NR 602 Final Exam Study Guide

 NR 602 Final Exam Study Guide July 2020

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● Eye disorders gabby burns 616-643

Eye Disorders:

Vision screening includes: fundoscopic exam, near and distance vision, ocular alignment, and clarity of ocular
media

Screenings:

· cover/uncover test

· Visual acuity test

· Hirschberg light reflex test

· Stereo acuity test-can be billed separately from primary care visit however specialized equipment
needed

· Autorefraction- can be billed separately from primary care visit however specialized equipment needed

· Photoscreening- can be billed separately from primary care visit however specialized equipment needed

Visual aquity screen

· use ten-foot vision charts,

· keep eyes open under the hand covering the eye,

· can miss two or less of the 20/20 vision line

Refer If

· 4/6 or less are correct

· two-line
NR 602 difference betweenStudy
Final Exam eyes even if in passing range
Guide

· abnormality in eye movement,

· abnormality in pupil color, size or brightness,

· dark or white spots in the pupil

· absent red-light reflex for those over 6

Strabismus: caused by an ocular alignment defect, or a defect in the position of the eyes in relation to each
other-muscles of the eyes are not coordinated

· phoria is an intermittent deviation in ocular alignment that is held latent by sensory fusion. The child
can maintain alignment on an object. Deviation occurs when binocular fusion is disrupted, most often during
the cover/uncover test.

· tropia is a consistent or intermittent deviation in ocular alignment. A child with a tropia is unable to
maintain alignment on an object of fixation. Intermittent tropia may occur when a child is tired.

Blepharoptosis or ptosis: drooping of the upper eyelids affecting one or both eyes. congenital or acquired,
secondary to trauma or inflammation.

Causes

· Congenital ptosis: an autosomal dominant trait.

· trauma to CN III during the birthing process

· trauma
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inflammation

· neurologic disorder (myasthenia gravis, botulism, muscular dystrophy)

Management:

• Correct any underlying systemic disease.

• Evaluate for anisometropia (unequal refractive errors in each eye), anisocoria, and decrease in pupillary light
reflex.

• If vision is compromised, surgery

Nystagmus: presence of involuntary, rhythmic movements that may be pendular oscillations or jerky drifts of
one or both eyes.

· horizontal, vertical, rotary, or mixed-congenital or acquired.

· Congenital nystagmus 6 weeks- 3 months of age

· acquired nystagmus occurs at a later age

· Nystagmus can occur in association with albinism, high refractive errors, CNS abnormalities, vitamin
B12 deficiency, tumors, after infection (e.g., coxsackievirus B, cytomegalovirus [CMV], Haemophilus
influenzae meningitis), various diseases of the inner ear and retina, middle ear trauma, visual loss before 2
years of age, and pharmacologic toxicity. The child may have a birth history of prematurity, intraventricular
hemorrhage, intrauterine psychogenic drug exposure, developmental delays, hydrocephaly, or the mother may
have had gestational diabetes. Nystagmus can be inherited, sometimes with a strong family history.

Management:

· Treat underlying condition

· Refer to ophthalmology

· acquired nystagmus requires prompt evaluation.

· Varied prognosis with a decreased acuity (20/50 or better) and at other times severe disability (20/200)
Cataract:
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Guide

· Most common cause of an abnormal pupillary reflex.

· They are categorized as congenital or acquired

· Cataracts may occur spontaneously or be genetic (e.g., Down syndrome, albinism).

· If a family history of cataracts, present in multiple family members, referral to a geneticist is

indicated.

· Cataracts can be the result of infection (e.g., congenital rubella, CMV, toxoplasmosis), trauma
to the eye, metabolic disease (e.g., galactosemia, hypocalcemia), long-term use of systemic
corticosteroids or ocular corticosteroid drops, prematurity, CNS anomalies (e.g., craniosynostosis,
cranial defects), and demyelinating sclerosis and ataxia-telangiectasia

· Can be seen in children who have other ocular abnormalities I.e. strabismus or pendular
nystagmus, and in those with diabetes mellitus, atopic dermatitis, or Marfan syndrome.

Management:

· titers for TORCH (toxoplasmosis, other, rubella, cytomegalovirus, herpes)

· syphilis (the Venereal Disease Research Laboratory [VDRL] test)

· serum calcium and phosphorus levels,

· urine testing

· Genetic testing is recommended if dysmorphic features.

· Monitor for progression to amblyopia

· Surgical removal of the lens/ intraocular implant

· contact lens, or glasses, although the lenses are often very thick

Glaucoma: circulation of aqueous fluid disturbance-resulting in IOP increase and damage to the optic
nerve
 NR 602 Final Exam Study Guide

· Primary congenital glaucoma is present at birth; infantile glaucoma develops in the first 1 to 2
years of life; juvenile glaucoma occurs after age 3.

· Primary glaucoma occurs because of a congenital abnormality of the structures that drain the
aqueous humor

· Glaucoma is also seen in association with dominantly inherited conditions, such as

neurofibromatosis or aniridia; diffuse facial nevus flammeus (port wine stain); Sturge-Weber,
Marfan, Hurler, or Pierre Robin syndromes; intraocular hemorrhage; or intraocular tumor.

· High incididence in children with a hx of cataract removal

· Secondary or juvenile glaucoma occurs when the drainage network for aqueous humor
becomes obstructed after ocular infection, trauma, systemic disease, or long-term corticosteroid use.

Glaucoma classic triad: tearing, photophobia, and excessive blinking/blepharospasm

• infant tends to turn away from light • Hazy corneas, corneal edema

Management:

· referral to an ophthalmologist

· IOP reading may require anesthesia

· Primary treatment is surgery as early as possible (often multiple surgeries are required).

· Systemic (azetazolamide or methazolamide) or topical (dorzolamide or brinzolamide

drops) carbonic anhydrase inhibitors will reduce IOP.

· Beta blocker (timolol) or combined beta blocker/carbonic anhydrase inhibitor drops may
be used Drug therapy may be difficult owing to its prolonged nature, side effects, and adverse
systemic effects

· discourage excessive physical or emotional stress as well as straining during defecation.

Retinopathy
NR of Prematurity
602 ROP: retinal
Final Exam Study vascular
Guide pathologic disease primarily caused by early gestational age
with low birth weight-abnormal growth of the retinal vessels in incompletely vascularized retinas of premature
infants.

ROP classifications:

1. distance to which the vascularization has progressed away from the optic nerve (zone I, II, or III)

2. severity of inflammatory changes (stages 1 through 5)

3. duration (clock hours)

4. presence of Plus disease (marked vascular dilation and tortuosity)

5. scarring patterns

6. presence of Rush disease (aggressive posterior ROP, or AP-ROP) Developing retinal vessels grow
outward from the optic nerve

· Higher oxygen concentrations produce lower VEGF levels, which slow vessel growth-
VEGF production is stimulated by hypoxia

· The increase in VEGF stimulates vessel growth but not necessarily in an ordered manner.

· target oxygen saturation of 90% to 95%

· premature infants born at or less than 28 weeks of gestation or weighing less than 1500 g.

· overall incidence of ROP in all newborns is 0.14%

· risk in infants under 1250 g is approximately 50%

· Other risk factors: poor weight gain, dopamine-resistant hypotension, white race,
hyperglycemia, insulin treatment, corticosteroid treatment, and insufficient intake of
docosahexaenoic acid

· Hypoxia, hemolytic disease, necrotizing enterocolitis, maternal preeclampsia, breast milk,

and adequate intake of lipids and calories may protect against developing ROP
 Management:
NR 602 Final Exam Study Guide

· Monitor for strabismus, pseudostrabismus, amblyopia, myopia, anisometropia,

leukokoria, and cataracts)

· Refer to intervention services for low-vision children, to low-vision community support

services, and to family support groups

· yearly ophthalmologic follow-up if ROP required tx, less frequent follow-up is needed if
no treatment was required.

· Cryosurgery or laser photocoagulation is used to arrest the progression of abnormally

growing blood vessels (argon and diode laser)

Retinoblastoma: intraocular malignant retinal tumor

· most common tumor in childhood (some 4% of cancers in children younger than 15 years of age)

· Approximately 300 children per year are diagnosed in the United States and Canada and 6000 children
worldwide

· Single (60% of cases) or multiple (40% of cases) tumors may be found in one or both eyes.

· Hereditary and nonhereditary formsMutation of the retinoblastoma susceptibility gene RB1 occurs in
hereditary retinoblastoma (40%) and is known as germinal retinoblastoma.

· RB1 germline mutation are at risk for additional retinoblastoma tumors and second primary malignancies
throughout life

· There is some evidence that HPV 16 and 18 contributes to retinoblastoma development

· The extraocular spread of retinoblastoma due to delayed diagnosis increases the risk of death.

· all infants and children should have a red reflex exam before discharge from the newborn nursery and
thereafter at every health maintenance visit

· • At-risk children should be screened from birth to age 7 years.

· RB1 carriers Q1-2 years after the age of 7

 NR 602 Final Exam Study Guide
Retinoblastoma clinical findings:

• Strabismus is the most common finding.

• decreased visual acuity.

• Uni- or bilateral white pupil (leukocoria), described often as an intermittent “glow, glint, gleam, or glare” by
parents, is usually seen in low-light settings or noted in photographs taken with a flash (e.g., cat’s eye reflex).

· abnormal red reflex, nystagmus, glaucoma, orbital cellulitis and photophobia (causes pain), hyphema,
hypopyon (pus in anterior chamber of eye); signs of global rupture

Diagnosis: ophthalmic exam (under anesthesia), ultrasound, or MRI. CT is no longer recommended d/t risk of
radiation-induced second cancers.

TX: cryotherapy, laser photocoagulation, episcleral plaque brachytherapy, systemic chemotherapy, or

enucleation. Children with germinal retinoblastoma have an increased risk of other cancers outside the eye and
require lifelong follow-up.

Conjunctivitis: inflammation of the palpebral and bulbar conjunctiva

· Most common ocular disorder in primary care caused by bacteria (50% to 75%) in children, occurring
from December to April.

· H. influenzae, Streptococcus pneumoniae, and Moraxella species, with both gram-negative and gram-
positive organisms implicated

· Conjunctivitis also occurs as a viral or fungal infection or as a response to allergens or chemical irritants.

· Bacterial-unilateral, viral-bilateral.

· Unilateral disease can also suggest a toxic, chemical, mechanical, or lacrimal cause.

· Ophthalmia Neonatorum: newborn conjunctivitis or neonatal blennorrhea occurs in the first month of life.

· Chlamydia trachomatis most common cause of ophthalmia neonatorum- Inclusion Conjunctivitis:

characterized by Conjunctival erythema and mild to severe mucopurulent to bloody discharge, usually bilateral-
requires systemic therapy tx
· Staphylococcus,
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Guide H. influenzae, Escherichia coli, Corynebacterium species,
Moraxella catarrhalis, Klebsiella pneumoniae, Pseudomonas aeruginosa).

· Neisseria gonorrhoeae and HSV

· Gonococcal conjunctivitis is concerning for blindness

• Chemically induced conjunctivitis-nonpurulent discharge and edematous bulbar and palpebral conjunctiva

• C. trachomatis: eyelid swelling and palpebral or bulbar conjunctival injection, moderate thick, purulent
discharge.

• N. gonorrhoeae: conjunctival inflammation, lid edema, erythema, and excessive, purulent discharge.

• Bacteria present with conjunctival erythema, purulent discharge.

• HSV specifically causes mild conjunctivitis, erythema, corneal opacity, serosanguineous discharge, and
vesicular rash on eyelids and is often unilateral.

DX: Swabs and scrapings: Gram and Giemsa staining, direct immunofluorescent monoclonal antibody staining,
cultures, enzyme-linked immunosorbent assay (ELISA), or polymerase chain reaction (PCR) testing. Any
infant younger than 2 weeks with ophthalmia neonatorum should be tested for gonorrhea. A culture for
gonorrhea (on chocolate agar or Thayer-Martin medium) or aggressive scraping for a Gram stain is used for
diagnosis. Culturing purulent discharge is not sufficient. If gonorrhea is suspected, also check for C.
trachomatis.

Management

• Irrigate the eyes, after obtaining cultures, with sterile normal saline until clear of exudate.

• Gonococcal conjunctivitis: (IM) ceftriaxone (25 to 50 mg/kg, not to exceed 125 mg) given once If there are
extraocular manifestations, a 7-day course of intramuscular or intravenous ceftriaxone is warranted.
Ceftriaxone is not given to neonates with hyperbilirubinemia; cefotaxime is an alternative

· Ocular morbidity (corneal infection with possible scarring or perforation) can result if infection is missed.

· Nongonococcal conjunctivitis: topical erythromycin 0.5% ointment, trimethoprim-polymyxin B, or

fluoroquinolone drops
· TheNReyes
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Guide
into the lower conjunctival sac.

· Herpes simplex conjunctivitis: Immediate referral for hospitalization and topical and systemic antivirals
are needed. Spread of virus to the CNS, mouth, and skin is of concern.

· Chlamydia: systemic erythromycin (50 mg/kg/day in four divided doses for 14 days) or azithromycin (20
mg/kg for 3 days)-Topical treatment is not indicated because it does not lower the risk for a subsequent
pneumonia caused by Chlamydia

· Chemically induced conjunctivitis resolves spontaneously within 3 to 4 days without specific treatment.

· Mothers and their sexual partners should receive treatment if gonococcal and/or chlamydial infections
occur in their newborns.

Prophylaxis required by law: erythromycin ointment 0.5% (a 0.25- to 0.5-inch strip to each eye) within 1 hour
of vaginal delivery or c-section

Bacterial Conjunctivitis: H. influenzae most common cause in children <7

· S. pneumoniae, M. catarrhalis, and adenovirus are also common pathogens.

· Erythema of one or both eyes, usually starting unilaterally and becoming bilateral (key finding)

· Yellow-green purulent discharge (key finding)

· Encrusted and matted eyelids on awakening (key finding)

· Burning, stinging, or itching of the eyes and a feeling of a foreign body

· Photophobia

· Petechiae on bulbar conjunctiva

· URI symptoms, otitis media, or acute pharyngitis

· Vision
NR screen shouldExam
602 Final be normal and documented
Study Guide

· Diagnostic Studies Routine culture testing is not necessary.

· Gram stain and culture can be done chronic and difficulty in treating

· Differential Diagnosis: nasolacrimal duct obstruction in infants, ear infection, Kawasaki disease, foreign
body, corneal abrasion, uveitis, herpetic conjunctivitis, poor compliance, or wrong choice of drug. Cultures or
scrapings are appropriate for unresolved infection. Management:

· conservatively without using antibiotics in teens and adolescents

· broad-spectrum coverage: Sodium sulfacetamide 10% ophthalmic solution or ointment; not effective
against H. influenzae

· Trimethoprim sulfate plus polymyxin B sulfate ophthalmic solution

· Erythromycin 0.5% ophthalmic ointment for patients with sulfa allergy

· infants Azithromycin drops for children older than 12 months

· Fluoroquinolone ophthalmic drops including besifloxacin, ciprofloxacin, gatifloxacin, levofloxacin,

moxifloxacin, or ofloxacin for children older than 12 months

· Avoid aminoglycosides (neomycin, tobramycin, and gentamicin)

Conjunctivitis-Otitis Syndrome caused by H. influenzae-treat for the otitis media. Concurrent use of a topical
antibiotic is not necessary.

Viral Conjunctivitis: usually caused by adenovirus (80%)

· Can be caused by herpes simplex, herpes zoster, enterovirus, molluscum contagiosum, or varicella virus.

· more common in children older than 6 years of age

· In-office testing is available

· profuse clear, watery discharge (key findings)

· NR headache,
Fever, 602 Final Exammalaise,
anorexia, Studyupper
Guiderespiratory symptoms (pharyngitis-conjunctivitis-fever triad
with adenovirus [key findings])

· Pharyngitis with enlarged preauricular nodes (key findings)

· Itchy, red, and swollen conjunctiva

· Hyperemia and swollen eyelids

· Photophobia with measles or varicella rashes

· Herpetic vesicles on the eyelid margins and eyelashes (marginal blepharitis) or on the conjunctiva and
cornea (keratoconjunctivitis)

Management: Good hygiene- should resolve in 7-14 days Viral conjunctivitis is self-limited and should
resolve in 7 to 14 days

· Warm or cold compresses and artificial tears can be used.

· Antihistamine or vasoconstrictive ophthalmic solutions

· If HSV infection- immediate referral to an ophthalmologist

Conjunctivitis-Pharyngitis Syndrome: caused by adenovirus and bacterium.

· Involvement of deeper layers of the cornea (keratitis) can occur and must be differentiated from
conjunctivitis.

· Scarring of the cornea resulting in blindness is a significant complication of HSV infection

· slit-lamp examination needed by ophthalmologist (refer)

Allergic conjunctivitis:

1. Acute sudden onset of symptoms (within 30 minutes) after exposure to an environmental

allergen, such as animal dander-itching, tearing, chemosis, and eyelid edema; the condition
resolves within 24 hours once exposure to allergen ends

2. Seasonal allergic conjunctivitis (hay fever)-mild injection and swelling caused by

outdoor pollens and may be associated with generalized allergic reaction including nasal
 congestion (allergic rhinoconjunctivitis). Seasonal allergens (e.g., grass pollens, ragweed) cause
NR 602
90%Final Exam
of allergic Study Guide
conjunctivitis in the United States.

3. Perennial conjunctivitis is chronic conjunctivitis related to year-round exposure to

allergens such as dust mites, animal dander, and molds-mild and waxes and wanes throughout
the year.

4. Vernal conjunctivitis is more severe, with peak incidence in 10- to 12-year-olds; boys>
girls

5. Atopic keratoconjunctivitis occurs in those with atopic dermatitis and/or asthma,

affecting the lower tarsal conjunctiva- late adolescence-significant itching, burning, and tearing
that is often chronic.

6. Giant papillary conjunctivitis occurs in contact lens wearers 10 times more frequent in
those wearing soft vs hard contacts

• Severe itching, tearing (key findings)

• Rhinitis

• Family or current history of atopy (eczema, asthma) and/or seasonal allergies

• Stringy, mucoid discharge

• Bilateral involvement most common

• Cobblestone papillary hypertrophy in the tarsal conjunctiva

DX: Conjunctival or nasal smears (using Wright stain) reveal numerous eosinophils.

Management: saline solution or artificial tears are administered along with cool compresses. Refrigerated eye
drops are more soothing.

topical decongestants, oral or topical antihistamines, topical mast cell stabilizers, or topical NSAIDs

· naphazoline hydrochloride plus antazoline ophthalmic solution can be used for irritation, and itching.
· OTC
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602 Final Examstabilizers
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Guide therapy

· Cromolyn sodium 4% on a regular basis.

· Nedocromil sodium 2% or lodoxamide tromethamine 0.1%.

· Topical NSAIDs, like ketorolac tromethamine 0.5%

· Ophthalmic histamine 1 (H1) blockers such as ketotifen or levocabastine

Complications- vernal conjunctivitis can lead to corneal ulceration, scarring and vision loss, corneal
degeneration, and changes in the corneal curvature.

Blepharitis: acute or chronic inflammation of the eyelash follicles or meibomian sebaceous glands of the
eyelids (or both)-usually bilateral.

Anterior: caused by seborrhea or staphylococcal bacteria-Demodex folliculorum is a parasite that may cause
chronic anterior blepharitis, presenting with cylindrical sleeves of dandruff around the eyelashes.

Posterior:-inner portion of the eyelid at the meibomian glands: rosacea or seborrheic dermatitis, may be source
of posterior blepharitis.

· allergic contact dermatitis, eczema, or psoriasis can cause blepharitis

· Swelling and erythema of the eyelid margins and palpebral conjunctiva

· Flaky, scaly debris over eyelid margins on awakening

· 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

Management:
· Scrub
NRthe602eyelashes
Final and
Exameyelids with aGuide
Study cotton-tipped applicator or clean washcloth containing a weak
(50%) solution of no-tears shampoo to maintain proper hygiene and debride the scales.

· warm compresses for 5 to 10 minutes at a time two to four times a day and wipe away lid debris.

· Massage the lids two to four times a day to express meibomian secretions.

· bacitracin or erythromycin 0.5% ophthalmic ointment at bedtime until symptoms subside and for at least
1 week thereafter. Ointment is preferable to eye drops-

· Azithromycin 1% ophthalmic solution for 4 weeks for posterior blepharitis

· 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.

· new eye makeup; minimize use of mascara and eyeliner

· artificial tears

Chronic staphylococcal blepharitis and meibomian keratoconjunctivitis:

Doxycycline or tetracycline can be used chronically in children older than 8 years of age. Azithromycin for
5 days may be used in younger children.

Hordeolum (Stye): infection of either the sebaceous glands, the eyelids (external hordeolum) or the
meibomian glands (internal hordeolum) caused by S. aureus or, rarely, P. aeruginosa

· tender, swollen red furuncle

· external hordeolum, the swelling is smaller, superficial, and located along the lid

· internal hordeolum is larger and may point through the skin or conjunctival surface

· c/o foreign body sensation. An internal hordeolum on the palpebral conjunctiva can be
inspected by rolling back the eyelid.
NRManagement:
602 Final Exam
Rupture Study Guide
often occurs spontaneously when the furuncle becomes large and a point
develops. Removal of an eyelash near the furuncle frequently promotes rupture.

· Warm, moist compresses three or four times daily, 10 to 15 minutes each time

· Hygiene for the eye can be maintained by scrubbing the eyelashes and eyelids with a cotton-
tipped applicator or clean washcloth containing a weak (50%) solution of no-tears shampoo once or
twice a day

· 0.5% erythromycin

· I&D by ophthalmology if it does not resolve

Chalazion: chronic sterile inflammation of the eyelid resulting from a lipogranuloma of the
meibomian glands, which line the posterior margins of the eyelids

deeper in the eyelid tissue than a hordeolum and may result from an internal hordeolum or retained
lipid granular secretions.

· mild erythema and slight swelling of the involved eyelid

· slow-growing, round, nonpigmented, painless (key finding) mass remains after inflammation
resolves.

· commonly acquired lid lesion seen in children and can persist for a long time. Management:
hot compresses for acute lesions

· ophthalmologist for surgical incision or topical intralesional corticosteroid injections if the

condition is unresolved or the lesion causes cosmetic concerns.

· can distort vision by causing astigmatism as a result of pressure on the orbit

· Recurrence is common

· pyogenic granuloma: fragile vascular granulation tissue that enlarges and bleeds rapidly if a
chalazion breaks through the conjunctival surface.
Nasolacrimal
NR 602Duct Final
Conditions:
Exam Study Guide

Dacryostenosis and Dacryocystitis: prevents tears from flowing into an opening in the nasal mucosa.

Dacryocystitis is an inflammation of the involved nasolacrimal duct; infection can result

Nasolacrimal duct obstruction: common in neonates, can occur secondary to trauma to the duct or to a chronic
duct obstruction complicated by an upper respiratory infection.

· more frequently in those with craniofacial disorders and Down syndrome d/t congenital failure of the duct
to canalize

· unilateral or bilateral-2 to 6 weeks after birth when tear production develops

· blockage usually resolves spontaneously in 90% of infants by 6 months of age and 96% of infants by 12
months

· Bacterial overgrowth may occur, resulting in excessive mucous production

· Continuous or intermittent tearing, stickiness, and mucoid discharge at the inner canthus that can become
purulent, with possible expression of purulent material

· Blepharitis in lids and lashes

· nasal obstruction and drainage

· thin mucopurulent exudate from the punctum lacrimale

· Tenderness and swelling over the lacrimal duct (can be exquisitely painful)

· Eyelids closed with dried mucous on awakening

· Edema and erythema of the tear sac (most prominent in the triangular area just below the medial canthus)

· Excoriation and thickening of the periorbital skin

· Mucocele of inner canthal tendon (presents as a bluish mass)

DX:
· Fluorescein
NR 602dye, instilled
Final Exam bilaterally
StudyinGuide
the inferior conjunctival sac and checked in 2 and 5 minutes with
a cobalt blue light source, will disappear if duct is patent.

· white blood cell (WBC) count (elevated) and cultures are obtained from the expressed exudate if the
inflammation is severe.

Management:

Daily massage of the lacrimal duct-2-3 times a day

· Bacterial conjunctivitis: erythromycin ophthalmic ointment, or a fluoroquinolone (moxifloxacin,

ciprofloxacin, ofloxacin, norfloxacin) for 1 to 3 weeks with massage and frequent cleansing

· Saline drops into the nose, followed by aspiration before feeding and at bedtime for nasal congestion

Preseptal cellulitis caused by trauma or infection i.e. eyelid abscess, or sinusitis is anterior to the orbit

· Orbital cellulitis involves tissues posterior to the orbital septum-and is more serious

Preseptal cellulitis is commonly seen in children up to 6 years of age

· infected lacerations, abrasions, insect stings or bites, impetigo, or a foreign body

· can be secondary to paranasal sinusitis

· streptococcal organisms, and S. aureus

· MRSA has been reported as a cause of periorbital cellulitis

· If fever is present-consider periorbital cellulitis

· Upper lid affected more than the lower lid

· Orbital discomfort or pain, proptosis, or paralysis of the extraocular muscles can occur with orbital
cellulitis.
· History
NR 602of sinusitis,
Final insect
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or eye Guide
trauma

· Bacteremia may indicate orbital cellulitis.

