PENYAKIT JANTUNG RHEUMA

Djoen Herdianto
SMF Jantung & Kedokteran Vaskular
RSUD A Wahab Sjahranie
Samarinda
 Batasan

 PENYAKIT KERADANGAN DIFUS YANG

MERUPAKAN KOMPLIKASI LAMBAT NON-
SUPURATIF DARI RADANG TENGGOROKAN
KARENA KUMAN STREPTOKOKUS GRUP A

( MELALUI PROSES "IMMUNOLOGI"), DENGAN

PERIODE LATEN I - 5 MINGGU.
 Batasan

 SUATU PENYAKIT SISTEMIK YANG MENGENAI

JARINGAN IKAT CONNECTIVE YANG MELIBATKAN
GANGGUAN MULTIORGAN.

 SEMUA MANIFESTASI KERADANGAN YANG TIMBUL

AKAN MEMBAIK, KECUALI PADA KARDITIS YANG
MENYEBABKAN KERUSAKAN PADA ORGAN
(BERSIFAT PERMANEN)
 PATOGENESIS/PATOFISIOLOGI
 INFEKSI KUMAN GABH STREPTOKOKUS
RADANG TENGGOROKAN BERAT KHAS DAN
TIDAK KHAS ATAU GEJALA (-)

 INFEKSI KUMAN GABH STREPTOKOKUS

ANTIGEN MIRIP JARINGAN PENYANGGA
MANUSIA ANTIBODI REAKSI
SILANG IMUNOLOGIS
 PATOGENESIS/PATOFISIOLOGI

 antibodi yang dihasilkan oleh sistem imun

tubuh untuk melawan aktifitas streptococcus
menyebabkan degenerasi fibrinoid jaringan
ikat, infiltrasi sel inflamasi dan proliferasi sel
spesisifik membentuk nodul Aschcoff :

- Cardiac cells → Pan Carditis.

PATOGENESIS/PATOFISIOLOGI

- Synovial membranes → Arthritis.

- Serosal membranes → Peritonitis

- Lesi pada Basal Gannglia → Chorea

Gambaran Morfologi
Demam Rheuma
Akut pada
Jantung.
 Patologi
Kelainan Jantung Rheuma dibagi 2 fase:
1. Fase akut
2. Fase kronis/ penyembuhan
 Karditis Rheumatik Akut
 Mengenai semua lapisan jantung
(pericarditis, miokarditis,
endokarditis),sinovial dan paru.
 Aschoff body : sel-sel plasma,limfosit &
eosinofil  reaksi perivaskular & vaskulitis.
 Katup-katup  vegetasi pengumpulan butir-
butir endapan trombosit dan fibrin. Letaknya
diujung daun katup  Stenosis
Karditis Rheumatik Kronis
Katup jantung yang paling sering
terkena komplikasi akibat reaksi
perivaskular dan vaskulitis adalah :
1. Katup Mitral ( 60 – 70 %)
2. Katup Aorta ( 25% )
3. Katup Trikuspid dan (10%)
4. Katup Pulmonal (jarang)
 GAMBARAN KLINIS :
1- CARDITIS:
- PANCARDITIS.
* Endocarditis and valvulitis.
* Myocarditis.
* Pericarditis.

- LESI KATUP JANTUNG RESIDUAL.

*MS.
*MR.
*AR.
*AS.
*TS.
*TR.
 GAMBARAN KLINIS :

2- ARTHRITIS:
A- Migratory.
B- Mengenai sendi-sendi besar.
Tanda-tanda inflammasi :
- Bengkak.
- Panas.
- Kemerahan.
- Nyeri.
- Immobilitas.
Tidak ada gejala-gejala residual.
 GAMBARAN KLINIS :

3- Chorea Rematik Sydenham :

-♀ > ♂ ( 7:1 ).
- Usia remaja
- Self limiting.
- Sekitar 50% dari kasus ini didapatkan Carditis.

4- Erythema marginatum (annularis):

- Sentral/tengahnya pucat.
- Trunk and thighs.
- Tidak nyeri.
- Self- limiting.
annular erythema
 GAMBARAN KLINIS :

5- Subcutaneous nodul:
- Didapatkan pada permukaan sendi-
sendi ekstensor.
- Diameter ± 1 cm .
- Tidak ada nyeri.

