Alexandria University

Faculty of medicine
Pediatrics Department

Type 1 diabetes
in children
 ETIOLOGY

Marwa Naguib Awad

Allah
1110
 Definition

common, chronic, metabolic syndrome

characterized by hyperglycemia as a cardinal
biochemical feature. caused by deficiency of
insulin secretion due to pancreatic β-cell damage

Polydipsia hyperglycemia Polyuria

 PREVALENCE
In 2006, the number of children globally aged 0–14 yr with type 1 diabetes was
estimated by the International Diabetes Federation to be 440 000, with an annual
increase of 3% per annum and 70 000 newly diagnosed cases a year.
 ETIOLOGY

Autoimmune

Genetic Environmental
Factors Triggers
Autoimmune

Islet cell antibodies (60-90%)

Islet cell antibodies (60-90%)
Glutamic acid decarboxylase antibodies (65-80%)
Glutamic acid decarboxylase antibodies (65-80%)

Insulin auto antibodies (30-40%)

Insulin auto antibodies (30-40%)

Type 1 diabetes is also associated with other autoimmune

disorders such as:-

Hashimoto’s and Graves’ disease (3–5%)

Celiac disease (2–5%)
Addison’s disease (>1%).
 Autoimmune

Numerous susceptibility loci(genes that predispose to type 1

diabetes)have been found.
Several of these loci are located in the major histocompatibility
complex (MHC) region on the short arm of chromosome 6 which
contains genes that regulate the immune response.
For example, the presence of DR3 and DR4 are associated with a
high risk of developing diabetes.
If a individual inherits the
HLA-DR3 type from one
parent and the HLA-DR4
type from the other
parent, they have a high
chance of developing type
1 diabetes

many people with this HLA

make-up (HLA-DR3/DR4)
never develop type 1
diabetes, even within the
same family

To add to the complexity,

it appears that a person
with the genetic make-up
HLA-DR2, DR5 has almost
no chance of developing
type 1 diabetes.

DR2 and DR5 are referred

to as 'diabetes resistance'
genes.
Environmental Triggers

infective
NutritionalToxic
 Bacterial infections act non-specifically to reduce glucose
tolerance, and thus to exacerbate a developing diabetes.
infective
Some viruses alternatively, they may act specifically on the β cells
of islets at various stages of a destructive process

Mumps Rubella
Mumps Rubella

Enteroviruses
Enteroviruses
(coxsackie
(coxsackie
&
&
Echovirus)
Echovirus)
 Nutritional

Whether this is a direct effect of breast milk or

is Whether
related tothis
theisdelayed
a directintroduction
effect of breast milk or
of cow’s
is related
milk to the delayed introduction of cow’s
is unclear
milk is unclear

Breast feeding Cow Milk

provide protection against the risk of IgG antibodies to bovine serum albumin
developing type 1 diabetes. molecular mimicry.
Toxic nitroso-
compound

They are rather unlikely to be important

triggers for initiating diabetes among children

They should not be entirely discounted

. Epidemiological studies have however

suggested that the onset of T1DM in children
may be related to an excess of nitrates in food
or drinking water.
PATHOPHYSIOLOGY

Marwa Marzouq zaki

1108
Pathophysiology of T1DM

95% of HLA-DQs
patients with →specific
T1DM have markers of
(HLA)-DR3 or T1DM
HLA-DR4. susceptibility.

High prevalence Graves disease,

in patients with Hashimoto
other thyroiditis
autoimmune Addison
.diseases .disease
Pathophysiology of T1DM

toxic
Viruses
chemicals

cytotoxins cow's milk

 Pathophysiology of T1DM
Damage Triggers Develop an
the autoimmun
to e response
pancreati immune
against
c β cells system in altered
a pancreatic β
from an
geneticall cell Ags or
infectiou y molecules
s or susceptibl in β cells
environ that
e resemble a
mental individual viral
agent. . protein.
Pathophysiology of T1DM
 T1DM