· Diagnostic studies not usually required

· Visual acuity, extraocular movement, and pupillary reaction testing • Complete blood count (CBC) with
differential • Blood cultures • CT scan to rule out sinusitis, orbital cellulitis or subperiosteal abscess

· Management: Refer if proptosis, ophthalmoplegia, or changes in visual acuity occur suggesting orbital
cellulitis

· Moderate to severe cellulitis, cellulitis in a child less than 1 year of age, a poor response to outpatient
management, or a purulent wound near the eyelid require hospitalization and intravenous administration of
antibiotics followed by a 10-day course of oral abx

· outpatient if older than 1 year, cellulitis is mild, the orbit is not involved (full eye movements are present,
no pain with eye movement, visual changes, or ptosis), and the child exhibits no symptoms of systemic
bacterial sepsis.

Outpatient management: Amoxicillin with clavulanic acid, cefdinir, and cefpodoxime are first-line choices for
treatment-x 7-14 days

· clindamycin or a combination regimen of trimethoprim/sulfamethoxazole (TMP-SMX) plus amoxicillin

or cefpodoxime or cefdinir for MRSA

· Warm soaks to the periorbital area every 2 to 4 hours for 15 minutes

· Reexamine the patient in 24 hours and if no improvement hospitalize for parenteral antibiotics, usually
ceftriaxone.

Complications: extension of the infection into the orbit, subperiosteal or orbital abscess, optic neuritis, retinal
vein thrombosis, panophthalmitis, meningitis, epidural and subdural abscesses, and cavernous sinus
thrombosis.

Keratitis and Corneal Ulcers Inflammation of the cornea (keratitis):

· alteration
NR 602 in visual
Finalacuity
Exam andStudy
may progress
Guide to corneal ulceration and blindness.

· medical emergency-refer to ophthalmology

· begins as a well-defined infiltration at the center or edge of the cornea and subsequently suppurates and
forms an ulcer that may penetrate deep into the corneal tissue or spread to involve the width of the cornea.
Involvement is usually unilateral.

· Caused by viruses (HSV-1, varicella zoster, hepatitis C), bacteria (H. influenzae, Moraxella, S. aureus, S.
pneumoniae, Pseudomonas, N. gonorrhoeae, Enterobacteriaceae [including Klebsiella, Enterobacter, Serratia,
and Proteus]), fungi (rare), and protozoa.

· Less common causes: allergic reaction, conjunctivitis, systemic infections, toxic chemicals, and the use of
corticosteroids

· most common risk factor for keratitis is trauma, which can also result from wearing extended-wear
contact lenses or having poor contact lens hygiene

White lesions on cornea; occasional corneal opacification

· Vesicles on the skin or eyelids; herpes lesions elsewhere on the body

· Severe pain, sensation of a foreign body (“gritty”), inflamed eye

· Photophobia, tearing, blurred vision, erythema, and spasms of the eyelid

· Area staining green with a fluorescein strip (if herpes, a dendritic ulcer is seen)

Management: slit lamp examination

• Steroids should never be used. • Treatment with antivirals, such as trifluridine or vidarabine, may speed
healing in herpes simplex infections.

Uveitis: Inflammation of the uveal tract (iris, ciliary body, choroids) and other ocular structures may be anterior
(affecting the iris, ciliary body, or both) or posterior (affecting the choroid). Adjacent ocular structures can also
be involved, including the retina, vitreous, sclera, lens, and optic nerve

· acute or chronic, infectious and non-infectious including viral/bacterial

· ocular
NR trauma, and infection
602 Final Exam elsewhere in the eye
Study Guide

· allergy, malignancy, and systemic diseases such as JIA, inflammatory bowel disease, Kawasaki disease,
herpes simplex, tuberculosis, Lyme disease, CMV, toxoplasmosis, syphilis, acquired immunodeficiency
syndrome (AIDS), ulcerative colitis, rubella retinitis, and Stevens-Johnson syndrome.

· Acute onset of pain (key finding)

· Red eye, photophobia, and blurred or decreased vision (key findings)

· Excessive tearing and eyelid edema

· Conjunctival erythema, circumcorneal injection

· Hypopyon (pus layer in the bottom of the anterior chamber)

· Cloudy appearance of the eye with a bulging iris and a contracted, irregular, or fixed pupil

· If chronic, there may be no ocular pain, photophobia, redness, or tearing

· Hx of prior viral infection, joint pain, trauma, or gastrointestinal problems

Definite diagnosis by slit lamp examination: treat underlying conditions

Management:

· Cycloplegics and topical or systemic corticosteroids

· NSAID’s adjunctive

Trachoma : chronic infectious, characterized by follicular keratoconjunctivitis with neovascularization of

the cornea.

· contagious—often spread by direct contact with eye, nose, or throat secretions of infected
persons; by contact with towels or washcloths contaminated by secretions; or by flies that are
attracted to the eyes.

· second leading cause of blindness in the world, caused by one of the two existing C.
trachomatis with a peak incidence in children 4 to 6 years
 NR· 602 inflammation,
Final Exampain, photophobia,
Study Guide excessive tearing, granulation follicles (large white or pale
yellow follicles 0.5 to 2 mm in size on the upper tarsal conjunctiva), and, in adults, eventual
entropion—inversion of the eyelid leading to corneal trauma, scarring, and blindness.

Management Consult with an ophthalmologist-recommendations vary.

· may be treated with a single dose of azithromycin (20 mg/kg)

Subconjunctival hemorrhage: splotchy bulbar conjunctival redness that occurs spontaneously or is secondary to
increased intrathoracic pressure (from coughing, sneezing, straining, or trauma) that results in the bursting of
conjunctival vessels.

· No treatment is indicated unless there is pain, vision loss, or photophobia-refer to

ophthalmology

Eyelid Contusion (“Black Eye”): bruising, swelling, and often an impressive appearance (“black eye”). For
increased pain or swelling, decrease in visual acuity, double vision, flashing lights or “floaters,” or develops a
bilateral “raccoon eyes” appearance-refer to r/o ruptured globe, basilar skull fracture, detached retina, hyphema

· All eye structures should be examined before excessive swelling sets in.

· Treatment consists of elevating the head and intermittent ice compresses for 48 hours

Corneal Abrasion: common-Scratches from forceps delivery, paper, brushes, fingernails, contact lens overuse,
improperly fitted cosmetic contact lenses, airbag deployment, plants, or foreign body in the conjunctival sac are
often responsible.

· Evidence and sensation of a foreign body; conjunctival erythema , Severe pain, photophobia, and
decreased vision

· Tearing, blepharospasm

· Disrupted tear film over the corneal epithelium (seen with a penlight)
· Fluorescein
NR 602 Finalstaining with superficial
Exam Study Guideuptake indicative of a minor corneal abrasion If the fluorescein
staining goes deeply into the cornea, subepithelial corneal damage (e.g., corneal ulceration or corneal tear) is
possible.

· Vertical striations on the cornea suggest a foreign body embedded under the eyelid. Management

· Refer severe corneal injuries or possible subepithelial damage to an ophthalmologist.

· Refer those who wear contact lenses and have an abrasion to an ophthalmologist to rule out bacterial
corneal infection (a prophylactic topical antibiotic [e.g., gentamicin or ciprofloxacin] may be prescribed in
these circumstances to cover Pseudomonas).

· topical antibiotics (0.5% erythromycin ointment or polymyxin/trimethoprim, ciprofloxacin or ofloxacin

drops) four times daily for 3 to 5 days

· patch for no longer than 24 hours

· heals in 24 to 48 hours.

· Elbow restraints for infant

· Oral analgesics or ophthalmologic NSAIDs (e.g., ketorolac 0.5%)

· NO topical steroids and antibiotics

Foreign body:

· Never remove an intraocular foreign body-refer immediately to ophthalmology

· Use of a topical anesthetic facilitates cooperation

· If an extraocular foreign body is not visualized but suspected, remove it via irrigation with
sterile saline or sterile eye solution.

· if the object is visualized, either irrigate or gently lift the object away with a moistened cotton-
tipped swab (after instillation of topical anesthetic).

· Treat with antibiotic ointment (erythromycin four times a day) until seen by an
ophthalmologist
 NR· 602After
Finalremoving
Examany extraocular
Study Guide object, instill fluorescein stain and inspect the cornea with
cobalt-blue light for corneal abrasion; check visual acuity

· Reschedule the patient in 24 hours or refer to an ophthalmologist for follow-up. • In the case
of an airbag deployment (i.e., talc, cornstarch, and/or baking soda released), irrigate the eyes with
sterile saline or sterile eye solution and carefully examine the eyes for further evidence of trauma.

Burns: Thermal (caused by exposure to steam, flame, intense heat [e.g., touching cornea with a curling iron],
cinders, or cigarettes) or chemical (e.g., cleaning agents, fertilizers, pesticides, battery fluid, or laboratory
products), or induced by UV light (e.g., from bright snow, laser pointers, or a sunlamp).

· Chemical burns are emergencies-Alkaline solutions are especially damaging.

· Burns on the eyelids are treated the same as burns elsewhere on the body.

· Fluorescein stain revealing pinpoint uptake

Management

· Chemical burns: immediate, ongoing, copious irrigation-tepid water, saline, or Ringer

irrigation for 20 to 30 minutes or until the pH of the tear film is 7.3 to 7.7.

· The pH should be rechecked after 30 minutes -Do not patch the eye; allow tearing to continue
to cleanse the eye.

· Cool compresses

· Thermal burns are often treated as corneal abrasions.

· UV burns are treated by using topical antibiotic prophylaxis, patches, and analgesics. Healing
should occur in 1 to 2 days.

Laceration of the orbit: perforation of the cornea and lead to uveal prolapse

· Anterior segment: irregular pupil (retracted or peaked), iris prolapsed

· Posterior segment: poor red-light reflex, decreased vision, black tissue or fluid seen under the conjunctiva

Management: eye shield-refer

 NR 602 Final Exam Study Guide

hyphema : accumulation of visible blood or blood products in the anterior chamber of the eye and is the result
of blunt trauma to the globe without penetration or perforation.

· caused by balls, fists or fingers, elbows, rocks, exploding airbags, and sticks.

· High-risk sports: baseball, hockey, racquetball, and squash

· in infants with birth trauma or in patients with retinoblastoma, abnormal iris vessels (rubeosis),
leukemia, juvenile xanthogranuloma of the iris, or abnormal hematologic profiles, such as sickle cell trait or
disease, or secondary to child abuse.

· An open globe must be excluded before any examination that would increase IOP

· somnolence (associated with intracranial trauma)

· Blood (appearing as a dark red fluid level between the cornea and iris) on gross examination or as a hazy-
appearing iris

· Inability to detect a bilateral red light reflex

· Pain, photophobia, and tearing; abnormal pupillary reflex

· Visual acuity changes and impaired vision

Management:

· Refer the patient immediately to an ophthalmologist.

· slit-lamp examination

· Restrict oral intake until the child has been seen by an ophthalmologist.

· perforated eye shield (not a patch) over the eye; avoid pressure to prevent reinjury. Outpatient
management for small (grade I) hyphemas.

· Parents should be told to elevate the head of the bed 30 degrees. The child should wear a Fox eye shield.
Bed rest with bathroom privileges must be maintained for 5 days; no strenuous activities for 10 days; daily eye
examinations required to check for blood staining and IOP. • Cycloplegic agents may be used.
· NRII602
grade or IIIFinal Exam
hyphema, with Study Guide
sickle cell disease, with an increase in IOP should be hospitalized

· Acetaminophen is the analgesic of choice; avoid aspirin and NSAIDs

· Sedatives may be necessary in pediatric patients.

· Treat nausea and prevent vomiting. • Surgery may be necessary to remove trapped blood from the
chamber

· Complications A second hemorrhage can occur within 3 to 5 days of the first, increasing the risk of
glaucoma, amblyopia, or corneal blood staining, which can result in permanent visual loss.

· The larger the hyphema, the more likely the child is to rebleed.

· abnormal hematologic profiles (e.g., sickle cell) are more likely to have visual loss because of optic
atrophy

Retinal detachment occurs when the neurosensory retina separates from its retinal pigment epithelium base
within the globe.

· Rare so suspicion should be high for traumatic causes (e.g., child abuse), a congenital abnormality or
syndrome (aphakia, cataracts, Ehlers-Danlos, Stickler, Marfan, Norrie syndromes), or specific disease (ROP,
viral retinitis, retinoblastoma, or various retinopathies

· Children who had prior cataract surgery are at increased risk

· Blurry vision that becomes progressively worse

· Dark cloud in one visual field, flashing lights, or a “shower of floaters”

· Darkening of retinal vessels on funduscopic examination

· Gray elevation at the site of detachment

Management NPO-refer
Orbital Hematoma
NR 602 Finaland Contusion
Exam ofStudy
the Globe:
Guide result of a blow to the globe from sports activities, motor
vehicle accidents, assault, BB gun accidents, or airbag deployment.

· Milky white appearance of the retina

· Visual acuity changes

· Severe bruising of the eyelids and periorbital tissues

· Lens dislocation, retinal detachment or edema, rupture of the eyeball

· Vitreous, retinal, or choroid hemorrhage

Management Refer-A closed head injury, damage to the skull, and facial bone fractures must be ruled out via
CT scan, MRI, or ultrasound radiography.

Orbital Fractures : walls of the orbit secondary to blunt trauma to the orbital rim or eyes

· common among adolescent and young adult males

· Pain, numbness below the orbit; trouble chewing; nosebleed • Diplopia, irregular pupil, limited ocular
movement (especially upward) • Corneal laceration, hyphema, and/or absent red light reflex • Globe
displacement (sunken or protruding) or enophthalmos (recession of the eyeball within the orbit) • Bony
discontinuity or “step-off” • Ecchymosis of the lids; subcutaneous emphysema in surrounding tissues, and
edema

Diagnostic Studies Plain film radiography and CT scan are the best imaging modalities. Management:
emergency- immediate intervention and referral.

· Diagnostic studies are performed to rule out injury to the skull and cranial contents.

· Open reduction may be necessary if any of the orbital bones are displaced or to rule out displacement of
the globe or enophthalmos.

· Ice the injury for 48 hours and have the patient sleep with the head of bed elevated
· Antibiotic
NR 602 prophylaxis
Final Examto cover nasal pathogens
Study Guide is recommended if the patient has an orbital fracture into
the sinus.

· Nasal decongestants may also be used to reduce nose blowing and sniffling.

Entropion: upper or lower eyelids invert so that the cilia or epithelium rubs against the corneal surface,
causing abrasion or irritation.

· Pain or irritation and photophobia are typical symptoms.

· lid laxity.

Management involves surgical intervention and referral to an ophthalmologist

Complications include corneal scarring and corneal infections.

Ectropion: eyelid margins evert-may be congenital; seen after infection; or secondary to scarring after trauma,
radiation, or prior surgery.

Management: lubrication for mild cases; surgery is indicated for chronic or symptomatic cases.

Euryblepharon: wide palpebral fissure with the appearance of a sagging half of the lower eyelid (temporal side)
or a pulling away of the lid from the orbit- a genetic etiology (e.g., Down syndrome), be associated with other
ocular anomalies (e.g., congenital cleft lip, strabismus, congenital ptosis)

· No treatment is indicated unless chronic tearing or exposure keratitis occurs

Pterygium: fibrovascular mass of thickened bulbar conjunctiva that extends beyond the limbus onto the cornea-
lesion is usually triangular and commonly found on the nasal side of the orbit.

· caused by irritation of the bulbar conjunctiva from sunlight, wind, dust, fumes, or airborne allergens; it
can also be hereditary.

A pinguecula may precede the pterygium, which occurs as a yellow-white, slightly raised mass on the bulbar
conjunctiva
·
NR 602 Final Exam Study Guide
painless, may itch, and may be accompanied by occasional complaints of blurred vision if the lesion
enlarges

· pterygium is uncommon in children, consider other causes: papillomas, dermoids, keratoacanthomas, an

epithelial inclusion or a dermoid cyst, or a rare malignancy

Treatment: protecting against irritants (use of goggles, sunglasses, or topical lubricants such as artificial tears)
and using mild vasoconstrictors or short-term steroids for inflammation

· exposure to UV light is a risk factor for the development of pterygium, children should wear sunglasses
and a hat

· surgical intervention if pterygium impedes vision

Vision impairment is defined as having vision that is 20/40 or worse in the better eye even with eyeglasses.

· Partial or low vision is defined as best corrected visual acuity between 20/70 and 20/200, whereas legal
blindness is distant visual acuity of 20/200 in the better eye or a visual field that includes an angle not greater
than 20 degrees.

Amaurosis= partial or total loss of vision.

More than half have comorbid chronic or neurologic conditions.

· Congenital cataracts, congenital glaucoma, high refractive errors, ROP, detached retina, neurologic
conditions involving CN II, cortical blindness, and optic atrophy are causative factors, as are retinoblastoma,
trauma, infection, hydrocephaly, and genetic conditions.

· increased risk for low-birth-weight, small-for-gestational age, and large-for-gestational age babies.

· According to the WHO, the number of blind children in the world is approximately 1.4 million

Allergy: discharge is usually clear-watery

 chronic dacrocystitis
NR 602 Final or nasolacrimal
Exam Study obstruction:
Guide mucoid or purulent discharge

conjunctivitis infection-chronic can have some mucoid production

● Musculoskeletal Injuries - assessment and treatment

● Rashes and Dermatologic conditions gabby MULTIPLE PEOPLE
○ Bacterial infection (Hye) (

■ Impetigo: bacterial colonization days to months before skin lesions appear. Via hands, towels,
clothes, nasal discharges, droplets. Poor hygiene. Warm, humid climates. lower socioeconomic groups.

1. Nonbullous w/ honey colored crusts-skin trauma (bites, abrasions, or varicella) or atopic

dermatitis.
 -phy exam: begins 1-2mm erythematous papules or pustules ->vesicles or bullae-
NR 602>rupture,
Final Examand
moist, honey
Study colored->crust->eroded skin. <2cm. Little pain, but
Guide
rapid spread
2. Bullous -sporadically common in infants and young kids. S. aureus
        -phy exam: large, accid, thin-wall, super cial, annular, oval pustular blisters or bullae-
>rupture->thin varnish-like coating or scale
*common on face, hands, neck, extremities, perineum, but can be anywhere, regional
lymphadenopathy
*dx study-gram stain and cx for organism (severe cases)
*management-topical abx (bacitracin, polymyxin B, neomycin), but mupirocin and retapamulin
are better choices d/t resistance. PO abx if infections in family, child care, or athletes.
        -infant w/ bullous -use methicillin, oxacillin, nafcillin
        -no response in 7 days->swab crust-> gram stain, cx, sensitivities.
Community acquired MRSA?->clinda or Bactrim.
-educate hand washing, cleanliness.
-No school until treated for 24 hours
-f/u in 2-3 days if not improving.
*complications - cellulitis with nonbullous-> ecthyma or erysipelas (cellulitis with enduration)
-Lymphangitis, suppurative lymphadenitis, guttate psoriasis,
erythema multiforme, scarlet fever, or glomerulonephritis ←--- Strep
-SSSS (staph scalded skin syndrome) -blistering disease (common in neonates:
Ritter disease), infants or children <5 yo. Fever, malaise, tender erythroderma on
neck folds axillae. RAPID crusty on eyes, nose, mouth. Nikolsky sign (peeling). ->IV
Abx
*Education- Thorough cleansing of breaks. Post In ammatory pigment change
(wks to mos)
● Cellulitis-common after bites, trauma or penetrating wound, children with DM and
immunosuppression. Strep penumoniae and S. aureus common.Buccal cellulitis over
joints by Hemophilius in uenzae <3mo to 3 yo, but decreased rate d/t vaccine.
● Clinical ndings-previous skin disruption or recent URI (H. in uenzae). Edema
w/i 24 hrs with insect bite->in ammatory. w/i 48-72 hrs->infectious. Fever, chill,
malaise, irritability, anorexia, vomiting, chills. Recent sore throat, pruritus, stool
retention, constipation, blood streaked stools. Erythematous, indurated, tender,
swollen, warm with poorly demarcated borders. Blue to purple tinge. Erysipelas-
orange peel
● Dx test-CBC, blood cx. Gram stain, cx for pus.
● Management-f/u in 24 hrs.
○ hospitalizations for infants for septic workup
○ strep?-PCN, Benzathine PCN IM, PCN V PO, Rocephin IM if allergic)
○ Staph-IM Rocephin+PO dicloxacillin or PO Ke ex
○ MRSA-clinda PO
○ H.In uenzae-Augmentin PO, methicillin or 3rd gene cephalosporin.
● Complications-Recurrent strep infection, septicemia, NF, TSS.
○ Education-cleansing and bandaged. Hand washing. HIB vaccine, not
shared bath water.
NR 602 Final Exam Study Guide

■ Folliculitis and furuncle-super cial bacterial in ammation of hair follicle

(folliculitis) and deeper infection with base of hair (furuncle). S. aureus common.
M>F
● Clinical ndings-pruritis for folliculitis, tenderness with furuncle.
Hot tub exposure?-most dense covered by swim suit after exposure.
 Fever, malaise, lymphadenopathy? Discrete, erythematous 1-2mm
papu;es or pustules. Face, scalp,thighs, upper arms, buttocks, back.

Nodules with furuncle.

● Dx test-gram stain, cx. MRSA?
● Management-warm compress with soap and water. Topical
keratolytics (benzoyl peroxide) for 5 days.
○ Topical abx, antistaph beta-lactamase-resistatn abx.-
>dicloxaccin.
○ Hand hygiene. No shaving. f/u in 1wk for folliculitis and 1 day
for furuncle or abscess.
● Complications-sycosis barbae.
○ Fungal infection
■ Candidiasis (Moniliasis)
■ Tinea Capitis (below)
■ Tinea corporis
■ Tinea cruris
■ Tinea pedis
■ Tinea vesicolor
○ Viral infection
■ Herpes simplex
■ Herpes Zoster
■ Molluscum contagiosum
■ Warts
○ Infestations of skin
■ Pediculosis
■ Scabies
○ Allergic and in ammatory reactions
■ Acne Vulgaris
■ Atopic dermatitis
■ Contact dermatitis
■ Diaper Dermatitis
■ Seborrheic dermatitis
○ Drug eruptions
 ○ Vascular reactions of skin
NR 602■ Urticaria
Final Examand angioedema
Study Guide
■ Erythema multiforme, Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis
○ Papulosquamous eruptions of skin
■ Pityriasis Rosea
■ Psoriasis
■ Lichen Striatus
■ Keratosis Pilaris
○ Congenital lesions of skin
■ Vascular and pigmented nevi
○ Cutaneous manifestations of underlying disease
■ Acanthosis nigricans
○ Other derm issues in peds
■ Vitiligo and hypopigmentation disorders
○ Hair and nail disorders
■ Tinea capitis
■ Traumatic Alopecia
■ Alopecia areata
■ Onychomycosis
■ Paronychia
○ Body art
■ Tattos and body piercing
● Mongolian spots(Donna lambert)  

○ Mongolian Spots- (also known as slate gray Nevi or dermal melancyotsis) pg609-610

○ -          Pigmentation that doesn’t develop completely, lying just under the skin.
Causing discoloration of the area that is underdeveloped.

○ -          Present at birth or shortly after birth. Usually self limiting within the
rst few
years of life. If present after onset of puberty, then disappear is unlikely. Usually fades
over time.

○ -          Most common in African American (90%), Hispanic (70%) and Asian ethnicity (62
to 86%). Usually only 10% of Caucasian infants develop this.

○ -          Usually located on the presacral or lumbosacral area, in dark skinned infants.

Also, on buttocks, shoulders, or upper and lower extremities.

○ -          Usually blue or slate gray, irregularly, variably size macules.

○ -          Important to document to distinguish from bruising.

○
Lead poisoning (Ali) (pg. 934 & Week 5 module)
Risk factors for lead poisoning:
● The child exhibits pica
●  Living near a lead smelter, battery recycling plant, or other industry likely to release
lead
●  A family member or caregiver works with lead-based materials
●  Household members engage in hobbies that might include ceramics, stained glass,
making own shing tackle
●  Painted or unusual materials are burned in wood stoves or replaces
● The family uses complementary, herbal, or folk remedies
 ● Food is prepared or stored in imported pottery or metal containers or water obtained
from contaminated
NR 602 Final Exam pipes
Study Guide
 
Mandatory screening questions:
● Does your child live in or regularly visit a house built before 1950? (This could include
a day care center, home of a babysitter, or a relative.)
● Does your child live in or regularly visit a house built before 1978 with recent, ongoing,
or planned renovations or remodeling (within the past six (6) months)?
● Does your child have a sibling or a playmate that has or did have lead poisoning?

