SlideShare a Scribd company logo
Infective Endocarditis
Kerolus Shehata, MD
Objectives
Recognize the current demographic characteristics of older and younger groups of
patients with endocarditis to facilitate early diagnosis and treatment strategies.
Synthesize the diagnostic criteria and imaging characteristics of endocarditis across a
range of patient populations to accurately diagnose this condition.
Enumerate important changes to the guideline for endocarditis prophylaxis to
reduce inappropriate antibiotic use.
Describe the clinical situations in which surgical referral is appropriate to treat
endocarditis and reduce mortality.
Introduction
In 1885, when Osler described the classic clinical presentation of infective endocarditis (IE),
rheumatic disease was the most common cause of valve dysfunction and IE usually presented as
a chronic condition.
Despite great progress in microbiology, diagnostic imaging, and cardiac surgery, the mortality
rates for IE remain very high, approaching 30% at 1 year.
Several factors have changed the clinical presentation of infective endocarditis over the last
several decades, including significant reduction of the incidence of rheumatic valve disease,
increased old age life expectancy, increased use of intracardiac devices, increased prevalence of
immune-compromised patients (e.g., organ transplantation), ubiquitous availability of
echocardiography, and earlier diagnosis.
Epidemiology
The overall incidence of IE continues to increase, with 11 episodes per 100,000 persons in the year 2000 and 15 episodes per 100,000 persons in 2011.
The median age of patients has steadily increased over the last 40 years. Currently, more than one-half of all cases of IE in the United States occur in patients
>60 years of age.
Only 40 years ago, rheumatic heart disease was the most common cardiac abnormality, being present in more than one-third of patients with IE. However,
recent series of IE have reported a rheumatic heart disease prevalence of only 6% in patients presenting with IE.
Although IE can involve almost any endocardial surface, there is a clear predilection for bacterial seeding and destruction of the heart valves. It has been
estimated that 38% of all cases of IE involve the aortic valve, with 34% involving the mitral valve, 8% involving both the aortic and mitral valves, and 4%
involving the tricuspid valve.
Congenital heart disease represents the underlying disorder in about 3.5% of all cases.
Only three-quarters of patients with infective endocarditis have known underlying heart disease.
Several organisms appear capable of infecting apparently normal valves, including S. aureus, some streptococci, Salmonella, Rickettsia, Borrelia, and Candida.
Pathogenesis of IE
Endothelial damage occurs first, followed by deposition of a platelet-fibrin matrix that
permits bacterial colonization.
The cycle of bacterial adherence, organism growth, and platelet-fibrin deposition is
repeated and again as the vegetation develops.
Vegetations occur where blood flow forces are greatest and valvular coaptation contact
occurs. This is where endothelial damage is most likely, namely the atrial side of the mitral
and tricuspid valves and the ventricular surface of the aortic and pulmonic valves.
The initial vegetation is a collection of fibrin and platelets. Microorganisms then adhere to
the vegetation and replicate to create extremely high concentrations of bacteria.
As the process continues, abscess formation may occur. Valvular destruction leads to
progressive regurgitation and perforation of the valve leaflet may occur
Microbiology of IE
Organisms such as viridans streptococci and S. aureus are more likely to cause endocarditis than are gram-negative rods such as Escherichia coli
and Proteus species.
The Modified Duke criteria define the following organisms as “Typical”: S. aureus, Viridans streptococci and Streptococcus bovis (S. bovis),
Enterococci, HACEK group organisms (Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella
corrodens, and Kingella kingae).
The risk of IE in patients with S. aureus bacteremia is especially high. In addition, S. aureus is associated with a highly destructive form of IE; as
such, all patients with S. aureus bacteremia should be clinically evaluated for IE.
S. bovis endocarditis is often associated with malignancy of the gastrointestinal (GI) track.
The microbiology of prosthetic valve endocarditis (PVE) is often predictable. Staphylococcus epidermidis (S. epidermidis) is a predominant
cause of PVE within the first 60 days after surgery (nosocomial source). S. aureus, gram-negative bacilli, diphtheroids, or fungi (particularly the
Candida species) are also causes of PVE during this early period that extends up to the first year after cardiac surgery.
In contrast, PVE after 1 year usually shares the same infectious organism profile as native valve endocarditis.
Epidemiologic factors associated with the development of
IE and the commonly associated organisms
IE in special patient populations
Elderly patients (ages >65 years) have a different clinical course of IE than do younger patients. They have lower rates of embolism, immune-
mediate phenomena, and septic complications. They tend to have fewer vegetations with more abscesses but are less likely to undergo
cardiac surgery. They have much higher mortality (25% vs. 13% in younger patients).
Patients undergoing chronic hemodialysis, especially those with diabetes mellitus, have a significant risk for IE. The predisposing factors in
this population include intravascular access, more frequent bacteremia, impairment of the immune system, and calcific valve disease. Since
valve thickening and calcification are commonly noted by echocardiography, the early identification of a vegetation can be challenging.
Injection drug use is a risk factor for IE, with a prevalence of 2-5% per year. he most common infecting organism in IDU patients is S. aureus
(60-90% of cases) with high prevalence of right-sided IE.
A prior history of endocarditis is an important predisposing cause for IE. Recurrent endocarditis occurred in 4.5% of one large cohort of
patients (excluding IDUs) who survived their initial episode.
Prosthetic valve endocarditis (PVE)
Having a prosthetic heart valve is the greatest risk for development of IE in
most clinical series. 1-3% of all patients with a prosthetic valve will develop
IE at 1 year and 3-6% of patients at 5 years.
PVE currently accounts for 10-30% of all cases of endocarditis, with S.
aureus being the culprit organism in 30% of cases.
The early period is generally defined as endocarditis in the first 60 days
after heart surgery, and most of the implicated organisms are considered
nosocomial. The late period involves organisms more like that of NVE.
Although there has been concern that mechanical valves are more
susceptible to IE, most series do not suggest a difference in the risk by
model, position, or type of valve
Prosthetic Vs. Native valve endocarditis
Similar presentations but different microbiology.
More invasive with higher rates of CHF, conduction
abnormalities, and CNS events.
Cardiac Implantable Electronic Device Infections
In the United States, >300,000 patients have been receiving new cardiac
implantable electronic device (CIED) implants every year.
The rate of CIED infection has increased, with a report that 1.9 per 1,000
pacemaker devices, and 9.5% of cardiac resynchronization therapy (CRT)
devices get infected over 2 years.
Currently, CIED IE accounts for 6.4% of all definite IE cases.
Most commonly (60% of cases), the infection involves the generator pocket;
however, blood stream infection is the only sign of device infection in
approximately 40% of cases.
The two most common organisms are coagulase-negative staphylococcus
followed by S. aureus.
Common underlying risk factors include an immune-suppressed state (renal
dysfunction, corticosteroid use), oral anticoagulant use, diabetes mellitus, and
indwelling hardware.
Clinical manifestations of IE
Endocarditis is a great mimic and patients may present with a wide variety of symptoms or findings that may
involve noncardiac organ systems.
Most commonly, the initial symptoms are related to persistent bacteremia with an indolent course from 2
weeks to several months.
Symptoms include fever, chills, night sweats, malaise, and weight loss. Less commonly, the initial
presentation is congestive heart failure (CHF; e.g., dyspnea and fatigue) due to significant valve dysfunction,
or a cardioembolic event such as stroke.
Fever is the most common symptom, occurring in >80% of patients with NVE or PVE. Fever is less common in
elderly patients, those with CHF, renal failure, severe disability, or previous antibiotic therapy.
A murmur of acute or chronic valve dysfunction is present in >80% of patients.
Petechiae of the mouth or conjunctivae, splinter hemorrhages within the proximal one-half of the nail bed,
and Roth spots by fundoscopy are all likely embolic phenomena. Osler’s nodes are painful nodules on the
pads of the fingers and toes.
Neurologic symptoms are common and are recognized in ≤50% of patients with IE. Embolic stroke is the
most common event. However, intracranial hemorrhage may occur due to a ruptured mycotic aneurysm
(MA) or bleeding into a thrombotic stroke territory
The modified Duke Criteria
Clinical Definition of IE According to the Duke Criteria
How to proceed if you suspect IE?
ESC diagnostic algorithm for IE
Echocardiographic features of IE
Findings can provide evidence for IE, including vegetations, leaflet perforation, annular abscess, aneurysm, fistula, and prosthetic valve dehiscence.
A vegetation is defined as a discrete echogenic mass adherent to an endocardial surface. The mass is usually irregularly shaped, with a characteristic high-
frequency motion described as an oscillation.
Vegetations typically occur on the higher-flow upstream surface of valves, but they may also appear on nonvalvular intravascular structures, such as the
intraventricular septum and atrial wall, or attached to prosthetic devices (e.g., pacemaker leads).
The identification of vegetations on prosthetic material is often difficult by TTE and transesophageal echocardiography TEE is usually required for
confirmation.
Many vegetations decrease in size (or completely resolve) with appropriate antibiotic therapy. However, some vegetations persist as less mobile structures
that become more echogenic with progressive fibrosis and/or calcification. Even after successful antimicrobial therapy, some sterile vegetations may
persist indefinitely.
Because the frequency of IE among patients with S. aureus bacteremia is reported to be approximately 30%, with many cases not being clinically
suspected, TEE should generally be pursued in the setting of S. aureus bacteremia to rule out IE.
A recent review identified clinical or transthoracic characteristics associated with low risk of IE (negative predictive values from 93-100%), where TEE may
be avoided in patients with S, Aureus bacteremia. These low-risk features included 1) absence of a permanent intracardiac device, 2) sterile follow-up
blood cultures within 4 days after the initial set, 3) no hemodialysis dependence, 4) nosocomial acquisition of S. aureus bacteremia, 5) absence of
secondary foci of infection, and 6) no clinical signs of IE.
Not every mass is a vegetation
As stated in the modified Duke Criteria, the presence of a mobile
intracardiac mass alone is not sufficient to make a definitive
diagnosis of IE.
Mobile masses visualized by echocardiography may be related to
alternate diagnoses, including Inflammatory mass lesion
(Libman-Sacks), sterile vegetations (marantic endocarditis),
cardiac tumors (e.g., papillary fibroelastoma), and myxomatous
valves with ruptured chordae/papillary muscle head.
Several normal intracardiac structures may also mimic the mobile
mass of an IE vegetation, including Lambl’s excrescences, Chiari
network or a prominent Eustachian valve.
Echocardiographic criteria for defining a vegetation
Positive features Negative features
Low reflectance High echogenicity
Attached to valve, upstream side Nonvalvular location
Irregular shape, amorphous Smooth surface or fibrillar
Mobile, oscillating Nonmobile
Associated tissue changes, valvular regurgitation Absence of regurgitation
Role of echocardiography in patients with IE
Appropriate use criteria of echocardiogram in
patients with known or suspected IE.
Imaging studies in PVE & NVE
Management of an Infected CIED
Cardiac CT in IE
The use of cardiac CT has evolved as a key adjunctive
imaging modality in IE workup. Its strength lies in
delineating paravalvular anatomy and complications
(abscesses, dehiscence, and fistulae).
Cardiac CT has incremental value in evaluating prosthetic
valve dysfunction and demonstrating prosthesis-related
vegetations, abscesses, or pseudoaneurysms.
2015 ESC guidelines include detection of paravalvular
lesions on cardiac CT as a major imaging criterion for IE.
18F-Fluorodeoxyglucose PET/CT in IE
Recently, there has been increased utilization of 18F-FDG PET/CT to show regions of
metabolic activity or inflammation.
PVE remains a diagnostic challenge, and abnormal 18F-FDG PET uptake around the
prosthetic valve is now considered a major imaging criterion for IE in the 2015 ESC
guidelines for IE.
In one study, adding positive FDG PET as a new major criterion significantly
increased the sensitivity of the modified Duke Criteria at admission, and allowed for
an earlier diagnosis, especially when echocardiography was normal or doubtful.
Lab studies in IE
Normochromic normocytic anemia, elevated ESR/CRP.
WBCs may be normal or elevated in patients with subacute IE.
Q-fever IE is diagnosed with an antiphase IgG titer >1:800 for Coxiella burnetii.
The presence of red blood cell casts on urinalysis is generally indicative of glomerulonephritis and is a minor diagnostic
criterion for IE.
A minimum of 3 blood cultures should be obtained over a 1-hour time period to demonstrate persistent bacteremia.
Negative blood cultures are seen in approximately 10% of infective endocarditis cases. Of those, approximately 50% had
prior therapy with antibiotics.
Culture-negative IE can be due to a noninfective endocarditis (Libman-Sacks) in patients with SLE.
Causes of culture-negative Endocarditis
Prior antibiotics.
Fastidious organisms: HACEK, Abiotrophia defectiva, etc., Brucella spp.
Non-cultivatable organism: Bartonella Quintana, Coxiella burnetii, Chlamydophila
psittaci, Tropheryma whipplei, Legionella spp, Mycoplasma.
