NR 602 / NR602 MIDTERM EXAM 2022 – 100% CORRECT AND VERIFIED

1. Chalazion
Chalazion is a chronic sterile inflammation of the eyelid resulting from a lipogranuloma of the meibomian
glands that line the posterior margins of the eyelids (see Fig. 29-7). It is deeper in the eyelid tissue than a
hordeolum and may result from an internal hordeolum or retained lipid granular secretions.
Clinical Findings
Initially, mild erythema and slight swelling of the involved eyelid are seen. After a few days the inflammation resolves, and a slow growing,
round, nonpigmented, painless (key finding) mass remains. It may persist for a long time and is a commonly acquired lid lesion seen in
children (see Fig. 29-7).
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Management
• Acute lesions are treated with hot compresses.
• Refer to an ophthalmologist for surgical incision or topical intralesional corticosteroid injections if the condition is unresolved or if the
lesion causes cosmetic concerns. A chalazion can distort vision by causing astigmatism as a result of pressure on the orbit.
Complications
Recurrence is common. Fragile, vascular granulation tissue called pyogenic granuloma that enlarges and bleeds rapidly can occur if a
chalazion breaks through the conjunctival surface.
Blepharitis
Blepharitis is an acute or chronic inflammation of the eyelash follicles or meibomian sebaceous glands of the eyelids (or both). It is usually
bilateral. There may be a history of contact lens wear or physical contact with another symptomatic person. It is commonly caused by
contaminated makeup or contact lens solution. Poor hygiene, tear deficiency, rosacea, and seborrheic dermatitis of the scalp and face are also
possible etiologic factors. The ulcerative form of blepharitis is usually caused by S. aureus. Nonulcerative blepharitis is occasionally seen in
children with psoriasis, seborrhea, eczema, allergies, lice infestation, or in children with trisomy 21.
Clinical Findings
• Swelling and erythema of the eyelid margins and palpebral conjunctiva
726
• Flaky, scaly debris over eyelid margins on awakening; presence of lice
• Gritty, burning feeling in eyes
• Mild bulbar conjunctival injection
• Ulcerative form: Hard scales at the base of the lashes (if the crust is removed, ulceration is seen at the hair follicles, the lashes fall out, and
an associated conjunctivitis is present)
Differential Diagnosis
Pediculosis of the eyelashes.
Management
Explain to the patient that this may be chronic or relapsing. Instructions for the patient include:
• Scrub the eyelashes and eyelids with a cotton-tipped applicator containing a weak (50%) solution of no-tears shampoo to maintain proper
hygiene and debride the scales.
• Use warm compresses for 5 to 10 minutes at a time two to four times a day and wipe away lid debris.
• At times antistaphylococcal antibiotic (e.g., erythromycin 0.5% ophthalmic ointment) is used until symptoms subside and for at least 1 week
thereafter. Ointment is preferable to eye drops because of increased duration of contact with the ocular tissue. Azithromycin 1% ophthalmic
solution for 4 weeks may also be used (Shtein, 2014).
• Treat associated seborrhea, psoriasis, eczema, or allergies as indicated.
• Remove contact lenses and wear eyeglasses for the duration of the treatment period. Sterilize or clean lenses before reinserting.
• Purchase new eye makeup; minimize use of mascara and eyeliner.
• Use artificial tears for patients with inadequate tear pools.
Chronic staphylococcal blepharitis and meibomian keratoconjunctivitis respond to oral erythromycin. Doxycycline, tetracycline, or
minocycline can be used chronically in children older than 8 years old.

2. Acute Otitis Media
AOM is an acute infection of the middle ear (Fig. 30-4). The AAP Clinical Practice Guideline requires the
presence of the following three components to diagnose AOM (Lieberthal et al, 2013):
• Recent, abrupt onset of signs and symptoms of middle ear inflammation and effusion (ear pain, irritability,
otorrhea, and/or fever)
• MEE as confirmed by bulging TM, limited or absent mobility by pneumatic otoscopy, air-fluid level behind
TM, and/or otorrhea
• Signs and symptoms of middle ear inflammation as confirmed by distinct erythema of the TM or onset of ear
pain (holding, tugging, rubbing of the ear in a nonverbal manner)
Characteristics of different types of AOM are defined in Table 30-4. AOM often follows eustachian tube dys-
function (ETD). Common causes of ETD include upper respiratory infections, allergies, and ETS. ETD leads
to 746functional eustachian tube obstruction and inflammation that decreases the protective ciliary action in
the eustachian tube. When the eustachian tube is obstructed, negative pressure develops as air is absorbed in
the middle ear (see Fig. 30-4). The negative pressure pulls fluid from the mucosal lining and causes an
accumulation of sterile fluid. Bacteria pulled in from the eustachian tube lead to the accumulation of purulent
fluid. Young children have shorter, more horizontal and more flaccid eustachian tubes that are easily disrupted
by viruses, which predisposes them to AOM. Respiratory syncytial virus and influenza are two of the viruses
most responsible for the increase in the incidence of AOM seen from January to April. Other risk factors
associated with AOM are listed in Boxes 30-1 and 30-2.
S. pneumoniae, nontypeable Haemophilus influenzae, Moraxella catarrhalis, and S. pyogenes (group A
streptococci) are the most common infecting organisms in AOM (Conover, 2013). S. pneumoniaecontinues to
be the most common bacteria responsible for AOM. The strains of S. pneumoniae in the heptavalent
pneumococcal conjugate vaccine (PCV7) have virtually disappeared from the middle ear fluid of children with
AOM (Lieberthal et al, 2013). With the introduction of the 13-valent S. pneumoniae vaccine, the bacteriology of
the middle ear is likely to continue to evolve. Bullous myringitis is almost always caused by S. pneumonia.
Nontypeable H. influenza remains a common cause of AOM. It is the most common cause of bilateral otitis
media, severe inflammation of the TM, and otitis-conjunctivitis syndrome. M. catarrhalis obtained from the
nasopharynx has become increasingly more beta-lactamase positive, but the high rate of clinical resolution in
children with AOM from M. catarrhalis makes amoxicillin a good choice for initial therapy (Lieberthal et al,
2013). M. catarrhalis rarely causes invasive disease. S. pyogenes is responsible for AOM in older children, is
responsible for more TM ruptures, and is more likely to cause mastoiditis.
Although a virus is usually the initial causative factor in AOM, strict diagnostic criteria, careful specimen
handling, and sensitive microbiologic techniques have shown that the majority of AOM is caused by bacteria or
bacteria and virus together (Lieberthal et al, 2013).
Clinical Findings
History
Rapid onset of signs and symptoms:
• Ear pain with possible ear pulling in the infant; may interfere with activity and/or sleep
• Irritability in an infant or toddler
• Otorrhea
• Fever
Other key factors or symptoms:
• Prematurity
• Craniofacial anomalies or congenital syndromes associated with craniofacial anomalies
• Exposure to risk factors
• Disrupted sleep or inability to sleep
• Lethargy, dizziness, tinnitus, and unsteady gait
• Diarrhea and vomiting
• Sudden hearing loss
• Stuffy nose, rhinorrhea, and sneezing
• Rare facial palsy and ataxia
Physical Examination
• Presence of MEE, confirmed by pneumatic otoscopy, tympanometry, or acoustic reflectometry, as evidenced by:
• Bulging TM (see Fig. 30-4)
• Decreased translucency of TM

3. • Absent or decreased mobility of the TM
• Air-fluid level behind the TM
• Otorrhea
747
• Signs and symptoms of middle ear inflammation indicated by either:
• Erythema of the TM (Amber is usually seen in otitis media with effusion [OME]; white or yellow may be seen in either AOM or OME
[Shaikh et al, 2010
].)
or
• Distinct otalgia that interferes with normal activity or sleep
• In addition, the following TM findings may be present:
• Increased vascularity with obscured or absent landmarks (see Fig. 30-4).
• Red, yellow, or purple TM (Redness alone should not be used to diagnose AOM, especially in a crying child.)
• Thin-walled, sagging bullae filled with straw-colored fluid seen with bullous myringitis
Diagnostic Studies
Pneumatic otoscopy is the simplest and most efficient way to diagnose AOM. Tympanometry reflects effusion (type B pattern).
Tympanocentesis to identify the infecting organism is helpful in the treatment of infants younger than 2 months old. In older infants and
children, tympanocentesis is rarely done and is useful only if the patient is toxic or immunocompromised or in the presence of resistant
infection or acute pain from bullous myringitis. If a tympanocentesis is warranted, refer the patient to an otolaryngologist for this procedure.
Differential Diagnosis
OME, mastoiditis, dental abscess, sinusitis, lymphadenitis, parotitis, peritonsillar abscess, trauma, ETD, impacted teeth, temporomandibular
joint dysfunction, and immune deficiency are differential diagnoses. Any infant 2 months old or younger with AOM should be evaluated for
fever without focus and not just treated for an ear infection.
Management
Many changes have been made in the treatment of AOM because of the increasing rate of antibiotic-resistant bacteria related to the
injudicious use of antibiotics. Ample evidence has been presented that symptom management may be all that is required in children with
MEE without other symptoms of AOM (Lieberthal et al, 2013
). Treatment guidelines are decided based on the child's age, illness severity,
and the certainty of diagnosis. Table 30-5 shows the recommendation for the diagnosis and subsequent treatment of AOM.
1. Pain management is the first principle of treatment.
• Weight-appropriate doses of ibuprofen or acetaminophen should be encouraged to decrease discomfort and fever.
• Topical analgesics, such as benzocaine or antipyrine/benzocaine otic preparations, can be added to systemic pain management if the
TM is known to be intact. Topical analgesics should not be used alone.
• Distraction, oil application, or external use of heat or cold may be of some use.
2. Antibiotics are also effective. (Table 30-6 lists dosage recommendations.)
• Amoxicillin remains the first-line antibiotic for AOM if there has not been a previous treated AOM in the previous 30 days, there is
no conjunctivitis, and no penicillin allergy (Lieberthal et al, 2013
). Beta-lactam coverage (amoxicillin/clavulanate, third-
generation cephalosporin) is recommended when the child has been treated with amoxicillin in the previous 30 days, there is an
allergy to penicillin, and the child has concurrent conjunctivitis or has recurrent otitis that has not responded to amoxicillin. If
there is a documented hypersensitivity reaction to amoxicillin, the following antibiotics are acceptable, follow the non-type 1
hypersensitivity and type 1 hypersensitivity recommendations in Table 30-6:
• Ceftriaxone may be effective for the vomiting child, the child unable to tolerate oral medications, or the child who has failed
amoxicillin/clavulanate.
748
• Clindamycin may be considered for ceftriaxone failure but should only be used if susceptibilities are known.
• Prophylactic antibiotics for chronic or recurrent AOM are not recommended.
3. Observation or “watchful waiting” for 48 to 72 hours (see Table 30-5) allows the patient to improve without antibiotic treatment. Pain
relief should be provided, and a means of follow-up must be in place. Options for follow-up include:
• Parent-initiated visit or phone call for worsening or no improvement
• Scheduled follow-up appointment
• Routine follow-up phone call
• Given a prescription to be started if the child's symptoms do not improve or if they worsen in 48 to 72 hours (Table 30-7)
• Communication with the parent, reevaluation, and the ability to obtain medication must be in place.
4. Recommendations for follow-up include:
• After 48 to 72 hours if a child has not showed improvement in ear symptomatology, the child should be seen to confirm or exclude
the presence of AOM. If the initial management option was an antibacterial agent, the agent should be changed.
Prevention and Education
The following interventions, shown to be helpful in preventing AOM, should be encouraged:
• Exclusive breastfeeding until at least 6 months of age seems to be protective against AOM

