Pediatric Emergencies

Al-Qadisiya Collage of Medicine

Iraq

Presented by : Ziyad Salih

INTRODUCTION

Accurate assessment of a child with an acute illness or injury requires special

knowledge and skills.

The majority of children presenting in the ED have mild moderate illness and

injury and remain alert.

For the critically ill child, determining the primary physiologic problem may

be difficult, because inadequate oxygenation, ventilation or perfusion from

any cause will eventually progress to the picture of cardiopulmonary failure.

CONTENTS :-

• Shock

• Status asthmatics

• Status epileptics

• Poisoning

SHOCK

Shock is a syndrome that results from inadequate oxygen

delivery to meet metabolic demands

If untreated metabolic acidosis, organ dysfunction and death

SHOCK

• Hemorrhage

• Serum/Plasma loss

• Sever diarrhea and vomiting Hypovolemic

• Analphylactic

• Neurogenic

• SepticDistributive

• Myocardial

• Dysrrhythmia

• CHD-(duct dependant)Cardiogenic

• Pneumothorax

• Tamponade

• DissectionObstructive

• Heat, CO, Cyanide

• EndocrineDissociative

SHOCK

Clinical Presentation

Early diagnosis requires a high index of suspicion

Diagnosis is made through the physical examination

focused on tissue perfusion

Extreme hypotension is a late and pre-morbid sign

SHOCK

Clinical Presentation

Neurological: Fluctuating mental status, sunken fontanel

Skin and extremities : Cool, pallor, cyanosis, poor cap refill,

weak pulses, poor muscle tone

Cardio-pulmonary: Hyperpnea, tachycardia

Renal: Scant, concentrated urine

SHOCK

Management

Airway If not protected or unable to be maintained, intubate

Breathing Always give 100% oxygen to start Saturation

monitor

Circulation Establish IV access rapidly Cardio-Respiratory

monitor & Frequent BP

SHOCK

Management

Draw blood and send for

1. ABG

2. Blood sugar

3. Electrolytes CBC

4. PT/PTT

5. Blood type and cross matching

SHOCKManagement

Treatment of hypovolemic shock

A . 20 cc/kg of NS over an appropriate period of time. If in

shock, get it in as rapidly as possible and give more as

needed. If the patient is unstable remember your ABC’s and

intubate patient.

B . This may be repeated once if patient still seems

hemodynamically compromised due to dehydration

C . Further fluid boluses should be guided by the CVP, BP.

SHOCK

Anaphylactic shock

A systemic reaction (usually life-threatening) that occurs

secondary to an IgE mediated antigen induced reaction

(allergen) or exposure to mast cell de-granulating agents

(anaphylactoid).

SHOCK

Anaphylactic shock

Both reactions cause mediator release (histamine,

leukotrienes, etc.) which produce the symptoms. While there

is often a history of prior exposure to a given antigen, in the

non-IgE mediated (anaphylactoid) reactions, symptoms may

occur during the first exposure.

SHOCK

Anaphylactic shock

A.Symptoms usually occur within seconds to 60 min. of Ag

exposure.

B.Variable: Initial symptoms may be mild or life threatening.

Generally, the earlier the onset, the more severe the reaction.

SHOCK

Anaphylactic shock

C .Symptoms :-

cutaneous (urticaria/angioedema, pruritus).

respiratory (bronchospasm, stridor, pulmonary edema.

laryngeal edema), rhinitis.

cardiovascular (hypotension, arrhythmias, myocardial

ischemia, vasodilation, flushing),

SHOCK

Anaphylactic shock

C .Symptoms :-

gastrointestinal (nausea, emesis, diarrhea, pain)

Also there could be asymmetric swelling of a limb or perioral

area.

SHOCK

Anaphylactic shock

Most Common Etiologic Agents

A.Antibiotics (for instance penicillin, although any could be

involved)

B.Insect (hymenoptera) stings

C.Foods (nuts, eggs, seafood)

SHOCK

Anaphylactic shock

D.Immunotherapy

E.Non-IgE (Anaphylactoid) mediated mast cell

degranulation:

1.Morphine

2.Codeine

3.Polymyxins

4.Radiocontrast dye

SHOCK

Anaphylactic shock

Management

A. ABC’s

B. Stop antigen administration - if insect bite or allergy shot,

isolate antigen site with tourniquets and inject 0.01 cc/kg epi.

