pediatric cardiology dysfunction for students--2011[1]
TRANSCRIPT
8/3/2019 Pediatric Cardiology Dysfunction for Students--2011[1]
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Cardiovascular
Dysfunction in the ChildN425
(ppt adapted from Norene Rouse, RN, MSN, CNS)Presented by:
Barbara Welton, RN, MSN CNS
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Cardiac Disease in Children: Statistics
Thousands of infants born each yearhave congenital cardiovasculardefects.
Of those who have these defects:² 4²10% have atrioventricular septal
defect.² 8²11% have coarctation of the aorta.² 9²14% have Tetrology of Fallot.² 10²11% have transposition of the
great arteries.
² 14²16% have ventricular septaldefects.² 4²8% percent have hypoplastic left
heart syndrome
Source: © 2011 American Heart Association
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Other Etiology«
Genetics Environment
Medications
Illegal drugs Alcohol
Chromosomal syndromes
Higher incidence if parent,(especially mother) had a defect.
Multi-factoral
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The Heart«
Muscular, four-chamberedorgan
Primary purpose is to pump
blood to the body by:² electrical stimulation
² rhythmic contraction of heartmuscle
² blood flows from an area of highpressure to area of low pressure
² valves prevent back flow
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Normal blood flow through the heart and lungs.
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Flow of Blood« 1.Blood enters into RAfrom body.
2.Blood flows from RA toRV.
3.RV blood goes to thelungs through the PA.
4.Blood enters lungs foroxygenation and returnsvia the PV into the LA.
5.Blood flows from LA toLV.
6.Blood moves from LV tothe body via the aorta.
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Assessment Priorities«
Abnormal heart sounds Color
Rales or crackles in lungs
Enlarged Liver (firm abdomen) Pulses and refill time
Edema
FTT
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Stroke Volume the amount of blood ejected from the ventricles witheach contraction
Is influenced by: Preload, Contractility, Afterload and HR
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Electrical Conduction of the Heart:
SA node (pacemaker), AV node, bundle of His (Leftand Right bundle branches), and the purkinje fibers.
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Frank-Starling
Law
Cardiacoutput
Strokevolume
Heartrate
Preload
Myocardialcontractility
Afterload
In cardiac physiology, the rulestating that cardiac outputincreases in proportion to the
diastolic stretch of heart musclefibers.
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Frank-Starling Law«
The preload in the intact heart isrelated to the resting length of themuscle fibers which in turn isdependent upon the amount of
filling of the chamber. Up to a point, an increase inpreload lengthens the myocyte andstimulates a more vigorouscontraction (Frank Starling Law) by
increasing the number of activatedmyosin-actin bridges and theamount of calcium released fromthe sarcoplamic reticulum.
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Diagnostic Testing«
Blood work (Hct?)
Echocardiogram
EKG/Holter monitor
Chest X-ray
Heart Catheterization
Electrophysiology (
EP)
Stress/Exercise Testing
MRI or CT scan
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Common Testing for CHD«
Echocardiography Can give information relating to
pressures, diameters,ventricular function
Hearth Catheterization Pros and Cons
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Echocardiography:Transthoracic
-M-Mode
-2-D
-Doppler
T EEFetal
Blue = away; Red = towards
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MRI
3D
4-D flowvectormapping
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Cardiac Catheterization«
Study various functions of the heart. Observe vessels and flow when dye injected. Measure Oxygen concentration across the valves
and walls (septa) of the heart. Measure pressures within each chamber of the
heart and across the valves. Procedure can even be performed in
small, newborn infants. Perform procedures once done in
surgery.
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The Child Going to Heart Cath
Answer questions
Keep things simple Validate anxiety Walk through the area
Prepare for procedure- Pre-op meds, monitoring- Insertion site prep- Equipment- Diversion activities- Time frame for procedure- Using pictures
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Post Heart Catheterization
Focus on child after procedure- bedside report, check site
- control/prevent bleeding at site
- keeping flat
- monitoring of VS- check leg pulses, perfusion, color
- light diet initially
- comfort measures
Ask parents what they know Reinforce/provide appropriate
information after MD has discussed withfamily
Home care instructions
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"Eisenmenger·s Syndrome"
When VSD defects go unrepaired into theteen or young adult years, increased pulmonaryblood flow can cause changes in the pulmonaryvasculature.
Eisenmenger Syndrome occurs when thenormal left to right shunting that occurs withseptal defects switches to a right to left shuntdue to the development of increased pulmonaryvascular damage leading to resistance.
