Infective Endocarditis

Infective Endocarditis
Dr. Meral SÖNMEZOĞLU Infectous Diseases Department YEDİTEPE UNIVERSITY HOSPITAL

Learning Objectives Recognize the risk factors, signs, and symptoms of infectious endocarditis. Understand the many approaches to diagnosing infectious endocarditis. Appreciate the necessity of rapid treatment. Anticipate possible complications. Know the indications for prophylaxis of infective endocarditis

Infective Endocarditis
Infective endocarditis (IE) is a deadly disease. Despite improvements in its management, IE remains associated with high mortality and severe complications

Definition IE should be suspected in a variety of very different clinical situations. It may present as an acute, rapidly progressive infection, but also as a subacute or chronic disease with low-grade fever and non-specific symptoms that may mislead or confuse initial assessment.

Definition Up to 90% of patients present with fever, often associated with systemic symptoms of chills, poor appetite and weight loss. Heart murmurs are found in up to 85% of patients. Up to 25% of patients have embolic complications at the time of diagnosis. Therefore IE has to be suspected in any patient presenting with fever and embolic phenomena.

Definition Infectious Endocarditis (IE): an infection of the heart’s endocardial surface Classified into four groups: Native Valve IE Prosthetic Valve IE Intravenous drug abuse (IVDA) IE Nosocomial IE (HCA- IE) 1/3

Sites of lesions Mitral Valve: 85% (Left atrium/ventricle)
Common site for Strep viridans group Aortic valve: 55% (Left ventricle) Emboli would effect systemic organs brain, kidneys, spleen Tricuspid valve: 20% (Right atrium/ventricle) Common site for IV drug users (Staph. spp) Emboli to lung Pulmonary valve: 1% (Right ventricle)

European Heart Journal (2015)

Classification Native valve endocarditis (NVE), acute and subacute
Prosthetic valve endocarditis (PVE), early and late Intravenous drug abuse (IVDA) endocarditis Other terms commonly used to classify types of IE include pacemaker IE and nosocomial IE (NIE).

Further Classification
Acute Affects normal heart valves Rapidly destructive Metastatic foci Commonly Staph. If not treated, usually fatal within 6 weeks Subacute Often affects damaged heart valves Indolent nature If not treated, usually fatal by one year

Further Classification
Acute Rapid progression of symptoms Less than 6 weeks duration Significant systemic signs/symptoms Fever Elevated systemic WBC/ left shift Subacute Slower, more chronic progression of symptoms Low grade fevers Vague clinical signs/symptoms weakness, anorexia, malaise,etc.

Acute NVE Frequently involves normal valves and usually has an aggressive course. Rapidly progressive illness in persons who are healthy or debilitated Virulent organisms, S aureus and group B streptococci are typically the causative agents

Subacute NVE Typically affects only abnormal valves.
Its course, even in untreated patients, is usually more indolent than that of the acute form and may extend over many months. Alpha-hemolytic streptococci or enterococci, usually in the setting of underlying structural valve disease

PVE Diagnosis is more difficult in PVE than in NVE.
Clinical presentation is frequently atypical, particularly in the early postoperative period, in which fever and inflammatory syndromes are common in the absence of IE. Persistent fever should trigger the suspicion of PVE.

PVE As in NVE, diagnosis of PVE is based mainly on the results of echocardiography and blood cultures. However, both are more frequently negative in PVE. Although TOE is mandatory in suspected PVE, its diagnostic value is lower than in NVE.

PVE A negative echocardiogram is frequently observed in PVE and does not rule out the diagnosis, but identification of a new periprosthetic leak is a major criterion CT or nuclear imaging is useful In PVE, staphylococcal and fungal infections are more frequent and streptococcal infection less frequent than in NVE.

PVE Staphylococci, fungi and Gram-negative bacilli are the main causes of early PVE, Staphylococci, oral streptococci, S. bovis and enterococci most frequent organisms of late PVE (community-acquired infections). Staphyloccoci and enteroccoci are the most common agents in prosthetic valve implantation endocarditis.