4. • Avoid bottle propping, feeding infants lying down, and passive smoke exposure
• Avoid the use of pacifiers: Although the relationship cannot be fully explained, multiple studies have shown
that pacifier use increases the incidence of AOM (Lieberthal et al, 2013).
• Pneumococcal vaccine; specifically PCV13, which contains subtype 19A
• Annual influenza vaccine may help prevent otitis media
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• Xylitol liquid or chewing gum as tolerated
• Choose licensed day care facilities with fewer children
• Educate regarding the problem of drug-resistant bacteria and the need to avoid the use of antibiotics unless
absolutely necessary; if antibiotics are used, the child needs to complete the entire course of the prescription
and follow up if symptoms do not resolve
Conjunctivitis
An estimated 6 million cases of bacterial conjunctivitis occur in the United States annually, at an estimated
cost of $377 million to $857 million (Azari and Barney, 2013). Conjunctivitis is an inflammation of the palpebral
and occasionally the bulbar conjunctiva (Fig. 29-5). It is the most frequently seen ocular disorder in pediatric
practice. In pediatric patients, bacteria are the most common cause of infection (50% to 75%) most commonly
from December to April. Pathogens include H. influenzae, Streptococcus pneumoniae, and Moraxella species
with both gram-negative and gram-positive organisms implicated (Azari and Barney, 2013).
Conjunctivitis also occurs as a viral or fungal infection or as a response to allergens or chemical irritants.
Bacterial conjunctivitis is often unilateral, whereas viral conjunctivitis is most often bilateral. Unilateral
disease can also suggest a toxic, chemical, mechanical, or lacrimal cause. Blockage of the tear drainage system
(e.g., from meibomianitis or blepharitis), injury, foreign body, abrasion or ulcers, keratitis, iritis, herpes simplex
virus (HSV), and infantile glaucoma are other known causes. Patient age is a major indicator of etiology (Table
29-6).
Types of Conjunctivitis
Type Incidence/Etiology Clinical Findings Diagnosis Management*
Ophthalmia
neonatorum
Neonates: Chlamydia trachomatis,
Staphylococcus aureus, Neisseria
gonorrhoeae, HSV (silver nitrate
reaction occurs in 10% of neonates)
Erythema,
chemosis,
purulent
exudate
with N.
gonorrhoeae;
clear to
mucoid
exudate with
chlamydia
Culture (ELISA, PCR),
Gram stain, R/O N.
gonorrhoeae,chlamydia
Saline irrigation to eyes
until exudate gone;
follow with
erythromycin ointment
For N.
gonorrhoeae:ceftriaxone
or IM or IV
For chlamydia:
erythromycin or possibly
azithromycin PO
For HSV: antivirals IV or
PO
Bacterial
conjunctivitis
In neonates 5 to 14 days old, preschoolers,
and sexually active teens: Haemophilus
influenzae(nontypeable), Streptococcus
pneumoniae, S. aureus, N.
gonorrhoeae
Erythema,
chemosis,
itching,
burning,
mucopurulent
exudate,
matter in
eyelashes; ↑
in winter
Cultures (required in
neonate); Gram stain
(optional); chocolate
agar (for N.
gonorrhoeae) R/O
pharyngitis, N.
gonorrhoeae, AOM,
URI, seborrhea
Neonates: Erythromycin
0.5% ophthalmic
ointment
≥1 year old: Fourth-
generation
fluoroquinolone
For concurrent AOM: Treat
accordingly for AOM
Warm soaks to eyes three
times a day until clear
No sharing towels, pillows
No school until treatment
begins
Chronic bacterial
conjunctivitis
(unresponsive
conjunctivitis
previously
School-age children and teens: Bacteria,
viruses, C. trachomatis
Same as above;
foreign body
sensation
Cultures, Gram stain; R/O
dacryostenosis,
blepharitis, corneal
ulcers, trachoma
Depends on prior
treatment, laboratory
results, and differential
diagnoses
Review compliance and
prior drug choices of
conjunctivitis treatment

5. Type Incidence/Etiology Clinical Findings Diagnosis Management*
treated as
bacterial in
etiology)
Consult with
ophthalmologist
Inclusion
conjunctivitis
Neonates 5 to 14 days old and sexually
active teens: C. trachomatis
Erythema,
chemosis,
clear or
mucoid
exudate,
palpebral
follicles
Cultures (ELISA, PCR), R/O
sexual activity
Neonates: Erythromycin or
azithromycin PO
Adolescents: Doxycycline,
azithromycin, EES,
erythromycin base,
levofloxacin PO
Viral conjunctivitis Adenovirus 3, 4, 7; HSV, herpes zoster,
varicella
Erythema,
chemosis,
tearing
(bilateral);
HSV and
herpes zoster:
unilateral
with
photophobia,
fever; zoster:
nose lesion;
spring and
fall
Cultures, R/O corneal
infiltration
Refer to ophthalmologist if
HSV or photophobia
present
Cool compresses three or
four times a day
Allergic and vernal
conjunctivitis
Atopy sufferers, seasonal Stringy, mucoid
exudate,
swollen
eyelids and
conjunctivae,
itching (key
finding),
tearing,
palpebral
follicles,
headache,
rhinitis
Eosinophils in conjunctival
scrapings
Naphazoline/pheniramine,
naphazoline/antazoline
ophthalmic solution (see
text)
Mast cell stabilizer (see
text)
Refer to allergist if needed
Otitis Externa
Otitis externa (OE), commonly called swimmer's ear, is a diffuse inflammation of the EAC and can involve the
pinna or TM. Inflammation is evidenced as (1) simple infection with edema, discharge, and erythema; (2)
furuncles or small abscesses that form in hair follicles; or (3) impetigo or infection of the superficial layers of
the epidermis. OE can also be classified as mycotic otitis externa, caused by fungus, or as chronic external
otitis, a diffuse low-grade infection of the EAC. Severe infection or systemic infection can be seen in children
who have diabetes mellitus, are immunocompromised, or have received head and neck irradiation.
OE results when the protective barriers in the EAC are damaged by mechanical or chemical mechanisms.
OE is most frequently caused by retained moisture in the EAC, which changes the usually acidic environment
to a neutral or basic environment, thereby promoting bacterial or fungal growth. Chlorine in swimming pools
adds to the 743problem because it kills the normal ear flora, allowing the growth of pathogens. Regular
cleaning of the EAC removes cerumen, which is an important barrier to water and infection. Soapy deposits,

6. alkaline drops, debris from skin conditions, local trauma, sweating, allergy, stress, and hearing aids can also be
responsible for causing OE (Rosenfeld et al, 2014).
OE is most often caused by Pseudomonas aeruginosa and Staphylococcus aureus, but it is not uncommon for
the infection to be polymicrobial. Furunculosis of the external canal is generally caused by S.
aureus and Streptococcus pyogenes. Otomycosis is caused by Aspergillus or Candida and can be the result of
systemic or topical antibiotics or steroids. Otomycosis is also more common in children with diabetes mellitus
or immune dysfunction and in these cases is most commonly caused by Aspergillus niger, Escherichia
coli, or Klebsiella pneumonia. Group B streptococci are a more common cause in neonates.
Long-standing ear drainage may suggest a foreign body, chronic middle ear pathology (such as, a
cholesteatoma), or granulomatous tissue. Bloody drainage may indicate trauma, severe otitis media, or
granulation tissue. Chronic or recurrent OE may result from eczema, seborrhea, or psoriasis. Eczematous
dermatitis, moist vesicles, and pustules are seen in acute infection, whereas crusting is more consistent with
chronic infection.
Clinical Findings
History
The following can be found:
• Itching and irritation
• Pain that seems disproportionate to what is seen on examination
• Pressure and fullness in ear and occasionally hearing loss that can be conductive or sensorineural
• Rare hearing loss and otorrhea or systemic complaints and symptoms
• Sagging of the superior canal, periauricular edema, and preauricular and postauricular lymphadenopathy with more severe disease
Extension to the surrounding soft tissue results in the obstruction of the canal with or without cellulitis.
Physical Examination
Findings on physical examination can include the following:
• Pain, often quite severe, with movement of the tragus (when pushed) or pinna (when pulled) or on attempts to examine the ear with an
otoscope
• Swollen EAC with debris, making visualization of the TM difficult or impossible
• Rare otorrhea
• Occasional regional lymphadenopathy
• Tragal tenderness with a red, raised area of induration that can be deep and diffuse or superficial and pointing, which is characteristic of
furunculosis
• Red, crusty, or pustular spreading lesions
• Pruritus associated with thick otorrhea that can be black, gray, blue-green, yellow, or white, and black spots over the TM are indicative of
mycotic infection
• Dry-appearing canal with some atrophy or thinning of the canal and virtually no cerumen visible with chronic OE
• Presence of pressure-equalizing tube or perforation of TM
Diagnostic Studies
Culturing the discharge from the ear is not customary but may be indicated if clinical improvement is not seen during or after treatment,
severe pain persists, the child is a neonate, the child is immunocompromised, or chronic or recurrent OE is suspected. Culturing requires a
swab premoistened with sterile nonbacteriostatic saline or water.
Differential Diagnosis
AOM with perforation, TTO, chronic suppurative otitis media (CSOM), necrotizing OE, cholesteatoma, mastoiditis, posterior auricular
lymphadenopathy, dental infection, and eczema are all possible differential diagnoses.
Management
The following steps outline the management of OE:
• Eardrops are the mainstay of therapy for OE (see Table 30-3). Eardrops containing acetic acid or antibiotic with and without corticosteroid
drops are the treatment of choice for OE. Symptoms should be markedly improved within 7 days, but resolution of the infection may take
up to 2 weeks. Drops should be used until all symptoms have resolved. Ototoxic drugs should not be used if there is a risk of TM
perforation.