T his pressure in the lungs can equal or exceedsystemic vascular resistance which causes thereversal of blood flow.
T
his is a cyanotic condition.
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Children born with Eisenmenger syndrome are born with a hole between the twochambers -- the left and right ventricles -- of the heart (ventricular septaldefect). T he hole allows blood that has already picked up oxygen from the lungs toflow back into the lungs, instead of going out to the rest of the body. T he
increased blood flow and high pressure damages the small blood vessels in thelungs.
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Heart Disease in Children«
The two types of heart disease inchildren are "congenital" and"acquired."
Congenital heart disease ispresent at birth.
Acquired heart disease developssometime during childhood oradulthood.
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Congenital Heart Disease«
These are structural problems About 40,000 children are born
with heart defects each year
At least 8 per 1000 are born
with a heart defect per year About 1 million Americans with
cardiovascular defects are alivetoday.
Many adults are being diagnosednow with heart defects
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Congenital Heart Disease«
Acyanotic
Systemic arterial
saturation isnormal.
Pulmonary bloodflow is normal or
increased. Oxygenation is
taking place
Cyanotic
Systemic arterialsaturation is low.
Pulmonary bloodflow can beincreased ordecreased.
Mixing of bloodwith and withoutoxygen
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Acyanotic Heart Defects
PDA ASD
VSD
AV canal Coarctation of the Aorta
Aortic Stenosis
Pulmonary Stenosis
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Cyanotic Heart Defects«
Tetralogy of Fallot (TOF) (has VSD)
Pulmonary Atresia with IVS (no VSD)
Transposition of the Great Vessels
Total Anomalous Pulmonary VenousReturn (TAPVR)
Truncus Arteriosus
Tricuspid Atresia Hypoplastic Left Heart Syndrome
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Atrial Septal Defect (ASD)
Abnormal holebetween the twoatria.
Excess blood movesfrom L to R throughhole causing increasedflow to RV and thento lungs.
This causes the heartto work harder
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Signs & Symptoms of ASD«
Usually asymptomatic ininfancy and early childhood,may wait to see if close onown.
May show s/s of CHF
Shortness of Breath Difficulty feeding Poor weight gain
Enlarged right heart Pulmonary hypertension can
occur in time Atrial dysrhythmias
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Treatment of ASD
Stitch repair
Amplatzer
Patch repairClosure recommendedbefore 5 years of age.
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Placing the Amplatzer
during Heart Catheterization
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Ventricular Septal Defect (VSD)
Most common cardiac lesion
Many close spontaneously
A hole or holes occurs between the
Left and Right ventricles Higher pressure on left causes
blood to leak back into the RV
Can cause enlargement of RV andthen weakening of the muscle
Repair to control CHF and maintainadequate growth
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VentricularSeptalDefect(VSD)
Sites
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Signs & Symptoms of a VSD«
Enlargement of the right heart fromincreased volume of blood. Possible lung congestion/CHF (moderate
sized defects)
Arrhythmias Inflammation
Treatment:
Stitches/Patches Closure device-not recommended-too
problematic
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Patent Ductus Arteriosus
Increased pulmonaryblood flow.
Ductus arteriosus fails toclose after birth.
Normal lungs releasebradykinin causingconstruction of smoothmuscle in ductus
Hypoxia problems prevent
the release of bradykininso remains open Oxygenated blood flows
from aorta back into thelungs.
Connects aorta & pulmonary arteries
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Signs & Symptoms of PDA«
May show no problems initially In time will show s/s of CHF Failure to thrive SOB on exertion
´Cold sweatµ Respiratory infections Bounding pulsesTreatment: Indomethacin or ibuprofen for
premature infants Surgery to tie off or divide if large Coil implantation
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Patent Ductus Arteriosus (PDA)
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Patent Ductus Arteriosus (PDA)
Size of thevesseldetermines
procedure used.
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Coarctation of the Aorta (COA)
Pinching or narrowing of part ofthe aorta that sends oxygenatedblood from the heart to the restof the body. Could extend to asection of the aorta. Increased
risk of stroke.May have hypoplastic aortic arch
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Signs & Symptoms of Coarc«
May not have anysymptoms until older orneed emergency surgery atbirth.
Higher BP to upper body sohigh risk of stroke. CheckBP in all 4 extremities.
Decreased or absent pulses
to lower body.
