7th BHAAAS ICU Symposium

Brčko 2015

Management of polytrauma patient

Jelena Veličkovid
Vesna Bumbaširevid
Clinical center of Serbia
Belgrade
 Trauma facts...

• Trauma is a disease
• Trauma is preventable,
predictable and treatable
• 5.8 million deaths each year
worldwide
• Trauma is a leading killer of
youth (5-44 years)
• 16% of disabilities caused by
trauma
• Huge economic impact
WHO report 2010.
 More facts...

Poorer people are more at risk of a trauma

Case
• Male, 37y, motorcycle accident
• Transferred to the closest (40km) level 1 trauma center
• Injuries at ED: GCS 14, rib fractures (V-VIII, left), lung
contusions, left femur and bilateral tibial fracture, soft tissue
contusions, distorted splenic shape on FAST, suspected
subcapsular hematoma on CT
• Hemodinamicaly stabile, temporary immobilized
• Transferred to the specialized orthopedic hospital in Belgrade
(80km) for definitive repair 4 hours later

• Day 2: During preparation for surgery, patient becomes

tachicardic, tachipneic, anxious, hypoxic, complains on chest
and abdominal pain.....
• Anesthesiologist refuses to anesthetize him and requests
CTPA as pulmonary embolism was suspected
• CT at the nearby hospital (1h later): Diffuse ground- glass
opacities, abdominal free fluid, signs of splenic rupture
• Transfer to the Emergency center (30 mins)
• Emergency center ED: somnolent, pale, Fr 135/min, TA 75/40,
tachypneic, hypoxic, intubated, immediately transferred to OR
• OR: Splenectomy, massive transfusion
• ICU: Severe ARDS (P/F ratio 34mmHg)
• Died on the 3rd day due to MOF

How many survival chances were missed?

 Trauma topics
Organization

Definition Trauma
Damage
control
Scoring

Inflammation
Transfusion
Coagulation Transport

Clinical Missed injuries

practice?
 Definition of polytrauma
The need for international consensus
1665 publications (1950-2008)
47 attempted to define polytrauma
8 groups of definitions:

Number of injuries, Injury severity Criterion

body regions or organ score (ISS) based
systems involved

Mechanism of Injuries representing Combination of ISS,

injury threat to life and systemic,
immune based
features

Consequent Combination
disability of 4 and 5

More than 40 definitions... Butcher,Balogh. Injury 2009

Butcher. J Trauma Acute Care Surg 2013
Until the establishment of a consensus definition...
MONOTRAUMA
 Injury to one body region
MULTITRAUMA
 Injury to more than one body region (not exeeding AIS≥3 in two regions)
without SIRS.
POLYTRAUMA
 Injury to at least two body regions with AIS≥ 3 in conjunction

with one or more of the listed physiologic parameters:

• Hypotension (SBP ≤ 90mmHg)
• Level of consciousness (GCS ≤ 8)
• Acidosis (BE≤ - 6)
• Coagulopathy (INR ≥ 1.4 or aPTT≥ 40s)
• Age (≥ 70years)
Butcher,Balogh. Eur J Trauma Emerg Surg 2014
Pape HC. Journal of Trauma and Acute Care Surgery 2014
 Trauma score systems: use(fulness)?

RATIONALE
• Classification and characterizing heterogenous trauma
patients
• Triage, resourcing
• Prognosis
• Quality care assessment
• Research
• Communication improvement

Lefering. Eur J Trauma. 2002

 Trauma score systems: use(fulness)?
• AIS: Abbreviated injury score
• ISS: Injury severity score
• AP/MAP: Anatomic profile/Maximal anatomic
profile
• NISS: New Injury Severity Score

• TS: Trauma score

• TI: Triage Index
CLASSIFICATION • PI: Prognostic Index
• GCS: Glasgow Coma Score
• RTS: Revised Trauma Score
 Anatomic profile of injury • CRAMS Scale
 Physiolocic response of trauma
• Trauma Index
victim
• TRISS: Trauma Injury Severity Score
 Combination • ASCOT: Severity Caracterisation of Trauma
• ICISS: International Classification of Disease-
based ISS
• HARM: Harborview assessment of risk of
mortality
 AIS: Abbreviated Injury Scale
Injury AIS Score Body regions:
0 No Injury Head
1 Minor Face
2 Moderate Neck
3 Serious
Thorax
Abdomen & Pelvic contents
4 Severe
Spine
5 Critical
Upper extremities
6 Unsurvivable
Lower extremities
9 Not further specified
External, burns and other
Inflammation
Host defense response during polytrauma

