Hyperphosphataemia

Phosphate disturbances are thankfully neglected in CICM SAQs. Fortunately for us all, up until Question 20.1 in the first paper of 2017 the college had never asked any questions about it. It appears in the Required Reading section purely for completeness (though the author is acute aware that the pursuit of completeness may lead one to contemplate disorders of molybdenum homeostasis, etc). Oh's Manual dwells briefly on phosphate and offers two Blue Boxes to describe its behaviour (Boxes 93.8 and 93.9, p. 957-958). Of the published literature, the best summary is offered by UpToDate. A highly detailed discussion is available behind another paywall, at Springer (Albaaj et al, 2003). Of free resources, the best turned out to be the eMedicine (Medscape) article by Eleanor Lederer and Vecihi Batuman (2015).

This list of clinical features was developed with the aid of articles describing accidental severe hyperphosphataemia, such as Fine et al (1997).  The authors offer two cases of their own, as well as summarising all case reports of adults with massive hyperphosphataemia. The blood results are offered in mg/dL, which is annoying, but with the use of an online calculator the author was able to determine that of the fatal overdoses, the highest recorded serum phosphate level was 19.0 mmol/L. Of the survivors, the highest recorded phosphate level was 10.0 mmol/L, reported by Zipser et al in 1975. The 41 year old male patient had ingested a sodium phosphate laxative, and had almost died as a consequence, with hypocalcemic tetany the dominant feature of presentation. Impaired renal function was implicated in the pathogenesis in almost all cases, leading one to believe that in the presence of normal renal function it would be difficult to fatally overdose on exogenous phosphate.