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Journal articles on the topic 'Hepatic Encephalopathy Caused By NAcetylcysteine'

Author: Grafiati

Published: 5 June 2025

Last updated: 12 July 2025

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Manas, Ranjan Mallick, Ranjan Behera Jyoti, Kumar Meher Alok, Behera Rupashree, and Kumar Giri Rupak. "Continuous Intravenous N- Acetylcysteine in iNon Acetaminophen Acute Liver Failure In Children." International Journal of Current Pharmaceutical Review and Research 15, no. 11 (2023): 448–53. https://doi.org/10.5281/zenodo.11580587.

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AbstractIntroduction: Assessing How Long-Term Intravenous N-Acetylcysteine Infusions Can Improve a Child's NonAcetaminophen Acute Liver Failure (Nai-Alf) Outcomes.Material and Methods: A predesigned proforma is used to conduct this observational research. Nacetylcysteine at a dosage of 150 mg/kg/day in 3 split doses by continuous intravenous infusion for up to 7consecutive days was given to 41 instances with non-acetaminophen caused acute liver failure in the age groupof 3 months to 14 years who came to VIMSAR's OPD & IPD, Burla. From the hospital registry, 37 patientswere chosen that did not receive N-acetylcysteine and had acute liver failure not caused by acetaminophen.Software called SPSS16v was used to analyse all of the data.Results: When compared to patients who did not receive NAC, those who had lower grades of hepaticencephalopathy (HE I & HE II) showed a reduction in the length of their ICU stay as well as an earlier recoveryin their liver function. In patients presenting with grades III or IV hepatic encephalopathy, NAC was found to beineffective in reducing hospital stays or ICU deaths. NAC use in youngsters has been determined to be safe.Conclusion: The current study's safety profile suggests that intravenous NAC should be investigated forpatients with early stage NAI-PALF. Nevertheless, further research is required to identify response predictorsand the ideal dosage and duration of NAC treatment.

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Salama, Fady, Anna Christina Leyson, Malay Shah, and Roberto Galuppo Monticelli. "A Challenging Case of Refractory Hepatic Encephalopathy in a Postliver Retransplant Patient with Thrombosed Portal Vein: A Shunt for a Shunt." Case Reports in Hepatology 2023 (February 25, 2023): 1–3. http://dx.doi.org/10.1155/2023/6765788.

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Hepatic encephalopathy (HE) is a frequent and serious complication of chronic liver disease. The mechanism of hepatic encephalopathy is not entirely clear. Hepatic encephalopathy is defined as brain dysfunction caused by liver insufficiency and/or portal-systemic blood shunting. It manifests as a wide spectrum of neurological or psychiatric abnormalities, ranging from subclinical alterations, detectable only by neuropsychological or neurophysiological assessment, to coma. Liver transplant (LT) is the definitive treatment for refractory hepatic encephalopathy. In this case, we present a challenging case of refractory hepatic encephalopathy in a postliver transplant patient with portal vein thrombosis and a splenorenal shunt treated with a novel technique to address his complex anatomy.

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Pisarek, Wojciech. "S100 Beta Protein as a Marker of Hepatic Encephalopathy: A Breakthrough in Diagnostics or a False Trail? Review of the Literature." Postępy Higieny i Medycyny Doświadczalnej 76, no. 1 (2022): 128–31. http://dx.doi.org/10.2478/ahem-2022-0018.

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Abstract Hepatic encephalopathy is a dysfunction of the central nervous system caused by chronic and acute liver disease. The dysfunction presents a wide spectrum of symptoms—from the undetectable in a standard clinical examination to hepatic coma—and could be caused by both chronic and acute liver diseases. For many years research has been conducted to find a marker that would allow for the accurate, quick, and possibly inexpensive detection of hepatic encephalopathy. Due to the pathogenesis of hepatic encephalopathy, researchers’ attention is focused on markers of damage to the central nervous system. One of the markers of astrocyte damage, known from research in neurology and neurosurgery, is the protein S100B. Published research results so far are inconclusive, but they allow us to look with optimism at the role of S100B as a marker of minimal hepatic encephalopathy (MHE).

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Komiljonovich, Ibragimov Nematjon, Murotov Temur Malik Nizomovich, and Igamkulov Behzod Zafar O’g’li. "HEPATIC ENCEPHALOPATHY CAUSED BY ENDOGENOUS INTOXICATION IN PATIENTS WITH DIABETES MELLITUS COMPLICATED BY PURULENT-SEPTIC LESIONS OF SOFT TISSUES, WAYS OF THEIR CORRECTION." American Journal of Medical Sciences and Pharmaceutical Research 5, no. 11 (2023): 20–29. http://dx.doi.org/10.37547/tajmspr/volume05issue11-04.

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Objective:to study hepatic encephalopathy caused by endogenous intoxication in patients with diabetes mellitus (DM) complicated by necrotic soft tissue lesion (PNSTL) and ways of their correction. Materials and methods:58 patients with diabetes mellitus complicated by purulent-necrotic soft tissue lesion and the effect of endotoxicosis on the functional state of the liver were examined in the intensive care unit, with optimization of correction of hepatic encephalopathy. In addition to traditional therapy, hepatoprotectionsand drugs that stop transaminase activity are included in patients. Conclusions:Early detection of hepatic encephalopathy before clinical manifestations and timely correction is pathogenetically justified and optimizes the outcomes of such a formidable complication as hepatic encephalopathy and coma.

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Jarmołowicz, Jakub, Agata Boczar, Patryk Dryja, Sven Solisch, Izabela Stawicka, and Izabela Orzołek. "Minimal hepatic encephalopathy - from cirrhosis to neurological disorders." Journal of Education, Health and Sport 76 (December 8, 2024): 56382. https://doi.org/10.12775/jehs.2024.76.56382.

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Introduction and aim Minimal hepatic encephalopathy (MHE) is a subtle but significant brain dysfunction resulting from chronic liver damage, with symptoms that can be difficult to detect. It affects patients' quality of life by causing problems with concentration, memory, and motor coordination. Untreated MHE may progress to more severe neurological disorders, such as overt hepatic encephalopathy. The importance of this condition lies in its impact on patients' daily functioning and the increased risk of accidents, particularly in situations requiring quick responses, such as driving.Neurological symptoms caused by the disease are potentially reversible with treatment. Materials and Methods Available literature from the PubMed and Google Scholar databases was reviewed using the following keywords: "minimal hepatic encephalopathy," "hepatic encephalopathy," "cirrhosis," and "SIBO." Conclusion The significance of Minimal Hepatic Encephalopathy is crucial from the perspective of preventing further progression and the onset of overt hepatic encephalopathy, as well as improving the quality of life for our patients. Patients and their families are often unaware of the condition, and the cognitive impairments are frequently underestimated. Enhancing diagnostic methods would enable physicians to identify these patients more promptly.

