Pediatrics Emergency in Children

Learning objectives
At the end of the course you will be able to:
Triage all sick children when they arrive at a health
facility

Assess and manage a child with trauma and Chocking

Assess and manage a child with acute poisoning and

burn

Asses and manage a child with DM & its Complication

 ETAT( Emergency, Triage
Assessment and Treatment)
 Triage is the process of rapidly examining all sick
children when they first arrive in health facility in
order to place them in one of the following
categories:
E=Emergency
P= Priority and
Q=Queue (non-urgent)
 Triage Categories
 All sick children are rapidly examined on arrival and sorted into 3

categories:

• EMERGENCY signs – who require immediate emergency

treatment

• PRIORITY signs – who should be given priority in the queue,

rapidly assessed and treated without delay

• NON-URGENT cases – who can wait their turn in the queue. The
majority of children seen will be non-urgent cases.
 Emergency Signs – ABCDO
 Triage involves looking for signs of serious illness or
injury
 Emergency signs are sorted in order of priority as:
 A = Airway
 B = Breathing
 C = Circulation, Coma, Convulsions
 D = Dehydration
 O= Others (bleeding child, major trauma with open
fracture, Acute poisoning )
 Priority Signs
These children need prompt, but not
emergency, assessment and treatment
These signs can be remembered with the
symbols:
3 TPR
MOB
 Priority signs – 3 TPR MOB
o Tiny baby
o Temperature 3T
o Trauma

o Pallor
o Poisoning 3P
o Pain

o Restless
o Respiratory distress 3R
o Referral

o Malnutrition/ marasmus M
o Oedema O
o Burns B
 Priority signs 3 TPR-MOB
• Tiny baby: any sick baby under 2 months
 Small babies difficult to assess, more prone to infection, more
likely to deteriorate quickly
• Temperature: child is very hot
 High fever may need prompt treatment and investigation e.g
paracetamol
• Trauma or other urgent surgical condition(not included as
other emergency condition)
 Includes acute abdomen, fractures, head injury
 Priority signs 3 TPR-MOB
• Pallor
 Severe pallor may indicate severe anaemia needing urgent
transfusion

• Poisoning
 Those who arrived after an hour of history of swallowing drugs or
poison but still s/he may deteriorate rapidly and may need specific
urgent treatment

• Pain
 Severe pain requires early full assessment and pain relief
 Priority Signs – 3 TPR- MOB
Restless, lethargy, irritable
 Child who is conscious but cries constantly and will not settle. May
have serious illness such as meningitis

Respiratory distress
 Moderate respiratory distress (chest indrawing or difficulty breathing
that is not severe) requires urgent but not emergency treatment. If in
doubt class as ‘E’

Referral
 Any urgent referral from another hospital or clinic should be seen as a
priority
 Priority Signs – 3 TPR-MOB
• Malnutrition/ marasmus
 Severe wasting may indicate severe malnutrition ( marasmus)

• Oedema
 Oedema of both feet may indicate another form of severe
malnutrition, Kwashiorkor

• Burn
 Major burns are very painful and children can deteriorate
rapidly
 Non-urgent
• Once assessment is complete if no emergency or priority signs are
found the child is classed ‘non-urgent’ and should wait their turn in
the queue
• However, if there is any change in the child’s condition, the child
will need to be triaged again and treated appropriately
 Treatment
• Emergency management
 Treatment must be started as soon as possible

 Ideally should be directed by senior health worker

 Needs good team work

 Needs frequent reassessment of ABCD

• Priority cases
 Can receive some treatments while waiting eg pain relief, anti-
pyretics
Pediatric Trauma
 Pediatric Trauma
Learning Objectives
At the end of the session students are able to
Assess a child with Trauma
Assess and manage immediate complications of
Trauma
Do life saving procedures in a child with Trauma
 Pediatric Trauma
Globally 50 million injuries occur per year.
Is a cause for 1.2 million deaths
Common in developing countries b/c of increase in
RTAs.
Pre-hospital care should focus on rapid assessment
and management of the airway, breathing, and
circulation as well as spinal immobilization.
Assessment and Management of
Trauma
Primary care and Resuscitation
Utilization of adjuncts to the primary care
Secondary care
Definitive care
Primary survey and Resuscitation

Airway maintenance with cervical spine protection

Breathing and ventilation

Circulation with hemorrhage control

Disability (evaluation of neurologic status)

Other/Exposure and environmental control

Assessment and Management of Trauma

A
ABCDO
B priorities !

