Friday, October 22, 2010

Every clinical detail about Acute rheumatic fever, especially in children

Rheumatic fever is an inflammatory disease affecting the heart, joints, central nervous system and subcutaneous tissue. It derives its name from involvement of joints and the presence of fever in acute stage. The major component of the rheumatic fever is heart damage, especially scarring of the mitral valve, which is than referred to as rheumatic heart disease.
Rheumatism (Rheumatismus - lat) or rheumatic fever (RF) is a systemic inflammatory illnessoff the connective tissue, with preferring of heart and vessels damaging. Besides this it is very often that others organs and system involved into pathological process. The development of this illness usually combined with group A beta hemolytic streptococcal (GABHS) pharyngitis in children and with congenital children organism peculiarities.
RF and its most serious complication, rheumatic heart disease (RHD), are believed to result from an autoimmune response; however, the exact pathogenesis remains unclear. Studies in the 1950s during an epidemic on a military base demonstrated 3% incidence of RF in adults with streptococcal pharyngitis not treated with antibiotics. Studies in children during the same period demonstrated an incidence of only 0.3%.
RF is very actually theme for today pediatrics because:
1) RF is widely spreading among the developing countries.Worldwide, incidence in developing countries incidence is > 100 cases/100,000 population.
2) It is diagnosed more often in schoolage childhood period ( 0.1 – 0,3 %).
3) Cardiac involvement is reported to occur in 30-70% of patients with their first attack of RF and in 73-90% of patients when all attacks are counted.
4) Invalidation of patient group, sometimes with death of the children.
5) Less antimicrobial treatment and access to health care, lower economic standards, lower hygiene and housing conditions, increased crowding, lower nutritional care etc. all reasons.

Pathophysiology:RF develops in children and adolescents following pharyngitis and tonsillitiswith GABHS (ie, Streptococcus pyogenes). The organisms attach to the epithelial cells of the upper respiratory tract and produce a battery of enzymes, which allows 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 elevated leukocyte count. In a small percent of patients, infection leads to RF several weeks after the sore throat has resolved. Only infections of the pharynx initiate or reactivate RF.
Direct contact with oral or respiratory secretions transmits the organism, and crowding enhances transmission. 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 prevents the major sequelae.
GABHS organisms are gram-positive cocci, which frequently colonize the skin and oropharynx. These organisms may cause suppurative diseases (eg, pharyngitis, impetigo, cellulitis, myositis, pneumonia, puerperal sepsis). GABHS organisms also may be associated with nonsuppurative diseases (eg, RF, acute poststreptococcal glomerulonephritis). Group A streptococci (GAS) elaborate the cytolytic toxins, streptolysins S and O. Of these 2 toxins, streptolysin O induces persistently high antibody titers that provide a useful marker of GAS infection and its nonsuppurative complications.
GAS, as identified using the Lancefield classification, has a group A carbohydrate antigen in the cell wall that is composed of a branched polymer of L-rhamnose and N-acetyl-D-glucosamine in a 2:1 ratio. GAS 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 GAS infection in humans. More than 90 Mserotypes 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 often are 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).

