A. Prevalence

Subacute bacterial endocarditis (SBE) affects 0.5:1000 to 1:1000 hospital patients, excluding those with postoperative endocarditis.

B. Pathology and Pathogenesis

• 1.
  

  Two factors are important in the pathogenesis of IE: (a) structural abnormalities of the heart or great arteries with a significant pressure gradient or turbulence, with resulting endothelial damage and platelet-fibrin thrombus formation; and (b) bacteremia, even if transient, with adherence of the organisms and eventual invasion of the underlying tissue.

  
  
• 2.
  

  Those with a prosthetic heart valve or prosthetic material in the heart are at particularly high risk for IE because these promote deposition of sterile thrombus.

  
  
• 3.
  

  Almost all patients who develop IE have a history of congenital or acquired heart disease. Drug addicts may develop endocarditis in the absence of known cardiac anomalies.

  
  
• 4.
  

  Dental procedures or chewing with diseased teeth or gums may be the most frequent cause of bacteremia.

C. Microbiology

• 1.
  

  In the past, Streptococcus viridans , enterococci, and Staphylococcus aureus were responsible for over 90% of cases of IE. In recent years, this frequency has decreased to 50% to 60%, with a concomitant increase in cases caused by fungus and HACEK organisms ( Haemophilus, Actinobacillus, Cardiobacterium, Eikenella , and Kingella ). HACEK organisms are particularly common in neonates and immunocompromised children.

  
  
• 2.
  

  α-Hemolytic streptococci ( S. viridans ) are the most common cause of IE following dental procedures or in those patients with carious teeth or periodontal disease.

  
  
• 3.
  

  Staphylococci ( S. aureus and coagulase-negative staphylococci) account for more cases than S. viridans in developed countries, usually health care–associated infections, such as postoperative endocarditis, indwelling vascular catheters, prosthetic material, prosthetic valve, among newborn infants, and intravenous drug abusers.

  
  
• 4.
  

  Enterococci are the organisms most often found after genitourinary or gastrointestinal surgery or instrumentation.

  
  
• 5.
  

  Fungal endocarditis (which has a poor prognosis) may occur in sick neonates, in patients receiving long-term antibiotic or steroid therapy, or after open heart surgery.

  
  
• 6.
  

  Culture-negative endocarditis. Diagnosis of this condition is made when a patient has clinical and/or echocardiographic evidence of endocarditis but persistently negative blood cultures. This occurs in about 5% to 7% of endocarditis in the United States. The most common cause of the condition is current or recent antibiotic therapy. It can be caused by a fastidious organism that grows poorly in vitro and rarely by fungus. At times, the diagnosis can be made only by removal of vegetation (during surgery).

D. Clinical Manifestations

• 1.
  

  Most patients are known to have an underlying heart disease. A history of toothache, recent dental procedure, or tonsillectomy is occasionally present. A history of recent cardiovascular procedures or surgeries may be present. The onset is usually insidious with prolonged low-grade fever of 38°C but fever may fluctuate up to 39.5°C.

  
  
• 2.
  

  Heart murmur is almost always present and splenomegaly is common (70%).

  
  
• 3.
  

  Skin manifestations (50%) may be present in the following forms:

  
  
  
  
  • a.
    

    Petechiae on the skin, mucous membranes, or conjunctivae are frequent.

    
    
  • b.
    

    Osler nodes (tender, pea-sized red nodes at the ends of the fingers or toes) are rare in children.

    
    
  • c.
    

    Janeway lesions (small, painless, hemorrhagic areas on the palms or soles) are rare.

    
    
  • d.
    

    Splinter hemorrhages (linear hemorrhagic streaks beneath the nails) also are rare.

  
  
  
  
• 4.
  

  Embolic or immunologic phenomena in other organs are present in about 50% of cases.

  
  
  
  
  • a.
    

    Pulmonary emboli or hematuria and renal failure may occur.