C D E
 Primary survey: A
Look/listen/feel

For secretions and foreign body or any evidence of

facial/mandibular or tracheal/laryngeal fractures with
potential for an unstable airway
Jaw thrust and avoid Chin lift
Maintain cervical support
Oropharyngeal airway if needed
If the airway is obstructed child may need endotracheal
or surgical airway eg cricothyroidotomy
Primary survey: A
 Primary survey: B
Assessment of breathing
Inspect the neck and thorax
Is the chest moving?
check if tracheal deviation
Absent air entry
Abnormal chest movement
The use of accessory muscles
Management of breathing
 Administer oxygen
 surgical consultation in case chest trauma
 Primary survey: C1, C2 & C3
External bleeding (e.g. large vessel injury)
Internal bleeding (e.g. in chest, abdomen, brain)
Spinal cord injury
Mgt :- Apply external pressure and elevation
20ml/kg of RL or NS as fast as possible
Suspected internal bleeding surgery
Look for coma and convulsion ( check AVPU ,GCS)
Treat or referral for intubation and further management if GCS <9

•
 Glasgow Coma Scale
Child Infant
Spontaneous 4 Spontaneous
To speech 3 To speech
Eye Opening (E)
To pain 2 To pain
None 1 None
Oriented 5 Coos/Babbles
Confused 4 Irritable Cry
Verbal (V) Inappropriate 3 Cries/Pain
Incomprehensible 2 Moans
None 1 None

Obeys commands 6 Spontaneous

Purposeful 5 Withdraws(touch)
Withdrawals(pain) 4 Withdraws (pain)
Motor (M)
Flexion(pain) 3 Abnormal flexion
Extension(pain) 2 Abnormal Extension
None 1 None
 Primary survey: D
Check for movement of the extremities
Neurologic deficit (pupillary size and reflexes,
posture)
Signs of increased ICP
Posture( decerebrate ,decorticate ) - suggests a
severe head injury
 Primary survey: O
ASSESS for Other Abnormalities

Look for spinal injury

Check temperature

Look for any visible bone or deformities

Log roll the patient with cervical spine immobilization

to fully assess the back, flank, and spine

Keep the patient warm throughout the initial trauma

assessment
 Adjuncts to primary survey
Laboratory Hct/Hgb
blood group and Rh
Random blood sugar
Urinary catheter ; NG tube
FAST u/s (Focused Assessment with Sonography for
Trauma)
Anti pain
 Secondary survey
Include a complete head to toe evaluation including
History
Complete examination
Laboratory studies
Radiographic studies
Problem identification
 Head Injury
TBI is the leading cause of death and disability in
pediatric trauma.
CLASSIFICATION
Primary vs secondary
Severity
– Mild: GCS 14-15
– Moderate : GCS 9-13
– Severe: GCS 3-8
Mechanism ( penetrating vs blunt)
 Management of head injury
primary survey (A,B,C,D,E) and resuscitation
Prevent secondary damage (hypoxia, hypotension,
hypoglycemia, hyperthermia, and ICP)

Endotracheal intubation & need referral urgently

Determine blood glucose level

Anticonvulsants
Elevate the head up to 30º & mannitol 0.5-1 gram
/kg for reduction of intracranial pressure(ICP)
 Chest Injuries
The chest wall of a child is more compliant than that of an adult so
significant force is required to cause rib fractures in children