7. • Antibiotic agents should be chosen based on efficacy, resistance patterns, low incidence of adverse effects, cost, and likelihood of
compliance. Neomycin, polymyxin, or hydrocortisone drops should not be used if the TM is not intact, because these drugs are
known to cause damage to the cochlea (Rosenfeld et al, 2014
).
• The quinolone products are effective against Pseudomonas, S. aureus, and Streptococcus pneumoniae, which may be a factor if the OE
is a complication of AOM.
• Systemic antibiotics should not be used unless there is extension of infection beyond the ear or host factors that require more systemic
treatment (severe OE, systemic illness, fever, lymphadenitis, or failed topical treatment).
• Treatment for OE must include thorough parent education regarding the instillation of otic drops so that they are effective in eradicating
infection. The drops should be administered with the child lying down with the affected ear upward. Drops should run into the EAC until it
is filled. Move the pinna in a to-and-fro movement or pump the tragus to remove any trapped air and ensure filling (Rosenfeld et al, 2014
).
The child should remain lying down for 3 to 5 minutes, leaving the ear open to the air.
744
• If the infection is severe and not improving in the first 5 to 7 days, aural irrigation with water, saline, or hydrogen peroxide may be tried, or
refer to the otolaryngologist for débridement and suction.
• If significant swelling is present, inserting a wick into the EAC is helpful. A wick made of compressed cellulose, hydrogel polymer
(Merocel XL), or gauze (0.25 inch) usually works well. The tip of the wick is lubricated with water or saline just before insertion into the
ear. Once in place, the wick should be impregnated with antibiotics for as long as it remains in the auditory canal. (This may require
reapplication of drops every 2 to 3 hours.) Wicks are usually removed after several days. The wick will fall out when the swelling has
subsided, and treatment with direct application of drops to the ear canal should continue for the entire course.
• Avoid cleaning, manipulating, and getting water into the ear. Swimming is prohibited during acute infection.
• Administer analgesics for pain. Narcotic analgesics may be necessary for severe pain but are only indicated for short-term use.
• Débridement with a cotton-tipped applicator, self-made cotton wick, or calcium alginate swabs is indicated once the inflammatory process
has subsided and can enhance the effectiveness of the ototopical antibiotic drops. Lance a furuncle that is superficial and pointed with a 14-
gauge needle. If it is deep and diffuse, a heating pad or warm oil-based drops can speed resolution.
• If impetigo is present, clear the canal by using water or an antiseptic solution followed by a warm-water rinse. Apply an antibiotic ointment
(mupirocin) twice a day for 5 to 7 days. There is increasing resistance to mupirocin, and retapamulin might be necessary in children over 9
months of age (Bangert et al, 2012
; Drucker, 2012). The child should avoid touching the ear. Fingernails should be short, and hands should
be cleansed with soap and water. Systemic antibiotics are generally unnecessary.
• Fungal OE is uncommon in primary OE. Fungal OE is more likely related to chronic OE or following treatment with topical and/or systemic
antibiotics. Aspergillus and Candida species are most commonly seen in mycotic OE (Rosenfeld et al, 2014
). Treatment consists of
antifungal solutions, such as clotrimazole-miconazole, nystatin, or other antifungal agents, including gentian violet and thimerosal 1 : 1000.
• The canal should be cleansed with a 5% boric acid in ethanol solution prior to antifungal solution.
If the child is not improved within 72 hours (relief of otalgia, itching, and fullness), recheck to confirm diagnosis. Lack of improvement
may be due to obstructed ear canal, foreign body, poor adherence, or contact sensitivity among other things. A follow-up visit may be
necessary after 1 to 2 weeks for reevaluation of the OE and removal of debris. If symptoms are worsening or there is no improvement in a
week, a referral to an otolaryngologist or dermatologist is indicated.
Complications
Infection of surrounding tissues with impetigo, irritated furunculosis, and malignant OE with progression and necrosis caused
by Pseudomonas are possible complications. Involvement of the parotid gland, mastoid bone, and infratemporal fossa is rare (Rosenfeld et al,
2014).
Prevention
The patient should be instructed to do the following:
• Avoid water in the ear canals.
• Use well-fitting earplugs for swimming especially in “dirty water.”
• Use alcohol vinegar otic mix (two parts rubbing alcohol, one part white vinegar, and one part distilled water) 3 to 5 drops daily, especially
after swimming or bathing, to prevent the recurrence of OE (Waitzman, 2015).
• Use a blow dryer on warm setting to dry the EAC.
• Avoid persistent scratching or cleaning of the external canal.
• Avoid prolonged use of ceruminolytic agents.
Hand-foot-mouth disease: This is a clinical entity evidenced by fever, vesicular eruptions in the oropharynx
that may ulcerate, and a maculopapular rash involving the hands and feet. The rash evolves to vesicles,
especially on the dorsa of the hands and the soles of the feet, and lasts 1 to 2 weeks (Fig. 24-1).

8. Pharyngiti
s
Acetaminophen or ibuprofen
Antibiotics if GABHS
Saltwater gargles
Anesthetic lozenges for older
child
Streptococcal Disease
Streptococci are gram-positive spherical cocci that are broadly classified based on their ability to hemolyze RBCs. Complete hemolysis is
known as beta-hemolytic. Partial hemolysis is alpha-hemolytic; non-hemolysis is gamma-hemolytic. Cell wall carbohydrate differences
further subdivide the streptococci. These differences are identified as Lancefield antigen subgroups A-H and K-V. Subgroups A-H and K-O
are associated with human disease. Group A beta-hemolytic streptococcus is the most virulent, although group B beta-hemolytic
streptococcus can cause bacteremia and meningitis in infants younger than 3 months old (rarely older). Group A streptococcus (GAS) are also
subdivided into more than 100 subtypes based upon their M protein antigen located on the cell surface and fimbriae on the cell's 535outer
edge. The virulence of GAS is greatly dependent upon their M protein. If the M protein is present, GAS strains are able to resist
phagocytosis; if the M protein is weak or absent, the strains are basically avirulent (e.g., chronic GAS pharyngeal carriers). GAS also
produces many varieties of enzymes and toxins that may stimulate specific antitoxin antibodies for immunity or serve as evidence of past
infection but not confer immunity. There may also not be cross-immunity between antibodies for different GAS strains (e.g., scarlet fever is
caused by three different pyrogenic exotoxins, so the illness can recur). Some general remarks about specific illnesses due to GAS and non-
group A and B streptococcus infection are discussed in this chapter; cross-references to specific chapters are noted for other GAS caused
infections.
Group A Streptococcus
Streptococcus microbes most commonly invade the respiratory tract, skin, soft tissues, and blood. Transmission is primarily through infected
upper respiratory tract secretions or, secondarily, through skin invasion. Fomites and household pets are not vectors. Food-borne outbreaks
from contamination by food handlers have been reported. Both streptococcus pharyngitis and impetigo are associated with crowding, whether
at home, school, or other institution. Streptococcal pharyngitis is rare in infants and children younger than 3 years old, but the incidence rises
with age and is most common in the winter and early spring in temperate climates when respiratory viruses circulate. Carrier rates in
asymptomatic children are up to 20% (Arnold and Nizet, 2012). By contrast, streptococcus skin infection (impetigo, pyoderma) is more
common in toddlers and preschool-age children. Those at increased risk for invasive GAS are individuals with varicella infection, IV drug
use, HIV, diabetes, chronic heart or lung disease, infants, and older adults.
The incubation period is 2 to 5 days for pharyngitis and 7 to 10 days from skin acquisition to development of impetiginous lesions. In
untreated individuals, the period of communicability is from the onset of symptoms up to a few months. Children are generally considered
non-infectious 24 hours after the start of appropriate antibiotic therapy.
Clinical Findings and Diagnostic Studies
The following may be seen in GAS:
• Respiratory tract infection: Streptococcal tonsillopharyngitis (GABHS) and pneumonia are described in Chapter 32. Peritonsillar abscess,
cervical lymphadenitis, retropharyngeal abscess, otitis media, mastoiditis, and sinusitis symptoms may be clinical features.
• Scarlet fever: This is caused by erythrogenic toxin. It is uncommon in children younger than 3 years old. The incubation period is
approximately 3 days (the range is 1 to 7 days). There is abrupt illness with sore throat, vomiting, headache, chills, and malaise. Fever can
reach 104° F (40° C). Tonsils are erythematous, swollen, and usually covered in exudate. The pharynx also is inflamed and can be covered
with a gray-white exudate. The palate and uvula are erythematous and reddened, and petechiae are present. The tongue is usually coated and
red. Desquamation of the coating leaves prominent papillae (strawberry tongue). The typical scarlatina rash appears 1 to 5 days following
onset of symptoms but may be the presenting symptom. The exanthema is red, blanches to pressure, and is finely papular, making the skin
feel coarse, with a sandpaper feel. The rash generally begins on the neck and spreads to the trunk and extremities becoming generalized
within 24 hours. The face may be spared (cheeks may be reddened with circumoral pallor), but the rash becomes denser on the neck, axilla,
and groin. Pastia lines, transverse linear hyperpigmented areas with tiny petechiae, are seen in the folds of the joints (see Fig. 24-3). In
severe disease, small vesicles (miliary sudamina) can be found on the hands, feet, and abdomen. There is circumoral pallor and the cheeks
are erythematous. The rash begins to fade and desquamate after 3 to 4 days starting on the face and slowly moving to the trunk and
extremities and may include fingernail margins, palms, and soles; this process can take up to 6 weeks. Sore throat and constitutional
symptoms resolve in approximately 5 to 7 days (average 3 to 4 days).
• Bacteremia: This can occur after respiratory (pharyngitis, tonsillitis, AOM) and localized skin infections. Some children have no obvious
source of infection. Meningitis, osteomyelitis, septic arthritis, pyelonephritis, pneumonia, peritonitis, and bacterial endocarditis are rare but
are associated with GAS bacteremia. (Neonatal sepsis due to group B streptococcus is discussed in Chapter 39.)
• Vaginitis and streptococcal toxic shock syndrome (see discussions in Chapter 36).
• Perianal streptococcal cellulitis: Symptoms include local itching, pain, blood-streaked stools, erythema, and proctitis. Fever and systemic
infections are uncommon. Although infection is usually the result of autoinoculation, sexual molestation is in the differential.
• Skin infections (see Chapter 37); rheumatic heart disease (see Chapter 25); and necrotizing fasciitis (see Chapter 37).
Refer to disease-specific chapters for diagnostic studies of disease-specific conditions.