    
    
  • b.
    

    Seizures and hemiparesis (20%) may occur.

    
    
  • c.
    

    Roth spots (oval, retinal hemorrhages with pale centers located near the optic disc) occur in <5% of patients.

  
  
  
  
• 5.
  

  Laboratory studies.

  
  
  
  
  • a.
    

    Positive blood cultures are obtained in more than 90% of patients in the absence of previous antimicrobial therapy.

    
    
  • b.
    

    Anemia and leukocytosis with a shift to the left are common.

    
    
  • c.
    

    The sedimentation rate is increased unless there is polycythemia.

    
    
  • d.
    

    Microscopic hematuria is found in 30% of patients.

  
  
  
  
• 6.
  

  Echocardiography. Although standard transthoracic echo (TTE) is sufficient in most cases, transesophageal echo (TEE) may be needed in obese or very muscular adolescents.

  
  
  
  
  • a.
    

    The following echo findings are included as major criteria in the modified Duke criteria: (1) oscillating intracardiac mass on valve or supporting structures, in the path of regurgitation jets or on implanted material; (2) abscesses; (3) new partial dehiscence of prosthetic valve; and (4) new valvular regurgitation.

    
    
  • b.
    

    The absence of vegetations on echo does not in itself rule out IE. False-negative diagnosis is possible if vegetations are small or have already embolized.

    
    
  • c.
    

    Conversely, a false-positive diagnosis is possible. An echogenic mass may represent a sterile thrombus, sterile prosthetic material, normal anatomic variation, an abnormal uninfected valve (previous scarring, severe myxomatous changes), or improper gain of the echo machine. Echo evidence of vegetation may persist for months or years after bacteriologic cure.

    
    
  • d.
    

    Certain echo features suggest a high-risk case or a need for surgery: (1) large vegetations (greatest risk when the vegetation is >10 mm), (2) severe valvular regurgitation, (3) abscess cavities, (4) pseudoaneurysm, (5) valvular perforation or dehiscence, or (6) decompensated heart failure.

  
  

E. Diagnosis

The diagnosis of infective endocarditis is challenging. The modified Duke criteria are used in the diagnosis. There are three categories of diagnostic possibilities using the modified Duke criteria: definite, possible, and rejected ( Box 12.1 ). Box 12.2 shows definitions of major and minor clinical criteria. It is imperative for readers to carefully read and understand the statements in these boxes ( Boxes 12.1 and Box 12.2 ).

• 1.
  

  A diagnosis of “ definite ” IE is made when (a) pathologic evidence and (b) fulfillment of certain clinical criteria (listed in Box 12.1 ) are present.

  
  
• 2.
  

  The category of “possible ” IE is made when (a) one major criterion and one minor criterion or (b) three minor criteria are present.

  
  
• 3.
  

  The category of “ rejected ” IE is made when one of the four statements in Box 12.1 is present.

F. Management

• 1.
  

  Blood cultures are indicated for all patients with fever of unexplained origin and a pathologic heart murmur, a history of heart disease, or previous endocarditis.

  
  
  
  
  • a.
    

    Usually three blood cultures are drawn over 24 hours, unless the patient is very ill. In 90% of cases, the causative agent is recovered from the first two cultures.

    
    
  • b.
    

    If there is no growth by the second day of incubation, two more cultures may be obtained. There is no value in obtaining more than five blood cultures over 2 days unless the patient received prior antibiotic therapy.

    
    
  • c.
    

    Aerobic incubation alone suffices because it is rare for IE to be due to anaerobic bacteria.

  
  
  
  
• 2.
  

  Initial empirical therapy is started with the following antibiotics while awaiting the results of blood cultures. Consultation from a local infectious disease specialist is strongly recommended.

  
  
  
  
  • a.
    