Acute RHD often produces a pancarditis, characterized by endocarditis, myocarditis, and pericarditis. Endocarditis is manifested as mitral and aortic valve insufficiency. Severe scarring of the valves develops during a period of months to years after an episode of acute RF, and recurrent episodes may cause progressive damage to the valves. The mitral valve is affected most commonly and severely (65-70% of patients); the aortic valve is affected second most commonly (25%). The tricuspid valve is deformed in only 10% of patients, almost always in association with mitral and aortic lesions, and the pulmonary valve rarely is affected. Severe valve insufficiency during the acute phase may result in congestive heart failure (CHF) and even death (1% of patients). Whether myocardial dysfunction during acute RF is related primarily to myocarditis or is secondary to CHF from severe valve insufficiency is not known. When pericarditis is present, it rarely affects cardiac function or results in constrictive pericarditis.
Chronic manifestations occur in adults with previous RHD from residual and progressive valve deformity. RHD is responsible for 99% of mitral valve stenosis in adults, and it may be associated with atrial fibrillation from chronic mitral valve disease and atrial enlargement.
Frequency:
· Internationally: In contrast to trends in the US, RF and RHD have not decreased in developing countries. Retrospective studies in developing countries demonstrate the highest figures for cardiac involvement and the highest recurrence rates of RF. Worldwide, an estimated 5-30 million children and young adults have chronic RHD, and 90,000 patients die from this disease each year.
Mortality/Morbidity: RHD is the major cause of morbidity from RF, and it is the major cause of mitral insufficiency and stenosis in the US and the world. Variables that correlate with severity of valve disease are the number of previous attacks of RF, the length of time between the onset of disease and start of therapy, and sex (the prognosis for females is worse than for males). Insufficiency from acute rheumatic valve disease resolves in 70-80% of patients if they adhere to antibiotic prophylaxis.
Sex: RF occurs in equal numbers in males and females. Females with RF fare worse than males and have a slightly higher incidence of chorea.
Age: RF is principally a disease of childhood, with a median age of 10 years; however, RF also occurs in adults (20% of cases).
CLINACAL FEATURES
History: Acute RF is a systemic disease. Thus, patients may present with a large variety of symptoms and complaints.
· History of an antecedent sore throat 1-5 weeks prior to onset is present in 70% of older children and young adults. Only 20% of younger children can recall an antecedent sore throat.
· Other symptoms on presentation may include fever, rash, headache, weight loss, epistaxis, fatigue, malaise, diaphoresis, and pallor.
· Patients also may have chest pain with orthopnea or abdominal pain and vomiting.
· Finally, history may reveal complaints more specific to RF.
· Migratory joint pain
· Nodules under the skin
· Increased irritability and shortened attention span with personality changes, such as pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections (PANDAS)
· Motor dysfunction
· History of previous RF
· Patients with previous RF are at a high risk of recurrence.
· Highest risk of recurrence within 5 years of the initial episode
· Greater risk of recurrence with younger age at the time of the initial episode
· Generally, recurrent attacks similar to the initial attack (however, risk of carditis and severity of valve damage increase with each attack)
Physical: Revised in 1992, the modified Kissell-Jones-Nesterov criteria provide guidelines for making the diagnosis of RF. Those criteria require the presence of 2 major or 1 major and 2 minor criteria for the diagnosis of RF. Having evidence of previous GAS pharyngitis is also necessary. These criteria are not absolute, and the diagnosis of RF can be made in patients with only confirmed streptococcal pharyngitis and chorea.
Major diagnostic criteria
· Carditis
· Polyarthritis
· Chorea
· Subcutaneous nodules
· Erythema marginatum
Minor diagnostic criteria (clinical)
· Fever
· Arthralgia
· Previous RF or rheumatic cardiac disease
(laboratory)
· Elevated acute-phase reactants (APRs), which are
a) erythrocyte sedimentation rate;
b) C-reactive protein
c) leukocitosis
· Three notable exceptions to strict adherence to the Jones criteria
· Chorea: It may occur late and be the only manifestation of RF.
· Indolent carditis: Patients presenting late to medical attention months after the onset of RF may have insufficient support to fulfill the criteria.
· Newly ill patients with a history of RF, especially RHD, who have supporting evidence of a recent GAS infection and who manifest either a single major or several minor criteria: Distinguishing recurrent carditis from preexisting significant RHD may be impossible.
· Evidence of previous GAS pharyngitis (One of the following must be present):
· Positive throat culture or rapid streptococcal antigen test
· Elevated or rising streptococcal antibody titer
Polyarthritis - usually with fever - is the presenting finding in about 75% of patients. The arthritis chiefly affected large joints, is distinctly migratory and is painful. Pathologic changers in the joints are mainly caused by edema, inflammation, and effusion of joint tissue. They are reversible and migratory in nature, favoring large joints, such as the knees, elbows, hips, shoulders, and wrists. The affected joint is swollen, hot, red, exquisitely painful for 1 to 2 days, after which a different joint is affected. The manifestations usually accompany the acute febrile period, usually the first 1 to 2 weeks.
Carditis - occurs in about 50% of the patients and may be asymptomatic. A pansystolic blowing mitral murmur is the hallmark. Less common is the diastolic aortic murmur heard along the left sternal border, murmurs may remain but often disappear if carditis does not recur. Rheumatic fever produces inflammatory hemorrhagic bullos lesions, called Aschoff bodies. The y cause swelling, fragmentation, alteration the connective tissue of the heart. Subsequent endocardities produces vegetations, which than healed become fibrous, scarred areas. The structures of the heart most affected are the mitral and aortic valves. If the scar tissue causes fusing of the leaflets, the valves are stenosed, causing obstruction to the blood flow into the left ventricle and aorta. If the valve edges are scarred so that they cannot completely close together, regurgitation (valvular insufficiency) or back flow of the blood occurs when the valves close. Signs of carditis are: 1) tachycardia, especially during rest or sleep that is out of proportion to the degree of fever; 2) cardiomegaly from increased workload and pericardial effusion; 3) a change in preexisting murmurs or new murmurs; 4) muffled heart sounds from pericardial effusion ; 5) an accentuated third sound (prediastolic gallop); 6) pericardial friction rub; 7) precordial pain from pericarditis; 8) changes in the conductivity of the heart, especially prolonged P-R interval ( first-degree heart block).
Borders of heart relative dullness
Until 2 years
Right- right parasternal line
Upper- the II rib
Left- 2cm outward from left mid-clavicular line
Transversal size- 6-9cm
2-7 years
Right- right parasternal line or something inward from right parasternal line.
Upper- the II intercostal space.
Left- 1cm outward from left mid-clavicular line.
Transversal size- 8- 12cm.
7- 12 years
Right- Between the right parasternal line and the right sternal line.
Upper- the III rib.
Left- 0.5cm outward from left mid-clavicular line.
Transversal size- 9- 14cm
Older than 12 years
Right- The right sternal line.
Upper- the III intercostal space.
Left- 0.5cm medially from left mid-clavicular line
Transversal size- 9- 14cm.

Borders of heart Absolute dullness
Until 2 years
Right- Left sternal line.
Upper- the II intercostal space.
Left- 1.0- 0.5cm outward from left mid-clavicular line.
Transversal size- 2-3cm.
2- 7 years
Right- Left sternal line
Upper- the III rib
Left- Left clavicular line
Transversal size- 4cm
7-12 years
Right- Left sternal line
Upper- the IIi intercostal space.
Left- Between the left mid-clavicular line and left parasternal line.
Transversal size- 5-5.5cm
Older 12 years
Right- Left sternal line
Upper- the IV rib
Left- left parasternal line
Transversal size- 5-5.5cm.

Average pulse rates at rest (beats per minute)
Newborn: 140-160
6 months: 130-135
1 year: 120-125
2 years: 110
3 years: 105
4 years: 100
5 years: 98-100
6-7 years: 85-90
10 years: 78-85
12 years: 70-75
*the normal rate is not more than 10% of average determined blood pressure.

Blood pressure, mmHg
Upper extrimity
Newborn
Systolic: 70-76
Diastolic: 35
For children younger than 12 months
Systolic: 76+ (2Xn); where n is age of child in months
Diastolic: 1/2 to 1/3 of systolic
1 year
systolic: 90-100
Diastolic: 60
For children Older than 1 year
Systolic: minimum [90+ (2Xn); where n is the age in years]. Maximum [100+(2Xn); where n is the age in years]
Diastole: 1/2 to 1/3 of systolic.
Lower extremity
Newborn
Systolic: 70-76
Diastolic: 35
For children younger than 9 months
systolic: 76 + (2Xn), where n is age in months
Diastolic: 1/2 to 1/3 of systolic
In children Older than 9-10 months
The blood pressure is 5-20 mmHg more than upper extremity.

