APP 1 Flashcards
1
Q
Name three types of intravascular infections?
A
-Infection of an artery (endarteritis)
-Endothelial site in the heart (endocarditis)
-The lumen of a vein (phlebitis).
2
Q
True or false, many microorganisms gain entry to the intravascular space and are passively carried throughout the circulatory system, either suspended in plasma or within various cellular components of blood. Usually, entry of microorganisms into the circulation represents a brief phase of an infection centered primarily in another organ system.
A
True
3
Q
Which three microbes produce disease by adhering to erythrocytes?
A
-Plasmodium species (the cause of malaria)
-Babesia microti (the cause of babesiosis)
-Bartonella bacilliformis (the agent of Oroya fever)
4
Q
How does infective phlebitis usually occur?
A
Infective phlebitis occurs mainly by direct spread when there is an adjacent focus of infection or when intravascular foreign bodies, such as catheters, implanted in veins become infected. Infective endarteritis arises in an analogous manner and, on rare occasions, when congenital arterial anomalies (eg, patent ductus arteriosus, coarctation of the aorta) or diseased arterial endothelium (eg, atherosclerotic plaques) become infected during transient bacteremia.
5
Q
What typically causes infective endocarditis?
A
With the exception of episodes that arise as a consequence of cardiac surgery or intracardiac instrumentation, infective endocarditis results from seeding of endothelial sites by microorganisms that are transiently present in the circulation.
6
Q
Are vascular endothelial infections typically caused by bactéries, fungi or viruses?
A
Vascular endothelial infections are caused mostly by bacteria, rarely by fungi, and never by viruses.
7
Q
What is endocarditis?
A
-Infection of the endocardial surface of the heart
8
Q
Where is endocarditis typically localized?
A
-Usually localized on the cardiac valves, but it can also occur on one or more of the chordae tendineae, on areas of the atrial or ventricular wall or in relation to malformations of the heart or implanted devices/prostheses
9
Q
How has endocarditis typically been classified?
A
Endocarditis has traditionally been classified according to the tempo of the clinical illness, for example, acute and subacute endocarditis. Patients presenting with markedly febrile, toxic courses lasting only days to a few weeks have acute endocarditis. In contrast, patients with subacute endocarditis often have lower fevers and illnesses marked by anorexia, weakness, and weight loss, and are symptomatic for longer than several weeks or even months.
10
Q
What is a more contemporary clinical classification?
A
However, a more contemporary and clinically relevant classification is based on the microbiological cause, the site of infection, and native valve vs intracardiac device, for example, a prosthetic valve or cardiac implanted electronic device (CIED). Occasionally endocarditis is further labeled by presumed predisposition, that is, injection drug use, health care associated.
11
Q
Has endocarditis increased or decreased in the past decade?
A
Increased from 2-5 cases per 100 000 person years to 6-10 cases per 100 000 person years.
12
Q
How has the age changed?
A
The median age of patients with endocarditis has increased steadily since the preantibiotic era; in the 1920s, the median age was <30 years, whereas currently median age is 65-70 years, and two out of three endocarditis patients are men.
13
Q
Acute rheumatic fever and subsequent rheumatic heart disease (see Chapter 12) has declined in developed countries as a predisposing factor for endocarditis, what are the current most common predisposing causes?
A
-Degenerative valvular disease (calcific valvular disease)
-Intracardiac devices (eg, pacemakers and prosthetic heart valves - high risk)
-Mitral valve prolapse with significant mitral regurgitation,
-Congenital cardiac defects (especially bicuspid aortic valves, ventricular septal defects, tetralogy of Fallot, and patent ductus arteriosus) (high risk)
-Previous endocarditis (high risk)
-hemodialysis (high risk)
DIM CPH
14
Q
Why has the rate of CIED infections increased?
A
As a consequence of the expanding indications for CIED implantation, for example, cardiac resynchronization therapy pacemaker (CRT-P) and defibrillator (CRT-D) in treatment of chronic heart failure, the rate of CIED infections has steadily increased during the last decades
15
Q
What percentage of endocarditis patients have no prior valvular abnormality?
