Recommendations
Key Recommendations
The management of IE is guided by identification of the causative organism and whether the infected valve is native or prosthetic.[7][36]
Refer any patient with suspected or confirmed IE for multidisciplinary evaluation. Ideally this will be within a specific endocarditis team, if available, including a cardiologist who is an accredited specialist in echocardiography (or a cardiologist and an additional accredited specialist in echocardiography who can be a cardiologist or clinical physiologist/scientist), a cardiac surgeon, an infectious disease or microbiology specialist, a neurologist, and a neurosurgeon.[7][50]
Patients with ‘red flags’ should be urgently transferred to the endocarditis team in a reference centre with rapid access to cardiac surgery facilities.[7][50] Red flags include:
Valve function complications and heart failure
Valve dehiscence
Prosthetic valve endocarditis
Infectious endocarditis in a patient with congenital heart disease
Neurological complications.
See also indications for surgery under Surgery below.
Start empirical antibiotic treatment once you have taken three sets of blood cultures at 30-minute intervals.[7] However, if the patient is unwell (e.g., with sepsis), do not delay empirical antibiotic therapy while waiting to take three sets of blood cultures.[27] Adjust antibiotic therapy accordingly when blood culture results are known (usually within 48 hours).[7]
Many patients require surgery; urgently refer any patient with acute heart failure for emergency surgery if they have persistent pulmonary oedema or cardiogenic shock despite medical treatment.[7] See Acute heart failure.
Refer any patient with suspected or confirmed IE for multidisciplinary evaluation. Ideally this will be within a specific ‘ endocarditis team’, if available, including a cardiologist who is an accredited specialist in echocardiography (or a cardiologist and an additional accredited specialist in echocardiography who can be a cardiologist or clinical physiologist/scientist), a cardiac surgeon, an infectious disease and/or microbiology specialist, a neurologist, and a neurosurgeon.[7][50]
Patients with ‘red flags’ should be urgently transferred to the endocarditis team in a reference centre with rapid access to cardiac surgery facilities.[7][50] Red flags include:
Valve function complications and heart failure
Valve dehiscence
Prosthetic valve endocarditis
Infectious endocarditis in a patient with congenital heart disease
Neurological complications.
Indications for non-urgent transfer include:[50]
Patients with prosthetic valve endocarditis
Patients with moderate/severe valve regurgitation (without heart failure or haemodynamic instability)
Those who have had a stroke (or other embolism)
Patients with a large residual vegetation.
Other patients (i.e., those with non-complicated IE) may be managed in a non-reference centre, in close consultation with the endocarditis team and the reference centre.[7][50]
Early discussion with the surgical team is paramount to optimal care; approximately 50% of IE patients will require surgical intervention.[4] See Surgery below for more information.
More info: The endocarditis team
The use of a specific multidisciplinary endocarditis team has proven vital in improving outcomes in IE with highly significant reductions in mortality rates, as well as reduced occurrence of culture-negative endocarditis, reduced rates of renal dysfunction, and improved surgical outcomes.[50] This strategy has been effective with both native and prosthetic valve IE.[51][52] In France, where this concept has been widely adopted, the 1-year mortality has reduced from 18.5% to 8.2%.[52]
The key roles of the multidisciplinary team are to:[50]
Review all patients with suspected IE to ensure prompt and accurate diagnosis
Formulate and oversee antibiotic plans, including considering the possibility of outpatient therapy
Discuss patients with the local heart centre within 12 hours of diagnosis, and then at least weekly, depending on clinical urgency; consider transfer, if indicated
Monitor daily progress in hospital, arrange outpatient follow-up
Communicate the diagnosis, treatment, and prognosis to patients.
Use an airway, breathing, and circulation (ABC) approach to guide initial management.
Monitor controlled oxygen therapy. An upper SpO 2 limit of 96% is reasonable when administering supplemental oxygen to most patients with acute illness who are not at risk of hypercapnia.
Evidence suggests that liberal use of supplemental oxygen (target SpO 2>96%) in acutely ill adults is associated with higher mortality than more conservative oxygen therapy.[53]
A lower target SpO 2 of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory failure.[54]
Evidence: Target oxygen saturation in acutely ill adults
Too much supplemental oxygen increases mortality.
Evidence from a large systematic review and meta-analysis supports conservative/controlled oxygen therapy versus liberal oxygen therapy in acutely ill adults who are not at risk of hypercapnia.
