DIAGNOSA DAN

TATALAKSANA SEPSIS
BAHAN BACAAN

• KEPUTUSAN MENTERI KESEHATAN REPUBLIK INDONESIA NOMOR HK.01.07/MENKES/342/2017

TENTANG PEDOMAN NASIONAL PELAYANAN KEDOKTERAN TATA LAKSANA SEPSIS
• Gotts J, Matthay M. Sepsis: pathophysiology and clinical management. BMJ. 2016;353:i1585.
• Jatin M. Vyas, a. (2016) Sepsis: MedlinePlus Medical Encyclopedia. [online] Nlm.nih.gov. Available at:
https://www.nlm.nih.gov/medlineplus/ency/article/000666.htm [Accessed 16 Jun. 2016]
• Dellinger RP, et al. Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup.
Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock:
2012. Crit Care Med. 2013 Feb;41:580-637.
• Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use
of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American
College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992;101(6):1644-1655.
doi:10.1378/chest.101.6.1644
DIAGNOSIS

• pada tahun 2016 the European Society of Intensive Care Medicine dan SCCM
merumuskan kriteria baru diagnosis sepsis yang didasarkan pada perubahan definisi
sepsis yang menekankan pada terjadinya disfungsi organ pada seorang yang
terinfeksi. Sistem skor Sequential Organ Failure Assessment (SOFA) digunakan
sebagai cara penilaian disfungsi organ.
• Kelompok ahli juga mengajukan kriteria baru yang dapat digunakan sebagai penapis
pasien sepsis yang dikenal dengan istilah quick SOFA (qSOFA). Tiga kriteria qSOFA
adalah laju napas lebih dari sama dengan 22 napas/menit, perubahan kesadaran,
tekanan darah sistolik kurang dari sama dengan 100 mmHg (cukup 2 dari 3 kriteria)
 Surviving Sepsis Campaign
2012
• Sepsis Definition
Systemic manifestation of infection and suspected infection; Severe sepsis: Severe sepsis + organ dysfunction

• Initial Resuscitation
Sepsis Induced hypoperfusion at least 30cc/kg in first 3 hours; Crystalloid fluid (no recommendation on 0.9%
NaCl vs balanced solution); Albumin if patient require “substantial” fluids (weak)
Protocolized care including: CVP, ScVO2, Normalize lactate

2016
• Sepsis Definition
Life threatening organ dysfunction caused by dysregulated response to infection; No category for severe sepsis

• Initial Resuscitation
Sepsis Induced hypoperfusion at least 30cc/kg in first 3 hours; Crystalloid fluid (no recommendation on 0.9%
NaCl vs balanced solution); Albumin if patient require “substantial” fluids (weak)
Use dynamic resuscitation markers (Passive leg raise)
Target MAP of 65 mmHg
Reassess hemodynamic status to guide resuscitation; Normalize lactate

Rhodes A, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017;43:304-77.
 Sepsis: New Definition 2016
Revised definitions
Definition

Category • Life threatening organ dysfunction* caused by a dysregulated host

response to infection
Sepsis

Definition

Category • Sepsis and vasopressor therapy needed to increase mean arterial

pressure to ≥65 mm Hg and lactate to >2 mmol/L despite adequate fluid
resuscitation
Septic
shock

*As assessed by an acute change of ≥2 points in the sequential organ failure assessment score
(components: partial pressure of oxygen in arterial blood/fractional inspired oxygen (PaO 2 /FIO 2 )
ratio, Glasgow coma scale, mean arterial pressure, vasopressor use, serum creatinine or urine output,
bilirubin, and platelet count).

Gotts J, Matthay M. Sepsis: pathophysiology and clinical management. BMJ. 2016;353:i1585.

SEPSIS (ACCORDING TO SEPSIS-3, 2016)
• a “life-threatening organ dysfunction caused by a dysregulated host response to
infection.”
• Recommendation: the use of sequential organ failure assessment (SOFA) score as clinical
criteria for sepsis in ICU encounters  Increase in SOFA score of t2 points or more .
• In non-ICU encounters, quick SOFA score was recommended as screening tool  qSOFA
score of two or more was set to identify high-risk patients. T
• Classical severe sepsis X
• Septic shock: sepsis with fluid-unresponsive hypotension, serum lactate level greater
than 2 mmol/L, and need for vasopressors to maintain mean arterial pressure of 65 mmHg
or greater
DIAGNOSIS SEPSIS
 Diagnostic Criteria for Sepsis