 
Physical exam:
● Clinical signs of lead toxicity may not be noted during the physical examination
because most lead retained by the body is stored in the bones and is not measured by
blood lead levels (BLLs).
● Clinical manifestations of poisoning are typically not visible until the lead level is
markedly elevated, however, a child can have high BLLs (e.g., 45 mcg/dL) with no obvious
clinical signs on physical exam.
● Most children have low level, chronic exposure with few or no symptoms
● Many children have subclinical e ects or have symptoms that are easily confused
with other conditions such as anemia (microcytic, hypochromic), constipation,
abdominal pain, impaired hearing, learning disabilities, delayed growth, and/or
hyperactivity.
● At higher levels, lead a ects vitamin D metabolism, nerve conduction velocities, and
hemoglobin synthesis that can lead to myocardial excitability, increased intracranial
pressure, seizures, coma, and death. Many children do not demonstrate signs of acute
toxicity until they have high lead levels.
Diagnostic Studies:
● All children at risk should be screened at 1 AND 2 years of age for lead.
● Immigrant children or other children from 3 to 6 years of age who have not been
previously tested should be screened.
● Normal level is <5 mcg/dL
● If an elevated lead level is present, an assessment of free erythrocyte protoporphyrin
(FEP) and zinc protoporphyrin (ZPP), and iron de ciency screening, including serum
ferritin, are helpful in determining diagnosis and management.
● There is compelling data that children of lower income families are at signi cantly
increased risk. In the non-Medicaid populations, many sources recommend continued
universal screening at 12 and 24 months. Other sources recommend a lead risk
assessment. The AAP recommends either, but a minimum of a risk assessment at 6, 9, 12,
18, 24 months, and yearly at 3, 4, 5 and 6 years.
 
Di erential Diagnosis:
GI infections, other causes of anemia, growth retardation, behavior disorders, attention de cit
hyperactivity disorder (ADHD), and CNS infections are included in the di erential diagnosis.
Management:
● Prevent the child’s exposure to lead in the environment—most common source is lead
based paint
● Monitor BLLs
● Correct dietary de ciencies (if any)
● Treat for toxicity (see below)
● Other children in the same household or environment where exposure could have
occurred should be tested and treated as indicated . In all cases of lead toxicity (≥5
mcg/dL):
○ Inform caregiver of level of toxicity
○ Provide caregiver dietary and environmental education
○ Remove child from source of lead if known
 ○ Report to public health department
NR ○ Initiate
602 Final environmental investigation (Some health department may do this)
Exam Study Guide
○ Initiate lead hazard control/abatement
○ Follow up BLL every 3 months until BLL declines
○ Refer to social services as appropriate
● Chelation therapy is recommended for levels higher than 45 mcg/dL to treat acute,
severe, and life-threatening poisoning. It is also critical that providers do follow-up
testing for children with positive lead screens until levels return to normal.
 Blood Lead Levels:
<5 mcg/dL
● Not considered lead poisoning
○ Provide caregiver/parent dietary and environmental education
○ Refer to social services as appropriate
○ Conduct environmental assessment to determine if child is exposed to a lead
source (e.g., pre-1978 housing)
● If high risk, retest in 6 months
● If low risk, no further testing necessary; ongoing monitoring for changes in
environment
≥5-9 mcg/dL
● Reference value requiring intervention:
○ Con rmatory venous blood test within 1-3 months
○ Early follow-up (two to four tests) by 3 months
○ Later follow-up (after BLLs decline) at 6-9 months
10-44 mcg/dL Con rmatory venous blood test within 1 week to 1 month a
● 10-19 mcg/dL
○ Early follow-up 1-3 months 
○ Later follow-up at 3-6 months
● 20-24 mcg/dL
○ Early follow-up 1-3 months 
○ Later follow-up at 1-3 months
● 25-44 mcg/dL
○ Early follow-up 2 weeks to 1 month
○ Later follow-up at 1 month
○ Retest every month until results <15 mcg/dL for at least 6 months, then retest
every 3 months until child is 36 months old
45-59 mcg/dL
● Con rmatory venous blood test within 48 hr
● Complete history and physical examination
● Complete neurologic examination
● Lab work: Hgb or Hct and iron status (FEP or ZPP)
● Abdominal x-ray with bowel decontamination if indicated
● Chelation therapy, may be oral in ambulatory setting
● Early follow-up as soon as possible
● Retest every month until results <15 mcg/dL for at least 6 months, then retest every 3
months until child is 36 months old
60-69 mcg/dL
● Con rmatory venous blood test within 24 h
● Complete history and physical examination
● Complete neurologic examination
● Lab work: Hgb or Hct and iron status (TIBC or SF)
● Abdominal x-ray with bowel decontamination if indicated
● Chelation therapy, may be oral in ambulatory setting
● Early follow-up as soon as possible
● Retest every month until results <15 mcg/dL for at least 6 months, then retest every 3
months until child is 36 months old
≥70 mcg/dL
● Medical emergency:
○ Retest immediately as an emergency lab test with venous blood sample
○ Hospitalize for IV chelation
 ○ Proceed according to action for 45-69 mcg/dL
Early
●NR 602follow-up as soon
Final Exam as possible
Study Guide
● Retest every month until results <15 mcg/dL for at least 6 months, then retest every 3
months until child is 36 months old

Patient and Family Education:

For lead poisoning to occur, there must be an intersection between the environmental hazard
and the child. In older homes, the point of greatest risk is the window because the windowsills
and putty may have high lead concentration. Because toddlers are the ideal height to reach
windowsills and are often drawn to open windows, the age of greatest risk is 2 to 3 years.
Summer is the season of greatest risk. Children can acquire lead through two major sources,
inhaled paint powder and ingested paint chips.
 
Parents need to be informed that it is critical to have professional assessment of the level of
home contamination and professional abatement may be necessary. Public health o cials
can work with parents to identify ways to control lead dust and paint chips in older homes
and can work with landlords on lead abatement of properties. Other strategies parents can
use include:
● Cover smaller peeling paint areas with sticky-backed paper
● Damp-mop and damp-dust with household cleaners or lead-speci c cleaning
products (e.g., Ledizolv) twice weekly to decrease lead dust in the air; do not dry mop or
sweep
● Pick up and dispose of paint chips with a disposable rag or paper towel soaked in
phosphate cleaner
● Run water until temperature changes to ush pipes of lead sediment
● Do not store or cook food in lead crystal or pottery that contains lead
● Remove work clothes and wash hands before returning home if job is lead-related
 
● Headaches - Angie King

Headaches - Pages 978-983

· Most common reason for referral to pediatric neurology

· Common during childhood

o Increases in frequency and incidence during adolescence

· Fall into two classi cations:

o Chronic

o Acute

· Common types that fall under chronic or acute and most commonly seen in PCP

· Pediatric Migraine Headache:

NRo 602
MoreFinal
than Exam Study
5 attacks with Guide
following indications

o Duration 2-72 hours

o At least two of the following

§ Bilateral or unilateral (common bilateral in young children; unilateral pain

usually emerges in late adolescence or early adult life)

§ Usually frontal/temporal

§ Occipital location is unusual and should be carefully evaluated (occipital

headache in children whether unilateral or bilateral is rare and calls for
diagnostic caution: many cases are attributable to structural lesions

§ Pulsating

§ Moderate to severe intensity aggravated by routine physical activity

§ Has either nausea or vomiting, or photophobia and phonophobia

§ Not attributed to another disorder

o Infrequent Episodic Tension Type Headache

o At least 10 episodes occurring on <1 day per month on average <12 days/year

o Headache lasting 30 mins – 7 days

o Headache at least has two of the following:

§ Bilateral location

§ Pressing/tightening (non pulsating)

§ Mild or moderate intensity

 NR 602 §Final
Not aggravated
Exam Studyby routine
Guide exercise such as walking or climbing stairs

o Has to have both the following

§ No nausea or vomiting (anorexia may occur)

§ No more than one photophobia or phonophobia

o Not attributed to another ICHD 3 diagnosis

· Chronic Tension Headache:

o Headache occurring on more than 15 days per month on average over 3 months

o Headache lasts hours to days and may be continuous

o Headache has at least two of the following:

§ Bilateral location

§ Pressing/tightening (non pulsating)

§ Mild to moderate intensity

§ Not aggravated by routine physical activity

o Must have both the following:

§ No more than one photophobia, phonophobia or mild nausea

§ Neither moderate or severe nausea or vomiting

o Not attributed to another ICHD 3 diagnosis

· Migraines are particularly di cult to diagnose

 Manifestations,
NRo 602 Final Examin Study
addition to description of symptoms, are expressed di erently
Guide
and with less clarity during childhood

· Exact physiologic mechanism and etiology for many headaches have not been
conclusively determined

· Headache pain occurs when pain sensitive intra-cranial structures are activated

o Structures include the arteries of the Circle of Willis and some of their branches,
Meningeal Arteries, large veins, and dural venous sinuses, and part of the dura near
blood vessels

o Muscles around the head, neck, scalp, eyes, jaw, teeth, sinuses, and external
carotid artery and its branches are external to the skull

o These structures result in localized pain, carried by CN V, VII, IX, X

· Children as young as 2 have been seen having migraine symptoms.

· Symptoms seen before 10 years old are more common in boys

· Symptoms seen during the teen years are more often seen in girls. This is related to
hormonal changes.

· Clinical ndings:

o History: it is important to ask the child as much as possible and not the parent.
Ask open-end questions.

o Duration and Severity: Severe onset warrants further investigation

§ Headache log may help identify triggers.

o Frequency and Trigger: Low intensity headaches, that the child recovers from is
less likely to have serious intracranial etiology. Triggers can include: ovulation,
menstruation, exercise, food, odors, stress, ca eine intake, shell sh, dairy products,
and some dried fruits.
 Location:
NRo 602 FinalOccipital or consistently
Exam Study Guide localized headaches can indicate an
underlying pathology.

§ Facial pain: might be sinusitis

o Oculomotor imbalance can produce a dull periorbital discomfort, whereas

temporomandibular joint pain tends to localize around the periauricular or
temporal areas.

§ Always ask if the pain is bifrontal or unilateral.

o Quality and Severity of Pain:

§ Sharp, throbbing or pounding may indicate a vascular migraine.

§ Dull and constant pain may be tension or organic.

§ Severity is assessed by limitations of life activities, missed days of school.

o Age of onset: Progression of the headaches over time and longest period of time
without symptoms.

o Home management and medication doses.

o Associated symptoms:

§ Nausea, vomiting, visual changes, dizziness, paresthesia, neck/shoulder

pain, back pain, otalgia, abdominal pain, hypersomnia, food cravings,
confusion, ataxia, pallor, photophobia and phonophobia.

o Head trauma: If associated with headache, a subdural hematoma or post

concussive syndrome must be considered.

o Psychologic Symptoms: Evaluate the presence of depression, school stressors, or

concerns about family functioning.

o Family history: Some children with headaches, especially migraines have a family
history of migraines.
· NR 602 FinalFeatures
Distinguishing Exam Study Guide Types:
of Headache

o Migraine and Migraine with aura:

§ With Aura:

· Represents 1/3 of children with migraines

· Prodrome may precede headache up to 24 hours characterized by

irritability, elation/sadness, talkativeness/social withdrawal, food
craving/anorexia, water retention, sleep disturbances

· Severe, unilateral often throbbing headache follows aura >30 min

later; lasts 5-20 min; may generalize

· About 5% of children with classic migraine do not have a headache

with their auras

§ Without Aura:

· Represents about 2/3 of children with migraines

· Also has similar prodrome features but more pronounces

· Headache in young children: commonly bilateral orbital, or

frontotemporal; pain may radiate to fact, occiput, neck

· Headache throbbing or pulsating; typically lasts < 4 hours but can

last up to 72 hours; moderate or severe intensity

· Activity aggravates, and sleeps relieves headache

· Nausea or vomiting or both

· Sensitivity to light, sound, and movement

§ Characteristics of migraines include:

NR 602 Final ·Exam Study
nausea, Guide pain, vomiting, unilateral pain, pulsating pain,
abdominal
relief with sleep, an aura, visual changes such as dark or blind spots,
and a history of family member (usually on the maternal side) with
migraine without aura, dizziness and motion sickness may be
described.

· Infants: May present with irritability, sleepiness, and pallor.

· Preadolescents: Nausea and vomiting may not occur, and the pain
can be more frontal with lethargy, and sleep to follow.

o Muscle contraction or Tension headaches: The pain is dull and bifrontal or

occipital with nausea and vomiting occurring only rarely. Characteristics of tension
headaches feel like a band squeezing the head. Tension headaches can last for
days or weeks but generally do not interfere with activities.

§ Psychosocial stress can be a major factor in tension and chronic daily

headaches in both children and adolescents.

o Medication overuse headaches: Resulting in the overuse of medications such as

acetaminophen, NSAIDs, and Excedrin migraine. These headaches are comorbid
with primary headache disorders and are increasing in the frequency in children.

§ Medication overuse is described as the use of the medication more than 15

days per month, manifested by gradual increase in headache frequency even
in the face of increasing analgesic treatment.

o Abdominal migraine: Midline pain, nausea and vomiting with minimal or no

headache. This rare and somewhat controversial diagnosis can be suggestive of
complex partial seizures and may merit further evaluation.

o Secondary Headaches: (or those headaches that have a pathologic process). Key
historical markers are sudden onset of hyper acute or increasing pain severity or
accompanying neurologic signs.

§ Red Flags suggestive of secondary headache:

· Headache upon awakening that then fades; increases in frequency

and severity over a period of only a few weeks; is persistent and
unilateral
NR 602 Final ·Exam Study Guide
First or worst headache

· Pain that awakens a child from sleep

· Vomiting but not nauseated that may relieve the headache, or

intractable vomiting

· Visual disturbances, diplopia, edema of the optic disc

· Increased pain with straining, sneezing, coughing, defecation or

changes in position

· Occipital region and neck pain

· Educational, mental, personality, or behavioral alterations;

irritability

· New onset seizures or facial or extremity numbness

· Unsteadiness or dramatic changes in balance, gait abnormalities

· Fever with or without nuchal rigidity

· Family history of neurologic disorders

· Child has a history of a ventriculoperitoneal shunt, meningitis,

hydrocephalus, tumor or prior history of a malignancy

§ Red Flags of Intracranial Structural Pathology

· Infants:

o Full anterior fontanelle

o Open metopic and coronal sutures

 Poor growth
NR 602 Final ExamoStudy Guide

o Impaired upward gaze

o Abnormal head growth

o Shrill cry

o Lethargy

o Vomiting

· Children:

o Headache described as severe, excruciating of recent onset,

unlike any previously experienced headache, no period of normal
functioning between episodes, or persistent and unilateral

o Papilledema or abnormal eye movements (or one or both eyes

suddenly turn in)

o Ataxia, hemiparesis, or abnormal deep tendon re exes

o Cranial bruits

o Personality changes

· Diagnostic Studies:

o Imaging studies are rarely indicated unless the history suggests intracranial
pressure, there is a sudden onset, increased severity, or change in headache
pattern, the neurologic examination is abnormal, or when a complaint of dizziness is
accompanied by double vision, a sensation of whirling, or confusion.

o CT is generally not in favor due to radiation.

 MRI is
NRo 602 the Exam
Final rst-lineStudy
treatment unless imaging is extremely urgent and cannot be
Guide
obtained immediately. Imaging should be done within 2-4 weeks to avoid
progression of symptoms or delay in treatment.

o EEG should be obtained if the history and physical suggest a seizure process.

o If history of external trauma (MVA), then cervical and spinal x-ray can be done

· Di erential Diagnosis:

o Sinusitis, trigeminal neuralgia, pseudotumor cerebri, sleep disorders,

hyperthyroidism, hypertension, cyclic vomiting, abdominal migraine, BPV, and
temporomandibular joint dysfunction

· Management:

o Individualized: may include: pharmacologic, and non-pharmacologic modalities

o Goals: Reduce frequency, reduce severity, duration, and disability to improve

quality of life

· Medications:

o Nonsteroidal anti-in ammatory drugs are rst line for acute treatment.
(Acetaminophen, naproxen sodium and ibuprofen).

o Zofran for nausea

o **Triptans have not been tested for safety and e cacy in children and
adolescents with the exception of sumatriptan and zolmitriptan.

o Prophylactic therapy is the use of speci c B-blockers, antidepressants,

anticonvulsants, or calcium channel blockers

· Di erential Diagnosis for Headaches in Children:

o Cocaine         
NR 602 §Final
Migraine
ExamlikeStudy
pain inGuide
patient with no history of migraines

o Marijuana

§ Frontal, mild

o Analgesics, oral contraceptive, steroids, cardiovascular agents              

§ Pain follows administration or withdraw of drug

o Food additives  

§ Pain occurs only individuals genetically sensitive, pain is di use, throbbing

after ingestion

o Vasculitis             

§ Uncommon in children; can occur as part of a collagen vascular disease

(lupus)

o Chronic HTN  

§ Low grade occipital pain on awakening or frontal during the day

o Eyestrain              

§ Dull, aching pain behind eyes, relieved when eyes are closed, muscular
fatigue

o TMJ                  

§ >8 years old, pain on one side of face and vertex of TMJ

o Whiplash             

§ Pain dull, aching in neck, shoulders, and upper arms with poor neck rotation.
 Following
NRo 602 Finalpartial
Examor gen. seizure
Study Guide          

§ Di use pain

o Infectious illness (meningitis)             

§ Pain may be nonspeci c

o Dental disease  

§ Uncommon

o Malfunctioning shunt             

§ History of ventriculoperitoneal, ventriculopleural, or ventriculoatrial shunt

o Toxins                                    

§ Dull aching pain

o Tumor (brain)                        

§ Progressive worsening, severe, worst early morning pain and lying down

o Exertional                             

§ Sharp and occurs after exercise

o Posttraumatic head injury  

§ Pain can be severe (epidural hematoma). Can start weeks after injury

· Medications:

o Acetaminophen
 NR 602 §Final
10-15mg/kg
ExamPO everyGuide
Study 4 h up to 500 mg every 4 h

§ For mild to moderate pain (acetaminophen has faster onset than ibuprofen)

o Ibuprofen

§ 7.5-10 mg/kg/dose PO every 6-8 h. Max dose 2400mg per day

§ Use at onset of attack. Greater headache resolution than acetaminophen.

§ Take with food

o Naproxen sodium

§ Children >2 years old; 5-7 mg/kg PO every 8-12 h

§ Adolescents: 400mg as initial dose; 200mg PO every 8-12 h (max dose

1000mg/24 h)

§ Safe and e ective

o Zofran

§ Ages 4-11 years old, on 4mg tablet or ODT tablet or 5mL

§ For vomiting associated with headache

· Migraine Speci c Abortive Acute Medications

o Sumatripton: Children >12 years old when no response to analgesics

§ Nasal spray 5mg/spray; 5-20mg each nostril once (can repeat every 2 h max
dose 40mg/24 h)

§ Subcutaneous 3-6mg single dose

 NR 602 §Final
Oral 25-100mg onceGuide
Exam Study (may repeat every 2 h; max 200mg/24 h) available in 25,
50 or 100mg tabs

§ FDA approved for >18 years old; regarded safe and well tolerated > 12 years
old. O label < 12          years old if not responded to other medications

§ Use with caution in patient with aura

§ Do not use in basilar type and hemiphlegic migraine or in those with

cardiovascular disease, uncontrolled hypertension, or who have use MAOI in
prior 2 weeks

· Prohylaxis Therapies for Pediatric Migraines

o Amitriptyline - Antidepressant

§ 0.25mg/kg/day PO at bedtime; may increase dose by 0.25mg/kg/day every 2

weeks; max dose 1mg/kg/day

§ One of the most widely used, but o label. Use caution in children <12

§ Order ECG if dosage exceeds 25mg/day

§ Adverse e ects: somnolence, dry mouth dysrhythmia

o Divalproex sodium – Anticonvulsant

§ Dosage depends on preparation and age

§ Not for use in children younger than 2

§ Adverse e ects: Weight gain, heartburn, hair loss, dizziness

o Topiramate – Anticonvulsant

§ Adolescent/adult immediate release oral; initially 25mg once daily (in

evening); may increase weekly by 25mg daily to 100 mg daily divided into two
 doses
NR 602 Final Exam Study Guide
§ This drug is gaining acceptance for e cacy. Indicated in epilepsy for
children as young as 2

§ Adverse e ects: Weight loss, episodes of paresthesia, cognitive slowing, loss

of appetite, dizziness, irritability; monitor any changes in school/cognitive
performance

o Cyproheptadine – Anti-serotonergic agents

§ Not recommended <2 years old

§ 3 years and adolescents: 0.2-0.4mg/kg/day divided in two equal doses; max

daily dose 0.5mg/day

§ E ective in migraine prophylaxis in ages 3-12

§ Adverse e ects: Weight gain (appetite stimulant) and somnolence; sedation

more problematic at doses higher than 4-8mg/24h

o Propranol – Antihypertensive

§ 35kg; 10-20mg three times daily

§ Over 35kg: 20-40 mg three times daily

§ Adults: 80mg/day divided every 6-8 hours with max of 160-240mg/day in

divided doses of 6-8 h

§ May take several weeks to a month to be e ective

§ Do not use in children with history of asthma; use with caution in children
with depression

§ Adverse e ect: lowers blood pressure, depressive e ects or exercise induced

asthma
· Complimentary
NR 602 Final Therapy
Exam Study Guide

o Biofeedback and cognitive therapies, acupressure and acupuncture, nerve block

or needling, yoga, physical therapy, massage therapy. Essential oils and
aromatherapy has also helped.

· Referral

o Persisting chronic headaches may bene t to see a headache subspecialist

· Complications

o School absence, anxiety, and depression

· Patient and Parent Education

oHeadache plan: Plan for rescue management, include ice, rest, dark room and
management in school

o Headache diary: Helpful to guring out triggers and monitoring progress

o Triggers Factor: Everyone is di erent, consider dietary physiologic, and

environment. Common food triggers tyramine, nitrates, MSG, aged cheese, arti cial
sweeteners, ca eine, chocolate, citrus fruits, cured meats, nuts, onions, and salty
foods. Physiologic triggers: hormonal changes, emotional anxiety, irregular eating,
or sleep or stress. Environmental triggers: weather changes, altitude, lighting, sun
odors, motion or activity

o Nutrition: Importance of eating breakfast, three meals a day at regular hours, and
no skipping of meals. Every meal should contain protein, high ber, low fat, and
normal levels of sodium and sugar.

o Fluid intake: 4-8 glasses of water daily to prevent dehydration headaches. Avoid
ca eine. Sports drinks without ca eine could help during a headache.

o Sleep: 8-12 hours of sleep at night, and do not oversleep. Go to bed and wake up
same time every day if possible. Turn o electronic devices 1-2 hours before bedtime.
 Exercise:
NRo 602 FinalAerobic
Examactivity
Study 30-45
Guidemin with increased heart rate and 5-10 mins of
stretching. Weight lifting does not count.

o School: Develop a home/school program

o Electronic use: Limit total use of devices

o Stress: Plan activities and avoid overcrowded schedules. Understand pain and
stress management techniques. Understand relaxation and muscle relaxation
techniques.
● Musculoskeletal assessment of the infant (Becky A.)
○ Week 6 ch43 (p 888)
Galeazzi Maneuver (leg length discrepancy)
Flex hips and knees while supine and place feet near butt. Look for knee height
equality- + sign if knee heights are unequal **not reliable for those with dislocatable
hips

Barlow Maneuver (Adduction potential for hip dislocation)

1st month of life, looking for laxity & instability
Baby is naked, supine, knees exed. Hip is exed & thigh is brought into adducted
position while applying gentle downward pressure- + femoral head slips or can e gently
pushed out of socket
 Ortolani
NRfew
602 Maneuver  (abduction)
FinalofExam
1st months life Study Guide
Like barlow but in reverse. Palpable clunk + sign. High pitch click at the end of
maneuver is common and not considered positive

 
Klisic test (observational sign of hip placement)
Place tip of 3rd nger of one hand over greater trochanter & index nger of same hand
on anterosuperior iliac spine. Imaginary line between the ngers should point to
umbilicus. + if points halfway btwn umbilibus & pubis