Guidelines differ in their recommendations on target oxygen saturation in acutely unwell adults who are receiving supplemental oxygen.
The 2017 British Thoracic Society (BTS) guideline recommends a target SpO 2 range of 94% to 98% for patients not at risk of hypercapnia, whereas the 2022 Thoracic Society of Australia and New Zealand (TSANZ) guideline recommends 92% to 96%.[54][55]
The Global Initiative For Asthma (GINA) guidelines recommend a target SpO 2 range of 93% to 96% in the context of a severe exacerbation of asthma.[56]
One systematic review including a meta-analysis of data from 25 randomised controlled trials published in 2018 found that in adults with acute illness, liberal oxygen therapy (broadly equivalent to a target saturation >96%) is associated with higher mortality than conservative oxygen therapy (broadly equivalent to a target saturation ≤96%).[53] In-hospital mortality was 11 per 1000 higher for the liberal oxygen therapy group versus the conservative therapy group (95% CI 2 to 22 per 1000 more). Mortality at 30 days was also higher in the group who had received liberal oxygen (relative risk 1.14, 95% CI 1.01 to 1.29). The trials included adults with sepsis, critical illness, stroke, trauma, myocardial infarction, or cardiac arrest, and patients who had emergency surgery. Studies that were limited to people with chronic respiratory illness or psychiatric illness, or patients on extracorporeal life support, receiving hyperbaric oxygen therapy, or having elective surgery, were all excluded from the review.
An upper SpO 2 limit of 96% is therefore reasonable when administering supplemental oxygen to patients with acute illness who are not at risk of hypercapnia. However, a higher target may be appropriate for some specific conditions (e.g., pneumothorax, carbon monoxide poisoning, cluster headache, or sickle cell crisis).[57]
In 2019 the BTS reviewed its guidance in response to this systematic review and meta-analysis and decided an interim update was not required.[58]
The committee noted that the systematic review supported the use of controlled oxygen therapy to a target.
While the systematic review showed an association between higher oxygen saturations and higher mortality, the BTS committee felt the review was not definitive on what the optimal target range should be. The suggested range of 94% to 96% in the review was based on the lower 95% confidence interval and the median baseline SpO 2 from the liberal oxygen groups, along with the earlier 2015 TSANZ guideline recommendation.
Subsequently, experience during the COVID-19 pandemic has also made clinicians more aware of the feasibility of permissive hypoxaemia.[59]
Management of oxygen therapy in patients in intensive care is specialised and informed by further evidence (not covered in this summary) that is more specific to this setting.[60][61][62]
If the patient requires fluid resuscitation, check local protocols for specific recommendations on fluid choice. There is debate, based on conflicting evidence, on whether there is a benefit in using normal saline or balanced crystalloid in critically ill patients.
Practical tip
Be aware that large volumes of normal saline as the sole fluid for resuscitation may lead to hyperchloraemic acidosis.
Also note that use of lactate-containing fluid in a patient with impaired liver metabolism may lead to a spuriously elevated lactate level, so results need to be interpreted with other markers of volume status.
Evidence: Choice of fluids
Evidence from two large randomised controlled trials (RCTs) suggests there is no difference between normal saline and a balanced crystalloid for critically ill patients in mortality at 90 days, although results from two meta-analyses including these RCTs point to a possible small benefit of balanced solutions compared with normal saline.
There has been extensive debate over the choice between normal saline (an unbalanced crystalloid) versus a balanced crystalloid (such as Hartmann’s solution [also known as Ringer’s lactate] or Plasma-Lyte®). Clinical practice varies widely, so you should check local protocols.
In 2021-2022 two large double-blind RCTs were published assessing intravenous fluid resuscitation in intensive care unit (ICU) patients with a balanced crystalloid solution (Plasma-Lyte) versus normal saline: the Plasma-Lyte 148 versus Saline (PLUS) trial (53 ICUs in Australia and New Zealand; n=5037) and the Balanced Solutions in Intensive Care Study (BaSICS) trial (75 ICUs in Brazil; n=11,052).[63][64]
In the PLUS study 45.2% of patients were admitted to ICU directly from surgery (emergency or elective), 42.3% had sepsis, and 79.0% were receiving mechanical ventilation at the time of randomisation.
In BaSICS almost half the patients (48.4%) were admitted to ICU after elective surgery and around 68% had some form of fluid resuscitation before being randomised.
