SYOK HIPOVOLEMIK PADA

TRAUMA
APAKAH ADA PERKEMBANGAN
BARU?
Warko Karnadihardja
05-09

PENDAHULUAN-1
Trauma adalah penyebab kematian nomor
satu di Amerika Serikat untuk golongan
usia 1-44 tahun
Selama periode tahun 1999 s/d 2003,
tercatat sebagai penyebab utama
kematian untuk usia < 65 tahun , melebihi
kematian akibat kanker dan penyakit
jantung
Pada traum berat timbul iskemia diseluruh
tubuh yang setelah resusitasi akan terjadi
cedera reperfusi, berupa reaksi inflamasi
yang berlebihan diluar kendali badan

Acute Care Surgeon = Total Care

( Acute Care + Traumatology + Intensive Care)

Three peaks of trauma related deaths

DEATHS

First peak
Laceration of brain
brainstem
aorta
spinal cord
heart

Second peak
Extradural
Subdural
Hemopneumothorax
Pelvic fractures
Long bone fractures
Abdominal injuries

ks
e
e
2w

1 hour

3 hours

Third peak
Sepsis
Multi organ failure
Secondary Brain Injury

ks
e
e
4w

PENDAHULUAN-2
Penyebab kematian yang segera
(early death) pada trauma, biasanya
diakibatkan syok hipovolemik atau
cedera otak berat.
Cedera otak bisa juga sebagai
penyebab kematian pada masa awal
setelah trauma, yaitu akibat cedera
otak sekunder yang disebabkan
perfusi serebral yang berkurang pada
syok hipovolemik yang dibiarkan.

PENDAHULUAN-3

Kematian yang terjadi

lambat setelah kejadian
trauma, yaitu setelah pasien
dirawat disebabkan oleh
infeksi nosokomial, dan
sepsis yang berujung pada
terjadinya MOF dan kematian

Massive dyshomeostasis induced by major trauma

Major Trauma

Hemorrhage

Central asphyxia

Low flow conditions

Airway obstruction

Debris
Bacterial/endotoxin
translocation

Severe chest injury

Immuno-inflammatory
response
dyshomeostasis

Inflammation

Sequential events

Bacterial invasion
Counter Inflammation
Immuno depression

SEPSIS

Faist E, Angele M & Wichmann M, Trauma 5th edit.

SYOK AKIBAT TRAUMA

Beberapa ahli berpendapat bahwa syok
akibat trauma berbeda dari syok lain, lebih
mempunyai sifat klinik tersendiri
Peitzman AB et al : Curr Probl Surg, 1995, 32 (11): 925-1002

Bersifat kompleks akibat perdarahan,

iskemi, reperfusi, crush injury, traumatic
shock atau kombinasi
Roumen RM et al : Ann Surg 1993, 218 (6): 769-776

Maka terapinya komprehensif : stop

perdarahan, koreksi volume, kontaminasi,
jaringan nekrotik dan fraktur tak stabil

TISSUE PERFUSION ALGORITHM IN

TRAUMA PATIENT

Harbrecht BG, Forsythe RM & Peitzman AB in

TISSUE HYPOPERFUSION
ALGORITHM IN TRAUMA PATIENT

Harbrecht BG, Forsythe RM & Peitzman AB in

APAKAH ADA PENGETAHUAN

BARU?
> 50% pasien yang meninggal
beberapa jam setelah perdarahan
masif, kebanyakan disebabkan oleh
koagulopati.
Dengan kemajuan sistem penanganan
trauma yang semakin baik di AS
selama 3 dekade ini, terbukti jelas
ada penurunan mortalitas akibat
trauma

BAGAIMANAKAH HASIL
PENERAPAN PENGETAHUAN
BARU ?
Dinegara bagian Georgia, mortalitas
akibat trauma untuk segala usia,
telah turun 29% dalam masa 20 tahun
terakhir (1981-2000)
Preventable death menurun 40%
dibanding 30 tahun yang lalu yaitu
menjadi < 5% apabila dirawat oleh
pusat trauma yang modern