    The usual initial regimen is an antistaphylococcal semisynthetic penicillin (nafcillin, oxacillin, or methicillin) and an aminoglycoside (gentamicin). This combination covers against S. viridans, S. aureus , and gram-negative organisms.

    
    
  • b.
    

    If a methicillin-resistant S. aureus is suspected, vancomycin should be substituted for the semisynthetic penicillin.

    
    
  • c.
    

    Vancomycin can be used in place of penicillin or a semisynthetic penicillin in penicillin-allergic patients.

  
  
  
  
• 3.
  

  The final selection of antibiotics for native valve IE depends on the organism isolated and the results of an antibiotic sensitivity test.

  
  
  
  
  • a.
    

    Streptococcal infective endocarditis

  
  
  
  
  • (1)
    

    For highly sensitive S. viridans , IV penicillin (or ceftriaxone given once daily) for 4 weeks is sufficient. Alternatively, penicillin, ampicillin, or ceftriaxone combined with gentamicin for 2 weeks may be used.

    
    
  • (2)
    

    For penicillin-resistant streptococci, 4 weeks of penicillin, ampicillin, or ceftriaxone combined with gentamicin for the first 2 weeks is recommended.

  
  
  
  
  • b.
    

    Staphylococcal endocarditis

  
  
  
  
  • (1)
    

    For methicillin-susceptible staphylococci IE, one of the semisynthetic β-lactamase–resistant penicillins (nafcillin, oxacillin, or methicillin) for a minimum of 6 weeks (with or without gentamicin for the first 3 to 5 days) is used.

    
    
  • (2)
    

    For patients with methicillin-resistant IE, vancomycin for 6 weeks (with or without gentamicin for the first 3 to 5 days) is used.

  
  
  
  
  • c.
    

    Enterococcus -caused endocarditis usually requires a combination of IV penicillin or ampicillin together with gentamicin for 4 to 6 weeks. If patients are allergic to penicillin, vancomycin combined with gentamicin for 6 weeks is required.

    
    
  • d.
    

    For HACEK organisms, ceftriaxone or another third-generation cephalosporin alone or ampicillin plus gentamicin for 4 weeks is recommended. IE caused by other gram-negative bacteria (such as Escherichia coli , Pseudomonas aeruginosa , or Serratia marcescens ) is treated with piperacillin or ceftazidime together with gentamicin for a minimum of 6 weeks.

    
    
  • e.
    

    Fungal endocarditis is very difficult to treat. Amphotericin B, with or without flucytosine, is most often used, but surgical replacement of the infected valve (native or prosthetic) is usually required.

    
    
  • f.
    

    In culture-negative endocarditis, treatment is directed against staphylococci, streptococci, and the HACEK organisms using ceftriaxone and gentamicin. When staphylococcal IE is suspected, nafcillin should be added to the above therapy.

  
  
  
  
• 4.
  

  Patients with prosthetic valve endocarditis should be treated for 6 weeks based on the organism isolated and the results of the sensitivity test. Operative intervention may be necessary before the antibiotic therapy is completed if the clinical situation warrants (such as progressive CHF, significant malfunction of prosthetic valves, persistently positive blood cultures after 2 weeks’ therapy). Bacteriologic relapse after an appropriate course of therapy also calls for operative intervention.

G. Prognosis

The overall recovery rate is 80% to 85%; it is 90% or better for S. viridans and enterococci, and about 50% for Staphylococcus organisms. Fungal endocarditis is associated with a very poor outcome.

H. Prevention

Until 2007, antibiotic prophylaxis for IE was routinely recommended before dental procedures for almost all CHDs (with exception of ASD), rheumatic and other valvular diseases, hypertrophic cardiomyopathy, and all other conditions included in the current recommendation. In 2007, the American Heart Association (AHA) made a major change in the antibiotic prophylaxis against IE.

• 1.
  

  The following are the updated recommendations for antibiotic prophylaxis.

  
  
  
  
  • a.
    

