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CHAPTER 156: Endocarditis 1043 medications, their major adverse effects, and their interacting drug effects. Concomitant antibiotic prophylaxis can compound adverse effects from antiretrovirals. Drug interactions are pharmacokinetic (changes in the level of one or more drugs) or pharmacodynamic (changes in effect, therapeutic response, or side effect of one or more drugs). 71,72 Consultation with a hospital pharmacologist and an infectious disease specialist helps man age those with a suspected drug reaction. REFERENCES The complete reference list is available online at www.TintinalliEM.com. TABLE 155-5 Antiretroviral Medications, Major Adverse Effects, and Interacting Drug Effects 70 (Continued) Antiretroviral Medications* Adverse Effects Interacting Drugs Effects of Interaction Ritonavir Nausea, vomiting, diarrhea, paresthesia (circumoral and extremi ties), hepatitis, taste perversion, possible increased bleeding episodes in patients with hemophilia Ritonavir/lopinavir Nausea, vomiting, pancreatitis, serum transaminase elevation, insulin resistance/diabetes mellitus, possible increased bleeding episodes in patients with hemophilia, PR interval prolongation Digoxin Increased digoxin concentration (monitor levels) Saquinavir Nausea, diarrhea, headache, serum transaminase elevation, possible increased bleeding episodes in patients with hemophilia, PR interval prolongation, QT interval prolongation, torsades de pointes Tipranavir Intracerebral hemorrhage, hepatotoxicity, rash, possible increased bleeding episodes in patients with hemophilia Proton pump inhibitors Decreased absorption of proton pump inhibitors; coadministration not recommended Entry and fusion inhibitors Enfuvirtide Bacterial pneumonia, injection site reaction, hypersensitivity reaction CCR-5 antagonist Maraviroc Abdominal pain, postural hypotension, cough, dizziness, pyrexia, rash, upper respiratory tract infection, hepatotoxicity Integrase inhibitors   Anticonvulsants Decreased antiretroviral concentrations (some contraindicated) Dolutegravir Hypersensitivity reaction, insomnia, headache, depression and suicidal ideation (rare) Raltegravir Increased creatine phosphokinase, rhabdomyolysis, muscle weakness, nausea, diarrhea, headache, rash (including Stevens- Johnson syndrome, hypersensitivity reaction, and toxic epidermal necrolysis), pyrexia, insomnia, depression, and suicidal ideation (rare)

Integrase inhibitors   Anticonvulsants Decreased antiretroviral concentrations (some contraindicated) Dolutegravir Hypersensitivity reaction, insomnia, headache, depression and suicidal ideation (rare) Raltegravir Increased creatine phosphokinase, rhabdomyolysis, muscle weakness, nausea, diarrhea, headache, rash (including Stevens- Johnson syndrome, hypersensitivity reaction, and toxic epidermal necrolysis), pyrexia, insomnia, depression, and suicidal ideation (rare) Abbreviations: HBV = hepatitis B virus; HCV = hepatitis C virus; HMG-CoA = 3-hydroxy-3-methylglutaryl-coenzyme A. *Some antiretroviral agents have interactions with buprenorphine and methadone, requiring modifications of the latter two agents. Source: http://www.aidsinfo.nih.gov/ContentFiles/AdultandAdolescentGL.pdf. (Panel on Antiretroviral Guidelines for Adults and Adolescents: Guidelines for the use of antiretroviral agents in adults and adolescents living with HIV. Department of Health and Human Services.) Accessed October 17, 2018. later Tables 156-3 and 156-4 in “Diagnosis” section). Unrecognized endocarditis has frequent complications and high mortality. In developed countries, the incidence of infective endocarditis ranges from 2 to 11.6 cases per 100,000 patient-years 1-7 and is higher in urban settings (likely reflecting the impact of injection drug use). Pediatric endocarditis is uncommon and is primarily associated with structural heart disease, postoperative congenital heart disease, rheumatic heart disease, or catheter-related bacteremia. 