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Changes in Serum phosphate during treatment of diabetic ketoacidosis: Predictive significance of severity of acidosis on presentation

机译:糖尿病酮症病治疗过程中血清磷酸盐的变化:酸中毒严重程度对呈现的预测意义

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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 ± 0.19mmol/L. Ninety percent of nadir phosphate levels were hypophosphataemic (<0.8mmol/L), and 11% were severely hypophosphataemic (<0.32mmol/L). Mean initial bicarbonate differed significantly between those with nadir phosphates <0.5mmol/L (9.26 ± 4.55) and those with nadir phosphates >0.5mmol/L (13.0 ± 4.59, P = 0.0031). Similar significant bicarbonate differences were noted between those with nadir phosphates less than and more than 0.32mmol/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.
机译:糖尿病酮酸期间(DKA)处理期间血清磷酸盐的变化并不具备很好的表征,尽管已知血清磷酸盐用处理落下。我们试图定义这些变化的性质以及对入院的酸中毒的严重程度是否影响了随后的脾磷吸血病症的严重程度。我们回顾性地审查了所有患有确认DKA的患者的数据,即2007年至2010年之间的单位包容。评估四十三名患有64个DKA发作的患者。在介绍时,62.5%的患者发作是高磷脂。所有患者中的初始血清磷酸盐与初始血清肌酐(R = 0.694,P <0.01)和初始血糖(r = 0.593,p <0.01)显着相关。在所有发作过程中治疗过程中血清磷酸盐下降(平均绝对下降1.28±0.77(SEM)mmol / L)。平均Nadir磷酸盐为0.58±0.19mmol / L.百分之九十的Nadir磷酸盐水平是脾脏血磷(<0.8mmol / L),11%是严重的低磷(<0.32mmol / L)。平均初始碳酸氢盐在磷酸萘吡吡磺酸酯<0.5mmol / L(9.26±4.55)的那些之间有显着不同,磷酸盐碱> 0.5mmol / L(13.0±4.59,p = 0.0031)。在磷酸胺分别小于且超过0.32mmol / L之间的那些之间的相似显着的碳酸氢盐差异(7.42±2.44和12.2±4.87,P <0.01)。初始高渗血症反映血管内体积耗竭和肾肾损伤。随后的咳嗽磷吸霉素的严重程度可以通过呈现的代谢酸中毒程度来预测。由于深吸次磷病毒可能与严重的并发症有关,临床医生应认识到这种生物化学紊乱在具有深厚酸中毒的DKA患者中的可能性。

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