A
Between 15% and 30% of patients with endocarditis do not have a prior valvular abnormality.
16
Q
Endocarditis can affect older people for the following reasons:
A
- The age of the general population and therefore the number of persons with degenerative valve disease has increased.
- Prosthetic valves to correct valve dysfunction are implanted more frequently in this age group.
- CIED devices are implanted more frequently in the elderly.
- Persons with congenital heart disease now live longer.
- The precipitating circumstances for transient bacteremia resulting in endocarditis, such as genitourinary tract infections and manipulations, colonic pathology (benign polyps and malignancy), hemodialysis, and health care–associated bloodstream infections (occurring both during hospitalization and among outpatients), are more common in the elderly.
17
Q
True or false injection drug use has also led to an increased incidence rate of endocarditis among younger persons.
A
True
18
Q
Endocarditis is caused by lots of different microbes: which are the most common?
A
-Staphylococcus aureus (S aureus - most common US), streptococci, Enterococcus faecalis (E faecalis), and coagulase-negative staphylococci (CoNS)
SSSE
19
Q
What events typically lead to S aureus bacteremia?
A
health care–associated infections and injection drug use
20
Q
True or false in other parts of the world, Scandinavian countries, South America, and Australia, streptococci species are still the most prevalent cause of endocarditis.
A
True
21
Q
Why has E faecalis endocartitis gone up?
A
reflecting the increasing age of the endocarditis population
22
Q
Organisms for acute endocarditis?
A
S aureus accounts for most of the cases
with the rest caused by:
- streptococci
-E faecalis
-pneumococci
-or aerobic Gram-negative bacilli.
23
Q
Organisms for subacute endocarditis?
A
-α-hemolytic and nonhemolytic streptococci are more prevalent than S aureus as causative microbial agent,
-with E faecalis, CoNS, and fastidious Gram-negative rods causing the remainder.
24
Q
Among patients with streptococci bloodstream infections what micro-organisms are most prevalent?
A
Streptococcus mitis, S gallolyticus, Streptococcus sanguinis, Streptococcus gordonii, and Streptococcus mutans. These species account for ~60%-70% of the isolates in patients with streptococcal endocarditis.
25
True or false since the risk of endocarditis is highly variable within different groups of streptococci, it is important from a clinical perspective to identify streptococcal bloodstream isolates at species level.
True
26
True or false the organisms that cause infection among injection drug users vary depending on whether the infection involves the tricuspid valve (or occasionally the pulmonic valve) or the valves of the left heart.
True
27
Among injection drug users which micro-organisms cause the most infections?
S aureus causes 70% of right-sided endocarditis, whereas in drug users a broader range of organisms cause left-sided infection (S aureus, 25%; streptococci, 15%; enterococci, 25%; fungi [usually Candida spp.], 10%; and Gram-negative bacilli, 8%).
28
True or false S aureus isolated from injection drug users with endocarditis are often resistant to methicillin.
True
29
Unidentified bacterial infection?
Advances in blood culture technology, molecular analysis (eg, polymerase chain reaction [PCR]) of surgically removed vegetations, and serologic testing have decreased the number of cases with culture-negative endocarditis. However, pitfalls have to be recognized, for example, PCR identifies bacterial DNA with high specificity but cannot identify the exact time of the infection. Bacterial DNA can remain in the heart valve tissue for years and may represent a previous episode of endocarditis. But even with contemporary diagnostics, ~10%-15% of endocarditis patients are still culture negative (ie, unknown cause).
30
True or false the microbiology of prosthetic valve endocarditis depends on the time after surgery when infection becomes symptomatic
True
31
Types of micro-organisms first year after placement?
In the first year after valve placement, many infections are health care associated and often the result of perioperative wound contamination or other nosocomial events.
As with other nosocomial infections,
staphylococci may cause more than 50% of endocarditis cases
streptococci and E faecalis are also prevalent
with Gram-negative rods, corynebacteria, and fungi each accounting for about 1%-5%.
32
Cause of endocarditis and micro-organisms in prosthetic valve endocarditis with symptoms beginning more than 1 year after valve surgery
Almost always health care related or community acquired and probably occurs as a consequence of transient bacteremia similar to the pathophysiology of native valve endocarditis.