Arch Surg. 2005;140:443-440

A 12-YEAR PROSPECTIVE STUDY OF

POSTINJURY MULTIPLE ORGAN FAILURE
David J. Ciesla, Ernest E. Moore, Jeffrey L Johnson, et al
Denver Health Medical Center and the University of Colorado
Health Sciences Center, Denver

Question : Has anything changed?

n : 1344 pts at risk for postinjury MOF
Conclusions:
The incidence, severity, and attendant mortality
of postinjury MOF decreased over the last 12
years despite an increased MOF risk.
Improvements in trauma and critical care and are
associated with decreased use of blood
transfusion during resuscitation

Transfusi Pasien Trauma

Trauma, Edisi VI (Felociano DV, Mattox KL, Moore, EE., tahun 2008)

Sunder-Plasman (1968)
Hb 7-15

Untuk
pasien
Kritis di ICU
Jika volume darah
normal
dan jantung sehat
Hb 7 atau 15 gm/dl
akan membawa O2
ke jaringan dalam kadar
yang sama banyak

BAGAIMANA CARA MENCEGAH

KEMATIAN AKIBAT SYOK
HIPOVOLEMIK ?
1. Mencegah kematian awal dengan
terfokus pada resusitasi untuk
hipovolemia
2. Mengurangi cedera otak sekunder
3. Mencegah kematian yang terjadi
kemudian setelah penanganan trauma
dengan melakukan usaha
imunomodulasi reaksi inflamasi

APAKAH SYOK ITU?

Keadaan perfusi jaringan yang berkurang
sehingga penyampaian oksigen kedalam
jaringan dan sel tidak mencukupi untuk
kebutuhan mempertahankan
metabolisme aerobik yang normal
Dapat juga diartikan sebagai
penyampaian oksigen dan nutriens ke
jaringan dan sel tidak cukup sehingga
jaringan dan sel tidak dapat berfungsi
normal.
Harbrecht BG et al, in Trauma 6th edit. Feliciano, Mattox,
Moore 2008

APAKAH YANG TERJADI

PADA SYOK HIPOVOLEMIK ?
Volume preload yang berkurang
mengakibatkan kinerja ventrikel
suboptimal
Volume intravaskular yang berkurang
juga akan menurunkan transport oksigen,
energi dan nutriens ke berbagai organ.
Volume intra vaskular yang berkurang
tersebut dapat disebabkan kehilangan
darah, permeabilitas yang meningkat
atau kehilangan kapasitans sistem vena

APAKAH YANG TERJADI PADA

HIPOPERFUSI SELULER ?
Jaringan dan sel yang mengalami
hipoperfusi akan menderita tekor oksigen
(oxygen debt).
Tetapi sulit mengukur oxygen debt pada
pasien trauma yang sedang diresusitasi
Meskipun tidak begitu akurat, kita dapat
menilai respons terhadap resusitasi
dengan mengukur
Base deficit
Kadar laktat
Feliciano DW, Mattox KL, Moore EI in Trauma,
VIth ed 2008
Gajic O et al : Crit Care Med, 2002, 30: 11871190

LABORATORY
Complete blood, shift to the left,
leucocytosis
Poor perfusion: electrolyte abnormalities,
rising creatinine, low bicarbonate
LFT, amylase, lipase
Serum lactate is sensitive in abdominal
disease elevated in
100% mesenteric ischemia
50% of bowel obstruction
The persistent lactate elevation is more
predictive of poor outcome than a
persistent base deficit
Gajic O et al : Crit Care Med, 2002, 30: 1187-1190
Husain FA et al : Am J Surg 2003, 185, 485-491
Lange H & Jackel R : Eur J Surg 1994, 160: 381-384