Blood flow to lower bodyalso reduced including the
kidneys and gut.
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Signs & Symptoms of Coarc cont«
Increased pressure above thenarrow area causing LV to workharder causing ventricle toenlarge then become weakened.
Blood then backs up into thelungs and CHF develops.
May present as a shelf-likeobstruction
May present as a tubularobstruction
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SubclavianFlap Repair
Repair of Coarctation of the AortaRepair approach dependent on proximity of other
structures, severity of side effects, and age ofchild at diagnosis
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Coarctation Repair
End to End
Anastomosis:
Uses lateral thoracotomy entryClosed heart procedure
End to end or end to side of
anastomosis preferred repairRe-coarctation after neonatalrepair not uncommon
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Balloon Angioplasty for Coarctation Repair«
Effective for reducing discrete coarctation and/or add stent
to keep open.Can develop tearing or aneurysm formation in the aorta
Heart Cath procedure:
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Coarctation of the Aorta«
Post op issues: Incision issues-picking child up
High blood pressure ² dam effect, willcome back from surgery with meds to
help and go home with meds. Body has adjusted to needing high
pressure to make blood flow.
Lower part of body may have adjustedto the lesser volume of blood and havesmaller vessels.
Development of collaterals
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Cyanotic Heart Defects«
Increasedpulmonary bloodflow
T
ransposition ofthe greatarteries(mixed defect)
T runcus
arteriosus T APVR
Decreasedpulmonary bloodflow
Pulmonaryatresia T ricuspid atresia **Tetrology of
Fallot (TOF)**
**Know for exam
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Tetrology of Fallot (TOF)1. PS - severity of
condition depends ondegree of obstruction.
2. VSD3. Overriding aorta
4. Hypertrophic RV
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Signs & Symptoms of TOF..
Cyanosis at birth Pink vs. Blue T et
Murmur
Crying leads to cyanosis
Leads to irritability and
then can become
unresponsive (´T et spellµ)
Pulmonary artery may be hypoplastic,nonconfluent, and supplied by aortopulmonarycollaterals.
Size dictates surgical repair
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Managing a ´Tet Spellµ«
A sudden change in blood flow from LR«to RL«
Prolonged spellsyncope, seizure, arrest
Knees to chest/squatting position to
decrease venous return from legs andraise systemic vascular resistance thusdecreasing R to L flow.
Oxygen
Morphine Inderal
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Repair of TOF
Palliative repair withBlalock-TaussigShunt getting blood
to the lungs. Open and patch
Pulmonary Artery
VSD patch
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Surgery for CHD (Pre-op)«
Knowledge deficit: child/family Promote nutrition (feeding tubes)
Altered cardiac output - fluid volumeexcess, pulmonary hypertension,
increased blood flow to lungs, CHF,frequent respiratory infections Activity intolerance ² fatigue,
weakness, disease process, circulatory
compromise Risk for infection ² debilitatedphysical status
Altered growth and development ²
decreased oxygenation
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The Post-Op Heart« Decreased Cardiac Output - surgical
complications, bleeding, fluid shifting Altered Comfort ² incision site,
treatments and procedures
Risk for infection ² from surgery,
and IV lines
Compromised Family Coping ² from
child·s surgery, child·s hospitalization,
lack of support systems, financial
considerations
Activity Intolerance ² post op status Altered Growth and Development ²
from underlying disease process
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Caring for the Child and Family...
Coping ² keeping family updatedat all times with the plan ofcare.
Educate regarding meds,therapies, and procedures
Allow family to help with care
when appropriate. ATC visiting. Encourage caringfor self.
Allow personal items at bedside.
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The Discharge«
Discuss with DischargeCoordinator
Wound care Medications Monitoring progress Nutrition needs
Activities Equipment needs Educational needs
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Congestive Heart Failure«CHF is a group of signs andsymptoms that reflect theheart·s inability to effectivelypump blood to meet the
metabolic requirements of thebody. The body wants equal amountsof blood going to the body
and the lungs to maintain afluid balance.
When one exceeds the other
heart failure occurs.