8 Overall, men are more com monly affected than women, and in-hospital mortality rate ranges from 18% to 32%. 1,2,9 Short-term mortality in medically managed endocar ditis increases with severe comorbid illnesses, abnormal mental status, congestive heart failure, or a bacterial etiology other than Streptococcus viridans. Most cases of endocarditis occur in those with a predisposing struc tural abnormality (congenital or acquired), prosthetic valve, or a risk factor for disease (e.g., injection drug use, intravascular device, poor dental hygiene, chronic hemodialysis, human immunodeficiency virus infection). Although the mitral valve is the most commonly affected site (followed by the aortic, tricuspid, and pulmonic valves), the incidence of tricuspid valve endocarditis has steadily increased, attributed principally to increased rates of injection drug use. For native valve endocarditis in the developed world, mitral valve prolapse is a common predisposing lesion. Other underlying structural factors include congenital defects (e.g., bicuspid aortic valve), degenerative cardiac lesions (calcific aortic stenosis), and rheumatic heart disease. In developing countries, rheumatic heart disease–related valvulopathy remains the leading risk factor. The estimated risk in injection drug users is 2% to 5% per year, with a mean age of diagnosis of 30 years old. Injection drug use–associated endocarditis often involves the tricuspid valve, has an increased susceptibility to recurrence (approximately 40%), and has increased mortality CHAPTER Endocarditis Daniel Saul Brenner Catherine A. Marco Richard E. Rothman INTRODUCTION AND EPIDEMIOLOGY Endocarditis patients often have nonspecific signs and symptoms, but endocarditis has the potential for multiorgan involvement. The clinical course of endocarditis can be indolent or fulminant. The majority of endocarditis is infective; diagnosis relies on a set of explicit criteria (see Tintinalli_Sec13_p0997-1100.indd 1043 8/2/19 8:12 PM

often have nonspecific signs and symptoms, but endocarditis has the potential for multiorgan involvement. The clinical course of endocarditis can be indolent or fulminant. The majority of endocarditis is infective; diagnosis relies on a set of explicit criteria (see Tintinalli_Sec13_p0997-1100.indd 1043 8/2/19 8:12 PM 1044 SECTION 13: Infectious Diseases in human immunodeficiency virus–positive patients with CD4+ count of <200/mm3. Large vegetation size and fungal organism are also associated with poor outcome.12 Indwelling vascular devices create increased risk that microorgan isms will attach to valves during bacteremia. Healthcare-associated endocarditis occurs when diagnosis is made >72 hours after admission without evidence of endocarditis on admission, endocarditis develops within 6 months after hospital discharge, or endocarditis develops within 6 months of cardiovascular manipulations including central venous catheter use, arteriovenous fistula for hemodialysis, invasive intravas cular techniques, or intracardiac devices such as pacemakers and left ventricular assist devices. 13,14 Prosthetic valve endocarditis occurs in 1% to 4% of recipients during the first year following replacement and in approximately 1% per year thereafter. There is no difference in infection risk between mechanical or bioprosthetic valves. Cases with onset within 60 days after surgery are termed early prosthetic valve endocarditis and are usually nosocomial. Cases starting beyond 60 days after surgery are termed late prosthetic valve endocarditis and are usually community acquired. Hospital mor tality rates are highest for those with early (30% to 80%) versus late (20% to 40%) prosthetic valve endocarditis, attributable to the greater virulence of the causative organisms involved. PATHOPHYSIOLOGY The normal endothelium is resistant to infection and thrombus for mation. Injury from high-pressure gradients and turbulent flow, as occurs with preexisting valvular or congenital cardiac lesions, lessens the natural defense. With