The relation between mortality

and serum lactate levels

Siegel JH, Rivkind AL, Dalal S et al: Arch Surg

125:498,1990

A RODEN MODEL OF HEMORRAGIC

SHOCK

Peitzman AB, Billor TR, Harbrecht BG, Curr Prob

Surg.1995

THE RELATION BETWEEN BASE

DEFISIT (NEGATIVE BASE EXCESS)
AND MORTALITY

Siegel JH, Rivkind AL, Dalal S et al: Arch Surg

125:498,1990

Major issues in restoring &

maintaining perfusion after initial
insult
Insult

Insult

Primary
Multiple Organ
Dysfunction

Systemic
Stress
Response

Secondary
Multiple Organ
Dysfunction

What Endpoints?
What Fluids?
When Inotropes?
When Blood?
What Results?

Demling et al. Surg Clin North Am 74(3); 1994.

RESUSITASI SIRKULASI SYOK

HEMORAGIK
( C nya-ATLS)
Pra-Rumah Sakit
Kristaloid (oxidative burst on neutrophil ?)
NaCl hipertonik +/- Dextran (small volume
resuscitation)
Permissive hypotension (penetrating
trauma)
Artificial O2 carriers (clinical trial phase III)
UGD Rumah Sakit
Koloid ? Kristaloid + koloid ?
Fresh whole Blood (terbaik)
Komponen darah: PRBC, FFP, Plt,
Fibrinogen, rFVIIa, dsb.

INTRAVITAL
VIDEOMICROSCOPY 90
MINUTES AFTER RL
RESUSCITATION
The Rolling
Adherent
Leucocytes

LEUCOCYTE ADHESION WITH

DIFFERENT FLUID
RESUSCITATION

Pascual J.L etal, J Trauma 2003 ;54 :

Class IV Hemorrhage
>2000 mL BVL (>40%)
Confused, lethargic
Hypotension
Heart rate > 140 / min

Definitive
Decreased pulse pressure control, blood
components
Respirations >35 / min
Urinary output negligible
ATLS 2008

Pitfalls
Complications of Shock and Shock
Management

Pitfalls

Hypothermia
Early coagulopathy
ATLS 2008

DIINGATKAN LAGI: GOALS DARI

RESUSITASI
Tindakan segera dan komprehensif
untuk mencegah kerusakan organ
sekunder akibat hipoksia, hipotensi
dan cedera reperfusi
DO NO MORE HARM dan CEGAH
INFEKSI

BAGAIMANA CARA MEMILIH

CAIRAN UNTUK RESUSITASI ?

Efek segera terhadap hemodinamik

Efek terhadap hemostasis
Mampu membawa oksigen
Bagaimana distribusinya dan efek
terhadap kebocoran endotel
Faktor keamanan
Kemampuan modulasi reaksi inflamasi
pH buffering (tidak memperberat asidosis)
Bagaimana cara ekskresi cairan dari tubuh
Apakah mudah didapat dan cost-effective

MASALAH SIRKULASI &

KOMPLIKASI
Penyebab cedera sirkulasi
Berat dan lamanya syok
Trauma multipel atau komorbiditas
Terjadi second hit
Apakah pendekatan resusitasinya
secara:
Alamiah?
Kecepatan tindakan?
Endpoints?

CURRENT AND FUTURE

RESUSCITATION FLUIDS
1. Isotonic Crystalloids
2. Hypertonic Crystalloids
3. Artificial Colloids
4. Plasma
5. Fresh whole blood
6. Artificial blood

7.Pharmacologic Resuscitation
8.Etc

APAKAH GOAL DARI RESUSITASI

YANG HENDAK DICAPAI ?
(END POINT = HASIL AKHIR)
Parameter yang paling sering
dipergunakan adalah BASE DEFISIT
yang selalu dimonitor sewaktu pasien
di UGD, OK dan ICU
Diperoleh dari analisa gas arterial
Tetapi yang paling penting:
Segera identifikasi syok dan segera
diresusitasi untuk mencegah oxygen
debt yang besar
Stop perdarahan

