CONTENTS

• Rapid Reference 🚀
• Diagnosis
  • When to suspect endocarditis
  • Lab workup
  • Septic pulmonary emboli
  • Echocardiography (TTE vs TEE)
  • Diagnostic strategies & Duke Criteria
• Manifestations include:
  • Metastatic infection
  • Neurologic complications
    • Septic embolic encephalitis
• Antibiotics
  • Empiric therapy
  • Definitive therapy
• Cardiothoracic surgery
• Anticoagulation
• Treatment for opioid use disorder
• Podcast
• Questions & discussion
• Pitfalls

---

rapid reference: endocarditis

(back to contents)

---

initial evaluation

• Peripheral blood cultures x3 (3 sets, at 3 different sites).
• Additional culture of any indwelling line in place >48 hours.
• Echocardiography. 📖
• Might consider CXR and/or CT chest if suspect right-sided endocarditis with septic pulmonary emboli.
• Might consider evaluation for metastatic infection, if suspected (e.g., joints, spleen, brain, spine).

empiric therapy 📖

• Acute, native valve: Consider vancomycin plus cefazolin.
• Subacute, native valve: Consider vancomycin plus ampicillin/sulbactam.
• Prosthetic valve, acute onset, <1 year post surgery: Consider vancomycin, gentamicin, and cefepime.
• Prosthetic valve, acute onset, >1 year post surgery: Consider vancomycin, gentamicin, and cefazolin.
• Prosthetic valve, subacute onset: Consider vancomycin, gentamicin, and ampicillin/sulbactam.

indications for surgical consultation 📖

• Valve regurgitation or fistula causing heart failure.
• Myocardial abscess.
• Vegetation enlargement, despite antibiotics.
• Persistent fever with positive cultures.
• Large vegetation with multiple embolic phenomena.

follow course

• Daily single blood culture to determine sterilization of blood.
• Telemetry monitoring +/- EKG to watch for heart block.
• Consider repeat echo (to evaluate for vegetation growth and/or worsening valvular dysfunction).
• Aggressive evaluation & management of any metastatic foci of infection (e.g., septic arthritis, splenic abscess).

---

when to suspect endocarditis

(back to contents)

---

at-risk patients

• Valvular heart disease, especially:
  • Prior endocarditis (Hazard Risk of 65).(31175343)
  • Prosthetic valve (Hazard Ratio of 19).(31175343)
    • Surgical prosthetic valve.
    • TAVR (transcatheter aortic valve replacement).
  • Aortic stenosis.
• Any other endovascular hardware, especially:
  • Pacemaker.
  • PICC line or subcutaneous port (e.g., used for chemotherapy).
• IV drug use.
• Hemodialysis patients (17-fold increase in endocarditis risk).(Vincent 2023)
• Older age, immunosuppression.

clinical presentation of left-sided endocarditis

• Fever (e.g., Strep viridans causing subacute bacterial endocarditis)
  • Fever plus IV drug use indicates ~15% risk of endocarditis.(30001813)
• Flu-like, nonspecific illness (e.g., chills, night sweats, headache).
• Septic shock (e.g., Staph aureus causing acute bacterial endocarditis).
• Acute heart failure from valve regurgitation.
• Systemic emboli (e.g., ischemic stroke, kidney infarction):
  • Stroke in a young patient is a classic endocarditis presentation.
  • Delirium due to multifocal emboli (with no clinically obvious focal neurologic lesion).

clinical features of right-sided endocarditis

• Fever.
• Septic pulmonary emboli:
  • Will often initially mimic pneumonia (with a constellation of respiratory failure, pulmonary infiltrates, and fever) or pulmonary embolism.
  • May eventually lead to hemoptysis, pneumothorax, or empyema.
  • The key radiologic finding is multiple pulmonary nodules that eventually cavitate (more on this below 📖).

traditional examination findings

• Fever (~85% sensitive).
• New regurgitant murmur.
• Signs of local infection at the site of a pacemaker or indwelling catheter.
• Classic findings for endocarditis (<5% sensitive, mostly seen in subacute endocarditis):
  • Splinter hemorrhages.
  • Conjunctival petechiae.
  • Janeway lesions (red/blue macules on palms and soles).
  • Osler's nodes (painful swelling in pulp of fingers).

point-of-care echocardiography findings

• Most sensitive findings:
  • (1) Valvular regurgitation. This raises a concern for endocarditis, but must be interpreted in clinical context:
    • Regurgitation is more worrisome if severe and found in a young patient with no prior cardiac disease (who shouldn't have regurgitation).
    • Regurgitation is most worrisome if there is a recent echocardiogram without any regurgitation.
    • Mild/trace regurgitation is nonspecific, especially in older patients.
  • (2) Valve looks “funny” (thickened, etc).
• More specific findings:
  • (1) Vegetation itself is seen.
  • (2) Prosthetic valve partial dehiscence.

