Endocrine abnormalities in lithium toxicity

Editor – Shanks et al¹ describe salient physiological lessons from their patient with severe sequelae of lithium toxicity. I wish to suggest further lessons that may be learned from their report to minimise harm in future similar cases. It appears that nephrogenic diabetes insipidus (DI) was not considered until day 10 of the admission. That sodium remained elevated despite fluid resuscitation clearly implicates impaired renal salt handling and the patient’s chronic lithium treatment was known. It is pertinent that 0.9% sodium chloride failed to correct the hypernatraemia from the start and so earlier suspicion of DI may have helped. There is no reason to stick doggedly to saline infusions to treat hypercalcaemia and 5% dextrose may have been the preferable resuscitation fluid.

One may justly wonder if the patient would have benefited from earlier ITU admission. Serum sodium was 172 mmol/L at day 4 – a severe medical emergency especially in a young patient – yet she was not transferred to ITU until almost a week later on day 10. This case must surely demonstrate that close monitoring and chasing of fluid and electrolyte goals is very hard on Level 1 wards. I would suggest that the refractory severe hypocalcaemia seen in this case was a known complication of unnecessary bisphosphonate treatment, as calcium will typically drop to safe levels (<3 mmol/L) with sufficient fluids alone. It would be pertinent to know how much improvement in fluid balance and what correction in serum calcium was achieved before the IV bisphosphonate was administered. Finally, with regards the patient’s neurological disorder, did the authors consider the possibility of thyrotoxic periodic paralysis?