MMohamad Supriatna Toto Saputraohamad Supriatna Toto Saputra, Dr, Sp.A, Dr, Sp.A

Place & Date of Birth : Sumedang, 15-09-1970 Marital Status : Married, 2 children Mailing Address : Jl. Puspowarno Selatan No.

10, Semarang Office Address : Child Health Department,

Faculty of Medicine

Diponegoro University / Dr. Kariadi Job position : Staff of Pediatric Intensive Care Unit Phone : 62-24-7613724 (home) Fax : 62-24-8414296 (office) e-mail : priandpri@yahoo.com

Educational History

Period (month/year)

School’s name and Place (city) Degrees obtained

1976 - 1982 Mandalaherang Elementary School Sumedang, West Java, Indonesia

-

1982 -1985 Cimalaka Junior High SchoolSumedang, WestJava, Indonesia

1985 - 1988 Bandung Senior High SchoolBandung, West Java, Indonesia

-

1988 - 1996 Faculty of Medicine Diponegoro University Semarang

Medical Doctor

2000 - 2005 Faculty of Medicine Diponegoro University

Pediatrician

Course / Fellowship / Workshop

No Name of Visit Experience, Course and Education

Location Period

1. International symposium and workshop on Infectious and Tropical Diseases

Semarang, Indonesia

2008

2. Seminar and Workshop The Role of Professional and Parents in Caring Children with Mental Retardation and Autism

Semarang, Indonesia

2008

3. Symposium and Workshop Toward Better Nutrition for Children Health

Semarang, Indonesia

2008

4. Symposium and Workshop Nutrisi & Metabolik, Endokrinologi, Nefrologi, dan Neurologi

Semarang,Indonesia

2008

5. Workshop NIF Scientific Workshop 2007 Semarang, Indonesia

2007

6. Workshop Early Detection on Neurodevelopmental Disorders

Semarang, Indonesia

2007

7. International Symposium on Liver Transplantation

Singapore 2007

8. Workshop InnovativeAssessment in Pediatrics Training Program & Seminar on New Trend in Residency Training Program

Yogyakarta, Indonesia

2007

8. Training Management of Emergency Patient Semarang, Indonesia

2006

9. Advanced Pediatric Resuscitation Couse (APRC) Jakarta, Indonesia

2006

10. Advanced Course of Mecanical Ventilation (ACMV)

Jakarta,Indonesia

2006

11. Pelatihan Vaksinologi Dasar bagi Dokter Spesialis Anak

Semarang 2006

12. Neonatal Resuscitation Course (NRP) Bandung, Indonesia

2005

Course / Fellowship / Workshop

8. Training Management of Emergency Patient

Semarang, Indonesia

2006

9. Advanced Pediatric Resuscitation Couse (APRC)

Jakarta, Indonesia

2006

10. Advanced Course of Mecanical Ventilation (ACMV)

Jakarta,Indonesia

2006

11. Pelatihan Vaksinologi Dasar bagi Dokter Spesialis Anak

Semarang 2006

12. Neonatal Resuscitation Course (NRP) Bandung, Indonesia

2005

13. Pediatric FCCS Jakarta 2010

Pengelolaan Kegawatan Pengelolaan Kegawatan DBD AnakDBD Anak

Moh.Supriatna, Moh.Supriatna, Tatty Ermin SetiatiTatty Ermin Setiati, Yusrina Istanti, Yusrina Istanti

Pediatric Department Dr Kariadi HospitalPediatric Department Dr Kariadi Hospital

Faculty of Medicine, Diponegoro University Faculty of Medicine, Diponegoro University

Semarang IndonesiaSemarang Indonesia

Warning Signs for Dengue ShockWarning Signs for Dengue Shock

Hemostatic & VascularHemostatic & VascularLeakage Factors Leakage Factors

Tatty ES ( 2004 ): Tatty ES ( 2004 ): hhemostatic & emostatic & vvascular ascular lleakage eakage ffactors actors ppredictor of redictor of sshock in hock in DHFDHF

PEI PEI ffirst irst rrank , followed by ank , followed by aalbumin, Ht, lbumin, Ht, pproteinrotein

In the non survivors: In the non survivors: hhemostatic emostatic ddisturbances & isturbances & vvascular leakage factors ascular leakage factors continued to be abnormal leading to MOF continued to be abnormal leading to MOF and bleeding ( DIC ) and bleeding ( DIC )