PVE The Duke criteria are helpful for the diagnosis of NVE (70–80%), but are less useful in PVE Nuclear techniques, particularly 18F-FDG PET/CT useful for the diagnosis of PVE An algorithm for evaluation of patients with suspected PVE, including echocardiography and PET/CT has been suggested

Early PVE Early PVE occurs within 60 days of valve implantation.
Traditionally, coagulase-negative staphylococci, gram-negative bacilli, and Candida species have been the common infecting organisms.

Late PVE Early PVE is defined as IE occurring within 1 year of surgery
Late PVE as IE occurring beyond 1 year, because of significant differences between the microbiological profiles

Pathophysiology Turbulent blood flow disrupts the endocardium making it “sticky” Bacteremia delivers the organisms to the endocardial surface Adherence of the organisms to the endocardial surface Eventual invasion of the valvular leaflets IE often occurs when there is an underlying cardiac abnormality that creates a high-low pressure gradient. The resultant turbulent blood flow disrupts the endocardial surface by peeling away the endothelium. The body’s natural response to endothelial damage is to repair it by laying down a sticky platelet-fibrin meshwork, which is a nidus for infection. Temporary bacteremia delivers the offending organism to the endocardial surface where is sticks to the platelet-fibrin meshwork. This festers into an infection that eventually invades the cardiac valves. The pathophysiology is slightly different with IVDA. It has been postulated that repeated injections of drugs and particulate material causes microtrauma to the cardiac valves, thereby starting the infection cascade.

Pathophysiology Formation of Non-Bacterial Thrombotic Endocarditis (NBTE) on surface of cardiac valve or site of endothelial damage Turbulent blood flow from certain congenital cardiac lesions traumatizes endothelium Traumatized endothelium predisposed to deposition of platelets and fibrin on endothelial surface resulting in NBTE Bacteremia with potentially pathogenic organism Adherence of bacteria in bloodstream to NBTE Proliferation of bacteria within a vegetation

Pathophysiology

Infectious Endocarditis Affecting the Mitral Valve:
Destruction of the Mitral Valve Fibrin Due to Haemophilus parainfluenzae Bacterial Infection

Pathogenesis Multiple independent pathophysiological processes
“Trauma” of the heart surfaces Platelet/fibrin deposition over traumatized tissue (non-bacterial thrombotic endocarditis) “Bacteremia” subsequent infection of the platelet/fibrin deposition (Bacterial endocarditis) Bacterial multiplication (10 9,10 cfu/gram of tissue)

Causes of Bacteremia Dental: Diagnostic Procedures
Procedures -Flossing/brushing Diagnostic Procedures Respiratory Bronchoscopy G.I. Barium enema Colonoscopy Genitourinary Prostatectomy

Epidemiology Incidence difficult to ascertain and varies according to location 3-9: in industrial countries Occurs in 1:1000 hospital admission Much more common in males than in females (2:1) May occur in persons of any age and increasingly common in elderly Mortality ranges from 20-30% There is an estimated 10-15,000 new cases of IE diagnosed in the U.S. each year, although the exact incidence of IE is difficult to ascertain. IE is a relatively uncommon disease, is not a reportable disease, and different case definitions have existed throughout the years. Furthermore, the incidence varies greatly depending on geographic regions. IE is more common among males. The male:female ratio varies from 2:1 to 9:1 depending on the source. In the past, IE was a disease of children and young adults. It predominantly affected children with congenital heart disease and adults with rheumatic heart disease. Today, IE commonly affects the elderly, with almost 50% of cases in the U.S. occurring in patients over the age of 60. This may be due to the decreasing incidence of rheumatic heart disease and the increasing proportion of elderly in the U.S. Mortality from IE remains high, and ranges from 20-30% despite newer antibiotics and surgical options.

