SUB. BAGIAN PEDIATRI GAWAT DARURAT FK. UNDIP/RSUP DR. KARIADI SEMARANG PENDAHULUAN SINDROM KLINIS KEGAGALAN 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 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 O 2 Content Hb Contentration O 2 Bound to Hb O 2 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
VR Fase dekompensasi Perfusi jaringan indekuat disertai hipotensi
Kesadaran menurun krn perfusi ke otak menurun
Hipotensi sebagai tanda terakhir dari syok Untuk anak 1-10 th : <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 Anuria GMO klinis PERJALANAN PATOFISIOLOGI SYOK Septic Shock Cardiogenic Shock Hypovolemic Shock Capillary 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 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
HYPO VOL SHOCK PRELOAD AFTERLOAD CONTRACTILITY N / 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 / Septic Shock
Distributive shock PRELOAD N / 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 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 <10 th
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 <5 th 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 III. SYOK KARDIOGENIK Etiologi : Pasca Bedah Penyakit Jantung Bawaan Miokarditis Infark / Iskemik Jantung Kardiomiopati Primer / Sekunder Hipoglikemia, Gangguan Metabolik Asfiksia, Sepsis
CARDIOGENIC SHOCK PRELOAD VARIABLE CONTRACTILITY DECREASED AFTERLOAD INCREASED MEKANISME SYOK KARDIOGENIK Cardiogenic Shock Contractility CO BP Metabolic acidosis, hypoxia, Myocardial depressant factor 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); 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 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
PENATALAKSANAAN SYOK 1. 2. Oksigenasi CaO 2
SaO 2 95 100 % Sistem K.V a. Preload ( resusitasi volume ) b. Atasi Disritmia c. Koreksi keseimbangan asam - basa
Jalan nafas Oksigen Anxietas 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 1 st 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 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 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 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 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 Fluid Therapy in Sepsis and Septic Shock Type of Fluid Colloid Crystalloid Volume 60 100 ml/kg (6 hours) CO , Restore BP MOF Inotropic Vasopressor (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 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 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 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) 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 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 Dose ( ug/kg/min ) Comment Inotropioc agents Norephrine ( - 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) 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 Vasodilators Nitroprusside
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 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 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/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 DO 2 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