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Penatalaksanaan Syok pada Anak
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PENATALAKSANAAN SYOK PENATALAKSANAAN SYOK PADA ANAK PADA ANAK
PENDAHULUAN
SINDROM KLINISKEGAGALAN SISTEM SIRKULASI
KEBUTUHAN OKSIGEN NUTRIEN JARINGAN
DEFISIENSI AKUT DITINGKAT SEL
:SYOK PADA ANAKØ Keadaan gawat darurat / morbiditas mortalitas
Ø % 80 hipovolemikØ / . Syok kompensasi sulit di D o k
manifestasi klinis tak jelas( refleks simpatis Redistribusi
. selektif al daerah dari organ perifer non- , , vital ke jantung paru
)otakØ :Tujuan Primer Pengelolaan Syok - ( )Preload resusitasi volume - Kontraktilitas - Resistensi pada sistemik
DEFINISI SYOK DEFINISI SYOK
SINDROM KLINIS AKIBAT KEGAGALAN SISTEM :SIRKULASI UNTUK MENCUKUPI
vNutrisivOksigen
Pasokanutilisasi
Metabolisme Jaringan tubuh
Defisiensi 02 Seluler
FUNGSI SISTEM SIRKULASI FUNGSI SISTEM SIRKULASI
Ø JantungØ Pembuluh DarahØ Volume Darah
Ø
Curah jantung & adekuatAliran darah
Metabolismejaringan
Metabolit
Eliminasi Di OrganPembuangan
PENGATURAN CURAH JANTUNG PENGATURAN CURAH JANTUNG DAN TEKANAN DARAH DAN TEKANAN DARAH
PRELOAD CONTRACTILITY AFTERLOAD
HEART RATE STROKE VOLUME
CARDIAC OUTPUT SYSTEMIC VASCULAR RESISTANCE
BLOOD PRESSURE
PENGANGKUTAN OKSIGEN PENGANGKUTAN OKSIGEN
Cardiac Out Put Blood flow
OxygenDelivery
Blood O2 Content
Hb Contentration
O2 Bound to Hb
O2 Dissolved in Plasma
KLASIFIKASI SYOK KLASIFIKASI SYOK MENURUT ETIOLOGI MENURUT ETIOLOGI
v SYOK HIPOVOLEMIKv SYOK DISTRIBUTIFv SYOK KARDIOGENIKv SYOK SEPTIKv SYOK OBSTRUKTIF
STADIUM SYOK STADIUM SYOK : FASE I KOMPENSASI : FASE I KOMPENSASI
Mekanisme Kompensasi Tubuh refleksi simpatis
- Resistensi sistemik : ; , , HR kulit dingin pucat
. , , cap refill terlambat nadi lemah
. tek nadi sempit - ( )Tekanan darah N - Tekanan Diastolik - Resistensi pembuluh darah
↑: ( <), splanknik Ginjal Diuresis Saluran ( , )cerna muntah ileus
: ( )FASE II DEKOMPENSASI 1 : ( )FASE II DEKOMPENSASI 1
- 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 DEKOMPENSASI 2 : ( )FASE II DEKOMPENSASI 2
Aliran darah lambat Agregasi Trombosit
Pembentukan TrombusPendarahan
Pelepasan Mediator
Vasodilatasi Arterial
Kenaikan Permeabilitas Kapiler VR
Fase dekompensasi
• Perfusi jaringan indekuat disertai hipotensi
•• Kesadaran menurun krn perfusi ke otak
menurun
•• Hipotensi sebagai tanda terakhir dari syok• Untuk anak 1-10th: <70 mmHg +(umur/thn
x 2) mmHg
: FASE III IREVERSIBEL
Ø Kerusakan / Kematian SelØ Disfungsi sistem multi organØ Cadangan fostat E. Tinggi ↓↓ ( Hepar, Jantung ) ↓ Tekanan darah tak
terukur Nadi tak teraba Kesadaran ↓↓ Anuria GMO
klinis
PERJALANAN PATOFISIOLOGI SYOK PERJALANAN PATOFISIOLOGI SYOK
Septic Shock Cardiogenic ShockHypovolemic Shock
Capillary Leak MediatorsMyocardial Depression
Preload Vasodilatation Contractility
Cardiac Output Blood Pressure
Sympathetic Discharge
Vasoconstriction,
HR Contractility
Improved Cardiac output and blood pressure
COMPENSATED
DECOMPENSATED Myocardial perfusion
Myocardial O 2 Consumption
Cardiac Output
Mediator Release
Cell Function
Cell Death Death of Organism
Tissue Ischemia
Loss of Auto regulation of
Microcirculation
COMPENSATED
Vasoconstriction HR Contractility
Syok Hipovolemik
• Etiologi: Diare, perdarahan, muntah, intake tak adekuat, diuresis osmotik, luka bakar
