Type1 diabetes mellitus Final yr MBBS Lecture

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

3. CAUSES
Progressive loss of islet-cell function
Insulin resistance
Iatrogenic - post pancreatic surgery

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)

7. Type 1- Diabetes Mellitus
T1DM

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

11. Hypothyroidism
affects 2-5% of children with diabetes
Addison disease
Celiac disease
Associated Autoimmune diseases

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

13. CLINICAL FEATURES
Acute onset
Usually preceded by infection
Polyuria
Polyphagia
Polydypsia
Weight loss
Nocturia
Diabetic coma

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 %

17. • Type 2 diabetes mellitus
• MODY
• Psychogenic polydipsia
• Nephrogenic diabetes insipidus
• High-output renal failure
• Transient hyperglycemia with illness / stress
• Factitious illness (Münchhausen syndrome by
proxy)
Differential Diagnosis

18. INVESTIGATIONS
1. Urine examination:
• glucosuria
• ketonuria
2. Blood sugar levels ( ↑BSR, ↑ BSF )
3.Serum electrolytes:
 Hyponatremia
 Hypokalemia
 Low chloride

19. 4. Acid Base Balance:
 pH is low
 Bicarbonate base deficit low
5. Blood examination:
 Hb and Hct ↑ due to dehydration
 ↑ TLC
Investigations

20. Management

21. Insulin Types 4 basic formulations
 Ultra-short acting insulin
 Lispro
 aspart
 Short acting insulin
 Regular Insulin
 Soluble Insulin
 Intermediate acting insulin
 NPH (Neutral Protamine Hagedorn)
 Lente
 Ultralente
 Long acting Insulin
 Glargine
 ultralente

22. INSULIN THERAPY
1. Insulin Replacement:

Insulin DOSE 0.75-1.0 U/kg S/C
(Range = 0.5 - 1.2 U/kg)
 Total daily dose divided into
NPH (2/3rd
of total)
Regular (1/3rd
of total)
 2/3rd
of daily dose- before breakfast
 1/3rd
- evening

23. Insulin- available forms

24. Insulin - available forms

25. Insulin Inj sites

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

30. Home Monitoring
Blood Sugar Monitoring:
• By Glucometer
Urin dipstick:
• Glucsuria
• Ketonuria

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

33. •Injection -site hypertrophy
•Retinopathy
•Cataracts
•Gastroparesis
•Hypertension
•Progressive renal failure
•Early coronary artery disease
•Peripheral vascular disease
•Peripheral and autonomic neuropathy
•Increased risk of infection
Complications:

34. COMPLICATIONS:
 Brittle Diabetes Mellitus:marked fluctuation in blood sugar
despite frequent adjustment of doses
 Diabetic Ketoacidosis
 Neuropathy
 Nephropathy
 Retinopathy and Blindness
 Hyperosmolar Diabetic Coma
 Lipoatrophy
 Growth Retardation and Emotional problem

35. HYPOGLYCEMIA
Major complication
Blood sugar level < 60mg/dl
Sign / Symptoms: Behavior changes ,
palpitation, pallor , diplopia , sweating
,nausea , vomiting , hunger,
disorientation tremors, may progress
to convulsion and coma
Treatment: lump of sugar, sweet drink
Severe hypoglycemia : Inj. Glucagon

36. DIABETIC KETOACIDOSIS
(DKA)
Hyperglycemia >300mg/dl
Ketonemia Plasma ketone >3mmol/l
Acidosis Bicarbonate<15meq/l
Ketonuria +ve

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

38. DKA
INVESTIGATIONS
1. CBC
2. ESR
3. BSR
4. Urine ketone
5. Urine sugar
6. ABG’S
7. Urea ,Creatinine
8. Electrolyte
9. Blood C/S
10. Urine C/S

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

45. ?