Introduction: Acute liver failure (ALF) is a syndrome defined by jaundice, coagulopathy (INR > 1.5) and hepatic encephalopathy in patients with no evidence of prior liver disease. Toxins and drugs are a frequent cause of ALF in children. Material and methods: The aim of our study was to establish the causes of toxic ALF in children followed up in our hospital in the period of January 2000 to August 2018. We retrospectively studied all hospital records of patients who developed ALF after mushroom/drug exposure and had been admitted to our hospital, the main pediatric toxicology center in northwestern Romania. Results: In the last 18 years, 123 patients were admitted to our clinic with toxic ALF (89 patients secondary to mushroom ingestion and 34 patients after drug exposure). In the 2000-2012 period accidental mushroom poisoning was the leading cause of toxic ALF. Unfortunately, during the last years, voluntary drug ingestions have increased dramatically. The most commonly incriminated drug was acetaminophen (52.94%). Conclusions: ALF in mushroom poisoning is associated with a high mortality in children, despite optimal medical therapy. This etiology was one of the most important causes of death in our cohort. The difficulty in accessing emergency liver transplantation is an obstacle common to many Eastern European pediatric centers. Fortunately, in the last 5 years the incidence of mushroom intoxications has decreased in our area. It is worrying that over the last few years there has been an increased incidence of toxic ALF after drug exposure (for suicidal purposes or due to lenient regulations for prescribing hepatotoxic medications).
The immune system of a child has a degree of immaturity that is maintained until 6–7 years of age. Immaturity may be due to age-related functional disorders in the immune response. A healthy child can contract a series of infections which contribute to the maturation of the immune system during the pre-pubertal period. If repeated infections with prolonged or severe complications occur during childhood, the presence of an immunodeficiency should then be considered. Much more frequent than primary immunodeficiency are recurrent infections (frequently involving the upper respiratory tract), which are less severe and occur under the conditions of an immune system with no apparent major defects. A child can present with 4 to 8 episodes of respiratory infections within a year, during the first 5 years of its life. The average duration of infection is 8 days and up to 2 weeks; if the child presents with 3 episodes of acute infections over a period of 6 months, the respiratory infections are then considered recurrent. The aim of this study was to identify the immunological changes or deviations that cause this clinical syndrome in children. For this purpose, 30 children with recurrent respiratory infections and 10 healthy children were included. Immunoglobulin levels were examined and immunophenotyping was performed. We found that the serum immunoglobulin levels were in the normal range in 70% of the children. On the contrary, our data revealed changes in peripheral cell populations, the most important being the decrease in the T-cluster of differentiation (CD)8 + and total B cell percentages and the increase in the number of memory B cells. The data obtained herein indicated that the decrease in the number of total B cells was mainly due to the decrease in the number of naive IgD + B cells. On the whole, the findings of this study indicate that recurrent respiratory infections may be associated with an altered cellular immune response. In such situations, the investigation of immunological parameters, such as T and B cell subtypes could complete the clinical diagnosis and guide the treatment strategy, thus increasing the quality of life of patients.
The purpose was to identify rapidly the etiology of toxic coma in children, to appreciate the severity of the coma, to detect elements of gravity based on associated clinical signs and symptoms and to evaluate the initial treatment. Toxic coma is a medical emergency, especially in a Pediatric Emergency Department, requiring rapid and precise evaluation. The key objectives in the evaluation and management of coma in children are: detecting severity characteristics, depth of coma, specific clinical signs and symptoms, etiological and differential diagnostic and also initializing supportive therapy and specific treatment. This is a retrospective study, where we analyzed all patients diagnosed with coma admitted to the ‘Grigore Alexandrescu’ Clinical Emergency Hospital for Children over a nine-year period from 2003 to 2011. We focused on toxic coma. A prospective component related to tracking certain signs and symptoms associated with toxic coma to diagnose and initiate appropriate therapy as early as possible was also included. In this nine-year study, 750 comatose patients were included. We found that toxicants represent the main cause of coma in children. There were 445 patients diagnosed with toxic coma, representing 59.3% and 305 cases of non-toxic coma, 40.7% of all coma cases presented in ER. The etiology of toxic coma in children is dominated by alcohol and abuse substances, followed by neurologic medication. Clinical manifestations were more frequent and more severe as the coma degree increases. Associating clinical manifestations in patients with altered neurologic status of toxic cause and toxicants has an important role in practice, because it helps us recognize the frequency of association of coma complications such as: aspiration syndrome, arrhythmias and seizures.
Most cases of envenomation by common European vipers (Vipera berus) have not been reported to have neurotoxic manifestations. However, these manifestations have been demonstrated in some cases of envenomation by subspecies of V. berus, found in the Carpathian Basin region of south-eastern Europe. Here, we report the case of a 5-year-old girl from the south of Romania who presented symptoms of neurotoxicity, as well as other systemic and local symptoms, after being bitten by an adder of the V. berus subspecies. Treatment consisted of monovalent antivenom, a corticosteroid, and prophylactic enoxaparin. Neurotoxic manifestations of envenomation as well as other local and systemic symptoms improved within 5 days of treatment. The presented case shows that venom from V. berus subspecies found in the Carpathian Basin can have neurotoxic effects. This case also confirmed the efficacy of monospecific antivenom treatment in bringing about rapid and complete remission, following envenomation.
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