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Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e

Chapter 155: Endocarditis Richard Rothman; Catherine A. Marco; Samuel Yang

INTRODUCTION AND EPIDEMIOLOGY

The clinical presentation of endocarditis is o�en nonspecific and variable, with potential to a�ect nearlyevery organ system in an indolent or fulminant course. The vast majority of endocarditis is infective;diagnosis relies on a set of explicit criteria, which include findings from blood culture, echocardiography, andclose clinical observation. Unrecognized infective endocarditis has frequent complications and highmortality.

In developed countries, the incidence of infective endocarditis ranges from 2 to 11.6 cases per 100,000

patient-years1,2,3,4,5,6,7 and is higher in urban versus rural settings, likely reflecting the impact of injectiondrug use. The disease is uncommon among children, where it is associated with structural congenital heartdisease, rheumatic heart disease, or nosocomial, catheter-related bacteremia. The disorder a�ects men morecommonly than women, and the hospital mortality rate is up to 18%, varying according to the

microorganism involved and presence of complications.1,2

Most cases occur either in those with a predisposing identifiable cardiac structural abnormality (congenitalor acquired), prosthetic valve, or a recognized risk factor for disease (including injection drug use,intravascular devices, poor dental hygiene, chronic hemodialysis, or infection with the humanimmunodeficiency virus). The mitral valve is the most commonly a�ected site, followed in decreasingfrequency by the aortic, tricuspid, and pulmonic valves.

For native valve–related infective endocarditis in the developed world, mitral valve prolapse is a commonpredisposing cardiac lesion. Other underlying structural defects include congenital defects (most commonlybicuspid aortic valve), degenerative cardiac lesions (particularly calcific aortic stenosis), and rheumatic heartdisease. In developing countries, rheumatic heart disease creating valvulopathy remains the leadingunderlying risk factor. For native valve–related lesions, le�-sided disease predominates, and mortality rangesfrom 16% to 27%. Short-term mortality increases in those with le�-sided native valve endocarditis whenaccompanied by other severe comorbid illnesses, abnormal mental status, congestive heart failure, or abacterial etiology other than Streptococcus viridans and Staphylococcus aureus, and when treated with

medical therapy absent valve surgery.8

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The estimated risk in injection drug users is 2% to 5% per year, with a mean age of diagnosis being 30 yearsold. When endocarditis occurs in injection drug users, it has a predilection for the tricuspid valve. Otherfeatures include increased susceptibility to recurrence (approximately 40%) and increased mortality in thosewith concurrent human immunodeficiency virus and evidence of immunosuppression (defined as a CD4+ T-

cell count of <200/mm3). Large vegetation size and fungal organism are predictive of poor outcome in

injection drug use–associated right-sided endocarditis.9

Indwelling vascular devices create greater risks that microorganisms will attach to valves during bacteremia.Healthcare-associated endocarditis occurs when (1) a diagnosis is made >72 hours a�er admission inpatients with no evidence of endocarditis on admission or in whom the disorder develops within 6 monthsa�er hospital discharge; or (2) cardiovascular manipulations have occurred in the ambulatory setting within6 months before endocarditis develops, including central venous catheter use, arteriovenous fistula forhemodialysis, invasive intravascular techniques, or intracardiac devices (e.g., prosthetic valves, pacemaker,

le� ventricular assist device).10,11

Prosthetic valve endocarditis occurs in 1% to 4% of recipients during the first year following valvereplacement and in approximately 1% per year therea�er. There is no di�erence in risk between mechanicalversus bioprosthetic valves. Cases with onset within 60 days a�er surgery are called early prosthetic valveendocarditis and are usually acquired in the hospital. Cases starting beyond 60 days a�er surgery are calledlate prosthetic valve endocarditis and are usually community acquired. Hospital mortality rates are highestfor those with early (30% to 80%) versus late (20% to 40%) prosthetic valve endocarditis, attributable to thegreater virulence of the causative organisms involved.