Serious intra thoracic trauma without rib fracture

Most of the chest injuries are blunt unless in adolescents

It a pneumothorax, heamothorax, flail chest or Cardiac tamponade

Air entry  on affected side

Movement on affected side

Dull on percussion

Rx: Insertion of a chest tube

 Abdominal Injuries
Life-threatening blood loss can occur due to internal bleeding.
Children are at greater due to immature musculoskeletal system
and a smaller body surface area
Classification
Blunt Vs. penetrating injury
Solid organ Vs. hollow organ
Management
Assess ABCD
hct and cross match
Ultrasound
Transfuse as necessary
Seek urgent surgical advice
 Musculoskeletal injuries
The most common fracture signs are pain, swelling,
tenderness, deformity, abnormal movement, and loss of
function
Fractures can be classified as closed (where the skin is intact)
Vs. open (where there is a wound which communicates the
fracture with the environment)
During the Primary Survey –The 3 S’s
Stop bleeding
Splint (immobilization)
Skin traction
Any material including cartoon or Plaster of Paris (POP) slab
Splinting and skin traction
Prevention of trauma in children
 Health Education, skills and behavioral change
 Prevention in Schools
 Playground safety
 School Bus safety
 Youth violence
 Environmental modification
 Product modification
 Supportive home visits
 Safety devices
 Community-based studies
 FOREIGN BODIES
Foreign bodies — Small children often choke on food or small
objects and usually clear the obstruction spontaneously with
coughing and choking.
The majority of pre hospital calls for airway obstruction in
children less than five years of age were caused by a foreign
object.
Ages at highest risk: 6months – 5 years
>90% of pediatric deaths due to foreign body aspiration occur
in children <5 years old; 65% in infants
Symptoms resolved in more than half of children prior to the
arrival of paramedics.
An intervention was required in 2 percent of cases.
 Diagnosis suspected in any previously well, afebrile
child with sudden onset respiratory distress and
associated coughing, choking, stridor or wheezing.
 <50% of children will have history of witnessed or
suspected foreign body aspiration
Esophageal foreign body — Foreign bodies lodged
in the esophagus in the area of the cricoid cartilage or
the tracheal bifurcation can compress the airway
causing partial airway obstruction.
 It is also possible that an esophageal foreign body
will become dislodged into the upper airway.
 Clinical manifestation
Mild obstruction
 the child abele to breath and cough effectively and speak.
 Children are fully responsive, crying and verbally respond to question; may
have loud cough.
Sever Obstruction
 The victim being unable to breath or speak
 Wheezy breath sound
 Attempt at cough that are quite and silent
 Cyanosis and diminishing consciousness (specially in children)
 Management of the Choking
 History of aspiration of foreign body plus increasing
respiratory distress requires immediate management
 Techniques are based on forced expiration rather
than mechanical means
 Techniques such as blind finger sweep of mouth
should be avoided in children as they may result in
trauma and are likely to push object further down into
airway
 Management of the choking (infant)

• Lay infant on your arm in head down position

• Give 5 blows to the infants back with heel of hand
• If obstruction persists turn over and give 5 chest
thrusts with 2 fingers, 1 finger breadth below nipple
level in midline
• If obstruction persists check infants mouth for any
object which can be easily removed
• If necessary repeat sequence with back slaps again
 Management of Choking (Child)
 Give 5 blows to the child’s back with heel of hand
with child sitting, kneeling or lying
 If obstruction persists, go behind the child and pass
your arms around the child’s body: form a fist with
one hand immediately below the child’s sternum;
place the other hand over the fist and pull upwards
into the abdomen; repeat this Heimlich manoeuvre 5
times
 If the obstruction persists, check the child’s mouth for
any obstruction which can be removed
 If necessary repeat sequence with back slaps again
Management of Choking in infants
and Children
Common Childhood Poisoning
 Learning Objective
At the end of this topic, you will be able to:

Assess a child with Acute Poisoning

Apply decontamination procedures in acute poisoning

Administer Charcoal and do gastric lavage

Identify specific poisons and manage accordingly

 POISONING
Suspect poisoning in any unexplained illness in a previously
healthy child

Primary survey: Assess ABCDO with additional consideration of

the poisoning agent

If the child arrives within 1hr of poisoning (especially ingestion

of substances to have gastric lavage), this child will be considered
as emergency because this needs urgent treatment
Airway: Remove excessive secretions, look for any inhalational
injury that might potentially worsen with time
• Check for signs of burns in or around the mouth or of stridor
(upper airway/laryngeal damage) suggesting ingestion of
corrosives
• Consider consultation for early intubation for patents if there is
sever airway compromise

Breathing: Look for signs of respiratory distress . Give oxygen and

manage accordingly
Circulation: Check the pulse, capillary refill and skin color.
If there is shock, treat accordingly

