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EXAM 4 PEDS STUDY GUIDE

CARDIAC
 Cardiac Assessment
o Normal pediatric vital signs HR
o Newborn
 100-180
o 1 wk-3 mo
 100-220
o 2 mo- 2 yr
 60-150
o 2-10 yr
 70-110
o 10 yr-adult
 55-90
 Cardiovascular disease has 2 major groups
o Congenital heart disease (CHD)
 Primarily anatomic abnormalities present at birth that result in
abnormal cardiac function
 2 types
 Heart failure (HF)
 Hypoxemia
o Acquired cardiac disorders
 Disease processes or abnormalities that occur after birth and can be
seen in normal heart or the presence of genital heart defects
 Various factors:
 Infection
 Autoimmune responses
 Environmental factors
 Familial tendencies
 History & physical exam
o HISTORY HISTORY HISTORY!!!!
o Inspection
 Nutritional state- failure to thrive or poor weight gain is associated
with heart disease
 Color- cyanosis –common feature of CHD
 Pallor associated with poor perfusion
 Chest deformities- enlarged hears distorts chest configuration
 Unusual pulsations- visible pulsations of the neck veins are seen
sometimes
 Respiratory excursion- refers to ease or difficulty of respiration
 Clubbing of fingers- associated with cyanosis
o Palpation and Percussion
 Chest- maneuvers help discern heart size and other characteristics
 Abdomen – hepatomegaly or spenomegaly
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 Peripheral pulses- rate, regularity, and amplitude
o Auscultation
 Heart rate and rhythm- listen for fast heart rates, slow, and irregular
rhythms
 Character of heart sounds- listen for distinct or muffled sounds,
murmurs, and additional heart sounds
o Diagnostic
 Electrocardiogram
 Nurse should assess the patient, not the monitor
 Echocardiography
 Most frequently used tests for detecting cardiac dysfunction
 Involves use of ultra-high-frequency sound waves to produce
an image of heart’s structure
 Transducer placed directly on chest wall delivers repetitive
pulses of ultrasound and processes the returned signals

Cardiac Catheterization
 Invasive diagnostic procedure in which a radiopaque catheter is inserted thru a
peripheral blood vessel into the heart
 Catheter is guided thru the heart with aid of fluoroscopy
 After tip of catheter is within a heart chamber, contrast material is injected, and
films are taken of the dilution and circulation of the material (angiography)
 Types:
o Diagnostic catheterizations:
 Used to diagnose congenital cardiac defects- particularly in
symptomatic infants & before surgical repair
 Divided into right-sided catheterizations, in which cateheter is
introduced through a vein & threaded into right atrium
 Left-sided catheterization- catheter is threaded thru an artery into
aorta and into the heart
o Interventional catheterizations:
 Therapeutic catheterization
 A balloon catheter or other device is used to alter the cardiac anatomy
 Interventions:
 Balloon atrioseptostomy
o Transposition of great arteries
o Some complex single-ventricle defects
 Balloon dilation
o Valvular pulmonic stenosis
o Branch pulmonary artery stenosis
o Congenital valvular aoritic stenosis
o Rheumatic mitral stenosis
o Recurrent coarctations of aorta
o Congential mitral stenosis
 Coil occlusion
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o PDA (<4mm(
 Transcatheter device closure
o ASD
 Amplatzer septal occluder
o ASD
 VSD devices
o VSDs
 Stent placement
o Pulmonary artery stenosis
o Coarctation of the aorta in adolescents
o Use to treat other lesions
 RF ablation
o Some tachydysrthymias
o Electrophysiology studies
 Catheters with tiny electrode that record the impulses of the heart
directly from conduction system are used to evaluate dysrthymias &
sometimes destroy accessory pathways that cause some
tachydsrthmias
 Possible side effects:
o Acute hemorrhage from entry site
o Low-grade fever
o Nausea
o Vomiting
o Loss of pulse in catheterized extreme
o Transient dysrhythmias
 Rare risks:
o Stroke
o Seiure
o Tamponade
o Death
 Preprocedural care:
o Prepare child & fam for procedure
o Use developmentally appropriate materials
o Assess & mark pulses
o Basline O2 sats
o NPO for 4-6 hours before procedure
 Postprocedural:
o Observe of the following for signs of complications:
 Pulses
 Temp & color of affected extremity
 Vital signs- q 15 minutes
 Blood pressure
 Dressing
 Fluid intake
 Bloog glucose levels- for hypoglycemia
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 Postpericardiotomy syndrome
o Symptoms:
 Fever
 Pericardial friction rub
 Pericardial & pleural effusion
o Occurs immediate post op
o Also can occur later (day 7-21)
o Cause=unknown