9. Differential Diagnosis, Management, and Complications
Many viral pathogens are on the differential for acute pharyngitis, including influenza, parainfluenza, rhinovirus, coronavirus, adenovirus,
and respiratory syncytial virus. EBV is common and is usually accompanied by other clinical findings (e.g., splenomegaly, generalized
lymphadenopathy). Other causes of bacterial upper respiratory disease include (though rare) diphtheria, tularemia, toxoplasmosis,
mycoplasma, tonsillar TB, salmonellosis, and brucellosis (Gerber, 2011). Staphylococcal impetigo must be differentiated from GABHS
pyoderma. Septicemia, meningitis, osteomyelitis, septic arthritis, pyelonephritis, and bacterial endocarditis can result from other bacteria
causing similar infections.
536
Antimicrobial therapy is recommended for GABHS-caused pharyngitis to decrease the risk of acute rheumatic fever, decrease the length
of the illness, prevent complications, and reduce transmission to others. See appropriate aforementioned site-specific chapters for
recommendations for managing specific infections.
Complications are usually caused by the spread of the disease from the localized infection. Upper respiratory complications include
cervical lymphadenitis, retropharyngeal abscess, otitis media, mastoiditis, and sinusitis if the primary infection is unrecognized or treatment
is inadequate. Acute poststreptococcal glomerulonephritis can occur following skin or upper respiratory GAS infection, whereas acute
rheumatic fever only occurs following GAS URIs. Poststreptococcal reactive arthritis can occur following GAS pharyngitis. Skin infection
with GAS may progress to cellulitis, myositis, or necrotizing fasciitis. Other complications may be associated with invasive infections
including pneumonia, pleural empyema, meningitis, osteomyelitis, and bacterial endocarditis.
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) is a group of neuropsychiatric
disorders thought to result from the production of autoimmune antibodies; these include obsessive-compulsive disorders, tic disorders, and
Tourette syndrome. See Chapter 19 for further discussion.
Non–Group A or B Streptococci
These streptococci or Lancefield groups (principally groups C and G) are associated with invasive disease in all age groups. They may cause
septicemia, UTIs, endocarditis, respiratory disease (upper and lower), skin soft tissue infection, pharyngitis, brain abscesses, and meningitis
in newborns, children, adolescents, and adults. The incubation period and communicability times are unknown. Positive culture from
normally sterile body fluids is adequate for diagnosis. Penicillin G is the drug of choice with modification based on culture sensitivities.
Pneumonia with empyema or abscess may respond slowly despite effective antimicrobial therapy with fevers lasting more than 7 days
(Haslam and St. Geme, 2012).
Kawasaki Disease
KD (also known as mucocutaneous lymph node syndrome or infantile polyarteritis) is the second most
common 563childhood vasculitis with a varying incidence from country to country, with Japan having the
highest incidence of 239.6 per 100,000. The incidence is increasing in Japan, the United Kingdom, and India
(Saundankar et al, 2014). The disease is characterized by an acute generalized systemic medium vessel
vasculitis occurring throughout the body. Although its cause is unknown, it is believed that an infectious agent
activates the immune system in a genetically susceptible host. Genetics may explain the higher incidence in
Asia as well as a higher incidence in children of parents or siblings with a history of the disease. Recent data
suggest T-cell activation plays a role in disease severity and susceptibility (Scuccimarri, 2012).
KD exhibits geographic and seasonal outbreaks, in the late winter and early spring. Person-to-person spread
is low. Referral of these children to a pediatrician is necessary. It is self-limited and the most common cause
of acquired heart disease in children in Japan and the United States (Saundankar et al, 2014). The
EULAR/PReS classification for KD includes a persistent fever for at least 5 days plus four of the following
(Ozen et al, 2010):
• Bilateral conjunctival injection
• Changes of the lips and oral cavity
• Cervical lymphadenopathy
• Polymorphous exanthema
• Changes in the peripheral extremities (swelling of the hands or feet) or perineal area
Clinical Findings
Despite accepted KD guidelines, children can have atypical or incomplete KD with coronary anomalies shown by echocardiogram. Children
younger than 6 to 12 months old may have more atypical findings. In atypical KD, the child may fulfill the criteria but has an additional
feature that is not usually seen in KD. In incomplete KD, the fever may last for 5 days or more, but the child will only meet two or three of
the other criteria. Incomplete KD is more common in children younger than 1 year old and older than 9 years old. Thus, incomplete KD
without nodal involvement is possible. Coronary artery involvement is found more frequently in children with incomplete KD, so based on
the frequency of the disease, an index of suspicion should be maintained in infancy and older school-age children (Scuccimarri, 2012). If KD
is untreated, the normal course of fever is 10 to 14 days.
Other clinical features associated with KD include irritability, aseptic meningitis, mild acute iridocyclitis or anterior uveitis, otitis media
due to inflammation rather than infection of the drum, urethritis, hydrops of the gallbladder, and facial nerve palsy. In children who have

10. received BCG, there may be erythema and induration at the site of injection. Two rare complications are MAS and peripheral gangrene
(Scuccimarri, 2012).
Stage 1: Acute Phase
The acute phase (days 0 to 14) begins with an abrupt onset of high fever (greater than 102.2° F [39° C]) that is unresponsive to antipyretics or
antibiotics. Significant irritability, bilateral nonpurulent conjunctival injection, erythema of the oropharynx, dryness and fissuring of the lips,
“strawberry tongue,” cervical lymphadenopathy, a polymorphous rash, erythema of the urethral meatus, tachycardia, and edema of the
extremities are typically noted. During the acute phase, there may be pericardial, myocardial, endocardial, and coronary artery inflammation.
The child typically is tachycardic and has a hyperdynamic precordium with a gallop rhythm and a flow murmur. Rarely, children have low
cardiac output syndrome from poor myocardial function.
Stage 2: Subacute Phase
The subacute phase (2 to 4 weeks after illness onset) begins with resolution of the fever and lasts until all other clinical signs have
disappeared. Irritability may be prolonged throughout this phase. Desquamation of the fingers (at the junction of nail tip and digit) occurs
first, followed by desquamation of the toes. Transient jaundice, abnormal liver function tests, arthralgia or arthritis, transient diarrhea,
orchitis, facial palsy, and sensorineural hearing loss may occur. Coronary artery aneurysms appear during this period—more so in untreated
children. Common sites for aneurysms, in order of frequency, are the proximal left anterior descending coronary, proximal right coronary, left
main coronary, left circumflex, and distal right coronary artery.
Stage 3: Convalescent Phase
During the convalescent phase, all clinical signs of KD have resolved, but laboratory values may not have returned to normal. This phase is
complete when all blood values are normal (6 to 8 weeks from onset). However, nail changes including Beau lines (deep transverse grooves
across the nails) may be seen (Scuccimari, 2012).
Although some researchers note a chronic phase lasting from 40 days to years after illness onset, this phase is not present in all patients.
Although coronary complications, if present, can persist into adulthood, a recent study of 564 patients with KD revealed a low incidence of
side effects in children who were followed to 21 years of age (Holve et al, 2014
).
Diagnostic Studies
KD is a diagnosis of exclusion. Results of lab investigations are not diagnostic but rather help rule in other diagnoses. Although the acute
phase reactants (ESR and CRP) are usually increased, they may be normal early in the course of the illness. A CBC may show an increased
WBC with a predominance of neutrophils with toxic granulation. Anemia may follow with prolonged inflammation. A marked
thrombocytosis with values greater than 1 million follow in the second week of illness in the subacute phase. The comprehensive metabolic
profile may show an increase in serum transaminases and hypoalbuminemia. Sterile pyuria may occur. Leukopenia and thrombocytopenia
in 564KD may occur in association with the life-threatening MAS.
• Stage 1 is typified by an elevated ESR and platelet count (as high as 700,000/mm3
), elevated CRP, leukocytosis with left shift, slight
decreases in red blood cells and hemoglobin, hypoalbuminemia, increased α2-globulin, and sterile pyuria. The platelet count may be initially
normal with gradual increase after the seventh day of fever.
• Blood, urine, cerebrospinal fluid, and group A beta-hemolytic streptococci (GABHS) pharyngeal cultures may be indicated given the
symptomatology (to rule out other sources of fever).
• Echocardiograms at acute illness, 2 weeks and 6 to 8 weeks after onset of fever, are performed to evaluate for coronary, myocardial, and
pericardial inflammation. Angiography, MRI, and cardiac stress testing may be considered.
Differential Diagnosis
The differential diagnosis includes viral infections (e.g., measles, adenovirus, EBV, enterovirus, influenza, or roseola) and bacterial infections
(e.g., cervical adenitis, scarlet fever, staphylococcal scalded skin syndrome, toxic shock syndrome, leptospirosis, or Rickettsia illness, such as
Rocky Mountain spotted fever). Immune-mediated diseases may need to be considered and include Steven-Johnson syndrome, serum
sickness, RF, SJIA or other JIA, or connective tissue diseases, such as SLE. Other differential diagnoses include mercury poisoning, or tumor
necrosis factor receptor–associated periodic syndromes, such as hyper IgM syndrome (Scuccimarri, 2012).
Management
• Early diagnosis is essential to prevent aneurysms in the coronary and extraparenchymal muscular arteries. Treatment goals include: (1)
evoking a rapid anti-inflammatory response, (2) preventing coronary thrombosis by inhibiting platelet aggregation, and (3) minimizing
long-term coronary risk factors by exercise, a heart healthy diet, and smoking prevention. The child should be referred for initial treatment
that includes the following medications and agents (Scuccimarri, 2012):
• Intravenous immunoglobulin (IVIG) therapy (a single dose of 2 g/kg over 12 hours, ideally in the first 10 days of the illness) to reduce
the incidence of coronary artery abnormalities. The use of immunoglobulin after the tenth day must be individualized. If a child is
found to have an abnormal echocardiogram, fever, tachycardia, or other signs of inflammation beyond the tenth day, then
immunoglobulin is still indicated. Retreatment with immunoglobulin may be useful for persistent or recurrent fevers.
• High-dose aspirin is given for its anti-inflammatory properties (80 to 100 mg/kg/day in four divided doses—every 6 hours initially)
until afebrile for at least 48 to 72 hours, then lowering the aspirin dose to 3 to 5 mg/kg/day until 6 to 8 weeks and then can

11. discontinue if the echocardiogram is normal. If significant coronary artery abnormalities develop and do not resolve, aspirin or other
antiplatelet therapy is used indefinitely.
• For patients with IVIG-resistant disease as indicated by a persistent fever 48 hours after treatment with IVIG and aspirin, a second
treatment of IVIG at 2 mg/kg over 12 hours is initiated. If this is not successful, then methylprednisone IV at 30 mg/kg over 3 hours
once a day for 1 to 3 days may be initiated. Infliximab 5 mg/kg may also be used. If the patient is still febrile, then the opposite anti-
inflammatory can be used. (Methylprednisone in the infliximab groups, or infliximab in the methylprednisone group.) Other options
include cyclosporine A, methotrexate or cyclophosphamide (Saneeymehri et al, 2015).
• An echocardiogram should be obtained as soon as the diagnosis is established as a baseline study, with subsequent studies at 2 weeks and 6
to 8 weeks after onset of illness. If a child is found to have abnormalities, more frequent evaluations may be indicated.
• All children on chronic aspirin therapy should receive inactivated influenza vaccination. If varicella or influenza develops, aspirin treatment
should be stopped for 6 weeks and another antiplatelet drug substituted to minimize the risk of Reye syndrome.
• Live virus vaccines should be delayed until 11 months after administration of IVIG (AAP Red Book, 2015).
• Children without coronary or cardiac changes should be followed by a cardiologist during the first year after the onset of KD. If there are
no cardiac changes during that first year, then the PCP may follow the patient with no activity restrictions imposed at that point.
• Patients with any range of transient coronary artery dilation (including giant aneurysms) should be followed by a cardiologist for years;
physical activity limitations may be imposed.
• Follow and counsel all KD patients about a heart-healthy diet.
Complications and Prognosis
The acute disease is self-limited; however, during the initial stage (acute phase), inflammation of the arterioles, venules, and capillaries of the
heart occurs and can later progress to coronary artery aneurysm in 15% to 25% of untreated children (less than 5% when treated
appropriately). The process of aneurysm formation and subsequent thrombosis or scarring of the coronary artery may occur as late as 6
months after the initial illness. Other possible complications include recurrence of KD (less than 2%); CHF or massive myocardial infarction;
myocarditis or pericarditis, or both (30%); pericardial effusion; and mitral valve insufficiency. Mortality (1.25%) from KD occurs from
cardiac sequelae 15 to 45 days after onset of fever. Children with coronary dilation or aneurysms (especially those greater than 4 mm) may
have long-term coronary endothelial changes that place the child at risk for early ischemic disease; 565they may also develop dyslipidemias
(Wood and Tulloh, 2009). Studies from Japan raise concern about risk of early atherosclerosis (due to arterial damage, ongoing inflammatory
process, and alteration in lipid profile and other atherosclerosis risk factors) even in children without coronary changes during acute febrile
illness (Fukazawa and Ogawa, 2009).
The risk of coronary aneurysm is reduced in patients older than 1 year old if IVIG is given within 10 days of the illness. Aneurysm
regression occurs in half of all patients who develop them, commonly by 1 year after the illness (80% resolve within 5 years), but vessels do
not dilate normally in response to increased oxygen demand by the myocardium. Prompt treatment of chest pain, dyspnea, extreme lethargy,
or syncope is always warranted. Surgical revascularization and transcatheter revascularization are used for some coronary sequelae of KD
(Wood and Tulloh, 2009).
Acute Rheumatic Fever
ARF is a nonsuppurative complication following a Lancefield GAS pharyngeal infection that results in an autoimmune inflammatory process
involving the joints (polyarthritis), heart (rheumatic heart disease), CNS (Sydenham chorea), and subcutaneous tissue (subcutaneous nodules
and erythema marginatum). Recurrent ARF with its multisystem responses can follow with subsequent GAS pharyngeal infections. Long-
term effects on tissues are generally minimal except for the damage done to cardiac valves that leaves fibrosis and scarring and results in
rheumatic heart disease. ARF is diagnosed based on a set of criteria called the revised Jones criteria (1992). These criteria are used for the
initial attack of ARF. Further modifications of the Jones criteria are used for recurrent ARF.
Clinical Findings and History
The diagnosis of an initial attack of ARF is based on the following revised Jones criteria:
• Evidence of documented (culture, rapid streptococcal antigen test, or ASO titer) GAS pharyngeal infection
• Findings of two major manifestations or one major and two minor manifestations of ARF (Berard, 2012; Burke and Chang, 2014)
Major Manifestations
Children with fewer manifestations can also have ARF. Arthritis of large joints occurs in 65% of cases, carditis
in 50%, chorea in 15% to 30%, cutaneous nodules in 5%, and subcutaneous nodules in less than 7%. There is
some controversy regarding the use of the Jones criteria in developing countries where the ability for
diagnostic testing may be limited; therefore, the World Health Organization (WHO) criteria (Box 25-2) may be
used (Ferrieri, 2002; Seckel and Hoke, 2011).
• Carditis is common (pancarditis, valves, pericardium, myocardium) and can cause chronic, life-threatening
disease (i.e., congestive heart failure [CHF]) with estimates of 30% to 80% of patients with ARF experiencing
carditis; it is more common in younger children than adolescents. The symptoms of carditis may be vague and
insidious with decreased appetite, fatigue, and pains. A high-pitched holosystolic murmur is heard at the apex
with radiation to the infrascapular area, as well as tachycardia and often a gallop rhythm. Mitral and possibly