HUBUNGAN ANTARA PERDARAHAN

MASIF DENGAN KEGAGALAN
METABOLIK
Pasien dengan perdarahan masif dengan
syok yang terlambat diatasi akan
menimbulkan kegagalan metabolik/trias
kematian berupa:
Hipotermi
Asidosis
Koagulopati
Pada suatu seri terdiri atas 17.000 pasien
trauma 82% kematian awal akibat trias
kematian
Hogt DB et al: J Trauma, 2004

The Lethal Triad

Severe Trauma
Prolonged
hypotension
Metabolic Acidosis

DEAT
H

Coagulopath
Hypotherm
y
ia
Rotondo MF, Zonies DH. Surg Clin North Am 1997; 77(4): 761-777

PATHOPHYSIOLOGY OF
LETHAL TRIAD OF DEATH
Coagulopathy

Acidosis
Severe trauma

Bleeding

Tissue
hypoxia
Hypothermia

Colloid and
Crystalloid infusion
Massive RBC
transfusion
Moore EE : Am J Surg 172: 405-410 1996

Dilution of
Coagulation factors
And platelets

BETULKAH KOAGULOPATI SUATU

PARADIGMA BARU DALAM TRAUMA
?
Kalau terjadi koagulopati,
apakah itu
Terjadi secara primer ?
atau
Akibat kejadian sekunder ?

THEORY OF TRAUMATIC
COAGULOPATHY
As primary event modified by
promoters

Mc Leod, JBA, Arch Surg 143, Aug.2008

THEORY OF TRAUMATIC
COAGULOPATHY
As secondary event

Mc Leod, JBA, Arch Surg 143, Aug.2008

COAGULOPATHY IN
TRAUMA vs DIC
The term DIC is incorrectly used to
define trauma related coagulopathy
Their pathophysiology is different
The use of the right terms is not only
a semantic issue but has major
implications for treatment
This was the main reason for the
delay in introduction of rFVIIa to
trauma patients

DIC
Hypercoagulable state with
loss localization of the
coagulation process
Leading to diffuse
depositisition of fibrin

COAGULOPATHY IN TRAUMA
Pathophysiology is complex and
multifactorial
Routine laboratory results resemble
those of DIC, because they detect
activation of coagulation and
fibrinolysis and consumption of
platelets and coagulation factors
Is hypocoagulable state with fibrin
deposition limited to the site of
injury

KESIMPULAN UNTUK PENCAPAIAN

AKHIR RESUSITASI
(ENDPOINTS RESUSITATION)
Tujuan akhir resusitasi syok, apapun
penyebabnya adalah
1. Mencapai kembali perfusi jaringan yang baik
2. Mencapai terselenggaranya fungsi sel yang
normal
3. Mencegah cedera organ, sehingga tidak
terjadi gagal organ
Endpoints dinilai atas dasar
Parameter sistemik atau global menurut
ATLS
Parameter yang spesifik jaringan
Parameter yang spesifik seluler

RESPONS TERHADAP RESUSITASI CAIRAN

RAPID RESPONSE

TRANSIENT
RESPONSE

NO RESPONSE

APA ITU DAMAGE CINTROL

RESUSCITATION?
TUJUAN:
Mengatasi segera koagulopati begitu pasien masuk
UGD
ALASANNYA
Pada pasien trauma berat dan perdarahan masif,
pada 30-35% kasus telah terjadi koagulopati
Koagulopati ini bisa terjadi tersendiri
Bisa juga disertai hipotermia dan asidosis atau
transfusi masif
Hess JR et al : Damage Control Resuscitation: Transfusion, 2006;46;
685-686
Mc Mullin NR et al: Hemostatic Resuscitation in YBICEM, 2006, PP
265-278