** thigh fold asymmetry is often present in infants with unilateral hip dislocation but
this is not diagnostic **
● Cystic brosis (Erin S.)
● Traumatic brain injury (Bri F)
● Sickle cell anemia (Jen H)
● Iron deNRciency
602anemia (Jen H.Study
Final Exam ) Guide
● Anemia of prematurity (MICHAEL S.)
Anemia of prematurity: week 6 ch39. (pg 750)
                Full-term infants accumulate almost 80% of their iron stores during the last trimester
of pregnancy. Delayed clamping of the umbilical cord also ensures that newborns receive the
maximal transfusion to begin life. Along with prematurity, maternal anemia, maternal
hypertension with intrauterine growth retardation, and/or gestational diabetes can result in
less iron transferred to the fetus. In the case of preterm births, the decreased iron stores are
depleted rapidly and the normal physiologic nadir occurs earlier, aggravated by a smaller
total blood volume at birth and poor GI absorption. The use of erythropoietin to prevent and
treat anemia of prematurity also increases the risk of iron de ciency. In general, preterm (<37
weeks’ gestation) infants require an oral supplement of elemental iron at 2 mg/kg per day
from 2 weeks through 12 months of age.
                      Breast milk provides an average iron content of 1.0 to 0.3 mg/L with a high
bioavailability. Because there is large variation in the iron content in human milk, the content
of maternal milk may not always provide for the needs of the growing infant. It is
recommended that the exclusively breastfed term infant receive elemental iron
supplementation of 1 mg/kg/day (15 mg maximum) beginning at 4 months of age and
continuing until iron-containing complementary foods are introduced and taken in adequate
quantities.
● Thalassemia Laci Patton
● Otitis media with and without e usion (Nicole)
○ Acute Otitis Media (AOM)
AOM is an acute infection of the middle ear (Fig 36.4) Burns (2020) Pediatric
Primary Care book-p656
○ The AAP Clinical Practice Guideline requires the presence of the following three
components to diagnose AOM:
■ Recent, abrupt onset of middle ear in ammation and e usion (ear pain,
irritability, otorrhea, and/or fever)
■ MEE con rmed by bulging TM, limited or absent mobility by pneumatic
otoscopy, air- uid level behind TM, and/or otorrhea
■ Signs and symptoms of middle ear in ammation con rmed by distinct TM
erythema or ear pain (holding, tugging, rubbing the ear)
○ AOM often follows eustachian tube dysfunction (ETD).
○ Common causes of ETD include upper respiratory infections, craniofacial anomalies
(cleft palate), allergies, adenoid hypertrophy, and tobacco smoke exposure.  ETD leads
to functional eustachian tube obstruction and in ammation that decreases the
protective ciliary action in the eustachian tube.
○ Eustachian tube obstruction causes negative pressure as air absorbs in the middle
ear (see Fig 36.4). The negative pressure pulls uid from the mucosal lining and causes
a sterile uid accumulation that may be colonized by bacteria and result in purulent
uid. Young children have shorter, more horizontal, and more accid eustachian tubes
that are easily disrupted by viruses, which predisposes them to AOM.
○ Respiratory syncytial virus and in uenza are two of the viruses most responsible for
the increase in the incidence of AOM seen from January to April.  Although a virus is
usually the initial causative factor in AOM, strict diagnostic criteria, careful specimen
ha’?9
○
○\
ndling, and sensitive microbiologic techniques have shown that the majority of AOM is
caused by bacteria or bacteria and virus together.
○ Most common infecting organisms in AOM:
■ S. pneumoniae-most common bacteria responsible for AOM
■ Nontypeable Haemophilus in uenza
■ Moraxella catarrhalis
■ S. pyogenes (group A streptococci)
Types of Acute Otitis Media
Type                                       Characteristics
AOM                                   Suppurative e usion of the middle ear
Bullous myringitis         AOM in which bullae form between the inner and middle layers of the
TM andNR bulge
602outward
Final Exam Study Guide
Persistent AOM                   AOM not resolved after antibiotic therapy or AOM recurs within
days of  Tx
Recurrent AOM                   3 separate bouts of AOM within 6-months or 4 within a 12-month
period;
                 often a positive family history of otitis media and other ENT disease
Risk Factors for Otitis Media, Chronic Otitis Media, or Otitis Media With E usion
BOX 36.3
Genetic susceptibility/sibling with history of otitis media
Native Americans and Native Alaskans
Non-Hispanic Caucasian
Prematurity
Younger than 2 years of age
Unimmunized
Day care attendance
Sharing a bedroom
Breastfeeding for less than 6 months
Parental smoking and other ETS exposure
Environmental pollution exposure
Overweight or obese
Feeding in supine position
Autumn season
Male gender
Early onset otitis media
Bilateral OME
Lower socioeconomic status
ETS, Environmental tobacco smoke; OME, otitis media with e usion.
Clinical Findings of AOM
History
Rapid onset of:
• Ear pain that may interfere with activity and/or sleep, especially when lying at
• Irritability and ear pulling in an infant or toddler
• Otorrhea
• Fever
Other key risk factors or symptoms include prematurity, craniofacial anomalies or congenital
syndromes associated with craniofacial anomalies, daycare attendance, disrupted sleep or
inability to sleep, lethargy, dizziness, tinnitus, unsteady gait, diarrhea and vomiting, sudden
hearing loss, stu y nose, rhinorrhea, and sneezing.
Physical Examination of AOM
• Presence of MEE, con rmed by pneumatic otoscopy, tympanometry, or acoustic
re ectometry, as evidenced by:
• Bulging TM (see Fig 36.4)
• Decreased TM translucency
• Absent or decreased TM mobility
• Air- uid level behind the TM
• Otorrhea
Signs and symptoms of middle ear in ammation indicated by TM (amber color is usually seen
in otitis media with e usion [OME]; white or yellow may be seen in either AOM or OME)
(Schilder et al., 2017).
In addition, the following TM ndings may be present:
• Increased vascularity with obscured or absent landmarks (see Fig 36.4).
• Red, yellow, or purple TM. (Redness alone should not be used to diagnose AOM,
especially in a crying child.)
• Thin-walled, sagging bullae lled with straw-colored uid seen with bullous myringitis
Diagnostic Studies for AOM
Pneumatic otoscopy is the simplest and most e cient way to diagnose AOM. Tympanometry
re ectsNRe usion (type BExam
602 Final pattern).
StudyTympanocentesis
Guide identi es the infecting organism and 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.
Di erential Diagnosis for AOM
OME, mastoiditis, dental abscess, sinusitis, lymphadenitis, parotitis, peritonsillar abscess,
trauma, ETD, impacted teeth, temporomandibular joint dysfunction, and immune de ciency
are di erential diagnoses. Any infant 2 months old or younger with AOM should be evaluated
for fever of unknown etiology and not just treated for an ear infection.
Management of AOM
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
demonstrates that symptom management may be all that is required in children with MEE
without other symptoms of AOM (Schilder et al., 2017). Treatment is based on the child’s age,
illness severity, and the certainty of diagnosis. Table 36.6 shows the recommendation for the
diagnosis and subsequent treatment of AOM.
Treatment Guidelines for Acute Otitis Media TABLE 36.6

1. Pain management is the rst principle of treatment with weight-appropriate doses of

children’s ibuprofen or acetaminophen to decrease discomfort and fever. Distraction, oil
application, or external use of heat or cold may be of some use.
2. Antibiotics are also e ective for AOM (Table 36.7).
• Amoxicillin remains the rst-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
(Schilder et al., 2017). β-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, or the child has concurrent
conjunctivitis or has recurrent otitis that has not responded to amoxicillin.
• If the child is younger than 2 years of age, treatment with amoxicillin or
amoxicillin/clavulanate for 10 days, or for children older than 2 years of age, treatment
for 5 to 7 days.
• Ceftriaxone may be e ective for the vomiting child, the child unable to tolerate oral
medications, or the child who has failed amoxicillin/clavulanate.
• 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 36.6) allows the patient to
improve without antibiotic treatment. Pain relief should be provided, and a means of follow-up
must be in place. Recommendations for follow-up include: parent-initiated visit or phone call
for worsening or no improvement; scheduled follow-up appointment; routine follow-up phone
call; or give a prescription to be started if the child’s symptoms do not improve or if they
worsenNR in 48 to 72
602 hours
Final (see Table
Exam Study36.6).
Guide
4. Routine follow-up is not needed if the child improves within 48 hours. If the child has not
shown improvement in ear symptomatology after 48 to 72 hours, the child should be seen to
con rm or exclude the presence of AOM. If the initial management option was an
antibacterial agent, the agent should be changed.
Management of Persistent and Recurrent Acute Otitis Media p658
• Persistent AOM occurs when antibiotic therapy is completed and AOM is still present
or AOM recurs within days of treatment. Retreatment with a broader-spectrum
antibiotic is suggested.
• Persistent MEE is common after resolution of acute symptoms and should not be seen
as a need for continuing antibiotics (see Otitis Media with E usion section).
• Recurrent AOM is de ned as more than three distinct and well-documented bouts of
AOM in 6 months or four or more episodes in 12 months.
An otolaryngology referral is indicated when appropriate therapy for otitis media fails.
Placement of tympanostomy or PE tubes can help relieve discomfort, reduce time with OME,
improve hearing, and decrease the likelihood of further infection (Wallace et al., 2014).
Indications for tympanostomy and the insertion of pressure-equalizing tubes is discussed
below.
Other Treatment Issues for AOM
• The PCP is encouraged to maintain understanding of current recommendations for AOM
management because of rapid changes in resistance patterns and newly developed
treatments.
• Decongestants and antihistamines are not indicated.
• Antimicrobial ototopical drops (o oxacin or cipro oxacin) or ophthalmic drops (tobramycin
or gentamicin) are indicated if the TM is perforated (Fig 36.5), the child has otorrhea, or the
child has patent, draining PE tubes.
• Xylitol, a sugar found in fruits and birch bark, has bacteriostatic e ects against S.
pneumoniae and interferes with bacterial adhesion to mucous membranes. It appears to
have some suppressive e ects in preventing ear infections. Xylitol is available in an oral
solution, lozenges, and chewing gum. The lozenges and chewing gum are more e ective than
the oral solution. Children younger than 2 years old cannot have chewing gum or lozenges.
Xylitol must be given three to ve times a day on a regular basis to be e ective.
• There is no safe or e ective herbal treatment for AOM or OME.
Complications of AOM
Persistent AOM, persistent OME, TM perforation, OE, mastoiditis, cholesteatoma,
tympanosclerosis (Fig 36.6), hearing loss of 25 to 30 dB for several months, ossicle necrosis,
pseudotumor cerebri, cerebral thrombophlebitis, and facial paralysis are possible
complications.
Medications Used to Treat Acute Otitis Media TABLE 36.7, p 658
 NR 602 Final Exam Study Guide

Prevention and Education for AOM

The following interventions, shown to be helpful in preventing AOM, should be encouraged:
• Exclusive breastfeeding until at least 6 months of age protects against AOM (Bowatte
et al., 2015)
• Avoid bottle propping, feeding infants lying down, and passive smoke exposure
• Pneumococcal vaccine; speci cally, PCV13, which contains subtype 19A
• Annual in uenza vaccine helps prevent otitis media
• 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
antibiotic use 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.
Otitis Media With E usion p 659
The diagnosis of OME is made in the presence of MEE without signs or symptoms of acute
ear infection (see Fig 36.7). MEE decreases the mobility of the TM and interferes with sound
conduction.
        OME can occur spontaneously with ETD caused by an in ammatory process after AOM,
viral illness, anatomic abnormalities, barotrauma, allergies, or a combination of these
conditions (Figs. 36.7 and 36.8). ETD changes the middle ear mucosa in the following sequence:
(1) the mucosa becomes secretory with increased mucus production, (2) the mucus absorbs
water as the mucosa becomes viscous, and (3) uid becomes stuck behind the TM. Bacterial
bio lms may explain the persistence of OME. Bio lms are mixed microorganisms enclosed in a
polymeric matrix that adhere to surfaces, such as the middle ear mucosa.
Risk Factors for Hearing Loss Caused by Otitis Media with E usion BOX 36.4p. 660
Bilateral Otitis media with e usion (OME) for 4 months or longer
If two or more present:
OME present for longer than 8 weeks
Speech development slower than peers
Speech less clear than previously
Child decreases amount of talking
Child less responsive to name and other familiar sounds
Child says “Huh?” or “What?” frequently
Child sits close to TV or wants volume louder
Child has di culty learning (reading, spelling)
Child is hyperactive or overly inattentive
OME, Otitis media with e usion.

Clinical Findings of OME

 History
ChildrenNRwith OME
602 FinalareExam
often afebrile and asymptomatic. However, some children may present
Study Guide
with intermittent complaints of mild ear pain, fullness in the ear (“popping” or feeling of
“talking in a barrel”), dizziness or impaired balance. The older child may complain of hearing
loss. The young child may request that you speak louder or require a higher volume than
usual for the radio or television.
Physical Examination of OME
Pneumatic otoscopy reveals decreased TM mobility. An abnormal-appearing TM, often
described as dull, varying from bulging and opaque with no visible landmarks to retracted
and translucent with visible landmarks and an air- uid level or bubble may be seen (Figs. 36.7
to 36.9). Examine head and neck structures for abnormalities.
Diagnostic Studies for OME
The tympanogram is at-type B. The audiogram can show hearing loss ranging from mild to
moderate (25 to 60 dB).
Di erential Diagnosis for OME
Di erential diagnoses include AOM, all causes of hearing loss and anatomic abnormalities,
and persistent unilateral OME can indicate a nasopharyngeal lesion or mass.

Management of OME
Recommendations for management of OME in children 2 months to 12 years of age include
(Rosenfeld et al., 2016):
1. Pneumatic otoscopy should be performed to document OME, particularly in children
with ear pain and/or hearing loss. Tympanometry may be indicated in children to
con rm OME diagnosis.
2. Manage the child with OME with watchful waiting for 3 months from date of
diagnosis.
3. Intranasal steroids or systemic steroids, system antibiotics, antihistamines, and
decongestants are not recommended for treatment of OME.
4. Children with OME who are at risk for speech, language, and learning problems
should be identi ed. An age-appropriate hearing test should be performed if OME
persists for 3 months or longer.
• At-risk children are de ned as having developmental delays because of sensory,
physical, cognitive, or behavioral factors (e.g., hearing loss independent of OME,
speech or language delays, pervasive or other developmental disorders,
syndromes or craniofacial disorders, blindness, and/or cleft palate). These
children should be promptly referred for hearing, speech, and language
evaluation.
5. Reevaluate a child with OME every 3 months until the e usion resolves, or every 3 to 6
months for children with chronic OME. When managing a child with OME, clinicians
should document resolution of OME in the medical record.
6. Communication is key to families understanding the duration and course of OME,
the need for follow-up, and the associated sequelae including potential hearing
impairment and impact on speech and language development.
7. Referral to an otolaryngologist is recommended when otoscopy suggests possible or
impending structural damage of the TM, signi cant hearing loss is identi ed, and/or
for chronic or persistent OME for more than 6 months. The need for referral should be
clearly communicated to the family.
8. In a child younger than 4 years old, insertion of tympanostomy tubes is performed
for persistent or chronic OME with associated sequelae; adenoidectomy is not
recommended unless an indication exists other than OME. In a child 4 years old or
older, insertion of tympanostomy tubes and/or adenoidectomy is recommended for
OME.
Complications or OME
Recurrent AOM and hearing loss that may be transient CHL, or with persistent OME,
permanent high-frequency SNHL.
● Urinary tract infection (Nicole)
Urinary Tract Infection
from Burns
NR(2020)
602 Pediatric Primary
Final Exam Care
Study book-p824
Guide
There are three kinds of UTI in children:
● asymptomatic bacteriuria
● cystitis
● pyelonephritis
Young children may have limited or unusual symptoms; therefore, a high degree of suspicion
must be maintained to diagnose UTI. In ammation and infection can occur at any point in the
urinary tract, so a UTI must be identi ed according to location.
Asymptomatic bacteriuria is bacteria in the urine without other symptoms, is benign, and does
not cause renal injury.
Cystitis is an infection of the bladder that produces lower tract symptoms but does not cause
fever or renal injury.
Pyelonephritis is the most severe type of UTI involving the renal parenchyma or kidneys and
must be readily identi ed and treated because of the potential irreversible renal damage.
Clinical signs thought to be consistent with pyelonephritis include fever, irritability, and
vomiting in an infant, and urinary symptoms associated with fever, bacteriuria, vomiting, and
renal tenderness in older children.
UTIs are the most common cause of serious bacterial infection in infants younger than 24
months old with fever without a focus.
A complicated UTI is de ned as a UTI with fever, toxicity, and dehydration, or a UTI occurring in
a child younger than 3 to 6 months old.
UTIs may be classi ed based on their association with other structural or functional
abnormality such as VUR, obstruction, dysfunctional voiding, or pregnancy.
Additionally, a UTI must be identi ed as a rst occurrence, recurrent (within 2 weeks with the
same organism or any reinfection with a di erent organism), or chronic (ongoing, unresolved,
often caused by a structural abnormality or resistant organism).
Age and gender of the pediatric patient are important factors in determining the evaluation
method and the course of treatment.
The organism most commonly associated with UTI is Escherichia coli (70%), although other
organisms (such as Enterobacter, Klebsiella, Pseudomonas, and Proteus) can cause infection.
UTI secondary to group B streptococcus is more common in neonates.
Factors contribute to the etiology of UTIs:
● Most UTIs are thought to be ascending (i.e., the infection begins with colonization of
the urethral area and ascends the urinary tract). If the infection progresses to the
kidney, intrarenal re ux deep into the kidneys can lead to scarring.
● However, the most important risk factor for the development of pyelonephritis in
children is VUR, which can be detected in 10% to 45% of young children who have
symptomatic UTIs.
● Furthermore, re ux of infected urine from the bladder increases the risk of
pyelonephritis. This kidney damage occurs in the compound papillae, which have wide
and gaping openings allowing intrarenal re ux. The compound papillae are located in
the upper and lower poles of the kidney, the usual site of scarring.
Host resistance factors and bacterial virulence factors are also important in the etiology of
UTIs:
● Presence of a structural abnormality or dysplasia (such as VUR, obstruction, or other
anatomic defect), or the presence of functional abnormalities (such as dysfunctional
voiding or constipation).
● Female gender (having a short urethra), poor hygiene, irritation, sexual activity or
sexual abuse, and pinworms.
● Several bacterial factors are known, but the two most important ones are adherence
and bacterial virulence. Bacteria that have mbriae or pili are able to adhere to the
 surface of the bladder mucosa; this allows the bacteria to resist the bladder’s defensive
cleansing ow ofExam
NR 602 Final urine and causes
Study Guidetissue in ammation and cell damage.
● Adherence may also play a role in bacteria ascending the urinary tract. Virulence
refers to the toxicity of substances released by bacteria. The greater the virulence, the
greater the damage to the urinary tract. Both of these factors enhance colonization of
the urinary tract and aid in the persistence and e ect of the bacteria.
Clinical Findings of Urinary Tract Infection in Children of Various Ages
table 41.3, p 825

The risk of UTI in infants 2 to 24 months old is about 5%. The incidence in females is more
than twice that of males (2.27%); uncircumcised boys have a rate 4 to 20 times greater than
circumcised boys (AAP Subcommittee on Urinary Tract Infection, 2016). There is a greater
frequency in premature and low-birth-weight infants. Females older than 12 months old have
2.1% prevalence; after the rst year of life, it is also more common to nd a UTI in females than
in males with an overall incidence of 1% to 3% in girls and 1% in boys (Elder, 2016d). The
incidence of UTI is often increased in sexually active adolescent girls. The risk of recurrence
within the rst year after an initial infection is common.
History and Clinical Findings of UTI p825
The following information should be obtained:
• Family history of VUR, recurrent UTI, or other kidney problems
• Prenatally diagnosed renal abnormality
• Previous infection: Request records from the past infection evaluation and diagnostic
studies
• Circumcision
• Risk factors for infants 2 to 24 months old with no other source of infection (AAP
Subcommittee on Urinary Tract Infection, 2016)
• Female—white race, age younger than 12 months old, temperature 39°C or higher,
fever for 2 days or more
• Male—nonblack race, temperature 39°C or higher, fever for more than 24 hours
• Hygiene habits: Wiping front to back
• Voiding patterns: Frequency, abnormal stream, complete emptying, dribbling,
enuresis, holding urine, incomplete emptying, and bathroom avoidance
• Constipation, perianal itching (pinworms)
• Irritants, such as nylon underwear or clothing (spandex, tight pants or shorts that
rub); bubble bath or sitting in soapy bath water
• Hypertension
• Sexual activity, masturbation, or sexual abuse
• Other infection: Pinworms, diaper rash
Physical Examination
See Table 41.3 for age-related symptoms.
• General appearance (toxic appearing?)
• Vital signs: Temperature, BP
• Growth parameters: Growth may be decreased with chronic UTI or renal insu ciency,
especially in infants
• Flank pain or costovertebral angle tenderness
• Abdominal examination: Suprapubic tenderness, bladder distention or a ank mass
(obstructive signs), mass from fecal impaction
• Genitalia: Vaginal erythema, edema, irritation, or discharge; labial adhesions;
uncircumcised male, urethral ballooning; weak, dribbling, threadlike stream
 • Neurologic examination (if voiding is dysfunctional): Perineal sensation, lower extremity
re
NRexes,
602sacral
Finaldimpling, or cutaneous
Exam Study Guide abnormality
Diagnostic Studies for UTI
The method used to collect urine has an e ect on the interpretation of results. Bagged urine
specimens, even after cleaning the external genitalia prior to placement, produce a high
incidence of false positive UA results due to contamination and thus must not be used to
determine UTI. If antimicrobial therapy must be initiated due to an ill-appearing child,
catheterization and urine culture must be obtained prior to administering antibiotics.
Older children who can void on command should be able to obtain a clean-catch void.
Having the female child sit with knees apart, feet supported, and torso leaned forward while
on the toilet separates the labia and decreases contamination.
Urine culture is essential to con rm the diagnosis. UTIs cause cultures with greater than
100,000 colonies of a single pathogen in a clean catch urine specimen, greater than 50,000 in a
catheterized or suprapubic specimen, or 10,000 colonies of a single pathogen in the
symptomatic.
• UA should be used only to raise or lower suspicion. Suspicious ndings include foul odor,
cloudiness, nitrites, leukocytes, alkaline pH, proteinuria, hematuria, pyuria, and bacteriuria.
• Leukocyte esterase chemical tests detect pyuria, but pyuria may arise from causes other
than UTI.
• Consider obtaining a lab UA with re exive gram stain and microscopy if dipstick ndings are
positive.
• Bacterial identi cation and determination of sensitivities are necessary in patients who
appear toxic or could have pyelonephritis, have relapses or recurrent UTI, or are
nonresponsive to medication.
• Complete blood count (CBC) (elevated WBC count), erythrocyte sedimentation rate (ESR), C-
reactive protein (CRP), BUN, and creatinine should be done if the child is younger than 1 year
old, appears ill, or if pyelonephritis is suspected.
• Blood culture should be done if sepsis is suspected (see Chapter 28).
FIG 41.1 Suspect Urinary Tract Infection (UTI) Algorithm.

FIG 41.1 Suspect Urinary Tract Infection (UTI) Algorithm. BBD, bowel and bladder dysfunction;
IM, intramuscular; IV, intravenous; UA, urinalysis; US, ultrasound; VCUG, Voiding
cystourethrogram; WBCs, white blood cells. Lower urinary tract symptoms include bladder
symptoms
NR (urinary frequency/urgency/incontinence/dysuria);
602 Final Exam Study Guide upper urinary tract symptoms
include fever, ank pain, gross hematuria, vomiting, malaise), abnormal renal ultrasound
includes ndings such as hydronephrosis, renal scarring, abnormal renal size (AAP
Subcommittee on UTI, 2016; AUA, 2010/2017).
Di erential Diagnosis for UTI
The di erential diagnosis includes urethritis, vaginitis, viral cystitis, foreign body, sexual
abuse, dysfunctional voiding, appendicitis, pelvic abscess, and pelvic in ammatory disease.
Any child who has acute fever without a focus, FTT, chronic diarrhea, or recurrent abdominal
pain should be evaluated for UTI.
Management for UTI
Goals of treatment are to quickly identify the extent and level of infection; to eradicate
infection; to provide symptomatic relief; to nd and correct anatomic or functional
abnormalities; and to prevent recurrence and renal damage (AAP Subcommittee on Urinary
Tract Infection, 2016). When deciding on a treatment plan, the child’s age, gender, symptoms,
the suspected location of the UTI, and antibiotic resistance patterns in the community must
be considered. Fig 41.1 outlines treatment of UTIs in the child.
Infants 2 to 24 Months Old
To diagnose UTI, the child should have both a UA suggesting infection (positive
leukocyte and/or nitrite tests) and urine culture from a sterile catheterization or
suprapubic aspiration (SPA) with at least 50,000 cfu/mL. Risk factors have been
identi ed to help steer management as judged by the clinician. Higher risk for girls is
white race, age younger than 12 months, temperature of at least 102.2°F (39°C), fever
lasting at least 2 days, and absence of another source of infection. Higher risk for boys
is nonblack race, temperature of at least 102.2°F (39°C), fever lasting more than 24 hours,
and absence of another source of infection ( Roberts, 2012; AAP, 2016).
Asymptomatic Bacteriuria
If there are no leukocytes on UA, no treatment is indicated.
Uncomplicated Cystitis
Use regional antibiotic resistance patterns and culture and sensitivity results when
choosing antibiotics. Short-term (3 to 5 days) antibiotics may be as e ective in treating
non-febrile bladder infections as standard 7- to 10-day dosing with no increased risk of
recurrence (Elder, 2016d). Children 2 to 24 months old and febrile children should have 7
to 14 days of antibiotics. Additional speci c recommendations for the febrile child less
than 24 months can be found in the AAP Guidelines. Recommended oral medications:
• Trimethoprim-sulfamethoxazole (TMP-SMX): More than 2 months old—8 to 12
mg/kg TMP component in two divided doses; adolescents, 160 mg TMP
component every 12 hours.
• Amoxicillin: Younger than 3 months old—20 to 30 mg/kg/day in two divided
doses every 12 hours; older than 3 months old—25 to 50 mg/kg/day in two divided
doses; adolescents, 250 to 500 mg every 8 hours or 875 mg every 12 hours.
• Amoxicillin clavulanate (doses for amoxicillin component): Younger than 3
months old—30 mg/kg/day in two divided doses; older than 3 months old—20 to
45 mg/kg/day in two or three divided doses; adolescents—250 to 500 mg every 8
hours or 875 mg every 12 hours.
• Cephalexin: 50 to 100 mg/kg/day divided in four doses and given every 6 hours
(maximum dose of 4 g/day).
• Ce xime: Older than 6 months old—16 mg/kg/day divided every 12 hours for rst
day, then 8 mg/kg/day divided every 12 hours to complete 13-day treatment;
adolescents—400 mg every 12 to 24 hours.
• Nitrofurantoin: Older than 1 month old—5 to 7 mg/kg/day divided every 6 hours
(maximum 400 mg/24 hours); adolescents—50 to 100 mg/dose every 6 hours
(macrocrystals) or 100 mg twice a day (dual release).
• Recurrent UTI: Further evaluation required. Prophylactic antibiotic use (Box 41.2)
is controversial and not routinely recommended.
• Acute pyelonephritis: Oral therapy is equally as e ective as parenteral therapy
in treating pyelonephritis and preventing kidney damage.
• Hospitalization is required if severity of symptoms warrants—dehydrated,
vomiting, or not drinking. Children 1 month old and younger should be admitted
and provided a parenteral regimen.
 • Infants over 1 month and children with uncomplicated pyelonephritis (well
hydrated,
NR 602 no vomiting,
Final Exam Studyno abdominal pain) can be e ectively treated with
Guide
ce xime, cephalexin, or amoxicillin clavulanate.
• Adolescents with uncomplicated pyelonephritis can be treated with either
amoxicillin clavulanate (875/125 mg twice a day) or cipro oxacin (500 mg twice a
day or extended release 1000 mg once a day).

