SEPSIS &

SEPTIC SHOCK
 Terminologi
Infeksi :
beradanya microorganisme seperti bakteri,
jamur, virus, protozoa, dengan disertai respon
inflamasi dan multiplikasi dari organisme
tersebut, pada jaringan Host yang dalam keadaan
normal seharusnya steril
Bakteremia :
adanya bakteri viabeldalam darah
 Terminologi
SIRS (Systemic Inflammatory Response Syndrome) :
Respon Inflamasi Sistemik terhadap berbagai clinical insult yang
berat, ditandai oleh dua atau lebih gejala-gejala berikut :
Suhu tubuh > 38o C atau < 36o C
Denyut jantung > 90 / menit
Respirasi > 20 / menit atau PaCO2
< 32 mm Hg
Sel darah putih > 12.000 / mm3 atau
< 4000 / mm3, atau > 10% bentuk imatur (stab =
band)
Sepsis : SIRS yang penyebabnya karena infeksi
 Terminologi
Severe Sepsis :
Sepsis yang disertai gangguan fungsi organ, hipoperfusi atau
hipotensi

Septic Shock :
Sepsis dengan hipotensi (sistolik < 90 mm Hg atau penurunan 40
mm Hg dari data dasar), setelah pemberian cairan resusitasi yang
adekwat, disertai tanda-tanda hipoperfusi

MODS (Multiple Organ Dysfunction Syndrome) :

Gangguan fungsi organ pada seorang yang sakit berat, dimana
homeostasis tidak dapat dipertahankan tanpa intervensi
Hubungan SEPSIS dan SIRS

Surgical

Sepsis DM
Severe
Infection Sepsis Pancreatitis
MOF
SIRS Trauma

Burn
 SEPSIS: DEFINING A DISEASE CONTINUUM

Infection/
Trauma SIRS Sepsis Severe Sepsis

SIRS related to
infection (suspected
A clinical response arising or confirmed)
from a nonspecific insult,
including 2 of the following:
Temperature 38oC or 36oC
HR 90 beats/min
Respirations 20/min
WBC count 12,000/mm3 or
4,000/mm3 or >10% immature
neutrophils

SIRS = systemic inflammatory response syndrome.

Bone et al. Chest. 1992;101:1644.
 SEPSIS: DEFINING A DISEASE CONTINUUM

Infection/ SIRS Sepsis Severe Sepsis

Trauma

Sepsis with organ failure

(one or more)
Cardiovascular
(hypotension)
Renal
Respiratory
Hepatic
Hematologic
CNS
Unexplained metabolic
acidosis

Bone et al. Chest. 1992;101:1644; Wheeler and Bernard. N Engl J Med. 1999;340:207.
 Injury
Infection
Non Infection
LPS ( lipopolysaccharide )

Complement System Rapid Inflammatory Reaction

Phagocyte cells

Monocytes and Macrophages

Sitokine pro inflammatory Delayed Inflammatory Response

secretion

Inflammatory Cascade
(Mediator, Neutrofil, Endothel
Platelet, Fibroblast)
 Tahap-tahap SEPSIS / SIRS 1

Tahap I
Injury Sitokin proinflamasi mediator dan sel
melawan organisme patogen

Tahap II
Sebagian sitokin ke sirkulasi merekrut
makrofag dan platelet stimulasi growth factor
rapid inflammatory reaction.
Sampai tahap II ini fisiologik, dikendalikan oleh
sitokin anti inflamasi
 Tahap-tahap SEPSIS / SIRS
Tahap III
Clinical insult terlalu besar
Sistem pengendalian tubuh tidak normal
homeostasis tak dapat dipertahankan
efek sitokin destruktif kerusakan organ yang
jauh dari tempat infeksi MODS MOFS
Perubahan yang terjadi
Progressive endhotelial dysfunctions
permeabilitas pembuluh darah meningkat.
Platelet sludging gangguan sirkulasi
maldistribusi aliran darah, iskemia dan reperfusion
injury
Aktivasi sistem koagulasi
Vasodilatasi, transudasi cairan dan maldistribusi
aliran darah syok
 Tahap-tahap SEPSIS / SIRS
Tahap IV
Terjadi kompensasi reaksi anti inflamasi yang
berlebihan imunosupresi / immune paralysis /
CARS ( Compensated Anti inflammatory Response
Syndrome)
CARS ditandai :
Penurunan ekspresi HLA DR < 30% pada
permukaan monosit penurunan sekresi TNF dan
IL-6 anergi mudah terkena infeksi.
Tahap V
Tahap akhir dari MODS immunologic dissonance
Penyebabnya :
Inflamasi yang berlebihan
Depresi imun yang persisten
 Pro-inflammatory anti-inflammatory
response response
Initial insult
(bacterial, viral, traumatic, thermal)

