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Hyperammonemia and Hepatic Encephalopathy in Pediatric and Adult Liver Intensive Care Unit
OBJECTIVES: The exact mechanism that causes the neurotoxicity of hepatic encephalopathy (HE) is still unknown. In this retrospective study, we aimed to define the frequency of hyperammonemia and its relationship with HE. METHODS: The records of 190 patients who were followed up in the Organ transpla...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Med Bull Sisli Etfal Hosp
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10098397/ https://www.ncbi.nlm.nih.gov/pubmed/37064852 http://dx.doi.org/10.14744/SEMB.2022.78872 |
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author | Ocak, Ilhan Colak, Mustafa Battal, Muharrem |
author_facet | Ocak, Ilhan Colak, Mustafa Battal, Muharrem |
author_sort | Ocak, Ilhan |
collection | PubMed |
description | OBJECTIVES: The exact mechanism that causes the neurotoxicity of hepatic encephalopathy (HE) is still unknown. In this retrospective study, we aimed to define the frequency of hyperammonemia and its relationship with HE. METHODS: The records of 190 patients who were followed up in the Organ transplantation and Hepato-pancreato-biliary surgery intensive care unit (ICU) between August 2021 and August 2022 were reviewed retrospectively. 111 adults and children whose ammonia levels were examined during their stay in the ICU were included in the study He was evaluated with West Haven Criteria. HE had grades 0–4 in the groups. RESULTS: The median age (range) was 5 (0–16) children and 60 (20–104) adults. The median ammonia value (range) was 42,2 (16–314). Hyperammonemia was present in 39 patients (35%) of all patients. Patients with hyperammonemia and grade 0 encephalopathy were 16 (14%), grade 1–2 patients were 11(10%), and grade 3 patients were 12 (11%). CONCLUSION: While our findings and literature evidence strongly support the view that ammonia is the primary factor responsible for, HE development, it shows that factors other than ammonia can only exacerbate HE. In addition, we think that the increased ammonia value in patients with acute liver failure and acute on chronic liver failure is correlated with the increase in the degree of encephalopathy. |
format | Online Article Text |
id | pubmed-10098397 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Med Bull Sisli Etfal Hosp |
record_format | MEDLINE/PubMed |
spelling | pubmed-100983972023-04-14 Hyperammonemia and Hepatic Encephalopathy in Pediatric and Adult Liver Intensive Care Unit Ocak, Ilhan Colak, Mustafa Battal, Muharrem Sisli Etfal Hastan Tip Bul Original Research OBJECTIVES: The exact mechanism that causes the neurotoxicity of hepatic encephalopathy (HE) is still unknown. In this retrospective study, we aimed to define the frequency of hyperammonemia and its relationship with HE. METHODS: The records of 190 patients who were followed up in the Organ transplantation and Hepato-pancreato-biliary surgery intensive care unit (ICU) between August 2021 and August 2022 were reviewed retrospectively. 111 adults and children whose ammonia levels were examined during their stay in the ICU were included in the study He was evaluated with West Haven Criteria. HE had grades 0–4 in the groups. RESULTS: The median age (range) was 5 (0–16) children and 60 (20–104) adults. The median ammonia value (range) was 42,2 (16–314). Hyperammonemia was present in 39 patients (35%) of all patients. Patients with hyperammonemia and grade 0 encephalopathy were 16 (14%), grade 1–2 patients were 11(10%), and grade 3 patients were 12 (11%). CONCLUSION: While our findings and literature evidence strongly support the view that ammonia is the primary factor responsible for, HE development, it shows that factors other than ammonia can only exacerbate HE. In addition, we think that the increased ammonia value in patients with acute liver failure and acute on chronic liver failure is correlated with the increase in the degree of encephalopathy. Med Bull Sisli Etfal Hosp 2023-03-21 /pmc/articles/PMC10098397/ /pubmed/37064852 http://dx.doi.org/10.14744/SEMB.2022.78872 Text en ©Copyright 2023 by The Medical Bulletin of Sisli Etfal Hospital https://creativecommons.org/licenses/by-nc/4.0/This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/) |
spellingShingle | Original Research Ocak, Ilhan Colak, Mustafa Battal, Muharrem Hyperammonemia and Hepatic Encephalopathy in Pediatric and Adult Liver Intensive Care Unit |
title | Hyperammonemia and Hepatic Encephalopathy in Pediatric and Adult Liver Intensive Care Unit |
title_full | Hyperammonemia and Hepatic Encephalopathy in Pediatric and Adult Liver Intensive Care Unit |
title_fullStr | Hyperammonemia and Hepatic Encephalopathy in Pediatric and Adult Liver Intensive Care Unit |
title_full_unstemmed | Hyperammonemia and Hepatic Encephalopathy in Pediatric and Adult Liver Intensive Care Unit |
title_short | Hyperammonemia and Hepatic Encephalopathy in Pediatric and Adult Liver Intensive Care Unit |
title_sort | hyperammonemia and hepatic encephalopathy in pediatric and adult liver intensive care unit |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10098397/ https://www.ncbi.nlm.nih.gov/pubmed/37064852 http://dx.doi.org/10.14744/SEMB.2022.78872 |
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