CONGENTIAL HEART DISEASE (CHD)
 Incidence:
o 5-8 per 1000 live births
o 2-3 are symptomatic in 1
st
year of life
o CHD=major cause of death in first year of life (after prematurity)
o Most common anomaly= ventricular septal defect
 Causes:
o Chromosomal/genetic 10-12%
o Maternal/environmental 1-2%
 Maternal drug use
 Infants that have FAS- 5-% have CHD
 Maternal illness
 Rubella infection  PDA & pulmonary branch stenosis
 Cytomegalovirus, toxoplasmosis, other viral illness
 Infants of diabetic mothers (IDMs)
o Multifactorial 8%%
 Normal fetal circulation changes
o When newborn takes 1
st
breath, the fetal vascular system undergoes abrupt
changes
 Umbilical vein & umbilical arteries
 Before birth, umbilical vein delivers O2 and nutrients to a fetus
 Foramen ovale
 Closes as pressure in left atrium exceed pressure in right
atrium
 Ductus arteriosus
 Starts to close in presence of increased O2
o The following are NO LONGER NEEDED:
 Foramen ovale
 Shunts highly oxygenated blood from RA to LA & supplies
upper extremities and head
 Ductus venosus
 Fetal blood vessel connecting UV to IVC
 Umbilical vessels
o WITH THE FIRST BREATH…
 Lungs expand causing dramatic fall in pulmonary vascular resistance
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 Market increase in pulmonary blood flow (raising LA pressure above
that of IVC)
 A progressive thinning of the walls of pulmonary arteries occurs
 Blood pressure is now high in the aorta & the baby’s systemic
circulation is well established
 The ductus arteriosus contstricts at birth, but there is often a small
shunt of blood from the aorta to the Left Pulmonary Artery for a few
days
 This decreases with increases PO2 which stimulates
bradykinin release
 Umbilical arteries constrict functionally, later become fibrous
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o History indicators of cardiac dysfunction
 Symptoms may appear 4-12 weeks after birth
 Failure to thrive, poor weight gain, activity intolerance
 Developmental delays
 Positive prenatal history
 Positive family history of cardiac disease
o Physical indicators of cardiac dysfunction:
 Poor feeding
 Tachypnea, tachydardia
 Diaphoresis
 Crackles
 Hepatomegaly
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 Cyanosis
 Murmur Sternal lift
 Impaired myocardial function
 Tachycardia
 Fatigue
 Weakness
 Restlessness
 Pale
 Cool extremities
 Decreased BP
 Decreased output
 Pulmonary congestion
 Tachypnea
 Dyspnea
 Respiratory distress
 Exercise intolerance
 Cyanosis
 Systemic venous congestion
 Peripheral & periorbital edema
 Weight gain
 Hepatomegaly
 Neck vein distention
 Goals of management
o Support maximal growth & nutrition
o Reduce cardiac workload
o Prevent & treat congestive heart failure
o Maintain optimal cardiac output
o Provide palliative procedures to protect lungs from too much bloow flow, or
too little blood flow
o Correct the underlying defect
o Maintain fluid & electrolyte balance
o Prevent secondary complications (failure to thrive, cardiogenic shock,
infection, respiratory compromise, cardiac dysrthythmia, thromboembolism)
 Diagnostic tests:
o H&P
o Chest x-ray
o Echocardiogram, EKG
o Labs:
 ABG’s
 CNC
 Electrolyte panel
 Therapeutic & diagnostic cardiac catheterization
 Therapeutic nursing management
o Avoid situations that increase cardiac demands (fever, pain, agitation)
o Avoid unnecessarily disturbing the infant
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o Monitor weights
o Small frequent feedings (increased calorie formula as needed)
o O2 as needed
o Administer pharmacologic agents as ordered; evaluate patient response to
treatment
o Portect from infection
o Accurate I&O
 Pharmacology:
o Depends on defect & MOST IMPORTANTLY patient’s clinical condition
 Digoxin
 Diuretics
 Prostaglandin
 Keep PDA open
 Indomethacin
 Close PDA
 Vasopressors
 Vasodilators
 Vaccinations as indicated
 Complications:
o Heart failure
o Postpericardiotomy syndrome
 Post-op period: fever, pericardial friction rub, pleural effusion
o Cerebral thrombosis
o Failure to thrive
o Death
 Older Classifications of CHD
o Acyanotic
 May become cyanotic
o Cyanotic
 May be pink
 May develop congestive heart failure
 Newer classification of CHD
o Hemodynamic characteristics (blood flow patterns within the heart):
1. Increased pulmonary blood flow
2. Decreased pulmonary blood flow
3. Obstruction of blood flow out of the heart
4. Mixed blood flow

