CASE REPORT CONGESTIVE HEART FAILURE CAUSED BY RHEUMATIC HEART DISEASE WITH SEVERE MALNUTRITION

Presenters

Jeffry Nugraha Fuji Khairunnisa

(070100327) (070100371)

CHAPTER 1 INTRODUCTION

1.1 Background Rheumatic heart disease is the most dreaded complication of rheumatic fever. The term rheumatic heart disease refers to the chronic heart valve damage that occurs after a person has had an episode of acute rheumatic fever. This valve damage can eventually lead to heart failure.1 Heart failure is a cardiac condition in which the heart is no longer able to function adequately to meet the bodys needs. Because heart failure can be produced by many kinds of cardiac disease, it is among the most prevalent of cardiac problems. Patients with heart failure often suffer from shortness of breath and fatigue, and have difficulty with physical exertion. Their life expectancy is often significantly reduced.2 Malnutrition, muscle wasting and cachexia are often present in congestive heart failure (CHF). However, malnutrition in CHF patients is not always as severe as muscle wasting. Data in the literature show that 24% of CHF patients have malnutrition (albumin < 3.5 mg/dl) but 68% have muscle atrophy.3
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1.2 Objective This paper is completed in order to fulfill one of the requirements in the Senior Clinical Assistances program in Department of Child Health of Haji Adam Malik General Hospital/University of Sumatera Utara. In addition, this paper provides readers with the knowledge of Congestive Heart Failure caused by Rheumatic Heart Disease with Severe Malnutrition and its management.

CHAPTER 2 LITERATURE REVIEW

2. 1 Rheumatic Heart Disease 2.1.1 Definition Rheumatic heart disease is a serious complication of rheumatic fever, a disease in which infection of the upper respiratory tract by streptococcal bacteria leads to heart disease. The infection typically affects the heart valves (valvular rheumatic heart disease), but it can also affect other heart structures.4 2.1.2 Epidemiology

The prevalence of rheumatic heart disease among school children aged 5-14 years varies from 1.36 to 6.4/1000. It is estimated that the prevalence of rheumatic heart disease in Indonesia is around 0.3-0.8 per 1000 school-age children aged between 5-15 years. Data from Department of Child Health, Medical School, University of Indonesia/Cipto Mangunkusomo Hospital showed that there is no significant decreased prevalence of rheumatic fever and rheumatic heart disease within 10 years (1983-1992).5 In the US, prevalence of rheumatic heart disease in the United States now is less than 0.05 per 1000 population. Internationally, the incidence of rheumatic fever and rheumatic heart disease has not decreased in developing countries. Retrospective studies reveal developing countries to have the highest figures for cardiac involvement and recurrence rates of rheumatic fever. Estimations worldwide are that 5-30 million children and young adults have chronic rheumatic heart disease, and 90,000 patients die from this disease each year. 4 Rheumatic fever occurs in equal numbers in males and females, but the prognosis is worse for females than for males. Rheumatic fever is principally a disease of childhood, with a median age of 10 years, although it also occurs in adults (20% of cases). It is well known that socioeconomic and environmental factors play an indirect, but important, role in the
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magnitude and severity of RF and RHD. Such factor as a shortage of resources for providing quality health care, inadequate expertise of health-care providers, and a low level of awareness of the disease in the community can all impact the expression of the disease in populations. Crowding adversely affects rheumatic fever incidence.4
2.1.3 Etiopathogenesis

The pathogenic mechanisms involved in the development of RF remain unclear. But it is evident that an abnormal humoral and cellular immune response occurs. Antigenic mimicry between streptococcal antigens, mainly M-protein epitopes and human tissues, such as heart valves, myosin and tropomyosin, brain proteins, synovial tissue and cartilage has been proposed as the triggering factor leading to autoimmunity in individuals with genetic predisposition. Several genetic markers of susceptibility have been studied but no consistent association found. Associations with different HLA class II antigens have been observed in several populations.4 Molecular mimicry was first demonstrated by humoral immune response. Streptococcal antibodies cross-react with several human tissues including heart, skin, brain, glomerular basement membrane, striated and smooth muscles. The presence of CD4+ T cells at lesions sites in the heart has been demonstrated, suggesting a direct role of these cells in the pathogenesis of RHD. Infiltrating T lymphocytes from heart lesions of severe RHD patients and peripheral T lymphocytes were capable of recognising immunodominant myocardium M5 peptides and valve proteins. These results showed the significance of molecular mimicry between beta hemolytic streptococci and heart tissue assessing the T-cell repertoire leading to local tissue damage in RHD. 4

2.1.4

Patophysiology

Rheumatic fever develops in some children and adolescents following pharyngitis with group A beta-hemolytic Streptococcus (ie, Streptococcus pyogenes). The organisms attach to the epithelial cells of the upper respiratory tract and produce a battery of enzymes allowing them to damage and invade human tissues. After an incubation period of 2-4 days, the invading organisms elicit an acute inflammatory response with 3-5 days of sore throat, fever, malaise, headache, and an elevated leukocyte count. In 0.3-3% of cases, infection leads to rheumatic
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fever several weeks after the sore throat has resolved. Only infections of the pharynx initiate or reactivate rheumatic fever. The organism spreads by direct contact with oral or respiratory secretions, and spread is enhanced by crowded living conditions. Patients remain infected for weeks after symptomatic resolution of pharyngitis and may serve as a reservoir for infecting others. Penicillin treatment shortens the clinical course of streptococcal pharyngitis and, more importantly, is effective in decreasing the incidence of major sequelae. 4 Group A Streptococcus is a gram-positive coccus that frequently colonizes the skin and oropharynxGroup A streptococci elaborate the cytolytic toxins streptolysins S and O. Of these, streptolysin O induces persistently high antibody titers that provide a useful marker of group A streptococcal infection and its nonsuppurative complications. Group A streptococci may be subserotyped by surface proteins on the cell wall of the organism. The presence of the M protein is the most important virulence factor for group A streptococcal infection in humans. More than 120 M protein serotypes or M protein genotypes have been identified, some of which have a long terminal antigenic domain (ie, epitopes) similar to antigens in various components of the human heart. Rheumatogenic strains are often encapsulated mucoid strains, rich in M proteins, and resistant to phagocytosis. These strains are strongly immunogenic, and anti-M antibodies against the streptococcal infection may cross-react with components of heart tissue (ie, sarcolemmal membranes, valve glycoproteins). Currently, emm typing is felt to be more discriminating than M typing. 4 Acute rheumatic heart disease often produces a pancarditis characterized by endocarditis, myocarditis, and pericarditis. Endocarditis is manifested as valve insufficiency. The mitral valve is most commonly and severely affected (65-70% of patients), and the aortic valve is second in frequency (25%). The tricuspid valve is deformed in only 10% of patients and is almost always associated with mitral and aortic lesions. The pulmonary valve is rarely affected. Severe valve insufficiency during the acute phase may result in congestive heart failure and even death (1% of patients). Whether myocardial dysfunction during acute rheumatic fever is primarily related to myocarditis or is secondary to congestive heart failure from severe valve insufficiency is not known. Pericarditis, when present, rarely affects cardiac function or results in constrictive pericarditis. 4

Chronic manifestations due to residual and progressive valve deformity occur in 9-39% of adults with previous rheumatic heart disease. Fusion of the valve apparatus resulting in stenosis or a combination of stenosis and insufficiency develops 2-10 years after an episode of acute rheumatic fever, and recurrent episodes may cause progressive damage to the valves. Fusion occurs at the level of the valve commissures, cusps, chordal attachments, or any combination of these. Rheumatic heart disease is responsible for 99% of mitral valve stenosis in adults in the United States. Associated atrial fibrillation or left atrial thrombus formation from chronic mitral valve involvement and atrial enlargement may be observed. 4
2.1.5 Diagnosis and Diagnostic Investigations

A diagnosis of rheumatic heart disease is made after confirming antecedent rheumatic fever. The modified Jones criteria (revised in 1992) provide guidelines for the diagnosis of rheumatic fever.2

Carditis (40%) The clinical picture of cariditis includes high pulse rate, congestive heart failure, arrhytmias and pericardial friction rubs. On the first attack, valvulitis is suspected in the presence of a new apical systolic murmur of mitral regurgitation (associated or not with an apical mid-diastolic murmur) and/or a basal diastolic murmur of aortic regurgitation.
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Cardiomegaly is noted on X-Ray and on echocardiogram. Myocarditis and/or pericarditis in the absence of valvular involvement is unlikely due to acute RF.6 Polyarthritis (70%) Arthritis is the most common manifestation, present in 60-80% of patients. It usually affects the peripheral large joints; small joints and axial skeleton are rarely involved. Knees, ankles, elbows and wrists are the most frequently affected. The joints are red, warm and swollen. Arthritis is characteristically asymmetrical, migratory, and very painful, although some patients may present mild joint complaints. It usually resolves spontaneously at the most in 2 or 3 weeks. Arthritis in ARF has an excellent response to salicylates. 6

Sydenham Chorea Sydenhams chorea is characterized by involuntary movements, specially of the face and limbs, muscle weakness, disturbances of speech and gait. Children usually exhibit concomitant psychologic dysfunction, especially obsessive-compulsive disorder, increased emotional lability, hyperactivity, irritablility and age-regressed behavior. It is usually a delayed manifestation, and is often the sole manifestation of ARF. 6

Erythema marginatum This is an evanescent, erythematous, non-pruritic rash with pale centers and rounded or serpiginous margins. Lesions occur mainly on the trunk and proximal extremities and may be induced by application of heat.6

Diagnostic Investigations for rheumatic heart disease : Laboratory Throat culture Throat culture findings for group A beta hemolytic Streptococcus are usually negative by the time symptoms of rheumatic fever or rheumatic heart disease appear. Attempts should be made to isolate the organism before the initiation of antibiotic therapy to help confirm a diagnosis of streptococcal pharyngitis and to allow typing of the organism if it is isolated successfully. 4