,treptococci, S aureus, E faecalis, and fastidious Gram-negative coccobacilli are the major causes of later-onset prosthetic valve endocarditis.
CoNS remain an important cause of infections that involve prosthetic valves. In persons who have acquired endocarditis in the first year after valve replacement, ~80% of CoNS are β-lactam antibiotic-resistant S epidermidis, whereas in patients who become infected later, other staphylococcal species, often those that are β-lactam sensitive, are more common.
33
Caracteristics of patient having undergone TAVR
transcatheter aortic valve replacement (TAVR) experience prosthetic valve endocarditis at rates comparable to those noted after surgical aortic valve replacement. Among the organisms usually causing late prosthetic valve endocarditis, E faecalis is overrepresented in those with TAVR endocarditis
34
What is transient bacteremia?
It occurs when heavily colonized mucosal surfaces are traumatized and spontaneously when mucosal surfaces are breached (Table 66-2). For example, spontaneous bacteremia was documented in 10% of patients with severe gingival disease who were studied before undergoing a dental procedure. Daily activities, such as tooth brushing, often cause transient bacteremia. Despite the frequency of bacteremia and the broad spectrum of organisms that gain entry into the circulation, endocarditis remains a relatively rare disease.
35
Where do most cases of endocarditis begin?
Most cases of endocarditis begin at an endocardial lesion that allows bacteria to adhere to and invade the heart valve. Damage to the endothelium results in exposure of the underlying extracellular matrix and production of tissue factor, which triggers coagulation and formation of sterile vegetations (nonbacterial thrombotic endocarditis). Such sterile vegetations facilitate bacterial adherence and infection during transient bacteremia. The colonization of the lesion is followed by further bacterial growth with extension of the lesion, formation of biofilm, tissue damage, vegetation growth, and dissemination of septic emboli to visceral organs and the brain.
36
How do inflammatory lesions contribute to endocarditis?
In response to local inflammation, endothelial cells express β1 integrins. The cell-surface integrins bind plasma fibronectin, which allows bacteria to adhere to the endothelial surface using fibronectin-binding adhesins. Attachment of bacteria to host cells triggers bacterial internalization and intracellular replication, thus allowing the bacteria to escape host defenses. In response to this invasion, further inflammation develops, promoting vegetation enlargement.
37
True or false normal vascular endothelium is resistant to bacterial infection, as can be inferred from the relative infrequency of endocarditis involving normal heart valves as well as from the difficulty of inducing endocarditis in laboratory animals
True
38
What role do non-bacterial vegetations play in the development of IE?
1- This type of vegetation is seen in persons with chronic disease and malignancy (marantic endocarditis) at the exact valve sites most commonly involved in infective endocarditis.
2-The cardiac abnormalities associated with endocarditis promote the formation of platelet-fibrin aggregates at these sites
3-Cardiac abnormalities that allow blood to flow from an area of very high pressure through a narrowing into a low-pressure reservoir (eg, ventricular septal defects and mitral and aortic valve regurgitation) are commonly associated with endocarditis. That flow pattern results in a Venturi effect, in which a low-pressure area is formed immediately downstream and to the sides of the narrowed orifice. When combined with turbulent flow, the Venturi effect allows platelet-fibrin aggregates to form on the endothelium at the low-pressure side of regurgitant aortic or mitral valves and ventricular septal defects. Additionally, high-velocity jet streams of blood flowing through the regurgitant valves and septal defects injure the endothelium on the wall of the left atrium, the right ventricle, or the chordae tendineae–anterior mitral valve leaflet. In turn, platelet-fibrin thrombi form at the sites of endothelial injury and serve as a niche for infective endocarditis (Fig. 66-1). Interestingly, cardiac lesions that result in low-pressure gradients (ostium secundum atrial septal defect) or low flow and reduced turbulence (chronic congestive heart failure) are rarely associated with infective endocarditis.
39
True or false only a limited number of bacteria that can go in the blood can produce endocarditis?
True
40
Steps to cause endocarditis?
