Acute Liver Failure In A Term Neonate After Repeated Paracetamol Administration.

Severe hepatotoxicity caused by paracetamol is rare in neonates. We report a case of paracetamol-induced acute liver failure in a term neonate. A 26-day-old boy was admitted with intestinal bleeding, shock signs, slight liver enlargement, coagulopathy, metabolic acidosis (pH=7.21; bicarbonate: 7.1 mEq/L), hypoglycemia (18 mg/dL), increased serum aminotransferase activity (AST=4,039 IU/L; ALT=1,087 IU/L) and hyperbilirubinemia (total: 9.57 mg/dL; direct: 6.18 mg/dL) after receiving oral paracetamol (10 mg/kg/dose every 4 hours) for three consecutive days (total dose around 180 mg/kg; serum concentration 36-48 hours after the last dose of 77 µg/ mL). Apart from supportive measures, the patient was successfully treated with intravenous N-acetylcysteine infusion during 11 consecutive days, and was discharged on day 34. The follow-up revealed full recovery of clinical and of laboratory findings of hepatic function. The paracetamol pharmacokinetics and pharmacodynamics in neonates and infants differ substantially from those in older children and adults. Despite the reduced rates of metabolism by the P-450 CYP2E1 enzyme system and the increased ability to synthesize glutathione--which provides greater resistance after overdoses--, it is possible to produce hepatotoxic metabolites (N-acetyl-p-benzoquinone) that cause hepatocellular damage, if glutathione sources are depleted. Paracetamol clearance is reduced and the half-life of elimination is prolonged. Therefore, a particular dosing regimen should be followed due to the toxicity risk of cumulative doses. This report highlights the risk for severe hepatotoxicity in neonates after paracetamol multiple doses for more than two to three days.32144-

Consecutive envenomation of two men bitten by the same coral snake (micrurus corallinus)

To report two patients who developed systemic neurotoxicity after consecutive bites by the same coral snake. Case report: Two previously healthy men (32-year-old and 34-year-old) found a coral snake in a woodpile while collecting wood for a barbecue. During the barbecue, both men became drunk and "played" with the snake, believing that they were handling a false coral snake, and were bitten within a few minutes of each other. Both patients were admitted to a referral tertiary care hospital (175 km from where the bites occurred) 16 hours and 19 hours postbite; both showed similar features of envenomation: palpebral ptosis, muscle weakness, dysphagia, and generalized myalgia. No fang marks or local pain were detected in either case. The patients were successfully treated with Brazilian coral snake antivenom (Fab '(2)) and discharged one-day postadmission, with improvement of myasthenia, but still showing palpebral ptosis. The offending snake was identified as a 42-cm-long Micrurus corallinus. During follow-up, both patients reported a transitory loss of taste that lasted approximately 3-4 weeks postbite. Conclusion: Consecutive bites by the same coral snake may cause systemic neurotoxicity (acute myasthenia) in more than one person, as well as transitory loss of taste, an underreported complication of snakebites58213213

EXPOSIÇÕES TÓXICAS EM CRIANÇAS A SANEANTES DE USO DOMICILIAR DE VENDA LEGAL E CLANDESTINA

RESUMO Objetivos: Analisar e comparar as repercussões clínicas dos acidentes com saneantes de uso domiciliar de origem legal e ilegal (clandestina) em crianças menores de 7 anos. Métodos: Estudo descritivo de corte transversal, com dados obtidos dos prontuários eletrônicos do Centro de Informações e Assistência Toxicológica de referência regional, no período de um ano completo. Foram realizadas análises estatísticas descritivas não paramétricas e de testes de associação. Resultados: A amostra foi constituída de 737 casos. A maioria das exposições ocorreu em crianças menores de 3 anos (mediana: 1 ano, intervalo interquartil: 1-3 anos) na residência habitual (92,9%) e por ingestão (97,2%). Os produtos envolvidos foram saneantes de baixa toxicidade sem efeito cáustico (38,9%), com efeito cáustico (24,1%), hidrocarbonetos (19,3%), inseticidas/raticidas (16,6%), e outros produtos (1,1%). Setenta casos decorreram de exposições a produtos clandestinos, principalmente cáusticos (n=47) e raticidas (n=15). Entre as 337 crianças que apresentaram manifestações clínicas pós-exposição, as ocorrências mais frequentes foram vômitos (n=125), queimaduras orais (n=74), tosse (n=35), salivação (n=26) e dor abdominal (n=25), significativamente mais comum com produtos clandestinos (55/70 versus 282/667; p<0,01). Dezenove crianças foram hospitalizadas (cáusticos, n=17; produtos clandestinos, n=12; mediana do tempo de internação: 2 dias), e 22 foram submetidas à endoscopia digestiva alta (hidróxido de sódio, n=14; produtos clandestinos, n=14), com alterações em 12 casos (grave=2). Não houve óbitos. Conclusões: Exposições tóxicas a saneantes de uso domiciliar de origem clandestina estão associadas com maior morbidade quando comparadas aos de venda autorizada