(1:1000) SQ into site after tourniquet applied. Flick off (do

not squeeze) any stinger present.

SHOCK

Anaphylactic shock

Management

C. Epinephrine:

1.Mainstay of treatment

2.Sc or IM 0.01 cc/kg of 1:1000, max 0.3 cc, may repeat

3. Rarely IV 1:10,000 by drip and titrate to achieve response,

begin at drip of 0.1 mcg/kg/min (only in refractory

hypotension requiring CPR).

SHOCK

Anaphylactic shock

Management

D.Immediate IV placement with IVF (LR/NS, bolus 20 cc/kg as needed for

shock).

E.Continue to observe for 24 hrs, as symptoms may recur.

1.Subjective: SOB, anxiety.

2.Objective: stridor, retractions, wheezing, cyanosis, pallor.

3.BP: q 5-10 min initially, then q 1 hr.

4.Continuous EKG monitor or A-line as needed.

SHOCK

Anaphylactic shock

Management

F. Other drugs as needed (NOT a substitute for epi.).

1.H1 Antihistamine - Benadryl 0.5-1.0 mg/kg po or slow IV

push.

2.Steroids - 1-2 mg/kg methylprednisolone to prevent late

phase response.

SHOCK

Anaphylactic shock

Management

3.Cimetidine IV 5-10 mg/kg given over 5 min - given in

association with H1 antihistamines may reverse profound

hypotension unresponsive to fluids/pressors (this is

controversial).

4.Glucagon may be effective in reversing hypotension in rare

cases, especially if beta-blockade is present. (Dose: < 10 kg:

0.1mg/kg IM, > 10 kg: 1 mg/dose IM).

STATUS ASTHMATICUS

is a life threatening form of asthma that is defined as a

condition in which a progressively worsening attack is

unresponsive to the usual appropriate therapy that leads to

pulmonary insufficiency. The primary mechanical event in

status asthmaticus is a progressive increase in airflow

resistance. Mucous plugging and mucosal edema or

inflammation are the major causes for the delayed recovery

in status asthmaticus.

STATUS ASTHMATICUS

The combination of hypoxia, hypercapnia, and acidosis may

result in cardiovascular depression and cardiopulmonary

arrest.

STATUS ASTHMATICUS

II. History:

A. Known asthmatic?

B. Asthma meds? Compliance? Time of last dose/nebulizer

Tx?

C. Previous clinic/ED visits?

D. Previous hospitalizations, intubations, steroid courses?

E. When did current wheezing/resp distress begin?

STATUS ASTHMATICUS

III.Physical Exam:

A.Vital Signs:

1.T: Fever may indicate URI, atelectasis or pneumonia

2.P: Usually elevated, especially if treated w/epi

3.R: Often tachypneic .

STATUS ASTHMATICUS

Treatment

1.Beta-agonist nebulizer treatment,

may give 5-10 mg nebs if minimal initial response.

a. Albuterol 0.15 mg/kg (max 10 mg/dose)

2.Atropine 250 mcg (<2 y.o.), 500 mcg (>2 y.o.), add to 2 nd or

3 rd beta-agonist neb

STATUS ASTHMATICUS

Treatment

3.Subcutaneous injection - subcutaneous epi. rarely done

today as nebulizers are so commonplace

A .Epinephrine: 1:1000 0.01 cc/kg/dose (0.3 cc max)

B .Terbutaline 0.05% solution, 0.01 mg/kg/dose with a max. of

0.25 mg q 20 - 30 minutes.

STATUS ASTHMATICUS

Treatment

4.Steroids: Solumedrol 2 mg/kg IV, then 1-2 mg/kg IV Q 6

hours. If mild exacerbation or quick response to above, may

consider oral prednisone 2 mg/kg.

5.Oxygen

A .In younger patients, the distress caused by fighting the

mask may only make the wheezing worse.

STATUS ASTHMATICUS

Treatment

B .Humidified 02 should be placed on all patients who show

evidence of hypoxia (O2 sat <90% on sat monitor/pulse

oximeter) or respiratory distress. Remember the sat monitor

gives no information regarding ventilation and pCO2.

STATUS EPILEPTICUS

STATUS EPILEPTICUS

Is an epileptic seizure of greater than 30 minutes

There are three major subtypes of status epilepticus in

children:

1- Prolonged febrile seizures lasting for >30 min, particularly

in a child younger than 3 yr of age, is the most common cause

of status epilepticus.