Systemic spillover of Systemic spillover of

pro-inflammatory anti-inflammatory
mediators Systemic mediators
Reaction

SIRS (pro-inflamma-
tory)

CARS (antipro-inflamma-
tory)

MARS
(mixed)

Cardiovascular Homeostais Apoptosis Organ Suppression

Compromise (cell death) dysfunction of the immune
(shock) system
SIRS CARS and Death with SIRS CARS
Predominates SIRS minimal Predominates Predominates
Balanced inflammation
Treatment of Sepsis
SEVERE SEPSIS: EARLY RECOGNITION

SIRS Criteria: Organ Failures:

Fever Respiratory
paO2:FiO2 < 300
Tachypnea
Cardiovascular
Tachycardia SBP < 90 mm Hg after IVF
Leukocytosis or Renal
leukopenia U/O < 30 mL/hr
CNS
Delirium
Metabolic
Lactate > 4 mmol/L, or anion gap
metabolic acidosis
 HOMEOSTASIS IS LOST IN SEPSIS

Proinflammatory
mediators
Endothelial injury
Tissue factor expression
Thrombin production

Increased PAl-1
Increased TAFIa
Reduced Protein C
(endogenous Activated
Protein C inhibits PAI-1)
Homeostasis

PAI-1= plasminogen activator inhibitor-1;TAFIa= thrombin activatable fibrinolysis inhibitor. Carvalho and Freeman.
J Crit Illness. 1994;9:51; Kidokoro et al. Shock. 1996;5:223; Vervloet et al. Semin Thromb Hemost. 1998;24:33.
Initial Resuscitation (first 6 hours)
Begin resuscitation immediately in patients with hypotension or
elevated serum lactate >4mmol/l; do not delay pending ICU
admission
Resuscitation goals:
- Central venous pressure (CVP) 812 mm Hg*
- Mean arterial pressure 65 mm Hg
- Urine output 0.5 mL.kg-1.hr-1
- Central venous (superior vena cava) oxygen
saturation 70%, or mixed venous 65%
If venous O2 saturation target not achieved: consider further
fluid transfuse packed red blood cells if required to hematocrit of
30% and/or
dobutamine infusion max 20 g.kg-1.min-1
A higher target CVP of 12-15 mmHg is recommended in the
presence of mechanical ventilation or pre-existing decreased
ventricular compliance
 Diagnosis
Obtain appropriate cultures before starting antibiotics
provided this does not significantly delay antimicrobial
administration
- Obtain two or more blood cultures (BCs)
- One or more BCs should be percutaneous
- One BC from each vascular access device in place
>48 hours
- Culture other sites as clinically indicated
Perform imaging studies promptly in order to confirm
and sample any source of infection (if safe to do so)
 Antibiotics
Begin intravenous antibiotics as early as
possible, and always within the first hour of
recognizing severe sepsis and septic shock

Broad-spectrum: one or more agents active

against likely bacterial/fungal pathogens and
with good penetration into presumed source

Reassess antimicrobial regimen daily to

optimize efficacy, prevent resistance, avoid
toxicity & minimize costs
 Antibiotics
Consider combination therapy in Pseudomonas infections

