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damage control resuscitation
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Damage Control
Resuscitation
Dr James Wheeler
Damage Control Resuscitation
• Definition:• A systematic approach to major exsanguinating trauma
incorporating several strategies to decrease mortality and morbidity:
1. Permissive hypotension (Minimal Normotension)
2. Haemostatic resuscitation (Massive Transfusion Protocol)
3. Haemorrhage Control (Damage control surgery)
Trauma Patient Mortality
• Head injury= leading cause of death
(largely determined at the time of
Injury)
• Haemorrhagic Shock= leading preventable
cause of death in trauma
Causes of Shock in Trauma
• Hypovolaemic• Haemorrhage
• Obstructive• Tension PTX• Cardiac tamponade
• Distributive• Neurogenic / Spinal
• Cardiogenic• Direct cardiac contusion
Cause of Haemorrhagic Shock
• Direct Tissue Damage• Dysruption of blood vessels with associated blood loss enough to
cause tissue hypoperfusion
• CoagulopathyIntrinsic Factors
• Trauma Induced Coagulopathy (TIC) / Acute Coagulopathy of Trauma (ACT)• 10-40% of trauma patients• Presence associated with 4-5 x increased mortality
Extrinsic Factors
• Hypothermia• Dilution (crystalloids, blood components)• Acidosis / Tissue Hypoperfusion
Trauma Induced Coagulopathy (TIC):
• Definition:• Intrinsic dysregulation of the blood coagulation in the setting
of trauma
• Pre-requisistes:• Tissue Hypoperfusion• Physical Tissue Damage
• Factors released by the tissue and endothelium in response to injury and hypoxia cause coagulopathy by several mechanisms:• Anticoagulation
• Thrombin-thrombomodulin Protein C system dysfn
• Platelet dysfunction• Hyperfibrinolysis
Principles of DCR• Rapid Physical Control of Haemorrhage
• Provide adequate tissue oxygenation while reducing the likelihood of UNCONTROLLED HAEMORRHAGE
• Recognise patients at risk of uncontrolled haemorrhage
• Introduce practices to reduce likelihood of:• Clot rupture & Excessive blood loss
• Avoid “Excessive” intravascular pressures but maintaining adequate tissue perfusion
= PERMISSIVE HYPOTENSION /
Minimal Normotension• Coagulopathy
• Haemodilution
• Hypothermia
• Acidosis
= HAEMOSTATIC RESUS /
Massive Transfusion Protocol
Recognising patients at risk of Uncontrolled Haemorrhage
• Clinically obvious / gestalt
• Scoring Systems:• Trauma Associated Severe Haemorrhage (TASH) Score:
• SBP < 100 mmHg
• HR > 120 bpm
• HB < 70 g/l
• Positive EFAST with haemodynamic instability
• Pelvic / long bone fracture
• BE <-10 mmol/L
• INR >1.5
• Assessment of Blood Consumption (ABC) Score• SBP < 90 mmHg
• HR >120 bpm
• Penetrating Mechanism
• Positive FAST
Score 2 = 38%, 3 = 45%, 4 = 100% chance of massive transfusion
• Thromboelastography / Coagulation testing
Prehospital Goals(Where trauma centre available)
1. Control Haemorrhage
2. Rapid transport to trauma centre (definitive control)
3. Initiate resuscitation guided by:• Mental status• Peripheral pulses
• Consider delayed resuscitation (= nil resus fluids)
Studies in patients with penetrating trauma needing
thoracotomy have shown a 2.63x increased risk of death with each prehospital procedure performed
Initial Mx in Trauma Centre
• Activation of trauma team• on or prior to arrival• Gen Surg / Anaes / ICU / Ortho / Blood Bank / Radiology
• Primary survey (ABC’s)• Exclude early life threats (tamponade, tension PTX…)&
establish presence or risk of HAEMORRHAGIC SHOCK• Manage Haemorrhage (immediate & plan definitive)• Resuscitate patient (DCR)
• Usually all happen concurrently
• Secondary Survey (may not get to this)….
