DIABETES MELLITUS, PEDIATRIC.ppt

DIABETES MELLITUS, PEDIATRIC
1

Session Outline
 Introduction
 Epidemiology
 Etiologic factors
 Pathogenesis & Pathophysiology
 Clinical Presentation
 Diagnosis
 Treatment
 Complications (Acute & Long term)
 Diabetic health education
2

Introduction
Diabetes mellitus (DM) is a chronic metabolic syndrome
having hyperglycemia as a cardinal biochemical feature.
There are two major types: Type – I and Type – II.
Type-I DM: Common endocrine-metabolic disorder of
childhood, caused by insulin deficiency due to damage to
pancreatic β-cells.
Type-II DM: Due to insulin resistance at the level of a
skeletal muscles, liver, and adipose tissue.
Morbidity and mortality from DM is related to acute and
long term complications.
Other types include: Gestational DM, Neonatal DM,
Maturity onset diabetes of the young (MODY).
3

Type-I Vs. Type-II DM: Differentiation
Demographics Type-I DM Type-II DM
Family History 3-5% 74-100%
Age Variable >10 years / Pubertal
Gender Male = Female Female > Male
Asymptomatic
Presentation Rare Common
BMI at Diagnosis < /=75 percentile >/= 85 percentile
Autoimmune
markers Common Uncommon
4

Epidemiology (Type-I DM)
It accounts for 10% of all diabetes.
Most cases of diabetes in children is type-I.
(This presentation focuses on type-I Diabetes)
However, it is not limited to children; 50% of individuals
with Type-I DM present as adults.
The incidence is currently on the rise.
Globally 400,000 total new cases of type-I diabetes
occur annually in all children under age 14 years.
5

Etiologic Factors (Type-I DM)
 Type-I DM is characterized by autoimmune-mediated destruction
of pancreatic beta cells culminating in absolute insulin deficiency.
 Diabetes develops as a result of an interplay between
both genetics and the environment.
1) Genetics: Evidences
 Prevalence in siblings is 6% compared to 0.4% in the
general population.
 Risk increases when parents have diabetes.
 Concordance rate among monozygotic twins is 30-65%.
However majority of patients with type-I DM do not have
family member with the disease (85%), so family
history alone is not a reliable tool to identify those at
risk of future diabetes.
6

2) The environment: several observations support the role
of the environment in the development of type-I DM:
50% monozygotic twins are discordant for type-I DM.
Variation in incidence between urban and rural areas
populated by the sane ethnic group.
Change in incidence that occurs with migration(see later).
Occurrence of seasonality
7

 The rate in Puerto Rico,17.4, is similar to that in Pennsylvania, but
the rate in neighboring and ethnically similar Cuba is only 2.9.
 Israeli children living in Canada have a fourfold greater incidence
than those in Israel.
 Where T1DM in the Indian population is very low, Indian children
migrating to England from South Africa developed incidence rates
comparable with those of English children in the community.
 Japanese living in Hawaii are five times more likely to have T1DM
than those in Japan.
 Ethnic French and Italian children in Montreal have twice the
incidence of diabetes as those in their native lands.
 Factors like viral infections, diet, & stressors are believed to play a
role in the causation of type-I DM.
8

Pathogenesis & Pathophysiology (Type-I DM)
 In type-I DM, a genetically susceptible host develops
autoimmunity to pancreatic β cells. What triggers this
autoimmunity is unknown.
 The natural history goes through the following events:
1) Initiation of autoimmunity: most occur before 2 years
of age, with presence of multiple autoantibodies. This
gap between appearance of antibodies & development
of the disease may offer an opportunity for prevention.
2) Preclinical autoimmunity with progressive β cell loss.
3) Onset of clinical disease: time of onset depends on the
number of autoantibodies, genetics, & environment.
4) Transient remission: Honeymoon period
5) Established disease
6) Development of complications.
9

Pathophysiology:
Insulin plays a major role in energy utilization by cells.
Post prandial its level rises for energy storage (anabolic)
and its level should drop during fasting state to mobilize
stored energy for use (catabolic).
Type-I DM is a progressive low insulin catabolic state.
With insulinopenia, glucose use by muscle & adipose
tissue decreases; plus glucose production by the liver via
glycogenolysis & gluconeogenesis increases, both leading
to hyperglycemia.
Hyperglycemia causes osmotic diuresis with loss of
calories, electrolytes → dehydration& physiologic stress.
Secretion of stress hormones then follow.
10