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Ridola, Lorenzo, Jessica Faccioli, Silvia Nardelli, Stefania Gioia, and Oliviero Riggio. "Hepatic encephalopathy: Diagnosis and management." Journal of Translational Internal Medicine 8, no. 4 (2020): 210–19. http://dx.doi.org/10.2478/jtim-2020-0034.

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Abstract Type C hepatic encephalopathy (HE) is a brain dysfunction caused by severe hepatocellular failure or presence of portal-systemic shunts in patients with liver cirrhosis. In its subclinical form, called “minimal hepatic encephalopathy (MHE), only psychometric tests or electrophysiological evaluation can reveal alterations in attention, working memory, psychomotor speed and visuospatial ability, while clinical neurological signs are lacking. The term “covert” (CHE) has been recently used to unify MHE and Grade I HE in order to refer to a condition that is not unapparent but also non overt. “Overt” HE (OHE) is characterized by personality changes, progressive disorientation in time and space, acute confusional state, stupor and coma. Based on its time course, OHE can be divided in Episodic, Recurrent or Persistent. Episodic HE is generally triggered by one or more precipitant factors that should be found and treated. Unlike MHE, clinical examination and clinical decision are crucial for OHE diagnosis and West Haven criteria are widely used to assess the severity of neurological dysfunction. Primary prophylaxis of OHE is indicated only in the patient with gastrointestinal bleeding using non-absorbable antibiotics (Rifaximin) or non-absorbable disaccharides (Lactulose). Treatment of OHE is based on the identification and correction of precipitating factors and starting empirical ammonia-lowering treatment with Rifaximin and Lactulose (per os and enemas). The latter should be used for secondary prophylaxis, adding Rifaximin if HE becomes recurrent. In recurrent/persistent HE, the treatment options include fecal transplantation, TIPS revision and closure of eventual splenorenal shunts. Treatment of MHE should be individualized on a case-by-case basis.

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Ishii, Yuji, Yoshinori Inagaki, Katuya Hirai, and Teruaki Aoki. "Hepatic encephalopathy caused by congenital extrahepatic portosystemic venous shunt." Journal of Hepato-Biliary-Pancreatic Surgery 7, no. 5 (2000): 524–28. http://dx.doi.org/10.1007/s005340070026.

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Shah, Ruchit N., Michael Makar, Nasir Akhtar, and Erin Forster. "Lactulose to the Rescue: A Case of Toxic Hepatic Encephalopathy Caused by Portosystemic Shunting and Epistaxis in a Patient with Hereditary Hemorrhagic Telangiectasia." Case Reports in Hepatology 2019 (March 26, 2019): 1–4. http://dx.doi.org/10.1155/2019/7573408.

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Hereditary hemorrhagic telangiectasia (HHT) is an uncommon autosomal dominant disorder characterized by telangiectasias and arteriovenous malformations. Multiple organ systems are involved including the skin, lungs, gastrointestinal tract, and brain. Hepatic encephalopathy is an extremely rare complication of HHT and early diagnosis and treatment can be life-saving. We present a rare case of hepatic encephalopathy caused by HHT-induced portosystemic shunting treated with lactulose.

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Amodio, Piero, and Sara Montagnese. "Lights and Shadows in Hepatic Encephalopathy Diagnosis." Journal of Clinical Medicine 10, no. 2 (2021): 341. http://dx.doi.org/10.3390/jcm10020341.

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Hepatic encephalopathy (HE) is a form of brain dysfunction that is caused by liver insufficiency and/or portal-systemic shunting. The exact nature of HE is debated; as such, conflicting uses of the term “HE” may cause inconsistencies in its detection and management. This review highlights the meaning of the term “HE” on the basis of its historical origins and current consensus. It also provides criteria for the diagnosis of the condition based on its phenotypes and risk factors for its occurrence. The procedure for differential diagnosis from other conditions which result in similar phenotypes is considered, together with precipitants and confounders. Finally, the current multidimensional approach for the correct clinical reporting of HE episodes is discussed.

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Setiorizaldi, Ilham, Amandianti Arimbi Tedjaningrum, Cindy Grace Panggabean, Enjelina Nangin, Jeffrey Christian Mahardhika, and Chandni P. Daryanani. "Pediatric Dengue Encephalopathy: A Review." Medical Clinical Update 1, no. 1 (2022): 5–7. http://dx.doi.org/10.58376/mcu.v1i1.5.

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Dengue encephalopathy is a very common neurological complication of dengue fever. Dengue encephalopathy or dengue hemorrhagic fever (DHF) with Central Nervous System (CNS) involvement used to be considered a relatively rare condition. However, the number of cases reported in human studies were increasing every year. Many factors caused the encephalopathy dengue. Possible mechanisms are hepatic failure (hepatic encephalopathy), cerebral hypoperfusion (shock), cerebral edema (vascular leakage) electrolyte disturbances, and intracranial hemorrhage due to thrombocytopenia or coagulopathy, which are secondary mechanisms of hepatic failure. Computed Tomography (CT) scan or Magnetic Resonance Imaging (MRI) of brain can be done to make certain of the diagnosis. The results can suggest the presence of extensive involvement of the bilateral cerebellar region, brain stem, and thalamus along with peculiar rim enhancement. Treatment in Intensive Care Unit (ICU) with a multidisciplinary team is required due to the patients’ decreased level of consciousness, underlying problems of airway, breathing, and circulation, comorbidities, and considerations of specific etiology.

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Singh, Tavankit, and Arthur McCullough. "Medical Management of Portal Hypertension and Its Complications." Digestive Disease Interventions 01, no. 04 (2017): 235–40. http://dx.doi.org/10.1055/s-0038-1629894.

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AbstractPortal hypertension, most commonly caused by cirrhosis, is defined as an elevated hepatic venous pressure gradient that can lead to complications including ascites, hepatic, esophageal/gastric varices, hepatic encephalopathy, and hepatorenal syndrome. While these complications are initially managed by medical and endoscopic treatments, progressive decompensation of liver disease may lead to liver transplantation.

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Moriyama, S., S. Chiba, K. Uesaka, et al. "Hepatic encephalopathy caused by portosystemic shunt in a Holstein calf." Japanese Journal of Large Animal Clinics 10, no. 2 (2019): 73–77. http://dx.doi.org/10.4190/jjlac.10.73.

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Mizumoto, Junki. "Disappearing into the Drug Crowd: Hepatic Encephalopathy Caused by Polypharmacy." American Journal of Medicine 132, no. 12 (2019): e856-e857. http://dx.doi.org/10.1016/j.amjmed.2019.05.052.