12. aortic regurgitation occur in 95% of cases, usually within 2 weeks of RF illness. The mitral valve becomes
leaky due to annular dilation and elongation of the chordate that attach leaflets to the left ventricle. With
moderate to severe mitral regurgitation CHF develops; recurrent episodes of RF lead to worsening valve
disease.
• Polyarthritis (migratory and painful) involving large joints and rarely small or unusual joints (e.g., vertebrae);
it is the most common manifestation of ARF.
• Sydenham chorea is uncommon.
560
• Erythema marginatum manifested as pink macules on the trunk and extremities; nonpruritic; this sign is
uncommon.
• Subcutaneous nodules associated with repeated episodes and severe carditis; this sign is uncommon.
Minor Manifestations
• Fever (101° F to 102° F [38.2° C to 38.9° C]), arthralgia, history of ARF
Diagnostic Studies
• Elevated acute-phase reactants (ESR, white blood cells [WBCs], CRP)
• Leukocytosis
• Prolonged PR interval on ECG
Children may be diagnosed with ARF without evidence of a preceding streptococcal infection in the following two situations: (1) a child
with Sydenham chorea or (2) with acquired heart disease (commonly mitral valve regurgitation without a congenitally abnormal or prolapsed
valve) that can only be linked to ARF. Approximately 80% of children with ARF have an elevated ASO titer. A combination of both DNase-B
testing and ASO rising may confirm the recent infection.
Differential Diagnosis
ARF is a clinical diagnosis associated with rising antibody titers. Arthritis and arthralgia can accompany a variety of diseases including JIA;
connective tissue diseases; viral infections, such as parvovirus; inflammatory bowel disease; bacterial infections, such as gonorrhea;
hemophilia; infective endocarditis; and Lyme disease (Berard, 2012). A complete history and physical examination with appropriate
diagnostic testing are critical to establish the diagnosis.
Management
The treatment of ARF includes the following:
• Antibiotic therapy to eradicate GAS infection: Primary prevention requires that a GAS infection be treated within 10 days of onset.
Benzathine penicillin G is the drug of choice unless there is an allergic history; erythromycin is then the drug of choice. Azithromycin and
cephalosporins are also sometimes used (Gerber, 2011). A patient with a history of ARF who has an upper respiratory infection should be
treated for GAS whether or not GAS is recovered as asymptomatic infection can trigger a recurrence.
• Anti-inflammatory therapy: Aspirin can be used for arthritis after the diagnosis is established; it is usually 561given only for 2 weeks and
then tapered. It is also used to treat mild to moderate carditis. Aspirin and steroids provide symptomatic relief but do not prevent the
incidence of chronic heart disease. Steroids have been beneficial in the management of severe carditis, reducing its morbidity and mortality.
The association of Reye syndrome with aspirin use is always a concern and must be addressed with parents. Yearly influenza immunization
is critical for children on aspirin therapy.
• Chest radiographs, ECG, and echocardiography are indicated; carditis usually develops within the first 3 weeks of symptoms.
• Referral for CHF treatment if needed: medical management and or valve replacement.
• Bed rest is generally indicated only for children with CHF. Children with Sydenham chorea may need to be protected from injury until their
choreiform movements are controlled. Steroids in the absence of other symptoms are not useful in the treatment of chorea.
• Children with severe chorea may benefit from the use of antiepileptic agents, such as sodium valproate or carbamazepine.
Prevention of Acute Rheumatic Fever
• Treat GAS pharyngeal infections with appropriate antibiotics. Antibacterial prophylaxis for those with a prior history of ARF is required
because of the greatly increased risk of recurrent ARF with subsequent inadequately treated GAS infections. Intramuscular penicillin G (1.2
million units) is more effective than daily penicillin V (Gerber, 2011) and must be given every 4 weeks (every 28 days) not monthly. It can
be given every 3 weeks in high-risk children.
• Antibacterial secondary prophylaxis with penicillin is given every 4 weeks for 5 years after the last ARF episode in children without carditis
or until 21 years old (whichever is longer). For those with carditis and persistent myocardial or valvular disease, treatment is 10 or more
years and may be lifelong (Gerber, 2011). In the majority of patients, valvular disease will resolve if they are compliant in taking antibiotic
prophylaxis after the first episode of rheumatic heart disease.
Complications

13. Chronic CHF can occur after an initial episode of ARF or follow recurrent episodes of ARF. Residual valvular damage is responsible for
CHF. The risk of significant cardiac disease increases dramatically with each subsequent episode of ARF; thus prevention of subsequent GAS
infections is critical. Engagement in the follow-up is essential to prevent the need for cardiac valvular repair.
Bronchiolitis
Bronchiolitis is also called infectious asthma, asthmatic bronchitis, wheezy bronchitis, or virus-induced
asthma. Bronchiolitis is a disease that causes inflammation, necrosis, and edema of the respiratory epithelial
cells in the lining of small airways, as well as copious mucus production (Ralston et al, 2014). Bronchiolitis is
characterized by the insidious onset of URI symptoms over 2 to 3 days that progresses to lower respiratory
symptoms that last as long as 10 days (Da Dalt et al, 2013). It is a communicable disease found primarily in
infancy to 2 years old (Teshome et al, 2013) that accounts for 10% of visits to a primary provider the first 2
years of life (Schroeder and Mansbach, 2014). Bronchiolitis is a common diagnosis used for an infant seen with
wheezing for the very first time and is the leading cause of hospitalizations for infants. The most common age
for severe disease occurs in infants between 2 to 3 months due to the natural postnatal nadir in maternal
immunoglobulins received via the placenta during the last trimester (Da Dalt et al, 2013). More than 80% of
the cases of bronchiolitis occur in infants younger than 1 year of age with a male-to-female ratio of 1.5 : 1
(Welliver, 2009). In mild cases, symptoms can last for 1 to 3 days. In severe cases, cyanosis, air hunger,
retractions, and nasal flaring with symptoms of severe respiratory distress within a few hours may be seen.
Apnea can occur with a wide range of prevalence reported (Ralston et al, 2014) and may require mechanical
ventilation.
Newer understanding of the pathophysiology in bronchiolitis points to airway obstruction as a result of
epithelial and inflammatory cellular debris due to infiltration of the virus into the small bronchiole epithelium
and alveolar epithelial cells (AEC), types I and II. Membranous pneumatoceles, or AEC type I, are dominant
and cover 96% of the respiratory tree. Their role is in gas exchange, whereas AEC type II are important to
surfactant production (Chuquimia et al, 2013). It is a disease of the small bronchioles that are 2 mm in size.
There is a sparing of basal cells in the bronchiole. The main lesion is epithelial necrosis, which leads to a dense
plugging of the bronchial lining. This results in increased airway resistance, atelectasis, hyperinflation, and
increased mucus production (Teshome et al, 2013).
Bronchiolitis is a viral illness predominantly caused by RSV, especially in outbreaks (Da Dalt et al,
2013; Welliver, 2009). Recent data suggest that up to 30% of infants with severe bronchiolitis are co-infected
with two or more viruses (Mansbach et al, 2012). In descending order after RSV, rhinovirus, parainfluenza,
adenovirus, and mycoplasma are causes (Teshome et al, 2013). Metapneumovirus was discovered in 2001 and
is a cause of bronchiolitis 7% of the time. Human bocavirus is a common co-infecting virus with RSV and is
found up to 80% of the time (Teshome et al, 2013). RSV-specific immunoglobulin E (IgE), eosinophils, and
chemokines may play a role in the pathogenesis of bronchiolitis (Welliver, 2009). Adenovirus and RSV can
cause long-term complications. The incubation period for RSV is 2 to 8 days and typically occurs from
November through March with virtually no outbreaks in the summer (Teshome et al, 2013; Welliver, 2009).
Fever tends to be higher with adenovirus versus RSV (Teshome et al, 2013).
Respiratory viruses are spread by close contact with infected respiratory secretions or fomites and can live
on 818surfaces for up to 30 minutes (Teshome et al, 2013). The most frequent mode of transmission is hand
carriage of contaminated secretion. The source of infection is an older child or adult family member with a
“mild” URI. Older children and adults have larger airways and tolerate the swelling associated with this
infection better than infants do. Most cases of bronchiolitis resolve completely, but recurrence of infection is
common, and symptoms tend to be mild.
Infants who are at higher risk of severe RSV include children with major chronic pulmonary disease, such as
CF, neuromuscular disorders, or bronchopulmonary dysplasia; premature birth before 35 weeks of gestational
age; and infants with significant hemodynamically difficulties due to congenital heart disease (Teshome et al,
2013). Other risk factors for severe RSV disease are male gender, crowded household, lack of breastfeeding,
smoke exposure, day care attendance, having siblings, birth during the winter months, and immunodeficiency
(Da Dalt et al, 2013).
Clinical Findings
History
The following are reported:
• Initial presentation: Typically the illness begins with URI symptoms of cough, coryza, and rhinorrhea and progresses over 3 to 7 days
(Smith, 2011).
• Gradual development of respiratory distress marked by noisy, raspy breathing with audible expiratory wheezing.
• Low-grade to moderate fever up to 102° F (38.9° C).
• Decrease in appetite.
• No prodrome in some infants; rather they have apnea as the initial symptom.