Consider combination empiric therapy in neutropenic

patients

Combination therapy no more than 3-5 days and de-

escalation following susceptibilities

Duration of therapy typically limited to 710 days; longer if

response slow, undrainable foci of infection, or
immunologic deficiencies

Stop antimicrobial therapy if cause is found to be non-

infectious
 Source Infection and Control
A specific anatomic site of infection should be established as
rapidly as possible and within the first 6 hours of presentation
Formally evaluate patient for a focus of infection amenable to
source control measures (e.g. abscess drainage, tissue
debridement)
Implement source control measures as soon as possible following
successful initial resuscitation
Exception: infected pancreatic necrosis, where surgical
intervention best delayed
Choose source control measure with maximum efficacy and
minimal physiologic upset
Remove intravascular access devices if potentially infected
 Fluid Therapy
Fluid-resuscitate using crystalloids or colloids
Target a CVP of 8mmHg (12mmHg if mechanically
ventilated)
Use a fluid challenge technique while associated with a
hemodynamic improvement
Give fluid challenges of 1000 ml of crystalloids or 300
500 ml of colloids over 30 minutes. More rapid and
larger volumes may be required in sepsis-induced
tissue hypoperfusion
Rate of fluid administration should be reduced if
cardiac filling pressures increase without concurrent
hemodynamic improvement
 Vasopressors
Maintain MAP 65mmHg
Norepinephrine or dopamine centrally administered are the initial
vasopressors of choice
Epinephrine, phenylephrine or vasopressin should not be administered
as the initial vasopressor in septic shock
Vasopressin 0.03 units/min maybe subsequently added to
norepinephrine with anticipation of an effect equivalent to
norepinephrine alone
Use epinephrine as the first alternative agent in septic shock when
blood pressure is poorly responsive to norepinephrine or dopamine
Do not use low-dose dopamine for renal protection
In patients requiring vasopressors, insert an arterial catheter as soon as
practical
 Inotropic Therapy
Use dobutamine in patients with
myocardial dysfunction as supported by
elevated cardiac filling pressures and low
cardiac output

Do not increase cardiac index to

predetermined supra-normal levels
 Steroids
Consider intravenous hydrocortisone for adult septic shock
when hypotension remains poorly responsive to adequate
fluid resuscitation and vasopressors
- ACTH stimulation test is not recommended to identify the subset
of adults with septic shock who should receive hydrocortisone
- Hydrocortisone is preferred to dexamethasone
- Fludrocortisone (50 g orally once a day) may be included if an
alternative to hydrocortisone is being used which lacks
significant mineralocorticoid activity
- Steroid therapy may be weaned once vasopressors are no longer
required
- Hydrocortisone dose should be <300mg/day

Do not use corticosteroids to treat sepsis in the absence of

shock unless the patients endocrine or corticosteroid
history warrants it
 Recombinant Human Activated Protein C (rhAPC)

Consider rhAPC in adult patients with sepsis-induced

organ dysfunction with clinical assessment of high risk
of death (typically APACHE II 25 or multiple organ
failure) if there are no contraindications

Adult patients with severe sepsis and low risk of

death (typically, APACHE II <20 or one organ failure)
should not receive rhAPC
 Blood Product Administration
Give red blood cells when hemoglobin decreases to <7.0 g/dl (<70
g/L) to target a hemoglobin of 7.0 9.0 g/dl in adults.
A higher hemoglobin level may be required in special
circumstances (eg: myocardial ischemia, severe hypoxemia, acute
hemorrhage, cyanotic heart disease or lactic acidosis)
Do not use erythropoietin to treat sepsis-related anemia. Erythropoietin
may be used for other accepted reasons
Do not use fresh frozen plasma to correct laboratory clotting abnormalities
unless there is bleeding or planned invasive procedures
Do not use anti-thrombin therapy
Administer platelets when:
Counts are <5000/mm3 (5 X 109/L) regardless of bleeding.
Counts are 5000 to 30,000/mm3 (530 X 109/L) and there is significant
bleeding risk. Higher platelet counts 50,000/mm3 (50 X 109/L) are
typically required for surgery or invasive procedures
 Mechanical Ventilation of Sepsis-induced
Acute Lung Injury (ALI)/ARDS
Target a tidal volume of 6ml/kg (predicted) body weight in patients with ALI/ARDS
Target an initial upper limit plateau pressure 30cmH2O. Consider chest wall
compliance when assessing plateau pressure
Allow PaCO2 to increase above normal, if needed to minimize plateau pressures and
tidal volumes
Positive end expiratory pressure (PEEP) should be set to avoid extensive lung collapse
at end-expiration
o Consider using the prone position for ARDS patients requiring potentially
injurious levels of FiO2 or plateau pressure, provided they are not put at risk from
positional changes
Maintain mechanically ventilated patients in a semi-recumbent position unless
contraindicated
Suggested target elevation 30 - 45 degrees
o Non invasive ventilation may be considered in the minority of ALI/ARDS
patients with mild-moderate hypoxemic respiratory failure. The patients need to
be haemodynamically stable, comfortable, easily arousable, able to protect/clear
their airway and expected to recover rapidly
 Mechanical Ventilation of Sepsis-induced
Acute Lung Injury (ALI)/ARDS
Use a weaning protocol and a spontaneous breathing trial (SBT)
regularly to evaluate the potential for discontinuing mechanical
ventilation
SBT options include a low level of pressure support with continuous
positive airway pressure 5 cm H2O or a T-piece.
Before the SBT, patients should:
Be arousable
Be hemodynamically stable without vasopressors
Have no new potentially serious conditions
Have low ventilatory and end-expiratory pressure requirement
Require FiO2 levels that can be safely delivered with a face mask
or nasal cannula
Do not use a pulmonary artery catheter for the routine monitoring of
patients with ALI/ARDS
Use a conservative fluid strategy for patients with established ALI
who do not have evidence of tissue hypoperfusion
 Sedation, Analgesia, and Neuromuscular
Blockade
Use sedation protocols with a sedation goal
for critically ill mechanically ventilated
patients