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Yuksel, Hatice, Osman Aydin, Derya Ari, Volkan Oter, Meral Akdogan, and Erdal Birol Bostanci. "Neurological disorders in liver transplantation." Ideggyógyászati szemle 75, no. 3-4 (2022): 129–35. http://dx.doi.org/10.18071/isz.75.0129.

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Liver transplantation is the only curative treatment in patients with end-stage liver failure. It has been associated with neurological disorders more frequently than other solid organ transplantations. We aimed to detect neurological disorders in liver transplantation patients and determine those that affect mortality. One hundred eighty-five patients, 105 with and 80 without neurological disorders, were included in this study. The follow-up was categorized into three periods: preoperative, early postoperative and late postoperative. We analyzed all medical records, including demographic, laboratory, radiological, and clinical data. Neurological disorders were observed in 52 (28.1%) patients in the preoperative period, in 45 (24.3%) in the early postoperative, and in 42 (22.7%) in the late postoperative period. Hepatic encephalopathy in the preoperative and altered mental state in the postoperative period were the most common neurological disorders. Both hepatic encephalopathy (37.5%) and altered mental state (57.7%) caused high mortality (p=0.019 and 0.001) and were determined as independent risk factors for mortality. Living donor transplantation caused less frequent mental deterioration (p=0.049). The mortality rate (53.8%) was high in patients with seizures (p=0.019). While mortality was 28.6% in Wilson’s disease patients with neurological disorders, no death was observed in patients without neurological disorders. We identified a wide variety of neurological disorders in liver transplantation patients. We also demonstrated that serious neurological disorders, including hepatic encephalopathy and seizures, are associated with high morbidity and mortality. Therefore, in order to avoid poor outcomes, hepatic encephalopathy should be considered as a prioritization criterion for liver transplantation.

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Inoue, Masayoshi, Toshihiro Tanaka, Hiroyuki Nakagawa, Tetsuya Yoshioka, and Kimihiko Kichikawa. "Splenic Vein Embolization Using Coil Anchors and Prophylactic Occlusion of a Hepatofugal Collateral for Hepatic Encephalopathy due to Splenorenal Shunt: Technical Note and Literature Review." Case Reports in Radiology 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/160653.

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Purpose. Interventional treatment strategies for patients with encephalopathy due to splenorenal shunt remain controversial. Portosplenic blood flow separation by occluding the splenic vein could avoid the complication of severe portal hypertension, but it would require repeated reintervention due to recurrence of symptoms. This paper describes occlusion of the splenic vein using coil anchors and prophylactic embolization of a collateral hepatofugal vessel with no recurrence of hyperammonemia.Materials and Methods. A 51-year-old woman with severe cirrhosis had hepatic encephalopathy due to a large splenorenal shunt. The serum ammonia level was 132 μg/dL. Via a transileocolic approach, the splenic vein was completely embolized with 0.035-inch metallic coils using coil anchors while preserving the splenorenal shunt. In addition, one of the collateral vessels of the portal vein, the retrogastric vein, was also embolized prophylactically.Results. After this procedure, the serum ammonia level decreased immediately to 24 μg/dL. The portal venous pressure increased by only 1.5 mmHg. Hepatic encephalopathy had not been observed for 25 months after the procedure, and neither retention of ascites nor worsening of esophageal varices and liver function was observed.Conclusion. This procedure appears to be safe and effective for hepatic encephalopathy caused by a splenorenal shunt.

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Nakadate, Kazuhiko, and Sumito Kamata. "Severe Acute Hepatic Dysfunction Induced by Ammonium Acetate Treatment Results in Choroid Plexus Swelling and Ventricle Enlargement in the Brain." International Journal of Molecular Sciences 23, no. 4 (2022): 2010. http://dx.doi.org/10.3390/ijms23042010.

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Hepatic encephalopathy is a major cause of liver failure. However, the pathophysiological role of ventricle enlargement in brain edema remains unclear. Here, we used an acute hepatic encephalopathy mouse model to examine the sequential pathological changes in the brain associated with this condition. We collected tissue samples from experimental animals treated with ammonium acetate at 3 and 24 h post-injection. Despite the normalization of the animal’s ammonia levels, samples taken at 24 h after injection exhibited distinct enlargement of lateral ventricles. The choroid plexus samples obtained at 3 h post-ammonium acetate treatment indicated enlargement; however, this swelling was reduced at the later timepoint. The aquaporin-1 proteins that regulate the choroid plexus were localized both in the apical membrane and the cytoplasm of the epithelia in the control; however, they translocated to the apical membranes of the epithelia in response to ammonia treatment. Therefore, severe acute hepatic encephalopathy induced by ammonium acetate administration caused enlargement of the ventricles, through swelling of the choroid plexus and aquaporin-1 transport and aggregation within the apical membranes.

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Direkze, Shamindra, and Rajiv Jalan. "Diagnosis and Treatment of Low-Grade Hepatic Encephalopathy." Digestive Diseases 33, no. 4 (2015): 562–69. http://dx.doi.org/10.1159/000375350.

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Minimal hepatic encephalopathy (mHE) is common among patients with cirrhotic liver disease and causes significant morbidity and mortality. It may present as cognitive impairment, behavioural changes and, less frequently, with neurological symptoms which make diagnosis of the disease challenging. A history of falls and accidents may also be suggestive of mHE. Diagnosis primarily relies on at least two positive psychometric tests of which the psychometric hepatic encephalopathy score (PHES) is essential. Alternatively, PHES and an electroencephalogram may be used to establish a diagnosis. Biochemical markers of encephalopathy currently have no role in the diagnosis of mHE. Treatment is not always advocated for a diagnosis of mHE but is dependent on the degree of impairment caused by the symptoms. After treatment of other metabolic abnormalities and co-morbidities associated with cirrhosis, more specific treatment for mHE largely relies on therapies used to lower ammonia levels. Laxatives and rifaximin are commonly used in treatment and work through decreasing ammonia absorption from the gut. Other therapies, such as BCAA, LOLA, L-carnitine and phenylbutyrate, modify responses to ammonia as well as enhancing metabolism and excretion. mHE resulting from spontaneous portosystemic shunts or transhepatic intraportal systemic shunts may require ablation or reduction of the shunt. Early detection and appropriate treatment of mHE is important to prevent significant cognitive impairments and progression to overt HE.

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Ross, P. F., A. E. Ledet, D. L. Owens, et al. "Experimental Equine Leukoencephalomalacia, Toxic Hepatosis, and Encephalopathy Caused by Corn Naturally Contaminated with Fumonisins." Journal of Veterinary Diagnostic Investigation 5, no. 1 (1993): 69–74. http://dx.doi.org/10.1177/104063879300500115.

