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Acute Fatty Liver of Pregnancy
Published in Sanjeewa Padumadasa, Malik Goonewardene, Obstetric Emergencies, 2021
Janaka de Silva, Sanjeewa Padumadasa
Steatosis of the liver impairs liver function and can activate fulminant liver failure and multiorgan dysfunction, which may result in the death of the woman and the fetus. Liver injury can be complicated by haematoma, infarction or rupture. Renal dysfunction can occur due to direct fatty infiltration, hypoperfusion and hepatorenal syndrome. Fatty acid metabolites are toxic to pancreatic tissue and may cause pancreatitis, which can be complicated by pseudocysts with secondary infection, haemorrhage and necrosis. Placental dysfunction results from the deposition of fatty acids as well as fibrin in the placenta. The reduced levels of fibrinogen, coagulation factors and antithrombin III (due to reduced production by the liver) together with endothelial cell dysfunction leads to coagulopathy. Transient diabetes insipidus may develop as a result of elevated levels of vasopressinase, the enzyme that metabolises vasopressin and is normally cleared by the liver. Encephalopathy may occur, and can lead to convulsions and coma.
Gastroenterology
Published in Faye Hill, Sash Noor, Neel Sharma, Tiago Villanueva, Medical and Surgical Emergencies for Students and Junior Doctors, 2021
Faye Hill, Sash Noor, Neel Sharma
Management is dependent on the grade of encephalopathy. A CT brain scan should be performed to exclude intracranial pathology and the presence of oedema. Lactulose has been shown to be merited in such patients. Patients with grade III or IV encephalopathy should ideally be intubated, with the use of mannitol for severe elevation of intracranial pressure or herniation. Antibiotics as per hospital protocol should be prescribed to reduce risk of sepsis.
Introduction to dementia
Published in Joanne Brooke, Dementia in Prison, 2020
Korsakoff’s syndrome is the most well-known form of ARBD, although is less common than other forms of ARBD such as alcoholic dementia (Ridley et al., 2013). Korsakoff’s syndrome often develops as part of a condition known as Wernicke-Korsakoff syndrome. This consists of two separate but related stages: Wernicke’s encephalopathy followed by Korsakoff’s syndrome and Wernicke-Korsakoff syndrome, which is diagnosed in 1 in 8 people with alcoholism. However, not everyone has a clear case of Wernicke’s encephalopathy before Korsakoff’s syndrome develops (Oudman et al., 2014). Encephalopathy refers to permanent or temporary brain damage, disorder or disease, which affects the brain’s function or structure and may be degenerative. The primary symptom is an altered mental status. Wernicke’s encephalopathy usually develops suddenly, often after abrupt and untreated withdrawal from alcohol. It has a range of different symptoms, but they may not be obvious, and it can be difficult to make a diagnosis (Oudman et al., 2014).
Long-term central nervous system (CNS) consequences of COVID-19 in children
Published in Expert Review of Neurotherapeutics, 2023
Saskia Howe de la Torre, Valeria Parlatini, Samuele Cortese
Overall, headache, cognitive deficits, anosmia, ageusia, and dizziness appear to be common neurological symptoms associated with long COVID in the pediatric population. Prevalence estimates are highly variable in the literature due to study heterogeneity in terms of design, sample size, inclusion of children with confirmed and non-confirmed infection, severity of primary COVID infection (mild vs severe symptoms requiring hospitalization), and method of case identification (e.g. general population vs specialized long COVID clinics). Pooled prevalence estimates range between 9.7% (fatigue) to 4.4% (dizziness) [19]. Similarly, symptom duration varies across studies and, although symptoms generally improve over time, they have been reported even after several months following initial infection. Increasing age has been identified as a risk factor, as well as female sex for some symptoms (ageusia and dizziness). Seizures typically present as acute SARS-CoV-2 sequela, but long-term risk warrants further investigation. Finally, encephalitis/encephalopathy are rare and often fatal acute complications but may be associated with long-term cognitive/neurological symptoms in survivors.
Pathogenesis and Management of Acute Necrotizing Encephalopathy
Published in Expert Review of Neurotherapeutics, 2023
Ningxiang Qin, Jing Wang, Xi Peng, Liang Wang
ANE is characterized by the rapid progression of acute encephalopathy [2]. Although ANE is frequently caused by multiple pathogen infections, studies have shown that different pathogens, races, adults, and children have similar clinical symptoms and laboratory and neuroimaging findings [2,30,55]. According to the existing case reports, the clinical course of most ANE patients can be divided into three stages: prodrome infection, acute encephalopathy, and recovery [56]. During the prodrome infection stage, which more than 90% of patients experience, fever, cough, vomiting, diarrhea, and other manifestations are characterized by febrile toxic diseases. Acute encephalopathy usually occurs 1–3 days after prodromal onset and is clinically characterized by rapid, progressive neurological deterioration, including sudden changes in mental status, deterioration of consciousness, rapid progression to coma, and possibly accompanied by seizures and focal neurological deficiency [1,36]. Patients at this stage often require ICU admission, but most have a poor prognosis. Although ANE is typically associated with viral infections, some patients may develop deteriorating mental status as a result of severe infections complicated by organ dysfunction, such as acute lung injury, disseminated intravascular coagulation, or shock. These complications can exacerbate the underlying pathology of ANE and may contribute to poor outcomes. Therefore, it is important to carefully monitor patients with ANE for signs of systemic infection and organ dysfunction and to provide prompt and appropriate management [57].
Hyperammonemia in acetaminophen toxicity
Published in Clinical Toxicology, 2022
Ryan T. Marino, Alexander M. Sidlak
Forty-six (45%) patients received one or multiple treatments for encephalopathy. The most common treatments were lactulose (44/46; 97%) and rifaximin (28/46, 61%). 15 (33%) patients had encephalopathy prior to treatment and 31 (67%) received treatment prior to or in the absence of encephalopathy. Six patients who were treated empirically developed encephalopathy. Three encephalopathic patients received no treatment for encephalopathy and none worsened. Of the patients not treated (56/102; 55%), none developed encephalopathy. 26 (52%) had ammonia concentrations obtained on presentation and those concentrations were similar to patients receiving treatment for encephalopathy (72 µmol/L (95% CI: 53–106) v 85 (65–185) [p = .09]. Overall, one patient required a liver transplantation and four patients died.