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INFECTIVE ENDOCARDITIS

ACQUIRED HEART • Acute and Subacute, non bacterial

DISEASE • Significant cause of morbidity and


mortality among children and
Maria Dolores B. Victor, M.D.
Department of Child Health
adolescents
FEU Hospital

EPIDEMIOLOGY ETIOLOGY
Streptococcus viridans leading causative agents
• Most often a complication of congenital Staphylococcus aureus in pediatric patients

or RHD Staph. Endo: No Heart Disease


S. viridans: After dental proc.
• Can occur in children without heart
Grp D. Enterococci: Lower bowel or G-U manipulation
disease Pseudomonas: IV drug users
Fungal organisms: After open heart surgery
• Rare in infancy

• Prevalence: 0.5 – 1 per 1000 hospital b. Predispose to endocarditis


admission -all CHDs except ASD secundum
• Pathogenesis: -rheumatic heart disease
a) Two factors are important: -prosthetic heart valves
1. presence of structural abnormalities of -MVP with mitral regurgitation
the heart
-HOCM
2. bacteremia
-drug addicts

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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

CLINICAL MANIFESTATIONS LABORATORY FINDINGS


 Signs:
• Blood culture
5. Embolic phenomena 90% of case (+) in 1st two blood cultures
a. Pulmonary emboli
b. Seizure • Culture other secretions
c. Hemiparesis • Echocardiography:
d. Hematuria
e. Roth spot ( retinal hemorrhage )
-valvular vegetations
-valve dysfunction
6. Clubbing of fingers
-embolic complications
7. Heart failure and arrhythmia

DIAGNOSIS PROGNOSIS

• High index of suspicion • Fatal in the pre-antibiotic era

• 20-25% mortality
• Blood culture
• 50-60%: serious morbidity 2º HF

• Pulmonary and systemic embolism

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TREATMENT PREVENTION

1.Treatment is started with penicilin or


Oxacillin plus Gentamycin • Antimicrobial prophylaxis prior to
2.Final selection of antibiotics is based on various procedures (dental,
the organism isolated and antibiotic
sensitivity respiratory, G-1 and g-U tracts)
3.Duration of treatment: 4-6 weeks
4.Operative intervention

Prophylactic regimens
A.For dental,oral,respiratory tract or esophageal
KAWASAKI DISEASE
procedures

Situation Agent Regimen • Acute febrile condition primarily affecting


Standard general Amoxicillin C:50mg/kg PO children
prophylaxis 1hr before procedure
A:2 g PO 1hr before • Association with vasculitis of coronary
procedure
blood vessels
Unable to take oral Ampicillin C:50mg/kg IM or IV within 30
medications min before procedure • Constellation of other systemic complaints
A:2 g IM or IV within 30 min
before procedure

ETIOLOGY EPIDEMIOLOGY
• 1st reported in Japanese children
• UNKNOWN • Leading cause of acquired heart disease in

• Bacterial toxins similar to staphylococcus US and recognized worldwide


• Peak age incidence : 1 – 2 years
toxins of TSS
- 50 % of cases occur before the age of 2 years
- ~80 % occur before the age of 5 years
- seldom beyond the age of 8 years

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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

Conjunctival injection Changes in the mouth


• Discrete vascular injection of bulbar
conjunctivae • Erythematous, fissuring, peeling, and
bleeding of lips
• Ocular discharge and corneal ulceration • Diffuse erythema of the oropharynx
do not occur • Strawberry tongue

Changes in the peripheral


Erythematous rash
extremities
• In the acute phase- firm induration of • Usually truncal, polymorphous,
hands and feet nonvesicular and without crusts
• Diffuse and deep erythema of hands and • Maybe morbilliform, maculopapular or
soles scarlatiniform
• Desquamation of fingertips and toenails on • May resemble erythema multiforme
the second week
• Transverse grooves across fingernails 2-3
months after onset ( Beau’s lines )

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Enlarged lymph node CHARACTERISTICS CLINICAL SIGNS

• Usually unilateral and cervical C. Illness not explained by other known


disease process
• Occurs in more than half of the patients
• The node usually measures more than 1.5
cms *Incomplete or Atypical Kawasaki: more
common in patients <1 yr of age
• Usually non-fluctuant, nontender or only
slightly tender
Cardiac involvement: 10-40%: Coronary
Vasculitis/ aneurysms

Incomplete ( Atypical ) Kawasaki LABORATORY FINDINGS


- patients who do not fulfill the criteria for 1. Leukocytosis- typical during acute stage ; 50 % of
patients have WBC count > 15,000
Kawasaki disease
2. Anemia
- more common in young infants 3. Elevated ESR and CRP – universal in KD,
returning to normal by 6 to 10 wks after onset of
illness

- should be considered in all children with 4. Abnormal plasma lipids


unexplained fever for >5 days associated 5. Hypoalbuminemia
with 2 or 3 of the principal features of KD 6. Hyponatremia

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

DISEASES OF THE • Long-standing volume/ pressure load


• Chronic hypoxia
MYOCARDIUM
• Others

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

All children: 36/100,000 (dilated cardiomyopathy)


• The classification is based on the
2/100,000 (hypertrophic & restrictive
anatomic and functional features of the
cardiomyopathy)
heart

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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.

