Page 484 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

354 PART 3: Cardiovascular Disorders

■ STRUCTURAL FAILURE OF PROSTHETIC VALVES seen around the aortic root. Fistulas can result from perforation of

This is a rare, but devastating complication in the case of mechanical valves. cardiac structures. The embolic potential is related to the particular
valve involvement (mitral more common than aortic), vegetation size
Treatment is emergent surgery. Structural failure of bioprosthetic
valves is common, and occurs due to progressive degeneration of (higher potential for vegetations >10 mm), and mobility (high mobility
having obviously higher potential). The embolic potential dramatically
the valve. Surveillance echocardiographic examination is recommended
annually 5 years after bioprostheses implantation, or whenever clinical decreases with appropriate antibiotic therapy regardless of location, size,
and mobility.
status changes. Treatment is usually reoperation. Transcatheter tech-
niques (valve-in-prosthesis implantation) are currently being evaluated. ■ CLINICAL PRESENTATION
The most important step for a timely diagnosis is a high index of sus-
picion. Indeed, presence of a febrile illness in combination with a new
KEY POINTS—PROSTHETIC VALVES valvular regurgitation, fever in patients with preexisting cardiac lesions
• Prosthetic valve thrombosis presents with thromboembolic events or intravascular hardware, persistently positive blood cultures, presence
or heart failure due to valve obstruction. Diagnosis is made by of unexplained peripheral abscesses (renal, splenic, vertebral, cerebral),
echocardiography or fluoroscopy. Treatment depends on location and the association of fever and embolic events should raise the suspi-
(left- vs right-sided valves) and thrombus burden. cion of bacterial endocarditis.
As etiology is highly variable, depending on both the causative micro-
• Structural failure of a mechanical prosthesis is rare and requires urgent organism and host, it is not surprising that clinical presentation does
reoperation. Failure of a bioprosthesis is frequent and progressive due not follow a single pattern. In broad terms, infectious endocarditis can
to degeneration. Reoperation after stabilization is recommended. present either as an acute, rapidly progressive disease, or as a subacute
or chronic disease. Fever is the most common symptom, occurring in
the majority of patients. Chills, weight loss, fatigue, and/or poor appe-
tite are also common. The classic immunologic phenomena (splinter
INFECTIVE ENDOCARDITIS hemorrhages, Roth spots, and glomerulonephritis) are less common, as
patients present earlier in the disease. Septic emboli to the spleen, brain,
Infective endocarditis (IE) is a disease caused by microbial infection of kidney, spine, or lung remain common, and are frequently the culprit
the endothelial lining of intracardiac structures. Despite advances in of the first medical evaluation. An elevated C-reactive protein and
diagnosis and antimicrobial therapy, mortality remains high, approach- sedimentation rate, leukocytosis, and anemia are common findings, but
ing 25% at 6 months. 39 nonspecific for infectious endocarditis. The cornerstone of laboratory
■ ETIOLOGY diagnosis is presence of positive blood cultures.
Cardiac examination shows frequently new or worsening heart mur-
A variety of microorganisms can cause IE, but staphylococci and murs. Such a finding in the appropriate clinical context should prompt
immediate echocardiographic evaluation. The choice of transthoracic
streptococci are responsible for ~80% of cases of native valve endo-
carditis, with gram-negative bacilli, HACEK group organisms, fungi, (TTE) versus transesophageal (TEE) echocardiography as a first imag-
ing modality depends on the clinical scenario. TTE is usually the first
polymicrobial or culture-negative endocarditis being responsible for the
rest. Prosthetic valve endocarditis is a serious complication that occurs triage step in the majority of cases, with vegetations larger than ∼3 mm
39
being usually well seen. TTE has excellent specificity, but lower sensi-
in 1% to 9% of patients. Early prosthetic valve endocarditis (within
40
60 days of implantation) is usually caused by Staphylococcus epidermidis tivity for diagnosis, especially for presence of perivalvular abscess or
prosthetic valve vegetations. TEE should be performed in patients with
and Staphylococcus aureus, while late prosthetic valve endocarditis is
caused most commonly by viridans streptococci. high clinical suspicion, as the sensitivity for detecting small lesions
is substantially improved. In patients with prosthetic heart valves,
■ PATHOPHYSIOLOGY intravascular devices, suspected valvular abscesses, or when planning
surgery it is best to start directly with a TEE. Repeat echocardiographic
Development of IE is a result of the complex interaction between blood- examination is recommended for assessment of patients with high index
stream pathogens and the matrix molecules and platelets at sites of endo- of suspicion in whom the initial study was negative, whenever clinical
cardial cell damage. The initial step consists of formation of nonbacterial deterioration occurs, or for monitoring disease progress in patients
thrombotic lesions at sites of endothelial damage (typically at sites of with high-risk features (large vegetations, paravalvular extension, severe
turbulent flow or of mechanical contact with intravascular/intracardiac regurgitation, or new ventricular dysfunction). Serial ECGs should be
devices), followed by transient bacteremia/fungemia with species of performed for assessment of atrioventricular conduction; presence of a
pathogenic potential, adherence to the sterile thrombus, and prolifera- new AV block of any degree should prompt thorough TEE examination
tion within the vegetation. Microorganisms adherent to the vegetation for probable perivalvular extension. Diagnosis is based on positive blood
stimulate further deposition of fibrin and platelets on their surface. cultures, echocardiographic findings, and clinical signs, according to the
Within this secluded focus, the buried microorganisms multiply rapidly. 41 Duke criteria.
The impact of IE is related to three factors: degree of valvular destruc- Beyond the infectious syndrome, patients present with acute cardiac
tion leading to hemodynamic alterations, extension into adjacent struc- decompensation secondary to hemodynamic alterations caused by endo-
ture (abscess/fistula formation), and embolization of infected material carditis; from a hemodynamic standpoint, these are treated similarly to
leading to peripheral organ abscess formation. The degree of valvular other causes of acute valvular regurgitation (see above). Complications
destruction depends largely on the balance between microorganism include abscesses, dehiscence (prosthetic valves)/destruction (native
virulence and host defense mechanisms. The potential for local exten- valves) with severe regurgitation, and embolization (Fig. 41-9). Immediate
sion depends on virulence (staphylococci being the most aggressive), surgery is indicated in patients who are hemodynamically unstable,
but also on the nature of the valve (significantly higher risk with valve have significant valve dysfunction, or fail to respond to antibiotic therapy.
prostheses), and position (aortic more frequent than mitral). Local Early surgery is advocated also to remove the infected foreign material in
extension leads initially to a cellulitic process (phlegmon); once cen- the case of prosthetic valves. Infected pacemakers/defibrillators should
tral necrosis ensues, fluid filled cavities appear, expand, and coalesce, be explanted completely (leads and generator); in patients who are pace-
leading to abscess formation. Pseudoaneurysms are formed when the maker dependent, a temporary pacing lead can be implanted from an
abscess cavity opens to the endocardial surface, and are most commonly internal jugular vein approach.

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