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 : [email protected]
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!)