BERDASAR BUKTI BARU

Pada pasien trauma berat, telah
terjadi koagulopati sewaktu masuk
ruang emergensi
Penelitian terbaru, menyokong
pentingnya mengatasi koagulopati
secepat dan seawal mungkin
Brohi K et al.J.Trauma 2003, 54 Hirshberg A et al, J Trauma 2003,
54 Mc Leod JB et al: J Trauma 2003, 54, Faringer PD et al.J.Trauma,
1993,34

BERDASAR BUKTI BARU

Infus dengan RL dan NaCl 0,9% menimbulkan
cedera reperfusi dan adhesi lekosit pada
pasien trauma berat
Akhirnya akan memperberat asidosis dan
koagulopati yang telah terjadi
Berakhir dengan komplikasi ARDS, SIRS & MOF
Maka harus ada revisi protokol resusitasi
PHTLS dan ATLS untuk kasus trauma tertentu.
Combra R et al.J. Trauma 1997,42, Cotton BA et al Shock,
2006,26,Rhee P et al: Crit Care Med 2000,28, Ayuste E L et al J
Trauma 2006,60 Rhee P et al: J. Trauma 2003.54 (Suppl)

BAGAIMANA PROTOKOL
RESUSITASI ATLS ?
LK 90% kasus trauma sehari-hari masih dapat
diatasi secara protokol ATLS, karena termasuk
syok yang rapid response atau transient
response.
Setelah resusitasi dengan RL + PRBC dan
ditindak lanjuti dengan terapi definitif,
umumnya cedera dapat diatasi.

Jadi ATLS masih dapat diterapkan

untuk menangani trauma seharihari

DENVER GROUPS POLICY IN THE

RESUSCITATION FOR BLEEDING PELVIC
TRAUMA

Resuscitate with 2 L crystalloid-place CVP line-MeasureBase Deficit- R/O Thoracic Source (Portable Chest X-Ray)
If beginning to transfuse PRBCs, start thinking about
pelvic packing
Transfuse PRBC and FFP 1:1 ;1 apheresis unit PLT for each
5 U PRBC
Immediate Notification: Attending Trauma Surgeon,
Attending Orthopaedic Surgeon, Blood Bank Resident, IR
Fellow
Cothren EC et al, Denver Group. USA, J.Trauma 2007, vol 62 N
4: 834-842

LOS ANGELES COUNTRY MEDICAL CENTER

Rapid Uncontrolled
Hemorrhagic Shock

HEMORRHAGE CONTROL
(surgical/endovascular)
Send type and crossmatch,
aPTT, INR and platelet count
Autotransfusion of shed
pleural blood
Hypotermia control
(Warm fluids & vent gases,
remove wet clothing, dry
patient, Bair Hugger, etc)

1. Start with 0 negative PRBC

Opening ER or OR fridge containing 8 units
of O negative blood automatically phones
blood bank to notify them of units taken
2. Switch to type specific or crossmatched blood as
soon as it is available

LAC-USC Trauma transfusion protocol. aPTT, activated partial thromboplastin time, FFP, fresh
frozen plasma, INR, International normalized ratio. PRBC, packed red blood cells

LOS ANGELES COUNTRY MEDICAL

CENTER
COMPONENT THERAPY TRIGGERS

EMPIRIC
1. >6 units of PRBC
2. History of coumadin

Request trauma cooler

6 units type specific FFP
(pre-thawed)
1 unit ABO/Rh matched
apheresis platelets

TARGETED
ABNORMAL:
aPTT/INR
Platelet < 50x103
Fibrinogen < 100

Request trauma cooler

6 units type specific FFP
(pre-thawed)
1 unit ABO/Rh matched
apheresis platelets
cryoprecitate