STATUS EPILEPTICUS

2- Idiopathic status epilepticus, in which a seizure develops

in the absence of an underlying CNS lesion or insult. It

includes :

• Sudden withdrawal of anticonvulsants.

• Anticonvulsants given on an irregular basis

STATUS EPILEPTICUS

3- Symptomatic status epilepticus: when the seizure occurs

as a result of an underlying neurologic disorder or a

metabolic abnormality.

Status epilepticus may also be the initial presentation of

epilepsy. Sleep deprivation and an intercurrent infection tend

to render epileptic patients more susceptible to status

epilepticus

STATUS EPILEPTICUS

I.Initial Management: position on side, protect from injury,

loosen clothing.

A.Airway

1.Jaw lift

2.Bite block or oral airway if able (no tongue blade or fingers

in mouth)

3.Suction secretions or emesis 4.Roll on side.

STATUS EPILEPTICUS

B.Breathing

1.O2 by mask

2.Intubate if needed

may need to intubate for respiratory depression secondary to

meds given.

C.Circulation - start IV, monitor BP, O2 SAT.

STATUS EPILEPTICUS

Quick history :

1.Description: [precipitating event, onset: focal/generalized,

duration], was child post-ictal ?

2.Fever? S/S illness?

3.Previous seizures? (degree, control, etc.)

4.Chronic seizure meds? (dose, compliance, levels)

5.Hx. trauma? (Accidental or non-accidental)

STATUS EPILEPTICUS

6.Toxin ingestion?

7.Chronic medical problems? Hx. of syncope?

8.Behavior changes?

9.Vomiting? / diarrhea? - Consider inborn error of metabolism

in infants.

STATUS EPILEPTICUS

III.Physical Exam

A.Vital Signs

1.Evidence of increased ICP / herniation ?

increased BP, tachycardia (early), bradycardia (occurs late

and is an ominous sign), dilated pupils, papilledema

2.Decreased BP from sepsis, toxins

3.Fever from meningitis

STATUS EPILEPTICUS

III.Physical Exam

A.Vital Signs

B.Mental Status / Level of Consciousness, Glasgow Coma

Scale

C.Respiratory Pattern

1.Assure good air exchange

2.Abnormal patterns with worsening level of consciousness

STATUS EPILEPTICUS

III.Physical Exam

Also examine

1.Pupils (size, reactivity)

2.Fundi (papilledema, hemorrhage)

3.Signs of head trauma

4.Signs of meningismus

5.Neuro. Exam - focal signs, level of consciousness

STATUS EPILEPTICUS

Treatment

Airway petency

Breathing

Circulation

STATUS EPILEPTICUS

POISONING

KEROSENE POISONING

This is a common problem among young children.

Over half of the children with all forms of poisoning admitted

to the ED.

This problem usually seems to arise from kerosene being kept

within reach of the child.

POISONING

KEROSENE POISONING

Kerosene is poorly absorbed by the GIT, but there is often

aspiration into the respiratory tract especially if the child

vomits. This causes pneumonitis which may be so severe as

to cause pulmonary oedema and hypoxaemia. Such features

usually occur within hours but may be seen a day or so after

ingestion when the child becomes breathless and feverish up

to 40ºC.

POISONING

KEROSENE POISONING

CNS complications most commonly include lethargy and

much less often semi-coma, coma and convulsions .

Bone marrow toxicity and haemolysis are not common.

Possibility of heart rhythm problems (such as atrial

fibrillation and ventricular fibrillation) and hepatic and renal

failure.

POISONING

KEROSENE POISONING

Treatment

Immediately remove the child from the source of the

poisoning and ensure the airway is open (this is always the

first priority).

Remove contaminated clothing and thoroughly wash the skin

with soap and water.

POISONING

KEROSENE POISONING

Treatment

If possible perform pulse oximetry and give supplemental

oxygen if indicated.

Intubation and mechanical ventilation may be needed in a

patient with severe hypoxia, respiratory distress or decreased

consciousness.

POISONING

KEROSENE POISONING

Treatment

Avoid gastric lavage because of the risk of inhalation and

hence pneumonitis. If very large amounts of kerosene have

been ingested less than an hour earlier then lavage may be

considered if the airway can be protected by expert

intubation.

POISONING

KEROSENE POISONING

Treatment

There is no evidence that corticosteroids are helpful. Some

texts recommend the routine use of antibiotics but this

remains controversial.

Thanks for your listening