LARYNGOTRACHEOBRONCHITIS
• inflammation of
the larynx and trachea and bronchial
passageways.
• it usually affects children between the
ages of 6 months and 3 years.
• a viral infection of the upper respiratory
tract that causes varying degrees of
airway obstruction.
• the disease is most often self-limited, but
it occasionally is severe and, rarely, fatal.
Causes
Croup can be caused by a number of
different viruses.
• In the fall, it is caused by
parainfluenza virus.
• In winter and spring, it is usually
caused by respiratory syncytial virus
or an influenza virus.
• In some cases it is diptheric in origin.
Pathophysiology
Infiltration of Para Influenza Virus through
the nose
↓spreads and eventually involves the larynx
and trachea
↓Inflammation and edema of the subglottic
larynx and trachea, especially near the
cricoid cartilage
↓Parainfluenzae virus activates chloride
secretion and inhibits sodium absorption
across the tracheal epithelium, contributing
to airway edema
↓limiting airflow
↓results in the barky cough, turbulent airflow
and stridor, and chest retractions
Signs and Symptoms
• Stridor- a harsh, raspy vibrating sound
heard when the child breathes in. This is
usually present when the child is agitated
but in severe cases may be present even
at rest. Stridor occurs when the opening
between the vocal cords becomes
narrower
• Fever
• The child's condition may improve in the
morning but worsen at night.
• Croup syndrome usually peaks 2 to 3
days after they start and the illness
generally last less than a week.
Progression of Symptoms
• STAGE 1 • Laryngoscopy  Provide and encourage fluid intake,
• Fear reveals inflammation in the larygeal IV fluids may be prescribed to
• Hoarseness spaces. maintain hydration.
• Croupy cough Medical Management  Keep the child comfortable in a semi-
• STAGE 2  Usually not necessary as croup is due seated position
• Use of accessory muscles to a viral infection.  Decrease the child's activity and
• Labored respiration  Antibiotics are prescribed if it is a encourage rest as long as croup
• STAGE 3 bacterial infection. attack persist.
• Restlessness • Fever is treated with acetaminophen.  Administer bronchodilators to relax
• Anxiety  Nebulized Epinephrine smooth muscles and relieve stridor.
• Pallor • adrenergic effects can cause mucosal  Administer acetaminophen as
• Sweating • vasoconstriction and subsequently prescribed to lower down fever.
• STAGE 4 decreases  Have a resuscitation equipment
• Permanent cyanosis • subglottic edema  Provide appropriate reassurance and
• Cessation of breathing • Onset is rapid education.
EARLY signs of impending airway • Peak is observed in 2hours
obstruction:  Frequent hand washing and avoiding
• Additional doses: Intensive Care Unit contact with people who have
1. Increase pulse and RR ( 20-30 minutes)
2. Increase restlessness respiratory infections can lessen the
• Regular Hospital Unit ( 3-4 hours) chance of spreading the viruses that
Telltale signs of croup:
 Corticosteroids (Dexamethasone) cause croup.
• BARKING COUGH
- anti inflammatory effects decrease  Avoidance of solid foods for first few
• STRIDOR
subglottic edema days
Steeple Sign- A sign on the frontal
- onset detectable as early as 6 hours OTITIS MEDIA - Latin for "Inflammation of
radiograph of tracheal narrowing and a
- continued improvement over 12- the Middle Ear"
suggestive for the DIAGNOSIS OF CROUP.
24hours Description
Risk Factors
PROGNOSIS (Expectations) • Otitis media is one of the most prevalent
o Allergies
• Viral croup usually goes away in 3 to diseases of early childhood.
o Repeated upper respiratory infections
7 days. The outlook for bacterial croup is • an infection of the middle ear, the area
o Previous croup
good with prompt treatment. just behind the eardrum. It happens
Possible Complications
• If an airway obstruction is not treated when the eustachian tubes, which
o Pneumonia
promptly, respiratory distress (severe connect the middle ear to the nose,
o Ear infection
difficulty breathing) and respiratory become blocked with fluid. With the
o Airway obstruction and death (rare) arrest can occur. infection, mucus, pus, and bacteria can
Diagnosis Nursing Considerations also pool behind the eardrum, causing
• Diagnosis is generally made on history and pressure and pain.
physical examination.
• Major Objective: Maintaining the airway
• Physical examination may show chest
and providing adequate respiratory • Ear infections usually begin with a cold.
exchange Although adults can get ear infections,
retraction and wheezing using a
• Children with severe respiratory distress they are most common in infants and
stethoscope.
should not be given anything by mouth to young children. That's because a child's
• Diagnostic tests may include: prevent aspiration and decrease work of eustachian tubes are narrower and
• Thoart Cultures breathing. shorter than an adults', and it's easier for
identify infecting organisms and their fluid to get trapped in the middle ear.
 Maintain patent airway
sensitivity to antibiotic when bacterial Etiology
 Assess respiration rate
infection is the cause Streptococcos pneumoniae, Haemophilus
• Blood Cultures  Monitor O2 saturation
influenzae, and Moraxella catarrhalis are
 Elevate HOB and provide bed rest
 Provide humidified o2 vial cool mist the three most common bacteria that
distinguish bacterial and viral infections causes AOM. The etiology of noninfectious
• X-ray of the neck tent for hospitalized child
OM is unknown, although OM may occur
may show upper airway narrowing and because of blocked eustachian tubes from
edema in subglottic folds. the edema of URIs, allergic rhintis, or
 hypertrophic adenoids. Chronic OM is
usually the extension of the Acute
episode.
Types Of Otitis
• Otitis media acuta - Myringitis bullosa
• Otitis media chronica
mesotympanalis - Influenza
• Acute otitis media is usually of rapid
onset and short duration. Acute otitis
media is typically associated with fluid
accumulation in the middle ear together
with signs or symptoms of ear infection;
a bulging eardrum usually accompanied
by pain, or a perforated eardrum, often
with drainage of purulent material
(pus).Fever can be present.
• The most common bacterial agents for
Acute Otitis Media are:
• Streptococcus pneumoniae
• Haemophilus influenzae
• Chronic Otitis Media is a persistent
inflammation of the middle ear, typically
for a minimum of a month. Chronic otitis
media may develop after a prolonged
period of time with fluid (effusion) or
negative pressure behind the eardrum
(tympanic membrane). Chronic otitis
media can cause ongoing damage to the
middle ear and eardrum and there may
be continuing drainage through a hole in
the eardrum.
• Chronic Otitis Media often starts
painlessly without fever. Ear pressure or
popping can be persistent for months.
Sometimes a subtle loss of hearing can
be due to chronic otitis media.
Pathophysiology
Predisposing Factors
• Age
• Sex
• Race
• Siblings or Parents with a history of
Chronic OM
Precipitating Factors
• URIs
Diagnostic Test
• Passive smoking
• Pneumatic Otoscopy - assessment of
• Attending daycare
• Using a pacifier
• Bottle feeding
↓Normal Eustachian tube is closed and
flat preventing organisms in the
pharyngeal cavity from entering the
middle ear.