Increased Pulmonary Blood Flow Defects
 Abnormal connection between the 2 side of the heart
o Either the septum or great vessels
 Increase blood volume on RIGHT side of heart
 Increased pulmonary blood flow
 Decreased systemic blood flow
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 Defects:
o Atrial Septal Defect (ASD)
 Acyanotic
 Hole between two atria
 Allowing blood from
higher pressure left
atrium to follow into the
lower pressure right
atrium
 Closes naturally, with
therapeutic catheterization of
surgery
 Loud, harsh murmur
 With fixed split second heart sound
 Enlarged right side of heart
 Increased oxygen saturiation in right atrium
 Mild congestive heart failure
 May be asymptomatc
 Surgical patch closure
o Ventricular Septal Defect (VSD)
 Acyanotic
 Hole between right & left ventricles
 Most common cardiac defect
 Closes naturally or with surgical
correction
 Loud, harsh murmur that begins at
about 4-8 weeks of age
 O2 saturation is higher that normal in
right ventricle
 Congestive heart failure
 Failure to thrive
 Dysrthymias
 Small defects may be asymptomatic
o Atrioventricular canal defect
 Combo of ASD & VSD
 Acyanotic
 Incomplete fusion of endocardium creating
a large central AV valve that allows blood
to flow between all four chambers of the
heart
 Most common cardiac defect in children
with Down syndrome
 Flow is determined by pulmonary and
systemic resistance
 Surgical repair required
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 CHF
 Loud systolic murmur
 Cyanosis increases with crying
 Pulmonary vascular obstructive disease
 Increased blood volume is pumped into the lungs, which may
eventually result in increased pulmonary vascular resistance
o Patent Ductus Arteriosus (PDA)
 Acyanotic
 Fetal vessel between the pulmonary
artery and the aorta that fails to
close
 PDA is common in premature
infants
 Closure occurs naturally, with
Indomethacin, therapeutic
catherization, or surgery
 Machinery-like murmur
 Patients at risk for BE and
pulmonary vascular obstructive
disease later in life from chronic excessive pulmonary blood flow
 Tachycardia
 Enlargement of left ventricle
 Wide pulse pressure
 Bounding pulses
 Tachypnea

OBSTRUCTIVE DEFECTS
 Blood exiting the heart meats an area of anatomic narrowing (stenosis) causing
obstruction to blood flow
 The pressure in ventricle and in great artery before obstruction is increased, and the
pressure in the area beyond the obstruction is decreased
 Location of narrowing is usually near the valve:
o Vavlular- at site of valve
o Subvalvular- narrowing in the ventricle below the valve (ventricular outflow
tract)
o Suprvalvular- narrowing in great artery above valve
 There is a pressure load on the ventricle and decreased cardiac output
 Clinically exhibit signs of HF
 Defects:
o Coarctation of the Aorta
 Acyanotic
 Narrowing of the aorta due to a
constricting band
 Increased blood pressure and
oxygen saturation in the upper
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extremities as compared with the lower extremities
 Headaches
 Vertigo
 Nosebleeds
 Absence of femoral pulses
 High blood pressure
 Leg pain
 Decreased cardiac output
 CHF
 Surgical repair & reconstruction
is usually needed
 Cool lower extremities
o Aortic Stenosis
 Acyanotic
 Narrowing of aortic valve
 Causing resistance to
blood flow in left
ventricle, decreased
cardiac output, left
ventricular hypertrophy,
& pulmonary vascular congestion
 Left ventricular enlargement
 Systolic ejection murmur
 Faint pulses, hypotension, tachycardia, poor feeding
 Exercise intolerance, chest pain, and dizziness
 Decreased cardiac output
 Opened with balloon procedure or surgery
 Risk for:
o BE, coronary insufficiency, & ventricular dysfunction
o Pulmonic Stenosis
 Acyanotic
 Narrowing of the pulmonary valve or pulmonary artery
 Resistance to blood flow causes right ventricular hypertrophy &
decreased pulmonary blood flow
 Right ventricular enlargement
 Systolic ejection murmur
 Exercise intolerance
 CHF, cyanosis
 Opened with balloon procedure or surgery

DECREASED PULMONARY BLOOD FLOW DEFECTS
 Tetralogy of Fallot
o Cyanotic
o Four anamolies are present:
 Pulmonary stenosis
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 VSD
 Dextroposition of aorta
 Enlargement of the right ventricle
o Palliative shunt may be placed until child is
able to have the surgical corrective repair
o Systolic murmur
o Cyanosis
o Polycthemia
o Clot formation
o Severe dyspnea
o Squatting position
o Hypercyanotic spells (“Tet Spells”)
o Acidosis
o Clubbing of the fingers
o Growth retardation
o Failure to thrive
 Tricuspid Atresia
o Cyanotic
o Tricuspid valve is completely closed
o Generally requires several complex
surgeries
o Incompatible with life if there is
inadequate pulmonary blood flow
o PGE infusion is used until an emergency
shunt procedure can be performed
o The Fontan procedure is the surgical
repair
o No blood flow from right atrium to right
ventricle
o Severe cyanosis within hours after birth (Increased as the PDA closes)
o CHF
o Failure to thrive