Risk Factors Intravenous drug abuse
Artificial heart valves and pacemakers Acquired heart defects Calcific aortic stenosis Mitral valve prolapse with regurgitation Congenital heart defects Intravascular catheters The top three risk factors for IE include, IVDA, prosthetic heart valves, and structural heart disease. IVDA – one large study of IVDAs found that the use of cocaine was associated with a higher risk of IE than other injectable drugs. The most significant risk factor for right-sided IE is IVDA, although left sided disease is quite common among IVDAs. The most common infecting organism is clearly S. aureus, particularly in right-sided infection. Prosthetic valve IE comprises a small proportion of all cases of IE and occurs in only 1% of all patients with artificial heart valves. The greatest risk is in the first year following valve replacement. Structural heart disease – approximately ¾ of all cases of IE occur in patients with preexisting structural heart abnormalities. The most common underlying heart abnormalities include mitral valve prolapse with mitral regurgitation and aortic stenosis. The most common congenital heart defects include Tetralogy of Fallot, bicuspid aortic valves, coarctation of the aorta, VSDs, and patent ductus arteriosus. In general, the higher the gradient of the valvular insufficiency, the higher the risk of IE. One of the greatest risk factors of all is a prior episode of IE. Some studies have documented recurrence as high as 9%.

Risk Factors Rheumatic heart disease
Currently accounts for 20-25% of cases Prosthetic heart valves 12-33% of cases: Staph common if IE occurs within 1 year of surgery; surgery required to replace infected material IV drug use Staph spp. most commonly isolated Intravenous catherization/shunt procedures Congenital heart defects patent ductus arteriosus, intraventricular shunts, etc Degenerative cardiac lesions The top three risk factors for IE include, IVDA, prosthetic heart valves, and structural heart disease. IVDA – one large study of IVDAs found that the use of cocaine was associated with a higher risk of IE than other injectable drugs. The most significant risk factor for right-sided IE is IVDA, although left sided disease is quite common among IVDAs. The most common infecting organism is clearly S. aureus, particularly in right-sided infection. Prosthetic valve IE comprises a small proportion of all cases of IE and occurs in only 1% of all patients with artificial heart valves. The greatest risk is in the first year following valve replacement. Structural heart disease – approximately ¾ of all cases of IE occur in patients with preexisting structural heart abnormalities. The most common underlying heart abnormalities include mitral valve prolapse with mitral regurgitation and aortic stenosis. The most common congenital heart defects include Tetralogy of Fallot, bicuspid aortic valves, coarctation of the aorta, VSDs, and patent ductus arteriosus. In general, the higher the gradient of the valvular insufficiency, the higher the risk of IE. One of the greatest risk factors of all is a prior episode of IE. Some studies have documented recurrence as high as 9%.

Infecting Organisms Common bacteria Not so common bacteria S. aureus
Streptococci Enterococci Not so common bacteria Fungi Pseudomonas HACEK Staphlococcal and Streptococcal organisms comprise over 80% of all infecting organisms.

Gram-Negatives All Rare
Streptococci Alpha-hemolytic Most common Beta-hemolytic Uncommon Enterococci Rare Pneumococci Rare Staphylococci S. aureus Second most common Coagulase negative Uncommon, but increasing Gram-Negatives All Rare Enterics, Pseudomonas species, Haemophilus, Actinobacillus,Cardiobacterium, Eikenella, Kingella, Neisseria sp Fungi Candida species Uncommon Others Rare

Infecting Organisms Overall, S aureus infection is the most common cause of IE, including PVE, acute IE, and IVDA IE. Approximately % of staphylococcal bacteremias are complicated by IE. More than half the cases are not associated with underlying valvular disease.

IE: Infecting organisms
Bacterial(80-90% of all causes due to strep & staph species) Streptococci: 55-60% Viridans strep: Strep species normally found in mouth Strep sanguis, oralis, salivarius, or mutans Rarely caused by Group A, B, C, strep

Staph. species: accounts for 20-35% of all bacterial causes Staph aureus: (coagulase positive staph) Coagulase is an enzyme capable of causing serum proteins to clot. A. Most common bacteria isolated from IV drug users B. Most common staph species isolated from I.E. infections C. Mortality is approximately 40% D. Therapy duration based on presence/absence of prosthetic material and antibiotic sensitivity

Staph epidermidis: (coagulase-negative) A. Most common staph species in patients with prosthetic valves and in neonates B. Often presents as subacute IE (SBE) Gram Negative Bacteria HACEK group: Hemophilus spp., Actinobacillus spp, Cardiobacterium spp, Eikenella spp, Kingella spp. Miscellaneous Gram Negative Organisms: Typical gram negative bacilli (E. coli, Klebsiella, etc) A. Frequently part of polymicrobial infections B. IV drug users or patients with prosthetic material C. High mortality rate: >65%