Alam H.B, P Rhee, Surg. Clin N Am, 2007

DIFFUSE
NONSURGICAL
BLEEDING

Recombinant factor VIIa

100 mcg/kg
Additional doses as require
(best if pH > 7.1 and T > 35

FLOW DIAGRAM OF MASSIVE TRANSFUSION/FRESH WHOLE BLOOD

TRANSFUSION PROTOCOL EMPLOYED
BY THE 31st COMBAT SUPPORT HOSPITAL IN BAGHDAD, IRAQ

Surgeon
Initial labs
Type & cross

Nursing supervisor

Immediately gets 4 donors

from holding area or from
CSH to prime pump
Notify
Command/ DCCS

Whole
blood drive
Walking Blood Bank

Time=0

Blood bank
Suspend
routne duties
Get help

4 Prbc
4 FFP

from phone list ~8 at a

Time

60 min

Any gaps in donors

donors

4 fresh whole
blood

4 fresh whole
blood
Provide extra runners
Provide extra nursing
For blood drawing or
screening
Repine TB, Perkins J, Kauvar D, Blackborne L, J Trauma,
2006

Massive
Transfusion pack
4 pRBC
4 FFP
10 cryoppt

30 min

Additional donors called

filled with additional

Emergency
Release pRBCs

90 min

120
min

4 pRBC
4 FFP
16pk platelets
(when available)

4 pRBC
4 FFP

Protocol terminated when no longer needed

INFORMATION OF Abbrv

PRBC
= Packed Red Blood Cells
FWB
= Fresh Whole Blood
FFP
= Fresh Frozen Plasma
Cryoppt
= Cryoprecipitate
CSH
= Combat Support Hospital
DCCS = Deputy Commander for
Clinical
Services

TRIAD
OF
DEAT
H

Moore EE Am J Surg,
1996, 172;405

IMPLEMENTING DCR IN VASCULAR

TRAUMA
Transfusions were started early,
warmed and infused rapidly
PRBC : FFP/thawed AB plasma = 1 : 1
to avoid dilutional coagulopathy
3 vials of rVIIIa ( 90-120g/kg or 2,4
mg x 3) was typically given in the ED,
OR and ICU
The goal was a normal INR in the OR

Aggressive DCR maneuvers for

successful limb salvage in combat
casualties with vascular trauma

THE PROTOCOL OF DCR

INITIAL ASSESSMENT AND
MANAGEMENT OF COMBAT
WOUNDED
First evaluated in a treatment resuscitation area
DCR was initiated in ED based on initial lab
studies and presentions vital signs and
continued intra operatively
Blood products were transfused within minutes
of arrival with an emerging release of 4 u PRBC,
2u thawed AB plasma
A massive transfusion protocol consisting
standardized release and transfusion of PRBCs
or fresh WB, thawed AB plasma, cryoprecipitate
and platelets for pts in-extremis

DCR + DC + RECONSTRUCTION
+ AMPUTATION

DCS & DCR

DCS: Is based on avoiding the lethal triad of
hypothermia, coagulopathy and progressive
acidosis in severely injured pts
(Stone, Strom and Feliciano the pioneer)
(Referensi) Cosgrift N, Moore EE, Sa uaia A et al. J. Trauma, 1997,
42: 857-861

DCR: Treats immediately the coagulopathy &

lethal triad of death as the patient was first
admitted
The essense of damage control is to achieve
an conclude an operative procedure before the
physiologic point of no return is reached

CONCLUSION
The presenting in severe trauma
physiologic condition that has
classically led us to perform DCS
may no longer be a
contraindication to complex and
prolonged extremity vascular
reconstruction when DCR
principles are employed

THE GOAL
The primary aim of this
study was to assess the
ability to use aggressive
DCR to enhance limb
salvage

THE PROTOCOL OF DCR

INITIAL ASSESSMENT AND
MANAGEMENT OF COMBAT
WOUNDED
First evaluated in a treatment resuscitation area
DCR was initiated in ED based on initial lab
studies and presentions vital signs and
continued intra operatively
Blood products were transfused within minutes
of arrival with an emerging release of 4 u PRBC,
2u thawed AB plasma
A massive transfusion protocol consisting
standardized release and transfusion of PRBCs
or fresh WB, thawed AB plasma, cryoprecipitate
and platelets for pts in-extremis

