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Diab Overview 23

The document provides an overview of pediatric diabetes, focusing on definitions, pathophysiology, diagnosis, and management of type 1 and type 2 diabetes in children and adolescents. It outlines the criteria for diagnosis, symptoms, complications, and treatment protocols, including insulin therapy and lifestyle modifications. Additionally, it discusses the importance of monitoring and follow-up care for managing diabetes effectively.
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0% found this document useful (0 votes)
12 views92 pages

Diab Overview 23

The document provides an overview of pediatric diabetes, focusing on definitions, pathophysiology, diagnosis, and management of type 1 and type 2 diabetes in children and adolescents. It outlines the criteria for diagnosis, symptoms, complications, and treatment protocols, including insulin therapy and lifestyle modifications. Additionally, it discusses the importance of monitoring and follow-up care for managing diabetes effectively.
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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Pediatric Diabetes

Overview
Randa Matter
Professor of Pediatrics
Ain Shams University
Intended learning outcomes; ILOs
• Define diabetes mellitus
• Describe pathophysiology of diabetes
• List criteria for diagnosis of type 1 diabetes
• Identify the most common types of diabetes.
• Plan management for type 1 and type 2
diabetes in children and adolescents.
Diabetes Mellitus
Definition

• A multisystem disease related to:


– Abnormal insulin production, or
– Impaired insulin utilization, or
– Both of the above
• Leading altered carbohydrate, fat and
protein metabolism.
Insulin Secretion

Fig. 47-1
Normal Insulin Metabolism

•  Insulin after a meal: anabolic


•Stimulates storage of glucose as
glycogen
•Inhibits gluconeogenesis
•Enhances fat deposition in adipose
tissue
•Increases protein synthesis
Normal Insulin Metabolism
• Fasting state
– Counter-regulatory hormones (especially
glucagon) stimulate glycogen → glucose
• When glucose unavailable during fasting
state
– Lipolysis (fat breakdown)
– Proteolysis (amino acid breakdown)
ALTERED CHO METABOLISM
 Insulin

 Glucose Utilization
+
 Glycogenolysis

Hyperglycemia

Glucosuria
(osmotic diuresis) 

Polyuria* 
(fluid and electrolyte imbalance)

Polydipsia*

* Hallmark symptoms of diabetes


ALTERED PROTEIN METABOLISM

 Insulin

 Protein Catabolism

 Gluconeogenesis
(amino acids → glucose)

Hyperglycemia

Weight Loss and Fatigue
(mid arm circumference)
ALTERED FAT METABOLISM

 Insulin

 Lipolysis

 Free fatty acids + ketones

Acidosis + Weight Loss
(skin fold thickness)
Intended learning outcomes; ILOs
• Define diabetes mellitus
• Describe pathophysiology of diabetes
• List criteria for diagnosis of type 1 diabetes
• Identify the most common types of diabetes.
• Plan management for type 1 and type 2
diabetes in children and adolescents.
Pathophysiology: Overview
Triggers:
-Poorly understood, plenty of theories.

-Molecular mimicry…
-Injury to islets…
-Random failure of tolerance…

Cell mediated response:


-Type 1 diabetes is caused by a T cell–mediated
autoimmune destruction of the pancreatic beta
cells.

KAI W. WUCHERPFENNIG1 AND GEORGE S. EISENBARTH.:Type 1 Diabetes


Pathophysiology: Triggers
Molecular mimicry: similar epitopes between pathogen and host.
HGAD65: auto antigen
Coxsackie & hCMV:
Viral peptides

-Viruses can produce proteins similar to those of the host.


3
-Immune cells present viral protein homologous to self protein.
Failure of tolerance and autoimmunity.
Injury to Islet cells: macrophages provoke insulinitis by release of
interleukin.
-Can lead to presentation of cryptic antigens....

Image from ROEP et al.: MOLECULAR MIMICRY IN TYPE 1 DIABETES


3
Pathogenesis of type 1 diabetes

-Type 1 diabetes is an autoimmune disease caused by a T cell–


mediated destruction of the pancreatic beta cells.
-It has genetic and environmental components
-Genetic factors:
-Association with HLA class II genes :B8, B15, DR3 &DR4
- Environmental Triggers:
-Viruses can produce proteins similar to those of the host.
- Molecular mimicry :Immune cells present viral protein
homologous to self protein.
autoimmunity
Coxsackie virus B19, mumps, rubella.
- Early exposure to cow’s milk.

