- Peds Exam 2 Blueprint CARDIAC
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Cardiac catheterization care
○ Uses
■ Transposition of great vessels
■ Some complex single ventricle defects
■ Atrial septal defect
■ Pulmonary artery stenosis
○ Process
■ Radiopaque catheter is peripherally inserted and threaded into the heart
under fluoroscopy
■ Contrast medium injected and images of blood vessels/heart taken
● Kids w/ shellfish or iodine allergy may react to dye
■ Routine, outpatient, risky
■ Diagnostic, interventional, and electrophysiological
■ May give digoxin before procedure to prevent arrhythmia
○ Complications
■ Nausea, vomiting, low grade fever, loss of pulse at catheter extremity,
transient dysrhythmias, acute hemorrhage at site
○ Procedure care
■ Preprocedural care
● Prepare the child and family for procedure
● Use developmentally appropriate materials to explain procedure to
the child
● Assess and mark pulses
● Baseline O2 saturation
● NPO prior to procedure
■ Postprocedural care
● Check the pulse distal to the site
● Monitor the temp and color of extremities
● Take vitals q15 min
● Monitor BP
● Monitor dressing for bleeding or hematoma
● Monitor intake and output
● Monitor blood glucose levels
■ After discharge
● Change dressing day after. Keep dry, and avoid bath for 3 days
● Inspect redness, irritation, swelling, drainage, bleeding
● Resume normal diet
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Check temp for 3 days: report over 100.4
Low activity for 3 days
Tylenol or Motrin for pain
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Kawasaki disease
○ An acute systemic vasculitis of unknown cause
○ In 75% of cases, the child is younger than 5 years of age
○ Causes inflammation in the coronary artery wall
● Three phases
○ Acute phase - sudden high fever, unresponsive to antipyretics and
antibiotics
○ Subacute phase - lasts from the end of fever through the end of all
Kawasaki disease clinical signs
○ Convalescent phase - clinical signs have resolved, but lab values have not
returned to normal
■ Ends when normal values have returned (6-8 weeks)
● Clinical manifestations
○ Bloodshot eyes, rash, strawberry tongue, red/cracked lips, swollen lymph
node in the neck, red palms/soles/swollen hands/feet
■ Two or more of these sx + fever = sign of KD
● Diagnosis
○ Fever for more than 5 days + 4/5 criteria
■ Changes in extremities - edema, peeling
■ Bilateral conjunctival injections w/o exudation
■ Changes in oral mucosa: cracked lips, strawberry tongue
■ Maculopapular rash
■ Cervical lymphadenopathy
● Therapeutic management
○ Acetylsalicylic acid (ASA) 80-100 mg/kg/day for fever
○ IV immunoglobulin (IVIG)
○ Then 3-5 mg/kg/day antiplatelet
○ Complications
■ Coronary artery aneurysms
■ Large aneurysm - MI
● Nursing management
○ Monitor cardiac status, I&O, daily weight
○ Comfort and symptom relief
○ Discharge teaching/follow up
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Coarctation of aorta
○ Patho
Narrowing near the insertion of the ductus arteriosus -> increased pressure
proximal to the defect (head and upper extremities) and decreased
pressure distal to the defect (body and lower extremities)
■ Like a pinched aorta
Clinical manifestations
■ High BP, bounding pulses in arms
● Upper body gets extensive blood flow
● Lower body gets weak blood flow
● This is why we do 4 extremity BP
■ Weak or absent femoral pulses
■ Cool lower extremities with lower BP
■ HF in infants
■ Older children: dizziness, headaches, fainting, epistaxis
Treatment
■ Surgical: resection of the coarcted portion
■ Non-surgical: balloon angioplasty to stretch it
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Tetralogy of Fallot
○ Four defects: VSD, PS, overriding aorta (going above pulmonary artery instead
of below), right ventricular hypertrophy
■ Kids don't have right or left sided heart failure, they have a combination of
both
● Patho
○ Vary depending on degree of PS and size of VSD
○ Shunt direction depends on difference between pulmonary and systemic
vascular resistance
■ Pulmonary vascular resistance higher than systemic -> shunts from
right to left
■ Systemic resistance higher than pulmonary -> shunts from left to
right
■ PS decreases blood flow to lungs and amount of oxygenated blood
that returns to the left side of the heart
● Clinical manifestations
○ Cyanosis
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CHF
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■ May be mild at first, progresses as PS worsens
○ Moderate murmur
○ Acute spells of cyanosis and hypoxia - blue spells or tet spells
■ Usually occur during crying or feeding
■ w/ infants, usually give morphine to calm down
■ Place child in knee chest position to decrease venous blood return
and improve oxygenation
○ Boot shaped heart
Treatment
○ Surgical
■ With cardiac surgery, infants usually have purple undertones
○ Mortality < 2-3%
Causes of CHF
■ Volume overload
● Left to right shunts that causes the RV to hypertrophy
■ Pressure overload
● Resulting from obstructive lesions
■ Decreased contractility - cardiomyopathy
■ High CO demands
CHF in children
○ Inability of heart to pump effectively
○ Inability to pump adequate amount of blood to systemic circulation at
normal filling pressure
Patho
○ RS failure
■ RV unable to pump effectively into PA -> increased pressure in RA
and systemic venous circulation -> hepatosplenomegaly,
occasionally edema
○ LS failure
■ LV unable to pump blood into systemic circulation -> increased
pressure in LA and pulmonary veins -> lungs become congested w
blood -> elevated pulmonary pressures and pulmonary edema
○ Although each type produces different signs and symptoms, it's unusual to
observe solely right or left sided failure in children
○ Compensatory mechanisms are used
Clinical manifestations
○ Impaired myocardial function
■ Tachycardia
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■ Gallop rhythm
■ Easily fatigued
■ Exercise intolerance
■ Irritable
■ Poor perfusion and slow cap refill
■ Weak pulses
■ Low BP
■ Mottled skin and cold extremities
■ Extreme pallor and duskiness
■ Big head, skinny body
Pulmonary congestion
○ Tachypnea
○ Hypoxemia/mild cyanosis
○ Impaired gas exchange
○ Dyspnea
○ Inability to feed
○ Poor weight gain/FTT
○ Intercostal retractions
○ Wheezing
○ Dry hacking cough
○ Gasping/grunting
○ Increased metabolic rate
○ Increased Kcal needs
Systemic venous congestion
○ Right to left failure results in increased pressure and pooling of
blood in venous circulation
○ Hepatomegaly
○ Sodium and fluid retention
○ Weight gain
○ Distended neck veins
Therapeutic management
○ Improve myocardial function
■ Digoxin (digitalis glycosides)
■ Improve myocardial contractility
■ Increases force of contraction (positive inotropic)
■ Decreases HR (negative chronotropic)
■ Indirectly enhances diuresis by increasing renal perfusion
■ Rapid onset
■ Administration
■ Prior to each dose count, take apical HR
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■ Don't give if HR < 90 in infant
■ Don’t give if HR < 60 in adolescent
Avoid giving oral form w meals
■ Decreases absorption
Give water after to prevent tooth decay
Monitor serum levels
■ 0.8-2 mcg/L
Given Q12h
Low K increases effect of digoxin (do you encourage
potassium diet on digoxin?)