Thrombotic microangiopathy following Bothrops jararaca snakebite: case report

Thrombotic microangiopathy (TMA) is an uncommon and severe complication of snakebites, and is similar, in general, to hemolytic-uremic syndrome (HUS). We describe a case of TMA following envenomation by Bothrops jararaca. Case details: A 56-y-old-woman with controlled hypertension was transferred from a primary hospital to our ER similar to 7 h after being bitten by B. jararaca in the distal left leg. She developed edema extending from the bite site to the proximal thigh, associated with intense radiating local pain, local paresthesia and ecchymosis at the bite site. Laboratory features upon admission revealed coagulopathy (20 min whole blood clotting time - WBCT20 > 20 min), thrombocytopenia (76,000 platelets/mm(3)) and slight increase in serum creatinine (1.58 mg/dL; RV < 1.2 mg/dL). Upon admission, the patient was treated with bothropic antivenom and fluids replacement. During evolution, her thrombocytopenia and anemia worsened, with blood films showing fragmented red cells, haptoglobin consumption, increase in serum lactate dehydrogenase, and progressive increase of serum creatinine (KDIGO stage = 3). No RBC transfusion, renal replacement therapy or plasmapheresis was done. The patient showed progressive improvement from day nine (D9) onwards and was discharged on D20; there was complete recovery of hemoglobin levels at follow-up (D50). ADAMTS-13 activity, assayed 10 months post-bite, was within reference values. Discussion: TMA following snakebite has been reported mainly in India, Sri Lanka and Australia, with several patients needing renal replacement therapy. Although controversial, plasmapheresis has also been used in some cases. Our patient developed microangiopathic hemolytic anemia, thrombocytopenia and acute kidney injury, a triad of features compatible with TMA similar to HUS. Despite the severity, the outcome following conservative treatment was good, with complete recovery57429429

Management of severe pain after dermal contact with caterpillars (erucism): a prospective case series

Erucism, envenomation caused by dermal contact with larval forms of moths, may result in intense local pain, mainly after contact with puss caterpillars (family Megalopygidae).To evaluate the response to different treatments for controlling severe pain in a case series of erucism in Campinas, southeastern Brazil. Prospective cohort study. A Numeric Pain Rating Scale (NPRS 0-10) was used to assess pain intensity in the Emergency Department (ED). Pain was considered as severe upon ED admission (T0) when the NPRS was >= 8. Inclusion criteria: age >= 8 years old, severe pain at T0, with continuous assessment of pain intensity in all patients using the NPRS during the ED stay (T5, T15, T30, T60 min and at discharge). Fifty-five patients fulfilled the inclusion criteria and were divided into three groups according to the initial treatment at T0: local anesthesia alone with 2% lidocaine (group 1, n = 15), local anesthesia and analgesics (group 2, n = 26) and analgesics without local anesthesia (group 3, n = 14). Most patients were admitted within 2 h after dermal contact with the stinging bristles of caterpillars (median =90 min, IQR: 40-125 min). In 22 cases (40%), the caterpillar was brought for identification (Podalia spp., n = 18; Megalopyge spp., n = 4). There was a significant decrease in pain from T5 onwards with all of the treatments. When the short-term response (T5 and T15) was considered, analgesia was more effective in groups 1 and 2 compared to group 3 (p < .01). Additional analgesia (from T5 until discharge) was frequently required (n = 25/55), mainly in group 1 (n = 11/15). The median length of stay in the ED was 120 min (IQR: 80-173 min). The association of local anesthesia with analgesics was apparently a good combination for the rapid management of severe pain in the ED57533834

Falencia hepatica aguda en neonato a termino despues de la ingestion de dosis repetidas de paracetamol