Keel M, Trentz O. Injury 2005

Host defense response during polytrauma
(two hit theory)
PRIMARY INSULT SECONDARY INSULT
Ischaemic/Reperfusion injury
Trauma organ injury, Interventional load,
tissue injury,
fractures surgery

Hyperinflamation

Hypoinflammation
SIRS, MOF... MARS

CARS
 Host response during polytrauma

Days 2-4: Hyperinflammatory phase (SIRS) / IL 6,8,12,18; TNFα

Days 11-21: Hypoinflammatory phase (CARS): IL 4,10,13, TGFβ
Brochner. Scand J of Trauma,
Resuscitation and Emergency Med.2009
 Days to operate

Day 1: Surgery (DCS)

Day 2-4 (Hyperinflammation): No surgery!
Day 5-10: Window of opportunity
Day 11-21 (Immunodepression): No surgery!
From week 4: Reconstructive surgery.
 Traumatic shock
• Complex ethiology
Hypovolemic – 59%
Obstructive – 16%
Distributive – 7%
Cardiogenic – 3%

In polytrauma patients shock is considered to be hypovolemic

until proven otherwise.

Kirkpatrick. Can J Surg 2010

Jain S. Medifocus 2010
Classification of hypovolemic shock

ATLS textbook.2012
Complex ethiology-think about it!

Don’t forget: iatrogenic causes,commorbidities, drugs...

What really matters
 The Lethal Triade
ISS >25 SBP <70 PH < 7.10 T < 34°C Mortality (%)

1
+ 10
+ + 39
+ + 58
+ + 49
+ + + 85
+ + + + 98

PH<7.10 (OR=12.3)
T<34°C (OR=8.7)
ISS>25 (OR=7.7)
SBP<70 (OR=5.8) Cosgriff. J trauma 1997
 Acidosis
• Poor tissue perfusion is the main contributor in trauma
patients
• Decreased cardiac output, hypoxia and anemia lead toward
cellular anaerobic metabolism and cause lactic acid
accumulation
• Resuscitation with normal saline induces hyperchloremic
acidosis
• Acidosis diminishes cardiac output leading to worse tissue
perfusion
• Aggravates coagulopathy
 PH drop from 7.4 to 7.0 reduces the effectiveness of coagulation cascade
by 50-75%
 Procoagulant drugs (rFVII) cannot work in acidotic environment
 Hypothermia
• The greatest contributor to hypothermia are environmental
temperature, cold crystalloids and PRBCs
• Tissue hypoperfusion and anaerobic metabolism exhaust ATP
which is required for maintenance of normothermia.
• Hypothermia causes coagulopathies:
 Coagulation cascade is temperature dependent
 Relative thrombocyopenia by plateled sequestration and
dysfunction
• Induces shivering with further depletion of ATP and
progression of acidosis
 Acute coagulopathy of trauma
• Present at admission in 25% of trauma patients
• 4 fold increase in mortality
PRIMARY – ENDOGENOUS
SECONDARY EVENTS
RESPONSE

Trauma Hemodilution

Shock Consumption
MacLeod JBA. Arch Surg 2008
 Synonims

• Trauma induced coagulopathy (TIC)

• Acute traumatic coagulopathy (ATC)
• Acute coagulopathy of traumatic shock (ACoTS)
• Endogenous acute coagulopathy (EAC)

MacLeod JBA. Arch Surg 2008

Hess JH.J Trauma 2008
Brohi R. J Trauma 2003
 TIC initiation

Tissue trauma
Shock with hypoperfusion

HYPOFIBRINOGENEMIA
HYPERFIBRINOLYSIS FIBRIN POLYMERISATION
DEFECTS

TIC features early in postinjury phase:

