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Introduction
• Injuries are the leading cause of death in American children
and young adults and are responsible for more childhood
deaths than all other causes combined
• Children are particularly vulnerable to injury for a number of
reasons, including their small size, relative physical
incoordination, and limited ability to predict understand
danger. In addition, the immaturity of their developing bones,
ligaments, and muscles; their thin body walls; and the
irrelatively large heads, compared with total body surface
area, make young children susceptible to serious or fatal
injury from falls and collisions.

CLINICAL APPROACH
• General Assessment
• Primary Assessment
• Secondary Assessment
• Tertiary Assessment

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General Assessment
• circumstances at the scene
• Rapid visual survey of the child, assessing the
child’s general appearance and
cardiopulmonary function.

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Primary Assessment
• Airway
• Breathing
• Circulation
• Disability
• Exposure

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Important Principals
• (1) no child’s respiratory rate should be >60
breaths/min for a sustained period.
• (2) normal heart rate is roughly 2-3 times normal
respiratory rate for age.
• (3) a simple guide for pediatric blood pressure is that
the lower limit of systolic blood pressure should be
≥60 mm Hg for neonates; ≥70 mm Hg for 1 mo-1 yr
olds; ≥70 mm Hg + (2 × age) for 1-10 yr olds; and ≥90
mm Hg for any child older than 10 yr.

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Airway and Breathing

• The most common precipitating event for cardiac instability in
infants and children is respiratory insufficiency. Therefore,
rapid assessment of respiratory failure and immediate
restoration of adequate ventilation and oxygenation remain
the first priority in the resuscitation of a child.

• Assessment of breathing includes evaluation of the child’s

respiratory rate, respiratory effort, abnormal sounds, and
pulse oximetry.

• Bradypnea and irregular respiratory patterns require urgent

attention, as they are often signs of impending respiratory
failure and apnea. Signs of increased respiratory effort
include nasal flaring, grunting, chest or neck muscle
retractions, head bobbing, and “seesaw” respirations.
Hemoglobin oxygen desaturation, as measured by pulse
oximetry, often accompanies parenchymal lung disease apnea
or airway obstruction.

• Central cyanosis is a sign of severe hypoxia and indicates an

emergent need for oxygen supplementation and respiratory
support.

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Circulation
• Cardiovascular function is assessed by evaluation of skin color
and temperature, heart rate, heart rhythm, pulses, capillary
refill time, and blood pressure.

• Tachycardia is the earliest and most reliable sign of shock, but

is itself fairly nonspecific and should be correlated with other
components of the exam, such as weakness, threadiness, and
absence of pulses. An age-specific approach to pulse
assessment will yield best results.

Disability

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Exposure
• The provider should undress the child (as is
feasible and reasonable) to perform a focused
physical exam, assessing for burns, bruising,
bleeding, joint laxity, and fractures. If possible,
the provider should assess the child’s
temperature. All maneuvers should be
performed with careful maintenance of
cervical spine precautions.

• Secondary Assessment
• Tertiary Assessment

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Airway Obstruction- Infant

Airway Obstruction- Child

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SHOCK

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Definition
• Shock is an acute process characterized by the
body’s inability to deliver adequate oxygen to
meet the metabolic demands of vital organs
and tissues.
• Shock occurs in approximately 2% of all
hospitalized infants, children, and adults in
developed countries.
• Most common cause of death is multiple
organ dysfunction syndrome (MODS).

Hypovolemic
the most Cardiogenic
common

Types of shock

Obstructive Distributive Septic

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Pathophysiology

Compensation
progressive
shift to less- responses that It may rapidly
Insufficient clinical
efficient attempt to progress to an
oxygen at the deterioration
anaerobic preserve uncompensated
tissue level and lactic
metabolism. oxygenation of state
acidosis.
the vital organs

Pathophysiology
All forms of shock affect cardiac output via several mechanisms, with
changes in heart rate, preload, afterload, and myocardial contractility
occurring separately or in combination

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Hypovolemic shock – blood

VOLUME problem

Cardiogenic shock - blood

PUMP problem

Distributive shock – blood

VESSEL problem

CLINICAL MANIFESTATIONS
• Shock may initially manifest as only
tachycardia, with or without tachypnea.
• Progression leads to decreased urine output,
poor peripheral perfusion, respiratory distress
or failure, alteration of mental status, and low
blood pressure

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A significant misconception is that shock occurs

only with low blood pressure; hypotension is
often a late finding and is not a criterion for the
diagnosis of shock because of a complex set of
compensatory mechanisms attempting to
preserve blood pressure. Hypotension reflects
an advanced state of decompensated shock and
is associated with increased morbidity and
mortality.