MIXED DEFECTS
 Transposition of the great arteries or transposition of the great vessels
o Cyanotic
o Aorta arises from the right ventricle instead of the left, and the pulmonary
artery arises from the left instead of the right
o Incompatible with life if there is no
connection between right and left sides
o Emergency septostomy is performed to
create a connection between the right and
left sides
o The surgical repair is the atrial switch
procedure
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o Severe cyanosis hours to days after birth (as PDA closes)
o Various murmurs
o Presence of ASD and VSD
o CHF
 Total anomalous pulmonary venous connection
o Cyanotic
o Total anomalous pulmonary venous
return
o Rare defect characterized by failure
of pulmonary veins to join the left
atrium; instead are connected with
the venous system
o Repaired surgically
o Cyanosis (inversely related to
amount to pulmonary blood flow)
o May initially be asymptomatic
o CHF, cardiac failure, death
 Truncus Arteriousus
o Cyanotic
o Failure of normal separation in development of the pulmonary artery and
aorta, resulting in a single vessel that
overrides both ventricles; mixing
pulmonary & systemic circulations
o Repaired in first few months of life
(closing VSD and hemographs-
modified Rastelli procedure)
o CHF
o Cyanosis
o Poor growth
o Activity intolerance
o Murmur
o Brain abscess
o Bacterial endocarditis
 Hypoplastic heart syndrome
o Left sided
 Cyanotic
 Left ventricle is NONFUNCTIONAL
 Requires several complex surgeries
or cardiac transplantation for
survival
 Right ventricular enlargement
 Severe cyanosis
 Severe decreases in cardiac output


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CHF IN CHILDREN
 Impaired myocardial function
o Tachycardia
o Fatigue
o Weakness
o Restlessness
o Pale
o Cool extremities
o Decreased blood pressure
o Decreased urinary output
 Pulmonary congestions
o Tachypnea
o Dyspnea
o Respiratory distress
o Exercise intolerance
o Cyanosis
 Systemic venous congestions
o Peripheral & periorbital edema
o Weight gain
o Ascites
o Hepatomegaly
o Neck vein distention


ENDOCARDITIS
 Bacterial endocarditis (BE) and subacute endocarditis (SBE) are now referred to as
infective endocarditis (IE)
 Often a sequela of bacteremia in children with CHD or AHD
 Most common causative agents:
o Streptococcus viridans or Staphylococcus aureus
o Fungal agents such as Candida albicans
 Prophylaxis for 1 hour before procedures (IV) or may use PO in some cases
o Antibiotics
 Clinical manifestations:
o Onset usually insidious
o Unexplained fever
o Anorexia
o Malaise
o Weight loss
o Characteristic findings caused by extracardiac emboli formation
 Splinter hemorrhage (think black lines) under the nails
 Osler nodes
 Janeway lesions
 Petechiae on oral mucous membranes
o May be present:
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 Heart failure
 Cardiac dysrthmias
 New murmur

RHEMATIC FEVER (RF) & RHEMATIC HEART DISEASE (RHD)
 Rheumatic Fever
o Inflammatory disease occurring after group A B-hemolytic stremptococcal
pharyngitis (GABHS)
o Infrequently seen in US
o Self-limiting
 Affects joints, skin, brain, serous surfaces, & heart
 Rheumatic heart disease
o Most common complication of RF
o Damage to valves as a result of RF
 Clinical manifestations:
o Jones criteria (Presence of 2 major manifestations or one major
manifestation & two minor manifestations)
 Carditis
 Polyarthritis
 Erythema Marginatum
 Subcutaneous Nodes
 Chorea (St. Vitus Dance, Sydenham Chorea)
 Treatment
o Prevention of GABHS
o Tx of streptococcal tonsillitis and pharyngitis
 Penicillin G IM once
 Penicillin V by mouth for 10 days
 Sulfa by mouth for 10 days
 Erythromycin (if patient is allergic to the above agent) by mouth for
10 days
o Tx of recurrent RF
 Same as above


KAWASAKI DISEASE (KD); Mucocutaneous lymph node syndrome
 An acute systemic vasculitis of unkown cause
 75% of cases, the child is younger than 5 years of age
 3 phases:
o Acute phase
 Sudden high fever, unresponsive to antipyretics & antibiotics
o Subacute phase
 Lasts from end of fever thru end of all KD clinical signs
o Convalescent phase:
 Clinical signs have resolved, but laboratory values have not returned
to normal
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 Ends when normal values have returned (6-8 weeks)
 Diagnostic criteria for Kawasaki disease
o Changes in extremities
 In acute phase: edema, erythema of palms and soles
 Subacute: periungual desquamation (peeling) of hands & fet
o Bilateral conjuctival injection (inflammation) without exudation
o Changes in the oral mucous membranes
o Polymorphous rash
o Cervical lymphadenopathy
 Treatment of KD
o Acetylsalicyclic acid (ASA) 80-11 mg/kg/day for fever
o IV immunoglobulin (IVIG)
o Then 3-5 mg/kg/day antiplatelet

Hyperlipidemia
 Identify kids at risk & treat early
 Tx is lifestyle modifcation
o Restrict intake of cholesterol & fats
o Increase intake of whole grains, fruits, & veggies
o Exercies for 60 min a day 5 days a week
o Stop smoking and avoid second-hand smoke
 If there is no response to diet changes & meds:
o Colestipol (Colestid)
o Cholestyramine (Questran)