1- Enter the circulation
2- Survive host defenses
3- Adhere to the thrombotic vegetation or valve endothelium
4- Replicate on the valve surface, and promote further vegetation formation
41
Organisms that cause endocarditis must be capable of what?
must be resistant to the complement-mediated bactericidal activity of serum and escape phagocytosis and killing by neutrophils.
42
Common bacteria found in endocarditis produce what to adhere?
Structures in the bacterial cell wall or extracellular polysaccharides have been implicated in interactions with host tissue receptors that facilitate the adherence of selected organisms. The common bacteria causing endocarditis, S mutans, Streptococcus sanguis, S mitis, and S gallolyticus, produce extracellular dextran, which mediates vigorous adherence of the organisms to platelet-fibrin aggregates on the heart valves.
43
Other molecule of adherence for streptococci?
By a bacterial protein, FimA, previously identified as an oral cavity adhesin. Furthermore, FimA is associated with the virulence of streptococcal strains in animal models of endocarditis. Cell wall lipoteichoic acid and a protein with major homology to the streptococcal oral adhesins may promote adherence of enterococci to platelet-fibrin aggregates.
44
Endocarditis-causing microbes bind to what?
Endocarditis-producing organisms, including E faecalis, S aureus, S mutans, and S sanguis, bind more vigorously to fibronectin than do organisms rarely implicated in the disease, suggesting a role for that host protein in mediating microbial adherence to cardiac valves
45
Role of fibronectin?
Binding of S aureus and CoNS to fibronectin-coated foreign devices correlates with device infection and may initiate prosthetic valve infection as a consequence of bacteremia. Fibronectin is present on the surface of nonbacterial thrombotic vegetations and exposed as subendothelial matrix when the endothelium is injured. However, the protein is not present on normal intact endothelium.
46
Cause of acute endocarditis without prior valvular disease?
Fibrinogen is both present in nonbacterial thrombotic vegetations and a key target for the adherence of S aureus. The initial adherence is mediated through a fibrinogen-binding protein of the S aureus cell surface (clumping factor) and may account for acute endocarditis without prior valvular disease.
47
Role of coagulase?
Interestingly, coagulase, which is used to identify S aureus (vs coagulase-negative species), does not promote adherence to thrombotic vegetations and is not a virulence factor associated with endocarditis.
48
What do S aureus and streptococci recognize?
aureus and streptococci possess surface components that recognize adhesive matrix molecules (MSCRAMM) that bind to extracellular matrix molecules acting as specific ligands, causing adherence of the organisms to thrombotic vegetations and injured endothelium
49
Role of tissue factor?
Fibronectin-binding proteins of S aureus facilitate invasion of endothelial cells and subsequent production of tissue factor, a glycoprotein that acts as a procoagulant for thrombin formation. S epidermidis and streptococci also induce tissue factor activity, but by interactions with locally recruited monocytes. Growth and maturation of the vegetation and the resulting envelopment of the microorganisms aid in organism survival and replication, which ultimately leads to overt endocarditis.
50
How do the microbes resist the antimicrobial factors secreted by the platelets?
Platelets activated by thrombin release low molecular weight, cationic, microbicidal proteins that kill some S aureus and α-hemolytic streptococci. Resistance of adherent organisms to the platelet microbicidal proteins, termed thrombocidins, may be an important factor in progression from valvular adherence to endocarditis.
51
How does vegetation formation et microbial growth feed each other?
When a vegetation is colonized by bacteria, it tends to grow by continued deposition of platelets and fibrin. S aureus and α-hemolytic streptococci promote platelet adhesion and aggregation and vegetation growth by complex unique and independent mechanisms unrelated to the elaboration of tissue factor and its procoagulant activity. Protected within the vegetation, bacterial proliferation proceeds unimpeded, leading to dense populations of organisms (108-109 bacteria per gram of tissue). The relative absence of phagocytic cells in vegetations is likely a factor that permits bacterial growth to continue without interruption.
52
Role of the biofilm?
