Presentation

1. Diabetes mellitus (DM) in children
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2. Diabetes mellitus (DM) in children
Objectives:
At the end of this lesson, learners will be able to:
 Define DM
 Explain the cause of child hood DM
 Discus the epidemiology of DM
 Discus the pathophysiology of type 1 DM
 List the clinical manifestations of type 1 DM
 Explain the diagnosis of type 1 DM
 Discus the management approaches of type 1 DM
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3. Diabetes mellitus (DM) in children
Is a common, chronic, metabolic syndrome
Characterized by hyperglycemia as a cardinal biochemical
feature.
Resulting from defects of insulin secretion, its action or
both.
Leading to abnormalities in carbohydrate, protein & fat
metabolism.
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4. Classification
According to the cause, the major forms are classified
 Type 1 DM (formerly called insulin dependent diabetes
mellitus(IDDM) or type I ) : deficiency of insulin
secretion due to pancreatic β-cell damage and
 Type 2 DM (formerly called non insulin dependent
diabetes mellitus(NIDDM) or type II) : Insulin resistance
with various degrees of β-cell impairment
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5. Type 2 diabetes
The children and adolescents with type 2 diabetes
are usually obese but are not insulin dependent
and infrequently develop ketosis(during severe
infections or other stresses)
Which is characterized by insulin resistance and
often a progressive defect in insulin secretion.
The incidence of T2DM in children has increased.
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6. Type1 Diabetes mellitus
T1DM is the most common endocrine-metabolic
disorder of childhood and adolescence
Individuals with T1DM confront serious lifestyle
alterations that include:
An absolute daily requirement for exogenous insulin
The need to monitor their own glucose level and
The need to pay attention to dietary intake.
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7. The natural history includes 4 distinct stages:
1. Preclinical β-cell autoimmunity with progressive defect
of insulin secretion
2. Onset of clinical diabetes
3. Transient remission “honeymoon period,” due to
regeneration of new islets has been detected at onset
of T1DM and
4.Established diabetes associated with acute and chronic
complications and decreased life expectancy.
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8. PATHOGENESIS
The main function of insulin:
1. Reduce blood glucose by:
Increase glucose uptake by the cells
Decrease glucogenolysis
Decrease gluconeogenesis
2. Inhibit protein breakdown(proteolysis)
3. Inhibit fat breakdown(lipolysis)
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9. PATHOPHYSIOLOGY…
 The autoimmune attack on the pancreatic islets leads
to a gradual and progressive destruction of β cells
 This results loss of insulin secretion & insulin
deficiency
 It is estimated that, at the onset of clinical DM, 80–90%
of the pancreatic islets are destroyed.
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10. PATHOPHYSIOLOGY…
Hyperglycemia produces an osmotic diuresis leads to
polyuria & (glycosuria) when the renal threshold is
exceeded (180 mg/dL; 10 mmol/L).
The polyuria leads to dehydration & compensatory
polydipsia
The resulting loss of calories as well as the persistent
dehydration, produce a physiologic stress
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11. PATHOPHYSIOLOGY…
This results hyper secretion of stress hormones
(epinephrine, cortisol, growth hormone, and glucagon).
These hormones, in turn, contribute to the metabolic
decompensation by further impairing insulin secretion &
antagonizing its action
Proteolysis resulting in weight loss and polyphagia
 Lipolysis: increases free FA(ketonemia,ketonuria)
&metabolic acidosis
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12. PATHOPHYSIOLOGY
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13. Clinical presentation
 Childhood type 1 diabetes can present in several different ways.
 Classic new onset
 Diabetic ketoacidosis
 Silent (asymptomatic) incidental discovery
 Classic new onset
 Hyperglycemia without acidosis is the most common presentation of
childhood type 1 diabetes.
 Symptoms are caused by hyperglycemia and include recurrent
infections(UTI), polyuria, polydipsia, weight loss despite increased
appetite initially (polyphagia) and lethargy.
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14.  Diabetic ketoacidosis
Children with type 1 diabetes often present with diabetic
ketoacidosis (hyperglycemia and ketoacidosis).
Symptoms are similar but usually more severe than those
of patients without acidosis.
Young children (<6 years of age) or from a low
socioeconomic background are more likely to have DKA as
their initial presentation of type 1 diabetes.
In our set up more than 80 % of patients will present with
DKA at the initial presentation.
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15. Diabetic ketoacidosis…
 When extremely low insulin levels are reached, ketoacids
accumulate & produce abdominal discomfort, nausea,
and emesis.
 Dehydration accelerates, causing weakness and polyuria
persists.
 Ketoacidosis exacerbates prior symptoms and leads to
Kussmaul respirations (deep, heavy, rapid breathing),
fruity breath odor (acetone), diminished neurocognitive
function.