Rapid antigen detection test This test allows rapid detection of group A streptococcal antigen and allows the diagnosis of streptococcal pharyngitis and the initiation of antibiotic therapy while the patient is still in the physician's office. Because the rapid antigen detection test has a specificity of greater than 95% but a sensitivity of only 60-90%, a throat culture should be obtained in conjunction with this test.4 Antistreptococcal antibodies The clinical features of rheumatic fever begin at the time antistreptococcal antibody levels are at their peak. Thus, antistreptococcal antibody testing is useful for confirming previous group A streptococcal infection. The elevated level of antistreptococcal antibodies is useful, particularly in patients that present with chorea as the only diagnostic criterion. Sensitivity for recent infections can be improved by testing for several antibodies. Antibody titers should be checked at 2-week intervals in order to detect a rising titer. 4 The most common extracellular antistreptococcal antibodies tested include antistreptolysin O (ASO), antideoxyribonuclease (DNAse) B, antihyaluronidase, antistreptokinase, antistreptococcal esterase, and anti-DNA. Antibody tests for cellular components of group A streptococcal antigens include antistreptococcal polysaccharide, antiteichoic acid antibody, and antiM protein antibody. 4 In general, the ratio of antibodies to extracellular streptococcal antigens rises during the first month after infection and then plateaus for 3-6 months before returning to normal levels after 612 months. When the ASO titer peaks (2-3 wk after the onset of rheumatic fever), the sensitivity of this test is 80-85%. The anti-DNAse B has a slightly higher sensitivity (90%) for detecting rheumatic fever or acute glomerulonephritis. Antihyaluronidase results are frequently abnormal in rheumatic fever patients with a normal level of ASO titer and may rise earlier and persist longer than elevated ASO titers during rheumatic fever. 4 Acute phase reactants The C-reactive protein and erythrocyte sedimentation rate are elevated in rheumatic fever due to the inflammatory nature of the disease. Both tests have a high sensitivity but low specificity for rheumatic fever. They may be used to monitor the resolution of inflammation, detect relapse when weaning aspirin, or identify the recurrence of disease. 4 Heart reactive antibodies Tropomyosin is elevated in acute rheumatic fever. 4 Rapid detection test for D8/17 This immunofluorescence technique for identifying the B cell marker D8/17 is positive in 90% of patients with rheumatic fever. It may be useful for identifying patients who are at risk for developing rheumatic fever. 4 Next Section: Imaging Studies

Imaging Studies Chest roentgenography Cardiomegaly, pulmonary congestion, and other findings consistent with heart failure may be seen on chest radiography. When the patient has fever and respiratory distress, chest radiography helps differentiate heart failure from rheumatic pneumonia. Doppler-echocardiogram In acute rheumatic heart disease, Doppler-echocardiography identifies and quantitates valve insufficiency and ventricular dysfunction. Studies in Cambodia and Mozambique demonstrated a 10-fold increase in the prevalence of rheumatic heart disease when echocardiography is used for clinical screening compared with strictly clinical findings.[4] With mild carditis, Doppler evidence of mitral regurgitation may be present during the acute phase of disease but resolves in weeks to months. In contrast, patients with moderate-to-severe carditis have persistent mitral and/or aortic regurgitation. The most important echocardiographic features of mitral regurgitation from acute rheumatic valvulitis are annular dilatation, elongation of the chordae to the anterior leaflet, and a posterolaterally directed mitral regurgitation jet. During acute rheumatic fever, the left ventricle is frequently dilated in association with a normal or increased fractional shortening. Thus, some cardiologists believe that valve insufficiency (from endocarditis), rather than myocardial dysfunction (from myocarditis), is the dominant cause of heart failure in acute rheumatic fever. In chronic rheumatic heart disease, echocardiography may be used to track the progression of valve stenosis and may help determine the time for surgical intervention. The leaflets of affected valves become diffusely thickened, with fusion of the commissures and chordae tendineae. Increased echodensity of the mitral valve may signify calcification. 4 Heart catheterization In acute rheumatic heart disease, this procedure is not indicated. With chronic disease, heart catheterization has been performed to evaluate mitral and aortic valve disease and to balloon stenotic mitral valves. 4 Postcatheterization precautions include hemorrhage, pain, nausea and vomiting, and arterial or venous obstruction from thrombosis or spasm.Complications may include mitral insufficiency after balloon dilation of the mitral valve, tachyarrhythmias, bradyarrhythmias, and vascular occlusion. 4 Previous Next Section: Imaging Studies Other Tests On ECG, sinus tachycardia most frequently accompanies acute rheumatic heart disease. Alternatively, some children develop sinus bradycardia from increased vagal tone. No correlation between bradycardia and the severity of the carditis is noted. 4
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First-degree atrioventricular (AV) block (prolongation of the PR interval) is observed in some patients with rheumatic heart disease. This abnormality may be related to localized myocardial inflammation involving the AV node or to vasculitis involving the AV nodal artery. First-degree AV block is a nonspecific finding and should not be used as a criterion for the diagnosis of rheumatic heart disease. Its presence does not correlate with the development of chronic rheumatic heart disease. 4 Second-degree (intermittent) and third-degree (complete) AV block with progression to ventricular standstill have been described. Heart block in the setting of rheumatic fever, however, typically resolves with the rest of the disease process. 4 When acute rheumatic fever is associated with pericarditis, ST segment elevation may be present and is marked most in lead II, III, aVF, and V4 -V6. 4 Patients with rheumatic heart disease also may develop atrial flutter, multifocal atrial tachycardia, or atrial fibrillation from chronic mitral valve disease and atrial dilation. Previous Next Section: Imaging Studies Histologic Findings Pathologic examination of the insufficient valves may reveal verrucous lesions at the line of closure. Aschoff bodies (perivascular foci of eosinophilic collagen surrounded by lymphocytes, plasma cells, and macrophages) are found in the pericardium, perivascular regions of the myocardium, and endocardium. The Aschoff bodies assume a granulomatous appearance with a central fibrinoid focus and eventually are replaced by nodules of scar tissue. Anitschkow cells are plump macrophages within Aschoff bodies. In the pericardium, fibrinous and serofibrinous exudates may produce an appearance of "bread and butter" pericarditis. 4 2.1.2 Management

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Therapy is directed towards eliminating the GABHS (group A beta hemolytic streptococci pharyngitis (if still present), suppressing inflammation from the autoimmune response, and providing supportive treatment of congestive heart failure. Treat residual GABHS pharyngitis as outlined above, if still present. Treatment of the acute inflammatory manifestations of acute rheumatic fever consists of salicylates and steroids. Aspirin in antiinflammatory doses effectively reduces all manifestations of the disease except chorea, and the response is typically dramatic. If rapid improvement is not observed after 24-36 hours of therapy, question the diagnosis of rheumatic fever. Attempt to obtain aspirin blood levels from 20-25 mg/dL, but stable levels may be difficult to achieve during the inflammatory phase because of variable GI absorption of the drug. Maintain aspirin at anti-inflammatory doses until the signs and symptoms of acute rheumatic fever are resolved or residing (6-8 wk) and the acute phase reactants (APRs) have returned to normal. Anti-inflammatory doses of aspirin may be associated with abnormal liver function tests and GI toxicity, and adjusting the aspirin dosage may be necessary. When discontinuing therapy, withdraw aspirin gradually over weeks while monitoring the APRs for evidence of rebound. 4 Chorea is most frequently self-limited but may be alleviated or partially controlled with phenobarbital or diazepam. If moderate to severe carditis is present as indicated by cardiomegaly, third-degree heart block or congestive heart failure, substitute PO prednisone for salicylate therapy. Continue prednisone for 2-6 weeks depending on the severity of the carditis, and taper prednisone during the final week(s) of therapy. Weaning prednisone therapy after a shorter period (2-4 weeks) while initiating and maintaining salicylates for several weeks can minimize adverse effects of the steroids while preventing rebound of the carditis. 4 Include digoxin and diuretics, afterload reduction, supplemental oxygen, bed rest, and sodium and fluid restriction as additional treatment for patients with acute rheumatic fever and heart failure. The diuretics most commonly used in conjunction with digoxin for children with heart failure include furosemide and spironolactone. Initiate digoxin only after checking electrolytes and correcting hypokalemia. The total digitalizing dose is 20-30 mcg/kg PO, with 50% of the dose administered initially, followed by 25% of the dose 12 hours and 24 hours after the initial dose. Maintenance doses typically are 8-10 mcg/kg/d PO in 2 divided
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doses. For older children and adults, the total loading dose is 1.25-1.5 mg PO, and the maintenance dose is 0.25-0.5 mg PO every day. Therapeutic digoxin levels are present at trough levels of 1.5-2 ng/mL. Afterload reduction (ie, using ACE inhibitor captopril) may be effective in improving cardiac output, particularly in the presence of mitral and aortic insufficiency. Start these agents judiciously. Use a small, initial test dose (some patients have an abnormally large response to these agents), and administer only after correcting hypovolemia. When heart failure persists or progresses during an episode of acute rheumatic fever in spite of aggressive medical therapy, surgery is indicated and may be life-saving for severe mitral and/or aortic insufficiency. 4 Preventive and prophylactic therapy is indicated after rheumatic fever and acute rheumatic heart disease to prevent further damage to valves. Primary prophylaxis (initial course of antibiotics administered to eradicate the streptococcal infection) also serves as the first course of secondary prophylaxis (prevention of recurrent rheumatic fever and rheumatic heart disease).4 Benzathine penicillin for patients who are unlikely to complete a 10-day course of oral therapy and patients with personal or family histories of rheumatic fever or rheumatic heart disease or other environmental factors (such as crowded living conditions or low socioeconomic status) that place them at substantial risk for the development of rheumatic fever. Benzathine penicillin should be given as a single injection in a large muscle mass. This formulation is painful; injections that contain procaine penicillin in addition to benzathine penicillin G are less painful. Less discomfort is associated with intramuscular benzathine penicillin G if the medication is warmed to room temperature before administration. The recommended dosage of benzathine penicillin G is 600 000 U intramuscularly for patients weighing 27 kg (60 lb) or less, and 1 200 000 U for patients weighing more than 27 kg. The combination of 900 000 U of benzathine penicilin G and 300 000 U of procaine penicillin G is satisfactory therapy for most children.7 An injection of 0.6-1.2 million units of benzathine penicillin G intramuscularly every 4 weeks is the recommended regimen for secondary prophylaxis for most US patients.