If missed dose: do not give extra or increase next
dose
If vomits: do not readminister
Signs of toxicity
■ N/V, diarrhea, lethargy, bradycardia
ACE inhibitors (captopril, enalapril)
○ Reduce the afterload on the heart by causing vasodilation
○ Makes it easier for heart to pump (decrease pulmonary/systemic
vascular resistance)
○ Inhibits normal function of renin angiotensin system
■ Blocks conversion of angiotensin I to II
■ Vasodilation occurs
■ Results in decreased pulmonary and systemic vascular
resistance, reduction in afterload and decreased RA and LA
pressures
■ Reduces secretion of aldosterone which reduces preload
by preventing volume expansion from fluid retention
■ Causes loss of sodium and water
○ Administration
■ Measure BP before and after administration
■ Notify MD if BP falls more than 15 mmHg
■ Monitor for signs of hyperkalemia
Beta blockers
Removed accumulated fluid and sodium
○ Diuretics (furosemide, chlorothiazide)
■ Potassium wasting diuretics remove excess fluid/sodium
■ Encourage a high potassium diet: bran cereal, potatoes,
tomatoes, bananas, melons, oranges
■ Monitor I&O
■ Adverse fx
Muscle weakness, irritability, drowsiness,
increased/decreased HR
■ Monitor daily weight
■ Mix oral elixir in juice to disguise bitter taste/intestinal
irritation
■ Watch if taking digoxin: low potassium increases the fx of
digoxin
● Fluid and sodium restriction
○ Diuretics
○ Possible fluid restriction (high calorie, low volume diet)
○ Lasix (not K+ sparing)
○ Potassium supplements may be needed
○ Fall in serum potassium enhances effects of digoxin (3.5-5.5 WNL)
● Decrease cardiac demands
○ Neutral thermal environment
○ Treat any existing infections
○ Semi fowler's
○ Calm the irritable child
○ Reduce breathing effort
○ Rest
○ Decreased environmental stimuli
○ Provide adequate nutrition
● Improve tissue oxygenation
○ Causes vasodilation
○ Supplemental cool humidified O2
■ Oxyhood, nasal cannula, facemask, tent
○ Suction as needed
Nursing management
○ Assess
■ Monitor temp closely
■ Respiratory distress
○ Administer meds
○ Rest/decrease stress
■ Cluster care to avoid sleep disturbance
■ Feed as soon as child is hungry
■ Minimize anxiety
○ Maintain nutritional status
○ Parental support
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PDA - patent ductus arteriosus
○ Failure of fetal ductus arteriosus to close
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■ Ideally closes in the first 24 hours of life. Takes longer in preterm infants
Patho
■ Depends on size of ductus and pulmonary vascular resistance
■ As systemic pressure exceeds pulmonary pressure, blood shunts from
aorta, across the duct to the pulmonary artery -> left to right shunt
■ Additional blood recirculated through lungs and returned to the LA and LV
-> increased workload on left side of heart, increased pulmonary vascular
congestion and resistance, and could lead to right ventricular pressure and
hypertrophy
Clinical manifestations
○ Asymptomatic or signs of HF
○ Machinery like murmur
○ Bounding pulses
■ d/t increased flow
Treatment
Nutrition of a pt w/ cardiovascular disease
HEMATOLOGY
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HIV
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Epidemiology
■ most common acquired from mother in utero
Patho
○ Primary infects a subset of T lymphocytes (CD4)
○ Virus takes over the CD4 cells and replicates, rendering CD4 dysfunction
-> CD4 cell count decreases to critical level -> risk of opportunistic illnesses
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Clinical manifestations
○ HIV
■ Lymphadenopathy
■ Hepatosplenomegaly
■ Oral candidiasis
■ FTT
■ Chronic/recurrent diarrhea
○ AIDS
■ PCP pneumonia
■ Recurrent bacterial infections
■ Wasting syndrome
■ CMV (cytomegalovirus)
■ Herpes simplex
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Diagnostic tests
○ In children > 18 mo, ELISA and Western blot immunoassay
○ Infants will be positive d/t maternal antibodies
■ HIV polymerase chain reaction (PCR) to detect proviral DNA
○ With the identification of HIV antigen, individuals may be diagnosed with
HIV infection prior to sx development
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Therapeutic management
○ Antiretroviral drugs to slow virus growth
○ Prevention/tx of opportunistic infections
○ Education - prevention of spread
Nursing management
○ Education - transmission/control
○ Prevention
○ Pain management
○ Emotional support
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Prognosis
○ Early recognition and treatment have changed HIV from a fatal to a chronic
illness
Hemophilia
○ A group of hereditary bleeding disorders that result from deficiencies of specific
clotting factors
○ Typically, an X linked recessive pattern
○ Forms
■ Hemophilia A
● Classic hemophilia (deficiency of factor VIII)
● Accounts for 80% of cases of hemophilia
■ Hemophilia B
● Christmas disease (deficiency of factor IX)
■ von Willebrand disease
● Deficiency, abnormality, or absence of vWF and factor VIII
● Affects both males and females
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Clinical manifestations
○ Bleeding tendencies range from mild to severe
○ Symptoms may not occur until 6 months of age
○ Hemarthrosis
■ Bleeding into joint spaces of the knee, ankle, or elbow leads to
impaired mobility and eventually bony changes and disability
■ Symptoms include warmth, pain, bruising, and decreased
movement
○ Epistaxis
○ Bleeding in the GI tract
○ Bleeding after procedures
■ Minor trauma, tooth extraction, minor surgeries
■ Large subQ and IM hemorrhages may occur
■ Bleeding into the neck, chest, or mouth may compromise the
airway
■ Bleeding in the spinal cord may cause paralysis
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Diagnostic eval
○ Can be diagnosed through amniocentesis
○ Genetic testing of family members is needed to ID carriers
○ Diagnosis is made on the basis of the hx, lab studies, and examination
■ Lab tests will show low levels of factor VIII or IX and a prolonged
PTT
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Platelet count, PT, and fibrinogen levels are normal
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Prognosis
○ No cure
○ Symptoms can be controlled
○ Average life expectancy
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Therapeutic management
○ Replacement of missing clotting factors
○ Desmopressin
■ Increases factor VIII activity by 2-4x (type A)
■ Used for mild hemophilia
○ Transfusions
○ Prompt intervention to reduce complications
○ Meds
■ Corticosteroids, NSAIDs
○ Exercise and PT
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Managing hemarthrosis
○ During bleeding episodes, elevate and immobilize the joint
○ Ice mild hemophilia
○ Factor VIII infusion for moderate hemophilia
○ Analgesics
○ Range of motion exercises after the bleeding stops will help to prevent
contractures
○ Physical therapy
○ Avoid obesity to minimize joint stress
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Nursing management
