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 PP. Perhimpunan Pengendalian Infeksi Indonesia (PP. PERDALIN)

Tim Panel Ahli PNPK Sepsis, Kemenkes RI

Kepala Bagian Ilmu Penyakit Dalam, FK TRISAKTI

Ketua PPRA, RS PONDOK INDAH – PURI INDAH

Wakil Ketua Komite Medik, RS PONDOK INDAH – PURI INDAH

Internist - Konsultan, RS PONDOK INDAH – PURI INDAH

CLABSI : How to predict?

RONALD IRWANTO

PP PERDALIN
 CLABSI : Central Line
Associated BSIs
Using Central Line BSIs SEPSIS
Primary BSIs
Hospital Settings
Majority causal :
- Gram Negative
MDR / XDR/PDR Gram Negative
(ESBL, Pseudomonas sp,Acinetobacter sp, etc)
- Gram Positive (MSSA/E, MRSA/E)
- Candida sp , Aspergillus sp (SFIs / IFIs)
Non Neutropenic Candidemia

Wenzel RP
M. Falagas
 CLABSI : Central Line
Associated BSIs
BSIs Blood Stream Infections  Sepsis
Bone et al criteria 1992
(Infection SITE + SIRS)

Surivival Sepsis Campaign 2010/2012

General variables
Inflammatory variables
Organ dysfunction
 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)

Sepsis : a Complex Clinical
Challenge

 High mortality rate

 Heterogeneous patient population
 Unpredictable disease progression
 Unclear etiology and pathogenesis

Wheeler, Bernard. N Eng J Med. 1999;340:207

 Systemic Inflammatory
Response Syndrome (SIRS)
Host response to
Inflammation include 2 of:

1. Temp >38oC or <36oC

2. Heart rate >90x/’
3. Respiratory rate >20x/’
or PaCO2<32mmHg
4. White blood cells count
>12.000/mm3, < 4.000
or bands >10%

Bone et al. Chest 1992;101:1644

 Updated Definition
Sepsis
– SIRS (systemic manifestations) + Infection (documented/
suspected)
Severe sepsis
– Sepsis + sepsis-induced organ dysfunction or tissue
hypoperfusion
Sepsis-induced hypotension
– a systolic BP(SBP) <90 mmHg or MAP <70 mmHg or SBP 
>40 mmHg or <2 SD below normal for age in the absence of
other cause of hypotension
Septic Shock
– Sepsis-induced hypotension persisting despite adequate
fluid resuscitation

Bone, et al. 1992 Chest 101:1644-1655

Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R, et al. Crit Care Med 2008; 36(1): 296-327
Infection SIRS Sepsis Severe Sepsis Septic Shock

Microorganism  A clinical response SIRS with a Sepsis with Refractory

invading arising from a presumed organ failure hypotension
sterile tissue nonspecific insult, or confirmed
with 2 of the Vascular collapse
infectious
following:
process
Renal
 T >38oC or Hemostasis
<36oC
 HR >90 Lung
beats/min LA
 RR >20/min
 WBC
>12,000/mm3 or
<4,000/mm3 or
>10% bands

Chest 1992;101:1644
 Criteria of Organ Dysfunction
 Aterial hypotension (MAP<70)
 SCVO2 >70%
 CI>3.5 L/mt/m2
 Arterial hypoxemia (PaO2/FiO2 <300)
 Acute oliguria (urine output<0.5ml/kg/h for at least 2
hours)
 Creatinin increase >0.5mg/dL
 Coagulation abnormalites (INR >1.5 or aPTT > 60 sec)
 Ileus
 Thombocytopenia <100.000/uL
 Hyperbilirubinemia >4 mg?dL
Tissue Perfusion
 Hyperlactatemia >3 mmol/L
 Decrease capilary fill SCCM/ESICM/ACCP/ATS/SIS
International Sepsis Definition Cofence,2001
Emergency Medicine 2010
How To Predict the Etiology of CLABSI?

Bacterial VS Fungal
Clinical parameter :
- Onset
- Progress
Laboratory parameter
- Procalcitonin
- Culture result
Risk Factors for Systemic Fungal Infections

Candida colonization
Prolonged used wide spectrum antibiotics
Iatrogenic : CVC
Ventilators
Urinary catethers
Hemodialysis
Surgery
Host Condition:
Malignancy
HIV-AIDS
Burns
COPD
Fungal infections have become increasingly
more frequent

Immunocompromised patients
AIDS organ transplantation

Increased use of invasive instruments

urinary catheters
CLABSI : When to Predict the SFIs?

CANDIDA IS
THE MOST
COMMON
OF
HUMAN FUNGAL
INFECTION

BOTH SUPERFICIAL
OR INVASIVE/
SYSTEMIC
INFECTION
 Invasive / Systemic Candida Infection
Risk Factors
Neutrophils count
<500
NEUTROPENIC
COLONIZATION
Febrile Neutropenia
Transplantation, MDS
Candida Post Chemotherapy, etc
Infection HIV/AIDS
Prolonged ICU Stay
>96 hours
NON
CVC
NEUTROPENIC
Broad Spec. AB
Non Immunocompromised GI Surgery, TPN, etc
Immunocompromised :
Primary COLONIZATION
Secondary : HIV/AIDS
Bassetti et al. Critical Care 2010
Non-Neutropenic Candida Infection
Prediction and Treatment Approach

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
 Conclusion
CLABSI need to be watch and observe for
every patient using central line device
BSIs showed by clinical symptoms and
conditions that fulfill the diagnosis criteria
Bacterial or fungal is the caused of
CLABSI
A few kind of criteria should be considered
to predict the etiology of CLABSI