Case Report



: dr. Sri Sofyani, SpA (K)


: Samuel Edhi Suranta
Theresa Shintauli



dr. Hopefully the content will be useful for everyone in the future. Sri Sofyani. Medical Faculty of North Sumatra University.“ Chronic Heart Failure (CHF) et causa Rheumatic Heart Disease (RHD)”. Adam Malik General Hospital.2 ACKNOWLEDGMENTS We are greatly indebted to the Almighty One for giving us blessing to finish this case report. There were critical but constructive comments and relevants suggestions from the reviewers. 26 November 2015 Presentators . Medan. This case report has gone through series of developments and corrections. and suggestions. SpA (K) for the time spent to give us guidances. We are also indebted to our supervisor and adviser.This case report is a requirement to complete the clinical assistance program in Department of Child Health in H. comments. We are grateful because without her guidance this case report wouldn’t have taken its present shape.

....18 REFERENCES............................. ........iii CHAPTER 1 INTRODUCTION........................................................................................................................................................................................3 TABLE OF CONTENTS ACKNOWLEDMENTS.........6 CHAPTER 3 CASE REPORT..................................................................... CHAPTER 4 DISCUSSION AND SUMMARY...............................................................................................................................................................................................................................4 CHAPTER 2 LITERATURE REVIEW..........ii TABLE OF CONTENTS............................................................................

The most plausible explanations for this geographic discrepancy of disease pattern are poor socio-economic status. this shows that our country.1 Syndrome of heart failure can be caused by various diseases that reduce the heart's pumping ability.696. chronic heart failure is a cardiovascular disease that the incidence and prevalence increase continuously. Heart failure is clinically difficult to recognized.and so it is often difficult to distinguish from other disease outside the heart.8 billion in US and 23 billion in the world. The doctor diagnose results.4 Severity and mortality of acute rheumatic fever and Rheumatic Heart Disease (RHD) has occured in developed country since the turn of 20 th century.2 Chronic heart failure is a serious health problem that have prevalence 5. cardiomyopathy and valvular heart disease. as well as the development of clinical treatments that improve symptoms and quality of life will slow down the progression of the disease and improve the quality of life.4 CHAPTER 1 INTRODUCTION 1. Indonesia. because of the diversity of the clinical situation. especially in infant and children. Infant and children is not a miniature adults size.Systematic study of heart failure in children in the mid-20 th century said thatthe most cause of pediatric heart failure remained rheumatic fever.1 Background Congestive heart failure is a collection of clinical symptoms as a result of structural or functional cardiac disorder that causes impaired ability ventricular filling and ejection of blood throughout the body. Diseases that often lead to heart failure include coronary artery disease. sub standard housing condition. chronic heart failure prevalence is 0. ineffective case finding and inadequate management of initial bacterial pharyngitis. and pharmacological aspects of the heart. Generally rheumatic fever accounts for third of cardiovascular disease in those countries. there are differences in the structure. is still having a very big burden of . According to WHO’s report in 1999 cardiovascular diseases contributes to a third of global deaths of which 78% occured in low and middle-income countries. function. hypertension. Recent developments allow the diagnosis to identify early heart failure. Therefore. and not specific signs in the early stages of the disease. assosiated over crowding. 2 Diagnosing of chronic heart failure is often associated with the mortality and morbidity of the patient that 5 year mortality is as equal as tumour disease. biochemical.this disease is an emergency that is very often encountered by health worker. so complaints and symptoms are often variable.13% or about around 229.3 Nowadays in Indonesia.

2 Objective This case report is the requirement to complete the clinical assistance program in Department of Child Health of H.5 infectious diseases. In addition.5 1. CHAPTER 2 LITERATURE REVIEW . So appropriate diagnosis treatment and public health interventions are very important to control the disease. prevention. Medical Faculty of Sumatra Utara University. and treatment of patient with rheumatic fever and RHD. clinical manifestations. and also the principles of management. diagnostic approaches. Adam Malik General Hospital. This can be effectively implemented by training the health center team as they operate mainly with in the community and have access to the public at large. this case report can be used as reference to know how to define rheumatic fever and RHD according to the epidemiology. pathogenesis.