Fungi.
Not IE (Libman-Sacks, myxoma, APLS, marantic, tumor)
Complications of IE
IE complicated by CHF
CHF is the complication of greatest impact on prognosis, in both NVE and PVE.
CHF is the most common indication for early surgery in IE. surgical treatment is associated with a 23%
mortality rate, compared with a 71% mortality rate with medical therapy.
Etiologies: Acute regurgitant lesion, chordal rupture, prosthetic valve dehiscence, fistula creating a
shunt or bulky vegetation obstructing a valve.
In mild presentations, delaying surgery may be an attractive strategy, especially in elderly patients or
those with significant comorbidity who carry an extreme risk of surgical complications.
Peri-annular extension of IE
Should always be suspected when fever and inflammatory markers do not resolve with appropriate antibiotic therapy.
Occurs when bacterial invasion (mostly staphylococci) weakens the periannular tissue and eventually leads to the
formation of tissue destruction with abscess, fistula, or valve dehiscence.
Complicates ≤40% of NVE and the majority of PVE.
In aortic valve IE, an expanding abscess may invade the membranous septum and the AV node causing differing degrees of
heart block.
Should always be suspected when fever and inflammatory markers do not resolve with appropriate antibiotic therapy.
A mortality rate of 40% is seen when it is associated with fistula and a new shunt. With such shunts, surgery is indicated,
even in the absence of any hemodynamic instability.
A very limited number of cases with are suitable for medical therapy alone, and these include abscess <1 cm, an isolated
organism that is drug-sensitive, and the absence of any evidence of valve destruction or heart block. Otherwise, surgery
should not be delayed.
Systemic embolization in IE
Dislodgment and embolization of a thrombus, vegetation, or friable necrotic tissue is the most common complication during IE.
Risk factors: previous embolism, first 2 weeks of Abx therapy, left sided IE (Mitral>Aortic), specific organisms (S. aureus, fungi, enterococci, HACEK),
and large mobile mitral vegetations >15 mm.
CNS is the most frequent clinically apparent site (65%), with 90% of affecting the middle cerebral artery territory.
No vascular bed is immune from potential cardioemboli.
Can lead to distal infarctions, abscesses (almost always with S. aureus) or rarely mycotic aneurysms.
The 2014 ACC/AHA guidelines recommend surgery as a class IIa indication only for those with recurrent emboli and persistent vegetations after
antibiotic therapy.
The 2015 ESC guidelines recommend urgent surgery as a class IIb indication for vegetations >15 mm and no other indications for surgery.
For right-sided IE, surgery is not indicated for simple pulmonary emboli but may be appropriate for pulmonary abscess formation.
Mycotic aneurysms occur as a result of microembolization into the vasa vasora of blood vessel walls. Branch point vessels are the most affected and,
unfortunately, this most frequently occurs within intracranial vessels. The mortality rate for a ruptured intracranial MA approaches 80% and there is
no accurate way to predict MA rupture. Intracranial MAs should be surgically ligated or treated by endovascular techniques.
Acute renal failure in IE
Occurs in 30% of cases of IE and indicates a poor prognosis.
Many factors may contribute to acute renal failure, including immune complex glomerulonephritis, embolic
renal infarcts, multiorgan failure associated with CHF or sepsis syndrome, and Interstitial nephritis
secondary to antibiotics (especially gentamicin and vancomycin).
Acute renal dysfunction is often reversible. However, renal replacement therapy may be required during the
acute phase illness.
Changes in renal function must be considered for appropriate dosing of antibiotic therapy.
Chronic complications of IE
Survivors of IE who are discharged from the hospital have an increased
risk of ischemic stroke, hemorrhagic stroke, myocardial infarction,
readmission for heart failure, ventricular arrhythmia, sudden death,
and all-cause death when compared with an age-matched cohort.
Risk factors for repeat IE include older age, male sex, drug abuse, and
valve replacement.
General principles for treatment of IE
Microbiologic eradication, whether achieved medically or surgically, is pivotal for successful treatment.
Antimicrobial therapy generally requires administration of high doses of bactericidal drugs, for at least 4 weeks through a parenteral route.
The choice of specific antimicrobials should be made while considering the following: Prior antibiotic treatment, Diagnosis of NVE, early PVE, or late PVE;
and Epidemiologic clues for pathogens and/or antibiotic resistance.
Except for staphylococcal infections, fever should resolve within days of starting therapy, and all patients should have surveillance blood cultures
obtained after 3-4 days of IV drug therapy.
After culture results are available, antibiotics should be modified, based on the sensitivity of the organism to the antimicrobial and the MIC of the drug to
the pathogen. This is particularly important with vancomycin therapy.
Bactericidal combinations are preferred to monotherapy against tolerant bacteria. For example, aminoglycosides synergize with B-lactams and
glycopeptides to enhance their efficacy and shorten their required duration of therapy. (N.B: 2015 ESC guidelines stated that aminoglycosides are no
longer recommended in Staph NVE).
Slow-growing/dormant microbes in vegetations and/or biofilms justify the need for rifampicin added to the regimen, and for prolonged periods.
PVE and device-related IE should have a much lower threshold for surgery compared with NVE.
In the setting of generator pocket infection, lead infection or endocarditis, complete and early removal of the device is recommended. Prolonged (6
weeks) antibiotic therapy is recommended, and a new device implantation should be delayed for 72h after repeat blood cultures remain negative.
Right-sided S. aureus, IE in IDU has 85% cure rate with antibiotics alone, with a short course of IV or oral treatment (2-4 w).
Surgical treatment of right-sided endocarditis is only limited to persistent bacteremia (>7 days) despite antibiotics or vegetations (>20 mm) after
recurrent pulmonary emboli.
Empiric antimicrobial therapy for IE
Indications for surgery in IE
Surgical treatment is used in approximately half of infective
endocarditis patients because of severe complications.
Congestive heart failure is the primary reason for surgical
intervention.
Other indications for surgery are extensive valvular destruction,
large vegetations, paravalvular abscess, ineffective
antimicrobial therapy, recurrent emboli on antibiotic therapy,
or the presence of a highly resistant organism.
Surgical management of infective endocarditis has the following
objectives: completely excise all infected and necrotic tissue,
remove and/or replace all infected prosthetic material, and
reconstruct cardiac structures to restore proper physiology.
Treatment of IE
Approach to management of IE
Prophylaxis against IE
Only indicated in certain cardiac conditions associated with the highest risk of
adverse outcomes from IE.
These conditions include cardiac transplant recipients who develop cardiac
valvulopathy, prosthetic cardiac valve or prosthetic material used for cardiac
valve repair, previous IE and certain congenital heart diseases (Unrepaired
cyanotic disease including palliative shunts and conduits, completed repair
during the first 6 months after the procedure, and repaired disease with
residual defect).
Reasonable for all dental procedures that involve manipulation of gingival
tissue or the periapical region of teeth or perforation of the oral mucosa.
Not recommended for patients who undergo GU or GI tract procedure.
Pearls for the boards
Only patients at the highest risk of complications from infective endocarditis require
prophylaxis.
Major clinical criteria for the diagnosis of infective endocarditis include multiple
positive blood cultures and echocardiographic evidence of endocardial involvement.
Patients with infective endocarditis and embolic CNS events should hold
anticoagulation.
Intracardiac device infections require complete removal of the device, including
generator and leads.
A 33-year-old man is admitted with a 1-week history of fever and shortness of breath. He has a history
of intravenous drug use.
On examination, he has a temperature of 102.5 degrees Fahrenheit, a heart rate of 110 bpm, and a
blood pressure of 102/60 mm Hg. He appears mildly dyspneic and diaphoretic. His jugular venous
pressure is 10 cm H20. His lungs have bibasilar rales. His cardiac exam demonstrates a hyperdynamic
precordium with a soft systolic murmur and S3 gallop. His extremities are warm without edema.
His echocardiogram on admission shows a left ventricular ejection fraction of 75%, a 1 cm vegetation on
the tricuspid valve with moderate to severe tricuspid regurgitation and thickening of the mitral valve
with severe mitral regurgitation. His chest X-ray shows pulmonary edema.
He is admitted to telemetry. Serial blood cultures are sent, and intravenous vancomycin is started. What
is the next best step in the management of this patient?
A. Intra-aortic balloon counterpulsation.
B. Urgent valve replacement.
C. Repeat transesophageal echocardiogram in 6 weeks.
D. Initiation of sacubitril/valsartan.
E. Addition of rifampin.
A 29-year-old woman is referred by her internist for evaluation of a newly identified murmur. The
patient reports no cardiovascular symptoms and has no significant medical history except for a
known penicillin allergy. Her only prescribed medicine is an oral contraceptive. She denies
recreational drug use.
On physical examination, there is a systolic click followed by a grade 2/6 late systolic
murmur.
Her transthoracic echocardiogram demonstrates myxomatous mitral valve disease with moderate
regurgitation and mild left atrial enlargement. The left ventricular end-systolic dimension is 32 mm
and ejection fraction is 65%.
Which of the following is required prior to dental procedures in this patient?
A. No antibiotic prophylaxis.
B. Clindamycin 600 mg.
C. Cephalexin 2 g.
D. Amoxicillin 2 g.
E. Metronidazole 500 mg.
A 34-year-old man is admitted with a fever. He has felt poorly for several months. He has had a 10-lb weight loss and
recurring night sweats. In the past few weeks, he has experienced progressive dyspnea. He is on no medications at this time.
His social history includes ongoing intravenous drug use. His temperature is 38.5° Celsius, heart rate is 103 bpm, blood
pressure is 95/50 mm Hg, and resting oxygen saturation on room air is 96%. His lungs reveal bibasilar fine rales. His jugular
venous pressure is not elevated. His apex is hyperdynamic, and there is a grade 2/6 systolic murmur and grade 2/4 diastolic
murmur along the left sternal border. The first heart sound (S1) is soft and there is an S3. He has no edema. There are
splinter hemorrhages under the nailbeds on his left fingers. His echocardiogram reveals a hyperdynamic left ventricle with
evidence for severe aortic regurgitation (AR) and vegetations on his aortic valve In addition to broad spectrum antibiotics,
which of the following is the most appropriate next step in the management of this patient?
A. Aortic valve replacement.
B. Intravenous esmolol 0.1 mg/kg/min.
C. Intra-aortic balloon pump.
D. Phenylephrine 40 mcg/min.
E. Transesophageal echocardiogram.
A 48-year-old man with a history of myxomatous valve disease and moderate mitralregurgitation
(MR) on echocardiogram presents today for his annual reassessment. He has a history of
hyperlipidemia and remote endocarditis. He feels well and rides his road bike most days of the week
without limiting symptoms. His exam is notable for a heart rate 52 bpm, blood pressure of 118/74
mm Hg, and pulse oximetry of 98%. His lungs are clear without rales. His cardiac exam reveals a soft,
late systolic murmur at the apex. There is no lower extremity edema.
Which of the following would be recommended for this patient?
A. Antibiotics prior to dental cleaning.
B. Aspirin 81 mg daily.
C. Cardiac magnetic resonance imaging.
D. Transesophageal echocardiogram.
E. Losartan 25 mg daily.
References
• Baddour LM, Wilson WR, Bayer AS, et al.; American Heart Association Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of
the Council on Cardiovascular Disease in the Young, Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and
Stroke Council. Infective endocarditis in adults: diagnosis, antimicrobial therapy, and management of complications: a scientific statement for
healthcare professionals from the American Heart Association. Circulation 2015;132:1435-86.
• Nishimura RA, Otto CM, Bonow RO, et al.; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2014
AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63:e57-185.
• Habib G, Lancellotti P, Antunes MJ, et al.; ESC Scientific Document Group. 2015 ESC guidelines for the management of infective endocarditis:
The Task Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association
for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM). Eur Heart J 2015;36:3075-128.
• Armstrong, W. F., Ryan, T., & Feigenbaum, H. (2018). Feigenbaum's echocardiography (8th ed.): Wolters Kluwer Health/Lippincott Williams &
Wilkins.
• Douglas PS, Khandheria B, Stainback RF, et al.; American College of Cardiology Foundation Quality Strategic Directions Committee
Appropriateness Criteria Working Group; American Society of Echocardiography; American College of Emergency Physicians; American Society
of Nuclear Cardiology; Society for Cardiovascular Angiography and Interventions; Society of Cardiovascular Computed Tomography; Society for
Cardiovascular Magnetic Resonance; American College of Chest Physicians; Society of Critical Care Medicine.
ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2007 appropriateness criteria for transthoracic and transesophageal echocardiography: a report of
the American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Criteria Working Group, American
Society of Echocardiography, American College of Emergency Physicians, American Society of Nuclear Cardiology, Society for Cardiovascular
Angiography and Interventions, Society of Cardiovascular Computed Tomography, and the Society for Cardiovascular Magnetic Resonance
endorsed by the American College of Chest Physicians and the Society of Critical Care Medicine. J Am Coll Cardiol 2007;50:187-204.
Thank You