Coma: check the AVPU and pupillary response

• Determine blood sugar and give Dextrose if
hypoglycemic or if the child has reduced level of
consciousness treat as if the child is hypoglycemic

Dehydration: Assess hydration status (dry tongue and

buccal mucosa, sunken eyes)

Exposure: Remove all clothing and wash with soap and

water and check body temperature
Secondary survey: more specific evaluation with history and
physical examination and laboratory to identify the exact cause
and extent with simultaneous detoxification of the patient
History and physical examination:
History
Find out full details of the poisoning agent
Attempt to identify the exact agent involved requesting to see
the container, were relevant
Try to find the best estimate of the agent dose or amount ( bear
in mind one pill can kill)
The rout of exposure ( inhalation ,injection, ingestion, contact )
 The time of ingestion to presentation (important for the
management of the child)
Check that no other children were involved
Physical exam:
Do detailed examination which help to identify the
causes: a breath odor ,temperature ,eye sign( dilated vs.
constricted pupil ), skin( hot flushed, dry), bowel sound
(absent or present)
 General Principles of Management
Gastrointestinal decontamination
Is most effective within 1hr of ingestion of poison
includes ipecac induced vomiting, use of cathartics,
gastric lavage, activated charcoal and whole bowel
irrigation (WBI)
Gastric lavage
Mostly done within one hour of ingestion of poisons
Perform lavage with 15 ml/kg body weight of normal saline
(0.9%) max 200 to 400ml
Lavage should be continued until the recovered lavage
solution is clear of particulate matter
Activated charcoal
Effective if used with in 1 hour
Usual dose 1 gm/kg; Max50 gm.
The amount of water is 8–10 times the amount of charcoal
Don’t force the child to take, you can insert NG tube to facilitate
If possible, give the whole amount at once.
Whole bowel irrigation (WBI)
Administration of large volume of polyethylene glycol solution
with balanced electrolyte.
Usually given by NGT
Effective in slowly absorbed substances(lithium, iron) and pills
For children 35ml/kg/hr can be given and adolescents can take
1-2 lt/hr
Decontamination of skin and eye
Remove all clothing and clean all exposed
areas with water and soap.
Rinse the eye for 10–15 minutes with clean running water
or saline
Antidote if this is available and indicated
Remove from the source of exposure
Supplemental oxygen if there is respiratory distress or
cyanosis
Keep unconscious children in the recovery position
 Specific poisons
1.Corrosive compounds
Acid and alkali are common agents including bleaches and
disinfectants
Do not induce vomiting or use activated charcoal or gastric
lavage
Give milk or water within 30 minutes
Secure IV line and arrange referral in sever cases
2. Hydrocarbons
Highly volatile substances (e.g. kerosene, benzene)
Do not induce vomiting or give activated charcoal or
gastric lavage as this increases aspiration
Oxygen therapy
3. Organophosphate poisoning
Commonly used insecticides and herbicides(eg malathion)
The effects of these poisons can be memorized as
"DUMBBELS”(Diarrhea, Urination, Meiosis, Bradycardia,
Bronchorrhea, Emesis, Lacrimation & Salivation)
Remove the poison by irrigating eye or washing skin
Decontaminate by activated charcoal or lavage within 1hr of
ingestion
After decontamination, antidotal therapy begins with
administration of atropine sulfate
Dose 0.05 to 0.1 mg per kg to children and 2 to 5 mg for
adolescents IV or IM.
4.Carbon monoxide poisoning
Remove patient from the source
Give 100% oxygen to accelerate removal of CO
can look pink but still be hypoxemic) until signs of hypoxia disappear
5.Snake bite
The child may present with local signs or systemic signs
Local signs include pain, swelling, tender lymph node enlargement
and local bleeding.
Initial systemic signs include nausea, vomiting, abdominal pain and
headache.
shock-tachycardia, hypotension
respiratory difficulty or paralysis
 Management
Assess and manage the ABCDO
Splint the limb below the level of the heart to
reduce movement and absorption of venom
Irrigate and dress the wound
Avoid cutting the wound or applying tourniquet
Paralysis of respiratory muscles can last for days
and requires intubation
Antivenom
Surgical Management_ incision o excision
1. Three years old boy was brought by his mother to emergency room after ingestion of liquid
from a container. What measures do you take in the right chronological order?
A. Take targeted history about ingested substance
B. Secure IV line and start resuscitation
C. Assess airway and breathing and give oxygen if in distress
D. Remove clothes and keep them in plastic container
E. Check AVPU
F. Do physical examination
G. Look for convulsion
H. Assess circulation
2. Put the actions in the right chronological order: what will you do first, what next, what after
that, and so on, and what last?
A. Ask about head or neck trauma
B. Call a senior health worker to see any emergency
C. Have blood specimens taken for laboratory analysis
D. Look for any priority signs
E. Look for emergency signs
F. Move on to the next patient
G. Place priority patients at the front of the queue
H. Start treatment of any emergency signs you find
BURN IN CHILDREN
At the end of the presentation ,you should be able to
Define burn

