Citation

Soderstrom JH, Fatovich DM, Mandelt C, Vasikaran S, McCoubrie DL, Daly FF, Stat SA. Br. J. Clin. Pharmacol. 2012; 74(1): 154-160.

Affiliation

Clinical Toxicologist, Emergency Physician Royal Perth Hospital Professor of Emergency Medicine Royal Perth Hospital, University of Western Australia and the Centre for Clinical Research in Emergency Medicine, Western Australian Institute for Medical Research Medical Scientist Biochemistry, PathWest, Royal Perth Hospital Medical Biochemist, Clinical Professor, University of Western Australia Clinical Toxicologist, Emergency Physician Royal Perth Hospital Clinical Toxicologist, Emergency Physician Royal Perth Hospital Biostatistician, School of Medicine and Pharmacology & Royal Perth Hospital, University of Western Australia.

Copyright

(Copyright © 2012, John Wiley and Sons)

DOI

10.1111/j.1365-2125.2011.04157.x

PMID

22122348

Abstract

What this paper adds: What is already known about this subject Paracetamol is commonly used in deliberate self poisoning (DSP) and this requires blood sampling to refine risk assessment. If saliva concentrations agreed with plasma concentrations, then this could support the development of non-invasive testing. Our pilot work supports this hypothesis, but was largely confined to non-toxic concentrations. What this study adds We found agreement between the indications for treatment of paracetamol DSP based on plasma and saliva paracetamol concentrations. Saliva may hold promise as a non-invasive method to risk stratify paracetamol poisoning. SUMMARY: Aims: Paracetamol is commonly used in deliberate self poisoning (DSP) and requires blood sampling to refine risk assessment. We aimed to test the agreement between plasma and saliva paracetamol concentrations in the toxic range in DSP. Methods: Contemporaneous paired plasma and saliva paracetamol concentrations were measured. Saliva was collected using a Sarstedt Salivette® device and the concentration was measured using a colorimetric method. Results: 56 patients (44, 78% female) median age 26 years (IQR 20-41) were enrolled. The median reported paracetamol ingestion was 10 g (IQR 6-14). Specimens were collected at a median of 4 hours (IQR 4-5.3) post ingestion. The median plasma and saliva paracetamol concentrations were 29 mg/L (IQR 8-110) and 38 mg/L (10-105) respectively (mean difference 8 mg/L, 95%CI 2-14). Lin's concordance correlation was 0.97 (95%CI 0.96-0.98). There were 15 patients who were treated with N-acetylcysteine. Their median reported paracetamol ingestion was 14 g (IQR 10-23) and samples were collected at a median of 4 hours post ingestion. The median plasma and saliva paracetamol concentrations were 167 mg/L (IQR 110-200) and 170 mg/L (IQR 103-210) respectively (mean difference 15 mg/L, 95%CI -4-35). Lin's concordance correlation was 0.94 (95% CI 0.88-0.99). No patient needing treatment would have been missed using saliva concentrations only. Conclusions: The agreement between the indications for treatment of paracetamol DSP based on plasma and saliva paracetamol concentrations extends into the toxic range, but with slightly lower agreement. Saliva may hold promise as a non-invasive method to risk stratify paracetamol poisoning.

Language: en