- Menghilang dalam beberapa minggu.

 PEMERIKSAAN PENUNJANG :
 LABORATORIUM :
- Darah Lengkap : Anemia, Leukositosis.
- LED meningkat.
- CRP positif.
- ASTO titer meningkat > 200 Todd Units (nilai puncak
dicapai dalam 3 minggu selanjutnya menurun hingga
normal setelah 6 minggu).
- Kultur apus tenggorokan positif terhadap GABH
Streptococci dan negatif bila sudah timbul Peny,
Jantung Rheuma
 PEMERIKSAAN PENUNJANG :
FOTO POLOS DADA:
- Normal.
- Kardiomegali.
- Tanda-tanda Gagal jantung.
 PEMERIKSAAN PENUNJANG :

 ECG:
- 1o AVB.
- ST.
- PAC.
- PVC.
 ECHOCARDIOGRAM.
- Pericardial effusion.
- Tanda-tanda kelainan pada katup jantung.
 Diagnosis
Kriteria Jones (1992)
Mayor Minor
 Karditis (perikarditis,mio-  Riwayat menderita DR
karditis, endokarditis) atau PJR
 Polyartritis  Artralgia
 Chorea Rematik Sydenham  Demam < 39 0 C
 Erytema marginatum  Anemia
 Nodul subkutan  Lekositosis

Dx positif  LED 

2 mayor + 1 minor  CRP positif

1 mayor + 2 minor  PR interval memanjang

 ASTO 
 Penatalaksanaan Medis

Tujuan :
1. Memberantas infeksi streptokokus
2. Mencegah komplikasi karditis
3. Mengurangi rasa sakit demam
 Penatalaksanaan Medis
 Memberantas Infeksi Streptokokus dengan
antibiotika.
 Mencegah komplikasi Carditis
 Analgesia.
 ASA (Acetyl Salicylic Acid)→ 100mg/kg/day. →
4 dosis terbagi + H2 Blockers or PPI.
 NSAIDs (Ibuprofen).
 Steroid.
 Rx untuk gagal jantung.
 Penatalaksanaan Medis

Indikasi pemberian steroid.

1- Resistant arthritis.
2- Pericarditis.
3- Myocarditis with 2o AVB or 3o AVB
 Penatalaksanaan Medis

1. Memberantas infeksi streptokokus

Pemberian Inj Penicilin G benzatin im dosis :
BB > 30 kg : 1,2 juta unit
BB < 30 kg 600.000 s/d 900.000 unit
Penicilin G oral 4 X 200.000 – 250.000 unit
atau
Erytromycin 50 mg/kg BB/hari dibagi dalam
4 dosis selama 10 hari
 Penatalaksanaan Medis

2. Mencegah komplikasi karditis

 Tirah baring selama serangan akut demam
rheuma
 Inj Penicilin benzatin sekali sebulan untuk
pencegahan sekunder
 Digitalis bila ada gagal jantung 0,04 s/d
0,06 mg/ kg BB
 Penatalaksanaan Medis

3. Mengurangi rasa sakit, demam dan anti

radang
 Salisilat 100 mg/kg BB /hari selama 2
minggu dilanjutkan 25 mg/kgBB/hari
selama 1 bulan
 Prednison 2mg/kgBB/hari selama 2
minggu dan dikurangi bertahap (tappering
off)
 PENCEGAHAN
I- Pencegahan Primer:
- Pengobatan Epidemi infeksi
streptokokus.
- Memperbaiki status sosioekonomi
masyarakat.
- Memperbaiki pusat-pusat
pelayanan kesehatan primer.
 PENCEGAHAN

II- Pencegahan Sekunder:

- Demam Rheuma disertai karditis
dan Penyakit Katup Jantung →
diberi profilaksis selama ≥ 10 tahun

setelah serangan terakhir atau

hingga usianya 40 tahun.
 PENCEGAHAN
II- Pencegahan Sekunder:
- Demam Rheuma disertai karditis
tanpa Peny Katup Jantung → diberi
profilaksis selama 10 tahun setelah
serangan terakhir atau hingga
mencapai usia dewasa (21 th).
- Demam Rheuma tanpa karditis →
diberi profilaksis selama 5 tahun
setelah serangan terakhir atau
hingga mencapai usia dewasa.
 PENCEGAHAN :
 Pencegahan terbaik:
- Benzathin penicillin 1.200.000 IU – IM setiap 4 minggu
(1 bulan) pada orang dewasa.
 Jika pasien hipersensitive terhadap penicillin:
- Erythromycin 250mg PO – OD.
 Miokarditis

Djoen Herdianto
SMF Jantung & Kedokteran Vaskular
RSUD A Wahab Sjahranie
Samarinda
 Miokarditis
 Proses inflamasi pada miokardium,
lapisan tebal otot jantung yang
merupakan bagian besar dari
jantung.
 Sering merupakan kelanjutan URI
 Epidemiologi
 Tidak ada angka Insiden yang akurat.
 Gold Standart untuk menegakkan
diagnosis melalui pemeriksaan non
invasif belum ada.
ETIOLOGI
 Infectious Noninfectious

Viruses – Systemic Diseases:

1. Coxsackie B 1. SLE
2. HIV 2. Sarcoidosis
3. Vasculitides(Wegener’s)
4. Celiac disease

Bacterial – Neoplastic infiltration

1. Corynebacterium diphtheriae

Protozoan – Drugs & toxins:

1. Trypanosoma cruzi (Chagas 1. Ethanol
disease) 2. Cocaine
3. Radiation
4. Chemotherapeutic agents -
Doxorubicin
Spirochete
1. Borrelia burgdorferi
(Lyme disease)
 Keluhan & Tanda Gejala

 Nyeri dada yang tidak spesifik

 Kadang nyeri dada spesifik yang
menyerupai Sindroma Koroner Akut
STEMI
 Keluhan dan tanda-tanda gagal jantung
 Keluhan & Tanda Gejala
 Timbul tanda- tanda keluhan gagal jantung
mendadak fulminant atau gradual dalam
beberapa hari atau minggu setelah sakit
demam akut
 Mirip Sindroma Koroner Akut STEMI,
peningkatan enzim cardiac markers,
gangguan kinetik miokard regional
PEMERIKSAAN PENUNJANG
 LABORATORIUM
 Peningkatan Lekosit
 Laju Endap Darah meningkat
 Troponin meningkat pada 1/3 dari kasus
 CK-MB meningkat pada 10% dari kasus
 Echocardiogram helps evaluate cardiac function
& exclude other causes
 Cardiac MRI improving in ability to see
abnormalities in myocardium
 EKG & FOTO POLOS DADA
Gambaran EKG :
sinus takikardi, kelainan repolarisasi
nonspesifik , dan kelainan konduksi
intraventrikular
 Foto Polos Dada :
Kardiomegali, hipertensi vena paru,
edema paru
 EKHOKARDIOGRAFI &
BIOPSI MIOKARDIUM
 Ekhokardiografi dapat ditemukan
kardiomegali & gangguan kontraktilitas
otot jantung.
 Biopsi Miokardiaum, meskipun kurang
sensitif, dapat menggambarkan
karakteristik pola inflammasi (misal.
Giant Cell)
 Biopsi Endomiokardium
 Gold standard untuk menegakkan
diagnosis Miokarditis
 Pathologic exam may reveal
lymphocytic inflammatory response with
necrosis, but this is not sensitive b/c of
the patchy areas of distribution.
 Biopsi Endomiokardium
 “Dallas” criteria for histopathologic dx
histopathological (acute myocarditis is
defined by lymphocytic infiltrates in
association with myocyte necrosis)
 “ Dallas” criteria for the detection of viral
genome was a predictor of poor outcome.
 May see “Giant cells”
 Treatment & Prognosis
 Fulminant myocarditis pt may present with
cardiogenic shock
– Ventricles are thickened, usually not dilated
 Subacute pt have dilated cardiomyopathy
 Chronic pt may have mildly dilated LV and
more of a restrictive cardiomyopathy
 Treatment
 Antibiotics if specific agent is identified
 Standard HF therapy
 Arrhythmia suppression
 Limited exercise role during recovery
 IVIG and steroids are controversial
 Fulminant myocarditis need aggressive short
term support from intra-aortic balloon
pumps &/or LVAD
 Pericardial Diseases
 Visceral – single layer mesothelial cells
 Parietal- fibrous < 2 mm thick
 Functions
– Limits motion
– Prevents dilatation during volume increase
– Barrier to infection
 15-50 ml serous fluid
 Well innervated
53
 Introduction
 The Pericardium is a fibroelastic tissue
made up of parietal and visceral layers
 These two layers are separated by the
pericardial cavity
 Pericardial cavity usually contains 15-50 ml
of plasma ultrafiltrate in healthy individuals
 Diseases of the Pericardium
 Acute Fibrinous Pericarditis
 Pericardial Effusion without major
hemodynamic compromise
 Cardiac Tamponade
 Constrictive Pericarditis
 Etiology of Pericardial
Diseases
 Viral Infections  Cardiac procedures
 Purulent Pericarditis  Drugs and Toxins
 TB  Metabolic disorders
 Mediastinal radiation  Malignancies (breast, lung,
 MI Hodgkin’s, mesothelioma)
 Cardiac surgery  Collagen Vascular Disease
 Trauma  Idiopathic
 Etiologies of Pericarditis
 Neoplastic-35%
 Immune Mediated- 23%
 Viral- 21%
 Bacterial-6%
 Uremia-6%
 TB- 4%
 Idiopathic-4%
 Viral Pericarditis
 Common bugs
– Cocksackie A and B
– Echovirus
– Adenovirus