Both found no difference in 90-day mortality overall or in pre-specified subgroups for patients with acute kidney injury (AKI), sepsis, or post-surgery. They also found no difference in the risk of AKI.
In BaSICS, for patients with traumatic brain injury, there was a small decrease in 90-day mortality with normal saline - however, the overall number of patients was small (<5% of total included in the study) so there is some uncertainty about this result. Patients with traumatic brain injury were excluded from PLUS as the authors felt these patients should be receiving saline or a solution of similar tonicity.
One meta-analysis of 13 RCTs (including PLUS and BaSICS) confirmed no overall difference, although the authors did highlight a non-significant trend towards a benefit of balanced solutions for risk of death.[65]
A subsequent individual patient data meta-analysis included six RCTs of which only PLUS and BaSICS were assessed as being at low risk of bias. There was no statistically significant difference in in-hospital mortality (odds ratio [OR] 0.96, 95% CI 0.91 to 1.02). However, the authors argued that using a Bayesian analysis there was a high probability that balanced solutions reduced in-hospital mortality, although they acknowledged that the absolute risk reduction was small.[66]
A prespecified subgroup analysis of patients with traumatic brain injury (n=1961) found that balanced solutions increased the risk of in-hospital mortality compared with normal saline (OR 1.42, 95% CI 1.10 to 1.82).
Previous evidence has been mixed.
One 2015 double-blind, cluster-randomised, double-crossover trial conducted in four ICUs in New Zealand (n=2278), the 0.9% Saline versus Plasma-Lyte for ICU fluid Therapy (SPLIT) trial, found no difference for in-hospital mortality, acute kidney injury, or use of renal-replacement therapy.[67]
However, a 2018 US multicentre unblinded cluster-randomised trial - the isotonic Solutions and Major Adverse Renal events Trial (SMART), among 15,802 critically ill adults receiving ICU care - found possible small benefits from balanced crystalloid (Ringer’s lactate or Plasma-Lyte) compared with normal saline. The 30-day outcomes showed a non-significant reduced mortality in the balanced crystalloid group versus the normal saline group (10.3% vs. 11.1%; OR 0.90, 95% CI 0.80 to 1.01) and a major adverse kidney event rate of 14.3% versus 15.4%, respectively (OR 0.91, 95% CI 0.84 to 0.99).[68]
One 2019 Cochrane review included 21 RCTs (n=20,213) assessing balanced crystalloids versus normal saline for resuscitation or maintenance in a critical care setting.[69]
The three largest RCTs in the Cochrane review (including SMART and SPLIT) all examined fluid resuscitation in adults and made up 94.2% of participants (n=19,054).
There was no difference in in‐hospital mortality (OR 0.91, 95% CI 0.83 to 1.01; high-quality evidence as assessed by GRADE), acute renal injury (OR 0.92, 95% CI 0.84 to 1.00; GRADE low), or organ system dysfunction (OR 0.80, 95% CI 0.40 to 1.61; GRADE very low).
Obtain blood cultures prior to starting antibiotic therapy; this is vital because one dose of an antibiotic often masks an underlying bacteraemia and delays appropriate therapy.
If the patient is unwell (e.g., with sepsis), do not delay empirical antibiotic therapy while waiting to take three sets of blood cultures.
When a micro-organism has been identified, repeat the blood cultures after 48 to 72 hours to check the effectiveness of treatment.[7]
Promptly give empirical broad-spectrum antibiotic therapy.[7] Check your local protocols and seek advice from an infectious disease or microbiology specialist because recommended empirical regimens may differ between regions.[50] The following factors should be taken into account when choosing the most appropriate empirical antibiotics:[7][36]
Whether the patient has received previous antibiotic therapy
Whether the infection involves a native or prosthetic valve
If a prosthetic valve is involved, when the patient had surgery
Local epidemiology and knowledge of antibiotic-resistant and culture-negative pathogens
Where the infection was acquired (community, nosocomial, or non-nosocomial healthcare-associated).
Adjust antibiotic therapy accordingly once blood culture results are known (usually within 48 hours).[7]
Think ' Could this be sepsis?' based on acute deterioration in a patient with suspected infective endocarditis.[22][23][24] See Sepsis in adults.
More info: Sepsis
Use a systematic approach, alongside your clinical judgement, for assessment; urgently consult a senior clinical decision-maker (e.g., ST4 level doctor in the UK) if you suspect sepsis.[22][24][25][26]
Refer to local guidelines for the recommended approach at your institution for assessment and management of the patient with suspected sepsis.
