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EPIDEMIOLOGY ETIOLOGY
Streptococcus viridans leading causative agents
• Most often a complication of congenital Staphylococcus aureus in pediatric patients
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CLINICAL MANIFESTATIONS CLINICAL MANIFESTATIONS
Signs:
Symptoms:
1. Fever ( 38 to 39 C in 80 – 90 % )
1. Fever
2. New heart murmur in 100 %
2. Chills
3. Fatigue
3. Splenomegaly
4. Loss of appetite
4. Skin manifestations from emboli in 50 %
a. Petecchiae
5. Pallor
b. Osler’s nodes- tender nodes at ends of
6. Chest and abdominal pain fingers
7. Arthralgia c. Janeway lesions- hemorrhagic areas at
8. Weight loss palms and soles
9. CNS manifestations – stroke, seizures, headache d. Splinter hemorrhages- linear lesions
berneath the nails
DIAGNOSIS PROGNOSIS
• 20-25% mortality
• Blood culture
• 50-60%: serious morbidity 2º HF
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TREATMENT PREVENTION
Prophylactic regimens
A.For dental,oral,respiratory tract or esophageal
KAWASAKI DISEASE
procedures
ETIOLOGY EPIDEMIOLOGY
• 1st reported in Japanese children
• UNKNOWN • Leading cause of acquired heart disease in
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CHARACTERISTIC CLINICAL SIGNS Fever
A. Fever for at least 5 days
• More than 5 days
PLUS • Generally high, abrupt, and sustained
B. Presence of four of the following: with peak temperatures exceeding 40 C
1. Bilateral nonpurulent conjunctival injection
2. Changes in the mucosa of oropharynx: • Persists for an average of 12 days
infected pharynx, dry fissured lips, strawberry tongue • May not respond to antipyretics
3. Changes of the peripheral extremities
-edema/ erythema of hands on feet • Usually resolves in 1-2 days after
-desquamation treatment with intravenous gamma
4. Rash-truncal, polymorphus, nonvesicular
5. Cervical lympahdenopathy
globulin
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Enlarged lymph node CHARACTERISTICS CLINICAL SIGNS
LABORATORY PROGNOSIS
7. Thrombocytosis- a characteristic feature of the later
• Complete recovery in those without
phase of illness; platelet counts ranging from 500,000 to >
1 million ; rarely present in the 1st week of illness, usually coronary vasculitis
appears in the 2nd week, and peaks in the 3rd week with
gradual return to normal by 4 to 8 weeks after onset
• 1-2% die with cardiac complications:
*A low platelet count at illness presentation is a risk HF, arrhythmia, MI
factor for coronary aneurysm
8. Sterile pyuria
9. Elevated serum transaminases
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TREATMENT
• IVIG during acute febrile disease : 2 gm/k • Measles and varicella immunizations
single dose over 10-12 hr infusion should be deferred for 11 months after a
child receives high dose IVIG
given within 10 days from onset of fever
• Salicylate : 80 – 100 mg/kg in 4 divided
doses
• Thrombolytic therapy
• Unoperated CHD
Cardiomyopathy CAUSES:
• CARDIOMYOPATHY:
• Is a disease of the heart muscle itself, not
Specific Gene Defects
associated with congenital, valvular or
Prior Viral Myocarditis
coronary heart disease
1.Primary or idiopathic Prevalence in newborn period:
2.Secondary 10 per 100,000 livebirths
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1. Dilated Cardiomyopathy 1. Dilated Cardiomyopathy
• Pathology and pathophysiology: • Clinical manifestations
1. Varying degrees of myocyte hypertrophy 1. Onset is insidious. History of fatigue,
and fibrosis weakness and symptoms of left-sided heart
failure.
2. Weakening of systolic contraction
associated with dilatation of all four 2. History of prior viral infection occasionally is
chambers. Although heart weight is elicited.
increased, the ventricular walls are not 3. Signs of CHF; tachycardia, crackles, weak
thickened peripheral pulses, distended neck veins,
hepatomegaly. Apical impulse is displaced.
