NR 602 MIDTERM EXAM STUDY GUIDE PURELY NEW ASSURED A++
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NR 602 (NR602)
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Chamberlain College Of Nursing
NR 602 MIDTERM EXAM STUDY GUIDE PURELY NEW ASSURED A++NR 602 MIDTERM EXAM STUDY GUIDE PURELY NEW ASSURED A++NR 602 MIDTERM EXAM STUDY GUIDE PURELY NEW ASSURED A++
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NR 602 MIDTERM EXAM STUDY GUIDE PURELY NEW
ASSURED A++
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.
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
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
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