The editors and current author would like to thank and acknowledge the significant contribution of the previous author of this chapter from the 2004 first edition, David K.M. Wong, MD. This current second edition chapter is a revision and update of the original author's work.
This is a 9 year old female, who present to the Emergency Department with fatigue, abdominal pain and loss of consciousness. She had no previous medical history and no previous cardiac problems. Four days prior, she started feeling tired, had intermittent headaches and abdominal pain, and vomited twice. Over the previous 24 hours her symptoms worsened, becoming increasingly tired and she continued to have abdominal pain. Tonight while sitting on a couch next to her mother, she lost consciousness and then her entire body became stiff. 911 was called. The episode resolved within a minute, but she had another three similar episodes within a short period of time.
In the ambulance, another episode was witnessed. Her eyes rolled up, she lost her posture, and her entire body became stiff for about 20 seconds. The episode resolved within 30 seconds and she regained consciousness. An ECG was obtained by EMS that showed bradycardia and arrhythmia, and since her blood pressure was marginal, she was given a bolus of normal saline en route to the hospital. On arrival in the ED, she continued to have a marginal blood pressure, poor perfusion and an abnormal ECG showing an irregular rhythm with wide complex QRS morphology.
Physical examination: VS T 37.6 degrees C, HR 52, RR 27, BP 82/58, oxygen saturation 98% on oxygen, weight 43.6 kg (96%ile). She is alert, but tired, and pale, with 5 out of 10 abdominal pain. Chest: symmetric, no deformity. Respiratory: fair air entry, fine crackles at both lung bases, no wheezing. Heart: irregular rhythm with bradycardia, normal precordial activity, no thrill, muffled S1 and S2, 1/6 holosystolic murmur, no diastolic murmur, no additional heart sounds, no gallop or rub. Abdomen: soft, tender at RUQ, epigastrium, and LUQ, not distended, liver soft, slightly enlarged, normal bowel sounds. Extremities: Normal range of motion, pulses thready in all four extremities, no pitting edema, no clubbing or cyanosis, no rash.
Clinical course: The ECG showed a complete (3rd degree) AV block with an irregular wide complex escape rhythm at a rate of 50-60 bpm. Cardiology was consulted in the ED. She was started on an epinephrine infusion. Her heart rate increased from the previous 50's to 150's with intact conduction due to the beta agonist medications. An echocardiogram was obtained at the bedside that showed mild left ventricular (LV) dilation, decreased LV systolic function, with an LVEF (LV ejection fraction) of 45%, and mild mitral regurgitation, so she was admitted to the PICU with the diagnosis of myocarditis and AV block. ECMO (extracorporeal membrane oxygenation)consultation was obtained due to the possibility of rapid deterioration.
In the PICU, epinephrine was discontinued and switched to isoproterenol and milrinone for beta-mimetic and positive inotrope activity. Laboratory tests were obtained and she was given intravenous immunoglobulin for presumed viral myocarditis. On the second day of hospitalization, her LV systolic function further decreased to an LVEF of 33% and she had non-sustained runs of ventricular tachycardia. Lidocaine was started to prevent sustained arrhythmia. Her blood pressure remained marginal. By the third day of hospitalization, laboratory tests showed elevated Mycoplasma IgM and she was started on azithromycin. Isoproterenol was discontinued two days after admission with complete recovery of AV conduction. Her LV function gradually improved. She was given ibuprofen for pericardial effusion and presumed pericarditis, which alleviated her chest and abdominal pain. As her blood pressure and LV function normalized by hospital day 7, milrinone was weaned off and she was transitioned to oral diuretics and afterload reduction. Since no further arrhythmias occurred, she was also weaned off lidocaine. She was finally discharged from the hospital with normal LV function (LVEF 64%) and no symptoms after 12 days of hospitalization. On subsequent follow-up, she remained in stable condition and all medications were discontinued. Holter monitoring showed no residual AV block.
Carditis (inflammation of the heart or its surrounding tissue) includes myocarditis, pericarditis, and endocarditis. Myocarditis is the inflammation of the myocardium, pericarditis is the inflammation of the serous membranes covering the heart (pericardium), and endocarditis is considered the inflammation of the inner endothelial layer of the heart including the heart valves. A certain degree of myocarditis can be frequently associated with pericarditis or endocarditis if the inflammation spreads to the myocardium. The etiology of carditis is vast. It may be due to various infections, rheumatic fever, or autoimmune conditions.
