DIABETES MELLITUS AND

HYPOGLYCEMIA IN CHILDREN

Prof Martin NDUWIMANA

KIU 08/11/2017
 Outlines
• Defintion
• Classification
• Epidemiology
• Diagnosis
• Management
• Diabete ketoacidosis
• Hypoglycemia
 Definition
• Diabetes mellitus is a group of metabolic diseases in
which a person has high blood sugar, either because the
body does not produce enough insulin, or because cells
do not respond to the insulin that is produced.
 Classification
• The differentiation between various forms of
diabetes has important implications for both
therapeutic decisions and educational approaches.
• Is no longer based on the type of treatment or age of
the patient and the terms “ insulin dependent”, “non
insulin dependant”, juvenile onset” and “ adult
onset” are obsolete.
 Classification
• The current classification is more appropriate and is
aetiology based.
I. Type 1
II. Type 2
III. Other specific types
IV. Gestational diabetes mellitus (GDM)
 I. DM type 1
• Characterized by beta cell destruction, usually
leading to absolute insulin deficiency.
• It has two forms:
– 1/ Immune-Mediated Diabetes Mellitus:
• Results from a cellular mediated autoimmune destruction of the
beta cells of the pancreas.
• One or more key antibodies are found in 85-90% of people with
this form of type 1 diabetes.
• People with this form of type 1 diabetes always require insulin
to survive.
• This is the most common form of type 1 diabetes and is
sometimes refered to as "Type 1A diabetes."
 I. DM type 1
• 1/Immune-Mediated Diabetes Mellitus:
• 2/ Idiopathic Diabetes Mellitus:
– Refers to forms of the disease that have no known
etiologies.
– These forms are much less common than immune-
mediated type 1 and are mostly found in people with
African or Asian ancestry.
– People with this form of type 1 diabetes often lack
antibodies found in immune-mediated type 1
diabetes, and may be able to go without insulin
therapy for some periods of time.
– This form of type 1 diabetes is sometimes refered to
as "Type 1B diabetes."
 Epidemiology of type 1 diabetes
• In most western countries, type 1 diabetes accounts
for over 90% of childhood and adolescent diabetes,
while across the lifespan, type 1 diabetes accounts
for 5–10% of individuals with diabetes.
• Approximately 80 000 children under 15 yr are
estimated to develop type 1 diabetes annually
worldwide
• Type 2 diabetes is becoming more common and
accounts for a significant proportion of youth onset
diabetes but population-based epidemiological data
 Epidemiology of type 1 diabetes
• A rise in type 1 diabetes incidence has been
observed globally in recent decades
• In some reports there has been a disproportionately
greater increase in those under the age of 5 yr and in
developing countries or those undergoing economic
transition in recent decades.
• In Africa, the reported incidence is also low, even
though diabetes overall is not rare in Africa, but
there is limited information from the region.
– A global incidence around 6.4/100.000/year has been
reported
Pathogenesis of type 1 diabetes
• Type 1 diabetes is characterized by chronic
immunomediated destruction of pancreatic β-cells,
leading to partial, or in most cases, absolute
insulin deficiency.
• Type 1 diabetes is an autoimmune disorder in
which the body attacks its pancreatic beta cells.
• That auto-pancreatic β-cell destruction, occurs at a
variable rate, and becomes clinically symptomatic
when approximately 90% of pancreatic β-cells are
destroyed.
Genetic issues
– Clear evidence suggests a genetic component in
type 1 diabetes mellitus.
– Monozygotic twins have a 60% lifetime
concordance for developing type 1 diabetes
mellitus, although only 30% do so within 10 years
after the first twin is diagnosed. In contrast,
dizygotic twins have only an 8% risk of
concordance, which is similar to the risk among
other siblings.
– The frequency of diabetes developing in children
with a diabetic mother is 2-3% and 5-6% if the
father has type 1 diabetes mellitus. The risk to
children rises to almost 30% if both parents are
diabetic.
 Type I – IDDM
• Human leukocyte antigen (HLA) genotype confers
approximately 50% of risk

• In the Caucasian population, specific

combinations of HLA DR and DQ alleles
determine genetic susceptibility
• Environmental factors