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A study to evaluate the effects of dietary fumonisin B, was conducted using 6 ponies (4 test and 2 control). A ration naturally contaminated with fumonisin B, was fed in 3 phases: 1) 44 ppm fumonisin B1, 2) less than 1 ppm fumonisin B1, and 3) 88 ppm fumonisin B,. All ponies were monitored daily, weighed weekly, and limit fed at a rate of 0.8% body weight plus hay. Feed intake was measured daily, and a serum chemistry panel was completed once or twice weekly. Four to 7 days after initiation of the trial (Phase 1), all 4 test ponies had decreased feed consumption, and selected serum chemistry parameters were markedly elevated. On day 9, 1 pony died acutely with mild encephalopathy and hepatic necrosis. Another pony, euthanized on day 45, also had mild encephalopathy and hepatic necrosis. The remaining 2 test ponies continued the 44 ppm fumonisin B, diet for 98 days. Phase 2 consisted of a diet with < 1 ppm fumonisin B, for 120 days. During this phase, the serum chemistry values of the 2 ponies returned to normal. Following Phase 2, the 2 ponies were fed a diet containing 88 ppm fumonisin B1. After 75 days, 1 animal died of equine leukoencephalomalacia with mild hepatic necrosis. On day 78, the remaining pony was euthanized after showing distress; it also had leukoencephalomalacia and hepatic lesions.

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Yang, Yang, Xueqing Liang, Shirui Yang, et al. "Preoperative prediction of overt hepatic encephalopathy caused by transjugular intrahepatic portosystemic shunt." European Journal of Radiology 154 (September 2022): 110384. http://dx.doi.org/10.1016/j.ejrad.2022.110384.

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Qazi Arisar, Fakhar Ali, Shameem Behram Khan, and Anam Umar. "Hepatic encephalopathy in chronic liver disease; predisposing factors in a developing country." Asian Journal of Medical Sciences 6, no. 2 (2014): 35–42. http://dx.doi.org/10.3126/ajms.v6i2.11099.

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Objective: To find out the risk factors for developing Hepatic Encephalopathy in patients suffering from Chronic liver disease.Background: Hepatic encephalopathy (HE) is a neuropsychiatric disorder that is caused by liver damage. In its pathology, alterations in normal brain function are associated with an increase in blood ammonia, benzodiazepine like substances, products of neurotoxic fatty acids, and other gut derived toxins, which gain access to the brain as a result of liver dysfunction. Study Design: Hospital based descriptive, cross sectional study. Setting: Medical Unit 1, Ward- 5, Jinnah Post Graduate Medical Centre, Karachi.Duration: July 2013 to December 2013Patients and Methods: About 150 patients admitted in medical unit 1 with a diagnosis of chronic liver disease in a state of hepatic encephalopathy were included in this study. Patients suffering from viral or bacterial encephalitis, stroke, brain tumor, Wernicke’s encephalopathy were excluded from the study.Results and Observations: There were 96 (64%) female and 54 (36%) were male patients. Mean age of the patients was 52.45 (±12.271) years. 80 (53.33%) patients were having constipation. Infection was found in 55 (36.66%) cases. Upper GI Bleed was present in 51 (34%) patients. 44 (29.33%) patients had moderate to severe electrolyte imbalance as the cause. Constipation alone was the cause in 11.33% of cases. More than one factor was found to be responsible in around 56% of patients while in 6.6% of cases none of these precipitating factors was isolated.Conclusion: Constipation is the commonest cause of hepatic encephalopathy followed by infection, upper GI bleed and electrolyte imbalance.DOI: http://dx.doi.org/10.3126/ajms.v6i2.11099Asian Journal of Medical Sciences Vol.6(2) 2015 36-43

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Gazda, Jakub, Peter Drotar, Sylvia Drazilova, et al. "Artificial Intelligence and Its Application to Minimal Hepatic Encephalopathy Diagnosis." Journal of Personalized Medicine 11, no. 11 (2021): 1090. http://dx.doi.org/10.3390/jpm11111090.

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Hepatic encephalopathy (HE) is a brain dysfunction caused by liver insufficiency and/or portosystemic shunting. HE manifests as a spectrum of neurological or psychiatric abnormalities. Diagnosis of overt HE (OHE) is based on the typical clinical manifestation, but covert HE (CHE) has only very subtle clinical signs and minimal HE (MHE) is detected only by specialized time-consuming psychometric tests, for which there is still no universally accepted gold standard. Significant progress has been made in artificial intelligence and its application to medicine. In this review, we introduce how artificial intelligence has been used to diagnose minimal hepatic encephalopathy thus far, and we discuss its further potential in analyzing speech and handwriting data, which are probably the most accessible data for evaluating the cognitive state of the patient.

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., Adnan, Sayad Ahmad Ahmad, and Muhammad Iqbal Qasim. "Hyponatremia and its Clinical Outcome Among Patients with Hepatic Encephalopathy Due to Liver Cirrhosis Presenting to ATH Abbottabad." Pakistan Journal of Medical and Health Sciences 17, no. 2 (2023): 357–59. http://dx.doi.org/10.53350/pjmhs2023172357.

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Introduction: Hepatic encephalopathy (HE) is a potentially reversible complication of liver cirrhosis causing significant mortality. Hyponatremia in cirrhosis is caused by hampered renal function to eliminate free water that results in water retention disproportionate to sodium retention leading to reduced plasma osmolality and is associated with significant morbidity and mortality. The purpose of study was to determine the frequency of hyponatremia among patients of liver cirrhosis with hepatic encephalopathy. Methods: The design of this study was an observational study design which was hospital-based survey and was conducted on 130 patients of liver cirrhosis. A specialized questionnaire was designed to collect all the study information. All data was analyzed using SPSS Statistics version 24. Chi-square test and Spearman's rank test were employed to correlate hyponatremia with HE and its severity. A p-value of <0.05 was considered statistically significant. Results: Among the patients, 92 (71%) males and 38 (29%) females; the mean age of the patients was 56±11.3 years. Hyponatremia was present in 48 (36.9%) patients. Among these, 25 (52%) were male and 23 (48%) were female; 12 (25%) patients had mild Hyponatremia, 28(58.3%) had moderate, and 8 (16.6%) had severe Hyponatremia. HE was significantly associated with hyponatremia with p value of lea than 0.001. Practical Implication: The benefit of our study was undertaken to determine the frequency of hyponatremia among patients of liver cirrhosis with hepatic encephalopathy to provide evidence for hyponatremia as a prognostic factor in HE so that early detection and management of hyponatremia in such patients will help reduce disease burden and mortality in liver cirrhosis. Conclusion: Patients with lower levels of sodium had higher grades/severity of HE. Significant association of hyponatremia was seen with liver cirrhosis and encephalopathy. Keywords: Abbottabad, Cirrhosis, Hepatic encephalopathy, Hyponatremia, Liver.

