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Pediatric Diabetes Mellitus Management
1. Dr. Muhammad Sajjad Sabir
MBBS, DCH, MCPS, FCPS
Assistant Professor of Paediatrics
Pediatric
Diabetes Mellitus
2. PEDIATRIC DIABETES
MELLITUS
Juvenile diabetes mellitus is a chronic
metabolic disorder resulting from absolute lack
of insulin
Most pediatric patients have type 1 diabetes
mellitus → lifetime dependence on exogenous
insulin
Abnormal metabolism of carbohydrate , protein
and fat
Characterized by hyperglycemia , glycosuria
and tendency to ketoacidosis
4. ETIOLOGY
Idiopathic:
95% belong to this category
Hereditary
Multi-factorial inheritance
Secondary:
Cushing syndrome
Hyperpituitarism
Surgical removal of pancreas
5. Type 1 - Insulin dependent
Insulin dependent
Most childhood diabetes
Prone to ketosis
Type 2 - Non-Insulin dependent
Usually Older children
Obesity-related
Positive family history
Not prone to ketosis
Classification of DM
according to Causes
6. CLASSIFICATION OF DM
ACCORDING TO CAUSES
Type 3 - Other Specific Types
Genetic defects in β-cell function( Maturity Onset
Diabetis of Young,MODY ) → responds to oral
hypoglycemic drugs
Genetic defect in insulin action
Infections - Congenital rubella
Drugs - Corticosteroids
Pancreatic exocrine insufficiency - Cystic fibrosis
Genetic/Chromosomal disorders
Type 4 - Gestational Diabetes Mellitus(GDM)
8. EPIDEMIOLOGY
UK- annual incidence 20 per 100,000
children
Incidence increasing in children < 5yr age
Under 1 - Extremely rare
Minor peak 4-6yr
Major peak 10-14yr
9. EPIDEMIOLOGY
No clear pattern of inheritance
Increased risk if 1 member of family
affected
Identical twin has 50% risk to develop DM
Individuals with HLA-DR3 and HLA-DR4
have increased risk
10. PHYSIOLOGY OF DIABETES IN Β
CELL FAILURE
Liver glycogen metabolism to
form glucose
Muscle protein breakdown to
form free amino acid
Adipose tissue breakdown or
triglycerides to form free fatty
acids which are oxidised to form
ketone bodies, ultimately leading
to Ketoacidosis
12. Natural history of T1DM
T1DM involves some or all following stages:
1) Initiation of autoimmunity
2) Preclinical autoimmunity with progressive
loss of β-cells
3) Onset of clinical disease
4) Transient remission
5) Established disease
6) Development of complication
14. The main symptoms of are secondary
to osmotic diuresis and glycosuria
Insulin deficiency→ hyperglycemia →
glycosuria→ osmotic diuresis
→Polyuria → ↑thurst →Polydipsia
Pathophysiology of T1DM
15. Insulin deficiency→ lack of glucose
utilization→ ↑ appetite→ Polyphagia
Insulin deficiency→ lack of glucose
utilization→ ↑utilization of fats → DKA
Impaired protein synthesis → Weight
loss
Pathophysiology of T1DM
16. DIAGNOSIS
Classic Symptoms: Polyuria, Polydypsia, Polyphagia, Weight loss
Diagnostic criterion Glucose level
Classic Symptoms plus BSR ≥ 200mg/dl
(11.1 mmol/L)
Fasting blood sugar ≥ 126mg/dl
(7.0 mmol/L)
2-hour plasma glucose level
during a 75-g oral glucose
tolerance test (OGTT)
≥ 200 mg/dL
(11.1 mmol/L)
HbA1c levels ≥ 6.5 %
26. DIET
Recent dietary recommendations
• Carbohydrates
• Should provide 50-55% of daily energy intake;
• no more than 10% of carbohydrates should be
from sucrose or other refined carbohydrates
• Fat - Should provide 30-35% of daily energy intake
