Oleh :

Fakhrina Nur F 170070201011030

Kurnia Auliana A.R 1700702010110

Supervisor: dr. Ali Haedar, SpEM

Introduction
Latar Belakang

In US, medical centers reported sepsis as 3 in 1000 cases.

51,1% of those cases admitted to ICU
The incidence of severe sepsis ranged from 0.2 cases per 1000 admissions in children to
26.2 per 1000 in individuals older than 85 years (Kalil, 2018)
In developing countries: 60-80% from all deaths every 3-4 second caused by sepsis
(GSA, 2016)
Indonesia: 48,96% death rate (Pradipta, 2009).
Literature Review
 Definition
Latest Definition 2016
Third International Consensus Definitions for Sepsis and Septic Shock
 Score criteria SOFA: Sequential Organ Failure Assessment
– SEPSIS: a life-threatening organ dysfunction caused by disregulation
host respond to infection. Organ dysfunction evaluated using SOFA
SCORE
– SEPTIC SHOCK: sepsis that causing circulation and cellular/metabo
llite abnormality which significant enough to cause mortality
 Fluid-unresponsive hypotension
 Need for vasopressors to keep MAP >65mmHg
 Serum lactate > 2mmol/L

(Singer, et al. JAMA 2016;315(8) 801-810)

Definition
 Etiology

Common source of
Bacterias:
infection: • Positive Gram bacteria
• Lungs (64%), • Negative Gram bacteria
• Abdomen (20%), • Mixed or others

• Blood Circulation (15%)

• Genitourinary tract
• Kidney (14%)
Hotchkiss et al, Sepsis and Septic Shock, ResearchGate, 2016 : vol. 2 : 1-21
(Singer M, 2016)

Pathophysiology
Pathophysiology

Antigen from bactera induces immune

01 system response

Inflammatory mediator secreted

02 → cytokine, neutrofil,complement, NO,
etc.

03 Failure to maintain homeostasis 

Maladaptive inflammation

04 Tissue hypoperfusion SHOCK

 Diagnosis

Anamnesis

Physical
Examination
Workup
Examiniation
qSOFA Mengenali pasien dengan infeksi yang
kemungkinan memiliki luaran yang buruk
1. Laju pernapasan 22x/menit atau lebih
2. Perubahan status mental (GCS<15)
3. Tekanan darah sistolik 100 mmHg atau kur
ang.
Jika 2 dari 3 komponen diatas ditemukan,
pasien dianggap memiliki qSOFA positif
Diagnosis Syok Septik :
Sepsis disertai
1. Diperlukan vasopresor untuk me
mpertahankan MAP >65 mmHg
2. Jumlah laktat serum >2 mmol/L ta
npa disertai hipovolemia (Keeley
et al., 2017).
 Clinical Manifestation
Hypotension,
Tachypnea Altered Mental Status
tachycardi
•Alveoli capillary membrane d •Myocardial depression Lethargy, confuse, delirium 
amage becaused of inflamm •Ejectionfraction decrease Airway (ETT)
ation  inotropic
•Respiratory alkalosis, hypox
emia, and/or hypercarbondio
xide

Hepar function Renal disturbance GI symptoms

Increase of ALT & bilirubin • Morbidity  renal failure

• Increasing creatinine
• Avoid  rescucitation

Hotchkiss et al, Sepsis and Septic Shock, ResearchGate, 2016 : vol. 2 : 1-21
 • qSOFA score - PaO2 : FiO2 < 300 mmHg
- Thrombocyte < 100.000/m
m3
- Bilirubin ≥ 2 mg/dL
1. Laju pernapasan 22x/men - Hypotention that require v
it atau lebih asopresor
2. Perubahan status mental - GCS ≤ 12
(GCS<15) - Creatinine ≥ 2 mg/dL or uri
3. Tekanan darah sistolik ne output < 500 mL/day
<90mmHg
Each indicator scored 0 (normal) – 4
(organ failure). Total score ≥2 indicat
es increase of organ dysfunction risk
or death

• SOFA score
Makic dan Bridges, Managing Sepsis and Septic Shock : Current Guidelines and Definitions, AJN, 2018 : 118 (2)
 Laboratorium Findings

Leucocytosis/Leucopenia Trombocytopenia
01 02

Increased CRP Hyperbilirubinemia

06 03

Hyperglicemia Increase lactat compound

05 04
 Hasil Pemeriksaan Penunjang
Tes laboratorium Temuan Keterangan

Hitung sel darah p Endotoksemia dapat menye

Leukositosis atau leukopenia
utih babkan early leukopenia

Nilai tinggi awal dapat dilihat

sebagai respon fase akut, ju
Hitung platelet Trombositosis atau trombositopenia
mlah trombosit yang rendah
terlihat pada DIC

Defisiensi Protein C; defisiensi antitro Kelainan dapat diamati sebe

Coagulation casca mbin; level D-dimer meningkat; PT (P lum timbulnya kegagalan or
de rothrombin Time) dan PTT (Partial Th gan dan tanpa perdarahan y
romboplastin Time) memanjang ang jelas.