KAI W. WUCHERPFENNIG1 AND GEORGE S. EISENBARTH.:Type 1 Diabetes


Intended learning outcomes; ILOs
• Define diabetes mellitus
• Describe pathophysiology of diabetes
• List criteria for diagnosis of type 1 diabetes
• Identify the most common types of diabetes.
• Plan management for type 1 and type 2
diabetes in children and adolescents.
Criteria for the diagnosis of diabetes mellitus

Symptoms of diabetes plus casual plasma glucose


concentration ≥ (200 mg/dl).
OR
Fasting plasma glucose (≥126 mg/dl).
OR
Two-hour post load glucose (≥200 mg/dl) during
an OGTT.
OR
Glycosylated haemoglobin (HbA1c) ≥6.5%
Diagnosis of pre-diabetes
• Impaired fasting glucose:
– FPG 100 – 125 mg/dl
• Impaired glucose tolerance:
– 2-hour plasma glucose 140 -199 mg/dl after the
OGTT
– HbA1c 5.7-6.4 %
Type 1 Diabetes Mellitus symptoms
More common Less common Severe
Diabetic Ketoacidosis*
Weight loss Table 2: Symptoms
Frequent and
Excessive hunger Signs:
vomiting •
and acute
abdominal pain
Polyuria-in younger Blurred vision Flushed cheeks Acetone smell
children bedwetting is on breath
common

Excessive thirst Mood changes Dehydration with continuing


polyuria
Tiredness-not wanting Skin infections Decreased level of consciousness
to play
Oral or vaginal Kussmaul respiration (rapid deep
thrush sighing)
Abdominal pain Coma Shock
Intended learning outcomes; ILOs
• Define diabetes mellitus
• Describe pathophysiology of diabetes
• List criteria for diagnosis of type 1 diabetes
• Identify the most common types of diabetes.
• Plan management for type 1 and type 2
diabetes in children and adolescents.
Etiological classification of diabetes
• Type 1 diabetes: It is characterized by β-Cell
destruction, usually leading to absolute insulin
deficiency. Onset occurs in childhood but may
occur at any age.
• Type 2 diabetes: May range from predominantly
insulin resistance with relative insulin deficiency
to a predominantly secretory defect with or
without insulin resistance.
• 3-Other types (atypical diabetes):
Etiological classification of diabetes
a) Genetic defects of β-cell function
Neonatal Diabetes (presenting in the first six months of
life) results from the inheritance of a mutation (s) in a
single gene. Two types; permanent which needs lifelong
treatment, and transient which will remit within a
median of 3 month, although it might relapse later in life.
Monogenic diabetes presents outside the neonatal
period, previously known as MODY (Maturity Onset
Diabetes of Young). They present with a strong family
history of diabetes (Autosomal dominant) with absence
of autoantibodies, especially if measured at diagnosis.
Etiological classification of diabetes

b) Genetic syndromes sometimes associated with diabetes: 1. Down


syndrome 2. Klinefelter syndrome 3. Turner
syndrome 4. Prader-Willi Syndrome
c) Diseases of the exocrine pancreas:
1. Pancreatitis 2. Trauma/pancreatectomy 3.Neoplasia
4. Cystic fibrosis 5. Hemochromatosis
d) Endocrinopathies
1. Acromegaly 2. Cushing’s syndrome 3.Glucagonoma
4. Pheochromocytoma 5. Hyperthyroidism
e) Infections: 1. Congenital rubella 2.Cytomegalovirus 3.Enterovirus
f) Gestational diabetes
Type 1 Diabetes Mellitus
Differential diagnosis
1. Urinary symptoms: 1. D.D. of diabetic ketoacidosis:
- Compulsive water - Pneumonia - Encephalitis.
intake. - Acute abdomen. - Salicylate intoxication.
- Urinary tract infection. - Intracranial lesion. - Lactic acidosis.
- Diabetes insipidus. - Gastroenteritis with metabolic acidosis.
- Hyperglycemic hyperosmolar nonketotic
(HHS) coma: extremely high blood glucose
(600-3000 mg/dl) without ketoacidosis.

