Management of polytrauma patient

Jelena Veličkovid Vesna Bumbaširevid Clinical center of Serbia Belgrade

7th BHAAAS ICU Symposium Brčko 2015

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

Trauma Definition

Scoring

Inflammation

Coagulation Transfusion

Damage control

Transport

Organization

Clinical practice?

Missed injuries

Definition of polytrauma The need for international consensus

1665 publications (1950-2008)

47 attempted to define polytrauma

8 groups of definitions:

Number of injuries, body regions or organ systems involved

Mechanism of injury

Consequent disability

Injuries representing threat to life

Injury severity score (ISS)

Combination of 4 and 5

Criterion based

Combination of ISS, and systemic, immune based features

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)?

CLASSIFICATION Anatomic profile of injury Physiolocic response of trauma

victim Combination

• 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 • PI: Prognostic Index • GCS: Glasgow Coma Score • RTS: Revised Trauma Score • CRAMS Scale • Trauma Index • TRISS: Trauma Injury Severity Score • 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

0 No Injury

1 Minor

2 Moderate

3 Serious

4 Severe

5 Critical

6 Unsurvivable

9 Not further specified

Body regions:

Head

Face

Neck

Thorax

Abdomen & Pelvic contents

Spine

Upper extremities

Lower extremities

External, burns and other

Inflammation

Host defense response during polytrauma

Keel M, Trentz O. Injury 2005

SIRS, MOF...

Host defense response during polytrauma (two hit theory)

PRIMARY INSULT

Trauma organ injury, tissue injury, fractures

SECONDARY INSULT

Ischaemic/Reperfusion injury

Interventional load,

surgery

Hyperinflamation

Hypoinflammation

CARS

MARS

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

Cosgriff. J trauma 1997

PH<7.10 (OR=12.3) T<34°C (OR=8.7) ISS>25 (OR=7.7) SBP<70 (OR=5.8)

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 RESPONSE

SECONDARY EVENTS

Trauma Shock

Hemodilution

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

HYPERFIBRINOLYSIS

Tissue trauma

Shock with hypoperfusion

HYPOFIBRINOGENEMIA

FIBRIN POLYMERISATION DEFECTS

TIC initiation

TIC features early in postinjury phase: • systemic anticoagulation • hyperfibrinolysis

Dilution, acidemia and consumption of coagulation proteins: not significant factors at early stage

Thrombomodulin

APC

VIIIa Va

PC

EPCR

TISSUE INJURY - HYPOPERFUSION

D dimer

Fibrin

t-PA release

PAI-1

inhibition

Primary

hyperfibrinolysis

Coagulopathy

Activated protein C pathway

low

TAFI

Thorsen.Br J Surg 2011, Brohi K. J Trauma 2008 Vučelić D. Bilt Transfuziol 2012

DEVELOPEMENT OF TRAUMATIC COAGULOPATHY

Tissue trauma + coagulopathy

Tissue trauma + hyperfibrinolysis/hypofibrinogenemia

INJURY WITH MULTIFOCAL BLEEDING BLOOD LOSS

Haemorrhagic

shock

• Haemodilution

• Resuscitation with

non-clotting fluids

Depletion

of clotting factors –

fibrinogen and

platelets

Diad of malfunction:

• hypothermia

• acidosis

Hyperfibrinolysis

EARLY EVENT

LATE EVENT

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.

ACIDOSIS from hypoperfusion

HYPOTHERMIA heat loss from environment and surgical exposure

COAGULOPATHY

Surgical control of bleeding is unlikely to be successful!

LETHAL TRIAD

Damage control resuscitation

• A systematic approach to exsanguinating trauma

• Strategies that target conditions that exacerbate haemorrhage in trauma patients

Damage control resuscitation

Permissive hypotension

Damage control 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

PLASMA

PLATELETS

1 1 1

Miller T. Perioperative Medicine 2013. Spinella PhC, Holcomb. Blood Reviews 2009.

Hematocrit ~ 30%

Coagulation factor activity > 30%

Platelet count > 80000

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

• 70-90g/l

• > 100g/l brain injury

PLATELETS

• > 50x109 /l

• > 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.

Trunkey. Sci Am 1983.

Distribution of deaths changes toward a bimodal distribution – elimination of late peak

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

. . .