SYOKSYOK

SINDROM KLINISSINDROM KLINIS

KEGAGALAN SISTEM SIRKULASIKEGAGALAN SISTEM SIRKULASI

KEBUTUHAN KEBUTUHAN OKSIGEN OKSIGEN NUTRIEN NUTRIEN JARINGANJARINGAN

DEFISIENSI AKUT DEFISIENSI AKUT

DITINGKAT SELDITINGKAT SEL

PENGATURAN CURAH JANTUNG PENGATURAN CURAH JANTUNG DAN TEKANAN DARAHDAN TEKANAN DARAH

PRELOAD CONTRACTILITY AFTERLOAD

HEART RATE STROKE VOLUME

CARDIAC OUTPUT SYSTEMIC VASCULAR RESISTANCE

BLOOD PRESSURE

PENGANGKUTAN OKSIGENPENGANGKUTAN OKSIGEN

Cardiac Out Put Blood flow

OxygenDelivery

Blood O2 Content

Hb Contentration

O2 Bound to Hb

O2 Dissolved in Plasma

Mekanisme Kompensasi Tubuh Mekanisme Kompensasi Tubuh refleksi refleksi simpatis simpatis

- Resistensi sistemik - Resistensi sistemik - Tekanan darah ( N )- Tekanan darah ( N )

- Tekanan Diastolik - Tekanan Diastolik - Tekanan Nadi Sempit - Tekanan Nadi Sempit

STADIUM SYOKSTADIUM SYOK

FASE I: KOMPENSASIFASE I: KOMPENSASI

FASE II : DEKOMPENSASIFASE II : DEKOMPENSASI

- Mekanisme kompensasi gagal

- Metabolisme anaerobik

- Asam laktat asidosis >>

terbentuk asam karbonat intraseluler

- Kontraktilitas otot jantung - Pompa Na – K sel

Integritas membran sel

Kerusakan sel

FASE II : LANJUTANFASE II : LANJUTAN

Aliran darah lambatAliran darah lambat

Agregasi TrombositAgregasi Trombosit

Pembentukan TrombusPembentukan Trombus

PendarahanPendarahan

Pelepasan MediatorPelepasan Mediator

Vasodilatasi ArterialVasodilatasi Arterial

Kenaikan Permeabilitas KapilerKenaikan Permeabilitas Kapiler

SSVR VR

FASE III : IREVERSIBELFASE III : IREVERSIBEL

Kerusakan / Kematian SelKerusakan / Kematian Sel Disfungsi sistem multi organDisfungsi sistem multi organ Cadangan fostat Cadangan fostat energienergi ttinggi inggi

( Hepar, Jantung )( Hepar, Jantung )

Tekanan darah tak terukurTekanan darah tak terukur Nadi tak terabaNadi tak teraba

Kesadaran Kesadaran AnuriaAnuriaGMOGMO

klinis

Tujuan Tujuan Pengelolaan SSDPengelolaan SSD

Meningkatkan transport OMeningkatkan transport O22 (DO (DO22) ke jaringan/sel: ) ke jaringan/sel:

Memperbaiki pra-beban dengan resusitasi volumeMemperbaiki pra-beban dengan resusitasi volume Meningkatkan kontraktilitas jantungMeningkatkan kontraktilitas jantung Menurunkan resistensi pembuluh darah Menurunkan resistensi pembuluh darah

Makro & MikroMakro & Mikrosirkulasisirkulasi

Oxygen Debt Oxygen Debt

Pemilihan Cairan ResusitasiPemilihan Cairan Resusitasi

KRISTALOID KOLOID

??

GELATINE, HES, ALBUMIN, PPF

< 100.000 D

100.000-300.000 D

> 300.000 D

TYPE OF FLUIDS:

CRYSTALOID

COLLOIDS

LOW MW

MEDIUM MW

HIGH MW

NaCl, RL, RA, Dextrose

HES

HESNa

Cl

H2O

H2O

The relative distribution of crystalloid and colloid solutions in the intra- and extravascular fluid space at equilibrium

(within 30 min to 1 hour of infusion)

FluidFluid IntravascularIntravascular ExtravascularExtravascularNormal capillary permeabilityNormal capillary permeability

CrystalloidCrystalloid

ColloidColloid

20%20%

70%70%

80%80%

30%30%

Increased capillary permeabilityIncreased capillary permeability

Crystalloid Crystalloid

ColloidColloid

15-20%15-20%

60-70%60-70%

80-85%80-85%

30-45%30-45%

Increased capillary permeability + cell membrane Increased capillary permeability + cell membrane dysfunctiondysfunction