– Viral infections (most important) probably by

initiating or modifying an autoimmune process.(
Mumps, coxsackie virus, CMV, congenital rubella)
– Dietary factors are also relevant
• Breastfed infants have a lower risk for Type 1 DM.
• Some cow's milk proteins (e.g., bovine serum albumin)
have antigenic similarities to an islet cell antigen.
Progression to Type 1 DM
Autoimmune markers
(ICA, IAA, GAD

Autoimmune destruction

Honeymoon

100% Islet loss

“Diabetes threshold”
 Honeymoon Period
• In patients with new onset of DM1 who do not have
DKA, the beta cell mass has not been completely
destroyed.
• The remaining functional beta cells seem to recover
with insulin treatment, and they are again able to
produce insulin.
• When this occurs, insulin requirements decrease, and
there is a period of stable blood glucose control, often
with nearly normal glucose concentrations.
• This phase of the disease, known as the honeymoon
period, usually starts in the first weeks of therapy and
usually continues for a few months at most, but can last
2 years
 II. DM type 2
• Refers to diseases that range from predominantly
insulin resistance with relative insulin deficiency to a
predominantly secretory defect with or without insulin
resistance.
• Type 2 diabetes is also a complex metabolic disorder of
heterogeneous aetiology with social, behavioural, and
environmental risk factors unmasking the effects of genetic
susceptibility.
• There is a strong hereditary (likely multigenic)
component to the disease, with the role of genetic
determinants illustrated by differences in the prevalence of
type 2 diabetes in various racial groups are considered.
 II. DM type 2
• The incidence of type 2 DM is increasing as more children
and adolescents in most societies become over weight or
obese and inactive.

• Most people with type 2 diabetes are obese.

• It is more common in certain racial and ethnic groups such

as African-Americans, American Indians,

• In Japanese school children, type 2 diabetes is now more

common than type 1
 Type 2 DM
• The first stage in the development of type 2 diabetes
is often insulin resistance, requiring increasing
amounts of insulin to be produced by the pancreas to
control blood glucose levels.
• Initially, the pancreas responds by producing more
insulin, but after several years, insulin production
decreases and diabetes develops.
• Type 2 diabetes usually develops slowly and
insidiously in children.
• Many people who have type 2 diabetes may pass
many years before being diagnosed.
 Natural History of Type 2 Diabetes
Genetic Complications
Onset of
susceptibility
diabetes Disability
Environmental
factors

P
Obesity Insulin resistance R Ongoing hyperglycemia Death
E
Risk for Metabolic
Disease Atherosclerosis Retinopathy Blindness
Syndrome
Hyperglycemia Nephropathy Renal failure
Neuropathy CHD
Hypertension
Amputation
 III. Other specific types of DM

A. Genetic defects of β-cell function:

– Monogenic DM( former MODDY)
– Transitional Neonatal DM(TNDM)
– Permanent Neonatal DM(PNDM)
– Others
B. Genetic defects in insulin action:
C. Diseases of the exocrine pancreas:
– Chronic pancreatitis, trauma, neoplasia etc.
 III. Other specific types of DM

D. Endocrine diseases
– Acromegaly, Cushing syndrome, etc.
E. Drug- or chemical-induced
– Pentamidine, glucorticoides, thyroide hormones
etc.
F. Infections:
– Congenital rubeola, CMV, enterovirus, etc.
G. Uncommon forms of immune-mediated
diabetes
 III. Other specific types of DM
D. Endocrine diseases
– Acromegaly, Cushing syndrome, etc.
E. Drug- or chemical-induced
– Pentamidine, glucorticoides, etc.
F. Infections:
– Congenital rubeola, CMV, enterovirus, etc.
G. Uncommon forms of immune-mediated
diabetes
– Anti-insulin receptor antibodies, etc.
H. Genetics syndromes:
– Down, Turner etc.
 Monogenic diabetes
• It is a familial form of mild, non-ketotic
diabetes presenting during adolescence or
early adulthood originally named “maturity-
onset diabetes of the young”(MODY).
• It is a group of disorders which result from
dominantly acting heterozygous mutations
in genes important for the development or
function of β cells
 Monogenic diabetes
• Within the diagnostic groups of monogenic diabetes,
there is great variation in the degree of hyperglycemia,
need for insulin, and risk for future complications.
• Making a specific molecular diagnosis:
– helps predict the expected clinical course of the disease,
– guide the most appropriate management for an individual,
– and has important implications for family members,
• enabling genetic counseling,
• and extended genetic testing in other diabetic family members,
whose diabetes may eventually be reclassified
 Neonatal diabetes
• It’s a monogenic form of diabetes which usually
starts in the first 6 months of life even though cases
may present as late 9–12 months of age.
• Thus the term “monogenic diabetes of infancy »
would be appropriate as many cases are diagnosed
beyond the neonatal period
• There is good evidence that it is not Type I DM as
neither auto-antibodies nor an excess of high Type I
HLA susceptibility are found in these patients.
 Neonatal diabetes