○ Close supervision and safe environment. Injury prevention
○ Dental procedures in a controlled situation
○ Prevent bleeding (shave only w/ electric razor)
○ For superficial bleeding, apply pressure for at least 15 min and ice to
promote vasoconstriction
○ If significant bleeding occurs, transfusion for factor replacement
○ Emotional support
Sickle cell anemia
○ Hereditary hemoglobinopathy
■ Occurs mainly in African Americans but also seen in South American,
Arabian, and East Indian descent
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Autosomal recessive - both parents w/ trait
● Each child has 1 in 4 chances of having disease
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Patho
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Partial or complete replacement of normal Hgb w/ abnormal Hgb S
Hgb in the RBCs takes on an elongated sickle shape
Sickled cells are rigid and obstruct capillary blood flow
Microscopic obstruction lead to vaso-occlusion
Absence of blood flow -> local hypoxia -> tissue ischemia and infarction
Clinical manifestations
○ Vary greatly. Occurs mainly during exacerbation periods
○ Crisis
■ Vaso-occlusive
■ Sequestration
■ Hyper-hemolytic
○ Acute chest syndrome
■ Serious complication
■ Clinically similar to pneumonia
■ New pulmonary infiltrate
■ Chest pain, fever, cough, tachypnea, wheezing, hypoxia
○ Cerebrovascular accident (CVA)
■ Sudden and severe complication, no related illness
■ Sickled cells block major blood vessels in brain -> cerebral infarct
-> neurological impairment
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Sickle cell crisis
○ Precipitating factors
■ Anything that increases the body's need for oxygen or alters the
transport of oxygen
■ Trauma
■ Fever, infection
■ Physical and emotional stress
■ Exposure to cold
■ Drug and alcohol use
■ Increased blood viscosity d/t dehydration
■ Hypoxia
■ Results from high altitude, poorly pressurized airplanes,
hypoventilation, vasoconstriction d/t hypothermia
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Vaso-occlusive (VOC) - pain episode
○ Most common type of crisis and is very painful
○ Stasis of blood w clumping of cells in the microcirculation leads to
ischemia and then infarction
○ Signs
■ Fever, pain, and tissue engorgement
Splenic sequestration
○ Life threatening type
■ Death within hours
○ Blood pools in the spleen, causing decreased blood volume and shock
○ Signs
■ Profound anemia, hypovolemia, shocks
Aplastic crisis
○ Diminished RBC production
○ Triggered by viral illness or depletion of folic acid
○ Signs
■ Profound anemia and pallor
Hyper-hemolytic crisis
○ Accelerated rate of RBC destruction
○ Signs
■ Anemia, jaundice, reticulocytosis
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Iron deficiency anemia
○ Caused by an inadequate supply of dietary iron
○ Generally preventable
○ Predictable at developmental periods
■ In premature infants, d/t low fetal supply
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■ At 12-36 months, d/t ingestion of large amounts of cow's milk and diet
■ In adolescents, d/t rapid growth and poor eating habits
Therapeutic management
■ Dietary counseling and supplements
■ Infants can add iron fortified cereal at 4-6 months
■ Bottle fed infants can have iron fortified formula
■ Supplements
● Can be given in vitamins - polyviflor
Nursing management
■ Educate family on proper way to give iron
● Avoid teeth/brush teeth after liquid iron
● Don't give milk/milk products
○ Wait 30 min
● Giving with citrus aids absorption
● Stools turn tarry green or black
● Diet
■ Iron rich foods
● Seafood, almonds, apricots, raisins, meat, pumpkin seeds, green
peas, spinach, broccoli
SCHOOL NURSING
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Direct caregiving
○ Administer meds
○ Perform routine screenings
○ Handle acute issues that
arise and assess critical
symptoms
○ Provide emotional support
○ Stay current on appropriate
EBP
Educator
○ Develop programs and
materials to teach students,
families, and other school
staff about health promotion
and injury prevention
○ Provide anticipatory guidance
about immunizations,
nutrition, meds, safety
○ Teach about
■ Hand hygiene,
helmets, sports
injuries, sex ed,
substance use,
STIs/safe practices,
driving safety
Case manager
○ Discussing home impact on
academics
○ Managing health impact on
academics and social
activities
○ Managing students w/
chronic health conditions
■ Daily meds,
assessments,
maintenance
Consultant
Influence the identified plan
Effect change
Enhance abilities of others
Examples - Talk to parents
about child’s vaccines or
illness / Talk to school admin
regarding staff training
Counselor
○ Emotional support
○ Mental and physical health
advocacy
○ Recognizing and addressing
underlying problems
○ Involvement in psychosocial
care
○ Referrals to community
○ Working alongside guidance
counselor
Community outreach
○ Screenings in the community
○ Assemblies
○ Vaccination clinics
○ Parent education sessions
○ Asthma and allergy action
plans
○ Hand hygiene
Research
○ Be familiar w/ kids’
acute/chronic health
conditions
○ Keep up w best current
practices
○ Research connection
between mental and physical
health
○ Data tracking
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GENITOURINARY
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Acute glomerulonephritis - glomeruli damaged by inflammation
○ Types
■ Most are postinfectious: streptococcal (most common), pneumococcal, or
viral
■ May be a primary event
○ May be manifestations of a systemic disorder
■ Systemic lupus erythematosus (SLE)
■ Sickle cell disease
■ Others
● Acute poststreptococcal glomerulonephritis (APSGN)
○ Immune complexes deposited in glomerular basement membrane ->
glomeruli become edematous and infiltrated w/ leukocytes -> capillary
lumen becomes occluded -> decreased plasma filtration -> excessive
accumulation of H2O and Na+ ->expands plasma and interstitial fluid
volume -> circulatory congestion and edema
○ Antigen-antibody complex from recent strep infection -> this complex in
the glomeruli causes
■ Inflammation
■ Decreased glomerular filtration rate
● Clinical manifestations
○ Headache
○ Increased BP
○ Facial and periorbital edema
○ Lethargic
○ Low grade fever
○ Weight gain (edema)
○ Urine
■ Proteinuria
■ Hematuria
■ Oliguria
■ Dysuria
● Lab testing
○ BUN
■ Newborn: 4-18 mg/dL
■ Child: 5-20 mg/dL
○ Creatinine
■ Infant: 0.2-0.4 mg/dL
■ Child: 0.3-0.7 mg/dL
■ Adolescent: 0.5-1.0 mg/dL
Throat culture: usually strep negative
Urinalysis
■ Proteinuria, tea-colored urine, hematuria, high specific gravity
○ Elevated BUN and creatinine
○ Positive ASO titer (antistreptolysin)
■ Serum antibodies to strep
Therapeutic management
○ Monitor for acute HTN, fluid balance
■ Monitor BP every 4-6 hours
■ Antihypertensives and diuretics to control HTN
○ Manage edema
■ Daily weights
■ Accurate I&O
■ Daily abdominal girth
○ Nutrition
■ Regular diet but no added salt
