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Hepatic Encephalopathy
Published in Charles Theisler, Adjuvant Medical Care, 2023
Hepatic encephalopathy (HE) is a neuropsychiatric condition characterized by transient, gradual, or complete loss of consciousness (hepatic coma) and decline in brain function as a result of liver failure. HE describes a range of reversible neuropsychiatric abnormalities. Hepatic encephalopathy as a result of cerebral edema and intracranial hypertension is a significant cause of morbidity and mortality in advanced cirrhotic patients. Acute HE usually develops in a clinically stable cirrhotic patient as the result of an acute precipitating event such as hypovolemia, metabolic disturbances, gastrointestinal bleeding, infection, and constipation. These precipitating factors should be managed and controlled. Chronic HE, by definition, occurs and persists in the absence of precipitating factors.1
No organ can make the body sick
Published in Dinesh Kumar Jain, Homeopathy, 2022
Body can become sick when the lung, liver, heart, kidney, or any other organ of the body is damaged. Liver disorder creates hepatic coma. Kidney failure is responsible for death. Heart failure also damages the whole body. Heart attack is the main cause of death. When pathology or disease in one organ can cause death, then how Kent can say that damage or disease of one organ cannot make the body sick. Now we can say this statement of Kent is also wrong.
Diagnostic Approach to Fulminant Hepatitis in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Yellow fever (YF) is a viral disease endemic to the tropical regions of Africa and South America; it is spread primarily by Aedes aegypti. It has a high case fatality rate and can manifest with life-threatening disease associated with fever, jaundice, renal failure, and hemorrhage. In severe cases, hepatic coma and death may develop. Laboratory abnormalities include marked transaminase elevations (AST > ALT), with mildly elevated ALP, direct bilirubin levels, and a prolonged INR [35]. Diagnosis is made by ELISA for IgM and is confirmed by a rise in titer between paired acute and convalescent samples. Rapid diagnostic test using PCR to detect virus in the blood and viral culture can also be used. Liver biopsy should be avoided in the acute phase of yellow fever, as fatal hemorrhage may occur [36]. There is no specific therapy for YF, and treatment includes fluids and supportive care.
Propranolol-induced hallucinations mimicking encephalopathy in a patient with liver cirrhosis
Published in Scandinavian Journal of Gastroenterology, 2021
Samer Al-Dury, Antonio Molinaro, Per Hedenström
HE results in a myriad of non-specific neurological and psychiatric manifestations that vary from minimal and undetectable symptoms upon physical examination to overt and severe symptoms, including hepatic coma and death [4]. HE is usually caused by an acute precipitating factor. In our case, it was an infection requiring hospitalization. Once the insulting factor was resolved, the patient was alert and showed no signs of cognitive dysfunction. In some cases where the liver function is severely impaired, HE can present intermittently without a clear precipitating factor, making diagnosis and treatment challenging and may lead to a lengthy and thorough assessment to investigate whether the patient is a suitable liver transplantation candidate [5,6]. Since the patient in this particular case had HE at presentation, we continued treatment with non-absorbable disaccharide Lactulose to achieve at least one bowel movement daily and the antibiotic Rifaximin 1100 mg/day to prevent further exacerbations of HE.
The development and hepatotoxicity of acetaminophen: reviewing over a century of progress
Published in Drug Metabolism Reviews, 2020
Mitchell R. McGill, Jack A. Hinson
Subsequently, there were a number of other reports of APAP toxicity in overdose patients (Thomson and Prescott 1966; Rose 1969; Proudfoot and Wright 1970; Boyer and Rouff 1971; Prescott et al. 1971). The clinical features of the toxicity were described by Boyer and Rouff (1971): nausea and vomiting within two to three hours followed by abdominal pain, chiefly in the upper right quadrant. Liver dysfunction is present within approximately 24 hours and peaks at four days after the overdose. The clinical biochemistry was summarized by Prescott et al. (1971): dramatic increases of circulating alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH); mild hyperbilirubinemia; increases in prothrombin time; and increased APAP half-life to greater than four hours. When the half-life was greater than 12 hours, hepatic coma frequently occurred.
A patent update on therapeutic applications of urease inhibitors (2012–2018)
Published in Expert Opinion on Therapeutic Patents, 2019
Abdul Hameed, Mariya Al-Rashida, Maliha Uroos, Syeda Uroos Qazi, Sadia Naz, Marium Ishtiaq, Khalid Mohammed Khan
Hydroxamic acids [18,19] and phosphoramidates are the most well-known urease inhibitors [20,21]. Hydroxamic acid and its analogs are known to be reversible inhibitors of both plant and bacterial ureases [22–24]. The importance of alkyl hydroxamic acid-mediated inhibition of urease for the possible treatment of hepatic coma is well documented in the literature [25]. Similarly, many other hydroxamic acid derivatives are also known to be active inhibitors of urease, wherein the –CONHOH structural moieties are known to be necessary for urease inhibition [26,27]. Fluoride ions are also capable of inactivating the enzyme, by acting as a noncompetitive inhibitor [22,28]. In another suggested mechanism, fluoride in the form of its acid, that is hydrofluoric acid, can provide a weak acidic environment that might be effective for countering urease activity. However, this mechanism was found to be much less effective as compared to direct inhibition by fluoride ions [29].