ABSTRACT
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.
Subject(s)
Acetaminophen/blood , Acetylcysteine/administration & dosage , Acute Disease , Analgesics, Non-Narcotic/blood , Antidotes/administration & dosage , Charcoal/administration & dosage , Emetics/administration & dosage , Evidence-Based Medicine , Female , Hospitals, Public , Humans , Male , Methionine/administration & dosage , Poisoning/therapy , Sodium Bicarbonate/administration & dosage , Sri Lanka , Time Factors , Treatment Outcome , Young AdultABSTRACT
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.