---

lab workup

(back to contents)

---

peripheral blood cultures

• This is the single most important test to order for suspected endocarditis. Cultures must be obtained prior to starting antibiotics in suspected endocarditis, even if this causes a short treatment delay.
• Number of cultures:
  • One “set” of cultures = two bottles (anaerobic & aerobic) drawn from a single location.
  • Ideally three sets should be obtained from three different locations (two sets are OK if this isn't possible).
• Location of cultures:
  • Ideally cultures should be obtained from a fresh peripheral stick.
  • If this isn't feasible, obtain blood wherever you can get it. For example, obtaining blood from a freshly placed central line is OK.
• Timing
  • In endocarditis, bacteremia is generally constant, so there is little rationale to space cultures out over time.
  • Don't worry about the timing of cultures – the key thing is to get a lot of cultures and fill the culture bottles fully. (Get a lot of blood; more blood removed = higher likelihood of capturing a causative pathogen).

additional culture of any indwelling lines

• In addition to the above peripheral cultures, any indwelling lines in place >48 hours should also be cultured.
• The intention here is to determine if there is an infection of the line. (more on line infection here)

other labs which may be considered (but not terribly helpful)

• Acute-phase reactants (ESR, CRP):
  • >95% sensitive for endocarditis.
  • These tests don't generally help guide initial patient management. They may be useful for subsequent follow-up, to help determine if the infection is responding adequately to therapy.
• Urinalysis consistent with glomerulonephritis (proteinuria, microscopic hematuria) is seen in ~60% of cases.

---

likelihood of endocarditis based on bacterial species 

Among streptococcal species, the risk of endocarditis may be estimated based on species:(32580572)And the following map may help clarify streptococcal phylogeny. (32580572) 

• Note that Streptococcus bovis has been renamed as Streptococcus gallolyticus (classically associated with bacteremia due to a colon cancer).
• Note that Streptococcus agalactiae is group B strep (GBS).  (This shouldn't be confused with Streptococcus dysgalactiae.)

---

septic pulmonary emboli

(back to contents)

---

Tricuspid endocarditis may present in a unique fashion, with septic pulmonary emboli.  These may mimic pneumonia or pulmonary embolism.

---

clinical features of septic pulmonary emboli

• Fever.
• Cough, hemoptysis.
• Pleuritic chest pain.
• Dyspnea (pleural irritation often cause disproportionately prominent tachypnea).

---

radiology of septic pulmonary emboli

lesion distribution:

• Multiple lesions are usually present.
• There is often a peripheral and lower lobe predominance (similar to other hematogenously disseminated lesions).
• Lesions are often based on the pleura (similar to sterile pulmonary infarcts).

initial lesion appearance

• Round or wedge-shaped.
• Usually ~0.5-3 cm.
• Often ill-defined (sometimes with a surrounding halo sign). This may reflect local hemorrhage into adjacent lung tissue.

subsequent cavitation

• About half of lesions eventually cavitate.
• Cavitation may occur early.  Thus, cavitation is usually seen in at least one lesion on CT scan.
• A characteristic feature is multiple lesions in different stages of cavitation (solid lesion ➡️ thick-walled cavity ➡️ thin-walled cavity).(29518379)
• There is usually no air-fluid level.

other radiologic findings that may occur

• Pleural effusion, which may include empyema.
• Pneumothorax.
• Mediastinal lymphadenopathy can be seen in ~20%.(Rosado-de-Christenson 2022)

radiological differential diagnosis includes:

• Pulmonary emboli.
• Pneumonia (including fungal pneumonia, necrotizing pneumonia).
• Pneumatoceles.
• Pulmonary metastases with subsequent cavitation.
• GPA (granulomatosis with polyangiitis).