injection drug use, endothelial damage occurs from repetitive bombardment with particulate matter (i.e., talc) present in injected material or from ischemia brought on by drug-induced vasospasm (cocaine use is particularly associated with endocarditis). The resultant endothelial damage promotes platelet/ fibrin deposition and the formation of sterile vegetations (nonbacterial thrombotic endocarditis). Nonbacterial thrombotic vegetations (also called marantic endocarditis) can result from hypercoagulable states, malignancy, or systemic lupus erythematosus (Libman-Sacks endocar ditis) and in areas surrounding foreign bodies (vascular catheters or prosthetic valves). Transient bacteremia (as little as 10 organisms per milliliter of blood for <30 minutes) may colonize and convert to infective endocarditis. Triggers include skin trauma or endogenously colonized surfaces of the oropharynx or GI or GU tract. Endocarditis can occur in the absence of trauma, and in normal hosts, it can be related to spontaneous bactere mia arising from brushing teeth, dental procedures, and both minor or systemic infections. 15-19 Coexistence of bacteremia and nonbacterial thrombotic endocar ditis does not uniformly result in infective endocarditis. The infecting organism must be able to adhere to the nonbacterial thrombus on the endothelium. Adherent organisms stimulate further deposition of platelets and fibrin, leading to generation of a “protected site” that phagocytic cells cannot easily penetrate. Although nonbacterial thrombotic endocarditis often precedes infective endocarditis, it not a prerequisite because highly invasive organisms ( Staphylococcus aureus) can directly invade the endocardium.

n of platelets and fibrin, leading to generation of a “protected site” that phagocytic cells cannot easily penetrate. Although nonbacterial thrombotic endocarditis often precedes infective endocarditis, it not a prerequisite because highly invasive organisms ( Staphylococcus aureus) can directly invade the endocardium. As the disease progresses, fragments from vegetation spread into the circulation and cause sustained bacteremia.  MICROBIOLOGY A wide range of pathogens cause infective endocarditis. Bacteria are the predominant cause, with a small number of species responsible for most of the cases ( Table 156-1). Staphylococcus is the single most common cause, followed by streptococci (including viridans group streptococci) and enterococci. 1,3,20-23 Other rarer causes of infectious endocarditis include Rickettsia, Chlamydophila, Bartonella, Coxiella burnetii, Legionella, Candida, and Aspergillus.23 The increase in staphylococcal endocarditis is linked to the increase in healthcare-associated endocarditis and increasing IV drug use. S. aureus is associated with rapid valve destruction, infection of structur ally normal heart valves (particularly tricuspid valves in patients who are IV drug abusers), and increased risk of in-hospital death. 1 The incidence of staphylococcal endocarditis related to pacemaker lead infection is also increasing and associated with severe morbidity and mortality. 24 In contrast, streptococcal endocarditis tends to be indolent. Enterococcal endocarditis is associated with underlying valvular disease and risk fac tors (diabetes mellitus, manipulation of the GU or lower GI tract). Early prosthetic valve endocarditis is most commonly caused by perioperative colonization from Staphylococcus epidermidis, Aspergillus, or Candida albicans. Blood cultures are the best method for detection of endocarditis but are negative in about 5% of patients; 33% to 50% of culture-negative endocarditis is attributed to prior antibiotic administration. For culturenegative cases without prior antibiotic administration, infection is most often due to fastidious organisms (usually from the HACEK group— Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella— and also Bartonella and Coxiella burnetii). CLINICAL FEATURES The clinical manifestations of endocarditis range from acute/fulminant to insidious/indolent. 20 Common presenting symptoms include fever, chills, weakness, and dyspnea. The most common complications are TABLE 156-1 Microbiology of Infective Endocarditis (IE) Native Valve IE (% of cases) Intracardiac Device IE (% cases) Normal Host Injection Drug Use 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 Abbreviation: HACEK = Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella group. *Including pacemakers and implantable cardioverter-defibrillators. Tintinalli_Sec13_p0997-1100.indd 1044 8/2/19 8:12 PM