Endocarditis.7 Clinical Definition: Clinically the term “heart failure” is applied to the syndrome of breathlessness and fatigue associated with cardiac disease.2. This leads to characteristic systemic pathophysiological responses (neural. anemia) may mimic the clinical signs of heart failure as may conditions causing fluid retention (eg. this requirement includes growth and development. Myocarditis virus Baby: VSD. Classification cancer treatment.2. as indicated by an elevated jugular venous pressure and oedema. acute hypertension. hypertension Neonatus: Cardiomyopathy asphyxia. Hemangioma.Cor pulmonale.7 2. COA. AV Block total Neonatus premature: fluid overload. renal and others).6 2. Conditions leading to a mismatch between tissue oxygen delivery and demand (eg. therefore. glomerulonefritis. tirotoksikosis. symptoms and signs. necessitates both the presence of significant cardiac disease and typical symptoms and signs. tachycardia supraventricular. myocarditis. Tachycardia supraventricular. with several definitions. hemokromtosis-hemosiderosis. the commonest being an abnormality of cardiac function whereby heart in unable to pump at a rate commensurate with the requirement of the metabolizing tissues. In case of children.7 2. Definition Congestive Heart failure (CHF) is a complex syndrome. It is often accompanied by fluid retention (“congestion”). . The clinical diagnosis of heart failure. Fetus: severe anemia.2.1. Congestive Heart Failure 2. Cardiomyopathy metabolic. cardiomyopathy. Etiology Etiology of congestive heart failure depending on the age of the child. tachycardia ventricular. hormonal. or does so only at elevated filling pressures.3. VSD.2. cystic fibrosis.6 Pathophysiological Definition: Cardiac failure is an inability of the heart to deliver blood (and therefore oxygen) at a rate commensurate with the requirements of the metabolizing tissues at rest or during light exercise. renal and hepatic failure).2. Kawasaki disease Children Teenagers: Rheumatic fever. PDA.

and symptoms of exercise intolerance into a numeric score comparable with the NYHA classification for adults more recently. The ROSS Heart Failure Classification was developed to provide a global assessment of heart failure severity in infants. but ordinary physical (Mild) activity results in fatigue. grunting. Class III Marked limitation of physical activity. Comfortable at rest. The well-established New York Heart Association (NYHA) Heart Failure Classification is not applicable to most of the pediatric population. and has subsequently been modified to apply to all pediatric ages. retraction. Comfortable at rest.8 Ross Heart Failure Classification For Children Class I Class II Asymptomatic Mild tachypnea or diaphoresis with feeding in infant Class III Dyspnea on exertion in older children Marked tachypnea or diaphoresis with feeding in infant Marked dispnea on exertion Class IV Prolonge feeding times with growth failure Symptome such as tachypnea. None of these measures has been validated as surrogate clinical end points in large numbers of children or patients with congenital heart disease. but neurohormonal activation and deteriorating clinical status have been shown to correlate with increasing class. or dyspnea. Symptoms of cardiac insufficiency at rest. or dyspnea. palpitation. growth problems. Pathophysiology . but less than ordinary (Moderate activity causes fatigue.2.7 Part of defining heart failure is defining a spectrum of severity. The modified Ross Classification incorporates feeding difficulties. or diaphoresis at rest New York Heart Association (NYHA) Functional Classification Class Class I Class Patient Symptoms No limitation of physical activity. II Slight limitation of physical activity. discomfort is increased. or dyspnea (shortness of breath). palpitation (feeling heart beats).4. palpitation. If any physical activity is undertaken. Ordinary physical activity does not cause undue fatigue. 2. ) Class (Severe) IV Unable to carry out any physical activity without discomfort.

