PENATALAKSANAAN SYOK PADA ANAK

PENDAHULUAN
SINDROM KLINIS KEGAGALAN SISTEM SIRKULASI

KEBUTUHAN NUTRIEN

OKSIGEN 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 SYOK
SINDROM KLINIS AKIBAT KEGAGALAN SISTEM SIRKULASI UNTUK MENCUKUPI :

Nutrisi Oksigen

Pasokan utilisasi

Metabolisme Jaringan tubuh

Defisiensi 02 Seluler

FUNGSI SISTEM SIRKULASI

Jantung Pembuluh Darah Volume Darah

Curah jantung & adekuat Aliran darah

Metabolisme jaringan Metabolit

Eliminasi Di Organ Pembuangan

PENGATURAN CURAH JANTUNG DAN TEKANAN DARAH

PRELOAD CONTRACTILITY AFTERLOAD

HEART RATE

STROKE VOLUME

CARDIAC OUTPUT

SYSTEMIC VASCULAR RESISTANCE

BLOOD PRESSURE

PENGANGKUTAN OKSIGEN
Cardiac Out Put Blood flow Oxygen Delivery Blood O2 Content

Hb Contentration O2 Bound to Hb

O2 Dissolved in Plasma

KLASIFIKASI SYOK MENURUT ETIOLOGI

SYOK HIPOVOLEMIK SYOK DISTRIBUTIF SYOK KARDIOGENIK SYOK SEPTIK SYOK OBSTRUKTIF

STADIUM SYOK 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)

- 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)

Aliran darah lambat Agregasi Trombosit Pembentukan Trombus Pendarahan 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

Kerusakan / Kematian Sel Disfungsi sistem multi organ Cadangan fostat E. Tinggi ( Hepar, Jantung ) Tekanan darah tak terukur Nadi tak teraba klinis Kesadaran Anuria GMO

PERJALANAN PATOFISIOLOGI SYOK

Hypovolemic Shock Septic Shock Cardiogenic Shock Myocardial Depression Contractility Blood Pressure

Capillary Leak
Preload

Mediators
Vasodilatation

Cardiac Output
Sympathetic Discharge

Improved Cardiac output and blood pressure

COMPENSATED

Vasoconstriction,

HR Contractility

Vasoconstriction HR Contractility COMPENSATED DECOMPENSATED Myocardial perfusion Myocardial O2 Consumption Cardiac Output Mediator Release Cell Function Cell Death Death of Organism Loss of Auto regulation of Microcirculation Tissue Ischemia

Syok Hipovolemik
Etiologi: Diare, perdarahan, muntah, intake tak adekuat, diuresis osmotik, luka bakar
PRELOAD HYPO VOL SHOCK

CONTRACTILITY N/

AFTERLOAD

Syok hipovolemik
Primary Assessment: A
B

Finding

Takhipneu tanpa pe WOB Takhikardi Tek.Drh N/ hipotensi dgn tek.nadi sempit Nadi lemah,kecil /tak teraba Pengisian kapiler lambat kulit dingin,pucat Kesadaran menurun Oliguria Kesadaran menurun

Distributive Shock
PRELOAD N/ Distributive shock CONTRACTILITY N/ AFTERLOAD Variable

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

CONTRACTILITY / 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 >38.5C or <36C 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 dysfunction in 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 > 3C

PRELOAD DECREASE

SEPTIC SHOCK

CONTRACTILITY N / DECREASED

AFTERLOAD VARIABLE

III. SYOK KARDIOGENIK

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

PRELOAD VARIABLE CONTRACTILITY DECREASED AFTERLOAD INCREASED

CARDIOGENIC SHOCK

MEKANISME SYOK KARDIOGENIK

Cardiogenic Shock Contractility

Metabolic acidosis, hypoxia, Myocardial depressant factor

CO BP

Compensatory mech. Afterload SVR

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); Endorgan 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 Sepsis New Concept about SIRS, SEPSIS, CARS, MARS
Pro-inflammatory response Initial insult (bacteria, viral, traumatic, thc, mal) Anti-inflammatory response

Systemic spillover of pro-inflammatory mediators

Systemic spillover of anti-inflammatory mediators

Systemic Reaction: SIRS (pro-inflammatory) CARS (anti-inflammatory) MARS (mixed)

Cardiovascular Homeostasis Compromise shock, CARS and SIRS SIRS pre-dominates balanced

Apoptosis (cell death) Death with minimal inflammation

Organ dysfunction SIRS Pre-dominated

Suppression of the immune system CARS pre-dominated

SEPSIS DAN GANGGUAN KOAGULASI

Sepsis Inflammatory cytokines

IL - 6
Tissue factor Mediated activation of coagulation

TNF -
Depression of fibrinolysis due to high levels of PAI-1

Inhibition of physiological anticoagulant pathways

Enhanced fibrin formation

Impaired fibrin removal

Microvascular thrombosis

CYTOKINE-MEDIATED PATHOGENETIC PATHWAYS of MICROVASCULAR THROMBOSIS in SEPSIS

Sepsis Activation of coagulation Widespread fibrin Deposition Consumption of platelets and clotting factor Bleeding (severe)

Microvascular thrombosis

MANIFESTASI KLINIS SYOK SEPTIK

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 Bacterial Sepsis

Age Group Pathogens Antimicrobial (Pending culture) Ampiciline + Gentamicin Cefotaxime Cefotaxime Ampiciline + Chlorampenicol Cefotaxime Cefriaxone Ampiciline + Chlorampenicol Vancomycin + Ceftazidime + Ticarcillin Initial dose (mg/kg) 50 2.5 5-0 50 50 25 50 50 50 25 25 50 75

0 1 months

Group B Strept. Enterobacteriaceae Staph. Aureus Listeria meningtides

1 24 months H. influenzae, Strept. Pneumoniae S. aureus, Neisseria meningtidis Group B Streptococcus > 24 months S. H. S. N. Pneumoniae Influenzae Aureus Meningtidis

Immuno compromised

S. aureus, Proteus Pseudomonas Enterobacteriaceae

PENATALAKSANAAN SYOK
1. Oksigenasi 2.