Haemorrhage Mx
• Localise source/s • Clinical / imaging
• Initial control / minimise bleeding • Pressure / Splinting / Traction /
Tourniquet….• DCR
• Plan for early definitive Mx of haemorrhage
DCR Evidence
• What we know!• Shock = BAD• Longer the period of Shock = Worse
• Haemorrhaging trauma patients develop coagulopathy
• What we are still trying to work out?!• How do we BEST maximise tissue perfusion without
exacerbating haemorrhage and coagulopathy
• Evidence = limited but developing• anecdotal / animal studies / human retrospective & RCT’s
The Evidence: Permissive Hypotension
• Multiple animal studies• Reliable rebleeding point in pigs at SBP 94mmHg• Hypotensive pigs aggressively resucitated (80ml/kg crystalloids)
• 3 x blood loss & greatly increased mortality compared with nil resucitation
• Review of fluid resus in animals (Mapstone) – Permissive Hypotension vs Normotension• RR death 0.37 in permissive hypotension group
• Anecdotal / Retrospective• WWI / WWII / Vietnam War
• Resuscitation in absence of bleeding control can be harmful
• Human Studies• Penetrating torso with BP<80 mmHg RCT (Houston): Delayed vs Immediate
resus• Delayed: lower mortality (30% vs 38%), less crystalloids (375ml vs 2.5L,
nil diff in MAP)• Hypotensive trauma patients RCT : SBP target 70mmHg vs 100mmHg
• No change in mortality (ie. No increased mortality)• Note no sig diff in SBP in the 2 groups
• Evidence suggests effect the same for Blunt & Penetrating
Permissive Hypotension Goals
• When to implement:• While there is, or the potential for, uncontrolled haemorrhage• Not when there is controlled haemorrhage (goal is normotension)
• How:• Titrate small bolus (250ml) fluid administration to a hypotensive
goal:• SBP of 70-90mmHg OR• normal mentation and palpable peripheral pulse (~radial
>80mmHg, ~brachial >60mmHg)• Consider fentanyl bolus to prevent hypertensive episodes
• Aim is to prevent clot dislodgement / decrease rate of blood loss in the immediate period after trauma, while maintaining “adequate” end organ perfusion
• Use in head injury is controversial• Some groups aim for normotension• Some advocate increased BP goals >100 mmHg• Some suggest nil change to other cases of haemorrhagic shock pt’s
Haemostatic ResuscitationCauses of coagulopathy in trauma
• Haemodilution:• Iatrogenic Dilutional
• excessive / any crystalloid use
• Physiologic Dilutional (extracellular fluid shifts)
• Acidosis• pH<7.1-7.2 impairs thrombin prodn
• Hypothermia • Impairs thrombin prodn & platelet fn• <33°C causes ~20%loos of coag fn
• Hypocalcaemia – citrate poisoning due to massive transfusion
• Acute Traumatic Coagulopathy (ATC)• Occurs if extensive tissue damage & hypoperfusion
• ?increased Activated Protein C• Inactivates factors Va & VIIIa• Promotes fibrinolysis• Functionally decreases thrombin
Haemostatic Resuscitation:The Evidence
• Massive transfusion protocol• Multiple studies show increased survival
• Higher crystalloid use >mortatlity• Higher ratio of FFP : RBC increased survival
• More recent wars (Afghanistan)
• Tranexamic Acid (TXA)• CRASH 2 (2010, 20000 patients, RCT)
• Antifibrinolytic• TXA increased survival, no increase in thrombotic episodes
• Recombinant Factor VIIa• Recent Cochrane review found no improvement in mortality
Haemostatic Resuscitation:Prevent / reduce coagulopathy
• Identify at risk group & act before coagulopathy develops:• Massive transfusion protocol
• Early use of blood components as the primary resuscitation fluid
• Use in the same ratio as they are lost through haemorrhage (exact ratio’s controversial)• PRBC : FFP 1:1• PRBC : Platelet (adult dose) 4:1• Fibrinogen
• Give TRANEXAMIC ACID
• Prevent hypothermia / significant acidosis
• Monitor and give maintain iCa2+
Mx of Haemorrhagic Shock - Crystalloids
• Historically resuscitation of trauma patients involved:• RAPID restoration of circulating blood volume with
CRYSTALLOID SOLUTIONS to maintain normotension / perfusion
• Advantages of crystalloids:• Cheap• Readily available / easy storage• No risk of transfusion reactions / infectious
agents / hyperkalaemia / hypocalcaemia…
• The above Mx may be appropriate / not harmful in most trauma patients
• But aggressive fluid resuscitation with crystalloids has disadvantages!