Clinically two subgroups were recognized:

– Transient neonatal diabetes mellitus (TNDM) &

– Permanent neonatal diabetes mellitus (PNDM)
 Transient neonatal diabetes
• Anomalies on 6q24 locus

• DM associated may start within the first week and

resolves around 12 weeks;

• However 50% of cases DM will reoccur during the

paediatric age range

• Initial glucose values can be very high (range12-57

mmol/L) and so insulin is used initially although the
dose can rapidly be reduced.
 Permanent neonatal diabetes
• Mutations concern Kir6.2

• Only 10% have a remitting form of DM that may

latter relapse
• Most patients have isolated DM

• However 20% have developmental delay of motor

and social function & generalized epilepsy

• Patients have all the clinical features of insulin

dependency
Clinical characteristics of type 1, type2 and monogenic DM
Obesity

Acanthosis
Nigricans
 Diagnostic criteria for DM

• Diagnostic criteria for diabetes are based on

blood glucose measurements and the presence
or absence of symptoms.
 Criteria for the Diagnosis of Diabetes

1. Classic symptoms of diabetes, with plasma glucose concentration

≥11.1 mmol/L (200 mg/dL)

OR
2. Fasting plasma glucose (FPG)

Fasting is defined as ≥126 mg/dL (7.0 mmol/L)no caloric intake for at

least 8 h
OR
3. Oral Glucose tolerance test(OGTT) :
2h post load plasma glucose ≥200 mg/dL (11.1 mmol/L) during an
OGTT
OR
American Diabetes Association Standards of Medical Care in Diabetes.
Classification and diagnosis of diabetes. Diabetes Care 2017; 40 (Suppl. 1): S11-S24
4. A1C ≥6.5%
 Diagnosis
• For most children, only urine testing for glucose and blood glucose
measurement are required for a diagnosis of diabetes.
• Other conditions associated with diabetes require several tests at
diagnosis and at later review
• Islet cell antibodies
• Thyroid function tests and antithyroid antibodies
• Antigliadin antibodies
• Lipid profiles
• Renal function tests and urin albumin
 Clinical manifestations

• Diabetes in young people usually presents with

characteristic symptoms such as polyuria,
polydipsia, nocturia, enuresis, weight loss – which
may be accompanied by polyphagia, and blurred
vision.
• Impairment of growth and susceptibility to certain
infections may also accompany chronic
hyperglycemia.
• Glycated Hemoglobin
– Glycosylated hemoglobin derivatives (HbA1a,
HbA1b, HbA1c) are the result of a
nonenzymatic reaction between glucose and
hemoglobin.
– A strong correlation exists between average
blood glucose concentrations over an 8- to 10-
week period and the proportion of glycated
hemoglobin.
– The percentage of HbA1c is more commonly
 Clinical manifestations
• In its most severe form, ketoacidosis or less
commonly non-ketotic hyperosmolar
syndrome may develop and lead to stupor,
coma and in the absence of effective
treatment, death.
• If symptoms are present, urinary ‘dipstick’
testing for glycosuria and ketonuria, or
measurement of glucose and ketones using
a bedside glucometer, provides a simple and
 Clinical manifestations
• If the blood glucose level is elevated, then
prompt referral to a center with experience
in managing children with diabetes is
essential.
• Waiting another day specifically to confirm
the hyperglycemia is unnecessary and if
ketones are present in blood or urine,
treatment is urgent, because ketoacidosis
can evolve rapidly.
 Complications
• Common complications:
– Hypoglycemia
– Diabetic keto-acidosis
• Long term complications
– Target organs/systems
 LONG TERM COMPLICATIONS
Amputations Heart disease Blindness
Loss of Sensations and strokes

