Infective Endocarditis

Student: Thaiane Yasmim de Oliveira Almeida

Group: 3
 Infective Endocarditis

• Infectious endocarditis refers to the colonization of cardiac valve endocardium by

virulent microorganisms. It is a rare condition that can lead to rapid and significant
morbidity and mortality of not efficiently diagnosed and treated. Infectious
endocarditis is the inflammation of the endocardium, their inner lining of the heart,
as well as the valves that separate each of the four chambers withing the heart.
 Etiology
• It is primarily a disease caused by bacteria and has a wide array of manifestations
and sequelae. The vast majority of infectious endocarditis cases stem from gram-
positive streptococci, staphylacocci and enterococci infection. Together, these 3
groups account for 80 to 90% of all cases.

• Staphylacoccus aureus speciallu responsable for around 30% of cases in developed

world.

• Numerous other bacteria have been previously indentified as well but compromise
only about 6% of total cases.
• Finally, fungal endocarditis represents only about 1% of cases but can be a
typically fatal complication of systemic Candida and Aspergillus infections in the
immunocompromised population.
 Risk Factors

• Risk factors and the enviromental setting of bacterial acquisition, healthcare

versus community, provide hints towards the underlying infectious etiology.

• The definition of nosocomial infections remains controversial, but in general,

healthcare-related cases emerge in the setting of early prosthetic valve endocarditis
or following recent vascular catherization, hemodialysis, hospitalization, or extra-
cardiac operative procedures. In these situations S. aureus represents the
predominant pathogen, responsible for around 50% of nosocomial infections.
• The less virulent coagulase-negative staphylacocci, such as S. epidermis,
stereotypically stem from indwelling vascular devides or recently implanted
prosthetic valves. Enterococcal infection emerges with similar frequency in both
nosocomial and non-nosocomial infections, compromising about 15% and 18% of
cases, respectively.

• Community-acquired infections tend to develop in the setting of

immunosupression, intravenous drug-use, poor dentition, degenerative valve
disease, and rheumatic heart disease.
 Pathophysiology
• The intact, healthy endocardium is typically resistant to bacterial seeding. Overall,
the development of infectious endocarditis requires prodromal endocardial injury
followed by a period of bacteremia. The preliminary endocardial disruption may
emerge secondary to turblent flow around diseased valves or from the direct
mechanical trauma caused by catheter or electrode insertion.

• In the setting of intravenous drug use, repetitive valvular barrage by co-injected

particulate matter generates the necessary injury. As evidenced by the predilection
for vegetations to form on the ventricular surface of the aortic valve and the atrial
surface of the mitral valve, hemodynamics plays an important role in the
pathogenesis.
• The vegetations are localized immediately downstream from regurgitant flow,
leading to the hypothesis that hypoperfusion of the intima predisposes these areas
to endocardial injury.

• Futhermore, infectious endocarditis is more common with high turbulence lesions

such as small ventricular sptal defect with a jet lesion or stenotic valves;
presumably, the high-pressure flow creates more local damage than defects
associated with large surface areas or low flow.
• The damaged endocardium serves as a nidus for platelet aggregation and
activation of the coagulation cascade, which fosters the formation of a sterile, non-
bacterial thrombotic vegetation.

• Subsequent bacteremia then alows for colonization of the vegetation. The

necessary bacteremia can stem from an established, distant source of infection or
emerge transiently secondary to intermittent hematogenous inoculation of oral
flora from dental/gingival manipulation.
 Signs and Symptoms
• Clinically, infective endocarditis may present with a myriad of signs and
symptoms, and clinicians should consider this diagnosis in any patient with risk
factors who present with fever or sepsis of unknown origin.

• Patients will often describe theinsidious onset of fevers, chills, malaise, and
fatigue that generally prompts medical evaluation within the first month.

• Fever typically over the 38.0ºC was found in 95% of all patients.
However, immunosuppression, old age, antypyretic use, or previous antibiotic
courses may prevent manifestation and lower the frequency of this finding.
• Nonspecific symptoms that is an indicative of systemic infection such as anorexia,
headache and generalized weakness may also be present.

• Symptoms that helo localize to the cardiopulmonary system such as chest pain,
dyspnea, decrease exercise tolerance, orthopnea, and paroxysmal nocturnal
dyspnea.
 History and physical examination

• Current or previous indwelling catheterization, intravenous drug use, recent

pacemaker placement, or history of prosthetic valves suggests predisposing
endocardial injury. The clinicial should also inquire about known degenerative
valve disease such as calcific aortic stenosis or mitral valve prolapse.

• Historical of rheumatic heart disease precedes the onset of less than 5% of

infective endocarditis cases in the developed world today.
• A thorough physical exam may identify stigmata that reinforce the diagnosis and
highlight complications of peripheral embolization. Fever will often be present.