    Antibiotic prophylaxis is recommended only for cardiac conditions listed in Box 12.3 , which was updated in 2017.

    
    
    
    

    Box 12.3

    
    

    2017 AHA/ACC Updated Recommendation on Cardiac Conditions for Which Prophylaxis with Dental Procedures is Recommended

    
    

    ^a The risk of IE is highest in the first 6 months after transplantation because of endothelial disruption, high-intensity immunosuppressive therapy, frequent central venous catheter access, and frequent endomyocardial biopsies. IE , infective endocarditis.Adapted from Nishimura RA, Otto CM, Bonow RO, et al: 217 AHA/ACC focused update of the 2014 AHA/ACC guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines, Circulation 2017;135(25): e1159-e1195.

    
    

    
    

    Prophylaxis against IE is reasonable before dental procedures that involve manipulation of gingival tissue, manipulation of the peripheral region of teeth, or perforation of the oral mucosa in patients with the following:

    
    

    
    
    • 1.
      

      Prosthetic cardiac valves, including transcatheter-implanted prostheses and homografts.

      
      
    • 2.
      

      Prosthetic material used for cardiac valve repair, such as annuloplasty rings and chords.

      
      
    • 3.
      

      Previous IE.

      
      
    • 4.
      

      Unrepaired cyanotic congenital heart disease or repaired congenital heart disease, with residual shunts or valvular regurgitation at the site of or adjacent to the site of a prosthetic patch or prosthetic device.

      
      
    • 5.
      

      Cardiac transplant with valve regurgitation due to a structurally abnormal valve. ^a

    
    

    
    
    
    
  • b.
    

    Procedures for which antibiotic prophylaxis is recommended and those not recommended are listed in Box 12.4 .

    
    
    
    

    Box 12.4

    
    

    Procedures for which Endocarditis Prophylaxis is Recommended

    
    

    GI , gastrointestinal; GU , genitourinary.

    
    

    
    

    
    

    
    
    • 1.
      

      Dental procedures

      
      

      All dental procedures that involve manipulation of gingival tissue of the periapical region of teeth or perforation of the oral mucosa. Antibiotic choices and dosages for dental procedures are shown in Table 12.1 .

      
      
    • 2.
      

      Respiratory tract procedures

      
      
      
      
      • a.
        

        Prophylaxis is recommended for the procedures that involve incision or biopsy of the respiratory mucosa, such as tonsillectomy and adenoidectomy.

        
        
      • b.
        

        Prophylaxis is not recommended for bronchoscopy (unless it involves incision of the mucosa, such as for abscess or empyema).

      
      
      
      
    • 3.
      

      GI and GU procedures

      
      
      
      
      • a.
        

        No prophylaxis for diagnostic esophagogastroduodenoscopy or colonoscopy.

        
        
      • b.
        

        Prophylaxis is reasonable in patients with infected GI or GU tract (with amoxicillin or ampicillin to cover against enterococci).

      
      
      
      
    • 4.
      

      Skin, skin structure, or musculoskeletal tissue.

      
      
      
      
      • a.
        

        Prophylaxis is recommended for surgical procedures that involve infected skin, skin structure, or musculoskeletal tissue (with antibiotics against Staphylococcus and β-hemolytic Streptococcus , such as antistaphylococcal penicillin or a cephalosporin).

        
        
      • b.
        

        Vancomycin or clindamycin is administered if unable to tolerate β-lactam or if infection is caused by methicillin-resistant Staphylococcus .

      
      

    
    

    
    
    
    
  • c.
    

    Antibiotic choices and dosages for dental procedures are shown in Table 12.1 .