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Management
• Clinical diagnosis.
• Start ABC.
• IV access and hydrate.
• Vasopressor therapy.
• When stable start to monitor metabolic state
and electrolyte .

Specific management

early administration of broad-

septic shock spectrum
antimicrobial agents

Distributive early initiation of a vasoconstrictive

shock agent to increase SVR (epinephrine)

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These patients may show poor response to fluid

resuscitation and may decompensate quickly
when fluids are administered.

Smaller boluses of fluid (5-10 mL/kg) should

cardiogenic
be given in cardiogenic shock to replace deficits
shock
and maintain preload.

myocardial support with epinephrine or

dopamine to improve cardiac output

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Infectious Upper Airway Obstruction

ETIOLOGY AND EPIDEMIOLOGY

• most acute infections of the upper airway are caused by
viruses. The parainfluenza viruses account for approximately
75% of cases.
• Most patients with croup are between the ages of 3 mo and 5
yr, with the peak in the 2nd yr of life.
• It occurs most commonly in the late fall and winter but can
occur throughout the year.

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Croup (Laryngotracheobronchitis)
• The term laryngotracheobronchitis refers to viral
infection of the glottic and subglottic regions.
• the most common form of acute upper
respiratory obstruction.
• Most patients have an upper respiratory tract
infection with some combination of rhinorrhea,
pharyngitis, mild cough, and low-grade fever for
1-3 days before the signs and symptoms of upper
airway obstruction become apparent. The child
then develops the characteristic “barking” cough,
hoarseness, and inspiratory stridor.

CLINICAL MANIFESTATIONS
• Most patients have an upper respiratory tract
infection with some combination of
rhinorrhea, pharyngitis, mild cough, and low-
grade fever for 1-3 days before the signs and
symptoms of upper airway obstruction
become apparent. The child then develops the
characteristic “barking” cough, hoarseness,
and inspiratory stridor.

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Physical examination
• Physical examination can reveal a hoarse voice,
coryza, normal to moderately inflamed pharynx,
and a slightly increased respiratory rate. Patients
vary substantially in their degrees of respiratory
distress.
• Rarely, the upper airway obstruction progresses
and is accompanied by an increasing respiratory
rate; nasal flaring; suprasternal, infrasternal, and
intercostal retractions; and continuous stridor.

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Treatment
• According to the severity

• Mild:
• Dexamethasone 0.5 mg/kg (IM)

• Moderate to Severe:
• Dexamethasone 0.5 mg/kg (IM)
• Epinephrine

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Acute Epiglottitis (Supraglottitis)

• potentially lethal, life threating condition.
• Most common organism is HiB, now
streptococcus.
• Most common age is 2-6 years.
• Incidence decreased after Hib vaccine.

CLINICAL MANIFESTATIONS
• acute rapidly progressive and potentially
fulminating course of high fever, sore throat,
dyspnea, and rapidly progressing respiratory
obstruction.
• The initial lack of respiratory distress can
deceive the unwary clinician.
• respiratory distress can also be the first
manifestation.

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Physical examination
• If the patient is obstructed send to OR for
intubation without examination
• Within a matter of hours, the patient appears
toxic, swallowing is difficult, and breathing is
labored.
• Drooling is usually present and the neck is
hyperextended in an attempt to maintain the
airway. The child may assume the tripod position
(sitting upright and leaning forward with the chin
up and mouth open while bracing on the arms).

diagnosis
• X-Ray (thumb sign)
• Laryngoscopy (large, cherry red, swollen
epiglottis)

Treatment
• IV antibiotics after you secure the airway

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Foreign Bodies in the

Airway
• Choking is a leading cause of morbidity and
mortality among children.
• The most common objects that children choke
on are food, coins, balloons, and toys.
• One-third of aspirated objects are nuts,
particularly peanuts.

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An infant is developmentally able to suck and swallow

and also is equipped with involuntary reflexes (gag, cough,
and glottis closure) that help to protect against aspiration
during swallowing.
• The smaller diameter is more likely to experience
significant blockage by small foreign bodies.
• Mucous and secretions may form a seal around the
foreign body, making it more difficult to dislodge by
forced air
• The most serious complication of foreign-body
aspiration is complete
obstruction of the airway.