• Follow-up cultures are not routinely needed. However, follow-up urine culture
should be done 48 to 72 hours after initiating treatment if symptoms persist or
organism resistance is found in the community.
• If the culture is not sterile or if no clinical improvement is seen, antibiotic
change should be based on sensitivity report. Urine should be sent for bacterial
identi cation and sensitivity studies if not performed initially, and an alternative
broad-spectrum antibiotic should be used pending those results. Culture should
again be repeated after 48 to 72 hours if response to therapy limited.
• Phenazopyridine may be given at 12 mg/kg/day for 6- to 12-year-olds and 200
mg for those older than 12 years old, three times a day for dysuria.
• Radiologic workup (Table 41.4) is recommended to identify any structural or
functional abnormality of the urinary tract and any renal scarring or damage.
• Children younger than 2 years old with the rst UTI should have a renal and
bladder ultrasound as soon as the urine is sterile or when the prescribed
antibiotic has been completed. Additionally, all children with fever, diagnosed
with pyelonephritis, or with recurrent UTIs should have a renal and bladder
ultrasound. VCUG does not need to be done routinely with rst febrile UTI.
However, if ultrasound reveals hydronephrosis, scarring, or other atypical or
concerning ndings, VCUG should be utilized (American Urological Association
[AUA], 2010/2017).
• DMSA scan ordered by the urological specialist may be obtained when renal
scarring is suspected or when diagnosis of pyelonephritis is uncertain (AUA,
2010/2017).

Radiologic Workup and Prophylaxis for Urinary Tract Infections Box 41.2, p 828
Why Do a Radiologic Workup?
• To identify any structural or functional abnormality of the urinary tract
• To identify any renal scarring or damage
Who Requires a Workup?
• Order a renal and bladder ultrasound on children with the rst positive urine culture
and with fever and systemic illness. In children with one or more infections of the lower
urinary tract (dysuria, urgency, frequency, suprapubic pain), renal and bladder
ultrasound may be considered; however, assessment and treatment of bladder and
bowel dysfunction is most important.
• If the renal ultrasound is abnormal, voiding cystourethrogram is indicated.
What about Prophylaxis?
• There is controversy about if and when prophylaxis should be used (AAP
Subcommittee on Urinary Tract Infection, 2016). If a decision to use prophylaxis is made
and depending on the source, between one-quarter to one-half of the treatment dose
of antibiotic may be given at bedtime.
• Nitrofurantoin: Older than 2 months old: 1-2 mg/kg as a single daily dose; expensive;
liquid form poorly tolerated; consider sprinkling capsules over applesauce, yogurt,
pudding
• TMP-SMX, trimethoprim-sulfamethoxazole:
 TMP 2 mg/kg as a single daily dose or 5 mg/kg twice per week (based on TMP
component) if older than 1 month
• Cephalexin: 10 mg/kg as a single daily dose
• Amoxicillin: 10 mg/kg as a single daily dose; can be used for a newborn or premature
infant; not used past the rst 2 postnatal months; shelf life for liquid is 14 days
 UTI Radiologic Studies Done for Evaluation of Urinary Tract Conditions table 41.4
NR 602 Final Exam Study Guide

UTI Patient and Family Education, Prevention, and Prognosis

Discuss the following with parents and/or patients:
• Clear explanation of the cause, potential complications, and overall treatment plan,
including short- and long-term plans.
• Frequent and complete voiding and increased uid intake, especially water. Scheduled
voiding times, voiding with knees spread apart, or double voiding (voiding and then
immediately attempting to void again) is helpful.
• Proper hygiene and avoiding irritants, such as bubble baths, sitting in soapy water,
and perfumed soaps. Avoid wearing tight pants, especially spandex pants. Wear cotton
underwear. Treat perineal in ammation to help prevent UTI.
• Treat constipation, pinworms.
• Encourage sexually active females to drink water before intercourse and void
immediately afterward.
• Decrease intake of bladder irritants, such as the “four Cs” (ca eine, carbonated
beverages, chocolate, citrus), aspartame (NutraSweet), alcohol, and spicy foods.
• Seek prompt medical attention with recurrence of fever and/or duration of fever for
more than 48 hours, especially if younger than 24 months old.
● Tourette syndrome (Bayless)
● Cerebral palsy (Bayless)
● Genitourinary anomalies (Yeonsil L).
        

Standards of Care
Urine dipstick or UA are not recommended at any age for screening of asymptomatic bacteremia or chronic kidney disease.
Routine BP check is recommended at any preventive health care visit starting at 3 YR old.

Anatomy and physiology

The urinary system begins forming and excreting urine at 3 months of gestational age. Glomerular filtration and
renal blood flow increase at birth and become stable by 1 to 2 years old. In infants, total extracellular fluid
volume is significantly greater than that of adults, and fluid composition tends to have a lower bicarbonate
concentration. Normal urine excretion is 1 to 2 mL/kg/h. The kidneys mature throughout infancy, and kidney
function approaches adult values between 6 and 12 months old.
Vesicoureteral Reflux (P829)
:retrograde regurgitation of urine from the bladder into the ureters and potentially the kidney. Major concern
with VUR is the exposure of the kidney to infected urine which may cause pyelonephritis.
Primary VUR: common and involves abnormally short ureter and ineffective valve
Secondary VUR: due to functional or structural bladder outlet obstruction
Grade I does not reach the renal pelvis
Grade II extends up to the renal pelvic without dilation
Grade III reflux to the renal pelvis with mild to moderate dilation of the ureter and the renal pelvis
Grade IV and V (high grade) distention of the ureter and renal pelvis and can include hydronephrosis
or reflux into the intrarenal collecting system.
Diagnostic studies
 Ultrasonography, VCUG (reflux and its grade), DMSA (renal scarring), BP and serum creatinine (when
NR 602areFinal
bil abnormalities Exam
present), Study
UA and Guide
culture if UTI is suggested
Management
The goal is to treat/prevent infection and subsequent scarring.
+ Most children outgrow their reflux secondary to an increase in the ureter intramural length. Grade I
and II reflux resolves spontaneously in up to 85% of children, grade III up to 50 %, lower chance of
cure for IV and V reflux. Very few children with low-grade VUR require surgery

FIG 41.2 Grading of Vesicoureteral Reflux.Grade I: Vesicoureteral reflux (VUR) into a nondilated ureter. Grade II: VUR into the upper collecting
system without dilation. Grade III: VUR into dilated ureter and/or blunting of calyceal fornices. Grade IV: VUR into a grossly dilated ureter. Grade
V: massive VUR, with significant ureteral dilation and tortuosity and loss of the papillary impression.
From Elder JS. Vesicoureteral reflux. In Kliegman RM, Stanton BF, St Geme JW, et al., eds. Nelson Textbook of Pediatrics. 20th ed. Elsevier; 2016:2562–2567.e. Fig
539.2.

Monitor Clinically Treat BBD CAP Yearly renal Surgical Correction

ultrasound +VCUG

Grade I Yes Yes Avoid Avoid Avoid

Grade II Yes Yes Consider Consider Consider

Grade III Not alone Yes Yes Yes Consider

Grade IV-V Not alone Yes Yes Yes Consider

Patient and Family Education, Prevention, and Prognosis

● • VUR does not cause scarring, infection does; but VUR is a risk factor for pyelonephritis and subsequent
scarring. Ensure prompt treatment of UTI. Emphasize the necessity of urine culture with any suspicious
symptoms. The potential for untreated, chronic UTI leading to chronic renal disease must be explained. BP and
growth should be monitored.
● • Treating
NR of 602
BBD Final
improves surgical
Exam outcomes.
Study Guide

● • Siblings are no longer routinely screened for presence of VUR (AUA 2010/2017).

● • Prophylactic medicines are best given at night because of urinary stasis while asleep. Recommended
medications used for prophylaxis are listed in Box 41.2.

● • Review the education discussed in the UTI section.

Physical Examination

• Growth parameters: FTT or falling growth curves (chronic renal insufficiency or long-standing
acidosis)

• Vital signs, especially BP

• Malformed ears (congenital renal disease)

• Oliguria or anuria

• Edema, hypertension, and proteinuria, which are suggestive of glomerular disease

• Flank pain, which is suggestive of an upper tract disorder

Box 41.3 Seven “Red Flags” for Chronic Renal Failure

1. Failure to thrive (poor growth, fatigue, anorexia, nausea, gastroesophageal reflux,

vomiting)

2. Chronic anemia (normochromic, normocytic, nonresponsive to medication)

3. Complicated enuresis (daytime frequency, urgency, incontinence, chronic constipation,

encopresis, infrequent voiding, straining to void, recurrent urinary tract infection)

4. Prolonged, unexplained vomiting or nausea (especially in the morning), anorexia,

weight loss without diarrhea
 NR 602 Final Exam Study Guide
5. Hypotension

6. Unusual bone disease (e.g., rickets, valgus deformity, fracture with minor trauma)

7. Poor school performance (e.g., headache, fatigue, inattention, withdrawal from

activities)

• Abdominal or flank mass, which suggests an obstruction, such as Wilms tumor, cystic disease, or
posterior valves

• External genitalia: Excoriation, bleeding, foreign body, abuse

Nephritis and Glomerulonephritis

Nephritis is a noninfectious, inflammatory kidney response characterized by varied degrees of hypertension,
edema, proteinuria, and hematuria that is either microscopic or macroscopic with dysmorphic RBCs and casts.
Nephritis is classified as acute, intermittent, or chronic. Primary GN occurs when the glomerulus is the original
and predominant structure impaired. Secondary GN occurs when renal involvement is secondary to systemic
disease (e.g., SLE,HSP, primary vasculitis, Goodpasture syndrome, or drug hypersensitivity reactions).
Involvement can be in the glomerulus, the interstitium, localized in one part of the kidney, or generalized
throughout. GN refers to inflammation primarily in the glomeruli; interstitial nephritis refers to inflammation in
the interstitium primarily caused by drug reactions. PSGN is the classic form of GN.

History and Clinical Findings

• Streptococcal skin (more likely) or pharyngeal infection within the past 2 to 3 weeks (PSGN). A
latent period of 7 to 10 days elapses between infection and the onset of symptoms; if fewer than 5
days or more than 14 days, consider other causes.

• Abrupt onset of gross hematuria.

• Reduced urine output (with diuresis in 5 to 7 days).

• Lethargy, anorexia, nausea, vomiting, abdominal pain.

• Chills, fever, backache (pyelonephritis).

• Medication taken in the past few weeks.

Physical Examination
 • Hypertension
NR 602 Final that is transient
Exam Studyand resolves in 1 to 2 weeks
Guide

• Edema, especially periorbital edema, or abrupt onset with weight gain

• Circulatory congestion—dyspnea, cough, pallor, pulmonary edema if severe

• Ear malformations

• Flank or abdominal pain or a mass (in polycystic kidney or malignancy [e.g., Wilms tumor])

• Costovertebral angle tenderness (in pyelonephritis)

• Rashes or arthralgias (with SLE, HSP, or impetigo)

• Evidence of trauma or abuse

Diagnostic Studies

• UA with microscopic examination—tea color; elevated specific gravity; macrohematuria and

microhematuria; proteinuria not exceeding the amount of hematuria; pyuria in PSGN; granular,
hyaline, WBC, or RBC casts; and dysmorphic RBCs

• Serum C3 or C4 (low early in disease, returning to normal in 6 to 8 weeks), total protein and
albumin (elevated)

• CBC, ESR, ASO titer (elevated), streptozyme test (positive), anti–deoxyribonucleic acid (DNA)
antibody titer

• Electrolytes, BUN, creatinine, and cholesterol

• Fluorescent antinuclear antibody (SLE), hepatitis titers, sickle cell or hemoglobin electrophoresis,
tuberculin PPD, and fluorescent treponemal antibody absorption (syphilis)

Wilms Tumor (P840)

Wilms tumor, the most common malignancy of the GU tract, is typically found as a firm, smooth mass in the
abdomen or flank. It is staged as follows:

• Stage I: The tumor is limited to the kidney and can be completely excised with the capsular surface
intact.

• Stage II: The tumor extends beyond the kidney but can still be completely excised.
 • Stage
NR 602III: ThereExam
Final is postsurgical
Study residual
Guide nonhematogenous extension confined to the abdomen.

• Stage IV: There is hematogenous metastasis, most frequently to the lung.

• Stage V: There is bilateral kidney involvement.

This malignancy manifests as a solitary growth in any part of either or both kidneys. There are approximately
8 cases of Wilms tumor per million in children younger than 15 years old with 500 new cases every year. Most
Wilms tumors occur in children between 2 and 5 years old. The peak incidence and median age at diagnosis is
3.5 years old (Densmore and Densmore, 2018). About 1% to 2% of children with Wilms tumor have a family
history of Wilms, and the tumor is inherited in an autosomal dominant manner. An important feature of Wilms
tumor is the occurrence of associated congenital anomalies including renal abnormalities, cryptorchidism,
hypospadias, duplication of the collecting system, ambiguous genitalia, hemihypertrophy, aniridia, cardiac
abnormalities, and Beckwith-Wiedemann, Denys-Drash, and Perlman syndromes. Wilms tumor occurs with
equal frequency in both sexes although males are usually diagnosed younger. There is a higher frequency in
African Americans and a lower frequency in Asians.

History and Clinical Findings

• The most frequent finding is increasing abdominal size or an actual palpable mass.

• Pain is reported if the mass has undergone rapid growth or hemorrhage.

• Fever, dyspnea, diarrhea, vomiting, weight loss, or malaise may be reported.

Physical Examination

• A firm, smooth abdominal or flank mass that does not cross the midline may be noted.

• BP is elevated if renal ischemia is present (rare).

• A left varicocele is found in males if the spermatic vein is obstructed.

• A careful examination is needed to rule out congenital anomalies.

Diagnostic Studies

• Chest and abdominal radiography are performed to differentiate neuroblastoma, which is usually
calcified.

• Abdominal ultrasonography is used to differentiate a solid from a cystic mass or hydronephrosis

and multicystic kidney.

• UA demonstrates hematuria in 25% to 33% of children.

 NR 602 Final Exam Study Guide
• Obtain a CBC, reticulocyte count, and liver and renal chemistry studies.

• A CT scan of the chest, abdomen, and pelvis to stage the disease and bone marrow is done by the
oncology team.

Differential Diagnosis
Neuroblastoma is the main differential diagnosis (the mass often crosses the midline). Multicystic kidney,
hydronephrosis, renal cyst, or other renal malignancies are additional conditions to consider.

Management
Diagnostic workup is the initial urgent priority, with concurrent referral to a pediatric cancer center for
treatment. Surgery removes the affected kidney and possibly the ureter and adrenal gland, and combined
chemotherapy and radiotherapy are instituted if the disease is advanced or has unfavorable histologic findings.
Coordinate close follow-up with the cancer team.

Complications
The lungs and liver are the most common sites of metastasis. Hypertension is possible because of renal
ischemia and occasionally leads to cardiac failure.

Patient and Family Education, Prevention, and Prognosis

The prognosis is determined by the histology of the neoplasm, the patient’s age (the younger the better), the
size of the tumor, positive nodes, and, most significantly, the extent or stage of the disease. The cure rate is about
80% to 90% for infants with stage 4S; reoccurrence of the disease has a less than 50% response to alternative
chemotherapeutic agents (Shohet and Foster, 2017). A pediatric urologist should determine if a child should be
allowed to participate in sports on an individual basis. Kidney protector use is highly recommended during
sports. The National Wilms Tumor Study is a good reference for information about management, sequela, and
prognosis.

Chronic Genitourinary Conditions in Males

Hypospadias
Hypospadias is a common congenital abnormality in which the urethral meatus is located anywhere from the
proximal glans to the perineum on the ventral surface (underside) of the penis. Chordee, a ventral bowing of the
penis, occurs when a tight band of fibrous tissue pulls on the penis. Torsion refers to rotation of the penis to the
right or left.
+Family hx (male relative)
+Report of unusual direction with urine stream

Physical Examination
In a newborn, the classic finding is a dorsally hooded foreskin. It is essential to visualize the urethral meatus,
which is facilitated by pulling the ventral shaft skin in a downward and outward direction. The deformity is
described by location—glanular, coronal, subcoronal, penoscrotal, scrotal, and as distal (60%), mid-penile
(25%), or proximal (15%).

Differential Diagnosis
The differential diagnosis includes intersex abnormalities.

Management
The goal of surgical repair is to have a functional penis that appears normal. Historically, circumcision was
avoided NR 602theFinal
because Exam
foreskin may Study
be used Guide
in the surgical repair. However, newer surgical techniques that do
not require the use of skin flaps change this standard of care. Physiologic phimosis may prevent visualization
of a urethral anomaly during a well-child exam, especially with a mild form of hypospadias. Surgical success is
not compromised in these cases. Referral should be made to a pediatric urologist at birth or at detection of the
anomaly. Surgery to correct hypospadias is best done around 6 to 12 months old. Repair is usually
accomplished in a one-stage outpatient procedure unless it is a complex defect.

Cryptorchidism (Undescended Testes)

Cryptorchidism is a testis that does not reside in and cannot be manipulated into the scrotum. A retractile testis
is out of the scrotum, but can be brought into the scrotum and remains there. A gliding testis can be brought
into the scrotum, but returns to a high position in the scrotum once released. An ectopic testis lies outside the
normal path of descent. An ascended testis is one that has fully descended, but has spontaneously re-ascended
and lies outside the scrotum. A trapped testis is one dislocated after herniorrhaphy. Any testis that is not in the
scrotum is subject to progressive deterioration. Undescended testes is a common disorder that often causes
great anxiety for parents.
+Fam hx of undescended testes or testicular malignancy
+Risk factors include prematurity, hypospadias, congenital hip subluxation, low birth wt, down syndrome,
klinefelter syndrome

Physical Examination
Having the child sit cross-legged, frog-legged, squat, or stand can facilitate testicle descent and palpation.

• Scrotal rugae less fully developed

• Bilateral or unilateral absence of a testicle

• Retractile testes, which move between the scrotum and external ring, but can be manipulated to the
lower part of the scrotum and remain there; in children 3 months to 7 years old, retraction is
especially common with tactile stimulation of the area or cold

• Gliding testes that lie between the scrotum and external ring and can be manipulated to the lower
part of the scrotum, but return to the high position

• Location of the testis is described as prescrotal (at the external inguinal ring); canalicular, high or
low (between the external and internal rings), the most common type; ectopic (superficial inguinal,
femoral, or perineal); or intraabdominal (above the internal inguinal ring), not palpable, occurring in
less than 15% of males with undescended testes.

Diagnostic Studies
None are indicated except in newborns with potential sex abnormalities, hypopituitarism, Down syndrome, or
congenital adrenal hyperplasia. The risk of intersex abnormality is 27% if hypospadias and unilateral or
bilateral cryptorchidism are present.

Differential Diagnosis
Anorchism and chromosomal abnormalities are the differential diagnoses.

Management
 The goals of treating undescended testes are to improve fertility outcome, decrease malignancy risk, and
minimizeNR the602 Final Exam
psychological stressStudy Guide
associated with an empty scrotum. Management is surgical intervention
between 9 and 15 months old. Hormonal therapy is not effective in stimulating testicular descent. Surgery at 6
months old is appropriate if orchiopexy is performed by a skilled pediatric urologist or surgeon with an
attendant and skilled pediatric anesthesiologist. In a child younger than 1 year old, regular examination to
assess the position of the testes should be performed at every well-child care visit. If the testes remain
undescended, referral to a pediatric urologist or surgeon should occur by 6 months old. Referral should also
occur if a retractile testis does not retain scrotal residence. If undescended testes are found after 1 year old, the
child should be immediately referred to a pediatric urologist or surgeon for treatment.

FIG 41.6 Hydroceles and Hernias.

From Katz A, Richardson W. Surgery. In: Zitelli BJ, McIntire SC, Nowalk AJ, eds. Zitelli and Davis’ Atlas of Pediatric Physical Diagnosis. 2018:616–657, Figure 18–
90.

● Diabetes (Michel-Ange)
Diabetes Mellitus P 952
Diabetes is one of the most common chronic diseases in childhood. Diabetes mellitus is a group of
conditions characterized by inadequate insulin secretion, insulin resistance, or both. These dynamics
lead to defective metabolism of carbohydrate, protein, and fat and subsequent hyperglycemia.
Diabetes (type 1 or 2) affects approximately 193,000 individuals younger than 20 years old in the
United States, which is approximately 0.24% of American youth younger than 20 years of age (CDC,
2017).

TABLE 45.3
 Type 1 Diabetes Type 2 Diabetes
NR 602 Final Exam Study Guide
Age at onset All ages ≥10 years old

Gender Equal distribution by gender More frequent in females

Race/ethnicity Most frequent in non-Hispanic More frequent in African Americans, Asians, Native
whites Americans, Hispanics

May occur in all racial and ethnic

groups

Obesity Similar to the general population; not >90%

related to type 1 diabetes

Family history of 5%-10% have first-degree relative Approximately 80% have first-degree relative affected
diabetes affected

Insulin secretion Very low Low, normal, or high

Insulin sensitivity Normal Decreased

Onset Acute, severe Subtle to severe

Ketosis, DKA Approximately one-third of new cases Uncommon

Hypertension Uncommon Common

Acanthosis nigricans Rare Common

Polycystic ovary Rare Common

syndrome

Islet autoimmunity Present Uncommon

● Among youth, the majority (87%) have type 1 diabetes, 10.5% have type 2 diabetes, and 2.5% have other types
(Pettitt et al., 2014). These include maturity-onset diabetes of youth (MODY), as well as diabetes related to
chronic conditions (e.g. cystic fibrosis), induced by chronic medication use (e.g. steroids), or correlated with
genetic disorders (e.g. Down syndrome).
● New cases of type 1 diabetes are more frequently diagnosed during the autumn and winter months. The
incidence of both type 1 and type 2 diabetes is increasing dramatically in children in the United States and other
countries throughout the world (Patterson et al., 2014; Pulgaron and Delamater, 2014). Table 45.3 shows the
distinguishing features of type 1 and type 2 diabetes

Type 1 Diabetes
● Type 1 diabetes is caused by autoimmune destruction of pancreatic beta cells in the islets
of Langerhans thought to be triggered by a preceding environmental event in genetically
susceptible individuals.
●  This destruction of beta cells results in an absolute de ciency in insulin secretion, reduced
biologic effectiveness, or both. Normal metabolic function depends upon su cient amounts
 of circulating insulin. Insulin de ciency results in uninhibited gluconeogenesis and a blockage
NR
in the602 Final
use and Exam
storage of Study Guide
circulating glucose.
●  Therefore high blood glucose levels are a result of the defective metabolism of
carbohydrate, protein, and fats. Based on 2009 data from the SEARCH for Diabetes in Youth
study, 6666 of 3.4 million youth were diagnosed with type 1 diabetes and 558 of 1.7 million
youth were diagnosed with type 2 diabetes in the United States (Dabelea, Mayer-Davis, et al.,
2014). Females and males were affected in equal numbers.
● The prevalence of type 1 diabetes varied by race and ethnicity and was highest among non-
Hispanic white youth (2.55/1000 children). Native American children had a much lower
prevalence of type 1 diabetes (0.35/1000 children), and only 32% of diabetes among Native
American children was type 1.
● The incidence of type 1 diabetes in the United States has increased. During the period 2002
to 2012, the incidence of type 1 diabetes increased from approximately 15,900 cases/year to
approximately 17,900 cases/year, an increase of 1.8% annually after adjusting for age, sex,
race, and ethnicity. The greatest increase in annual incidence was 4.2% in the Hispanic
population (Mayer-Davis et al., 2017). Although children were most often diagnosed during the
time of puberty and onset of symptoms can present at any age, increasing incidence occurred
in all age groups of children older than 4 years (Mayer-Davis et al., 2017).

