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Prosthetic Valve Endocarditis
Introduction
Prosthetic valve endocarditis (PVE) is a microbial infection of the endovascular that occurs on parts of a prosthetic valve or the reconstructed native valve of the heart.[1] PVE accounts for 20% of infective endocarditis. It is the most severe form of infective endocarditis and is associated with high morbidity and mortality.[2] Based on the time of the disease acquirement, this disease is classified into 2 types: early and late PVE. The early PVE is acquired within 1 year of the surgery, while the late PVE is acquired after 1 year. The clinical importance of this classification is the distinct microbiological profiles between the former and the latter.
Etiology
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Etiology
Early PVE occurs due to direct intraoperative contamination or hematogenous spread to the valve in the first days to weeks of the surgical procedure. Paravalvular abscess formation is common in both mechanical and bioprosthetic valves.[3] After 2 months of surgery and up to 12 months, the infection occurs due to late-onset nosocomial infection or a community-acquired infection. In the first 2 months after the surgical intervention, Staphylococcus aureus accounts for the highest number of PVE cases, followed by coagulase-negative staphylococci, gram-negative bacilli, and Candida species. In the period of 2 months to 12 months of the surgical intervention, streptococcus, staphylococcus aureus, and coagulase-negative staphylococcus are the most common pathogens. These are followed by enterococcus.[4] Staphylococcus epidermidis is the most common coagulase-negative staphylococcus in this period and is mostly methicillin-susceptible.[5][6] Late PVE occurs due to community-acquired infection; pathogens are similar to native valve endocarditis. The most frequent pathogens are streptococci and S. aureus, coagulase-negative staphylococci, and enterococci. Mortality in late PVE is high in patients with multiple comorbidities who acquire endocarditis when admitted to hospitals for other reasons.[7][6] Culture-negative endocarditis may occur with both early and late PVE. Other etiologies of PVE can be related to nontuberculosis mycobacteria ( Mycobacterium chimera) and enterovirus.[8][9]
Epidemiology
PVE is responsible for about 20% of endocarditis cases. It occurs in up to 6% of patients who have valve prostheses.[4] The epidemiology of the aortic PVE is different if the valve replacement was done surgically ( surgical aortic valve replacement SAVR) or transcatheter aortic valve replacement (TAVR). In SAVR, the incidence rate of PVE is 6 per 1000 cases.[10] the rate of PVE is higher in patients with bioprosthetic SAVR than in patients with mechanical SAVR.[11][12] In TVAR, the incidence rate of PVE in the bioprosthetic valve is similar to the SARV PVE with a bioprosthetic valve.[13] Healthcare-associated infection is associated with late PVE and occurs due to nosocomial infection when patients are admitted due to other medical conditions or due to exposure in an outpatient facility, such as in infusion centers, nursing homes, or during hemodialysis.[4]
Pathophysiology
In early PVE, the microorganism can directly invade the prosthetic vale intraoperatively due to contamination or spread hematogenous in the initial days to weeks after the procedure. The organisms during the first days after the valve implementation have direct access to the prothesis-annulus interface and the tissue along the suture in the paravalvular area. The organism can adhere to the fibrinogen and fibronectin in the paravalvular area, which causes the formation of abscesses in both mechanical and bioprosthetic valves. In late PVE, the prostheses do not allow the organism to adhere to leaflets as long as there is no evidence of thrombotic material. The sewing ring and sutures become endothelialized after a few months of the valve implementation. Alterations in the valve and the paravalvular surface can lead to the formation of microthrombus, to which the bacterial organisms can adhere and cause an infection.[14]
History and Physical
Patients with PVE present with symptoms similar to other types of infectious endocarditis (IE), including fever and chills, shortness of breath, pleuritic chest pains, anorexia, and weight loss. Patients may experience other symptoms such as malaise, headache, myalgias, arthralgias, night sweats, abdominal pain, and cough. Cardiac murmurs are more common in PVE than other types of IE. Splenomegaly and cutaneous manifestations such as petechiae or splinter hemorrhages are other common findings on physical exam. Petechiae are observed in up to 40 percent of patients; they can present as skin findings on an extremity or mucosal surfaces of the palate and conjunctivae. Findings on nail beds can include Splinter hemorrhages, which appear as red to brown lines that are non-blanching under the nail bed. Other less common clinical manifestations are Janeway lesions, which are non-tender erythematous macules on the palms and soles. Osler nodes are subcutaneous violaceous nodules, mainly on the pads of the fingers and toes. Additionally, Roth spots exudative, edematous hemorrhagic lesions of the retina with pale centers.