olymicrobial 1 3 Polymicrobial 1 0 Others 4 5 Others 7 6 Culture negative 9 3 Culture negative 12 10 Abbreviation: HACEK = Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella group. *Including pacemakers and implantable cardioverter-defibrillators. Tintinalli_Sec13_p0997-1100.indd 1044 8/2/19 8:12 PM CHAPTER 156: Endocarditis 1045 congestive heart failure (44%), CNS findings (30%), and peripheral arterial embolization (22%).22  FEVER Early bacteremia produces nonspecific signs and symptoms (Table 156-2), 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, >98% with injection drug use). 5,14,20,21 Fever may be absent in the elderly, those using antibiotics or antipyretics, and those with congestive heart failure, renal failure, or immunosuppression.  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 murmurs are common, heard in 50% to 85% of patients, although less so in rightsided endocarditis (<50%). Valvular abscesses and pericarditis can result from local extension. Other cardiac complications include heart blocks and dysrhythmias that result from extension of infection through the interventricular septum to the conduction system.  NEUROLOGIC MANIFESTATIONS About 20% to 40% of patients develop neurologic symptoms, including embolic cerebral ischemic events (often in multiple areas, a clinical clue), CNS abscess, intracranial hemorrhage, mycotic (or infected) aneurysm, meningitis, or seizures. 26 Rupture of a cerebral mycotic aneurysm results in subarachnoid hemorrhage. Embolic stroke involving the middle cerebral artery is the most common CNS complication.  ARTERIAL EMBOLIZATION Embolization of vegetation fragments is common (20% to 50% of patients), 27 resulting in infarction or abscess in remote tissues. Pulmo nary complications include pulmonary infarction, pneumonia, empy ema, or pleural effusion; multifocal pneumonia, like multifocal cerebral infarction, often is a clue to septic embolization. Coronary artery emboli usually arise from the aortic valve and may cause acute myocardial infarction or myocarditis. Embolic splenic infarction causes left upper quadrant abdominal pain with radiation to the left shoulder. Renal emboli result in flank pain and hematuria. Emboli to the mesenteric arteries cause acute abdominal pain, melena, or bowel ischemia. Emboli to arteries of the extremities may produce acute limb ischemia. Retinal artery embolism may cause acute monocular blindness.  CUTANEOUS FINDINGS Cutaneous embolic phenomena are less common due to early detection and treatment. Cutaneous findings may occur in 5% to 10% of cases and may include petechiae, splinter or subungual hemorrhages of digits, Osler nodes (small, tender subcutaneous nodules on the pads of the digits), and Janeway lesions (small hemorrhagic painless plaques on the digits). 28,29 Digital clubbing is infrequent, and occurs only in those with long-standing disease. Cutaneous signs are not specific and occur in other types of vasculitis or bacteremia. DIAGNOSIS Suspicion of endocarditis usually requires hospital admission for culture, echocardiography, and assessment of the clinical course. 1 Prolonged unexplained fever, malaise, or other constitutional symptoms should prompt evaluation for endocarditis. Thoroughly evaluate and admit febrile injection drug users since the prevalence of endocarditis is high (10% to 15%), follow-up is often challenging, and clinical find ings cannot reliably exclude the diagnosis.