causing heart failure who are not compensated. nervous and hormonal real as well as a pathological state of a decrease in heart function. In some circumstances found excessive load causing failure the heart as a pump without depression of the heart muscle are intrinsic. Heart failure is characterized with a hemodynamic response. the volume of the heart chamber. elevation of preload and cardiac muscle hypertrophy will further increase the burden of the heart.Response to the heart causing some compensation mechanism which aims to improve blood volume.Congestive heart failure occurs stagnation of blood flow. as well as the release of arginine vasopressin is everything a compensatory mechanism to maintain blood pressure adequate.8 When the ventricular end-diastolic volume increase. afterload elevation. . but also raise the wall strain and increase myocardial oxygen consumption. At the beginning of heart failure due to low cardiac output. systemic embolization of the mural thrombus. One of abnormal hemodynamic response is an increase in filling pressure of the heart or preload. This condition also causes activation of the body's compensatory mechanisms that acute form of hoarding water and salt by the kidneys and nervous system adrenergic activation.This will stimulate the neurohumoral compensatory mechanisms. in the body of an increase in activity of the sympathetic nervous system and the renin-angiotensinaldosterone system. On the contrary may also occur depression intrinsic cardiac muscle but is not clinically visible signs of heart failure due to cardiac load light. Heart failure is not a clinical situation involving only one body system but rather a clinical syndrome due to heart abnormalities so that the heart is unable to pump meet metabolic needs of the body. and refractory ventricular dysrhythmias. kidneys. Dilated cardiac mechanically inefficient will cause ventricular dysfunction. If this situation is not resolved soon. Important to distinguish between the heart's ability to pump with the contractility of the heart muscle. Vasoconstriction and water retention will temporarily increase blood pressure while the increase preload and increase cardiac contractility through Starling law. Increase in stroke volume achieved in this manner due to the strain of myocardial fibers. The decline will be followed by a decrease in ventricular contractility cardiac output which further decrease in blood pressure and a decrease in effective arterial blood volume.resistance peripheral blood and cardiac muscle hypertrophy. Dilated ventricle systolic dysfunction (decreased ejection fraction) and fluid retention increases the ventricular volume (dilatation). a healthy heart will increase up to a maximum cardiac output and cardiac output is achieved can not be enlarged again (FrankStarling principle).

Regardless of the etiology. Diagnosis Thorough history taking and physical examination.8 2.9 Mechanisms underlying heart failure include impaired ability cardiac contractility. the stroke volume must adjust to maintain cardiac output. are crucial in the evaluation of an infant or child with congestive heart failure. As the severity of congestive heart failure increases. The concept of cardiac output described by the equation CO = HR x SV where cardiac output is a function of heart rate multiplied by the stroke volume. the first manifestation of congestive heart failure is usually tachycardia. signs of venous congestion usually ensue.5. Left-sided heart failure is generally associated with signs of pulmonary venous congestion. Reduced cardiac output resulted in the sympathetic nervous system will increase heart rate to maintain normal cardiac output. including an assessment of the upper-extremity and lower-extremity blood pressures. If the compensation mechanism to maintain adequate tissue perfusion.2. But in heart failure all this happened so that the disturbances in cardiac output that is pumped by the ventricles is inadequate. which causes cardiac output is lower than normal cardiac output. whereas right-sided heart failure is associated with signs of systemic venous . An obvious exception to this finding occurs in congestive heart failure due to a primary bradyarrhythmia or complete heart block.

respiratory distress (retractions). nausea/vomiting. exercise intolerance. and/or pleural effusions. cool extremities with poor peripheral perfusion. and difficulty with feeding. less frequently. even when the individual is sitting upright. or syncope. a thready pulse.Signs of pulmonary venous congestion in an infant generally include tachypnea. particularly older children. by edema or ascites. which is possibly related to a catecholamine surge that occurs when they are challenged with eating while in respiratory distress. can affect the function of the other. Often. In older children. left-sided venous congestion causes tachypnea.9 Signs and symptoms of congestive heart failure include the following:  Tachycardia . Uncompensated congestive heart failure in an infant primarily manifests as a failure to thrive. In addition. ascites. Patients may complain of cool extremities. Clinical findings may include hypotension. dizziness. and decreased urine output. Right-sided venous congestion is characterized by hepatosplenomegaly and. failure to thrive may be followed by signs of renal and hepatic failure. children with congestive heart failure have diaphoresis during feedings.10 congestion. as well as a diminished level of consciousness. Older children with uncompensated congestive heart failure may have fatigue or lower-than-usual energy levels. Generally. and congestive heart failure with inadequate cardiac output is considered decompensated. Jugular venous distention is not a reliable indicator of systemic venous congestion in infants. Signs of congestive heart failure vary with the age of the child. however. Later stages of congestive heart failure are characterized by signs and symptoms of low cardiac output. leading to systemic and pulmonary venous congestion. Chemical evidence of renal and liver dysfunction may be present. congestive heart failure with normal cardiac output is called compensated congestive heart failure. because the jugular veins are difficult to observe. Children with uncompensated congestive heart failure. and wheezing. edema. respiratory distress. generally have a lower cardiac output than that which most experienced clinicians would estimate on the basis of the clinical signs. Marked failure of either ventricle. the distance from the right atrium to the angle of the jaw may be no more than 8-10 cm. grunting. abdominal pain. Right-sided congestion may result in hepatosplenomegaly. jugular venous distention. In severe cases.