Use either intermittent bolus sedation or

continuous infusion sedation to
predetermined end points (sedation scales),
with daily interruption/lightening to produce
awakening. Re-titrate if necessary

Avoid neuromuscular blockers where

possible. Monitor depth of block with train-of-
four when using continuous infusions
 Glucose Control
Use IV insulin to control hyperglycemia in patients with
severe sepsis following stabilization in the ICU

Aim to keep blood glucose 150 mg/dL (<8.3 mmol/L)

using a validated protocol for insulin dose adjustment

Provide a glucose calorie source and monitor blood

glucose values every 1-2 hours (4 hours when stable) in
patients receiving intravenous insulin

Interpret with caution low glucose levels obtained with

point of care testing, as these techniques may
overestimate arterial blood or plasma glucose values
 Renal Replacement
o Intermittent haemodialysis and
continuous veno-venous haemofiltration
(CVVH) are considered equivalent

o CVVH offers easier management in

hemodynamically unstable patients
 Bicarbonate Therapy

Do not use bicarbonate therapy for the

purpose of improving hemodynamics or
reducing vasopressor requirements
when treating hypoperfusion-induced
lactic academia with pH 7.15
 Deep Vein Thrombosis (DVT) Prophylaxis

Use either low-dose unfractionated

heparin (UFH) or low-molecular weight
heparin (LMWH), unless contra-indicated

Use a mechanical prophylactic device,

such as compression stockings or an
intermittent compression device, when
heparin is contra - indicated
o Use a combination of pharmacologic and mechanical
therapy for patients who are at very high risk for
DVT
o In patients at very high risk LMWH should be used
rather than UFH
 Stress Ulcer Prophylaxis
Provide stress ulcer prophylaxis using
H2 blocker or proton pump inhibitor

Benefits of prevention of upper GI bleed

must be weighed against the potential
for development of ventilator-associated
pneumonia
 Consideration for Limitation of Support

Discuss advance care planning with patients

and families

Describe likely outcomes and set realistic

expectations
 Laporan Kematian
Tn. RB
SMF Penyakit Dalam RS UKI
 Kronologis Kematian

Nama : Tn. RB
Usia : 61 th
TTL : 14 Februari 1955
Alamat : Jl. Cipinang 3 rt 14/ rw 8 Kebon
Pala
Datang ke IGD RS UKI tanggal 29 / 3/ 16
Meninggal pada tanggal 4/4/16
 29/3/2016
pukul 17.00 WIB
Alloanamnesa :
Pasien datang ke RS UKI dengan keluhan lemas, disertai
demam sejak 1 minggu SMRS. Demam awalnya dirasakan sejak
terasa nyeri pada anus dan keluar benjolan dari anus sejak 7
hari SMRS, Darah (+), keluar nanah dari benjolan (+). Nafsu
makan dan minum berkurang sejak 1 minggu yang lalu karena
pasien takut BAB, selain itu pasien mengeluh BAK sedikit
berwarna kuning
RPD: 6 hari yang lalu, pasien sudah berobat ke IGD RS UKI
dengan keluhan yang sama didiagnosis Haemorroid Interna
Grade III dan dianjurkan untuk rawat jalan dan di berikan obat :
Ketorolac 3x1tab
Sanmol 3x1tab
Ardium 2x3tab
Boraginol Supp 2x1
 Pemeriksaan Fisik
(tgl 29/3/2016)
Ku : TSB
Kes : Apatis
Tanda tanda vital :
TD : 100/60 mmHg
RR : 34 X/menit
S : 39,4C
N : 94 X/menit
 Pemeriksaan Fisik
(tgl 29/3/2016)
Mata : Abdomen :
CA +/+ SI-/- I :perut tampak datar.
Leher : A : BU (+) 4 x/menit
KGB tidak teraba membesar, P : timpani, nyeri ketok (-).
nyeri tekan(-) P : nyeri tekan (-), hepar limpa
Thorax : tidak teraba.
I : pergerakan dinding dada Ekstremitas :
simetris Edema -/-
P: vf kiri dan kanan sama Akral hangat
P :sonor pada kedua lapangan CRT<2 detik.
paru, batas paru jantung dbn, Rumple leede (-)
batas paru hati DBN
A : pernafasan vesikuler,
Anus :
RH+/+, Wh-/-, BJ I-II normal, Terdapat benjolan dengan
murmur (-), gallop (-). diameter, hiperemis, darah (+),
pus (+).