Pancreatic β
cells fail to
Circulating Plasma
Catabolic respond to all
insulin is very glucagon is
disorder insulin-
low or absent elevated secretory
stimuli
Clinical Picture of T1DM
 thisthis

condition
catabolic
Pathophysiology of T1DM
Prevent
condition
catabolic
Reverse

Prevent
ketosis
Reverse

ketosis

Patients need
exogenous insulin
to

Normalize
metabolism
andand
Normalize
a

metabolism
a
hyperglucagonemi

protein
hyperglucagonemi

protein
Decrease

lipid
Decrease

lipid
 Pathophysiology of T1DM
* In relatives & children from the general population with
positive ICA, a decline in the FPIR is a strong predictive
marker of impending diabetes.
* In evolving T1DM → rise in the fasting glucose level.
* Inability to keep Blood glucose level below 200mgs/dl.
* Uncontrolled lipolysis & ↓ levels of hepatic glucokinase and
GLUT 4 in adipocytes.
* Raised levels of FFAs.
* Transient insulin resistance.
* Force the onset of symptomatic DM.
 Partial recovery “Honeymo
in endogenous on" period
insulin
secretion
ultimately fails.
Initial excessive
secretion of
glucagon
relative to
insulin after
protein meals.

Infusion of somatostatin

Adjunctive therapy to insulin

Exacerbate effects of insulin deficiency and

promote lipolysis & ketoacidemia
MEDICAL NUTRITIONAL
THERAPY

Marwa Yusuf
1111
*Amount of calories needed /day:
1000 kcal/day for 1 year child and additional 100
kcal/day for each year of life.
*Goals of nutritional therapy:
1- Attain and maintain normal blood glucose and lipid
levels.
2- Attain and maintain ideal body weight and achieve
normal growth and development in children.

3- Prevent and treat diabetic complications e.g.

hypoglycemia, renal disease, cardiovascular diseases,
hypertension and neuropathy.
1-Carbohydrates (5o%-55%):
A) Simple carbohydrate (10%):
▪ has high glycemic index.
▪ e.g.: sugar (sucrose), honey, jam, chocolate……etc
B) Complex carbohydrate (40%):
▪ has low glycemic index
▪ e.g.: starch, bread, rice, vegetables, fruits……etc

2-Proteins (15%-20%):
▪ providing energy + play an important role in repair of body
tissues and growth.
▪ e.g.: fish, sea food, chicken, eggs, skimmed or low fat milk……etc
3-Fat (30%):

A) Saturated fat (10%):

▪ called bad fat.
▪ e.g.: butter, cheese, fat in meat………..etc.
B) Unsaturated fat (20%):
▪called good fat, help to lower blood cholesterol.
▪ e.g.* monounsaturated: olive oil, peanut oil…etc.
* polyunsaturated: corn oil, sunflower…etc.
• Diabetic food pyramid:
• Meal planning:
1- Provide well balanced diet with the main 3 meals 4-6 hours
apart with 3 small snacks in between.
2- Avoid hunger and over eating and no skipping meals (must
eat more than 3 meals a day).
3- In insulin treated diabetics, matching insulin to carbohydrate
content of a meal is recommended.
4- High fibers intake (cereals, fruits, vegetables) that decrease
rate of CHO digestion and absorption and so decrease the
need for insulin.
5-sweeteners can be used e.g.: saccharin, aspartame, sorbitol
and fructose.
6- Cheat days allowed in holidays.
MEDICAL THERAPY
INSULIN

Marwa Mustafa
1109
 Introduction
*All children with type 1 diabetes mellitus
(T1DM) require insulin therapy
*Source of insulin: extracts from pigs & cattle 
Human insulin by rDNA
* Mode of adminstration: SC
 Types of Insulin
Insulin has 4 basic formulations:
A) Ultra short-acting (eg, lispro, aspart, glulisine)
B) Traditional short-acting (eg, regular, soluble)
C) Medium-acting or intermediate-acting (eg, NPH,
isophane, lente, detemir)
D) Long-acting (eg, ultralente, glargine)
>> Mixture (Intermediate<NPH> :Ultrashort<Lispro> 70%:30%)
 A) Ultra short-acting
*Insulin lispro (Humalog)
with the reversal of the amino acids lysine and proline in the B
chain.
*Insulin aspart (NovoLog)
with the exception of single substitution of amino acid proline by
aspartic acid in position B28.
*Insulin glulisine (Apidra)
by replacement of asparagine at B3 position with lysine, and the
lysine at the B29 position is replaced by glutamic acid.
 Onset of action, peak activity & duration of
action:
*Both Aspart & Lispro have similar values:
Onset of action10-30 mins, peak activity 1-2 h
duration of action of Aspart is 2-4 h
duration of action of Lispro is 3-6 h
*As for glulisin:
Onset of action is 15mins, peak effect is in 1-1.5 h, and usual duration of
action is 1-2.5 h.
** Ultra short acting insulin due to rapid onset of action and short
duration they are more suitable for bolusing at mealtimes and for short-
term correction of hyperglycemia. They are also more suitable for use with
insulin pumps.
 Dose
0.5-1 U/kg/d SC initially
Adjust doses to achieve premeal and bedtime
blood glucose levels as follows:
<5 years: 100-200 mg/dL (5.5-10 mmol/L)
>5 years: 80-140 mg/dL (4-7.5 mmol/L)
 Interactions
*Medications that may decrease hypoglycemic effects of insulin
include
acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine, isoniazid,
diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid hormone,
estrogens, ethacrynic acid, calcitonin, PO contraceptives, diazoxide,
dobutamine, phenothiazines, cyclophosphamide, dextrothyroxine, lithium
carbonate, epinephrine, morphine sulfate, and niacin