Myocarditis is defined as the inflammation of the myocardium. We can classify myocarditis based on the etiologic factors, pathophysiology, and clinical presentation.
Among the etiologic factors, the most common cause of myocarditis in the pediatric population in the western world is viral in nature. Any virus may cause some degree of myocardial inflammation, but the most notable viruses are Coxsackie B virus, Parvovirus B19, adenoviruses, echoviruses, influenza viruses, and herpesviruses. Non-viral infectious myocarditis is more common in the less industrialized part of the world. Protozoal infections (Babesia), Chagas diseases (Trypanosoma cruzi), bacterial myocarditis due to diphtheria (Corynebacterium diphteriae) are common in Africa and South America, while Lyme disease and Mycoplasma myocarditis can be frequent in certain parts of United States. Autoimmune diseases are less common, and usually affect the myocardium via direct extension of the inflammatory process from the adjacent pericardium or endocardium. Pericarditis and endocarditis may be present in patients with systemic lupus erythematosus, CREST (calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome and other autoimmune disorders. Kawasaki disease is a medium-vessel vasculitis that also causes various degrees of myocarditis with ventricular dysfunction and pericardial involvement. Acute rheumatic fever can also induce inflammation of the myocardium with decreased LV function besides affecting the endocardium and the heart valves. Toxic myocarditis can be caused by alcohol, radiation, certain chemicals and cardiotoxic chemotherapy agents such as doxorubicin and adriamycin.
Whatever the suspected etiologic factor may be, the pathophysiology of myocarditis can be explained by a two-tier impact:
1) Infections or toxins cause direct cytotoxic damage to the cardiomyocytes, followed by:
2) A reaction of the immune system involving activation of macrophages and lymphocytes, which subsequently invade the myocardium resulting in myocardial dysfunction and necrosis. With certain viruses and autoimmune processes (Coxsackie B virus and acute rheumatic fever), even after the acute etiologic factor is eliminated, the immune system continues to invade the myocardium resulting in an ongoing inflammation and chronic gradual deterioration of the myocardial contractility and function.
The degree of direct damage and the severity of the immune response predict the manifestations of myocarditis. While several viral infections, such as HHV-6, EBV, or adenovirus may cause a mild and therefore subclinical inflammation of the heart, some viruses and bacteria can result in devastating damage with fulminant myocarditis and severely decreased myocardial function. Subclinical forms of myocarditis may never raise the suspicion and will not be clinically recognized. Acute myocarditis, depending on the severity, may present with symptoms of fatigue, decreased level of activity and generalized malaise. Fulminant myocarditis is the most severe form of acute myocarditis. It can present with fatigue, syncope, convulsions, atrioventricular block, generalized edema and leads to rapid deterioration of myocardial function with circulatory collapse and sometimes sudden death. Another presentation of acute myocarditis is focal myocarditis, where the global myocardial function is preserved and the inflammation is localized only to a certain discrete region of the heart. If the coronary arteries are affected in an area of inflammation, the focal myocarditis may cause transient coronary artery spasm and present as an acute coronary syndrome.
Chronic forms of myocarditis are due to ongoing damage whether by the inciting etiologic factor or by the immune response. It can lead to a gradual deterioration of myocardial function resulting in a dilated cardiomyopathy. Coxsackie B virus induced dilated cardiomyopathy is a well-recognized entity in adults as well as teenagers.
The clinical manifestations of myocarditis vary according to the underlying pathology; from the subclinical course with no symptoms to the severe fulminant myocarditis with acute heart failure, possibly accompanied by arrhythmias leading to syncope or sudden death. There is no single characteristic clinical profile for infectious myocarditis. However, typical symptoms of a viral upper respiratory infection can be recognized. A nonspecific systemic viral infection is usually followed by a latent period of a few days to weeks or even months. The latent period is followed by nonspecific signs and symptoms such as fatigue, anorexia, pallor, abdominal pain, mild jaundice, or lethargy. Diminished heart tones and hepatomegaly may be the only clinical clues pointing toward myocarditis. If the disease progresses, cardiac enlargement may ensue along with cardiac arrhythmias and worsening fatigue. The final stage of myocarditis may manifest with symptoms of heart failure, such as tachypnea, dyspnea, severe fatigue and generalized edema. Rarely, myocarditis may affect the subepicardial region involving the coronary arteries. The inflammation of coronary arteries presents with episodic spasm causing transient myocardial ischemia with typical chest pain, ST segment changes and elevation in cardiac enzymes. This entity can be mostly seen in teenagers and is labeled as focal myocarditis, and it usually does not cause myocardial dysfunction.