Evaluation
A workup should always involve obtaining blood cultures when a patient is suspected of having PVE due to clinical manifestations. Bacteremia in a febrile patient with a history of prosthetic valve replacement raises the probability of the PVE. Three blood cultures from different sites are required. A transthoracic echocardiogram (TTE) should follow this.[15] The modified Duke criteria are accepted criteria to establish the diagnosis of PVE.[16] Transesophageal echo (TEE) is recommended when TTE fails to make the diagnosis.[17] If the initial TEE is negative, repeating it in 3-5 days is recommended when the clinical suspicion is high for PVE. As shielding from the prosthesis prevents adequate images of TTE, TEE provides better diagnoses of PVE.[18][15] TEE's role is to help identify vegetation, characterize the valve dysfunction, identify the spread of infection in the periprosthetic area, determine the preoperative prognosis and timing for surgery, and follow up on PVE after management.[18] TEE has better sensitivity than TTE in diagnosing infectious endocarditis, especially PVE.[19] TEE should be done if there is suspicion about intracardiac complications in patients with positive IE on TTE.[15] TEE should be repeated if there are any clinical features of the development of new intracardiac complications.[15] Other diagnostic modalities may be required as part of the workup for patients with PVE; a chest X-ray can be ordered to evaluate lung infiltrates, and an electrocardiogram can be ordered to evaluate PR prolongation and possible AV blocks.
Cardiac computed tomography angiogram (CTA) can be used to diagnose PVE if the TEE fails to provide the diagnosis; cardiac CT is better than TEE for detecting perivalvular abscess; CTA can be used as the next step in diagnosis for patients who have negative TTE and have contraindications to perform TEE.[20][21][22] 18F-FDG PET/CT can be used to diagnose PVE if TTE/TEE fails to make the diagnosis and there is a high probability of the infection. It improves the diagnostic accuracy of the modified Duke criteria and yields high diagnostic performance.[23] Promising data showed 18F-FDG PET/CT to help as a follow-up modality after completing IE antibiotic treatment.[24][25] Magnetic resonance imaging (MRI) of the brain is considered the best diagnostic tool when septic emboli are suspected in the brain. CT of the chest and abdomen can also be considered when septic emboli are suspected.[25]
Treatment / Management
The valvular vegetations associated with PVE are usually larger than those found in native valve endocarditis (NVE). For the antibiotics to penetrate the total vegetation, they should be used in dosages that result in maximum, non-toxic serum concentrations.[1] When starting the treatment for a patient with PVE, it is required to identify the causing microorganism, select the appropriate antibiotic, evaluate for any complications of the endocarditis, and evaluate the need for surgical intervention if the antibiotics treatment fails, the infection causes a valvular abscess. Empiric treatment with antibiotics should be started after 3 blood cultures are obtained. This treatment should consider coverage of gram-positive and gram-negative bacteria. This empiric treatment should include vancomycin, gentamycin, and anti-pseudomonal carbapenem or cefepime. When the causing organism is identified, treatment should be tailored towards the coverage of this causative agent. American Heart Association recommends at least 6 weeks of antibiotic treatment.[25][15] When PVE is caused by staphylococcus, AHA recommends starting triple antibiotical treatment.[25][26] In the staphylococcus-induced PVE, either S. aureus or S. epidermidis, the susceptibility to methicillin is the main consideration when selecting combination therapy. When PVE is caused by methicillin-sensitive staphylococcus, the triple antibiotic regimen includes nafcillin or oxacillin (total of 6 weeks) combined with both gentamicin (which is given for the first 2 weeks of treatment only) and rifampin (total of 6 weeks of treatment). If the patient reports being allergic to penicillin without evidence of anaphylaxis, a first-generation cephalosporin should be the next choice.