Disadvantages of Crystalloids
• Increased Haemorrhage• Coagulopathy (Haemodilution / hypothermia / acidosis)• Clot rupture with restoration of normal blood pressure
• Compartment syndromes• abdo, limbs• Larger volumes needed when compared to blood products (3:1
rule)• Lowers plasma osmotic pressures – more extravasation in
damaged areas (Hartmann’s worse than N Saline)
• Increased inflammatory repsonse• Hartmann’s
• Acidosis• N Saline • Hartmann’s in those with impaired lactate metabolism
(DKA, liver failure)
Aggressive use associated with increased mortality in haemorrhagic shock
Haemostatic Resuscitation:Blood Products
Volume (ml) Contents Grouping Storage
PRBC 200 50-70% HCT ABO & Rh 42 days
FFP 250-330 All coag factors
~1/2 unit WB
ABO 12 months
Platelets 100-400 200 x 109
Platelets / bagABO & Rh 5 days
Cryo 30-40 Firinogen / VIII / XIII / VWF
~2 x unit WB
ABO 12 months
Whole Blood 24 hours
Remember:•temperature•citrate (hypoCa2+ after 4-6U PRBC in an hour)•potassium
Haemostatic Resuscitation
Whole Blood Component Therapy(1 PRBC / 1 FFP / 1 PLAT / 1 CRYO)
RBC (HCT) 38-50% 20%
COAGS 100% 50-60%
PLATELETS 150-400 X 103 / ul 280 x 103 / ul
FIBRINOGEN 1500mg 750 - 3000mg
Volume 450ml ~700ml (more with flush)
Damage Control Resuscitation(in a patient with haemorrhagic shock that cannot be controlled in the ED)
• Permissive Hypotension• No head injury
• Goal = SBP 70-90 mmHg (MAP 50-65) OR normal mentation & peripheral pulses
• Head injury• Controversial• Some suggest permissive hypotension is
contraindicated• Goal = normotension (depends on patient)
• Others use standard permissive hypotension• Others adjust goal to SBP >100 mmHg
Damage Control Resuscitation(in a patient with haemorrhagic shock that cannot be controlled in the ED)
• Haemostatic Resuscitation• If blood available:
• Initiate massive transfusion protocol• Fixed product ratio’s• Blood / FFP / Platelets / cryoprecipitate / calcium• Monitoring of coagulation
• If blood not immediately available:• Give 250-500ml boluses of crystalloids until blood available or resus goals met
• Warm Fluids / Cover Patient• TXA
• give early (best <3/24) once risk of haemorrhagic shock determined• 1g Stat and 1g over 8/24• Relative contraindications: thrombophilic disorder
• Early definitive control of bleeding
• Consider rVIIa?• If fibrinogen and platelets in sufficient numbers
SCGH Massive transfusion protocol
Things to monitor
• Physiological parameters:• Mental status• Urine output (>0.5ml/kg/hr)• Peripheral pulses / MAP• CVP• Temp (>35C)
• Haematological parameters• Hb (>90g/l)• Platelets (>50-80 x 109)• Coag’s: INR (<1.5), Fibrinogen(>1g/l)• CV SaO2 (>70%) / lactate (<4mmol/l) / pH (>7.2)• iCa2+ (>1.1mmol/l)• K+
The Future
• CryoStat
• Consensus on blood product use:• Accurate bedside monitoring of Coagulation
parameters to guide blood product use• Thromboelastography - ROTEM
Summary
• Identify those with / at risk of haemorrhagic shock on arrival
• Fluid resuscitation individualised for each patient
• Permissive hypotension in patients without head injury
• Early use of blood products as resus fluids• Massive transfusion protocol – with fixed product ratios• Monitor coagulation
• Use TXA in all patients requiring transfusion for uncontrolled haemorrhage
• Early definitive Mx of haemorrhage
• Once haemorrhage controlled – then aim for normal CV parameters
• monitor lactate / BE
Difficulties
• Alcohol / drug affected patients
• Head injured patient
• Delayed transfer to definitive care
• Complications of massive transfusion
References
• Bickell WH, Wall MJ Jr, Pepe PE, et al.: Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994, 331:1105-1109.
• Kaweski SM, Sise MJ, Virgilio RW, et al.: The effect of prehospital fluids on survival in trauma patients. J Trauma 1990, 30:1215-1218.
• Kowalenko T, Stern SA, Dronen SC, Wang x: Improved outcome with hypotensive resuscitation of uncontrolled hemorrhagic shock in a swine model. J Trauma 1992, 33:349-353
• Alberto S. Santibanez-Gallerani, M.D., Annabel E. Barber, M.D., Shelley J. Williams, M.S., Yan Zhao, B.S., G. Tom Shires, M.D. Improved Survival with Early Fluid Resuscitation Following Hemorrhagic Shock. World J. Surg. 25, 592–597, 2001
• Pek Ghe Tan, Marion Cincotta, Ornella Clavisi, Peter Bragge, Jason Wasiak, Loyal Pattuwage and Russell L Gruen. Review article: Prehospital fluid management in traumatic brain injury. Emergency Medicine Australasia (2011) 23, 665–676
• Philip F Stahel, Wade R Smith, Ernest E Moore. Current trends in resuscitation strategy for the multiply injured patient. Injury, Int. J. Care Injured (2009) 40S4, S27–S35