*Medications that may increase hypoglycemic effects of

insulin include
calcium, ACE inhibitors, alcohol, tetracyclines, beta blockers, lithium
carbonate, anabolic steroids, pyridoxine, salicylates, MAO inhibitors,
mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate,
fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone
 Precautions
>Hyperthyroidism may increase renal clearance of
insulin and may need more insulin to treat
hyperkalemia; hypothyroidism may delay insulin
turnover, requiring less insulin to treat hyperkalemia
>Due to prompt onset of action, administer within 15
min before or immediately after a meal; monitor
glucose carefully
>Dose adjustments may be necessary in renal and
hepatic dysfunction
 B) Traditional short-acting
Regular insulin (Humulin R, Novolin R)
preparation of zinc insulin crystals in solution
Onset of action is 0.25-1 h, peak activity is 1.5-4 h,
and duration of action is 5-9 h.
It is bound to either protamine (eg, isophane)
OR zinc (eg, lente, ultralente) in order to prolong the
duration of action.
C) Medium-acting or intermediate-acting
*Isophane insulin suspension (Novolin N):
Onset of action is 1-1.5 h, peak effect is in 4-12 h, and usual
duration of action is 24 h.
*Insulin zinc suspension (Lente):
Onset of action is 1-2.5 h, peak effect is in 8-12 h, and duration
of action is 18-24 h.
*Insulin NPH (Humulin N, Novolin N):
Neutral Protamine Hagedorn (NPH) insulin, which contains a
mixture of regular and protamine zinc insulin.
Onset of action is 3-4 h, peak effect is in 8-14 h, and usual
duration of action is 16-24 h.
*Insulin detemir (Levemir)
It is an insulin analogue in which a fatty acid is
bound to the lysin amino acid at position B29
it binds to albumin in the blood through the
fat acid at position B29It slowly dissociates
from this complex slow systemic absorption
Prolonged action (ranges from 5.7 to 23.2
h).
 D) Long-acting
*Extended insulin zinc suspension (Ultralente):
Onset of action is 4-8 h, peak effect is in 16-18 h, and usual
duration of action is >32 h.
Dose:
<6 years: Not established
>6 years: 10 U SC qd; adjust according to patient response
*Insulin glargine (Lantus):
A new long-acting insulin that has no peak and produces a
relatively stable level lasting more than 24 hours.
Glargine has a relatively flat profile of action, lasting some 18-
26 hours.
Dose: as Ultralente
 Precautions
* Administer at the same time each day, SC only, do not mix with any other
insulin or solution
* Use only if solution is clear and colorless
*Hyperthyroidism may increase renal clearance of insulin and may need more
insulin to treat hyperkalemia; hypothyroidism may delay insulin turnover,
requiring less insulin
* Dose adjustments of insulin may be necessary in patients diagnosed with
renal and hepatic dysfunction
* July 1, 2009 - The US Food and Drug Administration (FDA) has issued an
early communication regarding the association, based on 4 observational
studies, between insulin glargine and an increased cancer risk; further
evaluation is required before this association can be confirmed.
 Common insulin regimens
(1)Twice-daily Insulin Regimen (Split-Mixed and
Pre-Mixed Regimens):
Premixed insulins can be used or a mixture of a
short-acting insulin (e.g., regular, insulin lispro or
insulin aspart) and an intermediate-acting insulin
(e.g., NPH)
*2/3of the insulin dose is given in the morning before
breakfast and one-third is given before dinner
*For patients who experience nocturnal
hypoglycemia when NPH is administered at
dinner with a short-acting insulin, moving the
NPH dose to bedtime helps reduce the risk for
nocturnal hypoglycemia
Conversely, NPH at dinner can result in fasting hyperglycemia
due to dissipation of insulin activity and the dawn
phenomenon. Moving the NPH dose to bedtime can help
resolve this problem (limitation to using premixed insulin)
(2) Multiple Daily Insulin Injection Regimen:
Basal plus Prandial Insulin
Many different types of regimens are possible
with multiple daily injections
>Regular, insulin lispro or insulin aspart are used
to provide prandial insulin.
>NPH, lente, ultralente or insulin glargine is used
to provide basal insulin.
*Regular, insulin lispro/aspart before meals and NPH, lente,
ultralente, or insulin glargine at bedtime
*Insulin lispro/aspart before meals and NPH, lente, or
ultralente twice daily (breakfast and bedtime)
(3)Insulin Pumps
Continuous subcutaneous insulin infusion (CSII), rapid-acting
insulin infused continuously 24 hours a day through an insulin
pump at one or more basal rates, with additional boluses
given before each meal, and correction doses administered if
blood glucose levels exceed target levels.
COMPLICATIONS