---

causes of septic pulmonary emboli

• Right-sided endocarditis:
  • Tricuspid endocarditis.
  • Pacemaker-related endocarditis.
• Infected intravascular hardware, e.g.:
  • Central line infection.
  • Tunneled hemodialysis catheter infection.
  • Port infection.
• Septic thrombophlebitis anywhere in the body:
  • Septic internal jugular vein thrombosis (Lemierre's syndrome).
  • Septic pelvic thrombophlebitis (e.g., due to septic abortion or post-puerperal uterine infection).
  • Septic cavernous sinus thrombosis.
  • Septic portal venous thrombosis (pylephlebitis).

---

echocardiography

(back to contents)

---

performance

• Sensitivity of transthoracic echocardiogram (TTE) is ~70% for native valve endocarditis or 50% for prosthetic valve endocarditis.(26320109)
• Sensitivity of transesophageal echocardiogram (TEE) is ~96% for native valve endocarditis and ~92% for prosthetic valve endocarditis.(26320109)
• Specificity isn't perfect. For example, false-positive vegetation may occur due to thrombi or marantic (non-infectious) vegetations.
• Note: These numbers are population averages. The sensitivity of TTE is best appreciated by reviewing the images.
  • If the images are crystal clear, then the sensitivity is higher (and the added value of a TEE thus lower).
  • If the windows are poor and images are limited, then the sensitivity is poor.

advantages of transthoracic echocardiogram

• Noninvasive, useful to obtain as a baseline study.
• Easier to repeat serially if patient deteriorates.
• May be fully adequate to evaluate tricuspid endocarditis (without the need for TEE).(32299668)

advantages of transesophageal echocardiogram

• Greater sensitivity for endocarditis diagnosis, especially prosthetic valve endocarditis and left-sided endocarditis.
• Greater sensitivity for complications of endocarditis (e.g., aortic ring abscess, valve perforation).

2015 AHA/ACC guideline for which study to obtain

• (1) Everyone gets a baseline TTE to start.
• (2) TEE is usually indicated in the following situations.
  • TTE is negative and persistent suspicion for endocarditis remains (e.g., persistent bacteremia).
  • TTE is positive and shows high-risk features (large/mobile vegetations, valvular insufficiency, suggestion of perivalvular extension, or secondary ventricular dysfunction).
  • Patient has a prosthetic valve or complex congenital heart disease.
  • Patient has poor transthoracic imaging windows.

repeat echo: consider for hemodynamic deterioration or failure to improve clinically. Look for:

• Worsening valvular dysfunction.
• Development of aortic ring abscess.
• Enlarging vegetations despite antibiotics (associated with complications, need for surgery).

---

diagnostic strategies & Duke criteria

(back to contents)

---

approaches to the diagnosis of endocarditis?

• The modified Duke criteria are increasingly obsolete (especially for newer entities such as pacemaker or TAVR-associated endocarditis). These criteria are shown below, but in practice they aren't terribly helpful.
• The schematic above shows a more clinically useful approach to the diagnosis of endocarditis. Improvements in diagnostic radiology are increasingly helpful in ambiguous situations. When in doubt, further imaging data should be aggressively sought both to evaluate the diagnosis of endocarditis and also to look for competing diagnoses.

---

Duke criteria

modified Duke criteria for “definite” endocarditis

• Definite endocarditis:
  • Two major criteria.
  • One major criteria + 3 minor criteria.
  • Five minor criteria.
• Possible endocarditis:
  • One major and one minor.
  • Three minor criteria.

major criteria

• [1] Microbiologic data: any of the following
  • i) Two separate cultures with organisms typically involved in endocarditis:
    • Strep viridans, Strep. bovis (now renamed Strep. gallolyticus)
    • Staphylococcus aureus
    • Community-acquired enterococci, without primary focus
    • Haemophilus species
    • Aggregatibacter species
    • Cardiobacterium hominis
    • Eikenella corrodens
    • Kingella species
  • ii) Single culture of Coxiella burnetii or anti-phase 1 IgG antibody titer >1:800
  • iii) Bacteria consistent with endocarditis from persistently positive blood cultures:
    • At least two positive cultures drawn >12 hours apart.
    • 3 of 4 cultures positive, with first and last samples separated by >1 hour apart.
• [2] Echocardiographic data: any of the following
  • i) vegetation or myocardial abscess
  • ii) new valve regurgitation or dehiscence of prosthetic valve