Chorea occurs in 10-30% of patients with RF. Patients present with difficulty writing, involuntary grimacing, purposeless (ie, choreiform) movements of the arms and legs, speech impairment, generalized weakness, and emotional lability. Physical findings include hyperextended joints, hypotonia, diminished deep tendon reflexes, tongue fasciculations ("bag of worms"), and a "milk sign" or "relapsing grip" (ie, alternate increases and decreases in tension when the patient grips the examiner's hand). Occasionally, chorea is predominantly unilateral. Choreiform movements cease with sleep.
In the absence of a family history of Huntington chorea or findings consistent with systemic lupus erythematosus, the diagnosis of acute RF is almost certain. A long latency period exists between streptococcal pharyngitis (1-6 mo) and the onset of chorea, and a history of an antecedent sore throat frequently is not obtained. Patients with chorea often do not demonstrate other Jones criteria. Chorea is slightly more common in females than males. Chorea also is known as rheumatic chorea, Sydenham chorea, chorea minor, and St Vitus dance. Daily handwriting samples can be used as an indicator of progression or resolution of disease. Complete resolution of the symptoms typically occurs, with improvement in 1-2 weeks and full recovery in 2-3 months; however, incidents have been reported in which symptoms wax and wane for several years. The PANDAS disorder may be associated with chorea. Children have been identified in whom GAS infection appears to have triggered a relapsing-remitting symptom complex characterized by obsessive-compulsive personality disorder, and/or a tic disorder, and neurologic abnormalities (eg, cognitive defects, motoric hyperactivity). The symptoms may include emotional lability, separation anxiety, and oppositional behaviors, and they are prepubertal in onset. Some have proposed that the streptococcal infection triggers the formation of antibodies that cross-react with the basal ganglia of genetically susceptible hosts in a manner similar to the proposed mechanism for Sydenham chorea and causes the symptom complex.
Erythema marginatum: This characteristic rash, also known as erythema annulare, occurs in 5-13% of patients with acute RF. Erythema marginatum begins as 1- to 3-cm diameter, pink-to-red nonpruritic macules or papules located on the trunk and proximal limbs but never on the face. The lesions spread outward to form a serpiginous ring with erythematous raised margins and central clearing. The rash may fade and reappear within hours and is exacerbated by heat. Thus, if the lesions are not observed easily, they can be accentuated by the application of warm towels, a hot bath, or the use of tangential lighting. The rash occurs early in the course of the disease and remains long past the resolution of other symptoms. Erythema marginatum also has been reported in association with sepsis, drug reactions, and glomerulonephritis.
Subcutaneous nodules: Subcutaneous nodules are now an infrequent manifestation of RF. The frequency has declined during the past several years to 0-8% of patients with RF. When present, the nodules appear over the extensor surfaces of the elbows, knees, ankles, knuckles, scalp, and spinous processes of the lumbar and thoracic vertebrae (attached to the tendon sheath). The nodules are firm, nontender, and free from attachments to the overlying skin, and they range from a few millimeters to 1-2 cm. The nodules number from 1 to dozens, with a mean of 3-4. Histologically, the nodules contain areas resembling the Aschoff bodies observed in the heart. Subcutaneous nodules generally occur several weeks into the disease and resolve within a month. They are strongly associated with severe rheumatic carditis, and in the absence of carditis, question the diagnosis of subcutaneous nodules.
Other clinical manifestations
· Abdominal pain: Abdominal pain usually occurs at the onset of acute RF, resembles other conditions with acute microvascular mesenteric inflammation, and may mimic acute appendicitis.
· Arthralgias: Patients may complain of arthralgias on presentation. In the history, determining if the patient has taken aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) is important because these may suppress the full manifestations of the disease. Arthralgia cannot be considered a minor manifestation if arthritis is present.
· Epistaxis: Epistaxis may be associated with severe protracted rheumatic carditis.
· Fever: Fevers greater than 39°C with no characteristic pattern are present initially in almost every patient with acute RF. The fever may be low grade (38.0-38.5°C) in children with mild carditis or absent in patients with pure chorea. The fever decreases without antipyretic therapy in approximately 1 week, but low-grade fevers persist for 2-3 weeks.
· Rheumatic pneumonia: Patients present with the same signs as an infectious pneumonia.Differentiate rheumatic pneumonia from respiratory distress related to CHF.
Lab Studies:
· Throat culture
· Throat cultures for GABHS infections usually are negative by the time symptoms of RF or RHD appear.
· Make attempts to isolate the organism prior to 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.
· Rapid antigen detection test
· This test allows rapid detection of GAS antigen, allowing the diagnosis of streptococcal pharyngitis to be made and antibiotic therapy to be initiated while the patient is still in the physician’s office.
· This test reportedly has a specificity of greater than 95% but a sensitivity of only 60-90%. Thus, obtain a throat culture in conjunction with the rapid antigen detection test.
· Antistreptococcal antibodies
· Clinical features of RF begin when antistreptococcal antibody levels are at their peak. Thus, these tests are useful for confirming previous GAS infection. Antistreptococcal antibodies are particularly useful in patients who present with chorea as the only diagnostic criterion.
· Sensitivity for recent infections can be improved by testing for several antibodies. Check antibody titers 2 weeks apart to detect a rising titer. The most common extracellular antistreptococcal antibodies tested include antistreptolysin O (ASO) and anti-DNase B, antihyaluronidase, antistreptokinase, antistreptococcal esterase, and anti–nicotinamide adenine dinucleotide (anti-NAD). Antibody tests for cellular components of GAS antigens include antistreptococcal polysaccharide, antiteichoic acid antibody, and anti-M protein antibody.
· In general, the antibodies to extracellular streptococcal antigens rise during the first month after infection and then plateau for 3-6 months before returning to normal levels after 6-12 months. When the ASO titer peaks (2-3 wk after onset of RF), the sensitivity of this test is 80-85%.
· The anti-DNase B has a slightly higher sensitivity (90%) for detecting RF or acute glomerulonephritis. Antihyaluronidase frequently is abnormal in patients with RF with a normal ASO titer, may rise earlier, and persists longer than elevated ASO titers during incidents of RF.
· Acute-phase reactants: C-reactive protein and erythrocyte sedimentation rate are elevated in individuals with RF due to the inflammatory nature of the disease. Both tests have high sensitivity but low specificity for RF.
· Heart reactive antibodies: Tropomyosin is elevated in persons with acute RF.
· Rapid detection test for D8/17: This immunofluorescence technique for identifying the B-cell marker D8/17 is positive in 90% of patients with RF, and it may be useful for identifying patients who are at risk of developing RF.
Imaging Studies:
· Chest radiography
· Cardiomegaly, pulmonary congestion, and other findings consistent with heart failure may be observed on chest radiograph in individuals with RF.
· When the patient has fever and respiratory distress, the chest radiograph helps differentiate between CHF and rheumatic pneumonia.
· Echocardiography
· In individuals with acute RDH, echocardiography identifies and quantitates valve insufficiency and ventricular dysfunction.
· In persons 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 RF, the left ventricle frequently is dilated in association with a normal or increased fractional shortening. Thus, some cardiologists believe that valve insufficiency (eg, from endocarditis), rather than myocardial dysfunction (eg, from myocarditis), is the dominant cause of heart failure in individuals with acute RF.
· In individuals with chronic RHD, echocardiography tracks the progression of valve stenosis and may help determine the time for surgical intervention. The leaflets of affected valves become thickened diffusely, with fusion of the commissures and chordae tendineae. Increased echodensity of the mitral valve may signify calcification.
Other Tests:
· ECG Sinus tachycardia most frequently accompanies acute RHD. Alternatively, some children develop sinus bradycardia from increased vagal tone. No correlation exists between bradycardia and severity of carditis.
· First-degree atrioventricular (AV) block (prolongation of PR interval) is observed in some patients with RHD. 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 RHD. Its presence does not correlate with the development of chronic RHD.
· Second-degree (ie, intermittent) and third-degree (ie, complete) AV block with progression to ventricular standstill have been described. However, heart block in the setting of RF typically resolves with the rest of the disease process.
· In individuals with acute pericarditis, ST segment elevation may be present, most marked in leads II, III, aVF, and V4 through V6.
· Finally, patients with RHD may develop atrial flutter, multifocal atrial tachycardia, or atrial fibrillation from chronic mitral valve disease and atrial dilation.
Histologic FindingsPathologic examination of the insufficient valves may demonstrate verrucous lesions at the line of closure. Aschoff bodies (ie, 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.
Diagnosis.
The diagnosis must be based on the widely accepted Jones criteria, according to them we classify the manifestations as major and minor as to their diagnostic usefulness.
Major manifestations: Polyarthritis, carditis, chorea, subcutaneous nodules erythema marginatum.
Minor manifestations: Clinical - fever, arthralgia, previous rheumatic fever. Laboratory - leukocytosis, increasing erythrocyte sedimentation rate, C-reactive proteine, prolonged P-R interval.
Other - a) Streptococcal antibody tests ( antistreptolysin 0 ) are useful for documenting a resent Streptococcal infection, and the ESR and C-reactive protein test can provide evidence of an inflammatory process.
b) Positive throat culture for group A streptococcus .
c) Recent scarlet fever.
d) Doppler endocardiography has proven useful in identifying mitral insufficiency.
CLASSIFICATION OF RHEUMATISM (RHEUMATIC FEVER)
1. Criteria: Active (I, II, III stages) and non-active.
2. Clinical-anatomical characteristics of the damages
a. Heart (Active)
I. Primary rheumatic Carditis
II. Recurrent rheumatic Carditis (without valvulus defects, with defects).
III. Without visual heart changes.
(Non-active)
I. Heart defect
II. Rheumatic myocardiosclerosis.
b. Other systems and Organs (Active)
Polyarthritis, serousitis (pleuritis, peritonitis, abdominal syndrome), chorea, meningo-encephalitis, cerebral vasculitis, nephritis, hepatitis, pneumonia, dental problems, iritis, iridocyclitis, thyroiditis.
(non-active): Consequences and remaining effects after the main rheumatic process.