1. Differentiating between type 1 and type 2


Features suggesting the diagnosis of type 2 diabetes rather than type 1
diabetes at diagnosis include:
• Overweight or obesity • Age above 10 • Strong family history of type 2
diabetes • Acanthosis nigricans • High-risk racial or ethnic group
• Undetectable islet autoantibodies • Elevated C-peptide
Acanthosis Nigricans
11 8/12-Year-Old Female Patients
Type 1 Diabetes (T1) Type 2 Diabetes (T2)
• Chief complaint: Urinates 2 • Chief complaint: Urinates 2
to 3 times at night times 2 to 3 times at night times 2
weeks months
– A1C 8.2% at outside – A1C 8.2% at outside
clinic clinic
• Weight 63 kg, body mass • Weight 78 kg, BMI >95th
index (BMI) >85th percentile for age/gender
percentile for age/gender – Recent weight loss
– recent weight loss • BP 128/83
• Blood pressure (BP) 92/65 • Menses at age 10 years –
• Menses at 10 years – irregular
irregular
Complications of Type 1
Diabetes
Acute Chronic

− Diabetic ketoacidosis Microvascular


− Acute hypoglycemia − Nephropathy
− Infections − Retinopathy
− Neuropathy
− Macrovascular
− Poor growth and delayed
puberty
Type 1 Diabetes Mellitus
Investigations
At diagnosis
• C-peptide detecting endogenous insulin
secretion.
• Diabetes-associated autoantibodies; islet cell
antibody (ICA), insulin autoantibodies (IAA),
glutamic acid decarboxylase (GAD 65) and
specific zinc transporter antibodies.
These autoantibodies appear prior to insulin treatment
and are present in approximately 70% of children and
adolescents at the diagnosis of type 1 diabetes.
The levels of IAA show a strong inverse correlation with
age, being found in more than 90% of children under the
age of 5 years at diagnosis. The early appearance of IAA
makes them particularly useful for diabetes prediction in
young children.
Induction of insulin antibodies to exogenous insulin
means that IAA measurement is no longer informative
once insulin therapy has been given for more than 2
weeks.
Type 1 Diabetes Mellitus
Investigations
At diagnosis
• Comorbid conditions:
Autoimmune thyroid disease (Serum TSH level +
thyroperoxidase antibodies and annually thereafter;
Celiac disease (Tissue transglutaminase +
immunoglobulin A levels); Addison's disease (8 am
serum cortisol + serum sodium and potassium) as
indicated.
Type 1 Diabetes Mellitus
For follow up
After diagnosis:
• Daily blood glucose monitoring (self
monitoring).
• Intermediate monitoring every 2-4 wk. by
fructosamine.
• Long term metabolic control by glycosylated
Hb (HbA1c) every 3 months.
Type 1 Diabetes Mellitus
For follow up
Every year:
✓Blood urea, serum creatinine
✓SGOT, SGPT and alkaline phosphatase
✓Lipid profile and blood pressure annually
after age of 11 years for macrovascular
disease.
Type 1 Diabetes Mellitus
For follow up
Every year:
Screening for microvascular complications
Fundus examination: annually from age 11 years if
with 2 years duration and from 9 years if with 5
years duration.
Urinary albumin/creatinine ratio annually: same
as fundus indication.
Neurological examination to detect neuropathy.
Intended learning outcomes; ILOs
• Define diabetes mellitus
• Describe pathophysiology of diabetes
• List criteria for diagnosis of type 1 diabetes
• Identify the most common types of diabetes.
• Plan management for type 1 diabetes and
type 2 in children and adolescents.
Management of type 2 diabetes
• Weight reduction
• Diet
• exercise
• Lifestyle modification
• Drugs: Metformin
• Liraglutide injection (above 10 years)
Type 1 diabetes treatment
protocol

Insulin Diet Health education

Exercise Psychological Home glucose


management monitoring
A look at the past
In 1922,Banting and Best isolate insulin •
to became the treatment for diabetes.
Insulin

• Insulin types: Insulin used in children are


prepared by recombinant DNA technology
which includes; short-intermediate or long
acting insulin
Insulin Therapy: Mimicking Nature