PATHOPHYSIOLOGY

The normal endothelium is resistant to infection and thrombus formation unless it is injured by high-pressure gradients and turbulent flow states. Such abnormal hemodynamic states occur commonly in thosewith preexisting valvular or congenital cardiac defects. In injection drug use, endothelial damage likelyoccurs by a di�erent mechanism, such as from repetitive bombardment with particulate matter (i.e., talc)present in injected material or from ischemia brought on by vasospasm from the injected drug. Cocaine useis particularly associated with increased rates of endocarditis. The resultant endothelial damage promotesdeposition of platelets and fibrin and the formation of sterile vegetations (nonbacterial thromboticendocarditis).

Nonbacterial thrombotic endocarditis can also arise as a result of hypercoagulable states, such as in patientswith malignancy (marantic endocarditis) or systemic lupus erythematosus (Libman-Sacks endocarditis), andin areas surrounding foreign bodies like vascular catheters or prosthetic valves. In the setting of preexistentnonbacterial thrombotic endocarditis, transient bacteremia may result in colonization of vegetations andconversion to infective endocarditis.

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Transient bacteremia can occur from trauma to the skin or mucosal surfaces of the oropharynx or GI or GUtracts (all of which are normally laden with endogenous flora). Even in the absence of trauma, spontaneousbacteremia can occur in patients with periodontal disease or other localized infections. In cases ofbacteremia, the bacterial load usually does not exceed 10 organisms per milliliter of blood, and thebloodstream is usually sterilized in <30 minutes. In the presence of nonbacterial thrombotic endocarditis,this time interval is su�icient for bacteria to adhere to the vegetation and transform it into an infected lesion.

The coexistence of bacteremia and nonbacterial thrombotic endocarditis does not uniformly result ininfective endocarditis. To cause infective endocarditis, the infecting organism must be able to adhere to thenonbacterial thrombus on the endothelium. Di�erent organisms vary in this ability. Furthermore, althoughnonbacterial thrombotic endocarditis is o�en present in those who develop infective endocarditis, it not anabsolute prerequisite, and highly invasive organisms (e.g., S. aureus) can directly invade the endocardium.Adherent organisms stimulate further deposition of platelets and fibrin, leading to sequestration oforganisms into a "protected site" that phagocytic cells cannot easily penetrate. As the disease progresses,the vegetation continuously fragments, shedding surface organisms into the circulation and causingsustained bacteremia.

MICROBIOLOGY

A wide range of bacteria and fungi, as well as Rickettsia and Chlamydophila species, can cause infectiveendocarditis. Bacteria are the predominant cause overall, with a small number of species responsible for themajority of cases. Causative microorganisms vary based on the specific conditions (i.e., native vs prostheticvalve) and risk factors (injection drug use or intracardiac devices; Table 155-1). Overall, recent reports fromthe United States and European countries indicate that Staphylococcus is the single most common cause,

followed by streptococci and enterococci.1,3,12,13,14

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Abbreviation: HACEK = Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella group.

*Including pacemakers and implantable cardioverter-defibrillators.

TABLE 155-1

Microbiology of Infective Endocarditis (IE)

Native Valve IE (% of cases) Intracardiac Device IE (% cases)

  NonaddictIV Drug

Addict 

Prosthetic

Valve IE

Other

Devices*

Staphylococcus aureus 28 68 S. aureus 23 35

Coagulase-negative

Staphylococcus

9 3 Coagulase-negative

Staphylococcus

17 26

Viridans group

streptococci

21 10 Viridans group

streptococci

12 8

Other streptococci 14 3 Streptococcus bovis 10 7

Enterococcus species 11 4 Enterococcus species 12 6

HACEK 2 0 HACEK 2 1

Fungus 1 1 Fungus 4 1

Polymicrobial 1 3 Polymicrobial 1 0

Others 4 5 Others 7 6

Culture negative 9 3 Culture negative 12 10

The increase in the number of cases caused by staphylococci is likely linked to the observed increase inhealthcare-associated endocarditis and also more frequent intravenous drug use. Staphylococcalendocarditis can cause rapid destruction of valves, multiple distal abscesses, myocardial abscesses,

conduction defects, and pericarditis. Staphylococcal endocarditis has an increased risk of in-hospital death.1

In contrast, streptococcal endocarditis tends to be indolent. Patients with enterococcal endocarditisgenerally have underlying valvular disease and risk factors such as diabetes mellitus or manipulation of theGU or lower GI tract.