Microorganisms located deep in vegetations are often metabolically inactive, whereas the more superficial ones are actively proliferating, continuously shedding bacteria into the bloodstream. The bacteria most frequently found in endocarditis are able to form biofilm, a mucopolysaccharide film covering the vegetations and protecting the bacteria against the immune response and against antibiotics. The aggregation of organisms embedded in biofilm results in an accumulation of bacteria in the stationary phase of their growth cycle. In this condition, they are less susceptible to many antibiotics, particularly those agents that are bactericidal by virtue of action on the cell membrane or cell wall (β lactams, vancomycin, lipopeptides). The most convincing evidence of the role of biofilm in endocarditis is in intracardiac device–related infections.
53
Where do vegetations classically occur?
Classically, vegetations occur along the line of valve closure on the low-pressure surface of the regurgitant valve or septal defect or at the site of a jet stream lesion (see Fig. 66-1). Vegetations vary in Pg. 677size from a few millimeters to a centimeter or larger and may be single or multiple
54
How does the local lesion progress?
nitially the infection is limited to a local lesion, for example on a valve leaflet, but left untreated the cardiac damage will progress and may involve distortion and destruction of valve leaflets, possibly with perforation or rupture of chordae tendineae (Figs. 66-4 and 66-5).
55
How does the local lesion progress with prosthetics?
In the case of infected prosthetic valves, destruction of a valve leaflet of a bioprosthesis or impaired mobility of the valve mechanism in mechanical valves may occur. Infection can extend beyond the valve and into the annulus to cause perivalvular phlegmon or abscess leading to paravalvular destruction, formation of pseudoaneurysm, or fistulation. As a result, dehiscence of the prosthetic valve from the annulus with paravalvular flow may occur
56
True or false heart valve destruction with acute severe insufficiency can be a life-threatening condition with acute heart failure and unstable hemodynamics.
True
57
Sign or perivalvular involvement?
ominous sign of perivalvular involvement is new electrocardiographic conduction changes primarily in aortic valve endocarditis (a consequence of the anatomic proximity between the mitral and aortic annuli and the atrioventricular conduction system, the bundle of His, and the bundle branches).
58
2 complications of endocarditis
Pericarditis may develop as a consequence of infection extending into the pericardial space. Although intracardiac complications, such as myocardial abscesses, can occur with all microbial causes of endocarditis, they are more common when virulent pyogenic bacteria are responsible or when infection involves prosthetic valves, particularly within first year of surgery.
59
Emboli are recognized in how many patients?
Depending on the infective microbial organism, emboli are clinically recognized in 20%-40% of the patients, and approximately half of these patients will present with cerebral symptoms.
60
What increases risk of emboli?
In most cases the embolic complications are evident at the time of diagnosis with highest risk in S aureus endocarditis and in infections with larger vegetations (>10 mm in diameter) and especially those on the anterior mitral valve leaflet
61
Occult lesions?
However, occult lesions are present in up to 50%-60% of patients, and in S aureus endocarditis cerebral lesions has been observed in up to 70%-80% of the patients assessed with magnetic resonance imaging; half of the lesions were silent.
62
Are the emboli sterile or infectious?
In the early course of endocarditis, the emboli may be loaded with bacteria and spread the infection to peripheral sites with consequent abscess formation. Later, the emboli are sterile but may cause severe secondary ischemic complications. The risk of emboli decreases rapidly during the first 2-3 weeks of antibiotic treatment.
63
Complications left-sided endocarditis?
In left-sided endocarditis, cerebral complications include ischemic or hemorrhagic stroke, and more rarely meningitis and encephalitis. Vertebral spondylodiscitis and osteomyelitis are common, and abscesses/ischemic infarction of the spleen, the kidney, and other peripheral organ systems are also frequently seen. Infection in the vasa vasorum of larger arteries and arteritis beginning at the site of arterial occlusion from septic emboli especially in patients with S aureus endocarditis give rise to mycotic aneurysms. Those lesions, which can occur in any artery, are usually asymptomatic until they rupture.
64
Complications right-sided endocarditis?
In right-sided endocarditis, septic pulmonary artery emboli with secondary pneumonia, lung abscess, or pyopneumothorax may occur. These complications are prominent components of S aureus tricuspid valve endocarditis.
65
Consequences of immune-complexes?