Urgently refer any patient with acute heart failure for emergency surgery if they have persistent pulmonary oedema or cardiogenic shock despite medical therapy.[7] Give intravenous diuretics to manage pulmonary oedema prior to the surgery. See Acute heart failure.
Practical tip
Be aware that patients who are acutely unwell or present with symptoms of acute heart failure are often colonised with Staphylococcus aureus, and are at risk for deteriorating quickly. These patients often require urgent surgical intervention if the valvular lesion is beyond repair with medical treatment alone.
Oral streptococci (Streptococcus mitis, sanguinis, anginosus, salivarius, downei, and mutans) are generally penicillin-susceptible, although some have a relatively high minimum inhibitory concentration (MIC) and are therefore relatively penicillin-resistant; patients may be treated based on MIC values.[36] Cure rates of >95% can be achieved in patients treated with parenteral penicillin or ceftriaxone for IE caused by penicillin-susceptible oral streptococci or Streptococcus gallolyticus.[7][36]
If the patient has IE due to a penicillin-susceptible strain, antibiotic regimens include monotherapy with a beta-lactam (for 4 weeks), or a beta-lactam plus gentamicin (for 2 weeks).[7]
Although netilmicin is recommended by the European Society of Cardiology as an alternative to gentamicin, it is not available in the UK and some other European countries.
Vancomycin only (for 4 weeks) is recommended if the patient is unable to tolerate penicillin (type I hypersensitivity reaction).[7][36]
If the patient has a strain with some penicillin resistance or increased antibiotic exposure, gentamicin should be added to the beta-lactam.[7]
Staphylococcal endocarditis is an increasingly recognised entity, often resulting in acute and destructive disease.
If the patient has methicillin-sensitive Staphylococcus aureus (MSSA) infection, antibiotic regimens include beta-lactam monotherapy (e.g., flucloxacillin, cefazolin) for 4 to 6 weeks.[7]
If the patient has methicillin-resistant S aureus (MRSA) infection, they should be treated with vancomycin (same treatment duration as for MSSA).[7]
Other options include daptomycin combined with cloxacillin, ceftaroline, or fosfomycin.
S aureus is the most common cause of endocarditis on native valves of patients who use intravenous drugs. If these patients have right-sided endocarditis, gentamicin has been shown to increase the rate of microbial killing when used in combination with a beta-lactam.[71] However, aminoglycosides are no longer recommended in this scenario due to the increased risk of nephrotoxicity.[72][73]
If the patient is receiving treatment with aminoglycosides, monitor renal and liver function, and for possible ototoxicity continuously (before, during, and after treatment). Also monitor serum aminoglycoside level during treatment.[36][74]
The UK-based Medicines and Healthcare products Regulatory Agency has issued a drug safety alert about the increased risk of deafness associated with aminoglycoside treatment in patients with mitochondrial mutations.[74]
Follow your local protocols on genetic testing for mitochondrial mutations. Particularly consider mitochondrial mutation screening if the patient has a maternal history of deafness or mitochondrial mutations, or is having long-term or recurrent aminoglycoside treatment. Do not delay urgent antibiotic treatment for genetic testing.[74]
Practical tip
Beta haemolytic Streptococcus and Staphylococcus usually cause acute IE whereas Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella (HACEK) group is usually associated with an indolent presentation.
