management of polytrauma patientbhaaas.org/attachments/328_management-of-polytrauma-patient.pdf ·...
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Management of polytrauma patient
Jelena Veličkovid Vesna Bumbaširevid Clinical center of Serbia Belgrade
7th BHAAAS ICU Symposium Brčko 2015
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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.
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More facts...
Poorer people are more at risk of a trauma
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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.....
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• 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?
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Trauma topics
Trauma Definition
Scoring
Inflammation
Coagulation Transfusion
Damage control
Transport
Organization
Clinical practice?
Missed injuries
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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
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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
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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
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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
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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
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Inflammation
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Host defense response during polytrauma
Keel M, Trentz O. Injury 2005
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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
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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
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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.
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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
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Classification of hypovolemic shock
ATLS textbook.2012
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Complex ethiology-think about it!
Don’t forget: iatrogenic causes,commorbidities, drugs...
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What really matters
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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)
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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
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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
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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
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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
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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
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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
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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
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Additional contributing factors
Hypocalcemia:
ionized Ca <1mmol/L
Anemia:
Hb < 100g/L
Preexisting coagulation disorders
Drug effects
Rassain R. Crit Care 2010.
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ACIDOSIS from hypoperfusion
HYPOTHERMIA heat loss from environment and surgical exposure
COAGULOPATHY
Surgical control of bleeding is unlikely to be successful!
LETHAL TRIAD
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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
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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
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Permissive hypotension What is the evidence?
• Prospective, pseudorandomised study
• 598 patients with penetrating torso injury and SBP<90mmHg
• Immediate vs.delayed (until surgery) resuscitation
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• 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.
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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
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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
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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.
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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!
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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.
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Modified ratio of blood products
Lower PRBC:FFP ratio – less TIC –better outcome
Maegale. World J Emerg Med 2010.
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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
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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.
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Dilution and storage loss
Dutton RP. British Journal of Anaesthesia 2012
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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
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Only combined high/dose FFP, cryoprecipitate and platelet therapy with high total fibrinogen load appeared to produce a consistent improvement in coagulation.
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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
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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
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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
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Damage control surgery: stop the bleeding
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Damage control surgery: stop the contamination
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Damage control surgery: minimal stabilisation of fractures
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Angioembolisation
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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
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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.
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Time matters...
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Trimodal distribution of deaths in trauma
Trunkey. Sci Am 1983.
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Trunkey. Sci Am 1983.
Distribution of deaths changes toward a bimodal distribution – elimination of late peak
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Conclusions
Trauma patients should be managed in centers that treat a high volume of patients (trauma centers)
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Conclusions
Management should be pathophysiology based
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Conclusions
Trauma team plays a key role. There is no “I” in trauma management
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Conclusions
There is still a lot of space for establishment of optimal therapeutic approaches with clear objectives
Thank you
. . .