    
    
    
    

    Table 12.1

    
    

    Prophylactic Regimens for Dental Procedures

    
    

    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    

    		Single Dose 30-60 MIN Before Procedure
    Situation	Agent	Children	Adults
    Oral	Amoxicillin	50 mg/kg	2 g
    Unable to take oral medications	Ampicillin, or cefazolin or ceftriaxone	50 mg/kg (IM, IV)50 mg/kg (IM, IV)	2 g (IM, IV)1 g (IM, IV)
    Allergic to penicillin or ampicillin—oral	Cephalexin a,b or clindamycin, or azithromycin or clarithromycin	50 mg/kg 20 mg/kg 15 mg/kg 15 mg/kg	2 g 600 mg 500 mg 500 mg
    Allergic to penicillin or ampicillin and unable to take oral medication	Cefazolin, or ceftriaxone Clindamycin	50 mg/kg (IM, IV)20 mg/kg (IM, IV)	1 g (IM, IV)600 mg (IM, IV)

     
    

    IM, intramuscular; IV, intravenous

    
    

    a Or other first- or second-generation oral cephalosporin in equivalent adult or pediatric dosage.

    
    

    b Cephalosporins should not be used in an individual with a history of anaphylaxis, angioedema, or urticaria with penicillin or ampicillin.

    
    

  
  
  
  
• 2.
  

  Special situations.

  
  
  
  
  • a.
    

    For patients receiving rheumatic fever prophylaxis, use other antibiotics, such as clindamycin, azithromycin, or clarithromycin, rather than using a higher dose of the same antibiotic.

    
    
  • b.
    

    When the patient is already receiving a course of an antibiotic for other reasons (such as tonsillitis), delay a dental procedure, if possible, until at least 10 days after completion of the antibiotic therapy.

  
  
  
  
• 3.
  

  For patients who undergo cardiac surgery, the following applies:

  
  
  
  
  • a.
    

    A careful preoperative dental evaluation is recommended so that required dental treatment may be completed before cardiac surgery.

    
    
  • b.
    

    Prophylaxis at the time of surgery should be directed primarily against staphylococci and should be of short duration.

    
    
  • c.
    

    Prophylaxis should be initiated immediately before the operative procedure, repeated during prolonged procedures to maintain serum concentrations intraoperatively, and continued for no more than 48 hours postoperatively.

  
  

A. Prevalence

Myocarditis severe enough to be recognized clinically is rare, but the prevalence of mild and subclinical cases is probably much higher.

B. Etiology

• 1.
  

  Infections: Viruses (such as adenovirus, coxsackieviruses, echoviruses, and many others) are the most common cause of myocarditis in North America. In South America, Chagas disease (caused by Trypanosoma cruzi , a protozoan) is far more common. Rarely, bacteria, rickettsia, fungi, protozoa, and parasites are the causative agents.

  
  
• 2.
  

  Immune-mediated diseases: ARF, Kawasaki disease.

  
  
• 3.
  

  Autoimmune disorders: sarcoidosis, systemic lupus erythematosus.

  
  
• 4.
  

  Toxic myocarditis (drug ingestion, diphtheria exotoxin, and anoxic agents).

C. Pathology

• 1.
  

  The principal mechanism of cardiac involvement in viral myocarditis is believed to be a cell-mediated immunologic reaction, not merely myocardial damage from viral replication. Isolation of virus from the myocardium is unusual at autopsy.

  
  
• 2.
  

  Microscopic examination reveals patchy infiltrations by plasma cells, mononuclear leukocytes, and some eosinophils during the acute phase and giant cell infiltration in the later stages.

D. Clinical Manifestations

• 1.
  

  History of an upper respiratory tract infection may be present in older children. The onset of illness may be sudden in neonates and small infants, causing anorexia, vomiting, lethargy, and occasionally circulatory shock. In older children, a gradual onset of CHF and arrhythmia are commonly seen.

  
  
• 2.
  

  A soft, systolic ejection murmur and irregular rhythm caused by supraventricular or ventricular ectopic beats may be audible. Hepatomegaly (evidence of viral hepatitis) may be present.

  
  
• 3.
  