Symptoms Acute Subacute High grade fever and chills SOB
Arthralgias/ myalgias Abdominal pain Pleuritic chest pain Back pain Subacute Low grade fever Anorexia Weight loss Fatigue Arthralgias/ myalgias Abdominal pain N/V The onset of symptoms is usually ~2 weeks or less from the initiating bacteremia

Signs Fever Heart murmur
Nonspecific signs – petechiae, subungal or “splinter” hemorrhages, clubbing, splenomegaly, neurologic changes More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots

Petechiae Nonspecific Often located on extremities or mucous membranes
dermatology.about.com/.../ blpetechiaephoto.htm Harden Library for the Health Sciences hardin/ md/cdc/3184.html Photo credit, Josh Fierer, M.D. medicine.ucsd.edu/clinicalimg/ Eye-Petechiae.html

Splinter Hemorrhages Nonspecific Nonblanching
Subungal hemorrhages that extend the entire length of the nail or are primarily located at the proximal end of the nail (near the cuticle) are like due to trauma. Nonspecific Nonblanching Linear reddish-brown lesions found under the nail bed Usually do NOT extend the entire length of the nail

Splinter Hemorrhages

Osler’s Nodes More specific Painful and erythematous nodules
American College of Rheumatology webrheum.bham.ac.uk/.../ default/pages/3b5.htm Hand10/Hand10dx.html More specific Painful and erythematous nodules Located on pulp of fingers and toes More common in subacute IE

Janeway Lesions More specific Erythematous, blanching macules
Nonpainful Located on palms and soles

Roth spot •Non-specific for endocarditis, but
•“White-centered" hemorrhages, originally described in patients with bacterial endocarditis. •Non-specific for endocarditis, but discovering them in a patient who has other suggestive features of endocarditis constitutes strong support for the diagnosis

The Essential Blood Test
Blood Cultures Minimum of three blood cultures1 Three separate venipuncture sites Obtain 10-20mL in adults and 0.5-5mL in children2 Positive Result Typical organisms present in at least 2 separate samples Persistently positive blood culture (atypical organisms) Two positive blood cultures obtained at least 12 hours apart Three or a more positive blood cultures in which the first and last samples were collected at least one hour apart If you suspect the pt has subacute IE or is not critically ill, then the three samples can be collected over hours and antibiotics can be held until all three samples have been drawn. However, if the pt is acutely ill, critical, or unstable, the three cultures should be obtained over a 1 hour time span before beginning empiric therapy. There is no need to collect anaerobic blood cultures since virtually all cases of IE are caused by aerobic organisms. There is little additional diagnostic yield to collecting more than three blood cultures unless the pt was previously on antibiotics. In one study of 206 cases of IE, the initial blood culture was positive in 96% of streptococcal IE and one of the first two cultures were positive 98% of the time. For pt’s with IE cause by organisms other than strep, one of the first two blood culture was positive in 100% of the cases. The estimated diagnostic yield of a blood culture increases by about 3% per mL of blood cultured. One study found that the detection rate for bacteremia increased from 69% to 92% when at least 5mL of blood were used for culture. The most common cause of negative cultures in patients with IE is prior antibiotic use.

Additional Labs CBC ESR and CRP Complement levels (C3, C4, CH50) RF
Urinalysis Baseline chemistries and coags CBC – Look for a normochromic normocytic anemia and/or a leukocytosis. ESR and CRP - Look for an elevated erythrocyte sedimentation rate and/or an elevated C-reactive protein which are present % of the time. RF - Occasionally there will be an elevated levels of Rheumetoid Factor, particularly in patients who have been infected for six weeks or more. (Minor Duke’s Criteria) UA - Urinalysis may reveal microscopic or gross hematuria, proteinuria, and pyuria. These findings along with a low serum complement level indicate a glomerulonephritis or “immunologic phenomena”. (Minor Duke’s Criteria)