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2. Hypertrophic Cardiomyopathy 2. Hypertrophic Cardiomyopathy
• Clinical manifestations
• Diagnosis
1. Many children are asymptomatic
1. ECG : abnormal in majority of patients;
2. Family history is positive for the disease in 30 – LVH with or without ST depression,
60 %
abnormally deep Q waves
3. Easy fatigability, dyspnea, palpitation, or
anginal pain
2. CXR : mild cardiomegaly with
prominence of LV
4. Sudden death may occur with an incidence of
4 – 6 % a year 3. Echo : LVH predominantly affecting the
interventricular septum, concentric
5. Arterial pulse is characteristically brisk, hypertrophy of LV, left ventricular outflow
prominent LV lift obstruction
6. A soft systolic murmur of MR is often present
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3. Restrictive Cardiomyopathy CLASSIFICATION OF CARDIOMYOPATHIES ACCORDING TO
1. Supportive
2. Diuretics to relieve congestive symptoms DILATED HYPERTROPHIC RESTRICTIVE
3. Calcium channel blockers to increase diastolic PATHOPHYSIOLOG Massive Massive ventricular Poor ventricular
compliance Y cardiomegaly⇒ hypertrophy with compliance is the
extensive principal major abnormality⇒
4. Antiarrhythmia/ pacemaker
dilatation of involvement of simulate constrictive
5. Anticoagulation ventricle ventricular septum, pericarditis
6. Heart transplant LV & RV⇒
↑resistance to LV
filling ⇒ LVOTO in
• Prognosis : poor 25%⇒ MR
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CLASSIFICATION OF CARDIOMYOPATHIES ACCORDING TO Rheumatic Fever
STRUCTURAL AND FUNCTIONAL ABNORMALITIES
• Attack rate is 3 % with PR of 1/1000
DILATED HYPERTROPHIC RESTRICTIVE
• Secondary to Group A B-hemolytic
TREATMENT HEART FAILURE NO Heart failure relief streptococcus
treatment STANDARDIZED Calcium channel
Anti-arrhythmic THERAPY blockers
• Pathology and manifestations: found in different
drugs Discourage Anti-arrhythmic
organ systems
Systemic anti- competitive sports drugs a. Heart
coagulation and strenuous Anti-coagulation b. Brain
Heart physical activity c. Joints
Cardiac
transplantation Beta blocker, transplantation d. Skin
calcium channel
blockers • Others organs may be affected-no obvious
Pacemaker for manifestations
arrhythmias
Surgery
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Arthritis
Carditis
• Most serious , occurring in 40 – 50 % • Most common , 75 % ; least specific
• Varies: organic heart murmur, heart enlargement, • affects mostly of large joints ( knees, ankles,
tacchycardia, heart failure elbows, wrist )
• Indicated by apical systolic murmur, apical mid- • Rarely involves small joints
diastolic murmur , basal diastolic murmur, friction
• Asymmetric and polymigratory
rub , gallop rhythm
• Disappears spontaneously w/o leaving joint
• May present as chest pain, palpitations, dyspnea
deformity
• Involves all layers of the heart
• Very good response with salicylates (aspirin)
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Primary prevention- treatment of streptococcal Secondary Prevention- administration of long-
pharygitis to prevent RF acting penicillin for prolonged period of time to patients who
have developed RF to prevent recurrence of attacks
Advantages:
1. Allows eradication of disease
2. Duration of treatment is brief • Benzathine benzyl penicillin 1.2 M units deep IM
3. Prevents severe and irreversible heart damage ( RHD ) from initial every 21 to 28 days
attack of RF
• Benzathine Penicillin G 1.2 M units deep IM single • Penicillin V 250 mg twice daily
dose
• Penicillin V ( Phenoxymethyl Penicillin) 250 mg 3x
daily for 10 days • Erythromycin 250 mg daily
• Erythromycin estolate 20 – 40 mg/kg/day 2 to 4 times
daily for 10 days
The End
“ Med school provides perhaps the best substantiation for Charles Darwin's
Theory of Natural Selection. For here, we see in its cruelest form the survival
of the fittest. Not the smartest, as one should expect. But the fittest to cope
with inhuman pressures, the demands made not only on the brain but on the
psyche... “
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