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A severe degree of hypotension in children followed the intravenous administration of codeine phosphate in several case reports—histamine release was its presumed root cause [1–3]. We also report cardiovascular collapse following accidental bolus intravenous injection of 30 mg (74 μmol) codeine phosphate, but it was associated with a surprising profound degree of hypocalcaemia. A quantitative analysis is provided along with a novel hypothesis to explain the timing and the profound degree of hypocalcaemia that followed the administration of codeine phosphate.  We extend this observation to the initiation of kidney stone formation. The conundrum is that while calcium oxalate deposits grow progressively to form Randall's plaque, calcium oxalate does not precipitate in vitro at prevailing concentrations of ionized Ca2+ and oxalate [4]. Since the nidus of the commonest type of kidney stone, calcium oxalate, is hydroxyapatite, it has been postulated that this nidus permits the precipitation of calcium oxalate [5]. However, it is not known how the initial deposit of hydroxyapatite can occur on the basolateral aspect of the ascending thin limb of the loop of Henle in the inner medulla in patients with idiopathic hypocalciuria. We speculate that the first deposit is a precipitate of calcium carbonate (CaCO3).

Hypocalcaemia and a low cardiac output after intravenous codeine phosphate injection: need for an additional mechanism to remove ionized calcium