  The ECG may show any one or a combination of the following: low QRS voltages, ST-T changes, prolongation of the QT interval, and arrhythmias, especially premature contractions.

  
  
• 4.
  

  Cardiomegaly on chest radiograph is the most important clinical sign of myocarditis.

  
  
• 5.
  

  Echo studies reveal cardiac chamber enlargement and impaired LV systolic function. Occasionally, LV thrombi are found.

  
  
• 6.
  

  Laboratory studies. Cardiac troponin (I and T) levels and myocardial enzymes (creatine kinase [CK], MB isoenzyme of CK [CK-MB]) may be elevated. Troponin levels may be more sensitive than the cardiac enzymes. The normal value of cardiac troponin I in children is 2.0 ng/mL or less. B-type natriuretic peptide (BNP) and N-terminal-pro-BNP levels are elevated at the time of the diagnosis and they aid for management and evaluation of treatment progress.

  
  
• 7.
  

  Cardiac magnetic resonance imaging (MRI) has become the diagnostic tool of choice in diagnosis of acute or chronic phase of myocarditis. Cardiac MRI has mostly replaced radionuclide scanning in identifying inflammatory and necrotic changes characteristic of myocarditis. In additional, it aids the evaluation of cardiac function, pericardial effusion, and/or edema. Myocarditis can be confirmed by an endomyocardial biopsy.

  
  
• 8.
  

  Natural history. The mortality rate is as high as 75% in symptomatic neonates with acute viral myocarditis. In children, the majority of patients, especially those with mild inflammation, recover completely. Some patients develop subacute or chronic myocarditis with persistent cardiomegaly with or without signs of CHF and ECG evidence of LVH or BVH. Clinically, these patients are indistinguishable from those with dilated cardiomyopathy. Myocarditis may be a precursor to some cases of idiopathic dilated cardiomyopathy. Some patients develop refractory heart failure and may become candidates for heart transplantation.

E. Management

• 1.
  

  Virus identification by viral cultures from the blood, stool, or throat washing should be attempted, and comparison of acute and convalescent sera may be made for serologic titer rise.

  
  
• 2.
  

  Oxygen and bed rest are recommended. Use of a “cardiac chair” or “infant seat” relieves respiratory distress.

  
  
• 3.
  

  Bed rest and limitation in activities are recommended during the acute phase.

  
  
• 4.
  

  Anticongestive medications are used for symptomatic patient with heart failure.

  
  
  
  
  • a.
    

    Rapid-acting diuretics (furosemide or ethacrynic acid) and angiotensin-converting enzyme (ACE) inhibitors (captopril) or angiotensin receptor blockers are beneficial in the acute phase

    
    
  • b.
    

    Rapid-acting inotropic agents (such as dobutamine, dopamine, or inodilator, milrinone) are useful in critically ill children; however, they have the potential for arrhythmia.

    
    
  • c.
    

    Use of digoxin is not recommended, because some patients with myocarditis are found to be exquisitely sensitive to the drug.

    
    
  • d.
    

    β-Blockers are not recommended in the acute phase but may be required as long-term maintenance drug.

    
    
  • e.
    

    Nonsteroidal antiinflammatory agents are not recommended during acute and subacute phase.

    
    
  • f.
    

    The role of corticosteroids is unclear at this time, except in the treatment of severe rheumatic carditis.

  
  
  
  
• 5.
  

  Some centers have reported beneficial effects of intravenous immunoglobulin (IVIG) (2 g/kg, over 24 hours) (with better survival and better LV function by echo) as seen with Kawasaki disease; however, the routine use of IVIG remains controversial and is not recommended broadly.

  
  
• 6.
  

  Arrhythmias should be treated aggressively and may require the use of IV amiodarone. In patients with significant AV conduction disturbance, permanent pacemaker may be necessary

A. Etiology

• 1.
  

