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SEPSIS
Dr. Hadi Sulistyanto, SpPD,
MHKes, Finasim
RS BHAYANGKARA SEMARANG
3 JULI 2013
INFLAMATION AND SEPSIS
Inflammation is a vascular tissue reaction against all
forms of lesion. Basically a process of inflammation is
the body's defenses
SIRS : Systemic Inflamatory Response
Syndrome
SEPSIS : The systemic inflammatory response
to infection.
LESI
INFLAMASI
LOKAL SISTEMIK
+ INFEKSI SIRS
SEPSIS
bacterial Cardiac surgery
ROLE OF CYTOKINES
IL1,TNF, IL6, IL8, IL-10
netrofil
ENDOTHEL
(Guntur 2000)
INFLAMMATORY TRIAD
Fever
Tachycardia
Flushed skin
GRADASI SEPSIS
SIRS
SEPSIS
SEPSIS BERAT
SEPSIS DENGAN HIPOTENSI
SYOK SEPTIK
DEFINITION
Sepsis is an infection accompanied by
systemic response/inflamtion is marked by
two or more of the following :
Temperature >38°C or <36ºC
Pulse rate >90x/minute
Respiratory rate> 20/minute or PaCO2< 32
mmHg
Leucocyte >12000/mm3, <4000/mm3 or >10% of
immature/band leucocyte
SIRS/SEPSIS : CLINICAL
SYNDROM
COLD WARM
*Hypothermi : *< 35,6 0C *Hyperthermi : *38,3 0C
*Tachypneu ( resp > 20 /mnt) * Tachypneu ( resp > 20 /mnt)
*Tachycardi ( pulse > 100 / mnt) *Tachycardi ( pulse > 100 / mnt)
*Leukopenia < 4000 / mm3 *Leukocytosis > 12000 / mm3
*10% > cell imature *10% > cell imature
•Suspected infection (1992) • Suspected infection (1992)
• Biomarker dini PCT dan CRP • Biomarker dini PCT dan CRP
(2003) (2003)
INSIDEN SEPSIS & SEPSIS BERAT
Insiden sepsis USA 400.000 kasus sepsis;
200.000 kasus syok septik; 100.000 kematian
• More than 750,000 cases of severe sepsis in US
annually, more than 500 patients die of severe
sepsis daily.
• Indonesia data??
Mediator Inflamasi pada Sepsis
MEDIATORS
PRO ANTI
INFLAMMATORY INFLAMMATORY
•Bacterial Endotoxin •Interleukin10
•TNFα •PGE2
•Interleukin1 •Protein C
•Interleukin6 •Interleukin6
•Interleukin8 •Interleukin4
•Platelet Activating Factor •Interleukin12
(PAF) •Lipoxins
•InterferonGamma •GMCSF
•Prostaglandins •TGF
•Leukotrienes •IL1RA
COMMON MICROBIAL
ETIOLOGY OF SEPSIS
GRAM NEGATIVE : 6070%
E.coli, Enterobacteriaceae, Klebsiella sp,
Pseudomonas aeruginosa, Haemophillus influenzae
GRAM POSITIVE :
Streptococcus pneumoniae, Staphylococcus aureus,
Coagulase Negative Staphylococcus, Group B
Streptococcus
Yeast : Mucormycosis
Virus : CMV
Outer
membrane
Peptidoglycan
Periplasmic
space
Cytoplasmic
membrane
O antigen
Clinical condition PCT (ng/mL)
Health 0.05
Local Infection 0.05
Systemic Infection 2
(Sepsis)
Severe Sepsis 10
Septic Shock >>>
PCT = Pro Calcitonin
PCT AND SEPSIS, SEVERE SEPSIS
& SEPTIC SHOCK
PCT 1000
PENYEBAB DEMAM
8. PENY. ENDOKRIN
1. INFEKSI
9. TRAUMA FISIK
2. PENY. KOLLAGEN
3. PENY. SSP 10. BAHAN2 KIMIA
4. TUMOR GANAS 11. GGN BALANS CAIRAN
5. PENY. DARAH 12. PSIKOGENIK
6. PENY. KARDIOVASKULER 13. FAKSISI/FALSE
7. PENY. GASTROINTESTINAL FEVER/DEMAM PALSU
14. FUO (FEVER OF
UNKNOWN ORIGIN)
KAUSA FUO
40% INFEKSI
20% NEOPLASMA
15% PENYAKIT JARINGAN IKAT
SISANYA(25% BERBAGAI SEBAB
510% TETAP TIDAK DIKETAHUI
Clinical conditions associated with sepsis
Gastrointestinal Intravascular
Liver Central iv line
Gallbladder Infected prostetic device
Colon Septic thrombophlebitis
Intraabdominal abscess Lower respiratory tract
Intestinal obstruction Community acquired pneumonia
Intraabdominal instrumentation
Nosocomial pneumonia
Genitourinary Empyema
Acute pyelonephritis Lung abscess
Renal abscess
Renal calculi
Cardiovascular
Urinary tract obstruction Acute bacterial endocarditis
Prostatic abscess Myocardial abscess
Instrumentation Central nervous system
Pelvic Bacterial meningitis
Pelvic abscess, peritonitis Brain abscess
Perimeningeal infection
Cuncha B. In : Conn Current Therapy 2003
SYMPTOMS AND SIGNS
Fever
Tachycardia
Tachypnea
Hypotension
Organ dysfunction
MANAGEMENT OF SEPSIS
1. Terapi dasar
2. ANTIBIOTIKA DAN ELIMINASI SUMBER
INFEKSI
3. Resusitasi cairan
4. Nutrisi enteral – Imuno nutrisi
5. Terapi suplementatif
1. PENGOBATAN DASAR
Mengatasi penyebab vasodilatasi:
IL1 (Interneukin1)