General variables Inflammatory variables Hemodynamic variables

Fever (>38.3°C) Leukocytosis (WBC
count >12,000/µL)
Hypothermia (core
temperature >36°C)
Leukopenia (WBC
Heart rate >90/min or >2 SD count<4,000/µL)
above the normal value for Arterial hypotension
age (SBP <90 mmHg,
Normal WBC count MAP <70 mmHg, or
Tachypnea with greater than 10 % an SBP decrease >40
immature forms mmHg in adults or
Altered mental status
less than two SD
Significant edema or positive Plasma C-reactive below normal for
fluid balance (>20 mL/kg protein more than two age)
over 24 h) SD above the normal
value
Hyperglycemia (plasma Plasma procalcitonin
glucose >140 mg/dL or 7.7 more than two SD
mmol/L) in the absence of above the normal
diabetes value

Dellinger RP, et al. Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock:
2012. Crit Care Med. 2013 Feb;41:580-637. 1
 Diagnostic Criteria for Sepsis

Organ dysfunction variables Tissue perfusion variables

Arterial hypoxemia (PaO2 /FiO2 <300) Hyperlactatemia (>1
mmol/L)
Acute oliguria (urine output <0.5
mL/kg/h for at least 2h despite
Decreased capillary refill or
adequate fluid resuscitation)
mottling
Creatinine increase >0.5 mg/dL or
44.2 µmol/L
Coagulation abnormalities (INR >1.5
or aPTT >60 s)
Ileus (absent bowel sounds)

Thrombocytopenia (platelet count

<100,000/µL)

Hyperbilirubinemia (plasma total

bilirubin >4 mg/dL or 70 µmol/L)

Dellinger RP, et al. Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock:
2012. Crit Care Med. 2013 Feb;41:580-637. 1
ETIOLOGI

• Penyebab terbesar sepsis adalah bakteri Gram negatif (60-70% kasus).

Staphylococci, pneumococci, streptococci, dan bakteri Gram positif lain lebih jarang
menimbulkan sepsis dengan angka kejadian antara 20-40% dari seluruh angka
kejadian sepsis. Jamur oportunistik, virus, atau protozoa juga dilaporkan dapat
menimbulkan sepsis dengan kekerapan lebih jarang.
 CAUSES OF SEPSIS

Bloodstream
• Infection caused in any part of the
Places of Infection Origin Bones (common in children)
body, mainly skin, lungs, urinary tract,
Bowel (peritonitis) abdomen that can result in

Kidneys (pyelonephritis) bloodstream access to Gram positive

or Gram negative bacteria
Lining of brain (meningitis)
• In hospitals: IV lines, surgical wounds,
Liver or gallbladder surgical drains and sites of skin
breakdown (bedsores or pressure
Lungs (bacterial pneumonia)
ulcers)
Skin (cellulitis)

Jatin M. Vyas, a. (2016) Sepsis: MedlinePlus Medical Encyclopedia. [online] Nlm.nih.gov. Available at: https://www.nlm.nih.gov/medlineplus/ency/article/000666.htm [Accessed 16 Jun. 2016]
Patogenesis Sepsis
Faktor yang mempengaruhi respon imun pada
sepsis
1. Faktor genetik : Polimorphisme gen sitokin,
Mutasi TLR4 , MBP
2. Jenis organisme, Virulensi, Ukuran
inokulum
3. Faktor Host : Umur, status nutrisi,Comorbid
penyakit kronik
 Konsep Lewis Thomas Sepsis merupakan
respon yang tidak terkontrol
 Kegagalan sistem imun mengeliminasi MO :
-Pergeseran ke sitokin anti-inflamasi
-Anergy (ketidaktanggapan terhadap antigen)
-Kematian sel-sel imun
-Hilangnya ekpresi MHC kelas I Macropag
dan molekul costimulator.
Patofisiologi Sepsis
 Infection

Inflammatory Endothelial
Vasodilation
Mediators Dysfunction

Hypotension Microvascular Plugging Vasoconstriction Edema

Maldistribution of Microvascular Blood Flow

Ischemia

Cell Death

Organ Dysfunction
 Patofisiologi sepsis
Inflammatory cascade initiated during sepsis

LPS, PG monomers, DNA repeats, Lipoproteins, Teichoic

acid, Microbial toxins, other microbial components
(Superantigens)

Cytokine Stimulation

Coagulopathy TNF α Complement

Kinin IL-1 activation
Stimulation INF-γ C5a, C3a
Prostaglandins IL-6, IL-8 Leukocyte
Leukotrienss IL-10 chemotaxis
PAF Imfammation

Fibrin Deposition
DIC NO

Generalized endothelial damage

Vascular leak
Tissue edema
Vasodilatation
Bleeding
Temperature dysregulation (e.g. fever)