3. Course of disease
Acute, sub-acute, prolonged, recurrent, remittent.
4. Blood circulation insufficiency
CI- absent
CI1- I stage
CI2- II stage
CI3- III stage
*If it is possible, there is a necessity to point the main damage localization (myocarditis, pericarditis, pancarditis, coronaritis) and to stress the number of attacks.
Activity of the process
I stages
Leucocytosis: Less then 8 X 109/L
Erythrocyte sedimentation rate (ESR): Less then 20 mm/hr
C-reactive protein: - or +
Diphenilamine (DFA): less than 0.250
serrummucoid: 0.30
Antistreptolysin 0: less than 330
II stage
Leucocytosis: 8-10 X 109/L
Erythrocyte sedimentation rate (ESR): Less than 20-30 mm/hr
C-reactive protein: + or ++
Diphenilamine (DFA): Less than 0.250-0.330
serrummucoid: 0.30-0.60
Antistreptolysin 0: less than 330-660
III Stage
Leucocytosis: More than 10 X 109/L
Erythrocyte sedimentation rate (ESR): more than 30 mm/hr
C-reactive protein: +++ or ++++
Diphenilamine (DFA): More than 0.330
Serummucoid: More than 0.60
Antistreptolysin 0: Greater than 660
* the presence of 2 major criteria or of one major and two minor criteria indicates a high probability of the presence of rheumatic fever.
Heart Failure
Clinical symptoms
I. Failure of right ventricle which includes alteration in breath rates and pulse rates; cough and rales in the Lungs and the color of skin.
II. Failure of left ventricle which includes Hepatomegaly, splenomegaly, edema and Oliguria.
Degree of Heart failure
I. Clinical manifestation appears during physical activity (dyspnea, Tachycardia, acrocyanosis).
IIA: breath rates (>30-50%), pulse rate (>15-30%); Hepatomegaly (+3cm); edema (-); Oliguria (+).
IIB: breath rates (>50-70%); pulse rate (>30-50%); presence of cough and rales in the lungs; pale color of skin (+); Hepatomegaly (+3-5cm); edema and Oliguria (+).
III: Breath rates (>70%); Pulse rates (>50%); cough and rales in the Lungs (++) and also edema of Lung; pale color of skin (++); Hepatomegaly (>5cm); splenomegaly (+); edema, Oliguria (++).
Terms
1. Tachycardia: Increased heart rate
2. Bradycardia: Decreased heart rate.
3. Pulsus alternans: Strong beat followed by weak beat.
4. Pulsus bigeminus: coupled rhythm in which beat is felt in pairs.
5. Acrocyanosis: Persistent blue or cyanotic discoloration of the extremities, most commonly occuring in the hands although also occurring in the face and feet as well.
Differential diagnosis
1) rheumatoid arthritis
2) systemic lupus erythematosus
3) chronic tonsyllogenic intoxication
4) nonrheumatic cardities
5) infectious arthritis and
Treatment.
Antibiotic: Penicillin 30000-50000 IU\kg\day 10-14days or macrolids (eritromicin (20-40mg\kg\day
Hormone: prednisolone 0,8-1 mg\kg\day 10-14 days with decreasing dose every5-7 days on 5 mg till full stopping