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Shuliatnikova, Tetiana, and Valerii Tumanskyi. "BRAIN AQP4 DURING EXPERIMENTAL ACUTE LIVER FAILURE." Grail of Science, no. 16 (July 11, 2022): 559–61. http://dx.doi.org/10.36074/grail-of-science.17.06.2022.092.

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Hepatic encephalopathy (HE) was defined as a complex neuropsychiatric syndrome triggered by severe liver pathology and manifesting by covert and overt alterations up to hepatic coma and death [1]. Acute liver failure (ALF) results in acute hepatic encephalopathy (AHE) characterized by brain edema caused by complex mechanisms closely linked to ammonia toxicity [2]. Astrocytes are central brain cells the most sensitive to ammonia as being primarily source of glutamine synthetase (GS), therefore astrocyte swelling is a principal feature of AHE brain [1-3]. Aquaporin-4 (AQP4) is one of the central astrocyte molecules responsible for water homeostasis and cell volume in health and disease and presents the most abundant water channel in the CNS. According to current HE pathophysiology, alteration of AQP4 regulation can play a central role in the brain edema progression [1]. Considering high heterogeneity of astroglia populations in the CNS, AQP4 involvement to the links of HE can also sustain mentioned conventional diversity. The purpose of the study was determining the level of AQP4 in different rat brain regions in the conditions of ALF.

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Rodriguez, Guido, Roberto Testa, Guido Celle, et al. "Reduction of Cerebral Blood Flow in Subclinical Hepatic Encephalopathy and its Correlation with Plasma-Free Tryptophan." Journal of Cerebral Blood Flow & Metabolism 7, no. 6 (1987): 768–72. http://dx.doi.org/10.1038/jcbfm.1987.132.

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Cerebral blood flow (CBF), measured by the noninvasive xenon-133 inhalation method, EEG, and plasma levels of ammonia (NH3) and free tryptophan were determined in 18 hospitalized cirrhotic patients affected with subclinical hepatic encephalopathy, as diagnosed by the Kurtz test. CBF results were significantly lower (p < 0.001) in the patients' group as compared with a sex- and age-matched normal control population, although seven patients had values in the normal range. NH3 was increased only in six, while free tryptophan was increased in all but two patients. A significant negative correlation (p = 0.02) between CBF and free tryptophan was found, even though it appears to be difficult to interpret. We suggest that CBF impairment in some cirrhotic patients with subclinical hepatic encephalopathy may be related to the systemic metabolic derangement caused by the liver disease; free tryptophan could have some implication in producing CBF reduction.

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Huda, A., R. K. Gupta, N. Rajakumar, and M. A. Thomas. "Role of Magnetic Resonance in Understanding the Pathogenesis of Hepatic Encephalopathy." Magnetic Resonance Insights 2 (January 2008): MRI.S973. http://dx.doi.org/10.4137/mri.s973.

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A spectrum of neuropsychiatric abnormalities caused by portosystemic venous shunting occurs in hepatic encephalopathy (HE) patients with or without liver dysfunction. It is not completely clear how the astrocyte swelling leads to glial-neuronal dysfunction, and how the symptoms are manifested in HE. A major goal of this work is to review the current status of information available from the existing magnetic resonance (MR) modalities including MR imaging (MRI) and MR Spectroscopy (MRS) as well as other modalities in the understanding the pathogenesis of HE. First, we discuss briefly neuron-histopathology, neurotoxins, neuropsychological and neurophysiological tests. A short review on the progress with single-photon emission computed tomography (SPECT) and positron emission tomography (PET) is then presented. In the remaining part of the manuscript, the following topics pertinent to understanding the pathogenesis of HE are discussed: MRI, diffusion tensor imaging (DTI), one-dimensional MRS based single- and multi-voxel based spectroscopic imaging techniques and two-dimensional MRS.

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HAN, Jaryung, Young Seok HAN, and Yoon Jin HWANG. "Recurrent hepatic encephalopathy caused by the persistent porto-systemic shunt in liver transplant recipients." Annals of Hepato-Biliary-Pancreatic Surgery 25, no. 1 (2021): S275. http://dx.doi.org/10.14701/ahbps.ep-74.

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Takenaga, Shinsuke, and Yoshio Aizawa. "Efficacy and Safety of Transcatheter Embolization for Hepatic Encephalopathy Caused by Spontaneous Portosystemic Shunts." Interventional Radiology 2, no. 2 (2017): 51–58. http://dx.doi.org/10.22575/interventionalradiology.2016-0010.

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Grabner, A. "Enzootic liver cirrhosis and hepatic encephalopathy in horses after intoxication caused by senecio alpinus." Pferdeheilkunde Equine Medicine 6, no. 3 (1990): 119–24. http://dx.doi.org/10.21836/pem19900303.

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YANG, SIEN-SING, NAI-HSIN CHU, and CHI-HWA WU. "Subcortical somatosensory evoked potentials in patients with hepatic encephalopathy caused by severe acute hepatitis." Journal of Gastroenterology and Hepatology 8, no. 6 (1993): 545–49. http://dx.doi.org/10.1111/j.1440-1746.1993.tb01650.x.

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Yang, SS, NS Chu, and CH Wu. "Prognostic value of somatosensory evoked potentials in hepatic encephalopathy caused by severe acute hepatitis." Journal of Hepatology 13 (January 1991): S182. http://dx.doi.org/10.1016/0168-8278(91)91702-i.

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Younes, Kyan, Nicole R. Gonzales, Amrou Sarraj, Eliana Bonfante, and Amanda Jagolino-Cole. "Hepatic Encephalopathy Mimicking Acute Dominant Middle Cerebral Artery Ischemic Stroke: A Case Report." Case Reports in Neurology 11, no. 3 (2019): 304–11. http://dx.doi.org/10.1159/000504017.

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Hepatic encephalopathy and hyperammonemia are common in the setting of liver disease and have been associated with both generalized and focal neurological deficits. We report a case of hepatic encephalopathy with transaminitis in the setting of hyperammonemia clinically mimicking acute dominant middle cerebral artery (MCA) syndrome. A 59-year-old right-handed woman had new-onset expressive aphasia, left gaze deviation, and right hemiparesis consistent with MCA stroke. Her symptoms began 12 h after transarterial chemoembolization, a procedure to embolize blood supply and provide cytotoxic agents to a hepatocellular carcinoma tumor. Thrombocytopenia and age-indeterminate hypodensities on brain CT precluded intravenous thrombolytic administration. MRI revealed predominantly dominant hemisphere subcortical restricted diffusion with no cortical involvement. Due to a mismatch between the MRI findings and the neurological symptoms, she underwent digital subtraction cerebral angiography to assess candidacy for intra-arterial thrombectomy, which revealed completely patent MCAs with intact filling of the distal branches. Liver enzymes and ammonia were elevated. The patient was treated with lactulose and intravenous fluids. After normalization of liver enzymes, the patient’s neurological deficits resolved. Reversal of this patient’s focal symptoms with medical management could potentially be explained by the recovery of blood flow-metabolic demand mismatch caused by worsening liver dysfunction and hyperammonemia. As acute stroke therapies and interventions increase in utility for large artery acute ischemic stroke, it is vital to recognize hepatic encephalopathy and liver failure as part of the differential diagnosis for patients presenting with MCA syndrome.