Much like the clinical manifestations, results from laboratory and investigational tests are often variable. Erythrocyte sedimentation rate, white blood cell count, and cardiac enzymes may be normal or may be elevated, depending on the severity of the disease. Viral studies for Coxsackie B virus, adenoviruses, Parvovirus B19, EBV, HSV and influenza including viral culture, PCR, titers of IgG and IgM can be helpful to determine the etiology.
Chest radiographs may show an enlarged heart and, depending on the severity of the heart failure, pulmonary venous congestion may be present. Electrocardiographic (EKG) abnormalities are common, and may show sinus tachycardia, with low voltage QRS complexes in the standard leads and/or precordial leads. The T-waves may be flattened or inverted with changes in the ST segment depending on the myocardial strain or ischemia. Echocardiography is a very important part of the diagnosis evaluating for potential dilation of the heart chambers (which most commonly occurs in the left ventricle), with decreased left ventricular systolic function. Left atrial enlargement may be present if there is co-existent mitral insufficiency. However, the main importance of an echocardiogram is to assess myocardial contractility and pericardial effusion that could lead to tamponade. In many cases of subclinical inflammation or focal myocarditis, the left ventricular function is normal. Controversy remains on whether routine endomyocardial biopsies for suspected myocarditis should be performed, as the pathology is often patchy, therefore a negative biopsy cannot exclude the diagnosis. The sensitivity of endomyocardial biopsy is about 30%. Though not currently recognized as the gold standard in diagnosis, cardiac MRI is the most sensitive test and can show patches of myocardial dysfunction and subepicardial delayed enhancement consistent with myocarditis.
The treatment of myocarditis depends on the etiology. If known toxins or drugs are suspected, discontinuation of the etiologic factor is paramount. If an infectious agent is identified, appropriate disease-specific therapy should be instituted, however in most cases no infectious agent will be found. Bacterial causes are treated with proper antibiotics. Since the most common etiology is viral, there is no specific therapy available. Intravenous immunoglobulin (IVIG) has been shown to improve myocardial function and change clinical outcome in certain cases. Pooled IVIG will have lots of antibodies against viruses with ubiquitous infections of the population. Corticosteroids are not beneficial for myocarditis, and may decrease the innate immune response, prolonging and worsening the disease process. Besides IVIG treatment, the therapy of myocarditis focuses on alleviating the symptoms; arrhythmias and congestive heart failure. Arrhythmias should be treated aggressively, since ventricular tachycardia and fibrillation are the main causes of death. Treatment of heart failure consists of bed rest, oxygen administration, afterload reduction, positive inotrope and lusitrope (diastolic relaxation) therapy. Extracorporeal membrane oxygenation (ECMO) should be available for cases of fulminant myocarditis.
The prognosis also depends on the etiology and severity. Patients with a subclinical course of viral myocarditis usually recover completely without any residual problems. Similarly, focal myocarditis usually resolves without any sequelae. Coxsackie B virus has been shown to induce direct myocardial damage, so even after a subclinical form of acute infection, ongoing persistent myocarditis might result in dilated cardiomyopathy with poor prognosis. Most patients with acute but not severe myocarditis will recover in several weeks to months, with the heart size reverting back to normal within a year. Fulminant myocarditis can have devastating consequences with sudden death and/or multiorgan damage. If timely supportive measures are taken, which may include the utilization of ECMO, fulminant myocarditis can recover with complete resolution of myocardial function, just as it did in our case. However, in cases where heart failure persists, the prognosis is poor.
The most common form of endocarditis in children is infective endocarditis. This is a serious bacterial infectious process that usually affects the heart valves or the endothelium of the heart. Prior to the era of antibiotics, patients suffering from infective endocarditis had mortality rates of nearly 100%. However, with the introduction of antibiotics, the present day mortality rate for this disease in the pediatric population ranges between 5-20%.