↓The Eustachian tube opens to allow
drainage of secretions produced by the
middle ear mucosa and to equalize air
pressure between the middle ear and
the outside environment.
↓Blockage of the Eustachian tubes may
be caused by respiratory infection
(cold), allergies, exposure to cigarette
smoke, infected or overgrown adenoids
(tonsils),for infants, being fed lying
down (drinking a bottle while lying on
the back).
↓Passive smoking increases the risk of
persistent middle ear effusion by
enhancing attachment of the pathogens
that cause otitis to the respiratory
epithelium in the middle ear space, by
prolonging the inflammatory response
and by impeding drainage through the
Eustachian tube.
↓Impaired drainage of the Eustachian
tube causes retention of secretions in
the middle ear.
↓Air is unable to escape through the
obstructed tubes, is absorbed into the
circulation, and causes negative
pressure within the middle ear.
↓Negative pressure pulls interstitial fluid
into the tube and creates a serous
effusion. This effusion of the middle ear
provides a fertile media for microbial
growth. If growth is rapid, a middle ear
infection develops.
↓If the tube opens, a difference in
pressure causes bacteria to be swept
into the middle ear chamber, where the
organisms quickly proliferate and invade
the mucosa.
↓Complications include pain, fever, and
difficulty in hearing, otorrhea, tinnitus,
feeling of fullness and pulling of ear.
tympanic membrane mobility with a
pneumatic otoscope is essential to
differentiate AOM from otitis media with
ear effusion (OME). If an accumulation of
cerumen prevents adequate
visualization.So remove the cerumen
first.
• Diagnosis of AOM is made if visual
inspection of the tympanic
membranereveals a purulent discolored
effusion and a bulging or full, opacified,
or very reddened immmobile membrane.
An immobile tympanic membrane or an
orange discolored membrane indicates
OME.
Surgical Management
• Myringotomy – a surgical incision of the
eardrum may be necessary to alleviate
the severe pain of AOM. A myringotomy
is also performed to provide drainage of
infected middle ear fluid in the presence
of complications (mastoiditis,
labyrinthitis, or facial paralysis) or to
allow purulent middle ear fluid to drain
into the ear canal for culture.
• Tympanostomy tubes – are tubes placed
for equalizing pressure or grommets that
facilitate continued drainage of fluid and
allow ventilation of the middle ear.
• Adenoidectomy – removal of the
adenoids. Only performed in children
with recurrent AOM or chronic OME with
nasal obstruction.
Pharmacological Management
• Antibiotics -- If the doctor prescribes
antibiotics, be sure to give the child the
entire course. The antibiotic most often
prescribed for an ear infection is
amoxicillin, unless the child is allergic to
penicillin. If that's the case, there are
several options. Children who are treated
with antibiotics are more likely to
develop vomiting, diarrhea, or a rash.
• If the etiology is known then drug is used
aimed against the bacteria. If drug is
warranted, oral amoxicillin in high doses
(80-90mg/kg/day) is the treatment of
choice for initial episodes of AOM in
children who have not received
antibiotics within the past month.
Duration of antibiotic therapy is 10-14
days in children 6 years old and older,
shorter courses may be sufficient.
• Second-line antibiotics used to treat OM
include amoxicillin-clavulanate,
azithromycin, and cephalosporins such as
cefdinir, cefuroxime, and cefpodoxime.
IM ceftriaxone is used when the
causative organism is highly resistant
pneumococcus.
• Ibuprofen, acetaminophen -- Ask the
doctor about using over the counter oral
medications for pain and/or fever, such
as ibuprofen (Advil, Motrin) or
acetaminophen (Tylenol). Children under
18 should not take aspirin, due to the risk
of developing a rare but serious illness
called Reye's syndrome
• Ear drops – If the child has recurring ear
infections, a perforated eardrum, or
develops infection after ear tubes have
been placed, the doctor may prescribe
antibiotic ear drops instead of oral
antibiotics, to be used over a period of
time (like a few months). If the child
doesn't have ear tubes in place and
doesn't have any drainage from the ear,
the doctor may also prescribe anesthetic
ear drops to relieve pain.
Nursing Management
• Don't expose the child to secondhand
smoke.
• Keep the child away from other children
who are sick.
• Always hold the infant in an upright,
seated position during bottle feeding.
• Breastfeeding for at least 6 months can
make a child less prone to ear infections.
• Don't use a pacifier while laying the baby
in a crib.
• The pneumococcal vaccine (Prevnar)
prevents infections such as pneumonia
and meningitis, and studies show it
slightly reduces the risk of ear infections.
BRONCHIOLITIS
• swelling of the smallest air passages in
the lungs (bronchioles), usually due to a
viral infection (RSV)
• most common in infants between 2 and 6
months old
• Infection is spread by direct contact with
respiratory secretions
 • transmitted from person to person by
direct contact with nasal fluids, or by
airborne droplets. Although RSV
generally causes only mild symptoms in
an adult, it can cause severe illness in an
infant.
PATHOPHYSIOLOGY
• Risk factors:
• younger than 6 months old
• Never having been breast-fed
• Premature birth
• An underlying heart-lung condition
• A depressed immune system
• Exposure to tobacco smoke
• Contact with multiple children or
crowded place
• Having siblings who attend school or
child care
• due to a viral infection of the small
airways (Respiratory syncytial virus
(RSV)
– Respiratory syncitial virus-
considered the single most
important respiratory pathogen
in infancy and early childhood,
highly contagious
• Begins as a URI with symptoms of
rhinorrhea and low grade fever then
diseases progresses and becomes a
respiratory tract infection
• Infection of bronchiolar area and
ciliated epithelial cells produces
increased mucus secretion, cell death,
and sloughing, followed by a
peribronchiolar lymphocytic infiltrate
and submucosal edema.
• The combination of debris and edema
produces critical narrowing and
obstruction of small airways.