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Mun, Bo Gyung, Joo Hoon Lee, Young Seo Park, and Jiwon Jung. "A Case of Severe Hyperammonemic Encephalopathy Caused by Urinary Tract Infection in Obstructive Uropathy." Childhood Kidney Diseases 25, no. 2 (2021): 112–16. http://dx.doi.org/10.3339/jkspn.2021.25.2.112.

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Hyperammonemia is mainly caused by diseases related to liver failure. However, there are also non-hepatic causes of hyperammonemia, such as urinary tract infection (UTI) due to urease-producing organisms. Urease production by these bacteria induces a hydrolysis of urinary urea into ammonia that can cross the urothelial cell membrane and diffuse into blood vessels, leading to hyperammonemia. Delayed diagnosis and treatment of hyperammonemia can lead to lethal encephalopathy that can cause brain damage and life-threatening conditions. In the presence of obstructive uropathy, UTI by urease-producing bacteria can lead to more severe hyperammonemia due to enhanced resorption of ammonia into the systemic circulation. In this report, we present a case of acute severe hyperammonemic encephalopathy leading to brain death due to accumulation of ammonia in blood caused by Morganella morganii UTI in a 10-year-old girl with cloacal anomaly, causing obstructive uropathy even after multiple corrections.

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Donaldson, Janine, Tomasz Jacek, Piotr Wychowański, et al. "Rat Model of Endogenous and Exogenous Hyperammonaemia Induced by Different Diets." International Journal of Molecular Sciences 26, no. 5 (2025): 1818. https://doi.org/10.3390/ijms26051818.

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Two different diets able to induce dietary hyperammonaemia (a methionine–choline-deficient (MCD) diet and a methionine-deficient diet enriched with ammonium acetate (MAD + 20% ammonium acetate)) were tested in a rat model. The diets were shown to have different modes of action, inducing significant hyperammonaemia (HA) and growth retardation in the rats, with different metabolic consequences. The MCD diet resulted in the development of endogenous HA, with a decrease in bilirubin levels and an increase in hepatic fat content. In contrast, the MAD + 20% ammonium acetate diet increased circulating ALP and haptoglobin levels and decreased liver mass. The above results suggest that the MCD diet deteriorated the liver function of the rats, resulting in the development of endogenous HA, while the MAD diet caused moderate changes in liver metabolism, resulting in the development of exogenous HA. Interestingly, the commonly used oral treatments Lactulose and Rifaximin did not ameliorate hyperammonaemia during or after the treatment period. In conclusion, even though the diets used in the current study caused somewhat similar hyperammonaemia, they seemed to provoke different metabolic consequences. The latter can have an impact on the severity of the resulting hyperammonaemia and thus on the hyperammonaemia-induced encephalopathy, resulting in the development of distinguishing cognitive and metabolic (liver) effects compared to other forms of encephalopathy. We hypothesized that these rat models, with significantly increased serum ammonia levels, along with different liver injuries, could serve as a suitable double animal model for the testing of new, oral enzyme therapies for hepatic encephalopathy in future studies.

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I Bon, Elizaveta. "Indicators of Changes in Motor and Emotional Tests in A State of Ethanol Intoxication." Journal of Surgical Case Reports and Images 7, no. 9 (2024): 01–04. https://doi.org/10.31579/2690-1897/219.

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Alcohol intoxication refers to a clinically dangerous condition caused by recent alcohol consumption, in which alcohol and its metabolites accumulate in the bloodstream faster than they can be metabolized by the liver. Alcohol has a range of effects on the central nervous system at different doses. Acute effects include Wernicke's encephalopathy, traumatic brain injury, memory loss, seizures, stroke, and hepatic encephalopathy. We observe an increase in the mobility of rats after the introduction of alcohol and its sharp decline after the introduction of grapefruit juice. As for the number of short and long washings, as well as the "climbing" and "rering" stands, their number, after the introduction of alcohol, decreases somewhat, and after the introduction of grapefruit juice, also continues to decrease.

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Long, J., H. Vaughan-Williams, J. Moorhouse, H. Sethi, and N. Kumar. "Acute Budd–Chiari syndrome due to a simple liver cyst." Annals of The Royal College of Surgeons of England 96, no. 1 (2014): 000. http://dx.doi.org/10.1308/003588414x13824511649698.

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Simple liver cysts are common, rarely causing significant morbidity or mortality. Budd–Chiari syndrome (BCS) is caused by obstruction of hepatic venous outflow and is the leading cause of postsinusoidal liver failure. We present a rare case of BCS caused by a simple hepatic cyst. A 16cm × 16cm liver cyst was found on computed tomography of a 66-year-old woman presenting with abdominal pain. The cyst had become infected, thus enlarged, exerting mass effect with almost complete compression of the inferior vena cava. Shortly after admission, the patient developed acute liver failure, with deranged clotting and hepatic encephalopathy requiring full organ support on the intensive care unit. Cardiac output studies showed a low cardiac index of 1.4l/min/m2. An emergency laparotomy with fenestration of the cyst and drainage of 2l of purulent material led to a full recovery. Intraoperative cystic fluid aspirates later confirmed no evidence of Echinococcus. Histology confirmed a simple cyst. Liver biopsies showed severe, confluent, bridging necrosis, without background parenchymal liver disease. Acute BCS due to rapid compression of all major hepatic veins leading to fulminant hepatic failure is rare. Our case highlights a clinically significant complication of a simple liver cyst of which clinicians should be aware when managing these ‘innocent’ lesions.

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Haj, Mona, and Don C. Rockey. "Ammonia Levels Do Not Guide Clinical Management of Patients With Hepatic Encephalopathy Caused by Cirrhosis." American Journal of Gastroenterology 115, no. 5 (2020): 723–28. http://dx.doi.org/10.14309/ajg.0000000000000343.

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Nozaki, Harushige, Tomonori Shimada, Yoshirou Fukushima, Tsunamasa Inou, and Yasushi Takeda. "Successful Surgical Treatment for Hepatic Encephalopathy Caused by a Pancreatic Siphon: Report of a Case." Surgery Today 28, no. 10 (1998): 1069–72. http://dx.doi.org/10.1007/s005950050284.