Doubling-menandakan cede
Level kreatinin Meningkat
ra ginjal akut 16
 Hasil Pemeriksaan Penunjang
Tes laboratorium Temuan Keterangan

Mengindikasikan hipoksia jarin

Level asam laktat Lactic acid > 4 mmol/L (36 mg/dL)
gan

Mengindikasikan cedera hepat

Level alkaline phosphatase, AST, ALT, bi
Level enzim hepar oseluler akut yang disebabkan
lirubin meningkat
hipoperfusi

Berkorelasi terbalik dengan tin

Level serum fosfat Hipofosfatemia
gkat sitokin proinflamasi

Level C-reactive pro

Meningkat Respons fase akut
tein (CRP)

Membedakan SIRS yang infek

Level prokalsitonin Meningkat sius dari SIRS yang non-infeks
ius 17
Skor SOFA Mortalitas

0-6 <10%

7-9 15-20%

10-12 40-50%

13-14 50-60%

15 >80%

15-25 >90%
 Management Principles
Monitoring: ECG, vital signs q5min,
Early Recognition pulse oxymetry

Labs: RBS, CBC, Blood and urine

Source Control culture, Haemostasis functions, Serum
electrolyte, ABG, Ur/Cr

Early and adequate antibiotic CXR, consider echocardiography

therapy

Ventilatory support Urinary catheter

Early hemodynamic Maintain airway

resuscitation and support

Managed in resuscitation area Haemodynamic stabilization

(General Principle in Emergency Medicine 2nd edition, 2015)

(Singer, et al. JAMA 2016;315(8) 801-810)
Surviving Sepsis Campaign Update 2018
 Management

Fluid Rescucitation 1
Min. 30ml/kgBW crystaloid or
saline IV given in first 3 hour, reeva
luate hemodynamic status Antibiotic
2
Administered as soon as possible.
Empiric antibiotic must include 2 a
Define the Etiology ntibiotic from different derivats
3
Culture to define definitive antibiotic,
take the sample before administ
ration of empiric antibiotic
 4 Vasopressor if needed

•Norepinephrine (first line)

•Dopamine
Bicarbonat Therapy 5
For patient with lactat acidemia
Lactat production are induced by
hypoxic condition, pH < 7,15
6 Ventilation
•Sepsis + ARDS tidal volume target
→12 ml/kg
Stress ulcer profilactive •Sepsis + Respiratory failure witho
7 ut ARDS → tidal volume target 4-6
For patients with sepsis or septic shock
ml/kg
who have risk factors for gastrointestinal •Patient with mechanic ventilation
(GI) bleeding using PPIs or H2RAs → head up 30 degrees
 8 Glucose

If blood glucose level reach >180 mg/

dL for two times→ insulin therapy with
Nutrition 9 blood glucose target ≤180mg/dL

early enteral feeding whenever

possible

SSC Guidelines on Management for Sepsis & Septic Shock 2016

Tata Laksana
Hour-1 Surviving Sepsis Campaign Bundle of Care (Levy et al., 2018)

29
• Rekomendasi : 30ml/kgBB kristaloid seca
ra IV diberikan secepatnya pada 1 jam
pertama pada hipotensi atau kadar laktat
>4mmol/L.
• Kunci dari resusitasi adalah segera restor
asi kembali tekanan perfusi ke organ vital
Hal ini tidak boleh tertunda
• Tidak membaik  berikan vasopressor
• Pastikan saturasi O2 >94%

30
• Vasopresor (norepinefrin, epinefrin, vasopresin
dan inotropik (dobutamin) digunakan untuk me
ngoptimalkan cardiac afterload dan kontraktilita
s miokardial pada pasien dengan sepsis
(Saugel et al., 2015)
• Lini pertama : Norepinefrin
• harus diberikan dalam satu jam pertama untuk
mencapai MAP >65mmHg

31
• Mengembalikan kegagalan sirkulasi pada pasien
dengan syok septik parah (Saugel et al., 2015)
• Tidak direkomendasikan jika resusitasi cairan dan
pemberian vasopressor berhasil
• Hidrokortisone IV bisa diberikan dengan dosis
200 mg per hari.
• Pada pasien dengan asidemia laktat akibat hipop
erfusi (pH< 7,15), dapat diberikan terapi bikarbon
at dengan tujuan memperbaiki hemodinamik atau
menurunkan kebutuhan vasopressor
• (Rhodes et al., 2017)

