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Changes in serum phosphate during treatment of diabetic ketoacidosis: predictive significance of severity of acidosis on presentation
Author(s) -
Shen T.,
Braude S.
Publication year - 2012
Publication title -
internal medicine journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 1444-0903
DOI - 10.1111/imj.12001
Subject(s) - medicine , nadir , diabetic ketoacidosis , bicarbonate , metabolic acidosis , creatinine , phosphate , acidosis , ketoacidosis , endocrinology , diabetes mellitus , hypophosphatemia , gastroenterology , biochemistry , chemistry , type 1 diabetes , satellite , aerospace engineering , engineering
Changes in serum phosphate during diabetic ketoacidosis ( DKA ) treatment are not well characterised, although it is known that serum phosphate falls with treatment. We sought to define the nature of these changes and whether the severity of acidosis on admission influenced the severity of subsequent hypophosphataemia. We retrospectively reviewed data on all patients with confirmed DKA presenting to our unit between 2007 and 2010 inclusive. Forty‐three patients with 64 episodes of DKA were evaluated. At presentation, 62.5% of patient episodes were hyperphosphataemic. Initial serum phosphate in all patient episodes correlated significantly with the initial serum creatinine (r = 0.694, P < 0.01) and the initial blood glucose (r = 0.593, P < 0.01). Serum phosphate fell during the course of treatment in all episodes (mean absolute fall 1.28 ± 0.77 ( SEM ) mmol/ L ). The mean nadir phosphate was 0.58 ± 0.19 mmol/ L . Ninety per cent of nadir phosphate levels were hypophosphataemic (<0.8 mmol/ L ), and 11% were severely hypophosphataemic (<0.32 mmol/ L ). Mean initial bicarbonate differed significantly between those with nadir phosphates <0.5 mmol/ L (9.26 ± 4.55) and those with nadir phosphates >0.5 mmol/ L (13.0 ± 4.59, P = 0.0031). Similar significant bicarbonate differences were noted between those with nadir phosphates less than and more than 0.32 mmol/ L respectively (7.42 ± 2.44 and 12.2 ± 4.87, P < 0.01). The initial hyperphosphataemia is reflective of intravascular volume depletion and pre‐renal renal impairment. The severity of subsequent hypophosphataemia can be predicted by the degree of metabolic acidosis on presentation. As profound hypophosphataemia can be associated with serious complications, clinicians should recognise the likelihood of this biochemical derangement in those DKA patients presenting with profound acidosis.