  Viral infection is probably the most common cause of pericarditis, particularly in infancy. Viral causes include coxsackie virus, herpesvirus, mumps virus, and human immunodeficiency virus (HIV), among others.

  
  
• 2.
  

  Bacterial infection (purulent pericarditis) is rare. Commonly encountered are S. aureus, Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis , and streptococci.

  
  
• 3.
  

  ARF is a common cause of pericarditis in older children in certain parts of the world.

  
  
• 4.
  

  Tuberculosis (an occasional cause of constrictive pericarditis with insidious onset).

  
  
• 5.
  

  Heart surgery (postpericardiotomy syndrome).

  
  
• 6.
  

  Collagen disease such as rheumatoid arthritis.

  
  
• 7.
  

  A complication of oncologic disease or its therapy, including radiation.

  
  
• 8.
  

  Uremia (uremic pericarditis).

B. Pathology and Pathophysiology

• 1.
  

  Pericardial effusion may be serofibrinous, hemorrhagic, or purulent. Effusion may be completely reabsorbed or may result in pericardial thickening or chronic constriction (constrictive pericarditis). Findings of myocarditis are also present in about one-third of the patients.

  
  
• 2.
  

  Symptoms and signs of pericardial effusion are determined by two factors: speed of fluid accumulation and competence of the myocardium. A rapid accumulation of a large amount of pericardial fluid produces more serious circulatory embarrassment. A slow accumulation of a large amount of fluid may be well tolerated by stretching of the pericardium, if the myocardium is intact. A rapid accumulation of even a small amount of fluid in the presence of myocarditis can produce circulatory embarrassment.

  
  
• 3.
  

  When the pericardial effusion builds up, resulting in compression of the heart, it is called cardiac tamponade. Onset may be rapid or gradual. With the development of pericardial tamponade, several compensatory mechanisms are called on: systemic and pulmonary venous constriction (to improve diastolic filling), an increase in the SVR (to raise falling blood pressure), and tachycardia (to improve cardiac output).

C. Clinical Manifestations

• 1.
  

  Precordial or substernal pain (sharp, dull, aching, or stabbing) with occasional radiation to the shoulder and neck may be a presenting complaint. The pain may be relieved by leaning forward and made worse by supine position or deep inspiration.

  
  
• 2.
  

  Pericardial friction rub is the pathognomonic physical sign. The heart is hypodynamic, and heart murmur is usually absent. In children with purulent pericarditis, septic fever (101° to 105°F [38° to 41° C), tachycardia, chest pain, and dyspnea are almost always present. Signs of cardiac tamponade may be present (distant heart sounds, tachycardia, pulsus paradoxus, hepatomegaly, neck vein distention, and occasional hypotension with peripheral vasoconstriction).

  
  
• 3.
  

  The ECG may show a low-voltage QRS complex, ST-segment shift, and T-wave inversion.

  
  
• 4.
  

  Chest radiographs may show a varying degree of cardiomegaly. Water bottle–shaped heart and increased pulmonary venous markings are seen with large effusion.

  
  
• 5.
  

  Echo is the most useful tool in establishing the diagnosis of pericardial effusion. It appears as an echo-free space between the epicardium (visceral pericardium) and the parietal pericardium.

  
  
  
  
  • a.
    

    Small pericardial effusion first appears posteriorly in the dependent portion of the pericardial sac. A small amount of fluid, which appears only in systole, is normal. With larger effusion, the fluid also appears anteriorly. With very large effusions, the swinging motion of the heart may be imaged.

    
    
  • b.
    

    The following are helpful 2D echo findings of cardiac tamponade.

    
    
    
    
    • (1)
      

      Tamponade usually occurs with circumferential effusion.

      
      
    • (2)
      

      Collapse of the RA in late diastole ( Fig. 12.1 ) is seen in subcostal views (because the pressure in the pericardial sac exceeds the pressure within the RA at end-diastole when the atrium has emptied).

      
      

      
      

      
      

      

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