Physiologic Insulin Secretion


24-hr Profile
(µU/mL) 50
Insulin

25

0 Basal Insulin
Breakfast Lunch Dinner
150
(mg/dL)
Glucose

100

50
Basal Glucose
0
7 8 9 101112 1 2 3 4 5 6 7 8 9
AM Time of Day PM
Skyler JS. In: DeFronzo RA, ed. Current Therapy of Diabetes Mellitus. St. Louis: Mosby-
Year Book; 1998:108-116; Galloway JA, Chance RE. Horm Metab Res. 1994;26:591
The Basal/Bolus Insulin
Concept
• Basal Insulin
– Suppresses glucose production between
meals and overnight
– 50% of daily needs
• Bolus Insulin (Mealtime or Prandial)
– Limits hyperglycemia after meals
– Immediate rise and sharp peak at 1 hour
– 10% to 20% of total daily insulin requirement
at each meal
Continues subcutaneous insulin
infusion (CSII)
Pump therapy (Insulin pump is the best way of
achieving and maintaining strict control of blood
glucose concentrations in type 1 diabetes
patients through more physiological
insulinization than achieved with multiple daily
injections
Types of Insulin
• Rapid Acting:
– Insulin lispro (Humalog)
– Insulin aspart (Novolog)
– Insulin glulisine (Apidra)
• Short-acting:
– regular
• Intermediate-acting:
– NPH
• Long-acting:
– Insulin glargine 100(Lantus), 300(Toujeo)
– Insulin detemir (Levemir)
• Ultra-long basal:
- Insulin degludec (Tresiba)
Types of Insulin
Insulin Type Onset Peak Usual Effective Usual Maximum
(hours) Duration (hours) Duration (hours)

Aspart (Novolog) 5-10 minutes 1-3 3-5 4-6

Lispro (Humalog) <15 minutes 0.5-1.5 2-4 4-6

Glulisine (Apidra) <15 minutes Similar to apart/lispro

regular 0.5-1 hour 2-3 3-6 6-10

NPH 2-4 hours 4-10 10-16 14-18

Glargine (Lantus) 3 - 4 hours -- 24 24

Detemir (Levemir) similar to glargine


Insulin Preparations
Insulin dose
During the partial remission phase (honey
moon), the total daily insulin dose is often <0.5
IU/kg/d.
Prepubertal children (outside the partial
remission phase) usually require 0.7–1.0
IU/kg/d.
During puberty, requirements may rise
substantially above 1.2 IU/kg/d and even up to 2
IU/kg/d.
Insulin Injection Sites and method
Methods of Insulin Delivery
• Pens
• Jet injectors
• Insulin pumps—insulin is delivered at .5-2
units/hour. Most common risk of insulin pump
therapy is ketoacidosis.
• Implantable devices
• Transplantation of pancreatic cells
The first insulin pump
Complications of Insulin Therapy
• Local allergic reactions
• Systemic allergic reactions
• Insulin lipodystrophy (lipoatrophy or
lipohypertrophy)
• Insulin resistance
• Morning hyperglycemia—Dawn phenomenon
(nocturnal surges of growth hormone) so give
dose at HS not before dinner.
Nutritional Therapy

The major goals:


• to ensure ideal body weight and growth
similar to nondiabetic children,
• to help control of wide fluctuation of
blood glucose, and
• to reduce cardiovascular risk.
Nutrition
• CHO 45-55% of total calories
• Protein 15-20%
• Dietary fat <30% w/saturated fat
<10% and cholesterol
<300mg/day
Fiber intake 25-50g/day---blunts
the glycemic response.
Monounsaturated fatty acids (MUFA)
and polyunsaturated fatty acids
(PUFA) can be used as substitutes to
keep lipid intake within
recommended ranges or to improve
the lipid profile
Nutritional Therapy

Total daily caloric intake


may be divided to provide
- 20% at breakfast
- 30% at lunch
- 20% at dinner
- 10% at mid-morning,
mid-afternoon and
evening snacks.
Nutritional Therapy
Nutritional Therapy
Nutritional Guidelines
• Carbohydrate
Counting
– 1 carbohydrate
choice = 15 grams
carbohydrate
– 1 carbohydrate
choice = 1 starch
exchange(15g) or 1
fruit exchange(15g)
or 1 milk
exchange(15g)
Glycemic index and glycemic load