•
HYPOVOL
SHOCK
PRELOAD ↓
AFTERLOAD ↑
CONTRACTILITYN / ↑
Syok hipovolemik Primary Assessment: Finding• A
• B Takhipneu tanpa pe↑ WOB• C Takhikardi Tek.Drh N/ hipotensi dgn tek.nadi sempit Nadi lemah,kecil /tak teraba Pengisian kapiler lambat kulit dingin,pucat Kesadaran menurun Oliguria D Kesadaran menurun
Distributive Shock
Distributive
shock
PRELOAD N / ↑
CONTRACTILITYN / ↓
AFTERLOADVariable
Findings of Distributive Shock
• Primary Assessment Finding• A Patent airway, unless unconc.• B Tachypnea without ↑WOB, except
caused by pneumonia, ARDS, pulm edema• C Tachycardia, Hypotension with wide
pulse pressure(warm shock) or narrow p.pressure(cold shock) or normotension; Bounding perpheral pulse, Delayed cap.refill, Warm&flush skin(warm shock) or pale skin(cold shock): Changes in mental status; oliguria
• D Changes in mental status
Septic Shock
PRELOAD↓↓
CONTRACTI-
LITY ↓/ N
AFTERLOAD VARIABLE
Consensus Definitions and clinical Characteristic of Ped.Sepsis
• Systemic Inflammatory Response Syndrome ( SIRS )
• Sepsis• Severe Sepsis• Septic shock
SIRS
• Core temp of >38.5°C or <36°C• Tachycardia >2SD above normal for age,
for chhildren <1 year bradycardia <10th percentile for age
• Mean RR>2SD above normal for age• Leucocyte count ↑ or ↓ for age or 10%
immature neutrophils• ( At least 2 of the 4 criteria )
• SEPSIS :
• SIRS in the presence of, or as a result of,
suspected or proven infection
Severe sepsis
• Sepsis plus either cardiovascular dysfunction or ARDS
Or• Sepsis plus 2 or more other organ failures
RF as sign of organ dysfunctionin sepsis
• PaO2/FiO2 <300 in absence of CHD or lung disease
• PaCO2 >65 mmHg or 20 mmHg above baseline
• Proven need FiO2 >50% to maintain SaO2 >92%
• Need nonelective MV (invasive or noninvasive)
Septic shock
• Sepsis and
•• Cardiovascular dysfunction despite
administration of isotonic iv boluses > 40 ml/kg in 1 hour
Cardiovascular dysfunction
• Hypotension (SBP <5th percentile for age or SBP <2SD below normal for age or
• Need for vasoactive drug to maintain BP in normal range or
•• Two of the following characteristic of inadequate
organ perfusion:
Inadequate organ perfusion
• Unexplained metabolic acidosis: base deficit < 5meq/l
• Increase arterial lactate > twice the upper limit of normal
• Oliguria: Urine output0.5 ml/kg/hour• Prolonged cap refill: > 5 second• Cor to peripheral temp gap > 3°C
SEPTICSHOCK
PRELOADDECREASE
CONTRACTILITYN / DECREASED
AFTERLOADVARIABLE
. III SYOK KARDIOGENIK. III SYOK KARDIOGENIK
:EtiologiØ Pasca Bedah Penyakit Jantung BawaanØ MiokarditisØ / Infark Iskemik JantungØ / Kardiomiopati Primer SekunderØ , Hipoglikemia Gangguan MetabolikØ , Asfiksia Sepsis
CARDIOGENIC
SHOCK
PRELOADVARIABLE
CONTRACTILITYDECREASED
AFTERLOADINCREASED
MEKANISME SYOK KARDIOGENIK MEKANISME SYOK KARDIOGENIK
Cardiogenic Shock
Contractility
CO BP
Metabolic acidosis, hypoxia,Myocardial depressant factor
Compensatory mech. Afterload SVR
SYOK KARDIOGENIK SYOK KARDIOGENIK
Cardiac Ventricular Performance
:Factor Determinant . a Frekuensi dan Irama Jantung . b Preload dan Afterload . c Kontraktilitas Miokard Kompensasi Tubuh Self Perpetuating
Cycle Syok Progresif
Memburuk
Findings of Cardiogenic Shock• Primary Assessment Finding• A• B Tachypnea; WOB↑• C Tachycardia; N/low BP with
