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Paeds Vivasendocrinology-diabetes-and-growth

Paeds Vivas · endocrinology-diabetes-and-growth

Diabetic ketoacidosis — branching viva

Branching viva on paediatric diabetic ketoacidosis: diagnosing and grading DKA, delivering the ISPAD fluid and insulin protocol with the potassium and glucose logic, recognising and treating cerebral oedema at the bedside, and defining resolution and transition to subcutaneous insulin.

branching clinical structured oral4 min readVerification in progress

Target exams

RACP DCEMRCPCH ClinicalRCPSC Pediatrics
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Study tools

Target exams

RACP DCEMRCPCH ClinicalRCPSC Pediatrics
Prompt
Emergency department: a 5-year-old girl not known to have diabetes is brought in drowsy with a two-week history of drinking and passing urine excessively, now vomiting and breathing deeply with a sweet smell to her breath. Capillary glucose reads high, blood ketones are 5 mmol/L, and a venous gas shows pH 7.05 with a bicarbonate of 5 mmol/L. She is dehydrated but not shocked. The examiner asks: what is your diagnosis and how do you grade it, what is your fluid and insulin plan and in what order, why is her potassium misleading, and what complication must you watch for and how would you treat it — then branches to a pump user with unexplained ketosis, a persisting acidosis with a normalising glucose, and the resolution criteria for transition to subcutaneous insulin.

Opening framework

My framework has three layers. First, the diagnosis: this drowsy, dehydrated child breathing deeply with ketones on her breath has diabetic ketoacidosis, and I confirm it on the triad of hyperglycaemia, a venous pH below 7.3 or bicarbonate below 15, and ketonaemia. Second, the physiology that makes it dangerous: she is more dehydrated and more potassium-depleted than she looks, and correcting her too fast risks cerebral oedema. Third, the management in a fixed safety order: cautious fluids, then insulin by infusion an hour or two later at 0.05 to 0.1 units/kg/h with no bolus, early potassium, glucose-guided dextrose, and relentless neurological monitoring. [1]

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References6ShowHide
  1. [1]Glaser N, Fritsch M, Priyambada L, et al. ISPAD clinical practice consensus guidelines 2022: Diabetic ketoacidosis and hyperglycemic hyperosmolar state Pediatr Diabetes, 2022.PMID 36250645
  2. [2]Kuppermann N, Ghetti S, Schunk JE, et al. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis N Engl J Med, 2018.PMID 29897851
  3. [3]Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics N Engl J Med, 2001.PMID 11172153
  4. [6]Nallasamy K, Jayashree M, Singhi S, et al. Low-dose vs standard-dose insulin in pediatric diabetic ketoacidosis: a randomized clinical trial JAMA Pediatr, 2014.PMID 25264948
  5. [8]Wolfsdorf JI, Glaser N, Agus M, et al. ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state Pediatr Diabetes, 2018.PMID 29900641
  6. [9]Marcin JP, Glaser N, Barnett P, et al. Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema J Pediatr, 2002.PMID 12461495
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