Systemic Hypertension
 Essential hypertension has no known cause
 Secondary has an identifiable cause
 Pediatric hypertension is generally secondary to structural abnormality or an
underlying pathologic condition
o Renal disease
o Cardiovascular disease
o Endocrine or neurologic disorders
 Pharmacologic treatment:
o B-blockers
o Calcium channel blockers
o Angiotensin-converting enzyme (ACE) inhibitors
o Angiotensin receptor blockers
o Diuretics


MS

Immobilized patient
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 Atrophy
 Joint contracture
 Major musculoskeletal consequences of immobilization are:
o Significant decrease in muscle size, strength, and endurance
o Bone demineralization leading to osteoporosis
o Contractures and decreased joint mobility
 DVT


Developmental Dysplasia of the Hip (DDH)x
 Wide range of abnormal development of the hip leading to hip instability
 1 per 100 live births
 80% are female
 Lift hip affected most commonly
 Caucasion children most often affected
 Degrees of DDH
o Acetabular dysplasia
 Acetabular rool shallow; mildest form
o Subluxation
 Head of femur is partially displaced
 Flattened socket; most common form
o Dislocation
 Femoral head not in contact with acetabulum
 Clinical manifestations of DDH
o Infant:
 Shortened limb on affected side
 Restricted abduction of hip on affected side
 Unequal gluteal folds when infant prone
 Positive Ortolani test
 Positive Barlow test
o In older infant & child
 Affected leg shorter than other
 Telescoping or piston mobility of joint
 Trandelenburg sign
 Trandelenburg gait
 Greater tochanter is prominent and appears above line from
anterosuperior iliac spine to tuberosity of ischium
 Marked lordosis if bilateral dislocations
 Waddling gait if bilateral disclocations
 Sign of gluteus medius weakness or relative inhibition
 Sign is elicited by asking patient to stand on involved leg
 If sign is positive, the pelvis will drop on uninvolved side
 Ortolani & Barlow tests
o Barlow test shows that hip has potential to dislocate
o Ortolani test confirms its dislocation
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o
o Never do at the same time; do one knee then the other
 Diagnosis
o Newborn assessment tools most reliable in early infancy
o X-ray not reliable in infancy due to incomplete ossification of femoral head
o Ultrasound as adjunct to abnormal physical findings
 Therapeutic management of DDH
o Importance of early intervention
o Newborn to age 6 months:
 Palvik harness for abduction of hip
o Age 6-18 months:
 Dislocation unrecognized until child begins to stand and walk; use
traction and cast immobilization (spica)
o Older child:
 Operative reduction
 Tenotomy (muscle contracture)
 Osteotomy (rebuild acetabular roof)
 Difficult after 4 years
 Management: 0-6 months
o Splinting: Palvik harness
 Worn continuously x 3-5 months until hip stable
 Straps checked q 1-2 weeks for adjustment
o 95% effective if hips reducible at birth
o prevent adduction
o Nursing care of child in palvik harness
 Newborn hip assessment
 Management of reduction device
 Teaching application/use of harness
o Removal, adjustment discouraged
 Prevent skin breakdown
o Clothing, diaper under straps
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o Check for reddening under straps often
 Management: 6-18 months
o Gradual reduction by traction x 3 weeks
o Closed/open reduction under anesthesia
o Hip spica cast x 3 months
 Management: Older child
o Operative reduction
o Construction of acetabular roof
o Post-operative casting
o Successful reduction difficult after 4 years

TALIPES: Congenital Clubfoot
 Includes multiple foot, ankle deformity and malposition, and soft tissue
contractures
 Incidence: 1-2: 1000 live births
 Male: female= 2:1
 50% are bilateral
 increase risk of hip dysplasia
 Etiology
o Not well identified
o Strong family disposition
 Q:10 if parent affected
o Possible arrested fetal development of skeletal & soft tissue (9-10 weeks
gestation)
o Associated with other syndrome (myelomeningocele)
o Idiopathic clubfoot most common form
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o
o Talipes varus: inversion, or bending inward
o Talipes valgus: eversion, or bending out
o Talipes equinus: plantar flexion with toes lower than the heel
o Talipes calcaneus: dorsiflexion with toes higher than the heel
o Talipes equinovarus: when the foot turns inward and downward; most
common form
 Classification of clubfoot
o Mild or postural
 May correct spontaneously or require passive exercise or serial
casting
o Tetralogic
 Associated with other congenital anomalies
 Usually requires surgical correction with high incidence or
recurrence
o Idiopathic
 Bony abnormality almost always requiring surgical intervention
 Treatment
o Started as a neonate
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o Serial casting of affected leg(s)
o Recasting frequent until maximum correction achieved (~8-12 weeks)
o X-Ray to evaluate efficacy of casting
o If casting unsuccessful, surgery @6-12 months & casting/brace after surgery


Metatasus Adductus
 Most common
 Treatment usually not needed
 Due to abnormal intrauterine positioning
 Associated with pigeon toed gait
 Different from Talipes deformities because foot has full ROM