a narrow pulse pressure; weak or absent of peripheral pulse; N and then weak central pulses;Delayed cap refill with cool extremities; Signs of CHF; cyanosis(CHD/pulm.edema); End-organ Function ( Cold, pale skin, oliguria)
• D Changes of mental status••
Obstructive Shock
• Cardiac tamponade• Tension pneumothorax• Ductal – dependent congenital heart lesions• Massive pulmonary embolism
Cardiac tamponade
• Muffled or diminished heart sound• Pulsus paradoxus(decrease in systolic BP
by more than 10 mmHg during inspiration
• Distended neck vein• Note: Children following cardiac
surgery, D/ ndistinguishable from cardiogenic shock, Echo: important
Tension pneumothorax
• Patients with chest trauma, or any intubated child who deteorates suddenly during PPV
• Hyperresonance on the affected side• Diminished breath sounds on the affected side• Distended neck vein• Tracheal deviation towards contralateral side• Rapid deteoration in perfusion and rapi change
from tachycardia to bradicardia
Pathogenesis and Pathophysiology of SepsisNew Concept about SIRS, SEPSIS, CARS, MARS
Pro-inflammatory
response
Anti-inflammatory
response
Systemic Reaction:SIRS (pro-
inflammatory)CARS (anti-
inflammatory)MARS (mixed)
Systemic spillover of pro-inflammatory
mediators
Systemic spillover of anti-inflammatory
mediators
Initial insult (bacteria, viral, traumatic, thc, mal)
Cardiovascular Compromise
shock, SIRS pre-dominates
Homeostasis
CARS and SIRS
balanced
Apoptosis (cell death)
Death with minimal
inflammation
Organ dysfunction
SIRSPre-
dominated
Suppression of the
immune systemCARS pre-
dominated
SEPSIS DAN GANGGUAN KOAGULASI SEPSIS DAN GANGGUAN KOAGULASI
Sepsis
Inflammatorycytokines
- IL 6 - TNF
Tissue factor Mediated activation of
coagulation
Inhibition of physiological anticoagulant
pathways
Depression of
fibrinolysis due to high
levels of-PAI 1
Enhanced fibrinformation
Impaired fibrinremoval
Microvascularthrombosis
- CYTOKINE MEDIATED PATHOGENETIC- CYTOKINE MEDIATED PATHOGENETIC PATHWAYS of MICROVASCULAR THROMBOSIS PATHWAYS of MICROVASCULAR THROMBOSIS
in SEPSIS in SEPSIS
Sepsis
Activation ofcoagulation
Widespread fibrin
Deposition
Consumption of platelets and clottingfactor
Microvascularthrombosis Bleeding
( )severe
MANIFESTASI KLINIS SYOK SEPTIK MANIFESTASI KLINIS SYOK SEPTIK
v STADIUM KOMPENSASI - Resistensi Vaskuler - Curah Jantung - Takhikardia - Ekstermitas Hangat - Divresis Normalv STADIUM DEKOMPENSASI - Volume Intravaskuler - Depresi Miokard - Eksternal Dingin - Gelisah, Anuria, Distres Respirasi - Resistensi Vaskuler - Curah Jantung v STADIUM IREVERSIBEL - GMO
Most Common Pathogens in Childhood Bacterial Most Common Pathogens in Childhood BacterialSepsisSepsis
Age Group Pathogens Antimicrobial(Pending culture)
Initial dose (mg/kg)
0 – 1 months Group B Strept. EnterobacteriaceaeStaph. AureusListeria meningtides
Ampiciline +GentamicinCefotaxime
502.55-0
1 – 24 months H. influenzae, Strept. PneumoniaeS. aureus, Neisseria meningtidisGroup B Streptococcus
CefotaximeAmpiciline +Chlorampenicol
505025
> 24 months S. PneumoniaeH. InfluenzaeS. AureusN. Meningtidis
CefotaximeCefriaxoneAmpiciline +Chlorampenicol
50505025
Immuno compromised
S. aureus, ProteusPseudomonasEnterobacteriaceae
Vancomycin +Ceftazidime +Ticarcillin
255075
PENATALAKSANAAN SYOK PENATALAKSANAAN SYOK
1. 2.