 Viral infections uncommon in patients presenting

with pericardial effusion w/o pericarditis
– Exception is HIV- frequently presents with significant
effusion w/o pericaritis
– seen in 7 % of patients hospitalized with effusions
 Bacterial Pericarditis
 Staphylococcus
 Pneumococccus
 Streptococcus(rheumatic pancarditis)
 Haemophilus
 M.Tuberculosis
 Can occur as systemic spread or direct extension
 Frequently purulent
 Fungal Pericarditis
 Histoplasma- most common fungus in
immunocompetent patients
– Especially the Ohio River Valley
 In immunocompromised
– Aspergillus
– Candida
– Coccidoides
 Frequently purulent
 Other Infectious Etiologies
 Rickettsia Ricketsii
 Chlamydia Psittaci
 Borrelia burgdorferi
 Treponema Pallidum
 Actinomycosis
 Mycoplasma Pneumonia
 Nocardia
 Post MI
 Pericardial involvement is related to infarct size
 Early stage - inflammatory etiology
 Late stage
– Immune mediated weeks to months out
– Known as Post Cardiac Injury syndrome (PCIS) or
Dressler’s syndrome
– Rare in modern time due to reperfusion therapies
 Iatrogenic Causes
 Mediastinal Radiation-wide spectrum of
diseases seen
 Cardiac Surgeries
 Cardiac Procedures
 Traumatic
 Drugs
 Lupus like sydromes
– Procainamide
– Hydralazine
– Phenytoin
– INH
 Penicillins- Hypersensitivity Pericarditis
 Chemotherapy
– Doxorubicin/Daunorubicin-cardiomyopathy/pericardiopathy
 Bleomycin - sclerosing agent
 Toxins
 Asbestosis can cause pericardial lesions
 Scorpion fish venom can cause pericarditis
 Metabolic Disorders
 Uremia-
– Most common metabolic cause
– 6-10 % of ESRD patients not on HD can have Pericarditis
– Dialysis related Pericardial Effusions (seen in 13% of patients)
 Severe Hypothyroidism
– effusion – usually not significant
– rarely pericarditis
 Ovarian hyperstimulation syndrome
– complication of gonadotropin therapy
– Due to fluid shifts
 Malignancy
 Responsible for 6% of acute pericardial disease
(pericarditis and tamponade)
 Accounts for 15-20% of moderate to large pleural
effusions
 Mets - Lung, Breast, Hodgkin’s metastases
 Primary - Mesotheliomas and lipomas
 Collagen Vascular Disease
 SLE- pericardial involvement in up to 50%
 Rheumatoid Arthritis
 Progressive Systemic Sclerosis
 MCTD
 Polyarteritis
 Giant Cell Arteritis
 Inflammatory Bowel Disease
 Idiopathic
 In two large series (331 patients), only 16 %
had an identifiable cause of pericarditis
 Many of these cases are presumed viral
 Only 7-29% of patients have idiopathic
pericardial effusions
 Clinical Presentation of
Pericarditis
 Chest Pain-
– sudden onset over anterior chest
– sharp and pleuritic
– Improves by leaning forward
– Radiates commonly to trapezius ridges
 Pericardial Friction Rub
 EKG – findings depend on stage
 2 of 3 needed to make diagnosis +/- effusion.
 Diagnostic evaluation
 History  PPD
 Physical  HIV
 Search for systemic  BCx if febrile
disorders  No routine viral
cultures
 ECG
 Workup for malignancy
 CXR if history suggests
 ANA in selected cases  Echo-Class Ia
 Pericardial Friction Rub
 Auscutation
– Scratchy or squeaky sound
– LLSB most frequent site
– Use the diaphragm
– suspended respiration
 Highly specific for pericarditis (up to 85%).
 Intermittent – sensitivity can vary.
 Heard better in patients without effusion.
 Result of friction from 2 inflamed layers of
pericardium
 EKG Findings
Stage I
•ST elevation in most leads
•Exceptions aVR and V1
•Depression of PR segment
•Low voltage QRS – usually assoc with
tampanode