CLINICAL MANIFESTATIONS
• Three stages of symptoms may result from
aspiration of an object into the airway:
• Initial event: Violent paroxysms of coughing,
choking, gagging, and possibly airway obstruction
occur immediately when the foreign body is
aspirated.
• Asymptomatic interval: The foreign body
becomes lodged. This stage is most treacherous
and accounts for a large percentage of delayed
diagnoses and overlooked foreign bodies.

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• Complications: Obstruction, erosion, or

infection develops to direct attention again to
the presence of a foreign body. In this 3rd
stage, complications include fever, cough,
hemoptysis, pneumonia, and atelectasis.

DIAGNOSIS
• A positive history must never be ignored.

• Choking or coughing episodes accompanied by new onset

wheezing are highly suggestive of an airway foreign body.

• If there is any history of eating nuts, bronchoscopy is

carried out promptly

• Occasionally, fragments of a foreign body may produce

bilateral involvement or shifting infiltrates if it moves from
lobe to lobe.

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• Opaque foreign bodies occur in only 10-25% of cases.

• CT can help define radiolucent foreign bodies such as

fish bones.

• If there is a high index of suspicion, bronchoscopy

should be performed despite negative imaging studies.

• History is the most important factor in determining the

need for bronchoscopy.

• The treatment of choice for airway foreign

bodies is prompt endoscopic removal with
rigid instruments.

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Laryngeal Foreign Bodies

• Complete obstruction asphyxiates the child
unless it is promptly
relieved with the Heimlich maneuver.
• They lodge between the vocal cords in the
sagittal plane, causing symptoms of croup,
hoarseness, cough, stridor, and dyspnea.

Tracheal Foreign Bodies

• Choking and aspiration occurs in 90% of
patients with tracheal foreign bodies, stridor
in 60%, and wheezing in 50%.
• Posteroanterior and lateral soft tissue neck
radiographs (airway films) are abnormal in
92%

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Bronchial Foreign Bodies

• A good expiratory posteroanterior chest film is
most helpful. During expiration the bronchial
foreign body obstructs the exit of air from the
obstructed lung, producing obstructive
emphysema, air trapping, with persistent
inflation of the obstructed lung and shift of
the mediastinum toward the opposite

Approach to DKA (Diabetic ketoacidosis)

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• Diabetic ketoacidosis (DKA) are the most

serious acute complications of diabetes.

• (DKA) is characteristically associated with

type 1 diabetes

• It also occurs in type 2 diabetes under conditions

of extreme stress such as serious infection,
trauma, cardiovascular or other emergencies

1. Hyperglycemia > 200 mg/dl

2. Arterial PH < 7.3
3. Serum Bicarbonate is below 15 mEq/L
4. Ketones are elevated in serum and urine

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Pathophysiology DKA
• end result of the metabolic abnormalities
resulting from a
1. severe deficiency of insulin
2. insulin effectiveness occurs during stress as
counter regulatory hormones block insulin
action( Glucagon ,Growth hormone , cortisol ,
catecholamines)

Sign and Symptoms

• Polyuria
• Polydipsia
• Nausea
• Vomiting
• Abdominal pain
• Tachypnea with deep Kussmaul respirations
• Altered Mental status from Disorientation to
coma

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Laboratory tests
consider HbA1c to assess for chronic
hyperglycemia (normal values are 4.5%–5.9%);
in a new-onset diabetic, consider islet cell
antibodies, insulin antibodies, thyroid
antibodies, thyroid function tests, and celiac
screen (endomesial antibody or tissue
transglutaminase and total IgA)

Management
• the following guidelines are a starting point; therapy must
be individualized based on the dynamics of the patient
• a. Acidosis: pH is an indicator of insulin deficiency; if
acidosis is not resolving, the patient may need more insulin.
NOTE: Initial insulin administration will cause transient
worsening of acidosis as potassium is driven into the cells in
exchange for hydrogen ions
• b. Hyperglycemia: Blood glucose is an indicator of hydration
status
• C. Cerebral edema: Most severe complication of DKA.
Overly aggressive hydration and rapid correction of
hyperglycemia may play a role in its development

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Management

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Complications
1. Cerebral Edema
Cerebral edema complicating DKA remains the
major cause of morbidity and mortality in
children and adolescents with T1DM (20-80 %)
Occurs 6 to 12 hr after therapy of DKA is begun
often following period of apparent clinical
improvement

Risk factor of cerebral Edema

• Obtundation
• Papiledema
• Pupillary Dilation
• Hypertension
• Bradycardia
• Apnea