Oral streptococci (Streptococcus mitis, sanguinis, anginosus, salivarius, downei, and mutans) organisms are generally penicillin-susceptible although some have a relatively high minimum inhibitory concentration (MIC) and are therefore relatively penicillin-resistant; patients may be treated based on MIC values.[36] Cure rates of >95% can be achieved in patients treated with parenteral penicillin or ceftriaxone for IE caused by penicillin-susceptible oral streptococci or Streptococcus gallolyticus.[7][36]
If the patient has a penicillin-susceptible strain, the patient can be given beta-lactam therapy (e.g., benzylpenicillin, amoxicillin, or ceftriaxone).[7]
Vancomycin for 6 weeks with gentamicin for 2 weeks is recommended if the patient is unable to tolerate penicillin (type I hypersensitivity reaction).[7][36]
Patients with prosthetic valves are generally treated for 6 weeks.[7][36]
Staphylococcus aureus endocarditis infections are often rapidly progressive and carry a mortality rate greater than 45%.[75]
If the patient has methicillin-sensitive S aureus (MSSA) infection, treatment options include a beta-lactam plus rifampicin and gentamicin.[7]
If the patient has methicillin-resistant S aureus (MRSA) infection they should be treated with vancomycin plus rifampicin and gentamicin.[7]
If the patient is receiving treatment with aminoglycosides, monitor renal and liver function, and for possible ototoxicity continuously (before, during, and after treatment). Also monitor serum aminoglycoside level during treatment.[36][74]
The UK-based Medicines and Healthcare products Regulatory Agency has issued a drug safety alert about the increased risk of deafness associated with aminoglycoside treatment in patients with mitochondrial mutations.[74]
Follow your local protocols on genetic testing for mitochondrial mutations. Particularly consider mitochondrial mutation screening if the patient has a maternal history of deafness or mitochondrial mutations, or is having long-term or recurrent aminoglycoside treatment. Do not delay urgent antibiotic treatment for genetic testing.[74]
Multidrug resistance is an increasing problem and has a significant impact on the outcomes of patients with IE. More research is necessary to define appropriate treatments for resistant S aureus infections, as well as Streptococcus pneumoniae and vancomycin-resistant strains of Enterococcus faecium.
Practical tip
Beta haemolytic Streptococcus and Staphylococcus usually cause acute IE whereas Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella (HACEK) group is usually associated with an indolent presentation.
If the patient has enterococcal IE, they require prolonged administration (6 weeks) of antibiotics because enterococci are highly resistant to drug-induced killing by antibiotics.[7]
Treatment options for beta-lactam and gentamicin-susceptible strains include a beta-lactam (e.g., amoxicillin, ampicillin) plus ceftriaxone for 6 weeks or gentamicin for 2 weeks.
Treatment for beta-lactam resistant strains is vancomycin plus gentamicin.[7]
Enterococcus faecalis strains with high-level aminoglycoside resistance can be treated with ampicillin or amoxicillin plus ceftriaxone for 6 weeks, although this treatment is not active against Enterococcus faecium.[7][36] Faecium species that are multi-resistant to aminoglycosides, beta-lactams, and vancomycin have emerged in recent years; seek advice from an infectious disease or microbiology specialist.[36]
If the patient is receiving treatment with aminoglycosides, monitor renal and liver function, and for possible ototoxicity continuously (before, during, and after treatment). Also monitor serum aminoglycoside level during treatment.[36][74]
The UK-based Medicines and Healthcare products Regulatory Agency has issued a drug safety alert about the increased risk of deafness associated with aminoglycoside treatment in patients with mitochondrial mutations.[74]
Follow your local protocols on genetic testing for mitochondrial mutations. Particularly consider mitochondrial mutation screening if the patient has a maternal history of deafness or mitochondrial mutations, or is having long-term or recurrent aminoglycoside treatment. Do not delay urgent antibiotic treatment for genetic testing.[74]
Multidrug resistance is an increasing problem and has a significant impact on the outcomes of patients with IE. More research is necessary to define appropriate treatments for resistant Staphylococcus aureus infections, as well as Streptococcus pneumoniae and vancomycin-resistant strains of E faecium.
HACEK
Ceftriaxone is standard treatment if the patient has Haemophilus, Aggregatibacter (formerly Actinobacillus), Cardiobacterium, Eikenella, and Kingella (HACEK) endocarditis. Ceftriazone should be continued for 4 weeks for native valve IE.[7] It should be continued for 6 weeks for prosthetic valve IE.[7]
Ampicillin should not be used as first-line therapy for treatment of HACEK endocarditis because some HACEK-group bacilli produce beta-lactamases and are increasingly ampicillin-resistant.[7] However, if they do not produce beta-lactamase, ampicillin (for 4 weeks for native valve IE, and 6 weeks for prosthetic valve IE) plus gentamicin (for 2 weeks) is an option.[7]
HACEK strains are also susceptible to other third-generation cephalosporins and fluoroquinolones (e.g., ciprofloxacin).[7]
The European Medicines Agency and the UK-based Medicines and Healthcare products Regulatory Agency have issued warnings that fluoroquinolones have been associated with disabling and potentially irreversible musculoskeletal or nervous system adverse effects.[76][77]
In addition, the US Food and Drug Administration has issued warnings about the increased risk of aortic dissection, significant hypoglycaemia, and mental health adverse effects in patients taking fluoroquinolones.[78][79]
If the patient is receiving treatment with aminoglycosides, monitor renal and liver function, and for possible ototoxicity continuously (before, during, and after treatment). Also monitor serum aminoglycoside level during treatment.[36][74]
The UK-based Medicines and Healthcare products Regulatory Agency has issued a drug safety alert about the increased risk of deafness associated with aminoglycoside treatment in patients with mitochondrial mutations.[74]
Follow your local protocols on genetic testing for mitochondrial mutations. Particularly consider mitochondrial mutation screening if the patient has a maternal history of deafness or mitochondrial mutations, or is having long-term or recurrent aminoglycoside treatment. Do not delay urgent antibiotic treatment for genetic testing.[74]
Practical tip
Beta haemolytic Streptococcus and Staphylococcus usually cause acute IE whereas Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella (HACEK) group is usually associated with an indolent presentation.
