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Curriculum Vitae

NAMA : Dr. Ronald Irwanto Natadidjaja, SpPD – KPTI, FINASIM

PENDIDIKAN :
SMP - SMA : Kolese KANISIUS, 1994
Dokter Umum : FK TRISAKTI, 2002
Spesialis Penyakit Dalam (Internist) : FKUI, 2009
Konsultan Penyakit Tropik & Infeksi : FKUI / PAPDI, 2013

PEKERJAAN :
Bendahara Pengurus Besar Perhimpunan Konsultan Penyakit Tropik dan Infeksi Indonesia (PB PETRI)

SekJen Pengurus Pusat Perhimpunan Pengendalian Infeksi Indonesia (PP. PERDALIN)

Tim Panel Ahli PNPK Sepsis, Kemenkes RI

Anggota Pokja PPI, Kemenkes RI

Staf Pengajar Ilmu Penyakit Dalam, FK TRISAKTI

Ketua PPRA, RS PONDOK INDAH – PURI INDAH dan RS PONDOK INDAH – BINTARO JAYA

Wakil Ketua Komite Medik, RS PONDOK INDAH – PURI INDAH

Internist - Konsultan, RS PONDOK INDAH – PURI INDAH dan RS PONDOK INDAH – BINTARO JAYA
Catheter related Blood Stream Infection :
How to Prevent? How to Treat?

Ronald Irwanto
Infectious Disease (ID) Specialist
PERDALIN / INASIC
AGENDA
• Defining & Preventing the Catheter related
Blood Stream Infection (CRBSI)

• CRBSI focused on MRSA infection

• CRBSI : Systemic Invasive / Non Neutropenic


Candidemia
• Conclusion
• Defining & Preventing the Catheter related
Blood Stream Infection (CRBSI)
Catheter related BSIs
• Majority :Using Central Line BSIs SEPSIS
• Primary BSIs
• Hospital Settings
• Majority causal :
- Gram Positive (MSSA/E, MRSA/E) (Resident Flora)
- Candida sp ,Non Neutropenic Candidemia (Resident Flora)
- Gram Negative MDR / XDR/PDR Gram Negative
(ESBL, Pseudomonas sp,Acinetobacter sp, etc)
(Transient Flora)

Wenzel RP
M. Falagas
Preventing Catheter related BSIs
Do we need Prophylaxis?

No Study Established
Just Enhance the Bundles!!!
• CRBSI focused on MRSA infection
How To Predict the Etiology of CLABSI?

• Bacterial VS Fungal
• Clinical parameter :
- Onset
- Progress
• Laboratory parameter
- Procalcitonin
- Culture result
Microorganisms with Drug Resistance That are
Major Problems in Hospitals
Gram-positive Organism Gram-negative Organism
MRSA Klebsiella species  ESBL
MRSA (HRV)  VRSA Enterobacter species
VRE Pseudomonas aeruginosa
Acinetobacter baumanii
Note: HRV, heterogeneous resistance to vancomycin

Levy SB; CID 2001:33 (Suppl 3)


CA-MRSA
Host (-) in one year:
1. Hospitalization
2. Hospital Colonization
3. Invasive equipment

Microbiology :
High sensitive to cotrimoxazole

Higher PVL Toxin Producing

CRBSI???
Might be CA or HA MRSA
Treatment of MRSA

Susceptibility First choice Alternative

Methicillin(oxacillin) Vancomysin 1g bid iv Cotrimoxazole 60 mg/kg/day


resistant Teicoplanin 3 mg/kg (mild infection) in divide dose 2-4x iv
6 mg/kg (severe infection) (960 mg bid oral)
12 mg/kg (endocarditis) bid iv Minocyclin (or doxycyclin)
( MRSA ) for the first 2-5 day followed by 100 mg bid iv or oral
3-12 mg/kg qd Ciprofloxacin 400 mg bid iv
Linezolid 600 mg bid iv or oral or 500 mg bid oral
Quinopristin-Dalfopristin Levofloxacin 500 mg qd iv
7,5 mg/kg bid or tid iv or oral