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Administer the same dosage every 3 weeks in areas where rheumatic fever is endemic, in patients with residual carditis, and in high-risk patients. 4 Patients with rheumatic fever and carditis but no valve disease should receive prophylactic antibiotics for 10 years or well into adulthood, whichever is longer. Patients with mild carditis (eg, mild mitral regurgitation or healed carditis) should receive secondary prophylaxis for rheumatic fever for 10 years after the last attack, or at least until 25 years of age (whichever is longer). Patients with more severe valvular damage (eg, causing heart failure) or after valve surgery should receive lifelong secondary prophylaxis.8 Patients with rheumatic heart disease and valve damage require a single dose of antibiotics 1 hour before surgical and dental procedures to help prevent bacterial endocarditis. Patients who had rheumatic fever without valve damage do not need endocarditis prophylaxis. Do not use penicillin, ampicillin, or amoxicillin for endocarditis prophylaxis in patients already receiving penicillin for secondary rheumatic fever prophylaxis (relative resistance of PO streptococci to penicillin and aminopenicillins). Alternate drugs recommended by the American Heart Association for these patients include PO clindamycin (20 mg/kg in children, 600 mg in adults) and PO azithromycin or clarithromycin (15 mg/kg in children, 500 mg in adults).4 When heart failure persists or worsens after aggressive medical therapy for acute rheumatic heart disease, surgery to decrease valve insufficiency may be life-saving. Forty percent of patients with acute rheumatic heart disease subsequently develop mitral stenosis as adults.In patients with critical stenosis, mitral valvulotomy, percutaneous balloon valvuloplasty, or mitral valve replacement may be indicated. Due to high rates of recurrent symptoms after annuloplasty or other repair procedures, valve replacement appears to be the preferred surgical option.4 2.1.3 Prevention

For patients with GABHS pharyngitis, a meta-analysis supports a protective effect against rheumatic fever when penicillin is used following the diagnosis.4 Oral (PO) penicillin V remains the drug of choice for treatment of GABHS pharyngitis, but ampicillin and
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amoxicillin are equally effective. When PO penicillin is not feasible or dependable, a single dose of intramuscular benzathine penicillin G or benzathine/procaine penicillin combination is therapeutic. For patients who are allergic to penicillin, administer erythromycin or a firstgeneration cephalosporin. Other options include clarithromycin for 10 days, azithromycin for 5 days, or a narrow-spectrum (first-generation) cephalosporin for 10 days. As many as 15% of patients who are allergic to penicillin are also allergic to cephalosporins. Do not use tetracyclines or sulfonamides to treat GABHS pharyngitis.For recurrent group A streptococci (GAS) pharyngitis, a second 10-day course of the same antibiotic may be repeated. Alternate drugs include narrow-spectrum cephalosporins, amoxicillin-clavulanate, dicloxacillin, erythromycin, or other macrolides. 4 Control measures for patients with GABHS pharyngitis are as follows: Hospitalized patients, Place hospitalized patients with GABHS pharyngitis of pneumonia on droplet precautions, as well as standard precautions, until 24 hours after initiation of appropriate antibiotics. Exposed persons, People in contact with patients having documented cases of streptococcal infection first should undergo appropriate laboratory testing if they have clinical evidence of GABHS infection and should undergo antibiotic therapy if infected. School and childcare centers, Children with GABHS infection should not attend school or childcare centers for the first 24 hours after initiating antimicrobial therapy. GABHS carriage is difficult to eradicate with conventional penicillin therapy. Thus, PO clindamycin (20 mg/kg/d PO in 3 divided doses for 10 days) is recommended. 4

2.1.4

Complication

Potential complications include heart failure from valve insufficiency (acute rheumatic carditis) or stenosis (chronic rheumatic carditis). Associated cardiac complications include atrial arrhythmias, pulmonary edema, recurrent pulmonary emboli, infective endocarditis, intracardiac thrombus formation, and systemic emboli. 2.1.5 Prognosis

Manifestations of acute rheumatic fever resolve over a period of 12 weeks in 80% of patients and may extend as long as 15 weeks in the remaining patients.
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Rheumatic fever was the leading cause of death in people aged 5-20 years in the United States 100 years ago. At that time, the mortality rate was 8-30% from carditis and valvulitis but decreased to a 1-year mortality rate of 4% by the 1930s. Following the development of antibiotics, the mortality rate decreased to almost 0% by the 1960s in the United States; however, it has remained 1-10% in developing countries. The development of penicillin has also affected the likelihood of developing chronic valvular disease after an episode of acute rheumatic fever. Before penicillin, 60-70% of patients developed valve disease as compared to 9-39% of patients since penicillin was developed. In patients who develop murmurs from valve insufficiency from acute rheumatic fever, numerous factors, including the severity of the initial carditis, the presence or absence of recurrences, and the amount of time since the episode of rheumatic fever, affect the likelihood that valve abnormalities and the murmur will disappear. The type of treatment and the promptness with which treatment is initiated does not affect the likelihood of disappearance of the murmur. In general, the incidence of residual rheumatic heart disease at 10 years is 34% in patients without recurrences but 60% in patients with recurrent rheumatic fever. Disappearance of the murmur, when it occurs, happens within 5 years in 50% of patients. Thus, significant numbers of patients experience resolution of valve abnormalities even 5-10 years after their episode of rheumatic fever. The importance of preventing recurrences of rheumatic fever is evident. 2.2. Congestive Heart Failure 2.2.1. Definition Heart failure is the pathophysiologic state in which the heart, via an abnormality of cardiac function (detectable or not), fails to pump blood at a rate commensurate with the requirements of the metabolizing tissues or is able to do so only with an elevated diastolic filling pressure.9 2.2.2 Etiology Specific underlying factors cause various forms of heart failure, such as systolic heart failure (most commonly, left ventricular systolic dysfunction), diastolic heart failure, acute heart failure, high-output heart failure, and right heart failure. Underlying causes of systolic heart failure include the following:
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Coronary artery disease Diabetes mellitus Hypertension Valvular heart disease (stenosis or regurgitant lesions) Arrhythmia (supraventricular or ventricular) Infections and inflammation (myocarditis) Peripartum cardiomyopathy Congenital heart disease Drugs (either recreational, such as alcohol and cocaine, or therapeutic drugs with cardiac side effects, such as doxorubicin) Idiopathic cardiomyopathy Rare conditions (endocrine abnormalities, rheumatologic disease, neuromuscular conditions)

Underlying causes of diastolic heart failure include the following: Coronary artery disease Diabetes mellitus Hypertension Valvular heart disease (aortic stenosis) Hypertrophic cardiomyopathy Restrictive cardiomyopathy (amyloidosis, sarcoidosis) Constrictive pericarditis Acute valvular (mitral or aortic) regurgitation Myocardial infarction Myocarditis Arrhythmia Drugs (eg, cocaine, calcium channel blockers, or beta-blocker overdose) Sepsis Anemia Systemic arteriovenous fistulas Hyperthyroidism
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Underlying causes of acute heart failure include the following:

Underlying causes of high-output heart failure include the following:

Beriberi heart disease Paget disease of bone Albright syndrome (fibrous dysplasia) Multiple myeloma Pregnancy Glomerulonephritis Polycythemia vera Carcinoid syndrome Left ventricular failure Coronary artery disease (ischemia) Pulmonary hypertension Pulmonary valve stenosis Pulmonary embolism Chronic pulmonary disease Neuromuscular disease 9

Underlying causes of right heart failure include the following:

2.2.3 Patophysiology Congestive heart failure (CHF) occurs when the heart can no longer meet the metabolic demands of the body at normal physiologic venous pressures. Typically, the heart can respond to increased demands by means of one of the following: Increasing the heart rate, which is controlled by neural and humoral input Increasing the contractility of the ventricles, secondary to both circulating catecholamines and autonomic input Augmenting the preload, medicated by constriction of the venous capacitance vessels and the renal preservation of intravascular volume As the demands on the heart outstrip the normal range of physiologic compensatory mechanisms, signs of congestive heart failure occur. These signs include tachycardia; venous congestion; high catecholamine levels; and, ultimately, insufficient cardiac output with poor perfusion and endorgan compromise. 10

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Diminished cardiac output results from a complex interaction of various factors. Systolic dysfunction is characterized by diminished ventricular contractility that results in an impaired ability to increase the stroke volume to meet systemic demands. Factors such as anatomic stresses (eg, coarctation of the aorta) that contribute to an increased afterload (end-systolic wall stress) and those resulting from neurohormonal factors that increase systemic vascular resistance also lead to systolic dysfunction. 10 Diastolic dysfunction results from decreased ventricular compliance, necessitating an increase in venous pressure to maintain adequate ventricular filling. Causes of primary diastolic dysfunction include an anatomic obstruction that prevents ventricular filling (eg, pulmonary venous obstruction), a primary reduction in ventricular compliance (eg, cardiomyopathy, transplant rejection), external constraints (eg, pericardial effusion), and poor hemodynamics after the Fontan procedure (eg, elevated pulmonary vascular resistance). 10 In chronic heart failure, myocardial cells die from energy starvation, from cytotoxic mechanisms leading to necrosis, or from the acceleration of apoptosis or programmed cell death. Necrosis stimulates fibroblast proliferation, which results in the replacement of myocardial cells with collagen. The loss of myocytes leads to cardiac dilation and an increased afterload and wall tension, which results in further systolic dysfunction. In addition, the loss of mitochondrial mass leads to increased energy starvation. 10 During acute congestive heart failure, the sympathetic nervous system and renin-angiotensin system act to maintain blood flow and pressure to the vital organs. Increased neurohormonal activity results in increased myocardial contractility, selective peripheral vasoconstriction, salt and fluid retention, and blood pressure maintenance. As a chronic state of failure ensues, these same mechanisms cause adverse effects. The myocardial oxygen demand that exceeds the supply increases because of an increase in the heart rate, in contractility, and in wall stress. Alterations in calcium homeostasis and changes in contractile proteins occur, resulting in a hypertrophic response of the myocytes. Neurohormonal factors may lead to direct cardiotoxicity and necrosis.10 2.2.4 Diagnosis
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In the Framingham system, the diagnosis of heart failure requires that either 2 major criteria or 1 major and 2 minor criteria be present concurrently, as shown in Table 1 below. Minor criteria are accepted only if they cannot be attributed to another medical condition. Framingham criteria of heart Failure 11 Major Criteria Minor Criteria