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Nozaki, Harushige, Tomonori Shimada, Yoshirou Fukushima, Tsunamasa Inou, and Yasushi Takeda. "Successful surgical treatment for hepatic encephalopathy caused by a pancreatic siphon: Report of a case." Surgery Today 28, no. 10 (1998): 1069–72. http://dx.doi.org/10.1007/bf02483964.

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Podymova, S. D. "Wilson Wilson-Konovalov disease. Features of the debut, course of the disease, diagnostic difficulties, progression factors." Experimental and Clinical Gastroenterology, no. 8 (January 18, 2023): 77–83. http://dx.doi.org/10.31146/1682-8658-ecg-204-8-77-83.

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Modern genetic studies of the prevalence of Wilson-Konovalov disease show that the disease is much more common than previously thought. Of particular importance for early diagnosis is the knowledge of the first manifestations of the disease. The article discusses the features of the debut and clinical course, diagnostic approaches to various forms of Wilson-Konovalov disease. A survey, retrospective analysis and subsequent two-year follow-up of 24 patients with Wilson-Konovalov disease were carried out. During the observation, two variants of the debut of the hepatic form were identified: abdominal with severe pain in the abdomen, liver enlargement, pronounced cytolysis syndrome and high activity of alkaline phosphatase, and the second, manifested by a picture of chronic hepatitis with a moderate increase in the activity of aminotransferases, alkaline phosphatase and bilirubin levels. A feature of the course of the latent hepatic form was portal hypertension with an enlargement of the spleen to a huge size. With a mixed form of neurological and hepatic Wilson-Konovalov disease, four patients were diagnosed with “unexplained” encephalopathy caused by brain damage caused by Wilson-Konovalov’s disease.

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Niu, Chong, Qin, Li, Wei, and Zhao. "Mechanism of Fibrosis Induced by Echinococcus spp." Diseases 7, no. 3 (2019): 51. http://dx.doi.org/10.3390/diseases7030051.

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Infection with Echinococcus spp. causes fibrosis in various vital organs, including the liver and lungs. Hepatic fibrosis is a pathological feature of Echinococcus infection that destroys normal liver tissue, leading to jaundice, cholecystitis, portal hypertension, etc. Severe Echinococcus multilocularis infections lead to liver failure and hepatic encephalopathy. The formation of peripheral fiberboards around the metacestode is a major reason as to why antiparasitic drugs fail to be effectively transported to the lesion site. Studies on the mechanism of hepatic fibrosis caused by Echinococcus are important for treatment in patients. Recent studies have focused on miRNA and TGF-β. More recent findings have focused on the generation of collagen fibers around the metacestode. In this review paper we focus on the mechanism by which the Echinococcus parasite induces fibrosis in liver and some other organs in intermediate hosts—animals as well as human beings.

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Maharani, Baiq Nadya Putri, Aulia Dwi Hendriani, and Putu Wika Pramesti Iswari. "Liver Cirrhosis: Pathophysiology, Diagnosis, and Management." Jurnal Biologi Tropis 23, no. 1 (2023): 457–63. http://dx.doi.org/10.29303/jbt.v23i1.5763.

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Liver disease is still a concern in world health and liver cirrhosis is the eleventh leading cause of death in the world. Cirrhosis caused 1.32 million deaths in 2017. Liver cirrhosis is a fibrosis or nodule formation in the liver. The study was conducted on databases, such as PubMed, google scholar and gray literature. With inclusion criteria, that are free full text publications published in 2015-2022 and having relevant discussions. Fibrosis in cirrhosis of liver begins with the activation of Stellate and Kupffer cells, damaged hepatocytes and activated platelets are also invoved. Inflammatory cells will appear as a result of the damage and cause fibrosis due to the secretion of cytokines. In addition, there are pathological features, namely nodule regeneration and loss of normal lobular architecture within the nodule. The patient's diagnosis start from anamnesis to gather information related to risk factors, physical examination, laboratory tests, imaging, liver biopsy if necessary. Management can be carried out according from etiology of the cause of liver cirrhosis. Complications of liver cirrhosis are portal hypertension, ascites, hepatic encephalopathy, hepatocellular carcinoma, hyponatremia, and acute kidney injury. Liver cirrhosis is a liver fibrosis caused by Stellate, Kupffer cells, damaged hepatocytes, and activated platelets. Inflammatory cells cause fibrosis, leading to regenerating nodules and decreased blood flow. Diagnosis involves anamnesis, physical examination, laboratory tests, imaging, and liver biopsy if needed. Treatment is based on the etiology of liver cirrhosis, with complications including portal hypertension, ascites, and hepatic encephalopathy.

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Kim, Yongbang, Ju Hee Oh, Dae-Woong Bae, and Seonghoon Kim. "A Case of Central Pontine Myelinolysis Caused by Hyperbilirubinemia in Hepatic Encephalopathy without Significant Osmotic Stress." Journal of the Korean Neurological Association 40, no. 2 (2022): 192–94. http://dx.doi.org/10.17340/jkna.2022.2.18.

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Llansola, M., J. L. Cantero, E. Hita-Yañez, et al. "Progressive reduction of sleep time and quality in rats with hepatic encephalopathy caused by portacaval shunts." Neuroscience 201 (January 2012): 199–208. http://dx.doi.org/10.1016/j.neuroscience.2011.11.009.

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Ali, Akmat, Richmond Ronald Gomes, and Khadiza Begum. "Recovery from Leptospira-Related Acute Liver Failure and Acute Kidney Injury ― A Case Report from Bangladesh." Journal of Enam Medical College 9, no. 2 (2019): 136–39. http://dx.doi.org/10.3329/jemc.v9i2.41417.

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Leptospirosis is a zoonosis with protean manifestation caused by the spirochete, Leptospira interrogans. Here we report a 60-year-old male who presented with sudden onset of fever, rigors, myalgia and headache occasionally accompanied by nausea, vomiting and diarrhea. Later during the course of treatment he developed encephalopathy with fulminant hepatic failure and acute kidney injury and was diagnosed as a case of leptospirosis. A timely workup combined with early initiation of antibiotics and hemodialysis led to effective treatment for this patient. J Enam Med Col 2019; 9(2): 136-139

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Pearson, Erwin G. "Liver failure attributable to pyrrolizidine alkaloid toxicosis and associated with inspiratory dyspnea in ponies: Three cases (1982-1988)." Journal of the American Veterinary Medical Association 198, no. 9 (1991): 1651–54. http://dx.doi.org/10.2460/javma.1991.198.09.1651.