Pathophysiology: (Cont.)
The stress hormones then, decompensate the metabolic
process further:
1)Impair insulin secretion- Epinephrine
2)Antagonize insulin action – Epinephrine, Cortisol, GH.
3)Promote glucose production, lipolysis, and ketogenesis
– Glucagon, Epinephrine, Cortisol, Growth hormone.
4)Decrease glucose utilization & clearance- Epinephrine,
Cortisol, and Growth hormone (GH).
Insulin depletion coupled with glucagon excess leads to
further lipolysis and accumulation of free fatty acids
which is shunted towards production of ketone bodies →
METABOLIC ACIDOSIS.
11

Clinical Presentation (Type-I DM)
 The clinical picture correlates with progressive loss of β
cells.
 Polyuria develops with further loss of the cells.
 Nocturia
 Compensatory polydipsia and polyphagia then occurs.
 Weight loss follows when the dietary intake can not
cope with urinary calorie loss.
 With extremely low insulin level ketoacids accumulate
and patient develop diabetic ketoacidosis (DKA).
 About 20-40% of patients with type-I DM present with
DKA for the first time.
12

Diagnosis (Type-I DM)
The diagnosis of DM is usually straight forward.
Presence of poly-symptoms, with dehydration and weight
loss suggests the possibility of diabetes.
Diagnostic criteria:
1)Impaired Glucose tolerance (IGT): Fasting blood sugar
(FBS) 100-125mg/dL, or 2hour plasma glucose during
OGTT > 140mg/dL and < 200mg/dL.
2)Diabetes Mellitus: Symptoms of diabetes plus:
Random blood sugar (RBS) > 200mg/dL, or
Fasting blood sugar (FBS) > 126mg/dL or
2hour plasma glucose during OGTT > 200mg/dL.
NB: DKA must be looked for once diagnosis of DM is made.
OGTT: Oral Glucose Tolerance Test
13

Treatment (Type-I DM)
 Type of therapy depends on the patients initial clinical
presentation and whether DKA has occurred or not.
 Hence two groups of patients:
1) Patients with ketotic onset
2) Patients without ketosis on presentation.
 Principles of therapy:
 Insulin replacement
 Life style modification
 Regular follow up to assess glycemic control and look
for complications.
14

Treatment (Type-I DM): Insulin
1) Children with non ketotic onset: 60-80% of cases.
 These children have moderate symptoms, no/minimal
dehydration, and not yet progressed to DKA.
 The insulin dose required depends on pubertal status,
but needs to be manipulated based on glycemic control.
 The usual requirement is 0.7IU/Kg/day (Pre-pubertal),
1IU/Kg/day (Pubertal) & 1.2IU/Kg/day(Post-pubertal).
 Therapy may be started with 60-70% of the above dose
and adjusted as needed.
 Frequent blood sugar check needs to be done
especially during first few weeks, to adjust insulin
dosage.
 Self blood sugar monitoring is particularly helpful and
this must be thought to the patient as part of care.
15

Treatment (Type-I DM): Insulin
2) Children with DKA:
a)Those presenting with DKA for the 1st time: treatment
is transitioned to that described for those with non ketotic
onset once DKA has resolved.
b)Those with history of DM developing DKA: these will be
put on their previous insulin regimen used before the
onset of DKA after resolution of the DKA.
16

Treatment (Type-I DM): Diet
There is no much special dietary arrangement for the
diabetic child; however, the following points need to be
taken in to consideration:
The caloric mixture should comprise approximately 55%
carbohydrate, 30% fat, and 15% protein.
70% of the carbohydrate content should be derived from
complex carbohydrates such as starch.
Sucrose, highly refined sugars, & carbonated beverages
should be limited. These are absorbed rapidly & cause
wide swings in metabolic pattern.
17

Treatment (Type-I DM): Exercise
No form of exercise should be prohibited for the diabetic
child, but the following care needs to be taken:
For patients with poor glycemic control, vigorous exercise may
precipitate DKA.
When planning a vigorous exercise additional carbohydrate need to
be taken, and glucose from such sources as juice must be made
available during and after the exercise.
Watch for delayed hypoglycemia several hours after the exercise.
On the other hand regular exercise has a beneficial effect
on glycemic control by increasing the number of insulin
receptors, and therefore it has to be encouraged.
18