32
• Terapi antibiotik spektrum luas
empiris dengan satu jenis atau le
bih dilakukan untuk mencakup se
mua patogen yang memungkin
kan menyebabkan sepsis harus
dimulai segera pada pasien
dengan syok septik.
• Kultur harus diperoleh sebelum
pemberian antibiotik untuk meng
optimalkan identifikasi patogen d
an meningkatkan outcome pasien
• Gunakan antibiotic sesuai kultur
setelah hasil kultur keluar
33
Observasi ketat setiap 15 menit
Tanda overload cairan  peningkatan laju napas, penur
unan saturasi oksigen, dan ada distensi JVP.
Observasi ketat : tekanan darah sistolik dan MAP, penila
ian serum laktat dapat dilakukan maupun tidak. Pada pa
sien dengan overload cairan apabila tekanan darah sist
olik, MAP, dan serum laktat baik  diberikan diuretik unt
uk mengeluarkan cairan.
Namun jika tekanan sistolik, MAP, dan laktat mengalami
abnormalitas  segera berikan vasopressor, (diuretic tid
ak diberikan) (NCEC, 2014).

34
35
 Mortality
• About 20-30%.
• 40-60% patient died in 30 days after, oth
ers are 6 months after

Recovery
Patient often had physical malfunction
or neurocognitive disturbances. This s
Prognosis ituation brings patient to lower quality
of life.
Case Report
 Patient Identity

Name : Tn. S
No. Register : 1145xxxx
Sex : Laki-laki
Age : 46 thn
Job : swasta
Address : Singosari, Malang
Religion : Islam
Education : SMA
Primary Survey Primary Intervention

A : Paten
A : Head up 30°
B : Spontan, symetrical, RR 26x/minute
regular, Sat O2: 70 % on NRBM, retrac B : O2 on Jacson reese
tion(+), pembengkakan di rahang bawa C : Loading IVFD NaCl 0,9% 1500cc
h hingga leher. D:-
C : BP : 85/46 mmHg, Pulse: 72x/minute, E : warm blanket
regular, CRT >2 sec , warm and dry
acral
D : GCS 233
E : 370C

Triage category: P1
ANAMNESIS (Autoanamnesis)

Main complaint : Penurunan Kesadaran

Pasien rujukan dari RS Prima Husada dengan sejak 2 hari yang lalu disertai de
ngan luka terbuka dan pembengkakan pada area rahang bawah hingga leher.
Demam (+) sejak 2 hari yang lalu. Riwayat pasien datang ke RS Prima husada
dengan abses mandibula oleh Sp. B. kemudian dalam perawatan mengalami
penurunan kesadaran. Sempat di cek GDA dengan hasil 23 mg/dL dan dilaku
kan koreksi, tetapi kesadaran tidak membaik. Tekanan darah juga sempat turu
n yang kemudian stabi setelah di drip NE.
Past medical history :
• Patien riwayat DM sejak 8 Tahun yll, dan mengonsumsi obat …

History of treatment :
• Pasien rujukan dari RS Prima Husada, given: O2 NC 2-4 lpm, IVFD
NaCl 0,9% 1000 cc, Ciprofloxacin 400mg, Ceftriaxone 1 gram, urine
catheter (+)

Family history
• tidak ada yang punya riwayat serupa di keluarga, DM(-), HT(-)

Social history:
• Pasien merupakan pekerja swasta dan tinggal bersama istri dan 2
anak
PHYSICAL EXAMINATION
General Condition: tampak sakit berat BB : ?, TB ?

GCS: 233 BP: 85/46 mmHg PR: 72x/m RR: 26 x/m Tax: 37 0C

Head anemis(+/+) Icteric (-/-) pupil isokor

JVP sde, Lymphadenopathy (+) , luka terbuka dan bengkak pada rahang bawah hing -
Neck
ga leher. Retraksi supraklavikular (+)

Wall Ekspansi dinidng dada simetris, jejas (-)

Chest Ictus invisible, palpable at ICS V MCL S

Heart RHM ~ SL D LHM ~ ictus
S1 and S2 single, murmur (-), gallop (-)

Stem Fremitus D=S S S v v Rh - - Wh - -

Lung SS vv - - - -
SS vv - - - -

Abdomen Flat, soefl, BU (+) normal, nyeri epigastric (-)