Explain the different causes of burn

Identify the types of burn

Assess and manage burn wound

Definition
It is an injury to the skin or other human tissue caused by heat.

It occurs when some or all of the cells in the skin or other tissues

are destroyed by hot liquids (scalds), hot solids (contact burns), or

flames (flame burns).
Children are naturally curious. They are mobile and want to

explore their surroundings and play with new objects.

The peak incidence of burn injury occurs in toddlers (1 to 3 years

of age), and the injuries usually occur as the result of scalding from
hot liquids
 Causes of Burn
Thermal burn
Flame : fire injury(due to gasoline, kerosene)
Scald : moist heat/steam(hot water, liquids and foods).
Contact to hot surfaces(solids).
Chemical burns:-exposure to acid, alkali or organic substances
and common in industries and laboratories
Inhalation Injury (smoke and heated air)
Radiation:- overexposure to the sun, X-ray, radioactive
radiation, nuclear bomb explosions
Electrical:-Is the worst and deeper than the other types. Extent
depends on amount of voltage, length of exposure, type of
current, pathway of flow, and local tissue resistance
 CLASSIFICATION
1.First degree burn (superficial): It affects epidermis, red,
sunburn like appearance of the skin with no blisters. It is very
painful and heals without scaring.
2.Second degree burn( partial thickness ): in addition to the
epidermis, the dermis is involved . It is pink to dark and has
blisters. It is still painful and it is blanching. It heals with a scar
after many weeks.
3.Third degree burn (full thickness): are those full-thickness
injuries .it is not blanching, no blister, no pain sensation and have
a pale or charred color and a leathery appearance and heals by
scarring.
4.Fourth-degree burns: in addition to the three layers, the
underlying fascia, muscle, tendons and bone is involved
 Extent of body surface area injured
 Various methods are used to

estimate the TBSA affected by

burns; the most common
methods are :the rule of nines,
Lund and Browder method and
Palm method

1.Rule of nine
It is a quickest method to calculate
the extent of burns and
represents 9 and multiples of
nine.
 2. Lund and Browder method
A more precise (reliable) method; because it
adjusts for age
 3. Palm method
In patients with scattered burns, a method to estimate the

percentage of burn is the palm method.

The size of the patient’s palm from crease at wrist to tip of

extended fingers is approximately 1% of TBSA.

Indication for Hospital Admission
Burns >10% of TBSA (except 1st degree burn).
Burns over face ,neck ,hands ,feet ,perineum and joint.
Circumferential burns .
Inhalational and high tension electrical burns .
Suspected child abuse.
Associated injuries (fractures).
Burns in patients with preexisting medical conditions
that may complicate the acute recovery phase.
 Burn management
1. Emergency phase
2. Acute phase
3. Rehabilitative phase
Emergency treatment
Cool the burn area with cold tap water within 30 min for 20 min.
This stops the heat as well as decreases the progression of burn, but
avoid it for large area burn as it increases hypothermia and also
don’t use ice as is causes hypothermia
Similarly don’t use grease (e.g. butter, oil) since it predisposes for
infection and doesn’t disperse heat
If the burn is caused by hot tar, use mineral oil to remove the tar
Airway & Breathing:
Manage as trauma patient, since the airway swelling increases
in the next 24 hours, there is a need of early advanced airway
(intubation or tracheotomy)
Administer 100% oxygen to displace carbon monoxide during
inhalation burn
Circulation:
Secure urgently an IV line for burns of ≥10% of TBSA
If possible on the intact skin but access through burned areas
may be required. If IV access couldn’t be found, use
intraosseous
Don’t put adhesive plaster circumferentially to the body. As
swelling increases in the next 24 hours, it can cause
circulatory insufficiency
For children with severe burn (>20% BSA), give 20 mL/kg of
crystalloids still assessment of the extent of the burns and
calculation of the rest of the fluid of the 24 hours is completed