minor criteria

• [1] Patient at-risk for endocarditis (defined at top of this chapter).
• [2] Temperature >38C.
• [3] Vascular phenomena:
  • Major arterial emboli (e.g. ischemic stroke).
  • Septic pulmonary emboli.
  • Janeway lesions.
  • Conjunctival hemorrhage.
  • Infectious (mycotic) aneurysm.
• [4] Immunologic phenomena:
  • Glomerulonephritis.
  • Osler's nodes.
  • Positive rheumatoid factor.
• [5] Blood culture positivity not reaching the level of a major criterion.

---

metastatic infection

(back to contents)

---

• Recognizing distant sites of infection is important, because these may require surgical drainage.  Furthermore, such drainage should ideally be performed prior to valve replacement surgery, to avoid infection of the fresh valve.
• Common sites:
  • Joint infection(s).
  • Spinal infection, including discitis.
  • Splenic abscess.

---

neurologic complications

(back to contents)

---

range of neurological complications

• Ischemic stroke: MRI reveals ischemic stroke in ~70% of patients with left-sided endocarditis. However, these are often clinically silent. Only ~15% of patients have a clinical stroke.(31175343)
  • Patients can present with septic embolic encephalitis (section below).
• Cerebral hemorrhage occurs in ~4% of patients, including:
  • Hemorrhagic transformation of ischemic stroke.
  • Rupture of a mycotic aneurysm.
• Mycotic aneurysms occur in ~5% of patients.
  • The most common causes are Viridans group Streptococcus or Staphylococcus aureus.
  • Bacterial mycotic aneurysms are most often located within distal branches of the MCA (middle cerebral artery). Alternatively, fungal mycotic aneurysms tend to involve the circle of Willis.
  • Clinical presentation often results from subarachnoid hemorrhage or intracerebral hemorrhage (although infarction may also occur). Mycotic aneurysm rupture carries a mortality of 80%.(Louis 2021)
  • Large or enlarging mycotic aneurysms may require endovascular or neurosurgical intervention. However, many aneurysms may resolve with antibiotic therapy alone. 🌊
• Meningitis occurs in 1% of patients.
  • Most frequently due to S. aureus.(17290733)
• Brain abscess occurs in 0.1% of patients.

treatment implications include:

• Patients with meningitis or abscess may require antibiotics with good CNS penetration (e.g., ceftriaxone 2 grams IV Q12hr or nafcillin).

---

septic embolic encephalitis

(back to contents)

---

basics & epidemiology

• Commonly seen with endocarditis: (31964490)
  • 20-55% of patients present with a symptomatic ischemic stroke.
  • Patients are very often asymptomatic, yet with positive findings on MRI.
  • Risk factors include vegetation >3 cm, Staphylococcus aureus, mitral valve involvement, and anticoagulation therapy.
• Other causes of septic emboli include:
  • Pulmonary abscess or empyema.
• Consequences of septic emboli may include:
  • (1) Ischemic brain infarction.
  • (2) Brain abscess formation.
  • (3) Mycotic aneurysm formation.

imaging

• Ischemic infarcts tend to be small, multiple, of variable ages, distributed among various vascular territories, and often concentrated along peripheral watershed territory or the grey-white border.(31964490) They may also cause microbleeds in the cortical regions.(33741796)
• CT findings: Abscesses may be seen as low-attenuation foci, with or without microhemorrhagic transformation. Punctate or ring enhancement may occur following contrast administration.
• MRI findings:
  • Infarcts may cause T2/FLAIR hyperintensities with diffusion restriction.
  • Microbleeds will be notable on SWI/GRE sequences.
  • Abscesses may cause punctate or ring enhancement (similar to CT scan).

management

• Antibiotic therapy is needed for the management of endocarditis. Consideration should be given to selecting a regimen with adequate penetration of the brain.
• Anticoagulation may be contraindicated.
• Endovascular intervention can be used for the management of acute, large-vessel septic embolism or mycotic aneurysm.
• Cardiac surgery is safe in the context of embolic infarcts (and, indeed, repeated emboli may be an indication for surgery).