Circulating immune complexes that contain antigen from the causative organism are detectable in most patients. The concentration of these complexes correlates with prolonged duration of the disease, occurrence of extracardiac manifestations, and reduced serum complement concentration. Tissue injury mediated by deposition of circulating immune complexes occurs in the skin, choroid plexus, spleen, and synovium. Clinical findings such as Osler nodes, petechiae, vasculitic purpura, and arthralgia are caused by deposition of immune complexes in the skin, arterial wall, and synovium.
66
Pathogenesis of glomerulonephritis?
Glomerulonephritis is the best documented immune-mediated complication of endocarditis (see Chapter 12). Endocarditis is associated with a continuum of immune renal injuries from focal embolic glomerulonephritis (a lesion with few clinical consequences) to diffuse proliferative glomerulonephritis that results in an active urine sediment (ie, containing erythrocytes and erythrocyte casts) and is commonly associated with decreased creatinine clearance. In patients with prolonged episodes of subacute streptococcal endocarditis, circulating immune complexes, which form intravascularly under conditions of antibody excess, deposit in a subepithelial location along the glomerular basement membrane. Immunofluorescence studies reveal IgG and early complement components on the glomerular basement membrane in a lumpy distribution
67
Subacute endocarditis?
. Among patients with subacute endocarditis, glomerulonephritis is frequent, generally focal and mild, and remits with effective therapy of the infection. Acute staphylococcal endocarditis may cause an immune-mediated glomerulonephritis as a consequence of antigen deposition at the glomerular basement membrane and activation of the alternative complement pathway.
68
What does a diagnosis of endocarditis primarily rely on?
Non-specific symptoms + Whereas fever is present in more than 95% of the patients and a heart murmur is common, the classic peripheral signs of endocarditis like Osler nodes, Janeway lesions, and Roth spots are becoming increasingly rare as patients are presented at earlier stages of the disease.
Therefore, establishing a diagnosis of endocarditis depends primarily on blood cultures that yield microorganisms that commonly cause endocarditis and echocardiographic findings demonstrating characteristic lesions.
69
Symptoms and signs associated with endocarditis?
70
What is a cardinal finding with endocarditis?
A cardinal finding is documentation of persistent bacteremia through multiple positive blood cultures (at least three) for the same organisms over 24-48 hours. Blood cultures positive for organisms that are commonly the cause of endocarditis should raise the possibility of the diagnosis, even in the absence of other clinical findings. Without prior antibiotic therapy, at least 90%-95% of patients with endocarditis have positive blood cultures. In almost all cases, one of the initial two cultures is positive. Depending on the susceptibility of the organism, administration of antibiotics during the preceding 2 weeks may significantly reduce the frequency of positive blood cultures. Therefore, to avoid false-negative results, blood cultures should be obtained before antibiotics are given. In stable patients with apparent culture-negative endocarditis, ongoing antibiotic therapy may be held for several days in an attempt to obtain a pathogen.
71
Blood-culture negative endocarditis?
In patients with blood culture–negative endocarditis, serologic tests against rare causes like Coxiella burnetii, Bartonella spp., Brucella spp., and Mycoplasma spp. should be considered. Blood PCR is emerging as a promising method, but sensitivity is still too low. PCR of valve tissue removed at surgery can give a clue to diagnosis. In cases where all tests are negative, consideration should be given to autoimmune diseases as a cause of symptoms and vegetations.
72
TEE vs TTE?
The sensitivity and specificity of transesophageal echocardiography (TEE) are high and superior to those of transthoracic echocardiography (TTE), but TTE is more accessible and a better method for evaluation of left ventricular function and hemodynamics.
73
Major echographic findings?
The major echocardiographic criteria of endocarditis are vegetations and abscess. Vegetations are characterized by size, mobility, location, and numbers. False-negative findings may occur due to thrombi, cusp prolapse, loose chordae, or noninfected vegetations.
74
abcesses on echo?
Abscesses may be complicated by pseudoaneurysm, paravalvular leak, dehiscence of a prosthetic valve, perforation, or fistulation. Small abscesses in the early phase of the disease and abscesses located in the mitral valve annulus are difficult to diagnose, and repeat TTE/TEE after 5-7 days of treatment is recommended if early echocardiography is inconclusive but clinical suspicion remains high.