For methicillin-resistant staphylococcus, vancomycin should be combined with gentamycin and rifampin. If the bacteria is resistant to gentamycin, another aminoglycoside should be selected depending on the antibiotic susceptibilities.[25] A fluoroquinolone can be an alternative to the aminoglycoside in case of pan resistance to all aminoglycosides.[27] Rifampin uniquely affects staphylococcus invasion of foreign bodies and is used in staphylococcus-induced IE.[28] In streptococcal-induced PVE, combining a beta-lactam antibiotic and an aminoglycoside is the treatment of choice. This combination provides a synergistic killing of the causative bacteria.[17] If a penicillin-susceptible Streptococcus causes the PVE, the penicillin-gentamycin combination is recommended. For penicillin-allergic patients, vancomycin or cephalosporine are the choices. If the patient's penicillin allergy is not severe (does not include anaphylaxis), a cephalosporin should be used first. If the aminoglycoside is contraindicated, PVE can be treated with a single agent (penicillin, cephalosporine, or vancomycin). If the streptococcus resists penicillin, an aminoglycoside can be used alone for treatment.[15] If the organism is resistant to aminoglycoside, recommendations are for treatment with vancomycin as a single agent. In enterococcal-induced PVE, the combination of a cell wall-active agent (penicillin, ampicillin, or vancomycin) and an aminoglycoside (gentamycin or streptomycin) is considered. In penicillin allergy, vancomycin is a better alternative than cephalosporine combined with an aminoglycoside, as cephalosporins are ineffective against enterococcus.[29] In the setting of aminoglycoside resistance, the enterococcus PVE should be treated with a cell wall-active agent (penicillin, ampicillin, or vancomycin) alone for a longer period (8 to 12) weeks.[30] In the setting of vancomycin-resistant Enterococcus faecium (VRE), daptomycin and linezolid are considered acceptable choices for treatment.[31](B2)
When PVE is caused by Haemophilus, Aggregatibacter (previously Actinobacillus), Cardiobacterium, Eikenella, or Kingella (HACEK), third-generation cephalosporins are usually the first line of treatment and used for a total treatment period of 6 weeks. Ampicillin can be used if the organism shows sensitivity to the cultures. A fluoroquinolone can be used to treat an allergy to cephalosporins and ampicillin.[15] Treatment of gram-negative bacilli-induced PVE is usually combination therapy with a beta-lactam (penicillins, cephalosporins, or carbapenems) and either a fluoroquinolone or an aminoglycoside. The recommended duration of treatment is 6 weeks.[25] For patients with culture-negative PVE onset ≤1 year, the antibiotics coverage should consider the possibility of infection due to staphylococci, enterococci, and aerobic gram-negative bacilli. The antibiotic combination should include vancomycin, gentamicin, cefepime, and rifampin per AHA recommendations.[15] AHA recommends patients with culture-negative PVE onset >1 year after surgery receive infection coverage due to staphylococci, viridans group streptococci, enterococci, and HACEK organisms. The empiric combination should include vancomycin and ceftriaxone.[15] AHA recommends repeating 2 blood cultures every 24 to 48 hours till blood cultures are negative and starting the count of antibiotics treatment days after the first negative blood culture is achieved.
Early surgical intervention for PVE is indicated if:[15]
- The patient develops heart failure due to valve dehiscence, the development of intracardiac fistula, or the presence of severe prosthetic valve dysfunction.