More Related Content

What's hot

Eisenmenger syndrome
Eisenmenger syndromeEisenmenger syndrome
Eisenmenger syndrome
Feba
 
Dextrocardia
DextrocardiaDextrocardia
Dextrocardia
David Christian
 
Aortic regurgitation
Aortic regurgitationAortic regurgitation
Aortic regurgitation
Vitrag Shah
 
Tachyarrhythmias
TachyarrhythmiasTachyarrhythmias
Tachyarrhythmias
SCGH ED CME
 
Atrial fibrillation
Atrial fibrillation Atrial fibrillation
Atrial fibrillation
ikramdr01
 
Congenital heart diseases (Cyanotic CHD)
Congenital heart diseases (Cyanotic CHD)Congenital heart diseases (Cyanotic CHD)
Congenital heart diseases (Cyanotic CHD)
Deepak Chinagi
 
Atrial fibrillation causes,pathogenesis, clinical presentation 2013
Atrial fibrillation causes,pathogenesis, clinical presentation 2013Atrial fibrillation causes,pathogenesis, clinical presentation 2013
Atrial fibrillation causes,pathogenesis, clinical presentation 2013Basem Enany
 
Pulmonary Hypertension in Infants and Children
Pulmonary Hypertensionin Infants and ChildrenPulmonary Hypertensionin Infants and Children
Pulmonary Hypertension in Infants and Children
Pediatric Home Service
 
Prosthetic valve thrombosis
Prosthetic valve thrombosisProsthetic valve thrombosis
Prosthetic valve thrombosis
kazi alam nowaz
 
Congenital cyanotic heart disease approach
Congenital cyanotic heart disease approachCongenital cyanotic heart disease approach
Congenital cyanotic heart disease approachVarsha Shah
 
PSVT
PSVTPSVT
HEART FAILURE MANAGEMENT
HEART FAILURE MANAGEMENTHEART FAILURE MANAGEMENT
HEART FAILURE MANAGEMENT
dibufolio
 
Infective endocarditis guidelines 2015
Infective endocarditis guidelines 2015Infective endocarditis guidelines 2015
Infective endocarditis guidelines 2015
Rishi Bhargav
 
Valvular Heart Diseases - Final Year Lecture
Valvular Heart Diseases - Final Year LectureValvular Heart Diseases - Final Year Lecture
Valvular Heart Diseases - Final Year LectureMr Adeel Abbas
 
HOCM Hypertrophic cardiomyopathy
HOCM Hypertrophic cardiomyopathyHOCM Hypertrophic cardiomyopathy
HOCM Hypertrophic cardiomyopathy
Please hit like if you really liked my PPTs
 
Sudden cardiac death
Sudden cardiac deathSudden cardiac death
Sudden cardiac deathPuneet Shukla
 
Infective endocarditis
Infective endocarditisInfective endocarditis
Infective endocarditis
Mohamad Yaakub
 
Constrictive pericarditis
Constrictive pericarditisConstrictive pericarditis
Constrictive pericarditis
Waqas Khalid
 

What's hot (20)

Eisenmenger syndrome
Eisenmenger syndromeEisenmenger syndrome
Eisenmenger syndrome
 
Dextrocardia
DextrocardiaDextrocardia
Dextrocardia
 
Aortic regurgitation
Aortic regurgitationAortic regurgitation
Aortic regurgitation
 
Tachyarrhythmias
TachyarrhythmiasTachyarrhythmias
Tachyarrhythmias
 
Atrial fibrillation
Atrial fibrillation Atrial fibrillation
Atrial fibrillation
 
Congenital heart diseases (Cyanotic CHD)
Congenital heart diseases (Cyanotic CHD)Congenital heart diseases (Cyanotic CHD)
Congenital heart diseases (Cyanotic CHD)
 