Non-HACEK
Other culture-negative organisms (non-HACEK) that may cause endocarditis include: Chlamydia species, Coxiella species, Bartonella species, Brucella species, and Legionella species.
Seek early advice from an infectious disease or microbiology specialist, because these organisms are rare and can have severe consequences. Early surgery and long-term (at least 6 weeks) of antibiotic therapy is recommended.[7][36]
Seek early advice from an infectious disease or microbiology specialist if the patient has fungal IE.[7] Mortality is very high (>50%).[7]
Be aware that fungal infections most frequently affect patients with prosthetic valves and those who are immunocompromised or use intravenous drugs.[7]
The most common causative agents are Candida and Aspergillus.[7]
Treatment includes valve replacement and antifungal therapy.[7][80]
Penicillin allergy is commonly self-reported, but often found to be spurious following formal allergy assessment.[81] Determine the timing, extent, and nature of any previous reaction to penicillin.[36]
In general, if the patient has a history of type I hypersensitivity anaphylactoid reactions or severe excoriating rashes , do not give penicillins or cephalosporins (10% to 15% cross-reactivity).
If the patient has a low-risk penicillin allergy, consider giving a single dose of a penicillin or cephalosporin while monitoring the patient closely.[82] A low risk penicillin allergy includes:[82]
Unknown reaction >10 years previously
Type A adverse drug reaction (pharmacologically predictable intolerance) where direct de-labelling was not accepted by the patient
History of an unspecified childhood rash, localised injection-site reaction (only), or maculopapular exanthem >10 years ago.
Many patients require surgery. Timing of surgical intervention should be decided by a multidisciplinary endocarditis team, if available.[7][50][83] Be aware that some patients may need emergency surgery (e.g., those with acute heart failure with persistent pulmonary oedema or cardiogenic shock despite medical therapy).[7][50] See Acute heart failure.
The aims of surgery are to remove infected tissue completely and to repair or replace the affected valves, thus restoring cardiac anatomy.
Indications for surgery include:[7][50]
Heart failure with:
Cardiogenic shock or pulmonary oedema (requires emergency surgery), or
Poor haemodynamic tolerance (requires urgent surgery)
Uncontrolled infection with:
Local complications (e.g., abscess, false aneurysm, fistula, enlarging vegetation)
Persistent positive blood cultures (despite appropriate antibiotic therapy for more than 1 week)
Resistant bacteria or fungi
Prosthetic valve endocarditis caused by Staphylococcus aureus or non-HACEK gram-negative bacilli
High risk of embolism or established embolism:
Vegetation ≥10 mm and emboli despite appropriate antibiotic therapy
Vegetation ≥10 mm and another reason for surgery (e.g., patients with significant valvular dysfunction, whether a direct result of endocarditis process or not)
Vegetation ≥10 mm and no evidence of embolus.
More info: Surgery
One meta-analysis suggested that early surgery, at ≤7 days from diagnosis, affords mortality benefit in the long term.[84]
Treatment failures often occur in patients with multidrug-resistant organisms such as vancomycin-resistant enterococcus, and although these patients can present initially with a subacute course, persistent bacteraemia often leads to severe valvular abnormalities. Under these circumstances, surgical intervention is often required to maintain stability and aid in bacteraemic clearance.
Patients with peri-valvular abscess, fistula, valve dehiscence, perforation, or rupture should also be closely followed by a cardiothoracic surgical team.
Temporary cardiac pacing is recommended in patients with atrioventricular block secondary to an aortic root abscess.
