Non Valvular Cardiovascular Infections

Although non-valvular cardiovascular infections are much less common than valvular endocarditis, they nonetheless have the potential to be fatal. Certain cardiovascular infections, such as infected pacemakers and implantable defibrillators, as well as prosthetic graft infections, are discussed in other chapters. This chapter will focus on myocardial abscesses, mural endocarditis, and mycotic aneurysms.

Myocardial abscesses are rare but can develop by several mechanisms. A classification system by Chakrabarti [452] divides myocardial abscesses into the following categories: (A) endocarditis-related, (B) septicemia-related, or (C) miscellaneous (see Table 9.6). The most commonly identified cause of myocardial abscess (MA) is endocarditis-related, resulting from contiguous extension of valvular or mural endocarditis [452]. Hematogenous seeding during bacteremia or fungemia is also relatively common [452]. In this latter case, several areas of myocardium are often involved [453], and abscesses in multiple organs, typically the brain, lungs, and kidneys, also occur [452]. Miscellaneous causes of myocardial abscesses include trauma and penetrating injuries, iatro-

genic (e.g., catheterization, angioplasty), and anatomic abnormalities (e.g., aneurysm infection, infection of infarcted myocardium, infection of myxoma) [452]. S. aureus is the most frequently reported bacterial isolate in patients with MAs; other causes include streptococci, C. perfringens, Bacteroides spp., E. coli, Candida spp., and Aspergillus spp. [452,453]. Fungal MAs are more common in immunocompromised patients. Paravalvular MAs are usually recognized in the context of endocarditis that is failing to improve or clinically deteriorating. Non-paravalvular MAs are usually subtle, with most previous cases diagnosed at autopsy. The major complication of MAs is rupture. In MAs that develop in an area of recent myocardial infarction, the risk of rupture is increased sevenfold [454]. Rupture can result in tamponade, hemopericardium, and/or purulent pericarditis. Other complications include fistulae, cardiac arrhythmias, or septic shock. Although conduction disturbances detected by serial electrocardiograms in a patient with suspected or proven endocarditis is highly suggestive of a paravalvular MA, the diagnostic modality of choice for all MAs is TEE [452]. The management of non-par-avalvular MAs is poorly defined. No comparative studies have been reported in the English literature that compare differences in outcome between patients treated with medical therapy alone versus those treated with combined (medical/surgical) therapy. The management of peri-annular MA is more clearly defined. Identification of an abscess as an extension of valvular endocarditis is an indication for surgery [1,455], in conjunction with adequate antimicrobial coverage. Furthermore, early surgery is advocated, with the goal of achieving more rapid control of the infective process, to improve the chances of survival and to prevent the development of further perivalvular destruction [456]. Surgical intervention usually requires drainage of abscess, debridement of necrotic tissue, closure of any fistulous tracts that have developed, as well as valve replacement (for paravalvular MAs) [1,52]. There is some limited evidence that in select patients, paravalvular MAs may be treated successfully with medical therapy alone [52]. Recommended criteria for this form of management include those who have small (< 1 cm) abscess as well as those who do not have evidence of abscess-related complications (e.g., heart block, progression of abscess during therapy, valvular dehiscence, or valvular

Table 9.6. Antibiotic Treatment for NVE Due to Staphylococcusspp.

Category

First-line

Duration

Second-line

Duration

Comments

Penicillin S (MIC

High-dose penicillin

4 weeks if

Penicillin-sensitive Staphylococcus spp.

<0.1 |g/mL,and

G (e.g.,24 million

uncomplicated IE;

are very uncommon

P-lactamase negative)

units/day) IV

6 weeks if

complicated IE (e.g.,

metastatic septic

complications)

Vancomycin 30 mg/

6 weeks

Vancomycin indicated only for patients

kg/day IVq12h

unable to tolerate P-lactams

Penicillin R, Methicillin S

Nafcillin or oxacillin

P-lactam:4 weeks

Gentamicin therapy optional, and

(MSSA)

2 g IVq4h ±

if uncomplicated

when used, should be in divided

gentamicin 3 mg/

IE; 6 weeks if

daily doses (see text)

kg/day IV

complicated IE

(e.g., metastatic

Recommended duration is for

Cloxacillin 100-

septic complica-

left-sided IE or complicated

150 mg/kg/day

tions)

right-sided IE

(e.g.2 g IV q4h) ±

Gentamicin:3-5

gentamicin 3 mg/

days

Uncomplicated right-sided IE may be

kg/day IV

treated for 2 weeks (see text)