Clinical Findings
● Although the onset of type 1 diabetes is gradual with destruction of pancreatic islet cells
over time, children may become ill quite suddenly once symptoms manifest. As diabetes
develops, the symptomatology re ects the decreasing degree of beta cell mass, increasing
insulinopenia and hyperglycemia, and increasing ketoacids.
History
● With type 1 diabetes, the child may have had a viral infection, cold, or u; parents may notice
increased urination and thirst during the recovery period, with additional signs and symptoms
appearing over a period of days or weeks. The following early symptoms are often reported:
 • Polydipsia, polyphagia, polyuria
 • Nocturia, blurred vision
 • Weight loss or poor weight gain
 • Fatigue and lethargy
 • Vaginal moniliasis
As ketoacids accumulate, the following history is reported:
 • Abdominal pain, nausea and/or vomiting
 • Fruity-smelling breath
 • Weakness (caused by dehydration)
 • Mental confusion
 • Coma

Approximately 30% of children with new-onset type 1 diabetes present in diabetic ketoacidosis
(DKA). Younger age, ethnic/race minority status, lower socioeconomic status, and lack of private
health insurance are risk factors for presenting in DKA at diabetes onset (Dabelea, Rewers, et al.,
2014).

Physical Examination
Although children typically have polyuria, polydipsia, and weight loss, the physical examination of
children with new-onset type 1 diabetes may be remarkably benign. Findings can range from benign
to severe and can include:
 • Dehydration (child may not look clinically dehydrated unless actively vomiting)
 • Weight loss or slow weight gain
 • Muscle wasting
 • Tachycardia
  • Vaginal yeast, thrush, or other infection
NR 602 Final Exam Study Guide
If ketosis develops:
 • Slow, labored breathing (Kussmaul breathing)
 • Flushed cheeks and face
 • Fruity-smelling breath

Diagnostic Studies
Urine testing and blood glucose measurements are generally su cient to make the diagnosis:
 • Urine for glucose and ketones
 • Metabolic screen for acid-base status to exclude DKA
 • Hemoglobin A1c (HbA1c)
 • Blood glucose
 • Screen for the presence of pancreatic autoantibodies: This should be considered to con rm the diagnosis of type
1 diabetes, particularly in those cases where there may be uncertainty regarding type (Chiang, Kirkman, Laffel, and
Peters, 2014).

Capillary blood samples, reagent sticks, and glucose meters should be used only for monitoring diabetes control
and not for diagnosing diabetes mellitus.

Diagnostic Criteria for Diabetes

 The presence of one or more of the following criteria indicates a diagnosis of diabetes:
 • HbA1c ≥ 6.5%
 • Fasting plasma glucose 126 mg/dL (7 mmol/L) or greater
 • Random plasma glucose 200 mg/dL or greater plus presence of classic symptoms (polyuria, polydipsia,
polyphagia)
 • Postprandial (2 hours after eating) plasma glucose 200 mg/dL (11.1 mmol/L) or greater

● Epilepsy (Michel-Ange)

● Leukemia (Ashley D)
Leukemia (page 760-761)
Leukemias are a group of malignant hematological diseases in which normal bone marrow
elements are replaced by abnormal, poorly di erentiated lymphocytes called blast cells.
Leukemias are the most common form of childhood cancer accounting for up to 30% of all
pediatric cancers.  ALL (Acute Lymphoblastic Leukemia) accounts for 80% of leukemia cases
with peak incidence between 2 and 6 years of age, and 56% of leukemia cases in adolescents.
AML (Acute Myeloid Leukemia) is less common.

Clinical Findings: Anemia, pale, listless, irritable, or chronically tired.  A history of repeated
infections, fever, and weight loss.  Bleeding episodes mainly epistaxis, petechiae, and
hematomas.  Lymphadenopathy and hepatosplenomegaly. Bone and joint pain. Headache,
vomiting, or lethargy are rare at time of diagnosis.  All symptoms may be vague or
nonspeci c.

Diagnostics:  CBC with di erential, WBCs, platelet, and reticulocyte counts.

 Thrombocytopenia and anemia are present in most cases.  WBCs may be high, normal, or a
variation of low.   A peripheral smear may show malignant cells.  Bone marrow examination
showing an in ltration of blast cells replacing normal parts of the marrow.  Chromosomal and
genetic abnormalities are found in most children with ALL.

Management:  Approximately 90% of children diagnosed with ALL can now be cured.  They are
considered cured when they have been in remission over 10 years.  Treatment includes 4-6
 weeks of induction phase usually with vincristine, prednisone, and L-asparaginase.  This is
followedNRby602
a consolidation
Final Examphase
Studylasting
Guide several months and then a maintenance phase for
2 to 3 years.  Chemotherapy, CNS therapy or intrathecal administration of chemotherapy and
systemic administration of corticosteroids are the key interventions.  Those with AML,
treatment includes induction chemotherapy, CNS prophylaxis, and post remission therapy.
 Cranial (CNS) irradiation is decreasing in administration and only used for the high-risk child
as it has been linked to learning disabilities and impaired IQ.

The role of the PCP to facilitate proper referrals and interdisciplinary communication to assist
the family in their coping.  Regular health appointments should continue.  Immunizations
should be given as appropriate.

● ADHD (Ashley D)

ADHD (page 433-441)

Attention-De cit/Hyperactivity Disorder (ADHD) is one of the most commonly diagnosed
disorders in childhood.  ADHD is considered a neurodevelopmental disorder because it has a
clear neurologic base with symptoms that can profoundly a ect behavior of individuals in
many settings.  This is a chronic condition that can persist into adolescence and adulthood.
 Symptoms of ADHD a ect cognitive, educational, behavioral, emotional, and social
functioning and core symptoms include inattention, hyperactivity, and impulsivity which
occurs at a developmentally inappropriate level observed in at least two settings (home,
school, or work)with clear evidence of clinical impairment in social, academic, or occupational
functioning.  Prevalence rates vary The National Survey of Children’s Health reports 6.1%
overall prevalence of ADHD in children 2 to 17 in the US. There is no single cause for ADHD
research shows it is primarily a genetic disorder with environmental factors.

CLINICAL FINDINGS:   Many times, a child presents after a referral from a childcare provider,
school or parent/guardian.  Concerns may be related to the child’s memory, emotional
control, organization, planning or inhabiting thoughts or actions, di culty with peers,
following classroom rules, or regulating behavior.  A complete physical should be performed
with focus on the following:  weight, height, BMI, head circ, bp, pulse, vision, hearing, general
observation of child’s behavior with parent/guardian, dysmorphic stigmata, café au lait spots
(signs of abuse), recurrent otitis media, respiratory allergies, enlarged tonsils, sleep apnea,
heart sounds, murmur, mental status, speech, language, motor skills, cognition appropriate
for age.  Screen for iron de ciency, lead, and thyroid dysfunction as indicated.  ADHD speci c
behavior rating scales gives the most objective data to assess scope and severity of
symptoms while being able to monitor change once treatment starts.  Screeners include:
Vanderbilt ADHD scales, ADHD Rating Scale IV, Conner Parent and Teacher Rating Scales, and
the Child Attention Pro le.  Consistent use of one scale is recommended.

DIAGNOSING: TABLE 30.5 DSM-5 Criteria for Attention-De cit/Hyperactivity Disorder

A persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with

functioning or development, as characterized by (1) and/or (2):

1.           Inattention: Six (or more) of the following symptoms have persisted for at least 6 months
to a degree that is inconsistent with developmental level and that negatively impacts directly
on social and academic/occupational activities:
Note: The
NRsymptoms
602 Finalare not solely
Exam Studya Guide
manifestation of oppositional behavior, de ance,
hostility, or failure to understand tasks or instructions. For older adolescents and adults (age
17 and older), at least ve symptoms are required.

a.       Often fails to give close attention to details or makes careless

mistakes in schoolwork, at work, or during other activities (e.g., overlooks or
misses details, work is inaccurate).

b.       Often has di culty sustaining attention in tasks or play activities (e.g.,
has di culty remaining focused during lectures, conversations, or lengthy
reading).

c.       Often does not seem to listen when spoken to directly (e.g., mind seems
elsewhere, even in the absence of any obvious distraction).

d.       Often does not follow through on instructions and fails to nish
schoolwork, chores, or duties in the workplace (e.g., starts tasks but quickly
loses focus and is easily sidetracked).

e.       Often has di culty organizing tasks and activities (e.g., di culty
managing sequential tasks; di culty keeping materials and belongings in
order; messy, disorganized work; has poor time management; fails to meet
deadlines).

f.        Often avoids, dislikes, or is reluctant to engage in tasks that require

sustained mental e ort (e.g., schoolwork or homework; for older
adolescents and adults, preparing reports, completing forms, reviewing
lengthy papers).

g.       Often loses things necessary for tasks or activities (e.g., school
materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile
telephones).

h.       Is often easily distracted by extraneous stimuli (for older adolescents
and adults, may include unrelated thoughts).

i.         Is often forgetful in daily activities (e.g., doing chores, running errands;
for older adolescents and adults, returning calls, paying bills, keeping
appointments).

2.           Hyperactivity and impulsivity: Six (or more) of the following symptoms have persisted for
at least 6 months to a degree that is inconsistent with developmental level and that negatively
impacts directly on social and academic/occupational activities:

Note: The symptoms are not solely a manifestation of oppositional behavior, de ance,
hostility, or a failure to understand tasks or instructions. For older adolescents and adults
(age 17 and older), at least ve symptoms are required.
NR 602 Final Exam Study Guide
a.           Often dgets with or taps hands or feet or squirms in seat.

b.          Often leaves seat in situations when remaining seated is expected

(e.g., leaves his or her place in the classroom, in the o ce or other
workplace, or in other situations that require remaining in place).

c.           Often runs about or climbs in situations where it is inappropriate.

(Note: In adolescents or adults, may be limited to feeling restless.)

d.          Often unable to play or engage in leisure activities quietly.

e.           Is often “on the go,” acting as if “driven by a motor” (e.g., is unable to
be or uncomfortable being still for extended time, as in restaurants,
meetings; may be experienced by others as being restless or di cult to
keep up with).

f.        Often talks excessively.

g.           Often blurts out an answer before a question has been completed
(e.g., completes people’s sentences; cannot wait for turn in conversation).

h.          Often has di culty waiting his or her turn (e.g., while waiting in line).

i.        Often interrupts or intrudes on others (e.g., butts into conversations,

games, or activities; may start using other people’s things without asking
or receiving permission; for adolescents and adults, may intrude into or
take over what others are doing).

B. Several inattentive or hyperactive-impulsive symptoms were present prior to age 12 years.

C. Several inattentive or hyperactive-impulsive symptoms are present in two or more settings

(e.g., at home, school, or work; with friends or relatives; in other activities).

D. There is clear evidence that the symptoms interfere with, or reduce the quality of, social,
academic, or occupational functioning.

E. The symptoms do not occur exclusively during the course of schizophrenia or another
psychotic disorder and are not better explained by another mental disorder (e.g., mood
disorder, anxiety disorder, dissociative disorder, personality disorder, substance intoxication
or withdrawal).

MANAGEMENT:  Includes family education and support, behavior management, parent skills
training, and counselling.  It is also important that the PCP works with the family and the
school to set reasonable expectations and help develop a plan for the child’s success.
 PHARMACOLOGY
NR 602 FinalMANAGEMENT:
Exam Study  Medication
Guide alone is not as e ective as medication
combined with behavioral therapy.  Stimulants are the rst line medications for
uncomplicated ADHD which are methylphenidate and amphetamine conforms.  Between 70-
90% of children respond positively to stimulant meds.  When dealing with adolescents be sure
to assess for substance abuse prior to prescribing stimulants.  Non-stimulant medications
include Atomoxetine which is a non controlled norepinephrine reuptake inhibitor. The non-
stimulant medication may take up to 6 weeks before e ects are noted.  Many of the
medication side e ects can be minimized by having children eat a healthy meal before taking
their medication, ensuring meds are taken by 9am, taking medication with food or eating
soon after dose.  Complementary therapies include outdoor exercise, aerobic exercise,
adequate sleep, and good nutrition.  Keeping a clean uncluttered environment and learning
to manage stress is important.

FOLLOW UP AND REFERRAL:  Regular child and family follow up includes reassessment of
symptoms, functioning and target goals.  Review of medication, education, care coordination,
advocacy and assessment of family functioning and need for family support.  Referral to
specialist if things do not go as expected, poor medication response, or emergent
comorbidities.

● Dyslexia (MICHAEL S.)

Dyslexia: week 8 ch30
CH30 pg 441
Dyslexia refers to di culties with word recognition, decoding, and spelling. Di culties in
writing include spelling, punctuation, grammar, organization, and clarity of written expression.
Dyslexia is the most common Speci c Learning Disorder.  (pg 442) SLD a ects 5% to 15% of
school-aged children and is more common in males. Issues with learning and attention a ect
one in every ve children in the United States; about one-third have both disorders. SLDs
a ect children from all socioeconomic, racial, and ethnic groups, but they are less common in
upper-income children and children who are not of color
● Oppositional De ant Disorder (ODD) (Christina P.) Burns pg. 445-447
        Disruptive Behavior Disorders include CD, ADHD, and ODD. Approximately 2% to 8% of children
meet criteria for ODD. Males are more likely to be aggressive than females, and aggression peaks during
adolescence. Females are more likely to be socially or covertly aggressive, whereas males are more likely to be
physically aggressive. Acute, stressful life events or transitions can precipitate a brief period of social
aggression. Aggression has neurobiologic and socioenvironmental influences. Biologic changes noted include
alterations in dopamine, serotonin, and GABA, and multiple genes have been identified that contribute to
aggressiveness. Significant risk factors include a history of maltreatment or trauma with or without PTSD;
inconsistent or harsh discipline, or both; lack of maternal responsiveness; separations from parents; weak social
ties; bullying; peer influences (especially for older children and adolescents); and parental figure changes or
parental rejection. Social aggression can be a precursor to CD or ODD.
Making behavioral health diagnoses is often difficult. PCPs must decide whether behaviors are within
normal limits for age, temperament, family, health, and other factors. Comorbidities are common. In practice,
several things may need to be addressed: the behavior, the family effects, nutrition, sleep, and other interrelated
issues. In many cases, a behavioral health specialist such as a clinical psychologist or psychiatrist may be
required to assist in diagnostic decision-making.
Oppositional Defiant Disorder (ODD) is a pattern of negative, hostile, and defiant behavior that is
excessive compared with other children of the same age. Symptoms often occur in early childhood, from 3 to 7
years old with the disorder typically beginning by 8 years old. Etiologic factors include many of the parenting
and family dysfunctions identified for social aggression. Precursors to the disorder are common in early
childhood, especially defiance and negativism. More common in boys before puberty, the gender distribution is
approximately equal thereafter.
Clinical Findings
 The essential feature of ODD is a recurrent pattern of behavior that is negative, defiant, disobedient, and
NR 602
hostile toward Finalfigures.
authority ExamBehavior
Study is Guide
typically directed at family members, teachers, or peers that the
child knows well. The child manifests the following behaviors to an extent that leads to impairment:
• Actively defies or refuses adult requests or rules
• Is argumentative, angry, resentful, touchy, or easily annoyed
• Easily loses temper; is vindictive
• Blames others for own mistakes or difficulties
• Deliberately does things to annoy others
• Children often see their own behavior as justifiable, not oppositional or defiant
Differential Diagnosis
Conduct Disorder (CD) involves more serious violations of the rights of others and a more willful
disregard of authority.
Management
Attend to the early signs of defiant and oppositional behavior or aggression, or both, and educate
parents about positive parenting strategies and exercising consistent, healthy discipline, which is similar to the
management of CDs. Because these children typically do not perceive themselves as having a problem and
cause distress within the family system, referral for intervention is indicated. As described for CD, parent
training programs are more successful if they include information about child behavior in multiple
environments (e.g., school and home) and target dysfunctional family processes. Child training groups provide
added benefit if combined with parent training groups. Again, collaboration with the school is important. These
multiple approaches, conducted simultaneously, are most effective.

● Bipolar (lauren p)
● Depression (lauren p)
● Illegal substance use/abuse GABBY
● Pinworms  (Bhumika)
Incubation Period is 1 to 2 months, or longer from ingestion to migration to perianal area
Sign and Symptoms : Perirectal and/or vaginal pruritus; nervous irritability, hyperactivity,
insomnia; urethritis, vaginitis, salpingitis, and pelvic peritonitis have been reported
Duration of illness : Reinfection common in children
Route of Transmission : Ingested eggs from soil, water contamination, or direct fecal-oral route
from fomites on bedding, clothing, toys, baths; person-to- person. Female lays eggs in perianal
area and dies; ingested eggs hatch, become larvae in small intestine and migrate to rectum.
Lab Testing : 1 cm long white, threadlike worms can be visualized at anus during night after
child has been asleep for 2 to 3 hours. Microscopic examination: Use transparent adhesive tape
applied to anus to collect any eggs or pinworms present on three consecutive nights or
mornings before child arises. Direct stool examination usually not productive.
Treatment : Mebendazole, pyrantel pamoate or albendazole and repeated in 2 weeks; also treat
family members; vaginitis is self- limiting.
Easily spread among family members, in day care settings, and institutions (up to 50%
infestation rates in these populations).
Preventive: Morning baths, change bedding, hand hygiene, clip ngernails, avoid scratching
perianal region, avoid nail biting.
Day care precautions include hand hygiene, proper handling of underwear and diapers.         
● Congenital Heart Defects in Children GABBY BURDE
● Kawasaki Disease(Donna Lambert)  Kawasaki Disease (KD) (pg 560-561)

○ -known as mucocutaneous lymph node syndrome or infantile polyarteritis.

○ - acute febrile illness that can cause acquired heart disease.

○ - 2nd common childhood vasculitis. Characterized generalized systemic small to

medium vessel vasculitis occurring throughout the body.  In ltrates of macrophages in
the vasculature is unique to the disease.
NR 602 Final Exam Study Guide
○ -seasonal Peaks & suggestion of toxin release as a rash resembles erythroderma.  It
is thought that a superantigen is responsible for T cell activation = massive release of
cytokines and in turn in ammation= the in ammatory cascade.

○ Geographically- seasonal outbreaks in winter and early spring ( u season). No

usually person to person spread.

○ -          Six components required for suspected KD-albumin <3.0, urine >10 WBC/HPF,
platelet count > 450,000 after 7 days of fever, anemia consistent with age values, total
white blood cell count >15,000, and elevated alanine aminotransferase.

○ Clinical ndings-

-triphasic presentation

1st- acute phase- conjunctival hyperemia sparing the limbus, erythematous rash,
edema of hands and feet, a polymorphous erythematous rash and unilateral lymph
nodes.

○ 2nd- subacute phase- begins when fever, rash and cervical lymphadenopathy abate.
Arthralgias, w/ desquamation of the skin over the ngertips, thrombocytosis and
cardiac disease occur.

○ 3rd  nal phase- starts at day 25 of illness- s/s are absent, but there are still marked
elevations in ESR. Cardiac ndings include abnormalities of the coronary vessels and
myocarditis is almost universal.

○ -Other atypical criteria-involve multisystem- GI, GU, CNS, Resp, Musculoskeletal.

○ Findings on X-ray include- pulmonary nodules, interstitial in ltrates. Other ndings

can include hydrops of gallbladder, pancreatitis, diarrhea, vomiting, abdominal pain,
arthralgia, arthritis, and hepatitis jaundice. Speci c to the CNS- irritability, aseptic
meningitis, peripheral facial nerve palsy, sensorineural hearing loss. Other
occurrences- anterior uveitis, desquamating rash in the groin or erythema, induration
at the site of BCG vaccination.

○ Diagnostic Studies-

○ KD is a diagnosis of exclusion.  A CBC w/ di

, Platelet count, CMP, ESR, CRP should be
done.  Using the six components mentioned earlier should be used to elucidate the
diagnosis of incomplete KD.

○ Laboratory ndings include- neutrophilia w/ bands, elevation of acute phase

reaction- ESR, CRP and platelets, Elevated serum transaminase, hypoalbuminemia,
abnormal plasma lipids, anemia, and leukocytosis in synovial uid. Leukopenia and
thrombocytopenia
NR 602 Final Examin KD can occur
Study Guidewith life-threatening MAS.

○ DDx: Viral infections- measles, adenovirus, enterovirus, EBV, In uenza, roseola.;

bacterial infections- cervical adenitis, scarlet fever; Toxin-mediated diseases- scalded
skin syndrome, Toxic Shock syndrome. Hypersensitivity reactions- Stevens-Johnson
syndrome, acrodynia (mercury toxicity)

○ Management-

○ Early diagnosis prevents aneurysms in the coronaries & extra-parenchymal muscular

arteries. Treatment includes evoking rapid anti-in ammatory response, preventing
platelet aggregation and clot development, and minimizing modi able risk factors for
coronary disease- diet, exercise, and smoking.

○ -          IVIG therapy 2 single doses of 2mk/kg over 8 to 12 hours. Preferable in the early
stages of disease/ within 1st 10 days. This down regulates antibodies and
proin ammatory cytokines, suppresses t-cell activity.

○ -          If IVIG is unsuccessful in decreasing in ammation, then immunoglobulin is

used.

○ -          AHA recommends high dose ASA therapy for anti-platelet e ect. Dose 80-
100mg/kg/day in 4divided doses, until afebrile for 2-3 days, then lowering the dose to 3-
5mg/kg/day for 6-8 weeks.

○ -          2nd IVIG therapy- 2mg/kg over 12 hours. If unsuccessful then the use of

prednisolone is used.

○ -          IF Coronary aneurysm is present then use of anti-platelet and anti-coagulants

are used- coumadin or Plavix along with ASA.

○ -          Obtain baseline EKG, then repeat in 2 weeks and 6-8 weeks after onset of
illness.  Other studies used- cardiac MRI, CT angio’s.

○ -          Recommended to have inactivated

u vaccine if on chronic ASA. If u develops
then stop ASA x6eeks. And use another anti-platelet med = decreased risk of Reye
syndrome.

○ -          After IVIG vaccines should be delayed 11 months if live viruses are used.

○ -           Follow up with cardiology for 1st year post illness.

○ -          Physical limitation- if development of giant aneurysms from transient coronary

artery dilation.
 ○ Prognosis
NR 602 Final Exam Study Guide

○  Acute disease is self limited. With vascular strain development of aneurysm is 15% to
25% when untreated. Development can be up to 6 months post illness.  50% of
aneurysms regress within 2 years. IF ischemic heart develops then intervention
percutaneously or through bypass can take place.

○ Other complications include CHF or myocardial e usion, myocarditis, pericarditis

(30%), pericardial e usion, mitral valve insu ciency and reoccurrence of KD(2%).
● Rheumatic fever (Bhumika)

ARF is a nonsuppurative complication following a Lance eld GAS pharyngeal infection that
results in an autoimmune in ammatory 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 e ects on tissues are generally minimal
except for the damage done to cardiac valves that leaves brosis and scarring and results in
rheumatic heart disease.                        

2002-2003 World Health Organization Criteria for the Diagnosis of Rheumatic

Fever and Rheumatic Heart Disease—Based on the Revised Jones
Criteria                                                                                 

Diagnostic Categories

 Primary episode of RF*

 Recurrent attack of RF in a patient without established rheumatic heart disease†

Recurrent attack of RF in a patient with established rheumatic heart disease

Rheumatic chorea: Insidious onset rheumatic carditis†

Chronic valve lesions of rheumatic heart disease (patients presenting for the rst
time with pure mitral stenosis or mixed mitral valve disease)‡

Criteria

 Two major or one major and two minor manifestations plus evidence of a
preceding GAS infection • Two minor manifestations plus evidence of a preceding
GAS infection§

Other major manifestations or evidence of GAS infection not required

 Do not require any other criteria to be diagnosed as having rheumatic heart
disease and/or aortic valve disease
 Major NR 602 Final Exam Study Guide
Manifestations

 Carditis

 Polyarthritis

                                                        
                                                
                                        

                

                

                        

Chorea
 Erythema marginatum • Subcutaneous nodules
Minor Manifestations

 Clinical fever, polyarthralgia

 Laboratory elevated acute phase reactants (ESR or leukocyte count)

Supporting Evidence of a Preceding Group A Streptococcal Infection within the

Past 45 Days

ECG: Prolonged PR interval

Elevated or rising ASO or other streptococcal antibody or • A positive throat

culture or

Rapid antigen test for GAS or

Recent scarlet fever

                                                                

ASO, Anti-streptolysin O; ECG, electrocardiogram; ESR, erythrocyte sedimentation

rate; GAS, group A streptococcus; RF, rheumatic fever.                
         
NR 602 Final Exam Study Guide
                                        

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-in ammatory therapy: Aspirin can be used for arthritis after the diagnosis is
established; it is usually given 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 bene cial 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 in uenza
immunization is critical for children on aspirin therapy.                                

• Chest radiographs, ECG, and echocardiography are indicated; carditis usually develops
within the rst 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 bene t 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 e ective 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 rst episode of rheumatic heart
disease.NR 602 Final Exam Study Guide

Complications

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 signi cant 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.

