SHOCK ASSESSMENT AND MANAGEMENT

IN TRAUMA PATIENTS

dr. Prabowo Wicaksono Y.P., SpAn KMN., M. Biomed

A. BASIC SHOCK ASSESSMENT AND MANAGEMENT IN TRAUMA
PATIENT
1. DEFINITION OF SHOCK
Kegagalan sirkulasi akut: perfusi organ dan oksigenasi jaringan tidak adekuat:
disfungsi end organ.
Pengelolaan syok pada pasien trauma:
FIRST STEP:
RECOGNITION OF ITS PRESENCE !!!
Gejala dan tanda perfusi organ dan oksigenasi tidak adekuat

SECOND STEP:
IDENTIFY PROBABLE CAUSE
Pada kasus trauma: MECHANISM OF INJURY
90% syok in trauma: Hipovolemik syok karena perdarahan (hemoragik syok)
2. PRINCIPLES OF OXYGEN DELIVERY
Syok: penurunan pengiriman darah teroksigenasi ke jaringan (hipoperfusi)

RUMUS 1. PENGIRIMAN OKSIGEN KE JARINGAN TIAP MENIT (DO2) =

Jumlah oksigen dalam darah x Curah Jantung (CO)

Jumlah oksigen dalam darah =

[(Kapasitas pengikatan oksigen Hb x Konsentrasi Hb x Saturasi oksigen arteri) + jumlah
oksigen terlarut)] =
[[1,39 x Hb x SaO2) + (0.003x PaO2)] x CO
RUMUS 2. PENGARUH CURAH JANTUNG PADA TEKANAN DARAH
MAP = CO X SVR (systemic vascular resistance)
Penurunan MAP dibawah nilai kritis : penurunan CO; penurunan DO 2
RUMUS 3. CURAH JANTUNG
CO = SV X HR
SV: dipengaruhi oleh PRELOAD, AFTERLOAD dan KONTRAKTILITAS

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PRELOAD: STRECTH
Derajat peregangan serat otot miokard pada akhir fase diastolik.
Ditentukan oleh volume darah vena kembali ke jantung
Sistem vena : reservoir: 70% total volume darah

KONTRAKTILITAS
Kontraktilitas meningkat, CO meningkat.
Hukum Frank Starling: kekuatan kontraksi tergantung pada panjang serabut
miokard saat teregang

AFTERLOAD: SQUEZEE
Jumlah tekanan yang harus dilampaui jantung kiri untuk memompa darah ke
sirkulasi. Ditentukan oleh tekanan darah arteri dan tonus vaskular
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 KONSEP DASAR RESUSITASI CAIRAN :
PRELOAD mempengaruhi SV
SV mempengaruhi CO
CO mempengaruhi DO2

Perubahan PRELOAD, SV, SVR, CO : gangguan perfusi organ dan jaringan:

Metabolisme aerob  anaerob
Metabolisme anaerob : piruvat  laktat
Laktat : marker hipoksia jaringan dan beratnya shock
Kadar laktat ≥ 2 mmol/L: dihubungkan dengan peningkatan mortalitas
3. CLINICAL DIFFERENTIATION OF SHOCK AETIOLOGY
Klasifikasi: hemoragik dan non hemoragik
1. HAEMORRHAGIC SHOCK
THE MOST COMMON CAUSE OF SHOCK AFTER INJURY
Hampir semua pasien dengan multipel trauma akan menderita derajat tertentu
hipovolemia
If sign of shock are present, treatment should usually be initiated as if the
patient is hypovolaemic.
Once treatment is initiative other aetiologies should be identified and treated
accordingly
2. NON-HAEMORRHAGIC SHOCK
• Cardiogenic shock
• Tension Penumothorax
• Neurogenic shock
• Septic shock
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4. PATOPHYSIOLOGY OF BLOOD LOSS
• Respon awal: kompensasi : vasokonstriksi progresif kulit, otot dan visceral
• Tujuan: alihkan aliran darah ke ginjal, jantung, otak
• Berkurangnya volume sirkulasi akut + cedera: TAKIKARDI

Tachycardia is usually the EARLIEST measurable circulatory sign of shock

• Mekanisme kompensasi: terbatas
• Cara paling efektif: volume repletion with isotonic electrolyte solutions in sufficient
quantities
• Initial management goal:
PROVIDING ADEQUATE OXYGENATION,
VENTILATION AND APPROPIATE
FLUID RESUSCITATION
5. INITIAL ASSESSMENT OF SHOCKED PATIENT
RECOGNITION OF SHOCKED
Pastikan airway dan breathing clear
Penilaian sirkulasi: identifikasi awal manifestasi syok: takikardi dan vasokonstriksi kulit

