Toxicity of topical polyethylene glycol

An animal model was developed to study the potential toxicity resulting from repeated, topical applications of a polyethylene glycol-based antimicrobial cream. Applications of this cream to open wounds in rabbits produced the same syndrome observed in the burn patients treated with this agent. This syndrome was characterized by (1) elevated total calcium, (2) elevated osmolality gap, (3) high anion gap metabolic acidosis, and (4) renal failure. Ten of twelve treated animals died within one week of therapy. This syndrome appears to result from the absorption of polyethylene glycols and their metabolism to nephrotoxic compounds and to mono- and diacids. We propose that the increased serum osmolality reflects the absorption of glycols and their presence in the circulation, while the acidosis reflects the presence in plasma of mono- and diacid metabolites of the glycols. The diacid metabolities of low-molecular-weight polyethylene glycols are excellent calcium chelators and can account for the hypercalcemia. Finally, we suggest that polyethylene glycol metabolites produce renal destruction via mechanisms similar to those involved in the renal failure associated with ethylene glycol poisoning.