14. • Usually the patient's course is the worst by 48 to 72 hours after the wheezing starts and then the patient starts to improve. If the child has a
bacterial illness, the child will continue to worsen with a high fever.
Physical Examination
Findings include the following:
• Upper respiratory findings
• Coryza
• Mild conjunctivitis in 33% (Welliver, 2009)
• Pharyngitis
• Otitis media in up to 15% (Welliver, 2009)
• Lower respiratory findings (Teshome et al, 2013
)
• Tachypnea (approximately 40 to 80 breaths per minute)
• Substernal and/or intercostal retractions
• Heterophonous expiratory wheezing
• Fine or coarse crackles may be heard throughout the breathing cycle
• Varying signs of respiratory distress and pulmonary involvement (e.g., nasal flaring, grunting, retractions, cyanosis, prolonged
expiration)
• Abdominal distention
• Palpable liver and spleen, pushed down by hyperinflated lungs and a flattened diaphragm
Diagnostic Studies
A diagnosis of bronchiolitis should be based on the history and physical examination (Ralston et al, 2014
). Overuse of diagnostic testing
persists in clinical practice despite available guidelines on the diagnosis and management of bronchiolitis (Librizzi et al, 2014
; Ralston et al,
2014; Turner et al, 2014
). The routine use of chest radiographs in previously healthy infants with mild RSV bronchiolitis is not indicated.
Evidence-based guidelines from the AAP and the Scottish Intercollegiate Guidelines Network (SIGN) are strongly against routine chest
radiography, including those in previously healthy infants with mild RSV bronchiolitis (Ralston et al, 2014
; SIGN, 2006). In severe illness, a
chest x-ray may be ordered to rule out pneumonia or pneumothorax, but its use must be weighed against the dangers of radiation exposure.
The findings of chest radiography can vary, and even with severe illness the x-ray can be clear with a flattened diaphragm and an increase in
anteroposterior diameter. Areas of atelectasis can appear like a pneumonitis, but true pneumonia is uncommon (early bacterial pneumonia can
be difficult to detect and cannot be ruled out by radiographs).
Routine virologic testing is not recommended. In selected situations (hospitalization or if an infant has received monthly palivizumab
[Synagis]), enzyme-linked immunosorbent assays or fluorescent antibody techniques to look for RSV are the diagnostic procedures of choice
in most laboratories. Viral culture of nasal washings can be done in severe cases to confirm RSV, parainfluenza viruses, influenza viruses, and
adenoviruses. PCR is helpful in deciding about isolation of cohorts with the same infection in the hospital setting. The cost of the diagnostic
viral testing may outweigh the clinical usefulness of knowing which virus is infecting the patient.
Hematologic testing is not recommended in the latest guidelines. If a CBC is done for another reason, a mild leukocytosis may be seen
with 12,000 to 16,000/mm3
. Routine laboratory tests are usually not required to confirm the diagnosis, because they lack specificity.
However, young infants pose a diagnostic dilemma, because they are at greater risk of a serious bacterial infection (SBI) and, therefore, blood
cultures and CBC with differential are done with a higher rate of antibiotic use in infants who had these blood tests (Librizzi et al, 2014
).
Urine cultures actually have a higher rate of positive results in the young febrile infant (up to 2.3% in a bronchiolitis study conducted by
Librizzi and colleagues).
Differential Diagnosis
The diagnosis of bronchiolitis can be confused with asthma, but there are some differences that may be helpful. Asthma is an acute process
due to airway hyperreactivity and inflammation, whereas the onset of bronchiolitis is insidious. The response to the usual asthma therapies of
beta agonist and 819steroids is poor in infants with bronchiolitis. In contrast, certain viral illnesses in young children can induce wheezing
that will respond to a β-agonist with good results.
FB aspiration is discussed in greater detail later in this chapter, but this is usually a toddler with a history of choking who then develops
focal areas of wheezing. Although children with congestive heart failure can wheeze, they also show symptoms of sweating and the signs of
failure to thrive with a murmur and an S4 gallop rhythm. Other differentials include airway irritants, gastroesophageal reflux, pneumonia,
allergic pneumonitis, vascular rings, lung cysts, and lobar emphysema (Teshome et al, 2013
; Welliver, 2009).
Management
Evidence-based guidelines published by the AAP no longer support a trial of bronchodilators as an option for infants and children with
bronchiolitis because of the risk associated with its use and the lack of evidence of an effect (Ralston et al, 2014
; Schroeder and Mansbach,
2014). The use of epinephrine is also not recommended for infants and children. Administration of nebulized hypertonic saline to infants in
the emergency department is not recommended; however, nebulized hypertonic saline can be administered to infants and children diagnosed
with bronchiolitis and hospitalized. Systemic corticosteroids should not be administered in the treatment of bronchiolitis in infants; chest
physiotherapy is contraindicated in infants and children. Antibiotics have no place in the treatment of a viral disease (such as, bronchiolitis),
unless there is a concomitant bacterial infection or strong suspicion. Most infants with mild signs of respiratory distress can be treated as
outpatients if their oxygen level is within a normal range (Ralston et al, 2014
; Schroeder and Mansbach, 2014):
• Supportive care consists of adequate hydration and use of antipyretics.

15. • The need for supplemental oxygen administration is based on oxyhemoglobin saturation levels. If an infant's or child's oxyhemoglobin level
is greater than 90%, the decision to administer oxygen is left up to the provider (Ralston et al, 2014
).
• Transcutaneous oxygen saturation monitoring (continuous pulse oximetry) is also an individual provider's choice (Ralston et al, 2014
).
• Fluid intake is strongly recommended to prevent dehydration.
• Nasal suctioning to clear the upper nasal passages is recommended.
The inpatient management of bronchiolitis may include using heated, humidified, high-flow oxygen via nasal canula. The mechanism of
action is to improve mucous ciliary clearance and avoid nasal dryness. The high flow delivers positive airway pressure to keep the alveoli
open and reduce ventilation perfusion mismatch and small airway microatelectasis (Da Dalt et al, 2013
). This method needs more research
but is being regularly used in the inpatient basis (Schroeder and Mansbach, 2014; Teshome et al, 2013
).
Hypertonic saline (3%) is being used to treat bronchiolitis in hospitalized infants and children. The mechanism of action is due to
decreasing mucus viscosity, thus improving airway clearance. It is not recommended for outpatient use and does not reduce hospital
admission in patients being treated in the emergency department. However, its use does reduce length of hospital stay (Da Dalt et al,
2013; Zhang et al, 2008
). Research on this method is ongoing.
The use of deep airway suctioning is avoided, though continuing to keep the nasal airway clear on a regular basis may improve airflow.
This intervention is intuitive and does not need a randomized trial to show its benefit (Schroeder and Mansbach, 2014).
As stated previously, there is no evidence for the routine use of antibiotics, β-agonist, or corticosteroids. Ribavirin is no longer
recommended routinely and is presently only used in infants with severe illness due to underlying immunodeficiency, chronic lung disease, or
hemodynamically unstable cardiac conditions (Da Dalt et al, 2013
). Although leukotriene levels are high in bronchiolitis, the use of
antileukotriene inhibitors has not been adequately studied and, thus, is not recommended. A recent review showed an increased risk of
bronchiolitis with low cord blood vitamin D level (Belderbos et al, 2011
). At present, there is no evidence to show any pharmacologic therapy
is clearly superior.
Parents caring for infants and children at home need to understand:
• The management of rhinitis (use of saline drops and suctioning of nares)
• Indications for the use of antipyretics
• The use of home oxygen
• Signs of increasing respiratory distress or dehydration that call for hospitalization
• Guidelines for feeding an infant with signs of mild respiratory distress (amount of fluid needed per 24 hours; smaller, more frequent
feedings; monitoring of the respiratory rate; and guarding against vomiting)
• Education that infants and children with bronchiolitis typically have symptoms for 2 to 3 weeks
Infants younger than 2 months old and older infants with signs of severe respiratory distress should be hospitalized. Signs that suggest
increasing respiratory distress include the following (Smith, 2011):
• Progressive stridor or stridor at rest
• Apnea
• Increasing respiratory rate (sleeping rate of greater than 50 to 60 breaths per minute)
• Restlessness, pallor, or cyanosis
• Hypoxia recorded by either blood gas (partial pressure of oxygen [PO2] less than 60 mm Hg) or pulse oximetry (less than 92% on room air)
• Rising partial pressure of carbon dioxide (PCO2) (recorded by blood gas)
• Inability to tolerate oral feedings
• Depressed sensorium
820
• Presence of chronic cardiovascular or immunodeficiency disease
• Parent unable to manage at home for any reason
In-hospital management focuses on supportive care, focusing on suctioning of nares, humidified supplemental oxygen, and elevation of
the child to a sitting position at a 30- to 40-degree angle. IV hydration (or in infants nasogastric hydration) is needed when respiratory distress
interferes with nursing or bottle feeding.
Occasionally a hospitalized child is not able to be quickly weaned back to room air. Home management of these infants requiring oxygen
is sometimes difficult and may require a team approach, including involvement of a pediatric health care provider and home care nursing
visits. Strict outpatient follow-up is mandatory for as long as the child is receiving home oxygen.
Complications
The first 48 to 72 hours after the onset of cough are the most critical. Apneic spells are common in infants. The child is ill-appearing and
toxic but gradually improves. The fatality rate associated with bronchiolitis is about 1% to 2%. Infants younger than 12 weeks old and those
with underlying cardiorespiratory or immunodeficiency are at risk for severe disease.
Prolonged apnea, uncompensated respiratory acidosis, and profound dehydration secondary to loss of water from tachypnea and an
inability to drink are the factors leading to death in young infants with bronchiolitis. In some children, bronchiolitis can cause minor
pulmonary function problems and a tendency for bronchial hyperreactivity that lasts for years. RSV bronchiolitis has been associated with the
development of asthma, but its role in the causality of asthma is still debated. Recurrent episodes of wheezing can be seen during childhood