♦ Low GI carbohydrate foods (GI<55) may lower


post-prandial hyperglycemia when they are chosen
to replace higher GI foods (GI>70)
♦ Examples of low GI food sources include wholegrain
breads, pasta, temperate fruits and dairy products
Insulin-to-Carbohydrate Ratio

The carbohydrate coverage ratio:


An Insulin-to-Carbohydrate Ratios (I:C) ratio tells you
how many units of insulin you need to take to
"cover" a specified number of carbohydrate.

the amount of carbohydrate per one unit of insulin is


derived by dividing 500 by the total daily insulin
dose(TDD) in units if using rapid acting insulin, or
450 if using short acting insulin. Thus, for an adult
who typically takes 40 units per day, the I: C ratio
would be one unit of insulin to 12 gm of
carbohydrate
The carbohydrate coverage ratio:
500 ÷ Total Daily Insulin Dose
= 1 unit insulin covers so many grams of carbohydrate
This can be calculated using the Rule of “500”: Carbohydrate Bolus
Calculation
In this example :
Carbohydrate coverage ratio
= 500 ÷ TDI(40 units)
= 1unit insulin/ 12 g CHO
The insulin to carbohydrate ratio may vary during the day.
This example above assumes that you have a constant response to
insulin throughout the day. In reality, individual insulin
sensitivity varies. Someone who is resistant in the morning,
but sensitive at mid-day, will need to adjust the insulin-to-
carbohydrate ratio at different meal times. In such a case, the
background insulin dose would still be approximately 20 units;
however, the breakfast insulin-to-carbohydrate ratio might be
breakfast 1:8 grams, lunch 1:15 grams and dinner 1:12 grams.
The high blood sugar correction factor:
Correction Factor = 1800 ÷Total Daily Insulin Dose = 1 unit of insulin
will reduce the blood sugar so many mg/dl
This can be calculated using the Rule of “1800”.
Example:
Assume your total daily insulin dose (TDI) = 160 lbs ÷ 4 = 40 units
In this example:
Correction Factor
= 1800 ÷ TDI (40 units)
= 1 unit insulin will drop reduce the blood sugar level by 45 mg/dl
While the calculation is 1 unit will drop the blood sugar 45 mg/dl, to
make it easier most people will round up or round down the
number so the suggested correction factor may be 1 unit of rapid
acting insulin will drop the blood sugar 40-50 mg/dl.
Please keep in mind, the estimated insulin regimen is an initial “best
guess” and the dose may need to be modified to keep your blood
sugar on target.
Bolus – High blood sugar correction
(insulin sensitivity factor)
• The bolus dose for high blood sugar correction is
defined as how much one unit of rapid-acting
insulin will drop the blood sugar.
• Generally, to correct a high blood sugar, one unit
of insulin is needed to drop the blood glucose by
50 mg/dl. This drop in blood sugar can range
from 30-100 mg/dl or more, depending on
individual insulin sensitivities, and other
circumstances.
• • When using carbohydrate counting, persistent elevations of postmeal BG may require
adjustment in the insulin to carbohydrate ratio. The “500-rule” is often used to obtain
an initial ratio when starting with carbohydrate counting (divide 500 by the total daily
dose—basal and bolus insulin—to find the amount of carbohydrates in grams that 1
unit of insulin will cover).
• • The insulin: carbohydrate ratio for an individual meal, for example breakfast, can be
calculated by dividing the carbohydrate content in grams by the insulin dose in units.
This method often gives the most accurate results for an individual meal and can
preferably be used for breakfast when there usually is an increased insulin resistance. If
the glucose before and after the meal differ more than 2 to 3 mol/L (20-30 mg/dL), the
correction factor can be used to calculate out how much more (or less) insulin that
ideally should have been given for a certain meal.
• • Some centers also count protein and fat for calculating insulin requirements when
using a pump (FPU, fat-protein units). One FPU equals 100 kcal of fat or protein and
requires the same amount of insulin (as an extended bolus) as 10 g of carbohydrates.