Stage II
Transition or “pseudonormalization” or ST/PR
segments

Stage III
T wave inversions.

Stage IV
Normalization vs persistent changes

*No changes in metabolic causes

 EKG changes
 Arrhythmias uncommon. Arryhthmias
suggest myocarditis or ischemia
 Distinction From AMI

 ST elevations in pericarditis: begin at J point, rarely

exceed 5 mm, and retain normal concavity
 ST elevations / T wave changes are more generalized
 No reciprocal lead changes
 ST elevations and T wave inversions do not occur at
the same time
 PR segment changes common
 Q waves/QT prolongation/Hyperacute T waves
uncommon
 Cardiac Biomarkers
 Can see elevation in CK, MB, TpnI
 22% of patients with Acute Pericarditis in
one trial were above TpnI threshold
 Transient rise, resolving within the first 7
days
 Patients with higher TpnI did not have
higher complication rates
 CXR findings
 Typically normal in Pericarditis
 200ml of pericardial fluid needed to
accumulate before enlargement of the
cardiac silhouette seen
 Calcification in chronic cases may be
appreciated
Lateral CXR of a person with
chronic calcified pericarditis
due to TB

A – cystic mass
B – calcified pericardium
 Echocardiogram
 Should be done in all cases
 Often normal in patients with pericarditis,
unless associated with pericardial effusion
 Presence of pericardial effusion helps
support diagnosis, while absence does not
exclude it
Pericardial Effusion
 Diagnostic evaluation
 Not needed in all patients- Viral and
idiopathic usually follow a benign course
after treatment
 It is important to rule out significant
effusion and tamponade in patients
 Management
 Simple, uncomplicated pericarditis
– No high risk features
– Medical management
– outpatient if proper F/U is established
 High Risk Features
 Subacute onset  Immunosuppressed
 Fever >100.4  Hx of anticoagulation
 Leukocytosis  Acute Trauma
 Cardiac tamponade  Failure to respond to
 Large pericardial NSAIDS
effusion (>2cm) not
decreased after
NSAIDS
 Treatments
 ASA-Class I (2-6g/day) or
(800mg q6h tapered by
 Colchicine- Class IIa
800mg /week for 3-4 weeks)  Intrpericardial Steroids
 ASA resistance at 1 week should
prompt further investigation –Class IIa
 NSAIDS- ClassI (Ibuprofen 300-  Corticosteroids if
800mg q6h)
 GI prophylaxis refractory to NSAIDS
 Pericardiocentesis
 If moderate to severe tamponade is present
–Class IA recommendation
 If purulent, TB, or neoplastic pericarditis is
suspected- Class II a recommendation
 Persistent symptomatic pericardial effusion
 Complications
 Constriction
– scarring and consequent loss of elasticity of the
pericardial sac
 Tamponade
– accumulation of pericardial fluid under pressure
 Effusive-constrictive pericarditis
 Recurrent Pericarditis- seen in 15-30% of patients
with idiopathic pericarditis. Immune
autoreactivity thought to play a primary role.
 Pericardial Tamponade
 Increased Pericardial Pressures leading to
compression of all cardiac chambers
 Pericardial elasticity maybe limited (Acute vs
Chronic)
 Cardiac chambers become small and chamber
diastolic compliance is reduced
 Decreased cardiac filling
 Physiologic significance
 Early diastolic filling decreases, leading to
the majority of venous return occuring
during ventricular systole
 When tamponade is severe, total venous
return falls and cardiac chambers shrink
Physical Exam of Tamponade
 Sinus Tachycardia
 Elevated JVP
 Pulsus Paradoxus
 Rub possible
 Kussmaul's sign
– Less likely w/o
constrictive component
 Pulsus Paradoxus
 An exaggerated fall in systemic blood pressure during
inspiration
