyperammonemia, low blood urea concentration, hyperbilirubinemia and hypoalbuminemia. Many patients also have hypoprothrombinemia, another hepatocellular synthetic defect, and may have pathological bruising.
Neurological Dengue
Sunit K. Singh, Daniel Růžek in Neuroviral Infections, 2013
Current strategies to manage hepatic encephalopathy focus on control of the raised serum ammonia levels which result from impaired hepatic detoxification (Bernal et al. 2010). Lactulose is commonly given for this reason as it reduces the number of ammonia-forming gut bacteria, as well as acidifying the contents so as to convert NH-4 to NH3 and potentiate the excretion of ammonia. Antibiotics such as neomycin may also be given with the same purpose of reducing gut bacterial load. If these methods fail, serum ammonia concentrations may be reduced directly by hemofiltration. There is some evidence that therapeutic hypothermia slows cellular metabolism and production of ammonia, though this strategy is not yet widely used (Vaquero et al. 2005). Ultimately, however, the only effective treatment for severe hepatic encephalopathy is liver transplantation.
Endoscopic management of acute oesophageal variceal bleeding within 12 hours of admission is superior to 12–24 hours
Published in British Journal of Biomedical Science, 2021
N Mousa, A Abdel-Razik, T Sheta, A G Deiab, A Habib, M Diasty, A Eldesoky, A Taha, E Mousa, A Yassen, A Fathy, A Elgamal
Hepatic encephalopathy is a common consequence of liver cirrhosis [27]. Although there is an improvement in hepatic encephalopathy in both groups post-treatment, the results of this study showed an improvement in hepatic encephalopathy following endoscopic treatment at 12 hours post presentation versus endoscopic treatment at 12–24 hours-post presentation. These results could be explained by early cessation of bleeding and a reduction of the ammonia levels, the key factor of hepatic encephalopathy with early endoscopic treatment [28]. We speculate that early management with control of bleeding is the main source of ammonia with consequent reduction of the ammonia level that is responsible for the improvement of hepatic encephalopathy. This supports the view that early endoscopic management of acute variceal bleeding according to guidelines is an important measure to improve morbidity. Accordingly, we agree with Barkun et al. [29], who recommended early endoscopy to decrease morbidity and mortality, although some suggested that the time to endoscopy was not a significant predictor of outcome in patients with variceal bleeding [15].
Hyperammonemia in acetaminophen toxicity
Published in Clinical Toxicology, 2022
Ryan T. Marino, Alexander M. Sidlak
Another important observation drawn from the data in this cohort is that mental status did not worsen, and encephalopathy did not develop, in patients who were not treated for hyperammonemia. The same explanation for why hyperammonemia may develop in the absence of any clinical encephalopathy may also explain the lack of benefit for conventional therapies. Lactulose, which was initiated in a majority of those patients treated, provides its benefit in hepatic encephalopathy by reducing endogenous and dietary ammonia through a cathartic and pH-altering effect in the gut lumen. Rifaximin, the second most commonly used drug in this cohort reduces urease-producing bacteria in the gut lumen and thus endogenously produced ammonia [8]. The reduction in ammonia and other poorly metabolized molecules provided by lactulose or rifaximin may not benefit patients with acetaminophen toxicity given that these therapeutic targets may not be the main cause of hyperammonemia in toxicity and hyperammonemia may not be solely responsible for the encephalopathy that develops. Acetaminophen-induced hepatotoxicity can progress to hepatic failure, which may include encephalopathy, but using ammonia as an early marker of this possibility appears to be unwise. Using an ammonia concentration alone to initiate treatment for hepatic encephalopathy that has yet to develop may lead to patient discomfort or harm rather than any benefit [11].
Low free triiodothyronine levels are associated with frail phenotype in hospitalized inpatients with cirrhosis
Published in Postgraduate Medicine, 2022
Chaoqun Li, Chunshan Zhao, Zihan Yu, Wanting Yang, Mingyu Sun, Yifan Li, Gaoyue Guo, Yangyang Hui, Xiaoyu Wang, Xiaofei Fan, Bangmao Wang, Jie Zhang, Chao Sun
A cohort of adult patients with cirrhosis was consecutively recruited in our center (Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital) between 2018 and 2020. All patients were hospitalized most often because of cirrhosis-related complications. The diagnosis of cirrhosis corresponded to medical history, laboratory/imaging results, transient elastography or biopsy. The exclusion criteria were as follows: (i) prior diagnosis of thyroid disease and/or receiving drugs known to influence thyroid function; (ii) abnormal serum TSH concentration outside the normal range; (iii) primary hepatocellular carcinoma or extrahepatic cancer; (iv) acute on chronic liver failure (ACLF) on admission (v) severe hepatic encephalopathy and (vi) incomplete biochemical parameters and/or frail phenotype data. All patients provide informed consent and the current study was implemented according to the Declaration of Helsinki and was approved by the ethics committee of Tianjin Medical University General Hospital (IRB2021-YX-136-01).
Related Knowledge Centers
- Ammonia
- Coma
- Constipation
- Gastrointestinal Bleeding
- Personality
- Infection
- Altered Level of Consciousness
- Liver Failure
- Mood
- Electrolyte Imbalance