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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 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 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 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 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 - - 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