SYSTOLIC BLOOD PRESSURE SHOULD NOT BE USED AS SOLE INDICATOR OF SHOCK

DANGER OF DELAYED SHOCK RECOGNITION

Mekanisme kompensasi: TDS bisa normal sampai perdarahan 30% estimated blood
volume (EBV)
PERHATIKAN GEJALA DAN TANDA DINI SYOK:
• TAKIKARDI
• VASOKONSTRIKSI KULIT (LEMBAB, DINGIN, PUCAT)
• LAJU NAFAS MENINGKAT
• TEKANAN NADI (PULSE PRESSURE/ TDS-TDD) MENYEMPIT
 ANY PATIENT WHO IS COOL AND TACHYCARDIC IS IN SHOCK UNTIL PROVEN
OHTERWISE
Tachycardia by age:
Infants >160
Preschool >140
School to puberty >120
Adult >100

BEWARE IN ELDERLY PATIENT !!

Bisa tidak terjadi takikardi:
• respon jantung terhadap katekolamin menurun
• obat beta blocker
• pace maker
6. INITIAL MANAGEMENT OF HAEMORRHAGIC SHOCK
Diagnosis dan pengelolaan harus dilakukan simultan:
THE BASIC PRINCIPLE IS STOP THE BLEEDING AND REPLACE THE VOLUME LOSS
A. PHYSICAL EXAMINATION
Immediately diagnosing life-threatening injuries
Airway and breathing: Priority
Circulation:
• haemorrhage control : direct pressure to bleeding site
• assessment of perfusion
• may require operative intervention to control internal bleeding
• Disability: neurologic exam: GCS, pupil: light reflect, pupil size
• Exposure: complete exam, prevent hypothermia
• Gastric dilation: decompression with NG tube
• Urinary catheter insertion: renal function and haematuria
B. VASCULAR ACCESS LINES
• Must be gained promptly
• With two 16 G (minimum) peripheral IV cannulae (short large cannulae)
• Withdrawn blood: for type, cross match, full blood count
C. INITIAL FLUID THERAPY
• Isotonic crystalloid solutions for initial resuscitation
• Initial fluid bolus is given as rapidly as possible
• Dose: 1-2 L (adult), 20 ml/kg (paediatric)
• “3 for 1 rule” : 3L of crystalloid fluid needed to replace each litre of blood lost
• Warming fluids –Plasma and Crystaloid
• Almost all trauma patient suffered from some degree of hypothermia
• Warming crystalloid fluid to 39 C
• Evaluate patient respons:

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Evidence of adequate end organ perfusion and oxygenation:
• Urine output: adequate renal perfusion
• 0.5 ml/kg/hour (adult)
• 1 ml/kg/hour (paediatric)
• Level of consciousness
• Pulse rate
• Pulse pressure
• Blood pressure
Patient’s response to initial fluid therapy is the key to determining subsequent
therapy
7. BLOOD REPLACEMENT
A. PRC VS WB
• Either may be used in trauma patient
• Component therapy is usually used; maximise blood product available
• Purpose: to restore the O2 carrying capacity on the intravascular volume
• Crystalloid can be used for volume replacement itself

B. Crossmatched, Type-specific and Type O Blood

• Full crossmatched:
• Preferable.
• Availability: 1 hour
• For patient who stabilise rapidly (fast responder)
C. Type specific blood:
• Availability: 10 minutes,
• ABO and RH compatible
• For patient with transient response

D. O-neg blood
• Uses in exsanguinating haemorrhage
• Can not wait for type specific blood
• In multiple casualties; no risk of accidental wrong patient administration
B. RECENT DEVELOPMENT IN RESUSCITATIVE STRATEGIES FOR TRAUMATIC
HEMORRHAGIC SHOCK
• Perdarahan : masih merupakan penyebab utama kematian pada trauma
• Selama perdarahan belum dapat dikontrol, tujuan pengelolaan adalah:
Pertahankan oxygen delivery untuk membatasi hipoksia jaringan, inflamasi dan
disfungsi organ
1. CYRSTALLOIDS VS COLLOIDS
Berdasar EBM (Evidance Based Medicine):
Belum terbukti jenis cairan yang superior pada trauma
KOLOID:
Ekspansi plasma cepat dan persisten: peningkatan tekanan onkotik lebih cepat
Tujuan sirkulasi tercapai lebih cepat
KRISTALOID:
Lebih murah.
Resusitasi kristaloid jumlah besar: udem jaringan, asidosis hiperkloremik
Penelitian: meta analisis atau systematic review ??
Tidak terdapat bukti dari RCT’s bahwa resusitasi dengan koloid mengurangi resiko
kematian dibandingkan kristaloid
In light of shared pathophysiological pathway with inflammation activation between
sepsis and trauma, the use of HES raises serious concerns with respect to its safety in
trauma patient.