Oksigenasi
CaO2 ↑SaO2 95 – 100 %
Sistem K.V
a.Preload ↑( resusitasi volume )
b.Atasi Disritmiac.Koreksi keseimbangan
asam - basaJalan nafas Oksigen ↓ Α ν ξ ι ε τ α σ
TERAPI CAIRAN PADA SYOK TERAPI CAIRAN PADA SYOKØ AKSES VENA (90 detik); Tak berhasil IO
Ø KRISTALOID dan atau KOLOID 10 – 30 ml / kg B.B (6-10 menit) diulang 2 – 3 kaliØ SYOK SEPTIK 60 – 100 ml / kg B.B (dalam 6 jam pertama)Ø THE 1st CONSENSUS CONFERENCE on CCM 1997 (SYOK SEPTIK) a. Koloid terapi inisial, dilanjutkan
koloid/kristaloid b. Dipandu : respons klinis,perfusi, perifes, tvs,
tekanan sistem,MAP
Algoritme Terapi Cairan Pada Syok Algoritme Terapi Cairan Pada Syok
Suspected shock
Hypovolemia, Hypoperfusion, Tachycardia
10 – 30 mL Cryst/Colloid / kg / 6 – 10 min
Normotensive
Hypotensive
In Sepsis :
Antibiotics, Imunotheraphy
In Anaphylaksis :
Catekolamin, steroid, antihistamin
Urine > 1 ml/kg/hr
10-20 mL crys or coll/kg/10 min
AnuriaUrine < 1 ml/kg/hr
Urine output < 1 ml/kg/hr
Reevaluated 10 mL X.tal/kg 10 mL X.tal/kg 10–20 mL X.tal/kg
Reevaluated 10 mL X.tal/kg 10 mL X.tal/kg 10-20 mL X.tal/kg
Improved
Reevaluated
Improved
Reevaluated
Hypotensive, urine < 1 mL/kg/hr
CVP < 10 mmHg CVP, Cardiac status, chest X-Ray, Echocardiography
CVP > 10 mmHg
Afterload reduction, inotropic support, consider pulmonary
10-20 mL X.tal/kg
Reevaluated
Early Goal DirectedEarly Goal DirectedTherapy pada Syok SeptikTherapy pada Syok Septik
• Early aggressive fluid therapy (Crystaloid or colloid) n U w t n i hi ours o m ss onh f ad i i
• V sopr ssors notrop a e ic ru s w n r s st n d g he e i a ce
to lu t r pf id he a • n po ntsd i oo G d
p r p r l p r us on e i he a e f i on ousn ss ci e
p ll r l n a i a fee i g t m < ” rm i e a xtr m t s e e i ie
uls pr ssur N e e e or f age CVP 8-12 mmHg, ur s s mlDi e i > g SvcO2 >
70%• Admission to PICU when stabilized
Supplemental oxygen endotracheal intubation and
mechanical ventilation
Central venous and arterial
catheterization
Sedation, paralysis (if intubated), or both
Goals achieve
d
ScvO2
MAP
CVP
Hospital admission
8-12 mmHg
≥ 65 and ≤ 90 mmHg
≥ 70%
Yes
No
Crystalloid
Colloid
< 8 mmHg
Vasoactive agents< 65 mmHg> 90 mmHg
Transfusion of red cells until hematocrit ≥ 30%
Inotropic agents
< 70%
Protocol for Early Goal-Directed
Therapy
Fluid Therapy in Sepsis and Septic Shock
Type of Type of Fluid Fluid
Colloid Colloid CrystalloiCrystalloi
dd
Volume Volume 60 – 100 60 – 100
ml/kgml/kg(6 hours)(6 hours)
CO , Restore BPCO , Restore BP
MOFMOF
InotropicVasopressor
Ø (SYOK KARDIOGENIK) : Fluid Chalenge hati – hati :
a. memperbaiki kontraktilitas jantungb. dipantau ketat dengan TVS
Efek volume infus 1 L koloid pada Efek volume infus 1 L koloid pada ( )kompartemen tubuh 70 kg ( )kompartemen tubuh 70 kg