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Blood cultures are the best initial method for detection but are negative in about 5% of patients; in one thirdto one half of patients, cultures are negative because of prior antibiotic administration. For those casesassociated with negative blood cultures and without prior antibiotic administration, infection is due tofastidious organisms, such as the HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella,and Kingella), Bartonella species, or Coxiella burnetii.

Skin flora and contaminated injection devices are the most frequent sources of microorganisms in injectiondrug use–associated endocarditis. S. aureus accounts for >50% of cases, followed in decreasing frequency bystreptococcal species (including enterococci) and coagulase-negative staphylococci. The well-establishedpredilection for S. aureus to infect normal heart valves, particularly tricuspid valves, is seen in injectionaddicts, although streptococci and enterococci o�en infect abnormal mitral or aortic valves in these patients.

Microorganisms involved in prosthetic valve endocarditis o�en reflect contamination during theperioperative period, with Staphylococcus epidermidis being a commonly isolated organism. Aspergillus andCandida albicans account for the majority of cases of mycotic prosthetic valve endocarditis and o�en havelarge vegetations and emboli.

CLINICAL FEATURES

The clinical manifestations of endocarditis are on a continuum, from acute in onset to insidious and

indolent.12 Common presenting symptoms include fever, chills, weakness, and dyspnea. The most common

complications are congestive heart failure (44%), CNS disorder (30%), and peripheral embolization (22%).14

FEVER

Early bacteremia produces nonspecific signs and symptoms (Table 155-2), usually beginning within 2 weeks

of infection. Symptoms include fever, chills, nausea, vomiting, fatigue, and malaise.15 Fever (>38°C [100.4°F])is present in almost all patients (>90% overall and >98% in those with injection drug use–associated infective

endocarditis).5,11,12,13 Fever may be absent in the elderly, those with a history of antibiotic or antipyreticuse, and those with congestive heart failure, renal failure, or immunosuppression. Clinical symptoms ofsepsis may be present.

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TABLE 155-2

Clinical Features of Infective Endocarditis

Symptoms % Signs %

Fever 80 Fever 90

Chills 40 Heart murmur 85

Weakness 40 New murmur 3–5

Dyspnea 40 Changing murmur 5–10

Anorexia 25 Skin manifestations 18–50

Cough 25 Osler nodes 10–23

Malaise 25 Splinter hemorrhages 15

Skin lesions 20 Petechiae 20–40

Nausea/vomiting 20 Janeway lesions <10

Headache 20 Splenomegaly 20–57

Stroke 20 Embolic phenomena >50

Chest pain 15 Septic complications 20

Abdominal pain 15 Mycotic aneurysm 20

Mental status change 10–15 Renal failure 10

Back pain 10 Retinal lesions 2–10

CARDIAC MANIFESTATIONS

Congestive heart failure occurs in up to 70% of patients from distortion or perforation of valvular leaflets,rupture of the chordae tendineae or papillary muscles, or perforation of cardiac chambers. Heart murmursare common, heard in 50% to 85% of patients, although less so in cases of right-sided endocarditis (<50%).

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Valvular abscesses and pericarditis can result from local extension. Other cardiac complications includeheart blocks and dysrhythmias that result from extension of infection through the interventricular septum tothe conduction system.

NEUROLOGIC MANIFESTATIONS

About 20% to 40% of patients develop neurologic symptoms, notably cerebral ischemic events (o�en in

multiple areas), CNS abscess, intracranial hemorrhage, mycotic aneurysm, meningitis, or seizures.16 Embolic

stroke involving the middle cerebral artery is the most common CNS complication.15

ARTERIAL EMBOLIZATION

Friable vegetation fragments can embolize to any artery, resulting in infarction or abscess in remote tissues;finding multiple brain or lung abscesses should trigger a search for endocarditis. Pulmonary complicationsinclude pulmonary infarction, pneumonia, empyema, or pleural e�usion. Coronary artery emboli usuallyarise from the aortic valve and may cause acute myocardial infarction or myocarditis. Embolic splenicinfarction causes le� upper quadrant abdominal pain with radiation to the le� shoulder. Renal emboli resultin flank pain and hematuria. Emboli to the mesenteric arteries cause acute abdominal pain and guaiac-positive stool and can lead to bowel ischemia, whereas emboli to arteries of the extremities may produceacute limb ischemia. Rupture of a cerebral mycotic aneurysm results in subarachnoid hemorrhage. Retinalartery embolism may cause acute monocular blindness.