Marwa Shabaan
1112
 COMPLICATIONS

Acute Chronic

(1)Hypoglycemia (1)Macrovascular

(2)Microvascular
(2) Local allergic reactions
(3)miscellaneous
(3) Diabetic ketoacidosis

(4)-Psychosocial Problems
 Acute complications

(1)Hypoglycemia:

(blood glucose level below approximately 60 mg/dL)

Causes:
-change in insulin dose

-a small or missed meal

-strenuous exercise

In emergency, initial treatment is

a bolus injection of 25 mL of 50% glucose solution
followed by a continuous glucose infusion.
 (2) Local allergic reactions
-atthe site of insulin injections
-pain, burning, local erythema,and induration.
-less common with human insulin than with animal insulins.
-These reactions usually resolve spontaneously without any
intervention.
-Generalized insulin allergy is rare.
It may be treated with antihistamines. Some cases may require
epinephrine and IV steroids.
(3) Diabetic ketoacidosis:
-It is much more common among persons with (IDDM)
than (NIDDM).
-DKA is acute metabolic changes in the body

-It is characterized by hyperglycemia, ketosis, and

acidosis, leading to osmotic diuresis and dehydration.
4-Psychosocial Problems:
pain, hospitalization, changes in
These problems include
lifestyle, physical disabilities, and threatened survival.
Diabetes itself does not cause changes in
personality or psychiatric illness. Young people with
insulin- dependent diabetes mellitus (IDDM) may have a
higher prevalence of eating disorders, such as anorexia
nervosa and bulimia.
 Chronic complications

*Macrovascular complications
(1)- Atherosclerosis :
-People with diabetes experience accelerated atherosclerosis. It
affects small arterioles with the following predominant effects:
-Cardiovascular Disease
-Coronary atherosclerosis
Foot Problems:
Persons with diabetes are at significant risk for lower
extremity amputations; such procedures are 15 times more common among persons with diabetes than among those
without diabetes.

Pathophysiology: Peripheral neuropathy, peripheral vascular disease, and infection all may contribute to amputation in patients with diabetes.

Kidneys:
Atherosclerosis of the main renal arteries and their intrarenal branches causes chronic nephron ischemia.
*Microvascular complications:
Hyaline arteriosclerosis, a characteristic pattern of wall thickening of small
arterioles and capillaries is wide- spread

1-Diabetic retinopathy: People with diabetes are 25 times more

at risk for blindness than the general population. affects the eyes in
the following different ways:

-Background retinopathy
-Proliferative retinopathy
-Maculopathy
-Cataract
-Glaucoma
2-In the brain: the condition causes lacunar
infarction and ischemic white matter degeneration.

3-peripheral neuropathy: Four types of diabetic

neuropathies develop, including
(1) peripheral distal symmetrical polyneuropathy, predominantly
sensory;
(2) autonomic neuropathy;
(3) proximal painful motor neuropathy; and
(4) cranial mononeuropathy (ie, III, IV, VI).
*Miscellaneous complication:
1-Infections: People with diabetes are susceptible to various
types of infections. The most common sites affected are the skin
and urinary tract system.

2-Necrobiosis lipoidica: Local fat atrophy or hypertrophy at

injection sites is not unusual and usually improves by switching to
human insulin and injecting it directly into the affected area.

