What Is Endocarditis?
Endocarditis (infectious endocarditis) refers to an infection of the inner lining of the heart (the endocardium) and/or the valves that are covered with it. The source of the infections and inflammation can be from anywhere, such as bacteria of the mouth, cuts on the skin, contaminated needles and inadvertent injection of talc in IV drug abuse, sexually transmitted infections, etc. The mouth is an important concern, since poor dentition is a risk factor for endocarditis.
Bacteria–primarily Staphylococcus and Streptococcus–are particularly compatible with damaged or artificial heart valves, to the point that the incidence of endocarditis has fallen with the decrease in Rheumatic fever over the decades. Fungi can also cause endocarditis.
Whether heart valves are healthy or damaged, bacteria that take hold there cause new and/or further damage, leading to functional heart disease when the valves cannot perform optimally to prevent backflow into the heart chambers during each contraction.
Risk Factors for Endocarditis
- Age >60
- Male gender
- IV drug abuse
- Poor oral hygiene, poor dentition, or dental infection; alternately, excessive brushing and flossing; also, dental procedures involving instrumentation
- Structural abnormalities of the heart, such as congenital heart disease, valve damage from prior infection or surgical repair/replacement; mitral valve prolapse with mitral regurgitation, aortic valve disease, and other valvular disease
- Prosthetic valve replacement
Symptoms of endocarditis include fever (90%), anorexia and weight loss, headache, myalgia and arthralgia, abdominal pain, dyspnea, cough, and pleuritic pain.
Signs of endocarditis include heart murmurs (85%), enlarged spleen, and skin petechiae (splinter hemorrhages).
Complications of Endocarditis
Cardiac (up to 50%): heart failure, pericarditis, valve damage (valvular insufficiency) and valve abscess, and infectious emboli throughout the body.
Systemic (up to 25%): sepsis from infectious emboli (especially Staphylococcus and fungi), metastatic abscess (spleen, kidneys, brain, or lungs); fungal endocarditis can create mycotic aneurysms in the arterial (including cerebral) vessels.
Central Nervous System (up to 40%): stroke, brain abscess, and meningitis.
The seriousness of such complications contributes to an infectious endocarditis mortality rate of up to 25%.
How Is Endocarditis Diagnosed?
Endocarditis is an infectious disease; as such, diagnosis depends on both the microbiology involved and the damage that can result from it.
Diagnosis Is Based On
- Clinical presentation/signs and symptoms
- Three sets of blood cultures
- Cardiac ultrasonography
- Fever: Any patient with cardiac risk factors (structural abnormalities or valve disease) or IV drug abuse, indwelling IV lines, immunosuppression, or recent dental/surgical procedure who presents with fever should be considered for a diagnosis of endocarditis–at least to rule it out.
At least three sets of blood cultures are obtained to decrease the chance of a false negative result. If a patient is clinically unstable, empiric treatment (treatment based on observation and judgment in lieu of positive cultures) may need to begin even before the results of the cultures are ready.
Follow-up cultures are obtained after 2-3 days of antibiotic treatment, and then every 2-3 days thereafter until the bacteremia has cleared.
There are conditions that mimic infectious endocarditis but which result in negative cultures: antiphospholipid syndrome, non-infectious intracardiac vegetations from acute rheumatic fever, atrial myxoma, non-infectious lesions of the heart such as malignancy, lupus, and nonbacterial thrombotic endocarditis from a state of hypercoagulation.
Echocardiography (TTE and TEE)
A transthoracic (transducer over chest) cardiac echogram (TTE) is performed initially and if there is suspicion of infectious endocarditis, difficulty in imaging, or high risk factors for infective endocarditis, a transesophageal echocardiogram is the next step for better visualization and diagnostic accuracy. The findings of the TTE or the TTE/TEE sequence are compared with the microbiology garnered from the blood cultures.
Positive findings in echocardiography include
- pathologic lesions: “vegetations,” masses of platelets, fibrin, bacterial colonies, inflammatory cells, or–later–fibrosis and calcification
- intracardiac abscess
Echocardiography is also useful, in the absence of ultrasonic evidence of vegetations, of steering diagnostics away from endocarditis in pursuit of other conditions that may mimic its signs and symptoms, e.g., catheter infection, infections in implantable cardiac devices, prosthetic joint infection, osteomyelitis and other tissue infection, meningitis, pneumonia, or systemic sepsis.