Crystalloid Crystalloid

ColloidColloid

10-15%10-15%

50-60%50-60%

85-90%85-90%

40-50%40-50%

Sifat CairanSifat Cairan

Kristaloid (RL/RA/NaCl) Kristaloid (RL/RA/NaCl) Didistribusikan dan mengisisi kompartmen Didistribusikan dan mengisisi kompartmen

intersisialintersisial Tak memperbaiki sirkulasi mikroTak memperbaiki sirkulasi mikro Untuk mengisi volume intravaskuler perlu Untuk mengisi volume intravaskuler perlu

jumlah besarjumlah besar Dapat me Dapat me osmolaritas plasma & edema osmolaritas plasma & edema

serebri (1L RL membentuk 114 ml air)serebri (1L RL membentuk 114 ml air) Efek pro-koagulanEfek pro-koagulan efek samping efek samping

trombosis vena dalam dan emboli parutrombosis vena dalam dan emboli paru

Efek Koloid Sintetik yangEfek Koloid Sintetik yang MenguntungkanMenguntungkan

Kemampuan meningkatkan tekanan onkotikKemampuan meningkatkan tekanan onkotik

Mempertahankan volume intravaskulerMempertahankan volume intravaskuler

Efek menyumpal (Efek menyumpal (sealing effectsealing effect) untuk BM ) untuk BM

100.000100.000 –– 300.000 D300.000 D

Efek pada aliran darah regional splangnik & renalEfek pada aliran darah regional splangnik & renal

Efek terhadap mikrosirkulasiEfek terhadap mikrosirkulasi

Efek anti-inflamasi ( menurunkan ICAM-1 dan Efek anti-inflamasi ( menurunkan ICAM-1 dan

VCAM-1) VCAM-1) kebocoran vaskular ↓ kebocoran vaskular ↓

Zornow, MH et al.: Fluid Management In Zornow, MH et al.: Fluid Management In Patients With Traumatic Brain Injury. New Patients With Traumatic Brain Injury. New

Horizons 3:488-498, 1995Horizons 3:488-498, 1995

3,7003,700 4,7004,700 1,0001,000RLRL

9,3009,300 3,7003,700 14,00014,000 1,0001,0005% 5% DextroseDextrose

-750-750 250250 1,0001,00025% 25% AlbuminAlbumin

1,0001,000 1,0001,0005% 5% AlbuminAlbumin

IncreasIncreaseded

ICV (ml)ICV (ml)

IncreasIncreaseded

ISS ISS (ml)(ml)

Infused Infused volumevolume (ml) (ml)

Increased Increased PVPV (ml) (ml)

PV plasma volume; ISS interstitial fluid volume; ICV intracellular volume; RL lactated Ringer’s

solution; MFG=modified fluid gelatin

HES 200/0.5 6% 1,000 1,000

MFG 4% 1,000 1,000

Dextran-40 10% 1,000 500-600 -400/-

500

(added by presenter)(added by presenter)

Effects of Synthetic Colloids

Oncoticpressure

increased IVvolume

Venous flow back(preload)

Improvedrheology

Arterial oxygenconcentration

Flow resistance

Cardiac output

Retaining of fluidin the IVS

CO

Hematocrit

Hemodilution

CaO2 DO2

Penggunaan HES 200/0,5 pada SSDPenggunaan HES 200/0,5 pada SSD

Kelompok I Kelompok I

(kel. Kontrol/RL)(kel. Kontrol/RL)

Kelompok II Kelompok II

(kel. (kel. Perlakuan/HES)Perlakuan/HES)

Lama syok teratasiLama syok teratasi 7,9 jam7,9 jam 2,3 jam2,3 jam

Mortalitas (%)Mortalitas (%) 26,6726,67 6,676,67

Efusi pleura ringanEfusi pleura ringan 22 ----

Efusi pleura sedangEfusi pleura sedang 77 44

Efusi pleura beratEfusi pleura berat 2121 ----

Acute lung injury (ALI)Acute lung injury (ALI) 44 11

ARDSARDS 66 22

PIM beratPIM berat 88 ----

Lama rawat di PICULama rawat di PICU 13,513,5 66

Transfusi darahTransfusi darah 3030 88

Colloid DisadvantagesColloid Disadvantages

Gelatin HES Dextran

Anaphyl.Rx No No Severe

Coag.effect No Yes (HMW) Yes

Renal No Yes (HMW) High dose

Liver No May be No

Tissue Acc. No Yes (HMW) No

Dose restriction in RF

No Yes (HMW and MMW)

No

Effects of Effects of colloidcolloid solutions solutions on haemostasis and coagulationon haemostasis and coagulation

GelatinsGelatins HES HES DextranDextrans s

Factor VIII, vWF Factor VIII, vWF No effectNo effect

PlateletsPlatelets AdhesionAdhesion AggregationAggregation

No effectNo effect

Thrombus Thrombus formationformation

No clinical No clinical effecteffect

Blood typingBlood typing No effectNo effect In emergency In emergency

situation blood typing situation blood typing

prior to infusion prior to infusion

!