16. in patients with a history of bronchiolitis. This persists into adolescence with 10% of the children still wheezing. However, this figure may
not be different from the general population (Welliver, 2009).
Prevention
Palivizumab (Synagis) is an RSV-specific monoclonal antibody used to provide some protection from severe RSV infection for high-risk
infants (see Chapter 24 for guidelines). Educate caregivers about decreasing exposure to and transmission of RSV, especially those with high-
risk infants. Advice should include limiting exposure to child care centers whenever possible; use of alcohol-based hand sanitizers if available
or hand washing if the alcohol-based hand sanitizer is not available (Ralston et al, 2014
); avoiding tobacco smoke exposure; and scheduling
RSV prophylaxis vaccination, when indicated.
Asthma
Asthma is a chronic respiratory disease characterized by periods of coughing, wheezing, respiratory distress, and bronchospasm. Asthma can
occur with a persistent cough without significant wheezing. It is the most common chronic respiratory disease of children, with an incidence
as high as 30% of children in the Western world, and it is the leading cause of emergency department visits (Jackson et al, 2011
; Liu et al,
2011).
The pathophysiology is the result of immunohistopathologic responses that produce shedding of airway epithelium and collagen
deposition beneath the basement membrane, edema, mast cell activation and inflammatory infiltration by eosinophils, lymphocytes (Th2-like
cells), and neutrophils (especially in fatal asthma). The persistent inflammation can result in irreversible changes, such as airway wall
remodeling. Inflammation causes acute bronchoconstriction, airway edema, and mucous plug formation. In addition, airway inflammation
can trigger a hyperresponsiveness to a variety of stimuli, including allergens, exercise, cold air, and physical, chemical, or pharmacologic
agents. This results in bronchospasm, which presents as wheezing, breathlessness, chest tightness, and cough that can be worse at night or
with exercise. The airflow obstruction is often reversible, either spontaneously or with treatment. Remodeling of the airway can occur
secondary to persistent fibrotic changes in the airway lining. The fibrosis alters the airway caliber, leading to decreased airflow with
permanent changes starting in childhood, but become recognizable in adults. Recent advances have shown that there are different
“phenotypes” of this disease with different clinical manifestations, and data suggest that children who have symptoms before 3 years old are
more likely to have changes in lung functioning at 6 years old (Szefler et al, 2014
).
Asthma in children is classified as intermittent, mild persistent, moderate persistent, or severe persistent depending on symptoms,
recurrences, need for specific medications, and pulmonary function measurements (Table 25-2). Children classified at any level of asthma can
have episodes involving mild, moderate, or severe exacerbations. Exacerbations involve progressive worsening of shortness of breath, cough,
wheezing, chest tightness, or any combination of these symptoms. The degree of airway hyperresponsiveness is usually related to the severity
of asthma that can change over time. A well-controlled child with asthma has only one exacerbation in 3 years on average (Jackson et al,
2011).
TABLE 25-2
Classification of Asthma Severity in Children: Clinical Features Before Treatment
Classification and Step Symptoms* Nighttime Symptoms Lung Function
Step 1: Intermittent
Symptoms two times or less per week
Asymptomatic and normal PEF between
exacerbations
Requires SABA 2 days/week
Exacerbations brief (few hours or days); varying
intensity
No interference with normal activity
Two times or less per month FEV1 >80% predicted
Normal FEV1 between
exacerbations
Step 2: Mild persistent
Symptoms more than two times per week but less
than one time per day
Requires SABA more than two days/week but not
more than one per day
Exacerbations may affect activity (minor)
Three to four times per month FEV1 >80% predicted
Step 3: Moderate
persistent
Daily symptoms
Daily use of inhaled SABA
Some limitations
Exacerbations affect activity, two times or more
per week; may last days
More than one time per week
but not nightly
FEV1 >60% but <80% predicted
Step 4: Severe persistent
Continual symptoms
Requires SABA several times/day
Extremely limited physical activity
Frequent exacerbations
Often seven times per week FEV1 <60% predicted
*
Having at least one symptom in a particular step places the child in that particular classification.

17. FEV1, Forced expiratory volume in 1 second; PEF, peak expiratory flow; SABA, short-acting beta2-agonist.
Adapted from National Heart, Lung, and Blood Institute (NHLBI): Full report of the expert panel: guidelines for the diagnosis and management of
asthma, (EPR-3), Bethesda, MD, 2007, National Institutes of Health.
Many children experience early- and late-phase responses to their asthma episode. The early asthmatic response (EAR) phase is
characterized by activation of mast cells and their mediators, with bronchoconstriction being the key feature. EAR starts within 15 to 30
minutes of mast cell activation and resolves within approximately 1 hour if the individual is removed from the offending allergen. The late-
phase asthmatic response is a prolonged inflammatory state that usually follows the EAR within 4 to 12 hours after exposure to the allergen,
is often associated with airway hyperresponsiveness more severe than the EAR presentation, and can last from hours to several weeks.
Exercise-induced bronchospasm describes the phenomenon of airway narrowing during, or minutes after, the onset of vigorous activity. Most
asthmatics exhibit airway hyperirritability after vigorous activity and display exercise-induced bronchospasm. For some children, exercise is
the trigger for their asthma. Although asthma is not always associated with an allergic disorder in children, many pediatric patients with
chronic asthma have an allergic component. Increased weight gain in pregnancy and the first 2 years of life may increase TNF-α, a
proinflammatory cytokine implicated in asthma, which may be a predictive biomarker for asthma (Szefler et al, 2014
).
It is not known for certain whether hyperresponsiveness of the airways is present at birth or acquired later in genetically predisposed
children. However, the genetic predisposition for the development of an IgE-mediated response to common aeroallergens, known
as atopy,remains the strongest identifiable predisposing risk factor for asthma. A combination of genetic predisposition and exposure to
certain environmental factors are the necessary components responsible for the pathophysiologic response associated with asthma. Origins of
asthma exacerbations include exposure to respiratory virus, seasonal patterns, exposure to mycoplasma pneumonia and Chlamydophila
pneumoniae,pollution, smoking, pregnancy, and psychological stress (Jackson et al, 2011
; Szefler, 2013). Asthma is rarely diagnosed before
12 months old due to the high rate of viral illness causing bronchiolitis (Nelson and Zorc, 2013). A diagnosis of asthma should be made with
caution in a toddler who has only wheezing associated with viral infections (Mueller et al, 2013
).
The morbidity and mortality statistics of asthma in childhood demonstrate an alarming increasing incidence of asthma and its
complications with a lifetime prevalence of 13% (Nelson and Zorc, 2013). The prevalence rate for asthma is highest among children 5 to 17
years with the 566highest rate among black children (Centers for Disease Control and Prevention, 2015). Minority children have fewer
ambulatory care visits for asthma and are less likely to be on a controller medication. Occupational or environmental exposure can cause
airway inflammation associated with asthma. Factors known to precipitate or aggravate asthma in children include the following:
• Atopic individual response to allergens—inhaled, topical, ingested
• Viral infections and bacterial infections with atypical mycobacterium
• Exposure to known irritants (paint fumes, smoke, air pollutants) and occupational chemicals
• Gastroesophageal reflux
• Exposure to tobacco smoke (for infants, especially smoking by mother)
• Environmental changes—rapid changes in barometric pressure, temperature, especially cold air
• Exercise and psychological factors or emotional stresses (e.g., crying, laughter, anxiety attack, or panic or panic disorder)
• AR and sinusitis
• Drugs (e.g., acetaminophen, aspirin, beta-blockers)
• Food additives (sulfites)
• Endocrine factors (e.g., obesity)
Allergen-induced asthma results in hyperresponsive airways. The majority of children with asthma show evidence of sensitization to any
of the following inhalant allergens:
• House dust mites, cockroaches, indoor molds
• Saliva and dander of cats and dogs
• Outdoor seasonal molds
• Airborne pollens—trees, grasses, and weeds
• Food allergy, including egg and tree nut
Clinical Findings
History
In a primary care setting, asthma should be monitored using a standardized instrument, which may include the Asthma Control Test (ACT),
Asthma Control Questionnaire, Asthma Therapy Assessment Questionnaire, Asthma Control Score, and other instruments as found in the
guidelines summary (National Heart, Lung, and Blood Institute [NHLBI], 2007, p 17). The advantages of a standardized questionnaire are
that it allows the health care provider to assess changes in the patient's asthma and alter the management plan as needed. However, data
suggest the use of these tools is not effective in poorly controlled children in an acute setting (Szefler, 2014).
The assessment of asthma symptoms allows providers to determine if the asthma is well controlled, less well controlled, or poorly
controlled (Mueller et al, 2013
). Well-controlled children have symptoms less than 2 days a week and use short-acting beta2-agonists
(SABAs) less than twice 567a week, whereas less well-controlled patients have symptoms more than 2 days a week and likely need a step up
in treatments. Poorly controlled children have symptoms during the day and may utilize SABAs several times a day.
In primary care settings and the emergency department, the initial presentation is assessed based on the ability to talk in sentences,
breathlessness, and alertness (Nelson and Zorc, 2013). Critical points to cover in the history of a child being seen for asthma include the
following:

18. • Family history of asthma or other related allergic disorders (e.g., eczema or AR)
• Conditions associated with asthma (e.g., chronic sinusitis, nasal polyposis, gastroesophageal reflux, and chronic otitis media)
• Complaints of chest tightness or dyspnea
• Cough and wheezing particularly at night and in the early morning or shortness of breath with exercise or exertion (characteristic of asthma)
• Seasonal, continuous, or episodic pattern of symptoms that may be associated with certain allergens or triggering agents
• Episodes of recurrent “bronchitis” or pneumonia
• Precipitation of symptoms by known aggravating factors (upper respiratory infections, acetaminophen, aspirin)
• Level of alertness
Physical Examination
Table 25-3 outlines the physical assessment findings correlated with asthma severity. Broadly speaking, the
following may be seen on physical examination:
• Heterophonous wheezing (different pitches but may be absent if severe obstruction)
• Continuous and persistent coughing
• Prolonged expiratory phase, high-pitched rhonchi especially at the bases
• Diminished breath sounds
• Signs of respiratory distress, including tachypnea, retractions, nasal flaring, use of accessory muscles,
increasing restlessness, apprehension, agitation, drowsiness to coma
• Tachycardia, hypertension or hypotension, pulsus paradoxus
• Cyanosis of lips and nail beds if hypoxic
• Possible associated findings include sinusitis, AD, and AR.
Physical Assessment of Asthma and Asthma Severity
Severity of Asthma Physical Assessment Findings
Mild
Wheezing at the end of expiration or no wheezing
No or minimal intercostal retractions along posterior axillary line
Slight prolongation of expiratory phase
Normal aeration in all lung fields
Can talk in sentences
Moderate
Wheezing throughout expiration
Intercostal retractions
Prolonged expiratory phase
Decreased breath sounds at the base
Severe
Use of accessory muscles plus lower rib and suprasternal retractions; nasal flaring
Inspiratory and expiratory wheezing or no wheezing heard with poor air exchange
Suprasternal retractions with abdominal breathing
Decreased breath sounds throughout base
Impending respiratory arrest
Diminished breath sounds over entire lung filed
Tiring, inability to maintain respirations
Severely prolonged expiration if breath sounds are heard
Drowsy, confused
Diagnostic Studies
Laboratory and radiographic tests should be individualized and based on symptoms, severity or chronology of the disease, response to
therapy, and age. Tests to consider include the following:
• Oxygen saturation by pulse oximetry to assess severity of acute exacerbation. This should be a routine part of
every assessment of a child with asthma. Pulse oximetry measures the oxygen saturation (SaO2) of
hemoglobin—the percentage of total hemoglobin that is oxygenated.
• A CBC if secondary infection or anemia is suspected (also check for elevated numbers of eosinophils).
• Routine chest radiographs are not indicated in most children with asthma. Results are typically normal or
only show hyperinflation. Again imaging should be ordered judiciously with consideration of the long-term
risk. However, chest radiographs can be useful in the following situations: selected cases of asthma or
suspected asthma or if the child has persistent wheezing without a clinical explanation. Children with
hypoxia, fever, suspected pneumonia, and/or localized rales requiring admission are candidates for imaging.

