Dr. Muhammad Sajjad SabirMBBS, DCH, MCPS, FCPS

Assistant Professor of Paediatrics

Pediatric Diabetes Mellitus

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

CAUSES

Progressive loss of islet-cell functionInsulin resistanceIatrogenic - post pancreatic surgery

ETIOLOGY Idiopathic: 95% belong to this category Hereditary Multi-factorial inheritanceSecondary: Cushing syndrome Hyperpituitarism Surgical removal of pancreas

Type 1 - Insulin dependentInsulin 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

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)

Type 1- Diabetes Mellitus

T1DM

EPIDEMIOLOGY

UK- annual incidence 20 per 100,000 children

Incidence increasing in children < 5yr age Under 1 - Extremely rareMinor peak 4-6yrMajor peak 10-14yr

EPIDEMIOLOGY

No clear pattern of inheritanceIncreased risk if 1 member of family

affectedIdentical twin has 50% risk to develop DMIndividuals with HLA-DR3 and HLA-DR4

have increased risk

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

Hypothyroidism affects 2-5% of children with diabetes

Addison disease

Celiac disease

Associated Autoimmune diseases

Natural history of T1DM T1DM involves some or all following stages:

1) Initiation of autoimmunity2) Preclinical autoimmunity with progressive loss of β-cells

3) Onset of clinical disease

4) Transient remission

5) Established disease

6) Development of complication

CLINICAL FEATURESAcute onsetUsually preceded by infection

PolyuriaPolyphagiaPolydypsiaWeight lossNocturiaDiabetic coma

The main symptoms of are secondary to osmotic diuresis and glycosuria

Insulin deficiency→ hyperglycemia →

glycosuria→ osmotic diuresis

→Polyuria → ↑thurst →Polydipsia

Pathophysiology of T1DM

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

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 %

• 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

INVESTIGATIONS1. Urine examination:• glucosuria• ketonuria2. Blood sugar levels ( ↑BSR, ↑ BSF )3.Serum electrolytes: Hyponatremia Hypokalemia Low chloride

4. Acid Base Balance: pH is low Bicarbonate base deficit low5. Blood examination: Hb and Hct ↑ due to dehydration ↑ TLC

Investigations

Management

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

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

Insulin- available forms

Insulin - available forms

Insulin Inj sites

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

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

Patient and Parent EducationEducation 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

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

Home Monitoring

Blood Sugar Monitoring:

• By Glucometer

Urin dipstick:

• Glucsuria

• Ketonuria

(GLYCATED HEMOGLOBIN)HbA1c -best method for medium/long-term

diabetic control monitoringTarget 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

FOLLOW UP:Monitor GrowthBlood pressureSchool progressDietary complianceHbA1c levelJoint mobilityFundus examinationThyroid function testCheck insulin site

•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:

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

HYPOGLYCEMIAMajor complicationBlood sugar level < 60mg/dlSign / Symptoms: Behavior changes ,

palpitation, pallor , diplopia , sweating ,nausea , vomiting , hunger, disorientation tremors, may progress to convulsion and coma

Treatment: lump of sugar, sweet drinkSevere hypoglycemia : Inj. Glucagon

DIABETIC KETOACIDOSIS

(DKA)

Hyperglycemia >300mg/dl

Ketonemia Plasma ketone >3mmol/l

Acidosis Bicarbonate<15meq/l

Ketonuria +ve

PRESENTATION OF DKA

Polyuria , Polydipsia , Weight lossAcutely ill patient with fruity smell

due to ketosisNausea , Vomiting , LethargyHyperventilation , DehydrationAbdominal PainDrowsiness or Coma

DKA INVESTIGATIONS

1. CBC2. ESR3. BSR4. Urine ketone5. Urine sugar

6. ABG’S

7. Urea ,Creatinine

8. Electrolyte

9. Blood C/S

10. Urine C/S

DKA MANAGEMENT1. ABC2. Correction of fluid and electrolyte3. Correction of metabolic acidosis4. Provision of adequate insulin to prevent ketosis and

decrease hyperglycemia5. Prevention and monitoring of complications6. Identification of precipitating factors7. Insulin regimen8. Teaching of sick days

DKA PROTOCOL1st 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

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

D/D OF DIABETIC KETOACIDOSIS

1. Hyperosmolar Non Ketotic Coma2. Meningoencephalitis3. Salicylate Poisoning4. Gastroenteritis with Acidosis

SOMOGYI PHENOMENON

Due to ↑insulin dose in evening →Mid-night hypoglycemia → counter regulatory hormones → early morning ↑serum glucose (hyperglycemia)Management↓ evening insulin dose

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

?