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Etiology of CHF in Children«
Heart rate- Arrhythmias: SVT , VT ,
Bradycardia
Preload- Shunt lesions: VSD, AV canal,Single Ventricle; Anemia and Volume overload
Afterload- Left heart obstructive
lesions: Coarctation, Aortic Stenosis, HT N
Contractility- Myocardial disease:
Myocarditis, Cardiomyopathy
l l f
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Clinical Signs of CHF«
Tachycardia
Pale color
Feeding difficulties
Diaphoresis especially with feeding
Tachypnea with increased WOB Retracting and Grunting and wet lungs
Decreased distal pulses and coolextremities
Facial edema
Distended abdomen, enlarged spleenand liver with weight gain, but FTT
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Treatment of CHF«
Diuretics:- Furosemide (Lasix) 0.5 to 2 mg/kg/dose IV- Hydrochlorothiazide (HydroDiuril) 2-4
mg/kg/day- Chlorothiazide (Diuril) 20-40mg/kg/day- Ethacrynic acid (Edecrin) 1mg/kg/dose- Spironolactone (Aldactone) 1-3 mg/kg/day
Potassium sparing?
Electrolyte changes?
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Treatment of CHF
Digitalis ² Digoxin- T otal Digitalizing Dose 0.04 mg/kg
- Give ½ dose, then ¼ dose in 4-8 hoursand the last ¼ dose in 4-8 hours
- T oxicity: vomiting & arrhythmias- Rarely causes bradycardia (HR < 90)- More concern regarding heart block- T each parents to take HR?
- What should you teach?- Maintenance dose: 10 mcg/kg/daydivided
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Treatment of CHF«
Reducing Afterload (ACE Inhibitors)
- Enalapril: 0.1 mg/kg (may increase to 0.2-0.3mg/kg/day)
- Captopril: Neonates: 0.1-0.4 mg/kg/dose every6-24 hrInfants: 0.5-0.6 mg/kg/day dividedevery 6-24 hrChildren: 25 mg/day divided every 12
hrsAdolescents: begin 25 mg T ID, Max450 mg
Works by causing vasodilation of peripheral vessels.
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Nursing Care Plan for Child with CHF
Increased caloric requirements Infection control issues-handwashing
Energy conservation (frequent naps)
Balance fluids and electrolytes (labs) Do they have IV fluids running on
top of their feedings? Look at totalvolume intake.
Medication administration
Monitor results of above
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Acquired Heart Disease«
Rheumatic Fever
Bacterial Endocarditis
Kawasaki·s Disease
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Rheumatic Fever«
Autoimmune reaction to Group ABeta-hemolytic streptococcal(GABHS) pharyngitis.
It involves joints, skin, brain, heart
valves, blood vessels Major cardiac findings of RF is
inflammation of the heart in:endocardium, pericardium, and
myocardium Less frequent in US due to quickdiagnosis and antibiotic treatmentof strep throat or scarlet fever.
S/S Rh ti F
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S/S Rheumatic Fever«
Joint inflammation - swelling, tenderness,and redness over multiple joints. Usuallythe larger joints in the knees or ankles.T he inflammation "moves" from one joint toanother over several days.
Small nodules or hard, round bumps underthe skin Change in the child's neuromuscular
movements: chorea Rash - a pink rash with odd edges that is
usually seen on the trunk of the body orarms and legs. Fever, weight loss, fatigue, stomach pains
Jones Criteria
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Major Manifestations* Minor ManifestationsCarditis Clinical features:
Polyarthritis Arthralgia and Fever
Chorea Laboratory features:Erythema marginatum 1. Previous infection (ASO)
Subcutaneous nodules 2. Elevated Sed Rate (ESR)
Aschoff bodies 3. Positive C-reactive protein4. Prolonged PR interval
Supporting Evidence of Previous Group A Strep Infection:1. Positive throat culture or rapid streptococcal antigen test
2. Elevated or increasing streptococcal antibody titer
*The presence of two major or of one major and two minor manifestationsindicates a high probability of acute rheumatic fever if supported by
evidence of previous group A streptococcal infection.
Jones Criteria
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Jones Criteria Terminology«
C-Reactive Protein ² marker for acuteinflammation
Antistreptolysin-O titer (ASO) -streptococcal antibody tests for
previous infection Erythrocyte sedimentation rate
(ESR) ² used to monitor inflammatoryor malignant disease
Subcutaneous nodules (Aschoffbodies)
Histological findings
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Management of RF«
Administration of Penicillin Prevent permanent heartdamage
Treat other symptoms Prevent recurrences of RFthrough prophylactic use of
antibiotics
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Nursing management of RF«
Encourage compliance with medsespecially for long-term therapy.
