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UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
INFECTIOUS
ENDOCARDITIS
STUDENTS
William Cruz
Kevin Herrera
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018
INFECTIUS ENDOCARDITIS
 Concept.- Microbial infection of the endocardium, in most cases of bacterial
origin. The characteristic lesion is the vegetations that usually settle in the
valvular endocardium, although they can also affect the chordae tendineae, the
papillary muscles, or the mural endocardium. It usually affects men more than
women and has an approximate incidence of 1 per 1000 hospital admissions.
 Pathogeny.- Endocarditis on native valve: two fundamental facts determine
its appearance, the development of a fibrinoplaquetary thrombus, and its
colonization, which will cause a septic vegetation. Heart disease, rheumatic,
congenital, prolapse of the mitral valve, and degenerative heart disease
predispose the development of endocarditis.
 Endocarditis on valvular prostheses: If it occurs during the 12 months
following its implantation it is called early prosthetic endocarditis, it is usually
produced by colonization of the valvular prosthesis during the surgical
intervention, (by germs from the skin, from contamination of the
extracorporeal pump), or during the immediate postoperative period. After 12
months it is called late prosthetic endocarditis.
 Endocarditis on pacemakers: The infection of the generator bag or cables
originates during surgery or in the immediate postoperative period, usually by
staphylococci.
 Pathological anatomy.- The vegetation is a fibrinoplaquetary aggregate, not
vascularized, in whose matrix there are colonies of microorganisms and few
polymorphonuclear leukocytes and red blood cells. This can lead to abscesses,
fistulas, pericarditis or aneurysms of the sinus of Valsalva. Bacteremia can
cause septic metastases in any location, especially in the spleen, kidneys,
bones or joints and the CNS. The cutaneomucosal lesions characteristic of
endocarditis (petechiae, Osler's nodules, Janeway spots, splinter
hemorrhages), Roth's spots, and many musculoskeletal manifestations have an
immunological pathogenesis or septic emboli.
 Etiology.- Endocarditis on native valve; Streptococci, especially of the
viridans group, cause 30% -40% of endocarditis. Staphylococci cause 20% -
35%. And enterococci are responsible for 5% -15% of them. Endocarditis on
prosthetic valve; Coagulase-negative staphylococci (NEC) predominate in
precocity and, practically exclusively, by S. epidermidis,
 General symptoms: The initial symptom is usually fever, sometimes
preceded by a general picture consisting of asthenia, anorexia, weight loss and
nonspecific locomotor symptoms. Cardiac manifestations: The finding of a
regurgitant heart murmur is a basic element of diagnosis, the appearance of
signs of heart failure is of poor prognosis. Extracardiac Manifestations:
Petechiae and subungual hemorrhages are present in 20% of cases. Osler's
whitlow in subacute or slow forms. The Janeway spots are usually seen in
endocarditis due to S. aureus, Roth spots in the fundus examination are
usually in 5% of cases. Systemic embolisms are the most common
complication of the disease and occur in 20% -30% of cases, of which the
cerebral ones are more common and give focal signs or meningeal syndromes,
followed by splenic and renal. In endocarditis on valvular prostheses, fever,
toxic syndrome, possible embolic phenomena and signs of prosthetic
dysfunction are the predominant manifestations.
 Diagnosis.- The definitive diagnosis can only be established with absolute
certainty through the histological and microbiological examination of the
vegetations obtained in the surgical act or in the necropsy, for which
diagnostic criteria have been described that have been widely validated and
recognized. The diagnosis is considered definitive when there are two major
criteria, one major criterion and three minor or five minor criteria. Diagnosis
is considered possible when there is one major criterion and another minor or
three minor criteria.
 Complementary explorations.- Blood culture, together with the clinical
picture is the basis of the diagnosis, two blood cultures in aerobic and
anaerobic media isolate the etiological agent in more than 90% of cases, these
must be kept several weeks to detect the presence of germs of slow growth.