---

empiric therapy

(back to contents)

---

general concepts of endocarditis therapy

• Endocarditis is usually due to gram-positive infections (~90%), so empiric gram-negative coverage usually isn't necessary. However, there are some exceptions to this (e.g., IV drug use and early postoperative prosthetic valve endocarditis).
• Vancomycin monotherapy is often used, but it's not ideal for the following reasons:
  • (1) Vancomycin levels are often subtherapeutic for the first 1-2 days of therapy, before the dose is optimized.
  • (2) Vancomycin is a suboptimal antibiotic for the most common and virulent causes of endocarditis (e.g., MSSA and streptococcal species). Thus, vancomycin achieves a broad spectrum at the cost of reduced efficacy.
• If a single medication is desired for empiric therapy, daptomycin dosed at 10-12 mg/kg/day might be the best option. Compared to vancomycin, daptomycin has a broader spectrum of activity (e.g., covering vancomycin-resistant enterococci), lacks nephrotoxicity, and has more reliable pharmacokinetics.

acute, native-valve endocarditis

• Preferred regimens:
  • Vancomycin + cefazolin.
  • In cefazolin allergy, an alternative is vancomycin + ceftriaxone.(32757525) Please note that cefazolin is not cross-allergic with ceftriaxone or other beta-lactam antibiotics, so cefazolin is safe to use unless there is a specific cefazolin allergy.
  • Alternative: daptomycin monotherapy.
• Rationale:(23985343, 16505987, 17664322, 17173215, 28789974)
  • Cefazolin + Vancomycin as initial therapy seems to have better efficacy for methicillin-sensitive
    Staph aureus (MSSA).(23985343, 22006007)
  • Cefazolin plus Vancomycin might have improved efficacy against MRSA, compared to vancomycin alone.(Trinh et al., 22848719)
  • Cefazolin and vancomycin act at different stages of cell wall synthesis, so they function in a synergistic fashion.(10390234) This may partially explain the clinical evidence above.
  • The combination of vancomycin plus either cefazolin or nafcillin is guideline-recommended therapy for Staph. aureus before sensitivities are available (Class IIb recommendation of the AHA/IDSA). Over time, Staph aureus is becoming an increasingly common cause of endocarditis (especially among acutely ill patients) – so it makes sense to start this regimen up-front.

subacute, native-valve endocarditis

• Subacute endocarditis refers to gradual illness persisting over weeks. This doesn't usually cause critical illness, unless the endocarditis leads to a complication such as valvular dysfunction or embolic phenomena.
• Preferred regimens:
  • Vancomycin + ampicillin-sulbactam.
  • If ampicillin allergy: vancomycin + ceftriaxone.
• Rationale: Ampicillin-sulbactam isn't quite as good for Staph. aureus, but it provides better coverage for enterococcus and HACEK organisms (which typically cause subacute endocarditis).

prosthetic valve endocarditis

• American and European guidelines both recommend synergistic therapy with rifampin and gentamicin for prosthetic-valve endocarditis due to staphylococcus, streptococcus, and enterococcus. However, rifampin should be withheld until 3-5 days after initiation of treatment. Potential initial empiric regimens are as follows:
• [1] Conventional regimen: Vancomycin plus gentamicin.
• [2a] Preferred regimen for acute bacterial endocarditis occurring within months of valve surgery is vancomycin, gentamicin, and cefepime. Cefepime functions similarly to cefazolin, while also providing coverage for nosocomial gram-negative pathogens.
• [2b] Preferred regimen for acute bacterial endocarditis occurring >1 year after valve surgery is vancomycin, gentamicin, and cefazolin. The rationale for cefazolin is same as above for native valve endocarditis as discussed above.
• [3] Preferred regimen for subacute, prosthetic-valve endocarditis: Vancomycin, gentamicin, and ampicillin-sulbactam.