Surgical intervention in older patients is associated with lower in-hospital mortality. Moreover, complications and mortality in older patients undergoing surgery are similar to those in younger groups.[85] Age, therefore, should not be a contraindication to surgery where other indications for surgery exist.
Consider admission to the ICU if the patient has:
Undergone surgical intervention for IE
Sepsis
Heart failure
Valvular dysfunction
Multi-organ failure.
Nosocomial infection is also increasing in incidence and IE may develop during a hospital or ICU stay. The most common organisms to cause IE in the ICU are staphylococci, with streptococci being the second most common. Also specific to ICU is the increased incidence of fungal IE, which should therefore be considered if the patient does not improve with antibiotic therapy.
Decisions on anticoagulant and antiplatelet therapy should be made on an individual basis by the multidisciplinary endocarditis team, if available.[7]
More info: Anticoagulation/antiplatelet therapy
Although the majority of complications of IE occur as a result of emboli, there is no evidence that anticoagulation or antiplatelet therapy reduce this risk. In fact, data suggest that patients already on anticoagulants who develop prosthetic valve endocarditis are at higher risk of haemorrhagic transformation.[86] One double-blind, randomised controlled trial of high-dose aspirin in patients with IE demonstrated no benefit of antiplatelet therapy, with an accompanying increase in bleeding risk.[87]
Guidelines differ in their recommendations for antibiotic prophylaxis; check your local protocols. Decisions about antibiotic prophylaxis should only be made after careful evaluation of the individual patient’s circumstances, following discussion with the patient, taking into account the patient’s values and preferences, and using your clinical judgement.
The European Society of Cardiology (ESC) recommends that antibiotic prophylaxis should only be considered if the patient is at highest risk of IE and undergoing a dental procedure that requires manipulation of the gingival or periapical region of the teeth or perforation of the oral mucosa. The ESC considers a patient to be at highest risk of IE if they have:[7]
A prosthetic valve, including a transcatheter valve or a valve in which any prosthetic material was used for valve repair
A history of a previous episode of IE
Untreated cyanotic congenital heart disease, or congenital heart disease that has been repaired with a prosthetic material (including valved conduits or systemic-to-pulmonary shunts)
A ventricular assist device, as destination therapy (considered high risk because of the associated morbidity and mortality).
In the UK, the National Institute for Health and Care Excellence (NICE) recommends that an at-risk patient undergoing interventional procedures should not be given antibiotic prophylaxis against IE routinely. However, NICE emphasises that antibiotic therapy is still necessary to treat active or potential infections.[17] NICE considers a patient to be at-risk if they have:[17]
Acquired valvular heart disease with stenosis or regurgitation
Hypertrophic cardiomyopathy
Previous IE
Structural congenital heart disease, including surgically corrected or palliated structural conditions, but excluding isolated atrial septal defect, fully repaired ventricular septal defect, fully repaired patent ductus arteriosus, and closure devices that are judged to be endothelialised
Valve replacement.
NICE recommends giving clear information about prevention to any patient at risk of IE, which should include:[17]
The benefits and risks of antibiotic prophylaxis, and an explanation of why antibiotic prophylaxis is no longer routinely recommended
The importance of maintaining good oral health
Symptoms that may indicate IE and when to seek expert advice
The risks of undergoing invasive procedures, including non-medical procedures such as body piercing or tattooing.
The recommendations from the ESC and NICE may not be universally accepted in other countries.
The most common cause of infective endocarditis following dental, oral, respiratory tract, or oesophageal procedures is Streptococcus viridans (alpha-haemolytic streptococci). Therefore, antibiotics (if they are to be given for prophylaxis) are directed toward this organism, and administered as a single dose 30 to 60 minutes before the procedure.
Base your choice of antibiotic on your local hospital protocols.
The evidence for antibiotic prophylaxis preventing infection following dental procedures and instrumentation of the respiratory, genitourinary, or gastrointestinal tract is weak. Conflicting data suggest that a reduction in bacteraemia may not result in a lower incidence of infective endocarditis in low-risk individuals.[20] The risk of bacteraemia resulting from interventions such as dental procedures and instrumentation of the respiratory, genitourinary, or gastrointestinal tract is significantly smaller than from usual life-time activities such as toothbrushing or chewing.[21] Data indicate that, even if treatment with prophylactic antibiotics were 100% effective, only a small number of cases would be prevented.
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