Infective endocarditis stems from hemodynamically turbulent blood flow which causes endothelial trauma. This creates a predisposition for platelet and fibrin deposition on the endothelial surface. The platelet and fibrin deposits form a sterile thrombus on the endothelium known as non-bacterial thrombotic endocarditis. Bloodstream invasion of certain bacteria due to dental or upper respiratory procedures can result in transient bacteremia. The site of sterile thrombotic endocarditis becomes the nidus of bacterial growth for these susceptible adhesive microorganisms. Colonization and proliferation of bacteria in the thrombus creates an infected vegetation that can damage the invaded valve or myocardial tissue and serve as a constant source of bacteremia and septic emboli.
Conditions which predispose turbulent blood flow in the heart are risk factors for infective endocarditis. Such conditions include restrictive ventricular septal defects (VSD), patent ductus arteriosus (PDA), valvular disease of the mitral, aortic or tricuspid valves, and prosthetic valves. In underdeveloped countries where rheumatic heart disease is common, it is the most common cause for infective endocarditis. However, congenital heart disease is the most common risk factor in pediatric practices of the United States. The mitral valve is the most commonly affected region of the heart, followed by the aortic valve, then the tricuspid valve. Other risk factors include situations which increase the risk of bacteremia, such as IV drug use (which predisposes towards infective endocarditis of the right side of the heart), indwelling IV catheters, intra-arterial catheters, severe burns, dental procedures, or recent cardiac surgery.
It is estimated that 80% of all pediatric infective endocarditis are due to alpha-hemolytic streptococci (Streptococcus viridans group) and Staphylococcus aureus. Less common, but still not rare, are coagulase negative Staphylococcus (CONS or Staphylococcus epidermidis) and beta-hemolytic streptococci (Streptococcus pyogenes). HACEK organisms should always be considered when suspecting endocarditis. These are: Haemophilus, Aggregatibacter (formerly known as Actinobacillus), Cardiobacterium, Eikenella, and Kingella. Fungal and yeast infections are rare, but can cause severe damage and large vegetations.
The clinical course of infective endocarditis was historically divided to acute and subacute presentations. It was considered useful, because it was believed that certain bacteria present with a more rapid, acute clinical picture, while others cause a rather subacute course. This distinction does not hold true, so currently we do not differentiate between acute and subacute infective endocarditis except in describing the clinical course of the illness.
The acute course of infective endocarditis is usually characterized by a rapidly progressive clinical picture of sepsis, high fever, headaches, nausea, vomiting, diarrhea, cough, shortness of breath, and early cardiac decompensation. Subacute course due to less virulent infectious agents is characterized as an insidious, flu-like syndrome, associated with malaise, anorexia, and possible fever. In the pediatric population, it is rare to find splinter hemorrhages, Osler nodes (painful, red, nodular lesions most commonly found on fingers), Janeway lesions (small, erythematous, nontender areas of the palms and soles), and Roth spots (retinal hemorrhages with central clearing). If the course is prolonged, then splenomegaly, weight loss, night sweats, anemia, or petechiae may develop. In 20% of infective endocarditis, a new cardiac murmur or change in a preexisting murmur occurs.
Embolic episodes may also be a part of the clinical course; however this is more common in adults than in children. Emboli originating from left-sided endocarditis may cause renal infarcts resulting in frank hematuria, splenic infarcts resulting in left flank pain, or stroke-like symptoms resulting from cerebral emboli. Emboli from right-sided endocarditis may cause chest pain and shortness of breath due to pulmonary embolism.
Several sources describe diagnostic criteria (the Duke criteria) to allow early recognition of endocarditis, when vegetations are still too early to detect. A patient is considered to have infective endocarditis if 2 major criteria, 1 major plus 3 minor criteria or 5 minor criteria are met. The major criteria are:
- Two separate positive blood cultures for typical organisms
- Endocardial abnormalities on echocardiography (vegetation, abscess, new regurgitation).
The minor criteria are:
- Presence of a predisposing condition (i.e., valve abnormality)
- Fever greater than 38 degrees C
- Embolic episode (i.e., splenic infarct, renal infarct, cerebral infarct)
- Immunologic phenomena (i.e., Osler nodes, Janeway Lesions)
- One positive blood culture.