Atrial fibrillation causes,pathogenesis, clinical presentation 2013
Atrial fibrillation causes,pathogenesis, clinical presentation 2013Atrial fibrillation causes,pathogenesis, clinical presentation 2013
Atrial fibrillation causes,pathogenesis, clinical presentation 2013
 
Pulmonary Hypertension in Infants and Children
Pulmonary Hypertensionin Infants and ChildrenPulmonary Hypertensionin Infants and Children
Pulmonary Hypertension in Infants and Children
 
Atrial Fibrillation
Atrial FibrillationAtrial Fibrillation
Atrial Fibrillation
 
Prosthetic valve thrombosis
Prosthetic valve thrombosisProsthetic valve thrombosis
Prosthetic valve thrombosis
 
Congenital cyanotic heart disease approach
Congenital cyanotic heart disease approachCongenital cyanotic heart disease approach
Congenital cyanotic heart disease approach
 
PSVT
PSVTPSVT
PSVT
 
HEART FAILURE MANAGEMENT
HEART FAILURE MANAGEMENTHEART FAILURE MANAGEMENT
HEART FAILURE MANAGEMENT
 
Infective endocarditis guidelines 2015
Infective endocarditis guidelines 2015Infective endocarditis guidelines 2015
Infective endocarditis guidelines 2015
 
Valvular Heart Diseases - Final Year Lecture
Valvular Heart Diseases - Final Year LectureValvular Heart Diseases - Final Year Lecture
Valvular Heart Diseases - Final Year Lecture
 
HOCM Hypertrophic cardiomyopathy
HOCM Hypertrophic cardiomyopathyHOCM Hypertrophic cardiomyopathy
HOCM Hypertrophic cardiomyopathy
 
Pediatric arrhythmia
Pediatric arrhythmiaPediatric arrhythmia
Pediatric arrhythmia
 
Sudden cardiac death
Sudden cardiac deathSudden cardiac death
Sudden cardiac death
 
Infective endocarditis
Infective endocarditisInfective endocarditis
Infective endocarditis
 
Constrictive pericarditis
Constrictive pericarditisConstrictive pericarditis
Constrictive pericarditis
 

Similar to Infective Endocarditis

Infective endocarditis FINAL.pptx
Infective endocarditis FINAL.pptxInfective endocarditis FINAL.pptx
Infective endocarditis FINAL.pptx
RashiSrivastava62
 
Endocarditis review
Endocarditis reviewEndocarditis review
Endocarditis reviewscott homann
 
INFECTIVE ENDOCARDITIS.pptx
INFECTIVE ENDOCARDITIS.pptxINFECTIVE ENDOCARDITIS.pptx
INFECTIVE ENDOCARDITIS.pptx
BadarJamal4
 
4_6030689835172236523.pptx
4_6030689835172236523.pptx4_6030689835172236523.pptx
4_6030689835172236523.pptx
JibrilAliSe
 
Infective endocarditis updated
Infective endocarditis updatedInfective endocarditis updated
Infective endocarditis updated
Tasneem Bashir • تسنيم بشير
 
Infective Endocarditis- Prevention and Management
Infective Endocarditis- Prevention and ManagementInfective Endocarditis- Prevention and Management
Infective Endocarditis- Prevention and Management
Smarakranjan Rout
 
Infective endocarditis
Infective endocarditisInfective endocarditis
Infective endocarditis
Smarakranjan Rout
 
Nature ei
Nature   eiNature   ei
Nature ei
gisa_legal
 
ENDOCARDITIS - lecture.pptx
ENDOCARDITIS - lecture.pptxENDOCARDITIS - lecture.pptx
ENDOCARDITIS - lecture.pptx
Maina64
 
Infective endocarditis
Infective endocarditisInfective endocarditis
Infective endocarditispochao
 
Infective endocarditis.pptx
Infective endocarditis.pptxInfective endocarditis.pptx
Infective endocarditis.pptx
aishanteme
 
IEPPT-IIIstd (2).pptx
IEPPT-IIIstd (2).pptxIEPPT-IIIstd (2).pptx
IEPPT-IIIstd (2).pptx
yilkalmossie1
 
INFECTIVE ENDOCARDITIS.pptx
INFECTIVE ENDOCARDITIS.pptxINFECTIVE ENDOCARDITIS.pptx
INFECTIVE ENDOCARDITIS.pptx
HanaaMohamedSheikhOm
 
Slide Presentation on Endocarditis .pptx
Slide Presentation on Endocarditis .pptxSlide Presentation on Endocarditis .pptx
Slide Presentation on Endocarditis .pptx
UzomaBende
 
Bacterial endocarditis
Bacterial  endocarditisBacterial  endocarditis
Bacterial endocarditis
Sakina Musa
 
Infective Endocarditis - Indications of Surgery
Infective Endocarditis - Indications of SurgeryInfective Endocarditis - Indications of Surgery
Infective Endocarditis - Indications of Surgery
ZryanMejio1
 
Endocardite infecciosa
Endocardite infecciosaEndocardite infecciosa
Endocardite infecciosa
gisa_legal
 
Infective endocarditis 2020
Infective endocarditis 2020Infective endocarditis 2020
Infective endocarditis 2020
Nitin Das
 
Infective Endocarditis
Infective EndocarditisInfective Endocarditis
Infective Endocarditis
hospital
 
Infective endocarditis in children
Infective endocarditis in childrenInfective endocarditis in children
Infective endocarditis in children
birhanu abie
 

Similar to Infective Endocarditis (20)

Infective endocarditis FINAL.pptx
Infective endocarditis FINAL.pptxInfective endocarditis FINAL.pptx
Infective endocarditis FINAL.pptx
 
Endocarditis review
Endocarditis reviewEndocarditis review
Endocarditis review
 
INFECTIVE ENDOCARDITIS.pptx
INFECTIVE ENDOCARDITIS.pptxINFECTIVE ENDOCARDITIS.pptx
INFECTIVE ENDOCARDITIS.pptx
 
4_6030689835172236523.pptx
4_6030689835172236523.pptx4_6030689835172236523.pptx
4_6030689835172236523.pptx
 
Infective endocarditis updated
Infective endocarditis updatedInfective endocarditis updated
Infective endocarditis updated
 
Infective Endocarditis- Prevention and Management
Infective Endocarditis- Prevention and ManagementInfective Endocarditis- Prevention and Management
Infective Endocarditis- Prevention and Management
 
Infective endocarditis
Infective endocarditisInfective endocarditis
Infective endocarditis
 
Nature ei
Nature   eiNature   ei
Nature ei
 
ENDOCARDITIS - lecture.pptx
ENDOCARDITIS - lecture.pptxENDOCARDITIS - lecture.pptx
ENDOCARDITIS - lecture.pptx
 
Infective endocarditis
Infective endocarditisInfective endocarditis
Infective endocarditis
 
Infective endocarditis.pptx
Infective endocarditis.pptxInfective endocarditis.pptx
Infective endocarditis.pptx
 
IEPPT-IIIstd (2).pptx
IEPPT-IIIstd (2).pptxIEPPT-IIIstd (2).pptx
IEPPT-IIIstd (2).pptx
 
INFECTIVE ENDOCARDITIS.pptx
INFECTIVE ENDOCARDITIS.pptxINFECTIVE ENDOCARDITIS.pptx
INFECTIVE ENDOCARDITIS.pptx
 
Slide Presentation on Endocarditis .pptx
Slide Presentation on Endocarditis .pptxSlide Presentation on Endocarditis .pptx
Slide Presentation on Endocarditis .pptx
 
Bacterial endocarditis
Bacterial  endocarditisBacterial  endocarditis
Bacterial endocarditis
 
Infective Endocarditis - Indications of Surgery
Infective Endocarditis - Indications of SurgeryInfective Endocarditis - Indications of Surgery
Infective Endocarditis - Indications of Surgery
 
Endocardite infecciosa
Endocardite infecciosaEndocardite infecciosa
Endocardite infecciosa
 
Infective endocarditis 2020
Infective endocarditis 2020Infective endocarditis 2020
Infective endocarditis 2020
 
Infective Endocarditis
Infective EndocarditisInfective Endocarditis
Infective Endocarditis
 
Infective endocarditis in children
Infective endocarditis in childrenInfective endocarditis in children
Infective endocarditis in children
 

More from Kerolus Shehata

Invasive Hemodynamics: Assessment and interpretation
Invasive Hemodynamics: Assessment and interpretationInvasive Hemodynamics: Assessment and interpretation
Invasive Hemodynamics: Assessment and interpretation
Kerolus Shehata
 
Stress Echocardiography
Stress EchocardiographyStress Echocardiography
Stress Echocardiography
Kerolus Shehata
 
Exercise ECG Testing
Exercise ECG Testing Exercise ECG Testing
Exercise ECG Testing
Kerolus Shehata
 
Guideline‐Directed Medical Therapy in HFrEF
Guideline‐Directed Medical Therapy in HFrEFGuideline‐Directed Medical Therapy in HFrEF
Guideline‐Directed Medical Therapy in HFrEF
Kerolus Shehata
 
Atrial Fibrillation
Atrial FibrillationAtrial Fibrillation
Atrial Fibrillation
Kerolus Shehata
 
Preoperative evaluation
Preoperative evaluationPreoperative evaluation
Preoperative evaluation
Kerolus Shehata
 
Cholesterol Management Guidelines
Cholesterol Management GuidelinesCholesterol Management Guidelines
Cholesterol Management Guidelines
Kerolus Shehata
 
ASPREE Trial
ASPREE TrialASPREE Trial
ASPREE Trial
Kerolus Shehata
 
Complete EKG Interpretation Course
Complete EKG Interpretation Course Complete EKG Interpretation Course
Complete EKG Interpretation Course
Kerolus Shehata
 
