Management

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• 1st hour -> Infuse 10-20 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

2nd 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 > 7.30- Na 135-145 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: Mannitol0.5–1 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 DiabetesA 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!!!