• During expiration, the additional
dynamic narrowing produces
disproportionate airflow
• Trapping air in the alveoli that causes
hyperinflation that may lead to
atelectasis
• Inadequate gas exchange
• Patient experiences the following
symptoms:
• Tachypnea, greater than 70
breaths/min(most common physical
sign)
• Tachycardia
• Fever, usually in the range of 38.5-
39°C
• Nasal flaring
• Intercostal retractions
• Wheezing
• Cyanosis
• Apnea ( may be the first recognized
indicator in very young infants)
• In severe cases,: hypercapnia leading
to respiratory acidosis and
hypoxemia
DIAGNOSTIC TEST
• Enzyme-linked Immunosorbent Assay
(ELISA)- technique used mainly in
immunology to detect the presence of
an antibody or an antigen in a sample
• Immunflouresecent antibody (IFA) -
is a technique used for light
microscopy with a fluorescence
microscope and is primarily used
on biological samples. This
technique uses the specificity
of antibodies to their antigen to
target fluorescent dyes to
specific bimolecular targets within
a cell, and therefore allows
visualization of the distribution of
the target molecule through the
sample
• Blood gases
• Chest x-ray
• Patchy infiltrates
• Air trapping
• Focal atelectasis
MANAGEMENTS
Medical Management
• Chest clapping as supportive therapy
• Mechanical ventilation as necessary
• Provide cool humidified oxygen
Pharmacologic Management
Adrenergic agents- relieve reversible
bronchospasm by relaxing smooth
muscles on the bronchioles
• Albuterol (Proventil, Ventolin,
Salbutamol)
• Epinephrine (Adrenalin)
Cortecosteroids- blocks release of
inflammatory mediators
• Prednisone (Deltasone)
• Methylprednisolone (Medrol, Solu-
Medro
• Ribavirin (Virazole)- has an antiviral
activity against RSV by inhibiting the
synthesis of viral structural proteins,
but ribavirin aerosol treatment for RSV
infection is highly controversial
Nursing Management
• Provide patent airway
• Position at 30-40 degrees angle with
neck slightly extended
• Monitor O2 stat
• Encourage adequate intake and assess
for dehydration
• If fluids by mouth is contraindicated
given IV fluids are preferred until acute
crisis of the disease has passed
• Plenty of rest
Prevention
• RSV immunoglobulin (RSV-IGIV)-
provides neutralizing antibodies
against RSV
– I V preparation given monthly
– Have number of disadvantages that
have resulted in a decline in its use in
favor of palivizumab.
• Palivizumab- monoclonal antibody
– IM injection, monthly
– does not interfere with immune
response to vaccines, and can be
administered easily, without the need
for hospital admission.
• Handwashing
– Ensure that caregiver are not caring
other high risk patient
– isolate infected patients or nurse in
cohorts based on laboratory
confirmation of RSV stat
– Family members with an upper
respiratory infection should be
especially careful around infants.
– use of gloves, aprons or gowns when in
direct contact with the patient
ASTHMA
Asthma is the number one chronic illness
among school aged children and is the third
leading cause of hospital visits among
children under the age of fifteen. Asthma in
children is a chronic illness that is caused by
a number of different triggers.
 Asthma is a chronic disease that causes
the airways to become sore and swollen. It
is characterized by variable and recurring
symptoms, airflow obstruction, and
bronchospasm.
Types of asthma
• Acute severe asthma
• Refractory asthma
• Corticosteroid-Resistant asthma
• Brittle asthma
• Aspirin-Sensitive asthma
CLASSIFICATION
Asthma is clinically classified according to
the frequency of symptoms, forced
expiratory volume in 1 second (FEV1),
and peak expiratory flow rate.
It may also be classified as:
Atopic – extrinsic
Non-atopic - intrinsic
What causes asthma?
Things that cause asthma are called
triggers.
Allergens - pollens, foods, dust, molds,
feathers or animal dander
Irritants - dirt, cigarette smoke, gases and
air pollution
Odors - household cleaners, perfumes,
paints, varnishes, fabric softeners, laundry
detergents and cooking fumes
Irritants in the workplace - fumes and
vapors from wood products and metals
Metabisulfite - found in dried fruits, fruit
juices, beer, wine, salad bars and
vegetables
Respiratory infections - colds, flu, sore
throat and bronchitis
  Exercise can trigger an early asthmatic
response.
 Emotional stress - excessive fear or
excitement
 Weather conditions - very cold, windy
or sudden changes in the weather
 Medications - aspirin or related drugs,
as well as some drugs used to
treat glaucoma and high blood
pressure
Pathophysiology
Physical assessment
 Difficulty of breathing
 Wheezing
 Decreased O2Sat reading
 Hyperresonant upon percussion
 Expiration phase is longer than
inspiration
 Cyanosis may be present
 Pt is on sitting position
 Shield-like or barrel-shaped chest
 Clubbing of fingers
 Growth restriction
Signs and Symptoms
An acute exacerbation of asthma is
commonly referred to as an asthma attack.
Cardinal signs of asthma attack:
shortness of breath
Wheezing
chest tightness
Signs of asthma in a baby or toddler
include:
• Noisy breathing or breathing
increased 50 percent above normal
• Wheezing or panting with normal
activities
• Interrupted talking
• Pain or tight feeling in the chest
• Flaring of the nostrils when breathing
in
• Hyperinflation (appearance of
hunched shoulders, hunching forward
or preferring not to lie down)
• Lethargy, disinterest in normal or
favorite activities
• Difficulty sucking or eating
• Crying sounds softer, different
Diagnosis
• Diagnosing asthma in very young
children is difficult.
• To help the pediatrician make a correct
diagnosis, parents must provide
information about family history of
asthma or allergies, the child's overall
behavior, breathing patterns and
responses to foods or possible allergy
triggers.
• Lung function tests - often used to make
a definitive asthma diagnosis.
• Blood tests, allergy testing and x-rays
may be done to gather additional
information.
• The basic measurement is peak flow
rates and the following diagnostic
criteria:
 ≥20% difference on at least three
days in a week for at least two weeks;
 ≥20% improvement of peak flow
following treatment, for example:
 10 minutes of inhaled β-agonist
(e.g., salbutamol);
 six weeks of inhaled corticosteroid
(e.g., beclometasone)
 14 days of 30 mg prednisolone.
 ≥20% decrease in peak flow following
exposure to a trigger (e.g., exercise).
Peak expiratory flow rate monitoring
1. Place the indicator on the apparatus
at the bottom of the numbered scale.
2. Take a deep breath.
3. Place the meter in the mouth and
blows out as hard and as fast as
possible.
4. Repeat 2 or more times and record
the highest number achieved.
“ZONES” – rate of expiratory
compliance
• Green zone – 80%-100% of their personal
best; No asthma symptoms are present
• Yellow zone – 50%-80% of their personal
best; An episode of asthma may be
beginning
• Red zone – below 50%; Indicates an
asthma episode is beginning
Medical Management
Pharmacology
Medications used to treat asthma are
divided into two general classes:
• quick-relief medications used
to treat acute symptoms
• long-term control
medications
Babies or toddlers can use most
medications used for older children and
adults. The dosage is lower.
Medications to treat asthma symptoms in
infants and toddlers are usually given in a
tasty liquid form or with a nebulizer.
Fast acting
Short-acting - selective beta2-adrenoceptor
agonists,
salbutamol (albuterol USAN), levalbuterol, ter
butaline, ventolin and bitolterol
• Tremors, the major side effect, have
been greatly reduced by inhaled
delivery. There may also be cardiac side
effects at higher doses (due to Beta-1
agonist activity), such as elevated heart
rate or blood pressure.
• However, levalbuterol has been
shown to have fewer cardiac side effects
and significantly more anti-inflammatory
effects on bronchial smooth muscle.
• Older, less selective adrenergic
agonists, such as
inhaled epinephrine and ephedrine table
ts, have also been used. In
emergencies, these drugs were
sometimes administered by injection.
• Anticholinergic medications, such
as ipratropium bromide may be used
instead. They have no cardiac side
effects and thus can be used in patients
with heart disease.
Long term control
 Inhaled glucocorticoids are usually
considered preventive medications
while oral glucocorticoids are often
used to supplement treatment of a
severe attack.