Nonsteroid antiinflamation drug: aspirin 50-100 mg\kg\day but not more than 3,0;
voltaren (Š¾rtofen) 2,5-3 mg\kg\day brufen (ibubrofen) 20 mg\kg\day indometacin 2,5-3 mg\kg\day
full dose 3-4 weeks, then 2/3 of dose– 2 weeks, then 2-6 weeks of dose
Hinoline drugs: delagil 5 mg\kg\day
placvenil 8 mg\kg\day during 6-27months during recurrent course
Medical Care: Direct medical therapy toward eliminating the GAS pharyngitis (if still present), suppressing inflammation from the autoimmune response, and providing supportive treatment of CHF. Oral penicillin V remains the drug of choice for treatment of GAS pharyngitis. When oral penicillin is not feasible or dependable, a single dose of intramuscular benzathine penicillin G is therapeutic. For patients who are allergic to penicillin, administer erythromycin or a first-generation 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 penicillin-allergic patients also are allergic to cephalosporins. Do not use tetracyclines and sulfonamides to treat GAS pharyngitis.
· For recurrent 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.
· GAS carriage is difficult to eradicate with conventional penicillin therapy. Thus, oral clindamycin (20 mg/kg/d PO in 3 divided doses for 10 d) is recommended.
· In general, antimicrobial therapy is not indicated for pharyngeal carriers of GAS. Exceptions include the following:
· Outbreaks of RF or poststreptococcal glomerulonephritis
· Family history of RF
· During outbreaks of GAS pharyngitis in a closed community
· When tonsillectomy is considered for chronic GAS carriage
· When multiple episodes of documented GAS pharyngitis occur within a family despite appropriate therapy
· Following GAS toxic shock syndrome or necrotizing fasciitis in a household contact
· Treatment of the acute inflammatory manifestations of acute RF consists of salicylates and steroids. Aspirin in anti-inflammatory doses effectively reduces all manifestations of the disease except chorea, and the response typically is dramatic.
· If rapid improvement is not observed after 24-36 hours of therapy, question the diagnosis of RF.
· 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 RF are resolved or residing (6-8 wk) and the 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. Chorea most frequently is self-limited but may be alleviated or partially controlled with phenobarbital or diazepam.
· If moderate-to-severe carditis is present as indicated by cardiomegaly, CHF, or third-degree heart block, add oral prednisone to salicylate therapy.
· Continue prednisone for 2-6 weeks depending on the severity of the carditis, and taper prednisone during the last week of therapy.
· Discontinuing prednisone therapy after 2-4 weeks, while maintaining salicylates for an additional 2-4 weeks, can minimize adverse effects.
· Include digoxin and diuretics, afterload reduction, supplemental oxygen, bed rest, and sodium and fluid restriction as additional treatment for patients with acute RF and CHF. The diuretics most commonly used in conjunction with digoxin for children with CHF include furosemide and spironolactone.
· Initiate digoxin only after checking electrolytes and correcting abnormalities in serum potassium.
· The total loading dose is 20-30 mcg/kg PO qd, with 50% of the dose administered initially, followed by 25% of the dose 8 and 16 hours after the initial dose. Maintenance doses typically are 8-10 mcg/kg/d PO in 2 divided 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 qd. 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. Judiciously start these agents in the absence of hypovolemia.
· When heart failure persists or worsens during the acute phase after aggressive medical therapy, surgery is indicated to decrease valve insufficiency.
· Preventive and prophylactic therapy is indicated after RF and RHD 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 RF and RHD).
· 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. Administer the same dosage every 3 weeks in areas where RF is endemic, in patients with residual carditis, and in high-risk patients.
· While oral penicillin prophylaxis also is effective, data from the World Health Organization indicate that the recurrence risk of GAS pharyngitis is lower when penicillin is administered parentally.
· The duration of antibiotic prophylaxis is controversial. Continue antibiotic prophylaxis indefinitely for patients at high risk (eg, health care workers, teachers, daycare workers) for recurrent GAS infection. Ideally, continue prophylaxis indefinitely, because recurrent GAS infection and RF can occur at any age; however, the American Heart Association currently recommends that patients with RF without carditis receive prophylactic antibiotics for 5 years or until aged 21 years, whichever is longer. Patients with RF with carditis but no valve disease should receive prophylactic antibiotics for 10 years or well into adulthood, whichever is longer. Finally, patients with RF with carditis and valve disease should receive antibiotics at least 10 years or until aged 40 years.
· Patients with RHD and valve damage require a single dose of antibiotics 1 hour before surgical and dental procedures to help prevent bacterial endocarditis. Patients who had RF 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 RF prophylaxis (relative resistance of oral streptococci to penicillin and aminopenicillins). Alternate drugs recommended by the American Heart Association for these patients include oral clindamycin (children: 20 mg/kg; adults: 600 mg) and oral azithromycin or clarithromycin (children: 15 mg/kg; adults: 500 mg).
Control measures for patients with GAS pharyngitis are as follows:
· Hospitalized patients: Place hospitalized patients with GAS 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 GAS infection and should undergo antibiotic therapy if infected.
· School and childcare centers: Children with GAS infection should not attend school or childcare centers for the first 24 hours after initiating antimicrobial therapy.
Surgical Care: When heart failure persists or worsens after aggressive medical therapy for acute RHD, surgery to decrease valve insufficiency may be lifesaving. Approximately 40% of patients with acute RF subsequently develop mitral stenosis as adults. Mitral valvulotomy, percutaneous balloon valvuloplasty, or mitral valve replacement may be indicated in patients with critical stenosis. Valve replacement appears to be the preferred surgical option for patients with high rates of recurrent symptoms after annuloplasty or other repair procedures.
Diet: Advise nutritious diet without restrictions except in patients with CHF, who should follow a fluid-restricted and sodium-restricted diet. Potassium supplementation may be necessary because of the mineralocorticoid effect of corticosteroid and the diuretics, if used.
Activity: Initially, place patients on bed rest, followed by a period of indoor activity before they are permitted to return to school. Do not allow full activity until the APRs have returned to normal. Patients with chorea may require a wheelchair and should be on homebound instruction until the abnormal movements resolve.
Treatment and prevention of GAS pharyngitis outlined here are based on the current recommendations of the Committee on Infectious Disease (American Academy of Pediatrics). Medical therapy is directed toward elimination of GAS pharyngitis (if still present), suppression of inflammation from the autoimmune response, and supportive treatment of CHF.
Drug therapy
Drug Category: Antibiotics -- The roles for antibiotics are to (1) initially treat GAS pharyngitis, (2) prevent recurrent streptococcal pharyngitis, RF, and RHD, and (3) provide prophylaxis against bacterial endocarditis.
Drug Name: Penicillin VK (Beepen-VK, Pen.Vee K, V-Cillin K, Veetids) -- DOC for treatment of GAS pharyngitis. Although ampicillin or amoxicillin may be used instead, they have no microbiologic advantage. Do not use tetracyclines and sulfonamides to treat GAS pharyngitis. For recurrent GAS pharyngitis, a second 10-d course of same antibiotic may be repeated. Alternate drugs include narrow-spectrum cephalosporins, amoxicillin-clavulanate, dicloxacillin, erythromycin, or other macrolides.
Adult Dose: 500 mg PO bid/tid for 10 d
Pediatric Dose: Children:30-50mg/kg
Adolescents: Administer as in adults
Contraindications: Documented hypersensitivity
Interactions: Probenecid may increase effectiveness by decreasing clearance; tetracyclines are bacteriostatic, causing decrease in effectiveness of penicillins when administered concurrently
Precautions: Renal impairment, anaphylaxis, thrombocytopenia