nged unexplained fever, malaise, or other constitutional symptoms should prompt evaluation for endocarditis. Thoroughly evaluate and admit febrile injection drug users since the prevalence of endocarditis is high (10% to 15%), follow-up is often challenging, and clinical find ings cannot reliably exclude the diagnosis. Admit patients with a cardiac prosthetic valve and fever (or persistent malaise, vasculitis, or new murmur) given the high morbidity and mortality associated with prosthetic valve infections. In stable patients with a low suspicion of endocarditis who were initially discharged, admit immediately once positive blood cultures result. The Duke criteria 30,31 aid diagnosis of infective endocarditis (Tables 156-3 and 156-4). A more recent study demonstrated excel lent negative predictive value for the Prediction Rule for Endocarditis in Injection Drug Users, which assesses risk based on tachycardia, cardiac murmur, and absence of skin infection. 32 This latter tool requires more research before wider use in ED treatment and disposi tion decisions.  BLOOD CULTURES Obtain blood cultures (at least 10 mL per culture bottle) before begin ning antibiotics. Draw three sets from separate sites because fewer collections may not detect bacteremia. Those receiving any antibiotic therapy recently often require additional sets of blood cultures. Ideally, wait at least 1 hour between the first and last blood culture. Although administration of antibiotics prior to culture acquisition reduces recovery rate of TABLE 156-2 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 Tintinalli_Sec13_p0997-1100.indd 1045 8/2/19 8:12 PM

chiae 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 Tintinalli_Sec13_p0997-1100.indd 1045 8/2/19 8:12 PM 1046 SECTION 13: Infectious Diseases bacteria by 35% to 40%,33 in critically ill patients, do not withhold antibiotics to obtain cultures.34 In patients with confirmed endocarditis, repeat blood cultures every 48 to 72 hours to assess treatment progress. 23,35 For patients at risk for culture-negative infective endocarditis, advise the laboratory of the suspected diagnosis to prompt specialized test ing for fastidious organisms. Polymerase chain reaction techniques aid pathogen detection.  OTHER DIAGNOSTIC TESTS There are no definitive laboratory tests that diagnose endocarditis. Common findings are anemia (70% to 90%), hematuria, and eleva tion of erythrocyte sedimentation rate (>90%), C-reactive protein, or procalcitonin. ECG findings are also nonspecific but can identify conduction abnormalities resulting from infection. Prolonged PR interval, new left bundle branch block, or new right bundle branch block with left ante rior hemiblock suggests spread of infection into the conduction system. Junctional tachycardia, Wenckebach block, or complete heart block may indicate extension of infection from the mitral annulus into the atrio ventricular node or proximal bundle of His. Chest radiographs may demonstrate pulmonic emboli (often in mul tiple areas) in patients with right-sided valvular involvement or may show acute heart failure in those with left-sided valvular involvement.  ECHOCARDIOGRAPHY Echocardiographic abnormalities represent one of the two major criteria for definitive diagnosis. Two-dimensional transthoracic echocardiog raphy is the first choice for those with native valves. 35,36 The specificity of transthoracic echocardiography for vegetations is excellent (98%), although sensitivity varies according to patient population. Sensitivity of transthoracic echocardiography is highest in injection drug users (88% to 94%), who more often have larger vegetations, right-sided lesions, and favorable acoustic windows. For those with chest wall deformities, obesity, or chronic obstructive pulmonary disease, transthoracic echo cardiography is less sensitive. Transesophageal echocardiography is more sensitive and specific in detecting valvular abnormalities than transthoracic echocardiography due to improved image resolution but is less immediately available in the emergency setting. Use transesophageal echocardiography in patients with prosthetic valves or intracardiac devices, patients with inadequate transthoracic echocardiography imagery, and those with intermediate or high clinical probability of endocarditis. 35,36 Transesophageal echo cardiography is of particular value for assessing suspected complications such as myocardial abscess and perivalvular extension. TREATMENT  INITIAL STABILIZATION Patients with endocarditis may present with hemodynamic instability, respiratory compromise, pulmonary edema, diminished pulmonary capacity, altered mental status, and acidosis. Emergency stabilization with airway management and hemodynamic monitoring and support are priority interventions.

