Management

Laboratories Glucose electrolytes BUN Creatinine CBC ABG Urinalysis ECG

Management Goals of therapy Correct dehydration Correct acidosis and reverse ketosis Restore blood glucose to near normal Avoid complications of therapy Identify and treat any precipitating event

1. Correct dehydration 1 st hour -> Infuse ml/kg/hr IV bolus 0.9% NaCl or LR Use crystalloid not colloid Subsequent fluid management (deficit replacement) should be with 0.9% saline or Ringer’s acetate for at least 4–6 hours

2. Insulin therapy Dose: 0.1 unit/kg/hour Route of administration: IV An IV bolus is unnecessary, may increase the risk of cerebral edema Continue insulin drip until resolution of DKA

2. Insulin therapy To continue insulin infusion without causing hypoglycemia: -add 5% glucose if blood sugar <250mg/dl

3. Potassium replacement 2 nd hour -> 20 mmol/L Kphos + 20 mmol/L Kacetate Potassium replacement should continue throughout IV fluid therapy The maximum recommended rate is usually 0.5 mmol/kg/hr. If hypokalemia persists despite a maximum rate of potassium replacement, then the rate of insulin infusion can be reduced.

4. Phosphate replacement Prospective studies have not shown clinical benefit from phosphate replacement. Severe hypophosphatemia in conjunction with unexplained weakness should be treated Potassium phosphate salts careful monitoring of serum calcium is performed to avoid hypocalcemia

5. Correct acidosis Acidosis is reversible by fluid and insulin replacement Insulin stops further ketoacid production and allows ketoacids to be metabolized, which generates bicarbonate Controlled trials have shown no clinical benefit from bicarbonate administration except: -severe acidemia (ph <6.9)

Once DKA resolved Resolved DKA: - CO2 > 15 meq/L - pH > Na meq/L - no emesis Transition to: - oral intake - SC insulin - 15 –30 minutes (with rapid acting insulin) or 1–2 hours (with regular insulin) before stopping the insulin infusion

Complications of DKA Infection – Precipitates DKA – Fever – Leukocytosis can be secondary to acidosis Shock – If not improving with fluids r/o MI Vascular thrombosis – Severe dehydration – Cerebral vessels – Occurs hours to days after DKA Pulmonary Edema – Result of aggressive fluid resuscitation Cerebral Edema – Warning signs: - neurologic status changes - worsening headache - CN palsies - rising BP - decreased O2sat – Tx: Mannitol 0.5–1 g/kg IV over 20 minutes and repeat if there is no initial response in 30 minutes to 2 hours – May require intubation with hyperventilation

Long-Acting Insulin Analogs and the Risk of Diabetic Ketoacidosis in Children and Adolescents With Type 1 Diabetes A prospective study of 10,682 patients from 271 institutions Beate Karges, MD1, Thomas Kapellen, MD2, Andreas Neu, MD3, Sabine E. Hofer, MD4, Tilman Rohrer, MD5, Joachim Rosenbauer, MD6, Johannes Wolf, MD7, Reinhard W. Holl, MD8 and for the Diabetes Prospective Documentation (DPV) Initiative and the German Federal Ministry for Education and Research (BMBF) Competence Network of Diabetes Mellitus* + Author Affiliations

Objective To investigate if long-acting insulin analogs decrease the risk of diabetic ketoacidosis (DKA) in young individuals with type 1 diabetes.

Research Design Of 48,110 type 1 diabetic patients prospectively studied between 2001 and 2008, the incidence of DKA requiring hospitalization was analyzed in 10,682 individuals aged ≤20 years with a diabetes duration of ≥2 years.

Results The overall rate of DKA was 5.1 (SE ± 0.2)/100 patient-years. Patients using insulin glargine or detemir (n = 5,317) had a higher DKA incidence than individuals using NPH insulin (n = 5,365, 6.6 ± 0.4 vs. 3.6 ± 0.3, P < 0.001).

Conclusion Despite their long-acting pharmacokinetics, the use of insulin glargine or detemir is not associated with a lower incidence of DKA compared with NPH insulin.

THANK YOU!!!