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Crystalloids should be applied initially to treat the bleeding trauma patient and that
the addition of coloids should be considered in hemodynamically unstable patients
Use of the new HES: should be used within the prescribed limits because of the risk of
acute kidney injury and alteration of coagulation.

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2. VASOPRESSOR AGENTS
• Resusitasi cairan: strategi pertama untuk pulihkan MAP pada syok hemoragik
• Agen vasopressor: USE WITH CAUTION !!!
• Dibutuhkan SEMENTARA untuk pertahankan tekanan arterial dan perfusi jaringan;
• Apabila terdapat hipotensi persisten, meski resusitasi cairan sedang berjalan dan
hipovolemi belum terkoreksi.
• MAP adalah penentu utama perfusi jaringan

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• DOC: Norepinefrin (NE)
• Simpatomimetik, dominan vasokonstriktif.
• α-adrenergik stimulation: arterial and vena (splanchnic); alihkan volume darah vena
ke sirkulasi sistemik.
• β-adrenergik stimulation: menurunakan resistensi vena, meningkatkan venous
return.
• Rekomendasi target SBP (systolic blood pressure) : 80-90 mmHg
• Resusitasi cairan tetap dilanjutkan

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3. HOW MUCH FLUID AND MAP TARGET
Mean arterial pressure (MAP): tekanan perfusi ke semua organ
MAP: target resusitasi cairan dini
Resusitasi cairan terlalu agresif: BAHAYA MENINGKATKAN PERDARAHAN
Penyebab:
• Koagulopati: dilusi faktor koagulasi dan sebabkan hipotermia
• MAP terlalu tinggi: cegah pembentukan clot
Konsep “ resusitasi hipotensif” atau “ resusitasi volume rendah”

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• Resusitasi volume minimal lebih terpilih dibanding resusitasi cairan agresif sebelum
perdarahan aktif dapat dikontrol.
• Cegah hemodilusi dengan pembatasan cairan resusitasi dan tranfusi darah
• Hanya transfusi darah dapat memperbaiki oksigenasi jaringan

CONSIDER BLOOD TRANFUSION EARLY DURING THE MANAGEMENT OF

HEMORRHAGIC SHOCK TO IMPROVE MICROVASCULAR OXYGEN DELIVERY

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Target SBP: 80-100 mmHg until major bleeding has stopped in the initial phase after
trauma for patients without brain injury.
For traumatic hemorrhagic shock associated with severe brian injury, cerebral
perfussion pressure must be maintained by increasing arterial pressure to prevent
secondary brain injury

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4. TRANSFUSION AND PREVENTION OF ACUTE COAGULOPATHY OF TRAUMA (ACoT)
• Pencegahan koagulopati akut pada trauma telah menjadi tujuan utama pengelolaan
resusitasi awal syok hemoragik
• Pada traumatik hemoragik syok: 10-34 % alami koagulopati
• Penyebab : multifaktorial

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• Hindari penundaan transfusi darah dan komponen darah
• Tranfusi dini packed red cell (PRC) dan fresh frozen plasma (FFP):
• Prioritas untuk pertahankan arterial oxygen delivery dan pulihkan koagulasi efektif
• The administration of PRC is considered indispensible when HB level is < 7 g/dl:
Recommendation from study by Transfusion Requirements in Critical Care (TRICC)
• Pada pasien cedera kepala: Hb minimal 10 gr % : improved local cerebral oxygenation.
• Transfusi FFP 10-15 ml/kg harus diberikan segera untuk kompensasi defisit faktor
koagulasi pada tranfusi dengan PRC.
• Idealnya FFP diberikan bersama PRC.
• FFP direkomendasikan pada PT atau APTT 1,5 kali normal.

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C. SUMMARY
• Shock is acute circulatory failure leading to decrease organ perfusion
Management:
• First step: RECOGNITION OF ITS PRESENCE
• Second step: IDENTIFY THE PROBABLE CAUSE
• Tachycardia is usually the earliest measurable circulatory sign of shock
• Haemorrhagic shock: most common cause of shock in trauma

• Management of haemorrhagic shock: A – B–C–D–E

• C: STOP THE BLEEDING AND REPLACE VOLUME LOSS
• Crystalloids: First choice
• Colloids: consider in hemodynamically unstable patients: Gelatin, HES ( Caution: use
within prescribed limit)
• Vasopressor: use with CAUTION to transiently sustain MAP during persisten
hypotension, despite fluid resuscitation
• DOC: Norepinephrine
• Avoid excessive fluid resuscitation: danger of coagulopahty, hypothermia.
• Target SBP: 80-100 mmHg
• With Traumatic Brain Injury (TBI), GCS ≤ 8: Target SBP ≥ 120 mmHg
• Early tranfusion with PRC and FFP is a priority to maintain arterial oxgen delivery
and restore effective coagulation

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