Objective:Severe hepatotoxicity caused by paracetamol is rare in neonates. We report a case of paracetamol-induced acute liver failure in a term neonate.Case description:A 26-day-old boy was admitted with intestinal bleeding, shock signs, slight liver enlargement, coagulopathy, metabolic acidosis (pH=7.21; bicarbonate: 7.1mEq/L), hypoglycemia (18mg/dL), increased serum aminotransferase activity (AST=4,039IU/L; ALT=1,087IU/L) and hyperbilirubinemia (total: 9.57mg/dL; direct: 6.18mg/dL) after receiving oral paracetamol (10mg/kg/dose every 4 hours) for three consecutive days (total dose around 180mg/kg; serum concentration 36-48 hours after the last dose of 77&#181;g/ mL). Apart from supportive measures, the patient was successfully treated with intravenous N-acetylcysteine infusion during 11 consecutive days, and was discharged on day 34. The follow-up revealed full recovery of clinical and of laboratory findings of hepatic function.Comments:The paracetamol pharmacokinetics and pharmacodynamics in neonates and infants differ substantially from those in older children and adults. Despite the reduced rates of metabolism by the P-450 CYP2E1 enzyme system and the increased ability to synthesize glutathione - which provides greater resistance after overdoses -, it is possible to produce hepatotoxic metabolites (N-acetyl-p-benzoquinone) that cause hepatocellular damage, if glutathione sources are depleted. Paracetamol clearance is reduced and the half-life of elimination is prolonged. Therefore, a particular dosing regimen should be followed due to the toxicity risk of cumulative doses. This report highlights the risk for severe hepatotoxicity in neonates after paracetamol multiple doses for more than two to three days.Objetivo:A hepatoxicidade grave induzida pelo paracetamol é muito rara em neonatos. Relata-se o caso de um neonato de termo que desenvolveu falência hepática aguda após o uso de paracetamol.Descrição do caso:Menino, 26 dias, admitido com sangramento intestinal, sinais de choque, discreta hepatomegalia, coagulopatia, acidose metabólica (pH=7,21; bicarbonato: 7,1mEq/L), hipoglicemia (18mg/dL), aumento das aminotransferases séricas (AST=4.039UI/L; ALT=1.087UI/L) e hiperbilirrubinemia (total: 9,57mg/dL; direta: 6,18mg/dL), após uso de paracetamol via oral (10mg/kg/dose a cada quatro horas) por três dias consecutivos (dose total ao redor de 180mg/kg; nível sérico de 36-48 horas após a última dose de 77µg/mL). Além das medidas de suporte, o paciente foi tratado com N-acetilcisteína (infusão intravenosa contínua por 11 dias consecutivos), recebendo alta após 34 dias de internação. O seguimento mostrou recuperação clínica e dos parâmetros laboratoriais da função hepática.Comentários:A farmacocinética e a farmacodinâmica do paracetamol em neonatos e lactentes jovens (menores de um ano) diferem substancialmente de crianças maiores e adultos. Apesar de as taxas de metabolismo do sistema enzimático P-450 CYP2E1 estarem diminuídas e a capacidade de gerar glutationa, aumentadas - conferindo maior proteção após superdosagens -, existe a possibilidade de produção de metabólitos hepatotóxicos (N-acetil-p-benzoquinoneimina) que determinam lise celular, caso se esgotem as reservas de glutationa. A depuração é diminuída e a meia-vida de eliminação é prolongada, recomendando-se posologia distinta pelo risco de toxicidade de doses cumulativas. O presente relato destaca o risco de hepatotoxicidade grave em neonatos após o uso contínuo de paracetamol por mais de dois a três dias.Objetivo:La hepatotoxicidad grave inducida por el paracetamol es muy rara en neonatos. Se relata el caso de un neonato a t&#233;rmino que desarroll&#243; falencia hep&#225;tica aguda despu&#233;s del uso de paracetamol.Descripci&#243;n del caso:Ni&#241;o, 26 d&#237;as, admitido con sangrado intestinal, se&#241;ales de choque, discreta hepatomegalia, coagulopat&#237;a, acidosis metab&#243;lica (pH=7,21; bicarbonato: 7,1mEq/L), hipoglucemia (18mg/dL), aumento de las aminotransferasas s&#233;ricas (AST=4.039UI/L; ALT=1.087UI/L) e hiperbilirrubinemia (total: 9,75mg/dL; directa: 6,18mg/dL), despu&#233;s del uso de paracetamol por v&#237;a oral (10mg/kg/dosis a cada cuatro horas) durante tres d&#237;as consecutivos (dosis alrededor de 180mg/kg; nivel s&#233;rico de 36-48 horas despu&#233;s de la &#250;ltima dosis de 77&#181;g/mL). Adem&#225;s de las medidas de soporte, el paciente fue tratado con N-acetilciste&#237;na (infusi&#243;n intravenosa continua por 11 d&#237;as consecutivos), recibiendo alta despu&#233;s de 34 d&#237;as de internaci&#243;n. El seguimiento mostr&#243; recuperaci&#243;n cl&#237;nica y de los par&#225;metros laboratoriales de la funci&#243;n hep&#225;tica.Comentarios : La farmacocin&#233;tica y la farmacodin&#225;mica del paracetamol en neonatos y lactantes j&#243;venes (menores de un a&#241;o) difieren substancialmente de ni&#241;os m&#225;s grandes y adultos. A pesar de que las tasas de metabolismo del sistema enzim&#225;tico P-450 CYP2E1 est&#225;n reducidas y la capacidad de generar glutati&#243;n, aumentada - confiriendo m&#225;s protecci&#243;n despu&#233;s de superdosis -, existe la posibilidad de producci&#243;n de metab&#243;litos hepatot&#243;xicos (N-acetil-pbenzoquinoneimina) que determinan lisis celular, caso se agoten las reservas de glutati&#243;n. La depuraci&#243;n es reducida y la media vida de la eliminaci&#243;n, alargada, recomend&#225;ndose posolog&#237;a distinta por el riesgo de toxicidad de dosis cumulativas. El presente relato subraya el riesgo de hepatotoxicidad grave en neonatos despu&#233;s del uso continuo de paracetamol por m&#225;s de dos a tres d&#237;as.14414