75
Other roles of echo?
Echocardiography also carries important prognostic information and plays an essential role for determining whether to operate and deciding the optimal timing of surgery. Echocardiography is of crucial importance in evaluation of complications during the course of endocarditis and is a useful tool during follow-up after cessation of antibiotic treatment.
76
Other imaging?
Real-time 3D TEE has the advantage that intracardiac lesions can be presented “en face” to the surgeons. Intracardiac echocardiography (ICE) is another modality that may be an option in selected patients where TTE/TEE is inconclusive or a TEE cannot be performed
77
Imaging for foci?
Compared to TEE, multislice cardiac CT may be superior in the assessment of the perivalvular extent of the infection, particularly in the case of calcified or prosthetic valves. Cardiac CT can also be used to evaluate coronary arteries in younger patients. MRI is particularly useful in evaluation of cerebral lesions and as a supplement to CT in diagnosing the extent of osteogenic foci.
78
PET and CT?
F-FDG-PET/CT measures enhanced glucose uptake in addition to conventional CT. The method allows the detection of both morphologic and metabolic changes. In diagnosing endocarditis, it is helpful in cases of suspected prosthetic valve endocarditis or suspected CIED infection. The method also gives important information on extracardiac lesions, which may be infective and influence the choice and length of antibiotic treatment. This technique, however, is less sensitive than echocardiography for detecting vegetations and valve dysfunction. Additionally, to be useful, PET/CT must be utilized early when infection is active and in patients sufficiently distant from surgery to avoid confounding by postoperative changes.
79
Leukocyte PET
Leukocyte SPECT/CT uses radiolabeled leukocytes to detect infective foci. It is a tedious method with a lower sensitivity but higher specificity compared to PET/CT. It can be useful in patients who recently have undergone cardiac surgery (within 3 months). In this case, PET/CT is not useful as a diagnostic tool.
80
What is the treatment for endocarditis?
Treatment of endocarditis is primarily antibiotic, but 20%-50% of patients may need surgery, and initial diagnostics and assessments will focus on the decision regarding treatment strategy.
81
What is effective antibio treatment?
Effective antibiotic treatment for endocarditis requires identifying the causative agent and determining its antimicrobial susceptibility. That information enables the deployment of an effective antimicrobial regimen. Because host defenses are not very effective at inhibiting bacteria within vegetations, bactericidal antibiotics or combinations of antibiotics are required for optimal therapy. Antibiotics are administered parenterally to achieve high serum concentrations, which are necessary to penetrate the depths of relatively avascular vegetations. The reduced metabolic state of organisms deep in vegetations may render the bacteria difficult to eradicate and supports the use of prolonged antibiotic courses for most patients with infective endocarditis.
82
3 reasons for surgical treatment?
Heart failure
Uncontrolled infection
Prevention of embolism
83
Heart failure?
Heart failure due to valve destruction is a Class I recommendation in clinical guidelines, and patients with heart failure often undergo urgent or emergent surgery (<48 hours after diagnosis). Severe mitral or aortic valve regurgitation may cause hemodynamic instability with heart failure, and patients will quickly deteriorate further without valve repair or replacement.
84
Uncontrolled infections?
Uncontrolled infection may be associated with local abscess formation (aortic root abscess), which in most cases also will require surgery.
85
Prevention of embolism?
Prevention of embolism by surgery is controversial, and comorbidities and patients' operative risk play an important role when assessing the individual patient for surgery
For prevention of embolism, data suggest that early surgery (<48 hours) is better than later operations. Treatment guidelines therefore emphasize that urgent surgery should be the aim in these patients. In some cases, where the risk of embolism is low and the patient is without severe heart failure symptoms, surgery can be planned after antibiotic treatment is completed and thus performed in a low-risk elective setting.
86
Left-sided endo and surgery?
Consideration of surgery for left-sided endocarditis in PWID should follow guidance developed for surgery in endocarditis patients who do not inject drugs. In addition, treatment of endocarditis in PWID should include therapy for the predisposing opiate use disorder whenever possible.