MENT  INITIAL STABILIZATION Patients with endocarditis may present with hemodynamic instability, respiratory compromise, pulmonary edema, diminished pulmonary capacity, altered mental status, and acidosis. Emergency stabilization with airway management and hemodynamic monitoring and support are priority interventions. Intra-aortic balloon counterpulsation aids the TABLE 156-4 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 • Pathologic lesions: vegetation or intracardiac abscess present, confirmed by histology showing active endocarditis Clinical Criteria, Using Specific Definitions Listed in Table 156-3 • Two major criteria • One major and three minor criteria • Five minor criteria Possible infective endocarditis • One major criterion and one minor criterion • Three minor criteria Rejected • Firm alternate diagnosis for manifestations of endocarditis • Resolution of manifestations of endocarditis with antibiotic therapy for 4 d or less • No pathologic evidence of infective endocarditis at surgery or autopsy after antibiotic therapy for 4 d • Does not meet criteria for possible infective endocarditis TABLE 156-3 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 • Community-acquired Staphylococcus aureus or enterococci in the absence of a primary focus • Microorganisms consistent with IE from persistently positive blood cultures defined as: • At least two positive cultures of blood samples drawn >12 h apart • 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 • Abscess • New partial dehiscence of prosthetic valve • New valvular regurgitation (worsening or changing of preexisting murmur not sufficient) 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 hemor rhages, and Janeway lesions • Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots, and rheuma toid fever • Microbiologic evidence: positive blood culture but does not meet a major criterion as noted in Table 156-4 * or serologic evidence of active infection with organism consis tent with IE • Echocardiographic minor findings were eliminated in the modified Duke criteria Abbreviations: HACEK = Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella; IE = infective endocarditis. *Excludes single positive cultures for coagulase-negative staphylococci and organisms that do not cause IE. Tintinalli_Sec13_p0997-1100.indd 1046 8/2/19 8:12 PM

nated in the modified Duke criteria Abbreviations: HACEK = Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella; IE = infective endocarditis. *Excludes single positive cultures for coagulase-negative staphylococci and organisms that do not cause IE. Tintinalli_Sec13_p0997-1100.indd 1046 8/2/19 8:12 PM CHAPTER 156: Endocarditis 1047 emergency management of unstable mitral valve rupture but is contra indicated for aortic valve rupture. Definitive management requires a team approach, and that often includes experts from cardiology, infectious disease, and cardiac surgery. Systemic clot lysis or anticoagulation for treatment of endocarditisassociated stroke is controversial (concern of worsening underlying event) and best managed together with a stroke expert. Current guidelines for native valve endocarditis recommend withholding anticoagulation for at least 2 weeks after a CNS embolic event to reduce the risk of hemorrhagic transformation. 23,37,38 Patients with prosthetic valves being treated with anticoagulants may be maintained on established regimens as long as there is no evidence of bleeding. Patients with prosthetic valve endocarditis and evidence of embolic strokes should have anticoagulation and antiplatelet therapy withheld for at least 2 weeks to reduce the risk of hemorrhagic transformation. 23,39  EMPIRIC TREATMENT OF SUSPECTED ENDOCARDITIS OF NATIVE VALVES Antibiotic selection is based on patient characteristics and local resis tance patterns. Table 156-5 lists sample empiric treatment regimens.23,39-41 Although some recommend awaiting culture results before antibiotic therapy for patients with subacute bacterial endocarditis, we recom mend ED initiation of antibiotic therapy targeting the most common organisms for all patients suspected of endocarditis after obtaining blood cultures. For patients with suspected native valve infection, empiric antibiotic therapy includes a penicillinase-resistant penicillin, a cephalosporin, or daptomycin. 42 Gentamicin is no longer recommended for native valve staphylococcal infective endocarditis due to minimal benefit and significant nephrotoxicity. 23,41,43 For patients with complications (injection drug use, congenital heart disease, nosocomial infec tion, endocarditis developed while taking oral antibiotics, or suspected methicillin-resistant S. aureus), add vancomycin.  EMPIRIC TREATMENT OF SUSPECTED PROSTHETIC VALVE ENDOCARDITIS For patients with suspected artificial valve endocarditis, empiric therapy includes an antistaphylococcal β-lactam agent or vancomycin, with consideration of adding gentamicin and rifampin. 23,41  DEFINITIVE TREATMENT OF ENDOCARDITIS Base definitive antibiotic treatment on culture and sensitivity results. Most patients will require 4 to 6 weeks of antibiotic therapy. Surgical management is indicated in patients with severe valvular dysfunction, congestive heart failure, relapsing prosthetic valve endocarditis, major embolic complications, fungal endocarditis, new conduction defects or dysrhythmias, or persistent bacteremia after appropriate therapy. 23,39,44 Surgical risk increases in those >65 years old, on inotropes, with sepsis, or with cerebral emboli.45 Patients with concern for pacemaker lead infection may require removal of infected hardware in order to achieve source control. ENDOCARDITIS PROPHYLAXIS Because every day dental activities (brushing, flossing, chewing) cause bacteremia, dental hygiene is critical. Give antibiotic prophylaxis to those at risk (Table 156-6) prior to manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa.