may be useful. Significant tissue hypoxia increases serum lactate concentration and depletes the serum bicarbonate level. reduced renal blood flow may be expressed as increased BUN and creatinine levels. left-sided (tachypnea. rales. The CBC count can reveal signs of anemia or infection. as well as in noncardiac conditions in which cardiac perfusion may be compromised (sepsis). The systemic saturation on room air is a more reliable measure of oxygenation than are observations for cyanosis alone. altered consciousness. cool extremities. 12-lead electrocardiogram (ECG) may reveal evidence of structural or coronary artery disease or a complete atrioventricular block or arrhythmia. cardiac biomarkers. abdominal pain. blood urea nitrogen (BUN) level. which are often misleading. and syncope Appropriate laboratory testing includes assessment of the following: oxygen saturation. dizziness. electrolyte levels. nasal flaring or grunting. sweating. complete blood count (CBC). Brain natriuretic peptide (BNP) or N -terminal prohormone BNP (NT-proBNP) levels are elevated as a result of ventricular dilation. Blood . calcium level. Pulse oximetry. nausea/vomiting. as well as a hyperoxia test in newborns. jugular venous distention).Fatigue or low energy. ascites. creatinine level. Elevated potassium levels may represent renal compromise or even tissue destruction due to low cardiac output.11  Venous congestion . In more chronic congestive heart failure states. The evaluation of serum electrolyte levels in the patient with congestive heart failure may demonstrate hyponatremia secondary to water retention. Serial measurements of BNP levels in children with primary myocardial dysfunction and acute decompensated heart failure in which levels are persistently elevated and/or there is a lesser degree of decline in the first week of presentation are adverse prognostic factors. poor growth. edema. hemoglobin concentration. and renal and hepatic function. Normal levels may be slightly higher in neonates. The partial pressure of arterial oxygen (PaO 2) when the patient is receiving 100% oxygen (hyperoxia test) may help in distinguishing intracardiac mixing malformations from pulmonary disease in the setting of hypoxia. retractions. Cardiac troponin may be elevated in cases of myocarditis or after ischemic injury due to coronary anomaly or cardiomyopathy. pleural effusion.Right-sided (hepatomegaly. pallor. BNP levels of more than 100 pg/mL are associated with congestive heart failure in adults and children. pulmonary edema)  Low cardiac output . Elevation of serum BNP level is particularly useful in distinguishing patients with congestive heart failure from those with a primary respiratory process.

Echocardiography is indicated in any child with unexplained congestive heart failure to assess cardiac function and identify potential cardiovascular causes. note that children with a low cardiac output can depend on endogenous catecholamine levels to maintain tissue perfusion. cardiac enlargement may help to distinguish patients with congestive heart failure from those with respiratory disease. venous obstruction (total anomalous pulmonary venous obstruction). the cardiac silhouette is usually enlarged on the chest radiograph. congestive heart failure itself is not an echocardiographic diagnosis. and diastolic dysfunction due to high ventilator mean airway pressures.7 Radiography and Echocardiography In the presence of congestive heart failure.) Chest radiograph shows signs of congestive heart failure (CHF). along with pulmonary edema or venous congestion. . (See the image below. displaying a normal cardiac size on chest radiographs. therefore. particularly anatomic lesions and cardiomyopathy. On the other hand. As with BNP elevation. Sedation can cause withdrawal of the endogenous catecholamine drive. the underlying etiology is best identified by means of detailed history taking and physical examination and often by means of chest radiography. When oral sedation is performed for echocardiography. Increased pulmonary blood flow may be present. resulting in cardiac decompensation.12 gas abnormalities may show respiratory alkalosis in mild forms of congestive heart failure or metabolic acidosis in patients with evidence of low cardiac output or ductal-dependent congenital heart disease. However. exceptions may include restrictive cardiomyopathy.

