Age: 27 years
Gender: Male
Occupation: Graduate student
Working diagnosis: Residual ventricular septal defect after surgical closure
HISTORY
The patient was born with a perimembranous VSD. Because of severe aortic insufficiency at age 12 years, he underwent aortic valvuloplasty with plication of the noncoronary leaflet and direct suture closure of the VSD. Postoperatively there was a residual small VSD and mild to moderate aortic insufficiency. In the years following he was asymptomatic and had no activity restrictions. He participated in various sports as a student and frequently bicycled 60 to 80 miles a week. He was followed yearly in the congenital heart clinic with an echocardiogram. His VSD, aortic insufficiency, and left ventricular size and function were stable.
Six months ago, he developed fever and associated symptoms of fatigue, myalgias, shortness of breath, nonproductive cough, and wheezing. The patient was treated for a presumed bronchitis with a course of antibiotics and inhalers. His symptoms initially improved while taking antibiotics, but returned a few days after completing the antibiotic course. Over the next 6 months, he was placed on a series of antibiotics for a presumptive diagnosis of recurrent bronchitis.
The patient began to have predictable cycles of fevers up to 40° C and myalgias according to when he last took antibiotics. Approximately 5 days after completing a course of medication, he would have resumption of symptoms. The antibiotics he had been prescribed included penicillin, ampicillin, erythromycin, and tetracycline. His fevers and myalgias were relieved within 10 to 15 hours after starting the medications, except for tetracycline, which was never effective. Blood cultures were not drawn at any point.
He reported having one dental procedure for a loose dental filling a few weeks prior to his initial onset of symptoms. The patient took prophylactic antibiotics against endocarditis before dental procedures, but was not strict with the timing of the dose in relation to the procedure.
He was a nonsmoker, and had never used intravenous (IV) drugs.
Comments: Patients with residual VSD after early VSD repair warrant cardiology follow-up for signs of left ventricular dysfunction, aortic insufficiency, tricuspid insufficiency, pulmonary hypertension, LVOT obstruction, and infective endocarditis. Of patients who have undergone closure of their VSD, up to 5.5% needed a second operation to close residual or recurrent VSDs. However, if the residual VSD is small and restrictive, surgery is not necessary.
The clinical presentation of recurrent fevers in any patient with prior surgery and/or a turbulent lesion should obviously instigate a thorough workup for infective endocarditis. The most common presenting feature is fever, although it may be absent in up to 10% of patients. In right heart endocarditis, patients may present with hemoptysis or recurrent “chest infections” due to pulmonary emboli.
In infective endocarditis, fever is initially continuous, but may become intermittent particularly when short nonbactericidal courses of antibiotics have been given.
Cleaning, filling, or extracting teeth is associated with bacteremia with positive blood cultures in 12% to 85% of dental patients. The most common organisms are alpha-hemolytic streptococcus, in particular, the viridans streptococcus group. Although most patients receive instructions for endocarditis prophylaxis consistent with older American Heart Association guidelines, a study observed that only 22% of patients who were advised by their physician to take prophylactic antibiotics actually took prophylaxis as recommended.
CURRENT SYMPTOMS
A 6-month history of intermittent fevers, myalgias, and shortness of breath after a dental procedure.
He complained of headaches and neck soreness, but no joint pain or back pain.
He denied hemoptysis and hematuria.
He had no skin lesions.
NYHA class: I
Comments: The incidence of infective endocarditis is 0.38 cases per 10,000 person years. The major predisposing factors for the development of infective endocarditis are susceptible cardiovascular substrates and a source of bacteremia. Previously, a large proportion of patients who developed endocarditis had a history of rheumatic heart disease. Today, there is an increasing number of patients with congenital heart disease surviving into adulthood who present with infective endocarditis.
PHYSICAL EXAMINATION
Temperature 36.4, BP 122/68, HR 75, oxygen saturation 96% on room air
General: Height 138 cm (63 in), weight 63 kg (137 lb), BSA 1.55 m 2
HEENT: There was no conjunctival hemorrhage.
Neck veins: JVP was 6 cm above the sternal angle with a normal waveform.
Lungs/chest: End-expiratory wheezes, but no rales were heard.
Heart: The precordium was hyperdynamic with a left sternal border thrill. Heart sounds were normal. A grade 4/6 holosystolic murmur was heard best along the lower left sternal border. A high-pitched long diastolic decrescendo murmur was heard best at the left lower sternal border.
Abdomen: The abdomen was soft and nontender. There was no hepatosplenomegaly.
Extremities: Extremities were warm and without edema, clubbing, or cyanosis. There were no petechiae, splinter hemorrhages, Janeway lesions, or Osler nodes.
Pertinent Negatives
Neurologic exam was normal.
No spinal tenderness, costovertebral angle tenderness, or joint abnormalities were identified.
Comments: Fever will wax and wane particularly when there has been exposure to short nonbactericidal courses of antibiotics.
Conjunctival hemorrhage and Roth spots are the result of systemic septic emboli from infective endocarditis.
When present, congestive heart failure from infection-induced valvular destruction is a serious complication and portends a higher mortality.
Septic emboli to the lungs from right heart endocarditis can result in pulmonary infiltrates or pleural effusions.
Cardiac auscultation is consistent with the underlying cardiac anomaly. It is important to systematically note changes in auscultation from baseline exam as the changes may indicate valvular destruction.
Hepatomegaly is observed in many patients, and splenomegaly occurs in about 55% of patients. Splenic infarction or intra-abdominal abscess should be suspected if there is left upper quadrant pain and tenderness.
Clubbing of the nails may develop with subacute endocarditis. Skin lesions are also common with subacute endocarditis.
Neurologic involvement occurs in 30% to 40% of patients.
Involvement of the large joints may occur in up to 20% to 30% of patients.
LABORATORY DATA
| WBC count | 7 × 10 3 cells/L (4.3–10) |
| PMN | 48% (48–65) |
| Band cells | 11% (0–5) |
| Hemoglobin | 16 g/dL (13–17.0) |
| Hematocrit | 48% (41–51) |
| MCV | 90.7 fL (85–95) |
| Platelet count | 209 × 10 3 cells/L (150–420) |
| Sodium | 142 mg/dL (136–147) |
| Potassium | 4.2 mg/dL/dL (3.5–5.2) |
| Creatinine | 1.3 mg/dL (0.8–1.3) |
| Blood urea nitrogen | 11 mg/dL (6–23) |
| ESR | 1 mm/hr (0–5) |
| Urine analysis | No red or white blood cells, normal sediment |
Comments: Leukocytosis with bandemia is usually seen, although leukopenia can occur in overwhelming sepsis.
Anemia is seen in approximately 40% of patients as a manifestation of the anemia of chronic disease. Rarely is anemia due to hemolysis from large vegetations or valvular destruction.
The erythrocyte sedimentation rate (ESR) is usually elevated, but may be normal in 10% of cases, and therefore a normal result cannot exclude the diagnosis.
Microscopic hematuria is seen in more than 50% of cases.
ELECTROCARDIOGRAM
FINDINGS
Heart rate: 90 bpm
QRS axis: +35°
PR interval: 162 msec
QRS duration: 96 msec
Sinus rhythm, incomplete RBBB. There was no RA overload.
Comments: The presenting ECG is unchanged from previous studies. The incomplete right bundle branch block is not new.
Extension of infective endocarditis into the septum may lead to atrioventricular, fascicular, or bundle branch block, so lengthening of the PR interval or QRS duration may be an important sign. Rarely, embolization to the coronary arteries can lead to myocardial infarction.
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