Sepsis dan Septik Syok

Rama andyatma
201310330311166

Pendahuluan
- Sindroma respons inflamasi sistemik ( Systemic Inflammatory
Response Syndrome = SIRS) Peradangan tidak spesifik
yg disebabkan oleh infeksi maupun keadaan yg bukan
infeksius seperti emboli paru, luka bakar dan infark jantung.

Old paradigm of sepsis

Infection

Endotoxin and other microbial toxins

Proinflammatory state with cytokine release

and
Other proinflammatory mediators

Sepsis / SIRS
Shock and multiorgan dysfunction and possible death

Adaptasi dari Bone, 1997, hlm 239

New paradigm of sepsis

Local pro-inflammatory
response

Initial insult
(bacterial, viral,
traumatic, thermal)

Systemic spillover of proinflammatory mediators

Local anti-inflammatory
response

Systemic spillover of antiinflammatory mediators

Systemic
reaction:
SIRS (pro-inflammatory)
CARS (anti-inflammatory)
MARS
(mixed)

Adaptasi dari Jacobi, 2002, suppl 5

Homeostasis

Apoptosis
(cell death)

Organ
dysfunction

Suppression
of the
immune system

CARS and
SIRS balanced

SIRS
predominates

SIRS
predominates

CARS
predominates

Definitions used to describe the condition of septic patients

Bacteriemia

Presence of bacteria in blood (positive blood cultures)

Septicemia

Presence of microbes or their toxins in blood

SIRS

2 of these conditions: fever (oral temp. >380C) or hypothermia (<360C); tachypnea (>24 breath/min); tachycardia
(heart rate > 90 beats/min); leukocytosis (> 12.000/L); leukopenia (< 4.000/L) or > 10% bands; may have a
noninfectious etiology

Sepsis

SIRS that has a proven or suspected microbial etiology

Severe sepsis

= sepsis syndrome: sepsis with 0ne or more signs of organ dysfunction, e.g:
1.Cadiovascular: arterial systolic blood pressure 90mmHg or mean arterial pressure 70mmHg that respons to
administration of intravenous fluid
2.Renal: urine output < 0,5mL/kg per hour for 1 h despite adequate fluid resuscitation
3.Respiratory: PaO2/FIO2 250 or, if the lung is the only dysfunction organ, 200
4.Hematologic: platelet count < 80.000/L or 50% decrease in platelet count from highest value ercorded over
previous 3 days
5.Unexplained metabolic acidosis: a pH 7,30 or a base deficit 5,0mEq/L and a plasma lactate level > 1,5 times
upper limit of normal for reporting lab
6.Adequate fluid resuscitation: pulmonary artery wedge pressure 12mmHg or CVP 8mmHg

Septic shock

Sepsis with hypotention (arterial blood pressure < 90mmHg systolic, or 40mmHg less than patients normal blood
pressure) for at least 1 h despite adequate fluid resuscitation; or need for vasopressors to maintain systolic blood
pressure 90mmHg or mean arterial pressure 70mmHg

Refractory
septic shock

Septic shock that last for > 1 h and does not respond to fluid or pressor administration

MODS

Dysfunction of mor than one organ, requiring intervention to maintain homeostasis

SIRS: systemic inflammatory response syndrome

MODS: multiple-organ dysfunction syndrome

Berbagai jenis molekul pro- dan anti-inflamasi

Proinflammatory molecules
TNF-
IL-1
IL-2
IL-6
IL-8
IL-15
Neutrophil elastase
IFN-
Protein kinase
MCP-1*
MCP-2
Leukemia inhib.factor
(D-factor

Thromboxane
Platelet activating factor
Soluble Adhesion mol.
Vasoactive neuropeptides
Phospholipase
Tyrosine kinase
Plasminogen activator inhib.-1
Free radical generation
Neopterin
CD14
Prostacyclin
Prostaglandins

MCP = monocyte chemoattractant protein

(Adaptasi dari Bone, 1997, hlm 238)

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

Wenzell dkk definisi stadium sepsis :

I.

Systemic inflammatory response syndrome (SIRS)

Dua atau lebih gejala berikut :
1. Suhu > 38oC atau < 36o C
2. Nadi > 90 x/menit
3. Pernafasan > 20 x/menit
4. Lekosit > 12 ribu mm3 atau < 4 ribu /mm3 atau
ditemukan > 10% sel batang

II. Sepsis
SIRS disertai infeksi kuman yg dibuktikan dgn kultur.

III. Sepsis berat

Sepsis dgn disfungsi organ, hipotensi atau hipoperfusi
asidosis laktat, oligouri, perubahan status mental akut.

IV. Syok septik.

Sepsis berat dgn hipotensi yang tidak memberikan respon
terhadap resusitasi

cairan ( tekanan darah arteri < 90

mmHg atau turun > 40 mmHg dari tekanan darah yang

normal dari pasien.

Patogenesis
- Infeksi lokal bakteri aliran darah, bakteriemia
toksin aliran darah.
- Endotoksin lipopolysaccharide ( LPS) yang berasal
dari membran luar bakteri gram negatif.
- LPS sirkulasi darah protein plasma LPS Binding
Protein (LBP) LPS CD-14 (permukaan monosit,
makrofag,netrofil memacu sel fagosit mononuklear
mediator (Tumor necrosis factor (TNF),
Interleukin-1 (IL-1), Interleukin-6 (IL 6), Interleukin-8

Lanjutan ..

- Dikeluarkan Asam arakidonat dimetabolisir

menjadi lekotrin, tromboksan A 2, prostaglandin E 2
(PGE2) dan prostaglandin I2 (PGI2).
- IL-1, IL-6 mengaktifkan sel T memproduksi
interferon , IL-2, IL-4 dan Granulocyte colony
stimulating factor (GCSF).

Bakteri gram positif menyebabkan sepsis melalui 2

mekanisme: eksotoksin sebagai superantigen dan komponen
dinding sel yang menstimulasi imun

SEKIAN