RESUMO
OBJECTIVES: To compare the management of acute paracetamol poisoning with the best evidence available, and to determine the effect of plasma paracetamol level estimation on the management. DESIGN: Descriptive study with an intervention. SETTING: Medical wards of the National Hospital of Sri Lanka, Colombo. PATIENTS: Patients admitted with a history of acute paracetamol poisoning. INTERVENTION: Measurement of plasma paracetamol. METHODS: Data were obtained from the patients, medical staff and medical records. Plasma paracetamol was estimated between 4-24 hours of paracetamol ingestion. The current management practices were compared with the best evidence on acute paracetamol poisoning management. RESULTS: 157 patients were included. The mean ingested dose of paracetamol was 333 mg/kg body weight. Majority of the patients (84%) were transfers. Induced emesis and activated charcoal were given to 91% of patients. N-acetylcysteine was given to 66, methionine to 55, and both to 2. Aclinically important delay in the administration of antidotes was noted; 68% of patients received antidotes after 8 hours of the acute ingestion. Only 31 (26%) had paracetamol levels above the Rumack-Matthew normogram. 74 patients received an antidote despite having a plasma paracetamol level below the toxic level according to the normogram. INTERPRETATION: Management of acute paracetamol poisoning could be improved by following best available evidence and adapting cheaper methods for plasma paracetamol estimation.
Assuntos
Acetaminofen/sangue , Acetilcisteína/administração & dosagem , Doença Aguda , Analgésicos não Narcóticos/sangue , Antídotos/administração & dosagem , Carvão Vegetal/administração & dosagem , Eméticos/administração & dosagem , Medicina Baseada em Evidências , Feminino , Hospitais Públicos , Humanos , Masculino , Metionina/administração & dosagem , Intoxicação/terapia , Bicarbonato de Sódio/administração & dosagem , Sri Lanka , Fatores de Tempo , Resultado do Tratamento , Adulto JovemRESUMO
The aim of the present paper is to establish the possible role of serum TNF in the pathophysiology of three experimental models of liver injury: paracetamol intoxication, cholestasis followed by paracetamol intoxication and cholestasis. We concluded that under our experimental conditions the serum TNF-alpha levels were not responsible for the inflammatory phenomena described in our previous paper as apopt.