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Summary Of 41 equids referred to a veterinary teaching hospital in the Pacific northwest because of dyspnea and inspiratory noise, 3 ponies were diagnosed as having liver failure, most likely attributable to pyrroliziding alkaloid toxicosis. Dyspnea appeared to be caused by laryngeal and/or pharyngeal paralysis. It is proposed that this paralysis was a manifestation of hepatic encephalopathy. Although these clinical signs are not common for pyrrolizidine toxicosis, practitioners should be aware of the possibility so that misdiagnosis of other causes of inspiratory dyspnea may not be made.

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Hagen, Rachael, Minh Thu T. Nguyen, Danzhu Zhao, Melanie Orr, and Elizabeth Richardson. "Cerebral Edema and Super-Refractory Status Epilepticus After Transjugular Portosystemic Shunt Revision." ACG Case Reports Journal 12, no. 5 (2025): e01684. https://doi.org/10.14309/crj.0000000000001684.

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ABSTRACT We present a rare case of super-refractory status epilepticus directly after transjugular portosystemic shunt placement. Despite aggressive management with multiple antiepileptics, osmotic agents, and continuous veno-venous hemofiltration, the outcome was ultimately fatal. This case underscores the importance of maintaining a high index of suspicion when evaluating altered mental status in patients after recent transjugular portosystemic shunt placement and highlights the need for early diagnostic workup. Electroencephalogram and brain magnetic resonance imaging are valuable tools in distinguishing super-refractory status epilepticus caused by hepatic encephalopathy from other etiologies.

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Teksoy, Ozgun, Varol Sahinturk, Mustafa CENGİZ, Behcet İnal, and Adnan Ayhancı. "THE POSSIBLE EFFECTS OF SILYMARIN ON CEREBRUM WITH EXPERIMENTAL HEPATIC ENCEPHALOPATHY IN RATS." International Journal of Research -GRANTHAALAYAH 8, no. 8 (2020): 140–46. http://dx.doi.org/10.29121/granthaalayah.v8.i8.2020.946.

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Background: The relationship between liver diseases and neurological defects is well established. Hepatic encephalopathy (HE) has been seen both in people with acute liver failure (ALF) and chronic liver disease (CLF). HE is a complex neuropsychiatric syndrome that is seen in patients suffering from liver dysfunction. Silymarin (Sm) has antioxidant, anti-inflammatory, and anti-carcinogenic features. In this study, the possible protective effects of silymarin were investigated against dorsolateral prefrontal cortex (DLPFC) damage induced by thioacetamide (TAA). Method: To achieve this, male Sprague Dawley rats (200-250 g) were randomly divided into four groups, with 7 animals comprising each group: the control group, 50 mg/kg TAA group, 50 mg/kg Sm + TAA group, and 100 mg / kg Sm + TAA group. Results: Differences between the groups were determined by performing immunohistochemical analysis of the PFC. Bax, TNF-α, and TUNEL expression increased in the brain tissue of the experimental group where only TAA was administered. Conclusions: It was observed that in high doses in particular (100 mg/kg Sm + TAA group), Sm was effective in preventing PFC damage caused by TAA. It was determined that 100 mg/kg Sm significantly reduces TAA-induced inflammation (TNF-α and H&E) and apoptosis (Bax, TUNEL) in brain tissue.

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Kawale, Juhi B., and Kavita J. Rawat. "Study of etiology, clinical profile and predictive factors of spontaneous bacterial peritonitis in cirrhosis of liver." International Journal of Research in Medical Sciences 5, no. 6 (2017): 2326. http://dx.doi.org/10.18203/2320-6012.ijrms20172096.

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Background: Spontaneous bacterial peritonitis (SBP) is one of the potentially lethal complication of liver cirrhosis and is defined as infected ascites in the absence of any recognizable secondary cause of infection. Majority of the SBP cases are caused by organism from the gastrointestinal tract mainly aerobic gram-negative organisms- Escherichia coli being the most common etiological agent.Methods: It was a prospective observational study done over a period of 1 year in a tertiary care hospital. 50 patients from medical and gastroenterology wards were included in the study. Patients above 12 year of age with diagnosed cirrhosis of liver and documented evidence of SBP were included. Pregnant females, patients who refused to give consent, patients with a documented evidence of intra-abdominal source of infection or patients with ascitis due to non-hepatic causes were excluded.Results: The high serum bilirubin and creatinine levels were associated with higher mortality rate. Hepatic encephalopathy is associated with worse outcome. The outcome of the patient in relation to the grades of ascitis, liver enzymes, prothrombin time, international normalised ratio (INR), Child pugh grades, ascitic fluid polymorphonuclear leucocyte count, ascitic fluid culture and blood culture were not statistically significant.Conclusions: A high index of suspicion should exist for SBP in patients with cirrhosis and ascitis. Serum creatinine and bilirubin levels are strong predictors of mortality. Hepatic encephalopathy has a strong association with mortality in patients with spontaneous bacterial peritonitis.

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Danziger, Larry H., Steven J. Martin, and Robert A. Blum. "Central Nervous System Toxicity Associated With Meperidine Use in Hepatic Disease." Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 14, no. 2 (1994): 235–38. http://dx.doi.org/10.1002/j.1875-9114.1994.tb02815.x.

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Meperidine‐associated central nervous system (CNS) excitatory toxicities are believed to be caused by accumulation of the active metabolite normeperidine. Normeperidine is eliminated by the kidneys and accumulates in patients with renal insufficiency, sickle cell disease, and cancer. In patients with cirrhosis, the metabolism of meperidine is decreased, leading to accumulation of the parent drug and possible CNS depressive effects similar to hepatic encephalopathy. Although the elimination of normeperidine is decreased as well in these patients, the ratio of normeperidine to meperidine is generally low, and the narcotic effects of meperidine usually predominate. This is the first reported case of CNS excitatory toxicities in a patient with alcoholic hepatitis and cirrhosis, and normal renal function. Administration of multiple doses of meperidine in patients with hepatic disease should be discouraged.

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Zimmermann, Marcel, and Andreas S. Reichert. "Rapid metabolic and bioenergetic adaptations of astrocytes under hyperammonemia – a novel perspective on hepatic encephalopathy." Biological Chemistry 402, no. 9 (2021): 1103–13. http://dx.doi.org/10.1515/hsz-2021-0172.

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Abstract Hepatic encephalopathy (HE) is a well-studied, neurological syndrome caused by liver dysfunctions. Ammonia, the major toxin during HE pathogenesis, impairs many cellular processes within astrocytes. Yet, the molecular mechanisms causing HE are not fully understood. Here we will recapitulate possible underlying mechanisms with a clear focus on studies revealing a link between altered energy metabolism and HE in cellular models and in vivo. The role of the mitochondrial glutamate dehydrogenase and its role in metabolic rewiring of the TCA cycle will be discussed. We propose an updated model of ammonia-induced toxicity that may also be exploited for therapeutic strategies in the future.

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