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 Kyphosis
o Abnormally increased convex angulation of the curvature of the thoracic
spine
o Most common form is postural
o Can result from tuberculosis, arthritis, osteodystrophy, or compression
fracture
o PT w/ strengthening excercises
o Not associated with pain
 Lordosis
o Accentuation of the cervical or lumbar curvature beyond physiologic limits
o May be idiopathic or secondary complication or trauma
o May occur with flexion contractures of hip, congenital dislocated hip
o In obese children, abdominal fat alters center of gravity, causing lordosis
o Treat cause ie excess weight and manage pain; associated with pain
 Scoliosis
o Most common spinal deformity
o Complex spinal deformity in 3 planes:
 Lateral curvature
 Spinal rotation causing rib asymmetry
 Thoracic kyphosis
o Congenital or develop during childhood
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 Congenital associated w/ myelomeingocele
o Idiopathic scoliosis during growth spurt of early adolescence most common
form
o Early manifestations of Idiopathic scoliosis
 Seldom apparent before preadolescent growth spurt
 May be picked up in school screening
 Uneven pants length
 Rarely painful
 Right curvature is usually scoliosis
 Left curvature often associated with disorders and have a neurologic
component
o Diagnosis
 Physical exam
 Asymmetry of shoulder, hip height; flank, scapular shape when
standing
 Asymmetry of ribs & flanks with bend at waist
 Stand & twist to evaluate flexibility of curve
 X-Ray of spine to measure curve magnitude
 MRI if indications of other spinal abnormalities
 Spinal curvature and treatment
o 10 degree normal postural variation
o 10-20 – mild, no treatment if no progression
o 20-40- bracing
o >40 surgery
 Bracing/exercise
o Bracing can slow or stop progression of curvature
o TLSO (thoracolumbarsacral orthosis)
 Wear 16-23 hours per day; adjusted periodically
 Milwaukee brace; Boston brace (less visible)
o Daily exercises to prevent atrophy of spinal and abdominal muscle
 Operative management
o Curves >40, difficult sitting, breathing, pain require surgery
o Realignment and internal fixation with bony fusion or realigned spine
o Harrington rod system
 Immobilized postoperatively
 Post-Op Nursing care
o Pain management
 Considerable pain 2-3 days post-op
o Neurologic dysfunction
 Post-op paralysis a risk
o GI dysfunction
 Paralytic ileus
o GU dysfunction
 Urine retention & hypoperfusion possible
o Respiratory dysfunction
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 Anesthesia & immobility atelectasis
o Immobility consequences
 High potential for skin breakdown
 Potential for phlebitis
 Discharge education
o Recommended physical activity
o Pn meds & side effects
o Psychological adjustment to brace, altered body image
o Assess family, peer support
o Schooling
o National Scoliosis Foundation

Fractures
 Bone structure in a child
o Ossification incomplete until 18-21 years
o Epiphyseal plate
 Growth plate
o Periosteum
 Vascular membrane
 Critical for growth and healing of bone
 Bone healing in children
o Generally faster in children due to thick vascular periosteum
o Healing of bone
 Neonate: 2-3 weeks
 Early childhood: 4 weeks
 Later childhood: 5-8 weeks
 Adolescence: 8-12 weeks
 Adult: 10-16 weeks
o Remodeling
 Fractures in infant & small child:
o Infancy:
 Birth trauma
 MVA
 Child abuse (twisting, rough handling, pulling)
 Periosteal bleeding not visible on x-ray for weeks after injury
o Small child:
 Multiple fractures at varied stages of healing warrants investigation
for abuse
 Causes:
o Breaking a fall- clavicle, forearm
o Auto vs peds- femoral neck or femur
 Most commonly seen in 4-7 years old
 Triad of auto vs peds injuries:
 Femur fracture
 Trunk trauma
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 Head injury


 Epiphyseal fractures
o Epiphyseal plate weakest point of long bones
o Normally heals quick and completely
o Risk of damage to growth plate
o Can be mistaken for dislocation
o Early identification critical to minimize growth problems & angular
deformities
 Clinical course of fracture
o Muscles contract to “splint” broken bone
o Contusion or severe hemorrhage of surrounding soft tissue may occur
o Stable bone due to intact periosteum
o Neurovascular damage less common than in adults
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o
o 5 P’s of ischemia from vascular injury:
 Pain
 Pallor
 Pulselessness
 Paresthesia
 Paralysis
o Slight rise in WBC due to inflammation & hgb decreases
 Management
o Usually closed reduction & casting
o Femur, humerus fractures may require hospitalization and traction
o Internal fixation more quickly stabilizes injury (ORIF)
o Casting
 Bone will grown in the direction in which stress is placed on it- Wolff’s
law
 Critical to check for skin injury prior to application of cast
 Check for neurovascular compromise
 TRACTION
o Primary goals of traction
 To fatigue involved muscle and reduce muscle spasm
 To realign distal and proximal bone ends to promote satisfactory bone
healing
 To immobilize fracture until realignment has occurred and boen has
healed well enough to cast or splint
o Complications of fractures
 Circulatory impairment
 Nerve compression
 Compartment syndrome
 Epiphyseal damage
 Non union or malunion of bone
 Osteomyelitis
 Pulmonary emboli