Dilution, acidemia and consumption of coagulation proteins:
not significant
• systemic factors at early stage
anticoagulation
• hyperfibrinolysis
 Activated protein C pathway
Coagulopathy

VIIIa Va Fibrin
D dimer

t-PA release

TISSUE INJURY - HYPOPERFUSION APC PAI-1

inhibition

PC
Thrombomodulin low
TAFI
EPCR
Primary
hyperfibrinolysis

Thorsen.Br J Surg 2011, Brohi K. J Trauma 2008

Vučelić D. Bilt Transfuziol 2012
DEVELOPEMENT OF TRAUMATIC COAGULOPATHY
Tissue trauma + coagulopathy
Tissue trauma + EARLY EVENT
hyperfibrinolysis/hypofibrinogenemia

Haemorrhagic
shock

Depletion
INJURY WITH of clotting factors –
MULTIFOCAL BLEEDING fibrinogen and
BLOOD LOSS platelets

Hyperfibrinolysis • Haemodilution
LATE EVENT
• Resuscitation with
Diad of malfunction: non-clotting fluids
• hypothermia
• acidosis
Kozek-Langenecher.Min Anesth 2007
Vučelić D. Bilt Transfusiol 2012
Additional contributing factors
Hypocalcemia:
ionized Ca <1mmol/L

Anemia:
Hb < 100g/L

Preexisting
coagulation
disorders

Drug effects

Rassain R. Crit Care 2010.

 LETHAL TRIAD
HYPOTHERMIA
ACIDOSIS heat loss from environment and
from hypoperfusion surgical exposure

COAGULOPATHY

Surgical control of bleeding is unlikely to be successful!

 Damage control resuscitation
• A systematic approach to exsanguinating trauma
• Strategies that target conditions that exacerbate
haemorrhage in trauma patients

Damage control
resuscitation

Permissive Damage control

hypotension surgery

Haemostatic
resuscitation
 Permissive hypotension
• Keep the blood pressure low enough to avoid
exsanguination while maintaining perfusion of end-
organs.
• Injection of a fluid will increase blood pressure:
 Clot disruption
 Hemoglobin and clot factor dilution
 Hypothermia

Trauma patients without definitive hemorrhage control

should have a limited increase in blood pressure until
definitive surgical control of bleeding can be achieved
 Permissive hypotension
What is the evidence?

• Prospective, pseudorandomised study

• 598 patients with penetrating torso injury and SBP<90mmHg
• Immediate vs.delayed (until surgery) resuscitation
• Immediate group (Ringer acetate, mean 870ml):
 ↑ SBP on arrival to ED
 ↓Hb & Hct
 ↑PT & PTT
• Rate of survival significantly higher in the delayed
resuscitation group (70 vs. 62%, p=0.04)
• No difference in complication rate
Conclusion: For hypotensive patients with penetrating
torso injuries, delay of aggresive fluid resuscitation until
operative intervention improves the outcome.
 Permissive hypotension

• Safe strategy for use in the trauma population

• Results in significant reduction in blood product transfusion
and overall fluid administration
• Decreases postoperative coagulopathy and lowers the risk of
early postoperative death
• MAP 50mmHg better than 65 mmHg

Morrison CA.J Trauma-Injury

Infection and Critical Care.2011
 Permissive hypotension

Resuscitation end points:

1. Penetrating trauma – systolic 80-90mmHg or presence of
radial pulse
2. Blunt trauma – systolic 80-90 mmHg or presence of radial
pulse
3. Head injury – MAP ≥ 80 mmHg or systolic >100mmHg

Spahn DR. Crit Care 2013.

Cooper. JAMA 2004
The Brain Trauma Foundation. J Neurotrauma 2010
 Haemostatic resuscitation
• Very early use of blood and blood products as
primary resuscitation fluid
• Treatment of trauma induced coagulopathy
• Prevention of dilutional coagulopathy

Give no fluid that can’t either carry oxygen or

promote clotting

Jansen O. BMJ 2009.