CUTANEOUS FINDINGS

Cutaneous embolic phenomena are less common due to early clinical presentation and treatment.Cutaneous findings may occur in 5% to 10% of cases and may include petechiae, splinter or subungualhemorrhages of the finger or toenails, Osler nodes (small, tender subcutaneous nodules on the pads of the

fingers or toes), and Janeway lesions (small hemorrhagic painless plaques on the palms or soles).17,18 Digitalclubbing is infrequent and found only in those with long-standing disease. Cutaneous signs are not specificand may be seen in other disease states characterized by vasculitis or bacteremia.

ADMISSION

Suspicion of endocarditis usually requires hospital admission19,20 to allow the key diagnostic steps to occur

(culture, echocardiography, and clinical observation).1 Although prediction rules to exclude infective

endocarditis exist,21 none are currently robust enough to permit use in clinical practice. Considerendocarditis in patients with unexplained fever and with risk factors for the disease. Because the prevalenceof endocarditis among febrile injection drug users is high (10% to 15%), clinical findings cannot reliablyexclude the diagnosis, and follow-up is o�en a challenge, patients should be admitted to evaluate forbacteremia and endocarditis. Prolonged unexplained fever, malaise, or other constitutional symptomswithout another cause are symptoms concerning for endocarditis. Admit all patients with a cardiac

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prosthetic valve and fever (or persistent malaise, vasculitis, or new murmur) because of the increased risk forendocarditis and the high morbidity and mortality associated with prosthetic valve infections. Look for anynew or changed murmur, and seek evidence of vasculitis or embolization. In stable patients for whom thereis a low suspicion of endocarditis who were initially discharged, admit immediately once positive bloodcultures are found.

DIAGNOSTIC CRITERIA

The Duke criteria22,23 are widely used criteria for diagnosing infective endocarditis (Tables 155-3 and 155-4).

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Abbreviations: HACEK = Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella; IE = infective

endocarditis.

*Excludes single positive cultures for coagulase-negative staphylococci and organisms that do not cause IE.

TABLE 155-3

Duke Criteria* for Infective Endocarditis

Major Criteria

Positive blood culture for IE

Typical microorganism consistent with IE from two separate blood cultures* as noted below:

Streptococcus bovis, viridans streptococci, HACEK group

or

Community-acquired Staphylococcus aureus or enterococci in the absence of a primary focus

or

Microorganisms consistent with IE from persistently positive blood cultures defined as:

At least two positive cultures of blood samples drawn >12 h apart

or

All of three or a majority of four or more separate blood cultures (with first and last sample drawn at least 1 h

apart)

Single positive blood culture for Coxiella burnetii or antiphase I immunoglobulin G antibody titer of >1:800

Evidence of echocardiographic involvement

Positive ECG for IE defined as:

Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on

implanted material in the absence of an alternative anatomic explanation

or

Abscess

or

New partial dehiscence of prosthetic valve

New valvular regurgitation (worsening or changing of preexisting murmur not su�icient)

Minor Criteria

Predisposition: predisposing heart condition or injection drug use

Fever: temperature >38°C (100.4°F)

Vascular phenomena: major arterial emboli, septic pulmonary conjunctival hemorrhages, and Janeway

lesions

Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots, and rheumatoid fever

Microbiologic evidence: positive blood culture but does not meet a major criterion as noted in Table 155-4* or

serologic evidence of active infection with organism consistent with IE

Echocardiographic minor findings were eliminated in the modified Duke criteria

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TABLE 155-4

Modified Duke Criteria for Infective Endocarditis

Definite Infective Endocarditis

Pathologic criteria

Microorganisms demonstrated by culture or histologic examination of a vegetation or in a vegetation that has

embolized, or in an intracardiac abscess

or

Pathologic lesions: vegetation or intracardiac abscess present, confirmed by histology showing active

endocarditis

Clinical Criteria, Using Specific Definitions Listed in Table 155-3

Two major criteria

or

One major and three minor criteria

or

Five minor criteria

Possible infective endocarditis

One major criterion and one minor criterion

Three minor criteria

Rejected

Firm alternate diagnosis for manifestations of endocarditis

or

Resolution of manifestations of endocarditis with antibiotic therapy for 4 d or less

or

No pathologic evidence of infective endocarditis at surgery or autopsy a�er antibiotic therapy for 4 d

