PENATALAKSANAAN SYOK PADA ANAK Moh. Supriatna TS
Oct 22, 2014
PENATALAKSANAAN SYOK PADA ANAK
Moh. Supriatna TS
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 SYOK
SINDROM KLINIS AKIBAT KEGAGALAN SISTEM SIRKULASI UNTUK MENCUKUPI :
NutrisiOksigen
Pasokanutilisasi
Metabolisme Jaringan tubuh
Defisiensi 02 Seluler
FUNGSI SISTEM SIRKULASI
Jantung Pembuluh
Darah Volume
Darah
Curah jantung & adekuatAliran 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
KLASIFIKASI SYOK MENURUT ETIOLOGI
SYOK HIPOVOLEMIK SYOK DISTRIBUTIF SYOK KARDIOGENIK SYOK SEPTIK SYOK OBSTRUKTIF
PENGANGKUTAN OKSIGEN
Cardiac Out Put Blood flow
OxygenDelivery
Blood O2 Content
Hb Contentration
O2 Bound to Hb
O2 Dissolved in Plasma
STADIUM SYOKFASE I : KOMPENSASI
• Mekanisme Kompensasi Tubuh refleksi simpatis
- Resistensi sistemik - Tekanan darah ( N )
- Tekanan Diastolik - Tekanan Nadi Sempit
FASE II : DEKOMPENSASI
- 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 : LANJUTAN
Aliran darah lambat
Agregasi TrombositPembentukan Trombus
PendarahanPelepasan Mediator
Vasodilatasi Arterial
Kenaikan Permeabilitas Kapiler
VR
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 PATOFISIOLOGIS DARI SYOK
Septic Shock
Cardiogenic ShockHypovolemic
ShockCapilary Leak
Mediators
Myocardial Depression
Preload Vasodilatation
Contractility
Cardiac Output Blood Pressure
Sympathetic Discharge
Vasoconstriction,
HR Contractility
Improved Cardiac output and blood pressure
COMPENSATED
UNCOMPENSATED
Myocardial perfusion Myocardial O2
Consumption
Cardiac Output
Mediator Release
Cell Function
Cell Death Death of Organism
Tissue Ischemia
Loss of Autoregulation
of Mycrocirculation
COMPENSATED
Vasoconstriction HR Contractility
DIAGNOSIS SYOK
1. Riwayat Penyakit2. Pemeriksaan Klinis
a. Status KV- Freq. Jantung - Kualitas Nadi- Perfusi Kulit- Tekanan Darah
b. Gangguan Sirkulasi Organ Vital
- Status Mentalis / Respirasi- Produksi Urin
c. Penentuan B.B dan Estimasi kehilangan Volume Darah B.B ( kg ) = 2 x ( umur / th + 4 ) Estimasi Vol. Darah = 80 ml / kg B.B
I. SYOK HIPOVOLEMIK
a. Etiologi- Kehilangan Air dan Elektrolit- Kehilangan Plasma- Tindakan Bedah- Pendarahan Saluran Cerna
b. Manifestasi Klinis- Aliran Darah ke Organ Vital ( SSP, jantung, med. Adrenal )- ADH , Stim Renin – Aldosteron
Syok stadium dini ( kompensasi )
II. SYOK DISTRIBUTIF
a. Tonus Vasomotor Maldistribusi Abnormal Vol. Sirkulasi
Syok
b. Pooling Perifer HipovolemiShunting Vaskuler Relatif
( a dan b ) Hipotensi Berat
ETIOLOGI SYOK DISTRIBUTIFPenyebab Syok Distributif
Anafilakis :- Vaksin- Darah- Anestesi lokal
Neurologik :- Cedera kepala- Syok spinal
Syok Septik
Obat - obatan :- Barbiturat- Fenotiazin- Tranquilizer- Anti hipotensi
III. SYOK KARDIOGENIK
Etiologi : Pasca Bedah Penyakit Jantung Bawaan Miokarditis Infark / Iskemik Jantung Kardiomiopati Primer / Sekunder Hipoglikemia, Gangguan Metabolik Asfiksia, Sepsis
MEKANISME SYOK KARDIOGENIK
Cardiogenik 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 Jantungb. Preload dan Afterloadc. Kontraktilitas Miokard
• Kompensasi Tubuh Self Perpetuating Cycle
Syok Progresif Memburuk
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
SYOK SEPTIKPATOFISIOLOGI SYOK SEPTIK
Sumber infeksi
Organisme
Sintesa NO Sel endotel Toksin
Makrofag
TNF , IL–1, IL-2
Sel T PMN
TH 1
INF
TNF
IL - 2
TH 2
IL – 4
IL – 5
IL - 10
PAF Metab. Asam arakidonat
Kebocoran kapiler
Depresi miokard
SVR
SYOK SEPTIK
SEPSIS 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 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
Microvascular thrombosis
Bleeding ( severe )
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)
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
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 SYOK AKSES VENA ( 6 - 7 menit ) KRISTALOID dan atau KOLOID
10 – 30 ml / kg B.B ( < 20 menit )
diulang 2 – 3 kali SYOK SEPTIK 60 – 120 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
( SYOK KARDIOGENIK ) : Fluid Chalenge hati – hati :
a. memperbaiki kontraktilitas jantungb. dipantau ketat dengan TVS
Algoritme Terapi Cairan Pada Syok
Suspected shock
Hypovolemia, Hypoperfusion, Tachycardia
10 – 30 mL X.tal / kg / 6 – 10 min
Normotensive
Hypotensive
In Sepsis :
Antibiotics, Imunotheraphy
In Anaphylaksis :
Catekolamin, steroid, antihistamin
Urine > 1 ml/kg/hr
10-20 mL X.tal/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
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) -
Commonly Used Cardiovascular Drugs in Shock Syndromes
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 exxesive, 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
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
TERAPI ANTIINFLAMASI PADA SYOK
1. KORTIKOSTEROIDPada syok septik, bila ada INSUFISIENSI ADRENAL : Hydrocortisone 12,5 mg/m2/hari (dosis fisiologis) atau 50 – 100 mg/m2/hari (dosis untuk stress).
2. CHLOROQUIN dan METACLOFORAMIDEMerubah respons inflamasi pada syok septik.
MONITORING
• 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 A 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
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
Trombositopeni berat < 30.000 dengan pendarahan : - 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 dan mengurangi respons inflamasi sistemik (SIRS)
FUNGSI 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)
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- Doparmin dosis rendah (0,5 – 4 g/kg B.B/menit)
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 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