TNF (Tumor Necrosis Factor)
NO (Nitric oxide)
Prostaglandin
Aktivasi komplemen (C3a, C5a)
ABC (airway, breathing dan circulation):
Oksigen
Koloid dan kristaloid bergantian
Sodium bikarbonat koreksi asidosis
FACTORS TO BE CONSIDERED FOR
THE CHOICE OF ANTIBIOTICS
Community versus hospitalacquired
infections/ nosocomial
The anatomical site of the focus of
sepsis
The presence of underlying diseases
Diagnostic or surgical intervention
in the recent past
Samples have to be taken for culture before
the administration of antibiotics
Begin intravenous antibiotics as early
as possible & always within the first
hour of recognizing severe sepsis
/septic shock
Bactericidal antibiotics should be chosen
ANTIBIOTIC
The probability of effectivenes of antimicrobial
therapy should be at least 9095 % in severe
infections
Broad-spectrum empirical antimicrobials (3rd
Generation or 4th Generation Cephalosporin)
should be reviewed no later than 48 hours and
stepped down to narrow spectrum agents
promptly when appropriate
The Combination therapy de-escalation
following susceptibilities
Duration of therapy typically limited to 7-10
days: longer if response is slow or there are
undrainable foci of infection or immunologic
deficiencies/HIV
Virus : CMV
Perubahan hemodinamika sepsis
Permeabilitas kapiler
Cairan keluar ruang interstital
Cairan intravaskular berkurang
Dilatasi pembuluh darah resistensi
Tekanan darah menurun syok
Restorasi volume intravaskuler
Kristaloid + koloid
KRISTALOID:KOLOID = 4:1 ATAU 3:1;
KECEPATAN TETESAN KOLOID 1020
ML/KGBB/JAM
MAKSIMAL 10001500 ML/24 JAM
TUJUAN RESUSITASI
CAIRAN
Perbaikan volume darah
Mengoptimalkan Cardiac Output
Mengurangi resiko edema paru
Koreksi acidosis
VASOACTIVE THERAPY
Indikasi vasoaktif
Syok septik jika mengalami
hipoperfusi jaringan
Tidak merespon terapi cairan
VASOAKTIF
Dobutamine, ß-adrenergic agonist
Increasing contractility
Decreasing afterload
Initial dose: 0,5-1 mcg/kg/min/iv continous, then
titrated every few minutes (range 2-20
mcg/kg/min/iv)
Dopamine
Low doses: 23 mcg/kg/min, stimulation
of dopaminergec & ß-adrenergic
receptprs:
Glomerular filtration
Heart rate
Contratility Hight doses: > 5 mcg/kg/min,
adrenergiceffect
Peripheral vasoconstriction
Norepinephrine
Vasopressine (ADH=antidiuretic
hormone)
Pheripheral vasoconstriction
VASOPRESSOR AND INOTROPIC
Drug Activity to adrenergic
resceptor
1 2 1 2
DA
Dobutamin + + ++++ ++
0
Dopamine ++/+++ ? ++++ ++
++++
Epinephrin ++++ ++++ ++++ +++
0
Norepinephrin +++ +++ +++ +/++
0
Contractility Heart rate Vasoconstriction
Vasodilatation
IV. TERAPI SUPLEMENTATIF
Strategi Anti Eksotoksin dan Endotoksin
Monoklonal antibodi
Strategi Anti Mediator
Netralisasi NO
Terapi Herbal??
Intra Venus Immuno Globulin (IVIG)
Kortikosteroid ???
Some Immunomodulatory Therapy in Sepsis
Antiendotoxin therapy Immunostimulation
Monoclonal or polyconal antibodies Immunoglobulins
LPS analog, LPS elimination GCSF
Specific mediators IFN
anti TNF Immunonutrition
TNF receptors Non specific
IL1 RA Corticosteroids
Coagulants (AT, activated protein C) Pentoxifillin
Tissue factor pathway inhibitors Hemofiltration
PAF
Arachidonic metabolites
Bradikinin antagonist
Nitric oxide synthase inhibitors
Vincent JL, Sun Q, Duboid MJ. Clin Infec Dis 2002;34:108493
Supportive Therapy in Sepsis
Oxygenization
Fluid and volume resucitation
Vasopresor and inotropic
Albumine
Blood trasfusion
Nutrition
Blood glucose controlled
Renal dysfuction
Bicarbonate therapy
Corticosteroids
Coagulation disorders
Jindal N, Hollenberg SM, Dellinger RP. Crit Care Clin 2000;16(2):23349
KESIMPULAN
Sepsis merupakan penyebab utama kematian di
ruangan perawatan, oleh karena itu diperlukan
diagnosis yang lebih dini.
Untuk mencegah terjadinya kematian akibat sepsis
diperlukan penanganan yang adekuat.
Penanganan sepsis diantaranya:
Terapi dasar
Resusitasi cairan
Nutrisi parenteralimuno nutrisi
Pemberian Antibiotik yang adekuat dalam hal ini
dari golongan MEROPENEM, SEFALOSPORIN
GEN 3 ATAU 4.
Pemberian agen vasoaktif