This may result in postmeal hypoglycemia, and more recent studies have found a lower
need of insulin for protein, around 200 kcal equaling 10 g of carbs.
Examples:
• Example #1: Carbohydrate coverage at a meal
First, you have to calculate the carbohydrate coverage insulin dose using
this formula:
CHO insulin dose =
Total grams of CHO in the meal
÷ grams of CHO disposed by 1 unit of insulin
(the grams of CHO disposed of by 1 unit of insulin is the bottom number or
denominator of the Insulin:CHO ratio).
For Example #1, assume:
• You are going to eat 60 grams of carbohydrate for lunch
• Your Insulin: CHO ratio is 1:10
To get the CHO insulin dose, plug the numbers into the formula:
CHO insulin dose =
Total grams of CHO in the meal (60 g)
÷ grams of CHO disposed by 1 unit of insulin (10) = 6 units
You will need 6 units of rapid acting insulin to cover the carbohydrate.
Example #2: High blood sugar correction dose
• assume:
1 unit will drop your blood sugar 50 points (mg/dl) and the high blood
sugar correction factor is 50.
• Pre-meal blood sugar target is 120 mg/dl.
• Your actual blood sugar before lunch is 220 mg/dl.
Now, calculate the difference between your actual blood sugar and
target blood sugar:
220 minus 120 mg/dl = 100 mg/dl
To get the high blood sugar correction insulin dose, plug the numbers
into this formula:
Correction dose =
Difference between actual and target blood glucose (100mg/dl)
÷ correction factor (50) = 2 units of rapid acting insulin
So, you will need an additional 2 units of rapid acting insulin to
“correct” the blood sugar down to a target of 120 mg/dl.
Example #3: Total mealtime dose
Finally, to get the total mealtime insulin dose, add the CHO insulin
dose together with the high blood sugar correction insulin dose:
CHO Insulin Dose
+ High Blood Sugar Correction Dose
= Total Meal Insulin Dose
For Example #3, assume:
• The carbohydrate coverage dose is 6 units of rapid acting insulin.
• The high blood sugar correction dose is 2 units of rapid acting
insulin.
Now, add the two doses together to calculate your total meal dose.
Carbohydrate coverage dose (6 units)
+ high sugar correction dose (2 units)
= 8 units total meal dose!
The total lunch insulin dose is 8 units of rapid acting insulin.
Total Daily Insulin Requirement:
The general calculation for the body’s daily insulin requirement is:
Total Daily Insulin Requirement (in units of insulin)
= Weight in Pounds ÷ 4
Alternatively, if you measure your body weight in kilograms:
Total Daily Insulin Requirement (in units of insulin)
= 0.55 X Total Weight in Kilograms
Example 1:
If you are measuring your body weight in pounds:
• Assume you weigh 160 lbs.
In this example:
TOTAL DAILY INSULIN DOSE
= 160 lb ÷ 4 = 40 units of insulin/day
Example 2:
If you are measuring your body weight in kilograms:
• Assume your weight is 70Kg
In this example:
TOTAL DAILY INSULIN DOSE
= 0.55 x 70 Kg = 38.5 units of insulin/day
If your body is very resistant to insulin, you may require a higher dose. If your body
is sensitive to insulin, you may require a lower insulin dose.
Health education
• Based on self management, and is child-and
parent-centered.
• Where possible, diabetes education should be
delivered by a Multi- disciplinary pediatric
diabetes team (ideally a doctor, nurse,
dietitian, psychologist, social worker), with a
clear understanding of the special and
changing needs of young people and their
families.
Health education
Delivery tools
visual aids such as diagrams, drawings, written
guidelines, booklets, video, DVDs appropriate to
the child’s age, maturity and environment.
24 hour telephone support is extremely helpful
to families to reduce their isolation, helping to
develop confidence in their ability to manage
their child’s diabetes and cope with emergencies.
Health education ; Teaching Plan
• Simple pathophysiology
• Treatment modalities
• Recognition, treatment and prevention of
acute complications
• When to call the doctor
• Foot care, eye care, general hygiene, risk
factor management
Exercise Management

