PENATALAKSANAAN SYOK PENATALAKSANAAN SYOK

PADA ANAKPADA ANAK

PENDAHULUAN

SINDROM KLINISKEGAGALAN SISTEM SIRKULASI

KEBUTUHAN OKSIGEN NUTRIEN JARINGAN

DEFISIENSI AKUT DITINGKAT SEL

SYOK PADA ANAK : Keadaan gawat darurat

morbiditas / mortalitas 80 % hipovolemik 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, otak )

Tujuan Primer Pengelolaan Syok :- Preload ( resusitasi volume )- Kontraktilitas - Resistensi pada sistemik

DEFINISI SYOKDEFINISI SYOK

SINDROM KLINIS AKIBAT KEGAGALAN SISTEM SIRKULASI UNTUK MENCUKUPI :

NutrisiOksigen

Pasokanutilisasi

Metabolisme Jaringan tubuh

Defisiensi 02 Seluler

FUNGSI SISTEM SIRKULASIFUNGSI SISTEM SIRKULASI

Jantung Pembuluh

Darah Volume Darah

Curah jantung & adekuatAliran darah

Metabolisme

jaringan

Metabolit

Eliminasi Di Organ

Pembuangan

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

KLASIFIKASI SYOK KLASIFIKASI SYOK MENURUT ETIOLOGIMENURUT ETIOLOGI

SYOK HIPOVOLEMIK SYOK DISTRIBUTIF SYOK KARDIOGENIK SYOK SEPTIK SYOK OBSTRUKTIF

STADIUM SYOKSTADIUM SYOKFASE I : KOMPENSASIFASE 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 TrombositPembentukan Trombus

PendarahanPelepasan 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

Kerusakan / Kematian Sel Disfungsi sistem multi organ Cadangan fostat E. Tinggi

( Hepar, Jantung )

Tekanan darah tak terukur Nadi tak teraba

Kesadaran AnuriaGMO

klinis

PERJALANAN PATOFISIOLOGI PERJALANAN PATOFISIOLOGI SYOKSYOK

Septic Shock

Cardiogenic ShockHypovolemic

ShockCapillary Leak

Mediators

Myocardial Depression

Preload Vasodilatation

Contractility

Cardiac Output Blood Pressure

Sympathetic Discharge

Vasoconstriction,

HR Contractility

Improved Cardiac output and blood pressure

COMPENSATED

DECOMPENSATED

Myocardial perfusion Myocardial O2

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

Distributiveshock

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 KARDIOGENIKIII. SYOK KARDIOGENIK

Etiologi : Pasca Bedah Penyakit Jantung Bawaan Miokarditis Infark / Iskemik Jantung Kardiomiopati Primer / Sekunder Hipoglikemia, Gangguan Metabolik Asfiksia, Sepsis

CARDIOGENICSHOCK

PRELOADVARIABLE

CONTRACTILITYDECREASED

AFTERLOADINCREASED

MEKANISME SYOK KARDIOGENIKMEKANISME SYOK KARDIOGENIK

Cardiogenic Shock

Contractility

CO BP

Metabolic acidosis, hypoxia,Myocardial depressant factor

Compensatory mech. Afterload SVR

SYOK KARDIOGENIKSYOK KARDIOGENIK

• Cardiac Ventricular Performance • Factor Determinant :

a. Frekuensi dan Irama Jantungb. Preload dan Afterloadc. 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 SIRSbalanced

Apoptosis (cell death)

Death with minimal

inflammation

Organ dysfunction

SIRSPre-dominated

Suppression of the immune

systemCARS

pre-dominated

SEPSIS DAN GANGGUAN KOAGULASISEPSIS DAN GANGGUAN KOAGULASI

Sepsis

Inflammatory cytokines

IL - 6 TNF -

Tissue factor Mediated

activation of coagulation

Inhibition of physiological anticoagulant

pathways

Depression of

fibrinolysis due to high

levels of PAI-1Enhanced fibrin

formationImpaired fibrin

removal

Microvascular thrombosis

CYTOKINE-MEDIATED PATHOGENETIC CYTOKINE-MEDIATED PATHOGENETIC PATHWAYS of MICROVASCULAR PATHWAYS of MICROVASCULAR

THROMBOSIS in SEPSIS THROMBOSIS in SEPSIS

Sepsis

Activation of coagulation

Widespread fibrin

Deposition

Consumption of platelets and clotting

factorMicrovascular

thrombosis Bleeding (severe)

