Co-proxamol and suicide

Editor—We agree with Hawton et al that co-proxamol presents a major overdose hazard, their results illustrating the difficulties for licensing authorities in limiting availability of prescription medicines that are only hazardous in overdose. Co-proxamol is more likely to result in death; it causes prolongation of the QRS interval in an electrocardiogram in experimental animals and in humans. 3 This property is usually associated with sodium channel blockade and is a precursor to ventricular arrhythmia. We have shown a significant relation between estimated dextropropoxyphene dose (based on paracetamol concentration) and QRS prolongation in a case of co-proxamol poisoning, an effect not seen with other opioid combination products. Dextropropoxyphene is rapidly absorbed from the gastrointestinal tract, increasing early cardiac risk, with death happening within one hour after ingestion. Most patients probably die of co-proxamol poisoning as a result of its combined cardiac (non-opioid) and central nervous system (opioid) effects before hospital admission. Understanding these factors may also improve acute care. Prescribing patterns for co-proxamol may show geographical variation, which could alter the risk estimates calculated by Hawton et al. In Edinburgh co-proxamol poisoning accounted for 4.8% of 5583 patients admitted with self harm in the two years from July 2000 to June 2002 (overall 20% of patients took an opioid). These figures seem similar to those of Hawton et al.