IV drug use (IVDU)

• Patients at risk for broader spectrum of pathogens.
• [1] Vancomycin monotherapy is an acceptable therapy, although daptomycin might be preferable as monotherapy.
• [2] Vancomycin plus piperacillin-tazobactam is preferred:
  • Piperacillin-tazobactam improves coverage of enterococcus and gram-negatives compared to vancomycin monotherapy. The pharmacokinetics of piperacillin-tazobactam may be more predictable than vancomycin.

additional exposures to consider:

---

definitive therapy

(back to contents)

---

streptococcus pneumoniae

• Sensitivity unknown: ceftriaxone used initially for empiric therapy.
• Penicillin-sensitive: may treat with penicillin, cefazolin, or ceftriaxone.
• Penicillin-resistant, ceftriaxone sensitive: treat with ceftriaxone.
• Ceftriaxone-resistant (MIC >2 ug/mL): high-dose ceftriaxone seems to work regardless (e.g. 2 grams IV q12, as long as no meningeal involvement). For meningeal involvement, consider addition of vancomycin and rifampin (AHA guidelines).

beta-hemolytic streptococci (Groups A, B, C, F, and G)

• Group A streptococci: Penicillin G is the treatment of choice; ceftriaxone is a reasonable alternative.
• Groups B, C, F, G: May be slightly harder to kill than Group A streptococci. The cornerstone of therapy is still penicillin or ceftriaxone, but addition of gentamicin for the first two weeks may be considered (AHA guidelines) or recommended (ESC guidelines).

coagulase-negative staphylococci

• These are often methicillin-resistant. Methicillin-resistant strains are cross-resistant with cephalosporins and carbapenems (even though they may appear sensitive to these agents in vitro)(AHA guidelines).
• Staph lugdunensis (“slug”)
  • More virulent, with a high rate of perivalvular extension and metastatic infection.
  • Should always be taken seriously (less likely to be a contaminant)
  • Uniformly susceptible to most antibiotics (including methicillin, which may be used for treatment)(AHA, ESC guidelines).
• Native valve endocarditis: Nafcillin or vancomycin monotherapy (depending on sensitivity)
• Prosthetic valve endocarditis:
  • Methicillin-resistant: Vancomycin + rifampin + gentamicin
  • Methicillin-sensitive: {Nafcillin or cefazolin} + rifampin + gentamicin

methicillin-sensitive staphylococcus aureus (MSSA)

• Native valve, right-sided (often in context of IVDU): may be treated with two-week course of nafcillin/oxacillin in straightforward cases (e.g. no renal failure, extrapulmonary metastatic infection, or meningitis).
• Native valve, left-sided:
  • Without brain involvement: cefazolin or nafcillin. (further discussion of cefazolin vs. nafcillin for MSSA here)
  • With brain emboli: Nafcillin is the best agent (since cefazolin doesn't penetrate the CSF well). If nafcillin can't be tolerated, then vancomycin may be used instead.
• Prosthetic valve: Nafcillin + rifampin + gentamicin

methicillin-resistant staphylococcus aureus (MRSA)

• Native valve:
  • Vancomycin is 1st line (unless the vancomycin MIC is >1 mg/L, in which case daptomycin is probably superior)
  • Daptomycin is generally 2nd line. If daptomycin is used, combination of daptomycin plus a beta-lactam (e.g. ceftaroline) may enhance efficacy.
• Prosthetic valve:
  • Usually: Vancomycin + rifampin + gentamicin

enterococcus

• Third leading cause of endocarditis, accounting for ~10% of non-IVDU endocarditis. However, enterococcus tends to be indolent, so this may be somewhat less common (<10%) among critically ill patients. Unfortunately, enterococcus is rather difficult to kill (often requires synergistic combination of two drugs).
• Sensitive to both penicillin & gentamicin
  • i) {Ampicillin or Penicillin} + Gentamicin.
  • ii) Ampicillin + Ceftriaxone (2 grams IV q12hr) may be preferred if high risk of renal failure due to gentamicin.
• Sensitive to penicillin (but not gentamicin)
  • Ampicillin + Ceftriaxone (high-dose, 2 grams IV q12hr)
• Resistant to penicillin/ampicillin, but not vancomycin
  • {Vancomycin + Gentamicin}
• Resistant to penicillin, aminoglycosides, & vancomycin
  • Linezolid or daptomycin may be used.
  • Linezolid achieved cure in 17/22 patients with Enterococcus faecium.(12522747)
  • Daptomycin is not supported by much evidence. If used, consider high doses and combination with a beta-lactam (either ampicillin or ceftaroline; AHA guidelines IIb recommendation).