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16. Diabetic ketoacidosis…
 As an initial presentation or in a known case of DM when
they omit their insulin or when there is infection or stress.
 Can be classified as mild, moderate and severe DKA
Normal Mild Moderate Severe
Bicarbonate
meq/l(venous)
20-28 16-20 10-15 <10
PH(venous) 7.35-7.45 7.25-7.35 7.15-7.25 <7.15
Clinical No change Alert but
fatigued
Kussmal
breathing
,sleepy
comatose
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17.  Silent presentation
Some children will be diagnosed with type 1
diabetes before the onset of clinical symptoms.
This presentation is least common and typically
occurs in children who have another close family
member with type 1 diabetes and are being closely
monitored .
A rare presentation.
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18. Laboratory investigations
 Fasting or random blood glucose
 Urine ketones
 Urine protein
 Blood urea,
 Electrolytes and creatinine o
 Fasting lipid profile
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19. DIAGNOSIS
 Fasting plasma glucose (FPG) ≥126 mg/dl
 Hemoglobin A1C ≥6.5%
 A random plasma glucose ≥200 mg/dl, in patients with classic
symptoms of Hyperglycemia or hyperglycemic crisis
 Two-hour plasma glucose ≥200 mg/dl during an oral glucose
oral tolerance test after 75gm anhydrous glucose dissolved in
water of glucose
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20. Management
Goals
 To maintain balance b/n tight glucose control & avoiding
hypoglycemia
 To prevent ketoacidosis
 To permit normal growth & development with minimal effect on
lifestyle
Principles of Rx
 Initiation & adjustment of insulin
 Health education
 Reestablishment of the life routines
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21. New onset DM without DKA
Pharmacologic
 Mixed insulin (70% NPH insulin + 30% regular insulin)
 The dose of starting insulin depends on the age of the
patient and whether the patient has presented with DKA
or not.
 Initiation - 0.2 to 0.4units/ kg/ day twice daily injection-
before breakfast and before supper
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22. Management…
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23. Insulin Schedule
2/3 of insulin in morning subcutaneous (SC)
1/3 of insulin evening subcutaneous
For better glycemic control
Regular insulin 1/3 of dose
Lente insulin 2/3 of the dose
Monitoring
Frequent blood glucose monitoring
Insulin dose adjustment
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24. TX of DKA
 IV fluids: normal saline - 20 ml/kg bolus over the first hour
Regular Insulin after one hour of rehydration 0.05-0.l units/kg/hr if
continuous IV infusion, if not first dose of insulin 0.5u/kg/d give
½ IM and ½ IV, Subsequent doses should be 0.5u/kg/d SC every
4-6 hours.
 Provide K+ in the form of KCL 20-40 meq/L of fluid.
 Dose adjustment in case of a rapid fall in RBS>100mg/dl, and
hypokalemia that has persisted despite administration of K+ by ½
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25. TX of DKA…
Fluid administration in the first hour of therapy before
insulin administration has the following advantages:
 It allows time to obtain a serum potassium level on
presentation
 It corrects hypotension, which may increase if insulin
is used without hydration
 It improves insulin action
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26. Complications during treatment
 Hypoglycemia: RBS < 60mg/dl
 Characterized by
 Palpitation, sweating, tremor
 Dizziness, weakness ,Pallor, vomiting
 Anxiety, confusion ,convulsion, coma
 RX: Sweet drinks, glucose solution
– Glucagons – in severe cases
 Cerebral edema (Bed side mannitol 1gm/kg is important)
 Hypokalemia
 So we need to follow the child with V/S, frequent glucose and electrolyte
measurement to act accordingly.
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27. Other related events
 Somogyi phenomenon
 Hypoglycemia induced morning hyperglycemia
 Due to larger doses of evening insulin and an exaggerated counter-regulatory response
 RX: Reduce the dose of long acting Insulin at night .
 Dawn phenomenon
 In children with normal dose of insulin at night & normal midnight glucose
(normoglycemia), counter regulatory hormone may normally increase (early morning
hyperglycemia).
 Rx: Increase the dose of long acting insulin at night
 Brittle diabetes
 Marked fluctuation of blood glucose often with recurrent DKA despite frequent insulin
dose adjustment
 Hypoglycemia
 Hyperglycemia and ketosis
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28. Non-pharmacologic
Medical Nutrition Therapy (MNT)
• Avoid refined sugars as in soft drinks
• Be encouraged to have complex carbohydrates.
− Low in animal fat.
− Increase in the amount of fiber e.g., vegetables, fruits
Exercise
Regular moderate-intensity aerobic physical activity for at least 30
minutes at least 5 days a week or at least 150 min/week.
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29. .
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