‫داء السكر عند االطفال‬
CHILDHOOD DIABETES MELLITUS
‫الدكتور عبد المهدي عبد الرضا حسن الشحماني‬
‫ جامعة بابل‬/ ‫كلية التمريض‬
PhD, pediatric & Mental Health Nursing
DEFINITION
The term diabetes mellitus describes 
a metabolic disorder of multiple
etiologies characterized by chronic
hyperglycemia with disturbances of
carbohydrate, fat and protein
metabolism resulting from defects of
insulin secretion, insulin action or
both.
DIABETES EPIDEMIOLOGY
Diabetes is the most common endocrine problem & is a 
major health hazard worldwide.
Incidence of diabetes is alarmingly increasing all over the 
globe.
Incidence of childhood diabetes range between 3- 
50/100,000 worldwide; in Oman it is estimated as
4/100000 per year.
OLD CLASSIFICATION (1985)
Type 1, Insulin-dependent (IDDM) 
Type 2, Non Insulin-dependent (NIDDM) 
obese –
non-obese –
MODY –
IGT 
Gestational Diabetes 
WHO CLASSIFICATION 2000
Is based on etiology not on type of treatment or age of the 
patient.
Type 1 Diabetes 
-cell destruction)
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Type 2 Diabetes 
(defects in insulin secretion or action)
Other specific types 
WHO CLASSIFICATION/2
Both type 1 & type 2 can be further subdivided into: 
Not insulin requiring 
Insulin requiring for control 
Insulin requiring for survival 
Gestational diabetes is a separate entity 
Impaired Glucose Tolerance (IGT) indicates blood glucose 
levels between normal & diabetic cut off points during
glucose tolerance test.
DIAGNOSTIC CRITERIA
Fasting blood glucose level 
Diabetic 
Plasma >7.0 mmol 
Capillary >6.0 mmol 
IGT 
Plasma 6.0-6.9 mmol 
Capillary 5.6-6.0 mmol 
2 hours after glucose load 
(Plasma or capillary BS)
IGT 
7.8-11.0 
Diabetic level 
> 11.1 (200 mg) 
Types of Diabetes in Children
Type 1 diabetes mellitus accounts for >90% of cases. 
Type 2 diabetes is increasingly recognized in children with 
presentation like in adults.
Permanent neonatal diabetes 
Transient neonatal diabetes 
Maturity-onset diabetes of the young 
Secondary diabetes e.g. in cystic fibrosis or Cushing 
syndrome.
MODY
Usually affects older children & adolescents 
Not rare as previously considered 
2
5 subclasses are identified, one subclass has specific mode 
of inheritance (AD)
Not associated with immunologic or genetic markers 
Insulin resistance is present 
TRANSIENT NEONATAL DIABETES
Observed in both term & preterm babies, but more 
common in preterm
-cells 
Polyuria & dehydration are prominent, but baby looks well 
& suck vigorously
Highly sensitive to insulin 
Disappears in 4-6 weeks 
PERMANENT NEONATAL DIABETES
A familial form of diabetes that appear shortly after birth 
& continue for life
The usual genetic & immunologic markers of Type 1 
diabetes are absent
Insulin requiring, but ketosis resistant 
Is often associated with other congenital anomalies & 
syndromes e.g. Wolcott-Rallison syndrome.
TYPE 1 DIABETES: ETIOLOGY
Type 1 diabetes mellitus is an autoimmune disease. 
It is triggered by environmental factors in genetically 
susceptible individuals.
Both humoral & cell-mediated immunity are stimulated. 
GENETIC FACTORS
Evidence of genetics is shown in 
Ethnic differences 
Familial clustering 
High concordance rate in twins 
Specific genetic markers 
Higher incidence with genetic syndromes or chromosomal 
defects
AUTOIMMUNITY
-cells and insulin. 
Immunofluorescent antibodies & lymphocyte infiltration 
around pancreatic islet cells.
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Evidence of immune system activation. Circulating immune 
complexes with high IgA & low interferon levels.
Association with other autoimmune diseases. 
ENVIRONMENTAL INFLUENCE
Seasonal & geographical variation. 
Migrants take on risk of new home. 
Evidence for rapid temporal changes. 
Suspicion of environmental agents causing disease which 
is confirmed by case-control experimental animal studies.
