DKA - Younger patients known type 1 diabetic, rapid clinical course, non-compliance with insulin, abdomen. pain, SOB, tachypnoea, severe acidosis/ketosis, mild hyperglycaemia, AKI. Pathophysiology - lack of insulin in setting of glucagon release triggers breakdown of fatty acids into ketoacids which contribute to HAGMA. Precipitating factors include - infection, new diagnosis DM, poor treatment compliance, steroids, phenytoin, diuretics, MI, substance abuse. pH <7.25, HCO3- <18, urine/serum ketones +, AG >10. Clinically tachypnoeic, tachycardia, hypotensive, hypovolaemic, pseudohyponataemic (CALCULATE TRUE NA+ = (NA+ + BSL/4). HYPO-PHOS/MAG, HYPERKALAEMIC DUE TO ACIDOSIS (H+/K+ EXCHANGER) but K+ stores are depleted. Anxious/agitated, vomitting/diarrhoea/abdo. pain, ARF/polyuria. Complications include cardiac arrest (electrolytes, stroke, cerebral oedema, renal failure, DIC. Management - fluid 15-20ml/kg first hour, 4-14ml/kg in 2nd and third hour (with regular assessment - avoid N.Saline. Insulin - 7iu/hr (0.1u/kg/hr) until BSL <15 then start 5% dextrose and adjust to BSL. Time to reduce BSL 3mmol/L/hr, ketones by 0.5mmol/L/Hr, increase HCO3_ by 3/hr. Replace electrolytes PRN.