 Long-acting β2-agonists (LABA) are
similar in structure to short-acting
selective beta2-adrenoceptor agonists,
but have much longer side chains
resulting in a 12-hour effect.
Prevention
The only preventive agent known is allergen
immunotherapy. Controller medications
include the following:
 Inhaled glucocorticoids such
as beclomethasone normally come as
inhalers. Deposition of steroids in the
mouth may result in oral thrush.
Deposition near the vocal cords can
cause hoarse voice. (rinse mouth after
inhaler use or by using a spacer)
 Leukotriene modifiers such
as montelukast provide both anti-
spasm and anti-inflammatory effects.
 Mast cell stabilizers such as
(cromoglicate (cromolyn),
and nedocromil). These medications
are believed to prevent the initiation of
the allergy reaction, by stabilizing the
mast cell.
 Methylxanthines
(theophylline and aminophylline).
These agents are bronchodilators with
minimal anti-inflammatory effect.
 Antihistamines are often used to treat
the nasal allergies which can
accompany asthma.
  Asthmatic patients should avoid the
triggers as part of their preventive
measures.
• Concentrate on the bedroom, where
very young children spend as much
as 12-18 hours each day.
• Cover the pillows, mattress and box
springs in allergen-proof casings.
• Wash bed linens weekly in 130-
degree water. Use washable area
carpets.
• Buy only washable stuffed animals.
• Vacuum weekly or more. Don't allow
pets in the bedroom/house.
• Restrict smoking in the house (even
if someone smokes in the basement
of a multi-storied house, smoke
filters through the vents to all parts
of the house).
Can a child “out-grow” asthma?
Approximately 50 percent of children with
asthma appear to outgrow asthma when they
reach adolescence. Once someone develops
sensitive airways, they remain that way for
life, although asthma symptoms can vary
through the years. As a child's airways
mature, they are able to handle airway
inflammation and irritants better, so their
asthma symptoms may notably decrease.
About half of those children find their asthma
symptoms reappear in varying degrees when
they reach their late thirties or early forties.
Status Asthmaticus
- Children who continue to display
respiratory problems despite vigorous
therapeutic measures.
- May develop gradually or rapidly or
with complications such as pneumonia
- Is a medical emergency that can result
in respiratory failure and death if
untreated.
CYSTIC FIBROSIS - is an autosomal
recessive disorder affecting the exocrine
glands, in which their secretions become
abnormally viscous and liable to obstruct
glandular ducts.
 It primarily affects pulmonary and GI
function.
 The average life expectancy for the
cystic fibrosis patient is currently age 30
to 40.
 Death may occur because of respiratory
infection and failure.
 Other complications include esophageal
varices, diabetes, chronic sinusitis,
pancreatitis, rectal polyps,
intussusceptions, growth retardation,
and infertility.
OTHER NAMES
 CF
 Cystic fibrosis of the pancreas
 Fibrocystic disease of the pancreas
 Mucoviscidosis
 Mucoviscidosis of the pancreas
 Pancreas fibrocystic disease
 Pancreatic cystic fibrosis
PATHOPHYSIOLOGY
 A defective gene that leads to the
making of an abnormal protein.
àCFTR (cystic fibrosis transmembrane
regulator)
 Abnormal movement of sodium and
chloride in the body's cells.
 Leads to thicker secretions
 Exocrine glands become obstructed
 Appear histologically abnormal and
produce excessive secretions
(tracheobronchial and Brunner's
glands)
 Appear histologically normal but
secrete excessive Na and Cl (sweat,
parotid, and small salivary glands)
Assessment:
 Usually present before age 6 months
but severity varies and may present
later.
 Meconium ileus is found in neonate.
 usually present with respiratory
symptoms, chronic cough, and
wheezing.
 Parents may report salty taste when
skin is kissed.
 Recurrent pulmonary infections.
 Failure to gain weight or grow in the
presence of a good appetite.
 Frequent, bulky, and foul smelling stools
(steatorrhea)
 Protuberant abdomen, pot belly
 Bleeding disorders
 Clubbing of fingers in older child.
 Hyperglycemia, glucosuria with polyuria,
and weight loss.
 Sterility in males.
Diagnostic Evaluation:
 Sweat chloride test measures sodium
and chloride level in sweat.
 Chloride level of more than 60 mEq/L is
virtually diagnostic.
 Chloride level of 40 to 60 mEq/L is
borderline and should be repeated.
 Duodenal secretions: low trypsin
concentration is virtually diagnostic.
Nursing Interventions:
 Stool analysis:
 Reduced trypsin and chymotrypsin
levels-used for initial screening for
cystic fibrosis.
 Increased stool fat concentration.
 BMC ( Boehringer-Mannheim Corp.)
meconium strip test for stool includes
lactose and protein content; used for
screening.
 Chest X-ray may be normal initially;
later shows increased areas of infection,
over inflation, bronchial thickening and
plugging, atelectasis, and fibrosis.
 Pulmonary function studies (after age 4)
show decreased vital capacity and flow
rates
 Diagnosis is made when a positive
sweat test is seen
 Genetic screening may be done for
affected families.
Pharmacologic Interventions:
 Antimicrobial therapy as indicated for
pulmonary infection.
 Oral or I.V. antibiotics as required.
 Inhaled antibiotics, such as gentamicin
or tobramycin, may be used for severe
lung disease or colonization of
organisms.
 Bronchodilators to increase airway size
and assist in mucus clearance.
 Pulmozyme recombinant human DNase
(an enzyme) administered via
nebulization to decrease viscosity of
secretions.
 Pancreatic enzyme supplements with
each feeding.
 Favored preparation is pancrelipase.
 Occasionally, antacid is helpful to
improve tolerance of enzymes.
 Favorable response to enzymes is
based on tolerance of fatty foods,
decreased stool frequency, absence of
steatorrhea, improved appetite, and
lack of abdominal pain.
 Gene therapy, in which recombinant
DNA containing a corrected gene
sequence is introduced into the
diseased lung tissue by nebulization, is
in clinical trials.
 Monitor weight at least weekly to assess
effectiveness of nutritional
interventions.
 Monitor respiratory status and sputum
production, to evaluate response to
respiratory care measures.
 To promote airway clearance, employ
intermittent aerosol therapy three to
four times per day when the child is
symptomatic.
 Perform chest physical therapy three to
four times per day after aerosol therapy.
 Suction the infant or young child when
necessary, if not able to cough.
 Teach the child breathing exercises
using pursed lips to increase duration of
exhalation.
 Provide good skin care and position
changes to prevent skin breakdown in
malnourished child.
 Provide frequent mouth care to reduce
chances of infection because mucus is
present.
 Restrict contact with people with
respiratory infection.
 Encourage diet composed of foods high
in calories and protein and moderate to
high in fat because absorption of food is
incomplete.
 Administer fat-soluble vitamins, as
prescribed, to counteract
malabsorption.
 Provide opportunities for parents to
learn all aspects of care for the child.