Death
Kidney failure
Uncontrolled diabetes
can lead to…
DB Management
 What are the Goals?
• To give your child a loving, supportive
environment where each day is taken at a
time (not each blood sugar)
• Where your child can grow and thrive, learn
and explore
• Where blood sugars are corrected, not
interrogated
• Where the family is in balance – like a
mobile
• And where the long haul is what is
Diabetes Management Principles
• An effective insulin regimen
• Monitoring of glucose
• As flexible with food and activity as
possible
• Must remember
– Young children need routine and rules
– Young children need to develop autonomy
– Young children need to explore and experience
– Young children need to begin to make
 Treatment components
• Education
• Insulin therapy
• Diet and meal planning
• Exercise
• Monitoring
– HbA1c every 2-months
– Home regular BG monitoring
– Home urine ketones tests when indicated
 Criteria of DM compensation
• The aim of treatment –”QULITY OF
LIFE”
• The adequate growth & development of
child
• Active social position in life & society
• Decreasing acute complication and
prolong late complications of DM
• Normal life duration
 Criteria of DM compensation (c’d)
• Glucose level fasting 4-8 mmol/L
• Glucose after feeding 10-11mmol/L (3.3-8.3 mmol/L –
less than renal threshold)
• Night Glucose level 6-8 mmol/L
• Episodes of Hypoglycemia are absent
• Glucose absent in urine
• Glycated hemoglobine (HbA1c): less 7 %
– Measurement of HbA1c () levels is the best method
for medium-term to long-term diabetic control
monitoring.
 Criteria of DM compensation (c’d)
• Normal lipid, protein and mineral
metabolism
• Cholesterol mmol/L -< 5.2
• Triglicerids mmol/L - < 1.7
 EDUCATION
• Educate child & care givers about:
• Diabetes
• Insulin
• Life-saving skills
• Recognition of Hypo & DKA
• Meal plan
• Sick-day management
 Principles of insulin therapy
• Insulin therapy varies between individuals and
changes over time
• The correct dose of insulin is the dose that
achieves the best glycemic control without causing
obvious hypoglycemia problems and achieving
normal growth(height and weight)
• Dosage depends on,
• Age, weight, stage of puberty, duration and phase of
diabetes, state of injection sites, nutritional intake and
distribution, exercise pattern, daily routine
Hyperglycemia:
Microangiopathic
complications

Hypoglycemia:
Neuronal loss
Poor school
performance
seizures
 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
 Insulins analogues
• Ultra short acting
• Insulin Lispro
• Insulin Aspart
• Long acting without peak action to
simulate normal basal insulin
• Glargine
 Insulin management
• Most require 2 or more injections of insulin
daily, with doses adjusted on the basis of self-
monitoring of blood glucose levels.
• Insulin replacement is accomplished by giving a
basal insulin and a preprandial (premeal)
insulin.
• The basal insulin is either long-acting (glargine
or detemir) or intermediate-acting (NPH).
• The preprandial insulin is either short-acting
(regular) or ultra-rapid-acting (lispro, aspart,
glulisine)
 Frequently used regimes
Twice daily regimes
– 2 daily injections of a mixture of a short or rapid
insulin with an intermediate acting insulin (before
meal and before main evening meal).
– Approximately 1/3 of the total insulin dose is short
acting and 2/3 is intermediate.
– 2/3 of the total daily insulin is given in the
morning and 1/3 in the evening.