• Tachypnea and tachycardia mal also emerge in the setting of underlying valvular
insufficiency or systemic infection.

• Hypotension can similarly develop secondary to either septic or cardiogenic shock

in the event of acute valve perforation.

• Worsening murmurs presents in less than 50% of all cases.

• The dermatologic exam may show the classic immunologic and hemorrhagic
cutaneous sequela of infectious endocarditis.
• Osler nodes (painful subcutaneous nodules typically found on the palm),
subungual splinter hemorrhages and Janeway lesions (painless hemorrhagic
plaques on the palms/soles) sre each observed in less than 10% of all cases.

• The abdominal exam can reveal splenomegaly or even localized peritonitis, which
suggests bowel perforation from mesenteric arterial occlusion.

• Intracerebral embolization can present with focal motor or sensory deficits that
correspond to the impacted vascular territories.
 Evaluation
• 12-lead ECG- the typical ECG in IE appears normal. ST-elevation can be seen in
infectious endocarditis but should be considered a marker of MI .

• A two-view chest X-ray can reveal evidence of pulmonary abscesses, infiltrates, or

pleural effusions- in the case of severe left-sided valvular insufficiency, frank
cardiopulmonary edema, cardiomegaly, or cephalization of pulmonary vasculature
may be appreciated.

• CT scan or CT angiogram- possible pulmonary parenchymal disease, empyema, or

arterial embolization may require more advanced chest imaging.
• Broad laboratory workup is often indicated.

• Complete blood count often demonstrates a leukocytosis that points towards an

underlying infectious process.

• The second major criterion involves sonographic evidence of endocardial

involvement. An echocardiogram must demonstrate a vacillating intra-cardiac
mass fixed to a valve, supporting structure, or implanted material.

• However, the American Heart Association recommends obtaining a more sensitive

and specific transesophageal echocardiogram if suspicion for infectious
endocarditis remains high despite a negative TTE.
 Treatment

• Effective tratement hastens endocardial vegetation eradication and limits or

prevents secondary complications. However, those presenting in extremis with
acute decompensated heart failure, septic shock or stroke require stabilization and
resuscitation, prioritizing the tenets of airway, breathing, and circulation.
Following initial stabilization, subsequent treatment concetrates on prolonged
bactericidal antibiotic regimens and possible cardiothoracic surgical intervention.

• The antibiotic treatment duration and selection depend on the nature of the valve
involved and the resistance pattern of the infecting organism.
• In the case of native valve endocarditis with penicillin-susceptible viridans group
strep or S gallolyticus, the sortest proposed treatment regimen involves a two-
week course of ceftriaxone 2gm IV every 24 hours plus gentamicin 3mg/kg IV
every 24 hours.

• Other possible regimens include ceftriaxone 2mg every 24 hours via continuous
IV drip or in 4 to 6 equally divided doses. In the case of prosthetic valve
involvement, these same pathofens typically require a minimum of 6-week course
of 24 million unitis of penicillin G 24 hours or ceftriaxone 2gm with or without
gentamicin 3mg/kg every 24 hours.
• Patients at risk for staphylococcal infection typically require more prolonged
antibiotic therapy. Patients with native valve methicillin-sensitive S. aureus
infections can receive 6-week courses of either nafcillin 2gm every four hours or
cefazolin 2mg every 8 hours.

• Since beta-lactam monotherapy does not possess bactericidal activity against

enterococci, both native and prosthetic valve enterococcal infections require
combinations regimens.
• As an additional principle of medical management, two blood cultures should be
drawn evert 24 to 48 hours to ensure clearance of bloodstreem infection and direct
ongoing antimicrobial therapy.

• In general, early surgical intervention, including valve repair versus replacement,

is indicated in the event of acute heart failure, extensive infection with localized
complication, and recurrent arterial embolization.
• Acute valvular compromise manifesting with heart failure symptomatology
typically warrants operative intervention within 24 hours. However, AHA/ACC
also recommends early surgical treatment before completion of the initial
antibiotic course in the event of an associated atrioventricular block, paravalvular
abscess, or presence of destructive infiltrative lesions.
 Prognosis

• Prognosis can vary widely depending on the virulence of the infective pathogen,
the emergence of seconday complications, preexisting comorbidities, and the
presence of antive versus prosthetic valve. The initial mortality rate hovers around
18%, with one-year mortality reaching up to 40%.

• In general, cases of prosthetic valve endocarditis occuring within the first 60 days
of surgery demonstrate the highest in hopsital mortality rates.
• Although nearly 50% of infectious endocarditis cases now undergo surgical
intervention, in of itself, the surgical intervention does not appear to elevate the in-
hospital mortality risk.