Imaging Chest x-ray EKG Echocardiography
Look for multiple focal infiltrates and calcification of heart valves EKG Rarely diagnostic Look for evidence of ischemia, conduction delay, and arrhythmias Echocardiography CXR – A chest xray can contain multiple diagnostic clues such as calcification of heart valves, which should raise suspicion in a febrile patient without an obvious source. More commonly, the chest xray may reveal septic pulmonary emboli in a patient with right-sided IE (Minor Duke’s Criteria). EKG – An EKG alone cannot diagnose IE but it may show evidence of some of the disease’s complications. For example, EKG with ST changes may indicate ischemia or infarction from septic emboli. Arrhythmias such as heart block may indicated extension of the infection from the valves into the septum and surrounding cardiac tissue.

Indications for Echocardiography
Transthoracic echocardiography (TTE) First line if suspected IE Native valves Transesophageal echocardiography (TEE) Prosthetic valves Intracardiac complications Inadequate TTE Fungal or S. aureus or bacteremia TTE and TEE are complementary for evaluating cardiac hemodynamics and anatomy, but TEE has superior sensitivity, especially in detecting native valve vegetations, prosthetic valve vegetations, and local extension of infection. However, it is significantly more expensive and invasive. If there is any suspicion of IE, get a TTE. If there is staph or fungal bacteremia, a TEE should probably be obtained. If there is a high clinical suspicion for IE and the TTE is negative, you should proceed to a TEE. If there is a concern for intracardiac complications, a TEE is warranted. It’s important to remember that the negative predictive value of a TEE is between 96-98%, meaning that a TEE cannot definitively rule out endocarditis. If the initial TEE is negative in a patient with a high clinical suspicion for IE, a repeat examiniation should be done if the pt does not improve.

Making the Diagnosis Pelletier and Petersdorf criteria (1977)
Classification scheme of definite, probable, and possible IE Reasonably specific but lacked sensitivity Von Reyn criteria (1981) Added “rejected” as a category Added more clinical criteria Improved specificity and clinical utility Duke criteria (1994) Included the role of echocardiography in diagnosis Added IVDA as a “predisposing heart condition” Pelletier and Petersdorf criteria – 3 case categories: Definite – histologic evidence of endocardial vegetations on examination of tissue Probable - uniformly positive blood cultures with know underlying heart disease or embolic phenomena OR negative blood cultures in pts with fever, new regurgitant valvular heart murmur, and embolic phenomena Possible - uniformly positive blood cultures with know underlying heart disease or embolic phenomena OR negative blood cultures with fever and known underlying heart disease and embolic phenomena Von Reyn criteria – modified the above criteria to improve specificity and clinical utility. Duke Criteria – relies upon major and minor clinical and pathologic criteria to classify cases as definite, possible, and rejected

Modified Duke Criteria
Definite IE Microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or intracardiac abscess Histologic evidence of vegetation or intracardiac abscess Possible IE 2 major 1 major and 3 minor 5 minor Rejected IE Resolution of illness with four days or less of antibiotics Multiple studies have validated the Duke criteria. When applied and reapplied over the entire evaluation, these criteria are sensitive and specific and very rarely erroneously reject a true endocarditis.

dIAGNOSIS

Diagnosis of endocarditis is usually based on
clinical, microbiologic, and echocardiographic findings.

Criteria for consideration of IE

Indications for ECHO

Treatment Treatment involves antimicrobial therapy targeted to the identified organism. Surgical indications include heart failure, uncontrolled infection, and prevention of embolic events.

Treatment Parenteral antibiotics Surgery Surveillance blood cultures
High serum concentrations to penetrate vegetations Prolonged treatment to kill dormant bacteria clustered in vegetations Surgery Intracardiac complications Surveillance blood cultures

Treatment Multiple agents common due to synergy
Duration of therapy commonly 4-6 weeks Quick access to cardiothoracic surgery MIC’s/MBC’s determined for pathogens Effects drug selection, need for combination therapy Uncertain role for Schlicter test Unique Aminoglycoside “therapeutic” range AG’s dosed at 1mg/kg IV q 8hours; Peaks of 3 acceptable