Evaluation of Chest Pain in the Ambulatory Setting
Evaluation of Chest Pain in the Ambulatory SettingEvaluation of Chest Pain in the Ambulatory Setting
Evaluation of Chest Pain in the Ambulatory Setting
Kerolus Shehata
 
Management of hypertension
Management of hypertensionManagement of hypertension
Management of hypertension
Kerolus Shehata
 
Anticoagulation in venous thromboembolism
Anticoagulation in venous thromboembolismAnticoagulation in venous thromboembolism
Anticoagulation in venous thromboembolism
Kerolus Shehata
 
Hyperglycemic crises and hypoglycemia
Hyperglycemic crises and hypoglycemiaHyperglycemic crises and hypoglycemia
Hyperglycemic crises and hypoglycemia
Kerolus Shehata
 
Left Bundle Branch Block (LBBB)
Left Bundle Branch Block (LBBB)Left Bundle Branch Block (LBBB)
Left Bundle Branch Block (LBBB)
Kerolus Shehata
 
Non-Astherosclerotic Spontaneous Coronary Dissection
Non-Astherosclerotic Spontaneous Coronary DissectionNon-Astherosclerotic Spontaneous Coronary Dissection
Non-Astherosclerotic Spontaneous Coronary Dissection
Kerolus Shehata
 
Make your life worth living
Make your life worth livingMake your life worth living
Make your life worth living
Kerolus Shehata
 
First Aid, illustrated & simplified
First Aid, illustrated & simplified First Aid, illustrated & simplified
First Aid, illustrated & simplified
Kerolus Shehata
 
Get inspired and motivated
Get inspired and motivated Get inspired and motivated
Get inspired and motivated
Kerolus Shehata
 
General Toxicology, All In A Nutshell
General Toxicology, All In A NutshellGeneral Toxicology, All In A Nutshell
General Toxicology, All In A Nutshell
Kerolus Shehata
 
ABG, step by step approach (Updated)
ABG, step by step approach (Updated)ABG, step by step approach (Updated)
ABG, step by step approach (Updated)
Kerolus Shehata
 

More from Kerolus Shehata (20)

Invasive Hemodynamics: Assessment and interpretation
Invasive Hemodynamics: Assessment and interpretationInvasive Hemodynamics: Assessment and interpretation
Invasive Hemodynamics: Assessment and interpretation
 
Stress Echocardiography
Stress EchocardiographyStress Echocardiography
Stress Echocardiography
 
Exercise ECG Testing
Exercise ECG Testing Exercise ECG Testing
Exercise ECG Testing
 
Guideline‐Directed Medical Therapy in HFrEF
Guideline‐Directed Medical Therapy in HFrEFGuideline‐Directed Medical Therapy in HFrEF
Guideline‐Directed Medical Therapy in HFrEF
 
Atrial Fibrillation
Atrial FibrillationAtrial Fibrillation
Atrial Fibrillation
 
Preoperative evaluation
Preoperative evaluationPreoperative evaluation
Preoperative evaluation
 
Cholesterol Management Guidelines
Cholesterol Management GuidelinesCholesterol Management Guidelines
Cholesterol Management Guidelines
 
ASPREE Trial
ASPREE TrialASPREE Trial
ASPREE Trial
 
Complete EKG Interpretation Course
Complete EKG Interpretation Course Complete EKG Interpretation Course
Complete EKG Interpretation Course
 
Evaluation of Chest Pain in the Ambulatory Setting
Evaluation of Chest Pain in the Ambulatory SettingEvaluation of Chest Pain in the Ambulatory Setting
Evaluation of Chest Pain in the Ambulatory Setting
 
Management of hypertension
Management of hypertensionManagement of hypertension
Management of hypertension
 
Anticoagulation in venous thromboembolism
Anticoagulation in venous thromboembolismAnticoagulation in venous thromboembolism
Anticoagulation in venous thromboembolism
 
Hyperglycemic crises and hypoglycemia
Hyperglycemic crises and hypoglycemiaHyperglycemic crises and hypoglycemia
Hyperglycemic crises and hypoglycemia
 
Left Bundle Branch Block (LBBB)
Left Bundle Branch Block (LBBB)Left Bundle Branch Block (LBBB)
Left Bundle Branch Block (LBBB)
 
Non-Astherosclerotic Spontaneous Coronary Dissection
Non-Astherosclerotic Spontaneous Coronary DissectionNon-Astherosclerotic Spontaneous Coronary Dissection
Non-Astherosclerotic Spontaneous Coronary Dissection
 
Make your life worth living
Make your life worth livingMake your life worth living
Make your life worth living
 
First Aid, illustrated & simplified
First Aid, illustrated & simplified First Aid, illustrated & simplified
First Aid, illustrated & simplified
 
Get inspired and motivated
Get inspired and motivated Get inspired and motivated
Get inspired and motivated
 
General Toxicology, All In A Nutshell
General Toxicology, All In A NutshellGeneral Toxicology, All In A Nutshell
General Toxicology, All In A Nutshell
 
ABG, step by step approach (Updated)
ABG, step by step approach (Updated)ABG, step by step approach (Updated)
ABG, step by step approach (Updated)
 

Recently uploaded

For Better Surat #ℂall #Girl Service ❤85270-49040❤ Surat #ℂall #Girls
For Better Surat #ℂall #Girl Service ❤85270-49040❤ Surat #ℂall #GirlsFor Better Surat #ℂall #Girl Service ❤85270-49040❤ Surat #ℂall #Girls
For Better Surat #ℂall #Girl Service ❤85270-49040❤ Surat #ℂall #Girls
Savita Shen $i11
 
ARTHROLOGY PPT NCISM SYLLABUS AYURVEDA STUDENTS
ARTHROLOGY PPT NCISM SYLLABUS AYURVEDA STUDENTSARTHROLOGY PPT NCISM SYLLABUS AYURVEDA STUDENTS
ARTHROLOGY PPT NCISM SYLLABUS AYURVEDA STUDENTS
Dr. Vinay Pareek
 
Evaluation of antidepressant activity of clitoris ternatea in animals
Evaluation of antidepressant activity of clitoris ternatea in animalsEvaluation of antidepressant activity of clitoris ternatea in animals
Evaluation of antidepressant activity of clitoris ternatea in animals
Shweta
 
Non-respiratory Functions of the Lungs.pdf
Non-respiratory Functions of the Lungs.pdfNon-respiratory Functions of the Lungs.pdf
Non-respiratory Functions of the Lungs.pdf
MedicoseAcademics
 
POST OPERATIVE OLIGURIA and its management
POST OPERATIVE OLIGURIA and its managementPOST OPERATIVE OLIGURIA and its management
POST OPERATIVE OLIGURIA and its management
touseefaziz1
 
Physiology of Special Chemical Sensation of Taste
Physiology of Special Chemical Sensation of TastePhysiology of Special Chemical Sensation of Taste
Physiology of Special Chemical Sensation of Taste
MedicoseAcademics
 
24 Upakrama.pptx class ppt useful in all
24 Upakrama.pptx class ppt useful in all24 Upakrama.pptx class ppt useful in all
24 Upakrama.pptx class ppt useful in all
DrSathishMS1
 
Charaka Samhita Sutra sthana Chapter 15 Upakalpaniyaadhyaya
Charaka Samhita Sutra sthana Chapter 15 UpakalpaniyaadhyayaCharaka Samhita Sutra sthana Chapter 15 Upakalpaniyaadhyaya
Charaka Samhita Sutra sthana Chapter 15 Upakalpaniyaadhyaya
Dr KHALID B.M
 
Surat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model Safe
Surat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model SafeSurat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model Safe
Surat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model Safe
Savita Shen $i11
 
Triangles of Neck and Clinical Correlation by Dr. RIG.pptx
Triangles of Neck and Clinical Correlation by Dr. RIG.pptxTriangles of Neck and Clinical Correlation by Dr. RIG.pptx
Triangles of Neck and Clinical Correlation by Dr. RIG.pptx
Dr. Rabia Inam Gandapore
 
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness JourneyTom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
greendigital
 
KDIGO 2024 guidelines for diabetologists
KDIGO 2024 guidelines for diabetologistsKDIGO 2024 guidelines for diabetologists
KDIGO 2024 guidelines for diabetologists
د.محمود نجيب
 
micro teaching on communication m.sc nursing.pdf
micro teaching on communication m.sc nursing.pdfmicro teaching on communication m.sc nursing.pdf
micro teaching on communication m.sc nursing.pdf
Anurag Sharma
 
Prix Galien International 2024 Forum Program
Prix Galien International 2024 Forum ProgramPrix Galien International 2024 Forum Program
Prix Galien International 2024 Forum Program
Levi Shapiro
 
ANATOMY AND PHYSIOLOGY OF URINARY SYSTEM.pptx
ANATOMY AND PHYSIOLOGY OF URINARY SYSTEM.pptxANATOMY AND PHYSIOLOGY OF URINARY SYSTEM.pptx
ANATOMY AND PHYSIOLOGY OF URINARY SYSTEM.pptx
Swetaba Besh
 
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...
VarunMahajani
 
Physiology of Chemical Sensation of smell.pdf
Physiology of Chemical Sensation of smell.pdfPhysiology of Chemical Sensation of smell.pdf
Physiology of Chemical Sensation of smell.pdf
MedicoseAcademics
 
BENIGN PROSTATIC HYPERPLASIA.BPH. BPHpdf
BENIGN PROSTATIC HYPERPLASIA.BPH. BPHpdfBENIGN PROSTATIC HYPERPLASIA.BPH. BPHpdf
BENIGN PROSTATIC HYPERPLASIA.BPH. BPHpdf
DR SETH JOTHAM
 
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Oleg Kshivets
 
BRACHYTHERAPY OVERVIEW AND APPLICATORS
BRACHYTHERAPY OVERVIEW  AND  APPLICATORSBRACHYTHERAPY OVERVIEW  AND  APPLICATORS
BRACHYTHERAPY OVERVIEW AND APPLICATORS
Krishan Murari
 