KontraindikasiKontraindikasi KoloidKoloid

Kegagalan Jantung KongestifKegagalan Jantung KongestifGagal Ginjal ( serum Cr >2mg/dl U> Gagal Ginjal ( serum Cr >2mg/dl U>

177umol / l )177umol / l )Gangguan koagulasi berat ( kecuali pd Gangguan koagulasi berat ( kecuali pd

keadaan gawat mengancam jiwa )keadaan gawat mengancam jiwa )HiperhidrosisHiperhidrosis, d, dehidrasiehidrasiPerdarahan otakPerdarahan otak

ALGORITHM FOR FLUID MANAGMENT IN ALGORITHM FOR FLUID MANAGMENT IN COMPENSATED SHOCK ( WHO 2009)COMPENSATED SHOCK ( WHO 2009)

ISOTONIC CRYSTALLOID 5-10ML/KG 1 HR

IMPROVEMENT

NO

Ht increased:

2nd BOLUS OF FLUID10-20 ML/KG: 1 HR

Ht low

Significant occult/ overt bleeding

WB

CRYSTALOID5-7ML/KG 1-2 HRS3-5ML/KG 2-4 HRS2-3 ML/KG 2-4 HRS\MONITOR Ht 6-8 hr

Stop at 48 hours

YES

ALGORITHM FOR FLUID MANAGEMENT IN DECOMPENSATED SHOCK (WHO 2009)

Hypotensive ShockFluid resuscitation with 20mL/kg isotonic crystalloid or colloid over 15 minutes

Try to obtain a HCT level before fluid resuscitation

ImprovementYES NO

Crystalloid/colloid 10 mL/kg/hr for 1 hour, then continue with :IV crystalloid 5-7 mL/kg/hr for 1-2 hours; reduce to 3-5 mL/kg/hr for 2-4 hours; reduce to 2-3 mL/kg/hr for 2-4 hoursIf patient improve, fluid can be reducedMonitor HCT 6-hourly

Stop at 48 hours

Review 1st HCT

HCT ↑ or high HCT ↓

Administer 2nd fluid bolus (colloid)

Consider occult/overt bleed

10-20 mL/kg over ½ to 1 hourInitiate transfusion

with fresh WB

improvement

YES NO

improvement

Repeat 2nd HCT

HCT ↑ or high HCT ↓

Administer 3rd fluid bolus (colloid)10-20 mL/kg over 1 hour

YES NO Repeat 3rd HCT

HCT ↑ or high HCT ↓

Fluid bolus/increase fluid

Consider occult/overt bleed

Initiate transfusion with fresh WB

DENGUE STUDIES IN CHILDREN

DENGUE SHOCK SYNDROME: CRITICAL CARE PERSPECTIVEDENGUE SHOCK SYNDROME: CRITICAL CARE PERSPECTIVE

DSS = = Septic Shock which caused by dengue virusCombination of hypovolemic, distributive (+ cardiogenic) shock

MANAGEMENT OF DSS: UNIQUE - SIMILAR TO SEPTIC SHOCK

EARLY GOAL DIRECTED THERAPY (SSC)

WCPIC Geneva, 2007

SUGGESTEDFLUID RESUSCITATION IN

DSS

Macrocirculation: Macrocirculation: Mental status Mental status Pulse Pressure >20 mmHgPulse Pressure >20 mmHg MAP normal for ageMAP normal for age SaO2 >92%, SvcO2 >70% SaO2 >92%, SvcO2 >70% Warm extremities Warm extremities Temperature cor-toe < 2”Temperature cor-toe < 2” Capillary refill time <2” Capillary refill time <2” Diuresis >1 ml/kg/hrDiuresis >1 ml/kg/hr

End point of DSS rapid resuscitation:End point of DSS rapid resuscitation:

Microcirculation:Serum lactate

< 2mmol/l

Hypoperfusion Reperfusion

MMikrosirkulasiikrosirkulasi

deBaker, Am J Respir Crit Care Med 166:98–104,2002

Fluid responsive

Refractory shockPlace pulmonary artery catheter and direct fluid,

inotrope,vasopressor,vasodilator, and hormonal therapies to attain normal MAP-CVP and CI > 3.3 and < 6.0 L/min/m2

Place pulmonary artery catheter and direct fluid, inotrope,vasopressor,vasodilator, and hormonal therapies to attain normal

MAP-CVP and CI > 3.3 and < 6.0 L/min/m2

Figure 4. Stepwise management of hemodynamic support with goals of normal perfusion and perfusion pressure (MAP-CVP) in infants and children with septic shock. Proceed to next step if shock persists.

Give hydrocortisoneGive hydrocortisone

At Risk of Adrenal Insufficiency? Catecholamine-resistant shock Not at Risk?

Titrate epinephrine for cold shock, norepinephrine for warm shock to normal MAP-CVP and SVC O2 saturation > 70%

Titrate epinephrine for cold shock, norepinephrine for warm shock to normal MAP-CVP and SVC O2 saturation > 70%

Fluid refractory-dopamine resistant shock

Establish central venous access, begin dopamine therapy and establish arterial monitoring

Establish central venous access, begin dopamine therapy and establish arterial monitoring

Fluid refractory shock

Push 20cc/kg isotonic saline or colloid boluses up to and over 60 cc/kgCorrect hypoglycemia and hypocalcemia

Push 20cc/kg isotonic saline or colloid boluses up to and over 60 cc/kgCorrect hypoglycemia and hypocalcemia

Recognize decreased mental status and perfusion.Maintain airway and establish access according to PALS guidelines.

Recognize decreased mental status and perfusion.Maintain airway and establish access according to PALS guidelines.

Observe in PICUObserve in PICU

Consider ECMOConsider ECMO

0 min 5 min

60 min

15 min

Normal Blood Pressure Low Blood Pressure Low Blood Pressure Cold Shock Cold Shock Warm Shock SVC O2 sat < 70% SVC O2 sat < 70%

Do not give hydrocortisoneDo not give hydrocortisone

Add vasodilator or Type III PDE inhibitor Norepinephrine

with volume loading

Volume and Epinephrine Volume and (vasopressin or angiotensin)

Persistent Catecholamine-resistant shock

UNUSUAL MANIFESTATIONS AND COMPLICATIONS

Ensefalopati dengue Ensefalopati dengue

• Dijumpai pada 3% kasus DBD dengan mortalitas tinggi (50%)

• Insiden tersering pada anak < 2 tahun• Dicurigai ensefalopati dengue pada DBD disertai

penurunan kesadaran dengan syok maupun tidak dengan kejang maupun tidak

• Sering disertai dengan diare

Faktor Risiko Ensefalopati DengueFaktor Risiko Ensefalopati Dengue

• Syok berkepanjangan• Perdarahan saluran cerna berat• Gangguan fungsi hati berat• Overload cairan

Hasil lab yang menunjang diagnosisHasil lab yang menunjang diagnosis

SGOT dan SGPT ↑ (SGOT dan SGPT ↑ (> > 200 U/l)200 U/l) Bilirubin direk kadang meningkatBilirubin direk kadang meningkat PT dan PTT meningkatPT dan PTT meningkat Kadar gula darah ↑Kadar gula darah ↑ Kadar amoniak ↑Kadar amoniak ↑ AlkalosisAlkalosis Imbalance elektrolit (Na, K )Imbalance elektrolit (Na, K ) LP bila ada kecurigaan infeksi intrakranialLP bila ada kecurigaan infeksi intrakranial

Prinsip Tata Laksana Ensefalopati Dengue Prinsip Tata Laksana Ensefalopati Dengue