Three injections daily

Before breakfast – mixture of rapid or short with
intermediate
Before afternoon snack or evening meal – rapid or
short
Before bed – intermediate acting
 Insulin Dosage
• Prepubertal children usually require
• 0.7-1.0 IU/kg/day
• During puberty, requirements may rise above 1
and even up to 2 IU/kg/day
 Insulines 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.
 Adverses effects of insuline
• Hypoglycemia
• Lipoatrophy
• Lipohypertrophy
• Obesity
• Insulin allergy
• Insulin antibodies
• Insulin induced edema
 Practical issues
• 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
 Treatment made easier
• Insulin pens & new delivery products
• Handy insulin pumps
• fine micro needles
• Simple accurate glucometers
• Free educational material
• Computer programs for comprehensive
management & monitoring
• Diet
– On the standard twice daily regime, food intake is
divided into 3 main meals with snacks between
meals and before going to bed.
– Diet should be high in fibre which will provide a
sustained release of carbs.
 Type of Food
• The following are among the most recent
consensus recommendations:
• Should provide 50-55% of daily energy intake.
– No more than 10% of carbohydrates should be from
sucrose or other refined carbohydrates.

• Should provide 30-35% of daily energy intake.

• Should provide 10-15% of daily energy intake.
 Activity

• Diabetes mellitus requires no restrictions on

activity; exercise has real benefits for a child
with diabetes.
• Most children can adjust their insulin dosage
and diet to cope with all forms of exercise.
• The current guidelines are increasingly
sophisticated and allow children to compete at
the highest levels in sport.
 Monitoring strategies.

• Self Blood Glucose Monitoring – 2 to 4 / day

• Urine Testing – Ketones
• Glycosylated Hemoglobin - HbA1 C - quarterly
• Blood lipids - annually
• Thyroid function – annually
• Urine micro albumin – quarterly after 5 yr
• Dilated fundoscopy – age 10 yr + 3-5 yr
Clinical characteristics of type 1, type2 and monogenic DM
 Therapy of T2 DM in Children
• Reduce calories – weight loss
– NOT T1 DM diet with high complex CHO
• No Between meal snacks
– NOT T1 DM where hypoglycemia is frequent
• Reduce CHO intake
• Reduce fat intake
• Exercise – increase healthy
life style

• Drug treatment early x

 Therapy of T2 DM in Children
• Unless there are contraindications, all
children with T2DM should be started on
metformin.
– Metformin works by decreasing hepatic glucose
production and stimulating glucose uptake into
peripheral tissues
• When used appropriately, metformin lowers
A1c 1 to 2% and aids in weight loss.
Gastrointestinal adverse events may limit
achieving the target dose in some patients.
 Therapy of T2 DM in Children
• Other drugs
• Thiazolidinediones
– work to decrease blood glucose by increasing insulin
sensitivity in liver, muscle, and adipose tissue and to
decrease hepatic glucose synthesis output.
– Typically, long-term use of TZDs in adults will decrease A1c
an average of 1%.
– TZDs have been associated with a potential increased risk of
bladder cancer and fracture rates
• Sulfonylureas
– Work by stimulating pancreatic β-cells to secrete insulin.
– The use of sulfonylureas in adults provides lowering of A1c
approximately 1.25%.
• Others: Meglitinides, Alpha-Glucosidase Inhibitors, etc.
 Diagnosis
BG 250 mg/dL or 12 mmol/L Asymptomatic

Start with insulin

and diet, exercise
Diet and exercise

<7%

Monthly review, A1C q3mo <7%

Add metformin
Attempt to >7%
wean insulin
Add metformin
>7%

Add insulin, TZD, sulfonylurea

>7%

Add 3rd agent

TZD = thiazolidinedione
Silverstein JH, Rosenbloom AL.
J Pediatr Endcrinol Metab. 2000;13 Suppl 6:1406-1409.
DIABETIC KETO ACIDOSIS
 Diabetic ketoacidosis
• Ketoacidosis is a state of uncontrolled catabolism associated
with insulin deficiency
• Diabetic ketoacidosis tends to occur in individuals younger
than 19 years, but it may occur in patients with diabetes at any
age.
• Criteria
– Hyperglycemia: blood glucose
>11mmol/L(200mg/dL)
– Venous pH<7.3 or bicarbonate <15 mmol/L
– Ketonemia and ketonuria
 Diabetic ketoacidosis
• In the absence of insulin, hepatic glucose production
accelerates, and peripheral uptake by tissues such as muscle
is reduced.
• Rising glucose levels lead to an osmotic diuresis, loss of
fluid and electrolytes, and dehydration.
• Plasma osmolality rises and renal perfusion falls.
• In parallel, rapid lipolysis occurs, leading to elevated
circulating free fatty-acid levels.
• The free fatty acids are broken down to fatty acyl-CoA
within the liver cells, and this in turn is converted to
 Diabetic ketoacidosis