Paroxysmal nocturnal dyspnea Nocturnal cough Weight loss of 4.5 kg in 5 days in response Dyspnea on ordinary exertion to treatment Neck vein distention Rales Acute pulmonary edema Hepatojugular reflux S3 gallop Central venous pressure > 16 cm water Circulation time of 25 sec Radiographic cardiomegaly Pulmonary edema, visceral congestion, or cardiomegaly at autopsy A decrease in vital capacity by one third the maximal value recorded Pleural effusion Tachycardia (rate of 120 bpm) Hepatomegaly Bilateral ankle edema

NYHA classification of functional heart failure The New York Heart Association (NYHA) functional classification of heart failure is based on the patient's symptom severity and the amount of exertion that is needed to provoke their symptoms. 12 Class I II Functional Capacity Patients without limitation of physical activity Patients with slight limitation of physical activity, in which ordinary physical activity leads to fatigue, palpitation, dyspnea, or anginal pain; III they are comfortable at rest Patients with marked limitation of physical activity, in which less than ordinary activity results in fatigue, palpitation, dyspnea, or anginal pain; IV they are comfortable at rest Patients who are not only unable to carry on any physical activity without discomfort but who also have symptoms of heart failure or the anginal
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syndrome even at rest; the patient's discomfort increases if any physical activity is undertaken

ACC/AHA stages of heart failure

The American College of Cardiology/American Heart Association (ACC/AHA) developed a classification that described the development and progression of heart failure and that "recognizes that there are established risk factors and structural prerequisites for the development of HF and that therapeutic interventions introduced even before the appearance of LV dysfunction or symptoms can reduce the population morbidity and mortality of HF. 13 Level A B C D Description At high risk for heart failure but without structural heart disease or symptoms of heart failure Structural heart disease but without signs/symptoms of heart failure Structural heart disease with current or past symptoms of heart failure Refractory heart failure requiring specialized interventions

Modified Ross Heart Failure Classification for Children The Ross Heart Failure Classification was developed to provide a global assessment of heart failure severity in infants, and has subsequently been modified to apply to all pediatric ages. 14 Class I Class II Class III Asymptomatic Mild tachypnea or diaphoresis with feeding in infants Dyspnea on exertion in older children Marked tachypnea or diaphoresis with feeding in infants Marked dyspnea on exertion Class IV Prolonged feeding times with growth failure Symptoms such as tachypnea, retractions, grunting, or diaphoresis at rest 2.2.5. Management The management of congestive heart failure (CHF) is difficult and sometimes dangerous without knowledge of the underlying cause. Consequently, the first priority is acquiring a good understanding of the etiology. The goals of medical therapy for congestive heart failure include
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reducing the preload, enhancing cardiac contractility, reducing the afterload, improving oxygen delivery, and enhancing nutrition. As previously emphasized, the causes of congestive heart failure vary, and they appear in different patients to variable degrees. Thus, the medical management of congestive heart failure in children should be tailored to the specific details of each case. 10 Preload reduction can be achieved with oral (PO) or intravenous (IV) diuretics (eg, furosemide, thiazides, metolazone). Venous dilators (eg, nitroglycerin) can be administered, but their use is rare in common practice. Contractility can be supported with intravenous agents (eg, dopamine) or mixed agents (eg, dobutamine, inamrinone, milrinone). Digoxin appears to have some benefit in congestive heart failure, but the exact mechanism is unclear. Afterload reduction is obtained PO by administration of ACE inhibitors or IV by administration of other agents such as hydralazine, nitroprusside, and alprostadil.10 2.2.6 Prevention To help prevent recurrence of heart failure, counsel and educate patients in whom heart failure was caused by dietary factors or medication noncompliance with regard to the importance of proper diet and the necessity of medication compliance. A study by Dunlay et al examined medication use and adherence among community-dwelling patients with HF. The study found that medication adherence was suboptimal in many patients, often because of cost. 9 2.2.7. Prognosis In general, the mortality following hospitalization for patients with heart failure is 10.4% at 30 days, 22% at 1 year, and 42.3% at 5 years, despite marked improvement in medical and device therapy. Each rehospitalization increases mortality by about 20-22%. Mortality is greater than 50% for patients with NYHA class IV, ACC/AHA stage D heart failure. Heart failure associated with acute MI has an inpatient mortality of 20-40%; mortality approaches 80% in patients who are also hypotensive (eg, cardiogenic shock). (See Heart Failure Criteria and Classification). 9 A study by van Diepen et al suggests patients with heart failure or atrial fibrillation have a significantly higher risk of noncardiac postoperative mortality than patients with coronary artery disease; this risk should be considered even if a minor procedure is planned. 9
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2.3 SEVERE MALNUTRITION 2.3.1 Definition Malnutrisi is weight-for-height 3 Z scores below the WHO growth standards median, the diagnostic threshold of mid-upper-arm circumference below than 115 mm. There are 3 different types of malnutrition known worldwide, include: kwashiorkor. 15 2.3.2. Systems for assessing the severity of malnutrition in underweight children15 Method Mild Moderate Severe Marasmus, Kwashiorkor, and Marasmic-

Weight for age

90 %

75 to 89 %

60 to 74 %

<60 %

Weight for height

90 %

80 to 89 %

70 to 79 %

<70 %

Height for age

95 %

90 to 94 %

85 to 89 %

<85 %

Weight/height for age

90 %

85 to 89 %

75 to 84 %

<75 %

Clinical manifestation in marasmic malnutrition include absence of edema, inadequate intake of protein and calories.15 This picture below show the manifestation of marasmic malnutrition:

22

Clinical manifestation in Kwashiorkor include presence of edema, fair-to-normal calorie intake with inadequate protein intake.15 This picture below show the manifestation of Kwarshiorkor :

Marasmus-Kwashiorkor is A combination of both, kwashiorkor and marasmus. Signs and symptomps of marasmus could be found coincidently with kwashiorkor. The child look very thin with bones and ribs could be inspected very prominently, with mild edema found minimally, particularly in the lower extremities.15 Patients suffering from heart failure also have symptoms that can affect their food intake, for example, tiredness when strained, breathing difficulties and gastrointestinal symptoms like nausea, loss of appetite and ascites.17
23

There are many mechanisms whereby chronic cardiac failure may lead to malnutrition (Fig. 1). Elevated right-sided venous pressure produces hepatic and gastrointestinal congestion and, hence, anorexia, diminished synthetic capacity and malabsorption." Both hepatic congestion and diminished perfusion may produce a clinical picture resembling acute hepatitis. Splanchnic congestion can result in dyspepsia, malabsorption, maldigestion and protein-losing enteropathy. Elevated renal vein pressures lead to increased renal protein wastage. Pulmonary congestion can markedly increase lung stiffness, which increases the work of breathing. With congestive heart failure the metabolic demands of the respiratory musculature can increase from less than 5% to more than 25% of the total oxygen consumption of the body, thereby increasing energy expenditure and demands on cardiac output. Even minor degrees of pulmonary congestion can have significant effects on the requirements of the respiratory muscles for energy and oxygen. Decreased tissue perfusion or hypoxemia and, hence, diminished peripheral oxygen delivery can result in impaired aerobic glycolysis and inefficient use of energy. Low cardiac output itself produces fatigue and weakness, which may be compounded by the effects of diuretics on sodium, potassium and magnesium balance. These factors, in addition to the decreased palatability of a low-sodium diet, age, depression and the anorexigenic effect of cardiac drugs, may limit oral intake.16 2.3.3. MANAGEMENT OF SEVERE MALNUTRITION According to the Department of Health Republic of Indonesia, there are 5 aspects to be considered in managing children diagnosed with severe malnutrition : 1. Ten principal steps 2. Treatment of comorbidities 3. Failure of treatments 4. Patients dicharge before end of treatment 5. Emergency situation All these aspects should be well understood in order to manage severe malnutrition in children.15 1. Ten Principal Steps The ten principal steps in managing severe malnutrition should be conducted step by step based on the treatment phase. a. Step 1: Hypoglycemia correction
24

Children diagnosed with severe malnutrition are highly at risk to get hypoglycemia. This state is diagnosed when the level of blood glucose is below 54 mg/dl. Signs and symptomps of children developing hypoglycemia could be very not spesific. They can include gradually loss of consciousness, lethargic and weak arterial pulse. Symptomps such sweating and palpitation could occasionaly be identified, and the patient could pass away with the only symptomps is gradually loss of consciousness. It is essential to understand that in every health care facilities where it is pretty hard to detect blood glucose level, all children diagnosed with severe malnutrition should be assumed as hypoglymic children, hence hypoglycemia correction should be done immediately. 15 b. Step 2: Hypothermia correction Hypothermia is a condition potentially causing death to a severe malnourished child. This condition is diagnosed while axillar temperature is below 36,5oC. Hypothermia frequently occurs along with hypoglycemia and serious infection causing a large number of death among children. The simplest thing that can be done to a hypothermic child is called Kangoroo technique, in which the baby or child should be hugged tightly by mother and covered with blanket until the head. This will enable skin to skin contact between child and mother. Another thing to do is to place the child 50 cm below source of light and the body temperature should monitored once every 30 minutes. And the warming effort should be stopped while the temperature reaches 37oC. 15 c. Step 3: Dehydration correction It is sometimes difficut to identify dehydration signs on a severely malnourished child. Several things to identify include: 15 Lethargic. The children look apatis, not fully alert and unaware of circumstances. At the final stage, the children can get loss of consciousness. Sunken eye. It is important to take a detailed history to the parents aboout the appearence of eye, since several child do have a sunken eye even in a not dehydrated state. Tear production is frequently absent. Thirsty. Dehydrated patient is frequently very thristy and drinks very eagerly and this can be a very important and easily identified symptomps of dehydration in children. Lip mucose seems very dry.
25

Skin pinch returns slowly more than 2 seconds. But it can occur in a very malnourished child even not in a dehydrated state.