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Sprains & Strains
 Sprain:
o Ligament stretched or torn by force created as joint twisted
 Vessel, tendon, nerve damage common
 Joint laxity best indicator of severity of sprain
 Strain:
o Microscopic tear of tendon
 Painful & swollen
 Usually do not occur immediately but over time
 Management of soft tissue injuries
o RICE
 Rest
 Ice (some controversy about icing)
 Compression
 Elevation
 First 6-12 hours critical for treatment

Shin Splints
 Extensive running pressure on tibia
 Ligaments tear away from shaft of tibia
 Painful but rarely serious


Nursemaid’s elbow
 Most common dislocation in young children
 Usually <5
 Sudden jerk and pull of arm
 Tx: pop back into place just like a shoulder

Osgood-Schlatter disease
 Painful inflammatory disorder of proximal tibia at point of insertion of patellar
tendon
 Repeated stress and overuse of quadriceps causes irregularities of growth
 Presentation:
o Knee pain, inflammation at tibial tubercle
o Prominent tibial tubercle
o Pn exacerbated by activity, improved with rest
o Hip examination necessary to rule out hip abnormalities
o Knee x-ray findings variable
 Treatment:
o Self-limiting
o When growth of proximal tibia ceases, pain disappears
o Rest, avoiding activity that contract quadriceps


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Osteogenesis Imperfecta (OI)
 Group of heterogenous inherited disorders of connective tissue
 Characterized by excessive fragility and bone defects
 Defective periosteal bone formation and reduced cortical thickness of bones
 Hyperextensibility of ligaments
 Therapeutic management
o Primarily supportive care
o Drugs of limited benefit
o May rule out OI if multiple fractures occur
o Nursing care management:
 Caution with handling to prevent fractures
 Fam education
 Occupational panning and genetic counseling

Legg-Calve-Perthes disease
 Self-limiting, idiopathic, occurs in juveniles ages 3-12 , more cmmon in males 4-8 yo
 Avascular necrosis of femoral head
 10-15% of cases have bilateral hip involvement
 Most have delayed bone age
 Pathophysiology:
o Cause is unkown but involved disturbed circulation to the femoral head with
ischemic aseptic necrosis
 Treatment goal:
o Keep head of femur in acetabulum
o Containment with various appliances/devices
o Rest, no weight bearing initially
o Surgery in some cases
o Home traction in some cases
 Prognosis
o Self-limiting
o Outcome has wide variations due to multiple factors
 Nursing care management:
o Identification of affected children & referral teaching care and management
o Compliance issues with child and family

