Acute Care in Pediatrics

Francia C. Toledano
Clinical Instructor
 Learning Objectives
• Explain the different common acute life – threatening
conditions in pediatric population
• Enumerate the warning signs and symptoms needing
immediate medical attention
• Discuss the nursing responsibilities for each conditions
• Demonstrate the rescue breathing and basic life support
techniques in responding to acute life – threatening
conditions
 Shock
• Defined as a state in which the delivery of oxygen is
inadequate to meet the metabolic demands of vital
organs and tissues
• All types of shock can lead to impaired functioning of
vital organs such as the brain and kidneys
3 major classification of shock
• Hypovolemic shock
– Secondary to intravascular volume loss
• Maldistributive shock
– Maldistribution of blood flow
secondary to vasomotor instability or
capillary leak
• Cardiogenic shock
– Caused by cardiac pump disfunction
Incidence and Etiology
• Hypovolemic shock is the most common form of shock in
the pediatric population
– Dehydration with hypovolemic shock is the leading
cause of death in children worldwide

• Sepsis (systemic infection) is the most common cause of

Maldistributive shock. Anaphylactic shock is another form

• Preexisting congenital heart disease, cardiomyopathy,

myocarditis arrhythmias, drug toxicity and hemolytic
uremic syndrome are the major causes of cardiogenic
shock but it is less common in children
 Pathophysiology of Hypovolemic Shock
Decrease in Intravascular Volume leads to decrease in venous return to the heart with
subsequent fall in preload.

Inadequate cardiac output. HR increases (tachycardia) as early sign of shock.

If infection or inflammation is present subsequent release of toxins produces a

decrease in sympathetic tone with resulting vasodilation and a decrease in systemic
vascular resistance (SVR). Initial response of the body is increase cardiac output to
support BP. Excessive vasodilation leads to hypovolemia and hypotension

Endothelial damage also occurs leading to leaking of fluid from intravascular to

interstitial space known as capillary leak syndrome
 Pathophysiology of Maldistributive Shock
Septic (systemic infection) or anaphylactic (severe allergic reaction) shock origin

Child may develop disseminated intravascular coagulopathy (DIC) secondary to

inflammatory process.
DIC – abnormal response of the clotting system leading to prolonged and
inappropriate clotting. Manifested as petechiae, small purplish hemorrhagic
spots on the skin, bleeding from IV sites and puncture wounds.

One of the hallmark of septic shock is severe hypotension in the face of increased
cardiac output. Low diastolic pressure with wide pulse pressure is seen.
 Pathophysiology of Cardiogenic Shock
Ventricular pump dysfunction is seen. Can be due to structural heart disease, myocarditis, ischemia or
inflammatory mediators of septic shock.

Contractility is depressed so CO falls. Triggering sympathetic activation and the renin – angiotensin –
aldosterone system.

If CO remains low, oxygen delivery to the tissues will decrease.

Conversion of aerobic to anaerobic metabolism with ensuing metabolic acidosis.

Lungs attempt to compensate for metabolic acidosis by increasing the RR to exhale CO2, so respiratory
alkalosis may develop.

Metabolic acidosis lead to depress myocardial function. CO decreases further, compensatory mechanism fails
resulting in cardiovascular collapse and death.
Clinical Manifestation
• Cardiovascular signs are often the most prominent
• Poor perfusion manifest as cool extremities, diminished or
absent distal pulses, a capillary filling time >3s, mottling of
the skin
• Tachycardia and tachypnea in early shock
• BP normal to hypotensive
• Increase RR, retraction, nasal flaring
• Irritable and hard to console
• Lethargy
• In anaphylactic shock, child develop urticaria, have
swollen lips, and develop respiratory difficulties secondary
to airway swelling
Diagnosis
• Based on clinical findings, history of
preceding illness and results of diagnostic
test
• CBC, electrolytes, blood gases and blood
cultures are commonly obtained.
• Chest xray
• Echocardiograms
Treatment
• Early recognition and therapy
• Supplemental oxygen via nasal cannula or oxygen
mask
• Once airway is established, management is directed
toward volume replacement
• Whole blood or Packed RBC for transfusion
• Dopamine and dobutamine are frequently used to
improve CO.
• Epinephrine or norepinephrine is used to increase
systemic vascular resistance and support BP
• Antibiotics for sepsis
Nursing management
• Assessment and reassessment – assess the pulses,
perfusion, CFT, color and temperature of the skin, VS, UO,
LOC and respiratory effort.