Then use the Parkland formula (i.e. 4 mL /kg/% TBSA), in

addition to the patients calculated maintenance fluid

Lactated Ringer solution in 5% dextrose, normal saline with

5% glucose or half-normal saline with 5% glucose can be used

Half of the fluid is given over the 1st 8 hr, calculated from the
time of onset of burn

The remaining is given over the next 16 hr

Acute phase
Lasts until wound closure is complete
 Wound care and dressing 1-2 times/day.
Wound Debridement and skin graft
Prevent infection (by using Topical antibiotics, such as, silver
nitrate, silver sulfadiazine, gentian violet)
Tetanus toxoid for those who have not immunized.
A high-protein intake is also needed for wound healing

Rehabilitation phase
Provide psychosocial and emotional support
Health education
Assess home and environment
 Complications of burn
Hypovolemic shock
Electrolyte imbalance
Cardiac arrhythmias and cardiac
arrest
Metabolic Acidosis
Decrease temperature
Infection and Sepsis
Extensive and disabling scarring
Disfigurement
Contractures
 CHILDHOOD DM
OUTLINE
• Introduction
• Diagnostic criteria for DM
• DKA
• Management of DM and DM with DKA
• Nutritional management
• Long term complications
 DIABETES MELLITUS
• DM is a heterogeneous group of disorders in which there are distinct genetic
patterns as well as other etiologic and pathophysiologic mechanisms that
lead to impairment of glucose tolerance. Mainly two major forms:
A.Type1 DM
• Characterized by autoimmune destruction of pancreatic islet ß cells.
• Both genetic susceptibility and environmental factors contribute to the
pathogenesis
• Associated with other autoimmune diseases such as thyroiditis, celiac
disease, multiple sclerosis and Addison disease

B.TYPE2 DIABETES MELLITUS

• usually obese but are not insulin-dependent and infrequently develop ketosis
• Some may develop ketosis during severe infections or other stresses
• The presentation is typically more insidious than that with type 1 DM.
• often presents with excessive weight gain and fatigue as a result of insulin resistance
and/or incidental finding of glycosuria during routine physical examination
• A history of polyuria and polydipsia is relatively uncommon in these patients
• The incidence of type 2 DM in children has increased as a result of increased childhood
obesity.
 Diagnostic Criteria
Diabetes Mellitus (DM)
• Symptoms of DM plus random plasma glucose
>200mg/dL (11.1mmol/L)Or
• Fasting plasma glucose >126mg/dL (7.0mmol/L)
Impaired Glucose Tolerance (IGT)
• Fasting glucose 110–125mg/dL(6.1–7.0mmol/L)
or
• 2-hr plasma glucose during the OGTT<200mg/dL
(11.1mmol/L) but>140mg/dL
 DKA
• Definition: Exists when there is hyperglycemia (> 300
mg/dL), ketonemia, acidosis, glucosuria, and ketonuria
• Is the end result of the metabolic abnormalities
resulting from a severe deficiency of insulin or
insulin effectiveness
• Occurs in 20–40% of children with new-onset
diabetes and in children with known diabetes who
omit insulin doses or who do not successfully manage
an intercurrent illness
• May be arbitrarily classified as mild, moderate, or
severe.
 CLASSIFICATION OF DKA
Normal Mild Moderate Severe

CO2 20–28 16–20 10–15 <10

(mEq/L )

pH 7.35–7.45 7.25-7.35 7.15-7.25 <7.15

(venous)

