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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
. . .