Endocrine Abstracts (2017) 49 GP109 | DOI: 10.1530/endoabs.49.GP109

Treatment of diabetic ketoacidosis at type 1 diabetes mellitus presentation: 13 year experience from a tertiary centre (2004-2016)

Joana Serra-Caetano1, Lia Gata1, Alexandra Dinis1, Rita Cardoso1, Isabel Dinis1, Miguel Patrício2 & Alice Mirante1


1Pediatric Hospital, Coimbra Universitary Hospital Centre (CHUC), Coimbra, Portugal; 2Laboratory of Biostatistics and Medical Informatics and IBILI, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.


Introduction: Diabetic ketoacidosis (DKA) is an endocrine emergency and the leading cause of morbi-mortality in children with type 1 diabetes mellitus (1DM). DKA treatment is still controverse, mainly regarding hydroelectrolytic replacement and insulin dose.

Aims: To evaluate efectiveness and safety of our tertiary centre protocol in DKA treatment, which included initial volume expansion with isotonic saline in the first two hours followed by 0.45% sodium chloride with 5% glucose and insulin infusion (0.1 U/kg per h). Potassium replacement with potassium phosphate in the first 12 h.

Methods: Retrospective study of all children with moderate and severe DKA 1DM presented from 2004 to 2016. Data collected: insulin infusion dose, glycemia, pH. Osmolarity, corrected sodium, potassium and phosphate along the first 12 h of treatment. Statistic analysis with SPSS21 (P<0,05).

Results: 179 new cases of 1DM were admitted and 45 (25%) had DKA at presentation (15 severe, 12 moderate and 18 mild DKA). Within moderate and severe DKA (N=27), 18(67%) were female and mean age at diagnosis was 8.5±3.8 years. Means at admission were: 528±138 mg/dl glycemia, 310±12 mosm/kg osmolarity, 146±5 mmol/l corrected sodium, 4.5±0.73 mmol/l potassium and 1.5±0.5 mmol/l phosphate. Mean insulin infusion dose at treatment start was 0.08±0.03 U/kg per h. Along the first 12 h mean replacement doses were 4.3±1.3 gr/U per h of glucose, 0.13±0.04 mmol/kg per h of potassium, 0.33±0.1 mmol/kg per h of sodium and 0.06±0.02 mmol/kg per h of phosphate. There were 12(45%) cases of hypokalemia and 10(37%) of hypophosphatemia. There was no hypocalcemia nor cerebral edema. There was statistical significance in variation regarding glucose, pH, corrected sodium and osmolarity along the 12 h (P<0.0001). Sodium decreased in the first 8 h. Potassium decreased along the first 4 h and rose from 8 h forwards.

Conclusions: Our protocol allowed a safe treatment of DKA at 1DM presentation, with gradual correction of dehydration and acidosis. However, sodium and potassium replacement should be adjusted, leading to our actual protocol.

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