 Who needs it?
• 25% of trauma patients need transfusion
• 2-3% of civil and 7-8% of war trauma needs massive
transfusion
• Patients requiring massive transfusion (more than 10
units of PRBCs/24h) benefit the most from
haemostatic resuscitation
• Early detection of patients in need for massive
transfusion is essential!
 Prediction of massive transfusion
Simple as ABC
ABC Scoring
1. Penetrating mechanism
2. Positive FAST
3. SBP ≤ 90mmHg on arrival
4. Heart rate ≥ 120bpm on arrival

Score ≥ 2 is 75% sensitive and 86% specific for

predicting massive transfusion

Nunez TC. J Trauma 2009.

Modified ratio of blood products

Lower PRBC:FFP ratio – less TIC –better outcome

Maegale. World J Emerg Med 2010.
 RECONSTITUTED WHOLE BLOOD
RED BLOOD CELLS FRESH FROZEN PLATELETS
PLASMA
1 1 1

Hematocrit ~ 30%
Coagulation factor activity > 30%
Platelet count > 80000 Miller T. Perioperative Medicine 2013.
Spinella PhC, Holcomb. Blood Reviews 2009.
 Trauma blood packs

5 units of O Rh(D) negative/positive fresh RBC

(storage age < 14 days)
5 units of type AB Rh (D) negative/positive FFP
5 units (1 pool) of PC
Johansson PI. ISBT Science Series 2007.
Dilution and storage loss

Dutton RP. British Journal of Anaesthesia 2012

 Target values
HEMOGLOBIN PLATELETS

• 70-90g/l • > 50x109 /l

• > 100g/l brain injury • > 100x109/l

brain injury

Spahn DR et al. An updated European quideline.. Crit Care 2013

Only combined high/dose FFP, cryoprecipitate and
platelet therapy with high total fibrinogen load appeared
to produce a consistent improvement in coagulation.
 Other blood components

• Fibrinogen
• Cryoprecipitate
• PCC-Prothrombin complex concentrate
• F XIII
• F VIII, IX, vWF concentrate

Spahn DR et al. An updated European guideline. Crit Care 2013.

Nardi G et al. Critical Care 2015
 Tranexamic acid

• Randomised, placebo controlled trial

• 1g of tranexamic acid + 1g over 8h vs.placebo
• 20211 patients, 274 hospitals, 40 countries
• Primary outcome: death within 4 weeks of injury
• Improved survival by 10%
CONCLUSION: Tranexamic acid should be given as early as
possible to bleeding trauma patient.

CRASH-2 trial collaborators. Lancet 2011

 Damage control surgery
Planned temporary sacrifice of normal anatomy
to preserve vital physiology
PREDICTIVE INDICATORS FOR DCS
Major haemorrhage > 10 units
PRBCs
Severe wound contamination
An evolving lethal triade Hypothermia < 34°C
Acidosis, pH < 7.2 and base deficit ≥ 8
Coagulopathy, aPTT ≥ 60s

Shere-Wolfe R. Scand J of Trauma, Resusc and Emerg Med.2012

Damage control surgery: stop the
bleeding
Damage control surgery: stop the
contamination
Damage control surgery: minimal
stabilisation of fractures
Angioembolisation
 Golden hour

„There is a golden hour between life and

death. If you are critically injured you have
less than 60 minutes to survive. You might
not die right then; it may be three days or
two weeks later – but something has
happened in your body that is irreparable.“

R. Adams Cowley
Who coined the term and why?
The concept of “the golden hour” was a
marketing strategy by Dr. Cowley in
1963 in a letter to the Governor of
Maryland, the purpose of which was to
get ensure that police helicopters
would over-fly local hospitals and bring
severely injured pts to his Baltimore
Shock Trauma Centre.
…with no scientific evidence to support this
statement at the time!
Lockey. Resuscitation 2001.
Time matters...
Trimodal distribution of deaths in
trauma

Trunkey. Sci Am 1983.

Distribution of deaths changes toward a
bimodal distribution – elimination of late peak
Trunkey. Sci Am 1983.
 Conclusions
Trauma patients should be managed in centers that treat a
high volume of patients (trauma centers)
 Conclusions
Management should be pathophysiology based
 Conclusions
Trauma team plays a key role. There is no “I” in
trauma management
 Conclusions
There is still a lot of space for establishment of
optimal therapeutic approaches with clear
objectives

. . .

Thank you