■ Fluid restriction for HTN and edema
■ Potassium restriction during periods of oliguria
○ Assess for cerebral complications (e.g. seizures)
○ Bed rest is not necessary but activities should include frequent rest
periods to avoid fatigue
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Nephrotic syndrome - glomeruli damaged by non-inflammatory causes
○ Most common presentation of glomerular injury in children
○ Characteristics
■ Massive proteinuria
■ Hypoalbuminemia
■ Hyperlipidemia
■ Edema
○ Types of nephrotic syndrome
■ Minimal change nephrotic syndrome
● Aka idiopathic nephrosis, childhood nephrosis, minimal lesion
nephrosis
● Constitutes 80% of nephrotic syndrome cases
■ Secondary nephrotic syndrome
● Glomerular damage with known or presumed cause
■ Congenital nephrotic syndrome
● Inherited as autosomal recessive
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MCNS (minimal change nephrotic syndrome)
○ Patho
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Mostly in children 2-7 yo
Rare in children < 6 mo and > 8 yo
Cause and mechanisms are not truly known, but components are
thought to be
■ Metabolic
■ Biochemical
■ Physiochemical
■ Immune mediated
Glomerular membrane
■ Normally is impermeable to large proteins
■ Becomes permeable to proteins, especially albumin
■ Albumin is lost in the urine (hyperalbuminuria)
■ Serum albumin is decreased (hypoalbuminemia)
■ Fluid shifts from the plasma to the interstitial spaces
■ Hypovolemia
■ Edema
■ Ascites
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Diagnosis of MCNS
○ Suspected based on clinical manifestations
■ Facial edema
■ Ascites
■ Weight gain
■ Ankle or leg swelling
■ Diarrhea
■ Decreased urine output; frothy urine
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■ Anorexia
■ Irritability
■ Fatigue
■ Proteinuria 2+ on dipstick testing
■ Hypoalbuminemia
■ Hyperlipidemia
■ Low serum protein and sodium
May require renal biopsy to distinguish from other types of nephrotic
syndrome
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Management of MCNS
○ Reduce excretion of urinary protein
○ Reduce fluid retention in tissues
○ Prevent infection and minimize complications from therapies
○ Steroids - 1st line of tx
■ Prednisone = least expensive, safest
■ 2 mg/kg/day divided into twice a day dose over 6 weeks
■ Followed by 1.5 mg/kg/day every other day for 6 weeks
○ Diet
■ Sodium restriction
■ Fluid restriction if severe
■ Reduced fat
■ Adequate fluid intake
○ Immunosuppressant therapy when not responding to steroids
■ Cyclophosphamide (Cytoxan)
○ Diuretics for complications of edema
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Family issues with MCNS
○ Chronic condition w/ relapse
○ Developmental milestones
○ Social isolation
■ Lack of energy
■ Immunosuppression, protection
■ Change in appearance d/t edema affects the self image
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Nursing interventions for MCNS
○ Strict I&O
○ Monitor urine protein
○ Daily weight and abdominal girth
○ Monitor vitals and edema
○ Prevent infection
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■ Keep away from sick individuals
■ Pneumococcal vaccine
Encourage recreational and diversion activities
UTI
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Background
■ One of the most common conditions of childhood
● 75 of children have a febrile UTI in the first 2 years of life
■ Most important host factor is urinary stasis
■ Uncircumcised males are at higher risk
■ Girls have a higher prevalence than circumcised males
EBP
■ AAP reported significant UTI reduction in first year of life if males were
circumcised
■ Benefit of circumcisions outweighs risk
Classification of UTI
■ Bacteriuria - presence of bacteria in the urine
■ Pyuria - presence of white blood cells in the urine
■ Asymptomatic bacteriuria - significant bacteriuria (defined at > 100,000
colony forming units) with no clinical symptoms
■ Symptomatic bacteriuria - bacteriuria accompanied by physical signs of
UTI (dysuria, suprapubic discomfort, hematuria, fever)
■ Recurrent UTI - repeated episodes of bacteriuria or symptomatic UTI w/
the same strain of bacteria
■ Frequent UTI - more than 3 in a 6 month period
● Do not have to be infections characterized by the same strain of
bacteria
■ Persistent UTI - persistence of bacteriuria despite antibiotic treatment
■ Febrile UTI - bacteriuria accompanied by fever and other physical signs of
UTI
● Presence of fever typically implies pyelonephritis
■ Cystitis - inflammation of the bladder
■ Urethritis - inflammation of the urethra
■ Pyelonephritis - inflammation of the upper urinary tract and kidney
● Kidney infection usually characterized by presence of bacteriuria
and clinical symptoms that include fever
■ Urosepsis - febrile UTI coexisting w/ systemic signs of bacterial illness
● Blood culture reveals presence of urinary pathogen
Etiology and patho of UTI
■ Organisms that commonly cause UTIs
● E. coli is the most common
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● Streptococci
● Staph. Saprophyticus
● Occasionally, fungal and parasitic pathogens
■ Anatomic or physical causes
● Short urethra in girls
● Uncircumcised males
● Urinary stasis
● Incomplete emptying
● Increased fluid intake flushes bladder, decreases UTIs
Pediatric clinical manifestations
■ Infants
● Poor feeding
● Failure to gain weight
● Excess thirst
● Frequent urination
● Screaming with urination
● Foul smelling urine
● Fever
● Persistent diaper rash
■ Children
● Poor appetite
● Vomiting
● Growth failure
● Excessive thirst
● Painful urination
● Enuresis
● Blood in urine
● Fatigue
Normal characteristics of urine
■ Color
● Pale yellow to deep gold
■ Clear
■ In newborns
● 1-2 mL/kg/hr
■ In children
● 1 mL/kg/hr
Normal urinalysis
■ pH 5.0 - 8.0
■ Specific gravity 1.001-1.030
■ Urobilinogen up to 1 mg/dl
■ None of the following
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● Glucose
● Ketones
● Protein
● Bacteria (might be a few)
● WBCs
● RBCs
● Casts
● Nitrites
Diagnostic eval
■ Urinalysis
■ Urine culture w/ sensitivity
● Obtain specimen
○ < 2yo - sterile catheter/suprapubic aspiration
■ More accurate results
○ > 2 clean catch if possible
○ U bag
● Blood and protein
● Culture - gives you the organism
● Sensitivity - what antibiotic can be used as tx
■ Lab values
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UTI drug therapy
■ Trimethoprim-sulfamethoxazole (TMP-SMX) or nitrofurantoin
■ Amoxicillin
■ Cephalexin
■ Gentamycin
■ Carbenicillin
■ Pyridium (OTC)
● Turns urine dark orange
■ Combination agents (Urised) used to relieve pain
● Prep w/ methylene blue tint (will tint urine)
■ For repeated UTIs
● Prophylactic or suppressive antibiotics
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TMP-SMX administered every day to prevent recurrence or as a
single dose before events likely to cause UTIs
Prevention
■ Hygienic habits
■ Wipe front to back
■ Void when you feel the urge
■ Avoid tight clothing/diaper
