Chalazion
Chalazion is a chronic sterile inflammation of the eyelid resulting from a lipogranuloma of the meibomian glands that line
the posterior
... [Show More] 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
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• 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.
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 dysfunction
(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
• Absent or decreased mobility of the TM
• Air-fluid level behind the TM
• Otorrhea
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• 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 [Show Less]