Does not meet criteria for possible infective endocarditis

BLOOD CULTURES

Obtain blood cultures in the ED before beginning antibiotics, drawing three sets from separate sites becausefewer collections may not detect bacteremia. Obtain at least 10 mL of blood for each culture bottle.Additional sets of blood cultures may be needed in patients already receiving antibiotics. Ideally, wait at least1 hour between the first and last blood culture. In patients who are in septic shock or with systemiccomplications, do not withhold antibiotics to obtain delayed sets of cultures.

For patients who are at risk for culture-negative infective endocarditis, advise the laboratory of the suspecteddiagnosis to allow initiation of specialized testing to recover fastidious organisms. Polymerase chain reactiontechniques aid pathogen detection.

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OTHER DIAGNOSTIC TESTS

There are no definitive laboratory tests that diagnose endocarditis in the ED. Common findings are anemia(70% to 90% of cases), hematuria, and elevated erythrocyte sedimentation rate (>90% of cases), C-reactiveprotein, and procalcitonin.

ECG findings are also nonspecific but can identify conduction abnormalities resulting from infection.Prolonged PR interval, new le� bundle–branch block, or new right bundle-branch block with le� anteriorhemiblock suggests spread of infection from the aortic valve into the conduction system. Junctionaltachycardia, Wenckebach block, or complete heart block may indicate likely extension of infection from themitral annulus into the atrioventricular node or proximal bundle of His.

Chest radiographs may demonstrate other complications, such as pulmonic emboli in patients with right-sided valvular involvement or congestive heart failure in those with le�-sided valvular involvement.

ECHOCARDIOGRAPHY

Obtain echocardiography as soon as possible, because (1) echocardiographic abnormalities represent one ofthe two major criteria required for definitive diagnosis of endocarditis and (2) evaluation of the cardiacvalves and surrounding structures provides critical information for management decisions. Bedside EDechocardiography is one tool, in addition to formal inpatient testing.

Two-dimensional transthoracic echocardiography is the first choice for those with native valves. Thespecificity of transthoracic echocardiography for vegetations is excellent (98%), but sensitivity variesaccording to patient population. Sensitivity of transthoracic echocardiography is highest in injection drugusers (88% to 94%), who more o�en have larger vegetations, a preponderance of right-sided lesions, and afavorable acoustic precordial window characteristic of younger patients. For those with chest walldeformities, obesity, or chronic obstructive pulmonary disease, echocardiography is less sensitive.

Transesophageal echocardiography has greater sensitivity and specificity for valvular abnormalities thantransthoracic echocardiography due to improved image resolution, but it can be harder for an awake patientto tolerate. Use transesophageal echocardiography in (1) patients with prosthetic valves or intracardiacdevices; (2) those in whom inadequate images are likely to be obtained with transthoracic echocardiography,as described above; and (3) those with intermediate or high clinical probability of endocarditis.Transesophageal echocardiography is of particular value for assessing suspected complications such asmyocardial abscess and perivalvular extension.

TREATMENT

INITIAL STABILIZATION

Patients with endocarditis may present with hemodynamic instability, including hypotension, respiratorycompromise due to decreased cardiac output and/or pulmonary edema, diminished pulmonary capacity,

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altered mental status, or acidosis. Emergency stabilization with airway management and hemodynamicmonitoring and support are priority interventions. Intra-aortic balloon counterpulsation aids the emergencymanagement of unstable mitral valve rupture but is contraindicated for aortic valve rupture.

Definitive management requires a team approach and may include cardiology, infectious disease, andcardiac surgery. Systemic clot lysis or anticoagulation for treatment of endocarditis-associated stroke iscontroversial and best decided upon together with a stroke expert.