Sistem K.V

CaO2 SaO2 95 100 %

Jalan nafas Oksigen Anxietas

a. Preload ( resusitasi volume ) b. Atasi Disritmia c. Koreksi keseimbangan asam - basa

TERAPI 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/kristaloid b. Dipandu : respons klinis,perfusi, perifes, tvs, tekanan sistem,MAP

Algoritme Terapi Cairan Pada Syok

Suspected shock Hypovolemia, Hypoperfusion, Tachycardia 10 30 mL Cryst/Colloid / kg / 6 10 min In Sepsis : In Anaphylaksis : Antibiotics, Imunotheraphy Urine > 1 ml/kg/hr Catekolamin, steroid, antihistamin Hypotensive

Normotensive

10-20 mL crys or coll/kg/10 min Anuria

Urine < 1 ml/kg/hr

Urine output < 1 ml/kg/hr Reevaluated 10 mL X.tal/kg 10 mL X.tal/kg 1020 mL X.tal/kg

Reevaluated
Improved

10 mL X.tal/kg

10 mL X.tal/kg

10-20 mL X.tal/kg

Reevaluated
Improved

Reevaluated Hypotensive, urine < 1 mL/kg/hr

CVP < 10 mmHg

10-20 mL X.tal/kg

CVP, Cardiac status, chest X-Ray, Echocardiography

CVP > 10 mmHg

Reevaluated

Afterload reduction, inotropic support, consider pulmonary

Early Goal Directed Therapy 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 CVP 8-12 mmHg MAP 65 and 90 mmHg ScvO2 70% No Goals achieved < 8 mmHg

Protocol for Early Goal-Directed Therapy

Crystalloid Colloid

< 65 mmHg > 90 mmHg

Vasoactive agents

Transfusion of red cells until hematocrit 30% Inotropic agents

< 70%

Yes Hospital admission

Fluid Therapy in Sepsis and Septic Shock

Volume 60 100 ml/kg (6 hours) Type of Fluid Colloid Crystalloid

Inotropic Vasopressor

CO , Restore BP MOF

 (SYOK KARDIOGENIK) : Fluid Chalenge hati hati : a. memperbaiki kontraktilitas jantung b. dipantau ketat dengan TVS

Efek volume infus 1 L koloid pada kompartemen tubuh (70 kg)

Larutan Albumin 5% Hemacel Gelafundin Plasmafusin Dextran 40 Dextran 70 Expafusin Vol. Plasma 1000 700 1000 1000 1600 1300 1000 Vol. Inters 300 (-260) (-130) (-450) (-340) (-170) I.Intrasel

HAES steril 6% 1000 HAES steri10% 1450

ADRENAL INSUFFISIENSI PADA SYOK SEPTIK

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
Substitusi 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

IMUNOTERAPI
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
A. PARU : Suplai Oksigen adekuat - Intubasi/pemasangan V. mekanik dini pada syok septik - Pemberian cairan resusitasi, bila terlalu banyak/ agresif resiko tinggi edema paru 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

B.

FUNGSI ORGAN (lanjutan)

C. SIRKULASI SPLANKHNIK / SALURAN CERNA - Resusitasi volume, optimalisai CO, tekanan darah - Koreksi hipotensi (vasopresor/inotropik) - NUTRISI ENTERAL DINI GINJAL - Resusitasi volume, optimalisasi CO, tekanan darah - Koreksi hipotensi - Koreksi hipoksia dan anemia berat - Hindari obat-obatan nefrotoksik

D.

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 Syndromes

Drug Inotropioc agents Norephrine ( - adrenergic ) Dose ( ug/kg/min ) 0.05 1.0 Comment

For profound hypotension not responding to fluid or other inotropic drugs Dose related response, higher doses cause vasoconstriction. Useful in maintaining CO and BP inpatients unresponsive to dopamine or debutamine Indicated in bradycardia unresponsive to atropine if increase in heart rate is not excessive, may be helpful in reactive pulmonary hypertension Cardiovascular effects are complex and dose related. Low dose infusion can restore cardiovascular stability and improve renal function

Ephinephrine 0.05 1.0 ( - and - adrenergic )

Isoproterenol ( - adrenergic )

0.05 0.5

Dopamine ( - and dopaminergic )

1 20

Commonly Used Cardiovascular (lanjutan)

Drug Dobutamine ( - and - adrenergic ) Amrinone Dose ( ug/kg/min ) 1 20 Comment Positive inotropic effect with minimal changes in heart rate or systemic vascular resistance Initial bolus infusion may be required. Limited data available in children Balanced arterial and venous dilator. May result in thiocyanate or cyanide toxicity Causes dilatation of arterial and venus beds. Indirect inotropic effect may cause compensatory tachycardia Venus dilator. Dose not well established for infants and children

1 10

Vasodilators Nitroprusside

0.005 8

Phentolamine

1 20

Nitroglicerine

0.5 20

MONITORING
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 Body Weight Pulse Oximetry SvcO2

KEY POINTS IN MANAGEMENT

Remember BP and pulse are unreliable indicators in early septic shock Look for minor degrees (anxiety,restlessness) of mental impairment

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/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