RSV Bronchiolitis (Nida)

Burns pg. 685
Bronchiolitis  is the most common respiratory infection in infancy, causing cell death and
necrosis of respiratory epithelial cells lining small airways. There is increased destruction in the
lining of the bronchioles along with bronchospasm and copious mucous production.
Bronchiolitis is characterized by the insidious onset of URI symptoms, decreased feeding, and
mild fever, with apnea as a possible presentation in the younger infant. Usually after 1 to 2 days
of URI symptoms, wheezing and course crackles are heard with tachypnea and mild to severe
chest retractions that last as long as 12 days. Usually, the child improves by the 6th day of
illness. While older children can have viral induced wheezing, the classic picture of
bronchiolitis is an infant to 2 years old with upper respiratory prodrome followed by wheezing
and mild to severe respiratory distress. The peak incidence of this disease is in infants less than
6 months old; it is the most common cause of hospital admission in children less than 1 year. In
severe cases, cyanosis, air hunger, retractions, and nasal aring with symptoms of severe
respiratory distress can appear within a few hours. Apnea can occur with a wide range of
prevalence reported  and may require mechanical ventilation.
The pathophysiology in bronchiolitis  is due to shedding of bronchiole epithelium and
alveolar epithelial cells (AEC), types I and II, airway edema, and resultant dysfunction of the cilia.
Clinical Findings
History
The following are reported:
• Initial presentation: URI symptoms of cough, coryza, and rhinorrhea for 1 to 2 days
prior to lower respiratory disease

• Gradual development of respiratory distress with persistent coughing, tachypnea,

chest retractions, and 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

• Usually the course is the worst by 48 to 72 hours after wheezing starts. The disease
peaks at around 5 to 7 days. 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 ndings of coryza, mild conjunctivitis in 33%, and pharyngitis
 NR 602 Final
• Lower Exam ndings
respiratory Study Guide
of:

• Tachypnea (approximately 40 to 80 breaths per minute)

• Substernal and/or intercostal retractions

• Heterophonous expiratory wheezing (i.e., di erent pitches of wheezing in

di erent lung elds)

• Fine or coarse crackles may be heard throughout the breathing cycle

• Varying signs of respiratory distress and pulmonary involvement (e.g.,

nasal aring, grunting, retractions, cyanosis, prolonged expiration)

• Abdominal distention; palpable liver and spleen, pushed down by

hyperin ated lungs and a attened diaphragm

Diagnostic Studies
● Physical exam
● CXR
● Viral culture of nasal washings
● Hematologic testing is not recommended. If a CBC is done for another reason, a mild
leukocytosis may be seen with 12,000 to 16,000/mm
Di erential Diagnosis
The diagnosis of bronchiolitis  can be confused with asthma, although there are some
di erences that may be helpful. Asthma is an acute process due to airway hyperreactivity and
in ammation, whereas the onset of bronchiolitis is insidious. The response to the usual asthma
therapies of β agonist and steroids 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 usually found in 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 signs of failure to thrive with a murmur and an S4  gallop rhythm.
Other di erentials include airway irritants, gastroesophageal re ux, pneumonia, allergic
pneumonitis, vascular rings, lung cysts, and lobar emphysema.
Management
  Supportive care remains the primary therapy and includes fever control, maintaining
hydration and nutrition while keeping oxygen levels ≥90%. 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 their use and the lack of evidence of an
e ect. The use of epinephrine is also not recommended for infants and children. The use of
hypertonic saline in the outpatient department is not recommended and in hospitalized
children may show transient improvement in clinical scores without changing length of stay.
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:
 • Supportive care consists of adequate hydration, nutrition, fever control, and
maintaining oxygen.
NR 602 Final Exam Study Guide
• 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.

• Transcutaneous oxygen saturation monitoring (continuous pulse oximetry) is also

an individual provider’s choice. A recent study showed that continuous oxygen
monitoring leads to overdiagnosis of hypoxemia and delayed discharge. While
recurrent desaturations are common among infants with bronchiolitis, delayed
discharge is not needed due to these episodes and these infants can safely be sent
home

• Fluid intake is strongly recommended to prevent dehydration.

• Nasal suctioning to clear the upper nasal passages is recommended.

Complications
Complications of bronchiolitis  include apnea, respiratory failure, aspiration, and secondary
bacterial infections. The child is ill-appearing and toxic but gradually improves. The fatality rate
associated with bronchiolitis  is less than 0.05% and only 2% of infants who require
hospitalization need to be intubated. Infants younger than 12 weeks old and those with
underlying cardiorespiratory or immunode ciency 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.
Estimates of the risk of school-aged asthma and history of severe bronchiolitis in infancy range
from 20% to 60% with a recent study showing a rate of 27.6%.
Prevention
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 or hand washing, if hand sanitizer is not
available; avoiding tobacco smoke exposure; and scheduling RSV  prophylaxis vaccination,
when indicated. Recent literature support wearing a face mask to reduce the risk of respiratory
infections which, while common in Asia, is not a common practice in Western cultures.
Palivizumab (Synagis) is an RSV-speci c monoclonal antibody used to provide some protection
from severe RSV infection for a very small population of high-risk infants.

Croup (Nida) - burns pg. 482

Human parain uenza virus (hPIV), a paramyxovirus, is similar to the in uenza and mumps
viruses and is an important cause of laryngotracheobronchitis (croup), bronchitis,
bronchiolitis, and pneumonia.
There are four antigenic hPIV types. Types 1 and 2 usually strike children 1 to 5 years old and
are usually associated with croup; outbreaks are seen more in summer and fall and in odd-
numbered years; reinfections occur at any age. Type 3 is endemic, associated more with
bronchitis, bronchiolitis, and pneumonia in those younger than 12 months old, results in
shorter immunity (a particular problem for immunocompromised patients), and outbreaks peak
in the spring
NR 602 and summer
Final Exam(sometimes
Study Guide into fall months). Type 4 infections are less well
pathologically and clinically understood, may be more pervasive than once thought, and can
cause mild to severe respiratory illness. By the time most children are 5 years old, they have
been exposed to all of the types. An individual typically has repeated infections due to hPIV as
immunity is transient and limited.
This virus spreads by direct person-to-person contact through infected nasopharyngeal
secretions or from fomite contamination. It replicates in the super cial ciliated epithelial lining
the airways of the upper and lower respiratory tract and spreads readily. The incubation period
is 2 to 6 days. Healthy children shed virus for 4 to 7 days before symptom onset and up to 7 to
21 days after resolution of symptoms. The virus lives on nonporous surfaces for up to 10 hours.
Clinical Findings
Symptoms may include an acute onset of mild fever, sore throat, rhinitis, hoarseness, and
cough (including a typical “croup” cough). Lower respiratory involvement symptoms include
dyspnea, crackles, wheezing, and hyperaeration. In older children and adolescents, recurrent
infection may manifest as a mild URI.
Diagnostic Studies
Routine testing is not needed. Speci c RT-PCR assays are the standard diagnostic test when
needed. The virus can be isolated from nasopharyngeal secretions; culture results are usually
available within 4 to 7 days (or earlier). Sensitivities vary when rapid antigen identi cation is
performed by IFAs and enzyme immunoassays. WBC count may be normal or slightly elevated
with a mild lymphocyte elevation.
Di erential Diagnosis, Management, and Complications
The di erential diagnosis includes other viral URIs, allergic croup, laryngotracheitis, bacterial
tracheitis, retropharyngeal abscess, epiglottitis, laryngeal diphtheria, foreign body aspiration,
or GI re ux.
The treatment is supportive; recovery is uncomplicated in most cases. Reliable studies using
ribavirin are lacking; therefore, aerosolized ribavirin should only be considered for high-risk
patients with severe lower respiratory involvement. With the newer outpatient guidelines for
managing croup, few children need hospitalization. Antibiotics are reasonable in cases of
severe infection when secondary bacterial invasion is suspected (e.g., otitis media, bronchitis,
tracheitis, pneumonia). No vaccine is available; intravenous immune globulin is not helpful.
Good hand hygiene is important.
Complications are infrequent. Immunocompromised individuals are more prone to
developing secondary bacterial infections.
Symptoms management of croup: steroids, nebs, racemic epinephrine
● Asthma - all levels of severity---2 people might be easier gabby burde(Erica O. & Jenny S.)

- Asthma is characterized by varying degree of airow obstruction that presents as

coughing, wheezing, chest tightness, breathlessness, and respiratory distress
- In ammation causes acute bronchoconstriction, airway edema, and mucous plug formation.
- Asthma in children as intermittent, mild persistent, moderate persistent, or severe persistent depending on
symptoms, recurrences, need for speci c medications, and pulmonary function
 NR 602 Final Exam Study Guide

- Exercise-induced bronchospasm (EIB) describes the phenomenon of airway narrowing during, or minutes
after, the onset of vigorous activity
- Although asthma is not always associated with an allergic disorder in children, many children with
chronic asthma have an allergic component
- Asthma is rarely diagnosed before 12 months old due to the high rate of viral illnesses causing
bronchiolitis
- “all that wheezes is not asthma and all asthma does not wheeze”
- The development of an IgE-mediated response to common aeroallergens, known as atopy, remains the
strongest identi able predisposing risk factor for asthma
- Common triggers for an asthma exacerbation include:
- viral respiratory infections
- environmental allergens
- change in the weather
- Stress
- emotional expression
- Exercise
- sinusitis
- gastroesophageal re ex
- Majority of asthmatics show evidence of sensitization to any of the following inhalant allergens:
- House dust mites
- Cockroaches
- indoor molds
- Saliva
- dander of cats and dogs
- Outdoor seasonal molds
- Airborne pollens—trees, grasses, and weeds
-  Food allergy, including egg and tree nut

Diagnosis
- The new Global Initiative Guidelines (GINA) for 2018 recommend that PCPs query about a history of
wheezing, chest tightness, cough, and shortness of breath in children 6 years and older
- The latest AAP recommendations clearly advocate for the use of age-speci c asthma control tools as part
of assessment
- The advantages of a standardized questionnaire are that it allows the PCP to assess changes in
the patient’s asthma and alter the management plan as needed
- Objective measures of asthma control include
- assessment of lung function
- airway hyperresponsiveness assessmen
- Biomarkers
- Assessment of asthma severity in attack:
NR 602 Final Exam Study Guide

-
- History: Critical points to cover in the history include:
- 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
re ux, 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
- 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)
- Physical exam
- 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
- Altered level of alertness
- Tachycardia, hypertension, or hypotension
- Cyanosis of lips and nail beds if hypoxic
- Possible associated findings include sinusitis, AD, and AR
- Tests to consider include:
- SpO2
- CBC
- CXR (selectively)
- Allergy testing
- Sweat chloride testing (possible CF)
- Pulmonary function testing is the best way to evaluate obstructive respiratory pathology and remains
the gold standard for diagnosing asthma
- the GINA guidelines recommend spirometry every 1 to 2 years
- Children older than 5 years can typically perform spirometry
- FEV1 shows:
- >75%: Normal
- 60% to 75%: Mild obstruction
 - 50% to 59%: Moderate obstruction
NR 602 - <49%:
Final Exam Severe obstruction
Study Guide
- Reversibility with a bronchodilator is an increase in FEV1 of 12% or more or 100 mL from baseline
- If spirometry is not an option, peak expiratory flow (PEF) can be used in children as young as
4 to 5 years old
- child’s personal best value is the best guide to help detect possible changes in airway
obstruction
- 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.
- Red zone: Between 0% and 50% of personal best signals major airflow obstruction
- Exhaled nitric oxide has moderate accuracy when diagnosing children 5 and over

Differential Diagnosis of Asthma:

- acute bronchiolitis
- Laryngotracheobronchitis
- Bronchopneumonia
- Pneumothorax
- inhaled foreign body
- congenital malformations of the heart and pulmonary abnormalities or bronchopulmonary dysplasia or
bronchiectasis
- genetic disorders (e.g., cystic fibrosis and α-1-antitrypin deficiency)
- primary ciliary dyskinesia
- tracheal or foreign body compression (e.g., vascular aortic ring, enlarged lymph nodes, or tumors)
- chronic lower respiratory tract infections caused by immunodeficiency disorders
- congenital malformation of the GI system with resultant recurrent aspirations and gastroesophageal
reflux disease
- vocal cord dysfunction
- exposure to toxic substance
- Anaphylaxis

Classification / Management
NR 602 Final Exam Study Guide
NR 602 Final Exam Study Guide
NR 602 Final Exam Study Guide
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NR 602 Final Exam Study Guide

- Management tips:
- Avoid exposure to known allergens or irritants, especially when mold and pollen counts are at their
highest
- Use air conditioning, close windows and doors, and remain indoors as much as possible during
high pollen and mold season
- Consider allergen immunotherapy (AIT)
- Treat rhinitis, sinusitis, or gastroesophageal re ux
- If needed, refer to pulmonology for omalizumab; 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
- Administer yearly in uenza vaccine
- Provide a clear written asthma action plan using a tra c light approach of green, yellow, or red to
manage exacerbations
- Instruct parent to advance the asthma action plan to the yellow zone if the child has an
upper respiratory infection
- Educate regarding asthma basics, including triggers and prevention with environmental
modi cation, as well as the different treatment modalities including the techniques of
administration; dispel any myths regarding asthma medication
- Pharmacological tips:
- 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
- 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.
- The combination of ICS with a long-acting β2-agonist (LABA) can further control asthma
- Children with intermittent asthma may have long, symptom-free periods; they can also have
life-threatening exacerbations, often provoked by respiratory infection. In these situations, a
short course of systemic corticosteroids should be used
- A spacer or holding chamber with an attached mask enhances the delivery of MDI
medications to a child’s lower airways. Spacers eliminate the need to synchronize inhalation
with activation of MDI. Older children can use a spacer without the mask. It is important to
check technique at every asthma-related visit.
 - For treatment of exercise-induced asthma (EIA) or EIB:
NR 602 - WarmFinalup before
Examexercise
StudyforGuide
5 to 10 minutes
- As preventive, use a SABA 5 to 20 minutes prior to exercise
- A mast cell stabilizer such as Cromolyn can be added. Combination of both types of
drugs is the more effective therapy. Adding an anticholinergic may help if the SABA is
not working
- • If a SABA is used daily, a controller therapy should be instituted with either ICS ± LABA
and/or LTRA
- Using a scarf or mask around the mouth in cold weather may decrease EIA
- For treatment of acute asthma exacerbation:
- 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 in two divided doses to a maximum of 60 mg/day
- Magnesium sulfate intravenous (IV) is used in EDs; it causes bronchodilation due to respiratory
smooth muscle relaxation. The most signi cant side effect is hypotension
- The use of continuous infusion of terbutaline IV is limited to pediatric intensive care settings due
to the risk of sinus tachycardia, decreases in systolic and diastolic blood pressure, and myocardial
ischemia
- Theophylline, even at suboptimal doses, improves the lungs’ responsiveness to steroids
- Ketamine, a potent bronchodilator, may be used as an induction agent in critically ill children
with asthma and respiratory failure
- Ipratropium, an anticholinergic bronchodilator, via oral inhalation is used to treat
bronchospasms
- Epinephrine given subcutaneously or intramuscularly is an option in severe asthma where the
delivery of medication to smaller airways is limited due to bronchoconstriction
- Heliox, a mixture of oxygen and helium, can improve drug delivery in obstructed airways
because it has a lower density and less airway resistance
-
● Gastroenteritis  (LaDonna Russell)
● Genu Varum Laci Patton
● Cholesteatoma   (Nicole C.) Cholesteatoma  - Burns p.661
Cholesteatoma is usually the result of a chronic ear infection and involves the formation of an
epidermal inclusion cyst of the middle ear or mastoid consisting of desquamated debris from
the keratinizing, squamous epithelial lining of the middle ear (Fig 36.10). As the
cholesteatoma  grows in size, it can destroy the surrounding structures. Chronic otorrhea,
ossicular erosion, and hearing loss are common sequelae. Any child with chronic ear drainage
that does not resolve with appropriate antibiotic treatment should be referred to an
otolaryngologist to rule out cholesteatoma. Permanent hearing loss, facial nerve paralysis,
meningitis, and brain abscess are rare but potential complications of untreated
cholesteatoma.
Cholesteatomas can be congenital, primary acquired, or secondary acquired. Congenital
cholesteatomas are small and self-contained at birth and initially appear as a pearly white
mass behind the TM. Primary acquired cholesteatomas arise from negative middle ear pressure
that causes TM retraction and subsequent accumulation of an erosive keratin- lled cyst.
Secondary acquired cholesteatomas are the result of skin ingrowth from a perforated TM or
trapped epithelium due to ear trauma or a procedure.

nical Findings
History and Physical Examination
The history may be negative with congenital cholesteatomas. The history with an acquired
cholesteatoma might include:
• Chronic otitis media with malodorous purulent otorrhea

• Vertigo and hearing loss

 • History
NR or presence
602 Final of tympanostomy
Exam Study Guide or PE tubes

• A pearly white lesion is present on or behind the TM. Aural polyps are considered
cholesteatomas unless proven otherwise. Congenital cholesteatomas are often in the
most anteroinferior position behind the TM (see Fig 36.10).

erential Diagnosis
Tympanosclerosis (Fig 36.6), debris from chronic OME, malignant rhabdomyosarcoma, and
aural polyps are some of the di erential diagnoses.
nagement and Complications
Cholesteatoma  is managed surgically. Accurate diagnosis and immediate referral to an
otolaryngologist for surgical excision are needed. Complications include irreversible structural
damage, permanent bone damage, facial nerve palsy, hearing loss, and intracranial infection,
especially in untreated cases.
● Legg-Calve’-Perthes Disease (Kim S) signs and symptoms
○ self-limiting disease of femoral head comprising of necrosis, collapse, repair and
remodeling
○ Cause-familial, breech birth, prior trauma

○ Sx- acute or chronic onset, pain in hip, groin, knee sti ness (male).

○ + trendelenburg, shortening, decreased abduction, internal rotation, hip extension, +

radiographs but not early

○ Tx- BR, traction, PT, brace surgery may be needed

● Osgood-Schlatter (Kim S)

○ caused by micotrauma in deep bers of patellar tendor @ insertion to tibial

tuberosity

○ Dx- clinical h & p

○ Hx- recent physical activity, pain increase during and immed after,
running/jumping/kneeling/squatting, and up and down stairs exacerbates

○ Physical exam- pain reproduced by extending need against resistance, stressing

quad, squatting with knee full exed, focal swelling, heat and point tenderness, full
ROM of knee

○ Tx-self-limiting, modifying activity, ice/cold, stretching, NSAIDs, neoprene sleeve

● Developmental Dysplasia of the Hip (Thompson) (Burns, Ch.43 p.900)

● Developmental Dysplasia of the Hip (DDH) is a variety of anatomic abnormalities in which the
femoral head and the acetabulum are abnormally grown or not in correct alignment. Variations
of hip dysplasia include dysplastic, dislocatable, and dislocated hips. Dysplasia is noted by a
shallow, more
NR 602vertical
Finalacetabular socket
Exam Study with an immature hip/ acetabulum. Subluxation, the
Guide
hip is more unstable, and the femoral head will slide in and out of the acetabulum/hip. Hip
dysplasia is considered both congenital and even may develop throughout infancy and
childhood.
● The incidence of DDH is estimated to range from 1.5 to 20 per 1000 live births in the United
States. Risk factors include
○  breech delivery
○ female gender (4x more common than males)

○ a positive family history (genetic risk factors)

○ other congenital anomalies like oligohydramnios, torticollis, and lower limb

deformities (e.g. clubfoot, MA, and dislocated knee)
● Physiological factors include:
○   hormonal e ect of maternal estrogen and relaxin during delivery, which causes
temporary laxity in the hip joint.
● Mechanical factors:
○ from constant utero compression with restriction of movement late in gestational
age or when a fetal pelvis becomes locked in the maternal pelvis.
○ Mechanical factors are common in rst pregnancies, oligohydramnios, and breech
positioning.
● With unstable hip, the femoral head and acetabulum do not have a normal tight, anatomic
relationship, which leads to abnormal growth of the hip joint, causing permanent disability. In
newborns, the LEFT hip is most often a ected due to this hip is typically the one in the forced
abductions position against the mother sacrum.
● The hip can dislocate noncongenitally or in utero in children with certain muscular or
neurologic disorders that a ect the use of the lower extremities, such as cerebral palsy,
arthrogryposis, or myelomeningocele. Dislocation results from the abnormal use of the
extremity over time.
● Clinical Findings
● Risk factors for DDH
● ·       Female gender
● ·       Family history
● ·       High birth weight
● ·       Breech

● ·       Utero postural

● Physical Examination
● Hip examinations with appropriate tests should be performed on children as part of their
well-child supervision until the child begins to walk.
○ 1.  • Routine examinations of the hips and lower extremities until the infant is walking.
● ·       The Barlow and Ortolani tests are used to screen for DDH in neonates. Once an infant
reaches the second and third months of life, the soft tissue surrounding the hips begins to
tighten and the Barlow and Ortolani tests are less reliable.
○ 2.  The Klisic and Galeazzi tests are used to screen older infants. • Some 60% to 80% of
abnormal hips of newborns identi ed by physical examination resolve by 2 to 8 weeks.
  • In the older infant 6 to 18 months of age:
● 
○ 1.  • Limited abduction of the a ected hip and shortening of the thigh (unequal leg
lengths) are reliable signs (see Figs 43.3B  below). There should be a positive Galeazzi
sign (see Fig 43.3A).
● 2.
 • Normal abduction with comfort is 70 to 80 degrees bilaterally. Limited abduction includes
those cases with less than 60 degrees of abduction or unequal abduction from one side to the
other (see Fig 43.5; see below).
  • Other ndings include asymmetry of inguinal or gluteal folds (thigh fold asymmetry is
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not 602 Final Exam
to the Study
disorder andGuide
unequal leg lengths, shorter on the a ected side.
In the ambulatory child who was not diagnosed earlier or was not corrected, the following
might also be noted:
1.  • Short leg with toe walking on the a ected side

2.  • Positive Trendelenburg sign (see Fig 43.3C)

3.  • Marked lordosis or toe walking

4.  • Painless limping or waddling gait with child leaning to the a ected side
If the hips are dislocated bilaterally, asymmetries are not observed. Limited abduction is
the primary nding on examination (see Fig 43.5). Also in subluxation of the hip  (not frankly
dislocated), limited abduction again is the primary indicator. A waddling gait may also be
noted.

● 
● FIGURE 43 above
● FIG 43.3 Physical Findings in Congenital Hip Dislocation.(A) Leg-length inequality is a sign of
unilateral hip dislocation (Galeazzi sign). (B) Limitation of hip abduction is often present in older
infants with hip dislocation. Abduction of greater than 60 degrees is usually possible in infants.
Restriction or asymmetry indicates the need for careful radiologic examination. (C)
Trendelenburg sign. In single-leg stance, the abductor muscles of the normal hip support the
pelvis. Dislocation of the hip functionally shortens and weakens these muscles. When the child
attempts to stand on the dislocated hip, the opposite side of the pelvis drops. (D) Thigh-fold
asymmetry is often present in infants with unilateral hip dislocation. An extra fold can be seen
on the abnormal side. However, the nding is not diagnostic. It may be found in normal infants
and may be absent in children with hip dislocation or dislocatability.
 NR 602 Final Exam Study Guide

●  
Diagnostic Studies
Ultrasound is superior to radiographs for evaluating cartilaginous structures and is
recommended when the infant reaches 6 weeks of age. Ultrasound prior to 6 weeks of age has
a high incidence of false positive. Radiologic evaluation of the newborn to detect and
evaluate DDH is recommended once the proximal epiphysis ossi es, usually by 4 to 6 months.
Radiography prior to this is unreliable, because so much of the hip joint is cartilaginous in the
young infant. AP and lateral Lauenstein (frog-leg) position radiographs of the pelvis is
appropriate.
Management
The goal of management is to restore the articulation of the femur within the acetabulum.
Most neonatal hip instability ndings resolve spontaneously by 6 to 8 weeks.
•  Refer infant to an orthopedist if the newborn exam is positive. Follow up the newborn exam
again at 2 weeks of age with a thorough hip examination to check for DDH. If the exam is
positive or inconclusive, refer the infant to an orthopedist:
1.  • Refer infant if limited or asymmetric hip abduction is noted at 4 weeks or older.

2.   • For infants less than 6 months of age with a normal DDH examination and a
history of breech presentation in the third trimester, previous clinical hip
instability, improper swaddling, or a positive family history, or parental concern,
imaging is an option for con rmation.

3.   • The treatment of choice for persistent subluxation and reducible dislocations

identi ed in the early phase is a Pavlik harness. The harness is applied with hips
having greater than 90 degrees of exion and with adduction of the hip limited to
a neutral position. Radiographic or ultrasound documentation can be used
during treatment to verify the position of the hip.

4.  If the infant does not respond to treatment with the harness, surgical treatment
may be needed.

5.  • The earlier treatment is started with the Pavlik harness, the better the prognosis
for a successful outcome. The harness is worn 24 hours a day except for bathing.
The infant with a Pavlik harness should be seen weekly to make sure that it ts
properly, to identify complications associated with the use of the harness (e.g.,
avascular necrosis and femoral nerve palsy), and to ensure that the femur is
properly seated in the socket. Ultrasonography can be performed while the Pavlik
harness is worn to assess hip reduction and acetabular development. The length
of time the harness is worn depends on the age of the infant, when it was applied,
and whether reduction is successful. Typically, the harness is worn full time for 3 to
 6 weeks and then may be required only during waking hours for decreasing
periods
NR 602 of Exam
Final time. Study Guide

6.  • For a child in a Pavlik harness or spica cast, cast care, skin care, and car safety
when the child cannot easily be placed in a car seat are issues to be addressed.