Acute Complication of DM:DKA
INTRODUCTION:DKA
A common and life threatening medical emergency in
patients with type I diabetes.
May be an initial presentation of DM in a child in 20 –
40% of the time; for adults it is mostly a complication of
established diabetes.
Absolute/relative insulin deficiency resulting in
hyperglycemia, dehydration and accumulation of ketone
bodies in the blood with subsequent metabolic acidosis
(pH < 7.30; serum bicarbonate < 15 mmol/L). 19

Biochemical triad: ketonemia, hyperglycemia,
and acidemia.
One in 100 children with DKA dies in the USA.
The severe the DKA, the higher the mortality and
complications.
Severity is defined by venous blood PH:
 Mild DKA: PH 7.25 – 7.35
 Moderate DKA: PH 7.15 – 7.25
 Severe DKA: PH < 7.15 (Requires Intensive Care Rx)
20

Causes/Precipitating factors:
Initial presentation of type I diabetes mellitus (Delay in
diagnosis of DKA in a young child with no history of
diabetes)
 Missed insulin injections
Inadequate insulin dosage in a known diabetic patient
Stress: Emotional, trauma, surgery without adequate
insulin adjustment.
Intercurrent illness/infection without proper insulin
adjustment.
21

Risk Factors:
Low socioeconomic status/Less education
Poorly controlled diabetes
Previous history of DKA
Peripubertal ages and adolescents
Psychiatric illness
Unstable family dynamics
Use of insulin pump therapy
22

Pathophysiology of DKA:
A relative / absolute insulin deficiency is the factor.
Insulin helps move glucose in to cells as a source of
energy. In its absence body goes in to a catabolic state
with breakdown of glycogen, protein, and fat in muscle,
liver, and adipose tissue.
Counter regulatory hormones stimulate glycogenolysis,
gluconeogenesis, proteolysis, lipolysis, and ketogenesis in
an attempt to provide more fuel to cells.
Brain which consumes 20 % of body’s metabolic need
cannot use fatty acids as energy, and depends on ketones
produced by hepatic oxidation of fatty acids stimulated
by glucagon.
23

Hall Marks of DKA:
Metabolic acidosis: caused by elevated plasma
concentrations of the ketoacids acetoacetate and beta-
hydroxy butyrate. Lactic acidosis occurs in large part
from anaerobic glycolysis in hypoperfused tissues
secondary to hypovolemia from osmotic diuresis.
Hyperosmolality: in DKA, glucose is elevated about 400
mg/dL above normal, and the BUN is elevated by about
15 mg/dL. These elevations result in an additional
osmolar load of about 22 and 5 mOsm/L, respectively.
24

Hall Marks of DKA… Cont.
Dehydration: secondary to osmotic diuresis and glycosuria. May
progress to hypovolemic shock.
Electrolyte disturbance:
Hyponatremia: may be an artifact due to shift of water to ECF
secondary to hyperglycemia. Correct true value by adding 2.8 mEq/L to
obtained value for every 100mg/dL increase in serum glucose.
Potassium: Initially, artificially elevated b/c during acidosis, K+ is
exchanged for H+I (Intracellular K+ moves to ECF) Patients are
usually total body K+ depleted and serum K+ levels will drop rapidly
with correction of acidosis. Best way to confirm is to see U wave and
flat T wave on ECG.
Hypophosphatemia: due to osmotic diuresis.
25

Clinical evaluation:
History:
Triads of polydipsia, polyuria, polyphagia
Vomiting, abdominal pain, difficult
breathing
Symptoms of infection
Last insulin dose, ? Missed dose
Any stressful situation?
Physical:
Vital signs, Hydration status, 26

Diagnosis:
Diagnosis of DKA is established biochemically as:
A venous pH <7.3 or
Serum bicarbonate concentration <15 mmol/L,
Serum glucose concentration >200 mg/dL
together with ketonemia, glucosuria, & Ketonuria and
associated clinical features.
27

Work Up:
Blood sugar
Urine ketones
Serum electrolytes
CBC and infection screen
BUN and Creatinine
Imaging studies guided by clinical scenario
Venous blood PH
28