Edema -/- akral hangat kering, CRT >2 second

Extremities
 Hasil Laboratorium 15 Oktober 2019

Hemoglobin 15,0 11,4-15,1 g/dL

Leucocyte 4000 4700-11.300/µL

Hematocrite 47,1% 38-42

LABORATORIUM
Thrombocyte 217.000 142-424x103/µL

MCV 92,00 80-93 fl

MCH 29,40 27-31pg

Diff count -/-/77/21/2 0-4/0-1/51-67/25-33/2-5%

SGOT 65 0-40

SGPT 55 0-41

GDS 126 <200

Ur/Cr 160/5,61 16.6-48.5/<1,2

Albumin 2,50 3,5-5,2

Natrium 136 135-145

Kalium 6,00 3.5-5.1

Calsium 0,81 1,15-1,35

PTT/APTT 17,5/29 12-18/27-42

Chest X-Ray
Radiology

Chest X-Ray
Summary” Kardiomegali (LDH)”
 DIAGNOSIS

• Altered Mental Status dt syok Septik on NE

• Post Abses mandibula sinistra at Operative site
• Post Hipoglikemia
• AKI stage III
 Planning
PDx PTx :
• Serum Laktat • O2 on Jackson Reese 15lpm
• BGA • IVFD NaCL 0.9% loading 1500cc
• Kultur darah
continue maintenance 20 tpm
• IV metronidazole 3 x 500 mg
• IV. Ceftriaxone 2 x 1 gram
• IV. Omeprazole 1 x 40 mg
• IV Metoclopramide 3 x 10 mg
• IV Lansoprazole 30 mg
• Drip NE 0,6 mcg/kgBB/min -> 0,8
PMo
• Subjective mcg/kgBB/min
• Vital sign • Drip Dobutamin 10 mcg/kgBB/min
• Urine output • Pro ETT Ventilator
Discussion
 Clinical Manifestation
Hypotension,
Tachypnea Altered Mental Status
tachycardi
•Alveoli capillary membrane •Myocardial depression Lethargy, confuse, delirium 
damage becaused of inflam •Ejection fraction decrease Airway (ETT)
mation  inotropic
•Respiratory alkalosis, hypox
emia, and/or hypercarbondio
xide

Hepar function Renal disturbance GI symptoms

Increase of ALT & bilirubin • Morbidity  renal failure

• Increasing creatinine
• Avoid  rescucitation

Hotchkiss et al, Sepsis and Septic Shock, ResearchGate, 2016 : vol. 2 : 1-21
Physical Examination qSOFA Criteria:
• GCS: 456 1. Hypotension (Systolic BP <100mmHg)
• TD: 86/59 mmHg ; 2. Altered Mental Status
• PR: 121 bpm; 3. Tachypnea (RR>22x/minute)
• RR: 24 tpm;
• Tax: 37°C If qSOFA score >=2, it indicates high risk for
suffering sepsis

Consensus Definitions for Sepsis and Septic Shock, 2016

 • Alexander Butler
• Creative Director / Art Designer

• Te duo dolores intellegebat, ne ius eleifend cotidieque. Sea vitae

munere et. Aliquid luptatum invenire eam in, te has solet aperiam,
cu qui vidit noster periculis. Ad illum incorrupte qui, est decore vu
lputate appellantur ut. Cum ut insolens salutatus, impetus scripta
vocibus in pri. Fugit salutandi pri cu, ea pri nisl ignota, eu pro libri
s cetero.

The Power of PowerPoint | th 52

DIAGNOSIS OF SEPSIS

1. PaO2/FiO2 = 275,5
2. Platelet= 710
3. Bilirubin total = 1,02
4. MAP = 68
5. GCS = 15
6. Creatinin = 0,91

Total score = 2
SEPSIS
SEPTIC SHOCK: sepsis that causing circulation and cellular/metabollite abnormality which significant e
nough to cause mortality
• Fluid-unresponsive hypotension
• Need for vasopressors to keep MAP >65mmHg
• Serum lactate > 2mmol/L
(Singer et al., 2016)
Hotchkiss et al, Sepsis and Septic Shock, ResearchGate, 2016 : vol. 2 : 1-21
 Management Principles
Monitoring: ECG, vital signs q5min,
Early Recognition pulse oxymetry

Labs: RBS, CBC, Blood and urine

Source Control culture, Haemostasis functions, Serum
electrolyte, ABG, Ur/Cr

Early and adequate antibiotic CXR, consider echocardiography

therapy

Ventilatory support Urinary catheter

Early hemodynamic Maintain airway

resuscitation and support

Managed in resuscitation area Haemodynamic stabilization

(General Principle in Emergency Medicine 2nd edition, 2015)

Thank you