7.  An orthopedist should be immediately consulted for any infant seen in a primary
care setting who is in a Pavlik harness and exhibits excessive hip exion (beyond
100 degrees) or abduction (beyond 60 degrees).

8.   • The 6- to 18-month-old infant with a dislocated hip is likely to require either

closed manipulation or open reduction. Preoperative traction, adductor tenotomy,
and gentle reduction are especially helpful in preventing osteonecrosis of the
femoral head. After the closed or open reduction, a hip spica cast is applied in
order to maintain the hip in more than 90 degrees of exion and avoid excessive
internal or external rotation.

• Annual or biennial follow-up including radiographs to the point of skeletal maturity is

recommended to evaluate for the possibility of late asymmetric epiphyseal closure
Complications
The Pavlik harness and other positional devices may cause skin irritation, and a di erence in
leg length may remain. There may be delay in walking if the child is put in a body cast. The
long-term outcomes depend on the age at diagnosis, severity of the joint deformity, and
e ectiveness of therapy. Untreated cases may result in a permanent dislocation of the
femoral head so that it lies just under the iliac crest posteriorly. Adult degenerative arthritis is
associated with acetabular dysplasia. growth and development in infants and children.
Prevention
The condition cannot be prevented, but early identi cation resulting in early treatment
signi cantly reduces its long-term consequences. Screening of all neonates and infants
should include full hip abduction; examination for unequal inguinal and gluteal folds and
unequal leg lengths; and Barlow, Ortolani, and Galeazzi maneuvers at every examination. 

● Scoliosis( Dinara)
Scoliosis is a three-dimensional deformity most commonly described as a lateral curvature of
the spine in the frontal plane.
Two types of scoliosis:
1. Nonstructural (functional scoliosis) involves a curve in the spine without rotation of
the vertebrae. The curve is reversible, because it is caused by conditions such as poor
posture, muscle spasms, pain, or leg-length discrepancy.
2. Structural scoliosis involves a rotational element of the spine and has various
classi cations depending on the cause.
Ø  The diagnosis is based on a curvature of more than 10 degrees using the Cobb
method, measured by a radiologist. In most pediatric cases, the etiology is unknown
(idiopathic).
a.         Congenital, in which vertebrae fail to form (e.g., hemivertebrae). A structural
anomaly present at birth (e.g., hemivertebrae) often associated with other congenital
abnormalities, such as renal and cardiac anomalies; progression of curvature can
worsen rapidly, particularly during periods of rapid growth (e.g., rst 2 to 3 years of life
and adolescence).
 
b.        Neuromuscular (e.g., cerebral palsy, neuro bromatosis, Marfan syndrome).
 c.         Kyphosis, which results from disorders of sagittal alignment (such as postural
kyphosis
NR 602and Scheuermann
Final Exam Study disease).
Guide
d.        Idiopathic: Etiology is unknown and is likely multifactorial. It is the most common
type of scoliosis. There are three types classi ed by age at onset:
 
1. • Infantile (0 to 3 years of age)

2. • Juvenile (3 to 10 years of age)

3. • Adolescent (11 years of age and older)

(See table 43.2) pp 897 for more information about Scoliosis, Kyphosis, and Lordosis
 
Idiopathic scoliosis is the most common type.
The etiology is unknown, but it often has a familial or genetic pattern.
The incidence of idiopathic scoliosis is approximately 2% to 3%
__ 0.3% and 0.5% of children have curves greater than 20 degrees on radiography                          
                      
__ less than 0.1% have curves greater than a 40-degree Cobb angle.
 
Etiology:
➢   Hormonal changes and sexual
➢  Rapid growth period and gender. Females have a much higher risk of developing
curves greater than 30 degrees
o   Small to moderate scoliotic curves (10% to 30%) do not increase signi cantly
after skeletal growth is complete.
o   Double-S and more severe curves are more likely to progress during the
growth years. Monitor the curve on a regular basis.
o   In curves between 20 and 45 degrees, the risk for progression is high during
growth, and early intervention is of paramount importance.
o   In curves greater than 50 degrees, the spine loses its ability to compensate
and progression is expected. Young premenarchal females with large curves
are  vulnerable. The majority of adolescents with idiopathic scoliosis have a
right thoracic curve.
Clinical ndings.
Painless and insidious onset. No signi cant history.
Assess the following:
1. • Family history of scoliosis

2. • Age of menarche

3. • Etiologic factors related to the various causes of structural scoliosis

★ The presence of pain with a lateral curvature of the spine suggests an in ammatory
or neoplastic lesion as the cause of the scoliosis. Mild pain is activity-related. Severe,
constant, or night pain and point tenderness can be indicative of other pathologic
conditions (e.g., metastatic tumor or stenosis) and warrants further investigation.
Physical Examination
Children of all ages should be evaluated in the standing position, from both the front and the
side, to identify any asymmetry. Asymmetries to look for include:
1. • Unequal shoulder height.

2. • Unequal scapular prominences and heights: Note that the muscle masses may be
somewhat unequal, especially if the child uses one shoulder more than the other, as in
carrying books. Look for bony, not muscular, prominence.
3. • Unequal waist angles: The hip touches one arm and the contralateral arm hangs
free.
4. • Unequal rib prominences and chest asymmetry.
 5. • Asymmetry of the elbow-to-
ank distance and some deviation of the spine from a
straight head-to-toe line.
NR 602 Final Exam Study Guide
6. • Unequal rib heights when the child stands in the Adams forward bend position

During the Adams test the examiner looks for asymmetry of the posterior chest wall on forward
bending- the earliest abnormality seen.
★ Assess infant lying prone. Inspect for skin abnormalities, sacral dimple, and hairy
patches.
The physical examination should include the following:
1. • Observation for equal leg lengths

2. • Examination of the skin for hairy patches, nevi, café-au-lait spots, lipomas, dimples

3. • Neurologic examination checking for weakness or sensory disturbance

4. • Cardiac examination with diagnosis of Marfan syndrome

Diagnostic Studies
➢   Standing AP and lateral radiographs of the entire spine at the initial
evaluation of patients with clinical ndings of a spinal deformity.
On the PA radiographs, the degree of curvature is determined by the Cobb method.
➢  MRI is helpful when an underlying cause of the scoliosis is suspected based
on age (infantile and juvenile curves), abnormal ndings in the history and on
physical examination, and atypical radiographic features.
Di erential Diagnosis
➢ Structural scoliosis vs functional scoliosis.
➢ Persistent functional scoliosis to one side in a child with a neuromotor problem can
eventually become structural and must be managed with physical therapy or other
means to prevent progression.
 
Management:
 
❏ The goal is to stop the progression of curvature and improve pulmonary function.
❏ Treatment options include observation, bracing, and surgery.
❏ The ScoliScore is a genetic test that screens for more than 50 genetic markers of
idiopathic scoliosis, and identi es the patient as having a low, medium, or high risk for
curve progression.
Idiopathic Scoliosis (Dinara).
● Adolescent scoliosis can resolve, remain static, or increase.

● Progressive curves require bracing and surgery in an attempt to slow the curve
progression and prevent complications (e.g., thoracic insu ciency syndrome).
● Juvenile scoliosis is found more frequently in girls, are at high risk for progression
and often require surgical intervention.
● The treatment goal is to delay spinal fusion, allowing time for the pulmonary system
and thoracic cage to have matured and maximal trunk height to be achieved.
● for curves less than 20 degrees-observation is indicated.

● Brace treatment may reduce the need for surgery, restore the sagittal pro le, and
change vertebral rotation.
● Bracing is for curves more than 30 degrees. And for skeletally immature patients with
curves of 20 to 25 degrees that have shown more than 5 degrees of progression.
● Wear a brace as much as 23 hours per day; compliance is important.
 ● Surgical treatment is indicated for children and adolescents who do not respond to
bracing
NR 602and for Exam
Final those with curvature
Study Guide exceeding 45 to 50 degree.
● Vertical expandable prosthetic titanium rib (VEPTR). This procedure is indicated for
children with restricted pulmonary function due to the curvature of the thoracic spine.
Ø  The surgery involves implanting a prosthesis that serves to enlarge the constricted
thorax. The prosthesis can be adjusted approximately every 4 to 6 months, thereby
allowing for growth.
Ø  The “growing rod” is another surgical procedure, it involves inserting spinal rods
that are adjusted approximately every 6 months
Ø  Intervertebral spinal stapling does not require repeat adjustments and therefore
eliminates the need for repeat surgical procedures. Research on this technique is
limited, and clinical indications have not been universally agreed upon
 
● Referral to an orthopedist.

● Concerns of self-esteem problems, wondering about the long-term prognosis, and

concerns about clothing and participation in sports and other activities.
Complications
● severe deformity of the spinal column impair both respiratory and cardiovascular
function, limit physical activities, and impair comfort.
● The psychological consequences of an untreated scoliosis deformity

 
Prevention
● Prevention is not possible;

● Screening and early identi cation of scoliosis may help avoid more expensive,
invasive care and prevent the potential long-term consequences
Kyphosis
● The normal posterior curvature of the thoracic spine is excessive or exaggerated and
is outside the physiologic range of normal (normal is 20-45 degrees).
● Postural -the most common clinical type of kyphosis is (postural round back). The
curvature of the spinal column points backward and, when viewed from the side, gives
the appearance of a humpback.
● Postural kyphosis is the most common type and is more often seen in girls than in
boys. It rarely causes pain and the curvature is exible.
➢  Scheuermann kyphosis is an osteochondrosis that presents as an abnormality of
the vertebral epiphyseal growth plates.
o   Onset generally occurs in adolescence.
o   The kyphosis is rigid; the pain is located over the deformity and is worse at the
end of the day.
Management
● Exercise and physical therapy program that strengthens the supporting muscles. Ex:
dancing or swimming.
● Combination of a back brace, exercise, and physical therapy.

● Surgery may be required in children with structural problems that cause kyphosis and
in adolescents with curvature of the back that exceeds 50 to 60 degrees.
● Kyphosis caused by infections or tumors may also require surgery.

Lumbar Lordosis
Lumbar lordosis, or hyperlordosis, is an AP curve of the lumbar area of the spine (i.e., the child
stands with
NR the
602abdomen and buttocks
Final Exam Study Guideprotuberant).
● The least common of the congenital spinal deformities

● Is often associated with kyphosis or scoliosis.

● Congenital lordosis deformity is usually progressive. Lordosis can be a secondary

result of a hip problem.
● If lumbar lordosis is suspected, have the child bend forward. If the lumbar spine
attens and the lordosis disappears in the forward bending position, it indicates that
the spine is exible and the lordosis is only physiologic.
● This child should be seen for follow-up in 6 to 12 months.

● Lordosis resulting from hip exion contractures is absent while sitting; it is commonly
seen in children with cerebral palsy, spina bi da, and developmental dysplasia of the
hip.
● Febrile seizures (Kim S.)
○  most common type of seizures in children.
○ brief, generalized, clonic or tonic-clonic in nature, and can be either simple or
complex.
○ A concurrent illness is present with rapid fever rise to at least more than 102.2° F (39°
C), but the fever is not necessarily that high at the time of the seizure.
○ Minimal postictal confusion is associated with febrile seizures.

○ Simple febrile seizures last less than 15 minutes and may recur during the same
febrile illness period.

○   Complex febrile seizures last longer than 15 minutes, can recur on the same day,
and can have focal attributes (even during the postictal phase).

○ Febrile SE is uncommon, rarely stops spontaneously, is fairly resistant to

medications, and can persist for a long period of time.

○ Most children in febrile SE require one or more medications to end the seizure.

○ A report found that reducing the time from seizure onset to anticonvulsant
medication administration was key to reducing the seizure duration during an
episode.

○ Risk factors

■  Family medical history for febrile seizures or

■   in those with predisposing factors (e.g., neonatal intensive care unit [NICU]
stay more than 30 days, developmental delay, day care attendance).

■ Age 6 months to 60 months.

 ■ Male
NR 602 Finalgender
Exam Study Guide

■ lower sodium level.

■ Approximately 2% to 5% of neurologically healthy infants and young children

experience at least one simple febrile seizure with about 30% of this group
experiencing a second episode
○ Diagnostic Studies
■ A lumbar puncture may be done in infants younger than 12 months old and
who may also have used an antibiotic prior to seizure onset, and/or in those
who have signs of meningeal irritation.
■ Blood glucose in all children.
■  CBC, calcium, electrolytes, and urinalysis are optional but frequently included.
■ EEG if neurologic signs are present or seizure was atypical.
■ MRI for complex febrile seizure features or if any doubt exists about the
diagnosis.
○ Management
■ Protect the airway, breathing, and circulation if the seizure is still occurring.
Place the child in a side-lying position to prevent aspiration or airway
obstruction.
■ Reduce the fever with acetaminophen or ibuprofen (oral or suppository) after
the seizure has stopped, although the use of antipyretics will not necessarily
prevent another febrile seizure.
■ The child should be seen shortly after the seizure.  transport to an emergency
center if the seizure lasts more than 10 minutes.
■  anticonvulsants are not recommended for febrile seizures, but they may be
considered if the child has abnormal neurologic ndings or developmental
delays; the initial seizure was complex febrile, and there is a family history of
afebrile seizures or if the child has recurrent, prolonged simple febrile seizures.
○ Prophylaxis for Recurrent Febrile Seizures

■ Prolonged anticonvulsant prophylaxis is not recommended.

■ In the rare instance that prophylaxis is indicated, diazepam PO or Rectal can

be given over the course of the febrile illness (usually for 2 to 3 days).

■   Antipyretics can reduce the discomfort associated with a fever but do not
alter the risk of having another febrile seizure.
■ no long-term consequences are associated with febrile seizures, information
that febrile seizures recur in some children and that nothing can be done to
prevent the seizures (no serious impairment of any kind; recurrent higher
chance for epilepsy).
● Testicular torsion (Bev)  Page 846
Testicular torsion is the result of twisting of the spermatic cord, which subsequently
compromises the blood supply to the testicle. Generally, there is a 6-hour window before
signi cant ischemic damage and alteration in spermatic morphology and formation occurs.
 Normal xation of the testis is absent, so the testis rotates and blocks blood and lymphatic
ow. Torsion can occur after physical exertion, trauma, or on arising, and at any age but is most
common in adolescence and is uncommon before 10 years old. The left side is twice as likely to
be involved
NRbecause of the
602 Final longer
Exam spermatic
Study Guidecord.
History and Clinical Findings
        • Sudden onset of unilateral, unrelenting scrotal pain, often associated with nausea and
vomiting.
        • History of intermittent testicular pain. Prior episodes of transient pain are reported in
about half of patients.
        • Minor trauma, physical exertion, or onset of acute pain on arising is possible.
        • May be described as abdominal or inguinal pain by the embarrassed child.
        • Fever is minimal or absent.
Physical Examination
        • Ill-appearing and anxious male, resisting movement
        • Gradual, progressive swelling of involved scrotum with redness, warmth, and tenderness
        • The ipsilateral scrotum can be edematous, erythematous, and warm
        • “Blue dot” sign, which is a subtle blue mass visible through the scrotal skin
        • Testis larger than opposite side, elevated, lying transversely, exquisitely painful
        • Spermatic cord thickened, twisted, and tender
        • Slight elevation of the testis increases pain (in epididymitis it relieves pain)
        • The cremasteric re ex is absent on the side with torsion
        • Neonate—hard, painless, mass with edema or discolored scrotal skin
Diagnostic Studies
        • UA is usually normal; pyuria and bacteriuria indicate UTI, epididymitis, or orchitis.
        • Doppler ultrasound or testicular ow scan considered if Doppler ultrasound within
normal and time allows.
● Wilm’s tumor Bev PAGE 840
Wilms tumor, the most common malignancy of the GU tract, is typically found as a rm, smooth
mass in the abdomen or ank. It is staged as follows:
        • Stage I: The tumor is limited to the kidney and can be completely excised with the
capsular surface intact.
        • Stage II: The tumor extends beyond the kidney but can still be completely excised.
        • Stage III: There is postsurgical residual non hematogenous extension con ned to the
abdomen.
        • Stage IV: There is hematogenous metastasis, most frequently to the lung.
        • Stage V: There is bilateral kidney involvement.
This malignancy manifests as a solitary growth in any part of either or both kidneys. There are
approximately 8 cases of Wilms tumor per million in children younger than 15 years old with 500
new cases every year. Most Wilms tumors occur in children between 2 and 5 years old. The peak
incidence and median age at diagnosis is 3.5 years old (Densmore and Densmore, 2018). About
1% to 2% of children with Wilms tumor have a family history of Wilms, and the tumor is inherited
in an autosomal dominant manner. An important feature of Wilms tumor is the occurrence of
associated congenital anomalies including renal abnormalities, cryptorchidism, hypospadias,
duplication of the collecting system, ambiguous genitalia, hemihypertrophy, aniridia, cardiac
abnormalities, and Beckwith-Wiedemann, Denys-Drash, and Perlman syndromes. Wilms tumor
occurs with equal frequency in both sexes although males are usually diagnosed younger.
There is a higher frequency in African Americans and a lower frequency in Asians.
History and Clinical Findings
        • The most frequent nding is increasing abdominal size or an actual palpable mass.
        • Pain is reported if the mass has undergone rapid growth or hemorrhage.
        • Fever, dyspnea, diarrhea, vomiting, weight loss, or malaise may be reported.
Physical Examination
        • A rm, smooth abdominal or ank mass that does not cross the midline may be noted.
        • BP is elevated if renal ischemia is present (rare).
        • A left varicocele is found in males if the spermatic vein is obstructed.
        • A careful examination is needed to rule out congenital anomalies.
Diagnostic NRStudies
602 Final Exam Study Guide
        • Chest and abdominal radiography are performed to di erentiate neuroblastoma, which
is usually calci ed.
        • Abdominal ultrasonography is used to di erentiate a solid from a cystic mass or
hydronephrosis and multicystic kidney.
        • UA demonstrates hematuria in 25% to 33% of children.
        • Obtain a CBC, reticulocyte count, and liver and renal chemistry studies.
        • A CT scan of the chest, abdomen, and pelvis to stage the disease and bone marrow is
done by the oncology team.
Management
Diagnostic workup is the initial urgent priority, with concurrent referral to a pediatric cancer
center for treatment. Surgery removes the a ected kidney and possibly the ureter and adrenal
gland, and combined chemotherapy and radiotherapy are instituted if the disease is advanced
or has unfavorable histologic ndings. Coordinate close follow-up with the cancer team.
Complications
The lungs and liver are the most common sites of metastasis. Hypertension is possible because
of renal ischemia and occasionally leads to cardiac failure.
Patient and Family Education, Prevention, and Prognosis
The prognosis is determined by the histology of the neoplasm, the patient’s age (the younger
the better), the size of the tumor, positive nodes, and, most signi cantly, the extent or stage of
the disease. The cure rate is about 80% to 90% for infants with stage 4S; reoccurrence of the
disease has a less than 50% response to alternative chemotherapeutic agents (Shohet and
Foster, 2017). A pediatric urologist should determine if a child should be allowed to participate in
sports on an individual basis. Kidney protector use is highly recommended during sports. The
National Wilms Tumor Study is a good reference for information about management, sequela,
and prognosis.
● Turner Syndrome ( Bev)  Sex chromosome disorder (PAGE 518) AKA Monosomy X
  
• Monitor growth using syndrome-speci c growth chart; short stature is expected; GH treatment
typically begins early (∼4-5 years of age).
• Nonverbal (e.g., math) learning disabilities are common.
• Annual hearing exam; recurrent otitis media; progressive mid frequency sensorineural hearing
loss.
• Ongoing vision assessment; strabismus.
• Early onset osteo-penia/-porosis; vitamin D supplementation; appropriate estrogen therapy;
exercise.
• Monitor BP (hypertension).
• Annual thyroid screen (hypo-/hyperthyroidism); monitor for celiac disease.
• Ongoing assessment for celiac disease (tissue transglutaminase immunoglobulin A).
• Careful early monitoring for kyphosis, scoliosis, lordosis.
• Increased risk of hyperlipidemia; cardiac defects (e.g., aortic root dilatation; bicuspid aortic
valve; coarctation of aorta) and renal anomalies (e.g., horseshoe kidney, double collecting
system, increased urinary tract infection [UTI]).
• Supplemental estrogen therapy for sexual development and preservation of bone mineral
density (late childhood/early adolescence).
• Tendency to form keloids.
Turner syndrome is a chromosomal condition that a ects development in females. The most
commonNR 602of
feature Final Exam
Turner StudyisGuide
syndrome short stature, which becomes evident by about age 5.
An early loss of ovarian function (ovarian hypofunction or premature ovarian failure) is also
very common. The ovaries develop normally at rst, but egg cells (oocytes) usually die
prematurely and most ovarian tissue degenerates before birth. Many a ected girls do not
undergo puberty unless they receive hormone therapy,and most are unable to conceive
(infertile).
30 percent of females with Turner syndrome have extra folds of skin on the neck (webbed neck),
a low hairline at the back of the neck, pu ness or swelling(lymphedema) of the hands and feet,
skeletal abnormalities, or kidney problems.
One  third to one half of individuals with Turner syndrome are born with a heart defect,such as
a narrowing of the large artery leaving the heart (coarctation of the aorta) or abnormalities of
the valve that connects the aorta with the heart (the aortic valve).
Most with Turner syndrome have normal intelligence. Developmental delays, nonverbal learning
disabilities, and behavioral problems.
Frequency 
This condition occurs in about 1 in 2,500 newborn girls worldwide, but it is much more common
among pregnancies that do not survive to term (miscarriages and stillbirths).
Causes
Turner syndrome is related to the X chromosome, which is one of the two sex chromosomes.
Inheritance Pattern
Most cases of Turner syndrome are not inherited. When this condition results from monosomy
X, the chromosomal abnormality occurs as a random event during the formation of
reproductive cells (eggs and sperm) in the a ected person's parent. .An error in cell division
called nondisjunction can result in reproductive cells with an abnormal number of
chromosomes.
Other Names for This Condition
45,X•monosomy X•TS•Turner's syndrome•Ullrich-Turner syndrome
https://ghr.nlm.nih.gov/condition/turner-syndrome

● Down Syndrome ( Bev) Chromosomal disorder

 Down syndrome is caused by the addition of an entire chromosome (Chromosome 21).
Chromosome mutations usually result in multiorgan, large e ects, such as in Down syndrome,
in which the individual can have neurologic, eye, ear, orthopedic, cardiac, and other
abnormalities.  PAGE 15
Down (trisomy 21) Common Clinical Findings      PAGE 514
• Short stature
• Brachycephaly
• Midface hypoplasia with at nasal bridge
• Brush eld spots
• Epicanthal folds with upslanting palpebral ssures
• Small mouth with protruding tongue
• Myopia/cataracts
• Small ears/narrow canals
• Extra skin at nape of neck
• Lax joints (atlantoaxial instability)
• Short broad hands/feet/digits
• Single palmar crease
• Clinodactyly
• Exaggerated space/plantar groove between great and second toes
• Congenital heart disease
• At risk for
NRleukemia, hypothyroidism,
602 Final Exam Study Alzheimer
Guide disease
  
Neurodevelopmental Cues
• Intellectual/cognitive disability/developmental delays
• Hearing loss
• Hypotonia (infant)
Primary care Issues PAGE 518
• Careful review of newborn screen for hypothyroidism. Annual and/or systematic screening for
hypothyroidism.
• Careful review of newborn critical congenital heart disease (CCHD) with ongoing cardiac
evaluations.
• Monitor growth using a syndrome-speci c growth chart.
• Ongoing ophthalmologic exam for cataracts.
• Careful review of newborn hearing screening, followed by ongoing otologic/hearing
evaluation.
• Monitor for obstructive sleep apnea.
• Increased risk for duodenal atresia.
• High risk for atlantoaxial instability; if any signs of cervical myelopathy, obtain radiograph,
refer to neurosurgery.
• Monitor for neurologic conditions (e.g., infantile spasms, seizures, Moyamoya malformation).
• Systematic screening for celiac disease (CD).
• Increased risk for leukemia.
Children with Down syndrome are known to have low tone and loose ligaments that place them
at greater risk of having a compression of the spinal cord causing nerve damage referred to as
atlantoaxial instability.  Diagnosis includes an x-ray obtained with the individual’s neck in
neutral position with forward exion of the cervical spine.  Individuals with atlantoaxial
instability may exhibit changes in their ambulation, the ability to use upper extremities,
complaints of neck pain, a new xed head tilt, bowel or bladder dysfunction, or new
unexplained weakness
Sports Contraindicated for Youth With Down Syndrome and Conditions With Associated
Atlantoaxial or Atlanto-Occipital Joint Instability  PAGE 245
        • Gymnastics
        • Diving
        • Butter y stroke in swimming
        • Diving start in swimming
        • High jump
        • Pentathlon
        • Soccer
        • Alpine skiing
        • Equestrian
        • Squat lift
        • Judo
        • Snowboarding
        • Any warm-up exercises placing pressure on the head and neck muscles.