1. Airway + breathing management

2. Mencegah TIK ↑

3. Mencegah hipoglikemia

4. Mengurangi produksi amoniak

5. Memberikan vitamin K

6. Mengoreksi gangguan keseimbangan asam basa dan elektrolit

1. Airway + breathing management

2. Mencegah TIK ↑

3. Mencegah hipoglikemia

4. Mengurangi produksi amoniak

5. Memberikan vitamin K

6. Mengoreksi gangguan keseimbangan asam basa dan elektrolit

Tata Laksana Ensefalopati Dengue Tata Laksana Ensefalopati Dengue

- Vit K 0,3 mg/kgBB- Asam amino rantai pendek- Ringer asetat- Tranfusi darah bila ada indikasi- H2 blocker bila terjadi perdarahan

saluran cerna- Hemodialisis bila diperlukan

- Vit K 0,3 mg/kgBB- Asam amino rantai pendek- Ringer asetat- Tranfusi darah bila ada indikasi- H2 blocker bila terjadi perdarahan

saluran cerna- Hemodialisis bila diperlukan

Pengelolaan Pengelolaan TIK ↑TIK ↑

- Restriksi cairanRestriksi cairan- MMemperbaiki gangguan elektrolitemperbaiki gangguan elektrolit- Memperbaiki alkalosisMemperbaiki alkalosis- Kortikosteroid bila tidak ada perdarahanKortikosteroid bila tidak ada perdarahan- Manitol Manitol - Mempertahankan kadar gula darah > 60 mg%Mempertahankan kadar gula darah > 60 mg%

- Restriksi cairanRestriksi cairan- MMemperbaiki gangguan elektrolitemperbaiki gangguan elektrolit- Memperbaiki alkalosisMemperbaiki alkalosis- Kortikosteroid bila tidak ada perdarahanKortikosteroid bila tidak ada perdarahan- Manitol Manitol - Mempertahankan kadar gula darah > 60 mg%Mempertahankan kadar gula darah > 60 mg%

DENGUE vs JEDENGUE vs JEDenguDenguee

JEJE

•Defisit neurologisDefisit neurologis•Penurunan kesadaran atau Penurunan kesadaran atau

kejang terjadi sejak awal masuk kejang terjadi sejak awal masuk RSRS•Ig MIg M

±±±±

Ig M + Ig M + denguedengue

++++

Ig M Ig M + JE+ JE

Gagal Hati Akut Gagal Hati Akut

- Kerusakan hepatosit akibat virus dengueKerusakan hepatosit akibat virus dengue- Klinis : ikterik disertai peningkatan kadar Klinis : ikterik disertai peningkatan kadar

enzyme hatienzyme hati- Dapat disebabkan Dapat disebabkan overover--usesuses obat-obatan obat-obatan- Terdapat faktor genetik yang mendasari Terdapat faktor genetik yang mendasari

((Reye syndrome)Reye syndrome)- Dapat disebabkan syok berkepanjanganDapat disebabkan syok berkepanjangan

Gagal Ginjal Akut Gagal Ginjal Akut

Dapat disebabkan oleh :Dapat disebabkan oleh :- Syok berkepanjanganSyok berkepanjangan- Hemolisis akut dengan hemoglobulinuriaHemolisis akut dengan hemoglobulinuria

- G6PD Deficiency- G6PD Deficiency

- Hemoglobulinopathy- Hemoglobulinopathy- Dihubungkan dengan fase lanjut DBDDihubungkan dengan fase lanjut DBD- Obat – obatan Nephrotoxic Obat – obatan Nephrotoxic

Miokarditis Miokarditis Biasanya muncul saat recoveryBiasanya muncul saat recovery Sering terjadi pada anak berumur > 10 tahunSering terjadi pada anak berumur > 10 tahun Manifestasi klinis : Manifestasi klinis :

- Bradikardi Bradikardi - Irama iregulerIrama ireguler- DDapat terjadi gagal jantungapat terjadi gagal jantung Tidak ada terapi spesifik kecuali bila HR < 50x/’ Tidak ada terapi spesifik kecuali bila HR < 50x/’

(diberikan Isopril) → MONITORING(diberikan Isopril) → MONITORING Bersifat reversibelBersifat reversibel Gambaran EKG : QTc memanjangGambaran EKG : QTc memanjang

The rational used of fluid therapy in DSS is to The rational used of fluid therapy in DSS is to use the fluid that has good intravascular filling use the fluid that has good intravascular filling effect and safety profileeffect and safety profile..

EGDT can be adopted in the management of EGDT can be adopted in the management of DSSDSS..

End point of resuscitation is improvement of End point of resuscitation is improvement of macrocirculation and micricmacrocirculation and micricoorculation guidence rculation guidence by CVP, ScvO2,MAP, serum lactic acid levelby CVP, ScvO2,MAP, serum lactic acid level..

Unusual manifestasions: encephalopathy, liver Unusual manifestasions: encephalopathy, liver failure, renal failure, myocarditis. failure, renal failure, myocarditis.

ConclussionConclussion

THANK YOUTHANK YOU

Yummy! (Look, your blood is inside my

belly!)