■ Avoid prolonged wet bathing suits
■ Adequate fluid intake
■ Avoid constipation
Hemolytic uremic syndrome
○ Background
■ Uncommon acute renal disease characterized by
● Acute renal failure
● Hemolytic anemia
● Thrombocytopenia
■ Hx of gastroenteritis or URI followed by sudden onset of hemolysis and
renal failure
■ Primarily in 6 mo - 5yo
■ Cause
● E coli, shigella, salmonella, pneumococci, and viruses such as
coxsackie, adenovirus
■ Most common cause of acute renal failure in children
○ Patho
■ Endothelial lining of small glomerular arteries become swollen and
occluded w platelets and fibrin clots
■ RBCs are damaged as they move through occluded blood vessels
● They are removed by the spleen, causing acute hemolytic anemia
■ Platelet aggregation and damage causes thrombocytopenia
○ Clinical manifestations
■ Vomiting, diarrhea
■ Lethargy
■ Irritability
■ Pallor
■ Hemorrhagic: bruising, petechiae, jaundice, bloody diarrhea
■ Oliguria/anuria
■ CNS: seizures, stupor, coma
■ Acute HF
○ Lab testing
■ CBC - increased H+H
○
○
○
■ Increased rectic count
■ Hematuria
■ Proteinuria
■ Increased BUN and creatinine
■ Fibrin split in urine/serum (thrombocytopenia)
Diagnostic eval
■ Anemia, thrombocytopenia, and renal failure are sufficient for diagnosis
Therapeutic management
■ Supportive care
■ Treat HTN
■ Correct electrolyte imbalances
■ Blood transfusion for anemia
■ Fluid replacement
■ Enteral/parenteral nutrition after vomiting subsides
■ Dialysis (hemo or peritoneal) for anuria > 24h or seizures
Prognosis
■ Recovery rate 95% w/ prompt treatment
GASTROINTESTINAL
●
Dehydration
○ Types of dehydration
■ Isotonic
● Electrolyte and water deficits present in equal proportions
● Primary form of dehydration in children
● Serum sodium within normal limits: 130-150 mEq/L
■ Hypotonic
● Electrolyte deficits exceed water deficits
● s+s more severe
● Shock likely
● Na < 130 mEq/L
● Na+ deficit greater than H2O deficity; ICF fluid more concentrated
than ECF, so H2O shifts from extracellular to intracellular causing
increased ECF loss, where shock is a frequent result
■ Hypertonic
● Water loss exceeds electrolyte loss
● Most dangerous
● Shock less likely
● Neuro changes can occur
● Na > 150 mEq/L
● H2O loss greater than electrolyte loss; fluid shifts from lesser
concentration of ICF to higher concentration of ECF
●
Degrees of dehydration - weight loss in percentage (weight is the most important
determinant of dehydration)
○ Mild
■ 3-4% in children
■ 3-5% infants
■ S+S
■ Mucus membranes, anterior fontanel pulse, BP - all within
normal
■ Cap refill > 2s
■ Possible thirst
■ Rehydration therapy
■ Oral - 50mL/kg every 4-6 hours
○ Moderate
■ 6-8% in children
■ 6-9% in infants
■
■
○
S+S
■
■
Cap refill 2-4s
Thirst, irritability, slight pulse increase, orthostatic BP, dry
membranes, decrease tears, skin turgor, slight tachypnea,
normal/sunken fontanel
Rehydration
■ Oral - 100mL/kg every 4-6 hours
Severe
■ 10% children
■ Less than or equal to 10% infants
■ S+S
■ Cap refill > 4s
■ Tachypnea, orthostatic BP leading to shock, extreme thirst,
dry membranes, no tears and sunken eye, sunken fontanel,
oliguria/anuria
■ Rehydration
■ 40 mL/kg/hr until pulse and state returns to normal
■ Then 50-100 mL/kg or oral hydration
●
Diagnostic eval
○ Type and degree of dehydration
○ Body weight
○ Serum electrolytes
●
Clinical manifestation
○ Change in sensorium/response to stimuli
○ Skin changes/turgor
○ Cap refill
○ Sunken eyes/fontanelles
○ Lack of tears when crying
○ Wants to drink but may vomit, excessive thirst
○ Decreased urine output
■ Infants/babies
■ Indicated by no wet diapers in a 6-8 hr period or diapers w/
a little dark-yellow urine
■ Toddlers/older children
■ Very little dark yellow urine
○ Vitals
■ Rapid breathing
■ Increased HR
○ Restless/irritable
○
○
Lethargy/weakness
Poor skin turgor
●
Therapeutic management
○ Oral rehydration therapy
○ Parenteral fluid therapy
○ Treat underlying cause
○ Correct fluid imbalance
○ Oral - first treatment for mild to moderate dehydration
■ Over 4-6 hrs, about 50 mL/kg if tolerates
■ Give Pedialyte
■ No carbonated/caffeinated beverages
○ Zofran (ondansetron)
■ For N+V
○ IV therapy
■ When child is unable to take oral fluid
●
Nursing considerations
○ Monitor for signs of dehydration
■ Skin - color, temp, turgor, cap refill
■ Mucous membranes - moisture, color, secretions
■ Fontanel (infants) - sunken, soft, normal, flat
■ Alterations - mood, activity, thirst
○ Monitor vitals q 15-30 min
○ Monitor weight
■ During initial phase of therapy
○ Maintain accurate I+O
■ Urine - frequency, color, consistency, volume
■ Stools - frequency, volume, consistency
■ Sweating - estimate
●
Progression of symptoms
○ Earliest detectable sign - tachycardia
○ Dry skin/mucous membranes
○ Sunken fontanels (up to 18 months)
○ Coolness/mottling of extremities
○ Loss of skin elasticity
○ Prolonged capillary refill time
○ Increased pulse rate
○ Decrease to absence of tears
○ Oliguria and anuria
○
●
Low BP (late sign - onset of CV collapse)
Intussusception
○ Background
■ Most common cause of intestinal obstruction 3mo-6yo
■ Telescoping of one portion of the intestine into another
■ Cause unknown
○ Patho
■ Proximal segment telescopes into distal segment
■ Edema and obstruction -> increased pressure
■ Arterial blood flow stops -> ischemia
■
●
●
●
●
Diagnostic eval
○ Symptoms
○ Ultrasound - bullseye
○ Rectal exam - blood, mucus
Clinical man
○ Sudden acute abdominal pain
○ Screaming, drawing knees to chest
○ Vomiting
○ Lethargy
○ Currant jelly stools
○ Abdomen distended, tender
○ Palpable sausage-shaped mass RUQ
○ Empty RLQ (Dance sign)
Therapeutic management
○ Radiologist guided pneumo-enema or hydrostatic enema
○ IVF, NG decompression, antibiotics
○ Surgery
Nursing management
○ Education
○ Passage of normal brown stool prior to correction means it resolved itself
○ Post-op care
●
Diarrhea
○ Types
■ Acute: sudden increase and change in consistency of stool; infectious
(rotavirus, Norovirus), upper resp infec, UTI, antibiotics, laxative use
■ Chronic: increase in frequency and water content of stool for > 14 days;
malabsorption syndromes, IBD, immunodeficiency, food intolerance
■ Intractable: infancy; >2 weeks; inadequate mgmt. acute infectious diarrhea
■ Nonspecific: toddlers/children; loose stools, undigested food, >2 weeks;
may result from poor dietary habits, food sensitivities, excessive intake of
juice and artificial sweeteners
● Transmission - pathogens are fecal-oral route if infectious
○ Contaminated food/water
○ Lack of clean water
○ Overcrowding
○ Poor hygiene
○ Poor sanitation
● Diagnostic eval
○ Hx to determine possible cause
○ Symptoms
○ Lab tests only for severe dehydration
○ Prevention
● Prevention
○ Personal hygiene
○ Careful food prep
○ Disposal of soiled diapers
○ Handwashing
● Nursing considerations
○ Teaching
■ S+S of dehydration, ORT, introduction of regular diet
○ Monitor weight, I&O for hospitalized child
● Therapeutic management
○
●
Hirschsprung
○ Also called congenital aganglionic megacolon