Oxacillin resistant Quinopristin-Dalfopristin


Vancomycin intermediate 7,5 mg/kg bid or tid
( GRSA ) Linezolid 600 mg bid or oral
Dosed 100 mg loading, 50mg every
twelve hours, i.v. only
Tygecicline
Dosed 100 mg loading, 50mg every
twelve hours, i.v. only
Comparative In Vitro Activity of Glycopeptides Vs Staphylococcus spp And
Streptococcus spp
( From Spencer & Goering, With Permission From Elsevier Science-NL

Species No. of Minimum inhibitory concentration (mg/L)


isolates Teicoplanin vancomycin
50% 90% range 50% 90% range

S.Aureus (methicillin-
1250 0.5 0.5 < 0.03 – 8 1 2 0.03 – 8
sensitive)
S.Aureus (methicillin-
1083 0.5 0.5 < 0.06 – 16 1 2 0.06 – 4
resistant)
CNS (methicillin-sensitive) 885 1 2 < 0.06 – 32 2 4 0.06 – 16
CNS (methicillin-resistant) 428 2 4 < 0.125 – 32 2 4 0.125 – 4
s. haemolyticus 279 8 16 < 0.125 – 64 2 4 0.5 – 8
Strep. Agalactiae 127 0.06 0.125 < 0.03 – 0.5 0.25 0.5 0.25 – 0.5
Strep. Pneumoniae
256 0.06 0.125 < 0.03 – 0.5 0.25 0.5 < 0.03 – 1
(penicillin-sensitive)
Strep-pneumoniae
110 0.06 0.125 < 0.06 – 0.5 0.25 0.5 0.125-0.5
(penicillin-resistant)
Strep.pyogenes 196 0.06 0.12 < 0.03 – 0.12 0.5 1 0.25 – 1
Viridans streptococci 86 0.12 0.25 < 0.06 – 1 0.5 1 < 0.25 - 2
• CRBSI : Systemic Invasive / Non Neutropenic
Candidemia
Risk Factors for Systemic / Invasive Fungal
Infections
Candida colonization
Prolonged used wide spectrum antibiotics
Iatrogenic : CVC
Ventilators
Urinary catethers
Hemodialysis
Surgery
Host Condition:
Malignancy
HIV-AIDS
Burns
COPD
Dilemmas in Diagnosis Invasive
Fungal Infections
• Clinical symptoms are not characteristic
• Fungi can be both colonizers and
pathogens, and even laboratory
contamination
• Biopsy is often precluded by co-morbidity
• Objective evidence usually occurs late in
the course of infection
Diagnosis of Invasive Fungal Infection

• Proven/definite Host
factor
Clinical
feature Tissue Mycology
s

Is it VISIBLE for
• developing
Probable country?? Clinical

PLUS
Host
factor feature Mycology
s

High Specificity??
OR
Clinical

• Possible Host
factor
feature
s
Mycology

Invasive 
Fungal 
Infections 
Cooperative 
Group
Non-Neutropenic Candida Infection Treatment Approach

High Sensitivity??

Bassetti et al. Critical Care 2010


When to Start Antifungal Therapy ?
Colonization Invasiveness Dissemination
At risk

Time course Disease probability


No treatment Treatment

Overtreatment                            Undertreatment

Successful response
Ben E. dePauw. CID 2005;41:1251-3
CRBSI : Key of Treatment Performance
• Fast diagnosis
• Fast Remove catheter
• Fast Broad Spectrum AB (for both gram (+)ve & (-)ve)
+ Antifungal (If necessary) administered with
aggressive approach
• Fast microbiology result
• Fast De-escalation or step down when clinical going
well
Conclusion
• CRBSI should be diagnosed well
• The etiology : Gram (+)ve, Gram (-)ve, fungal
(majority is candida)
• Aggressive approach is needed
• Fast De-escalation should be done when it
proper
Thank You

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