Fungal IE Fungi are most frequently observed in PVE and in IE affecting IVDAs and immunocompromised patients. Candida and Aspergillus spp. predominate, the latter resulting in BCNIE. Mortality is very high (50%), and treatment necessitates dual antifungal administration and valve replacement. Most cases are treated with various forms of Amphotericin B with or without azoles, recent case reports describe successful therapy with the new echinocandin caspofungin

Cure rates for NVE For S viridans and S bovis infection, the rate is 98%. For enterococci and S aureus infection in individuals who abuse intravenous drugs, the rate is 90%. For community-acquired S aureus infection in individuals who do not abuse intravenous drugs, the rate is 60-70%. For infection with aerobic gram-negative organisms, the rate is 40-60%. For infection with fungal organisms, the rate is lower than 50%.

Cure rates for NVE Rates are 10-15% lower for each of the above categories, for both early and late PVE. Surgery is required far more frequently. Approximately 60% of early CoNS PVE cases and 70% of late CoNS PVE cases are curable.

Monitoring for complications
Valvular dysfunction, usually insufficiency of the mitral or aortic valves Myocardial or septal abscesses Congestive heart failure Metastatic infection Embolic phenomenon Organ dysfunction resulting from immunological processes

Complications Four etiologies Embolic Local spread of infection
Metastatic spread of infection Formation of immune complexes – glomerulonephritis and arthritis

Embolic Complications
Occur in up to 40% of patients with IE Predictors of embolization Size of vegetation Left-sided vegetations Fungal pathogens, S. aureus, and Strep. Bovis Incidence decreases significantly after initiation of effective antibiotics Systemic emboli are among the most common complications of IE, occurring in up to 40% of patients. Subclinical emboli are often found on autopsy.

Embolic Complications
Stroke Myocardial Infarction Fragments of valvular vegetation or vegetation-induced stenosis of coronary ostia Ischemic limbs Hypoxia from pulmonary emboli Abdominal pain (splenic or renal infarction)

Septic Pulmonary Emboli

Septic Retinal Embolus

Local Spread of Infection
Heart failure Extensive valvular damage Paravalvular abscess (30-40%) Most common in aortic valve, IVDA, and S. aureus May extend into adjacent conduction tissue causing arrythmias Higher rates of embolization and mortality Pericarditis Fistulous intracardiac connections

Local Spread of Infection
Acute S. aureus IE with perforation of the aortic valve and aortic valve vegetations. Acute S. aureus IE with mitral valve ring abscess extending into myocardium.

Metastatic Spread of Infection
Metastatic abscess Kidneys, spleen, brain, soft tissues Meningitis and/or encephalitis Vertebral osteomyelitis Septic arthritis

Complications requiring surgery
Infected prosthetic material: less than 1 year out from original heart surgery Refractory congestive heart failure (Leading cause of death) Unresponsive infection/ continued infection despite appropriate antibiotics Pt. experiences more than 1 major emboli

TUS 2012 Yüksek ateş şikâyetiyle başvuran 67 yaşındaki erkek hastada enfektif endokardit tanısı konulmuştur. Kan kültürlerinde Streptococcus bovis üreyen bu hastada aşağıdaki kanserlerden hangisinin taranması gerekir? A) Meme kanseri B) Prostat kanseri C) Kolon kanseri D) Perikardiyal mezotelyom E) Akciğer kanseri

TUS 2010 Aşağıdakilerden hangisi en sık karşılaşılan doğal kapak endokardit etkenidir? A) Koagülaz negatif stafilokoklar B) Pnömokoklar C) Mantarlar D) Enterokoklar E) Streptokoklar

TUS 2013 Aşağıdakilerden hangisi, enfektif endokardit tanısında kullanılan Duke kriterleri içerisinde minör kriterlerden biri olarak yer almaz? A) Yüksek ateş (≥38 °C) B) Osler nodülleri C) Roth lekeleri D) Janeway lezyonları E) Eritema marginatum

Infective Endocarditis

Similar presentations

Presentation on theme: "Infective Endocarditis"— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

Infective Endocarditis

Similar presentations

Presentation on theme: "Infective Endocarditis"— Presentation transcript:

Similar presentations

About project

Feedback