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Treatment of cerebral edema

• IV mannitol
• Endotracheal intubation
• Ventilation

2. Intracranial Thrombosis
3. ATN (severe dehydration)
4. Pancreatitis
5. Arrythmia by electrolytes abnormalities

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Approach to Anaphylaxis

Definition
1. A rapid-onset IgE-mediated systemic allergic reaction
involving multiple organ systems, including two or
more of the following:

a. Cutaneous/mucosal (flushing, urticaria, pruritus,

angioedema); seen in 90%

b. Respiratory (laryngeal edema, bronchospasm, dyspnea,

wheezing, stridor, hypoxemia); seen in ∼ 70%

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c. Gastrointestinal (GI) (vomiting, diarrhea,

crampy abdominal pain); seen in ∼ 40%–50%

d. Circulatory (tachycardia, hypotension,

syncope); seen in ∼ 30%–40%

2. Initial reaction may be delayed for several

hours AND symptoms may recur up to 72
hours after initial recovery. Patients should
therefore be observed for a minimum of 6–24
hours for late-phase symptoms

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Initial Management

1. Remove/stop exposure to precipitating

antigen
2. Give epinephrine intramuscular (IM)
immediately while performing ABCs. Delayed
administration is associated with increased
mortality

a. Establish airway and give O2 and PPV as needed.

b. Obtain IV access, Trendelenburg position with

head 30 degrees below feet, fluid boluses
followed by pressors as needed

3. Epinephrine = Mainstay of therapy. Immediately

give epinephrine, 0.01 mL/kg (1 : 1000) IM,
maximum dose 0.5 mL. Repeat every 5 min as
needed. The site of choice is the lateral aspect of
the thigh due to its vascularity

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4. Histamine-1 receptor antagonist such as

diphenhydramine, 1 to 2 mg/kg through IM, IV,
or oral (PO) route (maximum dose, 50 mg).
Also, consider a histamine-2 receptor
antagonist (e.g., ranitidine)

5. Corticosteroids help prevent the late phase of

the allergic response. Administer
methylprednisolone in a 2 mg/kg IV bolus,
followed by 2 mg/kg per day IV or IM divided
every 6 hours, or prednisone, 2 mg/kg PO
once daily
6. Albuterol 2.5 mg for <30 kg, 5 mg for >30 kg
for bronchospasm or wheezing repeated every
15 min as needed

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7. Racemic epinephrine 0.5 mL inhaled for signs

of upper airway obstruction
8. Patient should be discharged with an Epi-Pen
(>30 kg), Epi-Pen Junior (<30 kg), or
comparable injectable epinephrine product
with specific instructions on appropriate use
as well as an anaphylaxis action plan

Approach to Status Epilepticus

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• Status epilepticus is a medical emergency that should

be anticipated
in any patient who presents with an acute seizure.

• defined as continuous seizure activity or recurrent

seizure activity without regaining of consciousness
lasting for more than 5 min.

• In the past, the cutoff time was 30 min, but this has
been reduced to emphasize the risks involved with the
longer durations.

• Currently, with the recognition of status

epilepticus as a medical emergency, a lower
mortality rate of 4-5% is observed, most of it
secondary to the underlying etiology rather than
to the seizures.

• Status epilepticus carries an approximately 14%

risk of new neurologic deficits, most of this
(12.5%) secondary to the underlying pathology.

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Assessment: Common causes of childhood seizures

include
• electrolyte abnormalities, hypoglycemia, fever,
subtherapeutic anticonvulsant levels, central
nervous system (CNS) infections, trauma, toxic
ingestion, and metabolic abnormalities.
• Consider specific patient history such as shunt
malfunction in patient with ventriculoperitoneal
shunt. Less common causes include vascular,
neoplastic, and endocrine diseases

• Diagnostic workup: When stable, workup may

include CT or magnetic resonance imaging,
EEG, and lumbar puncture (LP)

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• Acute management of seizures

• If CNS infection is suspected, give antibiotics
and/or acyclovir early

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• Management of coma
• a. Airway (with C-spine immobilization),
Breathing, Circulation, D-stick, Oxygen,
Naloxone, Thiamine (ABC DON’T)

Pseudo–status epilepticus
• psychologic conversion reaction mimicking
status epilepticus or other movement
disorders (chorea, tics), rigors, clonus with
stimulation, and decerebrate/decorticate
posturing.

• EEG is helpful in ruling out pseudo–status

epilepticus

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