  Teach the parents about dietary
regimen and special need for calories,
fat, and vitamins.
 Discuss need for salt replacement,
especially on hot summer days or when
fever, vomiting, and diarrhea occur.
 Increase salt intake during hot weather,
fever, or excessive exercise to prevent
sodium depletion and cardiovascular
compromise.
TONSILS
Overview:
 Masses of lymphoid tissue located in
the pharyngeal cavity.
Function:
 Filter and protect the respiratory and
alimentary tracts from invasion by
pathogenic organisms and play a role
in antibody formation.
TONSILLECTOMY
 Surgical removal of one or both
tonsils, usually through a sharp wire
loop, scalpel, or electrocauterization.
 Performed under general anesthesia
either as an outpatient or with
overnight observation.
 Surgery takes 30-45 minutes
 Children remain at the hospital 2-4
hours after outpatient surgery or
overnight for observation.
Indications:
 Recurrent attacks of tonsillitis
 More than 7 times a year for one
year
 More than 5 times a year for 2
years
 More than 3 times a year for 3
years
 Peritonsillar abscess
 In children – done 4-6 weeks
after resolution of a peritonsillar
abscess
 In adults – done after the second
attack of peritonsillar abscess
 Enlarged tonsil causing obstructive
symptoms
 Difficulty in respiration
 Difficulty in swallowing
 Difficulty in speaking
Contraindications:
 Cleft palate
o Tonsils help prevent air escape
during speech
 Acute infection at the time of
surgery
Pre-Operative Care:
 Take a complete history with special
attention given to allergy symptoms,
difficulty swallowing, or airway
obstruction.
 Assess the child for any signs of
active infection and redness and
exudate of the throat.
 Review laboratory results
( Prothrombin time, PTT, platelet
count, Hgb, Hct).
 Check the child for loose teeth to
decrease the risk for aspiration
during the surgery.
 Explain the need for surgery in a
simple and nonthreatening manner.
 Have a calming and reassurig
attitude to ease the child’s anxiety.
 Let the child have a visit to the
surgical facility/hospital several days
in advance.
 Reassures the child that talking will
not be a problem after surgery.
 Instruct the patient to have nothing
by mouth for 6 hours prior to the
time of surgery.
Post – Operative Care:
 Assess the child for any excessive
swallowing, elevated pulse,
decreasing blood pressure, signs of
fresh bleeding in the back of the
throat and restlessness that does not
seem to be associated with the pain
which are an indicator of
postoperative bleeding.
 Place the child in a prone or side-
lying position.
 If bleeding occurs, turned the child to
the side and then notify the
physician.
 Provide clear, cool liquids when the
child is fully awake.
 If vomiting occurs, keep the child on
NPO status for 30 mins. and then
resume clear liquids.
 Use acetaminophen for pain relief.
Do not use aspirin or any medicine
containing aspirin.
 An ice collar can be applied for
comfort.
 Avoid giving milk and milk products. CLEFT LIP/PALATE
 Discourage the child from coughing, • are facial malformations that occur
clearing the throat or gargling. during embryonic development and are
the most common congenital deformity
 Encourage abundant liquid intake.
of the head and neck
Avoid citrus juices for 10 days.
 Avoid red liquids, which will give the • may appear separately or together
appearance of blood if the child WHAT’S THEIR DIFFERENCE?
vomits. CLEFT LIP
- results from failure of the maxillary and
 Add full liquids on the second day
median nasal processes to fuse
and soft foods as the child tolerates
(bet. 5&8wks of IU life)
them.
CLEFT PALATE
 Avoid rough or scratchy foods - is a midline fissure of the palate that
(bacon, chips, popcorn), citrus foods results from the failure of the 2 slides to
or spicy foods for 3 weeks. fuse
Before discharge, instruct the (9-12wks of IU life)
parents to:
CLEFTS….
 Encourage the child to chew and
• CL may vary from small notch to a
swallow. complete cleft; deformed dental
 Not to give the child any straws, structures
forks or sharp pointed toys that could • CP occurs in midline and may involve soft
be put in the mouth. & hard palate
 Call the physician for any bleeding, • When associated, may involve the
persistent earache, or fever greater midline & extend into the soft & hard
than 101 F (38.8 C). palates
 Child may return to school when • UNILATERAL OR BILATERAL
directed by the physician, usually in
about 10 days.
 Bring the child for a follow-up
appointment in 1-2 weeks.
ITS OCCURRENCE….
• CL/P is more common the CP
 • 60%-80% are male
• Females have a higher isolated clefts of
the 20 palate
• 86% in palatal; 68% unilateral CL assoc.
w/ palatal
DIAGNOSTIC TESTS:
• Thorough assessment of the mouth
• Prenatal: soft tissues of the face is
visualized until 13-14wks
• CL/P assoc with other structural
anomalies : 100%
• CL/P: 50% with CP
WHAT ARE THE CAUSES?
• Hereditary
• Environmental
• Teratogenic (phenytoin, smoking)
PATHOPHYSIOLOGY
Risk Factors:
Modifiable: teratogens and environment
Non-modifiable: environment
↓Genetic defects in cell migration
↓If tongue( separates the lip &palate) fails
to descend
↓Delay in merging of the upper lip @ the
midline (bet. 7th&11th wk IUL)
↓Delay in fusion of hard& soft palate (bet.
7th&12th wk IUL
↓Failure of the maxillary & premaxillary
processes to come together bet. 3rd&12th
wk of IUL
↓Palate /lip never fuses
↓Cleft lip/palate
MEDICAL & SURGICAL MNGT.
• Surgical Correction: CL
– Cheiloplasty (lip surgery)
(done @1-2mos)
– Tennison-Randall triangular flap
– Millard rotational advancement tech
• Surgical Correction: CP
– Palatoplasty (done 6-18mos)
NURSING MNGT.