MANIFESTASI KLINIS SYOK MANIFESTASI KLINIS SYOK SEPTIKSEPTIK

STADIUM KOMPENSASI- Resistensi Vaskuler - Curah Jantung - Takhikardia- Ekstermitas Hangat- Divresis Normal

STADIUM DEKOMPENSASI- Volume Intravaskuler - Depresi Miokard- Eksternal Dingin- Gelisah, Anuria, Distres Respirasi- Resistensi Vaskuler - Curah Jantung

STADIUM IREVERSIBEL- GMO

Most Common Pathogens in Childhood Most Common Pathogens in Childhood Bacterial SepsisBacterial Sepsis

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 SYOKPENATALAKSANAAN SYOK

1. 2.

Oksigenasi

CaO2 SaO2 95 – 100 %

Sistem K.V

a. Preload ( resusitasi volume )

b. Atasi Disritmiac. Koreksi keseimbangan

asam - basaJalan nafas Oksigen Anxietas

TERAPI CAIRAN PADA SYOKTERAPI CAIRAN PADA SYOK AKSES VENA (90 detik); Tak berhasil IO KRISTALOID dan atau KOLOID

10 – 30 ml / kg B.B (6-10 menit)

diulang 2 – 3 kali SYOK SEPTIK 60 – 100 ml / kg B.B

(dalam 6 jam pertama) THE 1st CONSENSUS CONFERENCE on CCM 1997

(SYOK SEPTIK)a. Koloid terapi inisial, dilanjutkan koloid/kristaloidb. Dipandu : respons klinis,perfusi, perifes, tvs, tekanan sistem,MAP

Algoritme Terapi Cairan Pada SyokAlgoritme 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) In EMU, within 6 hours of admission

• Vasopressors & Inotropic drugs when resistance to fluid therapy

• End points : Good peripheral perfusion Conciousness, Capillary feeling time < 2”, Warm extremities, MAP/Pulse pressure N for age, CVP 8-12 mmHg, Diuresis > 2ml/kg 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 achieved

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 Fluid Type of Fluid Colloid Colloid

CrystalloidCrystalloid

Volume Volume 60 – 100 ml/kg60 – 100 ml/kg

(6 hours)(6 hours)

CO CO , Restore BP, Restore BP MOFMOF

InotropicVasopressor

(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.Intrasel

Albumin 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 INSUFFISIENSIADRENAL INSUFFISIENSI PADA PADA SYOKSYOK

SEPTIKSEPTIKKORTIKOSTEROID

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 SUPORTIFTERAPI SUPORTIFSubstitusi faktor koagulasi (pada

Hemodilusi/PIM) :- Fresh Frozen Plasma- Cyroprecipitate

Tranfusi Masif setiap 5 – 6 unit PC ditambah 2 unit FFP

Fibrinogen < 100 mg/dl (tak respons terhadap FFP) : - Cyro precipitate 4 unit/10 kg BB

Konsentrat 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 ORGANFUNGSI ORGANA. 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 intravaskularb. COc. 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 KARDIOGENIKTATALAKSANA 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 Shock SyndromesSyndromes

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 hypertension

Dopamine( - 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 Differenceb. Pulse Rate and Volumec. Blood Pressured. Capillary Perfusion Timee. 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 Body Weight

• Pulse Oximetry• SvcO2

KEY POINTS IN MANAGEMENTKEY POINTS IN MANAGEMENT

Remember BP and pulse are unreliable indicators in early septic shock

Look for minor degrees of mental impairment (anxiety,restlessness)

Do not delay treatment, try to prevent the onset of hypotension, metabolic acidosis, and hypoxia

Give adequate fluids early in treatment, especially colloids

Do not use inotropic agents until the patients has received adequate fluid therapy

Monitor blood glucose, gases, and PH, and treat appropriately

RINGKASAN/KESIMPULANRINGKASAN/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 volume2. Me kontraktilitas jantung dan 3. Me SVR

• Dengan pemahaman patofisiologi, diagnosis dini dan memperhatikan “key management“ syok, diharapkan dapat me mortalitas syok