ource control. ENDOCARDITIS PROPHYLAXIS Because every day dental activities (brushing, flossing, chewing) cause bacteremia, dental hygiene is critical. Give antibiotic prophylaxis to those at risk (Table 156-6) prior to manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. 35,39,46 Prophylaxis is not needed in those at risk for nondental procedures , such as local injections, laceration suturing, IV placement, blood draw ing, endotracheal intubation, endoscopy, vaginal delivery, oral trauma, urethral catheterization, or uterine dilation and curettage. Some experts recommend prophylaxis for body art, such as tattooing and piercing, but this is not a standard practice. 35,47 Prophylaxis is not routinely indicated for patients with mitral valve prolapse, pacemakers, hypertrophic cardiomyopathy, physiologic mur murs, coronary artery bypass surgery or angioplasty, or surgical repair of atrial septal defect, ventricular septal defect, or patent ductus arteriosus. Recommendations for procedures that manipulate infected skin structures or musculoskeletal tissue are Class IIb (consider but useful ness not established); it is reasonable to administer antibiotics before the procedure for the highest-risk groups identified in Table 156-6. Choose an antibiotic active against staphylococci and β-hemolytic streptococci; vancomycin and clindamycin are options for those unable to tolerate a β-lactam or those suspected to have an infection caused by a methicillinresistant strain of Staphylococcus. The incidence of bacteremia with abscess incision and drainage is very low, which is one reason why many do not prophylaxis in this setting. A simplified strategy for antibiotic prophylaxis is provided in Table 156-7. With the endorsement of the National Institute for Health and Clinical Excellence of London, 48 the European College of Cardiology does not recommend prophylaxis before respiratory tract procedures, GI or GU procedures, or uncomplicated dermatologic or musculoskeletal procedures. TABLE 156-5 Empiric Therapy of Suspected Bacterial Endocarditis* Patient Characteristics Recommended Agents, Initial Dose Uncomplicated history Ceftriaxone, 1–2 grams IV Nafcillin, 2 grams IV Oxacillin, 2 grams IV Cefepime, 1 gram IV and Vancomycin, 15 milligrams/kg (if anaphylactic to penicillins) 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 Vancomycin, 15 milligrams/kg IV Daptomycin 8–10 milligrams/kg IV Concern for vancomycin-resistant Enterococcus infection Daptomycin 8–10 milligrams/kg Linezolid 600 milligrams Prosthetic heart valve Nafcillin 2 grams IV (if oxacillin-susceptible) Vancomycin, 15 milligrams/kg IV (if oxacillin resistance is suspected) plus Gentamicin, 1–2 milligrams/kg IV plus Rifampin, 300 milligrams PO *Based on American Heart Association, endorsed by the Infectious Diseases 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.

eases 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. TABLE 156-6 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 Tintinalli_Sec13_p0997-1100.indd 1047 8/2/19 8:12 PM