• Nsg DX:
✓ Decreased cardiac output related to dec cardiac function
or inadequate intravascular volume as evidenced by
hypotension, tachycardia, poor UO, lethargy or poor
perfusion
✓ Ineffective peripheral tissue perfusion r/t vasodilation and
coagulopathy as evidenced by altered neurologic status,
decreased UO and metabolic acidosis
 Respiratory
Distress Syndrome
• Premature infants born at less than 36 weeks gestation are at risk

• Occurs because the lungs of premature infants are underdeveloped and

lack enough surfactant to keep the alveoli open.

• Leads to dyspnea, hypoxia, and cyanosis and require immediate oxygen

administration
Incidence and Etiology
• The more premature the newborn, the
more likely that RDS will occur
• 60 – 80% of 28 – week gestation infants
develop RDS while only 15 – 30% of those
born at 32 – 36 weeks do so
Pathophysiology
• Infants with RDS have poor lung compliance

• Result is trauma to pulmonary structures, which leads to interstitial edema

and epithelial destruction.

• Inflammatory response and accumulation of cellular debris from tissue

necrosis causes airway obstruction

• Hyperinflation, atelectasis, and tissue fibrosis result

• Damage pulmonary vasculature

• Overall effect of the disease process is a ventilation – perfusion ratio

imbalance that leads to HYPERCAPNIA and HYPOXEMIA
Clinical Manifestations
• Dependency on supplemental oxygen for
more than 28 days and compensated
respiratory acidosis
• Pulmonary edema and cor pulmonale
• Crackles and wheezing on auscultation
• Fluid retention leading to heart failure
• Oxygen toxicity from long – term RDS
treatment leads to BRONCHOPULMONARY
DYSPLASIA
Diagnosis
• Based on infant’s history, PE, Lab results and
Chest xray.
• Diagnosis is suspected when the RDS has not
improved within 2 weeks, O2 therapy is
required beyond 28 days or prolonged
mechanical ventilation is necessary
• Rule out pneumonia and patent ductus
arteriosus
• Chest radiograph reveals alveolar
hyperinflation, atelectasis and fibrosis (scar)
Treatment
• Prevention is the primary focus of medical management of RDS

• Prenatal steroids promote the maturation of fetal lungs

(dexamethasone or betamethasone IV is given to the mother)

• Exogenous surfactant lowers alveolar surface tension, allowing

the alveoli to open mor easily with inspiration and preventing
collapse on expiration

• Diuretics, steroids and bronchodilators

• Tracheostomy for long – term ventilation

Nursing Management
• Physical assessment and provide
respiratory, nutritional and
developmental support
• Oxygenation
• Suctioning
• Nasogastric feeding
• Small frequent feeding with breastmilk
 Foreign
Body Aspiration
• Most common in children 6 months to 4 yrs
• Cough reflex protects the airway from
foreign body obstruction.
• Partial airway obstruction can cause
atelectasis and hyper expansion of alveoli
and resultant respiratory distress
• Complete airway obstruction leads to
hypoxia and death
Common causes of FBAO
• Coins
• Nuts
• Hot dogs
• Latex or rubber balloons
• Peanut butter
• Pieces of raw vegetables or fruit
• Chips
• Small toys
• Grapes
• Hard candies and popcorn
Clinical Manifestations
• Coughing or gaggling spells, cyanosis, and
restlessness or panic.
• Hoarseness, dyspnea, wheezing and stridor.
• Children may experience fever if they
develop pneumonia
• Children with complete obstructions are
unable to cough, speak or make vocalization.
• Cyanosis, loss of consciousness and death if
not relieved
 Poisoning
• Caustic Ingestion is most common in 1 to 3 yrs old
• Caustic substance: Strong acids/alkali capable of
corroding or burning organic tissue
• Most commonly ingested caustic substance: household
bleach
• May cause acute severe injury and long – term
complications such as esophageal strictures
Manifestations
• Upper airway injury: stridor, hoarseness,
nasal flaring, retractions
• GI tract injury: dysphagia (most
common), drooling, retrosternal or
abdominal pain, hematemesis
Pathophysiology
ALKALI ingestion ACID ingestion

