Abstract
We thank Drs Pakravan et al. for their commentary on our case report of two patients who had taken significant paracetamol overdoses and subsequently developed significant hypokalaemia within 8 h of presentation. 1 We would however like to make the following comments in reply:
We appreciate the authors' conviction with respect to their published retrospective and prospective studies relating to this phenomenon. 2 The authors have sought to extrapolate evidence gathered in an animal model, which certainly points towards a renal perfusion hypothesis as the cause of the hypokalaemia. Conclusive proof has however not yet been established that this model can be extrapolated into a human population.
The authors state that they believe a 36 h monitoring period is unnecessary and potentially wasteful of hospital resources for these patients. We would like to refute that claim as we believe it would be unwise from a clinical perspective to discharge a previously normokalaemic patient who had presented with this rare complication of paracetamol overdose back into the community immediately. The current level of evidence does not allow us to safely conclude that this hypokalaemia may be dismissed as unimportant in the context of their discharge from the hospital. Indeed a large number of our patients have concurrent cardiovascular pathology and addiction issues that may be significantly complicated by concurrent hypokalaemia. We would therefore advocate a more cautious approach until more robust evidence is available. Significant hypokalaemia remains an uncommon complication of the paracetamol toxidrome; it is therefore outside the norm and should be treated as such. Clinicians may find it hard to justify complications that arise in this group of patients, if discharged prior to normalization of their serum potassium concentration.