Drug Name: Benzathine (Bicillin L-A)/procaine penicillin (Crysticillin A.S., Wycillin) -- Used when PO administration of penicillin is not feasible or dependable. IM therapy with penicillin is painful, but discomfort may be minimized if penicillin G is brought to room temperature before injection or combination of benzathine penicillin G and procaine penicillin G is used. Initial course of antibiotics administered to eradicate streptococcal infection also serves as first course of prophylaxis. An injection of benzathine penicillin G IM q4wk is recommended regimen for secondary prevention for most United States patients. Administer same dosage q3wk in areas where RF is endemic, in patients with residual carditis, and in high-risk patients.
Adult Dose: Eradication: 1.2 million U of benzathine penicillin G or a combination of 900,000 U of benzathine penicillin G with 300,000 U of procaine penicillin G IM as a single dose
Secondary prevention: Administer eradication dose q3wk (in high-risk areas, high-risk patients) or q4wk (for most areas in United States)
Pediatric Dose: Eradication <60 lb: 600,000 U of benzathine penicillin G IM as a single dose
Secondary prevention: Administer eradication dose q3wk (in high-risk areas, high-risk patients) or q4wk (for most areas in United States)
Contraindications: Documented hypersensitivity
Interactions: Increases risk of bleeding when administered concurrently with warfarin; ethacrynic acid, aspirin, indomethacin, and furosemide may compete with penicillin G for renal tubular secretion, increasing penicillin serum concentrations
Precautions: Never use IV route to administer penicillin G procaine; impaired renal function; anaphylaxis; thrombocytopenia

