28151448 2010 Penatalaksanaan Syok Pada Anak

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PENATALAKSANAAN SYOK PADA ANAK

PENDAHULUANSINDROM 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 SYOKSINDROM 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 DARAHPRELOAD CONTRACTILITY AFTERLOAD

HEART RATE

STROKE VOLUME

CARDIAC OUTPUT

SYSTEMIC VASCULAR RESISTANCE

BLOOD PRESSURE

PENGANGKUTAN OKSIGENCardiac 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 > 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: 38.5C or 2SD above normal for age, for chhildren 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 5 second Cor to peripheral temp gap > 3C

PRELOAD DECREASE

SEPTIC SHOCK

CONTRACTILITY N / DECREASED

AFTERLOAD VARIABLE

III. SYOK KARDIOGENIKEtiologi : 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 KARDIOGENIKCardiogenic 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, MARSPro-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 KOAGULASISepsis Inflammatory cytokines

IL - 6Tissue 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 SEPSISSepsis 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 SepsisAge 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 SYOK1. 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 SyokSuspected 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

ReevaluatedImproved

10 mL X.tal/kg

10 mL X.tal/kg

10-20 mL X.tal/kg

ReevaluatedImproved

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 TherapyCrystalloid 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 ShockVolume 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 SEPTIKKORTIKOSTEROID Pada syok septik, bila refrakter thdp dopamin/adrenalin/nor-adrenalin mungkin terjadi INSUFISIE