Anticoagulation for prosthetic valve endocarditis may reduce the risk of thromboembolism without

increased risk of intracranial hemorrhage.24 Patients with prosthetic valves already being treated with

anticoagulants may be maintained on established regimens.25

EMPIRIC TREATMENT OF SUSPECTED ENDOCARDITIS OF NATIVE VALVES

Antibiotic selection is based on patient characteristics and local resistance patterns. Table 155-5 lists sample

empiric treatment regimens.25,26,27 Although some authors recommend awaiting culture results beforeantibiotic therapy for patients with subacute bacterial endocarditis, we recommend ED initiation of antibiotictherapy for all patients suspected of endocarditis a�er obtaining appropriate cultures, targeting the mostcommon organisms, Staphylococcus aureus and Streptococcus species. For patients with suspected nativevalve infection, empiric antibiotic therapy includes a penicillinase-resistant penicillin or a cephalosporin andan aminoglycoside. For patients with complications (including injection drug use, congenital heart disease,nosocomial infections, those who develop endocarditis while taking oral antibiotics, or those with suspectedmethicillin-resistant S. aureus), add vancomycin.

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TABLE 155-5

Empiric Therapy of Suspected Bacterial Endocarditis*

Patient CharacteristicsRecommended

Agents, Initial Dose

Uncomplicated history Ce�riaxone, 1–2

grams IV

or

Nafcillin, 2 grams

IV

or

Oxacillin, 2 grams

IV

or

Vancomycin, 15

milligrams/kg

plus

Gentamicin, 1–3

milligrams/kg IV

or

Tobramycin, 1

milligram/kg IV

Injection drug use, congenital heart disease, hospital-acquired, suspected methicillin-

resistant Staphylococcus aureus, or already on oral antibiotics

Nafcillin, 2 grams

IV

plus

Gentamicin, 1–3

milligrams/kg IV

plus

Vancomycin, 15

milligrams/kg IV

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*Based on American Heart Association, endorsed by the Infectious Disease Society of America,

http://www.idsociety.org/Organ_System/, accessed April 1, 2014. Because of controversy in the literature regarding the

optimal regimen for empiric treatment, antibiotic selection should be based on patient characteristics, local resistance

patterns, and current authoritative recommendations.

Patient CharacteristicsRecommended

Agents, Initial Dose

Prosthetic heart valve Vancomycin, 15

milligrams/kg IV

plus

Gentamicin, 1–3

milligrams/kg IV

plus

Rifampin, 300

milligrams PO

EMPIRIC TREATMENT OF SUSPECTED ENDOCARDITIS OF ARTIFICIAL VALVES

For patients with suspected artificial valve endocarditis, empiric therapy includes vancomycin, anaminoglycoside, and rifampin.

DEFINITIVE TREATMENT OF ENDOCARDITIS

Definitive antibiotic treatment is based on culture and sensitivity results. Most patients will require 4 to 6weeks of antibiotic therapy. Surgical management is indicated in patients with severe valvular dysfunction,congestive heart failure, relapsing prosthetic valve endocarditis, major embolic complications, fungalendocarditis, new conduction defects or dysrhythmias, or persistent bacteremia a�er appropriate antibiotic

therapy.28,29 Surgical risk increases in those older than 65 years, on inotropes, with sepsis or with cerebral

emboli.30

ENDOCARDITIS PROPHYLAXIS

Because everyday dental activities (brushing, flossing, chewing) create bacteremia, good dental care isimportant. Antibiotic prophylaxis should be given to those at risk (Table 155-6).

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TABLE 155-6

Highest Risk Conditions for Endocarditis31

Prosthetic heart valves

Prosthetic material used for valve repair

History of previous infective endocarditis

Unrepaired cyanotic congenital heart disease

Repaired congenital heart defect with prosthetic material or device

Repaired congenital heart disease with residual defects

Cardiac transplant recipients with valve regurgitation due to a structurally abnormal valve

Prophylaxis is not routinely indicated for patients with mitral valve prolapse (with or without regurgitation),pacemakers, hypertrophic cardiomyopathy, physiologic murmurs, prior coronary artery bypass surgery orangioplasty, or previous surgical repair of atrial septal defect, ventricular septal defect, or patent ductusarteriosus.

