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.¹

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.²,³ 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,⁴ 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.⁵ 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.