1) Type 1 diabetes (T1D) results from the autoimmune destruction of pancreatic beta cells, leading to insulin deficiency. It accounts for about 95% of diabetes cases in children. 2) Management of diabetic ketoacidosis (DKA) in T1D involves fluid resuscitation, continuous intravenous insulin infusion, monitoring of blood glucose and electrolytes, and treatment of the underlying precipitating cause. 3) Long-term management of T1D focuses on achieving optimal blood glucose control through multiple daily insulin injections or insulin pump therapy, along with carbohydrate counting and sick day rules. Close monitoring is needed to prevent complications.

1. When your child is too sweet
By Dr Liaw Siew Ching

3. IDDM/ Type I DM
• Introduction
• Physiology of diabetes in β cell failure in
type 1 DM
• DKA
• Long term management of diabetes

4. • Definition of DM:
- Symptoms of diabetes with random blood
sugar >11.1mmol/l or,
- Fasting plasma glucose >7.0mmol/l (fast
for 8H) or,
- 2 hour postload glucose >11.1mmol/l in
OGTT (glucose load with 75g anhydrous
glucose desolved in water or 1.75g/kg)
Introduction

5. • Type I DM (95%) – Autoimmune
destruction of the pancreatic islet cells
• Type 2 DM – A combination of β cell
failure and insulin resistant
• Cystic fibrosis-related diabetes
• Maturity onset diabetes of the young
• Genetic syndromes( Down’s syndrome,
Wolfram syndrome, neonatal diabetes
Aetiology of diabetes in children

6. • Europe: Scandinavia and the UK have the highest rates
of diabetes in Europe. There is a >10-fold difference in
incidence across Europe, which might be accounted for
in part by the distribution of high-risk HLA-DQ alleles.
• North America: Canada has incidence rates
comparable to those of Northern Europe (22/100,000
per year). The US has a lower rate (16/100,000 per
year), whereas Mexico has a rate of 1.5/100,000 per
year.
• South America: Rates are generally low, except in
Argentina and Uruguay.
• Africa (sub-Saharan): Estimated rates are generally
low.
• Eastern Mediterranean and the Middle East: Rates
vary between 1/100,000 per year (Pakistan) and
8/100,000 per year (Egypt).
• South-East Asia: A steady increase from a low
baseline in countries such as India and China. Due to
their vast populations, these will make a large
contribution to the future global incidence of type 1
diabetes.
• Western Pacific: Rates are low, with the exception of
Australia and New Zealand.
Epidemiology
http://www.diapedia.org/type-1-diabetes-mellitus/geography-of-type-1-diabetes#fn:4

7. Physiology of diabetes in β cell failure
in type 1 DM

8. Physiology of diabetes in β cell failure
in type 1 DM
• Lymphocytic infiltration destroying beta cells.
• After 80-90% of the beta cells are destroyed, hyperglycemia
develops.
• 85% patients have circulating islet cell antibodies and
detectable anti-insulin antibodies. Commonly found islet cell
antibodies are antibodies against glutamic acid decarboxylase
(GAD), an enzyme found within pancreatic beta cells.

9. Physiology of diabetes in β cell failure
in type 1 DM
• Insulin also increases the permiability of many cells
to potassium, magnesium and phosphate ions.
Insulin activates sodium-potassium ATPases in
many cells, causing a flux of potassium into cells.

10. Classic symptoms
Nausea
lethargy

11. Physiology of diabetes in β cell failure
in type 1 DM

12. Diabetic ketoacidosis
Low insulin leads to DKA
• Liver glycogen mobilization to form glucose
• Muscle protein breakdown to form free amino
acids
• Adipose tissue breakdown of triglycerides to
form free fatty acids which oxidized to form
ketone bodies
• Excess glucose in glomerular filtrate leads to
glucosuria.

13. DKA
Remember : children can die from DKA
Definition
• Blood glucose > 11
• Venous pH <7.3 or bicarbonate <15mmol/l
• Ketonaemia or ketonuria (ketone 2+)

14. Remember : children can die
from DKA
• BSPED Recommended DKA Guidelines 2009

15. Causes of DKA

16. Clinical presentation of DKA
• Dehydration, ketosis, acidosis,
infection.

17. Assessment of severity
• Present of one or more of the following may indicate severe DKA
• Blood ketone over 6mmol/l
• HCO3<5mmol/l
• pH <7
• Potassium <3.5mmol/l
• GCS < 12
• SPO2 <92%
• Low BP
• Tachycardia/bradycardia
• Anion gap >16

18. Principle of management
• General resuscitation
• Confirm diagnosis
• Full clinical assessment
• Fluid management
• Insulin