1. Dilated Cardiomyopathy 1. Dilated Cardiomyopathy


• Diagnosis
1. ECG: sinus tachycardia, combination of • Management
atrial enlargement, varying degrees of left 1. Aggressive treatment of CHF –
and right ventricular hypertrophy, non- digoxin, diuretics, vasodilators
specific T-wave abnormalities 2. Critically ill children: intubation, IV
2. CXR: cardiomegaly, with or without signs inotropes
of pulmonary edema 3. Antiarrhythmia
3. Echo: dilatation of heart and poor 4. Cardiac transplant
contractility

1. Dilated Cardiomyopathy 2. Hypertrophic Cardiomyopathy

• Familial disorder of the heart muscle


• Prognosis: progressive deterioration is • 30 – 60 % transmitted as autosomal
the rule rather than the exception. About dominant trait
2/3 of patients die from intractable heart
failure within 4 years after the onset of • Pathology and pathophysiology:
symptoms of CHF
1. Most characteristic abnormality is the
hypertrophied LV, with ventricular cavity
usually small or normal in size

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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

2. Hypertrophic Cardiomyopathy 3. Restrictive Cardiomyopathy


• Treatment
• Extremely rare form of cardiomyopathy
1. No standard treatment
• Maybe idiopathic, or associated with systemic
2. Moderate restriction of physical activities
diseases, malignancies, or radiation therapy
3. Digitalis and aggressive diuresis is
contraindicated • Characterized by markedly dilated atria and
generally normal ventricular dimensions.
4. B-blocking agents ( Propranolol) and calcium
channel blocking agents ( Verapamil ) have
Diastolic filling is impaired, resulting from
been use with success excessively stiff ventricular walls.
5. Pacemakers • Contractile function of the heart is normal
6. Surgery : ventricular septal myotomy

3. Restrictive Cardiomyopathy 3. Restrictive Cardiomyopathy


• Clinical manifestations • Diagnosis
1. History of exercise intolerance, 1. ECG : prominent P waves, atrial
weakness, chest pain fibrillation or supraventricular tachycardia
2. In its full-blown form: dyspnea, edema, 2. CXR : mild to moderate cardiomegaly,
pulmonary congestion, effusion
ascites, hepatomegaly, increase venous
pressure , pulmonary congestion 3. Echo : diagnostic; markedly enlarged
atria and small to normal sized ventricles.
Systolic function is normal. Atrial
thrombus maybe present

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3. Restrictive Cardiomyopathy CLASSIFICATION OF CARDIOMYOPATHIES ACCORDING TO

• Treatment STRUCTURAL AND FUNCTIONAL ABNORMALITIES

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

CLASSIFICATION OF CARDIOMYOPATHIES ACCORDING TO


STRUCTURAL AND FUNCTIONAL ABNORMALITIES
CLASSIFICATION OF CARDIOMYOPATHIES ACCORDING TO
STRUCTURAL AND FUNCTIONAL ABNORMALITIES DILATED HYPERTROPHIC RESTRICTIVE

CLINICAL  All age group  Many are  Dyspnea, edema,


MANIFESTATI affected with asymptomatic; ascites,
DILATED HYPERTROPHIC RESTRICTIVE ON insidious onset hepatomegaly,
 50%- heart murmur
EPIDEMIOLOGY Inherited in an  irritability, anorexia, or affected family ↑venous pressure,
autosomal dominant abdominal pain, member pulmonary
pattern cough, dyspnea on  Weakness, fatigue, congestion