○
○
○
○
○
○
Congenital anomaly that results in mechanical obstruction d/t the absence of
ganglionic cells in affected area of intestine
Risk - family hx
Clinical manifestations
■ Newborn
● Failure to pass meconium 24-48 hrs after birth
● Refusal to feed
● Bilious vomiting
● Abdominal distention
■ Infancy
● Failure to thrive
● Constipation/abdominal distention
● Diarrhea/vomiting
● Enterocolitis
■ Childhood
● Constipation
● Ribbon-like foul-smelling stools
● Abdominal distention
● Visible peristalsis
Diagnostic eval
■ Failure to pass meconium
■ Hx of constipation
■ x-ray, barium enema
■ Anorectal manometry
● Measures sphincter pressures w/ inflation of a balloon in the
rectum
■ Confirm the diagnosis w/ rectal biopsy
■
Therapeutic management
■ Surgery to remove aganglionic segment/colostomy
● Pre-op care
○ High protein, high calorie, low fiber diet
■
●
○ Emptying bowel w/ enemas
○ Antibiotics to decrease normal flora
● Post-op care
○ Monitor for wound infection
○ Monitor passage of stool
○ Pain relief
○ VS
○ Airway management
● Discharge planning and care
○ Education
Colostomy in an infant or child
● Nursing considerations
Pyloric stenosis
○ Constriction of the pyloric sphincter w/ obstruction of the gastric outlet
○ Patho
■ Muscle of pyloric sphincter thickens resulting in narrowing of pyloric canal
■ Obstruction occurs resulting in dilation, hypertrophy and hyperperistalsis
of stomach
■ Inflammation and edema result in complete obstruction
○ Diagnostic eval
■ H&P
■ Olive like mass palpated (hypertrophied pyloris)
■ Vomiting 30-60 min after feeding, becoming projectile
■ Ultrasound
○ Clinical manifestations
■ Projectile vomiting usually after feeding
■ Hungry, avid feeder
■ No evidence of pain
■ Weight loss
■ Dehydration
■ Distended upper abdomen
■ Olive shaped tumor to right of umbilicus
■ Visible peristalsis from L to R
○ Therapeutic management
■ Surgical repair
■ Small frequent feedings postop
○ Nursing management
■ Pre-op
● IV hydration, NPO
■ Post-op
●
●
●
○
IVF
Pain control
Feeding w/in 12-24 hours
CANCER
●
Leukemia
○ Background
■ Proliferation of immature, non functional blood cells, mainly WBC, crowds
out mature healthy cells
■ No "tumor" is present, but the same neoplastic properties are seen in solid
cancers
■ Infiltration and replacement of any body tissue w nonfunctional leukemic
cells
■ Liver and spleen are the most severely affected organs
●
ALL (acute lymphoblastic leukemia)
○ Most common form of childhood cancer
○ Bone marrow produces immature white cells that develop into
lymphoblasts which don't function properly; they build up and crowd out
the healthy cells
○ Peak onset is between 2 and 3 years of age
○ Survivability improved w use of antileukemic agents: close to 80%
○ Onset between age 1-9 of B cell better prognosis than younger than 1/10
and older
■ T cell prognosis is not affected by age
○ Very high WBC counts (>50,000) when diagnosed at higher risk
○ Risk factors
■ Prenatal exposure to x rays
■ Previous treatment w chemo
■ Genetic conditions
■ Down syndrome
■ Fanconi anemia
●
AML (acute myelogenous leukemia)
○ Affects a group of WBCs called myeloid cells, which normally develop into
mature RBCs, WBCs, and platelets
○ Like ALL, immature cells crowd out healthy cells
○ 20% of cases childhood leukemia
○ Higher rates during 1st year of life
○ WBC count <100,000 at diagnosis do better than those w/ higher counts
●
Acute leukemia
○
●
Clinical manifestations
○ Often few sx present initially
○ Fever
○ Frequent infections or infection that won't go away
○ Pale/listless/fatigue
○ Bone pain
○ Anorexia
○ Frequent or severe nosebleeds, bleeding gums
○ Excessive bruising
○ Enlarged lymph nodes
○ Shortness of breath
●
Consequences of leukemia
○ Depressed bone marrow function
■ Anemia from decreased RBCs
■ Infection from neutropenia
■ Bleeding tendencies from decreased platelet production
○ Weakening of bones may lead to fractures
■ Extramedullary (outside of bone marrow)
○ Spleen, liver and lymph glands show marked infiltration, enlargement, and
fibrosis
○ Extramedullary
○ CNS involvement
○ Testes
●
Diagnostic evaluation of leukemia
○ Based on the hx and physical manifestations
○ Peripheral blood smear
■ Immature leukocytes
■ Frequently, low blood counts
○
○
○
○
Lumbar puncture to evaluate CNS involvement: often asymptomatic
Chest x ray to determine if there's a mass of leukemic cells in the chest
Bone marrow aspiration or biopsy
■ Infiltrate of blast cells
Staging is now done w/ immunophenotyping using monoclonal antibodies
●
Prognosis
○ Age
■ >1 yr and less than or equal to 10 yrs more favorable
■ Infants not favorable
○ Initial WBC count
■ Less than or equal 50,000 favorable
○ Gene/chromosome abnormalities
■ Down syndrome and translocations at 4,11, 44 unfavorable
○ Response to chemo
■ Rapid response more favorable
○ Status of ALL during and after treatment
■ Remission w/ no residual leukemic cells more favorable
○ Increased susceptibility to infection
■ At the time of diagnosis and relapse
■ During immunosuppressive therapy
■ After prolonged antibiotic therapy that predisposes the pt to the
growth of a resistant organism
○ Prevention
■ Environment
■ Hand hygiene
■ Visitor restriction
■ Nutrition
■ Planning for home care
●
Therapeutic management of leukemia
○ Chemotherapy
■ Phase approach
■ First phase - induction
■ Increased risk of hemorrhage and infection
■ Second phase
■ To maintain remission
■ Third phase
■ Low dose to prevent relapse
○ Radiation therapy
○ Chemotherapy w stem cell transplant
Targeted therapy
■ Use of drugs to target specific molecules such as proteins on the
surface of cancer cells
Nursing management
○ Preparation for diagnostic and therapeutic procedures
○ Emotional support
○ Pain management
○ Monitoring/prevention of complications
○
●
●
Lymphomas
○ Neoplastic disease originating in the lymphoid and hematopoietic systems
● Hodgkin lymphoma (HL)
○ More prevalent in pts 15-19 years of age
○ EBV thought to have a role in causation
○ Primarily involves lymph nodes
○ Reed-Sternberg cancer cells are present
○ Often metastasizes to the spleen, liver, bone marrow, lungs, and other
tissues
○ Classified by histologic type
○ Increased risk for immunocompromised, those with history of HL among
immediate family members
○ Decreased risk in those exposed to infections in early childhood
○ Staging
○
■
Clinical manifestations
■ Painless enlargement of lymph nodes
■ Enlarged, firm, nontender, movable cervical or
supraclavicular nodes
■ Persistent non-productive cough
■ Unexplained abdominal pain
■ Low grade fever
■ Anorexia
■ Nausea
■ Weight loss
■ Night sweats
○
○
●
■ Pruritus
Diagnostic eval
■ H&P
■ CBC
■ Chem panel w/ albumin levels, ESR, C-reactive protein
■ ESR and CRP - indicate inflammation
■ CXR, CT, MRI, PET
■ Lymph node biopsy for diagnosis and staging
■ Presence of Hodgkin and Reed-Sternberg cells
■ Bone marrow aspiration if the stage is advanced
Management of Hodgkin Disease
■ Chemo and radiation