Kussmaul Kussmaul or
Clinical Normal Oriented, depressed
respirations;
alert but oriented but
respirations;
sleepy to
fatigued sleepy; depressed
sensorium to
arousable
coma
 MANAGEMENT OF DM
A. New-Onset Diabetes Without Ketoacidosis
Goals:
• To maintain a balance between tight glucose control and avoiding
hypoglycemia
• To eliminate polyuria and nocturia
• To prevent ketoacidosis, and
• To permit normal growth and development with minimal effect
on lifestyle.
Elements
• Initiation and adjustment of insulin
• Extensive teaching of the child and caretakers, and
• Reestablishment of the life routines
 New-Onset Diabetes Without Ketoacidosis
Insulin Therapy
• Most children with new-onset diabetes have some residual β-cell
function which reduces exogenous insulin needs
• Children with long-standing diabetes and no insulin reserve
require -about 0.7 U/kg/d if prepubertal,
-1.0 U/kg/d at midpuberty, and
- 1.2 U/kg/d by the end of puberty
• Dose in the newly diagnosed child, is about 60–70% of the full
replacement dose based on pubertal status
• The optimal insulin dose can only be determined empirically,
with frequent self-monitored blood glucose levels and insulin
adjustment
• Residual β-cell function usually fades within a few months and is
reflected as a steady increase in insulin requirements and wider
glucose excursions
 Insulin Therapy,cont’d
• The initial insulin schedule should be directed toward the
optimal degree of glucose control in an attempt to duplicate
the activity of the β cell
Limitations
Exogenous insulin does not have a 1st pass to the liver,
whereas 50% of pancreatic portal insulin is taken up by
the liver
absorption of an exogenous dose continues despite
hypoglycemia, whereas endogenous insulin release ceases
and serum levels quickly lower with a normally rapid
clearance
absorption rate from an injection varies by injection site
and patient activity level, whereas endogenous insulin is
secreted directly into the portal circulation.
 Insulin Therapy,cont’d
• All preanalog insulins form hexamers, which must
dissociate into monomers subcutaneously before being
absorbed into the circulation
• Thus, a detectable effect for regular (R) insulin is
delayed by 30–60 min after injection.
• This, in turn, requires delaying the meal 30–60 min
after the injection for optimal effect
• Frequent blood glucose monitoring and insulin
adjustment are necessary in the 1st weeks.
Continuous subcutaneous insulin infusion (CSII) via
battery-powered pumps provides a closer
approximation of normal plasma insulin profiles
Inhaled and Oral Insulin Therapies.
Basic Education
 B. DM with KETOACIDOSIS.
• Severe insulinopenia (or lack of effective insulin action)
results in a physiologic cascade of events in 3 general
pathways.
1.Excessive glucose production coupled with reduced
glucose utilization raises serum glucose
2.Increased catabolic processes result in cellular losses of
sodium, potassium, and phosphate
3.Increased release of free fatty acids from peripheral fat
stores supplies substrate for hepatic keto acid production.
Therapy must address both the initiating event in this
cascade (insulinopenia) and the subsequent physiologic
disruptions
Reversal of DKA is associated with inherent risks that
include hypoglycemia, hypokalemia, and cerebral edema
 DKA Treatment Protocol
TIME THERAPY COMMENTS
1st hour 10–20 mL/kg IV bolus 0.9% Quick volume expansion;may be
NaCl or LR repeated.NPO.Monitor I/O,
neurologic status.Use flow she
et.Have mannitol atbedside;1 g/kg
IV push for cerebral edema