Recently uploaded (20)

For Better Surat #ℂall #Girl Service ❤85270-49040❤ Surat #ℂall #Girls
For Better Surat #ℂall #Girl Service ❤85270-49040❤ Surat #ℂall #GirlsFor Better Surat #ℂall #Girl Service ❤85270-49040❤ Surat #ℂall #Girls
For Better Surat #ℂall #Girl Service ❤85270-49040❤ Surat #ℂall #Girls
 
ARTHROLOGY PPT NCISM SYLLABUS AYURVEDA STUDENTS
ARTHROLOGY PPT NCISM SYLLABUS AYURVEDA STUDENTSARTHROLOGY PPT NCISM SYLLABUS AYURVEDA STUDENTS
ARTHROLOGY PPT NCISM SYLLABUS AYURVEDA STUDENTS
 
Evaluation of antidepressant activity of clitoris ternatea in animals
Evaluation of antidepressant activity of clitoris ternatea in animalsEvaluation of antidepressant activity of clitoris ternatea in animals
Evaluation of antidepressant activity of clitoris ternatea in animals
 
Non-respiratory Functions of the Lungs.pdf
Non-respiratory Functions of the Lungs.pdfNon-respiratory Functions of the Lungs.pdf
Non-respiratory Functions of the Lungs.pdf
 
POST OPERATIVE OLIGURIA and its management
POST OPERATIVE OLIGURIA and its managementPOST OPERATIVE OLIGURIA and its management
POST OPERATIVE OLIGURIA and its management
 
Physiology of Special Chemical Sensation of Taste
Physiology of Special Chemical Sensation of TastePhysiology of Special Chemical Sensation of Taste
Physiology of Special Chemical Sensation of Taste
 
24 Upakrama.pptx class ppt useful in all
24 Upakrama.pptx class ppt useful in all24 Upakrama.pptx class ppt useful in all
24 Upakrama.pptx class ppt useful in all
 
Charaka Samhita Sutra sthana Chapter 15 Upakalpaniyaadhyaya
Charaka Samhita Sutra sthana Chapter 15 UpakalpaniyaadhyayaCharaka Samhita Sutra sthana Chapter 15 Upakalpaniyaadhyaya
Charaka Samhita Sutra sthana Chapter 15 Upakalpaniyaadhyaya
 
Surat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model Safe
Surat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model SafeSurat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model Safe
Surat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model Safe
 
Triangles of Neck and Clinical Correlation by Dr. RIG.pptx
Triangles of Neck and Clinical Correlation by Dr. RIG.pptxTriangles of Neck and Clinical Correlation by Dr. RIG.pptx
Triangles of Neck and Clinical Correlation by Dr. RIG.pptx
 
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness JourneyTom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
 
KDIGO 2024 guidelines for diabetologists
KDIGO 2024 guidelines for diabetologistsKDIGO 2024 guidelines for diabetologists
KDIGO 2024 guidelines for diabetologists
 
micro teaching on communication m.sc nursing.pdf
micro teaching on communication m.sc nursing.pdfmicro teaching on communication m.sc nursing.pdf
micro teaching on communication m.sc nursing.pdf
 
Prix Galien International 2024 Forum Program
Prix Galien International 2024 Forum ProgramPrix Galien International 2024 Forum Program
Prix Galien International 2024 Forum Program
 
ANATOMY AND PHYSIOLOGY OF URINARY SYSTEM.pptx
ANATOMY AND PHYSIOLOGY OF URINARY SYSTEM.pptxANATOMY AND PHYSIOLOGY OF URINARY SYSTEM.pptx
ANATOMY AND PHYSIOLOGY OF URINARY SYSTEM.pptx
 
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...
 
Physiology of Chemical Sensation of smell.pdf
Physiology of Chemical Sensation of smell.pdfPhysiology of Chemical Sensation of smell.pdf
Physiology of Chemical Sensation of smell.pdf
 
BENIGN PROSTATIC HYPERPLASIA.BPH. BPHpdf
BENIGN PROSTATIC HYPERPLASIA.BPH. BPHpdfBENIGN PROSTATIC HYPERPLASIA.BPH. BPHpdf
BENIGN PROSTATIC HYPERPLASIA.BPH. BPHpdf
 
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
 
BRACHYTHERAPY OVERVIEW AND APPLICATORS
BRACHYTHERAPY OVERVIEW  AND  APPLICATORSBRACHYTHERAPY OVERVIEW  AND  APPLICATORS
BRACHYTHERAPY OVERVIEW AND APPLICATORS
 