• Accumulation of ketone bodies produces a metabolic

acidosis. Vomiting leads to further loss of fluid and
electrolytes.
• The excess ketones are excreted in the urine but also appear
in the breath, producing a distinctive smell similar to that of
acetone.
• Respiratory compensation for the acidosis leads to
hyperventilation, graphically described as 'air hunger'.
• Progressive dehydration impairs renal excretion of
hydrogen ions and ketones, aggravating the acidosis
 Diabetic ketoacidosis
• Mostly the causes are
– Previous undiagnosed diabetes
– Interruption of insulin therapy
– The stress of intercurrent illness
• The management is depending on the level of
clinical and biological severity
•Mild (venous pH <7.3, bicarbonate <15 mmol/L)
•Moderate (venous pH <7.2, bicarbonate <10 mmol/L)
•Severe (venous pH <7.1, bicarbonate <5 mmol/L)
 DKA Clinical symptoms
Classic General symptoms Symptoms of
symptoms of associated
hyperglycemia infections
•Thirst • Generalized • Fever
• Polyuria weakness • Dysuria
• Polydipsia • Malaise/lethargy • Chills
• Nocturia • Nausea/vomiting • Chest pain
• Decreased • Abdominal pain
perspiration • Shortness of
• Fatigue breath
• Anorexia or
increased
appetite
 DKA clinical examination findings
Vital signs General signs Specific signs

• Tachycardia • Ill appearance • Ketotic breath

• Hypotension • Dry skin (fruity, with
• Tachypnea • Labored acetone smell)
• Hypothermia respirations • Confusion
• Fever, if • Dry mucous • Coma
infection membranes • Abdominal
• Decreased skin tenderness
turgor
• Decreased
reflexes
 Management
• Goals of therapy
– Correct dehydration
– Correct acidosis and reverse ketosis
– Restore blood glucose to near normal
– Avoid complications of therapy
– Identify and treat precipitating event
Confimed DKA
Confirmed DPA
HYPOGLYCEMIA
 DM and hypoglycemia
• Hypoglycaemia is one of the most common acute
complications of the treatment of type 1 diabetes,and
frightening for parents.
• E ffective treatment (and preferably prevention) are key
issues.
• Hypoglycaemia means ‘low blood glucose levels’.
• B lood glucose values <2.5 mmol/l (<45mg/dl) are too low
for normal neurological (brain) function.
• E ven people without diabetes may develop symptoms of
hypoglycaemia when the blood glucose level is <3.6 mmol/l
(about 65 mg/dl).
• People with diabetes should aim to keep blood glucose
levels >3.9 mmol/l (about 70 mg/dl).
 DM and hypoglycemia
• Symptoms
– The clinical symptoms of hypoglycaemia initially occur
as a result of adrenalin (autonomic activation) and
include:
– Trembling
– Rapid heart rate
– Pounding heart (palpitations)
– Sweating
– Pallor
– Hunger and/or nausea.
 Symptoms of neuroglycopenia
•Difficulty in concentrating •Dizziness and unsteady gait
•Irritability •Tiredness
•Blurred or double vision •Nightmares
•Disturbed colour vision •Inconsolable crying
•Difficulty hearing •Loss of consciousness
•S lurred speech •Seizures.
•Poor judgement and
confusion