Turgor Kulit : melambat

 Hasil Laboratorium
TANGGAL 29/3/16
Na 128 mmol/L
K 4,4 mmol/l
CL 11 mmol/L
Hb 12,1 g/dl
L 9,5 ribu/ul
Ht 34,7 %
T 101 ribu/ul
GDS 108 mg/dl
Ur 129 mg/dl
Cr 2,36 mg/dl
EKG
 RONTGEN THORAX
KESAN:
Hypertensive heart configuration dan
bronkopneumonia
 DIAGNOSA KERJA
(29/3/2016)
Diagnosa kerja :
Haemoroid interna gr. III
SIRS
Hiponatremia
AKI e.c. dehidrasi berat
Bronkopneumonia
 TATALAKSANA
(29/03/2016)

RAWAT INAP
Oksigenasi : nasal kanul 2-4 lpm
IVFD : III NS 0,9% / 24 JAM
II Futrolit / 24 JAM
MM/
OMZ 1 X 40 mg
Domperidone 1 X 10 mg
Paracetamol 3x500
Prorenal 3X2
CaCO3 3X1
BD Gard 2X1
Garam dapur 3 x 500 g
Px H2TL/24 JAM, Ur , Cr darah, dan elektrolit / 2 hari
Balance cairan ketat
Foto thorax PA
Konsul bedah
 (29/03/2016)

Diuresis
Urine output 500cc/8jam 62,5 cc/jam
Balance cairan :
Intake : 500 cc
Output : 750 cc
Balance : -250 cc
 Follow Up 30/3/2016
S/ Demam (+), lemas (+), P/
O/ Cek H2TL/24 jam, Cek ureum kreatinin per 2
KU : Tampak Sakit Sedang hari
Kes : Apatis IVFD : III NS 0,9% + II Futrolit
Td : 110/60 mmHg, Oksigenasi : nasal kanul 2-4 lpm
N : 81 kali/menit, Diet : Saring
S : 38 oC NGT : pasien menolak
RR : 18 kali/menit MM/
(Visit DR. dr. Sahala Panggabean,Sp.PD-
Thorax : Rh +/+, Wh -/- KGH) terapi lanjut
Diuresis
Prorenal 3x2(STOP)
CaCO3 3x1(STOP)
Urine output 1800cc/24jam 75 cc/jam
(+)Dexciclaf 3x1
Balance cairan :
A/ Abses Perianal
SIRS
Hiponatremia
AKI e.c. dehidrasi berat
Bronkopneumonia
 Follow Up 31/3/2016
S/ Demam (+) P/ Cek H2TL/24 jam, Cek ureum kreatinin per
O/ KU : Tampak Sakit Sedang 2 hari
Kes : Apatis IVFD : III NS 0,9% + II Futrolit
Td : 150/80 mmHg, Oksigenasi : nasal kanul 2-4 lpm
N : 82 kali/menit, Diet : Saring
S : 38,5 oC NGT : pasien menolak
RR : 20 kali/menit MM/
(Visit DR. dr. Sahala Panggabean,Sp.PD-
KGH) terapi lanjut
Thoraks : Rh +/+,
garam dapur 3x500mg (STOP)
Diuresis
Urine output 2650cc/24jam 110cc/jam Jawaban Konsul Bedah
Balance (dr. Stanley Ketting Oliver, Sp.B)
input : 2450 cc
A/ suspect haemorroid interna grade III-IV dd
output : 2500 cc
prolaps ani
balance : -50
P/ rendam PK sehari 2 kali (+ 10 menit)
Mm/ Lanmer 2x1gram (IV)
A/ -Abses Perianal
- SIRS tramadol 2x1 (IV)
- AKI ardium 2x1 tab (PO)
- Bronkopneumonia Saran : Optimalisasi KU, jika KU optimal
rencana Haemorroidektomi
Follow Up 31/3/2016
Hasil Lab :
- Na 135
- K 4,6
- Cl 108
- Hb 11,3
- Leu 7800
- Ht 31,8
- Tromb 109.0000
- Ureum 80
- Kreatinin 1,58
 Follow Up 1/4/2016
S/ Demam (+), P/ IVFD : III NS 0,9% + II Futrolit
O/ Oksigenasi : nasal kanul 2-4 lpm
Kes : somnolen
Diet : NGT 5x150cc bilas 50cc
KU : TSB
TD : 110/70 mmHg, MM/
Nadi : 82 kali/menit, (visit DR. dr. Sahala Panggabean, Sp.PD-
Suhu : 38,5 oC KGH) terapi lanjut
RR : 20 kali/menit paracetamol drip 3x1gram
Thoraks : Rh +/+
Diuresis Cek AGD, SGOT, SGPT
urin ouput: 1800cc/24 jam 75cc/jam
Balance
input : 2900 cc
output : 2950 cc
balance : -50