For highest risk patients, provide antibiotic prophylaxis before dental procedures that involve manipulationof gingival tissue, the periapical region of teeth, or perforation of the oral mucosa. Prophylaxis is not neededfor nondental procedures, such as local injections, laceration suturing, IV line placement, blood drawing,endotracheal intubation, endoscopy, vaginal delivery, oral trauma and bleeding, urethral catheterization, oruterine dilation and curettage. Some experts recommend prophylaxis for body art, such as tattooing andpiercing.

Recommendations for procedures that manipulate infected skin structures or musculoskeletal tissue areClass IIb (may be considered, usefulness is less well established); it is reasonable to administer antibioticsbefore the procedure for the highest risk groups identified in Table 155-6. The antibiotic should be activeagainst staphylococci and β-hemolytic streptococci. Vancomycin and clindamycin are options for thoseunable to tolerate a β-lactam or who are known or suspected to have an infection caused by a methicillin-resistant strain of Staphylococcus. The incidence of bacteremia with abscess incision and drainage is verylow; hence, clear data are lacking.

A simplified strategy for antibiotic prophylaxis is listed in Table 155-7.32 With the endorsement of the

National Institute for Health and Clinical Excellence of London,33 the European College of Cardiology doesnot recommend prophylaxis before respiratory tract procedures, GI or GU procedures, or uncomplicated

dermatologic or musculoskeletal procedures.34

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TABLE 155-7

Prophylaxis Against Endocarditis for Highest Risk Patients

Procedure Patient CharacteristicsAntibiotic

AgentDose

Dental procedures involving

manipulation of either gingival

tissue or the periapical region of

teeth or perforation of the oral

mucosa

Able to take oral antibiotics

 

Unable to take oral medication

 

 

Allergic to penicillins or ampicillin

 

 

 

 

Unable to take oral medication and

allergic to penicillins or ampicillin

 

 

Amoxicillin

or

Ampicillin

or

Cefazolin or

ce�riaxone

Cephalexin

or

Clindamycin

or

Azithromycin

or

clarithromycin

Cefazolin or

ce�riaxone

or

Clindamycin

2 grams

PO, 30–60

min

before

procedure

 

2 grams

IM or IV,

30–60 min

before

procedure

 

1 gram IM

or IV, 30–

60 min

before

procedure

2 grams

PO, 30–60

min

before

procedure

 

600

milligrams

PO, 30–60

min

before

procedure

 

500

milligrams

PO, 30–60

min

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Procedure Patient CharacteristicsAntibiotic

AgentDose

before

procedure

1 gram IM

or IV, 30–

60 min

before

procedure

 

600

milligrams

IM or IV,

30–60 min

before

procedure

Procedures on infected skin, skin

structure, or musculoskeletal

tissue

Non–methicillin-resistant strain of

Staphylococcus or β-hemolytic

Streptococcus suspected

 

 

Patients unable to tolerate a β-lactam

or who are known or suspected to

have an infection caused by a

methicillin-resistant strain of

Staphylococcus

 

 

Dicloxacillin

or

Cephalexin

Vancomycin

or

Clindamycin

2 grams

PO, 30–60

min

before

procedure

 

2 grams

PO, 30–60

min

before

procedure

1 gram IV,

30–60 min

before

procedure

600

milligrams

IM or IV,

30–60 min

before

procedure

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1. 

2. 

3. 

4. 

5. 

Procedure Patient CharacteristicsAntibiotic

AgentDose

Other procedures (respiratory; GI;

GU; noninfected dermatologic or

musculoskeletal procedures)

  Prophylaxis

not indicated

 

With good aseptic technique, prophylactic antibiotics are not recommended prior to invasive procedures

such as central lines.35

PRACTICE GUIDELINES

The American Heart Association has published guidelines on diagnosis and management(http://circ.ahajournals.org/cgi/reprint/111/23/e394) as well as prophylaxis(www.circ.ahajournals.org/content/lll/23/e394.full [accessed 8/17/2015])for infective endocarditis.

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