---

surgery

(back to contents)

---

potential indications for surgery in left-sided endocarditis

• (1) Heart failure (due to valve dysfunction or fistulae).
• (2) Uncontrolled infection:
  • Myocardial abscess, heart block.
  • Vegetation enlargement despite antibiotics.
  • Persistent fever and positive blood cultures for >7 days, with exclusion of other foci of infection (e.g., splenic abscess).
  • Fungal endocarditis or highly resistant organism.
• (3) Prevention of systemic embolization:
  • Huge vegetation (>15 mm).
  • Large vegetation (>10 mm) with one or more embolic episodes despite antibiotic therapy.

potential indications for surgery in right-sided endocarditis

• Surgery plays smaller role:
  • (a) Better outcomes compared to left-sided endocarditis.
  • (b) Many patients have ongoing IV drug abuse, may infect prosthetic valve.
• Indications to consider surgery:
  • Right heart failure due to severe tricuspid regurgitation with poor response to medical therapy.
  • Failure of antibiotics to clear infection.
  • Tricuspid valve vegetation >20 mm and recurrent pulmonary embolism despite antibiotics.

contraindications to surgery

• Inability to tolerate anticoagulation during bypass (e.g. due to recent intracranial hemorrhage or large ischemic stroke).
  • In this situation, surgery may need to be delayed by four weeks (if possible).

---

anticoagulation

(back to contents)

---

controversial, particularly for prosthetic valve endocarditis:

• Continuous anticoagulation is generally important for anyone with a mechanical prosthetic valve.
• Anticoagulation may increase the likelihood of hemorrhagic transformation following septic embolic stroke.
• Little high-quality evidence exists on this topic. In the absence of any solid evidence, be sure to discuss anticoagulation decisions with other specialists involved (e.g., cardiology and neurology).

current recommendations in AHA 2015 guidelines

• Patients with a mechanical valve who have experienced a CNS embolic event should stop all forms of anticoagulation for two weeks (Class IIa).
• Initiation of aspirin or anti-platelet agents as adjunctive therapy in endocarditis is not recommended.
• Continuation of long-term anti-platelet therapy may be considered for patients without bleeding complications (Class IIb).
• (No recommendation is made regarding continuation of anticoagulation.)

---

treatment for opioid use disorder

(back to contents)

---

• Endocarditis may in some ways be viewed as a symptom of the larger disease of opioid use disorder.
  • Patients with opioid use disorder are at enormous risk of endocarditis (e.g. 2-5% per year risk with active IV drug use).(30001813)
• One episode of endocarditis is a risk factor for recurrence (due to damage to the heart valves). Therefore, if patients continue to use IV drugs then they are at astronomically high risk of recurrent endocarditis.
  • Recurrent endocarditis is a common pathway whereby opioid use disorder leads to death.
• Medication-assisted therapy (MAT) is required for these patients.
• Unfortunately, inpatient medical systems often fail miserably to deliver medication-assisted therapy. One study from a top teaching hospital in 2016 reported that merely 8% of patients admitted with endocarditis and IV drug use were discharged with a plan for medication-assisted therapy.(26597670)
• 💡 For patients with endocarditis and opioid use disorder medication-assisted therapy is probably equally important as antibiotics.
  • Consult addiction psychiatry and connect patients with whatever services your hospital has to offer.
  • More on buprenorphine & medication-assisted therapy here.

---

podcast

(back to contents)

---

Follow us on iTunes

---

questions & discussion

(back to contents)

---

To keep this page small and fast, questions & discussion about this post can be found on another page here.

• Staph lugdunensis (“slug”) is a type of coagulase-negative staph which tends to cause invasive infections (more than other types of coagulase-negative Staph). Be careful about writing this off as a contaminant.
• Exactly which patients need surgery can be confusing. Infectious disease should always be consulted in these cases. If there is any consideration for possible surgery, then cardiology and cardiothoracic surgery should be involved as well.
• Thrombolytic therapy for ischemic stroke is contraindicated in the context of infectious endocarditis.
• Do not fail to provide aggressive medication-assisted therapy for associated opioid use disorder.
• Be careful about the use of vancomycin mono-therapy for empiric treatment of endocarditis. If you are going to pursue this, check levels early (ideally two levels following the initial dose) and make absolutely sure that the vancomycin is dosed properly.

Guide to emoji hyperlinks

• = Link to online calculator.
• = Link to Medscape monograph about a drug.
• = Link to IBCC section about a drug.
• = Link to IBCC section covering that topic.
• = Link to FOAMed site with related information.
• = Link to supplemental media.