the causes of congestive heart failure vary. Contractility can be supported with IV agents (eg. Treatment The management of congestive heart failure (CHF) is difficult and sometimes dangerous without knowledge of the underlying cause.2. the medical management of congestive heart failure in children should be tailored to the specific details of each case.13 2. furosemide. may Metolazone 0. and alprostadil.7 Pharmacologic Therapy Preload reduction can be achieved with oral (PO) or intravenous (IV) diuretics (eg. dopamine) or mixed agents (eg. Digoxin appears to have some benefit in congestive heart failure. milrinone). Consequently. Table. Pharmaceutical agents used in the treatment of congestive heart failure are summarized in the Table below. but their use is less common in pediatric practice.005 mg/kg/d PO .. nitroprusside. metolazone). thiazides. Thus. increase to bid . Afterload reduction is obtained orally through administration of angiotensinconverting enzyme (ACE) inhibitors or intravenously through administration of other agents. such as hydralazine. the first priority is acquiring a good understanding of the etiology. inamrinone. The goals of medical therapy for congestive heart failure include the following:  Reducing the preload  Enhancing cardiac contractility  Reducing the afterload  Improving oxygen delivery  Enhancing nutrition As previously discussed. nitroglycerin) can be administered. but the exact mechanism is unclear. dobutamine. divided bid or 75% of this dose IV. and they appear in different patients to variable degrees.6.2 mg/kg/dose PO Inotropic Digoxin Preterm infants: 0. Pharmaceutical Agents Used in the Treatment of Congestive Heart Failure Agent Pediatric Dose Preload Reduction Furosemide 1 mg/kg/dose PO or IV Hydrochlorothiazide 2 mg/kg/d PO divided bid Comment May increase to qid May increase to qid Used with loop diuretic.. Venous dilators (eg.

. not to exceed 0. titrate slowly at 1.. of dosage CHF is for Adults: 25-100 mg/d PO qd or not divided bid established in children Nitroprusside 0.01-0.005 mg/kg/d PO qd or 75% of this dose IV 5-10 mcg/kg/min IV (usual dosage.1-0. especially in unstable patients Milrinone 0.3 mcg/kg/min Typically used without loading dose.5 mg/kg/d .5-10 mcg/kg/min IV Nitroglycerin Nesiritide 0.03 mcg/kg/min IV upward to upward to desired effect Gradually Dobutamine titrate titrate desired effect Not to exceed 2wk intervals.1 mg/kg/d PO divided qd/bid.5 mcg/kg/min IV 0.03 mcg/kg/min IV May need to monitor cyanide level Vasodilator Initiate with 0. Dopamine maximal dosage may be up to 28 mcg/kg/min) Gradually 5-10 mcg/kg/min IV Epinephrine 0. target dose is 10-20 mg PO bid.3-1 mcg/kg/min IV Load: 50 mcg/kg IV over 15 min Afterload Reduction Captopril 0.5-5 mg/day PO qd/bid initially.14 age 10 y: 0.5 mg/kg/d PO divided q8h Enalapril Lisinopril 0.5-10 mg) Initial dose for hypertension is 0. not to exceed 40 mg/day Adults: Usual dosage is 10mg Not established PO qd (range.1 Losartan mg/kg/day treatment PO. Adults: 2.1-0. 2.1-0.01 mcg/kg/min .

Nitrates (nitroprusside. Management of acute decompensation involves treatment of presenting symptoms and adjustment or initiation of long-term therapy. However.5-25 mg PO bid Limited data suggest a therapeutic dosage range of 0.3-1 mcg/kg/min) infusion is appropriate until stabilization is achieved. Small studies have been conducted to measure hemodynamic effects of nesiritide in children with dilated cardiomyopathy. reduce dose to 25 mg qod if hyperkalemia occurs 25-50 mg PO qd Managing Acute Congestive Heart Failure in Child Long-standing but unrecognized congestive heart failure may present acutely. admit to the ICU for diuresis with IV furosemide.10 . Nesiritide carries the additional theoretical benefits of reversing deleterious neurohumoral responses and increasing natriuresis. Adults: 12. similarly.2-0. IV dopamine (5-10 mcg/kg/min) or milrinone (0. nitroglycerin) or nesiritide may be useful in patients with elevated pulmonary capillary wedge pressure and pulmonary congestion due to their venous dilating effects.5-50 mg PO qd.4 mg/kg/dose Carvedilol PO bid.1 mcg/kg/min IV cause dose-related hypotension . Adults: 25-100 mg PO qd Adults: 12. initiate with lower dose and gradually increase dose q2-3wk to Initiate with 3.3 mg/kg/day PO in single or divided doses Eplerenone Not established *Prostaglandin E1 (PGE1). an acute presentation may represent an acute onset of acquired cardiac disease (myocarditis or arrhythmia). For patients with significant hypotension.15 May Alprostadil* Beta-Blockade 0... Older children may require the placement of a central venous or pulmonary artery catheter to monitor venous pressure and cardiac output during stabilization. In older children with acute congestive heart failure.125 mg PO bid therapeutic range Metoprolol Not established Selective Aldosterone Antagonists Spironolactone 1-3.03-0. nesiritide has demonstrated no mortality advantage compared with nitroglycerin for acute decompensated heart failure in a large adult trial.