- The presence of persistent bacteremia 5 to 7 days after the appropriate antibiotic regimen, with other bacteremia sources, is excluded.
- Evidence of heart block, development of abscess (annular or aortic), or presence of destructive penetrating lesions
- Fungi or highly resistant bacterial organisms cause the PVE.
Early surgery is reasonable in PVE in the following scenarios: developing recurrent emboli despite the appropriate antibiotic treatment, relapsing PVE, or large mobile vegetations >10 mm.[15] Surgical intervention decreases mortality when performed on patients with PVE who develop heart failure.[32] Paravalvular PVE invasion can manifest as a complete heart block, annular or aortic abscess, destructive penetrating lesions, or an intracardiac fistula. These complications require early complex reconstructive surgery, improving the survival rate by 80%.[33] S. aureus PVE is associated with high mortality, and often, early surgery is indicated when complications are present. Such an early surgical approach was associated with decreased mortality in these patients. Other organisms that may require early surgical intervention are gram-negative (non-HACEK) microorganisms ( Pseudomonas aeruginosa and multidrug-resistant gram-negative bacilli), multidrug-resistant enterococci, and fungi.[34](B2)
After the surgical intervention is completed, 6 weeks of intravenous antibiotics are recommended if the intraoperative valve culture is positive.[35]
Differential Diagnosis
The differential diagnosis for PVE include the following:
- Native valve endocarditis: Patients usually have a clinical picture similar to PVE patients.
- Atrial myxoma: Patients present with constitutional symptoms secondary to cytokine release or may have systemic disease secondary to the embolic phenomenon.
- Libman-Sacks endocarditis: Patients are commonly asymptomatic and have a history suggestive of a diagnosis of systemic lupus erythematosus SLE.
- Nonbacterial thrombotic endocarditis (NBTE): Endocarditis is caused by sterile vegetation deposition on cardiac valves. NBTE can be caused by pancreatic, lung, and colon tumors or from SLE or tuberculosis.[36]
- Rheumatic fever: Jones criteria make the diagnosis: evidence of carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules, and evidence of preceding streptococcal infection.[37]
Prognosis
Despite the appropriate diagnosis and use of surgical treatment in PVE, morbidity and mortality remain high; PVE carries the highest mortality rates compared to other types of IE. The strongest predictors of mortality were persistent bacteremia, heart failure, intracardiac abscess, and stroke development.[4] Persistent bacteremia and healthcare-associated infection are associated with S aureus-induced IE.[38] S. aureus is associated with high mortality in both PVE and native valve endocarditis.[39] Healthcare-associated PVE is another predictor of high in-hospital mortality.[40] Other predictors for higher mortality are large vegetation, poor surgical candidacy, positive valve culture, embolization, and diabetes mellitus.[41][42]
Complications
The most common cardiac complication of PVE is heart failure. This can result from prosthetic valve dehiscence, which leads to valvular insufficiency or myocardial infarction from emboli.[43] Other cardiac complications are perivalvular abscess formation, intracardiac fistula, and pericarditis.[44] Non-cardiac complications are usually a result of an embolic event, metastatic abscess formation, or a mycotic aneurysm. Neurologic complications are stroke (due to an embolus), seizure (abscess or emboli), brain abscess formation, aseptic meningitis, acute encephalopathy, cerebral hemorrhage due to ruptured mycotic aneurysm, or meningoencephalitis.[45][46] Renal complications are renal infarction due to emboli, renal abscess, glomerulonephritis (due to immunoglobulins and complement deposition in the glomerular membrane), and acute interstitial nephritis. All these complications may present as acute renal failure.[47] Pulmonary complications occur due to right heart PVE; vegetations of the tricuspid or pulmonary valve can lead to embolization, which results in lung abscess, pneumonia, pleural effusion, or pneumothorax. Other complications are osteomyelitis, septic arthritis, persistent bacteremia, or candidemia in fungal PVE.[48] Mortality remains a serious concern after PVE despite appropriate treatment and surgical interventions.[4]
Consultations
To manage patients with VPE, the treating team must include the right interprofessional consultants. Early involvement of a cardiologist is essential to make the correct diagnosis, review the imaging studies, and give recommendations for the treatment plan. An infectious disease consult is necessary to direct the initial antibiotics treatment, review the cultures, and redirect the treatment according to the susceptibility results. Involving the radiologist in interpreting the imaging studies is an important step in managing patients with PVE. Some patients may require advanced imaging studies, and the radiologist recommends and directly chooses the appropriate type of imaging studies indicated to achieve the diagnosis. A cardiovascular surgeon should be part of the management team for patients with PVE. The cardiovascular surgeon needs to review the imaging studies, follow the patient's treatment progress, and follow the patient's blood culture response to the antibiotic treatment to determine the need for surgical intervention. A pharmacist's early involvement is important in managing PVE patients, directing the antibiotics treatment during hospitalization, checking the drug interactions, and following the patient's treatment course after discharge.