The treatment of a dehydrated and malnourished child include consumption of Rehydration Solution for Malnutrition (ReSoMal), with amount of fluid descriptions: 5 ml/kg bodyweight every 30 minutes for the first 2 hours Followed by another Resomal for as much as 5-10 ml/kg body weight/hour, given alternately with Formula 75 as the early diet. They are give every hour for 10 hours. If rehydration state has been reached, Formula 75 should be given every 2 hours.

a. Step 4: Electrolyte imbalance correction Electrolyte imbalance like a state of hypokalemia and hypomagnesemia is frequrntly occur to a patient with dehydration along with severe malnutrition. The potassium deficit will adversely affect cardiac function and gastric emptying ability, while magnesium is essential for potassium to enter cells and be retained. It is important to be realized that the mineral mix solution does not contain iron as this is withhels during the stabilization phase. The treatment includes admission of Rehydration solution for Malnutrition as well. This will fix both, the dehydration and electrolyte imbalance state. 15 The ORS can be used for watery diarrhea, at the recommended volume of 5-15 mL/kg/h, with a total of 70 mL/kg for the first 12 hours. Because the risk of cardiac failure is increased in children with marasmus, compliance with the rehydration regimen is even more critical than in children who are well nourished. Therefore, closely monitor the rehydration phase and promptly address signs of cardiac failure, such as tachypnea, tachycardia, edema, or hepatomegaly. Rehydration solution should be adapted to marasmic children with a low sodium content and a high potassium content. This can be prepared using standard WHO solution as a base or by directly administering a modified oral rehydration (ReSoMal) solution if available. 15 b. Step 5: Treatment of Infection Severely malnourished children is at a very great risk to develop infection, not only by community infection, but also the normal flora as well. This condition was brought on the
26

systemic manifestation of low protein intake of malnourished children. A state of hipoimmunoglobulinemia will predispose them to get opportunistic infection from normal flora. Infection of the lower respiratory tract infections is especially common, and although signs of infection should be carefully looked for, they are often difficult to detect. This is because unlike well nourished children who respond to infection with fever and inflammmation, malnourished children with even serious infection may only become drowsy or lethargic. Hence, antibiotic admission should be given to these patients, as a prophylaxis one and as a therapeutic as well. 15 For children without any clear evidence of infection, a broad spectrum antibiotic such Cotrimoxazole (trimethoprim 5 mg/kgBW + sulfamethoxazole 25 mg/kgBW orally twice daily for 5 days. Children with complications such septic shock, hypoglycemia, hypothermia, evidence of skin infections, respiratory tract and genitourinary tract infection or children who appear lethargic) should be given: First Line Treatments, include: Ampicillin, 50 mg/kgBW IM or IV for the first 2 days, followed by Amoxicillin 15 mg/kgBW orally every 8 hours for the next 5 days), along with Gentamycin 7,5 mg/kgBW IM or IV once daily for 7 days. If the child fails to improve within 48 hours, add Chloramphenicol 25 mg/kgBW IM or IV every 8 hours (or every 6 hours if meningitis is suspected) for the next 5 days. Some institutions routinely give malnourished children metronidazole 7,5 mg/kgBW every 8 hours for 7 days in addition to broad spectrum anti microbials. However, the efficacy of this treatment has not been estabilished yet by clinical trials. a. Step 6: Micronutrion Defficiency Severely malnourished children are at greater risk to develop vitamin and mineral deficiency, and therefore supplementation of multivitamin should be considered in the treatment of malnutrition as they serve as coenzyme and cofactor for daily metabolism. The supplementation include: 15
27

Second Line Treatments:

Folic Acid 5 mg on the first day, followed by 1 mg/day for the next several days. Zinc, 2 mg/kg body weight Cu, 0,3 mg/kg body weight Sulfas Ferrosus 3 mg/kg body weight, given after the stabilization and transitional phase are completed Vitamin A, given orally on the first day, with appropriate dose depending on age.

If there are evidences of vitamin A deficiency, or the patient was just suffered from measles in the last 3 months, vitamin A supplementation should be given on day 1, 2 and 15. 15 a. Step 7: Initial Refeeding Almost all severely malnourished children have infections, impaired liver and intestinal function along with problems related to electrolyte imbalance when first admitted to hospital. Because of these problems, they are unable to tolerate the usual amounts of dietary protein, fat and sodium as well. It is important, therefore, to begin feeding these children with a diet that is low in these nutrients, and high in carbohydrate. 15 There are three steps of giving diet to to the patients, adjusted to the treatment phase. Those in stabilization phase should get the early diet containg 75 kcal each 100 ml, which is well known as Formula 75 (F 75) WHO. While the patients who have already been in the transitional phase should get an alternating diet from F75 to F100. And for those who have reached the rehabilitation phase could consume F135 WHO as the correctional diet.15

b. Step 8: Correctional Refeeding Correctional refeeding should be given alternatingly from F 75 to F 100 in the transitional phase, and F 135 (but not recommended) in the rehabilitation phase. Children who are unwilling to eat should be fed by NGT. children who can eat should be given diet every 2, 3 or 4 hours, day and night. But is important to remeber, that eating orally is more recommended than NGT feeding. If the child could take three quarters of the days diet orally, then the NGT should be removed. 15
28

If the childs appetite improves, treatment has been successful then. The initial phase of treatment ends when the children becomes hungry, indicating that the child is now ready to begin the rehabilitation phase. Nevertheless, the transition should be gradual to avoid the risk of heart failure which can occur if children suddenly consume large amounts of feed. Replace the F75 with F 100 in the transitional phase. 15 Treatment Evaluation: Body weight should be measured daily to evaluate the efficacy of initial and correctional refeeding. 15 If weight gain is less than 5 gr/kgBW/day, the child should be reassesed If weight gain is between 5 to 10 gr/kgBW/day, an undetected infection should be suspected If weight gain is more than 10 gr/kgBW/day, then the therapeutic program has reached its target. a. Step 9: Stimulation Severely malnourished children have delayed mental and behavioural development, which,if not treated, can become the most serious long term result of malnutrition. Emotional and physical stimulation through play programmes that start during rehabilitation phase and continue after discharge can substantially reduce the risk of permanent mental retardation and emotional impairment. Care must be taken to avoid sensory deprivation. 15 Malnourished children need interaction with other children during rehabilitation. After the initial phase of treatment, the child should spend prolonged periods with other children. Activities should be selected to develop both motor and language skills, and new activities and materials should be introduced regularly. A childs effort to perform a task should always be praised and never criticized. 15 Physical activities promote the development of essential motor skills and may also enhance growth during rehabilitation. Play should include such activities as rolling on a matress,
29

climbing stairs and walking. The duration and intensity of physical activities should increase as the childs nutritional status and general condition improve. 15 b. Step 10: Prepare for Discharge During rehabilitation, preparation should be made to ensure that the child is fully reintegrated into the family and community after discharge. Criteria for discharge: A child may be considered to have recovered and be ready for discharge when the childs weight for height has no longer been in the severe malnutrition (BW/.BL > 70%). To achieve this goal, it is essential that the child receives as many meals as possible per day. In some instancies, a child may be discharged before he or she has reached the target weight for height for discharge, however, since the child is not yet recovered, he or she will need continuing care as an outpatient. 15 1. Treatment of Comorbidities a. Vitamin A deficiency If the patient is diagnosed with vitamin A deficinecy, vitamin A supplementation should be given according to patients age on day 1, 2 and 14. 15 b. Ulceration of the eye Any kind of eye problems should be evaluated to get the appropriate therapy, based on how severe the problem is, just like what listed below: 15 Eye Problems Treatment Bitots Spot only, without any Antibiotic eyedrops is not indicated other eye problem Suppurative and process Corneal ulcer inflamatory Chloramphenicol or tetrasiclin eyedrops

should be given Chloramphenicol 0,25 1% eyedrops, 1 gtt/6 hours for 7 to 10 days Atropine eyedrops 1%, 1gtt/8 hours for 3-5 days

c. Dermatosis
30

Zn defficiency is a common problem among malnourished children and causing a skin lesion called dermatosis. This should be treated with Zn supplementation orally, and the skin will respond effectively. 15 Additional treatment such KmnO4 solution 1% topically 10 minutes a day could be added as well. Diaper should be changed frequently to avoid diaper dermatitis in babies. 15 d. Parasitic Infections Stool examination should be done to look for worms egg that could possibly presents. If there are evidence of parasitic infections, pirantel pamoat 10 mg/kg body weight could be given orally. 9 If amebiasis or giardiasis is proven to be etiologies of diarrhea in children, administration of metronidaxole 7,5 mg/kg body weight /8 hours is indicated for 7 days. 15 e. Tuberculosis Children who got history of contact with tuberculosis patients should undergo evaluation and assesment to detect TB infection. TB scoring system should be assesed in those kind of children, and TB regimen should be started if the patients is diagnosed with TB. 15 1. Failure of Treatment Failure of treatment can be categorized into 2 kinds of conditions : a. Death Death in the first 24 to 72 hours is common among children diagnosed with hypoglycemia, hypothermia, dehydrated or sepsis. Thus, those conditions should be priorities in treating severely malnourished children. 15 b. Inadequacy of Weight Gain As much as 10 gr/kg body weight/ day or more is expected as a minimum weighy gain to reach the goal of treatments. Weight gain below that standard should raise suspicion of systemic infection that is still not detected. 15 1. Patient discharges before end of treatment For patient who ask to discharge before end of treatment, an education and counselling should be given about how to serve the food adequately, in a small protion but more frequently and how to overcome and give initial treatment to comorbidities. It is also important to explain about the importance of immunization to these kind of children. 15
31