• Pre-op:
– Feed infant in upright position, slowly &
burp frequently
– Use ESSR; (1) enlarged nipple
(2)stimulate sucking reflex (3)swallow
fluid appropriately (4)rest when infant
signals w/ facial expression
– Using special or modified nipples
• Post-op:
– Avoid oral thermometers
– Elbow restraints
– No straws, pacifiers, spoon or fork in and
around the mouth for 7-10days
– Place infants in side-lying position
– Stay in place while feeding
– Provide comfort to prevent crying
– Clean the suture lines w/ sterile H20 or
saline q after feeding
– Elbows may be restrained until palate is
healed (4-6wks)
– Teach parents to remove restraints q
2hrs
– Oral packing secured to the palate
(removed after 2-3d)
– Opiods may be given
– Acetaminophen
– Clear liquids then blenderized or soft diet
– Long term: good mouth care
Proper brushing defects
HIRSCHSPRUNG DISEASE
- also known as congenital aganglionic
megacolon
- mechanical obstruction caused by
inadequate motility of part of the
intestine
- congenital absence of or arrested
development of parasympathetic
ganglion cells in the intestinal wall,
usually in the distal colon
- four times more common in males than
in females
- usually isolated birth defect but has been
associated with other syndromes
including Down Syndrome
PATHOPHYSIOLOGY
During normal development, neuroblasts
will be found in the small intestine by the
7th week of gestation and will reach the
colon by the 12th week
↓In hirschsprung disease, there is a defect
in the migration of these neuroblasts
down their path to the distal intestine
↓Causes an abnormal migration of the
precursor ganglion cells
↓These ganglia control both the
contraction and relaxation of smooth
muscles in the intestine
↓There’s an impaired colonization of
ganglion cells in the distal portion of the
GI tract resulting in aganglionosis
↓Contraction and relaxation is absent in
the intestine
↓Lack of enervation produces the
functional defect that results in the
absence of propulsive movements
(peristalsis)
↓No peristaltic waves that move fecal
material throughout
↓Stool accumulates with the distention of
the bowel proximal to the defect
(megacolon)
↓The internal sphincter fails to relax
because the ganglion segment is missing
the inhibitory neurotransmitter, nitric
oxide
↓The result is an obstruction because the
evacuation of stool, gas, and liquid is
prevented
↓Intestinal distention and ischemia may
also occur as a result of distention of the
bowel wall
↓This contributes to the development of
enterocolitis (inflammation of the small
bowel and colon)
Clinical Manifestations
 Newborn period: anorexia, poor
feeding
 Infancy
o failure to thrive
o constipation
o abdominal distention
o episodes of diarrhea and
vomiting (including bile)
o signs of enterocolitis
o explosive, watery diarrhea
o fever
o appears significantly ill
 Childhood (symptoms may appear
more chronic)
o constipation
o stool appears ribbon like, fluid
like, or in pellet form
o abdominal distention
o visible peristalsis
o easily palpable fecal mass
o undernourished anemic
appearance
DiagnosticTests
Rectal examination
demonstrate absence of fecal
material in the long segment disease;
in short segment disease, rectal
impaction may be present and, when
the finger is removed, it may cause a
rush of stool as the obstruction is
temporary relieved
Abdominal x-ray
severe gaseous distention of the
bowel, with absence of gas in the
rectum; this may indicate a bowel
blockage
this study only allows physicians to
suspect the diagnosis, not
definitively diagnose it
Barium Enema
Barium, a chalky liquid, is inserted
through the anus into the colon, and
coats the inside of the colon. When
an x-ray of the abdomen is taken,
this part lights up. If hirschsprung
disease is present, a “transition
zone” may be apparent. In the
segment without nerve cells, the
colon will appear to be of normal size
or somewhat constricted. In the area
above, however, the colon will
appear dilated. The stool that cannot
be passed backs up and the colon is
stretched and enlarged. Visualizing
the funnel-like transition zone is a
clue that the individual may have
hirschsprung disease.
This is the most valuable radiologic
study for establishing the diagnosis.
Rectal Biopsy
-definitive diagnosis of hirschsprung
disease
-Involves removing a small piece of
tissue from the rectum. Doctor
examine the tissue sample under a
microscope and look for the presence
of ganglion cells (nerve cells). If no
nerve cells are visualized,
Hirschsprung disease is diagnosed.
In infants, a suction rectal biopsy can
be done at the bedside. Since there
are no sensory nerves at the site of
biopsy, this is not painful. When a
suction biopsy is inconclusive,
surgical biopsy is performed under
 general anesthesia in the operating
room.
Anorectal monometry
this determines whether normal
reflexes involving the rectum and the
anus are present. Used only in older
children, the test can be performed
at the bedside.
Ultrasonogram
may be done to demonstrate dilated
colon
Therapeutic Interventions
• Enema or colonic irrigation with
physiologic saline solution.
• Older child whose symptoms are chronic
but not severe may be treated with
isotonic enemas, stool softeners, and a
low residue diet.
Surgical Interventions
• Initially, a colostomy or ileostomy is
performed to decompress intestine,
divert fecal stream, and rest the normal
bowel. Created proximal to the
aganglionic segment to relieve
obstruction and allow the normally
enervated and dilated bowel to return to
its normal size
• Definitive surgery is done to remove the
non-functioning bowel segment with
various pull-through procedures
(abdominoperineal, endorectal, or
rectorectal).
• Complete corrective surgery is performed
usually when the child weighs
approximately 9 kilograms (20 pounds)
• The various surgical procedures that can
be performed are the Swenson,
Duhamel, Boley, and Soave procedures
• Swenson Procedure
– the original pull-through procedure
used to treat Hirschsprung disease
– the aganglionic segment is resected
down to the sigmoid colon and the
remaining rectum, and an oblique
anastamosis is performed between
the normal colon and low rectum.
• Duhamel procedure
- was first described in 1956 as a
modification to the Swenson
procedure
- Key points are that a retrorectal
approach is used and a significant
portion of aganglionic rectum is
retained
- The aganglionic bowel is resected
down to the rectum, and the rectum
is oversewn. The proximal bowel is
then brought through the retrorectal
space and an end-to-side
anastomosis is performed on the
remaining rectum
• Soave (endorectal) procedure
- was introduced in 1960’s and
consist of removing the mucosa and
submucosa of the rectum and pulling
the ganglionic bowel through the
aganglionic muscular cuff of the
rectum.
- the original operation did not
include a formal anastomosis, relying
on scar tissue formation between the
pull-through segment and the
surrounding aganglionic bowel. The
procedure has since been modified
by Boley to include a primary
anastomosis of the anus.
PRE-OPERATIVE CARE
1. Assist in emptying the bowel by giving
repeated enemas and colonic irrigations.
2. If abdominal distention is not relieved by
enemas, discomfort is significant, and
rectal tube insertion fails to give relief,
consult doctor for a nasogastric (NG) tube.
3. Offer pacifier for infant to suck if on
parenteral fluids.
4. Encourage parents to hold and rock the
infant.
5. Maintain position of comfort with head
elevated. Offer soothing stimulation (eg.
music, touch, play therapy).
6. Offer small frequent feedings. Low
residue diet will aid in keeping the stool
soft.
7. Administer parenteral nutrition if feeding
causes additional discomfort because of
distention and nausea.
8. For older child, provide demonstration
and written and verbal instruction to family
for saline enema administration and use of
stool softeners.
Enterocolitis -Most serious complication of
Hirschsprung disease.
Emergency preooperative care:
1. Monitor V/S and blood pressure for
signs of shock
2. Monitor fluid and electrolyte
replacements, as well as plasma or other
blood derivatives
3. Observing for symptoms of bowel
perforation such as fever, increasing
abdominal distention, vomiting,
increased tenderness, irritability,
dyspnea and cyanosis.
– Because, progressive distention of the
abdomen is a serious sign, the nurse
measures the abdominal circumference
with a paper tape measure, usually at
the level of the umbilicus or the widest
part of the abdomen.
Possible Complications:
• Inflammation and infection of the
intestines may occur before surgery, and
sometimes during the first 1-2 years
afterwards. Symptoms are severe,
including swelling of the abdomen, foul-
smelling watery diarrhea,lethargy and
poor feeding.