20. Management
• FM + deficit. Initially use 1/2NS with 3/4g KCL
• Continuous low dose intravenous infusion. No need bolus.
• Make up a solution of 1 unit per ml of human soluble insulin
(e.g. Actrapid) by adding 50 units (0.5 ml) insulin to 50 ml 0.9%
saline in a syringe pump. Attach this using a Y-connector to the
IV fluids already running. Do not add insulin directly to the fluid
bags.
• Run at 0.1 units/kg/hour (0.1ml/kg/hour). The insulin dose needs to
be maintained at 0.1 units/kg/hour to switch off ketogenesis.
• There are some paediatricians who believe that 0.05 units/kg/hour is
an adequate dose. There is no firm evidence to support this.

21. • Blood glucose level <14mmol/l, change the fluid to contain 5% glucose(generally
0.9% saline with glucose and potassium, see 1b above for type of fluid). DO NOT
reduce the insulin.
• Some suggest if the initial rate of fall of blood glucose is greater than 5-8 mmol/lper
hour, to help protect against cerebral oedema. There is no good evidence for this
practice, and blood glucose levels will often fall quickly purely because of rehydration.
• If the blood glucose falls below 4 mmol/l, give a bolus of 2 ml/kg of 10% glucose and
increase the glucose concentration of the infusion. Insulin can temporarily be reduced
for 1 hour.
• Once the pH is above 7.3, the blood glucose is down to 14 mmol/l, and a
glucosecontaining fluid has been started, consider reducing the insulin infusion rate,
but to no less than 0.05 units/kg/hour.
• If the blood glucose rises out of control, or the pH level is not improving after 4-6
hours consult senior medical staffand re-evaluate (possible sepsis, insulin errors or
other condition), and consider starting the whole protocol again.
• No role of bicarbonate.

22. HUSM DKA SOP 2009
• Although serum potassium appear normal,
but total body potassium is low and
worsened with insulin infusion.
Serum Potassium (mmol/l) Replacement
<2.5 Fast correction
2.5-3.0 1.5g KCL in each pint
3.0-4.0 1.0g KCL in each pint
4.0-5.5 0.5g KCL in each pint

23. Target of therapy
• Reduction of blood ketone by 0.5mmol/l/h
• Increase bicarb by 3mmol/l/h
• Reduce capillary blood sugar by
3.0mmol/l/h
• Maintain k+ between 4.0-5.5mmol/l

24. Resolution of DKA
• pH>7.3 units
• Bicarb >15mmol/l
• Blood ketone < 0.6mmol/l or urine ketone
nil.
• S/c insulin can be started.

25. Long Term Management of DM Type I
• Principles of insulin therapy
Guidelines on dosage:
• During the partial remission phase, total daily insulin dose is usually 0.5
IU/kg/day.
• Prepubertal children (outside the partial remission phase) usually require
insulin of 0.7–1.0 IU/kg/day.
• During puberty, requirements may rise to 1 - 2 IU/kg/day.
Frequently used regimens:
Twice Daily Regimens
• 2 daily injections of a mixture of a short or rapid acting insulin with and
• intermediate-acting insulins (before breakfast and the main evening meal)
• Approximately 2/3 intermediate-acting insulin and 1/3 of the total daily
insulin dose is short acting insulin. Ex: Mixtard 70/30
• 2/3 of the total daily dose is given in the morning and 1/3 in the evening

26. Three injections daily
•A mixture of short, rapid and intermediate-acting insulins before breakfast;
•A rapid-acting analogue or regular insulin alone before afternoon snack
•or the main evening meal. And an intermediate- acting insulin before bed.
Basal-bolus Regimen
•Of the total daily insulin requirements, 40 - 60% should be basal insulin, the rest pre-
prandial rapid-acting or regular insulin.
•If using regular insulin, inject 20 - 30 min before each main meal (breakfast, lunch; and
the main evening meal); if using rapid-acting insulin analogue inject immediately before
or after each main meal (e.g. breakfast, lunch; and the main evening meal).
•Basal cover is given once daily at bedtime. However sometimes twice daily injections
may be needed (the other dose usually before breakfast).
•Insulin pump regimens are regaining popularity with a fixed or a variable basal dose and
bolus doses with meals.
•Patient should learn about carbohydrate counting to adjust dose of pre-prandial insulin.
Long Term Management of DM Type I

27. Long Term Management of DM Type I

28. • Australian Clinical Practice Guidelines: Type 1 Diabetes in Children
and Adolescents

29. • Calorie counting
• Sick day management
• Fasting and surgery
Long Term Management of DM Type I