A/ - Abses Perianal
- SIRS
- AKI
- Bronkopneumonia
 Follow Up 1/4/2016

Hasil Lab : - SGOT 73 U/L

-AGD : - SGPT 43 U/L
- PH 7,546 - GDS 90 mg/dl
- PCO-2 17,8 mmHg - Hb 10,0 mg/dl
- PO2 110,4 mmHg - Leukosit 6,100 /ul
- Saturasi O2 98,6% - Hematokrit 28, 9%
- Base Excess -4,8 mmol/L - Trombosit 96.000/ul
- HCO3 15,6 mmol/L
- konsentrasi o2 12,6 vol%
 Follow Up 2/4/2016
S/ Demam (+), lemas (+)
P/ IVFD : III NS 0,9%
O/ Kes : somnolen II Futrolit
- KU: TSB Diet : NGT 5x150cc bilas 50cc
TD : 160/90 mmHg,
N : 82 X/M, Oksigenasi : nasal kanul 2-4 lpm
S : 38,7 oC MM/
RR : 30kali/menit
(visit DR. dr. Sahala Panggabean, Sp.PD-
Thoraks : Rh +/+
KGH) terapi lanjut
mm/
Diuresis (+) amlodipin 1x10 mg
urin ouput: 1800cc/24 jam 75cc/jam
Balance : lanmer usul ganti
Input : 3800 cc
Output : 2500 cc
Balance : +1.300 cc

A/ - Abses Perianal
- SIRS
- AKI
- Bronkopneumonia
 Follow Up 3/4/2016
Pkl. 23.30

S/ Demam (+),
O/ Kes : koma (+)
P/ Edukasi tentang kondisi
- KU : TSB pasien dan tindakan resusitasi
TD : 60 per palpatoir, intubasi serta perawatan ICU
N : 100 X/M lemah,
S : 39 oC pasien menolak
RR : 47 kali/menit
Status pasien DNR
Pkl 00.05 (tanggal 4/4/2016)
Thoraks : Rh +/+,
pasien dinyatakan meninggal
Diuresis dunia
urin ouput: 400cc/8 jam 50cc/jam
Balance
Input : 700 cc
Output : 500 cc
Balance : +200 cc

A/ - Abses Perianal
- Sepsis
- AKI
- Bronkopneumonia
 Tanggal 03 April 2016

Lab :
PH darah : 7,524
PCO-2 : 23,2 mmHg
PO2 : 67,4 mmHg
Saturasi : 95,1%
Base Excess : -1,5 mmol/L
HCO3 : 19,3 mmol/L
TCO2 : 20,0 mmol/L
Konsentrasi O2: 14,4 vol %

Elektrolit
Natrium : 141 mg/dl
Kalium : 3,9 mg/dl
Clorida : 109 mg/dl
TERIMA KASIH