• Protein - Should provide 10-15% of daily energy
intake
27. Important aspect of diabetes management
Real benefits for a child with diabetes
No form of exercise, including competitive sports,
should be forbidden to the diabetic child
25 min aerobic exercise- encourage regular daily
exercise
Exercise
28. Patient and Parent Education
Education is a continuing process involving the child,
family, and all members of the diabetes team
Recognition and treat hypoglycemia
How to mix insulin
How to inject / change sites
How to store insulin
How to check BSR/urine tests
Increase dose in acute illness
Complications
29. BLOOD SUGAR
MONITORING
4 readings (before meal, before snack
and in middle of night 3:00 am)
2 readings (before breakfast , before
dinner)
Good Control:
Fasting and Preprandial BSR – 70-
150mg/dl
Postprandial BSR – 180-200mg/dl
3:00 am Value – 65mg/dl
31. (GLYCATED HEMOGLOBIN)
HbA1c -best method for medium/long-term
diabetic control monitoring
Target HbA1c <7.5% (regardless of age)
Reflects average blood glucose level in preceding 2-3 months
HbA1c level Control
≤7% Intense
control
8-9% Average
≥11% Minimal
control
HbA1c level Control
6-7.5% Good control
7.6-9.9% Fair control
≥10% Poor control
HbA1c Level
32. FOLLOW UP:
Monitor Growth
Blood pressure
School progress
Dietary compliance
HbA1c level
Joint mobility
Fundus examination
Thyroid function test
Check insulin site
37. PRESENTATION OF
DKA
Polyuria , Polydipsia , Weight loss
Acutely ill patient with fruity smell
due to ketosis
Nausea , Vomiting , Lethargy
Hyperventilation , Dehydration
Abdominal Pain
Drowsiness or Coma
39. DKA MANAGEMENT
1. ABC
2. Correction of fluid and electrolyte
3. Correction of metabolic acidosis
4. Provision of adequate insulin to prevent ketosis and
decrease hyperglycemia
5. Prevention and monitoring of complications
6. Identification of precipitating factors
7. Insulin regimen
8. Teaching of sick days
40. DKA PROTOCOL
1st
hour :
10-20ml/kg iv bolus 0.9% NaCl or LR
Insulin drip at 0.05 - 0.10 units/kg/hr (Regular insulin)
2nd
hr until DKA resolution :
0.45% NaCl : plus continue insulin drip
I.V Rate= 85ml/kg + maintenance - bolus
23 hr
Note
(1) Initial IV bolus is considered part of total fluid allowed in 1st 24 hr
(2) Maintenance (24 hr) = 100 mL/kg (for the 1st 10 kg) + 50 mL/kg
(for the 2nd 10 kg) + 25 mL/kg (for all remaining kg)
(3) Cerebral edema major cause of morbidity and mortality
41. DKA PROTOCOL
20 mEq/L KCL (20ml in each Lit fluid)
Cerebral edema =1g/Kg Mannitol I.V push
5% glucose if blood sugar <250 mg/dl
Shift to subcutaneous insulin
• BSR is 180-240mg/dl
• Oral intake
• No emesis
• CO2 ≥16 mEq/L
• normal electrolytes
42. D/D OF DIABETIC KETOACIDOSIS
1. Hyperosmolar Non Ketotic Coma
2. Meningoencephalitis
3. Salicylate Poisoning
4. Gastroenteritis with Acidosis
43. SOMOGYI PHENOMENON
Due to ↑insulin dose in evening
→Mid-night hypoglycemia →
counter regulatory hormones →
early morning ↑serum glucose
(hyperglycemia)
Management
↓ evening insulin dose
44. DAWN PHENOMENON
Simple decline in insulin levels (seen in many
children using NPH insulin at supper or bedtime)
→ early morning hyperglycemia
Dawn phenomenon is due to overnight growth
hormone secretion and increased insulin
clearance
Management
↑ evening insulin dose