Deterrence and Patient Education
Endocarditis is an infection usually caused by bacteria or fungi and affects the heart's inner layer, including the heart's valves. The causative organism is most likely a bacteria but can also include some fungi that get to the heart through the bloodstream. PVE is 1 type of endocarditis that affects the replaced prosthetic valve. Getting infected heart valves causes damage to the valve and, hence, malfunction, which can cause major complications. Early treatment is necessary to prevent bad outcomes. Having surgery for a heart valve increases the risk of infection. Those who intravenously abuse drugs are at higher risk of this type of infection.
The patient should return to the emergency room if the patient experiences any of the following symptoms:
- Tiredness that persists for 2 to 3 days
- Decreased exercise tolerance
- Chest pain or shortness of breath
- Fever over 100.4 degrees F (38.0 degrees C)
- Extensive sweats, especially at night
- Palpitations
- Fainting
- Trouble speaking
- Weakness in any extremity or face
- Spots on fingernails, fingertips, whites of the eyes, or other skin areas
- Symptoms of a stroke include trouble speaking or inability to move 1 side of your body
Enhancing Healthcare Team Outcomes
PVE is associated with high morbidity and mortality. A comprehensive healthcare team must be cautious in the workup and treatment of this disease. Treatment of PVE needs to be started early, in an inpatient setting, and monitored by an interdisciplinary team of physicians, nurses, and pharmacists to ensure the appropriate treatment and prevent complications as treatment is usually extended over 6 to 8 weeks, patients complete treatment in an outpatient setting, at a short-term nursing facility, or home with home intravenous infusion. When a patient presents with suspected PVE, the physician starts the empiric antibiotics treatment, initiates the appropriate workup for confirmation of diagnosis, and identifies the causative organism. Antibiotics should be tailored to target the organism based on susceptibility results. Usually, physicians follow the necessary laboratory testing to prevent any possible renal or liver toxicity and monitor for signs or symptoms of PVE-related complications. The pharmacist has to check the antibiotic regimen, monitor for any possible drug-to-drug interaction, and monitor any possible toxicity. Nurses are responsible for appropriately administering the medications and monitoring for possible side effects during the hospital stay.
After discharge from the hospital, the team is responsible for appropriate follow-up on the patient’s adherence to treatment and monitoring possible side effects. The Doctor has to order appropriate laboratory tests to monitor possible toxicity and monitor drug levels in coordination with the pharmacist. The home visiting nurse ensures adherence, evaluates for appropriate intravenous administration of antibiotics, monitors the intravenous line side, monitors for any adverse reactions, and evaluates the patient for any possible signs or symptoms of PVE-related complications. Pharmacists and nurses should inform the clinician if medication compliance concerns a certain patient. This also includes drug adverse reactions or changes in a household environment. This comprehensive interprofessional team effort is needed to ensure high-quality patient care and to have the maximum benefits of the regimen.
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