87
Main drug groups for endocarditis?
Most endocarditis patients can be managed appropriately with antibiotics alone and the main drug groups are beta-lactam antibiotics, glycopeptide and lipopeptide agents, aminoglycosides, and also rifampicin. There is increasing prevalence of enterococci that are resistant to penicillins, vancomycin, and the aminoglycosides, that is, high-level resistance to streptomycin and gentamicin. In addition, there is increasing prevalence of staphylococci resistant to methicillin that are also resistant to all semisynthetic penicillinase-resistant penicillins, cephalosporins (except ceftaroline and ceftibiprole), and carbapenems. With these multiresistant bacteria circulating, endocarditis that is difficult to eradicate with antibiotics will be increasingly encountered
88
Empirical treatment?
Empirical antibiotic treatment must consider the common causes of endocarditis and always cover S aureus while taking the local prevalence of MRSA into account. In PWID and severely immunosuppressed patients, addition of antifungal therapy should be considered.
89
treatment for left-side endocarditis
Patients with uncomplicated left-sided endocarditis without embolization or valve destruction that is caused by streptococci or staphylococci can be effectively treated with 4-week regimens. Staphylococcal endocarditis, particularly that due to methicillin-resistant organisms, that does not respond promptly, or that is complicated by infection at remote sites, may require a longer course of therapy. Patients with embolization or prosthetic valve endocarditis should be treated for six weeks as are patients with infection by fastidious Gram-negative organisms or enterococci. Parenteral antibiotics are required in order to reach high enough concentrations to optimize killing. Once infection-related complications are controlled and patients are stabilized, a regimen using outpatient parental antibiotic therapy (OPAT) can be considered in suitable patients. A recent randomized clinical trial showed that after an initial phase of parental antibiotics, therapy in stabile patients infected with a common microorganism (streptococci, staphylococci, or enterococci), can be completed with oral antibiotics. Careful and frequent follow-up is required if one elects to switch to oral agents. With long courses of antimicrobial therapy, issues with drug toxicity and side effects often complicate treatment and force switching of drugs
90
treatment right-side endocarditis?
Endocarditis localized to the right-sided heart valves is most frequently seen in patients with CIEDs or central venous catheters or in PWID. Septic pulmonary emboli are common. In uncomplicated cases caused by methicillin-susceptible S aureus (but not MRSA), 2 weeks of parenteral antibiotics may be sufficient. Surgery is generally unnecessary in tricuspid valve endocarditis and should usually be avoided in PWID. An infected CIED, for example a pacemaker, should be extracted. This can be done by transvenous extraction in the vast majority of patients, yet surgery may sometimes be necessary for large vegetations
91
Other therapeutic issues?
kidney failure is common, and about 5% of endocarditis patients need dialysis during their infection. Neurological complications are also prevalent and may require neurologic or neurosurgical care. Long-term rehabilitation is often needed.
92
Prophylactic antibiotics?
The value of prophylactic antibiotics to prevent endocarditis in patients at risk is uncertain, because carefully controlled studies have never been performed. Although some animal studies support the use of antibiotic prophylaxis, it is now recognized that endocarditis more often is the result of transient bacteremia associated with routine daily activities such as tooth brushing, use of wooden toothpicks, or chewing food than to bacteremia during dental, gastrointestinal tract, or genitourinary tract procedures. In addition, even if highly effective, antibiotic prophylaxis at the time of dental procedures may prevent only an extremely small number of cases of endocarditis. Therefore, emphasis on improved oral health in patients at high risk of endocarditis may be much more important by reducing the incidence of transient bacteremia arising during activities of daily living.
93
Prophylactics in which situations?
Given these considerations, the American Heart Association now recommends prophylaxis only before high-risk dental procedures for the following high-risk patients: (1) prosthetic heart valve recipients; (2) those with a history of previous endocarditis; (3) persons with cyanotic congenital heart disease, which is unrepaired, repaired within 6 months, or incompletely corrected by surgery; or (4) cardiac transplant recipients who develop cardiac valvulopathy.
94
Incidence of endo?
incidence rate of 6-10 cases per 100 000 person-years.