Other tests can be helpful to discern tissue extension of disease and vascular involvement: cardiac MRI, CT angiography.
How Is Endocarditis Managed?
Blood culture and echocardiographic and proven infectious endocarditis is treated according to different protocols for specific populations.
Infectious Endocarditis Involving “Native” Valves
If infectious endocarditis involves a patient’s own (natural, or “native”) valves, bactericidal agents are selected that target the specific organisms.
If a patient is clinically stable, the few days without therapy until the results return from blood cultures is reasonable; for those who are unstable, empiric therapy can begin and then be reinforced or replaced based on the cultures that return later. Empiric therapy is based on the most likely organisms, statistically, such as Staphylococci, Streptococci, and enterococci, against which vancomycin is often used.
Repeat blood cultures are done to judge efficacy of the treatment. Treatment usually continues for 6 weeks after the blood cultures become negative to assure that the bacteria in the valvular vegetations are eradicated. Blood tests for anemia, toxicity, and inflammatory markers are done during therapy.
Since antibiotics in the aminoglycoside class often used to treat endocarditis can cause hearing loss, serial audiograms should be performed. Patients with endocarditis from organisms though to have originated orally should have scrupulous dental care.
Infectious Endocarditis Involving Prosthetic Valves (PVE)
Prosthetic valves, invasively implanted and remaining as foreign bodies, add additional avenues for pathology to the endocarditis process. Infection associated with prosthetic valves have an increased tendency toward invasive extension, which jeopardizes not only the valvular function and the valves themselves, but cardiac tissue.
Bactericidal agents are selected that target the specific organisms, as in native valve endocarditis–typically Staphylococci, Streptococci, and enterococci; however, due to the increased virulence associated with PVE, a triple-antibiotic regimen is implemented. Duration of therapy is typically longer than that for native valve endocarditis, i.e., > 6 weeks duration beyond when cultures become negative.
Treatment for Candida species fungal organisms that cause endocarditis consists of a combined approach of both antifungal therapy and surgical replacement of the valve(s). Other fungal organism may only require antifungal medications.
IV Drug Abusers
IV drug abusers present with special problems requiring extra considerations. One is that recurrence is more likely due to the relapse rate of those treated for addiction. Another consideration is that outpatient therapy is hazardous in a patient who is re-exposed to the availability of drugs and/or who has an indwelling line for out-patient administration of intravenous antibiotics. Such conditions may alter the paradigm toward oral medication. Longer hospitalizations are useful when the patient is compliant, but IV drug abusers, especially those who are not rehabilitated, often leave the hospital prematurely against medical advice.
Prevention of Endocarditis
Infectious endocarditis occurs from a sequence of events:
- An abnormal or damaged endothelial surface, such as on heart valves, cause the formation of a thrombus
- Transient circulation of bacteria in the bloodstream exposes this damaged area to the bacteria
- Seeding and proliferation of the bacteria which also causes the accrual of platelets and other inflammatory substances
The concept of preventing endocarditis with prophylactic antibiotics during times of theoretical introduction of bacteria into the bloodstream (during procedures) is not a fact; studies have ranged from helpful to inconclusive. But the rationale based on the sequence of events (above) makes prevention center on those who have the highest risks for it:
- Heart disease (excluding hypertrophic cardiomyopathy)
- Valvular disease (excluding bicuspid aortic valve and mitral valve prolapse)
- Prosthetic valves
- Previous endocarditis
- Repaired congenital cardiac anomalies
- IV drug abusers
- Extensive dental disease
- Renal and dialysis patients
As the theoretical cause of bacterial “seeding” of the heart valves is from introduction of bacteria into the bloodstream, those at increased risk should have prophylactic antibiotic coverage for any “instrumentation” that could result in this introduction into the bloodstream. The protocol for antibiotic prophylaxis includes beginning the antibiotics before a procedure, so that antibiotic blood levels are sufficient at the time of bacterial seeding to prevent valvular involvement.
- Dental procedures
- Respiratory tract surgical procedures (tonsillectomy, adenoidectomy, or bronchoscopy that includes biopsy)
- Gynecological procedures (dilation and curettage, terminations, endometrial biopsies)
- Obstetrical procedures (amniocentesis, chorionic villus sampling, and artificial rupture of membranes before vaginal delivery)
- Incision and drainage of abscesses
- Dialysis via an arteriovenous graft or shunt
- Arterial stenting procedures
- Other surgery