■ Nursing considerations
■ Same as leukemia and other cancers
Non Hodgkin lymphoma (NHL)
○ More prevalent in children younger than 14 yo
○ 10 children per 1 million
○ Absence of Reed-Sternberg cells
○ Risk factors
■ EBV infection
■ Inherited or acquired immunodeficiency
■ Previous cancer
○ Clinical manifestations
■ Same as HL
■ Usually diagnosed after metastasis to bone marrow or CNS
■ Lymphoid tumors may cause intestinal or airway obstruction, cranial
nerve palsies or spinal paralysis
○ NHL diagnosis and management
■ Diagnostic eval
■ Similar to HL
■ Most children with NHL have widespread disease at time of
diagnosis
■ Histology: mature B cell, lymphoblastic, aplastic large cell
■ Therapeutic management
■ Aggressive chemo, similar to leukemia therapy
■ Prognosis
■ Improved w/ younger age, no mediastinal involvement, low
tumor burden, good response to initial therapy
■ Cure 85-95% w/ limited disease, 70-90% w/ extensive
disease
■
●
Nursing considerations
■ Similar to HL
Wilms tumor
○ Most common kidney tumor of childhood
○ Most diagnosed between 2 and 3 years of age
○ 10% have congenital anomalies
○ Clin man
■ Swelling or mass w/in abdomen
● Firm, nontender, confined to one side, deep w/in flank (pain 40%)
● Often become quite large before they are noticed
■ Anemia secondary to hemorrhage w/in tumor
● Results in pallor, anorexia, and lethargy
■ Others
● Hematuria, HTN, weight loss, fever, sx of lung metastasis
■ Can spread, most often to abdominal lymph nodes and lungs
○ Diagnostic eval
■ H&P
● Congenital anomalies, family hx of cancer
● Signs of malignancy: weight loss, hepatosplenomegaly, anemia,
lymphadenopathy
■ Radiographic studies
■ Lab studies: CBC, biochemical studies, urinalysis
○ Prognosis
■ Unfavorable histology
● Anaplasia: look of the cancer cells may vary widely and the cells'
nuclei are large and distorted
● Only 10% of cases
● Poor prognosis
■ Favorable histology
● No anaplasia
● 5 year survival rate > 90%
○ Management
■ Therapeutic management
● Surgery: partial or total nephrectomy
● Chemo
● Radiation for metastatic disease
■ Nursing management
● Similar to care of other cancers
● Avoid palpation of tumor
● Surgery scheduled w/in 24 h of diagnosis
●
●
●
●
Pre-op care
○ surg usually within 24-48 hrs of admission
○ preop prep, labs, vitals especially BP due to HTN from
excess renin
○ NO PALPATION OF ABDOMEN (dissemination of cancer)
○ careful bathing
Post-op care
○ Monitor GI status
○ Risk for obstruction (from adhesions and ileus), BP, signs of
infection
Emotional support
Neuroblastoma
○ Background
■ Most common malignant extracranial solid tumor of childhood (infancy
through early childhood)
■ Majority of tumors develop in the adrenal gland or in neck, chest or spinal
cord
■ Silent tumor
● Often note diagnosed until metastasis has occurred
● Diagnostic eval
○ Locate primary site and sites of metastasis
■ Most common primary site is the abdomen
○ Radiologic studies and bone marrow eval
○ IVP (intravenous pyelogram) to eval renal involvement
●
Clinical manifestations
○ Depend on location and stage of disease
○ Abdominal
■ Firm, nontender, irregular mass that crosses the midline, pain,
vomiting, anorexia, resp. compromise, urinary frequency or
retention
○ Other sites
■ Head, neck, chest, pelvis
■ Neuro impairment, dyspnea, stridor, seizures, paralysis
●
Prognosis
○ Low risk group
■ Small tumors easily removed by surgery
■ 5 year survival rate > 95%
○ Intermediate risk group
Larger tumors that haven't spread or children younger than 18
months whose tumors have spread
■ 5 year survival rate 90-95%
High risk group
■ Disease that has spread after 18 months of age and those w a
genetic feature
■ 5 year survival rate approx 50%
■
○
●
●
●
Therapeutic management
○ Low risk
■ Surgery followed by observation or chemo
○ Intermediate risk
■ Chemo
■ Surgery
■ Observation (infants)
■ Radiation if progressive after chemo
○ High risk
■ Chemo
■ Surgery
■ Ablative therapy
■ HSCT
Nursing management
○ Psychological and physical prep for diagnostic and surgical procedures
○ Prevention of postop complications
○ Emotional/psych support and resources
Retinoblastoma
○ Background
■ Arises from the retina
■ 60% unilateral and non-hereditary
■ Diagnosed before age 2
■ In hereditary form, mutation in RB1 gene
○ Clin man
■ Whitish glow in pupil
■ Strabismus
■ Blindness is a late sign
■ Orbital cellulitis, glaucoma, pain (late signs)
○ Diagnostic eval
■ Detailed family hx
■ Recording of eye symptoms
■ Ophthalmoscopy, ultrasound, CT, MRI
○
■ Blood and tumor samples to test for RB1 gene mutation
■ Metastatic disease is rare
Staging
■
●
Prognosis and management
○ Prognosis
■ 10 yr survival rate nearly 90%
■ May spontaneously regress
■ Secondary tumors may arise especially w/ bilateral disease
○ Therapeutic management
■ Chemo and radiation
■ Enucleation for advanced disease w/ optic nerve invasion w no hope for
vision salvation
■ Photocoagulation and cryotherapy
■ Photocoagulation: laser beam to destroy retinal blood vessels that
supply the tumor
■ Cryotherapy: freezing the tumor
○ Nursing management
■ Prepare child and family for tests and procedures
■ Prepare family for facial appearance and post op care following
enucleation
■ Prepare family - loss of vision, appearance (prosthetic)
■ Emotional support
●
Chemotherapy
○ Interferes w/ nucleic acids, DNA, RNA
○ Classified by mechanism of action
○ Does not target only malignant cells. Affects other cells w/ high rate of
proliferation
○ Requires caution w/ handling/disposal and administration
INTEGUMENT
●
Lice
○
○
○
○
○
●
Scalp infection by Pediculus humanus capitis
■ Female lays eggs at night at junction of hair shaft
■ Eggs hatch in 7-10 days
■ Spread by sharing hats, combs
Clinical manifestations
■ Itching to occiput behind ears, nape of neck
Diagnostic eval
■ Observe nits adhered to hair shaft
Nursing care management
■ Pediculicide and manual removal
■ Education and prevent transmission
How to manage
■ Machine wash all washable clothing, towels, and bed linens in water hotter
than 130°F and dry them in a hot dryer for at least 20 minutes. Dry clean
non-washable items.
■ Thoroughly vacuum carpets, car seats, pillows, stuffed animals, rugs,
mattresses, and upholstered furniture.
■ Seal non-washable items in plastic bags for 14 days if unable to dry clean
or vacuum.
■ Soak combs, brushes, and hair accessories in lice-killing products for 1
hour or in boiling water for 10 minutes.
■ In daycare centers, store children’s clothing items such as hats and scarves
and other headgear in separate cubicles.
■ Discourage the sharing of items such as hats, scarves, hair accessories,
combs, and brushes among children in group settings such as daycare
centers and schools.
■ Avoid physical contact with infected individuals and their belongings,
especially clothing and bedding.
■ Inspect children in a group setting regularly for head lice.
■ Provide educational programs on the transmission of pediculosis, its
detection, and treatment.