 Inspiratory decline in thoracic pressure is transmitted
through the pericardium to the right side of the heart
 Systemic Venous return increases with inspiration
 In tamponade, the rigid pericardium prevents the RV free
wall from expanding during diastole causing the pressure
transmission to the septal wall and decreased LV filling
during inspiration
Acute vs chronic accumulation
 As little as 20-50 ml acutely can cause tamponade
acutely
 As much as 2 liters can accumulate chronically
prior to causing tamponade
 Conclusion
 Pericarditis has many causes
 A good history and physical will often lead to
diagnosis
 ECHO, EKG, HIV, CXR and PPD should be
done
 Outpatient management may be reasonable
 Anti-inflammatories key for medical
management
Endokarditis Infeksiosa
 roadmap
1. Definitions, general information
2. Clinical symptoms
3. Diagnosis
1. Duke criteria
2. Blood cultures
3. Echocardiography
4. Treatment basics
5. Complications
6. Prophylaxis
7. Summary
 Definitions, general
information

• Infective endocarditis
– inflammatory process on-going inside
endocardium
– due to infection after endothelium damage
– most often involving aortic and mitral valves
 Definitions, general information
- continued
Acording to localisation
• Left sided IE
– Native valve IE (NVE)
– Prosthetic valve IE(PVE)
• Early < 1 year after surgery
• Late >1 year after surgery
• Right sided IE
• Device- related IE (ICD)
 Definitions, general information
- continued
Acording to the mode of acquisition
• Health-care associated IE
– Nosocomial
– Non-nosocomial
• Community acquired IE
• Intravenous drug abuse-associated IE
 Definitions, general information
- continued
 Active IE
 Recurrence
– Relpse
– Reinfection
 Definitions, general information
- continued
 3-10/100 000/year
 Maximum at the age of 70-80
 More common in women
 Staphylococcus aureus is the most common
pathogen
 Streptococcal IE is still the most common
in developing countries
 roadmap
1. Definitions, general information
2. Clinical symptoms
3. Diagnosis
1. Duke criteria
2. Blood cultures
3. Echocardiography
4. Treatment basics
5. Complications
6. Prophylaxis
7. Summary
 Clinical symptoms
 Fever – over 90% of patients
 New intra-cardiac murmur - about 85% of
patients
 Roth spots, petechiae, glomerulonephritis –
up to 30% of patients
 Clinical symptoms – when to
suspect?
• Sepsis of unknown origin
• Fever coexsisting with:
– Intracardiac implantable material
– IE history
– Congenital heart disease or valve disease
– IE risk factors
– Congestive heart failure symptoms
– New heart block
– Positive blood cultures
– Focal neurological signs without known aetiology
– Periferal abscesess (kidney, spleen, brain, vertebral column)
 roadmap
1. Definitions
2. Clinical symptoms
3. Diagnosis
1. Duke criteria
2. Blood cultures
3. Echocardiography
4. Treatment basics
5. Complications
6. Prophylaxis
7. Summary
 Duke criteria
Major criteria
1. Blood culture positive for
typical IE-causing
microorganism
2. Evidence of endocardial
involvement
Diagnosis
• 2 major criteria
• 1 major and 3 minor
• 5 minor criteria
Minor criteria
1. Predisposition – heart
condition or i.v. drug abuse
2. Fever – temp. >38 °C
3. Vascular phenomena –
arterial emboli etc.
4. Immunologic phenomena –
glomerulonephritis, Osler’s
nodes, Roth’s spots
5. Microbiological evidence –
positive blood cultures but do
not meet major criteria
 roadmap
1. Definitions
2. Clinical symptoms
3. Diagnosis
1. Duke criteria
2. Blood cultures
3. Echocardiography
4. Treatment basics
5. Complications
6. Prophylaxis
7. Summary
 Blood cultures