Estreptococos
viridans o S.
bovis - sensibles
a la penicilina G
Penicilina G 12-18MU/dia EN 6 Dosis IV, O ceftriaxona 2gr/d IV
por 4 - 6 semanas puede ser asociado a gentamicina
3mg/kg/dia
Estreptococos
viridans o S. bovis -
sensibilidad
intermedia a la
penicilina G.
Penicilina G 12-18MU/dia EN 6 Dosis IV, O ceftriaxona 2gr/d
IV, mas gentamicina 3mg/kg/dia. por 4 - 6 semanas.
Enterococos o
estreptococos del
grupo viridans con
resistencia a la
penicilina
Penicilina G 24 MU/dia IV, mas gentamicina 1mg/kg.
c/8horas. O ceftriaxona 2gr. c/12h.IV, mas ampicilina
12gr./dia en 6 dosis. por 4 - 6 semanas.
Estafilococos (S.
aureus) o ECN (S.
epidermidis) sobre
válvula nativa.
Meticilín sensible:
Cloxacilina 12 g/d en 6
dosis i.v. ± gentamicina (3
mg/kg cada 24 h en 2-3
dosis)
Meticilín resistente:
Vancomicina 30-60
mg/kg cada 24 h dividida
en 2-4 dosis i.v.
Echocardiography allows to demonstrate the existence of vegetations in 60%
of the cases by the transtoracic technique and by 90% in the transesophageal,
in addition to assessing the severity of the valvular lesions, the functionalism
of the prostheses, the state of cardiac function and the presence of septic
complications such as perianular abscesses or fistulas between cavities.
 Prognosis.- The mortality figures are 15% -20% and depend mainly on the
responsible microorganism. Survival at 10 years of 81%
 Treatment.- Once the microorganism is isolated and its sensitivity known,
the treatment is based on the administration of the most appropriate
bactericidal antibiotic.
Bibliographic reference: J. M. Miró Meda, P. Tornos Mas. 2016. "Infectious
endocarditis". Valenti Farreras and C Rozman. Internal Medicine Farreras / Rozman.
Barcelona: Elsevier, 2016, pp.553-564

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Infectious Endocarditis Diagnosis, Treatment and Prognosis

  • 1. UNIVERSIDAD TECNICA DE MACHALA ACADEMIC UNIT OF CHEMICAL SCIENCES AND HEALTH MEDICINE SCHOOL ENGLISH INFECTIOUS ENDOCARDITIS STUDENTS William Cruz Kevin Herrera TEACHER: Mgs. Barreto Huilcapi Lina Maribel CLASS: EIGHTH SEMESTER ‘’A’’ Machala, El Oro 2018
  • 2. INFECTIUS ENDOCARDITIS  Concept.- Microbial infection of the endocardium, in most cases of bacterial origin. The characteristic lesion is the vegetations that usually settle in the valvular endocardium, although they can also affect the chordae tendineae, the papillary muscles, or the mural endocardium. It usually affects men more than women and has an approximate incidence of 1 per 1000 hospital admissions.  Pathogeny.- Endocarditis on native valve: two fundamental facts determine its appearance, the development of a fibrinoplaquetary thrombus, and its colonization, which will cause a septic vegetation. Heart disease, rheumatic, congenital, prolapse of the mitral valve, and degenerative heart disease predispose the development of endocarditis.  Endocarditis on valvular prostheses: If it occurs during the 12 months following its implantation it is called early prosthetic endocarditis, it is usually produced by colonization of the valvular prosthesis during the surgical intervention, (by germs from the skin, from contamination of the extracorporeal pump), or during the immediate postoperative period. After 12 months it is called late prosthetic endocarditis.
