Download clinical manifestations

Dr BASHAR HAGALI
Chief Of Public Hospitals In MOH
Introduction
 . Even in developed countries, rheumatic fever has not
been entirely eradicated.
 The overall incidence in the United States is less
than 1 per 100,000.
 There have been regional resurgences, such as in Utah
in the 1980s, with an incidence of nearly 12 per 100,000
children between the ages of 3 and 17 years.
ETIOLOGY AND EPIDEMIOLOGY
 acute rheumatic fever remains an important
preventable cause of cardiac disease.
 It is most common in children 6 to 15 years of age.
 It is due to an immunologic reaction that is a delayed
sequela of group A beta-hemolytic streptococcal
infections of the pharynx.
 A family history of rheumatic fever and lower
socioeconomic status are additional factors.
CLINICAL MANIFESTATIONS
 It is diagnosed using the clinical and laboratory findings of the revised
Jones criteria
 Arthritis is the most common major manifestation.
 Arthralgia cannot be used as a minor manifestation if
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arthritis is used as a major manifestation.
Carditis occurs in about 50% of patients.
Tachycardia, a new murmur (mitral or aortic
regurgitation), pericarditis, cardiomegaly, and signs of
heart failure are evidence of carditis.
Erythema marginatum, a serpiginous, nonpruritic, and
evanescent rash
Subcutaneous nodules are seen predominantly with
chronic or recurrent disease.
Chorea (Sydenham chorea or St. Vitus dance) consists of
neurologic and psychiatric signs
CLINICAL MANIFESTATIONS
 Previous rheumatic fever or rheumatic heart
disease Polyarthralgia Fever
Laboratory
 Laboratory :
Acute phase reaction: elevated
erythrocyte sedimentation rate, ESR
 C-reactive protein, CRP
 leukocytosis WBC
 Prolonged PR interval
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Supporting evidence of preceding streptococcal
infection
Diagnosis
 Clinical ( rare )
 Laboratory ???
 Over diagnosed in Clinical Practices
TREATMENT And PREVENTION
 Management : benzathine penicillin to eradicate the beta
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hemolytic streptococcus, anti-inflammatory therapy
Salicylates after the diagnosis is established,
Bed rest. Additional supportive therapy for heart failure or
chorea may be necessary during the acute presentation.
Long-term penicillin prophylaxis, preferably with
intramuscular benzathine penicillin G, 1.2 million U
every 28 days, is required.
Oral regimens for prophylaxis generally are not as effective.
TREATMENT And PREVENTION
 Treatment after the Acute Episode:
- Penicillin G Benzathine
600,000 units for less than 27 kg, 1.2 million units for
more than 27 kg intramuscularly every 4 weeks is the
drug of choice.
 Sulfadiazine
 Penicillin V
 Erythromycin
Prognosis
 The prognosis of acute rheumatic fever depends on the
degree of permanent cardiac damage.
 Cardiac involvement may resolve completely,
especially if it is the first episode and the prophylactic
regimen is followed.
 The severity of cardiac involvement worsens with
each recurrence of rheumatic fever.
Residual Valvular Damage
 the mitral and aortic valves are most commonly
affected by rheumatic fever and the severity of carditis
is quite variable
‫شكرا لكم‬
Dr BASHAR HAGALI
Chief Of Public Hospitals In MOH
Etiology of Heart Failure
 Fetus :
Severe anemia (hemolysis, fetal-maternal transfusion,
hypoplastic anemia) Supraventricular tachycardia
Ventricular tachycardia Complete heart block
Atrioventricular valve insufficiency High-output cardiac
failure (arteriovenous malformation, teratoma)
 Premature Neonate: Fluid overload PDA VSD Cor
pulmonale (BPD)
 Full-Term Neonate: Asphyxial cardiomyopathy
Arteriovenous malformation (vein of Galen, hepatic) Leftsided obstructive lesions (coarctation of aorta, hypoplastic
left heart, critical aortic stenosis) Transposition of great
arteries Large mixing cardiac defects (single ventricle,
truncus arteriosus) Viral myocarditis Anemia
Supraventricular tachycardia Complete heart block
Etiology of Heart Failure
 Infant-Toddler : Left-to-right cardiac shunts (VSD)
Hemangioma (arteriovenous malformation) Anomalous
left coronary artery Metabolic cardiomyopathy Acute
hypertension (hemolytic-uremic syndrome)
Supraventricular tachycardia Kawasaki disease
Postoperative repair of congenital heart disease
 Child-Adolescent :Rheumatic fever Acute hypertension
(glomerulonephritis) Viral myocarditis Thyrotoxicosis
Hemochromatosis-hemosiderosis Cancer therapy
(radiation, doxorubicin) Sickle cell anemia Endocarditis
Cor pulmonale (cystic fibrosis) Arrhythmias Chronic upper
airway obstruction (cor pulmonale) Unrepaired or palliated
congenital heart disease Cardiomyopathy
CLINICAL MANIFESTATIONS
poor feeding
 failure to thrive
, tachypnea, and diaphoresis with feeding.
 Older children may present with shortness of
breath, easy fatigability,
edema.
CLINICAL MANIFESTATIONS
Tachycardia, a gallop rhythm, and thready pulses
may be present with either cause.
 If left-sided failure is predominant, tachypnea,
orthopnea, wheezing, and pulmonary edema are
seen.
 If right-sided failure is present, hepatomegaly,
edema, and distended neck veins are present.
IMAGING STUDIES
 Chest radiography, are not specific
 An echocardiogram
Treatment of Heart Failure
 General Care:
- Rest : Reduces cardiac output
- Oxygen : Improves -oxygenation in presence of
pulmonary edema
- Sodium, fluid restrictions: Decreases vascular
congestion; decreases preload
- Diuretics( Furosemide) Salt excretion by ascending loop
of Henle: reduces preload; afterload reduced if
hypertension improves; may also cause venodilation
- Combination of distal tubule and loop diuretics :
Greater sodium excretion
Treatment of Heart Failure
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Inotropic Agents
-Digitalis Inhibits membrane Na+, K+-ATPase and increases intracellular Ca2+, improves cardiac
contractility, increases myocardial oxygen consumption
- Dopamine Releases myocardial norepinephrine plus direct effect on β-receptor, may increase
systemic blood pressure; at low infusion rates, dilates renal artery, facilitating diuresis
Dobutamine β1-receptor agent; often combined with dopamine
Amrinone/milrinone Nonsympathomimetic, noncardiac glycosides with inotropic effects; may
produce vasodilation
 Afterload Reduction
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Hydralazine Arteriolar vasodilator
Nitroprusside Arterial and venous relaxation; venodilation reduces preload
Captopril/enalapril Inhibition of angiotensin-converting enzyme; reduces angiotensin II
production
Other
Mechanical counterpulsation Improves coronary flow, afterload
Transplantation Removes diseased heart
Extracorporeal membrane oxygenation Bypasses heart
Carvedilol