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Case report

19 y.o Female with Infective Endocarditis

dr. Mario Tri Mulyono

dr. Yulius Patimang Sp.A,Sp.JP

Department of Cardiology and Vascular Disease

Medical Faculty of Hasanuddin University
Makassar
2020
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Patient Identity
 Name : Mrs. Nuranisa
 Age : 19 y.o.
 No.Register : 736592
 Admission Date : 12 February 2020
 History Taking
History of
Shortness Of
Shortness Breath and
Of Breath febris Family History of
since 4 Cough with intermittently cardiac disease was
days Sputum since 4 years denied
ago

DOE (+)
Febris
Birth history :
No history of syringe
Intermittenly, use
Normal, History
Fatique
of blue birth was
denied

No history of
hypertension,
diabetes mellitus and
chest pain
 Physical Examination
General status: mod-
ill
GCS 15 (E4M6V5) Vesicular breath
BMI : 17,33 sound, no ronchi and
(underweight) wheezing
BB : 39 kg TB 150 cm
Heart Sound
regular,
BP: 100/50 mmHg murmur diastolic
P : 90 bpm, regular grade 3/4 URSB,
R : 24 tpm murmur sistolic
T : 38,2 0C, grade 4/6 at ULSB,
LLSB, and apex
Pretibial edema
Conjungtiva anemic (-)
(-) Sclera ikterik (-) Warm acral
JVP R+2cm H2O Clubbing finger
(-)
 ECG at PJT 5

Sinus rhytm, HR 75 bpm, axis + 45 degree, Pr interval 0,16s, qrs duration 0,06s
Conclusion : Sinus rhythm, HR 75 bpm, normoaxis
 Laboratorium 12/02/2020
WBC 6,94 103/mm3 4-10 x 103/mm3 6
N/L/M/E/B 3,95/2,0/0,9/0/0 %
HGB 11,1 g/dl 12-16
PLT 217.000 103/mm3 150-400 x 103/mm3
PT 10,8 Second 10-14
INR 1,04
APTT 25,7 second 22,0-30,0
SGOT 21 U/L < 38
SGPT 8 U/L < 41
Ureum 33 mg/dl 10-50
Creatinin 0,53 mg/dl <1,1
RBG 120 gr/dl <140
Natrium 137 mmol/l 136 – 145
Kalium 4,0 mmol/l 3.5 – 5.1
Klorida 104 mmol/l 97 - 111
HbsAg, anti HCV Non reactive
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Thorax X Ray 13-02-
2020
Normal bronchovascular marking, no Conclusion : Cardiomegaly
specific process at both lungs
 Trachea at the midline
 Enlargement of cor, CTI 0.6, concave
Cardiac waist, Elevated apex ( RVE),
Aorta normal
 Both of sinus and diaphragm are normal
 Intact bones
 Normal soft tissue
Echocardiography (12-2-2020 ) 9

 Situs solitus Conclusion :

 AV-VA concordance • VSD perimembran L-R shunt
• Aorta regurgitasi severe
 Semua PV bermuara di LA • Tricuspid regurgitasi moderate
 Arcus aorta di kiri, CoA (-)
 PA konfluens, PDA (-)
 ASD (-), PFO (-)
 VSD perimembran ukuran 11 mm L-R shunt
 Dilatasi LA dan LV
 Aorta regurgitasi severe (AR PHT 180)
 Tricuspid regurgitasi moderate (TR VC 4 mm)
 Echocardiografi bedside 10

Terdapat vegetasi di katup Aorta ukuran 0,8 x 0,3 cm

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Diagnosis
 VSD perimembran L-R shunt
 Aorta regurgitasi severe
 Possible infective endocarditis
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Management
 Ceftriaxone 1 gr/12 hours/intravenous (1 month)
 Gentamisin 120 mg/24 hours/intravenous (2 weeks)
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PLAN
 Consult Thorasic surgery Division
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Introduction
 Infective endocarditis (IE) is a is a life-threatening disease

 Infective endocarditis (IE) is caused by damage to the endocardium

of the heart followed by microbial, usually bacterial  colonization

 Despiteimprovements in its management, IE remains associated with

high mortality and severe complications
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Epidemiology
 IE is a relatively rare but life-threatening disease
 Incidence ranged from 1,5 to 11,6 cases per 100,000 person-years
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Risk factors
 Prosthetic valves and cardiac devices (permanent pacemakers and cardioverter
defibrillators) are significant risk factors for IE
 Congenital heart disease also confers increased risk of IE
 Almost any type of structural heart disease can predispose to IE
 Other factors predisposing to IE include injection drug use (IDU), human
immunodeficiency virus (HIV) infection and extensive healthcare system
contact
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Microbiology
 Streptococci and staphylococci  approximately 80% of IE cases
 Enterococci are the third leading cause of IE
 In approximately 10% of cases of IE, blood cultures are negative, most
commonly due to patient receipt of antibiotics prior to the diagnostic work-up
 Serologic testing and polymerase-chain-reaction (PCR) using blood or valve
biopsies  suggest a causative pathogen in up to 60% of such cases
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Patofisiology
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End-Organ
Manifestasions
of IE
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Diagnosis
The diagnosis of IE typically requires a combination of :
 Clinical
 Microbiological and
 Echocardiography results
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Management
 All patients should receive antimicrobial therapy
 Duration of therapy
 Selection of the appropriate antimicrobial agent
 Considerations for prosthetic valves and implantable cardiac devices
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Surgery
 Indications for valve surgery are heart failure, uncontrolled infection and
prevention of embolic events in patients at high risk

 Uncontrolled infection may be related to paravalvular complications, such as

abscess, and enlarging vegetation

 Uncontrolled infection ongoing systemic illness with persistent fevers and

positive blood cultures, despite appropriate antibiotic therapy
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THANK YOU
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In summary, echocardiography (TTE and TOE),

positive blood cultures and clinical features remain the
cornerstone of IE diagnosis. When blood cultures are
negative, further microbiological studies are needed

The sensitivity of the Duke criteria can be improved

by new imaging modalities (MRI, CT, PET/CT) that
allow the diagnosis of embolic events and cardiac
involvement when TTE/TOE findings are negative or
doubtful