  • 3.  Endocarditis on pacemakers: The infection of the generator bag or cables originates during surgery or in the immediate postoperative period, usually by staphylococci.  Pathological anatomy.- The vegetation is a fibrinoplaquetary aggregate, not vascularized, in whose matrix there are colonies of microorganisms and few polymorphonuclear leukocytes and red blood cells. This can lead to abscesses, fistulas, pericarditis or aneurysms of the sinus of Valsalva. Bacteremia can cause septic metastases in any location, especially in the spleen, kidneys, bones or joints and the CNS. The cutaneomucosal lesions characteristic of endocarditis (petechiae, Osler's nodules, Janeway spots, splinter hemorrhages), Roth's spots, and many musculoskeletal manifestations have an immunological pathogenesis or septic emboli.  Etiology.- Endocarditis on native valve; Streptococci, especially of the viridans group, cause 30% -40% of endocarditis. Staphylococci cause 20% - 35%. And enterococci are responsible for 5% -15% of them. Endocarditis on prosthetic valve; Coagulase-negative staphylococci (NEC) predominate in precocity and, practically exclusively, by S. epidermidis,  General symptoms: The initial symptom is usually fever, sometimes preceded by a general picture consisting of asthenia, anorexia, weight loss and nonspecific locomotor symptoms. Cardiac manifestations: The finding of a regurgitant heart murmur is a basic element of diagnosis, the appearance of signs of heart failure is of poor prognosis. Extracardiac Manifestations: Petechiae and subungual hemorrhages are present in 20% of cases. Osler's whitlow in subacute or slow forms. The Janeway spots are usually seen in endocarditis due to S. aureus, Roth spots in the fundus examination are usually in 5% of cases. Systemic embolisms are the most common complication of the disease and occur in 20% -30% of cases, of which the cerebral ones are more common and give focal signs or meningeal syndromes, followed by splenic and renal. In endocarditis on valvular prostheses, fever,
  • 4. toxic syndrome, possible embolic phenomena and signs of prosthetic dysfunction are the predominant manifestations.  Diagnosis.- The definitive diagnosis can only be established with absolute certainty through the histological and microbiological examination of the vegetations obtained in the surgical act or in the necropsy, for which diagnostic criteria have been described that have been widely validated and recognized. The diagnosis is considered definitive when there are two major criteria, one major criterion and three minor or five minor criteria. Diagnosis is considered possible when there is one major criterion and another minor or three minor criteria.  Complementary explorations.- Blood culture, together with the clinical picture is the basis of the diagnosis, two blood cultures in aerobic and anaerobic media isolate the etiological agent in more than 90% of cases, these must be kept several weeks to detect the presence of germs of slow growth.
  • 5. Estreptococos viridans o S. bovis - sensibles a la penicilina G Penicilina G 12-18MU/dia EN 6 Dosis IV, O ceftriaxona 2gr/d IV por 4 - 6 semanas puede ser asociado a gentamicina 3mg/kg/dia Estreptococos viridans o S. bovis - sensibilidad intermedia a la penicilina G. Penicilina G 12-18MU/dia EN 6 Dosis IV, O ceftriaxona 2gr/d IV, mas gentamicina 3mg/kg/dia. por 4 - 6 semanas. Enterococos o estreptococos del grupo viridans con resistencia a la penicilina Penicilina G 24 MU/dia IV, mas gentamicina 1mg/kg. c/8horas. O ceftriaxona 2gr. c/12h.IV, mas ampicilina 12gr./dia en 6 dosis. por 4 - 6 semanas. Estafilococos (S. aureus) o ECN (S. epidermidis) sobre válvula nativa. Meticilín sensible: Cloxacilina 12 g/d en 6 dosis i.v. ± gentamicina (3 mg/kg cada 24 h en 2-3 dosis) Meticilín resistente: Vancomicina 30-60 mg/kg cada 24 h dividida en 2-4 dosis i.v. Echocardiography allows to demonstrate the existence of vegetations in 60% of the cases by the transtoracic technique and by 90% in the transesophageal, in addition to assessing the severity of the valvular lesions, the functionalism of the prostheses, the state of cardiac function and the presence of septic complications such as perianular abscesses or fistulas between cavities.  Prognosis.- The mortality figures are 15% -20% and depend mainly on the responsible microorganism. Survival at 10 years of 81%  Treatment.- Once the microorganism is isolated and its sensitivity known, the treatment is based on the administration of the most appropriate bactericidal antibiotic. Bibliographic reference: J. M. Miró Meda, P. Tornos Mas. 2016. "Infectious endocarditis". Valenti Farreras and C Rozman. Internal Medicine Farreras / Rozman. Barcelona: Elsevier, 2016, pp.553-564