Tachycardia, hyperventilation, Hypotension

Pallor, peripheral vasoconstriction
Cutaneous sign

MOF
Altered mental status
Shock
Death
 Patofisiologi sepsis
Inflammatory cascade initiated during sepsis

LPS, PG monomers, DNA repeats, Lipoproteins, Teichoic

acid, Microbial toxins, other microbial components
(Superantigens)

Cytokine Stimulation

Coagulopathy TNF α Complement

Kinin IL-1 activation
Stimulation INF-γ C5a, C3a
Prostaglandins IL-6, IL-8 Leukocyte
Leukotrienss IL-10 chemotaxis
PAF Imfammation

Fibrin Deposition
DIC NO

Generalized endothelial damage

Vascular leak
Tissue edema
Vasodilatation
Bleeding
Temperature dysregulation (e.g. fever)

Tachycardia, hyperventilation, Hypotension

Pallor, peripheral vasoconstriction
Cutaneous sign

MOF
Altered mental status
Shock
Death
Marker Sepsis
 Procalcitonin: Meningkat stlh 6 jam
Nilai normal < 0,05ng/ml
Nilai 0,5-2  suspek sepsis
Nilai 2-100 sepsis berat
 C Reaktif protein (CRP)
Sekresi CRP dimulai 4-6 jam setelah stimulasi & mencapai
puncak dalam waktu 36-48 jam  terus meningkat sampai
proses inflamasi teratasi

2
2
 Penatalaksanaan

 Tata laksana sepsis yg optimal mencakup:

 Mengenal secara dini tanda-tanda sepsis

 Mengontrol infeksi dengan terapi anti mikroba yang sesuai

 Perawatan suportif yang intensif pada ruang ICU

 Mengontrol kadar gula

 Vasopresor dan inotropik

 Terapi suportif thd kegagalan organ, ggn koagulasi

 Terapi imunologi bila tjd respon imun maladaptif host thd infeksi

2
TATALAKSANA SEPSIS

Terapi Antibiotik Rasional pada Sepsis. Aspek yang saling berkaitan erat, yaitu:
• a. Aspek antibiotik (Farmakokinetik dan farmakodinamik antibiotic)
• b. Aspek pejamu (derajat infeksi intensitas infeksi, tempat infeksi, usia, berat badan,
faktor genetik dan penyakit komorbid, status imun, kehamilan atau laktasi, riwayat
alergi dan faktor sosial ekonomi)
• c. Aspek bakteri (dimulai dengan pemberian antibiotik empiris kemudian disesuaikan
atau dihentikan sesuai dengan respons klinis atau hasil kultur)
ANTIBIOTIK PADA SEPSIS

• Terapi antibiotik empiris yakni pemberian antibiotik spektrum luas dapat diberikan
baik secara tunggal maupun kombinasi, dapat memiliki spektrum terhadap berbagai
kemungkinan kuman penyebab berdasarkan sindrom klinis dan pola kuman yang
telah dikumpulkan sebelumnya (antibiogram). Contoh antibiotik spektrum luas untuk
terapi empiris adalah golongan karbapenem, sefalosporin generasi 4, piperacilin
tazobactam. Obat-obat tersebut dapat diberikan secara tunggal atau dikombinasikan
dengan golongan kuinolon anti-pseudomonas (siprofloksasin, levofloksasin) atau
aminoglikosida.
TERAPI ANTIBIOTIK PADA
MIKROORGANISME RESISTEN ANTIBIOTIK

a. Patogenesis Resistensi Bakteri Secara mikrobiologik, resistensi bakteri dijelaskan

sebagai berikut:
1). Resistensi alami
• Kuman yang sejak awal memang tidak pernah sensitif terhadap antibiotik tertentu
dikatakan memiliki resistensi alami, misalnya: Pseudomonas aeruginosa resisten
terhadap kloramfenikol, dan sebagainya.
2). Resistensi didapat
• Suatu keadaan dimana kuman yang awalnya sensitif terhadap antibiotik tertentu
mengalami perubahan sifat menjadi resisten.
PILIHAN ANTIBIOTIK EMPIRIS MENURUT LOKASI INFEKSI
RESUSITASI AWAL DAN PENANGANAN INFEKSI
• ICU= intensive care unit ; VAP = ventilator-associated pneumonia
KELOMPOK TINDAKAN RESUSITASI
TATALAKSANA BANTUAN HEMODINAMIK
TERAPI PENUNJANG LAIN
PENANGANAN GANGGUAN KOAGULASI DAN KID
TERIMA KASIH