✓ Low pH with low viscosity

✓ Bleaches have pH of results in rapid transit to
9 – 11 the stomach leading to
gastric injury

✓ Causes liquefaction ✓ Coagulation necrosis

necrosis occurs

✓ Upper airway injury is

✓ Leading to common and may result in
thrombosis of blood gastric outlet obstruction
vessels or perforation in he antral
or pyloric area
Management
• Stabilization and supportive care
– Close observation with prevention of
vomiting, choking or aspiration
– Neutralizing the caustic agent, administer
activated charcoal or doing gastric lavage is
not recommended
• Endoscopic evaluation
– Performed within 24 hours of ingestion to
evaluate and stage the injury
– If strictures develop esophageal dilation is
performed to maintain normal swallowing
 Drowning
• Drowning is a major source of pediatric
mortality and morbidity worldwide

• Drowning is the process of experiencing

respiratory impairment from
submersion/immersion in liquid.

• Children who have seizure disorders

have a risk of drowning four times that
of the general population
 Head Trauma
• Most head trauma in childhood is minor
• Minor head trauma
– <2 yrs old – history or signs of blunt trauma to the scalp,
skull or brain. Infant or child is alert or awakens to voice or
light touch
– > 2 yrs old - GCS 14 or 15 at the initial assessment. No
abnormal findings on neurologic examination. No physical
evidence of skull fracture
Concussion
• From a direct blow to the head, face, neck or a
blow elsewhere with an “impulsive” force
transmitted to the head
• Results in rapid onset of short – lived
impairment of neurologic function that resolves
spontaneously
• Symptoms: Headache, confusion/disorientation,
difficulties with memory, blank stare or
“stunned” appearance, inattentiveness, slow or
incoherent speech, dizziness, gait abnormalities,
vomiting and emotional lability
Traumatic Brain injury (TBI)
• Associated with symptoms of brief LOC,
disorientation, vomiting
• Severity
– Mild TBI : GCS score 13 – 15
– Moderate TBI: GCS 9 – 12
– Severe: GCS is < or equal to 8
Basilar Skull Fracture
• This is a crack in the skull. Sometimes,
the broken skull bones can cut into brain.
This causes bleeding and can lead to
another injury.
• Symptoms: CSF rhinorrhea or otorrhea,
posterior auricular hematoma (battle
sign), hemotympanum, and periorbital
hematomas (racoon eyes)
Diagnosis
• Head CT scan
– Most children with minor head
trauma do not need head CT
scans
– Decision to obtain a head CT
should be made using clinical
predictors to determine risk for
TBI
Treatment
• A mild head injury may not require treatment.

• If the person is bleeding, stop it. Use gauze, a towel, or a piece of clothing. Do
not touch the wound. If the wound is open, do not apply pressure. Cover or
wrap the wound instead.

• If the person is vomiting, keep them upright. If they are lying down, roll their
body to the side to prevent choking.

• If the person is awake, instruct them not to move their head and neck. This
can help prevent further damage to their spine and brain.

• If the person is unconscious and breathing, try to stabilize their body. This
includes keeping their neck and head in line with their spine.

• If the person is unconscious and not breathing, begin the process of CPR
(cardiopulmonary resuscitation).
Nursing Responsibilities
• For patient with mild TBI and for discharge provide
instruction to the primary care taker to observe if the
patient develop the following signs and symptoms
needing immediate medical attention:

➢ Inability to awaken the child

➢ Persistent or worsening headache
➢ Vomiting that begins or continues 4 – 6 hrs after injury
➢ Change in mental status or behavior
➢ Unsteady gait, clumsiness or incoordination
➢ Seizure