ENVIRONMENTAL SUSPECTS
Viruses 
Coxaschie B 
Mumps 
Rubella 
Reoviruses 
Nutrition & dietary factors 
Cow’s milk protein 
Contaminated sea food 
OTHER MODIFYING FACTORS
The counter-regulatory hormones: 
glucagon
cortisol,
catecholamines
thyroxin,
GH & somatostatin
sex hormones
Emotional stress 
ETIOLOGIC MODEL
The etiologic model of type 1 diabetes resembles that of 
Rheumatic fever.
Rheumatic fever was prevented by elimination of the 
triggering environ. factor ( -streptococci).
Similarly type 1 diabetes may be prevented by controlling 
the triggering factors in high risk persons.
CLINICAL PRESENTATIONS
Classical symptom triad: 
polyuria, polydipsia and weight loss
DKA 
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Accidental diagnosis 
Anorexia nervosa like illness 
DIAGNOSIS
In symptomatic children a random plasma glucose >11 
mmol
(200 mg) is diagnostic.
A modified OGTT (fasting & 2h) may be needed in 
asymptomatic children with hyperglycemia if the cause is
not obvious.
Remember: acute infections in young non-diabetic children 
can cause hyperglycemia without ketoacidosis.
NATURAL HISTORY
Diagnosis & initiation of insulin 
Period of metabolic recovery 
Honeymoon phase 
State of total insulin dependency 
METABOLIC RECOVERY
During metabolic recovery the patient may
Develop one or more of the following:
Hepatomegaly•
Peripheral edema•
Loss of hair•
Problem with visual acuity•
These are caused by deposition of
glycogen &
metabolic re-balance.
HONEYMOON PERIOD
-cell reserve optimal function & initiation of insulin 
therapy.
Leads to normal blood glucose level without exogenous 
insulin.
Observed in 50-60% of newly diagnosed patients & it can last 
up to one year but it always ends.
Can confuse patients & parents if not educated about it 
early.
COMPLICATIONS OF DIABETES
Acute: 
DKA
Hypoglycemia
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Late-onset: 
Retinopathy 
Neuropathy
Nephropathy
Ischemic heart disease & stroke
TREATMENT GOALS
Prevent death & alleviate symptoms 
Achieve biochemical control 
Maintain growth & development 
Prevent acute complications 
Prevent or delay late-onset complications 
TREATMENT ELEMENTS
Education 
Insulin therapy 
Diet and meal planning 
Monitoring 
HbA1c every 2-months 
Home regular BG monitoring 
Home urine ketones tests when indicated 
EDUCATION
Educate child & care givers about: 
Diabetes
Insulin
Life-saving skills
Recognition of Hypo & DKA
Meal plan
Sick-day management
INSULIN
-chains. 
Discovered by Bants & Best in 1921. 
Animal types (porcine & bovine) were used before the 
introduction of human-like insulin (DNA-recombinant
types).
Recently more potent insulin analogs are produced by 
changing aminoacid sequence.
FUNCTION OF INSULIN
Insulin being an anabolic hormone stimulates protein &
fatty acids synthesis.

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Insulin decreases blood sugar 
By inhibiting hepatic glycogenolysis and 
gluconeogenesis.
By stimulating glucose uptake, utilization & storage by 
the liver, muscles & adipose tissue.
TYPES OF INSULIN
Short acting (neutral, soluble, regular) 
Peak 2-3 hours & duration up to 8 hours 
Intermediate acting 
Isophane (peak 6-8 h & duration 16-24 h) 
Biphasic (peak 4-6 h & duration 12-20 h) 
Semilente (peak 5-7 h & duration 12-18 h) 
Long acting (lente, ultralente & PZI) 
Peak 8-14 h & duration 20-36 h 
INSULIN CONCENTRATIONS
Insulin is available in different concentrations 40, 80 & 100 
Unit/ml.
WHO now recommends U 100 to be the only used insulin to 
prevent confusion.
Special preparation for infusion pumps is soluble insulin 
500 U/ml.
INSULIN REGIMENS
Twice daily: either NPH alone or NPH+SI. 
Thrice daily: SI before each meal and NPH only before 
dinner.
Intensive 4 times/day: SI before meals + NPH or Glargine 
at bed time.
Continuous s/c infusion using pumps loaded with SI. 
INSULIN ANALOGS
Ultra short acting 
Insulin Lispro
Insulin Aspart
Long acting without peak action to simulate normal basal 
insulin
Glargine
NEW INSULIN PREPARATIONS
Inhaled insulin proved to be effective & will be available 
within 2 years.