Insulin drip at 0.05 to 0.10 Iv

μ /kg/hr rate=85ml/kg+maint.-bolus/23hrs
2nd hour until DKA resolution 0.45% NaCl:plus continue
insulin drip
20 mEq/L KPhos and 20
mEq/L KAc
5% glucose if blood sugar
<250 mg/dL (14 mmol/L)
If K < 3 mEq/L, give 0.5 to 1.0
mEq/kg as oral K solution OR
increase IV K to 80 mEq/L
 DKA Treatment Protocol cont’d
Parameters to switch to sc insulin:No emesis;CO2 ≥ 16
mEq/L;normal electrolytes
Hyperglycemia and Dehydration.
• Insulin must be given at the beginning of therapy to accelerate
movement of glucose into cells, to subdue hepatic glucose
production, and to halt the movement of fatty acids from the
periphery to the liver
• No need to give initial bolus.
• Rehydration also lowers glucose levels by improving renal
perfusion and enhancing renal excretion.
• Repair of hyperglycemia occurs well before correction of acidosis.
Therefore, insulin is still needed to control fatty acid release after
normal glucose level.
 Hyperglycemia and Dehydration,cont…
• Repair of fluid deficits must be tempered by the
potential risk of cerebral edema
• Children with mild DKA rehydrate earlier and
can be switched to oral intake, whereas those
with severe DKA and a greater volume deficit
require 30–36 hr
• The initial serum sodium is usually normal or
low because of the osmolar dilution of
hyperglycemia
 Catabolic Losses
• Both the metabolic shift to a catabolic predominance and the
acidosis move potassium and phosphate from the cell to the
serum.
• The osmotic diuresis, the kaliuretic effect of the
hyperaldosteronism, and the ketonuria then accelerate renal
losses of potassium and phosphate.
• With prolonged illness and severe DKA, total body losses
can approach 10–13 mEq/kg of sodium, 5–6 mEq/kg of
potassium, and 4–5 mEq/kg of phosphate.
• The initial serum K level is often normal or elevated due
to the movement of potassium from the intracellular space
to the serum, both as part of the keto acid buffering process
and as part of the catabolic shift.
 Catabolic Losses,cont..t
• These effects are reversed with therapy, and potassium
returns to the cell
• Improved hydration increases renal blood flow, allowing
for increased excretion of potassium in the elevated
aldosterone state
• The net effect is often a dramatic decline in serum
potassium levels.
• It is unclear whether phosphate deficits contribute to
symptoms of DKA such as generalized muscle weakness
• It is prudent to use potassium phosphate rather than
potassium chloride as a potassium source. Potassium
acetate is also used, because it provides an additional
buffer
 Keto Acid Accumulationt
• Low insulin infusion rates (0.02–0.05 units/kg/h) are usually
sufficient to stop peripheral release of fatty acids, thereby
eliminating the flow of substrate for ketogenesis.
• The initial infusion rate may be decreased if blood glucose levels go
below 150 mg/dL (8 mmol/L) despite the addition of glucose to the
infusion
• Ketogenesis continues until fatty acid substrates already in the liver
are depleted
• There should be a steady increase in pH and serum bicarbonate as
therapy progresses. Kussmaul respirations should abate and
abdominal pain resolve
• All patients with DKA should be checked for initiating events that
may have triggered the metabolic decompensation
 RECOVERY FROM DKA
• Children with milder DKA recover in 10–20 hr
• Those with more severe DKA require 30–36 hr with
this protocol
• Any child can be easily transitioned to oral intake
and subcutaneous insulin when DKA has essentially
resolved (total CO2 >15 mEq/L; pH >7.30; sodium
stable between 135 and 145 mEq/L; no emesis).
• A flow sheet is mandatory for accurate monitoring
of changes in acidosis, electrolytes, fluid balance,
and clinical status
 Nutritional Management
• No special nutritional requirements for the diabetic child
other than those for optimal growth and devt.
• The caloric mixture should comprise approximately 55%
carbohydrate, 30% fat, and 15% protein.
• The total daily caloric intake is divided to provide 20% at
breakfast, 20% at lunch, and 30% at dinner
• 10% for each of the midmorning, midafternoon, and
evening snacks
• Approximately 70% of the carbohydrate content should be
derived from complex carbohydrates intake of sucrose and
highly refined sugars should be limited.
• Protein: High-protein intakes may contribute to diabetic
nephropathy
 Monitoring

•Compliance (check records)

•HBG tests
•HbA1 every 2 months
•Insulin & meal plan
•Growth & development
•Microalbuminuria
•Well being & life style
Although values of HbA1C may vary
according to the method used for
measurement,
in nondiabetic individuals, the HbA1C
fraction is usually less than 6%; in
diabetics
6–7.9% represent good metabolic control,
8.0–9.9%, fair control
 10.0% or higher, poor control.
 Long term complications:
Can be divided into 3 major categories:
(1) micro vascular complications:retinopathy and
nephropathy;
(2) macro vascular complications: particularly
accelerated coronary artery disease,
cerebrovascular disease, and peripheral vascular
disease; and
(3) neuropathies, both peripheral and autonomic,
affecting a variety of organs and systems
When to screen for these complications?
94