DCS & DCR

DCS: Is based on avoiding the lethal triad of
hypothermia, coagulopathy and progressive
acidosis in severely injured pts
(Stone, Strom and Feliciano the pioneer)
(Referensi) Cosgrift N, Moore EE, Sa uaia A et al. J. Trauma, 1997,
42: 857-861

DCR: Treats immediately the coagulopathy &

lethal triad of death as the patient was first
admitted
The essense of damage control is to achieve
an conclude an operative procedure before the
physiologic point of no return is reached

CONCLUSION
The presenting in severe trauma
physiologic condition that has
classically led us to perform DCS
may no longer be a
contraindication to complex and
prolonged extremity vascular
reconstruction when DCR
principles are employed

TAKE HOME MESSAGE

PESAN APA YANG BISA DIBAWA
PULANG?
PROTOKOL ATLS
Tetap berlaku untuk mengatasi sebagian
besar syok hipovolemik yang terjadi
sehari-hari
Pada syok hipovolemik berat yang no
response, maksimum infus RL adalah 2
liter, kemudian PRBC

(Sesuai ATLS 2004)

FOREWORD
EICBT : Educational Initiative on Critical
Bleeding in Trauma
Was formed in late 2006
To increase awareness among health
care professionals that coagulopathy
may play important role during the first
hour after traumatic injury
EICBT faculty :
Is an independent, international and
interdisciplinary panel of experts in
the fields of trauma management

DIAGRAM OF COAGULOPATHY IN
THE INJURED

ACoTS : Acute Coagulopathy of Trauma-Shock Hess JR et al, J

Trauma; 65 : 748-754

CONCLUSION
AWARENESS
25% to 30% of severely injured pts are
coagulopathic upon arrival in the ER
More than 50% of respondents are not aware
that early post traumatic coagulopathy is
present in their pts, diagnosis and treatment
is likely to begin too late
Damage control strategy must be
implemented to prevent post traumatic
coagulopathy, and treatment must begin as
early as possible, preventing secondary injury

TAKE HOME MESSAGE

PESAN APA YANG BISA DIBAWA
PULANG?
Damage Control Resuscitation
Trauma berat dan perdarahan masif (2-3%
trauma sipil, 7-10% trauma peperangan)
umumnya telah terjadi koagulopati sewaktu
masuk ruang emergensi RS
tidak boleh siberi kristaloid/koloid akan
memperburuk gangguan fisiologi
Sedang dikembangkan protokol yang akan
disetujui FDA, yang sekarang berlaku adalah
konsensus para ahli di lapangan
Endpoints DCR : Koreksi maksimal fisiologi dan
anatomi

TAKE HOME MASSAGE-2

The ultimate goal in the treatment of
shock from any etiology is to
Restore tissue perfusion
Re-establish normal cellular function,
and
Prevent damage to end-organs
Endpoint can be divided into
Systemic or global parameters (ATLS)
Tissue specific parameters
Celluler parameters

TAKE HOME MASSAGE-3

RESUSITASI KRISTALLOID
Pada kasus trauma dengan perdarahan masif,
infus awal dengan pemberian kristaloid + koloid
hanya boleh maksimal 2 liter saja
Bila setelah itu hemodinamik tetap tidak stabil,
maka infus selanjutnya adalah transfusi dengan
PRBC
Infus RL maupun NaCL 0,9% pada perdarahan
masif, merugikan karena merangsang reaksi
inflamasi, adhesi neutropil, kebocoran endotel,
bersifat immunosupren dan akhirnya terjadi ACS
sekunder, ARDS, MODS dan kematian (contoh
DA Nang Lung pada perang Vietnam)

TERIMA KASIH