Drug Name: Erythromycin (E.E.S., E-Mycin, Eryc, Ery-Tab, Erythrocin) -- Used for patients who are allergic to penicillin. Other options include clarithromycin, azithromycin, or a narrow-spectrum cephalosporin (ie, cephalexin). As many as 15% of penicillin-allergic patients also are allergic to cephalosporins.
Adult Dose: 250 mg erythromycin stearate/base (or 400 mg ethylsuccinate) q6h PO 1 h ac for 10 d
Pediatric Dose: 20-40 mg (as base, estolate, or stearate)/kg/d PO divided bid/qid for 10 d; not to exceed 1 g/d
Alternatively, 40 mg (as ethylsuccinate)/kg/d PO divided bid/qid for 10 d
Contraindications: Documented hypersensitivity; with terfenadine (off US market) or astemizole (use in combination with erythromycin may cause prolongation of QT interval, with increased risk of ventricular arrhythmias and sudden death)
Interactions: Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis
Precautions: Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (administer doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occurs

Drug Name: Clarithromycin (Biaxin) -- Alternate antibiotic for treating GAS pharyngitis in patients allergic to penicillin.
Adult Dose: 250-500 mg PO bid for 10 d
Pediatric Dose: 7.5 mg/kg PO bid for 10 d
Contraindications: Documented hypersensitivity; coadministration of pimozide; patients taking terfenadine (off US market); patients with long QT syndrome
Interactions: CYP450 1A2 and 3A4 inhibitor; toxicity increases with coadministration of fluconazole and pimozide; clarithromycin effects decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, and HMG CoA-reductase inhibitors; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents
Precautions: Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; administer one half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies

Drug Name: Azithromycin (Zithromax) -- Alternate antibiotic for treating GAS pharyngitis in patients allergic to penicillin.
Adult Dose: 12 mg/kg (not to exceed 500 mg) PO qd for 5 d
Pediatric Dose: Administer as in adults
Contraindications: Documented hypersensitivity; hepatic impairment; do not administer with pimozide
Interactions: May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine
Precautions: May increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in patients who are hospitalized, geriatric, or debilitated

Drug Name: Cephalexin (Keflex, Biocef, Keftab) -- Alternate antibiotic for treating GAS pharyngitis in patients allergic to penicillin.
Adult Dose: 250-500 mg PO qid for 10 d
Pediatric Dose: 25-50 mg/kg/d PO divided qid for 10 d
Contraindications: Documented hypersensitivity
Interactions: Coadministration with aminoglycosides increases nephrotoxic potential
Precautions: Adjust dose in renal impairment

Drug Name: Amoxicillin (Amoxil, Biomox, Trimox) -- DOC used for bacterial endocarditis prophylaxis. Administered as single PO dose 1 h before dental work or surgery.
Adult Dose: 2 g PO once as a single dose
Pediatric Dose: 50 mg/kg PO once as a single dose
Contraindications: Documented hypersensitivity
Interactions: None significant for prophylaxis
Precautions: Adjust dose in renal impairment

Drug Category: Anti-inflammatory agents -- Manifestations of acute RF (including carditis) typically respond rapidly to therapy with anti-inflammatory agents. Aspirin, in anti-inflammatory doses, is DOC. Prednisone is added when evidence of worsening carditis and heart failure exists.
Drug Name: Aspirin (Anacin, Ascriptin, Bayer Aspirin) -- Begin administration immediately after diagnosis of RF.Initiation of therapy may mask manifestations of disease.
Adult Dose: 4-8 g/d PO divided q4-6h; maintain aspirin levels in 20-25 mg/dL range until all symptoms have resolved and APRs have returned to normal
Pediatric Dose: 50-100 mg/kg/d PO divided q4-6h; maintain aspirin levels in 20-25 mg/dL range until all symptoms have resolved and APRs have returned to normal
Contraindications: Documented hypersensitivity; liver damage; hypoprothrombinemia, vitamin K deficiency; bleeding disorders; asthma
Interactions: Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs
Precautions: Risk of salicylate intoxication and poisoning; watch for hyperventilation with prolonged expiratory phase with respiratory alkalosis and metabolic acidosis; risk of tinnitus, GI discomfort, and ulceration; when taken during pregnancy, increased risk of pulmonary hypertension exists in fetus in neonatal period

Drug Name: Prednisone (Deltasone, Orasone) -- If moderate-to-severe carditis is present as indicated by cardiomegaly, CHF, or third-degree heart block, use 2 mg/kg/d PO prednisone in addition to or in lieu of salicylate therapy. Continue prednisone for 2-4 wk depending on severity of carditis and taper during last week of therapy. Discontinuing prednisone therapy after 2 wk while adding or maintaining salicylates for additional 2-4 wk may minimize adverse effects.
Adult Dose: 2 mg/kg/d PO for 2-4 wk
Pediatric Dose: Administer as in adults
Contraindications: Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease
Interactions: Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Precautions: Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