16 .


legs. the chest radiograph may show cardiomegaly. ceftriaxone. and abdomen Patient had experienced dyspnea -Shortness of breath. chest discomfort -Uncontrolled movements of arms. ankles. usually on the chest.Depending on the cause of heart Cardiomegaly failure. lattice-like rash. or facial muscles -Weakness and shortness of breath Accumulation of extra fluid in body and in heart and lungs makes it difficult for the heart to pump out all the blood leading to constant accumulation of blood in lungs leading to dyspnea Based on Chest X-Ray The Patient has . back.Benzatine Penicilline G is given Spironolactone. -Based on Jones Criteria which was revised in 1992. raised. red and extremely painful joints—particularly the knees.5 on the posterior film. defined as a cardiothoracic ratio of greater than 0. elbows. The patient treated with furosemide. and -Rheumatic fever develops in some has been experiencing pain in his joints children and adolescents following diagnose a Rheumatic fever patient has to have either 2 major or 1 major 2 minor symptoms. . tender. or wrists -Nodules over swollen joints -Red. Benzatine to prevent recurrence of 18 . Symptoms may include: -Fever -Swollen.Case Theory Patient has a history of sore throat.

et al. Jakarta: 1658-1662 Hsu. EGC. Concise Guide tothe Management of Heart Failure. Kesehatan Anak Nelson Ed. Jakarta : Media Aesculapius. American Heart 9. Dalam: Wahab.) Chris T.. Vol:2. Pearson. 2008. Collins T. World Health Organization: Departement Cardiology Western General Hospital. Heart failure. 2008. Jakarta: 1658-1662 . Debub University. Kapita selekta Kedokteran. Daphne. Assosiation . 15. Dalam: Wahab. edisi II. Arch intern Med. 2014. J.go. Departemen Kesehatan Republik Indonesia. Curtis LH. et al. 2000. Heart Failure in Children. Pa: WB Saunders Co. 3. Tesfaye G. Kronmal R. Kesehatan Anak Nelson Ed. Differences in the incidence of congestive heart failure by ethnicity. (Bahrami H. Edisi Kelima. Available from : www. 168: 418-24. Robbins Pathologic Basis of 10. 1999. jilid IV. 2000. Fifer MA. Ethiopian Health Center CHAPTER V REFERENCES 1.pdf. Daniel. A Samik. 6th ed. Arch Intern Med. Cotran RS. 490-8. Ilmu 6. Rheumatic Fever and Rheumatic Heart Disease for the 7. Hammill BG. Lippincott 2. Daniel. the Multi-Ethnic Study of Atherosclerosis. et al. Whellan DJ. 15. Bluemke DA. Gagal Jantung Kongestif. 2013. Kumar V. Frans L. Philadelphia. McMurray. Vol:2.depkes. Robbins SL. Dalam: Lilly LS. Jantung. Scotland. Info datin Situasi Kesehatan 5. 2005 June. 1994-2003. 168: 2138-45. Disease. Bernstein. et al. Williams & Wilkins. 2011. 226-230. failure in elderly persons. Hanifati S. EGC. Bernstein. Gagal Jantung Kongestif.) (Chatterjee NA. 2009. 2015. Ilmu 8. A Samik. Yadeta D. Incidence and prevalence of heart 4. 63-70. Pathophysiology of heart disease. Gail D.