PRINCIPLES OF THERAPY:
1) Maintain ABC of life
2) Correct Dehydration: Fluids & Electrolytes
3) Correct hyperglycemia: Insulin
4) Address any precipitating factor, if identified.
5) Prevent future recurrence: Patient education.
29

ABC of Life:
Assess air way, breathing and circulation.
Patients with GCS < 8 may need intubation to secure
air way and prevent aspiration.
Gastric decompression (NGT) to reduce risk of
aspiration.
Administer oxygen if patient is in shock or low oxygen
saturation.
30

FLUID THERAPY:
Critical part of treating patients with DKA.
The presence of even mild form of dehydration indicates
at least 3L of fluid has been lost !!
Give 10 – 20mL/Kg in the 1st hour; then replace deficit of
8.5% body weight and maintenance over next 23 hours.
Fluid type: NS / RL until blood sugar reaches 200mg/dL
when glucose containing fluid should be used.
ELECTROLYTE:
Potassium is the major concern.
Should be started after initial fluid bolus and before
commencing insulin therapy.
Add 20 – 40 mEq/L of KCL to each bag of fluid if serum
31

HYPERGLYCEMIA:
Goal: to reduce blood sugar at 70 – 100 mg/dL/hr.
The optimal administration of insulin is through insulin
infuser at 0.1 IU/Kg/Hr. Continue insulin infusion until
resolution of DKA (pH > 7.30, bicarbonate > 15 mEq/L), which
usually takes longer than normalization of blood glucose level.
Dose: Mix 50 IU of insulin in 50mL NS, and run at
0.1mL/Kg/Hr = 1mL per hour for a 10 Kg child.
In our setting, short of infuser we use the older system of
4hourly insulin based on blood sugar level: >600mg/dL –
1IU/Kg, 300 – 600mg/dL – 0.5IU/Kg, 180 – 300mg/dL –
0.25IU/Kg, No insulin when blood sugar is less than
180mg/dL.
32

Complication of DKA:
Cerebral edema is a feared complication, specially
related with therapy.
Mechanism not well known, may be osmotic or
vasogenic.
Avail mannitol at the bed side in every critically sick
DKA patient under therapy.
Consider intubation and mechanical ventilation
Alternative: hypertonic saline(3%) 5-10mL/Kg over 30
min can be used.
33

Chronic Complications of DM
 The development of these complications depend on the
extent of glycemic control, duration of diabetes and
genetics.
 How well the glycemic control has been is measured by
the level of glycosylated hemoglobin. HbA1c represents
the fraction of hemoglobin to which glucose has been
non enzymatically attached.
 HbA1c values of 6-7.9% represent good control, values
of 8.0-9.9%, fair control, and values of 10% or higher,
poor control.
 HbA1c measurement reflects glucose level of preceding
2-3 months.
 It has to be measured 3-4 times per year.
34

There are three major categories of chronic complications
of DM:
1)Microvascular: Retinopathy, Nephropathy
2)Macrovascular: Coronary artery disease, cerebrovascular
disease, & peripheral vascular disease.
3)Neuropathies: Peripheral and autonomic.
35

Pathogenesis of microvascular complications: several
mechanisms have been proposed:
Protein glycation: glucose binds irreversibly to proteins
(collagens) by non enzymatic means, giving advanced
glycation end products(AGE). The AGE accumulates in
vascular intracellular proteins &cause structural tissue
alterations with progressive occlusion of blood vessels.
Example: Binding to Hemoglobin, Renal basement membrane.
Polyol pathway: Sorbitol is formed from glucose by an
enzyme aldose reductase. High sorbitol level in tissues
(lens, nerves) causes and increased pressure & leakage in
blood vessels → decreased vessel wall elasticity and
microvascular hypertension, leading to local ischemia.
36

Diabetic Health Education
Should address the following issues:
Adherence to therapy & proper dosing.
Self injection techniques & injection site care.
Appropriate drug storage.
Symptoms of hypoglycemia.
Dietary management.
Regular exercise & caution with vigorous exercise.
Need for regular follow up & hygiene (oral, foot,…)
Self blood sugar monitoring & interpretation of results.
Awareness & avoidance of precipitating factors of DKA.
Psychosocial support & counseling.
37

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