Drug Category: Therapy for congestive heart failure -- Heart failure in RHD probably is related in part to severe insufficiency of the mitral and aortic valves and in part to pancarditis. Therapy traditionally has consisted of an inotropic agent (digitalis) in combination with diuretics (furosemide, spironolactone) and afterload reduction (captopril).
Drug Name: Digoxin (Lanoxin, Lanoxicaps) -- Inotropic agent widely used in past. Its efficacy in CHF is under review. Potential for toxicity is present. Therapeutic levels and clinical effects are observed more quickly if loading doses of digitalis are administered before routine maintenance doses. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure. Therapeutic digoxin levels are present at trough levels of 1.5-2 ng/mL.
Adult Dose: Total digitalizing dose (TDD) to be administered over 24 h; first dose is one half the TDD; second dose is one fourth the TDD, given 8 h later; third dose is one fourth the TDD, given 8 h after the second
TDD:0.75-1.5 mg PO
Maintenance dose: 0.125-0.5 mg PO qd
Pediatric Dose: TDD to be administered over 24 h; first dose is one half the TDD; second dose is one fourth the TDD, given 8 h later; third dose is one fourth the TDD, given 8 h after the second
TDD:
Preterm infant: 20-30 mcg/kg PO
Term infant: 25-35 mcg/kg PO
1 month to 2 years: 35-60 mcg/kg PO
2-5 years: 30-40 mcg/kg PO
5-10 years: 20-35 mcg/kg PO
>10 years: Administer as in adults
Maintenance dose:
Preterm infant: 5-7.5 mcg/kg/d PO divided bid
Term infant: 6-10 mcg/kg/d PO divided bid
1 month to 2 years: 10-15 mcg/kg/d PO divided bid
2-5 years: 7.5-10 mcg/kg/d PO divided bid
5-10 years: 5-10 mcg/kg/d PO divided bid
>10 years: Administer as in adults
Contraindications: Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome
Interactions: Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, PO amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil
Medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, PO colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (eg, carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid
Precautions: Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in patients receiving digitalis; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; caution in hypothyroidism, hypoxia, and acute myocarditis; initiate digoxin only after checking electrolytes and correcting abnormalities in serum potassium

Drug Name: Captopril (Capoten) -- Systemic afterload reduction may be helpful in improving cardiac output, particularly in setting of mitral and aortic valve insufficiency. Some patients have unusually large hypotensive response. Use small starting dose, particularly with hypovolemia.
Adult Dose: Starting dose: 6.25-12.5 mg PO tid
Typical dose: 50-100 mg PO tid
Pediatric Dose: Starting dose: 0.1-0.5 mg/kg/d PO divided tid; typically 1-2 mg/kg/d PO divided tid
Contraindications: Documented hypersensitivity; renal impairment
Interactions: NSAIDs may reduce hypotensive effects of captopril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases captopril levels; probenecid may increase captopril levels; hypotensive effects of ACE inhibitors may be enhanced when administered concurrently with diuretics
Precautions: Pregnancy category D in second and third trimesters; caution in renal impairment, valvular stenosis, or severe CHF.

Drug Name: Furosemide (Lasix) -- Diuretics frequently are used in conjunction with inotropic agents for patients with CHF. When used aggressively, may result in hypokalemia and hypovolemia. Risk of hearing loss in premature infants.
Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.
Adult Dose: 20-40 mg PO/IV/IM bid/tid
Pediatric Dose: 1-2 mg/kg/dose PO/IV/IM qd/tid
Contraindications: Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion
Interactions: Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced with concurrent administration; increased plasma lithium levels and toxicity are possible with concurrent administration
Precautions: Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter.

Drug Name: Spironolactone (Aldactone) -- Used in conjunction with furosemide as potassium-sparing diuretic.
Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.
Adult Dose: 100 mg PO divided qd/bid
Pediatric Dose: 2-4 mg/kg/d PO divided bid
Contraindications: Documented hypersensitivity; anuria; renal failure; hyperkalemia
Interactions: May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity of spironolactone
Precautions: Caution in renal and hepatic impairment
Patient Education:
· Direct patient education toward emphasizing measures that minimize further damage to the valves of the heart.
· Timely evaluation and treatment of pharyngitis in children help prevent RF.
· Secondary prophylaxis of patients with previous RF and valve involvement with penicillin injections every 3-4 weeks decrease the recurrence of RHD.
· Additional prophylactic antibiotics prior to dental and surgical procedures decrease the likelihood of bacterial endocarditis.
References and sources
1. Abernethy M, Bass N, Sharpe N: Doppler echocardiography and the early diagnosis of carditis in acute rheumatic fever. Aust N Z J Med 1994 Oct; 24(5): 530-5.
2. Circulation: The natural history of rheumatic fever and rheumatic heart disease. Ten-year report of a cooperative clinical trial of ACTH, cortisone, and aspirin. Circulation 1965 Sep; 32(3): 457-76.
3. Cotran RS, Kumar V, Collins T: Rheumatic fever. In: Robbins Pathologic Basis of Disease. 6th ed. WB Saunders Co; 1999: 570-73.
4. Dajani A, Taubert K, Ferrieri P: Treatment of acute streptococcal pharyngitis and prevention of rheumatic fever: a statement for health professionals. Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, the American. Pediatrics 1995 Oct; 96(4 Pt 1): 758-64.
5. Dajani AS, Taubert KA, Wilson W: Prevention of bacterial endocarditis. Recommendations by the American Heart Association. Circulation 1997 Jul 1; 96(1): 358-66.
6. Guidelines for the diagnosis of rheumatic fever: Jones Criteria, 1992 update. Special Writing Group of the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young of the American Heart Ass. JAMA 1992 Oct 21; 268(15): 2069-73.
7. Massell BF, Fyler DC, Roy SB: The clinical picture of rheumatic fever. Diagnosis, immediate prognosis, course and therapeutic implications. Am J Cardiol 1958; 1: 436-39.
8. Narula J, Virmani R, Reddy KS: Rheumatic Fever. American Registry of Pathology. Washington DC; 1999.
9. Pickering LK: Rheumatic Fever. 2000 Red Book: Report of the Committee on Infectious Diseases. 25th ed. American Academy of Pediatrics; Elk Grove Village, IL: 2000.
10. Swedo SE, Leonard HL, Garvey M, et al: A case of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. Am J Psychiatry 1998 Nov; 155(11): 1592-8.
11. Veasy LG, Wiedmeier SE, Orsmond GS, et al: Resurgence of acute rheumatic fever in the intermountain area of the United States. N Engl J Med 1987 Feb 19; 316(8): 421-7.



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