Lyme disease
○ Spirochete Borrelia burgdorferi enters skin and blood stream
○ Caused by tick bites
○ Clin man
■ Stage 1- early localized disease (tick bite)
○
○
○
○
●
● w/in 3-30 days erythema migrans ( "bullseye)")
■ Stage 2 - early disseminated disease
● Secondary annular lesions 3-10 wks after bite
● We don't test for Lyme disease until about 6 wks
■ Stage 3 - systemic involvement of neurologic, cardiac, musculoskeletal
systems 2-12 months after bite
Diagnostic eval
■ History, manifestations, lesions not always bullseye
■ Lab tests
Therapeutic management
■ Early tx if symptomatic to prevent complications
■ Oral antibiotics
● Doxycycline for over 8 yo
○ Causes discoloration of teeth so avoid in newly developing
teeth
● Amoxicillin for under 8yo
■ IV antibiotics later stages
Nursing care management
■ Prevention
● Avoid tick infested areas
● Cover arms and legs
● Insect repellants - caution w/ DEET products
○ Use sparingly w/ children under 2 d/t neuro complications
■ Tick removal education
Treatment
■ Pull tick out w/ tweezer
Burns
○ Causes
■ Extreme heat source
■ Cold, chemical, electric, radiation
○ Common patterns
■ Hot water scalds - most frequent in toddlers
■ Flame related burns - more in older children
■ Structural fires from playing w/ matches/lighters - more often in males
■ Nonaccidental burns indicate maltreatment
○ Etiology
■ Most result from contact w thermal agents
■ Fire and burns are the third leading COD age 5-9
■ Nonaccidental burns most common in 3 yo and under
○ Characteristics
■
●
●
Extent of injury
● % total body surface area
Depth of injury
○ Superficial (first-degree) burns are usually of minor significance. This type
of injury involves the epidermal layer only.
■ Epidermis intact and w/o blisters
■ Erythema: skin blanches w pressure
■ Painful
○ Partial-thickness (second-degree) burns involve the epidermis and
varying degrees of the dermal layer. These wounds are painful, moist, red,
and blistered; sensitive to temp changes, exposure to air, and light touch;
heals within 14-21 days
■ Wet, shiny, weeping surface
■ Blisters
■ Wound blanches w/ pressure
■ Painful, sensitive to touch and air currents
■ Can be superficial or deep
○ Full-thickness (third-degree) burns are serious injuries that involve the
entire epidermis and dermis and extend into subcutaneous tissue;
■ Affects nerve endings, sweat glands and hair follicles -> lack
sensation initially, but as peripheral fibers regenerate, becomes
severely painful
■ Color variable
■ Dry surface
■ Thrombosed vessels visible
■ No blanching
■ Autografting required for healing
○ Fourth-degree burns are full-thickness burns that involve underlying
structures such as muscle, fascia, and bone.
■ The wound appears dull and dry, and ligaments, tendons, and bone
may be exposed
■ Charring visible in deepest areas
■ Extremity movement limited
■ Insensate
■ Amputation of extremities is likely
■ Autografting required for healing
Severity of injury
○ minor (<5% TBSA in young children, <10% children >10 yrs old)
○ moderate (5-10 % TBSA in young children)
○ major (>10% TBSA in young children)
●
Management
○ Therapeutic management
■ Emergency care - stop the burning process
■ Minor burns
■ Stop the burning process:
■ Remove burned clothing and jewelry.
■ Apply cool water to the burn or hold the burned
area under cool running water.
■ Do not use ice.
■ Do not disturb any blisters that form unless the injury is
from a chemical substance.
■ Do not apply anything to the burn.
■ Cover with a clean cloth if risk of damage or contamination.
■ Major Burns
■ Stop the burning process:
■ Flame burns—smother the fire.
■ Place victim in the horizontal position.
■ Roll victim in a blanket or similar object; avoid
covering the head.
■ Remove burned clothing and jewelry.
■ Assess for an adequate airway and breathing.
■ Swelling happens immediately
■ If a child is not breathing, begin mouth-to-mouth
resuscitation.
■ Cover the burn with a clean dry cloth. No ointments/oils!
■ Keep victim warm.
■ Begin intravenous fluids and oxygen therapy as
prescribed.
■ Transport to medical aid.
■ Airway, fluids, nutrition (high protein, high cal), pain control,
antibiotics if infected, excision, debridement, skin grafts
○ Nursing care management
■ Acute phase
■ Manage shock and pulmonary status
■ VS, fluids, I&O
■ Management and rehab phases
■ Preventing infection, closing wound as quickly as possible,
managing complications
■ Restoring function
■ Comfort management
■ Prevention
●
Eczema
○ Seen in kids under 1 yo
■ Around the mouth d/t drooling, pacifier, etc.
■ Back of legs, around ankles
○ Chronic relapsing inflammatory skin disorder
■ Results in itching and lesions
■ More autoimmune
○ Clin man is age based
■ Infantile 2-6 mo of age, often resolves at 3 yo
● Erythema
● Vesicles
● Papules
● Weeping
● Oozing
● Crusting
● Scaling
● Often symmetric
■ Childhood 2-3 yr
● Symmetric involvement
● Clusters of small erythematous or flesh-colored papules or
minimally scaling patches
● Dry and may be hyperpigmented
● Lichenification (thickened skin with accentuation of creases)
○ Back of arms, elbow crease, back of legs
● Keratosis pilaris (follicular hyperkeratosis) common
■ Preadolescent and adolescent 12+ yo
● Same as childhood manifestations
● Dry, thick lesions (lichenified plaques) common
● Confluent papules
● Intense itching
● Unaffected skin dry and rough
● African American children likely to exhibit more papular or follicular
lesions than white children
● May exhibit one or more of the following:
○ Lymphadenopathy, especially near affected sites (around
neck)
○ Increased palmar creases (many cases)
○ Atopic pleats (extra line or groove of lower eyelid)
○ Prone to cold hands
○
○
○
○
○
○
○
●
Pityriasis alba (small, poorly defined areas of
hypopigmentation)
Facial pallor (especially around nose, mouth, and ears)
Bluish discoloration beneath eyes (“allergic shiners”)
Increased susceptibility to unusual cutaneous infections
(especially viral)
Diagnostic eval
■ History
■ Exam findings
Therapeutic management
■ Hydrate skin
● May use tepid baths to treat, but must apply emollient while skin
still moist
■ Relieve pruritus
● Benadryl or other allergy meds
■ Reduce flare ups or inflammation
● Can occur during periods of illness or stress
■ Prevent and control secondary infection
Nursing care management
■ Supportive care - hygiene, symptom relief
■ Keep skin from drying out
■ Prevent itch and infection
■ Family support
Diaper dermatitis
○ Most common in infants
■ Directly or indirectly caused by wearing diapers
■ Peak age 9-12 mo
○ Patho
■ increased pH of urine due to breakdown of urea in presence of fecal
urease which promotes activity of fecal enzymes that act as irritants and
increases permeability of skin to bile salts
● Clin man
○ Primarily on convex surfaces or in folds
● Nursing care
○ Address wetness, pH, fecal irritants
■ pH changes can occur when child tries new foods
○ Keep skin dry
○ Creams/ointments
■ Use barrier cream, Balmex, Decoden with sensitive skin
○ Cleanse w/ nonsoap cleanser (Cetaphil)
○
●
No powder
Retin A therapy - topical cream, gel liquid
○ Treats acne
○ can be irritating to skin; wait 20-30 min after washing skin to apply to decrease
irritation
○ avoid sun exposure/use sunscreen to avoid severe sunburn