Blood cultures are the most valuable laboratory tests in making the diagnosis of infective endocarditis. Controversy lingers as to the exact number of cultures that should be obtained for each patient with suspected infective endocarditis. However, the collection of 2 to 3 blood cultures over a 24 hour period will suffice in most cases. Approximately 5% of patients with endocarditis will have negative blood cultures. In some cases, the microorganisms contained in the vegetation are unexposed, encased in fibrin and platelets. Antibiotic therapy prior to obtaining blood cultures will reduce the likelihood of recovering the organism in the blood. Therefore, it is very important to obtain blood cultures prior to antibiotic treatment. Fungi or candida can cause endocarditis rarely, but these will eventually grow out of most blood cultures (though very slowly).
Other laboratory tests are not as helpful in making the diagnosis of infective endocarditis, but they may be helpful in monitoring clinical progress. Elevated erythrocyte sedimentation rate (ESR) is commonly found in endocarditis. During antibiotic therapy, a decrease of the ESR signifies that the treatment is most likely effective. Like many other infectious diseases, a leukocytosis with an accompanying left shift may be seen, although this is more common in the acute setting than the subacute course. Microscopic or macroscopic hematuria is also a common laboratory finding. Microscopic hematuria is most likely due to immune complex depositions in the glomeruli, whereas macroscopic hematuria is most likely a result from renal embolization. If the course is chronic, such as in the subacute cases, normocytic/microcytic anemia may occur.
A potentially helpful diagnostic procedure is echocardiography. Echocardiography is most helpful in children with normal cardiac anatomy or with isolated valvular abnormalities. However, this procedure is not 100% sensitive or specific, therefore a negative echocardiogram does not rule out endocarditis. Transesophageal echocardiography (TEE) has had better results than the transthoracic approach in adults; however the usefulness for this procedure in children with endocarditis remains uncertain.
The differential diagnosis for infective endocarditis is complex since this disease has variable clinical presentations. Because infective endocarditis commonly presents with fever, arthralgias, and a positive rheumatoid factor; juvenile idiopathic arthritis, Kawasaki disease, rheumatic fever, and other connective tissue disorders should be considered in the differential diagnosis. Neurologic manifestations from infective endocarditis may also mimic that of meningitis, cerebritis, or toxic encephalopathy. If hematuria is present, one must also consider other renal diseases. If S. aureus bacteremia along with an increasing ESR are present in a patient with infective endocarditis, one must consider osteomyelitis or septic arthritis. Cardiac myxomas or rheumatic carditis must also be considered if a patient presents with a new or changing heart murmur. The diagnosis of infective endocarditis should be considered in any child with persistent unexplained fevers especially if they are considered at high risk such as history of congenital heart defects or IV drug use.
Isolation of the infecting microorganism by blood culture is extremely important, not only in making the diagnosis, but also in planning for treatment. The microorganisms that are revealed from the blood cultures will strongly determine the type of antibiotic regimen to be used. The physician must be guided by the antibiotic susceptibility pattern. Although antibiotic regimens vary depending on the infective microorganism, one general principle is true in the treatment of infective endocarditis: complete eradication of the infecting microorganism with bactericidal agents will require at least 4 or 6 weeks of therapy. Initially when blood cultures are still pending, empiric antibiotics should be started. Empiric therapy includes coverage for the common bacteria, Streptococci and Staphylococcus aureus, but also for the less common MRSA (methicillin resistant Staphylococcus aureus) and Gram negatives, therefore vancomycin and gentamicin are the preferred regimen.
Obtaining occasional blood cultures during the first 8 weeks after cessation of treatment is warranted, because most relapses occur during this period. There are several common indications for surgery. These include a prior significant embolic event, persistent infection, and progressive congestive heart failure especially when the aortic or mitral valve is involved, large vegetation with the risk of a potentially fatal embolism and cardiac abscess.
The prognosis depends on the etiology and the availability of appropriate medical care. The mortality rate is between 2% and 20%. Mortality rates are slightly higher in patients with acute staphylococcal infection, fungal infection, and prosthetic valve endocarditis. Mortality may be caused by sudden perforation of the aortic valve with severe aortic insufficiency, chordal rupture with resultant mitral insufficiency, myocardial infarction, or intramyocardial abscess formation with the development of a myocarditis. If appropriate antibiotic therapy is administered, infective endocarditis can be eradicated potentially with no residual sequelae. Every patient after infective endocarditis should receive appropriate antibiotic prophylaxis during certain dental and surgical procedures to prevent recurrence.