 Always before starting antibiotics

 Always triple samples – aerobe, anaerobe and
mycotic , 10 ml each
 Three sets of samples required
 roadmap
1. Definitions
2. Clinical symptoms
3. Diagnosis
1. Duke criteria
2. Blood cultures
3. Echocardiography
4. Treatment basics
5. Complications
6. Prophylaxis
7. Summary
 Echocardiography
• Transthoracic (TTE) and transoesophageal
(TEE)
• fundamental importance in diagnosis,
management, and follow-up
• Should be performed as soon as the IE is
suspected
• Sensitivity of TEE is bigger than TTE (vs 90-
100% vs. 40-63% )
• TEE is first choice to find IE complications
 Echocardiography
Echocardiographic findings in
IE
• Vegetation
• Abscess
• Pseudoaneurysm
• Perforation
• Fistula
• Valve aneurysm
• Dishence of prosthetic valve
 roadmap
1. Definitions
2. Clinical symptoms
3. Diagnosis
1. Duke criteria
2. Blood cultures
3. Echocardiography
4. Treatment basics
5. Complications
6. Prophylaxis
7. Summary
 Treatment basics
 Sucess relies on eradication of pathogen
 Bactericidal regiment should be used
 Drug choice due to pathogen
 Surgery is used mainly to cope with
structural complications
 Treatment basics - continued
• NVE standard therapy - it takes 2-6 weeks to
eradicate the pathogen
• PVE – longer regime is necessery – over 6
weeks
• In Streptococcal IE shorter, 2 week course,
can be used when combining β-laktams with
aminoglycosides
• Most widely used drugs – amoxycylin,
gentamycin
• In case of β-laktams alergy - vancomycin
 roadmap
1. Definitions
2. Clinical symptoms
3. Diagnosis
1. Duke criteria
2. Blood cultures
3. Echocardiography
4. Treatment basics
5. Complications
6. Prophylaxis
7. Summary
 Complications
1. Congestive heart failure
• Most common complication
• Main indication to surgical treatment
• ~60% of IE patients
2. Uncontrolled infection
• Persisting infection
• Perivalvular extension in infective endocarditis
3. Systemic embolism
• Brain, spleen and lungs
• 30% of IE patients
• May be the first symptom
 Complications - continued

5. Neurologic events
6. Acute renal failure
7. Rheumatic problems
8. Myocarditis
 roadmap
1. Definitions
2. Clinical symptoms
3. Diagnosis
1. Duke criteria
2. Blood cultures
3. Echocardiography
4. Treatment basics
5. Complications
6. Prophylaxis
7. Summary
 Prophylaxis
• First and most important – proper oral hygiene
• Regular dental review
• Antibiotics only in high-risk group patients
– Prosthetic valve or foreign material used for heart
repair
– History of IE
– Congenital heart disease
• Cyanotic without correction or with residual lickeage
• CHD without lickeage but up to 6 months after surgery
– Use amoxycilin or ampicylin 30-60 min prior to
intervention
 roadmap
1. Definitions
2. Clinical symptoms
3. Diagnosis
1. Duke criteria
2. Blood cultures
3. Echocardiography
4. Treatment basics
5. Complications
6. Prophylaxis
7. Summary
 Summary
1. IE is rare but serious disease, with high mortality rate
2. Every case of fever of unknown origin should be
suspected for IE
3. Blood cultures are essential for diagnosis
4. TTE/TEE is the best method to monitor and follow-up
of IE
5. Antibiotics are main treatment
6. CHF is the most common complication
7. Pharmacological prophylaxis is reserved for a narrow
group of high risk patients