• Perforation or rupture of the intestine
• Short bowel syndrome
POSTOPERATIVE CARE
1. Change wound dressing using sterile
technique.
2. Prevent wound contamination from
diaper.
To prevent contamination of the
abdominal wound with urine in the
infant, the diaper should be pinned
below the dressing. Sometimes, a Foley
catheter is used in the immediate
postoperative period to divert the flow
of urine away from the abdomen.
3. Prevent perianal and anal excoriation by
thorough cleaning and use of ointments
after the infant soils (postoperative stools
can number 7 to 10 per day).
4. Use careful handwashing technique.
5. Report any wound redness, swelling or
drainage, evisceration, or dehiscence
immediately.
6. Suction oral secretions frequently to
prevent infection of the tracheobronchial
tree and lungs.
7. In older child, encourage frequent
coughing and deep breathing to maintain
respiratory status.
8. Allow the infant to cry for a short period
to prevent atelectasis.
9. Change position of infant frequently to
increase circulation and allow for aeration
of all lung areas.
10. Maintain patency of NG tube
immediately postoperatively.
11. Maintain NPO status until bowel sounds
return and the bowel is ready for feedings
as determined by the physician.
12. Provide frequent oral hygiene while on
NPO status.
13. Administer fluids to maintain hydration
and replace lost electrolytes. Begin oral
feedings as ordered.
14. Support the parents when teaching
them to care for their child’s colostomy.
Reassure parents that colostomy will not
cause delay in the child’s normal
development.
15. Involve the entire family in
teaching colostomy care to enhance
acceptance of body change of the child.
Assess stoma:
• Red in color (fully blood vessels)
• Moist (with mucous membranes
for lubrication)
• May bleed ( numerous large
vessels)
INTUSSUSCEPTION
-a condition in which one part of the
intestine becomes pushed into the lumen
of an adjoining segment
-invagination of one portion of the
intestine into another
INTUSSUSCEPTUM -the telescoping
PROXIMAL portion of the bowel
INTUSSUSCIPENS -the adjacent DISTAL
bowel
Medical Management
• Initial treatment of choice: NONSURGICAL
HYDROSTATIC REDUCTION
• BARIUM ENEMA-diagnostic and
therapeutic
Contraindicated: Perforation
• Water-soluble Contrast and Air
Pressure/Enema
• Carbon Dioxide Pressure
• SONOGRAM-preferred means of
diagnosis
• IV fluids, NGT decompression, Antibiotic
therapy may be used
Surgical Management
-if enema was unsuccessful
-pts who show signs of shock or peritonitis
-symptoms presented longer than 24 hrs
-manually reducing the invagination
-LAPAROTOMY – for multiple recurrences
-resection of any nonviable intestine
Nursing Management
– LISTEN to the parents’ description of the
child’s physical and behavioral symptoms
– Explain to the parents the need for
immediate hospitalization. Offer
emotional support: parents are
unprepared
– Observe/ monitor stools - normal BROWN
stool indicates that the intussusception
has reduced itself
– Monitor v/s. Infants may become
hypothermic at the onset of infection;
↑Temp: sepsis, ↑PR and dec BP:
peritonitis
Post-procedural care:
– Monitor v/s
– Check for the return of the bowel sounds
– Monitor pt who has undergone
hydrostatic reduction for passage of
stools and barium or water-soluble
contrast material
Pre-operative care:
– Maintain NPO status as ordered
– Routine laboratoy testing (CBC and UA)
– PARENTAL CONSENT
– Preanesthetic sedation
Post-operative care:
– Monitor V/S
– Check dressings and the return of bowel
sounds. Provide meticulous wound care.
– Preserve the parent-child relationship by
encouraging rooming-in or extended
visiting
– Parents’ reactions must be understood
and accepted
CELIAC DISEASE
o “Celiac sprue”, “Gluten-induced/sensitive
enteropathy”
o permanent intestinal intolerance to
gluten
o malabsorption syndrome
o 2nd to cystic fibrosis as a cause of
malabsorption in children
o More prevalent in women than in men
o More common among Caucasians
o It may occur in adults but usually affects
children, bet. ages 9 & 18 mos.
o primarily a childhood disorder
o More common among relatives,
especially siblings
Etiology
 Exact cause: Unknown
Genetic
Immunologic factors
Pathophysiology
Diagnostic Exam
*The major pathophysiologic char. of the
dse. are atrophy of villi in the upper small
intestine & malabsorption of nutrients.
Clinical Manifestation
• Diarrhea
• Abdominal pain
• Distended abdomen/protuberant
abdomen
• Steatorrhea
• Pale, foul-smelling bowel stools
• Mm wasting, weakness
• Athralgia/Bone pain
• Easy bruising, Bleeding problems
• Anemia, Smooth, red tongue
• Hypoprothrombinemia
• Hypomagnesemia & Hypocalcemia
S/Sx
- Irritability
- Tremor
- Convulsions
- Tetany
- Bone pain
- Osteomalacia
- Dental abnormalities
• Dermatitis herpetiformis
Intestinal biopsy
- confirmative test
- Serology
- detect antibodies to connective
tissue (endomysium & reticulin) &
gliadin
 Antireticulin Antibodies (ARA),IgA & IgG
 Antiendomysial Antibodies (EMA), IgA &
IgG
 Antigliadin antibodies (AGA), IgA & IgG
 The autoantibodies of IgA antireticulin
& antiendomysial IgA are more specific
markers for active celiac dse. than
circulating IgA antigliadin antibodies,
w/c may be present in other dses. &
conditions.
 Anti-tissue Transglutaminase Antibody
(tTG), IgA
- a more specific test recognized by
antiendomysial antibody
- tissue transglutaminase is an enzyme
responsible for linking certain
proteins. It has been identified as the
antigen that the body responds to
when it creates Anti-EMA antibodies.
Gliadin a peptide derivative of gluten,
triggers the dev’t. of tTG
autoantibodies. Although “tssue” is in
 the name of this autiantibody, it
nevertheless involves testing blood
NOT tissue.
Treatment
- Lifelong elimination of gluten
What is gluten?
- the protein component of cereal grains.
- each type of protein is slightly different
from the others. Gliadin in wheat,
hordein in barley, secalin in rye, avenin
in oats, zein in corn & oryzenin in rice.
- It is important to note that the gluten
found in corn & rice does not cause harm
to those w/ Celiac dse.
- Gluten-containing foods: “BROW”
• B arley
• R ye
• O ats
• W heat
Gluten-free foods: corn, potatoes, rice,
soybean flour
Gluten-free diet: ↑-calorie, ↑-protein,
↓-carbohydrate,↓-fat
Avoid foods containing “vegetable protein”
- In some children, who have more severe
mucosal damage, disaccharide digestion
is impaired, esp. LACTOSE. Therefore,
LACTOSE-FREE DIET is recommended,
w/c necessitates elimination all milk
products.
Supplemental Tx include: Vit. D, Iron,
Vit.B12, Folic acid
Nursing interventions:
 Observe pt.’s nutritional status &
progree by daily calorie counts & wt.
checks.