May need monthly IM injections if
non-compliant Assist with recovery from s/s--chorea movements are particularly
frustrating Emotional support
Prevent recurrence
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Bacterial Endocarditis
Bacteria in the bloodstream lodge onabnormal heart valves or otherdamaged heart tissue.
Certain normal bacteria that live onparts of your body can enter thesystem through surgical and dentalprocedures which cause a briefbacteremia.
Although bacteremia is common aftermany invasive procedures, only certainbacteria commonly cause endocarditis.
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Risks of Bacterial Endocarditis«
Microorganisms grow on theendocardium that is subjected toturbulence within the heart.
An artificial (prosthetic) heart valve
Heart valves damaged (scarred) byconditions such as rheumatic fever
Congenital heart or heart valve
defects (narrowing) Mitral valve prolapse with a murmur
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Risks of Bacterial Endocarditis«.
Hypertrophic cardiomyopathy Patients who already have somekind of heart problem have a
greater risk² Children with congenital, rheumatic,or degenerative heart diseases havea 60-80% risk
Drug abusers have a much higherrisk of getting endocarditis.
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S/S of BE«
Low-grade intermittent fever New heart murmur Anorexia, myalgias, HA
Enlarged spleen Petechiae oral mucosa Osler nodes: painful nodules--sign of vasculitis
Janeway spots/nodules: painlesshemorrhagic areas on palms and soles
Roth·s spots: retinal hemorrhages
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A ² C are Osler Nodes and were painful
D is a Janeway Lesion and was non-tender
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Bacterial Endocarditis
Treatment: Penicillin IVfor 4-6 weeks
70% streptococcal species
20% staph species 10% other: H flu, fungal,
gram negative bacteria
May need prophylaxis for
procedures but this ischanging
May need surgicalintervention
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Kawasaki·s Disease«
A.K.A. ´mucocutaneous lymphnode syndromeµ
This condition was described byDr Kawasaki in Japan in the
1960s and is an inflammation ofthe arteries of the body -probably triggered by a virusinfection. The danger in the
disease is that the inflammationcan cause damage to thecoronary arteries and affect theheart muscle.
k ·
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Kawasaki·s Disease«
80% are under 5 years of age Peak incidence in toddlers
Boys > Girls
Without treatment, 20-25% candevelop damage to blood vesselsthat supply the heart³esp.
Coronary dilation Greatest risk in <1 yr of age
Will form aneurysms
k · D
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Kawasaki·s Disease«
Specific cause is unknown(possibly a virus)
Progressive inflammation of small andmedium sized vessels (vasculitis).
Walls can become damaged to the pointof developing coronary artery
aneurysms in some which can lead toblood clot formation.
Ph f K k ·
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Phases of Kawasaki·s«
Acute phase: abrupt onset of highfever that doesn·t respond toantibiotics or antipyretics. Symptomsthen progress
Subacute phase: resolution of fever,high risk of developing coronary arteryaneurysms. Peeling begins
Convalescent phase: all clinical signshave resolved. Lab values altered.Resolved at the end of 6-8 weeksafter onset.
S/S f K ki· Di
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S/S of Kawasaki·s Disease«
Requires 5 of 6 principle criteria Fever ranging between 38-41° C Discrete conjunctival injection
without exudate
Changes in the mouth consistingof:--Erythema of lips--Strawberry tongue--Diffuse oropharyngeal
erythema
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S/S of Kawasaki·s Disease
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Polymorphous erythematous rash
Changes in the hands and feet consistingof:
--Firm indurative peripheral edema--Diffuse erythema of palms and soles--Convalescent desquamation of digits,
palms, and soles Unilateral cervical lymphadenopathy
S/S of Kawasaki s Disease
T t t f K ki·
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Treatment for Kawasaki·s«
Reduce fever, rash, joint inflammation,pain and to help prevent blood clots fromforming.
--Aspirin 80-100 mg/kg/day, every 6 hours(once fever resolved reduce aspirin to 3-5mg/kg/day, give daily)
Decrease the risk of developing coronaryartery abnormalities (when given early)
--IV Immune Globulin (2g/kg) give over10-12 hours (special blood product)
Treatment for Kawasaki·s
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Treatment for Kawasaki s
For patients with coronary arteryaneurysms, blood clots or high risk:
Warfarin (Coumadin),
Lovenox (injection)
High dose aspirin Once the fever has resolved aspirin
dose is reduced.
Once stable child can go home. Aspirinis usually continued for weeks orindefinitely.
F/U monitoring