Flucloxacillin 2 g IV

Recommended by BSAC (not available

q4 to 6 h

in N.America)

For "penicillin-allergy"

6 weeks

Use cefazolin with caution, as clinical

history (i.e., NOT type

failures associated with isolates

1/ immediate-type

producing P-lactamase type A have

hypersensitivity):

been reported (see text)

cefazolin 2 g IV q8h

± gentamicin 3 mg/

kg/day IV

For patients with type

Vancomycin has inferior efficacy

1 (immediate-type)

compared to P-lactams.AHA also

hypersensitivity

recommends considering P-lactam

reactions: Vancomycin

desensitization

30 mg/kg/day IV q12h

± gentamicin 3 mg/

kg/day IV

Methicillin R (i.e.,

Vancomycin 30 mg/

6 weeks

AHA recommendation; strongly

MRSA,MRSE)

kg/day IV q12h

consider consultation with an

infectious disease specialist.

Vancomycin 1 g IV

4-6 weeks

BSAC recommendation

q12h +1 ofthe

Vancomycin and gentamicin doses are

following: rifampin

modified for renal function

(300-600 mg po q12h)

Selection influenced by antimicrobial

OR Gentamicin 1 mg/kg

susceptibility testing

IV q8h OR Sodium

Strongly consider consultation with an

fusidate (500 mg

infectious disease specialist

po q8h)

Vancomycin-resistant

Strongly consider

staphylococci (i.e., VISA,

consultation with an

h-VISA,VRSA,VRSE)

infectious disease

specialist

S = susceptible; R = resistant

insufficiency) [52]. In these patients, the potential for complications does however continue to exist, and so it is recommended that such patients be monitored closely with serial TEEs (i.e., at 2, 4, and 8 weeks after completion of antimicrobial therapy) [52]. The duration of antimicrobial therapy after surgical intervention remains poorly defined. One review suggests the following approach [457]: Patients undergoing surgical intervention for NVE should be treated for a minimum of four to six weeks with appropriate intravenous antibiotics; the full duration of antibiotic therapy after valve replacement or repair is based on the intraoperative culture results. If the intraoperative cultures were negative and the patient preoperatively had already received a complete course of medical therapy, treatment with intravenous antibiotics for seven more days is sufficient. If the intraoperative cultures are negative but the patient had not received a full course of preoperative therapy, antibiotics are continued for a total of four to six weeks (including both the preoperative and postoperative period). If the intraoperative cultures were positive, the antibiotics should be continued for an additional four to six postoperative weeks. This latter recommendation is a conservative estimate, athough a retrospective single-center review of 358 patients concluded that it was unnecessary to continue treatment for patients with negative valve culture results for an arbitrary four- to six-week period after surgery [458]. The authors concluded that two weeks of treatment appears to be sufficient to prevent relapse, and, for those operated on near the end of the standard period of treatment, simply completing the planned course should suffice [458].

Mural endocarditis typically results from seeding of an abnormal area of endocardium during bacteremia or fungia; alternatively, it may develop as an extension of infection from underlying myocardial abscesses [453]. The organisms associated with mural endocarditis include Staphylococcus spp., viridans streptococci, Enterococcus spp., Salmonella spp., Klebsiella spp., Bacteroides fragilis group, Candida spp., and Aspergillus spp. [453]. Mural endocarditis most commonly presents with nonspecific constitutional symptoms, i.e., fever and chills. The diagnosis of mural endocarditis may be difficult. Blood cultures may be positive, although the data reflecting the sensitivity of this procedure on diagnosis is unknown. Echocardiography is likely the most useful diagnostic modality, with TEE probably superior to TTE [441,459-462]. Nonetheless, echocardiography may be negative in some cases. The complication most frequently associated with mural endocarditis is peripheral embolization, although cardiac rupture and the development of fistulae have been reported [453]. Although no studies exist to guide optimal therapy of this condition, it is likely that a combined approach is necessary, with early surgical intervention warranted to prevent the development of complications [453,459].

A mycotic vascular aneurysm is a localized dilation of the blood vessel wall that is infected.