Infective Endocarditis

  • 2. Objectives Recognize the current demographic characteristics of older and younger groups of patients with endocarditis to facilitate early diagnosis and treatment strategies. Synthesize the diagnostic criteria and imaging characteristics of endocarditis across a range of patient populations to accurately diagnose this condition. Enumerate important changes to the guideline for endocarditis prophylaxis to reduce inappropriate antibiotic use. Describe the clinical situations in which surgical referral is appropriate to treat endocarditis and reduce mortality.
  • 3. Introduction In 1885, when Osler described the classic clinical presentation of infective endocarditis (IE), rheumatic disease was the most common cause of valve dysfunction and IE usually presented as a chronic condition. Despite great progress in microbiology, diagnostic imaging, and cardiac surgery, the mortality rates for IE remain very high, approaching 30% at 1 year. Several factors have changed the clinical presentation of infective endocarditis over the last several decades, including significant reduction of the incidence of rheumatic valve disease, increased old age life expectancy, increased use of intracardiac devices, increased prevalence of immune-compromised patients (e.g., organ transplantation), ubiquitous availability of echocardiography, and earlier diagnosis.
  • 4. Epidemiology The overall incidence of IE continues to increase, with 11 episodes per 100,000 persons in the year 2000 and 15 episodes per 100,000 persons in 2011. The median age of patients has steadily increased over the last 40 years. Currently, more than one-half of all cases of IE in the United States occur in patients >60 years of age. Only 40 years ago, rheumatic heart disease was the most common cardiac abnormality, being present in more than one-third of patients with IE. However, recent series of IE have reported a rheumatic heart disease prevalence of only 6% in patients presenting with IE. Although IE can involve almost any endocardial surface, there is a clear predilection for bacterial seeding and destruction of the heart valves. It has been estimated that 38% of all cases of IE involve the aortic valve, with 34% involving the mitral valve, 8% involving both the aortic and mitral valves, and 4% involving the tricuspid valve. Congenital heart disease represents the underlying disorder in about 3.5% of all cases. Only three-quarters of patients with infective endocarditis have known underlying heart disease. Several organisms appear capable of infecting apparently normal valves, including S. aureus, some streptococci, Salmonella, Rickettsia, Borrelia, and Candida.
  • 5. Pathogenesis of IE Endothelial damage occurs first, followed by deposition of a platelet-fibrin matrix that permits bacterial colonization. The cycle of bacterial adherence, organism growth, and platelet-fibrin deposition is repeated and again as the vegetation develops. Vegetations occur where blood flow forces are greatest and valvular coaptation contact occurs. This is where endothelial damage is most likely, namely the atrial side of the mitral and tricuspid valves and the ventricular surface of the aortic and pulmonic valves. The initial vegetation is a collection of fibrin and platelets. Microorganisms then adhere to the vegetation and replicate to create extremely high concentrations of bacteria. As the process continues, abscess formation may occur. Valvular destruction leads to progressive regurgitation and perforation of the valve leaflet may occur
  • 6. Microbiology of IE Organisms such as viridans streptococci and S. aureus are more likely to cause endocarditis than are gram-negative rods such as Escherichia coli and Proteus species. The Modified Duke criteria define the following organisms as “Typical”: S. aureus, Viridans streptococci and Streptococcus bovis (S. bovis), Enterococci, HACEK group organisms (Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae). The risk of IE in patients with S. aureus bacteremia is especially high. In addition, S. aureus is associated with a highly destructive form of IE; as such, all patients with S. aureus bacteremia should be clinically evaluated for IE. S. bovis endocarditis is often associated with malignancy of the gastrointestinal (GI) track. The microbiology of prosthetic valve endocarditis (PVE) is often predictable. Staphylococcus epidermidis (S. epidermidis) is a predominant cause of PVE within the first 60 days after surgery (nosocomial source). S. aureus, gram-negative bacilli, diphtheroids, or fungi (particularly the Candida species) are also causes of PVE during this early period that extends up to the first year after cardiac surgery. In contrast, PVE after 1 year usually shares the same infectious organism profile as native valve endocarditis.
  • 7. Epidemiologic factors associated with the development of IE and the commonly associated organisms
  • 8. IE in special patient populations Elderly patients (ages >65 years) have a different clinical course of IE than do younger patients. They have lower rates of embolism, immune- mediate phenomena, and septic complications. They tend to have fewer vegetations with more abscesses but are less likely to undergo cardiac surgery. They have much higher mortality (25% vs. 13% in younger patients). Patients undergoing chronic hemodialysis, especially those with diabetes mellitus, have a significant risk for IE. The predisposing factors in this population include intravascular access, more frequent bacteremia, impairment of the immune system, and calcific valve disease. Since valve thickening and calcification are commonly noted by echocardiography, the early identification of a vegetation can be challenging. Injection drug use is a risk factor for IE, with a prevalence of 2-5% per year. he most common infecting organism in IDU patients is S. aureus (60-90% of cases) with high prevalence of right-sided IE. A prior history of endocarditis is an important predisposing cause for IE. Recurrent endocarditis occurred in 4.5% of one large cohort of patients (excluding IDUs) who survived their initial episode.
  • 9. Prosthetic valve endocarditis (PVE) Having a prosthetic heart valve is the greatest risk for development of IE in most clinical series. 1-3% of all patients with a prosthetic valve will develop IE at 1 year and 3-6% of patients at 5 years. PVE currently accounts for 10-30% of all cases of endocarditis, with S. aureus being the culprit organism in 30% of cases. The early period is generally defined as endocarditis in the first 60 days after heart surgery, and most of the implicated organisms are considered nosocomial. The late period involves organisms more like that of NVE. Although there has been concern that mechanical valves are more susceptible to IE, most series do not suggest a difference in the risk by model, position, or type of valve
  • 10. Prosthetic Vs. Native valve endocarditis Similar presentations but different microbiology. More invasive with higher rates of CHF, conduction abnormalities, and CNS events.
  • 11. Cardiac Implantable Electronic Device Infections In the United States, >300,000 patients have been receiving new cardiac implantable electronic device (CIED) implants every year. The rate of CIED infection has increased, with a report that 1.9 per 1,000 pacemaker devices, and 9.5% of cardiac resynchronization therapy (CRT) devices get infected over 2 years. Currently, CIED IE accounts for 6.4% of all definite IE cases. Most commonly (60% of cases), the infection involves the generator pocket; however, blood stream infection is the only sign of device infection in approximately 40% of cases. The two most common organisms are coagulase-negative staphylococcus followed by S. aureus. Common underlying risk factors include an immune-suppressed state (renal dysfunction, corticosteroid use), oral anticoagulant use, diabetes mellitus, and indwelling hardware.
  • 12. Clinical manifestations of IE Endocarditis is a great mimic and patients may present with a wide variety of symptoms or findings that may involve noncardiac organ systems. Most commonly, the initial symptoms are related to persistent bacteremia with an indolent course from 2 weeks to several months. Symptoms include fever, chills, night sweats, malaise, and weight loss. Less commonly, the initial presentation is congestive heart failure (CHF; e.g., dyspnea and fatigue) due to significant valve dysfunction, or a cardioembolic event such as stroke. Fever is the most common symptom, occurring in >80% of patients with NVE or PVE. Fever is less common in elderly patients, those with CHF, renal failure, severe disability, or previous antibiotic therapy. A murmur of acute or chronic valve dysfunction is present in >80% of patients. Petechiae of the mouth or conjunctivae, splinter hemorrhages within the proximal one-half of the nail bed, and Roth spots by fundoscopy are all likely embolic phenomena. Osler’s nodes are painful nodules on the pads of the fingers and toes. Neurologic symptoms are common and are recognized in ≤50% of patients with IE. Embolic stroke is the most common event. However, intracranial hemorrhage may occur due to a ruptured mycotic aneurysm (MA) or bleeding into a thrombotic stroke territory
  • 13. The modified Duke Criteria
  • 14. Clinical Definition of IE According to the Duke Criteria
  • 15. How to proceed if you suspect IE?
  • 17. Echocardiographic features of IE Findings can provide evidence for IE, including vegetations, leaflet perforation, annular abscess, aneurysm, fistula, and prosthetic valve dehiscence. A vegetation is defined as a discrete echogenic mass adherent to an endocardial surface. The mass is usually irregularly shaped, with a characteristic high- frequency motion described as an oscillation. Vegetations typically occur on the higher-flow upstream surface of valves, but they may also appear on nonvalvular intravascular structures, such as the intraventricular septum and atrial wall, or attached to prosthetic devices (e.g., pacemaker leads). The identification of vegetations on prosthetic material is often difficult by TTE and transesophageal echocardiography TEE is usually required for confirmation. Many vegetations decrease in size (or completely resolve) with appropriate antibiotic therapy. However, some vegetations persist as less mobile structures that become more echogenic with progressive fibrosis and/or calcification. Even after successful antimicrobial therapy, some sterile vegetations may persist indefinitely. Because the frequency of IE among patients with S. aureus bacteremia is reported to be approximately 30%, with many cases not being clinically suspected, TEE should generally be pursued in the setting of S. aureus bacteremia to rule out IE. A recent review identified clinical or transthoracic characteristics associated with low risk of IE (negative predictive values from 93-100%), where TEE may be avoided in patients with S, Aureus bacteremia. These low-risk features included 1) absence of a permanent intracardiac device, 2) sterile follow-up blood cultures within 4 days after the initial set, 3) no hemodialysis dependence, 4) nosocomial acquisition of S. aureus bacteremia, 5) absence of secondary foci of infection, and 6) no clinical signs of IE.
  • 18. Not every mass is a vegetation As stated in the modified Duke Criteria, the presence of a mobile intracardiac mass alone is not sufficient to make a definitive diagnosis of IE. Mobile masses visualized by echocardiography may be related to alternate diagnoses, including Inflammatory mass lesion (Libman-Sacks), sterile vegetations (marantic endocarditis), cardiac tumors (e.g., papillary fibroelastoma), and myxomatous valves with ruptured chordae/papillary muscle head. Several normal intracardiac structures may also mimic the mobile mass of an IE vegetation, including Lambl’s excrescences, Chiari network or a prominent Eustachian valve.
  • 19. Echocardiographic criteria for defining a vegetation Positive features Negative features Low reflectance High echogenicity Attached to valve, upstream side Nonvalvular location Irregular shape, amorphous Smooth surface or fibrillar Mobile, oscillating Nonmobile Associated tissue changes, valvular regurgitation Absence of regurgitation
  • 20. Role of echocardiography in patients with IE
  • 21. Appropriate use criteria of echocardiogram in patients with known or suspected IE.
  • 22. Imaging studies in PVE & NVE
  • 23. Management of an Infected CIED
  • 24. Cardiac CT in IE The use of cardiac CT has evolved as a key adjunctive imaging modality in IE workup. Its strength lies in delineating paravalvular anatomy and complications (abscesses, dehiscence, and fistulae). Cardiac CT has incremental value in evaluating prosthetic valve dysfunction and demonstrating prosthesis-related vegetations, abscesses, or pseudoaneurysms. 2015 ESC guidelines include detection of paravalvular lesions on cardiac CT as a major imaging criterion for IE.
  • 25. 18F-Fluorodeoxyglucose PET/CT in IE Recently, there has been increased utilization of 18F-FDG PET/CT to show regions of metabolic activity or inflammation. PVE remains a diagnostic challenge, and abnormal 18F-FDG PET uptake around the prosthetic valve is now considered a major imaging criterion for IE in the 2015 ESC guidelines for IE. In one study, adding positive FDG PET as a new major criterion significantly increased the sensitivity of the modified Duke Criteria at admission, and allowed for an earlier diagnosis, especially when echocardiography was normal or doubtful.
  • 26. Lab studies in IE Normochromic normocytic anemia, elevated ESR/CRP. WBCs may be normal or elevated in patients with subacute IE. Q-fever IE is diagnosed with an antiphase IgG titer >1:800 for Coxiella burnetii. The presence of red blood cell casts on urinalysis is generally indicative of glomerulonephritis and is a minor diagnostic criterion for IE. A minimum of 3 blood cultures should be obtained over a 1-hour time period to demonstrate persistent bacteremia. Negative blood cultures are seen in approximately 10% of infective endocarditis cases. Of those, approximately 50% had prior therapy with antibiotics. Culture-negative IE can be due to a noninfective endocarditis (Libman-Sacks) in patients with SLE.