3-Charcot joint: is a type of arthropathy observed in people with

diabetes. It is a progressive deterioration of foot joints
caused by underlying neuropathy.
 DKA

Marwa Abd El-Baki

1113
 Diabetic ketoacidosis (DKA)
• Is a complex metabolic state of
hyperglycemia , ketonuria ,
ketosis and acidosis.

• DKA results from untreated

absolute or relative deficiency of
insulin.
Pathophysiology
 Clinical features
Patient will represented by:
1. polyuria, polydipsia,
dehydration.
2. Vomiting, abdominal pain.
3. Kussmaul breathing and
acetone odor breath.
4. Altered consciousness:
drowsiness, coma
5. Evidence of precipitating
condition as infections.
 Does the child need to be on PICU ?
• Comatose or clinically unstable

• More than10% dehydrated with

shock

• Very young (age less than 2 years)

• Bicarbonate less than 10

• PH more than 900mg\dl

• Severe hyperkalaemia
Management of diabetic ketoacidosis:

A. General measures
B. Specific measures
 Investigations
• Child weight
• blood glucose
• PH
• K.B
• K level
• CBC
• urea and electrolytes
• arterial blood gases
• ECG
 1- fluid therapy
A) Type of fluid

Initially use 0.9% saline.

• Once the blood glucose has

fallen to 12 mmol/l
change the fluid to
0.45% saline / 5% dextrose.
• If the plasma Na
concentration at this time is
> 155 mmol/l,
use 0.45% saline.
B) Volume of the fluid
• Requirement = Maintenance + Deficit
• Deficit (liters) = % dehydration x body weight (kg)
• Hourly rate = (maintenance + deficit)/24

• Replace first 50% volume deficit in first 8 hours

• Replace remaining 50% deficit over next 16

hours
 example
A 20kg 6 years old boy who is 10% dehydrated
will require

Deficit = 10% x 20kg = 2000ml

plus
Maintenance = 60ml x 20kg = 1200 ml

Hourly rate = 3200ml over 24 hours =

146ml/hour.

It may be advisable to lengthen the period of rehydration

to 48 hours in very young children or those who are
hyperosmolar with high plasma sodium levels or very
high blood glucose levels.
 2. SODIUM BICARBONATE

• Indications: ABG pH < 7.0 after initial hour of

hydration

• Other contributing factors:

– Shock or Coma
– Severe Hyperkalemia
 3. POTASSIUM
• Potassium should be commenced immediately unless
anuria is suspected.
• Potassium is mainly an intracellular ion, and there is
always massive depletion of total body potassium
although initial plasma levels may be low, normal or
even high.
• Levels in the blood will fall once insulin is
commenced.
• Therefore add 20 mmol KCl to every 500 ml bag of
fluid.
 4- insulin
• Initial Insulin Dosing: IV Insulin infusion
starting at 0.1 unit/kg/hour

• Maintenance: Continue Insulin Infusion

until acidosis resolves

• When pH>7.3 and serum bicarbonate >15

• Decrease Insulin Infusion to 0.05 units/kg/hour

• Continue Insulin Infusion until SC Insulin started
 Glucose and electrolyte monitoring

• Check bedside glucose

every 1/2-2 hours until
stable

• Recheck 2-4 hours until

stable
 Initiate SC dosing

• For Known diabetic: Restart

prior program and readjust
Insulin

• New patient: Determine

Insulin requirements

• Regular 0.1 to 0.25 units per kg

every 6-8 hours
 DIABETIC
HYPOGLYCEMIA

Marian Makram
1114
 Definition:

Tight blood sugar (glucose) control increases the risk of

low blood sugar (hypoglycemia). Hypoglycemia occurs if
blood glucose levels fall below normal. It is generally
defined as a blood sugar below 70 mg/dL, although this
level may not necessarily cause symptoms in all patients.
Insufficient intake of food and excess exercise or alcohol
intake may cause hypoglycemia. Usually the condition is
manageable, but, occasionally, it can be severe or even
life threatening, particularly if the patient fails to
recognize the symptoms, especially while continuing to
take insulin or other hypoglycemic drugs.
 Main causes

• Common causes of diabetic hypoglycemia

include:
• Taking too much insulin or diabetes medication
• Not eating enough
• Postponing or skipping a meal or snack
• Increasing exercise or physical activity without
eating more or adjusting your medications
• Drinking alcohol
 Early warning signs
• Early signs and symptoms of diabetic hypoglycemia
include:
• Shakiness
• Dizziness
• Sweating
• Hunger
• Irritability or moodiness
• Anxiety or nervousness
• Headache
• Pounding heartbeat
Nighttime symptoms
• Diabetic hypoglycemia can also occur while
you sleep. Signs and symptoms include:
• Damp sheets or bed clothes due to
perspiration
• Nightmares
• Tiredness, irritability or confusion upon
waking
 Severe symptoms
• If early symptoms of diabetic hypoglycemia go untreated, signs
and symptoms of severe hypoglycemia can occur. These include:
• Clumsiness or jerky movements
• Muscle weakness
• Difficulty speaking or slurred speech
• Blurry or double vision
• Drowsiness
• Confusion
• Convulsions or seizures
• Unconsciousness
 Complication:

• If you ignore the symptoms of hypoglycemia too long, you may

lose consciousness. That's because your brain needs glucose to
function.
• Recognize the signs and symptoms of hypoglycemia early because
untreated, hypoglycemia can lead to:
• Seizure
• Loss of consciousness
• Death
• On the other hand, if you have diabetes, be careful not to over
treat your low blood sugar. If you do, you may cause your blood
sugar level to rise too high. This, too, can be dangerous and may
cause damage to your nerves, blood vessels and various organs.
 Tests and diagnosis:
• Signs and symptoms of hypoglycemia. You may not exhibit signs and
symptoms of hypoglycemia during your initial visit with your doctor.
In this case, your doctor may have you fast overnight. This will allow
hypoglycemic symptoms to occur so that he or she can make a
diagnosis. It's also possible that you'll need to undergo an extended
fast in a hospital setting. Or, if your symptoms occur after a meal,
your doctor will want to test your glucose levels after a meal.
• Documentation of low blood glucose when the signs and symptoms
occur. Your doctor will draw a sample of your blood to be analyzed in
the laboratory.
• Disappearance of the signs and symptoms. The third part of the
diagnostic triad involves whether your signs and symptoms go away
when blood glucose levels are raised.
 Expected Duration:

• An episode of hypoglycemia caused by exercise or by too much short-acting

insulin usually can be stopped within minutes by eating or drinking a food or
beverage that contains sugar (sugar tablets, candy, orange juice, nondiet soda).
Hypoglycemia caused by sulfonylurea or long-acting insulin can take one to two
days to go away.
• People with diabetes remain at risk for episodes of hypoglycemia throughout life
because they need medications that lower blood sugar. Hypoglycemic episodes at
night are particularly dangerous because the person often sleeps through the
early phase of low blood sugar. Over time, repeated episodes can lead to
impaired brain function.
• About 85% of patients with an insulinoma will be cured of hypoglycemia once the
insulin-secreting tumor is removed.
• In many people without diabetes who have hypoglycemic-like symptoms, the
symptoms can persist despite changes in diet. Often, the symptoms are caused by
something other than low blood glucose levels.
 Treatments and drugs:

•Treatment of hypoglycemia involves two basic approaches:

•Immediate initial treatment to raise your blood sugar level
•Treatment of the underlying condition that's causing your hypoglycemia, to prevent
it from recurring
•Immediate initial treatment
The initial treatment depends on your symptoms. Early symptoms can usually be
treated by consuming sugar, such as eating candy, drinking fruit juice or taking
glucose tablets to raise your blood sugar level. If your symptoms are more severe,
impairing your ability to take sugar by mouth, you may need intravenous glucose or
an injection of glucagon. If you're prone to severe episodes of hypoglycemia, ask
your doctor if a home glucagon kit might be appropriate for you.
•Treatment of the underlying condition
Preventing recurrent hypoglycemia requires your doctor to identify the underlying
condition and treat it. Depending on the underlying cause, treatment may involve:
•Medications. If a medication is the cause of your hypoglycemia, your doctor will
likely suggest changing the medication or adjusting the dosage.
•Tumor treatment. A tumor in your pancreas is treated by surgical removal.
Nesidioblastosis, enlargement of the pancreatic cells that make insulin, is often
treated by partial removal of the pancreas.
 Prevention:

• In people taking insulin, drinking alcohol can lead to an episode of

hypoglycemia . they should be very aware of this possible problem if
they drink.
• People with diabetes should always have ready access to emergency
supplies for treating unexpected episodes of hypoglycemia. These
supplies may include candy, sugar tablets, sugar paste in a tube
and/or a glucagon injection kit. A glucagon injection may be given if a
hypoglycemic patient is unconscious and cannot take sugar by mouth.
For diabetic children, emergency supplies can be kept in the school
nurse's office.
• ... The person also should eat at regular times during the day, never
skip meals and maintain a consistent exercise level. Like people with
diabetes, .