Larutan Vol. Plasma Vol. Inters I.IntraselAlbumin 5% 1000 - -Hemacel 700 300 -Gelafundin 1000 - -Plasmafusin 1000 - -Dextran 40 1600 (-260) (-340)Dextran 70 1300 (-130) (-170)Expafusin 1000 - -HAES steril 6% 1000 - -HAES steri10% 1450 (-450) -
ADRENAL INSUFFISIENSI ADRENAL INSUFFISIENSI PADA SYOK PADA SYOK
SEPTIKSEPTIK KORTIKOSTEROID Pada syok septik, bila refrakter thdp
dopamin/adrenalin/nor-adrenalin mungkin terjadi INSUFISIENSI ADRENAL Hydrocortisone 50mg (bolus), dilanjutkan 1-2 mg/kgBB/ 24 jam; 5-7 hari
TERAPI SUPORTIF TERAPI SUPORTIF
vSubstitusi faktor koagulasi (pada Hemodilusi/PIM) :
- Fresh Frozen Plasma - CyroprecipitatevTranfusi Masif setiap 5 – 6 unit PC ditambah 2
unit FFPvFibrinogen < 100 mg/dl (tak respons terhadap
FFP) : - Cyro precipitate 4 unit/10 kg BBvKonsentrat trombosit diberikan : Trombositopeni berat < 30.000 dengan
perdarahan atau tindakan invasif : - Konsentrat Trombosit
IMUNOTERAPIIMUNOTERAPI
• Tranfusi tukar pada sepsis : - memperbaiki oksigenasi jantung - mengeluarkan mediator dan endotokin
• Immunoglobulin (I.V) pada sepsis
• Hemofiltrasi dan Plasmafiltrasi :
– mengeluarkan endotoksin, mediator
– mengurangi respons inflamasi sistemik (SIRS)
FUNGSI ORGAN FUNGSI ORGAN.A :PARU
Suplai Oksigen adekuat - / . Intubasi pemasangan V mekanik dini pada
syok septik - , Pemberian cairan resusitasi bila terlalu
/ banyak agresif resiko tinggi edema paru .B :OTAK - , Hindari hipoksia hipoglikemia - ( )Hindari hiperkapnea dengan ventilator - :Pertahankan perfusi serebral . a volume intravaskular . b CO . / c Hb tekanan darah adekuat - , -Pemantauan kadar Na serum koreksi hati
hati
( )FUNGSI ORGAN lanjutan ( )FUNGSI ORGAN lanjutan.C / SIRKULASI SPLANKHNIK SALURAN CERNA
- , , Resusitasi volume optimalisai CO tekanan darah
- ( / )Koreksi hipotensi vasopresor inotropik - NUTRISI ENTERAL DINI.D GINJAL
- , , Resusitasi volume optimalisasi CO tekanan darah
- Koreksi hipotensi - Koreksi hipoksia dan anemia berat - Hindari obat- obatan nefrotoksik
TATALAKSANA SYOK KARDIOGENIK TATALAKSANA SYOK KARDIOGENIK
Oksigenasi Adekuat Koreksi GGN Asam Basa dan Elektrolit Kurangi Rasa Sakit dan Ansietas Atasi Disritmia Jantung : Kelebihan Preload Diuretika : Kontraktilitas Fluid Challenge
/ (+)Sesuai CVP POAP Obat Inotropik ( ) : Beban Afterload SVR Vasodilator
Koreksi Penyebab Primer
Commonly Used Cardiovascular Drugs in Shock Commonly Used Cardiovascular Drugs in ShockSyndromesSyndromes
Drug Dose ( ug/kg/min )
Comment
Inotropioc agentsNorephrine( - adrenergic )
0.05 – 1.0 For profound hypotension not responding to fluid or other inotropic drugs
Ephinephrine( - and - adrenergic )
0.05 – 1.0 Dose related response, higher doses cause vasoconstriction. Useful in maintaining CO and BP inpatients unresponsive to dopamine or debutamine