• Encourage children and adolescents to be


physically active, to be less sedentary and to
develop healthy lifestyle habits for the
following reasons;
a) Coronary heart disease risk reduction;
b) Weight control;
c) Self image; and
d) Reduction of insulin requirement.
Exercise Management

• Check blood glucose before, during and


after exercise.
• Eat before heavy exercise.
• Always carry a fast-acting carbohydrate
• Have extra carbohydrate snacks available.
• Approximately 1-1.5 g carbohydrate/kg body
weight/hour should be consumed during
strenuous exercise
Psychological management

Strategies to help the child and their family


cope with diabetes:
• Encourage the family to learn about diabetes
and to share their diabetes knowledge with
family and friends to engage support.
• Depending on their age and capability,
encourage the child to become involved in some
of their care, to be positive.
Home glucose monitoring
Blood glucose monitoring should ideally be
carried out 4-6 times a day, however, this is
dependent on the availability of testing strips.
Even two tests per day gives useful information.
Blood glucose testing delivers a picture of what
blood glucose levels are like over a period of 24
hours and helps to identify problems early.
MiniMed MiniMed
Guardian® Paradigm®
REAL-Time REAL-Time
System System

DexCom™ Abbott FreeStyle


SEVEN® PLUS Navigator®
CGM
Dexcom Eversense
Home glucose monitoring
Urine glucose testing may be used in;
a) presence of illness with fever and/or
vomiting,
b) blood glucose >270 mg/dl; and
persistent polyuria with elevated blood
glucose, especially if abdominal pain or
rapid breathing are present.
Self-
Monitoring
of Blood
Glucose
(SMBG)
Self-Monitoring of Blood Glucose
(SMBG)
Target indicators of metabolic control
Glycated Hemoglobin (Hb A1C )
• Measures blood levels over 2-3 months (per
text)
• High levels of glucose will attach to
hemoglobin
• Helps to ensure that the patient’s glucometer
is accurate
• The target HbA1c for all age-groups is a value
less than 7%.
Time in Range

Time in Range (TIR) ​indicates the percentage of how long the


glucose value was within the target range during a defined
period. This number can sometimes be described as “hours in
target range” as well.
If a person has a TIR of 50%, that would indicate that your
glucose levels were within the target range for approximately 12
hours on any given day.
Target range may vary from person to person, as best guided by
your primary care provider, but most official
recommendations range from 70 mg / dl -180 mg / dl.
The A1c only represents the average glucose value over the past 2 to 3
months as a single snapshot. It is devoid of any additional data or
explanations. Mapping the high's and low's, via TIR, offers a fuller view of
the day-to-day management for a person with diabetes.
https://diatribe.org/
Researchers at the ATTD Congress 2019 (Advanced
Technologies & Treatments for Diabetes) made the following
recommendations for people with type 1 and type 2 diabetes:
At least 70% of the day within 70 -180 mg / dl.
Less than 4% of the day below 70 mg / dl.
Reduction of time over 180 mg / dl per day.
The glucose data would be measured with a glucose sensor in
the previous 14 days.
If you are using a CGM system, the work is done for you since
the CGM systems determine a glucose value around the clock
giving you a consistent stream of measured values on average
every 5 minutes.
Glucose Management Indicator (GMI): A New Term for
Estimating A1C From Continuous Glucose Monitoring

CGM-derived mean glucose


GMI (%)*
(mg/dL)
100 5.7
125 6.3
150 6.9
175 7.5
200 8.1
225 8.7
250 9.3
275 9.9
300 10.5
350 11.7
Resources
• www.diabetes.org
• www.childrenwithdiabetes.com
• www.jdfcure.org
• www.cdc.gov
• http://care.diabetesjournals.org/
• www.barbaradaviscenter.org
– “Understanding Diabetes”
Test Yourself!
The lowest fasting plasma glucose level
suggestive of a diagnosis of DM is:
A. 90mg/dl
B. 115mg/dl
C. 126mg/dl
D. 140mg/dl
Test Yourself!

The risk factors for type 1 diabetes include all


of the following except:
a. Diet
b. Genetic
c. Autoimmune
d. Environmental
Test Yourself!

Blood sugar is controlled when Hemoglobin


A1C is:
a. Below 6%
b. Below 7%
c. Between 8-9%
d. Above 9%

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