BACTERIAL ENDOCARDITIS PROPHYLAXIS
Prophylactic antibiotics are recommended for children who are at high risk to develop infective endocarditis, while undergoing procedures that may induce a bacteremia. High risk patients include:
1) Patients with prosthetic cardiac valves or prosthetic material used for cardiac valve repair
2) Previous infective endocarditis
3) Unrepaired or palliated cyanotic heart disease
4) Repaired congenital heart disease with a prosthetic material for the first 6 months
5) Repaired congenital heart disease with residual defect at the site of prosthetic material
6) Cardiac valvulopathy in cardiac transplant recipients.
High risk individuals should receive antibiotic prophylaxis prior to dental procedures, invasive respiratory tract procedures and procedures involving infected skin.
The recommended antibiotic regimens for prophylaxis include amoxicillin 50 mg/kg PO 1 hour before the procedure or ampicillin or ceftriaxone 50 mg/kg IM or IV within 30 minutes of the procedure. If the patient is allergic to penicillin, an alternate drug may include clindamycin 20 mg/kg PO or cephalexin 50 mg/kg PO 1 hour before procedure, or clindamycin 20 mg/kg or cefazolin 25 mg/kg IM or IV within 30 minutes of the procedure.
Pericarditis is defined as an inflammatory reaction of the pericardium. Etiologies include acute bacterial pericarditis, acute viral pericarditis, postpericardiotomy syndrome, acute rheumatic fever and uremia. Electrocardiography (ECG) may be useful in the initial stage of the disease, when ST segments are elevated in almost all leads except V1 and aVR. After a few hours to days, the ST segments may return to baseline, and the T waves become flat. A low voltage (low amplitude) QRS may be seen if the pericardial effusion is large enough. Echocardiography is an important diagnostic test, which will reveal the presence of a pericardial effusion surrounding the heart. Moderate pericardial effusion secondary to pericarditis may also show up on x-ray as an enlarged cardiac silhouette with a triangular shape. In borderline cases, comparisons of previous x-rays may prove helpful.
Much like infective endocarditis, the incidence of acute bacterial pericarditis has dramatically declined since the development of antibiotics. The most common settings for acute bacterial pericarditis include septicemia or hematogenous or direct spread into the pericardium from another site, such as with pyelonephritis, osteomyelitis, tonsillitis, bacterial pneumonia, and empyema. The common microorganisms responsible for most acute bacterial pericarditis are Haemophilus influenzae type B, Staphylococcus aureus, pneumococcus, meningococcus, streptococcus species and tuberculosis infection. Patients with acute bacterial pericarditis will usually manifest with acute onset of chest pain, high fever, tachycardia, a friction rub, tachypnea, and toxemia. Acute bacterial pericarditis is often associated with an infection elsewhere, therefore an intensive search for the primary source is essential. Blood cultures are important and it is recommended that three to five sets should be obtained in the first 1 or 2 days after admission. These blood cultures are positive 40-80% of the time and the appropriate antimicrobial agent given for 4 to 6 weeks should be chosen based on the susceptibility testing. Acid-fast stains for tuberculosis of the sputum, gastric contents, or urine are considered if blood cultures come back negative.
Acute viral pericarditis is the most common etiology and is often associated with the aforementioned viral myocarditis. Like the viral myocarditis, the most common viral agents responsible for viral pericarditis include Coxsackie B virus, echoviruses, adenoviruses, and influenza virus. The clinical manifestations of the viral myocarditis usually dominate over the clinical manifestations of the viral pericarditis. The typical signs and symptoms of acute viral pericarditis include a low-grade temperature, chest pain, and a friction rub. The typical pathognomic sign of pericarditis is chest pain that is worse while supine and improves upon leaning forward. The therapy for acute viral pericarditis is symptomatic including NSAIDs. The prognosis of viral pericarditis is good and often self-limiting, with complete recovery in 3 to 4 weeks.