Greater tendency for exertion⇒ heart DOE, palpitations,  Heart: mildly


RVOTO failure angina pectoris, enlarged
 Holosystolic dizziness, syncope nonspecific
LV wall diffusely
murmurs of MR Brisk pulse, systolic murmurs
thickened 

and TR murmur at left


 Cardiomegaly sternal edge and
apex

CLASSIFICATION OF CARDIOMYOPATHIES ACCORDING TO


CLASSIFICATION OF CARDIOMYOPATHIES ACCORDING TO
STRUCTURAL AND FUNCTIONAL ABNORMALITIES
STRUCTURAL AND FUNCTIONAL ABNORMALITIES
LABORATORY DILATED HYPERTROPHIC RESTRICTIVE
DIAGNOSIS DILATED HYPERTROPHIC RESTRICTIVE
EKG  Bi-atrial enlargement  LVH with or without ST  Prominent P waves
segment depression ST segment PROGNOSIS Progressively Unpredictable, esp. Generally poor
LVH, nonspecific
Twave abnormalities and Twave inversion depression downhill course, in asymptomatic
T wave inversion survival beyond patient
Chest  Cardiomegaly,  Mild cardiomegaly with Mild to moderate one year is poor Progress to chronic
Roentgenogram pulmonary LV prominence cardiomegaly
congestion, pleural heart failure
effusion
Risk for sudden
Echocardiogram  Dilated LA, LV, poor  LVH affecting intravent, • Biatrial death caused by
contractility, septum, SAM of AMVL, enlargement,
LVOTO arrhythmia
pulmonary normal ventricular
hypertension chambers
Cardiac  Assess patient’s
Catheterization candidacy for surgery

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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

Rheumatic Fever Characteristics of Strep Throat


Clinical Strep throat Non-strep throat
• Valvular damage is one of the most serious Characteristics
complications of this disease, with a mitral valve
Age 5 – 15 years All ages
predilection, followed by aortic valve, TV, PV
Onset sudden gradual
• Aschoff bodies are the characteristic findings on
histopath Initial symptom Sore throat with pain on Mild sore throat
swallowing
• Symptoms are seen after 3-5 weeks , preceding
Appearance of Redness, hyperemia Redness of
strep throat infection Edema. Exudates,
throat pharnyx
- Average latent period: 3 weeks after infection enlargement of tonsils with
- Chorea has a longer latent period of 3-6 months exudates
Signs and symptoms which are characteristics of RF Fever High Not so high
maybe classified under Jones criteria Other signs Tender anterior cervical Cough,
LN,scabby erosions on hoarseness,watery
nostrils. Clinical picture of nasal discharge,
scarlet fever conjunctivitis

Jones Criteria Jones Criteria


• Major • Minor
1. Carditis 1. Clinical
• Two major criteria or 1 major plus 2
2. Polyarthritis - Fever minor criteria
- Arthralgia
3. Chorea - Plus evidence of a preceding strep
4. Erythema marginatum 2. Laboratory infection indicate a high probability of RF,
5. Subcutaneous nodules - Increase ESR/ CRP EXCEPT in 3 cases:
- Prolong PR interval
1. Chorea
2. Insidious or late-onset carditis
Plus : supporting evidence of antecedent group A strep infection
1. Positive throat culture or rapid streptococcal antigen test 3. Rheumatic recurrence
2. Elevated ASO titer

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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)

Chorea Subcutaneous Nodules

• St. Vitus’ dance • Small, non-tender pea-sized nodules that


• A triad of involuntary movements, muscular appear over the extensor surface of the joints
weakness, and emotional disturbance • Uncommonly seen, last only for 1 to 2 weeks
• More common in females • When present, is often in association with
• Characteristic involuntary movements usually carditis
begins in the face and affects the arms more
than the legs
• Disappears during sleep
• Long latent period of 3 – 6 months

Erythema Marginatum Management

• Rare, seen in less than 10 % • Rest


• Occurs only in patients with carditis • Anti inflammatory drugs
• A macular, non-pruritic, pink rash with pale - Aspirin
center - Prednisone
• Affects the trunk and proximal limbs, do not • Anti-decongestive- inotropes, diuretics,
involve the face afterloaders
• Application of heat may accentuate the • Primary prevention
appearance of lesions • Secondary prevention

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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

Duration of Secondary Prophylaxis Anti-inflammatory Therapy In RF


• Arthralgia or mild arthritis, no carditis – analgesics only
• RF without carditis -- 5 years or until age 21 years,
whichever is longer • Moderate or severe arthritis; no carditis, or carditis without
heart failure -- Aspirin 90 – 100 mg/kg/day for 2 weeks,
longer if necessary
• RF with carditis but no residual heart disease – 10 years
or well into adulthood whichever is longer
• Carditis with failure; with or w/o joint manifestations -
Prednisone 40 – 60 mg/day, after 2 – 3 wks slow
• RF with carditis and residual heart disease – at least 10 withdrawal to be completed in 3 more weeks
years since last episode and at least 40 years old,
- Aspirin to overlap for 4 – 6 weeks after discontinuation of
sometimes lifelong prophylaxis
Prednisone

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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