Infection of a vascular wall can occur as a complication of bacteremia by one of two mechanisms: Firstly, bacteria circulating in the intraluminal space can seed an atherosclerotic lesions, with subsequent local invasion, and formation of a true aneurysm. Alternatively, circulating bacteria can invade the vasa vasorum (the blood vessels ramifying on the outside of a major artery), leading to necrosis of the tunica intima, with subsequent pseudoaneurysm formation. Arterial bifurcation points are the most common sites of mycotic aneurysm formation [52], due to turbulence of blood flow that creates a temporary ebb, which permits circulating bacteria to adhere to the vascular wall. Mycotic aneurysms can be anatomically divided into two categories: Intracranial mycotic aneurysms (IMAs), which is the most frequent mycotic aneurismal complication of endocarditis [52], and extracranial mycotic aneurysms (EMAs), which include mycotic aneurysms of the aorta, of the visceral arteries, and the arteries of the extremities.

IMAs are an infrequent but potentially fatal complication of endocarditis. The overall mortality rate is approximately 60%, although this rate is dependent on the status of the aneurysm: for unruptured IMAs, the mortality rate is 30%, whereas the rate increases to ~80% once rupture has occurred [52,463]. IMAs occur more frequently in the anterior circulation, especially the distal middle cerebral artery and its branches, and may be multiple [463,464]. The clinical presentation of patients with IMAs is nonspecific, with the majority being asymptomatic until rupture occurs. The most common manifestations include fever and chills, headache, lethargy/altered level of consciousness; focal neurologic deficits (e.g., aphasia, hemiparesis) can also occur [52,463]. The variable presentation is likely a reflection of the location and progression of the aneurysm, and whether there is any mass effect.

The diagnosis of an IMA should be suspected in a patient with known endocarditis who develops neurological signs and symptoms, at which point rupture with either subarachnoid hemorrhage, intraventricular hemorrhage, or direct intracerebral destruction of the brain has probably occurred. Of note, the development of IMAs can be quite rapid. In an animal model, it has been demonstrated that the time interval from septic embolism to aneurismal dilatation can be as short as 24 hours [463]. The propensity of IMAs to bleed is the principal reason why anticoagulation should be avoided, if possible, in the management of patients with NVE. The differential diagnosis of new neurological deficit in such a patient should also include embolic infarction and, less commonly, bacterial meningitis. Cerebrovascular imaging is thus required. Computed tomodensitometry (CT) of the cere-brovascular system, without contrast, is useful as an initial diagnostic modality, with sensitivity of 90-95% for detecting an intracerebral hemorrhage (ICH) [52]; it may also be able to identify the location of the IMA. In the absence of an ICH, angiography should be performed (either magnetic resonance angiography (MRA) or CT angiography (CTA)) to detect IMAs. Both of these modalities have excellent sensitivities and specifi-ties (90-95% each) [52]. Both techniques may be false-negative, however, for aneurysms < 5 mm in diameter, in which case, conventional cerebral angiography may be used [52]. Examination of the cerebrospinal fluid (CSF) does not aid in diagnosing the presence of an IMA or in consistently identifying the etiologic pathogen [463].

The diagnosis of IMAs in a patient without known endocarditis may be more difficult. Clues suggestive of an infectious etiology when an incranial aneurysm is identified include a fusiform appearance or an atypical location [465]. In these situations, an IMA should be suspected and investigations for endocarditis should be pursued.

The management of IMAs primarily involves a prolonged course of appropriate antibiotics that achieve therapeutic levels in the central nervous sytem. The surgical management of IMAs remains controversial: its presence is not an unequivocal indication for surgical intervention. Resolution of IMAs with antimicrobial therapy alone is well documented. On the other hand, rupture of an IMA is associated with significant morbidity and unacceptable mortality. Unfortunately, no clinical data exist that have reliably identified patients at risk for rupture, in whom prophylactic surgery would be of greatest benefit. As such, the role of surgery in the management of IMAs must be individualized, based on the patient and aneurysm characteristics. One algorithm suggested, based on the authors' experiences at the Mayo Clinic, is as follows [463]: Patients with unruptured IMAs should be observed during antibiotic therapy, with a serial angiograms (MRA or CTA) at four to six weeks. If the IMA enlarges, surgical resection should be considered. If the IMA regresses, surgery can be deferred. If the IMA persists after an adequate course of antimicrobial therapy, surgical intervention could be considered if the residual aneurysm is large, if the patient wishes it, and if the patient's general condition permits. Of note, new IMAs can form after the initial ones have regressed, underscoring the need for regular follow-up of these patients until all of the aneurysms have regressed, or until > two serial angiograms have demonstrated stability in size.