Similar to the adult pericarditis following a myocardial infarction, known as Dressler's syndrome, an episode of acute pericarditis is well-recognized in children following cardiac surgery, including opening of the pericardium (post-pericardiotomy syndrome). The pathogenesis is unclear, however anti-myocardial antibodies and eosinophilia point toward an autoimmune etiology. Cardiac tamponade may occur, which may be treated with a pericardiocentesis, however in most cases of post-pericardiotomy syndrome, the disease is self-limiting in 2 to 3 weeks. NSAIDs may be used to lower the temperatures and improve chest pain. In the severely ill child, a course of prednisolone may be effective.
Cardiac tamponade is a serious complication that occurs due to the rather rapid collection of fluid in the pericardial sac causing compression of the atria and impairing diastolic filling and thus cardiac function. Typical findings of cardiac tamponade are jugular venous distention, hepatomegaly, occasionally generalized edema, hypotension, tachycardia, and pulsus paradoxus (more than 20 mmHg decrease in BP during inspiration). Cardiac tamponade is a potentially life-threatening condition and should prompt urgent pericardiocentesis.
1. What is the most common microorganism found in pediatric infective endocarditis?
. . . . . a. Staph aureus
. . . . . b. Strep viridans
. . . . . c. E. coli
. . . . . d. Pneumococci
. . . . . e. Strep pyogenes
2. What is the most common etiologic factor of myocarditis?
. . . . . a. viral
. . . . . b. Mycoplasma
. . . . . c. Lyme disease
3. Among the following, which is not a minor criteria for infective endocarditis based on the Duke Criteria?
. . . . . a. Osler nodes
. . . . . b. single positive blood culture of S. aureus
. . . . . c. Roth spots
. . . . . d. vegetation on echocardiography
. . . . . e. fever above 38 C
4. What type of prophylactic antibiotic against infective endocarditis would you prescribe to a 9-year old female, with a past medical history of a repaired VSD with no residual defect, and a history of allergic reaction to penicillin, scheduled for a tooth extraction the next day?
. . . . . a. Amoxicillin
. . . . . b. Ampicillin
. . . . . c. Clindamycin
. . . . . d. Cefazolin
. . . . . e. None
5. Which one of the following represents the most severe clinical manifestation commonly found in pediatric myocarditis?
. . . . . a. Myocardial infarction
. . . . . b. Acute congestive heart failure
. . . . . c. Pericarditis
. . . . . d. Valve regurgitation
. . . . . e. None of the above
6. Which is the most helpful test to diagnose myocarditis?
. . . . . a. Cardiac enzymes
. . . . . b. EKG
. . . . . c. Echocardiogram
. . . . . d. CXR
. . . . . e. Cardiac MRI
7. Which of the following is/are treatment options for pediatric postpericardiotomy syndrome?
. . . . . a. Salicylates
. . . . . b. Pericardiocentesis
. . . . . c. Bed rest
. . . . . d. Prednisolone
. . . . . e. All of the above
1. Towbin JA. Chapter 58 - Myocarditis. In: Allen HD, Driscoll DJ, Shaddy RE, Feltes TF (eds). Heart Disease in Infants, Children, and Adolescents, 7th edition. 2008, Baltimore: Lippincott Williams and Wilkins, pp. 1207-1224.
2. Baddour LM, Wilson WR, Bayer AS, et al. Infective Endocarditis: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Statement for Healthcare Professionals From the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: Endorsed by the Infectious Diseases Society of America. Circulation. 2005; 111: e394-e434.
3. Taubert KA, Gewitz MH. Chapter 65 - Infective Endocarditis. In: Allen HD, Driscoll DJ, Shaddy RE, Feltes TF (eds). Heart Disease in Infants, Children, and Adolescents, 7th edition. 2008, Baltimore: Lippincott Williams and Wilkins, pp. 1299-1311.
4. Sagar S, Liu PP, Cooper LT Jr. Myocarditis. Lancet. 2012; 379: 738-747.
5. Wilson W, Taubert KA, Gewitz M et al. Prevention of infective endocarditis: guidelines from the American Heart Association. Circulation. 2007; 116:1736-1754.
Answers to questions
1. b. Strep viridans
2. a. viral
3. d. vegetation on echocardiography
4. e. no prophylaxis is indicated
5. b. Acute congestive heart failure
6. e. Cardiac MRI
7. e. All of the above