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Nasal insulin was not successful because of variable nasal 
absorption.
Oral insulin preparations are under trials. 
ADVERSE EFFECTS OF INSULIN
Hypoglycemia 
Lipoatrophy 
Lipohypertrophy 
Obesity 
Insulin allergy 
Insulin antibodies 
Insulin induced edema 
PRACTICAL PROBLEMS
Non-availability of insulin in poor countries 
injection sites & technique 
Insulin storage & transfer 
Mixing insulin preparations 
Insulin & school hours 
Adjusting insulin dose at home 
Sick-day management 
Recognition & Rx of hypo at home 
DIET REGULATION
Regular meal plans with calorie exchange options are 
encouraged.
50-60% of required energy to be obtained from complex 
carbohydrates.
Distribute carbohydrate load evenly during the day 
preferably 3 meals & 2 snacks with avoidance of simple
sugars.
Encouraged low salt, low saturated fats and high fiber diet. 
EXERCISE
Decreases insulin requirement in diabetic subjects by 
increasing both sensitivity of muscle cells to insulin &
glucose utilization.
It can precipitate hypoglycemia in the unprepared diabetic 
patient.
It may worsen pre-existing diabetic retinopathy. 
MONITORING
Compliance (check records) 
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HBG tests 
HbA1 every 2 months 
Insulin & meal plan 
Growth & development 
Well being & life style 
School & hobbies 
ADVANCES IN MONITORING
Smaller & accurate meters for intermittent BG monitoring 
Glucowatch continuous monitoring using reverse 
iontophoresis to measure interstitial fluid glucose every 20
minutes
Glucosensor that measures s/c capillary BG every 5 
minutes
Implantable sensor with high & low BG alarm 
ADVANCES IN MANAGEMENT
Better understanding of diabetes allows more rational 
approach to therapy.
Primary prevention could be possible if the triggering 
factors are identified.
The DCCT studies proves beyond doubt that chronic 
diabetic complication can be controlled or prevented by
strict glycemic control.
TREATMENT MADE EASY
Insulin pens & new delivery products 
Handy insulin pumps 
fine micro needles 
Simple accurate glucometers 
Free educational material 
computer programs for comprehensive management & 
monitoring
TELECARE SYSTEMS
IT has improved diabetes care 
Internet sites for education & support 
Web-based systems for telecare are now available. The 
patient feeds his HBGM data and get the physician, nurse &
dietician advice on the required modification to diet &
insulin treatment.
PITFALLS OF MANAGEMENT
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Delayed diagnosis of IDDM 
The honey-moon period 
Detection & treatment of NIDDY 
Problems with diagnosis & treatment of DKA & 
hypoglycemia
Somogi’s effect (dawn phenomenon) may go unrecognized. 
FUTURE PROMISES
The cure for IDDM is successful islet cell transplantation, 
which will be available in the near future.
Primary prevention by a vaccine or drug will be offered to 
at risk subjects identified by genetic studies.
Gene modulation therapy for susceptible subjects is a 
promising preventive measure.
Pancreas & Islet Cell Transplantation
Pancreas transplants are usually given to diabetics with 
end stage renal disease.
Islet cell transplants, the ultimate treatment of type 1 
diabetes is under trial in many centers in the US & Europe
with encouraging results but graft rejection & recurrence
of autoimmunity are serious limitations.
IMMUNE MODULATION
Immunosuppressive therapy for 
Newly diagnosed
Prolonged the honey moon
For high risk children
Immune modulating drugs 
Nicotinamide
mycophenolate
GENE THERAPY
Blocks the immunologic attack against islet-cells by DNA- 
plasmids encoding self antigen.
Gene encode cytokine inhibitors. 
Modifying gene expressed islet-cell antigens like GAD. 
PREDICTION OF DIABETES
Sensitive & specific immunologic markers 
GAD Antibodies 
GLIMA antibodies 
IA-2 antibodies 
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Sensitive genetic markers 
HLA haplotypes •
DQ molecular markers •
PREVENTION OF DIABETES
Primary prevention
Identification of diabetes gene •
Tampering with the immune system •
Elimination of environmental factor •
Secondary prevention
Immunosuppressive therapy •
Tertiary prevention
Tight metabolic control & good monitoring •
Dreams are the seedlings of realities
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