19. Infants with wheezing during the winter who have clinical bronchiolitis do not need imaging (Nelson and
Zorc, 2013).
• If sinusitis is suspected as the trigger, no diagnostic radiographic testing is needed.
• Allergy evaluation should be considered, keeping in mind that history and physical examination are key in
this consideration. (Refer child to pediatric allergist.)
• Sweat test should be considered based on history in every patient with asthma.
• Pulmonary function tests:
• Spirometry testing is the gold standard for diagnosing asthma and should be used on a regular basis to
monitor, evaluate, and manage asthma. Exercise challenges using spirometry can also be done to
evaluate the child with exercised-induced asthma. Children older than 5 years can typically perform
spirometry.
568
• To evaluate the accuracy of the spirometry, look for an initial sharp peak with an extension down to the
baseline at the end of expiration that is reproducible at least two times. Compare the child's values with
the predicted value for the child's age, height, sex, and race.
• Look at the forced expiratory volume in 1 second (FEV1), which represents the amount of air exhaled in 1
second. The interpretation of percentage predicted is:
• >75%: Normal
• 60% to 75%: Mild obstruction
• 50% to 59%: Moderate obstruction
• <49%: Severe obstruction
• The forced vital capacity (FVC) represents the amount of air expelled:
• 80% to 120%: Normal
• 70% to 79%: Mild reduction
• 50% to 69%: Moderate reduction
• <50%: Severe reduction
• The FEV1/FVC represents the amount of air expelled in the first second over the total amount of air
expelled and should be greater than 90% of the predicted value. Spirometry testing is done prior to a
breathing treatment and 10 minutes after the treatment. If the child's FEV1 improves by 12%, the child
likely has asthma because this illustrates hyperresponsiveness.
• The forced expiratory flow (FEF) (FEF25 to FEF75) reflects the middle portion of the downward limb of the
curve and is a good measure of smaller airway function. The interpretation of percentage predicted is:
• >60%: Normal
• 40% to 60%: Mild obstruction
• 20% to 40%: Moderate obstruction
• <10%: Severe obstruction
• Doing spirometry during well-child checks and for sick visits gives the practitioner an excellent indication
of the amount of inflammation and bronchospasm present in the airway (Kamakshya, 2012). Table 25-
4 represents abnormal spirometry patterns.
TABLE 25-4
Abnormal Spirometry Findings
Obstructive Restrictive
FVC Normal or ↓ ↓
FEV1 ↓ ↓
FEV1/FVC ↓ Normal or ↑
FEV1, Forced expiratory volume in 1 second; FVC, forced vital capacity.

20. • Consider the use of more sophisticated pulmonary laboratory studies for the child with severe asthma.
• Peak flow measurements:
• If spirometry is not an option, peak expiratory flow (PEF) can be used.
• PEF can be used in some children as young as 4 to 5 years old. The values are instrument specific, so the
child's personal best value is the best guide to help detect possible changes in airway obstruction. The
predicted range for height and age can be substituted if personal best rate is not available (Table 25-5).
Interpretation of PEF reading is as follows if PEF is in the:
• Green zone: More than 80% to 100% of personal best signals good control.
• Yellow zone: Between 50% and 79% of personal best signals a caution.
569
• Red zone: Between 0% and 50% of personal best signals major airflow obstruction.
• Box 25-3 describes use of peak flowmeter and interpretation of results.
Exhaled nitric oxide (Dweik et al, 2011
):
• A biomarker for the children with asthma is exhaled nitric oxide testing, which measures a fraction of exhaled nitric oxide (FEno).
• The test measures eosinophilic airway inflammation and helps to determine whether corticosteroids would be helpful in the
management of the patient. It may support the diagnosis of asthma and can help determine compliance with corticosteroid therapy.
• A FEno value of more than 35 ppb in children indicates eosinophilic inflammation and likely responsiveness to corticosteroids, whereas
25 to 35 ppb should be interpreted with caution. There is still controversy about this test, although guidelines have been published.
Management
Management strategies are based on whether the child has intermittent, mild persistent, moderate persistent, or severe persistent asthma
(see Table 25-3). A stepwise approach is recommended. If control of symptoms is not maintained at a particular step of classification and
management, the health care provider first should reevaluate for adherence and administration factors. If these factors do not appear to be
responsible for the lack of symptom control, go to the next treatment step. Likewise, gradual step-downs in pharmacologic therapy may be
considered when the child is well controlled for 3 months. Inhaled corticosteroids may be reduced about 25% to 50% every 3 months to the
lowest possible dose needed to control the child's asthma (NHLBI, 2007; Szefler et al, 2014
).
Chronic Asthma
Treatment of chronic asthma in children is based on general control measures and pharmacotherapy. Control
measures can include the following:
• Avoid exposure to known allergens or irritants.
• Avoid use of acetaminophen in children at risk for asthma (Jackson et al, 2011; McBride, 2011).
• Administer yearly influenza vaccine.
• Control environment to eliminate or reduce offending allergen.
• Consider allergen immunotherapy. Studies have pointed to reduction in health care cost and improved
outcomes associated with allergy immunotherapy (Dretzke et al, 2013; Hankin et al, 2013).
• Treat rhinitis, sinusitis, or gastroesophageal reflux.
• Other pharmacologic agents that may need to be considered include:
• Anticholinergics—to reduce vagal tone in the airways (may also decrease mucus gland secretion)
• Cromolyn sodium—to inhibit mast cell release of histamine
• Leukotriene modifiers—to disrupt the synthesis or function of leukotrienes
• If needed, refer to pulmonology for omalizumab, a recombinant DNA-derived, humanized IgG monoclonal
antibody that binds to human IgE on the 570surface of mast cells and basophils. This anti-IgE monoclonal
antibody is used as a second-line treatment for children older than 12 who have moderate to severe
allergy-related asthma and react to perennial allergens. It is used when symptoms are not controlled by
inhaled corticosteroids.
• Follow up with PCP after an exacerbation requiring emergency department care, and obtain a clear written
asthma action plan.
• Education regarding asthma basics, including triggers and prevention with environmental modification, as
well as the different treatment modalities includes the techniques of administration and dispelling any myths
regarding asthma medication. In terms of coping, the child and family need to be able to understand their
emotions, worries, and uncertainty, as well as when to contact their PCP
. Developing and understanding the
asthma action plan is very important during a well-child visit (Archibald and Scott, 2014).
The pharmacologic management of asthma in children is based on the severity of asthma and the child's
age. The stepwise approach to treatment (Figs. 25-1 and 25-2) is based on severity of symptoms and the use of
pharmacotherapy to control chronic symptoms, maintain normal activity, prevent recurrent exacerbations, and
minimize adverse side effects and nearly “normal” pulmonary function. Within any classification, a child may
experience mild, moderate, or severe exacerbations. NHLBI guidelines for assessing asthma control and

21. initiating and adjusting asthma therapy for the various pediatric age groups are found in Figures 25-3 and 25-
4.
Important considerations to note in the pharmacologic treatment of asthma include the following:
• Control of asthma should be gained as quickly as possible by starting at the classification step most
appropriate to the initial severity of the child's symptoms or at a higher level (e.g., a course of systemic
corticosteroids or higher dose of inhaled corticosteroid). After control of symptoms, decrease treatment to the
least amount of medication needed to maintain control.
• Systemic corticosteroids may be needed at any time and stepped up if there is a major flare-up of
symptoms. 573Control of inflammation is a key principle in the management of asthma.
• The combination of inhaled corticosteroids with a long-acting beta2-agonist (LABA) can further control asthma
(Szefler, 2013).
• Children with intermittent asthma may have long periods in which they are symptom-free; they can also have
life-threatening exacerbations, often provoked by respiratory infection. In these situations, a short course of
systemic corticosteroids should be used.
• Variations in asthma necessitate individualized treatment plans.
• β2 agonists can be administered with metered dose inhaler (MDI) therapy via spacer for children with mild
and moderate exacerbations of asthma, but for children with severe airway obstruction who may have
decreased deposition of drug in the base of the lung, a nebulizer may be better (Nelson and Zorc, 2013).
There is need for more research on the use of MDI therapy and nebulizer therapy in the pediatric population
(Szefler et al, 2014). A spacer or holding chamber with an attached mask enhances the delivery of MDI
medications to the lower airways of a child. Spacers eliminate the need to synchronize inhalation with
activation of MDI. Older children can use a spacer without the mask.
• Dry powder inhalers (DPIs) do not need spacers or shaking before use. Instruct children to rinse their mouth
with water and spit after inhalation. DPIs should not be used in children younger than 4 years old.
• Different inhaled corticosteroids are not equal in potency to each other on a per puff or microgram
basis. Tables 25-6 and 25-7 compare daily low, medium, and high doses of various inhaled corticosteroids
used for children. Combination inhaled corticosteroid and LABA can be used in children from 4 years old
(Taketomo et al, 2014).
For treatment of exercise-induced bronchospasm:
• Warm up before exercise for 5 to 10 minutes.
• Use either an inhaled SABA or a mast cell stabilizer (cromolyn) or both prior to exercise. Combination of
both types of drugs is the more effective therapy. A LABA can be used in older children.
• Use two puffs of a β2 agonist and/or cromolyn MDI 15 to 30 minutes before exercise. Tolerance may
develop if a β2 agonist is used more than a few times 574a week; it should not be used as a controller
monotherapy. Those who exercise regularly and develop symptoms of asthma should use controller
medication, preferably an inhaled corticosteroid.
• Using a scarf or mask around the mouth may decrease exercise-induced asthma (EIA) induced by cold.
Table 25-8 identifies the usual dosages for long-term control medications (exclusive of inhaled
corticosteroids) used to treat asthma in children. Quick-relief medications are listed in Table 25-9. Practice
parameters are guides and should not replace individualized treatment based on clinical judgment and unique
differences among children.
Acute Exacerbations of Asthma
The treatment of acute episodes of asthma is also based on classification of the severity of the episode. Acute
episodes 579are classified as mild, moderate, and severe. Signs and symptoms are summarized in Table 25-10.
Early recognition of warning signs and treatment should be stressed in both patient or parent education, or
both.
The initial pharmacologic treatment for acute asthma exacerbations is shown in Figure 25-5. It consists of
inhaled SABAs (albuterol), two to six puffs every 20 minutes for three treatments by way of MDI with a spacer,
or a single nebulizer treatment (0.15 mg/kg; minimum 1.25 to 2.5 mg of 0.5% solution of albuterol in 2 to 3 mL
of normal saline).
If the initial treatment results in a good response (PEF/FEV1 > 70% of the patient's best), the inhaled SABAs can be continued every 3 to 4
hours for 24 to 48 hours with a 3-day course of oral steroids at 1 to 2 mg/kg/day to a maximum of 60 mg per day. Reassessment is important
to ensure an adequate response and to further assess asthma severity.
An incomplete response (PEF or FEV1 between 40% and 69% of personal best or symptoms recur within 4 hours of therapy) is treated by
continuing β2 agonists and adding an oral corticosteroid. The β2 agonist can be given by nebulizer or MDI with spacer. Parents should be
taught to call their PCP for additional instructions. If there is marked distress (severe acute symptoms) or a poor response (PEF or
FEV1 <40%) to treatment, the child should have the β2 agonist repeated immediately and should be taken to the emergency department.
Emergency medical rescue (911) transportation should be used if the distress is severe and the child is agitated and unable to talk. If children
experience acute asthma exacerbations more than once every 4 to 6 weeks, their treatment plan should be reevaluated.
581