In severe circumstances, especially if it is prolonged,

hypoglycaemia can cause death.
Grading the seriousness of hypoglycaemia

Mild Moderate Severe

The child The child or parent The patient either

recognises is aware of, responds loses
hypoglycaemia to, and treats the consciousness
and is able to self-hypoglycaemia, but or has a
treat without the needs someone convulsion (fit)
assistance of others.
else to assist. associated with
Blood glucose values low blood
Blood glucose are again around glucose.
values are around ≤ ≤3.9 mmol/l (<70
3.9 mmol/l mg/dl) but the person
(<70 mg/dl). is not able to
help himself or
 Treatment of hypoglycaemia
• The aim of treatment is to get glucose
values back to normal and to prevent
progression to loss of consciousness or
convulsions.
• This is achieved by feeding the child.
– The initial intake of food has to be a rapid-
acting carbohydrate food, which includes
sweetened drinks like glucose water, canned or
bottled drinks, fruit juices and also glucose-
containing sweets.
 Treatment of hypoglycaemia
• It is recommended that the child consumes 0.3-0.5 g/ kg or
9-15 grams of such rapid-acting carbohydrates for a child
weighing 30 kg.
• The lower the glucose value, the more glucose is needed.
• In practice:
– Parents should be advised to continue supplying rapid-acting
carbohydrate until the symptoms have resolved.
– If blood glucose testing is available, test after 10-15 minutes. If
glucose values are still low, continue giving rapid-acting
carbohydrates.
 Treatment of hypoglycaemia

• If the child is having severe symptoms (is not able to

eat), is unconscious, nauseated or having a
convulsion, give either:
– intravenous glucose (eg 10% glucose drip or 1ml/kg of
25% dextrose)
OR

– I V, IM or subcutaneous glucagon (0.25 mg for small

children; 0.5 mg for children up to 40-50 kg and 1 mg for
older ).
• After an injection of glucagon,the blood glucose would be
expected to rise within 10-15 minutes.
 Preventing hypoglycaemia
• Remind the child and parents often about
the symptoms of hypoglycaemia.
• Remind them about what might cause
hypoglycaemia:
– Missing a meal or eating less than usual
– Delaying a meal after giving the insulin injection
– A ctivity of longer duration or intensity, eg school
vacations, parties, training for games etc
– A t night – the risk of hypo is higher after an active day
– When taking alcohol – which also blocks liver
gluconeogenesis
– When appetite is poor because of illness – eg with
vomiting or flu.
 Preventing hypoglycaemia
• Repeated episodes of hypoglycaemia should
result in a review of the management of the
child, including insulin doses and eating
plan, with specific advice to parents about
adapting these in advance, to prevent
recurrences.
 Other causes of hyoglycemia
• Hypoglycemia is one of the most common
metabolic disorder in children
• The causes for hypoglycemia are many and
diverse.
• Hyperinsulinemia, hypopituitarism, and inborn errors of
metabolism are frequent causes of hypoglycemia in infancy.
• In toddlers, ketotic hypoglycemia is most common. In
adolescents, insulin-producing pancreatic tumors are the most
common cause of true hypoglycemia.
 Other causes of hypoglycemia

Low glycogen stores

Very frequent in ewbons : small for gestational age,prematurity
Fasting : Ketotic hypoglycemia
Is the most common cause of hypoglycemia in children from 1 year to 5 years of age
Malnutrition : Severe acute malnutrition : may lead to death!!!!!!
Diarrhea+++
Hormone abnormalities
 Growth hormone deficiency
 Cortisol deficiency
 Other causes of hyoglycemia
Inborn errors of metabolism
 Carbohydrates
oGlycogen storage diseases
oGalactosemia
oHereditary fructose intolerance
 Amino acid
oTyrosinemia
 Fatty acid
oCarnitine deficiency
oFatty acid transport deficiency
 Other causes of hyoglycemia
Increased use of insulin
• Hyperinsulinism
•Beta cell hyperplasia
•Insulin dysregulation
 Infant of diabetic mother
 Beckwith-Weidemann Syndrome
Stressors associated with hypoglycemia
 Specific infections
o Malaria++++
o Sepsis++++
 Other causes of hyoglycemia
 Miscellaneous
•Congenital heart disease Shock
•Burns
•Tumors
•Reye Syndrome
• Surgery
•Hepatitis
•Alpha-1-antitrypsin deficiency
•Pharmacologic causes of hypoglycemia
• Of course insulin therapy & oral hypoglycemics
•But also others such as Methanol, Salicylates, Beta blockers
Pentamidine etc.