Acute ammonia-induced intoxication is a kind of acute irritant gas poisoning, which mainly causes systemic inflammatory reaction and immune dysfunction through direct and indirect lung injury, leading to chemogenic pulmonary edema and acute respiratory distress syndrome (ARDS). The mechanism of its toxic injury is complex, and the fatality rate of patients increases significantly once ARDS occurs. In this paper, the patient with acute and severe ammonia-induced intoxication was successfully treated by extracorporeal membrane oxygenation (ECMO) combined with fiberoptic bronchoscopy and other critical technologies, and achieved good results. By analyzing the diagnosis and treatment process of severe ammonia-induced intoxication complicated with ARDS patients, this paper summarizes the clinical characteristics of ammonia-induced intoxication injury, and the application opportunities of ECMO and various critical medical technologies, so as to facilitate the efficient intervention and treatment of ammonia-induced intoxication according to the clinical opportunity and improve the survival rate of patients.
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http://dx.doi.org/10.3760/cma.j.cn121094-20231103-00100 | DOI Listing |
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
September 2024
Center of Emergency & Intensive Care Unit, Jinshan Hospital, Fudan University; Medical Research Center for Chemical Injury, Emergency and Critical Care of Chemical Injury, Fudan University; Key Laboratory of Chemical Injury, Emergency and Critical Medicine of Shanghai Municipal Health Commission, Shanghai 201508, China.
Animals (Basel)
July 2021
Clinical Pathology Department, Faculty of Veterinary Medicine, Kafrelsheikh University, KafrelSheikh 33516, Egypt.
Ammonia is a critical hazardous nitrogen metabolic product in aquaculture. Despite trials for its control, ammonia intoxication remains one of the most critical issues to overcome. In this study, we explored the modulatory effect and potential mechanism by which extract (YSE) can ameliorate ammonia intoxication-induced adverse effects on tilapia health and metabolism.
View Article and Find Full Text PDFEBioMedicine
October 2019
Institute of Biochemistry and Molecular Biology I, Heinrich Heine University Düsseldorf, Medical Faculty, Düsseldorf, Germany. Electronic address:
Background: Hepatic encephalopathy (HE) is a severe neuropsychiatric syndrome caused by various types of liver failure resulting in hyperammonemia-induced dysfunction of astrocytes. It is unclear whether autophagy, an important pro-survival pathway, is altered in the brains of ammonia-intoxicated animals as well as in HE patients.
Methods: Using primary rat astrocytes, a co-culture model of primary mouse astrocytes and neurons, an in vivo rat HE model, and post mortem brain samples of liver cirrhosis patients with HE we analyzed whether and how hyperammonemia modulates autophagy.
Inhal Toxicol
December 2016
a Analytical Toxicology Division , US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground , MD , USA.
This study examined acute toxicity and lung injury following inhalation exposure to ammonia. Male Sprague-Dawley rats (300-350 g) were exposed to 9000, 20,000, 23,000, 26,000, 30,000 or 35,000 ppm of ammonia for 20 min in a custom head-out exposure system. The exposure atmosphere, which attained steady state within 3 min for all ammonia concentrations, was monitored and verified using a Fourier transform infrared spectroscopy (FTIR) gas analyzer.
View Article and Find Full Text PDFHepatology
July 2011
Clinic for Gastroenterology, Hepatology, and Infectiology, Heinrich-Heine University, Düsseldorf, Germany.
Unlabelled: Astrocytes play an important role in the pathogenesis of hepatic encephalopathy (HE) and ammonia toxicity, whereas little is known about microglia and neuroinflammation under these conditions. We therefore studied the effects of ammonia on rat microglia in vitro and in vivo and analyzed markers of neuroinflammation in post mortem brain tissue from patients with cirrhosis with and without HE and non-cirrhotic controls. In cultured rat microglia, ammonia stimulated cell migration and induced oxidative stress and an up-regulation of the microglial activation marker ionized calcium-binding adaptor molecule-1 (Iba-1).
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