OSTEOMYELITIS
 Inflammation and infection of bony tissue
 May be caused by exogenous or hematogenous sources
 Signs and symptoms begin abruptly, resemble symptoms of arthritis and leukemia
 Marked leukocytosis
 Bone cultures obtained from biopsy or aspirate
 Early x-rays may appear normal
 Bone scans for diagnosis
 Exogenous Osteomyelitis
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o Infectious agent invades bone following penetrating wound, open fracture,
contamination in surgery, or secondary from extension from abscess or burn
 Hematogenous osteomyelitis
o Preexisting infection
o Source may be furuncles, skin infections, upper respiratory tract infection,
abscessed teeth, pyelonephritis
o Any organism can cause osteomyelitis
o Infective emboli travel to artiers in bone metaphysis, causing abscess
formation and bone destruction
 Therapeutic management of osteomyeleitis
o May have subacute presentation with walled off abscess rather than
spreading infection
o Prompt, vigorous IV antibiotics for extended period (3-4 weeks or up to
several months)
o Monitor hematologic, renal, hepatic responses to treatment
 Nursing care:
o COMPLETE bed rest & immobility of limb
o Pn management concerns
o Long-term IV access (for antibiotic administration)
o Nutritional considerations
o Long-term hospitilzation, therapy
o Psychosocial needs
Juvenile Idiopathic Arthritis (JIA)
 AKA juvenile rheumatoid arthritis, juvenile chronic arthritis, or idiopathic arthritis
of childhood
 Possible causes
 Peak ages: 1-3 years and 8-10 years
 Often undiagnosed
 Actually a heterogenous group of diseases:
o Pauciarticular onset – involves 4 or more joints
o Polyarticular onset- involves 5 or more joints
o Systemic onset- high fever, rash, hepatosplenomegaly, pericarditis, pleuritis,
lymphadenopathy)
 Symptoms may “burn out” and become inactive
 Chronic inflammation of synovium with joing effusion, destruction of cartilage, and
ankylosis of joints as disease progresses
 Symptoms:
o Stiffness
o Swelling
o Loss of mobility in affected joints
o Warm to touch, usually without erythema
o Tender to touch in some cases
o Symptoms increase with stressors
o Growth retardation
 Diagnostic evaluation of JIA
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o No definitive diagnostic tests
o Elevated sedimentation rate in some cases
o Antinuclear antibodies common, but not specific for JIA
o Leukocytosis during exacerbations
o Diagnosis based on criteria of American College of Rheumatology
 Their diagnostic criteria:
 Age of onset <16 years
 1 or more affected joints
 Duration of arthritis >6 weeks
 Exclusion of other forms of arthritis
 Therapeutic management:
o No cure
o Goals of therapy:
 Preserve function
 Prevent deformities
 Relieve symptoms
o Iridocyclitis, uveitis:
 Inflammation of iris & ciliary body
 Unique to JIA
 Requires opthalmologist
 MEDS
o NSAIDs
o SSARDs
o Corticosteroids
o Cytotoxic agents
o Immunologic modulators
 Management of JIA
o Therapy individualized to child
o Physical & occupational therapy
o Nutrition, exercise
o Splinting devices
o Pn management
o Prognosis
Systemic Lupus Erythematosus (SLE)
 A chronic, multisystem, autoimmune disease of the CT and blood vessels characterized
by inflammation on potentially any body issue
 Course and symptoms: unpredictable, mild to life threatening complications
o Clinical manifestations of systemic lupus erythematosus related to tissues
involved:
 Constitutional- fever, fatigue, weight loss, anorexia
 Cutaneous- erythematous butterfly rash over bridge of nose and
across cheeks, discoid rash, photosensitivity, mucocutaneous
ulceration, alopecia, periungual telangiectasias
 Musculoskeletal- arthritis, arthralgia, myositis, myalgia, tenosynovitis
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 Neurologic- headache, seizure, forgetfulness, behavior change, change
in school performance, psychosis, chorea, stroke, cranial and
peripheral neuropathy, pseudotumor cerebri
 Pulmonary and cardiac- pleuritis, basilar pneumonitis, atelactasis,
pericarditis, myocarditis, endocarditis
 Renal- Glomerulonephritis, nephritic syndrome, hypertension
 GI- abdominal pain, NV, blood in stool, abdominal crisis, esophageal
dysfuntion, colitis
 Hepatic, splenic, and nodal- hepatomegaly, splenomegaly,
lymphadenopathy
 Hematologic- anemia, cytopenia
 Ophthalmologic- cotton wool spots, papilledema, retinopathy
 Vascular- Raynaud phenomenon, thrombophleitis, livedo reticularis
o Diagnostic Criteria for SLE:
1. Malar rash- fixed malar erythema
2. Discoid rash- patchy erythematous lesions
3. Photosensitivity- pain with sun exposure
4. Oronasal ulcers- painless ulcers in mouth or nose
5. Arthritis- swelling, tenderness, or effusion in two or more peripheral
joints (nonerosive)
6. Serositis- pleuritis, pericarditis
7. Renal disorder- proteinuria, casts
8. Neuro disorder- psychosis, seizures
9. Hematologic disorder- hemolytic anemia, thrombocytopenia,
leucopenia, lymphopenia
10. Immunologic disorder- anti double stranded DNA, anti Sm,
antiphospholipid antibodiesl lupus anticoagulant; false positive
syphilis test (rapid plasma reagin [RPR])
11. Antinuclear antibodies
 Neonatal lupus: another form of lupus, which occurs when maternal auto antibodies
 cross the placenta and cause transient lupus like symptoms in a newborn, with
potential complications of heart block
 Therapeutic management
o Ensure child’s health by balancing meds necessary to avoid exacerbation and
complications while preventing or minimizing treatment associated
morbidity.
o MEDS
 Corticosteroids-to control inflammation administered in doses
sufficient to control and then taper to lowest suppressive dose
 Antimalarial (rash and arthritis)
 NSAIDS (relieve muscle and joint inflammation)
 Immunosuppressive agents
 such as cyclophosphamide- renal and CNS disease
 mycophenolate, azathioprine, and methotrexate-effective, may
be used to control SLE and allow steroids to be reduced
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 Antihypertensives, aspirin, antibiotics, may be needed to treat or
avoid complications
 General supportive care: sufficient nutrition, sleep and rest, exercise.
o Limit exposure to sun and ultraviolet B (UVB) light is limited bc of
association with SLE exacerbation
 Sunscreens, wearing sun resistant clothes, and altering outdoor
activities; must be provided with great sensitivity to ensure
compliance while minimizing the associated feeling of being different
from peers
 Nursing Care Management
o Principal nursing goal: help child and fam positively adjust to disease and
therapy
o Learn S/S of exacerbation
o Key issues:
 Therapy compliance, body-image problems associated with rash, hair
loss, and steroid therapy; school attendance; vocational activities,
social relationships; sexual activity; and pregnancy.
 Maintain reg med supervision, seek attention quickly when ill, or
before elective surgical procedures, such as dental extraction, bc of
potential needs for increasd steroids or prophylactic antibiotics
o Carry ID for disease and steroid dependence