2. Emergency case Two conditions that should obtain serious care include shock and severe anemia. Patients presenting with shock should be ressucitated with initial crystalloid RL 15 ml/kg body weight for the first one hour, followed by Rehydration Solution for Malnutrition (ReSoMal) for the next several hours. Patients presenting with severe anemia (those with Hb levels below 4 gr/l) should get a whole blood transfusion 10 ml/kg body weights. While those with Hb levels between 4 to 6 gr/l should receive transfusion of packed red cells as much as 10 ml/kg body weight if respiratory distress evidences are found. 15 2.3.4. Management of Malnutrition in Patients with Heart Failure Patients suffering from heart failure have an increased need for nutrition and should eat a diet high in fat and carbohydrates. Beyond the normal diet, patients suffering from heart failure often need additional nutrition, such as nutritional drinks with a higher calorie level. Small regular meals or continuous nutrient supply is preferable, as it decreases the need for oxygen in the heart muscle. Patients with heart failure suffer from hypermetabolism as well as an increased loss of nutrition through the forced diuresis. The nutritional need is higher the more severe the heart failure is. To stimulate the appetite in patients suffering from chronic heart failure it is important that the food is appetising. The importance of good oral health has also been pointed out. Salt restrictions vary with regard to daily intake from 1.6 to 4.0 g for mild to moderate heart failure. With a deterioration of the heart failure, the recommendation is 0.8 1.6 g salt/day. Elderly patients rate taste and flavour as the most important for their choice of which food to eat, and they find it hard to accept a diet poor in salt. The quality of life is affected negatively if the food is tasteless. Therefore, alternative ways of flavouring the food, for example using herbs and other spices, should be suggested to them.17

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CHAPTER 3 CASE REPORT 3.1 Case SA, four teen years old girl, weight 30 kg, height 157 cm, admitted to Adam Malik Hospital on 17th September 2011 at 03.30 pm with chief complain of breathlessness. Breathlessness experienced by the patient in the last 7 days, increasing in severity within 1 day before admittance after exercising. Even at rest, breathlessness still occurs. Breathlessness accompanying with palpitation Weather not influence breathlessness. Cyanotic history not found. Chest pain not found. Cough at night not found. Foot swelling history not found. Joint pain history found at her both shoulder since last month. Fever has last for 7 days. The fever is intermittent and cured with antipyretic drugs. There is no history of seizure and shivering. Pain when swallowing not found. History of Pregnancy : During pregnancy her mother never got fever and took drugs or herbs. Her mother said that she has never checked if she had diabetes mellitus and hypertension. Her mother checked the pregnancy regularly (every month) to the midwife. According to the midwife, the pregnancy was okay. History of Delivery : Patient was born spontaneously in term helped by midwife. Her mother forgot the body weight and body length of the patient at birth. According to her mother, the patient cry right after birth, and there was no cyanosis found. History of Immunization : Patient never take any immunization. History of previous disease : RHD History of previous drugs : Furosemide, Spironolakton, Digoxin. Physical examination Presence Status: Sensorium: Compos mentis; temperature: 37,8 oC; BW: 30 kg; BL: 157 cm; BW/BL: 65% Anemic (-), Dyspnea (+), Icteric (-), Cyanosis (-), Oedema (-)

33

Localized Status: Head : Eye: Light reflexes (+/+), isochoric pupil, pale conjunctiva palpebra inferior (-/-) Ear and Mouth: within normal limit; Nose: nasal canul (+) Neck : Lymph node enlargement (-), jugular vein pressure: R+2 cmH2O Chest : Symetric, Epigastrical retraction (+) HR : 138 bpm, regular, pansistolik murmur grade IV/VI intercostal space III linea mid clavicularis sinistra RR : 42 tpm, regular, rales (-/-) Abdomen Extremities Genitalia Therapy: - Bed rest semifowler - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10 gtt/mnt (micro) Laboratory Result 17st September 2011: Complete Blood Count Hemoglobin (Hb) Erytrocyte (RBC) Leukocyte (WBC) Hematocrite Trombocyte (PLT) MCV MCH MCHC Results 11,30 g % 4,51 x 106/mm3 10,03x103/mm3 35,60 % 400x103/mm3 78,90Fl 25,10 pg 31,70 g % Normal Value 12,0 14,4g % 4,20 4,87 x106/mm3 4,5 11,0 x103/mm3 38 44 % 150 450 x103/mm3 85 95 fL 28 32 pg 33 35 g %
34

: Soepel, Ascites (-), undulation (-), : :

shifting dullness (-), smilling

umbillicus (-) , Hepar/Lien: non palpable Pols: 138 bpm, regular, adequate pressure/volume, CFT<3, warm, female, within normal range : CHF ec DD : - RHD, AHD oedem (-). BP : 120/70 mmHg Working Diagnosis

RDW MPV PCT PDW Neutrofil Limfosit Monosit Eosinophil Basophil Neutrophil absolute Limfosit absolute Monosit absolute Eosinophil absolute Basophil absolute LIVER SGOT SGPT GLUCOSE Ad Random Blood glucose KIDNEY Ureum Kreatinin ELECTROLITE Natrium Kalium Klorida IMUNOSEROLOGI

14,10 10,10 Fl 0,41 % 11,3 fL 65,50 % 22,30 % 9,30 % 2,70 % 0,200 % 6,57 x 103/L 2,24 x 103/L 0,93 x 103/L 0,27 x 103/L 0,02 x 103/L

11,6 14,8 % 7,0 10,2 fL

37 80 % 20 40 % 28% 16% 01% 2,7 6,5 x103/L 1,5 3,7 x103/L 0,2 0,4 x103/L 0 0,10 x103/L 0 0,1 x103/L

16 U/l 7 U/l

<32 U/l <31 U/l

94,10 mg/dl

<200 mg/dl

21,60 mg/dl 0,47 mg/dl

<50 0,57 0,87

140 mEq/L 4,4 mEq/L 105 mEq/L

135 155 3,6 - 5,5 96 106

35

ASTO AUTOIMMUNE CRP Kualitatif

800

Positif

Chest X-ray Result:

Follow Up 18th September 2011 S : Dyspnea (+), fever (-) O: Presence status cm, Anemic (-), Dyspnea (+) , Icteric (-), Cyanosis (-), Oedema (-) Localized status :
36

Sensorium : Compos mentis, Body temperature : 37,2C, BW : 30 kg, BL : 157

Head

Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit

palpebra inferior (-/-). Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (+) : Symmetric Fusiform , epigastrical retraction (+) HR : 132 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra RR : 26 tpm, regular, rales (-/-), wheezing (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 132 bpm, regular, adequate pressure/volume, CFT<3, warm, oedem extremities (-). BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec DD : - RHD - AHD P : - Bed rest semifowler position - O2 1-2 l/i (nasal kanul) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatine Penicillin 1200000 IV/IM/28days - Diet MBRG 1700 + 60 gr protein R/ >>Consult radiology div; Result = > CHF stage II

Follow Up 19th September 2011 S : Dyspnea (+), fever (-) O: Presence status cm,
37

Sensorium : Compos mentis, Body temperature : 36,8C, BW : 30 kg, BL : 157

Anemic (-), Dyspnea (+) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (+) : Symetric, epigastrical retraction (+) HR : 104 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 24 tpm, regular, rales (-/-), wheezing (-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 104 bpm, regular, adequate pressure/volume, oedem (-) on extremities. BP : 110/60 mmHg Anogenital : Female, within normal limit. A: CHD ec suspect RHD P : - Bed rest semifowler position - O2 1-2 l/i (nasal kanul) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj Benzatin Penicillin 1200000 IU/IM28days - MBRG diet 1700 kkal + 60 gr Protein R/ - Throat swab, LED (22/09/2011), Echo (20/09/2011)

palpebra inferior (-/-).

Follow Up 20th September 2011 S : Dyspnea (-), fever (-) O: Presence status cm,
38

Sensorium : Compos mentis, Body temperature : 36,9C, BW : 30 kg, BL : 157

Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (+) : Symetric, epigastrical retriction (-) HR : 98 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 28 tpm, regular, rales (-/-), wheezing (-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 98 bpm, regular, adequate pressure/volume, oedem (-) on extremities, warm, CRT <3 BP : 100/60 mmHg Anogenital : Female, within normal limit. A: CHD ec suspect RHD P : - Bed rest semifowler position - Diet MBRG 1700 kkal + 60 gr Protein - O2 1-2 l/i (nasal kanul) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days - Prednisone 60 mg/day 4-4-4 (Day 1) - Antasida Syr 3 x CI R/ - Echo (20/09/2011) Results : MS mild + MI moderate + AI Moderate + Dilatation LA-LV

palpebra inferior (-/-).

Follow Up 21st September 2011 S : Dyspnea (-), fever (-) O:

39

Presence status cm, BW/BL : 65%

Sensorium : Compos mentis, Body temperature : 36,9C, BW : 30 kg, BL : 157 Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (+) : Symetric, epigastrical retriction (-) HR : 102 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 24 tpm, regular, rales (-/-), wheezing (-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 102 bpm, regular, adequate pressure/volume, oedem (-) on extremities, warm, CRT <3 BP : 100/60 mmHg Anogenital : Female, within normal limit. A: CHD ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition P : - Bed rest semifowler position - Diet MBRG 1700 kkal + 60 gr Protein - O2 1-2 l/i (nasal kanul) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days - Prednisone 60 mg/day 4-4-4 (D2) - Antacid Syr 3 x CI R/ - Throat swab (22/09/2011) - Konsul Gizi
40

palpebra inferior (-/-).

- Konsul THTResult : Tonsilitis - LED, DLLaboratory results : Hb/Ht/Leu/Tromb : 11,9 g%/36,60% /14,73.103/mm3/369.103/mm3 LED : 56mm/hour Blood Culture : No Bactery found

Follow Up 22nd September 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 100 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 24 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 100 bpm, regular, adequate pressure/volume, oedem (-), extremities warm, CRT <3 BP : 120/50 mmHg Anogenital : Female, within normal limit. A: CHD ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position
41

Sensorium : Compos mentis, Body temperature : 36,9C, BW : 30 kg, BL : 157

palpebra inferior (-/-).

- Diet MBRG 1700 kkal + 60 gr Protein - O2 1-2 l/i (nasal kanul) - Inj. Ceftriaxone 1 gr/12h/IV (D1) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/11) - Prednisone 60 mg/day 4-4-4 (D3) - Antacid Syr 3 x CI R/ - Throat Swab result : Roultella ornithimolytica bactery was found. - Konsul PedSos

Follow Up 23rd September 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 110 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 24 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable
42

Sensorium : Compos mentis, Body temperature : 36,7C, BW : 30 kg, BL : 157

palpebra inferior (-/-).