For IMAs that are peripherally located that have ruptured, surgical resection should be performed, provided that the patient's condition can allow for surgical anesthesia. For IMAs that are proximately located, a more conservative approach may be considered, because clipping of these aneurysms in the acute stage may be difficult. In these situations, a trial of antibiotic therapy can be pursued. This will allow fibrosis of the vascular wall, which may make subsequent clipping feasible. If the patient has multiple aneurysms, then the ruptured one should be resected, along with other accessible peripheral aneurysms. The remaining ones are treated with antimicrobial therapy, with serial angiographic imaging; if there is evidence of enlargement, resection should be considered.

The role of endovascular occlusion of IMAs has been described in case series, although the limited power and follow-up of the patients prevents any robust conclusion about the efficacy of this modality [463].

Extracranial mycotic aneurysms (EMAs) can involve the aorta, the visceral arteries, or the arteries of the extremities. Infected aneurysm or pseudo-aneurysm of the aorta is a rate but life-threatetning condition. The overall hospital mortality ranges from 5-40%, although the anatomic location of the EMA, the infecting pathogen, and accompanying comordities are important factors affecting prognosis. In a single-center retrospective study of 17 patients over 20 years, the operative mortality for supra-renal EMAs was 43%, while that for infra-renal EMAs was 10% [466].

The most common organisms involved in EMAs are S. aureus and Salmonella spp. [321,467,468]. The latter is discussed in the section on Salmonella NVE. Other common pathogens include Streptococcus spp. (S. pneumoniae [469], viridans streptococci [470], P-hemolytic streptococci [471]), Gram-negative rods (e.g., E. coli [472]), and anaerobes (e.g., B. fragilis group, Peptostreptococcus spp., and P. acnes) [468].

The standard management of EMAs involves a combined approach. Medical therapy (i.e., adequate antimicrobial coverage of long-term duration) is required, but in itself is not sufficient because of the difficulty of antibiotics to penetrate into aneurysms [473]. Therefore, debride-ment/resectionof the infected aorta and the surrounding infected tissue, followed by revas-cularization (either in situ or extra-anatomic grafting) is also required [474]. Traditionally, aortic ligation with extra-anatomic bypass was the standard treatment for mycotic aortic aneurysms [474]. However, extra-anatomic bypass may not be practical or feasible if visceral arterial involvement is present; for example, in mycotic aneurysms of the suprarenal aorta, no remote or extraanatomic routes may be available to maintain perfusion to the viscera. As well, in the presence of bacteremia, even a remote graft may be at risk for hematogenous seeding. Furthermore, long-term patency may be compromised. An alternative procedure is in situ reconstruction of the infected aorta with a prosthetic graft. Placement of a foreign body into an infected surgical field seems counter-intuitive, as it has potential for developing early- and late-graft infection. Indeed, such a complication has been previously reported, necessitating a high rate of reoperation [475-477]. However, reports of the safety, durability, and efficacy of in situ reconstruction in the presence of a mycotic aortic aneurysm have also been described [478,479]. To further decrease the risk of in situ graft infection, various modifications (e.g., omental wrapping [477], antimicrobial-coated graft [480,481], cry-opreserved allograft [482,483]) have been used. Although there are no guidelines regarding the proper indication for in situ reconstruction, the presence of gross purulent infection at the aortic site is likely a contraindication to this procedure.

The optimal duration of antibiotic treatment for aortic EMAs is not well defined. Recommendations have varied from > 4-6 weeks to lifelong therapy [474], the latter being especially recommended in the presence of an in situ prosthetic graft.

Endovascular repair is an emerging field in vascular surgery. Although most experience is in the repair of sterile aneurysms, cases of successful treatment of infected aneurysms have been reported [479,484]. In the absence of more robust evidence, it has been suggested that this modality may be currently best suited as a temporalizing measure to rapidly stop the bleeding of a ruptured aortic EMA, followed by definitive surgery [474].

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