 Assess fluid status: record intake, urine
output, & # of stools. Watch for signs
of DHN, i.e., dry skin & mucous
membranes & poor skin turgor.
 Check serum electrolyte levels. Watch
for signs of hypokalemia (weakness,
lethargy, rapid pulse, & diarrhea), &
low Ca levels (mm twitching & tetany).
 Monitor PT & Hgb & Hct. Protect pt.
from bleeding & bruising. Administer
Vit.K, iron,folic acid, & Vit.B12 as
ordered. If pt. can tolerate iron, give it
bet. meals, when absorption is best.
 Provide a gluten-free diet.
 Assess the pt.’s acceptance &
understanding of the dse. & encourage
pt. to participate in a local Celiac dse.
support group.
 Six (6) key elements:
 C onsultation with a skilled dietitian
 E ducation about the disease
 L ifelong adherence to gluten-free
diet
 I dentification & tx of nutritional
deficiencies
 A ccess to an advocacy group
 C ontinuous long-term ff-up by a
multidisciplinary team
POISONING
Poison – either ingested, inhaled or
absorbed in the body injures the body by
its chemical action
Goals:
1. to remove poison before absorbed
2. to provided supportive care (i.e. vital
organs)
3. to administer antidotes to neutralize
the poison
4. to implement treatment that hastens
elimination of absorbed poison
Common accident in infants – falls
Common accident in toddlers – poisoning
PRINCIPLES
 Determine the substance taken and
assess LOC
 Unless poisoning was corrosive,
caustic(strong alkali such as lye) or
hydrocarbon = vomiting (most
effective)
 Strong acid or alkali poisoning
(corrosive type)
- dilute with water or milk (120cc [4
ounces])
- do not induce vomiting/do not
neutralize
- airway management(priority)
- e.g. lye, acid
 Syrup of Ipecac – oral antiemetic to
cause vomiting after drug overdose or
poisoning; stimulates vomiting in the
brain
Contraindication of Ipecac or no emetic
induction if:
 comatose victim, in shock, convulsing
or has lost gag reflex
 corrosive ingestion
NSG -> side-lying, sitting or kneeling
position with head below the chest to avoid
aspiration
Ipecac dose:
15 ml – adolescent, school age and
pre-school; repeat dosage once if
vomiting does not occur within 20
minutes
10 ml – infant; do not repeat
Administer with 200-300 cc warm water
 Universal antidote: 1.) activated
charcoal 2.) milk of magnesia 3.)
burned toast
Remember:
 Never administer the charcoal before
ipecac
 Tracheostomy set should always be at
bed side
 Kerosene/Gasoline poisoning: give
mineral oil
 Caustic poisoning (muriatic acid): give
vinegar(low % acidity), don’t induce
emesis, prepare tracheostomy set,
lavage ->cuffed endotracheal tube
TYLENOL POISONING - Causes liver
damage: cell damage, liver dysfunction, liver
failure
PHASES of tylenol poisoning
 Initial phase(>150mg/kg-TOXIC; 2-4
hours after ingestion) - n/v, pallor,
malaise, vomiting, sweating
 Latent phase(24-36 hours) - feel
relatively well, may recover
 Hepatic involvement(may last up to 7
days & be permanent) - RUQ pain,
jaundice, confusion, stupor,
coagulation abdnormalities, hepatic
failure, coma, death
- Monitor for? liver enzymes
- Patients who do not die in hepatic stage
gradually recover
Medical Management
 Induce emesis (NSG! No charcoal if
giving antidote)
 Gastric lavage
 N-acetylcysteine(mucomyst): antidote for
tylenol poisoning
-alters metabolism & decreases liver
damage
-S/E: bad taste and smell->NSG dilute in
juice/soda
-A/E: watch for bronchospasm
ASPIRIN POISONING
S/sx:
 Metabolic acidosis -> lung stimulation ->
blows off excess C02 ->tachypnea-
Kussmaul respirations(initial response)
 Hypoglycemia, thirst
 Loss of fluids/electrolytes – dec Na+, K+
 GI irritation
 Bleeding -> monitor? Bleeding time
 most frequently accidentally ingested by
toddlers
 acute ingestion: 300-500 mg/kg->severe
TOXICITY
 chronic ingestion: >100 mg/kg per day x
2days or more
 requires treatment: 1.5 to 5 grains per
pound
Medical Management/Treatment
 Induce emesis-syrup of Ipecac/lavage
with activated charcoal (important in
early toxicity)(if not in
coma/convulsing)!!!
 Cathartics to speed through GI tract
 Possible dialysis (if unresponsive)
 Fluids->DHN
 Assisted ventilation, PRN
 Seizure precautions
 Administer as ordered: IVF, NaHCO3,
electrolytes, volume expander,
glucose, Vita K, anticonvulsants, O2
Prognosis
 with prompt treatment: GOOD
 if with seizures: POOR
LEAD TOXICITY
Sources: pain, varnish, battery, crayons,
pencil, smoke-belching vehicles via
ingestion or inhalation
Assessment
  beginning symptoms of lethargy -6 doses/day for 7 days: therapy: never as
 impulsiveness and learning difficulty single-agent therapy; with EDTA
 as lead increases, severe  Succimer(Chemet)-19-day tx; may be with
encephalopathy with seizures and food/whole
permanent MR ] All meds S/E: nephrotoxicity
NSG ->force fluids, chelates are excreted
Risk Factors: via kidneys
• Poverty Monitor for? Creatinine levels, BUN
• Age less than 6 years old Prognosis:
• Dwelling in the city Massive amounts: encephalopathy,
What happens in lead toxicity? seizures, coma,possible death
pencil, paint, crayon(lead) ->interferes iron Smaller amounts: risk for neurologic
binding onto heme molecule->destruction impairment
of RBC functioning (releases erythrocyte
protoporphyrin -> hypochromic, microcytic
anemia ->lead competes with Ca ->
destroys bones, teeth & kidneys
->accumulation of NH->destroys
endothelial cells in the brain -> crosses the
blood-brain barrier
->encephalopathy
Diagnostic tests
 Blood smear: >20mcg/dL: acute
poisoning
 Erythrocyte protoporphyrin test N:
<35mcg/100ml blood
 Abdominal x-ray
 Long bones
Medical management
 Remove child from source
 If >20mcg/dL: needs chelation therapy
– removes lead from body by binding
with lead & excreted via kidneys
 If >45mcg/dL, CaNa2EDTA/EDTA and
Succimer are used
 If >70mcg/dL, British Anti-Lewisite is
used with EDTA
MEDS:
 Calcium disodium
edetate(CaNa2EDTA/EDTA) po: for
>20mcg/dL lead in blood -helps excrete
in urine 20-50 times the normal rate
-inject procaine with drug/site rotation
-give DEEP IM or IV
!!! MIO, U/A ->nsg: maintain OIF
 Dimercaprol(BAL ‘British Anti-Lewisite
Calcium’ in peanut oil)
NSG -> do not give if allergic to peanuts;
DEEP IM