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Septic shock
Etiology
Microorganism and condition that may predispose to infection
Microorganism
Gram-negative bacteria:
Enterobacteriaceae, pseudomonads, Haemophillus spp., other gram-negative bacteria
Condition
Diabetes mellitus Lymphoproliferative diseases Cirrhosis of the lever Burns Invassive procedures or devices Neutropenia Indwelling urinary catheter Diverticulitis, perforated viscus Intravascular catheter Indwelling mechanical devices Burns Neutropenia Intravenous drug use Infection with superantigen-producing S. pyogenes Neutropenia Broad-spectrum antimicrobial therapy
Gram-positive bacteria:
Staphylococcus aureus, coagulase-negative staphylococcus, enterococci, Streptococcus pneumoniae, other streptococci, other gram-positive bacteria
Epidemiology
Incidence of sepsis and septic shock over the past 20 years Annual number of cases: > 300.000 2/3 of cases occur in pts hospitalized for other illnesses The increasing incidence of severe sepsis is attributable to:
The aging of the population
Imunopatogenesis
Mekanisme imunosupresi
2. Anergi
Erat kaitannya dengan kematian Limfosit, sel epitel usus Apoptotic cell death apoptosis sitokin anti-inflamasi anergi
Sepsis / SIRS
Systemic spillover of proinflammatory mediators Systemic reaction: SIRS (pro-inflammatory) CARS (anti-inflammatory) MARS (mixed)
C
Cardiovascular compromise (shock) SIRS predominates
H
Homeostasis
A
Apoptosis (cell death) SIRS predominates
O
Organ dysfunction SIRS predominates
S
Suppression of the immune system CARS predominates
Anti-inflammatory molecules
IL-1 ra IL-4 IL-10 IL-13 Type II IL-1 receptor Transforming growth factor- Epinephrine Soluble TNF- receptors Leukotriene B4-receptor antagonism Soluble recombinant CD-14 LPS binding protein
Merusak organ
(e.g. ARDS)
Temuan penelitian:
G-CSF produksi nuetrofil survival
Otopsi
Limfosit, epitel sel usus: menghilang (apoptosis) Sel imun adaptif turun secara progresif dan dalam jumlah besar Penyebab kematian (gagal organ), secara histologis: tidak sesuai
?
cell hibernation (cell stunning)
Follow up: konsentrasi, base defisit, pH, saturasi oksigen vena sentral 6 jam pertama sangat menentukan keberhasilan tindakan
2. Diagnosis
Penting menentukan sumber dan mikroba penyebab infeksi Bahan yang diperiksa: darah, urin, cairan serebrospinal, luka, sputum, dll
3. Antibiotic therapy
sebelum tersedia hasil kultur: sesuai pola antibiotika se tempat
4. Source control
Drainase abses, debridement jaringan nekrosis Alat bantu (kateter, dll), benda potensial sumber infeksi disingkirkan
5. Vasopressors
Diberikan selama pemberian fluid chalengge dan hipovolemik belum teratasi Pemberian dopamin harus dalam dosis teurapetik
6. Inotropic therapy
Bagi pasien dengan isi semenit rendah: beri dopamin Bagi pasien dengan tekanan darah rendah: kombinasi dengan vasopresor
7. Steroid
Pemberian dosis tinggi memperjelek kondisi (infeksi sekunder) Temuan penelitian: pemberian hidrokortison 200- 300mg/hr selama 1 minggu perbaikan kondisi Perlu pemberian dosis rendah kortikosteroid (Dellinger, 2004; Hotchkiss, 2003) Kortikosteroid tidak direkomendasikan (Chambers, 2003)
8. Activated protein C
Pemberian Rh APC Relative risk of death 19,4%; absolut risk of death 6,1% Harus memenuhi sistem scoring APACHE Menghambat faktor Va dan VIIIa trombin tak terbentuk penghambatan aktivitas trombosit, pematangan neutrofil, degranulasi sel mast Pumya kemampuan direct anti-inflammatory
Rh APC:
Pasien dengan kemungkinana DVT: beri low-dose unfractionated heparin / low-molecular weight heparin
Pasien dengan resiko perdarahan:pakai intermittent compression device e.g.
Trombositopenia Koagulasi Perdarahan aktif
Central venous and arterial catheterization Sedation, paralysis (if intubated), or both
CVP 812mmHg
<8mmHg
Crystalloid Colloid
Vasoactive agents
70%
<70%
70%
No
Goal achieved
Yes
Hospital admission
Adaptasi dari Rivers, 2001, hlm. 1371
Kesimpulan:
Anti-inflamasi diberikan pada fase hiperinflamasi Immune stimulant diberikan pada fase hipoinflamasi
Survival
Ab terhadap MMIF peritonitis Inhibisi produk mikroba toll like receptor (TLR)
PARP - inhibotor
Kesimpulan
Terjadi pergeseran besar dalam sikap peneliti mengenai masalah sepsis Sepsis tidak sekedar immune system gone haywire melainkan kemungkinan severely compromised immune system (mikroba patogen ) Hasil otopsi menunjukkan focal necrosis
Terimakasih