Extremities : Pols: 110 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHD ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D4) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D2) - Antacid Syr 3 x CI - Folic acid 1 x 5 mg next day 1 x 1 mg - Vitamin A 1 x 200000 - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI R/ - Urinalysis results : Normal

Follow Up 24th September 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva
43

Sensorium : Compos mentis, Body temperature : 36,8C, BW : 30 kg, BL : 157

palpebra inferior (-/-). Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 112 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 30 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 112 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D3) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D5) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI R/ - Modul Cardiology : Dx : CHF ec MI Moedrate + MV Prolaps + MS Mild + AI Mild ec RHD
44

- Modul Gizi : Dx : Severe Malnutrition Type Marasmic + RHD

Follow Up 25th September 2011 S : Dyspnea (-), fever (-) O: Presence status : Sensorium : Compos mentis, Body temperature : 36,8C, BW : 30 kg, BL : 157 cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva

palpebra inferior (-/-). Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 110 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 28 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 110 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul)
45

- IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D4) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D6) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI R/ - Modul Cardiology : Dx : CHF ec MI Moedrate + MV Prolaps + MS Mild + AI Mild ec RHD - Modul Gizi : Dx : Severe Malnutrition Type Marasmic + RHD Follow Up 26th September 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 110 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 28 tpm, regular, rales (-/-)
46

Sensorium : Compos mentis, Body temperature : 36,7C, BW : 30 kg, BL : 157

palpebra inferior (-/-).

Abdomen

: Soepel, Peristaltic (+) N Hepar/Lien: non palpable

Extremities : Pols: 110 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D5) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D7) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI R/ - Modul Cardiology : Dx : CHF ec MI Moedrate + MV Prolaps + MS Mild + AI Mild ec RHD - Modul Gizi : Dx : Severe Malnutrition Type Marasmic + RHD

Follow Up 27th September 2011 S : Dyspnea (-), fever (-) O: Presence status :
47

Sensorium : Compos mentis, Body temperature : 36,8C, BW : 30 kg, BL : 157

cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 110 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 30 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 110 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D6) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D8) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI
48

palpebra inferior (-/-).

R/ - Modul Cardiology : Dx : CHF ec MI Moedrate + MV Prolaps + MS Mild + AI Mild ec RHD - Modul Gizi : Dx : Severe Malnutrition Type Marasmic + RHD

Follow Up 28th September 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 118 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 32 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 110 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position
49

Sensorium : Compos mentis, Body temperature : 36,7C, BW : 30 kg, BL : 157

palpebra inferior (-/-).

- Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D7) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D9) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI R/ - Modul Cardiology : Dx : CHF ec MI Moedrate + MV Prolaps + MS Mild + AI Mild ec RHD - Modul Gizi : Dx : Severe Malnutrition Type Marasmic + RHD

Follow Up 29th September 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-)
50

Sensorium : Compos mentis, Body temperature : 36,8C, BW : 30 kg, BL : 157

palpebra inferior (-/-).

Chest

: Symetric, epigastrical retriction (-) HR : 110 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 36 tpm, regular, rales (-/-)

Abdomen

: Soepel, Peristaltic (+) N Hepar/Lien: non palpable

Extremities : Pols: 110 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition marasmus type+ Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D8) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D10) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI

Follow Up 30th September 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65%
51

Sensorium : Compos mentis, Body temperature : 36,4C, BW : 30 kg, BL : 157

Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 100 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 30 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 110 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D9) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D11) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI
52

palpebra inferior (-/-).

R/ - Modul Cardiology : Dx : CHF ec MI Moedrate + MV Prolaps + MS Mild + AI Mild ec RHD - Modul Gizi : Dx : Severe Malnutrition Type Marasmic + RHD

Follow Up 1st October 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 82 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 24 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 110 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day)
53

Sensorium : Compos mentis, Body temperature : 36,8C, BW : 30 kg, BL : 157

palpebra inferior (-/-).

- O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D10) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D12) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI

Follow Up 2nd October 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 94 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 24 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N
54

Sensorium : Compos mentis, Body temperature : 37,0C, BW : 30 kg, BL : 157

palpebra inferior (-/-).

Hepar/Lien: non palpable Extremities : Pols: 94 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D11) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D13) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI

Follow Up 3rd October 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva
55

Sensorium : Compos mentis, Body temperature : 37,0C, BW : 30 kg, BL : 157

palpebra inferior (-/-).

Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 98 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 24 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 98 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D12) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D14) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI

Follow Up 4st October 2011 S : Dyspnea (-), fever (-)

56

O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 96 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 28 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 96 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D13) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D15)
57

Sensorium : Compos mentis, Body temperature : 36,8C, BW : 30 kg, BL : 157

palpebra inferior (-/-).

- Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI

Follow Up 5st October 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 96 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 28 tpm, regular, rales (-/-) Abdomen : Soepel, Peristaltic (+) N Hepar/Lien: non palpable Extremities : Pols: 96 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position
58

Sensorium : Compos mentis, Body temperature : 36,8C, BW : 30 kg, BL : 157

palpebra inferior (-/-).

- Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D14) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D16) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI

Follow Up 6st October 2011 S : Dyspnea (-), fever (-) O: Presence status cm, BW/BL : 65% Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-) Localized status Head : : Eye : Light reflexes (+/+), isochoric pupil, pale conjunctiva Ear/ Mouth/ Nose: within normal limit Neck Chest : Lymph node enlargement (-), jugular vein pressure : R+2 cmH2O. Cannon wave (-) : Symetric, epigastrical retriction (-) HR : 96 bpm, regular, pansistolik murmur grade IV/VI intercostal space II-III linea mid clavicularis sinistra, Thrill (+) RR : 28 tpm, regular, rales (-/-)
59

Sensorium : Compos mentis, Body temperature : 36,8C, BW : 30 kg, BL : 157

palpebra inferior (-/-).

Abdomen

: Soepel, Peristaltic (+) N Hepar/Lien: non palpable

Extremities : Pols: 96 bpm, regular, adequate pressure/volume, oedem(-) extremities warm, CRT <3 BP : 110/70 mmHg Anogenital : Female, within normal limit. A: CHF ec MI Moderate + MS Mild + AI Moderate ec RHD + Severe Malnutrition + Tonsilitis P : - Bed rest semifowler position - Diet F75 325 cc/2jam/oral (kalori 2400 kkal/day) - O2 1-2 l/i (nasal canul) - IVFD D5% NaCl 0,45% 10gtt/i micro - Inj. Ceftriaxone 1 gr/12h/IV (D15) - Furosemide 2 x 25 mg - Spironolacton 2 x 25 mg - Inj. Benzatin Penicillin 1200000 IU/IM/28 days (18/10/2011) - Prednisone 60 mg/day 4-4-4 (D17) - Antacid Syr 3 x CI - Folic acid 1 x 1 mg - Zinc 1 x 20 mg - Multivitamin without Fe 1 x CI

60

3.2

3.2

DISCUSSION

SA, 14 years old girl, weight 30 kg, height 157 cm, admitted to Adam Malik Hospital on 17th September 2011 at 03.30 pm with chief complain of breathlessness. Breathlessness experienced by the patient in the last 7 days, increasing in severity within 1 day before admittance after exercising. Even at rest, breathlessness still occurs. Breathlessness accompanying with palpitation. Joint pain history found at her both shoulder since last month. Fever has last for 7 days. The fever is intermittent and cured with antipyretic drugs. History of previous disease is RHD. History of previous drugs are Furosemide, Spironolakton, Digoxin. Last echocardiography examination done on September 20th 2011 and the result of echocardiogram is MI Moderate, MS Mild, AI Moderate.

Epidemiology of RHD shows that the highest number of incidences is in equal numbers in males and females. The prevalence of rheumatic heart disease among school children aged 5-14 years varies from 1.36 to 6.4/1000 children. It is estimated that the prevalence of rheumatic heart disease in Indonesia is around 0.3-0.8 per 1000 school-age children aged between 5-15 years. In this case the patient is a girl and came with the chief complain of breathlessness. The aged of this boy is 14 years old. Patients with RHD typically present with from the Jones criteria require the presence of 2 major or 1 major and 2 minor criteria for the diagnosis of rheumathic disease. The major diagnostic criteria include carditis, polyarthritis, chorea, subcutaneous nodule, and erythema marginatum. The minor diagnostic criteria include fever, arthralgia, prolonged PR interval on ECG, elevated acute phase reactants (increased erythrocyte sedimentation rate [ESR]), presence of C-reactive protein, and leukocytosis. This patient presents with mayor criteria from the Jones criteria include Polyarthritis, and minor criteria include continous fever, LED increased, and presence of C-reactive protein.

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Due to the various problems with RHD, besides using The Jones Criteria, examnination should be done to diagnose RHD such as throat culture, Doppler echocardiogram, histologic findings blood test, and ECG. In this case, besides using The Jones Criteria, the test had been done to this patient to diagnose RHD were Doppler Echocardiogram and the result was MI Moderate, MS Mild, and AI Moderate. Roultella ornithimolytica bactery was found from the throat swab. Treatment of RHD is prophylaxis. Preventive and prophylactic therapy is indicated after rheumatic fever and acute rheumatic heart disease to prevent further damage to valves. Primary prophylaxis (initial course of antibiotics administered to eradicate the streptococcal infection) also serves as the first course of secondary prophylaxis (prevention of recurrent rheumatic fever and rheumatic heart disease). An injection of 0.6-1.2 million units of benzathine penicillin G intramuscularly every 4 weeks is the recommended regimen for secondary prophylaxis for most patients. In patients with critical stenosis, mitral valvulotomy, percutaneous balloon valvuloplasty, or mitral valve replacement may be indicated. This patient had been given an injection of 0.6-1.2 million units of benzathine penicillin G intramuscularly every 4 weeks. Heart failure occurs when the heart cannot deliver adequate cardiac output to meet the metabolic needs of the body. Congestive heart failure (CHF) is a clinical syndrome in which the heart is unable to pump enough blood to the body to meet its needs, to dispose of venous return adequately, or a combination of the two. Framingham criteria usually used to diagnose CHF, and its relies on several sources of clinical findings, including history, physical examination, and chest-x-ray films. This criteria consists of major criteria and minor criteria, heart failure diagnosed when 2 major criteria, or 1 major criteria + 2 minor criteria were found.