Isoproterenol( - adrenergic )
0.05 – 0.5 Indicated in bradycardia unresponsive to atropine if increase in heart rate is not excessive, may be helpful in reactive pulmonary hypertensionDopamine
( - and - dopaminergic )
1 – 20 Cardiovascular effects are complex and dose related. Low dose infusion can restore cardiovascular stability and improve renal function
…( )Commonly Used Cardiovascular lanjutan …( )Commonly Used Cardiovascular lanjutan
Drug Dose( ug/kg/min )
Comment
Dobutamine( - and - adrenergic )
1 – 20 Positive inotropic effect with minimal changes in heart rate or systemic vascular resistance
Amrinone 1 – 10 Initial bolus infusion may be required. Limited data available in children
VasodilatorsNitroprusside 0.005 – 8 Balanced arterial and venous dilator.
May result in thiocyanate or cyanide toxicity
Phentolamine 1 – 20 Causes dilatation of arterial and venus beds. Indirect inotropic effect may cause compensatory tachycardia
Nitroglicerine 0.5 – 20 Venus dilator. Dose not well established for infants and children
MONITORINGMONITORING - State of Consiousness Glasgow Coma Scale Respiratory Rate and Character :Cardiovascular Parameters . a Skin and Core Temperature Difference . b Pulse Rate and Volume . c Blood Pressure . d Capillary Perfusion Time . e Central Venous Pressure Should Be
Monitored in Patient Where There Has Been Poor
Response To Fluid Therapy Or With Established
Shock Urinary Output- , Urine Bag Or Preferably
; - / Catheter Output Should Be 1 2 ml kg BodyWeight
Pulse Oximetry SvcO2
KEY POINTS IN MANAGEMENT KEY POINTS IN MANAGEMENT
Ø Remember BP and pulse are unreliable indicators in early septic shock
Ø Look for minor degrees of mental impairment (anxiety,restlessness)
Ø Do not delay treatment, try to prevent the onset of hypotension, metabolic acidosis, and hypoxia
Ø Give adequate fluids early in treatment, especially colloids
Ø Do not use inotropic agents until the patients has received adequate fluid therapy
Ø Monitor blood glucose, gases, and PH, and treat appropriately
/RINGKASAN KESIMPULAN/RINGKASAN KESIMPULAN• Syok merupakan keadaan gawat darurat, sering ditemukan
pada anak• Morbiditas dan mortalitas syok masih tinggi• Syok hipovolemik, paling sering terjadi pada anak
(80%), sisanya syok kardiogenik• Diagnosis syok dini sulit, tetapi penting diketahui melalui
pemahaman patofisiologi syok (stadium kompensasi, dekompensasi dan ireversibel)
• Pengelolaan syok bertujuan meningkatkan DO2 melalui pe CO yaitu :
1. Memperbaiki prabeban dengan resusitasi volume 2. Me kontraktilitas jantung dan 3. Me SVR
• Dengan pemahaman patofisiologi, diagnosis dini dan memperhatikan “key management“ syok, diharapkan dapat me mortalitas syok