  • 27. Causes of culture-negative Endocarditis Prior antibiotics. Fastidious organisms: HACEK, Abiotrophia defectiva, etc., Brucella spp. Non-cultivatable organism: Bartonella Quintana, Coxiella burnetii, Chlamydophila psittaci, Tropheryma whipplei, Legionella spp, Mycoplasma. Fungi. Not IE (Libman-Sacks, myxoma, APLS, marantic, tumor)
  • 29. IE complicated by CHF CHF is the complication of greatest impact on prognosis, in both NVE and PVE. CHF is the most common indication for early surgery in IE. surgical treatment is associated with a 23% mortality rate, compared with a 71% mortality rate with medical therapy. Etiologies: Acute regurgitant lesion, chordal rupture, prosthetic valve dehiscence, fistula creating a shunt or bulky vegetation obstructing a valve. In mild presentations, delaying surgery may be an attractive strategy, especially in elderly patients or those with significant comorbidity who carry an extreme risk of surgical complications.
  • 30. Peri-annular extension of IE Should always be suspected when fever and inflammatory markers do not resolve with appropriate antibiotic therapy. Occurs when bacterial invasion (mostly staphylococci) weakens the periannular tissue and eventually leads to the formation of tissue destruction with abscess, fistula, or valve dehiscence. Complicates ≤40% of NVE and the majority of PVE. In aortic valve IE, an expanding abscess may invade the membranous septum and the AV node causing differing degrees of heart block. Should always be suspected when fever and inflammatory markers do not resolve with appropriate antibiotic therapy. A mortality rate of 40% is seen when it is associated with fistula and a new shunt. With such shunts, surgery is indicated, even in the absence of any hemodynamic instability. A very limited number of cases with are suitable for medical therapy alone, and these include abscess <1 cm, an isolated organism that is drug-sensitive, and the absence of any evidence of valve destruction or heart block. Otherwise, surgery should not be delayed.
  • 31. Systemic embolization in IE Dislodgment and embolization of a thrombus, vegetation, or friable necrotic tissue is the most common complication during IE. Risk factors: previous embolism, first 2 weeks of Abx therapy, left sided IE (Mitral>Aortic), specific organisms (S. aureus, fungi, enterococci, HACEK), and large mobile mitral vegetations >15 mm. CNS is the most frequent clinically apparent site (65%), with 90% of affecting the middle cerebral artery territory. No vascular bed is immune from potential cardioemboli. Can lead to distal infarctions, abscesses (almost always with S. aureus) or rarely mycotic aneurysms. The 2014 ACC/AHA guidelines recommend surgery as a class IIa indication only for those with recurrent emboli and persistent vegetations after antibiotic therapy. The 2015 ESC guidelines recommend urgent surgery as a class IIb indication for vegetations >15 mm and no other indications for surgery. For right-sided IE, surgery is not indicated for simple pulmonary emboli but may be appropriate for pulmonary abscess formation. Mycotic aneurysms occur as a result of microembolization into the vasa vasora of blood vessel walls. Branch point vessels are the most affected and, unfortunately, this most frequently occurs within intracranial vessels. The mortality rate for a ruptured intracranial MA approaches 80% and there is no accurate way to predict MA rupture. Intracranial MAs should be surgically ligated or treated by endovascular techniques.
  • 32. Acute renal failure in IE Occurs in 30% of cases of IE and indicates a poor prognosis. Many factors may contribute to acute renal failure, including immune complex glomerulonephritis, embolic renal infarcts, multiorgan failure associated with CHF or sepsis syndrome, and Interstitial nephritis secondary to antibiotics (especially gentamicin and vancomycin). Acute renal dysfunction is often reversible. However, renal replacement therapy may be required during the acute phase illness. Changes in renal function must be considered for appropriate dosing of antibiotic therapy.
  • 33. Chronic complications of IE Survivors of IE who are discharged from the hospital have an increased risk of ischemic stroke, hemorrhagic stroke, myocardial infarction, readmission for heart failure, ventricular arrhythmia, sudden death, and all-cause death when compared with an age-matched cohort. Risk factors for repeat IE include older age, male sex, drug abuse, and valve replacement.
  • 34. General principles for treatment of IE Microbiologic eradication, whether achieved medically or surgically, is pivotal for successful treatment. Antimicrobial therapy generally requires administration of high doses of bactericidal drugs, for at least 4 weeks through a parenteral route. The choice of specific antimicrobials should be made while considering the following: Prior antibiotic treatment, Diagnosis of NVE, early PVE, or late PVE; and Epidemiologic clues for pathogens and/or antibiotic resistance. Except for staphylococcal infections, fever should resolve within days of starting therapy, and all patients should have surveillance blood cultures obtained after 3-4 days of IV drug therapy. After culture results are available, antibiotics should be modified, based on the sensitivity of the organism to the antimicrobial and the MIC of the drug to the pathogen. This is particularly important with vancomycin therapy. Bactericidal combinations are preferred to monotherapy against tolerant bacteria. For example, aminoglycosides synergize with B-lactams and glycopeptides to enhance their efficacy and shorten their required duration of therapy. (N.B: 2015 ESC guidelines stated that aminoglycosides are no longer recommended in Staph NVE). Slow-growing/dormant microbes in vegetations and/or biofilms justify the need for rifampicin added to the regimen, and for prolonged periods. PVE and device-related IE should have a much lower threshold for surgery compared with NVE. In the setting of generator pocket infection, lead infection or endocarditis, complete and early removal of the device is recommended. Prolonged (6 weeks) antibiotic therapy is recommended, and a new device implantation should be delayed for 72h after repeat blood cultures remain negative. Right-sided S. aureus, IE in IDU has 85% cure rate with antibiotics alone, with a short course of IV or oral treatment (2-4 w). Surgical treatment of right-sided endocarditis is only limited to persistent bacteremia (>7 days) despite antibiotics or vegetations (>20 mm) after recurrent pulmonary emboli.
  • 36. Indications for surgery in IE Surgical treatment is used in approximately half of infective endocarditis patients because of severe complications. Congestive heart failure is the primary reason for surgical intervention. Other indications for surgery are extensive valvular destruction, large vegetations, paravalvular abscess, ineffective antimicrobial therapy, recurrent emboli on antibiotic therapy, or the presence of a highly resistant organism. Surgical management of infective endocarditis has the following objectives: completely excise all infected and necrotic tissue, remove and/or replace all infected prosthetic material, and reconstruct cardiac structures to restore proper physiology.
  • 39. Prophylaxis against IE Only indicated in certain cardiac conditions associated with the highest risk of adverse outcomes from IE. These conditions include cardiac transplant recipients who develop cardiac valvulopathy, prosthetic cardiac valve or prosthetic material used for cardiac valve repair, previous IE and certain congenital heart diseases (Unrepaired cyanotic disease including palliative shunts and conduits, completed repair during the first 6 months after the procedure, and repaired disease with residual defect). Reasonable for all dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. Not recommended for patients who undergo GU or GI tract procedure.
  • 40. Pearls for the boards Only patients at the highest risk of complications from infective endocarditis require prophylaxis. Major clinical criteria for the diagnosis of infective endocarditis include multiple positive blood cultures and echocardiographic evidence of endocardial involvement. Patients with infective endocarditis and embolic CNS events should hold anticoagulation. Intracardiac device infections require complete removal of the device, including generator and leads.
  • 41. A 33-year-old man is admitted with a 1-week history of fever and shortness of breath. He has a history of intravenous drug use. On examination, he has a temperature of 102.5 degrees Fahrenheit, a heart rate of 110 bpm, and a blood pressure of 102/60 mm Hg. He appears mildly dyspneic and diaphoretic. His jugular venous pressure is 10 cm H20. His lungs have bibasilar rales. His cardiac exam demonstrates a hyperdynamic precordium with a soft systolic murmur and S3 gallop. His extremities are warm without edema. His echocardiogram on admission shows a left ventricular ejection fraction of 75%, a 1 cm vegetation on the tricuspid valve with moderate to severe tricuspid regurgitation and thickening of the mitral valve with severe mitral regurgitation. His chest X-ray shows pulmonary edema. He is admitted to telemetry. Serial blood cultures are sent, and intravenous vancomycin is started. What is the next best step in the management of this patient? A. Intra-aortic balloon counterpulsation. B. Urgent valve replacement. C. Repeat transesophageal echocardiogram in 6 weeks. D. Initiation of sacubitril/valsartan. E. Addition of rifampin.
  • 42. A 29-year-old woman is referred by her internist for evaluation of a newly identified murmur. The patient reports no cardiovascular symptoms and has no significant medical history except for a known penicillin allergy. Her only prescribed medicine is an oral contraceptive. She denies recreational drug use. On physical examination, there is a systolic click followed by a grade 2/6 late systolic murmur. Her transthoracic echocardiogram demonstrates myxomatous mitral valve disease with moderate regurgitation and mild left atrial enlargement. The left ventricular end-systolic dimension is 32 mm and ejection fraction is 65%. Which of the following is required prior to dental procedures in this patient? A. No antibiotic prophylaxis. B. Clindamycin 600 mg. C. Cephalexin 2 g. D. Amoxicillin 2 g. E. Metronidazole 500 mg.
  • 43. A 34-year-old man is admitted with a fever. He has felt poorly for several months. He has had a 10-lb weight loss and recurring night sweats. In the past few weeks, he has experienced progressive dyspnea. He is on no medications at this time. His social history includes ongoing intravenous drug use. His temperature is 38.5° Celsius, heart rate is 103 bpm, blood pressure is 95/50 mm Hg, and resting oxygen saturation on room air is 96%. His lungs reveal bibasilar fine rales. His jugular venous pressure is not elevated. His apex is hyperdynamic, and there is a grade 2/6 systolic murmur and grade 2/4 diastolic murmur along the left sternal border. The first heart sound (S1) is soft and there is an S3. He has no edema. There are splinter hemorrhages under the nailbeds on his left fingers. His echocardiogram reveals a hyperdynamic left ventricle with evidence for severe aortic regurgitation (AR) and vegetations on his aortic valve In addition to broad spectrum antibiotics, which of the following is the most appropriate next step in the management of this patient? A. Aortic valve replacement. B. Intravenous esmolol 0.1 mg/kg/min. C. Intra-aortic balloon pump. D. Phenylephrine 40 mcg/min. E. Transesophageal echocardiogram.
  • 44. A 48-year-old man with a history of myxomatous valve disease and moderate mitralregurgitation (MR) on echocardiogram presents today for his annual reassessment. He has a history of hyperlipidemia and remote endocarditis. He feels well and rides his road bike most days of the week without limiting symptoms. His exam is notable for a heart rate 52 bpm, blood pressure of 118/74 mm Hg, and pulse oximetry of 98%. His lungs are clear without rales. His cardiac exam reveals a soft, late systolic murmur at the apex. There is no lower extremity edema. Which of the following would be recommended for this patient? A. Antibiotics prior to dental cleaning. B. Aspirin 81 mg daily. C. Cardiac magnetic resonance imaging. D. Transesophageal echocardiogram. E. Losartan 25 mg daily.
  • 45. References • Baddour LM, Wilson WR, Bayer AS, et al.; American Heart Association Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and Stroke Council. Infective endocarditis in adults: diagnosis, antimicrobial therapy, and management of complications: a scientific statement for healthcare professionals from the American Heart Association. Circulation 2015;132:1435-86. • Nishimura RA, Otto CM, Bonow RO, et al.; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63:e57-185. • Habib G, Lancellotti P, Antunes MJ, et al.; ESC Scientific Document Group. 2015 ESC guidelines for the management of infective endocarditis: The Task Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM). Eur Heart J 2015;36:3075-128. • Armstrong, W. F., Ryan, T., & Feigenbaum, H. (2018). Feigenbaum's echocardiography (8th ed.): Wolters Kluwer Health/Lippincott Williams & Wilkins. • Douglas PS, Khandheria B, Stainback RF, et al.; American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Criteria Working Group; American Society of Echocardiography; American College of Emergency Physicians; American Society of Nuclear Cardiology; Society for Cardiovascular Angiography and Interventions; Society of Cardiovascular Computed Tomography; Society for Cardiovascular Magnetic Resonance; American College of Chest Physicians; Society of Critical Care Medicine. ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2007 appropriateness criteria for transthoracic and transesophageal echocardiography: a report of the American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Criteria Working Group, American Society of Echocardiography, American College of Emergency Physicians, American Society of Nuclear Cardiology, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, and the Society for Cardiovascular Magnetic Resonance endorsed by the American College of Chest Physicians and the Society of Critical Care Medicine. J Am Coll Cardiol 2007;50:187-204.