The major criteria consists of: Paroxysmal nocturnal dyspnea or orthopnoe, distension of jugular vein, rales, rontgen: cardiomegaly, acute pulmonary oedem, S3 gallop, central vein pressure > 16 cm H2O, circulation time 25 seconds, hepatojugular reflux,
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pulmonalry oedem or visceral congestion or cardiomegaly in autopsy, decreasing of body weight > 4.5 kg in 5 days which response to heart failure therapy. While the minor criteria consist of: edema of bilateral foot, nocturnal cough, dyspnea at daily or routine activities, hepatomegaly, pleural effusion, vital capacity decrease greater than one-third of maximal value, tachycardia (pulse > 120 times/minute) In this case, dyspnea admittance after exercising and even at rest, dyspnea still occurs. There were distension of jugular vein, cardiomegaly, and tachycardia. This patient had 3 major and 1 minor criteria. The treatment of CHF include reducing the preload, enhancing cardiac contractility, reducing the afterload, improving oxygen delivery, and enhancing nutrition. Preload reduction can be achieved with oral (PO) or intravenous (IV) diuretics (eg, furosemide, thiazides, metolazone). Venous dilators (eg, nitroglycerin) can be administered, but their use is rare in common practice. Contractility can be supported with intravenous agents (eg, dopamine) or mixed agents (eg, dobutamine, inamrinone, milrinone). Digoxin appears to have some benefit in congestive heart failure, but the exact mechanism is unclear. Afterload reduction is obtained PO by administration of ACE inhibitors or IV by administration of other agents such as hydralazine, nitroprusside, and alprostadil. The patient was given with prednisone to eliminated of the underlying causes of the disease (rheumatic heart disease). The patient also was given furosemide and spironolactone to control patients heart failure state. Besides that, the patient also had severe malnutrition and the management of nutrition for severe malnutrition was given to this patient as elimination of the precipitating or contributing causes. Severe malnutrition is both a medical and a social disorder. Malnutrition is the end result of chronic nutritional and, frequently, emotional deprivation by carers who, because of poor understanding, poverty or family problems, are unable to provide the child with the nutrition and care he/she requires. Malnutrition is globally the most important risk factor for illness and death, contributing to more than half of deaths in children worldwide. In developing countries, more than 50% of the 10 million deaths each year are either
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directly or indirectly secondary to malnutrition in children younger than 5 years. Malnutrition is directly responsible for 300,000 deaths per year in children younger than 5 years in developing countries and contributes indirectly to over half the deaths in childhood worldwide (32%) in developing countries. Protein-energy malnutrition (PEM) is observed most frequently in developing countries. The term of PEM used to describe a deficiency in carbohydrate, protein and fat, now also can include deficiencies in vitamins, minerals and trace elements. PEM may range in severity from mild to severe, and severe forms may present as any of the following syndromes include khwarsiorkor, marasmus, and the mix type between khwarsiorkor and marasmus type. Distinction between the 2 forms of PEM is based on the presence of edema (kwashiorkor) or absence of edema (marasmus). Marasmus involves inadequate intake of protein and calories, whereas a child with kwashiorkor has fair-to-normal calorie intake with inadequate protein intake. Although significant clinical differences between kwashiorkor and marasmus are noted, some studies suggest that marasmus represents an adaptation to starvation whereas kwashiorkor represents a dysadaptation to starvation. The diagnosis of malnutrition can be made from history taking, physical examination, antropometrical measurement and laboratory finding. From history taking, we must concern about the recent intake of food and fluids, usual diet, breastfeeding, diarrhea, loss of appetite and weight loss. In physical examination, we look for sign of dehydration, fever, skin changes, muscle hypotrophy, and oedema.The antropometrical measurement will show the growth failure of the child. We diagnosed this patient with severe malnutrition physical examination, and antropometrical measurement. From the physical examination, patient look like very thin, costal seen clearly but no oedema both of his extremities. In antropometrical measurement. The child's weight for her height is 65 % which indicates of severe malnutrition. Management of the child with severe malnutrition is divided into three phases. These are:
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 Initial treatment: life-threatening problems are identified and treated in a hospital or a residential care facility, specific deficiencies are corrected, metabolic abnormalities are reversed and feeding is begun. Rehabilitation: intensive feeding is given to recover most of the lost weight, emotional and physical stimulation are increased, the mother or carer is trained to continue care at home, and preparations are made for discharge of the child. Follow-up: after discharge, the child and the childs family are followed to prevent relapse and assure the continued physical, mental and emotional development of the child. The treatment had 10 steps conducted to this patient had already been in line with the guideline of malnutrition management from Department of Health Republic of Indonesia. The requirement of the fluid and food was adjusted to the stabilization phase requirement. Fom the guideline of malnutrition management from Department of Health Republic of Indonesia, this patient was include in second planning of the treatment, This patient was firstly treated in the stabilization phase in which dehydration were assesed and treated subsequently. IVFD D5% NaCl 0.45% was given for electrolyte balance. The diet F-75 was given to this patient until the last 1 day before she back home. In stabilization phase, vitamin A, folat acid, Zinc, and multivitamin without Fe was given to this patient.

3.3.

Summary

It has been reported a case of 14 years old girl with main complain breathlessness. From history taking, physical examination, antropometrical measurement, and laboratorium this patient was diagnosed chronic heart failure caused by rheumatic heart disease and severe malnutrition. Treatment of this patient is intravenous fluid drips D5% NaCl 0.45%, furosemide, spironolactone, prednisone, zinc, vitamin A, multivitamin without Fe, and F75 reguler diet. Further follow up is still needed to evaluate the growth impairment, such as weight gain, and return to age-appropriate developmental status. Doctors advise patients to do valvuloplasti, but
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her parents do not agree. The patient went home at 7th October 2011 due to doctors permit and suggested to control every month.

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REFERENCES
1. Fogoros, R.N, 2011. Rheumatic Heart Disease. Available from:

http://heartdisease.about.com/od/heartvalvedisease/a/rheumatic_heart_disease.htm. [Accessed on September 30th, 2011]

2. Fogoros, R.N, 2011. Heart Failure - The Basics. Available from:

http://heartdisease.about.com/od/livingwithheartfailure/a/heart_failure.htm. [Accessed on September 30th, 2011]

3. E. Pasini, R. Aquilani, M. Gheorghiade, F. S., Dioguardi., 2003. Malnutrition, muscle

wasting and cachexia in chronic heart failure: the nutritional approach. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12784775. [Accessed on September 30th, 2011]
4. Chin, T. K., 2010. Pediatric Rheumatic Heart Disease. Available from:

http://emedicine.medscape.com/article/891897-overview#showall. September 30th, 2011]

[Accesed

on

5. Iskandar, B., et al, 2008. Comparison of minimal inhibitory and bactericidal capacity of

oral penicillin V with benzathine penicillin G to Streptococcus beta-hemolyticus group A in children with rheumatic heart disease. Available from: http://www.paediatricaindonesiana.org/pdffile/48-3-5.pdf . [Accessed on September 30th, 2011]
6. AHA. Guidelines for the diagnosis of rheumatic fever. Jones Criteria, 1992 update.

Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council. on Cardiovascular Disease in the Young, the American Heart Association; JAMA 1992 Oct 21; 268(15):2069-73.
7. Dajani, A., et al., 1995. Treatment of Acute Streptococcal Pharyngitis and Prevention of

Rheumatic

Fever:

Statement

for

Health

Professionals.

Available
th

from:

http://pediatrics.aappublications.org/content/96/4/758 [Accessed on October 7 , 2011] 8. Mayosi, B., 2010. Natural history, screening, and management of rheumatic heart

disease. Available from:

http://www.uptodate.com/contents/natural-history-screening-and-management-ofrheumatic-heart disease?source=search_result&search=Natural+history%2C+screening 67

%2C+and+management+of+rheumatic+heart+disease&selectedTitle=1~66 [Accessed on

October 7th, 2011]

9. Dumitru, I., 2011. Heart Disease. Available from:

http://emedicine.medscape.com/article/163062-overview#showall. [Accessed on October 7th, 2011]

10. Satou, G.M., 2009. Pediatric Congestive Heart Failure. Available from:

http://emedicine.medscape.com/article/901307-overview#showall. [Accessed on October 7th, 2011]

11. Roger, V.L., et al., 2004.

Trends in Heart Failure Incidence and Survival in a

Community-Based Population. Available from: http://jama.ama-assn.org/content/292/3/344.full [Accessed on September 8th, 2011]

12. American

Heart

Association.

Classes

of

heart

failure.

Available

from:

http://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Classesof-Heart-Failure_UCM_306328_Article.jsp. [Accesed on October 8th, 2011]

13. Shah, R.V., Fifer, M.A., 2007. Heart Failure. In : Lilly, L.S., ed. Pathophysiology of

Heart Disease : A Collaborative Project of Medical Students and Faculty. BaltimorePhiladelpia. Lippincott Williams & Wilkins, 2007; 243
14. Hsu, D.T., Pearson, G.D., 2009. Heart Failure in Children. Available from:

http://circheartfailure.ahajournals.org/content/2/1/63.full#T1 [Accessed on October 9th, 2011]

15. Direktorat Gizi Masyarakat-Direktorat Janderal Bina Keseharan Masyarakat. Translated

from: Direktorat Gizi Masyarakat-Direktorat Janderal Bina Kesehatan Masyarakat, 2005. Buku Bagan Tatalaksana Anak Gizi Buruk. Jakarta : Direktorat Gizi MasyarakatDirektorat Janderal Bina Kesehatan Masyarakat,
16. Webb, J.G., Kies, M.C., Chan-Yan, C.C., 1986. Malnutrition and the heart. Available

from : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1491347/ [Accessed on October 9th, 2011]

17. Jacobsson, A., Pihl-Lindgren, E., Fridlund, B., 2001. Malnutrition in patients

suffering from chronic heart failure; the nurses care. Available from : http://eurjhf.oxfordjournals.org/content/3/4/449.full [Accessed on October 8th 2011]

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